Decompressive Craniectomy and Hydrocephalus

De Bonis, Pasquale; Mangiola, Annunziato; Pompucci, Angelo; Anile, Carmelo

doi: 10.1227/NEU.0b013e31821787b6
Author Information

Rome, Italy

Article Outline

To the Editor:

We read with interest the article by Rahme et al1 reporting a study that included patients who underwent decompressive craniectomy for medically refractory elevated intracranial pressure resulting from a cerebrovascular accident. Patients with subarachnoid hemorrhage, intraventricular hemorrhage, or head trauma were excluded because of the potential relationship between those diagnoses and the development of hydrocephalus. None of the 14 patients of this series developed hydrocephalus requiring a cerebrospinal fluid shunt. The authors are to be commended for their contribution to this intriguing and timely aspect of neurosurgery (In addition to the aforementioned article, from May to September 2010, 2 articles were published on this topic).2,3 These results are in contrast with previous reports.2,4-6

We believe that the key to understanding why different authors have found different results is the definition of decompressive craniectomy. In fact, we have noticed that there is considerable variation in “standard hemicraniectomy” among centers. In the published series on decompressive hemicraniectomy, some surgeons always decompress the temporal fossa through a temporal craniectomy; others perform a much higher craniectomy (close to the midline); some authors extend craniectomy more posteriorly; others extend it more anteriorly; and most authors talk only about “large/wide” or “larger/wider” craniectomies without clearly defining the limits and width of craniectomy. Not to mention the expansive duraplasty. Some authors, including Taylor et al,7 the authors of the only randomized trial on decompressive craniectomy in the pediatric population, leave the dura intact (which is nonsense in terms of effectiveness of intracranial pressure lowering), whereas others perform an external delamination or longitudinal incisions.

We would like to provide information from our article on decompressive hemicraniectomy for traumatic brain injury as an adjunct to this article's questions.2 In a multivariate model including variables described by other authors to be associated with posttraumatic hydrocephalus (older age, longer timing of cranioplasty, higher score at Fisher grading system, low postresuscitation Glasgow Coma Scale score, cerebrospinal fluid infection), area of craniotomy, and distance of craniotomy from midline, we found that the only factor independently associated with the development of hydrocephalus was the distance from the midline. We therefore concluded that a craniectomy with a superior limit that is too close (< 25 mm) to the midline can predispose patients undergoing decompressive craniectomy to the development of hydrocephalus.

This new hypothesis may explain the very high incidence of hydrocephalus (88% of patients, half of whom harbored persistent hydrocephalus after cranioplasty and required a ventriculoperitoneal shunt) reported in the series of Waziri and associates6 (discussed by Rahme et al). In fact, the superior margin of the craniotomy used by these authors was within 1 to 2 cm of the sagittal sinus, as they clearly stated (Reference 3 in the Methods). Moreover, in that study, the authors had no confounding factors (traumatic brain injury, subarachnoid hemorrhage), so they probably observed a pure influence of decompressive craniectomy on the development of hydrocephalus.

We think that Rahme et al had no cases developing hydrocephalus because the superior limit of hemicraniectomy in their series was probably > 25 mm. We therefore suggest that the authors analyze their data in this light to confirm or refute our hypothesis.

Pasquale De Bonis

Annunziato Mangiola

Angelo Pompucci

Carmelo Anile

Rome, Italy

1. Rahme R, Weil AG, Sabbagh M, Moumdjian R, Bouthillier A, Bojanowski MW. Decompressive craniectomy is not an independent risk factor for communicating hydrocephalus in patients with increased intracranial pressure. Neurosurgery. 2010;67(3):675-678.
2. De Bonis P, Pompucci A, Mangiola A, Rigante L, Anile C. Post-traumatic hydrocephalus after decompressive craniectomy: an underestimated risk factor. J Neurotrauma. 2010;27(11):1965-1970.
3. Kaen A, Jimenez-Roldan L, Alday R, et al. Interhemispheric hygroma after decompressive craniectomy: does it predict posttraumatic hydrocephalus? J Neurosurg. 2010;113(6):1287-1293.
4. Yang XF, Wen L, Shen F, et al. Surgical complications secondary to decompressive craniectomy in patients with a head injury: a series of 108 consecutive cases. Acta Neurochir (Wien). 2008;150(12):1241-1247.
5. Mazzini L, Campini R, Angelino E, Rognone F, Pastore I, Oliveri G. Posttraumatic hydrocephalus: a clinical, neuroradiologic, and neuropsychologic assessment of long-term outcome. Arch Phys Med Rehabil. 2003;84(11):1637-1641.
6. Waziri A, Fusco D, Mayer SA, McKhann GM, Connolly ES. Postoperative hydrocephalus in patients undergoing decompressive hemicraniectomy for ischemic or hemorrhagic stroke. Neurosurgery. 2007;61(3):489-493.
7. Taylor A, Butt W, Rosenfeld J, et al. A randomized trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension. Childs Nerv Syst. 2001;17(3):154-162.
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