First Edition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: 1m Text books Review books 1 Didactic lectures and conferences ™ Primary and review articles 1m Points made by attendings and other residents on rounds or in the OR 1 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 woll. 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 dimoalismail@gmailcom alismailmo@ngha.med.sa Mohemmed Abdulwahab Buhalim Senior Registrar, General Surgery and Vascular Surgery King Faisal University, Al Ansa, Saudi Arabia drmohammed_abdulwahab@hotmail.comReviewers Dr. Abdulwahed Meshikhes FRCSI, FACS, Medical Director and Senior Consultant Surgeon Al Zahra General Hospital, Qatif, Saudi Arabia Chapter: Small bowel Dr. Hamad Hadi AlQahtani 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 Al-Harbi Assistant Consultant, Adult Hematology and Stem Cell transplant, King Fahad Specialist Hospital, Dammam, Saudi Arabia Chapter: Hematology and Blood products Dr. Haytham Alartaj 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 / Trauma, Head of Trauma Unit, Dopartment of Surgery, College of Medicine, Imam Abdulrahman bin Faisal Univorsity, Dammam, Saudi Arabia Chapter: Trauma Dr. Fahied AlQahtani 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 Meaicine, King Faisal University, Al Ahsa, Saudi Arabia Chaptor: Hoad and Nock Dr. Mamdouh Abdulassib Head of General Surgery Department, Al Osrah Intl. Hospital, Riyadh, Saudi Arabia Chapter: Appenaix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-Colorectal Consultant Chapter: Anorectal Dr. Shadi AlShammary Assistant Professor, Hepatobiliary and Liver Trensplant, 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. Al-Buainain Assistant Professor of Surgery, Consultant Pediatric Surgeon Immam Abdulrahman bin Faisal University Chapter: Pediatric surgery Dr. Omar Al Rasheed Assistant Professor, Orthopedics, College of Medicine, King Feisal 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@omail.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 reference 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. Itis 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. Itis 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 Ca Biolgy = 5 Hematology and Blood products... - 13 Immunology 8 2 Infection n Awtibioties. Ez a Fluids and Electrolytes, so as Nutrition, a : “ Inflammation and Cytokines... 15 Woung #eating ss rs ea Bure - .. 86 ‘Teams 9% Critical Care. = a saa 161 Anesthesia 7 190 Minimal Lavasive Surgery and Surgical Technelogy rene 200 Perioperative Care 208 Oncology. . sacl ‘Transpl = 2a ‘Skin and Soft tissues - renee 3A Hand and Neck as Adrenal gland. EE ES oS 252 ‘Thyroid os co 264 Parathyroid ee SRR : 300 Breast a ‘Thoracic Surgery 5s . 358 Vascular Surgery. 7 er) Esophagus. - a 404 Stomach . 443 ‘Small bowel . zl xo Appendix - cree SST Large bowel : sm Anorectal - erence 83 Liver . oxo Portal Hypertension . wees Biliary System no Pancreas _ sisi M Spleen = sso Hernia and abdominal w - erence BT Pediatrie Surgery soe Epidemiology and Ethie Se 2931 Approach sheet - 7 ne 939 ‘Tubes, Drains, and Catheters... onCell BiologyCELL BIOLOGY CELL CYCLE Cell Cycle (By order G1__| Determine cell cycle length, Most Vanable, Growin Hormones work here: 'S__| DNA replication/duplication, Protein Synthesis, RadioResistance (G2_[ DNA Stabiity (Repair Phase) ‘M__| Mitosis (Coll divsion), RadioSonsitive 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 © Gentriole: a specialized microtubule involved in cel! division CELL MEMBRANE Desmosomes > Cellular adhesion “Anchor” molecules “No communication’ ™ Tight junctions > impermeable barrier “No communication” Gap junctions (Most common type) > Allow call-cell communication (connexin subunits) ABO blood-type antigens: (glycoLipids on cell membrane) © Needed in Liver and Renal transplants ™ HLA-type antigens (glycoProteins on cell membrane} NUCLEUS, TRANSCRIPTION, AND TRANSLATION Steroid hormone > binds receptor in Gytoplasm, then enters nucieus = Thyroid hormone > binds receptor in NucleusCELLULAR METABOLISM ™ Giycolysis (Krebs cycle): 2 ATP and 2 pyruvate (from breakdown of 1 glucose} © NADH/FADH2 in mitochondria © 4 molecule of glucose produces 36 ATP | Gluconeoaenesis (Cori cycle): mechanism by lactic acid © Instarvation or stress © Liver converts muscle lactate into glucose (mediated by: pyruvate) Glucose > Lactate > Pyruvate > Glucose (aluconeogenesis) ™ Lactate level © Generated by conversion of Pyruvate Lactate by “Lactate dehydrogenase (LDH)” © Increased lactate level happened during anabolic metabolism © 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 © Serial Lactate level ‘Measurement of tissue perfusion and end-point resuscitation + Causes of } Lactate level: Bowel ischemia Renal failure DM Pancreatitis Malignancy Pheochromocytoma Infection PROTEIN SYNTHESIS: (Functional genomics) 1) Transcription: ‘By translation of DNA to > RNA Take place in: Ribosome © Introns are segments removed from DNA by 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 © Kinesin for movement away from centrosome © Dynein for movement toward it ™ Protein kinase C: activated by Ca and diacylglycerol (DAG) Protein kinase A‘: activated by CAMPDNA ENZYMES ™ Holicase: ‘© Unwinds DNA at replication point Topoisomerase: ‘© Create single or double-stranded break in the helix © Fluoroquinolones inhibits DNA gyrase (topoisomerase I!) ™ Polymerase: © Used for duplication of DNA/RNA + Elongates the strand = Replace RNAwith DNA ™ Ligase (© Catalyzes the formation of phosphodiester bond DNA MUTATION Point (Silent) mutation: Change base 1 Missense mutation: Change amino acid “SCD" Non-sense mutation: Stop Codon BLOTTING PROCEDURES = Southern blot: DNA = Northemblot RNA Western: ProteinOTHERS 25,000 genes found in the human genome Apoptosis accomplished by activation of Caspases Rough endoplasmic reticulum: Synthesizes proteins Smooth endoplasmic reticulum: Synthesizes lipid and steroids © Detoxifies drugs and poisoning © Contain G6P enzyme which convert G6P to glucose in gluconeogenesis © Sactoplasmic reticulum (subtype of smooth endoplasmic reticulum) Found in striated and smooth muscles IP3 generally + cytoplasmic calcium concentration Contains large store of calcium Malignant hyperthermia happens due to defect of sacroplasmic reticulumHematology and Blood Products Reviewed by: Dr. Salman Al-HarbiHEMATOLOGY AND BLOOD PRODUCTS History and physical examination are the best way to predict bleeding risk in normal people Safest blood group: O - All blood products carry the risk of HIV and viral hepatitis except: Albumin and Globulins ABO: glycolipid HLA: glycoprotein = Mechanism of coagulation: 4) Vascular vasoconstriction 2) Primary (Platelet adhesion) 3) Secondary (Coagulation cascade and thrombin generation) Starts when: Measured Exclusive inGiae pah ways) | Expoced colageriend ecioe val (79) Vil en Shy | TEE HE Factor 7) Er rei Oude vil trinsic pathway Best for iver synthetic function PY measures 1972: I Vil XX = Common pathway 0 Measured by PT & PTT oI V.X. Xill and fibrinogen (10 + 5—2 = 13) . © Antithrombin ill: Inhibits thrombin, 1X, X, X! ©. Protein C: (Vitamin K-dependent) * Degrades factors V, Vill, fibrinogen + Aciivaied protein C in sepsis: Fibrinolysis ‘+ Contraindicated to use in recent hemomhage © Plasmin: + Degrades V, Vill, fibrinogen, fibrin + Alpha-2 antipiasmin natural inhibitor of plasmin from endothelium Coagulation factors: (© Factors V and Vill (labile factors): Not found In stored blood ‘+ Factor V, Vill loss activity in blood but not in FFP ‘Factor Vili (Antichemophilic}: The only factor made by endothelium © Factor Vil: Shortest half life © Factor XI: Not found in eryoprecipitate © Factor Xill: Deficiency leads to delayed bleeding (Normal PT and PTT)Q; - Hemoglobin Association Curve Hb Curve | O2 binding pH K_[_W [23DPG | Temp co2 | Ca RIGHT SHIFTING J J (Acidosis) | | | 7. 1 1 t [ft LEFT SHIFTING t 1 (Alkalosis) | t | | 4 4 4 fe Causes of Left shifting Causes of Right shifting Causes of False High pulse oximetry Causes of False Low pulse oximetry ‘Carboxyhemogiobinemia Hemogiooin S (CO poising) Methemoglobinemia Methemogiobinemia (if Sa0,< 85%) (S00, > 85%) Skin pigmentation Dark tattoo or Henna (if Sa0, = 65%) Fetal Hb Pregnancy Stored blood ethylene blue (Associated with acidosis) Dark nail polish Hyperventilation ‘Anemia, Fever. Hypoxia ABP. ypotension ‘= Hypoventilation lead to right shifting by increasing the PacOz > Improve tissue Or uptake BLOOD TYPES: © Most common blood procuct 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 = Blood can be stored for maximum of 3 weeks © Maximum rate of blood transfusion to avoid citrate toxicity is 66.5 mL/minFresh Frozen DDAVP ‘ABOIRh Compatible | All groups Vasopressin is preferable acceptable analogue Life span:5=7days _| Life span: year atelets : FFP Crystalloids : RBCs Normal level of fibrinogen: 2 — 4 gid © Fibrinogen level's low in primary fibrinolysis and DIC. © Platelets count used to help to differentiate between them (Low in DIC) = Thrombolytic or Fibrinolytics: (+ Plasmin > Degrade the fibrin) ‘0 Tissue plasminogen activator (1PA) © Urokinase ® Anti. Thrombolytic or Anti- fibrinolytics: (| Plasmin > Increase fibrin level) © Tranexamic acid, Aprotinin © &-Aminocaproic acid: better than FFP in case of fibrinolytics reversal is needed © ‘as Post transurethral prolapse (Urokinase releasing)" © But FFP is better than e-Aminocaproic acid in case of fibrinolytics overdose to replace all coagulation factorsHEMOLYSIS REACTIONS | Most common cause of death ‘rom transfusion reaction’ Clerical error = Most common fatal infectious complication of blood transfusion: Viral hepatitis (HBV) Reaction Etiology Febrile Non-hemolytic transfusion reaction __| Most common transfusion reaction WA Due recipient antibody reaction against donor WBCs, (Donor WBC > Recipient antibody) ‘Acute hemolytic transfusion reaction ‘Due ABO incompatibility (Type Il hypersensitivity) © Tachycardia, Hypotension, Oligouria, no syncope © Associated with hemolysis (Dropped Hb) © Managed by stop transfusion and supportive measures Delayed hemolytic transfusion reaction Dus to HLAincompatibilty (7 ~10 days post-transfusion) Transfusion-elated acute lung injury (TRALI) | Most common cause of transfusion-related death aw Caused by donor antibodies to recipient's WECS (Donor antibody > Recipient WBC) #1 Capillary permeability Type and Screen: © Todetect ABO and Rh phenotype = Forward type: Antiserum against patient's ABO antigen Reverse type: Isoagglutinins in patient's serum Type and Cross (Cross-match): © Used before transfusion © By mixing recipient serum with donor lymphooytes (indirect Coombs tes!) Investigations for hemolysi © | Haptogiobin < 50 ma/dL. © 1 Free hemoglobin > 5 g/dL. © 1 Reticulocytes 7 Unconjugated bilirubin, and LDH in delayed reaction Methemoglobinemia Peripheral blood smear 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: ns: Replacement of 1 unit of total blood volume (One blood volume) within 24 hours Replacement of 50%% of total blood volume within 3 hours 210 units PRECs in 24 hours 2-10 units of stored blood over 4 6 hours 2 6 units PRBCs in 12 hours 24 units PRBCs int hour = Complications: © Hyperkalemia (Most common) = Due to lysis of stored blood (especially if > 21 days) ‘Thrombocytopenia (Coagulopathy) + Dilutional thrombocytopenia end coagulation factors deficiency Metabolic acidosis + Due to presence of lactic acid +The pH of unit of blood at time of collection is 7.10 when due to citric acid + Falls 0.1 pH unitiwaek due to production of lactic and pyruvic acids © Metabolic alkalosis = Due to citrate metabolism in the liver and conversion to bicarbonate Hypomagnesaemia © Hypocalcemia Poor clotting and persistent hypotension Rule for replacement in massive transtusior + 10 to 20 mL of 10% Ca gluconate IV for each 500 mL of blood infused or = 210 5 mL of 10% Ca chloride IV’ for each 500 mL of blood infusedBLEEDING DISORDERS Most common cause of surgical bleeding: Incomplete hemostasi Best assessment of bieeding disorders in normal people: History and examination Best assessment of clot strength: Thromboelastogram © Assess platelet function, clot strength, and fibrinolysis © Assess for defects in clotting factor (FFP, Cryoprecipitate, platelets, or tranexamic acid) ©. Used in liver transplantation, cardiac surgery, major obstetric surgery and trauma = Von Willebrand's disease ‘© Most common congenital bleeding disorder © Most common symptom: Epistaxis © Leads to: + Failure of platelets aggregation = | Gplb, ¢ BT (ristocetin test) 7 PTT o Twes: Type! Type Type Mostcomman = Most severe form ‘AD ‘AD AR Partial QuaNitative defidency ‘Qualitative deficiency ‘Complete deficency. DDAVP + DDAVP in mild form TWF & Factor 8 (Humate-P) Antifipnnolytic therapy (aminocaproic acid) VWF + Factor 8 (Humate-P) | Recombinant factor Vil VWF + Factor 8 (Humate-P) Used in refractory 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 avolded and used in life threatening situations where is no other treatment available (Large volume required in FFP, and + infections with Cryoprecioitate) § Hemophili © Sexlinked recessive, } PTT only © Most common symptom: Hemarthrosis © Types ‘= A(\VIll deficiency) factor 8 + B (IX deficiency) factor 9 “Christmas disease” = © (WX deficiency) factor 11 © Crosses placenta (newborns may not bleed at circumcision} © Target level pre-operatively = 30-40% for minor operations + > 50% for major operations or trauma > 80% for life-threatening bleecing int Factor VIII or IX = DDAVP with e-aminocarpoic acidm= Uremia (ESRD) | Platelets (1 bleeding time) with normal PT, PTT and fibrinogen © | Gplb | Gplibitlia | VWF = DIC: 6 Investigations: Fibrinolysis (| Fibrinogen | PT + PTT) + Fibrin split produots 1 D-dimer | Platelets © Management: = Hoparin-induced thrombocytope: Treat the cause wm ‘© Most common complication: Thrombosis (Not bleeding) Antiplatelet antibodies (IgG PF4 AB) > White clot Caused by UFH (Not related to the dose) or LMWH (Minimal risk) Detected on day 5-7 (life of platelets) 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 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 (Exereted by Liver) ‘© Dose: 2 meg/kgimin ‘+ Lepirudine: reversible direct thrombin inhibitor (Excreted by Kidney) ‘+ Hirudin: IRreversible direct thrombin inhibitor © From saliva of leeches, most potent direct inhibitor of thrombin Direct Factor Xa inhibitor ‘= Foncaparinux © VTE prophylactic dose: 2.5 mg SC OD © VTE therapeutic dose: 5 — 10 mg SC OD (No-FDA approved) Bernard Soulier: Gplb receptor deficiency ® Glanzmann’s thrombocytopenia: Gplib/lila receptor deficiencyANTICOAGULANTS: Mechanism Dose ‘Activates of AT Il (Augmentation) Inhibits X & 1 Prophylactic Dose: | Low-ri 5000 IU SC BID/TID | 12 - 24 hours Therapeutic Dose: | High-risk: 80 units/kg IV bolus | 48 ~ 72 hours Doesnt cross placental | Protamine sulfate (Used in pregnancy) Long term: ‘Osteoporosis, alopecia and thrombocytopenia Not preferred in case of liver disease (metabolized by liver) Use Ideal body weight (IBW) for obese patientsNOTES = Protamine sulfate © Indications and dosage: ‘= Heparin overdose (Consider t% of heparin: 