Introduction

This "manual" is a compilation of study notes we have made over the past 5 years
based on a number of sources, including those listed here:

■ Text books
■ Review books
■ Didactic lectures and conferences
■ Primary and review articles
■ Points made by attendings and other residents on rounds or in the OR
■ UpToDate®

Disclaimer: Individual illustrations and material may belong to a third party.

Unless otherwise stated all figures and tables by Mohammed Alismail

Hopefully, these notes will provide you with some benefit as well.

I welcome all criticism and correction and look forward to supplementing and
augmenting this first edition many times over.

Mohammed Abdulraof Alismail

Assistant Consultant, General Surgery
National Guard, King Abdulaziz Hospital, Al Ahsa, Saudi Arabia
dr.moalismail@gmail.com
alismailmo@ngha.med.sa

Mohammed Abdulwahab Buhalim

Senior Registrar, General Surgery and Vascular Surgery
King Faisal University, Al Ahsa, Saudi Arabia
dr.mohammed abdulwahab@hotmail.com
 Reviewers

Dr. Abdulwahed Meshikhes

FRCSI, FAGS, Medical Director and Senior Consultant Surgeon
Al Zahra General Hospital, Qatif, Saudi Arabia
Chapter: Small bowel

Dr. Hamad Hadi AIQahtani MD, FRCS

Professor of Surgery, Consultant Hepato-Pancreato-Biliary Surgeon
Chairman department of surgery, College of Medicine, King Saud University, Saudi
Arabia
Chapter: Liver

Dr. Salman AI-Harbi

Assistant Consultant, Adult Hematology and Stem Cell transplant, King Fahad
Specialist Hospital, Dammam, Saudi Arabia
Chapter: Hematology and Blood products

Dr. Haytham Alarfaj

Assistant Professor, General Surgery, College of Medicine, King Faisal University, Al
Ahsa, Saudi Arabia
Chapter: Perioperative Care
Chapter: Fluids and Electrolytes

Dr. Mohammed Al Duhileb

MD, MRCS, SBGS, KFBES, Consultant Breast and Endocrine Surgeon, King Fahad
Specialist Hospital, Dammam, Saudi Arabia
Chapter: Nutrition
Chapter: Breast
Dr. Mamoun Nabri
Assistant Professor, Consultant General Surgery I Trauma, Head of Trauma Unit,
Department of Surgery, College of Medicine, Imam Abdulrahman bin Faisal University,
Dammam, Saudi Arabia
Chapter: Trauma

Dr. Fahied AIQahtani

Consultant Anesthesia and Pain Management, King Abdulaziz Medical City, National
Guard, Al Ahsa, Saudi Arabia
Chapter: Anesthesia

Dr. Ahmed Mosa

Assistant Professor, Vascular Surgery, College of Medicine, King Faisal University, Al
Ahsa, Saudi Arabia
Chapter: Vascular Surgery

Dr. Saeed Shomimi

Consultant Upper GI Surgery, Department of Surgery, College of Medicine, Imam
Abdulrahman bin Faisal University, Dammam, Saudi Arabia
Chapter: Stomach

Dr. Mohammed Bubshait

Assistant Professor, General Surgery, College of Medicine, King Faisal University, Al
Ahsa, Saudi Arabia
Chapter: Head and Neck

Dr. Mamdouh Abdulassib

Head of General Surgery Department, Al Osrah Intl. Hospital, Riyadh, Saudi Arabia
Chapter: Appendix
Dr. Zakir K Mohamed
MBBS, MRCSed, CCBST, MSc(Leeds), FRCSEd, FRCSEng, CCT(UK), Consultant
Colorectal and General Surgeon, Adjunct Associate Professor of Surgery, College of
Medicine, MBRU, Mediclinic Parkview Hospital, Dubai, UAE
Chapter: Large Bowel

Dr. Neamat Al Turki

MBBS, MD, SB-SURG, SB-Co/orectal Consultant
Chapter: Anorectal

Dr. Shadi AIShammary

Assistant Professor, Hepatobiliary and Liver Transplant, Department of Surgery,
College of Medicine, Imam Abdulrahman bin Faisal University, Dammam, Saudi Arabia
Chapter: Liver

Dr. Ahmed M El Damati

Consultant General Surgery, Department of Surgery, College of Medicine, Imam
Abdulrahman bin Faisal University, Dammam, Saudi Arabia
Chapter: Spleen

Dr. Ahmed Muhammed Odeh

MBChB, GBGS, MRCS (Ire/), FRCS (Eng}, Consultant General Surgery, Assistant
Professor, College of Medicine, Al Ahsa, King Faisal University, Saudi Arabia
Chapter: Hernia and Abdominal Wall

Dr. Hussah M. AI-Buainain

Assistant Professor of Surgery, Consultant Pediatric Surgeon
lmmam Abdu/rahman bin Faisal University
Chapter: Pediatric surgery

Dr. Omar Al Rasheed

Assistant Professor, Orthopedics, College of Medicine, King Faisal University, Al Ahsa,
Saudi Arabia
Chapter: Orthopedics-Trauma
 Copyright

All rights reserved. No part of this publication may be reproduced, stored in a retrieval
system, or transmitted, in any form or by any means, electronic, mechanical,
photocopying, recording, or otherwise, without the written prior permission of the
author.

All the efforts have been made to provide in this book accurate indications and dosage
for drugs. The reader has to read and review the package data of each drug provided
by the manufacturer for indications, dosage, warning and precaution

Copyright© First edition 2020

For any inquiries, please contact via email at dr.moalismail@gmail.com

This work is no substitute for individual patient assessment based on health care
professionals' examination of each patient and consideration of, among other things,
age, weight, gender, current or prior medical conditions, medication history, laboratory
data, and other factors unique to the patient.

The publisher does not provide medical advice or guidance, and this work is merely a
referenee tool.

Health care professionals, and not the publisher, are solely responsible for the use of
this work including all medical judgments and for
any resulting diagnosis and treatments

Copyright© First edition 2020

 Preface
Surgery is about knowledge and skills.

Books and literature are the main sources of knowledge.

It is not always convenient to go through a big textbook to look for a small piece of
information.

It is about time to change the way surgical books are written.

The author went through many textbooks, handbooks, and articles during medical
school and residency to come to a decision to write his own notes that are up-to-date
and concise but thorough.

This book provides medical students, surgical residents, and junior surgeons all the
important pieces of information they need for each surgical topic.

It is easy to read and memorize. It discusses in depth all aspects of

a disease in a systematic and to-the-point fashion.

It provides a quick but thorough review before any surgical examination of all
levels.
 Table of.Contents
Ctll Biology .................................. .. .....8
f-ltmatolo_gyand Blood products.. ..... 13
Immunology ...... . .. ...24
Infection ..... .....27
A1,tihiotics .. .....37
Fluids and t:ltctrolytts .....43
Nutrition ... -····················- .....63
lnflammation and Cytokinc:s ...... . .....75
\Vound Htaling... .. ...79
8Ul'll ..... . .....86
Tr auma.. .....93
Critical Care....... ... 161
Ane-sthesia ............... ... 190
Min.imal Jm,asive Surgery and Surgical Technology..... ...200
Perioptr-ative. Care .. ...208
Oncology.................. ...218
Transplant .............. . ...227
Skin and Soft tissues........ ...234
Hand and Neck... ...245
Adrtnal gland.... ................ 252
Thyl'oid......................................................................................................................................................................................... 264
Parathyroid ....................300
Brust ......... ...311
Thoracic Surgery ...358
Vascular Surgery ...378
Esophagus .. ...404
Stomach..... . ...443
Small bowel ...486
Appendix .... ...557
Large. bowel............. ... 573
Anorectal ...653
Lh•er ...... ...680
Portal Hypertension ... 718
Biliary System ......... ...730
Pancreas ... 797
Spleen .... ...850
Hernia and abdominal wall. ...867
Pediatric Sur·gery ............ ...909
£pidtiuiology and Ethics. ...931
Approach Sheet.. ............. ...939
1\lbes, Drains, and Catheters...... . ... 947
Cell Biology
CELL BIOLOGY
CELL CYCLE

Cell Cycle
(Bv order) Description
G1 Determine cell cvcle lenath, Most Variable, Growth Hormones work here
s DNA reolicationlduolication, Protein Svnthesis, RadioResistance
G2 DNA Stabilitv IReoair PhaseI
M Mitosis (Cell division), RadioSensitive

CELL PHASES
■ Prophase -+ centromere attachment, spindle formation, nucleus disappears
■ Metaphase -+ chromosome alignment
■ Anaphase -+ chromosomes pulled apart
■ Telophase -+ separate nucleus reforms around each set of chromosomes
o Centriole: a specialized microtubule involved in cell division

CELL MEMBRANE
■ Desmosomes -+
Cellular adhesion "Anchor" molecules "No communication"
■ Tight junctions -+
Impermeable barrier "No communication"
■ Gap junctions (Most common type) -+
Allow cell-cell communication (connexin subunits)

■ ABO blood-type antigens: (glycoLipids on cell membrane)

o Needed in Liver and Renal transRlanls

■ HLA-type antigens (glycoProteins on cell membrane)

NUCLEUS, TRANSCRIPTION, AND TRANSLATION

-+
■ Steroid hormone binds receptor in Cytoplasm, then enters nucleus
-+
■ Thyroid hormone binds receptor in Nucleus
CELLULAR METABOLISM
■ Glycolysis (Krebs cycle): 2 ATP and 2 pyruvate (from breakdown of 1 glucose)
C) NADH/FADH2 in mitochondria
C) 1 molecule of glucose produces 36 ATP

■ Gluconeogenesis (Cori cycle): mechanism by lactic acid

o In starvation or stress
o Liver converts muscle lactate into glucose (mediated by: pyruvate)

Glucose+ Lactate+ Pyruvate + Glucose (gluconeogenesis}

■ Lactate level
o Generated by conversion of Pyruvate + Lactate by "Lactate dehydrogenase (LOH)"
o Increased lactate level happened during anabolic metabolism
o Uptake of lactate by liver 50% and kidney 30%
• L-Lactate is the only form produced in human metabolism
• D-Lactate is produced by bacterial metabolism and found in patients with gastric
bypass or small bowel resection

o Serial Lactate level

• Measuremenlof tissue perfusion and end-point resuscitation
• Causes of f Lactate level:
• Bowel is.chemia
• Renal failure
• OM
• Pancrealitis
• Malignancy
• Pheochromocytoma
• Infection

PROTEIN SYNTHESIS: (Functional genomics)

1} Transcription:
• By translation of DNAto + RNIA
• Take place in: Ribosome
o Intrans are segments removed from DNAby splicing before the transcription

2} Translation: of messenger RNA (mRNA + protein)

• Take place in: Ribosome

3} Processing of the protein

■ Proteins kinesin/dynein required for directional transport along the microtubules

o Kinesin for movement away from centrosome
o Dynein for movement toward it

■ Protein kinase C: activated by Ca and diacylglycerol (DAG}

■ Protein kinase A: activated by cAMP
DNA ENZYMES
■ Helicase:
o Unwinds DNA at replication point

■ Topoisomerase:
o Create single or double-stranded break in the helix
o Fluoroquinolones inhibits DNA gyrase (topoisomerase II)

■ Polymerase:
o Used for duplication of DNA/RNA
• Elongates the strand
• Replace RNA with DNA
■ Liqase
o Catalyzes the formation of phosphodiester bond

DNA MUTATION
■ Point (Silent) mutation: Change base
■ Missense mutation: Change amino acid "SCO"
■ Non-sense mutation: Stop Codon

BLOTTING PROCEDURES
■ Southern blot: DNA
■ Northern blot: Rf\JA
■ Western: Protein
OTHERS
■ 25,000 genes found in the human genome

■ Apoptosis accomplished by activation of Caspases

■ Rough endoplasmic reticulum: Synthesizes proteins

■ Smooth endop lasm ic reticulum· Synthesizes lipid and steroid�

o Detoxifies drugs and poisoning
o Contain G6P enzyme which convert G6P to glucose in gluconeogenesis
o Sacroplasmic reticulum (subtype of smooth endoplasmic reticulum)
• Found in striated and smooth muscles
• IP3 generally f cytoplasmic calcium concentration
• Contains large store of calcium
• Malignant nypertnermia happens aue to defect of sacroplasmic reticulum
Hematology and Blood
Products
Reviewed by:

Dr. Salman AI-Harbi

HEMATOLOGY AND BLOOD PRODUCTS
■ History and physical examination are the best way to predict bleeding risk in normal people
■ Safest blood group: 0 -
■ All blood products carry the risk of HIV and viral hepatitis except: Albumin and Globulins
■ ABO: glycolipid
■ HLA: glycoprotein

■ Mechanism of coagulation:
1} Vascular vasoconstriction
2} Primary (Platelet adhesion)
3) Secondary (Coagulation cascade and thrombin generation}

Starts when: Measured by Exclusive

Intrinsic pathway Exposed collagen and factor XII (12) PTT (Table Tennis: Inside) VIII
Tissue factor -1- factor VII (7) VII
PT (Tennis: Outside)
Ex trinsic pathway
Best for liver synthetic function
PT measures 1972: II. VII IX. X
■ Common pathway
0 Measured by PT & PTT
0 II V X XII I and fibrino=n 110 -1- 5 2-13,

■ Mechanism of ant;coagulalioo·
o Antithrombin 111: Inhibits thrombin, IX, X, XI

o Protein C: (Vitamin K-dependent)

• Degrades factors V, VIII, fibrinogen
• Activated protein C in sepsis: Fibrinolysis
• Contraindicated to use in recent hemorrhage

o Plasmin:
• Degrades V, VIII, fibrinogen, fibrin
• Alpha-2 antiplasmin -+
natural inhibitor of plasmin from endothelium

■ Coagulation factors:
o Factors V and VIII (labile factors): No! founa in stored blood
• Factor V, VIII loss activity in blood but not in FFP
• Factor VIII (Anti-hemophilic): The only factor made by endothelium

o Factor VII: Shortest half life

o Factor XI: Not found in cryoprecipitate
o Factor XIII: Deficiency leads to delayed bleeding (Normal PT and PTT)
 02 - Hemoglobin Association Curve

Hb Curve 02 binding pH K w 2.3 DPG Temp PS0 (N=27) CO2 Ca

RIGHT SHIFTING ! ! {Acidosis) l l l l l l l

LEFT SHIFTING l f (Alkalosis) l ! ! ! ! ! l

Causes of Left shifting Causes of Right shifting

Causes of False High pulse oximetry Causes of False Low pulse oximetry
Carboxyhemoglobinemia Hemoglobin S
(CO poising)
Methemoglobinemia Methemoglobinemia
(if Sao, < 85%) (if Sao,> 85%)
Skin pigmentation Dark tattoo or Henna
(if sao 2 < 85%)
Fetal Hb Pregnanc)ol
Stored blood Methylene blue
{Associated with acidosis) Dark nail polish
Hyperventilation Anemia, Fever. Hypoxia
IABP Hypotension

■ Hypoventilation lead to right shifting by increasing the PaC02

� Improve tissue 02 uptake

BLOOD TYPES:
■ Most common blood product source of contamination: Platelets
■ Most common cause of infection-related mortality: Bacterial contamination

■ Most common bacterial contaminate in blood: Gram-positive (S. epidermidis)

■ Most common type of hepatitis related to blood transfusion: Hepatitis B Virus

■ Most common viral agent transmitted: CMV

■ BJooclcan be stored for maximum of 3 weeks

■ Maximum rate of blood transfusion to avoid -citrate toxicity is 66.5 mUmin

 Fresh Frozen DDAVP
Packed RBCs Platelets Cryoprecipitate
Plasma (Desmopressin)
Stored in citrate All factors Factor Vlll-vWF Release VII I-vWF
_,.!Ca Protein C, S Factor XIII from endothelium
.,. Refractory I BP Anti-thrombin Ill Fibrinogen
.,. Metabolic atka/osis Fibronectin
ABO/Rh Compatible ABO Compatible is ABO/Rn-compatiole All groups Vasopressin
Life span: 42 clays preferable is preferable acceptable analogue
Half.life is longer on shelf
than whole blood Life�sp�n�
.. 1 year Life �pan: 5 - 7 da11s Li� �pan�.1 ye�
1 unit t Hb by 1 g/dl 1 unit of platelets 1 unit: Decrease UOP
1 platelets by 10000 t fibrinogen 5 - 10 mg/di
Factor V, VIII not
available
� � � �
2:1:1/1:1:1 RBCs : Platelets : FFP 10 units 1 unit/2 units PRBCs 0.3mcg/kg IV
3:1 Crystalloids : RBCs
Used in: Used in: Used in: Used in: Used in:
Hb < 7 g/dl Dilutiooal coagulopathy < 50,000 + bleeding I FibrinQgen Uremic
DIC or Liver disease
< 1.5- 2 g /di !,Qllg!,!IQJ2al!!ll
Hb < 10 g/dl in cardiac < 10,000 (< 100- 200 mg/ di)
patient/ SCD vWD (Type I)
Warfarin rev!;!rs,!I
Pre-operatively, with vWD
Fibrinolll!i!.S reversal target level of: Hemophilia A
(Uroklnase, tPA) Hemoehilia A
> 100,000 in Dilutional
coagulopathy
neurosurgery
resulted from MOF
refractory to FFP
> 50,000 in major
surgery Diabetes insipidus
Patient on NSAIDs
> 20, 000 in minor
surgery

■ Normal level of fibrinogen: 2 - 4 g/dl

o Fibrinogen level is low in primary fibrinolysis and DIC
o Platelets count used to help to differentiate between them (Low in DIC)

■ Thrombolytic or Fibrinolytics: (t Plasmin -+

[)egrade the fibrin)
o Tissue plasminogen activator (IPA}
o Urokinase

■ Anti- Thrombolytic or Anti- fibrinolytics: (! Plasmin -+ Increase fibrin level)

o Tranexamic acid, Aprotinin
o t-Aminocaproic acid: better than FFP in case of fibrinolytics reversal is needed
o "as Post transurethral prolapse (Urokinase releasing)"
o But FFP is better than t-Aminocaproic acid in case of fibrinoly1ics overdose to replace
all coagulation factors
HEMOLYSIS REACTIONS
■ Most common cause of death from transfusion reaction: Clerical error

■ Most common fatal infectious complication of blood transfusion: Viral hepatitis (HBV)

Reaction
Febrile Non-hemolytic transfusion reaction
W➔A
(Donor WBC➔Recipient antibody)
Acute hemolytic transfusion reaction
Delayed hemolytic transfusion reaction
(7 - 10 days post-transfusion)
Transfusion-rel<1ted acute lung injury (TRALI)
A➔W
(Donor antibody ➔Recipient WBC}
Etiology
Most common transfusion reaction
Due recipient antibody reaction against donor WBCs
Due ABO incompatibility (Type II hypersensitivity)
c:, Tagiycardia,l;[yi:iote sion=Oligouria, no synco12e
c:, Associated with hemolysis (Dropped Hb)
c:, Managed by stop transfusion and supportive
measures
Due to HLA incompatibility
Most common cause of transfusion-related death
Caused by donor antibodies to recipient's WBCs
<:> 1' Capillary permeability

■ Type and Screen:

o To detect ABO and Rh phenotype
• Forward type: '.Antiserum agains[ patients ABO antfgen
• Reverse type: lsoagglutinins in patient's serum

■ Type and Cross (Cross-match):

o Used before transfusion
o By mixing recipient serum with donor lymphocytes (indirect Coombs test)

■ Investigations for hemolysis:

o l Haptoglobin < 50 mg/dl
o j Free hemoglobin > 5 g/dl
o t Reticulocytes
o t Unconjugated bilirubin, and LDH in delayed reaction
o Methemoglobinemia
o Peripheral blood smear
o Positive Coombs test
• Direct Coombs test: (Performed on patient's RBCs} for autoimmune hemolysis
• Indirect Coombs test: (Performed on patient's serum) used before transfusion
MASSIVE TRANSFUSION:
■ Definitions:
o Replacement of 1 unit of total blood volume (One blood volume) within 24 hours
o Replacement of50%% of total blood volume within 3 hours
o 2: 10 units PRBCs in 24 hours
o 2: 10 units of stored blood over 4 - 6 hours
o 2: 6 units PRBCs in 12 hours
o 2: 4 units PRBCs in 1 hour

■ Complications:
o Hyperkalemia (Most common}
• Due lo lysis of stored blood (especially if> 21 days)

o T,hrombocytopenia (Coagulopathy)
• Dilutional thrombocytopenia and coagulation factors deficiency

o Metabolic acidosis
• Due to presence of lactic acid
• The pH of unit of blood at time of collection is 7.10 when due lo citric acid
• Falls 0.1 pH uniVweek due to production of lactic and pyruvic acids

o Metabolic alkalosis
• Due to citrate metabolism in the liver and conversion to bicarbonate

o Hypomagnesaemia

o Hypocalcemia
• Poor clotting and persistent hypotension

Rule for replacement in massive transfusion:

• 10 lo 20 ml of 10% Ca gluconate IV for each500 ml of blood infused or
• 2 to5 ml of 10% Ca chloride IV for each500 ml of blood infused
 BLEEDING DISORDERS
■ Most common cause of surgical bleeding: Incomplete hemostasis
■ Best assessment of bleeding disorders in normal people: History and examination
■ Best assessment of clot strength: Thromboelastogram
o Assess platelet function, clot strength, and fibrinolysis
o Assess for defects in clotting factor (FFP, Cryoprecipitate, platelets, or tranexamic acid}
o Used in liver transplantation, cardiac surgery, major obstetric surgery and trauma

■ Von Willebrand's disease

o Most common congenital bleeding disorder
o Most common symptom: Epistaxis
o Leads to:
• Failure of platelets aggregation
r
• t Gplb, BT (ristocetin test} t PTT

o Types:

Tv= J Tvne II Tvne Ill

Most common - Most severe form
AD AD AR
Partial QuaNtitative deficiency Qualitative deficiency Complete deficiency
DDAVP ± DDAVP in mild form r vWF ± Factor 8 (Humate-P)
Antifibrinolytic therapy (aminocaproic acid)
r vWF ± Factor 8 (Humate-P) Recombinant factor VII:
r vWF + Factor 8 /Humate-PI Used in refractorv cases

DDAVP used in mild form and only for 3- 4 doses, can't be used> 72 hours due to
tachyphylaxis (rapid increased response)

FFP or Cryoprecipitate should be avoided and used in life threatening situations where
r
is no other treatment available (Large volume required in FFP, and infections with
Cryoprecipitate)

■ Hemophilia
r
o Sex-linked recessive, PTT only
o Most common symptom: Hemarthrosis
o Types:
• A (VIII deficiency) factor 8
• B (IX deficiency) factor 9 "Christmas disease•
• C (IX deficiency} factor 11

o Crosses placenta (newborns may not bleed at circumcision)

o Target level pre-operatively:

• 30 - 40% for minor operations
• > 50% for major operations or 'trauma
• > 80% for life-threatening bleeding

o Treatment:
• Recombinant Factor VIII or IX
• DDAVP with e-aminocarpoic acid
■ Uremia (ESRD)
o t Platelets{t bleeding time) with normal PT, PTT and fibrinogen
o ! Gplb ! Gpllb/llla ! VWF

■ DIC:
o Investigations:
• Fibrinolysis (! Fibrinogen t PT t PTT)
• t Fibrin split products
• t D-dimer
• t Platelets

o Management:
• Treat the cause

■ Heparin-induced thrombocytopenia (HIT)

o Most common complication: Thrombosis{Not bleeding)
o Antiplatelet antibodies (lgG PF4 AB) ,+ White clot
o Caused by UFH (Not related to the dose) or LMWH{Minimal risk)
• Detected on day 5 - 7{life of platelets}

o lovest;gat;on·
• Falling of platelets count > 50% from baseline
• Serotonin Assay
• Anti-PF4 ELISA
• Fibrinogen level
• Bilateral duplex U/S of lower extremities to exclude silent DVT

o Management:
• Stop heparin and LMWH for life
• Warfarin should be postpone until platelet recovery{< 150,000)
• Avoid platelets transfusion{thrombogenic effect)
• For patient with thrombosis:
• Therapeutic doses of alternative anticoagulant until recovery of platelets
followed by transition to warfarin
• Treatment:
Direct thrombin inhibitor
• Argatroban: reversible direct thrombin inhibitor{Excreted by Liver)
o Dose: 2 mcg/kg/min
• Lepirudine: reversible direct thrombin inhibitor (Excreted by Kidney)
• Hirudin: /Rreversible direct thrombin inhibitor
o From saliva of leeches, most potent direct inhibitor of thrombin

Direct Factor Xa inhibitor

• Fondaparinux
o VTE prophylactic dose: 2.5 mg SC OD
o VTE therapeutic dose: 5 -10 mg SC OD (No-FDA approved)

■ Bernard Soulier: Gplb receptor deficiency

■ Glanzmann's thrombocytopenia: Gpllb/llla receptor deficiency

 ANTI-COAGULANTS
Drua Mechanism / Dose Perio~rative Measures Comolication Reversal
Prevents vitamin K- Pre-op: PT (INR) Cross the placental 1) Stop drug
dependent Hold 5 days (Contraindication in
decarboxylation of pregnancy) 2) Vitamin K
glutamic acids PO (6 hours to effect)
Post-op· Warfarin skin necrosis 1 -2.5 mg if INR 5 - 9
Factors· Resume within Due to short half-life of with risk of bleeding
II, VII, IX, X (1972), 12 -24 hours proteins C and S
Proteins C and S 2.5 - 5 mg if INR > 9
Occurs when start with no risk
Dose: warfarin without starting
Warfarin Start by 5 - 10 mg heparin before it Intravenously 10 mg
once daily (1 -2 hours to effect)
In serious bleeding

3) In emergency:
FFP

Or

Prothrombin complex
Ill. VII. IX and X\
Activates of AT Ill Pre-op: PTT Doesn't cross placental Pro/amine sulfate
(Augmentation) Hold 6 hours T½ 60 -90 (Used in pregnancy)
min
Inhibits X & II Long term:
Post-op: Osteoporosis, alopecia
Heparin
Prophylactic Dose: Low-risk: and thrombocytopenia
5000 IU SC BID/TID 12-24 hours
Not preferred in case of
Therapeutic Dose: High-risk: liver disease
80 units/kg IV bolus 48- 72 hours (metabolized by liver)
Then 18 units/kQ IV
Activates of AT 111 Pre-op: Anti-X Not preferred in case of Protamine sulfate
(Augmentation) Hold24 hours assay renal failure (Partial reversal)
(excreted by kidneys)
Inhibits X only Post-op: T½4.5h
Low-risk: Best anti-coagulant in
LMWH
Prophylactic Dose: 12-24 hours pregnancy and
40 mg SCOD malignancy, and less risk
High-risk: of HIT
Therapeutic Dose: 48- 72 hours
1 mg/kg SC BID
1.5 ma/ka SCOD
Use Ideal body weight {IBW) for obese patients
NOTES
■ Protamine sulfate
o Indications and dosage:
• Heparin overdose (Consider t½ of heparin: 60 - 90 min}
• 1 - 1.5 mg per 100 U of heparin (Not exceeding 50 mg/ day)
• Half the dose if> 30 minute for last dose of heparin

• Enoxaparin overdose
• 1 mg/ mg if last dose < 8 hours
• 0.5 mg/ mg if last dose> 8 hours

• Counteract effect of anticoagulant preoperative, after dialysis or heart

surgery
• Reversal of Heparin/ LMWH
• Approach: Hold further doses, volume resuscitation, control source of
bleeding, transfusion (PRBCs, Platelets, or FFP} as indicated, Consider
antidote
• Consider antidote for severe bleeding with prolonged PTT
• Protamine reverse heparin 100%, and LMWH only 60 - 80%

o Rout:
• Slow IV push over 10 minutes at least

o Monitor:
• PTT and anti Xa level after 4 hours, consider another dose if bleeding continue
and PTT still prolonged

o Side effect:
• Allergy, hypotension, bradycardia, nausea and vomiting, flushing, teratogenic

■ Bridging:
o Using of short-acting anticoagulant during interruption of warfarin when INR not in
therapeutic range

1) Warfarin stopped 4 - 5 days before surgery

2) Heparin initiated 2 days after stopping (3 days pre-op)

Stopped 4 - 6 hours preoperatively, restarted 12 - 24 hours postoperatively

o Indications:
• Recent (within 30 days) myocardial infarction
• Mechanical heart valves
• Stroke
• Pulmonary embolism
 ■ Heparin does not work in Anti-Thrombin Ill deficiency patients
o If DVT happens in heparinized-patient -+ starts FFP then AT-Ill then heparin

■ t-Aminocaproic acid "Procoagulant agents:" (anti-fibrinolytics):

o Inhibits fibrinolysis by inhibiting plasmin
o Used in thrombolytic overdoses (reversal of IPA and urokinase)

■ Compression devices: improve venous return, and induce fibrinolysis by release IPA
• Used in moderate and high risk of DVT

HYP ERCOAGULABILITY DISORDERS

■ Most common factor causing acquired hypercoagulability -+ Smoking
■ Factor V Leiden mutation
o Most common congenital hypercoagulability disorder
o Causes resistance to activated protein C; the defect is on factor V
o Leads to inability to inactivate factor V

■ Anti-Phospholipid Antibody syndrome

o Procoagulant (prolonged PTT but hypercoagulable)
o Antibodies to cardiolipin and lupus anticoagulant
• Cardiolipin is mitochondrial membrane phospholipid

■ Homocysteinemia: Treated with folic acid, 812

■ Yirchow's triad· hypercoagulability, endothelial injury, stasis of blood flow

POST HEMODIALYSIS
■ Dialysis on the day of surgery -+ Heparin-free dialysis
■ Elective surgery: > 24 hours after hemodialysis
o To avoid risk of hyperkalemia

■ For emergency surgery: Proceed if K < 5.5 and no ECG changes

Immunology
IMMUNOLOGY
Primary lymphoid organs: Bone marrow Thymus and liver
Secondary lymphoid organs: Spleen and Lymph nodes

■ B cells (Bone): Antibody mediated immunity (humeral)

o Produced by Bone ma"ow, Matured in Bone marrow

■ T cells (Thymus): Cell mediated immunity

o Produced by Bone ma"ow, Matured in Thymus
o Helper T cells (CD4)
• Release IL-2 -+ cytotoxic T cells
• Release IL-4 -+ B-cell maturation to plasma cells
o lntradermal skin test (TB skin test): Used to test cell-mediated immunity

MHC Classes:
■ MHC class I
o Single chain + 5 domains
o CD8, on all nucleated cells
o Cytotoxic T cells + Viral infection

■ MHC class II
o 2 Chains + 4 domains
o CD4, on antigen-presenting cells only
o Helper T cells + Bacterial infection

■ NK cells lack self-MHC

ANTIBODIES

Antibody Description
1AM Initial LarQest antibody (5 domains: 10 bindinQ sites) and Opsonin
laG Most abundant antibodv. Cross olacenta and Oosonin
In& Produced bv GIT IPe•=r's catches I and breast milk
l!IE Allerqic reactions, parasite infections
laD Membrane-bound receotor on B cells

VACCINES

Tvne Diseases
Live Attenuated Measles. Mumos. Rubella. Polio /Sabin\. Yellow fever Influenza
Inactivated /killed) Cholera Influenza HAV. Polio /Salk). Rabies
Toxoid Diohtheria. Tetanus
Subunit HBV, Pertussis, HPV
Coiuaate Hib S. oneumania

■ Vaccined: Patient received vaccine± immuned

■ lmmuned: Patient received vaccine and antilbodies titer to the immunity level
TETANUS
Tetanus Drone wounds Non-Tetanus Drone wounds
3 doses and < 5 vears None None
3 doses and > 5 years Td None
3 doses and > 10 years Td (1 dose)± TIG (Controversial) Td (1 dose)
Or immunocompromised
< 3 doses or unknown Td (3 doses\+ TIG Td 13 doses\
TIG: Tetanus immunoglobulin (Anti-toxin)
Td: Tetanus toxoid (Vaccine)
'Tdao is oreferred to Td for adult who never received Tdao"

■ Tetanus prone wounds:

o > 6 hours old
o > 1 cm depth
o Contamination (infected)
o lschemia or devitalized tissue
o Burn

■ Doses:
o Tetanus toxoid: 0.5 ml intramuscular
o Tetanus immune globulin: 250 units intramuscular

■ Vaccination:
o Tetanus toxoid (vaccine) given at age of 2, 4, and 6 months
o Booster doses of tetanus toxoid given at age of 1 and 5 years

OTHERS

■ Surgical Histopathology specimens:

o Fixed: (10% buffered formalin)
• For all routine specimens (including lymph node}

Paraffin: fit for fixed specimen (permanent section), for special stains

o Fresh:
• For aspirated fluid, any organ or lesion need to be in frozen section

Frozen section allowed for rapid examination of section for immuno-histo/ogy and
immuno-onco/ogy, used for fresh unfixed specimen
Infection
INFECTION
Personal Protective Equipment (PPE) should be worn by all personnel for all patients
■ To be worn in order:
o Shoe covers + Gowns + Mask + Goggles / Face shield + Head cover
o Hand hygiene
o Gloves

■ To be removed in order:
o Shoe covers
o Gloves + Hand hygiene
o Goggles I Face shield + Hand hygiene
o Gowns + Hand hygiene
o Mask (Lower part first) + Hand hygiene
o Inside the room: Airborne transmission
o Outside the room: Droplets transmission

N95 mask should be worn for all aiirborne transmission

o Open pulmonary TB
o Measles
o Varicella
o MERSCoV
Re-used for 5 times, but single use for MERS CoV

■ Hand rub (Alcohol) for 20 - 30 seconds

■ Hand wash (Water and Soap) for 40 - 60 seconds

o 5moments:
o Before touching a patient
o Before clean/aseptic procedure
o After touching a patient
o After touching patient surroundings
o After body fluid exposure

o Other iodications·
o For soiled hand contamination
o After bathroom
o Before eating
o Clostridium difficile
 BACTERIA

Classification of Bacteria
Aerobes Anaerobes
Cocci Bacilli Clostridia spc.
Gram+ Gram- Gram+ Gram- Bacteroides
Staohvlococci Gonococci Diohtheria E. Coli
Streotococci Meninaococci Anthrax Klebsiella
Pneumococci Neisseria Mvcobacterium Proteus
Enterococci Salmonella
IAmnicillinl
Gram+: Pum/e stain due to oresence of oeotidoalvcan /aver

FEVER
■ Most common source within 48 hours: Atelectasis
■ Most common source within 5 days: Urinary tract infection
■ Most common source after 5 days: Wound infection
WOUND INFECTION (SURGICAL SITE INFECTION)
■ Definition:
o Infection at the site of surgical incision within 1 month of operation or within 1 year of
operation if foreign body implanted

■ 2: 105 organisms is diagnostic for wound infe.ction and burn wound infection
o > 103 organisms is diagnostic for central line infection

■ Most common nosocomial infection overall: UTI

■ Most common nosocomial infection in surgical patient: Surgical site Infection

o Most common organism: Staphylococcus aureus
o Most common gram -ve organism: E. coli
o Most common anaerobes organism: Bacteroides

Staohvlococcus Streotococcus
Most common cause of SSI overall
Most common cause of cellulitis postoperative > 24 hour Most common cause of cellulitis postoperative < 24 hour
/a Iona with Clostridia)
Mast common causative organism of abscess Most common causative organism of non-operative
cellulitis

■ Most common bacteria in the colon: Anaerobes

o Most common anaerobe in the colon: Bacteroides
o Most common aerobic bacteria in the colon: E. Coli

■ Leading cause of infectious death after surgery: Nosocomial pneumonia

■ Decrease risk of wound infection by: Normal saljne jrrjgat;on

o Water irrigation used only in burn wound

■ Remote infection (e.g. UTI) t the risk of surgical site infection by at least 7%
■ Malignancy suspected in chronic wound if: Overturned edges ➔ Biopsy (BCC vs. SCC)
LINE INFECTIONS
■ Most common organism overall of line/graft infection: Staphylococcus epidermidis
o Most common early organism: S. aureus (GPC coagulase positive)
o Most common late organism: S. epidermidis (GPC coagulase negative}

■ Highest infection with: Femoral line

■ Lowest infection with: Subclavian line
■ Most common complications of subclavian vein catheterization:
o Pneumothorax and thrombosis

FUNGAL INFECTION
■ Indications for systemic anti-fungal therapy:
o Candida endophthalmitis
o Osteomyelitis
o Septic arthritis
o Endocarditis
o Any patient with single positive blood culture
o Colonization from multiple sites

Candida isolated from surgical drain is not an indication as it due to colonization

■ Options for anti-fungal:

o Amphotericin B (associated with t Kand t Mg)
o Caspofungin
o Voriconazole
NECROTIZING SOFT TISSUE INFECTIONS
■ Mortality ranges from 25% - 40% (higher in truncal and perinea!)
■ Necrotizing myositis primarily involves the muscle but can spread to surrounding tissue as well
■ Clinical Presentation:
o Bullae, skin necrosis, crepitus, SIRS or Septic shock
o Renal failure (! Na, ! Cl) in advanced disease
o Pain beyond the margins of erythema
o Gas on imaging

■ Common sites:
o Genitalia, Perineum "Fournier's gangrene" (Colle's fascia prevent infection to reach}
o Abdominal wall

■ Types:
o Type 1: Polymicrobial (Commonest)
• Presented in immunocompromised patients (diabetes mellitus}
• Most common sites: Perineum, Trunk, OM foot, and Pressure sore
• Most common organisms:
o Bacteroides and Streptococcus

o Type 2: Monomicrobial
• Presented in healthy patients with history of trauma, but more Aggressive
• Most common sites: Extremities, and Trunk
• Most common organism:
o Group A 13-hemolytic Streptococci or Staphylococci (Exotoxin)
o Clostridium perfringens (alpha toxin} "Most common organism"
Gas-gangrene -+ Myon ecrosis
Large pleomorphic Gram-positive rods anaerobes

o Type 3: Marine organisms

• V. vulnificus infection of traumatized skin in sea divers
• Associated with severe infection (required Penicillin G, Tetracycline, Ceftazidime)

o Type 4: Fungal infection

■ Management:
o Early Surgical Debridement {definitive treatment)
• Incisions should be made over involved skin parallel to neurovascular bundles
• Necrotic tissue will appear dull, gray, and avascular with characteristic
"murky dishwater" fluid
• Revision surgery should be planned ("second look") within 24 to 48 hours

o IV antibiotics
• Broad-spectrum antibiotics until culture results
(Piperaci/Jin/tazobactam, Carbapenem, and Ampicillin/su/bactam)

• Penicillin G (4 million units IV every 4 hours)± Clindamycin for Clostridium

• 3rd Cephalosporin or Aminoglycoside (Gentamicin} for gram-negative
• Va ncomycin for resistant Staphylococcus aureus (MRSA)
Clindamycin or Linezo/id used to inhibit toxin synthesis
PRIMARY (SPONTANEOUS) BACTERIAL PERITONITIS
■ Definition: ascitic fluid infection without evident intra-abdominal surgical cause

■ Usually monobacterial: E. Coli (most common) or Klebsiella

■ Risk factors:
o Ascitic fluid total protein< 1 g/dL (<10 g/L)
o Serum total bilirubin > 2.5 mg/dl
o Variceal hemorrhage
o Malnutrition
o Usage of PPI

■ Clinical presentation:
o Fever, abdominal pain, altered mental status
o Associated with cirrhosis, and sometimes nephrotic syndrome

■ i
Investigat on:
o Ab dominal paracentesis
• > 100 WBCs/mL
• PMNs > 250 ceUs/ml is diagnostic
• PMNs > 500 more specmc, but less sensitive compared to > 250

• Microbes with a single morphology on Gram's stain

• Aerobic and anaerobic culture
• Albumin, protein, glucose, LOH, amylase, and bilirubin

o Laboratory
• Metabolic acidosis
• Impaired renal function

o Imaging
• Rule out secondary causes
• Absence of pneumoperitoneum on an imaging study

■ Management:
o 3rd generation Cephalosporin, followed by Culture-based antibiotics for 2 - 3 weeks
o Removal of indwelling devices
o Prophylaxis antibiotics: Fluoroquinolones or Trimethoprim-sulfamethoxazole
• Cefotaxime
• Ceftriaxone used in advanced cirrhosis or history of UGI bleeding
• Ciprofloxacin used as secondary prophylaxis as weekly dose
• Indications·
• Upper GI hemorrhage
• Ascitic fluid total protein < 1 g/dl (<10 g/L)

SECONDARY BACTERIAL PERITONITIS

■ Due to intra-abdominal source (Transmucosal migration)
o Usually due to perforation or severe inflammation

■ Polymicrobial (Bacteroides, E. Coli, and enterococcus)

■ Treatment:
o Surgical intervention and treat the source
HEPATITIS
■ Hepatitis B /DNA)
o Most common hepatitis leads to HCC
• Hepatitis B lead to HCC due to Cirrhosis
o Most common hepatitis related to blood transfusion
o Can cause fulminant hepatic failure

HBsAq Anti-HBs HBeAq Anti-HBe Anti-HBc

Acute HBV • • laM
•
Window
Chronic lhiah infectivi"'' • •
laM
laG
Chronic llow infectiviM • • laG
Recove~ • • laG
Immunized • None

■ Hepatitis C (RNA)
o Most common hepatitis related to drug abuse
o Most common hepatitis leads to Cirrhosis
• Hepatitis C can lead to HCC without cirrhosis
o Most common hepatitis leading to liver TXP

■ Hepatitis E:
o Can cause hepatitis in pregnancy

HIV
■ Most common involved organ: Stomach
■ Most common cause for laparotomy in HIV patients: Opportunistic infections (CMV)
o Most common intestinal manifestation of AIDS: CMV cojjtjs

■ Most common neoplasm in AIDS patients: Kaposi's sarcoma

■ Most common cause of upper GI bleeds: Kaposi's sarcoma

■ Most common cause of lower GI bleeds: CMV

■ CD4 (Normal > 800}

o < 200 leads to development of opportunistic infections
o Best for morbidity and prediction of immunity

■ Viral load
o Best for mortality and risk of transmission
OTHERS
■ Staphylococcus aureus produces exotoxins: hemolysin and leukocidin
■ Abscess that do not wait for fluctuation:
o Hand infection
o Parotid abscess
o Breast abscess
o Buttock abscess
o Perianal abscess

■ Infective Endocarditis
o Most common involved native valve: Mitral
o Most common involved prosthetic valve: Aortic
o High-risk conditions (requiring pro-phylaxis)
• Prosthetic cardiac valve
• Previous infective endocarditis
• Cyanotic congenital heart diseases

o No longer recommended for antibiotics prophylaxis

• Mitral valve prolapse
• Rheumatic heart disease
• Congenital heart disease
• Bicuspid valve disease

■ Ludwig's angina:
o Submandibular space infection (emergency situation)
o Treatment:
• Maintain airway, Antibiotics, Surgery± transection of mylohyoid

■ TB ulcer: Apple jelly granulation

■ Smells of some organisms:

o Pseudomonas: Grape, sweet, fruity, tortillas or com chips to some people
o Escherichia coli: Floral or flowery odor
o Candida or Yeast: Bread baking or beer
o Proteus: Rancid or rotten chicken soup, chocolate cake or brownies
o Gram-negative anaerobes: Bad breath, morning breath, just smell bad
o Clostridium or gas-gangrene: Sweet odor (decayed apple)
o Bacteroides: Over ripe cheese odor
 ■ Toxic shock syndrome:
Staohvlococcus Strentococcus

••
Associated with:
Surgical site infection and wounds ••
Associated with:
Non-surgical cellulitis or surgical < 24 hours

• Abscess
Line infection ••Lymphangttis (Red streaks, Lymphadenopathy)
Necrotizing fasciitis

•GAS gangrene
Communitv-aMuired oneumonia
Hiqh fever hvootension and malaise are more
Multioroan failure Associated with bacteremia. sore throat
Earlv rash and desauamation after 2 weeks Rarelv develoo rash
Penicillin G ± Clindamycin Penicillin G ± Clindamycin
Nafcillin or oxacillin Varncomycin
Vancomvcin

■ Cal/dog/human bites (polymicrobial)

o Staphylococcus aureus: most common organism in infected human bite wound
o Eikenella: most common organism cultured specifically from human bite wounds
o Pasteurella multocida: most common found in cat and dog bites

■ Snake Bite:
o Snake venom is 90% protein
• Enzymes (Phospholipase A, Procoagulant enzymes)
• Non-enzymatic polypeptide toxins
• Non-toxic proteins

o Presentation:
• Local: pain, swelling, tenderness, enlarged lymph nodes, bleeding, or necrosis
• General:
• Nausea, vomiting, weakness
• Cardiovascular: Dizziness, hypotension, arrhythmia
• Bleeding (Epistaxis, gums, intracranial bleeding, GI bleeding)
• Neurological (Paraesthesia, ptosis, numbness, paralysis}
• Musculoskeletal (Stiffness, Myoglobinuria, hyperkalemia, cardiac arrest}
• Renal (Loin pain, hematouria, myoglobinuria, uremia)
• Endocrine (adrenal insufficiency, hypothyroidism, hypopituitarism)

o Management:
• First-aid treatment and transport to hospital (ABCDE)
• Traditional treatment proven to be useless (local incision/pricks, attempts to suck
the venom, tourniquets, topical instillation or application of herbs or chemical)
• Immobilization helps to decrease the absorption of venom
• Avoid any interference with bite wound
• Antivenom (lmmunoglobulin purified from plasma of horse, donkey or sheep}
• Either as monovalent (specific venom) or polyvalent (multiple venom)
• Indicated if patient developed systemic symptoms, or local symptoms
(rapid extension, large lymph nodes,> 50% of bitten limb} within 48 hours
• Given IV (bolus or infusion), not recommended to apply it locally
• Anaphylactic reaction is most common side effects
• 2nd dose indicated if bleeding, neurotoxic or cardiovascular signs persists
after 1 - 2 hours
 NEEDLE-STICK INJURIES
■ Types:
0 Percutaneous injury (e.g. needle stick or cut with a sharp object
0 Contact with mucous membranes or non-intact skin

■ Immediate irrigation with saline or water

■ Antiseptic (chlorhexidine) or wound squeezing showed not to decrease risk of transmission

■ HIV
0
..
Risk:
0.3% for percutaneous exposure
0.09% for mucous membrane exposure

0 Post-exposure medications: Tenofovir-emtricitabine + raltegravir (or dolutegravir)

■ HBV
0
.
Risk:
Patient:
• HBsAg and HBeAg +ve: 37 - 62%
. • HBsAg +ve only:
Nonimmunized is 6 - 24%
23- 37%

0 Post-exposure medications:

Health-Care Provider Post-exposure investigation Postexposure prophylaxis Postvaccination

IHCPl serolonv
Patient HCP HBIG Vaccine
(HBsAn\ (Anti-HBs)
Vaccine responder
(anti-HBs > 10 m/UlmL No action needed
after 3 - 6 HB vaccines)
Positive/ . 2 doses No No
Vaccine non-responder Unknown separated by 1
(anti-HBs < 10 m/UlmL month
after 3 - 6 HB vaccines) Negative No action needed
Positive/ <10 mlU/ml 1 dose Revaccination Yes
Unknown
Response is unknown
Neaative <10 mlU/mL None Revaccination Yes
Anv >10 mlU/mL No action needed No
Positive/ . 1 dose Complete vaccination Yes
Unvaccinated Unknown
Neoative . None Complete vaccination Yes

■ HCV
0 Risk: 1.8% (Much less than HBV)
0 Post-exposure medications: No effective medications
Antibiotics
ANTIBIOTICS
MECHANISM OF ACTION
■ Inhibitors of cell wall synthesis:
o Penicillin, Cephalosporins, Carbapenems, Vancomycin

■ Inhibitors of 30s ribosome:

o Aminoglycosides, Tetracycline

■ Inhibitors of 50s ribosome:

o Clindamycin, Linezolid, Macrolide

■ Inhibitor of DNA gyrase ffopoisomerase II):

o Fluoroquinolones

■ Inhibitor of RNA polymerase:

o Rifampcin

■ Produces oxygen free radicals (to damage DNA):

o Metronidazole

■ Inhibitor of DihydroFolate Reductase (inhibits purine synthesis):

o Trimethoprim

Bacteriostatic antibiotics: Tetracycline, C/indamycin, Erythromycin

Bactericidal antibiotics: Aminog/ycosides and Fluoroquinolones

MECHANISM OF ANTIBIOTIC RESISTANCE

■ Most common method of antibiotic resistance:
o Transfer of plasmids (penicillin resistance}

■ Aminoglycosides: Decrease in active transport

■ MRSA / VRE: Mutation of cell wall binding protein

ANTIBIOTICS COVERAGE

Gram Positive Gram Nei ative Anaerobes

MRSA MSSA Streotococci E. Coli, Klebsiella Pseudomonas
Penicillin Metronidazole
Amoxvcillin
Ciindamvcin Clindamvcin
Vancom ,cin Linezolid Daotomvcin
Ciprofloxacin
Gentamicin
Cefuroxime
Amoxvcillin/Clavulanate I Amoxvcillin/Clavulanate
Pioeracillin/Tazobectam
Meron<>nema and lmioenem
 INHIBIT CLASIFICATION ANTIBIOTICS
Penicinillase - Sens;b/e
Natural Penicillins Penicillin G: Na, K, Procainic, Benzathine (IV, IM)
(narl'ow spectrum) Penicillin V: VO
Aminopenidllins Ampicillin
(broad spectrum) Amoxicillin
Penlclnillase - Resistant {tlffYnanow sptttn,m}
Penicillins Nafcillin Oxacillin I
Anti,:,seudomonal (eKttndttlsptttrum)
Oidoxacillin

Ticarcillin
C,/1 CarboxipenicilHns Carbenicillin
Piperacillin
Ureidopenicillins Azlocillin
Wall

Mezlocillin
s 1• Generation Cefazolin Cephalexine Cephapirin
Cefadroxil Cephadrine Cephalotin
y
n Beta
Cefuroxime Cefamandole Cefprozil
t Lactams
h
r Generation Cefoxitin Cefonicid Cefmetazole
• Cefotetan Cefaclor
s
Cephafosporins Cefoperazone Ceftriaxone Ceftazidime
i 3· Generation Cefpodoxime Ceftizoxime Cefotaxime
s Cefdinir Ceftibuten Cefixime
Cefditoren
4• Generation Cefepime Cefpirome •
s• Generation Ceftaroline
Carbapenems Meropenem I Ertapenem I Ooripenem I lmipenem + Cylastatine
Monobaetoms Aztreonam
•• • Beta•lactamase Jnhlb. Sulbactam I Tazobactam I Clawlanic Acid
No Glycop,ptld•s Vaneomycin I Bacitr.acin
lactam
Amine,.
Teicoplanin
Gentamycin
I
Neomycin
PolymyxinB
St1ep1omycin
305 glycosid�s Amikacin Tobramycin
Tetrac-yclins Doxycycline Oemedocylin • Minocycfine
T etracyclin Tigecyclin
Protein Oxazolidonones linezolid
Synthesis Streptoqramins Quinupristin/D 1alfopristin
sos CloramphenJco/
Macro/Ides Ery1hromyc.in Az.ithromycin Clarithromycin
Llntosamfdes Clindamycin Unoomycin
DNA Fluorqulnolones Oprofloxacin I Norfloxacin Levofloxacin Ofloxacin
topoisomerases
Quino/ones
Sparfloxacin
Nalidixic Acid
I Moxifloxacin Gemifloxacin Enofloxacin

Sulfamethoxaiole Ag Sulfadiatine Sulfasalaiine Sulfisoxaiole

I
Folic Acid Sulfonamides
Synthesis (SMX)
DHFR Inhibitors Trimethroprim (TMP) Pirymethamine
ONA (damage) Metronidazo/e
mRNAsynth. Rifampim
 COMMONLY USED ANTIBIOTICS IN SURGERY
Disease
Best for SSI prophylaxis
Mild OM foot infection
Skin, Bone infection
Post-operative infection
Community-Biliary inf.
Primary Peritonitis
SSI prophylaxis
Biliary infections
(Acute cholecystitis)
Pancreatitis + sepsis
Polybacterial necrotizing fasciitis
Severe diverticulitis
Severe OM foot infection
Mild diverticulitis or cellulitis
Abscess
Mild CDF infection
Abscess, anaerobic infections
Prophylaxis for colorectal suraerv
PCN-allergic SSI prophylaxis for
(hernia and breast)
Mild-Moderate CDF infection
Severe CDF infection
MRSA skin/subcutaneous infection
H. Pylori infection
Monobacterial necrotizing fasciitis
Mild OM foot infection
PCN-allergic cellulitis
PCN-alleraic SSI oroohvlaxis
Skin or intra-abdominal infections
Severe OM foot infection
Bacterial septicemia
Necrotizing pancreatitis
Intra-abdominal infection I Tigecycline load: 100 mg IVthen 50 mg IVq12
Multi-<lrua resistance Colistin load: 5 ma/ka IVthen 2.5 ma/ka IVa12
MRSA, VRSA
Camplicated skin infection
Nosocomial Pneumonia
Prokinetic (stomach clearance)
Severe UTI
Skin, bone infection
Intra-abdominal infection
Bacteria seoticemia
Gram - septicemia
UT I skin infection
Antibiotic / Dose Side-effect / Notes
Cefazolin (1" Cephalosporins) longest half-life
2 a IVa24h
Cefuroxime (2"" Cephalosporins) Diarrhea
500 mg PO q12h Nephrotoxicity
750 ma or 1.5 a IVa8h
Ceftriaxone (3'" Cephalosporins) Cholestatic jaundice
1 g IVq 24h Gallbladder sludging
Piperacillin/tazobectam (Tazocin) Inhibits platelets
3.37 g IVq6h PCN allergy·
4.5 g IV (in severe infection) Cefepime 1 g IVq8h or
Ciprofloxacin + Metronidazole
Amoxaicillin/clavulanate 875 mg PO q 12h
Or Ceftriaxone + Metronidazole
Metronidazole 500 -1000 mg IVq8h Peripheral neuropathy
+ Cefazolin PCN allergy:
Gentamicin instead of cefazolin
Vancomycin HTN, Redman syndrome
(histamine release) if not given
125 mg PO q6h slowly
500mg P0q6h
30 mntka/dav IV(divided to a12h\
Amoxacillin1g PO q12h PCN allergy:
Clarithromycin 500 mg PO q12h Metronidazole instead of
Omeorazole 40 ma PO a 12h Amoxacillin
Clindamycin 600 mg IVq8h Pseudomembranous colitis
Ciprofloxacin + Clindamycin Tendon rupture
500 - 750 mg PO q12h
400 ma IVa12h
lmipenem 500 -1000 mg IVq8h Seizures (also Mepridine)
+ cilastatin (to prevent renal
hvdrolvsis\
Nephrotoxicity
Linezolid 600 mg IV/PO q12h Should not be 1" antibiotics
Should be combined with other
- BM sunnression
Erythromycin
50 -100 mg PO q8h
100 ma IVa8h
Gentamicin Decrease biliary concentration
3 - 5 mg/kg/day IV/IM divided q8hr Nephrotoxicity
Ototoxicity
Bactr im (Tri/Sulf)10 - 15 mg/kg/day Erythema multifom1,
divided a8h Teratoaenic, Neohrotoxicitv
 PENICILLIN ALLERGY
■ Most common medication allergy
■ Penicillin by itself is not allergen, and allergy from complex break-down

■ Types:

Immediate Delaved
Within 1 hour of administration (up to 6 hours) Begin after multiple doses, after
. Re-exposure associated with life-threatening days of administration (classically
anaphylaxis after 6 hours)
Time . But lgE antibodies sensitivity decreased overtime
. 50% of patients lost sensitivity after 5 years from last
reaction
Pruritus, urticaria, angioedema, flushing, laryngeal edema, and Most common allergic:
hypotension
Presentation Delayed cutaneous reactions
(Maculopapular cutaneous rash
and eruotion)
Mediated by lgE Mediated by T Cells
Pathogenesis
/Tvne I hvnersensitivitv\ /Tv= IV hvnersensitivitv\
. Penicillin skin test for Positive features of past immediate reaction
0 Positive skin test have 5 - 10% cross-reaction to cephalosporins
Investigations
- Graded challenge (test dosing): for patents believed to be non-allergic
0 By aiven 1%, then 10% then 100% of dose at 30 min interval
- Avoidance of all Penicillin Discontinue: Cutaneous reactions
usually resolve within 1 - 2 weeks
- Caution use of other Beta-ladam antibiotics: after discontinue
Carbapenem
Cephalosporins (due to cross reaction) Antihistamines: if associated with
Management pruritic component
- Desensitization: by starting with 1/1000 to 1/100 dilution
of the drug Glucocorticoids: for severe
0 Used in patient with immediate allergy and no eruptions, no response to
acceotable alternate antibiotics antihistamines

■ Alternative prophylactic antibiotics:

o Non-severe allergy: (Non-type I hypersensitivity)
• Cefazolin: used for prophylaxis of most general surgery procedures
• Ceftriaxone: used for prophylaxis of hepatobiliary surgery (less cross-sensitivty)

o Severe allergy: (Type I hypersensitivity))

• Clindamycin + Gentamicin: used for prophylaxis of most surgical procedures
• Fluoroguinolones {Cipro): prophylaxis o f Gastroduodenal, Biliary surgery
• Gentamicin: prophylaxis of Colorectal surgery
• Vancomycin: used for prophylaxis of breast, hernia, and vascular procedures
• If allergic to vancomycin: Daptomycin or Linezolid

+ Metronidazole
OTHERS
■ Ideal body weight = 50 kg + 2.3 kg for each inch over 5 feet

■ Dosing weight = IBW + 0.4 (Actual weight - IBW)

o Used for all medications (including antibiotics, anticoagulants and analgesia}

■ Maintain glucose level by: Decrease length of antibiotics

■ Side effects of antituberculosis drugs

o lsoniazid: Hepatotoxicity, B6 deficiency
o Rifampin: Hepatotoxicity and GIT symptoms
o Pyrazinamide: Hepatotoxicity
o Ethamb utol: Retrobulbar neuritis

■ Orugs to avoid in Pregnancy: (M-CAT)

o Metronidazole
o Ciprofloxacin
o Aminolycosides
o Tetracyclin

■ Antibiotics used to treat UTI:

o Best: Ciprofloxacin 500 mg PO q 12 hours for 1 week

o Options for Pregnant:

• Nitrofurantoin 100 mg PO q 12 hours for 1 week
• Amoxicillin (augmentin} 625 mg PO q 12 hours for 1 week
• Cephalexin 500 mg PO q 12 hours for 1 week

Type Anti-MRSA antibiotics Anti-Pseudomonal antibiotics

(Gram +ve) (Gram-ve/
Beta-Lactam Ploeraclllln and tazobactam Ploeraclllin and tazobactam
Ceftaroline /5th ceohalosoorin\ Cefeoime 14th ceohalosoorin\
- Ceftazidime /3<d ceohalosoorin l
- Merooenem / lmioenem
Fluoroauinolones - Ciorofloxacin
Aminoglycosides (Anti . Gentamicin
30S)
Tetracyclines (Anti 30S) Doxycycline Doxycycllne
Minocycline Minocycline
Tiaecvclin
Others Trimethoprim/sulfamethoxazole Trimethoprim/sulfamethoxazole
Vancomycin (Glycopeptide} Colistin
linezolid (Oxazolidinone "Anti 50S") Acetic acid
Clindamycin (Lincosam ides "Anti
50S")
Daotomvcin
Fluids and Electrolytes
Reviewed by:

Dr. Haytham Alarfaj

FLUIDS AND ELECTROLYTES
■ Body is made of 42 L water (28L intracellular, 14L extracellular}

■ Fluid compartments:
o Intra-cellular: 40% of body weight and 70% of body water" 100kg x 0.07 = 7 L of water"
• C,ystalloids can increases intra-cellular compartment 75% (25% intravascu/ar)

o Extra-cellular: 20% of body weight and 30% of body water

• Interstitial: 2/3 of extra-cellular compartment

• Intra-vascular (plasma): 1/3 of extra-cellular compartment

• Colloids (including blood} can increases intra-vascular compartment 100%

• Trans-cellular
• CSF, P leural fluid, Synov
, ial fluid, Peritoneal fluid

Athlete male need more fluid maintenance than obese male

Major Cation/Anions
Cation/+\ Anion 1-l
Extra-Cellular Na Cl
Intra-Cellular K P04

■ F luid spacing:
o 1•• spacing: intracellular and extracellular fluid compartments

o 2nd spacing: excess accumulation of fluid in interstitial spaces (edema}

o 3rd spacing: accumulation of fluid in "no fluid" areas such as ascites, and in burns
A sudden weight gain or loss is best indicator of fluid status
■ Osmolarity
o Number of solute per solution (mOsmol/Liter)
o Volume of plasma including volume of solutes
o Examples:
• Hypotonic solution (0.45% NS, 0.33% NS) decreases osmolarity
• Hypertonic solution (D5 ½ NS, D5 NS, DS RL) increases osmolarity

■ Osmolality
o Number of solute per solvent (mOsmol/Kg)
o Weight of the plasma without solutes
o The principal determinants of osmolality are the concentrations of sodium, glucose, and
urea that dissolved in the fluid
o Determined by (Albumin and Na)
• Proteins: determine plasma/interstitial osmotic pressures
• Na: determines intracellular/extracellular osmotic pressure
• Hypernatremia: ! Extracellular fluid volume as in dehydration, DI
• Hyponatremia: l Extracellular fluid space as in over-hydration, SIADH

■ Pressures
o Colloid osmotic "Oncotic" pressure (Pulling force)
• lntravascular -+ Interstitial tissue
• Determined by Proteins
Decreased in hypoalbuminemi.a leads to tissue edema

• Highest in Capillary (Venous)

Oncotic pressure 25 mm Hg > Hydrostatic pressure 18 mm Hg

o Hydrostatic pressure (Pushing force)

• Interstitial -+ lntravascular
• Highest in Capillaries (Arterial)
Hydrostatic pressure 35 mm H g > Oncotic pressure 25 mm Hg
IV FLUIDS
■ Highest temperature for IV fluids should be < 65 degree centigrade

■ Crystalloids :
o 75% will distribute into extracellular (interstitial compartment)
o Only 25% will stay intravascular due to Hydrostatic pressure > Oncotic pressure
o Hypotonic solution (Dextrose 5%) distribute into intracellular

0.9% Normal Saline RinQer Lactate

Na 154 and Cl 154 Na 130 Cl 109 K 4 Ca 3 Lactate 28
Hvperosmolar, isotonic pH 5.5 Hvooosmolar, isotonic, pH 6.5
Osmolaritv = 308 Osmolaritv = 270
Most Acidic solution Leads to + Apoptosis & inflammatory response
Leads to +Hyperchloremic metabolic Acidosis � Metabolic Alkalosis

Ringer lactate metabolized by liver to sodium

bicarbonate + metabolic acidosis in liver failure
Used in: Used in:
Dehydration (vomiting, diarrhea) Post-operative Day O
Trauma with head injury: Burn and Trauma
. Instead use hypertonlc saline Pancreatic and biliary loss
Enterocutanous fistula, Diarrhea
CDF-dlarrhea lit will not cause acidosis\
- NS preferred over LR when blood is being - LR preferred over NS during initial
transfused simultaneously resuscitation {1 Metabolic acidosis)

"because citrate can lead t o calcium precipitate - LR should not be infused through same
(hypocafcemia) and coagufopathy'' IV line durina blood transfusion

■ Balanced crystalloids (Chloride level< 110): showed no! mortality or risk of AKI
■ D5 ½ NS + 20 KCI: Used in 1•1 day post-operative, and Pyloric stenosis
■ Addition of dextrose + Stimulate insulin release

■ Colloids:
o Increases intravascular volume (70% will stay intravascular)
o Albumin: Can leads to pulmonary edema
o Starch: Inhibits platelets and decreases vWF
+ Coagulopathy, and renal failure
ESTIMATES OF VOLUME REPLACEMENT
■ Dehydration physiology:
o Hypotonic fluid loss � t Serum osmolality
o Stimulation of ADH, Renin, and Angiotensin
o Inhibit ANP (Atrial natriuretic peptide)
o Resulting in:
• Vasoconstriction
• Salt and water retention
• ! Urine volume, ! Na excretion, t Osmolality
Increased extra-cellular space is a sign of over-hydration (due to t Na excretion)

■ Lactate:
o Indicator of adequate resuscitation in trauma
o Indicator for tissue perfusion / ischemia (if still high > 24 hours � PCWP)

■ UOP: Best indicator of adequate volume replacement

o End-Point of resuscitation: Base-deficit (indirect measure of COP and 02)

■ Insensible fluid losses: 10 cc/kg/day; 75% skin, 25% respiratory (around 600 ml)
o Average stool loss = 250 ml of water

■ During open abdominal operations, Fluid loss is: 0.5-1.0 Uhour

■ GIT fluid secretion:

o Stomach 1 - 2 Uday
• Gastric juice: Na 60 Cl 110

o Biliary system, Pancreas, and duodenum: 500-1,000 mUday

■ GIT electrolyte losses:

o Saliva: K• (highest concentration of K• in body)
o Stomach: Wand c1-
o Pancreas and bile: HC03-
o Large intestine: K•
o Sweat: hypotonic (Na concentration 35 - 65)

■ Changes with age:

o t Residual volume
o tADH
o ! Aldosterone
 ELECTROLYTES IMBALANCE
Clinical presentation

General signs Musculoskeletal ABG ECG Associated with

tK Hypotension Muscle weakness Respiratory alkalosis WideQRS Nausea
Arrhythmia Peaked T
Seizures Muscle spasm Metabolic acidosis Flat P waves Vomiting
Prolong PR
Fatigue Elevated ST Diarrhea

Flaccid paralysis Oliguria

lorogressive ascendina\
!K Bradycardia t Deep tendon reflexes Metabolic alkalosis Flat / inverted T Constipation
Arrhythmia
Hypertension Muscleweakness Uwaves Polyuria
Confusion
Soastic oaralvsis Polvdiosia
t Na Tachycardia Ataxia, restless Dehydration
Hypertensian Muscle twitching
Fever Tonic spasm Edema
Delirium f Deep tendon reflexes
Cama
! Na Tachycardia Weakness, fatigue Enterocutanous fistula
Diarrhea
Orthostatic Muscle spasm Cerebral edema
hypotension Oliguria
t Deep tendon reflexes TURB procedure
Seizure
t Ca Bradycardia Muscle weakness Respiratory alkalosis WideQRS Hyper PTH
Dehydration (Hyperventilation) ShortQT Pancreatitis
Weight loss t Deep tendon reflexes Depressed ST Malignancy
Constioation
! Ca Bradycardia f Deep tendon reflexes ProlongQT Diarrhea

Arrhythmia Perioral numbness

Seizures Fingertips, toes tingling

Carpopedal spasm

Tetanv. Convulsions
t PO, High anion gap Malignancy
metabolic acidosis
Crush iniurv
! PO, Respiratory alkalosis Refeeding syndrome
(Hyperventilauon)
Hvoerglycemia
t Mg Hypotension t Deep tendon reflex WideQRS
Cardiac arrest
Prolona PR
! Mg Hypertension t Deep tendon reflexes ProlongQT Constipation
Arrhythmia
Tetanv TallTwave lieus
POTASSIUM (Normal 3.5 - 5)
■ Daily K requirements: 3500 - 4700 mg (0.5 -1.0 mEq/kg/day)
■ Usual recommendation rate of IV K replacement: 10 - 20 mEq / hour

HYPERKALEMIA
■ Causes:

Excess release from cells Decreased elimination Medications Others

Blood transfusion Renal failure NSAIDs Excess intake
Rhabdomvolvsis I Aldosterone: K-Soarina diuretics
Tumor lvsis svndrome ■ Addison's ACEi
Metabolic acidosis ■ Congenital adrenal Digoxin
/throuah exchanae of H' with Kl hyperplasia
Hemolvsis Beta-blockers

■ Management:
o < 6.5 meq/L:
� Kexalate 15-30 g PO every 4 - 6 hours or as enema
• Polystyrene sulfonate is K binder to excrete more potassium
• Used in emergency if other modality failed and hemodialysis can't be done
• Contraindicated in patient receiving opioids, bowel disease or obstruction,
can lead to intestinal necrosis

o Acute management:
• Diuretics
• Used as concurrent treatment in emergency with preserved renal function
• Used with NS maintenance if patient not hypervolemic
• 40 mg of intravenous fu rosemide every 12 hours

• Hemodialysis
• Indicated in patient with hyperkalemia and severe renal impairment
• Should be done < 6 hours or use GI cation exchangers

• Rapidly acting agents

RAPIDLY ACTING AGENTS
■ Indications:
o Hyperkalemia and ECG changes
o Potassium level> 6.5 to 7 meq/L

1} Ca gluconate
o 1g infused over 2 - 3 minutes
o Rule of 10· 10 mlof 10% solution over 10 minutes
� Followed by continues calcium infusion as 0.3 - 2 mg/kg/hr
o Calcium gluconate (membrane stabilizer for heart) without reduction of serum K level
o Ca Chloride need central line (thrombophlebitis)
o Cardiac monitor

2} Insulin with glucose:

o 10 units of regular insulin in 500 mlof D10, given over 60 minutes
o 10 units of regular insulin, followed by 50 ml of D50 (25 g of glucose)
� Greater reduction, but more risk of hypoglycemia
o Insulin should be given alone if the serum glucose is .:250 mg/dl
o Close monitoring of blood glucose

3} B2 agonists:
o Salbutamol (Albuterol) 10 to 20 mg in 4 ml of saline by nebulization over 10 minutes
HYPOKALEMIA
■ Causes:

Increased losses Urinarv loss Others

Vomiting Diuretics Inadequate intake
Diarrhea t Aldosterone level: Low Mg level
■ Cushing's (due to concurrent loss)
■ Conn's
Excess sweatina Hvoothermia

■ Clinical presentation:
o Muscle weakness
o Nephropathy
o Glucose intolerance
o Metabolic alkalosis
� by increased excretion of K with HCO3
� by increased exchange of K with H'

o ECG changes: U waves, Depress ST wave

■ Management:
o Correct the Mg first

o 3,0 to 3.4 meq/L;

� Orally KCI 10 to 20 meq 2 - 4 times/day (20 to 80 meq/day)

o < 2.5 - 3 meq/L or Symptomatic:

� Orally KCI PO 40 meq 3 - 4 times/day

� IV KCI 20 meq in 200 ml of NaCl over 2 hours

• Rate should not exceed 10 meq/hr (peripheral line-+ phlebitis)

o Potassium-sparing diuretics used in potassium wasting patients

o Cardiac monitor

o Use HCOa in case of metabolic acidosis

 SODIUM (Normal 135 - 145)
■ Daily Na requirement: 1 - 2 mEq/kg/day
■ Avoid Na in Cirrhosis (Sodium retention by the kidney increases the ascites)

HYPERNATREMIA
■ Causes:

Water loss Urinary loss Hiah volume Others

Skin losses Osmotic dieuresis Hypertonic saline Restrict water intake
Gastrointestinal losses Diabetes lnsipidus Salt poisoning Post-operative
(due to transient increase in ADHJ
Acute tubular necrosis 1Aldosterone level:
■ Cushing's
■ Conn's
■ Management:
o NaCl to correct High Na slowly to avoid cerebral edema

o Free water for hypovolemic patient with urine osmolarity > 800
• Restrict water intake (! UOP)
• Osmotic dieuresis (t UOP)

o DDAVP for Central Diabetes lnsipidus

o Treat the underlying cause for Nephrogenic Diabetes lnsipidus

HYPONATREMIA

■ Assessment:
1) Serum Osmolality
• lsotonjc (280 - 295 mOsm/kg) "Pseudohyponatremia"
-+ Hyperprotienemia / Hyperlipidemia

• Hypertonic (>295 mOsm/kg)

-+ Hyperglycemia / Mannitol / Radiocontrast agent

• Hypotonic (<280 mOsm/kg)

2) Volume status (Used for hypotonic osmolality)

• Hypovolemic
o Urine Na>20-+ Renal causes ( Diuretics, ACEi, Nephropathy)
o Urine Na<20-+ Extra-renal (lleostomy, Dehydration, Vomiting, Diarrhea)

• Euvolemic
o SIADH, Glucocorticosteroid deficiency
o Diuretics, Hypothyroidism, Postoperative, Polydipsia

• HypervoJemjc
o Urine Na>20 mEq/L-+ Renal failure
o Urine Na<20 mEq/L-+ Heart failure, Cirrhosis, Nephrotic syndrome

■ Management:
o Correct Low Na slowly to avoid central pontine myelinosis ( no more than 1 mEq/h)
o NaCl or 3% NaCl
o Fluid restriction if f ADH

DIFFERENCES BETWEEN SIAOH ANO 01:

AOH Serum Na Urine Na Urine Gravity Management

"1'.!l!M la QQZ: Osmolality· Osmolality
CT
t
SIAOH
/J UOP)
l
J l Fluid restriction

!
i ! !
Diabetes lnsipidus D5 Water
(t UOP) DDAVP
SIADH caused b)l: Lung_ cancer. meniag_itis, infection, Drugs: ciQrofloxacin, ox'iJ_ocin

SIADH differentiated from adrenal insufficiency by! K

CALCIUM
HYPERCALCEMIA
■ Causes:

Hyperparathyroidism
l PTH
Druo-induced {e.Q. lithum)
Hyperthyroidism
Thiazide diuretics
Addison
t PTH Sarcoidosis
Neoplasm
■ Osteolytic malignancy
■ lvmohoma
Most common cause of hvnercalcemia Hvneroarathvroidism
Most common cause of out-oatient t Ca Hvr>erDarathvroldlsm
Most common cause of in-oatient t Ca Osteolvtic m alianancv
Most common cause of hvnArcalcemia crisis Metastatic Mallanancv
Most common malianant cause of hvoercalcemia Breast cancer
Most common mortalih, risk of hvnercalcemia in SCLC

■ Treatment·
o >14 mg/dl (3.5 mmol/l): IV Normal saline
NaCl 200 to 300 mUhour and maintain urine output at 100 to 150 mUhour

o Fursomide 40 mg over 2 hour

o IV Bisphosphonate / Calcitonin/hydrocortisone
• Both are used in malignancy or severe acute
• Inhibits osteoclastic bone resorption

o Dialysis

■ No lactated Ringer's or thiazide diuretics in Hypercalcemia

HYPOCALCEMIA

■ Localized numbness I tingling in hypocalcemia due to:

o Peripheral vasoconstriction
+ Decreasing the action potential of the digits due to decreasing the threshold
+ Perioral numbness and digits tingling
■ Localized numbness I tingling in local anesthesia toxicity due to:
o High concentration of local anesthesia in highly vascular tissue on free nerve endings

■ Signs:
o Chvostek's sign:
• lpsilateral facial twitching
• Induced by tapping at point 1 cm anterior to ear (tragus) and 2 cm below
zygomatic bone

o Trousseau's sign:
• Carpal spasm due to neuromuscular excitabilijy
• Induced by inflation of BP cuff 20 mmHg above patient's systolic BP for 3 min
• Positive: Flexion of metacarpophalangeal joint with extension of distal
interphalangeal and finger adduction

■ Causes:

Hypoparathyroidism
! PTH
Abnormal Ma+
Chronic renal> failure (Uremia)
t PTH
Liver disease 11 Vitamin Ol
Pancreatitis
Variable Rhabdomyolysis
Tumor lvsis svndrome
Hyperventilation � Respiratory alkalosis
Respiratory alkalosls
� Increase calcium-albumin bindina (redistribution/

■ Management:
o ECG + Check Mg level
o Check Albumin level

o Oral Calcium carbonate 1250 mg PO TID

• Non-symptomatic patient with Calcium > 8 mg/di

o Oral Calcium carbonate 2500 mg PO TID

• Mild Symptomatic or Calcium < 8 mg/dL

o IV Calcium gluconate 2 g IV over 1 h infusion

• Severe Symptomatic (Seizure, tetany, stridor, laryngospasm)
• Calcium < 4 mg/dL
PHOSPHOROUS

HYPERPHOSPHATEMIA
■ Causes:
o Low Urine P04 < 1500:
• Renal failure (Most common cause) � High anion gap metabolic acidosis
• 1 PTH

o High Urine P04 > 1500:

• Rhabdomyolysis
• Tumor lysis syndrome

■ Management:
o IV NaCl + Acetazolamide
o Dialysis in renal failure
o P04 binder (in chronic): Sucralfate

HYPOPHOSPHATEMIA
■ Causes:
o Refeeding syndrome (Most common cause)
o i PTH
o t Vitamin D
o 1 Ca level
o GI loss
o Rhabdomyolysis

■ Conseouence·
o Prolong Ventilation
o Hyperglycemia

■ Management·
o For Phosphorous level <0.5 mg/dl: 0.5 mmol/kg IV infused over 4-6 hr

o For Phosphorous level 0.5-1 mg/dL: 0.25 mmol/kg IV infused over 4-6 hr
MAGNESIUM
HYPERMAGNESEMIA
■ Causes:
o OKA
o t PTH
o Addison
o Renal failure
o TPN

■ Management:
o Stop magnesium, ECG
o IV calcium chloride or gluconate

HYPOMAGNESEMIA
■ Causes:
o Most common cause of in-patient: Diuretics (Thiazide, Amphotericin B)
o Most common cause of out-patient: Alcoholism
o Most commonly associated with:
• Dietary deficiency, GI loss, OKA, ! K ! P04 ! Ca, Hypothyroidism

■ Management:
o Unstable (arrhytmia) -+ 1 - 2 g MgS04 over 2 - 15 minutes
o Stable (symptomatic)
• Severe < 1 mg/di or 0.4 mmol/L or 0.8 meq/L:
1 - 2 g MgS04 in 50 to 100 ml of D5W over 1 hour followed by infusion of 4 - 8 g
MgS04 over 12 to 24 hours

• Mild> 1 mg/di or 0.4 mmol/L or 0.8 meq/L:

Mg Oxide 400mg every 12 hours
ABG
■ Normal level:
o pH: 7.35- 7.45
o HC03: 22 - 26
o PaC02: 35 - 45

■ Calculation:
o Respiratory: ! pH : t PaC02
o Metabolic: ! pH : ! HC03

METABOLIC ACIDOSIS
■ Most common acid-base disorder(! pH with ! HC03 or t H+}
■ High anion gap acjdosjs· OKA, isoniazid, lactic acidosis, salicylates, renal failure/ uremia,
Alcohol
■ Normal anion gap acidosis: Duodenal and small bowel fistulas, Pancreatic fistula, lleostomy,
Normal saline, and Severe diarrhea
o Drugs associated with normal anion gap acidosis: Spironolactone & Lactulose

METABOLIC ALKALOSIS
o Due to:
o t H+
o t HC03 (Caused by citrate in massive blood transfusion)
o Contraction alkalosis(Most common)
• By indirect gaining of HC03 through loss of HC03-free water
• As diuretics or GI losses guided by Aldosterone which leads to
• Reabsorption of Na, Water, and HC03
• Excretion of K and H+

• Most potent stimulator for aldosterone release in injured patient: ACTH

Followed by: Extracellular fluid K

o Nasogastric suction, Vomiting and Gastric fistula results in:

� Hypochloremic, Hypokalemic, Metabolic alkalosis, and paradoxical aciduria
• Stomach losses H+ and Cl + Hypochloremic metabolic a/ka/osis
o Due to high loss of H+ and Cl with obstructed pylorus
• Kidney excrete NaHC03 (Alkali} to compensate alkalosis
• Kidney compensate Na losses by reabsorption of Na and excretion of K
and H+ + Hypokalemic aciduria
• Paradoxical aciduria:
o Contradictory term because kidney excrete acid (H+) instead of
alkali during metabolic alkalosis due to Na losses

■ Resuscitation with NS leads to hyperchloremic metabolic acidosis

BASE EXCESS
o Normal level: (-2) - (+2)
o Base excess: > +2
o Amount of acid required to restore 1 liter of blood to normal pH 7.4
o Metabolic alkalosis

BASE DEFICIT
o Base deficit: < -2
o Amount of alkali required to restore 1 liter of blood to normal pH 7.4
o Metabolic acidosis

SUMMARY OF THE CAUSES OF ACID-BASE IMBALANCE

Acid-base Caused bv
Metabollc acidosis HighAGAP NormalAGAP
IMost/v medical causesl IMost/v sumica/ causesl
Renal failure, Uremia Small bowel and duodenal fistulas
(l PO4)
High-output Pancreatic fistula
DKA
lleostomy
lsoniazid
Normal saline
Laclic acidosis
Severe diarrhea
Late NSAIDs
Late sepsis Addison's (l K}

Alcohol l PTH

Drugs:
Lactulose, Spironolactone
Sulfamvlon, Prooofol
Metabollc alkalosis Gastric fistula
Conn's (t K, Aldosterone}
Cushing syndrome
Diuretics (Thiazlde)
Vomiting or Nasogastric suction
Ringer Lactate
Massive blood transfusion
Respiratory acidosis Hypoventilation
! Minute ventilation (Respiratory rate x Tidal volume)
CNS deoression
Respiratory alkalosis Hyperventilation
t Minute ventilation (Respiratory rate x Tidal volume)
! PO4, l Ca, t K (c:> lead to l K)
Early PE
Early S epsis
Earlv NSAIDs
 DIURETICS
Aldosterone
Antagonist
■ Spironolacton
■ Amiloride
■ PTH
------------------

Proximal Tubule Proximal Mid Distal

,----------------
Osmotic diuretics ', ....,,
..,. E11ter K : Distal tubules
(Reduce absorption of , -+ Exit Na, Cl
o I

Na,H20)
■ Mannitol ■ Thiazide
■ ----------------•
I

-----------------------·
Acerazolamide

Loop of Henle
Descending thin limb (permeable to : Ascending thick limb (permeable 10 : -------------------,
wate,) : salt) ,I Aldosterone
: Competition with Cl -+ Na/K block ,
•
, Antago111st
■ Osmotic diuresis (Mannitol) : ■ Loop diuresis (Furosemide) 0
I : ■ K+ sparing diuretics
I
I ■ ADH
0 I
I
I
L----------------------------! L------------------'

o Loop diuretics are contraindicated in rhabdomyolysis

o Acetazolamide: ! K, Metabolic acidosis
o Furosemide: ! K, Ototoxic, Nephrotoxic
o Thiazide: t K, Metabolic alkalosis (Contraindicated in t Ca or ! Na)
o Spironolactone: t K, Metabolic acidosis

CONTRAST-INDUCED NEPHROPATHY
o Increase of serum creatinine 25% from baseline after contrast given within 48 - 72 hours

Pcevention-
o IV fluid with NS started 6 - 12 hours pre-procedure and continue for 24 hours post-procedure
at rate 1 - 1.5 ml/kg/hour (Most effective method)
o N-Acetylcystein: 1200 mg twice daily pre-procedure and the day of procedure
o Low cost, no adverse effect and potential beneficial effects
o Use iodixanol (iso-osmolal), low-osmolal contrast, or non-ionic contrast
o Sodium bicarbonate
o Avoid diuretics
o Renal-replacement therapy
 EQUATIONS

Normal level
2 Na � K + Glucose + BUN 280-295 mg/di
Plasma osmolarlty 18 2.8
0.6 kg x(Na/140) - 1 0. 6 used in male
Water deficit 0.5 used in female
Na-140/140 xTotal bod water Some used TBW instead of IBW
0.6 kg x(140-Na)
Na deficit Total body water:
50% in men an 40% in women

Na+ 1.6 x (Glucose level-100) / 100

Corrected Na For every 100 mg/di increased of glucose above normal (100 mg/di)
Na will decrease b 1.6 - 3 mE
Ca+ 0.8 (4-Albumin) -+ Mg/di
Corrected Ca
Ca+ 40-Albumin -+ Mmol/1
0.4 kg x(3.5 - K) ! K by 0.3 mEq/L for every 0.1
increase of H above normal

Serum albumin -Ascitic fluid albumin < 11g/L: Non-PHTN causes

SAAG > 11 : Portal HTN
= Cardiac output (HR xSV) x SVR Most sensitive for Shock
MAP o Diastole+ 1/3 Pulse pressure (S - D)
o Diastolic+ (Systolic - Diastolic) I 3)
o 2 Diastole + S tole I 3

COMMONLY USED UNITS CONVERSION

From To

Weight Kg x2.2 Lb

Albumin g/dl x10 g/L

Bilirubln mg/di X 17.1 umol/1

mg/di x0.25 mmol/1

Calcium
mmol/1 x4 mg/di
mg/di x88.3 umol/1
Creatinine
Umol/1 X 0.013 mg/di

Glucose mmol/1 x18 mg/di

TUMOR LYSIS SYNDROME
o Release of purines and pyrimidines -+ f PO..., f K, f Uric acid, l Ca (Don't give Ca)
o Mediated by cytotoxic T cells
o Leads to renal failure

SUMMARY OF SOME ELECTROLYTES CHANGES

- -
K Na Ma PO• Ca Uric acid
Tumor lysls syndrome l l 1 l
No reolacement
Refeeding syndrome ! i ! l -
Acute Renal failure l ! - Monitor
t -
Nutrition
Reviewed by:

Dr. Mohammed Al Duhileb

NUTRITION
■ Most common nutritional allergy: Nut
■ Most common nutrient deficiency: Iron
■ Most common trace element deficiency: Zinc
■ Protein requirement: 0.8 - 1.5 g/kg/day
Mean: 1.2 g/kg/day with 20% ofessential amino acids
o Mild stress: 1 - 1.2 g/kg/day
o Moderate stress: 1.3 - 1.5 g/kg/day (hypercatabolism status)
o Critically ill patient: 1 .5 - 2 g/kg/day

■ Caloric requirements "Resting energy": 25 - 30 calories/kg/day

o Trauma, surgery, or sepsis stress increase kcal requirement: 20% - 40%
• Caloric requirements in severe injury: 30 - 40 calories/kg/day
• Caloric requirements in Extensive trauma or burn: 45 - 50 calories/kg/day
o Pregnancy increases kcal: 300 kcal/day
o Lactation increases kcal: 500 kcal/day

■ Nutrition in Bums:
o Calories: 25 kcal/kg/day + (30 kcal/day x % burn}
o Protein: 1-1.5 g/kg/day + (3 g x % burn)

■ Calories of macronutrient:
o Fat 9 kcal/g
o Protein 4 kcal/g
o Carbohydrates 4 kcal/g (dextrose 3.4 kcal/g)

Calculation: How many grams of10% dextrose in 1 liter:

10% = 10g I 100ml
so, 100g 11000ml � 100 grams

Calculation: How many calories in 100 grams ofdextrose:

1g = 3. 4 calories x 100 gram = 340 calories

Calculation· How many calories are needed per day for 70-kg person:
70 kg x 25 calories = 1800 calories I day

Calculation: How many calories per day in 70-kg person receiving 5 qlkg/day of carbohydrate.
0.6 glkqlday oflipids and 0. 2 qlkqlday ofnitrogen:
6. 25g ofproteins = 1 g ofnitrogen
(5 x 4) + (0.6 x 9) + (6.25 x 0.2 x 4) x 70 kg= (2128) - 2100 kcal/day

Calculation: How many grams of glucose are needed daily to maintain optimal nitrogen
balance tor the above person:
1800 calories I 4 gram = 450 g of glucose daily

Calculation· How many grams offatin the 2so ml of 20% lipid solution
20% = 20g I 100 ml (250 ml I 100 = 2.5)
2.5 x 20g = 50 grams offal
 ■ Harris Benedict equation calculates "Resting metabolic rate" based on
o Weight, Height, Age, and Gender

■ Best predictor of Resting metabolic rate in critically ill: Penn State 2003 equation
■ Fever increases basal metabolic rate {10% for each degree above 3s.o•c)

■ Nutritional assessment:
o Pre-albumin: Half-life: 24 hours (Most accurate test)
• Retinol-binding prealbumin: Shortest half-life (12 hours)
o Albumin: Half -life: 18 days
o Transferrin: Half-life 8 - 9 days
• Transferrin: transporter of iron
• Ferritin: storage form of iron

CARBOHYDRATE DIGESTION
■ Begins with salivary amylase
o Sucrose = fructose + glucose
o Lactose = galactose + glucose
o Maltose = glucose + glucose

■ During starvation
1) Glycogenolysis

2) Gluconeogenesis done by Liver and Kidneys only /Alanine)

• Gluconeogenesis occurs in Kidneys only (not liver) in: Late starvation
• Glucose produced by gluconeogenesis not used by: Skeletal muscle and Bone
• Primary source of fuel during acute starvation:
• < 1 week: Fat
• > 1 week: Ketones

3) Lipolysis (after 24 - 36 hours)

• Fat "Ketones" (by G6P = not found in muscle)
• Main fuel uses by the brain, heart and skeletal muscles

• Lactate is released by glycolysis {Skeletal muscles, RBCs, WBCs) and used by

liver to be converted to glucose via Cori cycle

■ Obligate glucose users:

o Brain ➔ Switches to ketones in > 48 hours starvation and > 3 weeks in most organs
o Adrenal medulla
o Peripheral nerves
o RBCs& WBCs
RESPIRATORY QUOTIENT (RQ) CO2 produced
■ RQ measures energy expenditure =
02 consumed
Process Resoiratorv Quotient
Letosis and fat oxidation lstarvinn\ < 0.7
Fat utilization 0.7
Protein utilization 0.8
Normal /Balanced feedina l: 0.825
Carbohvdrate utilization 1
Lipogenesis (Overfeeding) >1
- Increases risk of infection
- Ventilator problems
0 ! alucose, t fat -+ ! Minute ventilation

POSTOPERATIVE PHASES
■ Catabolic phase "Day O - 3" (negative nitrogen balance) "! Lean body mass"
o Lean body mass: Fat-free body weight {decreased in catabo/ic phase and critical ill)

■ Diuresis phase "Day 2 - 5"

■ Anabolic phase "Day 3 - 6" (positive nitrogen balance)
FAT DIGESTION
■ 90% of fat in body in forms of: Glycerides
■ Glycerides, Cholesterol, lipids are digested by lipase, bile salts, and cholesterol esterase
� Forms Micelles (Micelles contains long-chain FAs, Fat-soluble vitamins)

■ Micelles + chylomicrons + lymphatics

o Long chain fatty acids enter enterocyte by membrane fusing + Lymphatics
o Short chain fatty acids enter enterocyte by simple diffusion + Portal vein
■ Essential Fatty Acids: Linoleic (Omega 6), Linolenic (Omega 3), Arachidonic
o Not synthesized by body
o Used for prostaglandin synthesis

■ Short-chain fatty acids: Acetate (Acetic acid), Propionic acid, Butyric acid
o Main nutrient of colonocytes

■ Insulin inhibits lipolysis (Anabolic: t Lipid and protein)

AMINO ACIDS
■ Fuel during sepsis: Only amino acids
■ Only amino acids to increase during times ot stress: Alanine and phenylalanine

■ Simplest amino acid precursor for gluconeogenesis: Alanine

■ Primary substrate for gluconeogenesis: Alanine

■ Amino acid that enhances immune system: Glutamine

■ Amino acid that enhances immune system in critical ill patient: Arginine

■ Most common amino acid in bloodstream and tissue (most abundant): Glutamine
o Glutamine produced by lung in liver failure
o Glutamine increases intestinal cellularity + Enhance bowel absorption
o Glutamine is the fuel of Enterocytes and Cancer cells

■ Aromatic Amino Acids: Tyrosine, Tryptophan, Phenylalanine

■ Branched-chain amino acids: Leucine, lsoleucine, Valine
o Only A.A metabolized outside the liver (in muscle)
o All are essential amino acids
• Other essential amino acids: Arginine, Phenylalanine
• Non-Essential amino acids: Glutamine, Alanine
NITROGEN BALANCE
■ 6.25 g of protein contains 1 g of nitrogen
■ 6 .25 g of protein = 25 g of glucose = 4 kcal
■ Non-protein calories : Nitrogen (NPC:N}
o Normal -+ 150:1 (Range: 100:1-200:1)
o Moderate stress -+ 120:1
o Severe stress -+ 90-120: 1
o Burn .+90-100:1

Calculation: What is NPC:N in 2000 calories with 100qproteins

100 g x 4 = 400 calories
2000 - 400 = 1600 non-protein calories
100 g I 6. 25=16 grams of nitrogen
NPC 1600/16=100
NPC·N=100:1

Calculation: How many grams of protein needed for 70kg to maintain Normal NPC:N f150:1l
1) 70 kg x 25 = 1750 kcal I day
2) 17501150 = 11. 6 g of nitrogen needed daily
3) 11. 6 x 6. 25 = 72 grams of protein needed to maintain 150:1 (NPC:N)

Calculation: How many grams of protein needed for a person taking 450g glucose daily to
maintain Normal NPC:N (150:11
1) 450/25=18
2) 18 x 6.25 = 112 grams of proteins

■ Nitrogen balance= (N in-N out)

o Nitrogen In = protein/ 6.25
o Nitrogen Out = 24 hour urine N + 4 gram

■ Positive N balance (anabolism): by increasing protein diet

o Hypokalemia -+ Glycosuria -+ potential effect

■ Negative N balance (catabolism}

■ Total protein synthesis for a healthy, normal 70-kg male is 250 glday
o Urea production from liver to get rid of ammonia from amino acid
o Majority of protein breakdown from skeletal muscle into Glutamine and Alanine
ENTERAL NUTRITION
■ Best to start feeding by enteral nutrition as long no contraindications as early as 24 hours
■ Modes of feeding:
o Bolus: used for gastric feeding by hypertonic feeds at higher rate
o Intermittent: used for post-gastric feeding
• Should be started as soon as possible
o Continuous: have risk of aspiration and should stopped overnight
• Used in initiation of feeding in critical ill patients

■ Route of tube feeding:

o Short-Term:(< 4 weeks)
• Nasogastric: for patients with functional stomach and low risk of aspiration
• Nasoenteric - Post-pyloric: for sepsis, pancreatitis, GERD, aspiration, proximal
fistula, and prolong feeding, br.ain injury with gastroparesis (usually first 3 days)

o Long-term: {> 4 weeks)

• Gastrostomy: for mechanical obstruction , swallowing dysfunction, and long
term failure of intestinal function (short bowel, fistula), Maxillofacial injuries
• Jejunostomy: for patients with aspiration risk or dysfunction gastric motility
{as patients with head injury}

■ Prevention of aspiration with enteral feeding:

o Always elevate head 30 degree
o Hold feeding if residual gastric volume> 200 ml {check every 4 hours}

■ Types of enteral formulas:

o Monomeric (Elemental)
• Small molecular weight compounds
• Contains individual amino acids, glucose polymer and low fat with 2 - 3% long
chain triglycerides (LCTs}

o Oligomeric (Semi-elemental)
• Contains peptides with varying chain length, primary as medium chain
triglycerides

o Polymeric
• Contains intact proteins, complex carbohydrates and mainly LCTs

o Specialized formula

■ Using of enteral formulas·

o Initial Enteral formula for surgical pati,ent: Low-residue isotonic formula

o Formula for patient NPO > 7 days witlh functioning GIT: Elemental formula /Monomeric)

o Formula for pancreatic disease: Polymeric

o Formula for renal dysfunction: Nepro, Suplena

o Formula for liver disease: NutriHep
o Formula for hypoalbuminemia: Ensure +
o Formula for diabetic patients: Glucerna
 ■ Gastrostomy techniques:
o Types: Temporary or Permanent

o Methods:
• Open (Direct, Roux limb)
• Laparoscopic
• Endoscopic (PEG tube)
• Needle-catheter gastrostomy or jejunostomy

o Surgical techniques:
• Stamm: serous-lined temporary method with inversion of gastric wall
• Depage-Janeway: mucus-lined permanent method with horizontal flap
• Witzel: either transverse or longitudinal (used for feeding jejunostomy tube)
• Tave!

o Site of gastrostomy:
• At midpoint of stomach close to greater curvature

Fig. 20 • 21 : Summ g,,suost'Omy is a ampor,1,y Cattl'OSlOl'l'lj Fig. JO,:U: W\uel's lempOf8ry gallfOSIOmy.

Ga!itr�tomy
Upper sire Po:;ierior wall
mldlint gastric mucosa
irw;ision
--+ --+

Horizontal fastric Aap Raised flap with base

at greater curvature

Abdominal wall

In

Gasttostomy tu� rS placed

afong the flap into the gastric: h.,m•n Ant«ior g,utric wall and tube flap
End of the tastric tube flap is broud1t
are sutured around the ga.strOStomy tube
out through � !l.eparate wound �d is.
Figs 20 • 25 A itnd 8: J.\ne....-ay',s pernunent gastrostomy suturl!d to the skin iHf,ge
TOTAL PARENTERAL NUTRITION
■ Most common indications for TPN:
o Nonfunctioning GIT (short bowel syndrome, intractable vomiting, or diarrhea "IBD")

o Need for bowel rest (severe pancreatitis, enterocutaneous fistulas, prolonged ileus)

o Severe malnutrition (e.g. TPN pre-op if weight loss> 20% during last 6 months)
• TPN is given 7 days pre-operative

o NPO > 7 days with no plan for enteral feeding

■ Nutritional requirements for average adult male: 20% Protein+ 30% Fat+ 50% Carbohydrate

■ Peripheral line TPN: Fat-based with low-osmlarity solution (for< 1 week)

o Maximum lipids infusion: 2.5 g/kg/h

■ Central line TPN: Glucose-based (for> 1 week)

o Maximum glucose infusion: 5 g/kg/h (Add insulin if patient having hyperglycemia)
o Can be inserted by PICC line

■ TPN weaning rate = 50 ml/ hour

Lipid emulsions
■ 10% lipid solution contains 1.1 kcal/cc

■ 20% lipid solution contains 2 kcal/cc

Calculation: How many grams of fat in the 250 ml of 20¾ lipid solution
20% = 20g 1 100 ml (250 ml l 100 = 2.5)
2.5 x 20g = 50 grams offat

Calculation: How many Kcal in 500 ml of 10% lipid solution:

500 X 0.1 = 50 9 fat
50 x 9 = 450 kcal

Calculation: How many calories for patient receiving 1000 ml bag of TPN contains 10% of
dextrose and 7% of proteins and also receiving 250 ml of 20% fat emulsion:
Dextrose: 101100 x 1000 = 100 gm x 3. 4 = 340 calories
Proteins: 71100 x 1000 = 70 gm x 4 = 280 calories
Fat: 201100 x 250 = 50 gm x 9 = 450 calories
Total: 1070 calories

Calculation: Create TPN for healthy 70 kg patient

1) Calculate fluid amount (30 ml x 70 kg) = 2100 ml

2) Caloric requirement: 30 x 70 = 2100 kcal I day

Use IBW for this person (70kg for example)

3) Protein requirement: 1 x 70 = 70 g I day x 4 = 280 kcal I day

4) Remaining= 2100- 280 = 1820 kcal/day

70%(1260 kcal/day) CHO

1260 kcal I 3.4 = 370 glday

30% (540 kcal/day) Lipids

420 kcal I 9 = 46.6 glday
Lipid emulsion 20% contains: 1000 kcal in 500 ml (500 x 2)
Lipid emulsion 10% contains: 550 kcal in 500 ml (500 x 1. 1)

5) Measure total calories again

420 kcal (lipid) + 280 kcal (protein) + 1260 kcal (CHO) = 1960 kcal
If total amount > Total caloric requirement � Re-adjust the amount of dextrose

6) Add trace elements. vitamins and electrolytes

Vitamin K is not present in commercially prepared formula, and should be supplemented
Complications of TPN:
■ Catheter-related infection:
Type Catheter tip Blood Management
culture culture
Catheter Colonization Positive Neoative Remove catheter
Catheter-related infection Positive Positive Remove catheter+ IV Antibiotics

o Positive result:
• > 1000 CFU (quantitative method) or> 15 CFU (semiquantitative method)
• Most common organism: Staphylococcus epidermidis
• Most common early organism: Staphylococcus aureus

o Least risk of infection: Subclavian line

o Highest risk of infection and DVT/PE: Femoral line

■ Metabolic complications
o Most common electrolyte disturbance: ! P04

o Hyperglycemia
• Maintaining of glucose< 110 mg/dl improves mortality and reduces infections

o Refeeding Syndrome
• l PO., l K, J Mg, j Na
• Prevented by starting feeding at a low rate (10-15 kcal/kg/day)

o In renal failure you should -+ ! K, ! Proteins

o In respiratory failure you should -+ ! Carbohydrates

■ Acalculous Cholecystitis

■ Cholestatic liver disease: within 1 - 2 weelks (reversible)

■ Cholestasis: within 2 -4 weeks (irreversible)

o Management: Change to hepatic formula and l Lipid content of TPN

■ Acid-base abnormalities: {Hypercapnia)

■ Gastrointestinal atrophy
o Enteral feeding is better to prevent bacterial translocation
OTHERS

NUTRITIONAL DEFICIENCIES

Nutritional deficiencv Comolication

Chromium .. cemia and neurooathv
Selenium Cardiomvopathv
Conner Pancvto=nia
Zinc Poor wound healing, Diffuse Dry eczematoid rash,
Loss taste sensation skin & hair oroblems. and oeri-oral rash
Essential fatty acids (Lineolic acid) Reddish dermatitis (Scaly acrodermatitis), Alopecia, vision
chanoes Thrombocvtooenia
Vitamin B 1 (Thiamine) Encephalopathy, Cardiomyopathy, and Thigh numbness
More with Billroth sumerv
Vitamin 86 /Pvridoxine) Anemia Glossitis and Neurooathv
Vitamin 812 (Cobalamin) Beefy tongue, anemia, Peripheral neuropathy
More with crohn disease with S80
Vitamin 83 /Niacin) /Pellaora I: Diarrhea Dermatitis Dementia
Vitamin C (Ascorbic acid) Scurvy
- General weakness
- Anemia
- Gingivitis
- Skin hemorrhaae

■ Types of roalovlcilioo·
o Marasmus: inadequate protein and caloric intake
o Kwashiorkor: catabolic protein loss ➔ hypoalbuminemia and generalized edema

■ Protein-sparing effect after administration of: 2 L of DSW

■ Trace elements:
o Iron, iodine, cobalt, zinc, copper, selenium and chromium

■ Propofol delivers 1 kcal/cc in the form of lipid

■ Vitamin C (Ascorbic acid):

o Cross-linked lysine and praline
o t Resuscitation volume and edema
o Increases absorption of iron
Inflammation and
Cytokines
INFLAMMATION AND CYTOKINES
GROWTH AND ACTIVATING FACTORS
■ PDGF (Platelet-derived growth factor)
o Key factor for wound healing
o Accelerate wound healing in chronic wound
o Chemotactic and activates inflammatory cells & fibroblasts

■ EGF / EPGF (Epidermal growth factor)

o Epithelialization
o Accelerate healing of donor graft
o Accelerate epithelization of split-thickness skin graft
■ PAF (Platelet-activating factor)
o Generated by phospholipase in endothelium
o Increased platelets aggregation
o Bronchoconstrictor

■ VEGF (Vascular epidermal growth factor)

o For neovascularization (angiogenesis) involved in tumor metastasis

■ FGF (Fibroblastic growth factor)

o Stimulate wound contraction

HYPERSENSITIVITY REACTIONS
■ Basophils: source of histamine in blood
■ Mast cells: source of histamine in tissue
o Release histamine & Bradykinin-+ Vasodilation

■ Types:
Tune Mediated bv Examole
I lgE -+ Mast cells & Eosinophils Penicillin allergy
(Immediate) Lymphazurin allergy
Bee stino
II lgG, lgM Hyperacute rejection
(Cytotoxic) -+ l BP, t HR, diffuse bleedinq ABO incompatibility
Ill Antigen-antibody complex Rheumatoid Arthritis, SLE
(Como/ex)
IV Delayed type hypersensitivity Vitamin K injection
(Delayed) DM type 1
TB skin test (PPD)
Crohn's disease
Delaved oenicillin allerov

NITRIC OXIDE (NO)

■ Arginine precursor-+ Activates guanylate cyclase (l cGMP)
■ Vascular smooth muscle dilation (with no decreasing of protein permeability)
o Vascular smooth muscle constriction by Endothelin
CYTOKINES
■ Cytokines derived from Polypeptide hotmones
■ Most of them produced by macrophages
■ Macrophages: dominant role in wound healing; release (PDGF) and (IL-1 and TNF-a)

Cvtokine Function
TNF-a • Most potent stinulus: lipopolysaccharide (Lipid A)
• Causes + Cachexia (increases muscle catabolism)
• Stimulate Eicosanoids (Thromboxane)
• Requlate E-Selectin
IL-1 • Causes fever postoperative (alveolar macrophages)
0 NSAIDs decrease fever by PGE2 synthesis
• Blocked bv steroids
IL-2 • Activates NK-T cells, in Renal cell carcinoma
• Inhibited bv Cvclos=rine Zenaoax
IL-4 • Activates B cells
IL-6 • Increases Hepatic Acute Phase proteins (C-reactive protein, amy1oid A)
• In SIRS and seosis
IL-8 • In ARDS. Attracts PMNs
IL-10 • Reflects severitv in trauma

ANTI-INFLAMMATORY CYTOKINES
■ IL4
■ IL 10
■ IL 13
■ TGF-B
o Increases collagen
o Inhibit T-Cells and immunosuppressor (inhibit plasminogen inhibitor)
o Important mediator for angiogenesis in wound healing

HEPATIC ACUTE PHASE

■ Increased: CRP, amyloids, fibrinogen, haptoglobin, ceruloplasmin, a-1 antitrypsin, and C3
■ Decreased: albumin, pre-albumin, and transferrin

CELL ADHESION MOLECULES

■ Selectins: "Rolling adhesion" (L - on Leukocytes, P - on Platelets, E - on Endothelium)
■ Beta-2 integrins (ICAM, VCAM) on leukocytes: anchoring adhesion "Firm adhesion"
■ � cell Adhesion
■ P53: cell Regulation
COMPLEMENT
■ Classic pathway (lgG or lgM): Factors C1, C2, and C4
■ C3: Convergence point for both pathways (Critical step: Activation C3)
■ Mg: required for both pathways
■ Anaphylatoxins: C3a, C4a, csa
■ Opsonization: C3b and C4b
■ Membrane attack complex: C5b-9b
■ Chemotaxis for inflammatory cells: C3a and C5a

CYCLOOXYGENASE (COX)
■ Produced from arachidonic precursors
■ Prostaglandins. Prostacyclin: (by endothelium)
o l Platelets aggregation
o Systemic and pulmonary vasodilation {! SVR, ! PVR)
o Bronchodilation

■ Thromboxane: (by platelets)

o Stimulated by TNF - a
o t Platelets aggregation by increasing release of calcium in platelets
o Systemic and pulmonary vasoconstriction (t SVR, t PVR)
o Bronchoconstriction

■ NSAIDs: inhibit cyclooxygenase (reversible)

■ Aspirin: inhibits cyclooxygenase (irreversible)

■ Steroids: inhibit phospholipase

LEUKOTRIENES
■ Produced from arachidonic precursors (Lipoxygenase)
c::> Vasoconstriction, Bronchoconstriction

MISCELLANEOUS
■ Thyroid hormone: does not play a major role in injury or inflammation
■ Reperfusion injury: PMNs are the primary mediator
■ Interferons: released by lymphocytes in response to viral infection
■ Platelets granules:
o Alpha:
• Fibronectin
• Fibrinogen
• Platelet factor 4
• Heparin-Induced Thrombocytopenia (HIT} due to antibodies against PF4

o Dense:
• Adenosine
• Calcium
■ Serotonin
Wound Healing and
Dressing
 WOUND HEALING AND DRESSING
■ Order of cell arrival to the wound:
o Platelets (Not true cell)
o PMNs (Neutrophils)
o Macrophages (3 - 4 days}
o Fibroblasts (Day 6}

■ Peripheral nerves regenerate at 1 mm/day

■ Epithelization occurs at rate 1 - 2 mm/day
INFLAMMATION PHASES

Phase Descriotion Time Notes

0 Vasoconstriction Dav 1
I Inflammation Day 1 -4 PMNs (Neutrophils) are the first infiltrating cells
in wound site durina first 24 -48 hours
II Proliferation & Enithelialization Dav5 2nd Week Fibroblasts acts for colla=n deoosition 1111 + II
Ill Maturation and Remodelina
f'C- --� ·--·--
3'd week - 1 81 Year Decreased vascularitv cross-linkina collaaen
_.,___, ·- •k-

■ Collagens:
Tvne Descriotion Time Most common site
I Most common, primarv collaoen in healed wound Dav 3-4 Bone, Scar Healed wound
II Cartilaae
Ill Increased in healina wounds Dav 1 -2 Vessels Healina wound
IV In basement membrane
V In smooth muscle Cornea
Diseases associated with abnormal wound healing:
• Osteogenesis imperfect: Type I collagen
• Ehlers-Danlos syndrome: type Ill collagen
• Marian's svndrome: Fibrillin defect

■ 48 hours (2 days): time for re-epithelialization

■ 3 - 4 days: time for production of collagen and starting of tensile strength
¢ At 3 weeks: maximum collagen accumulation occurs (Maturation phase)

¢ At 8 weeks: maximum tensile strength (80% only) after collagen cross-linked

■ Tensile strength: most important factor in healing closed incisions (primary intention)
o Early: Fibrin
o Late: Collagen cross-linking (inhibited by d-Penicillamine)
o Regain tensile strength rapidly: Bladder> Stomach > Colon
o Regain tensile strength slowly: Skin, Fascia, and Tendons
o Usually completed at 8 weeks, but can be gradually increased up to 2 years (80% only)

■ Epithelial integrity: most important factor in healing open wounds (secondary intention}
o Any contaminate wound > 6 hours preferable to be closed by secondary intention
o Myofibroblasts ( communicate by gap junctions} involved in wound contraction
 ■ PDF- BB showed to improve healing in DM foot ulcer
■ Weakest time point for small bowel anastomosis: 3 - 5 days
o Due to increased collagenolysis when resolving the edema
o Collagenolysis appears more in large bowel (higher risk of leakage)
o Submucosal layer has the greatest tensile strength (Ability to hold stitches)
o Serosal layer gives watertight seal (More risk of leakage in esophagus and rectum}

■ Signs of malignant transformation in a chronic wound: Overturned wound edges

■ Irrigation of lacerated wound best with Normal Saline

■ Scar revision should be delayed approximately 1 year to allow maturation.

■ Reopening of the midline scar without excision gives most rapid gain in strength than excision

Factors associated with increased wound healing

■ Moist environment
■ Tight glucose control
Factors associated with decreased wound healing
■ Local tissue infection (Most major)
o Bacterial infection (> 105 / cm2)

■ Vitamin C deficiency, Hypoalbuminemia, Malignancy, Smoking

■ Diabetes
o Several defects:
• Hyperglycemia-associated glycosylation
• Tissue hypoxia, and ! angiogenesis
• Sorbitol accumulation
• Thick basement membrane -+ Increased dermal vascular permeability
-+ Albumin deposition -+ impairs diffusion of oxygen and nutrients
o Decreased collagen and collagen maturation, decreased fibroblasts, impaired
Lymphocyte and Leukocyte

■ Steroids
o Inhibits macrophages, and t migration of macrophages
o Impair fibroblast proliferation and collagen synthesis
o Inhibits T-cell function
o t Angiogenesis
o Steroids usage should be delayed post-injury at least 3 - 4 days

■ Chemoradiation
o Free radicals -+ DNA Damage -+ loc .al fibrosis and vascular effects
o Impaired fibroblasts
o Chemotherapy least effective in wound healing if stopped > 2 weeks perioperative
o Radiation least effective in wound healing if stopped > 3 weeks perioperative

■ Tamoxifen: ! TGF-B
Nutr. itional effects
■ Vitamin A: improve the wound healing, and counteracts effects of steroids on wound healing

■ Vitamin E: increases tensile strength, but excess amount inhibits wound healing

■ Vitamin C: hydroxylation of lysine and proline in collagen synthesis

o Daily supplement 60 mg for healthy, and > 1g in cr itically ill patient

■ Vitamin D serves an immunomodulatory role in wound healing

■ Zinc deficiency results in delayed early wound healing

- Although supplement of any of the above will not promote wound healing in normal people
Vitamin A promote wound healing in normal people with no nutritional deficiency (Schwartz)

EXCESS HEALING

Hypertrophic scar Keloid

Etiolonu due t neovascularih, Autosomal dominant Tu= 1 Collaaen
Risk factors Bum. Lona standina non-healina wound Burn. Trauma
Timina 4 - 6 weeks oost iniurv (uo to 3 months\ Can an,...ars vears after iniurv
Sites On flexor surfaces uooer torso dar1< skinned On neck chest. ear lobes and shoulders
Mechanism Excessive cross-linking of collagen and chronic Altered ratio of:
inflammation Collaaen production / Collaaenase aclivitv
Collagen Collagen stays within confines of original scar Collagen goes beyond original scar
Parallel orientation of collaaen Random orientation and thick collaaen
Chanaes Mvofibroblasts. t fibroblast t collaaen Nonnal fibroblast. t TGF-B
Rearession Freauent Never
Management Pressure gannents, Silicone gel sheets Surgical excision followed by
Intra-lesion steroid injection intra-lesion steroid injection (Triamcinolone)
If suraerv indicated: minimum 1 vear

PRESSURE SORE
■ Skin injured if pressure of 60 mmHg/ 1 hour (sacral pressure 120 mmHg)
■ Stages:
o Stage I: Erythema
o Stage II: Partial thickness skin loss
o Stage Ill: Full thickness skin loss
o Stage IV: Exposed muscles or bone (beyond the fascia)
PYODERMA GANGRENOSUM
■ Neutrophilic dermatosis -+ inflammatory and ulcerative disorder
■ Most common presentation: inflammatory papule or pustule (not infectious nor gangrenous}
■ Pathogenesis:
o Neutrophil dysfunction
o PAPA syndrome
o Auto-inflammatory disorders (eg, inflammatory bowel disease and arthritis}

■ Associated with:
o Inflammatory bowel disease, lgA monoclonal gammopathy, hematoloical malignancies,
Arthritis, PAPA syndrome

■ Types:
o Ulcerative (classic): tender, inflammatory papule (lower extremities and trunk)
o Bullous: (arms and face)
o Pustular: associated with inflammatory bowel disease
o Vegetative: localized, solitary, superficial (head and neck)

■ Piagnosjs·
o Biopsy to rule out malignancy

o Major criteria (must have both):

• Rapid progression of painful, necrolytic cutaneous ulcer
• Other causes of cutaneous ulceration have been excluded

o Minor criteria (must have two):

• History suggestive of pathergy
• Association with systemic dise .ase
• Histopathologic findings (sterile dermal neutrophilia, ± mixed inflammation, ±
lymphocytic vasculitis)

■ Treatment:
o Limited disease:
• Local corticosteroids
• Local calcineurin inhibitors

o Extensive disease
• Systemic glucocorticoids or cyclosporine

o Adjunctive therapies: infliximab

Wound Dressing
o Moisture Environment

Types:
Types Agents Used in Comments
Films Tegaderm, Secondary dressing
Bioclusive
Foams Allevyn, Mebpilex , Moderate exudate Consist of 2 layers:
Lyofoam Hydrophilic silicone or polyurethane layer
Hvdroohobic. aas oermeable !aver
Alginates Slivercel, Sliverlon Heavily exudate Non-adherent polysaccharides
For open surgical wound Insoluble in water
Hydrocolloids DuoDERM, Promote epithelialization
Tegasorb and wound maturation by
creatina moist environment
Hydrogels Nu-Gel, lntrasite Necrotic. yellowish sloughy For dry wound
Gel. Vigilon, or Granulating clean
Elast"""I
Hydro active DuoDERM Polyurethane matrix

■ Specjfic dressing·
o Honey: significantly reduced need of amputation and improve healing of chronic ulcer
o Acetic acid: bactericidal to most bacteria+ anti-pseudomonas effect
o Aquacel: must be ionized by soaking in NaCl
o Iodine povidione: not used in dry necrotic areas

• Mepilex'Borderlrle

Film Dressing Foam Dressing Alginates Dressing

__ __--,.,._­,..
l•••n !lcJo!ol!n

.,--=--·--··
�.. I --
5

Hydrocolloid Dressing Hydrogel Dressing Hydroactive Dressing

 ■ Hemostatic agent.s:

Tvne Trend name Sol!lrce Absorotion Used in

Absorbable gelatin Gelfoam, Surgifoam Porcine 4 to 6 weeks Organ surface bleeding

Oxidized All Surgicel Plant 1 to 2 weeks Organ surface bleeding

regenerated
cellulose Venous oozina
Microfibrillar Avitene Bovine > 8weeks Cavity unamenable to
collagen cautery or compression as
nerve
Fibrin sealant TachoSil Human fibrinogen Immediate External arterial bleeding
and thrombin
Venous oozina
Zeolite Quikclot Calcium-loaded External arterial bleeding
aluminosilicate
mineral
Microporaus Arista Potato starch 48 hours Needle hale bleeding in
polysaccharide vascular graft or adentitia
spheres
Organ surface bleeding

Cavity unamenable to
cautery or compression as
nerve
Bovine albumin- Bioglue Bovine Large artery bleeding
glutaraldehyde Fibrin-9lue
tissue adhesive

Absorbable gelatin Tissue adhesive

Fibrin sealant

fi'lrl?ii\rr ti'ii13Jit fi·j;j9iM•

FIBRILI..A.R

Oxidized cellulose Microfibrillar collagen

Burn
BURN
■ Zones of burn wound:
o Coagulation
o Surrounded by zone of Stasis (most amenable to salvage)
o Surrounded by zone of Hyperemia

■ lmbibition: blood supply to skin graft for O - 3 days

■ Neovascularization: starts around day 3

■ Most common cause of free flap failure: Venous thrombosis

■ Most common cause of skin graft loss: Hematoma I Seroma

■ Most common type of burn is Scald burns

o 140° F water causes burn in 3 seconds

■ Most common type of burn come to hospital and be admitted is Flame burns

Admission Criteria:
■ 2nd degree> 20% TBSA, or> 10% TBSA in> 50 or< 10 years of age
■ 2nd degree in hands, face, feet, genitalia, perineum, or skin overlying major joints
■ 3rd degree
■ Electrical and chemical burns
■ Concomitant conditions:
o lnhalational injury, mechanical traumas or pre-existing medical condition

Assessment of total body svrtace area·

■ Lund and Browder chart (Most accurate)
■ Palm method (1% equal to patient's palm)

■ Rule of 9
o Circumferential leg = 18, Circumferential forearm = 9
o Anterior Right thigh = 9
•in Children: head= 18 and lower limbs= 14 each"

Parkland formula:
■ Used for all burn patient who need admission
u V
■ UOP as best measure of resuscitation (> 0.5 ml/kg/hour)

■ Ringer lactate 3- 4 ml/ kg/ %TBSA

o Started from the time of the burn
o ½ volume should be given in 1st 8 hours and the remaining½ over the 16 hours
o Can be used up to 6 ml/ kg / %TBSA in children< 2 years old
o Additional maintenance fluid is required for children< 20 kg

■ Colloid of 5% albumin usually given for burn > 40% TBSA 8 - 24 hours post-injury

Most common cause of death in first 24h in burn: Inadequate fluid resuscitation
Hypermetabolic response:
■ Oxidation of lipids, t Proteolysis, gluconeogenesis, Temperature
■ Best indicator for hypermetabolic response is: Negative Metabolic rate

■ Burn release cytokines and activates SIRS if> 20 - 25%

Nutrition in burn:
■ Caloric need: 25 kcal/kg/day + (30 kcal x % burn)
■ Protein need: 1 g/kg/day + (3 g x % burn)

■ Non-Protein calories: Nitrogen (normal 150:1) in burn 100:1

■ Glucose: Best source of non-protein calories in patients with burns (primary fuel)

■ Protein: Most important for healing of severe burns

■ Feeding in critical ill patient with burn is best with: Nasoieiynal feeding
■ Best nutritional assessment by: Daily weight measure

■ Assessment of protein status (or during administration of protein): Nitrogen Balance

■ Serum albumin: marker of nutritional status after patient recovery

Microbial infection in burn:

■ Most common infection in patients with severe burn (> 30% BSA)
o Pneumonia (most common cause of death}

■ Most common organism in burn wound: Pseudomonas

■ Most common organism isolated from blood in burn patient: S. aureus

■ Most common viral infection in burn wound: HSV

■ Most common opportunistic infection in burn wound: Candida

■ Best way to detect bum wound infection vs. colonization:

o Biopsy of burn wound including normal skin

o Positive result if > 105

� Need surgical excision of infected wound
TOPICAL ANTIMICROBIAL
Tvoe Description
Most common
Do not use in patients with sulfa allergy
Sliver Sulfadlazlne
Side effects:
(Sllvadene)
Neutropenia
Thrombocytopenia
Inhibit eoithelialization
Side effects:
�. ! Cl, ! K, ! Ca
Silver nitrate Discoloration
Methemoglobinemia
t CVP (contraindicated in G6PD\
Best for eschar penetration
Sulfamylon
Side effects:
(Mafenlde sodium)
Painful application
Metabolic acidosis <carbonic anhvdrase inhibition\

■ Management of wound and wound care:

o 1 st degree and superficial 2nd degree:
• Continue wound dressing for 2 - 3 weeks
• May be used for deep 2nd burn wound for few days and re-assess

o Deep 2nd and 3rd degree:

• Early excision and grafting

■ Skin grafting:
o Sufficient autologous skin graft (< 40% TBSA):
• Autologus partial-thickness skin graft:
• Used mainly for large area need to be covered

• Contraindicated in presence of wound infection

• Autologus full-thickness skin graft:
• Used in areas susceptible for trauma
(face, foot, weight bearing surfaces "Joints")

• Associated with less wound contraction

• Requires addition coverage to donor sites

o Insufficient autologus skin graft (> 40% TBSA):

• Allograft (Cadaveric skin) or porcine skin graft as temporary coverage
• Staged wound excision and skin graft

Dressing changes as definitive management is not preferred for 2nd or 3rd degree burn wound
due to healing with secondary intention lead to poor cosmetic results and more wound infection
Inhalation injury:
■ Clinical signs:
o Carbonaceous sputum (Most indicative)
o Singed nasal hair

■ Most common cause of the death: ARDS / Pneumonia

o Early: Airway compromised
o Late: Pneumonia

■ Affinity of Carbon monoxide for hemoglobin 200 - 250 times greater than oxygen
o Pulse oximetry reading-+ False High

■ Half-life of carboxyhemoglobin in patient breathing 100% 02: 1 hour

■ CO poisoning should be treated until carboxyhemoglobin level < 10% and no symptoms

■ Indications for intubation:

o Associated with:
• Severe upper airway edema (Hoarseness, wheezing, or strider)
• Supraglottic inhalation injury
• Deep bums to the face
• >40% TBSA

o Respiratory parameters:
• Pa02 < 60 mm Hg
• PaC02 > 50 mm Hg
• Pa02/F 102 ratio < 200

Electrical burn:
■ Cataract is one of the complications of electrical burn
■ Management:
o Oxygen supplement

o Adequate fluid resuscitation with maintain UOP of 100 ml/hour (> 1 ml/kg/hour)

o Osmotic diuresis with Mannitol (25 g every 6 hours)

o Intravenous NaHCO3 (5% continuous infusion) for alkalinization of urine

o 1% methylene blue used to treat Methemoglobinemia

o Colloid administration (albumin or fresh frozen plasma)

• 12 - 72 hours after injury may restore intravascular volume in patient with
persistent low urine output despite adequate crystalloid administration

o Plasmapheresis may reduce intravenous fluid requirements in patients who do not

respond to standard crystalloid resuscitation

± Fasciotomy

± Debridement
Chemical burn:
■ Management of Hydrofluoric acid burn:
o Copious irrigation with water and Calcium gluconate gel application

■ Lye powdered should be wiping or sweeping with no irrigation

■ Acid and alkali burns (chemical burn}: Water iffigation

(Normal saline in non-burn wound}

o Alkalis -+ deeper burns (liquefaction necrosis)

o Acid -+ coagulation necrosis

Skin complications of burn:

■ Erythema multiforme: least severe form
■ Stevens Johnson syndrome (more serious}: < 10% BSA

■ Toxic epidermal necrolysis (TEN): > 30% BSA (most severe form)
� Staph scalded skin syndrome:
o Skin epidermal-dermal separation seen in all
o No steroids
OTHERS
■ Frostbite: Treated with warm water immersion ''99 - 108 F (37 - 42 C)"

■ Ma�olin's ulcer: squamous cell cancer in chronic non-healing burn wound

o In patient suspected malignancy of chronic wounds (overturned edges), biopsy must be
repeated to rule out malignancy (SCC vs. BCC)

■ Curling's ulcer: gastric or duodenal ulcer witlh bums

■ Pain in burn: Antecubital vein and IV Morphine

■ Seizures: usually due to ! Na

■ Escharotomy
o Indication:
• Circumferential deep burns with suspected compartment

• For compartment pressure > 25 - 30 mm Hg

• Signs of vascular impairment
• Decreased peripheral blood flow
o Delayed capillary refill
o Neurologic deficits

• Decreased or absent Doppler ultrasonic pulse detection.

o Thoracic Escharotomy may be needed if patient have circumferential thoracic pain with
increasing PC02 and PIP (peak inspi ratory pressure)

o Patient with no improvement after escharotomy may need fasciotomy

• Escharotomy: surgical incision through eschar only
• Fasciotomy: surgical incision through all layer including the fascia
Trauma
Reviewed by:

Dr. Mamoun Nabri

Dr. Omar Al Rasheed

TRAUMA
■ Assembling the trauma team
■ Personal Protective Equipment (PPE) should be worn by all personnel

■ Assigning rules and prepare equipment's (Intubation set, FAST, Chest tube, ED
Thoracotomy, Suction)

■ ATLS Protocol
Primary survey
o A: Airway with protection of cervical spine
o Helmet removed by 2-persons technique
o Ask patient any question
o Open airway with protection of cervical
• Jaw-thrust is preferred method if suspected cervical injury

Jaw-thrust He.ad tilt· chin

moneuver lirt moneover

o Suction
o Oropharyngeal airway, nasoph.aryngeal airway if not contraindicated, pre-
intubation oxygenation
o Endotracheal intubation (rapid sequence induction) and 100% oxygen ventilation
o Cricothyroidotomy if obstruction or failure of TEE
o Tracheostomy if cricothyroidotomy contraindicated
o Hard collar or sandbags to protect cervical spine (unless penetrating neck injury)

Patient become unstable when finish � Re-assessment (ABCDE)

o B: Breathing and ventilation

o Respiratory rate, Oxygen saturation
o Examination of the chest
• Inspection
• Palpation
• Percussion (dullness, hyper-resonance)
• Auscultation

± Neck examination (Tracheal shifting, Neck veins)

± Chest x-ray

Patient become unstable when finish � Re-assessment (ABCDE)

o C: Circulation
o Examination of the pulse, blood pressure and 4 pulses

o Exclude external bleeding

• Simple pressure, pack and apply pressure
• Liberal use of tourniquet for limbs bleeding
• Reduction and splinting for long bone
• Check pulse after reduction -+ Doppler -+ Angiography -+ Exploration

o Exctude iotecoal b!eedjng

• Abdominal examination for distension
• Pelvic examination for stability
o Manual palpation of the pelvis for assess pelvic ring and crepitus
o Manual compression along iliac crest over ASIS, then assess pelvic
ring stability and pubis symphysis
o Contralateral push-pull examinations of the lower extremities are
rarely necessary to identify instability

• FAST± Pelvic x-ray

o Insertion of 2 Large IV cannula for blood extraction

• Adult:
o Preferable route by order:
• Peripheral upper limb (antecubital fossa)
• Peripheral lower limb
Failed? Central line or lntraosseous line (Tibia/Humerus)

Subclavian venous catheter not preferred in trauma

Unless patient has pneumothorax:
� Do ipsilateral subclavian catheterization

Best site for venous cut down: Saphenous vein at ankle

• Children:
o Preferable route by order:
• Peripheral upper limb
• Peripheral lower limb
Failed? lntraosseous line (Proximal tibia -+ Distal femur)
o Blood withdraw before resuscitation (to prevent dilution of the blood)
• For CBC, RFT, LFT, Coagulation profile, Pregnancy test, RBS, Lactic acid
± Blood Culture, Urine culture, ABG, Type and screen, Cross Match

o Fluid resuscitation with 1 Liter Ringer lactate or Normal saline, then re­
assessment

o Massive transfusion guideline (1:1:1) should be initiated as soon as it is

anticipated that patient will require massive transfusion (after 2 units PRBCs)

Patient become unstable when finish � Re-assessment (ABCDE)

 o D: Disability
o GCS (Level of consciousness)
o Reflexes "Pupil"
o Lateralization signs
• Sensory function
• Motor function

o Leg roll and examination of spine and to assess digital rectal examination (DRE)
• Conscious: Spine tenderness
• Comatose: Step deformity

o DRE used to assess sphincter. high-grade prostate, and blood on finger

Patient become unstable when finish � Re-assessment (ABCDE)

o E: Exposure and prevent hypothermia

Patient become unstable when finish -+ Re-assessment (ABCDE)

Resuscitation

Adjuncts to primary survey {ABCDEFG)

o ABG, Pelvis x-ray, Chest x-ray, DPL, ECG, Foley's, FAST, NGT ± X-ray extremities
No Foley's catheter before DRE

Re-evaluation

Consider need for transfer

Secondary survey
o AMPLE (Allergy, Medications. Past medical and surgical, Last meal, Event history)
o Time of injury
o Mechanism of injury
o Type and speed of vehicle
o Location of the victim in the vehicle
o Seat belt, Air bag, Helmet
o Number and status of the passengers
o History of loss of consciousness or vomiting

o Full systemic examination from head to toe (Including pelvis and long bones)

Adjuncts to secondary survey

o CT scan
o Bronchoscopy

Definitive management

Tertiary survey
Full body examination 24 hours after admission to rule out missed injuries
■ Hemorrhage is the most common cause of <leath in 1•1 hour
o Resuscitation with 1-liter Ringer lactate
o Due to asymptomatic grade 1 hemorrhagic shock = 750 ml
• 1 ml blood = 3 ml crystalloids (750 x 3 = 2250 ml) = almost 2 liters

o Serial lactate level is useful in trending success of the resuscitation

o Unstable patients:
• Non-responder or transient responder after the 2 liters of crystalloids

■ Mean Arterial Pressure (MAP)·

o Equations:
o Diastole+ 1/3 Pulse pressure
o Diastolic + (Systolic - Diastolic} / 3}
o (2 Diastole+ Systole) / 3

o Assessment of tissue perfusion and oxygenation

o More sensitive indicator for shock
o Hypotension: Systolic BP:'.> 90 mm Hg, or MAP:'.> 65 mm Hg

■ Pvlse pressure·
o Systolic - Diastolic pressures
o Narrow pulse pressure: < 25% of systolic pressure
o Blood loss, cardiac tamponade or aortic valve stenosis
o More sensitive indicator for blood loss

■ Permissive hypotension technique: (SBP < 80 mmHg)

o Do not use it in traumatic brain injury
o Used as selective technique to limit further bleeding, coagulopathy, and hypothermia
o Still there is no RCT supporting using this technique yet
o Although it used by selective centers during transfer patient from accident site to OR for
penetrating trauma
 ■ Tissue injury response (Stress hormones}:

Increased Decreased
Hormonal ACTH
Aldosterone •
Insulin
Increased during flow phase as
anabolic effects

••
ADH
Mesenteric vasoconstrictor TSH in brain injury and after surgery
Blood shunting from splanchnic organs
T3 and T4
Cortisol
Catecholamines (Epinephrine, Norepi, Dopamine)

Glucagon
Growth Hormone
TSH in hvn1>rthvroid oatients
Hormones that usually have no role in tissue iniurv: TSH, LH. and FSH
Metabolism pH (Contract Alkalosis) GFR
Blood sugar (Hyperglycemia) Oxygen
Insulin resistance Impaired glutamine melabolism

Gluconeogenesis Glycogenolysis

Proteolysis Transport proteins

Lioolvsis (Albumin, Transferrin)
Nutritional Copper Iron
Zinc /Due to heoatic seauestration l
Immunity WBC, and inflammatory markers CD3
Neutrophils CD4
lmoaired macrophaaes

■ First hormone to release during stress: Corticotrophin-releasing hormone (CRH)

■ Order of hormone release:
o Immediate: Epinephrine (Peak 1 - 2 days after injury)
o After 20 minutes: Glucagon
o After 30 minutes: Insulin and ADH
o After 2 - 4 hours: Cortisol
o After 24 hours: Growth hormone
PENETRATING INJURIES
■ Types:
o High velocity (> 600 m/sec) + Projectile, Destructive
o Like rifles, or shotgun {close distance)
o Leads to form primary and secondary temporary cavitations (pressure waves}

o Low velocity(< 300 m/sec) + Propelled, Less severe

o Like knife, or airgun
o May travel for long distance in subcutaneous
o Creates primary permanent cavitation

Inlet Exit
Sha"" Round (oval in obliaue firinal lrreaular /Destructivel
Size Small (micro-tears at skin marainl Larae
Loss of substance More Less
Powder marks Yes No
(tattooinal
Ettne Inverted Everted
Bevelina Internal External
DIAGNOSTIC PERITONEAL LAVAGE (DPL)
■ Indicated in hypotensive trauma patient after responding by IV fluid or in unstable patient with
equivocal or negative FAST (Nowadays CT scan replace the DPL)

■ Access:
o Infra-umbilical: Standard
o Supra-umbilical: for pelvic fracture, retroperitoneal hematoma suspicion, or pregnancy

■ Method:
o Closed technique:
o Anesthetize the skin
o Access the peritoneum via needle with syringe infra-umbilical at midline
o Pass the guidewire over the needle and remove the needle
o Small stab incision at the entry of the wire
o Pass the catheter over guidewire with direction toward left or right pelvic gutter
o Aspiration for blood with 10 ml syringe
o If negative, Lavage with 1 liter normal saline and withdraw it under gravity
o Send :? 300 ml fluid for analysis

o Open technique:
o Anesthetize the skin
o Access the peritoneum via 4 - 6 cm infra-umbilical incision
o Retraction of the skin and dissect until opening of linea alba
o Place towel clips over both sides of rectus muscle and lift it up
o Pass the catheter and trocar 45 - 60 degree caudally into peritoneum
o Retract the trocar within the catheter, and advance the catheter to the pelvis
o Aspiration for blood with 10 ml syringe
o If negative, Lavage with 1 liter normal saline and withdraw it under gravity
o Send :? 300 ml fluid for analysis

■ Positive findings (patient should be shifted to the OR theater):

o > 100,000 RBCs/cc in general or in blunt abdominal trauma
> 10,000 RBCs/cc in penetrating abdominothroacic trauma
o > 10 ml of blood
o > 500 WBC/cc
o t levels of Amylase, ALP, and Bilirubin level
o Food particles, bile, bacteria

■ Pitfalls:
o High false-positive rate
o Risk of visceral injury
o Poor sensitivity to detect retroperitoneal injuries

■ DPL / FAST positive -+ Laparotomy

■ DPL / FAST negative -+ CT abdomen I Observation
HEAD INJURY
■ Cerebral perfusion pressure
o Goal: ICP < 12, CPP > 60
o CPP = MAP - ICP
o ICP > 20: need immediate treatment (Contraindication for laparoscopy)

o Maneuvers to treat High ICP:

o Raise head of bed for 30 degree
o Relative hypeNentilation -+ Cerebral vasoconstriction (CO2 30 - 35)
o 3% Normal saline
o ± Mannitol {1 g/kg IV for 3 days), Barbiturates, Phenytoin
o Steroid have no role
o Keep Na 140 - 150 (can use hypertonic saline)

■ Glasgow Coma Scale /GCS}

Score Motor (6 ooints) Verbal (5 points) Eve (4 points)

1 No response No resoonse No response
2 Decerebration Inappropriate sounds To pain
(Abnormal extension)
3 Decortication Inappropriate words To voice
{Abnormal flexion)
4 Withdraw from oain Confused or disoriented Soontaneous
5 Localized oainful stimulus Aoorooriate and oriented
6 Obev commands

o Motor part is the most reliable measure

o GCS s 8:
o Intubation
• Most common indication in trauma: altered mental status
o ICP monitor (Peak ICP occurs 48 - 72 hours after injury)
o Ventriculostomy (external ventricular drainage)
• Used in: lntraventricular hemorrhage, or hydrocephalous

o GCS score in pediatric age group:

Score Motor (6 ooints) Verbal (5 ooints) Eve 14 ooints)

1 No resoonse No resoonse No resoonse
2 Decerebration Grunts I Agitated To pain
(Abnormal extension)
3 Decortication Inappropriate screaming or crying To voice I shout
(Abnormal flexion)
4 Withdraw from pain Inappropriate interaction Spontaneous
Irritable Cries
5 Withdraw from touch Coos I Babbles
Cries annrooriatelv
6 Move soontaneouslv

o GCS score in intubated patients:

• Maximum soore is 10 and minimum is 2 (No verbal scores)
• Verbal scores can also derived from the motor and eye components
• Alternative scores: FOUR soore, AVPU, and Simplified motor score
 ■ FOUR score

Score Eve Motor Brainstem reflexes Resoiration

0 No response No response Absent Pupil, Corneal Breaths at ventilator rate or
and Couah reflex Aonea
1 To pain Extension response Pupil and Corneal Above ventilator rate
reflexes absent
2 To voice I shout Flexion response Pupil or Corneal reflexes (Not intubated)
absent lrreaular breathina
3 Open but not Localizing to pain 1 Pupil wide and fixed (Not intubated)
trackina Chevne Stokes breathina
4 Spontaneous Thumbs-up, Fist, Pupil and Corneal (Not intubated)
Peace sion reflexes oresent Reoular breathino oattern

■ Cerebral hematoma·
Eoidural hematoma Subdural hematoma
Presentation Lucid interval between Loss of consciousness Falling in elderly patients

Kemohan's phenomenon:
Contralateral dilated pupil and ipsilateral More dangerous due to associated injuries
hemiparesis (brain compression)
+ Transtentorial herniation
Vascular iniurv Middle meninaeal arterv Venous olexus
CT finding Lens shape (biconcave) Crescent shape

Treatment lmm�diale bu[c bcl�s aod sucgh;al ��ag.iatico gf b�wats;nna iodh;at� tt·
- Focal neurologic deficit
-Asymmetric or fixed dilated pupils
- Midline shift > 5 mm
- GCS ,; 8 or 2 points decreased from time of injury until hospitalization
- Hematoma volume > 30 cm 3
- Hematoma Thickness > 1.5 cm of epidural or > 1 cm of subdural hematoma
- ICP > 20 mm Ha

■ Signs of basal skull fracture:

o Otorrhea, Rhinorrhea (due to cribriform plate fracture)
o Dilated pupil (Due to CN Ill compression)
o Raccoon eyes (associated with anterior Iossa fracture)
o Battle's sign: Posterior fossa fracture
• Bruising over mastoid process
• Associated with ataxia and nystagmus
■ Target: Halo: Ring sign:
o A way to differentiate between CSF and other ear discharges
o By using a tissue you find a central non-clotted blood surrounded by clear fluid
• Non-clotted due to streptokinase activity

Blood

CSF

■ Examination of the cranial nerves

CNI 0lfactorv Test each nostril to smell

Visual acuity of each eye
CNII Optic
Fundus examination
CNIll 0culomotor Pupils examination
CNIV Trochlear Ptosis
CNVI Abducens Follow finer at H pattern
Corneal reflex
Jawjerl<
CNV Trigeminal
Facial sensation
Facial motor (Ooen mouth, Clench teeth I
Facial asymmetry or drop
CNVII Facial Facial expressions
Grins Shuts eves Frown Show teeth Puff out checks
Weber's test for lateralization
CNVIII Vestibulococlear Rinne's test for air and bone conduction
Examination of external canal and eardrums
Gag reflex
CNIX Glossopharyngeal
Voice
Swallow, Cough
CNX Vagus
Palate examination for uvular disolacement
Trapezius examination
CNXI Accessory Shrugs shoulders
Tums head aaainst resistance
Articulation
CNXII Hypoglossal Inspect tongue for wasting or fasciculation
Protrude tonaue and look for deviation
 NECK TRAUMA
■ Neck zones based on penetrating iniury:

Zone Definition Content Incision

Thoracic ouUet or Clavicle to Cricoid Lung apex, Trachea Median sternotomy
Zone 1
Subclavian vessels Anterolateral thoracotornv
Cricoid to Angle of mandible Vertebral vessels Cervical incision medial to
Carotid vessels SCM
Zone 2 Jugular vein
Esophagus, Trachea (Don't joining both incision if
bilateral exoosure reauired\
Angle of mandible to Base of skull External or internal carotid High cervical incision with
vessels subluxation of mandible
Zone 3 Jugular vein
Cranial nerve
Hvoooharvnoeal

■ Management of penetrating neck iniuries:

Manaaement Zone I / Zane II Zone Ill

Asvmotomatic CTA Chest and Neck Observation
Symptomatic CTA Chest and Neck CTA Chest and Neck
(Soft signs)
T

Ell[ lil/OlllWWali� gali!!DI !lDl)r Positive CTA ➔ Angioembolization

Angiography ± embolization
± esophagogram and bronchoscopy

Failed -+ Exploration
Positive CTA-+ Exploration
Instability or
Symptomatic Exploration
/Hard sions\

Soft sians Hard sians

Voice chanoes Laroe Exoandina. Pulsatile hematoma
Couah Active external bleedina
Dvsohaaia Internal bleedina into trachea or esoohaaus
Venous bleedina Hoarseness. dyspnea, stridor
Subcutaneous emoh=erna
Massive Hemootvsis
Neuroloaical deficit
■ Thyroid gland injury:
o Control bleeding and drain (no thyroidectomy)

■ Esophageal injury:
o Nasogastric tube

o Left neck exploration

o Access:
Front door
• Retract carotid sheath laterally and enter the plane to find esophagus behind the
trachea

Back door (in case of carotid hematoma)

• Retract carotid sheath medially and enter the plane to find esophagus

o Divide 3 structures cross the esophagus for visualization:

• Omohyoid muscle
• Middle thyroid vein
• Inferior thyroid artery

o In case of poor visualization:

• Contra lateral neck exploration through separate incision
• Intra-operative esophagoscopy
CEREBRAL VASCULAR INJURY (CVI)
■ Including carotid or vertebral artery injury
■ Including dissection, thrombosis, or pseudoaneurysm
■ Risk of stroke 20% in untreated patients
■ Risk factors:
o Displaced mid-face fracture (LeFort II or Ill}
o Mandible fracture
o Complex skull fracture or Basilar skull fracture
o Closed head injury with diffuse axonal injury
o Cervical subluxation or ligamentous injury
o Cervical spine fractures
o T horacic vascular injury

■ Clinical presentation:
o Potential arterial hemorrhage
o Cervical bruit
o Expanding cervical hematoma
o Focal neurologic defect (TIA, hemiparesis, Homer's Syndrome}
o Stroke on CT or MRI

■ Investigations:
o CT angiogram (initial test of choice} if clinical suspicious or risk factor for CVI

o Arteriogram (used for equivocal results)

■ Grades:
o Grade I: Irregularity of vessel wall, dissection or intramural hematoma with <25%
luminal stenosis

o Grade II: Visualized thrombus or raised intimal flap. or dissection or intramural

hematoma with 25% or more luminal narrowing

o Grade Ill: Pseudoaneurysm

o Grade IV: Vessel occlusion
o Grade V: Vessel transaction with extravasation

■ Management:
o Unstable or penetrating: Open surgical repair

o Stable and blunt injury:

• Grade I: Anti-Thrombotic if no contraindications
• Heparin 15 units/kg/hour (without loading dose} Target PTT: 40- 50 s
• Anti-platelets (Aspirin 325 mg/day or Clopidogrel 75 mg/day)
Repeat CTA after 7 - 10 days if healed stopped, if not use for 6 months
• Grade II - V
• Surgically accessible: Operative repair
• Non surgically accessible:
o Grade II - IV: Anti- Thrombotic
o Grade V: Endovascular treatment
SPINE TRAUMA

■ Criteria to remove C-spine collar with no images required: (all points are required)
o National Emergency X-Radiology Utilization Study (NEXUS) criteria
• No midline tenderness
• No focal neurologic deficit
• Normal alertness
• No intoxication
• No painful distracting injury

o Canadian C-Spine Rule

• No midline tenderness
• No paresthesia in extremities
• Ambulatory or sitting upright
• Able to rotate the neck 45 degrees to the left and right
• Low-impact mechanism
• < 65 years

c::, CT scan if not cleared

■ C1:
o Burst (Jefferson fracture): Axial loading
o Most commonly missed
o Risk of neurological injury is low
o Radiological views: open-mouth odontoid and lateral

■ C2:
o Most common in cervical fracture
o Hangman's fracture: Distraction and extension
o Odontoid fracture
• Types:
• Type I: above base (stable)
• Type II: at base (unstable)
• Type Ill: behind the base (unstable)

■ Stable fracture:
o Compression (wedge) fractures
o Only 1 column is disrupted (anterior column only)
• Anterior column: anterior spinous ligament (in stable fracture)
• Middle column: vertebral body, posterior spinous ligament (in unstable fracture)
• Posterior column: faceUlamina interface (in unstable fracture)

■ Unstable fracture:
o > 1 column disrupted
o Fracture involving middle or posterior columns
o Burst fractures
o C2 odontoid fracture type II and 111
 ■ Accessory spinal nerve injury:
o Following neck dissection, lymph node excision, or trauma
o Affected trapezius muscle + Shrug shoulders

■ Chance Fracture:
o Flexion-distraclion injury (seatbelt injury)
o May be a bony injury or ligamentous injury (ftexion-distraction injury)

■ Cauda eguina syndrome:

o Defined by a constellation of symptoms that result from terminal spinal nerve root
compression in the lumbosacral region

o Characterized by:
• Bilateral leg pain
• Bowel and bladder dysfunction
• Saddle anesthesia
• Lower extremity sensorimotor changes

o Urgent surgical decompression within 48 hours

Reflexes:

Root Reflex Associated Sensory Associated Motor

cs Biceos reflex Lateral un=r ann Shoulder and elbow flexors
C6 Brachioradialis Lateral forearm dorsum 1•1 web soace and thumb Wrist extensors
C7 Triceos Middle finaer Elbow extensors ltriceosI
ca - Ulnar side of little finger Finger flexors, extensors and
intrinsic
T1 Medial side of foreann Finaer abduction
T8-T10 Above umbilicus lntercostal and trunk
Deviation of umbilicus toward area stroked
T10-T12 Below umbilicus Abdominal muscles
L1 Cremasteric reflex losilateral rise of testes Hio ffexors
L2-L3 - Anterior and inner thigh Hip ffexian
Hio adduction
L4 Knee jerk Anterior knee, and medial leg Quadriceps "L4"
Knee extensors
LS Dorsiflexion foot Foat 1•1 web space Ankle darsiflexion
Toe extensors
S1 Plantar ffexion foot Posterior leg Foot plantar flexion
Ankle ierk Foot aversion
S2 - Plantar foot Toe olantar flexion
S3 - Perianal Ankle olanterflexors
S2-SS Anal wink Perianal Contraction af anal sohincter
 Peroneal nerves injury:

Nerve Root Associated wl Svmotoms

Common peroneal nerve L4-S2 Fracture head or neck of fibula Both
(Most common) Lithotomy position
Deep peroneal nerve L4-S2 Knee dislocation Loss of dorsiflextion (foot Drop)

Loss of sensation of dorsal

aspect of the foot (1., web space)

Superficial peroneal nerve LS-S1 Compartment syndrome Loss eversion

(Moving foot laterally; outward)

Sensory:
Lateral aspect of foot dorsum

Spinal cord injury syndromes:

Syndrome Pro!lnosis Motor S1 S2 p

Anterior cord syndrome Worst Loss Preserve
Posterior cord
Preserve Preserve Preserve Loss
syndrome
Central cord syndrome Loss of upper
Good Loss (Upper> Lower) Preserve extremities only Preserve
(Most common hme)
Brawn Squard lpsilateral
Best lpsilateral loss Contralateral loss
svndrome loss
S 1: Sensation
S2: Pain and Temperature
P: P�0ri'oceol/on vibration and touch

■ Spinal cord injury increases the risk of DVTIPE

■ Cervical injury: Nasal intubation

o Nasal intubation is contraindicated in Apneic patients

Steroids for blunt trauma to prevent neurogenic shock is used for 48 hours only

■ Types of nerve injury:

o Neuropraxia: (Most mild)
• Physiological block of nerve conduction without anatomical interruption
• By focal segmental demyelination
• Occurs after transient ischemia, stretch or external compression to the nerve

o Axonotmesis
• Anatomical interruption of axon without interruption of connective tissue
• Occurs mainly after traction or crush injury, or severe compression as well
• Endoneurium remains intact

o Neurotmesis: (Most severe)

• Complete anatomical interruption of axon and connective tissue (epineurium)
MAXILLOFACIAL TRAUMA
■ Temporal skull fracture: Facial nerve injury (at geniculate ganglion)
o Most common facial bone fracture: Nasal bone

■ Maxillary fracture: Trigeminal nerve injury

■ Mandible fracture most commonly at condyle (Angle & Subcondyl)

■ Le FortClassification
o Type I: Maxilla fracture transversely
o Type 11: Lateral to nose
o Type Ill: Lateral orbital walls

II Ill

Orbital floor iniury � Upward gaze

■ Management of facial nerve injury:

o Penetrating:
• Surgical exploration

o Blunt:
• Non-operative management is the goal

• Early and complete:

• Medial to lateral canthus of eye: Surgical exploration within 72 hours
• Lateral to lateral canthus of eye: Non-operative management

• Late or incomplete:
• Non-operative management
■ Facial injury: Cricothyroidotomy intubation
o Contraindication:
• < 12 years old
• Laryngeal trauma or fracture
• Subglotlic stenosis

+ Tracheostomy

o Technique:
• Percutaneous cricothyroidotomy (Seldinger Technique}

• Needle cricothyroidotomy:
• Palpate thyroid and criooid cartilage by thumb and 3rd finger
• Insert catheter-needle with NS directed caudally at 45 degree
• Aspirate during insertion (ensure air-bubbles)
• Advance the catheter and remove the needle
• Attach ventilation {15 Umin) or bag mask can be used

• Surgjcal crjcothyrojdotomy·
• Palpate thyroid and criooid cartilage by thumb and 3rd finger
• Make 3 cm vertical midline skin incision on top of cricothyroid membrane
• Palpate the membrane during opening the midline incision
• Make horizontal incision over cricothyroid membrane
• Retract the trachea superiorly and inferiorly
• Insert tracheostomy tub,e through the membrane
• Remove retractor and rotate the tracheostomy 90 degree and advanced
caudally
• Remove the obturator, and insert the cannula
• Inflate the balloon and attach it to ventilator

• FONA (Front of the Neck Access)

CARDIOTHORACIC TRAUMA
■ Thoracotomy in trauma should be done after ABCD of ATLS, which includes decompression by
chest lube followed by lhoracotomy

■ ER thoracotomy
o Perfect patient is one with recordable pulse and single anterior thoracic stab wound with
pericardia! tamponade who lose vitals in front of emergency department staff
o Survival rate 15 - 50%, should be done selectively based on injury and transport time
o Indications:
• Patient sustaining witnessed penetrating trauma< 15 min pre-hospital CPR

• Patient sustaining witnessed blunt trauma< 5 min pre-hospital CPR

• Persistent severe hypotensio •n (SBP < 60)

o Cardiac tamponade, intra-thoracic or abdominal bleeding, air embolism

o Steps:
• Left anterior thoracotomy
• Open pericardium anterior to th.e phrenic nerve
• Cardiac repair followed by Cardiac massage (Two-Hands}
• Cross clamp the descending thoracic aorta
• Cross clamp the hilum in pulmonary hemorrhage or lung twist

■ OR Thoracotomy
o Indications:
• > 1,500 ml initially for any type of injury, other definition exist as well:
• > 1,500 ml initially for blunt trauma
• > 1000 ml initially for penetrating trauma

• > 200 ml/h for 2 - 4 hours

• Associated with other injuries:
• Esophageal injury -+ Gastric content in tube
• Tracheal or bronchial injury -+ Massive air leak
• Open pneumothorax
• Air embolism
• Great vessel injury
• Pericardia! tamponade

Most common source of bleeding: Intern al thoracic artery ± intercostal arteries

■ Diaphragmatic injury
o More common on the left (Bronchus injuries more common on the right)
o Investigations:
• CXR: Initial tool (NGT coil to the chest, and elevation of hemidiaphragm)
• Can miss 20 - 50% on injuries

• CT scan
• Low sensitivity
• Sions.;
o Collar sign
o Dependent viscus sign
o Dangling sign of diaphragmatic flap

• Can detect viscus herniation, but can't detect laceration of stab wounds

• Diagnostic Laparoscopy
• For suspicious findings on CT with no indications for laparotomy

• VATS
• Best investigation to detect minimal stab wounds
• Can detect injury in retroperitoneal diaphragm
• Indicated if laparotomy is not indicated

o Treatment:
• Acute < 1 - 2 weeks: Laparotomy
• Laparoscopy can be alternative if no other indications for laparotomy

• Chronic> 1 - 2 weeks: Thoracotomy

• Mechanical ventilation with positive pressure may prevent herniation or at least

chest tube should be in placed

• Tension pneumothorax can developed during insufflation of CO2 during

laparoscopy in diaphragmatic injury

• Repair:
• Linear injury: Continuous 1 locking polypropylene suture

• Damage control surgery· No repair, cover the defect with folded pad

• T issue loss with defect: Mesh repair

o Biological mesh: for temporary repair if infection present
o Prosthetic mesh: for definitive repair
o Alternative: omentum, fascia lata, or latissimus flap

• Detach from chest wall:

o Interrupted 1 polypropylene suture through the edge of detached
diaphragm, then around the adjacent rib, and then through
the edge of the diaphragm again before tying
■ Flail chest:
o ;,, 2 consecutive ribs broken at ;,, 2 sites -+ paradoxical motion
o Underlying pulmonary contusion

■ Tension pneumothorax (one way valve)

o t BP, t Breath sounds
o t Venous return (IVC, SVC compression)
o t Airway pressures
o Distended neck veins
o Tracheal shift

o Treatment:
• Needle decompression at 2nd I ntercostal space, then chest tube insertion

■ Open pneumothorax
o Associated with inspiratory rushing breath sound

o Cover the hole with sterile dressing as 3-sides adhesive non-occlusive dressing to
prevent tension pneumothorax

o Insertion of chest tube

■ Pulmonary contusion
o Usually early within 12 - 24 hours (ARDS can developed late)
o Appears as localized patchy infiltration
o Associated with rib fractures (Unilateral or bilateral)
o Followed by alveolar damage, edema and hemorrhage

■ Retained hemothorax (10 - 20%}

o Residual hemothorax despite attempted evacuation by tube thoracostomy
o 26% risk to develop empyema (which may need for decortication)

o Options for management:

i
• Initial observat on (80% successful if< 300 ml remaining}
• Video-assisted thoracoscopy "VATS" ± decortication
(for> 300 ml remaining) if< 1 week
• Thoracotomy (if associated with other injuries as diaphragmatic injury)

o Other Options: (Often ineffective methods)

• Placement of additional chest tube
• lmage-9uide chest drainage
• Instillation of fibrinolytics through existing chest tube
■ Air embolism (CO2 embolism}
o Pathophysiology:
• Direct communication between air and vascular system
• Pressure gradient

o Etiology and risk factors:

• Surgical procedures (open or laparoscopy) ''Most common"
• Trauma to the chest, neck, or abdomen
• Central venous catheterization
• Positive pressure ventilation
(Ventilator-introduced barotrauma)

o Signs:
• End-Tidal CO2
� Initial abrupt increased, Followed by sudden drop (Most important)

• End-Tidal Nitrogen
� More sensitive test to air and associated with earlier detection

• Cardiogenic shock

• Hypotension, machinery (harsh, crunching, Mill, Cog or Water -wheel) murmur

• Air leak if associated with bronchial injury

o Management·
• Resuscitation
� ICU management
� IV fluids ± inotropes
� Ventilation with 100% 02
� Intubation if required

• Maneuvers to prevent turthe:r complication

� Stop CO2, deflate abdomen, remove instruments during laparoscopy

� Turn to Left lateral decubitus, Trendelenburg position (Durant maneuver)

• Associated with central line ,catheterization /No trauma) � Air aspiration

� Swan-Ganz or Bunegin-albin (Better) catheter through right internal

jugular vein and aspirate

� Aspirate from right atrium by introduce syringe below left costal margin
• Associated with blunt thoracic trauma

Q Bronchoscopy to evaluate bronchial tree

• Associated with penetrating thoracic trauma

1) Intubation with one-lung ventilation

2} Emergency Left anterolateral thoracotomy

Q Clamshell thoracotomy may consider if air embolism diagnosed
preoperatively

3) Control pulmonary hilum to control bleeding and prevent further embolism

Q Clamping or digital pressure of the hilum
Q Twisting the affected lung 180 degree
Q Aortic clamp is also applied for extra-thoracic bleeding

4} If above methods failed, Open the pericardium and direct air aspiration
Q Heart apex of left ventricle or aortic root by 16 - 18 gauge needle
Q Right coronary artery by tuberculin syringe

5) Continue operative resuscitation

Q Vigorous cardiac massage
Q Keep in Trendelenburg IPOSition with pulmonary hilum clamped

6} Primary repair of tracheobronchial injury or lung laceration by

absorbable sutures though opening the presented tract of injury
(Pulmonary tractotomy) and repair of injured vessels or bronchi
■ Myocardial contusion
o Most common at: Anterior right ventricle
o Most common arrhythmia: Supraventricular Tachycardia and PVCs
o Most common causes of death: Ventricular tachycardia and Ventricular fibrillation

■ Aortic dissection
o Clinical presentation:
• Dyspnea and chest pain
• Pseudo-coarctation syndrome:
• Upper Extremity BP > Lower Extremity BP
• Decreased femoral pulses

o Imaging findings:
• Widened mediastinum > 8 cm
• NGT and Trachea deviation to right, and deviation of left bronchus
• Left apical capping
• P' and 2 nd rib fractures
• Obliteration of the aortic nob
• Left hemothorax

o Tear is usually at ligamentum arteriosum, at aortic isthmus

(before beginning of descending thoracic aorta)

o Investigations:
• Unstable:
• Trans-esophageal Echocardiogram

• Stable:
• CXR
• Spiral CT chest with IV contrast (if abnormal CXR)
o Direct signs: Pseudoaneurysm, extravasation, irregular intima
o Indirect sign: Periaortic hematoma

• Angiography is the gold standard (if abnormal CT)

o Treatment:
• Left thoracotomy: for most descending thoracic aortic dissection

• Median sternotomy: for ascending thoracic aortic dissection

• Laparotomy: for abdominal aorta

• All other abdominal injury should be controlled first before addressing
aortic injury

Q Definitive repair
Q Interposition PTFE graft
■ Cardiac injury and tamponade:
o Constriction of the heart(! Cardiac output) as result of compression from pericardia!
bleeding

o Beck's triad:
• Hypotension
• Jugular venous distention
• Muffled heart sounds

o Kussmaul's sign:
• Jugular venous distention during inspiration

o Management:
• Stable with negative FAST:
• ECG, Echocardiogram, Troponin I + Any abnormality mandates monitor
• Unstable:
• Initial as temporary method before definitive repair:
o Pericariocentesis

