Hemocephalus and Not Hydrocephalus as a Predictor of Poor Outcome From Supratentorial Intracerebral Hemorrhage
To the Editor:
I was interested to see the study by Diringer et al1 on supratentorial intracerebral hemorrhage, which indicated that the poor prognosis conferred by hydrocephalus had not been previously recognized. As a one-time staff member of the Washington University School of Medicine, I felt impelled to correct some pathological misconceptions.
Internal hydrocephalus implies increased ventricular volume associated with accumulation of cerebrospinal fluid. Preexisting hydrocephalus was not excluded. It is unfortunate that this was not a clinicopathological study. The authors seemingly allude to acute hemocephalus, since ventricular enlargement in their patients with supratentorial intracerebral hemorrhage correlated with intraventricular hemorrhage and complementary evidence of raised intracranial pressure due to a localized space-occupying effect. The more vigorous the hemorrhage into the ventricles, irrespective of source, the more likely it is that blood clot will form and obstruct the ventricular system, particularly with compression and displacement of the brain parenchyma and rapidly rising intracranial pressure. The more severe the bleeding the greater the tamponade effect, sometimes even with tearing of the ventricular wall. However, acute hemocephalus, as a poor prognostic sign, is certainly not a novel finding in such patients. Intraventricular hemorrhage has long been recognized in pathology to be a terminal event accompanied by deep coma and high mortality as a consequence of the hemocephalus and tamponade effect.2 It is incorrect to regard the ventricular volumetic expansion as hydrocephalus.
The submission exemplifies a major problem in modern clinical medicine, whereby the importance of pathological detail in medical education and the relevance of autopsy confirmation have been significantly downgraded.
- Copyright © 1998 by American Heart Association
We thank Dr Stehbens for his thoughtful comments regarding our recent publication. In his letter he suggests that there were pathological misconceptions that might limit the interpretation of our study and points out that the term “hydrocephalus” implies ventricular enlargement with accumulation of CSF. We, however, applied a clinical definition that describes ventricular enlargement regardless of mechanism.
Preexisting hydrocephalus was not excluded in our study. While establishing the absence of preexisting hydrocephalus would have absolutely confirmed that our patients suffered from acute hydrocephalus, the natural history of intracerebral hemorrhage and the demands of the management of these patients make obtaining such information impossible and probably irrelevant.
In his letter, Dr Stehbens describes how intraventricular hemorrhage (hemocephalus) leads to the development of hydrocephalus and how acute hemocephalus is a well-known poor prognostic sign. The focus of our study, however, was hydrocephalus (clinically defined), not hemocephalus. This is an important distinction, since 25% of our patients with hydrocephalus did not have intraventricular hemorrhage. Finally, while we agree that there has been decreased emphasis on autopsy confirmation in medical education, the purpose of our study was to define prognosis rather than pathology.