Cerebral blood flow, vasoreactivity, and oxygen consumption during barbiturate therapy in severe traumatic brain lesions

Abstract

Mean hemispheric cerebral blood flow (CBF) and intracranial pressure (ICP) were measured in 19 severely head-injured patients treated with barbiturate coma. The CBF was calculated from the clearance of tracer substance monitored by extracranial scintillation detectors after intravenous administration of xenon-133. In 11 of the patients cerebral arteriovenous oxygen differences were measured simultaneously. In all patients the effects of pronounced hyperventilation were recorded prior to initiation of barbiturate treatment. A normal CBF response to hyperventilation (delta CBF/delta PaCO2 greater than or equal to 1) was obtained in eight patients. In these patients induction of barbiturate coma was accompanied by physiological decreases in CBF and in the calculated cerebral metabolic rate of oxygen (CMRO2); they also exhibited a rapid and lasting decrease in ICP. A decreased or an abolished CO2 reactivity was recorded (delta CBF/delta PaCO2 less than 1) in 11 patients. In 10 of these 11 patients the physiological decreases in CBF and CMRO2 were not obtained during barbiturate treatment and the decrease in ICP was transitory. This study demonstrates a correlation between cerebral vasoreactivity, physiological effects of barbiturate therapy, and clinical outcome.

Therapeutic hypothermia for severe adult Herpes simplex virus encephalitis

“…It has been proven that in patients with brain edema and reduced carbon dioxide reactivity (CO 2 R) the usual treatment options such as administration of hyperosmolar solutions, hyperventilation, barbiturate induced coma and steroids are of humble efficacy or completely useless [2]. Furthermore, in traumatic brain injury and central nervous system infections reduction in CO 2 R was a single most accurate predictor variable for poor outcome [2,3].…”

The Lund concept: is this logical?

“…CH Nordström 5 A lasting vasoconstriction and reduction of CBV can be achieved through reduction of cerebral energy metabolism e.g. by barbiturates (15). This mechanism appears to be effective only in patients with preserved cerebrovascular CO 2 -reactivity (15).…”

“…by barbiturates (15). This mechanism appears to be effective only in patients with preserved cerebrovascular CO 2 -reactivity (15). In addition, prolonged high-dose barbiturate treatment is associated with pulmonary, cardiovascular and other serious complications (22).…”

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“…[4,[36][37][38]43] Similarly, therapeutic manipulations that decrease or increase CBF are associated with an increase and decrease in AVDO 2 , respectively. [35,43] The initial pretreatment AVDO 2 value, therefore, indicates that the brain is compensating for reduced flow by extracting more oxygen. Where sufficient aerobic reserve existed, the AVDO 2 improved after treatment, but in those patients with an exhausted reserve, no improvement in AVDO 2 was observed and delayed infarction occurred.…”

“…[14,46] Despite these limitations, jugular saturation monitoring can help guide therapy, optimize CPP, and measure the effects of therapeutic interventions, such as ventilation or mannitol administration, to ensure adequate CBF to meet metabolic demands. [8,10,11,35,49] Jugular saturation monitors may also detect transient episodes of cerebral hypoxia from potentially preventable systemic causes such as hypotension, hypoxia, fever, or seizures. [11,18,40] The identification of inadequate cerebral oxygenation is important in the management of cases of head injury.…”