Background-Routine coagulation tests do not necessarily reflect haemostasis in vivo in cirrhotic patients, particularly those who have bleeding varices. Thrombelastography (TEG) can provide a global assessment of haemostatic function from initial clot formation to clot dissolution. Aim-To evaluate TEG changes in cirrhotic patients with variceal bleeding and their association with early rebleeding. Patients/Methods-Twenty cirrhotic patients with active variceal bleeding had serial TEG and routine coagulation tests daily for seven days. The TEG variables before the day of rebleeding (n = 6) were compared with those of patients without rebleeding (n = 14). Results-Baseline characteristics of the rebleeding and non-rebleeding groups were comparable apart from a higher incidence of uncontrolled infection on the day of rebleeding in the rebleeding group (p = 0.007). The patients in the rebleeding group were more hypocoagulable before the day of rebleeding as shown by longer r (42 v 24 mm, p<0.001) and k (48 v 13 mm, p<0.001) and smaller a (12 v 38°, p<0.001) compared with the mean of daily results of the non-rebleeding group. Routine coagulation tests, however, showed no significant diVerences between the two groups. Conclusion-The results of serial TEG measurements suggest that hypocoagulability may be associated with early rebleeding in cirrhotic patients. (Gut 1998;43:267-271)
In a prospective study to correlate admission glucose level with neurologic outcome in stroke, 252 acute stroke patients without prior disability and admitted within 24 hours of onset of ictus were assessed. The stroke was classified into one of three types -cortical infarct, lacunar infarct, or intracerebral hemorrhage -by clinical, computed tomographic, and necropsy findings. Fifty-one diabetic patients were excluded from the entire cohort to form a nondiabetic category for analysis. We found that admission glucose level showed a significantly higher degree of correlation with mortality and morbidity (measured as arm function, leg function, and activities of daily living) when cortical (n = 118) and lacunar (n = 58) infarcts were pooled compared with when they were assessed separately. E pidemiologic data' have shown that hyperglycemia is associated with an increased incidence of cerebrovascular diseases. Animal experiments using controlled degrees of cerebral ischemia have demonstrated that elevated blood glucose concentrations enhance the degree of neurologic deficit 2 and morphologic brain damage.34 Clinical observations have also indicated that patients with hyperglycemia with or without diabetes mellitus have poorer neurologic outcome than their normoglycemic counterparts. 5 The adverse effect of hyperglycemia on energy metabolism in the ischemic brain is postulated to be the result of severe lactic acidosis.
67On the other hand, cerebral blood flow studies 8 indicate that hyperglycemia is not necessarily an unfavorable condition in acute cerebral ischemia. Moreover, in out-of-hospital cardiac arrests, a high glucose level may simply reflect prolonged cardiopulmonary resuscitation rather than be the primary determinant of poor neurologic outcome. Such controversy prompted us to examine, in a prospective manner, the relation between admission glucose level and the outcome in a large cohort of stroke patients. We report our preliminary observations on 252 acute stroke patients admitted over the first 6 months of our study.
In an attempt to determine whether the dose of an antiepileptic drug should be increased in epileptic patients who were seizure-free and had subtherapeutic serum levels, 79 patients with idiopathic generalized tonic-clonic seizures treated with monotherapy [phenytoin (PHT) or phenobarbital (PB)] and with a subtherapeutic serum level were prospectively studied. Their last seizure was at least 3 months prior to entry, and no patient had any clinical evidence of toxicity. They were randomized to study arm A (keeping the level in the subtherapeutic range) or study arm B (increasing the dose until the level reached and stayed at the therapeutic range). Over a mean follow-up period of 24 months, there was no significant difference between the two study arms in the occurrence of seizures, but arm B patients had an increased incidence of neurotoxic side effects from the dose increment. These results confirm the clinical impression that it is unnecessary to increase the dose of the antiepileptic drug despite a subtherapeutic serum concentration in a relatively well-stabilized patient, thus minimizing the frequency of dose adjustment and the need for expensive therapeutic drug monitoring.
SUMMARY Visual evoked responses (VERs) were recorded on 52 chronic alcoholic patients without Wernicke-Korsakoff syndrome, 22 ofwhom had cerebellar ataxia, and eight chronic alcoholics with Wernicke-Korsakoff syndrome. Abnormal VERs were found in 23% of patients without and 37% of patients with Wernicke-Korsakoff syndrome. The main VER abnormalities of all the alcoholic groups were prolonged latency and reduced amplitude of the P100 component. Improvement followed a six month period of abstinence. VERs may be useful in the early detection of alcohol induced brain damage, and in following the progress of patients with the condition.
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