Massive Brain Swelling After Cranioplasty: Could Anesthesia Play a Role?

Author Type(s)

Faculty

Document Type

Abstract

Publication Date

2022

DOI

10.1097/ANA.0000000000000863

Journal Title

Journal of Neurosurgical Anesthesiology

Department

Anesthesiology

Abstract

Cranioplasty following decompressive craniectomy is a step towards recovery. 1 Although considered a low-risk surgery, complications occur in up to 40% of cases, including infection, graft resorption, and hematoma. 2, 3 Occurring in up to 2.4% of cases, massive brain swelling after cranioplasty (MBSC) is among the most catastrophic complications, resulting in death or permanent disability.3 While the etiology of MBSC remains unknown, preoperative sinking skin flap syndrome, use of negative pressure drains, and autoregulatory dysfunction may play a role.2, 3 Limited studies and case reports on MBSC focus on patient and surgical risk factors - there are currently no studies examining the role of anesthesia on MBSC. With the goal of improving safety for patients undergoing anesthesia for cranioplasties, we reviewed the anesthetic records of four patients who developed MBSC at our institution to determine if elements of anesthetic care may have an impact on the development or prevention of this complication. A review of complications following cranioplasties found four patients who had developed massive cerebral edema following cranioplasty (Table 1). The patients ranged in age from 25-58, three initially presented with traumatic brain injuries (TBI) and one with a stroke, and all had decompressive hemicraniectomies (DHC). Three patients had cranioplasty within 3 months of DHC, the fourth patient was 3 years out and undergoing his third cranioplasty after a recurrent infection had necessitated prior reversals. All four patients underwent general anesthesia using sevoflurane, three received synthetic grafts, one autologous, and sub-galeal drains were placed in each case. IV fluid administration, estimated blood loss, and urine output were within routine values. Two patients received intraoperative mannitol. Three patients had midline shift prior to cranioplasty (the fourth patient did not have recent imaging). One patient had confirmed sinking skin flap syndrome and a second likely had it based on imaging. Among the anesthetic variables reviewed, we were interested in those that impact cerebral blood flow, particularly in the setting of impaired autoregulation, including blood pressure trends and ETCO2 levels. Three patients required antihypertensive medications. Two patients became acutely hypertensive following emergence, both of whom were immediately given opioids and antihypertensives. The onset of hypertension coincided with other signs of increased intracranial pressure (ICP), including fixed dilated pupils and a seizure suggesting an etiology for hypertension. The third patient was both hypertensive and hypercapnic during emergence and was given metoprolol with resolution of high blood pressure. He was transported to PACU, although sleepy, he received no additional intervention. Shortly thereafter, he was found to be hypertensive and bradycardic, likely from increased ICP from cerebral edema. In the other cases, ETCO2 levels were within normal limits. A review of these four cases suggests areas where anesthetic management may either mitigate risk of MBSC or indicate impending MBSC. Severe cerebral injury secondary to TBI or anoxic insult disrupts normal autoregulation, rendering patients vulnerable to injury from hyper- and hypotension, hypercapnia, and fluid shifts. While cranioplasties are performed once patients have recovered from the acute phase of their injury, this does not guarantee return of normal autoregulation. From an anesthetic standpoint, tight control of blood pressure, arterial or ETCO2, and intrathoracic pressures may help decrease the risk of MBSC. In patients with known autoregulatory dysfunction, avoidance of high volatile concentrations may also be considered. Caution should be taken to avoid large fluid shifts with crystalloids, hypertonic saline, mannitol, or albumin. Providers should remain vigilant for acute hypertension, which necessitates an immediate physical exam to look for signs of increased ICP. Patients with sunken flap syndrome or those in whom a negative pressure drain was plac d should be considered at higher risk for MBSC (Fig. 1). (Figure Presented).

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