Gw. Roach et al., Ineffectiveness of burst suppression therapy in mitigating perioperative cerebrovascular dysfunction, ANESTHESIOL, 90(5), 1999, pp. 1255-1264
Citations number
47
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Background: Cerebral injury is among the most common and disabling complica
tions of open heart surgery, Attempts to provide neuroprotection have yield
ed conflicting results. We assessed the potential of propofol-induced burst
suppression during open heart surgery to provide cerebral protection as de
termined by postoperative neuropsychologic function.
Methods: Two hundred twenty-five patients undergoing valve surgery were ran
domized to receive either sufentanil or sufentanil plus propofol titrated t
o electroencephalographic burst suppression. Blinded investigators performe
d neurologic and neuropsychologic testing at baseline, postoperative day (P
OD) 1 (neurologic testing only), PODs 5-7, and PODs 50-70. Neuropsychologic
tests were compared with the results of 40 nonsurgical patients matched fo
r age and education.
Results: Electroencephalographic burst suppression was successfully achieve
d in all 109 propofol patients. However, these patients sustained at least
as many adverse neurologic outcomes as the 116 controls: POD 1, 40% versus
25%, P = 0.06; PODs 5-7, -18% versus 8%, P = 0.07; PODs 50-70, -6% versus 6
%, P = 0.80. No differences in the incidence of neuropsychologic deficits w
ere detected, with 91% of the propofol patients versus 92% of the control p
atients being impaired at PODs 5-7, decreasing to 52 and 47%, respectively,
by PODs 50-70, No significant differences in the severity of neuropsycholo
gic dysfunction, depression, or anxiety were noted.
Conclusions: Electroencephalographic burst suppression sur gery with propof
ol during cardiac valve replacement did not significantly reduce the incide
nce or severity of neurologic or neuropsychologic dysfunction, The authors'
results suggest that neither cerebral metabolic suppression nor reduction
in cerebral blood flow reliably provide neuroprotection during open heart s
urgery. Other therapeutic approaches must be evaluated to address this impo
rtant medical problem.