Oesophageal Pathology:

X-Ray features of Oesophageal Tumours

 Malignancy - Mediastinal expansion
Squamous (upper 1/3)
Dysphagia
- Tracheal bowing
Mixed (middle 1/3) - Air-fluid levels
Adeno (lower 1/3) - Type I lower oesophagus
- Type II cardia
- Type III fundus Difficulty
Scope findings for Oesophagitis Swallowin
g
 Oesophagitis - Red, inflammed oesophageal mucosa
Reflux oesophagitis Hx of heartburn - May see signs of Barret’s oesophagus
Various aetiologies
Non-Reflux oesophagitis C - Caustic ingestion
I - Infection (e.g. candida) Oropharyngeal Oesophageal
T - Tetracyclines (drugs) Can’t form a bolus Liquids + Solids
R - Radiation Achalaisa
I - Iatrogenic (e.g. N.G. Tubes) Solids only
S - Systemic diseases Malignancy
Solids  both
 Strictures Barium Swallow
- May see filling defects Advanced malignancy
Oesophagitis
CITRIS - benign - May see Bird’s beak (achalasia)
Reflux - benign cause for non-benign changes - May see apple core (malignancy)
Management:
- Shouldering (malignancy)
- Compare lesion length to vertebral bodies  Surgery - 10cm margins needed to clear
 Motility Disorders
 Neoadjuvant theraphy if lymph spread is present
Primary (in oesophagus)
- Achalasia
 Chemoradio therapy for all squamous Ca
- Uncooridnated contractions
CT Scan  Oesophagectomy may be necessary
- Look for mets
- Hypercontractility “nutcracker”
- Staging
- Hypocontractility “ineffective oesophagus”
Secondary (outside oesophagus)
- CNS disorders e.g. stroke
- Chagas infection
- Caustic ingestion
- Connective Tissue Disease (Scleroderma)
- Carcinoma
Idiopathic
 Motility Disorder of Oesophagus
Primary Secondary Idiopathic Achalasia
Problem in oesophagus Problem d/t other causes Unknown cause
Motility d
isorder o
fo esophagu
 Inadequate relaxation of L..O.S.  CNS disorders  No primary or secondary cause s
 Uncoordinated contraction  Chagas infections can be found
(D.E.S.)  Caustic ingestion
 Hypercontraction - “nutcracker”  Connective Tissue diseases (e.g.
 Hypocontraction “ineffective Scleroderma)
oesophageal motility  Carcinoma

Achalasia Pathophysiology: Inhibitory Fibres

- Nitric oxide
1. Oesophageal Body - VIP
Destruction of myenteric nn plexus  Motility
2. Oesophageal Sphincter Excitatory Fibres
Selective destruction of inhibitory fibres  unopposed excitatory action - Acetylcholine

S&S: Diagnosis:

 Dysphagia Dysphagia  Chest X-ray CT scan

Dysphagia May see air fluid levels
Achalasia
 Heartburn May see “sigmoid oesophagus” -
 Regurgitation of food very large oesophagus Management:
 Respiratory Sx d/t aspiration Gastric bubble may be absent
 Respiratory Sx d/t pharyngeal  Barium Swallow
 Ach inhibitors
irritation by reflux  Manometry
 Botox injections
 Hypetensive L.E.S
Retrosternal pain - good prognosis  Sphincterotomy / Heller’s Myotomy
(nn preserved) Incomplete relaxation of L.E.S. Pseudoachalasia Prevent reflux - DOR (ant) or Toupet (post)
Aperistalsis of oesophageal body
 Longstanding Hx of symptoms (not Not as “complete” as Nissin
 CT scan
usually acute)  Dilatation - Risk of rupture
See tumours
F/U - for life!!!