60 - 90 min) ‘= 1—1.5mg per 100 U of heparin (Not exceeding 50 mg / day) ‘+ Half the dose if > 30 minute for last dose of heparin + Enoxaparin overdose © img /mg iflast 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% © Rout = Slow IV push over 10 minutes at least © Monitor: ‘+ PTT and anti Xa level after 4 hours, consider another dose if bleeding continue and PTT still prolonged © Side effect: = Allergy. hypotension, bradycardia, nausea and vomiting, flushing, teratogenic ™ Bridging: © Using of short-acting anticoagulant during interruption of warfarin when INR not in therapeutic range 4) 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 © Indication ‘Recent (within 30 days) myocardial infarction + Mechanical heart valves = Stroke + Pulmonary embolismHeparin does not work in Anti-Thrombin lil deficiency patients © IEDVT happens in heparinized -pationt > starts FFP then AT-lll then hepari | c-Aminocaproic acid “Procoagulant agents" (anti-ibrinalytics): Inhibits fibrinolysis by inhibiting plasmin ©. Used in thrombolytic overdoses (reversal of tPA and urokinase) | Compression devices: improve venous return, and induce fibrinolysis by release tPA = Used in moderate and high risk of DVT HYPERCOAGULABILITY DISORDERS Most common factor causing acquired hypercoagulability Smoking m= Factor V Leiden mutation © Most common congenital hynercoaqulabilty disorder © Causes resistance to activated protein C; the defect o Leads to inability to inactivate factor V on factor V | Anti-Phospholipid Antibody syndrome © Procoagulant (prolonged PTT but hypercoagulable) © Antibodies to cardiolipin and lupus anticoagulant * Carciclipin is mitochondrial membrane phospholipi § Homacysteinemia: Treated with folic acid, B12 ™ Virchow'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 © Toavoid 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 (humoral) © Produced by Bone marrow, Matured in Bone marrow ™ T cells (Thymus): Cell mediated immunity © Produced by Bone marrow, Matured in Thymus © Helper T cells (CD4) + Release IL-2 > cytotoxic T cells «Release IL-4 > B-cell maturation to plasma cells © Intradermal skin test (TB skin test): Used to test cell-mediated immunity MHC Classes: MHC class I © Single chain + 5 domains © €DB, on all nucleated cells © Cytotoxic T calls € Viral infection MHC class Il © 2Chains + 4 domains © CD4, on antigen-presenting cells only © Helper T cells € Bacterial infection NK cells lack self-MHC. ANTIBODIES ‘Antibody |__lom__| IgG ___| Most abundant antibody, Cross placenta, and Opsonin IgA | Produced by GIT (Peyer's patches), and breast milk IgE | Allergic reactions, parasite infections Igd__ [Membrane-bound receptor on 8 cells: VACCINES. 7 Diseases Live Attenuated Measles, Mumps, Rubella, Polo (Sabin), Yellow fever, Influenza Inactivated (kiled) | Cholera, Influenza, HAV, Polio (Salk), Rabies TToxcid Diphtheria, Tetanus ‘Subunit HBV. Pertussis, HPV Cojugate Hib, S. pneumonia ™ Vaccined: Patient received vaccine + immuned © Immuned: Patient received vaccine and antibodies titer to the immunity levelTETANUS ‘Tetanus prone wounds Non-Tetanus prone wounds doses and = 5 yoars None None 3 doses and > 5 years Ta. None 3dosesand> 10 years _| Td (1 dose) # TIG (Controversial) Te (1 dose) (Or immunocompromised <3 doses or unknown Td G doses] + TIG Td (3 doses) TIG: Tetanus immunoglobulin (Anti-toxin) ‘Td: Tetanus toxoid (Vaccine) ‘Tiap is preferred to Td for adult who never received Tdap" = Tetanus prone wounds: > 6 hours old >1 om depth Contamination (infected) Ischemia or devitalized tissue Burn = Doses: (© Tetanus toxoid: 0.5 ml intramuscular © Tetanus immune globulin: 250 units intramuscular © Vaccinatiot (0 Tetanus toxoid (vaccine) given at age of 2, 4, and 6 months © Booster doses of tetanus toxoid given at age of 1 and 5 years OTHERS ™ Surgical Histopathology specimens: © Fixed: (10% buffered formalin) + For all routine specimens (including lymph node) Paraffin: ft for fixed specimen (permanent section), for special stains Fresh: For aspirated fluid, any organ or lesion need to be in frozen section Frozen section allowed for rapid examination of section for immuno-histology and immuno-oncology, used for fresh unfixed specimenInfectionINFECTION Personal Protective Equipment (PPE) should be worn by all personnel for all pationts = Tobe worn in order: ‘© Shoe covers > Gowns > Mask > Goggles / Face shield > Head cover © Hand hygiene © Gloves = Tobe removed in order: © Shoe covers © Gloves ‘> Hand hygiene © Goggles /Face shield > Hand hygiene © Gowns > Hand hygiene © Mask (Lower part first) _ > Hand hygiene © Inside the room: Airbome transmission © Outside the room: Droplets transmission N95 mask should be worn for all airbome transmission ‘© Open pulmonary TB © Measles ©. Varicella o MERS Cov Ro-usod for 5 tim ;, but single use for MERS CoV = Hand rub (Alcohol) for 20 - 30 seconds = Hand wash (Water and Soap) for 40 ~ 60 seconds © Smomenis: © Before touching a patient © Before clean/aseptic procedure © After touching a patient © After touching patient surroundings ©. After body fluid exposure © Other indications: For soiled hand contamination After bathroom Before eating Clostridium difficileBACTERIA jon of Bacteria ‘Anaerob Cocsi Bacilli Clostridia spe. Gram + Gram= Gram Gram = Bacteroides Staphylococci ‘Gonococsi Diphtheria. E.Coli ‘Streptococci Meningococel Anthrax Klebsiella Pneumococci Neisseria Mycobacterium, Protous Enterococci ‘Salmonella (Ampicilin) (Gram +: Purple stain due to presence of peptidoglycan layer 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, ‘© Infection at the site of surgical incision within 1 month of operation or within 1 year of operation if foreign body implanted > 10° organisms is diagnostic for wound infection and burn wound infection © > 10° organisms is diagnostic for central line infection Most common nosocer infection overall: UTI © Most common nosocomial infection in surgical patient: Surgical site Infection © Most common organism: Staphylococcus aureus © Most common gram —ve organism: E. coli ‘© Most common anaerobes organism: Bacteroides ‘Staphylococcus ‘Most common cause of SSI overall Streptococcus ‘Most common cause of cellulitis postoperative > 24 hour ‘Most common cause of cellulitis postoperative < 24 hour (along with Costiidia) Most common causative organism of absoess ‘Most common causative organism of non-operative: cellulitis | Most common bacteria in the colon: Anaerabes ‘© Most common anaerobe in the colon: Bacteroides © Most common aerobic bactena in the colon: E. Coli ™ Leading cause of infectious death after surgery: Nosocomial pneumonia Decrease risk of wound infection by: Normal saline irrigation © Water irrigation used only in burn wound Remote infection (e.g. UTI) 1 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 © Most common early organism: S. aureus (GPC coagulase positive) © 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: © Pneumothorax and thrombosis FUNGAL INFECTION Indications for systemic anti-fungal therapy: © Candida endophthalmitis Osteomyelitis, Septic arthritis, Endocarditis Any patient with single positive blood culture Colonization from mutiple sites Candida isolated from surgical drain is not an indication as it due to colonization Options for anti-fungal ‘o Amphotericin B (associated with | K and | Mg) © Caspofungin © VoriconazoleNEGROTIZING SOFT TISSUE INFECTIONS Mortality ranges from 25% - 40% (higher in truncal and perineal) = Necrotizing myositis primarily involves the muscle but can spread to surrounding tissue as well Clinical Presentation: © Bullae, skin necrosis, crepitus, SIRS or Septic shock © Renal failure (| Na, | Cl) in advanced disease © Pain beyond the margins of erythema © Gas on imaging = Common sites: ‘© Genitalia, Perineum “Fournier's gangrene” (Colle's fascia prevent infection to reach) © Abdominal wall = Typos: (© Type 1: Polymicrobial (Commonest) Presented in immunocompromised patients (diabetes mellitus) ‘= Most common sites: Perineum, Trunk, OM foot, and Pressure sore Most common organisms: © Bacteroides and Streptococcus © Type 2: Monomicrobial ‘Presented in healthy patients with history of trauma, but more Aggressive + Most common sites: Extremities, and Trunk = Mest common organism: © Group A B-hemolytic Streptococci or Staphylococci (Exotoxin) © Clostridium perfringens (alpha toxin) “Most common organism” Gas-gangrene 3 Myonecrosis Large pleomorphic Gram-positive rods anaerobes © Type 3: ‘ V. vulnificus infection of traumatized skin in sea divers + Associated with severe infection (required Peniciliin G, Tetracycline, Ceftazidime) © Type 4: Fungal infection = Managemen © Early Surgical Debridement (definitive treatment) * Incisions should be made over involved skin parallel to neurovascular bundles + Neorotic tissue will appear dull, gray, and avascular with characteristic “murky dishwater” fluid + Revision surgery should be planned (“second look’) within 24 to 48 hours © Wantbiotics + Broad-spectrum antibiotics until culture results (Piperacilintazobactam, Carbapenem, and Ampicillin/sulbactam) Penicillin G (4 million units IV every 4 hours) + Clindamycin for Clostridium 3" Cephalosporin or Aminoglycoside (Gentarricin) for gram-negative Vancomycin for resistant Staphylococcus aureus (MRSA) Clindamycin or Linezolid 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: © Ascitic fluid total protein <1 g/dL (<10 giL) Serum total bilirubin > 25 mg/dL. Variceal hemorrhage Malnutrition Usage of PPI Cinical presentation: © Fever, abdominal pain, altered mental status © Associated with cirrhosis, and sometimes nephrotic syndrome © Investigation: ‘© Abdominal paracentesis = > 100 WBCs/mL. = PMNs > 250 cells/ml is diagnostic ‘+ PMNs > 500 more specific, but less sensitive compared to > 250 ‘Microbes with a single morphology on Gram’s stain Aerobic and anaerobic culture Albumin, protein, glucose, LDH, amylase, and bilirubin © Laboratory + Metabolic acidosis ‘+ Impaired renal function © Imaging Rule out secondary causes ‘+ Absence of pneumoperitoneum on an imaging study = Managemen ‘© 3 generation Cephalosporin, followed by Culture-based antibiotics for 2-3 weeks © Removal of indwelling devices © Prophylaxis antibiotics: Fluoroquinolones or Trimethoprim-sulfamethoxazole * Cofotaxime + Ceftriaxone used in advanced cirthosis or history of UGI bleeding + Ciprofloxacin used as secondary prophylaxis as weekly dose + Upper GI hemorrhage © Ascitc fluid total prot <1 gidL (s10 g/L) SECONDARY BACTERIAL PERITONITIS Due to intra-abdominal source (Transmucosal migration) © Usually due to perioration or severe inflammation ™ Polymicrobial (Bacteroides, E. Coli, and enterococous) = Treatment: © Surgical intervention and treat the sourceHEPATITIS Hepatitis B (DNA\ ‘© Most common hepatitis leads to HCC + Hepatitis B lead to HCC due to Cirthosis © Most common hepatitis related to blood transfusion © Can cause fulminant hepatic failure HBsAg | Anti-HBs [HBeAg | Anti-HBe | Anti-HBc ‘Acute HBV gM ‘Window : IgM ‘Chronic (high infectivity) |__« : lg ‘Chronic (low infectivity) . * 1g Recovery - . la immunized . ‘None Hepatitis C (RNA) © Most common hepatitis related to drug abuse © Most common hepatitis leads to Cirrhosis ‘Hepatitis C can lead to HCC without cirrhosis, © Most common hepatitis leading to Liver TXP = Hepatitis E: © Can cause hepatitis in pregnancy Most common involved organ: Stomach Most common cause for laparotomy in HIV patients: Opportunistic infections (CMV: © Most common intestinal manifestation of AIDS: CMV colitis Most common neoplasm in AIDS patients: Kaposi's sarcoma Most common cause of upper Gi bleeds: Kaposi's sarcoma Most common cause of lower Gl bleeds: CMV © CD4 (Normal > 800) © < 200 leads to development of opportunistic infections © Best for morbidity and prediction of immunity Viral load © Best for mortality and risk of transmissionOTHERS = Staphylococcus aureus produces exotoxins: hemolysin and leukocidin ™ Abscess that do not wait for fluctuation: © Hand infection © Parotid abscess © Breast abscess © Buttock abscess © Perianal abscess infective Endocarditis ‘© Most common involved native valve: Mitral © Most common involved prosthetic valve: Aortic © High-risk conditions (requiring prophylaxis) Prosthetic cardiac valve Previous infective endocarditis + Cyanotic congenital heart diseases © No longer recommended for antibiotics prophylaxis «Mitral valve prolapse + Rheumatic heart disease Congenital neart disease + Bicuspid valve disease Ludwig's angina: © Submandibular space infection (emergency situation) © Treatment: + Maintain airway, Antibiotics, Surgery + transection of mylohyoid TB ulcer: Apple jelly granulation = Smells of some organisms: ‘© Pseudomonas: Grape, sweet, frulty, tortilas or com chips to some people Escherichia coli: Floral or flowery odor Candida or Yeast: Bread baking or beer Proteus: Rancid or rotten chicken soup, chocolate cake or brownies Gram-negative anaerobes: Bac breath, moming breath, just smell bad Clostridium or gas-gangrene: Sweet odor (decayed apple) Bacteroides: Over ripe cheese odor™ Toxic shock syndrome: ‘Staphylococcus Streptococcus: Associated with: vated with: = Surgical site infection and wounds = Non-surgical cellulitis or surgical < 24 hours Abscess © Lymphanaitis (Red streaks, Lymphadenopathy) 1m Line infection Necrotizing fascitis GAS gangrene §_Community-acquired pneumonia High fever, hypotension and malaise are more Multiorgan failure ‘Associated with bacteremia, sore throat Early rash and desquamation after 2 weeks Rarely develop rash Penicilin G + Clindamycin Penicilin G « Clindemycin Nafcilin or oxacilin Vancomycin Vancomycin = Catidoghhuman bites (polymicrobial) © Staphylococcus aureus: most common organism in infected human bite wound © Eikenolla: most common organism cultured specifically from human bite wounds © Pasteurella multocida: most common found in cat and dog bites ™ Snake Bite: ‘© Snake venom is 90% protein + Enzymes (Phospholipase A, Procoagulant enzymes) ‘+ Non-enzymatic polypeptide toxins + Non-toxic proteins ©. Presentation: = Local: pain, swelling, tenderness, enlarged lymph nodes, bleeding, or necrosis * General ‘+ Nausea, vomiting, weakness Cardiovascular: Dizziness, hypotension, arrhythmia Bleeding (Epistaxis, gums, intracranial bleeding, Gl bleeding) Neurological (Paraesthesia, ptosis, numbness, paralysis) ‘Musculoskeletal (Stifiness, Myogiobinuria, hyperkalemia, cardiac arrest) Renal (Loin pain, hematouria, myoglobinuria, uremia} Endocrine (adrenal insufficiency. hypothyroidism. hypopituitarism) © Management: ‘+ First-aid treatment and transport to hospital (ABCDE} Traditional treatment proven to be useless (iocal incision/prioks, 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 (Immunoglobulin 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 2° dose indicated if bleeding, neurotoxic or cardiovascular signs persists after 1—2 hoursNEEDLE-STICK INJURIES m= Types: (© Percutaneous injury (e.g. needle stick or cut with a sharp object © 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 © Risk: * 0.3% for percutaneous exposure 0.09% for mucous membrane exposure © Post-exposute medications: Tenofovir-emtricitabine + raltegravir (or