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NEWS: Risk Factors for Post-Traumatic Hydrocephalus Following Decompressive Craniectomy

By Currents Editor posted 12-07-2018 08:38

  
Authors: Nasi D, Gladi M, Di Rienzo A, et al. Risk factors for post-traumatic hydrocephalus following decompressive craniectomy. Acta neurochirurgica. 2018 Sep 1;160(9):1691-8.

Reviewed by: Wazim Mohamed, MD, Assistant Professor of Neurology, Division of Neurotrauma and Critical Care Neurology, Wayne State University

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Methods

Post-traumatic hydrocephalus (PTH) occurs in up to a third of patients with traumatic brain injury (TBI) that undergo decompressive craniectomy (DC) and has been linked to unfavorable outcomes. This study analyzed the risk factors associated with PTH after decompressive craniectomy for TBI. Patients undergoing DC for TBI at a single center over eight years were included in the study. Indications for DC were based on Brain Trauma Foundation guidelines, 4th ed. PTH was defined as progressive ventricular dilation with a modified Frontal Horn Index ≥ 33 percent associated with narrowed CSF space at the convexity, third ventricular enlargement and periventricular lucencies on serial CT scans. Clinical deterioration was used in non-comatose patients to define symptomatic PTH. The primary end point of the study was the development of PTH after DC and the need for surgical intervention. A review of the literature was done to identify risk factors for the development of PTH, including timing of cranioplasty, and included in univariate and multivariate logistic regression analysis. Secondary outcomes included clinical status at six-month follow up with Glasgow outcome scale (GOS) 1-3 as unfavorable outcome and GOS 4 and 5 as favorable outcome.

Results

Out of 190 patients who underwent DC, 130 patients were alive at 30 days and 37 (19.5 percent) developed PTH. The median interval from DC to development of PTH requiring surgical treatment was 6.43 months (range one to 15 months). In 28 out of 37 patients (75.7 percent), PTH was diagnosed on the basis of clinical and radiologic determinants. In the remaining nine patients, the diagnosis was purely radiological due to the comatose or minimally conscious state of the patients. A ventriculoperitoneal shunt (VPS) was required in 34 of out 37 patients (91.9 percent) while in three patients, the PTH resolved after cranioplasty and temporary lumbar drain placement. On univariate analysis, patients requiring a VPS were significantly younger (<65 years; p<0.01), had subarachnoid hemorrhage on their CT scans (p=0.027) and underwent a bifrontal craniectomy rather than a unilateral decompression (p=0.03). An interhemispheric hygroma was present in 35.1 percent of patients with PTH compared to only 6.5 percent of patients that did not develop PTH (p<0.0001) and remained significant in the multivariate logistic regression analysis (p<0.001). Delayed reconstruction cranioplasty was strongly associated with the development of PTH; 92 percent of patients that developed PTH received a cranioplasty after three months (p<0.0001). On the multiple logistic regression model, delayed cranioplasty was significantly associated with the development of PTH (p<0.001). The baseline characteristics between patients who received an early versus delayed cranioplasty were similar. In the analysis of secondary outcomes, an unfavorable outcome was seen in 78.4 percent of patients with PTH compared to 40.8 percent of patients without PTH (p<0.0001).

Commentary

Delayed cranioplasty was associated with higher rates of PTH in patients with TBI that undergo DC. In addition, the presence of an interhemispheric hygroma was independently associated with the development of PTH. Previous DC trials for TBI have shown a mortality benefit at the cost of increased morbidity (severely disabled or vegetative states) among survivors. The increased morbidity may be due to the complications sustained secondary to DC, with a high proportion of these patients developing PTH. Mechanistically, the arachnoid granulations responsible for CSF resorption act as a one-way pressure dependent valve. The conversion of a closed cranial vault to an open box can cause a disruption in the pulsatile cerebrospinal fluid dynamics leading to PTH. This could explain the utility of cranioplasties in restoring intracranial pressure dynamics and resolution of PTH. Delayed cranial reconstruction could cause permanent dysfunction of the arachnoid granulations, by prolonging the injury, and lead to irreversible injury, even after cranioplasty. Previous studies have also demonstrated the association between interhemispheric hygromas and hydrocephalus. The authors believe that this may be an epiphenomenon due to alterations in the CSF dynamics secondary to damage of arachnoid–dura interface layer after TBI or secondary to the craniectomy site that is close to the midline. Although not clearly stated as a prospective study, the authors do state that an informed consent was obtained from all the patients, and the potential prospective nature of the study adds to its strength. There seemed to be a few print errors in the results section with the multiple logistic regression table containing odds ratios that were outside the confidence intervals. Among the limitations, the authors have mentioned that the association between PTH and poor outcome may be an indication of disease severity and not necessarily causal. Another limitation is that the results of cranioplasty on PTH could be partially affected by overall disease severity and health status between the two groups. Future studies targeting preventative strategies for the development of PTH in TBI patients undergoing DC may help decrease the morbidity among the survivors.

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