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Pavan K Bhatraju, Jignesh P Shah and Luis S Marsano A case of ileal diverticulitis causing pylephlebitis
Pavan K Bhatraju, Jignesh P Shah and Luis S Marsano, 20 September 2010


A woman who initially was noted to have a right lower quadrant inflammatory process on computer tomography (CT) presented 1 week later with worsening abdominal pain. She was non-compliant with her initial discharge medications and re-presented to the emergency room in sepsis. Following an initial evaluation, a diagnosis of pylephlebitis was made.

We will discuss one of the few cases reported in the literature of right-sided ileal diverticulitis causing pylephlebitis. The following case report is an overview of the causes, diagnosis, and management of pylephlebitis.


A 57-year-old female initially presented to University of Louisville emergency room with symptoms of right lower quadrant abdominal tenderness. Her past medical history included type 2 insulin dependent diabetes mellitus, hypertension, coronary artery disease status-post 3 vessel coronary artery bypass graft 7 years prior, drug eluting stent placement 2 years prior, and a history of alcohol abuse for over 20 years, but sobriety for last 5 years. She denied any recent operations, procedures or trauma.

Her admission white blood cell count (5.66* 109/L) was within normal limits, and she was afebrile. She had a CT scan in the emergency room that supported an inflammatory process in the ileum/cecum. At that point she was diagnosed with inflammatory bowel disease vs ileal diverticulutis (Fig 1). She was discharged on oral antibiotics and was scheduled for an outpatient colonoscopy.

Figure 1 CT scan showing inflammation in the ileum.

She returned to our emergency room after 9 days for symptoms of right upper quadrant abdominal pain with nausea, vomiting, and confusion. She denied diarrhea, hematochezia, melena, and constipation. She had been noncompliant with her initial antibiotics.

During her evaluation by the emergency medical services, she was ill appearing and found to have a temperature of 97.8o F (36.6oC) with subsequent temperature spikes as high as 103.1oF (39.5oC) over the following 24 hours. Her blood pressure was 154/78 and heart rate was 108. There was prominent right upper quadrant tenderness with mild diffuse abdominal tenderness. Her white blood cell count, hemoglobin, and platelets were within normal limits. Her BUN was 27 mg/dL (normal, 7-20mg/dL), creatinine 0.7 mg/dL (normal, 0.5-1.2mg/dL), total bilirubin 2.1 mg/dL (normal, 0.2-1.0), direct bilirubin of 1.4 mg/dL (normal, 0.0 -0.4mg/dL), and alkaline phosphatase 207 U/L (normal, 38-126 U/L).

Within 24 hours she had a profound leukocytosis (29.42 * 109/L), increasing alkaline phosphatase (430 U/L maximum on Day 6) and rising total bilirubin (4.1 mg/dL maximum on day 5).

With the increasing total bilirubin, consistently elevated alkaline phosphatase and worsening white blood cell count, there was an increased suspicion of a concurrent biliary etiology of disease. She underwent a HIDA scan & abdominal ultrasound that showed no evidence of acute cholecystitis or common bile duct dilation. There was no definitive flow within the intrahepatic portal vein (concerning for thrombosis) and gallbladder sludge and minimal wall thickening with pericholecystic fluid were noted.

After obtaining blood cultures, she was started on piperacillin/tazobactam, metronidazole and ampicillin.

Repeat CT scan of the abdomen was performed that showed extensive left portal vein thrombosis, suspected thrombosis of the superior mesenteric vein, normal appendix, and tiny diverticulae arising from the terminal ileum which were no longer inflamed compared with the prior study, findings suggestive of resolution of ileal

Figure 2 Thrombosis within portal vein (arrow).


Over her hospital course her fever was the first sign of improvement on hospital day 3. The first organisms isolated from both blood cultures after 48 hours showed Streptococcus anginosus and Fusobacterium species. The second set of blood cultures collected on day 2 reported growth of Clostridium clostridiiforme. She was switched to IV ampicillin/sulbactam based on her cultures & sensitivities and was started on a heparin drip. Oral metronidazole was added on day 6 to treat the Clostridium species.