• Cardiac arrest or Pulseless electrical activity (PEA)

o Emergency thoracotomy

• Positive FAST pericardia! window in unstable patient in spite fluid

resuscitation
o Pericardia! window incision (to confirm diagnosis)
(10 cm midline vertical incision over sub-xiphoid)

Positive result + Sternotomy (Better) or Thoracotomy

o Pericardiocentesis
• Indications:
• Emergency: Suspicions of cardiac tamponade
As temporary method for later definitive operation

• Steps:
• Ensure NGT and IV line are connected
• Antiseptic of sub-xiphoid area
• Infiltration of local anesthesia
• Position the patient in semirecumbent position at 30 - 45 degree
• Puncture the area between xiphoid process and left subcostal area
• Connect ECG at base of insertion
• Advance the spinal needle connected to 50 ml syringe at 45 degree
• Toward the left shoulder for depth of 5 cm (can be more in obese patient)
• If ST elevation (injury) withdraw the needle backward
• Aspirate as much as fluid
 Type of Thoracotomy Site of injury

- Ascendin!'.I aorta
- lnnominate artery
Median sternotomy
- Proximal right subclavian artery
- Proximal left common carotid artery

For i:1roximal RIGHT injuries:

- Trachea and proximal both bronchus
Right Posteriolateral thoracotomy - Right bronchus
- Proximal or Middle esophagus (Malignancy)

for distal LEFT lnlurjes;

- Descending aorta
Left Posteriolateral thoracotomy - L,eftsubclavian artery
- Distal left bronchus

For specific LEFT injuries:

- ER thoracotomy
Left Anteriolateral thoracotomy
- Proximal left subclavian artery (Most difficult exposure)

- Distal left esophagus (Perforation, Malignancy)

For proximal LEFT Injuries:

Right Anteriolateral thoracotomy
- Lung and chest wall
ABDOMINAL TRAUMA
■ Most common organ injured with blunt trauma: Liver
■ Most common organ injured with penetrating trauma: Small bowel

■ Penetrating injury:
o Gunshot injuries:
o Unstable: Immediate exploration (Standard of care)
o Stable: CT scan with triple contrast followed by exploration

o Stab abdominal injuries:

o Back or flank:
• Unstable: Immediate exploration (Standard of care)
• Stable: CT scan with triple contrast followed by exploration

o Anterior abdomen:
• Unstable, evisceration or peritonitis: Laparotomy

• Stable:
o CT scan followed by local wound exploration (Alternative)
• Intact fascia:
• Clean and close the wound if< 12 hours
• Keep the wound open if > 12 hours
± CT abdomen
± L.aparoscopy
(if associated with other injury as rectal bleeding)

• Penetrated fascia:
• Unstable: Laparotomy
• Stable:
Laparotomy (Standard of care)
Alternative
• CT scan with triple contrast
• 24 hours observation
• Serial abdominal examination
• Serial Hb and WBC

■ Blunt injury: Trauma CT scan

o CT Chest/ Abdomen / Pelvis ± Head or Cervical with IV contrast
o IV contrast is a must, to evaluate solid organs
o Oral water-soluble contrast used selectively to rule out leakage, but might miss
bleeding from bowel lumen
o Rectal contrast used in flank or back injury or suspicious of large bowel
perforation

o Fluid density:
o 0- 10 HU: Ascites, Bile, Urine, or Intestinal contents
o 30 - 40 HU: Unclotted blood
o 40 - 60 HU: Clotted blood
o 80 - 300 HU: Active bleeding
PREPARATION OF THE THEATER FOR TRAUMA PATIENT
■ Consent for exploration:
o Exploratory laparotomy ± thoracotomy ± splenectomy ± bowel resection ± stoma

■ Warm room 80- 85'F (27 - 29.4'C)

■ Cell saver
■ Level one rapid infuser
■ Fluids and blood cross match
■ Massive blood transfusion protocol
■ Make sure patient in supine position with arms extended
■ Ask previous team about what happens (Orthopedics, Vascular)
■ Consider consultations
■ Prepare tubes and catheters
o Nasogastric tube
o Foley's catheter
o IV line catheters

Anesthesia equipment:
Oral/nasal airways
Ambu bags
Medication and catheters: ETT
CVP catheter kit - Suction device
PA catheter kit - Laryngoscope

Tray 1 eaujpment:
Intravenous access
.�.
•• •• Mechanical ventilator

- Arterial blood gases

,,- .t, /, ... ' Portable monitor: ECG, BP, 0 2
Rapid infusion / Warming device
• Stretcher ;
Tray 2 Instrument trays: •
: ,,
• • With f P cuff ', Autologous blood saver
,,. \
Basic surgical trays

.,,, .. .
.,,,
- Trauma set auto-transfusion device
, (salvage)

.,..,',',.. .
'•
. . -...
I tI tI I
Thoracotomy set Irrigation and suction
Chest tube set
- Vascular set \\', .
• ' •
•-' • I. ' •••
,i,
i
I tI .'
Miscellaneous: Blankets anJ(oley ca!Mf1.r

•.
Trauma/ laparotomy pads
•I
t
•t t•
stored on underoarriage

o
Self-retaining retractors

. :. .,· •
I
Topical hemostatic agents
I I
Argon beam coagulator
J \: '
I II \
'..} �-' Pneumatic compression devices
EXPLORATORY LAPAROTOMY
■ Steps:
o Supine position with arms extended

o Prep and drape from the chin to the knees and laterally to posterior axillary lines

o Exposure and control of bleeding

• Midline incision from xiphoid to symphysis pubis (One strike by a Knife)
• Preferable supra-umbilical entrance (quickest way due to thin peritoneum)
• For previous scar:
o Skin incision beyond the previous scar into "virgin" territory
o Skin incision byp.ass the scar "Bilateral subcostal incision"
• Division of ligamentum teres, falciform, triangular, and coronary ligaments if liver
mobilization is needed
• Evisceration of the bowel

• Large self-retaining retractors for exposure

• Packing of the 4 Quadrants and Pelvis with trauma or laparotomy pads
• Starting by: most injured area (unstable quadrant)
• Finishing by: least injured area (stable quadrant)
• Sites of packing:
o Sandwich the liver (above and below packing}
o Sandwich the spleen {above and below packing)
o Paracolic gutters
o Pelvis

± Resuscitative maneuver (Aortic control}

• Supra-diaphragmatic aortic control "Through left thoracotomy•
o Used for uncontrolled or expanding supra-mesocolic hematoma

• Supra-celiac (infra-diaphragmatic) aortic control

o Access lesser sac
c:> Through gastrocolic ligament
c:, Through gastrohepatic ligament
• By mobilization of left liver lobe, dividing the left crus
taking care not to injure the phrenic nerve,

o Manual compression with pressure against the spines

Controlled:
• Inform the anesthesia to catch-up

Not controlled:
• Check the packing areas and control packing first
• Check unpacked areas, mesentery from the root up to both surfaces of the bowel
o Exploration:
• Identify and control source of bleeding: (Solid organs or vascular structures)
• Liver and gallbladder
• Right kidney
• Anterior stomach and duodenum
• Spleen and left kidney
• Missing parts:
o Both hemidiaphragm
o Posterior peritoneum, bowel, and mesentery
o Bladder, ureters and posterior wall of transverse colon and stomach

• Identify and control source of contamination

(Small bowel, colon, stomach, then lesser sac)
• lnfra-mesocolic exploration
o Pull transverse colon cranially, and run the bowel from ligament of
Treitz to rectum, examine bowel (mesenteric and anti-mesenteric)
and mesentery

• Supra-mesocolic exploration
o Pull transverse colon caudally and examination of supramesocolon
o Entering the less ,er sac:
• Through left greater omentum "thinner and less vascular"
• Identify any fluid collection
• Posterior stomach, duodenum, and pancreas

± Kocherization

± Exploration of retroperitoneum

o Decision:
• Definitive repair
• Damage control
Maneuvers to exposure of retroperitoneum:
Right side:

Classic Kocher

■ Maneuver:
o Incise lateral peritoneal attachment of 1 st, and 2nd duodenum and retract it along with
head of pancreas medially until left lateral edge of aorta

Care to preserve right renal artery

■ Exposure: IVC, distal CBD, aorta, right kidney, duodenum, and head of pancreas

Extended Kocher: (Part of Cattell-Braasch)

U!OJ:m
Division of
parietal ,peritoneum

■ Maneuver:
o Mobilize D3 and continue by standard kocher along white line of Told! until the cecum

o Extension up to the porta hepatis, and posteriorly to the level of left renal vein

Care to preserve replaced right hepatic artery

■ Exposure: SMA, Infra-hepatic IVC, right kidney, right iliac vessels

 Cattell-Braasch: (Right medial visceral rotation}:: Super-Extended kocher

■ Maneuver: CBD - DJjunction

o Kocher maneuver by mobilizJng the duodenal loop from CBD to SMV inferiorly

o Extended Kocher maneuver by incising the posterior peritoneum along the white line of
Toldt and mobilizing the right colon medially

o Incise the avascular line of fusion of the small bowel mesentery to the posterior
peritoneum from cecum up along the "white line" between cecum and ligament of Treitz

■ Most common complications:

o SMV injury at the root of mesentery
o Avulsion of middle colic vein

■ Exposure:
o lnfra-mesocolic retroperitoneum
o IVC
o Celiac trunk
o Renal and iliac vessels
o Infra-renal aorta and aortic bifurcation
o 3'•, 4th part of duodenum
o Head of pancreas
Left side:
Mattox: (Left medial visceral rotation)

II
�
- I
)I
//
,,
I
t

■ Maneuver
o Mobilize descending colon by incise sigmoid colon to splenic flexure along lateral
peritoneal reflection

o Retract the descending colon, left kidney spleen, pancreas, and stomach medially
• Modified mattox maneuver by keeping the kidney in Gerota's fascia

o Continue dissection upward lateral to spleen for mobilization of spleen medially

■ Most common compUcations·

o Splenic injury
o Avulsion of the descending lumbar vein

■ Exposure:
o Supra-mesocolic retroperitoneum (Central)
o Aorta
o Celiac trunk
o SMA/SMV
o Left renal and iliac vessels
o Tail of pancreas
DAMAGECONTROLLAPAROTOMY
■ Definition: rapid termination of an operation after control of life-threatening bleeding and
contamination followed by correction of physiologic abnormalities and definitive management

■ Used in patient with borderline of lethal triad (Coagulopathy, Metabolic Acidosis, Hypothermia)
o Arterial pH of ,s; 7.2
o Lactic acid > 5 mmol/L
o Base deficit < - 15 in < 55 years, < - 6 in > 55 years
o Temperature < 35 degree centigrade
o PT and/or PTT > 50% normal

■ Examples:
o Ligation of uncontrollable venous bleeding (No venous repair)

o Bleeding duodenal/gastric ulcer

o Direct suture, resection, or by direct packing , with no reconstruction

o Gastrointestinal perforation with generalized peritonitis

o Peritoneal lavage with transection of proximal intestines and no reconstruction

o Acute mesenteric ischemia

o Staged laparotomy with resection of necrotic bowel and no anastomosis

o Toxic megacolon
o Subtotal colectomy with distal sigmoid and rectum left in situ

o Acute cholecystitis
o Percutaneous cholecystostomy, Subtotal cholecystectomy
 PELVIC TRAUMA
■ Associated with 15% Urethral injury, 7% Bladder rupture, and Rectal injury
■ Pelvic fracture associated with supra-pubic tenderness and pelvic lateral wall tenderness
■ Open book: diastases of> 2.5 cm
■ Anterior pelvic fractures: Venous bleeding 80%
o Inspection for open wound, scrotum, and penile meatus
o Bimanual and speculum examinations in female
o Gentle compression on ASIS toward midline with mild anteroposterior movement

■ Posterior pelvic fractures: Arterial bleeding 10 - 20%

o Most common artery injured: Superior gluteal artery
o Inspection for open wound, perineum, and perianal
o Palpation of the sacrum, sacroiliac joint, and DRE and assessment of prostate

■ Management:

Stable Unstable

FAST positive FAST negative

laparotomy
Conservative management Pelvic Fixation Unstable Stable
Pelvic Packing

Pelvic Packing CT scan

Post-operative status Pelvic Fixation 1) Pelvic Binder
Re-do FAST 2) External Fixation
�-----,---�1 3) Angioembolization

Stable Unstable ±

Continue conservative management Angioembolization

Consider external fixation
o Pelvic packing:
• Through 10 cm midline incision from pubic symphysis extended superiorly
• 3 laparotomy pads placed on each side deep within preperitoneal space
• Fascia is closed with O polydioxanone monofilament suture
• Skin closed with staples

I
o Indications for angiography:
• Ongoing transfusion> 4 units [n first 12 hours after the coagulopathy is corrected
• Pelvic ex1ravasation of the contrast on CT imaging
• Persistent instability after packing (arterial source}

o Open pelvic fracture:

• Diverting sigmoid colostomy used to reduce risk of infection
• The perineal wound left to heal by secondary intention with VAC device
o Pelvic binder/sheet:
• Indicated as initial management of an unstable ring injury

• Contraindications:
• Hypothetical risk of over-rotation of hemipelvis and hollow viscus injury
(bladder) in pelvic fractures

• Technique:
• Centered over greater trochanters to effect indirect reduction
• Do not place over iliac crest/abdomen
• May augment with internal rotation of lower extremities and taping at
ankles
• Prolonged pressure from binder or sheet may cause skin necrosis

• Pitfalls:
• Binder can mask pelvic ring injuries, creating false negative radiographs
and CT images

o External fixation of the pelvis:

• Indicated in unstable ring injury with ongoing blood loss

• Contraindications:
• Ilium fracture that precludes safe application
• Acetabular fracture

• Technique:
• Stability of bleeding bone surfaces and venous plexus in order to form clot
• Pins inserted into ilium
• Supra-acetabular pin insertion
o Single pin in column of supracetabular bone from AIIS towards
PSIS
o AIIS pins can place the lateral femoral cutaneous nerve at risk

• Superior iliac crest pin insertion

o Multiple half pins in the superior iliac crest
o Place in thickest portion of ilium (gluteal pillar)
o May be placed with minimal fluoroscopy
o Should be placed before emergent laparotomy
GASTRIC TRAUMA
■ Techniques:
o Primary repair (For most gastric injuri,es)

o Excision and primary repair (For perforated stress ulcer in trauma patients)

o Distal gastrectomy (For destructive injuries Stage IV "Billroth procedure"}

o Total gastrectomy (For rupture or dev .ascularization of> 50% of the stomach)

o Drainage procedure (For injuries involving the Latarjet nerves)

SMALL BOWEL/DUODENAL TRAUMA
■ Most common site of duodenal trauma: 2nd part
■ Most common site of duodenal hematoma: 3"' part
■ Associated with seat-belt sign (which also associated with mesenteric tears)
■ CT findings:
o Extra-luminal contrast or air "lung window"
o Bowel discontinuity
o Mesenteric stranding
o Sentinel clot (can cover the injured area}

■ Para-duodenal hematoma
o Usually presented on 2nd CT
o Clinical scenario: 1 st CT normal, after 24 hours patient still complain + CT
o Associated with Coiled spring sign (Appears also with intussusception}
o Management:
• As CT findings:
• Conservation (NGT + TPN) for duration of 2 weeks
• Most of them resolved within 3 - 4 weeks
• Start enteral feeding after 2 weeks:
o Tolerate + Continue conservative
o Not tolerate + Repeat CT
• Disappeared: Continue conservative
• Persistent after 4 weeks: Open, Check for laceration

• As intraoperative findings:
• All hematomas should be opened to rule out perforation
• For laceration associated with hematoma
o Should be closed in direction results in largest residual lumen by
primary repair transverse running monofilament absorbable suture

• Needle-catheter jejunostomy for medium to large hematoma

• Closed-suction drain and omental buttress for support duodenal repair

■ Mesenteric hematoma or injury:

o Assess the mesentery
• Expanding or not

o Assess the bowel

• Color
• Pulsation
• Peristalsis

Bucket handle: mesentery is stripped away from the bowel

Leading to bleeding and ischemic bowel

o Management of mesenteric injury:

• Conservative management (Control bleeding)
• Resection and anastomosis of the bowel: if associated with bowel ischemia
Grade Descriotion
Grade I Hematoma 1 portion
Partial-thickness Laceration
Grade II Hematoma > 1 portion
Laceration < 50% circumference
Grade Ill Disruption
50 - 75% 2nd part of duodenum
With no involvement of ampulla
50 - 100% other parts or small
bowel
Grade IV Transaction
Disruption ;, 75% 2"" part
lnvolvina amoulla or distal CBD
Grade V Transection with tissue loss
Duodenal devascularization
Disruption of duodenopancreatic
complex
Manaaement
La,�raliao:
■ Clean:
Primary repair, transversely (Single or double layers)
Omental buttress by Continuous 3--0 absorbable suture
Resection and anastomosis for multiple injuries in
short segment
■ A:;i;w;isilffll will! 1.2ats1miailli2!l·
Debridement (Trimming of the edges/
:t Duodenal diversion :t feedina ieiunostomv
1 11 part duodenum:
■ Debridement or resection and end-to-end repair
"Duodenoduodenostomy·
2nd part duodenum:
■ Proximal to ampulla:
Roux-en-Y Gastrojejunostomy (Preferable)
Repair with Jejunal serosal patch technique
± Pyloric exclusion
■ Distal to ampulla: (Proximal to mesenteric vessels)
Roux-en-Y Duodenojejunostomy
3'" 14'" part duodenum: (Distal to mesenteric vessels)
Remaining ofsmall bowel:
■ Resection and anastomosis (duodenojejunostomy)
■ Resection and stoma for high-risk patients
(Shock. severe contamination. de/av suraerv. > 6 PRBCs)
Unstable:
■ 1 - 2 stages repair:
0 Close suction drainage followed by repair
0 CBD ligation followed by reconstruction or repair
Stable:
■ Duodenal injury:
0 Duodenal diverticulization
0 Pyloric exclusion
■ Associated CBD injury:
0 < 50% circumference: Repair over T tube
0 > 50% circumference: choledochoenteric anastomosis
■ Ampulla injury:
0 Minor: Primary repair
0 Detach:
Re-implantation into duodenum
Re-implantation into roux loop of jejunum
■ P ancreaticoduodenectom:)! "Whipple procedure•:
0 Associated with complex pancreatic injury
0 Extensive amoulla or CBD iniurv
 - Duodenotomy:
- Cootinuou.s
�inglebyc<
POS sutures

Injury oo the inner/medial

P¥'l ofdw duocl�1.1m

Closure of ruodenotomy
using POS/Pot,t!Ktic acid soture
Pyloric exclusion + Gastrojejunostomy + NCJ
Injury of medial wall closed by PDS
Duodenotomy closed by Vicryl

Ouode..al
in_iu.ry sutured

Ttube
duodenostomy

Primary closure over T-tube + gastrostomy + NCJ Roux-en-Y duodenojejunostomy ± Tube jejunostomy

1.0l0ftlllld�w➔
Haemn-oa, OuochNfir,il;,ry ��
lh'iaYKoi$80!GIIJ

Primary repair with serosal patch of jejunum Pancreaticoduodenectomy

■ Duodenal diversion:
Used in complex pancreaticoduodenal injuries or isolated duodenal injury with non-optimal
repair or to protect duodenal anastomosis

o Roux-en-y duodenojejunostomy

o Retrograde jejunostomy
• Not recommended anymore

o Duodenal diverticulization (Berne procedure}: "3 tubes drainage"

• Primary closure of the duodenal wound
• Antrectomy ± Vagotomy
• Lateral tube duodenostomy
• Distal feeding jejunostomy tube
+ Nasogastric tube
± External drainage

�
± T-tube common bile duct drainage
± End-to-side gastrojejunostomy

Effective approach for grade IV duodenal trauma for duodenal injury without repair

o Pyloric exclusion+ Gastrojejunostomy (Jordan procedure)

• Should not performed if other diversion procedure was used
(as Roux-en-y duodenojejunostomy)

• Preferable option if duodenum can be satisfactory closed

• Pylorus opened by itself after 2 weeks - 2 months (within 3 months)

• Possibility of end-fistula (duodenal, or pancreatic 20%)

• Techniques:
• Suture:
o Gastrostomy then closure of pylorus with O PDS absorbable suture

• Stapler: (Alternative, less preferable)

o TA stapler: No g,astric transaction
• No need for re-operation for re-anastomosis

o GIA stapler: Associated with gastric transaction

• Need re-operation for re-anastomosis if no diversion

± Tube duodenostomy
+ Drain
PANCREATIC TRAUMA
■ Most common site of pancreatic trauma: Neck (against vertebra)
■ More common type of injury: Penetrating injury
■ Location of the duct:
o Between the 2/3 and 1/3 of the pancreas, posteriorly

■ i
Investigat ons:
o Serum amylase:
• Not sensitive or specific, repeated measurement increases its accuracy

o Pancreatography to identify ductal injuries

• ERCP
• Used for early (< 3 months) pancreatic pseudocyst
• To exclude ductal injury

• MRCP
• Operative (Trans-cystic or Trans-duodenal)

o Trauma CT:
• Can miss up to 30% of pancreatic injuries, can't detect ductal injury

• Findings:
Direct: laceration, hematoma, transection, head disruption, diffuse swelling

Indirect: hematoma at transverse colon, fluid in lesser sac, duodenal injury

lumbar spine fracture (chance fracture) against L1 spine

o lntraoperative assessment:!: intra-operative U/S

• Findings associated with pancreatic injury: central retroperitoneal hematoma, bile
staining or air in surrounding tissues, fluid collection in lesser sac

■ Exposure of pancreas:
o Kocherization: For inspection posterior surface

o Opening the lesser sac: For inspection upper and lower borders

o Mattox maneuver: For long pancreas

■ Damage control procedure: (Critically ill, massive bleeding, can't tolerate Jong procedure)
o External drainage, and distal feeding jejunostomy ± Pyloric exclusion
Followed by ERCP or MRCP to assess pancreatic duct injury
 Grade Contusion Tear
Ductal Management
disruotion
Grade I Minor <3cm No As CT finding:
- Non-operative management for most patients
- Drainage for persistent symptomatic patient
- ERCP may needed for patient who developed early
complications (as Pseudocyst) to exclude ductal injury

Grade II Major > 3cm No As Intra-operative finding:

- Open capsule to check the duct
Suspicion of injury? Operative Pancreatography, ERCP
- Repair for major(> 3cm) tear
- Close-suction drainage
± Needle catheter or tube ieiunostomv
Hemodynamically unstable
Closed-suction drainage

Hemodynamjcanv stable
Grade Ill
Distal transection
To the left of SMA/SMV
To the left of Portal vein
Yes ••
Distal Pancreatectomy with Splenectomy
With closure of the proximal duct
Distal pancreas either to be removed or anastomosis as
pancreaticojejunostomy

:1: Spleen preserving(low-risk)

+ Needle catheter or tube "'iunostomv
Proximal transaction Hennodynamically stable
Grade IV
To the right of SMAISMV
Yes Viable tissues
• lntra-t1ancreatic CBD injurt onl)!
0 Roux-en-y choledochojejunostomy
With closure of distal CBD

• Pancreatic duct injurt on!\t (Isolated pancreatic body)

0 External drainage, distal feeding access
ERCP next day ± Stent

0 Central pancreatectomy with closure of

proximal duct and distal pancreaticojejunostomy

0 Distal pancreatectomy � risk of brittle diabetes

Grade V Disruption of pancreatic head

• Both injured � Whipple

• Both non-injured � Primary repair, duodenal diversion,

external drainage and distal jejunostomy tube

Nonviable tissues
Associated with comelex duodenal or ameulla injuries

•
Associated with SMA/SMV injuries
Whipple or Staged-Whipple

••
Hennodynamically unstable
Closed-suction drainage
Temporary packinQ and return after 24 hours
■ Operative Panereatography:

1) Retrograde pancreatography "Trans-duodenal catheterization of pancreatic duct"

2} Mid-duct needle catheterization

3) Antegrade pancreatography "Catheterization of distal pancreatic duct"

Alternative: Intra-operative ERCP, MRCP, ERCP

 COLON TRAUMA
Manaaement
Non-Destructive wound Destructive wound
Grade Description
(tissue loss, devascularization,
mesenteric vascular iniurv)
Grade I Hematoma 1 portion
Seromusclar closure -
laceration of partial thickness
Grade II Hematoma > 1 portion

Laceration Primary closure Resection and anastomosis

< 50% circumference
re.a. Thro•�h and /hrouoh lnlurlesl
Grade Ill laceration Resection and anastomosis
> 50% circumference Resection and anastomosis
Resection and diversion
Grade IV Transection Resection and anastomosis
Grade V Transection with tissue loss
Resection and diversion

■ Pivertjna colostomy
o Indications:
• Shock
• > 6 PRBCs
• Multiple comorbidities
• Delay surgery
• Severe contamination

o Options:
• End colostomy: for destructive wound

• Proximal diversion: for non-destructive wound

■ Colonoscopy or Siqmoidoscopy:
o Should not be used to identify colonic injury, as it may worsen bowel injury
o It might be used selectively for gluteal injury to identify injury of pelvic organs along with
bladder catheterization

■ Hepatic flexure non-amenable to primary repair + Resection of right colon with ileocolostomy
 RECTAL TRAUMA
■ Most common type: penetrating trauma

I Intra-peritoneal I Extra-peritoneal I

I Proximal rectal injury I Distal rectal injury

I Not identified
Non-amenable for repair
I I
Non-Destructive Destructive
( < 50% of Circumference} (> 50% of Circumference}

! !
Primary repair Resection and anastomosis Proximal loop diverting colostomy
± Presacral drainage ± Proximal diverting colostomy Primary repair (for accessible wound)

± Presacral drainage
(For destructive wound, or posterior distal injury)

■ APR is reserved for devastating anorectal injuries, or severely damaged anal sphincters
LIVER TRAUMA
■ Most common injured organ in abdominal trauma

■ Most common type on injury: Blunt injury

■ CT findings:
o Periportal edema (Earliest sign)
o Contusion or laceration
o Hematoma or biloma
o Active bleeding
o Abscess in late stage

■ Stages:

Liver iniurv
Grade Description
Hematoma Subcapsular < 10%
Laceration Capsular tear < 1 cm depth
Hematoma Subcapsular, 10 - 50%
II
Laceration 1 -3 cm depth
Hematoma > 50% or expanding or intraparenchymal
Ill
Laceration >3 cm depth or involving trabecular vessels
25 - 75% Parenchymal devascularization
IV Laceration or 1 -3 Couinaud's segments within a single lobe
> 75% Parenchymal devascularization
Laceration or > 3 Couinaud's segments within a single lobe
V
Juxtahepatic venous injuries
Vascular (Retrohepatic IVC / Major hepatic veins)
VI Vascular Hepatic avulsion
■ Management:
o Blunt:
• Conservative: Stable patient (any stage, except stage IV, and V)
• With no other indications for laparotomy
• Stage IV and IV: highly selective patients

• Exploration: unstable patient

o Penetrating: Exploration

■ Conservative measures:
o Bed rest
o Fluid resuscitation
o ICU management
o Serial abdominal examination
o Serial Hemoglobin level every 6 - 8 hours
o Anticoagulation should be started within 48 hours
o Angioembolization

■ Non contraindication situations for non-operative management:

o Contrast blush: can managed with selective angiography and embolization

o Massive retroperitoneum
• Liver parenchymal bleeding "Low-pressure" and eventually will stop (unlike spleen)

■ Role of interventional radiology:

o For stable patient with low-grade liver injury or with active blush to increases successful
rate of non-operative management

o Indications:
• Contrast blush
• Hemobilia
• Pseudoaneurysm

■ Indications for operative intervention:

o Unstable patient
o Drop of hemoglobin
o Blood requirement 2: 6 units
o Signs of peritonitis
Operative Techniques for Hepatic Trauma
■ Exploratory laparotomy and control of bleeding (Sandwich packing of the liver)
■ Mobilization:
o Clamping and division of ligamentum teres, falciform, triangular, and coronary ligaments

■ Techniques to control liver injury:

Mild to moderate
o Peri-hepatic compressive packing (Best and initial step)
• Surgical sponges packing (keep if planned for second laparotomy: 48 - 72 hours}
• Hemostatic tampon
• Absorbable gelatin-com pressed sponge wrapped in hemostatic fabric

• Persistent bleeding despite packing:

• Injury to the hepatic artery, portal vein, or retrohepatic vessels

o Manual compression of the liver between both hands

o Electrocautery (for vessels < 0.5 mm in diameter)

o Direct liver suturing (0 Chromic on blunt needle)

o Topical hemostatic agents

• Oxidized regenerated cellulose
• Gelatin matrix
• Topical thrombin
• Fibrin sealant
• Microporous polysaccharide spheres

Moderate to severe
o Figure of 8 suturing

o Omental packing
• Used for packing of deep laceration for hemostasis and migration of immune
mediators into the injury
• Care to preserve right gastroepip/oic vessels

o Parenchymal vessel ligation

o Finger fracture/ Clamp-and-crush technique followed by definitive repair

for deep laceration to identify major vascular or ductal structure

o Constructed balloon tamponade (large Penrose drain and red rubber catheter}:
for large trans-hepatic penetrating injury

Massive after removal of packing

o Pringle maneuver

o Selective hepatic artery ligation

o Liver resection (Non-anatomical):

• Used for devascularized segment (Resection should not be at initial laparotomy)
■ Pringle maneuver:
o Indicated if bleeding is too brisk to allow visualization and control
o By digital pressure by left index and thumb to porta hepatis (hepatoduodenal ligament)
o Followed by clamping with vascular clamp, Penrose, or Rummel tourniquet
• CBO (lateral} � Most Anterior (to the right of hepatic artery)
• Portal vein (posterior)
• Proper hepatic artery (medial} � (right hepatic artery cross posteriorly to CBO)

0 Method:
1} Enter of lesser sac
2} Rotation of hand clockwise to access Foramen of Winslow
3} Manual compression of porta hepatis
4} Followed by Rommel tourniquet or vascular clamp "non-crushing clamp"

o Does not stop bleeding from:

• IVC
• Hepatic veins
• Aberrant left hepatic artery (doesn't enter the porta hepatis}
• Aberrant right hepatic artery if runs posterior and to the right of porta hepatis

o Cycle:
• Continuous:
• Up to 45 - 60 minutes

• Intermittent:
• 15 minutes with 5 minutes off for reperfusion (maximum 30 - 60 minutes)
• Associated more with re-perfusion injury
■ Methods to control injury that controlled only by Pringle maneuver
o Selective artery ligation and Omental pack
• Ligation of left or right hepatic artery
• Beyond bifurcation of proper hepatic artery
• Need prophylactic cholecystectomy if right hepatic artery ligated

• Proper hepatic artery should not be ligated

• Common hepatic artery

• Can be ligated due to extensive collaterals (GOA backflow ➔ Uver)
• Can be attempted if portal vein intact
• Assessment done by release of Pringle after occlusion of the artery
• Angiography may considered when patient shifted to ICU post-operatively

o Portal vein ligation

• Used in critical ill patient with non-amenable portal vein for repair
• If ligated, need second look to check viability of liver and bowel
• If repair is amenable, Primary repair with lateral venorrhaphy by 5 - 0 Prolene
suture is preferred

■ Methods to control iniury that Uncontrolled by Pringle maneuver

o Peri-hepatic packing for hepatic veins
• Controlled:
• Shift to ICU ± Hepatic vein stent by radiology

• uncontroned·
• Direct repair with distal (supra-renal) and proximal IVC clamping and
stapled-assisted parenchymal resection

• Temporary shunting of the retrohepatic vena cava (Atriocaval shunting)

o Associated with mortality rates as high as 90%
o 36 Fr chest tube is prepared by creating hole in its proximal-end
o Place the distal holes in IVC below renal veins
o Open the chest
o Clamp the proximal end of the tube
o Insert the tube in1o right atrium and secure with purse-string
o Advance the tube down to infra-hepatic vena cava

• Venovenous bypass and repair of the liver injury

o Jugular to Femoral vein bypass

o Temporary Supra-celiac aortic control

■ Complications of liver injury:
o Delayed or recurrent bleeding
• Most common complication of non-operative management for liver injury

o Abdominal compartment syndrome (lihe only complication treated non-conservatively)

o Pseudoaneurysm
o Biloma
o AV fistula
o Abscess
o Infarction

■ Gallbladder injury:
o Treated by cholecystectomy

■ Common bile duct injury

o < 50% of circumference -+ Repair over T tube

o > 50% circumference (e.g. CBD transeclion):

• Choledochojejunostomy ± Cholecystectomy
• Used for isolated CBD injury
• Used for intra-pancreati-c CBD injury with no pancreatic injury

• Whipple
• If associated with other injuries

lntraoperative cholangiogram if injury not identified or bile oozing only from liver bed
SPLEEN TRAUMA
■ Most common type of injury: Blunt injury
■ Most common early post-splenectomy complication: Bleeding
■ Associated with OPSI up to 8%

■ Keh r's sign: Acute pain at tip of left shoulder due to diaphragmatic irritation by blood or other
contents or in rupture spleen during supine position with leg elevation

■ Infectious mononucleosis -+ presented with fever, leukocytosis, hepatosplenomegaly

o Atypical lymphocytes and very high bilirubin
o Can be presented after blunt trauma

■ Imaging findings associated with splenic trauma:

o Left lower ribs fracture in 20%
o Left lower lobe atelectasis
o Pleural effusion

■ Grades:

Solenic iniun,
Grade li>escriotion
Hematoma Subcapsular < 10%
Laceration Capsular tear < 1 cm depth
Hematoma Subcapsular, 10 -50%
II 1 -3 cm depth
Laceration
Hematoma > 50% or expanding or intraparenchymal
Ill > 3 cm depth or involving trabecular vessels
Laceration

IV Laceration Segmental or hilar

> 25% devascularization
V Laceration Complete shuttered spleen
Advance one stage for > 1 injury of same grade

■ Delayed splenic rupture after 48 hours can happen due to rupture of subcapsular splenic
hematoma and may need to repeat CT

■ Management of all grades is conservative as long as patient is stable

o ± ICU management
o Bed rest
o IV fluid
o Cross-match and blood standby
o NGT

■ Stable patient with blush of contrast on CT:

o Decreased significantly the non-operative management outcome
o Selective Angioembolization can be used with risk of complications
■ Risk factors of non-operative failure:
o > 40 year old
o Need for blood transfusion
o High-grade injuries

■ Indications for splenectomy: /Failure of conservative measures)

o Patient remains unstable
o Hilar injuries
o > 6 Units of PRBCs in 24 hours
o Active blush or pseudoaneurysm after failure or non-available angioembolization
o > Grade II associated with coagulopathy or multiple injuries
o No ICU / Blood available
o Unable to shift the patient to OR quickly

■ Principles for splenectomy in trauma:

o Exploration must be done for other injuries as well
o Lateral to medial approach
o Hilar divided combined not separately (with risk of pseudoaneurysm}
o No need to search for accessory spleen as in elective
o Vaccines should be given after 2 wee ks or upon discharge
o Antibiotics should be given if patient having high WBC or fever to prevent OPSI

■ Splenic artery embolization

Indications
o Trauma
• Borderline hemodynamically unstable with documented isolated splenic injuries
in high-risk patient for surgery
• Hemodynamically stable splenic injury grade IV-V ± contrast extravasation ±
splenic vascular injury (arterial injury on CT scan)

o Hypersplenism
• Used for massive spleen {>20 cm) before laparoscopic splenectomy

o Splenic artery aneurysm and pseudoaneurysm

Technique
o Proximal coil embolization: is the technique of choice

o Selective or Distal embolization (beyond hilar vessels):

+ Associated with splenic necrosis and infarctions
o Both

Complications:
o Splenic infarction
o Abscess or rupture
o Splenic vein thrombosis
o Sepsis
o Pancreatitis
Splenic preservation (Splenorrhaphy)
■ Indication:
o Selected hemodynamic stable patients with no other injury

■ Method:
o Mobilization

o For splenic capsule tear:

• Applying hemostatic clips or suture ligation (continuous) with care not to tear
capsule

• By insert suture into strips or pledgets of Teflon felt, omental pedicle, or oxidized
cellulose gauze

o For Multiple splenic superficial injury (intact hilum)

• Argon beam
• Horizontal mattress sutures
• Fibrin glue
• Topical hemostatic agents
• With pressure, and for oozing, need to be applied on dry surface
• Double sheath of oxidized cellulose gauze covered by gauze
• Avitene

• Absorbable Dacron mesh wrap + pressure and purse string (PDS 2-0}
• For high grade splenic injury

■ Partial Splenectomy
o Used for:
• Selected hemodynamic stable patients with no other injury
• Patient with injury limited to superior or inferior pole

o Temporarily occlude the splenic artery with a Silastic loop

o Ligate the traumatized vessel from hilum
o Release splenic artery and observe the line of demarcation
o Remove the devascularize part by electrocautery along capsule line

■ Partial or total splenectomy with auto-transplantation

o To achieve partial immunocompetence in younger patients who do not have associated
enteric injury

o Performed by placing sections of splenic parenchyma into pouches in the greater

omentum
RETROPERITONEAL ZONES

■ Zone I (Central zone) Medial to psoas muscle

o Supra-mesocolic area
o lnfra-mesocolic area

■ Zone II (Peri-nephric or Para-colic zone} Lateral to psoas muscle

■ Zone Ill (Pelvis zone)

Management approach:
o Penetrating: Exploration (any zone}

o Blunt:
• Zone I: Exploration
• Exposed by Mattox maneuver (Left-sided medial visceral rotation)

• Zone II: Observation/ Explore if expanding/ pulsatile or extravasation

• Exposed by Mattox maneuver (Left-sided medial visceral rotation)

• Exposed by Cattell maneuver (Right-sided medial visceral rotation)

o For IVC, or right renal vessels injury
• Zone Ill: Observation/ Explore if expanding/ pulsatile or extravasation
• Exposed by rapid exposure of distal aorta at root of mesentery to identify
iliac vessels

Aortic clamp·
o Supra-diaphragmatic aortic control •Through left thoracotomy"
• Used for uncontrolled or expanding supra-mesocolic hematoma

o Supra-celiac (infra-diaphragmatic) aortic control "Through /aparotomy"

• Used for expanding hematoma above celiac level
• Access lesser sac
• Through gastrocolic ligament
• Through gastrohepatic Iigament
o By mobilization of left liver lobe, dividing the left crus taking care not
to injure the phrenic nerve,
• Manual compression with pres sure against the spines
• Followed by exposure and repair in zone I or II

o lnfra-celiac (and above the renal arteries)

• No occlusion
VASCULAR TRAUMA
■ Palpable radial pulse: Systolic blood pressure > 80 mm Hg
■ Palpable femoral pulse: Systolic blood pressure > 70 mm Hg
■ Palpable carotid pulse: Systolic blood pressure > 60 mm Hg

Hard sians Soft sians

Pulsatile or exoandina hematoma Non-oulsatile non-exruondina hematoma
Absent distal oulse Diminished oulse
Bruit or Thrill lniuru in oroximitv to name vessel
lschemia (ABI < 0.4) ABI < 0.9
(Pulselessness, Pain, Pallor, Paresthesia,
Paralysis, and Poikilothermia)
Management: Management:
+ OR exploration +ABI
< 1.0: CT Anaioaranhv

■ No venous repair in damage control surgery -+ Ligation (e.g. popliteal vein, IVC)
■ Vascular repair performed before orthopedic repair
o Primary repair always (if< 2 cm)
o Saphenous vein graft (if 2: 2 cm)
(Use contralatera/ saphenous vein, if you ligate concurrent vein)

Tolerate to be liqated Not tolerate to be ligated

Internal iuaular vein Aorta
External or internal carotid arterv Common carotid
SMA tCollateral will be from Celiac) "Preferred not to be liaated"
SMV (Risk of bowel edema 2 - 3 months) "Preferred not to be ligated"
Portal vein "Preferred not to be ligated"
IVC "Preferred not to be ligated, especially supra-renal IVC"
Riaht or left or Common heoatic arterv Heoatic oro=r arterv
Left renal vein Riaht renal vein
Pooliteal vein
Internal iliac arterv

■ foe difficunof exposure of confluence of common mac vein-

+ Divide the right common iliac artery and mobilize aortic bifurcation to left for exposure
followed by definitive repair

■ IVC iniuries:
o Primary repair if< 50% of the diameter
o Saphenous vein or synthetic patch if> 50% of the diameter
o Repair posterior wall through anterior wall (if intact anterior wall -+
cut through it)
o Ligation of IVC is tolerated below the renal veins (due to presence of collaterals)

■ Mangled extremities severity score: used in extremities amputation in trauma

 ABDOMINAL COMPARTMENT SYNDROME (ACS)
■ Definitions:
o Intra-abdominal hypertension> 12 mm Hg
o Abdominal compartment syndrome:
o > 20 mm Hg, and usually resu Its in organ failure
o Any intra-abdominal hypertension with organ failure

■ Measured by: Bladder pressure

■ Technique: (showed be done every 4 hours in presence of risk factors)

o Transducer zeroed in the mid-axillary line at the level of the iliac crest
o Patient should be in: Supine position
o Insert Foley's catheter and attach it to 3 stopcocks connected to each other's
NS infusion bag 60 ml syringe Pressure tube

� D ra ina g tube
Foley's Catheter 'I--------.....� � --
----- _ _ _ _
_,j

■ Clamp drainage tube

o Stopcock 1: OFF and Stopcock 2: ON -+ Aspirate 25 ml (maximum)
o Stopcock 2: OFF and Stopcock 1: ON -+ Instill 25 ml to bladder
Wait 30 - 60 seconds (to allow relaxation of detrusor muscle)

o Stopcock 1 & 2: OFF and Stopcock 3: ON -+ measure pressure

Measure !AP at end�xpiration with no abdominal contractions

o Unclamp drainage tube

■ Physiological effects:

Increased Decreased
CVP COP
Heart
PCWP
Vascular Peripheral resistance Venous return

Peak Pressure Compliance

Pulmonary
FRC
Renal blood flow
Renal GFR
UOP
ICP
Others Potassium level
■ Treatment:
o DECOMPRESSION LAPAROTOMY
o Associated with 60% Mortality
o Can be done as bed-side for ICU patients
o Indications:
• Intra-abdominal pressure > 35 mm Hg
• Any intra-abdominal pressure resulting in end-organ dysfunction

o PERCUTANEOUS DRAINAGE
o For significant ascitic component of abdominal compartment syndrome
o Ultrasound should be done to determine amenability for drainage

■ Techniques for closure after decompression laparotomy:

o 10- 10 loban closure

o Vacuum-assisted devices

o "Towel clips" over the skin only

o Bogota bag closure "Named for Colombian surgeon"

o Sterile open urological irrigation bag

o Sequential fascia! closure technique (Denver technique)

o Preferred for laparotomy not closed at second laparotomy

o Split-thickness skin grafts

o Prosthetic fascia! closure with mesh and skin closure

o Serial closure of upper and lower aspects of the fascia

LIMB COMPARTMENT SYNDROME

■ Risk factors:
o Volkmann's contraction
• Permanent flexion contracture of the hand at the wrist (claw)
• Due to supracondylar fracture of the humerus -+ Obstruction of brachia! artery

o Crush injury
o Reperfusion after time of ischemia
o Fracture (Most commonly tibial fracture)

■ Mediated by PMNs (Polymorphonuclear cells}

■ Most common site:

o Anterior compartment of the leg

■ Most common assocjated nerve injury·

o Superficial peroneal nerve

■ Earliest sign:
o Paresthesia between 1 st and 2nd toes (by pressure on deep peronea/ neNe)
o Pain with passive motion

■ Diagnosis:
o Compartment pressure > 20 mm Hg

■ Treatment:

o 4 - QUARDANT FASCIOTOMY for all compartments

o Indications:
• Compartment pressure > 25 mm Hg

• Gradient pressure < 35 (Diastolic pressure - Compartment pressure)

o Medial incision:
• Used to allows decompression of superficial and deep posterior compartments

o Lateral incision:
• Used to allows decompression of anterior and lateral compartments
ORTHOPEDIC TRAUMA

■ Most common missed injury: Bone fracture (Mostly rib fracture)

■ Most common missed fracture: Phalangeal fracture

■ Long bone fractures:

o Traction and Splinting

o External fixation: in Contaminated/ Open fractures

• Temporary method, used in trauma with multiple injuries (hemodynamically
unstable) as bridging for definitive management

o Internal fixation (lntra-medullary nailing within 24 hours):

• Definitive management in adults for close long bone fracture

o Spica casting: in< 5 years old patients

Definitive management in < 24 hours decreased the morbidity and mortality

Femoral neck fractures associated with avascu/ar necrosis

■ Knee Ligaments injury :

o Anterior cruciate ligament: Most injured ligament
• History of pop or snap with immediate effusion

o Medial collateral ligament:

• When knee forced medially to leg by lateral injury (Medial pain)

o Lateral collateral ligament:

• When knee forced laterally to l,eg by medial injury (Lateral pain)

o Patella ligament:
• Injured when falls on partially flexed knee

■ Knee dislocation+ Reduction and checkABI

o Pulse present + ABI if< 0.9 + Angiography
o Pulse absent + OR

■ Shoulder dislocation
o Anterior + Axillary nerve
o Posterior+ Axillary artery

■ Hip dislocation
o Anterior + Femoral vein
o Posterior+ Sciatic nerve (Findings: Flexed, Internal rotated, Adducted lower limb)

■ Colle's fracture+ Posterior angulation of radius

■ Smith fracture -t Anterior angulation of radius
NERVES INJURY OF UPPER EXTREMITY
Motor Sensorv Deformitv Mechanism
Radial nerve Extension and Web space Wrist drop Fracture of

·1
�,,· f
/Most common/ flexion of the between thumb proximal
wrist and index with humerus
C5-T1 dorsal fingers
All extensor
muscles of the
hand, triceps
muscle
�-�
Median nerve Thenar muscles Web space Ape thumb Supracondylar
(thumb, index) between thumb fracture of

��.:I.
C5-T1 and most and index with humerus

-
anterior group palmar fingers
of forearm
f;-

�.,
Ulnar nerve Abduction of Dorsal and Claw hand Supracondylar
all fingers planter of little fracture of
C8-T1 and ring finger humerus
All intrinsic
muscles
�-
RENAL TRAUMA
■ Hematuria is the best indicator of renal trauma

■ Anterior-+ posterior renal hilum structures: (Vein-Artery-Pelvis}

■ Investigation: CT scan with contrast

■ Management:
o Associated with renal vascular injury: Nephrectomy (Unless it is the only kidney}
o Not associated with renal vascular injury: Nephrorraphy or Partial nephrectomy
Ureter should be identified and confirm continuity from pelvis to bladder

BLADDER TRAUMA
■ Associated with pelvic fracture
■ Management:

CT Cystogram (Most accurate test)

o Extra-peritoneal (Extravasation surrounding the bladder}

• Foley's catheter 7-14 days

o Intra-peritoneal (Contrast leak and outlining loops of bowel}

• Primary repair of the defect

■ Most common cause of bladder neck obstruction: Posterior valves

URETERAL TRAUMA
■ Associated with pelvic fracture
■ lovestjgations·
o CT scan with delayed phase
o IVP and retrograde urethrogram (RUG)

■ Technique of retrograde urethrogram:

o Position:
Obliquely 45 degree with bottom leg flexed 90 degree at the knee and top leg kept
straight

o Fluoroscopic C-arm positioned just below pubic bone

o Foley catheter flushed with radiopaque contrast and inserted just inside urethral meatus
resting over fossa navicularis

o Catheter balloon is filled with 1 - 2 ml of radiopaque contrast or saline solution

o Take pre-injection image

o Catheter-tipped syringe is then filled with 50 ml of radiopaque contrast, and 20 - 30 ml

of contrast is injected in retrograde fa shion

o TaKe retrograde urethrogram image

 ■ Management of ureteral injury:
Unstable patient or associate with other injuries
o Ligation of both ends of ureter
o Percutaneous nephrostomy
o Uretero-ureterostomy as delayed reconstruction after 3 months

Stable patient
o Partial transaction: Repair over the stent

o Complete transection
• Upper and middle (above pelvic brim)
• < 2 cm: Primary repair
• > 2 cm:
o Initially: Percutaneous nephrostomy and tie both ends
o Later: Uretero-ureterostomy or ileal interposition
• Lower (below pelvic brim)
• Re-implant into the bladder± psoas hitch or Boari flap

Leave drains for all uretera/ injuries

URETHRAL TRAUMA
■ Presentation:
o Hematuria or blood at meatus

■ Investigation:
o Retrograde urethrogram (RUG)

■ Treatment:
o No Foley if this injury is suspected

o Suprapubic cystostomy and repair in 2 - 3 months

PEDIATRIC TRAUMA
■ Blood pressure is not a good indicator of blood loss in children
■ t risk of head injury
■ t risk of hypothermia
■ Normal pulse:
o < 1 year: 160 bpm
o < 5 years: 140 bpm
o > 10 years: 120 bpm

TRAUMA DURING PREGNANCY

■ Pregnant patients can have up to 30% total lblood volume loss without signs
■ Estimate pregnancy based on fundal height (20 cm = 20 weeks = at level of umbilicus)
■ Pelvis protect uterus up to 12 weeks
■ Recommended position:
o Left lateral decubitus

■ Alteration in pregnancy:
o t Cardiac output
o t 2.3 DPG
o Partial IVC obstruction

■ Indications for C-section during exploratory laparotomy for trauma:

o Unstable spinal injury

o Persistent maternal shock or severe injuries and pregnancy near term (> 34 weeks)

o Threat to the mother's life (hemorrhage, DIC)

o Risk of fetal distress exceeds risk of immaturity

o Maternal death
 TETANUS

Tetanus prone wounds Non-Tetanus prone wounds

3 doses and < 5 vears None None
3 doses and > 5 vears Td None
3 doses and > 10 years Td (1 dose) :1: TIG (Controversial) Td (1 dose)
Or immunocomoromised
< 3 doses or unknown Td (3 doses\+ TIG Td (3 doses\
TIG: Tetanus immunoglobulin (Anti-toxin)
Td: Tetanus toxoid (Vaccine)
'7dap is preferred to Td for adult who never received Tdap"

■ Tetanus prone wounds:

o > 6 hours old
o > 1 cm depth
o Contamination (infected)
o lschemia or devitalized tissue
o Burn

■ Doses:
o Tetanus toxoid: 0.5 ml intramuscular
o Tetanus immune globulin: 250 units intramuscular

■ Vaccination:
o Tetanus toxoid (vaccine) given at age of 2, 4, and 6 months
o Booster doses of tetanus toxoid given at age of 1 and 5 years

RABIES
■ Given after bite of wild animal
■ HRIG and HDCV given both as soon as possible after exposure
■ HDCV given also on days 3, 7, 14, and 28
■ Always in deltoid area
o if given into gluteal area -+
leads to lower neutralizing antibody titers

OTHERS
■ Absorbable sutures used in:
o CBD repair
o Ureteric repair
o Lung repair
o Tracheal injury
o Bronchial injury
o Small bowel injury
o Solid organ injury

■ Non-absorbable sutures used in:

o Heart (Pledgeted non-absorbable suture)
o Pancreas
o Diaphragm
o Pyloric exclusion
o Vascular structures
Critical Care
CRITICAL CARE
■ Preload = LVEDV = End Diastolic Volume (estimated by CVP, or PCWP)
■ Afterload = SVR
■ Cardiac Output (CO) estimated by: Partial CO2 re-breathing
■ r 02: closes ductus arterosus
■ ! PVR: closes foramen ovale

Central Chemoreceotors Perioheral Chemoreceotors

Location Ventral surface of brainstem Aortic arch bodies
Carotid bodv
Sensitive to pH of CSF 02, CO,, H+ (pH)
Indirect: CO, of plasma Pressure alteration
Stretch of vascular wall
Influence Resoiratorv drive to breathe Acute chan=d in blood oases
Effects Increased respiratory rate I depth In response to t CO,, ! O,, acidosis
In response to f CO2 Inhibition of autonomic nervous system
Leading to:
- Increased respiratory rate / depth
- Svstemic vasoconstriction

■ Aortic bOdy:
o Peripheral chemoreceptor in between aortic arch and pulmonary artery
o Send signals through: Vagus nerve (X)
o 02 sensor

■ Carotid bOdy:
o Peripheral chemoreceptor in common carotid {al carotid bifurcation) "Adventitia"
o Send signals through: Glossopharyngeal nerve {IX)
o 02 sensor
o Glossopharyngeal & Vagus
o Most common site of paraganglionoma: carotid body

■ Carotid Sinus: Pressure sensor

PULMONARY ARTERY CATHETERIZATION "Swan Ganz catheter"
o Indications
• Diagnostic: Coronary artery disease (complicated Ml)
• Therapeutic:
• Aspiration of air emboli
• Assessment of fluid requirement in shock patient

Monitor with PA catheter will no decrease mortality, ICU length of stay or Post-op Ml
Dysrhythmia is the most common complication

o Technique
• Insertion into pulmonary artery in zone Ill (lower lung)
• Because alveolar pressure is lowest (no interruption of flow) f accuracy

o Through:

Distance to right atrium Distance to wedge

ln ulmonarv arterv oressureI
Riaht subclavian vein 10-15cm 45cm
Right Internal jugular vein
15-20cm 50cm
IStraiohtest and lowest comollcationt
Left subclavian vein 10-15cm 55cm
Left Internal iuaular vein 15-20cm 60cm
Femoral or brachial vein

o Measurement:
• Pulmonary artery pressure:
• Pressure transducer must be calibrated and zeroed to level of left atrium
• Best placed at level of right atrium
• Normal level: ( 15/5 - 30/15) mm Hg

• Pulmonary artery wedge pressure:

• Measuring left ventricle pressure (reflected Left atrium pressure)
• Measured at end-expiration after inflation of the balloon
• Non-pulsatile pressure, Normal level: 5 - 15 mm Hg (preload)
• Not affected by PEEP if < 10
• Pulmonary Embolism /PE}: l PA pressure ! PCWP

• CVP = Right atrium: 2 - 6 mm Hg (afterload)

• Sv02 , Cl, SV, SVR, PVR and temperature

o Interpretation:

CVP/PCWP CO/Cl SVR/PVR SvO,

Distributive lseoticl shock I t I t
Cardioaenic shock t I t J
Hvnnvolemic shock I I t I
Neuroqenic shock l l l t
• Septic shock presented without signs of hypovolemia "oliguria" (Nonmal COP)
• Cardiogenic shock presented with distended neck veins (Elevated CVP/PCWP)
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)
■ Definition:
o Dysregulated inflammatory response to non-infectious stimuli
• Such as trauma, burns, pancreatitis, surgery, and autoimmune disorders.
o Endotoxin (lipopolysaccharide: lipid A) is the most potent stimulus for SIRS
� TNF-a release
o Inflammatory response mediated by: Macrophages

■ SIRS Criteria: Presence of:? 2

o Temperature > 38 or< 36 •c
o Heart rate > 90 BPM
o Respiratory rate > 20 or PaCO2 < 32
o WBC > 12000 or < 4000 mm3 or> 10% bands

■ Quick Sequential Organ failure assessment (qSOFA Score):

o Presence of> 2 of:
• Respiratory rate :? 22 breaths/min
• Alter mental status
• Systolic BP s 100 mmHg

SOFA score better than SIRS in prediction of mortality (with 20% difference)

■ SEPSIS:
o Definition:
• Body's overwhelming and life-threatening response to an infection, which can
lead to tissue damage, organ failure and death
• Presence of SIRS resulting from infection "Documented infection•
� Most common overall infection cause sepsis: Pneumonia
o Sepsis should be identified within 6 hours (early recognition)
o Most common organism: E. coli

o Predictors of mortality in sepsis:

• Platelets level: Thrombocytopenia t mortality
• Chloride level: t Chloride level> 110 t mortality and may leads to renal failure
• Mortality in septic shock: 40%

■ Severe Sepsis:
o Sepsis + Organic dysfunction by dysregulated host response to the infection
• Examples: Hypotension, Lactate> 4 mmol, Coagulopalhy, Oliguria,
Thrombocytopenia, Hypoxemia (Pa02 / Fi02 < 300), Decreases level of
consciousness

■ Septic Shock:
o Sepsis with refractory hypotension despite adequate fluid resuscitation requiring
vasoactive medication to maintain MAP> 65 mmHg and lactate> 2 mmol/L

■ Multi-Organ Dysfunctions /MODS): Failure of:? 2 organ dysfunction

MANAGEMENT OF SEPSIS
■ 1 st hour:
o Initial resuscitation (30 ml /kg): 2 L crystalloids "as 500 ml every 10 - 15 minutes·
• After given of 2 L NS check response and switch to RL (to ! metabolic acidosis}

o Serial Lactate level {as measurement of tissue perfusion and end-point resuscitation)
• Measure lactate level upon presentation, and repeat it after 2 - 4 hours if lactate
> 2 mmol/L
• Causes oft Lactate level:
Q Bowel ischemia
Q Renal failure
QOM
Q Pancreatitis
Q Malignancy
Q Pheochromocytoma
Q Infection
• Base deficit is associated with metabolic acidosis and predict mortality
Q Less accurate and affected by renal dysfunction, alcohol,
hypoalbuminemia, and large volume resuscitation

o Blood culture before IV Antibiotics

o IV Broad-spectrum Antibiotics within 1 hour of diagnosis

• Mortality is increased 10% for every 1-hour delay in septic shock

o Maintain MAP:? 65 mm Hg (> 80- 85 in known HTN to ! risk of renal failure)

• Combined with measurement of UOP > 0.5 mVkg/hour
• If< 65 despite fluid resuscitation: Start Vasopressors
Q Drug of choice: Norepinephrine or Dopamine
Q 2nd line drug: Vasopressin can be added
Arterial catheterization required in patient in need for vasopressor therapy

o Ongoing hemodynamic assessment (Repeat full examination including vital signs,

bedside U/S, Assess fluid responsiveness by using passive leg raise or fluid challenge)

o Maintain CVP :? 8 - 12 mm Hg � 12- 15 in intubated patients)

o Maintain Sv02 or Scv02 > 70% (because O, extraction by tissue is 20- 30%)
Sv02 "mixed venous oxygen saturation" (Pulmonary artery)
Scv02 ·'superior vena cava oxygen saturation" (Central vein)
• If< 70%: 1) Increase Fi02 and check Pa02 level
2) Blood transfusion if Hematocrit< 30%
3) If failed or normal level -+ Start Dobutamine
• Can be replaced by measure of Lactate clearance (goal> 20% over 6 hours)

o Control of the source: e.g. surgical site (with multiple fluid culture)
Supportive care
■ Blood transfusion if Hb < 7 g/dl (or< 9 in cardiac patients)

■ Nutrition: low-calorie enteral feeding within 48 hours (if no contraindication for enteral feeding)
o Albumin infusion: given in hypoalbuminemia patients (contraindicated in head injury)

■ Tight glucose control and monitor with goal of< 180 mg/dl

■ Anticoagulant prophylaxis: Heparin or LMWH (in acute renal injury) + Mechanical compression

■ Stress ulcer prophylaxis: Histamine blocker or proton pump inhibitor

■ VAP prophylaxis: Elevation head of bed >30 degrees in intubated patient

■ Consider low-dose steroid therapy (ACTH stimulation test is not recommended in septic shock)
o Because 20% of septic patient develops adrenal insufficiency
o Used in septic shock despite fluid resuscitation and vasopressor (Improve shock status)
o Dose: Hydrocortisone< 300 mg/day

■ Ventilation: (for ARDS)

o Tidal volume 6 ml / kg
o Plateau pressure< 30 cm H2O

■ Recombinant human activated protein C {APC)

o In the past: Recommended, decreased rates of mortality in septic patients
o Currently: Failed to show a mortality benefit and used in sepsis-induced MOF only
SHOCK
■ Inadequate tissue oxygenation due to inadequate tissue perfusion
o Measured by Mean arterial pressure (MAP) = CO x SVR = (2 Diastole+ Systole)/ 3
• Hypotension: Systolic BP ,, 90 mm Hg, or MAP ,, 65 mm Hg
• Blood pressure is maintained until 30% of total blood volume is lost

■ Hypovolemic shock
o Types: hemorrhagic, traumatic, and non-hemorrhagic
o r
Initial change: Diastolic pressure
o Earliest acid-gas abnormality: Respiratory Alkalosis
o 7% associated with pure neurological findings as neurogenic shock

o Compensatory mechanism:
• Systemic and Splanchnic Vasoconstriction and Bronchodilation

• Increased:
• Heart rate � Decreased venous return
• Cardiac output and contractility
• Cerebral and coronary blood flow
• Na and water reabsorption (By releasing of aldosterone)
• Respiratory rate (Respiratory alkalosis followed by metabolic acidosis)

o Classification of Hemorrhage:

I II Ill IV
Blood loss (ml) < 750 750 -1500 1500-2000 >2000
Blood loss l¼l < 15% 15-30 % 30-40% >40 %
Resnirato~ rate 15 20 20 30 30 40 >35
Heart rate Normal Tachycardia (100- Tachycardia (120 - Tachycardia (> 140)
120) 140)
Pulse nressure Normal Decreased Decreased Decreased
Blood pressure Normal Normal Hypotensive Hypotensive
Orthostatic
hvnntension
Urine outnut Normal 20 30ml/hr 5 15ml/hr N=lioible
CNS symptom Normal Anxious Confused Lethamic
Fluid management Crystalloids Crystalloids Crystalloids and Blood Crystalloids and
Blood
■ Management of hypovolemic shock
o Initial Management:
ABCDE
Rewarming hypothermic patient should be 1 st step before medical management

o Medical Management:
1) IV fluids (crystalloids) -+ Rule: 3 crystalloids: 1 RBCs
• Goal of SBP:
o With brain injury: > 120 mm Hg (to prevent secondary brain injury)
o Without brain injury: 80- 100 mm Hg

2) Blood components (Rule: 2:1:1 or 1:1 :1 of RBCs : Platelets : FFP)

• RBCs if Hb < 7 or < 10 in brain injury
• FFP:
o Transfuse with 1st PRBCs in ongoing bleeding or if> 6 units of PRBCs
o Increase survival rate, but some studies showed also increased risk of
thromboembolic events and multiorgan failure
• Platelets: Used if platelets < 50,000 or after 6 units of PRBCs

3) Tranexamic acid
• Synthetic analogue of amino acid lysine
• Anti-fibrinolytic by inhibiting plasminogen activation
o Other example: 1:-Aminocaproic acid and aprotinin
o Tranexamic acid is 1O times more potent than aminocaproic acid

• Used in: Early traumatic hemorrhage(< 3 hours), Post cardiac bypass

• Decreased mortality rate (16% to 14.5%) without increase of
thromboembolic complications
• Loading dose: 1 g over 10 min, then infusion 1 g over 8 hours
• Excreted by renal (Need renal adjustment dose if used for long time)

4) Recombinant Factor VIia

• Used in traumatic hemorrhagic shock failed to be controlled by surgical or
angiographic hemostasis
• Dose: 200 ug/kg IV followed by 100 ug/kg at 1 and 3 hours later
• Does not decrease mortality rate

Vasopressors: should not be used as it can decrease tissue perfusion

Activated Protein C is contraindicated in hypovolemic shock

o Definitive management: (Control source of bleeding)

• Upper GI endoscopy: for Upper GI bleeding
• Pelvic compression or stabilization: for pelvic injuries
• Surgery:
• Packing and surgical bleeding control
• Damage control surgery: in unstable patient

• Angioembolization: in stable patient

■ Cardiogenic shock
o Impaired diastolic filling of right atrium, ! ventricular filling

o Criteria:
• SBP < 90 mmHg
• Cardiac Index < 2.2 Um/m2 (C.I = HR x SVI)
• PCWP > 18 mmHg

o Causes of cardiogenic shock:

• Tension pneumothorax
• Pericardia! tamponade
• Myocardial contusion
• Air embolism

o Beck's triad:
• Hypotension
• Jugular venous distention
• Muffled heart sounds

o Kussmaul's sign:
• Jugular venous distention during inspiration

o Management:
• Ventilator support
• Avoid barbiturates, morphine, propofol and benzodiazepines
• 1 st agent inotrope: Dopamine
• 2nd agent inotropes: Dobutamine and Milrinone
• Treat the cause

■ Intra-aortic balloon pump (IABP)

o Place lip of the catheter just Distal to left subclavian (2 cm below the top of the arch)

o Inflates on T wave (during diastole) and deflates on P wave (during systole)

o Diastolic Augmentation

o l Preload, ! Afterload, j COP, t Coronary flow

o Used for cardiogenic shock

o Aortic regurgitation is a contraindication to IABP

■ Septic Shock
o t Coagulation and inflammation
o t Fibrinolysis, t Plasma iron
o Remember:
• Insulin helps peripheral neuropathy
• Insulin resistance if t PO4

Pulse BP Extremities RBS level Insulin ABG

Earlv seosis t Normal Warm t I Resoirato~ alkalosis
Late seosis t I Cold t t Metabolic acidosis

■ Anaphylactic shock
o lgE mediated
o Histamine release + Smooth muscle- re-laxation, Bronchial contraction, Capillary leak
o Presented with: Pruritus, flushing, urticaria appear
o Recurrence rate:
• 40 - 60% for insect stings
• 20 - 40% for radiocontrast agents
• 10 - 20% for penicillin

o Management:
• First line: Epinephrine 0.01 mg/kg IM of 1:1000 (repeat q 5 - 15 min if needed)
• Antihistamines (diphenhydramine 25 - 50 mg IV over 5 min)
• Steroids and Bronchodilators
• Monitor V/S, 02 Support

■ Neurogenic shock
o Loss of sympathetic tone + t HR, t BP, Poikilothermia (changing temperature)
o Spinal shock: temporary loss of spinal reflex activity and sensation below cord injury

o Treatment:
• Airway support, Fluids, and Atropine if bradycardia
• Steroids used in blunt injury wi:thin first 8 hours for 24 - 48 hours of high-dose
• Mainstay treatment: Fluid resuscitation
• The only type of shock that benefits from trendelenburg position for vasoactive
drug administration

o Adjuvant therapy:
• Low (Below T4}: Dopamine or Norepinephrine
• High (Above T4): alpha - agonist: Phenylephrine 100-180 µg/min
• Alternative: Ephedrine 10 mg IV bolus

■ Adrenal insufficiency
o Most common cause: withdrawal of exogenous steroids (as patients with /8D)
o Most sensitive test: Corticotrophin stimulation test (< 5 mgld)
o Cortisol level (> 15 mgld)
o t Glucose, t K
o Treatment: Steroid (1x hydrocortisone 5x prednisone 30x dexamethasone}
 Algorithm of Shock
'Check SVR

f SVR 1 SVR

CheckCVP Check Cardiac index

f CVP ! CVP f Cl, f Sv02 1 Cl, f Sv02

Cardiogenic Hemorrhagic Septic Neurogenic
RECEPTORS
■ Adrenergic Receptors

Receotor Effects on muscle Other effects

Alpha 1 Contract: Gluconeogenesis, Glycogenolysis
- Vascular/ Bronchial smooth muscle Ejaculation
- Pupillarv dilator muscle+ Dilation (Mvdriasis)
Alpha 2 Contract: l Norepinephrine, Ach, insulin, cAMP
- Vascular/ Bronchial smooth muscle t Glucaqon
Beta 1 Increases Mvocardial contraction and rate of contractions r Renin Hunoer /Ghrelin). cAMP
Beta 2 Relaxes: f Insulin, Glucagon, Renin
Vascular/ Bronchial / Uterine smooth muscle f Lipolysis, cAMP
Contract: Urethral sohincter Gluconeoaenesis Glvcoaenolvsis 'B > ,,;·
Dopamine ReJaxes·
Renal / Solanchnic smooth muscle

■ Cholinergic receptors (Acts by Acetylcholine)

Muscarinic receotors Nicotinic receotors

Type G-Protein receptors with 5 subtypes Ligand-9ated Ion channels with 2 subtypes
Post / Pre aanalionic Post.,,analionic receotors
Location Smooth muscle Skeletal muscle
Effects - Stimulate smooth muscle I glands (Bronchospasm) - Stimulate skeletal muscle
- Stimulate Adrenal medulla:
Cholineroic actiyity: + Epinephrine / Norepinephrine
- l HR, BP, RR, Temperature, Constrict Pupils
- t Peristalsis
Blocked by Atropine Curare (Tubocurarine)

■ Other muscarinic antagonists:

o Atropine:
• Used in: anticholinesterase poisoning, bradycardia, antispasmodic, anesthesia
(CNS depression)

o lpratropium
• Used in: asthma and bronchitis

o Diphenhydramine
• Used in: extrapyramidal symptoms from antipsychotic, antihistamine, asthma,
insomnia

o Mebeverine
• Selective action on the smooth muscle, without other anticholinergic effects
• Used in: irritable bowel syndrome
 INOTROPIC DRUGS
■ lnotropic � increases contractility
■ Chronotropic � increases heart rate
0 Positive: Atropine, Dopamine, Epinephrine, lsoproterenol , Milrinone
0 Negative: Beta blockers , CCB

Receotor activitv
Drug Dose Effect Use
Aloha 1 Beta 2 Beta 1
2-5 µg/kg/min Dopaminergic activity VD. l UOP (renal dose) Cardiogenic shock or
Rarelv used neurogenic shock
Dopamine < 10 µg/kg/mln ++ . +·++ l SV, T HR, l COP 1" agent for cardiogenic
shock
> 1 0 µg/kglmin +++ . ++ VC, l BP, l SVR Side effect: Armythmia

Dobutamine
3-15 µglkg/min
. + +++
T COP, ! SVR, VD
No effect on BP
2"" agent, cardiogenic shock
1" agent by some references
0.2-5 µg/kg/mln T HR / BP, T COP, ! SVR Cardiac arrest (1 mg JV)
(Most common) + ++ ++++ T SVR, VC (Alpha-dose) Pulseless VT, PEA
Epinephrine T Lactate Anaphylaxis
C�asa12c�iS�ad Massive PE
> 5 µg/kglmin :t±±± + ++
I Glucose level: HF with low BP
0.05- 5 • Glycogenolysis Septic or cardiogenic
Norepinephrine
(Vasogressod
µglkg/min ++++ . ++
• T Glucagon
- ! Insulin
shock
- Inhibits bowel motility
lsooroterenol . +++ +·++ t SVR. t COP. t HR VD Hvnotension and J HR
10 µg/min VC, Only lnotrope !COP Hypotension with ! SVR
Phenylephrine
(VasQJ1re11sod
++ . . (hyperdynamic sepsis,
neuroaenic oroblemI
NON-ADRENERGIC AGENTS
Phosphodiesterase ! COP
Milrinone inhibitor (l cAMP) 2"" agent in cardiogenic
shock
0.01 - 0.04 Can be released from Vasoconstriction 2"" agent in septic or
Vasopressin units/min posterior pttuitary Water reabsorption anaphylactic shock
(Vasogressoa
Acts on V, - V,

Epinephrine
■ &!ailabl11 ll:2cm:r
0 1: 1000 (1 mg/ml) mainly in anaphylaxis
0 1: 10000 (0.1 mg/ml) mainly in other i ndications

••■ Dosage: 0 .01 mg/kg of 1: 10000 up to 0.1 mg/kg of 1:1000

H alf-life: 2 - 4 minutes
Rout:
0 IM (Preferable due to rapid absorption) and SC
0 IV used in caution with only (1:10000) and more diluted concentrations

■ lrn:!iQaliQ0li'
0 Anaphylaxis
0 Cardiac arrest and Bradycardia
0 Shock
0 Asthma
0 Local effect (Peptic ulcer disease, adjacent to Local anesthesia)
 EMBOLI
Pulmonarv embolism Fat embolism
Risk factors Wall: Aging, Vasulary injury Trauma
Fracture, Joint reconstruction
Flow (stasis): Bed rest, Surgery, Cardiac failure
Systemic
Constituents: Bums, OM, Pancreatitis,
Polvcvthemia, Malignancy, Dehydration, Coaqulopathy Cardiopulmonary bvoass
Pathophysiology Thrombus emboli from deep veins or right atrium Mechanical
Damaged vessels lead to fat droplets
Propagate into circulation

Obstruct pulmonary artery Biochemical

Stress hormones released
Produces right ventricular strain Activate lipases
Hydrolyse lipids into FFAs
Most commonly from the iliofemoral region FFAs induce pulmonary damage and
increase capillary permeabilijy
Clinical features Swelling or tenderness of calf Tachycardia, tachypnea
Pleuritic chest pain Encepalopathy (hypoxia, confusion)
Tachycardia, tachypnea Petechial rash
Shock (outflow obstruction) Pyrexia
Paradoxial embolisation Retinopathy
Renal imoairment
Investigations CBC, PT/PTT, Type and Screen CBC, PT/PTT, Type and Screen
Electrolytes, ABG (V/Q mismatch) Electrolytes, ABG
■ T Pulmonary artery pressure, l CVP, l PCWP Urinlysis (Lipiduria)
■ l P02 and PC02 respiratory alkalosis ECG: Tachycardia and RV strain
CXR
Plasma 0-dimer Nodular (ground-glass) opacities
ECG (Sinus Tachycardia, S1 Q3T3) Snow•storm appearance:
CXR (Westermark sign; focal oligemia) Diffuse bilateral pulmonary infiltrates
VQ scan (Consistent with lung contusion, acute
Spiral CT lung injury, or ARDS)
Pulmonarv anaioaraohv
Management Early mobilization Respiratory support
TED stockin9s
Anti-DVT machine Fluid/Electrolyte resuscitation
T herapeutic anticoagulation (UFH, LMWH)
transition to oral or LMHW after 24 h after acute injury DVT prophylaxis

Anti-fibrinolytic agents or catheter-directed therapy Nutritional support

for massive PE with hypotension or systemic shock

Surgical or Percutaneous embolectomy + IVC filter

for high-risk of bleeding with massive PE
for contraindications to thrombolysis (intracrania or
uncontrolled bleeding, recent surgery/trauma)

IVC filter (if used) should be below renal veins

lthrouah rioht IJV)
 PULMONARY SYSTEM
■ Aging: ! FEV1 and vital capacity, f FRC
■ V/Q ratio: highest in upper lobes, lowest in lower lobes (changes with posture)
■ PEEP (Positive end-expiratory pressure)
0 Normal PEEP:
• 5 cm H20 (in closed glottis in non-ventilated patient)

o Advantages:
• Improve oxygenation (by improving t FRC)
• t Mean alveolar pressure, f Lung compliance
o Disadvantages: Barotrauma, ! Preload and f Afterload (Right-side HF), r ICP
o Contraindication: Hypotension, lntracranial disease, focal lung disease

o Changes:
• Increase: PaO2(0xygenation),, Dead Space, PVR , PCWP, Compliance, FRC
• Decreases: Renal blood flow, UOP, COP, ANP, A-a 02 gradient, RA filling

o Auto-PEEP (intrinsic PEEP):

• Failure to expire full Tidal volume (VT} + dynamic hyperinflation
• t lnspiratory time and failure to return to baseline on waveform
• Complications: Hypotension, t venous return, respiratory fatigue, and agitation
r
• Management: t Rate and tida.l volume, l:E ratio (by t lnspiratory time), treat
bronchospasm

Plateau pressure Peak pressure

Intrinsic PEEP (Barotraumal t I> 30) t /> 501
Obstructed tube I Small or kinked Normal t
Bronchosoasm tor Normal t

Indications for intubations Parameters for weanina

Apnea or respiratory distress Stable, no tachypnea (< 30), no inotropes
VIS
Tachvnnea I> 30) or bradvnnea
<8 GCS >10
- pH 7.35 -7.45 - pH 7.35 -7.45
- PaO2<60 mm Hg ABG - PaO2> 60 - 70 mm Hg
- Paco,>50 mm Ho - Paco,< 50 mm Ho
- FIO2 ,; 40%
- Ventilator - PEEP<5-8
- Mode: Pressure sunnort or SIMV
- Tidal volume < 5 ml /kg - Tidal volume >5 ml /kg
- Vital capacity < 15 mUkg or< 1 L - Vital capacity> 10 -15 mUkg or > 1 L
- Pa02/ Fi02< 200 - Pa02/ Fi02> 200
Ratio
- Minute ventilation>10 Umin - Minute ventilation < 10 Umin
- PIA-al O,> 350 - P /A-al 02< 350
Other indications: Order of weanino: FiO2 + PEEP + RR
- Anticipated deterioration Indicators of weanioo·
0 e.g. inhalation injury 0 Rapid shallow breathing (RSBI) < 100
- Airway protection Most sensitive test
- Failure to ventilate (obstruction) = RR + Tidal volume
- Failure to oxygenate ( contusion) 0 Negative inspiratory force (NIF) < • 20 cm
- Need to use neuromuscular blockers 0 Tobin Index and Pre,-oo FEV1
Cuff-leak: should be used prior to extubation especially in neck surgery or bum
� By deflate tube and check for airflow around tube to exclude laryngeal edema or secretions

PULMONARY FUNCTION MEASUREMENTS

■ Total lung capacity (TLC) = FVC+ RV
o Lung volume after maximal inspiration

■ Vital capacity (VC)

o Largest amount of air expired after maximal inspiratory effort

■ Forced vital capacity (FVC)

o Amount of gas exhaled following maximal inspiration and expiration

■ lnspiratory Reserve Volume (I RV)

o Air inspired with maximal inspiratory effort

■ Expiratory Reserve Volume (ERV)

o Volume expelled by active expiratory effort after passive expiration

■ Residual volume (RV)

o Lung volume after maximal expiration

■ Forced Expiratory Volume (FEV)

o Normal 5- 7 L
o FEV1: fraction of VC expired during 1 •1 second of forced expiration with maximal effort
after maximal inhalation

■ Functional residual capacity (FRC) = RV+ ERV

o Lung volume after normal exhalation
o t FRC in Surgery (atelectasis), sepsis (ARDS), and trauma

■ Tidal volume (TV)

o Volume of air with normal inspiration and expiration

■ Minute ventilation = TV x RR
o Amount of air inspired per minute (6 L) = (500ml/breath X 12 breaths/minute)

-
■ COPD f work of breathing due to prolonged expiratory phase
■ Dead space: Ventilated area but not perfused
�.oooma

--
ln�r.ltion lnS!)inllory Vit.11 1n.,,..1ery T°""
'5,000<rl reserve casmeity c:apai0ily
-mo "'P"dly

--
4,000ml

:3,000<rl
M: . ::M:::tnr: 1J ...
:i,ooom E.xpi,ntory
f9HIVI F
Mo,dmum
,.000.. V oxplrAtton
-m•
�
0
Timo
ABNORMAL BREATHING PATTERNS
■ Kussmaul's respiration
o Hyperventilation that deep and rapid respiratory pattern
o Causes: Metabolic acidosis as DKA, Renal failure

■ Cheyne Stokes respiration

o Progressive deeper and shallow breathing followed by gradual decreasing until apnea
o Causes: Traumatic brain injury, Brain tumors, Stroke, Heart failure

■ Biot's respiration
o Periods of rapid breathing near equal depth followed by regular periods of apnea
o Causes: Trauma, Stroke, or Opioids

■ Apneustic respiration

■ Ataxia respiration
ACUTE RESPIRATORY FAILURE
■ Type I: Hypoxemic respiratory failure (most common)
o Examples: ARDS and pneumonia
o Pa02 < 60 mm Hg on room air

■ Type II: Hypercapnic respiratory failure

o Examples: Asthma and COPD
o PaC02 > 50 mm Hg on room air
o Should increase alveolar ventilation by achieving adequate minute ventilation

■ Aspiration pneumonia
o Most common sites:
• Posterior segments of the upper lobes
• Apical segments of the lower lobes

■ Acute lung injury:

o Bilateral infiltration on CXR
o Pa02 I Fi02 s 300 mm Hg
o PCWP s 18 mm Hg

■ ARDS (mediated by PMNs)

o Initial histology: Influx of protein-rich fluid and leukocytes

o Most common cause: Pneumonia

• Other causes: Shock, sepsis, trauma, DIC, burn, pancreatitis
• Usually appears late (24 - 72 hours after injury)

o Most common cause of death in ARDS: Sepsis and MOF

o Definition:
• Bilateral fluffy infiltration on CXR
Associated also with pulmonary edema

• Pa02 I Fi02 s 200 mm Hg

• PCWP s 18 mm Hg
• t A-a 02 gradient, t pulmonary shunt
• ! FRC, ! PVR, ! PCWP

o Supportive Care:
"ARDS Protocol"
• Pressure support ventilator
• Tidal volume: Low between 6 and 8 ml/kg
• Plateau pressure < 30 cm H20
• PEEP: 5 mm Hg
• High FI02
 ■ Management of ARF:
o Noninvasive ventilation INIV)
• First-line therapy in ARF type 11
• Weaning strategy for intubated patients with ARF
• Noninvasive positive pressure ventilation (NIPPV}:
o Indications:
• Acute hypoxemic respiratory failure (ARDS}
• Cardiogenic pulmonary edema
• Exacerbation of COPD
• Obstructed sleep apnea

o CPAP: Continuous positive airway pressure

c> Starting by 4 cm H20

o BiPAP: Bilevel positive airway pressure

c> IPAP (inspiratory pressure): started by 8 - 15 cm H20
c> EPAP (expiratory pressure): started by 4 - 5 cm H20

• Contraindications:
o Uncooperative patient
o Unprotected airway
o Hemodynamically unstable
o Gastric distension

o Endotracheal intubation
• By direct laryngoscopy or the GlideScope
• Length of insertion:
o From incisors: 23 cm in men and 21 cm in women

• Short-acting sedative with neuromuscular blockade awake patient

o Propofol: may cause hypotension
o Etomidate: may cause adrenal insufficiency

• Deterioration (hypotension) after intubation: DOPE

c> Displaced or Obstructed tube, Pneumothorax, Equipment malfunction

Ventilation Oxvaenation
Determined by Minute ventilation (Normal = 6 L / min) Determined either by:
- A-a 02 gradient: Normal = < 10 mm Hg
- PaO2/FiO2: Normal = 500
MECHANICAL VENTILATION
■ Volume modes: (Tidal volume and rate are preset)
o Controlled Mechanical Ventilation (CMV)
• Does not allow patient interaction "Tidal volume and rate are presef'
• Can cause diaphragmatic inactivity, atrophy and contractility dysfunction

o Assist-Control Ventilation {ACV)

• Most common mode, patient-triggered I time-triggered
• inspiratory effort by the patient triggers delivery of pre-set tidal volume

o Synchronous Intermittent Mandatory Ventilation (SIMV)

• Patient initiate breathing + mandatory set pressure, tidal volume and rate in
coordination with the respiratory effort
• Patient not initiate breathing � Change to control-mode automatically

■ Pressure modes: (Pressure is preset)

o Close monitoring of the minute ventilation
+ Sudden decrease in pulmonary compliance leads to acute respiratory acidosis
o Pressure Control:
• Set inspiratory pressure and inspiratory time
• Used in any patient with risk of barotrauma:
� ARDS, trauma, lung procedure, and Bronchopleural fistula

o Pressure Support:
• Breaths assisted by set inspiratory pressure
• Delivered when inspiratory flow drops below predetermined threshold
• Apnea alarms are required to ensure patient safety
• Used in weaning {limit barotrauma and decrease the work of breathing)

o Inverse-ratio pressure mode: "l:E = 2:1"

• Leads to Permissive hypercapnia, and Auto-PEEP
• Alternate between high, low PEEP with long inspiratory time "7:1 -10:1"
• Used for severe hypoxemia

■ Strategies use in mechanical ventilation:

o Low Tidal Volume: (4 - 6 ml/kg} to lower the plateau pressures in ALI or ARDS
• To achieve hypocapnia

o Permissive Hypercapnia: (by! volume ventilation}

• To reduce alveolar overdistension and pressures in ARDS patients
• Avoided in patients with traumatic brain injury
� Try to increase respiratory rate (30 -35} to prevent acidosis

o Open Lung Strategy:

• By using lung recruitment manoeuvres with high PEEP and low tidal volume
• Improve oxygenation in ARDS patients
■ Starting ventilation:
1) Assist-control mode and FiO2 = 100%

2) Set initial tidal volume 8 ml/kg and reduce it 1 ml/kg every 2 hours until 6 ml/kg

3) Select RR 12 - 15 breaths/min, and increase it if still t PaCO2 (not> 35 breaths/min)

• Now measure the Plateau pressure and arterial PaCO2 and pH

4) Add PEEP 5 - 7 cm H2O

5) Adjust PEEP and FiO2 -+ PaO2 > 55 mm Hg and SaO2 > 88%
• Try to keep FiO2 s 60% to prevent 02 radical toxicity, absorptive atelectasis, and
pulmonary fibrosis
Ventilator-Associated Pneumonia (VAP)
■ Definition: pneumonia develops 48 hours after intubation
o Most common nosocomial infection: Pneumonia
o Most common organism associated with VAP: Staphylococcus aureus

■ Incidence: 9% - 27% (70% chance at day 30 of ventilator support)

■ Diagnosis:
o Fiberoptic bronchoscopy with quantitative culture:
• Protected specimen brush (PSB) > 10 3 CFU/ml
• Bronchoalveolar lavage (BAL)> 104 CFU/mL
• Endotracheal aspiration > 10 5 CFU/mL

o CPIS "Clinical pulmonary infection score"

0 1 2
Tracheal secretion Rare Abundant Abundant and ourulent
CXR infiltration None Diffuse Localized
Tem.,..rature Normal > 38.5 and< 38.9 > 39 or< 36.5
WBC count Normal < 4 or> 11 < 4 or > 11 or > 1 0% bands
Pa02/ Fi02 > 240 or ARDS < 240 or no ARDS

o Recommendation:
• CPIS > 5 is diagnostic for VAP
• Discontinue Antibiotics if maintain CPIS s 6 after 72 hours of antibiotics

■ Management·
o Empiric antibiotic therapy
o Early VAP (< 4 days): Gram-positive (S.aureus, Strep., H. influenza)
• Ceftriaxone, ftuoroquinolone, or ertapenem ± macrolide

o Late VAP (> 4 days): Gram-negative and multidrug-resistant organisms

• Antipseudomonal cephalosporin or carbapenem
+ Antipseudomonal ftuoroquinolone or aminoglycoside
+ Linezolid or vancomycin

o Duration of antibiotics:
• Past: 14 - 21 days
• Currently: until organism/ sensitivity identified or after 72 hours with CPIS s 6

■ Prevention:
o Elevate the head 30 degree
o Daily "sedation vacations"
o Daily oral care with chlorhexidine gluconate
o Peptic ulcer disease prophylaxis
o Deep venous thrombosis prophylaxis
o Tracheostomy if indicated may decrease the incidence of VAP if performed before the
10th day of ventilator support
Air embolism (CO2 embolism}
■ Pathophysiology:
o Direct communication between air and vascular system
o Pressure gradient

■ Etiology and risk factors:

o Surgical procedures (open or laparoscopy) •Most common"
o Trauma to the chest, neck, or abdomen
o Central venous catheterization
o Positive pressure ventilation
o Ventilator-introduced barotrauma
o Argon beam coagulation (lead to increases intra-abdominal pressure)

■ Signs:
o End-Tidal CO2
• Initial abrupt increased, Followed by sudden drop (Most important)

o End-Tidal Nitrogen
• More sensitive test to air and associated with earlier detection

o Cardiogenic shock
o Hypotension, machinery (harsh, crunching, Mill, Cog or Water-wheel) murmur
o Air leak if associated with bronchial injury
o t PaC02, ! Pa0 2, ! Sa02

■ Management:
o Resuscjtaljon
• ICU management
• IV fluids ± inotropes
• Ventilation with 100% 02
• Intubation if required

o Maneuvers to prevent further complication

• Stop CO2, deflate abdomen, remove instruments during laparoscopy
• Turn to Left lateral decubitus, Trendelenburg position (Durant maneuver)

o Associated with central line catheterization (No trauma) -+ Air aspiration

• Swan-Ganz or Bunegin-albin (!Better) catheter through right internal jugular vein
and aspirate
• Aspirate from right atrium by introduce syringe below left costal margin

o Associated with blunt thoracic trauma

• Bronchoscopy to evaluate bronchial tree
o Associated with penetrating thoracic trauma

7} Intubation with one-lung ventilation

8} Emergency Left anterolateral thoracotomy

� Clamshell thoracotomy may consider if air embolism diagnosed
preoperatively

9} Control pulmonary hilum to control bleeding and prevent further embolism

� Clamping or digital pressure of the hilum
� Twisting the affected lung 180 degree
� Aortic clamp is also applied for extra-thoracic bleeding

10)If above methods failed, Open the pericardium and direct air aspiration
� Heart apex of left ventricle or aortic root by 16 - 18 gauge needle
� Right coronary artery by tuberculin syringe

11 )Continue operative resuscitation

� Vigorous cardiac massage
� Keep in Trendelenburg position with pulmonary hilum clamped

12)Primary repair of tracheobronchial injury or lung laceration by

absorbable sutures though opening the presented tract of injury
(Pulmonary tractotomy) and repair of injured vessels or bronchi
RENAL SYSTEM
■ Most common cause of postoperative renal failure: Intra-op hypotension
■ U/S renal help to differentiate the etiology of AKI

■ Electrolytes associated with renal failure: f P04 ! Na !K

RAAS System:
■ Angiotensingoen {produced by Liver) + A1ngiotensin I (converted by Renin)
o Renin released by Afferent juxtaglomerular in response to t Na {by macula densa)

■ Angiotensin I + Angiotensin II (converted by ACE from lungs)

■ Functions of angiotensin II:
o Increases sympathetic activity
o Increases Na, Cl reabsorption and K excretion
o Increases Aldosterone secretion from adrenal cortex
• Acts on Distal convoluted tubule
• Na and water reabsorption

o Increases ADH secretion

• Acts on Collecting tubules

o Vasoconstrictor

ACUTE RENAL FAILURE

Pre-renal Azotemia Acute tubular necrosis

Rule: 1- 20- 20-500
FeNa (Best test/ <1%
Urine Na <20
BUN/Cr ratio >20 Opposite
Urine osmolality > 500mOsm

FeNa = (Urfne Na) (Plasma Na)

(Urine Cr) (Plasma Cr)
Types of renal failure:
■ Anuria" < 100 ml/day" or Oliguria "100- 400 ml/day•
o Complete obstruction
o Glomerulonephritis
o Necrosis
o Hepatorenal syndrome
o Pre-renal failure

■ High-output• > 400 mVday"

o lschemia
• Pre-renal azotemia
• Acute tubular necrosis
o Nephrotoxic
• Contrast-induced renal failure
• Rhabdomyolysis
• Drugs

o Glomerulonephritis
o Partial obstructive neuropathy

Nephroto xic drugs

Direct effect Indirect effect

ATN Interstitial nenhritis Glomerular iniu~
Aminoalvcosides Allopurinol
Amohotericin B PPls Clooidnnrel
Acetaminoohein NSAIDs NSAIDs Retroperitoneal fibrosis
Iodine contrasts Vancomvcin Methotrexate
Mannitol Thiazide / looo diuretics Diuretics
IVIG Quinolones

Strategies for prevention of AKI:

o Volume expansion: Primary preventive measure for contrast-induced nephrotoxicity (CIN)

o N-acetylcysteine: free radical scavenger showed to prevent CIN

o Most recent studies showed no benefit, but can be used as it's safe and inexpensive

o Atrial natriuretic peptide (ANP): inhibit agents that reduce blood flow (usage is controversial)
o Dilates Afferent glomerular arterioles and Constricts Efferent glomerular arterioles

o Erythrop oietin: in research, showed effects in animal models

o Diuretics:
o No benefits on duration of AKI, surviv.al or outcome

o D opamine (renal d ose): studies showed no evidence of usefulness in AKI

Management of AKI:
o Management of volume hemostasis and electrolytes imbalance
o Management of acid-base abnormality
o Nutritional support:
o Sodium intake < 2 g/day
o Protein intake to 0.6 - 0.8 g/kg

o Avoid neurotoxic drugs

o Aggressive glucose control
o Low-volume low-pressure ventilation

o Renal Replacement Therapy

o Timing: Early is better
o Indications:
• Severe acidemia
• Severe hyperkalemia
• Ingestion of dialyzable substance -+ renal failure
• Volume overload with no oliguria
• Signs of uremia

0�
• Intensive strategy: IHD 6 times I week or continuous at 35 ml/kg/h
• Moderate strategy: IHD 3 times/ week or continuous at 20 ml/kg/h
No significant differences between them

o Modalities:
• Peritoneal dialysis:
• Should be intact peritoneum, can compromise respiratory status

• Ultrafiltration:
• Rapid removal of volume without significant solute removal
• Used for treating volume overload in the presence of oliguria

• Intermittent hemodialysis (IHO):

• Most common used method in USA
• Uses semipermeable biocompatible synthetic membrane and
electrochemical gradient maintained with continuous dialysate flow
• Allows for rapid remova I of solute
• Disadvantages: removal of volume limited (due to hypotension), hypoxia
• Continuous renal replacement therapy (CRRT)
• Most common used method international
• By hemofiltration, removal of volume and solute
• Replacement fluid infused continuously to avoid hemodynamic instability

• Continuous venovenous hemofiltration (CVVH)

• Continuous venovenous hemodiafiltration (CWHOF)

• Initially thought to be safe for hemodynamically unstable, but studies
showed opposite effects
OTHER CONDITIONS
■ Capnography:
o CO2 in exhale air (in waves only) used for monitor
o Determination of arterial to end-tidal CO2 gradient
o Allows confirmation of endotracheal tube and airway integrity

■ Capnometer:
o CO2 measurement (in number only)
o Determination of partial pressure of CO2

■ Reperfusion injury:
0 Mediated by PMNs
o Xanthine oxidase in endothelial cells -+ oxygen radicals
■ -+ coronary sinus
Lowest 02 tension

■ Highest 02 tension -+ renal veins & IVC

■ Width of pressure cuff should be 40% of the arm circumference

■ Normal 02 delivery-to-consumption ratio -+ 5:1

■ Vasovagal attack: ! Peripheral resistance

■ Brain death
o Apnea test
• Positive test: pC02 > 60 mm Hg

o Absent brainstem reflexes and DTRs (DTRs can be present!)

 SUMMARY OF PRESSURE MENTIONED
Heart Resoiratorv Renal
t HR tPCWP tAldosterone
tMAP t PIP tADH
t CVP t PAP t Cortisol
tSVR t PaC02 tCatecholamine
t PVR t Airway pressure t Renin
1 After/oad (Right-side HF) t Mean airway pressure
Increased 1 ICP
Pneumoperitoneum PEEP:
t Pa02 (Oxygenation)
PEEP t Compliance
t Dead space
Abdominal 1 FRC
Compartment ! HR Pneumo12eritQn!;!um: ! Renal flow
Syndrome
(Most common) !FRC ! UOP
! Compliance t pH (Acidosis}
!COP ! Vital capacity
De�reased !ANP
t Right atrium filling
! Peripheral blood lilow
! Pre-load (LVEDV)
(Venous return)

1 FRC J FRC
Aaina Atelectasis
PEEP ARDS
Pneumoperitoneum
Abdominal comoartment svndrome

t ETCO, ! ETCO,
Earlv air embolism Embolism IPulmonan, Air\
Tracheal intubation Esoohaaeal intubation
Malianant hvnerthermia Obstruction
Atelectasis Disconnection from the ventilator
Hypoventilation Nitrous oxide
H,motension H,movolemia
Metabolic acidosis
Anesthesia
Reviewed by:

Dr. Fahied A/Qahtani

ANESTHESIA
INHALATIONAL INDUCTION AGENTS
■ Most common cause of intraoperative bradycardia
■ ! MAC -+ t Lipid soluble -+ t Potency

Nitrous oxide
o Fastest but f MAC (Low potency), weak analgesia

Halothane
o Side effects: Hepatitis, Post-anesthesia shivering, Highest myocardial depression
• Shivering caused by t CO2 Production and ! 02 Consumption

lsoflurane
o Lowers brain 02 consumption with no increasing in ICP

Sevoflurane
o Safest drug, have some risk of malignant hyperthemia

Desflurane
o Can cause mucus trapping, airway resistant and irritation (contraindicated in asthma)

All inha/afion agents have risk of malignant hy,perlhermia

INTRAVENOUS INDUCTION AGENTS (Works on GABA)

Druq Uses Characters Effects

Closed head injury Analgesic - ! CBF
Thiopental
(barbiturate)
- ! BP
Most patient Amnesia, Non-analgesic - 1 BP, Hypertriglyceridemia
Respiratory depression - Respiratory depression, Apnea
Propofol -
Bronchodilator, Sedative Injection-site pain
- Metabolic acidosis
Asthmatic patient Analaesic - Hallucinations
Ketamine No respiratory depression (Psychotomimetic effects)
(works on Contraindicated i, Bronchodilator - f airway secretions
NMDAJ head injury - t HR t BP t COP
- t CBF t ICP
Rapid sequence Fast-acting, Short duration - No changes of HR, COP, BP
intubation Doesn't cause vasodilatation - Nausea / Vomiting
Etomidate -
(In patient with risk of Adrenocortical insufficiency
hvnotenslon)
All are fast onset. except Ketamine (slow-onset/
�ll am fil.� atMQk:�CG li�tmt 'fb.klatw.tal (�{Q»:::m,s:2�
All are I BP. except Ketamine f1 BPI

■ Drug of Choice in Asthmatic patient:

o Etomidate in: Normal BP
o Propofol: in HTN
o Ketamine: in Hypotensive
RAPID SEQUENCE INTUBATION
o Used in full stomach (recent oral intake), GERO, Intestinal obstruction, Morbid obesity,
and in emergency (as trauma)

■ Steps:
1) Preparation

2) Position: Sniff position (8 to 10 cm head elevation with pads under occiput and
atlanto-occipital extension), avoid over-extension in traumatic patients

3) Pre-oxygenation 100% for 3 minutes

• ± Cricoid pressure (Sellick's maneuver)

4) Premedication
• Lidocaine 100 mg: in head injury
• Fentanyl 2 - 3 mcg/kg: Cardiovascular disease, head injury
• Rocuronium 0.1 mg/kg: in head injury

5) Induction
• Etomidate
• Ketamine
• Midazolam
• Propofol (Most commonly)
• Thiopental

6) Muscle paralysis
• Succinylcholine 1 to 1.5 mg/kg: (recommended)
• Alternative: Rocuronium .. Non-depolarizing NMBAs"

7) Placement of endotracheal intubation

• Men: 23 cm from incisors
• Women: 21 cm from incisors
• Children: Age/2 + 12 cm

8) Confirmation of endotracheal intubation

(Inspection, Auscultation, Capnography, X-ray)

9) Inhalation agent or sedation

NARCOTICS (OPIOIDS)
■ Act on Mu receptors in brain, metabolized by the liver
■ Avoid use of narcotics in patients on MAOls (monoamine oxidase inhibitors)
-+ Hyperpyrexic coma

Morphine
o Histamine release (causes hypotension)-+ Contraindicated in Asthmatic patient
o ! Cough, ! BP
o Dosage:
• Continuous: 0.05 -0.5 mg/kg/hr IV
• Intermittent: 0.1 mg/kg (maximum: 20 - 30 mg/day)

Fentanyl
o Dosage:
• as analgesia: 1 - 2 mcg/kg IV/UM q1 - 2 hours PRN
• as anesthesia: 2 - 20 mcg/kg/dose initially, then 1 - 2 mcg/kg/hour IV

Pethidine (Meperidine)
o Dosage:
• 50 - 150 mg IM/ SC q3 -4 hours PRN (not used in renal impairment-+ Seizure)

■ Most potent narcotic: Sufentanil

■ Overdose treatment: Naloxone

o Dosage: 0.4 - 2 mg IM / SC; repeat q2 - 3 min PRN (not> 10 mg)
MUSCLE RELAXANTS (PARALYTICS)
■ 1 st muscle to recover from paralytics and last muscle to get paralyzed:
o Diaphragm

■ 1 st muscle to get paralyzed and last muscle to get recover:

o Neck and face muscles

■ Depolarizing agents: Succi nylcholine Only

o Characters·
• Fasciculations, f ICP, malignant hyperthermia, hyperkalemia

o Contraindicated in:
• Burns
• Neurologic injury
• Massive trauma
• Acute renal failure (hyperkalemia)
• Open angle glaucoma
• Previous history of prolonged paralysis
• Due to Atypical pseudocholinesterases
c:) Avoid Succinylcholine / Mivacurium

o Management of succinylcholine cardiac arrest: IV Calcium gluconate

■ Non-Depolarizing agents:
o Mechanism: Inhibit neuromuscular junction by competing with Acetylcholine

Cis-atracurium: by Hoffman degradation (Histamine release)

o Safe for kidney I liver

Mivacurium: by Plasma cholinesterase (Shortest half-life)

Rocuronium: by Liver
o Rapid acting, Short duration

Pancuronium: by Kidneys
o Longest duration
o Most common side effect: Tachycardia

■ Reversing drugs for Non-Depolarizing agents: Neostigmine

o Blocks acetylcholinesterase, increasing acetylcholine level
o Atropine should be given with neostigmine to counteract effects of generalized
acetylcholine overdose

MALIGNANT HYPERTHERMIA (Contraction syndrome)

o Defect in calcium metabolism
o 1 st sign is tend-tidal CO2
o Risk increased when use: Succinylcholine, Sevoflurane, MAOls, TAD
o Treatment:
• Stop the procedure
• Hyperventilation 100% 02
• Dantrolene ( 10 mg/kg) -+
inhibits Calcium release
■ Avoid hypothermia
BENZODIAZEPINES (Works on GABA)
■ Midazolam, Diazepam, Lorazepam
o Midazolam cross placenta (contraindicated in pregnancy)
• Dose: 0.5-1 mg (10-50 mcg/kg) over 2 minutes (not exceed 2.5 mg/dose)

o Diazepam: 5-10 mg IV/ IM q 6 -12 hours

■ � for Sedation, Anxiety, Panic disorders, and Seizures

■ Characters: Amnesic, Anxiolytic, Respiratory depression, not analgesic

■ Metabolized by liver

■ Side effects:
o Cognitive effects: drowsiness, dizziness, and decreased alertness and concentration
o Paradoxical effects: increased seizures, violence, irritability
o Others: somnolence, decreased libido and erection

■ Symptoms of overdose:
o Drowsiness
o Nystagmus
o Ataxia
o Hypotension
o Respiratory depression
o Cardiorespiratory arrest

■ Treatment of overdose: Flumazenil

o Dosage: 0.2 mg IV over 15 - 30 seconds
o Contraindicated in elevated ICP
EPIDURAL AND SPINAL ANESTHESIA

EPIDURAL ANESTHESIA SPINAL ANESTHESIA

Site of injection Outside dura (No CSF obtained) Subarachnoid space (CSF obtained)
Location TS - T9: Thoracotomy Below L2
TS - T10: Laparotomy Most common at L4 - L5

Avoid insertion at;;, T5 /risk of bradvcardiaI

Characters Sympathetic denervation, vasodilation Associated with significant neuromuscular
blockage (Sensory and motor)
No Parasympathetic block
(intact motor function) Vasodilation
Onset Slower Faster
Duration Lonaer Sharter 12 hours\
Usage Anesthesia as combined with others Spinal anesthesia alone for any surgery
below umbilicus
Analgesia for postoperative pain
Caudal block for oostooerative oain control
Side effects - Epidural hematoma - Respiratory distress
- Epidural abscess - Urinary retention
- Urinary retention - Spinal headache (by CSF leakage)
- Headache if dura entered
Lowest respiratory and cardiac
comolications
Contraindications - Hypertrophic cardiomyopathy
- Cyanotic heart disease
- Aortic stenosis
- Cirrhosis
- Coagulopathy
- Elevated ICP
- Systemic infection
- Severe Hvnovolemia lean worsen the hvnotension\
LOCAL ANESTHETICS
■ Work by increasing action potential threshold, preventing Na influx
■ Excreted by: kidney
■ Side effects:
o Tremors (1st), seizures, tinnitus, arrhythmias

■ Treatment of overdose:
o IV 20% fat emulsion (intralipid) 1.5 mUkg bolus, then infusion of 0.25 mUkg/min

■ Onset of all local anesthetics: 5 - 15 minutes

■ Amides: (metabolized in liver)

Lidocaine (short acting: 1 - 2 hours, with epinephrine: up to 4 hours)

• Maximum dose without epinephrine: 5 mg/kg (Maximum: 300 mg)
• Maximum dose with epinephrine: 7 mg/kg (Maximum: 500 mg)

Bupivacaine (long acting: 3 - 12 hours)

• Maximum dose without epinephrine: 3 mg/kg
• Maximum dose with epinephrine: 35mg/kg

Prilocaine

Mepivacaine

■ Esters: (metabolized by pseudocholinesterase)

o t allergic potential due PABA analogue
o Most of them are vasodilating agents
o Cocaine (vasoconstrictor), procaine, amethocaine and chloroprocaine

ADDITIVES:

Epinephrine
o Maximum dose is 4 micrograms/kg
o Adding epinephrine will increase the safety dose and duration of local anesthesia

o Contraindicated in:
• Arrhythmias
• Unstable angina
• Uncontrolled HTN
• Poor collaterals (penis and ear, toes, fingers, nose)

Clonidine

Sodium bicarbonate
o Raise the pH -+ increases onset and prolong the duration and reduces pain of injection
Example:
■ Maximum dose of 1% lidocaine without epinephrine in 100 kg person:
o as 1 % lidocaine contains 10 ml/solution
o 3 mg x 100 kg= 300;, 10 = 30 ml of 1% lidocaine is the maximum to use
ASA CLASSES

Class Description Example Mortality

Class I Healthy patient 0.05%
Class II - Controlled DM or HTN
Mild disease - BMI > 30 and < 40 0.5%
- Smoker
Class Ill - Uncontrolled DM or HTN
- BMI > 40
- Stable angina
Severe disease - Previous Ml or CVA (> 3 months)
5%
- ESRD undergoing regular dialysis
- Active- heoatitis
Class IV - Unstable angina
- Recent Ml or CVA (< 3 months)
- Cardiac failure (Very low EF)
Organ failure - Liver ffailure 8 -20%
- ESRD not undergoing regular dialysis
- Severe COPD
- Sepsis or DIC
Class V Moribund - Ruptured aortic aneurysm
(Not expected to - Saddle pulmonary embolus
9.5-50%
survive without
intervention)
Class VI Oraan Donor

MALLAMPATI SCORE
■ Class I: Complete visualization of soft palate
■ Class II: Complete visualization of uvula
■ Class Ill: Visualization of only base of uvula
■ Class IV: Non-visualized uvula

Class I Class II Class Ill Class IV

OTHERS
■ Pattern of recovery from general anesthesia:
Small bowel + Stomach + Large bowel

■ Cerebrovascular accidents happened during recovery stage

■ Endotracheal tube should be placed 2 cm above the carina

■ Best determinant of esophageal vs. tracheal intubation: End-tidal CO2

t ETC02 ! ETCO2
Earlv air embolism Embolism (Pulmonarv. Air\
Tracheal intubation Obstruction
Malianant hvnerthermia Disconnection from the ventilator
Atelectasis Nitrous oxide
Hvnoventilation Hvnotension, Hvnnvolemia
Metabolic acidosis

■ NPO status
o Clear liquid: allows up to 2 hours preoperative
o Full liquid: allows up to 4 hours preoperative
o Solid food: allows up to 6 hours preoperative

■ Gastric aspiration best managed with:

o Suctioning and controlled ventilation with positive end-expiratory pressure (PEEP)

■ Drugs which contraindicated in asthmatic patients:

o Beta blockers
o Morphine "Narcotics" (Histamine release and respiratory depression)
o Neostigmine (Acetylcholinesterase inhibitors)
o Desflurane (Induction agent)
o Mivacurium (Muscle relaxant)
Minimal Invasive and
Surgical Technology
MINIMAL INVASIVE AND SURGICAL TECHNOLOGY

PERITONEAL MEMBRANE (Surface area: 1.8 m2)

■ NH3, Ca, Fe, and lead are removed
■ Most drugs are not removed with peritoneal dialysis

Peritoneum + Serous membrane lines walls of the abdominal cavities and covers viscera
Composed of Mesothelium (simple squamous cells on basement membrane)

1) Parietal: (outer) lines the walls of the abdominal and pelvic cavities
2) Visceral: (inner) covers the organs

■ Greater sac: extends from diaphragm to pelvis

■ Lesser sac: behind the stomach -+ Divided into Greater and Lesser OMENTUM
o Right margin -+ Connected to greater sac by epiploic foramen (foramen of winslow)

Borders of lesser sac:

■ Anteriorly: Free border of lesser omentum, bile duct, hepatic artery, and portal vein
■ Posteriorly: Inferior vena cava
■ Superiorly: Caudate lobe of the liver
■ Inferiorly: 1•1 part of the duodenum

Omentum + 2 layered folds of visceral peritoneum connect stomach to another viscus

-+ Omentum supplied by: Left and right gastroepiploic artery
1) Greater omentum: connects greater curvature of stomach to transverse colon
(policmanl �Jocalization of infection
2) Lesser omentum: suspends lesser curvature of stomach from the fissure of ligamentum
venosum and the porta hepatis

Mesentery + 2 layered folds of visceral peritoneum connecting intestines to posterior abdominal wall
1) Dorsal: from splanchnopleuric mesoderm
-+ Greater omenum and all ligaments and intestinal mesenteries
2) Ventral: from septum transversum
-+ Lesser omentum, falciform ligament, and coronary and triangular ligaments of the liver
SURGICAL TECHNOLOGY
■ Maneuvers to exposure of retroperitoneum:
Right side:
Classic Kocher:
Maneuver: Incise lateral peritoneal attachment of 1'1, and 2nd
duodenum and retract it along with head of pancreas medially
c:, Until left lateral edge of aorta
Care to preserve right renal artery

Exposure: IVC, distal CBD, aorta, right kidney, duodenum, and

head of pancreas

Extended Kocher: (Part of Cattell-Braasch}

Maneuver: Mobilize transverse (3rd ) part of duodenum and continue
by standard kocher along white line of Told! until the cecum

-
Exposure: SMA, Infra-hepatic IVC, right kidney, right iliac vessels

Associated with risk of injury to the replaced right hepatic artery

Cattell-Braasch: (Right medial visceral rotation)= Super-Extended

kocher
Maneuver: Begun at CBD until ligament ofTreitz
Extended kocher then, incise visceral peritoneum of small bowel
mesentery medial to the cecum until ligament of Treitz
Exposure: IVC, SMA, SMV, IMA. IMV, infra-renal aorta, 3rd , 4th part
of duodenum, and Head of pancreas

Left side:
Mattox: (Left medial visceral rotation)

)
o Maneuver: Mobilize descending colon to midline, by
incise sigmoid colon to splenic flexure along lateral
' peritoneal reflection

o Exposure: Aorta, Celiac trunk, and left renal and iliac

vessels, andTail of pancreas
CO2 PNEUMOPERITONEUM
■ CO2 Characters:
Inert gas with highly soluble and not support combustion
- Low risk of gas embolism, cheap and available

■ Nitrous oxide:
- Bowel dilatation
• 1 End-Tidal CO2

■ Argon beam:
- f risk of gas embolus

■ Changes related to pneumoper;toneum·

Increased Decreased
Heart l HR 1 HR (Most common)
fMAP 1 COP
l CVP lANP
l SVR 1 Right atrium filling
l PVR 1 Peripheral blood flow
1 Pre-load
/Venous return l
Respiratory f PCWP 1 Vital capacity
f Airway pressure LFRC
l PIP 1 Complirmce
l PAP
t Mean airway pressure
Renal fAldosterone 1 Renal flow
fADH 1 UOP
fCortisol 1 pH
fCatecholamine
t Renin

■ PEEP worsens effects of pneumoperitoneum

■ Cardiopulmonary dysfunction occur with intra-abdominal pressure > 20

■ Most common arrthymia during laparoscopy: Bradycardia

Ergonomics:
1- Table Height: instruments level should be at elbow level, with rest of the shoulder
Table Height = 0.45 x Surgeon high
• If patient on trendelenburg position = table more down
2- Distance between surgeon and monitor should be 5 diagonal times= ( 5 x Inches of screen )
3- Level of monitor should be at resting eye level 10 degree down "20 lax meter)
4- Manipulation angle between two instrument = 60 degree
5- Azimth Angle between instrument and telescope (camera)= 30 degree' 2 = 60 degree
(manipulation angle}
6- Elevation angle between instrument and body = 30 degree
7 - Instrument Length is:
20 cm junior pedia, 28 cm senior pedia, 36 cm in adult, 45 cm in obese patient
8- Distance between target and instrument = 1/2 instrument length. 18 in 36 instruments
9- Length of intra-abdominal instrument = 113 irnstrument length
10-To find the lost instrument: elevation angle must be 60, and azimuth angle should be 30

Umbilical Incisions:
■ Superior Crease (Crying incision)
■ Inferior Crease (Smiling incision) Best
o Site of obliteration vitellointestinal duct -+ high capacity of closure
o So, less chance of hernia, and most of them do not close it
■ Trans-umbilical: usually avoided, because of s.epidermides and high chance of hernia
o But used in obese patient because too less fat layer
■ Longitudinal inferior crease
■ Supra of Infra Umbilical: 5 cm far from umbilicus

Any tissue extraction from any port � you have to close it /high risk of port-site hernia)
Access techniques of Primary (first port):
1- Closed: by Verss needle
Palmars point: left midclavicular line, ·subcostal (Only contraindication: splenomegaly)
2- Open: under vision by hasson technique (Best)

Dissection of the fascia of 1 st port incision should be transverse dissection to prevent bleeding
f
Abdomen lited by the hand not the clamps (clamps iust to make the umbilicus averted)

Distal abdominal aorta and right common iliac artery have greatest risk of injury during first trocar
insertion inferior to the umbilicus
Verss needle:
■ Closed(-) Open(I)
■ Consist of: style! & simple needle of 1.2 mm width
■ Sizes: 8cm & 10cm for pedia, 12cm Adult, 20cm Bariatric
■ Hold it like a dart(best) or a pencil
o If patient supine: enter perpendicular (in Obese patient)
o If patient trendelenburg position: enter oblique

Tests:
■ Test the Spring before usage
■ 2 pricks you should hear: Rectus, Peritoneal(tinting it 4 cm)
■ Injection and aspiration of same amount normal saline
■ Hanging test or Drop test: the floated drop will go in after lifting abdomen
■ Plunger Test: after introduce verss with syringe, remove plunger then lift abdomen to
watch the saline goes inside
■ Needle Movement Test: verss should move freely, but don't do it cause it can do bowel
laceration

Safest trocar: Sharp pyramidal trocar

Flow rate should be 1Umin in 1st 500ml of gas: to prevent gas embolism and vasovagal attack
Minimum Gas to introduce 1st trocar: 1.5 - 6 L
Pressure set: 13 - 15 in adult. 8 - 10 in children

IVC Preperitoneum SC, or Aorta, bowel, or

muscle Block, bladder, or
closed wall stomach
or valve
Preset Pressure 12 12 12 12 12
Actual Pressure 6 12 12 30 12
Flow Rate 1L/min 0.5L/min 0 0 0.5L/min
Total Gas used 12L 500ml 200ml 200ml 1L
Present. Nulliparous Max of Unilateral
verus with no Preperitoneum is dilatation
distension 1L
Coagulation types:
1- Fulguration: Spray mode (0.5 cm far) by Monopolar only
- 1.6 less time injury, used in structure above vessels, mild endometriosis, and liver bed
bleeding

2- Desiccation: can be done by bipolar

- By holding the tubular tissue, and desiccated until become sealed

3) Harmonic Scalpel: Ultrasonic Generator

- 55,500 vibrations/second, 80 - 100 degree (instead of 200-300 in mono-bi polar)
- Works by friction energy
- Seal vessels up to 5mm
- Best instrument for dissection

4} Liqasure:
Best instrument for hemostasis
Seal vessels up to 7mm
Extracorporeal Knots
■ Roder's knot: (1-3-1) = 1 hitch 3 winds 1 locking hitch

Stacked
&11.ldon
Tail the long
threata

■ Meltzer's knot: (2-3-2)

"""
.......
........
.......
,,._..
l'lalf\l'IOl

■ Tayside knot

■ Tumble square knot

o Used when tissue is under tension, do Square knot not surgical knot, then stretch one
end from right or left ( both side pre-knot, post-knot), Most secured knot but you have to
double lock it, you have to see buttock sign

■ Others:
o Mishra's knot: (Triple 1-1-1}
o Weston knot
Perioperative Care
Reviewed by:

Dr. Haytham Alarfaj

PERIOPERATIVE CARE

PERIOPERATIVE ASSESSMENT

■ APPROACH TO PERIOPERATIVE CARE

o Identify and assess the high-risk patients
• ASA (American Society of Ane·sthesiologists)
• RCRI (revised cardiac risk index)
• CPET (cardiopulmonary exercise testing)

o Detailed preoperative assessment

• Performance assessment:
• Eastern Cooperative Oncology group (ECOG) status

Grade Performance status

0 Fully active. able to carry_ on all ore-disease f)erformance without restriction
1 I Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or
sedentarv nature e.o.,_Ji_ght house work office work
Ambulatory and capable of all selfcare but unable to carry out any work activities; up and about
2
more than 50% of wakinQ hours
3 Caoable of onlv limited self care; confined to bed or chair more than 50% of waking hours
4 Comoletelv disabled; cannot carry on anv selfcare: totallv confined to bed or chair
5 I Dead

• Karnofsky Performance Status Scale

Condition Value Level of functional caoacitv

Able to carry on normal activity and 100% No comolaints: no evidence of disease
to work; no special care needed 90% Able to carry on normal activity; minor signs or symptoms of
disease
80% _Normal activi!}'. with effort; some signs or symptoms of disease
Unable to work; able to live at 70% Cares for self; unable to carry on normal activity or to do active
home and care for most personal work
needs; varying amount of 60% Requires occasional assistance but is able to care for most
assistance needed oersonal needs
50% Reouires considerable assistance and freouent medical care
Unable to care for self; requires 40% Disabled· reouires cnecial care and assistance
equivalent of institutional or 30% Severely disabled; hospital admission indicated although death
hospital care; diseases may be not imminent
progressing rapidly 20% Very sick; hospttal admission necessary; active supportive
treatment necessarv
10% Moribund· fatal orocesses ornnressina raoidlv
0% Dead

Both scores used to identify quality of life and referral to palliative care in malignancy
Karnofsky < 50% or ECOG > 3

o Optimize medical management

o lntraoperative considerations
o Consider specific strategies, e.g. b-blockade or goal-directed therapy
o Consider admission to a critical care facility postoperatively
■ PULMONARY FUNCTION TESTS
o Most important investigation to predict post-operative pulmonary complications:
• Pulmonary function tests (FEV 1)

o FEV1: Forced expiratory volume in 1 second

• > 2 Lcan tolerate pneumonectomy
• > 1.5 Lcan tolerate lobectomy
• > 1.25 L can tolerate thoracotomy

o Need predicted post-operative FEV1 > 0.8 Lor> 40% predicted postoperative

o No resection if preoperative levels:

• pCO2> 50
• pO2< 60
• VO2 max< 10-12 ml/min/kg
• FEV1 < 1.6 L (1600) or< 50%

o Pulmonary function tests have positive predictive value for postoperative pulmonary
complications in patients undergoing lung resection only

■ RISK FACTORS FOR POSTPONING THE ELECTIVE SURGERY

Risk factor Time waitinq for elective surnerv

Hvnnthvroidism / H"""rthvroidism Till euthvroid achieved
Smokinq 6 - 8 weeks cessation
CABG 4weeks
Mvocardial infarction 6 months
PCI anaioolastv with stent 4-6weeks
PCI anaioolastv without stent 1 week
Cardiological risk factors: Until optimization
- CHF (S3 gallOJ>)
- Aortic stenosis
- Distended JVP
- Unstable angina (Class 4)
- Premature Ventricular Contractions (PVC)
of> 5 contractions/min

H:.!lli!rtension with !;!nd-organ d:.!sfunction:

- Left ventricular hypertrophy
- Renal failure
- CVA
- Svstolic or Diastolic dvsfunction
■ PERIOPERATIVE MEDICATIONS (in moderate and high risk surgery)

Medication Pre-ooerative Post-ooerative

Warfarin Hold for 3 - 5 days Start within 12 - 24 hours
Hold for 6 hours Start after:
Heparin 12 - 24 hours for minor procedures
48 - 72 hours for maier orocedures
Hold for 24 hours Start after:
LMWH 12 - 24 hours for minor procedures
48 - 72 hours for maier orocedures
NSAIDs Hold for 3 days
Aspirin Hold for 5 - 7 days
Clopidogrel (Plavix)
fADP inhibitor!
Apixaban Hold for 2 - 3 days
fFactor Xa inhibitor!
Oabigatran Hold for 2 - 5 days
fFactor Ila inhibitorl
Oral Contraceotives Hold for 4 - 6 weeks
Anti TNF medications Hold for 6 - 8 weeks Start after 4 weeks
(Controversial/ 2 weeks for Adalimumab
Methotrexate Hold for 1 - 2 weeks Start after 1 - 2 weeks
Corticosteroids Hold for 2 weeks Start after 2 - 4 weeks

■ Bridging:
o Using of short-acting anticoagulant during interruption of warfarin when INR not in
therapeutic range

o Steps:
3) Warfarin stopped 4 • 5 days before surgery

4) Heparin initiated 2 days after stopping (3 days pre-op)

o Indications:
• Recent (within 30 days) myocardial infarction
• Mechanical heart valves
• Stroke
• Pulmonary embolism

o INR > 1.5: No elective surgical procedures

o INR > 1.3: No bed-side procedures (central line, biopsy)

PERIOPERATIVE MANAGEMENT
■ DAVID

D (Diet) A (activitvl V N/SJ I (lnvesti ation IVF) D (Drugs)

Now Later Ambulation Incentive Trend RBS PT/PTT Antiemetic
soirometer
Regular NPO Physiotherapy Chest Weight Type and CBC Antibiotics
diet midniqht physiotheraov screen
BMI RFT LFT Antiulcer
Urinalysis Septic Anticoagulant
work-uo
1/0 chart Ana"'esia

■ MAINTENANCE OF IV FLUID: (examples for 70kg patient )

o 100- 50- 20rule (Per day)
• 100x 1°1 10kg= 1000+ {50 X 2nd 10kg } (500)
• = 1500+ {20x remaining 50} {1000) = 2500ml/ day
• 2500/ 24 -+ 104ml/ hr

o 4- 2- 1rule (Per hour)

• 4x 1st 10kg =40+{2x 2nd 10kg) (20)
• =60 + {1x remaining 50} (50) -+ 110ml /hour
• Alternative: Weight+ 40

Healthy patient can tolerate 10 days of partial starvation (/VF only) without signs ofprotein catabo/ism

■ ANTISEPTIC
o poyjdone-iodine (9- 12% active iodine)
• Mechanism: destroying microbial protein and DNA /as Hydrogen peroxide)
• Most significant in reducing microorganisms when allow to dry
• Best for skin preparation pre-operative
• Works against gram+ and -. aerobes and anaerobes

o Chlorhexidine
• Mechanism: Disruption of cytoplasmic membrane "cell wall" /as alcohol)
• Salts of dihydrochloride, diacetate, and digluconate
• Works against gram+ and -, aerobes and anaerobes, and antjfungal

o Most of studies showed no difference between them in reducing surgical site infection
 ■ VENOUS THROMBOEMBOLISM PROPHYLAXIS
o Low: "Early Ambulation"
• Minor surgery I Laparoscopic with no risk factor
• Obesity, Smoking, Varicose vein, Immobility> 3 days

o Moderate: "Heparin 5000 SC q 12 hours / LMWH 40 mg q 24 hours"

• Bedridden
• Comorbidities (Congestive heart failure)
• Oral contraceptives, Pregnancy, or postpartum

o High: "Heparin 5000 SC q 8 hours/ LMWH 40 mg q 24 hours"

• Major general surgery or major orthopedic surgery
• Spinal cord injury or Long bone fracture
• Active malignancy, or Previous DVT/PE

o Caprini risk assessment for VTE:

1 Point each 2 Points each 3 Points each 5 Points each

Aae > 40vear Aae> 60 vear Aae > 75 vear Stroke
Minor sumerv Orthooedic suroen• Histon, ofDVT/PE Elective arthroolastv
BMI > 30 Maior sumerv Family history of VTE Hip, Pelvis, Leo fracture
Preanancv Laoaroscooic suraeru Factor V Leiden Acute soinal iniurv
Varicose vein Malignancy
OCPs Bedridden
Acute Ml Central vein
Low 1-2 Heoarin
Moderate 3-4 LMWH or Heparin
Hiah 5 and above LMWH + IPC

o weus score system for OYI probabmty·

Disease Score
Active cancer +1
Paralysis of extremities +1
Maior suraerv in less than 4 weeks orior +1
Bedridden for> 3 davs +1
Entire lea swellina +1
Localized tenderness alona distribution of deeo venous svstem +1
Pittino edema +1
Previous DVT +1
Calf swellino more than 3 cm comoared with asvmntomatic ,..,., +1
Collateral superficial veins (non varicose) +1
Alternative diaanosis las likelv or areater than that of DVT\ -2
Low risk 0 score 5 %DVT
Moderate risk 1 -2 scores 17 %DVT
Hioh risk > 2 scores 53%DVT

o Unfractionated Heparin is alternative to LMWH if contraindicated (as renal failure)

o IPC (intermittent pneumatic compression) or GCS (graduating compression stocking)

Should be used for all Moderate and high risk
 o Indications for IVC filter:
• Contraindicat ons for anti-coagulation therapy
i
• Recurrent DVT
• Pulmonary embolus while on therapeutic anticoagulation
• Free floating iliofemoral , IVC or femoral DVT
• Patients who have had pulmonary embolectomy

IVG filter should be placed below the level of renal veins

■ PERIOPERATIVE ANTIBIOTICS FOR 551

o Used for all classes (Class ID, II, Ill and IV}, except Class I
• Class ID: Clean+ prosthetic part (e.g. mesh, valve, or implant)

o Prophylactic antibiotics: used to prevent surgical site infections only (Gram+)

o 30- 60 minutes before skin incision, stop post-operative within< 24 hours

o Second dose of prophylactic antibiotic should be given if procedure lasts > 3 hours

o Best for hair removal to prevent SSI ➔ Clippers (not razors}

o Classification of surgical site wound based on surgical operation:

Class Class I Class II Class Ill Class IV

Type Clean Clean Contaminated Contaminated Dirty
For only skin flora Hollow viscus Gross spillage of Old traumatic wounds with
entered with NO viscus contents retained devitalized tissue
Description
No hollow viscus spillage of contents with existing infection or
entered perforated viscera
Hernia surgery Cholecystectorny Penetrating trauma Perforated diverticulitis
(if no mesh applied)
Elective GI surgery Enterotomy in bowel Necrotizing infections
Breast surgery obstruction
Example
(if no implant) Colorectal surgery
Non-perforated non- Gangrenous I Perforated
gangrenous appendicitis
annendicitis
Colorectal: 10- 15¾
Infection rate 1-5% 3-17% >30%
Rest: 1 - 10%
Infection rate
With antibiotics <2% 2-3% <7% 7-10%

Irrigation of the wound with Normal Saline, prior to closure shown to decrease wound infection in
clean contaminated wound
 o Prophylactic antibiotic based on type of surgery:
Tvne of suraerv Proohvlactic antibiotics PCN Allernv
Gastroduodenal area
Cefazolin 2g Vancomycin, Clindamycin
Non-obstructinn
Ciprofloxacin or Cefazolin
+ Metronidazole
Gentamycin + Clindamycin
Neomycin + Erythromycin
Colorectal surgery
Ampicillin/Sulbactam
Obstructing small bowel Gentamicin or Ciprofloxacin
+ Metronidazole
Piperacillin
Carbapenem
Colistin
Clindamycin or Vancomycin
Cefazolin
Biliary tract + Aminoglycosides
Cefoxitin
(Open, Lab "high-risk")
Ceftriaxone
Ciprofloxacin + Metronidazole
Biliary tract
None None
(Lab "low-risk")
Cardiovascular Cefazolin, Cefurox.ime Vancomvcin, Clindamvcin
Breast, Hernia Cefazolin Vancomycin, Clindamycin
 ■ GLUCOCORTICOID COVERAGE PERIOPERATIVE:
No Need to give Continue same dose Additional dose
additional dose /No HPAA sunnressionl IHPAA sunnressionl

If patient stop -Any dose < 3 weeks - Dose > 20 mg/day for ;;, 3 weeks
glucocorticoids > 3 weeks - Dose 5 - 20 mg daily ;;, 3 weeks

o For uncertain adrenal suppression

• For patient taken 5 - 20 mg/day for;,, 3 weeks
• Either to do testing by: Low-ACTH test
• Positive results:
o Cortisol 8 am < 5 mcg/dL
0 ACTH test -+
Cortisol < 18 mcg/dl

• Or give additional dose if there is moderate-major surgical stress

o Glucocorticoid coverage:
• Minor procedures: No extra supplementation

• Moderate surgical stress: 50 mg hydrocortisone IV pre-induction and 25 mg

hydrocortisone q 8 hours for 24 hours, then resume usual dose

• Major surgical stress: 100 mg hydrocortisone IV pre-induction and 50 mg q 8

hours for 24 hours, then resume usual dose

o Cessation of corticosteroids:
• Any dose < 1 week: No need for tapering

• 1 - 3 weeks: Tapering for> 7.5 mg/day prednisolone or> 30 mg/day

hydrocortisone

• > 3 weeks:
• Taper prednisolone 2.5/hydrocortisone 10 mg every 3 -4 days down to
physiological dose
• Followed by reduction of hydrocortisone 2.5 mg every 2 - 4 weeks
• Cortisol level or suppression test recommended when hydrocortisone
reach 10 mg/day

• If steroids stopped suddenly perioperative -+

risk of Addison crisis
• t K, t Ca, l Na
• Metabolic acidosis (! HC03)
• Hypoglycemia , hypotension, hyperpigmentation
OTHERS
■ Hand scrubs should be done for at least 120 seconds

■ Recommended range of temperature for operating room: 20 - 25 degree centigrade

■ Best way to prevent hypothermia: Warm air

■ Only medication decreases mortality and morbidity perioperative: Beta-Blocker

■ Strong risk factor for morbidity and mortality postoperative: Albumin level

■ Most common association with postoperative mortality: Pre-op renal failure

■ Complications of obstructed sleep apnea (OSA}:

o Right ventricular failure
o Hypoxemia
o Hypercapnia
o Polycythemia

■ Prostate surgery + release urokinase, activates plasminogen

o Treatment: e-aminocaproic acid (Amicar}

■ Bladder training
o Used if> 2 weeks on Foley's catheter
o Training to reinforce the detrusor muscles
o By clamping the catheter every 4 hours for duration of 20 minutes for 48 hours
Oncology
 ONCOLOGY
■ STAGE: for location "TNM Classification, or Classical staging'
■ GRADE: for histological characters (on Microscope)
0
..
Qllarni:;1erislii. fim!iogs !lf maligoa□I (aoai:1Iasia) le�iQD
Invasion

.. Monoclonal origin
Cellular pleomorphism
Nuclear pleomorphism (Can present in benign lesion as well)
• Loss of cell polarity (atypia)

...
0 Grades:
( 1) Well-differentiated tumor
(2) Moderately-dif ferentiated tumor
(3) Poorly-differentiated tumor

■ Most common cancer worldwide: Lung cancer

0 Most common cause of cancer-related death in male and female
■ Most common cause of cancer in female: Breast cancer
■ Most common cause of cancer in male: Prostate cancer

■ Terminology:
0 Hyperplasia: increased number of eel Is
0 Metaplasia: replacement of tissue with another
0 Dysplasia: altered size, shape, and organization (eg Barrett's dysplasia)

PET scan (positron emission tomography}

■ Identify metastases, by detects "Fluorodeoxyglucose" by using C-11
0 Infuse 18-FDG-+ Detect 6-FDG by hexokinase
0 Difficult in patients with uncontrolled diabetes, and in brain lesions

Tumor markers:
Marker Descriotion Associated with
Glycoprotein from embryonic endoderm Colon cancer, Breast cancer. Lung cancer
Half-life: 18 days Medullary thyroid cancer, Seminoma
CEA
COPD, Pancreatitis, Smoking
lnflammaton, bowel disease
Monoclonal antibody Pancreatic cancer, Esophagus cancer
CA 19-9
Bile duct cancer
CA 15-3 Glvcoorotein mucin tvne Breast cancer
CA 125 Glvcoorotein mucin tvne Ovarian cancer, Endometrial cancer
Glycoprotein from placenta Testicular cancer, Choriocarcinoma
Beta-HCG
Half-life: 1 - 2 davs Seminoma
AFP (alpha Glycoprotein from yolk sac Liver cancer
fetooroteinl Half-life: 5 davs Germ cells cancer
Calcitonin Hormone from parafollicular C cells Medullarv thyroid cancer
Thvroalobulin Read thvroid chaoter Thvroid cancer lexceot medullarv and anaolastic)
Chrom-ranin A Carcinoid tumor
Highest sensitivity, but low specificity Prostate cancer
PSA
Half-life: 18 days
NSE Small cell luna cancer Neuroblastoma
 Cancer: Loss Tumor suppressor gene + Gain oncogene
■ Geneticaueration·
o Activation of Oncogenes
o Inactivation of Tumor suppressor gen·es
o Reduction of cellular adhesions (E-Cadherin)
o Reactivation of telomerase
o Presence of mic rosatellite instability

■ Tumor suppressor genes :

o Mutated gene ➔ Loss of its function ➔ cancer development
Gene Chromosome Descriotion Associated with
Short arm Ch. 17 Most common gene 50% of all human cancers
Initiate apoptosis Li-Fraumeni syndrome
p53 (Sarcomas, breast cancer, brain
tumors, leukemiaI
Long arm Ch. 5 Cell cycle regulation and movement FAP
- Regulate B-catenin function Gardner's syndrome
APC
Most common mutatiorn is loss of 2'"' allele
Initial mutated aene to develon in CRC
DCC Lona arm Ch. 18 Cell adhesion Colorectal cancer
hMSH2 DNA mismatch Lvnch svndrome HNPCC
DPC4 Ch. 18 SMAD orotein Pancreatic cancer
Ch. 17 Associated more with hormone -ve receptors 60% Breast cancer
BRCAI Lost more in sporadic breast cancer 40% Ovarian cancer
Colon and Prostate cancer
Ch. 13 More common than BRCA I 60% Breast cancer
10% Ovarian cancer
BRCAII 10% Male Breast cancer
Melanoma
Rb1 Ch. 13 Cell cycle regulation Retinoblastoma
 ■ Proto-oncogenes:
o Oncogene: gene can lead to transform cell into a tumor cell under certain circumstances
o Proto-oncogene: gene gives rise to oncogene after genetic alteration

Gene Descriotion Tv= of mutation Associated with

G protein defect Point mutation Colon, Lung, Pancreas cancers
K-RAS Most commonly mutated oncogene in
sooradic colonic maliQnancies
Tyrosine kinase receptor Point mutation Familial/ MEN of MTC
Located in chromosome 10 Papillary thyroid cancer
RET
Pheochromocytoma
Hirschsoruna's disease
Tyrosine kinase defect Amplification Breast cancer
HER2/neu Gene amplification + suppressing apoptosis
and increasino oroliferation and arowth
Tyrosine kinase receptor Amplification GIST, Seminoma, Melanoma
KIT
Stem cell arowth factor receotor
Non-receptor Tyrosine kinase defect Point mutatian Colan, Breast, Prostate cancers
Src
1" onc=ene discovered
Regulate cell cycle Amplification Parathyroid adenoma
PRAD-1
Breast and salivan, cancers
PDGF receptor defect Overexpression Breast cancer, and Melanoma
Sis
Erb B EGF receotor defect Breast. salivarv ovaries cancers
Transcription factors Translacation Burkitt's lymphomas
Myc
Regulate cell cycle and apoptosis Translocation Chronic myeloid leukemia
ABL (9:22)

Risk modifier genes:

■ Phospholipase A2
■ COX2 (cyclooxygenase 2)
o Overexpression has been linked to resistance to apoptotic signals
o COX2-specific NSAIDs have been shown to increase apoptosis

■ CD44v
o Involved in cell-cell adhesion activities
o Associated with advanced disease and metastasis (multiple myeloma)
 ■ Radiation therapy /XRTl:
0 Target: DNA
o Most vulnerable stage of cell cycle for XRT: M phase
o Most damage done by formation of: 02 radicals
• The effectiveness of radiation therapy decreased by low-tissue oxygen tension

Radio-Sensitive tumors Radio-Resistant tumors

Ewina sarcoma Melanoma
Semino mas Most sarcoma (except Ewing)
- Epithelial sarcomas
Lymphomas - Osteosarcoma
-GISTs
Merkel cell carcinoma Pancreatic cancer
Multiole mveloma
SCLC
Larrm tumors are less resoonsive to XRT due to Jack of oxvnen

■ Chemotherapy agents:

Mechanism of action Side effects

ANTIMETABOLITE
Methotrexate Inhibits Dihydrofolate Reductase Renal toxicity, Radiation recall, BM suppression
-+ inhibits purine and DNA synthesis Leucovorin reverses effects bv resuoolvinq folate
5-Fluorouracil Inhibits Thymidy1ate Synthase BM suppression
-+ inhibits purine and DNA synthesis Hand-foot syndrome: Soreness, redness, and
peeling of palms and soles
Leucovorin (folinic acid) increases toxicitv of 5FU
Azathioprine -+ (6-mercaptopurine)
-+ inhibits purine and DNA synthesis
ANTI-TUMOR ANTIBIOTICS
Bleomycin Pulmonary fibrosis
Busulfan
Doxorubicin 02 radical formation Cardiac toxicity
VINCA or PLANT ALKALOIDS
Vincristine Binding tubulin protein Perioheral neurooathv
Vin!llastine -+ Inhibit microtubules formation !lone suppression
-+ Aoootosis
ALKYLATING AGENT
(Effective durina all ohases of cell cvcle)
Cyclo11hos11hamide Acrolein: active metabolite SIADH
Hemorrhaaic cvstitis
Cisplatin Nephrotoxic, Neurotoxic, Ototoxic
Carboolatin Bone sunnression

■ Ovarian cancer: only tumor that the surgical debulking improves chemotherapy

■ Lymphoma: Curable solid tumors with chemotherapy only

■ Chemoresistant tumors:
o Gastric, Bladder, and Soft tissue SCC cancers
a D
B
Key
B = Bleomytin, Bu•ulfan
Pulmonary Fib�ts
@: = Cit.platin, c.arboplatin
Nephro/ototoxk
D = Ooxorubldn
Cardiotoxic
• • Methotrexate and 5-Fluorouracll
Myeloouppreolon
00 • Nltro�urea� ( lomuotlne, airmuc:.tine}
Neurotoxlc ( xBBB )
P • CycloPho,phamlde
Hemorragic Cystiti$
Y = Vine• Alkaloid ( Vincrlstlne, Vinblastlne )
Peripheral Neuropathy
OTHERS

■ ECOG assess ment: (Eastern Cooperative Oncology Group)

Grade ECOG Performance Status
0 Fully active. able to carrv on all pre-disease oerformance without restriction
Restricted in physically strenuous activity but ambulatory and able to carry out work of a
1
liaht or sedentarv nature, e.a., liaht house work, office work
Ambulatory and capable of all selfcare but unable to carry out any work activities; up and
2
about more than 50% of wakina hours
3 Capable of only limited selfcare: confined to bed or chair more than 50% of wakina hours
4 Completely disabled; cannot carry on any selfcare; totally confined to bed or chair
5 Dead

■ Neoadjuvant therapy:
o Therapy that given prior to the main treatment (e.g. surgical resection)

■ Adjuvant therapy:
o Therapy that given during or after the main treatment

■ Metachronous tumors
o Tumors occurring at different times
o Non-anastomotic new tumors developing at least 6 months after the initial diagnosis

■ Synchronous tumors
o Tumors occurring at the same time
o 2 or more primary tumors separated by normal bowel and not due direct extension

■ Carcinogens:
o Asbestos: Mesothelioma
o Arsenic and Vinyl chloride: Liver Angiosarcoma
o Alfatoxin B 1: Liver cancer
o Beta-naphthylamine: Bladder cancer
o Benzene: Leukemia
o Coal tar: Scrotal, Larynx, skin, bronchial cancer

■ Resection of a normal organ to prevent cancer:

o Breast: BRCA I or II with strong family history
o Thyroid: RET proto-oncogene with family history thyroid cancers
o Colon: in patients with FAP

■ Some cancer spreads:

o Virchow's node: Stomach -+
Supraclavicular nodes
o Sister Mary Joseph's node: Pancreas -+
Periumbilical node
o Krukenberg tumor: Ovarian -+
Stomach
■ The first step in carcinogenesis produced by RNA virus -+ Transcription into cellular DNA
■ Malignant cells do not enter Go stage after proliferation

■ Cytotoxic T cells need MHC complex to attack tumor

o Natural killer cells independently attack tumor cells

■ Kaposi sarcoma
o Most common site: Palate
o Treatment: Radiation
PATHOLOGICAL CALCIFICATIONS
■ Oystrophic calcification:
o Necrotic or degenerated tissue, calcifiication by calcium salt (normal calcium level)
o Due to damaged membrane, lead to bind Ca to PO -+ Calcium phosphate
o Examples:
• Scars
• TB, fat necrosis, hemorrhagic infarction
• Calcified thrombus, atherosclerosis, calcified Valvular disease
• Degenerate colloid goiter, degenerate tumor
• Psammoma body: single necrotic cells constitute seed crystals encrusted by
mineral deposits

■ Metastatic calcification:
o Normal tissue, calcification due to hypercalcemia in alkaline environment
o Examples:
• Chronic renal failure
• Hyperparathyroidism
• Destructive bone lesion
• Malignancy (Breast, lymphoma, leukemia, and parathyroid cancer)
Transplant
TRANSPLANT
■ Autoaraft: same individual
■ lsoaraft: different individual, genetically identical
■ AUograft· different individual, same species
■ Xenoaraft: different individual, different species
Transplant immunology:
■ ABO blood compatibility:
o Most important in recipient/donor matching
o Required for all transplants (less important in liver TXP)

■ HLA (human leukocyte antigen):

o HLA-DR should be positive in renal TXP

■ Cross-match: mixing recipient serum with donor lymphocytes

lmmunosuppressive Medications
■ Steroids
o First line, inhibit macrophages , lymphocyte proliferation, cytokine and prostaglandin

■ Cyclosporin:
o Binds cyclophilin and inhibits ca/cineurin
o Inhibits cytokine synthesis (IL-2), inhibits T-Cell proliferation
o Side effects: Hirsutism, gingival hyperplasia, nephrotoxicity

■ Jacronmus:
o Anti- /L2
o Most commonly used as maintenance immunosuppressive agent
o Side effects: Alopecia, Post-transplant DM

■ Monoclonal antibodies (OKT3}:

o Example: Zenapax:
o Block CD3, antagonist
i
IL-2 receptors
o Used for induct on and acute rejection episodes

■ Azathioprine
o Antimetabolite, inhibit DNA synthesis
o Inhibiting T- and B-lymphocyte proliferation
o Side effects: BM suppression

■ Sirolimus:
o Anti-T cells (mTOR)
o Side effects: Thrombocytopenia, an,emia

■ Mycophenol ate:
o inhibits purine synthesis, inhibits growth of T cells

University of Wisconsin preservation solution:

■ Most commonly used fluid worldwide
■ Contents: Raffinose, Hydroxyethyl starch and lactobionate
Types of rejection
■ Hyperacute reiection (occurs within minutes)
o Caused by preformed antibodies to ABO or HLA
• Activates complement cascade and thrombosis
• Risk factors: Perioperative blood transfusion, prior transplant or pregnancy
• Treatment: Emergent re-transplant (or removal of organ if kidney)

■ Accelerated reiection (occurs< 1 week)

o Caused by sensitized T cells to donor antigens
o Best way to determine acute rejection: Duplex U/S and Tissue biopsy
o Treated by t immunosuppression + steroids

■ Acute reiection (1 week to 1 month}

o Most common type
o Caused by T cells (cytotoxic and helper T cells) or Humoral {Antibody-mediated)
o Treated as accelerated rejection

■ Chronic reiecti on
o Replacement of parenchyma with fibrosis and vascular fibromuscular hyperplasia
o Type IV hypersensitivity reaction

Contraindications for transplantation

■ Active uncontrolled infection
o Chronic infections as HIV is not considered absolute contraindication

■ Untreated Malignancy:
o Wait at least 2 years after treated low- risk malignancy
• Examples as excision of colon cancer in polyp without invasion

o Wait at least 5 years after treated high-risk malignancy

• Examples as lymphoma, melanoma, renal cell carcinoma, breast/ colon cancer

o HCC is not considered contraindication for liver transplant

■ Acute viral hepatitis

■ Active substance abuse

■ Insufficient cardiopulmonary reserve

■ Poorly controlled psychiatric illness

 (stored up to 72 hours)
Kidney transplantation
■ Most common cause for kidney transplant: OM
■ Most common cause of transplant rejection: DM
■ First sign of rejection: High CPK, then hyperglycemia
■ 5-year graft survival: 75% - 80%
■ The left kidney has longer renal vein, which allows for easier anastomosis

■ Advantages of retroperitoneal placement of transplanted kidney:

o Close to bladder (less risk of ischemia due to short ureter)
o Close to iliac vessels (allows for multiple options for vascular reconstruction)
o Avoids peritoneal contamination
o Allows for easy biopsy

■ Complications:
o Acute tubular necrosis (Tubulitis)
• Acute rejection
• Associated with low urine output
• Treated by aggressive fluid therapy

o Urine leaks
• Treated by PCD and ureteral stent

o Renal vein thrombosis (Proteinuria}

o Renal artery stenosls

• Treated by angiography and stenting

o Infection
• Most common early infection by: CMV virus
• Presentation may include: Fever, malaise, or myalgia
• 2 phases:
• Early: Immediately post-transplant (risk of rejection)
• Late: 3 - 6 months post-transplant (peak of immunosuppression)

• Treated by
• Prophylaxis against common organisms
• Acyclovir or Ganciclovir

o Lymphocele (most common cause o·f external ureter compression)

• Lymphocele happens 2 - 4 weeks after surgery

• Management:
• Percutaneous drainage alone (initial management)
• Percutaneous drainage with sclerosing agent
o Better result but associated with toxicity to transplanted kidney
• If associated with re-accumulation after drain removal:
• Internal drainage "Lap/open peritoneal window (marsupialization)"
o Most effective management for recurrent lymphocele
Heart transplantation (stored up to 6 hours)
■ Most common diagnosis requires heart transplant: lschemic dilated cardiomyopathy

Pancreas transplantation
■ Need both donor celiac artery and SMA for arterial supply
■ Need donor portal vein for venous drainage, attach to iliac vessels
■ Most common transplant site for pancreatic islet transplantation: Liver
■ Drainage of pancreatic transplant by anastomosis to: Bladder or small bowel
■ Complications:
o Venous thrombosis or rejection

Lung transplantation (stored up to 6 hours)

■ Most common cause of early mortality: Reperfusion injury

■ Most common cause of late death and death overall following lung TXP: Chronic rejection

■ Acute rejection: Perivascular lymphocytosis

■ Chronic rejection: Bronchiolitis obliterans

■ Indication for double-lung TXP: Cystic fibrosis

Liver transplantation (stored up to 24 hours)
■ Most common cause for liver transplant:
o Chronic hepatitis C
o Biliary atresia in pediatrics

■ Criteria for urgent transplantation: Fulminant hepatic failure

■ Indications for liver transplant

o Acute liver failure
• Acetaminophen toxicity
• Acidosis: pH< 7.30
• Bleeding: PT> 100 / INR> 6.5
• Creatinine> 300 mmol/L

• Non- Acetaminophen toxicity

• Age< 10 or> 40
• Bleeding: PT> 100 / INR> 6.5
• Creatinine> 300 mmol/L
• No Hepatitis A / B
• Jaundice> 7 days before encephalopathy

o Hepatocellular carcinoma
Milan criteria
• 1 Lesion < 5 cm
• 3 Lesions< 3 cm
• Child A/ B / C
• No gross vascular or lymphatic invasion, No thrombosis
• No metastasis

■ MELD score: Creatinine, INR, Bilirubin (Albumin in not one of the criteria)
o Predict 3-months mortality and if patients with benefit from liver transplant in cirrhosis
o MELD> 15 benefits from liver transplant

■ Complications:
o Bile leak (Most common)

o Primary Non-functional
• P' 24 hours -+ Total bilirubin > 10, bile output< 20 cc/12 h, f PT and PTT
o Hepatic artery thrombosis
• Most common early vascular complication
• Fulminant hepatic failure
• Requires re-transplantation

o Hepatitis B re-infection
• Lamivudine (protease inhibitor) used to help prevent reinfection

o Chronic rejection
• Associated with elevated liver enzymes and hyperbilirubinemia
• Usually asymptomatic
OTHERS
■ Blood transfusion preoperative decreases rejection rate of transplanted organs (Positive effect)

■ Most commonly involved segment for bowel transplantation: mid to distal ileum

■ Skin cancer: most common malignancy following transplant (Squamous cell carcinoma)
o Anal cancer is the second most common

■ 2nd most common malignancy: Post-transplant Lymphoproliferative disorder

o Related to EPV virus which associated also with B Cells, Burkitt's lymphoma
o Presented with abdominal pain and small bowel mass on CT scan

■ Routine screening by Panel Reactive Antibody (PRA) predict presence of donor antibodies
o High PRA contraindicated to perform TXP: High risk of hyperacute rejection

■ Cardiopulmonary complications:
o Recipient: Myocardial Infarction
o Donor: Pulmonary embolism
Skin and S,oft tissues
SKIN, AND SOFT TISSUES
■ Skin layers: (from outside to inside)
o Stratum corneum
o Stratum lucidum
o Stratum granulosum
o Stratum spinosum
o Stratum basalis

■ Keratinocytes: main cell type in epidermis; originate from basal layer

■ Melanocytes: neuroectodermal origin (neural crest cells); in basal layer of epidermis

■ Dermis: primarily structural proteins (collagen) for the epidermis

■ Langerhans cells: antigen-presenting cells (MHC class 11), originate from bone marrow

■ Sensory nerves
o Pacinian corpuscles: pressure
o Ruffini's endings: warmth
o Krause's end-bulbs: cold
o Meissner's corpuscles: tactile sense

■ Eccrine sweat glands: aqueous sweat

■ Apocrine sweat glands: milky sweat

■ Cushlng's striae: caused by loss of tensile strength and elasticity

■ Furuncle: infection of the hair follicle in which purulent material extends through the dermis into
the subcutaneous tissue

■ Carbuncle: several inflamed follicles "clusters of boil" into a single inflammatory mass with
purulent drainage from multiple follicles

■ Hidradenitis suppurative:
o Chronic follicular occlusion and hyperkeratosis
o Inflammation of Apocrine sweat glands
� Chronic scaring

o Usually in axilla and groin regions

• Can happens in perianal and perinea! regions
• May mimic complex anal fistula

o Most common organisms: Staphylococcus and Streptococcus

o Management:
• Improve hygiene
• Antibiotics {Clindamycin}
• Surgery for refractory disease
• Incision and drainage of abscess
• Unroofing fistula and debridement of the granulation tissues

■ True Sebaceous cyst· originate from sebaceous glands and contain sebum
o Epidermoid cyst: originates from epidennis and contain keratin
o Pilar cyst: originate from hair follicles and contain keratin
• No sebaceous cyst in the soles

■ Dermoid cyst: benign cystic teratoma, contains mature solid tissues "some malignant potential"

■ Lipoma: Mature benign tumor of fat cells enclosed by thin fibrous capsules

■ Ingrown toenail "Onychocryptosis": nail grows and cut the side of nail bed "paronychium•
■ Congenital nevi
o Consist of hamartomas which consisting of nevus cells

o Most common location: Trunk, followed by the extremities and head and neck

o Large is> 10 cm and giant is> 20 cm

o Risk of melanoma is up to 10% in large and giant nevi and occurs in first 3 years of life

o Patients with large or giant CMNs are at risk for neurocutaneous melanocytosis
(leptomeningeal melanosis)

o Management:
• Early excision and reconstruction is the gold standard

• Serial examination for worrisome features is an option

(Ulceration, uneven pigmentation, change in shape, and nodu/arity)
+ lncisional biopsy
To address malignant potential, only complete excision is a possible solution

• Options for removal of larger nevi include:

• Serial excision

• Excision and full-thickness skin grafting

o Best for ear and eyelid reconstruction

• Excision and closure with distant flaps

• Tissue expansion and excision

o Best for scalp lesions
o Associated with increased morbidity in lower extremity
FLAPS
■ Most common cause of pedicled or anastomosed free flap necrosis: venous thrombosis

■ TRAM flap
o Based on superior epigastric vessels
o Periumbilical perforators most important determinant of TRAM flap viability

Flap Based on
Traoezius flao Transverse cervical arterv
Latissimus flao Thoracodorsal arterv
Pectoralis maior flao Thoracoacromial arterv
TRAM flao Suoerior eoiaastric arten,
Axial flao Deeo eoiaastric arterv

UV RADIATION
■ Damages DNA and repair mechanisms
■ Melanin single best factor for protecting skin from UV radiation
■ Ultraviolet B-light absorbed by DNA, and responsible for chronic sun damage

SKIN GRAFT
■ Full Thickness Skin Graft:
o Used in areas susceptible for trauma
{face, foot, weight bearing surfaces ''Joints")

o Associated with less wound contraction

o Requires addition coverage to donor sites
o High primary contraction {less wound contraction overall)

■ Split-Thickness Skin Graft:

o All epidermis and part of dermis
o High secondary contraction
o Used mainly for large area need to be covered
o Contraindicated in presence of wound infection

Blood supply of skin graft during first 3 days by imbibition then by neovascularization
 SKIN CANCER
Melanoma Basal cell carcinoma Squamous cell carcinoma
(Most common mortality- (Most common) (2"d most common)
related SCl
Lesion Asymmetrical Pink or skin-colored pea�y waxy- Flesh-colored papule or nodule
Irregular borer appearance papule or nodule Hyperl<eratotic
Multi-color Rolled borders Raised borders
.e 6 mm diameter Central scar and depression Scaly patch
Changing Branching Sore that does not heal
Umbilication or ulceration Could be crusted or ulcerated
Su,...rficial telanoiectases
Pathognomonic Palisading nuclei of peripheral Keratin pearls
features cells and stromal retraction
Location Anywhere Anywhere, sun-damaged areas Anywhere, sun-damaged areas
Skin, Eyes, and Anus Most common head, neck, arms (Face, neck, arms, ears, chest,
(back in men, legs in and lower lip back and upper lip)
women), (Upper ch est)
Post-XRT areas
Include scalp, nails, Old burn scars
oenitalia
Origin Neural crest cells Stratum basale of epidermis and Epidermidis
(melanocytes) hair follicles Extending beyond stratum

Risk factors
in basal laver eoidermis
■ Previous XRT • Sun exposure
basale
••
Sun exposure
■ Previous skin CA
■ Intermittent sun • PATCHED gene •
Previous XRT
Previous skin CA
■ Fair skin
exposure
(UV type A)
•
(mutated in 90%)
••
HPV

•••
p53 lmmunosuppression
■ Dysplastic nevi (mutated in 50%) Arsenics
■ Atypical nevi Bowen's disease
■
■
Congenttal nevi
•
Atrophic epidermis
Xeroderma
•
Actinic keratosis
pigmentosum
••
Xeroderma pigmentosum
Hydrocarbons (coal tar)
Chloroohenols
Types Revise melanoma section Nodular (most common)
Moroheaform /most annressiveI
Spread :1: Metastasis Locally invasive Lymphatic or perineural
(Most common: Lung) Metastasis more than BCC

Metastasis to small bowel

most common from
melanoma
Management Revise melanoma section lncisional biopsy of suspicious skin lesion to confirm diagnosis

Surgical excision with .e 4 mm margin

Regional lymphadenectomy for clinically positive nodes

XRT and chemotherapy: for inoperable or metastases or

lymphatic/vessel invasion

MOHS suraerv for hiah risk

MELANOMA
■ Patient need to be examined from the head 10 toe (including perinea!, perianal, scrotal or labia}
o Including neurological examination

■ Most common site for distant metastasis: Lung followed by Liver

■ Most common extra-intestinal malignancy metastasized to the small bowel

■ Increased risk to develop intussusception

■ ABCDE rule of Diagnosis:

o A: Asymmetry + Angulations, indentation, notching
o B: Border + Irregular, notched or ragged
o C: Color + Asymmetrical, and darkening
o D: Diameter + > 6 millimeters and increasing
o E: Evolving + Change in size, shape and color
■ Dia gnosis:
o < 2 cm lesion: Excisional biopsy with 1 - 2 mm margin
o > 2 cm lesions or cosmetically sensitive area: lncisional biopsy (or punch biopsy)
Shave biopsy may be used for small, flat lesion (inappropriate if melanoma is suspected)

■ Types:
o Melanoma in situ or thin lentigo maligna (Hutchinson's freckle):
• Superficial papillary dermis; 0.5 cm margins

o Superficial spreading melanoma (Most common)

Appears in trunks and proximal extremities

o Lentigo maligna (Least aggressive)

Appears in sun-exposed areas in elderly patients

o Nodular (Most aggressive)

Associated with vertical growth and atypical presentation

o Acral lentiginous (more in dark skin people}

Appears in mucous surfaces sub-ungual areas beneath fingernails and toenails

■ Clark level "histological characters" Breslow thickness 'Most accurate for

prognosis"
o Level 1: Confined to epidermis 0.75 mm
o Level 2: Invasion of Papillary derm'is 0.76-1.5 mm
o Level 3: Filling the Papillary dermis 1.5-3mm
o Level 4: Invasion of Reticular dermis >3mm
o Level 5: Invasion of deep subcutaneous tissue
■ Management of melanoma:
o Staging (for patients with biopsy-proven melanoma and nodal disease)
• Full blood workups including liver enzymes and LDH
• Full body CT scan

...
0 Excision with Margin:
TIS: 0.5 cm
< 1 mm depth: 1 cm
. 1 - 4 mm depth: 2 cm
> 4 mm depth: 3 cm

o Lymph nodes:
• SLNB
• Indications:
o Negative nodes clinically and melanoma depth.: 0.75 mm (Level 2)
o T1 melanoma{< 1mm) but with ulceration, or high mitotic rate

• Technique:
o Preoperative lymphoscintigraphy
+ lntradermal injections of technetium-sulfur colloid

o lntraoperative intradermal injection of 1 ml of isosulfan or

methylene blue dye near the tumor or biopsy site

• Used in melanoma and breast cancers to avoid radical lymphadenectomy

• Used in colorectal cancer to improve staging

• Resection if positive clinically

• For axillary dissection all levels should be dissected
{Therapeutic, not only staging as breast cancer)
• 1 - 2 - 3 (Even lymph nodes medial to pectoralis minor)

• Line of Saooey· (2 cm above umbilicus)

Determine direction of lymphatic spread

o + Superficial parotidectomy for all anterior head/neck melanomas.: 1 mm deep

o Administration of a recombinant cytokine (interferon-a-2b) showed increased survival in

high-risk group
SOFT TISSUE SARCOMA
■ Origin: Mesoderm
■ Hematogenous spread
■ 50% arise from extremities; 50% in children
■ Most important prognostic factor: Histological grade
■ Usually Chemoresistant, Radiosensitive

■ Most common type: Malignant fibrous histjosarcoma then Liposarcoma

o Rhabdomyosarcoma in head and neck sarcomas (most common sarcoma in pediatric)
o Leiomyosarcomas and liposarcoma in visceral and retroperitoneal sarcomas
• Liposarcoma is the most common retroperitoneal sarcoma

■ Most common site for metastasis: Lung

■ Risk factors:
o Asbestos: Mesothelioma
o PVC and arsenic: Angiosarcoma
o Chronic lymphedema: Lymphangiosarcoma
o Kaposi's sarcoma (KS): Vascular sarcoma
• Oral and pharyngeal mucosa are the most common sites

■ Symptoms:
o Asymptomatic mass (most common presentation)
o GI bleeding, or bowel obstruction in intra-abdominal sarcoma

■ Investigation:
o Chest x-ray (lung metastasis)

o CT scan for lesions other that extremities

o MRI for lesions in the extremities

o Biopsy "Should be done after the MRI" -+ Spindle cells

• FNA
• Used only to confirm or rule out presence of metastatic or local recurrence

• Core-biopsy
• Preferred technique to diagnose soft tissue sarcoma> 4 - 5 cm

• lncisional (longitudinal) biopsy

• Gold standard historically for> 4 cm lesions if core biopsy non-diagnostic

• Excisional biopsy
• For superficial lesion < 4 - 5 cm that not involving hands or feet
■ Management:
o Wide local excision with 1 - 2 cm margin and at least 1 uninvolved fascial plane

o Radiotherapy
• For large tumors> 5 cm(> T1)

• For intermediate or high grade tumors

• Close margin < 1 cm or positive margin not feasible for re-excision

o Neoadjuvant Chemotherapy (Doxorubicin-based)

• For locally advanced high-grade tumors
(Rhabdomyosarcoma or Ewing's sarcoma any size)
• > 5 cm Pleomorphic liposarcoma, Round cell liposarcoma, or Synovial sarcoma

• > 10 cm other high-grade tumors

• Metastasis

o Lymphadenectomy
• Most common tumor requires lymphadenectomy: Angiosarcoma
• Lymph node metastasis should be confirmed by FNA
• Treated by radical lymphadenectomy

■ Best predictor for recurrence:

o Surgical margin followed by Histolo,gical Grading
OTHER CONDITIONS
■ Xanthoma: yellow, contains histiocytes

■ Keratoses
o Actinic keratosis: premalignant in sun-damaged areas
o Seborrheic keratosis: not premalignant; trunk on elderly
o Arsenical keratosis: associated with squamous cell carcinoma

■ Merkel cell carcinoma: are neuroendocrine

o Very aggressive malignant tumor

■ Glomus cell tumor

o Painful tumor composed of blood vessels and nerves
o Benign; most common in the terminal aspect of the digit

■ Desmoid tumors: occur in fascial planes

o Anterior abdominal wall (most common location)
o Intra-abdominal desmoids associated with Gardner's syndrome

■ Bowen's disease: SCCA in situ; 10% turn into invasive SCCA; associated with HPV
o Treatment: imiquimod, cautery ablation, topical 5-FU, avoid wide local excision

■ Keratoacanthoma
o Rapid growth, rolled edges, filled with keratin
o Not malignant but can be confused with SCCA

■ Hyperhidrosis: f sweating, especially noticeable in the palms

o Treatment: thoracic sympathectomy if refractory

■ Benign cysts
o Trichilemmal cyst: in scalp, no epidermis
o Ganglion cyst: over tendons, filled with collagen
o Pilonidal cyst: congenital coccygeal s inus with ingrown hair
• Options for management:
• Unroofing sinus tract and secondary intention healing (most conservative)
• Incision and drainage for pilonidal abscess
• Wide excision and primary repair
• Wide exci sion and secondary intention healing
(associated with least infection)
Head and Neck
Reviewed by:

Dr. Mohammed Bubshait

HEAD AND NECK
ANATOMY AND PHYSIOLOGY
■ Narrowest area in adult: Glottis
■ Narrowest area in children: Subglottic
■ Tracheostomy: usually consider in patients who will require intubation longer than 14 days

Arteries
■ External carotid artery
o 1 '' branch is superior thyroid artery

■ Internal carotid artery

o 1'' branch is ophthalmic artery
"No branches at the neck"

■ carotid sheath contains·

o Common carotid artery
o Internal jugular vein
o Vagus nerve

■ Carotid Sinus: Pressure sensor

■ Carotid bOdy: Chemoreceptor in Adventitia, 02 sensor

o Glossopharyngeal & Vagus
o Most common site of paraganglionoma: carotid body

Veins
■ Internal jugular vein
o Runs within the carotid sheath
o Formed by union of the inferior petrosal sinus and the sigmoid sinus
o United with subclavian vein to form brachiocephalic veins

■ External jugular vein

o Runs superficially to slemocleidomastoid muscle
o Formed by union of posterior division of retromandibular vein with posterior auricular
vein
o Drains to subclavian vein

Nerves
■ Vagus nerve: posteriorly between internal jugular (IJ) vein and carotid artery

■ Trigeminal nerve: sensation lo most of face & anterior½ of tongue

■ Glossopharyngeal nerve: Sensory to posterior 1/, tongue, and Gag reflex

■ Hypoglossal nerve: Motor to all of tongue except pa/atoq/ossus

o Tongue deviates lo the same side of a hypoglossal nerve injury
Triangles of the neck

Superior Inferior Lateral/ Posterior Medial/ Anterior

Anterior Inferior border Clavicle Anterior border of Vertical midline
(Submentle, Carotid, of mandible Sternocleidomastoid (Mental symphysis to
Muscular, suprastemal notch)
Submandibularl
Posterior Clavicle Trapezius muscle Posterior border of
(OccipUal, Subclavian) Sternocleidomastoid

SCALENUS MUSCLE
■ Attached to 1'1 rib

■ Subclavian Vein
Anterior
■ Phrenic nerve
o Anterior Scalenus Muscle
■ Subclavian Artery
■ Brachia! plexus
o Middle Scalenus Muscle
■ Thoracodorsal nerve
o Posterior Scalenus Muscle
Posterior

SALIVARY GLANDS
■ Stensen's duct: {duct of parotid gland}
o Opened into vestibule opposite upper 2 nd molar
o Mostly serous fluid

■ Wharton duct: (duct of submandibular gland}

o Opened into sublingual caruncle at the base of the tongue
o 50/50 serous/mucin

■ Bartholin duct (By duct of Rivinus): {duct of sublingual gland)

o Mostly mucin

SIALADENITIS (inflammation of salivary glands)

■ Usually presented as postoperative, due to dehydration, mostly after GIT procedure
■ Associated with high mortality rate
■ Submandibular is more common than parntid sialadenitis due to calculi
■ Most common organism: Staphylococcus aureus
o Bacterial is unilateral and is associated with tense and tender gland

■ Presentat;oo·
o Sudden onset of salivary gland pain and swelling
o Dehydration and xerostomia

■ Purulent material expressed from Wharton or Stensen duct during bimanual palpation
■ Management:
o Aggressive hydration, massage, warm compresses
o Antibiotics {Clindamycin}
o Sialogogues such as sour candy and lemons
o If persist > 48 - 72 hours -+ Incision and drainage for intraparotid abscess
OROPHARYNGEALCANCER
■ Erythroplakia is premalignant lesion with hi,gher rate of malignant transformation than
leukoplakia
■ Most common site for oral cavity cancer: Lower lip

■ Squamous cell carcinoma:

o Most common source: Tonsil
o Most common distant metastases for head and neck tumors: Lung
o Associated with:
• EBV + posterior cervical neck nodes in nasopharyngeal cancer
• Staphylococcus aureus following wound infection

o Management:
• FNA is the 1st step to confirm the diagnosis
• If not diagnostic + Exciisional biopsy
• CT scan I MRI Chest (to rule out distant metastasis}
• EUA + Pan endoscopy with multiple biopsy

If diagnosis confirmed with malignant and primary lesion can't be identified:

+ MRND followed by radiation therapy

SALIVARY GLAND TUMORS

Type Characteristics
Pleomorphlc adenoma Most common benign tumor in adult
(May undergoes malignant degeneration)

Most common cause of facial nerve oaralvsis

Warthin's tumor
(Papillary cystadenoma)
Mucoepldermold cancer
Adenoid cystic CA
2nd most common benign tumor
Most common tumor to be bilateral
Mainly in men / smoker
Most common malignant tumor
Most commonlv invadina suoerficial and deeo nnrtions
2nd most common malignant tumor
Associated with Perineural invasion a/ona facial nerve "Painful"

■ Management:
o Benign: Superficial parotidectomy
o Malignant: Total parotidectomy with facial nerve sparing (resects & graft if involved)
ASSOCIATED NERVE INJURIES
Nerve
Greater auricular nerve
Transient facial nerve iniurv
Frey's syndrome
Most common injured nerve with parotid surgery
c(> Numbness over
lower portion of ear
Most common early complication associated with nerve iniurv
Most common late-complication after parotidectomy

Auriculotemporal nerve cross-innervates with sympathetic

Marginal mandibular nerve
and lingual nerve
fibers to sweat glands of skin
c(> Gustatorv sweatina
Most common nerve injury following submandibular surgery
c(> Dropping of the lip
at angle of the
mouth

■ Other tumors·
o Papilloma
• Most common benign neoplasm of Nose, Para-nasal sinuses, and Larynx

o Lymphoma
• Most common tumor of the nasopharynx in children

o Hemangioma
• Most common benign head and neck tumor in adult
• Most common salivary gland tumor in children
PITUITARY GLAND
■ Most common pituitary adenoma: Prolactinoma
■ Most common extra-pituitary ACTH: SCLC (Bronchial tumors)

■ Dopamine: inhibits prolactin secretion

■ Anterior pituitary (80% of gland, adenohypophysis): No direct blood supply

■ Posterior pituitary (neurohypophysis): Does not contain cell bodies, No Blood-Brain-Barrier

o ADH: Supra-Optic nuclei
o Oxytocin: Para-Ventricular nuclei

■ All pituitary tumors respond to bromocriptine (dopamine agonist) except: ACTH

■ Treatment of most pituitary tumors:
o < 1 cm: Bromocriptine
o > 1 cm or mass effect: Transsphenoidal resection

■ Bitemporal hemianopsia is classic visual change with pituitary mass effect

■ Sheehan's syndrome
o Post-partum trouble lactating (1'' sign)
� amenorrhea, adrenal insufficiency, and hypothyroidism

■ Craniopharyngioma: benign calcified cyst, remnants of Rathke's pouch

� Treatment: resection
OTHERS
■ Most common organism of otitis externa: Pseudomonas aeruginosa

■ Acoustic neuroma -+ CN VIII, tinnitus, hearing loss

■ Ludwig'si angina: acute infection of mouth floor (mylohyoid muscle}
-+ Debr dement
■ Cleft palate: repair at 12 months (1 year}

■ Cleft lip: repair at 3 months (10 weeks)

■ Tracheoinnominate fistula:
o Avoided by making tracheostomy not lower than 3rd ring
o Occurs 2 - 3 weeks post tracheostomy
o Digital compression should be done against manubrium to stop bleeding
o Persist bleeding:
• Re-intubate the patient with an endotracheal tube
• Bronchoscopy should be done in OR
• Inflate tracheostomy balloon
• Remove the tracheostomy in case of persist bleeding
• Perform anterior compression on the innominate artery
Adrenal gland
Adrenal Gland
ANATOMY AND PHYSIOLOGY
R inf phlenlt a

R.pnteniev. L�v.

