Middle-Aged Woman With Severe Abdominal Pain

A 48-year-old woman is evaluated for transfer to the ICU. She presented to the emergency department 48 hours ago with severe abdominal pain and emesis. The pain had started several days earlier and was located in the upper abdomen with some radiation to the back. No position--even the fetal position--provided relief. After admission, she was given intravenous fluids and analgesics; in the last several hours, her condition has deteriorated. She now complains of thirst and is somewhat agitated.

PHYSICAL EXAMINATION

This thin woman weighs 60 kg (132 lb). Temperature is normal; heart rate is 132 beats per minute, and respiration rate is 20 breaths per minute. Mucosae are dry, but she has no scleral icterus. Chest is clear. Bowel sounds are markedly diminished, and there is diffuse tenderness, with rebound and the greatest tenderness noted in the upper mid epigastrium.

LABORATORY AND IMAGING RESULTS

Currently, hematocrit is 48% (level on admission, 39%), white blood cell (WBC) count is 19,000/µL (count on admission, 16,700/µL), and platelet count is 91,000/µL (count on admission, 171,000/µL). Blood glucose level is 253 mg/dL, which is essentially unchanged from the level on admission. Levels of serum amylase and lipase are both significantly elevated at 680 U/L and 1011 U/L, respectively. The lactate dehydrogenase level is 510 U/dL. Results of a measurement of C-reactive protein that was sent to the laboratory the morning after admission have now come in: the level is 211 mg/dL.

A CT scan obtained on admission revealed streaking and necrosis of about one third to one half the pancreas and a single small fluid collection near its tail. Abdominal ultrasonography shows no gallstones or bile duct dilation.

Which finding in this patient is least predictive of severe acute pancreatitis with associated complications and/or mortality?A. Presentation CT scan.
B. Ranson score.
C. Current C-reactive protein level.
D. Body mass index (BMI).

CORRECT ANSWER: D

In the United States, the most common causes of acute pancreatitis are:

• (Small) gallstone disease, typically in women older than 60 years.
• Alcohol abuse, usually in men and usually at younger ages than are generally seen with gallstone disease-related pancreatitis.

Pathophysiology of acute pancreatitis. In both these patient populations, a central factor in the development of the disease is inappropriate transformation of trypsinogen into trypsin and subsequent activation of digestive enzymes within the pancreas. This process results in local pancreatic injury and an intensive body-wide inflammatory response that causes systemic effects and additional tissue damage; these effects can eventuate in multiorgan failure and sometimes death.¹

This patient's history included no mention of either gallstone disease or alcoholism, but in the absence of gallstones on imaging, alcoholism is statistically the most likely cause of her pancreatitis.

Predictors of a severe course. Severe disease develops in roughly 20% of patients with acute pancreatitis. Of these patients, 10% to 30% (or 2% to 6% of all patients with pancreatitis) die of the disease. Despite advances in intensive care medicine, these numbers have changed little in the past 30 years.²

Which manifestations of disease in this patient predict a severe course? A variety of markers--for which years of evidence are available--can accurately gauge the risk of severe disease in a patient with acute pancreatitis. These include specific laboratory values that reflect the systemic inflammatory response of severe disease and scoring systems that incorporate measures of systemic inflammatory response and organ failure, as well as imaging scores.^1,3,4

An index of the severity of acute pancreatitis can be compiled based on CT evidence of fluid collections, fat stranding, and extent of necrosis (choice A).¹ In this patient, 5 to 7 points would be assigned for fluid collection and necrosis; scores of greater than 6 are associated with a high risk of severe pancreatitis.

Since their publication in 1982, the Ranson criteria for the evaluation of acute pancreatitis (choice B) have been commonly used and are still quite helpful.⁴ The criteria assign 1 point for each of the following at presentation:

• Age older than 55 years.
• Blood glucose level greater than 200 mg/dL.
• WBC count greater than 16,000/µL.
• Lactate dehydrogenase level greater than 350 U/L.
• Alanine aminotransferase level greater than 250 U/L.

In addition, 1 point is assigned for the presence of each of the following within 48 hours of admission:

• Decrease in hematocrit of more than 10%.
• Serum calcium level less than 8 mg/dL.
• Base deficit of more than 4 mEq/L.
• Increase in blood urea nitrogen level of more than 5 mg/dL.
• Fluid sequestration of more than 6 L.
• Oxygen saturation (with partial pressure) of less than 60 mm Hg.

At a minimum, this patient scores points for her admission WBC count, blood glucose level, and lactate dehydrogenase level. In addition, her vital signs and hydration status suggest massive fluid sequestration. Thus, her Ranson score is at least 3--a score that is quite sensitive for the presence of severe disease and that has a high negative predictive value. Moreover, other laboratory results are still pending.

A patient's C-reactive protein level 24 to 48 hours after symptom onset (choice C) is an excellent prognostic indicator of disease severity, with sensitivity, specificity, and overall accuracy (72%) equivalent to those of the Ranson criteria. A C-reactive protein level of more than 150 mg/dL correlates with severe acute pancreatitis.

Other markers and clinical findings also have predictive value. These include thirst, progressive tachycardia, agitation, rising hematocrit level, poor urine output, tachypnea, and lack of improvement in 48 hours.¹

Body habitus has a statistical association with the risk of severe disease. However, an elevated BMI (greater than 30)--rather than a normal or a low BMI, such as this patient has--is the indicator of a poor prognosis.⁵ Thus, choice D is the finding least predictive of severe disease here.

Outcome of this case. The patient was transferred to the ICU. After a stormy course of hypertension, acute respiratory distress syndrome, and disseminated intravascular coagulation, she died on the fifth hospital day. Postmortem findings included evidence of profound, extensive hemorrhagic pancreatitis. No gallstones were found.

References:

REFERENCES:1. Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med. 2006;354:2142-2150.
2. McKay CJ, Imrie CW. The continuing challenge of early mortality in acute pancreatitis. Br J Surg. 2004;91:1243-1244.
3. Papachristou GI, Whitcomb DC. Predictors of severity and necrosis in acute pancreatitis. Gastroenterol Clin North Am. 2004;33:871-890.
4. Ranson H. Biological and prognostic factors in human acute pancreatitis: a review. Am J Gastroenterol. 1982;77:633-638.
5. Martinez J, Sanchez-Paya J, Palazon JM, et al. Is obesity a risk factor in acute pancreatitis? A meta-analysis. Pancreatology. 2004;4:42-48.