Notes:
Pseudo-achalasia - e.g. submucosal tumours ---- short Hx with wt loss, etc.
Signs & Symptoms:
 Recurrent well-localised epigastric pain
 Pain may radiate to the back
 Pain radiating to shoulder - affected diaphragm Rule of Thumb:
Peptic Ulceration (PUD)
 Duodenal ulcer - pain when hungry, relieved by food/antacids/milk/vomiting Gastric ulcers = always chronic
Ulceratio
 Gastric ulcer - pain during eating, relieved by vomiting Duodenal ulcers = acute/chronic n of the g
astric mu
cosa (exp
 May have heartburn, anorexia, waterbrash (sudden flow of saliva into mouth) osed to a
cid).

Causes:
 H. pylori Infects mucosa of antrum of stomach  inflammatory response = gastritis
Inflammations stimulates gastrin production  hypersecretion of gastrin  hypersecretion of acid Typical Atypical
Excess acid  gastric metaplasia of duodenal mucosa & colonisation  damaged mucosa - Lesser curve - Cardiac region
Irradication therapy needed (PPI + 2x Abs) - Multiple ulcers - Fundus
 NSAIDS Cox inhibition  inhibits prostaglandin synthesis  decreased mucous & bicarb in stomach mucosal damage (in NSAID use) - Greater curve
- Antrum
 Smoking More NB in gastric ulceration than duodenal ulceration
Typical ulcers don’t need - Pylorus
Delayed healing of ulcers and increases risk of complications (e.g. bleeding/perf)
to be biopsied necessarily. Always biopsy these!!
 Genetic factors
 Zollinger-Ellison syndr Gastrin-secreting tumour (gastrinoma) - mostly found in pancreas but can be in duodenum/stomach
Large volume of acid secreted into small intestines  diarrhoea
Inactivation of pancreatic lipase  steatorrhoea
 Blood group O
 Hyperparathyroidism  Ca2+ levels  stimulate acid secretion

Complications:
 Perforation
 Acute haemorrhage
 Chronic haemorrhage
 Pyloric stenosis
Management:
 Resus - fluids/NG tube if needed/nutrition/blood TF
 Admit
 G-scope with biopsy
Acute onset of sever unremitting epigastric pain
Pt may be pale, shocked, peripherally shut down (d/t generalised peritonitis)
Erect CXR needed - free air under the diaphragm!!
Upper GI Bleeding
Types of Gastric Surgery:
Upper GI Bleeding often leads to anaemia and blood in stool may be totally occult
Narrowing of pyloric channel  gastric outlet obstruction Billroth I
Fullness Preserves duodenal passage
Constant dull epigastric pain Preserves pancreatic fx
Projectile vomiting of large volumes undigested food Less incidence of gastritis & reflux
± visible peristalsis in thin patient (gastric peristalsis) Only suitable for distal limited gastric resections
Succusion splash (audible splashing noise when pt gently rocked from side to side) Billroth II
Can be used for larger gastric resections
Can result in dumping syndr
Treatment:
Roux-en-Y
 Surgery (various procedures can be done) Better control of enterogastric reflux
 Eradicate H.pylori Method of choice for early dumping or reflux
DDx for Upper GI Bleeds Management:
Oesophagus
 Varicose veins Portal Hpt d/t alcohol
Initial Care
Stable patient without signs of exsanguination
Upper GI Bleeds
Portal Hpt d/t hepatitis - don’t give blood TF
 Mallory Weiss Tears - resus appropriately
 Erosive Reflux disease - stop bleeding during scope
 Oesophageal Ca
Patient in shock


Blood tests

Scans

Examination
Hx

Upper GI Bleeds: Investigations

Infections Always remember Candida in Immunococompromise - give 4U blood TF immediately
- fluid resus
- try to stop bleeding during scope
Stomach
 PUD H.pylori Patient with anaemia
NSAIDS - Transfuse 1U per g/dl bellow 10g/dl if the patient has symptoms
Stress

