Fulminant ulcerative colitis complicated by treatment-refractory bacteremia

Abstract

Severe ulcerative colitis is defined by more than six bloody stools daily and evidence of toxicity, demonstrated by fever, tachycardia, anemia, or an elevated erythrocyte sedimentation rate. Fulminant disease represents a subset of severe disease with signs and symptoms suggestive of increased toxicity. Treatment of severe colitis includes intravenous corticosteroid administration, with consideration of intravenous infliximab 5 mg/kg. Failure to show improvement after 3 to 5 days is an indication for colectomy or treatment with intravenous cyclosporine. We report a 23-year-old Hispanic woman with decompensated cirrhosis presenting with new-onset fulminant ulcerative colitis and resulting polymicrobial bacteremia, requiring colectomy for infection source control and colitis treatment.

Disease severity in ulcerative colitis (UC) is based on clinical and endoscopic findings and is classified as mild, moderate, severe, or fulminant. Fulminant colitis occurs in a portion of patients with severe UC who have more than 10 stools per day, continuous bleeding, abdominal pain, distention, and acute, severe toxic symptoms including fever and anorexia (1). In fulminant UC with extensive ulceration, the altered colonic mucosa may represent a potential source of infection, particularly in those with a preexisting state of increased intestinal permeability and impaired immune function such as cirrhosis. Patients with cirrhosis also have delayed intestinal motility, which can lead to intestinal bacterial overgrowth. In conjunction with portal hypertension, this overgrowth enables perpetuation of bacteria and can facilitate the spread of bacteria to extraintestinal sites (2). Forty-five percent of hospitalized patients with cirrhosis and gastrointestinal hemorrhage develop bacterial infections, the most common being spontaneous bacterial peritonitis (SBP) (2, 3).

CASE REPORT

A 23-year-old Hispanic woman with prior systemic lupus erythematosus and decompensated cirrhosis secondary to autoimmune hepatitis presented to an outlying facility with a 2-day history of hematochezia and intermittent abdominal pain. Esophagogastroduodenoscopy and colonoscopy revealed nonbleeding esophageal varices and pancolitis, respectively. The patient was discharged on prednisone 40 mg daily. She was readmitted to our facility because of an increase in the frequency of rectal bleeding and worsening abdominal pain. On examination, she was afebrile, with a heart rate of 118 beats per minute and a blood pressure of 110/70 mm Hg. Her mucous membranes were dry. Her abdomen was soft, mildly tender to palpation, and bowel sounds were present. The blood hemoglobin was 8.9 g/dL; platelets, 128,000/μL; and international normalized ratio, 2.1. Abdominal ultrasound showed a small amount of ascites, nonamenable to paracentesis. Following admission, she had several more episodes of hematochezia. Repeat colonoscopy revealed severe ulcerating lesions throughout the entire colon (Figure 1). Colon biopsies demonstrated chronic colitis, cryptitis with crypt abscess formation, basal cell plasmacytosis, and early glandular distortion. Stool was obtained during colonoscopy and was negative for infectious etiologies. The patient was started on methylprednisolone 50 mg intravenously twice daily for treatment of suspected ulcerative colitis. Despite this therapy, hematochezia persisted with declining hemoglobin and persistent coagulopathy. Endotracheal intubation was performed.

Figure 1.

Colonoscopy showing erythema, necrosis, and ulcerating lesions in (a) transverse colon, (b) ascending colon, and (c) cecum.

Approximately 96 hours into admission, the patient's temperature rose to 102°F, her heart rate rose to 140 beats per minute, and her blood pressure fell to 86/52 mm Hg. Due to suspicion of ensuing sepsis, immunosuppressive therapy with infliximab was decided against. A fecal management system collected 2000 mL of maroon-colored fluid over the following 24 hours. Aggressive blood product support continued. She was empirically started on piperacillin/tazobactam. Blood cultures revealed growth of gram-negative bacilli and gram-positive cocci. Vancomycin was added to the antibiotic regimen. Repeat blood cultures revealed gram-positive cocci in chains, gram-positive cocci in clusters, and two different gram-negative bacilli. Subsequent identification demonstrated Streptococcus pneumoniae, methicillin-sensitive Staphylococcus aureus, Escherichia coli, and an unidentifiable anaerobic gram-negative bacillus. The patient's clinical condition progressively worsened, requiring increasing levels of vasopressor support and further administration of blood products. Despite adequate antimicrobial coverage, multispecies bacteremia failed to clear.

The patient underwent total abdominal colectomy with ileostomy. Postoperatively, she improved markedly. Restoration of hemodynamics, stabilization of blood counts, and clearance of bacteremia were achieved within 36 hours. Examination of the resected colon revealed numerous areas of cryptitis and crypt architectural distortion, as well as multiple foci of mucosal erosions with extravasation of erythrocytes through the length of the colon specimen. No obvious perforation was identified. At 1-month follow up after hospital discharge, the patient was doing well, with toleration of a normal diet, resumption of activities of daily living, and progression towards hepatic transplant evaluation.

DISCUSSION

Fulminant UC is uncommon and requires institution of potent intravenous immunosuppression or colectomy for adequate control. We present a patient with fulminant UC superimposed on decompensated cirrhosis, who developed resulting treatment-refractory polymicrobial bacteremia. Total abdominal colectomy was required to treat both bacteremia and fulminant colitis. Given the presence of ascites at the time of admission, it is postulated that severe mucosal friability, in combination with cirrhosis-associated immune dysfunction, led to the development of polymicrobial SBP and subsequent bacteremia. Pathogens isolated from blood cultures support this hypothesis. S. pneumoniae, E. coli, and anaerobic gram-negative bacilli represent usual gut flora and are among the most common causes of SBP. While S. aureus is not a typical cause of SBP, it has been demonstrated that the epidemiology of nosocomial SBP and bacteremia in hospitalized cirrhotic patients is characterized by a decreased prevalence of Enterobacteriaceae and a predominance of gram-positive cocci, namely S. aureus (4).