R �renalv,
L Sl.4). adrenal a.
L-glal,O

L miadle ac:1rena1 a
R. middle adrenal a.
L a.drenalv.
Accessory
r. adrenalv. Lint adrenal a

L. ren�� &v
Lrenal a. & V

L kidney
R. kidney

Sup. mesenterk .i

■ Vascular supply
o Superior adrenal artery + Inferior phrenic artery
o Middle adrenal artery + Aorta
o Inferior adrenal artery + Renal artery

o Left adrenal vein -+ Left renal vein

o Right adrenal vein (shorter} -+ IVC
(Right adrenal associated with life-threatening bleeding)

■ Arrangement of renal vessels (Anterior -+ Posterior): VA P (pelvis}

o Right renal vein is posterior to Inferior Vena Cava
o Left renal artery is anterior and directly connected to the abdominal aorta

■ Juxtaglomerular cells found in: Afferent

■ Most common metastases to adrenal gland: Lung CA
o Others of common metastases to adrenal gland: Breast. and melanoma

■ Adrenal Cortex:
o No innervation to the cortex, from mesoderm
• Glomerulosa ➔ aldosterone
• Fasciculata ➔ glucocorticoids
• Reticularis ➔ androgens/estrogens

■ Adrenal Medulla:
o Developed from neural crest and migrate through para-aorta
o Innervated by sympathetic splanchnic nerves, from ectoderm

■ ACTH, and Cortisol has a diurnal peak at late night "early morning" (4- 6 a.m)
 FUNCTIONAL ADRENAL TUMORS • ADRENAL CORTEX
Conn's syndrome Addison's disease Cushing's disease
Hvneraldosteronism Hvoocortisolism Hvnercortisolism
Causes Adrenal adenoma 70% Withdrawal of steroids Pituitary adenoma (Cushing's disease)
Adrenal hyperplasia 30% Autoimmune disease Exogenous steroids "Most common•
EctopicACTH
Adrenal adenoma 15%
Adrenal hunemlasia
Presentation Diastolic refractory HTN Hypotension Truncal Obesity
Hyperglycemia Hypoglycemia Hyperpigmentation (if l ACTH)
Hyperpigmentation Proximal muscle wasting and weakness
"Most common cause of Fatigue and weight loss Fat pad "buffalo hump", Moon face
Secondary HTN" Hypertension, hyperglycemia
Dyslipidemia, psychosis, kidney stones
Insomnia, Hirsutism, lnfertilitv, DVT / PE
Electrolytes t Na, ! K < 40%, t Urine K ! Na, t K, 1Ca t Na,! K, ! Ca
Metabolic alkalosis Metabolic acidosis Metabolic alkalosis
Investigation PlasmaAldosterone > 15 mcg Cortisol morning level Most s12ecific test: (Best for screening)
Plasma Renin < 0.5 Low-dose dexamethasone suppression
Screening: f ACTH test
t Aldosterone I renin > 25
False positive: Renal failure Most sensitive test: Most s ens itive test·
ACTH stimulating test 24 hour urine cortisol level
Confirmation b)t "Corticotropin test" Associated with high false-positive result
Na-loading suppression test in pregnant, liver disease or alcoholic
➔ 24h urine K,Na,aldosterone
l:J.e.'li. �s.t {QC ,,isb.iag:s,.
Avoid BB ACEi diuretics Late-Niaht Salivarv cortisol test
Secondary t Renin ! or NormalACTH !ACTH: Adrenal
disease Renal artery stenosis Panhypopituitarism t ACTH: Extra-adrenal
CHF. Cirrhosis, Nephrotic Steroid use/withdrawal EctopicACTH: SCLC Bronchial tumors
Localization NP-59 scintigraphy "1311-6B-iodomethyl Noriodocholesterol"
Selective adrenal vein sampling for aldosterone and cortisol
■ AdministrationACTH
■ ObtainingAldosterone and Cortisol from both adrenal veins and vena cava
■ le 4:1 increase inAldosterone / Cortisol ration + Unilateral tumor
Used For:
■ Abnormal bilateral adrenal glands (To differentiate between adenoma and hyperplasia)
■ Abnormal unilateral < 1 cm nodule
■ Aae >40
Management Eac bilal�cal b��ccla�ia Replacement of: eilUWilY
Not-fit for surge!Y . Fluids. Glucose Trans-sphenoidal excision
Fi!ilure for loQl!lization: . Glucocorticoid Persistent or recurrent + Irradiation
1) Selective vein sample . Mineralocorticoid Failed? Medical adrenalectomy
2) Medical management (Ketoconazole)
(Spironolactone) Adrenal insufficiency:
"Refractory hypotension" EctooicATCH: Treat primary tumor
Vailatera1· Treated by:
For confirmed adenoma: 1) Fluids Adceaal;
Adrenalectomy 2) Glucocorticoids Unilateral or Bilateral Adrenalectomy
(Correct HTN i n 30% only) - Followed by steroid supplement
- Measure cortisol level
- Taoerino the steroid sunnlement
 Algorithm for Cushing's
Screening tests:
Low-dose dexamethasone suppression test (1 mg at 11pm and cortisol level at 8am)
24 hour urine cortisol level x 2 times

Normal 1 - 2 folds > 3 folds

I Late-Night Salivary cortisol test x 2 times II ACTH level

High Very High Low

15 - 500pg/mL > 1000pg/ml < 5pg/mL

Adrenal hyperplasia CT Adrenal

I I
CRH-secreting tumors Adrenal Cushing's

High-dose dexamethasone test

8 mg overnight or 2 mg q 6 h x 2 days I MRI Head
I
Not suppressed Partial suppression > 50%
Equivocal-+ ACTH gradient -+ No Equivocal-+ ACTH gradient-+ Yes

!
Pituitary Cushing's

�
Negi3tive CT Neck, Abdo.men and Pelvis

■ Indications for bilateral adrenalectomy

o Bilateral Cushing's disease
o Bilateral adrenal hyperplasia if failed medically (20 - 30% only benefits from surgery)
o Palliative treatment for unresectable or not localized ectopic ACTH-producing tumors
o Palliative treatment for pituitary adenoma

■ 30% after bilateral adrenalectomy develops Nelson's syndrome

(overgrowth pre-existing pituitary tumor)
-+ t ACTH (pigmentation), Visual field defects, headaches, and extra-ocular muscle palsies
Congenital adrenal hyperplasia (enzyme defect in cortisol synthesis)
1) 21-Hydroxylase deficiency: (Most common 90%)
o Precocious puberty in males, virilization (ambiguous genitalia) in females
r
o t 17-0H progesterone testosterone, Salt wasting (!Na tK) and hypotension
• Testosterone produced by leydig cell

2) 11-Hydroxylase deficiency:
o t 11-Deoxycortisone, Salt saving -+ hypertension
o Etomidate (11-hydroxylase inhibitor of steroid synthesis} used in hypercortisolism crisis

Patient need to be ruled out from associated MTC and pheochromocytoma

ADRENAL MEDULLA
■ Catecholamine precursor: Tyrosine
■ PNMT "phenylethanolamine N-methyltransferase•
o Converts Norepinephrine -+ Epinephrine
o Found only in the adrenal medulla

■ MAO "monoamine oxidase": Breaks catecholamines -+ metanephrines & VMA

■ Most common location of extra-adrenal rests of neural crest:
o Retroperitoneum at organ of Zuckerkandl (at the aortic bifurcation)

Pheochromocytoma
■ Neuroendocrine tumor of adrenal medulla -+ Catecholamine secreting tumors
■ Originates from chromaffin cells "as carcinoid tumors"
■ Most common found at right-side
■ 30 - 40% of pheochromocytoma detected as incidentaloma
■ Clinical presentation:
o Hypertension is the most common presentation
• Associated with headache, palpitations, sweating, or anxiety
• Orthostatic hypotension happens from volume contraction

Due to desensitized norepinephrine receptors (due tot norepinephrine leveO

o 10% Tumor:
• 10% Malignant, 10% Bilateral, 10% in Children, 10% Familial
• 10% Extra-adrenal (30 - 40% malignant)

Malignant pheochromocytoma is extra-adrenal neuroectodermal tissue or

associated with invasion to surrounding structures

■ Investigations:
o Pheochromocytoma occurred as familial in 10% (50% of them associated with MEN)
• U/S Neck, TSH, PTH, Calcitonin and Calcium levels

o Most Sensitive initial test: Plasma Metanephrines

• Plasma metanephrines used to exclude pheochromocytoma

o Most Specific test (screening test): 24-hours Urine Metanephrines

• Urine VMA is not used due to low sensitivity and specificity
• False t VMA: coffee, tea, fruits, vanilla, iodine contrast, labetalol, a & � blockers
• Fractionated urinary catecholamines are very sensitive but low specificity
� Due to extra-adrenal lack of PN MT
o Adrenal pheochromocytomas secretes "Epinephrine"
o Extra-adrenal pheochromocytomas secretes ''Norepinephrine"

o Chromogranin A:
• Highly specific and used in conjunction with catecholamine
• Used also to diagnose recurrence
 o Clonldine suppression test
• Oral 0.3 mg clonidine -+ Decrease catecholamine< 500 pg/ml after 2 - 3 h
• Suppresses catecholamine excess but not secretion
• Used if plasma or urine tests a re equivocal

o Metaiodobenzylguanidine (MIBG) scan:

• Used for localization of recurrent, metastatic, or multifocal disease

o Adrenal vein sampling or venography: Contraindicated (Can cause HTN crisis)

■ Imaging:
o CT scan Neck, Chest, Abdomen an d Pelvis :t IV contrast
• Should be done to exclude extra-adrenal paragangliomas
• Especially if< 40 years, SDHx mutations or positive family history

o MRI
• Test of choice for pregnant, pediatric age group, or patient allergic to contrast

o PET scan
• Associated with false positive when assess retroperitoneal area due to presence
of brown fat

■ Imaging features:
o Large heterogeneous with cystic and hemorrhagic changes
o Increased attenuation on non-enhanced CT> 20 HU
o Increased vascularity
o Contrast washout < 50%
o Hyperintense on T2
■ Pre-operative management:
o Exclude MEN

o Adequate hydration 3 - 4 days pre-operative to avoid postoperative hypotension

o a-blocker "Phenoxybenzamine: Non-selective irreversible long-acting a-blocker"

• Initial dose: 10 mg BID initially" for 1 - 3 weeks pre-operative
• Used to allow for expansion of blood volume
• Last doses of a or � blockers: in the morning of surgery
• Selective alpha 1 blockers "Prazosin, terazosin, and doxazosin"
used in long-term therapy (metastatic pheochromocytoma)

o �-blocker "Propranolol 10 mg QID initially" at 3 - 4 days pre-operative

• Used after alpha blockers for persistent tachycardia, and arrhythmia
Due to unopposed beta receptor stimulation
• �-blocker should never be started before a-blocker
Leads to worsening of vasoconstriction � HTN crisis, Ml, Pulmonary edema
Due to unopposed alpha receptor stimulation

o Blood pressure monitoring (twice daily) with target blood pressure is < 120/80 mmHg

o Encourage salt intake

o No diuretics, No steroids (can cause HTN crisis)

■ Treatment:
o Adrenalectomy for all incidentally pheochromocytoma
• Retro-peritoneal (Posterior approach):
Q Best approach as lowest morbidity and mortality
• Trans-peritoneal
Q Anterior approach: for bilateral adrenalectomy
Q Lateral approach: for obese or large(> 6 cm) unilateral adrenalectomy
• Thoracoabdominal approach: for en-bloc resection as malignant tumors
• Bilateral cortical-sparing subtotal adrenalectomy may be used for bilateral
disease

o Open Adrenalectomy for:

• Suspicion for malignancy with possible local invasion
• > 6 cm size in suspicious of malignancy(No upper size limit in benign)
• Invasive adrenal cortical carcinoma
• Evidence of clinical feminization
• Hypersecretion of multiple sex hormones
• Contraindication to laparoscopy

■ Intra-operative:
o CCB(Nicardipine) or Nitroprusside infusion used to control HTN crisis
o lsoflurane or enflurane used as inhalation agents
o Avoid fentanyl, morphine and ketamine

■ Post-operative management·
o IV isotonic solution as bolus for hypotension (Don'/ use a-blocker)
o Correct hypoglycemia(as a result of rebound hyperinsulinemia)
o Test plasma free metanephrines after 2 weeks, 6 weeks and at 6 months to confirm
o patient's biochemical response
o ICU monitor
NEUROBLASTOMA
■ Most common solid abdominal malignancy in children
■ Most common in 1 '' 2 years of life
■ Derived from neural crest cells
o Located on adrenal
o Can occur any sites along sympathetic chain

■ Presented with:
o Left flank mass
o Secretory diarrhea
o Hypertension
o Weight loss and failure to thrive
o Raccoon eyes (orbital metastases)
o Opsomyoclonus syndrome (unsteady gait)
i
■ Investigat ons:
o t Catecholamines, VMA and metanephrines
o AXR: Stippled fine calcifications in the tumor

■ worse prognosis it associated with:

o Neuron-specific enolase (NSE)
o LOH
o N-myc amplification

■ Treatment: resection {adrenal gland and kidney taken; 40% cured)

o Initially unresectable tumors may be resectable after doxorubicin-based chemo
 ADRENAL INCIDENTALOMA
■ 1 - 5% for patient undergoing abdominal CT for other reasons (excluding malignancy)

■ Causes:

Non-functional Functional Malignancy (Primary or metastasis)

''Most common•
Cortical adenoma 'Most common•
Myelolipoma (Mature adipose tissue)
"Can be observed r=ardless the size''
Ganglloneuromas
"Sumica/ excision for svmotomatic"
Cvst or Hemorrhaae
•Functional or Non-functional"
Subcllnical Cushing's Biopsy not indicated unless for non-
(Cortisol-producing tumor) candidate for surgery
"Most common•
Pheochromocytoma PET useful for extra-adrenal
malignancy
Conn's (Aldosteronoma)

■ Benign features: (Imaging features of benign adenoma}

o Non-Functional, round and smooth contour, and homogenous characters

o < 4 cm in diameter
• Malignancy potential "based on size":
o < 3 cm (or< 4 cm): < 5%
o 3-Scm (or4-6cm): 5-10%
o > 5 cm (or> 6 cm): 25%

o Attenuation of< 10 HU in non-contrast CT

o Contrast was-out > 50% after 10 min

■ Investigations:
1) CT CAP with IV contrast + Adrenal mass (Size, Character, and Contralateral)

2) Biochemical test:
• Plasma metanephrines /24-hour urine VMA, metanephrines & catecholamines
• Low-dose DST/ 24-hour urinary free cortisol or Late-night salivary cortisol
• Plasma aldosterone / Potassium level / Renin
 ■ Management of adrenal incidentaloma:

Unilateral
I
I Bilateral

I
Functional Non-functional
(regardless the size)

i
Pre-operative optimization
Follow algorithm of disease
I I
Benign <4cm 2: 4 cm or > 1 cm / year
Asymptomatic Suspicious (regardless the size)
Symptomatic (regardless the size)

I
! I
Adrenalectomy
Serial Follow-up

Serial imaging every 3 - 6 months for 2 years

Biochemical testing every 12 months for 5 years

"Adrenal tumor tends to grow in 20% and 10%

to be functional over a period of 10 years•
Open Laparoscopic
(Standard of

- Suspicion for invasive cancer Congenital

- > 6 cm size (relative) Adrenal
- Evidence of clinical feminization Hyperplasia
- Hypersecretion of multiple sex hormones
- Contraindication to laparoscopy

Spironolactone alone
Selective venous catheterization
Surgery
(20 - 30% only benefits from surgery)

Expectant management rather than adrenalectomy is an option for patient with high-risk, elderly with
multiple comorbidities, who not candidate for surgical intervention
Thyroid
Thyroid
ANATOMY
■ From 1"' and 2nd pharyngeal Arches (3"1, and 4th Pouches in parathyroid gland)
■ Thyroid measures 15 - 25 g, each lobe 4 - 6 cm length, and 1 - 2 cm in thickness
■ Originate from foramen cecum, migrate caudally and rest over 2nd - 3rd tracheal ring
■ Ligament of Berry: posterior medial suspensory ligament close to entry of RLN
Muscles
■ Platysma
o Origin: Deep fascia of pectoralis major and deltoid
o Insertion: Body of mandible and angle of mouth
o Nerve supply: Cervical branch of facial nerve
o Action: Depresses mandible and angle of mouth (Neck expression)
• Important to suture in closure or bad scar can happen

■ Strap muscles {lnfrahyoid muscles)

o Including: Omohyoid, Thyrohyoid, Sternohyoid, Sternothyroid
• Sternohyoid is most superficial
o Nerve supply: Ansa cervicalis (C1, C2, C3)
o Action: Depresses hyoid bone

■ Cricothyroid muscle
o Nerve supply: External branch of Superior laryngeal nerve
o Action: Tension and elongation of the vocal folds � high pitch phonation

Blood Supply
■ Arterial:
1) Superior thyroid artery + 1•1 branch off external carotid artery
2} Inferior thyroid artery + "Thyrocervical trunk" from 1 ' 1 part of subclavian artery
• Branches of thyrocervical trunk:
• Inferior thyroid artery
• Suprascapular artery
• Ascending cervical artery
• Transverse cervical artery

3} Thyroid ima artery "unpaired and inconstant"

• From aortic arch, brachiocephalic artery, or right common carotid artery
• Anterior to the trachea (careful during tracheostomy)

■ Venous:
1} Superior thyroid vein
� lnterna I jugular vein

2} Middle thyroid vein "Anterior to the carotid artery"

� lnterna I jugular vein

3} Inferior thyroid vein "Posterior to the carotid artery, largest, most variable"
� lnnominate vein (brachiocephalic vein) � SVC
NERVE SUPPLY
Superior laryngeal nerve
■ Originate from vagus nerve at the neck during descending pathway
■ External "Motor''
o Supply cricothyroid muscle, Supraglottis
o Tense the cord

■ Internal "Sensory"
o Above vocal cords, cough reflex
o Can lead to aspiration

■ Risk of injury: 15%

o Injury results in loss of high-pitch sound and easy voice fatigability (opera singer)
o Tested by repeat a word for 10 times (tone will decrease)

■ Cross superior thyroid artery 1 cm from superior pole of thyroid

■ cernea and coHeagues

o Type 1: Nerve crosses the artery �1 cm above the superior aspect of the thyroid lobe
o Type 2:
• A: Nerve crosses the artery < 1 cm above the superior aspect of the thyroid lobe
• B: Nerve crosses the artery below the superior aspect of the thyroid lobe

■ Type 2A (20%) has the greatest risk of injury

Recurrent laryngeal nerves !RLNsl
■ Originate from vagus nerve at the mediastinum during ascending pathway
■ Medial -+ motor to all of larynx except cricothyroid muscle
■ Run in the tracheoesophageal groove (posterior to cricothyroid)
■ Related to inferior thyroid artery:
o Anterior to ITA
o Posterior to /TA (Commonest)
o Between the branches

■ Right RLN:
o More short, lateral, and non-oblique
o Loops around right subclavian artery
o Descending Anteriorly -+ and ascending Posteriorly

o Non-recurrent (2%} which is associated with vascular anomaly and high risk of injury
• Vascular anomaly: absence of innominate artery (Right subclavian and Right
common carotid arise directly from aortic arch) -+ Retro-esophageal subclavian

■ Left RLN:
o Loops around aortic arch
o Descending Anteriorly -+ and ascending Posteriorly

o Non-recurrent (< 1 %) which is associated with vascular anomaly

• Vascular anomaly: Right-sided aortic arch, or abnormal location of left subclavian

■ Risk of injury of the RLN: 1 - 2% (80% transient)

o Most common site of injury:
• At insertion into cricothyroid membrane
• At entrance of Larynx
• Near Ligament of Berry

o Highest risk of injury of RLN:

• During ligation of ITA
• Right RLN during ascending
Right RLN more common to be injured than left RLN

o Most common type of injury: Stretch injury

o Repair primary or by grafting from: Ansa Cervicalis

o If you cut RLN during planned total thyroidectomy:

• Repair the nerve and do lobectomy only (even if the other lobe have a nodule)
• Refer the patient to another surgeon to do the other diseased lobe
COURSE OF VAGUS NERVE (101H CRANIAL NERVE)
■ Cranial:
o Exit the brain from medulla oblongata
o Travel through basal cistern
o Exit the cranial through jugular foramen
o Branches:
• Auricular branch
• Meningeal branch

■ Cervical:
o Descends posteriorly vertically within carotid sheath posteriolateral to common carotid
artery, medial to internal jugular vein (Between them)

o Right vagus:
• Cross anterior to the right subclavian artery behind innominate vessels
• Travel medially toward esophagus

o Left vagus
• Cross anterior to the left subclavian behind innominate vessels
• Travel medially toward esophagus

o Branches:
• Pharyngeal branches
• Superior laryngeal nerve
• Right recurrent laryngeal nerve

■ Jhoracjc-
o Right vagus: Posterior vagal trunk
• Celiac plexus
• Posterior gastric plexus

o Left vagus: Anterior vagal trunk

• Left recurrent laryngeal nerve
• Anterior gastric plexus
• Hepatic plexus
• Cardiac branches

o Esophageal plexus by meeting of righUleft vagus at esophageal hiatus

■ Abdomen:
o Enter the abdomen through esophageal hiatus
o Terminates by supplying esophagus, ·stomach, small and large bowel
 HISTORY AND EXAMINATION
History of thyroid nodule:
■ Mass: Site, size, shape, skin, symmetry, time, changes in size or character
■ Function:

Hvnerthvroidism Hvnothvroidism
Nervous system Anxiety Fatigue
Insomnia Depression
Tremors Peripheral neuropathy
Myxedema coma
Memorv loss
Cardiovascular Tachycardia and Palpitations Bradycardia
Increased systolic pressure Decreased systolic pressure
Atrial fibrillation Flat or inverted T wave
Dyspnea
Perioheral swellino
Metabolic Weight loss Weight gain
Diarrhea Constipation
Increase appetite Cold intolerance
Heat intolerance
SweatinQ
Skin and musculoskeletal Warm moist soft skin Dry, rough skin
Hyperpigmentation Coarse, brittle hair
Proximal myopathy Thin, brittle nails
Alopecia
Muscle cramps
Non-oittino Mvxedema
Menstrual cycle Menorrhagia Irregular cycle
Lioht or absent menstrual oeriod loss of libido
Extra-thyroidal manifestation Exophthalmos ID Ce�1,u2iog ,bilgrJ:a ·
Thyroid acropathy (Periosteal hypertrophy) • Cretinism
Pretibial myxedema • Umbilical hernia
''Due to glycosaminoglycans deposition• • Rectal orolaose

■ Compressive symptoms:
o Dysphagia, dyspnea and dysphonia

■ Invasion symptoms:
o Hoarseness
o Homer's syndrome (Ptosis, Miosis, Anhidrosis, Enophthalmosis)

■ Family history (MEN, or cancers)

■ Allergy and drug history:
o ! Thyroid (Lithium "associated with t Parathyroid", Amiodarone, Anti-thyroid, IL-2)

o t Thyroid
• Amiodarone "iodine-base" by f destruction of follicles � release of T4

• Thyroxine: Used for weight loss, or induce energy for bodybuilding

o Factitious thyrotoxicosis: ! TSH, ! Thyroglobulin
Examination
■ General appearance (Hyperthyroidism, Hypothyroidism)
■ Vital signs and systemic examination

■ Local examination:
o Inspection (Ask patient to swallow, and to protrude the tongue)
o Palpation
• Thyroid
• From behind the patient first (ask patient to swallow)
• From front of the patient (ask patient to swallow)
• Thyroglossal cyst
� Comment on location (Sub-hyoid is the most common site}
� Transillumination test
• Retrosternal extension
� Pemberton's test: Elevate arm to check thoracic outlet obstruction
• Trachea (40% of thyroid goiter associated with trachea shifting)
• By index at suprastema I notch

• Lymph nodes

o Percussion (Percuss the manubrium sterni for dullness in retrosternal extension}

o Auscultation (For Bruit)

Ophthalmological examination; (For patient with grave's disease}

■ lid lag
o Due to sympathetic overactivity
o Von Graefe's sign
• Hold patient head by left hand
• Ask patient to follow your right index
• Move the index from forehead downward, and follow the eyelids
• Positive test: White sclera will appear and the eyelid will not move

■ lid retraction
o Due to sympathetic overactivity "Levator palpebrae muscle"
o Dalrymple's sign: upper sclera is visible above iris during inspection

■ Exophthalmos
o Due to retro-orbital fibrosis by fat accumulation and edema
o Look to the patient from front, side, and above
o sclera is visible around iris (mild degree will showed sclera visible from below iris}

■ Chemosis
o Swelling of the conjunctiva
o Due to obstruction of venous and lymphatic drainage of conjunctiva by increased retro­
orbital pressure

■ Ophthalmoplegia
o Due to muscle weakness (especially internal oblique muscle)
o Double vision / blurred, inability to look upward and outward
PHYSIOLOGY OF THYROID HORMONES
■ The only amino acid hormones: Insulin and Thyroid hormones

■ TSH: most important initial investigation (most sensitive indicator of gland function)

■ T4:T3 ratio is 15:1 {T3 is the active form)= tyrosine+ iodine

■ Production is inhibited by glucocorticoids

■ Synthesis:
1) Transportation of iodide

2) Oxidation of iodide to iodine and iodination of tyrosine on Thyroglobulin to from MIT/ DIT

3) Coupling of 2 DIT "Di-iodotyrosine• to form T4 "Thyroxine= Tetraiodothyronine•

4) Coupling of 1 MIT "Mono-iodotyrosine" and 1 DIT to form T3 "Triiodothyronine"

■ T3 produced in periphery (liver, renal, and muscles) from T4 converted by Oe-iodinases

o Free T3, T4: Active, and most accurate

o Bounded T3, T4: (Albumin 20%, Thyroxine-binding globulin "TBG" 70%): Inactive form
T3 bindings to thyroid receptors found inside the Nucleus

In contrast to Total T4, Total T3 can be measured (fess bounded form)

■ Jhyroglobulio-
o Glycoprotein (Storage form of T3 and T4 in colloid)

o Synthesized by thyroid follicular cells in the rough ER & ionized by peroxidase

o Not ordered routinely unless indicated

o Tumor maker of papillary/follicular cancers, metastasis, and recurrence

• Not good for medullary/ anaplastic cancers due to poorly differentiated cells

o Most sensitive tumor marker after total thyroidectomy for follicular-derived tumors
• Thyroglobulin should ordered along with "Anti-Thyroglobulin" preoperatively

o Follow up after suppressive treatment (1 131 or medications)

• Every 3 months during 1 •1 year
• Every 6 months during 2nd year
• Then, Yearly
Positive value: > 100 ng/ml
 ■ Thyroid hormones changes:
o In Sepsis or shock: (Euthyroid sick)
• Normal or ! TSH
•
tT3 ! T4
• t rT3
o In Pregnancy:
• tTBG -+tT3fT4
• t B-hCG -+ l TSH
• t Nodule size

■ Antithyroid medications used to lower:

o T3 -+ in 3 weeks before using 1 131
o T4-+in 6 weeks before using 1 131

■ Half-life time of thyroid hormones:

o T ½ ofTSH-+ 1 hour
o T ½ ofT3-+ 1 - 3 days
o T ½ of T4-+ 7 days

The thyroid gland has storage reserve of 3 weeks of T4, That's why thyroxine may not needed at few
days post total thyroidectomy

TSH INTERPRETATION
■ High TSH
o HighT4
• Pituitary tumor, Thyroxine-replacement therapy

o NormalT4
• Subclinical hypothyroidism

o LowT4
• Primary hypothyroidism (Treat then continue investigation}
-+Neck thyroid U/S ± FNA

■ LowTSH
o HighT4
• Hyperthyroidism (Toxic goiter, factitious, thyroiditis}
-+Thyroid scan

o LowT4
• Central hypothyroidism (LowTRH)

Remember:
Hypothyroidism can increase risk of perioperative complications (Infection, bowel recovery),
and non-emergency surgery should be postponed until achieving euthyroid status
ABNORMALITIES OF THYROID DESCENT
■ Lingual thyroid (inability to descend)
o Persists in foramen cecum at base of the tongue

o Found as posterior pharyngeal mass

o 2% malignancy risk (70% of patients have only thyroid tissue)

o Treatment:
• RAI ablation by 1 131 (Best) & Thyroxine

■ Thyroglossal duct cyst (Upper tract not obliterated during descending)

o From the descent of the thyroid glancl from the foramen cecum

o Susceptible to infection and may be premalignant

o Most common location: Subhyoid

o Diagnosjs·
• Clinically (1 - 2 cm, smooth, well-defined midline neck mass that moves upward
with protrusion of the tongue), if not midline mass think about + PTC
• U/S preferred only to document the presence of normal thyroid tissue in the neck

o Treatment:
• Sistrunk procedure + resection along with hyoid bone
Enough for patient with papillary cancer associated-disease

■ Pyramidal lobe: (Lower tract not obliterated during descending)

o 10% from the isthmus toward the thymus
ASYMPTOMATIC THYROID NODULE
■ Malignant risk of any thyroid nodule: 5%
INDICATIONS FOR FNA
■ FNA is the single most important test and initial test to evaluate thyroid masses (after TSH)
■ Technique:
o At least 25 guage, U/S guided is preferable
o Suction / No-suction technique
o Alcohol/ Dry sample
o Sufficient sample: 6 groups follicular cells (10 cells each group) at each slide
o Maximum FNA: 3 times in one session
o Nodule selection: Most suspicious or Largest diameter (if no suspicious)
o U/S guided is more sensitive, avoiding the fat and the necrotic areas

■ Indications:
o Cold nodule by thyroid scan
o Thyroid nodule > 1 cm or growth during follow-up
o Thyroid nodule < 1 cm if associated with high-risk features
• Clinically (Symptomatic, Radiation, family history, prior thyroidectomy)
• Radiologically

Susoicious features on Ultrasound Suspicious features of nodal metastasis

Heteroaeneous lrreQular borders
Thick caosule Cvstic
Non-compressible Round
lrre�ular borders (Ill-defined) Loss of central fattv hilum
Hvnoecho=nicitv Calcifications
Microcalcification / Microlobulation t Central vascularitv
"Perioheral calcification: benian features·
"Taller ldee=r\ than wide" nodule
Posterior acoustic shadow
Anaular marains
Incomplete halo "Invasion" (halo = Hvooechoic rim)

■ Non-indications for FNA for thyroid nodule:

o Any thyroid nodule < 1 cm with no high-risk and no suspicious features on U/S
o Purely cystic nodule
o Hyperthyroidism "Can trigger thyroid storm"
o Pregnant woman with hyperthyroidism {> 16 GW)

■ Indications for Core biopsy I lncisional biops.y:

o Suspicion of anaplastic thyroid carcin-0ma
o Thyroid lymphoma
o Metastatic disease to the thyroid
o U nresectable primary thyroid carcinoma

Core biopsy not done routinely due to disadvantage:

Due to risk of nerve injury, vascular injury, and changing the architecture

FNA or lntraoperative frozen section unreliable in Follicular or HiJrthle CA due to vascular and
capsular invasion
 BETHESDA CLASSIFICATION
Types Meaning Example Risk of Management
malignancy
Type I Incomplete study Cyst fluid 1" trial: Repeat UIS guided FNA within 3 months
Indeterminate Acellular 2"" trial: Repeat U/S FNA vs. Lobectomy
Non-diagnostic Blood 1-7%
Consider thyroglobulin test from recurrent
asoirated cvst
Type II Benign Follicular nodule Follow-up by U/S
Hyperplastic For asymptomatic
nodule Every 6 months for 1st year then annually
Colloid cyst 0-3 %
Lobectomy
For high-risk patient,> 4 an, grows, or associated
with comoressive svmotoms
Type Ill Atypia (FLUS/AUS) Follicular lesion Repeat FNA after 3 -6 months:
Mild atypia -+ Follicular cells If 2"" biQl!S� is FLUS/AUS:
Microfollicular -+ Follicular Molecular testing vs. Thyroid lobectomy
Macrofollicular adenoma
-+ Follicular CA Observation & follow-up U/S in 12 months for:
-+ Hurthle CA > 50% macrofollicular lesions and no risk factors
-+ PTC
FLUS: Follicular s-1s•t. Diagnostic lobectomy: definitive management
lesion of Reserved as initial step for:
undetermined -> 1 cm lesions
significance - High-risk patients or patient preference
- High-risk lesion (Pure follicular pattern)
AUS: Atypia of
undetermined Radionuclide scanning may be used to
sianificance determine the function of the nodule here
Type IV Follicular neoplasm Follicular CA Lobectomy
1 5-30 %
Hurthle CA Total thvroidectomv /Hiah-risk oatients)
Type V Suspicious of Papillary CA Total thyroidectomy vs. Lobectomy
60-75 %
malianancv Medullary CA ± intra�rative frozen section
Type VI Malignant Anaplastic CA Total thyroidectomy and proceed
Lvmohoma 97-99%

Molecular testing
■ Used for patients with indeterminate nodules (Bethesda Ill and IV}
■ Mutational analysis "Specific 7-gene mut.ations" (point mutations):
o BRAF, RAS, RET/PTC, and PAX8/PPARy
o False positive: 20%
o False negative: 5 - 28% (down to 5% with ThySeq II panel}
c::, For patient with benign patter: Observation
c::> For patient with point mutation:: Total thyroidectomy

■ Gene expression classifer (GEC)

o Used if negative mutational analysis
o By microRNA analysis of 142 genes
o Positive test associated with 37 -44% malignancy
o Negative test drop the risk of cancer to 5%
o For patient with positive test: Diagnostic lobectomy
THYROID SCAN
■ By using 1 123 or Tc-99m
o Hot nodule {15%): < 1% cancer risk + send to endocrinologist
o Cold nodule (85%}: 5 - 10% cancer risk

■ Used before U/S in hyperthyroidism, and after U/S in euthyroidism

■ Most commonly impact the treatment in Bethesda 11, 111, IV (follicular neoplasm)

■ Indications: "Recommended in hyperthyroidism•

o Thyroid nodule > 1 cm with hyperthyroidism "f free T4 and ! TSH"
• Especially for follicular lesions

o Grave's disease with atypical presentation (without exophthalmos)

o Detection of ectopic thyroid tissue
o Detection of residual tissue post thyroid surgery with cancer

■ Interpretation:
o Diffuse unifocal uptake: Grave's disease
o Heterogeneous uptake: Toxic multinodular goiter
o No uptake:
• Thyroiditis (f Thyroglobulin)
• Factitious thyrotoxicosis (!Thyroglobulin)

CT SCAN
■ Neck, Chest Abdomen and Pelvis:
o For large bulky mass, anaplastic or medullary cancer, lymphadenopathy

■ Neck and Chestonly·

o For substemal extension

■ Without contrast

■ Disadvantage of iodine contrast:

o Interfere with radioactive iodine for treatment
• Urinary iodine assessed within 2- 3 months, and 1 131 administered after that

o Can precipitate thyroid storm

PET SCAN
■ Limited rule
■ Detect only 50% of thyroid cancer

■ Indications:
o Localization of recurrent or persistent thyroid cancer with lg-positive, RAI scan
negative disease
o Detection of poorly differentiated cancers and Hurthle cell tumors
o Detection of distant metastasis
 THYROID GOITER
NONTOXIC GOITER
■ Non-toxic Multinodular Goiter:
o Benign condition (but may contain up to 20% microcarcinomas)
o Treatment modalities:
• TSH-suppression (No rule recently, except in patient with radiation history)
• Observation/ Follow-up
• Radioiodine therapy (can reduce the size 40% - 60% within 2 years)
• Lobectomy vs. Subtotal thyroidectomy (Preferable in symptomatic goiter)
• > 4 cm in benign condition
• > 1 cm in suspicious of malignancy

TOXIC GOITER (Hyperthyroidism)

Toxic Diffuse goiter Toxic Multinodular goiter Toxic Nodular goiter 30%
11 11
"Graves' disease "Plummer's disease
Most common cause of Associated with Mostly follicular adenoma
hyperthyroidism with extra-thyroidal hyperthyroidism with no
manifestations extra-thyroidal manifestations

Associated with family history

Associated with autoimmune diseases:
DM1. Addison's Mvasthenia aravis
Investigations Thyroid function tests Thyroid function tests Thyroid function tests
Thyroid scan (112J) if no eye symptoms Thyroid scan (112J) Thyroid scan (Im)
Diffuse unifocal uptake Heterogeneous uptake

Anti-TSH antibodies "TSH-R"

Diagnostic 90%
Also called TSI
"Thyroid-stimulating immunoglobulin·

lgG antibodies to TSH receptor

Management 1) Achieve Euthyroid

2} Definitive management
Continue anti-thyroid medications for 1 - 2 years (18 months)
Associated with relapse in 40 - 60%
Peak: 6 weeks
Can decrease life-long thyroxine if used before thyroidectomy

Radioactive iodine ablation

Mainstay treatment for Grave's disease in USA
Preferred with anti-thyroid medications for small toxic nodular goiter
Need higher dose for toxic multinodular goiter> Grave's
Associated with relapse in 50%
Peak: 6 months

Total I near-total I Subtotal thyroidectomy

 HYPERTHYROIDISM THERAPY
Treatment Mechanism Side effects Notes
Hepatitis "Safest antithyroid in pregnancy"
Inhibits peroxidases and
Propylthiouracil
peripheral conversion T4 to T3
(Cholestatic liver failure) + Less crossing to the placenta
Preferable to use in 1" trimester
Inhibits peroxidases only Agranulocytosis Contraindicated in pregnancy
"Fever, sore throat, limb + More crossing to the placenta
(Both of them inhibits binding weakness and mouth ulcer" Used in 2•• and 3'" trimester only
and coupling) Used in breastfeeding patients
Surgery should be postPone
Methimazole uni/I grenu/ocytes > 1000
cells/mm

Vasculitis
Aplastic anemia
Cretinism
lnhibtts peripheral conversion l risk of stillbirth Should be given for all
only fetal growth retardation symptomatic thyrotoxicosis with
HR> 90
Beta Blockers
Proprano/ol Contraindicated in:
- 3"' trimester pregnancy
- Bronchial asthma
- Heart failure /not due to thvroid)
Steroids Inhibits both oeroxidases and peripheral conversion
Decrease releasing of thyroid Used in > 40 years, high risk for surgery, and recurrent
honnones hyperthyroidism after surgery

Sideeffects;
- Most common: Dryness, Sialadenitis, Nausea, Vomiting
- Most serious: BM depression
- Progression of opthalmopathy
Radioactive 1 131 - Thyroid cancer
ablation - Hyperparathyroidism

Contraindicated in:
- Pregnancy and lactation
- Desire to get pregnant in the coming 6 months
- Confirmed cancer or suspected nodule
- Severe reactions to anti-thyroid medications
- Lame goiter with compressive symptoms
Toxic nodular goiter: Lobectomy
Multinodular goiter or Grave's: Total or Near-total thyroidectomy
Indicated as first line for Grave's in:
• Age < 15 years
• Large goiter
• Pregnant women or desiring to become pregnant
• Presence of suspicious nodule of malignancy
T hyroidectomy • Failure of medical treatment/ Persistent hyperthyroidism
• Intolerance of side effects of the medications
I2tal Q[ t::l!l!![ -121111 ru:gf!lcrnd Qll!l[ �Yblatal ia;
• Severe opthalmopathy
• Side effects of antithyroid medications
• Thvroid cancer
THYROID STORM
■ Massive release of intra-thyroid thyroxine
■ Risk factors:
o Anxiety, Sepsis, Infection
o Amiodarone
o Hyperthyroidism (Most common: Graves' disease)
Elective surgery should be postponed until euthyroid state
i
■ Presentat on:
o Tachycardia
o Fever
o Changing of the mentality
o Numbness
o Vomiting
o Diarrhea
o High-output cardiac failure (most common cause of death)

■ Treatment:
o Achieve euthyroid status:
• Initial: Hydration & Propylthiouracil
• Adjuvant: Beta-blockers to control high-output cardiac symptoms

• No Aspirin: because it makesT4 unbounded and increased its level

• Iodine solutions: To l Vascularity (contraindicated in pregnancy)
• Lugol's solution (8 mg of iodide per drop)
• Potassium iodide (SSKI; 50 mg iodide per drop)

Iodine solution given 10 days preoperatively concurrently with thionamide to decrease risk of
hyperthyroidism after withdrawal of iodine solution

Jod-Basedow effect: hyperthyroidism following administration of iodine

Q in endemic goiter (due to iodine deficiency)

Wolff-Chaikoff effect: giving high dose of iodine (Lugo/'s solution) to inhibits TSH
Q in normal population and grave's disease
Q This principle is used sometime to treat thyroid storm

o Emergent thyroidectomy
 THYROIDITIS
■ Usually painless euthyroid, with 4 phases:
o Hyperthyroidism -+
Euthyroidism � Hypothyroidism -+ Euthyroidism
Hashimoto's De Quervain's Sunnurative Riedel's
Characteristics Most common cause of Most common Infectious Invasive fibrotic
goitrous hypothyroidism cause of
painful thyroid
Painless firm and rubben, aland
Nature Chronic Sub-acute Acute Chronic
Pathophysiology Autoimmune disease Painful Left Pyriform sinus fistula in Sclerosing
(Humeral and cell- Viral infection children cholangitis
mediated) (URT infection)
Pre-existing thyroid disease Fibrotic diseases
Painless
Post-partum Preceded by URT infection or Retroperitoneal
otttis media fibrosis
Pathology Lymphocytic infiltration Granulomatous Bacterial Woody (fibrous)
Plasma cells Giant cells Streptococcus
Follicular destruction Bacteroides Involving strap
Smaller follicles lined by muscles and
Hurthel or Askanazy cells carotid sheath
(Not pre-malignant lesion)

-+ Risk of papillary CA
-+ Risk of Lymphoma
(Rapid enlarged, long-
standing, painful due to
compression)
Investigations t ESR in painful thyroiditis, t TSH and l T4
lmmunacompromised war1<-ups in painless thyroiditis
Hashimoto's th:,!raiditis:
• Anti-TPO antibodies (Thyroid peroxidase antibodies) 90%
• Thyroglobulin antibody (TgAB antibodies) 60%
• TSH-R (Anti TSH receptors) 60%
• Microsomal antibody
FNA if associated with suspicious nodule (Nat used in Riedel's thyroiditis ar suspected lymphoma)
Direct endoscoov if suspected Pvriform fistula
Management Hashimoto's: Self-limited, Thyroid replacement hormones if hypothyroidism
(Self-limited) De Quervain's or Riedel's
• NSAIDs or Prednisone ± Tamoxifen (in refractory to steroids)
• Levothyroxine with TSH > 10 IU/ml or> 5 IU/ml with goiter or positive Anti-TPO
TSH rechecked 6 weeks after therapy and every 6 to 12 months
• Wedge excision of isthmus in Riedel's to decompress trachea and for tissue diagnosis

Open/Care biopsy ta rule out thyroid cancer in Hashimato's, or Riedel's thyroiditis

Suppurative:
• U/S with needle aspiration and Broad spectrum antibiotics for 14 days if indicated
• Emergent drainage if abscess found ± thyroidectomy in compressive abscess
• Complete resection of the sinus in Pyriform sinus fistula

Total thyroidectomy reserved for.

Enlamina aoiter, comoression. recurrence, not resnondina to medical, SUS""Cted malianancv
 THYROID CANCER
■ Most common endocrine malignancy
■ Most common cancer metastasis to thyroid: Renal Cell Carcinoma
0 Others: Lung and breast cancers {Cowden: hamartomas in skin, thyroid and breast)
FOLLICULAR CELL-DERIVED
1) W!!II !2itt!!reati;it!u! t 1.1m2rl!
Papillary carcinoma
{Most common)
Risk factors Radiation "Most commonly''
Family history
"BRAF I Proto-oncogene"
Familial adenomatous polyposis
Ulcerative colitis
Thyroglossal duct cyst
Hashimoto's thvroiditis
Route of soread lvmchatics {Cervical in 50%)
Distant metastasis Luna
Characteristics Best prognosis based on the Age
Multicentric 60% "same lobe"
Multifocal 80% "both lobes"
Pathognomonic Cystic & Salid components
features Cuboidal cells
Papillary projections
lntra-fluclear cytoplasmic
Inclusion body
Psammoma bodies 40%
Central Microcalcifications
Calcified clumps
(Seen also in Mesothelioma,
Somatostatinoma, Serous
cystadenoma/
Orphan Annie nuclei
Prominent nucleoli
Radioiodine ablation Uc to 90%
Management Thyroid lobectomy
low risks, < 1 cm lesion
Total thyroidectomy
High-risks, > 1 cm lesions
lateral aberrant thyroid
BRAF cositive =ne
Follicular carcinoma Hurthle cell carcinoma
{Variant of follicular CA)
Iodine-deficiency Same as Follicular thyroid
carcinoma (FTC)
Cowden disease "PTEN"
(Skin hyperpigmentation,
hemartomas, melanoma,
endometrium, colorectal,
breast and thyroid tumors)
Hematoaenous Lvmchatic I Hematoaenous
Bone Bone
Solitary Oxyphilic variant of FTC
Encapsulated (majority) Multifocal 30%
Worst prognosis of the well-
differentiated tumors
Adenoma80% Adenoma
Carcinoma Carcinoma
Capsular invasion Capsular invasion
Vascular invasion Vascular invasion
(Microscopic or (Microscopic or macroscopic)
macroscopic)
Ucto 70% Uc to 5%
Diagnostic lobectomy Diagnostic lobectomy
Low risks, < 4 cm lesion low risks, < 4 cm lesion
Total thyroidectomy Total thyroidectomy + CLND
High-risks, > 4 cm lesions High-risks, > 4 cm lesions
Hurthle cell carcinoma on final
catholonv
 Treatment of well-differentiated tumors:

I Follicular hyperplasia < 1 cm of unifocal carcinoma in

Low risk patient
> 1 cm of carcinoma
> 4 cm follicular lesions

Hiirthle cell adenoma Hiirthle cell carcinoma

< 1 cm in High-risk patient

■ Stages Ill/IV (T3 / T4)
■ Multi-focal
■ Extra-thyroidal disease
■ Extra-capsular extension
■ Radiation to head or neck
■ Lymph nodes metastasis
■ BRAF positive gene

Male, and > 45 or < 15 years in old

risk classifications

J Observation I Follicular lesion: (Diagnostic lobectomy)

Thyroid Lobectomy without isthmusectomy
J Total Thyroidectomy I
Other differentiated thyroid neoplasm:
Thyroid Lobectomy ± isthmusectomy
± removal of pyramidal lobe if present

Completion thyroidectomy usually performed for cancers on frozen section or at final pathology
especially for frankly angioinvasion even without capsular invasion

■ Papillary thyroid microcarcinoma

o Observation is acceptable option in absence of worrisome features for patient with:
• < 1 cm detected preoperatively or post lobectomy
• No clinically involved cervical lymph nodes
• No extrathyroidal extension
• No history of head and neck irradiation
2) Poorly Differentiated tumors
■ Anaplastic thyroid cancer
o Most aggressive thyroid CA
o Hematogenous spread
o Associated with euthyroid status, and Superior Vena cava syndrome

o Risk factors:
• Patients with known well-differentiated follicular-derived cancers
• Family history "BRAF gene"
• Elderly patient with rapid growing mass

o Histopathological features:
• Foci of well-differentiated tumors
• Features of anaplasia
• Vesicular nuclei
• Giant cells and multinucleated cells

o Management· Palliative
• CT chest and neck with PET scan to assess the extent of the disease

• Debulking thyroidectomy ± tracheostomy (Only for compromised airways)

• Curative Thyroidectomy (limited rule)
• Resectable disease with no distant metastasis "Localized to neck"
• Fit for surgery

• Adjuvant radiotherapy 2 - 4 weeks postoperative due to edema

• Adjuvant chemotherapy based on CT/PET scan after radiotherapy sessions

NON-FOLLICULAR CELL-DERIVED

1) Para-follicular

■ Medullary thyroid carcinoma

o Proliferation of cells derived from the neural crest (Never came with Thyrog/ossa/ cyst)

o Lymphatic spread, with more aggressive behavior

o Evaluation:

History and examination

• Palpable thyroid nodule with euthyroid status ± Obstructive symptoms
• Positive family history in case of inherited MTC
• Symptoms of high calcitonin level: Flushing, diarrhea and weight loss
• Metastatic symptoms: Brain, Bone, Lung, Liver
• Associated with other disorders in case of inherited MTG:
Hyperparathyroidism (20 - 30%)
Pheochromocytoma 50%
Marfanoid habitus with mucosal neuromas

Laboratory evaluation
• TSH level

• Calcitonin level(> 10 pg/ml) "Most sensitive for staging and prognosis"

• Pentagastrin-stimulated peak plasma calcitonin level is most sensitive
• CEA risk of D-differentiation to anaplastic cancer "Better predictor for prognosis"

• Rule out other disorders associated with inherited MTC:

� PTH level and calcium level, 24-h VMA and metanephrines
• Genetic testing for RET proto-oncogene in family members
• Associated with medullary, papillary, pheochromocytoma, hirschsprung's

Radiological evaluation
• U/S neck, CT neck and chest, CT/MRI liver and bone scan

FNA of thyroid nodule

• Pleomorphic cells without follicle development
• Arises from parafollicular C cells "C-cell hyperplasia"
• Granular eosinophilic cytoplasm staining for calcitonin
• Amyloid deposition is pathognomonic
o Types:
Sporadic 75%:
• Focal C-Cell hyperplasia and unilateral
• Associated with para-neoplastic (Cushing's Syndrome, Diarrhea from VIP)

Hereditary 25%
• Familial: RET Proto-oncogene
• Associated with familial MTC and MEN medullary thyroid cancer
• Multifocal and bilateral tumors, neoplastic C-Cell

• MEN-Associated
MEN 2A: Medullary thyroid cancer, Pheochromocytoma, Hyperparathyroidism
MEN 2B: Medullary thyroid cancer, Pheochromocytoma, Mucosa! neuroma

o Prognosis (From best to worst):

• Familial MTC ( Non-MEN)
• MEN 2 AMTC
• Sporadic MTC
• MEN 2 BMTC

o Management of medullary thyroid cancer:

• Rule out pheochromocytoma and otherMEN-associated diseases

• Total thyroidectomy and bilateral central node dissection (risk of multicentricity)

• Step-ahead approach
� Remove central nodes if negative
� Remove ipsilateral neck lymph nodes if central nodes are positive

• Prophylactic thyroidectomy at ( 1st year in MEN2B, 3 - 5 years inMEN2A)

±Central LN dissection highly indicated if high calcitonin or positive by U/S

• Aggressive management is required due to aggressiveness of the disease and

useless of the RAI (No follicle cells)
2) Stromal

■ Thyroid lymphoma
o B-Cells lymphadenopathy (Non-Hodgkin lymphomas)
o Tumor marker: LOH

o Risk factors:
• Hashimoto's disease
• Hypothyroidism

o CT Scan:
• Donut sign (in airway compression)

o Management:
• Chemoradiation
• ADVP

• R-CHOP
� Rituximab
Q Cyclophosphamide
� Doxorubicin
� Vincristine
� Prednisolone

One cycle R-CHOP -+ Radiation -+ 5 cycles of R-CHOP

Initiation of chemotherapy will help impending airway obstruction

• Surgery
• Options for patient with airway obstruction and no benefits of
chemotherapy:
� Thyroid isthmusectomy
� Near-total thyroidectomy
c:> Total thyroidectomy
GENERAL INDICATIONS FOR THYROIDECTOMY
■ Toxic multinodular goiter, unreasoned to treatment
■ Toxic solitary nodule
■ Persistent hyperthyroidism
■ Pregnant female with allergy to anti-thyroid medications
■ No response to treatment, or develop side effects
■ Follicular/Papillary/Medullary neoplasms
■ Goiter with·
o Malignancy features, compressive symptoms, Large (or enlarging during follow-up)
o High-risk patients: male, > 45 or< 15 years, > 4 cm, extrathyroidal disease
o Develop complications as exophthalmos
o For Cosmesis

RISK STAGING SYSTEMS

■ TNM
■ MACIS: Metastasis, Age, Complete excision, Invasion (Extra-thyroidal), Size
■ AGES: Age, Grade of histology, Extension of tumor (Extra-thyroidal), Size
■ AMES: Age, Metastasis, Extension of tumor (Extra-thyroidal), Size
■ EORTC
Proanostic variable MACIS AGES AMES EORTC
Patient factor
Age X X X X
3.1 (if<40 year) 0.05 x age(if>40 year)
0.08 x aae (if> 40 vear)
Sex - - X X

Tumor factor
Size X X X
+ 0.3 x tumor size + 0.2 x tumor size

Multicentricitv - - - -
Histologic grade - X - -
+ 1 (if grade 2)
... 3 (ifarade 3-41
Histoloaic tvne Onlv for PTC Onlv for PTC X X
Extrathyroidal invasion X X X X
+ 1 (if locally invasive) + 1 (if extrathyroid)
+ 1 /if incomoletelv resected)
Nodal metastasis - - - -
Distant metastasis X X X X
+ 3 (if distant spread) + 3 (if distant spread)

MACIS AGES AMES

Low risk: 99%
<6=99% < 4=99% Young(<40 male,<50 female)
<5cm
6-7=89% 4-5=80% No metastases
Survival (20-year) High risk: 61%
7-8 =56% 5-6=67% >Sm
Distant metastases
>8= 24% > 6= 13% Extrathyroid papillary
Caosular invasion
INDICATIONS OF MRND (LATERAL NECK DISSECTION): "Level 2, 3, 4 ± 5•
■ Positive clinically or radiological nodes (Frozen section is used if suspicious intraoperatively)
■ Positive central nodes in medullary cancer may requires ipsilateral MRND
■ Most common involvement: Level 3 and 4

Hyoid bone

Cricoid cartilage

INDICATIONS FOR CENTRAL NODE DISSECTION: "Level 6"

■ Indications as prophylactic:
o High-risk patients(> 1 cm cancer with tall cells)

Controversial and not routinely recommended

(due tot risk of RLN and parathyroid injury)

■ Indications as therapeutic :
o Positive central nodes
o Positive lateral nodes
o Medullary thyroid cancer
o Hiirthle cell carcinoma
o Parathyroid cancer

■ Level of dissection: from hyoid bone lo manubrium and carotid to carotid

o Delphian nodes "Prelaryngeal nodes" are found within anterior suspensory ligament

Consequence oflymph nodesinvotyement·

Jpsilateral Central � lpsilateral Lateral � Contralateral Central � Contralateral Lateral
c:> If MRND planned, central lymph node dissection should be done before the lateral dissection
c:> Level 1 and 5 dissections are rarely indicated
TSH SUPPRESSION THERAPY Qevothvroxine)
■ Benefit: Decrease growth of thyroid tissue, used in follicular-derived tumors

■ Target:
o Pre-existing disease: TSH < 0.1 mU/L
0 High-risk: TSH < 0.5- mU/L
o Low-risk: TSH < 2 mU/L

■ Duration:
o 6- 12 months
Should be stopped 2 weeks before radioiodine scan or ablation

■ Side effects:
o Bone density loss (osteoporosis) and atrial arrhythmias

■ High risk:
o Macroscopic invasion, Incomplete tumor resection, Distant metastases, high
thyroglobulin, vascular invasion, N1

■ Intermediate risk:
o Microscopic invasion, cervical lymph nodes metastasis, aggressive histology, multifocal
papillary cancer with extra-thyroidal extension
Radiotherapy
■ Indications for 1 131 <Radioactive ablation therapy}:
o Nodal involvement
o Remnant thyroid tissue (l Thyroglobulin level)
o Extra-thyroidal extension
o Distant metastases
o Hurthle cell carcinoma
o > 4 cm cancers
o < 4 cm cancers with high-risk features
• Tall / Columnar cells on pathology, or vascular invasion are considered as well

Consider / 131 for most of papillary thyroid cancer> 1 cm (90% avid)

■ 1 131 effective for:

o Papillary cancer 90%

-�
o Follicular cancer 70%
o Hurthle cell cancer 30%

o 1 131 ablation 4 - 6 weeks after thyroidectomy

• Repeat ablation after 6 - 12 months for intermediate and high risk
• Repeat ablation for elevated thyroglobulin

■ Indication for XRT: (all tumors)

o Metastasis
o Locally invasive cancer
o Recurrent cancer

■ Dose-dependent: fixed-dose between 30 and 150 mCi (1.1 and 5.6 GBq)
o High dose (5.6 - 7.4 GBq} = 150 - 200 mCi Most effective for high risk
o Medium dose (3.7 GBq) = 100 mCi Most effective for intermediate risk
o Low dose (1.1 GBq} = < 100 mCi Recommended for low risk

Follow-up
■ History and Physical examination every 6 months for 3 years then annually
■ Thyroid function test, Thyroglobulin, and Anti- Thyroglobulin every 6 months
o Thyroglobulin every 3 months in 1 st year, then every 6 months in 2nd year, then annually
o Calcitonin, CEA instead of Thyroglobulin in cases of Para-follicular carcinoma

■ U/S neck 6 months after thyroidectomy, then annually

■ 1 123 whole body scan annually or 6 months after ablation, if negative every 2 years for 5 years
o 1 123 whole body scan 5 - 7 days after thyroidectomy for intermediate and high risk

■ CT scan or MRI if needed

■ PET scan for poorly differentiated thyroid cancer or Tg-positive and RAI scan negative disease
CALCIUM/ VITAMIN D SUPPLEMENT AFTER THYROIOECTOMY
■ Risk of hypocalcemia post thyroidectomy 20% and increased with:
o Total thyroidectomy
o Central neck dissection
o Grave's disease (due to hunger bone syndrome post-operative)
o Parathyroid injury or devascularization
o Thyroxine supplement along calcium supplement with interval < 2 hours

■ lntraoperative PTH asses sment:

o First reading before the incision, Second reading 15 minutes after thyroidectomy
o If PTH drop> 70% � Supplemental oral calcium and vitamin D needed

■ Management of hypocalcemia:
o ECG + Check Mg level

o Oral Calcium carbonate 1250 mg PO TIO

• Non-symptomatic patient with Calcium > 8 mg/di
• Some prefer to place all patients with total thyroidectomy on supplements

o Oral Calcium carbonate 2500 mg PO TID

• Mild Symptomatic
• Calcium < 8 mg/dl

o IV Calcium gluconate 2 g IV over 1 h infusion

• Severe Symptomatic (Seizure, tetany, stridor, laryngospasm)
• Calcium < 4 mg/dl
• Osteitis fibrosa cystica

■ > 1 Parathyroid gland were grafted: Calcitriol 0.5 -1.0 mcg PO in 2 divided dose

■ Thyroxine and calcium should not be given at the same time

o Interval: 2 - 4 hours to allow absorption of calcium
VOCAL CORDS
■ Most patients have some immediate voice changes, resolve within 2 weeks postoperative
■ Vocal cord assessment preoperatively should be done for all patients
o Recently, advised for patient with previous neck surgery or history of voice change

■ Recurrent Laryngeal nerve injury

o Severe respiratory stress and stridor if bilateral complete injured

losilateral Bilateral
Partial Adducted /loss of abduction •midline of iniured nerve"\ Adducted + Re-intubate
Comolete Paramedian oosition /loss of abduction & adduction I Paramedian + Traclleostomv

■ Superior Laryngeal nerve injury + Asymmetric glottis opening

o Bowing and inferior displacement of the affected cord and rotation of posterior glottis
toward injured side

■ Both nerves injuries + Cadaveric position (Bilateral paramedian)

DIFFERENT TYPES OF THYROIOECTOMY

Ace
No risk of bilateral R

Subtotal thvroidectomv: keep thyroid tissue bilaterally

Tubercles of Zuckerkandl (posterior extension of thyroid tissue)
Near to RLN (Rotate medially to find it)

Near-total thyroidectomv: keep thyroid tissue unilaterally (either at upper pole, or near RLN)

■ Thyroxine dose:
o After total thyroidectomy: 1.5 mcg/kg + around 100 mcg once daily
o After lobectomy: 1.3 mcg/kg

Some surgeon believed to start thyroxine early to keep TSH low, for suspicious diseases
STEPS OF THYROIDECTOMY
■ Position:
o Reverse Trendelenburg (Head-up 30 - 45 degree}

o Semi-Fowler's position (Head-up 15 - 30 degree with hip fiexi on}

o Supine position
Roll placed below shoulder -+ extend the neck
{lo decrease the venous return and bleeding)

■ Incision:
o "Collar incision"
• Made on skin creases
• 2 fingerbreadth above sternal notch
• 1 cm below cricoid cartilage (More accurate)
• From medial borders of SCM muscle to SCM muscle for 4 - 5 cm

o Deepen the incision and divide the platysma horizontal/y (supplied by facial nerve)
• Superior flap to thyroid cartilage
• Inferior flap to sternal notch
• Avoid injury to anterior jugular veins (risk of bleeding and air embolism)

o Divide the strap muscles longitudinalfy in midline and retracted laterally

• Along the cervical linea alba
• In case of need for division (large goiter}, it should divide high up, as the
innervation came from below
■ Thyroid lobe mobilization (starting by pathological side)
Sharp dissection is better than blunt to prevent oozing intraoperative

o Middle thyroid vein: as it's short, it's the 1 st vein to be ligated during the procedure

o Upper pole dissection: (Some preferred to be dissected after the lower pole)
• Approached by multiple ways:
• Lateral (Back-<loor)
Q By retracting strap muscles laterally± partial resection (or cutting
the sternothyroid only), then retraction of carotid artery laterally
• Anteromedial
Q By blunt dissection into avascular cricothyroid space
(Reeve or Joll space) all the way to the prevertebral fascia

• Posteromedial
• Mobilize inferiomedially, ligate, divide the superior thyroid artery then the vein
• Artery should be ligated before the vein to prevent lobe congestion
• Most bleeding coming from superior pole, need double ligation
• Dissection and ligation should be as close as to the capsule

• External branch of SLN: identified by crossing superior thyroid artery 1 cm above

superior pole

o Lower pole dissection:

• Retract medially -+ Identify, ligate, and divide Inferior thyroid artery then vein
• Ligate the inferior thyroid artery close to thyroid to prevent transient parathyroid
ischemia or injury to RLN
• RLN:
• Need to be identified and preserved before ligation of any structures
• Identified at:
Q Tracheoesophageal groove by mobilize tubercles of Zuckerkandl
(posteriolateral extension)
Q Posterior to ITA
Q Most consistently identified at level of cricoid cartilage

■ Intra-operative nerve monitor

o Controversial (Meta-analysis study failed to how protective effect)
o Requires specialized electrode integrated endotracheal tube
o Help to evaluation of nerve function and improve recognition of nerve injury
o Doesn't reduce risk of injury
o Intact nerve associated with high rate of return functionality of cord paresis
■ Identify. check status and preserve the superior and inferior parathyroid glands
o Usually between true and false capsules of thyroid
• Superior parathyroid -+ posteriolateral to the RLN
• Inferior parathyroid -+ anteromedial to the RLN

o Dissection of thyroid from parathyroid should be done medial to lateral

■ Complete dissection posteriorly from ligament of Berry (to isthmus if lobectomy planned)
o True capsule: interior, removed with thyroid during thyroidectomy
o False capsule (surgical capsule): external, from pretracheal fascia, not removed during
thyroidectomy

■ Dexamethasone given by some surgeons intra-operatively to decrease the neck edema

-+ Decreases risk of vomiting -+ Decreases capillary leak -+ Decreases the hematoma risk
■ Hemostasis can be assessed by:
o Trendelenburg position
o Valsalva maneuver

■ Specimen marked with suture at superior pole for orientation

■ Closure
o Closure of strap muscles:
• 3-0 continuous absorbable suture and keep small window from below
• Advantage of quick rele .ase if hematoma developed

o Closure of platysma:
• 3-0 interrupted absorbable suture
• Inappropriate closure of platysma leads to bad scar

o Closure of the skin by 4-0 absorbable subcuticular suture

■ Drain doesn't affect mortality, decreasing hematoma size, or decreasing symptoms of

compression (Might be preferable in case of large dead space)

■ No Bandage should be places (especially in recovery unit) to allow discover early complication
COMPLICATION OF THYROIDECTOMY
■ Early / Late

■ General Complications:
o Atelectasis
o UTI
o DVT / PE
o Wound infection
o Complications of the anesthesia

■ Complications of surgery:
o Hematoma {1 -2 %)
• Airway compression happens in 6 - 8 hours -+ Open bedside then OR
• Compression due to edema not due hematoma itself
• Edema happens due to ! venous return

o Voice changes (15 -30 %)

• Usually transient and resolved within 2 weeks
• Due to vocal cord edema

o Hypocalcemia (20 %)
• Resolves in 80% in about 12 months
• < 2% due to permanent hypoparathyroidism

o Parathyroid injury
• Parathyroid which appears devascularized intra-op should be autotransplant of 1-
mm fragments into pocket-made of sternocleidomastoid or brachioradialis

o RLN injury (1 - 2 %)
• Dissection is most difficult in Grave's disease
• Most common site of injury: at the insertion
• Most common type of injury: Stretch injury

o SLN injury (15-20 %)

• Especially if superior pole ligated en mass

o Infection (1 - 2 %)
• Very low rate due to t vascularity
• Drain doesn't affect mortality, ! hematoma size, or ! symptoms of compression

o Life-long thyroxine:
• After total thyroidectomy: 100%
• After lobectomy: 1 0 - 15%
 ■ Cervical lymph nodes classification

Level Grou s
LevelI Submental and submandibular I m h nodes
LevelII U er IJ nodes "Anterior and Posterior"
Level Ill Middle IJ nodes H oid bone to Cricoid
LevelIV Lower IJ nodes Cricoid to clavicle
LevelV Posterior triangle lymph nodes Base of skull to cricoid
� S inal accesso Sub-occi tal Su raclavicular nodes
Anterior triangle lymph nodes Hyoid bone to manubrium
"Central Com artmenr medial to the carotid sheath
Superior mediastinal nodes Manubrium to brachiocephalic veins,
between common carotid arteries

■ Radical Neck Dissection (RND):

o Removal of all ipsilateral cervical lymph node from levels I through V, together with
SAN, SCM and IJV

■ Modified Radical Neck Dissection (MRND):

o Removal of level 11, 111, IV, and V lymph node groups with preservation of one or more:
• Type 1: Preservation of spinal accessory nerve (SAN) CN= 12
• Type 2: Preservation of SAN + internal jugular vein (/JV)
• Type 3: Preservation of SAN+ /JV+ sternocleidomastoid muscle (SCM)

No mortality difference compared with RND

Most morbidity occurs from accessory nerve resection

Functional neck dissection Removal of level 11, Ill, IV, V (MRND type 3)

■ Selective Neck dissection (For NO)

o Anterior or Central neck dissection: Removal of level VI
o Lateral necK dissection: Removal of level II, Ill, IV
■ Modified Radical Neck dissection
o Removal of all fibro-fatty tissue along the internal jugular vein (levels 11, 111, and IV) and
the posterior triangle (level V)

o With preservation of the internal jugular vein, spinal accessory and cervical sensory
nerves, and the sternocleidomastoid muscle, unless adherent or invaded by tumor

o Incision:
• Extended low transverse collar incision {for thyroidectomy)
± Extended up along anterior border of the sternocleidomastoid muscle

• YI H IT incision, Hockey stick incision, McFee incision or Apron incision

Mclee

V
lncisloo

o Open the plane by dissection between Strap muscles and SCM

o Sub-platysmal plane created

• Superiorly: Mandible
• Inferiorly: Clavicle
• Medially: Midline
• Laterally: Anterior margin of the trapezius muscle

o The posterior aspect of superior flap retracted away from external jugular vein, great
auricular nerve, and parotid gland

o Incise the deep cervical fascia overlying the submandibular gland 1 cm anterior and 1
cm inferior to the angle of the mandible

(Care to preserve the marginal mandibular branch of facial nerve and phrenic nerve)

o Retract the sternocleidomastoid superiorly

 o Dissection:
• Started at uppermost area near angle o f the mandible

• Direction of dissection: Superior lateral + Inferior medial

along the anterior scalenus muscle, the phrenic nerve, and the brachia! plexus
• Borders of dissection:
• Superior: Angle of mandible
• Inferior: Clavicle
• Medial: Carotid sheath and internal jugular vein
• Lateral Posterior edge of Sternocleidomastoid muscle
• Posterior: Deep cervical fascia and trapezius muscle

• Continue dissection until carotid sheath, open the sheath and dissect fibro-fatty
contents away
• Be careful on the left side not to injure the thoracic duct

• Level V dissected lateral to medial along posterior edge of SCM

o Spinal accessory nerve identified superior and lateral (Frequent site of metastasis)
• Identified in the posterior triangle as it enters the trapezius muscle
• Identified beneath posterior belly of digastric muscle

o Send specimen to pathology

o Check for hemostasis

o Drain

o Closure (including platysma)

■ Complications of MRND:
o Infection
o Seroma
o Lymphocele
o Anterior jugular vein thrombosis
o Injury to:
• Thoracic duct
• Vagus nerve
• Phrenic nerve
• Great auricular nerve
• Accessory spinal nerve
• Sympathetic chain injury (Hornor's syndrome)
Parathyroid
PARATHYROID
ANATOMY AND PHYSIOLOGY
Superior parathyroid gland Inferior parathyroid gland
Pharvnaeal pouch 4"" Pouch 3"' Pouch
Most common ectopic location Retro-esophagral space Thyrothymic ligament
Carotid sheath lntra-tlwmus
Relation to RLNs Pos1eriolateral Anteriomedial
Relation to inferior thyroid artery Above lTA BelowlTA

Within 1 cm of junction of:

ITA- RLN
Constancv More like Iv to be constant More likelv to be ectooic

Grosslv a,nearance
Nonna! oarathvroid Abnonnal oarathvroid Lvmoh node
Size <?mm >7 mm <7 mm
Color Yellow-brown non-alossv Dark White alossv
Consistencv Soft Firm Firmer

■ Parathyroid glands migrates caudally

■ Normal weight: 20 - 40 mg
■ Blood supply:
o Inferior thyroid artery: supply both superior and inferior parathyroid glands
o Superior, Middle, and inferior thyroid veins

PTH / VITAMIN D (CHOLECALCIFEROL)

■ Produced and stored by Chief cells
■ Half-life of PTH is 2 - 4 minutes
■ Vitamin Dprevent osteoporosis
■ Vitamin Dmade first in skin + UV sunlight converts 7-dehydrocholesterol to cholecalciferol
� Hydroxylation of "Cholecalciferol" in the liver + Calcidiol {25-OH)
� Hydroxylation of "Calcidiot {25-OH)" in the kidney + Calcitriol (1-OH) ''Active form"

■ Action of PTH:
o Bone: t resorption (osteoclasts) + t Ca t PO.
o Kidney:
• PTH: t Ca reabsorption and t PO. excretion
• V. D: t Ca reabsorption and t PO4 reabsorption

o GIT:
• PTH: indirect by enhance 25 hydroxylation of Vitamin Din the kidney
• V. D: t Ca reabsorption and t PO. reabsorption

CALCITONIN:
■ Produced by thyroid parafollicular C cells
■ ! Serum Ca
o Inhibit osteoclast bone resorption
o Inhibit reabsorption of calcium and phosphate and inhibit excretion of phosphate
 PRIMARY HYPERPARATHYROIDISM
■ Most common cause of hypercalcemia
■ Most common caused by parathyroid adenoma
o 10- 15% parathyroid hyperplasia
o 2- 5% double adenoma
o 1% parathyroid cancer

■ Etiology·
o Thyroid or renal diseases, Radiation, Lithium
o Genetic:
• PRAD1 oncogene (associated with neoplastic lesion, and 18% of adenoma)
• MEN-associated (MENIN, RET proto-oncogene)

■ Clinical presentation:
o Asymptomatic 80%
o Symptomatic: (Hypercalcemia)

Gastrointestinal Musculoskeletal Renal Metabolic

Nausea, Vomiting Proximal muscular weakness Polyuria Fatigue
Diffuse oain and irritabilitv
Abdominal pain Pathological fracture Nephrolithiasis 10 - 20% Gallstones
(Most common) /Ca bilirubinate\
Constipation Bone pain Nephrocalcinosis < 5% Hyperchloremic
Bone c=ts (renal oarenchvmal calcification) Metabolic acidosis
Peotic ulcer Osteooorosis Gout
Pancreatitis Osteitis fibrosa cystica 10 - 20% Pseudogout
(brown tumors) pathognornonic

Findings on h!!nds x-r!!�:

Sub-periosteal resorption
On radial aspect of middle phalanx
of 2nd/ 3"' finaers
Chondrocalcinosis Calciohvlaxix /Non-Uremic\

■ Diagnosis:
o Based on laboratory investigations only

Electrolvtes Primarv PTH Secondarv Tertian, PTH

PTH t t t
Serum Ca t Normal or 1 t
j (Renal failure)
Serum PO. l Normal Mtamin D deficiencv\
j or l
Serum Cl t (Cl:PO, > 33)
Urinarv Ca t t
Urinarv PO. t
RenalcAMP t
GFR J
HCO, t
ALP t /Bone disease\ t t

Vitamin D level should be normalized before assigning a diagnosis of hyperparathyroidism

! Mg level in patients with Osteitis fibrosa c ystica
Indications for parathyroidectomy:
■ Symptomatic
■ Asymptomatic
o Serum calcium> 1 mg/di (0.25 mmol/L} above upper limit of normal level
o Bone mass (Osteoporosis} T-score < - 2.5 or vertebral fracture
o 24-h urinary calcium> 400 mg/di as it increases stone risk (recently by NIH 2014)
o < 50 years
o Creatinine clearance (GFR) < 60 mUmin
o Not desired for long-term medical surveillance

Persistent hyperparathyroidism:
■ Non-resolve hyperparathyroidism or recurrence within 6 months after surgery
■ Caused by inadequate exploration or failure to recognize adenoma during initial operation.
■ Most common cause: parathyroid adenoma
Recurrent hyperparathyroidism:
■ Return of disease after an apparent cure more than 6 months
■ Most common cause: parathyroid hyperplasia

Most common sjte of persjstent or recurrent hyperparathyrojdjsm·

■ Retro/Para esophageal groove (Most common)
■ Mediastinal (,!"d most common)
SECONDARY HYPERPARATHYROIDISM
■ Due to parathyroid hyperplasia (Not adenoma}

■ Etiology:
o Metabolic diseases
• Renal failure
• Vitamin D deficiency
• Post-bariatric surgery

■ Medical management:
o Vitamin D correction
o Cinacalcet (Sensipar)
• Initial treatment of choice for secondary hyperparathyroidism

o Prevent hyperphosphatemia
• Aluminum salts
• Ca-contained phosphate binder: Ca carbonate and acetate
• Ca-free phosphate binders: Sevelamer hydrochloride and lanthanum carbonate

o Decrease PTH secretion

■ Indications for surgery: {Subtotal parathyroidectomy)

o Symptomatic hyperparathyroidism (bone pain, pruritus) uncontrolled medically
• Bone fracture, pancreatitis, peptic ulcer or kidney stones are not indications for
parathyroidectomy as primary hyperparathyroidism, unless failure of treatment

o Tumoral calcinosis (Peri-articular masses} and calcium depositions

o Calcium >11 mg/dl and uncontrolled PTH level(> 600 pg/ml)

o Calcium-phosphate products� 55 (70 in some sources)

o Calciphylaxis (uremic arteriolopathy and pruritus):

• Calcification of small to medium arteries -+ Erythematous, painful skin lesions
• Diagnosed by skin biopsy

o Progressive intractable renal osteodystrophy

• Osteitis fibrosa cystica
• Osteomalacia
• Adynamic bone disease
TERTIARY HYPERPARATHYROIDISM
■ Caused by hyperfunctioning of parathyroid after treatment of secondary hyperparathyroidism
o Example: Renal transplant in CKD

■ Medical management: Cinacalcet (Sensipar)

o Calcimimetic agent used mainly in tertiary hyperparathyrodism
o Used in primary hyperparathyroidism in case of non-operative candidate

■ Indications for surgery: /Subtotal parathyroidectomy)

o Severe hypercalcemia(> 12.5 mg/dl)
o Persistent hypercalcemia ;,, 2 years after renal transplantation, associated with:
• Decline in renal function, Nephrolithiasis, Progressive bone disease, Pancreatitis

FAMILIAL HYPERCALCEMIC HYPOCALCIURIA

■ Autosomal dominant
■ Defect in PTH receptor in distal convoluted tubule of the kidney
■ l Ca and t Urine Ca
■ Negative U/S and Sestamibi scans
■ 24-hour Urine calcium is indicated for all patients
o Indicated for patients with chronic hypercalcemia and positive family history
o Not indicated routinely in patients with primary hyperparathyroidism
o Positive result for familial hypercalcemic hypocalciuria < 100 mg / 24 hours

■ Treatment: No parathyroidectomy

PARATHYROID CANCER
■ PRAD1 oncogene, Tumor marker: hCG
■ Rare cause of hypercalcemia
■ Associated with palpable neck mass(must be differentiated from thyroid mass)
■ Most common location for metastases: Lung
■ Pathology:
o Focal chief cell hyperplasia extending through the capsule

■ Very high l Ca(> 13 -14 mg/di), PTH, and alkaline phosphatase

■ Management:
o En-bloc gland resection with ipsilateral thyroid lobectomy and central neck dissection
± Lateral neck dissection if grossly involved

HUNGER BONE SYNDROME

■ After parathyroidectomy
■ Caused by severe hypocalcemia
■ Risk factors:
o Tertiary hyperparathyroidism
o Grave's disease
o Large adenoma

■ Normal PTH, 1 HC03, l Ca, 1 P04-+ Laryngospasm

LOCALIZATION AND MISSING PARATHYROID GLAND
■ Most common location at reoperation: normal anatomic position Tracheoesophageal groove
■ Most common location of ectopic parathyroid gland: Thymus

■ Preoperative localization:
o Mandatory for all primary parathyroidism planning for surgery (20% ectopic disease}

o Not mandatory for patient undergoing bilateral exploration (Cancer, MEN, Hyperplasia)
• But can be used to identify supernumerary or ectopic gland

o Non-invasive:
• Sestamibi scan "Technetium-99m" as initial test to be used
• False-positive: Thyroid disease or lymphadenopathy
• Normal parathyroid: Not seen
• Adenoma or hyperplasia: Delayed or slow uptake

• U/S neck: to rule out concurrent thyroid disease and intra-thyroidal parathyroid
Concordant (UIS and M/8/ suggest the same site) � 95% accuracy
• 40 CT (for re-operative cases}: Most sensitive single test
• Provide anatomical and functional information

• MRI or SPECT (Single-proton emission CT ) for ectopic

• MRI has low sensitivity due similar characteristics of cervical lymph nodes
• CT and MRI is used to localize mediastinal or ectopic parathyroid glands

o Invasive:
• U/S guided neck FNA (for re-operative cases}
• Selective angiography in conjunction with venous sampling
• For re-operative cases with non-convincing non-invasive localization

■ lntraoperative adjuncts:
o lntraoperative PTH monitor:
• For all patients
• At baseline (pre-incision or pre-pedicle ligation)
• 5, 10, 15, and 20 minutes intervals after removal

• Positive value:
• 2: 50% drop from pre-removal or baseline
o At 10 minutes (Miami criteria)
o At 20 minutes (R·ome criteria)
• Reaching positive value indicate closure and postoperative follow-up
• Some criteria require normal or following a kinetic trend toward normal level

o lntraoperative RLN monitor:

• Improves recognition of nerve injury
• Help to localize parathyroid gland

o lntraoperative gamma probe to detect pre-operative Tc 99: Controversial

Surgical localization steps:
■ Superior:
o Dissect and look in Retro/Para-esophageal, pharyngeal spaces
o Carotid sheath exploration (from bifurcation to the base of the neck)
o Superior intrathyroidal
• Check thyroid by intra-op U/S to confirm the location as intra-thyroidal
• Either hemi-thyroidectomy or ligation only of inferior thyroid artery
• If hemi-thyroidectomy planned, make it at the last option and should be
discussed with all patients before surgery

■ Inferior:
o Majority are found in proximity to the lower thyroid pole
o Explore thyrothymic ligament or tail ot Thymus (Cervical thymectomy)
o Carotid sheath exploration
o Inferior intra-thyroidal, (same as previous steps)
� Achieve 50% drop in PTH:
Close and follow calcium level

� Failure to achieve 50% drop after ipsilateral exploration (Superior/inferior):

Bilateral neck exploration

� Failure to achieve 50% drop after bilateral exploration:

Close and follow PTH level with sestamibi scan

Frozen section used to confirm parathyroid gland and it's weight

CaPTHUS scori na model Points

Total serum calcium ;, 3 mmoVL 1212 ma/di\ 1
Intact PTH level ;, 2 times the unner limit of normal valu,e 1
Neck UIS nnsitive for one enlar"" oarathvroid eland 1
Sestamibi scan oositive for one enlarae oarathvroid eland 1
Concordant sestamibi scan and neck U/S results for one enlar= oarathvroid aland on same side 1
> 3 nnints has sensitivitv of 44% and soecificm1of100%

UNILATERAL VS. BILATERAL NECK EXPLORATION

■ Unilateral neck exploration
o If both sestamibi and U/S showed its location pre-operatively
o Lower the risk of complications, as injury to RLN or hypoparathyroidism
(recent studies showed no difference in rates)

■ Bilateral neck exploration (4-gland exploration)

o Failure of preoperative localization
o Failure of PTH to decrease after excision of preoperative localized enlarged gland
o MEN 1, MEN 2 A. Familial hyperparathyroidism
o Suspected parathyroid hyperplasia
(SecondaryfTertiary hyperparathyroidilsm, Mild PTH/Ca elevation)

■ Median sternotomy reserved for:

o Calcium level> 13 mg/dl (as initial operation)
o Localized mediastinal gland
POSTOPERATIVE CARE
■ History and Physical examination
■ PTH, Calcium and vitamin D level 1 - 2 weeks postoperative to establish baseline level
o At 2- 3 days postoperative, then at day 10
■ PTH and calcium level annual to identify recurrence (2%)
■ Calcium supplement: for symptomatic only or calcium level < 8 mg/di for one-gland resection
■ Calcium supplement and calcitriol started immediately post subtotal or total parathyroidectomy
Surgical cure is defined by normal calcium level /not by normal PTH level)

PARATHYROID HYPERPLASIA OR OOUBLE-ADENOMA

o Parathyroid hyperplasia are lobulated, and lack the rim of normal parathyroid gland
which seen in adenomas

o Options for parathyroid hyperplasia /Secondary or Tertiary hyperparathyroidisml:

• Total parathyroidectomy with autoimplantation
'Less recurrence rate•
• Removal of all identified parathyroid glands + Supernumerary gland
• Best for recurrent hyperparathyroidism
• Need for forearm incision for reimplantation into non-dominant
brachioradialis (rather than ipsilateral SCM)

• Subtotal parathyroidectomy
"Preferred option, less post-operative hypocalcemia"
• Resection of 3 and ½ off parathyroid glans + Supernumerary gland
• No forearm incision for auto-transplantation
• Preservation of a viable, histologically confirmed 50 mg remnant
• Inferior gland more preferable to be preserved (easily accessible)
• If adenoma found:
o Adenoma + ipsilateral parathyroid glands are resected
o Normal glands contralateral are biopsied and marked
(If recurrence developed � Only one side will be explored)

o Intra-op PTH

o Frozen section or biopsy from the normal glands after oontralateral exploration are
needed to exclude asymmetric hyperplasia in double adenoma

o Check missing gland location if available

o ± Bilateral neck exploration

 MULTIPLE ENDOCRINE NEOPLASIA SYNDROMES
MENI MEN II A MEN II B
Werner's Svndrome Sinnle's Svndrome
Components Hyperparathyroidism 100% Medullary thyroid cancer 100% Medullary thyroid cancer
Parathyroid hyperplasia Bilateral 100%
Earliest onset and high recurrence Multicentric

Pancreatic tumors 30 - 80% Pheochromocytorna 40 - 50% Pheochromocytoma

Non-functional "Most common" Benign 50% Benign
Functional Bilateral Bilateral

••
- Gastrinoma "Most common• Multicentric Multicentric
Most common site: duodenum

•• Multifocal and multicentric

Malignant (Lymph node, Liver)
20% of gastrinoma have MEN
- lnsulinoma 10 - 15%
Pituitary adenoma 15 - 50%
Prolactinoma "Most common"
Growth hormone. Cushina's disease
Other Facial angiofibromas
features Lipomas
Carcinoid tumors·
Thymus. Bronchi GIT or Pancreas
Gene MENIN
"Tumor suppressor gene"
Autosomal dominant
Chromosome 11
Svmotomatic Hvneroarathvroidism
First to treat Hvneroarathvroidism
Mortality Pancreatic tumor
Morbiditv
Proanosis Better
Management Hyperparathyroidism (Familial, MEN)
Bilateral neck exploration with subtotal
or total parathyroidectomy and
autotransplantation
-1- Bilateral Thymectomy
(Incidence of Supernumerary gland)
Pancreatic tumor
For identified > 2 cm tumor
Distal pancreatectomy (body, tail)
Enucleation of palpable head tumor
Peri-pancreatic lymph node sampling
Duodenotomy and excision
Pituitary adenoma
Bromocriptine "Dopamine agonist"
± Radiation
Trans-sphenoidal resection for:
- Non-prolactinoma
- Compressive symptoms
- Failure of medical treatment
Hyperparathyroidism 20 - 30%
Parathyroid hyperplasia
Mucosa! neuromas
100%
(Marfan's habitus)
"Neurofibromatosis"
Sites: Lip, Tongue, Eyelids
Cutaenous lichen amyloidosis S�!lllllsl '1�f2Dllili!l�
Hirschsprung's disease Pectus exacavatum
Kyphosis
Conoenital hip dislocation
RET prato-oncogene RET proto-oncogene
"Tumor suppressor gene• "Tumor suppressor gene"
Autosomal dominant Autosomal dominant
Chromosome 10 Chromosome 10
Medullarv thvroid cancer Medullarv thvroid cancer
Pheochromocvtoma Pheochromocvtoma
Medullary thyroid cancer Medullary thyroid cancer
Worse Worst
Pheochromocytoma
Unilateral: Unilateral adrenalectomy
Follow-up every 6 - 12 months with metanephrines
Bilateral
Cortical-sparing subtotal adrenalectomy
Bilateral adrenalectomy
Medullary thyroid cancer:
Total thyroidectomy and bilateral central node dissection
Parathyroidectomy done if indicated in the same operation
Progh:,!lactic th)!!:oidectom:,!
MEN IIA: At 3 - 5 years
MEN 11B: 1" year
± Central LN dissection if high calcitonin or positive by UIS
Hyperparathyroidism
Bilateral neck exploration with subtotal or total
parathyroidectomy and autotransplantation
-1- Thvmectomv (Incidence of suoranumerv aland\
OTHERS
■ Most common cause of hypoparathyroidism: previous thyroid surgery

■ Primary hyperparathyroidism t risk of stillbirth if not resected in pregnant women

o Surgery planned in 2nd trimester

■ Parathyromatosis:
o Recurrent or persistent hyperparathyroidism following multiple resections
o Etiology:
• Fracture of parathyroid capsule
• Low-grade parathyroid malignancy
• Overgrowth of embryologic rests of parathyroid tissue

o Managed with serial debulking and phanmacological treatment

■ Very high hypercalcemia associated with:

o MEN-Hyperparathyroidism
o Parathyroid cancer

■ Thiazide and Ringer lactate contraindicated in hypercalcemia

o Alternative: Fursomide after proper hydration

■ Bisphosphonate indicated in refractory hypo.calcemia associated with bradycardia or asystole

 Breast
Reviewed by:

Dr. Mohammed Al Duhileb

BREAST
ANATOMY AND PHYSIOLOGY
■ Breast developed at 5th - 6th weeks of fetal development, from 2 ventral bands of thickened
ectoderm { mammary ridges, milk lines}
o Derived from sweat gland, and composed of 15 - 20 lobes
o Accessory breasts {polymastia) or accessory nipples {polythelia) may occur along the
milk line

■ Breast boarders:
o Superior: 2nd rib
o Inferior: 6th rib (infra-mammary fold}
o �: Lateral boarder of sternum
o Lateral: Anterior axillary line

■ Breast divides into 5 segments:

o 4 Quadrants
• Upper outer quadrant contains greatest volume of breast (most lesions occurred)

o Tail of Spence: extends laterally across the anterior axillary fold

• Contains most of glandular tissue

■ MontgomeN glands:
o Accessory areolar glands (Modified sebaceous glands) to lubricate the nipple during the
breast feeding

■ Cooper's ligaments:
o Suspensory ligaments; divide breast into segments
o Skin dimpling if Cooper's ligament involved (Shorten or distorted)

■ Multi-Focality
o Presence of 2: 2 tumor foci within a single quadrant of the breast (within 4 - 5 cm)

■ Multi-Centricity
o Presence of 2: 2 tumor foci within different quadrants of same breast {4 - 5 cm away)
 Blood Supply
Arterial Source
Internal thoracic (mammary) artery 1" part of subclavian artery
+ Medial side of the breast
lateral branches of posterior 2"", 3"', 4"' intercostal arteries Aorta
+ Medial mammarv arterv {Alona with internal mamman,l
Lateral thoracic artery Axillary artery
+ lateral side of the breast

Thoracoacromial arte~
Venous
Internal thoracic vein
Posterior intercostal veins
Tributaries of the axilla~ vein

• Batson's plexus:
0 Valveless vein plexus extends from the base of the skull to the sacrum
0 Allows direct hematogenous metastasis of breast cancer to spine
0 Other tumors can spread through Batson's plexus: Prostate and Rectal cancers

Lymphatic drainage:

••
■ 97% to axillary nodes (Central and Lateral portions)
2% to internal mammary nodes.(Medial portiion)
Most common cause of primary axillary adenopathy is: Lymphoma (Not breast cancer)

Nerves
■ Motor
Nerve Muscle Associated disorder Arterial sunnlv
MEDIAL BORDER OF AXILLA
Long thoracic nerve Serratus Winged Scapula lateral thoracic artery
Shoulder pain
Examined by making the patient Inability to raise arm above
oushina with extended arms shoulder level
POSTERIOR BORDER OF AXlLLA
Thoracodorsal nerve latissimus dorsi Weak Adduction, internal rotation Thoracodorsal artery
Esoeciallv for swimmino climbino
ANTERIOR BORDER OF AXILLA
Medial oectoral nerve Pectoralis maior and minor
Lateral pectoral nerve Pectoralis major only Pectoralis muscles atrophy
(Wrapping around pectoralis Weakness of shoulder motion
minor)

■ Sensory
th
0 Anterolateral: Lateral cutaneous branches and 3"' - 6 intercostal nerves
0 Upper b reast: Cutaneous branches of cervical plexus
0 Medial arm and axilla· lntercostobrachial nerve
PHYSIOLOGY
■ Estrogen:
o Initiate Ductal development (columnar cells)
o Increases breast size

■ Progesterone:
o Initiate Lobular development
o Differentiation of ductal development
o Lobular hyperplasia happens during pregnancy

■ Prolactin:
o Synergizes estrogen and progesterone
o Synthesis of milk

■ Oxytocin:
o Milk lit down (contraction myoepithelial, compression of alveoli)
TRIPLE ASSESSMENT
1) History
• Systemic symptoms:
o Early satiety, Anorexia, weight loss
o Anemia, fatigue, fever± rigors, lower limb edema, ascites
o Bone pain
o Dyspnea, cough, hemoptysis
o Jaundice
o Fever

• Personal symptoms:
o Current age
o Gender
o Radiation
o Smoking(associated more with periductal mastitis)
0 Alcohol
o Obesity

• Breast symptoms:
o History of the mass and pain
o History of nipple discharge
o LMP and menstrual pattern
o History of prolonged estrogen exposure:
• Age of menarche(< 12 years)
• Age of menopause (> 55 years)
• Drugs(OCPs, or Hormonal therapy) > 5 years
• Number and pattern of pregnancies
• Age of 1'' birth(full-term after 30 years)
• Breast-feeding (Risk factor if< 6 months)
Breast feeding decreases risk of breast CA by decreasing numbers of menstrual cycles

• Family history:
o History of Breast CA or other cancers in family (Most important risk factor)
• (Number, degree relative and age of onset, and age of death)

• Past medical. surgical history

• Allergy and drug history

• Social history

■ GAIL Model to estimate risk of breast cancer includes:

o Race
o Age
o Age of menarche
o Age of 1st live birth
o Number of biopsy specimen including benign or atypical hyperplasia
o Number of 1st degree relatives with breast cancer
2) Examination
• General appearance
• Vital signs
• Systemic examination:
o Abdomen examination
o Chest examination
o Extremities examination

Local examination of the breast:

• Inspect and compare both breasts:
o Positions:
• Ask patient to sit with arms at sides
• Ask patient to press on her hips to contract pectorals
• Ask patient to elevate arm above the head
• Ask patient to lean forward with breast pendulous

o Skin for color and thickness

o Breast for symmetry, size and contour (masses, dimpling, flattening)
o Nipple for size, shape, direction, ulceration, or discharge

• Palpate and compare both breasts:

o Position:
• Ask patient to lie supine on the bed with ipsilateral hand behind the head
• Best pattern for palpation of masses: Vertical strip pattern

o Palpate for consistency, tenderness, nodules

• Nodules: site, size, shape, consistency, tenderness, mobility

o Don't forget to exam the breast tail, nipple-areola, and infra-mammary folds
• Areola examined as radial palpation by index finger to asses discharge

o Examination of axilla and supraclavicular

• Lymph node palpation and comment on: location, size, delimination, mobility,
consistency and tenderness
• Order or groups for examination
• Central group
• Apical group
• Lateral group
• Anterior group
• Delimination:
• Discrete: Non-adherent lymph nodes, can be moved against each other
• Matted: Adherent lymph nodes, due to peri-adenitis, countable
• Amalgamated: Adherent lymph nodes, due to infiltration, non-countable

o Don't forget to exam the: Abdomen, Lumbar spines and Arms

2) Mammogram and US of the Breasts

3) Pathological assessment
SKIN MANIFESTATIONS OF BREAST
■ Skin tethering and dimpling (indentation)
o Indentation happens during lump movement
o Skin tethering (Retraction)
• When lump suited deeply and distorts Cooper ligament
• When lump suited superficially due extension of tumor or fibrosis (Mondor's
disease)
• Not consider as skin infiltration, it is just a warrant sign

o Skin dimpling (Puckering)

• When lump suited deeply due to shortening of Cooper ligament
• Usually after skin tethering

o Causes:
• Traumatic fat necrosis
• Breast Cancer

■ Peau d'orange
o Appears mostly at lower portion of the breast
o Edema of skin between hair follicles due to lymphatic blockage
o Causes:
• Infection
• Traumatic fat necrosis
• Breast cancer

■ Nipple retraction (Inversion)

o Due to fibrosis, calcification
o causes·
• Breast infection
• Breast cancer
• Duct ectasia
• Traumatic fat necrosis
• Pregnancy or Breast feeding
• Congenital

Nipple inversion should be distinguish from primary nipple inversion

(Started since birth and bilaterally in most cases)

■ Eczema-like
o As weep, crust or erode of nipple-areola complex
o Causes:
• Paget disease
• Breast cancer

■ Others:
o Obvious lump
o Redness
o Ulceration
NIPPLE DISCHARGE
■ Causes:
o Most common cause of physiological nipple discharge: Galactorrhea
• Causes:
• Physiological (Lactating or during pregnancy)
• Drugs
o OCPs
o Phenothiazine
o Tricyclic antidepressants
o Metoclopramide

• Pituitary adenoma
o Persistent galactorrhea > 2 years postpartum need to
o Non-lactating female
1 st test: Serum pregnancy, if negative: Serum prolactin level

• Other causes including medication usage and neurogenic stimulation

o Most common cause of abnormal nipple discharge: lntraductal papilloma

• Unilateral > Bilateral bloody or brown discharge

o Second most common cause of nipple discharge: Duct ectasia

• Bilateral > Unilateral bloody or creamy cheesy discharge

o Other causes:
• Breast cancer
• Fibrocystic diseases
• Pregnancy I Breastfeeding
• Breast infection

■ Malignant features of nipple discharge:

o Unilateral
o Spontaneously, Non-cyclic
o Bloody or clear discharge
• Bloody discharge seen in 20% of women in pregnancy and lactation
• Due to hypervascularity of developing breast
• Can be unilateral or bilateral
• Benign and require no treatment

o Arise from single duct

o Associated with mass

■ Management:
o Clear/ Green, Cyclic, Non-spontaneous:
• Reassurance with (cytology not needed)

o Anything else:
• U/S and Mammogram of both breasts and manage accordingly
• ± Ductography
BENIGN BREAST DISEASES
■ ANDI classification:
o Disease: Fibroadenoma > 3 cm, Atypua
o Disorder: Fibroadenoma 1 - 3 cm, Nipple inversion/ retraction, Bloody discharge
o Normal: Fibroadenoma < 1 cm, Nipple eversion

1) NON-PROLIFERATIVE BREAST LESIONS

o The most common non-proliferative breast lesions is Breast Cyst
o Derived from terminal duct lobular unit
o Types:
• Breast cysts
• Fibroadenoma

o No risk of malignancy

o Types of breast cyst:

• Simple
• Conservative
• Aspirate only if symptomatic (Most common lesion associated with pain)
c:> Rule: Aspirate , Aspirate, Excise
c:> Interval: 6 months
c:> Re-examination for residual mass after aspiration
c:> Cytology is needed for bloody aspirated fluid only

• Complex (Irregular border, associated with solid components)

• Core biopsy from solid component {to rule out DCIS}
• Malignancy associated with breast cyst is: Mucinous cancer

• Galactocele
• Round, well circumscribed, mobile, milk-filled cyst
• Occurs after or during cessation of lactation
• May occurs 6 - 12 months after breastfeeding
• Usually located in the central portion of the breast
• Pathophysiology:
c:> Ruptured alveoli containing milk, after ductal obstruction

• Aspiration:
c:> Thick, creamy material that may be tinged dark green or brown

o Indication for excisionof breast cyst:

• Symptomatic or infected
• Complex (Residual mass after aspiration)
• Bloody aspiration (Straw-colored is not an indication for excision)
• 3rd Recurrence
2) FIBRO-EPITHELIAL LESIONS (Proliferation without Atypia}
o No risk of malignancy (although some references agree for minimal 2-fold risk)
o Types:
• Ductal hyperplasia
• Mild ductal hyperplasia: 3 - 4 cells above basement membrane
• Moderate ductal hyperplasia: 2: 5 cells above basement membrane

• lntraductal papillomas

• Sclerosing adenosis
• Most common pathologic diagnosis in patients undergoing biopsy of
microcalcifcations
• May presented as mass and mimics malignancy
• Adenosis: Increased number of small terminal ductules or acini
• Proliferation of stromal tissue produces -+ Sclerosing adenosis

• Radial scars
• Originate at sites of terminal duct branching
• May presented as mass and mimics malignancy
• Pathology:
� Irregular spiculated masses with prominent architectural distortion
c:> Stellate arrangement of ductal structures
� Central fibroelastic core

o Imaging:
• Mass density with spiculated margins (Radial scar or sclerosing adenosis) ±
Benign calcifications (microcalcifications)

o Histolo gy:
• Proliferative (ductal proliferation)
• lnvolutional (stromal fibrosis, epithelial regression)

o Management:
• Follow-up as screening
• Avoid nicotine, caffeine, and alcohol, and Ibuprofen regular for 2 - 3 weeks
3) INTRA-DUCTAL HYPERPLASIA (Proliferation with Atypial
o Risk of malignancy increased by 4-fold
• Increased by 9-fold if associated with strong family history of breast cancer

o Types:
• Atypical Ductal hyperplasia (ADH)
• Atypical Lobular hyperplasia {ALH)

o Have some features of DCIS or LCIS "DCIS is an ADH > 3 mm"

o ADH, ALH, LCIS are markers for breast cancer of both breasts (Not pre-malignant)
• DCIS is pre-malignant lesion
• LCIS / DCIS increased risk of malignancy by 10-fold

o Management:
1} Excisional biopsy to confirm the diagnosis and to rule out DCIS
2) Definitive management options:
• Observation
• Tamoxifen for 5 years
• Prophylactic bilateral mastectomy
BENIGN BREAST DISEASES
■ Congenital breast diseases:
o Neonatal breast enlargement: Due to circulating maternal estrogens

o Accessory nippl es: Most common breast anomaly

o Accessory breast tissue (polythelia}: Most common location is axilla

■ Mastodynia (Mastalgia):
o Cyclic pain: Decreased or disappears after menopause or during pregnancy
o Non-cyclic pain: Musculoskeletal in origin
o Most common location: Upper outer quadrant

o Risk factors: Caffeine, nicotine, methylxanthines.

• Fibrocystic disease -+ Cyclic mastodynia
• Infection -+ Non-cyclic mastodynia

o lovestjgatjon·
• Bilateral mammogram to exclude malignancy in non-cyclic pain

o Treatment:
• Danazol (Synthetic steroids)
• Side effects: Amenorrhea, acne, Hirsutism, Weight gain and Deep voice

• Evening primrose oil

• Tamoxifen up to 5 years
• OCPs
• NSAIDs

■ Mondor's disease
o Superficial vein thrombophlebitis of breast ( Cord-like)

o Associated with trauma, usually in lower outer quadrant

o Other sites:
• Brachia!
• Femoral
• Calf veins
• Dorsal vein of the penis

o Treatment:
• NSAIDs
• Restrict arm movements
• Warm compression
 ■ Traumatic fat necrosis
o Mimic carcinoma even in skin tethering & nipple retraction (No risk of malignancy)
o A history of trauma alone is not diagnostic
o Risk factors
• Breast reduction surgery
• Breast irradiation
• Post-operative or post-traumatic breast hematoma

o Imaging:
• Oil cyst, Circumscribed spiculated mass of mixed soft tissue and fat with
calcified rim and calcifications or microcalcifications, and architectural
distortion

o Pathology:
• Fragments of degenerate necrotic adipocytes with loss of nuclear staining
• Lucent-centered with coars.e calcifications
• Foamy macrophages with multiple nucleoli giant cells
(Lipid-laden macrophages)

o Management·
• Regress spontaneously
• Excisional biopsy is needed to diagnose in absence of trauma history or
atypical radiological finding

■ Breast abscess:
o Due to blockage of engorged lactiferous ducts + milk stasis
o Mostly at upper outer quadrant
o Classified as:
• Lactational: Related to S. aureus
• Non-Lactational: Usually multi-bacterial

Lactating Non-Lactating

I I
Normal skin Pathological skin
Small abscess < 5 cm Persistent abscess Repeated needle
t t aspiration

Needle or UIS-guided aspiration Incision & Drainage Incision & Drainage

(Can be repeated twice) + Tissue biopsy + Tissue biopsy
"risk of milk fistula" + Antibiotics
Continue breastfeeding Antibiotics
Continue breastfeeding
Milk fistula: between the skin and a lacliferous duct, resolve spontaneous with cessation of lactation
 ■ Duct ectasia
o Presented with nipple discharge, subareolar mass, mammary duct fistula, and
Nipple retraction "due to peri-ductal filbrosis"

o More common in smokers, (No risk of malignancy)

o Characters of nipple discharge

• Serous or serosanguineous "Creamy cheesy"
(Color ranged from yellow to blue-green brown)

• Mostly bilateral, and could be unilateral

0 Pathology:
• Dilatation of breast ducts
• Periductal inflammation
• Plasma cells

o Management·
• Usually resolves spontaneously

• Surgery indicated in persistent or recurrent symptoms or associated with

persistent cyst
• Microductectomy in single localized duct
• Complete duct excision for multiple or non-localized duct

o Management of recurrence peri-ductal subareolar mastitis: (Zuska's disease)

• Antibiotics for 2 - 4 weeks before total duct excision

• Incision and drainage

Fistulectomy and primary closure Total duct excision

(Preferred initiallv)
Youna ru>tient
Small abscess localized to 1 S""ment
Recurrence involvinQ same seQment
No discharae from other ducts
No orior fistulectomv
No or mild nioole inversion
Patient unconcerned about ninnle inversion
Elderlv oatient
Larae abscess affect > 50% of areolar circumference
Recurrence involvinQ different seamen!
Purulent discharae from other ducts
Recurrence after fistulectomv
Marked nioole inversion
Patient reauests correction of ninnle inversion
■ Granulomatous mastitis
o Chronic inflammatory breast disease, and may recur
• Tuberculosis (acid-fast bacilli)
• Sarcoidosis

o Associated with painful mass and inflammation ± fistula ± abscess

o Radiologic findings are similar to breast cancer

0 Pathology:
• Non-caseating granulomas, chronic inflammation, giant cells and micro-abscess
confined to the lobule

o Management options:
• Core biopsy to rule out associated diseases
• Observation and reassurance
• Antibiotics
• Prolactin-lowering medications
• Steroids
• If persistent (May associated with autoimmune or connective tissue
diseases)

• Incision and drainage if associated with abscess

• Surgical excision for steroid-refractory disease

■ lntraductal papilloma:
o True polyps, Bloody nipple discharge

o Not premalignant and no risk for cancer (unless associated with atypia)
• But you have to rule out invasive papillary carcinoma

o Unilateral in 75% of patients (Bilateral in 25%}

o Cytology � Ductal cells

o Types:
• Central
• Peripheral (greater incidence of malignancy)

o Management·
• U/S and Mammogram bilateral

• Ductogram used for localization if failed to be seen by U/S or Mammogram

• Wire-guided subareolar major duct excision

Patient will lose the ability of breast feeding
FIBROAOENOMA
■ Most common breast lesion in adolescents and young women; 10% multiple
■ From hyperplasia of single Lobule
■ Painless, slow growing, well circumscribed, firm, and rubbery
■ Not associated with increased risk of malignancy
■ Giant fibroadenoma when size > 5 cm
■ Fibrocystic disease associated with high estrogen level
o Pathology: Adenosis with apocrine metaplasia

■ Investigations:
o U/S or Mammogram + Core Biopsy
• Hypoechoic mass with posterior enhancement
• Coarse calcifications (popcorn lesions)

■ Pathology of fibroadenoma:
o Firm, Lobulated, with ductal and stromal fragments as whorl-like pattern, with
projections of epithelial cells

■ Management oot;ons·
o Observation and Follow up every 6 months with U/S and clinical examination
o Indications for resection:
• > 3 cm or increasing in size
• Symptomatic (Pain, discomfort or anxiety)
• Increased cellularity on biopsy
• Change characters on U/S

■ Indications tor Excjsional biopsy £no need forNegative margin)·

o ADH/ALH
o LCIS
o Papillary lesions
o Radial Scar (Sclerosing adenosis not an indication)
o Atypia
o Suspicious (BIRADS IV I VJ
CYSTOSARCOMA PHYLLODES
■ Presented with very large and rapid growing mass ± skin erosions at perimenopausal age
■ 10% are malignant, with hematogenous spread
■ High risk of recurrence in 10 - 20% of patients with benign phyllodes (50% in malignant)

■ Usually benign tumor with increasing of:

o Mitotic activity
o Stromal hyperplasia
o Nuclear pleomorphism

■ Imaging:
o Similar to fibroadenoma
o Lobulated leaf-like 5 cm mass± calcifications± necrosis

■ Pathology:
o Stromal and epithelial elements (mesenchymal tissue}, and spindle cells
o Malignant phyllodes degenerates into sarcomatous lesions with non-epithelial elements

■ Pathology needed to differentiate between benign and malignant:

o Benign: Fibrosarcomatous elements
o Malignant: Liposarcomatous or rhabdomyosarcomatous elements
Associated with increase mitotic activity > 5 - 10 mitosis per HPF

■ Most common site of metastasis in malignant phyllodes: Lung

■ Treatment
o Wide local excision with 1 - 2 cm negative margins
• Used for small size phyllodes (benign and malignant)

o Simple mastectomy
• Used for phyllodes of large size with respect to size of the breast
• Used for high-grade phyllodes

o Radiotherapy to the breast

• For all patient underwent wide local excision

o Radiotherapy to the chest wall

• Indicated for all malignant phyllodes
• Involving fascia or chest wall
• Very large > 5 cm
• Recurrence
• Unable to obtain negative margins or closed margins
SCREENING
■ Clinical:

o Breast self-examination
• Started at age of 20, done monthly, 5 -10 days after cycle for premenopausal
• Done at same date every month for postmenopausal women
• Not recommended recently by most guidelines (Increases false-positive rates)
• Has value for mammogram occult lesions, and to be first identification method

o Clinical breast examination

• Done every 1 - 3 years from 2 5 years
• Done annual after age of 40 years
• Every 6 months at age of 25 years in patients with BRCA mutation

■ Imaging:

o Mammogram
• Radiation dose of 0.1 cGy per study (equal 4 chest x-ray}
• 2: 5 mm for the lump to be detected
• 10 - 20% Palpable, but not detected by mammogram
• 10 - 50% Detected by mammogram, not palpable ➔ 25% is malignant
• Routine mammography decreases mortality from breast cancer by 33%
• Guidelines:
• Started at 40 years or 10 years before earliest case, then annual

No mammography in patients < 40 years (Dense parenchyma)

• Standard views of mammography:

• Cranial-Caudal (CC): best for medial area
• Mediolateral-Oblique (MLO): best for upper outer and axillary areas

• Advantage of Mammogram:
• Calcifications, Lymph node status, Multicentric, and Multifocal

o Ultrasound
• Used for screening in patient < 40 years
• Advantage of U/S:
• Cystic vs. Solid, Size of mass, Lymph nodes features

UIS is needed for any abnormal results in mammogram

Mammogram is needed for any abnormal results in UIS

Maliqnant features on Mammoqram Malianant features on Ultrasound

Soiculation Thick caosule
lrreaular borders Incomplete Halo
Hvnoecho=nicitv Non-comoressible
Microcalcification / Microlobulation Heteroaeneous or irr=ular borders /Ill-defined)
Anaular mamins Hvooechoaenicitv
Duct extension "Taller (dee=r\ -than -wide" nodule
Posterior acoustic shadow "Not Enhancement"
Hiah acoustic attenuation
 o MRI
• Low specificity {Associated with f false-positive results and mastectomy)
• Screening tool for high-risk patients
-+Annual, started at age of 25 years in BRCA mutation patients

• Indications of MRI of breasts:

As Screenina tool As Diaanostic tool

BRCA positive BRCA positive with malignancy for contralateral breast
Breast implant Breast implant with malignancy
Screening of contralateral occult breast diseases for Metastatic axillary lymph nodes with no primary breast
new breast malignancy lesions detected radiologically
History of chest radiation Equivocal mammogram
•• Cowden syndrome
li-Fraumeni syndrome ••
Pre-ollerative evaluation of high-risk llatients:
Invasive Lobular cancer
Planning for Breast-Conserving Surgery

•• 0 Post-BCS with positive margins

Dense breast

• Extensive DCIS

• ADH or ALH with a mass

Extent of the disease

Bl-RADS {Breast Imaging Reporting and Data System)

Cateaorv Descriotion Risk of malianancv Recommendation

0 lncomolete studv 0 10% Reoeat / r=uest another imaoe
1 Neqative 0-0.1% Routine screeninq
2 Benian findinas 0-0.1% Routine screenina
3 Probably benign findings <2% Mammogram every 6months/ 2years
Bioosv for oaloable mass
4 Susoicious 20-50% Excisional biopsy
5 Hiahlv susoicious of malianancv 60-90% Excisional bioosv. follow the treatment
6 Malinnant lbioosv orovenl 100% Follow the treatment

■ Indications for genetic counseling

o Pedigree score of ;? 8
o Strong family history of breast or ovarian cancers
o Breast cancer under age of 45
o Triple negative under age of 60
o Personal history of ovarian cancer at any age
o Male breast cancer

Ped igree Tool Score

Risk factors
Breast cancer at aae ;? 50 vears 3
Breast cancer at aae < 50vears 4
Ovarian cancer at anv a= 5
Male breast cancer at anv aae 8
Jewish 4
BIOPSY
■ Fine-Needle Aspiration (FNA):
o Obtains Cells only (Can't obtain receptors status}
o Should be avoided to diagnose breas .t cancer
o Used for:
• Axilla: Metastasis to lymph node
• Breast tissue: Recurrence or Metastasis

■ Core biopsy:
o Obtains Cells + architecture
o Best for breast tissue for assessment of:
• Cellular type(Ductal vs. Lobular} and grade
• In-situ and invasive tumors, and % of DCIS
• Receptors status "ER/PR and HER"
• Lymphovascular invasion
• Multifocal / Multicentric lesions
• Mitotic index(> 2 is aggressive) and Ki67 (Nuclear cellular proliferation)
• Low Ki67 -+ Lesser benefits of chemotherapy

o Types:
• Blind (Tru-Cut)
• US-guided
• Vacuum-Assisted: Multiple tissue sampling {good for calcifications}
• MRI-guided
• Stereotactic: Mammogram-guided
• Used when there is no mass
(only microcalcification or architectural distortion)

• For Mammogram findings that not visualized on U/S

■ Excisional biopsy {without negative margins)

o Indicated after failure of biopsy to obtain microcalcification seen by image
(Normal epithelium or fatty tissue)

■ Skin punch or wedge biopsy

o Indicated when worrisome skin or nipple changes even in normal imaging

Marker should be placed for each biopsy under image guidance for further inte,vention or radiation
{clip is alternative for excisional biopsy)
DUCTAL CARCINOMA IN SITU (DCIS)
■ lntraductal carcinoma is term applied to DCIS
■ Malignant cells of the ductal epithelium without invasion of basement membrane
■ Appears as Microcalcifications and may extend beyond that area on mammography
■ Most aggressive type: Comedo (Multicentric, Central necrosis)
■ Pathology:
o Proliferation of the epithelium, papillary projections
o Hyperchromasia (Clumping of chromatin)
o Nuclear crowding and Loss of polarity (cribriform growth pattern)
o Prominent nucleoli with poorly cohesive intact cells
o No pleomorphism, mitoses, atypia or invasion
o Calcium deposition in necrotic area

■ Premalignant lesion (lntra-ductal carcinoma)

o 50% developed into invasive ductal carcinoma in 10 years (lpsilateral breast)

Necrosis Nuclear grade DCIS grade

Comedo -�E�xt� e�ns� �w�e___,H'-"igh High
Intermediate Focal Intermediate Intermediate
Non-Comedo: Absent Low Low
Solid, Cribriform, Papillary

Management:
■ 45% recurrence rate for lumpectomy only without XRT
■ 20% incidence of invasive breast cancer on final pathology report
■ Tamoxifen is used for 5 years in (ER/PR+} t.o decrease the recurrence risk
■ Chemotherapy is not indicated as there is no invasion of the basement membrane
■ Surgical options:
o Breast-conserving surgery (BCS) "Lumpectomy with negative margin and post-op XRT'
• For localized DCIS with acceptable negative margins of 2 mm at least

o Breast-conserving surgery+ SLNB

• Suspicious of IDC (Palpable mass, at axillary tail, or micro-invasion)
• SLNB done post-operatively when final pathology show invasion (20%)

o Total (Simple) mastectomy+ SLNB (Associated with lowest recurrence)

• Contraindicated to use radiotherapy
(Pregnancy, connective tissue diseases, history of radiation)
• Persistent DCIS after BCS
• Extensive DCIS: (BCS also an appropriate option)
• > 4 cm or > 25% of the main tumor
• High nuclear grade± Necrosis
• Multicentric (> 1 quadrant)
• Unable to obtain negative margins

■ SLNB indicated during mastectomy due to difficulty to do it post-operatively

(Lack of breast tissue to trace lymph node)

■ If SLNB not done during mastectomy, and final pathology showed invasion
� Axillary lymph node dissection (Inability to do SLNB)
LOBULAR CARCINOMA IN SITU (LCIS)
■ Originates from terminal duct lobular units (Found only in female)
■ Not premalignant lesion
■ Considered a marker for breast cancer
o Malignancy can happen anywhere in both breasts, but not the site of LCIS lesion
o 70% are Invasive DUCTAL Cancer
o 25- 35% get cancer, need for excisional biopsy to confirm the diagnosis
• Core biopsy is not enough, and excisional biopsy is needed

■ On examination:
o Not palpable (Asymptomatic)

■ On imaging:
o No calcifications
o Not detected radiologically
o Associated with:
• Neighborhood Calcification on mammogram
• Calcifications without Pattern

■ Jnyasjve Lobular cancer on pathology·

o Indistinct mas with poorly defined borders and infiltrating cells in linear arrangement
which might grow circumferentially around ducts and lobules
o No calcifications, No mass

■ Investigation:
o Excisional biopsy is indicated to rule out associated malignancy and to confirm the
diagnosis

o No need for negative margin (except for pleomorphic LCIS to rule out DCIS)

■ Treatment options:
o Observation and mammogram every 6 months
+ Tamoxifen "Raloxifene is better" (Chemoprevention) for hormone positive receptors
'Best option"

o Bilateral simple mastectomy (no ALND)

• For patients with family history of breast cancer

LCIS DCIS
Incidence 5% 10%
Gender OnlvFemale 95% Female. 5% Male
Age 45 years 55 years
IPremenonausan IPostmenonausall
Axillarv metastasis 1% 1%
Mammoaram None Microcalcifications
Multicentricitv 60- 90% 40-80%
Laterallty Bilateral 60% Unilateral 85%, Bilateral 15%
Lateralltv as subseauent Ca. Bilateral losilateral
Incidence as subseauent Ca. 25% 50%
BREAST CANCER
■ 10% of breast cancer have Negative mammogram, and Negative ultrasound
■ Tumor marker: CA 15-3, and CEA
■ Most common symptom: Asymptomatic
■ Most common site for metastasis: Lymph nodes.
■ Most common site for distant metastasis: (1) Bone (2) Lung (3) Pleura (4) soft tissue (5) Liver
■ Symptoms of metastasis: back pain, jaundic ,e, and headache
■ Most important prognostic staging factor: Lymph nodes

ADENOCARCINOMAS (> 90%}

o Ductal type
• 85% of all breast CA, Positive(+) E-Cadherin
• Includes:
• DCIS, Invasive ductal carcinoma, and Paget's disease

• IDC subtypes: "Papillary, Tubu�ar, Mucinous cribriform, and solid"

• Tubular (Columnar lesions with stromal invasion} has better prognosis
� Lumpectomy + SLNB

• Cribriform (Hyperchromatic nuclei, Punched-out spaces "Swiss cheese"}

� Lumpectomy alone

• Mucinous has good prognosis(associated more with breast cyst}

• Medullary has Lymphoplasmacylic reaction(Lymphoid cells) and

vesicular cells within tumor with benign features on U/S and better
prognosis "low risk of lymph node metastasis" with high mitotic rate and
poorly differentiated

o Lobular type
• Usually Bilateral, Multifocal, and Multicentric
• Positive ER receptor in 90%, Negative(-) Cadherin "No mass"
• Includes:
• LCIS, and Invasive lobular carcinoma

• Imaging:
• Asymmetric density on mammogram

• Pathology:
• Indistinct mas with poorly defined borders and infiltrating cells in linear
arrangement which might grow circumferentially around ducts and lobules
No calcifications, No mass

• Patient need MRI due to diffuse calcifications of the breast

• Associated with difficulty to detect metastasis on SLNB or frozen section
• Management options: (as invasive ductal carcinoma)
• Breast conservative surgery(Lumpectomy + radiation} + SLNB
• Total mastectomy + SLNB± Chemotherapy± Hormonal therapy
 o Inflammatory breast cancer
• Considered T4d disease or Stage 111B
• Adenocarcinoma in dermal lymphatics is diagnostic
• Criteria for diagnosis:
• Rapid onset erythema ± Peau d'orange (Lymphatic obstruction} in less
than 6 months
• Erythema covers 1/3 of the breast size
• Biopsy shows invasive carcinoma

• Management: Neoadjuvant chemotherapy, MRM then Chemoradiation

• Neoadjuvant chemotherapy associated with better survival
• Patient response re-assessed after the neoadjuvant chemotherapy
o Response: MRM followed by radiotherapy
o No- Response: radiotherapy followed by MRM if respond

Radiotherapy include radiation to the chest wall, axillary, supraclavicular, and internal
mammary nodes

o No special type (NST)

• Have worse prognosis

NON-ADENOCARCINOMAS (2 - 5%)
o Malignant phyllodes
o Sarcomas
o Squamous cell carcinoma
o Lymphoma
■ Paget's disease
o Intra-dermal cancer cells of nipple-areola complex '"Carcinoma in situ"
o Presented with chronic, eczematous eruption of the nipple and scaly skin lesion
o 95% associated with breast mass, Not associated with Peau d'orange
o Pathology:
• Resemble DCIS
• Large cells with pale cytoplasm and prominent nucleoli

o Can be differentiated between melanoma by:

• Positive CEA
• Positive mucine
• Negative S-100 antigen
• Vacuolated cells (Pathognomonic)

o Best to differentiate between Paget's and Inflammatory Breast Cancer:

• Wedge biopsy of the skin or nipple

o Management Options:
Should be resected (Due to underlying malignancy 25 - 30%)

• Central lumpectomy (Resection of nipple-areola complex) ± XRT

• For Paget's with No DCIS, No mass
• For Paget's with Retro-areolar Mass or OCIS
• Indications for SLNB: In IOC or OCIS with:
o Palpable mass
o Located at axillary tail
o Micro-invasion

• Simple mastectomy (No SLNB)

• For Paget's with peripherally located OCIS
• No suspicious signs of invasion
(Palpable mass, Located at axillary tail, Micro-invasion

• If discovered invasive cancer post-mastectomy

� Axillary lymph node dissection (Inability to do SLNB)

• Total (Simple) Mastectomy+ SLNB (Most preferred procedure for all Paget's)
• For Paget's with invasive ductal carcinoma
• For Paget's with extensive DCIS or suspicious of invasive cancer:
o Palpable mass
o Located at axillary tail
o Micro-invasion

• Modified radical mastectomy

• For Paget's with invasive ductal carcinoma with Positive nodes
BREAST CANCER GENES
■ BRCA mutation /Tumor suppressor genes)
o Breast cancer is: Sporadic 70%, Familial 25%, Hereditary 5%
o Breast cancer associated with BRCA have same prognosis to patient with non-BRCA

■ BRCA I(Ch. 17}

o Most common hereditary cause of breast cancer
o Female breast cancer: 60 - 70%
o Associated Cancers:
• Ovarian cancer40%
• Colon and Prostate cancer
o Associated with hormone negative receptors (Worse prognosis}

■ BRCA II (Ch. 13)

o Most common genetic cause of breast cancer (Most common overall)
o More common associated with breast cancer(> 60 %}
o Female breast cancer: 60 - 80%
o Associated with Male: 6%
o Associated Cancers:
• Melanoma
• Ovarian cancer 20%
• Gastric cancers
• Pancreatic, gallbladder and bile ducts cancers
• Prostate

■ Other genes: CHEK2, STK11, PALB 2, PTEN, ATM, TP53

Test the affected members of the family first (before the patient) with BRCA for any mutations, then
test the screening members for that specific mutation only

■ Options for patients with BRCA mutation

o Prophylactic bilateral mastectomy
o Continue Surveillance
• Clinical breast examination every 6 months
• Imaging screening yearly, at age of 25 years

o Prophylactic bilateral oophorectomy

• After complete childbearing (Ti me of menopause}
• Reduces the risk of breast cancer by 50%
• Reduces the risk of ovarian cancer by 98%
RECEPTORS

■ ER/PR receptors
o Receptor-positive tumors have better prognosis than negative receptors
o Receptor-positive tumors are more common in postmenopausal women
o Progesterone receptors have better prognosis than estrogen receptors

■ HER2/neu: "Human epidermal growth factor" Proto-oncogene

o Designed as CD340 (Cluster of differentiation}, and Erb-2 protein
o HER2 (+) have worse prognosis, and more to be metastasized (Opposite to ER/PR}
o Not hereditary, and overexpressed in 25% of all breast cancers
o Tyrosine kinase receptor, blocked by Trastuzumab (Herceptin}
• Humanized monoclonal antibody against Erb-2 protein
• Dose:
• Loading dose: 8 mg/kg UV / 90 min
• Maintenance: 6 mg/kg IV every 3 weeks for 52 weeks (1 year only)

• Side effects:
• Cardiotoxicity (Decreased Left ventricular EF)
• Fetal risk
• GI symptoms
• Rush and edema

■ EGFR "Epidermal growth factor"

o Related to acquired Tamoxifen resistance
o Lapatinib is dual tyrosine kinase inhibitor that target HER2 and EGFR

■ VEGF: "Vascular endothelial growth factor"

o Blocked by Bevacizumab "Angiogenesis inhibitor"
• Used in metastatic colorectal cancer, and breast cancer
• Side effect: Hypertensjon

■ E-Cadherin:
o lntercellular adhesion molecules (Positive in Mass-forming cancers}
o Presented in ductal type only

BREAST CANCER-RELATED RECEPTORS

ER PR HER2 Ki67 Prognosis Response to Response to

endocrine therapy chemotheraov
Luminal A (50%) HiQh + :I: - < 14% Best HiQh low
Luminal B (20%) low+ + :I: > 14% Worse low Hioh
HER2-enriched - - + Worse Response to anti-HER2
Higher response to dual therapy
/Chemotheranv + anti-HER21: 65%
Basal-like - - - Worst Most response to chemotherapy
fTriole neaative>
HORMONAL THERAPY
Postmenopausal:
■ Aromatase inhibitor (to prevent peripheral conversion to estrogen}
o Examples: Letrozole, Anastrozole, Exemestane
o Increased risk of osteoporosis, myalgia, and arthralgia
o No DVT risk
o Decrease the incidence of contralateral breast cancer in postmenopausal
o Not used as chemoprevention for premenopausal due to intact ovarian function

Premenopausal:
■ Tamoxifen (Competitive inhibitor: Selective Estrogen Receptor Modulator}
o Decrease the recurrence of breast cancers (up to 50%)
o Decrease the incidence of DCIS I LCIS
o Improve the survival in IDC only
o Used mainly for premenopausal, and few study suggested to started for 1 - 2 years for
postmenopausal before starting aromatase inhibitor

o Dose: 20 mg/day for 5 - 10 years

• Increases risk of:
• Uterine & Endometrial cancers 0.2% � 1.6%
• Thromboembolic events (DVT - PE}< 3%
• Sarcoma
• Stroke
• Cataract
• Bone fracture

• Decreases risk of: Osteoporosis

• Contraindications:
• Pregnancy
• Liver failure
• DVT / PE events (Raloxifene is alternative)
o Raloxifene maintained 76% of the efficacy of tamoxifen to prevent
recurrence of inv.asive cancer
o Raloxifen is given only for post-menopausal women
o Doesn't showed decrease of the incidence of DCIS / LCIS

Hormonal therapy can be given during radiotherapy treatment

Hormonal therapy can't be given during chemotherapy treatment (Counteract each other)

Hormonal therapy alone is appropriate for patients with local invasive ductal cancer who is non­
operative candidate (> 70 years, with multiple co-morbidities)
BREAST CANCER STAGING

Staqe TNM Description

Staae O Tis Carcinoma in situ "DCIS, LCIS, Paaet's"
Staqe 1 T1 s 2 cm

2A T2 2-Scm
Stage 2
2B T3 >5cm

3A N2 Fixed matted nodes or 4- 9 LN

Axillarv or internal mammary (IM) nodes

3B T4a Extension to chest wall

T4b Extension to the skin
T4c Extension to chest wall and skin
Stage 3
T4d lnflammatorv breast cancer

3C N3 > 10 LN
Axilla and IM nodes
Supraclavicular I lnfraclavicular

Staae 4 M1 Distant metastasis

Remember: any Stage + N1 � Upgrade to the next stage
Example: T1 + N1 (< 4 ipsilateral mobile axillary lymph nodes) = Staqe 2A "Size S 2 cm"

■ Metastatic work-ups

Indicated for <? Stage Ill or symptomatically suspicious

o CBC, Liver enzymes and calcium level

o CT Chest/Abdomen/ and Pelvis with IV contrast
o Bone scan
o Brain CT, indicated only in:
• Positive(+} HER2/Neu
• Triple Negative(-)
• Symptomatic (Headache, Blurred vision, or Seizure)
SENTINEL LYMPH NODE BIOPSY (SLNB)
■ Sentinel node: 1"' node in the axilla to receive lymphatic drainage from breast
o Reflect the status of axilla in 97% (8 - 12% false-negative rate)
o SLNB used for staging only (not for control as ALND)
o The ideal numbers of SLN: 2 - 3 nodes

■ Indications:
o IDC: Node-negative T1 - T2
o DCIS:
• Plan for mastectomy
• Suspicious of invasive cancer

■ Relative indications:
o Selective T3

-�
o Mullifocal, or multicentric
o Prior radiation therapy or prior breast/axilla surgery (Controversial}

o Methylene blue, Lymphazurin blue dye, or lsosulfan blue dye

o Associated with type I hypersensitivity and anaphylactic shock
lsosulfan blue dye associated more with anaphylactic shock and false oximetry reading
Patient must be informed that urine may tums into blue, due to blue dye

■ Contraindications:
o Clinically positive nodes
o Inflammatory breast cancer
o Pregnancy
• Options: MRM, UIS guided FNA, After delivery (if 3rd trimester}, or Technetium
• Never use blue dye (Due to anaphylactic shock and teratogenicity}

Accuracy of SLNB doesn't affected by neoadjuvant systemic therapy

■ For patient with early breast cancer <T1 - T2) and clinically negative lymph nodes who are
found to have positive < 3SLNB without extra-capsular extension:

o AMAROS trial:
• Showed no difference in survival for patients assigned to radiotherapy without
axillary dissection comparing to axillary dissection

o ACOSOG 20010 trial:

• Showed that axillary dissection is not required for patient who agreed to complete
whole breast radiation and adjuvant systemic therapies
SLN IDENTIFICATION
■ By blue dye:
o Any blue node or any non-blue node with a blue afferent lymphatic
o Incision is made below hair line

■ By radioactivity: (Sulfur colloid)

o Remove of all SLN with highest count, and > 10% of most radioactive node
o Incision is made over the hot nodes

Highest sensitivity "99¾" if combined both "blue dye and radioactive material"

20¾ of patients with non-palpable cancer had axillary metastasis

50¾ of patients with palpable cancer had axillary metastasis

■ Complications of SLNB:
o Anaphylaxis
o Seroma
o Nerve injury
o Failure of SLNB
o Need to conversion of ALND (With complications of ALND)

LYMPHOSCINTIGRAPHY (sentinel lymph node mapping)

■ Standard in melanoma, Controversial in breast
■ The dose is higher in breast cancer
■ By injecting radioisotopes:
o Intra-dermal "Tc-99m" for 15 - 30 minutes before mapping

■ Performed using a gamma camera to identify areas of increased radioactivity

■ Lymphoscintigraphy at minimal dose is alternative for blue dye in pregnant patients

AXILLARY LYMPH NODES DISSECTION (ALND)
■ ::: 1 O lymph nodes are needed for proper ALND

■ Dissection for Level I and II only (take level Ill nodes "Supra/infra clavicular" if involved)

■ Indications:
o Positive nodes (With no plan for neoadjuvant chemotherapy or after chemotherapy)
o Positive SLNB
o Failure of SLN mapping (No blue dye or tracer on SLN)
o Invasive cancer discovered post total mastectomy with no SLNB
o ::: T4 breast cancer
o Occult breast cancer
• Axillary metastasis without bre .ast lesion
• Investigation:
• Bilateral U/S and Mammogram
• Bilateral breast MRI
• Whole body image (CT CAP, PET scan)
• FNA, Core biopsy, Excisional biopsy
• lncisional biopsy (for matted, adherent to major vascular structures)

• Management:
• Modified radical mastectomy± Neoadjuvant chemotherapy (Best option)
• Axillary lymph node dissection
± Whole-breast radiotherapy and follow-up of the breast
± Hormonal therapy

■ Not indicated it negative SLNB ioclvdes·

o Histological evidence of isolated tumor cells (ITCs)
• ITCs: < 0.2 mm
• Located in lymphatic sinuses, No malignant activity (No proliferation, no
stromal reaction), and Nlo recurrence risk
• Micro-metastases 0.2 mm - 2 mm
• Located outside the lymphatic sinuses, "in the nodal tissue"
• No need for further action in solitary, ALND if 2: 2
• Macro-metastases > 2 mm -+ Need for ALND

■ Complications:
o Lymphedema (13 - 20% in ALND) and (2% in SLNB}
o Lymphangiosarcoma
o Nerve injury
o Shoulder weakness
i
15%
o Loss sensat on posterior upper arm (Most common)
The only sacrificed ne,ve (not preseNed) in ALND: lntercostobrachia/ nerve
 ■ Axillary groups of lymph Nodes:
Levels 13\ Grouos 16\ Vessel Receive from
Level I Lateral (axillary or humeral) Medial or posterior to Most upper extremity
/Lateral to (Jectora/1s minor) axillarv vein
Anterior Lateral thoracic vessels Lateral breast
lnectoral or extra-mammarv\ 1" node to receive
Posterior (subscapular) Subscapular vessels Posterior neck, trunk
and shoulder
Level II Central All of the other groups
/SuoerficlaVdeeo to oectora/is minor)
Rotter's Thoracoacromial
(inter-pectoral node between vessels
maior and minorl
Level Ill Apical Central node
(Medial to pectoralls minor muscle) (sub-clavicular)
linfra-clavicu/ar\
■ Recurrence:
o Breast Cancer:
• 20% recur as local cancer, 60% as distant metastasis and 20% both

o Axillary lymph nodes metastasis:

• 30% in Negative nodes and 75% in Positive nodes

o Di stant metastasis
• ER Negative: Within 3 - 5 years
• ER Positive: After 5 years

o Factors decreases the recurrence

, :
• Postoperative Radiation
• Chemotherapy
• Hormonal therapy {Tamoxifien)
Hormonal receptor status does not affect the recurrence

o Factors improve the survival:

• Less number of involved positive nodes (direct relation)
• Hormonal therapy {Tamoxifien) in IDC only

o If margins are involved post-operative:

After lumpectomy

• Re-excision and obtain negative margin:

o After DCIS if negative margins< 2 mm
o After IDC if one margin only

• Total mastectomy:
o After invasive cancer or recurrent DCIS after repeated resection

200 axillary staging or dissection is not needed, unless positive

preoperatively

After mastectomy:

• If skin flaps involved

+ Wide local excision
• If muscles are involved
+ Radiotherapy (No muscles excision}
■ Multi-drugs Chemotherapy
o Given before the radiotherapy
o Indications:
• Neoadjuvant
• Down-staging

• Down-sizing
o For > 5 cm breast tumor or large compared to breast size to make
BCS feasible

• Adjuvant
• Positive lymph nodes for systemic control

• Negative lymph nodes in High-risk patients:

"for systemic control of locally advanced cancer•
o > 1 cm lesions
o > 5 mm lesions with adverse prognostic features:
• Triple Negative
• HER -2 positive
• Lymph vessel invasion
• High nuclear/ histological grade

o Types:
• Taxane-based (microtubute inhibitors)
• Docetaxel or Paclitaxel .associated with cardiotoxicity

• Anthracycline-based (topoisomerase II inhibitors)

• Doxorubicin (Adriamycin) associated with cardiotoxicity and hair loss
• Epirubicin

• Antimetabolite-based
• 5-Fluorouracil
• Methotrexate
• Cyclophosphamide associated with hair and nail damage, hemorrhagic
cystitis

o Used for 4 - 6 cycles, for duration of 6 - 12 weeks (2 - 3 months)

o Oncotype Ox (21-gene assay) to estimate benefits of chemotherapy in ER/PR positive

in node-negative breast cancer by SLNB

o After complete response by neoadjuvant chemotherapy:

• Axillary lymph nodes:
• To proceed directly with ALND is controversial
• Do SLNB if positive + ALND

• Breast:
• Partial mastectomy (Lumpectomy}
■ Radiotherapy (XRT)
o Should be given after the chemotherapy
o Thick skin flaps can affect the radiotherapy dose and effect

o Indications:
• Whole breast± boost to the tumor bed
• Given at 50 Gray with or without a boost)
• Given for duration of 5 - 6 weeks
• Post BCS for all patient with DCIS or invasive cancer
• Chest wall
• Post mastectomy with recurrence or unable to obtain negative margins
• Positive nodes with no neoadjuvant chemotherapy
• T3 - T4 primary lesions (> 5 cm size)
• Regional {nodal including supra/infra clavicular) XRT:
• > 3 involved axillary lymph nodes, or residual nodal disease
• T3 - T4 primary lesions
• T2 lesion with high-risk features{< 10 ALND, high-grade, LV invasion)

Regional (nodal) XRT may not indicated if complete ALND was done

Regional (nodal) XRT is controversial for 1 - 3 involved axillary nodes

• Accelerated partial breast irradiation
• Used selectively for patients with DCIS or early invasive cancers
• Given at lower dose than standard whole breast irradiation
• Given twice daily for 5 days
• Types:
o lntraoperative breast irradiation (IORT)

o External beam radiotherapy (EBRT)

Less recurrence rate by 2%

• Criteria:
o <? 60 years
o Unifocal T1 (s 2 cm) ER-positive tumor
o No lymphovascular invasion
o Negative tumor margins by <? 2 mm
o NO by SLNB or followed axillary dissection
o Not allowed neoadjuvant therapy

o Contraindications of radiotherapy:
• Pregnancy
• Connective tissue diseases (SLE, Scleroderma, except RA)
• History of radiation (lymphoma)
• Cardiotoxicity
MANAGEMENT OF BREAST CANCER BY STAGE
■ Stage I and II:
o Breast conserving surgery with axillary staging
o Mastectomy and axillary staging
± Radiation therapy
± Immediate reconstruction
± Hormonal treatment (ER/PR and HER2)

■ Stage Ill (Locally advanced breast cancer)

o Neoadjuvant chemotherapy followed by
• Breast conservative surgery and axillary staging
• Modified radical mastectomy
o ± Radiation therapy
o ± Hormonal treatment (ER/PR and HIER2)

■ Stage IV (Distant metastasis)

o Palliative chemotherapy
o Palliative radiation therapy
o Palliative hormonal therapy (ER/PR and HER2)
o Palliative surgery (indicated in presence of fungating or ulcerating breast cancer)
o Bisphosphonates for bone metastasis
o PCD for pleural effusion

MANAGEMENT OF BREAST CANCER IN PREGNANCY

■ 1 st and 2nd trimester:
o Abort the pregnancy (in very early pregnancy if patient agreed)
o Simple Mastectomy + SLNB
o MRM (Risk of spontaneous abortion of anesthesia in 1 st trimester)

■ 2nd and 3rd trimester:

o Lumpectomy + SLNB / ALNO
o Simple mastectomy + SLNB
o MRM
± Immediate Chemotherapy
± Postpartum Radiotherapy

■ SLNB can be performed by using Tc99 sulfur colloid

■ Neoadjuvant Anthracycline-based chemotherapy can be used in 2nd trimester
■ No XRT while pregnant
■ No breastfeeding after delivery if XRT performed
MALE BREAST CANCER
■ Ductal type, commonly at age of 60 - 70 years
■ BRCA mutation in 6 - 12% (More likely to be BRCA II)
■ Associated with steroid, previous XRT
■ Higher risk of contralateral breast cancer than women
■ Associated more with hormonal positive disease
■ Risk factors
o Familial and BRCA II mutation
o Klinefelter's syndrome
o Testicular cancer
o Cirrhosis
o Obesity
o Alcoholism
o Jewish

■ Treatment:
o Simple mastectomy+ SLNB (Standard of care)
o Modified radical mastectomy
o Breast conserving surgery+ Radiatio:n + SLNB
(Usually unfeasible due to central tumor and small breast)

± Hormonal therapy
± Chemotherapy
± Radiation therapy

GYNECOMASTIA
■ Most commonly due to physiologically changes
■ Etiology:
o Decrease testosterone
• Klinefelter's syndrome
• Renal failure

o High estrogen production

• Tumors (Testicular and Non-testicular tumors; Hepatocel/ular tumor)
• Endocrine disorders (Hyperthyroidism, Hypothyroidism)
• Hepatic diseases (Cirrhosis)

o Androgen insufficiency

o Drugs (Digitalis, Spironolactone, lsoniazid, Ketoconazole, and Steroids)

■ Treatment:
o Androgen replacement
o Anti-estrogen (Tamoxifen)
o Subcutaneous mastectomy
SUMMARY OF BREAST CANCER MANAGEMENT
■ Multidisciplinary meeting
■ Family meeting
■ Tumor Board meeting
■ Guideline-based /Hospital vs. NCCIN)

Loco-regional Systemic
Breast
Chemotherapy
�
'--
Surgery
- - - - - - --'�Axilla
HER21Neu
'-.._j
/1 Biological Therapy
Radiation
VEGF

Pre-Menopausal
Hormonal Therapy
,......,.----j�- ---------�
'----..J

Post-Menopausa1

Order of management:
■ Surgery ➔ Chemotherapy ➔ Radiation ➔ Hormonal I Target therapy
■ Chemotherapy ➔ Surgery ➔ Radiation ➔ Hormonal I Target therapy
Surgery postponed 4 - 6 weeks from last dose of chemotherapy

SURVEILLANCE AFTER MANAGEMENT

■ History and examination
o Every 6 months for 5 years, then annually

■ Mammogram
o 6 months after BCS radiation then annual

■ Pelvic examination
o Annual for all patients with intact uterus on Tamoxifen

■ Bone density
o Every 1 - 2 years for selected patients on Aromatase inhibitors

■ Chest X-ray
o Not routinely recommended
STEWART TREVES SYNDROME
■ Lymphangiosarcoma usually developed 7 - 10 years after chronic lymphedema
■ Usually presented 4 - 8 years postoperative
■ Presented with unilateral, well-defined, large, painless, firm mass, and rapid increase in size
■ Angiosarcoma can involve nipple-areola complex (other types are rare) with skin thickening,
erythema, or skin discoloration after radiation therapy
■ Treatment:
o Open biopsy and wide excision of nodules for diagnosis
o Aggressive surgical debridement and possible amputation

LI-FRAUMENI SYNDROME
■ Autosomal dominant, P53 mutation
■ Associated disease:
o GLASB -+
Glioblastoma, Leukemia, Adrenal cancer, Sarcomas, Breast/ Brain cancer

POLAND'S SYNDROME
■ No pectoralis muscle
■ Hypoplasia of chest wall, amastia, hypoplastic shoulder
■ Male are more affected

COWDEN SYNDROME
■ Autosomal dominant (PTEN mutation)
■ Hamartomas arises from all 3 embryonic lay·ers
■ Associated with:
o Hamartomatous lesions of the skin and mucous membranes
o Cancerous lesions:
• Skin (Melanoma)
• Breast
• Thyroid
• Endometrium
• Colon
• Brain
TYPES OF MASTECTOMY
Breast-conserving surgery
■ Segmental or partial mastectomy (Lumpectomy) "+ Radiation± Chemotherapy"
o Indications:
• For clinical stages I and II DCIS or IDC resectable with clear surgical margin

o Contraindication: "Indications of MRM"

• Multicentricity or diffuse microcalcifications (as extensive DCIS)
• Persistent positive margins after adequate resection
• Previous radiation history
• Inflammatory breast cancer
• Any contraindications for radia1ion therapy (as pregnancy, except 3rd trimester)

Involvement of axillary lymph nodes or Nipple-areolar complex is not contraindication

Simple mastectomy/ Total mastectomy

■ Complete breast removal± removal of fascia of pectoralis major± SLNB (With no ALND)
■ Simple mastectomy differs from total mastectomy in preserving the axillary tail
■ Subcategory· Nipple-areolar sparing, and Skin sparing mastectomy
o Indications without SLNB
1} Paget's disease without DCIS or IDC

2} Malignant phyllodes tumor

o Indications with SLNB or ALND

1} Locally advanced breast cancer
• Preferable option for subareolar mass

2} Multifocal breast cancer

3} Paget"s disease + DCIS (SLNB) or IDC (ALND}

Modified radical mastectomy "Paley mastectomy"

■ Complete breast removal with fascia of the pectoralis major and level I, II, and Ill axillary
lymph nodes dissection (Level Ill is rarely indicated)
■ Indications:
o Multicentricity or diffuse microcalcifications (as extensive DCIS)
o Persistent positive margins after adequate resection
o Previous radiation history
o Inflammatory breast cancer
o Any contraindications for radiation therapy (as pregnancy, except 3,d trimester)

Radical mastectomy "Halsted mastectomy"

■ Complete breast removal including pectoralis major and minor, and level I, 11, and Ill axillary
lymph nodes
BREAST RECONSTRUCTION
■ Methods:

o Implant (Tissue expander; saline or silicone)

• May be used as initial step for delayed reconstruction (if radiotherapy planned)

. �
• Immediate:
o If no radiotherapy planned
o Less pain but need adequate skin
o Used as permanent type at subcutaneous level superficial to
pectoralis major

• Delayed: (Most common type)

o If radiotherapy planned (6 - 12 months after complete XRT}
o Also for lesions in medial or central portions with > 2 cm size
o Doesn't need adequate skin, more control of final breast size
o At level of submuscular deep to pectoralis major
o Usually as staged procedure

o Autologous
• Types: (Based on the site)

• Abdomen (Most common)

o TRAM (Superior and deep inferior epigastric artery)
• Most common type

o DIEP (Deep inferior epigastric perforators)

o SIEA (Superficial inferior epigastric artery)

• Trunk
o Latissimus dorsi flap (Thoracodorsal artery)
• Used if unavailable abdominal donor site, or small breast
• Used also to cover implant against radiation
• Contraindicated if ALND, or locoregional radiation done

o Thoracodorsal artery perforators

• Thigh
o Transverse upper gracilis

• Gluteal
o SGAP (Superior gluteal artery perforators}
o !GAP (Inferior gluteal artery perforators)
OTHERS
■ Skin-Sparing or Nipple-Sparing mastectomy:
o Breast reconstruction is needed:

o Incision is made inferior and lateral (to prevent flap necrosis)

o Skin-sparing mastectomy sacrifices only 5%-10% of the breast skin

o Indications for nipple-sparing mastectomy:

• > 2 cm distance of tumor from nipple and < 5 cm tumor
• No skin involvement, no prior breast surgery and no radiation to the breast
• As prophylactic mastectomy (for BRCA or DCIS)
• For Phyllodes and giant Fibroadenoma

o Contraindications for nipple-sparing mastectomy:

• Paget's disease or inflammatory breast cancer
• < 2 cm tumor distance from nipple-areola complex
• Contraindications for BCS:
• Multicentricity or Extensive disease
• Contraindications of radiotherapy
o Pregnancy
o Previous radiation
o Connective tissue diseases

■ Central lumpectomy:
o Lumpectomy + Removal of nipple-areola complex

■ Subcutaneous mastectomy:
o Simple or Total mastectomy without skin excision

■ Wide local Excision= Lumpectomy = Quadrantectomy= Tylectomy

¢ Excision with negative margin

■ Enucleation: Excision without negative mar.gin

■ Wire-localization lumpectomy: for non-palpable lesions
o Incision is made on the tip of the wire (not near the tail}
o Specimen radiology should be obtain for every lesion to ensure complete excision

■ Completion mastectomy: Removal of remnant part without ALNO

■ Completion ALND: Initial SLNB was negative, followed by pathological lymph nodes

■ Indications for antibiotics use in breast siurgery:

o Foreign body "guide-wire"
o Re-excision
o Axillary surgery
OPERATIVE NOTES
■ Simple mastectomy/Modified radical mastectomy
o Five nerves should be protected:
• Thoracodorsal nerve (Supply latissimus dorsi)
• Medial to latissimus dorsi and subscapular vessels
• Beneath axillary vein
• In front of thoracodorsal artery

• Long thoracic nerve (Supply serratus anterior)

• Superficial to serratus anterior on medial side

• Medial anterior thoracic (pectoral) nerve -+ superficial to axillary vein

• Lateral anterior thoracic (pectoral) nerve -+ medial to pectoralis minor
• Subscapular nerve

■ Steps:
o Position: Supine, with arm extended and abducted 90 degree, forearm pronated (to
prevent brachia! plexus injury}

o Incision:
Circumareolar, Curvilinear "Parallel to Langer's line", Radial "vertical at inferior half of
the breast", or Transverse elliptical ''if nipple-areola complex included"

• Radial incision best used at lower part of the breast

• Curvilinear incision best used at upper part of the breast

o Creation of superior/inferior or medial/lateral flaps including nipple-areola complex

