Mr. B, a 77-year-old African American, was admitted through the hospital clinic with complaints of a 20-lb weight loss and fatigue over the past six weeks. His medical history was significant for 17 years of diabetes mellitus and hypertension. He also had glaucoma and suffered an ischemic stroke one year before this encounter.
Surgical history included a partial colostomy with subsequent takedown secondary to a bowel obstruction 20 years ago. He had no drug allergies. Mr. B had drunk whiskey and smoked a pack of cigarettes daily for 40 years, but he had done neither for 20 years. He denied IV drug abuse. Medications were hydrochlorothiazide, simvastatin, extended-release glipizide, enalapril, aspirin, felodipine, insulin, and pilocarpine eyedrops.  

1. Examination findings

On admission, Mr. B’s temperature was 98.6°F, pulse 54 beats per minute, respiration rate 20 breaths per minute, and BP 106/58 mm Hg. Mr. B was well-nourished and in no apparent distress. Examination revealed pale conjunctivae and a left facial droop (upper motor neuron) due to the old stroke. Heart exam showed a normal S1 and S2, without murmur. Lungs were clear. His abdomen was soft, nontender, and mildly distended, without palpable masses or organomegaly; no shifting dullness was detected. Bowel sounds were normal. Examination of the extremities was benign. 

2. Lab results

Mr. B’s laboratory findings (Table 1) suggested a cholestatic picture (high levels of direct bilirubin, alkaline phosphatase, and γ-glutamyltransferase), necessitating ultrasound (US) or CT of the abdomen. Based on the weight loss and the patient’s age, we suspected a malignant process. 

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The initial US of the abdomen revealed a common bile duct measuring 12 mm and mild ascites. A mass was seen in the head of the pancreas. Subsequent abdominal paracentesis yielded only 30 cc of yellow/straw-colored fluid containing both atypical epithelial cells and WBCs (Table 2).

The serum and ascites protein levels were 5.9 and 1 g/dL, respectively, while serum and ascites albumin levels were 3.4 and 0.4 g/dL, resulting in a serum-to-ascites albumin gradient (SAAG) >1.1 (high). In addition, the WBC count in the peritoneal fluid was low ( 90/µL), indicating a noninfectious source for the ascites. Cytology was negative for any malignant cells, which presented a diagnostic dilemma: Why was the fluid transudative when there was an obvious cancer in the pancreas? 

3. Treatment

Because the treatment of pancreatic cancer depends on the involvement of the surrounding structures, a spiral CT of the abdomen was done to evaluate the extension of the tumor. Imaging demonstrated a 4.9-cm x 3.7-cm low-attenuating mass in the neck of the pancreas and invading the surrounding soft tissues. The mass also extended posteriorly and occluded the superior mesenteric artery and the superior mesenteric vein. In addition, there was invasion of the portal vein, which also showed thrombosis, and dilatation of the intrahepatic ducts.
The mass was unresectable. Stent placement by endoscopic retrograde cholangiopancreatography was unsuccessful secondary to stenosis. Mr. B refused further evaluation and expired two weeks after discharge.

4. Discussion

Pancreatic carcinoma is responsible for more than 30,000 deaths in the United States each year. The mean survival is 8-12 months for patients with locally advanced, unresectable disease and 3-6 months for those with metastatic disease at presentation.

Ascites is defined by the accumulation of excess fluid within the peritoneal cavity.1 Diagnostic paracentesis is an integral part of the evaluation. The difference between the albumin concentration in the serum and the ascites fluid is thought to reflect directly the colloid osmotic pressure and indirectly the degree of portal hypertension. Generally, patients with a high SAAG (>1.1) have portal hypertension, while patients with a low SAAG (<1.1) do not. When describing ascites, high SAAG and low SAAG have replaced the terms “transudative” and “exudative,” respectively, in most recent publications.2

An overwhelming majority of patients with ascites have an exudate, i.e., low SAAG, indicating an inflammatory process secondary to metastasis. This usually signals a stage IV cancer, and palliative therapy might be appropriate.

Mr. B’s surprising high SAAG is explained by portal-vein invasion and thrombosis causing portal hypertension. A review of portal-vein thrombosis noted that portal-vein obstruction can result from one or more of the following: thrombosis, invasion by a malignant tumor, or constriction within a malignant tumor (adenocarcinoma of the pancreas or bile ducts).3 Inflammatory changes in the wall of the vein induce spasm, produce venous stasis, and cause intimal damage, factors that predispose to thrombosis.2 Mr. B had inflammatory changes in his portal vein from the adjacent cancer and the cancer itself that contributed to the formation of a deep venous thrombosis of the portal vein.

In conclusion, pancreatic carcinoma usually presents with low SAAG ascites, but it is important to recognize that pancreatic carcinoma can also present with high SAAG ascites secondary to portal-vein invasion and thrombosis causing portal hypertension. This case should remind physicians to challenge unexpected laboratory results and create differentials for atypical presentations of disease.

Dr. Brodkin is a hospitalist with Aurora Healthcare in Kenosha, Wis. Dr. Murali is a gastroenterologist with Berkshire Medical Center in Pittsfield, Mass.

1. Little AG, Moossa AR. Gastrointestinal hemorrhage from left-sided portal hypertension. Am J Surg. 1981;141:153-158.
2. Valla DC, Condat B. Portal vein thrombosis in adults: pathophysiology, pathogenesis and management. J Hepatol. 2000;32:865-871.
3. Hoefs JC. Serum protein concentration and portal pressure determine the ascitic fluid protein concentration in patients with chronic liver disease. J Lab Clin Med. 1983;102:260-273.