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ACUTE PANCREATITIS

ACUTE PANCREATITIS. SHABNA.A 2002 BATCH. DEFINITION. NON-BACTERIAL INFLAMMATION OF PANCREAS CAUSED BY ACTIVATION,INTERSTITIAL LIBERATION AND DIGESTION OF GLAND BY ITS OWN ENZYMES MILD PARENCHYMAL OEDEMA → SEVERE HAEMORRHAGIC PANCREATITIS → GANGRENE AND NECROSIS. ETIOLOGY.

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ACUTE PANCREATITIS

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  1. ACUTE PANCREATITIS SHABNA.A 2002 BATCH

  2. DEFINITION • NON-BACTERIAL INFLAMMATION OF PANCREAS CAUSED BY ACTIVATION,INTERSTITIAL LIBERATION AND DIGESTION OF GLAND BY ITS OWN ENZYMES • MILD PARENCHYMAL OEDEMA→SEVERE HAEMORRHAGIC PANCREATITIS→GANGRENE AND NECROSIS

  3. ETIOLOGY

  4. 1) GALL-STONE PANCREATITIS • 40% of all cases • 90% of a/c pancreatitis • Transient obstruction of pancreatic duct by a gall stone in CBD at Ampulla of Vater • Brief obstruction • Middle→late forties • Women

  5. 2)ALCOHOLIC PANCREATITIS • 40% of all cases of pancreatitis • 75% of c/c pancreatitis • Diagnosed after patients have consumed alcohol for atleast 20 yrs(b/w 6-10 yrs),daily consumption averages 100-150 gm/day • Diet richer in fat & protien

  6. MECHANISM OF ALCOHOL-RELATED INJURY • Alcohol is a known stimulant of gastric acid secretion→ duodenal acidification→ stimulates secretin release→ ↑exocrine secretion of pancreatic water & HCO3→parenchymal injury • Ethanol induces spasm of sphincter of Oddi → obstruction to pancreatic juice outflow

  7. Ethanol→↑ed conc: of enzyme protein in pancreatic juice→ precipitation in pancreatic ducts→ multiple ductal obstruction • ↑es pancreatic duct permeability→ leaking of enzymes→ damage to pancreas • a/c ethanol ingestion→ ↓es pancreatic blood flow→ ischaemia→ cellular damage

  8. 3) HYPERCALCEMIC STATES • Commonly hyperparathyroidism • Favour intraductal precipitation of calcium stones • ↑es permeability of ducts→ enzyme leakage 4) HYPERLIPIDEMIA • With ↑ed chylomicrons & VLDL • Release of large amounts of toxic fatty acids by pancreatic lipase

  9. 5)HEREDITARY PANCREATITIS • Dominant trait • Mutation in gene for trypsinogen→ interferes with normal trypsin degradation→ digest pancreas • Rare • b/w 12-14 yrs • Recurrent a/c attacks

  10. 6)POST-OPERATIVE (IATROGENIC) PANCREATITIS • Occurs after so many procedures • Direct injury to the gland Pancreatic biopsy,Pancreatic resection • Obstruction of pancreatic duct Long-arm T-tube through sphincter,forceful dilatation of sphincter to >5 mm diameter

  11. Follows endoscopic sphincterotomy • Follows surgical sphincteroplasty • Follows Billroth II gastrectomy

  12. Definite cause Azathioprine Estrogen Probable cause Thiazide diuretics Furosemide Ethacrynic acid Sulfonamides Tetracycline L-asparginase Corticosteroids Phenformin Procinamide Valproate Clonidine Pentamidine 7)DRUGS

  13. 8) PANCREATIC DIVISUM • Failure of dorsal & ventral duct system to join • Young adulthood • Recurrent episodes of acute pancreatitis DORSAL PANCREAS VENTRAL PANCREAS

  14. 9) MISCELLANEOUS CAUSES • Follows scorpion venom poisoning • Infections(mumps, group B coxsackie viruses, herpes simplex, IMN) • Exposure to anticholinesterase insecticides 10) IDIOPATHIC • 15-20 % of total • Other causes should be ruled out before confirmation

  15. PATHOGENESIS

  16. 1) OBSTRUCTION-SECRETION • Partial duct obstruction+Stimulation of pancreatic secretionMore severe pancreatic inflammation • Biliary pancreatitis gall stone obstructs pancreatic duct • A/c alcoholic pancreatitis Alcohol stimulates gastric acid secretion which then releases secretin stimulates pancreatic secretion • Alcoholspasm of sphincterobstructs pancreatic flow

  17. 2)COMMON-CHANNEL THEORY • Gall-stone in Ampulla of Vater obstructs CBD & pancreatic duct common channel b/w them bile reflux into pancreatic duct. • Infected bile contains deconjugated bile salts & bile incubated with pancreatic juice contains lysolecithine injure lining of pancreatic ducts es permeability leakage of pancreatic enzymes to surrounding parenchyma pancreatitis