• Superior flap -+ to clavicle
• Inferior flap -+ to inframammary line (anterior rectus sheath)
• Medial -+ to sternum
• Lateral-+ to anterior border of latissmus dorsi (anterior axillary line)

Flap thickness of 1 cm is better to avoid skin dimpling, for superficial tumor,

thickness can be less and skin can be excised as well

o Continue by electrocautery to dissect the breast from medial to lateral until removal from
pectoralis fascia

o Ligate the perforaters from internal mammary vessel with vicryl 2-0 and divide them

o Dissect axillary tail of spence by introducing finger into foramen of Langer (defect in
deep pectoralis fascia}

o Drains
• Superior flap
• Inferior flap with axilla (MRM) or Axilla alone (lumpectomy + ALND}
Removal of drain if< 25 - 30 ml/day for 7 days

■ Most common nerve injurypost mastectomy:

o lntercostal brachiocutaneous nerve injury (2nd IC n.)
-+ Hyperesthesia of inner arm and lateral chest
Axillary lymph node dissection (ALND)
■ Standard ALND: Removal of level I and II only
o Take level Ill nodes only if grossly involved

-�
o Axillary vein is the limit for level I and II dissection
(Dissection lateral or posterior to axillary vein if not involved increases risk of edema)

o Incision

• At skin crease distal to the hair-bearing skin of the axilla

• Lazy S 1 cm below hair-bearing between pectoralis major and latissimus dorsi
• Anterior axillary incision (dashed line) parallel and posterior to pectoralis major

o Retract pectoralis major medially from lateral boarder

o Enter the axilla by incise clavicopectoral fascia with preserving of medial pectoral nerve
± cutting the pectoa/is minor

o Identify the border of axmary djssecHon·

• Superior: Axillary Vein
• Anterior: Pectoralis major, minor and Clavipectoral fascia
• Posterior: Subscapularis and Latissimus dorsi (Thoracodorsal artery and nerve)

• Medially: Serratus anterior and chest wall (Long thoracic nerve)

• Laterally: Medial boarder of Latissimus dorsi

o ldentjfy the axjUary yejn (by clearing the latissimus dorsi from fat along anterior surface)
Axillary vein is identified by locating the lateral border of the pectoralis major
Axillary vein is identified as it runs posterior to the pectoralis
Axillary vein is inferior and medial to axillary artery and brachia/ plexus
Axillary vein is superio/ateral boarder of axil/a

o Identify and preserve:

• lntercostobrachial nerve is encountered 2/3 of the way to the axillary vein
• Medial pectoral nerve
o Dissection of axillary area:
• Begins along the inferior border of the axillary vein, lateral to medial

• Angular vein (to subscapular vein) found at lower extent of dissection

• Ligate the small branches from the axillary vein

• The thoracoepigastric vein identified
(Landmark to preseNe the Thoracodorsa/ nerve •deep to the vein")

• Continue dissection along pectoralis minor and preserve medial pectoral nerve

• Retraction of pectoralis minor medially to allow dissection of level II

• The intercostobrachial nerve identified laterally, and retracted superiorly

• The long thoracic nerve of B,ell exposed by retraction of the axillary fat laterally,
and identified posterior to intercostobrachial nerve
• The axillary lymph nodes (fat) dissected away starting at the inferior border of the
axillary vein between the both nerves proceeding caudally and sent to pathology

o Check for level Ill if grossly involved, 1ake it out

o Clip the small lymphatic channels to minimi.ze lymphocele formation

o Check for hemostasis

o Drain
• Dose not prevent seroma, but decrease the complications of seroma

o Closure
 Summarv
Spiculated margins
Imaging
BeniQn calcifications (microcalcifications)
Sclerosing adenosis
Proliferation of stromal tissue
Radial scar
Pathology Proliferative (ductal proliferation)
lnvolutional (stromal fibrosis, epithelial rearession)
Oil cyst, Circumscribed spiculated mass of mixed soft tissue and fat with
Imaging
calcified rim and calcifications or microcalcifications, and architectural distortion
Fragments of degenerate necrotic adipocytes with loss of nuclear staining
Traumatic fat necrosis
Lucent-centered with coarse calcifications
Pathology
Foamy macrophages with multiple nucleoli giant cells
/Lioid-laden macroohaaes I
Hypoechoic mass with posterior enhancement
Imaging
Coarse calcifications fnoocorn lesions)
Fibroadenoma Arise from hyperplasia of single Lobule
Pathology Firm, Lobulated, with ductal and stromal fragments as whort-like pattern, with
oroiections of eoithelial cells
Similar to fibroadenoma
Imaging
Lobulated leaf-like 5 cm mass ± calcifications ± necrosis
BenigQ'
Strom al and epithelial elements (mesenchymal tissue), and spindle cells
Fibrosarcomatous elements
Phyllodes
Associated with inc·rease mitotic activity> 5 - 10 mitosis per HPF
Pathology
Malignant:
Sarcomatous lesions with non-epithelial elements
Lioosarcomatous or rhabdomvnsarcomatous elements
lmaaina Microcalcifications and mav extend bevond that area on mammoaraohv
Proliferation of the epithelium, papillary projections
Hyperchromasia (Clumping of chromatin)
DCIS Nuclear crowding and Loss of polarity (cribriform growth pattern)
"lntraductal carcinoma• Pathology Prominent nucleoli with poorly cohesive intact cells
No pleamorphism, mitoses, atypia or invasion
Calcium deposition in necrotic area
Maliqnant cells of ductal epithelium without invasion of basement membrane
No calcifications, Not detected radiologically
Imaging
Associated with:
Neiahborhood Calcification on mamm=ram Calcifications without Pattern
LCIS
Invasive lobular:
Indistinct mas with poorly defined borders and infiltrating cells in linear
Pathology
arrangement which might grow circumferentially around ducts and lobules
No calcifications No mass
Resemble DCIS
Paget's disease Large cells with pale cytoplasm, and prominent nucleoli
Pathology
"Intra-dermal cancer'' Vacuolated cells (Pathognomonic)
Positive CEA mucine Neaative S-100 anti=n
Inflammatory breast Adenocarcinoma in dermal lymphatics is diagnostic
Pathology
cancer
Resemble DCIS with invasion of basement membrane
Tubular: Columnar lesions with stromal invasion
Invasive ductal
Pathology Cribriform: Hyperchromatic nuclei, Punched-out spaces "Swiss cheese"
carcinoma
Medullary: Lymphoplasmacytic reaction (Lymphoid cells) and vesicular cells
within tumor with hiqh mitotic rate and poorly differentiated
Thoracic Surgery
THORACIC SURGERY
ANATOMY AND PHYSIOLOGY
■ Right lung + 3 lobes+ 10 segments
■ Left lung + 2 lobes+ 8 segments

■ Type I pneumocytes: Gas exchange

■ Type II pneumocytes: Surfactant production

PULMONARY FUNCTION TESTS

■ FEV1: Forced expiratory volume in 1 second
o > 2 L can tolerate pneumonectomy
o > 1.5 L can tolerate lobectomy
o > 1.25 L can tolerate thoracotomy

■ Need predicted post-operative FEV1 > 0.8 Lor> 40% predicted postoperative

■ No resection if preoperative levels:

o pCO2> 50
o pO2< 60
o VO2 max< 10-12 ml/min/kg
o FEV1 < 1.6 L (1600) or< 50%

■ Most common complication of lobectomy: Atelectasis

■ Most common complication of pneumonectomy: Arrhythmias

PLEURAL DISEASES
SPONTANEOUS PNEUMOTHORAX
■ Definition:
o Accumulation of gas in pleural cavity
Normally pleural space has negative pressure
(5 cm H20 lower than atmospheric pressure)

■ Classification:

Types Subtypes Differential diagnosis

Primarv Suboleural bleb ruoture
Secondary Lung diseases
COPD, Asthma
Cystic fibrosis, Sarcoidosis
Spontaneous
Malignancy, Esophageal rupture

Catamenial (endometrial deposits) pneumothorax is

rare tvne which occurs within 72 hours of menses
Iatrogenic Trans-thoracic needle aspiration or biopsy
Central vein catheterization
Acquired
Thoracentesis
Traumatic Blunt or oenetratina

Ooen
Simple
Closed
Tension

■ Most recurrences develop between 6 months - 2 years after initial episode

o After 1 st pneumothorax -+ 20%
o After 2nd pneumothorax -+ 60%
o After 3,d pneumothorax -+ 80%
■ Clinically:
o Primary spontaneous pneumothorax more common in tall, thin men who are smokers
• Smoking increase the risk of pneumothorax by 20-fold

o Most symptomatic patient complaints of chest pain, dry cough, or dyspnea

o Signs of pneumothorax:
• Tachypneic, Decreased chest wall motion
• Hyperresonance on percussion, Subcutaneous emphysema

o Signs of tension pneumothorax

• Tachycardia, Hypotension
• Tracheal deviation, Jugular venous distension

■ Investigations:
o Chest X-ray (Not specific, help to detect pneumothorax)
• Posteroanterior or lateral view (affected side up)
• Convex white line representing visceral pleura
• Gas most often accumulates in apicolateral
• 50 ml volume needed to be visible in upright position (500 ml in supine)
• Size of the pneumothorax can be estimated as:
• Small pneumothorax:
o < 3cm between apical parietal pleura and thoracic cupula (< 15%
of hemithorax)
o No lateral component

• Large pneumothorax:
o > 3cm
o Complete separation of the visceral and parietal pleura

o CT chest with IV contrast

• CT is the best to estimate the size of pneumothorax
• Indicated in complex cases of in uncertain diagnosis
• Occult pneumothorax discovered on CT but not in chest x-ray

o VATS
■ Management:
o Conservatively
• For small pneumothorax
• Usually resolved within 10 days (1.25 - 2.2% of the volume/ day)
• Management consist of:
• Hospitalization
Preferable to admit patient for 24 hours, otherwise patient can be
discharged with follow-up within 12- 24 hours

• Close monitor
• 100% 02 supplement
• Repeat chest x-ray within 3 - 6 hours

o Chest tube
• Indicated in large, symptomatic, or tension pneumothorax after decompression
• Types:
• Regular chest tube (28 Fr) through 5th intercostal space directed to apex
• Pig tail (7 - 14 Fr) as Seldinger technique may be used for small primary
pneumothorax with few symptoms
• Chest tube left in place for 24 - 48 hours
• Suction usually not required, and air-leak should not persist
• Chest tube placed under water seal once lung expansion confirmed
• Effective in 90% in 1 st time, 50% in 2nd time, 15% in 3 rd time pneumothorax
• Chemical pleurodesis (Sterile talc slurry and doxycycline solution)
• Dose should me limited to 5 g to prevent ARDS
• 500 mg of doxycycline combined with lidocaine infused through chest tube
• Patient is shifted from side to side
• Suction is placed for 48 hours

Chemical pleurodesis reserved for patient with secondary

pneumothorax unfit for surgical intervention

o Surgery (VATS/Open, Pulmonary blebectomy, and mechanical pleurodesis)

• Recurrence
• Large of persistence air leak > 3 - 7 days
• Undrained concomitant hemithorax
• Tension pneumothorax
• Bilateral pneumothorax
• Identification of large or multiple subpleural blebs on C T on initial episode
• Absence of medical facilities in isolated areas
• High-risk occupation (Pilots, Scuba divers, High-altitude)
• LaPlace law: Pressure =Tension/ Radius
• Low pressure -+ Increase radius
Q Air trapping and exp.ansion
Q Rupture -+ pneumothorax
Q Can lead to Tension pneumothorax
PLEURAL EFFUSION
■ Causes of white-out lung
o Trachea pulled toward the opacified side
• Pneumonectomy, collapsed, agenesis, hypoplasia

o Trachea remains central in position

• Consolidation, edema, ARDS, pleural or chest wall mass

o Trachea pushed away from the opacified side

• Pleural effusion, diaphragmatic hernia, large pulmonary mass

■ Pleural aspiration:
o Most likely to be caused by anaerobes
o Bronchoscopy used for assessment

■ Malignant pleural effusion best treated with VATS chemical pleurdesis

■ Pleural fluid analysis·

Test Transudate Exudate

An=arance Clear Straw -Turbid
RBC <5000 >5000
WBC < 1000 > 1000
DH 7.45- 7.55 < 7.45 (Acidosis)
Protein <3a >3a
LOH <200 >200
Gravitv <1 >1
Glucose > 60 <60
Pleural fluid I serum protein <0.5 >0.5
Pleural fluid/ serum LOH <0.6 >0.6
Causes CHF High am�ase: Hl11!QQll£cemia:
Liver cirrhosis - Esophageal rupture - Infection
Renal failure - Pancreaticopleural fistula -Empyema
- Malignancy -TB
- Malianancv

Empyema treated with thoracotomy and decortication

LUNG CANCER
■ Most common site of distant metastasis: Brain

■ SCLC:
o Most common lung cancer in smokers
o Most common cause of malignancy-related SVC syndrome
o Neuroendocrine in origin (SCLC and Carcinoid from same origin)
o Paraneoplastic: ADH, ACTH (most common paraneoplastic syndrome)

■ Non SCLC:
o Most common lung cancer overall
• Adenocarcinoma: Peripheral (Most common lung cancer overall)
• sec: Central
o Paraneoplastic: PTH

■ Pancoast tumor: invasion of the apex of chest wall (invasion of T1)

o Homer's syndrome (invasion of sympathetic chain - ptosis, miosis, anhidrosis)

■ Asbestos exposure increases lung CA risk 90X

■ Positive paratracheal lymph nodes -+ Unresectable

■ Radiological characterizes of pulmonary metastasis:

o Multiple(;? 2 nodules)
o Peripherally located
o Sharply circumscribed
o Calcified nodules
o Enhance > 20 HU

■ Biopsy:
o Central (Near to bronchial tree): Fiberoptic bronchoscopy and biopsy
o Peripheral: Percutaneous image-guided biopsy

■ Criteria for pulmonary metastatectomy:

o No unresectable nodules (ability to resect them all) ''Most important factor"
o Appears resectable on imaging based
o No disease at primary tumor
o No metastasis outside lung
o Adequate cardiopulmonary function
o No non-surgical alternative
MEDIASTINAL MASS
■ Most common mediastinal tumor in adults and children: Neurogenic tumors
■ Most common germ cell tumor in mediastinum: Teratoma
■ Most common malignant germ cell tumor in mediastinum: Seminoma (XRT sensitive)

■ Borders:
o Superior: Thoracic inlet
o Inferior: Diaphragm
o Lateral: Medial reflections of the visceral pleura
o Posterior: Paravertebral sulci

■ Presentation of mediastinal mass:

o Usually asymptomatic
o Symptomatic if enlarged
• Local symptoms: shortness of breath, cough, and chest pain
• Systemic:
• Paraneoplastic syndromes
o Myasthenia gravis
o Hypercalcemia from parathyroid adenomas
o Gynecomastia from germ-cell tumors

o Examination findings:
• Facial plethora from superior vena cava compression (SVC syndrome)
• Head, neck, and arm swelling
• Headache, Conjunctiva! edema
• Pemberton's sign: leading to facial plethora, swelling and dilated veins
when patient raise their arms above the head (thoracic inlet pressure)
• Associated also with small cell lung cancer

• Homer's syndrome with involvement of the sympathetic chain

• Diaphragmatic paralysis from phrenic nerve invasion
• Hoarseness from involvement of the recurrent laryngeal nerve

■ Investigations:
o Laboratory
• Functional: TSH, Adrenocorticotropic hormone, catecholamines, and VIP level
• Tumor markers: AFP, beta-hCG, and LDH

o Imaging
• CT scan is the most specific and sensitive test
• MRI used for posterior mediastinal mass for involvement of the neural foramen
• PET scan used to evaluate extra-thoracic disease or extent of lymph nodes

o CT-guided Biopsy
• Indicated only for:
• > 5 cm large mass
• No characteristic features
• Unresectable (Evidence of invasion)
■ Compartments:
o Anterior compartment:
• Borders:
• Posterior surface of sternum
• Superior to diaphragm
• Anterior to innominate vessels, great vessels and pericardium

• Masses:
• Thymic mass (Most common anterior mediastinal mass}
o Thymomas (Most common, associated with myasthenia gravis)
• 15 - 20% of patients with myasthenia gravis have thymoma
• Associated with para-neoplastic syndromes:
• Myasthenia gravis
• Apl .astic anemia

• Imaging: Discrete mass in thymic bed

• Treatment: Complete surgical resection without biopsy

o Thymic carcinoma
• Not associated with para-neoplastic syndromes:

• Lymphoma
o Usually multicentric
o Hodgkin's lymphoma usually asymptomaitc
o Non-Hodgkin's lymphoma usually associated with SVC syndrome
o Imaging:
• Extensive unresectable mediastinal disease
• Lymphadenopathy

o Treatment: Chemotherapy and radiation

• Substernal thyroid
o Most common caused by benign multinodular goiters
o Presentation:
• Asymptomatic
• Most commonly, presented as extension of cervical
thyroid into mediastinum
• Symptomatic (Compression symptoms)
• Dyspnea, dysphagia, and chest pain

o Imaging:
• CT scan used to evaluate the extension preoperatively

o Treatment:
• Cervical incision ± upper manubriotomy and complete
resection

• Parathyroid adenoma
• Germ-cell tumor
o Teratoma
• Most common type
• Benign germ-cell neoplasm
• Contain tissue from all 3 germ-cell lines
• Mesoderm, ectoderm, and endoderm, with
ectodermal predominance

• Imaging:
• Heterogenous appearance

• Treatment:
• Complete surgical resection without biopsy

o Seminoma
• Slow-growing tumors
• 60 - 70% metastasized to local lymph nodes, lung, or bone

• Treatment·
• Systemic chemotherapy (Cisplatin, Bleomycin)
combined with radiotherapy

• Surgery used only as excisional biopsy for isolated

small seminoma

o Non-seminomatous germ-cell tumors

• Presentation:
• SVC syndrome and dyspnea and signs of
• Compression symptoms
• Invasion to surrounding structures (lungs}

• Associated with elevation of AFP and beta-hCG

• Imaging:
• Heterogenous anterior mediastinal mass

• Treatment:
• Like seminoma
o Middle compartment:
• Borders:
• Extends from the thoracic inlet to the diaphragm
• Anterior to vertebra, and posterior to innominate vessels and pericardium

• Masses:
• Lymphoma
o Mediastinal lymphadenopathy is the most common mass of the
middle mediastinum

• Bronchogenic cyst
o Most common mediastinal cysts

• Pericardia! or Neuroenteric cyst

• Lymphangioma
• Fibroma

o Posterior compartment:
• Borders·
• Within the paravertebra! sulci bilaterally
• Contains intercostal vessels I nerves, sympathetic trunk, and azygos vein

• Masses:
• Schwannoma and Neurofibroma
• Ganglioneurorna
• Neuroblastoma
• Pheochromocytoma
TRACHEA
■ Most common ear1y complication after tracheal surgery: Laryngeal edema

■ Most common late complication after tracheal surgery: Granulation tissue formation

BRONCHIAL ADENOMAS
■ Adenoid cystic adenoma: Spreads along perineural lymphatics (XRT sensitive)

HAMARTOMAS
■ Most common benign adult lung tumor (popcorn lesion)

LUNG ABSCESS
■ Most common site: Superior segment of RLL
OTHER CONDITIONS
■ Tuberculosis: Caseating granulomas usually at the apex

■ Sarcoidosis: Non-caseating granulomas

■ Intra-lobar pulmonary sequestration: by aorta

■ Most common cause of calcified granuloma: Thoracic histoplasmosis

■ Most common benign chest wall tumor: Osteochondroma

■ Most common malignant chest wall tumor: Chondrosarcoma

HYPERHIDROSIS
■ Sweating in excess of physiologic requirements
■ Concomitant axillary hyperhidrosis with garment staining and odor (bromhidrosis) in 50%

Anatomy
■ Autonomic nervous system (sympathetic) via T1-T8-+ stellate ganglia-+ brachia! plexus
■ Sympathetic ganglia between medial border of rib head and collus longus muscle
■ Sympathetic chain descends vertically within thorax over the rib heads
o 2nd rib is the most proximal rib identified during thoracoscopy
• by crossing of 2nd intercostal artery from subclavian artery

Management
■ Antiperspirant: Aluminum chloride hexahydrate 20%
■ lontophoresis
■ Botulinum toxin A
Surgery:
■ Sympathectomy: ablation of sympathetic ganglion with transection of sympathetic chain above
and below ganglion
■ Sympathicotomy: transection of the sympathetic chain at the indicated level
■ Clipping: application of a clip at a specific level
■ Blocking: placement of clips above and below the cited ganglion
■ For Palmar hyperhidrosis:
o Transection of sympathetic chain over 2nd and 3rd ribs (T2 and T3}
• if concomitant axillary hyperhidrosis is present-+ T4 also

■ For Axillary sweating:

o Transection of sympathetic chain at the T3-T4 level

■ To decrease the side effects of surgery, perform a more distal sympathicotomy at T3-T4

Complications:
■ Immediate
o lncisional and retrosternal pain
o Anhidrosis of upper chest and face
o Homer's syndrome

■ Chronic
o Compensatory Sweating
o Reduced HR
OPERATIVE NOTES
Posterolateral Thoracotomy
■ Used for pulmonary surgery, extrapleural pneumonectomy, and access to the intrathoracic
esophagus, trachea, and mainstem bronchi

Serratua
anterior
muscle---.----

Latissimus
dorsal Malor mutde

Scapula Incision line

lati�imus dor:.i
mu5cle

.•

Trap,ezlus mu:.c�

■ Preparation
o One-lung ventilation through intubation with double-lumen endothracheal tube or
bronchial blocker
o Patient is placed in the lateral decubitus position and the bed is flexed
• Helps to widening the rib interspaces and keep the hip out of the field
o The knees are padded to prevent injury to the peroneal nerves
o Axillary roll is placed under axilla to prevent injury to axillary structures, brachia! plexus
o The ipslateral arm is supported with an airplane splint to permit exposure to the
posterolateral chest wall
 DiYldtd IIUsl:imus
don.al mu:1cle

serratua
antetlor

Anl4<1of tnd

■ Incision
o Started 1 or 2 cm under the scapular tip
o Extended anteriorly along the rib in curvilinear fashion, 2 fingerbreadths below the level
of the nipple
o Extended posteriorly at the midpoint between the medial border of the scapula and the
spinous processes
o Latissimus dorsi divided laterally
• Latissimus dorsi may be mobilized and retracted in small thoracotomy
o Serratus anterior swept anteromedially or divided in case of difficult exposure
• Usually not divided to avoid postoperative shoulder dysfunction
o The trapezius, rhomboid major, and minor muscles can be divided posteriorly in case of
high curve incision

■ Intra-Pleural space and mobilization

o The 5th intercostal space is entered through dissection above the lower rib
o The intercostal muscle flap is harvest by periosteal elevator
• The ribs above and below the intercostal muscle are scored and the periosteum
is scraped toward the muscle
• Electrocautery may be used to, harvest the muscle flap to avoid taking the
periosteum with the flap

o The rib is retracted away from the field by:

• Rib retraction (Finochietto retractor)
• Rib shingling (posteriorly at the level of paraspinous ligament by sliding rib cutter)
• Rib resection (extensive pleural disease, extensive adhesions, rib disease)
• Periosteal elevator is used to free the rib from the intercostal muscles after
scoring and scraping the pleura off the bone, then rib cutter is used

o The lung is deflated as the anesthesiologist employs one-lung ventilation

o The lung is reflected posteriorly
■ Vascular ligation (in case of lobectomy)
o The pulmonary artery is identified in the pulmonary hilum
o The pulmonary arterial blood supply to the specific lobe is dissected out and the
branches ligated in continuity and divided
o The pulmonary venous drainage is identified, upper lobes drain into the superior veins
and lower lobes drain into the inferior veins
o The appropriate vein is dissected, ligated in continuity, and divided
o The vein is oversewn with 4-0 polypropylene suture

■ Lung resection (if planned)

o The lobar bronchus is sharply dissected out and stapled with an automatic stapling
device
o The bronchus is divided distal to the staple line and the lobe removed

■ Before closure
o The anesthesiolgist is requested to inflate the remaining lung and to hold inflated under
20 cm H20 pressure
o The bronchial staple line is submerged in saline, and an air leak ruled out
o Anterior and posterior chest tubes are placed.

■ Closure
o The intercostal space is closed with paracostal sutures
o The incision is closed in layers
o The chest tubes should be kept on suction and removed when the patient has no air
leak and < 100 ml/day
CHEST TUBE (Options: 1 bottle, 2 bottles, or 3 bottle system "PLEUR-EVAC or ATRIUM')

o Collection chamber
o Water-seal chamber: 2 cm
o Suction chamber:
• (in Wet-suction system only)-+ Fill with sterile water - 15 to - 20 cm H20
• Suction: Low (60 - 80) mmHg, or High (80 - 100) mmHg

ANATOMY
■ Safe Triangle: between latissimus dorsi, lateral of pectoralis major, and upper boarder of 5th rib
■ Neurovascular bundle (intercostal nerve) pass just below the rib
■ Positions:
o Patient supine or at 45• angle with arm abducted and externally rotated placed behind
patient's head
o Anterior: used in blunt trauma, to prevent blockage by tissue and progression to tension
pneumothorax
o Posterior: used in penetrating trauma, to drain the blood

■ Length: measured by cm from the last hole (which should be inside), can be measured by
calculate the distance between skin incision and apex of the lung

■ Indications: Pneumothorax, Hemothorax, Hydrothorax, Chylothorax, Empyema, Pleural

effusion, Patients with penetrating chest wall injury who are intubated or about to be intubated

■ contrajndjcations·
o The need for emergent thoracotomy
o Relative: Coagulopathy, Pulmonary bullae, Pulmonary, pleural, or thoracic adhesions,
Loculated pleural effusion or empyerrna, Skin infection over the chest tube insertion
■ Steps:
1) Patient consent
2) Aseptic precautions
3} Local anesthetics -+ infiltrate all layers {pleura is the most important}
4} Incision at 4th - 5th IC pace between .anterior and mid-axillary line
• Over a rib that is below interco,stal level for chest tube insertion
• Inside safety triangle to avoid long thoracic nerve injury
• 2nd rib identified by Angle of Louis (2nd rib), or Suprasternal notch (1'' IC space)

5) Perform blunt dissection ''Kelly clamp or artery forceps" over the rib
• Should be near to superior boarder of the rib, avoiding injury of neurovascular bundle
6) Finger exploration to confirm intra-pleural placement
7) Direct clamped drain to the base in effusion and apical in pneumothorax
8} Connect the drain to the underwater seal then unclamp it
9} Skin closure over the tube
10) Occlusive dressing

-a:t••--
P•t,.._• .....,__..,�

11) Chest x-ray

12) Monitor the chest tube system
• After insertion there must be bubbling until evacuate pneumothorax
• If there is no tidalling (fluctuation of water level during respirations)
• Tube may be kinked, clamped, blocked, or no more air leak

■ Clamping:
• General rule: chest tubes for pneumothorax should never be clamped
• Clamping chest tube 12 - 24 hours before removal of chest tube

■ Rules of Removal·
• Normal V/S with equal air entry bilaterally
• Chest x-ray normal and lung should be completely expanded
• Tube should not be > 1 week
• No Air leak
• Drainage is <200 ml in 24 hours(< 2 ml/kg/day)
• Chest x-ray must obtained after removal and 24 hours later
• At end-inspiration (studies showed no difference between end-expiration)
Bubbling Swinging (Oscillation)
"Tidallina"
Yes Yes Air leak or still air inside pleura
Note: You have to stnn the suction first !
Yes No Svstem / Connection air leak
No Yes After partial/total pneumonectomy due
to decrease luno comoliance
No No Tube may be kinked, clamped, blocked
Luna exoanded !no more air leak\
Tidalling: fluctuation of water level during respirations
Indicates enlamed oleural soace
Vascular Surgery
Reviewed by:

Dr. Ahmed Mosa

VASCULAR SURGERY
■ Most sensitive tissue for the ischemia: Nerve

■ Most common congenital hypercoagulable disorder:

o Resistance to activated protein C (Fa.ctor V Leiden)

■ Most common acquired hypercoagulable disorder: Smoking

■ Most common type of aneurysm: Degenerative
■ Bruit: Continuous low-pitch by stethoscope
■ Thrill: Continuous vibration by palpation

FOOT ARCHES
1) Longitudinal
o Medial: Calcaneus, 3 cuneiform, Talus, l51, 2nd, 3rd metatarsals, Navicular
o Lateral: Calcaneus, cuboid, 4th, and 5th metatarsals

2} Transverse
o Between cuneiform and cuboid

Planter arches -+ Deep and lateral arches

DIABETIC FOOT

■ Chronic ulcer: > 3 - 4 months

o Most common site of diabetic ulcer: 2 nd metatarsal bone
o Range of motion of the ankle and 1 '' MTP joint should be evaluated

■ Charcot foot: (Osteoarthropathy)

o Fracture or dislocation of interphalangeal or metatarsophalangeal joints
o Leading to pressure on areas with little protection -+ foot deformation
o Signs: Hot, red, swollen foot or collapsed arch
o Ulcers often occur at these sites because of the abnormal pressure and shear forces
created by the collapse of the arch

■ Pseudoepitheliomatous hyperplasia is benign condition with similarity of squamous cell

carcinoma features, biopsy should be repeated to rule out SCC in other areas

■ Osteomyelitis (no biopsy)

o Associated factors· 2
• Ulcer> 2 cm in size or> 3 mm in depth
• Non-healing ulcer after appropriate management
• Sausage toe
• ESR> 70 mm/hour
• Radiographic evidence of bony destruction below the ulcer

o Clinical sign:
• Hot, pain, red, tenderness, joint stiffness

o X-Ray: (negative during first 1 - 2 weeks)

• Localized osteopenia and trabecular destruction
• Periosteal reactions
• Cortical thickening
Can help to rule out gas-forming infections

o MRI (Most sensitive test)

■ Neuropathy theory:
o t Blood glucose -+ t nerve glucose concentrations -+ Glucose converted to sorbitol
o Chronic intracellular hyperglycemia � Glycosylation end products deposition
o Sensory neuropathy: Distal -+ Proximal

■ Callus: nonviable, hyperkeratotic tissue -+ subcutaneous hemorrhage -+ ulcer

o Debridement of the callus improved healing of neuropathic foot ulcer

■ IV Antibiotics
o Broad-spectrum antibiotics until culture results
(Piperaci/Jin/tazobactam, Carbapenem, and Ampici/Jin/sulbactam) ± Metronidazole

o Anaerobic coverage may needed (Cli:ndamycin, Metronidazole) for patient with infected
and ischemic foot
 ■ University Of Texas Diabetic Wound Classification
Grade
Stage
0 I II Ill
A Ulcerative lesion Superficial wound Tendon/capsule BonefJOint
(No infection / completely epithelized penetration penetration
No ischemia)
B Infection Infection Infection Infection
C lschemia lschemia lschemia lschemia
D Infection + ischemia Infection + ischemia Infection + ischemia Infection + ischemia

■ Wagner's classification:
o Grade 0: No ulceration
o Grade 1: Superficial ulceration
o Grade 2: Deep ulceration
o Grade 3: Osteomyelitis or deep abscess
o Grade 4: Localized gangrene
o Grade 5: Extensive gangrene
 ■ Types of ulcer (Based on etiology}:

Venous Stasis Neurotroohic Arterial

Pathophysiology Venous stasis Sensory: Unrecognized Peripheral vascular
traumatic injury disease
Distention of dermal capillaries
with leakage and polymerization Motor: Charcot's foot
of fibrinoaen + Fibrin cuffs
Location Lower third of the leg High pressure points Over bony prominences
Medial aspect (Planar aspect of 1 •1 / 5'" Most distal of the extremities
Proximal to medial malleolus metatarsophalangeal Feet (heels and tips of toes)
ioints) Nail bed
Borders Shallow with irregular edges Punched Out Punched Out
Sharp demarcation
Shallow with smooth
marnins
Base Granulating Deep sinus Poor granulation
With failure of re- Variable depth Dry necrotic or pale base
eoithelialization
Surroundings Lipoderrnatosclerosis Calloused Erythema
(Brownish pigmentation, Edematous
Loss of subcutaneous fat) ± Infection

Edematous
Risk factors History of DVTNaricose veins DM Smoking
Trauma Bum Intermittent claudication
Surgery Neuropathy
Multiole oreanancv
Pain Usually painless None Severe, more at night
Relieved bv elevation
Association Pigmentation Can associate with Minimal bleeding
Telangiectasis osteomyelitis
Cbi:acii:; i�gJ�mia
Pale, Hair loss
Atrophic scaling skin, Cold
feet
No pulses
ABI < 0.5
Prolong capillary refill > 4s
(Normal: < 3 seconds\
Management Compression therapy Glucose control Wound care

Foot and wound care Revascularization

± Antibiotics ± Surgery ± Antibiotics ± Surgery

± Amoutation

■ T ranscutaneous oxygen tension (TcP02) must be > 40 mmHg to achieve wound closure
A-V FISTULA
1) Native
2) AV shunt by graft
3) Tunneled double lumen catheter
Or
1) Congenital
2) Acquired
3) Surgically created
o Urgent
0 Chronic: in CKD I V
4) External AVF: through subclavian, jugular or femoral veins

Rules:
■ As short to hand
■ Non-dominant hand
■ 1 cm from skin surface
■ Adequate flow
■ Should fit for repeated cannulation
■ Accessible in sitting position
Tjmes to functjon (mature}: minimum 1 month, and 4 months before dialysis (30- 20- 10 GFR rule)
Mature fistula: if> 6 mm in diameter, < 6 mm in depth after 6 weeks

Patency: 3 years

Cannulation: Not recommended before 14 days

Types:
■ External
■ Internal:
1) Simple direct:
o Radiocephalic "Cimino fistula" (most common) -+ Superficial radial nerve injury
o Brachiocephalic
o Brachiobasilic
o AV graft
i
o Art ficial PTFE
2) Vein transposition
3) Vein translocation

Steps to create ra diocephalic A-V fistula:

1) Evaluate cephalic vein by duplex +/- venous mapping or venogram
2) Check Allen test & distal pulses
3) Transverse incision over ArteryNein
4) Longitudinal incision between ArteryNein
5) Mobilize at least 2 cm segment of radial artery and measure it's diameter
6) Mobilize the vein and measure it's diameter
7) Proximal and distal control of both
8) Arteriotomy and heparinization
9) Side-to-side, or end-to-end anastomosis
10) Check thrill and distal pulses
11) Ligate any branches from artery or vein by 4-0 Silk
Requirements of the artery:
1) Unobstructed artery
2) > 2 mm luminal diameter
3) Patent palmar arch

Requirements of the vein:

1) Straight segment
2) > 2.5 mm luminal diameter
3) Depth < 1 cm from skin

Complications:
■ Failure to mature (in small vein)
■ Vascular steal (in proximal fistulas)
■ Vein stenosis
o Most common A-V fistula failure: Vein obstruction

■ Aneurysm
■ Seroma
■ Thrombosis
■ High out-put heart failure
■ Infection
■ Catheter-induced DVT
o Anticoagulant for 3 months

o No thrombolysis

o Catheter
• Functional: Keep it

• Occluded: Change the catheter

• Infected:
• Exit-site infection: Antibiotics only for S. aureus ± Anti-Pseudomonas

• Pus or Tunnel infection: Remove and change catheter site

• Positive blood culture: Change line over wire

CEREBROVASCULAR DISEASE
■ Most important risk factor for stroke: Hypertension

■ Most common site of stenosis: Carotid bifurcation

■ 1'1 branch of internal carotid artery: Ophthalmic artery

■ 1 st branch of external carotid artery: Superior thyroid artery

■ Communication between the internal carotid artery and external carotid artery occurs through
ophthalmic artery and internal maxillary artery

■ Most commonly diseased intracranial artery: Middle cerebral artery

■ Cerebral ischemic events most commonly from embolization from the internal carotid artery

■ Internal Carotid endarterectomy (CEA)

o Done between intima and media
o Wait 4 - 6 weeks for patient with recent stroke
o Use a shunt during CEA for stump pressures < 50 or if contralateral side is stenotic
o Carotid stenting used alternatively for high-risk patients
(previous CEA and restenosis, multipJe comorbidities, previous neck XRT)

o Indications:
• Symptomatic:
• Highly considered: Severe Stenosis > 70%
• Less considered: Moderate Stenosis > 50%

• Asymptomatic:
• Highly considered: Severe Stenosis > 80%
• Less considered: Moderate Stenosis > 60%

o Complications from repair:

• Vagus nerve injury (most common cranial nerve injury with CEA)

• Myocardial infarction
(most common cause of non-stroke morbidity and mortality after CEA)
• Hypertension due to carotid body injury (treated with Nipride)
• Hypoglossal nerve injury: tongue deviates to the same side of injury
• Glossopharyngeal nerve injury
• Ansa cervicalis injury
• Mandibular branch of facial nerve: affects comer of mouth (smile)
• Pseudoaneurysm

VERTEBROBASILAR ARTERY DISEASE

■ 2 vertebral arteries arise from the subclavian arteries and combine -+ single basilar artery
■ Basilar splits -+ 2 posterior cerebral arteries
THORACIC AORTIC DISEASE
■ Branches of thoracic aorta:
o Ascending aorta:
• 2 Coronary arteries

o Aortic arch fin order/:

1) lnnominate artery (Brachiocephalic)
• Right subclavian artery
• Right common carotid artery
• Thyroid ima artery

2) Left common carotid artery

3) Left subclavian artery

• 1 st part: Vertebral artery, Internal thoracic artery, Thyrocervical trunk
• Branches of thyrocervical trunk:
� Inferior thyroid artery
� Suprascapular artery
� Ascending cervical artery
� Transverse cervical artery

• 2nd part: Costocervical trunk + superior intercostal and deep cervical artery

• 3rd part: Dorsal scapular artery

o Axillary artery branches: (Continues as brachia! artery)

• After lateral 1 st rib Subclavian ➔ Axillary artery
• Branches:
• 1st part; Superior thoracic artery

• 2nd part: Thoracoacromial artery and Lateral thoracic artery

• 3rd part: Subscapular artery+ Thoracodorsal artery

Axillary vein is superiolateral .boarder of axil/a

Axillary artery and brachia/ plexus are superiolateral to axillary vein

o Descending Thoracic aorta:

• Bronchial arteries
• Mediastinal arteries
• Esophageal arteries
• Pericardia! arteries
• Superior phrenic arteries
Ascending aortic aneurysms
■ Presented with back pain, voice changes, dyspnea, or dysphagia
■ Most common site of rupture: Near left subclavian artery
■ Indications for repair:
o Symptomatic
o 2: 5.5 cm
o Rapid f in size (> 0.5 cm/year)

Descending aortic aneurysms

■ Indications for repair
o If endovascular repair possible -+ 5.5 cm
o If open repair needed -+ 6.5 cm

Risk of mortality or paraplegia is less with endovascular (2'Ya-3%) compared to open repair (20%)
Re-implant intercostal arteries below TB to help prevent paraplegia with open repair

■ Endoleak: persistent flow of blood into aneurysm sac after device placement
o Usually managed with placement of stent or embolization
0 �
• Type I: Incompetent seal at proximal or distal attachment sites
• Type II: Patent inferior mesenteric artery or lumbar artery branches
Retrograde flow into the aneurysm sac through patient's IMA or lumbar artery
(Most common type)

• Type Ill: junctional leak or disconnect of the endograft components

• Type IV: due to graft porosity and is self-limited, typically resolving in 24 hours
• Type V (endotension): continued aneurysm sac expansion without a
demonstrable endoleak on any imaging modality
Treated by relining the existing endograft with a newer
Aortic dissections
■ Stanford classification
o Class A: involvement of ascending aortic
o Class B: descending aortic involvement only

■ DeBakey classification
o Type I: ascending and descending
o Type II: ascending only
o Type Ill: descending only

■ Most dissections start in: Ascending aorta

■ Most common location of tear: Media

■ 95% of patients have severe hypertension a1 presentation

■ Operate on all ascending aortic dissections

■ Operate on descending aortic dissections if visceral or extremity ischemia or if contained

rupture

Paraplegia caused by spinal cord ischemia due to occlusion of intercostal arteries and artery of
Adamkiewicz that occurs with descending thoracic aortic surgery
ABDOMINAL AORTIC DISEASE
■ Branches of abdominal aorta:
o 3 single anterior visceral branches: C eliac, SMA, IMA
o 3 terminal branches: 2 Common iliac, and Median sacral branches
o 5 paired lateral branches:
• Inferior Phrenic
• Renal
• Middle Adrenal
• Gonadal
• 4 Lumbar

ABDOMINAL AORTIC ANEURYSMS

■ Normal diameter of aorta: 2 - 3 cm
■ Result from degeneration of the medial layer
■ Most common site of rupture: Left posterolateral wall 2 - 4 cm below renal arteries
■ Most common risk factors associated with rlJlpture: Diastolic hypertension or COPO
■ 50% mortality with rupture
■ Indications for repair:
o Symptomatic
o > 5.5 cm
o > 5 cm in female or high-risks for rupture (severe COPD, Uncontrolled HTN)
o Growth > 1 cm / year

■ Endovascular aneurysm repair (EVAR} should be done before any other intervention (as
hemicolectomy) if the indications met{> 5.5 cm diameter}, otherwise follow-up after 6 months

■ Reimplant inferior mesenteric artery if back-pressure < 40 mm Hg

■ complications·
o Major vein injury with proximal cross-clamp: retro-aortic left renal vein

o Impotence
• Ensure flow of at least 1 intern.al iliac artery to prevent vasculogenic impotence

o Myocardial infarction (Most common cause of early death after surgery)

o Renal failure (Most common cause of late death after surgery)

o lschemic colitis
• Inferior mesenteric artery often sacrificed with AAA repair and can cause
ischemia of left colon

• Diagnosed with endoscopy or abdominal CT; middle and distal rectum are spared
from ischemia (middle and inferior rectal arteries are branches off internal iliac
artery)

o Inflammatory aneurysms: adhesions to the 3rd and 4th portions of the duodenum

o Ureteral entrapment 25%

o Mycotic aneurysms: Salmonella, Staphylococcus

Aortic graft infections
■ Most common caused by Staphylococcus
■ More common with grafts going to the groin (aorto-bifemoral grafts)

Aortoenteric fistula
■ Usually occurs > 6 months after abdominal aortic surgery
■ Graft erodes into 3rd or 4th portion of duodenum near proximal suture line

Aortic Coarctation:
■ Most common site: Aortic arch distal to left subclavian

TASC Classification of aortoiliac lesions:

■ Type A: (Endovascular)
o Stenosis of common iliac artery

■ Type B: (Endovascular)
o Stenosis of infra-renal aortic artery
o Unilateral occlusion of common iliac artery

■ Type C: (Surgery)
o Bilateral occlusion of common iliac artery
o Bilateral stenosis of external iliac artery

■ Type D: (Surgery)
o Occlusion of infra-renal aortic artery
o Diffuse disease involving aorta and both iliac
o Bilateral occlusion of external iliac art,ery
PERIPHERAL ARTERIAL DISEASE
Rutherford Symptomatic Classification of Peripheral Arterial Diseases:
■ Stage 0: Asymptomatic
■ Stage 1: Mild claudication
■ Stage 2: Moderate claudication
■ Stage 3: Severe claudication
■ Stage 4: Rest pain
■ Stage 5: Minor tissue loss with ischemic non-healing ulcer or focal gangrene
■ Stage 6: Major tissue loss: extending above trans-metatarsal level, non-salvageable foot

Leg compartments
■ Anterior: Deep peroneal nerve {dorsiflexion, sensation between 1st and 2nd toes}
o Supplied by Anterior tibial artery

■ Lateral: Superficial peroneal nerve (eversion, lateral foot sensation}

■ Posterior:
o Deep: Tibial nerve {plantar flexion), p osterior tibial artery, peroneal artery
o Superficial: Sural nerve

■ Leriche syndrome: No femoral pulses, Buttock or thigh claudication, Impotence

o Lesion at aortic bifurcation or above
o Treatment: Aorto-bifemoral bypass graft

■ Most common atherosclerotic occlusion in lower ex1remities:

o Hunter's canal (distal superficial femoral artery exits here)
• Sartorius muscle covers Hunter's canal
o Earliest event of atherosclerosis: LDL oxidation (Fat streak)
o Preventive agent for atherosclerosis: Stalin drugs
o Homocystinuria can f risk of atherosclerosis

■ Ankle brachia! index (ABI)

Normal level 1-1.2

Mild ischemia (Claudication} < 0.9
Moderate ischemia < 0.7
Severe ischemia /Rest nain. Ulceration\ < 0.5-0.4
Ganarene < 0.3

■ Unreliable ABI reading:

o Vascular injury to deep femoral artery or profunda brachii
o Intimal flap
o Transected artery that maintained in continuity
o AV fistula

■ Critical limb ischemia:

o ABI < 0.4
o Ankle pressure < 50
o Toe pressure < 30
ACUTE LIMB ISCHEMIA
■ Definition: Sudden loss of limb perfusion for up to 2 weeks from initial event
i
■ Presentat on of ischemia:
o Pain, pallor, poikilothermia (coldness}. pulselessness. paresthesia, and paralysis
o Thrombus: History of PAD. signs of chronic ischemia, pulses in contralateral limb effected
• Signs of chronic limb ischemia: Hair loss, shiny skin. hypertrophic nails, wounds
o Embolus: Sudden onset, history of arrhythmia, Ml. valvular disease, or multiple sites 15%

■ lovest;gatjons·
o Source of the event: ECG, Echo
o Specific: Doppler U/S, Arteriography (invasive)

■ Classified due to etiology:

o Thrombus (60%)

Rutherford Description Sensory loss Muscle Arterial Venous

Classification weak
Viable No immediate threatenino No No Audible Audible
Threatened Associated with minor or maior sensorimotor loss (cold and mottledl
- Marainallv Salvaoeable if oromotlv treated Minimal /toes) No Inaudible Audible
- Immediately Salvageable with immediate Moderate Mild Inaudible Audible
revascularization /bevond toesl
Irreversible Major tissue loss or permanent Profound Profound Inaudible Inaudible
nerve damaoe

o Embolus (40%)
• Most common cause: atrial fibrillation, recent Ml with left ventricular thrombus
• Most common site: Common femoral artery
• Renal artery most common site of atheroma embolization {by cholesterol clefts)

■ Management of acute limb ischemia:

o Anticoagulation initially. and alone if viable (only narrowing with good collaterals}

o Intra-arterial thrombolysis for viable with no or mild sensorimotor deficits < 14 days

o Surgical thrombectomy: for threatened limb by thrombus

o Open embolectomy: for threatened limb by embolus

o Fasciotomy: considered if ischemia > 4-6 hours with postoperative anticoagulant

o Amputation for non-salvageable limb (irreversible stage)

■ Contraindication to anticoagulation or thrombolytic therapy:

o Acute bleeding
o Recent GI bleeding in last 10 days
o Brain or spinal trauma or intervention within last 3 months
o Cerebrovascular accident (CVA) in last 2 months
o lntracranial disease (malignancy or metastasis)
o Eye surgery
o Malignant or uncontrolled hypertension
o Pregnancy
AMPUTATIONS
■ BKA: 80% heal, 70% walk again, 5% mortality
■ AKA: 90% heal, 30% walk again, 10% mortality
BELOW KNEE AMPUTATION
o Posterior Flap technique: (others: sagittal, skew, medial, and fish-mouth flaps)

Superficial peroneal nerve (SPN)

Anterior tibial artery/vein

LateraJ Tiibial nerve (TN)
(SPN) Deep peroneal nerve (DPN)
Great Saphenous vein
Posterior Tibialis muscle
Po.stel'ior Posterior tibial artery/vein
Com1mn Includes: SOLEUS, and deep GASTROCNEMIUS
(TN)
ShorVsmall Saphenous vein

Anterior Compartment: (Deep peroneal nerve)

■ Tibialis anterior, Extensor hallucis longus, Extensor digitorum longus

Posterior Compartment: (Tibial nerve)

■ Gastrocnemius, Soleus, Tibialis posterior, Fl,exor hallucis and digitorum longus

Lateral Compartment: (Superficial peroneal nerve)

■ Fibularis longus, Fibularis brevis

Steps:
■ Physiotherapy, Glucose control, DVT prophylaxis, ICU if required, Consent for BKA ± AKA
■ Marker, Shaving, Tourniquet if non-ischemic limb
■ Anterior flap should be 12 cm below tibial tuberosity for the prosthesis
■ Posterior flap should be 10- 12 cm below anterior incision, 1.5 diameter of leg
■ Skin incised, greater and lesser saphenous veins identified anteromedially, ligated, and divided
■ Divide anterior and lateral compartments by electrocautery
■ Anterior tibial artery and vein, identified, ligated and divided
■ Tibial periosteum incised by blade, and by elevator 2 cm proximal to incision
Amputation Jeve[' 12 - 17 cm of tibia below knee ioint
■ By electrical saw the bone is amputated 2 cm proximal to incision with slightly oblique direction
■ Apply Rasp to remove sharp edges, then apply wax for hemostasis
■ Same for fibula but 1 • 1.5 cm proximal to tibia
■ Tibial nerve, Superficial and Deep peroneal nerves are retracted and divided sharply
■ If posterior flap bulky, soleus can partially or totally divided but not beyond the level of
Gastrocnemius fascia to preserve the blood supply for the posterior flap
■ Closure by adjusting the posterior flap with absorbable sutures
■ Drain inserted if required, and skin closure by skin clips
ABOVE KNEE AMPUTATION
o Fish-Mouth flap technique: (others: sagittal, skew, medial)

Femoral artery and vein

,,--;,Jft(--fo��"Jt--- Greater Saphenous vein

Deep femoral artery and vein

Sciatic nerve

Anterior Compartment: (Femoral nerve)

■ Sartorius, Quadriceps

Posterior Compartment: (Tibial nerve)

■ Hamstrings muscles 'biceps femoris, semitendinosus, semimembranosus"

Medial Compartment: (Obturator nerve)

■ Gracilis, adductor longus, adductor brevis, adductor magnus

Steps:
■ Physiotherapy, Glucose control, DVT prophylaxis, ICU if required, Consent
■ Marker, Shaving, Tourniquet if non-ischemic limb
■ Fish-mouth incision with equal anterior and posterior flaps (112 diameter of the limb+ 1 cm)
■ The greater saphenous vein is identified, ligated, and divided
■ The fascia and muscles of the anterior thigh are divided
■ Superficial femoral artery and vein are identified medially, divided separately
■ The femur is exposed and periosteal elevated for 10 cm above the incision
■ The femur is transected 7 - 10 cm proximal to skin incision by oscillating or Gigli saw
Amputation level: > 12 cm above knee and > 18 cm (25 - 30 cm) below greater trochanter

■ Deep femoral artery and vein are identified medially, divided separately
■ Sciatic nerve is pulled gently of 2 cm, divided sharply, and allowed to retract
No ligation of the nerve to prevent neuroma formation

■ The edges of the transected femur are smoothed with a rasp or file
■ Flex the hip prior to closing, if hip flexion leads to tension, femur should be shortened

■ Myopexy of posteromedial musculature should be performed prior to skin closure

By sewing the muse/es of posterior and medial compartments anterolateral/y to the periosteum

■ Closure then drain inserted if required, and skin by skin clips

UPPER EXTREMITY
■ Most common site of upper extremity stenosis: Subclavian artery

■ Subclavian steal syndrome: proximal subclavian artery stenosis resulting in reversal of flow
through ipsilateral vertebral artery into the subclavian artery

■ Treatment: Percutaneous transluminal angioplasty(PTA} and stenting

Paradoxical embolism (crossed embolism):

■ Arterial thrombosis caused by embolism of thrombus of venous origin through lateral opening
of the heart (patent foramen ovale) • ASD"

Example: upper limb thrombosis � pulmonary embolism

Thoracic outlet syndrome (CS - T1)

■ Subclavian vein: passes over 1st rib anterior to anterior scalene muscle, then behind clavicle
■ Brachia! plexus and subclavian artery: pass over 1st rib posterior to anterior scalene muscle
and anterior to the middle scalene muscle
■ Presented with back, neck, and/or arm pain/weakness/tingling(Neurological symptoms}
■ Neurologic involvement
■ Most common anatomic abnormality: Cervical rib
■ Most common cause of pain: Brachia! plexus irritation
o Ulnar nerve � triceps weakness and atrophy, weakness of intrinsic muscles of hand,
weak wrist flexion

■ Treatment:
o Cervical rib and 1st rib resection, divide anterior scalene muscle

RENAL VASCULAR DISEASE

■ Right renal artery runs posterior to IVC
■ Renal atherosclerosis: left side, proximal½, men
■ Fibromuscular dysplasia: right side, distal½, women
■ Treated with percutaneous transluminal angioplasty(PTA)

VISCERAL AND PERIPHERAL ANEURYSMS

■ Rupture: most common complication of aneurysms above inguinal ligament
■ Thrombosis and emboli: most common complications of aneurysms below inguinal ligament

Visceral artery aneurysms

■ Repair all splanchnic artery aneurysms(> 2 cm} when diagnosed(50% risk for rupture)

Splenic artery aneurysm

■ Most common visceral aneurysm(more common in women}

Renal(> 1.5 cm) artery aneurysm, Iliac(> 3.0 cm} or femoral(> 2.5 cm} artery aneurysms
■ Treated with covered stent
Popliteal artery aneurysm
■ Most common peripheral aneurysm
■ Most common symptom: Thrombosis
■ ½ are bilateral, ½ have another aneurysm (AAA, femoral, etc.}
■ Indications for repair:
o Symptomatic
o >2 cm

■ By exclusion and bypass of all popliteal aneurysms, covered stent not recommended

Pseudoaneurysm
■ Most common location is the femoral artery

Summary of the indications for open surgical repair of the aneurysms:

Site Size Other factors

Visceral >2cm
Symptomatic
Spleen >2cm
Preanant
Popllteal >2cm Symptomatic
Renal > 1.5 cm
Iliac >3cm
Femoral >2.5 cm
Symptomatic
Ascending thoracic aorta >5.5 cm
Raoid t in size (> 0.5 cm/vear)
Descending thoracic aorta > 6.5 cm
Symptomatic

>5.5 cm >5 cm in female or high-risks for rupture

Abdominal aorta
(severe COPD, Unc ontrolled HTN)

Growth > 1 cm / vear

OTHER VASCULAR DISEASES
■ Fibromuscular dysplasia
o Renal artery most commonly involved
o Most common variant: Medial fibrodysplasia
o Treated with PTA

■ Buerger's disease
o Young men, smokers
o Severe rest pain with bilateral ulceration, gangrene of digits
o Corkscrew collaterals on angiogram and severe distal disease
o Treatment by stop smoking or will require continued amputations

■ Embolic Blue toe syndrome (Trash foot)

o Embolus of atherosclerotic debris that blocks distal arteries

o Most common site of origin: Distal aorta

o Presentatjon·
• Sudden cool, painful, cyanotic to livedo reticularis forefoot or toes
• Palpable distal pulses

o Biopsy:
• From skin or muscles (Gastrocnemius or Quadriceps)
• Pathology: Cholesterol crystals

Arteritis
■ Temporal arteritis (large artery)
o Women, > 55 years, headache, fever, blurred vision (risk of blindness)

o Temporal artery biopsy

-+ Giant cell arteritis, granulomas
o Treatment:
• Steroids only
• Bypass vessel if needed

■ Polyarteritis nodosa (medium artery)

o Weight loss, rash, arthralgia, hypertension, kidney dysfunction
o Renal artery most commonly involved
o Treated by steroids

■ Kawasaki's disease (medium artery)

o Children
o Aneurysms of coronary arteries and brachiocephalic vessels
o Treated by steroids ± CABG

■ Hypersensitivity angiitis (small artery)

o Rash (palpable purpura), fever
o Treated by calcium channel blockers, pentoxifylline
VENOUS DISEASE
■ Greater saphenous vein joins femoral vein near groin and runs medially

■ Saphenous landmark:
o 1.5 cm anterior to medial malleolus

■ No clamps on IVC or it will tear

■ Left renal vein can be ligated near IVC, have collaterals (left gonadal vein, left adrenal vein)
■ Right renal vein does not have these collaterals

■ Most common failure of A-V grafts for dialysis:

o Venous obstruction due intimal hyperplasia

■ Migrating thrombophlebitis in pancreatic and gastric cancer

■ Normal venous Doppler U/S:
o Augmentation of now with distal compression or release of proximal compression

■ Sequential compression devices help prevent blood clots by:

o ! Venous stasis
o t tPA release
■ Deep venous thrombosis (DVT)
o Most common in calf
o Pain, tenderness, calf swelling
o Left leg more involved than right in May-Thurner syndrome
(Left common iliac vein compressed by right common iliac artery)

o Management:
• Knee-high compression stockings (30 to 40 mm Hg)

• IV Anticoagulation (for first 10 days} weight-based dosing of:

• In-patient options:
o Unfractionated Heparin
• UFH should not be used in liver failure
• Reduces the incidence of DVT by 25% and fatal PE by 50%

o LMWH
• LMWH associated with lower mortality, bleeding risk, and
recurrence when compared with UFH
• More effective than UFH for high-risk patient
• LMWH should not be used in patient with renal failure

o Fondaparinux SC (factor Xa inhibitor}

o Rivaroxaban
o Direct thrombin inhibitors (Hirudin, Argatroban, and Bivalirudin)
• Used in high-suspicious of HIT or previous HIT

• Out-patient options:
o LMWH and Warfarin
o LMWH followed by dabigatran {direct lhrombin inhibitor) or
Edoxaban
o Rivaroxaban or Apixaban (factor Xa inhibitors)

Indicated if (No PE, Non-massive DVT, No renal insufficiency, low risk

of bleeding, hemodynamical/y stable, No need for in-hospital care)

• Transition to long oral anticoagulation: (after 10 days}

o Vitamin K antagonists (warfarin) with INR 2 - 3

o Factor Xa inhibitors (Rivaroxaban, apixaban, or edoxaban}

o Direct thrombin inhibitors (dabigatran)
Both of them do not require monitor of INR

Warfarin started while patient on anticoagulant until INR 2: 2 for 24

hours or 5 days in case of direct thrombin inhibitors

o Duration: for at least 3 months

• 6 months or lifetime for provoked DVT
(identified major risk factors or hormonal therapy)
• Thrombolysis or Pharmacomechanlcal thrombectomy
• Mechanical, pharmacological or Catheter-directed
o Altep/ase "Tissue plasminogen activator" (IPA)
o Streptokinase
o Urokinase

• Convert plasminogen to plasmin which leads to degradation of fibrin

• Indications·
o Extensive proximal DVT as iliofemoral DVT {< 1 week duration)
as massive swollen leg with severe pain, edema and tenderness

o Phlegmasia Cerulea Dolens (impending venous gangrene)

• Severe swelling, pain and cyanosis

o Patient should have good life-expectancy (< 70 year old)

o Low bleeding risk

o Failure of anticoagulation, thrombolysis or both may indicate

pharmacomecha nical thrombectomy

Septic thrombi is contraindication for thrombectomy

• IVC filter
• Indications:
o Recurrent DVT or PE despite anticoagulation therapy

o Free floating iliofemoral or IVC thrombi

o After pulmonary embolectomy

o Septic or chronic PE in high-risk patients

o Contraindication to anticoagulation or thrombolytic therapy

• Acute bleeding
• Recent GI bleeding in last 1 O days
• Brain or spinal trauma or intervention within last 3 months
• Cerebrovascular accident (CVA) in last 2 months
• lntracranial disease (malignancy or metastasis)
• Eye surgery
• Malignant or uncontrolled hypertension
• Pregnancy
 HEMATOLOGIC DRUGS
Drua Mechanism/ Dose Perio=rative Measures Comolication Reversal
Prevents vitamin K- Pre-op: PT (INR) Cross the placental 1) Stop drug
dependent decarboxylation Hold 5days (Contraindication in
of glutamic acids pregnancy) 2) Vitamin K
Minor: 1-2.5mg
factors· Post-00· �atfacic :ikio ce"cgsi� INR >1 0: 2.5-5mg
Bleeding: 5-10mg
Warfarin II, VII, IX. X (1972) & Resume within Due to short half-life of
proteins C and S 12 -24 hours proteins C and S IV in 50 ml IVF

(Take 6 hours for

Dose: Occurs when start effects/
Start by 5- 10 mg /OD warfarin without starting
heparin before it 3\FFP
Activates of AT 111 Pre-op: PTT Doesn't cross placental Protamine sulfate
(Augmentation) Hold 6hours T½= 60-90 (Used in pregnancy)
min
c:> Inhibits X & II Long term:
Heparin
Post-op Osteoporosis, alopecia
Prophylactic Dose: 48- 72h major and thrombocytopenia
5000IU SCBID/TIO 24h for minor
Not preferred in case of
Therapeutic Dose: liver disease
80units/kg IV bolus (metabolized by liver)
Then. 18units/ka IV
Activates of AT Ill Pre -op: Anti - X assay Not preferred in case of Protami:le sulfate
(Augmentation) Hold 24 hours renal failure
T½ = 4.5h (excreted by kidneys)
c:> Inhibits X only Post -op
48- 72h major Best anti-coagulant in
LMWH Prophylactic Dose: 24h for minor pregnancy and
30mg SCBID malignancy, and less
4 0mg SCOD risk of HIT

Therapeutic Dose:
1 mg/kg SC BID
1.5ma/ka SCOD
Use Ideal body weight (IBW) for obese patients
 EMBOLI
Pulmonarv embolism Fat embolism
Risk factors Wall: Aging, Vascular injury Trauma
Fracture, Joint reconstruction
Flow (stasis): Bed rest, Surgery, Cardiac failure
Systemic
Constituents: Bums, OM, Pancreatitis,
Polvcvthemia, Malignancy, Dehydration, Coaqulopathy Cardiopulmonary bvoass
Pathophysiology Thrombus emboli from deep veins or right atrium Mechanical
Damaged vessels lead to fat droplets
Propagate into circulation

Obstruct pulmonary artery Biochemical

Stress hormones released
Produces right ventricular strain Activate lipases
Hydrolyses lipids into FFAs
Most commonly from the iliofemoral region FFAs induce pulmonary damage and
increase capillary permeability
Clinical features Swelling or tenderness of calf Tachycardia, tachypnea
Pleuritic chest pain Encepalopathy (hypoxia, confusion)
Paradoxial embolization Petechial rash
Pyrexia
Shock (Tachycardia, tachypnea, hypotension) Retinopathy
Due to outflow obstruction Renal imoairment
Investigations CBC, PT/PTT, Type and Screen CBC, PT/PTT, Type and Screen
Electrolytes, ABG (V/Q mismatch) Electrolytes, ABG
■ T Pulmonary artery pressure, l CVP, ! PCWP Urinlysis (Lipiduria)
ECG: Tachycardia and RV strain
■ l P02 and PC02 respiratory alkalosis CXR
Nodular (ground-glass) opacities
Plasma 0-dimer Snow-storm a1111earance:
ECG (Sinus Tachycardia, S1Q3T3) Diffuse bilateral pulmonary infiltrates
CXR (Westermark sign; focal oligemia) (Consistent with lung contusion, acute
VO scan lung injury, pulmonary edema, or
Spiral CT ARDS)
Pulmonarv anaioaraohv
Management Early mobilization Respiratory support
TED stockings
Anti-DVT machine Fluid/Electrolyte resuscitation
T herapeutic anticoagulation (UFH, LMWH)
transition to oral or LMHW after 24 h after acute injury DVT prophylaxis

Anti-fibrinolytic agents or catheter-directed therapy Nutritional support

Massive PE
Unstable patient (hypotension or systemic shock)

Surgical or Percutaneous embolectomy + IVC filter

Massive PE with contraindications to thrombolysis
"high-risk of bleeding• (intracranial or uncontrolled
bleeding, recent surgery/trauma)

IVC filter (if used) should be below renal veins (through

right IJV)
LYMPHATICS
■ Do not contain a basement membrane
■ Not found in bone, muscle, tendon, cartilage, brain, or cornea
■ Deep lymphatics have valves, and endothelium
■ Most common organism related to infection: Streptococcus (Red streaks, Lymphadenopathy)
■ Lymphocele following surgery usually after dissection in the groin

OTHERS
■ Angio-contrast osmolarity: 600 - 900 mOsm
■ Management of acute contrast reaction: Epinephrine

■ Femoropopliteal grafts
o 75% 5-year patency
o Popliteal artery exposure below knee: posterior muscle is gastrocnemius, anterior is
popliteus

■ Femoral-distal grafts
o 50% 5-year patency

■ Swelling following lower extremity bypass:

o Early: reperfusion injury and compartment syndrome (Treated with fasciotomy)
o Late: DVT

■ Complications of reperfusion of ischemic tissue:

o Local: Compartment syndrome
o Systemic:
• Lactic acidosis
• Hypotension
• Hyperkalemia
• Myoglobinuria
• Renal failure

Popliteal entrapment syndrome

■ Most present with mild intermittent claudication
■ Medial deviation of artery around medial head of gastrocnemius muscle (Most common)

-+ Loss of pulses with dorsiflexion

■ Investigation: Arteriogram (to make decision for exploration)

■ Treatment: Resection of medial head of gastrocnemius muscle

Acute ligation of pop/ilea/ artery have higher risk of limb loss (75%) compared to brachia/ artery (25%)
Esophagus
Esophagus
ANATOMY AND PHYSIOLOGY
■ Esophageal layers:
o Mucosa (Strongest layer) -+ Epithelium, lamina properia, and muscularis mucosa
o Submucosa -+ Meissner's "Submucosal plexus" lymphatic plexus
o Muscularis properia or exlemia
• Inner Circular (Helical)
• Auerbach ''Myenleric plexus" (Parasympathetic; Interstitial cells of Cajal)
• Outer Longitudinal
Striated Skeletal muscle in upper½ and Smooth muscle in tower½

o Adventitia (No serosa)

■ Esophageal parts: (Total length: 25 - 30 cm from incisors)

o Cervical 15 - 20 cm "Cricopharyngeus lo the supraslernal notch (Thoracic inlet)"
o Thoracic (Retroperitoneal) 20 cm "Suprastemal notch to Diaphragm"
• Upper thoracic: 20 - 25 cm "Thoracic inlet to Azygos vein"
• Middle thoracic: 25 - 30 cm "Azygos vein to Inferior pulmonary vein"
• Lower thoracic: 30 - 40 cm "Inferior pulmonary vein to the GEJ"

o Abdominal (lntraperitoneal) 1 - 2 cm "from the diaphragm to the cardia"

■ Blood Supply:

Part Arterial suoolv Venous drainaae

Cervical Inferior thvrold arterv Inferior thvrold vein
Thoracic Bronchial artery (1 right, 2 left) Bronchial vein

Descending thoracic aorta Azygos or hemiazygos veins

Azvnos vein runs a/ona the riaht side and dumos into SVC
Abdominal Left gastric artery Left gastric vein (Coronary vein)

Inferior ohrenlc arterv

■ Lymphatics drainage:
o Upper½ drains cephalad, lower½ drains caudal
Left vagus is anterior to esophagus, and Right vagus is posterior to esophagus

■ Diaphragmatic hiatus

Level Hiatus Associated with

TS IVC /anterior riaht\ Riaht ohrenic nerve
T10 Esophagus (anterior left) Vaous nerve
T12 Aorta loosterior) Thoracic duct, and azvaos vein

Esophagus & azygos vein passed through the right crus ofdiaphragm
ESOPHAGEAL SPHINCTERS
UES LES Causes of

Position from incisors 15cm /cricooharvnaeus muscle) 40cm ••

t LES Pressure
Gastrin
Pressure at rest 70 15
(! in GERO) •• Motilin
Achalasia
Pressure at swallowing 15
(t in Zenker)
0
• Protein
Distension
Lenath 2-3cm 2-5cm
Most common cause of deficient LES is inad=uate of intra-abdominal /enmh

ANATOMIC AREAS OF ESOPHAGEAL NARROWING

■ Distance from incisors (add 3cm if from nostril)
o 15cm: Cricopharyngeus muscle "narrowest GIT zone"
o 25cm: Aortic arch and Left bronchus
o 40cm: Diaphragm

SWALLOWING
■ Swallowing center is located in the medulla
■ Swallowing waves:
o Primary peristalsis: occurs with food bolus and swallow initiation
o Secondary peristalsis: propagating only (incomplete emptying)
o Tertiary peristalsis: non-propagating, non-peristalsing (dysfunctional)

■ Swallowing mechanism: (initial swallowing leads to t LES}

1} Soft palate occludes nasopharynx
2} Anterosuperior movement of the hyoid bone
3} Elevation of the larynx and airway opening is blocked by epiglottis
4} Cricopharyngeus relaxes
5} Pharyngeal contraction
THORACIC DUCT
■ Originates from Cistema Chyli at T2, ascending on the right side of midline
o Below T5 - T6 -+ To the right of aorta
o Above T5 - T6 -+ To the left of aorta

■ Collects lymph from entire body below diaphragm, and left thorax

■ Drain into Left supraclavicular lymph node (Virchow lymph node)

■ Empty into Union of the left internal jugular and left subclavian vein
o To the left of azygos vein, and esophagus

■ Right lymphatic duct:

o Received from right thorax, right arm, and right head and neck and
o Drain into right supraclavicular lymph node
o Empty into Union of the right internal jugular and right subclavian vein

■ Investigations:
o Chyle leak is increased tube output on reintroduction of enteral feeding
o Drain cytology:
• Chylomicrons
• High triglyceride levels (> 110 mg/ml)
• High lymphocyte count

■ Management:
o lntraoperative: Repair or ligation

o Postoperative:
• Diet modification (Medium-chain fatty acids)
• ± NPO ±TPN
• Somatostatin analogues advocated by some authors
• Chest tube for pleural effusion
• Thoracotomy and surgical duct ligation or embolization
• Used if drainage> 500 - 1000 ml/day despite TPN and NPO
 DIVERTICULA

Zenker {Most common tvoe) Traction Epiphrenic

Tvne False True False
Site Upper esophagus 15 cm Mid esophagus 25 Distal esophagus
cm
Left posterior Lateral
Lateral
At level of:
Cricopharyngeus muscle Cricothyroid
cartilage

Inside Killian triangle, between inferior

pharyngeal constrictors and
cricooharvnaeus
Nature Pulsion, Paraesophageal Non-Puls/on Pulsion
Parabronchial
Etiology Failure of cricopharyngeus and UES to Inflammatory Motility disorder
relax (mediastlna/ (achalas/a, or DES)
aranulomatous, TBJ
Presentation Elderly patient with dysphagia (Most common symptom)
Choking, cough, halitosis and hoarseness can be associated
Rarely it may harbor malignancy
Bovce's sinn: Cervical borborvamus in oaloable neck mass and emaciation
lnvestiaations Esonhaaram /UGI endosCO"" if findinas suooests of malionanc,
Treatment Myotomy should be perfonned for all Excision & primary Myotomy
patients to avoid risk of recurrence, by closure
dividing cr/copharyngeus completely + Dlverticulectomy
extending to cervical esophagus Indications:
Large> 2 cm
Myotomy alone may sufficient for Symptomatic
treatment of small diverticulum (< 2 cm) Motility disorder

Surgery (preferred for < 3 cm)

Throughout left neck incision

Q1210 ll�1l1l1.11l11.112mll
It eliminate risk of malignancv and risk
of retained food
Preferable option for 2 3 cm

Oeen Divertlculoeexll
Mucosa is not divided so no risk of leak

Endoscopic Diverticulotomy
Rigid option for > 3 cm
Fl1xlbl1 for poor candidate with multiple
sessions

Salivary fistula is associated with -

ectomv and -oexv
 MOTILITY DISORDERS
■ Most common primary motility disorder of esophagus: Achalasia (Cameron)
■ Nutcracker is the most common primary motility disorder (Schwartz)
■ Most common secondary motility disorder off esophagus: GERO
o Other secondary disorders: Scleroderma

■ Psychiatric history as: Anxiety, depression, somatoform disorder associated with major motility
disorders as DES

■ Investigations needed:
o Contrast esophagogram: To assess esophageal anatomy, length, and presence
o pH study: To identify GERO
o Upper Endoscopy: To identify Barrett's esophagus, malignancy, or stricture
o High-resolution manometry (HRM): Standard of care

■ Esophageal motility disorders classified used 3rd Chicago Classification System based on high­
resolution manometry:

Disease lntecirated relaxation pressure Peristalsis

Achalasia > Unner nonnal limit Failed or soastic
EGJOO > Unner nonnal limit Normal

Disease Integrated relaxation pr·essure Distal contractile integral Distal

latencv
Major motilitit: disorder Nonna! High Short
DES
i!: 20% premature

Jackhammer
i!: 20% DC/ > 8000

Absent contractllitv
Minor motility disorder Normal Normal
But > 50% ineffective swallows
Normal Nonna! Normal Normal
 ■ Esophageal motility disorders classified into:
o Achalasia
• Most common primary motility disorder of esophagus

• Pathophysiology:
• Autoimmune response triggered by infection
o Trypanosomacru.zi (Chagas disease)
• Leading to destruction of inhibitory postganglionic neuron "Aurbach
plexus" of distal esophagus and LES
• Leading to failure of LES to relax and lack of coordinated peristalsis

• Clinical presentation:
• Progressive dysphagia to liquid an solids
• Heartburn, Regurgitation, and Retention of food up to 40%
• Weight loss due to low oral intake and sitophobia

• Investigations:
• Contrast esophagogram
o Bird's Beak or Corkscrew appearance, air-fluid level, dilatation
o Sigmoid esophagus: dilated tortuous deviated esophagus

• Upper GI endoscopy
o Esophagitis, Dila1ed esophagus with food retention

• Manometry (Gold standard)

o Incomplete LES relaxation and no peristalsis
o Hypertensive LES is not one of criteria to diagnose achalasia

. �

Incidence Impaired LES Peristalsis Characteristic

relaxation

Type I 55% Yes Absent Complete loss of contractile activity in

the body of the esophaaus
Tvoe II 40% Yes Absent Increased esophaoeal pressure
Type Ill 5% Yes Abnormal Premature simultaneous spastic
contractions "Corkscrew annAarance"
o Management of achalasia:
• Achalasia has no cure

• Medical management (For poor risk patients for intervention)

• Nitrates (lsosorbide dinitrate}

• CCB (Nifedipine)

• Phosphodiestrase-5 inhibitors (Sildenafil) -+ blocks degradation of NO

Taking 30 minutes before the meal

• Endoscopic management
• Botulin um Toxin (For poor risk patients for dilatation or myotomy)
o Block Ach release from nerve endings leading to paralysis
o Temporary effects for 3 - 4 months due to axonal regeneration

• Pneumatic dilatation
o Initial line and most effective non-operative treatment if not
associated with hiatal hernia or tortuous esophagus

o By using handheld manometer with balloon (30 - 40 mm}, inflated

to pressure of 7 - 15 psi until waist is fully flattened, and held for 15
- 60 seconds

o Leads to disrupts the circular fibers of the LES

o Produces relief up to 90%

o > 25% of patient will relapse within 5 years and need dilatation

o GERO can occur in 15% to 30% of patients after PD

o Best to be used in patients> 45 year, female, post-dilatation LES

pressure < 10 mm Hg, and type II achalasia

• Myotomy: Equivalent s!hort-term outcomes compared with LHM

■ Surgical management
• Laparoscopic Heller Myotomy with partial fundoplication
o Most effective treatment (Gold standard) for the achalasia

o Started by Ernst Heller {1913) with anterior and posterior myotomy

of distal esophagus

o Modified by Zaaijer (1923) to anterior extramucosal myotomy only

with equivalent results

o If posterior dissection done + Toupe! fundoplication (270-Post)

o If posterior dissection not done + Dor fundoplication (200-Ant)

o Steps:
• Rapid sequence approach is preferable due to risk of
aspiration of retained esophageal contents
• Endoscopy used to evacuate any residual material
• Esophagomyotomy 2 cm above GEJ by sharp dissection

• Circular muscle fibers, identified, elevated and divided until

submucosal plane identified

• Now myotomy is carried upward 5 cm from GEJ and 2.5 cm

distally to -cardia

• Separate muscle fibers from underlying mucosa

• Repeat endoscopy to confinn integrity of mucosa

• Transthoracic myotomy

• Esophagectomy
o Reserved for advanced achalasia with dilated, tortuous sigmoid
esophagus with diameter > 6 cm and failed to be treated by other
modalities or require resection due to presence of esophageal
pathology
■ Special cases with achalasia:
o Associated with GERO:
• Partial fundoplication with myotomy

o Associated with epiphrenic diverticulum:

• Diverticulectomy with myotomy extending from proximal diverticulum

o Associated with SCC: (mass proximally)

• Esophagectomy if resectable

o Associated with perforation:

• Primary repair
• Opposite-site longitudinal myotomy
• Partial fundoplication
■ Esophageal motility disorders classified into: (Non-Achalasia types}
o Esophagogastric junction outflow obstruction (EGJOO)
• Incomplete relaxation of GEJ defined by elevated Integrated relaxation pressure
{IRP) with preserved peristalsis

o Major motility disorders (always symptomatic; chest pain, dysphagia, regurgitation)

• Distal or diffuse Esophageal Spasm (DES)
• Premature smooth muscle contractions > 20% of swallows
• Due to impaired neurologic inhibitory pathway
• Symptoms similar to coronary artery disease (myocardial infarction)
• Barium showed •corkscrew" pattern of simultaneous contractions
• Management:
o Dietary and behavioral modifications
o If failed or persist follow achalasia management

• Jackhammer esophagus
• Excessive cholinergic drive causing asynchronous hypercontractions of
circular and longitudinal muscle
• Differentiated from nutcracker esophagus, as hypertensive peristalsis with
distal contractile integral (DCI) between 5000 - 8000 mm Hg.s.cm

• Systemic sclerosis (scleroderma)

• Hypocontraction of esophageal smooth muscle, with preserved skeletal
muscle contraction in upper esophageal sphincter
• In very carefully selected cases, RYGBP may be considered for primary
management of refractory GERO in scleroderma
• Edrophonium (cholinesterase inhibitor) causes f LES pressure
• Anti-reflux surgery most likely to failed due to absence of contractility
 o Minor esophageal motility disorders (Can be symptomatic or asymptomatic)
• Ineffective esophageal motility
• 2: 50% of ineffective swallows (low or absent contractile vigor)
• Distal contractile integral (DCI) < 450 mm Hg.s.cm
• Treatment should be targeted to control of GERO

• Fragmented peristalsis
• 2: 50% of fragmented swallows
• With defect in peristaltic contraction of at least 5 cm

Disease Etioloav Manometrv

Achalasla Destruction of inhibitory postganglionic No peristalsis
neuron (Aurbach plexus) of distal Failure or incomplete LES relaxation
esoohaaus and LES f LES pressure but not one of the criteria
DES Impaired neurologic inhibitory pathway f amplitude (> 30 mm Hg) non-peristaltic
Normal LES relax
Nutcracker Excessive cholinergic drive t amplitude peristaltic
(> 200 mm Hg amplitude pressure)
Normal LES relax
Scleroderma Excessive cholinergic drive l peristalsis
Loss of LES pressure

Normal peristalsis in proximal striated muscles

Absent peristalsis in distal smooth muscles
Fibrous replacement of smooth muscles
Dilated esoohaaeal lumen
CONGENITAL DIAPHRAGMATIC HERNIA

Bochdalek Foramen of Morgagni

(Most common)
Site Posteior, Lateral Anterior, Medial
More on Left side More on Right side

Presentation Resoiratorv distress Mostlv asvmotomalic

Sac No sac Well-formed sac
Content Omentum or Transverse colon
Associated anomalies Rare Down or Turner syndrome
(Pulmonary hypoplasia) Malrotation
Genitourinary malformations
Cardiac or neural tube defects

FOfamen of
Bochdalek

Crura
' . . .,
HIATAL HERNIA
■ Associated symptoms:
o Heartburn, regurgitation, postprandial epigastric fullness or pain, dysphagia, vomiting,
weight loss, or dyspnea

■ Preoperative investigations:
o CT chest and abdomen with IV andl oral contrasts

o Assessment of esophageal motility (for patients with dysphagia}

• Cine-esophagogram
• Esophageal manometry (for abnormal esophagogram)
• 24-hour pH test (to assess for reflux if fundoplication is not planned)

o Barium study (Initial test of choice)

o Upper GI endoscopy (Most important investigation)

• To evaluate distal esophagus and stomach and exclude PUD, Barrett's
esophagus, stricture, or neoplasm

Tvoe Tvoe of hernia Associated with Mana<1ement

Type I SI/ding hem/a -GERO Conservative
(most common) - Schatzki ring ± Nissen fundoplication
GE junction above diaphragm ± Collis gastroplasty
Cardia is posterior
No hernia sac
Type II True Paraesophageal - Hiigh risk of Urgent OR
incarceration For symptomatic and
GE junction below diaphragm asymptomatic hernias
Gastric fundus/body herniation -Gastric volvulus
(organoaxial volvulus) ± Nissen fundoplication

-Anemia Conservative management

Type Ill Paraesophagea/ In elderly asymptomatic
Combined (GE junction above diaphragm) patients
Both cardia and fundus of the stomach are herniated
Type IV Paraesophageal
Entire stomach in the chest olus another oraan

■ Approach:
o Laparoscopic approach (Standard of-care)
o Left thoracotomy approach

■ Principles of surgical technique:

o Reduction of herniated abdominal contents
o Excision of hernia sac
o Return ofGastroesophageal junction into abdomen
o Mobilization of intrathoracic esophagus to ensure 2 to 3 cm of tension-free, intra­
abdominal esophagus
o Repair of diaphragmatic hernia defect (esophageal hiatus}
 ■ Controversies:
o Anti-reflux surgery should be used for most patients, even if there is no clear cut reflux
symptoms preoperatively
• By wrapping over tension-free intra-abdominal EG junction over 56F bougie
• Because LES function is not guaranteed after reconstruction

o Posterior onlay polytetrafluoroethylene (PTFE} mesh reinforcement

• Can reduce the recurrence rate
• Associated with long-term complications (stenosis, erosion, perforation)
• Primary repair preferred over prosthetic reinforcement
• Biological material preferred if crura too attenuated for tension-free repair

■ Post-operative care:
o Clear liquid for 72 hours
o Soft diet for 1 weak
o Avoid eating large volumes early in postoperative period to avoid gastric.distension

SCHATZKI RING
■ Submucosal circumferential ring at distal esophagus, at squamocolumnar junction
■ Presented with dysphagia after rapid ingestion of solid foot
o Dysphagia happens if diameter < 1.3 cm

■ Associated with history of drug ingestion

■ No malignant potential
■ Management:
o Observation for asymptomatic patients
o Oral dilatation
o Excision of ring should be avoided

LEIOMYOMA
■ Most common benign esophageal tumor; located in submucosa or muscularis propria
■ Most common site: Distal esophagus
■ Presented with pain and dysphagia
■ Minimal risk of malignancy (preferred to remove it rather than observation)
■ Investigations
o Barium swallow (Most useful method)
o Endoscopic U/S to rule out malignancy
fhypoechoic mass in submucosa or muscularis properia/

o No Biopsy (to avoid perforation if plan for enucleation)

■ Management:
o Small s 3 cm (most of leiomyoma}:
• Extra-mucosal Enucleation ± Primary repair of the defect
• By doing:
• Left thoracotomy for distal esophageal lesions
• Right thoracotomy for proximal or middle esophageal lesions

o Large > 3 cm, or involving GEJ: Esophageal resection

GASTROESOPHAGEAL REFLUX DISEASE (GERO)
■ GERO happens due to incompetent lower esophageal sphincter (LES), resulting from:
o Transient or permanent relaxation
o Increased intra-abdominal pressure

■ Risk factors:
o Obesity, hiatal hernia, pregnancy, delayed gastric emptying, and connective tissue
disorders, H.py/ori have no association

■ Clinical presentation:
o Different than physiological reflux in nocturnal or while supine and may be associated
with mucosal injury (A/ginic acid works as esophageal barrier)
• Physiological reflux happens when person is awake and standing

o Typical (esophageal)
• Burning chest pain, regurgitation of tasteless fluid into mouth (water brash)
• Sensation of lump or tightness in the throat, pain on swallowing {odynophagia)

o Atypical (extra-esophageal)
• Cough, wheezing, hoarseness, sore throat, postnasal drip and ear pain
• Silent reflux if happens without typical symptoms

o Complications (alarms)
• Dysphagia, early satiety, hematemesis, melena, vomiting, and weight loss

■ Complications:
o Erosive esophagitis (Most common complication) and stricture
o Aspiration and asthma
o Barrett's esophagus, and adenocarcinoma
Investigations

■ Confirmatory Investigations:
o Upper GI endoscopy (Initial test)
• To diagnose GERO
• To rule out complications of GERO (Barrett's esophagus, stricture)
• To rule out esophageal disease (Hiatal hernia, short esophagus)

o 24-h esophageal pH probe (Most specific)

• Esophageal pH< 4 is diagnostic

■ Investigati ons to rule out motility disorders:

o Contrast esophagogram
• Used to assess for hiatal hemi.a, short esophagus, dysmotility, and reflux

o Esophageal manometry
• Used to rule out other diagnosis (achalasia) if not improved on treatment
• Used preoperatively to determine type of surgery

• Manometry fjndjno· Incompetent LES

• Hypotensive UES / LES: Resting LES< 6 mmHg
• Overall length< 2 cm (abdominal length< 1 cm)
Stop PP/ 1 week at least before manometry

■ Laryngoscopy if associated with extra-esophageal symptoms

■ Malignancy work-up if alarms symptoms
 ■ Management:
1) Life style modification+ Protein Pump Inhibitors
2) Endoscopic management
3) Surgery

■ Life-style modifications:
o Weight loss
o Avoid chocolate, peppermint, fat, onion, garlic, alcohol, caffeine and nicotine
o Nothing by mouth 2 - 3 hours before sleep
o Elevation head of the bed 6 - 10 in
o Limitation of specific activity such as bending over or strenuous exercises

Endoscopic management (Preserved for poor-ris!k patients)

■ Types of endoscopic anti-reflux repair:
o Synthetic implant injection technique
o Radiofrequency ablation
o Cryoablation and YAG laser
o Argon beam coagulation
o Photodynamic therapy (5-aminolevulinic acid)
o Plicating, suturing, and stapling devices

■ Indications for endoscopic anti-reflux repair:

o Failure of surgical treatment
o Atypical GERD symptom
o PPl-responsive typical GERD symptoms
o Small hiatal hernia < 2 cm
o Mild esophagitis
o Normal esophageal motility
o No Barrett's esophagus
o Unwilling to undergo surgery

■ Contraindication for endoscopic anti-reflux repair:

o Large hiatal hernia > 2 cm
o Severe esophagitis / Barrett's
o Impaired esophageal motility
Surgery
■ Types of fundoplications:
o Posterior fundoplications:
• Nissen 360° (The only total fundoplication type}
• Toupet 270°

o Anterior fundoplications:
• Dor 180 - 200•
• Thal 270°
• Belsey 270° (Trans-thoracic}

o All types of fundoplications are effective and durable anti-reflux repairs, and generate
excellent outcome in 90% of patient

■ Indications for anti-reflux surgery:

o Failure of therapy
o Young patient unwilling to take lifelong medication, or patient preference
o Certain populations, if associated with
• Large hiatal hernia
• Risk of osteoporosis
• Children with GERO
• Associated complications
• Lung transplant candidates

o Silent reflux
o Complications of GERO:
• Structurally defective LES ± Severe endoscopic esophagitis
• Barrett's esophagus (for reflux symptoms not for cancer progression)
• Stricture
• Biopsy to exclude malignancy and trial of dilation with 50 to 60F bougie

■ Indications for partial fundoplication:

o Poor esophageal motility (as in patients with DES)
o Insufficient gastric fundus
o In association with Heller myotomy for achalasia

■ Contraindication of anti-reflux surgery:

Absolute
o Barrett's esophagus with high grade dysplasia or malignancy
o Inability to tolerate general anesthesia
o Uncorrected coagulopathy
o Severe COPD
o Advanced pregnancy

Relative
o Previous upper abdominal surgery
o Morbid obesity
o Severe esophagitis ± stricture
o Short esophagus
o Large para-esophageal hiatal hernia
■ Principles of anti-reflux surgery:
o Restore the pressure of LES to twice resting gastric pressure and ;? 3 cm in length
o Placing adequate length of LES intra-abdominal (as positive pressure}
o Ability of reconstructed cardia to relax with swallowing
o Do not exceed peristaltic ability of distal esophagus
o Fundoplication should be maintained intra-abdominal without tension

■ Technique of fundoplication
o Left posterolateral thoracotomy in the 6th intercostal space

o Proper exposure and elevation of the liver until caudate lobe visualized

o Exploration and reduction of hiatal hernia if present

• Dissection of the sac and hiatal closure posterior to esophagus
• PTFE mesh is used only for large hernia and tension crural repair

o Open the lesser omentum to gain access to the right crus of diaphragm

o Gastrohepatic ligament is identified initially, courses toward right crus of diaphragm

o Replaced left hepatic artery (from left gastric artery} may be encountered before dividing
the gastrohepatic ligament

o Dissection always medial to left crus (to prevent injury to IVC}

The key maneuver for wrap is identification of the left crura

o Vagus nerve should be identified and preserved during distal esophageal dissection

o Achieve a tension free abdominal esophagus

o Creation of flap valve with short intra--abdominal length of 3 cm at least

To increase resting gastric pressure level twice

o Loose wrap and maintain position of the gastric fundus close to distal esophagus

o Ensure relaxation of the sphincter

• Only the fundus of the stomach should be used
• Gastric wrap should be properly placed around the sphincter
• Prevent damage to vagal nerves during dissection

o 360° gastric wrap should be no > 2 cm and constructed over large (50 to 56F) bougie

o Approximation of the crura posteriorly above the repair

■ Laparoscopic port positions for fundoplicatio n:

Sor JO mm
(Surg'<0n's r1gh1 Jund)

I
•.
' ...... ... .
■ Collis gastroplasty:
o Used for short esophagus as lengthening procedure
• As sliding hernia that does not reduced in standing position
• > 5 cm between diaphragmatic crura and GEJ on endoscopy

o By divide the cardia and upper stomach, parallel to lesser curvature of the stomach

Patients with morbid obesity advised to consider Roux en-Y gastric bypass but not sleeve
gastrectomy (may worsen pre-existing GERO)

■ Complications of anti-reflux surgery:

o Pneumothorax: Most common intraoperative complication
o Recurrent GERO
o Gas bloat syndrome: Usually self-limited and resolved within 6 weeks
o Esophageal dysmotility: Either present preoperative or due to obstructive wrap
o Dysphagia
• Mostly because of postoperative edema
• Most common cause of persistent dysphagia: wrap too light

o Gastroparesis
• Options for treatment includes:
• Medical treatment {e.g., domperidone)
• Pyloric Botox injection
• Gastric pacing
• Pyloric drainage procedures

o Esophageal perforation

o Anatomical failure
• Herniated wrap
• Slipped wrap
• Disrupted wrap
• Para-esophageal hernia
• Wrap too tight

■ Most common complications:

o Pneumothorax: Most common intraoperative complication
o Dysphagia
o Slipped wrap
o Most common operative finding on re;peated fundoplication: Herniated wrap

Patients that not responding well to PP/ are unlikely to get benefits from anti-reflux surgery
BARRETT'S ESOPHAGUS
■ Definitions:
o Presence of endoscopically-visible segment of columnar lined esophagus with goblet
cells as consequence of gastroesophageal reflux disease (GERO)

o 2: 3 cm intestinal metaplasia (Squamous -+ Columnar)

At squamocolumnar junction •3 cm proximal to Gastroesophageal junction (GEJ)"

■ Associated with upper-mid esophagus strictures

■ Cancer risk f 30 times-+ Adenocarcinoma (Not SCC)

o Increases risk 0.7% / year for low-grade
o Increases risk 7% / year for high-grade

■ Screening:
o Chronic (>5 years) and/or frequent (weekly or more) symptoms of heartburn or acid
regurgitation and 2: 2 risk factors
o If initial endoscopy is negative-+ No repeat
o If endoscopy is negative but esophagitis-+ PPI and repeat endoscopy in 3 months 10
% risk of BE on repeated endoscopy in esophagitis
o Repeat endoscopy for any nodules or lesions in the columnar mucosa

■ Risk factors:
o > 50 years
o Caucasian race
o Central obesity
o History of BE or esophageal cancer in 1 st degree relatives (P53 mutation)
o Smoking
0 Alcohol

■ Mana gement options:

No dysplasia
o Management of GERO medically
o Surveillance after 1 year then every 3 - 5 years
o Surgery indicated only if GERO is inadequately controlled

With dysplasia
o Low-grade:
• PPI
• Nissen fundoplication (can help in regression to non-dysplastic BE)
• Mucosa! ablation (for persistant low-grade dysplasia)
• Surveillance every 6 -12 months until 2 sessions are negative for dysplasia
• Endoscopy should be repeated to rule out high-grade dysplasia or cancer
• Topical acetic acid spray also may help delineate areas of concern
• Endoscopy follow-up should be after 6 months to assess the response
• 4-quadrant biopsies every 1 to 2 cm throughout columnar segment
(Especially the irregularity part of columnar segment)
o High-grade (severe dysplasia}: Should be confirmed by 2 pathologists
• Endoscopic resection (for small lesions)
• Used for highly selected patients (unfit for thoracotomy)

• Excises full-thickness mucosa, submucosa leaving muscularis properia

• Size: > 1 - 2 cm � EUS for depth of invasion and lymph nodes

• Depth of invasion:
o Mucosa only (T1a): Esophagectomy or endoscopic resection
• Risk of lymph node metastasis: < 2%

o Submucosa (T1 b): Esophagectomy and lymph node dissection

• Risk of lymph node metastasis: 25%

• Techniques of endoscopic ablation:

o Radiofrequency Ablation
• Most common and initial method to be used
• Replaced esophagectomy which was the standard of care
• By using high thermal injury (10- 12 joules) superficially of
0.5 mm depth allow for tissue necrosis and destruction of
500 - 1000 um of superficial tissue, allow for mucosal
regeneration
• Most common complication: Chest pain

o Argon Plasma Coagulation

• By using high-frequency monopolar electrical current
conducted via ionize argon gas
• Depth of penetration from 1 - 3 mm

o Cryotherapy
• Non-contact ablation by using alternating cycles of rapid
freezing by liquid nitrogen or rapidly expanding CO2
• Associated with stricture formation

o Photodynamic Therapy
• Administration of photosensitizing drug "Photofrin or
Porfimer sodium" followed by applying red laser light at 630
nm, 24 - 72 hours later results in generation or reactive 02
and complete tissue destruction in 50 - 75%
• Most common complications: Stricture, Cutaneous
photosensitivity, and AF
 o Endoscopic Mucosa I Resection {Diagnostic and therapeutic)
• Unable to remove > 2 cm lesion as one piece leading to left
residual tissues if removed a piecemeal
• After EMR:
• RFA is used to ablate remaining abnormal mucosa
• Esophagectomy if pathology high-risk tumor
• Repeat EMR and ablation if high-grade dysplasia
persists

o Endoscopic Submucosal Dissection (as therapeutic only)

• Allow to remove > 2 cm lesion as en bloc or ulcerated lesion
involved mucosa and submucosa
• Difficulty of both to treat long-segment BE
• Complications: Stricture, Bleeding, or Perforation

• Esophagectomy ± Lymph node dissection

• Option for high-grade dysplasia and T1 a adenocarcinoma

• Strongly considered ( Standard of care) for:

o Associated with nodules > 3 cm

o Ultra-long segment BE

o Poor esophageal body function with large hiatal hernia or

dysphagia symptoms

o GERD poorly controlled on twice-daily PPI

o Associated with malignancy if:

• > T1 b SM1 adenocarcinoma
• Multifocal adenocarcinoma
• Poorly differentiated tumors
• Lymphovascular invasion
• Squamous histology any grade
(higher propensity for lymph node involvement)

PPls may reduce the risk of progression in patients with BE

Anti-reflux surgery may leads to regression of dysplasia and may reduce the risk of progression
But also there is evidence that failed anti-reflux surgery for reduce progression of the disease
 ESOPHAGEAL CANCER
■ Most common worldwide: sec (Adenocarcinoma in USA)
■ Most common metastasis: Lymph node (60% involved)
■ Most common distant metastasis: Lungs
■ Most preoperative predictor for mortality and morbidity: Nutritional status
o Jejunostomy is the method of choice for feeding of advanced esophageal cancer

o Gastrostomy should be avoided because it may compromise gastric conduit during

reconstruction and will delay chemotherapy for 2 - 4 weeks

Squamous Cell Carcinoma {SCC) Adenocarcinoma

(Most common overall) (Most common in USA)
Risk factors Smoking, Alcohol, More in black men Barrett's Esophagus
GERO
HPV Obesity
Lye stricture (Corrosive ingestion) Smoking
Achalasla Male
Leiomyoma Caucasian
Diverticulum
Nutritional: (Increased intake)
Nutritional: - Red meats
- -
- Zinc and selenium deficiency
Nitrous compounds in food - Iron
Saturated fat

Plummer vlnson syndrome

(dysphagia, iron defteiency anemia, glossitis, and
esophageal web)

Tvlosis fAD of h•=erl<eratosisl

Pathophyslology Metaplasia � Dysplasia
c:, Invasive cancer
Histopathology Hyperkeratosis (Squamous dysplasia) Barrett's mucosa
Columnar epithelium
Goblet cells
Site Proximal and middle esoohaaus Distal and middle esoohaaus
AnnAarance Pearlv-white Salmon-oink
Radiosensitivitv Hinher Lower
Lymph node Higher Lower
involvement

■ Presentation:
o Symptomatic: dysphagia, regurgitation, weight loss (Usually advanced)

o Surveillance: in patients with GERO or Barrett's esophagus

 ■ i
Investigat ons:
o Esophagogram (Barium swallow}: Initial test to guide the UGI endoscopy
• Asymmetrical bulge with an infiltrative appearance
• Apple-core fling defect for symmetrical, circumferential narrowing

o Upper GI endoscopy: Gold standard

• Seattle protocol: 4-quadrants multiple biopsy along every cm of apparent disease
by jumbo forceps ''2.7 mm (1.8 mm in large forceps)"

o CT C hest and Abdomen with IV and Oral contrasts: for unresectability

• Can't differentiate between T3 /T4 (thickness> 5 mm considered abnormal}
• Lymph node> 1 cm in short axis considered abnormal

o PETscan
• Higher sensitivity to detect metastasis
{20% in patient with negative findings on CT or bone scan)

o EUS
• Best for depth of the tumor and para-esophageal lymph nodes
• Suspicious nodes: irregular, distinct border, rounded, hypoechoic,> 1 cm
• Unable to detect nodes> 2 cm from esophageal wall

o Endoscopic mucosa! resection (EMR)

• Diagnostic and therapeutic for lesions < 2 cm (T1a)

o Laparoscopy
• For patient with tumors at GEJ, to asses peritoneal surface, liver, and sampling of
celiac nodes

o Bronchoscopy

■ Staging:

Description Stacie TNM

Tis: Carcinoma In situ 0 Tis
T1a: Lamina propria or mucosa IA T1
T1 b: Submucosa
T2: Muscularis propria IB T2 /T3
T3: Adventltia (Periesophacieal tissue) II A T2 /T3 (NO)
T4: Adjacent structures II B T1 /T2 (N1)
T4a invade adjacent structures usually resectable
(Pleura, diaphragm, pericardium}
T4b invade adiacent structures usuallv unresectable (trachea and aorta)
N1: 1 - 2 Regional lymph nodes Ill T3 N1
N2: 3 - 6 Regional lymph nodes T4
N3: � 7 Realonal lvmoh nodes
Distant metastasis IV M1
 ■ Factors suggest unresectability of esophageal cancer
o Physiological fitness:
• Age > 75 years
• FEV1 < 1.25
• Ejection fraction < 40%
• > 20% weight loss (albumin< 3.5 gldL)

o Physical symptoms:
• Dysphagia or obstruction
• Pain or ulceration
• Bleeding or infection

o Physical signs:
• Stridor, Hoarseness (Laryngeal nerve invasion; most common is left side)
+ Associated with aspiration if not treated
• Hiccups (Phrenic nerve invasfon)
• Horner's syndrome (brachia/ plexus invasion)
• Malignant pleural effusion or Malignant fistula
• Airway invasion or Vertebral invasion
• Distant metastasis (as jaundice)

o Barium signs:
• Tumor length > 8 cm
• Abnormal esophageal axis

o CT signs:
• Contact with aorta > 90 degree
• Bulging into posterior membranous portion of airway
• Loss of retrocrural fat planes
• Peritoneal studding or omental caking
• Multiple enlarged > 4 nodes
• Extra-regional lymph node spread (mediastinal, or suprac/avicu/ar)
• Distant metastasis

Regional lymph nodes: Any pen-esophageal lymph nodes from cervical to ce/iac node

In the previous classifications, ce/iac or cervical nodes for upper thoracic esophagus is considered as
M1 a, nowadays they considered as regional regardless the location of the primary tumor
o Endoscopic signs of unresectability:
• T4b: Transmural tumor invade unresectable adjacent structures
• Aorta, Trachea, Bronchus, or Vertebral body

• T4a involving transmural invasion of resectable adjacent structures

• Diaphragm, Pleura, or Pericardium (is NOT considered unresectable}

o Intra-operative signs of unresectability:

• Unresectable primary
• Cavitary spread
• Extension through mediastinal wall
• Multiple gross lymph node metastases
• Microscopic nodal metastasis at margins of resection
• Distant metastasis
■ Management of resectable esophageal cancer:

o Esophagus-preserving endoscopic management

• Tis or High-grade dysplasia "Confined to mucosa"
• T1 a "Tumor invades lamina properia or muscularis mucosa"
• T1 b SM1 "Tumor invades superficial 1/3 of submucosa"
• Contraindications for Esophagus-preserving therapy
• >T1bSM1
• Nodules >3 cm
• Multifocal
• Squamous histology (higher propensity for lymph node involvement)
• Poorly differentiated tumors
• Lymphovascular invasion

o Esophagectomy with regional lymphadenectomy "with 1 cm negative margin"

• :!: T1 a historically, "due associated with 40% synchronous invasive carcinoma"
• T1 b SM2 / SM3 "Tumor invades submucosa"

o Neoadjuvant chemoradiation ''5FU and Cisplatin" for 6 - 8 weeks

• Positive nodes
• :!: T2 "Locally advanced resectable esophageal cancer"
• Reaching to muscularis propria layer

• If complete response happens:

• Adenocarcinoma: Surgery (No enough study yet)
• sec:
o Salvage esophagectomy: No longer recommended routinely
o Observation: Preferred
• After discussing with the patient benefits/risks
• Less risk of complication
• Minimal risk of recurrence in 1 - 5 years

o Adjuvant chemotherapy
• High-risk of local or systemic recurrence
• T3- T4 tumors
• R1 or R2 resection (residual disease or positive margins)
• Multiple positive lymph nodes

■ Postoperative:
o Allow mucosal healing by reducing acidity
• High-dose PPI
• H2 blocker twice daily
• Sucralfate
• Anti-reflux surgery

■ Follow-up:
o Every 3 - 6 months for 1 year with 4-quadrant biopsies at every 1 cm of treated
mucosa, followed by increase the interval after negative 2 sessions
■ Management of unresectable esophageal cancer: "T4b or M1"
o Chemotherapy for advanced disseminated disease
• Cervical lymph nodes metastasis for lower-mid esophageal cancer
• Celiac nodes for cervical esophageal cancer
• > 4 lymph node involvement

o Radiotherapy for control of local symptoms

o Endoscopic palliation as stenting or dilatation

• Unfit for surgery
• Cardiac, pulmonary or hepatic failure
• Associated trachea-esophageal fistula
 ■ Surgical approach:
o Cervical (8%):
o Upper thoracic (3%):
o Mid thoracic (32%): Right
o Lower thoracic (25%):
o Abdominal:
Left •usually unresectable, different lymphatics•
Right "Avoid the aorta•
"Most common site of adenocarcinoma"
Left
Midline laparotomy

■ Options ofesoohagectomy:
Type Tri-incisional Transhiatal Ivor-Lewis Left Thoracoabdominal
Three-holes
/McKeownl
Location of Preferred for Preferred for middle For middle or lower Tumor beyond 30 - 35 cm
tumor proximal esophagus thoracic esophagus esophagus

Can be used for all For upper, middle or

location lower esophagus
Order of 1) Right Abdominal with left 1) Abdominal Left thoracoabdominal
operation posteriorlateral cervical incision
thoracotomy 2) Right
posteriorlateral
2) Abdominal and left thoracotomy
cervical
Anastomosis Left cervical Left cervical Right chest Left chest
Advantages Used for all tumors No thoracic Good exposure of
incision or thoracic esophagus
Adequate anastomosis
lymphadenectomy Good nodal access
Maximum margins
Maximum margins Low risk of RLN
No need for one- injury
No thoracic lung ventilation
anastomosis Low risk of stricture
Low mortality and and leak
pulmonary
comolications rates
Disadvantages Thoracic incision Inadequate Thoracic incision Large incision
lymphadenectomy and anastomosis
Risk of pulmonary Thoracic anastomosis
complications Risk of bleeding, Not good for tumor
tracheal injury in proximal Risk of GERO
Risk of RLN injury esophagus
Risk of RLN injury Risk of residual tissue and
Need to change Higher mortality rate margins
ruotient oos�ion
■ Primary blood supply to gastric conduit after esophagectomy: Right gastroepiploic artery

■ Interposition:
o Stomach:
• 1 st option to be used
• Best to use for short segment
• Inability to use as conduit if diseased stomach, or previous surgery

o Colonic:
• Left colon is preferable (better size, more reliable blood supply}
• Used for long segment of esophagus and end stage GERD with high Barrett's (to
preserve gastric function}

o Jejunum:
• 3"' option

■ comoijcations ofEsoohagectomy·
o Respiratory complications (Most common}
o Recurrent laryngeal nerve injury
o Chyle leak, Stricture, Atrial fibrillation
CAUSTIC ESOPHAGEAL INJURY
■ Most common site: Antrum, followed by Middle of esophagus

■ Types:
o Alkalis:
• More frequency to be swallowed
• Leads to deeper burns (liquefaction necrosis)

o Acid:
• Causes immediate burns in the mouth
• Leads to superficial burns ( coagulation necrosis)

■ Phases:
o Acute necrotic phase (1 -4 days)

o Ulceration and granulation phase (3 -12 days)

o Cicatrization and scarring (Started at 3rd week}

• Stricture developed in this phase

■ Degree of injury:

Dearee Death Descriotion

pt I Suoerficial mucosa! burn Hvneremia and edema
2nd superficial II A Non-circumferential full thickness
lsuoerficial ulcerations. exudates. slouahina <1/3 lenath\
Transmucosal injury
2nd deep II B Circumferential full thickness
ldeeo ulcerations. exudates slouahina of >1/3 lenoth)
3"' Ill Transmucosal injury Deep ulceration with full-thickness necrosis
± periesoohaoeal

■ Management:
o UGI endoscopy (Investigation of choice)
• Should not introduced beyond the proximal lesion
• Esophagogram with gastrografin swallow and CXR should be done in 48 - 72
hours to rule out consequence of esophageal perforation

o IV fluid and antibiotics to reduce the inflammatory reaction

o NPO, No NG tube
• Oral feeding started when dysphagia regressed

o Neutralization
• Acid: by Milk, egg, antacids
• Alkali: by Vinegar, lemon or orange juice

o Na bicarbonate should be avoided � Risk of perforation

■ Management based on degree of injury:
o 1 st degree: Observation

o 2nd or 3rd degree: Laparotomy

Viable esophagus and stomach

• lntraluminal Stent (Constructed from chest tube)
• Should be keep for 21 days followed by esophagogram

• Biopsy from posterior gastri-c wall

• Air in esophageal/gastri,c wall indicate necrosis and mandates resection

• Jejunostomy

Questionable viability
• 2nd look after 36 hours

Eull-thickness necrosis
• Esophagogast.ric resection
• Indicated in:
o Full-thickness necrosis (as presence of air in the wall)
o Complete stenosis
o Marked irregularity and pocketing
o Fistula

• Order of preference of esophageal substjtute·

o Colon
o Stomach
o Jejunum

• Cervical esophagostomy

• Jejunostomy

• Resection of involved organs

■ comoijcations·
o 24 - 48 hours: Perforation

o 2 - 3 weeks: Stricture (Most common)

o Tracheoesophageal fistula

o Squamous cell carcinoma

o Mediastinal abscess
ESOPHAGEAL PERFORATION
■ Causes:
o Iatrogenic diagnostic (Most common 60%)
• By Upper endoscopy and trans-esophageal echocardiography
• Patient may have underlying pathology that require UGE as esophagitis, stricture
or hiatal hernia
• Site: Upper esophagus. at crioophazyngeus muscle (through killian triangle)

o Spontaneous rupture (Boerhaave's esophagus 15 - 30%)

• Site: Distal esophagus 3 - 5 cm proximal to GE junction at posterior
{Left lower lateral esophagus)

o Other causes: trauma, malignancy, caustic ingestion or foreign body

■ Presentation:
o Vague complains including pain, dysphagia or nausea
o Could be asymptomatic or septic shock (Mortality rate 10 - 40%)

■ Investigations:
o Chest x-ray (Non-specific)
• Pneumomediastinum, pleural effusion, pneumothorax, or SC emphysema

o Esophagography:
• Gastrografin swallow if the initial test of choice
• Barium should be done after gastrografin if contained leak (higher sensitivity)

Agent of choice Contraindicated agent Due to risk

of
Suspe cted Gastrografln Barium (initially) Mediastinitis
oerforatlon
Suspected Barium Gastrografin Pneumonitis
aspiration (water insoluble) (high osmolality iodinated water-soluble agent)

Omnipaque
(nonionic, isotonic
iodinated aoent)

o CT chest and upper abdomen with oral contrast

• Fat stranding, pneumomediastinum, extravasation, effusion, or empyema

o Upper flexible endoscopy

• Used only fori patients with high suspicious of perforation with negative images
• High insufflat on pressure in case of free perforation can lead to tension
pneumothorax

o Pleural fluid > 6.5, and Leukocytosis

 ■ Management of esophageal perforation:

I Perforation

I Contained
I I Free perforation I

Diseased Unstable � Unstable Stable

esophagus or failed Not Visualized Visualized
(Malignancy) non-operative HR< 100 or Contaminated No Contaminated

!
WBC 12- 14
Norma/BP
i
Surgery Non-operative
or management
Diversion

I I Cervical I I Thoracic
I No Contamination I I Contamination
! !
! I Closed drainage
I I Diversion
I
I Stenting
I Diversion
"Loop esophagostomy
I
and open jejunostomy or
gastrostomy" I Early(< 24 h) I I Late (> 24 h) I
!
Primary repair Primary repair "preferable"
(2-layers) (1-layer)

Esophagectomy
''if associated with necrosis or
inflamed esophagus"
■ Special conditions:

o Perforation associated with achalasia:

• Opposite-site longitudinal myotomy is required along with repair
• Partial fundoplication

o Perforation after Nissen fundopljcation:

• Laparotomy
• Dismantling of the fundoplication
• Primary repair of the esophagus
• Repeat Nissen fundoplication

o Perforation after esophaqectomy:

• Diagnostic thoracoscopy or thoracotomy
• Viable Gastric conduit:
• Chest tube placement for all patients with free leak
• Wide drain the anastomosis for cervical leak
• Primary repair of small tear
• Revision for larger tear
• Stent placement can be used

• Necrotic. or gangrenous Gastric conduit:

• Right thoracotomy and reduce gastric remnant into the abdomen
• Cervical esophagoslomy and gastrostomy
• Delayed reconstruction of the esophagus

o Perforation associated with malignancy:

• Addressing the mass at time of OR is required

• Options:
• Esophagectomy with immediate reconstruction:
o For stable patient without contamination

• Esophgogastrostomy:
o For unstable pati,ent or massive contamination

• Esophageal stenting:
o For stable patient with contained perforation
■ Approach to esophageal perforation:
o Upper and Middle Thoracic: Right Posteriolateral Thoracotomy
o Lower Thoracic: (Most common) Left Posteriolateral Thoracotomy
o GE junction: Midline laparotomy

■ Non-operative management includes:

o ICU admission
o NPO and head elevation
o IV antibiotics ± anlifungal if located at distal esophagus
o PPI
o Consider TPN
o Start liquid diet if no perforation on repeated images 72 - 96 hours

■ Primary repair:
o Buttressed with intercostal or diaphragmatic flaps for thoracic esophagus
o Buttressed with omentum or rotational flap for abdominal esophagus

■ Esophageal stenting ·
o indications·
• Palliative for malignancy
• Iatrogenic perforation
• Boerhaave's syndrome
• Anastomotic leak

o Complications:
• GERO and globus sensation
• Bleeding, perforation or migration 30%
• Late complications: Tumor ingrowth, fistula, occlusion, or stricture
Stomach
Reviewed by:

Dr. Saeed Shomimi

Stomach
ANATOMY AND PHYSIOLOGY
Right GEA
Gastroduodenalartery
SPDA
Common Hepatic Artery Proper Hepatic Artery

Right gastric artery

CELIAC TRUNK

(From Ventral of Splenic Artery Left GEA

supra-renal aorta)
Short Gastric Artery

Left Gastric Artery Pancreatic artery

Posterior gastric artery

"supply posterior fundus'1
Right, Middle colic arteries
SMA
lleocolic artery
(From Ventral of
supra-renal aorta)
IPDA

Left colic artery

-l:==============:
IMA
Sigmoid artery
(From Left lateral
infra-renal aorta)
Superior rectal artery

■ Greater curvature:
o Proximal part: Left gastroepiploic artery
Short gastric artery supply the fundus and proximal part above splenic artery
o Distal part: Right gastroepiploic artery

■ Lesser curvature:
o Proximal part: Left gastric artery
o Distal part: Right gastric artery
Left gastric artery ligation can cause transient left hepatic ischemia (in replaced left
hepatic artery)

■ Pylorus: Gastroduodenal artery

Anatomical angles:
■ Angle of His: angle of leak
■ Insurance angularis: angle of stricture
■ Gastrosplenic ligament: angle of bleed
Lymphatic drainage
■ Divided into 4 zones:

Cel,ac nodes

Zone From Groups

Zone I (Inferior gastric) Pylorus and distal greater curvature 0 Inferior Qastric node
0 Subpyloric node

+ Rlaht aastroeplplolc node

Zone II (splenic) Proximal greater curvature 0 Pancreaticosplenic node

+ Left aastroecicloic node

Zone Ill (superior gastric) Proximal lesser curvature 0 Superior Qastric node
0 Pericardia node

+ Left aastric node

Zone IV (Hepatic) Pylorus and distal lesser curvature 0 Suprapyloric node

+ Riaht aastric node

All four zones of lymph nodes drain into the celiac group and into the thoracic duct

■ Gastric lymph nodes divided into 20 stations

-..---·-l·-.,.• .....
(First 12 stations classified as regional lymph nodes)

...
.{
•
-�� -·-····---------··
..... �
.•·
A:!\.,
($ / '
-'!ttl- - , �
 GASTROINTESTINAL HORMONES

Source Source Tvoe of Cell Honnones Activity Notes

NSAIDs inhibit
Cardia HCO3
HCO3
Chief cells Pensinonen 1 st enzvme in oroteolvsis
Fundus and Release HCI Acidification
body Parietal cells H' Antral distension
intrinsic factor IF binds B12 (absorbed in Stimulates:
terminal ileum) -+Somatostatin
Stomach Release HCI -+Secretin
Peristalsis -+CCK
G cells Gastrin
Stimulate parietal cells -+Motilin
Antrum and -+GIP
pylorus ''Universal-off switch" Used in:
D cells Inhibit all GIT hormones Pancreatic disease
Somatostatln
(Pancreas) t bile secretion UGIB
1 exocrine pancreas
M cells Gastric emptying Motilin receptors
i
Motil n GB contraction in fasting located on smooth
(Antrum)
MMC activation muscle cells
Delay Qastric emptyinQ Half-life•
GB contraction in meal 2-3 minutes
Intestines Duodenum Relaxation sphincter
I cells CCK
Oddi
t exocrine pancreas
1 bile secretion
HCO3 secretion
S cells Secretin
t bile secretion Stimulated bv bile

■ Gastrin-release peptide "Bombesin": universal-on switch for all GI hormones except secretin

■ Stomach -+ Gherlin -+l Appetite

■ Duodenum -+ Leptin (works on ileum) -+ ! Appetite
■ Satiety hormones:
o CCK and Leptin

■ Peristalsis: occurs only in antrum (distal stomach)

■ Drugs:
o Ranitidine blocks gastrin receptors (IH2-recceptor blockers)
o Omeprazole irreversibly blocks H'/K• ATPase in parietal cell
� The only drug that induce achlorhydria
� halt-time: 24 hours

o Erythromycin: Motilin agonist

o Metoclopramide: Dopamine antagonist
o Domperidone: Dopamine antagonist
 ■ Causes of changes in gastrin level:
t Gastrin
Acid Suppression Acid production ! Gastrin
(BAO < 10 mErt oH > 2) (BAO> 10 mErt aH < 2)
Vaaotomv Antral hvnero/asia Antral distension
Atroohic or chronic aastritis Retained antrum {in B/1/roth //J Acidification
Protein oumo inhibitor Secretin fin aastrin oma\ Secretin
Short bowel svndrome Gastrinoma Somatostatin
Massive bowel resection Luminal oeotides. amino acids <ootent stimulator\ Luminal acids
Renal failure DM Gastric outlet obstruction Hvnothvroidism
Pernicious anemia H. Pvlori

■ Gast ric emptying:

"Dumping• "Gastropariesis"
Increased emntvina Delav emotvina
Zollinaer Ellison svndrome (ZES) Duodenal distension
t Gastrin Alkaline environment
Previous surgery Previous surgery
- Retained antrum (In B/1/roth II) - Previous vagotomy
- Massive bowel resection (without drainaae orocedure)
DruQs Hormones:
- Metoclopramide - CCK
- Erythromycin - Secretin
- Somatostatin
Nutritional:
- Lipid
- Proteins
Hvoeralvcemia
Hvookalemia
Gastric outlet obstruction
Ooioids
ACID-REDUCING SURGERY

ANTRECTOMY

VAGOTOMIES
■ Vagotomy used to eliminate parasympathetic innervation of any remaining acid-producing
stomach tissue to decrease acidity in gastric outlet obstruction and PUD

■ Anatomy:
o Right vagus: Posterior to esophagus
Q Posterior gastric branch
• Criminal nerve of Grassi: branch of posterior gastric -+ recurrent ulcer
Q Celiac branch

o Left vagus: Anterior to esophagus

Q Anterior gastric branch: along the lesser curvature with posterior branch
Q Hepatic branch

o Nerves of Latarjet: Terminal branches of anterior and posterior gastric branches

■ Most common indication to perform vagotomy: Patient on Protein pump inhibitor (PPI}
■ Most common complication of vagotomy: Diarrhea
■ Most common cause of recurrent PUD: Incomplete vagotomy (if posterior vagus not divided)
■ Incomplete vagotomy can be assessed by: Pancreatic polypeptide level
■ Truncal vagotomy
o t Basal acid output by 90%, f gastrin, f Intra-gastric pressure
o Need for drainage procedure (antrectomy, pyloroplasty, or gastrojejunostomy}
o 10 - 20% have bile reflux gastritis (treated by conversion of billroth II to Rouex-en-Y)

■ Proxjmal yagotomy "Highly selective vagotomy or Parietal cell vagotomy'

o No need for drainage procedure
o Taylor operation (posterior truncal vagotomy and anterior highly selective vagotomy} is
alternative to parietal cell vagotomy.

Comparison of different types of vagotomy:

Truncal vagotomy Highly selective Truncal vagotomy

with Antrectomv vaqotomv with Pvloroplastv
Indications Refractory duodenal ulcer, Intractable symptoms Emeraency
aastric ulcer tvnA II and 111 Perforated ulcers /Perforation bleedinal
Mortalitv rate Hiahest 12%l Lowest Averaae
Liauid emotvina t t t
Solid emptying ! Normal 1
(Postprandial hvoerinsulinemia) (Dumpinol
Diarrhea Averaae Lowest Hiahest
Dumplna Hiahest Lowest Averaae
PUD recurrence Lowest Hiahest Averaae
 Comparison of different types of vagotomy:

Divide Preserve
Truncal Divide vagal trunks at level of esophagus
before celiac and heoatic branches 4 cm oroxlmal to GEJ
Selective Anterior and posterior gastric Preserve celiac and hepatic branches
branches

Divide vagal trunks distal to level of

esophagus just below the posterior
celiac branches
Highly Divide terminal branches of anterior and Preserved Crow's foot during branching 6 cm
selective posterior Qastric branches of proximal proximal to pylorus on lesser curvature
2/3 of the stomach (Which are the end branches of Latarjet nerves)

Divide Anterior nerve of Latarjet Preserve main anterior and posterior branches of
"Terminal left vagal branch" vagal trunks
+ Provide motor function to the pylorus
Located on lesser curvature Preserve celiac and hepatic branches

Divide Posterior nerve of Latarjet
"Terminal right vagal branch"
Divide Criminal nerve of Grassl
Preserve vagal branches to antrum and pylorus
Preserve innervation of pyloroantral reQion
(gastric emptying)
Preserve distal 1/3 of the stomach to maintain
antral function

•Truncal

.Selective
(Total gastric)
1::;.Proximal
(Jll4h1Yaelectivo,
Parietal cell)
\��cl�::::.--:".':':::::..
Steps of open truncal vagotomy: {Can be done laparoscopica/ly)
■ Midline laparotomy extended to xiphoid process (with good light source)

■ Retraction of greater curvature on the gastroesophageal junction and lower esophagus

■ Incise peritoneal cover horizontally from angle of lesser curvature to cardiac notch
o by retraction of peritoneum with forceps to avoid injury of anterior vagus nerve

■ Mobilize the esophagus by blunt dissection of thumb and index encircle the esophagus
■ Anterior vagal trunk is identified in anterior midportion of esophagus, 2 - 4 cm above GEJ

■ 2 - 4 cm segments separated from surrounding tissue, and resection of 2 cm by applying clips

at most superior and most inferior parts and send to histopathology

■ Posterior vagal trunk identified along the right edge of the esophagus
■ By applying gentle tension on GEJ, lead to "bowstring" of posterior vagus, then 2 cm resected
by the same maneuver and send to histopathology
UPPER GASTROINTESTINAL BLEEDING
■ Obscure bleeding:
o Bleeding persists or recurs after negative evaluation by endoscopy

■ Occult bleeding:
o Bleeding not apparent to the patient, only related complications (such as anemia)

■ Causes of upper GI bJeeding·

o Non-Variceal bleeding: PUD, Gastritis or Esophagitis, Mallory Weiss tear or tumors

o Variceal bleeding
Q Gastroesophageal varices
Q Hypertensive portal gastropathy
Q Isolated gastric varices (IGV): Not in continuation with esophageal varices
• Isolated GV are related to gastroepiploic (GEV) veins
• Types:
o IGV-1: located in fundus (Treated as esophageal varices)
0 IGV-2: located distally

• Management:
o Conservative: for non-bleeding varices
o Balloon tamponade by Sengstaken-Blakemore tube
• Temporary for life-threatening uncontrolled bleeding

o Endoscopic management:
• By sclerotherapy, varix ligation or cyanoacrylate injection
• Should not be used if there is splenic vein thrombosis

o Depend on the type of portal hypertension:

• Non-segmental portal hypertension: TIPS shunt
• Segmental or left sided (Sinistral) portal hypertension:
• Caused by splenic vein thrombosis as result of
chronic pancreatitis
• Managed by splenectomy

o Liver transplant: for cirrhotic patient

■ Forrest Classification of endoscopic findings and risk of rebleeding in PUD:

Grade
Grade I
(Active hemorrhage)
 Alaorithm of manaaement of uooer aastrointestinal bleedina·
Supportive Care
Resuscitation + NGT and Foley's ± Intubation ± ICU management
(Cold lavage is not recommended anymore)

Pre-Endoscopy

I
I
I I
Variceal bleeding Non-Variceal bleeding

• (Susllicious of llOrtal hJ,:'.llertension}

Somatostatin analogue (Octreotide) • IV PPI (Omeprazole)
(50 µg bolus IV over 5 min) 80 mg bolus followed by
followed by continuous infusion 8 mg/hour for 72 hours
25 g/hour for 72 hours post-endoscopy
0 if active bleeding at endoscopy + 12 mg/day
+ Then change it to orally

0 ! portal pressure by ! blood flow • IV Erythromycin

• Long-acting vasopressin analogue {Terlipressin)
3 mg/kg over 20 -30 min
30-90 min prior to endoscopy
Efficacy to control acute variceal bleeding: 70 - 80%
Side effects: vasoconstriction (ischemia, infarction) Binds to motilin receptor and
Best (Octreotide + Terlipressin)

•
stimulate smooth muscle
contraction
No oral medications (Including beta blockers)

1) Endoscopy (within 4 - 24 hours)

Endoscopy
(within 4 - 24 hours)

I
I I
Variceal bleeding Non-Variceal bleeding

1) Band ligation: (Most common method and the best)

- Begin with largest column of varices at most distal point
- NGT or feeding tubes avoided as not to dislodge any elastic bands 1) Mechanical treatment
- Repeat band ligation 10-14 days interval (3-4 sessions) until the
varices are eradicated
2) Thermal treatment
2) Sclerotherapy:
- Sclerosants: (1 - 5 ml for each varix)
• Ethanolamine 3} Injection of epinephrine
• Na morrhuate or Na tetradecyl sulfate
· l:;Q[lJ!liiQiillis:m:i' Rebleeding, Perforation
 I Uncontrolled (Refractory) Variceal bleeding
I
I
Mild • Moderate
I
Severe

Repeat endoscopy within 72 hours Balloon tamponade as temporary method

(Sengstaken-Blakemore tube)
- Most common complication: Aspiration pneumonia
- Reb leeding in: 50%
- Duration should be < 36 hours

I Uncontrolled by tamponade, Recurrent bleeding

Isolated gastric varices
- Endoscopic ablation (obturation)
- Cyanoacrylate glue
- Thrombin
I
I I
I No liver diseases
Child A f B (Without ascites)
Child B (with ascites)
Child C
Refractory ascites
I
I
Splenic vein;,, 1 cm Splenic vein < 1 cm
or Thrombosed and no thrombosis

- TIPS (alternative) !
DSRS

I
If(+) si:1lenic vein thrombosis: '

11
- Splenic artery embolization
- Splenectomy {TIPS is alternative) Surgical shunt Emergency TIPS

I
♦ ♦
I ♦
As definitive treatment Anatomy not suitable Oecompensation

Sugiura procedure Liver transplant

■ Peri-endoscopy for Non-variceal bleeding:

o Resuscitation
o Platelets infusion if< 30,000
o Blood transfusion if Hb< 7 g/dl (< 10 g/dl in high-risk patients)
PEPTIC ULCER
■ Defects in the gastrointestinal mucosa that extend through the muscularis mucosae with
hypersecretion of acid

■ Pathophysiology:
o Gastric ulcer: defect in gastric mucosa
o Duodenal ulcer: increased acid-peptide action on mucosa
Q Not associated with l gastrin level (associated with t Basal pentagastrin)

■ Risk factors:
o Helicobacter pylori infection

o Antral gastritis

o Gastrinoma (Zollinger-Ellison syndrome)

o Crohn's disease

0 Alcohol

o Smoking

o Stress

o Chemotherapy

o Radiation

o Steroids

o NSAIDs
Q Daily low-dose aspirin can be taken with PPI

Gastric ulcer Duodenal ulcer

Associated with weight loss Most common
Pain increased with meal Pain decreased with meal
.lnitialll( decreased but ecurs a e short ·nterva
Pain started 30 min after the meal Pain started 2 - 3 hours after meal and at night
70°0 associated with H. m,lori 100% associated with H. m,,,l"' ori._______
Blood ty,_,1',_e A, -- -- B loo
_ d,
. t
., y__f)e 0, non-secretor
__ __,-c.,..,-,---
,___potential ra;:, _, haroor malignancy
1 - 3 % malignancy Rarely
DUODENAL ULCER
■ Most common type of peptic ulcer

■ Most common site: 1•• part of the duodenum

o Anterior ulcer associated with perforation (Most common type)
o Posterior ulcers associated with bleeding (GOA is most common source)

■ Perforated duodenal ulcer:

o Most common indication for surgery in duodenal ulcer

o Tachycardia is the only early symptom

o Pneumoperitoneum absent in 10 - 15% in cases on upright x-ray

o Culture should be taken (biopsy only for suspicious of malignancy •mass")

o PPI and IV antibiotics for all patients

i
o Post ERCP perforat on associated with different causes:
� Post Sphincterotomy (small, retroperitoneal perforation)
� Perforation by the scope
c:> Perforation due to manipulation
� Perforation by guide-wire (associated with large air, and small perforation)
■ Management of perforated duodenal ulcer:
o Sealed perforation
� Clinically: Stable vital signs, No peritonitis
� Radiologically: No free air, contained fluid, no defect, no contrast extravasation,
enhanced thin wall
� Managed conservatively

o Small free perforation

� Peritoneal washout and Graham patch
� No closure by suture, only omental plug and fixation
• Friable tissue can make defect bigger
• May narrow scarred gastric outlet

o Large free perforation (> 2 cm)

� Anastomosis with Roux limb
� Jejunal "serosal patch"

o Definitive procedure:
� Indications:
• Large, multiple or intrac1able duodenal ulcer
• Giant perforation
• Gastric ulcer
• Gastric outlet obstruction
• Bleeding associated with perforation
• Unable to afford medications

� Options:
• Gastrojejunstomy and vagotomy
• TV and antrectomy
• HSV

o Types of patch:
� Graham's patch ID): Plugging the perforation with free omental plug

� Modified Graham's omentopex:y /B}:

• after primary repair, placing omental flap and tie the same stitches over
the vascularized omentum

� CeUan jones repair- Plugging the perforation with omental pedicle

b primary ctosur. wkb C Clffl911Cal pecJde bo, , cl FtN oroentat plug :

a primary closure omental pedlcle flap Cen. ·Jones� Orahem pach
■ Bleeding duodenal ulcer:
o Most common reason for hospitalization in duodenal ulcer
o Deep posterior bleeding ulcers in the proximal duodenum are worrisome because may
involve gastroduodenal artery (GOA)

■ Management of bleeding duodenal ulcer:

o Conservative
• 75% will stops by only IV fluid and PPI infusion

o Endoscopic management
• Mechanical
• Hemoclip
• Endoscopic band ligation
• Balloon tamponade

• Thermal
• Bipolar electrocautery
• Argon plasma coagulation

• Injection
• Epinephrine injection (1 :10000) ± sclerotherapy (may leads to necrosis)
• Fibrin sealant injection

o Repeat endoscopic managem,ent ± Angioembolization

o Surgery
• Bleeding in low-risk patient:
• Oversewing with vagotomy and pyloroplasty

• Kissing duodenal ulcer (Perforated + Bleeding, or signs of bleeding)

• Closure of the perforation with omental patch and duodenotomy with
oversewing of posterior ulcer
o Surgery
Indications: Re-bleeding in unstable patient or> 6 units PRBCs /24 hours

Options:
Oversewing alone
Oversewing with vagotomy and drainage ;'Lowest mortality"
Antrectomy and vagotomy ;towest rebleeding rate"

Steps:
• Make sure NGT inserted
• Upper midline incision ± left to xiphoid extension
• Mobilization
• Kocherization ± Take down triangular ligament to mobilize left lobe liver
o Replaced right hepatic artery can be injured during kocherization
o Kocherization should be done in all patients for tension-free closure

• Identify pylorus either by:

o Palpation of pyloric ring
o Before vein of Mayo {Tributary of right gastric vein)

• 2 Traction sutures placed cephalad and caudal just after pylorus or by

using Babcock
• 6 cm Longitudinal (Horizontal) enterotomy to expose posterior bleeding ulcer
• GDA runs from cephalic to caudal

• By using finger pressure till resuscitation of the patient

• 4-quadrant suture ligation for bleeding anterior ulcer

• U stitch or Figure of 8 used to control bleeding from anterior aspect

• It should be deep enough at ulcer bed to include deep transverse
pancreatic artery (Posterior branch of GOA), but not that deep to prevent
CBD injury

• Control bleeding from:

o Proximal and distal gastroduodenal artery (GDA)
o Deep transverse pancreatic artery

• If bleeding still not stop:

o Make sure kocherization is performed
o Expose posterior duodenum
o Apply figure of 8 from posterior aspect
 • Closure of duodenotomy by Heineke-Mikulicz pyloroplasty
• By traction cephalic and caudal
• Then close it Transverse (Vertical) by taking full thickness
• Take a 2 nd layer to prevent dog-ear
• If there is tension -+ perform kocherization

---------
A B

• ± Truncal vagotomy

o Unstable patient:
• Midline incision, and duodenotomy followed by digital pressure
• U-stitch in clean healthy edge (for transverse pancreatic artery)
 ■ Surgical indications for peptic ulcer diseases:

Duodenal ulcer Gastric ulcer

Bleeding (Stable) (Stable)
Not on PPI Oversaw, biopsy and TV pyloroplasty
Oversaw of GDA only
"Not controlled by Distal gastrectomy (Best option)
endoscopic measures"
On PPI
Oversaw of GDA + TV + Pyloroplasty /Unstable or high-risk)
Oversaw and biopsy
/Unstable or high-risk)
Oversaw of GDA only

ILal.t QRlllm "Deflnltlllt"l ILHl Qptlon "Defln!11llt"l

TV + Antrectomy Total vs. Subtotal gastrectomy
"Used after rebleeding" "Used for diffuse life-threatening
bleedina"
Free Perforation (La5t 2pti20 "D11fioitill11"l (Stabl11 Q[ IOlll·[i:ils "D11fioitillll")
TV + Antrectomy
Small ulcer

•
/Stable)
Not on PPI
Graham Patch
Wedge excision and TV + Pyloroplasty
■ On PPI
Formal gastric resection
± TV + Pyloroplasty
■ Not on PPI (Negative biOQS)l}
■ On PPI Left alone, oversewn, or patched
Graham Patch + HSV
(Best option for patient with Large ulcer
treated or negative H. pylori) Distal gastrectomy
(Antrectomy ± Vagotomy)
Large ulcer> 2 cm
Jejuna! patch Stress ulcer
Anastomosis with Roux limb Wedge excision and primary closure

Giant ulcer
Definitive surgery {Unstable or high-risk)
Biopsy and Graham patch
{Unstable or hig!]-risk)
Graham patch ± Pyloric exclusion
with aastroenterostomv
Obstruction (Laat 2ml2n "Deflnltllle") (Stable Q[ IQlll·tllll "Deflnltllle")
T V + Antrectomy Distal gastrectomy

(Unstable or high-risk) /Unstable or high-risk)

Gastroieiunostomv + HSV Biopsy + Gastroieiunostomv + HSV
Intractability /Oeeration of choice): HSV (Stable or low-risk "De finitive")
Distal gastrectomy
(Non-healing> 3 months /Other oetionsl
after completion of PP/ TV + Pyloroplasty Wedge excision + HSV
therano,l TV + Antrectomy
Upper endoscopy should be repeated 6 weeks after treatment of PUD to rule out malignancy
 GASTRIC ULCER
■ Most common location: on lesser curvature of the stomach (at Insurance angularis)
■ Most common complication: Perforation

■ Definitive management for gastric ulcer is: Excision (Considered as malignant)

o Even in negative biopsy

■ Ulcer located at lesser curvature is likely to cause •tea por and hourglass stomach

■ Ulcer located at the pylorus is likely to cause f Acid

■ Johnson Classification of gastric ulcers:

Location Acidity Association Manaqement

Type I Distal lesser curve Normal Blood group A Distal gastrectomy + Blllroth I
"Most common" at incisura Antral aastritis
Type II Two Ulcers: l TV + Billroth I
(Drag_stedt! Lesser curve •vagotomy indicated only if failed
Duodenum antacids or unreliable patients•
Type Ill Pre-pyloric l TV+ Blllroth I (preferable)
TV + Blllroth II or Roux-en-y GJ
•vagotomy indicated only if failed
antacids or unreliable =tients•
Type IV Proximal lesser Normal T risk of > 2 cm from GEJ:
curve near GEJ bleeding Pauchet 12roC!!dUr!!
Distal gastrectomy + Billroth I

< 2 cm from GEJ:

Csends erocedure
Subtotal gastrectomy + roux-en-y
ieiunal reconstruction
Type V Diffuse ulcer Normal NSAIDs Stop NSAIDs
Steroids Misoprostol "prostaglandin analogue"
May help prevent NSAIDs-ulcer

PPI or anti-histamine

Anterior gastrostomy and

oversewlng major sites of
bleeding

Total gastrectomy
in life-threatenina bleedina
 Features of benian aastric ulcer
On lesser curvature
Small ulcer I< 1 cm)
Reaular shape
Ulcer niche
Hiah acid /TvnA 11. Ill)
Not comolicated
Treated with medical treatment
!features of malianant aastric ulcer
On areater curvature
Giant ulcer(> 2 cm diameter\
lrreaular shape
Ulcer notch
Low acid /Tvne I. IV V ulcers and ulcers not located in nvtorus)
Perforated > Obstructed ulcers
Do not heal at 12 weeks desoite medical treatment

■ Upper endoscopy + Biopsy

o 8 biopsies from 4 quadrants should be taken from the base and the rim of the ulcer
o Most accurate if taken from the rim of the ulcer, and from antrum area
o Endoscopy should be repeated after 6 - 8 weeks

■ Frozen section at time of surgery may change extent of resection and lymphadenectomy

■ Low-acid gastric ulcer /Lesser or Greater curvature) can be managed by either:

o Biopsy, edges debridement and primary repair

o Wedge excision and frozen section

� For small perforated gastric ulcer in low-risk stable patients not on PPI
� For ulcer located on anterior wall of the stomach
� For ulcer located > 2 cm far from pylorus and gastroesophageal junction

o Formal resection {Antrectomy ± acid-reducing operation)

� For most types of gastric ulcer, or complicated gastric ulcer
� For large perforated gastric ulcer or in patients on PPI
HELICOBACTER PYLORI
■ Gram Negative(-) aerobes, motile rods
■ Risk factor for both PUD and gastric cancer
o Treatment will decrease the recurrence rate of PUD and risk of malignancy
o Not associated with Achalasia and GERD

■ Pathophysiology:
o Hypergastrinemia
Q Inhibit antral D cells (inhibition of somatostatin)
Q Hypersecretion of acid

o Antral alkalinization
Q Inhibit Somatostatin release

o Colonization in duodenum
Q Inhibit HC03 release

■ Test for screening "initial test": Rapid urease test

■ Test for diagnosis "100% accurate": Culture and histological examination from "antrum•
■ Eradication test: Urea breath test in 4 - 6 weeks
■ H.Pylori examination is not needed for complicated ulcer {bleeding, perforation) but eradication
test after treatment should be used in all cases

■ Management:
o Clarithromycin 500 mg q 8 hours for 2 weeks
o Metronidazole or Amoxacillin 1 q 12 hours (q 8 hours if used alone) for 2 weeks
o PPI with endoscopy in 8 - 12 weeks (discontinue if ulcer healed by endoscopy)

Consider lifelong PP/ if vagotomy not performed

Long-term gastric acid suppression is associated with C. difficile colitis

OTHER TYPES OF ULCER

■ Cameron ulcer:
o Gastric ulcer with paraesophageal hernia

■ Stress ulcer
o Most common site: Fundus (along with autoimmune gastritis)

o Findings on endoscopy:
Q Multiple sallow lesions with discrete areas of erythema with focal hemorrhage

o Sucralfate: t duodenal HC03 used in stress ulcer & PUD in pregnancy

o Perforated stress ulcer treated with excision and primary repair only
GASTROINTESTINAL RECONSTRUCTION
■ Indications:
o After distal gastrectomy or antrectomy
c:> Urgent surgery for peptic ulcer, or Gastric ulcer
c:> Recurrent ulcer despites anti-secretory medications

■ Billroth I (Anatomical)
o Antrectomy and gastroduodenostomy
o Indications:
c:> Preferred operation for most benign gastric ulcer
c:> Duodenal ulcer if recurrent or bleeding when pyloroplasy not feasible

o Advantages:
c:> Most anatomical and physiological anastomosis
c:> Technical easy

o Disadvantages:
c:> Alkaline reflux syndrome (Most common)
c:> Dumping syndrome
� Associated with extensive duodenal mobilization

■ Billroth II (Non-anatomical)
o Antrectomy and loop gastrojejunostomy
o Indications:
� Distal gastric ulcer or cancer that requires extensive duodenal mobilization
� Scarred duodenum or tension associated with Billroth I

o Advantage: One anastomosis, and ease of construction

o Disadvantages:
c:> Alkaline reflux syndrome (Most common)
� Retained antrum syndrome
� Duodenal stump leak "blow-out''
� Afferent or efferent loop obstruct ion
� Marginal ulcer, Internal hernia, lntussusception, or Stricture
c:> Malabsorption and anemia (Most common)

■ Roux-en-Y gastrojejunostomy (Least preferable)

o Reserved for patients who have complications associated with Billroth II
o Preferred in patients without previous vagotomy
o Roux limb should be 45 - 60 cm long to ensure the absence of bile in gastric pouch
o Advantage: Less reflux esophagitis, gastritis and less dumping
o Disadvantages:
� Gastric atony "Roux stasis syndrome", especially in patients had vagotomy
c:> Same as Billroth II

Gastrotomy done by incision near to pylorus close to greater cuNature in longitudinal direction
(to prevent compromising of blood supply)

Local resection of stomach near to lesser cuNature may vagotomize the an/rum and pylorus leading
to gastric stasis, which may need drainage procedure
■ Duodenal stump leak:
o Extensive inflammation and, or scar may render secure duodenal closure

o Duodenal stump leak usually happends as result of afferent limb obstruction

• After Billroth I -+ As lateral duodenal leak (in continuity with stomach)
• After Billroth II -+ As end duodenal leak

o Gastrostomy and feeding jejunostomy should be considered in patients with diffcult

duodenal closure

o Management:
• Percutaneous drainage
• Can be successful along lbowel rest lateral duodenal leak (after Billroth I)

• Bowel rest, NGT, and TPN

• NGT positioned with the tip in the afferent limb near distal duodenum

• Re-exploration (Definitive management}

• Indications:
o Failure of conerv.ative management for 6 weeks
o Peritonitis

• Options for repair:

o Primary repair with omental patch
• Used for lateral duodenal leak

o Retrograde tube duodenostomy + Wide drainage "Preferred"

• To create controlled duodenocutanous fistula
• To be fixed as Witzel retrograde jejunostomy
• Omentum is sewn over the closure
• Used for end duodenal leak

o Lateral tube duodenostomy

o Duodenotomy closed around a tube "end duodenostomy"

• Used as last option

o Roux limb anastomosed to the end of the open duodenum

GASTRIC DRAINAGE PROCEDURE

1lGASTROJEJUNOSTOMY
■ Most common indication: Gastric outlet obstruction (GOO}
o By stethoscope: "Succussion splash" can be heard
o Some patient with (GOO} may benefits from TPN as pre-op preparation

■ For resectable cancer of antropyloric region after subtotal gastrectomy

■ For nonresectable cancer of stomach as palliative treatment
o Roux-en-Y gastrojejunostomy
• Used in bariatric surgery, dumping syndrome, alkaline reflux gastritis

Types:
■ According to relation of transverse colon:
o Anteocolic -+ easy, preferred in malignancy
o Risk of volvulus, delayed gastric emptying

o Retrocolic -+ preferred in simple obstruction

o Lower rate of afferent loop syndrome "minimizes length of afferent limb"
o Risk of GJ-colic fistula, obstruction in malignancy

2) PYLORIC DILATION
3) PYLOROMYOTOMY

4) PYLOROPLASTY
■ Pyloroplasty is superior to gastrojejunostomy but should not be performed in presence of
fibrosed and scarred pyloroduodenum in chronic duodenal ulcer

■ Indications:
o Gastric drainage procedure for PUD as adjunctive to vagotomy
o Surgical control of bleeding duodenal ulcer

■ Types:
o Heineke-Mikulicz pyloroplasty (Most common type)
Q Longitudinal incision across the pylorus and D1, then closed transversely
Q Used in duodenal bleeding ulcer, short stricture segment(< 7 m)

o Finney pyloroplasty
Q Side-to-side gastroduodenostomy with pylorus incision
Q Used in medium stricture segment (7 - 15 cm)

o Jaboulay pyloroplasty

J�Qi�
Q Side-to-side gastroduodenostomy without pylorus incision
Q Used in multiple short stricture segments over a healthy segment

G.astroj@iunostomy Heinoko-Mikulicz Jaboulay Finney

GASTROINTESTINAL STROMAL TUMORS (GISTS)
■ Most common gastric neoplasm (GISTS/Leiomyoma), but can be malignant
■ Most common sarcoma of the GI tract

■ Most common site: Stomach (Body)

o 2nd most common site: Small bowel fjejunum and ileum)

■ Characteristics:
o Submucosal, Slow growing, Solitary
o Radio-resistance
o Stromal cells (Epithelial stromal cells, Interstitial cells of Cajal and Spindle cells)
o 75% positive for C-KIT (CD117) "Proto-Oncogene"
o 10% positive for PDGF receptor

■ Clinical presentation:
o Non-specific abdominal pain, bleeding or rupture
� Bleeding due to erosions of mucosa (unlike adenocarcinoma; all-layer mass)
o Metastatic to liver or peritoneum
o Carney's syndrome triad (GIST, paraganglioma, and pulmonary chondroma)
o Neurofibromatosis 1 (GIST, neurofibroma, glioma, malignant nerve sheath tumor)

■ i
Investigat ons:

o CT abdomen and pelvis (Oral and IV contrast):

� Enhanced mass arising in the wall
� ± Heterogeneous components (Central ulceration and necrosis)

o MRI: Hypervascular mass and to assess for difficult location

o PET scan: for assessment of metastatic disease and no response to therapy

o Endoscopy: can detect GISTs initially as submucosal mass

o Barium study: Ulceration with "Doughnut sign"

o FNA Biopsy used differentiate between GIST, leiomyoma, and leiomyosarcoma

� GIST -+ Interstitial cells of Cajal and spindle cells and positive C-KIT
� Leiomyoma -+ Smooth muscles (actin and desmin)

No need for FNA if radiological appearance is typical of GIST

 ■ Risk Stratification:

Points 0 10 20 30 40 50 60 70 80 90 100

Size (cm) 0 5 10 15 25 35 45
'le5/50HPF
Mitotic index
<5/SOHPF
Colon/rectum
Site
Stomach/other Small intestine
Total points 0 20 40 60 80 100 120 140 160 180 200

Probabllty of 2-year RFS 90 80 70 60 50403020 10

Probabllly of 5--year RFS 90 80 70 6050403020 10

■ Management of GISTs:
0 Wedge resection with negative margins: for all GISTs especially if> 2 cm
� Tumor rupture is associated with inevitable peritoneal recurrence

o Observation with serial endoscopy/imaging: is an option for< 2 cm

■ lmatjnjb (Gleevec: tyrosine kinase inhibitor)

o Neoadiuvant therapy (for 6 months and continued up until time of surgery)
• Locally advance GISTs who need multiple resection
• Difficult anatomic locations (GEJ, periampullary and rectal tumor}

CT repeated usually in 4 weeks, 3 months, and 6 months to assess resectability

o Adiuvant therapy (at least 3 years)

• Metastatic unresectable GISTS
• High-risk of recurrence:
• > 5 cm and > 5/50 HPF
• > 10 cm with any mitotic rate
• > 10/50 HPF with any size
• Non-gastric site

Adjuvant imatinib is preferred for most cases of GISTs unless there is minimal risk of recurrence

■ Management of Leiomyoma:
o < 2 cm, Asymptomatic: Observation or Enucleation
o 2: 2 cm, Symptomatic: Wedge resection (due to greater malignant potential)

■ Management of Leiomyosarcoma:
o Stomach: Local resection with an adequate margin
o Small bowel: en bloc segmental resection with negative margins
GASTRIC CANCER
■ Incidence of distal gastric cancer decreased while incidence of proximal (cardia) gastric cancer
in increasing
■ Most common site: Antrum
■ Risk factors:
o Atrophic gastritis (intestinal type)
Q Gastric bacteria in atrophic gastritis convert nitrate into nitrite

o Adenomatous polyps
Q Most common gastric polyp: Hyperplastic polyp
(Associated with atrophic gastritis)

Q Most common malignant gastric polyp: Adenomatous polyp

Q Most common site of gastric polyp: Fundus

Q Treatment of antral polyp -+ Wedge gastrectomy

o Helicobacter pylori infection increas.es the risk only for distal cancers

o Diet
Q Starchy diet high in pickled, salted , or smoked food

Q Dietary nitrates
• Nitrosamines resulted from food during storage
• Reduce consumption of nitrate-rich preserved food decrease gastric CA

o Family history (15%}

Q (P53 suppression / COX-2 overexpression) for sporadic gastric CA
• Aspirin may be protective

Q (E-cadherin/CDH1 mutation), FAP, and HNPCC for diffuse gastric CA

• Prophylactic total gastrectomy recommended for CDH1 carrier between
18 - 40 years

o Others:
Q EBVvirus
Q Pernicious anemia
Q Type A blood group
Q Partial gastrectomy
Q Intestinal metaplasia
■ Associated extra-gastric nodes or tumors:
o Virchow's node (Left supraclavicular node)
Q By blocking the thoracic duct leading to regurgitation into the surrounding nodes

o Irish node (Left anterior axillary node)

o Sister Mary Joseph's node

Q Through lymphatic vessels which runs along obliterated umbilical vein
(ligamentum teres) to umbilicus

o Blumer's shelf (Pre-rectal metastasis in rectovesical or rectouterine pouch)

o Krukenberg tumor (Metastasis to ovary)

Q Via trans-coelomic spread (across body cavity as peritoneum, or pleura)
Q Associated with colloid mucin-secreting signet-ring gastric carcinoma

■ Investigations:
o Endoscopy

o Endoscopic U/S for determine depth of the tumor and lymph node status

o CT CAP or PET scan for metastasis

o Diagnostic laparoscopy can identify metastasis up to 40% in negative CT findings

o Peritoneal washing during laparoscopy

■ Stages:

TNM Invades
T1a Mucosa (Lamina properla, Muscularis mucosa}
T1b Submucsoa
T2 Muscularis properia
TJ Subserosa, Including:
- Gastrocolic ligament
- Gastrohepatic ligament
- Greater or lesser omentum

Without oerforation of the visceral oeritoneal

T4a Serosa

Associated with oerforation of the visceral oeritoneal

T4b Adiacent st ructures

Lvmoh node status Metastasis

N1 1 - 2 rAnional lvmoh nodes
N2 3 - 6 reaional lvmoh nodes
NJa 7 - 15 regional lymph
nodes
N3b > 15 reoional lvmoh nodes

7th American Joint Committee on Cancer Staalna System

Staae Subtvoe TNM TotalT +NI
A T1 NO 1
Invade mucosa and submucosa regardless
Stage I B T1 N1 2 lymph node status (Early gastric cancer)
T2 NO
A T1 N2 3
T2 N1
T3 NO
Stage II B T1 N3 4
T2 N2
T3 N1
T4
A T2 N3 5
T3 N2
T4 N1
Stage Ill
B T3 N3 6
T4 N2
C T4 N3 7
M1 Involving of non-regional lymph nodes
Stage IV
rretrooeritoneal or mesenteric nodes)
 ■ Classifications:
o Siewert Classification for GEJ tumors:

Siewert Classification
Siewert Description
I Tumor located 1 - 5 cm proximal to GEJ/Cardia
II Tumor located 1 cm proximal to 2 cm distal to GEJ/Cardia
Ill Tumor located 2 - 5 cm distal to GEJ/Cardia

Q Siewert I and II treated as esophageal cancer

Q Siewert Ill treated as gastric cancer
(In most recent studies, tumor located within 5 cm and crossing GEJ are treated
as esophageal cancer)

o Borrmann classification of advanced gastric cancer "Gross Classification"

Q Type 1: Polypoid
Q Type 2: Fungating (ulcerative with elevated distinct borders)
Q Type 3: Ulcerated (ulcerative with indistinct borders)
Q Type 4: Diffusely infiltrative

Protruded type
Type 1

Type 2 4.17
Type3 �s Depressed type

Type4 �-1:'Wij
The bon'maM dassUicadon system developed In 1926
o Pathological /Macroscopic} classification for early gastric cancer:
� Type I: Exophytic lesion
� Type II: Superficial lesion
• Type IIA: Elevated lesion
• Type 11B: Flat lesion
• Type IIC: Depressed lesion

� Type Ill: Excavated lesion (May extend to muscularis properia)

T:,p,1=========­
n,,.,,,,..,1,.1)

1),-11-========== IIHFl•IJ
<s•,-rjku11J

I=
o Lauren classification "Histological Classification"
� Intestinal type (53%) •well-differentiated"
• Associated with
o Atrophic gastritis
o Intestinal metaplasia
o Dysplasia

� Diffuse type (33%) "poor-differentiated"

• Associated with
o Female, Younger patients with positive family history
0 Blood type A
o CDH1, and E-cadherin mutations
o Diffuse large proximal tumors
o Early metastatic spread via transmural and lymphatic invasion

• Not associated with chronic gastritis

• Associated with linilis pl astica finding
• Prophylactic total gastrectomy should be considered in patients with
genetic mutations

� Unclassified (14%)
■ Management:
o Endoscopic resection criteria:
Q For all polyps > 1 c m and < 2 cm diameter, with no ulceration
Q Pedunculated (non-sessile) polyps
Q Tumor confined to the mucosa
Q No foci of invasive carcinoma
Q Well, or moderately well differentiated histopathology
Q Absence of lymphovascular invasion
Unfit � Surgery

o EMR
Q Elevation of the tumor by saline injection, snare encircling mucosa to excise

o ESD
Q By marking the borders with electrocautery and epinephrine injected with indigo
carmine hydrodissection of the submucosal plane (Used up to SM1 submucosal
lesions)

o Surgery
Q Radical subtotal gastrectomy
• Standard for resectable gastric cancer
• No difference in survival comparing total to subtotal gastrectomy
• RO resection (preferable with 5 cm margin)
• Frozen section of resection margins
• Reoperation after R1 is not recommended
o R1; Residual microscopic pathology
o R2: Residual grossly pathology

Q Distal gastrectomy with Billroth II reconstruction

• Used for distal 2/3 gastric cancer
• Preferred over Billroth I, as less risk of obstruction if recurrence happen

Q Total gastrectomy with Roux-en-Y esophagojejunostomy

• Used for proximal gastric cancer or diffuse (Linitis plastica)
• Proximal gastrectomy is equivalent from an oncologic perspective

o Neoadjuvant Chemoradiation
Q Used for locoregionally advanced disease
• > T2
• Positive lymph nodes

Q Used as palliative for unresectable gastric cancer

■ Lymphadenectomy:
o 2: 15 nodes should be resected with the gastrectomy specimen

o DO (No resection of lymph nodes}

Q Used in palliative gastrectomy

o 01 lymphadenectomy
Q Removal of perigastric lymph nodes along lesser and greater curvature (stations
1 to 7}
Q "D1+" including stations 8, 9 ± 11 (in total gastrectomy)
Q Standard for "Radical subtotal gastrectomy"
Q Indicated in T1 tumors (early gastric cancer) that unfit for endoscopic resection

o D2 lymphadenectomy (extended lymph node dissection) Preferred option

Q Removal of perigastric lymph nodes + nodes along the axis of celiac, common
hepatic, left gastric, and splenic hilum (stations 1 to 12}
Q Comparable morbidity and improved survival compared to D1
Q Standard operation for gastric cancer in Asia and specialized U.S. centers
Q Splenectomy is recommended due to removal of station 10 (splenic hilar lymph
node}
Q Used during total or distal gastrectomy
• Not used in proximal or pylorus preserving gastrectomy

Both 01 and 02 (stations 1 - 12) classified as regional lymphadenectomy

o D2+ ID3 previously) lymphadenectomy (superextended lymphadenectomy)

Q Including removal of para-aortic nodes (stations 1 to 16)
Q Classified as distant metastasis (M1) and not recommended anymore

■ complicated gastric cancer­

o Perforation
Q Primary closure with omentum in high-risk patient with no necrosis
Q Gastrectomy based on location

o Obstruction
Q Total gastrectomy with roux-en-Y esophagojejunostomy for proximal lesion
Q Endoscopic dilation and stent ffor high-risk patient with short-term survival

o Bleeding
Q Endoscopic management as 1st line
Q Angiography with coil embolization if endoscopic management failed
Q Gastrectomy (based on location) for unstable patient
• limited resection in patient with short-term survival
• Aggressive resection for more localized disease
MUCOSA-ASSOCIATED LYMPHOID TISSUE LYMPHOMA (MALT)
■ Lymphoproliferative mucosal disease

■ Arises from B-cells lymphocytes

■ Related to H. pylori infection

■ Most common site: Stomach

■ Treatment:
o Low-grade
Q Triple-therapy antibiotics for H. pylori eradication and surveillance

o High-grade, or does not regress

Q XRT ± Chemotherapy

o Associated with complications (Gastric outlet obstruction)

Q Gastrectomy

GASTRIC LYMPHOMAS
■ Most common location for extra-nodal lymphoma: Stomach
■ Most common site of primary GI lymphoma: Stomach
■ 95% are Non-Hodgkin lymphoma (B-cell type)
■ 50% associated with symptomatic symptoms (fever, weight loss, night sweating)
■ Diagnosis:
o Upper GI endoscopy and biopsy
•Nodular appearance and enlarged gastric folds associated with primary lymphoma•

■ Treatment:
o Chemotherapy (Best) and XRT
Q CHOP regimen
• Cyclophosphamide
• Doxorubicin
• Vincristine
• Prednisolone

o Surgery (radical subtotal gastrectomy) preserved for tumor localized to stomach and
regional lymph nodes or if associated with obstruction or bleeding
MORBID OBESITY
■ Indications:
o BMI .: 40 kg/m2
o BMI > 35 kg/m2 with significant obesity-related comorbidities(diabetes, hypertension)
o Unsuccessful attempts at weight loss by non-operative means
o Clearance by dietician and mental health professional
o No medical contraindications to surgery

TuRll
■ Restrictive procedure
o Gastric banding

o Sleeve gastrectomy
• Vertical gastrectomy
• Started 4 cm from pylorus at level of incisura angularis up to the angle of His
• Volume of stomach to be reduced from(> 1500 ml) to(< 200 ml)

o Vertical banded gastroplasty

• Abandoned due to weight regain
• Lesser curvature is used as restrictive pouch

■ i
Malabsorpt ve procedures
o Roux-en-Y gastric bypass
• Combined restrictive and malabsorptive procedure
• Most effective procedure when used 15 ml pouch and 75 - 150 cm roux-en-y
limb, connected to jejunum 30 -50 cm proximal to ligament of Treitz

o Biliopancreatic diversion with duodenal switch

• Lengths·
• Alimantry limb(roux limb}: 200 - 300 cm
• BP limb: 80 -100 cm (150 cm proximal to the ileocecal valve)
• Common limb: 50 cm up to 100 cm(revision if you add 150 cm here}

• Duodenal switch used to eliminates dumping syndrome and peptic ulceration

o Jejunoileal bypass
• Not used anymore due to higher rate of liver cirrhosis
• Jejunoileostomy at 10 cm proxjmal to ileocecal valve
• Associated with hyperoxaluria, liver cirrhosis, kidney stones, and osteoporosis

