Post-Operative Hydrocephalus in Patients Undergoing Emergent Hemicraniectomy for Elevated Intracranial Pressure (ICP): a retrospective case series of 40 patients

Elevated intracranial pressure (i.e. intracranial hypertension) is a potentially devastating sequela of neurologic injury, often complicating catastrophic brain injury such as deep intracerebral hematoma and hemispheric ischemic stroke. Despite initial compensatory mechanisms, elevated ICP directly leads to mechanical compression and distortion of brain tissue as well as hypoxic-ischemic injury. These changes result in transtentorial or tonsillar herniation with cranial nerve and respiratory dysfunction, coma, and if left unchecked, ultimately death. Regardless of proximate cause, ICH (intracranial hypertension) is a medical emergency which requires immediate attention. Following early establishment of invasive monitoring of ICP, non-invasive ICP reduction can be achieved medically through a combination of head elevation, hyperventilation, hypertonic therapy, propofol sedation with intubation, mannitol diuresis, and therapeutic hypothermia. Medical ICP reduction therapy for hemispheric ischemic stroke and deep cerebral hematoma may fail for several reasons. In a minority of cases, failure can be attributed to the fact that most medical therapies lose their efficacy with prolonged use. However, in the majority of cases, failure is simply a consequence of the inability of medical therapy to control the rapid (< 24 hours) increases in ICP seen in hemispheric ischemic stroke and deep intracerebral hematoma. Large hemispheric infarction has a particularly poor response to optimal medical management, with mortality estimated to be between 50 and 78%. At the point where the medical therapies noted above can no longer maintain ICP in acceptable ranges for a given patient, and surgical correction of the offending insult in not an option (predominantly hemispheric stroke, deep intracerebral hematoma, acute head trauma), attempts to increase the intracranial volume can be implemented. Usually employed as a ‘last-ditch’ effort to control refractory ICH, hemicraniectomy with durotomy is one such procedure designed to increase intracranial volume. Hemicraniectomy involves removal of the skull over approximately one-half of the head ipsilateral to the lesion, always to the level of the origin of the zygomatic arch/floor of the middle cranial fossa (to afford adequate decompression of the temporal lobe and middle cranial fossa) while avoiding the sigmoid and superior sagittal sinuses (to prevent the possibility of sinus thrombosis). Furthermore, care must be taken to perform a decompression large enough so as not to have the freely swelling brain trap and occlude surface blood vessels (particularly cortical draining veins) against the skull edge. The rationale of this procedure is to permit brain swelling into a durotomy ‘bag’, outside the confines of the usual boundary of the skull. Opening the skull vault and allowing the brain to freely ‘herniate’ outward can allow a reduction in ICP and prevent continuing brain damage by hypoxicischemic injury or mechanical distortion of brain tissue. The scalp is then sutured with minimal tension; this removes pressure from the edematous brain on the midline (e.g. brainstem) and contralateral structures. The bone is either kept frozen in antibiotic solution or stored under the patient’s own abdominal skin. To improve cosmetic defects and restore cerebral protection, the bone is replaced at the earliest appropriate time period, which is primarily dependent on the extent of resolution of the patient’s intracranial hypertension. Observational data suggest that rapid and sustained control of ICP via decompressive hemicraniectomy improves outcomes in trauma, hemispheric cerebral infarction, and subarachnoid hemorrhage in carefully selected cases. Decompressive craniectomy also appears to improve brain tissue oxygenation. A retrospective analysis evaluating the effects of decompressive hemicraniectomy for traumatic brain injury at one year found that 25% of patients at very high risk of brain death prior to