Increased oro-cecal transit time in grade I or II hepatic encephalopathy.

UNLABELLED: The pathogenic mechanisms of hepatic encephalopathy remain to be elucidated. It has been suggested that a digestive motor disorder could promote the absorption of toxins produced within the lumen and thus enhance hepatic encephalopathy. AIM: To evaluate oro-cecal transit time in cirrhotic patients with and without hepatic encephalopathy. METHODS: Hospitalized patients with alcoholic cirrhosis without encephalopathy and with spontaneous grade I and II encephalopathy were included. Severity of hepatic encephalopathy was assessed clinically and the Child-Pugh score was used to describe cirrhosis severity. Nine healthy volunteers constituted a control group. Oro-cecal transit time was measured with the sulfasalazine test. RESULTS: Twenty-eight patients (mean age 62.5 +/- 8.5 years) were included. Ten had hepatic encephalopathy of unknown cause and 18 were free of hepatic encephalopathy. Oro-cecal transit time was significantly longer in patients with hepatic encephalopathy (641 +/- 350 min) compared to patients without hepatic encephalopathy (298 +/- 96; P<0.05) and to controls (354 +/- 90; P<0.05). Oro-cecal transit time was comparable for each Child-Pugh score and was not different between the two grades of hepatic encephalopathy. CONCLUSION: Oro-cecal transit time is longer in alcoholic cirrhosis patients with hepatic encephalopathy. This digestive motor disorder provides a partial explanation of hepatic encephalopathy of unknown etiology.

Cardiac sources of embolism should be routinely screened in ischemic colitis.

OBJECTIVE: Potential cardiac sources of embolism may promote ischemic colitis. The aim of this study was to evaluate their role in segmental, nongangrenous ischemic colitis and to determine the usefulness of routine cardiac evaluation in patients with this disease. METHODS: Sixty case and 60 control patients matched for age and gender were included and questioned regarding treatment and prior cardiovascular history or risk factors. Potential cardiac sources of embolism, classified as "proven" or " still debated," were screened using an electrocardiogram, rhythmic Holter monitoring over 24 h, and transthoracic echocardiography. RESULTS: Sex ratio (male:female) was 1:2, and mean age was 70 +/- 14 yr. Case and control patients had similar drug use, prior cardiovascular history, and risk factors. A potential cardiac source of embolism was found in 26/60 case (43%), compared with 14/60 control patients (23%) (p = 0.02; OR = 2.5, 95% CI = 1.2-5.5). Excluding the "still debated," 21/60 case (35%), compared with 8/60 control patients (13%), had a "proven" cardiac source of embolism (p < 0.01; OR = 3.5, 95% CI = 1.4-8.4). Electrocardiogram alone misdiagnosed 72% of the "proven" cardiac sources of embolism, whereas the combination electrocardiogram plus Holter monitoring detected 71%, and electrocardiogram plus echocardiography 62%. Twelve of 21 case patients with at least one proven cardiac source of embolism, were previously unknown. Anticoagulant therapy was required in 32% of case patients and antiarrhythmic therapy in 25% of cases. CONCLUSIONS: Potential cardiac sources of embolism were more common in patients with segmental, nongangrenous ischemic colitis than in control patients. Therefore, these patients should undergo a routine electrocardiogram, rhythmic Holter monitoring, and transthoracic echocardiography. Anticoagulant therapy should also be considered for this patient population.