Outcome

Sleeve aastrectomv Gastric bvoass

Excess weiaht loss durlna 1 •• vear 40-60% 60-80%
Resolution of GERO/ Venous stasis 50% 90%
Tv""'2DM 50% > 70-80%
Hvnertension 50% 50%to 65%
Hvnertloidemla 50% 70%

Resolution of comorbidities is within 5 years after bariatric surgery

COMPLICATIONS OF GASTRECTOMY AND BARIATRIC SURGERY
■ Anastomotic leak: Most serious complication following sleeve gastrectomy
o Most common sites of leak:
Sleeve -+ Angle of His
LRYGB -+ Proximal 1/3 gastrojejunostomy (others: pouch staple lines and
jejunojejunal anastomosis)

o Most reliable indicator: tachycardia (associated with fever and abdominal pain)
o Most common cause of leak: lschemia (presented 4 -5 days post-operative)
Q Other causes: Mechanical (presented 2
nd
day post-operative)

o Most common cause of death post bariatric surgery: Pulmonary embolism

o Investigations:
Q Upper GI series: can detect leak early post-operative with low sensitivity

Q CT Abdomen: can detect leak late post-operative with more sensitivity than UGI,
and can differentiate between leak and abscess

Q Upper GI endoscopy: have highest sensitivity to detect leak

■ Gastroparesis
o Most common complication of LRYGB
o Gold standard investigation: Nuclear medicine scan

■ Stricture/ Stenosis
o Most common early complication of LRYGB
o Mostly happen 4 -10 weeks post-operative
o Risk: 1% with linear stapler and 30% with circular stapler
o Presented with post-prandial epigastric pain and vomiting
o Investigated by barium, UGI endoscopy (best for diagnosis)
o Treat by upper GI endoscopy and dilatation

■ Marginal ulcer
o Risk factors:
Q Gastric bypass (Retained antrum, leak, necrosis)
Q Long afferent limb (Billroth 11), Uncomplete vagotomy
Q Gastrinoma, H.pylori infection, Smoking, NSAIDs, Vitamin B12 deficiency

o Investigations:
Q Upper GI study in first 2 weeks (to avoid staple line disruption}
Q Upper GI endoscopy

o Management:
Q PPI, Smoking cessation, Cholestyramine if bile reflux
■ Internal hernia
o Most common cause of obstruction post LRYGB

o Types:
c:> Para-duodenal
• Most common type: Left para-duodenal hernia
• Lateral boundary of paraduodenal hernia: Inferior mesenteric vein
� Para-cecal
c:> Para-mesenteric
� Foramen of winslow
� Post Roux-en-Y

■ Sites of internal hernia:

A) Petersen's: Most common site of internal hernia post retrocolic LRYGB
Q Petersen's space: between small bowel and transverse mesocolic
B) Jejunojejunostomy: Most common site of internal hernia post antecolic LRYGB

C) Mesocolic of transverse colon

■ CT Sign:
o Whirl sign or Whirlpool sign {Mesenteric Swirl)
� Best single predictor sign of internal hernia
� Also associated with volvulus

■ Nutritional
o Most common complication of BPD: anemia
o Microcytic hypochromic anemia and fatigue: Iron deficiency
� Most common nutritional deficiency post gastrectomy
� Due to absence of acidic environment
� Presented with anemia and fatigue

o Macrocytic hypochromic anemia: due to loss of function of intrinsic factors due to loss of
acidity (in antrectomy) + Low Vitamin B 12

o Vitamin B 1 deficiency (thigh numbness, and cardiomyopathy) in Billroth II

� Most common cause of neuropathy post bypass (thiamine deficiency)

o Replacement of Vitamin B deficiency should be intravenously

 ■ Others
o Gall stones
� U/S abdomen is recommended preoperatively
� Controversial
• Option 1: Patient should undergoing gastric bypass with laparoscopic
cholecystectomy if incidental gallstones are found

• Option 2: Patient should undergoing gastric bypass only, and

laparoscopic cholecystectomy later on if become symptomatic
{Associated with less hospital stay and operative time}

o GERO
� UGI endoscopy is recommended preoperatively
� To rule out Barrett esophagus and hiatal hernia, and to evaluate the distal part of
stomach in patient undergoing gastric bypass

o Weight regain
o Malnutrition
o Internal bleeding
o Duodenal stump leak
o Gastrogastric fistula
o Alkaline reflux gastritis
o Afferent or efferent loop obstruction

o Dumping syndrome (Most common complication of gastrectomy)

� Caused by the destruction or bypass of the pyloric sphincter

Earlv dumoina Late dumoina

Time 15 - 30 min after the meal 2 - 3 hours after the meal
Manifestations Nausea and vomiting Profound hypoglycemia
Cramping abdominal pain
Diarrhea
Palpitations, tachycardia,
diaphoresis,
fainting, dizziness, flushing, blurred
vision
Mechanism Hyperosmolar load into small bowel Reactive hyperglycemia

Rapid passage of high osmolarity Carbohydrates delivered rapidly into small

food into small bowel inducing rapid bowel and quickly absorbed, resulting in
shift of extracellular fluid into hyperglycemia, followed by hypoglycemia
intestinal lumen to achieve isotonicity responding to the insulin, leading to activates
the adrenal to release catecholamines
Management Dietary modifications
• Avoiding foods containing llarge amounts of sugar
• Frequent feeding of small meals rich in protein and fat
• Separate liquids from solids during the meal

Octreotide 100 ua subcutaneouslv twice dailv if above measures are failed

 Dumping syndrome Alkaline reflux gastritis
Presentation Postprandial dizziness Postprandial pain
Non-bilious vomiting Bilious vomiting not relieved
by vomiting
Etiology Following Billroth II Following Billroth II, and
least by Billroth I
Investigation CT scan CT scan
Upper GI series Upper GI series
Upper GI endoscopy Upper GI endoscopy
Gastric emptying scan Gastric emptying scan
Management Avoids liquids during Surgery (for intractable)
meals
Conversion to Roux-en-Y
Octreotide gastrojejunostomy
(Roux limb> 40 cm)
Roux-en-Y
gastrojejunostomy Other options:
Interposition of 40-cm
isoperistaltic jejunal loop
between gastric remnant and
duodenum (Henley loop)
Billroth II gastrojejunostomy
with Braun enteroenterostomy
Total gastrectomy with Roux
esoohaaoieiunostomv
Afferent-loop obstruction
/Blind looo\
Abdominal pain, weight loss
No vomiting
Non-bilious vomiting relieved
by bilious vomiting
Megaloblastic anemia
Neurologic disorders
Following Antecolic Billroth II
CT scan
(Dilated biliopancreatic limb
proximal to gastrojejunostomy)
UGI is test of choice for efferent
looo obstruction
IV Vitamin B12 therapy
IV Antibiotics (Tetracyclines)
(High-risk of duodenal stump
blowout)
Surgery (for most patients)
Conversion to Billroth I or
Rouex-en-y gastroenterostomy
OTHERS
■ Mallory Weiss tear: (Arterial bleeding)
o Partial thickness mucosal or submucosal longitudinal tear
o Located on lesser curvature {near GE junction)
o Due to increase intra-gastric pressure
o Etiology:
Q Forceful repeated vomiting
Q Coughing
Q Seizures

o Management options·
Q Anti-emetics (Most appropriate}
Q EGD and clips

Q Gastrostomy and oversewing the vessel {Definitive management}

■ Dieulafoy's ulcer: (Arterial bleeding}

o Congenital submucosal vascular (AV) malformation
o Located in gastric fundus or near to gastroesophageal junction {GEJ)
o Difficult to identified on endoscopy (Due to normal mucosa and intermittent bleeding)
o Management·
Q Endoscopic hemostatic therapy
Q Angiographic embolization
Q Surgery

■ Hypertrophic Gastropathy (Menetrier's disease):

o May caused by CMV. and may increa.se risk of gastric cancer (Not premalignant}
o f TGF-B
o ! Protein, ! Acid, Achlorhydria
o Characteristics: (By UGI endoscopy and biopsy)
Q Giant gastric folds (t rugal folds} in proximal stomach
Q Mucosal cell hyperplasia
Q Loss of parietal cells

Giant gastric folds and mucosa/ hyperplasia is also associated with ZES

o Management:
Q t Protein diet
Q Indications for gastric resection:
• Bleeding
• Severe hypoproteinemia
• Malignancy
 ■ (Gastric antral vascular ectasia) Watermelon stomach
o More in elderly women with chronic GI blood loss requiring transfusion

o Predominantly affects distal stomach

o Characteristics:
Q Dilated mucosa! blood vessels with thrombi in lamina propria
Q Mucosa! fibromuscular hyperplasia and hyalinization

o Management:
Q Estrogen and progesterone
Q Endoscopic treatment with neodymium yttrium-aluminum garnet (Nd:YAG) laser
or argon plasma coagulator
Q Antrectomy
Q Consider TIPSS

Beta blockers and nitrates are useful in portal hypertensive gastropathy but ineffective in gastric
antral vascular ectasia

■ Gastric volvulus
o Borchardt's triad:
Q Sudden onset of severe upper abdominal pain
Q Recurrent retching without vomitus
Q Inability to pass a nasogastric tube

o Associated with:
Q Diaphragmatic defect
• Para-esophageal hernia in adult
• Congenital diaphragmatic hernia in children

Q Congenital absence of intraperitoneal visceral attachments

Q Wandering spleen

o Management:
Q Emergent exploration (laparotomy or laparoscopy)
Operative Note

Gastrectomy with 02 Lymphadenectomy

■ Diagnostic laparoscopy should be offered for patients with high-risk for occult metastasis

■ Position: Supine position

■ Incision: Mid line or Chevron incision

■ Steps:
o Exploration for undiagnosed metastasis in liver, peritoneum or omentum ± Liver U/S

o Mobilize the Greater omentum from the transverse colon to be removed as en bloc

Consideration of splenectomy
o Enter lesser sac by dividing the gastrocolic ligament through the greater omentum

o Examine the posterior stomach if invading short gastric vessels or splenic capsule

o Splenectomy must be performed in total gastrectomy to include station 10 node

o Splenectomy performed by
� Ligation of splenic artery at the origin to include all lymph nodes
c:> Ligation of splenic vein at the hilum

o Divide short gastric vessels at the hilum of spleen (in case no plan for splenectomy)

Dissection of infra-pyloric lymph nodes

o Kocherization of the duodenum

o Divide the right gastroepiploic vessels far from gastric wall

o Subpyloric nodes are separated from pancreatic head, and pyloric vein is ligated at the
junction with middle colic vein

Dissection of supra-pyloric lymph nodes

o Divide the right gastric artery at the left edge of porta hepatis (distal to pylorus)

o Supra-pyloric lymph nodes dissected to be removed with the specimen

Distal transaction
o Dissect the duodenum circumferentially 2 cm distal to thy pylorus

o The duodenum transected by linear stapler distal to the pylorus

o The stapled duodenal stump is over sewn with 3-0 silk

Dissection
o Dissect all lymph nodes surrounding hepatic artery, para-aortic and celiac plexus to be
removed with specimen (superior to pancreas, anterior to aorta and celiac plexus}

o Dissect all lymph nodes away from splenic artery if no plan to perform splenectomy

o Divide Left gastric artery at origin and dissect lymph nodes along lesser curvature

o Divide Left gastroepiploic artery and dissect lymph nodes along greater curvature

o Divide the gastrohepatic ligament close to the liver

Subtotal gastrectomy
o Greater curvature transected straight by linear stapler (5 cm margin from tumor}

o Lesser curvature transected as angle up to the top (2 - 3 cm from esophagus)

Q Stapled lesser curvature is over sewn by suture and kept closed

Total gastrectomy + so1eoectomy

Mobilize the left lobe of the liver to exipose the gastroesophageal junction
0
o Transect the esophagus 2 cm above gross tumor margin

o Send the specimen to the pathology as Frozen section to the margins

Reconstruction
Total gastrectomy
o 50 - 60 cm Roux-en-y esophagojejunostomy by Circular stapler {diameter 2: 25 mm)
Q Jejunum is transected by linear stapler 10 cm distal to the ligament of Treitz
Q Either as antecolic or retocolic through defect in transverse mesocolon

o Hunt Lawrence pouch {J pouch) with functional end-to-side jejunojejunostomy

Subtotal gastrectomy
o Billroth I or II according to the remnant part

Finishing the operation

o ± Feeding jejunostomy tube
o Close mesenteric defect of transverse mesocolon
o Irrigation with normal saline
o Check for hemostasis
o Drain
o Closure
o Keep NGT for few days
o Vaccination if splenectomy performed
Small Bowel
Reviewed by:

Dr. Abdulwahed Meshikhes

SMALL BOWEL
ANATOMY AND PHYSIOLOGY
■ Submucosa is the strongest layer of bowel
■ Gut rotates 270 degree counterclockwise around SMA in the 4 th week of development
■ lgA: most immunoglobulin produced in the gut

■ Germ layers·
o Endoderm -+ Epithelium of the bowel, Lungs, Liver, Pancreas, Thyroid
o Mesoderm-+ Muscular layer of the bowel, Bone, Mesentery, Connective tissue, Spleen
o Ectoderm -+ Skin, Hair, Nails, Brain, Spinal cord, Adrenal medulla

■ Primitive gut tube:

o Foregut -+ Esophagus, Stomach, until DJ junction, Liver, Pancreas, and Gallbladder
o Midg ut -+ From DJ junction until proximal 2/3 transverse colon
o Hindgut-+ Distal 1/3 of transverse colon down to anal canal
Midgut rotates 270 degrees counterclockwise normally

■ Normal diameter:
o Small bowel: 3 cm
o Transverse colon: 6 cm
o Cecum: 9 cm

■ Cells:
o Lamina properia: contains all cells except enterochromaffin cells
• Enterochromaffin cells (carcinoid precursor)

o Enteroglucagon -+ Induce small bowel hypertrophy

o Goblet cells: mucin secretion
o Paneth cells: located at the base of the crypt
o Brunner's glands (secretes alkaline mucus) in duodenum
• Prevent marginal ulcer
• Not found in jejunum

■ Ligament of Treitz: "Suspensory muscle of duodenum•

o Fixes duodenum to retroperioneum
o Surgical landmark for separation of duodenum from jejunum "DJ junction"
o DJ junction found at the base of mesocolon of transverse colon
o Attaches from diaphragm to either:
• Duodenojejunal flexure
• Duodenojejunal flexure and 3rd, 4th part of duodenum
• 3rd and 4th part of duodenum

■ Migrating motor complex (gut motility):

o Phase I: Rest
o Phase II: Gallbladder contraction
o Phase Ill: Peristalsis
o Phase IV: Deceleration

Mediated by: Motilin during fasting (acts on phase Ill)

Motilin receptors located in the Antrum
 Duodenum + SPDA (GOA} & IPDA (SMA)
■ Most common site of adenoma
■ Most common site of adenocarcinoma
■ Most common site of intestinal atresia

1" oart lbulbl 2°• oart ldescendinn1 3"' oart ltransversel 4th oart lasce ndinn1
Most common site of Retroperitoneum
duodenal ulcer Contains ampulla of Valer Most common site of compression:
At posteriomedial aspect - Hematoma
- SMA syndrome
NG T inserted to 1" part Most common site of trauma
can decreases the
regurgitation risk Associated with:
- Gallstone fistula
- Annular pancreas
- Diverticula
- Gastrinoma

Jejunum
■ Most common site of pneumatosis intestinalis
ileum
■ Most common site of Crohn's disease
■ Most common site of Perforation in Crohn's disease
■ Most common site of Perforation in typhoid enteritis
■ Most common site of Adenocarcinoma in Crohn's disease
■ Most common site of Lymphoma
■ Most common site of Carcinoid syndrome
■ Most common site of Duplication cyst
■ lleal break:
o Inhibition of jejunal motility by ileum "induced by fat meal and mediated by peptide YY"

Jejunum Ileum
Plica circularis More Less
IValvulae conniventesl
Vascular arcades Less More
Mesenteric fat less More
Pever's oatches less More
Vasa recta Lona Short
Circumference Larae Small
Villi size Lanie Small
Wall thickness Thick Thin

■ Absorption:

Duodenum Jejunum Ileum Terminal ileum

(Last 30 cm of ileum/
Calcium Water B12 + intrinsic factor B12 + intrinsic factor
Iron Fat Unconjugated bile acids Conjugate bile acids
(Both requires acidic envirooment) (Fatty acids absorbed in colon) loassive absomtion) (active absomtion)
Proteins Folate
Vitamins A. D. E K Calcium-oxalate bindina
SMALL BOWEL OBSTRUCTION
■ Most common cause with history of previous abdominal surgery:
o Small bowel: Adhesions (Most common cause)
• Fibrinous: Early (7 hours -10 days)
• Avascular and flimsy
• Usually resolved completely

• Fibrous: Late (10 days -1 month}

• Due to poor blood supply and sepsis
• Dense vascular adhesions
• Usually sub-acute and recurrent

o Large bowel: Primary neoplasm

■ Most common cause without previous abdominal surgery:

o Small bowel: Hernia
• Metastatic disease (melanoma, ovarian cancer) is commoner than primary neoplasm

o Large bowel: Primary neoplasm

■ Pathophysiology:
Proximal small bowel has secretory function, but distal small bowel has absorptive function

o Obstruction-+ Dilation proximally and collapse distally

o Bacterial fermentation-+ More distension

o Edematous bowel -+ Fluid sequestration -+ Increased intraluminal pressure -+ bacterial

translocation

o Vomiting -+ More fluid loss -+ Metabolic alkalosis and hypovolemia -+ Dehydration

• Feculent vomitus associated with late presentation and established obstruction

Metabolic acidosis associated with distal bowel obstruction

o More dilation-+ Compromised perfusion-+ lschemia-+ Necrosis-+ Perforation

o ± Sepsis, Shock -+ Death

■ Signs of strangulation:
o Constant severe pain, tachycardia, fever, leukocytosis, and acidosis
o t Amylase, D-lactate, and intestinal fatty acid binding protein level
 Classification of intestinal obstruction
Mechanical lntraluminal Proximal Low-Grade
Foreign bodies, gall stone, Pylorus to proximal jejunum . Partial obstruction
intussusception, bezoars, . Complete obstruction
oarasites. nnlvnnid lesions
Functional Intramural Intermediate High-Grade
Postoperative ileus, Inflammation (Crohn's, TB), tumor, Mid-jejunum to Mid-ileum - Strangulated
Drugs diverticulum, intussusception - Closed loop
Extraluminal Distal
Adhesions, hernias, bands, Distal ileum to ileocecal
volvulus, or cancer valve

Proximal Distal (Small or Large bowel) Closed-loop

Intermittent Intermittent to Consistent Progressive
Pain Colicky Deep localized visceral Rapidly worsen
Central
Vomitina Larae. Bilious Low. Feculent Prominent /Reflex)
Dehvdration Severe Moderate to Low
Tenderness Eoiaastric Diffuse Diffuse and proaressive
Distension Absent Moderate to severe Often absent
Obstioation Mav not oresent Alwavs oresent and ear1v feature Mav not oresent
Bowel sounds Normal Hvoeractive HYJ>eractive
Central located Peripheral located Non-specific gas pattern
> 3 cm diameter > 6 cm diameter U-shape sign
Radiological signs Valvulae conniventes Haustra spanning par1
No air in the rectum No air in the rectum
Air fluid levels Air fluid levels
■ Rule of X-ray:
o Upright CXR: Detection of perforation {air under diaphragm)

o ErectAXR: Help to differentiate between: Small/Large, Complete/Partial

• Findings:
• Dilated loops of small bowel > 3 cm {most specific finding)
• Multiple air-fluid levels> 3
• Pneumoperitoneum
• No air in rectum

o SupineAXR
• Help to differentiate between levels of obstruction Oejunum versus ileum)
• Gas distribution: Continue to management
• No-gas: Abdominal CT with IV contrast

o Rule of "3":
• 3 Folds
• 3 Air-fluid levels
• > 3 cm Diameter of small bowel

o Signs of small bowel obstruction:

• String of beads sign (obstruction)
• Pseudotumor sign (strangulated)
• Rigler's sign (double wall sign)� Pneumoperitoneum + air inside bowel
Air with bowel obstruction could be from swallowed nitrogen

o Signs of duodenal obstruction:

• Double bubble sign
• Stacked coins
• Coiled spring sign
(Due to duodenal hematoma or intussusception)
■ Rule of CT:
o Assessment of:
• Transitional zone, level of obstruction, mass staging, viability of the bowel,
synchronous tumors, status of proximal bowel

o Used with IV and oral contrast

• Dose of oral or enema contrast 250 ml (90 g) iodine in 1000 ml water
• Rectal contrast only used for colonic obstruction, especially partial obstruction

o Signs:
• Obstruction:
• String of beads sign
• Small bowel feces sign
• U-shape sign "closed loop obstruction"

• Strangulation:
• Pneumatosis lntestinalis
• Target sign or Beak sign "transitional point"
• Whirl sign "Mesenteric rotation"

o Assessment of bowel wall thickening:

• Focal thickening(< 5 cm): Adenocarcinoma
• Focal thickening (5 - 10 cm}: Diverticulitis, Crohn's disease, Bowel ischemia
• Segmental thickening (10 - 20 cm): Bowel ischemia, 180, infection, radiation
• Diffuse thickening: UC, SLE, Infectious enteritis

o Enhancement:

1) Portal HTN
1) Acute IBD 1) Chronic Crohn's 1) Chronic IBD
2) Infection
2) Bowel ischemia 2) Bowel ischemia 2) Chemotherapy
3) Acute IBD
3) Hemorrhage 3) Neoplasm 3) Celiac disease
4) Bowel ischemia

■ Rule of Endoscopy:
o Contraindicated (except for gastric outlet obstruction, non-optimized for surgery)
Can causes perforation
PNEUMATOSIS INTESTINALIS
■ Multiple gas-filled cysts of the gastrointestinal tract
o Spontaneous rupture gives rise to pneumoperitoneum

■ Most common site: Jejunum, followed by ileocecal region and colon

■ Types:
o Cystic (foamy or granular appearanoe) located in submucosa
o Linear located in subserosa and rarely muscularis layer

■ Etiology:
o Most cases are associated with COPD or the immunocompromised state
o Pneumatosis in neonates is usually associated with necrotizing enterocolitis

Life-threateninq Non Life-threateninq

Bowel ischemia Iatrogenic
- Post endoscopy
- Post-surgical anastomosis
- Post-organ transplant
- Post ieiunostomv
Bowel stranaulation Post chlemotheranv or steroids
Inflammation Barium enema
Toxic meaacolon Inflammatory bowel disease
Connective tissue disease Connective tissue disease
Trauma Asthma or COPD

■ Diagnosis· Usually radiologically by plain abdominal or barium studies

Pneumatosis lntestinalis Pseudo-pneumatosis lntestinalis

(intra-mural gas) (lntra-luminal gas)

■ Treatment:
o No treatment is necessary unless complications developed
• Rectal bleeding, Volvulus, Tension pneumoperitoneum

o Treatment of underlying cause if required

• Bowel ischemia or infarction
• Inflammatory bowel disease
EVALUATION OF POSTOPERATIVE SMALL BOWEL OBSTRUCTION

■ CT enterography
o Administration of oral contrast (water-methylcellulose solution} to achieve intraluminal
distension
o Best to use in patients with Crohn's disease to rule out strictures

■ Enteroclysis
o Fluoroscopic study: Instillation of barium followed by methylcellulose and air
• It is less widely used now due 10 discomfort to patients
• It is replaced nowadays by CT enteroclysis

o Detects minimal adhesions and mucosal changes

o Contraindicated in complete obstruction

■ Small bowel series

o Barium:
• Contraindicated in suspected perforation, strangulation, complete or closed loop
obstruction

o Gastrograffin:
• High osmolality iodinated water-soluble contrast
• Used in partial adhesive obstruction
• Not in virgin or complete
• Contrast appears in colon after 4 - 24 hours
o If no contrast in colon and no improvement -+ 90% need surgery
• Can differentiate between partial and complete
• It is therapeutic as well as diagnostic in adhesive small bowel obstruction

Small bowel series may delay CT examination and surgery

MANAGEMENT OF SMALL BOWEL OBSTRUCTION
■ Conservative therapy:
o Offered for most cases of partial SBO, or early postoperative period, and in patients
showing improvement over the first 12 to 24 hours

1) Aggressive fluid resuscitation and electrolytes correction

• Most patients with vomiting will have:
Hypoch/oremic, hypoka/emic metabolic a/ka/osis with
concomitant paradoxical aciduria

2) Nasogastric tube and monitor Urine Output

• NGT -+ for symptomatic relief, gastrointestinal decompression, and allow for
serial assessment of antegrade bowel movement

3) Medications:
• Patient will be NPO with IV medications including:
• Antibiotics (Ampicillin} if indicated
• Analgesia
o Narcotic medication should not be used in non-operative period as
can mask worsening symptoms

■ Surgical intervention
o Indications:
• Failure of conservative treatment
• Worsening symptoms (fever, tachycardia, leukocytosis)
• Hemodynamically unstable
• Peritonitis
• Obstructed or strangulated hernia
• Complicated obstruction (Perforation)
• High-grade obstruction (Strangulated or Closed-loop}
• Fever, tachycardia, distended tender abdomen with guarding and rigidity
• CT findings of
o U-shape sign "closed loop obstruction"
o Pneumatosis Intestinalis with suspicious of bowel ischemia
o Target sign or Beak sign "transitional point"
o Whirl sign "Mesenteric rotation"

o Options:
• Exploration for primary lesions or metastasis
• Viable bowel:
• Adhesions: adhesiolysis or release of adhesion band
• Hernia: reduce and repair
• Perforation: repair

• Non-viable bowel: Segmental resection and primary anastomosis

• Questionable viability: Warm packs and increased oxygenation. If no
improvement either resection or closure with 2 nd look after 24 - 48 hours
• Diffuse (entire) non-viable small bowel: Close and terminate
• Laparoscopy has limited role
 o Hernia repair in bowel obstruction:
• Strangulated: Primary repair I VAC-dressing / Biological mesh
• Non-Strangulated: Non-absorbable mesh

■ Timing of surgery
o Complicated or High-grade (Strangulated, Closed-loop)
• Immediately with no need for CT scan

o Low-grade
• Virgin abdomen:
• Small bowel: 24 hours max (25% of all SBO patients need operation)
• Large bowel: 12 hours max

• Non-Virgin abdomen: 48 - 72 hours

Nowadays, patient can be treated with non-operative measures up to day 5 (increased risk of bowel
resection) and contrast study need to be done pre-operative if> 48 hours with no improvement

■ Adhesive barrier:
o Solid barrier:
• lnterceed (Oxidized cellulose)
• Seprafilm (Hyaluronate-based, sodium hyaluronate and carboxymethyl
cellulose)
• SurgiWrap (polylactide)
• ePTFE: non-absorbable

o uaujd barrier:
• lcodextrin solution
• Spraygel (Polyethelene glycol)
• Hyaluronic acid solution

o Associated with decreased adhesion but doesn't decrease rate of SBO

o Should not wrap intestinal anastomosis, may increase risk of leak

o Solid barriers best to use for patients having laparotomy with high-risk to develop
adhesions

o Liquid barriers best to use for patients undergoing laparoscopic lysis of adhesions
INTUSSUSCEPTION
■ lnvagination of one segment "lntussuceptum" of the gastrointestinal tract into the lumen of an
adjoining segment "lntussuscipien"

■ Age of presentation: 6 months - 2 years (Consider pathological disease if> 2 years)

■ Most common site:

o ileocolic "Terminal ileum and extends distally into colon"

■ Pathophysiology:
o Inhomogeneity in a bowel segment
(Undergoes sudden change in diameter, flaccidity, or induration)

o Mechanical linkage (Intramural or extramural)

Unbalanced forces happen when normal peristaltic wave encounters a focal abnormality
in the bowel wall "lead poinr which known as secondary intussusception

o Peristaltic activity
The intussusceptum telescopes into distal bowel by peristaltic activity, as the mesentery
of proximal bowel drawn into distal bowel, compressed and resulting in venous
obstruction and bowel wall edema, arterial insufficiency can happen later if not reduced,
leading to ischemia and necrosis

■ Etiology:
o Primary intussusception (Usually after upper respiratory tract infections or enteritis)
• Hypertrophy of Payer's patches (Viral infection)
• Hyperplasia of lymphoid tissue

o Secondary intussusception (due to leading point}

• Meckel's diverticulum ''Most common lead poinr
• Polyp, lipoma, or cecal adenocarcinoma
• Ectopic pancreas or gastric mucosa, hemartomas
• Enteric duplication cyst, Lymphoma

■ Clinical presentation:
o Long history of intermittent obstruction
o Bloody mucus diarrhea "Currant jelly ·stools" (from vascular congestion)
o On examination:
• 0ance's sign (Elongated Sausage mass in RUQ, and absence in RLQ)

■ Associated diseases:
o Melanoma
o Cystic fibrosis, purpura
o Celiac disease
o CDF infection
■ i
Investigat ons:
o Abdominal X-Ray:
• Non-specific
• Can diagnose intussusception in 60%
• Coiled spring sign associated also with small bowel intramural hematoma

o Diagnostic enema (Diagnostic tool for children only}

• By air or contrast enema

o U/S:
• Best initial study
• Signs: Target or Pseudo-kidney signs

o CT Scan (Diagnostic tool for adult)

• Mainly used for adult patients
• Signs: Target sign, Crescent (meniscus) sign, Sausage sign, Claw sign

lnlUSSuSdplen

Ned<
■ Management of intussusception:
o IV fluids and antibiotics

o Stable/ No peritonitis/ Child:

• Air enema only "Success rate: 60 - 90%"

• Max pressure with air-contrast enema: 120 mm Hg
• Max column height with barium enema: 1 meter {3 feet}

• Failure or suspicious of complete reduction: Repeat air enema / Barium enema

o Unstable/ Peritonitis/ Failure of reduction I Adult:

• Resection and anastomosis with segmental lymphadenectomy
• Preferred method for adult patients (Due to malignant lead point)
• Should be done if there is necrotic bowel in children

• Reduction without resection

• Preferred method for children
• Reduction is done by pushing not pulling {squeezing distal to proximal)
• For patients with retrograde intussusception (post gastric bypass}

■ Recurrence rate:
o 5 - 10% in radiological or surgical management
o Post-operative recurrence: Air enema
POST-OPERATIVE ILEUS
■ Symptoms and signs of intestinal obstruction in the absence of mechanical obstruction

■ Clinical presentation:
o Vomiting, constipation and abdominal distension
o Diminish bowel sounds (Hyperactive in intestinal obstruction)

■ Time to return motilitypost-operative:

o O - 24 hours in small intestine
o 24 - 48 hours in stomach
o 48 - 72 hours in colon

Prolonged postoperative ileus if> 4 - 6 days

■ Risk factors:
o Open abdominal surgery (most common)
o Infection (sepsis)
o Trauma (Spinal cord injury, retroperitoneal hemorrhage)
o Drugs (Anti-cholinergic, opiates, anti-histamine, tricyclic antidepressants, CCB)
o Uremia
i
o Pancreat tis
o Diabetes
o Stroke
o Myocardial infarction
o Vinca alkaloids

■ Medications that decreases postoperative ileus:

o Erythromycin, Alviomopan, Ketorolac (-+ renal failure)

■ lovesJigatjons;
o CBC, Electrolytes panel, Liver and renal function tests, amylase level
o AXR (Dilated loops of bowel, paucity of colonic gas, and no air-fluid levels)
o CT (if suspicious of mechanical obstr1Uction or failed management > 48 hours)

■ Management:
o Supportive care:
• Limitation of oral intake
• Early post-operative enteral feeding decreases the risk of ileus
• TPN for prolonged ileus
• NGT decompression if vomiting or prominent distension
• Pain management with NSAIDs
• Maintain of fluid therapy
• Electrolytes replacement IV
• Bowel rest or sips of water
SHORT BOWEL SYNDROME
■ Defined as< 30% of normal bowel length(< 75 cm in children and< 200 cm in adults)
■ Most common cause:
o Adult: Massive single resection ( associated with AMI, and Crohn's disease)
o Children: Resection secondary to necrotizing enterocolitis

■ After massive resection adaptation: by Lengthening and hypertrophy of the villi

■ Diagnosis is made on symptoms, not by remaining length of bowel
■ Schilling test: checks for B12 absorption (radiolabeled B12 in urine)
■ Risk factors:
o Bowel length:< 180 - 200 cm of vialble small bowel or loss of� 50% of small intestine

o Absence of ileocecal valve

• Permanent TPN in Presence il,eocecal valve with small bowel< 50 cm
• Permanent TPN in Absence ileocecal valve with small bowel< 75 cm

o Absence of the colon

• Permanent TPN in Presence of colon with small bowel length < 60 cm
• Permanent TPN in Absence of colon with small bowel length< 100 cm

o Diseased remaining bowel (Crohn's disease)

o Ilea/ resection: Fat malabsorption occurs when> 100 cm of terminal ileum resected

■ Complications:
o Therapy-related
• Metabolic: can lead to dehydration and renal dysfunction
• Hypocalcemia: related to poor absorption and binding by intraluminal fat
• Metabolic acidosis/alkalosis
• Hyperglycemia / Hypoglycemia

• Catheter-related sepsis or thrombosis

• Liver disease: Steatosis, Cholestasis and Liver failure
• Source for morbidity and usually leads to liver with small bowel transplant
• Minimized by providing .as large a portion of calories enterally, avoiding
overfeeding, using mixed fuels (<30% fat)

o Physiological
• Gastric hypersecretion
• Dietary deficiency
• Bacterial overgrowth
• Bile acid diarrhea
• Nephrolithiasis
• Due to calcium malabsorption leads to
o Binding of Calcium to Long-chain fatty acids instead of oxalate
o Absorb oxalate from colon and forms calcium oxalate stones
( Cholestyramine binds oxalic acid in colon)

• Cho/elithiasis (30 - 40%)

• As complication of TPN (due to cholestasis) or diseased ileum (less
absorption of bile acids)
■ Management:
MULTIDISCIPLINARY APPROACH
o Prevent complications:
• Hydration
• Correction of electrolytes

o Diet modification:
• Maximize enteral feeding (High Carbohydrates/Proteins)
• Oxalate and fat restriction to 20 - 30% (provide more of long-chain triglyceride)
• Continuous feeding rather than intermittent
• Separating solid and liquid
• Vitamin D supplementation
• Monitor iron and trace elements

o TPN + E nteral feeding

• 50 - 70% of SBS patient achieve independence from TPN

o Improve absorption: (first 1 - 2 years post-operative before adaptation}

• Reduce hypergastrinema (acidity}: PPI or H2 antagonists

o Delay small bowel transit lime·

• Antimotility: Narcotics, loperamide, diphenoxy1ate or octreotide
• Octreotide side effects: steatorrhea and inhibit adaptation

o Growth factors (growth hormone and GLP-2 analogue "Teduglutide"} may stimulate
adaptation

o Surgery:
• Non-transplant:
Improve function of existing bowel
• Strictureplasty for stenotic segments causes partial obstruction
• Tapering enteroplasty for dilated dysfunctional segments
• Restoration of bowel continuity (avoid stoma)

Fasten intestinal transit time procedures

• Segmental reversal of the small bowel
• Interposition of a segment of colon between segments of small bowel
• Construction of small-intestinal valves
• Electrical pacing of the small intestine

Intestinal lengthening operation

Used for short intestinal remnant and dilated segment(> 3 - 4 cm)
• LILT: longitudinal intestinal lengthening and tailoring procedure
• STEP: serial transverse enteroplasty procedure (STEP}
o Outcome is more favorable than LILT

• Transplant:
• Indicated for life-threatening complications and/or long-term TPN
• Indicated with liver transplant in patients with liver failure
o Approach to small bowel syndrome:
• Non-<lilated segment
• Tolerate enteral feeding
o Conservative management

• Not tolerating enteral feeding (on TPN)

o Non-functional distal bowel
• Restoration of bowel continuity

o Bowel length > 90 cm

• Fasten intestinal transit time procedures
(Segmental reversal of the small bowel)

o Bowel length < 60 cm with TPN complications

• Bowel transplant

• Dilated segment > 4 cm

• Bowel length > 120 cm
o Improve function of existing bowel procedures
(Strictureplasty, or Tapering)

• Bowel length < 90 cm

o Improve function of existing bowel procedures
(Strictureplasty <>r Tapering)

o Intestinal lengthening operation

(LILT, STEP)
 MECKEL'S DIVERTICULUM
■ Derived from persistent vitelline duct (failure of closure of the omphalomesenteric duct)
■ True diverticulum, found on anti-mesenteric border of small bowel
■ Most common cause of painless lower GI bleeding in children
■ Most common presentation in adults: Obstruction
■ Most common tumor found in Meckel's diverticulum: Carcino id t m u o r
■ Most common cause of small bowel hemorrhage: Angiodysplasia
o Most common cause of obscure upper GI bleeding

■ Rule of 2: 2 feet from ileocecal valve, 2% population, 2% symptomatic, 2 tissue types

(pancreatic, gastric), and 2 presentations {diverticulitis and bleeding); presents in P' 2 years
o Gastric mucosa: most common to be found and to be symptomatic (bleeding)
o Pancreas tissue: most common tissue found that causes diverticulitis

■ Localization:
Me ckel'sscan (Tc99)
If failed to localized in symptomatic patient-+ D ia gnostic Laparos co py
o

■ Treatment:

Asymptomatic I Symptomatic
I
I
A dult Chi ldren Complicated
- Bleeding
I Smple
i I
-Perforated
Complicated -Tumor
Simple - Inflamed base

l
or Involving the base

•
Co ntro v e rsial I
._I
__D_iv_e_rt_i_c _u _le_c_to_m_Y _ __,I ._I
__s_e _g_
m_e_n_t_a _l R_es_ e_ c_t_io_n _ ___,11 Diverticule ctomy

■ Observation is preferred for adult with incidental diverticulum to decrease morbidity

■ Prophylactic diverticulectomy is preserved for:

o Narrow base (neck)
o Longer > 2 cm
o Thickened
o Associated with fibrous band
o Associated with Inflamed base of signs of diverticulitis
o Associated with palpable ectopic tissue (gastric mucosa)
o Children and young population < 40 - 50 years
• Due to mild risk of malignant transformation and to decrease oomplications

Segmental resection used if the base is indurated, contained palpable abnormality or

>2 cm wide that make small vowel lumen at risk of narrowing

Appendectomy should be considered for all patients with symptomatic Meckel's diverticulum
DUODENAL DIVERTICULA
■ Most common site: 2 nd part of duodenum
■ Frequency of diverticula: duodenal> jejunal > ilea!
■ False diverticulum, found near to ampulla of Vater
■ Located on mesenteric border (Meckel's diverticulum located on anti-mesenteric border)
■ Treatment:
o For symptomatic diverticula (diverticulitis, pancreatitis) non-surgical management
should be done, at least initially

o Endoscopic sphincterotomy and stent placement should be attempted first for

diverticulum near the ampulla

o Operative management should not be done until failure or inability to perform

endoscopic management

o Resection with Choledochoduodenostomy or Choledochojejunostomy used if ampulla

inside the diverticulum

Asymptomatic
(Any size)
I
I Symptomatic
'
I
Bleeding

I
Obstruction
Pancreatitis I Perforation
Cholangitis

Observation
•
Diverticulectomy
or I Gastrojejunotomy
I
Seamental Resection

IIEOJEJUNAL DIVERTICULA
■ Treatment:
o Asymptomatic: Observation
o Symptomatic: Segmental resection

DUODENAL ATRESIA
■ Duodenoduodenostomy
INFLAMMATORY BOWEL DISEASES
CROHN'S DISEASE
■ Bi-modal disease
o 1'' peak at 15 - 30 years
o 2nd peak at 60 years

■ Etiology·
o Infectious:
• Mycobacterium paratuberculosis
• Chlamydia, Listeria monocytogenes, Pseudomonas species, Reovirus

o Immunological:
• Poor barrier with exposure of lamina propria lymphocytes to antigens
• Defects in immune regulatory mechanisms
• Over-responsiveness off mucosa! T cells to enteric flora

o Genetic:
• Presence of a locus on chromosome 16
• DR5 alleles (NOD2 I CARD15) genes
• 50% concordance with monozygotic twins

■ Investigations:
o CBC, ESR, CRP, Electrolytes, Albumin and Vitamin B12
• CRP can predict patient response to biological therapy

o Antibody markers:
• Perinuclear anti-neutrophil cytoplasmic antibodies (pANCA)
• Anti-Saccharomyces Cerevisiae antibody (ASCA}
• Anti-ftagellin antibody (CBir1) is a marker for complicated disease

o Leukocyte scintigraphy (WBC scan}

o CT enterography
• Thick bowel wall (terminal ileum) or Segmental colitis with skip lesions
• Comb sign (Increased vascularity of mesentery}
• Fat halo sign, Creeping fat wrapping
• Abscess, phlegmon, ulceration, stricture or fistula

o MR enterography

o Endoscopy
• Colonoscopy should visualize terminal ileum
• Capsule enteroscopy is contraindicated in stricture or obstruction
• ERCP used if IBD associated with Primary sclerosing cholangitis (PSC)
■ Medical treatment approach:
o Step-up: By starting with 5-ASA
• 5-ASA is a chemoprevention
• Associated with developing strictures or penetrating disease

o Top-down: By starting with Monoclo11al antibodies or IL-2 inhibitors

• Superior to step-up approach
• Improve quality of life as steroid sparing

■ Indications for antibiotics:

o Abscess
o Fistula
o Colonic Colitis
 ■ Medical Treatment:
Tvnes Mechanism
Anti•lnflammatary Anti-inflammato!)'. effects:
• Inhibits prostaglandines, leukotrienes
5-ASA • Decrease neutrophil chemotaxis
uAminosalicylates" • Antioxidant activity
Side effects of sulfa(ll,'.ridine:
Crystalluria, BM depression
Megaloblastic anemia
Oligospermia
Interstitial nephritis
Glucocorticoids Inhibits phospholipase A2
Inhibits transcription of NO, and COX2
Inhibit production of cytokines
Sjde effects·
OM, HTN, Osteoporosis,
Neuropathy, Myopathy, Cataract,
Glaucoma, Acne, Hirsutism
lmmunitv and adrenal sunnression
lmmunomodulators Inhibit purine synthesis
Inhibit synthesis of DNA, RNA, Protein
Reduce steroid demand
Side effects:
BM depression, Pancreatitis, Infections Methotrexate
Gastrointestinal toxicity
Hepatic dysfunction
Contraindicated in pregnancy
(Azalhioorine is safe in n""'nancvl
Monoclonal TNF-0 inhibitor
antibodies
"Biological therapy" Associated with 50% reduction of
urgent surgery, and superior to
immunomodulators for recurrence rate
Side effeci•
Anaphylaxis (Most common)
"Adalimumab is alternative"
Tuberculosis (PPD test pre-treatment),
HBV. Seosis, Heoatic failure
ll•2 inhibitors Fungal macrolide antibiotic
Cyclosporine binds to cyclophilin
Inhibits inte�eukin-2 production
Inhibits proliferation of T cells
Binds to mTOR
Antibiotics
Tvnes
Sulfasalazine
5-ASA + sulfapyridine
Mesalamines
Release 5-ASA in the distal
small bowel
Tirnes of mesalamines:
- Asacol
• Salofalk: pH-dependent,
Colonic release
• Pentasa: Sustained release
• Canasa: Suppository
• Rowasa: Enema
Qllll
Prednisolone
Budesonide
(Controlled ileal release)
With first-pass liver
metabolism "less side effects"
IV Hydrocortisone
Azathioprine (lmuran)
"Pro 6-mercaptopurine•
Dose: 2 - 3 mg/kg/day
(Folic acid antagonist)
Inhibit dihydrofolate
reductase
SC Adalimumab (Humira)
fully humanized
Dose: 160 mg induction dose
followed by 40 mg q 2 weeks
IV lnfliximab
Dose: 10 mg/kg q 8 weeks
Certolizumab
Calcineurin inhibitors
(Cyclosporine, Tacrolimus)
Sirolimus
Ciprofloxacin
Metronidazole
Usaae
Induction / Maintenance
Mild to moderate UC
Colonic CD
Sylfl!ss1ls1;1:ia1t:
for mild colonic IBD
Be!.lal flllIDUla
M1tss1lamines:
For distal UC
Induction only
Not for maintenance
Extra-intestinal disease
(Pyoderma gangrenosum)
Hold 2 weeks pre-op and
restarl 2 - 4 weeks postop
Maintenance only
Not for induction
(Need for 6 - 8 weeks
to be active)
Hold 1 - 2 weeks pre-<Jf>
and restarl 1 - 2 weeks
postop
Induction and
Maintenance
For moderate to severe
active IBD, Steroid
resistant, or fistulas
Hold 6 - 8 weeks pre--0p
(2 weeks for Humira) and
restarl 4 weeks postop
Refractory IBD
Extensive involvement
of small bowel
Induction only
UC: Pouchitis
CD: After ileal resection
for oerianal abscesses
■ Surgical Treatment:
o Indications for surgery:
• Elective:
• Intractability, Complications of medications
• Abscess, Fistula, Stricture, Dysplasia, Malignancy

• Emergency:
• Toxic colitis, Toxic megacolon
• Massive bleeding, Perforation

• Most common indication:

• Intestinal obstruction and chronic deputy

lmmunomodulators and monoclonal antibodies should not be stopped during the

per/operative period for /BO surgery

o Surgical options:
• Segmental resection and anastomosis
• No need for negative margin microscopically, just resection of grossly
involvement area with 2 cm margin
• Recurrence is always proximal to the anastomosis
• 50% recurrence rate requiring surgery after resection
• Preferable for colonic CD
o Isolated short segment or colonic stricture should be resected
o Stenling used only for anastomotic colonic stricture
• Cecum should be resected for involved terminal ileum
o Except if there is > 6 inches uninvolved proximal to cecum
• Total colectomy with anastomosis
• Used for multiple colonic diseases
• Total colectomy with end ileostomy
• Used as urgent operation for emergency indications
• Retained rectal mucosa have risk of malignancy
o Bleeding, pain or mucus discharge � Proctoscopy
• Proctitis: Proctectomy with intersphincteric anal dissection
• Cancer: Staging, followed by abdomino-perineal resection
(APR) with total mesorectal excision (TME)
• Total proctocolectomy and iteostomy
• Restorative operation for extensive small bowel involvement
• Indicated for colon and rectum involvement or malignancy
• Useful in emergency situations
• Restoration later by ileo-anal anastomosis

o Anastomotic technique:
• Side-to-side anastomosis associated with lower leak rate and postoperative
complications compared to end-to-end anastomosis

• Stapled anastomosis associated with lower leak rate compared to hand-sewn

anastomosis
STRICTURES

Indications of each option for manaciement of strictures

■ No previous resection
Segmental resection ■ Presence of contraindication for stricturoplasty
■ Multiple small bowel strictures within> 1 segment of bowel
■ Multiple small bowel strictures within long segment of bowel
Stricturoplasty
■ Multiple prior resection of> 100 cm of small bowel
■ Rapid recurren,ce of Crohn disease with obstructive symptoms
■ Obstructing fibrotic small-bowel stricture without associated sepsis

■ Poor-risk patients with obstructive GIT stricture

■ Previous extensive small bowel resection
Surgical bypass ■ Severe Crohn's disease not amenable for other option due to
association with abscess or risk of injury to other structures

■ Used for small stricture < 4 - 5 cm with no contraindications

0 Symptomatic stricture
Endoscopic Dilatation 0 Colonic stricture < 4 - 5 cm
0 Anastomotic stricture

■ Multiple biopsy are needed due to risk of malignancy

■ Active Crohn's disease without complete obstruction (fibrotic stricture}

-=> Should be treated medically first

■ Contraindications for non-resection methods /Stricturoplasty, Dilatation}

o Acute inflammation
o Dysplasia or suspicious of malignancy at stricture site
o Extensive tension due to inflamed bowel segment
o Multiple stricture over short segment
o Colonic stricture
o Sepsis
o Abscess or phlegmon
o Hemorrhage, Fistula
o Malnutrition or hypoalbuminemia
 ■ Techniques of Stricturoplasty: (Based on location)
1 •t and 2nd parts duodenum or small bowel 3rd and 4th part
duodenum

< 10 cm > 10 cm

Heinecke Mickulicz Stricturoplasty Side-to-side Gastrojejunostomy

For stricture length < 12 cm (+ pyloroplasty and vagotomy) Duodenojejunostomy
(Longttudinal at anti-mesentric followed
by transverse closure)
Michelassi Side-to-side
Finney or Jaboulay Stricturoplasty isoperistaltic Stricturop/asty
For stricture length 10 - 25 cm For multiple short strictures
over> 20 cm lengthy small bowel

Heinecke Mickulicz Finney Jabou/ay

Michelassi Side-to-side isoperistattic Stricturoplasty

■ Management of Collection (abscess} in Crohn's
o Most of patient will require surgical intervention after 4 - 6 weeks
o Operating too soon may put normal bowel at risk for resection
o Drainage and delayed surgery lead to decrease morbidity and avoid stoma creation
o Medical management only for small abscess < 4 cm
o Percutaneous drainage for large abscess > 4 cm or small abscess after failure of
medical management if accessible

o Indications for surgical intervention:

• Metabolic derangement (sepsis, metabolic disturbance)
• Associated with Peritonitis (Obstruction, Perforation, Bleeding, or Fistula)
• Failure of medical management in < 4 cm collection
• Failure of percutaneous drainage in > 4 cm collection
(lntra-mesenteric and intra-loop abscesses)

■ Fistula in Crohn's:
o lleovesical fistula
• Usually not associated with history of previous surgery
• Presented with pneumaturia, and fecaluria
• CT scan usually diagnostic
• 50 - 70% associated with simultaneous ileosigmoid fistula

o Colovesical or lleoduodenal fistula

• Rare, usually associated with history of previous surgery

o Enterocutaneous fistula
• Resection and anastomosis with suturing the site of entrance of adjacent organs
• lnftiximab not shown to decrease the need of operative management

■ Anal fissures io Crohn's·

o Topical nitroglycerin (0.2%)

■ Perianal fistula in Crohn's:

o Asymptomatic or mild � Antibiotics if needed + Topical nitroglycerin
o Symptomatic or severe � lnfliximab

Above Dentate Below Dentate

Stable/ Unstable/
Drained Not drained

Anti-TNF Seton Metronidazole

(infliximab) & Ciprofloxacin

o Surgery: (for low intersphincteric fistulas or fistulas refractory to medical therapy)

• Fistulotomy: for intersphincteric or low transsphincteric fistula
• Drainage non-cutting silastic seton: for complex fistula
• Diverting stoma and proctectomy: for associated severe rectal disease
ULCERATIVE COLITIS
■ Characterized by remission and exacerbation, started distally (rectum) and extend proximally
o Chronic relapse
o Acute exacerbation or fulminant course in 10- 15%

■ Clinical presentation:
o Bloody diarrhea
o Tenesmus
o Passage of mucus
o Weight loss

■ Screening for malignancy:

o Risk of malignancy:
• 2% at 10 years, 8 - 10% at 20 years, 18 - 50% at 30 years

o Endoscopic surveillance:
• 4 quadrant random biopsies at 10 cm intervals (32 biopsies)+ suspicious lesions
• 8 - 10 years after symptoms, then annually
• Annually if associated with PSC, family history of CRC, Stricture or Pseudopolyp

■ Associated lesion: (Need 2 pathologist consultants to confirm)

o Microscopic pattern:
High-grade dysplasia (Associated cancer: 40%)
• Histology: Marked atypia, hyperchromasia and pleomorphism
• Managed by oncological resection

Low-grade dysplasia (Associated cancer: 20%)

• Histology: Densely packed, enlarged nuclei with mucin depletion
• Managed by oncological resec.tion or close surveillance (every 3 to 6 months)

o Macroscopic pattern:

Paris classification of GIT polvos based on endoscopic aooearance

TuneO Superfkial polypoid, flat/depressed, or excavated tumours
Tvoe 1 Polypoid carcinomas, usually attached on a wide base
Tune2 Ulcerated carcinomas with sharolv demarcated and raised marains
Tvoe 3 Ulcerated, infiltrating carcinomas without definite limits
Tvne4 Non-ulcerated, diffusely infiltrating carcinomas
Type 5 Unclassifiable advanced carcinomas
 Paris type O:
• Polypoid (Lesion protrude from mucosa into the lumen 2: 2.5 mm)
• Paris type Ip: Pedunculated
• Paris type Is: Sessile
Endoscopica/ly removable (even in high-grade dysplasia)

• Non-Polypoid
• Paris type Ila: Superficially elevated (< 2.5 mm)
• Paris type llb: Flat
• Paris type lie: Depressed
• Paris type Ill: Excavated
Non-amenable for endoscopic removal

• Stricture
• 60% after 20 years of the disease
• Most common location: proximal to splenic flexure
• Presented with large bowel obstruction
• Managed by oncological resection

• Invisible

■ Indications for surgery:

o Elective:
• Intractability (failure of medical treatment): most common indication
• Dysplasia (Low or High grades} or Cancer
• Chronic bleeding
• Extra-colonic manifestations: erythema nodosum, arthritis, and eye diseases
• Growth failure in children

o Emergency:
• Toxic colitis: > 6 bloody stools/d, fever, t HR, drop in Hemoglobin, leukocytosis
• Toxic megacolon, Massive b !leeding, Perforation
If not improved with non-operative measures (NPO, NGT, bowel decompression,
I.V fluids, steroids and antibiotics) within 48 - 72 hours

■ Surgical options:
o Total abdominal colectomy with end ileostomy (Urgent Surgery)

o Restorative Proctocolectomy + lleal pouch-anal anastomosis :!: diverting stoma

(Curative elective surgery)
• Maximum length of anorectal mucosa between dentate line and anastomosis
should be < 2 cm

o Total proctocolectomy with end ileostomy or (kock pouch) ileostomy

(Curative surgery with anal incontinence)

o Total colectomy with lleo-rectal anastomosis

(alternative for leal-pouch anal anastomosis, but it need annual surveillance for rectal
stump, and for high-risk patients)
 ■ Intermediate colitis
o Patient with equivocal findings of ulcerative colitis versus Crohn's disease

o Complete colonoscopy with evaluation of terminal ileum with biopsy should be repeated

o If still undetermined, then 3-stages procedure should be performed to allow complete

pathological examination

o Never do proctectomy as emergent surgery

t Operation length (due to pouch construction), nerve injury (due to pelvic dissection)

Ulcerative colitis Crohn's disease

lleoanal anastomosis (IPAA) Curative Contraindicated
(Risk of recurrence)
Pouches (continent ileostomy) Used in anal incontinence Contraindicated
/Risk of recurrence)
Seamental colectomv Contraindicated Used for isolated colonic disease

■ Management of rectal remnant/stump:

Intra-operative
o Transect distal colon in area with minimal inflammation

o Placement of suture or staple intraperitoneally to 'hitch' stump to the sacral promontory

or psoas muscle

o Stump can be brought to level of subcutaneous tissue an fixed by Silk (above the
fascia) lower risk of pelvic abscess (Best for short rectal stump)

o (Safest) To fashion formal mucus fistula in case of long end (difficult for the patient)

Post-operative
o Insert rectal tube (Malecot drain) transanally for stump decompression for couple of
days and kept in place on top of the stump

o Rectal tube removed on 5 - 7 days postoperative

o If patient have peritonitis due to rectal stump leakage postoperative, then he might need
to be reoperated for washout and drainage
 DIFFERENCES OF INFLAMMATORY BOWEL DISEASES

Ulcerative colitis. Crohn's disease

Ethnicity Jewish > non-Jewish white > African American > Asian
Smokin!l Protective Risk factor
AnnAndectomv Protective Risk factor
Location Colon (extend proximally} Mouth to anus
Commonest site: ileocecal area
Most common site Rectum 40% lleal and lleocecal
Rectosigmoid 40% Small bowel
20% Crohn's colitis
Site of nerforation Transverse colon Terminal ileum
Serolonu P-ANCA+ve ASCA+ve
Radiological Thin bowel wall Thick bowel wall

Lead-pipe appearance Creeping fat wrapping

Target sign Involvement of small bowel

(SeQmental colitis, Strictures)
Endoscopy Continuous Skip lesion

Mucosa/ friable, edema and atrophy Aphthous ulcer

with exudate (earliest lesion)
(earliest lesion)
Mucosa/ ulceration

Mucosal slouQhinQ in severe UC Cobbelstone annearance

Macroscopic Rectum-Involvement Rectal-sparing
(Then extend proximally)
Anus- Involvement
Anus-sparing (Fissure and fistula)
Pseudo-polyps
Toxic megacolon Perianal involvement
Backwash ileitis (Most commonly: skin taal
Microscopic Mucosal and submucosal Transmural
(Histology)
Superficial erosions Granuloma

Crypt abscess Goblet cells

Non-caseating Granulomatous

Lvmohanaiectasia
Risk of Very high Increased
adenocarcinoma
Extra-Intestinal More Less
manifestation Pyoderma QanQrenosum Erythema nodosum
Arthritis Peripheral arthritis
Gallstones (common) Amyloidosis
Primarv sclerosinQ cholanaitis (rare)
■ Extra-intestinal manifestations of inflammatory bowel diseases:
o Ocular:
• Uveitis, lridis and episcleritis
(Most common manifestations and most respond to steroids)

o Dermatological:
• Erythema nodosum
• Pyoderma gangrenosum

o Rheumatologic:
• Peripheral arthritis
• Ankylosing spondylitis
• Sacroilitis

o Urological:
• Kidney stones
• Ureteral obstruction

o Hepatobiliary:
• Gallstones (Most common)
i
• Pr mary sclerosing cholangitis
• Hepatosteatosis
• Pericholangitis
• Cholangiocarcinoma

■ Extra-intestinal manifestations parallel to disease activity:

o Peripheral arthritis
o Episclerilis
o Erythema nodosum
o Aphthous ulcer

■ Most common extraintestinal manifestation requiring total colectomy:

o Failure to thrive

■ Most common extraintestinal manifestation do NOT improved with colectomy:

o Ankylosing spondylitis
o Primary sclerosing cholangitis
CARCINOID DISEASE
■ Serotonin is produced by Kulchitsky cells (enterochromaffin cell)
-+ 5- HydroxylndoleAcetic Acid "5-HIAA"
■ Gastric carcinoid:
o All foregut carcinoid are atypical carcinoid
o Types:

Type Tvoe I Tvoe II Type Ill

Size Small<2cm Small <2cm Larae> 2 cm
Number Multiole Multiole Solitarv
Acid h"=roastrinemia hvneroastrinemia Normal
Associated with Most common type Higher malignant potential (10%) - Sporadic
- Metastasis
- Pernicious anemia - MEN 1 - Carcinoid syndrome
-Atrophic gastritis -ZES

o Diagnosis:
• Plasma Chromogranin A
• Upper GI endoscopy and biopsy
• EUS may be helpful to assess the depth of invasion
• CT scan and Octreotide scan helpful for staging

o Management:
• Endoscopical resection (EMR): for small, < 5 lesions and confined to mucosa
• 01/02 Gastrectomy: for larger lesions
• Surgical debulking: used in selected patients with metastasis
• Somatostatin analogue (Octreotide):
• Useful to control symptoms of carcinoid syndrome
• Does not prolong survival in metastatic carcinoid disease
• Should be started before anesthesia induction to avoid carcinoid crisis
If crisis developed -+ Giive Octreotide and don't abort the procedure

■ Small bowel carcinoid:

o Most common site: Ileum (Appendix in some sources}
o Most common site that causes carcinoid syndrome: Ileum
o Most common site that associated with high metastatic potential: Ileum
o More aggressive than appendicular carcinoid
o 25 - 50% of liver metastasis will developed carcinoid syndrome

o Management:
• Examination of entire small bowel
• Segmental resection only: for< 1 cm carcinoid tumor
• Wide excision with lymphadenectomy: for> 1 cm localized disease
• Right hemicolectomy: for carcinoid in terminal ileum
• Surgical debulking: for metastasis disease
• Somatostatin analogue (Octreotide)
■ Appendicular carcinoid: (Revise appendix chapter)

■ Colorectal carcinoid:
o Up to 25% of carcinoid tumors are found in rectum
o Right colon carcinoid (less common than left) are more likely to be malignant
o Most small carcinoid tumors are benign
o > 2 cm carcinoid tumors (60%) associated with distant metastasis
o Management:
• Transanal resection: for small carcinoids
• Radical surgery: for large tumor> 2 cm or invasion to muscularis
• Oebulking + Radical surgery: for metastasis colon carcinoids

■ Pancreatic carcinoid:
o Mostly malignant
o Most common site: Body and tail of pancreas
o High incidence of carcinoid syndrome
■ Careinold syndrome:
o High risk of synchronous and metasynchronous tumors

o Etiology:
• Gastrointestinal disease with liver metastasis (Most common from: Ileum)
• Extra-gastrointestinal disease (Bronchial, Retroperitoneal)

o Mediators: Serotonin, Bradykinin, Substance P

o Presentation:
• Intermittent flushing (kallikrein) and diarrhea (serotonin)
• Hypotension, tachycardia
• Fibrosis of endocardium and valves of right heart (Tricuspid regurgitation)

o Investigations:
• 24-hour urinary 5-HIAA (Most sensitive test and initial test)
• Chromogranin A (Most sensitive and specific test)
• Best for prognosis and follow-up
• Octreotide scan
• Most specific test for localization, with higher sensitivity than CT for
localization and detect extra-abdominal metastasis or non-identified
primary disease
• 68-Ga-OOTATATE PET/CT
• Superior to octreotide scan with regard to ability to detect metastases, as
well as to define existence and extent of metastatic disease

o Management options:
• Somatostatin analogue (Octreotide) started before the induction and continue
until next day postoperatively to avoid carcinoid crises

• Liver resection (Debulking is the goal)

• Resection of primary tumor with concurrent liver resection
• Octreotide scan used before resection to rule out extra-hepatic metastasis
• Criteria:
o Resectable liver disease with acceptable morbidity and mortality
o Absence of right heart insufficiency
o Absence of extra-abdominal or diffuse peritoneal disease

• 1 Stage for early disease

• 2 Stages for advanced disease (Extensive or bilobar)
o Resection of the left lobe metastasis + right portal vein ligation
o Extended right hepatectomy after 8 weeks of hypertrophy
• Liver transplant: in selected patients with extensive disease (High recurrence)

• Other modalities used also in advanced unresectable metastasis disease:

• Radiofrequency ablation
• Trans-arterial chemoembolization or radioembolization
BENIGN SMALL BOWEL TUMORS
■ Adenomas:
o Most common benign small bowel tumor
o Most common site: duodenum

■ GI stromal tumors /GISTs)

o Most common mesenchymal tumors arising in the small intestine
o Most common presentation of GISTs or Leiomyoma: Vigorus GI bleeding
o Subdivided to: Leiomyomas, Leiomyosarcomas, and Smooth muscle tumors
• Leiomyosarcoma usually in jejunum and ileum (extraluminal)
Leiomyosarcoma is the most common sarcoma of the small bowel

■ Peutz Jeghers syndrome

o Autosomal dominant {All first-degree should be tested}

o Characteristics:
• Hamartomas polyps (2 - 20 polyps)
• Mucocutaneous melanotic skin pigmentation
• Common presentations: GI bleeding, lntussusception -+ Intestinal obstruction
• Associated with
• Low-risk of malignancy
• Colon, stomach, and pancreatic cancer
• Extra-intestinal malignancies (most common: breast Cancer)

o Hamartomas polyps associated also with:

• Juvenile polyposis syndrome
• Phosphate and Tensin {PTEN) Hamrtoma Tumor Syndromes (PHTS) (as
Cowden syndrome or multiple hamartoma disease)
MALIGNANT SMALL BOWEL TUMORS
■ Adenocarcinoma: most common malignant small bowel tumor
o Most common site: duodenum
o Most common site in Crohn's: ileum
o Treatment:
• Jejunum or ileum: Segmental resection and primary anastomosis
• Duodenum:
1 st and 2nd parts 3rd and 4th parts Unresectable
(proximal to ligament of Treitz}

Whipple Procedure Duodenojejunostomy Gastrojejunostomy

Jejunojejunostomy
■ Most common malignancies of small bowel in order:
o Adenocarcinoma > Carcinoid > Lymphoma > GISTs

■ Most common extraintestinal cancer metastatic to small bowel: Melanoma

■ Most common polyp: Hyperplastic
■ Villous adenoma is highest risk for cancer (Most common site: Periampullary)

■ Lymphoma
o Most common site: ileum
o Lugano staging system for Gastrointestinal lymphoma:

Staae Extent of lvmohoma

I Confined to GI tract (Sing�rimarv or multiple non-contiguous lesions)
II Extending into the abdomen from primary GI site
Iii: Local nodal involvement
112: Distant nodal involvement
IIE Penetration of serosa to involve adiacent organs or tissues
IIV Disseminated extra-nodal involvement or concomitant suora-diaohraamatic nodal involvement

o Treatment:
• Surgical resection
• For localized disease (Lugano stage I or II)
• Involves segmental resection with;,, 12 mesenteric nodes

• Chemotherapy
• As adjuvant CHOP or R-CHOP chemotherapy after resection
• As primary treatment for non-operable disease
STOMAS
■ Definition:
i
o Art ficial opening created surgically used for multiple purpose

■ Indications:
o Feeding
o Diversion
• Hemodynamically unstable (Trauma, sepsis)
• Perforation, Obstruction
• High risk for anastomotic leak (Malnutrition, high dose steroids, radiation)
• To protect distal anastomosis
• Low rectal anastomosis{< 5 - 7 cm from anal verge)

o Decompression as defunctioning of distal bowel

-+ CRC, Diverticular disease, IBD

■ Principles:
o Flat area of skin
o 5 cm away from umbilicus
o Away from:
• Skin creases
• Folds
• Previous scars
• Bony prominences and costal margin

o Below the waist/belt line (away from belt, away from primary tumor "radiation effect")
o Above the waist/belt line in emergency sittings
o Within the rectus sheath
o Separate incision to prevent wound infection
o Tension free in supine, sitting, and standing positions
o Easily accessible by the patient during supine and standing positions
o Mark the site during supine and lying forward positions (for elective cases)
• Marker should be done by tattoo, skin scratch, or permanent marker

■ Techniques of construction:
o Open laparotomy
o Laparoscopic-assisted
o Blind trephine
• Adhesions are the most common cause of trephine failure
• Resection and anastomosis after blind trephine is worrisome due to adhesions
around the bowel which may lead to inadequate vascularity

■ Types:
o Anatomical location{lleostomy / Colostomy)
o Loop or End stoma
o Temporary or Permanent stoma
o Double barreled stoma (Paul Mikulicz)
o Split or divided stoma (Devine operation)
o Defunctioning stoma
o Mucus fistula
COLOSTOMIES
■ Begins to function: postoperative day 5

■ End colostomy:
o Site -+
Left iliac fossa, by sigmoid or descending colon
o Interrupted absorbable sutures
o Full thickness colon
o ± Mucus fistula (in long distal colon ornly)
• In Hartmann, no mucus fistula, and mucus discharged through anus
o Highest risk of parastomal hernia (40%)

1) Temporary:
o To protect distal anastomosis
o To achieve bowel rest (as perinea! Crohn's)
o If primary anastomosis is not possible after resection (as perforation, sepsis, ischemia
or obstruction)

2) Permanent:
o After APR for low rectal tumors

■ Loop colostomy:
o No spout, quick and temporary stoma, but not favorable
o Usually in sigmoid or right transverse colon in right upper or left lower quadrants
o Disadvantages:
• Requires larger fascia defect
• 2nd highest risk of parastomal hernia (30%)

• More prone to prolapse than end colostomy

o Technical consideration·
• Skin incision: T ransverse
• Colon incision: Transverse (longitudinal) parallel or within anterior tenia

■ Double barrel colostomy:

o Used in midsigmoid perforation or volvulus
o After resection, proximal & distal limbs of colon are sutured together along
antimesenteric border
ILEOSTOMIES
■ Begins to function: 24 - 72 hours
■ Spout (everting the bowel wall}
■ Should protrude more than colostomy by 0.5 cm
■ End ileostomy:
o Performed after colectomy for IBD
o Most distal segment of the ileum is used

1) Temporary
o To protect an ileorectal anastomosis
o Persistent low anal fistula
o Right sided colonic trauma
o Preliminary to obstruction of ileo-anal reservoir

2) Permanent :
o Total proctocolectomy for UC, Severe Crohn's disease, FAP
o Radical cystectomy for urinary bladder with urine diversion to ileal conduit (Urostomy)

■ Loop ileostomy:
o Most preferred type to protect low pelvic rectal anastomosis
o Lowest risk of parastomal hernia

■ Continent ileostomy: (Kock pouch}

o Stoma pouch (reservoir) inside abdomen with catheter outside
o Indicated for patient undergone total proctocolectomy and ileostomy and thus not
candidates for IPAA, or failed IPAA
o Complications: Obstruction, incontinence, Pouchitis, Nipple valve extrusion
• Most common complication of continent ileostomy: Nipple-valve failure

Indiana pouch: Similar to Kock pouch except it is made of terminal ileum and ascending colon
■ lleoanal Reservoir; ilea! pouch (J or S Pouch):
o J or W pouch usually no need for pouch intubation (in contrast to S or H pouch)

■ Brooke-technique ileostomy
o Everted end ileostomy: (Nippling the stoma= Spouting the stoma)
• By placing 4 stitches through edge of the bowel, then 2 - 4 cm at serosa to the
skin, with 1 cm more of superior part of the bowel
• Do not take mucosa in seromusclar bite, or fistula will happen

rr
 ■ ELECTROLYTES COMPARISON:

Fluid Na• c1· K• HC0 3· H•

mEa/L mEa/L mEa/L mE"'L mEa/L
Gastric 60 -100 90- 140 10-20 N/A 30-100
Duodenum 140 80 5 50 N/A
Jejunum 100 100 5 10-20 N/A
Ileum 130 110 10 30 N/A
Colon 60 40 30 20 N/A

■ ILEOSTOMY versus COLOSTOMY:

lleostomy Colostomy
Site Usuallv on the Riaht Usuallv on the left or RUQ
Snoutina Yes No
Caliber Smaller laraer
Content Greenish fluid Brownish semi-solid
Output Average: 500 ml/day 200-700 ml/day
low: < 500 ml/day K output more
High: > 1.5 U day
Na cutout more (3 times)

■ STOMA CONSTRUCTION:
o Prepare the patient with stoma marking and stoma nurse for education

o Deliver bowel through the abdominal wall

• Create the aperture by full-thickness circular skin incision
• 2 cm cruciate incision in anterior rectus fascia to allows 2 finger breadths to pass
• Make sure not to become tight (ischemia) or wide (parastomal hernia)
• Mobilize the selected bowel segment to achieve tension-free
• lleostomy: 10 -15 cm away from ileocecal valve

• Make sure the bowel segment oriented not twisted

o Closure of the abdomen

o Mature the stoma

• Loop stoma: Elevate the bowel and create small mesenteric defect for plastic rod
• Open the stoma end (distal limb for loop stoma, along tenia line for colon)
• Place 4 absorbable stay sutures at 3, 6, 9, 12 o'clock
• Evert bowel by gently pulling on the sutures, then tie in place (Spouting)
• Fix the stoma by taking seromuscular layer to dermis layer

Prophylactic mesh may prevent parastomal hernia (in case of permanent stoma)
■ STOMA CLOSURE:
o Done after diagnostic studies
o Contrast or Barium enema used for assessment of distal bowel before closure to
exclude any recurrence of tumor, inflammation, or stricture

o Time:
• Stoma closure should not be done before appropriate time
• Due to edema, and inflammation

Divertina looo colostomv 2 months /6 - 8 weeks)

lleostomv 2 - 3 months
End colostomy 3 -6 months

o Steps:
• Take down of residual circumferential adhesions ± Laparoscopy or Laparotomy

• Abdominal incision:
• Elliptical incision around the stoma for loop stoma
• Midline incision or reopening laparotomy incision for end stoma

• Stoma:
• The stoma is separated from surrounding skin, subcutaneous tissue, and
fascia until finger pass into peritoneal cavity circumferentially

• Mobilize the proximal and distal segment of the bowel for tension-free
reanastomosis

• T he bowel edges should be resected prior to anastomosis in end stoma

(May be preserved for loop stoma)

• Hand sewn or stapler anastomosis between both ends of the bowel

• Closure:
• Abdominal wound closure
• Skin site of stoma left open for dressing to be healed by secondary
intention
• Abdominal wound closure
■ STOMA CARE:
o Appliance:
• Choose type of pouch, measure the stoma and cut the pouch 0.3 cm larger
• During comfortable position, gentle pushing the skin from face plate, while pulling
the pouch away from the stoma (Stoma paste should not be in ilea! conduit)
• Bag is pressed over the stoma for 30 seconds
• Skin barrier paste or powder

o Removal:
• Empty pouch when 1 /4 to 1 /3 full
• Change pouch when leaking

r
o Food output: (Fruit juice, Fired, Spicy food, Chocolate, Milk and Caffeine)
o Food ! output: (Banana, Cheese, Starchy carbohydrates, Jelly, and Soluble fiber)

o Vinegar can help removing alkaline crystals in urostomy

r·--,�·-··1
One-piece type

Urile collection bag

/
Two-piece type

Range
Stool colleaion bag
( connection part )

Non-rel\lm valve

Urinary vent stopcock

l
-1-Cap ( Stool ) vent Vent closure device
( dip)
Urinary vent
■ STOMA COMPLICATIONS:
o Early complications:
• Technical: Inappropriate site, bad construction (no spout}
• Bleeding

• lschemia
• Due to poor vascularity or tension.
• Edematous with bluish discoloration and can progress to necrosis
• Depth of the ischemia can be assessed by endoscopy or glass test tube
with external light, or puncture with a needle (no bleeding after puncture)
o Inserting small lubricated test tube and shining flashlight into tube

• Management:
o Limited to the stoma and mucosa only + observation
• ± Debridement
• Full thickness superficial necrosis> 1 cm can associated
with steno sis which urgent operation may be required
o Proximal to anterior fascia -+ immediate revision

• Mucocutaneous separation
• Risk factors:
Improper approximation, excess tension (traction}, infection, steroid or
malnutrition

• Management:
o Partial separation:
• Probe gently to determine depth of separation
• Irrigate and if> 1 cm depth packed with barrier powder,
alginate, or hydrofiber, then covered with solid skin barrier

o Complete separation:
• Local revision

• Retraction
• > 0.5 cm below skin surface
• Either stomal or skin retraction
• Presented with leakage, decreased appliance wear time, and skin irritation
• Stoma should be evaluated while the patient sitting and standing

• Management:
o Convex faceplate pouching system and Support tight belt may
be used to control leakage around the appliance
o Significant retrac1ion may requires operative revision
o Late complications:
• Stenosis
• Due to ischemia, retraction, mucocutaneous separation, or recurrence of
Crohn's disease

• Management:
o Low residue diet, stool softeners
o Dilatation of stoma is not preferred over long time due to scar
formation and more stenosis
o Surgical revision is advisable for severe stenosis
o Local excision of scar and formation of new mucocutaneous
junction can resolve the stenosis

• Prolapse
• Full-thickness protrusion (normal prolapse is 5 - 10 cm}
• Most common: Distal non-functional loop stoma
• 50% associated with pa rastomal hernia
• Risk factors·
o Construction outside rectus muscle
o Large opening of abdominal wall
o Insufficient fixation
o Weak abdominal muscles
o Distended redundant distal bowel
o Increased intra-abdominal pressure

• Types:
o Fixed type: by improper construction
o Sliding type: susceptible for incarceration

• Management:
o Normal stoma color and function: Conservative
o Severe painful or non-functional stoma: Revision
o lschemic, strangulation or obstruction: Urgent intervention

• Conservative measures:
o Continuous pressure to distal part of the stoma
o Ice pack or osmotic material can help reduce the prolapse (sugar or
salt}
o Binder or hernia support belt with prolapse flap may be used

• Surgical option:
o Temporary stoma: Take down and restore bowel continuity
o Permanent stoma:
• Local parastomal procedure
• Intra-abdominal procedure
(Convert loop stoma to end stoma}
 ■ Pouchitis:
• Inflammation of ileal pouch reservoir of an ilea! pouch-anal anastomosis
{IPAA)
o Acute(< 4 weeks) or chronic(> 4 weeks)
o Usually happens after chemotherapy (5-FU)

• Most common complication of ileal-pouch anal anastomosis for UC

• Clinical history: Diarrhea, urgency, incontinence, abdominal pain, ±

infection (fever, chills, weight loss)

• Investigations:
o Pouchoscopy + Biopsy
Diffuse: fecal culture, CDF culture, LFT, celiac and AMA, CMV
Asymmetric pouchitis -+ lschemic pouchitis

• Management:
o Stop NSAIDs
o Ciprofloxacin or Metronidazole for 2 weeks for active pouchitis
o Topical 5-aminos .alicylic acids (5-ASAs) for idiopathic pouchitis
o Treat underlying cause (CDF: Metronidazole I Vancomycin, CMV:
ganciclovir)
o lmmunomodulators(6-mercaptopurine or azathioprine) or Anti-TNF
usually used after 8 weeks
o Oral budesonide or budesonide enema used in primary sclerosing
cholangitis

• High Output Stoma:

• > 1 ,500 mUday for ileostomy
• Leads to hyponatremia, hypokalemia
• Treated with rehydration and replacement

• Other complications:
• Skin irritation
• Diversion colitis
• Parastomal fistula or hernia

■ Stoma prevent the complications of leak, but does not prevent leak

■ Risk factors for leak: Male, Malnutrition, Anemia, Tension, Difficult dissection

■ Most common complication after ileostomy reversal: Small bowel obstruction

■ Most common cause of fistula near stoma site: Crohn's disease

■ Most common cause of stenosis of stoma: /schemia

■ Most common stoma infection: Candida

ENTERIC FISTULA
■ Definition:
o Abnormal communication between two epithelialized surfaces
• Internal fistula
• External fistula (enterocutaneous, rectovaginal fistula)

■ Causes:
o 80% of enteric fistula are postoperative due to iatrogenic injury
• Examples: adhesiolysis in open abdominal surgery or in laparoscopic ventral
hernia repair

o 30% caused by Crohn's disease

o Other causes including adhesiolysis, and neoplasm

■ Fistula out-put:
o Low output < 500 ml/day
o High output> 500 ml/day (more likely from small bowel}

o Factors inhibits spontaneous closure

• "FRIENDS"
• Foreign body
• Radiation
• Inflammatory bowel disease
• Epithelialization
• Neoplasm
• Distal obstruction
• Sepsis / Short tract < 2 cm

• Unlikely to close:
• Gastric fistula
• Distal small bowel fistula (ileal)
• Tract length < 2 cm
• Defect> 1 cm
• High output fistula
• Malnourished state or sepsis

■ 30 - 35% of fistula undergoes spontaneous closure up to 60 days (2 months)

■ Management of enteral fistula:
o Recognition and Stabilization (first 24 - 48 hours)
• Minimize fluid and electrolyte loss by crystalloids and electrolytes replacement
• Albumin and FFP when needed
• Control of fistula output
• NGT
• Oral rehydration solutions:
o Gastrolyte, Pedialyte, Ceralyte (For moderate-high output)
o Diluted electrolytes beverages: Gatorade, Tomato or Clamato juice
• H2 antagonist, PPI, or Sucralfate reduces the gastric output
• Anti-TNF (lnfliximab) ± Tacrolimus used for fistula secondary to Crohn's
• Anti-motility drugs:
o Loperamide (up to 4 mg QID)
o Codeine (up to 100 mg QID)
o Others: Diphenoxylate, Paregoric, and Tincture of opium

• Somatostatin analogue (Octreotide) specially biliary, or pancreatic fistulas

o Half-life: 2 hours
o Side effects: gallstones, cholecystitis, hyperglycemia, mucosal
atrophy and interruption of intestinal adaptation

• Control of sepsis
• Patient can develop high-grade fever, and > 500 g protein catabolism
• Recognition and drainage of abscess within 24 - 48 hours
• Antibiotics preferred to continue for > 7 days

o Investigation (after 7 days)

• CBC including hematocrit {> 30%), albumin(> 3 g) and transferrin levels, CRP
• U/S, CT and MRI
• Fistulogram + catheter for water-soluble dye injection through external opening

o Nutritional support
• Combination of TPN with enteral feeding(± fistulocylsis)
• 80 - 120 g protein, 2200 - 3600 calories, 20% fat, vitamins and trace elements
• Avoid hyperglycemia

o Wound care
• Keep edges protected and clean with stump and gentile closure
• Wound-care and stoma nurse
• Drainage catheter with ± suction system(VAC dressing: Ring vs. Silo method)

o Operatjon (after 4 - 6 weeks of conseNative measures)

• 50 - 60% of patients will require surgery
• Indicated when failure of non-operative management for > 60 days
• Adhesiolysis, and bowel resection (risk of short bowel syndrome)
• Incision must be closed

o Rehabilitation and postoperative care

• TPN ± Enteral feeding
• ± Antibiotics
• ± Suction for drainage
INTESTINAL DUPLICATION CYSTS
■ Congenital cyst with epithelial lining similar to intestinal mucosa, and smooth muscle layer
± Heterotrophic tissue (gastric mucosa, pancreatic tissue)

■ Location: Throughout all GI tract (45% small bowel + most commonly: ileum)
■ Types:
o Tubular: occur on mesenteric side, Gastric mucosa found in 80%
o Cystic: occur at ileocecal junction

■ Investigation:
o CT is the preferred method for diagnosis
o Sodium pertechnetate Tcgg scan is us.ed to differentiate between Meckel's diverticulum
and duplication cyst

■ Management:
o Asymptomatic: Observation and follow-up
o Symptomatic: Surgical resection is the preferred method for all duplication cysts

TYPHOID ENTERITIS (SALMONELLA)

■ Associated with mesenteric lymphadenopathy and involvement of Peyer's patches (ulceration)
■ Most common complication: GIT hemorrhage
■ Most common complication associated with high Morbidity/ Mortality: GIT perforation (ileum)
■ Treatment: Bactrim

TUBERCULOUS ENTERITIS
■ Most common symptom: Nonspecific chronic abdominal pain and fever

■ CT abdomen + mural thickening with contiguous ileocecal valve and hypodense lymph nodes
with peripheral enhancement of mesentery (suggested TB more than Crohn disease)

■ Colonoscopy with biopsy + ulcers, strictures, nodules, pseudopolyps, fibrous bands, fistulas
■ Management
o Unstable (complicated; obstruction, f)erforation, ischemia): Exploration
o Stable: Anti-tuberculous chemotherapy (RIPE)
• Rifampicin
• lsoniazid
• Pyrazinamide
• Ethambutol
For 2months

Followed by
• Rifampicin
• lsoniazid
For 4 - 6 months
ACUTE MESENTERIC ISCHEMIA
■ Mortality 60%, usually involves the superior mesenteric artery

■ Watershed areas (Griffith's: splenic flexure/ Sudeck's: upper rectum) are most vulnerable

■ Most common involved vessel: SMA

i
■ Presentat ons:
o Elderly patient with multiple comorbidities heart diseases {AF, Valvular disease)

o Sudden abdominal pain out of proportion to physical examination

• Usually postprandial pain

o Associated with immediate bowel evacuation, and sometimes bloody diarrhea

o Diffuse tenderness, rebound, and rigidity are late signs (infarction and necrosis)

o In absence of pain (unresponsiveness patients}:

• Progressive abdominal distension and acidosis is the early sign of ischemia and
impending bowel infarction

■ Investigations:
o Hemoconcentralion with t Hb and Hct, Leukocytosis with left shifting
o Metabolic acidosis, t Lactate, t K, t ALP and amylase (advanced ischemia or necrosis)
o AXR, and Endoscopy are not helpful

o Barium contrast is contraindicated

• May limit visualization of the mesenteric arteries during angiography
• Leakage of barium in bowel perforation can make revascularization more difficult

o Duplex U/5:
• Non-invasive assessment of the patency of the mesenteric vessels
• Used for follow-up after open surgical reconstruction or endovascular treatment
of the mesenteric vessels to assess recurrence of the disease

o Spiral CT Abdomen with IV contrast:

• Most common modality used for AMI
• Findings:
• Bowel wall (Decreased and delayed enhancement, mural thickening)
• Mesentery (Venous congestion and engorgement, mesenteric edema and
hemorrhage)
• Others:
o Adynamic ileus with gasless abdomen (most common finding}
o F ree fluid or ascites
o Signs of bowel infarction
• Pneumoperitoneum
• Pneumatosis intestinalis
• Gas in portal vein

o CT angiography can replace conventional angiography to confirm the diagnosis

 o Conventional angiography "Gold standard":
• Used if diagnosis not clear or plan for revascularization

• Should not be used in patient with surgical abdomen, and patient should proceed
directly to the theater

• Embolus:
• Meniscus sign "Emboli l'odge at branch points"
• Usually at the orifice of the middle colic artery
• With an abrupt cutoff of a normal proximal SMA several centimeters from
its origin on the aorta

• Thrombus:
• In contrast, Lesion occurs near origin and tapers off 1 - 2 cm distally

• Chronic mesenteric thrombosis:

• Associated with diffuse collateral circulation

• Non-occlusive mesenteric ischemia:

• Normal SMA with segments of vasospasm
• If diagnosed + infusion catheter placed at SMA orifice for (Papaverine)

• SMV thrombosis:
• Intact arterial circulation with no delayed images of mesenteric veins

SMA Thrombosis (25 %) SMA Embolism (50 %) SMV Thrombosis

Risk factors Atherosclerosis "Most common"
(PAD or Coronary disease)
Chronic mesenteric ischemia
Presentation Hypotension, Collateral circulations Origin: Heart
Postprandial pain, weight loss
Destination
- at origin
- in proximal mesenteric artery
Entire middle gut may involved
Management IV Heparin :I: Thrombolysis
Improve + Conservative with
- PTA± stent
- Surgical revascularization
Q!lfiai!ive WslDilll!lW!l!JI:
Thrombus/ Symptomatic:
Bypass procedure
(surgical vs. endovascular)
''Most common tvoe''
Cardiac diseases
(MI, AF, Valve disease)
Aortic atherosclerosis
Prior arterial emboli
Destination:
3 - 10 cm distal to origin of
SMA
Proximal jejunum is spared
IV Heparin :I: Thrombolysis
Improve + Conservative
Defiai!iY.!l Wsl□iW!l!D!IDI°
Embolus/ Symptomatic:
Embolectomy
(suroical vs. endovascular)
Hypercoagulable syndromes
PEorDVT
Oral contraception
Malignancy
Intra-abdominal inflammation
/An,,..ndicitis. Diverticulitis\
Abdominal pain
Vomiting and diarrhea
Portal hypertension (Chronic)
Involvement of short
segments of bowel
Any_ bowel draining veins:
SMV, IMV, Splenic or Portal
veins
Resuscitation + IV Heparin
Catheter-Thrombolysis:
Used for refractory abdominal
pain despite anticoagulation
Angiography repeated in 24
hours
 ■ Management of acute mesenteric ischemia:
o Fluid resuscitation and hemodynamic monitoring at ICU unit
• Central venous catheter
• Peripheral arterial catheter
• Foley catheter

o Correction of refractory acidosis with ·sodium bicarbonate

o IV Antibiotics

o IV therapeutic heparin to prevent further progression of thrombus

o Revascularization should be used before any surgical intervention in stable patient

• Endovascular vs. surgical management depend on patient's condition

o Peritonitis mandates immediate open surgical intervention in any type of ischemia

DEFINITIVE MANAGEMENT OF ACUTE MESENTERIC ISCHEMIA

■ Diagnostic laparoscopy

■ Endovascular + Intra-arterial thrombolytic therapy for acute mesenteric ischemia

o Used selectively for acute and chronic mesenteric ischemia in non-contraindicated pis

o Higher probability of successful when performed within 12 hours of symptom onset

o After resolution, identify the underlying pathology

o Elective correction of mesenteric stenosis by:
• Operative mesenteric revascularization
• Mesenteric balloon angioplasty ± stenting

o Approach through:
• Common femoral artery
• Left brachia! artery: if SMA branching in acute angle from aorta

o Disadvantages:
• Does not allow to inspection off ischemic bowel after mesenteric flow restoration
• Prolonged time to achieve successful thrombolysis
• Incomplete or unsuccessful thrombolysis may lead to delayed operative
revascularization

■ Surgical bypass for mesenteric thrombosis:

o Vascular: Antegrade vs. Retrograde

• Retrograde is better as less atherosclerosis, but need supra-celiac exposure

• Vascular conduit: Greater saphenous vein or Dacron graft

'.
• Prosthetic materials should be avoided in patients with nonviable bowel

o �: Duodenojejunostomy if bowel compromised

■ Surgical embolectomy:
o Midline laparotomy

o Abdominal exploration

o Mobilization of transverse colon and reflected upwards, small bowel to RUQ

o Division of ligament of Treitz and mobilization of 4 th part duodenum

o SMA palpated at the root, beneath pancreas, between 3rd/4th part junction of duodenum

o SMA identified medial to SMV and dissected from surrounding structures and
lymphatics

o Middle colic artery excised horizontally at the root

o Proximal and distal vascular control is obtained

o Longitudinal arteriotomy preferred over Transverse arteriotomy

• Which used for distal anastomosis of the bypass graft if embolectomy failed

o Extract the embolus by balloon embolectomy catheter passed proximally and distally

o If embolectomy failed:
• Expose the distal SMA in the root of small bowel mesentery
• Arteriotomy is used for distal anastomosis of bypass graft

o Assess the bowel for viability:

• lntraoperative intravenous fluorescein injection
• Inspection with a Wood's lamp
• Doppler assessment of antimesenteric intestinal arterial pulsations

o ± bowel resection and anastomosis for any non-viable bowel

o 2nd look laparotomy after 24 - 48 hours should be considered in:

• Questionable viability small lbowel
• To allow complete demarcation of nonviable small bowel
• To prevent major resection that may cause short bowel syndrome
• May show some vascular recovery

• Small bowel ischemia due to venous disease

• To allow resection of all nonviable ischemic bowel after 1 st resection

Alternatively resection and stoma is used in critical-ill patient, perforated or frankly

gangrenous segment of the bowel

o Terminate the procedure for diffuse (entire) non-viable small bowel

Non-Obstructed mesenteric ischemia (NOMI)
■ Caused by low-flow state resulting from shock or use of vasoconstrictors
■ Risk factors:
o Hypotension, severe liver or renal dis ,ease, or recent major cardiac or abdominal
surgery, drugs (Vasopressors, Ergotamines, Cocaine and Digitalis)
i
■ Presentat on·
o Diffuse gradual-onset abdominal pain

Progressive worsening is associated with embolic or thrombotic events

Progressive abdominal distension with worsening acidosis in unresponsiveness patients

■ Management:
o Resuscitation, Systemic anticoagulant (Heparin)

o Stop vasoconstricting agents

o Systemic anticoagulation through IV heparin

o Catheter-directed infusion of vasodilator agents (Papaverine, Tolazoline) through SMA

• Phosphodiesterase inhibitor, antispasmodic
• The only treatment for NOMI
• Can be used for mesenteric embolism (Not curative in mesenteric thrombosis)
• Used in diffuse spasm on mesenteric angiography
• Used at 30 - 60 mg / hour for at least 24 hours
• Side effect:
• Hypotension

• Other agents·
• Nitroglycerin
• Glycerol trinitrate
• Prostaglandin E1

• Improved: Repeat angiography

• Deteriorate (peritonitis): Laparotomy

• Rebound tenderness or involuntary guarding

• Papaverine infusion should be continued intraoperatively and

postoperatively

• Warm irrigation '1uid and laparotomy pads should be used to

prevent further intestinal vasoconstriction
Chronic mesenteric ischemia
■ From long-standing atherosclerotic disease of� 2 mesenteric vessels, or arteritis
o Leading to collaterals that developed between Celiac / SMA, and SMA / IMA
(arch of Riolan centrally and marginal arteries of Drummond at the periphery)

■ Typical lesions are located at the vessels origin (within 2 cm from celiac or SMA)

■ Etiology:
o Atherosclerotic arterial occlusive disease (Most common cause)
• Associated with renal artery stenosis and dyslipidemia

o Median arcuate ligament syndrome (Celiac artery compression syndrome)

• Extrinsic compression of the celiac artery by the median arcuate ligament of the
diaphragm

■ Risk factors:
0 Smoking, DM, HTN, and dyslipidemia

■ Pcesentatjon·
o Asymptomatic (most common)
o Symptomatic (if 2 out of 3 of splanchnic arteries involved "Celiac, SMA, IMA")
• Postprandial pain (most common), and weight loss due to food fear "sitophobia"
• SMA is always diseased as occluded or stenosis > 70%

■ Investigations:
o Duplex U/S
o CT abdomen with IV contrast: for atherosclerosis
o Angiography
■ Management of chronic mesenteric ischemia:
o Conservative:
• Smoke cessation and secondary prevention to limit progression of atherosclerotic
disease (antiplatelet therapy)
• IV Heparin indicated in acute thrombus

o Revascularization
• Indicated in presence of symptoms (abdominal pain and weight loss) in
documented splanchnic artery stenosis.

• Options:
• Open surgery (in Celia.c artery compression syndrome)
o Release the ligamentous structure that compresses proximal CA

• Percutaneous transluminal stent angioplasty (PTA)

o Balloon angioplasty is not recommended due to recoil potential

o Used for:
• Focal short segment lesions
• High-risk patients for surgical intervention
• Recurrent disease
• Anastomotic stenosis after mesenteric revascularization

o Consider stent placement in:

• Calcified ostial stenosis
• High-grade eccentric stenosis
• Chronic occlusions
• Significant residual stenosis >30%
• Presence of dissection after angioplasty

• Open surgical reconstruction

o Trans-aortic endarterectomy
• For ostial lesions of patent CA and SMA

o Mesenteric artery bypass

• For lesions located 1 - 2 cm distal to mesenteric origin
• Antegrade from the supraceliac aorta
• Retrograde from either the infrarenal aorta or iliac artery

o Mesenteric re-implantation
SUPERIOR MESENTERIC ARTERY (SMA) SYNDROME
■ Compression of the 3rd part of duodenum by the SMA

■ Usually developed 6 - 12 days after scoliosis surgery

■ Pain relieved by left lateral decubitus, prone or knee to chest position

o Due to decrease tension on aorto-mesenteric artery angle

■ Diagnostic criteria:
o Duodenal obstruction with abrupt cutoff in 3rd part
o Aorto-mesenteric artery angle s 2s• {most sensitive measure)
o High fixation of duodenum by the ligament of Treitz

■ Management:
o Conservative (NGT, Correct electrolytes, High Caloric intake, NJ feeding, ± TPN)

o If failed conservative (or no improvement after 4 - 6 weeks): Surgical

(Strong's procedure "Mobilization of Treitz ligamenr, Gastrojejunostomy,
Duodenojejunostomy)
TECHNIQUES OF BOWEL RESECTION AND ANASTOMOSIS
■ Principles:
o Adequate exposure:
• Wound heals from side-to-side not from end-to-end

o Assessment of safety:
• Indication of resection
• Identify margins
• Assess whole bowel for secondary lesions

o Prepare bowel for resection and anastomosis

• Asses blood supply of margins for anastomosis (color and pulsation)
• Achieve tension-free
• Avoid contamination
• Milking back intestinal contents
• Apply non-crushing clamps
• Use non-traumatic suction

o Bowel anastomosis:
• Make sure to clean mesenteric fat at both serosal edges for 1 cm
• Bowel anastomosis should be in Inversion fashion
• Anti-mesenteric border have least blood supply and should be cut obliquely
• This method also used to widen a narrow lumen "Cheatle's cut"
• Approximation without strangulation
• Avoid taking posterior layer while suturing anterior layer � Stricture I Obstruction
• Sutures placed < 5 mm from edge
• Sutures placed 2 - 3 mm between each other
• Sutures is tied at anti-mesenteric border
■ Anastomotic leak
o Most commonly at day 3 - 5 {after subside of the edema)
o Distal leak as colorectal can presented up to 10 days
o Early anastomotic leak defined as leakage within 30 days postoperative
o Mortality rate increased up to 18% if leak recognized after 5th post-operative day
o Most anastomotic leaks occur on mesenteric side of bowel
o Theory: lschemia to the anastomosis

o Risk factors:
• Patient risks: COPD, smoking, obesity, male, elderly, and radiation
• Nature of disease
o Crohn's/Diverticulitis
o Colo-colic and Coloanal > ileocolic {Up to 20% compared to 3%)

• Drugs (NSAIDs "Ketorolac", Steroids, immunomodulators,

immunosuppressants, and VEGF inhibitors)

• Surgeon risks: Blood loss, Vasopressors, Prolonged procedure, Contamination

o cun;car oresentatjon·
• Leak started from intraoperative period is difficult to diagnose during
postoperative period especially if patient has diverting stoma or prolonged ileus
• Not specific signs and symptoms {abdominal pain, fever, vomiting) ± peritonitis
• Patient can presented with sepsis or septic shock
• Proximal anastomosis usually presented with more severe signs and
symptoms
• lntraperitoneal leak usually present with fever and sepsis with peritonitis
than patient with extraperitoneal leak

o p;agnos;s:
• Most sensitive sign: Tachycardia
• Most sensitive investigation: C RP {Remains elevated > 3 days)
• Best imaging to diagnose leak: CT (Oral/rectal and IV contrasts)
• If questionable leak during imaging, and clinically suspected, it is best to confirm
by: Laparoscopy

o Surgicalpoints:
• Bowel prep vs. No bowel prep doesn't affect the rate of leak, but minimizes the
effects of the leak
• Drain still controversial
• Adhesive barrier {Such as Seprafilm) can increase risk of leak when wrap the
suture or staple line with it
• Some studies showed hand-sewn anastomosis has higher leak rate in ileocolic
anastomosis compared to stapled anastomosis
• Superior rectal artery should be spared in sigmoid resection to minimize the risk
of anastomotic leak
o Management of anastomotic leak:
Based on the leak
• Free leak: Operative management

• Small contained leak:

o Intravenous antibiotics and close observation
(especially if they have proximal diversion)

o Percutaneous drainage (PCD) if associated with peri-anastomotic

abscess, especially if > 3 cm

o Open, Washout, Repair and Divert

(if PCD failed or unavailable while patient in sepsis)

Based on the location

• Small bowel or ileocolic or colo-colic:
o Resection and re-anastomosis ± proximal diversion
o Takedown the anastomosis and end colostomy

• Colo-rectal: (as LAR)

o Loop ileostomy and drainage of the anastomosis only

Resection and end stoma is associated with high morbidity and

permanent stoma

Short Hartmann's stump may be followed with pull-through colo­

anal anastomosis

• lntraperitoneal / Extraperitoneal:
o lntraperitoneal:
• Resection and re-anastomosis ± Diverting stoma
• Hartmann's procedure if suspected ischemia
• Repair of the anastomosis and proximal defunctiong stoma:
in highly s,elected patients with minor tissue defect and
adequate blood supply

o Extraperitoneal:
• Revision of anastomosis only if defect can be seen and risk
of disruption is small

Based on the patient factors

• Hemodynamically Stabl,e: Resection and re-anastomosis ± stoma
• Hemodynamically Unstable: Takedown the anastomosis and perform
ileostomy with mucus fistula or end stoma

Based on the time of presentation

• Early
• Late(> 7 - 10 days)
o Re-operation is usually unnecessary due to peritoneal reaction and
adhesions
o IV antibiotics, close observation, and percutaneous drainage
Preparation for Hand-Sewn
■ Instruments:
o Fine needle holder
o DeBakey forceps
o Crushing and non-crushing bowel clamps
o Non-traumatic Babcock clamp "Don't use Allis or any toothed forceps"

■ Sut ure Material:

o Absorbable multifilament sutures (Avoid Catgut)
o Absorbable monofilament sutures are used in gastrointestinal surgery
o Absorbable monofilament suture materials with retain 70% tensile strength: PDS, and
Maxon -+ Prolong absorption time

■ Suture size:
o 2-0 •·· 4-0 (Optimal 3-0)

■ Needle:
o Reversed cutting "atraumatic", narrow taper point
SUTURING TECHNIQUES
■ Lambert: Deep seromuscular (submucosal) sutures "Most common type"
■ Connell: Full thickness Out-In -+
In-Out at One end
■ Cushing: As Connell suture but seromuscular depth
■ Gambee: Full thickness suture to achieve aversion
■ Halsted: Seromuscular horizontal mattress
■ Horizontal mattress: encourage adhesions and stenosis -+ NOT recommended
Lambert Cushing and Connell

-
Cushmg \.

"" J __,,..
inlenupted
Com-el

Halsted Gambee

serosa
:::'I � muscularis
submucosa
� .mucosa
I
Shapes of anastomosis:
■ End-to-End:
■ End-to-Side or Side-to-End:
o Anastomosis should not> 2.5 - 5 cm from blind end -+ to prevent blind loop syndrome
■ Side-to-Side:
o Stapler: Best to use for ileocolic anastomosis after right hemicolectomy (fewer leaks)

Alternative ways for anastomosis:

■ Compression nitinol clip / ring
■ Biofragmentable ring
HAND SEWN BOWEL ANASTOMOSIS
■ Types: (No superior type)
o Continuous: On animal studies showed decrease oxygen tension -+ impaired healing
o Interrupted: Best to use in acute cases when edema is present

■ Layers:
o Single layer:
• Best type -+ Less time, less narrowing
o Double laye rs:
• Believed to be more safe in decreasing leak rate
• Most studies showed no difference in decreasing leak rate
• Pathological reports showed signs of necrosis and sloughing due to strangulation
• By using inner continuous and outer interrupted sutures

STEPS:
1) Assigned margins for resection

2) CONTROLLING MESENTERY:
■ Opened by:
o Scoring: incise the overlying peritoneum from both sides, and divide mesenteric vessels
• Benign cases: No need to extend to base of mesentery (only vertical scoring)
• Malignant cases: liberal V-shape wedge excision to involve lymph nodes

o Controlling branches: by inserting closed fine tip artery forceps between arcades, then
insertion of artery forceps inside opening and tie each branch
o By using high energy electrosurgical devices: LigaSure or Ultracision
3) DIVISION OF THE BOWEL
■ Apply crushing clamps from anti-mesenteric sides at points of resection obliquely 30 degree
■ Apply non-crushing clamps proximal and distal to crushing clamp to avoid contamination
■ Divide bowel by sharp blade as one cut along the edge of bowel clamps obliquely
Single layer technique:
■ Anastomosis of the bowel "End-to-End technique"
o Two cut ends of the bowel are brought in close "Tension-free'
o Apply stay sutures at serosa of both mesenteric and anti-mesenteric ends (Don't ligate)

■ Interrupted method: (Outer closure)

o Starting from mesenteric side at anterior wall a interrupted Lambert sutures
o When reaching anti-mesenteric➔ Tie both stay sutures but don't cut to rotate the bowel

o Continue suturing the posterior wall from outside as interrupted sutures

■ Continuous method: (Posterior➔ Anterior closure)

o Either by stay sutures at ends or at middle anterior wall, or Babcocks to visualize
posterior wall
o Starting by closing posterior wall from middle as full thickness continuous suture
o Anchoring the first knot with another suture to start on other side later on
o Now continue to anti-mesenteric by switch to Connell inverting stitch and continue
suturing anterior wall as Lambert stitch until mid-point of anterior wall
o Start another suture from anchoring posterior knot and continue as same manner
o Tie both threads when reach to mid-point anterior wall

■ Starting as continuous single layer by using Lambert stitch at mesenteric border

■ Connell stitch is made in both ends at anti-mesenteric angles
■ Outside in➔ Inside out (on same end) "continuous U-shape"
■ Suture tied at anti-mesenteric border
Double layer technique:
■ Outer first technique (Standard) : ''Less traumatic to bowel wall"
o Starting by Lambert suture at anti-mesenteric border then mesenteric border
o Tie both sutures, and don't cut them (for retraction purpose)
o Close the anterior wall between them by interrupted Lambert suture

o Rotate the bowel by passing the stay suture behind the anastomosis

o Close the posterior wall by using double needle suture or 2 sutures inserted in the
middle of posterior wall taking full thickness and tie the knots, then continue as
continuous suture of both sides until reach the angles
 o Continue suturing the angle by using Connell or Cushing
• Bring the needle from inside-outside through anterior wall
• Continue suture anterior wall starting from same edge

o Now reinforce this posterior wall by interrupted Lambert 2 nd layer suture

■ Inner first technique:

o as single layer technique, then reinforce suture line by taking interrupted Lambert
stitches as fat 5 - 7 mm from suture line

5) Check and Close

■ Check water-tight anastomosis by close one end and milking bowel from other end
■ Check lumen for patency

■ Mesenteric defect closed at last with interrupted or continuous sutures at edges with minimal
sutures just to close the defect for prevention of internal hernia
■ ± Abdominal drain
■ Abdominal wall closure
■ Subcutaneous and skin closure
STAPLER ANASTOMOSIS
■ Not preferable in trauma patients (risk of leak an intra-abdominal abscess)
■ Results in good blood supply counter effect the eversion due to stapler
■ No significant different between stapler and lhand sewn except:
o Short timing and more strictures result with stapler

■ Types:
o Linear "6 rows ofstaples"
• Linear GIA cuttini:i stapler (Gastrointestinal anastomosis)

• Linear TA stapler (Transverse anastomosis/ Thoraco-abdominal anastomosis)

• Used in stapling bowel lumens prior to resection and anastomosis, and in

'
closure of open ends of side-to-side stapled anastomosis

Color Used as Closed staole heiaht

White Vascular anastomosis 1 mm
Blue Standard anastomosis 1.5mm
Green Thick tissue anastomosis 2mm

o Circular (EEA: End-to-end anastomosis)

• Sizes of outer diameter: 21 mm, 25 mm, 28 mm, 31 mm, and 33 mm
• Standard for colorectal surgery and low pelvis: 28 or 31 mm
• Large diameter (31, and 33 mm) associated with higher rate of
anastomotic leakage
• Small diameter (25, and 28 mm} associated more with strictures
END-TO-END ANASTOMOSIS

SIDE-TO-SIDE ANASTOMOSIS
ERCP Lengths
■ Length:
o From incisors to GE junction: 40 cm
o Stomach length: 30 cm (gastric pouch 3 - 7 cm}
o Duodenum
• 1st part: 5 cm
• 2nd part: 7 .5 cm

■ Altered length:
o Roux-en-y
• Short roux limb: 40 cm+ 75 cm (roux-limb)+ 80-100 cm (BP limb)= 215 cm
• Long roux limb: 40 cm+ 150 cm (roux-limb}+ 80 - 100 cm (BP limb}= 290 cm
o Biliopancreatic diversion
• Alimantry limb (roux limb}: 200 - 250 cm
• BP limb: 80-100 cm (150 cm proximal to the ileocecal valve}
• Common limb: 50 cm (revision if you add 150 cm here}

■ Approaches:
o Transorally
o Through a gastrostomy or jejunostomy tract
• Gastrostomy tract allowed to mature for 2 weeks, then wire-guided dilation of
tract performed, permitting insertion of the duodenoscope
o Laparoscopy-assisted ERCP
• Superior to Balloon-assisted ERCP with regard to papilla identification,
cannulation rate, and therapeutic success
• Balloon-assisted ERCP preferred strategy when only patients with roux limbs
less than 150 cm were considered (savings of $2388}, but when patients with
roux limbs 150 cm or longer, it will be more expensive (increased cost of $593).

■ Scopes:
o ERCP using standard duodenoscope:
• Side-viewing duodenoscope (125 cm length} is the ideal to perform ERCP
• Short wire: 180 - 260 cm
• Long wire: 420-480 cm

o ERCP using an enteroscope or colonoscope:

• Pediatric colonoscope (164 cm length} and enteroscope (240 cm length}
• Used for short Roux limb
• Forward-viewing and lack of instrument elevator, make duct cannulation difficult
• Solution: once the papilla is reached, a guidewire is placed, over which a
duodenoscope is subsequently advanced

o ERCP using deep enteroscopy techniques:

• Used for biliopancreatic diversion or long roux limb
• Double-balloon enteroscopy, single-balloon enteroscopy, and spiral enteroscopy
• Balloon-assisted ERCP preferred when roux limbs < 150 cm
• Forward-viewing -+ unfavorable orientation of the native papilla, lack of an
instrument elevator
 ■ Papilla:
o Native papilla: standard duodenoscope
• Short Roux limb 75 cm from gastrojejunostomy: standard duodenoscope
• Long Roux limb 150 cm: through a gastrostomy or jejunostomy or a laparoscopy­
assisted ERCP
o Bilioenteric or pancreatoenteric anastomosis: forward-viewing endoscopes
• Short Roux limb: enteroscopes or colonoscopies
• Long Roux limb: deep enteroscopy techniques such as balloon-assisted
enteroscopy or spiral enteroscopy

RELATIVE CONTRAINDICATIONS
■ Alter anatomy of GIT tract
■ Portal hypertension with esophageal+/. gastric varices
■ Acute pancreatitis except gallstone pancreatitis
■ Recent myocardial infarction
■ Repeated failed attempts at ERCP therapy
■ Patient cannot be adequately sedated
■ Anaphylactic reaction
ABSOLUTE CONTRAINDICATIONS
■ Pharyngeal or esophageal obstruction
■ Severe uncorrected coagulopathy
■ Existing bowel perforation
■ Unstable cardiopulmonary status
Appendix
Reviewed by:

Dr. Mamdouh Abdulassib

APPENDIX

■ Appendix functions:
o May play role in secretion of immunoglobulin A
o As reservoir for recolonize the colon with healthy bacteria

■ Blood supply:
o Appendicualr artery
• Originate posterior to terminal ileum
• Enter the appendix along its medial aspect

o Arises from:
• Posterior cecal artery (Most common) + lleocolic artery + SMA
• Ilea! artery + lleocolic artery + SMA
• lleocolic artery (directly) +SMA
• Right colic artery (directly) +SMA

■ Innervation:
o Sympathetic: Superior mesenteric plexus T10-L 1

o Parasympathetic: Vagus

■ Layers of appendix:
o Serosa
o Muscularis layer (absent in some locations)
o Submucosa and mucosa

■ Appendicular tip location:

o Retrocecal 65%
• Associated with iliopsoas sign

o Pelvic 30%
• Associated with obturator sign
• Associate with urinary symptoms, diarrhea, or dysentery

o Retroperitoneal 7%

o Subhepatic

o Pre or Post ilea!

■ Appendicular base location:

o At the McBurney point in 4 % of patients
o Within 3 cm of McBurney point in 36% of patients
o 3 - 5 cm from McBurney point in 28% of patients
o > 5 cm from the McBurney point in 36% of patients
ACUTE APPENDICITIS
■ Pathophysiology:
o Obstruction of lumen by:
• Fecolith 30 - 40% (Most common cause in adults)
• 80% calcified fecolith

• Lymphoid hyperplasia (Most common cause in children)

• Bacterial infection

• Foreign material

• Neoplasm

o Obstruction leads to increases intraluminal pressure by accumulated mucosal

secretions

o Leads to stretch of visceral afferent nerve fibers (Vague abdominal pain)

o Bacterial overgrowth ➔ Inflammation ➔ Increased secretion

o Inflammation extend to serosa + reach to parietal peritoneum (Localized pain)

o Increasing intraluminal pressure eventually leads to venous obstruction followed by
arterial obstruction + Full-thickness ischemia

o lschemia followed by necrosis and perforation

+ Appendicular abscess or generalized peritonistis
o Timing of progression:
• Perforation {12 - 36 hours "18 hours")
• Mass (48 hours)
• Abscess (72 hours)

o Most common site of perforation:

• Midpoint of anti-mesenteric border
• Just beyond the point of obstruction
■ Clinical presentation:
o Order of the symptoms:
1) Anorexia
2) Abdominal pain (periumbilical) that peak at 4 hours
3) Pain localizes at Right iliac fossa
4) Nausea
5) Vomiting

o Vomiting before the abdominal pain siuggests gastroenteritis

o Migrating pain is the most discriminating features of acute appendicitis

o Perforation usually presented at extremities of age (due to misdiagnosis)

o Tachycardia is the earliest sign of perforation and peritonitis

o Symptoms in relation to the location:

• Diarrhea: Pre or post ileal appendicitis
• Burning micturition: Pelvic appendicitis
• Inability to extend the hip: Retrocecal appendicitis

o Valentino's syndrome:
• Pain at the right iliac fossa caused by perforated peptic ulcer and retroperitoneal
extension leads to inflammation around appendix (reactive appendicitis)

■ Examination Signs:
o RIF tenderness is the most sensitive but present in other abdominal conditions

o Rebound tenderness or percussion tenderness

o Cough tenderness

o Guarding or Rigidity

o Rovsing's sign:
• Palpation of LIF produce pain in RIF

o Obturator sign:
• Pain with passive internal rotation of flexed right thigh
Suggestive of pelvic appendicitis

o Psoas sign:
• Pain when extending the right thigh while patient on his left side
Suggestive of Retrocecal appendicitis
■ Differential diagnosis:
o Pelvic Inflammatory disease (PIO) or tubo-ovarian abscess
o Endometriosis
o Ovarian cyst or torsion
o Diverticulitis
o Crohn's Disease
o Colonic Carcinoma
o Mesenteric adenitis
o Omental Torsion
o Renal Colic
o Urinary Tract Infection
o Epiploic appendagitis
o Typhilitis

■ Investigations:
o Laboratory
• Increased WBC level
• Most sensitive lab test: Left shifting of differential WBC counts
• Total WBCs >10,500 (present in 80% of patients)
• > 15,000 suggestive of complicated appendicitis
• WBCs level is unreliable in infants, elderly (blunt immune response}, and
pregnant patients (physiologic leukocytosis)

• Increased inflammatory markers

• CRP, ESR (highly sensitive but not specific)

• Urine analysis to rule out urinary tract conditions

• Beta-HCG level to rule out ectopic pregnancy

o U/S:
• Diameter> 7 cm, absent peristalsis, fluid collection, or fecolith detection
• Non-compressibility is the most specific sign in US

o CT scan:
• Diameter> 7 mm or wall thickness> 2 mm
• Fat stranding, enhancement off the wall, periappendicular fluid
• No contrast in lumen ± fecolith

o Diagnostic laparoscopy
• Useful in equivocal cases & when CT scan is contraindicated
• Especially in women of childbearing age
■ Appendicular scores:
o Appendicitis inflammatory response (AIR) score
• Same sensitivity with more specificity compare to Alvarado score
• Better to use for pediatric age group

o Alvarado score

Svmptoms Alvarado score AIR score

Miorato~ RIF nain 1
RIF oain 1
Vomitino 1
Nausea or VomitinQ 1
Anorexia 1
$ions Alvarado score AIR score
RIF Tenderness 2
RIF Rebound tenderness 1 1 - 3 /Deoend on severitv)
Fever> 37 .5 °C 1
Fever> 38.5 °C 1
Laboratorv Alvarado score AIR score
Leukocytosis 2 1 for 10 - 14.9
2forle15
Left shifting of neutrophils 1 1 for70-84%
2 for;, 85%
C-reactive protein (CRP) 1 for 10 -49 g/1
2for le50 o/1
Total Score;
< 5: Appendicitis unlikely (30%) � Discharge

5-6: Appendicitis is possible (66%) + CT scan I Admission and observation

7-8: Appendicitis is likely + Possible surgery
;,9: Appendicitis is highly likely (93%) + Surgery
■ Management of acute appendicitis:
o Open/ Lap appendectomy
• Up to 20% is the acceptable rate of negative appendectomy
(increased in women)

o Conservative management± Interval appendectomy

• Not the standard of care, interval appendectomy no longer recommended
• Medical management alone associated with recurrence 7 - 14% at 1 st year
• Interval appendectomy associated with decreased risk of obstruction, wound
infection and reoperation
• Colonoscopy should be done prior to interval appendectomy for> 50 years
• Interval appendectomy usually done in 6 - 10 weeks

• Indications: "Controversial"
• Localized peritonitis (Abscess or phlegmon)
• Children with complicated appendicitis
• Mild early acute appendicitis in educated patient lives near to hospital

■ Antibiotics:
o Acute appendicitis: 3ro generation cephalosporin + metronidazole or cefazoline as
single pre-operative dose, and discontinue postoperative< 24 hours

o Perforated appendicitis or abscess: 3'd generation cephalosporin + metronidazole for

48 hours at least followed by oral up to 7 days

■ Complications of acute appendicitis or post-appendectomy:

o Abscess or Mucocele

o Perforation

o Gangrene

o Bowel obstruction

o Cecal fistula: Most likely to resolve spontaneously

o Septic seeding (Pylephlebitis)

• Septic thrombophlebitis of Portal vein (Portal Pyemia), SMV, or Splenic vein
• May presented post-appendectomy or hemorrhoidectomy
• Can associated with multiple small liver abscesses
• Associated with elevated ALP, without jaundice
• CT Scan:
• Surrounding stranding, air bubbles or thrombi within SMV or portal vein

• Management:
• Antibiotics
• Appendectomy
• Anticoagulation if suspect thrombosis
 ■ Perforated appendicitis:
o Generalized peritonitis with sepsis
• Patient usually requires midline laparotomy

o Localized peritonitis with contained mass

Phlegmon
"matted loops of bowel adherent to
inflamed appendix" Abscess > 4 cm
Abscess < 4 cm

I
I
I Afebrile
I No Improvement
despite antibiotics.
Fever/ Sepsis

Conservative
Colonoscopy in 2 - 4 weeks
No interval appendectomy if adult
i i
I Open Appendectomy
I Antibiotics + PCD
CT-guided or by Laparoscopic
"Standard of care"

Colonoscopy in 2 - 4 weeks

Patients with a multicomparlmental abscess required open drainage and washout

■ Most common bacteria isolated in perforated appendix: Bacteroides

■ i
Mortality of appendicit s:
o Acute appendicitis: 0.1 %
o Perforated appendix: 5%
o Fetal loss in acute appendicitis 3 - 5% and 25% in perforated appendicitis
■ Appendicitis during pregnancy
o Appendix is displaced superiorly
o 1 st Trimester: Most common cause of acute abdominal pain
o 2nd Trimester: Most common time for acute appendicitis
o 3"' Trimester: Most common time for perforated appendicitis {25% risk of fetal loss)

o MRI may indicated for clinically suspicious patient and negative U/S result
o Management·
• Confirmed appendicitis: Appendectomy
• Hasson technique and minimal insufflation should be used if laparoscopic
appendectomy planned

• Incision should be raised if open appendectomy is planned (cecum is

pushed upward by the gravid uterus)

• Diffuse peritonitis: Laparotomy

• Walled-off (contained) perforation:

, Phlegmon:
o Afebrile patient: IV antibiotics
o Febrile patient despite antibiotics: Appendectomy

• Abscess:
o IV antibiotic± U/S guided drainage

•"·;

·�
,,/ ' .r'''"
..··
l :.•

'•,,
,.

·­
.,
,_,... -:::::::-_.1,
·­
·-
• Molliths ' fl.Al �...... ....·

--�2Z!.
"'_____.;....b-�,-

--
AS/S---- ' "�--.
■ During appendectomy in case of normal appendix:
o Examine the cecum up to 1 meter of distal ileum and examine the pelvic structures to
identify any pathology

o Always perform appendectomy in open cases (to avoid future confusion)

o Regional enteritis not involving cecum -+ Appendectomy

o Ovarian cyst
• Clear cyst:
• > 5 cm: Aspirate the cyst + Appendectomy
• < 5 cm: Don't aspirate, most likely Graafian follicle

• Ruptured cyst
• Stable: Appendectomy + control bleeding
• Unstable: Oophrectomy

• Cystic mass
• < 5 cm: appendectomy + follow up the mass
• > 5 cm: Consent for unilateral salpingo-oophorectomy + Appendectomy
Never biopsy an ovarian mass (Risk of pseudomyxoma peritonei)

o Thick fallopian tube and exudates -+ appendectomy + post op PIO antibiotics

o Inflamed ileum -+ Appendectomy

o Inflamed cecum -+ Closed without any intervention

o Cecal mass -+ Right hemicolectomy, or biopsy if resection is not feasible

o Endometrial tissue "Pelvic endometriosis"

(Blue-colored lesion involvement of ovaries, uterus, peritoneal surfaces, etc.)
• Medical management
• Laser ablation if failed medical treatment
• Hysterectomy and bilateral salpingo-oophorectomy for refractory, extensive or
recurrent disease
Careinoid tumor of the appendix

<1cm 1-2cm >2cm

- Tip of appendix - Base

Post-operative
- Middle of appendix
Lymphovascular invasion
- Mesoappendix
- Lymph node metastasis
- Grade II (High proliferation rate)
- Mixed histology
(Goblet cell, adenocarcinoma)

Open Appendectomy Right hemicolectomy

No Yes with regional lymphadenctomy

Observation

■ Frozen section should be submitted for atypical inflamed appendicitis

■ 5-HIAA and chromogranin A post-operatively should be done for every carcinoid tumors to rule
out distant metastasis

■ Cystadenocarcinoma or adenocarcinoma of the appendix: (any size)

-+Right hemicolectomy
-+Appendectomy only preserved for:
o (Tis} adenocarcinoma
o Lymphoma of the appendix

■ Most common malignant tumor of the appendix: Adenocarcinoma (Not carcinoid)

 Mucocele of the appendix
■ Distension of the appendix (filled with mucus)
■ Caused by:
o Retention cysts (lntraluminal mucin production)
o Mucosa! hyperplasia (No atypia)
o Cystadenoma (Few atypia)
o Cystadenocarcinoma (Stromal invasion)

■ Management:
o Convert laparoscopy to open is recommended to avoid the risk of disseminating cancer
cells (spillage) in case of malignant mucocele
• EndoBag is alternative way before dissect cecum and appendix to avoid spillage
and rupture

o Intact mucocele without rupture have no risk

o Rupture benign mucocele will not be converted to malignant

o Rupture malignant mucocele will lead to pseudomyxoma peritonei

o Colonoscopy to rule out synchronous or metachronous lesions in 25%

o For Mucocele diagnosed during laparoscopic appendectomy:

• Perform diagnostic laparoscopy and closure with no resection for suspicious or
large > 2 cm mucocele

• Conversion to open procedure is the standard of care for Mucocele s 2 cm

• Although most cases can be performed laparoscopically, with attempt not
to rupture the mucocele

• CT scan staging

• Perform therapeutic procedure for resectable disease

Malignant
Benign
Cystadenocarcinoma
Cecal or terminal ileum involvement
Positive peri-appendicular lymph node
Positive margins

Open Laparotomy Cecectomy with removal of

Appendectomy + Frozen section -Appendix
Wide excision of mesoappendix / peri-appendicular lymph node - Mesoappendix
- Peri-appendicular lymph node
lleocecectomy or Cecectomy (Typhlectomy)
Preserved for base involvement or compromised by mucocele > 2 cm Right hemicolectomy

Right hemicolectomy (Historically)

Pseudomyxoma peritonei
■ Intra-peritoneal diffuse collections of gelatinous material and mucinous implants on peritoneal
surfaces "jelly belly"

■ Due to rupture of cystadenoma, or adenocarcinomas -+ peritoneal studding

■ Most common caused by: Appendix

■ Most common symptoms: increased abdominal girth

■ Overall 5-year survival: 70¼

■ CT scan: Liver and spleen scalloping, redistribution phenomenon:

o Peripheral location of tumor in abdomen with sparing and central displacement of small
bowel and mesentery

■ Treatment:
o Aggressive cytoreduction and intraperitoneal heated chemotherapy "IPHC"
• All gross disease and the omentum should be removed
• Appendectomy is routinely performed
• Hysterectomy with bilateral salpingo-oophorectomy is performed in women
• If diagnosed intraoperatively, then closure with staging should be done

o Heated chemotherapy to penetrate large tumor deposits (not larger than 2.5 mm)

■ Paul sugarbaker technique

Cytoreductive surgery (CRS) by Hyperthermic intraperitoneal chemotherapy (HIPEC)

o Heated chemotherapy (42 - 43 degrees C) for 90 minutes
• As tumor cells dies at 40 degree C, while normal cells dies at 44 degree C

o Used for treatment of:

• Pseudomyxoma Peritonei from disseminated mucinous of cystadenoma
• Peritoneal carcinomatosis dissemination from GIT cancers (CRC, gastric}
• Peritoneal mesothelioma
• Ovarian cancer

o Time to use: after resection of bowel, and before anastomosis of bowel

o Heated to penetrate tumor deposits (not larger than 2.5 mm)

Operative Note
Appendectomy

■ After finishing induction and before drapping, examine the abdomen to rule out any mass
o No mass felt: Continue with appendectomy
o If mass felt & patient is not toxic: Consider abandoning the procedure and continuing
conservative management

■ Incisions for open appendectomy:

Oblique incisions
o McBurney's or Grid Iron (Muscle splitting)
• Skin incision perpendicular to McBurney' point
• (a point between Lateral 1/3 - Medial 2/3 of an imaginary line connecting ASIS
and umbilicus}

o Rutherford Morison's (Muscle cutting)

• Extension of the wound upward and laterally to cut internal oblique and
transversus abdominis
• Used in difficult cases in which more exposure is needed (subhepatic appendix)

Transverse incisions
o Lanz (Muscle splitting)
• 2 cm below umbilicus centered between mid-clavicular and mid-inguinal
• Between ASIS and umbilicus

o Rocky Davis (Muscle cutting)

• Extension of the wound medial and downwards

o Fowler Weir incision (Muscle cutting)

• Extension of the wound medianly to cut rectus muscles

Vertical incisions
o Lower midline
• Used in generalized peritonitis or pelvic appendix

o Right paramedian
■ Steps of open appendectomy:
o After skin and subcutaneous incision
o External oblique divided at line of incision at direction of its fibers
• Incise it first by scalpel followed by partially closed Mayo's scissor
o Internal oblique and transversus abdominis split by using straight Mayo's scissor or
Artery forceps to expose peritoneum
o Peritoneum is grasped between two artery forceps and scissor used to make sure of
transparency followed by small snip to open the peritoneum
o Fluid taken for culture

o Abdominal exploration if done throlJlgh midline incision or laparoscopy

o Confirm right ovary and fallopian tube are normal in female patients

o Deliver the appendix:

• Place index inside peritoneal cavity medially and hook the appendix
• Cecum held by moist gauze an delivered into wound gradually and gentle side to
side motion, or by Babcock with caution if previous method failed
• Appendix identified following the taenia distally or follow the small bowel to find
the cecum, or by reaching posterior peritoneum and move medially to hold the
cecum
• It is advisable not to grasp the appendix itself
• Grasping by Babcock around the appendix or at level of mesoappendix
• If appendix tip unable to visualized -+ Tilt the patient to Trendelenburg position

o Complete mobilization of cecum, is indicated in:

• Retrocecal completely with difficult exposure
• Appendicular phlegmon
• Severely inflamed, or gangrenous appendix for proper transaction

o Confirm diagnosis:
• Acute appendicitis: swollen congested inflamed tip ± pus
• Gangrenous appendix: if extend into cecum, excise and perform cecostomy
• Perforated appendicitis
• Appendicular mass
• Normal shape appendix: examine the tip for carcinoid, cecum and other organs

o Transection methods of appendicular base:

• Classical
• Divide the mesentery first between 2 Kelly clamps and ligation of free
ends by 3-0 silk
• Base identified and then crushed with Kelly clamp and moved 1 cm toward
the tip, divide the base using the scalpel and ligate the crushed segment
with 0 or 2-0 Vicryl
• Endo-loop

• Stapler
 o Retrograde appendectomy
• Indicated if the tip is not clearly visible
• Creation of window between the base and cecum followed by transection of
mesoappendix
• Followed by completion of appendectomy from base to tip

o Ways of dealing with appendicular stump

• Simple ligation and irrigation with saline (Preferred method)
• lnvagination of appendicular base into the cecum followed by purse string suture
• Cauterize the mucosa remaining in the stump of the appendix (controversial)
avoiding development of mucocele

o Closure
• Peritoneum and transversalis fascia: continuous absorbable suture
• Rectus sheath and internal oblique with interrupted suture
• Closure of external oblique
• Closure of skin by subcuticular suture, or interrupted in case of perforated
appendix

■ Ports insertion for laparoscopic appendectomy:

V <I

' ..

J \
Large Bowel
Reviewed by:

Dr. Zakir
 LARGE BOWEL
ANATOMY AND PHYSIOLOGY
■ The large bowel consists of cecum and colon
o Cecum is 6 cm long, fixed and widest part (7.5 cm}
(t risk of perforation in patient with competent ileocecal valve}

o The colon measured 135 -150 cm and divided into 4 segments:

Seamen! Lenath
Ascendina colon 15 -25 cm from ileocecal iunction - Heoatic flexure
Midgut Hepatic flexure
Transverse colon 50 cm from heoatic to solenic flexures
Solenic flexure
Descending colon 15 - 30 cm from solenic flexure to oelvic brim (iliac crest)
Sigmoid colon 40 cm from pelvic brim to the rectosigmoid junction which located against 3'•
Hindgut
sacral vertebra (10 -15 cm from anal verge)

Siamoid is mobile and narrowest oart /risk of obstruction and volvulusl

■ Plicae semilunaris: T ransverse bands -+ Haustra

■ Taenia coli: Longitudinal 3 bands (from outer longitudinal muscle layer}
o The taenia encircle the bowel completely at rectosigmoid junction
o No diverticulum in the rectum

lntra-oeritoneal structures Extra-oeritoneal structures

Esoohaaus Abdominal esoohaaus Thoracic esoohaaus
Abdomen Small bowel - liver - Spleen 2nd and 3'• part duodenum - Pancreas
Kidnevs Adrenal alands, Aorta and IVC
Large bowel Transverse colon Ascending colon
Siamoid colon Descendina colon
Anorectal Upper rectum Middle rectum (Only anterior; partial)
(Covered bv oeritoneum anterior and lateral) Distal rectum /No oeritoneal coveraaeI

Locations of some diseases

Cecum Ascendina colon Transverse colon Descendina colon Siamoid

Site of oerforation Attenuated FAP Site of dis1ension FAP Site of obstruction
Volvulus Sessile polvos Toxic meaacolon Hvoernlastic polvos Volvulus
Angiodysplasia HNPCC Malignant I UC Pseudomembranous Colonic stricture
stricture colitis
Actinomyces Toxic megacolon lschemic colitis lschemic colitis Diverticulitis
(Distal/vi (Proximallvl
Lvmohoma UC oerforation Malianan~
Tuberculosis
Tvnhlitis
Pneumatosis intestinalis
 Arterial supply

From lateral aspect of the infra-

From ventral aspect of the supra-
renal aorta
renal aorta
SMA IMA
(proximal to distal) Supplying distal ½ transverse,
Supplying small bowel, ascending
descending colon, sigmoid.
and proximal ½ of transverse colon
unner rectum
Left colic artery (Ascending and descending
Middle colic artery (Main supply for transverse colon)
branches/
Riaht colic arterv (Ascendina and descendinnl Siamoidal arterv
lleocolic artery (Terminal branch) Superior rectal artery (Terminal branch)
0 Descending branch
0 Cecal artery (Anterior and posterior)
0 Appendicular artery from posterior cecal artery

0 lleal arterv

■ Collateral pathways:
o Arch of Buhler -+ connecting Celiac to SMA
o Arc of Riolan (meandering mesenteric) -+ SMA (middle oolic) to /MA (left oolic)
o Marginal artery of Drummond {15 - 20%) -+ SMA (descending ileocolic) to /MA

■ Watershed areas:
o Griffith's point (Splenic flexure): SMAand IMAjunction
• Between ascending left colic artery and marginal artery of Drummond

o Sudeck's point (Rectosigmoid junction): Between sigmoidal and superior rectal arteries

Colon is more sensitive to isch'emia than small bowel (due to lesser co/laterals)

Venous d rainage

SMV IMV
ITo the left of /MAI
Jeiunal and ileal veins Left colic vein
ileocolic vein Siomoidal vein
Rioht colic vein Superior rectal vein
Gastrocolic trunk of Henle
0 Middle colic vein
0 Right gastroepiploic vein
0 IPDV (Anterior and posterior branches)
0 SPDV (Anterior branch only)
Posterior SPDV -+ Portal vein

c:> SMV joins IMV-Splenic vein to form confluence of portal c:> Drains into splenic vein
vein c:> Confluence of SMV-Solenic vein in 30%
 Nerve supply

Svmoathetic Parasvmoathetic
Right colon Superior mesenteric and celiac ganglia Vagus
Transverse colon
Distal colon Inferior mesenteric and h'=oaastric alexus S2 - S4 /Pelvic salanchnic nerve\

■ Sensory neurotransmitters: Substance P & Calcitonin

■ Main nutrient of colonocytes: Short-chain fatty acids

''Acetate (Acetic acid), Propionic acid, Butyric acid"

■ Colon absorption:
o Water passively (1 - 2 Uday and up lo 5 L/day)
o Na actively by Na/K ATPase (Colon secretes K)
o Cl actively by CI/HC03 exchange (Colon secretes HC03)
o Short-chain fatty acids
LARGE BOWEL OBSTRUCTION
■ Definition: Intestinal obstruction distal to ileocecal valve

■ Most common mechanical cause: colorectal carcinoma

o Followed by volvulus then diverticulitis

■ Most common adynamic cause:

o Acute colonic pseudo-obstruction (Ogilvie's syndrome).

■ Most common site of perforation: cecum

■ Management:
Surgery is the definitive therapy for most causes

o INFLAMMATION:
• Usually due to strictures from diverticulitis, Crohn's disease, or at points of prior
anastomoses

• Management:
Non-operative:
• In diverticulitis (hemodynamic stable, no purulent or feculent peritonitis)
• Conservation+ follow up colonoscopy and biopsy (to rule out malignancy)
± Stenting

• Operative
• j risk of injury of surrounding structures
• Options:
o Temporary loop colostomy (in case of severe inflammation}
o Resection and anastomosis ± stoma
o Hartmann's procedure
o Subtotal colectomy with end ileo-anal anastomosis
o Colonoscopy and stenting

o VOLVULUS

o INTUSSUSCEPTION

o INCARCERATED HERNIA

o OGILVIE'$ SYNDROME
o COLORECTAL CANCER:
• Partial obstruction
Conservative management + Staging + Single-stage procedure
• Complete obstruction
• Right-side lesion:
o Right hemicolectomy :!: diverting stoma
o Right hemicolectomy with mucus fistula and ileostomy
• Used for rectal mass with suspicious proximal viability
(ischemia, necrosis or perforation)

• Splenic flexure lesion:

o Left hemicolectomy
• Associated with non-oncological resection, and resection of
non-drained lymph nodes from splenic flexure

o Extended left hemicolectomy

• Associated with difficult mobilization of transverse
mesocolon and less lymphatic dissection

o Extended right hemicolectomy

• Adequate lymphadenectomy and tension-free anastomosis

o Segmental resection and anastomosis

• Associated with inadequate blood supply for resection and
anastomosis and non-oncological resection

• Left-side lesion:
o Stent
o Hartmann's procedure
• Used for high-risk patient, unstable, or perforated

o Resection and anastomosis :!: diverting stoma

• Used as oncological resection, after exclude ischemia
necrosis or perforation of right colon and cecum
• Keeping in mind risk of synchronous tumor 5% and need for
proper staging postoperative

o Subtotal or Total colectomy

• Used for left colonic mass with suspicious proximal viability
(ischemia, necrosis or perforation) or synchronous tumor

o Diverting loop stoma

• Diverting sigmoid colostomy: best for distal lesion
• Stoma can be resected later for definitive surgery
• Diverting transverse colostomy
• Diverting ileostomy: 2nd option, used with risk of dehydration

• Advanced: /Met astatic resect abte CRC}

o Stent + Staging + Surgery if resectable or down-staged
o Subtotal vs. Total colectomy
Colonoseopy Stenting
■ Indications for stenting:
o Palliative
o Bridge to definitive surgery
• To allow proper chemotherapy preoperatively
• To perform colonoscopy for synchronous tumors
• Mainly used for intermitted, partial obstruction (Not in complete obstruction)

o Benign diseases (Controversial)

• Most common benign indication for stenting:
Anastomotic and diverticular stricture

o No stenting for right colon

o No stenting for rectal malignancy (risk of migration and affect radiotherapy}

■ Contraindications:
o Peritonitis
o Perforation
o lschemia

■ Types of stent:
o Covered: Less tumor ingrowth but more risk to be migrated
o Non-covered:
Stent should be extended 2 cm proximal and distal to the tumor

■ Complications:
o Perforation 5%: Mostly at colonic segment with sharp angulation, patients on
bevacizumab

o Migration 11 %: Short narrow stent, or due to shrinkage of tumor

o Obstruction: By
• Fecal matter
• Early migration
• Synchronous lesion
• Tumor ingrowth
• Slow expansion of stent (up to 72 hours}
OGILVIE'S SYNDROME
■ Definition: Acute colonic pseudo-obstruction(motility disorder} presented with signs and
symptoms of a mechanical obstruction of colon in the absence of a mechanical cause
(anatomic lesion}

■ Risk factors:
o Opiate, elderly, bedridden, recent surgery, infection, or trauma
i
■ Presentat on:
o Post-operative day 4 abdominal pain, constipation and distension
o Distended abdomen with positive bowel sounds
Serial examination needed eve,y 12 - 24 hours
i
■ Investigat ons:
o CT Scan showing proximal colonic dilatation with no signs of mechanical obstruction
o Contrast enema may be helpful but carry risk of perforation

■ Management jn order:
1) Supportive care
o Adequate hydration
o NGT is used for decompression
o Alter position hourly
o Maintain K level > 4, and Mg level > 2 mg/di
o Discontinue opiates, laxatives, anti-diarrhea, anti-cholinergic, anti-psychotics, CCB

2} Neostigmine: (acetylcholinesterase inhibitor)

o Indications:
• Failure of conservative measures(> 24 - 48 hours}
• Cecal diameter of > 12 cm

o Dose:
• 2 - 2.5 mg IV over 3 minutes
• 2nd dose can be given with 24 lhours interval
Dose must be adjusted for patient with renal insufficiency

o Side effects: Bradycardia, Hypotension, and Ml

(Atropine must be available at bedside)

o Contraindjcations:
• Asthma or Bronchospasm
• Acute coronary artery syndrome
• Acute urinary retention
• Obstruction(Intestinal or Urinary)
• 2nd or 3,d degree heart block
• Peritonitis

o Relative contraindications:
• Creatinine > 3 mg/di (Renal failure) + Need dose adjustment
• Recent Myocardial infarction
• Concomitant beta blocker
3) Colonoscopic decompression
o For patient not improving with conservative measures and neostigmine or can't tolerate
o Contraindicated in peritonitis or perforation
o No need for bowel prep, with minimal air insufflation
o Advanced to the cecum or at least up to hepatic flexure
o If ischemic mucosa was visualized, immediate withdrawal is indicated
o Effective in 50% of patients, and 80% if used tube decompression
• Tube usually fall spontaneously, it should be manually removed after 72 hours
• Flush every 4 - 6 hours and connect it to low-suction system

4) Percutaneous tube cecostomy

o Used for proximal colonic decompression who fail steps above
o For patients without ischemia or perforation

5) Surgery
o Indications:
• Perforation, mechanical obstruction or ischemia
• Failure for non-operative measure > 6 days

o Options:
• Cecostomy or colostomy
• Subtotal or total colectomy
• Right hemicolectomy
ISCHEMIC COLITIS
■ Clinical presentation:
o Rapid onset of abdominal pain and tenderness, tenesmus, and bright red diarrhea

o These symptoms usually started within 24 hours from onset of abdominal pain

■ R isk f actors:
• Medical disease:
• OM, HTN, Atherosclerosis
• CHF, Arterial fibrillation, myocardial infarction
• RA, SLE, SCD

• Intervention:
• Surgery (ligation of IMA)
• Aorto-iliac (endovascular or surgery), Cardiopulmonary bypass
• Colonoscopy, or Hemodialysis

Predictive fact or tor ischemic colitis after intervention­

Preoperative shock

• Drugs:
• Constipation-induced (Cathartics, Opioids), OCPs, or Chemotherapy
• Antibiotics, lmmunomodulators (Anti-TNF), Vasoconstrictors (Cocaine,
methamphetamines)

■ Most vulnerable /watershed} areas:

o Splenic flexure (Griffth's point)
• Most common site of IC ;,Proximal left colon - Distal transverse colon•

• Marginal artery of Drummond may play role in the segment of colon

o Rectosigmoid junction (Sudeck's point).

• Superior hemorrhoidal artery are termination of IMA

o Right colon: lleocolic artery is terminal branch of SMA

 i
■ Investigat on:
o Anemia, leukocytosis, hypoalbuminemia, increased BUN and LDH

o Stool culture for suspected infectious colitis

o Metabolic acidosis suggestive of intestinal infarction

o AXR
• Round density along the sides of gas-filled colon "Thumb printing"
• Most common radiological non-specific finding (75%)
• Seen on barium study x -ray and CT scan
• Indicates bowel wall (haustra) thickening
• Due to submucosal edema from infection or inflammation (colitis)
• Differential diagnosis:
o lschemic colitis, CDF, Diverticulitis, Ulcerative colitis
o Mesenteric ischemia, Hemorrhage
o Lymphoma, Leukemia

o Barium enema
• Previously was used as diagnostic tool that done early "Thumb printing" sign
• Water-soluble or barium are relatively contraindicated during the acute phase
• Because of danger of barium peritonitis if extravasation happens or during
surgery, barium study replaced nowadays with CT scan

o CT abdomen (with IV and Oral contrasts)

• Bowel thickening, mural thickening, or fat stranding
• Pneumatosis, portal venous gas, megacolon and ascites indicate severe
diseases

o CT angiography to exclude mesenteric ischemia

(if pain sudden and out of proportion to physical exam)

o Flexible Endoscopy
• Gold standard and should be performed within 48 hours except in peritonitis
• Relatively contraindicated in acute phase
• Don't go beyond the ischemic area, and do it with minimal insufflation

• Colonoscopy used for suspected right ischemic colitis and along with biopsy
used postoperatively to exclude infectious or malignant causes
• Flexible sigmoidoscopy used for suspected left ischemic colitis

• Findings: Single strip sign (Single longitudinal ulcer)

• Specific for ischemic co Iitis but not commonly seen
• Signs of ischemia: edema, dusky mucosa covered with exudates,
petechial hemorrhage, with no active bleeding
• Biopsy should be taken: Mucosal infarction, ghost cells (Pathognomonic)
■ Management of ischemic colitis:
o Conservative
• Resuscitation with IV fluids
• Bowel rest ± NGT ± TPN
• Broad-spectrum IV Antibiotics 2: 1 week "due to bacterial trans/ocation"
• Avoid Cathartics and Steroids (unless used for other medical diseases)
• Avoid Endoscopy and contrast studies in acute ischemic colitis

Response rate: 80%

Recurrence rate: 10%

o Surgery (Only 20% of patients)

• Indications for urgent surgery:
• Peritonitis, Perforation, IBleeding or Hemodynamically unstable
• Transmural necrosis on:
o CT (pneumatosis or portal venous gas)
o Endoscopy (gray-appearing mucosa)

• Surgical options as urgent surgery:

• Anatomical segmental resection + diverting end stoma

• Temporary closure and 2nd look laparotomy after 24 hours

o For extensive or patchy involvement of large bowel

• Subtotal colectomy wiith end ileostomy

o If entire colon is i nvolved, or massive non-localized hemorrhage

• Indications for elective resection and anastomosis:

• Stricture
o Presenting with intermittent abdominal pain
o Constipation alternating with diarrhea

• Non-resolving segmental colitis for> 2 weeks

o Including pain, bloody diarrhea or recurrence of sepsis
TOXIC MEGACOLON
■ Risk factors:
o Inflammatory bowel disease (5% in UC}, and Clostridium difficile infection
o Salmonella, Shigella, and Campylobacter colitis are rare causes

■ Pathophysiology:
o Acute transmural inflammation of the colon leading to smooth muscle relaxation (due to
NO} and inhibits motility, leads to necrosis due to bacterial and inflammatory mediators
■ Pathology
o Proximal dilatation of inflamed colon, thinning of the bowel wall, and deep ulcers
o In C. difficile:
• Diffuse ulcerations, raised mucosa! nodules, yellowish-white superficial plaques
with normal mucosa (pseudo-membrane appearance}, and extensive denudation

o In fulminant amoebic colitis:,

• "wet-blotting paper" appearance, punched-out ulcers, and trophozoites

o In Cytomegalovirus colitis: Inclusion bodies

■ CHnjcal presentation
o Severe bloody diarrhea, abdominal pain and distention
o Toxic appearance (altered sensorium, tachycardia, fever, postural hypotension), lower
abdominal distension and tenderness ± peritonitis
o Jalan criteria for diagnosis:
• Fever> 38.6
• HR> 120
• WBC > 10.5

■ tnvesJigation
o Leukocytosis, Anemia, f ESR and CRP, hypoalbuminemia, septic and CDF work-up
o Colonoscopy should be avoided in toxic status
• Limited endoscopy (only to visualize the diseased part with minimal insufflation)
To rule out IBD, CDF or CMV

o AXR and CT
• Most common involvement segments: ascending and transverse colon
• CT findings:
• Colonic wall thickening, and submucosal edema
• Pericolic stranding, and thickened haustra
• T ransverse colon diameter> 6 cm

Colonic distension is more prominent in transverse colon

■ Management of toxic megacolon:
o Conservative with bowel rest, and changing patient posture
o Discontinue all anti-motility agents, opiates, and anti-cholinergics
o Discontinue all other antibiotics if CDF suspected
o Enteral feeding begun as soon as patient shows signs of improvement
o IV hydrocortisone 100 mg every 6 - 8 hours (for IBD patients with fulminant colitis}
o Oral Vancomycin 500 mg 6 hourly ± Metronidazole 500 mg 8 hourly (for CDF)

o Indications of surgery:
• Perforation, hemorrhage, progress dilatation
• Failure of medical treatment 48 - 72 hours (relative indication)
• IBD-Toxic megacolon
• CMV-Toxic megacolon
• CDF-Toxic megacolon

• Procedure of choice: Total colectomy with end-ileostomy (No bowel prep)

• Used after failure of conservative management

• Inflamed rectosigmoid ➔ Mucous fistula with part of sigmoid colon

proximal to inflammation

• Rectal stump management:

Intra-operative
o Transect distal colon in area with minimally inflamed

o Placement of suture or staple intraperitoneally to the sacral

promontory or psoas muscle

o Stump can brought to level of subcutaneous tissue an fixed by Silk

(above the fascia} lower risk of pelvic abscess
• Best for short rectal stump

o (Safest) To fashion a formal mucus fistula (difficult for the patient)

• Best for lo-ng rectal stump

Post-operative
o Insert rectal tube (Malecot drain} transanally for decompression for
couple of days and kept in place on top of the stump

o Rectal tube removed on 5 - 7 days postoperative

o If patient have peritonitis due to rectal stump leakage postoperative,

then he might need to be reoperated for washout and drainage
 SIGMOID VOLVULUS
■ Risk factors:
o High-fiber diets
o Parkinson's
o Elderly patients

■ Sigmoid > Right colon > Transverse colon

■ Manifests as acute large bowel obstruction (Constipation and obstipation)

■ Pathophysiology:
o Narrow mesenteric base and colon becomes elongated
o Without normal lateral attachments to right or left walls

■ Imaging findings:
o Abdominal x-ray: Bent inner tube sign and Omega sign
o Gastrografin enema: Bird's beak sign
o CT scan

■ Management options:
Stable Unstable

No peritonitis Peritonitis Peritonitis No peritonitis

(Perforation, Gangrene)

Rigid Proctoscopy / Sigmoidoscopy Hartmann 's procedure Resection and diversion

+ rectal tube {maintain deoompression) by colostomy

Elective open sigmoid colectomy Resection and anastomosis Resection & anastomosis
{due to 50% - 70% recurrence) (Option for non-perforated :!: Loop ileostomy
sigmoid}
Co/opexy I Cecopexy atone or
Cecostomy I Sigmoidstomy tube
carries 25% recurrence risk

■ Decompression is contraindication if gangrenous or strangulation is suspected

o Symptoms and signs of sepsis
o Severe abdominal pain
o Tachycardia
o Tenderness, rebound tenderness, and guarding
o Presence of necrotic mucosa, ulceration or dark blood on endoscopy

■ If resection and anastomosis planned

o Proximal margin: bases on level of ischemia
o Distal margin: at rectosigmoid junction

■ Patient must screen postoperative with elective colonoscopy to rule out neoplastic lesions

■ Total colectomy is an option if synchronous tumor found

 CECAL VOLVULUS
■ Associated with history of previous operations, distal colonic obstruction and mobile cecum
■ Mostly as congenital cause, Manifests as small bowel obstruction
■ Types:
o Axial ileocolic volvulus 70 - 90%
o Cecal bascule "Fold upon itself' 10 - 30%

■ Imaging findings:
o Bird beak and whirl signs on CT scan, and axial torsion sign on KUB
o Dilated cecum in the left upper quadrant

■ Management:

Stable Unstable

Gangrenous Non Gangrenous Peritonitis No Peritonitis

(Leukocytosis, acidosis,
i
fever, peritonit s)

Right hemicolectomy Resection Cecopexy

with primary anastomosis anastomosis ·suturing cecum to
Right hemicolectomy abdominal wall"
+ Loop ileostomy + ileostomy
lleocolic resection with
+ Mucus fistula Cecostomv tube
colopexy
"Suturing right colon to
posterior peritoneum"

Current! most common to use Traditional!

