Acute pancreatitis is an inflammatory condition, which results in severe abdominal pain along with elevated pancreatic enzymes. Though the exact pathogenesis is not well known, there are several etiologies that have been linked to acute attacks.
Biliary tract disease (i.e. gallstones) and chronic alcohol use are the two most common causes of acute pancreatitis.
The various causes of acute pancreatitis can be remembered with the mnemonic GET SMASHED:
Patients with acute pancreatitis will typically present with severe epigastric abdominal pain that radiates straight to their back, nausea, vomiting, and inability to get comfortable on the examination table.
Depending on the etiology, patients will usually present to the hospital within 24-48 hours of the event.
On physical exam patients will often have tachycardia, fever, vomiting, severe tenderness in the epigastric area, and pale mucosa.
Other signs to watch for include: dyspnea, hypotension, and bruising around the umbilicus (Cullen sign) and flanks (Grey-Turner sign), which is seen in hemorrhagic pancreatitis.
When acute pancreatitis is suspected, the best initial step is to obtain amylase and lipase levels. These levels are typically 3-4 times the upper limit, with lipase being more sensitive and specific for acute pancreatitis.
Other laboratory tests, which may be elevated, include:
In patients with a clinical diagnosis of pancreatitis, imaging is not typically required for confirmation. Imaging should be performed in patients where:
Contrast-enhanced computed tomography (CECT) is the standard imaging modality for the evaluation of acute pancreatitis and its complications, including necrosis and vascular complications. Non-contrast CT scan can be used, however, it cannot assess for necrosis or vascular complications.
Ultrasound is used to look for gallstones, biliary sludge or a blockage.
Once stones and a dilated common bile duct are detected on ultrasound, endoscopic retrograde cholangiopancreatography (ERCP) may be used to confirm a diagnosis of choledocholithiasis and also for therapeutic purposes by removing the stone(s) responsible for symptoms.
Ranson's criteria are commonly used to estimate the mortality of patients with pancreatitis based on initial and 48 hour lab values. They include:
On Admission:
48 hours after admission:
Each additional criterion a patient has coincides with an increased risk of mortality.
The most frequently evaluated single-item predictors that have been found to correlate with severity include older age, obesity, hematocrit, C-reactive protein, and blood urea nitrogen (BUN). An elevated hematocrit (>44%) on admission is predictive of more severe disease, as it reflects greater hemoconcentration from third-space losses. Similarly, a BUN >20 mg/dL at the time of admission is associated with an increased risk of death. In addition, increases in BUN on serial measurement are associated with worse outcomes. An elevated C-reactive protein level (>150 mg/dL), which rises more slowly than BUN or other acute markers (eg, hematocrit), has also been shown to correlate with severe AP 24-48 hours after admission.
Treatment of acute pancreatitis consists of:
Pharmacologic pain control consists of IV hydromorphone, fentanyl, or meperidine. Empiric antibiotics are not used, unless pancreatic necrosis is suspected.
Surgical intervention is typically not required in the treatment of acute pancreatitis, but drainage may be performed if an abscess or pseudocyst is present.
ERCP is incorporated when gallstone pancreatitis is suspected. This procedure uses an endoscope to dilate and remove stones within the pancreatic duct.
Ursodeoxycholic acid treatment can be considered as a second-line option for patients with symptomatic cholelithiasis (eg, biliary colic) who do not desire surgery, but it does not have a role in the treatment of patients with GP.
The management of gallstone pancreatitis depends on its severity. Patients with mild disease, which is characterized by the lack of both organ failure and local or systemic complications (eg, acute necrotic collection, heart failure), should undergo cholecystectomy within 7 days of clinical improvement; this is usually performed during the same hospitalization (eg, this patient could be scheduled for surgery the next day). Patients who do not have their gallbladders removed have a 25%-30% risk of recurrent acute pancreatitis, cholecystitis, or cholangitis during the next 6-18 weeks.
Delayed cholecystectomy should be considered for patients with severe GP, which is characterized by persistent failure of one or more organ systems (eg, hypotension not responsive to fluid resuscitation). Waiting allows for the resolution of active inflammation and complications (eg, walled-off necrosis), facilitating surgical management. In addition to having a cholecystectomy, patients should also undergo evaluation of the biliary system to ensure no gallstones remain. This can be performed through intraoperative cholangiogram in low-risk patients; alternatively, endoscopic retrograde cholangiopancreatography can be obtained prior to cholecystectomy in patients with evidence of persistent biliary obstruction (eg, elevated alkaline phosphatase, hyperbilirubinemia).
The most high-yield complications of acute pancreatitis are:
Early acute pancreatitis complications: GRASS
Late acute pancreatitis complications: NAP