Post-Traumatic Hydrocephalus after Decompressive Craniectomy: An Underestimated Risk Factor

Abstract

The incidence of post-traumatic hydrocephalus (PTH) has been reported to be 0.7-51.4%, and we have frequently observed the development of PTH in patients undergoing decompressive craniectomy (DC). For this reason we performed a retrospective review of a consecutive series of patients undergoing DC after traumatic brain injury (TBI). From January 2006 to December 2009, 41 patients underwent DC after closed head injury. Study outcomes focused specifically on the development of hydrocephalus after DC. Variables described by other authors to be associated with PTH were studied, including advanced age, the timing of cranioplasty, higher score on the Fisher grading system, low post-resuscitation Glasgow Coma Scale (GCS) score, and cerebrospinal fluid (CSF) infection. We also analyzed the influence of the area of craniotomy and the distance of craniotomy from the midline. Logistic regression was used with hydrocephalus as the primary outcome measure. Of the nine patients who developed hydrocephalus, eight patients (89%) had undergone craniotomy with the superior limit <25 mm from the midline. This association was statistically significant (p = 0.01 - Fisher's exact test). Logistic regression analysis showed that the only factor independently associated with the development of hydrocephalus was the distance from the midline. Patients with craniotomy whose superior limit was <25 mm from the midline had a markedly increased risk of developing hydrocephalus (OR = 17). Craniectomy with a superior limit too close to the midline can predispose patients undergoing DC to the development of hydrocephalus. We therefore suggest performing wide DCs with the superior limit >25 mm from the midline.

The influence of decompressive craniectomy on the development of hydrocephalus: a review

“…Injury severity is another impact factor for hydrocephalus. In a multivariate analysis, Honeybul et al found that maximum ICP prior to decompression (p=0.012) and admission Glasgow Coma Score (GCS) (p=0.009), which are indicators of injury severity, are significant independent risk factors for development of hydrocephalus after DC, but they found no relationship between the craniectomy margin and hydrocephalus 11 , which differs from a report by De Bonis et al 28 . Their results suggest that damage to the CSF drainage pathways contributes to the primary brain injury, rather than the craniectomy margin, as a factor responsible for hydrocephalus.…”

“…Lee et al reported a 41.2% incidence of hydrocephalus in patients who suffer from malignant middle cerebral artery infarction and underwent DC 27 . De Bonis and colleagues found a lower incidence of hydrocephalus after DC (34.5%) according to more strict criteria: radiographic evidence of progressive ventricular dilatation with an Evan index .0.3, associated with narrowed CSF spaces at the convexity on serial CT imaging 28 . Others defined hydrocephalus as progressive ventricular dilatation with trans-ependymal edema, together with (1) the presence of either clinical deterioration or failure to make neurological progress over time, and (2) some evidence of clinical improvement after insertion of a ventriculo-peritoneal shunt (V-P shunt).…”

“…De Bonis et al reported that the distance from the midline is the only factor associated with hydrocephalus after TBI 28 . They considered that extracellular fluid is absorbed during the diastolic phase of the cardiac cycle, and that this causes a decrease in brain parenchyma volume and a consequent increase in ventricular volume, which causes hydrocephalus.…”

Cerebral venous overdrainage: an under-recognized complication of cerebrospinal fluid diversion

“…One study that may explain this discrepancy was performed by De Bonis et al, 24 who reported their experience with posttraumatic hydrocephalus in patients who had undergone decompressive hemicraniectomy after traumatic brain injury. They analyzed the area of craniotomy and the distance of the craniotomy from the midline.…”

“…They hypothesized, based on the Starling resistor concept, that during each cardiac cycle in which extracellular fluid is produced during systole and absorbed in diastole, an imbalance between the production and absorption of extracellular fluid in favor of absorption would cause a decrease in brain parenchyma volume and consequently increase the size of the ventricles. 24 Thus in patients with craniectomies too close to the midline, the loss of CSF pressure surrounding the cortical draining veins in diastole would cause an increase in venous outflow. In turn, cerebral venous overdrainage would cause an increase in extracellular fluid absorption, leading to a loss of brain parenchyma volume and ventriculomegaly.…”