Evaluation of the management of hepatic encephalopathy.
Evaluation of the management of hepatic encephalopathy.
复制标题
肝性脑病治疗的评估。
DOI：
10.1016/s0022-3476(72)80146-x
复制
发表时间：
1972
期刊：
影响因子：
--
通讯作者：
Iris F. Litt
中科院分区：
文献类型：
--
作者：
Michael I. Cohen;Iris F. Litt
IN 1969, we described briefly in the JOURNAL 1 our method for plasmapheresis of whole blood and the use of this technique in the management of hepatic encephalopathy. Four children were initially reported. An additional 16 patients have been seen subsequently. Between 0.22 and 20 per cent a of adult patients with acute serum hepatitis develop hepatic encephalQpathy during the course of their illness. The mortality rate associated with this complication approximates 80 per cent. 4 With the recent rise in the incidence of drug abuse among teen-agers, a complementary increase in hepatitis has been observed2, G Therefore, it would seem prudent to anticipate similarly high morbidity and mortality rates among adolescent patients who develop hepatic encephalopathy. A re-evaluation of current therapeutic approaches to this problem in children and adolescents therefore seems timely. In a 4 year period, the Division of Adolescent Medicine has cared for 2,373 teenagers with hepatitis, approximately 90 per cent of whom were drug abusers. Eighteen of these patients developed hepatic encephalopathy. In addition, two toddlers also became encephalopathic and are included in this commentary because of similar therapeutic modalities utilized in their care. Pertinent clinical data on these patients appear in Table I. The diagnosis of serum hepatitis was made only when Australia antigenemia or Australia antibody was identified. Upon admission, 2 patients were obtunded intermittently with bouts of irrational, wild, and aggressive behavior (stage 2 hepatic coma); 10 patients were stuporous and would only respond to deep painful stimuli (stage 3 hepatic coma); and 8 children were comatose, totally unresponsive to stimuli, but had a spontaneous respiratory pattern (stage 4 hepatic coma). With the exception of two, all patients progressed to a totally unresponsive state within 24 hours of admission. Determination of the prothrombin time in 20 patients revealed a prolongation in all of them. A standard battery of analyses of serum relating to liver disease were similarly abnormal in all subjects, but the degree of abnormality did not prognosticate the eventual outcome. Electroencephalography was performed in nine patients, and although each was abnormal, the results did not appear to indicate a good or poor prognosis. Similarly, electrolyte and acid-base imbalance although present in all subjects failed to differentiate the survivor from the nonsurvivor.
