Ning Chou

A retrospective analysis and review of an institution's experience with the complications of cranioplasty

Abstract Introduction. Cranial reconstruction with a cranioplasty is performed to repair skull defects after decompressive craniectomies. Aims. To retrospectively review all cranioplasties performed in our institution over 10 years and analyse the complications and the factors that cause complications. Patient and methods. Two hundred and forty-three cranioplasties were performed from 2000 to 2010, with a follow-up of at least 1 year. Age, sex, comorbidities, material, site of skull defect, time between decompression and cranioplasty, and rate of complications were collected from our database. Fischers T-test and direct logistical regression were performed to identify factors that contributed to the rate of complications. p < 0.05 was considered significant. Results. Post-cranioplasty seizures (14.81%), infection and exposed implant (9.05%), haemorrhage (1.65%) and others (0.82%) were identified complications. Total percentage of complications was 25.92%. Previous trauma (p = 0.034) and intracranial haemorrhage (p = 0.019) as well as pre-cranioplasty neurological deficit (p = 0.046) were related to seizures, while pre-cranioplasty neurological deficit (p = 0.036) and exposed implant extrusion (p = 0.048) contributed to infection of cranioplasties. Discussion. Most of the seizures may be post-traumatic seizures or scar epilepsy from intracranial haemorrhage. Implant extrusions were found to be associated with infection of the implant, and they should therefore be treated early. Patient selection is important as patients with neurological deficits were susceptible to seizures and infection. Intracranial haemorrhage was caused by persistant bleeding, trauma or shunt overdrainge. Conclusion. Cranioplasty has significant complications. A thorough understanding of factors that contribute to the different types of complications will benefit the management of cranioplasty patients.

Mapping the incidence of focal tissue hypoxia after decompressive craniectomy

The ‘cut off’ for determination of focal cerebral tissue hypoxia is variously given as <20, <15 or <10 mmHg. Recent developments in micro-sensor technology using fluorimetric oxygen quenching methods is available. It is not yet clear whether hypoxia cut-off’s are comparable across different tissue oxygen measurement systems. The objective therefore, was to determine the temporal profile of brain tissue hypoxia in a cohort of patients requiring decompressive craniectomy or surgical management of severe traumatic brain injury (TBI).