Pancreas

Foundations

Acute pancreatitis is an inflammatory condition leading to enzymatic autodigestion and the destruction of pancreatic tissue. Its presentation ranges widely from mild, self-limited disease to sepsis and multiorgan failure. Recurrent episodes of acute pancreatitis can result in the progressive fibrosis of chronic pancreatitis. Acute pancreatitis is the most common pancreatic disease worldwide and one of the top reasons for hospitalization due to gastrointestinal disease in the United States. ^, Mortality can run as high as 30% in severe cases; however, although hospital admissions continue to increase, the overall mortality of acute pancreatitis has decreased.

There are numerous causes of acute pancreatitis ( Box 77.1 ), with gallstones (40% to 70%) and chronic alcohol consumption (25% to 35%) accounting for the majority of cases. Other common causes include hypertriglyceridemia (serum triglyceride levels > 1000 mg/dL), complications from endoscopic retrograde cholangiopancreatography (ERCP), medications, trauma, and idiopathic. It is thought that many idiopathic cases may be due to occult to microlithiasis. Smoking and diabetes are independent risk factors for the development of pancreatitis.

Acute pancreatitis can be classified by type—interstitial edematous versus necrotizing pancreatitis—and by local complications. Most patients have the interstitial edematous type, which usually resolves within the first week of illness. Approximately 5% to 10% of patients develop necrotizing pancreatitis, which can involve the pancreatic parenchyma and surrounding tissue. Necrotic tissue may remain sterile, liquefy, or become infected. Infected lesions are associated with increased morbidity. Local complications usually occur after the first week and should be suspected in patients with prolonged or recurrent symptoms, secondary elevation of pancreatic serum markers, or signs of sepsis, such as fever and leukocytosis. The local complications of acute pancreatitis are summarized in Box 77.2 .

Clinical Features

Patients with acute pancreatitis typically present with persistent epigastric or left upper quadrant pain that may radiate to the back, chest, or flanks. The pain is usually moderate to severe in intensity; however, the intensity of pain does not correlate with clinical severity. Associated symptoms include nausea, vomiting, and anorexia as oral intake may exacerbate pain. The pain may be alleviated by sitting up or bending forward.

Vital signs may be normal in cases of mild or early disease. Abnormalities commonly reflect patient discomfort or an existing inflammatory process, with rises in temperature, heart rate, or respiratory rate. Blood pressure may be slightly elevated secondary to pain, although in severe or complicated cases, hypotension and signs of shock may be present. Jaundice suggests an obstructive process such as a gallstone or tumor. Respirations may be shallow due to splinting from pain, and pulmonary auscultation may reveal decreased breath sounds or basilar crackles in the setting of pulmonary complications.

The abdomen can appear normal or distended. The classic clinical findings of Cullen sign (bluish periumbilical discoloration due to hemoperitoneum) and Grey Turner sign (reddish-brown discoloration around the flanks due to retroperitoneal bleeding) are rare and neither sensitive nor specific for acute pancreatitis but, when present, may confer a poor prognosis. Auscultation of the abdomen may reveal normal, diminished, or absent bowel sounds if the patient has concomitant ileus. Palpation of the abdomen often reveals epigastric tenderness with or without guarding and with rebound tenderness being a less common finding. Right upper quadrant tenderness and the presence of Murphy sign may be seen in cases of gallstone pancreatitis.

In addition to direct injury to the pancreas, patients may have local complications involving surrounding structures (e.g., bowel necrosis, splenic or portal vein thrombosis, gastrointestinal bleeding, or gastric outlet obstruction). Most of these tend to be late findings.

Systemic complications are related to the progression of local inflammation and may result in SIRS. Although in most cases these conditions resolve within days, if persistent there may be progression to fulminant sepsis, shock, and organ failure, especially if there is underlying chronic disease. The pulmonary, cardiovascular, and renal systems are the most important when assessing for organ failure. Increased microvascular permeability is the primary cause of pulmonary sequelae, although enzymatic degradation of surfactant may also play a role. Patients may develop ARDS, atelectasis, or pleural effusion, manifested as hypoxemia or respiratory distress. Pleural effusions are present in up to 50% of patients and tend to develop more frequently on the left side. Cardiovascular collapse, as evidenced by decreased mean arterial pressure or the need for inotropic support, may develop as shock results from fluid shifts and volume loss. Renal failure, demonstrated by an elevated creatinine level, may arise from a combination of hypoperfusion and the effects of inflammatory mediators.

In addition, coagulopathy occurs from cytokine-mediated activation of the coagulation cascade, potentially leading to thrombocytopenia or disseminated intravascular coagulation. Metabolic abnormalities are also common. Hyperglycemia results from decreased insulin production and hypocalcemia from low albumin and magnesium levels.

Differential Diagnoses

A number of disease processes have the ability to mimic the presentation of acute pancreatitis and should be considered in the differential diagnosis ( Box 77.3 ). Inflammation of nearby intra-abdominal organs, such as the gallbladder, stomach, and duodenum, is often characterized by a similar pattern of epigastric or upper quadrant abdominal pain. Myocardial infarction, pneumonia, and aortic pathology may also present as lower thoracic or upper abdominal pain, with radiation to the back.