Upon discharge 12 days after admission, her liver tests and white blood cell count normalized. She was discharged on antibiotic treatment for 4 more weeks of penicillin-G continuous infusion of 18 million units daily and oral metronidazole 750 milligrams 3 times daily. She was also converted from IV heparin to oral anticoagulation with warfarin for 3 months with follow-up imaging.


We have reported a case of acute pylephlebitis associated with portal vein thrombosis as a result of ileal diverticulitis. Pylephlebitis is defined as septic thrombophlebitis of the portal vein or one of its tributaries and is a rare complication usually of an intra-abdominal inflammatory process.

It was a previously well-defined complication of appendicitis but the condition is now rare, owing to better recognition and early treatment with antibiotic therapy. However, the number of case reports dealing with pylephlebitis seems to have increased [1], with diverticular disease replacing appendicitis as the most common cause [2].

The mortality rate of pylephlebitis has been estimated as 50% overall, with a mortality as high as 80% when the etiology is other than appendicitis [2].

In our case, a previously healthy subject presented with nonspecific symptoms of nausea, vomiting, and fatigue with a rising white blood count and fever. Blood cultures ultimately grew Fusobacterium, Streptococcus anginosus and Clostridium clostridiiforme which supported an intra-abdominal origin of infection.

It is important for the clinician to have early suspicion of this diagnosis to promptly institute broad-spectrum antibiotic coverage. Delaying in initiation of broad-spectrum antibiotics has been associated with unfavorable outcomes in multiple cases [3]. Furthermore, it is imperative to maintain broad spectrum coverage until days 4-5 or until anaerobic and slow growing abdominal organisms can grow on culture media.

Empirical antibiotic therapy for a patient with suspected pylephlebitis should include broad coverage for enteric facultative gram-negative bacilli, an agent active against anaerobes (especially B fragilis) and coverage for aerobic Streptococcus species [1]. Furthermore, patients with clostridial bacteremia, an unlikely organism in pylephlebitis, have had mortality rates reported from 30% to 58% [4,5]. Due to these reports, our patient initially received piperacillin/tazobactam and ampicillin until specific antibiotic therapy was instituted.

Ideal length of time for antibiotic therapy is still undefined. In a series of 19 patients with pylephlebitis described by Plemmons et al. [1] data regarding the duration of antibiotic therapy were available for 6 of the 13 patients that survived. All 6 received at least 2 weeks of therapy, with a mean of 4.2 weeks and a median of 4 weeks.

Based on the frequency of hepatic abscesses as a complication of pylephlebitis, and since developing abscesses may not be visualized on early CT scans, a minimum of 6 weeks antibiotic therapy seems necessary [5].

Our patient received an additional 4 weeks of antibiotic therapy with penicillin G and metronidazole to achieve a total of 6 weeks of therapy.

The role of anticoagulation has not been clearly defined in the treatment of pylephlebitis. The largest series to date evaluating the role of anticoagulation treatment in patients with pylephlebitis was by Baril et al. [6] in 1996 and included 44 cases. They concluded that patients with pylephlebitis, normal clotting function and mesenteric vein involvement would benefit from anticoagulation therapy. However, the study was unable to provide recommendations for a clinical endpoint to anticoagulation treatment or length of time for follow-up imaging to evaluate for recanalization. Follow-up imaging showed a variance in recanalization from months to more than a year.

Due to the well characterized benefits of antibiotics upon improvement of clinical course, no reports were described in which a patient received only anticoagulation and no antibiotics. Also in no case was improvement in a patientís clinical status clearly attributed to the addition of IV heparin [1]. Further Condat et al. [7] reported 8 patients in a series of 33 patients with portal vein or mesenteric thrombosis directly linked to abdominal sepsis and showed that early anticoagulation led to 31% of the patients achieving complete thrombus resolution and 46% achieving partial thrombus resolution. Based on these findings as well as our patient having no contraindications to anticoagulation therapy we chose to start her on day 2 on an IV heparin drip.

