In Reply: Dural Tenting in Elective Craniotomies: A Randomized Clinical Trial

To the Editor: We thank Wang et al for their letter1 and in-depth analysis of our recent study published in Neurosurgery.2 Those authors raised questions regarding the randomized controlled trial in which we evaluated the necessity of prophylactic dural tenting sutures in adults undergoing elective supratentorial craniotomies. Wang et al argued that the mass effect of cerebral edema prevented the formation of postoperative extradural hematoma (EDH), rather than the surgical technique, as evaluated in our trial. In response, we would like to note the following points. Those authors present a hypothetical mechanism whereby postoperative brain edema, observed in a portion of our patients, may prevent the formation of EDH. However, the rate of reoperations due to EDH in our population was not statistically different compared with one of the largest external studies (3 events in 490 patients, 0.61%; 10 events in 1055 patients, 0.95%; respectively, 2-tailed test, P = .56).3 Second, Zeng et al,4 based on their case series of 25 postoperative EDHs, speculated that a decrease in intracranial pressure after tumor resection and cerebrospinal fluid (CSF) loss might lead to dural detachment and subsequent formation of postoperative EDH. Yet, this mechanism, however speculative, is not identical with what Wang et al proposed in their letter (decreased pressure contributing to the formation of EDH vs increased pressure preventing the formation of EDH). In our practice, including cases from our randomized controlled trial,2 we have encountered instances of hemorrhage into the tumor resection cavity occurring in the presence of cerebral edema. This observation indirectly contradicts the hypothesis proposed by Wang et al, ie that cerebral edema prevents hemorrhage formation. Moreover, we would like to note that one of the purposes of randomization is to minimize the effect of confounding factors, one of which could be brain edema.5 Nonetheless, if we were to include only patients without brain edema, the generalizability of our results would be unnecessarily and artificially reduced. Furthermore, such an approach would still fail to account for intraoperative or postoperative edema. Finally, extradural bleeding is a well-established cause of EDH. We believe that in the setting of reduced intracranial pressure (such as after tumor resection) extradural bleeding may lead to dural detachment and thus the formation of EDH. In this view, decreased intracranial pressure would be a contributing factor, but not the primary cause, of postoperative EDH. Yet, as previously stated, these speculations require further investigation. The second comment by Wang et al concerns the use of drainage techniques and their potential impact on the development of postoperative EDH. In our cohort, the primary indication for subgaleal drainage was excessive bleeding, although some surgeons used wound drains routinely. The decision to place a drain was based on individual surgeon and participating center preferences and was not randomized. In the available literature, Bonney et al6 analyzed the effect of drainage on radiographic outcomes after traumatic EDH and found no association between drain use and residual extradural collections. The authors of the letter also inquire about our definition of CSF leak, which was one of the secondary outcomes in our trial. According to the study protocol, the definition of a CSF leak demanding treatment encompasses both external and internal CSF leaks that require intervention.7 Treatment includes both invasive and noninvasive measures: medical therapy with acetazolamide, CSF puncture and aspiration, pressure dressing, external CSF drainage, and surgical repair. We sincerely thank Wang et al for their detailed analysis of our study. We have made every effort to ensure that our responses are supported by the available scientific evidence. Those authors' comments underscore the need for further research.