Acute Pancreatitis  Abdominal aortic dissection  Cholangitis

 Basal pneumonia  Acute cholecystitis

Pathophysiology
 Progression Complications
Pancreatic complications
1. Acute oedematous pancreatitis: interstitial inflammation &
oedema with peripancreatic fat necrosis. Sparing of acinar cells
Pancreatic  Initial fragile pseudocapsule matures into a fibrous capsule over 6 wks
pseudocyst  Usually asymptomatic & resolves if small
2. Necrotising pancreatitis: destruction of acinar cells
 Large pseudocyst may cause abdo pain, and compress / erode
3. Acute haemorrhagic pancreatitis: bleeding into pancreas and surrounding structures
retroperitoneum. Pancreatic ascites  Leakage of pancreatic secretion into peritoneal cavity
 Involvement of adjacent structures: CBD, duodenum, splenic veins,  May leak into thoracic cavity causing pleural effusion or
transverse colon bronchopancreatic fistula
 Severity dependent on balance between proteolytic enzymes & Abscess  Infection of necrotic pancreatic tissue
antiproteolytic factors (eg trypsin inhibitor, 1-antitrypsin) Gastrointestinal complications
 Factors influencing acute pancreatitis: UGI bleed  Gastric / duodenal erosion
1. Defective intracellular tpt & secretion of pancreatic zymogens Variceal  Splenic or portal vein thrombosis causes portal hpt, resulting in
haemorrhage oesophageal varices. Treat with thrombolysis.
2. Hyperstimulation of pancreas eg EtOH, fat erosion into colon
3. Pancreatic duct obstruction eg choledocholithiasis Duodenal  Compression by pancreatic mass
4. Reflux of infected bile/duodenal contents into pancreatic duct eg obstruction
sphincter of Oddi, disruption by gallstones Obstructive  Compression of CBD by pancreatic mass
jaundice
Causes: “GET SMASHED” Systemic complications
 Gallstones  Scorpion venom
Shock, renal  Increased vascular permeability
failure, DIC
 Ethanol  Hyperlipidaemia / HyperCa / Hypoxia  ARDS due to microthrombi in pulmonary vessels
 Trauma Hypothermia Hyperglycaemia  Disruption of Islets of Langerhans with altered insulin/glucagon axis
 Steroids  ERCP Hypocalcaemia  Sequestration of Ca in fat necrosis resulting in decreased ionized Ca++
 Mumps  Drugs (azathioprine, thiazides  serum albumin  Increased capillary permeability
 Autoimmune (PAN) diuretics, Na valproate)
Diagnosis
Clinical features  Based on clinical pic, elevated serum amylase or lipase and U/S
 Severe upper abdominal pain radiating  Epigastric tenderness
evidence of pancreatic swelling
to back, better on sitting forward.  Absent / quiet bowel sounds due to
 Nausea / vomiting paralytic ileus
 Fever  Hypovolaemic shock + oliguria Investigations
 Jaundice  Signs of haemorrhagic pancreatitis – Serum  > 1000 U/L or > 4 times the normal range. May be less in acute exacerbation of
Amylase chronic pancreatitis due to reduced vol. of functioning tissue.
 No guarding/rebound (c.f. perforated discoloration of flanks (Grey Turner’s
peptic ulcer) sign) or periumbilicus (Cullen’s sign)  Returns to normal within 24-48 hrs. Dx by raised urinary amylase: creatinine
ratio thereafter
 Persistently elevated amylase suggests pseudocyst formation
DDx  Mild elevations in intestinal ischaemia, perforated peptic ulcer & ruptured
 Perforated viscus  Perforated peptic ulcer ovarian cyst
 Myocardial infarction  Acute exacerbation of peptic ulcer  NO prognostic value
 Abdominal aortic aneurysm  Biliary colic AXR  Loss of psoas shadow (retroperitoneal fluid)