dolutegravir) = HBV © Patient: ‘+ HBsAg and HBeAg +ve: 37 - 62% «HBsAg 4ve only: 23-37% = Nonimmunized is 6 - 24% © Post-exposure medications: Hoalth-Care Provider | Poat-exposure investigation | Postexposure prophylaxis Postvaccination (HCP) serology Pationt HCP HEIG Vaccine (HBsAg) (Anti-HBs) Vaccine responder (antHBs > 10 mii No action noeded after 3~ 6 HB vaccines) Posiivel zs doses No No Vaccine non-responder | Unknown Separated by 1 (anti Bs < 10 mln. month after 3-6 HB vaccines) Negative No action needed Pasiival =O IU | Tae Ravaccination Yer ke je unknown [Unknown response is unknown | Negative <19 miUimL | None Revaccination ‘Yes ‘Any. 310 miUimL | No action neaded No Positive! : 1 dose ‘Complete vaccination Yes Unvaceinated | Unknown Negative = None Complete vaccination Yes = HcV © Risk: 1.8% (Much less than HBV) © Post-exposure medications: No effective medicationsAntibioticsANTIBIOTICS MECHANISM OF ACTION © Inhibitors of cell wall synthesis: © Penicillin, Cephalosporins, Carbapenems, Vancomycin Inhibitors of 30s ribosome: ‘0 Aminoglycosides, Tetracycline Inhibitors of 50s ribosome. ‘© Clindamycin, Linezolid, Macrolide Inhibitor of DNA avrase (Topoisomerase Il): © Fluoroquinolones Inhibitor of RNA polymerase: © Rifampcin Produces oxygen free radicals (to damage DNA): © Metronidazole Inhibitor of DihydroF oiate Reductase (inhibits purine synthesis): © Trimethoprim, Bacteriostatic antibiotics: Tetracycline, Clindamycin, Erythromycin Bactericidal antibiotics: Aminoglycosides and Fiuoroquinolones MECHANISM OF ANTIBIOTIC RESISTANCE Most common method of antibiotic resistance: 0 Transfer of plasmids (penicillin resistance) ™ Aminoglycosides: Decrease in active transport 1 MRSA/ VRE: Mutation of cell wall binding protein ANTIBIOTICS COVERAGE Gram Positive Gram Negative ‘Anaerobes: MRSA | MSSA | Streptococci | E. Coli, Klebsiella | Pseudomon: Penicillin Metronidazole “Amoxyeilin Clindamyein. Clindamycin. ‘Vancomycin, Linezolid, Daptomycin Ciprofloxacin ‘Gentamicin Cefuroxime “Amoxyellin/Glavuianate ‘Amoxyelin/Glavulanaie: Piperacillin/Tazobectam Meropenema and ImipenemINHIBIT CLASIFICATION I ANTIBIOTICS Pericinillese ~ Sensible Natural Penicilins | PenicilinG: Na, K, Procainic,Benzathine (WV, IM) (oarowssecren| _ | PenicilinV: VO "Aminopenicilins | Ampicilin (erosdspecrum) | Amoxicilin Penicinilase ~ Resistant (ery narrow spec) Penicilins Wain | Oaacilin | _‘Didoxacilin ‘Aniipseudomonal(extnded peta) Tcarcilin cell Carboxipenicitine | Carbericilin Piperailin sil Ureidopenizlins | Azlodlin . Meziocilin ¥ Generation | Cefarolin | Cepholexine | Cephapivin S| eee Cefadroxt | Cephadnine | Cephalotin © lies Cefuroxime | Cefamandole | Cefprosil i 2 Generation [cefoxitin | Cefoniid Cefmerarsle : Cofotetan | Cefaclor . Cephalosporine Cefoperarone | Ceftriaxone | Ceftatime i 3*Generation | Cefpodosime | Ceftizoxime | Cefotaxime i Cefdinie Ceftbuten | Cefbime ‘Cefditoren F Generation | Cefepime Cefpirome * ‘7 Generation | Ceftarline Carbapenems Meropenem | Ertapenem | Ooripenem | imipenem + Cylastatine Monobactams | Ratreonam sf Betorlectomese in| Sulbactam Tazobactam ClavulanicAeid Wo ‘lycopeptides Vancomycin Bacitracin lactam “Ticopl Polyeryxin & “nino ‘Gentaryein Neomycin Sureptomyain 305 | olycosides ‘Amikacin Tobramycin Tetrecyelins Doxycycline Demecdocylin = Minocyaine Tetracycin Tigecycln Protein Oxazalidonones | Unezokd Synthesis ‘Streptogramins | Quinupristin/Dalfopristin $05 cleramphenicol Macroldes Erythromycin [azithromycin [Clarithromycin Uncosemides Clindamycin Lincomyein DNA | Fluorquinolones Gprofiexscin | Norfioxecin | _Levofloxacn | Offoxacin topoisomerases Sparfloracin | Morifloxacin | Gemifloacin | Enofloxacin ‘Quinolones Nalidxi Ad Folie Al Sulfonamides Sulfamethorazole | Ag Sulfadiazine | Sulfasalazine | Sulfisoxazole Synthesis (NX) DHFR Iaibiters “Trimethoprim (TMP) Pirymethamine ‘DWA (damage) | Metronidazole ‘mRNA synth. | RifampinCOMMONLY USED ANTIBIOTICS IN SURGERY Disease “Antibiotic / Dose ‘Side-effect /Notes Boat for SSI prophylaxis Mild DM foot infection Cefazolin (7 Cophalosporins) 2a Nazar Longest half-life ‘Skin, Bone infection Post-operative infection Cefuroxime (2° Cephalosporins) 500 mg PO q12h 150 mg or 1.5 1V o8h Diarhea Nophrotoxicity Community Biliary nt Primary Peiitoritis, Ceftriaxone (3° Cephalosparins) tglVq2an Gholestaticjaundice Gallbladder siudging SSI prophyaxis Biliary infoctions jeracillinitazobectam (Tazocin) Inhibits platolots (Acute cholecystitis) 3.37 g IV g6n Pow al Pancreatitis + sepsis Polybacterial necrotizing fasciitis Severe diverticullis Severe DM foo! infection, 4.5 9 IV (in severe infection} PCN allergy: Cefepime 1 IV q8h or Ciprofloxacin + Metronidazole Mild diverticulitis or collultis ‘Abscess ‘Amoxaicilliniclavulanate 675 mg PO qi2h Or Geftriaxone + Metronidazole Mild CDF infection Metronidazole 500 - 1000 mg IV qh Peripheral neuropathy Abscess, anaerobic infections + Cefazolin PON allergy: Prophylaxis for colorectal surgery Gentamicin instead of cefazolin PCN-allergio SSI prophylaxis for | Vancomycin HTN, Rodman syndrome (hemia and breast) (histamine release) if not given ‘Moderate CDF infection 125mg PO qéh slowly Sovoro CDF infection 500 mg PO qéh MRSA skin/subcutaneous infection 30 mghkg/day IV (divided to 12h) H_Pyioni infection “Amoxacillin 1g PO q12h Clarithromycin 500 mg PO q12h Omeprazole 40 mg PO qin PCN allenay: Metronidazole instead of ‘Amoxacilin Monabacterial necrolizing fascitis Mild DM foot infection PCN-alleraic cellulitis PCN-allergic SSI prophylaxis, Clindamyein 600 mg IV 8h Pseudomembranous collie ‘Skin or intra-abdominal infecions ‘Severe DM foo! infection Ciprofloxacin + Clindamycin 500 - 750 mg PO q12h 400 mg IV qi2h Tendon ruplure Bacterial sepiicemia Necrotizing pancreatitis, imipenem 500 - 1000 mg IV gan Seizures (also Mepridine) + cilastatin (fo prevent renal hydrolysis) Intra-abdominal infection Muti-ciug resistance line Load: 100 mg IV then 50 mg IV q12, Load: 5 mgikg IV then 2.5 mg/kg IV q12 Nephrotoxicity MRSA, VRSA Complicated skin infection Nosocomial Pnoumonia jezolid 600 mg IV/PO q 12h Should not be Tantibiotes ‘Should be combined with other = BM suppression Prokinetic (stomach clearance) | Erythromycin 50-100 mg PO qh 400 mg IV gh ‘Severe UTT ‘Gentamicin Decrease biliary concentration Skin, bona infection Intra-atsdominal infection Bacteria septicemia 4- Smglkg/day IN/IM divided q&hr Nephroioxicity Ototoxicity ‘Gram — septicemia UTI, skin infection Bactrim (Tri/Sulf) 10 — 16 mg/kgiday divided a8h Erythema multifomm, Teratogenic, NephrotoxicityPENICILLIN ALLERGY Most common medication allergy = Penicillin by itself is not allergen, and allergy from complex break-down = Twes: Immediate Thour ofadministration (up to 6 hours) ~ Re-exposure associated with life-threatening anaphylaxis = But IgE antioodies sensitivity decreased overtime = 50% of patients lost sensitivity after § years from last reaction days of administration (classically aiter 6 hours) Presentation Pruritus, urticaria, angioedema, fushing, laryngeal edema, and hypotension Most common allergic: Delayed cutaneous reactions (Meculopapular cutanoous rach and eruption) Pathogenesis Wediated by IgE (Type | hypersensitivity) Mediated by T Cells (Type IV hypersensitivity] 9 Positive skin tast have § - 10% cross-reaction to 9 By given 1%, than 10%, then 100% of dose at 30 = Penicilin skin test for Positive features of past immediate reaction cephalosporins ~ Grailed challenge (test dosing): for patents believed to be non-allergic ‘min intorval Management = Avoidance of all Peni = Caution use of other Beta-lactam antbiotics: Carbapenem Cephalosporins (due to cross reaction) - Desensitization: by starting with 1/1000 to 1/100 dilution Discentinue, Cutaneous reactions usually resolve within 1-2 weeks after discontinue Antihistamines: if associated with prurite component of the drug Glucocorticoids: for severe 2 Used in pationt with immediate allergy andno | eruptions, no response to accepiable allemate aniibiotics antihistamines © Alternative proohylactic antibiotics: © Non-severe allergy: (Non-type | hypersensitivity) * Cefazolin: used for prophylaxis of most general surgery procedures + Ceftriaxone: used for prophylaxis of hepatobiliary surgery (less cross-sensitivty) © Severe allerg (Type | hypersensitivity)) Gentamicin: prophylaxis of Colorectal surgery ‘Clindamycin + Gentamicin: used for prophylaxis of most surgical procedures Fluoroquinolanes (Cipro): prophylaxis of Gastroduodenal, Biliary surgery ‘Vancomycin: used for prophylaxis of breast, hernia, and vascular procedures ‘+ Ifallergic 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 - BW) ©. Used for all medications (including antibiotics, anticoagulants and analgesia) Maintain glucose level by: Decrease length of antibiotics Side effects of antituberculosis drugs © Isoniazid: Hepatotoxicity, B6 deficiency © Ritampin: Hepatotoxicity and GIT symptoms © Pyrazinamide: Hepatotoxicity © Ethambutol: Retrobubar neuritis Drugs to avoid in Pregnancy: (M-CAT) Metronidazole © Ciprofloxacin © Aminolycosides © Tetracyelin Antibiotics used to treat UTI: (© Best: Ciprofloxacin 500 mg PO q 12 hours for 1 week © 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 antibioti (Gram +ve) (Gram—ve} BetaLaciam Piperacillin and tazobactam Piperacillin and tazobactam Ceftaroline (5" cephalosporin) Cefepime (48 cephalosporin’ = ‘Ceftazidime [3% cephalosporin) - Meropenem / imipenem Fiuoroquinoiones = Ciprofloxacin ‘Aminoglycosides (Anti - Gentamicin 30S) Tetracyelines (Anti30S) | Doxyeyeline Doxyeyeline Minooyctine Minocyoline eye ‘Others Trimethoprimisultamethoxazole Trimethoprim/sulfamethoxazole Vancomycin (Glycopeptide) Colistin Linezolid (Oxazolidinone “Anti 50S") | Acetic acid Clindamyein (Lincosamides “Anti 508") DaptomycinFluids and Electrolytes Reviewed by: Dr. Haytham AlartajFLUIDS AND ELECTROLYTES Body is made of 42 L water (28L intracellular, 14L extracellular) @ Fluid compartments. © Intra-cellular: 40% of body weight and 70% of body water “100kg x 0.07 = 7 L of water” * Crystalloids can increases intra-cellular compartment 75% (25% intravascular) © Extra-callular: 20% of body weight and 30% of body water + Interstitial: 2/3 of extra-cellular compartment + Intra-vaseular (plasma): 1/3 of extra-cellular compartment © Colloids (including blood) can increases intra-vascular compartment 100% = Trans-collular © CSF, Pleural fluid, Synovial fluid, Peritoneal fluid Athlete male need more fluid maintenance than obese male Major Cation/Anions Cation (+) [Anion (=) Extra-Cellular Na cl Intra-Cellular K POs ™ Eluid spacing: © 1* spacing: intracellular and extracellular fluid compartments © 2 spacing: excess accumulation of fluid in interstitial spaces (edema) © 3 gpacing: accumulation of fluid in “no fluid’ areas such as ascites, and in bums A sudden weight gain or loss is best indicator of fluid status= Osmolarity © Number of solute per solution (mOsmol/Liter) © Volume of plasma including volume of solutes o Examples: + Hypotonic solution (0.45% NS, 0.33% NS) decreases osmolarity + Hypertonic solution (D5 ¥% NS, D5 NS, D5 RL) increases osmolarity = Osmolality © Number of solute per solvent (mOsmol/Kg) © Weight of the plasma without solutes © The principal determinants of osmolality are the concentrations of sodium, glucose, and urea that dissolved in the fluid © Determined by (Albumin and Na) + Proteins: determine plasmalinterstitial osmotic pressures Na: determines intracellulariextracellular osmotic pressure ‘+ Aypernatremia: | Extracellular fluid volume as in dehydration, DI + Hyponatremia: | Extracellular fluid space as in over-hydration, SIADH ™ Pressures © Colloid osmotic “Oncotic” pressure (Pulling force) = Intravascular > Interstitial tissue = Determined by Proteins Decreased in hypoalbuminemia leads to tissue edema ‘Highest in Capillary (Venous) Oncotic pressure 25 mm Hg > Hydrostatic pressure 18 mm Hg © Hydrostatic pressure (Pushing force) Interstitial > intravascular ‘+ Highest in Capillaries (Arterial) Hydrostatic pressure 35 mm Hg > Oncotic pressure 26 mm HgIV FLUIDS Highest temperature for IV fluids should be < 65 degree centigrade © Crystalloids: 6 75% ll distribute into extracellular (interstitial compartment) © Only 25% will stay intravascular due to Hydrostatic pressure > Oncotic pressure © Hypotonic solution (Dextrose 5%) distribute into intracellular 0.9% Normal Saline Ringer Lactate Na 164 and C1154 Na 130 C1109 K 4 Ca 3 Lactate 28 Hyperosmolar, isotonic pH 5.5 Hypoosmolar, isotonic, pH 6.5 ‘Osmolarity = 308 ‘Osmolarity = 270 Most Acidic solution Leads to Hyperchloremic metabolic Acidosis Leads 10 > Apoptosis & inflammatory response > Metabolic Alkalosis. Ringer lactate metabolized by liver to sodium bicarbonate > metabolic acidosis in liver failure Usedinz Dehydration (vomit ee diarrhea) Trauma with heat Instead use hypertonic satine Used in: Post-operative Day 0 Bum and Trauma Pancreatic and biliary loss Enterocutanous fistula, Diarrhea CDF-diarrhea (it will not cause acidosis) ~ NS preferred over LR when blood is being transfused simultaneously ‘because citrate can lead to calcium precipitate (nypocalcemia) and coagulopathy’ ~ LR preferred over NS during initial resuscitation (| Metabolic acidosis) = LR should not be infused through same IV line during blood transfusion Balanced crystalloids (Chloride level < 110): showed no | mortality or risk of AKI D5 %NS + 20 KCI: Used in 1* day post-operative, and Pyloric stenosis Addition of dextrose > Stimulate insulin release = Colloids: © Increases intravascular volume (70% will stay intravascular] © Albumin: Can leads to pulmonary edema ©. Starch: Inhibits platelets and decreases vWF > Coagulopathy, and renal failureESTIMATES OF VOLUME REPLACEMENT Dehydration physiology: Hypotonic fiuid loss > 1 Serum osmolality Stimulation of ADH, Renin, and Angiotensin Inhibit ANP (Atrial natriuretic peptide) Resulting in: + Vasoconstriction + Salt and water retention = [Urine volume, | Na excretion, + Osmolality Increased extra-cellular space is a sign of over-hydration (due to } Na excretion) ™ Lactate: © Indicator of adequate resuscitation in trauma © Indicator for tissue perfusion { ischemia (if still high > 24 hours PCWP) '™ _UOP: Best indicator of adequate volume replacement © End-Point of resuscitation: Base-deficit (indirect measure of COP and 02) ™ Insensible fluid losses: 10 ccika/day: 75% skin, 25% respiratory (around 600 ml) © Average stool loss = 250 mi of water = During open abdominal operations, Fluid loss is: 0.5-1.0 L/hour = GIT fluid secretion: © Stomach 1-2 Liday * Gastric juice: Na 60 Cl 110 © Biliary system, Pancreas, and duodenum: 500—1,000 mLiday Gif electrolyte losses: © Saliva: K* (highest concentration of Kin body} © Stomach: H* and CI © Penereas and bile: HCOS- © Large intestine: K* © Sweat: hypotonic (Na concentration 35 ~ 65) ™ Changes with age: © 1 Residual volume © 1ADH © {AldosteroneELECTROLYTES IMBALANCE Clinical presentation 1K {Na 1 POs General signs Bradycardia Arrhythy Hypertension Confusion “Tachycardia Orthosiatic Bradycardia Arrhythmia Seizures, Hypertension Arrhythmia Musculoskeletal | Deep tendon reflexes Muscle weakness: ‘Weakness, fatigue Muscle spasm | Deep tendon reflexes 