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Original Article

Occurrence of Adenylate Kinase in Cerebrospinal Fluid after Isoflurane Anaesthesia and Orthognathic Surgery

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Pages 97-112 | Published online: 18 Jan 2010
 

Abstract

The study objective was, firstly, to investigate whether anaesthesia with induced arterial hypotension would cause leakage of a biochemical marker of neuronal injury, adenylate kinase (AK), into the cerebrospinal fluid (CSF). (Definition: arterial hypotension = mean arterial pressure (MAP) 50–65 mmHg during ≥ 10 rnin). Secondly, a subgroup of patients was examined with a limited battery of psychometric tests.

Patients, scheduled for orthognathic surgery, were allocated to either hypotension (n=20) or normotension (n=20). Seventeen patients were subjected to psychometry.

Arterial blood pressure was recorded continuously and controlled by adjustments of the administered concentration of the inhalational anaesthetic isoflurane. Fentanyl, an opioid, was given equally in both groups. A lumbar puncture was performed approximately 20 h post-operatively for a CSF sample, later analysed for AK activity. Neuropsychological tests were performed the day before surgery and the fourteenth day postoperatively.

The CSF-AK value was pathologically increased (>0.040 U/L) in 24 patients (65%), of whom 9 were normotensive. There was no significant difference between the CSF-AK values in the hypotensive and normotensive groups, mean values were 0.082 (s.d. 0.051) and 0.066 (s.d. 0.059) U/L, respectively. The overall correlation between the 10 rnin MAP levels and the CSF-AK values was close to zero. In the pilot neuropsychological investigation some abnormalities were observed, indicating clinically significant adverse effects in four hypotensive patients, of whom two displayed pathologically increased CSF-AK values. At the group level, the correlation between the changes in psychometry and the measured CSF-AK values was poor.

Increases in CSF-AK activities may be a non-specific occurrence in the perioperative interval, possibly indicating an adverse effect on the brain. Arterial hypotension could not be proven to explain the CSF-AK outcome.

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