FBC / U&E / INR

If no source found - think of Bleeding that stopped

CT scans
U/Sound
Oesophageal-gastro-duodenoscope (OGD)
Look for signs of liver pathology - can be a source of the bleeding
Look for signs of blood loss severity
Used to exclude items on the common-causes-list
- Asymptomatic patient - no transfusion needed
Smoking
Caustic ingestion Re-bleeds
Malignancy Patient over 60yrs
 Malignancy Carcinoma - transfuse if >4U blood needed to resus or >8U needed in 48hrs
Lymphoma Patient under 60yrs
Melanoma - transfuse if >8U needed to resus or >12U needed during 48hrs
Kaposi Sarcoma
 Gastritis Haemorrhagic (severe cases)
Indications for Surgery

Extra-GI Bleedings
- Bleeding not controllable during scope & patient in shock
Duodenum
- >1 re-bleed in one admission (patient over 60yrs)
 Erosions (ulcers) - >2 re-bleeds in one admission (patient under 60yrs)
 Malignancy (rare in the duodenum)

Secondary Bleeds Techniques for controlling a bleed:

 Pancreatic Pseudocyst  Band ligation
 Aorto-enteric fistula  Cauterisation
 Haemobilia (trauma in liver -- bile duct)  Adrenaline inj into the ulcer base

Fistulae
Pancreas
Liver
Aorto-enteric fistula
GIT tumours
Mallory-Weiss Tears
 ENT  Sengtaken Blakemore tube
 Medical disorders (bleeding problems)  Open surgery

Notes:
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Complications from Resection:
 Dumping Syndrome
 Decreased Calcium absorption - os-
teoporosis
Post-gastrectomy Syndromes
 Anaemia - iron deficiency
 B12 deficiency

Dumping Syndrome: Anaemia:

Caused by - Bleeding Complications of Gastrectomy with Vagotomy:
Early - 15-30min after a meal  intake - appetite low  Denervation
Incr transit time  absorption - Decreased HCl
 Impaired storage
Hypertonic solution released into intestine
Intestines suck water into lumen (osmosis)  Impaired gastric digestion
Hypovolaemia  catecholamine release  Impaired sphincter control - transit time increased
B12 Deficiency:
Tachycardia Caused by - Lacking intrinsic factor - poor absorption
 Hormone / acid secretion imbalance
Palpitations  intake - poor appetite
Flushing
Sweating
Etc. Types of Gastric Surgery:
Intestinal lumen distended - major aspect of Early Dumping Hypocalcaemia:
Pain Caused by - Decr fatty acid absorption Billroth I
Bloating  decr calcium absorption Preserves duodenal passage
Full sensation  osteoporosis Preserves pancreatic fx
Diarrhoea Rx: give Calcium + Vit B12 together Less incidence of gastritis & reflux
Only suitable for distal limited gastric resections
Late - 40-50min after a meal Billroth II
 transit time - quick release of all gastric contents at once Can be used for larger gastric resections
 carbs absorbed from duodenum Can result in dumping syndr
 blood glucose levels Roux-en-Y
 insulin release Better control of enterogastric reflux
Sudden  in glucose Method of choice for early dumping or reflux
Hypoglycaemia  Catecholamine release
Tachycardia
Flushing
Palpitations
Sweating

Rx: Low carb meals (rather protein/other)

Small, frequent meals rather than big meals
Complications from Reconstruction:
 Afferent Loop syndrome
 Efferent Loop syndrome
 Alkaline gastritis
Post-gastrectomy Syndromes
 Gastroparesis

Afferent Loop Syndrome: Gastroparesis:

Obstruction caused by - Twisting Gastric atony - leftover stomach is atonic Complications of Gastrectomy with Vagotomy:
Herniation  emptying ? d/t denervation and lacking hormone secretions  Denervation
Strictures  Pain after eating  Impaired storage
Adhesions  Early satiety  Impaired gastric digestion
Anastomosis stenosis  Nausea
 1-2litres of fluid build up in the Afferent Loop  Impaired sphincter control - transit time increased
 Vomiting  Hormone / acid secretion imbalance
 Distension
 Pressure - fullness/pain Dx: Exclude other possibilities Electrolyte imbalances
 Reflux into stomach rather than outflow into intestines Strictures
 Vomiting of intestinal contents - immediate relief of pain Diabetes Mellitus Types of Gastric Surgery:
Etc.
Dx: Radio isotope studies = gold standard Billroth I
Rx: Erythromycin Preserves duodenal passage
Rx: Re-operate Metoclopramide Preserves pancreatic fx
Convert to Roux-en-Y Less incidence of gastritis & reflux
Enteroenterostomy - better/easier option Only suitable for distal limited gastric resections
Billroth II
Can be used for larger gastric resections
Efferent Loop Syndrome: Vagotomy: Can result in dumping syndr
Usually occurs within 30days  Atony of the stomach Roux-en-Y
Very uncommon  Pumping abnormalities Better control of enterogastric reflux
Method of choice for early dumping or reflux
 Secretion abnormalities
Gastric content does not empty
Anastomosis stenosis (gastric outlet obstruction)
 Pressure
 Fullness
 Nausea
 Pain
 Vomiting (undigested food)

Dx: Beefy red mucosa seen when doing a scope

History of gastric surgery present

Rx: Surgery - Roux-en-Y

Presentation: Primary Stones Asymptomatic
Stones originate in - Usually no Rx required 1 - 2 % convert per year
Gallbladder or CBD stones can cause:
 Pain
the gallbladder
(usually pigmented
- Majority of stones
Cholelithiasis
 Nausea stones) < 0.5% per year Symptomatic
 Vomiting - Rx usually required
± 50% convert per year
 Tender RUQ Secondary Stones
Stones in
the biliary
Complicated tree.
Stones originate in - Choledo
- Require urgent treatment lithiasis
Obstruction of any structure can cause: the ducts - Cholecy
stolithiasis
 Pain (usually cholesterol
 Nausea stones)
 Vomiting
 Tender RUQ Investigations:
 Persistence of pain Bloods Inflammatory markers (e.g. ESR, CRP, WCC)
 RUQ mass LFTs (stone in GB vs CBD)
 May have jaundice… Amylase / Lipase (?gallstone pancreatitis) Indications for Prophylactic Surgery:
Treatment:
- Haematological diseases
Obstruction that becomes infected may cause: U/S Cholecystitis Acute Hereditary spherocytosis
Stones
- thickened wall
 Above sx - Lapscope surgery (single vs double) Sickle Cell disease
- pericholecystic fluid
 Swinging fever - Murphy’s U/S sign
- Open surgery
 Tachycardia - ERCP stone removal - Immunocompromise
- Distended GB ± stones Transplant patients
 Neutrophilia (later cholecystectomy)
Cholecystitis Chronic Diabetes Mellitus
 Rigors - Stones HIV +
On-table cholangiogram - very useful
- Thickened wall Chemotherapy
Inflammation & infections can cause: - No perichlecystic fluid or pain
Stones in the CBD Long term corticosteroid Rx
 Pain Simple Biliary Colic
- Transcystic approach (small stones)
 Nausea - Clinically no Sx (no pain)
- Cut in the CBD (big stones) Surgery of choice:
 Vomiting - See stones (but none of the other signs) - Laparoscopic cholecystectomy
Obstruction
 RUQ tenderness - Open cholecystectomy
- See stone in duct
 Fever - dilated bile ducts
- ERCP therapeutic
 Tachycardia - abN LFT’s seen on bloods
 Neutrophilia Lecithin Cholesterol:
ERCP Remember risk factors during procedure - Soliaire stones
- Mulberry
- Crystalline
Constant Pain / Vomiting / Nausea / Fever / Murphy’s Sign Cholesterol Diabetes mellitus
80%
Mixed: Pregnancy
Complications: - Faceted
Diet
 Biliary colic  Cholecystitis (acute)  empyema  Gangrene  Perforation  Biliary Peritonitis (or Mucocele) - Concentric
 Obstruction  stasis  cholecystitis  Jaundice Genetics
 RUQ pain Bile salts:
 Obstructive Jaundice  Stasis  Cholangitis
 Fever Triad Bile Acids - Pigment (Calcium) Haematological disease
 Obstructive Jaundice  Stasis  Pancreatitis
 Jaundice Dark/Black
 Large stone  erodes through to duodenum (fistula)  Gallstone ileus / Small bowel obstruction Crohn’s disease
 Organ failure / shock Light / Brown
 Adenocarcinoma gallbladder - Jacks
S&S: Obstruction:
 Dark urine d/t unconjugated bilirubin circulating & excreted in the urine (urobilinogen absent)  Obstruction of the biliary