7 Deep tendon refles Perioral aurbness Fingertips, toes tingling Carpopedal spasm Tetany, Convulsions 7 Deep tendon reflexes Tetany Metabolc alkalosis Respiratory alkalosis| (Hyporvontilation) ECG Flat / inverted T Uwaves Protong QT Prolong QT. Tall T wave ‘Associated with ‘Constipation Polyuria Polydipsia Enterocutanous fistula, Diarthea Cerebral edema Oliguia TURB procedure Diarthea Refeeding syndrome Hyperglycemia ‘Constipation lleusPOTASSIUM (Normal 3.5 - 5) Daily K requirements: 3500 ~ 4700 mg (0.5 4.0 mEq/kg/day) ™ Usual recommendation rate of lV K replacement: 10 - 20 mEq/ hour HYPERKALEMIA = Causes: Excess release from cells | Decreased elimination Medications ‘Others Blood transfusion Renal failure NSAIDs Rhabdomyolysis idosteron K-Sparing diuretics Tumor lysis syndrome. ™ Addison's ‘ACE! Metabolic acidosis, ™ Congenital adrenal | Digoxin (through exchange of H” with K) hyperplasia Hemolysis Bota blockers ™ Management: © <6.5 maqi = 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, © 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 furosemide 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. © Hyperkalemia and ECG changes © Potassium level > 6.5107 meq/L 1) Ga gluconate © Aginfused over 2 - 3 minutes © Rule of 10: 10 mL of 10% solution over 10 minutes = Followed by continues calcium infusion as 0.3 - 2 mg/kg/hr Calcium gluconate (membrane stabilizer for heart) without reduction of serum K level Ca Chloride need central line (thrombophlebitis) Cardiac monitor 2) Insulin with glucose: © 10 units of regular insulin in 500 mL of D10, given over 60 minutes © 10 units of regular insulin, followed by 50 mL of D50 (25 g of glucose) © Greater reduction, but more risk of hypoglycemia © Insulin should be given alone if the serum glucose is 250 mg/dL. © Close monitoring of blood glucose 3) B2 agonists: © Salbutamol (Albuterol) 10 to 20 mg in 4 mL of saline by nebulization over 10 minutesHYPOKALEMIA = Causes: Increased losse: los: ‘Others Vorniting juretios Thadequate intake Diarrhea Aldosterone level. Low Mg level Cushing's (due to concurrent loss) m_Conn’s Excess sweating Hypothermia © Clinical presentatior © Muscle weakness © Nephropathy © Glucose intolerance © Metabolic alkalo: © by Increased excretion of K with HCO3 = by increased exchange of K with H* © ECG changes: U waves, Depress ST wave = Management: © Correct the Mg first 3.0 to 3.4 meq/L: © Orally KCI 10 to 20 meq 2 - 4 times/day (20 to 80 meqiday) © <2.5-3 meqiL or Symptomatic © Orally KCI PO 40 meq 3 - 4 times/day © IVKC120 meg in 200 mL of NaCl over 2 hours + Rate should not exceed 10 meq/hr (peripheral line > phiebitis) © Potassium-sparing diuretics used in potassium wasting patients © Cardiac monitor © Use HCOs in case of metabolic acidosisSODIUM © Dail (Normal 135 - 145) ly Na requirement: 4 ~ 2 mEq/kglday Avoid Na in Cirrhosis (Sodium retention by the kidney increases the ascites) HYPERNATREMIA = Causes: Water loss Urinary loss: High volume On ‘Skin losses, ‘Osmotic dieuresis | Hypertonic saline | Restrict water intake Gastrointestinal losses | Diabetes insipidus Salt poisoning Post-operative (due to transient increase in ADH) Raute tubular necro: [Aldosterone level ™ Cushing's '§_Conn’s ™ Management NaC! to correct High Na slowly to avoid cerebral edema = Restrict water intake (| UOP) + Osmotic dieuresis (t UOP) © DDAVP for Central Diabetes insipidus Froe water for hypovolemic patient with urine osmolarity > 800 Treat the underlying cause for Nephrogenic Diabetes insipidusHYPONATREMIA, Assessment: 1) Serum Osmolality ‘+ Isotonic (280 - 295 mOsm/kg) “Pseudohyponatremia” > Hyperprotienemia / Hyperlipidemia + Hypertonic (> 295 mOsmikg) > Hyperglycemia / Mannitol / Radiocontrast agont + Hypotonic (< 280 mOsm/kg) 2) Volume status (Used for hypotonic osmolality) + Hypovolemic © Urine Na > 20 % Renal causes (Diuretics, ACEI, Nephropathy) © Urine Na < 20 % Extra-renal (lleostomy, Dehydration, Vomiting, Diarrhea) + Euvolemic © SIADH, Glucocorticosteroid deficiency © Diuretics, Hypothyroidism, Postoperative, Polydipsia + Hypervolemic © Urine Na > 20 mEq/L > Renal failure © Urine Na < 20 mEq/L > Heart failure, Cirrhosis, Nephrotic syndrome = Managemen © Cortect Low Na slowly to avoid central pontine myelinosis (no more than 1 mEq/h) © NaCl or 3% NaCl © Fluid restriction if 1 ADH DIFFERENCES BETWEEN SIADH AND DI: ‘ADH ‘Serum Na | Urine Na | Urine Gravity] Management Watkin CT. | Osmolality | Osmolality ‘SIADH i T 7 Fluid restriction |. UOP) Li Diabetes insipidus Y 1 Y DS Water (OP) t DDAVP. ADH. Lung cancer. meningitis, infection, Drugs: ciprofloxacin, oxytocin SIADH differentiated from adrenal insufficiency by | KCALCIUM HYPERCALCEMIA. ™ Causes, Hyperparathyroidism PTH Sarcoidosis Neoplasm ‘= Lymphoma 1 PTH Drug-induced (e.g, lithum: Osteolytic malignancy ‘Most common cause of hypercalcemia Hyperparathyroidism Most common cause of out-patient | Ca Hyperparathyroidism_ ‘Most common cause of in-patient | Ca Osteolytic malignancy ‘Most common cause of hypercalcemia crisis. Metastatic Malignancy ‘Most common malignant cause of hypercaloemia Breast cancer Most common mortality risk of hypercalcemia in SCLC = Treatment: © >14 mg/dL (3.5 mmol/L): IV Normal saline NaCl 200 to 300 mLhour and maintain urine output at 100 to 150 mL/hour © Fursomide 40 mg over 2 hour © IVBisphosphonate / Calcitonin’hydrocortisone Both are used in malignancy or severe acute = Inhibits osteoclastic bone resorption © Dialysis = No lactated Ringer's or thiazide diuretics in HypercalcemiaHYPOCALCEMIA ™ Localized numbness / tingling in hypocalcemia due to: © Peripheral vasoconstriction > Decreasing the action potential of the digits due to decreasing the threshold > Perioral numbness and digits tingling ™ Localized numbness /tingling in local anesthesia toxicity due to: ‘© High concentration of local anesthesia in highly vascular tissue on free nerve endings m= Signs: © Chvostek’s sign: ‘Ipsilateral facial twitching ‘+ Induced by tapping at point 1 cm anterior to ear (tragus) and 2 cm below zygomatic bone © Trousseau’s sign: + Carpal spasm due to neuromuscular excitability + 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: aii Hypoparathyroidiem Abnormal Mg+ ‘Chronic renal failure (Uremia) ETE Liver disease (1 Vitamin D) Pancreatitis Variable Rhabdomyolysis Tumor lysis syndrome ‘Hyperventilation > Respiratory alkalosis. 2 Increase calcium-albumin binding (redistribution) Respiratory alkalosis ™ Management © ECG + Check Mg level © Check Albumin level © Oral Calcium carbonate 1250 mg PO TID + Non-symptomatic patient with Calcium > & mg/dl © Oral Calcium carbonate 2500 mg PO TID ‘Mild Symptomatic or Calcium < 8 mg/dL. © IV Galcium gluconate 2 g IV over 1 h infusion * Severe Symptomatic (Seizure, tetany, stridor, laryngospasm) = Calcium <4 mg/dLPHOSPHOROUS HYPERPHOSPHATEMIA ™ Cause: © Low Urine PO4 < 1500: + Renal failure (Most common cause) > High anion gap metabolic acidosis + (PTH © High Urine PO4 > 1500: = Rhabdomyolysis, = Tumor lysis syndrome ™ Management © IVNaCI+Acetazolamide © Dialysis in renal failure © P04 binder (in chronic): Sucralfate HYPOPHOSPHATEMIA ™ Causes: © Refeeding syndrome (Most common cause} © 1PTH © | Vitamin D © | Calevel Glloss Rhabdomyolysis = Consequence: © Prolong Ventilation © Hyperglycemia ™ Management: ‘© For Phosphorous level <0.5 mg/dL: 0.5 mmol/kg IV’ infused aver 4-6 hr © For Phosphorous lo 1.0.5-1 mgldL: 0.25 mmol/kg IV infused over 4-6 hrMAGNESIUM HYPERMAGNESEMIA ™ Cause: DKA PTH Addison Renal failure TPN = Management: © Stop magnesium, ECG © calcium chloride or gluconate HYPOMAGNESEMIA = Causes: ‘© Most common cause of in-patient: Diuretics (Thiazide, Amphotericin B) © Most common cause of out-patient: Alcoholism © Most commonly associated with: + Dietary deficiency, Gl loss, DKA, | K | POs | Ca, Hypothyroidism = Management: © Unstable (arshytmia) > 1 - 2 g MgSO4 over 2 - 15 minutes © Stable (symptomatic) + Severe <1 mgidi or 0.4 mmol/L or 0.8 meqiL: 4-2. MgSO4 in 50 to 100 ml of DSW over 1 hour followed by infusion of 4 - 8g MgSO4 over 12 to 24 hours ‘= Mild > 1 mo/al or 0.4 mmol/L oF 0.8 meqyL: Mg Oxide 400mg every 12 hoursABG = Normal lovel: 0 pH: 7.35 ~ 7.45 © HCOS: 22 - 26 © PaCO2: 35 ~ 45 ™ Calculation © Respiratory: | pH: t Paco2 © Metabolic: | pH : | HCO3 METABOLIC ACIDOSIS Most common acid-base disorder (| pH with | HCO3 or 1 H+) = High anion gan acidosis: DKA. 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 © Drugs associated with normal anion gap acidosis: Spironolactone & Lactulose METABOLIC ALKALOSIS © Due to: o LHe © 7 HCO3 (Caused by citrate in massive blood transfusion) © Contraction alkalosis (Most common) * Byiindirect gaining of HCO3 through loss of HCO3-free water + As diuretics or GI losses guided by Aldosterone which leads to ‘+ Reabsorption of Na, Water, and HCO = Excretion of K and H+ + Most potent stimulator for aldosterone release in injured patient. ACTH Followed by: Extracellular fluid K © Nasogastric suction, Voriting and Gastric fistula results in: = Hypochloremic, Hypokalemic, Metabolic alkalosis, and paradoxical aciduria ‘+ Stomach losses H+ and Cl > Hypochloremic metabolic alkalosis ‘© Due to high loss of H+ and Cl with obstructed pylorus + Kidney excrete NaHCO: (Alkali) to compensate alkalosis + Kidney compensate Na losses by reabsorption of Na and excretion of K and H+ > Hypokalemic aciduria + Paradoxical aciduria: © 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 © Normal level: (-2) ~ (+2) © Base excess: > +2 © Amount of acid required to restore 1 liter of blood to normal pH 7.4 © Metabolic alkalosis BASE DEFICIT © Base deficit: <-2 © Amount of alkali required to restore 1 liter of blood to normal pH 7.4 © Metabolic acid: SUMMARY OF THE CAUSES OF ACID-BASE IMBALANCE Renal failure, Uremia ‘Small bowel and duodenal fistulas (1 P04) DKA. output Pancreatic fistula Ileostomy Isoniazid Normal saline Lactic acidosis Severe diarthea Late NSAIDs Late sepsis Addison's (1 K) Alcohol PTH Drug Lactulose, Spironolactone Respiratory acidosis | Hypoventilation fi ion (Respiratory rate x Tidal volurn CNS depressionDIURETICS | Aldesterone 1 “Antagonist | i Spironolacton { m Aniloride @ PTH Proximal Tubule Proximal Mid Osmotic diuretics > Enter K > Exit Na, Cl Distal tubules (Reduce absorption of Mannitol m Acetazolamide Nal20) | Des water) "Aldosterone Antagonist Osmotic diuresis (Mannitol) i K® sparing diurcties Loop diuretics are contraindicated in rhabdomyolysis, Acetazolamide: | K, Metabolic acidosis Furosemide: | K, Ototoxic, Nephrotoxic Thiazide: | K, Metabolic alkalosis (Contraindicated in t Ca or | Na} Spironolactone: + K, Metabolic acidosis CONTRAST-INDUCED NEPHROPATHY © Increase of serum creatinine 25% from baseline after contrast given within 48 ~ 72 hours © IV fluid with NS started 6 - 12 hours pre-procedure and continue for 24 hours post-procedure atrate 1 - 1.5 mi/kg/hour (Most effective method) © N-Acetyleystein: 1200 mg twice daily pre-procedure and the day of procedure © Low cost, no adverse effect and potential beneficial effects Use iodixanol (iso-osmolal), low-osmolal contrast, or non-ionic contrast Sodium bicarbonate Avoid diuretics Renabreplacement therapyEQUATIONS a toe Plasma osmolarity 2Na 7 Glugese + BUN 280 — 295 mg/dl 0.6 kg x (Na/140) = 1 0.6 used in male 0.5 used in female (Na — 140)/140 x Total body water Someuced [EYE ato of EW. 0.6 kg x (140-Na) Total body water: 50% in men an 40% in women Na + 1.6 x (Glucose level - 100) / 100 Conected Ne For every 100 maid) increased of glucose above normal (100 mg/dl) Na will decrease by 16—3mEq Canrecpad'Ga Ca +08 (4—Albumin) > Mgidl Ca+ (40 ~Aloumin) > Mmol/t coma S585 Se ‘AGAP Na = (HCO; + Cl) 1242 FeNa (Urine Na) _ (Plasma Na < 1% in pre-renal Urine Cr) Plasma Cr > 1% in acuto tubular necrosis SAAG Serum albumin — Ascitic fluid albumin < 11g/L: Non-PHTN causes > 11 g/L: Portal HTN = Cardiac output (HRx SV) x SVR ‘Most sensitive for Shook MAP © Diastole + 1/3 Pulse pressure (S - D) © Diastolic + (Systolic — Diastolic) / 3) 2 (2 Diastole + Systole)/ 3 COMMONLY USED UNITS CONVERSION From To Weight kg | x22 Lb Albumin gidk | x10 git Bilirubin mg/dl} x17.4 | umol maid! | x0.25 | mmol Calcium mmol | x4 mg/dl mgidt_ | x88.3 | umoWl Creatinine Umom | x0.013 | moja Glucose mmol | x18 | mg/dlTUMOR LYSIS SYNDROME © Release of purines and pyrimidines % + POs, 7K, 1 Uric acid, | Ca (Don't give Ca) © Mediated by cytotoxic T cells © Leads to renal failure SUMMARY OF SOME ELECTROLYTES CHANGES K [Na [Mg | PO. imor lysis syndrome | t Refeeding syndrome | | | 7 4 Monitor Acute Renalfailure | t | 1 | - t aNutrition Reviewed by: Dr. Mohammed Al DuhilebNUTRITION Most common nutritional allergy: Nut Most common nutrient deficiency: Iron Most common trace element deficiency: Zine Protein requirement: 0.8 ~ 1.5 gikg/day Mean: 1.2 g/kg/day with 20% of essential amino acids © Mid stress: 1 - 1.2 g/ka/day © Moderate stress: 1.3 — 1.5 g/kg/day (hypercatabolism status) © Critically il patient: 1.5 - 2 g/ka/day Caloric requirements “Resting energy": 25 - 30 calories/kg/day © Trauma, surgery, or sepsis stress increase kcal requirement: 20% — 40% + Caloric requirements in severe injury: 30 - 40 caloriesikg/day * Caloric requirements in Extensive trauma or burn: 45 — 50 caloriesikg/day © Pregnancy increases kcal: 300 kcal/day © Lactation increases keal: 500 keal/day ‘Nutrition in Bums: ‘© Calories: 25 keallkgiday + (30 keal/day * % burn) © Protein: 1-1.5 g/ka/day + (3 9 x % burn) Calories of macronutrient: © Fat 9 kcallg © Protein 4 kcal/g © Carbohydrates 4 keallg (dextrose 3.4 kcal/g) lation: y ‘i 10% = 10g / 100ml 0, 1009 / 100m! 9 100 grams Calculation: How many calories in 100 arams of dextrose: 4g = 3.4 calories x 100 gram = 340 calories 70 kg x 25 calories = 1800 calories / day Calculation: How many calories per day in 70-kg person receiving 5 a/ka/day of carbohydrate, 6.259 of proteins = 1g of nitrogen (9X 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 for the above person: 1800 calories /4 gram = 450 g of glucose daily 20% = 20g / 100 mil (250 mi/ 100 = 2.5) 2.5 x 209 = 50 grams of fat= Harris Benedict equation calculates “Resting metabolic rate” based on © Weight, Height, Age, and Gender Best predictor of Resting metabolic rate in critically il: Penn State 2003 equation = Fever increases basal metabolic rate (10% for each degree above 38.0°C) = Nutritional assessment: © Pre-albumin: Halt-ife: 24 hours (Mest accurate test) + Retinol-binding prealbumin: Shortest halt-lfe (12 hours) © Albumin: Half-life: 18 days © Transferrin: Half-life 8-9 days ‘Transferrin: transporter of iron + Ferritin: storage form of iron CARBOHYDRATE DIGESTION Begins with salivary amylase © Sucrose = fructose + glucose © Lactose = galactose + glucose © 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’ © St 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 alycolysis (Skeletal muscles, RBCs. WBCs) and used by liver to be converted to glucose via Cori cycle ™ Obligate glucose users: © Brain > Switches to ketones in > 48 hours starvation and > 3 weeks in most organs © Adrenal medulla © Peripheral nerves © RBCs & WBCsRESPIRATORY QUOTIENT (RQ) RQ measures energy expenditure = CO? produced consumed Process