What is Acute Pancreatitis?
Acute Pancreatitis is an inflammatory process of variable severity. Most episodes of acute pancreatitis are self-limiting and associated with mild transitory symptoms that remit within 3 to 5 days. . The exact mechanism by which various etiologic factors induce acute pancreatitis and with such variable severity is unclear. However, the chain of events begins with pancreatic acinar cell injury. Afflicted acinar cells locally release activated pancreatic digestive enzymes that result in parenchymal autodigestion along with the recruitment of inflammatory cell mediators, eventually leading to a systemic inflammatory response.
The two most common causes of acute pancreatitis in the United States are gallstones and alcoholism, collectively accounting for 80% of pancreatitis hospital admissions.
Drug induced (definite association: isoniazid, estrogens; probable association: thiazides, furosemide, sulfonamides, tetracycline, corticosteroids).
Patients typically present with epigastric pain, often radiating to the back. Tenderness is usually limited to the upper abdomen but may be associated with signs of diffuse peritonitis. Occasionally, irritation from intraperitoneal pancreatic enzymes results in impressive peritoneal signs, simulating other causes of an acute abdomen. Nausea, vomiting, and a low-grade fever are frequent, as are tachycardia and hypotension secondary to hypovolemia. Asymptomatic hypoxemia, renal failure, hypocalcemia, and hyperglycemia are evidence of severe systemic effects. Flank ecchymosis (Gray-turner sign) or periumbilical ecchymosis (Cullensign) are almost always manifestations of severe pancreatitis and have been associated with a 40% mortality rate. However, these signs are present in only 1% to 3% of cases and do not usually develop until 48 hours after the onset of symptoms.
Serum amylase is the most useful test. Levels rise within 2 to 12 hours of symptoms and may return to normal over the following 2 to 5 days. Persistent elevations of levels for longer than 10 days indicate complications, such as pseudocyst formation. Normal levels can indicate resolution of acute pancreatitis, pancreatic hemorrhage, or pancreatic necrosis.
Serum lipase generally is considered more sensitive for pancreatic disease (95%), but its specificity varies from 55% to 95%.
Trypsin-activated peptide (TAP) is elevated in the urine of patients with acute pancreatitis within 12 hours of symptom onset and has a sensitivity and specificity of 96% and 95%, respectively.
Radiologic imaging complements clinical history and exam because no single modality provides a perfect diagnostic index of pancreatitis severity.
Ultrasonography’s (US) specificity in pancreatitis can be greater than 95%, yet its sensitivity ranges between 62% and 95%. The pancreas is not visualized in up to 40% of patients due to overlying bowel gas and body habitus. The primary utility of US in acute pancreatitis is to determine whether gallstones or choledocholithiasis are present.
Computed tomography (CT) is superior to ultrasonography in evaluating the pancreas and is not limited by bowel gas. The sensitivity and specificity of CT are 90% and 100%, respectively. Iodinated contrast enhancement is essential to detect the presence of pancreatic necrosis. CT may also be helpful in differentiating acute pancreatitis from conditions such as malignancy, small-bowel obstruction, or acute cholecystitis.
Magnetic resonance imaging (MRI) is a useful substitute for CT scan in patients allergic to iodinated contrast or in acute renal failure. In addition, MRI/MR cholangiopancreatography (MRCP) is better than CT at visualizing cholelithiasis, choledocholithiasis, and anomalies of the pancreatic duct.
ERCP is not routinely indicated for the evaluation of patients during an attack of acute pancreatitis. Indications for ERCP are as follows:
Because the associated mortality of severe acute pancreatitis approaches 40% and randomized studies have shown that early aggressive supportive care improves outcomes, attempts have been made to identify clinical parameters that predict patients at higher risk of developing severe outcomes.
Necrotizing pancreatitis occurs in about 10% to 20% of acute pancreatitis cases, and its presence correlates with prognosis. It can be present at initial presentation or develop later in the clinical course. Necrosis is diagnosed on CT as failure to enhance with intravenous contrast.
One of the key predictors of poor outcome in acute pancreatitis is end-organ dysfunction resulting from circulatory collapse. Therefore, the initial approach to managing acute pancreatitis focuses on fluid resuscitation and close monitoring for evolving organ dysfunction
Volume resuscitation with isotonic fluids is crucial; urinary output is monitored with a Foley catheter.
Gastric rest with nutritional support. Nasogastric decompression is performed to decrease neurohormonal stimulation of pancreatic secretion. Acute pancreatitis is a hypercatabolic state, and nutritional support has been shown to have a significant impact on outcomes in critically ill patients.
Analgesics are required for pain relief.
Antibiotics. The routine use of antibiotic prophylaxis in acute pancreatitis, especially in mild to moderate cases, is not supported in the literature. although they certainly should be used when infected necrosis is suspected.
Surgical treatment must be entertained for the small percentage of patients who continue to deteriorate despite aggressive supportive therapy. Although there is not a clear consensus of the indications for operative intervention, some of the incontrovertible indications include (1) diagnostic uncertainty in the face of clinical deterioration, (2) related life-threatening complications (i.e., intra-abdominal hemorrhage, viscus perforation, abdominal compartment syndrome), and (3) infected pancreatic necrosis.
In necrotizing pancreatitis, percutaneous drainage can be an effective therapy in a very select group of patients
Wide débridement (necrosectomy), supplemented by either open packing or closed drainage, is the standard operative approach for managing infected necrotizing pancreatitis.
Gallstone-induced pancreatitis. Ongoing choledocholithiasis is found in only 25% of biliary acute pancreatitis cases. Nonetheless, all patients with pancreatitis should be evaluated for the presence of gallstones because the etiology has specific therapeutic implications.