Pylephlebitis and Pyogenic Liver Abscesses: a Complication of Hemorrhoidal Banding

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Pylephlebitis and pyogenic liver abscesses: A complication of hemorrhoidal banding

Nicole G Chau BSc MD1, Sacha Bhatia MD MBA1, Maitreyi Raman MD FRCPC2

NG Chau, S Bhatia, M Raman. Pylephlebitis and pyogenic La pyléphlébite et les abcès hépatiques liver abscesses: A complication of hemorrhoidal banding. pyogènes : Une complication du cerclage des Can J Gastroenterol 2007;21(9):601-603. hémorroïdes Hemorrhoidal banding is a well-established and safe outpatient procedure. Septic complications of hemorrhoidal banding are rare Le cerclage des hémorroïdes est une intervention établie et sécuritaire en consultations externes. Les complications septiques du cerclage des but can be fatal. The first case of pylephlebitis (septic portal vein hémorroïdes sont rares mais peuvent être fatales. La présente étude rend thrombosis) and pyogenic liver abscess following hemorrhoidal compte du premier cas de pyléphlébite (thrombose de la veine porte avec banding in a 49-year-old man with diabetes is reported in the present septicémie) et d’abcès hépatique pyogène après un cerclage d’hémorroïdes study. Risk factors, management and the role of prophylaxis in chez un homme diabétique de 49 ans. On discute des facteurs de risque, de immunocompromised patients are discussed. Caution against hemor- la prise en charge et du rôle de la prophylaxie chez les patients immuno- rhoidal banding in immunosuppressed patients, including patients compromis. Il faut faire preuve de prudence lors du cerclage d’hémor- with diabetes, is warranted. roïdes de patients immunosupprimés, y compris les patients diabétiques.

Key Words: Hemorrhoidal banding; Pylephlebitis; Pyogenic liver abscess CASE PRESENTATION was abnormal with albumin at 17 g/L, an international nor- A 49-year-old Vietnamese man presented to the emergency malized ratio of 1.1 and total bilirubin of 17 μmol/L. department of the Toronto Western Hospital, University Creatinine was elevated at 170 μmol/L but normalized with Health Network (Toronto, Ontario) with a five-day history hydration. Doppler abdominal ultrasound revealed cirrhosis of fever, right upper quadrant pain, ascites, vomiting and with extensive portal vein thrombosis, ascites, two hypoechoic hematochezia following hemorrhoidal banding treatment for liver lesions consistent with hepatic abscesses and an unre- symptomatic internal hemorrhoids with normal colonoscopy markable biliary tree. at an outpatient community clinic. Rectal varices were Empiric piperacillin/tazobactam (4.5 g given intravenously absent on colonoscopy. Past history included type II diabetes every 8 h) was quickly initiated for pylephlebitis (septic portal with retinopathy, hypertension, dyslipidemia, minor lacunar vein thrombosis) and pyogenic liver abscesses (PLA). There stroke and remotely treated pulmonary tuberculosis. His only was immediate defervescence. A computed tomography (CT) medications were oral hypoglycemics (metformin and gly- scan of the abdomen confirmed right, left and main portal vein buride) and antihypertensives (amlodipine). He denied alco- thrombosis, splenic and superior mesenteric vein thrombosis hol, illicit drug use, known liver disease or risk factors for and five small, hypodense liver lesions in segments 1, 4A and liver disease. The family physician denied previous liver dis- 5 that were consistent with multifocal abscesses (Figure 1). ease, abdominal imaging or abnormal liver enzymes. A Blood cultures and ultrasound-guided aspirate from the largest review of the University Health Network records confirmed abscess (2.5 cm) grew Klebsiella pneumoniae sensitive to the same. ciprofloxacin. Therapeutic CT-guided aspiration was unsuc- Examination revealed a temperature of 38.7°C, tachycar- cessful. Gastroscopy performed for melena revealed grade 2 to dia, mild right upper quadrant tenderness and ascites. 3 esophageal varices that were banded. Colonoscopy con- Jaundice, hepatosplenomegaly, asterixis, stigmata of liver firmed no mass or rectal varices. Cirrhotic workup revealed disease and signs of local complications were absent. only a positive hepatitis B core and surface antibody. Bloodwork revealed microcytic anemia with a hemoglobin Hypercoagulable workup was negative. Induced sputum for acid- level of 104 g/L and a leukocytosis level of 16.0×109/L with fast bacilli was negative. Oral ciprofloxacin 500 mg twice daily neutrophilia. Transaminases were mildly elevated with aspar- was continued for six weeks after discharge. Follow-up imaging tate aminotransferase at 160 U/L, alanine aminotransferase at showed resolution of abscesses and improvement in portal vein 96 U/L and alkaline phosphatase at 330 U/L. Liver function thrombosis. 1Department of Medicine, University of Toronto; 2Division of General Internal Medicine and Gastroenterology, University Health Network, Toronto, Ontario Correspondence: Dr Maitreyi Raman, University of Calgary, 234 Scenic Acres Terrace, Calgary, Alberta T3L 1Y4. Telephone 403-241-2183, fax 403-210-9368, e-mail [email protected] Received for publication August 16, 2006. Accepted August 21, 2006

