We thank De Bonis et al for their interest in our article.1 In our series of 17 patients who underwent decompressive hemicraniectomy (DH) for cerebrovascular accident-related, medically refractory increased intracranial pressure, a full standard hemicraniectomy was performed in 13 patients, whereas only 4 received large craniectomy flaps. Clinically significant hydrocephalus necessitating cerebrospinal fluid (CSF) diversion developed in none of the 14 survivors. Unfortunately, we are unable to provide the authors with the information that they request because exact measurements of the hemicraniectomy flaps, particularly the distance between their medial edge and the superior sagittal sinus, were difficult to determine in our retrospective study. However, it has been our standard practice to perform wide bony decompressions extending from the floor of the middle fossa laterally to within 1 to 2 cm of the sagittal suture medially and from the floor of the anterior fossa anteriorly to approximately 5 to 6 cm behind the pinna posteriorly.2 Therefore, we would expect that the vast majority of patients in our series had hemicraniectomy flaps extending to within 2.5 cm of the superior sagittal sinus. When analyzing the incidence of hydrocephalus after DH, it is important to distinguish between complications of the underlying cerebral insult and those resulting from the surgical procedure itself. This is particularly true in patients with head trauma and those with subarachnoid and/or intraventricular hemorrhage who are naturally prone to the development of hydrocephalus, regardless of whether DH is performed. For this reason, we have strived to eliminate these major confounding factors and exclude such patients from our analysis. We read the authors' recent article on posttraumatic hydrocephalus after decompressive craniectomy in patients with traumatic brain injury.3 Although we find the authors' hypothesis interesting in general, there are nonetheless several issues that merit discussion. Their patient cohort was particularly small, with only 26 survivors included in the final analysis. Such a small sample size is unlikely to have a high enough statistical power to allow firm conclusions regarding prognostic factors, particularly when a 6-variable multivariate analysis is performed. Moreover, numerical variables were not analyzed as such and instead were dichotomized using arbitrary cutoff values (30 d for cranioplasty, 40 yr for age, 162 cm2 for cranioplasty, and 25 mm for distance from midline). This raises significant concerns about the validity of their statistical analysis. Clinical examination was not included in the definition of hydrocephalus for many comatose patients, which may have significantly affected their results. In our series, in 2 patients, asymptomatic extra-axial CSF collections developed after DH, which resolved spontaneously after cranioplasty. We believe that such collections are the result of increased intracranial compliance after the removal of a large piece of cranium rather than an actual mismatch between CSF production and absorption.1 Most importantly, the presence of a statistically significant association between a DH extending close to midline and hydrocephalus is in no way proof of a causal relationship, particularly in severely head-injured patients. It is noteworthy that all but 2 of their patients had evidence of subarachnoid and/or intraventricular blood on computed tomography (Fisher grade 2). A major confounding factor was thus present in the absolute majority of patients, which makes it difficult to attribute the development of hydrocephalus to the surgical procedure itself. Is it possible that patients who underwent DH closer to the midline had more severe structural damage to the cerebral hemisphere on CT, which may account for their increased rate of posttraumatic hydrocephalus? This is definitely a possibility in the setting of a retrospective study that may be subject to all kinds of inherent biases. In conclusion, to establish a cause-and-effect relationship between DH and hydrocephalus, one has to study the incidence of the latter in patients undergoing DH for conditions not known to be associated with hydrocephalus (eg, ischemic stroke). Alternatively, a randomized, controlled trial comparing the incidence of hydrocephalus in severe traumatic brain injury survivors who underwent DH and those who did not may provide the answer. Until then, we have no reason to believe that DH is a risk factor for hydrocephalus, independently of the patient's underlying cerebral insult. Michel Bojanowski Ralph Rahme Montreal, Quebec
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