Pale stools
Pruritus
d/t bile that cannot pass into GIT to act on stool
d/t inability to secrete bile salts into obstructed biliary system (bile salts in dermis)
tree
 Jaundice Obstructive Jaundice
 Malaise (hyperbilirubinaemia
 Jaundice >2.5) from obstruction of
bile flow to duodenum Cholestati
 Anorexia & Nausea c Jaundice
obstructio -
n to the fl
ow of bile
fr om liver
Investigations:
 Bloods LFT  ALP - more specific for obstruction - Formation of ALP from cells in lining of biliary canaliculi

minal
Intralu-
Gradual decrease in levels once obstr relieved Gallstones
 ƴGT - can also be  in intrahepatic obstruction Cholidocholithiasis (stone in CBD)
 Transaminases Mirrizzi Syndr (enlarged GB obstructing CBD)
 Lactic dehydrogenase (LDH)

Intramural
Stricture - stones, trauma, post-procedural
FBC
Coagulation screen (prolonged prothrombin time) Sclerosing Cholangitis - fibrosis of biliary tree
Ratio between total and conjugated bilirubin > 50%
Cholangiocarcinoma - adenocarcinoma of biliary tree
 Ultrasound Safe, non-invasive & reliable - GOLD STANDARD Congenital Causes (biliary atresia) - jaundice 2-3 wks of life
Detects the following: Duct dilatation (in acute cases or intrahepatic obstr, ducts won’t be dilated)
Gallbladder distension Choledochal cysts - 5 types of cysts in biliary tree
Stones (indication to do ERCP) - No stones - consider CaPancreas
Parasitic worms / infx
SOL in liver
SOL in pancreas (overlying bowel gas can obstruct view) Trauma

 MRCP MRI - non-invasive, no radiation but expensive Post-procedural

No intro of infection into obstructed biliary system or pancreatic ducts

Extramural
Pancreatic pseudocyst - not epithelialized
Enables vascular assessment & parenchymal assessment of the liver & pancreas - NB in malignancy
Chronic pancreatitis - calcifications seen on imaging
 ERCP Outlines biliary & pancreatic system - inject dye into papilla of Vater - often d/t alcohol intake
More detailed info than US Peri-ampulary pathology (tumours)
Endoscopic Rx of gallstones, biopsy & periampularry tumours can be done - relieve obstruction by e.g. stents
Complications Retroperitoneal path
- acute pancreatitis - sarcoma
- cholangitis (administer prophylactic Abs) - TB lymphadenopathy (peri-aortic)
- haemorrhage - lymphoma
- perforation
Duodenal path (inflammation / fibrosis)
- scarring - structures
Malignancies (head of pancreas, GB, Duo)
 Percutaneous Transhepatic Cholangiography (PTC) - assess obstruction of biliary tree (not used commonly) - invariably associated with stones if in GB
 CT scan Identify hepatic ducts, bile ducts, pancreatic tumours & demonstrates dilated biliary tree to level of obstr. - 90% adenocarcinoma
May detect dissemination to adjacent lymph nodes - 10% squamous carcinoma
 Lapscope Under GA - role in staging tumours with malignant obstruction of biliary tree (as well as mets) Direct invasion of bile ducts cause obstruction
 Laparotomy Used to remove causal lesion / relieve biliary obstruction - intraoperative U/S is also helpful for neoplasia & obstr. Early lymph/haem dissemination

