Cerebral edema and intracranial pressure monitoring

Abstract

With the wide acceptance of liver transplantation as a therapeutic alternative in fulminant hepatic failure (FHF), the successful management of patients with this syndrome has acquired a new urgency. Topping the list of medical problems is the development of brain swelling. Two decades after the recognition of its importance,1 brain edema and intracranial hypertension still constitute a major cause of death in these patients. In a more recent classification of FHF, brain edema was especially prominent in those subjects with “hyperacute failure,”2 in whom a period of 7 days or less elapsed between the development of jaundice and encephalopathy. The goal of this review is to discuss two aspects of this clinical problem. On one hand, elucidation of its pathogenesis should lead to a more rational therapeutic approach; such an information would also be valuable to understand the relationship between hepatic encephalopathy and brain edema, a source of controversy. Studies of pathogenic mechanisms are difficult to perform in humans and animal models of FHF have proven valuable, as brain swelling can be detected with some regularity.3 On the other hand, an increasing array of techniques is now available in the intensive care setting to monitor patients with FHF. Of these, intracranial pressure monitoring has received the most critical attention. However, concerns with the risks of craniotomy and the need to acquire more dynamic information has led several groups to explore non‐invasive methods that evaluate the consequences of intracranial hypertension. Their role, though potentially exciting, is still uncertain. Copyright © 1995 by the American Association for the Study of Liver Diseases.

Transparent nanocrystalline yttria-stabilized-zirconia calvarium prosthesis

“…For example, opportunity may arise for chronic monitoring of cerebral edema, which is largely precluded by the invasiveness of current techniques. 18 Similarly, it may enable chronic monitoring and more precise targeting of photodynamic therapies for residual gliomas, 19 which could prolong survival and improve quality of life for many suffering from brain cancer. Finally, it could provide a platform for development of new optical neuromodulation modalities, with potential applications ranging from fundamental neurophysiology studies to clinical psychiatry.…”

Selective increase of brain lactate synthesis in experimental acute liver failure: Results of a [1H-13C] nuclear magnetic resonance study

“…39 Brain edema and the resulting increased intracranial pressure constitute a major cause of death in patients with ALF. 40,41 The cause of the decreased TCA cycle flux and subsequently increased lactate production in brain in ALF is unknown. However, brain ammonia increases to millimolar levels in experimental ALF, 2,3 and comparable concentrations of ammonia cause inhibition of ␣-ketoglutarate dehydrogenase, 7 a rate-limiting TCA cycle enzyme.…”

Recombinant activated factor VII for coagulopathy in fulminant hepatic failure compared with conventional therapy

“…2 Although precise guidelines for safe coagulation parameters in patients with FHF for the performance of invasive procedures do not exist, the presence of coagulopathy is widely believed to increase the risk for procedurerelated bleeding. Common invasive procedures in this setting include placement of catheters for dialysis or ultrafiltration or placement of intracranial pressure (ICP) monitors that, although still controversial, 3 are considered valuable tools in many centers.…”