Subdural effusion in decompressive craniectomy.

Abstract

Dear Editor I have read with great interest the article BAnother treatment choice for subdural effusion with ventricle dilation^ by Fang et al. The authors report their experience treating subdural effusions (SE) in two patients with decompressive craniectomy (DC) using lumboperitoneal shunt [7]. Traumatic SE is an alteration of the cerebrospinal fluid (CSF) circulation that is associated with traumatic brain injury (TBI). However, SE has also been associated with DC for traumatic and non-traumatic conditions [11, 18, 22]. The underlying pathogenesis of SE in both conditions (DC and TBI) is different; therefore, the management of this condition could be largely different [3, 10, 13]. Traumatic SE is a relatively common complication of TBI with a benign course in the majority of cases [23]. As the authors mentioned, the origin of TSE has been related with a tear in the subarachnoid layer probably due to the head trauma producing egress of the CSF to the subdural space in a valve-like manner [1, 7, 23]. Other theories have been also proposed such as the presence of a neomembrane with increased capillary permeability leading to the development of the SE [1, 8]. Furthermore, due to the head trauma or disturbances in CSF absorption, alterations in intracranial compliance could also contribute to this complication [9, 12, 13, 15]. I agree with the authors that most SE cases are self-limited, but in rare cases SE manifests with mass effect and ventricular dilation and even in those cases the surgical management is variable [4, 16, 17, 23]. Accordingly, it is not clear if shunting procedures are the Bonly cure^ for this type of CSF alterations in the setting of DC for TBI, as stated by the authors [7]. On the other hand, CSF disturbances after DC could be caused by intracranial hypotension and the effect of atmospheric pressure [2, 5, 10]. After a large bone flap is removed from the cranium, atmospheric pressure is applied onto the brain parenchyma producing a significant alteration in the intracranial dynamics [2]. CSF absorption is carried out in a pressure-dependant manner through the arachnoid granulations with a directly proportional relationship between subarachnoid pressure and CSF absorption rate [14, 18]. Therefore, pressurerelated alterations take place into the subarachnoid space with the subsequent alteration of the CSF absorption. This mechanism is aggravated by any communication between the subdural and subarachnoid space [10] producing the SE after DC. As the authors stated, the SE acts as compensatory mechanism of the disturbed CSF circulation due to the subarachnoid/subdural gradient. Furthermore, ventricular dilation may also occur by the same mechanism [6, 18], and this event may further dis turb the CSF dynamics thus increasing the subarachnoid/subdural gradient. SE is not a common finding in patients who have undergone DC for traumatic and non-traumatic conditions [1, 11, 21]. Therefore, other factors may play a role in the development of SE after DC. Despite that the authors report a good outcome of their patients, it is necessary to bear in mind that the same radiological picture could be related to different pathophysiological mechanisms. SE could also be * Josue M. Avecillas-Chasin josue.avecillas@salud.madrid.org; josueavecillas@hotmail.com