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Excerpt
Cerebral hemorrhage is a form of acute stroke that is particularly resistant to effective therapy. Intracranial bleeding is usually a dramatic acute event that is easily recognized by the patient and any nearby observer. Classification of intracranial hemorrhages includes: a) the extra-axial epidural and subdural hematomas; b) subarachnoid hemorrhage predominantly from ruptured berry aneurysms; c) arteriovenous malformations; and d) parenchymal intracerebral hematomas (ICH). This last group has a broad set of etiologies, the most frequent of which is primary hypertensive hemorrhage. While surgical and intensive care therapies are clearly indicated and commonly perceived to be effective for extra-axial hematomas, arteriovenous malformations and ruptured berry aneurysms, the precise role of surgical intervention and intensive care medicine is less clear for ICH.
For the last three decades, the role of surgical clot removal of ICH has not been clear [1]. Recent controlled studies have been limited and do not convincingly argue for a surgical therapeutic imperative [2,3,4]. Supportive therapies for ICH in the intensive care unit have been developed from general principles of neurosurgical care, particularly the care of the acute subarachnoid hemorrhage patient. Unfortunately, the effectiveness of these elements of care has not been specifically evaluated. Despite high-quality intensive care, the morbidity and mortality for ICH remain unacceptably high [5].
Observational epidemiologic studies have defined the morbidity and mortality for hypertensive intracerebral hemorrhage [6-8]. It is not uncommon to see a 30% to 50% mortality rate for a large group of primary brain hemorrhages. These prospective studies have consistently demonstrated that at least three patient factors (e.g., Glasgow Coma Scale score, volume of hemorrhage, and intraventricular extension) identified at the initial clinical presentation appear to relate directly to severity of illness. This issue of Critical Care Medicine presents important new work in this area. Dr. Tuhrim and colleagues have prospectively evaluated patients with ICH and demonstrated that the presence of intraventricular hemorrhage (IVH) relates directly to mortality [9]. Remarkably, this relationship holds over a wide range of IVH sizes. Furthermore, this relationship appears to be independent of initial parenchymal hematoma size or Glasgow Coma Scale score at time of presentation. Previous work has defined the volume of ICH as a continuous variable that proportionately increases its effect on mortality as the hematoma size increases [7]. The findings in this series of patients from Mt. Sinai Medical Center demonstrate the same effect of IVH size on probability of 30-day mortality. Thus, as IVH increases in size from 10 to 40 cc, the likelihood of mortality increases substantially. Taken together, these data demonstrate the direct influence of total hematoma size (ICH and IVH) on mortality. This "dose-injury" relationship suggests strongly that a safe and effective method for removing blood clots should have substantial potential to alter mortality and perhaps morbidity.
In the worlds of clinical medicine and experimental brain injury, there is rarely biological evidence stronger than a dose-effect curve that demonstrates a continuous relationship between an injury factor and an outcome event. The biological argument for removal of all or part of an intracerebral or intraventricular hematoma could not be more compelling. The ingredients for a successful therapeutic intervention are now well defined and readily available in the clinical domain.
