Acute Pancreatitis

Recognizing patients with severe acute pancreatitis as soon as possible is critical for achieving optimal outcomes. Management depends largely on severity. Medical treatment of mild acute pancreatitis is relatively straightforward. Treatment of severe acute pancreatitis involves intensive care. Surgical intervention (open or minimally invasive) is indicated in selected cases.

Essential update: AGA releases new guidelines for diagnosis/management of asymptomatic neoplastic pancreatic cysts

The American Gastroenterological Association recommends the following in the diagnosis and management of asymptomatic neoplastic pancreatic cysts^[1] :

• For asymptomatic mucinous cysts, a 2-year interval is recommended for a cyst of any size undergoing surveillance, with surveillance being stopped after 5 years if there is no change.
• Perform surgery only if there is more than one concerning feature on MRI confirmed on endoscopic ultrasonography (EUS) and only in centers with high volumes of pancreatic surgery, and there should be no surveillance after surgery if there is no invasive cancer or dysplasia.
• The risk of malignant transformation of pancreatic cysts is approximately 0.24% per year, and the risk of cancer in cysts without a significant change over a 5-year period is likely to be lower.
• The small risk of malignant progression in stable cysts is likely outweighed by the costs of surveillance and the risks of surgery.
• Positive cytology on EUS-guided fine-needle aspiration (FNA) has the highest specificity for diagnosing malignancy; if there is a combination of high-risk features on imaging, then this is likely to increase the risk of malignancy even further. Similarly, if a cyst has both a solid component and a dilated pancreatic duct (confirmed on both EUS and MRI), the specificity for malignancy is likely to be high even in the absence of positive cytology.
• There is lower immediate postoperative mortality, as well as long-term mortality, for patients who undergo surgery in high-volume pancreatic centers.
• It seems sensible to offer screening even after the cyst has been resected, provided the patients have not undergone total pancreatectomy. Surveillance should continue as long as the patient remains a good candidate for surgery. MRI every 2 years may be a reasonable approach for these patients. The clinician may elect to offer more frequent surveillance in the case of invasive cancer resection, particularly if there is concern that the lesion has not been fully resected.

Signs and symptoms

Symptoms of acute pancreatitis include the following:

• Abdominal pain (cardinal symptom): Characteristically dull, boring, and steady; usually sudden in onset and gradually becoming more severe until reaching a constant ache; most often located in the upper abdomen and may radiate directly through to the back
• Nausea and vomiting, sometimes with anorexia
• Diarrhea

Patients may have a history of the following:

• Recent operative or other invasive procedures
• Family history of hypertriglyceridemia
• Previous biliary colic and binge alcohol consumption (major causes of acute pancreatitis)

The following physical findings may be noted, varying with the severity of the disease:

• Fever (76%) and tachycardia (65%); hypotension
• Abdominal tenderness, muscular guarding (68%), and distention (65%); diminished or absent bowel sounds
• Jaundice (28%)
• Dyspnea (10%); tachypnea; basilar rales, especially in the left lung
• In severe cases, hemodynamic instability (10%) and hematemesis or melena (5%); pale, diaphoretic, and listless appearance
• Occasionally, extremity muscular spasm secondary to hypocalcemia

The following uncommon physical findings are associated with severe necrotizing pancreatitis:

• Cullen sign (bluish discoloration around the umbilicus resulting from hemoperitoneum)
• Grey-Turner sign (reddish-brown discoloration along the flanks resulting from retroperitoneal blood dissecting along tissue planes); more commonly, patients may have a ruddy erythema in the flanks secondary to extravasated pancreatic exudate
• Erythematous skin nodules, usually no larger than 1 cm and typically located on extensor skin surfaces; polyarthritis

See Clinical Presentation for more detail.

Diagnosis

Once a working diagnosis of acute pancreatitis is reached, laboratory tests are obtained to support the clinical impression, such as the following:

• Serum amylase and lipase
• Liver-associated enzymes
• Blood urea nitrogen (BUN), creatinine, and electrolytes
• Blood glucose
• Serum cholesterol and triglyceride
• Complete blood count (CBC) and hematocrit; NLR
• C-reactive protein (CRP)
• Arterial blood gas values
• Serum lactic dehydrogenase (LDH) and bicarbonate
• Immunoglobulin G4 (IgG4)

Diagnostic imaging is unnecessary in most cases but may be obtained when the diagnosis is in doubt, when pancreatitis is severe, or when a given study might provide specific information required. Modalities employed include the following:

• Abdominal radiography (limited role): Kidneys-ureters-bladder (KUB) radiography with the patient upright is primarily performed to detect free air in the abdomen
• Abdominal ultrasonography (most useful initial test in determining the etiology, and is the technique of choice for detecting gallstones)
• Endoscopic ultrasonography (EUS) (used mainly for detection of microlithiasis and periampullary lesions not easily revealed by other methods)
• Abdominal computed tomography (CT) scanning (generally not indicated for patients with mild pancreatitis but always indicated for those with severe acute pancreatitis)
• Endoscopic retrograde cholangiopancreatography (ERCP; to be used with extreme caution in this disease and never as a first-line diagnostic tool ^[2] )
• Magnetic resonance cholangiopancreatography (MRCP; not as sensitive as ERCP but safer and noninvasive)

Other diagnostic modalities include the following:

• CT-guided or EUS-guided aspiration and drainage
• Genetic testing

Acute pancreatitis is broadly classified as either mild or severe. According to the Atlanta classification, severe acute pancreatitis is signaled by the following^[3] :

• Evidence of organ failure (eg, systolic blood pressure below 90 mm Hg, arterial partial pressure of oxygen [P a O 2] 60 mm Hg or lower, serum creatinine level 2 mg/dL or higher, GI bleeding amounting to 500 mL or more in 24 hours)
• Local complications (eg, necrosis, abscess, pseudocyst)
• Ranson score of 3 or higher or APACHE score of 8 or higher

See Workup for more detail.

Management

Medical management of mild acute pancreatitis is relatively straightforward; however, patients with severe acute pancreatitis require intensive care.

Initial supportive care includes the following:

• Fluid resuscitation ^[4]
• Nutritional support

Antibiotic therapy is employed as follows:

• Antibiotics (usually of the imipenem class) should be used in any case of pancreatitis complicated by infected pancreatic necrosis but should not be given routinely for fever, especially early
• Antibiotic prophylaxis in severe pancreatitis is controversial; routine use of antibiotics as prophylaxis against infection in severe acute pancreatitis is not currently recommended

Surgical intervention (open or minimally invasive) is indicated when an anatomic complication amenable to a mechanical solution is present. Procedures appropriate for specific conditions involving pancreatitis include the following:

• Gallstone pancreatitis: Cholecystectomy
• Pancreatic duct disruption: Image-guided percutaneous placement of a drainage tube into the fluid collection ^[5] ; stent or tube placement via ERCP; in refractory cases, distal pancreatectomy or a Whipple procedure
• Pseudocysts: None necessary in most cases; for large or symptomatic pseudocysts, percutaneous aspiration, endoscopic transpapillary or transmural techniques, or surgical management
• Infected pancreatic necrosis: Image-guided aspiration; necrosectomy
• Pancreatic abscess: Percutaneous catheter drainage and antibiotics; if no response, surgical debridement and drainage