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Abstract

Chatauret, N. et al., 2001. Mild hypothermia prevents cerebral edema and CSF lactate accumulation in acute liver failure. Metabolic Brain Disease, ABSTRACT Evidence from both clinical and experimental studies demonstrates that mild hypothermia prevents encephalopathy and brain edema in acute liver failure (ALF). As part of a series of studies to elucidate the mechanism(s) involved in this protective effect, groups of rats with ALF resulting from hepatic devascularization were maintained at either 37°C (normothermic) or 35°C (hypothermic), and neurological status was monitored in relation to cerebrospinal fluid (CSF) concentrations of ammonia and lactate. CSF was removed via implanted cisterna magna catheters. Mild hypothermia resulted in a delay in onset of encephalopathy and prevention of brain edema; CSF concentrations of ammonia and lactate were concomitantly decreased. Blood ammonia concentrations, on the other hand, were not affected by hypothermia in ALF rats. These findings suggest that brain edema and encephalopathy in ALF are the consequence of ammonia-induced impairment of brain energy metabolism and open the way for magnetic resonance spectroscopic monitoring of cerebral function in ALF. Mild hypothermia could be beneficial in the prevention of severe encephalopathy and brain edema in patients with ALF awaiting liver transplantation.

Better lactate clearance associated with good neurologic outcome in survivors who treated with therapeutic hypothermia after out-of-hospital cardiac arrest

“…However, previous studies showed that hypothermia was associated with increased cerebral lactate clearance [32] and also with reduced intracranial pressure and decreased brain edema [33]. The lactate level and its clearance might be affected by overproduction of lactate from skeletal muscle in PCAS patients with seizures or shivering.…”

Acute liver failure in adults

“…Умеренная гипотермия пациентов (32-34°С) может предотвращать или контролировать повышение ВЧД у па циентов с ОПН. Данные эффекты были доказаны в экспе риментальных моделях на животных [94,95], возможно, за счет предотвращения развития гиперемии, изменения метаболизма аммиака в головном мозге или глюкозы или комбинации этих механизмов. В то же время эффекты ги потермии у пациентов с ОПН не изучались в РКИ, од нако небольшой подтверждающий их клинический опыт существует [96].…”

Hemiballistisch-choreatiforme Bewegungsstörung durch eine nicht-ketotische Hyperglykämie

“…Die hepatische Enzephalopathie ist u. a. durch einen erhöhten serologischen Ammoniakspiegel charakterisiert. Ammoniak kann im Gehirn nur durch Astrozyten verstoffwechselt werden, da sie als einzige Zellen des ZNS mittels Glutaminsynthetase Ammoniak zu Glutamin verstoffwechseln können [8]. Durch eine Überproduktion osmotisch aktiven Glutamins schwellen die Astrozyten zu Gemistozyten an.…”