Etomidate May Cause Cerebral Hypoxia
January 1, 1998 3 minutes read
Etomidate May Cause Cerebral Hypoxia
ABSTRACT & COMMENTARY
Synopsis: During cerebral vascular surgery, a dose of etomidate that produced burst suppression on EEG resulted in a fall in brain tissue PaO2 from 27 ± 4 to 19 ± 4 mmHg. Increased FIO2 restored baseline values in some patients, but placement of a temporary arterial occlusion clip resulted in hypoxia and acidosis in most patients.
Source: Edelman GJ, et al. Anesth Analg 1997;85(10): 821-825.
Etomidate is frequently used to provide brain protection during intubation or manipulation of patients with cerebral ischemia since it lowers ICP and maintains arterial pressure while inducing anesthesia. It can be used to suppress EEG activity and, since it is less of a myocardial depressant than other agents, it may favorably affect cerebral blood flow. Conflicting evidence from animal experiments led Edelman and colleagues to study the effects of etomidate on directly measured cerebral tissue blood gases in nine patients undergoing cerebral vascular procedures that would require temporary vascular occlusions.
After induction of general anesthesia with isoflurane and in the presence of mild hypothermia (35.6°C), a Paratrend 7 (a fiberoptic continuous blood gas sensor) catheter was inserted directly into a cortical gyrus within the distribution of the vessel to be occluded. After 30 minutes of equilibration, bolus doses of etomidate repeated every 1-2 minutes were administered until burst suppression on the EEG was obtained. Five minutes later, measurements of tissue gas tensions were recorded. FIO2 was increased to restore tissue PO2 to baseline, and the vascular clip was applied. Repeated measurements were recorded after the clip was applied.
Administration of etomidate resulted in a fall in tissue PO2 (27 to 19 mmHg) but no change in PCO2 (50 to 51 mmHg) or pH (7.14 to 7.15) prior to clip placement. Increasing the FIO2 restored tissue PO2 in most patients, but, in two patients, PO2 fell to below 10 mmHg after etomidate was given and did not return to baseline after FIO2 was increased. After an average of four minutes of ischemia, all patients developed further hypoxia (25 down to 17 mmHg), a rise in CO2 (53 to 65 mmHg), and acidosis (7.13 to 7.04). Four patients developed anoxia (PO2 = 0); however, all patients recovered without neurological injury.
By decreasing cerebral PO2, etomidate may not provide cerebral protection during ischemia. Use of the drug in patients at risk of cerebral ischemia should be reconsidered.
COMMENT BY CHARLES G. DURBIN, Jr., MD, FCCM
This paper presents provocative data regarding the use of etomidate in critically ill patients. The benefits of a stable blood pressure and the ability to suppress EEG activity have led to widespread support of this agent in head injured patients to cover the stimulus of intubation or other noxious procedures. A concern with etomidate is its suppression of endogenous steroid production. Prolonged use may suppress adrenal function to a point of developing Addison’s disease. This new concern of inducing cerebral hypoxia may justify reevaluating this agent’s place in neurological injury.
There are several problems with this study. The first is with the device used to measure tissue gas values. It is an intra-arterial continuous blood gas analyzer, which has not been evaluated for use to measure tissue gas concentrations. The sensor’s surface area is large compared to that of the capillary bed, and the meaning of the values obtained is not known. It is also a time-averaged measurement, and tissue blood flow changes may change more rapidly than the device is capable of tracking. The data from this study may fit our preconceived notion of what should happen, but the output from the device has not been validated in a controlled way.
These data would be more meaningful if some patients had received barbiturates for brain protection. It would be helpful to know if these drugs behaved differently with this model. It is possible that all drugs that produce electrical suppression decrease cerebral PO2 as measured in this study, and that this phenomenon may not be a specific effect of etomidate (or even deleterious). Extrapolation of the oxygen levels seen with this technique to imply a problem with tissue oxygenation related only to etomidate is unwarranted without further study, but, the results raise some concerns.
Etomidate may be inappropriate for use in patients with head injury because:
a. it decreases cerebral PO2.
b. it markedly lowers blood pressure.
c. it directly raises ICP.
d. it causes strange movements.
e. it depresses immune function.
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