Respiratory Quotient = Increases tisk of infection = Ventilator problems Tetosis and fat oxidation (Gtarving) 07 Fat utilization 0.7, Protein utilization 08 Normal (Balanced feeding) 0.625 Carbohydrate utilization 1 Lipogenesis (Overfeeding) >t 2 _{ glucose, | fat > | Minute ventilation POSTOPERATIVE PHASES ™ Catabolic phase “Day 0— 3° (negative nitrogen balance) “| Lean body mass” © Lean body mass: Fat-free body weight (decreased in catabolic phase and critical il) ™ Diuresis phase “Day 2-5 Anabolic phase “Day 3 - 6" (postive 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) 1 Micelles % chylomicrons > lymphatics © Long chain fatty acids enter enterocyte by membrane fusing > Lymphatics © Short chain fatty acids enter enterocyte by simple diffusion > Portal vein = Essential Fatty Acids: Linoleic (Omega €), Linolenic (Omega 3), Arachidonic © Not synthesized by body © Used for prostaglandin synthesis, ™ Short-chain fatty acids: Acetate (Acetic acid), Propionic acid, Butyric acid © Main nutrient of colonocytes '& Insulin inhibits lipolysis (Anabolic: + Lipid and protein) ‘AMINO ACIDS ™ Fuel during sepsis: Only amino acids = Only amino acids to inctease during tines of 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 © Glutamine produced by Iung in liver failure © Glutamine increases intestinal cellularity > Enhance bowel absorption © Glutamine is the fuel of Enterocytes and Cancer cells = Aromatic Amino Acids: Tyrosine, Tryptophan, Phenylalanine = Branched-chain amino acids: Leucine, Isoleucine, Valine © Only A.A metabolized outside the liver (in muscle) © Allare 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 ofprotein = 25 g of glucose = 4 kcal ™Non-protein calories : Nitrogen (NPC:N) © Normal > 150:1 (Range: 100.1 — 200:1) © Moderate stress 31204 o Severe stress > 90-120:1 © Burn > 90-100:1 Calculation: What is NPC: in 2000 calories with 100 q proteins 100 9 x 4 = 400 calories 2000 - 400 = 1600 non-protein calories 100 g / 6.25 = 16 grams of nitrogen NPC 1600/16 = 100 “N= 10:1 1) 70kg x 25 = 1750 cacy 2) 1750/150 = 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 450 9 glucose daily to ‘maintain Normal NPC:N (150-7, 1) 450/25 = 18 2) 18x 6.25 = 112 grams of proteins Nitrogen balance = (N in - N out) © Nitrogen In = protein / 6.25, © Nitrogen Out = 24 hour urine N +4 gram ™ Positive N belance (anebolism): by increasing protein diet © Hypokalemia > Glycosuria > potential effect ™ Negi /e N balance (catabolism) © Total protein synthesis for 2 healthy, normal 70-kg male is 250 giday ‘© Urea production from liver to get rid of ammonia from amino acid © 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: © Bolus: used for gastric feeding by hypertonic feeds at higher rate © Intermittent: used for post-gastric feeding + Should be started as soon as possible © Continuous: have risk of aspiration and should stopped overnight Used in initiation of feeding in critical il patients Route of tube feeding: ‘© 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, brain injury with gastroparesis (usually first 3 days) © 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: © Always elevate head 30 degree © Hold feeding ifresidual gastric volume > 200 mi (check every 4 hours) = Types of enteral formulas: ‘© Monomeric (Elemental) + Small molecular weight compounds = Contains individual amino acids, glucose polymer and low fat with 2 ~ 3% long chain triglycerides (LCTs) © Oligomeric (Semi-elemental) = Contains peptides with varying chain length, primary as medium chain triglycerides © Polymeric + Contains intact proteins, complex carbohydrates and mainly LCTs © Specialized formula © Initial Enteral formula for surgical patient: Low-residue isotonic formula © Formula for patient NPO > 7 days with functioning GIT: Elementel formula (Monomeric) © Formula for pancreatic disease: Polymeric Formula for renal dysfunction: Nepro, Suplena Formula for liver disease: NutriHtep Formula for hypoalbuminemia: Ensure + Formula for diabetic patients: Glucemam™ Gastrostomy techniques: ‘© Types: Temporary or Permanent © Methods: Open (Direct, Roux limb) * Laparoscopic + Endoscopic (PEG tube) * Needle-catheter gastrostomy or jejunostomy © 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) Tavel © Sile of gastrostomy: ‘= At midpoint of stomach close to greater curvature Fi. 2022: Went terry gastostony, fail fay with oe Seprenerconere ‘Adoni wall eemeaieea ane slong the Mapa the gastric lumen Anterior ease wal and tube lao End ofthe gastrictube apis brought 5 Se tae creeghs puree Figs 20 - 25 A and B : Janeway’s permanent gastrostomyTOTAL PARENTERAL NUTRITION ost common indications for TPN: ‘© Nonfunctioning GIT (short bowel syndrome, intractable voriting, or diarthea “IBD") © Need for bowel rest (severe pancreatitis, enterocutaneous fistulas, prolonged ileus) © Severe malnutrition (e.g. TPN pre-op if weight loss > 20% during last 6 months) «= TPNis given 7 days pre-operative © NPO > days with no pian for enteral feeding = Nutritional requirements for average adult male: 20% Protein + 30% Fat + 50% Carbohydrate ™ Peripheral ine TPN: Fat-based with low-osmiarity solution (for < 1 week) © Maximum lipids infusion: 2.5 g/kg/h = Central ine TPN: Glucose-based (for > 4 week) ‘© Maximum glucose infusion: 5 g/kgih (Add insulin if patient having hyperglycemia) © Can be inserted by PIC line TPN weaning rate = 50 ml hour Lipid emulsions, 10% lipid solution contains 1.1 keal/ec 20% lipid solution contains 2 keal/ecCalculation: How many grams of fat in the 250 mi of 20% lipid solution ‘20% = 20g / 100 mil (250 mi/ 100 = 2.5) 2.5 x 20g = 50 grams of fat Calculation: How many Keal in 500 ml of 10% linid solution: 500 x 0.1 = 50 g fat 50 x 9 = 450 kcal Calculation: How many calories for patient receiving 1000 rl bag of TPN contains 10% of dextrose and 7% of proteins and also receiving 250 ml of 20% fat emulsion: Dextrose: 10/100 x 1000 = 100 gm x 3.4 = 340 calories Proteins: 7/100 x 1000 = 70 gm x 4 = 280 calories Fat: 20/100 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 mi 2) Caloric requirement: 30 x 70 = 2100 keal /day Use IBW for this person (70kg for example) 3) Protein requirement: 1 x 70 = 70 g/day x 4 = 260 kcal / day 4) Remaining = 2100 = 280 = 1820 kcal/day 70% (1260 kcal/day) CHO 1260 kcal/3.4 = 370 giday 30% (540 kcallday) Lipids 420 kcal /9 = 46.6 g/day Lipid ernulsion 20% contains: 1000 kcal in 500 mI (500 x 2) Lipid emulsion 10% contains: §50 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) Vitamin Kis 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 Negative: Remove calheler Catheter-related infection Positive Positive Remove catheter + IV Antibiotics © Positive result: ‘= > 1000 CFU (quantitative method) or > 15 CFU (semiquantitative method) Most common organism: Staphylococcus epidermidis = Most common early organism: Staphylococcus aureus © Least risk of infection: Subelavian line © Highest risk of infection and DVT/PE: Femoral line Metabolic complications ‘© Most common electrolyte disturbance: | POx Hyperglycemia ‘Maintaining of glucose < 110 mg/dL improves mortality and reduces infections © Refeeding Syndrome = PO. 1K, | Mg, t Na Prevented by starting feeding at a low rate (10-15 kcal/kgiday) © Inrenal feilure you should > LK, | Proteins In respiratory failure you should > | Carbohydrates ™ Acalculous Cholecys ™ Cholestatic liver disease: within 1 - 2 weeks (reversible) ™ Cholestasis: within 2 — 4 weeks (irreversible) © Management: Change to hepatic formula and | Lipid content of TPN ™ Acid-base abnormalities: (Hypercapnia) ™ Gastrointestinal atrophy © Enteral feeding is better to prevent bacterial translocationOTHERS NUTRITIONAL DEFICIENCIES Nutritional deficiency Complication Chromium “Hyperglycemia and neuropathy Selenium Cardiomyopathy Copper Pancytopenia Zine Poor wound healing, Diffuse Dry eczemetoid rash, Loss taste sensation, skin & hair problems, and per-oral rash Essential fatty acids (Lineolo acid) Reddish dermaiits (Sealy acrodermatitis), Alopecia, vision changes Thrombocytopenia Vitamin B1 (Thiamine) Moro with Bilroth surgery Encaphalopathy, Cardiomyopathy, and Thigh numbness Vitamin BS (Pyridoxine) ‘Anemia, Glossiis, and Neuropathy, Vitamin B12 (Cobalamin) More with crohn disease with SBO Boofy tongue, anomia, Poriphoral nouropathy Vitamin B3 (Niacin) (Pellagra: Diarmhea, Demmatiis, Dementia Vitamin C (Ascorbic acid) ‘Scurvy - General weakness = Anemia = Gingivitis ~_Skin hemorthage ‘© Types of malnutrition; © Marasmus: inadequate protein and caloric intake © Kwashiorkor: catabolic protein loss hypoalbuminemia and generalized edema Trace elements: Protein-sparing effect after administration of: 2 L of DSW © Iron, iodine, cobalt, zinc, copper, selenium and chromium Vitamin C (Ascorbic acid): Propofol delivers 1 kcallcc in the form of lipid © Crosslinked lysine and proline © { Resuscitation volume and edema © Increases absorption of ironInflammation and CytokinesINFLAMMATION AND CYTOKINES GROWTH AND ACTIVATING FACTORS PDGF (Platelet-derived growth factor) © Key factor for wound healing © Accelerate wound healing in chronic wound © Chemotactic and activates inflammatory cells & fibroblasts, ™@ EGF /EPGF (Epidermal growth factor) © Epithelialization © Accelerate healing of donor graft © Accelerate epithelization of split-thickness skin graft PAE (Platelet-activating factor) (© Generated by phospholipase in endothelium © Increased platelets aggregation © Bronchoconstrictor = VEGE (Vascular epidermal growth factor) (© For neovascularization (angiogenesis) involved in tumor metastasis EGE (Fibroblastic growth factor) ‘© Stimulate wound contraction HYPERSENSITIVITY REACTIONS '™ Basophils: source of histamine in blood Mast cells: source of histamine in tissue © Release histamine & Bradykinin > Vasocilation = Types: Type Mediated by Example, v IgE > Mast cols & Eosinophils Penicilin allergy (immediate) Lymphazurin allergy Bee u IgG, IgM Hyperacute rejection (Cytotoxic) | | BP. 1 HR, diffuse bleeding ABO incompatibility ti ‘Antigon-antibody compiox Rhoumatoid Arihrits, SLE (Complex) Vv Delayed type hypersensitivity Vitamin K injection (Delayed) DM type 1 ‘TB skin test (PPD) Crohn's disease Delayed penicilin allorg NITRIC OXIDE (NO) Arginine procursor > Activates guanylate cyclase (t cGMP) = Vascular smooth muscle diiation (with no decreasing of protein permeability) © Vascular smooth muscle constriction by EndothelinCYTOKINES Cytokines derived from Polypeptide hormones = Most of them produced by macrophages Macrophages: dominant role in wound healing; release (PDGF) and (IL-1 and TNF-a) = Types Function ‘Most potent stimulus: Lipopolysaccharide (Lipid A) ‘+ Causes > Cachesia (inoreases muscle catabolism) ‘+ Stimulate Eicosanoids (Thromboxane) + Regulate E-Selectin w-4 ‘Causes fever postoperative (alveolar macrophages) (© NSAIDS decrease fever by PGEZ syntnesis + Blocked by steroids 1-2 + Aciivates NK-T cells in Renal cell carcinoma ‘+ Inhibited by Cyclosporine, Zenapax iL—4 = Aciivates B cells 1-6 Increases Hepatic Acute Phase proteins (C-reactive protein, amyloid A) + _In SIRS and sepsis 1-8 ‘+ InARDS, Attracts PMNS iL=10 + Reflects severity n trauma ANTI-INFLAMMATORY CYTOKINES m4 = iLt0 mw iLtg = TGFB ©. Increases collagen © Inhibit T-Cells and immunosuppressor (inhibit plasminogen inhibitor) ©. Important mediator for angiogenesis in wound healing HEPATIC ACUTE PHASE @ Increased: CRP. amyloids. fibrinogen. haptoglobin, ceruloplasmin, 2-1 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” APC: cell Adhesion ™ P53: cell RegulationCOMPLEMENT Classic pathway (Ig or IgM): Factors C1, C2, and C4 3: Convergence point for both pathways (Critical step: Activation C3) Mg: required for both pathways Anaphylatoxins: C3a, C4a, C5a Opsonization: C3b and C4b Membrane attack complex: C5b-9b Chemotaxis for inflammatory cells: C3a and CSa CYCLOOXYGENASE (COX) ™ Produced from arachidonic precursors = Prostaglandins, Prostacyclin: (by endothelium) © | Platelets aggregation ©. Systemic and pulmonary vasodilation (J SVR, | PVR) © Bronchodilation = Thromboxane: (by platelets) Stimulated by TNF - a + Platelets aggregation by increasing release of calcium in platelets ‘Systemic and pulmonary vasoconstriction (+ SVR, t PVR) Bronchoconstriction = NSAIDs: inhibit cyclooxygenase (reversible) © Aspirin: inhibits cyclooxygenase (irreversible) Steroids: inhibit phospholipase LEUKOTRIENES ™ Produced from arachidonic precursors © 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: © 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: Platelets (Not true cell) PNINs (Neutrophils) Macrophages (3 - 4 days) Fibroblasts (Day 6) '™ Perioheral nerves regenerate at 1 mmi/day ™ Epithelization occurs at rate 1 — 2 mm/day INFLAMMATION PHASES Phase Description Time Notes 0 | Vasoconstriction Day i 1 [Inflammation Day 1-4 PMNs (Noutrophils) are the first infltrating oolls in wound site during first 24 — 48 hours il__| Proliferation & Epithelialization | Day 5-2 Week_| Fibroblasts acts for collagen deposition (il > [Maturation and Remodeling _| 3° week — 1" Year | Decreased vascularity, cross-linking collagen ™ Collagons: q Description Time. Most common site 1 [Most common, primary colagenin healed wound | Day3—4 | Bone, Soar, Healed wound W Cartlago [Increased in healing wounds Day 12 | Vessels, Healing wound 1V__[In basement membrane V__[Insmooth muscle Comea = Osteogenesis mperfect: Type | collagen ‘+ Ehlers—Danlos syndrome: type ill collagen ¢__Marfan's syndrome: Fibrin 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) © Eorly: Fibrin © Late: Collagen cross-linking (inhibited by d-Pericillamine) © Regain tensile strength rapidly: Bladder > Stomach > Colon © Regain tensile sength slowly: Skin, Fascia, and Tendons © Usually completed at 8 weeks, but can be gradually increased up to 2 years (80% only) = Epitholial integrity: most important factor in healing open wounds (secondary intention) © Any contaminate wound > 6 hours preferable to be closed by secondary intention © Myofibroblasts (communicate by gap junctions) involved in wound contractionFactors PDF- BB showed to improve healing in DM foot ulcer ‘Weakest time point for small bowel anastomosis: 3 - 5 days © Due to increased collagenolysis when resolving the edema © Collagenolysis appears more in large bowel (higher risk of leakage) © Submucosal layer has the greatest tensile strength (Ability to hold stitches) © 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 4 year to allow maturation. Reopening of the midline scar without excision gives most rapid gain in strength than excision sociated with increased wound healing Moist environment Tight glucose control Factors associated with decreased wound healing Local tissue infection (Most major) © Bacterial infection (> 10°/ cm?) Vitamin C deficiency, Hypoalbuminemia, Malignancy, Smoking Diabetes © 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, © Decreased collagen and collagen maturation, decreased fibroblasts, impaired Lymphocyte and Leukooyte Steroids © Inhibits macrophages, and | migration of macrophages © Impair fibroblast proliferation and collagen synthesis © Inhibits T-cell function © | Angiogenesis © Steroids usage should be delayed