Complications: Cholangitis (triad - RUQ pain, fever, jaundice) / if not treated may lead to shock. Rx: Vit K to prevent bleeding. Liver Damage also occurs.
Obstruction of cystic duct  Stasis  Culture for bacterial growth  Complications

Cholecystits
Most often stones Poor infection control Organisms can come from anywhere - Pancreatitis
- gallstones situation!! Inflammation - Hepatorenal syndrome
- pancreatic Can cause scarring - Gallstone ileus
- Empyema - rupture - peritonitis
Can be acalculus - Mirrizzi syndrome
Inflamma
- immobility (no CCK) Narrow angle between CBD tion of the
gallbladde
and cystic duct r
Vascular
- inotropes (vasodilation,
Types:
fluid translocation, oedema)
 Acute
 Chronic

S&S:  Complicated
 RUQ pain  Uncomplicated
 Fever
 Malaise
 Calculi
 Murphy’s sign
 Acalculi

Investigations:
- U/S See stones
Distended gallbladder - mucosal fluid
Peri-cholecystatic fluid - multi-factorial
Thickened wall - inflammation
Dilated ducts - outlet obstruction

- ERCP Not safe if there is already infection

Can introduce more infection
 Presentation Liver abscess:
Liver Masses - Pain RUQ

Tumours Cysts Infective

- Fever
- Rigors Liver Masses
Benign Simple  Pyogenic abscess (most - Jaundice
 Liver cell adenoma Complex Adenoma common infective liver - Anorexia, nausea, wt loss
- ± Palpable liver abscess
 Focal Nodular Hyperplasia Adenocarcinoma mass)
- ± May have tenderness
 Haemangioma Biliary  Fungal
 Biliary Haematomas  Amoebic
Malignant Primary  Parasitic (often forms X-ray features of liver abscess:
 Hepatocellular “Hepatoma” cysts) - raised hemidiaphragms
 Cholangiocarcinoma - air-fluid levels
Sources of infection: - pneumobilia
 Sarcomas
 Neuroendocrine  Pyelophlebitis of
portovenous vessels
 Germ cell
(from appendicitis)
Malignant Secondary / Mets
 Trauma
 Colorectal Indications for Surgery Focal Nodular Hyperplasia of the Liver
for Abscess:  Direct extension - from
 Neurendocrine - More common in females
- Rupture cholangtitis (etc.)
 Non-colorectal Non-
- Ascites  Arteria - from any other Sx: Usually asymptomatic
neuroendocrine
- Peritonitis source in body.
 GIT - Imminent rupture
May regress with time
 Ovaries - Failed conservative Rx Rx:
May regress on withdrawal of contraceptive pill
 Etc. - If abd surgery - Ab’s
Dx: Hyperplasia vs Adenoma - central fibrous scar in hyperplasia (usually seen on U/S or CT)
necessary anyways.. - Aspiration / surgical drain
- pig tail catheters
Rx: No malignant transformation thus no treatment unless symptomatic.

