Abstract
Low- and middle-income countries (LMICs) bear most of the global burden of traumatic brain injury (TBI), but they lack the resources to address this public health crisis. For TBI guidelines and innovations to be effective, they must consider the context in LMICs; keeping this in mind, this article will focus on the history, pathophysiology, practice, evidence, and implications of cisternostomy. In this narrative review, the author discusses the history, pathophysiology, practice, evidence, and implications of cisternostomy. Cisternostomy for the management of TBI is an innovation developed in LMICs, primarily for LMICs. Its practice is based on the cerebrospinal fluid shift edema theory that attributes injury to increased pressure within the subarachnoid space due to subarachnoid hemorrhage and subsequent dysfunction of glymphatic drainage. Early reports of the technique report significant improvements in the Glasgow Outcome Scale, lower mortality rates, and shorter intensive care unit durations. Most reports are single-center studies with small sample sizes, and the technique requires experience and skill. These limitations have led to criticisms and slow adoption of the technique. Further research is needed to establish the effect of cisternostomy on TBI outcomes.
Highlights
Low- and middle-income countries (LMICs) bear most of the global burden of traumatic brain injury (TBI), but they lack the resources to address this public health crisis
For TBI guidelines and innovations to be effective, they must consider the context in LMICs; keeping this in mind, this article will focus on the history, pathophysiology, practice, evidence, and implications of cisternostomy
TBI causes 111 years of life lived with disability per 100 000, and 80% of its burden occurs in low- and middle-income countries (LMICs) [1]
Summary
Cisternostomy in the context of severe TBI aims at opening the basal cisterns to atmospheric pressure and tackle the vicious process leading to posttraumatic brain swelling [11]. Acute TBI causes the translocation of type 4 aquaporin channels away from astrocytes’ endfeet, thereby altering the flow of extracellular CNS fluid (glymphatic and interstitial) and causing reactive astrogliosis [20] Based on these facts, the concept of CSF shift edema started to emerge, as it was suggested that, following posttraumatic subarachnoid bleeding which impairs the normal CSF flow and resorption, the interstitial and intracellular fluid could increase as a result of the shift from the rising pressure of the basal cisterns into the brain parenchyma [11]. The role of cisternotomy on glymphatic flow and TBI was studied in mice models by Plog et al [22] who used horizontal cisternotomy to drain CSF from mice that had acute TBI continually Of note, they found no evidence in favor of cisternostomy preventing the secondary cascade of TBI. Glymphatic disruption occurs between days 3 and 28 in mice models, in a small number of cases, it occurs as early as day 1 [19]. erefore, if cisternostomy could in the future prove its effectiveness in all TBI cases, some of its effects could not be explained by the CSF shift edema theory alone and should perhaps be attributable to the reduced intracranial pressure and the overall optimization of the CSF flow as seen following decompressive craniectomy [25]
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