For diagnostic purpose and some therapeutic
auent comfort dia nostic value and ease of
Length: 35 cm (Short-Standard = Fiberoptic)
60 - 80 cm for Ion flexible si moidosco
Indications:
Examination of entire sigmoid
Screening of colorectal cancer
Biopsy
Currently used for some procedures:
o Decompression of sigmoid volvulus
o Endoluminal stenting
o Balloon dilation
Position: Left lateral
Caution: Should be done with minimal insufflation to
For therapeutic purpose and some diagnostic
Length: 30 cm
Indications:
Accurate measurement of mass from anal
verge
Decompression of sigmoid volvulus
Banding of hemorrtioids
During anterior resection of rectum to
gauge lower resection margin

No endoscopy in acute settings

Use of CO2 rather than air insufflation is preferable to decrease risk of proximal colon over-distension
 MANAGEMENT OF LOWER GI BLEEDING

Resuscitation ± PRBCs transfusion I

Nasogastri� tybe I
Negative Positive
Bile to r/o post-pyloric bleeding (Bleeding, or can't rule out /
Clear lavaoe unavailable NGT)
c:, Saline irrigation
c:, Upper GI endoscopy

I Hemod'if)amica/lv_ Stable :
♦
Hemodv_namicallv_ Unstable
Despites fluid resuscitation
> 6 units PRBCs 124h

Proctoscopy
(R/O anorectal diseases}
♦
Angiography
"Most specific test followed
by colonoscopy"
Not visualized Visualized Visualized
(or intermittent} (from above) (anorectal)

! ProctoscoE?iC control
Not successful or
Negative findings

I !
{Hemoclips, cautery

I
Elective Colonoscopy or epinephrine- injection)
Exploration
I
I I
Mila_ • f:t:1.Qd§.al.tll
Moderate - Severe
"> 4 units PRBCs•
,.
I Severe life-threatening
I
I
Urgent Colonoscopy ± CTA Angiography
With bowel preparation For bleeding > 0.5 - 1 ml/min
Moderate - Severe: 6 - 12 h r-+ "Most specific test"
Milg M2Q!:[s!I�: 24 h No colonoscopy in massive bleeding
Minimal: 1 week
I
I I
I
Positive Negative

I
Control by epinephrine, endo-clip, c:, UGIE (if not done)
band ligation or cautery
Positive
Not visualized
Not controlled
I Visualized

-(
"Tagged RBCs scan"
� Angiography or Failure

*
Meckel scan (T99 scan)
- Technetium sulfur colloid scan

I I
- For bleeding .: 0.1 ml/min Negative
"Most sensitive test" c:, Exploration Exploration Embolization
- For intermittent bleeding
(Can be seen for 24 hours) Vasopressin infusion
LGIB
- Not controlled by angiography I endoscopy
- Not visualized by Tagged RBCs or Urgent colonoscopy

Subtotal colectomy with

Exploration �
Non-Localized end ileostomy
Examination from DJ junction - rectum
-
c:, Rule out masses / lesions - Localized
(Pre-op or intra-op) r+
Segmental resection
(5 - 10% re-bleeding)

■ i
LGIB controlled post-ang ography:
o Colonoscopy is a must, to rule out necoplastic lesions (5 - 30%)
o Colonic resection is no mandatory, due to < 20% will develop mucosal ischemia

■ CT angiography
o Detects bleeding at rate 0.3 mUmin
o Have rule in acute massive LGIB in stable patients
• Because bleeding can be too copious for colonoscopy to be visualized
o Can be used evaulation the small bowel
• Capsule endoscopy (CE) and double-balloon endoscopy (DBE) are preferred

■ Stool guaiac test "FOBT"

o Used to detect occult blood loss
o Can stay positive up to 3 weeks after bleed
o "FIT" is more specific than "FOBT"
• Used to detect the False-positive guaiac "FOBT'
• False-positive: due to beef, vitamin C, iron, cimetidine
SURGERY FOR LOWER GI BLEEDING
■ Before incision:
o Resuscitation and correction of coagulopathy
o Nasogastric tube
o Rigid sigmoidoscopy

■ Steps of the operation:

o Lithotomy or supine position with split-leg posttion
o Incision and explore the abdomen
o Identify the source of bleeding:
• lntraoperative Colonoscopy
• Through enterotomy in the proximal jejunum {Should be sterilized)
• Through the mouth:
o Small bowel manually reduced over the scope with transillumination

• Bimanual palpation and tran sillumination proximal to ileocecal valve

• To exclude Meckel's diverticulum or palpable mass

• Serial clamping

o Mobilize ascending colon and hepatic flexure, ligate ileocolic pedicle and divide ileum
• Avoid duodenal injury
• Avoid excessive traction on the hepatic flexure -+ Avulsion of middle colic vein
o Preserve or divide the omentum from transverse colon (divide gastroepiploic if resected)
o Mobilize sigmoid, descending colon, and splenic flexure {Avoid splenic injury)
o Ligate the inferior mesenteric and middle colic vascular pedicles {Avoid ureteric injury)
o Mobilize and ligate upper mesorectum, and divide across upper rectum
• Avoid hypogastric nerve injury

o Construction:
• With ileorectal anastomosis:
• For stable low-risk patient

• Without anastomosis (Stoma):

• Massive hemorrhage with instability despite resuscitation and blood
transfusions
• Malnutrition or major co morbidity
• Inflammatory disease of the terminal ileum or rectum
• Poor anal sphincter function and fecal incontinence

Better for patient with high-risk for re-bleeding for post-operative localization

■ Alternatives to subtotal colectomy (unknown source} or segmental resection {known source}

o Blind segmental resection (Should not be performed)
o Blind right hemicolectomy (may be used if suggested right-sided bleeding)
• Associated with lowest mortality but associated with rebleeding

■ Post-operatively:
o Total parenteral nutrition for patients required subtotal colectomy
o Prophylaxis for deep venous thrombosis
o Bulking agents + antidiarrheal medications
ANGIODYSPLASIA BLEEDING "Arteriovenous malformation" {Venous bleeding}
■ More common on the right side

■ Most common site: Cecum

■ Due to dilatation of blood vessels in submucosa

■ Associated with 80% recurrence

■ Associated with:
o Aortic stenosis (Post aortic valve surgery)
o Renal failure
o Von Willebrand's disease
o Heart failure

■ Investigations:
o Colonoscopy
o Angiography: Dilated slow emptying veins

■ Management·
o Conservative: for incidentally discovered lesions

o Endoscopic management
• Argon plasma coagulation followed by endoclips (Standard of care)
• Intra-arterial vasopressin
• Selective gel foam
• Sclerosing agents

o Pharmacological management (No proven effective medical therapy)

• Thalidomide
• Octreotide
• Estrogen I Progesterone

o Segmental resection (Right hemicol,ectomy): for failure of treatment or recurrence

DIVERTICULAR DISEASES
■ US and European has more prevalence of diverticulosis at sigmoid colon
■ Asian patients > 70% associated with right colon diverticulosis
■ Diverticular disease: symptomatic diverticula
o Symptomatic diverticulosis
o Diverticulitis

DIVERTICULAR SLEDDING (false diverticulum, Arterial)

■ False diverticulum (Mucosa and submucosa ± serosa, Lacking muscularis layer)
o True diverticulum is rare, congenital, and more at right colon

■ Most common cause of lower GI bleeding is diverticulosis

o Melena can happen with slowly bleeding from right side colon

■ Most common site: Left (sigmoid)

o Law of Laplace: Pressure =Tension/ Radius
o Sigmoid colon has small diameter -+ highest pressure

■ Most common symptom of left-side diverticula: Diverticulitis

■ Most common symptom of right-side diverticula: Bleeding (15% risk of bleeding)

■ Risk factors for diverticulosis:

o Hypertension
o Atherosclerosis
o Smoking and alcohol consumption
o Regular use of NSAIDs, or antiplatelet medications
o Low-fiber diet

■ Pathophvsiology:
o Due to segmentation -+ increased intraluminal pressure -+ mucosal herniation
o Herniation through weak points of mucosa at sites of vasa recti penetrate the bowel wall
o Over time vessel draped over the dome of diverticulum separated only by mucosa
-+ Ruptures and bleeds
■ Management:
o Usually self-limited (70 - 80% stopped spontaneously}
o The risk of re-bleeding after non-operative management is 25¾
o No rule for elective surgery

o Indications for urgent surgery·

• Ongoing hemodynamic instability
• > 4 - 6 units of blood transfusion within 24 hours
• Continue bleeding after 72 hours
• Re-bleeding after 1 week of initial episode
DIVERTICULITIS
■ The mean time for diverticulitis to develop in diverticular disease patient is 7 years

■ Erosion of diverticular wall from increased intraluminal pressure

-+ inflammation and focal necrosis -+ perforation
■ Clinical presentation:
o Abdominal pain (mostly on left side), tenderness, and fever± vomiting
o Seeds, corn, and nuts were previously avoided
• Recently no studies shows any increased risk to develop diverticulitis

■ Investigations:
o CBC (Leukocytosis), Urinalysis
o CT scan have high sensitivity and specificity
o Interval colonoscopy (avoid in acute setting} 6 - 8 weeks after subside inflammation
• To confirms diagnosis and excludes malignancy 3 - 5%
(usually in complicated diverticulitis)

o CT colonography used after subside of acute event and can replace colonoscopy in
high-risk patient, with equivalent resu It to colonoscopy in identify synchronous lesions

o Barium enema (avoid in acute setting}

■ Classifications:

Hinchey classification Modified Hinchey classification

Stage I Pericolic abscess or phlegmon StaaeO Mild clinical diverticulitis
Staae la Confined oericolic inflammation. ohl=mon
Staae lb Confined oericolic abscess
Staae II Retro=ritoneal or oelvic abscess
Staae Ill Purulent oeritonitis (Morta/itv rate 6%/
Staae IV Fecal oeritonitis {Mortalitv rate 35%1

■ Complicated diverticulitis:
o Abscess
• Most common complication
• Most common surgical indication

o Fistula 12 - 20%
• Colovesical fistula 65%
• Colovaginal fistula 25%
• Coloenteric fistula
• Colouterine fistula

o Obstruction

o Perforation
 MANAGEMENT OF DIVERTICULITIS

Uncomplicated Complicated

I
I
Bowel rest I
Oral Antibiotics Perforation Abscess
Interval colonoscopy Obstruction

I Fistula I
Successful of medical therapy 75 - 90%

I I
Follow as outpatient with:
Clear liquid high fiber diet
Oral antibiotics:
-
<2-4cm
11 >2-4cm

Ciprofloxacin + Metronidazole
for 7 -10 days Surgery
I
Some studies shows improvement when used
anti-inflammatory agents: (mesalamine)
IV antibiotics
I
Relative indications for hospitalization:
. lmmunocompromised CT-guided PCD
. Renal or heart disease (keep drain 7 - 10 days)
Followed by elective resection
Recurrence rate: up to 40%

Colonoscopy should be done for all complicated diverticulitis before surgical resection
 ■ Surgical options:

Indications Disadvantaaes
Resection and primary anastomosis Operation of choice in elective settings, Associated with higher
± Colonic lavage ± Diversion and nowadays for acute phase as well morbidity compared to
diversion
Morbidity: 30%
Mortal;,.,: 4%
Hartmann's procedure Historically used in acute phase Associated with high
(Sigmoid resection, end colostomy, complications rate
closure of distal stump) Morbidity: 50%
Followed by reversal in 3 - 6 months Mortality: 17% 30- 45% end with
oem1anent colostomy
Laparoscopic peritoneal lavage Hinchey Ill Guidelines doesn't support
Hinchey II if PC.D unhelpful this approach and used only
as bridge for definitive
suraerv

■ Surgical considerations:
o Indications for surgical resection:
• 1 episode of complicated diverticulitis
• Hinchey 1 - 2: 6 - 8 weeks after recovery
• Hinchey 3 - 4 : during same admission

• Uncomplicated diverticulitis "during same admission"

• 2: 2 episodes (Historically)
• 2: 4 episodes (In some guidelines only}
• > 50 years
• lmmunocompromised patients
o Diabetic patients
o Chronic renal failure
o Collagen vascular disease
o Transplant patients on chronic steroids

• Can't rule out malignancy

o Most important predictor for recurrence is:

• Incomplete resection of sigmoid colon (Colosigmoid anastomosis)

o Proximal margin:
• Normal colon (No thick inflamed colon, No hypertrophy of muscularis propria)
• No need to resect all the diffuse diverticulums if presented
• Resection should include entire sigmoid colon (in left-side diverticulitis)

o Distal margin·
• Proximal rectum (where the taenia splay out)
■ Management of Colovesical fistula:
o Most common cause of colovesical fistula is Diverticulitis
o 2nd most common cause of colovesical fistula is malignancy

o Presentation:
• Recurrent UTI
• Pneumouria
• Fecaluria
More common in males

o Investigations:
• CT Cystogram (diagnostic test)
• Findings: Air within the bladder (with no instrumentation or catheter)

• Cystoscopy: to rule out malignant fistula (bladder involvement)

• CT scan (with rectal enema only) used as diagnostic test for colovaginal fistula

o Management:
• Up to 50% of colovesical fistulas will close spontaneously
• Initially intravenous antibiotics and colonoscopy
• Benign fistula:
• Single stage elective resection: Sigmoidectomy with primary anastomosis
• Hartmann's procedure for associated pelvic sepsis or high-risk patients
• Resection of the fistula tract
• No closure of bladder defect unless large defect

• Malignant fistula:
• En bloc resection of colon and bladder wall with primary repair

• Postoperative:
• Foley's catheter for bladder drainage for 7 - 10 days
• Cystogram to verify fistula closure

■ Management of Colovaginal fistula:

o May presents with passing gas or sto-OI through the vagina

o Anorectal examination should be don-e to rule out anovaginal fistula

o Management:
• Single stage sigmoidectomy
• No closure of vaginal defect unless large defect
• Closure of fistula tract
• Placing well-vascularized tissue (omentum} interposition
± Loop ileostomy in patient with malnutrition
COLONIC STRICTURES
■ Most common locations: Sigmoid colon, Transverse colon (proximal to splenic flexure)
■ 7% harbor an occult adenocarcinoma
■ Worsening constipation associated with development of colonic stricture

■ Malignant stricture features:

o Proximal to splenic flexure
o Associated with large bowel obstruction
o Abrupt self-like borders (Tapered border is a benign feature)
o Obliterated mucosa! folds

■ Etiology:
o Diverticulitis, IBD, anastomotic stricture, radiation
o lschemic colitis
o Colorectal cancer

■ Management:
o RESECTION AND ANASTOMOSIS is definitive treatment for symptomatic stricture as:
• Obstructive symptoms
• Unable to rule out malignancy
• Unable to survey colon proximal to stricture

o Stricture associated with IBD:

• Any strictures associated with UC is malignant until prove otherwise
• Biopsy should be taken to exclude malignant (difficult due to fibrotic nature)
• 10 random biopsies should be taken
• Proctocolectomy indicated in stricture in UC
• Segmental resection indicated in colonic stricture in CD
• Stricturoplasty is alternative way for short stricture with 7% risk of
malignancy
• Contraindications for stricturoplasty:
o Perforation
o Multiple strictures in short segment
o Hypoalbuminemi ,a

o Stricture associated with ischemic colitis:

• Repeated colonoscopy to exclude malignancy
• Endoscopic dilation used for symptomatic stricture
• Resection and anastomosis (Definitive treatment)
• Used in young patients with minimal comorbidities, or if cannot exclude
malignancy

o Stricture associated with Diverticulitis / Anastomotic stricture:

• Colonic stenting is used as bridge preoperative to allow inflammation to resolve
• Should be used in caution in multiple, > 10 cm, or extraluminal obstruction
• Endoscopic dilation used for symptomatic anastomotic.stricture
• Resection and anastomosis (Definitive treatment)
• Temporary loop colostomy used in significant inflammation with difficulty for
dissection for resection and anastomosis
• Hartmann procedure is used in hemodynamically instability/ purulent peritonitis
POLYPS
■ Polyp: protuberance into lumen from overgrowth of the epithelial lining of mucosa
■ Malignant polyp: adenocarcinoma invades submucosa (T1) but not beyond
o Carcinoma in situ or high-grade dysplasia are confined to muscosa and lamina properia

■ Polyps more in Proximal colon: HNPCC, Attenuated FAP, and sessile polyps
■ Polyps more in Distal colon: FAP, and Hyperplastic polyps

Types:
Non-neoplastic
o Hyperplastic: (most common polyp overall)
• Normal epithelial cells accumulating on mucosa! surface
• Hyperplasia: enlargement of tissue by increase reproduction rate
• Most common polyp found on colonoscopy
• Most common found on rectum
• Mostly sessile polyp, No malignant potential

o Mucosal: No clinical significance

o Inflammatory pseudo-polyps
• Irregular, associated with neighboring areas of mucosal ulceration (IBD)
• Associated with dysplasia if found in clusters (biopsy indicated)

o Hamartomas
• Non-malignant mix1ure of normal tissue in disorganized mass
• Have higher risk of developing colorectal carcinoma
• Types:
Sporadic: Juvenile

Non-Sporadic: Autosomal dominant syndromes

• Juvenile polyposis syndrome or coli:
o Autosomal dominant (SMAD4)
o 2 5 juvenile hamartoma polyps
o CRC is the most common malignancy (40%)
o Extra-intestinal manifestation in 15%

• Peutz Jeghers syndrome

o Autosomal dominant (STK11)
o Multiple polyps throughout the small bowel and colon
o Mucosal hyperpigmentation
o Presented as intussusception, bleeding or obstruction
o Associated with colorectal 15%, pancreatic, genitourinary, breast,
and cervical mali,gnancies
o Colonoscopy, EGD started at 10 years then every 3 years
o Breast MRI and Cervical smear started at age of 25 years

• Cowden's syndrome
o Autosomal dominant (PTEN)
o Hamartomas arises from all 3 embryonic layers
o Follicular epithelium and Facial trichilemmomas
o Melanoma, mucosa, GIT, CRC 15%, Thyroid , Breast, Endometrium
 o Neoplastic lesions (Adenoma}
• Adenoma: tumor from glandular structures in epithelial tissue
• Associated with cellular atypia, pre-malignant lesion
• Most common neoplastic polyp found on colonoscopy

• Incidence of synchronous adenoma in colon cancer resection specimen: 30%

• Findings of polyp in sigmoidoscopy should prompt full colonoscopy

• More than 80% of CRC are known to develop from adenomas

Adenoma-Carcinoma sequence:
• 7 - 10 years to develop CRC from polyp
• Short duration (1 year} in high-risk: UC, FAP, HNPCC
• Suppressive genes: (Inactivation}
o APC "adenomatous polyposis coli gene"
(Most common, initial, predict severity}
o DCC "deleted in colon cancer"; occurs late in advanced disease
o p53

• Oncogene: (Activation): K-RAS (associated also with pancreatic CA)

• Order: APC ➔ K-RAS ➔ DCC ➔ P53

• Types of adenoma:

Tvne Incidence Risk of malianancv Histolonv

Tubular 85% Most common 5% Branching tubules embedded
in lamina orooeria
Tubulovillous 10-25% 20% Mixture of tubular and villous
oattems
Villous 10% 40% Most common malignant polyp Epithelial projections over
lamina ornneria

• Advanced adenoma /high-risk of malignancy or synchronous cancer):

• > 1 cm
• 2: 3 adenomas
• Villous lesions or severe dysplasia
• Focus of invasive malignancy
■ Lymph node metastases depends on:
o Haggitt classification for carcinoma invasion in polyp:
• Level 0: in-situ or intramucosal "No risk of lymph node metastasis"
• Level 1: invades muscularis mucosae (head)
• Level 2: invades level of the neck of polyp
• Level 3: invades any part of the stalk
• Level 4: invades submucosa below stalk at base, or in sessile polyp

o Submucosal invasion in sessile polyp:

• Sm1 (upper third)
• Sm2 (middle third)
• Sm3 (lower third) + formal colonic resection

o Tumor grade: Well, moderately or poorly differentiated

o Tumor budding: Presence or absence of remote submucosal invasion

Paris classification of GIT oolvos based on endoscopic aooearance

TuneO Suoerficial 001,=oid flat/deoressed or excavated tumours
Tune 1 Polvnnid carcinomas usuallv attached on a wide base
Tune2 Ulcerated carcinomas with sharni v demarcated and raised maroins
Tvoe 3 Ulcerated infiltratina carcinomas without definite limits
Tvne4 Non-ulcerated diffuse Iv infiltrati na carcinomas
Tvne 5 Unclassifiable advanced carcinomas

Paris type 0:
• Polypoid (Lesion protrude from mucosa into the lumen .: 2.5 mm)
• Paris type Ip: Pedunculated
• Paris type Is: Sessile
Endoscopica/ly removable (even in high-grade dysplasia)

• Non-Polypoid
• Paris type Ila: Superficially elevated (< 2.5 mm)
• Paris type llb: Flat
• Paris type lie: Depressed
• Paris type Ill: Excavated
Non-amenable for endoscopic removal

• Stricture
• 60% after 20 years of the disease
• Most common location: proximal to splenic flexure
• Presented with large bowel obstruction
• Managed by oncological resection

• Invisible
 ■ Management:

Rectal polyp Colonic polyp

o Pedunculated or sessile polyps o Pedunculated or sessile polyps

(Benign, Tis, or T1) (Benign, Tis, orT1)

o Amenable for endoscopic excision o Amenable for endoscopic excision

Within 15 cm from anal verge
- Diameter < 3 cm
- < 1/3 of rectal circumference
Mobile, non-fixed

•
Local rectal resection
- TAE (Transanal excision)
Endoscopic resection
- TEM (Transanal Endoscopic Microsurgery)

- TAMIS (Transanal Minimally Invasive Surgery)

Colorectal polyp

■ Focus of invasive carcinoma

> T1(invading muscu/aris properia)

T1 (submucosa) in selected cases:

o SM3 invasion or Haggitt level 4
Radical surgery
■ Lesion removed with margin of< 2 mm
■ Lymphovascular (N1) or perineural invasion - Segmental resection
■ Poorly differentiated - Colectomy
■ Sessile lesion -LAR
o Removed as piecemeal -APR
o Located in distal third of the rectum

■ Mucinous or signet cell components

■ Non-amenable or incomplete excision for:
o Tis or Invasive cancer
o High risk {Sessile lesion > 2 cm)

Colonoscopy should be performed for all patients to exclude synchronous polyps or cancer
 ■ Techniques for polypectomy:
o Biopsy forceps (Hot or Cold): for< 3 mm polyps

o Snare excision (Hot or Cold): for> 4 mm polyps ;;Preferred technique•

• Not preferred in sessile polyp (Risk of perforation)

o Fulguration with argon plasma coagulation

• Can be used after incomplete polypectomy by EMR or ESD

o Piecemeal excision

o Endoscopic mucosa! resection (EMR), Endoscopic submucosal dissection (ESD)

• Used for> 2 cm polyps
• EMR: injecting the submucosa I layer with saline under the lesion followed by
snare excision in one or multiple pieces
• ESD: en block excision by injecting the submucosal layer at the edges of the
lesion, then incising the edge, and performing dissection of the submucosal layer
with endoscopic knives until the entire lesion is removed

Tattoo the area with india ink at time of polypectomy for further evaluation or resection

■ Complications of polypectomy:
o Bleeding (Most common) 0.5 - 2.2%

o Post-polypectomy syndrome 0.3%

• Signs and symptoms of perforation:
• Abdominal pain and tenderness
• Fever, and leukocytosis
• Without diffuse peritonitis
• CT scan: Fat stranding and thick colonic wall without pneumoperitoneum
• Management: Bowel rest, antibiotics, and close observation

o Benign pneumoperitoneum
• Associated with no abdominal pain and no systemic signs of perforation
• Management: Bowel rest, antibiotics, and close observation

o Colonic perforation
• 0.1% in hot biopsy forceps or snare excision. 1% in EMR, and 4% in ESD
• Management: Laparotomy and closure of the perforation

■ Screening and follow-up with colonoscopy for polyps:

3-6 months < 3 years 3 years 5 -10 years

Sessile adenomas removed piecemeal > 10 polyps ;;, 3 polyps < 3 polyps

After excision of polyp > 1 cm polyp < 1 cm polyp

High-9rade dysplasia No polyps

Villous polvo
COLORECTAL CANCER
■ Risk factors:
o Age (major risk factor for sporadic CRC)
o Adenomatous polyps > 1 cm, villous or tubulovillous polyps
o C.septicum, C.bovis, family history, smoking, IBD
o Red meat, Saturated and Polyunsaturated fat (O/eic acid; olive, coconut, fish are safe)

■ Most common site: Sigmoid

o Right colon cancer is more in Asian population and > 60 year old patients

■ Mostly sporadic (6 - 8 % are hereditary disease)

■ Most important prognostic factor: Lymph nodes status {then serosal extension)
■ Most common site of metastasis: Lymph nodes
■ Most common site of distant metastasis: Liver {by portal vein), then Lungs
o lntraoperative ultrasound have highest sensitivity to detect liver metastasis

■ Rectal cancer has worse prognosis:

o Higher recurrence rate
o Metastasize to spine directly via Batson's plexus (venous)

■ Sentinel lymph node used in:

o CRC to improve staging
o Breast CA and melanoma to avoid radical lymphadenectomy

■ Approach to patient with CRC:

o History and examination (including PR and PV assessment for rectal cancers)
o CT CAP, Colonoscopy, Rigid proctoscope (rectal cancer) and biopsy
o PET scan may be used in positive lymph nodes to assess distant metastasis
o MRI pelvis for rectal cancers (For assessment of the N; Lymph nodes)
o Endo-rectal U/S (For assessment of the T; depth of invasion)

■ Endo-rectal ultrasound:
o Assessing depth of invasion (sphincter involvement), recurrence, and lymph nodes
o Can't identify internal opening of a fistula
o Showed 5 layers
• 1"' layer "White": Mucosa! surface
• 2nd layer "Black": Mucosa
• 3rd layer "White": Submucosa
• 4lh layer "Black": Musclaris propria
• 5lh layer "White": Serosa (Peri-rectal fat)

............
l ;•••ff..,• ll'fttt .. ,� I ._ to ...•••••fU JII
,�-=�••••
ft�• • ...-••u
..,l'•• ,..,._. t.ri,.roc•IHU. • lfuc•1uh
1, f••••• 1•1 t•� !•u••
 ■ Screening for patients with no risk-factors:
Everv 10 vears Everv 5 vears Everv 1 vear
Colonoscopy Flexible Sigmoidoscopy ± FOBT Fecal occult blood test (FOBT)
"Best to be combined with siamoidosconv"
Double-contrast barium enema Fecal immunochemical test /FIT\
CT ColonoQraphy

■ Colonoscopy:
o Colonoscopy is a form of secondary prevention not a primary
o Should be done until age of 75 years

Startina at aqe Condition Repeat everv

50 =ars No risk factors or averaae risk factors 13"' deareel 10 vears
40 years 1" or 2nd dearee with non-oolvns CRC aae 2: 60 vears 10 vears
10 years before youngest case 1" or 2nd dearee with oolvos or CRC at a"" S 60 vears 5 vears
20-25 years Known case of aFAP 1 -2 years
10 years before youngest case
Known case of HNPC C
Required screening at age 30 - 35 years for:
- Annual endometrial biopsy
- Trans-vaginal lJI/S
- EGO with antrum biopsy
- Urinalvsis
10- 12 years (Puberty) Known case of FAP (EGD at 20 years) 1 year until
-Age of 25 years
Known case of PJS (EGD at 10 years) - Surgery

Then everv 1 - 5 years based on SpiQelman score

8 - 12 years after symptoms Known case of UC 1 year
Immediately in:
0 PSC
0 Family history of CRC
0 Stricture or Pseudooolvn

■ Serum CEA/CA 19 - 9
o Not useful for screening
o Used for follow-up and prognosis
o Initial pre-operative CEA level is obtained for post-operative follow-up
o Worse prognosis if preoperative level > 5 ng/ml
o Should be done every 3 - 6 months postoperatively
o Should be done even if normal level pre-operatively
• Advanced recurrent non-localized tumor may secretes CEA
• Metachronous tumor may secretes CEA

o High CA 19 - 9 may reflect nodal disease in colorectal cancer

 ■ Staging for colorectal cancer:
o CT Chest, Abdomen, and Pelvis with IV and Oral contrasts

o CT head in symptomatic patients only

T Invades N Metastasis to
Tis Carcinoma in situ (lntra�pithelial) N1 1 -3 pericolic or perirectal lymph nodes
Mucosal / lamina orooeria invasion
T1 Submucosa N2 ., 4 pericolic or perirectal lymph nodes
T2 Into muscularis oro,...ria N3 Anv lvmnh node alone maier vascular trunk
T3 Through muscularis propria
Transmural involvement
Subserosa

Invading peri-rectal fat

/In non-oeritoneal covered rectum\
T4 Adjacent structures (fixed mass)

lnvadino oeritoneal surface

Peritoneum
Omentum
M1 Metastasis liver
Para-aortic lymph nodes
Peri-oortal l•=nh nodes

Staae Subtvne TNM

Staae I T1 /T2
Stage II A ll
B T4
Stage Ill A N1
T1 /T2 N2
B
T3N1
C T3N2
T4 N1 -2

Modified Duke's classification

No nodal involvement With nodal involvement
Tis/ T1 Duke's A
Duke's C1
T2 Duke's B1
T3 Duke's B2 Duke's C2
M1 Duke's D
MANAGEMENT OF COLORECTAL CANCER
■ Multidisciplinary meeting
■ Family meeting
■ Tumor Board meeting

Based on stage:

■ Stage O (Polyp with Tis}

o Endoscopically removal with free margin
o Radical resection if failure of removal

■ Stage 1 (T1-T2)
o Trans-anal excision
• For high-risk patients or refusal radical resection

o Radical resection ± neoadjuvant or adjuvant chemoradiation

■ Stage 2 (T3-T4)
o Localized colon cancer:
• Adjuvant chemotherapy for high-risk group only
• Obstructed I Perforated cancer
• T4 tumor
• Lymphovascular invasion
• Poorly differentiated tumors

• Radical resection

o Localized rectal cancer:

• Neoadjuvant chemoradiation for all patients
• Re-staging after chemotherapy course
• Radical resection
• Adjuvant chemoradiation for hi gh-risk group

■ Stage 3 (N1}
o Adjuvant chemotherapy for all colon cancer
o Re-staging after chemotherapy course
o Radical resection

■ Stage 4 (M1)
o Chemotherapy (therapeutic or palliative}
o Radiotherapy in symptomatic patients
o Re-staging after chemotherapy course
o Radical resection if resectable
1) Radical resection
o Used for isolated colorectal cancer, stable patients
o Segmental resection of local structures involved by tumor with major vascular pedicle
and lymphatic drainage (at /east 12 lymph nodes) with at least 5 cm negative proximal
and distal margins in colon cancer

o Right-side lesion:
• Right hemicolectomy :!: diverting stoma
• Right hemicolectomy with mucus fistula and ileostomy
• Used for rectal mass with suspicious proximal viability (ischemia, necrosis
or perforation)

o Hepatic flexure lesion: Extended right hemicolectomy

o Transverse colon lesion:

• Segmental resection of transverse colon
• Extended right hemicolectomy

o Splenic flexure lesion:

• Left hemicolectomy
• Associated with non-oncological resection, and resection of non-drained
lymph nodes from splenic flexure
• Extended left hemicolectomy
• Associated with difficult mobilization of transverse mesocolon and less
lymphatic dissection
• Extended right hemicolectomy
• Better for adequate lymphatic dissection and for tension-free anastomosis

• Segmental resection and anastomosis

• Associated with inadequate blood supply for resection and anastomosis
and non-oncological resection

o Left-side lesion:
• Hartmann's procedure
• Used for high-risk patient, unstable, or perforated

• Resection and anastomosis :!: diverting stoma

• Left hemicolectomy
• Sigmoidectomy
• Used as oncological resection, after exclude ischemia necrosis or
perforation of right colon and cecum
• Risk of synchronous tumor 5% and need for staging postoperative

o Associated with synchronous tumors or questionable viability of proximal colon:

(Colonic mass with suspicious proximal viability as ischemia, necrosis or perforation, or
synchronous tumor)
• Total or subtotal colectomy
 o Perforated:
• Colonic perforation usually proximal to the tumor or at the cecum
• Contained
• Intra-peritoneal: Percutaneous drainage
Extra-peritoneal: Proximal fecal diversion with drainage of sepsis
Followed by neoadjuvant chemoradiation then elective surgery

• Free
• Right hemicolectomy
• Hartmann's procedure
• Proximal diverting stoma with washout followed by elective surgery
Used to control contamination for perforated rectal mass with sepsis

o Obstructed:
• Right Colon: Right hemicolectomy and primary anastomosis
• Left Colon: Resection and primary anastomosis
• Rectal:
• Stenting (Proximal rectal cancer, Widely metastasis)
• Chemoradiation (Can relieve obstruction if partially obstructed)
• Loop transverse colostomy (Lesions that cannot be passed by scope)
• Diverting loop ileostomy (For lesions that can be passed by scope)
o Can be left in situ following the low anterior resection if needed

2) Diverting loop stoma

o Stoma can be resected later for definiltive surgery
o Stoma can be reversed after down-staging in unresectable tumor or as permanent
o Stoma marking used preoperatively maybe twice in low rectal cancer for LAR / APR
o Does not prevent leak, but decrease contamination if leak happens
o Needed in patients with high-risk of leak (Previous radiation, Comorbidities)
o Diverting transverse colostomy
• Best for obstructed colorectal cancer
• Used in unstable patient with high rectal cancer
• To make the patient benefits from chemoradiation for rectosigmoid lesions
• To be used as defunctioning stoma after LAR

o Diverting sigmoid colostomy:

• Best for obstructed distal colorectal cancer
• Indications:
• Unstable patient with low rectal cancer
• Frozen pelvis
• Unable to obtain safe margin
• Obstructed tumors with inability for 1 stage surgery (as metastasis)

• Advantages:
• Used to assess proximal colon by colonoscopy
• To be used later for APR after chemotherapy
• To be used as permanent colostomy in unresectable cancer

o Diverting ileostomy: 2nd option, used with risk of dehydration

• May divert the fecal stream in patients with incompetent ileocecal valve
• Barium study may be used to evaluate distal bowel
 3) Hartmann's procedure
o Used for high-risk patient, unstable, or perforated
o Oncological resection

4) Colonic stent
o Used for left-colonic intermittent, partial obstruction
o Not used for rectal cancer (High risk of migration, and tenesmus}
• Can be used for proximal rectal lesion if the bottom of stent above anorectal ring

o If perforated colon cancer during stenting, may lead to advance the stage of tumor
o Chemoradiation in presence of stent associated withf risk of perforation

■ Rectal cancer
o Classified based on the location:
• Upper rectum: 12 - 16 cm from anal verge up to teania flare
• Middle rectum: 8 - 12 cm from anal verge
• Lower rectum: Anorectal ring and 4 - 8 cm from anal verge

o Low anterior resection (LAR)

• Used for upper and middle rectal cancer
• To allow for 2 cm distal margin
• Distal extend of the tumor should be > 6 cm from anal verge
• Distal extend of the tumor should be > 2 cm from levator ani muscle

• Sigmoidectomy: Removal of sigmoid and part of upper rectum

• Anterior resection:
• Removal of sigmoid and upper rectum down to peritoneal reflection

o Abdominoperineal resection (APR)

• Used for middle and lower rectal cancer
• Inability to achieve negative distal margin in LAR
• Local recurrent or advanced rectal cancer
• Invasion into the anal sphincter or levator muscles
• Ultra-low LAR is alternative for APR
• 2 stoma marking done pre-operatively before assessment
• Right side: for diversion if LAR done
• Left side: if APR is a must

Lower rectal cancer

June Description I Manaaement
I I Suora-anal tumors /> 1 cm from anal rinaj I Coloanal anastomosis
II Juxta-anal tumors (< 1 c from anal ring_)_ Partial intersohincteric resection
Ill I Intra-anal tumors (Invasion of internal anal sphincter) I Total intersphincteric resection
IV Trans-anal tumors /Invasion of external anal sohincterY IAPR
 ■ Indications of adjuncts therapy:

Chemotheranv Radiotheranv
Neoadjuvant: No role in isolated colon cancer due to
- Unresectable Stage IV (as down staging) frequent complications:
- Radiation enteritis
Adjuvant: - Renal injury
- Stage II "High-risk group"
Colon 0 Obstructed / Perforated cancer
0 T4 tumor
0 Lymphovascular invasion
0 Poorly differentiated tumors

- Stage Ill (N 1 )
Neoadjuvant: Neoadjuvant:
- Stage II (T3/T4) - Stage II (T3/T4)
- N1 - N1

Adjuvant: Adjuvant:
Rectum - Stage II (T3/T4) "High-risk groups" - Positive resection margins
0 Poorly differentiated - Perforation or abscess formation
0 Lymphovascular invasion
0 Perineural invasion

- N1

■ Chemotherapy:
o FOLFOX (folinic acid+ fluorouracil + oxaliplatin}
o lnfusional 5-FU/LV or Capecitabine for 6 months
• Used for patients with comorbi•dities, Peripheral neuropathy, > 70 years

o Working as radiosensitizer for rectal cancers

o Decreases the recurrence by 40%

o Neoadjuvant therapy for rectal cancer:

• Induction chemotherapy {Chemotherapy -+CRT-+ TME)

• Consolidation chemotherapy (CRT-+Chemotherapy -+ TME)

• Well tolerated and increase the pathologic response rate

o Adjuvant therapy:
• Colon
• 4 - 6 months FOLFOX

• Rectal
• Chemo "2 months" -+CRT ''6 weeks" -+Chemo "2 months"
• Chemo "4 months" -+CRT "6 weeks"

No adjuvant chemotherapy if complete pathological response after neoadjuvant therapy

■ Radiotherapy:
o Used along with IV 5-FU based or oral capecitabine chemotherapy as chemoradiation

o Used if rectum is involved, as:

• Neoadjuvant therapy (Preferred)
• Adjuvant therapy for high-risk pathology

o t Local recurrence with no effect on survival

• t Survival rate in rectal cancer in old studies
o Courses:
• Short Course:
• 5 Gy/day for 5 days followed by surgery within 1 week
Associated with higher toxicity rate

• Long Course: (Preferable)

• 2 Gy/day for 5 - 6 weeks followed by surgery after 3 - 6 weeks
Longer duration (> 10 weeks) may be used to subside the inflammation

o complications·
• Neoadjuvant chemoradiation associated with increased risk of leak

• Acute radiation enteritis

• Risk factors:
o Limited splanchnic perfusion (Hypertension, OM, heart disease)
o Concomitant che motherapy (Radiation sensitizers)

• Presentat;on·
o Nausea, Anorexia, Diarrhea, and abdominal pain
o Hypokalemia caused also from the effect of chemotherapy, or by
villous adenoma in the colon

• Treatment:
o Supportive

• Chronic radiation enteritis

• Progressive occlusive v.asculitis, leads to chronic ischemia and fibrosis
• Usually after 6 months from radiation effect
• Indications for surgery· (Resection and anastomosis)
o Obstruction, perforation, hemorrhage or fistula
FOLLOW-UP OF COLORECTAL CANCER
Clinical evaluation Every 3 months for 2 years, then
CEA level Every 6 months for 3 years, then
Annual
CT CAP Annual for 5 years
Colonoscopy "1 - 3 - 5" RULE
After 6 months post-operative if not done pre-operative completely
After 12 months post-operative if done preoperative
Then 3'• year
Then 5'" year

- If Positive findings: Management + Annual

- If Neaative findinas: Everv 4 - 5 vears
Proctoscnnv Everv 6 months for 3 - 5 vears /After resection of rectal cancer)

■ Synchronous tumor: 6 - 8%
o 2 or more primary tumors separated by normal bowel and not due direct extension
o Colonoscopy should be done for entire colon to exclude synchronous tumors

■ Metachronous tumor: 1 - 3% in first 5 years

o Non-anastomotic new tumors developing at least 6 months after the initial diagnosis
FAMILIAL ADENOMATOUS POLYPOSIS (FAP)
■ FAP is > 100 synchronous adenomas or < 1-00 with a positive family history
■ Risk of malignancy is 100% by age of 40 years
■ Colon cancer is the 1 '1 most common cause of death in FAP
■ Autosomal dominant
o APC gene mutation (70% of the case·s) on Chromosome 5 {5q21)

■ Clinical presentation:
o Bleeding, diarrhea, abdominal pain, and mucous discharge
o Colorectal polyps more in distal colon and rectum
o 25% to 30% do not have a family history

o Extra-colonic disease:
• Gastric hyperplastic polyps at fundus in 80% - 90% (low malignant potential)

• Gastric adenomas at antrum

• Duodenal per-ampullary tumors

• 2nd most common cause of death in FAP
• 95% of patients, developed 16 years post colonic polyps
• 5% to 10% developing duodenal cancer
• Management:
o Excised for biopsy and follow up in 6 months, then yearly
• For Small tubular adenomas or low-grade dysplasia

NSA/Ds as chemoprevention can help in polyp regression

o Whipple procedure
• For cancer-proven polyp

o Pancreas-preserving duodenectomy
• Indications:
• High-risk adenomas (villous, >1 cm)
• High-grade dysplasia
• Spigelman classification� Stage IV (9 - 12 points)

Soi elman classification

1 ooint 2 nnints 3 nnints
Number of polvo 1-4 5-20 > 20
Size of oofvn 1-4mm 0.5-1 cm > 1 cm
Histolonv Tubulous Tubulovillous Villous
Dvsolasia Mild Moderate Severe
 o Extra-intestinal disease:
• Osteomas 80% "Most common extra-intestinal finding"
• Found at mandible, skull and tibia
• CHRPE (Congenital hypertrophy of the retinal pigment epithelium) 75%
• 2: 4 patchy area discoloration at fundoscopy (pathognomonic)
• Epidermoid cyst 50%
• Papillary thyroid cancer
• Dermoid cysts

o Desmoid Tumors: 30%

• Developed 2 to 3 years after surgery
• 3nl most common cause of death in FAP
• 10% grow, 10% resolve, 30% grow and regress, 50% stable
• Management:
• Extra-abdominal
o Early excision with 1 cm margin
o Recurrence rate 20% - 50%

• Intra-abdominal
o Tamoxifen, NSAIDs, Estrogen antagonists, and Chemotherapy
o Radiotherapy as palliative measures
o Diversion or bypass in case of obstruction or ischemia

■ Gardner's syndrome: i
o FAP + Extra-intest nal manifestations
• Epidermoid cyst, Desmoid tumors, Hemartomas, Osteomas

■ Turcot's syndrome:
o FAP + Brain tumors

■ Attenuated Familial Adenomatous Polyposis

o APC mutation in 30% only
o < 100 polyps, and more at proximal colon
o Presented at later age (30 - 40 )
o No extra-colonic or intestinal manifestation (Gastric adenomas, Desmoids, and CHRP)
o Risk of CRC 100% at 60 years if not treated

■ Screening of FAP:
o Colonoscopy screening started at 10 - 12 years, followed by annual colonoscopy

o Colonoscopy screening started at 20 years for aFAP, followed by annual colonoscopy

o Upper endoscopy at 20 years then every 1 - 5 years based on Spigelman score

 ■ Management:
o Chemoprevention with NSAIDs (Not an alternative to prophylactic surgery)
• Indications:
• lleal pouch anal anastomosis polyps
• High family risk of desmoid tumors
• Delayed surgery or inability to tolerate polypectomy or proctectomy

o Surgery
• Indications:
• Once polyps detected
• Before age of 20 years

Total abdominal colectomy Total proctocolectomy with lleal Total proctocolectomy with
with ileorectal anastomosis pouch-anal anastomosis end (Brooke) ileostomy
(TAC with IRA) (IPAA)
Most common, safest procedure
"Continence-oreservina•
Indications - Young patients - Young patients - Old patient

- Intact sphincter mechanism - Intact sphincter mechanism - Poor sphincter function

-< 3 an rectal polyps -> 3 cm rectal polyps - Patient preference

-Alternative procedure for UC - Curative for UC - Inability to create 1PM

-HNPCC
- aFAP
- FAP with mild polyposis:
< 20 rectal polyps
< 1000 colonic adenoma
-Severe polyposis
> 20 rectal polyps
> 1000 colonic adenoma
- Severe rectal disease
- Colorectal dysplasia or cancer
(inadequate mesenteric
length)
- low rectal cancer requiring
APR
- Rectal cancer requiring
postoperative radiation

- No colorectal dvsolasialcancer No rectal mucosa left behind

Advantage No permanent stoma lowest morbidity
"Restorative J, S, W, H pouch"
Disadvantage Retained 15 an of rectum Complex surgery with risk of Permanent stoma
(40% cancer within 30 years) damage pelvic nerves Valve slippage

Requires Rectal surveillance Highest morbidity

/6 -12 months\

• Anal mucosectomy and hand-sewn IPAA

• Alternative to double-stapled IPAA
• Used for high-risk patients of retained rectal cuff in UC or FAP
• For adenoma of anal transitional zone or dysplasia at lower rectum

• Total proctocolectomy with continent (Kock) ileostomy:

• Alternative to end ileostomy in non-candidate patients for IPAA
• Contraindications
o Crohn's disease, Obesity, Marginal small bowel length
o Inability to perform daily stomal intubation
LYNCH SYNDROMES "HNPCC" (Hereditary nonpolyposis colon cancer)
■ Most common inherited large bowel cancer syndrome
■ Autosomal dominant, DNA mismatch repair gene and microsatellite instability
o MSH2 (hMSH2)
o MLH1

■ Associated with same prognosis to sporadic CRC

■ Associated with Early age of cancer (Age of 45 years)
■ All newly diagnosed CRC < 50 year should be evaluated for mismatch repair deficiency
■ More in proximal colon (Right-side}
■ Associated with Genitourinary and Extra-colonic malignancy:
o t Risk of ovarian, endometrial, bladder, pancreas, small bowel and stomach cancer
o Most common extraintestinal malignancy: Endometrial cancer

■ Pathological features:
o High risk of synchronous and metasynchronous tumors 40% (multiple)
o Mucinous, poorly differentiated, and 'signet-ring' appearance

■ Amsterdam Criteria II: 3/2/1 < 50

o 3 relatives with Lynch-syndrome associated CA (endometrial, CRC, small bowel, ureter)
o 2 generations affected
o 1 of first degree and < 50 year old

Amsterdam criteria used to assess the risk for HNPCC based on family history
Tumors should be verified by pathological examination (Exclude FAP)

■ Types:
o Lynch I: Familial colorectal cancer
o Lynch II: Associated with extra-colonic cancers
o familial coforectaf cancer ty_pe x-
• Meet Amsterdam criteria but� No DNA mismatch (No microsatellite instability}
• Doesn't appear to increased risk of Lynch-associated cancers

■ Screening:
o Annual colonoscopy started at age 25 or 10 years before youngest case
o Annual endometrial biopsy, transvagirnal U/S, EGD with antrum biopsy, and urinalysis
• Started at age 30 - 35 years

■ Surgery:
Total proctocolectomy with i/eorectal anastomosis (risk of metachronous tumors)

o Indicated in all HNPCC with endoscopically unresectable lesion

o Segmental resection preserved for elderly or young if accepted high surveillance with
close follow-up

■ Chemoprevention
o Aspirin: decrease risk of CRC and extra-colonic cancer in lynch syndrome
o Oral contraceptive
o Resistant starch

COX-2 inhibitors and anti-inflammatory shown to decrease adenoma size and number
in large bowel
PSEUDOMEMBRANOUS COLITIS
■ Clostridium diffcile is a gram-positive, spore-forming anaerobic bacillus
■ Transmission route: Fecal-oral route

■ Mechanism: Colonization, change in intestinal microflora, and altered immunity

o PMN inflammation of mucosa and submucosal

■ Risk factors:
o Elderly, ICU patients, IBD, history of PP!, NGT, immunosuppressive
o Bowel preparation and chemotherapy
o Antibiotics used in last 3 months
• Fuoroquinolones and Cephalosporins
(C/indamycin, Ceftriaxone, Ciprofloxacin, Amoxicillin)

■ Presentation:
o Most common in: Distal colon

o Mild- Severe:
• Diarrhea, fever, nausea, abdominal pain, leukocytosis, distention

o Fulminant COi:
• Severe colitis, septicemia, need for vasopressors / ventilator
• Mortality rate of fulminant COi: 30 - 90 %

■ Investigation:
o CBC, Lactate level, Albumin level

o Stool studies:
1} ELISA ''Highly specific"
"Immunoassay" for CDF Toxins A "Endotoxic", B "Cytotoxic" and GOH antigen
• GOH antigen: Most sensitive
• Can be used as initial test for 2-stage approach
• Because positivity can't distinguish toxigenic from non-toxigenic

• Both toxins + GOH antigen Positive: CDF confirmed

• Both toxins + GOH antigen Ne ,gative: CDF excluded
• One of the toxins or one of the tests only positive: Next step

2} PCR (emerging as test of choice) "Highly sensitive"

• PCR used for Cytolethal distending toxin CDT

3} Most specific· Cytotoxin assay stool culture over 24 hours "Gold-standard"

o CT Abdomen:
• Localized or diffuse colonic thickening and ascites
• Accordion sign: intraluminal contrast or air outlined by thickened mucosa

o Colonoscopy:
• Findings: Pseudomembranes, white plaques, and ring lesions
• Right colon involved in 30% of CDF patients
• To insert tube in transverse colon for vancomycin enema needed
■ Management of CDF:
o Resuscitation with Ringer Lactate (No Normal saline which can increases the acidosis)
o Infection control (Private room, gloves, hand-wash with chlorhexidine not alcohol)
o Avoid bowel preps, narcotics and anti-diarrhea (can causes toxic megacolon)
o Avoid Broad-spectrum long course antibiotics
o Minimize GI intubation

o Medical treatment
• Duration: 10 - 14 days

• Oral Metronidazole
• 1 °1 line treatment for CDF
• For mild to moderate disease

• IV Metronidazole
• For patient not feasible for enteral administration (ileus)

• Oral Vancomycin
• Recurrence (2 nd episode of recurrence)
• For moderate to severe disease
o Pulse> 120 and systolic blood pressure< 100
o WBC> 15000
o Renal failure (Creatinine> 1.5 x baseline)
o Lactate> 2, Albumin< 2

• Non-responding to metronidazole
• For CDF in IBD (as 1st line treatment)
• For pregnant or breast feeding patient

IV vancomycin does not result in adequate intraluminal levels

Vancomycin enemas or irrigations through a colonic tube (inserted

proximal to transverse colon during colonoscopy) used for patient who
indicated to use vancomycin and not feasible for enteral administration

• IV Tigecycline
• Used for patients who need broad-spectrum antibiotics and active against
C. diffcile.

• Fdaxomicin
• New macrocyclic antibiotic with narrow therapeutic spectrum associated
with decreased recurrence
• Fecal microbiota transplant indicated for:
• 2: 3 episodes of unresponsive COi to standard treatment
• COi not responding to therapy after 1 week
• Recurrent nonresponsive severe COi
o Surgical management:
• Indications:
• Fulminant disease
o Severe disease PLUS one of the following:
• Hypotensi,on requiring vasopressor support
• Ventilator -dependence
• WBC :2: 50,000 cells/µL
• Lactate > 5 mmol/L

• Complicated:
o Toxic megacolon failed to resolved medically> 72 hours
• (Cecum> 12 cm or colon> 6 cm)
• Severe bloody diarrhea
• Abdominal pain and distention ±tenderness±peritonitis
• Toxic (Tachycardia, fever, postural hypotension)

o Colonic perforation

• Operation:
• Open total colectomy + end ileostomy

• Loop ileostomy
o Antegrade irrigation of vancomycin for 10 days
o Associated with decreased mortality and high stoma closure rates

No segmental resection I No anastomosis

CECAL DISEASES
■ Actinomyces
o Granulomatous
o Associated with yellow-white sulfur granules
o Treated by antibiotics (Penicillin} and drainage

■ Angiodysplasia

■ Lymphoma
o Most common site of large bowel lymphoma
o Most common cause of large bowel bleeding in patients with HIV

■ Tuberculosis

■ Pneumatosis intestinalis
o Antibiotics and observation only if no peritonitis

■ Typhlitis (Neutropenic necrotizing enterocol'itis) "life-threatening"

o Risk factors·
• HIV, Leukemia, aplastic anemia
• Candida, Pseudomonas

o Presentation:
• RLQ abdominal pain
• Fever
• Diarrhea
• Vomiting

o er findings·
• Bowel wall thickening and edema of the cecum
• Mesenteric stranding, bowel di latation, mucosal enhancement
• Pneumatosis intestinalis

o Management:
• IV fluids, antibiotics, NGT and bowel rest only
• Blood culture and CDF culture
• Avoid ileus (Avoid narcotics, anti-cholinergic, anti-diarrhea}
• Granulocyte colony-stimulating factor (G-CSF) to accelerate leukocyte count
• Indication for surgical intervention:
• Perforation
• Persistent lower GI bleeding
Colonic inertia and Chronic constipation
■ Definition of colonic inertia:
o Chronically constipated patient with markedly prolonged colonic transit time in the
absence of anorectal dysfunction
o Retention of ;, 20% of the markers in the colon on 5th day after ingestion
o Total transit time > 72 hours

■ Normal transjt time: 31 hours in men, and 39 hours in women

■ Definition of functional constipation:

o Based on Rome Ill Criteria(" 2 out of 6 symptoms for;, 12 months without laxatives)
• Straining on > 25% of defecations
• Sensation of incomplete evacuation on > 25% of defecations
• Sensation of anorectal obstruction/blockage for at least 25% of defecations
• Hard-like stools on > 25% of defecations
• Manual maneuvers to facilitate at least 25% of defecations
• < 3 bowel movements per week

■ Etiology:
o Diet and behavioral lifestyle
o Endocrine and metabolic causes (Hypercalcemia, Hypothyroidism, OM)
o Colonic pathology (Stricture, Malignancy, Hirschsprung's disease)
o Anorectal Pathology (lntussusception, Rectocele, Proctitis, fissure)
o Psychiatric disorders, Paradoxical puborectalis contraction, or Drugs

■ Approach:
1) History and examination
2) Serum chemistry and thyroid function tests and exclude metabolic causes

Colonos•copy ± Barium enema

Normal Abnormal

l
Conservative Management Treat the cause
■ Dietary modifications and exercise
■ Fiber supplementation (25 g/d)
■ Increase fluid intake to 1.5 to 2 liters
■ Catharti cs and enemas
o Psyllium and lactulose
o Low-volume polyethylene glycol electrolyte solution

I I
I

I Failed
I I Improve
I
Assess transit time Continue conservative management
 Assess the transit tim,e (Sitz marker study)
■ 24 radio-opaque markers
o As single capsule and daily serial imaging starting on day 3 after ingestion
o As multiple sets of differently shaped markers for 3 consecutive days

■ Nuclear scintigraphy (Traceable radio-nucleotide)

o Patient eats dual-labeled meal (Scrambled eggs with T99 sulfur colloid
and 300 ml water with indium-111)
o Gamma camera used to follow every 30 minutes in upright position until
gastric emptying

Abnormal Normal

Defecogram (F/uoroscopy or MRI) Psychological consideration

Anal manometry and Balloon expulsion ± Biopsy

Normal Abnormal

Small bowel follow through Treat the cause

Slow transit Consider Gastric pacemaker

Normal transit Consider Total colectomy with ileorectal anastomosis

 ■ Summary:
Normal transit Slow transit
constioation constioation
Pelvic floor dysfunction
Colonic Transit Normal Delayed Normal

20% of radiologic
markers remain in
colon at 5 da=
Defecography Normal Normal lliUHiitDdiag 12ittiDitUW �llDdt2m1·
Generalized descent of the perineum below the
pubococcygeal line during defecation, with thinning of
the pelvic musculature

Obstructed defecation Sl£ndrome:

(rectocele, prolapse and intussusception)
Increased anorectal angle during defecation and
inability to expel contrast

Paradoxical euborectalis contraction:

Contraction of the puborectalis durinQ defecation
Manometry Normal Normal Varies

Abnormal if t Restino anal oressure > 90 mm Ho

OTHERS
■ Colonic perforation in HIV: due to CMV infection

■ Chilaiditi syndrome
o Transposition of transverse colon or hepatic flexure to above the liver
o Due to absence or laxity of ligament suspending transverse colon or falciforrn ligament
o Mistaken for pneumoperitoneum

■ Epiploic appendagitis
o Due to venous thrombosis -+ torsion of appendage -+ inflammation
o Management: Conservative (as infarcted omentum)
o Indication of surgery: -+ligated and resected of inflamed appendage
• Failure of conservative
• Worsening symptoms
• Complications (intussusception, bowel obstruction, abscess)

■ Stercoral ulcer and perforation

o Due to pressure and irritation resulting from severe prolonged constipation
o Perforation by internal contents (foreign objects, fecalomas)
o Most common site: Rectum
o Risk factors:
• NSAIDs usage
• Chagas disease
• Hirschprung's disease
• Toxic colitis and megacolon

o Criteria to diagnose stercoral perforation:

• Anti-mesenteric > 1 cm colonic perforation
• Colon full of stool protruding through perforation site
• Evidence of multiple pressure ulcer with acute surrounding inflammation
• Absence of external injury ( Diverticulitis or neoplasm)

o Management:
• Hartmann's procedure rather tlnan primary closure

■ Blumer's shelf
o Metastasis to pouch of Douglas (anterior to rectum - Recto-uterine pouch)
o Felt during rectal examination
o Most common source: GISTs (Stomach), lung, pancreas, and stomach
Bowel preparation
■ Mechanism:
o Decrease the fecal load of the colon and facilitate the action of non-absorbable
antibiotics

■ Mechanical bowel prep alone is not recommended for routinely colon operations
o Used for Sigmoid (left distal) colon, rectal, and right colon if stoma planned
o Used for colonoscopy for better visualization
o Don't do bowel preparation in obstructing bowel
o Improving the ability to manipulate and remove colon by removing solid material

■ Only clear liquid on day of surgery and NPO midnight

■ Mechanical:

Tvoe Dosaae Characteristic

Polyethylene glycol 20 sachets on Osmotically balanced
solution - 4l as 250 ml every 10 minutes Sulfate-free has better taste
(Movipreol - 2l + Sisacodv/ and small
Oral sodium phosphate 32 - 40 tablets: Hyperosmotic
- 20 tablets on evening preoperative Cellulose based
- 12 - 20 tablets 3 - 5 hours oreooerative
Aqueous NaP - 30 - 45 ml orally twice May cause fluid shift
- 10 - 12 hours interval with last dose 3 Not for IBD, obstruction, or
hours oreooerativelv renal failure
Senna Adjuvant as 8mg/5ml Activated by colonic bacteria
(Anthraquinone and increases colonic
derivatives) motility

Bisacodyl Adjuvant as 4 tablets of 5 mg at noon Poo�y absorbable

diphenylmethane
Stimulate colonic motilitv

■ Oral antibiotic preparation:

o No need of antibiotic preparation for colonoscopy

o For all patient with distal colonic resection: Mechanical + Oral antibiotics preparation

o Metronidazole 500mg {3 doses) with ciprofloxacin 500mg {2 doses) pre-op

■ Benefits and disadvantages:

o Studies showed no difference between prep and no prep bowel surgery for post­
operative complications including anastomotic leak and SSI

o Recent studies showed combined preparation associated with reduction in SSI,

anastomotic leak, ileus and length of !hospital stay

o Associated with risk factor for pseudomembranous colitis

OPERATIVE NOTES
Principles in Colon Surgery

■ Pre-operative:
o Assess resectability:
• Imaging-based and staging
• Multidisciplinary meeting
• Tumor Board meeting for possible neoadjuvant therapy

o Assess fitness:
• ICU and consultations if required
• Functional tests
• Correction of anemia

o Pre-operative preparation:
• Clear liquid diet for 24 hours
• Bowel preparation for left colectomy, and right if stoma was planned
• Colonoscopy for elective cases (can be done postoperative in emergency)
• Stoma marking in elective cases
• Baseline CEA
• Type and cross-match of blood
• Antibiotics, DVT prophylaxis and pneumatic compression boots
• NGT in obstructed settings, Foley's catheter, Central line if indicated
• Ureteric stent in case of difficult pelvic dissection (previous surgery, diverticulitis)
• Mobilization, and chest physiotherapy
• Informed consent

■ Steps:
o Position: Supine position or Loyid Davis (Modified Lithotomy) for distal tumors
o Incision: Midline Laparotomy
o Place self-retaining retractor
o Abdominal exploration (liver, peritoneum and rest of the colon) ± lntraoperative liver U/S
A+C lleocecectomv
A+D Ascendina colectomv
A+F Riaht hemicolectomv
A+G Extended rioht hemicolectomv
E+H Transverse colectomv
G+I Left hemicolectomv
F+I Extended left hemicolectomv
J+K SiQmoid colectomv
A+ J Subtotal colectomv
A+K Total colectomv
A+L Total oroctocolectomv
RIGHT COLECTOMY
■ Indications: ileocecal, ascending, and proximal 2/3 of transverse colon lesions

Medial-to-Lateral approach (No-Touch Technique)

o By identifying and ligating the lymphovascular pedicle (inferior mesenteric vessels), and
dividing the mesocolon before manipulating the tumor (feeding vessels from the root)
o No superior oncological results
o Used during laparoscopic resection

Lateral-to-Medial approach
o Mobilization
• Retract the small bowel away ffrom the colon by wrapping over warm wet pad

• Retract the colon medially by incising along avascular white line of Toldt
• Retract the colon medially to expose the right ureter and gonadal vessels
Right ureter identified by crossing pelvic brim over the right common iliac vessels
• Divide the hepatocolic ligament to release the hepatic flexure
• Opening the lesser sac by dividing the omentum of transverse colon distally
through gastrocolic ligament
• Identify the duodenum and separate it from the colon

o Bowel resection
• Proximal and distal resection margins should be at least 5 cm from the tumor

• Transect the terminal ileum by GIA "Gastrointestinal anastomosis" stapler

• 5 - 10 cm from ileocecal valve due to common blood supply with cecum
Should be with good margins in patients with cecal tumors
• Transection of the distal colon "Transverse colon" by GIA stapler
• Standard right hemicolectomy: Just after the hepatic flexure
• Extended right hemicolectomy: Just before the splenic flexure

• Check for patency of the lumen and any bleeding points

o Vascular resection
• Expose the root of mesentery by retracting the small bowel to the left side
• Score the peritoneum over mesocolon between transected points
• Elevate the colon and do trans.illumination test to identify the vessles
• Standard right hemicolectomy: lleocolic, right colic, and right branch of middle
colic vessels divided at origins just below the 3"' part of duodenum
• Extended right hemicolectomy: lleocolic, right and middle colic vessels
Vascularity of remaining transverse colon depends on marginal arteries
• Complete mesenteric excision with proximal and distal margin of at least 5 cm
with regional lymphadenectomy (2 12 lymph nodes)
o Send the specimen to the pathology
o Re-anastomosis between terminal ileum and transverse colon by hand sewn end-to-end
or TA "Transverse stapler'' side-to-side functional end-to-end anastomosis at the
antimesenteric borders

o Cheatle slit is performed on anti-mesenteric border if there is disparity between small

bowel and colon

Cheotle slit

o Before closure of the abdomen:

• Closure of mesenteric defect
± Stoma if indicated
• Irrigation with sterile saline
• Check for hemostasis
± Drain if indicated

o Abdominal wall and skin closure

■ Laparoscopic port positions for right hemicolectomy:

5mmpon
surgeon
5mm port surgeon

5/ 12 mm
pCN'tsurg-eon
5 mm camera pon

■ Specimen removal:
o Through 5 cm incision lateral to rectus muscle, retract the rectus medially, and rectus­
sparing split-incision through the posterior rectus sheath for removal of specimen

o Through Pfannenstiel incision

LEFT COLECTOMY
■ Indications: Cancer in distal 1/3 of transverse colon, splenic flexure, descending, and sigmoid
colon till upper rectum (2 to 3 cm above the ·sacral promontory)

Medial-to-Lateral approach (No-Touch Technique)

o By identifying and ligating the lymphovascular pedicle (inferior mesenteric vessels}, and
dividing the mesocolon before manipulating the tumor (feeding vessels from the root}

o No superior oncological results

o Used during laparoscopic resection
o More difficult to apply to lesions of the left colon

Lateral-to-Medial approach
o Mobilization
• Retract the small bowel away ffrom the colon by wrapping over warm wet pad

• Retract the colon medially by incising along the avascular white line of Told! at
level of rectosigmoid until splenic flexure
• Retract the colon medially to expose the left ureter and gonadal vessels
• Left ureter identified by:
• Medial and deep to gonadal vessels
• Crossing the pelvic brim over the bifurcation of common iliac vessels
• Anterior to the external iliac vessels
• At intersigmoid fossa
• By incising the peritoneum over psoas muscle to find ureter medially
• By peristalsis "Vermiculation•

• Opening the lesser sac by dividing the omentum of transverse colon distally
through gastrocolic ligament
o Bowel resection
• Proximal and distal resection margins should be at least 5 cm from the tumor
• Proximal point: Proximal to splenic flexure
• Distal point:
o Standard left hemicolectomy: Before the sigmoid
o Sigmoidectomy: Rectosigmoid junction (at Sacral promontory)

• Transect proximal and distal colon points by stapler based on vascular division
• Check for patency of the lumen and any bleeding points

o Vascular resection
• Expose the root of mesentery by retracting the small bowel to the right side

• Score the peritoneum over mesocolon between transected points on the medial
aspect from duodenum down to promontory of sacrum

• Sigmoidectomy without descending colectomy:

• Sigmoidal, superior rectal vessels (distal to left colic artery)
• Left hemicolectomy: (Tumor at splenic Oexure)
• Left colic, Left branch of middle colic. and first branches of sigmoid
vessels

• Left hemicolectomy with sigmoidectomy:

• IMAand IMV
o IMA divided at aorta, lateral and inferior to ligament of Treitz
o IMV divided at lower border of pancreas

• Extended left hemicolectomy:

• IMAand IMV
• Middle colic vessels

• Complete mesenteric excision with proximal and distal margin of at least 5 cm

with regional lymphadenectomy (� 12 lymph nodes)

o Send specimen to the pathology with marked proximal and distal margins for orientation

o Re-anastomosis by hand sewn, or EEACircular stapler for anastomosis at the sigmoid

o Before closure of the a bdomen:

• Closure of mesenteric defect
± Stoma if indicated
• Irrigation with sterile saline
• Check for hemostasis
± Drain

o Abdominal wall and skin closure

 ■ Laparoscopic port positions for left hemicolectomy:

■ Specimen removal:
o Through 5 cm incision lateral to rectus muscle, retract the rectus medially, and rectus­
sparing split-incision through the posterior rectus sheath for removal of specimen

o Through Pfannenstiel incision

SubtotalfTotal colectomy:
■ Indications: in synchronous neoplasms on right and left colon
■ Subtotal colectomy:
o American: by keeping part of sigmoid colon
o British: by keeping part of upper rectum

■ Total colectomy used also in HNPCC

Principles in Rectal Surgery

■ Pre-operative:
o Assess resectability:
• Imaging-based and staging
• Multidisciplinary meeting
• Tumor Board meeting for possible neoadjuvant therapy

o A ssess fitness:
• ICU and consultations if required
• Functional tests
• Correction of anemia

o Pre-operative preparation:
• Clear liquid diet for 24 hours
• Bowel preparation
• Stoma marking for patient undergoes APR
• 2 Stoma marking for patient undergoes LAR (For possible APR}
• Colonoscopy for elective cases (can be done postoperative in emergency)
• Baseline CEA
• Type and cross-match of blood
• Antibiotics, DVT prophylaxis and pneumatic compression boots
• NGT in obstructed settings, Foley's catheter, Central line if indicated
• Ureteric stent in case of:
• Hydronephrosis
• Expected difficult pelvic dissection (previous surgery, diverticulitis)

• Mobilization, and chest physiotherapy

• Informed consent (LAR / APR)
■ Goals of surgery:
o Removal of primary tumor + Regional lymphadenectomy and superior hemorrhoidal
artery pedicle (at least 12 lymph nodes)
• Low rectal anastomosis have highest anastomotic leak of all GI anastomosis

■ Types of surgery:
o Anterior resection (Sphincter-preserving procedure)
• Resection of the rectum from abdominal approach

o High anterior resection

• Resection of distal sigmoid colon and upper rectum (above peritoneal reflection)

o Low anterior resection

• Resection of the upper and middle rectum (below peritoneal reflection) with 6 cm
from anal verge and 2 cm margin proximal to levator muscle (Total of 8 cm)

o Ultralow or Extended low anterior resection ± J pouch

• Extended distal margin for tumor located at distal rectum above the sphincter
• Anterior dissection is extended along:
• Rectovaginal septum in women
• Distal to the seminal vesicles and prostate in men

o Abdominoperineal resection (APR)

• Resection of sigmoid, rectum, anus, and construction of permanent colostomy
• Used for:
• Low rectal adenocarcinoma (< 6 cm from anal verge)
• Inability to achieve negative distal margin by anterior resection
• Local recurrent or advanced rectal cancer

■ Margins:
o Radial margins: Obtaining circumferential margins by (Total mesorectal excision)

o Proximal margin: 5 cm, for proper lymphadenectomy and viable proximal bowel

o Distal margin: 2 cm or 1 cm for tumor located below mesorectal margin (historically)

• Nowadays negative margins accepted
Total mesorectal excision ITMEl
■ Was first introduced by Bill Heald in 1982

■ Circumferential removal of mesorectum and its enveloping fascia with lymph nodes

■ Decrease recurrence rate and improves the survival

■ Used for curative resection in middle and distal rectum

■ Partial mesorectal excision with 5 cm mesorectal margin from primary tumor used for upper
rectum or rectosigmoid junction

■ Steps:
o Divide superior hemorrhoidal artery

o Sharp incision at peritoneal reflection of Waldeyer's fascia posterior to the rectum

o Sharp incision at peritoneal reflection of Denonvilliers' fascia anterior to the rectum, and
separation of rectal wall from the seminal vesicles and prostate anteriorly

o Continue anterior dissection at lateral side (anterolateral dissection)

• Lateral stalk are found and ligated (middle hemorrhoidal vessels)
• Dissection should be medial to parasympathetic (inferior hypogastric nerves)

o Remove the mesorectum with its fascia and lymph nodes

■ Steps of the operation (Anterior resection I Abdominoperineal resection}:
o Position: Modified lithotomy (supine with slightly trendelenburg position} with either:

• Moderate legs abduction at 45' degrees and elevated at 15 degrees

(Right leg toward left shoulder and left leg toward right shoulder)
• Lithotomv stirrups (some authors advice to avoid stirrups which leads to
excessive flexion of the hip and vascular complications can happen in long
procedure)

Excessive pressure on the calves or lateral aspect of the leg may lead to
compartmental syndrome or common peroneal nerve injury

o DRE and Proctoscopy to determine the distance of the tumor from anal verge

o The abdomen and perineum are draped for LAR and possible APR

o Incision: Lower midline incision (above umbilicus down to pubic symphysis}

o Place self-retaining retractor

o Abdominal exploration (liver, peritoneum and rest of the colon for synchronous lesions}
± lntraoperative liver U/S

o Retract the small bowel upward and laterally, and covered with wet pads
■ Steps for open anterior resection:
1) Proximal dissection: {Lateral-to-medial dissection)
o Incise the Lateral peritoneal attachment along the avascular white line of Toldt to
mobilize left colon from rectosigmoid junction up to splenic flexure

o Mobilize splenic flexure if needed

• Keep the patient on Reverse Trendelenburg position
• Mobilization done from proximal and distal directions (antegrade and retrograde)
• By grasping the greater omentum and retracted upward
• With the countertraction, incises the peritoneum and enters the lesser sac by
dividing the gastrocolic omentum to enter the lesser sac
• Divide the splenocolic ligamen1 to fully release the splenic flexure
• Do not pull down on the splenic flexure
• Packing may be placed at retrocollc space to continue full dissection

o Identify left ureter

o Displace the ureter laterally along with the gonadal vessels (without skeletonization)

o Dissection continue up until reach IMA if high-ligation planned

2) Vascular division:
o High ligation:
• Division of IMA at level of aorta (2 cm from origin)
Q Most of the surgeon prefer this method
Q Doesn't improve survival and associated with injury to sympathetic trunks
Q Done selectively to sigmoid cancer, or rectal cancer T3fr4
Q Can affect blood supply of right colon due to dissection

• Division of IMV
• If mobilization beyond splenic flexure is needed
• Below pancreatic margin or behind the DJ junction (at level of duodenum)
• If more mobilization is needed
+ Stripping of the mesentery of transverse mesocolon before mobilization
of the hepatic flexure

o Low ligation:
• Isolation and division of superior rectal artery and distal sigmoidal vessels
(Distal to left colic artery) "May prevent neNe injury"

3) Proximal Resection
o Proximal resection of distal descending colon 5 cm proximal to the tumor by GIA 60
• Approximately at midpoint or proximal 113 of the sigmoid colon
4) Distal dissection "Total mesorectal excision"
o Posteriorly:
• Incise Waldeyer's fascia and oontinue dissection downwards
• Superficial to sacral promontory down to the level of coccygeus (tip of coccyx)
• Superficial to hypogastric plexus, to prevent injury to middle sacral artery or
pre-sacral venous plexus
• Evaluate the distal margin again

Waldeye- r's fascaa

( Pre---sacral )

Oenonviltier's
fascia

tncorrect ancle

o Laterally:
• Mobilize the mesorectal laterally, and divide the lateral rectal ligaments
• Lateral ligaments oonsist of nerves with branches of middle rectal artery in 25%
• Taking care of ureters and hypOQastric plexus
 o Anteriorly:
• Incise the peritoneal laterally, and retract the bladder superiorly:
• Male: Denonvillier's fascia to mobilized off seminal vesicles and prostate
across the rectovesical reflection
• Female: Rectum is mobilized off the posterior vaginal wall across the
rectovaginal reflection
i
o Continue dissect on until the level of IL.evator ani muscle

Assess the ability of performing sphincter-preserving surgery

■ Steps to continue for anterior resection:

Distal resection
o With taking care for both ureters
o Proximal rectum is clamped and rese ,cted 2 cm distal to the tumor by linear stapler
o Hold the rectum by right angle and place 2 stay sutures below transection level
o Mesentery is excised with proper lymphadenectomy
o Send specimen to histopathology

Anastomosis
o Check vascularity of proximal colon by color, and looking for spurt

o Enterotomy of descending colon is made and take purse string suture

o Anvil of circular stapler is placed and purse suture is tied over the anvil

o Circular EEA stapler introduced through the anus by the assistant, deploying the "spike"
just anterior to the staple line of the rectum

o Check small bowel and exclude internal hernia

o Anastomosis is completed by attach the anvil to circular stapler (28 - 30) and stapling

o Assess the anastomosis

i
by air-leak test through proctoscopy or sigmoidoscopy, or
povidone-iodine solut on injection while anastomosis submerged with saline

o Donuts are inspected for any defect and send to histopathology

o Before closure of the abdomen:

• Closure of mesenteric defect
± Proximal diverting stoma if indicated
• Irrigation with sterile saline
• Check for hemostasis
± Drain if indicated

o Abdominal wall and skin closure

o Foley's catheter to be in place 3 - 5 days (due to edema and urinary retention)

■ Steps to continue for abdominoperineal resection (APR}:
Perinea! excision
• Closure of the anus by purse-string silk

Posterior dissection (First)

• Marking elliptical incision of 2 cm
• Anterior perinea! body to posterior coccyx and ischial tuberosities laterally
• Superficial to hypogastric plexus and divide inferior rectal vessels at
anteriolaterally
• Hook the puborectalis from abdominal incision and continue dissection posterior
to transverse perinea I muscle until reach the tip of the coccyx

• Entering the peritoneal cavity by cutting the anococcygeal fascia anterior to the
tip of coccyx and /evator ani bilaterally to enter the pelvis
Anterior dissection
• Palpate the transverse perineal muscle
• Anterior limit of dissection in male, to prevent injury to urethra
• Continue dissection from perineal body to the levator ani (Levator sling)
• Divide rectourethralis ligament (male) transverse perineal musculature (female)

• Deliver the abdominal part of rectum through the perineal opening by grasping
the proximal end of the specimen and deliver it through the perineal wound

Rbetourolht-:11.is
Median raphe

0 0

'l'r•11...�c,nd stump o oi AnlO co

and 1>ro.dnu1I re4":Juun drawn lhN•u
o,,.ming in IC'\rator,ml mu,-.cle and
Pert.(mrum
o Send to the histopathology

o Before closure of the abdomen:

• Irrigation with sterile saline
• Check for hemostasis
• Presacral drainage by 1 or 2 drains and brought through anterior wall
• ± Proximal diverting stoma if indicated

o Closure:
• Peritoneal closure should be performed
• Closure of perinea! wound in layers starting from levator muscle
• The preoperative colostomy site is excised
• The proximal sigmoid end is brought through trans-rectus opening and sutured to
the anterior abdominal wall while the end of colostomy is closed
• Closure of midline wound
• Mature the colostomy by sewing as full thickness to the dermis circumferentially

o Foley's catheter to be in place 3 - 5 days {due to edema and urinary retention)

■ Laparoscopic anterior resection:

■ Specimen removal:
o Through 5 cm incision lateral to rectus muscle, retract the rectus medially, and rectus­
sparing split-incision through the posterior rectus sheath for removal of specimen

o Through Pfannenstiel incision

HARTMANN PROCEDURE
■ Sigmoidectomy and end colostomy with closure of rectal stump as blind pouch ± mucus fistula

■ Restoration of continuity requires second operation

■ Alternative procedure: Primary anastomosis with temporary diverting proximal loop stoma

■ Advantages of Hartmann's procedure:

o Short operation
o Avoiding the risk of anastomotic leak

■ Indications:
o Complicated diverticulitis: perforation, abscess with peritonitis
o Distal colorectal cancer
o Distal injury with hemodynamically unstable, malnourished, or inability for repair

■ Position:
o Supine position
o Trendelenburg position if more exposure needed

■ Steps:
o Lower Midline incision
o Abdominal exploration and retraction
o Fluid culture if present
o Retract the small bowel with warm pads upwards and laterally

o Mobilization
• Retract the colon medially, and incise along the avascular white line of Told!
• In severe inflammation, dissec1ion along mesenteric border of the colon
• Identify and avoid injury to the ureter
• Dissection should carried out proximally and distally to achieve tension-free
• For suspected malignancy, lymphadenectomy including mesentery is necessary

o Bowel resection
• Divide the proximal bowel first, away from the pathology or inflammation
• Proximally: Beginning of sigmoid colon (identified by left colic artery)
• Distally: Rectosigmoid junction (identified by loss of teania coli)

o Vascular division
• Mesenteric vessels or Sigmoidal and superior rectal vessels

o Send specimen to histopathology

o Irrigation with warm saline

o Inspect for hemostasis

 o Distal colon "Hartmann's pouch"
• Tacked to the sacral promontory or psoas muscle to prevent retraction
• Long polypropylene suture attached to help future identification

o Creation of colostomy
• Excise the pre-operative marked stoma site circular
• Cruciate incision in the anterior rectus sheath without division of the muscle
• Incise the peritoneum and make sure allowing passage of 2 fingers
• Proximal colon brought through the stomal site without tension
(may need mobilization of proximal colon)

o Closure
• Closed-suction drain
• Close the fascia
• Closure of the skin should be loosely and packed with moist gauze

o Mature the colostomy

• Excise the staple line on the proximal colon
• Sew the edges of the colostomy to the skin with 3 - 0 absorbable suture
• Full-thickness colon to the dermis
• Apply stomal applicant

■ Rectal stump management to prevent leakage ''blowout":

Intra-operative
o Transect distal colon in area with minimally inflamed

o Placement of suture or staple intraperitoneally to sacral promontory or psoas muscle

o Stump can brought to level of subcutaneous tissue (above the fascia) this will prevent
mucus fistula and help to lower risk ot pelvic abscess (best for short rectal stump)

o (Safest) To fashion formal mucus fistula in case of long end (difficult for the patient)

Post-operative
o Insert rectal tube (Malecot drain) transanally for decompression for couple of days and
kept in place on top of the stump

o Rectal tube removed on 5 - 7 days postoperative

o If patient have peritonitis due to rectal stump leakage postoperative, then he might need
to be reoperated for washout and drainage

■ Complications:
o Wound infection (most common)
o Stump leak
o Fistula
o Ureteral injury
o Paralytic ileus
REVERSAL OF HARTMANN PROCEDURE
■ 40% of patient associated with failure of reversal due to short stump or frozen pelvis

■ Timing:
o Optimal: 3 - 6 months
• Early: < 3 months
• Used in stoma complications, patient request
• Disadvantage: inflammation, difficult to identify the stump

• Late: > 3 months

• Disadvantage: fibrosis

■ Steps:
o Colonoscopy should be done before the reversal if not done before Hartmann's

o Position: Modified lithotomy position

• Bladder catheter should be ins.erted and stents placed at this time if desired
• Stoma is closed by suture to minimize any contamination and covered by gauze
• Cover the entire abdomen with antimicrobial adhesive covering

o Incision: Through previous scar, Lower midline incision down to symphysis pubis

o Mobilization - Resection of distal colon

• Adhesiolysis of small bowel (especially from the pelvis)
• Free the distal colon is circumferentially at the fascial level
• Divide the distal colon just beneath the anterior abdominal wall
• Now place the retractors
• Complete the remainder of the adhesiolysis

o Identify and mobilize Hartmann pouch

• Long stump usually sutured to anterior or lateral wall at previous operation
• Short stump or retracted stump can by identified by the following maneuvers:
• Rigid proctocopy inserted and advanced
• Air insufflation by rigid procotscopy

• Mobilization of most proximal end is needed if rectum associated with angulation

• Evaluate the pouch for any remnant of sigmoid part
• The proximal colon must be anastomosed to the rectum

o Anastomosis
By EEA stapler:
• Anvil on proximal bowel with purse string
• Stapler through anus with no tension and make the opening through previous
stapler line of the stump for introduction of the anvil
• Test the anastomosis by clamping proximal bowel and introduce air through anus

o Stoma site closed partially by placing 3 - 0 absorbable purse string at dermal level with
small Penrose drain in the center, or to be healed by secondary intention

o Closure
Complications of colorectal surgery
■ Ureteric injury
o Identify location of the ureters
• Crossing the pelvic brim over the common iliac vessels
• Medial and deep to gonadal vessels
• Courses over the right iliac vessels "Right ureter"
• At intersigmoid fossa (Recess at the base of the mesosigmoid) "Left ureter"
• Peristalsis "Vermiculation" can be observed after stimulation for confirmation

Ureteric catheterization help to identify the ureter in re-do as reversal of

Hartmann's procedure or in patients with large size tumor

o High-risk sites for injury during:

• Ligation of the inferior mesenteric artery
• Incision of the pelvic peritoneum lateral to the rectum
• Division of the lateral stalks of the rectum deep in the pelvis
(Particularly if done from below during APR)

o Complications of missed ureteral injury:

• Abscess, sepsis, ileus, urinary obstruction, and flank pain

o Diagnosis of ureteral injury:

• Pack the suspected injured area with sponges
• Techniques used to look for ex1ravasation:
• IV methylene blue or indigo carmine
• Direct injection into renal pelvis or ureter of contrasts
• Retrograde injection of methylene blue
• On-table intravenous pyelogram (IVP}

• Post-operatively:
• Yellow fluid with high Creatinine level from abdominal drain

o Management of ureteral inj ury:

• Call urologist

• Intra-operatively:
• Managed based on location and extent of the injury

• Post-operatively:
• Percutaneous nephrostomy tube placement for diversion
± Percutaneous drainage

• Managed based on location and extent of the injury

 ■ Nerve injury during anterior resection or abdominoperineal resection:

Nerve Site of i niurv Disorder

(Sympathetic)
Hypogastric p lexus
"Joining the para-sympathetic
to from pelvic plexus"
At origin of IMA in aorta Retrograde ejaculation (Infertility)
"Infertility in women due adhesion
Sacral promontory (Posteriorly) around fallopian tube"
lateral stalks (Laterally) Impotence and bladder dysfunction

Mobilization of uooer mesorectum

(Para-sympathetic)
Pelvic splanchnic injury
"nervi erioentes"
Pudenda! nerve injury
lateral ligaments of the rectum Impotence and bladder dysfunction
Anterior dissection behind prostate Ejaculation failure
and seminal vesicle

■ Presacral bleeding /Low pressure venous plexus)

o Sites of bleeding
• Presacral and lateral sacral veins
• Internal iliac vein
• Rectovaginal, retroprostatic, or paravesical veins
• Sacral or presacral artery

o Techniques to control bleeding:

• Early packing
• Argon beam coagulation
• Suturing for localized bleeding site
• Sterile thumbtack over sacral foramen ± Surgicel
• Ligation for veins, small arterial branches, or internal iliac artery
• Repair for external iliac artery, or the vein if it easily exposed
• Rectus muscle welding
• 2 x 2 cm segment of rectus muscle is harvested as free flap and sewn
over bleeding area
• Packing with Surgicel for 24 - 48 hours, then patient shifted from ICU lo the
operating room for removal in persistent uncontrolled bleeding
Circular Stapler

■ Head Color:
o White: for 25mm
o Blue: for 28 mm
o Green: for 31/33 mm

■ Head Diameter: (21 - 33 mm •29 mm is optimal")

o 25mm associated with higher stricture rate for end-to-end anastomosis
o 31 / 33 mm associated with higher anastomotic leak

■ Staple leg length:

o 3.5 mm
o 4.8 mm
o 5.5mm

■ Steps:
o Remove the red plastic cap (accessory tip) tilting top anvil by rotating the wing nut CCW
o Open the instrument by rotating wing nut CCW until red band is fully visible
o Remove the detachable head to expose the trocar
o Retract the trocar by rotating wing nut CW until trocar is fully disappear
Head along the trocar can introduced without removing anvil as alternative approach

o Opening the proximal lumen end and insert the Anvil and close it as purse string suture
• Ensure the purse string tied above the Tying notch

o Insert the instrument up to the closed lumen with detachable head

o Fully extend the trocar and pierce tissue by rotating the wing nut CCW
o Push the tissue down until red-orange band (Base of trocar) is visible
o Reattach the detachable head by sliding the anvil shaft over the trocar {Click sound)
o Turn the wing nut CW to close the instrument
• Make sure no extra-lumen tissue in included
• Make sure for proper orientation for both lumen to prevent twisting

o Do not plan to fire until the red band is visible within green range of gap scale
• Preferable to be between last 2 markers

o Draw red safety layer back toward adjusting knob until it seats into body of instrument
o If the safety cannot be released, the instrument is not in the safe firing range
o Once released, squeeze the firing handle with firm steady pressure
• The surgeon will feel reduced trigger pressure and hear crunch
• Remember, Do not fire if there is tension on the tissues

o After firing, release the firing handle and re-engage the safety
o Open instrument by turning wing nut CCW one-half to three-quarters for easy remove
(two full turns)
• If you open more than that, it will make vacuum-like effect and difficult removal
o To assure the anvil is free from tissue rotate the instrument 90 degree in both directions
o To withdraw the open instrument, apply rearward traction while simultaneously rotating
o Inspect your anastomosis and inspect the donut tissue
• If donut is not complete -+ Anastomosis defect
 C

ln�rtiori and a.uembly

of naplint devKe
E
Anastomosts
Ano rectal
Reviewed by:

Dr. Nemat
 ANORECTAL
ANATOMY AND PHYSIOLOGY
Anus
■ Su rgical anal canal: From anorectal ring -+ Anal verge
■ Anatomical anal canal: From dentate line -+ Anal verge
■ Dentate lioe (Pectjnate lioe): Separate columnar from squamous epithelium
o The lining of the anal canal consists of an line
o Separating columnar from squamous epithelium
o Separating the upper mucosal (endoderm) and lower cutaneous (ectoderm) segment
o It corresponds to a line of anal valves that represent remnants of the proctodeal
membrane
o Above each valve, there is small pocket (anal sinus or crypt), connected to anal glands
o 8-14 longitudinal folds (rectal columns or columns of Morgagni) located above the
dentate line, which anal crypts or sinuses empty

■ Hilton's white jjne {below dentate line): Separate non-keratinized from keratinized stratified
squamous epithelium

Surgical anal canal based on dentate line:

Above dentate line Below dentate line

,.Anal canal11 ''Anal marain 11
Endoderm Ectoderm (Anoderm)
Origin 3 - 5 cm length Started at level of anal verge including perianal skin over
5 - 6 cm radius from sauamous mucocutaneous iunction
Eoithelium Columnar Stratified sauamous
Superior rectal artery Inferior rectal artery
Arterial supply
c:> Sunnle lower anus and both sohincters
Venous drainaqe Portal (Superior rectal vein) Systemic (Inferior rectal vein)
Inferior mesenteric and Superficial inguinal lymph nodes
Lymphatic drainage
internal iliac nodes
"Visceral" "Somatic·
Nerve supply Autonomic fibers of inferior Inferior rectal nerve (from Internal pudenda! nerve)
hvooqastric plexus
Sensation Insensitive Sens�ive
Adenocarcinoma Squamous cell carcinoma
Pathology
Internal Hemorrhoids External Hemorrhoids

Anal sphincters:

Internal sphincter External sphincter

Muscle Circular smooth muscle lmuscularis orooeriaI Extension of ouborectalis muscle
Sphincter Involuntary Voluntary (S3- S4)

Responsible for 50 - 80% of Resting pressure: Responsible for Squeeze pressure

Normal: 40 - 80 mm Ha
Innervation Sympathetic nerve fibers "LS·
from inferior hypogastric plexus
Parasympathetic nerve fibers "S2, S3, S4"
Normal: 40 - 80 mm Ha above restina oressure
Inferior rectal nerve (from internal pudendaI nerve)
S4 Perinea! branch (as somatic nerve supply)
Rectum
■ Serosa found in upper rectum only
■ Identified by absence of teania coli, no segmentation
■ Rectal muscles consists of inner circular and outer longitudinal
■ Rectum length is 12-15 cm
o Upper rectum: Covered by peritoneum on anterior & lateral sides
12 - 16 cm from anal verge up to teania flare

o Middle rectum: Covered by peritoneum on anterior side (partial retroperitoneum)

8 - 12 cm from anal verge

o Lower rectum: not covered (totally retroperitoneum)

Anorectal ring and 4 - 8 cm from anal verge

■ Oenonvilliers fascia (Anterior): rectovesical fascia / rectovaginal fascia

■ Waldeyer's fascia (Posterior): rectosacral fascia

o Anteroinferior1y directed thick fascial reflection from the presacral fascia at the S4 level
to the fascia propria of the rectum just above the anorectal ring

■ Lateral ligaments of the rectum (Lateral stalks):

o Condensation of pelvic fascia that supports distal rectum
o Related structures:
• Pelvic plexus
• Middle rectal artery
� Do not pass through lateral stalks, but branches are courses through in 25%

■ Levator ani (Pelvic floor muscles): Transition between anal canal and rectum
o Support rectum from lateral borders
o Consist of: Puborectalis, Pubococcygus, and lleococcygus
• Anorectal ring (5 cm from anal verge, 1 cm above dentate line):
• Formed by Levator-External sphincter complex (Puborectalis)
• Puborectalis partially encircle the anus (No anterior coverage)
� Forms angulation of Anorectal area to maintain continence

■ Houston's valves
o 3 Transverse folds of rectum
• Upper and lower convex to the right
• Middle is convex to the left
o Support the weight of fecal matter, and prevent its urging toward the anus
o Rectum normally holds between 200 and 250 ml
o Good location to perform rectal biopsy (does not contain all muscle wall layers}
■ lsehioreetal boundaries:
o Medial: Levator ani muscles and external sphincter
o Lateral: Obturator internus (Contains pudenda! nerve}
o Roof: Junction of medial and lateral walls
o Floor: Superficial fascia and skin

■ Arterial supply of the rectum:

o Superior rectal artery:
� Continuation of inferior mesenteric artery

o Middle rectal artery

� From internal iliac artery
� Related to lateral stalks

o Inferior rectal artery: From internal pudenda! artery (from internal iliac artery)

■ Lymphatic drainage of the rectum:

o Upper&middle rectum·
• Drains upwards -+
Inferior mesenteric nodes -+ Para-aortic nodes
o Lower rectum:
• Drains upwards -+ Inferior mesenteric nodes
• Drains laterally -+ Internal iliac nodes
HEMORRHOIDS (arterial)
■ Hemo"hoids: Blood flow, Piles: Balls
■ Submucosal vascular cushions of the anal canal, protect anal sphincters during defecation
o Clusters of:
• Vascular tissue (arterioles, venules, arteriolar-venular connection)
• Smooth muscle
• Connective tissue
• Elastic tissue

■ Hemorrhoids are sinusoids (lack muscular wall on histology), Not veins or artery
o Hemorrhoidal bleeding classified as arterial bleeding due to:
• Bright red colon
• Well oxygenated blood
• Arterial pH analysis

■ Location:
o Left lateral, right anterior, and right posterior fibromuscular cushions (3, 7, 11)
o Due to left inferior rectal vessel is straight and right one branched into anterior/posterior

External hemorrhoids Internal hemorrhoids

Location Distal to dentate line
Coveraae Covered bv anoderm
Anodenn Abnormal
/bluish discoloration and conaestion\
Blood SUDDIY Inferior hemorrhoidal vessels
Presentation Pain> Bleeding
Proximal to dentate line
Covered bv columnar eoithelium
Normal
Superior hemorrhoidal vessels
Fresh bright bleeding after defecation> pain

■ Pathophysiology:
o Increase venous pressure and venous congestion with hypertrophy of internal
hemorrhoids due to increased intra-abdominal pressure
o Weakness of fibromuscular stroma
o Increased internal sphincter tone

■ Risk factors:
o Constipation and straining, aging, pregnancy, malignancy, rectal or spinal cord surgery

■ Classification of internal hemorrhoids:

Gradina Descriotion Manaaement

Grade 1 No prolapse (bleeding only) Conservative
Internal buloe into the anus without orolaose
Grade 2 Prolapse and spontaneously reduced Conservative
Non-ooerative manaaement
Grade 3 Prolapse and manually reduced Hemorrhoidectomy
Non-ooerative manaaement
Grade 4 Irreducible orolapse Hemorrhoidectomv
 Management of hemorrhoids:

■ Conservative measures: 'For all type 1 and 2, and some of type 3 hemorrhoids"
o Dietary and Behavioral Therapies
o Analgesia and vasoactive agent:
• Hydroxyethylrutoside (Daflon) improves venous tone, microvascular
permeability, lymphatic activity, and microcirculatory nutritive flow
• Dose: 500 mg PO 6 tablets x 4 days, 4 tablets x 3 days (2 tablets for chronic)

o Topical agents:
• GTN Nitroglycerine and Nifedipine relieve spasm of the sphincter
• Steroids for short period (1 week) can relieve perianal inflammation

• Tribenoside (promote healing of basement membrane and improve local

microcirculation and vascular tone)
• Lidocaine (used in combination with Tribenoside as Procto-glyvenol)

o Adequate fluid intake and high fiber diet (Psyllium seed & Methylcellulose)
o Avoid straining and avoid suppositories (can stimulate pruritus}

o Proper hygiene and sitz baths after bowel movement and 2 - 3 times / day
• May alleviate sphincter and pelvic floor muscle spasms
• Warm bath for thrombosed h&morrhoids

o Stool softener /Laxative):

Tvn e Examoles Action Usaae

Bulk forming Sterculia "Normacol" High-fiber diet, Best for hemorrhoids and chronic constipation
Psyllium reabsorb water Not good for acute constipation
Need to drink copious amount of fluid
Increase size of Contraindication in:
stool bolus, make Intestinal obstruction, stroke, spinal injury,
stool softer imoaired =ristalsis
Stimulant laxative Bisacodyl "Dulcolex· Increase peristalsis Used in l frequency of defecation
Senna Can be used for short period "aggravate
Castor oil constipation in long term"
Contraindicated in:
Intestinal obstruction/ =rforation
Osmotic laxative Lactulose Hypertonic increase Best 1•1 choice for constipation
Macrogol "Movicol" fluid toward stool Used in hard constipation
(Polyethylene glycol) Need adequate fluid intake

Glycerin supposijory Lactulose "Non-digestible sugar"

Mg Citrate -+ Increases blood glucose, reduce ammonia
Na Biphosphate -+ Gaseous abdominal distension

Contraindicated in:
Intestinal obstruction/ perforation
lmoaired renal function/ dehvrlration
Stool softeners I Docusate Hold fat and water As retention enema
Surfactants I Mineral oil within stool No role in chronic constipation / anorectal
Lubricant diseases
■ Non-Operative procedure: (Office-based procedures)
Indicated for: grade 1 - 2, some grade 3

o Rubber-band ligation: by elastic band (1 - 2 quadrants are banded per visit)

• Used for grade 1 and 2 (do not use it in external hemorrhoids -+ Painful)

o Infrared coagulation: not effective in treating large piles (for grade 1, some 2)

o Sclerotherapy: injected into anorectal submucosa to induce fibrosis

• Mitchell technique: by using carbolic acid as sclerosing agent
• Phenol in oil is the most common agent used

■ Operative:
Indicated for: Recurrent bleeding, Large, piles grade 3 - 4, Thrombosed

o Open hemorrhoidectomy (Milligan-Morgan) "Most common used and effective•

• Grasping external hemorrhoids with hemostat and retracted caudally
• Grasping internal hemorrhoids and traction applied
• V-incision made on andoderm till mucocutaneous junction
• Apex of hemorrhoids pedicle retracted away from sphincter fibers
• Suture ligated and hemorrhoid amputated, and wound left open
Need to resect down to the internal anal sphincter (do not go through ii)

o Closed hemorrhoidectomy (Ferguson's technique)

• Same as milligan-morgan but wound closed with absorbable suture

o Submucosal hemorrhoidectomy (Parks procedure)

o Stapled hemorrhoidectomy (Circumferential mucosectomy; Anoplasty)

• Complications: Pain, perforation, rectovaginal fistula, urinary retention

o Whitehead's circumferential hemorrhoidectomy (high complications)

o Ligasure and Starion hemorrhoidecto:my with submucosal dissection

o Lord's procedure: (Manual anal dilatation) maintain sphincter laxity by dilatation

o LASER hemorrhoidectomy: vaporized / excised by carbon dioxide or NdYag LASER

o Doppler-guided ligation of branches of superior hemorrhoidal artery

• Not effective for external hemorrhoids
• Associated with recurrence
 ■ Thrombosed Internal hemorrhoid:
o Conservative (Usually doesn't require surgery)

o For persistent or recurrent cases:

• "3 quadrant hemorrhoidectomy'' Milligan-Morgan

■ Thrombosed external hemorrhoid:

o < 72 hours:
• Excision of the thrombosed hemorrhoid by elliptical incision
Lance open (lancing the skin Lancing)
By incise the skin to evacuate the clot, to relieve the pressure
Excision has better result from evacuation only

o > 72 hours:
• Conservative management

■ Acute strangulated hemorrhoids:

o Presented with irreducible hemorrhoids, with ischemia necrosis and ulceration

o Urgent standard hemorrhoidectomy

Complications of hemorrhoidectomy:
■ Urinary retention
o Due to pelvic floor muscle spasm

■ Bleeding

■ Anal stenosis

■ Incontinence
■ Infection / Sepsis
o Necrotizing infection must be ruled out by examination under anesthesia
o Retroperitoneal or Pelvic sepsis may indicate rectal perforation
ANAL FISSURE
■ Split in the anoderm, 90% located posteriorly at midline
o Due to less blood supply and angulation of the anus

■ Etiology:
o Trauma as passage of hard stool associated with increased intra-anal pressure
o Other causes: "Associated with multiple fissure, or off-mid/ine anal fissure"
• IBD, TB, HIV, Syphilis, Chronic infection, or Anal cancer

■ Clinical presentation
o Chronic Constipation
o Pain and bleeding of red streaks mixed with stool, or after defecation
o Chronic anal fissure: (> 4 - 6 weeks}
• Fibrosis and Hypertrophy anal papilla inside the anus
• Skin tag (Sentinel pile) outside the anus

■ Management:
o Conservative:
• Heals 90% of acute anal fissure
• Sitz bath, stool softener, hi gh-fibers diet and topical agents
• Topjcal appljcatjons: (used for 6 - 8 weeks)
• Nitroglycerin
o 0.2% GTN (neurogenic relaxation of internal sphincter)

• Calcium channel blockers

o Nifedipine gel (reduce 02 demand and contraction of muscle)
o 2% Oiltiazem with 1% lidocaine

Side effects for both (More with GTN): Headache

• Botulinum toxin
Binds to presynaptic nerve terminals of the neuromuscular junction preventing
release of acetylcholine and te mporarily
� Paralyzing the muscle, reducing the spasm and contraction of the sphincter

• Injected to internal sphincter or trans-sphincteric plane as

10 units/ 4 quadrants or 20 units at 3 and 9 O'clock

Many studies recommend to inject 20 units on either side of the anterior

midline in the intersphincteric groove which provides the best results

• 1 cm spread, and last for 3 - 4 months due to axonal regeneration

• Associated with greatest healing rate as non-operative method, but also

associated with high recurrence rate as well

50% of anal fissure healed conservatively

18 - 27% recur within 5 years
o Surgery:
Goal: Decreased the elevated anal resting tone

1) Lateral subcutaneous internal sphincterotomy at "Right lateral column"

• Used for:
Chronic anal fissure after failure of medical management in hypertonic sphincter

• Types:
• Closed: by inserting index in anal canal and blade in inter-sphincteric
groove followed by change direction of blade to cut muscles towards the
finger while going out

• Open: by making incision over inter-sphincteric groove, delivery of muscle

fibers by forceps and cutting the fibers at the length of the fissure
o Options: Cutting 2/3 length of the fissure, or all internal sphincter

• Done laterally at 3 or 9 O'clock

• Contralateral side is used for 2nd trial of sphincterotomy

• If not done laterally (e.g. posterior sphincterotomy):

• Associated with more risk of keyhole sphincter deformity (alteration of the
shape), stenosis and poor wound healing

• Don't do these:
• Don't go above dentate
• Don't cut external sphincter, or mucosa
• Don't do it in Crohn's + Do colonoscopy and biopsy

• Most serious complication: Fecal incontinence

• Usually to flatus
• Range between 5 -15% (3% affect quality of life)

2) Fissurectomy ± advancement flap IAnoplastyl

• For low baseline sphincter resting pressure (hypotonic sphincter) with chronic
anal fissure after failure of medical management

o Recurrence after surgery (Mostly due to incomplete division of internal sphincter)

• Rule out other etiology (Colonoscopy, PPD and HIV tests)
• Anal manometry or TRUS
• Biopsy of fissure edges
• 2nd trial of surgical therapy at contralateral side if no other etiology found
ANO RECTAL ABSCESS
■ 30% of anorectal abscess developed into fistula-in-ano
■ Pathophysiology: Obstruction of anal crypts of Morgagni's
(10- 15 crypts located at dentate line, empty anal glands into rectum)

Submu,c:,owl �• Ottp �I 'Patt ---->��.,C

El!llffllat� A.flOOO«)'pt.. �l"',.l!t --�--'�•
�sphinci.

■ �
o Perianal (60%), lschiorectal (20%), Submucosal
o lnter-sphincteric
• Lack external findings, diagnosed by tenderness on PR
• Tran-anal drainage by dividing internal sphincter

o Post-anal (between levators and external sphincter)

o Supralevator abscess:
• Trans-sphincteric abscess: Drained through skin incision
Extra-sphincteric fistula developed if drained trans-rectally
• lnter-sphincteric abscess: Drained trans-rectally
Supra-sphincteric fistula developed if drained through skin

■ Management: vn No
o Antibiotics: Indicated only for:
• Cellulitis, Sepsis, Prosthetic heart valves, Recurrent infection
• lmmunocompromised: DM, HIV, BM transplant, Chemotherapy, Steroids

o Culture: for all (E.Coli associated more with perianal fistula)

o Biopsy: in perianal lesion, suspicious nodule, recurrence, fistula tract, IBD, malignancy
o Drainage:
• CT-gyided drajnage· for high supralevator abscesses
• Catheter-drainage: for prolonged period (recurrent or large infections)
• Surgical drainage:
• PR should be done to asses extension into post-anal space and
contralateral Iossa
• Bedside: for most perianal and small ischiorectal abscesses
• Incision should be as close as to anal verge
(if fistula developed, it will be short simple fistula)
• Counter elliptical incision for horseshoe abscess as lateral extension to
ischiorectal fossa (e.g. lschiorectal abscess)
• Fistulotomy at time of I & D used for only for simple fistula
o Contraindicated in complex fistula
 FISTULA-IN-ANO
■ Etiology:
o Anorectal abscess (most common), IBD, Diverticulitis, TB, Trauma, Radiation, CRC

■ Goodsa/1's rule (in lithotomy position, less accurate in anterior fistula in women}
o Anterior:
• External opening is < 3 cm anterior to imaginary line: Straight line
• External opening is> 3 cm anterior to imaginary line: Curves and terminated
posteriorly at the midline

o Posterior: all external opening curved and terminated at 6 O'clock (midline)

" Long anterl<lf "
fi,:\ula
Anterior
Secondary openng � V.
Primary opening
in crypt

■ Parks classification:
Tvne of fistula lnter-sohincteric Trans-sohincteric Suora-sohincteric Extra-sohincteric
Prevalence 70% 20% 5% <5%
/Most common)
Tvoe of fistula low-LvinQ fistula low-Hiah lvinQ fistula Hiqh-lvinQ fistula HiQh-lvinQ fistula
Description Between anal Through external Encompasses entire Outside the sphincter
sphincters sphincter sphincter

Associated with:
- Radiation
- Infectious diseases
- Anal incontinence
Origin Perianal abscess lschiorectal abscess Supralevator abscess Trauma, IBD
(anal crypts) Pelvic inflammation
Appendiceal or
diverticular abscess
Management Fistulotomy Uooer 2'1· Fistulectomy Varies
> 30"/4 of sphincter length
- Seton Advancement flap
- Advancement flap
- LIFT

lower½:
< 30"/4 of sphincter length
- Fistulotomy
- Seton
 Complex fistula
(Associated with recurrence or incontinence after intervention/
Based on anatomv Based on association
Multiple fistula Fecal incontinence
Anterior fistula in women (Less fibers\
Suora-sohincteric fistula lnflammatorv bowel disease
Extra-sphincteric fistula Immunodeficiency or compromised wound healing
High Trans-sphincteric fistula Including radiation and prior surgery
(> 20 - 30% of external anal snhincter lenothl
High fistula: Internal opening is away from anal verge (above anorectal ring)

■ Management:
Simple fistula Complex fistula
Best to be transferred to CoJorectal surgeon
- Fistulotomy - Seton
Division of internal sphincter or distal 1/3 of
external sphincter is tolerable - Advancement flaps
Gold-standard 2nd stage procedure in complex fistula
Options
- Fibrin sealant injection
- Ligation of intersphincteric tract (LIFT)
- Collagen plug For High Trans-sphincteric fistula only
For simple fistula as well as extra-sphincteric fistula
- Fistulectomy (Least appropriate)

o Seton: thread introduced along the tr.ack of fistula and left in situ
• Indicated in complex fistula
• Definitive procedure done 6 - 10 weeks later
(Can be the definitive management alone in IBD patients)

• Types:
• Non-cutting (Loose) or drainage seton:
As silastic band, or vessel loop

• Cutting seton:
By using non-absorbable suture, with progressive sliding knot (Roeder's,
Meltzer's knots) and interval pushing the knot in the outpatient clinic

-+ To achieve gradual necrosis (starting from the base)

o fistula associated with iaflammatory bowel disease·
• Non-cutting (drainage) seton
• No fistulotomy, flaps or LIFT (except for highly-selected patients)
• If fistula well-drain -+
treat IBD medically (e.g. Ant-TNF: infliximab for Crohn's)
• TPN can help induce fistula closure
• Diverting stoma and proctectomy used in refractory associated with rectal
disease
PILONIDAL DISEASE
■ Pilonidal is derived from the roots "pilus• (hair} and "nidus" (nest)
■ Infection of skin and subcutaneous tissue at upper natal cleft of buttocks
■ Ranging from simple sinus to multiple draining sinuses and infection
■ Due to hair penetrates into the subcutaneous tissues through dilated hair follicles leads to local
trauma and inflammation
■ Risk factors:
o Hirsute individuals
o Deep natal clefts
o Obese
o Poor hygiene
o Prolonged sitting
i
o Excessive sweat ng

■ i
Sinus track ng: methylene blue to identify associated sinus tracts

■ Principle of management:
1} Control of sepsis ± drainage
2} Avoid too much excision (excision down to post-sacral fascia should be avoided if possible)
3} Unroof all disease, debridement and remove hairs
4} Use off-midline excision and closure when possible
5} Minimal tension if closed

■ Management:
o Non-operative: ''Main treatment for minor non-infected disease"
• Meticulous hair control (natal cleft shaving)
• Improved perinea! hygiene
• Limited lateral incision and drainage for treatment of abscess

o Excision:
• Used mainly for multiple sinuses
• En bloc excision of entire pilonidal sinus and epithelialized tracts down to level of
sacrococcygeal fascia

o Closure:
• Recurrence rate 7% with primary closure (Much less in delayed closure}
• Primary closure
• Delayed closure if infected, or extensive disease (Preferable)

o Off-midline techniques:
• Z-plasty
• V-Y advancement flap
• Rhomboid (Limberg} flap
• Bascom cleft closure

o Associated with abscess

• Incision and drainage lateral to intergluteal cleft
FECAL INCONTINENCE
■ Oefinition:
o Inability to control passage of gas, liquid, or stool until socially acceptable time or place
for evacuation

■ Types:
o Mechanical
• Oue to obstetric injury, or trauma

o Neurogenic incontinence
• Oue to stretching of pudenda! nerves during labor, descent of the perineum and
nerve stretch during straining at stool or rectal prolapse, or systemic disease
such as multiple sclerosis, scleroderma, or spinal cord injury

o Idiopathic
• Due to medical disease such as diarrhea with limited rectal capacity, irritable
bowel syndrome, or sedation

■ Investigations:
o Needle electromyography (EMG} most accurate but painful
o Transrectal ultrasound: most sensitive for sphincter injury

■ Management:
o Neurogenic: Biofeedback therapy (Pelvic floor exercise and training)
� If not improved: Artificial bowel sphincter, Neurostimulation, Colostomy

o Mechanical: Anal sphincter reconstruction

• Done anteriorly (To prevent injury of pudenda! nerves on lateral sides}
RECTAL/ RECTOSIGMOID PROLAPSE
■ Risk factors:
o Laxative abuse
o Straining
o COPD
o Female
o Multiparous
0 Elderly
Not associated with volvulus

■ Types:
o Full thickness {True; Procidentia): all layers of the rectum ;;Most common type"
� Appears as Circular folds "Concentric rings•

o Mucosa! prolapse (External prolapse): partial thickness protrusion

� Appears as Radial folds "as hemorrhoids"

Internal prolapse is an internal intussusception of rectal wall without protrusion

(Associated with SRUS "Solitary rectal ulcer syndrome)

■ Evaluation:
o Clinical diagnosis

o Cindefecography is diagnostic test to differentiate between mucosal and true prolapse

o Anorectal manometry to assess any sphincter damage

o Colonic transit studies to assess patient with history of constipation

o Colonoscopy, Air-contrast barium enema, or CT colonography to exclude

neoplasms or diverticular disease

■ Treatment:
o Reduction:
• By sedation, field block with local anesthesia, or sprinkling with Sugar/ Salt to
reduce edema, and covering with wet gauze

o Conservative is the main therapy for internal and reducible prolapse

• High-fiber diet/ Bulk-forming laxatives
• Biofeedback

o Surgery is the main therapy for full thickness rectal prolapse

• Usually avoided in internal prolapse
• Indications for repair:
• Full thickness rectal prolapse± Constipation± Incontinence
"Presence of only rectal prolapse is an indication for surgery"
Surgical options

Abdominal procedure (Best for young, Lowest recurrence)

Suture rectopexy with slgmoldectomy Constipation Incontinence
'by fixing the rectum to pre-sacral fascia'
Improved Improved
Lowest recurrence IBestl. but indicated onlv if associated with constioation
Worsening Improved
Rectopexy without sigmoidectomy
Rlpsteln's / Marlex procedure / Prosthetic Sling Worsening Improved
Fixing rectum to presacral fascia by using fascia lata as sling
- By Marlex mesh / lvalon sponge "Marlex rectopexy"
Hiahest Morbiditv(Not recommended anvmore)

Perianal procedure (Best for elderly, Highest recurrence)

Altemeler procedure Incontinence
Perianal rectosigmoidectomy
Worsening
Usedfor
- Full-thickness long segment(> 3 - 4 cm)

Delorme procedure (Mucosa/ sleeve resection; Reefing the rectal mucosa) Improved

Mucosal proctectomy followed by muscular plication and anastomosing the proximal extent of
mucosal resection

Used for:
- Full-thickness short segment(< 3 - 4 cm)
- Mucosal orolaose
Anal encirclement "Thlersch wire" No rule

High morbidity rate

No lonoer =rformed currentlv

Recurrence of rectal prolapse

Previous operation
Resection + Rectooevv
Rectooexv alone
Altemeler orocedure
Delorme procedure
Ooeratlon of choice
With comorbidities Without comorbidities
Delorme orocedure Reoeat Rectooexv onlv
Altemeier orocedure Reoeat Rectooexv + resection
Altemeier orocedure Reoeat Rectooexv onlv
Delorme procedure Repeat Rectopexy ± resection
Altemeier orocedure
 FIGURE I 11ucOAI p,oa� �\�).
A, SubnilcOAt infiluanan wlch .,...,._. �
•• Ciro.i""'nnml mutOMI � C. Ouecdon of ffllilC(IN. _..,
from ll'MQII¥ .. 0 #Id E. l'liaoiw: 1llUII � c...: ... ol
INICO».-.d�wll.F.�---v-­
C&IIKIDl,.,,.....0/WNl/ll
........ illlld.D[ ..... �
olcolortcal�Scl.M..lffl,0--,....,_�
17.__lNJ

E
FIGURE l Perineal rKtosf,mold«tomy (Altemeiet's procedure).
A co C, Full-thickness exdMOn of the outer cylinder ol the probpse..
0, Me:senteric �ssels ligated: St3)' sutures placed .-i dlsQI edp ol
inner cyDnder. E, Anan.omosk of che dlml :upea of CM �
""°" t<> th• .-.<121 ,..,,,,_ (hom Wl,;tlow C&, R,crd p,olops< ond
inMsvsapt,om, In kk OE. tdiu,r. Hi.ndbook of � IM'J'l-1'1•
St louk, f997, Qwlty Mtd,l:af Miah..,, 274-298-j
SOLITARY RECTAL ULCER
■ Most prominent in female
■ Most common site: Anterior wall of distal rec.tum
■ Presented with:
o Rectal bleeding
o Tenesmus (sense of incomplete evacuation)
o Anismus; Dyssynergia (failure of relaxation of pelvic floor muscle after defecation)

■ Pathogenesis:
o Etiology is unknown, most likely relate to rectal prolapse
o Paradoxical contraction of puborectal:is muscle -+ trauma -+ ischemia
o Associated with:
• Sexual history
• Herpes Simplex virus (Herpes proctitis) in HIV patients
• lntussusception
i
■ Investigat ons:
o Colonoscopy and Jumbo biopsy
• Exclude malignancy or colitis
• Appear as Polypoid lesion 25%, Multiple lesions 30%
• Findings:
• Hyperemic changes, ulcer covered by slough
• Friable thickened patches of rectal wall (5 - 12 cm from anal verge)
• "Colitis cystics profunda"
o Mucus-filled glands trapped in submucosal with normal epithelium
o Confused with cancer

o Barium enema (Non-specific)

• Mucosal granularity, polypoid lesion, stricture, ulceration, thickened rectal folds

o Defecography or Dynamic pelvic MRI

• Used to exclude pelvic or rectal prolapse, or internal intussusception

o Anorectal manometry
• Should be done in all children

o EMG or Balloon expulsion test for paradoxical contraction of puborectalis

■ Crjterja for djagnosjs·

o Straining and tenesmus
o Internal or external rectal prolapse
o Solitary multiple erythematous ulceration or polypoid lesions in endoscopy
o Histology of fibrotic obliteration of the lamina propria
■ Management:
o Conservative measures for most patients
• High-fiber diet, including supplement with .: 6 glasses of water daily
• Bulk laxatives, and elimination of suppositories

o Associated with:
• Rectal prolapse -+
Cystocolpoproctography -+ Rectopexy ± sigmoidectomy
• Pelvic prolapse -+
Multidisciplinary pelvic floor repair
• Paradoxical puborectalis -+
Biofeedback

Avoid surgical resection of the ulcer

ANORECTAL STRICTURE
■ Etiology:
o Iatrogenic (Most common) as previous rectal surgery, or trauma from instrumentation
o Inflammatory bowel disease, TB, infectious proctitis, radiation proctitis
o Malignancy

■ Management:
o Resection and anastomosis for suspicious malignancy

o Benign condition:
• Medical Treatment
• Mechanical Dilation
• Rectal strictures:
• Stricturectomy (anterior resection) if not responding with dilation

• Anal strictures: Anoplasty

• Transverse closure

• Simple random flaps

(Mucosal advancement flap, Y-V advancement flap, Rotational S flap)

• Full-thickness advanc-ement flaps

(Diamond flap, House ft.ap, V-Y advancement flap)

CARCINOID OF RECTUM
■ Low rectal carcinoids
o < 2 cm: Trans-anal excision (wide local excision with negative margins)
o > 2 cm or invasion of muscularis properia: APR

■ Colon or high rectal carcinoids:

o Formal resection with lymph node dis.section
RECTOVAGINAL FISTULA
■ Etiology:
o Obstetric injury (most common}, followed by Crohn's disease
o Iatrogenic (low anterior resection, hysterectomy or vaginal surgery}
o Neoplasm, infection or radiation

■ Presentation:
o Passage of stool or gas through the vagina, vaginal discharge
o Repeated UTI, dyspareunia

■ Classification:
o High fistula: at the level of the cervix

o Low fistula (anovaginal}: at or below the dentate line

•associated with trauma and sphincter injury"

o Simple fistula: at middle - lower rectovaginal septum, Low, < 2.5 cm in diameter

o Complex fistula: at upper rectovaginal septum, High, > 2.5 cm in diameter

■ Investigations:
o Anoscopy or vaginal examination
• In Trendelenburg and lithotomy position, the vagina can be filled with saline while
the rectum is insufflated with air
• Air bubbling through the rectovaginal septum can elucidate the fistula's location

o Tampon test: by placing tampon in vagina, methylene blue enema and ask the patient to
ambulate for 20 - 30 minutes, then re-examination for blue stain

o EUA under GA for patients with 18D

o Pelvic MRI or endorectal coil MRI to identify sphincter defects

■ Management:
o 50% of obstetric related fistula mostly will close spontaneously within 6 months

o Initial treatment: Conservative for 3 - 6 months to allow inflammation to subside

o Abscess or infection: Drainage and treat infection ± draining seton

o No repair should be undertaken for at least 6 months for radiated tissue

o Pre-operative:
• Phosphate enema on the morning preoperative for simple repair
• Full mechanical and antibiotic bowel preparation for extensive repair
o Surgery:
• Trans-anal: (for low fistula)
• Endo-rectal Advancement Flap
• Fistulotomy
• Fibrin glue
• Trans-abdominal: (for high fistula)
• Rectal resection
• Primary repair with omental interposition

• Trans-vaginal

• Trans-perinea!

Fecal diversion (Colostomy) used in recurrent cases, and radiation-related

ANAL CANCER
■ Most common site of distant metastasis: inguinal lymph nodes
0 Confirmed by FNA
o Associated with malignancy distal to dentate line
o Inguinal lymph nodes dissection:
• 24% rate of wound infection
• 40% rate of lower limb lymphedema
• Reserved for recurrent or persistent disease in the groin

■ Classification:
o Anal margin (distal to dentate) and anal canal (proximal to dentate)
o Peri-anal (completely visualized with gentle eversion of buttocks) and Intra-anal

■ Squamous or anal intraepithelial lesions

o Associated with HPV infection, sexual history, HIV or previous radiation
0 Pathology:
• Nuclear pleomorphism and enlargement, hyperchromasia, increased mitotic
activity with intact basement membrane

o c1assjfied iota;
• High-grade squamous intraepithelial lesions (HSIL)
• High grade dysplasia, AIN2, and AIN3
• Treated with ablation with close surveillance

• Low- grade squamous intraepithelial lesions (LSIL)

• Low grade dysplasia, and AIN1

o Perianal skin lesions: treated with electron beam radiation

■ Epidermoid tumors (Squamous cell carcinoma)

o Wide local excision: Peri-anal, Anal margin, s T1, < 2 cm, Negative LN

o Nigro protocol: Intra-anal, Anal canal, Invading the sphincter, 2: T2, > 5 cm, Positive LN
• Nigro protocol (5-FU, Mitomycin C, and 45 Gy external beam radiation)
• Standard treatment for Cloacogenic cancer (Variant of SCC)

o APR indicated for recurrent, persistent, or involving sphincter

■ Adenocarcinoma:
o Associated with synchronous GI adenocarcinoma

o Small T1 (Not beyond submucosa): Wide local excision

o Remaining adenocarcinomas: As rectal cancers

Stage I: Surgery

Stage II/ Ill:

1) Neoadjuvant chemotherapy (5-FU based)
2) APR
3) Adjuvant chemotherapy
 ■ Melanoma:
o Usually not pigmented
o Presented with rectal bleeding
o Management:
• Wide local excision: as initial treatment, regardless the site
• APR: if Involving sphincter, large, fungating, or necrotic

■ Bowen's disease:
o Squamous cell carcinoma in situ of the anus

o Management:
• Biopsy from 4 quadrants at dentate line, anal verge, and perianal skin
• Wide local excision (recurrence rate 30%)

■ Extra-mammary Paget's:
o Paget's disease: Breast, bone and anal

o Adenocarcinoma in situ ( lntraderrnal apocrine gland cancer)

• Typically extended microscopically beyond visible lesion
• Associated with underlying carcinoma in 30% - 45%

o Presentation:
• Most common presentation is intractable severe itching
• Eczematous, well demarcated plaque with ulceration and scaling

o Investigations:
• lncisional biopsy
• Positive Periodic acid-S-chiff (PAS) stain due to significant mucin
• Paget cells (Large vacuolated cytoplasm with eccentric nuclei)

• CTabdomen
• Colonoscopy
50% associated with internal malignancy

o Management:
• WLE with clear margin: Localized or peri-anal Paget's
• APR: Invasive apocrine cancer
• Recurrence rate: 30 - 70%
± Chemotherapy
± Radiotherapy (unfit patient, or multifocal disease)

Lowest recurrence in Mohs micrographic surgery (sending margins as frozen section until negativity)
OTHER DISEASES
■ Anorectal diseases in AIDS patients:
o Kaposi's sarcoma: Nodule with ulceration
o HSV: Rectal ulcer
o CMV: Shallow ulcers

■ Anogenital warts (Condyloma acuminata)

o Caused by Human papilloma virus (HPV)
• Types 6 and 11 appears to cause warts
• Types 16 and 18 appears to predispose malignancy an flat dysplasia

o Verrucous carcinoma is locally aggressive form of condyloma acuminate

o Associated with squamous intraepithelial lesions and squamous cell carcinoma

o 5% acetic acid help to guide the biopsy in Bowen's disease or condyloma acuminate
• Dehydrates the neoplastic cells with dense nuclei to appears white
• Acetowhite appearance in Bowen's disease, AIN

o Appearance:
• Small, solitary flesh-colored plaques to distinct 1 - 2 mm flesh-colored papules

o Management:
• Evaluate the extent of involvement
• By examination, EUA, anoscopy, sigmoid or colposcopy, vaginal speculum

• Small:
• Topical application of local agent: (Can be used as mainstay treatment)
o lmiquimod (immunomodulator}:
• Lead to Induction of pro-inflammatory cytokines

o Biochloracetic acid or Trichloroacetic acid:

• Keratolytic {Chemical cauterization)

o Agents Interrupts mitosis:

• Podophyllin
• Podoflox
• 5-Fluorouracil

• Surgical Excision ± Fulguration of the remaining condyloma

• Larger or Multiple (Extensive):

• Surgical excision with no negative margin (Macroscopic} ± fulguration
• APR may need if involved the anal sphincter
■ Radiation proctitis:
o Most common site of radiation injury i n GI tract: rectum
• Complication of Radiotherapy -+ Radiation proctitis
• Complication of Chemotherapy -+ Perirectal abscess

o Caused by N. gonorrhoeae

o Treatment:
• Early: Sucralfate (Butyrate) enema
• Late:
• Argon beam plasma coagulation
o For patient not responding to Sucralfate enema

• Formalin fixation
o High success rate, but associated with stricture

• Epinephrine injection
 Liver
Reviewed by:

Dr. Hamad Hadi A/Qahtani

Dr. Shadi A/Shammary

LIVER
ANATOMY
■ Liver weight 1500 g
■ Liver segments divided based on: Hepatic venous system
■ Liver divided as:

ltftlo� Left lobe

IVC Caudate lobe

First level 2 Lobes Second level 4 sections Third level 8 segments

(Divided by Cantlie's line) (Divided by 3 Portal scissurae) C0uioauc s:.1assifis:.ali00

"Between gallbladder and IVG" "Divided by 3 hepatic veins· {clockwise direction)
Middle hepatic vein travel along this
line
Rioht anterior V. VIII
Right lobe V, VI, VII, VIII
Rioht posterior VI, VII
Left medial (Quadrate lobe) IV
11, 111, IV
Left lobe
Left lateral 11, Ill
Caudate lobe I

o Gallbladder lies on segments (IVb and V)

o Bare area: posterior surface of liver not covered by Glisson's capsule (peritoneum
coverage of the liver), between anterior and posterior coronary ligaments
o Riedel lobe: inferior projection (extension) of right lobe of the liver

■ Falciform ligament:
o Divide segments Ill and IV
o Contains round ligament (ligamentum teres): Obliterated umbilical vein
o Separate Left medial & left lateral section of the liver

■ Liqamentum venosum:
o Contains remnant of ductus venosus -+ separates left lobe from caudate
o Marker for Left portal vein
CT image of liver segments

TRIPHASIC CT LIVER
■ Dynamic postcontrast imaging (3 phases) with precontrast:
o Early arterial phase (30 second)
o Portal venous phase (60 second)
o Equilibrium phase (90 second)

■ Gadoxetic acid, Primovist contrast (Eov/st):

-+
o Liver-cell specific MRI contrast 50% cleared by hepatobiliary excretion
o Help to differentiate between FNH, and adenoma
Blood supply:
■ Portal vein (75% of hepatic blood flow, 50% of hepatic oxygenation}
o Divided into right and left portal veins
o Right portal vein divided into:
• Right anterior (V, VIII)
• Right posterior (VI, VII)
o Left portal vein supplies segments (II, 111, IV)

8 3

RlQhl antenor
5

Right portal

■ Portal vein
o Forms from superior mesenteric vein joining splenic vein behind NECK of the pancreas
o Portal veins accounts 70% of hepatic blood flow
o Hepatic veins and portal vein differentiated by extension of Glisson's capsule
o No valves

■ Portal triad in the hepatoduodenal ligament (porta hepatis)

o CBD (lateral) -+ Most Anterior (to the right of hepatic artery)
o Portal vein (posterior)
o Proper hepatic artery (medial) -+ (right hepatic artery cross posteriorly to CBD)
Cystic duct is outside port hepatis

■ Foramen of Winslow = Epiploic Foramen

o Entrance to lesser sac (to the right of porta hepatis)
o Anterior: Portal triad (Free border of lesser sac; just behind hepatoduodenal ligament)
o Posterior 1vc
o Inferior: Duodenum
o Superior: Liver
 ■ Hepatic artery (25% of hepatic blood flow, 50% of hepatic oxygenation}
o Arises from celiac trunk

o Right hepatic artery

• 80% posterior to CHD
• Right anterior branch (V, VIII)
• BiQbl posterior branch (VI, VII}

o Middle hepatic artery

• Usually arising from left hepatic artery
• Supplies segment IV

o Left hepatic artery supplies segments I, 11, Ill

o Most liver tumors are supplied by: Hepatic artery (rather than portal vein}

o Ligation of hepatic artery proximal to GDA will not affect the liver because backflow from
the GDA goes to the liver

o Hepatic artery variants:

• Right hepatic artery:
• From SMA (Most common hepatic artery variant} 10- 15%
• Posteriolateral to CBD, hepatoduodenal ligament and head of pancreas
Gives -+ Right gastric artery (instead from proper hepatic artery)
• Left hepatic artery:
• From Left gastric artery (located in gastrohepatic ligament medially)

Venous drainage: "All drains to JVC"

■ Right hepatic vein
o Divide the right lobe into: Right anterior •v, VIII" and right posterior ''VI, VII"
■ Middle hepatic vein
o Divide the liver into: Right and Left lobe "IV and V, VIII"

■ Left hepatic vein

o Divide the liver into: Left medial "IV" and left lateral •11, Ill"
o Middle and left hepatic veins may join together and forms common trunk before enter
IVC

■ Caudate lobe drains directly to -+ IVC

■ Hepatic veins hemorrhage is the most common site for life threatening hemorrhage during liver
resection
PHYSIOLOGY AND LIVER ENZYMES
■ Total bilirubin: including direct bilirubin

■ Alkaline phosphatase (ALP -ALK):

o Source from liver (canalicular membrane), bone, and placenta
o More sensitive in predicting biliary obstruction
o Causes of elevation of ALP in Normall population:
• Infants, Late pregnancy, and after fatty meal

o Causes of elevation of ALP as a disease:

Elevated GGT Normal GGT
Normal CBD DIiated CBD Bone causes Other causes
Hepatitis CBD stone Fracture Renal failure
Heart failure
Primary biliary cirrhosis Hepatobiliary malignancy Vitamin D deficiency Hyperparathyroidism
MEN
Sarcoidosis Pancreatitis Metastasis Renal cell carcinoma
Lymphoma/Leukemia

■ Alanine aminotransferase (ALTl:

o Hepatic specific enzyme
o Correlate with abdominal adiposity
o Elevated in: NAFLD, Drug-induced liver injury, Hepatitis, Alcoholic liver disease

■ Aspartate aminotransferase (AST\

o Elevated in: Cirrhosis, Hepatitis, Biliarry diseases

■ 5-Nucleotidase: Most specific test for hepatobiliary disorders

■ Gamma glutamyltransferase /GGT\

o Most sensitive test for hepatobiliary d isorder
o Absent in bone and placenta

■ coaoulooathy
o As result of prolonged biliary obstruction
o Due to malabsorption of fat-soluble vitamin K, decrease production of coagulation
factors from the liver, and thrombocytopenia secondary to hypersplenism as a result of
liver cirrhosis/portal hypertension

■ Kupffer cells
o Liver macrophages {Primary defense against Lipopolysaccharide}

■ Ito cells (hepatic stellate cells)

o Principle mediator of fibrosis in cirrhotic liver
o Located in the space of Disse
o Characterized by presence of lipid droplets (Due to vitamin A storage)
■ Nutrient uptake: occurs in sinusoidal membrane
■ B12: the only water-soluble vitamin stored in the liver

■ i
Hepatic function after resect on: Synthesis & glucose metabolism

■ Hepatic function reserve:

o ICG test
o MEGX (for exocrine function also)
o Aminopyrine breath test

■ Hepatic synthesis function: PT (Best test for liver function)

■ Endoscopic sclerotherapy preserves hepatic synthesis perfusion

■ Acute Hepatic phase:

o t CRP, t Ceruloplasmin
t CRP in stress in patients with liver failure

o t Albumin, t Transferrin

■ Histology of liver cells·

o Consists of:
• Acini: around terminal portal venules, defined by blood flow and metabolism
• Lobules: around central hepatic venules, defined by venous inflow

o The hepatocytes of the acinus are divided into:

• Acinar zone 1
• Closest to the afferent portal venule where the sinusoids are smaller and
have many collaterals
• Receive blood with the highest concentration of oxygen
• Rich in Golgi apparatus (required for bile salt transport)

• Acinar zone 2
• Away from the portal venule

• Acinar zone 3 (Central lobular)

• Away from the portal venule, but closest to the central hepatic venule
• Less resistant to hepatotoxins (due to receive nutritionally depleted blood}
• 1 st zone to be compromised in low-flow or low-oxygenation state
(Hepatocytes most sensitive to ischemia in this zone)
■ Courvoisier's law
o Palpable non-tender gallbladder with jaundice is unlikely due to gall stones
o In patient with obstruction as CBD stone, gallbladder will be contracted, fibrotic and non­
distensible

o Associated with:
• Malignancy (Head of pancreas or uncinate process, distal CBD or Periampullary
tumors)
• Pancreatic stricture in chronic pancreatitis
• Portal lymphadenopathy

• Exception to this rule: (Not applicable in}

• Absence of gallbladder (post cholecystectomy)
• Intra-hepatic gallbladder
• Double impacted stone (Cystic and CBD stones+ GB mucocele)
• Large stone at Hartmann's pouch (Mirizzi syndrome)
• Empyemia of gallbladder with CBD stone
• Pancreatic calculus obstructing ampulla of Valer
LIVER FAILURE
■ Most common cause of liver failure: Cirrhosis
■ Most common cause of acute liver failure: Drugs or toxins (including acetaminophen}

■ Cirrhosis defined as end-stage liver damage with hepatocyte death and disruption of hepatic
parenchyma by diffuse fibrosis (Dense matrix material deposition in the perisinusoidal space)

■ Factors associated wjth improve prognosis and outcome of liverfailure·

o t Phosphate associated with improve prognosis of acute liver failure
o t Sodium (Na}
o t Protein intake < 50 g/day (to decrease ammonia rate and encephalopathy}
o Lactulose to inhibit absorption of ammonia by acidifying the colon
o Neomycin (non-absorbable antibiotics} reduce colonic flora and production of ammonia

■ Physiological changes:
o t Resting energy expenditure
o t Cardiac output
o t Systemic vascular resistance
o t Muscle and fat storage

■ Jmagjng findings io cjrrhosjs·

o Caudate lobe hypertrophy, and Right lobe atrophy
o Recanalization of umbilical vein
o Enlargement of portal vein diameter
o Ascites and Splenomegaly

■ Hemorrhoidectomy is relatively contraindicated in cirrhosis

■ t Lactate, t aldosterone, Glutamine produced by the lungs in liver failure

Child-Pugh score to assess severity of Cirrhosi s

Points
Clinical and Lab Criteria
1 2 3
Encephalopathy None Controlled Refractory
Ascites Absent Controlled Refractory
< 2 mg/dL 2 • 3 mg/dL > 3 mg/dL
Bilirubin
< 34 uMoVL 34 - 51 uMol/L > 51 uMol/L
> 3.5 g/dl 2.8 • 3.5 g/dl < 2.8 g/dl
Albumin
> 35 28- 35 < 28
< 4 seconds 4 - 6 seconds > 6 seconds
Prothrombin time INR > 2.3
I INR < 1.7 INR 1.7 • 2.3
Child A 5-6 points + Mortality 10% (FLR 50% = tolerate up to 50% resection}
Child B 7-9 points + Mortality 30% (FLR 75% = tolerate up to 25% resection}
Child C 10-15 points + Mortality 75% (Liver resection contraindicated)
■ Fulminant hepatic failure
o Caused by hepatic artery thrombosis
o Could be happens after liver transplantation
o Complications: Cerebral edema and intracranial hypertension
o Treatment: re-transplantation

■ Budd-Chiari syndrome (Hepatic vein thrombosis}

o Etiology:
• Hypercoagulable conditions (Most common in west}
• Myeloproliferative disorders "Most common•
• Polycythemia vera
• Protein C or S deficiency

• High estrogen (Pregnancy or postpartum, OCPs}

• Membranous venous web {Most common in Asia)
• Others (trauma, tumor, postoperative)

o Pathophysiology:
• Obstruction at level of IVC, hepatic veins or central veins in the liver
• Leads to post-hepatic (Post-sinusoidal) portal hypertension
• Leads to Caudate lobe (segment I) hypertrophy and atrophy of right lobe

o Presentation:
• Abdominal pain, Ascites (Most common}, and Hepatomegaly
• Lower leg edema if caudate lobe obstructing the IVC

o Investigations:
• Doppler U/S •initial test of choice•
• Hepatic venography "Most specific tesr
• Spider-like appearance of multiple hepatic veins on venogram

• CT scan: Central + Delayed peripheral enhancement (unlike hemangioma}

o Management:
1) Anticoagulant (used initially in early acute obstruction}
2) Thrombolysis and angioplasty (for venous web obstruction)
3) Associated with liver damage

Reversible liver damage:

• Side-to-side portocavel shunt: Replaced nowadays with TIPS
• Patent IVC + TIPS
• Obstructed IVC + Mesoatrial shunt
Irreversible liver damage: "thrombosis of all hepatic veins"
• Liver transplant
HEPATORENAL SYNDROME
■ Liver cirrhosis associated with progressive renal failure in absence of intrinsic renal disease
■ Poor prognosis for patient with liver cirrhosis
■ Investigations:
o t Urine Na, FeNa < 1%
o ! GFR
o t Osmlarity
o Proteinuria

■ Types:
o Type 1:
• Progress rapidly
• Pathophysio!ogy:
• Precipitated by event th.at causes acute on top of chronic liver failure
• Leading to multiorgan failure (renal failure is a part of multiorgan failure}
• Splanchnic vasodilation and renal arterial vasoconstriction
� Renal hypoperfusion and renal failure

• Treatment:
• Treat the cause

o Type 2:
• Progress slowly
• Pathophysiology:
• Fluid shift from intravascular to extravascular (as ascites)

• Treatment:
• Exclude primary renal causes
• Treat the liver failure
• Treating the ascites (as TIPS) may help in treatment of type 2 HRS
• Sodium and water restriction
• IV fluids, Octreotide, Midodrine, and Vasopressin analogs
• Diuretics (Only if caused by ascites}
BENIGN LIVER TUMORS
LIVER CYST LESIONS
■ Traumatic cysts
o False cyst (no epithelial lining)

o Management:
• Asymptomatic: Conservative
• Symptomatic:
• Bile leak:
o ERCP and sphincterotomy
o Surgical ligation of leaking bile duct if ERCP failed

• Pain, Compression, or Hemorrhage

o Surgical resection

■ Simple cyst
o Most common benign liver lesion overall, and most common type of cyst
o Single layer of cuboidal or columnar cells without atypia lines
o Contain serous fluid, do not communicate with the biliary tree, with no septations
o Usually asymptomatic
Symptoms appears in: > 5 cm size, peduncu/ated, or hemorrhagic

o CT findings:
• Well-demarcated homogeneous anechoic lesions with smooth borders, oval or
round in shape, without internal structure and no contrast-enhancement

• Signs of suspicious neoplasm:

• High-density fluid(> 10 Hounsfield units)
• Wall enhancement(irregular thickened wall), Internal septation
• Mural nodularity, and papillary projections

• Signs of infection:
• Wall thickening
• Debris inside lesion
• Multiloculation

• Signs of hydatid cyst:

• Endocysl/pericyst interface
• Calcification
• Daughter cyst
 o Management of simple liver cyst:
• Asymptomatic: Observation
• Symptomatic (vague abdominal pain, early satiety)
• Aspiration only (As temporary method; not-preferable)

• Aspiration and contrast instillation (After re-occurrence)

o Biliary or perjtonea! commynjcations
• MRCP, No sclerosing agent (Contraindicated)

o No biliary or peritoneal communications:

• Sclerotherapy (95% ethanol or minocycline hydrochloride)
• Alcohol retained for 2 to 4 hours, then aspirated
• 10% recurrence rate

• Surgical deroofing (Fenestration, Marsupialization)

o Gold standard
o Steps:
• Cyst is punctured
Bile -+ intraoperative cholangiogram
• Anterior wall is excised completely with no resection of liver
• Cyst wall sent to histopathology
Cystadenoma or cystadenocarcinoma -+ Further resection

■ Polycystic liver disease

o Usually associated with multiple cysts in the liver and kidney
o Usually asymptomatic. but associated symptoms could be:
• Pain
• Compression
• Early satiety (Stomach)
• Dyspnea (Diaphragm}
• Peripheral edema (IVC}
• Portal hypertension (Portal vein or hepatic venous outflow)
o Ascites or varices as complications of portal hypertension
• Jaundice (Biliary)

o Management of symptomatic disease:

• Aspiration alone: for infected cyst
• Sclerotherapy: Usually not effective
• Open cyst fenestration: For few very large cysts
• Combined resection and fenestration: For massive cystic disease
• Liver transplant :!: renal transplant: Most effective treatment
 ■ Cystadenomas and Cystadenoeareinomas
o Pathology:
• Mucin-secreting columnar/ cuboidal epithelium with atypical spindle cells

o Investigations:
• CBC, Blood culture, Echinococcus serology, Amebic titer
• Stool analysis for parasites
• CEA, and CA19- 9
• U/S and MRI (CT not useful for internal septation)

o Signs of suspicious neoplasm:

• Large Multi-locular septated cystic mass (10 - 20 cm)
• High-density fluid (> 10 Hounsfield units)
• Wall enhancement (irregular thickened wall)
• Internal septation, Mural nodul.arity, and papillary projections

o Cystadenomas (premalignant lesion)

• Most common primary cystic tumor of the liver
• Consist of3 layers:
• Inner epithelium (Cuboidal or Columnar)
• Middle mesenchymal stroma
• Outer collagen connective tissue layer (pseudocapsule)
Which separate the cyst from liver parenchyma
• Types:

With ovarian stroma (true cystadenomas) 80% Without ovarian stroma (IPMN-B)
lntraductal Paoillarv Mucinous Neoolasm of bile duct
Exclusivelv in women Affect both aender
Usuallv contains ER and PR receotors Usuallv communicates with the biliarv tree
More favorable oroanosis Less favorable oroanosis /Premalianant ,v,tential\
Management options:
■ Enucleation •
Management options:

•• Partial liver resection

Partial liver resection
± lntraoperative cholangiogram
± lntraoperative cholangiogram ± Extrahepatic biliary resection
+ Portal lvmohadenectomv
Communication with bile duct -+ Bile duct resection with bllioenterlc reconstruction

o Cystadenocarcinomas
• Usually do not communicate with the biliary tree
• Rupture of the cyst should be avoided, as it may lead to carcinomatosis
• Early changes of malignant progression: intestinal metaplasia
• Management:
• Formal resection + lntraoperative cholangiogram
To rule out other diagnosis if communicates with biliary tree
(fPMN-8 or Cholangiocarcinoma)
 ■ HYDATID CYST
o Zoonosis caused by: Canine tapewo•rm
o Most common site: Right lobe of the liver (inferior segments)
o Associated with biliary fistula in 20 - 30%
o Jaundice appeared if the cyst rupture<! into biliary tree

o Primary host: Dogs

o Intermediate hosts: Sheep , goats, camels, and humans
o Portal circulation -+ Liver (80%), lungs, brain and bones
o Route of infection: Fecal-oral transmission of larval form of dog tapeworm (Canines)
• Echinococcus granulosus
• Echinococcus multilocularis more at north areas, with multiloculated cysts

o Consist of 2 layers:
• Inner (endocyst, Scolices): Single germinal layer (Active layer)
• Outer (pericyst): Thick acellular layer (Calcified in 50%)

o Investigations:

Specific Non-specific
ELISA Eosinophilla in 30 - 40%
Sensitivity of 85%

Negative in infected cyst if no leak or non,viable

Can be positive 4 years post-treatment

(Not suitable for follow-uni
lmmunoelectrophoresis Indirect hemagglutination test
Used for oost-treatrnent follow-uo Sensitivitv of 90%
Hydatid antigen western blotting 95% Casoni's skin test
■ Antigen B (intradermal injection of sterilized fluid from hydatid cyst)
■ Arc antigen 5
Sensitivity of 70%
Used as confirrnatoN test and best for diaanosis

o Imaging: "U/S, CT, ERCP (in cholangitis or jaundice)"

• Well-defined hypodense lesions with a distinct wall
• Ring-like calcifications of the p,ericysts (25 - 30%)
• ERCP used only to rule out communication with biliary tract (20 - 30%)
• Radiological signs:
• Water lily sign "floating membrane": Detached membrane (rupture)
• Spin or Whirl sign: Detached membrane
• Snowflake sign: Free-ffloating protoscoleces
• Serpent sign: Internal rupture of the cyst with collapsed membrane
• Hydatid sand: Daughter cyst
• Honeycomb: Granddaughter cysts (Rosette appearance)
 Management:

■ Albendazole followed by surgical treatment (Gold standard}

Monotherapy Indications Contraindications Side effects

Initial treatment for< 5 cm cyst in Complicated inactive Neutropenia
poor patient for intervention CE1 (CE 4/5 Calcified cyst)
Medical only
BM suppression
Asymptomatic non-complicated cyst Pregnancy
(Albendazole,
Hepatotoxicity
Mebendazo/e)
BM suppression

Chronic liver disease

Initial treatment for:
■ Small< 5 cm High-risk locations Chemically-induced
■ Uni-locular (should be avoided in sclerosing cholangitis
■ Anterior cyst peripheral cyst due to
■ Peripheral cyst risk of leak) if sclerosing agent
PAIR
introduced in biliary fistula
CE1, CE2, CE3
Cyst with biliary fistula
High risk patient for surgery
Infected or recurrent disease Complicated cyst
/inactive or calcified\

••
Indications:
Biliary tract fistula

••
Near to major structure (portal, hepatic veins, or bile ducts)
Mass effect

•••
Surgery Rupture or infected
Difficult sites for PAIR (Posterior or non-peripheral cyst)
(Liver Resection,
Multiple daughter cysts
Transplantation)
Large > 5 cm calcified cyst

•• Recurrent diseases with failure of other management

Technicallv not feasible to remove aerminal laminated laver bv cvstectomv onlv

■ Surgical techniques:
o Laparoscopic: Small< 5 cm, uni-locular, anterior and peripheral cysts
o Open: Large> 5 cm, multiple> 3 cysts, posterior or central, Heavy calcified

Caoitonnaae Evacuation of the cvst and closure of the cavitv

Fenestration Evacuation of the cvst and leave a hole in it
Marsupialization Partial enucleation (Evacuation of the cvst and excision of superficial walls}
Cvstectomv Enucleation of the cvst /Excision of the cvst comoletelv with the caosule\
Pericystectomy Excision of the cyst completely with a rim of liver tissue
■ Closed: without entering the cyst (without aspirating cyst content)
(Associated with ■ Open (Preferable): aspirating the cyst content followed by injection of
lowest recurrence) sclerosina aaent i20% hvnertonic saline) for 15 min followed bv oericvstectomv
Liver resection Non-anatomical or anatomical
Mainlv used for: Larae size or recurrence
Liver transplant In E. multilocularis with multiple cysts resulting in concurrent fulminant liver failure
from sclerosina cholanaitis Budd-Chiari svndrome or biliarv sclerosis
Management of Hydatid cyst:

■ Medical treatment: (Albendazole, Mebendazole)

o As monotherapy successful rate only 30%
• {10 - 15 mg/kg/d divided BID) for 3 - 6 months or stop postoperative

o Combined with Praziquantel (40 mg/kg once a week) is more effective

■ PAIR (Percutaneous puncture, Aspiration, Injection, and Re-aspiration)

o Albendazole given 4 hours pre-intervention and 1 month post-intervention

o Percutaneous drainage is not preferred (high risk of peritoneal leak and anaphylaxis}
unless large cyst (>10 cm), unilocular, uncomplicated disease with drainage catheter
left in place until output < 10 ml / day

0 Steps of PAIR:
• U/S guided PCA

• Injection of indwelling scolicidal solution for 10- 30 minutes, then re-aspiration of

the agent as sclerosing agents:
• 20% Hypertonic NS {risk of hypernatremia), Ethyl alcohol
• 95% Ethanol, Nitrate solutions, Tetracycline
• Hydrogen peroxide, Povidone iodine, Chlorhexidine, or Formalin

• Irrigation with NS

Sc/erosing agents are contraindicated if cysts are communicating with biliary tract because
chemically-induced sc/erosing cho/angitis

■ surgical intervention
o Preoperative Albendazole followed by surgery then, Albendazole for 1 month post-op
o Cystic leakage puts the patient at risk of anaphylactic reaction (release of protoscolices)
o Plane at level of xiphoid is important for hydatid cyst resection
o Assessment of biliary communication:
• Preoperative MRCP
• Postoperative ERCP (for persistent postoperative bile leak)
• lntraoperative application of diluted hydrogen peroxide in the cyst cavity

o Options for bile duct communication:

• Placement of an external drain along the cyst cavity
• Direct suture ligation with absorbable sutures followed by omentoplasty
• Bilioenteric anastomosis: for large bile duct fistula
 ■ Management based on WHO classification:

Gharbi tvoe Cvst tvne Status lmaaina Manaaement

Type I CE1 Unilocular (Simple cyst) < 5 cm: Albendazole or PAIR

> 5 cm: Both

Type Ill CE2 Active Multilocular
With daughter cysts

(Rosette-like appearance)
(Honeycomb aooearance)
Albendazole + PAIR
Type II CE3 Complex cyst
Surgery
With daughter cysts
Transitional
Water li/Jt_ sign:
(Detached membraneI
Type IV CE4 Heterogeneous
No d.aughter cysts
Watch and wait
Inactive (Ball of wool)
"Complicated cyst' Surgery + Albendazole
TypeV CES Thick calcified wall

fCone-shaoe shadow)

Completely calcified hydatid cyst associated with eggshell appearance

 LIVER ABSCESSES {all fin right lobe)
Pyogenic
Most common liver abscess in
USA
Pain, Fever, Jaundice
SecondaQl to infection:
- Biliary tree (Most common)
c:> Cholangitis
Presentation
Past history of: (Routes)
- Diverticulitis, Appendicitis
- Post liver transplant
- Subcutaneous abscess
- Endocarditis
Gram -ve (E.Coll, Klebsiella)
Organism
Anaerobic (Bacteroides)
Leukocytosis, t ALP level
Positive blood culture (50%)
Imaging:
Well-defined hypoechoic /
Investigation hypodense round lesion with
well-defined wall
(Peripheral enhancement)
More likely to be multiple
± Internal echoes
+ air-fluid levels
IV antibiotics
First line of therapy, for 4 - 6
weeks
Management Drainage
(if no response to antibiotics)
- Percutaneous drainage
- Closed aspiration
- Suraerv
Amebic Schistosomiasis
{Not an Abscess)
Most common liver abscess overall Most common cause of
portal hvnertension
Travel to Mexico, Alcoholic Pre-sinusoidal portal
hypertension
Pain and fever
Maculopapular rash
Within a year of colitis
Hypersplenism
Most common site: (No sp/enectomy unless
hemato/oglcal disease)
Superior-anterior right lobe of the
liver
Entamoeba histolytica in pus / serum
t ALP level Normal AST, ALT
Mildly f ALP
Serology tests "Enzyme immunoassay"
(Positive amebic fluorescent antibody)
Complement fixation
gi
Ima n :g test
Well-defined hypoechoic / hypodense
round lesion with wall enhancement t Portal vein pressure
(Peripheral rim edema)
± Central necrotic area Periportal fibrosis
± reddish-brown material "Pipe-stem"
(Anchovy paste, Chocolate sauce)
Metronldazole Prazlquantel
40- 75 mg/kg
As single dose
Percutaneous closed-aspiration
(if medical treatment failed) Surgical
decompression for:
- Advanced stas:ie
- Recurrent bleeding

■ Elevation of right diaphragm on CXR favors diagnosis of abscess rather than cholangitis
■ Necrotic hepatic malignancy must not be mistaken for hepatic abscess

■ Most common organisms related to hepatic abscess:

o E. coli: Most common organism isolated from hepatic abscess
o Klebsiella: Associated with multiple liver abscesses, more in eastern region

■ Septic work-up including blood culture should be obtained for all abscesses
Management of liver abscess:
■ Pyogenic abscess:
o IV antibiotics :!: 8 weeks (< 4 weeks if proper drainage done)
• Mainstay therapy for multiple small abscesses
• Choice of antibiotics in pyogenic abscess depends on presumed source·
• Colonic source: Fluoroquinolone / 3rd cephalosporin + metronidazole
• Biliary source: Piperacillin-tazobactam
• Malignant biliary obstruction: Meropenem and linezolid
• Liver transplant: + Fluconazole
• Subcutaneous abscess or endocarditis: Vancomycin

o Percutaneous drainage
• Aspiration was the standard because high viscosity, but recently drainage
showed more effective than aspiration alone

o Surgical intervention and drainage

• Failure of drainage or Rupture
• Contraindication of percutaneous drainage:
• Ascites
• Intra-abdominal source of infection
• Need for trans-pleural d rainage
• Multiple large pyogenic abscesses

o Steps of drainage:
• Midline or right subcostal incision
• Localized of liver abscesses by intraoperative U/S
• Isolate the area by cover the rest of abdomen with towels
• Aspirate the abscess and send fluid for culture for directed antibiotics
• Irrigation and suction of the cavity
• Tract is enlarged and debridement done with breaking all pockets
• nssue culture is taken to exclude malignancy
• Drains placed inside abscess cavity an peri-hepatic area

■ Amebic abscess
o IY antibiotics
• Metronidazole: 750 mg TIO for 7 - 10 days
• Paromomycin, diiodohydrox.yquin, or diloxanide furoate (for 1 - 3 weeks)
Used for intra-Juminal cysts eradication (if not used � 10% relapse)

o Percutaneousdrainage
• No response after 5 - 7 days of antibiotics
• Ruptured, or High risk for rupture{> 5 cm, Located in the Left lobe)

o Surgery
• For hemorrhage, erosion into surround organs, or sepsis with failure of PCD
 LIVER BENIGN LESIONS
Adenoma
OCPs in young women
Anabolic steroid in men
t rupture & bleeding
Presentation t malignant risk in women
ft t malignant risk in men
30% Multiple (Not due OCPs)
Monoclonal proliferation of
Pathology heoatocvtes onlv
Vacuolated hepatocytes
(glycogen & lipid deposition)
Histology No bile ducts
No Kupffer cells
Capsulated lesion
Arterlal
phase Early peripheral
Homogeneous enhancement
(Heterogeneous if recent
{Hypervascular hemorrhage or necrosis)
lesions)
lntra-lesional fat or bleeding
Hypodense lesion
(Hyperdense if inflamed)
Venous
phase
Focal nodular hvoerplasia
Associated in young patient
No malignancy risk
Equally disturbed throughout the liver
and usually located peripherally
Thought to be cause due to
developmental vascular malformation
Benign polyclonal proliferation of all
cellular elements
Central stellate scar with septa
Bile canaliculi
Kupffer cells
lmaaina
Homogeneous enhancement
Non-capsulated lesion
No calcifications
lsodense lesion
Rapid washout
Central stellate scar that
enhanced on arterial phase
(20% have absence of the scar)
Hemanqioma
Most common benign
hepatic tumor
20% Multiple
No malignancy risk
Spontaneous rupture is rare
+ AV fistula, Heart failure
+ Kasabach-Merritt svndrome
Endothelial vascular channels
enclosed within fibroblastic
stroma, fed by hepatic artery
Peripheral nodular discrete
enhancement
light-bulb sign on MRI
Centripetal progression
(peripheral to central)
- Peripheral enhancement
- Peripheral puddling
Associated with return of
contrast in blood pool in
delaved ohase

• i
Investigat ons:
0 Triphasic CT scan of the liver
0 MRI liver if equivocal findings
0 RBCs scan is the most specific test for hemangioma
99
0 T Sulfur colloid/ Eovist uptake

.
• t in FNH as ''hot nodule" due to presence of Kupffer cells
! in adenoma as "cold nodule

■ Bile duct hamartomas are the most common benign lesions of the liver seen during laparotomy
Management of benign liver lesions:

1) Hemangioma
o Asymptomatic: Observation (No biopsy)
o Symptomatic (Usually large, peripheral located hemangioma � capsule stretching)
• Symptoms:
• Pain, Hemorrhage
• Kasabach-Merritt syndrome
o > 10 cm, Coagulopathy (!Platelets,! Fibrin, t Fibrin degradation)

• Treatment:
• Rule out other causes (Upper GI endoscopy, U/S)
• Angioembolization (Only in case of bleeding)
• Resection (Enuc/eation for small, peripheral site, or Partial resection)
o For failure of embolization
o After embolization for complications-related
(Rupture, Hemorrhage, or Twisting)

2) Adenoma
o Treatment:
• Surgical Resection (Wedge resection or Formal resection "No Enucleation'1
• Standard of care for all adenoma, regardless the size

• Discontinue OCPs and anabolic steroid and life-long follow-up, Option for:
• Asymptomatic adenoma < 5 cm lesion that regress on follow-up

o Adenoma with hepatocyte nuclear factor-1 (HNF) associated with no risk of bleeding or
malignancy, and should not be resected

o Adenomatosis: (> 10 adenomas)

• Discontinue OCPs first
• Resection for > 5 cm lesions
• RFA for residual lesions
• Liver TXP for aggressive disease

3) FNH
o Treatment:
• Observation
• Indication for resection:
• Symptomatic (Persistent pain)
• Rupture and hemorrhage (resection after the embolization)
• Inability to rule out malignancy
MALIGNANT LIVER TUMORS
■ Most common solid tumor worldwide: Hepatocellular carcinoma
■ Most common malignant liver tumor in children: Hepatoblastoma
■ Survival rate depend on size of liver tumor
■ Recurrence depends on vascular invasion
■ Risk factors:
o HBV (most common risk factor) and HCV

o Non-alcoholic fatty liver disease (NAFLO)

o Aflatoxins (carcinogenic toxins from Aspergil/us), azo dyes, aromatic amines

o Arsenic and Vinyl chloride (Liver angiosarcoma)

o N-nitrose compounds, pesticides, and porphyria

o Hemochromatosis

o Alpha anti-trypsin deficiency

o Budd-Chiari syndrome

o Oral contraceptives, anabolic steroids, radiation, smoking

■ lovestjgatjons·
o Tumor marker for HCC:
• Alpha-fetoprotein (> 400 ng/ml), CEA, and CA 19-9
• Used for screening but not for diagnosis
o Not an accurate tool for screening because usually normal in early
HCC, and the recommended screening tool is Ultrasound

• Alpha-fetoprotein along with U/S used for screening in patients with HCV

o Ultrasound abdomen

o Triphasic CT scan of the liver

o MRI liver

o Image-guided FNA biopsy of liver mass

• Used for> 1 cm but< 2 cm liver mass with atypical combined findings by CT
scan and MRI
Types of primary malignant liver tumors

■ Hepatocellular carcinoma
o HCC usually invades toward portal vein (Unlike metastasis)
o Associated with: Liver cirrhosis and PVT
o Most sensitive and specific investigation: AFP and U/S
o Biopsy is not indicated if diagnosed by imaging and AFP
o Adenomatous hyperplasia � atypical hyperplasia � HCC
o Causes of elevated alpha-fetoprotein:
• Inside Liver: HCC, Hepatoblastoma, Metastasis, Cirrhosis, liver failure, Carcinoid
• Outside Liver: Germ cells tumor, Pregnancy

■ Fibrolamellar hepatocellular carcinoma

o Primary neuroendocrine tumor of the liver (in young patients)
• No parenchymal liver injury or cirrhosis

o Imaging:
• Capsulated lesion with hetero,genous enhancement
• Non-enhanced scar
• Associated with Calcification 70%

o Histology:
• Polygonal tumor cells embedded in fibrous stoma
• Abundant mitochondria (Eosinophilic appearance)
• Bile canaliculi

o Doesn't produce AFP (Associated witih elevation of neurotensin level)

o Best prognosis
• 5-year survival rate after surgical resection: 30% - 50%
• Nodal metastases: 15% - 30%

■ lntrahepatic Cholangiocarcinoma
o Associated with sclerosing cholangitis, choledochal cyst, viral hepatitis and cirrhosis
o Does not associated with High AFP
o Types:
• Mass forming
• Periductal infiltrating: Most common type, and worst prognosis
• lntra-ductal

o Management:
• Mistaken for metastases of unknown origin
• Upper GI endoscopy, Lower GI endoscopy, Mammogram
• ± Liver FNA to rule out metastasis
• Diagnostic laparoscopy {To rule out peritoneal metastases)
• Surgical resection is potentially curative (5-year survival rate: 44% - 63%)
Triphasie CT findings of Liver mass

HYPERVASCULAR lesions "Hyper-attenuation" of the liver

Benign lesion
Associated with return of contrast in blood pool in delayed phase
Centripetal filling (peripheral to central) on delayed phase
Hemangioms - Peripheral enhancement, puddling
- Perioheral to central nodular enhancement /Liaht-bulb sian\
Arterial phase:
lntra-lesional fat or bleeding
Adenoma Capsuled heterogenous with early peripheral enhancement

Venous ohase: Hvnodense lesion /Hvoerdense if inflamed)

Arterial phase;
Non-capsulated hypervascular lesion with homogeneous enhancement,
and no calcifications
FNH
Venous phase:
Rapid washout isodense lesion with central stellate scar that enhanced
on arterial phase
Malignant lesions (Prima0£)
Capsulated lesion with heterogenous enhancement
Fibrolamellar HCC Non-enhanced scar
Associated with calcification 70%
Capsulated (pseudocapsule) rapid-enhanced lesion with early wash out
(Hypodense in venous phase)

HCC 90% Early wash-out malignancy:

- Hepatocellular carcinoma
- Renal cell carcinoma
- Functional neuroendocrine tumors
Metastasis Carcinoid, Leiomyosarcoma, Breast, Renal or Thyroid metastasis

HYPOVASCULAR lesions of the liver

Hypodense lesion in Portal phase
Slow washout with irres:iular border
CRC Metastasis
(Most of metastasis) Differentiated between hemangiomas and FNH by:
■ Peripheral ring enhancement
■ Perioheral wash-out
Delay heterogenous enhancement
Intra-hepatic Retraction of liver capsule
cholangiocarcinoma Peripheral biliary dilatation
Fibrous stroma
HCC 10%
Others Lymphoma, Hepatic infarction, Focal fatty infiltration
■ Markers for fibrogenic activity:

o Invasive:
• Liver biopsy
• Gold standard for fibrosis and cirrhosis, can predict degree of liver fibrosis
• Not preferred in:
o Highly suspicious of metastasis (from colorectal cancer)
o Highly suspicious of HCC (by imaging and elevated AFP)
o Imaging findings of Simple cyst, Adenoma, FNH or Hemangioma
o High lesions (as in dome of segment VII) -+ Pneumothorax
o Near adjacent organs (as tip of segment Ill) -+ Stomach injury
o Near to IVC (as in caudate lobe or posterior segment V)

o Non-invasive:
• Serum markers
• AST/ALT ratio

• Fibrometer (Age, platelet count, prothrombin index, AST, a2-macro­

globulin, hyaluronan, urea}: Highest specificity than AST/ALT ratio

• Clinical scoring:
• Forns Index: (Age, platelet count, yGT, cholesterol)
o Highest sensitivity (predict patients with low risk of fibrosis only}

• Child Pugh score: (Ascites, Encephalopathy, Bilirubin, PT, Albumin)

o Predict mortality in chronic liver disease exceeding 1 year

• MELD score: (Creatinine, INR, Bilirubin}

o Predict 3 months mortality for patient with chronic liver disease
o Predict if patients with benefit from liver transplant in cirrhosis
o MELD score > 15 benefits from liver transplant

• Transient Elastography (Fibroscan): similar sensitivity and specificity as liver

biopsy, can predict mild vs. advanced liver disease (poor for intermediate stages)
■ Assessment of hepatic reserve and function preoperatively:
o Static tests
• Child-Pugh score
• Bilirubin for excretion
• Alkaline phosphatase for cholestasis
• AST / ALT for hepatoce llular integrity
• Albumin and Coagulation profile (PT) for hepatic synthesis

o Dynamic tests
Clearance half-life
• lndocyanine green clearance test (ICG)
• Most widely used test
• lndocyanine green retained in plasma after 15 minutes
o 15% - 20% dye remaining: Tolerate 2 segments resection
o 21 % - 30% dye remaining: Tolerate 1 segment resection
o > 40% dye remai:ning: Post-operative liver failure

• Galactose elimination test

• Caffeine clearance test

Metabolite formation
• CO2 exhalation
• Aminopyrine breath test
• Erythromycin test

• Metabolite in serum
• Lidocaine test (MEGX)
• Midazolam test

o Volumetric estimation /CT Scan or MRI}

• Adequate Future Liver Remnant (FLR)
• > 20% For healthy, non-cirrhotic liver
• > 30% For liver-induced injury (Post-chemotherapy)
• > 40% For evidence of cirrhosis or chronic liver disease

FLR volume should be 2: 2 segments near to each other with intact inflow, outflow "> 300 mUm2"
■ Management approach:
o SURGICAL RESECTION
• Treatment of choice of HCC and most CRC metastasis
• HCC usually invades toward portal vein
• Usually requires segmental resection unlike metastasis (wedge resection)

• Rules for surgical resection:

• Single lesion with adequate Future Liver Remnant (FLR)
• No cirrhosis or Cirrhosis with preserved liver function (Child A)
• No associated diseases (portal pressures s 10 mm Hg)

• Alternative for resection who meet above criteria:

• RFA for < 3 - 4 cm ancl < 3 lesions
• Thermal or Ethanol ablation for < 2 - 3 cm and < 3 lesions
• Transplant for Child A best if> 3 cm lesion who meet Milan criteria

Atrophy-Hypertrophy complex:
• Controlled restoration of liver parenchyma following hepatocyte loss
• Due to impairment of bile flow, portal or hepatic venous blood flow
(Mostly due to malignancy)
� lpsilateral liver atrophy and contralateral liver hypertrophy
• Some ways were invented to create the AHC, as Portal vein embolization
t
• Leading to depletion of electrolytes(! Mg ! PO. Platelets)

Portal vein embolization for contralateral hypertrophy:

• Transhepatic route is the preferred technique
• Used to allow extensive resection or for patients with inadequate FLR
• FLR < 20% in normal liver
• FLR < 40% in compromised liver

• Surgery planned after 4 weeks from PVE

• Liver reservoir increases within 6 weeks:
• 10 - 15% in non-embolized liver
• 20 - 25% in embolized liver

o OR THOTOPIC LIVER TRANSPLANTATION

• For cirrhosis with no cardiopulmonary conditions
• Milan criteria
• 1 lesion < 5 cm
• 1 - 3 lesions < 3 cm
• No extrahepatic spread (including lymph nodes)
• No vascular invasion

Not fit ? -+ RFA / TACE

o RADIOFREQUENCY ABLATION IRFAl
• Radiofrequency ablation by generating of heat > 60 degree C
• Crye-ablation by generation of cold energy
• Ethanol ablation used for s 3 nodules or s 3 cm associated with liver disease

• Indications:
• Child A I B / C not fit for Surgery or Transplantation
• Non-resectable metastasis
• As bridge before Transplant

• Relative contraindications:
• Near vascular structures (low effectiveness due to "heat sink" effect)
• Near biliary ducts (risk of stricture, fistula, or bile leak)
• Severe cirrhosis (Child C)
• > 3 lesions or > 3 cm size

• Bi-polar RFA can be used for lesions up to 5 cm)

• Occlusion of the hepatic artery, or portal triad (Pringle maneuver) used to

minimize "heat-sink" effects during ablation

o EMBOLIZATION
• Indications:
• Intermediate stage on Barcelona Clinic Liver Cancer (BCLC)
o Multinodular> 3 lesions in Child A - B

• Surgically unresectable without vascular invasion or extrahepatic spread

o Inadequate FLR
o Child B waiting for liver transplant

• Relative Contraindication:
• Portal vein thrombosis
• Child C (risk of hepatic decompensation)

• Options:
• Transarterial chemoembolization (TACE) by cisplatin / doxorubicin
• Transarterial embolization (TAE)
• Radioembolization

• Complications;
• Post-embolization syndrome (Post TACE Syndrome)
o Abdominal pain, nausea, vomiting, and mild fever
o Treatment: Supportive
o The most serious consequence: Hepatic failure
HCC WITH PORTAL VEIN THROMBOSIS
■ PVT associated with HCC in 10 - 40%
o Most common cause of PVT in children is umbilical vein infection

■ Management options:
o Surgical resection
• Controversial and associated with recurrence and poor outcome, especially if
involving the main bronchus

o Transplantation
• Contraindicated due to high rate of recurrence

o Transarterial embolizatlon
• Transarterial chemoembolization (TACE) is contraindicated due to high embolic
effects leading to hepatic necrosis and hepatic insufficiency

• Transarterial radioembolization (TARE) is an option

• Recently, it improves outcome in selective patients

(Non-occlusive with preseNe liver function I Not involving the main bronchus)

o Systemic therapy "Sorafenib: oral multikinase inhibitor" the only therapy specifically
recommended for unresectable HCC with PVT
• Indicated in:
• Not surgical/ transplant candidate
• 2: 4 lesions
• Gross Vascular/ Lymphatic invasion
• Metastasis
 ■ Summary according to Barcelona Clinic Liver Cancer (BCLC} for HCC:

Chi\d A I I Child A/B

I
I.
Very early stage Early stage
I
Intermediate stage Advanced stage
Single< 2 cm Solitary, Multinodular Portal invasion

.. ..
3 nodules s 3 cm (> 3 lesions) N1, M1

Portal hypertension
l Bilirubin
Associated Diseases ?