Liver Cell Adenomas Biliary Hamartomas

- Relatively uncommon - Small fibrous lesions - usually beneath capsule of liver
- Almost exclusively woman (may be ass with contraceptives - high *oestrogen+)
Dx: Do biopsy - can be mistaken for small metastatic lesion
Sx: May be asymptomatic
May present with R.U.Q pain d/t haemorrhage within tumour
May have signs of haemoperitonium (rupture)
Cavernous Heamangioma
- Most common benign liver tumour
Dx: Usually solitary, encapsulated lesion
- mostly asymptomatic (don’t reach sufficient size to cause abd pain / swelling / haemorrhage)
Malignant transformation has been reported - F/U regularly
U/S or CT scan may show adenomas
Dx: Dense hyperechoic lesion so on ultrasound
Usually normal LFT’s
Incidental finding on lapscope
Avoid PCBiopsy
Needle biopsy can be hazardous
Rx: Formal hepatic resection (difficulties distinguishing adenoma from well-diff hepatoma)
Rx: Resect only large lesions (by experienced surgeons)
Also risk of malignant transformation & risk of spontaneous haemorrhage = resect!
Leave incidental findings alone if small
Clinical Features:
 Constant severe / agonising epigastric pain
 Pain ± radiates to the back - severe necrotising / deep peptic ulcer can also radiate to back
 Nausea & vomiting & retching Acute Pancreatitis
 Less tenderness, guarding & rigidity than expected from Hx
± shock Inflamma
tion of th
± Cullen’s sign - bruising around umbilicus / drawny discolouration of flanks (retroperitoneal haemorrhage) normal an e Pancrea
atomical s with retu
± obstructive jaundice (transient) & functio rn to
nal norm
± pleural effusion - almost always Lt fided (d/t inflammation tracking retroperitoneally to involve pleura) ality.

Pathophys: Causes: Unknown

4.
3.

2. Severe necrosis - leads to

1. mild oedema
Different forms of Pancreatitis
General Effects: Metabolic Hypothermia Known
 Organ failure Alcohol

Necrotising septio
Severe haemorrhage
complications if not operated on)
 Hypovolaemic shock - Fluid/protein/electrolyte loss from capillary permeability Hyperlipidaemia
- Metabolic upset d/t cytokine release Hypercalcaemia
 Endotoxins in systemic circulation - bacteria & their products implicated
Iatrogenic Drugs - steroids
 Other - Acute Renal failure
- ARVs
- ARDS
Toxins - scorpion stings
- Consumptive coagulopathy
- Altered liver Fx - hepatocyte depression
Vascular Thromboembolism
- obstruction of common bile duct with gallstones
- pancreatic oedema causing obstruction
Mechanical Gallstones/slush - common bile duct
- cholecystitis
Local Effects:
- pancreatic duct
 Reflux of duodenal juices &/ bile into pancreatic duct Post-op - ileus
 Obstr to flow of pancreatic enzymes within the duct system - stasis
 intraductal activation of trypsin, chymotrypsin, phospholipase, catalase, elastase - increased pressure
 cell necrosis Pancreatic Ca
 further enzyme release form necrotic cells - microcirculatory changes Previous poly-gastrectomy
Activated proteolytic enzymes Haemorrhage
 Incr capillary permeability Pancreatic divisum - congenital & - annular pancreas
 Incr protein exudation Blunt/penetrating traumatic injury
 Retroperitoneal oedema ERCP / angiography
 Peritoneal exudation
Infections Mumps
Complications: Coxsackie
 Pancreatic pseudocyst
- not enclosed by epithelial layer (not true cyst)
- collection of pancreatic secretions & inflamm exudate enclosed in wall of fibrous/granular tissue
- occurs >4wks from onset of acute pancreatitis
- persistent/intermittent abd discomfort - mild-mod hyperamylasaemia  Pancreatic necrosis
- compressing neighbouring structures to cause vomiting & obstructive jaundice  Progressive jaundice
 Pancreatic abscess  Persistent duodenal ieus
~ circumscribed intr-abd collection of puss (usually in proximity to pancreas, conetaining little/no pancr fluid)  GI bleeding
~ more ill pt with pyrexia & leucocytosis (worse than pseudocyst)  Pancreatic ascites
~ UC or CT confirmation
Diagnosis:
Non-pancreatic causes for
 Biochemistry Serum amylase ± >1000 u/l - 3x the normal upper limit
May  rapidly & return to Normal within 48 yrs
hyperamylasaemia
(usually not >1000)
Acute Pancreatitis
Hyperlipidaemia may influence results
Reflects rupture of acinar cells & parts of ductal system  Acute cholecystitis
Amylase released into system  Perforated duodenal ulcer
Normal value does not exclude pancreatitis
 High intestinal obstruction
Serum lipase  - rise slower & more sustained
Most commonly tested for  Mesenteric vascular occlusion
Longer 1/2 life  Bowel strangulation
Not only  in pancreatitis (poor specificity)  Dissecting aortic aneurysm
Blood sugar HGT  Ruptured aortic aneurysm
 Ruptured ectopic pregnancy
 Gastroscopy Include ulcers
Exclude ulcers

