Case Reports

Diffuse abdominal pain, vomiting

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The patient had undergone a cholecystectomy years earlier following an episode of gallstone pancreatitis. So what was causing the pain this time around?


 

References

PRACTICE POINTERS

• Use the APACHE-II scoring system early on to help predict the severity of pancreatitis.

• Consider early enteral nutrition in patients with severe disease; taking this step has been linked to lower infection rates and shorter lengths of stay.

• Consider patient factors and the risk of severe infection when deciding whether or not to use prophylactic antibiotics in cases of severe necrotizing pancreatitis.

CASE A 57-year-old Caucasian woman sought care at our emergency department (ED) for diffuse abdominal pain and nausea. She said that the pain began after eating lunch earlier that day, and localized periumbilically, with radiation to the back. She had several episodes of nonbilious, nonbloody vomiting, but denied fever, chills, or diarrhea.

Her past medical history was notable only for an episode of gallstone pancreatitis 11 years earlier, after which she underwent a cholecystectomy. Her only medications were ibandronate sodium (Boniva) taken for osteoporosis (diagnosed 2 years earlier), a multivitamin, calcium, magnesium, and vitamin E supplements. Her family history was notable for a brother who had pancreatic cancer in his 50s. The patient reported infrequent alcohol use.

The abdominal exam was notable for diffuse tenderness to palpation, most prominent in the epigastric region. The patient exhibited voluntary guarding, without rebound, and positive bowel sounds throughout.

The patient’s laboratory studies on admission included leukocytosis of 21,300 cells/mcL and hemoglobin and hematocrit of 17.3 g/dL and 52.1%, respectively. She had an amylase of 1733 U/L and lipase of 4288 U/L. Lactate and lactic dehydrogenase were 1.83 mg/dL and 265 U/L, respectively. Liver function tests and a basic metabolic panel were within normal limits. A noncontrast computed tomography (CT) scan of the abdomen and pelvis was notable for an enlarged pancreas with peripancreatic edema and free fluid in the abdomen.

The patient underwent aggressive fluid resuscitation throughout the first 6 hours of her hospital stay. Urine output was noted to be incongruent with fluid intake, at just over 60 cc/h. Over the next 4 hours, she became progressively tachycardic, tachypneic, and somnolent, with increasing abdominal tenderness. Her serum potassium level rose to 4.9 mEq/L, while serum bicarbonate declined to 13 mEq/L and serum calcium, to 6.2 mg/dL. Arterial blood gas revealed metabolic acidosis with a pH of 7.22.

Our patient was subsequently transferred to the medical intensive care unit, where she required endotracheal intubation.

WHAT IS THE MOST LIKELY EXPLANATION FOR HER CONDITION?

Acute necrotizing pancreatitis

A repeat CT scan of the abdomen and pelvis with IV contrast taken on the second day of admission revealed extensive pancreatitis with complete disintegration of the pancreatic tissue and absence of pancreatic enhancement (FIGURE), as well as a large amount of abdominal ascites.

Pancreatitis is a common inpatient diagnosis, with approximately 200,000 hospitalizations yearly.1 Most cases are mild and self-limiting, requiring minimal intervention including parenteral fluid resuscitation, pain control, and restriction of oral intake. Most cases can be attributed to gallstones or excessive alcohol use, but approximately 25% of cases are idiopathic.1 Other causes include hypertriglyceridemia, infection, hypercalcemia, and medications such as azathioprine, 6-mercaptopurine, trimethoprim sulfa-methoxazole, and furosemide. Severe necrotizing pancreatitis represents about 20% of all cases, but carries a mortality rate of between 10% and 30%.1

Diagnosis is based on clinical features in conjunction with biochemical markers. Amylase is nonspecific, but levels 3 times the upper limit of normal are usually diagnostic of acute pancreatitis. Lipase is 85% to 100% sensitive for pancreatitis, and is more specific than amylase. Alanine aminotransferase >150 IU/L is 96% specific for gallstone pancreatitis.2 Of note: there is no evidence to support daily monitoring of these enzyme levels as predictors of clinical improvement or disease severity.

FIGURE
CT scan of abdomen taken on second day of admission

Predicting severity at time of presentation can be difficult

As was true with our patient, predicting the severity of acute pancreatitis at the time of presentation can be difficult. Scoring systems that are commonly used to evaluate disease severity include Ranson’s score, APACHE-II (Acute Physiology and Chronic Health Evaluation-II), and CT severity index, among others (TABLE). Of these, the APACHE-II score has been found to be most predictive of progression to severe disease, with accuracy of up to 75%.3

Recent studies have shown that a body mass index >30 kg/m2 is an independent risk factor for progression to severe pancreatitis.4 Other clinical predictors include poor urine output, rising hematocrit, agitation or confusion, and lack of improvement in symptoms within 48 hours.1

Though our patient came in with symptoms that were initially mild, she quickly manifested several clinical predictors for severe pancreatitis, including poor urine output and increasing confusion, as well as an APACHE-II score of 12 at 6 hours after presentation (values ≥8 indicate high risk for progression to severe disease).

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