The appropriate length of time for anticoagulation therapy for pylephlebitis is not well defined. Some studies recommend systemic anticoagulation for a minimum of 6 months while others recommend 3 months [8,9]. We chose to anticoagulate our patient for 3 months and re-evaluate based on imaging for further therapy.

We disagree with previous reports indicating that clinical or laboratory jaundice is rare in pylephlebitis except in cases complicated by multiple liver abscesses and that the relative absence of jaundice early in the illness helps distinguish pylephlebitis from ascending cholangitis [1]. Our patient had a rising bilirubin that reached a maximum of 4.1 mg/dL, but on repeated imaging demonstrated no signs of liver abscesses. Similarly another case report by Jaber [10] commented on a case of pylephlebitis presenting initially as an obstructive biliary picture. Based on these reports we feel clinical suspicion for cholangitis should remain high early in the patientís treatment no matter if the patient presents with or without laboratory or clinical jaundice.


A patient who initially complained of nonspecific abdominal tenderness eventually re-presented with worsening pain, fever, and sepsis. Blood cultures ultimately grew Streptococcus anginosus, Fusobacterium and Clostridium clostridiiforme, which clearly suggested an intra-abdominal origin.

Results of abdominal ultrasonography, 2 different computed tomography scans taken 9 days apart confirmed the most likely source of sepsis was diverticulitis with seeding of the portal vein. No emergency surgical treatment was warranted since the infectious process resolved upon repeat imaging and patient demonstrates clinical improvement. Our patient was scheduled to receive outpatient antibiotic therapy for 4 more weeks with penicillin-G and metronidazole.

This article was first published on on the 15 of September 2010.


Pavan K Bhatraju, MD, Jignesh P Shah, MD, and Luis S Marsano, MD.
Division of Gastroenterology
Hepatology & Nutrition
University of Louisville School Of Medicine
Louisville, KY, USA

Corresponding author

Dr Pavan Bhatraju
Email: [email protected]


  1. Plemmons R, Dooley D, Longfield R. Septic thrombophlebitis of the portal vein (pylephlebitis): diagnosis and management in the modern era. Clin Infect Dis 1995; 21: 1114-20.
  2. [No authors listed]. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 18-1977. N Engl J Med 1977; 296: 1051-7.
  3. Perez-Cruet M, Grable E, Drapkin M, et al. Pylephlebitis associated with diverticulitis. South Med J 1993; 86: 578-80.
  4. Bodey GP, Rodriguez S, Fainstein V, et al. Clostridial bacteremia in cancer patients. A 12 year experience. Cancer 1991; 67: 1928-42.
  5. Singh P, Yadav N, Visvalingam V, et al. Pylephlebitis Ė diagnosis and management. Am J Gastroenterol 2001; 96: 1312-3.
  6. Baril N, Wren S, Radin R, et al. The role of anticoagulation in the pylephlebitis. Am J Surg 1996; 172: 449-52.
  7. Condat B, Pessione F, Helene Denninger M, et al. Recent portal or mesenteric venous thrombosis: Increased recognition and frequent recanalization on anticoagulant therapy. Hepatology 2000; 32: 466-70.
  8. Aguas M, Bastida G, Nos P, et al. Septic thrombophlebitis of the superior mesenteric vein and multiple liver abscesses in a patient with Crohnís disease at onset. BMC Gastroenterology 2007; 7: 22-6.
  9. Sywak M, Romano C, Raber E, et al. Septic thrombophlebitis of the inferior mesenteric vein from sigmoid diverticulitis. J Am Coll Surg 2003; 196(2): 326-7.
  10. Jaber MR, Holland C. Septic pylephlebitis mimicking biliary obstruction. Am J Gastroenterol 2008; 103(3): 807-8.

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