 Radiology Chest Xray Pleural effusions

Features of ARDS - effusion / air-fluid levels if bowel perf / lower lobe pneumonia
Abd Xray Erect - see air-fluid levels
Supine - show typical small bowel signs
Bowel empty of gas except sentinel loop of jejunum
± gas seen in hepatic & splenic flexures but not transverse colon
- local ileus OR radiopaque stones
U/Sound Swelling of pancreas with peri-pancreatic fluid collections & oedema
± stones
CT scan Pancreatic & peri-pancreatic swelling / necrosis / stones

Management:

 Resus if not done - haemorrhagic can develop into necrotising

Monitor fluid output and input
 Nutrition NGT if vomiting
TPN for severe cases - least lipids possible
Enteral feeding may be better - duodenal feeds through a PEG
Rest the bowel - keep pt NPO
 Antibiotics controversial
 ERCP If gallstones / mechanical causes suspected
If patient is stable enough to cope through procedure
 Surgery Certain indications for surgery:
- deteriorating condition on max support - do necrosectomy
- septic pancreatitis
- gallstone associated - do cholecystectomy
- missed diagnosis
Causes:
 Alcohol - most common
 Hyperparathyroidism Chronic
 Truamatic duct strictures
 Gallstones (primary / secondary)
 Pancreas divisum
Pancreatitis
NB: Smoking is an important Co-factor!! Chronic In
fla
characteri mmatory conditio
sed by fib n
Pancreatic inflammation of exocrin rosis & de
Pathophys: e pancrea struction
Associate tic tissue
 Secretion of viscid pancreatic juices  Acute fluid collection dw
derangem ith permanent
 Protein plugs formed in duct system  Not a pseudocyst - pseudocysts ent of stru
cture & fu
 Calcification occurs to form duct stones don’t happen very acutely. nction.
 Impaired flow of pancreatic juices
 Inflammation / stricture formation of duct system

Acute Pancreatitis  recurrent acute  chronic relapsing  chronic pancreatitis

 Replacement of gland by fibrous tissue
 Entire ductal system can be constricted

Loss of acinar tissue  steatorrhoea

Loss of islets tissue  diabetes mellitus

S&S: Pancreatic Pseudocyst

 Pain d/t fluid around pancreas  splanchnic nn - perineural fibrosis  Commonest place = lesser sack
Or
Complications include
d/t pseudocyst causing pain
 infx (with abscess)
Or
Acute attack (d/t alcohol) with incr ductal pressure  ruptured vessels (with haemorrhage)
- epigastric  Rupture (with peritonitis)
- radiates to back - eased by leaning forward / getting down on all 4’s  Obstructive jaundice (very rare)
- may be precipitated by eating (some people learn to avoid fatty foods)
 Weight loss d/t  food intake
d/t poor diet Much less common than Pain/Wt loss
d/t malabsorption and steatorrhoea
 Steatorrhoea - Pale, bulky, offensive, floating, difficult to flush
 Transient / intermittent obstructive jaundice
 Duodenal obstruction
 Splenic vv thrombosis - splenomegaly / hypersplenism / gastric & oesophageal varices.