How many lives does an ulcerative colitis patient have?

In May, 2009, a 41-year-old man presented with continuous rectal bleeding. 9 days before this presentation he had been diagnosed with ulcerative colitis after investigations for bloody diarrhoea (with more than 20 stools per day), and abdominal cramps. At the initial diagnosis, he was treated with regular mesalazine, azathioprine, and prednisolone; butylscopolamine and metamizole were prescribed for symptomatic relief. His symptoms did not improve and infl iximab was added to his regimen. However, after the fi rst infusion he discharged himself from hospital before any follow-up was arranged. When he presented again, his blood pressure was 130/70 mm Hg; heart rate 110 beats/min; respiratory rate 24 breaths/min; and temperature 42°C. His abdomen was generally tender, and a high-frequency diastolic murmur, loudest at the left lower sternal border, was heard. His haemoglobin was 92·8 g/L; white blood cell count 14·7×109/L; and concentration of C-reactive protein (CRP) 65 mg/L. Cytomegalovirus pp65 antigen was undetectable. Abdominal ultrasonography and contrast-enhanced CT (fi gure A) showed fulminant pancolitis. The bowel wall thickness was estimated at 15 mm. Transoesophageal echocardiography was done to investigate the murmur (fi gure B, videos 1 and 2); this showed a large endocardial abscess cavity adjacent to his aortic valve, third-degree aortic insuffi ciency, and globally diminished left-ventricular function. The patient was treated empirically with intravenous gentamicin and vancomycin; his mesalazine, azathioprine, and infl iximab treatments were stopped, and his prednisolone was quickly tapered. The next day, blood cultures grew Streptococcus anginosus. An aortic valve replacement (with a homograft) and aortic root replacement was done as an emergency. On the 6th postoperative day, he developed ventricular fi brillation and had a cardiac arrest. After successful resuscitation, an echocardiogram showed a central homograft failure with paravalvular leak; a new homograft was therefore implanted and the abscess cavity was fl ushed and sealed. 3 days later he had another cardiac arrest, with complete atrioventricular block which was thought to be See Online for webvideos 1 and 2 due to erosion of the sinus node; this conduction abnormality was successfully treated by insertion of a DDD pacemaker. After he had recovered from surgery the patient was discharged to a rehabilitation facility. A month after discharge, the patient again presented with fulminant colitis and was referred for proctocolectomy. He made an uneventful recovery and was well at last follow-up in June, 2010. Infl ammatory bowel disease is an independent risk factor for native valve endocarditis. The likely mechanism is bacterial translocation of the gut resulting in bacteraemia, which can be undetectable by standard blood culture methods in febrile ulcerative colitis patients. The two key components of the Duke criteria for infective endocarditis (bacteraemia resulting from typical organisms [viridans streptococci] and evidence of cardiac valvular involvement) were quickly established in this case, once the murmur was heard. Several factors contributed to the lifethreatening course in this patient; the immunosuppressive treatments, administration of an analgesic with antipyretic properties to a patient at high risk of infection, and circumstances that led to initial tests which focused exclusively on the gut. The risk of opportunistic infection is increased when corticosteroids, azathioprine, or infl iximab are prescribed individually. However, when these treatments are used in combination, the risk increases in a synergistic manner, and such combinations should be avoided. Instead, fast-acting, single agents with short half-lives are preferable in this setting. In addition, if medical treatment of ulcerative colitis fails, proctocolectomy surgery should not be delayed.