I
I I
' '
Np
II ,Yes I Yes
. No I
I Solit�ry
+
II Multi-nodular
♦
I
I Resection
11 RFA
11 Resection
11 Transplant
11 TAC_
I I Sorafenib

�------- C_u_ra_ tiv

_ _e_ t_rea
_ _ tm
_ _ e_n_t_______ L.I _ _ _P_ a_ll_ia_tiv_ _e_ tre_ _ a_tm_ _e_n_
�I _ t
_ _ __,
_

■ For patients not fit for transplant or surgery:

Not-Candidate for
Surgery
Fit to Milan criteria
1 lesion< 5 cm
7 Yes
I
I
.
I Transplant
I
1 - 3 lesions< 3 cm
Candidate for
Transplant
No Extrahepatic spread
No Lymphovascular invasion ----j No I
'
I
> 3 lesions < 3 lesions Severe cirrhosis
> 5 cm lesion S 5 cm lesion (Child B > 8, Child C)
Near vascular structure Far from vascular structure Vascular invasion
Near biliary duct Far from biliary duct Extra-hepatic spread
Associated with: Portal HTN, Jaundice
I
I
--. t
TACE RIFA Symptomatic treatment
METASTASIS FROM COLORECTAL ORIGIN
■ Synchronous metastasis
o Resectable
• Simultaneous resection "Preferable"
• Used in favorable risk factors (as low-risk patient, < 70 years)
• Isolated liver metastasis are 10 - 25% resectable

• Colonic resection + Adjuvant chemotherapy + Liver resection "Safest"

• liver resection usually in 6 weeks after chemotherapy if resectable
• Used if associated with unfavorable risk factors:
o High-risk patients or> 70 years
o > 1 liver lesion
o Extra-hepatic dis ,ease
o Requires > 1 lobectomy

• Liver resection + Chemotherapy± Radiation + Colonic resection

• Used in:
o Rectal cancer (long time between radiation and resection of tumor)
o Extensive liver disease (may progress to unresectability)

• Preoperative chemotherapy followed by 1-stage or 2-stages surgery

• Controversial (because it can make liver metastasis disappears)
• Indicated only for;? 5 metastases

Others advice for 2 - 3 .courses of neoadjuvant chemotherapy in all

patients with resectab/e liver metastases

o Unresectable
• Down-staging by neoadjuvant chemotherapy for 4 - 6 months (12 weeks)

■ Metachronous metastasis
o Resectable
• Associated with favorable risk profile:
• Solitary < 5 cm tumor
• Disease-free interval (DFI)> 12 months
• No extra-hepatic disease
• No lymphatic invasion
• CEA < 200 ng/ml

• Yes + Resection
• No + Neoadjuvant chemotherapy
o Unresectable
• Down-staging is the goal by neoadjuvant chemotherapy
■ Disappeared liver lesions after neoadjuvant chemotherapy
o Rarely represents a pathologic complete response

o Management:
• MRI liver and lntraoperative U/S
• lntraoperative UIS is most sensitive test to detect liver lesions

• If still negative (Truly missed lesions):

• Non-multiple lesions:
o Anatomical resection

• Multiple small lesions:

o Follow-up post-operatively
• Segmental resection
• Percutaneous ablation

o Postoperative hepatic artery infusion of chemotherapy

Blind major hepatectomy for small deeply located lesion is not advised
HEPATIC RESECTION
■ Non-anatomical resection
o For most of benign diseases
o For some of malignant diseases:
• Cirrhosis
• Not tolerate resection of> 2 segments of functional parenchyma
• Neuroendocrine metastasis

■ Anatomical resection
o For most of malignant diseases
o Types:
• LEFT HEPATECTOMY
• Resection of segment 11, 111, IV
Left medial segmentectomy
Resection of medial segment (Segment IV) to the right of falciform

Left lateral segmentectomy

Resection of lateral segments (Segment II, Ill) to the left of falciform

• Extended left hepatectomy

o Left hepatectomy including segments V, VIII

• RIGHT HEPATECTOMY
• Resection of segments V, VI, VII, VIII

• Extended right hepatectomy

o Right hepatectomy including segment IV and middle hepatic vein

o eciociple of anatomjcal resectjon·

1} Control of inflow vessels
2} Control of outflow vessels
3} Parenchymal transection
• Maintain 1 CVP to prevent backflow during resection
• Trendelenburg position + to maintain adequate cardiac preload and ! risk of air
embolism via opening hepatic veins during transection

■ Complications of liver resection:

o Hemorrhage 10%
• Occlusion of the portal triad (Pringle maneuver) in major and minor liver
resections during the transection of the parenchyma to decrease blood loss
o Bile leak 6 - 20%
o Liver failure, Ascites, Infection
HEPATECTOMY
Preparation
■ Assess resectability:
o Imaging-based (Local disease, and adequate FLR "Future Liver Remnant")
o Multidisciplinary meeting
o Tumor Board meeting

■ Assess fitness:
o Correction of anemia and of coagulopathy
o Investigations for cirrhosis
o Functional tests

■ Pre-operative preparation:
o ICU and consultations if required
o DVT prophylaxis and pneumatic compression boots
o Antibiotics prophylaxis
o Type and cross-match of blood
o NGT, Foley's catheter, Central line if indicated (For CVP monitoring}
o Mobilization, and chest physiotherapy
o Informed consent

Initial Steps:
Position: Supine or trendelenburg position
Incisions:
o Right subcostal incision with midline extension (Hockey stick incision)
o Chevron or Mercedes incision

1} Divide the round (ligamentum teres) and falciform ligaments to the dome of the liver

2} Abdominal exploration

3} Intra-operative U/S and bimanual examination of the liver in case of malignancy

4} Control the inflow of the liver before the outflow

Right Hepatectomy
o Right hepatectomy: Segments 5 - 8
o Right lobectomy: Segments 4 - 8
o Right lateral-posterior sectorectomy: Segments 6 - 7

1} Further Mobilization by retraction of the liver medially and divide retroperitoneal attachments
(Right coronary and triangular ligaments)

2} Fundus-first cholecystectomy, with ligation of cystic stump

3} Perform intra-operative ultrasound, for evaluation and rule out communication to bile system

4} Control of the right structures (extra-hepatic: most common method)

o Perform right hilar dissection and divide the right hepatic artery
o Divide the right hepatic duct and both retracted medially to expose right portal vein
(Bile duct should be transected intra-hepatic to avoid injury of the confluence)
o Divide the inflow (right portal vein) with vascular stapler
o Divide the outflow (right hepatic vein) with vascular stapler

Right hepatic vein exposed at the base of segment 8 superiorly entering the IVG
Can be divided before (preferable) or after parenchymal transaction

Intra-hepatic vascular control: for tumor> 2 cm away from hi/us of liver

By 2 incision at gallbladder bed and caudate process and control pedic/es by TA stapler

5} Mobilize the right lobe medially then ligate and divide the short hepatic veins and caudate
veins that enter the retrohepatic IVC

6} Tunneling behind the live by make counter-irncision at right base of gallbladder fossa; pass
Kelly clamp deep to hilar plate anterior to IVC, then place umbilical tape (Hanging method)

5} Open the gastrohepatic ligament and assess for replaced hepatic arteries (selected cases)

7} Prepare for Parenchymal transaction

o By asking the anesthesiologist to lower the CVP < 5 H20

o Prepare for Pringle maneuver to be encircle by umbilical tape to control hepatoduodenal

ligament in in case of bleeding while performing parenchymal transaction
8) Parenchymal transection
o Along line of demarcation {along Cantlie's line} until segment V/VIII MHV branches
o From anteroinferior to posterosuperio r fashion

o Techniques:
• Clamp-crush technique
• Finger fracture with suture hemostasis
• Water-jet
• Harmonic scalper
• LigaSure
• Vascular stapling
• Radiofrequency dissector
• CUSA (Cavitron Ultrasonic aspirator} ± Argon beam coagulation "Most preferred"

9) Control and divide the right hepatic vein if not divided before, avoiding injury to IVC or middle
hepatic vein

± Saline cholangiogram via the cystic duct stump to confirm that the cut edge is watertight
± Contrast fluoroscopic cholangiogram to confirm patency of right hepatic duct and distal CBD
± Place omentum pack, or Taco-seal dressing over the liver edge

10) Fixation of the liver, by tacking the falciform ligament back to the diaphragm

11) Before closure

o Frozen section of the specimen to assess resection margin in malignancy
o Irrigate cavity with saline
o Check for hemostasis or bile leak
• By asking the anesthesiologist to elevate CVP ;? 8 H20
± Closed-suction drainage if indicated

12) Closure in layers

Left Hepatectomy
1) Divide the left triangular ligament and ligamentum venosum (Arantius ligament) caudally

2) Mobilize the left lobe laterally

3) Open the gastrohepatic ligament and assess for replaced hepatic arteries

4) Control of the left structures:

o Incise the peritoneum overlying the hilum medially and divide Left hepatic artery
Confirm the patency by temporarily occluding the left hepatic artery before division
o Dissect portal vein at base of umbilical fissure, divide Left portal vein
o Divide the Left hepatjcduct

5) Make counter-incision in segment IVB 1 cm above base of umbilical fissure and pass Kelly
clamp behind left hilar plate and exiting anterior to caudate lobe

6) Place umbilical tape in the tunnel behind the left hilar plate

7) Retract the left lobe laterally to expose the left hepatic vein

8) Pass right angle clamp between right and left hepatic veins and advance umbilical tape

9) Divide Left hepatic yein after parenchymal transection (due to inadequate extrahepatic
exposure)

13) Prepare for Parenchymal transection

o By asking the anesthesiologist to lower the CVP < 5 H20
o Prepare for Pringle maneuver to be encircle by umbilical tape to control hepatoduodenal
ligament in in case of bleeding while performing parenchymal transection

10) Parenchymal transection until segment VNIIII MHV encountered

11) Divide the left hepatic vein if not divided before

± Place omentum pack, or Taco-seal dressing over the liver edge

12) Fixation of the liver, by tacking the falciform ligament back to the diaphragm

14)Before closure
o Frozen section of the specimen to assess resection margin in malignancy
o Irrigate cavity with saline
o Check for hemostasis or bile leak
• By asking the anesthesiologist. to elevate CVP � 8 H20
± Closed-suction drainage if indicated

13) Closure in layers

Portal Hypertension
PORTAL HYPERTENSION
ANATOMY AND PHYSIOLOGY
■ Portal hypertension
o Normal portal vein pressure 5- 10mm Hg
o No valves in portal vein
o lndocyanine used to measure portal pressure before liver TXP
o Most common cause of portal hypertension: Cirrhosis
o Cirrhosis and portal hypertension -+ Metabolic alkalosis

■ i
Investigat ons:

Test Value
Wedged hepatic venous pressure (WHVP) > 5mmHg
Direct portal venous pressure

"Most sensitive and accurate test"

Hepatic venous pressure gradient (HVPG) > 10mm Hg
= WHVP - Free hepatic venous pressure

Splenlc pressure > 15mmHa

Portal venous pressure measured at surcierv > 20 mmHo

Portal pressure > 12 mm Hg is necessary for varices to form

Normal pressure measurement during shunting, should not terminate the procedure
As the pressure measurement is inaccurate especially in pre-sinusoidal portal hypertension

o UIS abdomen
• Used to assess for liver cirrhosis, splenomegaly, or liver mass
 ■ Types of portal hypertension:
o Central (Most common)
o Left-sided (Sinistral} "Gastrosplenic side"

ortal vein
Extrahepatic lotrahepatie

■ Etiology:

Pre-Hepatic Intra-Hepatic Post-Hepatic

/Sinistral\
Splenomegaly Hepatic vein occlusion
e.m-:.in11.1.P.ill.1l S.in11.:.P.i.ll.1I e.P.11t·:.ia1111P.i.ll.1l 1B udd-Chiari svndromel
Splenic vein ocdusion Schistosomiasis Cirrhosis Venoocclusive IVG thrombosis
disease
(Most common as
ore-sinusoida/l
Portal vein occlusion Myeloproliferative Sclerosing cholangitis Heart failure
disorders
AV fistula Granulomatous Primary biliary cirrhosis
diseases 1TB)
Heoatic metastasis Heoatitis
 Portosvstemlc collaterals (Common sites of varices)
Site Portal /Afferent) Svstemic
Gastroesophageal Left gastric vein Azygos vein
junction (anastomosis to caval system � varices) (intercostal, diaphragmatic and
esoohaaeal veinsI
Anterior abdominal Paraumbilical veins Superficial epigastric vein
wall Left portal vein Umbilical vein (Falciform ligament)

Anal canal Suoerlor rectal vein Middle and inferior rectal veins
Colonic lleocolic vein, right and middle colic veins Veins of Retzius (Right gonadal and
renal vein)
Omental SMV/IMV Retroperitoneal or pelvic veins
Solenic bed
Left renal vein

■ Yeios ofsappey·
o Superior veins of Sappey -+ Upper part of falciform ligament
o Inferior veins of Sappey -+ Lower part of falciform ligament
o Left inferior phrenic vein and intercostal vein -+ Left triangular ligament
o Right inferior phrenic vein -+ Right triangular ligament
o Recanalized umbilical vein -+ Ligamentum teres
o Cystic veins and branches of left gastric veins -+ Gastrohepatic omentum
o Diaphragmatic veins -+ Bare area of liver
o Ligamentum venosum -+ Patent ductus venosus
Child-Pugh score to assess severity of cirrhosis

Points
Clinical and Lab Criteria
1 2 3
Encephalopathy None Controlled Refractory
Ascltes Absent Controlled Refractory
< 2 mg/dL 2 - 3 mg/dL > 3 mg/dL
Bilirubin
< 34 uMoVL 34 - 51 uMol/L > 51 uMol/L
> 3.5 g/dL 2.8 - 3.5 g/dl < 2.8 g/dL
Albumin
> 35 28- 35 <28
< 4 seconds 4 - 6 seconds > 6 seconds
Prothrombin time
UNR<1.7 INR 1.7 - 2.3 INR > 2.3
Child A 5-6 points + Mortality 10% (FLR 50% = tolerate up to 50% resection)
Child B 7 -9 points + Mortality 30% (FLR 75% = tolerate up to 25% resection)
Child C 10 - 15 points + Mortality 75% (Liver resection contraindicated)
■ Child-Pugh Score correlates with mortality a�er open shunt placement
Ascites
■ Pathophysiology:
o Due to high intravascular pressure {Hydrostatic pressure) -+ capillary leakage
o Due to low oncotic pressure {low albumin)
o Due to local release of vasodilators (Nitric oxide)
o Pseudohyperaldosteronism

■ lovestjgatjon·
o Diagnostic paracentesis for all patient with new onset ascites

SAAG = (serum albumin) - (albumin level of ascitic fluid)

WBC > 500 WBC > 250 Lymphocytes > 250

Neutrophils > 250
SAAG ;!: 11 g/L (1.1 g/dL) Cirrhosis SBP with PHTN TB
"Ascites due to PHTN" Acute liver failure Malignancy
Portal vein thrombosis
SAAG < 11 g/L {1.1 g/dL) Malnutrition Pancreatitis TB
"Ascites not due to PHTN" Nephrotic syndrome Peritonitis Malignancy
SBPand !Alb Connective tissue disease

■ Management:
o Medical optimization (Furosemide, Spirono/actone, Na restriction) is initial step

o Large-volume (4-6 L) Paracentesis

• Preferred site: 3 cm medial and 3 cm superior to ASIS in left lower quadrant

o 25% of albumin is used to replace every 100 ml with 1 g

o Correction of coagulopathy

o TIPS is alternative in uncontrolled ascites used for good liver function to decrease risk
of encephalopathy

o Liver transplant used in Child C patients

 Management of Upper Gastrointestinal Bleeding:

Supportive Care
Resuscitation + NGT and Foley's± Intubation ± ICU management
(Cold lavage is not recommended anymore)

Pre-Endoscopy
I
I
Variceal bleeding Non-Variceal bleeding
{Sus12icious of 1:!Qrlal h:i112ertension)
■ Somatostatin analogue (Octreotide} ■ IV PPI (Omeprazole)
{50 µg bolus IV over 5 min}
followed by continuous infusion + 80 mg bolus followed by
8 mg/hour for 72 hours
26 g/hour for 72 hours post-endoscopy Then change it to orally
0 if active bleeding at endoscopy ➔ 12 mg/day
0 t portal pressure by t blood flow
■ IV Erythromycin
■ Long-acting vasopressin analogue {Terlipressin) 3 mg/kg over 20 - 30 min
Efficacy to control acute variceal bleeding: 70 - 80% 30 - 90 min prior to endoscopy
Side effects: vasoconstriction (ischemia, infarction)
Best (Octreotide + Terlipressin) Binds to motilin receptor and
stimulate smooth muscle
■ No oral medications (Including beta blockers) contraction

Endoscopy
(within 4 - 24 hours)

I
I I
Variceal bleeding Non-Variceal bleeding

1) Band ligation: (Most common method and the best)

- Begin with largest column of varices at most distal point 1) Mechanical treatment
- NGT or feeding tubes avoided as not to dislodge any elastic bands
- Repeat band ligation 10 - 14 days interval (3- 4 sessions) until the 2) Thermal treatment
varices are eradicated
3) Injection of epinephrine
2) Sclerotherapy:
- Sclerosants: {1 - 5 ml for each varix)
• Ethanolamine
• Na morrhuate or Na tetradecyl sulfate
- Com12lications: Rebleeding, Perforation
 I Uncontrolled (Refractory) Variceal bleeding
I
I
I I
Mild - Moderate Severe

Repeat endoscopy within 72 hours Balloon tamponade as temporary method

(Sengstaken-Blakemore tube)
- Most common complication: Aspiration pneumonia
- Rebleeding in: 50%
- Duration should be < 36 hours

I Uncontrolled by tamponade, Recurrent bleeding I

I
I
I Isolated gastric varices I I Esophageal or Gastroesophageal varices
I
I I
No liver diseases Child B (with ascites)
Child A/ B (Without ascites) Child C
Refractory ascites
I
Endoscopic ablation {obturation)
I
Splenic vein > 1 cm
I
Splenic vein < 1 cm
- Cyanoacrylate glue or Thrombosed No thrombosis
- Thrombin
TIPS (alternative)

If(+} s12lenic vein thrombosis:

Splenic artery embolization DSRS

11
Splenectomy (TIPS is alternative)
Surgical shunt Emergency TIPS
I I

As definitive treatment Anatomy not suitable for Decompensation

!
shunting

! Mesocaval shunt (temporary)

Liver transplant
Sugiura procedure
■ Peri-endoscopy for variceal bleeding:
o Resuscitation should be with 05 water
• Normal saline associated with t ascites due to t Na along with t aldosterone
• Due to presence of Pseudohyperaldosteronism

o IV PPI (Omeprazole) should be given in variceal bleeding in case of portal gastropathy

to prevent ulcer formation

o Broad-spectrum antibiotic: 3rd cephalosporin (especially in cirrhosis) for 5 days

o Platelets infusion if < 30,000
o Repeat upper endoscopy 1 - 3 months after varices eradication
o Blood transfusion if Hb < 7 g/dl (< 10 g/dl in high-risk patients)
o Lactulose, Colonic wash may be used to decrease the risk of hepatic encephalopathy

■ Prevention of bleeding
o Primary prophylaxis:
• Prevention of the first portal hypertensive bleeding episode in an individual with
cirrhosis and esophageal varices

• Non-selective beta-blocker
o Mainstay medical treatment for non-bleeding varices
o Non-selective is more effective than selective beta-blockers
o Reduce rebleeding risk: 40%
o Improve overall survival rate: 20%
o Not preferred in advanced cirrhosis (hepatorenal syndrome)

• Endoscopic band ligation

o More effective in non-bleeding medium to large varices

Small vessels Medium - Large vessels

Or associated with Red wale marks
ChlldA None BB (Preferred initially)
Child B / C BB Or
Endoscoolc band llaatlon /Best\

o Secondary prophylaxis
• Prevention of recurrent episodes of variceal hemorrhage following an initial
bleeding event and should be given to all patients

• Recommended therapy:
o Beta-blocker+ Endoscopic variceal ligation
o Beta-blocker+ Nitrates (Alternative)

• TIPS is recommended only in patients with recurrent variceal bleeding refractory

to pharmacologic and endoscopic therapy
Shunts
lnterventional radiological shunt
■ Transjuqular lntrahepatic Portosystemic Shunt (TIPS)
o From percutaneous jugular venous approach through Right jugular vein
o Tract between hepatic vein and portal vein covered by stent of PTFE

Hepauc vein

Stent

Portal vein

Gaflllladder

o Indications:
• Refractory ascites
• Budd-Chiari syndrome not responsive to anticoagulation
• Childs-Pugh B and C with acute esophageal variceal bleeding refractory to
medical or endoscopic management
• Hepatic hydrothorax refractory to diuretics and salt restriction

o Contraindications:

Absolute Relative
{TIPS a/so mav benefits these patients)
Severe encephalopathy Hepatic vein thrombosis
Uncontrollable bleeding Non-cirrhotic oortal vein thrombosis
Unrelieved biliarv obstruction Gastric antral variceal ectasia
Active systemic or hepatic bacterial infection Polycystic liver disease
Severe cardiopulmonary comorbidity Central liver mass
(pulmonary hypertension, tricuspid regurgitation,
elevated riaht heart oressure conaestive heart failureI

o compHcations·
• Risk of encephalopathy (30%) "Most common complication"
• Recurrent bleeding: 18% - 32%
• Stenosis or occlusion 50% by 1 st year

o Contraindication or after failure of TIPS: Surgical shunt

• Obstructed IVC _,. Mesoatrial shunt
• Plan for Liver transplant -+ Mesocaval shunt
• No plan for Liver transplant _,. Side to side portocavel shunt
Surgical shunts
Used in recurrent variceal bleeding and preserved liver function (Child A/B) with liver transplant
anticipated in > 1 year

■ Total portal systemic shunts

o Portocaval shunt
Discouraged in liver transplant candidates, due to dissection of porta hepatis and
leading to sclerotic portal vein -+ alternatively use Mesocavel shunt

1) End to end portocavel shunt

2) End to side portocavel shunt (Eck fistula)
3) Side to side portocavel shunt
• Used in Budd Chiari (Replaced nowadays with TIPS/ Mesoatrial shunts)
• Partial preservation of portal blood flow
• Most effective for prevent recurrent varicea/ bleeding and ascites

o Mesocaval shunt (H-graft)

• Used after failure of TIPS
• It avoids dissection of portal vein, thus avoiding the complication of difficult
reoperation for future liver transplantation

o Central splenorenal shunt

■ Partial portal systemic shunts

o Interposition shunt (Portocavel, Mesocavel, and Mesorenal)
• Shunt diameter :s 10 mm

■ Selective shunts
o Distal splenorenal shunt:
• Used in reduced hepatoportal flow (preseNe the perfusion of portal to liver)
-+ Reduced rates of encephalopathy and liver failure
• Distal splenic vein is anastomosed to the Left renal vein

• Used only for Child's A, ± hypersplenism with Upper GI variceal bleeding, in

reduced hepatoportal flow

• Used also for patient who may later become candidates for liver transplantation

• Less risk of encephalopathy, but may cause worsening of ascites or

encephalopathy if presented

• Not used in emergency settings

Esophageal devascularization procedures:
■ Used in extensive portal and splenic vein thrombosis (portal hypertension} who are not fit
for shunt and failed medical and endoscopic management (Refractory ascites}

■ Do not interfere with hepatopetal blood flow (No risk of hepatic encephalopathy}

■ Suajura procedure:
o Oevascularization of upper stomach and esophagus with esophageal transection and
splenectomy via thoracic and abdominal incisions

o Preserve left gastric vein (coronary veins)

■ Hassab's decongestion procedure:

o Oevascularization of the distal 7 cm of the esophagus, and proximal part of stomach
without esophageal transection then splenectomy, vagotomy and pyeloroplasty via
single abdominal incision
Biliary System
BILIARY SYSTEM
ANATOMY AND PHYSIOLOGY
GALLBLADDER
■ Lies on segments IVb, and V
■ Mucosa consist of: Columnar cells epithelium (Greatest absorptive structure in the body)
■ No submucosa, No muscularis mucosa, No peristalsis
■ Completely covered by peritoneum (Except for intra-hepatic gallbladder)
■ Mucus secreted by lnfundibulum and neck
o Fundus -+ Smooth muscle
o Body -+ Elastic fibers
o Hartmann's pouch located in infundibulum (impacted stone and cause cholecystitis)

■ Function:
o Concentrate bile 50 - 100 times
o Bile storage with capacity of 50 ml (Up to JOO ml)
o Actively reabsorb NaCl and water (absorption based on Na concentration)

■ Gallbladder contracts in stage II (MMC) during:

o Fasting (between meals} by: Motilin
o Meal by: CCK and Vagal input (Parasympathetic)
Postprandial gallbladder emptying is maximum at 2 hours

■ Triangle of Calot's "Hepatocystic triangle"

• Boundaries: Cystic duct laterally, CHO medially, Liver superiorly

• Contains:
c::> Calot's lymph node (Lund's or Mascagni's node)
c::> Cystic artery

ffill/lt-O(HA

--·-·--�11'1
lllt<octat .J
-='--- Common hop11llc

---
IW
.....
■ Vascular supply:
o Arterial:
• Cystic artery (anterior and posterior) is end artery from:
c:) Right hepatic artery "Cross posterior to CBD'
• Retroduodenal branches from Gastroduodenal artery medially

o \/enous:
• Small veins -+ Right portal vein
o Vascular variants: (anomalies present in 50% of population)
• Cystic artery from:
c:) Right hepatic artery· (80- 90%)

c:) Accessory or replaced right hepatic artery (10%) "from SMA"

Replaced arlery felt deep to transected cystic duct

c:) 2 Cystic arteries (Right hepatic artery, Common hepatic artery)

c:) 2 Cystic arteries (Right hepatic artery, Left hepatic artery)
c:) 2 Cystic arteries (Both from Right hepatic artery}

c:) Cystic artery cross anterior to CBD

■ Biliary tree: (Proximal to distal)

o Intra-hepatic (Sectoral} ducts

o Right and Left hepatic ducts

• Left hepatic duct is longer than right hepatic duct
• Most common anatomical varjant:
c:) Right anterior or posterior hepatic duct drain into left hepatic duct

o Common hepatic duct "1 - 4 cm in length, 4 mm in diameter"

o Common bile duct "7 - 10 cm in length, 5- 10 mm in diameter"

(Joining of cystic duct and common h,epatic duct)
• Supraduodenal
c:) In front of Winslow foramen (supplied by GDA} anterior to portal vein

c:) Has longitudinal blood supply (at 3 and 9 o'clock)

-+ proximal bile injury t strictures

• Retroduodenal (Between 1 st part duodenum and head of pancreas)
• lntrapancreatic (behind the head of the pancreas)
• lntraduodenal
CBD and pancreatic duct united outside duodenal wall as single duct 70%
CBD and pancreatic duct united within duodenal wall 20%
CBD and Pancreatic duct enter the duodenal wall separately 10%
■ Lymphatic drainage of biliary t.ree:
o Superior duct -+ Hilar nodes
o Inferior duct -+ Peripancreatic nodes
■ Gallbladder variants:
o Normal gallbladder
o Intra-hepatic gallbladder
o Duplicated gallbladder
o Absent gallbladder
0 Left-sided gallbladder

■ Cystic duct variants:

o Cystic duct join CHD at Low junction
o Cystic duct join CHD at High junction
o Cystic duct adherent to CHD
o Cystic duct long joining CHD posterior to the duodenum
o Cystic duct drains into right hepatic duct instead of CHD
o Absence of cystic duct
o Spiral cystic duct crossing CHD anterior and joining it at posterior surface
o Spiral cystic duct crossing CHD posterior and joining it at anterior surface

■ Spiral valves of Heister:

o Mucosal folds located in:
• Proximal mucosa of the cystic duct at gallbladder neck

o Help passage of bile to and from gallbladder and regulate gallbladder distension
o Make the endoscopic cannulation and catheterization difficult

■ Ducts of Luschka:
o Accessory biliary ducts in liver bed that can leak after a cholecystectomy
o 2nd most common cause of bile leak after cystic duct leak
o Usually ,;; 3 mm, originates from right hepatic ductal system
o Management:
• Sphincterotomy (for decompre ssion}± Trans-ampullary stenting

■ Sphincter of Oddi:
o Thick coat of circular smooth muscle encircle CBD at ampulla of Valer
o Regulated by interstitial cells of Cajal

o Ampulla of Yater-
• Located at posteriomedial aspect of 2nd part of duodenum
• Papilla of mucous membrane

o Basal pressure:
• 5-15 mm Hg greater than CBD pressure
• 15-30 mm Hg greater than duodenal pressure

o Contracted by: Morphine

o Relaxed by: Glucagon, CCK

Biliary pressure < Pancreatic pressure

BILE
■ Bile contents: Bilirubin, bile salts, phospholipids (Lecithin), and cholesterol
■ Pigmentation of the bile is primarily due to Bilirubin dig/ucuronide
■ Function: Absorption of the lipid

■ Regulation of bile excretion:

o t Bile excretion: CCK (t ½: 2 - 3 min}, Secretin (Most potent), and Vagus input
• Hydrochloric acid, partly digested proteins, and fatty acids+ Secretin

o t Bile excretion: Somatostatin, VIP, Atropine, Splanchnic nerve stimulation

■ Bile secreted from Hepatocytes (80%) and Bile canalicular cells (20%}
o Secretion rate: 40 ml/ hour (500 ml - 1 L / day)
o Pool of 5 g
o Normal pH (Acidic if protein consumption increased}
o Encircle every 4 hours
• Bile is sterile 100% in cholecystectomy for gallstones
• Bile is sterile 80% in Acute cholecystitis and 0% in Cholangitis

BILE METABOLISM
1} Hemolysis of RBCs in spleen: Heme converted to+ Biliverdin, CO, and Fe (II)
2} Biliverdin + Unconjugated (indirect) bilirubin (by biliverdin reductase)
"Water-insoluble/ Fat-soluble"

3} Albumin carries unconjugated bilirubin to, liver+ Conjugation to glucuronic acid

4} Conjugated (direct) bilirubin •·water-soluble/ Fat-insoluble" released in bile

5} Enter the gut and converted by bacteria into:

o Stercobilinogen (stercobilin)+ Brown feces
o Urobilinogen (urobilin}+ Reabsorbed and excreted by kidney+ Yellow urine
Both decreased in presence of biliary obstruction

BILE ACID SYNTHESIS

■ HMG CoA+ (HMG CoA reductase)+ Cholesterol+ (?-alpha hydroxylase)+ Bile salts
o t HMG CoA reductase: Gallstones in obese
o t 7-alpha-hydroxylase: Gallstones in thin

■ Primary (Conjugated) bile acids

o Synthesized in the liver by cholesterol, conjugated by Glycine and Taurine
o Active reabsorption in terminal ileum (can't be reabsorb in gallbladder)
o Types: Cholic acid and Chenodoxycholic acid

■ Secondary (Unconjugated) bile acids

i
o Synthesized by intest nal bacteria
o Passive reabsorption in colon
o Cholestyramine prevent reabsorption of unconjugated bilirubin
o Types:
• Deoxycholic acid � Cholic acid
• Lithocholic acid � Chenodoxycholic acid
GALLSTONES
■ Risk factors:
o Female, Forty(> 40 years), Fertile(;? 1 children), Fat(BMI >30), Fair (Caucasian)

■ Incidence:
o 10% the risk in population to have gallstones
o 20 - 30% of all incidental gallstones to be symptomatic

■ Pathophysiology:
o Biliary sludge and stasis
• Hypersecretion of cholesterol (decreased degradation of mucin)

• Hypomotility of gallbladder and excessive sphincteric contraction

� Accumulation of bile and increased predisposnion for stone formation

■ comoonents of gallstone·
o Bilirubin
o Bile salts
o Phospholipids (Lecithin)
o Cholesterol or Calcium bilirubinate or both

■ Investigations:
o UIS abdomen (Higher sensitivity than CT scan)
• For symptomatic patient with negative UIS findings
� Repeat UIS after 2 weeks

o CT scan

o HIDA scan(Most sensitive test)

• For symptomatic patient with negative UIS findings 2 times
� Upper GI endoscopy

• For symptomatic patient with negative UIS findings and UGIE

� HIDA scan+ CCK for ejection fraction (Biliary dyskinesia)

■ UIS findings:
o Hyperechoic intraluminal structure
o Mobility of the intraluminal structure during changes in position
o Shadowing posterior to the structure
o No posterior enhancement (Presence in cyst)

Patient should be fasting for 6 hours

-+ To limit gallbladder contraction and excessive bowel gases
■ Types of the gallstones

1} Mixed stones: Most common type

2) Non-pigmented stones:

o Cholesterol stones
• Found only in gallbladder (Single, Large, Smooth stone}

• Caused by:
f Cholesterol hypersecretion "Most common"
! Phospholipid (Lecithin)
! Bile salts

• > 90% are radiolucent

o Pathophysiotogy:
• Cholesterol is held by micelles ( conjugated bile salt)
• Phospholipid (Lecithin} increases capacity for cholesterol to be solubilized
in phospholipid vesicles (Primary form in bile}

• Phospholipid vesicles conjoin micelles more rapid than cholesterol vesicles

• Cholesterol vesicles accumulate and become unstable

• Cholesterol crystals formation (Super-saturation of cholesterol)

3} Pigmented stones (most common worldwide}

o Found in gallbladder or CBD (Multiple, Small, Spiculated stones)

o Calcium bilirubinate
• Main component of pigmented stones

o Types:
Black stones:
c:> Caused by solubilization of unconjugated bilirubin
c:> Caused by:
o Hemolytic disorders, Cirrhosis, TPN, ilea/ resection, Crohn's
disease, and Cystic fibrosis

Brown stones:
c:> Most common Primary CBD stones
c:, Formed inside the bile ducts
c:, Associated with biliary infection
c:> Infection (E. coli} causing deconjugation of bilirubin

o Dissolution agents {mono-octanoin) do not work on pigmented stones

INDICATIONS FOR CHOLECYSTECTOMY
■ Symptomatic Cholelithiasis:
o Biliary colic
o Acute or chronic (Calculus or Acalculous) cholecystitis
o Emphysematous, Perforated, or Gangrene gallbladder
o Mucocele or Empyema of gallbladder
o Gallstone pancreatitis

■ Asymptomatic Cholelithiasis:
o Patients on Total parenteral nutritio:n (TPN)
o Heart transplant
o No immediate access to health care facility
o Sickle cell disease
• Higher rate of biliary complications, and hard to distinguish between vaso­
occlusive crisis
• Cholecystectomy is not considered for other hemolytic disorders as thalassemia
or hereditary spherocytosis

o For patient undergoing other abdominal surgery

• Patient undergoing splenectomy for hemolytic anemia (SCD)
• Patient undergoing gastric bypass with asymptomatic gallstones
• Patient undergoing total gastrectomy
• Patient undergoing massive bowel resection
• Patient undergoing resection and anastomosis of small bowel carcinoid with
planning for life-ling somatostatin analogue

o Gallbladder disorders:
• Gallbladder trauma
• Gallbladder stone > 2.5 cm
• Gallbladder polyp
• > 1 cm or < 1 cm but increasing in size
• Associated with stones, regardless polyp size or symptoms
• Associated with primary sclerosing cholangitis
• Age > 60 years (Controversial)

• Porcelain gallbladder
• Proven or concern for gallbladder cancer
• Long common channel of bile and pancreatic ducts (Choledochal cyst)

■ Relative indications for asymptomatic Cholelithiasis:

o Life expectancy >20 years (children)
o Calculi > 2 cm in diameter or < 3 mm with patent cystic duct
o Non-functioning gallbladder
o Hemolytic disorders
o Vague dyspeptic symptoms in the presence of gallstones

CONTRAINDICATIONS
■ Uncorrected coagulopathy

■ Liver cirrhosis (Child C)

o Laparoscopic cholecystectomy f mortality and morbidity in cirrhosis patient
ACUTE CHOLECYSTITIS
■ Inflammatory process with bacterial contamination
o Most common organism: E. coli

■ Most sensitive test: HIDA scan ± CCK (CCK-CS)

■ Most common route of biliary infection: Hematogenous through portal system

■ Pathophysiology:
o Obstruction of the cystic duct
• By impacted of gallstones in the Neck, Hartmann's pouch, or Cystic duct
• Increase intraluminal pressure
• Initiate inflammatory event
-+ Enlarge, thick wall of the gallbladder -+ lschemia
-+ Secondary bacterial infection
o Earliest event: t Biliary Lysolecithin

o Mucocele developed after long-standing obstruction

-+ Slowly absorption of bile pigment
-+ Continuous secretion from mucosa of gallbladder
c:) Mucoid content (White bile - Hydrops gallbladder}

■ Clinical picture:
o Persistent severe pain> 6 hours, febrile, anorexia, nausea, and vomiting
o Focal tenderness and guarding in RUQ area
o Murphy's sign: inspiratory arrest with deep palpation in RUQ area
• May be absent in obese, DM, Steroids, lmmunosuppressed

o Mild leukocytosis (12 - 15,000 cells/mm3), t Alkaline phosphatase

• WBC> 20,000 is suggestive of a complicated form of cholecystitis
• Jaundice is suggestive of CBD stones or obstruction of bile ducts

o Clinical picture of chronic cholecystitis (Biliary colic)

Long-standing gallbladder inflammation usually due to gallstones
• Episodic moderate pain for 1 - 5 hours during night or after fatty meal
• Located in epigastrium or RUQ radiating to upper back (shoulder)
• ± Nausea or vomiting, with mild tenderness over RUQ or epigastrium
• Normal labs

■ U/S findings:
o Gallbladder stones or sludge (absence in acalculous cholecystitis}
o Gallbladder wall thickening> 3 mm
o Gallbladder distension> 5 cm
o Subserosal halo sign
o Pericholecystic fluid, or infiltration of f.at
o Intramural gas for emphysematous cholecystitis
o Rokitansky-Aschoff sinus (epithelial invaginations in the gallbladder wall = Intramural
diverticula) for chronic cholecystitis

■ CT scan is more sensitive than U/S for signs of acute cholecystitis (not stones}, and U/S
should not be done in patient diagnosed with acute cholecystitis by CT scan
■ Complications:
o Gangrene, Perforation, Mucocele, Empyema, Emphysematous cholecystilis
o Cholangitis, Sepsis
o Cholecystoenleric fistula
o Gallstone ileus

■ Antibiotics
o Should cover gram negative and anaerobes
o Options:
• 3rd generation Cephalosporhn with good anaerobic coverage

• 2nd generation Cephalospori1n + Metronidazole

• Aminoglycosides (Gentamicin) + Metronidazole

c:, For patients allergic to Cephalosporin

■ Treatment options:
o Conservative and antibiotics with interval cholecystectomy in 6 - 12 weeks
• Better option for mild form of acute cholecyslitis in high-risk patients

o Emergent cholecystectomy within 1 - 3 days "Preferred option"

• Preferred time: During first 72 hours of attack
(Studies showed no l mortality or morbidity)
• Studies showed no different between the two depends on surgeon experience

• Convert to open risk factors: Male, Obesity, and Cirrhosis

o Cholecystostomy tube
• For Crjtica! ill patient
• Unstable patient (ICU or on inotropes) with
o Acute cholecystitis
o Emphysematous cholecystilis

• For Contraindication for surgery

c:, Uncorrected coagulopathy, Cirrhosis (Child C liver cirrhosis)
c:, Early for intervention (Early Ml "ST or non-ST elevation")
• Perforation or gangrenous gall bladder are emergency situation which need to be
operated rather than cholecystostomy tube

• Failure lo improve after Cholecystostomy tube:

c:> Suspect perforated or gangrenous gallbladder
c:, Proceed with Emergent Cholecysteclomy

• Removal of Cholecystostomy tube

c:, After positive results and patent cystic duct on cholangiography
Which performed after 4 - 6 weeks

c:, Keep tube in patient with non-patent cystic duct until surgery time
c:, After stone extraction for patients not tolerating delayed surgery
PREGNANCY WITH GALLSTONES
■ BiliaN colic
o Conservative management with diet modification and follow-up after delivery (Mainstay
treatment)

For recurrent and failure of conservative management:

• Lap cholecystectomy: 2nd trimester
(Delay the surgery if patient still in 1 st trimester)

• Open cholecystectomy: 3rd trimester

(Delay the surgery post-delivery if near term)

i
■ Acute cholecyst tis
o Lap cholecystectomy during admission: 2nd trimester in low-risk patient

o Medical management followed by percutaneous cholecytosotomy as bridge for

definitive cholecystectomy: 1 st , 3rd trimester or 2nd trimester in high-risk patient
ACALCULOUS CHOLECYSTITIS
■ Symptoms and signs of acute cholecystitis with no stones or sludge inside gallbladder

■ Associated with more risk of gallbladder gangrene and perforation

■ Risk factors:
o Severe burns, Dehydration, Prolonged TPN
o Transfusion, Trauma or major surgery, or ileus

■ Pathophysiology:
o Biliary stasis (f Viscosity)
o lschemia

■ Pathology:
o Transmural edema of gallbladder
o Patchy thrombosis of arterioles and venules

■ Management:
o Cholecystostomy tube
• Due to low risk to develop recurrence of symptoms
(Elderly patients with no stones)

• For Critical ill patient

c:, Unstable patient (ICU or on inotropes}
• For Contraindication for laparoscopic surgery
c:, Coagulopathy, Cirrhosis (Child C liver cirrhosis)
c:, Early for intervention (Early Ml "ST or non-ST elevation")

o Cholecystectomy (Laparoscopic or open)

• Indicated if failed to improve or associated with perforated or gangrene
• Not absolute indicated after relieved by cholecystostomy due to lower risk of
recurrence than calculous cholecystitis
EMPHYSEMATOUS GALLBLADDER DISEASE (Male)
■ Acute life-threatening anaerobic infection of gallbladder wall by gas-forming organisms

■ Most common organisms: Clostridium perfringens followed by E. coli

■ Increased risk in diabetics elderly male patienls

■ Mortality rate: 15 - 25%

■ Criteria to diagnose:
o Presence of air within the gallbladder wall or lumen ± biliary ducts
• Without recent biliary instrumentation

o Absence of abnormal communication with gastrointestinal tract

■ Management:
o IV antibiotics
• Penicillin-based (Piperacillin and Tazobectam)
• Alternative: 3rd generation Cephalosporin and quinolones + Metronidazole

o Emergent cholecystectomy
• Operation of choice also for perforated or gangrenous gallbladder

o Percutaneous drainage if unstable

HIDA Scan (Hepatobiliary lminoDiacelic Acid Scan) "Cholescintigraphy"
■ lminodiacetic acid is derivatives from technetium T99(Nuclear study)
■ Nuclear study of bile flow, uptake by liver in 10 minutes and cleared by Kupffer cells
■ Visualized in duodenum within 60 minutes(after 20 minutes if gallbladder removed}
■ Evaluate anatomical and functional of liver, gallbladder bile ducts and duodenum
■ Sensitivity and specificity of 95%
o False-positive in:
• Gallbladder stasis(as patient f.asting or receiving TPN}
• Impaired clearance(severe liver disease or hyperbilirubinemia)
• Biliary sphincterotomy

■ Used for assessment of:

o Non-visualized Gallbladder
• Contracted gallbladder(if postprandial< 2 hours}
• Acute cholecystitis(cystic duct obstruction after 60 - 120 minutes)

O Biliary leak
o Biliary reflux(into stomach or biliary-enteric anastomosis)
o Biliary-enteric bypass
o Biliary dilatation including choledochal cyst
o Biliary obstruction or stasis
o Ampulla obstruction (delayed or absent filling of duodenum)
o Differentiation of FNH from other hepatic lesion

■ Addition of other medications as pharmacologic enhancement:

o Used in patient with stasis; NPO > 24 hours, or on TPN
1) Morphine sulfate:
• Used after 30 - 60 minutes if gallbladder not visualized to increase sphincter of
Oddi tone and CBD pressure(! False-positive rate of HIDA scan}

2) Cholecystokinin analogues (Sincalide) "CCK-CS"

• Help by increases bile flow, gallbladder contraction, relax of sphincter of Oddi
• Assessment of gallbladder ejection fraction(Normal level > 50%}
• Help for emptying of the gallbladder

3) Nitroglycerin: Help for relaxation of the sphincter of Oddi

4) Phenobarabital
• Improve specificity for diagnosis of biliary atresia in neonates by increases
production of bile

5) Fatty meal: Help emptying of bile into duodenum for confirmation of CBD patency

■ Indications for cholecystectomy after CCK-CS /HIDA scan}:

o Chronic cholecystitis
• > 60 minutes to empty
• Ejection fraction < 40%
• Symptoms developed during CCK administration

o Acute or Chronic(Calculous or acalculous) cholecystitis

• Not-visualized(non-filling) gallbladder in patients with gallbladder
MIRIZZI SYNDROME
■ Common hepatic duct obstruction by extrinsic compression from impacted stone in the cystic
duct or Hartmann's pouch of the gallbladder
o By mechanical obstruction
o By inflammation and edema

� Recurrent Cholangitis

■ Incidence: 0.7 - 1.8%, and increases the risk of gallbladder cancer

■ Investigation:
o ERCP, MRCP, or PTC to identify the anatomy and rule out malignancy
(if urgent cholecystectomy not needed)

■ Types:
o Type I: Impacted stone at infundibulum or cystic duct compress at level of CHO
o Type II: Stone erode into CH resulting in cholecystocholedochal fistula

■ Csendes C!assjficatjon: (account the presence of cholecystobiliary fistula)

o Type I: External compression of common hepatic duct due to impacted stone at neck of
gallbladder or cystic duct without fistula

o Type II: The fistula involves< 1/3 of circumference of common hepatic duct

o Type Ill: Involvement up to 2/3 of ciroumference of common hepatic duct

o Type IV: Destruction of the entire wall of common hepatic duct

■ Standard management

Type I:
o Open cholecystectomy (Standard of care)
• Laparoscopic cholecystectomy is not contraindicated (controversial)

o Subtotal cholecystectomy if inflammation has obliterated the triangle of Calot

o Biliary drainage procedure may be indicated if stricture developed later on

Type II. Ill or IV:

o Open subtotal/ partial cholecystectomy + Fistula closure (as CBD exploration)
• Type II: By absorbable material or repair over T tube

• Types II Ill: Choledochoplasty by remnant gallbladder or cystic duct stump

• Types Ill IV: Biliary drainage

o How to exam a fistula: Open the fund us, Clear fluid/stones, Look for bile gush
 GALLSTONE ILEUS (Female)
■ More in elderly female
■ Air in the biliary tree with small bowel obstruction
■ Fistula between gallbladder Fundus and
o 2nd part of duodenum (Most common)
o Transverse colon at hepatic flexure
-+ Obstruction of terminal ileum (in cholecystoduodenal fistula)

■ Investigat ions:
o X-ray: (Rigler's triad} presented in 20 - 30%
• Gallstones outside gallbladder
• Air in bile ducts {Pneumobilia)
• Small bowel obstruction

o CT Scan: Preferred diagnostic tool

■ Treatment:
o Proximal Longitudinal Enterotomy on antimesenteric, proximal to impacted point
• Milking and extraction of the stone, and bowel examination for other stones
• Transverse closure of enterotomy to avoid residual bowel stenosis
• Bowel resection and anastomosis if perforated or ischemic segment

o Cholecystectomy and biliary-enteric fistula takedown and biliary reconstruction

• As delayed procedure (Preferable option)
• As single procedure (For low-nisk stable patient)

Pneumobilia Portal vein gas

Causes Recent biliary Instrumentation (ERCPI most common Bowel dilatation
"Post endoscopic, acute gastric
Incompetent sphincter of Oddi dilatation, paralytic ileus"
"Sphincterotomy, passing stone, chronic pancreatitis"
Bowel necrosis
Blllary-enterlc anastomosis "Infection, Mesenteric occlusion,
"Cholecystoenterostomy, choledochoduodenostomy, Mechanical obstruction, CRC"
Whipple procedure"
Abdominal Infection
Blllary-enterlc fistula "Diverticulitis, Cholecystitis,
"i:iallstone ileus, traumatic, neoplasm" Pancreatitis, Appendicitis"

IBD or Perforated bowel

CT Isolated bubbles Branching
Features Centrally located Peripherally located " > on left lobe"
> 2 cm from liver capsule < 2 cm from liver capsule
CT
Image
OBSTRUCTED JAUNDICE AND CBD STONES
■ Definition of jaundice:
o Increased of bilirubin in the blood 2 - 3 folds than the normal limit, manifested by
yellowish discoloration of the skin and the sclera

■ Increases risk of infection by increase bacteria overgrowth and translocation

o Leading to altering pH of the bowel
o Lactulose decrease the risk by reducing the intestinal permeability

■ Causes of obstructed jaundice:

Benign Malignant
Choledocholithiasis /CBD Stone\ Pancreatic adenocarcinoma
Paoillarv stenosis Cholanaiocarcinoma
Choledochal cvstic disease Gallbladder carcinoma
Post-suraical stricture Amoullan, carcinoma
Mirizzi's svndrome Neuroendocrine disease
Pancreatic oseudocvst Metastatic disease
Sclerosina Cholanaitis

Pre-hepatic Hepatic Post-hepatic

(Liqht jaundice; indirect) (Deeo jaundice) (Verv deeo iaundiceJ
Hemotysls
••
lofecuon:
Hepatitis ••
lolca:beoaljc bile g1,u,1:.-
DruQS
Cholangitis
••Biliary cirrhosis
CholanQitis
Liver malianancv
Congenjta1·
■ Gilbert syndrome ••
E�tca-tieoalic bile guct:r
CBD stones or stricture
■ Crigler Najjar syndrome
•Cholangiocarcinoma
Duodenal or oancrealic mass

••
Toxins:
Alcohol
Paracetamol poisoning
-+ Cirrhosis

■ i
Indications for antibiot cs in jaundiced patient:
o Cholangitis
o CBD stone
o Biliary instrumentation
■ Types of CBD stones:
o Primary CBD stones
• Forms inside the bile ducts
• Brown pigment stones (formed by calcium bilirubinate)
• Associated with biliary stasis and infection

• Causes of bjliary stasis·

c:> Stricture
c:> Papillary stenosis
c:> Tumors
c:> Secondary stones

o Secondary CBD stones "Most common"

• Forms inside the gallbladder
• Cholesterol stones

■ Retained ceo stone·

o Stone left in place at time of surgery or diagnosed after cholecystectomy up to 2 years

■ Recurrent CBD stone:

o CBD stone diagnosed after CBD stone removal or after cholecystectomy > 2 years

■ Presentation:
o Could be silent (asymptomatic)

o Yellowish discoloration of eye (icterus), skin and mucosal membrane

• 1 st evident of jaundice appears: under the tongue
• Progressive jaundice with impacted stone or pancreatic malignancy
• Fluctuating jaundice with periampullary tumors or primary sclerosing cholangitis

o Diarrhea
• Due to malabsorption of Fat soluble vitamins (ADEK)
c:> Vitamins ADE need long time to be deficient
• Pre-op coagulation profile needed (malabsorption of vitamin K)

o Acholic (clay color - pale) stool/ Biluria (dark urine)

• Upper GI bleeding or hemolysis: f Urobilin
• CBD stone: .! Urobilin (! bile entering the gut)

o Complications of obstruction
• Cholangitis
• Gallstone pancreatitis
• Gallstone ileus
• Stricture
■ Laboratory investigations:
o Hyperbilirubinemia (mainly Direct "conjugated")
• Highest test with positive predictive value for CBD stones

Causes
Direct billrubin Sepsis (Predictive factor for perforated appendicitis)
TPN
Cirrhosis
Biliary obstruction
- Internal:
0 Stone
0 Strictures
0 Cholestatic diseases (PBC, PSC)
0 Cholangiocarcinoma

- External:
0 Gallbladder carcinoma
0 Pancreatic head CA
Indirect bilirubin SCD or Thalassemia
Hemolytic reaction
Reabsorplion of hematoma
Ineffective erythropoiesis
Right-side HF
Gilbert's syndrome or Crigler Najjar syndrome
Both Viral or Drug-induced Hepatitis

o j Alkaline phosphatase (ALP)

• Increased also in:
c:> Pregnancy and bone disease

• Increased with normal bilirubin if common bile duct not involved

c:> As in unilateral hepatic duct stricture

o 5-Nucleotidase: most specific test for hepatobiliary disorders

o Gamma glutamyltransferase (GGT): most sensitive test for hepatobiliary disorder

c:, Absent in bone and placenta, and help in isolated rise in ALP
 ■ Radiological investigations:
o U/S
• Initial test to identify gallbladder stone, and size, number of CBD stones
• Dilated CBD diameter(> 8 mrrn) "Normal diameter is< 6 mm"
c:, > 6 mm CBD diameter in elderly patient, and post cholecystectomy

ERCP is the most sensitive lest for cho/edocholithiasis

o CT Scan
• Can evaluate CBD stones with different densities, especially at distal CBD
• Can rule out other causes of obstructed jaundice

o MRCP
• General indications for MRCP:
Biliary
c:, Choledocholithiasis (for intermediate-risk group)
o Can miss stones < 5 mm

c:> Post-surgical altered biliary anatomy complications

c:> Biliary injuries
c:> Benign or malignant biliary stricture (Cholangiocarcinoma)
c:> Identification of congenital anomaly of cystic and hepatic ducts

Pancreatic
c:, Pancreatic divisum
c:> Anomalous Pancreaticobiliary junction (Cho/edocha/ cysts)
c:> Chronic pancreatitis (Can detect side branches changes)
c:> Pancreatic adenocarcinoma
(Double duct sign: dilatation of pancreatic an common bile ducts)
c:> Pancreatic cystic lesions communication with duct
(Pseudocyst, IPMN)

Grouo Criteria Ootions for next steo

Presence of an:,! ver:,! strong credictors: Pre-operative ERCP
■ CBD stone on radiological images
■ Clinical ascending cholangitis
High risk
■ Total bilirubin > 4 mg/di
Etfllif!CQfl g( bolb g( slcgag Q[flgjQt!l[li:
■ Dilated CBD diameter > 6 mm
■ Bilirubin 1.8 - 4 ma/di
Presence of an:i of strong credictors: MRCP
■ Dilated CBD diameter > 6 mm
■ Bilirubin 1.8 - 4 mg/di Laparoscopic Cholecystectomy
with intraoperative cholangiogram
Intermediate risk Presence of moderate i;!redictors: (Preferred option)
■ Abnormal liver tests other than bilirubin
■ Age > 55 years Positive cholangiQgram:
■ Clinical gallstone pancreatitis ■ CBD exploration
■ Post-ooerative ERCP
Low risk No presence of anv predictors Cholecvstectomv
o Endoscopic Cholangiography (ERCP)
• ERCP is the gold standard for diagnosing and treating CBD stones
• As definitive modality with no cholecystectomy for > 70 year old patients
• Risk of recurrent symptoms from gallbladder stones is 15%

• Methods for difficult CBD cannulalion:

• Rendezvous Technique "Kissing technique"
o Percutaneous UIS-guided PTC + ERCP
• Endoscopic UIS-guided Antegrade Biliary Drainage
• Endoscopic UIS-guided Transluminal Biliary Drainage

o Percutaneous Transhepatic Cholecystostomy (PTC) "Diagnostic± Therapeutic"

• Cannulation of peripheral biliary tree followed by contrast injection
• Proximal biliary tree best visualized by PTC rather than ERCP
• Indications:
• Failed ERCP I ERCP not feasible
• Used mainly for primary CBD stones
• Identify level of obstruction of biliary tree (strictures, tumors, or others)
• Anatomic evaluation of complications of ERCP
• Demonstrate site of bile leaks

o Percutaneous Transhepatic Biliary Drainage (PTO) "Therapeutic"

• Cannulalion of peripheral biliary tree after percutaneous puncture followed by
wire insertion and catheter manipulation
• Indications:
• Provide adequate biliary drainage
• Remove stone
• Stenting or biopsy

o Percutaneous Cholecystostomy "Therapeutic"

• Cannulation of gallbladder (for drainage of gallbladder contents)

o lntraoperative UIS

o lntraoperative Cholangiography
• Used to confirm the diagnosis and outline the biliary anatomy before the CBD
exploration is undertaken

• Indications:
• Dilated CBD diameter
• Wide cystic duct
• Palpable CBD stones
• Elevated liver enzymes and bilirubin
• History of pancreatitis

• Positive result (No proximal or distal fill)

"Duct is clipped, injured, intra-hepatic or distal stones"

c:> Convert to open and proceed with CBD exploration

c:> Performs hepaticojejunostomy
■ Order of management of non-complicated choledocholithiasis:
1) ERCP and sphincterotomy

Failed, or Non-visualized stone?

2) Laparoscopic cholecystectomy with intraoperative cholangiogram

o After clipping the distal cystic duct and before cystic duct division

o Open cystic duct via partial transverse incision

o Introduce Cholangiogram catheter (4 - 5 Fr) and clip over it or clamp it by "Olsen

cholangiogram clamp" which catheter located between the jaws

o Take plain pre-contrast fluoroscopy image and check for location and size of stones
(15-20 ml of contrast dye diluted 1:1 with saline is injected under fluoroscopy)

o Flushed with 2 - 3 ml of saline while tilting the table slightly to the right side

o Administer 1 mg glucagon IV (Avoided in patients taking beta-blockers) or nitroglycerin

to induce relaxation of the sphincter of Oddi

o Repeat flushing with saline after glucagon

o Repeat cholangiogram

Success � Closure of cystic duct by clipping proximal to the incision or ligation

Failed?

3) Balloon-catheter stone retrieval via Iran-cystic

Failed?

4) Wire Dorrnia basket stone extractor under fluoroscopic guidance

Failed?

5) Flexible choledochoscope ± cystic duct dilatation

o Alternatively post-op ERCP
• If used and failed � Postoperative T-tube as radiological intervention

o Used for:
• Catch the stone via wire basket under vision or push it to duodenum
• Electrohydraulic lithotripsy for impacted stones
• Check for retained stones before T-tube removal

Success � Ligated the dilated cystic duct and completion of cholecystectomy

Failed?

6) CBD exploration (Trans-CBD Choledochotomy)

o 2 cm longitudinal incision on anterior aspect of distal CBD at 12 O' Clock
o Flexible choledochoscope passed through the incision to clear the stone
o Suture the choledochotomy over T tube

Failure?

7) CBD drainage procedure (Choledochoduodenostomy)

o Need to be converted from laparoscopic to open CBD exploration
o Randall stones forceps or Desjardin forceps are forceps used in open exploration to
catch the stone
o When stones cannot be cleared and/or when the CBD > 1.5 cm diameter
If not familiar with open CBD exploration -+ Place T-tube and transfer
■ Management options for Choledocholithiasis:
o Pre-operative ERCP
• Indications: (High-risk groups)
c:) Acute Cholangitis
c:) Worsening gallstone pancreatitis

c:) Multiple comorbidities

c:) Rule out malignancy

• Relative indications: (Intermediate-risk groups}

c:) Visualized CBD stones on UIS, EUS, CT, MRCP or Cholangiogram

c:) Recurrent CBD stones or gallstone pancreatitis

c:) High suspicious of CBD stones

(Dilated CBD, Cholelithiasis, elevated LFT}

• Alternative approach for intermediate-risk groups:

c:) Laparoscopic cholecystectomy with intraoperative cholangiogram

c:) For impacted stone, can be managed either by CBD exploration or

postoperative ERCP {with risk of retained stone}

• Standard ERCP sphincterotomy

c:) By incision of musculature of biliary portion of sphincter of Oddi
c:) After deep cannulation of the bile duct

c:) Length of sphincterotomy should be tailored to size of stone (preferred

completely unroofs the papilla}

o Post-operative ERCP
• Indications:
c:) Non-impacted < 2 cm CBD stone

c:) Retained or recurrent CBD stones

c:) Small CBD diameter for CBD exploration

c:) Surgeon less familiar of CBD exploration

c:) Unavailability of 3-mm choledochoscope, biliary stents, or T-tubes

There is risk of unsuccessful or retained stones (Up to 10%) if this technique is

used over CBD exploration

Post-operative ERCP has similar morbidity of pre-operative ERCP

o Post-operative T-tube (as radiological intervention)

• Indication:
c:) For retained CBD sto-nes as alternative if post-operative ERCP failed

o Cholecystectomy
• At same admission if no stent
• Interval after 6 weeks if stent inserted
 o CBD exploration
• Indications:

Laoaroscooic CBD exoloration Ooen CBD exoloration

Positive intraoperative cholangiogram
CBD stone with absence of ERCP
lmoacted stone
Palpable CBD stones who are undergoing open
cholecystectomy
Failure of stone extraction by ERCP or laparoscopic
methods
When concomitant biliarv drainaae is rAnuired

Trans-cystic {1 st line/ Trans-choledochal

Contraindications Stones proximal to cystic duct Small CBD diameter(< 7 mm)
(Due to cystic duct angle) (risk of stricture)

Small, friable cystic duct{< 4 mm) Severe inflammation of porta

hepatis
Multiple CBD stones(> 8 stones)

large CBD stone

I> 1 cm or more than cvstic duct diameter\
Location of stone Distal to cystic duct Entire duct
Dralnaae Optional cystic duct tube T-tube

• Similar ductal clearance, morbidity and mortality rate to ERCP

• Preferable approach as single-stage laparoscopic approach over ERCP

c::, ERCP is indicated if single-stage approach is contraindicated:
o Acute cholangitis
o Suspicious of malignancy
o Contraindications for laparoscopy (coagulopathy, instability)

• If no experience with CBD exploration:

c::, Place T-tube and terminate procedure then transfer

• For small distal CBD stone (:s 3 mm) could be flushed past the ampulla with
saline while administering IV 1 mg glucagon (Avoided in patients taking beta­
blockers) or nitroglycerin to induce relaxation of the sphincter of Oddi

• Options for severely impacted stone: (After failure of other methods)

c::, Electrohydraulic lithotripsy via Choledochoscope
c::> CBD drainage procedure
c::, Place T-tube and terminate the operation if not familiar with CBD
exploration and refer for stone treatment

c::> Duodenotomy and sphincteroplasty

(Almost never required anymore)

Post-op ERCP used for retained non-impacted

o CBD drainage procedures
• Indications:
c::, CBD stone associated with stricture

c::, Inability to remove intra-hepatic or CBD stones by other methods

(including ERCP)

c::, Persistent CBD stone with dilated CBD > 1.5 cm

c::, Multiple(> 5) or prirrnary CBD stones

• Types
c::, Trans-duodenal Sphincteroplasty
o Preferred option for Non-dilated CBD diameter(< 1.5 cm)

o Morphine-neostigmine(Nardi) test is used to identify patients who

will get the benefits of this procedure

o Associated with decreased incidence of re-stenosis

o Transampullary septectomy should be performed to decreased the

risk of pancreatitis

c::, Choledochoduodenostomy (COD)

o Most favorable drainage procedure to prevent recurrence

o Used for:
• Impacted distal CBD stones
• Funnel syndrome(CBD stone with distal CBD stenosis)
• lntraoperative failure of CBD stone extraction throughout
CBD exploration

c::, Choledochojejunostomy (CDJ)

o For patient with CBD stones who underwent CDD complicated by
Sump syndrome which failed to managed endoscopically

o CDD and CDJ should not be performed If patient having gallbladder

disease and no plan for cholecystectomy or questionable cystic
duct patency

c::, Hepaticojejunostomy (HJ)

o For patient found to have significant duodenal inflammation or
inadequate mobility of duodenum to do CDD

o Most superior drainage procedure

o Lowest rate of stricture due to rich blood supply

CHOLANGITIS
■ Pathophysiology:
o Obstruction of the bile duct (Partial> Complete)
o lntraluminal pressure> 20 cm H2O
o Sepsis when colovenous reflux occurs at> 200 mm Hg

■ Most common causes:

o Gallstones
o Secondary CBD stone

■ Most sensitive test: MRCP

■ Most common organisms: E. coli and Klebsiella

■ Complications:
o Renal failure (Most common serious complication)
o Liver abscess
o Sclerosing i
cholangitis
o Pancreat tis
o Portal vein thrombosis
o Sepsis and septic shock

■ Clinical presentations:
o Charcot's triad: (in 50%)
• RUQ pain
• Fever with Chills
• Jaundice

o Reynolds' pentad: (suggests septic shock)

Charcot's triad plus
• Mental status changes
• Shock

■ Treatment:
1) Fluid resuscitation and antibiotics (Piperacillin-based)

2) Emergent ERCP with sphincterotomy for decompression and stone extraction

c::> If failed
-+ Emergent PTC
c::> lf failed
-+ Emergent OR and insert T-tube

Elective cholecystectomy (after 6 weeks) for patients with gallbladder, after resolving of sepsis
STEPS OF ERCP:
1) Inserting the duodenoscope and positioning over the papilla

2) Locating the papilla, Cannulating the major papilla followed by minor papilla

3) Sphincterotomy at 11 O'clock
o 3 and 9 O'clock: Vessels entry to CBD
o 4 O'clock: Site of pancreatic duct

Absolute contraindications of ERCP Relative contraindications of ERCP

Pharyngeal or esophageal obstruction
Severe uncorrected coagulopathv
Existing bowel perforation
Unstable cardiopulmonary status
Alter anatomy of GIT tract
(Biliary - enteric anastomosis)
Portal hvoertension with esophageal + gastric varices
Acute pancreatitis except gallstone pancreatitis
Recent mvocardial infarction
ReDeated failed attempts at ERCP theraov
Patient cannot be adeguatelv sedated
AnaPhvlactic reaction

HEMOBILIA
■ Etiology:
o Iatrogenic injury (Mostly blunt trauma) of right hepatic artery "Most common''
o Post liver biopsy
o Post liver transplant
o Infection

■ Pathophysiology:
o Fistula between bile duct and hepatic arterial system (arterial pseudoaneurysm)
o Bleeding into biliary tree, then to the gastrointestinal system

■ Presentation:
o Right upper quadrant abdominal pain
0 Upper GI bleeding
o Jaundice
o Acute pancreatitis (Rare)

■ Treatment:
o Conservative (mild cases)
o Angioembolization

Bilhemia is passage of bile into the bloodstream through bile duct-venous system fistula after
blunt liver trauma
COMMON BILE DUCT INJURIES
■ Most commonly occur after elective laparoscopic cholecystectomy for chronic calcular
cholecystitis, f in elderly
o Risk in laparoscopic cholecystectomy � 0.5-3%
o Risk in open cholecystectomy � 0.2-0.5%

■ Operative risk factors·

o Retraction of the gallbladder fundus
• Excess cephalad retraction make cystic duct and CBD in one line
(Most common risk factor)

• Insufficient upward retraction can make CBD to be divided twice to remove the
gallbladder

o Retraction of the gallbladder infundibulum

• Upward retraction make cystic duct in line of CBD and more risk of CBD injury
• Insufficient lateral retraction can make CBD look like cystic duct
• Excessive retraction can lead to CBD Tenting (high risk of injury during cystic
duct division}

o Injury to the CBD most commonly occur at: Dissection of triangle of Calot's

■ Factors suggest clipping CBD instead of cystic duct

o Non-fully encompassed by standard clip (9 - 10 mm}
o Persistent bile leak from liver
o Identification of second ductal structure
o Extra soft tissue adjacent to porta hepatis
o Duct can be traced behind duodenum
o Large artery behind the presumed cystic duct

■ Presentation:
o Elevated liver enzymes

o Abdominal pain with bile collection

• No collection if the duct was ligated

o Nausea, vomiting, jaundice

o ± Cholangitis
■ Investigations of biliary injury:
o CBC and Liver enzymes, Septic workup for patients in sepsis

o lntraoperative cholangiogram
• To characterize the anatomy of bile duct injury

o U/5 to rule out collection

• Drainage of fluid: if bilious fluid± Transfer

o HIDAscan
• Used to confirm site and persistence bile leak noninvasively

o ERCP
• Used to assess biliary tree (distally)
• ± Sphincterotomy
• ± Stenting

o PTC
• Used to assess biliary tree proximally in jaundice patient with proximal dilated
duct and allow for decompression by stent or catheter (PTD}

o MRCP with gadolinium contrast (80% accuracy to detect site of leak)

• May identify injury alone without ERCP/PTC and ERCP/PTC can be used as
therapeutic modality or if MRCP failed to identify extent of injury

o MRAorCTA
• 10 - 30% the incidence of concurrent vascular injury
• Most common vascular injury is right hepatic artery
• Vascular injury associated with pseudoaneurysm, delayed hemorrhage, bile
ducts (necrosis, stenosis and cholangitis), liver (necrosis, atrophy)
• CT also can identify lobar atrophy
■ Approach:

Drain and Transfer

o Intra-operative: 25% of major bile duct injury identified at time of operation
• Call for help from hepatobiliary or expert surgeon
• Identify the site of bile leak if post-operatively
c:, Cystic duct stump, liver bed, bowel running, kocherization

• Perform cholangiogram
• Insert external drain
• Do not attempt to remove gallbladder unless if no structure will be divided
• Do not ligated proximal transected duct, but insert retrograde catheter to control
leak
• If satisfactory repair by expert surgeon is possible, it is ideal to perform it at time
of original operation

o Post-operative:
• Avoid early reoperation and perform complete assessment

• Control sepsis
c:> Drain the abdomen: Percutaneous drainage

c:, Drain the liver: Percutaneous transhepatic drainage (PTD)

c:, Antibiotics ± antifungal

• Investigate
c:> HIDA, MRCP, PTC, CTA

c:> ERCP ± Stenting ± Stphincterotomy

o Help to reduce risk of leak, stricture, and help identification and
dissection of hepatic ducts

• Transfer
c:> To hepatobiliary center for delayed reconstruction after 6 - 12 weeks to
allow subside of inflammation

• Patient may need

c:> Liver transplant
o if associated with Portal hypertension, intrahepatic stenosis

c:> Hepatic resection

o if associated with concurrent vascular injury or recurrent stricture
and cholangitis
■ Classifications:
o Bismuth, Strasberg, Amsterdam, Neuhaus, Hannover, Lau

■ Strasberg classification:
o A: Cystic duct leak or from liver bed of subvesical duct of Luschka

o B: Occlusion {almost aberrant right hepatic duct)

• Doesn't associated with collection
• Associated with cholestasis and lobar atrophy

o C: Transection of aberrant right hepatic ducts

o D: Non-circumferential Lateral injury of CBD

o E: Injury to the Main duct ''Bismuth-Cor/ette classification"

• 1: Transection > 2 cm from bifurcation
• 2: Transection < 2 cm from bifurcation
• 3: Transection of hilum with int.act hilar plate
• 4: Separation of CBD in hilum
• 5: Type C + Hilum injury

>2cm >2an E3
E1 E2

E4
Tvne of iniurv Manaciement of biliarv iniurv based on Strasberci Classification

A
Percutaneous drainage (initial)

ERCP±Slanting±Sphincterotomy (definitive)

Mild: Conservative± Percutaneous drainage (For type C)

B Severe or Cholangitis: Percutaneous transhepatic biliary drainage (PTD)

lntraoperative or Recurrent sepsis or cholangitis

■ < 3 mm: Simple ligation
■

C
�4mm:
0 Re-implant to their multiple segments
0 Hepalicojejunostomy
0 Right posterior hepatic sectionectomy (definitive option)
-
> 50°6, involvement of circumfere nce or due thermal inju!Jl or near bifurcation
■ Roux-en y Hepaticojejunostomy (definitive option)
< 50% involvement of circumference
Minor:
■ Dilatation and stenting (by endoscopy or radiology)
0 Used for short segment stricture
C Used as temporary method (post-op} or permanent in high risk patents

■ Primary repair Over "T tube"

(T tube placed through same incision as formal choledochotomy)

Extensive or due to thermal inju!::l'. or small < 1 cm far from bifurcation:

■ Primary repair Over "T tube - end"

..
(T tube place through separate choledochotomy and injury closed over
"T tube - end" to minimize risk of stricture) �
No tissue loss, or minimal and far from the bifurcation:
■ Duct to duct primary repair over "T tube - end"
(through separate choledochotomy)
If stricture happens -# Balloon dilatation and stenting

Major tissue loss or Qroximal inju!Jl near bifurcation:

■ Ligation of distal bile duct

E
■ Debridement of proximal bile duct
■ Definitive
0 E1, E2, E3: Roux-en y Hepaticojejunostomy or Choledochojejunostomy
Cho/edochoduodenostomy is an option for distal CBD injury
In E3 Lower the hilar plate and extend the choledocotomv along left hepatic
duct to ensure large common channel

0 E4options
• Create common back wall and jejuna! lump Hepaticojejunostomy
• Double riaht and left heoaticojejunostomv
GALLBLADDER ADENOCARCINOMA (Female)

■ Most common cancer of the biliary tract (90% are adenocarcinoma)

■ Most common site of metastasis: Liver (segments IVb and V)

■ Most prognostic factor: Depth of invasion

■ Initial nodes to be involved: Cystic duct nodes

■ Risk factors:
o Female, Ulcerative colitis, Infection (Salmonella typhi}

o Choledochal cysts, Mirizzi syndrome

o Gallstones (Large stone > 2.5 cm) "Highest risk associated with GB cancer"

o Gallbladder wall calcifications

• Types:
c::, Diffuse calcifications (Porcelain gallbladder) 15% risk of malignancy
• Less risk of malignancy due to Transmural calcifications and
no remnant mucosa to develop carcinoma

c::, Focal calcification (35% risk of malignancy)

• Selective calcification in part of mucosa

• Risk of malignancy on pathological specimen was found to be 6% compared to

1%, which is less than what literature reported
• Prophylactic cholecystectomy was absolute indication in the past, currently it is
individualized to the patients, risks/benefits, and more with focal type

o Gallbladder polyp
• Cholesterol polyp /Cholesterolosis):
c::, Most common type ot polyp (comet tail) "usually multiple"

c::, U/5 Findings:

o Multiple, Hyperechoic, pedunculated, non-mobile,< 5 mm lesions
with no posterior shadowing

c::, Speckled cholesterol deposits in macrophages on the gallbladder

mucosa (Strawberry gallbladder}

• Granulomatous polyps
c::, Usually developed at fundus
c::, Thick gallbladder wall with septation or stricture

• Adenomyomatosis (cholecystitis glandularis proliferans):

c::, Hypertrophy of the smooth muscle -+ Sinuses
c::, Sessile lesion, microcysts •usually> 10 mm"
c::, Cholecystectomy is the treatment of choice
• Adenoma (The only pre-malignant polyp)

• Management of gallbladder polyps:

c:) Laparoscopic Cholecystectomy
o For> 10 mm polyp (88% risk of malignancy)
o Increasing in size, associated with gallstone, Age> 60 years
o Suspicious of malignancy by U/S
(Open approach to avoid perforation of gallbladder)

c:) Follow-up with U/5 every 6 months - yearly

o < 10 mm and asymptomatic with no suspicious of malignancy
■ i
Investigat on:
o U/S abdomen
o CTCAP
• Preoperati ve as staging for high-risk patients {> 50 years, > 10 mm polyp or
suspicious of malignancy)

• Postoperative for tumor 2: T1 b

■ Staging:
o Stage I: T1
• T1a Invading lamina properia only
• T1b "Invading muscularis layer" 30% involving the lymph nodes

o Stage II: T2 "Invading peri-muscular connective tissue: subserosaf'

• 60% involving of lymph nodes
• Dissemination of GB cancer can occurs when dissecting into subserosal space
by hook in laparosoopic cholecystectomy for incidental GB cancer

o Stage Illa: T3 "Invading the serosa, liver, or adjacent organs; stomach, duodenum"

o Stage lllb: N1

o Stage IVa: T4 "Invading main portal vein, hepatic artery or 2: 2 extrahepatic organs"

o Stage IVb: N2 / M1

■ Stage-based management·
o Stage Tis and T1a: SimpleCholecystectomy

o Stage T1b: (Confined, Limited to, Extending into, Invading but not penetrating, Invasion
of muscular layer)
• Radical cholecystectomy regardless the risks (Cameron) "Preferable"

• Radical cholecystectomy only if associated with perineural, lymphatic or vascular

invasion {Sabiston}

o Stage T2: (Extending into and through, invading and penetrating muscular layer)
c:> Radical cholecystectomy and Portal lymphadenectomy

o Selective T3: Radical cholecystectomy and Portal lymphadenectomy

■ Lymphadenectomy:
o N1: "Cystic nodes, CBD or portal vein nodes"
• Should be excised if involved in stage T1b or T2

o N2: "Celiac, Para-aortic, SMA, Peri-pancreatic" biopsied for frozen section if suspicious
• No surgery if N2 involved
■ Management of gallbladder cancer:
o Suspicious of gallbladder cancer (fundal hard mass , severe wall thickening)
+ Conversion to open surgery is the standard of care
+ Doesn't mandate immediate radical cholecystectomy
+ Tissue biopsy for frozen section (High risk of peritoneal dissemination)
c:> Positjve: Radical cholecystectomy
c:> Negative or not-diagnostic: Closed and wait for final pathology

Re-exploration and achieve RO resection should be within 2 weeks

o Radical Cholecystectomy, involved open cholecystectomy and either:

o Wedge resection of segments /Vb and V "preferable"
o Hepatic wedge resection
o Right hepatic /obectomy
o Trisectionectomy with RO resection

o Risk of ports involvement 10 - 20% in T2 / T3

• Previously was recommended to do excision for all laparoscopic ports
• Current guidelines recommend against port site resection which showed no
improve of patient outcome

o Cystic duct margin should be sent to frozen section

• Positive: excise and excise CBD margins as frozen section until achieving
negative margins, followed by hepaticojejunostomy

o Gallbladder perforation I iatrogenic bile leak has poor prognostic value

o No recommendations regarding neo-adjuvant therapy

o Unresectable or metastatic disease: (M1, N2)

• Chemotherapy (Gemcitabine .and Cisplatin)

• Biliary stenting rather than bypass

BILE DUCT CANCER (CHOLANGIOCARCINOMA) (Male)
■ Most common primary bile duct cancer

■ 2nd most common primary hepatic malignancy

■ Arise from the biliary epithelium

o Most tumors are adenocarcinoma (>90%)
o Most common location: at bifurcation of CHO confluence
o Carcinoid is rare and arising within biliary system leading to obstruction

■ Most patients are found to have unresectable disease at presentation

o Tumor recurrence occurs at 37 - 70%

■ Risk factors:
o Male
o Ulcerativei colitis
o Pancreat tis
o Infection
• Parasite: Clonorchis sinensis, Opisthorchis viverrini
• Bacteria: Salmonella
• Viral: Hepatitis C and B

o Primary sclerosing cholangitis

o Choledochal cysts

■ Types:
o Perihilar cholangiocarcinoma (Klatskin tumors) "most common type"
o Distal cholangiocarcinoma 20 - 40% "2nd most common type"
o lntrahepatic cholangiocarcinoma

■ Histological classification: (From most common and most favorable histology)

o Nodular (Most common type)
o Papillary
o Scirrhous
o Diffusely infiltrating

■ Investigations:
o CBC (for sepsis, cholangitis)
o Liver function profile (for obstructed jaundice)
o CA 19 - 9 (98% specific and 79% sensitive}
o Other tumor markers: CEA, Chromogranin A
o Tissue diagnosis difficult to obtain non-operatively, except in advanced cases
• Percutaneous FNA biopsy, biliary brush or scrape biopsy, and cytological
examination have a low sensitivity and associated with spreading intro the tract
■ Imaging:
o U/S liver
o CT scan
o MRCP
o ERCP (superior for distal cholangiocarcinoma}
o PTC (superior for perihilar and proximal cholangiocarcinoma)
• Help to identify proximal extent of the tumor
(most important factor in determining resectability)

■ Bismuth-Corlette classification: (for Klatiskin tumors "perihi/ar cholangiocarcinomas")

o Type I: Limited to CHO

o Type II: Involve bifurcation of right and left hepatic ducts

o Type Ill:
• Illa: Type II and extend to right hepatic duct
• 111 b: Type II and extend to left hepatic duct

o Type IV:
• Extending to both right and left hepatic ducts
• Multifocal

o Type V: Stricture at junction of CBD a.nd cystic duct

 ■ Management of cholangiocarcinoma:

Upper½ "Klatiskin tumors" Lower 1/,

(Most common) (More resectable)

I I I
Unresectable Resectable
(Most common)
Resectable Unresectable (Most common)

Roux-en Y
Hepaticojejunostomy I Whipple procedure
I
Cholecystectomy

Gastroieiunostomv

I At bifurcation of CHD or proximal part I

l
Excision of bile duct I Right hepatic duct I Left hepatic duct
I
Portal lymphadenectomy
l !
II
Bypass p rocedure
Cholecystectomy
Right lobectomy Left lobectomy
Bilateral Roux-en Y
Hepaticojejunostomy
■ Resectability:
o Resectable:
• Tumor invades constructible venous structures including portal vein
• Tumor invades Porta-hepatis nodes; Cystic nodes, CBD or Peri-portal nodes
• Unilobar vascular structures
Tumor requires resection of liver segments, including segments I, IV, or V
• Involvement of both extra-hepatic right and left hepatic ducts

o Unresectable

• Bilateral involvement of portal vein (Right and Left or main vein)

• Bilateral involvement of hepatic lobar artery
• Bilateral lobar metastasis of the liver
• Bilateral intra-hepatic biliary duct (as right hepatic duct and segment 3 duct}
• Lobar atrophy + Involvement of contralateral Portal vein/ Biliary radicals

• Extra-hepatic metastasis
c::> Tumor invades Celiac, Para-aortic, or SMA nodes
c::> Peritoneal implants

-# Biliary bypass and cho/ecystectomy

■ Palliative options:
o Biliary bypass and cholecystectomy for decompression and to prevent risk of acute
cholecystitis
• > 50% found to have peritoneal implants, nodal or hepatic metastasis
intraoperatively
• Segment Ill or IV bypass with hepaticojejunostomy or choledochojejunostomy

o Biliary stenting (Internal drainage; Biliary Endoprostheses)

• Used in high-risk patient or in sepsis, but can predisposing biliary infection
• Mainly used for:
c:, Unresectable malignancy (metallic stent, or plastic stent as temporary)
c:, Borderline resectable malignancy (polymer; plastic stent)

o Liver transplantation
• Mayo Clinic Criteria (University of Nebraska strategy)
1) Chemoradiation "5-Fluorouracil, and extra-beam 4,500 cGy"
2) Transcatheter-iridium-192 brachytherapy "2000 - 3000 cGy"
3) Oral Capecitabine
4) Liver transplant
• Inclusion criteria
c:, Locally advanced unresectab/e disease (with no local metastasis)
(hilar or extra-hepatic cholangiocarcinoma)

c:> Primary sclerosing cholangitis with resectable disease

c:, Absence of medical contraindications

• Exclusion criteria:
c:> Extra-hepatic disease (including regional lymph nodes)
c:, Uncontrolled infection
c:> Prior attempt at resection
c:> Prior treatment with radiation or chemotherapy
c:> Previous malignancy within 5 years

o Chemotherapy or Radiation (studies showed no improvement of survival)

o Photodynamic therapy used for unresectable cholangiocarcinoma without evidence of

metastasis and non-candidate for TXP

o Radioembolization (for intra-hepatic cholangiocarcinoma)

CHOLEDOCHAL CYSTS (Female)
■ Risk factor for:
o Cancer throughout biliary tree (More common at gallbladder) 20%
o Cholangiocarcinoma 10 - 30%
i
o Pancreat tis 30%

■ Etiology:
o Abnormal pancreaticobiliary duct junction (Babbitt's theory ofthe common channel)
i
o Pancreat c duct joins CBD 1 cm proximal to ampulla as common channel
• Enter duodenum as single duct in 70% of population "Common channel"
• Long common channel > 1 cm is predisposing factor for choledochal cyst
• Long common channel leads to reflux of pancreatic juice to biliary tree

■ Presentation: (Triad in < 50% of patients)

o Right upper quadrant mass
o Abdominal pain
o Jaundice

■ Jovest;gatioos·
o U/S Only 70% sensitivity -+ CT scan
o Biliary mapping
• MRCP -+
for proximal biliary tree
• ERCP -+
for distal biliary tree

■ Histological types:

-�
o Glandular
o Fibrotic

o Type I: (commonest)
• Fusiform or Cystic dilation of extrahepatic ducts

o Type II:
• True Saccular diverticulum of extrahepatic bile ducts

o Type Ill (Choledochocele):

• Dilation limited to intraduodenal portion of distal CBD

o Type IV: Multiple cysts

• IVa: lntrahepatic and extrahepatic cystic dilations
• IVb: Extrahepatic cysts witho-ut intrahepatic cysts

o Type V (Caroli)
• lntrahepatic saccular cystic dilatations± Peri-portal fibrosis
• 70% are bilateral
• 30 - 40% associated with renal disorders (renal cysts and nephrospongiosis)
• Complications:
c:> Cholangiocarcinoma should be ruled out with imaging and CA 19 - 9
c:, Cholangitis and sepsis
c:, Amyloidosis
■ Management of choledochal cyst:
TuR.L!
o Complete cyst excision including bile duct, Cholecystectomy, and Roux-en-y
hepaticojejunostomy
• Hepaticoduodenostomy is an option but can cause bile reflux in 30%
• Frozen section of the proximal and distal bile duct margins needed to exclude
cholangiocarcinoma

o Partial cyst excision and fulguration of remnant mucosa, cholecystectomy and

roux-en-y hepaticojejunostomy
• If the cyst is adherent to portal vein or major vascular structure

Type II
o Simple diverticulectomy with closure of CBO at cystic neck

Type Ill ICholedochocelel

o < 3 cm: ERCP with sphincterotomy

o > 3 cm:
• Transduodenal excision (Preferred)
• Drainage into duodenum

TypelY
o Extra-hepatic
• Complete cyst excision including bile duct, Cholecystectomy, and Roux-en­
y hepaticojejunostomy

o Intra-hepatic
• Segmental resection

TypeY(Caroli disease)
o Simple:
• Segmental resection

o Complex:
(> 1 segment, Bilobar, Portal hypertension, suspicion of cholangiocarcinoma)

• Liver transplant if> 1 segment or bilaterally involved

BILE DUCT STRICTURES
■ Risk factors:
o Ulcerative colitis
o Primary sclerosing cholangitis

■ Bile duct stricture without history of pancreatitis I biliary surgery is cancer until prove otherwise

■ Etiology·
o Benign
• lschemia (Most commonly, due to iatrogenic event)
• Chronic obstruction
• Infection
• Chemical agents

o Non-benign
• Primary sclerosing cholangitis
• Cholangiocarcinoma
• Hepatocellular carcinoma
• Gallbladder cancer

■ Highest incidence of positive bile cultures:

Strictures > CBD stone > acute cholecystitis > chronic cholecystitis

■ Investigations
o Liver function tests
• Unilateral (as right hepatic duct stricture)
c::> f ALP with normal bilirubin level

• Bilateral (as CBD stricture)

c::> f ALP and f Bilirubin

0 MRCP (Best)

■ Management:
o Initial: ERCP with dilatation and ste:nting (for benign conditions)
if fail -+ PTC

o Definitive treatment: Excision with

• Choledochojejunostomy (associated with lowest recurrence of jaundice)

• Hepaticojejunostomy

• Choledochoduodenostomy
c::> Associated with stenosis of the anastomosis (Cholangitis)
c::> May be preferable option for distal CBD stricture
o Dose not divert the bile, easy to perform, and it leave the jejunum
for gut I pancreatic decompression if needed

•sump syndrome"
c::> by collecting debris at distal segment of bile duct lead to obstruction I
recurrent ascending cholangilis
PRIMARY SCLEROSING CHOLANGITIS (Male)
■ Chronic inflammation and destruction of both intrahepatic and extrahepatic bile ducts
■ Immune-mediated disorder
-+ Multifocal strictures of the biliary tree
-+ biliary cirrhosis
-+ Bloody diarrhea and symptoms of inflammatory bowel disease
-+ Fluctuating jaundice
Hepatic duct bifurcation is the most severely strictured segment

■ Associated with increased risk for cancer:

o Cholangiocarcinoma 14%
o Independent risk factor for CRC in ulcerative colitis 2%
o Gallbladder cancer
o Hepatocellular carcinoma

■ Associated wilb ·
o Ulcerative colitis (80%}
o Retroperitoneal fibrosis
o Thyroid disease
o Autoimmune hepatitis (DM type 1, Pancreatitis} 17%
o Gallstones 25%

■ Diagnosed by:
o ERCP (Best), MRCP or PTC
• "Beads on a string• on ERCP
c:> Segmental fibrosis areas separated by saccular dilatation areas

o j ALP "biochemical hallmark"

■ Follow-up investigations:
o Annual ultrasound scan for gallbladder is recommended

o Thyroid function tests for follow-up thyroid status

o Colonoscopy is warranted to exclude the diagnosis of IBD

o Cytological examination of biliary brushing and biopsy should be obtained for all
Sensitivity of ERCP brush cytology and biopsy to detect malignancy is: 30 - 50%

o CA 19-9 follow-up recommended (false-positive in bacterial cholangitis}

o Liver biopsy non-specific for PSC

■ Management:
o PSC must be distinguished from secondary sclerosing cholangitis
� Due to biliary tree injury (obstruction, infection, chemical agents, and ischemia)

o Surgical resection of extrahepatic ducts needed to exclude cancer in dominant biliary

strictures

o Strong suspicion for malignancy in dominant stricture

o Liver transplant indicated if liver cirrhosis developed

Dominant stricture
CBD diameters 1.5 mm
Asymptomatic Symptomatic CHO diameters 1 mm
I
No treatment I I
Cancer suspected
II No cancer suspected
I
Pruritus Steatorrhea

Cholestyramine or UDCA
± Anti-histamines
Fat-soluble vitamins
I Endoscopic balloon dilation ±
stenting {risk of cholangitis)

Resection of hilar and extrahepatic biliary tree

Cholecystectomy
Frozen sections
± Stents with transient Roux-en-Y hepaticojejunostomy
PRIMARY BILIARY CIRRHOSIS (Female)
■ Women; medium-sized hepatic ducts

■ Cholestasis -+ cirrhosis -+ portal hypertension

■ Positive Anti-mitochondrial antibodies (AMA)

■ No increased risk for cancer

■ Treatment:
o Ursodeoxycholic acid

o Liver transplant

POSTCHOLECYSTECTOMY SYNDROME
■ RUQ pain, vomiting and diarrhea

■ In up to 40% post cholecystectomy patient

■ Post-cholecystectomy changes:
o ! Total bile salt pools only

■ Etiology:
o Biliary microlithiasis (Most common}
o Dysfunction of sphincter of oddi
o Remaining stone
o Biliary injury
o Dysmotility
o Choledochocyst

■ Management:
o Ursodeoxycholic acid

o Cholestyramine if associated with di.arrhea

• Prevent reabsorption of unconjugated bilirubin
OTHER CONDITIONS
■ Ursodeoxycholic acid (UDCA)
o Tertiary bile acid converted from 7• Ketolithocholic (Secondary bile acid)

o Mechanism of action
• Reduce duodenal absorption leading to disruption of micelles and reduce
cholesterol absorption leading to decrease cholesterol concentration

o Used for:
• Primary biliary cirrhosis
• Post obesity surgery
• Post cholecystectomy syndrome
• Most of biliary anastomosis (risk of stricture and cholangitis)
• Gallstones:
c:> Small stone size (< 0 .5 to 1 cm)
c:> Mild symptoms and non-candidate for cholecystectomy
c:> Good gallbladder function (Normal filling and emptying)
c:> Non-calcified non-pigments stones

o Dissolution rate:
• 40-60%
• Reaching up to 90% in ideal patients
45% recurrence in 5 years

o Dose:
• 10 - 15 mg/kg/day for 6 months

■ Delta bilirubin:
o Bound to albumin covalently
o Half-life of 18 days{> 2 weeks)
+ May take a while to clear long-standing jaundice

■ Drugs that causes cholestasis:

o Ceftriaxone
o Ciprofloxacin
o Augmentin

■ Gentamicin + ! biliary contraction, less biliary concentration than serum

■ Extra-biliary fistula:
o t Bile synthesis
o t Bile-acid Dependent flow
OPERATIVE NOTES
First Open Cholecystectomy was done by: Karl Langenbuch 1882

First Lap Cholecystectomy was done by: Erich Muhe 1985 (Germany)

Laparoscopic Cholecystectomy
■ Ports Jocation: "in order·
o 5- 10 mm telescope (Infra or lateral to umbilicus)
Dissection of umbilical port should be- in horizontal way to prevent bleeding

o 10 mm (Epigastric area - Midline)

o 5 mm (Right mid-clavicular line} around 2 cm below costal margin

o 5 mm (Right anterior axillary line) 5 cm far from mid-clavicular port

Any ports should not be in line between telescope and gallbladder

Al/ accessory ports should be directed to gallbladder as it penetrates abdominal wall to

prevent trauma of abdominal wall with angulation

■ Position
o Supine
o Reverse trendelenburg and right-side up during cystic dissection

■ Steps:
1) Exploration of the abdomen
• Easy operation: Smooth non-cirrhotic liver, protruded gallbladder, and no adhesions

2) Retraction of gallbladder fundus

• Grasp the fundus of gallbladder and retract it upward and laterally

• Excess cephalad retraction make cystic duel and CBD in one line and more risk for injury
• Insufficient upward retraction can make CBD to be divided twice to remove the gallbladder
• Dissect and cauterize any adhesions preventing adequate retraction
• Distended gallbladder may need needle aspiration for proper retraction
• Thick wall better to retract it with tooth forceps

3) Retraction of gallbladder infundibulum

• Should be retracted downward and (Laterally/ Medially)
• Upward retraction of Hartmann's pouch make cystic duct in line of CBD and t risk of injury
• Insufficient lateral retraction can make CBD look like cystic duct
4) Dissection of Cystic pedicle:
• Dissect the anterior peritoneum:
o Grasp posterior leaf of Hartmann's pouch and retract it downward/laterally
Retraction done by left hand and dissection carried out with right hand
• Dissect the posterior peritoneum: (Preferred to start with "less vascular")
o Grasp anterior leaf of Hartmann's pouch and retract it downward/medially
• Dissect peritoneum done by starting proximally and go as far back as the liver with Maryland
grasper as blunt dissection (Don't use cauteiy before identify cystic structures)

• Medial wall of Hartmann's pouch should be cleared completely

• Rouviere's sulcus
o Fissure between right lobe and caudate process during posterior dissection

o Corresponds to level of porta hepatis where right pedicle enters the liver

o Recommended that all dissection to be above (or anterior) to the sulcus to avoid injury
of bile duct

5) Separation and division of cystic vessels

Obtaining the Critical View of Safety (CVS) by Sffasberg "Liver edge, Gallbladder, Cystic duct"
■ Dissection of Calot's triangle (cleared from fat and fibrous)
■ Dissection of lower 1/3 of gallbladder from cystic plate (liver bed}

■ 2 and only 2 structures should be seen entering the neck of gall bladder

By using Maryland's grasper, gently opening of the jaw in the line of cystic duct between the
duct and artery

Operative cholangiogram (if planned) should be done prior to clipping, cutting or transecting
any ductal structures
Cystic artery:
■ Divided after complete distal skeletonization and make sure to be enter to gallbladder
■ Should be clipped before the duct
o If duct divided before, may lead to dissection of cystic artery as stretch injury

■ 2 clips applied proximal and 1 clip distally

o Alternative: One clip and hook with cautery above it (in small artery)

■ Skeletonization done by:

o Maryland vertical opening in line of the structure
o Hook up and down
o Hook cauterization of bands in vertical direction
(Should be minimal with low cauterization power)

■ AnteriorI Posterior branches

o Sometimes cystic proper artery divides into anterior and posterior branches before enter
gallbladder
o Most common cause of intraoperative bleeding is clipping of anterior branch and failure
to identify posterior branch
(Posterior branch should be identified in all cases)

■ Right hepatic artery

o Injury to it associated with right hepatic duct injury/ right liver ischemia
o Can be prevented by completely dissection of artery up to:
• Entrance level to gallbladder

• Proximal 1/3 of gallbladder to make sure it is not looped right hepatic artery with
short cystic artery leading to division of right hepatic artery
Cystic duct:
■ Skeletonized up to the gallbladder and 1 cm away from CBD
o Cystic duct should be completely stripped from anterior and posterior aspects
o Stone should be milked up to gallbladder before clipping

■ 2 clips applied proximal and 1 clip distally

o The distal clip preferred to be directed opposite to previous clips for good stump
o Cystic duct stump should be short enough to prevent another gallbladder and long
enough to control complications if developed postoperative

■ Should be clipped without excessive retraction + Tenting of CBD

■ Some preferred to clip the duct after "elephant head appearance• or ''elephant trunk sign•
which is visualized after proximal dissection of peritoneal folds medially and laterally

■ Alternative ways for to divide cystic duct:

+ Extra-corporeal ligation, Endo-GIA stapler, or Endoloop
o Used in> 5 mm size of cystic duct
o Some sources preferred ligation over the clip, as clip can be displaced into CBD and
forms CBD stone over years

■ Factors suggest clipping CBD instead of cystic duct

o Non-fully encompassed by standard clip (9 - 10 mm}
o Persistent bile leak from liver
o Identification of second ductal structure
o Extra soft tissue adjacent to porta hepatis
o Duct can be traced behind duodenum
o Large artery behind the presumed cystic duct

6} Scissor to divide cystic artery followed by cystic duct

7} Dissection of gallbladder from liver bed should be carried out in avascular plane

8} Extraction of gallbladder
• Preferred to be through 10 mm epigastric port (to prevent port-side hernia)
• Neck of the gallbladder should be engaged first

9} Irrigation and suction of any clot, bleeding, bile

10} Remove any remaining stones to prevent abscess collection

11} Inspect liver bed for any bleeding or bile

• Can be controlled by hook and cautery, silvercil gauze, hemostatic agents
• Gallbladder bed may be filled with omentum and a drain placed over omentum

12} ± Drain and deflate the abdomen

• May used if suspicious of bile leak or injury, severely inflamed or gangrenous gallbladder
• Drain must be removed after 24 - 48 hours if no suspicion of bile leak or bleeding with
recommended amount of< 100 ml/ day

13} Endo-fascia! closure of extraction port, and umbilical port if> 5 mm, followed by skin closure
Open Cholecystectomy
1) Right subcostal incision
o 2 fingerbreadths below costar margin from xiphoid to the anterior axillary line

2) Divide the falciform ligament

0 Doubly ligated with 2-0 silk and divided

3) Inspect the abdomen

4) Decompress the gallbladder with 16-gauge needle or a suction trocar if needed

Open Cholecystectomy from Above Downward:. (Retrograde) Gallbladder+ Calot's

(Fundus-first technique) "Preferred method in open cho/ecystectomy"
■ Decrease conversion in difficult cases

■ Steps:
1) Grasp the gall bladder and retracted downward and anteriorly

2) Dissect gallbladder from liver from fundus above downward until hepatoduodenal ligament
o Inspect the gallbladder fossa for leakage or bleeding

3) Dissect the area of the cystic duct and the common bile duct
o Identify cystic duct and it's union to CIBD
o Identify the cystic artery (Ligate proximally and distally with 2-0 silk and divide)

4) Isolate the cystic duct by double pass a 2-0 silk around it

Nonabsorbab/e sutures are acceptable for use cystic duct stump, but not recommended for biliary­
enteric anastomosis or cho/edochotomy suture lines, as they can be lithogenic and incite a chronic
inflammatory reaction

Best for bi/iary-enteric anastomosis: Monofilament absorbab/e sutures

5) ± Cholangiogram
o Clamp the cystic duct proximally and distally between two clamps, divide and ligate
o ± Jackson-Pratt drain

6) Remove gallbladder

Open Cholecystectomy from Below Upward (Antegrade) Calot's + Gallbladder

■ More bleeding is encountered using this technique than using the retrograde method

1) Dissect the area of the cystic duct and the common duct
o Identify cystic duct and artery

2) Doubly ligate the cystic duct and cystic artery with 2-0 silk and divided ± Cholangiogram

3) Dissect gallbladder away from liver bed ± Jackson-Pratt drain

Radical cholecystectomy
■ Same steps mentioned above + abdominal exploration for metastasis
■ Dissection of hepatoduodenal ligament and send lymph nodes including periportal to
histopathology ± celiac lymph node
o Foramen of Winslow is behind hepatoduodenal ligament (entering to lesser sac)

■ Umbilical tape with suction tube is used to encircle hepatoduodenal structure for applying of
Pringle maneuver during liver resection

■ Excise liver segments of IVb and V

■ Cystic duct sump excised and send to histopathology with cystic duct margin as frozen section
± CBD excision and hepaticojejunostomy if margin involved

■ Don't excise laparoscopic ports if laparosoopic cholecystectomy was done

Partial Cholecysteetomy
■ Definition:
o Cholecystectomy with leaving part of posterior wall of gallbladder ± fulguration

Subtotal Cholecystectomy
■ Definition:
o Cholecystectomy with leaving portion of the infundibulum in situ along cystic duct
o Used if the cystic duct cannot be diss,ected safely out from porta hepatis

■ Essential part:
o Removal all of the stones, and irrigation of the remnant part

■ Indications: (Also indications for drains)

o Difficult cases
• Severe inflammation:
c:> Acute or Chronic Cholecystitis, Mirizzi's syndrome

• Empyema or perforated gallbladder

• lntrahepatic gallbladder

o High risk patient for bleeding

• Cirrhosis
• Portal hypertension

■ Types:
A) Fenestrating
• By left the posterior part of gallbladder in situ, with cauterization of the mucosa
• Cystic duct closed internally by purse-string
• High risk of postoperative fistula, but not associated with cholecystolithiasis

B) Reconstituting
• Closure of the infundibulum "Hartmann's pouch• by sutures or staples
• Low risk of postoperative fistula, but associated with cholecystolithiasis

..
Cholecystostomy Tube
■ Indications:
o For Critical ill patient
• Unstable patient (ICU or on inotropes) with
• Acute cholecystitis
• Emphysematous cholecystitis

o For Contraindication for surgery

• Uncorrected coagulopathy, Cinrhosis (Child C liver cirrhosis)
• Early for intervention (Early Ml "ST or non-ST elevation")

■ Types:
o Trans-Hepatic
• Preferred route overall
• Associated with early tract maturation

o Trans-Peritoneal
• Preferred route to remove stone through a large tract
• Used when anatomical inaccessible through trans-hepatic approach
• Used in liver disease or coagulopathy

Size of pigtail tube: at least 8 Fr

■ Types of technique: (through UIS or CT guided)

o Direct trocar technique

o Seldinger technique through a guide-wire

• Preferred technique due to usage of fine needle
(Less risk of perforation or bleeding)

■ Technique:
o After insertion of the pigtail, bile and pus aspirated for culture

o Connect the tube to gravity drainage

o After drainage of bile, clamp the tube for 24 - 48 hours and re-assess the patient

o Discharge patient with the tube clamped

o Cholecystogram through the tube after 4 - 6 weeks

o Remove the cholecystostomy tube if

• Clear cholangiography (Patent cystic duct)
• Positive results:
• Bile drainage instead of pus
• Resolution of symptoms and signs
• Reduction in WBC > 25%
■ Status of cystic tube:
o Patent
• Can tolerate the surgeN later on:
• Interval cholecystectomy when patient become stable, individualized on
the basis of patient age and surgical risk (Recurrence rate: 10-50%)
• Can't tolerate the surgeN later on:
• Stone extraction before removal of cholecystostomy

o Occluded
• Stable: Keep the tube in place until the time of cholecystectomy
• Unstable (gangrene, or perforation): Emergent cholecystectomy
• Cholangitis: ERCP or PTC if failed -+ Emergent OR and insert T-tube
CHOLANGIOGRAM
■ Routine use is controversial and may limit the extend of injury but will not prevent injury
o Because injuries occur before cholangiogram

■ It helps to identify anatomy and can help repair injury if occurred

■ lntraoperative cholangiography may be performed to confirm the diagnosis and outline the
biliary anatomy before the CBD exploration is undertaken

■ Criteria for selective IOC:

o History of jaundice, History of pancreatitis, Elevation of hepatic enzyme levels
o Dilated CBD diameter, Wide cystic duct, Palpable CBD stones

■ Steps:
o Dissection of Calot's triangle
o Identify cystic duct
o Putting clip on cystic duct close to neck of gallbladder (without divide the duct)
o Incision made in cystic duct or rarely at the Common bile duct
o If at cystic duct -+ transverse incision at anterolateral boarder below the clip
o Insertion of cholangiogram catheter (4 - 5 Fr) at RUQ area and direct it to the incision
and cover over it by the clamp or clips or by Olsen cholangiogram clamp which catheter
located between the jaws
o Take a plain pre-contrast fluoroscopy image
• Flushed with 2 - 3 ml of saline to confirm there is no leaks at catheter opening

• Steep Trendelenburg position with table lilt to the right (left lateral position)
So the images will not superimposed by the vertebra
• 15-20 ml of diluted contrast dye 1 :1 with saline is injected under fluoroscopy

■ Completi on if
o Flow contrast into duodenum
o Filling of both right and left hepatic ducts (secondary biliary ducts)
• Change position to Trendelenburg position
Morphine used for contraction of the sphincter of Oddi

o Flow into CBD with absence of:

• Biliary tree dilatation
• Filling defects within the biliary· tree
G/ucagon used to relax sphincter of Oddi

o Tapering of the distal CBD

"With no filling defect or extravasation to be normal Cholangiogram"

■ Positive result (No proximal or distal fill)

"Duct is clipped, injured, intra-hepatic or distal stones•

o Convert to open and proceed with CBD exploration

o Performs hepaticojejunostomy
CBD Exploration

Indications:
■ Impacted stone
■ Positive intraoperative cholangiogram
■ CBD stone with absence of ERCP

Laparoscopic CBD exploration

■ Perform laparoscopic cholecystectomy without division of cystic duct (as retraction}

■ Put a clip near to the neck of gallbladder to avoid spillage

■ Contraindication for trans-cystic:

o Stones proximal to cystic duct(at common hepatic duct) "Due to cystic duct angle"
o Small, friable cystic duct(< 4 mm}
o Multiple CBD stones(> 8 stones)
o Large CBD stone(> 1 cm or more than diameter of cystic duct)

■ contrajndjcatjon tor trans-choledochal·

o Small CBD diameter(< 7 mm) (risk of stricture)
o Severe inflammation of porta hepatis

■ Steps:
o Positive cholangiogram

o Trans-cystic approach
• Transverse incision at cystic d1Uct(Ductotomy) if not done for cholangiogram

Flushing step
• Flush with 2 - 3 ml normal saline through cholangiography catheter
• Ensure all staff wearing radiation-protective clothes
• Repeat the cholangiogram
• IV 1 mg of Glucagon(in patients who are not on Beta-blockers)
• Repeat flush with repeat image
Clear by cholangiogram? Clip the proximal cystic duct

Mechanical step
• Insert guidewire while cholangiogram catheter in-place
• Balloon Dilatation of the cystic duct for 3 minutes
• Balloon catheter passing down to CBD, inflated and trial to retrieve the stone
• Wire Dormia basket stone extractor
• Choledochoscope(2.5 or 3-mm} Inserted directly or over guide wire
c::> With trial of retrieval or pushing of the stone

Clear by cholangiogram? Ligate the proximal cystic duct (No T-tube)

o Trans-choledochal approach
• Retract cystic duct upward and laterally expose anterior supra-duodenal CBD

• Confirmation by bile aspiration through 21-gauge needle on syringe

• 4 - 0 sutures laterally and medially (3 and 9 o'clock) on CBD for traction

• Longitudinal incision of 2 cm over anterior aspect of distal CBD at 12 O'Clock

• 4 Fr Fogarty catheter to remove stones after saline flushing
• Choledochoscope used and directed proximally and distally to ensure complete
removal of stones

• Insertion of 14 Fr T-tube
• Keep the T tube at the inferior end of choledochotomy
• Closure of CBD above the T tube with interrupted 4 - 0 absorbable sutures

• The tube brought out linearly through the abdominal wall

Open CBD exploration
Indications:
■ CBD stone in patient undergoing open cholecystectomy
■ When endoscopic or laparoscopic techniques failed or unavailable
■ When concomitant biliary drainage is required

Steps:
■ Right subcostal incision or upper midline incision
■ Cholangiogram for assess the indication for CBD exploration

■ Kocher maneuver by incision of lateral peritoneum of duodenum to expose distal CBD

■ Ligate proximal cystic duct to prevent migraLing stones from gallbladder

■ Dissect anterolateral of CBD 2 cm distal to cystic stump to open hepatoduodenal ligament

o Skeletonization of > 2 -3 cm can result in ischemia to the duct
o Dissection of hepatoduodenal ligament should be Lateral to hepatic artery

■ Aspirate the CBD to make sure you are in the right place ± send culture

■ Place 4 - 0 absorbable stay sutures medial and lateral to the supraduodenal CBD

■ Longitudinal incision of 2 cm of anterior wall of the CBD at 12 O'Clock (Choledochotomy)

o Never incise CHO due to risk of stricture and for the chance of hepaticojejunostomy
o Incision should be at level of cystic duct entry slightly to the left of mid-plane of CBD to
prevent opening of septum of fused cystic/CBD due to parallel insertion of cystic duct to
CBD in 20% of patients

■ Remove stones by·

o Extrinsic pressure by milking the stones to the upward choledochotomy
o Extraction of any obvious stones
o Explore the duct by using Randall stones forceps, Desjardin forceps, irrigation catheter,
biliary Fogarty catheter, Choledochoscope
• Instrument introduced closely, then introduced open and close to grasp stones

■ For severely impacted stone:

o Electrohydraulic lithotripsy via Choledochoscope
o Duodenotomy and sphincteroplasty (Almost never required anymore)
o Place T-tube and terminate the operation (and referral for stone treatment)
o CBD drainage procedure

■ Demonstrate ampullary patency by using a small French catheter

o If doubt, use a Bakes No. 3 dilator ve,y carefully or by Cho/edochoscopy

■ Conduct repeated irrigation of the biliary ducts to remove small stones or sludge

■ Drainage procedure if required

■ Performs cholecystectomy and repeat the cholangiogram

■ Close the defect over T-tube and bring the Hube straight out through separate incision
Common Bile Duct Drainage Procedures

General indications for biliary bypass procedures:

■ Persistent CBD stone with dilated CBD > 1.5 cm
■ Multiple (> 5) or primary CBD stones
■ Intra-hepatic stones
■ Choledochal cyst
■ CBD injury
■ CBD stricture/ obstruction
■ Malignancy(GB cancer, Cholangiocarcinoma, Periampullary cancers "palliative")

■ Trans-duodenal Sphincteroplasty
o Preferred option for Non-dilated CBD diameter(< 1.5 cm)

o Morphine-neostigmine(Nardi) test is used to identify patients who will get the benefits of
this procedure

o Associated with decreased incidence of re-stenosis

o Transampullary septectomy should be performed to decreased the risk of pancreatitis

■ Side-to-side Choledochoduodenostomy (COD)

o Easy and less operative time
o Most favorable drainage procedure to prevent recurrence

o Used for·
• Impacted distal CBD stones
• Recurrent stones requiring repeated interventions
• Funnel syndrome(CBD stone with distal CBD stenosis)
• lntraoperative failure of extraction CBD stone throughout CBD exploration
• Stricture leading to distal obstruction
• Distal obstruction from stricture
• Malignancy (Controversial)
Some preferred to avoid it in malignancy, as risk of re-obstruction, and others
found to be effective if CBD and duodenum are dilated and non-obstructed

o Side effects:
• Sump syndrome
• Recurrent ascending cholangitis
• High risk of stasis
Which managed by ERCP and sphincterotomy, or definitive as HJ
■ Choledochojejunostomy (COJ)
o More difficult and more operative lime

o For patient with CBO stones who underwent COD complicated by Sump syndrome
which failed to managed endoscopically

o Used for:
• Malignancy
• Strictures, and CBD stones as COD

o Types:
• Roux-en-Y end-to-side (retrocolic) jejunostomy
(40- 50 cm roux limb, jejunostomy limb 20 cm from ligament of Treitz}

• Loop side-to-side jejunostomy

Used for palliative (can lead to reflux and recurrent cholangitis)

COO and COJ should not be performed If patient having gallbladder disease (and no plan for
cholecystectomy) or questionable cystic duct patency

■ Hepaticojejunostomy (HJ)
o Most superior drainage procedure

o Lowest rate of stricture, due to rich blood supply

o For patient found to have significant duodenal inflammation or inadequate mobility of

duodenum to do COD

o Used for: (Benign/ iatrogenic I Malignancy)

• CBD strictures, injured or transected

• lntraoperative failure of extraction CBO stone throughout CBD exploration

• Palliative for malignant obstruction in periampullary region

• Intra-hepatic stones
 T-tube
■ Made of rubber to enhance fibrosis
■ T-tube sizes varies from 10- 16 French (12 - 14 Fr usually used)
■ Split one end of straight silastic catheter if T-tube not available
o Customized Silastic catheter T-tube prone to be dislodged

■ Short arm: CHO Long arm: CBD

■ T-tube-end directed straight outside abdomen for choledochoscopy if needed

■ Secure to skin with 2-0 silk and maturation need at least 2 weeks (4 - 8 weeks}

■ Usage:
o Decompression:
• Cholangitis who failed other methods
• As tract for re-stenting
• After repair of injury or after trans-choledochal CBD incision
• Impacted stone with non-familiar surgeon with CBD exploration

o Retained stone
• ERCP is alternative
• Cholangiogram postoperative 7 - 10 days to reveal CBD for retained stones

■ Removal:
Clinical and lab work-ups
Cholangiogram 7 - 10 days
I
I Clear
I Retained stone

Clamp the tube

re-assess with 24 hours
I '
Asymptomatic Symptomatic Keep the tube unclamp
Normal liver functions Obstructive symptoms
Discharge patient with T-tube for 4 - 6 weeks

Perform choledochoscope with basket

retrieval of the stone
Discharge Unclamp
Removal after 2 - 4 weeks

Cholangitis No Cholangitis
Gradually elevated LFT

ERCP
 T-tube

Common bile duel

Figure 14.18.

G,llbl..ddMr
,tff'W>V't<J at thit tiu

Hepatic
ducu

T ·wl><

To cn1vi� draina.t,e
 Biliary and Pancreatic stent

■ Indications:
o Leakage (pancreatic, biliary)
i
o Pancreat c fistula
o Obstructed jaundice
• Benign: benign biliary strictures, CBD stone
• Malignant: Pancreatic cancer, Cholangiocarcinoma

■ Relative contraindications: Bleeding, or Ascites

Metallic Plastic
For Malignant diseases (long-term) For Benign diseases
Indication - Unresectable pancreatic/ biliary cancer - CBD stones
- Malionant disease underooina neoadiuvant theranv - Bile/ oancreatic leak
Diameter 6-10 mm 2-4 mm (5Fr-12Fr)
Patency 6-9 months 2-6 months
- Balloon-mounted stents - Carey-Coons stent
Types - Silicone stents
- Self-exnandinn ISEMSI:
Uncovered Full covered Composed of:
Externally by silicon or PTFE - Polyethylene
- Polytetraftuoroethylene
- Teflon
1 Migration f Patency Cheapest

Advantage t Tissue ingrowth Can be used for multiple

times for benign diseases
Used for benion as well
Difficult to extract t Migration Require endoscopic
Limit use for benian causes dilatation before stent
Disadvantage
- t morbidity j Pancreatitis, Cholecystitis
- Poor Jona-term natencv t Stent occlusion lsludoel
Mia ration 1% 20% 6%
Occ lusion 4% 7% 33%

■ Complications:
o Stent occlusion
• Biliary sludge
• Tumor ingrow1h

Plastic stent: Removal and replacement evel)I 2-3 months or when occluded

Metallic stent:
- Removal and insertion of plastic stent (in life-expectancy< 3 months)
- Insertion of second SEMS within the occluded one more
effective than mechanical cleansing

o Stent migration
o Pancreatilis / Cholecystitis
Pancreas
PANCREAS
ANATOMY AND PHYSIOLOGY
■ Pancreas is totally retroperitoneal organ, located against L1 - L2
■ Ventral buds � Wirsung duct (major}, uncinate and inferior head
■ Dorsal buds � Santorini duct (minor), body, tail, and superior head
� Communicate with CBD before duodenal ampulla with 1 cm common channel (70%)
� Normal duct size is < 4 mm and located at 4 o'clock on sphincter of Oddi

Anatomical considerations:
■ Uncinate process:
o Anterior to it: Portal vein, Mesenteric vessels (Both are Posterior to the neck)
o Posterior to it: IVC and CBD (Both are Posterior to the head)

Blood supply:
■ Superior Pancreaticoduodenal Artery (SPDA) � GOA
■ Inferior Pancreaticoduodenal Artery {IPDA} � SMA
■ Pancreatic (least important) � Splenic artery
■ Venous drainage � Portal system

Summary of pancreatic part and relation to diseases / structures:

Distal pancreas
Head Neck
(Body I tail)
Diseases related Pancreatic adenocarcinoma Trauma Glucagonorna

Pancreatic pseudocysts Vipoma

IPMNs Other pancreatic cystic

neoplasms
Somatostatinoma
Structures related Posteriorly: Posteriorly:
IVC &CBD SMV &portal vein

HiQhest concentration of PP
 Exocrine Pancreas:

Ouctal Acinar
Stimulated by Secreti'n CCK
HCO3 related to Cl level Pancreatic enzymes and Cl
Secretes
■ Lipase
■ Amylase
■ Proteases
■ Amylase and Lipase are the only enzymes i111 the body secreted in active form

■ Most pancreatic enzymes excreted through dorsal duct (Santorini duct)

■ Pancreatic juice:
o Odorless
o Clear
o Alkaline
o Output of 1.5 - 2.5 l / day

■ Any pancreatic stimulation leads to: t Serum Cl

o High pancreatic output -+ t HCO3 t Cl
o Low pancreatic output -+ t HCO3 t Cl

Endocrine Pancreas:

Aloha Beta Delta Pancreatic Polvneotide VIP

Secretes Glucagon Insulin Somatostatin Pancreatic polypeptide
fMain/v in the head!
Function t Exocrine -+ Hyperglycemia GB relaxation
function -+ GB contracts
-+ t Exocrine function t Bowel secretion
and motility

■ Trypsin is the common activator of the pancreatic proenzymes

o Activated by enterokinase (released from duodenum)
o Inhibits activation of Trypsinogen -+ Familial pancreatitis

■ Insulin is stimulated by Lysine

■ Inhibits both exocrine and endocrine functions of pancreas:

o Somatostatin
o Sympathetic stimulation

■ Oral glucose t response more than IV glucose due to: Gastric inhibitory peptide
PANCREAS DIVISUM
■ Most common congenital anomaly of the pancreas (10 - 20¼ of population)
o CFTR mutations in 47% of patients

■ Pathophysiology of pancreatitis:
o Failed fusion of the 2 pancreatic ducts
• Santorini duct become dominant duct and drain all pancreas into minor papilla

o Small papilla -+ Partial obstruction

-+ Dilated dorsal duct
-+ Recurrent or chronic pancreatitis 5%
■ Types:
o Complete divisum
• Ventral duct (Wirsung duct) and CBD enter duodenum through major papilla
• Dorsal duct (Santorini duct) enter duodenum via minor papilla "proximal"
With no communication

o Incomplete divisum
• Associated with partial commu nication between Wirsung and Santorini ducts

■ Minor papilla:
o Located 2 cm proximal to ampulla of Vater
o Identified by endoscopy through:
• Retraction of overlying duodenal fold
• Spray with dilute dye (methylene blue, India ink) ± IV Secretin

■ Management·
o ERCP and minor papilla sphincteroplasty
• Balloon dilatation, Papillotomy, stenting, or botulinum toxin injection

o Surgery
• Indication:
• Failure to cannulate the minor papilla
• Chronic pancreatitis

• Options:
• Dilated duct > 7 mm: Lateral pancreaticojejunostomy (Puestow)

• Familial: Total pancreatectomy with islet autotransplantation

• Non-dilated duct with recurrent acute pancreatitis:

o Endoscopic minor papillotomy
o Failed -+ Operative sphincteroplasty
o Failed -+ Whipplle

• Chronic pancreatitis involving the head:

o Whipple
o Failed -+ Total pancreatectomy with islet autotransplantation
HETEROTOPIC (ECTOPIC) PANCREAS
■ Arise anywhere along primitive foregut
■ Most common sites:
o Duodenum, Jejunum, Stomach, Meckel's diverticulum, Gallbladder

■ Presentation:
o Asymptomatic (Most common)
o Associated with intussusception (May present with bowel obstruction)

■ Gross appearance:
o Normal pancreas with firm, yellow, well circ umscribed, lobulated nodules from the
submucosa
o May have central umbilication due to a central duct if below mucosa (can detect
radiographically)

■ Microscopically:
o Usually in submucosa
o Almost always acinar cells and ducts; islets present in 1/3
o May be pyloric type mucous glands
o May have convoluted branching pattern mimicking invasive carcinoma
o Rarely retains mucus and resembles mucinous carcinoma

■ Investigations and management:

o Usually diagnosed after open surgery
o Usually resected during surgery due to difficult diagnosis
o Upper GI endoscopy help to diagnose in 36%
• U/S guided core biopsy for the submucosal lesion

o Usually not required resection unless:

• Symptomatic
• Can't reach to diagnosis (to ex.elude malignancy)

ANNULAR PANCREAS
■ Ventral bud failed to clockwise rotation and migrates
� Circumferential or Near-circumferential surrounding of the 2 nd part duodenum

■ May associated with other congenital disorders (Down syndrome, malrotation, or atresia)

■ Treatment
o No resection of pancreas

o Bypass surgery
1) Duodenoduodenostomy

2) Duodenojejunostomy

3) Gastrojejunostomy (Higher incidence of marginal ulcer and bleeding)

ACUTE PANCREATITIS
■ Definition:
o Interstitial pancreatitis which characterized by edematous change in the parenchyma
with or without peripancreatic fluid collection

■ Etiology
o Gallstones (Most common)
o Alcohol (2nd most common)
o Medications (Azathioprine, Furosemide, Steroids, Cimetidine)
o Electrolytes and Nutritional (t Lipid "pseudohyponatremia", t Ca)
o Surgical operations (CABG, CBD exploration, Distal gastrectomy)
o ERCP (In sphincter of Oddi dysfunction)
o Trauma
o Viral infection
o Autoimmune

■ Pathogenesis:
o Obstruction of pancreatic duct
• Leads to auto-digestion by activation of Proteolytic enzymes
(Phospholipase A, Lysolecithins)

o Common channel theory

• Obstruction of the ampulla in presence of long common channel can lead to
biliary-pancreatic reflux

o Duodenal reflux
• Closed loop of duodenum as in Billroth II gastrectomy can lead to activation of
enterokinase which activates Trypsin

o Back diffusion
• Alcohol and bile acids can injure the barrier of pancreatic duct leading to back
effusion and activation of lysosomal hydrolase (Cathepsin B) in acinar cells

� Activation of Trypsinogen
o Cathespin B, Hypercalcemia -+ Colocalization
o Acidic pH -+ Autoactivation of proteolytic enzymes (Phospholipase A, Lysolecithins)

� Inactivation of trypsin inhibitors

o As in hereditary pancreatitis

Hypoca/cemia can result from acute pancreatilis due to fat necrosis "Fat Saponification" of the
retroperitoneal and omental fat appears as whitish patches due to calcium deposition
■ Signs of retroperitoneal hemorrhage: (Associated with hemorrhagic pancreatitis)
o Cullen's sign ''Peri-umbilical bruising"
• By spreading along fa/ciform ligament

o Grey Turner sign "Flank bruising"

• By spreading into pararenal space along quadratus lamborum muscle

o Fox's sign "bruising inferior to inguinal ligament"

• By spreading along psoas and iliac muscles

o Walzel sign "livedo reticularis"

• Due to trypsin-induced damage to venous plexus
• Seen on extremities and trunk

o Bryant's sign "Blue scrotum"

■ Djagnosjs· (2 Out of 3)
o Severe constant epigastric abdominal pain radiating to the back which associate with
nausea, vomiting, anorexia and exacerbated by oral intake

o Elevated serum Amylase or Lipase

o CT Scan findings suggestive for acute pancreatitis ± complications

■ Local comoHcat;ons·
<4 weeks
o Acute pancreatic fluid collection: Interstitial pancreatitis with peripancreatic fluid

o Acute necrotizing pancreatitis: Non-capsulated fluid collection with necrosis

> 4 weeks
o Walled-off pancreatic necrosis: Encapsulated mature collection of necrosis

o Pancreatic pseudocyst
• Encapsulated, homogenous, enzyme-rich fluid collection with well-defined wall
"Usually outside pancreatic parenchyma"

o Pancreatic abscess: infected pancreatic pseudocyst

■ Classification of gallstone pancrealitis depends on the severity
o Mild acute gallstone pancreatitis (Edematous)
• Picture of acute pancreatitis without SIRS that abate within 24 - 48 hours
• CT scan is not indicated as no fluid collection or local complications

o Moderately severe gallstone pancreatitis (Necrotizing)

• Associated with transient SIRS (fever, leukocytosis) or persistent increased
pancreatic/liver enzymes which pancreatitis do not regress over 48 hours
• Associated with transient organ failure{< 48 hours}± local complications
• CT is indicated for persistent symptoms > 3 days
• MRCP or ERCP may indicated in biliary obstruction

o Severe acute gallstone pancreatitis (Necrotizing)

• Associated with progressive organ failure (> 48 hours) and local complications
• U/S is the only imaging needed to confirm gallstones and exclude biliary
dilatation suggestive for choledocholithiasis (CBD diameter > 11 mm)
• Usually requires intubation and ventilation, renal replacement therapy, or
inotropic administration

Atlanta criteria (1992\ Revised Atlanta criteria (2012\

Mild acute pancreatltis Mild acute pancreatitls
- No organ failure - No organ failure
- No local complications - No local complications
Severe acute J;!ancreatitis Moderatelll severe acute J;!3ncreatitis
-
- ± Local complications - Transient organ failure < 48 hours
- Ranson score > 2 or APACHE > 7 - ± Local complications
- Organ failure:
0 SBP<90mmHg
0 PaO2< 60mmHg
0 GI bleedina > 500ml/ dav

stvece acute pancreatttls

- Persistent oraan failure > 48 hours
 ■ i
Investigat ons:
o Amylase and lipase need to be elevated 3 times above the upper limit
• Found also in salivary glands (S-Amylase) and Fallopian tubes

• When Lipase is normal and amylase is elevated, Non-pancreatic causes of

hyperamylasemia are more likely
• Urine amylase is most useful in Macroamylasemia and pancreatitis with normal
amylase level
• High amylase level doesn't mean increased severity
(actually mild pancreatitis have higher serum amylase level)

Causes of Hvoeramvlasemia Pancreatitis with normal amvlase level

Pancreatitis. Cholecvstitis. Aooendicitis Salpinaitis. Hepatitis Alcoholism
PUD, lnflammatorv bowel disease, Bowel obstruction Acute on top of chronic pancreatitis
Pneumonia, PE, Luna cancer Hvoertrialvceridemia
Parotilis, DKA, Trauma, Ectopic preanancv, Renal failure Late presentation

Rises within Normalized after

Serum Amvlase 6-24 hours 3-5davs
Urine Amvlase /More sensitive} 6- 8 hours 7-10davs
Serum lloase /Most sensitive and most soecificl 4-8 hours 8-14 davs
Lioase is onlv oroduced bv oancreas and Iota/Iv absorbed bv the kidnev /No urine Uoasel

o Amylase/Creatinine Clearance Ratio

• Can used to confirm macroamylasemia
• Used sometimes to differentiate between cholecystitis and pancreatitis
• Can be used up to 30days

o ABG, Renal profile, Liver profile, Calcium level, Plasma Glucose, Triglycerides

o Serum methemalbumin (differentiate lbetween edematous/hemorrhagic pancreatitis)

o CRP

o Lactate level

o Septic work-up if suspect infection

o Upright CXR

o Abdominal X-ray

o CT scan

o U/S abdomen

o MRCP
o Chest and Abdomen X-ray findings:
• Jejunal sentinel loop, Central or localized ileus, Colon Cut-off sign
• Pancreatic calcifications
• Pancreatic complications
• Local (Pseudocyst, Abscess}
• Adjacent structures (Du odenal obstruction}
• Pulmonary (ARDS, effusion, pneumonia, fistula}

o Triphasic CT Abdomen "Pancreatic protocol"

• CT with oral water (negative intraluminal contrast} and IV iodinated contrast
• Section thickness < 3 mm
• Arterial "Pancreatic parenchymal phase• 15 - 30 s
• Portal venous phase "Liver phase" 45 - 60 s
• Delayed phase > 60 s

• Indications:
• Severe abdominal pain where ischemia or perforation is suspected

• Moderate or severe pancreatitis 72 hours after onset of symptoms to

asses for complications if patient deteriorated

CT has highest sensitivity if performed at least after 72 hours from symptoms

(after relieving of pancreatic edema)
 BISAP Score Points
(Bedside index for severitv of acute oancreatitisl
BUN> 25 1
lmoaired mental status 1
Aae> 60 vears 1
SIRS I> 2 criteria: Temoerature PaO2 . Pulse RR WBCl 1
Pleural effusion 1
Total score Mortalitv
0 0.1%
1 0.4%
2 1.6%
3 3.6%
4 7.4%
5 9.5%

Ranson's criteria
Non-Biliarv Pancreatitis Biliarv Pancreatitis
On Admission
Age> 55 vear Age> 70 vear
WBC> 16000 mm2 WBC> 18000 mm2
Glucose> 200 mg/di (> 11 mmol/L} Glucose> 220 mg/di (> 12 mmol/L}
LDH > 350 IU/L LDH > 400 IU/L
AST> 250 IU/L
After 48 hours from admission
Hematocrit decreases > 10 %
Serum Ca < 8 m..,/dl I< 2 mmol/Ll
Base deficit> 4 mEa/L Base deficit> 5 mEa/L
BUN> 5 mg/di BUN > 2 mg/di
Fluid seauestration > 6 L Fluid seauestration > 4 L
PO2< 60 mm Hg NA
Mortal tty Rate
Score 0 - 2: 2% Score 3 - 4: 15%
Score 5 - 6: 40% Score 7 - 8: 100%
Grade CT Severity Index (Balthazar score) Points
A Normal pancreas 0
B Pancreatic enlarqement 1
C Pancreatic inflammation ± oerioancreatic fat 2
D Sinqle peripancreatic fluid collection 3
E > 2 fluid collections or retrooeritoneal air 4
Necrosis oercentaae
0 0
< 30 2
30-50 4
> 50 6
CT Severitv index
Lowarade 0-3
Middle arade (6% mortalitvl 4-6
Hioh orade (17% mortalitvl 7 -10
MANAGEMENT OF ACUTE PANCREATITIS
■ Predict the severity:
o Ranson's criteria
o APACHE (Acute Physiology and Chronic Health Evaluation) score
o Balthazar score(CT index of Severity)
o HAPS score

■ Assess the systemic response:

o SIRS score "Most predictive"
o SOFA for "organ failure"

■ ICU admission:
o Severe pancreatitis
o Organ dysfunction
o High-mortality scores(:? 3 BISAP,:? 5 Ranson, > 7 APACHE scores}

■ Hydration:
o IV RL bolus of 500 -1000 ml, maintenance 10 -20 ml/kg/hour for first 24 -48 hours

o Asses resuscitation and prevent overload to avoid ARDS, Compartment syndrome

o Monitor the patient SIRS, BUN, Hct and UOP with goal of 0.5 - 1 ml/kg/hour

■ Broad-spectrum antibiotic:
o Indicated only if suspected infected pancreatitis either by imaging or culture

o FNA should obtained only if clinical suspicious of infection is high or not improving
clinically in pancreatic necrosis, and should be sent for gram stain and culture

■ Analgesia
o NSAIDS for most mild abdominal pain

o Opioids(except morphine) as bupren-0rphine, pentazocine, procaine hydrochloride, and

meperidine used for severe abdominal pain

o Morphine give longer pain relieve(although some textbook mentioned to avoid it due to
contraction of sphincter of Oddi, but no study shows contraindication to use or
worsening of the attack}

■ Nutrition
o Low fat solid enteral diet with Polymeric formula(No elemental or immune-enhancing
formulas) should be started immediately within 24 - 48 hours of admission if there is no
SIRS or ICU care in mild acute pancreatitis, to prevent bacterial translocation and
atrophy of GI mucosa

o Nasojejunal tube feeding was considered optimal to avoid pancreatic stimulation

Nowadays even nasogastric feeding showed to be safe and effective in pancreatitis

o Bowel rest with TPN preserved for chronic pancreatitis if tube feeding not feasible
(Severe pancreatitis, Severe ileus, high output fistula)
■ ERCP with sphincterotomy
o Not recommended as routine practice and indicated only for:
• Cholangitis within 24 hours
• Evidence of biliary obstruction not resolved within 24 - 48 hours
• Patient with comorbidities, High-risk for cholecystectomy after 6 weeks

o Can be done during pregnancy (Choledochoscopy used to minimize radiation using)

■ Cholecystectomy with intraoperative cholanqioqram

o Recommended during admission (within 48 - 72 hours) for mild biliary pancreatitis

o Not recommended until 6 weeks after severe pancreatitis with peripancreatic fluid

o 10 Cholangiogram should be done routinely even for mild gallstones pancreatitis

because there is no indications for preoperative ERCP or MRCP

■ Open surgery
o Reserved for selected infected pancreatic necrosis or other local complications (gastric
outlet or biliary obstruction) after failure of 4 weeks conservative measures

■ Management of local complications:

o Pancreatic: phlegmon, abscess, pseudocyst, ascites, thrombosis or pseudoaneurysm

o Adjacent organs: bowel obstruction, obstructed jaundice, thrombosis or fistula

PANCREATIC NECROSIS
■ 10% - 25% of all cases of acute pancreatitis

■ Most important risk factor for necrotizing pancreatitis: Obesity

■ Mortality rate comparing infected pancreatic necrosis to sterile necrosis is 30% vs. 15%
i
■ Presentat on·
o Asymptomatic
o Symptomatic
• Obstruction: Failure to thrive 40%, Biliary obstruction, or Gastric obstruction
• Sepsis: Fever, tachycardia, ileus, organ dysfunction

■ Imaging:
o CT with IV Contrast 72 - 96 hours after onset of symptoms
• Diffuse of focal non-enhanced areas with low attenuation (< 50 HU)
• Involvement> 30% of the pancreas or measure 3 cm in maximal dimension
• Peripancreatic fat necrosis
• Gas or gas-fluid level in case of infection

o MRI: Can detect necrosis without gadolinium infusion

o EUS

■ Management:
Step-up approach help to reduce major complications such as incidence of mu/Ii-organ failure
(from 40% to 12%), new-onset OM (from 38% to 16%), incisional hernia, mortality (by delaying
surgical intervention) as well as costs

o Conservative with early fluid resuscitation within first 24 hours

o IV Antibiotics (if suspicious of infection clinically, radiologically or by sampling)

• FNA for gram stain and culture for bacteria and fungal
• Associated with 40% False-negative
• Pancreatic penetrating antibiotics (Carpapenam or Fluoroquinolones)
for 6 weeks
• Aminoglycosides are unable to penetrate into pancreatic tissue
• Culture-directed antibiotic therapy
• Parenteral antibiotics, selective gut decontamination, and probiotics are not
recommended routinely

o Percutaneous drainage (Sufficient as only procedure in 24%)

• Used in persistent infection, failure to thrive or gastric outlet obstruction
• May prevent up to 50% the need of surgical intervention
• Collection should be accessed through retroperitoneal
• Vigorous flushing may address small-to-moderate size collections
o Endoscopic drainage
• For collection locate within 2 cm of stomach or duodenum
• Used after failure of percutane-0us drainage
• EUS with duplex is recommended to avoid vascular injury
• Not feasible for necrosis with retroperitoneal extension
• Mechanical debridement by using irrigation, alligator forceps, baskets, nets
• Slanting by SEMS or pig-tail and nasocystic catheter left in place for irrigation
• Slanting may be required to be placed indefinitely for patient with
disconnected pancreatic duct syndrome

o Minimal invasive debridement

• Divided into:
• Lap Trans-peritoneal Debridement
o Risk of distant contamination
o Re-operation rate is 20%

• Video-assisted Retro-peritoneal Debridement (VARD)

o Preferred method
o Necrosectomy (Necrosectomy)
• Indications:
• Infected necrotizing pancreatitis with clinical deterioration
• Unresolving organ failure > 4 weeks after symptom onset

• Performed after 4 - 6 weeks from symptom onset

• 75% mortality if perform within first 2 weeks, and 25% after 2 weeks

• Because it lead to overwhelming inflammatory response

• And may lead to removal of viable pancreatic tissue

(Endocrine and exocrine insufficiency)

• Techniques of packing after necrosectomy:

• Open packing
o Packing of lesser sac whereas the abdomen is left open for
reassessment every 24 - 48 hours

o Closure usually as secondary intention, or by primary repair

• Close packing
o Laparotomy and debridement of necrotic tissue followed by primary
closure over 2 - 12 gauze-stuffed Penrose or Abramson drains via
separate stab incisions which removed gradually one every other
day to allow for s.low collapse of the cavity

o Addition silicone drain inserted in pancreatic bed and lesser sac

• Postoperative continuous lavage

o Large 2 - 3 lumen drains for debridement after closure
o Superior to open and close packing regarding morbidity

• Drains and packing for � 7 days to allow for the slow collapse of the necrotic
cavity and resolution of pancreatic fistula
o Life-saving procedure (Laparotomy, Angioembolization) should be used any time if
clinical deterioration due to collateral damage from severe pancreatitis
• lschemia, perforation, bleeding, or compartment syndrome
• Surgical debridement of sterile necrosis during live-saving procedure should be
avoided except for:
• Interactive gastric outlet obstruction

• Bowel or biliary obstruction

• Persistent abdominal pain

• Disconnected duct syndrome

Intervention should be delayed 8 weeks after symptoms onset

CT follow-up may be needed for pancreatic necrosis to asses for local complications
CHRONIC PANCREATITIS
■ Definition:
o Progressive disease that lead to destruction of normal pancreas with loss of its exocrine
and endocrine functions

■ Etiology:
o Toxic
• Alcohol (Most common cause)
• Metabolic (f Ca, f Lipid, f PTH)

o Obstructed
• Pancreatic divisum
• Trauma
• Gallstones
• Malignancy (IPMN, Ductal adenocarcinoma)

o Genetic mutation
• PRSS1 (Cationic Trypsin)
• Associated with Hereditary pancreatitis

• SPINK1: Pancreatic Secretory Trypsin Inhibitor

• Associated with Nutritional (Tropical pancreatitis) in 40 - 50%
• CFTR (Cystic fibrosis transmembrane conductance regulator)
• Associated with Pancreatic 0ivisum

• Alpha-1 antitrypsin deficiency

o Autoimmune pancreatitis
• Elevation of lgG, lgG4, and CA 19-9
• Imaging: Diffuse edema with long segment stricture and no ductal dilatation
• Pathology: Lymphoplasmacytic infiltrate, storiform fibrosis, obliterative phlebitis
• Treatment: Steroids

o Others
• Post necrotic pancreatitis
• lschemic or vascular, or idiopathic (2nd most common cause)

■ Glioical presentatjon:
o Pain (Most common symptom and surgical indication)
• Persistent and aggravated by food or alcohol drinking (Post-prandial)
• 20 - 45% of patients have no pain
• May associated with weight loss, anorexia, nausea and vomiting

o Jaundice (in case of migrating stone to obstruct the CBD)

• CBD stricture is the most common cause of jaundice in chronic pancreatitis

o Exocrine insufficiency (40 - 50%): Steatorrhea (foul-smelling loose stool)

• Fat Malabsorption (Long-chain fatty acids) + ! Ca and! Vitamin K

o Endocrine insufficiency: Diabetes 3c in 20% (impaired glucose tolerance in 75%)

 i
■ Investigat ons:
o Postprandial pancreatic polypeptide hormone is most sensitive test
o Bentiromide test (to measure urinary PABA) 1 00% sensitive for severe fibrosis
o Amylase and lipase not helpful in chronic pancreatitis
o Others: Fecal elastase, Serum trypsin, RBS, HgB A1C, and GTT

■ Histology:
o Islet cells hyperplasia
o Irreversible parenchymal fibrosis
o Loss of Acinar cells

■ Imaging:
o CT, MRI, and MRCP are used to confirm the diagnosis

o EUS used to diagnose very early pancrealitis and to rule out any pancreatic masses
• Best to asses vascular involvement when in doubt by CT or MRI

o ERCP is the best investigation to detect early chronic pancreatitis

• Gold standard for diagnosis and staging {Most sensitive and specific test)
• Severity can be assessed based on abnormality of main or branch ducts
• Also help as therapeutic: drain cyst, stent, brush cytology or biopsy

■ CT / MRI features of chronic pancreatitis:

o Ductal Dilatation (68%)
o Fibrosis and distortion (51%), Pancreatic edema
o Dilation and stenosis in pancreatic duct "Chain of Lakes•
• "Double-duct" sign associated with pancreatic malignancy
i
o Pancreat c Calcifications (55%)
• Associated with Chronic pancr-eatitis {68%), IPMN, Serous cytsadenoma,
Neuroendocrine tumors, and adenocarcinoma

o Features of complications of pancreatitis "Mass, cyst or pseudocyst (32%)"

o Features of malignancy

■ Rosemont criteria for chronic pancreatitis bv /EUS}:

Parenchvmal features
MaiorA
Hyperechoic foci with shadowing
Maior B
Lobularity with honevcombina
Ductal features
MaiorA
Main duct calculi
Minor
Lobularitv onlv
Hvnerechoic foci onlv
Cvsts
Stranding
Minor
lrreaular main duct
Dilated main duct
> 3.5 mm in body
> 1.5 mm in tail
Dilated side branches
Hvnerechoic duct marain
■ Management:
o Medical management
• Alcohol cessation
• Analgesia
• Somatostatin associated with 65% pain relief "CCK inhibitor"
• Opioids as buprenorphine, pentazocine, procaine hydrochloride, and
meperidine used for severe abdominal pain
• Pregablin can leads to reduction of opioid use

• Oral enzyme therapy, Selective antisecretory therapy

• Should be offered for all patient with steatorrhea or weight loss
• Non-enteric coated enzyme replacement used during each meal

• Blockage of visceral afferent nerve (Celiac plexus block with alcohol injection}

o Endoscopic management
• Used in obstructive chronic pancreatitis

• Leads to pain relief in 74% of patients {But it is less than surgical therapy)

• Options:
• Dilatation of strictures

• Papillotomy of papilla off Valer

• Slanting (Every 3 months for 2 years usually)

o Stent removal as,sociated with 30 - 40% recurrence

• Removal of stone (if< 5 mm) ± lithotripsy

Pancreatic duct decompression is the only therapy that shown to prevent progression of chronic
pancreatitis
 o Surgical management
• Indicated as pain relief after failure of medical and endoscopic management

• 40 - 70% of patients required surgery

• Options:

Inflammatory head mass Dilated duct > 6 mm Small duct disease< 6 mm

Duodenum-preserving Endoscopic thera[Py Continue medical treatment

pancreatic head resection
(DPPHR)
■ Frey's procedure
■ Beger procedure
■ Berne procedure
Puestow proced1ure Beger procedure
Frey's procedure Total pancreatectomy with
autotransplantation

Whipple procedure

o Puestow procedure:
• Roux-en-Y longitudinal (lateral) pancreaticojejunostomy

• Recommended for patient with chronic pain and main duct 2: 7 mm

• You have to rule out signs of inflammatory pancreatic head:

• Biliary dilatation (30 - 50%)
• Duodenal narrowing (5%)

Positive � Patient need surgery that involving head resection

 o Frey's procedure: (duodenal preserving drainage procedure}
• Local resection (encoring) of ventral part of the head
+ Longitudinal {Lateral} pancreaticojejunostomy
• Most preferable in case of dilated duct with mild inflammation of the head

Most favorable procedure to surgeon because the neck of pancreas is not transected as
in Beger procedure, so inflammation near to SMA and vein is not a problem
St�rtof
running -------..
wtures
common tiae dl.lCl

.,,_,..
-..,,,,..,le -f-�

B A

o Beger procedure:
• Duodenum-preserving pancreatic head resection and performing 2
pancreaticojejunostomies
1) Pancreaticojejunostomy to distal pancreas
2) Pancreaticojejunostomy to remnant pancreatic tissue on the duodenum
• Associated with 2 major risks:
1) Duodenal ischemia
o Due to damage of posterior branch of GOA

2) Pancreatic leak from pancreatic neck transection and 2 anastomosis

 o Resection-Onlyprocedures:
• Distal pancreatectomy:
• Associated with very short-term pain relief
• Used for:
o Rare cases in isolated pancreatic tail strictures
o Complications such as pseudoaneurysm
o Focal inflammation of body/tail with no significant ductal dilatation

• Whipple procedure:
• For suspicious of malignancy or localized disease at head of pancreas
• For patient with extensive fibrosis including pancreatic duct, CBD ±
duodenum

• Total pancreatectomy with autotransplantation

• 30 - 50% of patients will continue to have pain postoperative

o Biliary drainage:
• Choledochoduodenostomy / choledochojejunostomy for biliary strictures
• Choledochojejunostomy have lowest recurrence of jaundice

■ Pain relief after surgical intervention for chronic pancreatitis (From highest to lowest)
o Isolated beta islet cells transplantation
o Frey's procedure
o Beger procedure
o Puestow procedure
o Whipple procedure

Celiac plexus block used to treat refractory malignancy-associated chronic pancreatitis

with 90% effective for short term (3 - 6 months)

■ Complications of chronic pancreatitis:

o Local complications: Pseudocyst, Pseudoaneurysm, Abscess

o Complication of inflammatory pancreatic head:

• Bile duct stenosis
• Duodenal obstruction
• Pancreatic carcinoma
Should be ruled out before surgery that not involving head resection

o Sinistral portal hypertension

• Splenic vein thrombosis (Treated by splenectomy)
• Upper GI bleeding "due to pseudoaneurysm"

o Pulmonary complications:
• Atelectasis (most common pulmonary complication of pancreatitis)
• ARDS (related to release of phospholipases)
• Pleural effusion
• Pneumonia
• Pancreaticopleural effusion
PANCREATIC FISTULA/ LEAK
■ Pancreatic fistula: leakage of pancreatic fluid as a result of disruption of pancreatic ducts

■ Pancreatic leak diagnosed if surgical drain near anastomosis > 30 mL/day, with amylase level
x 3 normal level after 3rd postoperative day (need serum and drain amylase level)
■ Classification:
o External:
• High output > 200 ml/ day -+ Usually needs Endoscopic therapy ± Octreotide
• Low output < 200 ml/ day -+ Usually needs conservative management
High-output pancreatic fistula usually associated with metabolic acidosis

o Internal:
• Pancreatic ascites, pleural effusion, communicate with other visceral organs

o Based on underlying diseases:

• Pancreatitis, Malignancy, Normal pancreas

o Based on immediate predisposing cause:

• Postoperative, PCD, Trauma
• 20% after Distal pancreatectomy (95% resolve spontaneously)
• 12% after Whipple procedure (May need MRCP or ERCP ± stent)

■ Grading: "ISGPF: International Study Group of Pancreatic Fistula"

A B C
Clinical condition Well Often well ill
Drain amvlase level > 3 times of normal serum amvlase level
Persistent draln=e > 3 weeks No Usuallv Yes
UIS or CT Neaative Neaative I Positive Positive
Re-o=ratlon No No Yes
Sians of infection No Yes Yes
Management: Na Yes/ No Yes
TPN, Somatostatln analoaue

■ Management:
1} NPO and Nasojejunal feeding for High-output fistula (B/ C}, Otherwise enteral feeding

2} IV fluid and electrolytes correction ± antibiotics if fever or leukocytosis

3} CT abdomen "pancreatic protocol" of any signs of sepsis

4} Somatostatin analogue: Octreotide •used in high output fistula"

o 100 mcg (up to 300 mcg) q 8 hours SQ starting on day of surgery (as prophylactic) and
to be continue for 5 - 8 days (stopped after that if no reduce in fistula output)
o Octreotide showed to reduce the output only without reducing the rate of closure

5} ERCP with sphincterotomy + pancreatic stent

6) Percutaneous drainage: if endoscopy not feasible or failed

7) Surgery: (By Hepatobiliary surgeon)
o Indications:
• Failure of conservative measures (Persistent chronic pancreatic fistula}
• Infected fluid
• Enlarging collection despite conservative measures
• External fistula,
• Recurrent pain or pancreatitis during attempts of feeding

o Options·
• Distal pancreatectomy
• Pancreatojejunostomy
• Fistulojejunostomy
 FUNCTIONAL PANCREATIC NEUROENDOCRINE TUMORS
■ Represents ½ of pancreatic endocrine neoplasms
■ Associated with hereditary syndromes:
o MENI
o Neurofibromatosis 1 (Associated with duodenal Somatostatinoma}
o VHL (Associated with Somatostatinonna)
o Tuberous sclerosis (Associated with non-functional pancreatic tumors}

■ Characteristics of functional pancreaticneuroendocrine tumor s:

lnsulinoma Glucagonoma VIPoma Somatostatinoma

(Verner Morrison
svndrome)
Origin Beta cells Alpha cells Neural crest cells Delta cells
-+ APUD cells

"Amine Precursor
Uptake, and
Decarboxv/astion"
Secretes Insulin Glucagon Vasoactive intestinal Somatostatin
peptide (VIP)
Malignant Benign Malignant Malignant Malignant
potential
70% are metastatic
at time of diaanosis
Proanosis Best Variable Variable Worse
Genetic Sporadic Sporadic Sporadic Sporadic
5%with MEN 20%with MEN
Site Evenly distributed Tail Tail Head
throughout pancreas
Peri-ganglionic Duodenum
"Adrenal, Colon,
liver or bronchus"
Solitary Solitary Solitary Solitary Solitary

Multifocal in MEN-
associated
Size Small <2 cm Variable larqe > 2 cm Variable
Effectiveness of Minimal 90% possess 90% possess 90% possess
Octreotide scan 25% possess Somatostatin Sornatostatin Sornatostatin
Somatostatin receotors receotors receotors receotors
Presentation Whipple's triad 40 Syndrome WDHA SGDA
DVT, Diabetes Watery diarrhea Steatorrhea
Fasting hypoglycemia Diarrhea, Dermatitis
Wecrolytic migratory Hyperglycemia Gallstones
erythema•
Hypoglycemia < 40 lK f Ca
mg/di Diabetes
Hyperpigmentation Achlorhydria
Relief by glucose Stomatitis Achlorhydria
Hypoamine acidemia Metabolic acidosis
Diagnosis Vacoulated Serum VIP Sornatostatin level >
keratinocytes on > 200 pg/ml 3 times of normal
bioosv level
lnsulinoma
■ Most common functional endocrine pancreatic tumors
■ Diagnosis:
o Fasting for 72 hours with every 6 hours measurement of:
• Insulin / glucose> 0.4
• C peptide>200pmol/L (?. 0.2 nmol/1)
• Proinsulin> 5 pmol/L

o Exclude factitious insulinoma

• Absence of sulfonylurea in plasma and urine: Insulin / glucose< 1
• Exogenous insulin: Insulin / glucose> 1

■ Localization:
o CT I MRI
o Octreotide scan
o EUS
o Intro-operative U/S (Best for localization} with manual palpation
o Pre-operative Selective Intra-arterial Calcium with hepatic vein sampling
• Used for localization of difficult cases or for recurrent disease

Directing the injecting-catheter into Ce/iac for localization insulinoma in tail

Directing the injecting-catheter into GOA for localization insulinoma in head

■ Management:

<2cm >2cm

Close to the duct Far from the duct Head Tail

Distal pancreatectomy I Enucleation I I Whipple procedure 11 Distal pancreatectomy

o In multi-focal disease /MEN-associated}:

• Aggressive treatment may be required for identified tumor> 2 cm
• Including distal pancreatectomy and enucleation of pancreatic head mass

o Intra-operative glucose monitor (Stop dextrose infusion preoperatively)

o Blind distal pancreatectomy for non-localized insulinoma is not recommended

o For refractory or metastasis: (as palliative)

• Hepatic artery embolization
• Somatostatin analogue
• 5-FU or interferon-alpha
 Gastrinoma (Zollinger-Ellison syndrome)
■ Syndrome of severe peptic ulcer disease and diarrhea caused by gastrin hypersecretion
■ 2nd most common functional neuroendocrine tumor of pancreas
■ Most common functional pancreatic tumor in MEN-1(followed by insulinoma)
■ Most common site of gastrinoma: Duodenum (Not pancreas)
■ 50 % Malignant, 50 % Multiple, 70% Sporadic
■ Clinical presentation:
o MEN-1 associated symptoms in familial type
• Primary hyperparathyroidism, kidney stones, pituitary tumors, thyroid tumors,
adrenocortical tumors, lipomas, and cutaneous angiofibromas

o Refractory ulcer, diarrhea, malabsorption, and reflux with esophagitis ± stricture

• Hypergastrinemia leading to acid hypersecretion and peptic ulceration
• Typically as solitary ulcer in proximal duodenum

The mean time from symptoms to diagnosis is 8 years

Sooradic aastrinoma Familial Gastrinoma /MEN 11

Prevalence 80 % 20 %
Gastrinoma size > 2 cm <2cm
Number of tumors Sinale Multiole in 50%
Most common location Pancreas Duodenum
Malianant ootentlal Hiah Rare

Duodenal aastrinoma Pancreatic aastrinoma

Prevalence Common 170- 90% l
Associated with 85% of MEN 1
Most common site Proximal duodenum •01•
(Most common site overall)
Less common
Sooradic aastrinoma
Inside Passaro's triangle in 80%
0 CBD/Cystic duct junction
0 Neck/Body pancreatic junction
o 2rnJ/3rd duodenum junction

Most common metastasis to Lvmoh nodes 150- 80%1 Liver

lmoact of metastasis on survival Low Hlah

■ Atypical presentation includes:

o Multiple ulcers

o As lymph node only in 10% of sporadic gastrinoma

o Distal sites in duodenal gastrinoma as D2or jejunum

o Outside passaro's triangle (to the left of mesenteric vessels)

• Examples: stomach, bile duct, ovary, lung, heart, and lymph nodes
• Higher risk of metastasis than tumor located inside triangle

o Any patient with unusual peptic ulcer disease should be screened for ZES
■ Causes of hypergastrinemia:
Hvoersecretorv hyperqastrinemia Hvoosecretorv hyperqastrinemia
Gastrinoma (ZES) Pernicious anemia
Gastric outlet obstruction Atrophic gastritis
Retained antrum Previous vaootomv
Antral hvnerolasia DM
H. Pvlori infection Renal failure

■ Diagnosis:
o Fasting serum gastrin level> 100 pg/ml(> 10 folds)
• False-positive results due to:
• Achlorhydria
• Antacid medications
o All acid secretion reducing medications(PPls and H2 receptor
antagonists) must be stopped before measuring serum gastrin, acid
output or stomach pH levels

• Should be confirmed if high, by measuring:

• Stomach pH level
• Basal acid output "Gastric acid secretion"(Highest sensitivity)

o Basal acid output > 15 mEq/hour (Normal: 2 to 5 mEq/hour)

o Endoscopy (Gastric pH,;; 2, Prominent gastric folds "due to trophic gastrin effect")

o Investigate MEN(Calcium level, PTH, Prolactin level)

o Provocative tests:(for equivocal results)

• Secretin stimulation test "Confirmatory test"
• t Gastrin(> 200) in ZES
• t Gastrin in normal patients

• Calcium infusion test

• Standard meal test
■ Localization:
o CT /MRI
• CT detects around 50% of primary gastrinomas and 50% of liver metastases
• Can detects gastrinomas if> 3 cm (sensitivity 20 - 30% for tumors < 1 cm)
• MRI detects around 25% only of primary gastrinomas and 85% of liver
metastases
• Gastrinomas are relatively hypervascular mass

o EUS
• Best to detect pancreatic gastrinoma (85%) but less for duodenal (40%)
• Combination of both EUS and SRS leading to detect> 90% of gastrinoma

o lntraoperative U/S
• Very useful for localizing pancreatic gastrinoma and liver metastases as 5 mm
• Poor at detecting duodenal gastrinoma

o Octreotide (Somatostatin) scan "Somatostatin receptor scintigraphy" (SRS)

• Most useful test for localization and metastases detection "highest sensitivity''
• Better in gastrinoma than insulinoma

o DOTAscan
• By using gallium as whole body test
• Newest and highest sensitivity test than octreotide scan
• Pre-operative test of choice for localization and metastases detection

o Duodenotomy and Palpation at the time of surgery

• Highest sensitivity (100%) to d•etect small duodenal gastrinoma
• Causes dimpling of the mucosa as firm nodule between thumb and forefinger
■ Management of Gastrinoma:
o Proton pump inhibitor
• Adjust the dose to BAO levels < 15 mEq/hour is necessary, and symptoms relief
alone is not reliable indicator

o Subtotal parathyroidectomy
• MEN-1 ZES patients should be done 1st before gastrinoma resection
• Treating hyperparathyroidism leads to more favor management of gastrinoma

o Surgical resection of gastrinoma

• MEN-1: indicated for identifiable tumor > 2 cm

• Sporadic: for all patient diagnosed with ZES

• Types of surgery:
• Enucleation of palpable pancreatic head tumors
o If not involving major ductal or vascular structures

• Distal pancreatectomy
o For disease in the body and tail of the pancreas

• Whipple procedure
o For large duodenal tumors or ampullary involvement
o For bulky large tumor localized to pancreatic head

• Proximal duodenotomy with "Full-thickness" resection

o For all patients without identifiable tumor on preoperative imaging
(risk of occult duodenal gastrinoma)

+ Peri-pancreatic and regional lymph node sampling and excision

• Cytoreductive surgery
o 25 - 30% patients will have liver metastasis
o Debulking of the primary tumor with complete removal for liver
metastases if can be removed safely
o In contrasts to adenocarcinoma, Liver metastasis in ZES is not
contraindicating resection
o Most metastasis can be removed safely without the need of
vascular reconstruction

• UnresectableINon-localized gastrinoma·
• Long-term PPI therapy

• Highly selective vagotomy

• Total gastrectomy
o Best long term quality of life than vagotomy
• Recurrence or metastatic disease:
• Chemotherapy (Strept.ozotocin + 5-Fluorouracil I Doxorubicin)
• Octreotide
NON FUNCTIONAL ENDOCRINE TUMORS
■ 40% of neuroendocrine tumors are non-functional
■ 90% of the nonfunctional tumors are malignant
o OM associated with malignancy
o 90% of solid tumors are malignant
o 50% of mixed tumors are malignant
o 30% of cystic tumors are malignant

■ Most common site of metastases: Liver

■ Serum Chromogranin A
o Marker for most of neuroendocrine tumors (especially non-functional types)
o Other markers:
• Polypeptide neurotensin,
• Neuron-specific enolase

PANCREATIC CYSTS
1} JoOammatocy fluid couectjons (False)·
Acute peripancreatic fluid collections: pseudocysts, acute necrotic collections, and walled­
off pancreatic necrosis

2) Non-neoplastic pancreatic cysts

o True cysts "benign epithelial cysts"
o Retention cysts (due to obstruction by neoplasia, cystic fibrosis, or pancreatitis)
o Mucinous non-neoplastic cysts

3) Pancreatic cystic neoplasms

o Not associated with painful pancreatitis, or trauma
PANCREATIC PSEUDOCYSTS
■ Chronic fluid collection surrounded by non-epithelialized wall of granulation tissue, developed
from peripancreatic fluid collection which due to duct leakage in pancreatitis

■ Most common cystic lesion of the pancreas

■ Most common complication of chronic pancreatitis
■ Most common site: HEAD of pancreas
o Other sites: spleen, kidney, sub-hepatic, pleura, mediastinum, and others
o Mid-BODY of pancreas is the most common of disconnected duct syndrome

■ Consequence:
1) Chronic pancreatilis with duct leak and extravasation

2) Peripancreatic fluid collection

o Acute pancreatic necrosis non-capsulated fluid collection with necrosis < 4 weeks

o Walled-off pancreatic necrosis encapsulated collection of necrosis > 4 weeks

• Infected pancreatic necrosis

o Acute pseudocyst (encapsulated by early granulation tissue)> 4 weeks

• Pancreatic abscess: infected pancreatic pseudocyst

o Chronic pseudocyst (encapsulated by granulation tissue or fibrosis)> 6 weeks

■ Risk factors:
o Acute pancreatitis (up to 10%)
o Chronic pancreatitis (20 - 38%)
o Trauma "Patient need ERCP to exclude ductal injury"

■ Presentation:
o 50% of pancreatic pseudocyst associated with hyperamylasemia
o Key factor for diagnosis of pseudocyst is persistent symptoms after 3 - 5 days
o Post-prandial pain may associated with pancreatic ductal disruption
o Symptoms of gastric of bowel obstruction
o Exclude neoplasm symptoms

■ Imaging:
o CT with contrast
• Repeated CT scan should not be done < 4 weeks or if there is no deterioration
• If Contrast contraindicated � MRI or EUS

o MRI/ MRCP ± Contrast

• To assess for duct communication (Pancreatitis, Rapidly enlarged, Persistent)

o EUS
• Can assess pancreatic duct, mural nodules, and can aspirate fluid (Amylase,
CEA. and mucin)
■ Findings on imaging:
o Immature cyst on initial presentation (unlike IPMN)

o Communication to the pancreatic duct

o Walled-off pancreatic necrosis have more thicker wall with necrotic debris, and irregular
cavity (sausage shape)

o Exclude findings of neoplasm or chronic pancreatitis {dilated duct, calcifications)

o Exclude other complications of chronic pancreatitis as splenic vein thrombosis

■ Complications:
o Obstruction (Bowel, Biliary, or Vascular)
• Biliary obstruction either by compression or as stricture from pancreatitis
• Choledochojejunostomy or choledochoduodenostomy can be added to definitive
procedure of pancreatitis if not. resolved with drainage

o Infection

o Rupture (Pancreatic ascites)

• Especially in patient with alcohol abuse
• Paracentesis is diagnostic (Amylase> 3 times serum, > 3 g protein)
• Managed by NPO, NGT, Octreotide, and TPN

o Bleeding
• Splenic artery is the most common source of bleeding

o Fistula (Bowel, Colon, Pleura)

o Suspicious of malignancy (IPMN)

■ Management of pancreatic pseudocyst

o Conservative management± TPN is mainstay therapy for asymptomatic pseudocyst
• Enteral feeding should be started unless compress on stomach or duodenum

o Indications for drainage

• Symptomatic or associated with complications
• Pain or fullness, gastric or biliary obstruction, infection, vein thrombosis,
nutritional failure or early satiety, fistula, bleeding, or rupture
• Persistent or progressive enlargement of the pseudocyst
• 2: 6 weeks to ensure maturation of the cyst or size> 6 cm
■ Methods of drainage of pancreatic pseudocyst:

o Immature: 'Non-calcified wall(< 6 weeks}, or Walled-off necrosis(> 4 weeks}"

• External drainage/ Open Necrosectomy
• Less recurrence rate with external drainage in normal duct
• Internal drainage is difficult due to thin wall that unable to hold the stitches

o Mature: "Calcified wall(> 6 weeks}"

• Internal drainage
• Internal drainage always preferable than external drainage, because
pseudocyst communicates with pancreatic ductal system in 80%
• Wall biopsy is required to rule out cystic neoplasms

o Assocjate wilb infected necrosis or vein thrombosjs ·

• External drainage ± Oebridement
• Associated with 10% recurrence rate
• Used after documentation of the infection by CT or US guided-aspiration
for gram stain and culture

■ Methods of internal drainage:

o Percutaneouscatheter-method
• as temporary method for infected pseudocyst
• High failure and recurrence rate

o Endoscopic methods
• Trans-papillary stenting: indicated in:
• Communicated pseudocyst with main duct
• Strictures of the duct in pancreatic pseudocyst

• Trans-mural drainage: indicated in:

• Large pseudocyst with enteric lumen indentation
• Large pseudocyst with ductal obstruction
• Trans-papillary method not feasible

o Open/ Laparoscopic surgical

• True cystoenterostomy(Duct involvement)
• Cystogastrostomy or cystoduodenostomy
o Cystogastrostomy associated with higher risk of bleeding compared
to cystojejunosto my
o Cystogastrostomy should be avoided in walled-off necrosis

• Roux-en-Y cystojeiunostomy
o Can be added to drainage of walled-off necrosis due to thick
capsule

• Distal pancreatectomy
o For pseudocyst in the tail or with ductal disruption
 ■ Management of pancreatic pseudocyst based on ductal anatomy:
Ductal anatomy after episode of pancreatitis
Type Description Best manaaement
Type 1 Normal duct PCD or Endoscopic drainage
"Only aspiration without drain can by sufficient"

Suraerv onlv after failure of non-suraical methods

Type2 Stricture to main duct
Type 3 Complete obstruction to main duct
Complete disruption
"Disconnected duct syndrome"
Type4 Chronic pancreatitis
Trans-papillary drainage or Surgery
Associated with 25% failure rate of non-suraical methods
Surgery
■ Roux-en-y l ateral pancreatojejunostomy
■ Roux-en-y cystoenterostomy
■ Distal pancreatectomy ± splenectomy
Drainaae can be used as alternative or initial steo
Definitive procedure for chronic pancreatltis

No need for true surnical drainaae of the cvst

Tvoe 2 and 3 are associated with oersistent pseudocvst or waifed-off necrosis
 PANCREATIC CYSTIC NEOPLASMS
Serous cystic tumors Mucinous cystic lntraductal papillary Solid
neoplasms (MCNs) mucinous neoplasms Pseudopapillary
'Most Common tvoe• OPMNs) Neoplasms (SPNs)
Prevalence 30% 10-45% 25% 10%
Elderlv Female Younn Female Elderlv Male Female /exdusivelvl
Site Evenly distributed Body or Tail Head of pancreas (Main-duct) Body or Tail
Bodv / Tail /Branch ducll
DNA Absent K-RAS mutation K-RAS mutation Absent
Malignant No Yes Yes in 40% Indolent malignancy
potential 60% in main-duct type (10-15%)
20% in branch-duct type
c> Mucinous adenocarcinoma
CEA& CA19-9 I l t J
Viscosity J f (Mucin) t (Mucin) J
Communication No No Yes (as pseudocysts) No
with the duct t Amylase level
Obstructed jaundice
40% aresented as aancreat/11s
Cytology Glycogen-rich Mucin-rich Mucin-rich Polygonal epithelial
Cuboidal cells Columnar cells Columnar cells cells
Positive (PAS) Prominent stalks
Periodic-acid Schiff Branchina oaoillae
Sub-types Serous Mutinous non- Main-duct type (lnteS!ina/)
cystadenocarcinoma dysplastic cyst + Express CDX2, MUC2 (Better prognosis)
Branch-duct type (Gastric)
Due to malignant Mixed type
degeneration ••ovarian Stroma�'
Strama of spindle cells Histological s u bt��es:
-
Gastric (Most common) + Ductal adenocarcinoma
Intestinal � Mucinous adenocarcinoma
Pancreaticobiliary + Ductal adenocarcinoma
Oncocvtic + Ductal adenocarcinoma
Imaging Thin capsule with Large unHocular or Main !!uct 2r Mixed llal•: Large mass with:
microcystic pattern septated mulli-locular Dilated main duct > 5 mm
(Based on cyst with internal Mural nodules Circumscribed
Triphasic CT, Appearance: papillary projections Mullifocal if not in the head
MRIIMRCP) Honeycomb Cystic-solid
(Polycystic Thick wall with Branch duct: (Most common) component
Microcystic) calclficatlons Dilated slde branches only
(as pseudocyst) (Bunch of grapes) Capsule
Sunburst sign 40-60% multifocal
(Central calcified scar) EUS +FNA Calcifications Inside
May needed to Upper endoscopy
Ground Glass differentiated ii from Enlarged ampulla w�h mucin
Cluster of aranas oseudocvst "fish-e= anru,arance"
Management Observation Resection is the rule Main duct: Resection Resection

Surgery Observation/Follow-up Branch d11ct·

(Enucleation/Resection) is an option for < 3 cm - Observation
for symptomatic lesion cyst size with low-risk - Resection if suspicious
or larae > 4 cm rvsts features
Notes Associated with VHL Extra-pancreatic CA In 1O-
syndrome in 15-30% 45% (Breast, colon, prostate)

■ Peripheral eggshell calcifications presented in:

o Mucinous cystic neoplasms (suggestive for malignancy)
o Calcified hydatid cyst, Wilm's tumor a.nd Meconium ileus
 Management of IPMN and MCN:

High-risk stigma Symptomatic

Obstruction jaundice Pancreatitis
Main duct 2: 10 mm
Enhanced solid component Worrisome features !MRCPl
- Cyst 2: 3 cm
- Non-enhanced mural nodule
- Dilated main duct> 5 mm
- Thick wall
Yes No
Yes No

Resection EUS + FNA biopsy

t Non definitive diagnosis

Changing in size
Change in character
High-risk features:
- Definitive (enhanced) mural nodule
- Dilated main duct> 10 mm
- Cytology suspicious for malignancy
(CEA > 200 nglml, Solid component, Mucin)

'---------------1 Yes No

Size of the cyst?