  Sentinel loop of proximal jejunum (solitary air-filled dilatation) 8. pts with signs of cholangitis (fever, TWC, cholestatic LFT): Blood
U/S  Confirm diagnosis C/S + start IV ABx (3rd generation cephalosporin eg ceftriaxone +
 Show gallstones, biliary obstruction or pseudocysts metronidazole). ABx not necessary if not complicated.
Endoscopic  DGIM – Last updated March 2005
Show gallstones, biliary obstruction or pseudocysts 9. I/O charting
U/S, ERCP
or MRCP
10. Admit
CT scan  Assess viability of pancreas
 Necrotising pancreatitis shows decreased enhancement on IV contrast injection  Severe pancreatitis: CVP monitoring if in shock. Intubate and
 Gas within necrotic material suggests infection and impending abscess ventilate if necessary, start prophylactic ABx
formation – percutaneous aspiration of material for culture required.  Non-acute Mx:
 Assess peripancreatic organ involvement  Feeding: withhold enteral feeding, but start parenteral
Serial CRP  Indicator of progress of pancreatitis nutrition early due to catabolic state
 Thromboembolism prophylaxis: SQ heparin
Assessing severity  Necrotising pancreatitis / pancreatic abscess: surgical
1. 3rd space fluid loss /  clinical dehydration  haemoconcentration >10% debridement + drainage
reduced end-organ  confusion  raised urea/creatinine
perfusion  ascites  metabolic acidosis
 Pancreatic pseudocyst: drainage into stomach / duodenum
2. Signs of organ failure  Coagulopathy (DIC screen +) after 6 wks when pseudocapsule has matured.
 Renal failure ( creatinine, metab acidosis, K+)  Pancreatic ascites: distal pancreatectomy
 Respiratory distress & hypoxia ( PaO2 & SaO2)  PT presenting with jaundice or cholangitis: ERCP to dx
3. Signs of sepsis  Local septic Cx (eg pancreatic abscess, infected pancreatic and treat choledocholithiasis.
necrosis) usually occurs only after 1 wk
 Consider non-pancreatic cause of sepsis eg cholangitis
secondary to biliary obstruction – look for cholestatic LFT Prognostic factors: Modified Glasgow Criteria (predicts mortality)
picture  PO2 < 8kPa  Glucose > 10mmol/L
4. Signs of severe  Grey-Turner’s sign, Cullen’s sign  WBC > 15 X 109/L  Urea > 16mmol/L (post rehydration)
pancreatitis  Signs of hypo Ca: carpopedal spasm, tetany
 Albumin < 30 g/L  ALT > 200U/L
 Blood glucose <10 mmol/L
 Serum Ca < 2 mmol/L (corrected)  LDH > 600U/L
Acute Management  c.f. Ranson’s criteria, which is only valid for alcoholic pancreatitis. However, Modified
 Main aims: restore blood volume, rest gut, treat underlying cause Glasgow criteria does not allow for easy follow up assessment of PT’s progress.
1. Keep pt fasted  Overall mortality: 10%
2. ABC and monitoring  Necrotising pancreatitis / pancreatic abscess mortality: 50%
3. Drip and suck
4. Supplemental O2 Ranson’s criteria:
5. Inx: Serum amylase, FBC, U/E/Cr, Ca, Glucose, LFT, LDH, ABG  On admission After 48h
blood C/S; CXR – assess for respiratory compromise, exclude basal  > 55 y.o  Serum Ca < 2 mmol/L
pneumonia and perforated viscus, ECG + cardiac enzymes –  bld glucose >11 mmol/L  Bld urea increase by 10 mmol/L
exclude AMI/atypical angina  TW > 16 x 10 ^9/L  Hct falls by > 10%
 LDH > 70 IU/L  Base excess > -4
6. Analgesia – Pethidine (avoid NSAIDs due to nephrotoxicity),  AST > 60 IU/L  PaO2 < 60mmHg (8kPa)
antispamodics. Not advisable if PT is in shock.  Estimated fluid sequestration > 6L
7. in pt w hx of PUD: Prophylactic acid suppressive Rx

DGIM – Last updated March 2005