post-injury at least 3 ~ 4 days Chemoradiation © Free radicals > DNA Damage > local fibrosis and vascular effects ©. Impaired fibroblasts © Chemotherapy least effective in wound healing if stopped > 2 weeks perioperative © Radiation least effective in wound healing if stopped > 3 weeks perioperative Tamoxifen: | TGF-BNutritional effects improve the wound healing, and counteracts effects of steroids on wound healing : increases tensile strength, but excess amount inhibits wound h = Vitamin C: hydroxylation of lysine and proline in collagen synthesis © Daily supplement 60 mg for healthy, and > 4g in critically il 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 + Vilamin A promote wound healing in normal people with no nutritional deficiency (Schwartz) EXCESS HEALING Hypertrophic scar Kel Etiology, due | neovascularity ‘Auiosomal dominant, Type 1 Golagen Risk factors _| Burn, Long standing non-healing wound Burn, Trauma Timing 4 6 weeks post injury (up to 3 months) ‘Can appears years after injury Sites (On fiexor surfaces upper torso, dark skinned __| On neck, chest, ear lobes and shoulders Mechanism _ | Excessive cross-linking of collagen and chrori | Altered ratio of: inftammation ‘Collagen production / Collagenase activity Collagen | Collagen stays within confines of orginal scar | Collagen goes beyond original scar Parallel orientation of collagen Random orientation and thick collagen ‘Changes | Myofibroblasts, ¢ fibroblast, ¢ collagen Normal fibroblast, t TGF-B Regression __| Froquent Novor Management | Pressure garments, Silicone gel sheets ‘Surgical excision followed by Intravlesion steroid injection intraresion steroid injection (Triamcnolone) JF surgery indicated: minimum 4 year PRESSURE SORE Skin injured if proscure of 60 mmHg! 1 hour (sacral pressure 120 mmHg) ™ Stages: ©. Stage |: Erythema 6. Stage II: Partial thicknass skin loss © Stage Ill: Full thickness skin loss © 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: © Neutrophil dysfunction 0 PAPA syndrome © Auto-inflammatory disorders (eg, inflammatory bowel disease end arthritis) Associated with: 0 Inflammatory bowel disease, IGA monoclonal gammopathy, hematoloical malignancies, Arthritis, PAPA syndrome = Typos: Ulcerative (classic): tender, inflammatory papule (lower extremities and trunk) Bullous: (arms and face) Pustular: associated with inflammatory bowel disease Vegetative: localized, solitary, superficial (head and neck) ™ Diagnosis: © Biopsy to rule out malignancy © Major criteria (must have both): ‘= Rapid progression of painful, necrolytic cutaneous ulcer Other causes of cutaneous ulceration have been excluded © Minor criteria (must have two): + History suggestive of pathergy Association with systemic disease + Histopathologic findings (sterile dermal neutrophilia, + mixed inflammation, + lymphocytic vasculitis) = Treatment: ©. Limited disease: Local corticosteroids = Local calcineurin inhibitors © Extensive disease + Systemic glucocorticoids or cyclosporine © Adjunctive therapies: infliximabWound Dressing (© Moisture Environment Type: D Us ‘Com Fims Teaaderm. ‘Secondary dressing Bioclusive, Foams ‘Allevyn, Mebpilex, | Moderate exudate ‘Consist of 2 layers Lyofoam Hydrophilic silicone or polyurethane layer Hydrophobic, gas permeable layer ‘Aiginates | Sliverosl, Sliverion | Heavily exudate ‘Non-adherent polysaccharides For epen surgical wound __| insoluble in water Hydrocolloids | DuoDERM, Promote epithelialization Tegasorb and wound maturation by creating moist environment Hydrogels | Nu-Gel, iniraste | Necrotio, yellowish sioughy | For dry wound Gel, Viaion, or Granuiating clean Elasiogel Hydroactive | DuODERM Polyurethane matrix, @ Specific dressing: Honey: significantly reduced need of amputation and improve healing of chronic ulcer Acelic acid: bactericidal to most bacteria + anti-pseudomonas effect ‘Aquacel: must be ionized by soaking in NaCl Iodine povidione: not used in dry necrotic areas Film Dressing = Pec abit Dressing @Mepilex:BorderLite Foam Dressing Hydrogel Dressing Alginates Dressing 5 TRCER Hydroactive Dressing= Hemostatic agent Type Trend name ‘Source “Absorption Used in ‘Absorbable gelatin | Gelfoam, Surgifoam | Porcine to 6 wooks | Organ surface blooding Oxidized ‘All Surgicel Plant 1 to 2weeks | Organ surface bleeding regenerated cellulose Venous oozing Microfiber Aiitene Bovine SBweeks | Cavity unamenable io collagen ‘cautery or compression as nerve Fibrin sealant TachoSil Human fiorinogen | Immediate | Exiomal arterial bleeding and thrombin Venous oozing Zeolite ‘Quikclot Calcium-loaded Exiemal arterial bleeding aluminosilicate mineral Microporous Arista Polato starch “46 hours Needle hole bleeding in polysaccharide vascular gratt or adentitia spheros " (Organ surface bieeding Cavity unamenable to cautery or compression as rene Bovine albumin- Biogiuo Large ariery bleeding glutaraldehyde Fibrin-glue tissue adhesive pe eS= e Absorbable gelatin Tissue adhesive Fibrin sealant eS = , Oxidized cellulose Microfibrillar collagenBurnBURN = Zones of burn wound: © Coagulation © Surrounded by zone of Stasis (most amenable to salvage) © Surrounded by zone of Hyperemia = imbibition: blood supply to skin graft for 0-3 days 1 Neovascularization: starts around day 3 Most common cause of free ‘lap failure: Venous thrombosis Most common cause of skin graft loss: Hematoma / Seroma Most common type of burn is Seald burns © 140°F water causes bum in 3 seconds Most common type of burn come to hospital and be admitted is Flame burns ion Criteria m2" degree > 20% TBSA, of > 10% TBSAin > 50 or < 10 years of age m2"! degree in hands, face, feet, genitalia, perineum, or skin overlying major joints m3" degree Electrical and chemical burns ™ Concomitant conditions: © Inhalational injury, mechanical traumas or pre-existing medical condition Assessment of lotal body surface area: = Lund and Browder chart (Most accurete) = Palm method (1% equal to patient's palm) ™ Rule of 9 ‘© Citcumferential leq = 18, Circumferential forearm = 9 © Anterior Right thigh = 9 “In Children: head = 18 and lower limbs = 14 each” Used for all burn patient who need admission ® UOP as best measure of resuscitation ( > 0.5 mi/kg/nour) Ringer lactate 3 — 4 ml /kg/ %TBSA © Started from the time of the burn. © %volume should be given in 1* 8 hours and the remaining ¥: over the 16 hours © Can be used up to 6 ml/ kg / %TBSA in children <2 years old © Additional maintenance fluid is required for children < 20 kg Colloid of 5% albumin usuelly given for burn > 40% TBSA 8 — 24 hours post-injury Most common cause of death in first 24h in burn: Inadequate fluid resuscitation'ypermetabolic response Oxidation of ipids, } Proteolysis, gluconesgene: Temperature Best indicator for hypermetabolic response is: Negative Metabolic rate Burn release cytokines and activates SIRS if > 20 — 25% sition i Caloric need: 25 kcallka/day + (30 kcal x % burn) Protein need: 1 gikg/day + (3 9 % bum) | 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 bums Feeding in critical ill patient with burn is best with: Nasojejunal feeding ™ Best nutritional assessment by: Daily weight measure Assessment of protein status (or during adi istration 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) © 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 bum wound: HSV Most common opportunistic infection in burn wound: Candida Best way to detect burn wound infection vs. colonization: © Biopsy of burn wound including normal skin, © Positive result if > 105 > Need surgical excision of infected woundTOPICAL ANTIMICROBIAL, Typ Description Most common Do not use in patients with sulfa allergy Side effects: Neutrop Thrombocytopenia Inhibit epithelialization Side effects: Na, | Cl. LK, | Ca Silver nitrate Discoloration Methemoglobinamia {_CVP (contraindicated in GSPD) Best for eschar penetration Silver Sulfadiazine (Silvadene) Sulfamylon Side effects: (Mafenide sodium) | Psinfut application Metabolic acidosis (carbonic anhydrase inhibition) . f © 1'degree and superficial 2 degree: * Continue wound dressing for 2-3 weeks + May be used for deep 2"! burn wound for few days and re-assess © Deep 2% and 3" degree: Early excision and grafting = Skin grafting © 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 © Insufficient autologus skin graft (> 40% TBSA) = Allograft (Cadaveric skin) of 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: (© Carbonaceous sputum (Most indicative) © Singed nasal hair Most common cause of the death: ARDS / Pneumonia © Early: Airway compromised © Late: Pneumonia Affinity of Carbon monoxide for hemoglobin 200 - 250 times greater than oxygen © Pulse oximetry reading > False High Half-life of carboxyhemoglobin in patient breathing 100% O2: 1 hour CO poisoning should be treated until carboxyhemoglobin level < 10% and no symptoms Indications for intubation: 0 Associated with: Severe upper airway edema (Hoarseness, wheezing, or stridor) + Supraglottic inhalation injury Deep burns to the face + > 40% TBSA © Respiratory parameters: = PaO < 60 mm Hg = PaCO2 > 50 mm Hg + PaQz/FIOz ratio < 200 Electrical bum: '™ Cataract is one of the complications of electrical bum ™ Managemen © Oxygen supplement © Adequate fluid resuscitation with maintain UOP of 100 mL/hour (> 1 mLikg/hour) © Osmotic diuresis with Mannitol (25 g every 6 hours) © Intravenous NaHCO; (5% continuous infusion) for alkalinization of urine © 1% methylene blue used to treat Methemoglobinemia © 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 administraton © Plasmapheresis may reduce intravenous fluid requirements in patients who do not respond to standard crystalloid resuscitation 4 Fasci omy + DebridementChemical burn: Management of Hydrofluoric acid burn: © Copious irrigation with water and Calcium gluconate gel application m= Lye powdered should be wiping or sweeping with no irrigation Acid and alkali bums (chemical burn): Water irrigation (Normal saline in non-burn wound) © Alkalis > deeper burns (liquefaction necrosis) © 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: ©. Skin epidermal-dermal separation seen in all © NosteraidsOTHERS Frostbite: Treated with warm water immersion “99 ~ 108 F (37 ~ 42 Cy’ ™ Marjolin’s ulcer: squamous cell cancer in chronic non-healing burn wound © Inpatient suspected malignancy of chronic wounds (overtumed edges), biopsy must be repeated to rule out malignancy (SCC vs. BCC) Curling’s ulcer: gastric or duodenal ulcer with bums Pain in burn: Antecubital vein and IV Morphine Selzures: usually due to | Na Escharotomy © Indication ‘Circumferential deep burns with suspected compartment + For compartment pressure > 25-30 mm Hg + Signs of vascular impairment ‘+ Decreased peripheral blood flow © Delayed capillary refill ‘© Neurolocic ceficits ‘+ Decreased or absent Doppler ultrasonic pulse detection © Thoracic Escharotomy may be needed if patient have circumferential thoracic pain with increasing PCO2 and PIP (peak inspiratory pressure) © 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 © A: Airway with protection of cervical spine ‘© Helmet removed by 2-persons technique © Ask pationt any question © Open airway with protection of cervical + Jaw-thrust is preferred method if suspected cervical injury | aw -theust Head tit hin maneuver Tit maneuver © Suction Oropharyngeal airway, nasopharyngeal airway if not contraindicated, pre- intubation oxygenation Endotracheal intubation (rapid sequence induction) and 100% oxygen ventilation Cricothyroidotomy if obstruction or failure of TEE Tracheostomy if cricothyroidotomy contraindicated Hard collar or sandbags to protect cervical spine (unless penetrating neck injury) Patient become unstable when finish > Re-assessment (A BCDE) © B: Breathing and ventilation © Respiratory rate, Oxygen saturation © Examination of the chest Inspection Palpation Percussion (duliness, hyper-resonance) ‘Auscuttation + Neck examination (Tracheal shifting, Neck veins) Chest xray Patient become unstable when finish > Re-assessment (ABCDE)© ©: Circulation © Examination of the pulse, blood pressure and 4 pulses © Exclude extemal 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 ‘+ Abdominal examination for distension ‘= Pelvic examination for stability © Manual palpation of the pelvis for assess pelvic ring and crepitus © Manual compression along iliac crest over ASIS, then assess pelvic ring stability and pubis symphysis © Contralateral push-pull examinations of the lower extremities are rarely necessary to identify instability © FAST + Pelvic x-ray © Insertion of 2 Large IV cannula for blood extraction © Adult: © Preferable route by orde: "Peripheral upper limb (antecubital fossa) + Peripheral lower limb Failed? Central line or Intraosseous line (Tibia/Humerus) Subelavian venous catheter not preferred in trauma Unless patient has pneumothorex: © Do ipsilateral subclavian catheterization Best site for venous cut down: Saphenous vein at ankle + Children: © Preferable route by order: ‘= Peripheral upper limb * Peripheral lower limb Failed? Intraosseous line (Proximal tibia > Distal femur) © Blood withdraw before resuscitation (to prevent dilution of the biood) ‘* For CBC, RFT, LFT, Coagulation profile, Pregnancy test, RBS, Lactic acid + Blood Culture, Urine culture, ABG, Type and screen, Cross Match Fluid resuscitation with 4 Liter Ringer lactate or Normal saline, then ro- assessment © 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)oD: Disability © GCS (Level of consciousness) ©. Reflexes “Pupil” ce Lateralization signs ‘+ Sensory function = Motor function 2 Leg roll and examination of spine and to assess digital rectal examination (DRE) ‘+ Conscious: Spine tendemess ‘= Comatose: Step deformity © DRE used to assess sphincter, high-grade prostate, and blood on finger © E: Exposure and prevent hypothermia Resuscitation Adjuncts to primary survey (ABCDEFG) © ABG, Pelvis x-ray, Chest x-ray, DPL, ECG, Foley’s, FAST, NGT+ X-ray extremities Re-evaluation Consider need for transfer Secondary survey © AMPLE (Allergy, Medications, Past medical and surgical, Last meal, Event history) © Time of injury Mechanism of injury ‘Type and speed of vehicle Location of the victim in the vehicle Seat belt, Airbag, Helmet Number and status of the passengers History of loss of consciousness or vomiting © Full systemic examination from head to toe (Including pelvis and long bones) Adjuncts to secondary survey CT scan © Bronchoscopy Definitive management Tertiary survey Full body examination 24 hours after admission to rule out missed injuries| Hemorrhage Is the most common cause of death in 1**hour ‘© Resuscitation with ‘-liter Ringer lactate © Due to asymptomatic grade 1 hemorrhagic shock = 750 mi ‘= 1 ml blood = 3 ml crystalloids (750 x 3 = 2250 ml almost 2 liters © Serial lactate level is useful in trending success of the resuscitation © Unstable patients: ‘+ Non-responder or transient responder after the 2 liters of crystalloids . © Equations: © Diastole + 1/3 Pulse pressure © Diastolic + (Systolic — Diastolic) /3) © (2 Diastole + Systole) / 3 © Assessment of tissue perfusion and oxygenation © More sensitive indicator for shock © Hypotension: Systolic BP < 90 mm Hg, or MAP < 65 mm Hg . © Systolic - Diastolic pressures 