Effects of Cranioplasty on Cerebral Blood Flow Following Decompressive Craniectomy: A Systematic Review of the Literature

Neurosurgery ◽  
2017 ◽  
Vol 81 (2) ◽  
pp. 204-216 ◽  
Author(s):  
Sameer H. Halani ◽  
Jason K. Chu ◽  
James G. Malcolm ◽  
Rima S. Rindler ◽  
Jason W. Allen ◽  
...  
Resuscitation ◽  
2019 ◽  
Vol 138 ◽  
pp. 46-52
Author(s):  
Luca Lucchetta ◽  
Timothy N. Kwan ◽  
Junko Kosaka ◽  
Aiko Tanaka ◽  
Glenn M. Eastwood ◽  
...  

2018 ◽  
Vol 129 (1) ◽  
pp. 241-246 ◽  
Author(s):  
Aditya Vedantam ◽  
Claudia S. Robertson ◽  
Shankar P. Gopinath

OBJECTIVEFew studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI).METHODSThe authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed.RESULTSTwenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001).CONCLUSIONSIn the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.


2018 ◽  
Vol 241 ◽  
pp. 505-513 ◽  
Author(s):  
Simina Toma ◽  
Bradley J. MacIntosh ◽  
Walter Swardfager ◽  
Benjamin I. Goldstein

2014 ◽  
Vol 37 (6) ◽  
pp. 401-408 ◽  
Author(s):  
Verónica V. Olavarría ◽  
Hisatomi Arima ◽  
Craig S. Anderson ◽  
Alejandro M. Brunser ◽  
Paula Muñoz-Venturelli ◽  
...  

2010 ◽  
Vol 36 (12) ◽  
pp. 2163-2164 ◽  
Author(s):  
E. Vicenzini ◽  
S. Pro ◽  
F. Randi ◽  
P. Pulitano ◽  
G. Spadetta ◽  
...  

2017 ◽  
Vol 38 (2) ◽  
pp. 189-203 ◽  
Author(s):  
Mathilde MH Pauls ◽  
Barry Moynihan ◽  
Thomas R Barrick ◽  
Christina Kruuse ◽  
Jeremy B Madigan ◽  
...  

Agents that augment cerebral blood flow (CBF) could be potential treatments for vascular cognitive impairment. Phosphodiesterase-5 inhibitors are vasodilating drugs established in the treatment of erectile dysfunction (ED) and pulmonary hypertension. We reviewed published data on the effects of phosphodiesterase-5 inhibitors on CBF in adult humans. A systematic review according to PRISMA guidelines was performed. Embase, Medline and Cochrane Library Trials databases were searched. Sixteen studies with 353 participants in total were retrieved. Studies included healthy volunteers and patients with migraine, ED, type 2 diabetes, stroke, pulmonary hypertension, Becker muscular dystrophy and subarachnoid haemorrhage. Most studies used middle cerebral artery flow velocity to estimate CBF. Few studies employed direct measurements of tissue perfusion. Resting CBF velocity was unaffected by phosphodiesterase-5 inhibitors, but cerebrovascular regulation was improved in ED, pulmonary hypertension, diabetes, Becker's and a group of healthy volunteers. This evidence suggests that phosphodiesterase-5 inhibitors improve responsiveness of the cerebral vasculature, particularly in disease states associated with an impaired endothelial dilatory response. This supports the potential therapeutic use of phosphodiesterase-5 inhibitors in vascular cognitive impairment where CBF is reduced. Further studies with better resolution of deep CBF are warranted. The review is registered on the PROSPERO database (registration number CRD42016029668).


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