Diffuse abdominal pain, vomiting

TABLE
Predictors for progression to severe pancreatitis¹

Role of antibiotics? A source of debate

Infection represents the leading cause of morbidity and mortality in patients with pancreatic necrosis. Approximately 40% of patients with necrosis develop infection, with a 20% mortality rate.⁵ Signs of infection usually develop relatively late in the clinical course and rates increase drastically each week a patient remains hospitalized (71% of patients have signs of infection at 3 weeks).⁵

Interestingly, the role for antibiotics in such patients has been a source of debate in practice, as well as in the medical literature. Two recent large meta-analyses came to different conclusions regarding the use of antibiotics. A 2006 study by Heinrich et al concluded that patients with pancreatic necrosis demonstrated by contrast-enhanced CT scans should receive antibiotic prophylaxis with imipenem or meropenem for 14 days, and that prophylactic antibiotics do not increase rates of subsequent fungal infection.⁶ Conversely, as noted in a 2008 study published in the American Journal of Gastroenterology, “prophylactic antibiotics cannot reduce infected pancreatic necrosis and mortality in patients with acute necrotizing pancreatitis.”⁷

Two leading professional groups have similarly contradictory recommendations on the topic, with the American Gastroenterological Association (AGA) supporting antibiotic use for patients with >30% pancreatic necrosis noted on CT and the American College of Gastroenterology (ACG) recommending against the use of prophylactic antibiotics.⁸

As with any clinical dilemma, it seems prudent to make the decision for or against prophylactic antibiotics based on available clinical information and the particular patient’s risk factors. Clearly, in the most high-risk patients, it would be difficult to justify withholding antibiotic therapy.

Complete bowel rest—or not?
In the past, it was thought necessary to allow for complete bowel rest and suppression of pancreatic exocrine secretion during acute pancreatitis by providing total parenteral nutrition.^6,9 More recently, though, the use of early nasojejunal enteral feeding (which was initiated for our patient) has been advocated by several large meta-analyses,⁶ as well as by the AGA and ACG.²

The use of enteral feeding has been associated with improved outcomes, including lower infection rates (due to maintenance of the intestinal barrier and prevention of bacterial translocation), decreased length of stay, reduced rates of organ failure, and fewer deaths among patients who require surgical intervention.⁶

A lengthy road to recovery for our patient
After 7 days of mechanical ventilation, our patient was extubated. However, she developed significant bilateral pleural effusions as a result of fluid third spacing, and required thoracentesis.

She completed a 14-day course of imipenem, followed by an additional 10-day course due to hypotension and a suspected infected pseudocyst. Subsequent imaging studies confirmed our suspicions: She had developed a large pseudocyst (>13 cm), which remained under observation by both a gastroenterologist and general surgeon. Six weeks after admission, our patient was discharged to home with family.

But what was the cause? Although we were unable to clearly delineate an inciting cause for her pancreatitis during the admission, she was to undergo further investigation as an outpatient. There were also plans to drain the pseudocyst 6 weeks after discharge.

A learning opportunity. This patient’s case provided an excellent opportunity for our team to review the important clinical predictors for progression to severe pancreatitis, and the rapid nature of clinical decline in such patients. In hindsight, the predictors of severity in our patient were few, but included the rapid onset and clinical progression of her symptoms, as well as her elevated hematocrit on presentation and poor urine output over the first 6 hours of admission.