| JOURNAL HOME | CME HOME | THIS MONTH | PAST ISSUES | ETOC | COLLECTIONS |
| AUTHORS | REVIEWERS | EDITORIAL BOARD | FEEDBACK | RSS | HELP |
| ||||||||||||||
| ||||||||||||||
|
|
|
|
||||||||||||
|
||||||||||||||
Department of Anesthesiology, University of Alabama School of Medicine, Birmingham, AL Department of Anesthesiology, University of Texas Health Science Center,, San Antonio, TX
To the Editor:
We would like to congratulate Bruder et al. (1) for their cerebral blood flow velocity study indicating that the observed hyperemia during the recovery from neurosurgical anesthesia appears to be "independent of the anesthetic technique or hemodynamic or ventilatory changes" (1). They suggest that the causative factor may involve a stress response. Schubert, in the accompanying editorial, wisely cautions that other factors may also be involved including the return to normocapnia after prolonged hypocapnia, intraoperative and/or postoperative hypertension and defective autoregulation (2). We would like to mention another important factor, iatrogenic in nature, and touched upon briefly by Schubert, namely, brain retraction pressure (BRP).
While brain retraction may be needed to ensure good exposure in many neurosurgical procedures, the resulting sequelae of contusion followed by infarction certainly is not unusual. Andrews and Bringas (3) reported that the incidence of contusion or infarction from "overzealous brain retraction" was probably 10% in cranial based surgery and about 5% in intracranial aneurysms. Rosenorn described a 22% incidence of infarction located beneath the tip of the retractor blade as demonstrated by CT scans (4). With this troubling high incidence of sequelae following BRP, it appears that the subtle physiological consequences of BRP are not appreciated by the neurosurgeon in general because he or she does not measure the moment to moment changes in BRP during the course of the neurosurgical procedure.
We have noted (5) that in the normotensive animal (dog), the application of 20 mm Hg BRP to the temporal lobe produced an immediate increase in epidural intracranial pressure (ICP) of 10 mm Hg on the contralateral side as well as an increase in cisterna magna pressure to 14.5 mm Hg. A significant decrease in mean hemispheric blood flows occurred in both the retracted and contralateral hemispheres under normotensive and hypotensive conditions. This indicates that retraction forces are transmitted throughout the brain and can also affect the distribution of regional blood flow. The relationship of somatosensory evoked potential (SEP) to cortical blood flow indicated that a 50% or greater decrease in the SEP correlated with a marked diminution of rCBF and the development of a focal ischemic lesion (5,6). The problem of BRP can be markedly enhanced because of the excessive mechanical shear stresses that can be generated by the edge pressures of the retractor blade. A further hazard can occur when constant fixed retraction is applied to brain. Initially, "creep" occurs as the brain bulk adjusts by moving away from the retractor into the adjacent area (7). After the period of adjustment, BRP and contralateral ICP may even increase as brain mass moves against the retractor. This is a possible explanation of the appearance of intracerebral hemorrhage or ischemia distant from the retracted area after retractor release. The cerebrovascular dynamic changes under induced or iatrogenic hypotension under a BRP 
20.0 mm Hg can involve ischemia and infarction. In a patient study involving 50 patients, the BRP often exceeded 25 mm Hg for times ranging from 30 to 120 min (8). These data seem to indicate that BRP may be a major contributing factor to the cerebral hyperemia found by Bruder et al. postoperatively. It would be important to evaluate the factors noted by Dr. Schubert in further controlled studies where BRP is monitored throughout the neurosurgical procedure. Perhaps we have identified another "smoking gun"!
References
Département d’Anesthésie-Réanimation, CHU Timone, Bd J Moulin, Marseille, France
In Response:
We appreciate the interest and the comments of Drs. Albin and Bunegin on the mechanisms of postoperative cerebral hyperemia. We agree that brain retraction pressure (BRP) and cerebral ischemia may contribute to cerebral hyperemia. Transient cerebral hyperemia has been described after subdural hematoma surgery. This may be related to the compression of the brain by the hematoma, a mechanism similar to BRP (1,2). Hypoperfusion of the brain, due to carotid artery stenosis for example, may be complicated by severe hyperemia and cerebral hemorrhage after the revascularization (3–5). Thus, cerebral ischemia probably explains most cases of severe postoperative hyperperfusion published in the neurosurgical setting. However, our neurosurgeons almost never use retractors in brain tumor surgery and try to limit its use as much as possible in aneurysm surgery. Although we did not record the use of retractors in this study, they were probably not used in most patients. Since this study, we have measured cerebral blood flow velocities (CBFV) during emergence in many neurosurgical patients. Occasionally, we have found very large CBFV increase (>100 % over baseline). It is possible that intraoperative factors, as the one described by Drs. Albin and Bunegin, may amplify postoperative hyperemia. It is probably the sum of several factors contributing to cerebral hyperemia that may lead to clinical complications as cerebral hemorrhage or edema.
References
Department of General Anesthesiology, The Cleveland Clinic Foundation, Cleveland, OH
In Response:
Albin and Bunegin call attention to an interesting, yet poorly appreciated mechanism of brain injury during elective intracranial surgery, namely excessive brain retraction pressure (BRP). They convincingly argue that the injury may be quite common and that it may affect not only the locally retracted brain region but also remote cerebral tissue.
Although the notion that BRP may contribute to the early cerebral hyperemia observed by Bruder et al. (1) is worthy of serious consideration, it also evokes several questions. First, if BRP is responsible for postcraniotomy emergence hyperemia, why was the hyperemic response observed in both tumor and aneurysm surgery, when the latter presumably associates with BRP injury more frequently than the former because relatively more retraction is required in operations where little brain tissue is removed? The mechanism by which BRP would produce hyperemia is not addressed by Albin & Bunegin. Depending on the extent of ischemia, a transient luxury reperfusion phase is said to occur after ischemia brain injury (2). Yet postischemic hyperemia is frequently not observed after focal ischemia (3). Thus, BRP-related ischemia and injury might be expected to result in regions of coexisting adequate and low flow brain regions, (4) not unlikely the situation seen in closed head injury, but unlike the fairly uniform hyperemia observed by Bruder et al. If BRP is similar to traumatic cerebral contusion in its cerebral hemodynamic signature, hyperemia would not be expected, even as early as 4 hours after injury (5).
The suggestion that BRP may represent another "smoking gun" in postcraniotomy hyperemia is intriguing; but to clear the smoke, the fresh winds of further mechanistic investigation need to blow even harder.
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
