PATHOPHYSIOLOGY
Acute pancreatitis is typically a mild disease, which often resolves spontaneously. However, about 20% of those cases develop into severe acute pancreatitis. Pancreatitis develops because of obstruction to the outflow of pancreatic digestive enzymes caused by bile duct or pancreatic duct obstruction. Acute pancreatitis can also result from a direct cellular injury from drugs or viral infection.
In obstructive disease, the backup of pancreatic secretions or duodenal content, or both, triggers activation and release of enzymes within the pancreatic acinar cells. The activated enzymes cause autodigestion of pancreatic cells and tissue, resulting in inflammation and release of inflammatory cytokines. The autodigestion causes vascular damage, coagulative necrosis, fat necrosis, and formation pseudocysts. Edema within the pancreatic capsule leads to ischemia and can contribute to necrosis. There also can be an independent activation of inflammation within acinar cells contributing to the local and systemic response occurring in acute pancreatitis in the case of alcohol abuse, the pancreatic acinar cells metabolize ethanol with the generation of toxic metabolites that injure pancreatic acinar cells, causing the release of activated enzymes. Chronic alcohol use also may cause the formation of protein plugs in the pancreatic ducts and spasm of the sphincter of Oddi, resulting in obstruction.
System effects are associated with moderately severe and severe acute pancreatitis. Proinflammatory cytokines and vasoactive peptides are released into the bloodstream. There is activation of leukocytes, injury to vessel walls, and coagulation abnormalities within the development of vasodilation, hypotension, and shock. Complications can include acute respiratory distress syndrome, heart failure, renal failure, coagulopathies, intraabdominal hypertension, and systemic inflammatory response syndrome. Paralytic ileus and gastrointestinal bleeding can occur. Translocation of intestinal bacteria to the bloodstream causes peritonitis or sepsis. Recurrent inflammation activates pancreatic stellate cells, causing pancreatic fibrosis, strictures, and duct obstruction that lead to chronic pancreatitis (McCance & Huether, 2019).
CLINICAL MANIFESTATIONS
The cardinal manifestation of acute Pancreatitis is epigastric or midabdominal constant pain ranging from mild abdominal discomfort too severe, incapacitating pain. The pain may radiate to the back because of the retroperitoneal location of the pancreas. Pain is caused by (1) edema, which distends the pancreatic ducts and capsule; (2) chemical irritation and inflammation of the peritoneum; (3) irritation or obstruction of the biliary tract; and (4) inflammation of nerves. Fever and Leukocytosis accompany the inflammatory response. Nausea and vomiting are caused by paralytic ileus secondary to pancreatitis or peritonitis. Jaundice can result from obstruction of the bile duct or from pancreatic edema pressing on the duct. Abdominal distention accompanies bowel hypermotility or paralytic ileus in the accumulation of fluid in the peritoneal and retroperitoneal cavity. Abdominal compartment syndrome is a potentially life-threatening complication. Hypovolemia, hypertension, tachycardia, myocardial insufficiency, and shock occur because plasma volume is lost as inflammatory mediators released into the circulation increase vascular permeability and dilate vessels. Tachypnea and hypoxia developed secondary to ascites, pulmonary edema, atelectasis, or pleural effusion. Hypovolemia can decrease renal blood flow sufficiently to impair renal function and cause renal failure. Tetany may develop as a result of hypocalcemia when calcium is deposited into areas of fat necrosis or as a result of decreased response to parathormone. Transient hyperglycemia also can occur if glucagon is released from damaged Alpha cells in the pancreatic islets. in severe acute pancreatitis, some individuals develop flank or paraumbilical ecchymosis, a sign of poor prognosis. Multiple organ failure or SIRS account for most deaths of those with severe acute pancreatitis (McCance & Huether, 2019).
EVALUATION & TREATMENT
Diagnosis is based on clinical findings, identification of associated disorders, laboratory studies, and imaging results. Elevated serum amylase concentration is characteristic but is not diagnostic of severity or specificity of disease. Elevated serum lipase level is the primary diagnostic marker for acute pancreatitis. Both enzymes are elevated to a least three times their normal value. An elevated C-reactive protein is suggestive of severe disease (McCance & Huether, 2019).
The goal of treatment is to stop the process of autodigestion and prevent systemic complications. Narcotics, nonsteroidal anti-inflammatory drugs, and acetaminophen are used to relieve pain. Hemodynamic monitory and parenteral fluids are essential to restore blood volume and prevent hypotension and shock, particularly in the first 24 to 48 hours if ileus is not present. In severe acute pancreatitis, enteral nutrition with the use of jejunal tube feeding is usually well-tolerated and may decrease pancreatic enzyme secretion, prevent gut bacterial overgrowth, and maintain gut barrier function. Parenteral hyperalimentation should be initiated only when enteral feeding is not tolerated. Drugs that decrease gastric acid production can decrease the stimulation of the pancreas by secretin (McCance & Huether, 2019).