Abstract

Purpose: Pylephlebitis is septic thrombophlebitis of portal vein or its tributaries. It is a rare but potentially fatal condition. We are reporting a case of pylephlebitis and superior mesenteric vein (SMV) thrombosis. There were no GI symptoms or identifiable risk factors on presentation. Final diagnosis could only be reached as case unfolded. Methods: Case report and review of literature. Results: A 70-year-old female with history of hypertension, GERD, dyslipidemia and diverticulosis presented with fever of 1 day duration. She had no dysuria, diarrhea, abdominal pain or cough. She denied substance abuse. She had no personal or family history of clotting disorder. Vital signs: temperature 39.3 C, HR 110/min, RR 20/min, and BP 126/60. Exam was unremarkable. CBC showed WBC 5200/cubic mm with 94% PMNs. Creatinine was 2.3 mg/dL. Anion gap, LFT, lipase, UA, chest x-ray were all normal. Blood culture grew gram negative bacilli and gram positive cocci at 13 hours. Vancomycin, metronidazole, and cefepime were started. Non-contrast CT of chest, abdomen and pelvis showed mesenteric infiltration surrounding ileocolic branch of SMV and colonic diverticulosis. Colonoscopy revealed pan-colonic and terminal ileum diverticulosis. Blood culture grew E. coli, Strep. bovis, Citrobacter koseri and Bacteroides caccae. Given polymicrobial bacteremia and CT finding, it was postulated that she had pylephlebitis due to silent episode of diverticulitis. She was treated with 4 weeks of ceftriaxone and metronidazole. Follow-up contrast enhanced CT scan showed resolution of mesenteric infiltration but there was SMV thrombosis. She was started on anticoagulation with warfarin. Conclusion: A high index of suspicion is needed for prompt diagnosis of pylephlebitis. Delayed diagnosis contributes to high mortality rate (30-50%). Risk factors include intra-abdominal inflammatory conditions and hypercoagulability. In about 32% of cases, etiology could not be identified. CT scan is the preferred diagnostic tool. It can detect the source as well as complications of pylephlebitis--hepatic septic emboli and bowel ischemia. Antibiotic therapy is the mainstay of treatment. The role of anticoagulation is controversial. In uncomplicated cases, anticoagulation is not recommended because observational studies showed no additional benefit. In our case, we did not start anticoagulation at the beginning because there was no evidence of bowel ischemia nor of antibiotic failure. But the follow-up scan showed the development of SMV thrombosis prompting anticoagulation. Our case is unique for two reasons: 1) the presentation was non-specific, and 2) although uncomplicated at beginning, later on she was found to have developed SMV thrombosis requiring anticoagulation.

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