  18. 3)DUODENAL REFLUX After Billroth II gastrectomy duodenal reflux occurs through papilla of Vaterpancreatitis 4)ED PANCREATIC DUCT PERMEABILITY Acute alcohol ingestion,direct exposure of duct to deconjugated bile salts,pancreatic secretion against an obstruction,acute hypercalcemia   duct permeability enzyme leakage pancreatitis

  19. 5)ENZYME AUTOACTIVATION

  20. PATHOLOGY

  21. Hemorrhagic Pancreatitis and Fat Necrosis Saponification  chelation of Ca with fatty acids liberated by pancreatic enzymes

  22. Changes due to action of pancreatic enzymes • Microvascular leakageoedema • Fat necrosis by lipase • Proteolytic destruction of pancreas • Destruction of blood vessels - interstitial hemorrhage

  23. Milder– a/c interstitial pancreatitis or acute edematous pancreatitis • Histology • Interstitial edema • Focal areas of fat necrosis in pancreas & peripancreatic fat • No pancreatic necrosis

  24. Severe –a/c necrotizing pancreatitis • Necrosis of pancreatic tissue affect acinar, ductal tissue & islets • Damage to vessel hemorrhage into parenchyma

  25. CLINICAL FEATURES

  26. Diverse spectrum of illness • Mild,short-lived,self-limiting illness severe toxic condition

  27. ABDOMINAL PAIN • Predominant feature • Begins in mid-epigastrium • Penetrating,radiating to back • Also in right or left upper quadrant • Also as generalized non-localized pain • Variable intensity-less severe with oedematous than necrotizing form of disease

  28. Alcohol associated pancreatitispain onset b/w 12-48 hours after an episode of inebriation Gall-stone associated pancreatitispain follows ingestion of a large meal nausea,vomiting & retching severe,protracted vomiting

  29. RARE PRESENTATION • Severe systemic illness hypotension,hypoperfusion & mental depression {signs of profound fluid loss}

  30. SIGNS • Fever(100-101ºF) • Tachycardia • Epigastric tenderness • Abdominal distension paralytic ileus from retroperitoneal phlegmon distension with intraperitoneal fluid in necrotizing pancreatitis

  31. Guarding & rigidity • Bowel sounds ed or absent • No palpable mass usually • If palpable A swollen pancreas (phlegmon, pseudocyst or abscess)

  32. Severe haemorrhagic pancreatitis In < 3% of patients • GREY-TURNER’S SIGN-bluish discolouration in left flank

  33. GREY TURNER’S SIGN

  34. CULLEN’S SIGN-bluish discolouration in periumbilical region • Results of tracking of blood-stained retroperitoneal fluid through tissue planes of abdominal wall to the flank or along the falciform ligament to the umbilical area • Indicates presence of severe episode of a/c haemorrhagic pancreatitis

  35. Grey turner’s sign Cullen’s sign

  36. Jaundice uncommon finding seen in patients with gall-stone pancreatitis also follow compression of distal CBD by oedema of head of pancreas • Major circulatory derangements in severe pancreatitis hypotension,hypoperfusion related to hypovolemia & ed preload to heart

  37. Extraabdominal manifestations • Left pleural effusion or left hemidiaphragm elevation(1/3 patients) • Signs of a/c pulmonary failure tachypnoea,dyspnoea,cyanosis • Subcutaneous fat necrosis • Cerebral abnormalities confusion,psychosis & coma follow hyperosmolarity,hypoperfusion & hypoxia,cerebral fat embolism or DIC

  38. DIFFERENTIAL DIAGNOSIS • Perforated peptic ulcer • Acute cholecystitis • Gangrenous small bowel obstruction • Cholangitis • Gastroenteritis • Vascular occlusion • Pancreatic cancer • Renal colic

  39. DIAGNOSIS

  40. SERUM AMYLASE • 90% of patients • Most widely used • Hyperamylasemia observed from 24 hrs to 7 days • es to > 2.5 times • Values > 1000 IU/dl  Biliary pancreatitis • Lower values  a/c alcoholic pancreatitis • P-type isoamylase  more diagnostic • 10% have normal serum amylase level

  41. 2) SERUM LIPASE • More reliable to diagnose • Pancreas is the main source of lipase in blood • Duration of hyperlipasemia exceeds that of hyperamylasemia • Time consuming & difficult  not preferred 3) SERUM TRYPSIN & ELASTASE CONCENTRATION • Sensitive markers of pancreatic inflammation • Radioimmunoassay kits are available

  42. 4) ADDITIONAL LAB TESTS • Haematocrit ed due to dehydration or ed due to pancreatic or retroperitoneal blood loss in necrotizing pancreatitis • ed WBC count >10000 cells/mm³ • Hyperglycemia,mild azotemia,hypocalcemia • LFT Normal or mild  in S.bilirubin (< 2 mg%) Common in gall-stone pancreatitis Also due to partial obstruction CBD by swollen pancreatic head

  43. 5) RADIOLOGICAL PROCEDURES Supportive to clinical and lab diagnosis

  44. Plain chest X-ray • Supportive of diagnosis • Left basal atelectasis, elevation of left hemidiaphragm, left pleural effusion • Reflect significant inflammatory process • Helpful to eliminate other diagnosis

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