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ACUTE PANCREATITIS. By: Maj.Gen.Badshah khan Prof. & HOD Medicine YMDC. INTRODUCTION. Pancreatitis is divided into acute and chronic.
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ACUTE PANCREATITIS By: Maj.Gen.Badshah khan Prof. & HOD Medicine YMDC
INTRODUCTION • Pancreatitis is divided into acute and chronic. • By definition, acute pancreatitis is an inflammatory process that occurs on the background of previously normal pancreas and can return to normal after resolution of the episode. • In chronic pancreatitis there is continuing inflammation with irreversible structural changes.
INCIDENCE Acute pancreatitis occurs in approximately 10 per 100,000 population per year. It accounts for about 3% of all abdominal pain cases admitted to the hospital.
CAUSES OF ACUTE PANCREATITIS Common (90% of cases): • Gallstones • Idiopathic • Alcohol • Post-ERCP Rare: • Post-surgical(abdominal,cardiopulmonary bypass) • Trauma • Drugs (azathioprine,thiazide diuretics, sodium valproate) •Metabolic(hypercalcaemia,hypertriglyceridaemia) • Pancreas divisum
• Sphincter of Oddi dysfunction • Infection (mumps, Coxsackie virus) • Hereditary • Renal failure • Organ transplantation (kidney, liver) • Severe hypothermia • Petrochemical exposure
PATHOPHYSIOLOGY Mechanisms by which pancreatic necrosis occurs remain speculative. Any theory must take into account how a very diverse group of etiological factors can produce the same endpoint. There is some suggestion that the final common pathway is a marked elevation of intracellular calcium which in turn leads to activation of intracellular proteases which digest the pancreas and surrounding tissue.
CLINICAL FEATURES • Upper abdominal pain which radiates to the back • Nauseaand vomiting • Epigastric tenderness • Signs of peritonitis • Hypotension • Cullen's sign • Grey Turner’s sign
COURSE AND PROGNOSIS About 80% cases are mild with mortality less than 5% while 20% cases are severe with mortality upto 50%.
INVESTIGATIONS Blood • blood CP • serum amylase • serum lipase • CRP • RFTS • LFTS • blood sugar • coagulation profile
Urinary amylase Radiology • Erect chest x-ray to exclude visceral perforation. • Supine abdominal x-ray to look for gallstones and calcification of pancreas. • ultrasound abdomen • CT scan abdomen with contrast • MRI • MRCP • ERCP
ASSESSMENT OF DISEASE SEVERITY GLASGOW CRITERIA • Age > 55 years • PO2 < 8 kPa (60 mmHg) • White blood cell count (WBC) > 15 × 109/L • Albumin < 32 g/L • Serum calcium < 2 mmol/L (8 mg/dL) (corrected) • Glucose > 10 mmol/L (180 mg/dL) • Urea > 16 mmol/L (after rehydration) • Alanineaminotransferase (ALT) > 200 U/L • Lactate dehydrogenase (LDH) > 600 U/L
The APACHE II scoring system parameters Physiological • Temperature • Heart rate • Respiratory rate • Mean arterial pressure • Glasgow Coma Scale
Laboratory • Oxygenation (PaO2) • Arterial pH • Serum: sodium, potassium ,creatinine • Haematocrit • White blood cell count
Factors That May Predict Severe Pancreatitis Within 48 Hours Of Admission Initial assessment • Clinical impression of severity • Body mass index > 30 • Pleural effusion on chest X-ray • APACHE II score > 8
24 hrs after admission • Clinical impression of severity • APACHE II score > 8 • Glasgow score ≥ 3 • Persisting organ failure, especially if multiple • CRP > 150 mg/L 48 hrs after admission • Clinical impression of severity • Glasgow score ≥ 3 • CRP > 150 mg/L • Persisting organ failure for 48 hrs • Multiple or progressive organ failure
MANAGEMENT • Analgesics • Antiemetics • IV fluids • Prophylactic antibiotics • Prophylactic anticoagulants • Detection and management of complication • Treating the underlying cause e.g.gallstones
COMPLICATIONS SYSTEMIC : • Systemic inflammatory response syndrome (SIRS) • Hypoxia • Hyperglycaemia • Hypocalcaemia • Reduced serum albumin conc. PANCREATIC: • Necrosis • Abscess • Pseudocyst • Pancreatic ascites or pleural effusion
GASTROINTESTINAL • Upper gastrointestinal bleeding • Variceal haemorrhage • Erosion into colon • Duodenal obstruction • Obstructive jaundice