Autologous cranioplasty following decompressive craniectomy in the trauma setting.

BACKGROUND: Decompressive craniectomy (DC) is an option for the treatment of increased intracranial pressure resulting from an acute neurological insult, including insults caused by trauma. When the brain swelling has receded, the skull is reconstructed with a wide choice of materials, each with its own advantages and disadvantages in terms of cost, cosmetic appearance, biocompatibility, implant strength and complication rate. Autologous cranioplasty (AC), where the patient's own bone flap is stored and reutilised, is common in many countries. No outcome studies have, however, been published on this technique for traumatic injuries. METHODS: A retrospective study was conducted including all AC operations performed following DC due to traumatic brain injury. All operations were performed in one institution during a 4-year time period. Results were analysed for complication rates. RESULTS: 44 cases were included. The mean time from craniotomy to cranioplasty was 86 (95% CI: 63-109) days. Complications severe enough to warrant readmission or further surgery were found in 13 cases (30%). No statistically significant predictor of complication from cranioplasty was detected. The complication rate was similar to published data on cranioplasty using artificial prosthetic materials. CONCLUSIONS: AC in the trauma setting is a valid treatment option with a complication rate that seems no worse than other alternatives.

Post-traumatic head injury pituitary dysfunction.

Partial or complete pituitary dysfunction affects 33-50% of all traumatic brain injury (TBI) survivors and is a significant contributor to the overall disability burden. The hypophyseal vessels are anatomically vulnerable to shearing injuries, raised intracranial pressure and anterior base of skull fractures, and pituitary ischaemia or haemorrhage is a common finding at autopsy. Post-traumatic hypopituitarism (PTHP) can affect all grades of severity of injury and is often difficult to diagnose, as its features largely overlap with common post-concussive symptoms. PTHP has a wide range of manifestations, including fatigue, myopathy, cognitive difficulties, depression, behavioural changes or life-threatening complications such as sodium dysregulation and adrenal crisis. In some instances, mild PTHP can recover, at least partially, but cases of late onset are also known. At present, there is no consensus on whether all TBI patients should be screened (including mild TBI) and at what time points, given that neuroendocrine tests in the acute phase are simply likely to reflect a non-specific trauma response rather than true pituitary damage and that the time course of PTHP is unclear. A full investigation of the hypothalamic-pituitary axis requires specialized neuroendocrine assessment, including stimulation tests, as random hormone levels can be misleading in this context. Given the high incidence of TBI, this may have significant resource implications for Endocrinology services but, on the other hand, patients with PTHP may receive suboptimal rehabilitation unless the underlying hormone deficiency is identified and treated.