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Band-like epigastric pain was the first indication of a potentially deadly disorder for a 56-year-old man. He presented to the emergency department 2 weeks after first developing the pain, which was now accompanied by worsening nausea, diarrhea, chills, anorexia, and dizziness. Before the onset of symptoms, he had been in his usual state of health. His past medical history was significant for hepatitis C, hypertension, diabetes mellitus, alcohol abuse of 6 beers per day, and a 30 pack-year smoking history. The patient, having denied drinking over the previous 2 weeks due to abdominal discomfort, did not report any withdrawal symptoms. He was not taking any medications and had no significant family history.
On physical examination, the patient had a blood pressure of 118/68 mm Hg, a regular heart rate of 80 beats per minute, a respiratory rate of 18 breaths per minute, an oral temperature of 98° F (36.6° C), and an oxygen saturation of 98% on room air. He had mild scleral icterus. An abdominal examination revealed a flat abdomen with normal bowel sounds, tenderness to the epigastrium without rebound, and hepatomegaly, with the liver edge 2 centimeters below the costal margin. Laboratory testing demonstrated a leukocyte count of 16.3 x 109 cells/L with neutrophils at 96% and bands at 1%. His platelet count was 158 x 109/L. Total bilirubin was measured at 2.1 mg/dL; direct bilirubin, at 1.2 mg/dL. Results from his coagulation profile were within normal ranges, as were levels of creatinine, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lipase.
Computed tomography (CT) with contrast of the abdomen and pelvis showed thrombosis of the main portal vein extending into the left portal vein and asymmetric sigmoid colonic wall thickening (Figures 1 and 2). In the absence of systemic inflammatory response syndrome, we could not justify empiric antibiotic treatment until the initial set of blood cultures returned; these grew Bacteroides uniformis and Peptococcus saccharolyticus.
Given the portal vein thrombosis, combined with the patient's history of alcohol use and probable cirrhosis, a colonoscopy was performed 1 week later to rule out a malignancy that could have spurred thrombosis. This revealed inflammatory thickening of the rectosigmoid junction (Figure 3). The corresponding biopsy showed moderate chronic colitis with chronic hemorrhage, eosinophils, and rare neutrophils consistent with chronic diverticulitis. No granulomas or malignancies were identified.
Pylephlebitis, a rare and serious complication of intraabdominal infections, is characterized by suppurative thrombosis of the portal vein or a tributary, fever, abdominal pain, hepatic dysfunction, and bacteremia. It was universally fatal before the availability of antibiotics.
The source of pylephlebitis is most commonly appendicitis or diverticulitis, though it can occur also as a complication of ascending cholangitis, septic choledocholithiasis, inflammatory bowel disease, pancreatitis, or gastrointestinal perforations from cancer or trauma.
Isolates are usually normal bowel flora, such as Bacteroides fragilis and Escherichia coli. Aeromonas hydrophila, Streptococcus and Staphylococcus species, Proteus mirabilis, Klebsiella pneumoniae, Clostridium species, yeasts, Citrobacter species, and rarely, Enterococcus species have been described as well.
Therapy should last 4-6 weeks; parenteral antibiotics are administered for the first 1-3 weeks until clinical improvement is noted, and then oral antibiotics are used for the duration of the treatment period.
Initially, the patient was treated with IV piperacillin-tazobactam and a heparin drip. Abdominal pain and leukocytosis quickly subsided, and his blood cultures cleared the following day. Due to his generally mild and uncomplicated clinical course, he continued piperacillin-tazobactam for 1 week and was then discharged with instructions to complete a 3-week regimen of oral ciprofloxacin and metronidazole. In addition, because B. uniformis was identified, we chose to prescribe warfarin for 6 months. No consensus exists on the optimal length of time to administer anticoagulation in patients with pylephlebitis, so we based our decision on the recommended duration of anticoagulation in patients with provoked deep venous thrombosis. We cannot be certain if anticoagulation reduced the severity of our patient's illness, but given his etiology, it might have reduced the risk for further complications.
On outpatient follow-up at 2 and 6 weeks and at 3 and 6 months, the patient remained asymptomatic. During this time, results from his liver function panel normalized. Because the patient was clinically stable, no further imaging was carried out to assess for recanalization of the portal vein.
We recommend that the diagnosis of pylephlebitis be considered in any patient presenting with an infectious focus in the abdomen and evidence of portal vein thrombosis on abdominal CT. Treatment is comprised of broad-spectrum antibiotic therapy, along with consideration of anticoagulation and surgical intervention in selected patients. This disease, once universally fatal, now carries an estimated mortality of 11-32%.