Chau et al

varices confirmed by endoscopy. However, colonoscopy at the community clinic and colonoscopy at the Toronto Western Hospital did not show rectal varices. If rectal varices indeed were missed in our patient, it would be intuitive to think that the presence of pre-existing liver disease and portal vein thrombosis would result in a higher complication rate following endoscopic rectal variceal ligation compared with internal hemorrhoidal banding in a patient without pre-existing liver disease or portal vein thrombosis. A thorough MEDLINE liter- ature search to date did not reveal clear data to ascertain the actual difference in complication rate. Pylephlebitis (septic portal vein thrombosis) is a rare but serious condition that can complicate any intra-abdominal infection that is often secondary to diverticulitis, appendicitis, biliary tree infection or inflammatory bowel disease. Clinical presentation is often nonspecific; however, pylephlebitis Figure 1) Computed tomography scan of the abdomen showing right, should be suspected in patients with fever, right upper left and main portal vein thrombosis, splenic and superior mesenteric quadrant tenderness or jaundice. Diagnosis is best confirmed vein thrombosis and small, hypodense liver lesions consistent with mul- by CT scan or colour flow Doppler ultrasonography to demon- tifocal abscesses. Arrow indicates a lobulated hepatic abscess above the strate portal vein thrombosis in a patient with bacteremia. hilum Mortality ranges from 11% to 32%, even with the use of antibiotics (9,10). The mainstay of treatment is early initiation of parenteral broad-spectrum antibiotics followed by specific antibiotics against the bacterial isolates that may lead to DISCUSSION resolution of both portal vein thrombosis and hepatic abscess. Septic complications of hemorrhoidal banding are rare but The median duration of therapy in surviving patients is can be fatal. A review (1) of 39 studies including 4.2 weeks (9). Bacteroides fragilis and E coli are the most common 8060 patients undergoing hemorrhoidal banding revealed a isolates. Portal vein thrombosis may progress to fatal mesenteric rate of infection of 0.05%, and a retrospective study (2) of vein thrombosis (10) but the role of anticoagulation is contro- 805 patients undergoing hemorrhoidal banding revealed only versial. In the absence of malignancy, hypercoagulable disorder one case of bacteremia (0.09% sepsis). However, at least and multiple thromboses, we elected not to anticoagulate this six deaths due to septic complications following hemorrhoidal patient, who also had melena secondary to esophageal varices. banding have been published in nine papers (3). Septic com- Colonoscopy confirmed the absence of diverticulitis or malig- plications posthemorrhoidal banding include abdominal pain, nancy in this patient. fever, urinary retention, local perineal edema and cellulitis PLA is rare, with an incidence rate of 2.3 per 100,000 peo- extending to the pelvis and thighs that occurred two to ple; incidence is higher in men, immunodeficient states and seven days following hemorrhoidal banding treatment (3). diabetes patients (11). Mortality ranges from 10% to 12% Responsible organisms confirmed at autopsy have included (12). Clinical manifestations are nonspecific and include fever, Escherichia coli and Clostridium species (4,5). Prevention of abdominal pain and emesis; diagnosis is confirmed by CT scan local septic complications include the use of enemas before or ultrasound. The etiology of PLA is frequently from biliary banding, sterile instruments and povidine-iodine preparation pathology (often polymicrobial), hematogenous (portal system (3). Early review of patients within a few days posthemor- entry or hepatic artery from intestinal focus such as diverticuli- rhoidal banding is advised in patients with previous septic tis or inflammatory bowel disease), direct (percutanous inter- complications (6). vention or trauma) or by contiguity. PLA may be the first Risk factors for septic complications include HIV infection manifestation of colorectal cancer, even in the absence of (6,7), immunosupression, phenothiazines, intravenous drug hepatic metastases. Therefore, colorectal cancer screening is abuse (4), diabetes and rheumatic diseases (6,7). warranted in patients with PLA in the absence of biliary To our knowledge, this is the first reported case of pathology (13). PLA has been reported in two patients follow- pylephlebitis following hemorrhoidal banding and the second ing hemorrhoidectomy, and liver isolates grew Streptococcus reported case of PLA following hemorrhoidal banding treat- viridans and K pneumoniae (14). PLA has also been reported ment. Interestingly, the only other case (8) of PLA following following surveillance colonoscopy in a patient with inflam- hemorrhoidal banding was also in a Vietnamese male with dia- matory bowel disease (15). betes and a remote history of tuberculosis. Although K pneu- K pneumoniae is the predominant cause of PLA in people of moniae was isolated, the patient required right hepatectomy to Asian origin (16,17), with rising incidence in Western coun- control sepsis. These cases highlight the increased risk of PLAs tries (18,19). Minor mucosal injuries of the gastrointestinal due to K pneumoniae in patients with diabetes who experience tract are thought to allow entry of K pneumoniae into the gastrointestinal mucosal injury through hemorrhoidal banding. bloodstream, with passage through the portal vein resulting in It is possible that the present patient had pre-existing sequestration by Kupffer cells in the liver, leading to liver chronic liver disease secondary to hepatitis B or nonalcoholic abscess formation. K pneumoniae liver abscesses (KLA) are fatty liver disease, and portal vein thrombosis that potentially usually monobacterial with bacteremia occurring in 95% of resulted in rectal varices. Certainly, the presence of significant cases (20); however, 64% of KLA are cryptogenic (21). portal hypertension is supported by the presence of esophageal Standard ampicillin/gentamicin/metronidazole regimens can

