Worsening Abdominal Pain in Man With History of Alcohol Abuse

October 1, 2007
Ronald N. Rubin, MD
Ronald N. Rubin, MD

Forty-eight hours ago, a 39-year-old man presented to the emergency department with emesis and severe upper abdominal pain of semi-acute onset, which radiated slightly to the back.

Forty-eight hours ago, a 39-year-old man presented to the emergency department with emesis and severe upper abdominal pain of semi-acute onset, which radiated slightly to the back. He was admitted and has been managed conservatively with intravenous fluids, analgesics, and nothing to eat or drink.

In the past several hours, however, his condition has significantly deteriorated. He has assumed a fetal position but still seems unable to get comfortable. He now complains of thirst, is quite agitated, and is becoming confused.

HISTORY

The patient has had similar episodes in the past and was told they resulted from pancreatic inflammation. He has a long history of alcohol abuse and had been drinking at least half a bottle of vodka daily during the week before his admission. He also had been hospitalized previously for heart failure and atrial fibrillation that were thought to be alcohol-related.

PHYSICAL EXAMINATION

Temperature is 38.3°C (101°F ); heart rate, 150 beats per minute; and respiration rate, 20 breaths per minute. The mucosae are dry, but there is no scleral icterus. Chest is clear. Bowel sounds are markedly diminished, and the abdomen is diffusely tender, with the greatest tenderness in the upper mid-epigastrium; rebound tenderness is noted as well.

LABORATORY AND IMAGING STUDIES

Hematocrit is 50% (on admission, it was 39%); leukocyte count is 19,000/µL (on admission, 16,700/µL), with 11% band forms; and platelet count is 91,000/µL (on admission, 171,000/µL). Blood glucose level is 253 mg/dL, which is essentially unchanged from the level on admission. Serum amylase and lipase levels are both significantly elevated at 906 U/L and 2011 U/L, respectively. Lactate dehydrogenase level is 510 U/L. The C-reactive protein level in a sample obtained the morning after admission is 191 mg/dL.

The admission CT scan revealed significant streaking and necrosis of the pancreas and a single small fluid collection near the tail. Abdominal ultrasonography shows no gallstones or dilation of the bile ducts.

Which of the following would be least beneficial for the patient at this time?

A.

Transfer the patient to an ICU for fluid resuscitation and monitoring.

B.

Empirically initiate broad-spectrum antibiotics.

C.

Arrange for immediate surgical debridement of necrotic pancreatic tissue.

D.

Provide nutritional support if necessary-enteral if possible, or totalparenteral.

CORRECT ANSWER: C

This patient has acute pancreatitis that is evolving into severe, morbid disease. Acute pancreatitis is common; in the United States, those affected tend to be either elderly (older than 60 years), predominantly female patients with (small) gallstone pancreatitis or younger, predominantly male patients with alcohol-related pancreatitis. In disease of either origin, activation of digestive enzymes within the pancreas causes local injury and an intense, body-wide inflammatory response. The latter produces its own tissue damage and systemic effects that can culminate in multi-organ failure and even death.1

Severe disease develops in roughly 20% of patients with acute pancreatitis; about 10% to 30% of these patients die (2% to 6% of all patients with pancreatitis). Despite advances in ICU medicine and medical care generally, these percentages have changed little in the past 30 years.2 Still, certain management maneuvers are more effective than others at reducing the morbidity and mortality associated with severe acute disease.

Identifying patients at risk for severe acute pancreatitis. Various time- and data-tested markers can accurately quantitate the risk of severe disease in patients with acute pancreatitis. These include specific laboratory values that indicate the systemic inflammatory response, scoring systems that assess the same response as well as organ failure, and imaging scores.1-3

This patient fulfills several sets of criteria for severe pancreatitis:

  • The traditional Ranson criteria.
  • C-reactive protein level greater than 150 mg/dL.
  • CT severity index (most likely fulfilled).

He also displays other markers not included in traditional risk profiles but reported to be prognostic (eg, rising hematocrit, progressive tachycardia, agitation, and confusion).1 In addition, his history of ill-defined cardiac disease introduces enough doubt about his hemodynamic stability to make it prudent to transfer him to the ICU for monitoring of the aggressive and complicated volume resuscitation he obviously will require (choice A).

Management of severe disease. When a patient fails to improve within 48 hours (and this man is actually worsening), further diagnostic and therapeutic maneuvers need be considered. Most experts suggest a second imaging study (eg, CT with contrast) to detect new necrosis, fluid collections, or other pertinent findings.

Antibiotics. The use of antibiotics in severe acute pancreatitis (choice B) remains controversial. Infection of pseudocysts or pancreatic necrosis are dreaded complications that increase mortality to around 50%.1,4 However, several randomized trials of prophylactic antibiotic therapy have produced conflicting results.4 Here, the use of antibiotics would not be strictly "prophylactic": this man has a fever, and although the fever has other possible causes (eg, delirium tremens), most experts would consider using antibiotics, possibly in conjunction with fine-needle aspiration to confirm infection.

Nutritional support. A preponderance of data suggest that nutritional support in severe or complicated pancreatitis (choice D) is associated with improved outcomes (eg, decreased rates of infection, less surgery, and shorter hospital stays). There is debate over which method is superior-enteral or parenteral.5

Delayed surgery. Drainage of infected pseudocysts and debridement of infected, necrotic pancreatic tissue is indicated and potentially lifesaving. However, the timing of surgery is crucial. Early surgery-in the first 48 to 96 hours-is associated with increased mortality, as high as 65%.6 Most authorities agree that even in disease complicated by infection, postponement of surgery for about 2 weeks permits demarcation of necrotic or infected tissue to occur and allows for optimization of the patient's medical condition. Thus, choice C is least likely to benefit this patient. Immediate surgery would be too early and would likely be counterproductive.

Outcome of this case. The patient was transferred to the ICU. He tolerated enteral nutrition and underwent debridement on day 16. After a long recovery, he was discharged on day 44.

References:


REFERENCES:


1.

Whitcomb DC. Clinical practice. Acute pancreatitis.

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2006;354: 2142-2150.

2.

McKay CJ, Imrie CW. The continuing challenge of early mortality in acute pancreatitis.

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3.

Papachristou GI, Whitcomb DC. Predictors of severity and necrosis in acute pancreatitis.

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2004;33:871-890.

4.

Nathens AB, Curtis JR, Beal RJ, et al. Management of the critically ill patient with severe acute pancreatitis.

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5.

Marik PE, Zaloga GP. Meta-analysis of parenteral versus enteral nutrition in patients with acute pancreatitis.

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6.

Uhl W, Warshaw A, Imrie C, et al. IAP Guidelines for the Surgical Management of Acute Pancreatitis.

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