Acute Pancreatitis

(AP)

Dr. A. R. Nitin Rao

Surgical Gastroenterologist
Bangalore, India
 Pancreas - anatomy
Weight – 75 – 125 gms
Length – 10 – 20 cms
Width – 3 – 5 cms
Thickest in the head (1.5 –
3.5 cms) & thinnest in the
tail (0.8 – 2.5 cms)
Head (includes uncinate
process), neck, body & tail
 Histology & Physiology
ENDOCRINE
 Islets of Langerhans
α cells (constitue 20 -25%) – produce glucagon
Β cells (constitute majority ) – produce insulin
δ cells (constitute 5%) – produce somatostatin
Others – Pancreatic polypeptide (PP), Gastrin,
Vasoactive intestinal polypeptide (VIP)
EXOCRINE (>1ml/minute)
 Acinar cells (contain zymogen granules) - secrete
enzymes
 Centroacinar & Intercalated duct cells – secrete
water & electrolytes
 Enzymes produced – Trypsin, Chymotrypsin,
Elastase, Lipase, Amylase etc.
Cholecystokinin (CCK) – most potent endogenous
hormone to stimulate pancreatic enzyme
 Acute Pancreatitis (AP)
 AP includes a broad spectrum of
pancreatic disease, varying from mild
parenchymal edema to severe
hemorrhagic pancreatitis with loss of
parenchymal viability , subsequent
gangrene & death
 Present as mild abdominal pain to severe
hypotension, metabolic derangement,
sepsis, fluid sequestration, multiorgan
failure & death
 9/10 patients have mild course managed
by supportive care. 1/10 patients have a
severe form.
 In PM studies 95% of patients dying within
 Etiology
 Alcohol 90%
 Trauma
 Biliary tract disease External
 Hyperlipidemia Operative
 Hypercalcemia ERCP
 Familial  Ischaemia
 Viral infection Hypotension
 Scorpion venom Cardiopulmonary bypass
 Drugs (Azathioprine, Vasculitis
Estrogens)  Pancreas duct
 Idiopathic obstruction
Tumor
Pancreatic divisum
Ascaris infestation
Ampullary stenosis
 Clinical Presentation
 Abdominal pain (predominant)
Epigastrium/ radiates to back
 Nausea, Vomiting
 Fever
 Tachycardia
 Epigastric tenderness
 Abdominal distension
 Hypotension
 Severe episode of acute hemorrhagic pancreatitis
Turners sign (bluish discoloration of (L) flank
Cullen’s sign (bluish discoloration of periumblical
region)
 Jaundice
 Diagnosis
LABORATORY TESTS RADIOLOGY
 Serum amylase  CXR
 Serum amylase  AXR
isoenzymes  US
 Urinary amylase  CT
 Serum lipase  MRI +/- MRCP
 Serum
methemalbumin
 Peritoneal fluid
analysis
 Hyperamylasemia
Amylase isoenzymes P type (pancreas) & S type
(salivary glands, fallopian tubes, ovaries,
prostate, breast, lung)
 In nearly all pancreatic disorders
 Biliary tract disease
 Intestinal obstruction
 Mesenteric infarction
 Perforated peptic ulcer
 Peritonitis
 Ac Appendicitis
 Ruptured AA
 Mumps
 Pneumonia
 Pregnancy
 Severity – Ranson’s criteria
ON ADMISSION WITHIN 48 HRS
Age > 55 yrs BUN rise > 5 md/dl
WBC > 16,000/mm3 PaO2 (<8kPa)
Blood glucose > S Calcium <8 mg/dl
200mg/dl Hematocrit fall >
LDH > 350 IU/L 10%
AST > 250 U/dl Base deficit > 4
mEq/L care
2 or less criteria – no mortality, supportive
Fluid
5 - 6 criteria ICU support required, sequestration
mortality upto 50% >
7 or more criteria – higher mortality6predicted
L
 Supportive therapy for
severe AP
CARDIOVASCULAR
 Adequate volume resuscitation
 Avoid hypotension/hypoxia/poor
perfusion
METABOLIC
 Replacement of calcium/electrolytes
as needed
NUTRITIONAL
 Enteral feeding
PAIN
 Supportive therapy for
severe AP
PULMONARY
 Oxygen supplementation in mild case
 Ventilatory support
RENAL
 Adequate perfusion
 CVVHD/HD if ATN and in renal failure
INFECTIOUS
 Broad spectrum antibiotics
 Imipenem if suspect pancreatic infection
 Operative Mx for AP
 ERCP & sphincterotomy
 Cholecystectomy in same admission
 Necrosectomy
 Acute fluid collection if infected
external drainage
(percutaneous or open method)