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be hazardous because K pneumoniae is intrinsically resistant to SUMMARY ampicillin and metronidazole is ineffective against aerobes. Patients presenting with sepsis following hemorrhoidal banding The preferred empirical regimen for KLA is a combination of without local signs of infection should undergo evaluation for aminoglycoside and extended-spectrum beta-lactams (19). pylephlebitis and PLA. Early diagnosis by ultrasound or CT Drainage is essential for treatment in most cases; however, scan, followed by prompt initiation of broad-spectrum antibi- antibiotic therapy alone may be effective. One study (22) otics, is recommended to avoid morbidity and mortality. found percutaneous transhepatic drainage to be as effective as Percutaneous drainage and specific antibiotic therapy based on surgery to treat KLA. bacterial isolates should be continued for at least four weeks. As Diabetes is the most common concomitant disease in evidenced by the present case, diabetes is a risk factor for septic patients with KLA (16,17,19-21). Of 160 patients with PLA, complications from hemorrhoidal banding and formation of diabetes was present in 67.5% of patients with KLA com- KLA. Caution against hemorrhoidal banding is warranted in pared with only 4.5% of patients with polymicrobial liver immunocompromised patients, including those with diabetes. abscesses (RR of 11.1) (16). Diabetes is also a risk factor for Careful history and physical examination to screen for immuno- extrahepatic metastases from KLA, including endophthalmi- compromised patients in addition to adequate colonic prepara- tis (16,23) and septic pulmonary emboli (20). The increased tion with an enema and use of sterile instruments are key steps risk of PLA in patients with diabetes may be related to the to prevent septic complications; however, no evidence exists for interference with neutrophil chemotaxis and phagocytosis antibiotic prophylaxis for hemorrhoidal banding. Close follow- (24-26). up of immunocompromised patients is imperative.

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