Acute Pancreatitis

Acute Pancreatitis

• Sudden onset of unrelenting upper abdominal pain resulting from inflammation of the pancreas

• Patients commonly present to ER due to severe abdominal pain

• Requires admission to the hospital for medical management

Pathophysiology

• Release of kallikrein and chymotrypsin results in increased capillary membrane permeability, leading to leakage of fluid into the interstitium and development of edema and relative hypovolemia

• Elastase is the most harmful in terms of direct cell damage, it causes dissolution of the elastic fibers of blood vessels and cuts, leading to hemorrhage

• Phospholipase A destroys phosholipids of cell membranes causing severe pancreatic and adipose tissue necrosis

• Lipase flows into damaged tissue and is absorbed into systemic circulation, resulting in fat necrosis of the pancreas and surrounding tissues

Acute Pancreatitis

• Inflammation of the pancreas that produces exocrine and endocrine dysfunction

• Results from premature activation of pancreatic exocrine enzymes (trypsin, phospholipase A, and elastase)

Edematous (Interstitial) Pancreatitis

• Usually mild

• Resolves in about 7 days

• Results in fluid accumulation and swelling

Severe or Necrotizing Pancreatitis

• Associated with a high degree of complications and mortality

• Caused by the release of cytokines and other proinflammatory mediators that produce a hyperinflammatory reaction, resulting in cell death and tissue damage

Causes of Acute Pancreatitis

• Ethanol abuse• Biliary diseases

– Gallstones– Choledocholithiasis– Biliary sludge– Microlithiasis

• Mechanical/structural injury– Sphincter of Oddi dysfunction– Pancreas divisum– Trauma– Postendoscopic retrograde

cholangiopancreatography– Pancreatic malignancy– PUD– IBD

• Medications– Azathiprine/6-mercaptopurine– Dideoxyinosine– Pentamidine– Sulfonamides– Thiazide diuretics– ACEI

• Metabolic– Hypertriglyceridemia– Hypercalcemia

• Infectious– Viral– Bacterial– Parasitic

• Vascular– Vasculitis

• Genetic predisposition• idiopathic

Acute Pancreatitis: Damage and Destruction

• Inflammation is caused by premature activation of enzymes which leads to tissue damage

• If pancreatitis damages the islets of Langerhans, diabetes mellitus may result

• Severe sudden pancreatitis causes massive hemorrhage and total destruction of the pancreas, manifested as diabetic acidosis, shock and coma

Clinical Presentation

• Upper abdominal pain rapidly increasing in severity, often within 60 minutes

• Epigastric pain• Right-sided pain• Diffuse abdominal pain with radiation to back• Pain rarely only in left upper quadrant• Restless• Prefer to sit and lean• N/V• Fever• Tachycardia

Abdominal Examination

• Decreased or absent bowel sounds• Abdominal tenderness• Guarding• Palpable mass in epigastric area• Biliary colic • Jaundice if there’s obstruction of the bile duct• Cullen’s sign• Grey Turner’s Sign

Clinical Manifestations

• Abdominal distention• Abdominal guarding• Abdominal tympany• Hypoactive bowel

sounds• Severe disease:

peritoneal signs, ascites, jaundice, palpable abdominal mass, Grey Turner’s sign, Cullen’s sign, and signs of hypovolemic shock

Diagnostic Evaluation

• Patient’s history• Physical examination• Diagnostic findings

– Serum amylase levels greater than three times the upper limit

– Serum amylase levels may be normal in patients with pancreatitis related to alcohol abuse or hypertriglyceridemia

– Levels greater than five times the top normal value should be expected in patients with renal failure because amylase is cleared by the kidneys

Imaging Modalities

• Plain abdominal x-rays for visualizing gallstones or a gas-filled transverse colon ending at the area of pancreatic inflammation– colon cut-off sign

• Abdominal ultrasound– Cholelithiasis, biliary sludge, bile duct dilation, and

pseudocysts• CT of abdomen• MRCP (magnetic resonance

cholangiopancreatography)

Ranson’s Criteria

• The severity of acute pancreatitis is determined by the existence of certain criteria, called Ranson’s criteria

• The more criteria met by the patient, the more severe the episode of pancreatitis

• 1% mortality: fewer than three• 16%: three or four criteria• 40% with five or six criteria• 100%: seven or eight criteria

Ranson’s Criteria

• On admission– Patient older than 55– WBC > 16,000– Serum glucose >200– Serum lactate dehydrogenase >350– Aspartate aminotransferase > 250

• During initial 48 hours after admission– 10% decrease in Hct– BUN increase > 5– Serum calcium < 8– Base deficit > 4– PaO2 < 60– Estimated fluid sequestration > 6 liters

Common Complications of Acute Pancreatitis

• Pulmonary– Atelactasis– Pleural effusions– ARDS

• Cardiovascular– Cardiogenic shock

• Neurologic– Pancreatic encephalopathy

• Metabolic– Metabolic acidosis– Hypocalcemia– Altered glucose metabolism

• Hematologic– DIC– GI bleeding

• Renal– Prerenal failure

Management

• Fluid Management

• Nutritional support– Rest gut– TPN

• Pain management

• Supporting other organ systems

Treatment

• IV replacement of fluids, proteins, and electrolytes

• Fluid volume replacement and blood transfusions

• Withholding food and fluids to rest the pancreas

• NG tube suctioning• Drugs• Peritoneal lavage• Surgical drainage• Laparotomy to remove

obstruction