0 Narrow pulse pressure: < 25% of systolic pressure © Blood loss. cardiac tamponade or aortic valve stenosis © More sensitive indicator for blood loss = Permissive hypotension technique: (SBP < 80 mmHg) © Do not use it in traumatic brain injury Used as selective technique to limit further bleeding, coagulopathy, and hypothermia Still there is no RCT supporting using this technique yet Although it used by selective centers during transfer patient from accident site to OR for penetrating trauma™ Tissue injury response (Stress hormones) increased ave No role in tissue injul | First hormone to release during stress: Corticotrophin-+ Order of hormone release: © Immediate: Epinophrine © After 20 minutes: Glucagon © After 30 minutes: Insulin and ADH © Afler 2-4 hours: Cortisol © After 24 hours: Growth hormone Decreased TSH, LH, and FSH ing hormone (CRH) (Poak 1 — 2 days aftor injury)PENETRATING INJURIES = Typos: ‘© High velocity (> 600 misec) > Projectile, Destructive © Like rifles, or shotgun (close distance) © Leads to form primary and secondary temporary cavitations (pressure waves) © Low velocity (< 300 m/sec) > Propelled, Less severe co Like knife, or airgun © May travel for long distance in subcutaneous © Creates primary permanent cavitation pe. Round (oval in oblique fina) Treqular (Destructive) izo ‘Small (miro-tears at skin margin) | Large ‘Loss of substance | More Less. Powder marks | Yos, No (tattooing) [Edge inverted Everied Beveling Intermal ExtemalDIAGNOSTIC PERITONEAL LAVAGE (DPL) 1 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) . al: Standard © Supra-umbilical: for pelvic fracture, retroperitoneal hematoma suspicion, or pregnancy = Method: © Closed technique: © Anesthetize the skin © Access the peritoneum via needle with syringe infra-umbilical at midline © Pass the guidewire over the needle and remove the needle © Small stab incision at the entry of the wire ©. Pass the catheter over guidewire with direction toward left or right pelvic gutter © Aspiration for blood with 10 ml syringe © negative, Lavage with 4 liter normal saline and withdraw it under gravity © Send 2 300 mi fluid for analysis © Open technique: co Anesthetize the skin © Access the peritoneum via 4 — 6 cm infra-umbilical incision © Retraction of the skin and dissect until opening of linea alba © Place towel cips over both sides of rectus muscle and litt it up ©. Pass the catheter and trocar 45 - 60 degree caudally into peritoneum ©. Retract the trocar within the catheter, and advance the catheter to the pelvis ©. Aspiration for blood with 10 ml syringe © Ifnegative, Lavage with 4 liter normal saline and withdraw it under gravity © Send 2 300 mi fluid for analysis Positive findings (patient should be shifted to the OR theater} > 100,000 RBCs/cc in general or in blunt abdominal trauma, > 10,000 RBCs/cc in penetrating abdominothroacic trauma > 10 ml of blood > 500 WBC/oc 1 levels of Amylase, ALP, and Bilirubin level Food particles, bile, bacteria High false-positive rate Risk of visceral injury Poor sensitivity to detect retroperitoneal injuries DPL/ FAST positive > Laparotomy DPL/FAST negative > CT abdomen / ObservationHEAD INJURY Cerebral perfusion pressure © Goal: ICP < 12, CPP > 60 @ CPP=MAP - ICP © ICP > 20: need immediate treatment (Contraindication for laparoscopy) © Maneuvers to treat High ICP: Raise head of bed for 30 degree Relative hyperventilation > Cerebral vasoconstriction (COz 30-35) 3% Normal saline Mannitol (1 gikg IV for 3 days), Barbiturates, Phenytoin Steroid have no role Keep Na 140 — 150 (can use hypertonic saline) ™ Glasgow Coma Scale (GCS) Score Motor (6 poinis Verbal (S points Eye (4 paints) 1 _ | Noresponse No response. No response: 2 | Decerebration Inappropriate sounds "To pain (Abrommal extonsion) T_| Decoriicaton Thappropriate words To voice (Abnormal fioxion) 4 [Withdraw from pain ‘Confused or disoriented | Spontaneous 5 _| Localized painful ‘Appropriate and onented 6 | Obey commands © Motor part is the most reliable measure © GCS <8: ©. Intubation ‘+ Most common indication in trauma: altered mental status © ICP monitor (Peak ICP occurs 48 - 72 hours after injury) © Ventriculostomy (external ventricular drainage) ‘+ Used in: Intraventricular hemorthage, or hycrocephalous © GCS score in pediatric age group: Score Motor (6 paints) Verbal (6 points) Eye (4 points) 1_[ No response. No response. No response. 2 | Docorebration Grunts / Agitated Topan (Abnormal extension) 3__| Decortication Tnappropriate screaming or erying | To voice /shout (Abnormal floxion) 4 | Withdraw from pain Inappropriate interaction ‘Spontaneous Irritable Cries 3 _| Withdraw from touch Coos / Babies Cries appropriately 6 | Move spontaneously © GCS score in intubated patients: ‘Maximum score is 10 and minimum is 2 (No verbal scores) Verbal scores can also derived from the motor and eye components + Alternative scores: FOUR score, AVPU, and Simplified motor score™ FOUR score ‘Score Eye ‘Motor Brainstem reflexes Respiration ‘0 |Novesponso | No response ‘Absent Pupil, Corneal | Breaths at vontlator rate or and Cough reflex Apnea 1 |Topan Extension response | Pupil and Corneal ‘Above ventilator rate reflexes absont 2 [To voice /shout | Flexion response Pupi or Comeal reflexes. | (Not intubated) ‘absent Irreguiar breathing 3 |Openbutnot _ | Localizing to pain 7 Pupi wide and fixed | (Not intubated) tracking Cheyne Stokes breathing % [Spontaneous | Thumbs-up, Fisi, Pupi and Comeal (Not intubated) Peace sign reflexes present Regular breathing pattem ™ Cerebral hematoma: Epidural hematoma ‘Subdural hematoma Presentation | Lucid interval between Loss of consciousness | Faling in ederly patients Kermohan's phenomenon: Contraiateral dilated pupil and ipsilateral More dangerous due to associated injuries hemiparesis (brain compression) > Transtentorial herniation Vascular injury | Middle meningeal artery Venous plexus CT finding | Lens shape (biconcave) ‘Crescent shape Treatment = Focal neurologic deficit = Asymmetric or fixed dilated pupils =Midiine shift > § mm - GCS <8 or2 points decreased from time of injury until hospitalization =Hematoma volume > 30 cm? -Hematoma Thickness > 1.5 cm of epidural or > 4 om of subdural hematoma =IGP > 20 mm Hg igns of basal skull fractu (© Otorrhea, Rhinorrhea (due to ibriform plate fracture) © Dilated pupil (Due to CN Ill compression) © Raccoon eyes (associated with anterior fossa fracture) © Battle's sign: Posterior fossa fracture + Bruising over mastoid process * Associated with ataxia and nystagmusTarget; Halo; Ring sian: ‘© Away to differentiate between CSF and other ear discharges © By using a tissue you find a central non-clotted blood surrounded by clear fluid + Non-clotted due to streptokinase activity Bloed os © Examination of the cranial nerves: ch ‘Offack “esteach nestle arel ; Visual acuity of each eye ny ore Fundus examination CNII_|Oculomotar | Pupis examination NIV | Trochiear | Poss CNVI_| —Abducens | Folow finer at H pattem ‘Gomneal flex cNY Trigeminal ee ae Facial motor (Open mouth, Clench weth) Facial asymmetry or drop cnt Facial Facial exprescions Grns, Shuts eyes, Frown, Show teeth, Puff out checks Weber's test fr lateralization CVI | Vestibulococtear | Rinne’s test for ar and tone conduction Examination of extemal canal and eardrums Gag reflex CNIK | Glossopharyngeal | C28" Swallow, Couch ene anus Palate examination for uvular displacement “Trapezius examination CNX! | Accessory | Shrugs shoulders “Turns head against resistance "Ariculation CNXiI | Hypogtossal | inspect tongue for wasting or ‘asciculation Protrude tongue and look for deviationNECK TRAUMA '™ Neck zones based on penetrating injury: Zone Definition Content incision Zone 1 | TREPscie oullet or Ciavicle 6 Caeaid | Lung apex, Trachea Median sternotomy Subclavian vessels Anierolateral thoracotomy Cricoid to Angle of mandible Vertebral vessels Cervical incision medial to Carotid vessos scM Zone 2 Jugular vein Esophagus, Trachea (Don't joining both incision if bilateral oxpocuro coquirod) ‘Angle of mandibie to Base of skull | External or niemal careta High cervical inosion wih vessels subluxation of mandible Zone 3 dluguler vein Cranial nerve Hypopharyngeal . f nenetrati i Management Zone |! Zone It Zone iil Asymptomatic | GTA Chest and Neck ‘Observation ‘Symptomatic | CTA Chest and Neck CTA Chest and Neck (Soft signs) Angiography + embolization + esophagogram and bronchoscopy Positive CTA > Exploration Positive CTA > Angioombolization Failed > Exploration Symptomatic Exploration (Hard signs) Soft signs Hard signs Voice changes Large, Expanding, Pulsatile hematoma ‘Active external bleeding Tntemal bleeding into trachea or esophaqus Venous bleoding Hoarseness, dyspnea, stridor ‘Suboutaneous emphysema, Massive Homoptysis Neurological deficitThyroid gland injury: Control bleeding and drain (no thyroidectomy) = Esophageal injury: Nasogastric tube Left neck exploration 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 Divide 3 structures cross the esophagus for visualization: = Omohyoid muscle + Midcle thyroid vein Inferior thyroid artery In case of poor visualization: = Contralateral neck exploration through separate incision Intraoperative 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: © Displaced mid-face fracture (LeFort Il or til) Mandible fracture Complex skull fracture or Basilar skull fracture Closed head injury with diffuse axonal injury Cervical subluxation or ligamentous injury Cervical spine fractures Thoracic vascular injury Clinical presentation: Potential arterial hemorthage Cervical bruit Expanding cervical hematoma Focal neurologic defect (TIA, hemiparesis, Horner's Syndrome) Stroke on CT or MRI Investigations: (© CT angiogram (initial test of choice) if clinical suspicious or risk factor for CVI © Arteriogram (used for equivocal results) Grades, © Grade I: irregularity of vessel wall, dissection or intramural hematoma with <25% luminal stenosis © Grade Il: Visualized thrombus or caised intimal flap, or dissection or intramural hematoma with 25% or more luminal narrowing © Grade Ill: Pseudoaneurysm © Grade IV: Vessel ocolusion © Grade V: Vessel transection with extravasation ™ Management, © Unstable or penetrating: Open surgical repair © Stable and blunt injury Grade I: Anti-Thrombotie if no contraindication ‘+ Heparin 15 unitsikg/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 ll-V ‘+ Surgically accessible: Operative repair ‘* Non surgically accessible: © Grade ll - IV: Anti- Thrombotic © Grade V: Endovascular treatmentSPINE TRAUMA Criteria to remove C-spine collar with no images required: (all points are required) © National Emergency X-Radiology Utilization Study (NEXUS) criteria + No midline tenderness No focal neurologic deficit Normal alertness. No intoxication No paintul distracting injury © Ganadian C-Spine Rule No midline tenderness No paresthesia in extremities Ambulatory o” sitting upright Abie to rotate the neck 45 degrees to the left and right, Low-impact mechanism <65 years > CT scan if not cleared mcr: © Burst (Jefferson fracture): Axial loading © Most commonly missed © Risk of neurological injury is low © Radiological views: open-mouth odontoid and lateral = C2: Most common in carvical fracture Hangman’s fracture: Distraction and extension © Odontoid fracture + Types: Type I: above base (stable) + Type Il: at base (unstable) ‘+ Type Il: behind the base (unstable) Stable fracture: ‘© Compression (wedge) fractures © Only 1 columnis disrupted (anterior column only} + Anterior column: anterior spinous ligament (in stable fracture) + Midcle column: vertebral body, posterior spinous ligament (in unstable fracture) + Posterior column: facel/lamina interface (in unstable fracture) ™ Unstable fracture: > t column disrupted Fracture involving middle or posterior columns Burst fractures C2 odontoid fracture type I! and IlAccessory spinal nerve injut ‘© Following neck dissection, lymph node excision, or trauma © Affected trapezius muscle > Shrug shoulders Chance Fracture: © Flexion-distraction injury (seatbett injury) © May be a bony injury or ligamentous injury (flexion-distraction injury) ™ Cauda equina syndrome: ‘© Defined by a constellation of symptoms that result from terminal spinal nerve root compression in the lumbosacral region © Characterized by: Bilateral leg pain Bowel and bladder dysfunction + Saddle anesthesia Lower extremity sensorimotor changes © Urgent surgical decompression within 48 hours Rofloxes: Root flex ‘Associated Senso: ‘Associated Motor C5 Biceps refex Lateral upperarm ‘Shoulder end elbow flexors cs Brachioradialis | Lateral forearm, dorsum 1® web space and thumb _| Wrst extensors Gr Triceps ‘Middle finger Elbow extensors (Wiceos) cB Uinar side of ite finger Finger fiexors, extensors and intrinsio TH Wedial side of forearm Finger abduction FE ree StS — Deviation of unblicus toward area stroked ene ut Cremasteric reflex | Ipsiateral rise of testes Hip flexors, 2-13 |- ‘Anterior and inner thigt Hip flexion Hip adduction La Knee jerk ‘Anterior knee, and medial log ‘Quadriceps ‘Li” Knee exiensors is Davaifiexion foot | Foot 1" web space ‘Anile dorsflexion ‘Toe extensors si Plantar flexion foot | Posterior lag Foot plantar flexon ‘Ankle jerk Foot eversion 2 a Piantar foot “Toe plantar flexion 53 2 Periansl “Ankle planterflexors $2=S5_| Analwink Peranal ‘Gontracton of anal sphincterPeroneal nerves injury: Nene Root ‘Associated w) Sympioms ‘Common peroneal nerve | L482] Fracture head or neck of fbula Both (Most common) Lithotomy postion Deep peroneal nerve [4-82 Knee dislocation Loss of dorsifextion (oot Drop] Loss of sensation of dorsal aspect of the foot (1* web space] Superficial peroneal nerve | LEST] Comparmentayndrome | Lass everson {Aovng fot latray, outward) ‘Sensory: {tral apoct of foot dorsum Spinal cord injury syndromes: Syndrome [Prognosis | fotor 31 = P Tiferiar cord syndrome | — Worst Tess Fran Postestoccord, Proserve Preserve Preserve Loss syndrome Canal eord eyndrame Teas of unoer Moat) Good _| Loss (Upper> Lower) | Preserve | extremities only Preserve eon Soars Best | ipstoterat oss Contralateral loss ‘eauaarat $7 Sereaton '$2:Pain and Temperature : Progriocepticn, vibration and touch Spinal cord injury increases the risk of DVT/PE = Cervical injury: Nasal Nasal intubation is cont itubation traindicated in Apneic patients ‘Steroids for biunt trauma to prevent neurogenic shock is used for 48 hours only ™ Twes of nerve injury: © 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 © 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 © Neurotmesi: (Most severe) = Complete anatomical interruption of axon and connective tissue (epineurium)MAXILLOFACIAL TRAUMA Temporal skull fracture: Facial nerve injury (at geniculate ganglion) © Most common facial bone fracture: Nasal bone = Maxillary fracture: Trigeminal nerve injury = Mandible fracture most commonly at condyle (Angle & Subcondyl) . © Type I: Maxilla fracture transversely © Type Il: Lateral to nose © Type Ill: Lateral orbital walls, Orbital floor injury > Upward gaze Management of facial narve injury + Surgical exploration 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: Cricothyroldotomy intubation © Contraindi =< 12 years old + Laryngeal