1-2 cm >3cm

Repeat CT/MRI Repeat CT/MRI MRI/EUS every 3 - 6 months

2- 3 years Yearly for 2 years Consider surgery in young fit patient
Then every 2 - 3 years

■ ERCP for sampling of fluid or brushings in IPMN or pancreatic CA is not recommended

■ Due to high risk of dysplastic implantation {due to communication with pancreatic duct)

■ Sensitivity of ERCP brush cytology and biopsy to detect malignancy is: 30 - 50%

■ Resection of IPMN is associated with more risk of pancreatic leak than resection in chronic
pancreatitis or adenocarcinoma, due to soft fragile pancreas

■ Distal pancreatectomy without splenectomy used for benign lesion (serous cystic lesions) and
splenectomy is used for malignant lesion to include peripancreatic lymph nodes
PANCREATIC ADENOCARCINOMA
■ 98% exocrine, 80% in Head

■ Most commonly arise from Ductal (from Main duct}

o Ductal adenocarcinoma has "Pancreaticobiliary phenotype"
o Double duct sign: dilatation of both pancreatic duct and CBD
• Associated with pancreatic malignancy

■ Most common gene mutation: K-RAS

■ Serum marker: CA 19 - 9 with p16 mutation
o CA 19-9 is not diagnostic, and not elevated in all types of pancreatic cancer
o Increased in pancreatic biliary obstruction
o Marker of unresectability

■ Route of spread: Lymphatic

■ Most common site of distant metastasis: Liver
■ Most common symptom: Weight loss

■ Risk factors:
o Smoking (Most associated risk factor}
o Chronic pancreatitis
o Diabetes
o K-RAS or p53 mutation

■ Resectable rate: 20%

o Cure rate of resectable pancreatic cancer: 20%
o Cure rate of all pancreatic cancer: 5%

■ Clinical presentation:
o Weight loss (Most common)

o Jaundice (2 nd most common in pancreatic head tumor)

o Pain (2nd most common in pancreatic body/tail tumor}

• Worse in supine position and relieved by leaning forward
• Due to:
• Invasion into splanchnic plexus and retroperitoneum
• Obstruction of the pancreatic duct

o Nausea and vomiting

• Mostly due to infiltration of celiac nodes plexus
<:> Motility disturbance of stomach and duodenum

• Other causes:
• Extensive scarring of the head leading to duodenal obstruction
• Infiltration of the duodenum
■ Resectable (Triphasic CT with Triple-contrast I pancreatic protocol or intraoperatively)
o Arterial:
• No connection with SMA, celiac, CHA

o Venous:
• No connection with SMV or PV
• Abutment {loss of fat separation) < 180° of SMV/PV with no contour irregularity

■ Borderline resectability
o Lymph nodes:
• Peri-pancreatic lymph nodes
• Porta hepatis lymph nodes

o Extra-pancreatic:
• Invasion to duodenum or distal stomach
• Biliary obstruction
• Duodenal obstruction (But usu.ally as late findings)
• Suspicious but not diagnostic of metastatic
(sma/1 indeterminate liver lesions that are too sma/1 to characterize)

o Arterial:
• Abutment,;; 1 so• of SMA or celiac artery
• Abutment,;; 180° or short-segment encasement> 1 so• of CHA

o Venous:
• Encasement> 1 so• of SMV/PV
• Abutment,;; 180° of SMV/PV with vein contour irregularity
• Short segment thrombosis of SMV/PV amenable for reconstruction
• Connecti on with IVC

■ Unresectable {Locally advanced)

o Arterial:
• Encasement> 1 so• of SMA, Celiac artery
i
• Connect on with Aorta

o Venous:
• Unconstructable occlusion of SMV/PV

■ Metastatic:
o Lymph nodes:
• Celiac lymph nodes
• Hepatic hilar lymph nodes
• Retroperitoneal lymph nodes
• Periaortic lymph nodes

o Extra-pancreatic:
• Metastases to Liver
• Metastasis to Peritoneum, Retroperitoneum, or Omentum
• Ascites, or mesenteric infiltration
• Distant metastasis
Management of Pancreatic cancer
■ Stage I and II (Resectable)
� Neoadjuvant chemoradiation is controversial
� Whipple procedure± Adjuvant chemoradiation for 4 months

No need for Biopsy in solid pancreatic mass unless it is unresectable for those in a neoadjuvant trial
or before starting chemotherapy or target therapy

■ Stage Ill (Staging) ➔ EUS (Best to assess vascular resectability)

o Borderline resectable
• Neoadjuvant chemotherapy for 2 months
• FOLFIRINOX (5-fluorouracil, leucovorin, irinotecan, and oxaliplatin)
• Gemcitabine/nab-paclitaxel
• Re-staging (Dual-phase CT, CA19-9 level)
± Neoadjuvant chemoradiation if no response
• Re-staging (Dual-phase CT, CA19-9 level)
• 4 weeks with no therapy, followed by surgery
± Adjuvant chemoradiation 4 months

o Locany advanced unresectable

• Neoadjuvant chemotherapy for 4 - 6 months followed by chemoradiation
• Re-staging (Dual-phase CT, CA19-9 level)
• Only 25% resectable after chemotherapy (75% recurrence)

■ Stage IV (Metastasis or unresectable) ➔ EUS + FNA for targeted-chemotherapy

o Chemotherapy
o Palliative management:
o Associated with Biliary obstruction:
• Life expectancy < 6 months or preoperative: Stenting
• Life expectancy > 6 months or intraoperative: Biliary bypass

o Associated with Duodenal obstruction:

• Life expectancy < 6 months or preoperative: Stenting
• Life expectancy > 6 months or intraoperative:
Gastrojejunostomy ± Celiac plexus block

Indications for pre-operative biliary drainage for resectable pancreatic cancer: (ERCP + Stent)
■ Delayed surgery > 10 days for neoadjuvant chemotherapy

■ Cholangitis or Severe hyperbilirubinemia (> 20 mg/di)

■ Multiple Comorbidities (Renal failure) or Malnutrition patient
■ Coagulopathy
Defer the operation after drainage by 3 - •6 weeks to allow jaundice to resolve

Preoperative drainage for liver resection may be necessary in case of severe jaundice, because
cholestasis can impairs liver regeneration

Routine ERCP preoperative not preferred in cases of resectable pancreatic mass with obstructed
jaundice, due to high risk of complications with no difference in mortality rate
PERIAMPULLARY TUMORS
■ Consist of 4 tumors: "From commonest to rarest"
o Main pancreatic duct tumor
• Most common periampullary tumor
• Median survival rate after resection: 20 months
• 5-year survival: 20%

o Distal CBD tumor

• Most common primary cancer of biliary tract
i
• Ar ses between cystic duct and ampulla of Valer
• 5-year survival: 25 - 40%
• Imaging finding:
• No mass, or short segment of asymmetric CBD wall thickening

o Ampullary tumor
• Higher resectability rate
• 5-year survival: 35 - 70%
• Imaging finding:
• Nodular mass, bulging ampulla or irregular thickening
• Consists of2 pathorogica1 subtypes·
• Intestinal
• Pancreaticobiliary

o Duodenal tumor
• Most common site of small bowel adenocarcinoma
• Developed by adenoma- carcinoma theory
• 5-year survival: 45 - 70% (Best Prognosis)
• Imaging finding:
• Masslike thickening of duodenal wall or polypoid mass

■ Presentation:
o Painless Progressive jaundice
• May associated with mild dull epigastric pain radiating to the back
• May associated with Cholangitis
• Severe pain may indicate invasion to celiac plexus

o Constitutional symptoms: Anorexia, weight loss, fatigue

o Symptoms of pancreatic endocrine and exocrine insufficiency, anemia or melena
o Physical examination non-specific and may shows signs of advanced disease as
hepatomegaly, Courvoisier's sign, Virchow's node, and Sister Mary Joseph's nodule

■ Investigation:
o CBC, Basic screen, Liver and renal profiles, CA 19-9
o CT
• High predicative of unresectable disease
• Low predicative of resectable disease

o MRI: for assessment of resectability based on T stage and vascular structures

o ERCP ± EUS

■ Management: Whipple procedure (Pancreaticoduodenectomy)

Operative Note
■ Lesser curvature is entered by division one or more of these ligaments:
o Gastrocolic ligament
o Gastrohepatic ligament
o Gastrosplenic ligament

Faldfres ligament

Right
triangular
llgamenl

Hepatoga Stomach
( lessee

Hepatoduodenal
ligament
DISTAL PANCREATECTOMY
■ Pre-operative vaccination if planned for splenectomy

■ Diagnostic laparoscopy should be offered for patients with high-risk for occult metastasis

■ Incision: Midline or Bilateral subcostal incision (Preferred)

■ Abdominal exploration for suspicious of metastasis

■ Mobilization:
o The lesser sac is entered by division of gastrocolic omentum (expose by
elevation of transverse mesocolon) and gastrosplenic ligament
o Preserve the middle colic vein
o The peritoneum along the inferior border of the pancreas is incised
o The retroperitoneal space entered by elevation of the body and tail of the pancreas by
gentle dissection behind the gland

■ Splenic p art: (Distal pancreatectomy with splenectomy)

o The short gastric vessels at gastrosplenic ligament are ligated and divided
o Lateral peritoneal attachments (splenorenal ligament) are divided and the spleen
mobilized anteriorly and medially
o Splenophrenic and splenocolic ligaments are divided
o Divide the short gastric vessels if not divided before exposure

■ Vascular part: (Distal pancreatectomy with s:plenectomy)

o The pancreas and spleen are mobilized upwards and towards the patient's right by blunt
dissection between the kidney and the tail of the pancreas
o IMV identified and divided if it drains into the splenic vein
o Dissection of peripancreatic soft tissues continues until Splenic vein/SMV confluence
SMV located at the base of middle ,colic vein

o Splenic artery identified at upper border of the pancreas, then ligated and divided
o Splenic vein divided after the artery

■ Splenic-preserving distal pancreatectomy:

o Develop plane deep to the pancreas but superficial to the splenic vessels
o Divide the branches between pancreatic tail and body with splenic vessels

■ Pancreatic part:
o The pancreatic parenchyma is divided using electrocautery or linear stapler ± 1 cm
margin in suspicious of neoplasm
o The specimen sent for frozen section in case of malignant etiology
o Clip is placed if possible postoperative radiotherapy
o 3 - 0 monofilament non-absorbable to ligate the main pancreatic duct
o Interrupted horizontal mattress sutures are placed through the edge of the pancreatic
parenchyma to close the cut edge

■ Check for hemostasis

■ Closed-suction drain is placed near the edge of pancreas

■ Closure
WHIPPLE PROCEDURE
■ Removal of pancreatic head, duodenum, jejunum, gallbladder, bile duct± gastric antrum
■ Diagnostic laparoscopy should be offered for patients with high-risk for occult metastasis
Indications:
■ Periampullary adenocarcinomas arising in:
o Head of pancreas
o Ampulla
o Distal bile duct
• •
o Duodenum
Steps:
1} Incision:
o Upper midline •
o Mercedes benz incision
o Hockey stick incision

o Chevron incision Mercedes benz Hockey stick Chevron

• For patients with previous lower abdominal surgery or wide costal margin

2) Abdominal exotoration·
o For extrapancreatic metastasis in the liver, peritoneum or omentum± Liver U/S
o Peri-pancreatic lymph nodes metastasis is not a contraindication in low-risk patients
o If suspect metastasis -+ send for a frozen section
Positive -+ One or Triple bypass (Choledochojejunostomy, Gastrojejunostomy,
Jejunojejunostomy)

3} Mobilization & Exposure of the pancreas:

o Transverse mesocolon is retracted inferiorly
o Omentum and the stomach are retracted superiorly and anteriorly
o Enter lesser sac by dividing the gastrocolic ligament through the greater omentum
o Divide the gastrocolic trunk, and avoid injury to middle colic vein
o Middle colic vein identified on anterior surface of SMV posterior to transverse
mesocolon, can be divided in obese patients, or large tumor for further exposure and to
prevent vein injury during traction
4} Assess resectability:
o Inspect the inferior neck of pancreas for any tumor extension

o Attempts to palpate plane between tumor and

• Posterior pulsation of the SMA
• The relationship to right lateral wall of SMA is most critical aspect

• Anterior surface of SMV / PV and posterior surface of neck of pancreas

• Tumor prone to invade l'ateral or posterior wall of SMPV confluence

5} Complete Kocher maneuver:

o Extended Kocher maneuver
• 3rn part of duodenum and uncinate process are retracted superiorly and the
hepatic flexure and transverse mesocolon are retracted inferiorly
• Identify the IVC, and all tissue medial to the right ureter and right gonadal vessels
are retracted to the left side anterior to IVC, until left lateral edge of the aorta
exposed
• Care to preserve right renal artery, and replaced right hepatic artery
• Reassess the relationship of tumor to SMA by manual palpation
• IVC identified and posterior pancreatic soft tissues and lymph nodes are
completely dissected off from I VC and aorta
• Extension of the Kocher maneuver up to the porta hepatis
• En bloc dissection of the retroperitoneal soft tissues is accomplished up to the
level of the left renal vein

o Cattell Maneuver: Right medial visceral rotation (Selective)

• To expose 3rd, and 4th part of duodenum, infra-hepatic IVC, SMA
• By incise the visceral peritoneum of small bowel mesentery the ligament of Treitz
(from ileocecal to hepatic flexure along white line of Toldt)
6} Biliary dissection:
o Gallbladder is retracted superiorly and anteriorly
o The cystic duct is identified and dissected down to its junction with the CBD
o The anterior peritoneum of porta hepatis is completely divided across CBD and hepatic
artery
o Circumferential dissection at the level of the cystic duct and CBD confluence
o Vessel loop is placed around CBD and retracted laterally

7} Portal dissection:
o Dissect common hepatic artery
• Proximally to the celiac trunk
• Distally to right gastric artery and GOA
• The right gastric artery preserved if pylorus-preserving is planned
• Common hepatic artery lymph nodes are dissected and sent as frozen section

o Divide right gastric artery and GOA+ Mobilize common hepatic artery
• Assess for a replaced/accessory right or common hepatic artery (origin: SMA}
Usually located posterior and lateral to portal vein
• If replaced hepatic artery + need to be dissected until origin to prevent injury
• By palpation of porta hepatis through foramen of Winslow
• Clamp GOA 5 minutes and try to feed pulsation at hepatic proper artery
o Due to retrograde flow (in celiac trunk extensive calcification)
"GOA-Dependent flow" 1 - 2 % of population affected
o Should be with adequate stump if need for embolization post-op

o Expose portal vein

• Common hepatic artery retracted medially, and CBD is retracted laterally
• Soft tissues between the CHA and CBD dissected toward the main specimen
• The anterior surface of portal vein is identified and dissected down to the
superior neck of the pancreas
• The posterior lymph nodes of porta hepatis dissected from the portal vein
• Care not to injure aberrant right hepatic artery (posterolateral to the vein)
• Gallbladder dissected from posterior surface of the liver
• Divide the CHO 1 cm distal to the hepatic duct bifurcation
• The middle colic vein identified and followed to the inferior border of pancreas to
identify the SMV

--
8) Stomach dissection:
o Standard Whipple:
• Greater omentum is dissected from transverse mesocolon up to the level of the
confluence of left and right gastroepiploic arteries on the greater curvature of the
stomach, and greater curvature divide at the bare area
• At the level of 2nd , and 3rd branches of left gastric artery, the lesser omentum is
dissected and lesser curvature divided
• Assess for replaced left hepatic artery during opening lesser omentum
• The distal stomach is retracted to the right of the porta hepatis

o Pylorus preservation Whipple: may be considered in small periampullary tumors

• At this case, subpyloric lymph nodes dissected from inferior part of duodenum
• Duodenojejunostomy created 2 - 3 cm from pylorus
• Thought to decrease delayed gastric emptying by maintaing normal gastric
hormones release
• Erythromycin is used in case of delayed gastric emptying
• Less oncological procedure, with similar complications

9} Duodenojejunal dissection:
o Dissect loose attachments of ligament of Treitz
o Transect jejunum 15 cm distal to ligament of Treitz and divide the mesentery
o Continue dissection proximally to involve 3,a and 4th parts of duodenum, divide its
mesentery to level of aorta
o Reflect duodenojejunal section underneath the level of superior mesenteric vessels
o 4th part of duodenum and first portion of jejunum delivered by dissection from the

retroperitoneum from left to right beneath the mesenteric vessels

1 O)Pancreatic dissection:
o 4 separate polypropylene figure of 8 stitches are placed on either side of the inferior and
superior neck of the pancreas

o Tunneling:
• The neck of pancreas is dissected from Mesenteric vessels and Portal vein
• If tumor adhere to portal vein/SMV
-+ Transect pancreas more distally + segmental venous resection
o The uncinate process is retracted to tihe right, the portal vein retracted to the left

o Dissect the uncinate process from SMA with its branches, and SMV

o The specimen is removed and sent to pathology for frozen sections on:
• Bile duct margin
• Uncinate process margin
• Pancreatic neck margin

o Titanium clips are placed along the retroperitoneal margin on the lateral edge of SMA

11} Vascular Resection (Selective)

o If tumor adhere to SMV / SMPV and no evidence of extension to SMA or celiac axis
o Divide the splenic vein to expose SMA
o Systemic heparinization and occlude the SMA (to prevent bowel edema)
o Resect SMPV part that attached to tumor (2 - 3 cm proximal and distal)
o Followed by end-to-end anastomosis
o Arterial reconstruction is controversial

Best venous donor site: Left renal vein (Due to presence of collaterals)
12) Reconstruction

1. Pancreaticojejunostomy:
o Mobilize transected jejunum by incision of transverse mesocolon to right of middle colic
vessel (retrocolic better than retroperitoneal = posterior to mesenteric vessels)

o Pancreaticojejunostomy 15 cm from ligament of Treitz

• By full thickness end-to-side anastomosis between pancreatic duct and anti­
mesenteric enterotomy over a small Silastic stent (if not dilated duct) with
interrupted 4-0 polypropylene non-absorbable sutures
• Dunking method: Two-layer end-to-end or end-to-side invagination cut end of
pancreas into jejunum (for small duct with soft pancreas)

• Duct-to-mucosa: Two-layer end-to-side full-thickness pancreatic duct to jejunal

wall (Best for large duct with fibrotic pancreas)
1) Suture posterior pancreas to jejuna! wall
2} Suture pancreatic duct to jejunal window at 3 - 6 - 9 - 12 O'clock
3} Suture the anterior pancreas to jejunal wall

None decreases the risk ofpancreatic anastomotic leak

2. Hepaticojejunostomy
o End-to-side CHO to antimesenteric border of the jejunum 15 cm distal to
pancreaticojejunostomy
o As single layer with interrupted 4-0 absorbable monofilament sutures
 3. Gastrojejunostomy
o Antecolic end-to-side or side-to-side gastrojejunostomy in two layers, starting from
greater curvature

o Antecolic position is preferred as it may minimize postoperative radiation injury to the

anastomosis or subsequent blockage from local recurrent cancer.

o The distance between the biliary and gastric anastomoses should be " 30 cm

o Cuff of duodenum revised, preserving at least 1.5 cm of postpyloric duodenum to

preserve blood supply to the anastomosis

o Feeding jejunostomy tube may be placed 30 cm distal to the gastrojejunostomy, by

using Witzel technique

■ Place falciform ligament between hepatic artery, at level of GOA stump, and afferent jejunal
limb to cover and protect GOA stump

■ Irrigation of the abdomen

■ Check for hemostasis

■ Drains insertion
o Inferior drain is placed posterior to the biliary anastomosis, and a
o Superior drain is placed between the pancreatic anastomosis and the incision

■ Closure the abdomen

Life expectancy post-Whipple: 20 months

Survival rate of patients who underwent Whipple procedure is around 20%

Complications of Whipple procedure:
■ Delayed gastric emptying (14 -45%}: most common complication
o NG decompression and stop enteral feeding
o Start prokinetics
o Start jejunostomy feeding or TPN for (Prolonged cases

■ Pancreatic/Biliary fistula (7%)

o Risk factors:
• Small pancreatic duct
• Soft or normal parenchyma (non-malignancy}
o Manifested as abdominal pain, fever, tachycardia leukocytosis
o Diagnosed by:
• Drain amylase > 3 times of serum amylase on Day 3

■ Bleeding
o Early post-pancreatectomy bleeding: within 24 hours
• Due to inadequate hemostasis
• Management:
• Retum to OR

o Late post-pancreatectomy bleeding: any time after 24 hours

• Due to inflammatory process (leak} leading to vascular erosion
• Lead to formation of pseudoaneurysm that rupture
• Most common site: GOA stump followed by hepatic, SMA, and splenic artery
• Management:
• Angioembolization
• Because of fragile tissue after 24 hours and difficult to control surgically

Remember to rule out intraluminal bleeding (Anastomotic bleeding, Stress ulcer)

■ Pancreatitis

■ Diabetes mellitus

■ Steatorrhea

■ Pancreatic abscess

■ Renal failure

■ Sepsis

■ Pleural effusion

■ Coagulopathy

■ Wound infection/Intra-abdominal collection (pancreatic leak}

■ Most common nutritional complication of Whipple:

o t Zinc
o f Copper
 Spleen
Reviewed by:

Dr. Ahmed M El Demati

SPLEEN
ANATOMY AND PHYSIOLOGY
■ Arises from mesoderm by the 5th week of gestation
■ Only solid visceral abdominal organ covered completely with visceral peritoneum
■ Size of the spleen size between 7 -11 cm (up to 13 cm)
o Moderate splenomegaly: > 15 cm (or > 500 mg)
o Massive splenomegaly: > 22 cm ( or > 1 kg) "Early satiety is important symptom"

Vascular supply
■ Splenic artery
Branches:
o Left GEA (ligation affects left GEA, leads to -+ ischemia of the fundus)
o Short gastric, posterior gastric, and to pancreas

Types:
o Distributive (commonest) -+ Short trunk
o Magistral -+ Dividing near hilum

Magls1,ol
Distributed Simple - .....
30�

■ Splenic vein:
o Joining SMV behind the neck of the pancreas to form the Portal vein
o Located posterior and inferior to the splenic artery

Splenic ligaments:
■ Chief ligaments (Vascular ligaments)
o Gastrosplenic ligament -+ Held Short Gastric, Left GEA, and splenic vessels
• Short gastric vessel is most commonly cause of bleeding "short stump"

• 1"' to divide during splenectomy to open lesser sac (Anterior approach)

c::, Splenic pedicle

Splenorenal ligament held splenic vessels in case of portal hypertension

■ Minor ligaments
o Splenocolic ligament -+ 1 •• to divide during splenectomy (Posterior approach)
o Splenophrenic ligament, Pancreatosplenic, and Pancreatocolic ligaments
Function of the spleen:
■ Red pulp (85%): Filtering, including damaged RBCs

■ White pulp {15%): immunologic function; produce lgM

■ Extra medullary site for Hematopoiesis

■ Opsonization by producing: Tuftsin, Properdin, and Fibronectin {Adhesive glycoprotein)

Initiating alternative complement pathway which enhancing the macrophages to kill
encapsulated bacteria

Splenic anomalies
■ AccessoN spleen (20%):
o Most commonly associated with: Hereditary Spherocytosis

o Most commonly found at: Splenic hifum

• 2nd most common is Gastroco/ic ligament
• 3rd most common: Tail of pancreas
Other locations: Bowel mesentery, Broad ligament, Spermatic cord

o Localized by technetium T99 tagged RBCs scan

■ Wandering Spleen:
o Failure to from 1 or more of suspensory ligaments of spleen -+ long splenic pedicle
o CT findings:
• Absence of spleen in its normal position, and ectopic spleen

o Treatment:
• Mostly asymptomatic
• Symptomatic: {due to torsion of splenic vessels)
• Splenectomy or splenopexy
IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP)
■ Anti-Platelets lgG
■ Petechial, gingival bleeding, bruising, soft tissue ecchymosis
■ Spleen size is usually not enlarged

■ Treatment:
o Observation

o First line: Steroids for 8 weeks

• Response is seen within 3 weeks
• For asymptomatic patient with platelets< 20,000/mm3
• For symptomatic patient with platelets< 50,000/mm3

o 2nd line: IV gammaglobulin used for:

• Bleeding with platelets < 5000/mm3
• Steroid resistant
• Extensive purpura
• Need to increase platelets preoperatively
• Pregnant

o 3th line:
• Rituximab (monoclonal antibody)
• Eltrombopag (thrombopoietin-receptor antagonists)

o 4'd line: Splenectomy

• For patients with failure of steroids after 12 months and continue bleeding

• Most common non-traumatic condition requiring splenectomy: ITP

Hereditary Spherocytosis in United States
• Most common condition treated effectively with splenectomy: ITP
• Predictor for effectiveness of splenectomy:
o Good response to steroid (90% over 60% in non-responding)
o Age < 40 years
• Most common cause of failed splenectomy: missed accessory spleen

THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP)

■ Thrombocytopenia, fever, purpura, neurological symptoms, alter mental changes, renal
dysfunction, hematuria

■ Death most commonly due to intracerebral hemorrhage or acute renal failure

■ Peri pheral smear shows:

o Basophilic stippling
o Nucleated RBCs
o Schistocy1es
o Hyaline around membrane

■ Treatment:
o Plasmapheresis (primary); immunosuppression
OVERWHELMING POST-SPLENECTOMY INFECTION (OPSI)
■ 0.1% risk after splenectomy, and up to 8% in traumatic spleen
■ f risk in children, and highest risk in Tha/assemia

■ Most episodes occur within 2 years of splenectomy

■ Not responding to antibiotics with mortality rate 50%

■ Secondary to specific lack of immunity to capsulated bacteria (Due to loss of Opsonization)

■ Capsulated gram negative organisms:

S. pneumonia (most common}, H. influenzae, N. meningitides and Klebsiella pneumonia

■ Strategy used to reduce mortality rate:

o Partial splenectomy
o Vaccination 2 weeks before splenectomy to avoid transient immunosuppression

VACCINATION AND ANTIBIOTICS

Meninaococcal Pneumococcal Hemoohilius influenza
MCV4 PCV13 Vaccination if not previously vaccined
+ PPSV23 after 8 weeks
MPV is alternative and used Recommended yearly
for> 55 year + Booster after 5 year
± Booster

■ Vaccines given 2 weeks before elective sple nectomy:

o For maturation of vaccine and optimizing antigen-antibody recognition

■ Vaccines given after 2 weeks "preferred" or upon discharge ( day 5 - 7} after emergency
splenectomy:
o To avoid transient immunosuppression

ANTIBIOTICS
■ Prophylactic Antibiotics: Controversial (Different recommendations)
o Daily oral antibiotics with oral penicillin VK or amoxicillin or monthly penicillin G
• Different recommendations:
• Until age of 5 years, or 5 years after splenectomy (Schwartz}
• For 1 - 2 years after splenectomy in children (< 16 years}
• Until adulthood

o Life-long antibiotics considered for low response to vaccines and immunocompromised

POST SPLENECTOMY CHANGES

■ Increased:
o WBCs, RBCs, Platelets
o Heinz bodies (Hb), Howell-Jolly bodies (nuclear remnants}
o Target Cells, Spur cells, stippling
o Irregular shaped fragmented RBCs

■ Loss of
o Tuftsin, Properdin, Fibronectin and Schistocytes
HEMOLYTIC ANEMIAS
MEMBRANE PROTEIN DEFECTS

Spherocytosis
■ Most common congenital hemolytic anemia requiring splenectomy
■ Loss Spectrin, Ankyrin (membrane protein)-+ Splenic sequestration (hypersplenism)

■ Presentation:
o Leg ulcers
o Pigmented stones
o Anemia, reticulocytosis, jaundice, splenomegaly

■ Splenectomy with cholecystectomy at age ot 5, after immunizations

Elliotocytosis
■ Spectrin and protein 4.1 deficit (membrane protein)

NON-MEMBRANE PROTEIN DEFECTS

Pyruvate kinase deficiency

■ Most common congenital hemolytic anemia overall
■ Most common congenital hemolytic anemia not involving membrane protein that requires
splenectomy

G6PD deficiency
■ Precipitated by infection, certain drugs, fava beans
■ Warm antibody is indication for splenectomy

Sickle cell anemia

■ AR, Qualitative hemoglobinopathy of Hb in Chromosome 11 in 6th codon in B-Chain
c:, Replace Glutamic (Hb B) with Valine (Hb S)
c:, Point mutation (amino acid),: Adenine with Thymine

■ Hb Electrophoresis: Hb S to determine severity and response to treatment

o Blood transfusion may indicated if Hb < 10 g or HbS > 60%

■ Sickler test: RBC's + Na dentonate

■ Splenectomy indicated for:

o Recurrent acute sequestration crises (after 1 major acute sequestration crises)
o Hypersplenism
o Splenic complications (abscess)
Beta thalassemia
■ Most common type of thalassemia; due to persistent Hb F
o Major: both chains affected
o Minor: 1 chain affected

■ Most die as premature secondary to hemosiderosis

■ Associated with increasing risk of:

o OPS!
o DVT / PE
o Pulmonary hypertension following splenectomy
HODGKIN'S DISEASE
■ Neoplastic cells: Reed-Sternberg cells
■ Types:
o Nodular sclerosing (Most common)
o Mixed Cellularity
o Lymphocyte predominant (Best prognosis)
o Lymphocyte depleted (Worst prognosis)
o Nodular lymphocyte-predominant

■ Most common cause of chylous ascites: Lymphoma

■ Arbor classification:
o Stage I: 1 area or 2 contiguous areas on the same side of diaphragm
o Stage II: 2 non-contiguous areas on the same side of diaphragm
o Stage Ill: involved on both sides of diaphragm
o Stage IV: Disseminated or multiple involvement of extranodal organs

• 0

" /
I I I I

Stage I Stage II Stage Ills Stage IV

■ Chemotherapy used in Hodgkin lymphoma

o ABVD (Doxorubicin, Bleomycin, Vinb!astine, Dacarbazine)

NON-HODGKIN'S LYMPHOMA
■ Most common malignant splenic tumor
■ 90% B-cell lymphomas
■ Worse prognosis than Hodgkin's
■ No need for surgical staging
■ Chemotherapy used in Non-Hodgkin lymphoma
o ADVP
o R-CHOP
• Rituximab
• Cyclophosphamide
• Doxorubicin
• Vincristine
• Prednisolone

One cycle R-CHOP -+ Radiation -+ 5 cycles of R-CHOP

SPLENIC VASCULAR DISEASES

■ Splenic artery aneurysm

o Most common visceral aneurysm (more common in women)
o Associate with: portal hypertension, female, multipartum

o Double rupture phenomena

(Lesser sac bleeding, followed by peritoneum bleeding)

o High rate of pregnancy-related rupture and mortality in 3rd trimester

o Management:

<2cm 2: 2 cm
Asymptomatic Symptomatic
Not pregnant Pregnant or want to be pregnant

Proximal or Middle Distal (Near to spleen)

Follow up
(Far from spleen)

Ligation and resection of the aneurysm

I ._I __ s_p le _ t_ o_ m_ _
_ _ n_ec Y_ __,

■ Splenic artery pseudoaneurysm

o Most common visceral pseudoaneurysm
o Etiology·
• Trauma
• Pancreatilis
• Postoperative causes

o Most common clinical symptom: Abdominal pain

o Gold standard investigation: CT angiography

o Management·
• as above (some recommend repair of all splenic pseudoaneurysm)

■ Splenic vein thrombosis:

o Most common cause: Pancreatitis
o Presentation:
• Upper GI bleeding
• Pancreatitis
• No esophageal varices

o Can cause portal hypertension

o Treatment: Splenectomy
SPLENIC ARTERY EMBOLIZATION
■ Indications
o Trauma
• Borderline hemodynamically unstable with documented isolated splenic injuries
in high-risk patient for surgery
• Hemodynamically stable splenic injury grade IV-V ± contrast extravasation ±
splenic vascular injury (arterial injury on CT scan)

o Hypersplenism
• Used for massive spleen (>20 cm) before laparoscopic splenectomy

o Splenic artery aneurysm and pseudoaneurysm

■ Technique
o Proximal embolization is the technique of choice
• Distal embolization associated with splenic infarcts

■ Complications:
o Splenic abscess, splenic rupture, splenic vein thrombosis, sepsis and pancreatitis
■ SPLENIC CYSTS
o Pseudocysts (false)
• Most common type of splenic cyst
• Due to trauma, or pancreatitis

o Primary (true}

Non-Parasitic
• Most common primary splenic cyst

• Management:
• Asymptomatic/ < 5 cm: Conservative

• Symptomatic/> 5 cm:
o Partial splenectomy

o Total splenectomy if polycystic or inaccessible for partial

o Laparoscopic unroofing or fenestration for peripherally located

c:, Higher chance of recurrence

o Avoid PCD due to high risk of recurrence

Parasitic
• Most common etiology of splenic cyst

• Most common organism is: Echinococcus granulosus

• Unilocular cyst, wall calcifications and internal daughter cysts

• Management:
• Total splenectomy + Medical treatment
■ SPLENIC ABSCESS
o Caused by hematogenous spread from distant primary septic focus

o Most common organisms: Streptococcus and E. Coli

o Mortality rate:
• 15 - 20% in healthy patients
• Up to 80% in immunocompromised patients

o Investigation:
• CT scan with IV contrast -+ Lesion does not enhance with contrast
o Management:
• IV broad-spectrum antibiotics � 14 days

• Total splenectomy (Open/Laparoscopic)

• Standard of care
• Indications:
o Multi-locular abscess
o Unlocular abscess as isolated or prominent cause of sepsis
o Failure of percutaneous drainage

• Percutaneous drainage
• Failure rate: 50 - 60%
• Indications:
o Selected unilocular abscess (high-risk, multiple causes of sepsis)
o Patients who cannot tolerate splenectomy

• Contraindications:
o Multilocular abscess
o Multiple small ab·scesses
o Multiple sites of infection
o No safe route for drainage
o Coagulopathy or diffuse ascites
OTHER CONDITIONS
■ Associated with High morbidity: Myeloid Dysplasia

■ Associated with Rupture: Malaria

■ Most common primary splenic tumor:

o Vascular tumor (angiosarcoma, hemangioma)
• Most common splenic tumor overall: Hemangioma

■ Most common tumor spread to spleen: Lung cancer

■ Most predict for hemolysis with hypersplenism: Reticulocytes

■ Hyposplenism not associated with atrophy

■ Felty's syndrome:
o Rheumatoid arthritis, Hepatomegaly, .Splenomegaly and Neutropenia
OPERATIVE NOTE
■ Most common indication for splenectomy: Trauma

■ Most common organ injury during splenectomy: Pancreas (Tail)

■ Standard of care: Laparoscopic splenectomy

■ Indications for hand-assist laparoscopic splenectomy: Massive splenomegaly

■ Indications for open splenectomy:

o Trauma (most common)
o Massive splenomegaly
o Ascites and portal hypertension
(Splenic vein thrombosis ➔ isolated gastric varices)

o Multiple prior operations

o Extensive splenic irradiation
o Splenic abscess

■ Peri-operative:
o Pre-operative vaccination for elective cases (and post-operative in emergency)
o ICU bed in case of trauma
o Type and cross-match of blood
o Antibiotics prophylaxis
o DVT prophylaxis and pneumatic compression boots
o NGT intraoperative
o Mobilization, and chest physiotherapy
o Informed consent
 Differences between Elective and Emergency Open Splenectomy:

Elective Emerciencv
Pre- Vaccination at least 2 weeks pre-op
ooeratlve Solenic arterv embolizalion if needed
Incision Left subcoslal incision Midline incision
Midline incision (massive solenomeaalvl
Exploration For accessory spleen Must be done for other iniuries
Medial Approach {Anterior approach) Lateral Approach

- Lesser sac is entered through the left part - 4 quadrants packing and
of gastrocolic omentum (gastrocolic
ligament) and divide the Gastrosplenic
ligament as near as to spleen to prevent
ischemia of stomach fundus
- Divide splenocolic ligament
- Retract colon downward
- Retract the spleen medially
Intra-
Approach
operative - Divide lateral ligaments
(Splenorenal, Splenophrenic)
abdominal pads below spleen
- Lesser sac is entered through
division of gastrocolic omentum
followed by division of
Splenocolic ligament and
Gastrosplenic ligament
- Control hilum by finger if
continuous bleeding
- Mobilize spleen laterally bluntly
by fingers

• Retract the stomach medially, and expose • Higher short gastric vessels
splenic vessels divided after splenic mobilization
0 Splenic artery isoI1ated and divided
just distal to the ta ii of pancreas - Dissect and divide lateral
0 Splenic vein runs below artery and attachments
behind pancreas, and then divided
- Divide hilar vessels combined
- Check for hemostasis in the
retropertioneal space at splenic bed - Check for hemostasis in the
retropertioneal space at splenic
bed
Accessory Search and remove Don't search, keep it
soleen
Drain - For susoected oraan iniurv /Pancreas Stomach. Colon)
Post- Antibiotics Vaccination 2 weeks or upon
operative discharae

■ Post-operative:
o Platelets should infuse after ligation of the artery if indicated{< 50,000}

o FFP if there is t INR or ongoing bleeding

o Aspirin if platelets> 106 (600,000 by other sources)
LAPAROSCOPIC SPLENECTOMY
■ Position: Right lateral decubitus position at 45• (left-side UP) "Hanging spleen"
o Beanbag under right flank
o Protective roll under right axilla
o Hyperextend left arm

■ Ports insertion: (3- 4 ports)

o Preferred as open technique
• Supra-umbilical incision with insufflate to 15 mm Hg pressure
• Abdominal exploration

o 1 st port (12 mm; for stapling} under 11 th rib at mid-axillary line

o 2nd port (10 mm) 2 cm below costal margin medial to left anterior axillary line
o 3"' port (5 mm} medial and anterior to first trocar at mid-clavicular line

■ Steps: Lateral Approach

o Abdominal exploration for accessory spleen before obscured by bleeding or diathermy
marks

o Divide splenocolic ligament

o Posterior dissection and divide lateral ligaments (Splenophrenic and Splenorenal) until
visualize the left crus of diaphragm

o Enter lesser sac by dividing the greater omentum between the stomach and spleen
(gastrosplenic ligament)

o Mobilize the spleen inferomedially and divide high gastrosplenic attachments

o Identify and divide the hilar vessels separately after separation from tail of pancreas

o Divide the remaining posterior attachments of the spleen

o Place the spleen into large specimen bag and remove it by either morcellization or
hand-assisted port (in case of malignancy)

o Check for hemostasis in the retroperitoneal space

o Inspection for accessory spleen

o Drain placement only for concern of pancreatic injury

o Closure of the fascia at all port sites 10 mm in size or larger

o Skin closure
■ Complications of Splenectomy:
o Intra-operative:
• Hemorrhage (1 't)
• Pancreatic injury
• Tail of pancreas is proximal to splenic hilum by 1 cm in 75%

• Bowel injury (Colon, Stomach)

• Diaphragmatic injury
• Left kidney and left Supra-renal injury

o Post-operative:
• Early:
• Pulmonary complications
o Atelectasis "Most common complication after open splenectomy"
o Pneumothorax

• lleus
• Subphrenic abscess
• Thrombocytosis (Can lead to portal vein thrombosis)

• Thromboembolic events (5 - 37%)

o Usually in first 2 weeks postoperative
o DVT prophylaxis indicated for all patient undergoing splenectomy
o Highest risk in patient with thalassemia
o Portal vein thrombosis associated in 40% for splenomegaly and
myeloproliferative disorders

• Acute gastric dilatation:

o Due to occupying space and delay recovery of distended stomach
o Presentation:
• Tachypnea, tachycardia, and hypotension
• Abdominal pain, non-projectile vomiting
• Vasovagal reaction

o NGT should inserted intra-operatively and kept for 24 - 48 hours

. �
• OPSI

• Splenosis
o Splenic implants, related to trauma
(autotransplantation -+ help in OPSI and may cause recurrence of
hematological disorders)
Hernia, and Abdominal
Wall
Reviewed by:

Dr. Ahmed Muhammed Odeh

HERNIA, AND ABDOMINAL WALL
ABDOMINAL WALL
■ Blood supply of abdominal wall:
o Femoral artery: (medial to lateral)
1) Superficial external pudenda/ artery
2) Superficial epigastric artery
3) Superficial circumflex iliac artery
Provide supply to inguinal area

o Internal thoracic artery: (from 1st part of subclavian)

1) Superior epigastric artery: terminal branch
• Anastomosis with inferior epiga stric artery at umbilicus
2) Musclophrenic artery

o External iliac artery:

1) Inferior epigastric artery
• Travel between transversalis fascia layers and pierce rectus sheath at arcuate line
• Medial to the bowel, compensate internal thoracic (internal mammary} artery

2) Deep circumflex artery

• Anastomosis with inferior epigastric artery between transversalis abdominis and
internal oblique muscles
• Innervate skin of flank area along with lumbar, intercostal arteries

■ Innervation:
o From anterior rami of spinal nerves T6 - T12

■ Lymphatic drainage:
o Superficial lymph vessels
• Above umbilicus: Anterior axillary nodes
• Below umbilicus: Superficial inguinal nodes

o Deep lymph vessels

• Internal thoracic, external iliac, posterior mediastinal and para-aortic lymph nodes
 ■ Layers of abdominal wall: (superficial to deep)

o Skin

o Superficial fatty layer (Camper's fascia)

o Deep membranous fibrous layer (Scarpa's fascia)

• Fascia lata
• Celle's fascia

o External abdominal oblique fascia (Hands in pocket) is the direction of fibers

• Inguinal ligament
o Shelving edge connecting l liopubic tract to inguinal ligament

• Lacunar ligament (Ligament of Gimbernat)

o Medial extension of inguinal ligament (Lateral reflection of external oblique)

• Cooper's ligament
o Lateral extension of Lacunar ligament

o Internal abdominal oblique Direction against external oblique (upward and medially)
• Cremasteric muscles
• Conjoin tendon

o Transversalis fascia, which forms:

• Conjoined tendon (along with i oblique) inserted into iliopectineal line
• Cooper's (ileopectineal) ligament (posterior to femoral vessel)
• lliopectineal arch (lower border)
• lliopubic tract

■ Arcuate line "Semicircularis Douglas line" (3 - 4 cm below umbilicus)

Anterior rectus sheath Posterior rectus sheath

Above arcuate line External oblique aponeurosis Internal lamina of internal oblique
aponeurosis

External lamina of internal oblique aponeurosis Transversus abdominis

aooneurosis
Below arcuate line External oblique aponeurosis Absent (Moves anterior)

Both laminae of internal oblique aponeurosis

Transversus abdominis aooneurosis

INGUINAL AREA
■ Inguinal ligament (Poupart"s ligament):
o Inguinal points:
• MidPoint of inguinal ligament: A.S.1.S -+ Pubic tubercle
• Mid inguinal point: AS.I.$ � symphysis pubis

o Length of inguinal canal:

• 4 cm from Lateral: AS.LS {deep ring) to Medial: Pubic tubercle (Superficial ring)

o Rings:
• External (superficial) inguinal ring: opening of external oblique aponeurosis
o Location:
• Above and medial to pubic tubercle

o Exit of:
• Spermatic cord and its content
• llioinguinal nerve (passes through this ring only)
• Indirect inguinal hernia

• Internal (deep) inguinal ring: opening of fascia transversalis

o Locat;oo·
• 1/2 inch above mid point of inguinal ligament
(lateral to inferior epigastric vessels)

o Inlet of:
• Spermatic cord and its content
• Round ligament (female)
• Indirect inguinal hernia

• On media side, TF condensed '"U-shaped" -+ Shutter mechanism during cough

o Boundaries:
• Anterior: Extemal oblique aponeurosis (Enforced laterally by internal oblique)

• Posterior: Transversalis fascia (Enforced medially by conjoint tendon)

Must be repaired during hernia repair

• Roof: Conjoined tendon

• Floor: Inguinal ligament, and Lacunar ligament
• Medial: Superficial ring
• Lateral: Deep ring
• Content: Spermatic cord (male), Round ligament (female)
 ■ HESSELBACH'S TRIANGLE:
o Medially: Rectus muscle
o lnferiomedial: Inguinal ligament
o Laterally: Inferior epigastric artery

■ MYOPECTINEAL ORIFICE OF FRUCHAUD (MPO)

o Any groin hernia occur through this area

o In Laparoscopic (TEP, TAPP) the myopeclineal orifice should be covered completely

o Boundaries:
• Superior: Internal oblique
• Inferior: Cooper's ligament
• Medial: Rectus sheath
• Lateral: lliopsoas muscle

o Divided into:
• Superior part
• Inferior part (Triangle of Doom, Triangle of Pain)

■ Differences between direct and indirect inguilnal hernia:

Direct hernia Indirect hernia

Risk factors Weakness of abdominal wall
r
Intra-abdominal pressure
f Elastase, f TGF-B
1 hvdroxvoroline
Defect Transversalis fascia
Relation to Inferior eolaastrlc Inferior and Medial to IEA
Relation to Soermatic cord Behind the cord
Relation to Hesselbach's trlanale Throuah it
Coveraae Abdominal wall coveraae
Complication Less
Most common hernia overall
Persistently patent processus
vaainalis
Throuah deep rina
Suoerior and Lateral to IEA
Anterior and Lateral to the cord
Outside the trianale
Internal soermatic fascia
More
- Higher risk of incarceration
- Scrotal hematoma

Inguinal hernia is more common on the right side due to slower descent of right testis during fetal
development because of delay in atrophy of processus vagina/is
■ Coverings of the spermatic cord: (from external to intemal)
o External spermatic fascia (from external oblique aponeurosis)
o Cremasteric muscle (from internal oblique muscle)
o Internal spermatic fascia (from fascia transversalis}
• Cover the indirect inguinal hernia

o Contents:
• Pampiniform plexus of veins
• 2 Maior structures:
o Vas deferens: medial to spermatic cord
o Round ligament in female

• 3 Arteries:
o Artery to vas deferens (from inferior vesical artery)
o Cremasteric vessels (from inferior epigastric artery)
o Testicular artery (from aorta)

• 3 Nerves:
o Genital branch of genitofemoral nerve
o Nerve to Cremasteric
o Sympathetic nerves

o Relations:
• Anterior and Lateral to the cord: Indirect hernia
• Anterior and medial to the cord: llioinguinal nerve
• Medial to the cord: Vas deferens
• Lateral to the cord: Genitofemoral nerve
• Behind the cord: Direct hernia

■ Composition of a hernia:
1) Sac:
• Neck (narrowest part): absent in direct hernia
• Body
• Tail

2) Content:
• Direct hernia: Retroperitoneal fat± omentum or bowel
• Indirect hernia: Peritoneal sac± omentum or bowel

3) Covering
 ■ NYHUS CLASSIFICATION
o I: Indirect with normal ring

o II: Indirect with enlarged ring

• But not extend to scrotum

o 111 (Associated with defect)

• A: Direct
• B: Indirect & posterior wall defect "Direct" (Pantaloons hernia)
• C: Femoral

o IV Recurrent
• A: Direct
• B: Indirect
• C: Femoral
• D: Pantaloon

Types of pain may associated with hernia:

■ Nociceptive pain: Reproduced with abdominal muscle contraction
o Most common type
o Result of ligamentous or muscular trauma and inflammation

■ Neuropathic pain: Localized sharp burning or tearing sensation

■ Visceral pain: Diffuse and poorly localized
SPECIFIC EXAMINATION TESTS FOR INGUINAL HERNIA
1} Expansile cough impulse: cough while reduce hernia content and look for expanding

2} Neck holding test: (Standing position)

o Hold neck of scrotum by index and thumb
• If you can get above it + scrotal swelling
• If you can't get above it + inguinoscrotal swelling

3) Reducibility: (Lying position)

o Ask patient to reduce it by himself
o Locate deep inguinal ring, press on hernia from inferior until complete reduction

4) Internal (deep) ring occlusion test

o Ask patient to cough while maintain pressure + reappears in direct hernia
o Remove your finger + hernia slide down obliquely in indirect hernia

5) Three finger test (Zieman's technique)

o Index on deep ring + indirect
o Middle on superficial ring + direct
o Ring finger on saphenous opening + femoral
o Ask patient to cough

6) Exanimation of superficial ring (Very painful, avoid it)

7) lnvagination test
o Scrotum inverted and enter inguinal canal by index finger or 5th finger
o Assess size of external ring and finger introduced until deep ring
o Ask patient to cough
• Swelling on the tip + indirect hernia
• Swelling on the pulp + direct hernia

8) Ring occlusion test

o Reduce the hernia content
o Occlusion of deep ring by thumb and ask patient to cough
o Direct hernia will protrude but indirect hernia will not

9) Location of the swelling in relation to pubic tubercle:

o Above and medial: inguinal hernia
o Below and lateral: femoral hernia

10)Percussion and auscultation:

o For bowel content

11)Transillumination test
ROLE OF IMAGING IN ABDOMINAL HERNIA
■ Hernia is clinical diagnosis

■ Indications for imaging:

o Occult primary or recurrent hernia
(Groin pain with normal or equivocal examination)

o Athletic pubalgia

■ Types of imaging:
o U/S
• Initial test of choice
• Patient is asked to cough during the exam to elicit herniation of the content

o CT scan
• Have a sensitivity of 80% and specificity of 65%

o MRI
• Highest sensitivity and specificity
INGUINAL HERNIA REPAIR:
1) Skin incision: 1 cm above (ASIS ➔ Pubic t ubercle) for good closure at the end
o Parallel to inguinal ligament, although horizontal incision is more cosmetic
o Starting from pubic tubercle to midinguinal point
o Skin incision should be over the hernia
o Divided the 3 veins: (Ligate. Don't cauterize the veins)
• Superficial epigastric vein
• Superficial external pudenda/ vein
• Superficial external (circumflex) iliac vein

2) Dissection of External oblique:

o Scarpa's fascia (deep fascia) dissected along line of the incision
• Deep fascia below and medial to inguinal ligament opened and exposure of
femoral canal indicated in absence of inguinal hernia and in women

o External oblique opened by blade as snip, then extended parallel to inguinal ligament
• llioinguinal nerve located underneath external oblique (anterior and medial to the
cord}, and should be identified and reserved
• Should be opened over the hernia exactly and parallel to its fibers
• Till reach to external (superficial) ring medially
• Boundaries of external oblique = skin edges

o Separation of superior and inferior external oblique flaps from internal oblique and cord
• Superior flap:
Up to Conjoint tendon (ilioinguinal and iliohypogastric nerves}

• Inferior flap:
Down to Inguinal ligament (inguinal ligament and iliopubic tract)

o Both flaps should be dissected from surrounding tissues anteriorly and posteriorly

3) Delivery of Spermatic cord

o Mobilize the cord with sharp dissection under vision separating it from posterior wall
o Blunt dissection by index finger at pubic tubercle for 2 cm (risk of injury to structures}

o Penrose drain used to hold medial to external ring along with ilioinguinal nerve,
genitofemoral nerve, and spermatic vessels

o Blue line: External spermatic vein

• Landmark for preservation genitofemoral nerve
4) Division of Cremaster muscle:
• Should be done routinely for examination of indirect hernia

• Divide the muscle longitudinally along the anterior surface

• If division done transverse or excision
➔ Low-lying testes and dysejaculation

• The creamster can be left open or closed by interrupted suture

• Resection of creamster is essential part of shouldice repair to prevent recurrence
of indirect inguinal hernia

5) Management of hernia sac

o Indirect:
• Identify peritoneal sac and separation from spermatic vessels and vas deferens
• Small sac:
Isolate it and inverted without open it or suture ligation {to prevent post-op pain)

• Large sac:
Transected at the ring with suture-ligation by 2-0 silk of the proximal part without
excessive dissection of the sac from the cord (to prevent ischemic orchitis)
This method associated more with post-operative pain

Distal sac left in place with incision of anterior wall (or excision} to prevent
hydrocele (Excision have lowest recurrence than division or invagination)

• Wide deep ring narrowed by re-enforce with stitches, or mesh plug

o Direct: High ligation or reduction of the sac into retroperitoneal space

• No Sac {only bulge):
Plication of posterior wall by taking the posterior wall to posterior wall (not inguinal
ligament} to overlap the hernia

• Normal neck:
Sac pushed behind fascia transversalis without open it

Defect closed by interrupted suture to maintain reduction of the sac, but have to
rule for strength

• Narrow neck:
Sac isolated and cleared, then excise and transfix the defect by absorbable suture

o No Content:
• If extend beyond pubic tubercle ➔ Transect the sac, leave distal sac in situ
• If not extend beyond pubic tubercle ➔ Transfix with absorbable suture
 o Sliding hernia: (sigmoid, cecum, appendix, bladder)
• Don't remove appendix or appendices epiplocae
• Organ wall forms part of the sac, so no attempt to separate organ from sac!
• Defect closed by purse-string pushed behind fascia transversalis

6) Reconstruction:
o Repair of inguinal floor (Described below in details)

o Parietalization of the cord

• By dissect the cord to achieve sufficient length to prevent split of the mesh (used
mainly in Stoppa repair)

o Relaxing incision
• Through anterior rectus sheath (vertical incision)

7) Closure:
o In laparotomy: (as layer-by-layer closure)
• Peritoneum not always closed, but if closed (continuous)
• Internal oblique closed along transversalis (interrupted)
• External oblique closed (continuous)

o In hernia:
• External oblique closed (continuous)
o Closure is done by taking the edge (and only the edge) of the aponeurosis

o Reconstruct the superficial ring to be loose enough to prevent strangulation of the cord

Round ligament separated and retracted, ca·n be divided and excised and internal ring
obliterated during repair in female

Pulling the testes downwards

Repair of inguinal floor:
■ Lichtenstein repair:
o Tension-free overlay mesh repair of posterior wall without incising transversalis fascia
o 15 x 7.5 mesh placed with first stitch just medial to pubic tubercle
o Sutured along inguinal ligament, till 1 cm lateral to internal ring
o Sutured superior and medial to internal oblique and rectus sheath
o Creation of shatter valve by slit the mesh into two tails, to prevent recurrence of indirect
hernia
o Secure prosthesis

■ Bassini repair:
1) Divide the cremasteric and posterio:r wall of
inguinal canal

2) Opening the transversalis fascia

From deep ring to pubic tubercle

3) 3 Layers ➔ 1 Layer by imbrication

• Internal oblique
• Transversalis abdominis
• Transversus abdominis

To the Inguinal ligament

Tanner slide: vertical release of anterior rectus sheath to reduce the tension
Because external oblique aponeurosis fuse to internal oblique aponeurosis very medially, at lower
abdomen

■ McVay (Cooper's) repair:

o Can be used for inguinal or femoral hernia repair
o Used for large direct hernia and abse:nce of caudal margin of fascia transversalis

3 Layers ➔ 1 Layer by imbrication

• Internal oblique
• Transversalis abdominis
• Transversus abdominis

To the
Medial to femoral canal: Cooper's ligament (pectineal ligament)
Transitional stitch
Lateral to femoral canal: iliopubic tract and inguinal ligament

o Relaxing incision is needed, which made along anterior rectus sheath vertically from
pubic tubercle for 2 - 4 cm (Risk of postoperative pain and ventral hernia)
■ Shouldice repair (Lowest recurrence rate in tension repairs}
4 /aver-overlapping technique after incising the transversalis fascia:
At pubic tubercle
o Medial -+ Lateral
1) lliopubic tract + Posterior aspect of Superior flap of the transversalis
(Transversalis fascia, Internal oblique and Transverus abdominis)

At i nternal ring
o Lateral -+ Medial (pubic tubercle)
2) Superior flap+ Inguinal ligament

3) Internal oblique, transversus abdominis -+ External oblique aponeurosis

4) Repeat 3rd step from medial to lateral

■ Maloney Darn Repair

o After placation of transversalis fascia
o Continuous "Partial approximating" nylon suture
between conioined tendon and inguinal ligament
o By starting laterally, just medial to internal ring
o The 2nd layer is darn "Plicated"

■ Anatomical Repair
o Used for small ventral hernia, including umbilical, Paraumbilical and incisional hernia
o After skin incision and redundant sac excised, the hernia sac open and content reduced
o Repair of the defect by
• Simple interrupted non-absorbable suture
To be tied at the end as tying while keeping tension on both holding sutures
beside it
• Simple continuous non-absorbable suture
 ■ Mayo repair: (More tension)
o For Umbilical and Paraumbilical hernia of defect< 3 cm
• For small defects that can't closed by figure-of-8

o Flaps of fascia are overlapped with 3 cm overlap by

Non-absorbable suture
o Upper flap taken 2 - 3 cm out the margin
o Lower flap taken 1 - 2 cm out the margin
o Second layer of stitches to suture both edges of the flaps
With 1 cm margin
o ± Relaxing incision which placed 5 cm lateral to the defect

2 1

■ Marcy repair:
o Used in nyhus type 1, for indirect hernia
o High ligation of sac, and narrowing of internal ring
o Posterior wall augmented by single continuous
suture fixation of IOA and TM to inguinal ligament

OPEN POSTERIOR REPAIR:

■ lliopubic tract repair
■ Nyhus repair
MESH
■ Mesh is used to allow for tension-free hernia repair
■ Sizes:
o Current recommended size: 7.5 x 15 cm (12 x 15 cm for laparoscopic mesh}
o Size of mesh should be 8 cm + size of defect (if less than 4 cm)
o Size of mesh should be 12 cm + size of defect (if more than 4 cm)
o Should overlap at least 2 cm of fascia {due to 30-50% shrinkage of the mesh)

■ Indicated for almost all the hernia unless contraindicated

o Previously was recommended for ventral hernia if defect 2: 3 cm
(associated with 43% recurrence, and 24% only if mesh is used)
o For umbilical hernia, mesh is used if defect > 2 cm

■ Planes for mesh:

o On lay: Above anterior rectus sheath
o Inlay: Bridging the gap, interposition between layers of rectus sheaths
• Alternative to inlay either anterior or posterior component separation
o Sublay (Retro-rectus): Above posterior rectus sheath (Most recommended plane)
o Pre-peritoneal: above peritoneal layer
o Underlay: intra-peritoneal (2nd most recommended plane)

Overlay

Unde<lay
( 1n1ta,pe�ton,u1 )

Retrorecrus
Poaari« t1huth r.nd P9ritoneum
can be appro:,cim..lt.cl \\nd do$N with sot:t.•

/ Prepenton��
P9riton•um �te,ic,,- tedl;n;
and pefitoneol la-Jer
■ Mesh fixation:
o Anchor the mesh to Pubic tubercle, Cooper ligament, or Inguinal ligament
o No suture should be taken beyond periosteum of pubic tubercle
-+ Osteitis pubic (Perostitis) and postoperative pain
-+ Confirmed by Bone scan, and CT/MRI used to exclude hernia recurrence
-+ Bone resection and curettage (Definitive treatment for intractable pain)
o In open surgery:
• Medially to Transversus abdorminis, and laterally to Inguinal ligament

o In laparoscopic surgery:
• Medially to Cooper's ligament. and laterally to ASIS

o Mesh should be fixed, unfolded, no tension, with folded edges and fixed by 2-0 prolene

■ Characteristic of mesh:

Standard 70 -140 g/ m2
Light weight < 70 g/m2
Weight Q Less pain
Heavy weight> 140 g/m2
Q More shrink and reaction
Tensile strength 82 N/cm (horizontal)
/Maxi 32 N/cm /vertical)
Macroporous> 75 µ
-+ Suitable for contaminated defect
-+ Migration of macrophages
Pore size
Microporous < 10 µ
-+Adherent granulomas (t shrinkage)
-+Less adhesions
-+Remove immediatelv when infected
Monofllament
Q Less infection rate
Filaments
Multlfllaments
Q More infection rate
Integrity
Others Pliability (flexibility)
Transcarencv

■ Patient can lift weight post hernia repair:

o + mesh: 2 - 3 weeks
o - mesh: 6 - 8 weeks
 ■ Ideal mesh: {Not availablel
o Inert, Non-allergic, Non-inflammatory, Non-carcinogenic, Non-infected, Non-degradable
o High tensile strength, Pliable, Sterilizable, Barrier to adhesions, and Cost-effective

■ Alternative to mesh in infected hernia or perforation:

o Primary repair
o Biological mesh
o Rotational flap
o VAC dressing
■ If mesh got infected: IV antibiotics and:
o Mesh removal (Standard of care}
o Excision of the exposed part
o Keep the mesh (if macroporous)

■ Types of mesh:

Svnthetic
Absorbable
Polyglycolic mesh
(Vicryl, Dexon}
- Knitted structure
- Maintain tensile strength
70% of 21 days
POIJ!lactlc acid
Used for maintain strength
far 9 months not for closure
of the defect
Bioloqical
■ Expensive
■ Can be used in infection
■ Associated with allergy
Non-Absorbable ■ Used for reinforcement (bridging)
0 Sublay in ventral hernia
0 lnlav in inauinal hernia
Poly(!ro11ylene mesh Human: (Alloderm}
(prolene, marlex, physiomesh}
Porcine: (Surgisis)
- Wove structure
Source
- Most common type Bovine: (Periguard)
- Macroporous, Monofilament
- Avoid it if near internal viscera
- Hiah shrinkina rate /> 75%)
PTFE Paly-tetra-fluoro-ethylene Dermis: (Alladerm)
(Gare-Tex, Dualmesh)
Pericardium (Periguard}
- Microporaus
- Non-adherent (No adhesions} Submucosal (Surgisis)
Organ
- Medium shrinking rate (40 - 50%)

(Gore-Tex) is double layer mesh

"PTFE - Polypropylene"
Used in contact with internal viscera
Polyester mesh Cross-linked (Periguard)
(Mersilene}
- Wove structure Progression Non (Alloderm, Surgisis}
- Hydrophilic (can get infected)
- Hiah shrinkina rate
NOTES:
■ Complications:
o Hematoma or seroma
• Abdominal binder after hernia can be used to minimize the seroma development
o Has no role to repair or prevent complications of hernia

• Close-suction drain can reduce seroma after open surgery for obese patients

• If seroma developed, don't aspirate unless become symptomatic or wait for 2 - 3

months to ensure scarring of the mesh

o Hernia recurrence
• Most common cause of recurrent ventral hernia repair: Separation of the mesh
• Most common location of recurrent hernia (most common site of mesh
separation}: Medial
• Lichtenstein repair associated with lowest recurrence in open approach
• Use of mesh is associated with 50% to 75% reduction in the risk of recurrence
• Recurrence after open anterior approach -+ Do laparoscopy or open posterior
• Recurrence after laparoscopic approach -+ Do open anterior approach
• Risk factors:
o Medical issues:
• Malnutrition, immunosuppression, diabetes, steroid, obesity, and
smoking

o Technical causes:
• Improper mesh size, tissue ischemia, infection, and tension
• Incorrect placement of the mesh
• (Sublay mesh "Retro-muscular" is the best, and lowest recurrence")
• Inlay mesh is not recommended
• Inadequate overlap of mesh in the inferomedial side of inguinal
canal near the pubic tubercle, where the medial recurrence
classically occurs after open hernia repair.
• Resection of creamster is essential part of shouldice repair to
prevent recurrence of indirect inguinal hernia

• Management: Watchful waiting unless symptomatic or complicated

o Urinary retention (Most common early complication following hernia repair}

• Most common cause: General anesthesia
• Treatment·
o Insertion Foley's catheter
o Overnight admission and trial of normal voiding before discharge
o If failed, discharge the pati'ent with Foley's catheter for about 1 week
o lsehemie orehitis
• Injury (thrombosis) of spermatic cord veins (Pampiniform plexus) "most common"
o Due to excessive dissection of the cord distally

• Injury to the testicular artery also can causes Testicular atrophy

• Treatment:
o Reassurance, NSAIDs
o Intra-operatively:
• Proximal ligation of the sac
• Avoid distal excessive, dissection of the cord

o Testicular pain
• Due to compression of ilioinguinal nerve

o Femoral vein
• Most common vascular injury
• Located laterally in femoral hernia repair

o Nerve entrapment
• Usually because of stapling, tacking the nerve
• Lateral femoral cutaneous nerve most common during laparoscopic repair
• llioinguinal nerve is the most common during open repair

• Characteristic of pain:
o Acute Neuropathic pain
o At dermatome distribution

• Treatment:
o Immediately post-operative:
• Immediate return the patient for re-exploration and removal of offending
tacks (Standard of Caire)

o During follow-up:
• Observation, bed rest, ice packs
• NSAIDs
• Local nerve block injection or local steroid injection
• Laparoscopic exploration, Triple neurectomy, and removal of meshoma
• Selective neurectomy or neurolysis, mesh removal and fixation
material, or revision of the repair are options for treatment
 o Nerve injury

Nerves iniurv
More in 012en inguinal hernia re12air
Most commonly injured during hernia repair
(Could be injured during appendectomy)
� Lead to develop hernia postoperative (Most common cause)

Location:
llioinguinal nerve - Below external oblique muscle, anterior and medial to the cord
IL1 fibers) - Pass through superficial external ring only (Common site of injury)

Presentation of injury:
- Numbness of base of penis & medial inner thigh (Superiomedial)
- Loss of Cremasteric reflex
Most commonly injured during appendectomy
(Could be injured durin!'.I hernia repair)
� Lead to develop hernia postoperative
lllohypogastric nerve
Location: Below external oblique muscle

Presentation of injury:
Same as ilioinauinal nerve + Suoraoubic numbness
More in La12arosco12ic inguinal hernia re12air
Most common nerve Injury by tacking the mesh
Lateral femoral cutaneous nerve Lateral thigh numbness
Usually injured with laparoscopic hernia repair, by
Genitofemoral nerve ■ Clips beUow and lateral to iliopubic tract
O{_entral rami of L 1, L21 ■ Clips lateral to cord
Along Psoas muscle Genital branch (Open} ➔ Cremaster, anterior and lateral scrotum
Femoral branch (Laoaroscooic) ➔ Uooer anterior and lateral thioh
Intermediate cutaneous of anterior femoral nerve
■ 22% of patients have undiagnosed contralat.eral hernia

■ Cord lipomas: should be removed

■ Open preferred over laparoscopic repair in case of:

o Pelvic radiation
o Preperitoneal surgery {radical prostatectomy, kidney transplant)
o Primary inguinal hernia repair {Equivalent to laparoscopy in some sources)
o Recurrent hernia after laparoscopic repair
o Non-tolerate of GA, or pneumoperitoneum {Cardiopulmonary disease}
o Previous lower abdominal surgery or pelvic lymph nodes dissection
o Systemic anticoagulants

■ Laparoscopic hernia repair associated with:

o Fewer surgical site infections (Most important advantage)
o Fewer postoperative seroma
o Less recurrence rate (or similar rate to open by different studies}
o Less postoperative pain
o Less postoperative ileus
o Longer operative time
o Higher cost despite shorter hospital stay
o Higher enterotomy rate

■ Inguinal block: 60 - 80 ml of local anesthesia is used

o Location of iniection: 1 cm medial and 1 cm inferior to ASIS
{between internal oblique and transversus abdominis)
• 20ml injected vertically to block iliohypogastric and ilioinguinal nerves

o lntradermal: 2 cm above and medial to ASIS

• 20ml injected as weal by spinal needle of the line of incision

o Subdermal and subfascial of 10 ml inifiltration can be used

o 5 ml injected into pubic tubercle and origin of rectus muscle

o 20 ml injected along direction of spermatic cord beginning by deep ring

■ Cirrhosis and Ascites:
o Repair of umbilical hernia associated with ascites have higher risk for complications
• Groin hernia not markedly influence by ascites

o Indications for emergency repair: (With no mesh)

• Associated with complications:
o Infected, Necrotic, Perforated, Incarcerated, or Strangulated

• Associated with spontaneous rupture (with peritonitis)

• Associated with overlying skin necrosis, and ulceration

o Indications for repair on same admission in Child A/B: (With synthetic mesh)
• Symptomatic
• Associated with leakage (without peritonitis)
• Controlled ascites (well-compensated cirrhosis)
• Uncontrolled (Refractory) ascites "Recur after paracentesis"
o Hernia repair only at time or later after TIPS or Liver transplant

o Management:
• Medical optimization (Furosemide, Spironolactone, Na restriction) is initial step
• Large-volume (4-6 L) Paracentesis
• 25% of albumin is used to replace every 100 ml with 1 g
• Correction of coagulopathy
• Umbilical hernia repair
• Control of the ascites
• TIPS is alternative in uncontrolled ascites used for good liver function to decrease
risk of encephalopathy
• Liver transplant used in Child C patients
ANATOMICAL LANDMARKS IN LAPAROSCOPY
■ Retroinguinal spaces
o The posterior lamina of fascia transversalis divide anterior lamina and peritoneum:
• Vascular space "anterior": Contains inferior epigastric vessels

• Space of Bogros "posterior"

o Between posterior lamina of fascia transversalis & peritoneum
o Mesh is placed here

• Space of Retzius
o Located at most medial aspect of Space of Bogros
o Behind supravesical fossa and medial umbilical ligament
o Contains normal and aberrant obturator arteries and accessory pudenda!
vessels
o This space should be exposed to proper fixation of the mesh

■ 5 Peritoneal folds:
o Median umbilical ligament -+ Urachus
o 2 Medial umbilical ligaments -+ Umbilical artery
• Medial umbilical fossa: Site of direct inguinal hernia and femoral hernia

o 2 Lateral umbilical ligaments -+ Inferior epigastric artery

• Lateral umbilical fossa: Site of indirect inguinal hernia

Ligamentum teres � Umbilical vein (2 Umbilical arteries and only 1 vein)

■ Landmarks:
o Trapezoid of Disaster:
1) Triangle of doom: (medial) Dee Superolateral:
Contains: P Oiopubic tract
■ External iliac vessels Pain
■ Inferior epigastric vessels.
2) Triangle of pain: (lateral)
Contains:
■ Femoral nerve
■ Femoral branch of genito!emoral n.
■ Lateral femoral cutaneous. nerve
3) Corona Mortis:
■ Formed by anastomosis between
o Pubic branch of inferior epigastric artery
o Obturator artery (from internal iliac artery)
o Aberrant obturator artery (20 - 30%)
Found at neck of femoral hernia sac

4) Mercedes-Benz sign:
■ Formed by identification of inferior epigastric vessel, internal ring and vas
deferens
LAPAROSCOPIC HERNIA REPAIR
■ Indications:
o Bilateral or recurrent hernia
o Associated with umbilical hernia, paraumbilical hernia, or Obesity
o Patient/Surgeon preference

■ Mesh should cover at least 5 cm lateral to deep inguinal ring

o Always fix the mesh (Self-anchoring mesh is NOT a standard of care)

■ Types of laparoscopic surgery:

o Trans-Abdominal Preperitoneal Procedure (TAPP)
• Preperitoneal approach with intraperitoneal perspective
• Useful in:
o Bilateral hernias
o Large hernia defects
o Scarring from previous lower abdominal surgery

o Totally extraperitoneal Procedure (TEP)

• Access to preperitoneal space without intraperitoneal infiltration
• Minimizes the risk intra-abdominal organs injury and port site herniation
• Useful in:
o Bilateral inguinal hernias
o Unilateral hernia with preperitoneal scarring for anterior approach

o lntraperitoneal Onlay Mesh Procedure

• Permits posterior approach without preperitoneal dissection
• Useful if anterior approach is unfeasible:
o Recurrent refractory hernias
o Extensive preperitoneal scarring

• Similar to TAPP without inverting sac, mesh is placed and fixed over the defect

• Disadvantages:
o Lateral cutaneous nerve and genitofemoral nerve injuries
o Mesh complications
STEPS OF TAPP

■ The abdominal cavity is accessed using dissecting trocar or open Hasson technique
■ Pneumoperitoneum is instilled to 15 mmHg
■ Two of 5 mm trocars are placed lateral and slightly inferior to the umbilical trocar

■ The patient is placed in the Trendelenburg position

■ Abdominal exploration

■ Peritoneal incision
o Medially: Lateral aspect of medial umbilical ligament, 3 - 4 cm superior to hernia defect
o Laterally: Anterior Superior Iliac Spine (ASIS) or 5 cm posterolateral to internal ring
o The inferior edge of incised peritoneum is retracted, and the preperitoneum is dissected
along space of Bogros to expose the spermatic cord

■ Medial Dissection (For origin of direct hernia sac)

o The aim is to enter space of Retzius
o Dissection begin laterally (lateral to lateral umbilical ligament)
o Starting in Cooper's ligament (not beyond it� Corona mortis) until pubic symphysis
o Gentle traction of peritoneum to separate it from transversalis fascia (pseudosac)
o After reduction of sac, fix it to Cooper's ligament to prevent hematoma or seroma
o Complete dissection of peritoneum until contralateral pubic tubercle

■ Lateral Dissection (For origin of indirect hernia sac) "More difficult"

o Indirect hernia usually protrude anterior and lateral to the cord
o Sac separation should be from upper half of internal ring to prevent injury of the cord
o The sac is grasped and elevated superiorly from the cord and the space below is
developed bluntly to allow for mesh placement
o Lateral dissection should be carried out till iliopsoas muscle

■ Parietalization of spermatic fascia to dissect hernia sac

o By separation of peritoneum from vas and gonadal vessels towards cranial aspect
o Extensive parietalization is important until mid-psoas for placement of mesh

■ Mesh placement and Closure

o The mesh usually 10 x 15 cm to completely cover the myopeclineal orifice
o Secured medially to Cooper's ligament by spiral tacker and secured laterally to ASIS
o Tacks should be placed above and medial to the iliopubic tract to avoid injury to the
lateral cutaneous nerve of the thigh and the femoral branch of the genitofemoral nerve
o The peritoneum should be closed completely to avoid contact between the mesh and
the bowel
o The abdomen is deflated and Closure
STEPS OF TEP
■ Small incision is made inferior to the umbilicus

■ Subcutaneous tissue is dissected to the level of anterior rectus sheath

■ Anterior rectus sheath incised lateral to lin,ea alba and retracted superolaterally

■ Dissecting balloon is advanced through the incision toward the pubic symphysis

■ Under direct visualization with a 30° laparoscope, the balloon is inflated slowly to bluntly
dissect the preperitoneal space

■ The dissecting balloon is replaced with 12 mm balloon trocar

■ Pneumopreperitoneum by insufflation to 15 mmHg

■ Patient is placed in Trendelenburg position

■ 5 mm trocar is placed suprapubically in the midline

■ 5 mm trocar is placed inferior to the insufflation port

■ Similar remaining steps to TAPP

■ Closure with anterior rectus sheath is closed with an interrupted suture

FEMORAL HERNIA
■ Most common in females (Indirect inguinal hernia is the most common hernia overall)
■ Defect in transversalis fascia
■ Highest risk (40%} of incarceration and strangulation
■ Associate with Richter's hernia (non-circumferential incarceration of anti-mesenteric bowel}
■ Location of femoral hernia:
o At anteromedial thigh
o Below the inguinal ligament
o Below and lateral to pubic tubercle

■ Femoral canal/ring boundaries:

o Posterior: Cooper's ligament
o Anterior: Inguinal ligament / iliopubic tract
o Lateral: Femoral vein
o Medial: Lacunar ligament

1) Femoral neck is closed to iliopectinea/ ligament and aberrant obturator artery

• Curves along free border of lacunar ligament
• Might be injured during exposing the cooper's ligament

2) Contains lymph node of Cloquet

■ Layers of femoral sheath:

o Skin, Subcutaneous tissue, Superficial fascia and deep fascia
o Fascia transversalis forming the anterior part of femoral sheath
o Fascia iliacus forming the posterior part of femoral sheath
o Femoral ring: from fossa ovalis
o Contains: (from medial to lateral}
• Femoral canal-Vein-Artery- Nerve
• Femoral nerve located outside the femoral sheath
■ Surgery:
o Should be done in all cases (Asymptomatic and symptomatic}

o Laparoscopic hernia repair

o Open approach:
• Low approach (infra-inguinal): Lookwood repair
o Used in elective cases "Transverse incision"

• Mid approach "preperitoneal" (trans-inguinal): Lotheissen's repair

o Can repair both inguinal and femoral through this approach
o No longer used, because of disruption of the canal (need to be repaired}

• High approach "preperitoneal" (supra-inguinal): McEvedy's repair

o Used in emergency cases "Vertical incision in para-rectus line"

• Cooper's repair (McVay repair):

o Used for inguinal/ femoral hernia repairs
o Approximation of conjoined tendon to cooper's ligament

■ Steps:
o After incision if there is no femoral hernia, external oblique showed be incised to rule out
inguinal hernia
o Reduce the femoral hernia content into femoral canal
o Closure of the canal by non-absorbable suture without constriction of the femoral vein
o Closure

■ Difficulties for reduce femoral hernia:

1) Transverses fascia must be divided first
2) Opening the canal by divide inguinal ligament
3) Dilate the neck
4) Divide lacunar ligament (20% presence of abberant obturator artery)
INCISIONAL HERNIA
■ Most common type of hernia to recur after primary closure
■ Most common cause: Inadequate closure
■ Highest risk to develop incisional hernia: Infection

■ Factors to decrease incisional hernia development:

o Closure of abdominal fascia with continuous non-absorbable
o Interrupted for otherwise
o Sharp cutting
o Tension free

■ Subtypes·
o Port-side hernia
o Extraction site hernia
o Post TRAM flap hernia
o Post-transplant hernia

■ Stages:

Stage I < 10 cm and clean

{Lowest risk of recurrence and small bowel obstruction/
Stage II < 1 O cm and contaminated
10- 20 cm and clean
Stage Ill 2: 10 cm and contaminated
/Hiahest risk of recurrence and small bowel obstruction) 2: 20 cm

■ Management techniques:
o Hernia sac, need to be isolated, opened for reduction of contents, then excised
o Primary repair+ mesh
(Sublay mesh ''Retro-muscular" is the best, and lowest recurrence")
Inlay mesh is not recommended � due to develop ECF and recurrence

o Component separation (lateral release) for large defect

o ± relaxing incision in anterior rectus s!heath to reduce seroma
o Preoperative Progressive Pneumoperitoneum is an option for treatment of giant ventral
hernia, by inflation for couple of weeks
COMPONENT SEPARATION
■ Used for massive, complex incisional hernia if there is contamination or bowel surgery required
■ Provides tensionless closure of large, full thickness anterior abdominal wall defects with
autologous tissue
■ Can restore abdominal wall functionality for defects up to 20 cm at the level of the umbilicus

■ General Techniques:
1) Translation of muscular layer of the abdominal wall to enlarge the tissue surface area
2) Separation of muscle layers to allow maximal individual expansion of each muscle unit
3) Disconnection of muscle unit from its fascial sheath envelope to facilitate expansion
4) Use of abdominal wall musculature to cover intra-abdominal contents
5) Use of bilateral mobilization rather tihan unilateral advancement for equilibrating forces
of the abdominal wall and centralizirng the midline

■ Steps:

1} Skin and SC are dissected free from the

anterior rectus sheath and external oblique A
(EO) aponeurosis -+ Laterally (A}

2} The EOA is incised longitudinally about 2

cm lateral to the rectus abdominis (RA) (B)

3} The EO muscle are separated from

internal oblique (10} muscle (C, D}
-+ laterally to mid-axillary line RA
5 cm upper abdomen
10 cm mid-abdomen
3 cm lower-abdomen

4} The posterior rectus sheath is incised ""'��.:--.u.. D

longitudinally and separated from the RA - ◄H►
◄10
RA muscle to provide medial advancement ◄'I\
of the RA-IO myofascial complex (E)
-+ Provide additional 2-4 cm

::
e
RA ___..
_
+��"E
:= 410
--.....__----•TA
r
PARASTOMAL HERNIA
■ Definition: Hernia through abdominal wall defect "trephine• created during stoma formation
■ Most common late complication of colostomy (40%)
o Occur within 2 years of constriction
■ Subtype of incisional hernia
■ Most sensitive test for detection: CT Scan

■ Risk factors·
o Patient: old age, COPD, weight gain postoperatively, malnutrition, /8D, and malignancy
o Technique: Emergency, Large diameter of the trephine (wide defect> 2 fingerbreadth),
construction outside rectus sheath
• Highest risk: End-colostomy {40%), then loop colostomy
• Lowest risk: Loop ileostomy

■ Types of parastomal hernia /Based on intra-<0perative findings}:

Subcutaneous Most common type

Hernia sac within subcutaneous
Interstitial Highest risk of strangulation
Hernia sac within Javers of abdominal wall
Peristomal Hernia sac circumferential enclosing the stoma
{Prolapse)
lntrastoma Hernia sac between the bowel wall and averted intestinal laver

■ Classifications of parastomal hernia:

Phvsical exam CT findinas

Isolated small PH No sac
Small PH with CIH Bowel formino the colostomy with < 5 cm sac
Isolated larae PH Bowel formina the colostomv with > 5 cm sac
Larae PH with CIH Sac containina omentum
lntestinal looo other than bowel formina stoma
PH: Parastomal Hernia
C/H: Concomitant incisional hernia
■ Management of parastomal hernia:
o Asymptomatic: Conservative
o Symptomatic: Repair
• Absolute indications: Strangulated, or Obstructed
• Relative indications: Incarcerated, Prolapse, Stenosis, Large, Pain, Interfere with
quality of life

■ Management options:
1) Fascia! repair (Historically)
2) Relocation of the stoma
• Used if patient had complications of the stoma (excoriation, stenosis, prolapse)
• Disadvantage: Laparotomy, May not address the hernia, May develop new hernia

3) Prosthetic repair "Open or Laparoscopic" (Most effective)

• Standard of Care

■ Approach:
o Open: May associated with failure rate up to 60%
o Laparoscopic: Preferred option for small parastomal hernia who do not require
relocation with no concurrent ventral hernia

■ Jechnjaues <Open or Laparoscopjc)·

o Sugar-baker technique:
• Repair with intra-peritoneal mesh over aperture with 3 - 5 cm overlap
• Laparoscopic Sugar-baker is the most effective and lowest recurrence rate

o Keyhole technique:
• Slit placed within mesh and stoma passes through the slit before traversing
abdominal wall

o Sandwich technique:
• Combination between Sugar-baker and Keyhole techniques to reinforce the
complete lateral abdominal wall

■ Options for mesh site:

o Sublay: Within retrorectus space {Lowest recurrence rate)
o Onlay: Above the anterior rectus fascia (Higher rate of mesh infection and excision)
o Inlay
o Underlay (Intra-peritoneal inlay)

■ Operative consideration:
o Uncoated monofilament polyprolene mesh is the most superior type of mesh
o Stoma site, fascia! fixation or closure of lateral space have no effect on parastomal
hernia
INTERNAL HERNIA
■ Most common cause of obstruction post LRYGB
■ Types:
o Para-duodenal
c:> Most common type: Left para-duodenal hernia
• Lateral boundary of paraduodenal hernia: Inferior mesenteric vein
o Para-cecal
o Para-mesenteric
o Foramen of winslow
o Post Roux-en-Y
C

■ Sites of internal hernia:

A) Petersen's: Most common site of internal hernia post retrocolic LRYGB
c:> Petersen's space: between small bowel and transverse mesocolic

B) Jejunojejunostomy: Most common site of internal hernia post antecolic LRYGB

C) Mesocolic of transverse colon

■ CJ Sjgn·
o Whirl sign or Whirlpool sign (Mesenteric Swirl)
c:> Best single predictor sign of internal hernia
c:> Also associated with volvulus
INCARCERATED HERNIA
■ Definition: Hernia that can't be reduced
■ Tapping of hernia contents in the hernia defect (irreducible)
■ Mild tenderness (venous congestion) ± intestinal obstruction
■ Management:
o Suspicious of strangulation/ Failure of reduction: (Preferred way of management)
• Urgent operation with no reduction within 6 - 12 hours of presentation
• Open hernia repair± bowel resection and anastomosis

o No suspicious of strangulation or obstruction: •Exclude femoral hernia"

• Attempt of reduction (if presented < 6 hours} followed by repair 24 - 48 hours
(same admission) to minimize risk of recurrence
o Apply ice or cold compression
o Supine or trendelenburg position (frog leg position in children}
o Sedation and strong analgesia

• Preferred method in pediatric age group

STRANGULATED HERNIA
o Signs and symptoms:
• More common in indirect inguinal hernia
• Tender, warm and red skin, fever, tachycardia, hypotension, and leukocytosis

o OR techniques:
1) Groin incision {laparotomy indicated if slipped bowel and failure of withdrawal)
For doubt hernia (femoral vs. inguinal}:
Pfannenstiel incision 2 cm above pubic ramus, extending laterally down lateral to the
scrotum

For strangulated scrotal hernia

Groin incision for bowel retrieval and hernia repair, laparotomy if failed

2) Incision deepen to reach the sac

3) Open the sac while holding the content

• Evacuate toxic fluid
• Check the neck of the hernia and release the content (dilatation vs. division)
• Check bowel viability:
o Peristalsis, Color & Shines, Competency, Mesenteric vessels

• If in doubt: 02100% and warm, moist packs for 5-10 minutes

• Infiltration of mesentery by 1 % procaine may help overcome vascular spasm
• ± Dilatation of the neck
o If the contents slipped into peritoneum or sac was not opened first:
• Narrow internal ring + Laparotomy
• Wide internal ring:
o Try to pull the bowel without tension
o Balloon-port and laparoscopy
o Standard laparotomy

4) Reduce the content (in bowel viable, or resection anastomosis done)

• In this point, if bowel difficult to .assess: cut the ring and do bowel running
• For direct hernia: division of transversalis fascia laterally or medially
• For indirect hernias: cut the deep ring laterally to avoid injury of vas
• For femoral hernia: cut the lacunar ligament medially or iliopubic tract superiorly
Laterally. the external iliac vessels prevent extensive dissection

5) Excise the sac

6) Repair the defect and closure

OTHER TYPES OF HERNIA
■ Pantaloon hernia: direct and indirect inguinal hernias

■ Sliding hemjas· retroperitoneal organ wall m akes up part of the hernia sac (hernia sac formed
secondary)
o Ovaries or fallopian tubes most common in females
o Cecum or sigmoid most common in male

■ Epigastric hernia
o Occurs at site of nerves and vessels perforating linea alba, usually multiple
o Need to be open in vertical incision, to rule out other epigastric hernias
o Fatty hernia (usually extraperitoneal fat)
o More common in male

■ Spigelian hernia
o Defect of transverse abdominis along linea semicircularis
o Located between:
• Lateral border of rectus sheath
• Linea semicircularis ''Douglas' line" (Inferior to arcuate line)
o Presented as obstruction + lump
o Surgical repair should be done for all cases

Rectus Sheath

Arcuate Line

■ Pediatric hernia:
o Umbilical hernia
• Unlike adult, does not associated with risk of incarceration
• Repair should be delayed until age of 5 years or if associated with complications

o Inguinal hernia
• Presence of inguinal hernia is an indication of repair
• Herniorrhaphy: High ligation only to close the patent processus vaginalis without
reconstruction of inguinal 0oor (always indirect)
■ Obturator hernia (anterior pelvis)
o Presented as elderly multiparous female with intermittent obstruction without a lump
• Some cases presented with tender mass at upper inner thigh or anterolaterally on
digital rectal exam

o Herniation through obturator foramen

o Howshlp Romberg sign:

• Inner thigh pain with internal rotation due to pressure on obturator nerve
• Relieved with tight flexion
• Exacerbated by hip extension, adduction or external rotation

o Surgical repair should be done for all cases

■ Sciatic hernia (posterior pelvis)

o Herniation through the greater sciatic foramen; high rate of strangulation

■ Lumbar hernia
o Superior (Geynfelttl "More common·
• Superior: 12th rib
• Medial: Sacrospinalis (Quadratus lumborum)
• Lateral: Internal oblique

o Inferior /Petit hernia)

• Inferior: Ileum crest
• Medial: Latissimus dorsi
• Lateral: External oblique

■ Perinea! hernia
o Risk factors: APR, Multiparous, sacral excision

■ Litter's hernia:
o Mickie's diverticulum

■ Maydl's hernia:
o 2 loops of the bowel ( hernia in W)

■ Amyand hernia:
o Appendix

■ Sports hernia:
o Tear or weakness of posterior inguinal canal components (dilated superficial ring)
RECTUS SHEATH
■ Anterior: complete
■ Posterior: absent below semicircularis = Arcuate line (3 - 4 cm below umbilicus)
o Moves anterior below this line
1) Above it: Anterior lamella of internal oblique and external oblique are in front of rectus
2) Below it: Internal and external oblique and transversus abdominis in front of rectus

■ Pivarjcat;oo of rectj·
o Intact transversalis fascia
o Management: Physiotherapy, weight reduction
o Operative intervention: Abdominoplasty

■ Rectus Sheath Hematomas

o Due to inferior epigastric vessel injury
o Positive Carnett's sign -+ Abdominal pain not changes or increased during flexion
o Positive Fothergill's sign -+ Mass doesn't cross midline and doesn't change with flexion
o More likely to cause severe bleeding, if located below umbilicus
o Types:
• Type I; Small and confined within the rectus muscle

• Type II: Confined within rectus but dissect along transversalis or cross midline

• Type Ill: Below arcuate line with retroperitoneal extension

± hemoperitoneum, ± blood within space of Retzius

o Management:
• Conservative management, Correction of coagulopathy ± PRBCs
o Indications for bridging warfarin with heparin:
• Recent (within 30 days) myocardial infarction
• Mechanical heart valves
• Stroke
• Pulmonary embolism

o Correc tion of coagulop athy should be considered for all patients except :
• Recent mechanical heart valve
• Recent saddle embolus

• Angioembolization:
o For hemodynamically unstable, free bleeding, enlarged hematoma or clinical
deterioration

• Surgical intervention:
o Failure of drainage (in infected hematoma), Failure of embolization, or
Abdominal compartment syndrome
DESMOID TUMORS (Fibrosareoma)
■ More in female, benign but locally invasive; t recurrences
■ Associated with Gardner's syndrome
■ Treated with excision

RETROPERITONEAL FIBROSIS
■ Associated with using of methysergide (for migraine), Ceroid antibodies
■ IVP most sensitive test (constricted ureters)
■ Trapped ureters and lymphatic obstruction � Ureteric obstruction and renal failure
■ Treatment:
o High-dose of Steroid
o Surgery indicated in renal compromised

RETROPERITONEAL TUMORS
■ Mostly malignant
■ Most common malignant retroperitoneal tumor: Lymphoma followed by Liposarcoma
o Lymphoma usually associated with multiple adenopathy and constitutional symptoms
o Liposarcomas and leiomyosarcomas arising from vascular structures
o Large size tumor can displace and encase viscera

■ Most common sarcoma of retroperitoneum: Liposarcoma

■ Most common site for liposarcoma: Extremities (Thigh)
■ Most common metastases: Lung
■ Most common symptom of retroperitoneal sarcomas: Abdominal mass (not ureteric
obstruction)
■ Most common site of recurrent sarcoma: Peritoneal or Retroperitoneal space
■ The most commonly resected organ during liposarcoma resection: lpsilateral kidney

MESENTERIC TUMORS
■ Most common malignant: Liposarcoma
■ Most common site of malignant tumors: Close to the root of the mesentery

OMENTAL TUMORS
■ Mostly metastati c
■ No biopsy

CHYLOUS ASCITES
■ Associated with lymphoma
■ Cisterna chyli, anterior L 1-L2
■ Mortality rate > 40%
■ Paracentesis:
o t Triglycerides, Protein, and Lymphocytes
SCLEROSING MESENTERITIS (mesenteric lipodystrophy or mesenteric panniculitis)
■ Etiology:
o Autoimmune, abdominal surgery, para-neoplastic syndrome, ischemia and infection

■ Presentation: abdominal pain, diarrhea, and weight loss

o Abdominal mass in LUQ or epigastric areas

■ Investigation
o CT: soft tissue mass in the small bowel mesentery
• Specific signs are: "fat ring sign• and •tumor pseudo-capsule"

■ Management:
o Asymptomatic: Conservative

o Symptomatic
• Without bowel obstruction:
Tamoxifen 10 mg BID (Alternative: azathioprine)
+ Prednisone 40 mg daily for 3 months

• With bowel obstruction: Surgery

Pediatric Surgery
Reviewed by:

Dr. Hussah M. AI-Buainain

PEDIATRIC SURGERY
ANATOMY AND PHYSIOLOGY
■ Suggested Age Grouping:
o Neonate/Newborn: 0 - 28 or 30 days
• Premature < 38 gestational age
• Term > 38 gestational age
Low birth weight < 2,500 g

o Infant/Baby: 1 - 12 months
o Toddler: 1 - 2 or 3 years
o Child: > 5 years

■ Embryological origin of the gut system:

o Foregut + Esophagus, Stomach, until DJ junction, Liver, Pancreas, and Gallbladder

o Midgut + From DJ junction until proximal 213 transverse colon

o Hindgut + Distal 113 of transverse colon down to anal canal

Midgut rotates 270 degrees counterclockwise normally

■ Immunity at birth:
o lgA from mother's milk
o lgG crosses the placenta

■ T rauma bolus: 20 ml/kg X 2, then give blood 10 ml/kg

o Target urine output > 2 - 4 ml/kg/hour

■ f alkaline phosphatase in children compared with adults + bone growth

CONGENITAL CYSTIC DISEASE OF THE LUNG
■ Pulmonary sequestration
o Lung tissue has anomalous systemic arterial supply (thoracic aorta or abdominal aorta
through inferior pulmonary ligament)
o Types:
• Extra-lobar: venous drainage via systemic circulation (azygous system)
• Intra-lobar: venous drainage via pulmonary circulation

Both are more common on left side

o Do not communicate with tracheobronchial tree

o Most commonly presents with infection
o Treatment: Lobectomy

■ Congenital lobar overinflation (emphysema)

o Cartilage fails to develop in bronchus, leading to air trapping with expiration
o Vascular supply and other lobes are normal (except compressed by hyperinflated lobe)
o LUL most commonly affected
o Treatment: Lobectomy

■ Bronchiogenic cyst
o Most common cysts of the mediastinum; usually posterior to the carina
o Extra-pulmonary cysts formed from bronchial tissue and cartilage wall
o Usually present with a mediastinal mass filled with milky liquid
o Can compress adjacent structures or become infected
o Malignant potential
o Treatment: Resection

MEDIASTINAL MASSES IN CHILDREN

■ Most common medjastinal tumor in children:
o Neurogenic tumors (neurofibroma, neuroganglioma, neuroblastoma)
o Usually located posteriorly

■ Presenting symptoms:
o Respiratory symptoms, and dysphagi.a

■ Anterior: T cell lymphoma, teratoma, and other germ cell tumors, thyroid cancer
■ Middle: T cell lymphoma, teratoma, cyst (cardiogenic or bronchiogenic)
■ Posterior: T cell lymphoma, neuroblastoma, neurogenic tumor
Thymoma is rare in children

LYMPHADENOPATHY
■ Cystic hyqroma (lymphangioma):
o Usually found in lateral cervical regions in neck
o Due to sequestration or obstruction of developing lymph vessels
+ Multiloculated cystic mass with overlying vesicles
o Most common sites: Neck, axilla, groin, and mediastinum
o Usually lateral to the sternocleidomastoid (SCM) muscle
o Treatment: Surgical excision and image.guided sclerotherapy
DIAPHRAGMATIC HERNIAS AND CHEST WALL
■ Overall survival 50%
■ Prenatal prediction of survival: by using Lung-to-Head ratio
■ Treatment: High-frequency ventilation; inhaled nitric oxide; may need ECMO
o Need to reduce bowel and repair defect± mesh (abdominal approach)
Bochdalek Foramen of Morgagni
(Most common)
Site Posteior, Lateral Anterior, Medial
More on Left side More on Right side

Presentation Resoiratorv distress Mostlv asvmotomatic

Sac No sac Well-formed sac
Content Omentum or Transverse colon
Associated anomalies Rare Down or Turner syndrome
(Pulmonary hypoplasia) Malrotation
Genitourinary malformations
Cardiac or neural tube defects

BRANCHIAL CLEFT CYST

■ Consist of 6 arches, 5 clefts
■ Treatment for all branchial cysts: Complete resection

Tvne Location Co ,nnected with Note

1" Cleft Anole of mandible External auditorv canal Associated with facial nerve
2nd Cleft Anterior border of SCM Tonsillar oillar Most common tvne
3•• Cleft Medial or throuoh SCM Piriform sinus
INFANTILE HYPERTROPHIC PYLORIC STENOS IS (IHPS)
■ Characterized by hypertrophy of the circular muscle, causing pyloric narrowing and elongation
of pyloric channel

■ Produce partial or complete gastric outlet obstruction

■ The cause of hypertrophic circular muscle of the pylorus in IHPS is thought to result from the
failure to relax the smooth muscle sphincter.

■ Incidence 1 :250 live births, most common in Caucasian populations

■ Male-to-female ratio 4:1

■ Etiology:
o Unknown

o The classic studies of Carter and Evans defined the disease as a paradigm for
multifactorial, sex-modified threshold model of inheritance

o Genetic predisposition as it is associated with inherited syndromes (e.g., Smith-Lemli-

Opitz and Cornelia de Lange syndromes)

o Non syndromic IHPS shows familial aggregation

o Developmental abnormality in which the pyloric muscle hypertrophies started after birth.

o Environmental factors (the changing rates of IHPS, which have been reported in several
areas and countries)

o Other hypothesis:
• A decrease in immunoreactivities of the neurotransmitter such as substance-P,
somatostatin
• Epidermal growth factors (EGF), platelet-derived growth factor subtype BB
(PDGF-BB), Platelet derived endothelial cell growth factor (PDEGF). and insulin­
like growth factor-1
• Altered expression of neuronal nitric oxide synthesis
■ Clinical presentation
o History:
• Typically a full-term baby, 2-8 weeks old
• Rarely reported in premature infants
• Non-bilious projectile vomiting soon after feeds
• Jaundice associated with indirect hyperbilirubimemia (2-5%)
• Associated anomalies (6-20%)
• Rarely: failure to thrive, constipation, seizures

o Physical examination:
• Pyloric "tumor" in right upper quadrant or epigastric area ("olive• like mass)
Method of palpation: need quite environment, identify the edge of the with the
fingertip, apply gentle pressure deep to the liver and progress caudally to reveal
an enlarged pylorus
• An enlarged pylorus located just above the umbilicus at the lateral border of the
rectal muscle below the liver edge

• Visible peristalsis (after test feed}

• Dehydration (late presentation)

■ Investigations:
o Metabolic disturbances:
• Hypochloremic hypokalemic metabolic alkalosis
• Paradoxical aciduria due to renal conservation of Na+ leading to loss of H+
• CO2 increase due to the respiratory compensation

o Diagnostic Imaging
• Ultrasound:
• Criteria for diagnosis:
o Pyloric muscle thickness 2' 4 mm
o Pyloric channel length 2' 16 mm

• Barium study:
• Narrowed elongated pyloric canal giving a "string• or "double track" sign
• Caused by compressed invaginated folds of mucosa
■ Management:
o Operation never an emergency

o Resuscitation:
• Airway, breathing, circulation (ABC)
• Nasogastric tube, gastric washouts (0.9% saline) "controversial"
• Monitor urine output, blood gases and electrolytes
• NS until dehydration resolved, then:
• 05 ½ NS + 20 KCI: in clhildren (with total fluid intake: 120-150 ml/kg/day)
• 010 NS+ 10 KCI: in adults
• Try to avoid K-containing, non-salt containing, and non-glucose containing fluids

o Definitive management:
• Ramstedt's pyloromyotomy was first described in 1911
• Pyloromyotomy (RUQ incision; proximal extent should be the circular muscles
of stomach)

• Complications of surgery:
o Persistent vomiting
o Mucosa! perforation (1%-4%)
o Incomplete myotomy: wait 10 days before reoperation
o Wound infection and dehiscence
o lncisional hernia (rare)
TRACHEOESOPHAGEAL FISTULAS (TEF)
■ 5 Types, most common type: Type C
o Type A: Pure esophageal atresia "Second most common"
o Type C: Proximal esophageal atresia (blind pouch} and distal TE fistula

■ Clinical presentation:
o Excessive drooling, spits up feeds
o Respiratory symptoms with feeding (Coughing and Chocking)
o Cannot introduce NGT in stomach
o VACTERL syndrome:
• Vertebral, Anorectal (imperforate anus}, Cardiac, TE fistula, radius/Renal, and
Limb anomalies

■ Management:
o Chromosomal analysis
o Resuscitate and prepare patients for definitive management:
o Delay operative in premature or sick infants
o Gastrostomy initially, used for pure atresia without fistula
o Right thoracotomy + OR Bronchoscopy:
• Division of Azygous vein
• Transect tracheoesophageal fistula
• Primary esophagoesophagostomy ± Primary repair of trachea
• Most common postoperative complication: GERO

IMPERFORATE ANUS
■ Embryological theory: Failure of descent of the urorectal septum
■ More common in males
■ Most common defect:
o Male: rectouretheral defect
o Female: rectovestibular defect

■ Classification:
o Depends on level of rectal pouch toward levator ani muscle

o High level:
• Male: End as fistula to membranous urethra
• Female: End as persistent cloaca
• Management: Colostomy followed by pull-through procedure at 2 months
Pull-through procedure· Posterior sagittal anorectoplasty

Patient with high level imperforated anus have high risk of incontinence

o Low level:
• Male I Female: End as fistula to perineum
• Management: perinea! operation with NO colostomy

■ Associated with VACTERL anomalies in 60%

■ Lateral abdominal x-ray inverted position with radiopaque marker of the perineum
'* Allows distance between most distal extent of air in rectum and perinea! surface to be
measured
INTUSSUSCEPTION
■ lnvagination of one segment "lntussuceptum" of the gastrointestinal tract into the lumen of an
adjoining segment "lntussuscipien"

■ Age of presentation: 6 months - 2 years (Consider pathological disease if> 2 years)

■ Most common site:

o ileocolic "Terminal ileum and extends distally into colon"

■ Pathophysiology:
o Inhomogeneity in a bowel segment
(Undergoes sudden change in diameter, flaccidity, or induration)

o Mechanical linkage (Intramural or extramural)

Unbalanced forces happen when normal peristaltic wave encounters a focal abnormality
in the bowel wall "lead point" which known as secondary intussusception

o Peristaltic activity
The intussusceptum telescopes into distal bowel by peristaltic activity, as the mesentery
of proximal bowel drawn into distal bowel, compressed and resulting in venous
obstruction and bowel wall edema, arterial insufficiency can happen later if not reduced,
leading to ischemia and necrosis

■ Etiology:
o Primary intussusception (Usually after upper respiratory tract infections or enteritis)
• Hypertrophy of Payer's patches (Viral infection)
• Hyperplasia of lymphoid tissue

o Secondary intussusception (due to leading point)

• Meckel's diverticulum ''Most common lead point''
• Polyp, lipoma, or cecal adenocarcinoma
• Ectopic pancreas or gastric mucosa, hemartomas
• Enteric duplication cyst, Lymphoma

■ Clinical presentation:
o Long history of intermittent obstruction
o Bloody mucus diarrhea "Currant jelly ·stools" (from vascular congestion)
o On examination:
• 0ance's sign (Elongated Sausage mass in RUQ, and absence in RLQ)

■ Associated diseases:
o Melanoma
o Cystic fibrosis, purpura
o Celiac disease
o CDF infection
■ i
Investigat ons:
o Abdominal X-Ray:
• Non-specific
• Can diagnose intussusception in 60%
• Coiled spring sign associated also with small bowel intramural hematoma

o Diagnostic enema (Diagnostic tool for children only}

• By air or contrast enema

o U/S:
• Best initial study
• Signs: Target or Pseudo-kidney signs

o CT Scan (Diagnostic tool for adult)

• Mainly used for adult patients
• Signs: Target sign, Crescent (meniscus) sign, Sausage sign, Claw sign

IJITUSSUSCIPl!N

APEX

INTIJSSUSCl!PTIJM

-�
INTIJSSUSQPIEN
■ Management of intussusception:
o IV fluids and antibiotics

o Stable/ No peritonitis/ Child:

• Air enema only "Success rate: 60 - 90%"

• Max pressure with air-contrast enema: 120 mm Hg
• Max column height with barium enema: 1 meter {3 feet}

• Failure or suspicious of complete reduction: Repeat air enema / Barium enema

o Unstable/ Peritonitis/ Failure of reduction I Adult:

• Resection and anastomosis
• Preferred method for adult group (Due to malignant lead point)
• Should be done if there is necrotic bowel in children

• Reduction without resection

• Preferred method for children
• Reduction is done by pushing not pulling {squeezing distal to proximal)
• For patients with retrograde intussusception (post gastric bypass}

■ Recurrence rate:
o 5 - 10% in radiological or surgical management
o Post-operative recurrence: Air enema
PYLORIC ATRESIA
■ Rare disease (1 :100,000 live births)
■ Presents with symptoms of gastric outlet obstruction
■ May be associated with epidermolysis bullosa and other gastrointestinal anomalies, such as
duplications
■ May occur as a web, a cord or gap between the antrum of the stomach and the first part of the
duodenum
■ Diagnosed with a "single bubble" on the abdominal radiograph
■ The diagnosis may be confirmed with a contrast study

■ Management:
o Resuscitation
o Correct electrolyte abnormalities
o Repair with a Billroth type I (gastroduodenostomy) anastomosis
o Morbidity & mortality are usually related to the associated anomalies

INTESTINAL ATRESIAS
■ Develop as a result of intrauterine mesenteric vascular accidents
c::> Segmental loss of the intestinal lumen

■ Symptoms:
o Bilious vomiting, distention, failure to pass meconium

■ Investigation:
o Barium enema

■ Treatment:
o Resection
DUODENAL ATRESIA
■ Most common cause of duodenal obstruction in newborns (< 1 week)
■ Associated with polyhydramnios, and Down's syndrome in 30%

■ Clinical presentation:
o Bilious vomiting
o Feeding intolerance

■ Investigation·
o Prenatal U/S
o Abdominal x-ray: Double-bubble sign
o Upper GI series: in partial obstruction

■ Management:
o Resuscitation, Orogastric tube, Duodenoduodenostomy or duodenojejunostomy

MALROTATION
■ Due to failure of normal counterclockwise rotation (270 degrees) around SMA at 10 -12 GW
o Volvulus is clockwise rotation
o Creation of Ladd's band (extend from cecum to lateral abdominal wall crossing the
duodenum -+ Duodenal obstruction)

■ Clinical presentation:
o Bilious vomiting and failure to thrive
o Abdominal tenderness

■ Diagnostic test:
o Upper GI endoscopy: Malrotation and corkscrew appearance of duodenum
o CT Scan: SMA located to the right (instead from to the left) of SMV

■ Treatment:
o Ladd's procedure: resect Ladd's bands, counterclockwise rotation
o Appendectomy
• Because after counterclockwise rotation the Cecum will be on left side
Which may delay the diagnosis of appendicitis
NECROTIZING ENTEROCOLITIS (NEC)
■ Classically presents with bloody stools after 1 st feeding in premature neonate
■ Risk factors:
o Prematurity
o Hypoxia
o Sepsis

■ Symptoms:
o Lethargy
o Abdominal distention
o Vomiting
o Blood per rectum

■ Abdominal x-ray:
o Pneumatosis intestinalis
o Portal vein air
o Free air

■ Joitial Treatment·
o Resuscitation, NPO, antibiotics, TPN, and orogastric tube

■ Indications for operation:

o Perforation (Pneumoperitoneum}
o Peritonitis
o Clinical deterioration despite medical management
HIRSCHSPRUNG'S DISEASE:
■ Congenital, Acquired (most common due to trypanosoma cruzi)
■ Most common site: Rectosigmoid

■ Pathophysiology:
o Absence of ganglion cells in Auerbach (myenteric) and Meissner plexuses due to
failure to progress in caudal direction
o Hypertrophy of nerve trunks (bundles)
o Increased acetylcholinesterase staining

■ Clinical presentation:
o Most common cause of colonic obstruction in infants
o Fail to pass meconium in 1st 24 hours
o Explosive release of watery stool
o Enterocolitis (abdominal distention, tenderness with fever, failure to thrive, and lethargy)

■ Investigations:
o Barium enema: transition zone between dilated ganglionic colon and distal constricted
aganglionic rectal segment
o Slow transit time
o Anal manometry: No relaxation of internal sphincter
o Rectal biopsy: (Gold standard)
• Suction biopsy of mucosa/ submucosal samples at 1, 2, 3 cm from dentate line
• Full thickness biopsy is required under GA for older children
• Absence of ganglion should be at least 2 cm from dentate line to diagnose

■ Management·
1) Medical management
o Rehydration, Systemic antibiotics, Nasogastric decompression, Rectal irrigations

2) Decompressive Colostomy
o lf failed medical management
o Frozen section required to place the stoma in ganglion containing bowel

Multi-staged approach (Preferred)

o Colostomy in newborn period
• Proximal to the histologic transition zone
Identified by series of frozen section biopsies to find correct level of diversion

o Followed by definitive pull-through •operation after the child weighed >10 kg

(Duhamel, Swenson's, and Soave operations)

Single-stage approach
o Option for newborn who does not have enterocolitis, or multiple medical anomalies or
diseases

-+
If persistent constipation or partial obstruction after pull-through procedure:

-+ Surgery may be needed if persist after age of 4

Observation and re-evaluation every 6 months
MECONIUM ILEUS
■ Clinical presentation:
o Bilious vomiting, failure to pass meconium, and abdominal distention
o Cystic fibrosis associated with meconium ileus in 10%

■ Investigations:
o Abdominal x-ray: dilated bowel loop with no air-fluid levels (too thick meconium}
o Contrast enema: Confirmatory diagnostic study which showed microcolon
o Sweat Cl test or PCR for Cl channel defect

■ Management:
o Uncomplicated: Gastrografin enema
• Can be used as 12 hour intervals over several days until meconium evacuated

o Complicated: Failure to resolve with gastrografin

• Enterotomy (purse-string} and irrigation with N-acetylcysteine / Saline
• Resection of distal ileum± ileostomy

OMPHALOCELE GASTROSCHISIS
Embryology Primary failure of lateral ventral folds to Primary body folds develop normally
form the orimitive umbilical rina Vascular ruoture of riaht umbilical vein
Stage of anomaly 3 -5 weeks 5-6 weeks

Genetics Familial Sporadic

Oraan herniation Small bowel. liver. aallbladder Small bowel
Membrane I Sac Coverina sac No Sac on defect
Location of defect Midline To riaht of umbilicus and umbilical cord
Umbilical cord Midline To left of defect
Other anomalies Common 1so -Zo°/41 Less common
Associated also with malrotation (intestinal atresia, malrotation)

Cantrell pentalogy
- Cardiac defects (Mo.st common)
- Pericardium defects
- Sternal cleft
- Diaphragmatic defects
- Omohalocele
Bowel comnlication Rare Obstruction
Abnormal karvotvoe 30-40% Rare
Management - Saline-soaked gauzes
- Resuscitation, NPO :1:: TPN
- Packing :f: Vicryl mesh silo
- Primarv closure later on
Proqnosis Worse (due to associated anomalies) Better
UMBILICAL HERNIA
■ Unlike adult, does not associated with risk of incarceration
■ Repair should be delayed until age of 5 years or if associated with complications, or VP shunt

INGUINAL HERNIA
■ Extension of the hernia into the internal ring differentiates hernia from hydrocele
■ Presence of inguinal hernia is an indication of repair
■ Ma nagement:

o Bilateral exploration for unilateral hernia (asymptomatic opposite side)

• Controversial, Standard of care in infants for most surgeon
• Frequency of patent processus vaginalis on the opposite side 30 - 50%
• Especially in premature infants or associated with incarceration

o Herniorrhaphy
• High ligation only to close the patent processus vaginalis without reconstruction
of inguinal floor (always indirect}

HYDROCELE
■ Most disappear by 1 year
■ Management:
o Non-communicating hydrocele
• Usually resolve without operation, and aspiration is not required

o Communicating hydrocele
• Usually requires operation at age of 1 year
• Groin incision, and resection with hydrocelectomy and excision of processus
vaginalis
UNDESCENDED TESTICLES
■ 30% in premature infants

■ Associated with:
o Malignant potential (Seminoma)

o Decreased fertility
• Fertility is not changed if undescended testis is unilateral
• Orchidopexy improve fertility (never back to normal), and doesn't change
malignant potential

■ Investigations:
o Scrotal U/S
o MRI (in absence of scrotal and inguinal testis bilaterally)
o Chromosomal studies (in bilateral cases)
o Diagnostic laparoscopy if failed to identify the location of undescended testis

■ Treatment·
o No surgery in first 6 months (Testis may descend)

o Orchidopexy through inguinal incision

• If undescended testis found at inguinal area clinically
• If spermatic cord found to traverse the internal ring or testis is found at the ring

o 2-stage Fowler-Stephens procedure, if unable to scrotum (too far)

• Testicular vessels clipped to promotes neovasculogenesis, followed by 2nd stage
6 months later (will depend on vasal artery)

o Orchidectomy (in atrophic testis of po-st- pubertal)

Scrotal incision done for suspicious of testicular torsion

NEUROBLASTOMA
■ Most common solid abdominal malignancy in children
■ Most common in 1 '' 2 years of life
■ Derived from neural crest cells
o Located on adrenal
o Can occur any sites along sympathetic chain

■ Presented with:
o Left flank mass
o Secretory diarrhea
o Hypertension
o Weight loss and failure to thrive
o Raccoon eyes (orbital metastases)
o Opsomyoclonus syndrome (unsteady gait)

■ Investigati ons:
o t Catecholamines, VMA and metanephrines
o AXR: Stippled fine calcifications in the tumor
o Bone marrow biopsy

■ Worse prognosis if associated with:

o Neuron-specific enolase (NSE)
o LOH
o N-myc amplification

■ Treatment: Resection (adrenal gland and kidney taken; 40% cured)

o Initially unresectable tumors may be resectable after doxorubicin-based chemo

WILMS TUMOR {NEPHROBLASTOMA)

■ Most common primary malignant tumor of kidney in children
■ Bilateral in 10%
■ Mean age at diagnosis: 3 years
■ Prognosis based on: Tumor grade
■ Most common sites of metastasis: Bone or Lung
■ i
Presentat on:
o Asymptomatic mass
o Hematuria
o Hypertension

■ Abdominal CT:
o Replacement of renal parenchyma and not displacement
{differentiates it from neuroblastoma)

■ Treatment:
o Nephrectomy
o Actinomycin and vincristine based chemo in all unless Stage I and < 500 g tumor
BILIARY ATRESIA
■ Most common cause of neonatal jaundice requiring surgery
■ Presentation:
o Progressive jaundice persisting > 2 weeks after birth
• Involving either the extrahepatic or intrahepatic biliary tree or both

o Cholangitis
o Continued cirrhosis
o Hepatic failure

■ Investigation:
o Liver biopsy: periportal fibrosis, bile plugging, eventual cirrhosis

o lntraoperative Cholangiography

o Ultrasound

■ Management:
o Kasai procedure (hepatoportoenterostomy)
• Done at age 3 months, or on s,ame settings if diagnosed intraoperatively
• Involves resecting the atretic extrahepatic bile duct segment

HEPATOBLASTOMA
■ Most common malignant liver tumor in children
■ Associated with t AFP and t beta-HCG (Fractures, precocious puberty)
■ Treatment:
o Resection
o Doxorubicin and Cisplatin based chemotherapy for downstaging

TERATOMA
■ Associated with t AFP and j beta-HCG
■ Treatment: Excision
■ Sacrococcygeal teratomas
o 90% benign at birth and more malignant potential after 2 months
o (almost all have exophytic component)
o Treatment: Coccygectomy

TRACHEOMALACIA
■ Elliptical, fragmented tracheal rings instead of C-shaped
■ Wheezing, usually get better after 1-2 years
■ Surgical indications:
o Dying spell, failure to wean from ventfilator, recurrent infections

■ Surgery: Aortopexy (aorta sutured to the back of the sternum, opens up trachea)
LARYNGOMALACIA
■ Most common cause of airway obstruction in infants
■ Symptoms:
o Intermittent respiratory distress
o Stridor exacerbation in the supine position

■ Caused by immature epiglottis cartilage with intermittent collapse of the epiglottis airway
■ Surgical tracheostomy reserved for selected patients

CHOANAL ATRESIA
■ Obstruction of choanal opening (nasal passage} by either bone or mucous membrane
■ Symptoms:
o Intermittent respiratory distress
o Poor suckling

■ Treatment: Surgery

LARYNGEAL PAPILLOMATOSIS
■ Most common tumor of the pediatric larynx
■ Frequently involutes after puberty
■ Can treat with endoscopic removal or laser but frequently comes back
■ Thought to be caused from HPV in the mother during passage through the birth canal
OTHERS
Presented at aae of Wait for reoair until aae of lat least\
Pvloric stenosis 3 weeks - 3 months -
lntussusception 6 months -2 years -
Duodenal atresia < 1 week
Malrotation > 1 week
Neuroblastoma 0-2 years
Neohroblastoma > 2 vears
Bilia~ atresia Wrthin 1 month of life
ln11uinal hernia - Immediate
Hvdrocele - 1 vear
Undescended testicles - 2 vears
Umbilical hernia - 5 vears

■ Causes of Bilious vomiting

o Intestinal or duodenal atresias
o Annular pancreas
o Meconium ileus
o Malrotation
o Hirschsprung's disease

■ Causes of Failure to pass meconium

o Intestinal atresias
o Meconium ileus
o Hirschsprung's disease

MOST COMMON
■ Most common children's malignancy overall: Leukemia {ALL)
■ Most common solid tumor class: CNS tumors

■ Most common general surgery tumor: Neuroblastoma

■ Most common in child< 2 years: Neuroblastoma
■ Most common in child > 2 years: Wilms tumor
■ Most common cause of duodenal obstruction< 1 week: Duodenal atresia
■ Most common cause of duodenal obstruction > 1 week and overall: Malrotation

■ Most common intestinal obstruction in Children: lntussusption

■ Most common cause of colon obstruction: Hirschsprung's disease
■ Most common liver tumor in children: Hepatoblastoma
■ Most common lung tumor in children: Carcinoid

■ Most common cause of painful lower GI bleeding: Benign anorectal lesions

■ Most common cause of painless lower GI bleeding: Meckel's diverticulum
Epidemiology and
Ethics
EPIDEMIOLOGY AND ETHICS
■ Incidence: number of new cases diagnosed over a certain time frame in a population
(Number of new cases of a disease in a given time)
(Total population at risk)

■ Prevalence: number of individuals with a certain condition at a given time

/Number of existing cases of a disease )
(Total population)

Risk of Disease

■ Relative risk = incidence in exposed/incidence in unexposed

Incidence in exposed group
Incidence in unexposed group

■ Odds ratio = (Estimated the relative risk if prevalence low)

Odds of exposure among patients with a disease
Odds of exposure among patients without a disease

Risk Disease status

Present Absent
Smoker A B
Non-smoker C D

Al (A+ B) A/C A/B A xD

RR=
C I (C + D) OR_
- B/D = CID = BxC

Result >1 suggests positive relationship (0 suggests no relationship)

■ Attributable risk= Difference in rates

= (incidence in exposed population) - (incidence in unexposed population)

■ Independent risk factor:

o Risk factor than can increase the risk of the disease by itself only
o Examples:
• Smoking (for lung cancer)
• NGT (for nosocomial infection)
• Renal failure,CVA, Valve surgery (for mortality in elderly patients)
• BM failure (for mortality)
• Hyperglycemia, Hypertension, Obesity (for cerebrovascular accidents)
• Corticosteroids (for fractures, pressure ulcer, infection)
Statistics of diagnostic tests
■ Sensitivity: ability of the screening test to detect disease
o Proportion of patients with the disease who have Positive test

■ Specificity: ability of the screening test to rule out the disease

o Proportion of patients without the disease who have Negative test

o High sensitivity: like ELISA test for HIV infection

o High specificity: like Western blot confirmatory HIV test
o Sensitivity and specificity: are independent of prevalence

■ Positive predictive value: probability that a patient with a positive test has a disease
■ Negative predictive value: Probability that a patient with a negative test does not have a
disease

Test/Disease + -
Yes True+ IA\ False-IC\
No False+ /B\ True- (D)

• Sensitivity = A/ A+ C
• Specificity = D I D+ B
• Positive Predictive value =A/ A+ B
• Negative Predictive value = DID + C
• Accuracy = A + D /A+ B + C + D

Types of error
■ Null hypothesis: hypothesis that no difference exists between groups (exposure and disease or
treatment and response)
o Probability value (P value)
• p < 0.05 rejects the null hypothesis (chance of Type I error)
• p < 0.05 = > 95% likelihood that the difference between the populations is true

■ Type I error: rejects null hypothesis incorrectly (False Positive)

o Falsely assumed there was a difference when no difference exists

■ Type II error: accepts null hypothesis incorrectly (False Negative)

■ Power of test = probability of making the correct conclusion = 1 - Type II error

Prevention
■ Primary prevention: Preventive measures to decrease the incidence

■ Secondary prevention: Identifying disease early to treat and reduce the disease progression

■ Tertiary prevention: Measures to decrease the morbidity or mortality

TRIALS AND STUDIES

Type of the study Description Outcome Disadvantaae

Randomized Prospective comparison of Causal relationship Costly, Time
clinical trial experimental treatment with placebo Minimal bias consuming

"Gold standard" (Single or blind or open-label triaV

"Controlled studv"
Case control Retrospective comparison of patient Odds ratio Recall and
"Observational study" with disease with healthy control Used for rare cases selection bias
Cross sectional Survey of large number of people to Prevalence No risk or
"Observational study" assess disease prevalence incidence
Cohort study Prospective or retrospective study for Relative risk Costly, Time
"Observational study" exposed patients Odds ratio consuming
Incidence
Prevalence
Meta-analysis Pooling of multiple studies

TYPE OF BIAS

Bias Descriotion Examoles Strateav to reduce bias

Selection bias Error in assigning Sampling bias Randomization
sample Healthy-worker effect
Non-resoonse bias
Recall Bias Common in Decrease time from
retrosoective studv exoosure to follow-uo
Others: Verification Bias Publication Bias Interviewer Bias
Measurement
Procedure
Observer-exoectancv
Confound Ina
Lead-time

Level of Evidence
■ Level 1: Meta-analysis
■ Level 2: RCTs
■ Level 3: Cohort study
■ Level 4: Case control study
■ Level 5: Case report study
Phases of clinical research
■ Phase 0: Pharmacodynamics and pharmacokinetics
■ Phase 1: Screening for safety
■ Phase 2: Efficacy
■ Phase 3: Confirmation of safety and efficacy
■ Phase 4: Safety studies during sales
Univariate Descriptive Statistics
Central Tendency
■ Numeric terms: 2,3,6,5,8,9,9
o � mathematical average = 5 (Normally distributed)
o Mode: most frequently occurring value = 9
o Median: middle value of a set of data (50th percentile)= 6
In order of central tendency: Mean > Mode > Median

Dispers ion
o Variance: Measure of how spread out a distribution
o Standard Deviation: Measures scores deviation from the mean

Bi- and Multivariate Inferential Statistical Tests

Differences of Groups

Quantitative variables
■ Student's T-TEST: Compares 2 groups with 1 quantitative variable
o Examples:
• Difference in hours consuming between male and female
• AB/ between OM and non-OM patients
• Weight reduction between sleeve and gastric bypass

■ Paired T-TEST: variable is quantitative; before and after studies

o Examples·
• Weight reduction rate before and after sleeve gastrectomy
• Fluid loss preoperative and postoperative for intestinal obstruction
• Drug versus placebo

■ ANOVA: Compares 2: 2 groups with 2: 1 qualitative variables

o Examples·
• Smoking and hypertension in different age groups
• Effects of 3 different anti-hypertensive medication (on 3 groups of patients)
• BM/, and growth charts

Qualitative variables
■ Nonparametric statistics: compare categorical (qualitative) variables (race, sex, medical
problems and diseases, medications)

■ CHI-SQUARED TEST: Compares 2 groups with 1 categorical (qualitative) variables

o Examples
• Number of obese patients with and without OM versus non-obese patients with
and without OM
• Drug effects on 2 experimental groups
Relationships
■ Multiple Regression
o Used with several independent variables and one dependent variable
o For prediction
• e.g. Between (independent) drug use, alcohol use, child abuse and (dependent)
suicidal tendencies

■ Logistic Regression
o Same multiple regression but dependent variable is categorical "dichotomous variable"
• e.g. Odds of a suicide occurring at various levels of alcohol use

■ Measure of association·
o By correlation and chi-square

■ Correlation:
o Measure of association appropriate for continuous and discrete "ordinal scale" variables
o Measure between two variables to determine a relationship/association
• e.g. amount of damage to a house on fire and number of firefighters at the fire

Variable Test
Deoendent lnde=ndent
Categorical Categorical Chi-sauare
Categorical Quantitative Logistic regression
/Dichotomous = "onlv 2")
Quantitative Categorical T-Test (2 outcomes)
(Continuous) (Dichotomous in I-test) ■ BP in gender
ANOVA (3 outcomes)
■ BP in blood group
Quantitative Quantitative Correlation
(Continuous) (Continuous\
Categorical: sex, education, blood group, death
Qualitative Data: color, smell, appearance
Quantitative Data: size, weight, surface, cost, temperature
■ Discrete: Numbers of cars you have
■ Continuous: Your heiaht. blood oressure
Ethics and Patient safety
■ Terminology:
o Respect for autonomy: respect patients as individuals
• To make patient take self-determination decision
o Beneficence: acting in patient's best interest
o Nonmaleficence: "Do no harm" avoid recommending treatments where the risks are
high and the benefits are negligible

■ Consent:
o Not required in
• Emergency therapy
• Patient lacking decision-making capacity (consent taken from designated
surrogate decision maker)
• Minors(< 18 years) if(Emergent therapy needed, STDs, or refusal treatment
(except if parents refused))

■ Do-not-resuscitate IDNR} order

o Refuse all non-palliative therapies or can only restrict use of specific therapy
o Physicians can remove respiratory care in cases in which no living will exists and the
patient is incapable of voicing a decision

■ confjdentjality is not mandated when the patient·

o Allows the physician to share information with designated others (family, etc.)
o Has a disease that is legally reportable
o Suicidal or homicidal
o Assault due to gunshot or other type of penetrating wound
o Adolescent with harmful condition to self or others
■ Malpractice
o Events:
• Medical Error: adverse event or near-miss that is preventable with the current
state of medical knowledge.

• Adverse Event: (either preventable or unpreventable}

• Injury related to medical management rather than by underlying
disease/condition of the patient (diagnosis and treatment, failure to
diagnose or treat, and the systems and equipment used to deliver care)

• Near-miss: event or situation that could have resulted in an accident, injury or

illness but did not

• Sentinel Event (JCAHO): unexpected occurrence involving death or serious

injury includes loss of limb or function leg wrong site surgery/
• If recurrence happens it would carry a significant chance of a serious
adverse outcome.
• Hospital need to report it with immediate investigation and response

o National Surgical Quality Improvement Program (NSQIP): collect outcome data to

measure and improve surgical quality in the United States

o Risk factors for retained object after surgery (Most common: sponge): emergency
procedure, unplanned change in procedure, obesity, towel used for closure
Approach Sheet
 Approach Sheet
Wash hands, Greeting, Introduce yourself, Permission
Prepare your instruments
Approach Utilize the Personal Protective Equipment (PPE)
Inform nurse staff about what you going to do
Ensure Privacv
Assess stability: ABC
Unstable

NPO (Diet)

IV Line
o Investigation "General, Critical, Specific, Septic workups, Type and Screen, Cross match"
o Fluids after the investigations

Tubes, Input/ Output Chart

Monitor VIS

± ECG, CXR

Medications (Prophylactic, Therapeutic "Antibiotics, Analgesia", Specific)

Serial examination

± Consider ICU admission

± Consultations

Re-assess
 If relative (Relation? Most responsible person? What he knows?)

Demographic data (Name, Age, Gender, Residency, Occupation, Marital and pregnancy status)

Chief complains and History of present illness

1) Current symptoms analysis of the pain, mass or discharge

2) Related symptoms
General Nausea, VomitinQ, Chanqe bowel habijs, Distention, Trauma
Upper GI Heartburn, Obstructed jaundice, Odynophagia, Halitosis, Hiccups
Dvsphaqia {Proqress ive. liquid. solid) + Wheezinq, Hoarseness
Lower GI Tenesmus. PR bleedina
Genitourina~ Urinarv svmotoms Vaainal discharae Menstrual �•cle and LMP
Endocrine Functionality

3) Risk factors
(DR. M)
General
Dietary intake. Radiation {When and How\ Massive blood or fluid resuscitation
< 12 year menarche, > 55 year menopause, OCPs or hormonal, Lactation
Breast
Preanancv /Number oattem aae at 1st birth\ Trauma
Hernia Chronic couqh, SmokinQ, Heaw weiqht liftinq, Urinary retention

4) Complications
(A B C D E F - NWJ)
General Anorexia/Ascites, Bone pain, Cough, Dyspnea, Edema/Early satiety
History Fever± rigors, Night sweating, Weight loss, Jaundic-e
Breast Bone pain. Back pain, Headache, Jaundice, Skin chanqes
Compression (dysphagia, dyspnea, dysphonia)
Invasion (Hoarseness, Homer's syndrome, Strider)
Exclude MEN:
- HTN, Palpitation, Sweating
Endocrine - Calcitonin (Flushing, Diarrhea, Weight loss)
- Hypercalcemia
0 Musculoskeletal (pain, weakness, or fracture)
0 Urinary (Renal stones, polyuria, polydipsia)
0 GIT (Constioation, Ulcer, Pancreatitis, Gallstones)
Hernia Fever Obstruction svmotoms Skin chanaes

Past medical, and past surgical history

- Similar attack or hospitalization (Colitis, Pain)
- Previous biopsy or mammogram
- Recent Viral URTI (Thyroiditis, Appendicitis)
- Comorbidities or malignancy
- Intervention or procedures (Where, When, "Elective or emergency", What, Difficulty, Drain)
Allergy and drug history
- Including history of recent usage of Antibiotics, OCPs (Name, Duration)
Family history
- Number, degree relative and age of onset, and age of death
Social history
- Alcohol. Obesitv. Smokinn Sexual historv Travel historv Tattoo
 Ask for female nurse before examination a female patient

General appearance(Dehydration, pale, jaundice, toxicity)

Vital signs
- General: Pulse, Blood pressure, Respiratory rate, Temperature, Oxygen saturation, RBS
- Specific: Abdominal girth, weight, drains, tubes

General examination(Level of consciousness, BMI, Signs of hepatic failure)

Examination
Local examination of ipsilateral and contralateral side ± Wound ± Stoma
- Inspection, Palpation (superficial and deep), Percussion, and Auscultation
± Missing parts: Left supraclavicular node, Groins, Scrotum, Perineum, Back, and DRE

Systemic examination (Abdomen, Chest, All lymph nodes including supraclavicular nodes)
- Specific examinations(Ophthalmological, Hands and arms)

Performance status IECOG score)

Differential diagnosis
Laboratory:
- General: CBC , Liver, Renal, Coagulation profiles, RBS, Pregnancy test, Bone panel
- Critical: Lactic acid, LOH, ABG, CRP, Culture Blood/ Urine, Urinalysis
Amylase level, Lipid profile
Pancreas
Fastina aastrin insulin alucose levels
Heoatitis orofile Seroloav /Blood Stool\. ELISA Liver or Biliarv
ESR TSH Free T3 and T4 Anti-TPO/TSH Thvroid disease
Calcium (Urine Serum I. PTH level Parathvroid
Cortisol, Low-dose dexamethasone
Adrenal
ACTH Aldosterone Metaneohrines

Imaging:
Borderline VIS (Fever! ➔ Acute Manaaement ➔ Re-Assess
Investigations X-ray (Upright Chest, Abdomen), U/S abdomen
Short-time
UIS neck(thyroid, lymph nodes)
UIS and Mammoaram for bilateral breast axilla
Triphasic CT Abdomen(± Chest I Pelvis) + IV Contrast
MRI liver + IV Contrast
Long-time MRCP
CT neck (thyroid, lymph nodes)± Chest ± IV contrast
1 123 whole bodv thvroid scan

Endoscopy:
- Laryngoscopy, Bronchoscopy
- Colonoscopy after bowel preparation± biopsy
- EUS or/and ERCP :I: Stent :I: biopsy(AFP, CEA, CA 19- 9, Mucin, Amylase)
Precaution is needed for all investiaations that reauires radiauon (Cholanaioaraohv. ERCP!
Diagnosis and expected management
/Review his/on, and examination if diaanosis chanaed at anv umel
 Admission orders (Also for patient deteriorating in the Ward)
- NPO (Diet), IV Catheter (Labs "Type and Screen, Cross match•, then Fluids), Tubes, Input I Output Chart
- Monitor VIS, ECG, CXR
- Medications (Prophylactic, Therapeutic "Antibiotics, Analgesia•, Specific)
- Serial examination±Consider ICU admission± Consultations

Definitive management

0 Markers tumor (AFP, CEA, CA 19 -9, CA 15-3, Thyroglobulin, Anti-Thyroglobulin, LDH)

N
MEN Ruled out (Metanephrines, Calcitonin, CEA, PTH, Ca and electrolytes, UIS, CT scan)
C
0
L Metastasis (Staging CT CAP ±Brain± IV contrast , Bone Scan, MRI, PET scan)
0 Meetings (Genetic counseling (Specific gene), Family, Multidisciplinary, Tumor Board)
G
I Medications+ Complications of each
C - Vaccination, Neoadjuvant Chemotherapy± Radiotherapy
A
L
Before Review resectabili!X (Clinical, Radiological, Endoscopic, Pathological)
Admission Non
0
N Medjcal management+ Complications of each
C
0
L lnterventional management

G
I Surgjcal management
C
A
L
Consent (With complrcations of each, laparoscopy, surgery, stoma)
- Diagnostic laparoscopy (for high-risk patient for occult metastasis)
- Operation name (Laparoscopic, Open)±OPEN±Abortion± Re-Operation± Reconstruction
Indication (Diagnosis), Benefits/Complications, Alternatives
± Take Completion consent from the relatives if needed

Education
- Diet, Chest and physical physiotherapy
- Stoma care, Stoma nurse
After Preparation
Admission
ICU
Fitness Consultations (Endocrinologist, ENT, Cardiology, Plastic surgery)
Functional tests /ECG Chest x-rav. PFTs Pre-oo echocardioaraml
Radiology (Cholangiogram, DJ stent, Wire-localization, Breast radiation)
Arrangement Pathology (Frozen section)
Endoscoov (ERCP, Intra-op endosconvl
Intestines
Bowel prep
Stoma marking
Last Day DAVID - Cross match
 Confirm presence of:
Correct Consen� Operation and patient names, Correct Site by Sign-in, time-out, sign-out
Equipment and arrangements
Administration:
Inside the OR GA Considerations (CVP, Central, Arterial, Epidural lines, Trans-esophageal echocardiogram)
Medications (Antibiotics, DVT prophylaxis, and P neumatic compression)
Tubes (Foley's catheter, NGT)

GA - Position (Body and Hands) Prepare and drape the area of the operation
 Recove!:l( monitoring

VIS
Tubes and Drains (Positive vs. Negative)
General
1/0 Chart
Dressinq
Voice
Specific
Wound {hematoma \

Shift l!l!!ient to !!le :i!li!lll 2r ICU

Historv I Examination DailvSOAP

DAVID
VIS
Management Tubes and Drains (Positive vs. Negative)
1/0 Chart
Dressinq

Discharge orders

Drains
Post-operative Removal Tubes
Staoles Stitches /Date of removal\
RSD - Avoidance of risk factors
- Dressing, Stoma care, Stoma nurse
Education - Come back to ER if symptoms persists
- Chest and Physical physiotherapy
- Chanqes that may developed {urine may return blue)
Adjuvant therapy (Vaccination, TSH suppression)
Medications Analgesia
Antibiotics
General Surgery
- History and examination of ipsilateral, contralateral organ
- Review of histopathology and endoscopy
- Labs and Tumor marker
- Imaging and Endoscopy
OPO follow-up - Complication's management
Oncology (Chemotherapy, Radiotherapy, RAI)

Endocrine
Markers tumor
Metastasis exclusion
Malignancy Meetings (Genetic counseling, Family, Multidisciplinary, Tumor Board)
diagnosed post-op Medications + Complications of each
- Vaccination, Neoadjuvant Chemotherapy± Radiotherapy
Review resectabilitv {Clinical, Radioloqical, Endoscopic , Patholoqical)
 ComQlications
Anesthesia Surgetl£
Post-operative
Atelectasis Intra-operative
Early Late
Hemorrhage Seroma or hematoma
DVT/PE thrombosis
Urinarv retention Wound infection
During Insertions of Trocars
Acute aastric dilatation UTI
Allergy
DVT/PE thrombosis Nutritional deficiencv
During pneumoperitonum lieus Recurrence
- Bowel injury
Prolong recovery - Solid organ injury
- Vascular injury General Specific
- CO, embolism
Hemorrhage Thyroid:
Atelectasis -Voice changes
Wound infection - Hypocalcemia
Nerve injury DVT/PE thrombosis - Hematoma
Diaphragm injury Acute gastric dilatation - Life-long thyroxine
Nutritional deficiency
lieus, UTI
Recurrence
Mesenteric ischemia: Splenic:
- lschemia - OPSI
-Abscess - Splenosis
Nearby structures injury - Bleeding -Acute gastric dilatation
(Spermatic cord, Parathyroid) - Short bowel syndrome
-TPN need
- Mortalitv
Anti-reflux surgei:v: Pancreatic:
- Pneumothorax - Delayed gastric
-Recurrent GERD emptying
Hemorrhage - Dysphagia - Pancreatitis
- Gastroparesis - Fistula, leak, abscess
- Esophageal perforation -Pleural effusion
- Failure of wrao
Gastric:
Esoehagectomy:
- Leak
-Respiratory complications (Most common)
-Duodenal stump leak
-Retained antrum
-RLN injury
- Marginal ulcer
- Stricture / Stenosis
- Chyle leak
-Alkaline reflux syndrome
(Chylomicrons, triglyceride, lymphocyte)
- Blind loop obstruction
- Dumping syndrome
- Stricture
- Gastrooaresis
Breast: MRND: Liver:
- Lymphadema - Infection, Seroma or Lymphocele - Peritoneal leak
- Sarcoma - Anterior jugular vein thrombosis - Bile leak
- Shoulder -Thoracic duct injury -Anaphylaxis
weakness - Sympathetic chain injury (Hornor's syndrome) -Recurrence
- Loss sensation - Phrenic nerve or Great auricular nerve injury
- Vaaus nerve or Accessarv nerve iniurv
Tubes, Drains, and
Catheters
TUBES' DRAINS ' AND CATHETERS
■ Size of inner diameter: depends on the material
■ Size of outer diameter: by French unit
o 12 Fr /3 = 4 mm diameter (Large number is bigger diameter)
• Smaller gauge bigger diameter (10 gauge is largest diameter)

Classification-
■ Active: (with pressure gradient = suction)
o Redivac Drain, Jackson pratt drain

■ Passive:
o Open: Courrgated drain, plastic sheath

o Closed: Nasogastric, Foley catheter

Material:
■ Polyvinylchloride (PVC)
o Larger inner diameter, used in short duration
■ Polyurethane (PUR)
o Flexible, less irritant
■ Polyethylene (PE)
■ Fluoropolomers (PTFE)
■ Silicon (Foley)
■ Red rubber (Sengstaken, Courrgated drain)
■ Plastic (Nasogastric tube)
■ Latex (T-tube, Robinson)
o Not inert, or induce inflammation

Ranae Preferable I Adult Children

Nasnnastric tube 6-18Fr I12-18Fr 6-12Fr
Foley's catheter 6-26Fr 14-18Fr 6-12Fr
20 - 24Fr for prostate enlargement
or for 3-wavs catheter
Drains 6-14 Fr 10-12 Fr I
Chest tube 12-32Fr 24-28Fr for clear effusion and air 18Fr
28-32Fr for blood or PUS
T-tube 12-18Fr 12-14Fr I
Seldinger 10-32Ga 18-21Ga
At least 18 in trauma oatients
r.:,•--- 78 - 1/78 ;nrh
Drains
■ Simple drain (Robinson drain) ■ Courrgated drain
o Passive open drain
o Best to use in limb wound/abscess

---
-·

■ Redivac Drain ■ Penrose drain

(Increases risk of infection in clean
wound)

---
■ Jackson pratt drain (Vaccum drain)
o One-way closed system with low negative pressure•
o best to use in closed spaces; thyroid, parotid, breast
TUBES
NASOGASTRIC TUBE
■ Indications:
o Diagnostic
• Upper GI bleeding
• Aspiration of gastric content
• Identification of esophagus or stomach on CXR
• Administration of radiographic contrast
o Therapeutic
• Gastric decompression (after splenectomy)
• Relief of symptoms and bowel rest (bowel obstruction)
• Stomach lavage
• Feeding
• Administration of medication

■ Contraindications:
o Absolute
• Severe facial trauma
• Basilar skull fracture
• Esophageal stricture
• Recent nasal surgery
o Relative
• Esophageal varices
• Abnormal coagulopathy

■ Technique
o Position: Sitting upright with neck partially flexed
o Length:
• Measured from nasal tip, around the ear, down to subcostal area (or xiphoid)
• between 2nd and 3"' black dot
o Ask patient to drink water or swallow during insertion
o Verification:
• Aspiration of gastric content
• Pushing air and auscultate gush of air in stomach (not confirmatory method)
• Chest x-ray
o NGT must be drained under gravity
TYPES
■ RYLE'S TUBE
o Most common type, used for short du ration
o Best for aspiration (intra-operative)

■ ENTRIFLEX
o Radioopaque with central guide-wire, used for long duration, best for feeding

■ Levin (single lumen)

■ Sump (double lumen; for suction) "Made of PVC"

■ Sengstaken-Blakemore tube (3 channels, 2 Balloons: gastric and esophageal)
o Minnesota tube is SBT with additional channel for esophageal aspiration (4 channels)

o Indications: For temporary(< 24 hours) hemostasis of esophageal or gastric varices

o Contraindications:
• Variceal bleeding stops or slows
• Recent surgery involving gastroesophageal junction
• Known esophageal stricture

-----
--

o Steps:
• Intubation
• Positioning at 45 degree
• Check tube for leak by inflation with 100 ml to maximal recommended volume
(300 - 500 ml}
• Insert the tube orally or through the nose for 50 cm
• Inflate gastric balloon 100 ml
• AXR and check the balloon
• Continue inflation of gastric ba !loon up 250 ml ( 450 - 500 ml for Minnesota tube)
• Withdraw the tube until feel resistance (at 30 - 35 cm)
• Aspirate gastric and esophageal port to check for bleeding
• For esophageal varices only (after failure to control by gastric balloon):
• Inflate esophageal balloon to 25 - 30 mmHg
• Check bleeding either by
o Aspiration of esophageal port in Minnesota tube
o Introducing Salem sump in SBT until marked depth
(2 cm above gastric balloon}
• Deflate the balloon 10 mmHg every 2 hours
• Apply traction to the tube (1 kg, or suspended over by 1L fluid bag}

o Monitoring:
• Gastric balloon (by Volume)
• Esophageal balloon (by Pressure)
• Perforation I Esophageal necrosis happen if pressure > 40 - 50 mmHg
FLATUS TUBE (RECTAL TUBE)
■ Indications:
o Decompression of large bowel in pseudo-obstruction
o Prevent immediate recurrence of sigmoid volvulus

■ Contraindications:
o Paralytic ileus, acute surgical abdomen, recent rectal or prostatic surgery
o Relative: rectal disease (abscess, inft.ammation, fistula), rectosigmoid obstruction
CHEST TUBE (Options: 1 bottle, 2 bottles, or 3 bottle system "PLEUR-EVAC or ATRIUM')

o Collection chamber
o Water-seal chamber: 2 cm
o Suction chamber:
• (in Wet-suction system only)-+ Fill with sterile water - 15 to - 20 cm H20
• Suction: Low (60 - 80) mmHg, or High (80 - 100) mmHg

ANATOMY
■ Safe Triangle: between latissimus dorsi, lateral of pectoralis major, and upper boarder of 5th rib
■ Neurovascular bundle (intercostal nerve) pass just below the rib
■ Positions:
o Patient supine or at 45• angle with arm abducted and externally rotated placed behind
patient's head
o Anterior: used in blunt trauma, to prevent blockage by tissue and progression to tension
pneumothorax
o Posterior: used in penetrating trauma, to drain the blood

■ Length: measured by cm from the last hole (which should be inside), can be measured by
calculate the distance between skin incision and apex of the lung

■ Indications: Pneumothorax, Hemothorax, Hydrothorax, Chylothorax, Empyema, Pleural

effusion, Patients with penetrating chest wall injury who are intubated or about to be intubated

■ contrajndjcations·
o The need for emergent thoracotomy
o Relative: Coagulopathy, Pulmonary bullae, Pulmonary, pleural, or thoracic adhesions,
Loculated pleural effusion or empyerrna, Skin infection over the chest tube insertion
■ Steps:
2) Patient consent
3) Aseptic precautions
4) Local anesthetics -+ infiltrate all layers {pleura is the most important)
5) Incision at 4th - 5th IC pace between .anterior and mid-axillary line
• Over a rib that is below interco,stal level for chest tube insertion
• Inside safety triangle to avoid long thoracic nerve injury
• 2nd rib identified by Angle of Louis

6) Perform blunt dissection ''Kelly clamp or artery forceps" over the rib
• Should be near to superior boarder of the rib, avoiding injury of neurovascular bundle
7) Finger exploration to confirm intra-pleural placement
8) Direct clamped drain to the base in effusion and apical in pneumothorax
9} Connect the drain to the underwater seal then unclamp it
10)Skin closure over the tube
11) Occlusive dressing

....._.,_,_.._..
12) Chest x-ray
13) Monitor the chest tube system
• After insertion there must be bubbling until evacuate pneumothorax
• If there is no tidalling (fluctuation of water level during respirations)
• Tube may be kinked, clamped, blocked, or no more air leak

■ Clamping:
• General rule: chest tubes for pneumothorax should never be clamped
• Clamping chest tube 12 - 24 hours before removal of chest tube

■ Rules of Removal:
• Normal V/S with equal air entry bilaterally
• Chest x-ray normal and lung should be completely expanded
• Tube should not be > 1 week
• No Air leak
• Drainage is <200 ml in 24 hours(< 2 ml/kg/day)
• Chest x-ray must obtained after removal and 24 hours later
• At end-inspiration(studies showed no difference between end-expiration)
 Bubbling Swinging (Oscillation)
"Tidallina"
Yes Yes Air leak or still air inside pleura
Note: You have to stnn the suction first !
Yes No Svstem / Connection air leak
No Yes After partial/total pneumonectomy due
to decrease luna comoliance
No No Tube may be kinked, clamped, blocked
Luna exoanded !no more air leak\
Tidal/ina: fluctuation of water level durina re•nirations

HEPATOBILIARY TUBES
■ Percutaneous transhepatic biliary drainage
o Indications: (Nowadays PCTBD reserved if ERCP fails or not available)
• Relieving obstructive symptoms
• Treating benign strictures, cholangitis secondary to biliary obstruction, diversion
for bile leaks

o Contraindications:
• Massive ascites
• Multiple intrahepatic obstructio -ns
• Bleeding diathesis

l/J
■ T-tube
Cholecystostomy Tube
■ Indications:
o For Critical ill patient
• Unstable patient (ICU or on inotropes) with acute cholecystitis, or
Emphysematous cholecystitis

o For Contraindication for surgeN

• Uncorrected coagulopathy, Cinrhosis (Child C liver cirrhosis)
• Early for intervention (Early Ml "ST or non-ST elevation"}

■ Types:
o Trans-Hepatic
• Preferred route overall, and associated with early tract maturation

o Trans-Peritoneal
• Preferred route to remove stone through a large tract
• Used when anatomical inaccessible through trans-hepatic approach
• Used in liver disease or coagulopathy
Size of pigtail tube: at least 8 Fr
■ Types of technjaye· (through UIS or CT guided)
o Direct trocar technique
o Seldinger technique through a guide-wire
• Preferred, due to usage of fine needle (Less risk of perforation or bleeding)

■ Technique:
o After insertion of the pigtail, bile and pus aspirated for culture
o Connect the tube to gravity drainage
o After drainage of bile, clamp the tube for 24 - 48 hours and re-assess the patient
o Discharge patient with the tube clamped
o Cholecystogram through the tube after 4 - 6 weeks
o Remove the cholecystostomy tube if
• Clear cholangiography (Patent cystic duct)
• Positive results:
• Bile drainage instead of pus
• Resolution of symptoms and signs
• Reduction in WBC > 25'%

■ Status of cystic tube:

o Patent
• Can tolerate the surgery later on·
• Interval cholecystectomy when patient become stable, individualized on
the basis of patient age and surgical risk (Recurrence rate: 10-50%)
• Can't tolerate the surgeN later on:
• Stone extraction before removal of cholecystostomy

o Occluded
• Stable: Keep the tube in place until the time of cholecystectomy
• Unstable (gangrene, or perforation): Emergent cholecystectomy
• Cholangitis: ERCP or PTC if failed -+ Emergent OR and insert T-tube
CATHETERS
■ Straight catheter

■ Balloon

■ PIGTAIL
o Curve side holes, to prevent trauma
o For deep drainage

■ Butterfly

1
■ Seldinger
FOLEY CATHETER
■ Indications:
o Diagnostic
• Collection of urine sample
• Monitor urine output
• Imaging of urinary tract

o Therapeutic
• Acute urinary retention
• Bladder irrigation
• Hygiene care of bedridden patient

■ Contraindications:
o Presence of lower urinary tract injury (urethral injury) -+ associated with pelvic fracture
-+ Retrograde urethrogram
o Relative contraindications: urethral stricture, recent urinary tract surgery

TYPES
o Rubber: For short duration(< 1 week) o Silicon: For long duration(> 1 week)

o 3-way Foley: For flushing(as in hematuria)

Inflate balloon with water
Saline should not be used to inflate balloon � crystalize and block the tube