Acute Pancreatitis by Dr. Patricia Chipalabwe - Surgery-unza

ACUTE PANCREATITIS Presenter: Dr. Patricia Chipalabwe Supervisor: Dr. Sihem Moderator: Dr. Mbambiko Functions Islets of langerhans Endocrine Alpha cells-glucagon 20% Beta cells- insulin 75% Delta cells- somatostatin Exocrine Pancreatic juice Amylase Lipase Trypsin Chymotrypsin Carboxypeptidase Definition Acute pancreatitis is a reversible condition in which activated pancreatic enzymes leak into the substance of the pancreas and initiate the auto-digestion of the gland. It varies from mild edema to severe hemorrhagic necrosis. EPIDEMIOLOGY Gender predilection Generally – M>F In males-more often related to alcohol In females-more often related to biliary tract disease Idiopathic pancreatitis has no clear gender predilection ETIOLOGY I GET SMASHED I-Idiopathic G-Gallstones E-Ethanol T-Trauma (Blunt / Penetrating trauma) S-Steroids M- Mumps ; EBV, CMV A-Autoimmune : Hereditary pancreatitis S-Scorpions and Snakes H- Hyperlipidemia, hypercalcemia E- ERCP (Back pressure of contrast) D- Drugs (Steroids, Furosemide, Thiazide, Estrogen, Metronidazole) OTHERS Congenital: Pancreatic Divisum, Annular Pancreas Vascular: Ischemia, vasculitis Pathophysiology The underlying mechanism of injury in pancreatitis is thought to be due to premature activation of pancreatic enzymes within the pancreas leading to autodigestion. Anything that injures the acinar cells and impairs the secretion of zymogen granules or damages the duct epithelium and thus delays enzyme secretion can trigger acute pancreatitis. Once cellular injury has been initiated, the inflammatory process can lead to pancreatic edema, hemorrhage and eventually necrosis. As inflammatory mediators are released into the circulation, the systemic complications can arise such as hemodynamic instability, bacteremia (due to translocation of gut flora), ARDS, pleural effusion, GI hemorrhage, renal failure and DIC. The pathophysiologic involvement of acute pancreatitis ranges from edematous pancreatitis (which is self limiting) to necrotizing pancreatitis. Classification of Acute Pancreatitis The Revised Atlanta Classification The Two Phases Early Phase (<1 week) Characterized by SIRS +/- organ failure Severity assessed by functional/clinical severity scoring system (Ranson/Glasgow etc) Late Phase (> 1week) Characterized by local complications Severity assessed by morphological scoring system (Balthazar scoring) Severity of Acute Pancreatitis 1. Mild: No organ failure, no local complications 2. Moderate: Organ failure less than 48hrs, +/- local complications 3. Severe: Severe organ failure longer than 48hrs and/or death Morphological classification of Acute Pancreatitis 1. Interstitial edematous Pancreatitis 2. Necrotizing Pancreatitis Parenchymal Peripancreatic necrosis Combined type INTERSTITIAL EDEMATOUS PANCREATITIS Pancreatic enlargement due to edema. On CT, pancreatic parenchyma shows negatively homogeneous enhancement and peripancreatic fat standing. Outcome: Symptoms usually resolve within first week. NECROTIZING PANCREATITIS Inflammation associated with pancreatic parenchymal necrosis or peripancreatic necrosis Cause impairment of pancreatic perfusion Impairment evolve over several days. Early CT may underestimate the extent of the disease. CLINICAL PRESENTATION Symptoms Pain (SOCRATES) Site: usually epigastrium but it may be in Upper quadrants or whole abdomen Onset: sudden and the pain has no upper limit Character: dull, boring and steady Radiation: to the back in 50% Associated with: nausea, vomiting, retching, anorexia, hiccups Time duration: persist for hours to days Exacerbate in the supine position, refractory to the usual analgesics and may be relieved by sitting and leaning forward (Muhammedan Prayer sign) Nausea, non projectile vomiting, retching Anorexia Fever Weakness Tachycardia, Tachypnea Pale, diaphoretic Shallow breathing Abdominal distension (ileus, ascites) Inspection- Grey Turner’s sign, Cullen’s sign, Fox’s sign, Panniculitis ( subcutaneous nodular fat necrosis, tender red nodules usually over the extremities). Palpation-Rebound tenderness, Rigidity Korte’s sign: pain and resistance in the zone where the head of the pancreas is located (in Epigastrium 6-7cm above the umbilicus) Mayo-Robson’s sign: tenderness at the Mayo-Robson point Percussion-Shifting dullness Auscultation-Absence of bowel sounds due to ileus Other- Purtscher retinopathy (on Fundoscopy) Activation of compliment and agglutination of blood cells within retinal vessels causing ischemic injury to retina. At this point, the tail of the pancreas is projected on the abdominal wall INVESTIGATIONS BLOOD TESTS FBC Serum Amylase and Lipase C-reactive Protein Serum electrolytes Blood glucose Renal Function tests Liver Function tests LDH Coagulation profile Arterial Blood Gas Analysis Serum Amylase Sensitivity is about 72% Release within 6 to 12 hours of the onset and remains elevated for 3-5 days. Elevation > 3X normal is significant High Amylase levels are also seen in I.O, perforated ulcer, ruptured ectopic pregnancy, salpingitis, renal failure, salivary gland disorders and diabetic ketoacidosis. Serum Lipase More pancreatic-specific than S.Amylase Sensitivity is about 100% Remains elevated longer than Amylase ( …