trauma or fracture * Subglottic stenosis tion > Tracheostomy © Technique: Percutaneous cricothyroidotomy (Seldinger Technique) = Needle cricothyroidotomy: Palpate thyroid and cricoid cartilage by thumb and 3" finger Insert catheter-needie with NS directed caudally at 45 degree Aspirate during insertion (ensure air-bubbles) ‘Advance the catheter and remove the needle Attach ventilation (16 Limin) or bag mask can be used Palpate thyroid anc cricoid cartilage by thumb and 3" 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 oricothyroid membrane Retract the trachea superiorly and inferiorly Insert tracheostomy tube 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 tube followed by thoracotomy = ER thoracotomy © Perfect patient is one with recordable pulse and single anterior thoracic stab wound with pericardial tamponade who lose vitals in front of emergency department staff © Survival rate 15 ~ 50%, should be done selectively based on injury and transport time © Indications: Patient sustaining witnessed penetrating trauma < 15 min pre-hospital CPR = Patient sustaining witnessed blunt trauma <5 min pre-hospital CPR * Persistent severe hypotension (SBP < 60) © Cardiac tamponade, intra-thoracic or abdominal bleeding, air embolism © Steps: Left anterior thoracotomy ‘Open pericardium anterior to the 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 © Indications: ‘+ > 4,500 ml initially for any type of injury, other definition exist as well: ‘= > 4,500 ml initially for blunt trauma ‘+> 1000 mi initally for penetrating trauma = 200 milh 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 Pericardial tamponade ‘Most common source of bleeding: Internal thoracic artery + intercostal arteries™ Diaphragmatic injury More common on the feft (Bronchus injuries more commen on the right) Investigations: * CXR: Initial tool (NGT coil to the chest, and elevation of hemidiaphragm) + Can miss 20 ~ 50% on injuries + CT scan = Low sensitivity © Collar sign © Dependent viscus sign © 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 Treatment = Acute < 1-2 weeks: Laparotomy ‘+ Laparoscopy cen be alternative if no other indications for laparotomy + Chronic > 1 — 2 weeks: Thoracotomy + Mechanical ventilation with positive pressure may prevent hemiation or at least chest tube should be in placed + Tension pneumothorax can developed during insuftlation of COz during laparoscopy in diaphragmatic injury Repair: ‘+ Linear injury: Continuous 1 locking polypropylene suture ‘+ Damage control surgery: No repair, cover the defect with folded pad + Tissue loss with defect: Mesh repair ‘© Biological mesh: for temporary repair if infection present © Prosthetic mesh: for definitive repair © Alternative: omentum, fascia lata, or latissimus flap ‘+ Detach from chest wall: © Interrupted 4 polypropylene suture through the edge of detached diaphragm, then around the adjacent rib, and then through, the edge of the diaphragm again before tying1m Flail chest: © 22 consecutive ribs broken at 2 2 sites > paradoxical motion © Underlying pulmonary contusion 1 Tension pneumothorax (one way valve) © { BP, | Breath sounds © | Venous return (IVC, SVC compression) © Airway pressures © Distended neck veins © Tracheal shift © Treatment Needle decompression at 2 intercostal space, then chest tube insertion = Open pneumothorax © Associated with inspiratory rushing breath sound © Cover the hole with sterile dressing as 3-sides adhesive non-occlusive dressing to prevent tension pneumethorax © Insertion of chest tube = Pulmonary contusion © Usually earty within 12 ~ 24 hours (ARDS can developed late) © Appears as localized patchy infiltration © Associated with rib fractures (Unilateral or bilateral) © Followed by alveolar damage, edema and hemorrhage Retained hemothorax (10 — 20 © Residual nemothorax despite attempted evacuation by tube thoracostomy © 26% risk to develop empyema (which may need for decortication) © Options for management: ‘+ Initial observation (80% successful if < 300 mi remaining) + Video-assisted thoracoscopy “VATS” + decortication (for > 300 ml remaining) if < 1 week * Thoracotomy if associated with other injuries as diaphragmatic injury) © Other Options: (Often ineffective methods) ‘= Placement of additional chest tube * Image-guide chest drainage ‘+ _Instillation of fibrinolytics through existing chest tube= Air embolism (CO; embolism) © Pathophysiolo: Direct communication between air and vascular system Pressure gradient © 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) © Signs: * End-Tidal CO, © 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 * Airleak if associated with bronchial injury = tPaCOs, | PaO2, | Sa02 © Management + Resuscitation = ICU management © IN fluids # inotropes = Ventilation with 100% O2 © Intubation if required © Stop COz, deflate abdomen, remove instruments during laparoscopy © Tum 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 © Bronchoscopy to evaluate bronchial tree = Associated with penetrating thoracic trauma 1) Intubation with one-lung ventilation 2) Emergency Left anterolateral thoracotomy > Clamshell thoracotomy may consider if air embolism diagnosed preoperatively 3) 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 4) 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 5) Continue operative resuscitation © Vigorous cardiac massage © Keep in Trencelenburg position 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 © Most common at: Anterior right ventricle © Most common arrhythmia: Supraventricular Tachycardia and PVCs © Most common causes of death: Ventricular tachycardia and Ventricular fibrillation Aortic dissection © Clinical presentation: ‘+ Dyspnea and chest pain + Pseudo-coarctation syndrome: ‘© Upper Extremity BP > Lower Extremity BP ‘© Decreased femoral pulses © Imagina findinas: ‘+ Widened mediastinum > 8 cm NNGT and Trachea deviation to right, and deviation of left bronchus, Lett apical capping 1 and 2” rib fractures Obliteration of the aortic nob Lett hemothorax © Tear'is usually at ligamentum arteriosum, at aortic isthmus (before beginning of descending thoracic aorta) © Investigations: = Unstable: + Trans-esophageal Echocardiogram + Stable © CXR ‘= Spiral CT chest with IV contrast (if abnormal CXR) ©. Direct signs: Pseudoaneurysm, extravasation, regular intima © 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 + Allother abdo jury should be controlled first before addressing aortic injury © Definitive repair © Interposition PTFE graft™ Cardiac injury and tamponade: © Constriction of the heart (| Cardiac output) as result of compression from pericardial bleeding © Beck's triad: * Hypotension + Jugular venous distention = Muffied heart sounds © Kussmauts sign: + Jugular venous distention during inspiration, © Management = Stable with negative FAST: = ECG, Echocardiogram, Troponin | > Any abnormality mandates monitor + Unstable ‘Initial as temporary method before definitive repair: © Pericariocentesis © Cardiac arrest or Pulseless electrical activity (PEA) © Emergency thoracotomy ‘+ Positive FAST pericardial window in unstable patient in spite fluid window incision (to confirm ciagnosis) (10 cm midline vertical incision over sub-xiphoid) Positive result > Sternotomy (Better) or Thoracotomy © Pericardiocentesis + Indications: ‘* Emergency: Suspicions of cardiac tamponade As temporary method for later definitive operation Ensure NGT and IV line are connected Antiseptic of sub-xiphoid area Infiltration of local anesthesia Position the patent 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 mi 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 ~ Trachea and proximal both bronchus Right Posteriolateral thoracotomy = Right bronchus = Proximal or Middle esophagus (Malignancy) For specific LEFT injuries: R thoracotomy Left Anteriolateral thoracotomy - Proximal left subclavian artery (Most difficult exposure) - Distal left esophagus (Perforation, Malignancy)ABDOMINAL TRAUMA © Most common organ injured with blunt trauma: Liver = Most common organ injured with penetrating trauma: Small bowel Penetrating injury: © Gunshot injuries: © Unstable: Immediate exploration (Standard of care) ©. Stable: CT scan with triple contrast followed by exploration © Stab abdominal injuries: © Back or flank: + Unstable: Immediate exploration (Standard of care) ‘+ Stable: CT scan with triple contrast followed by exploration ©. Anterior abdomen: ‘+ Unstable, evisceration or peritonitis: Laparotomy + Stable: © 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 + Laparoscopy (associated with other injury as rectal bleeding) + Penetrated fascia: ‘+ Unstable: Laparotomy + Stable. - Laparotomy (Standard of care) = Alternative = CT scan with triple contrast = 24hours observation "Serial abdominal examination = Serial Hb and WBC Blunt injury: Trauma CT scan © CT Chest / Abdomen / Pelvis + Head or Cervical with IV contrast co IV contrast is a must, to evaluate solid organs © Oral water-soluble contrast used selectively to rule out leakage, but might miss bleeding from bowel lumen © Reotal contrast used in flank or back injury or suspicious of large bowel perforation © Fluid density: 0-10HU: Ascites, Bile, Urine, or Intestinal contents © 30-40HU: Unclotied blood © 40-60 HU: Clotted blood © 80 ~300 HU: Active bleedingPREPARATION OF THE THEATER FOR TRAUMA PATIENT Consent for exploration: © 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 consutiations Prepare tubes and catheters, © Nasogastric tube © Foley's catheter © IVline catheters Anesthesia equipm = Oral/nasal airways - Ambu bags ‘ - EIT = CVP catheter kit = Suction device = PAcatheter kit = Laryngoscope ‘Tray 1 equipment; Mechanical ventilator ~ Intravenous access = Arterial blood gases Portable monitor: ECG, BP, 0, Sircithen Rapid infusion / Warming device ‘ray 2 Instrument trays: ~ Basic surgical trays Mars oP ett ‘Autologous blood saver - Trauma set auto-transfusion device (salvage) = Thoracotomy set = Chest tube set Irrigation and suction - Vascular set cellaneou! ‘Trauma laparotomy pads Self-retaining retractors Topical hemostatic agents ‘Argon beam coagulator Pneumatic compression devicesEXPLORATORY LAPAROTOMY m Stops: ‘© Supine position with arms extended © Prep and drape from the chin to the knees and laterally to posterior axillary lines © 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: © Skin incision beyond the previous scar into “virgin’ territory © Skin incision bypass 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-rataining 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: ‘© Sandwich the liver (above and below packing) Sandwich the spleen (above and below packing) Paracolic gutters Pelvis ooo 4 Resuscitative maneuver (Aortic control) ‘+ Supra-diaphragmatic aortic control “Through left thoracotomy" ‘© Used for uncontrolled or expanding supra-mesocolic hematoma + Supra-celiac (infra-diaphragmatic) aortic control © Access lesser sac © Through gastrocolic ligament © Through gastrohepatic ligament + By mobilization of left liver lobe, dividing the left crus, taking care not to injure the phrenic nerve, © 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© 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: © Both hemidiaphragm ©. Posterior peritoneum, bowel, and mesentery © Bladder, ureters and posterior wall of transverse colon and stomach + Identify and control source of contamination (Small bowel, colon, stomach, then lesser sac) ‘+ Infra-mesocolic exploration ‘© Pull transverse colen cranially, and run the bowel from ligament of Treitz to rectum, examine bowel (mesenteric and anti-mesenteric) and mesentery ‘© Pull transverse colon caudally and examination of supramesocoion © Entering the lesser sac: + Through left greater omentum “thinner and less vascular’ ‘+ Identity any fluid collection + Posterior stomach, duodenum, and pancreas £Kochorization + Exploration of retroperitoneum © Decisio Definitive repair = Damage controlManeuvers to exposure of retroperitoneum: Right side: Classic Kocher = Maneuver: (© Incise lateral peritoneal attachment of 1", and 2" 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) Cacum Division of parietal peritoneum ‘© Mobilize D3 and continue by standard kocher along white line of Toldt until the cecum © 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 . ree CBD - DJ junction Kocher maneuver by mobilizing the duodenal loop from CBD to SMV inferiorly Extended Kocher maneuver by incising the posterior peritoneum along the white line of ‘Toldt and mobilizing the right colon medially 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: ‘SMV injuty at the root of mesentery Avulsion of middle colic vein m Exposure: Infra-mesocolic retroperitoneum vc Celiac trunk Renal and iliac vessels Infra-renal aorta and aortic bifurcation 3%, 4 part of duodenum Head of pancreasLeft side: Mattox: (Left medial visceral rotation) Mobilize descending colon by incise sigmoid colon to splenic flexure along lateral peritoneal refiecton Retract the descending colon, left kidney spleen, pancreas, and stomach medially Modified mattox maneuver by keeping the kidney in Gerota’s fascia Continue dissection upward lateral to spleen for mobilization of spleen medially Most common complications: ° Splenic injury Avulsion of the descending lumbar vein m Exposure: ‘Supra-mesocolic retroperitoneum (Central) Aorta Celiac trunk ‘SMA/SMV Left renal an Tail of pancreasDAMAGE CONTROL LAPAROTOMY ™ Del 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 borderiine of lethal triad (Coagulopathy, Metabolic Acidosis, Hypotherrria) Arterial pH of 7.2 Lactic acid > 5 mmol/L Base deficit < - 15 in < 55 years, <~ 6 in > 55 years Temperature < 35 degree centigrade PT and/or PTT > 50% normal = Example (© Ligation of uncontrollable venous bleeding (No venous repair) © Bleeding duodenai/gastiic ulcer © Direct suture, resection, or by direct packing , with no reconstruction © Gastrointestinal perforation with generalized peritonitis © Peritoneal lavage with transection of proximal intestines and no reconstruction © Acute mesenteric ischemia © Staged laparotomy with resection of necrotic bowel and no anastomosis © Toxic megacolon © Subtotal colectomy with distal sigmoid and rectum left in situ © Acute cholecystitis ©. 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 tendemess Open book diastases of > 2.5 cm Anterior pelvic fractures: Venous bleeding 80% © Inspection for open wound, scrotum, and penile meatus © Bimanual and speculum examinations in female © Gentle compression on ASIS toward midline with mild anteroposterior movement ™ Posterior pelvic fractures: Arterial bleeding 10 - 20% © Most common artery injured: Superior gluteal artery © Inspection for open wound, perineum, and perianal © Palpation of the sacrum, sacroiliac joint, and DRE and assessment of prostate = Management, =< —s [_FAST positive FAST negative Laparotomy Conservative management Polvic Fixation Unstable Stable Pelvic Packing ’ ’ Polvic Packing CT scan Post-operative status Pelvic Fixation 1) Pelvic Binder Re-do FAST || 2) External Fixation 3) Angioembolization Stable [Unstable] | + + t Continue conservative management Angioembolization Consider external fixation