Induced arterial hypotension for interventional thoracic aortic stent-graft placement: impact on intracranial haemodynamics and cognitive function.
OBJECTIVE
The study investigated the impact of induced arterial hypotension for the facilitation of endovascular stent-graft placement in patients with thoracic aortic aneurysm on cerebral blood flow velocity and neurological/neurocognitive outcome.


METHODS
In 27 ASA III patients, cerebral blood flow velocity was recorded during induced arterial hypotension for endovascular stent-graft placement using transcranial Doppler sonography and the Folstein Mini Mental State Examination and the National Institute of Health Stroke Scale were performed before and after the intervention.


RESULTS
Mean arterial pressure was decreased <50 mmHg, and in 22 patients it was <40 mmHg. Diastolic cerebral blood flow velocity decreased by 59%. Postoperatively, six of 21 patients exhibited changes in the Folstein Mini Mental State Examination and four of these six patients in the National Institute of Health Stroke Scale as indices of new-found neurocognitive dysfunction, but there were no signs of stroke. Loss of the diastolic blood flow profile was detected in two of six patients with new-found neurocognitive dysfunctions and in 18 of 21 patients with no new-found neurocognitive dysfunction. Changes in the Folstein Mini Mental State Examination on postoperative day 1 were correlated to the pre-procedural Folstein Mini Mental State Examination, but not to the time spent with a mean arterial pressure <50 mmHg, <40 mmHg or with a loss of diastolic blood flow profile.


CONCLUSIONS
Transcranial Doppler sonography visualizes the individual effect of induced hypotension and the period of intracranial circulatory arrest during aortic stent-graft placement. However, transient new-found neurocognitive dysfunctions occur independently of the transcranial Doppler data, and are in close correlation to the neurocognitive state before the procedure. The results suggest that induced arterial hypotension is not the major factor for postoperative new-found neurocognitive dysfunction.
von Knobelsdorff
G
G
University Hospital Hamburg-Eppendorf, Department of Anaesthesiology, Hamburg, Germany. pd.dr.g.von.knobelsdorff@bernward-khs.de
Höppner
R M
RM
Tonner
P H
PH
Paris
A
A
Nienaber
C A
CA
Scholz
J
J
Schulte am Esch
J
J
D001013:Aorta, Thoracic / Q000601:surgery; D002560:Cerebrovascular Circulation / Q000502:physiology*; D003071:Cognition / Q000502:physiology*; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007022:Hypotension / Q000139:chemically induced*; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests; D015607:Stents; D017585:Ultrasonography, Doppler, Transcranial