Cerebral hemodynamic and metabolic changes in fulminant hepatic failure: A retrospective study

Abstract

The purpose of this retrospective study was to determine cerebral hemodynamic and metabolic changes in comatose patients with fulminant hepatic failure. Computerized tomography of the brain and cerebral blood flow measurements by the xenon-computerized tomography scan or intravenous xenon-133 methods were obtained in 33 patients with fulminant hepatic failure. In a subgroup of 22 patients, arteriojugular venous oxygen content difference and cerebral metabolic rate for oxygen were determined. Carbon dioxide reactivity was tested in 17 patients, and intracranial pressure was recorded by an epidural monitor in 8 patients. Cerebral blood flow and arteriojugular venous oxygen content difference were adjusted to the average arterial carbon dioxide pressure of the sample (32 mm Hg). Adjusted cerebral blood flow varied from 16.5 to 94.7 ml/100 gm/min; 52% of the patients had reduced adjusted cerebral blood flows (less than 33 ml/100 gm/min), whereas 24% had hyperemic values (greater than 50 ml/100 gm/min). Patients with higher adjusted cerebral blood flows showed cerebral swelling on computerized tomography scan (p < 0.002), were in deeper coma (p < 0.05) and had greater mortality (p < 0.002). The adjusted arteriojugular venous oxygen content difference was negatively correlated with adjusted cerebral blood flow (r = -0.61, p < 0.002). The majority of patients with reduced adjusted cerebral blood flows had low adjusted arteriojugular venous oxygen content differences (less than 5 vol%), indicating hyperemia rather than ischemia. The average cerebral metabolic rate for oxygen was 50% of normal (1.6 +/- 0.4 ml/100 gm/min); even patients with low cerebral metabolic rates for oxygen recovered neurologically.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenesis of Hepatic Encephalopathy: Role of Ammonia and Systemic Inflammation

“…It has been shown that increasing inflammation has a direct correlation with increasing CBF 64 which in turn is known to raise intracranial pressure. 65 This has been further demonstrated by studies which have examined therapeutic strategies that reduce systemic inflammation and cerebral hyperemia.…”

Transcranial Doppler is valid for determination of the lower limit of cerebral blood flow autoregulation.

“…2 Traditionally, cerebral perfusion in critically ill patients has been indirectly evaluated by measure of cerebral perfusion pressure (MAP minus intracranial pressure) or by internal jugular venous oxygen content, where a constant cerebral oxygen consumption is assumed. 3 Obviously, these invasive measures do not provide sufficient insight in cerebrovascular hemodynamics. Repeated measurements every day of CBF by, for example, I33 Xe technique is a cumbersome and a measured in the right middle cerebral artery by a 2-MHz probe, and blood samples were drawn at intervals of 5 mm Hg.…”

Keeping cool in acute liver failure: Rationale for the use of mild hypothermia

“…Loss of cerebrovascular autoregulation and development of cerebral hyperemia, described in patients with advanced ALF [111], [112], [113], [114] and [115], are relevant to the pathogenesis of brain edema and intracranial hypertension [116]. Loss of cerebrovascular autoregulation may cause luxury perfusion or hypoxia during increases or decreases of systemic arterial pressure, respectively.…”

“…Loss of cerebrovascular autoregulation may cause luxury perfusion or hypoxia during increases or decreases of systemic arterial pressure, respectively. Cerebral hyperemia is associated with brain edema and mortality in ALF [113] and [117]. The mechanisms by which cerebral hyperemia enhances brain edema and ICP in ALF have been reviewed by Larsen and Wendon [116].…”