Morbid obesity, defined as a body mass index greater than 40 kg/m2, has an estimated prevalence of 7.7% in the United States.1 The term bariatric surgery comprises surgical techniques including Roux-en-Y gastric bypass, sleeve gastrectomy, and gastric banding. Unfortunately, numerous complications can arise both early and late in the postoperative course.2
Fusobacterium species, gram-negative anaerobic bacilli that commonly inhabit the oropharynx, are well known for causing Lemierre syndrome, a thrombophlebitis of the internal jugular veins that usually occurs from the contiguous spread of oropharyngeal infections.3 Recent evidence suggests that Fusobacterium also colonizes the gastrointestinal mucosa, with case reports demonstrating a gastrointestinal variant of Lemierre syndrome presenting as septic thrombosis of the portal vein.4,5
We present a rare case of acute pylephlebitis complicated by hepatic abscess formation secondary to Fusobacterium nucleatum in a patient who recently underwent a Roux-en-Y gastric bypass surgery.
A 48-year-old woman who recently underwent a laparoscopic Roux-en-y gastric bypass surgery (body mass index 44.2 kg/m2) presented with abdominal discomfort for 3 months following surgery. A contrast computed tomography (CT) scan of her abdomen at that time showed phlegmon at the surgical site, and she was instructed to follow up with her surgeon outpatient. However, over the next 3 weeks, she continued to have worsening abdominal pain.
On presentation, she was tachycardic and mildly hypotensive and had right upper quadrant tenderness. Laboratory work revealed a white blood cell count of 14,400 cells/mm3, aspartate aminotransferase 58 U/L, alanine aminotransferase 44 U/L, total bilirubin 2.1 mg/dL, alkaline phosphatase of 178 U/L, blood urea nitrogen 23 mg/dL, and creatinine 1.0 mg/dL. Sedimentation rate was 140 mm/h, and C-reactive protein was 30 mg/dL. A CT scan with contrast demonstrated the portal vein thrombosis (PVT) (Fig. 1) and complex cystic masses in the liver (Fig. 2), which were not seen on the CT scan 3 weeks earlier. A magnetic resonance imaging of the liver confirmed that these lesions were hepatic abscesses. The patient was started on ceftriaxone, metronidazole, and also a therapeutic dose of enoxaparin for anticoagulation. A tagged white blood cell scan confirmed acute pylephlebitis. The liver abscess was aspirated.
An esophagogastroduodenoscopy and colonoscopy showed a healthy anastomosis of the Roux-en-Y gastric bypass as well as nonbleeding diverticulosis. The liver abscess culture grew F. nucleatum. The patient was transitioned to rivaroxaban with a 6-week course of ceftriaxone and metronidazole.
A follow-up CT scan of the abdomen 4 months later showed resolution of the hepatic abscesses, persistence of PVT, and formation of collateral venous channels around the portal vein. Anticoagulation was continued for 6 months.
Laparoscopic Roux-en-Y surgery is a popular intervention for treatment of morbid obesity with a more sustained weight loss compared with other bariatric surgical techniques. Complications of this operation include anastomotic leakage, strictures, bowel obstruction, fistulae, and internal hernias.2 However, similar to other abdominal surgeries, bariatric surgery is also associated with an increased risk of postoperative infections. There exists 1 case in the literature of gastric banding complicated by septic thrombophlebitis of the portal vein and hepatic abscesses.6 However, our case is the first description of pylephlebitis with multiple liver abscesses as a consequence of laparoscopic Roux-en-Y gastric bypass surgery.
Pylephlebitis is described as septic thrombophlebitis involving the portal vein, occurring as a complication of an intra-abdominal infectious source or a recent surgery in an area drained by portal venous system.5,7 In our case, the patient had a recent Roux-en-Y gastric bypass surgery, which was complicated by a phlegmon at the surgical site. The diagnostic criteria for pylephlebitis include demonstration of a thrombus in portal vein on imaging along with positive blood or tissue cultures. A contrast-enhanced CT scan is preferred over ultrasound because of its better sensitivity and specificity, especially in delineating the extension of the thrombus and detecting suppurative foci within organs.8
Fusobacterium species, anaerobic gram-negative bacilli, are normal residents of the oropharyngeal cavity but uncommonly reside in the gastrointestinal tract. Lemierre syndrome, septic venous thrombosis of the internal jugular vein caused by an upper respiratory tract infection, is classically associated with Fusobacterium necrophorum.4,9 It predominantly affects young, healthy adults.4 In contrast, F. nucleatum is the culprit in the majority of abdominal and pelvic infections and typically affects the elderly population with multiple comorbid conditions and/or malignancies.3,4,10–13
A suggested mechanism for thrombophlebitis can be attributed to F. nucleatum's ability to bind to and activate the plasminogen to plasmin that results in localized proteolysis and allows it to invade locoregional veins.11 Also, the lipid A component of the bacterial endotoxin has been shown to activate the intrinsic pathway of the coagulation cascade in vitro, which imparts its thrombogenic potential.14
Review of the literature suggests that among the 17 existing cases linking Fusobacterium species to PVT, more than 50% were secondary to F. nucleatum infection. Of the 17 cases, only 5 were complicated by hepatic abscesses. The majority of cases were males (13 of 17), and 50% of cases did not have an identifiable source of infection. A portal cavernous transformation developed in 30% of cases.3,4,7,8 Other complications included splenomegaly,15 splenic abscesses, hepatic venous infarct, and decompensated liver disease.5,10,14 However, approximately half of the cases had no PVT-associated acute or chronic complications.3,7,8,11–13
Treatment includes antibiotics, and in cases with a hepatic abscess, surgical drainage may be required. Because of increasing resistance to penicillins, complete identification and testing for antimicrobial susceptibility are important for tailoring antibiotic therapy.8 In most cases, Fusobacterium species respond well to combinations of β-lactam/β-lactamase inhibitors, cephalosporins, carbapenems, clindamycin, metronidazole, fluoroquinolones, and tetracycline.5,8,9 Usually, 4 to 6 weeks of antibiotic therapy is preferred because of slower penetration and sterilization of the infected thrombus.7
Concomitant treatment with anticoagulants is still debatable but generally favored. Indications for anticoagulant therapy include progression of the thrombosis, nonresolving fevers despite appropriate antibiotic therapy, and prevention of septic embolization to various organs.7,8 Review of the existing cases of pylephlebitis secondary to Fusobacterium revealed that more than 80% of the patients received anticoagulation ranging between 3 and 6 months.3,8,12 Of the 2 patients who did not receive any anticoagulation therapy, one had persistence of the portal vein thrombus.13 However, another patient who remained on anticoagulants for 9 months had failed recanalization of his portal vein.12 Hence, inconclusive evidence exists for the beneficial impact of anticoagulation.
In conclusion, our patient had the first known Fusobacterium-associated pylephlebitis complicated by hepatic abscesses after Roux-en-Y gastric bypass surgery. Pylephlebitis is a possible and potentially fatal complication that can follow bariatric surgery. With the growing number of bariatric surgeries, physicians should be vigilant of this condition as a delayed complication of an intervention. Anticoagulation therapy is controversial but seems to benefit most patients with pylephlebitis.
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