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Traumatic brain injury (TBI) is associated with high morbidity and mortality rates despite all recent advances in its diagnosis and management. One of the main complications of TBI patients is post-traumatic hydrocephalus (PTH). Hydrocephalus after brain injury is considered to be multi-factorial, the exact underlying pathophysiologic mechanisms remain unclear, and any risk factors related to its development have remained ill-defined. In our current narrative review, we overview the proposed pathophysiologic mechanisms for PTH, PTH following decompressive craniectomy, de novo post-cranioplasty PTH, and review the pertinent literature regarding any PTH predisposing factors. Advanced patient’s age in adults and the presence of any comorbidities, the severity of the initial brain injury, as well as the presence of subarachnoid and/or intraventricular hemorrhages, the necessity for prolonged mechanical ventilation and the need for vasopressors’ administration have all been identified as predisposing factors for PTH. Furthermore, the necessity for decompressive craniectomy (DC), its extent and its proximity to the anatomical midline, the presence of subdural hygroma and/or interhemispheric hygroma following DC, as well as the presence of transcalvarial herniation seem to play a role in post-DC PTH. Moreover, there is an equipoise regarding the association of restorative cranioplasty (CP) and PTH. Several studies report development of PTH after CP with varying rates, while others postulate that CP may improve a pre-existing PTH. The role of timing of CP in the development or the improvement of pre-existing PTH remains highly controversial. Thorough knowledge and proper identification of predisposing factors may lead to early recognition and optimal treatment of PTH, thereby improving the overall functional outcome of TBI patients. On the contrary, misdiagnosis or delayed diagnosis of PTH may lead to severe disability and/or death.
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Tarousa et al. (2026) studied this question.
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