Decompressive Cranioplasty (Osteoplastic Hinged Craniectomy): A Novel Technique for Increased Intracranial Pressure-Initial Experience and Outcome.

BACKGROUND: We redesigned decompressive craniectomy and cranioplasty procedures to decrease the inherent risk of complications. This novel technique, called decompressive cranioplasty, not only may decrease the complication rate but also may improve the cosmetic result, obviate the need for artificial skull implant, and increase the decompressive volume compared with traditional craniectomy. METHODS: In decompressive cranioplasty, the Agnes Fast craniotomy was adopted without cutting the temporalis muscle from the underlying bone flap. After opening the dura with or without removal of intracranial hematomas, duraplasty was performed with an intracranial pressure monitor inserted. Four miniplates were bent into a "Z" shape, and the vascularized bone flap was elevated approximately 1.2-1.5 cm above the outer cortex of the skull and fixed with the miniplates. Subsequent cranioplasty was done with a mini-incision on the miniplate sites and reshaping of the miniplate to align the outer cortex of the bone flap. RESULTS: We successfully performed decompressive cranioplasty in 3 emergent cases-2 traumatic subdural hematomas and 1 malignant middle cerebral artery infarction. Postoperative brain computed tomography demonstrated adequate decompression in all cases. Cosmetic outcome was excellent, and there was no temporal hallowing. Mastication function was not affected. At 6-month follow-up, there was no bone flap shrinkage and no hydrocephalus. CONCLUSIONS: Decompressive cranioplasty is a safe and effective method in the management of patients with brain edema and intracranial hypertension. It is simple to perform and may reduce the morbidity associated with traditional decompressive craniectomy and subsequent cranioplasty.

Direct visualization of microcirculation impairment after acute subdural hemorrhage in a novel animal model.

OBJECTIVE: Direct brain compression and secondary injury due to increased intracranial pressure are believed to be the pathognomic causes of a grave outcome in acute subdural hemorrhage (aSDH). However, ischemic damage from aSDH has received limited attention. The authors hypothesized that cerebral microcirculation is altered after aSDH. Direct visualization of microcirculation was conducted in a novel rat model. METHODS: A craniectomy was performed on each of the 18 experimental adult Wistar rats, followed by superfusion of autologous arterial blood onto the cortical surface. Changes in microcirculation were recorded by capillary videoscopy. Blood flow and the partial pressure of oxygen in the brain tissue (PbtO2) were measured at various depths from the cortex. The brain was then sectioned for pathological examination. The effects of aspirin pretreatment were also examined. RESULTS: Instantaneous vasospasm of small cortical arteries after aSDH was observed; thrombosis also developed 120 minutes after aSDH. Reductions in blood flow and PbtO2 were found at depths of 2-4 mm. Blood-brain barrier disruption and thrombi formation were confirmed using immunohistochemical staining, while aspirin pretreatment reduced thrombosis and the impairment of microcirculation. CONCLUSIONS: Microcirculation impairment was demonstrated in this aSDH model. Aspirin pretreatment prevented the diffuse thrombosis of cortical and subcortical vessels after aSDH.