scholarly journals Midline shift in patients with closed traumatic brain injury may be driven by cerebral perfusion pressure not intracranial pressure

2021 ◽  
Vol 65 (4) ◽  
Author(s):  
Danilo CARDIM ◽  
Chiara ROBBA ◽  
Bernhard SCHMIDT ◽  
Joseph DONNELLY ◽  
Eric A. SCHMIDT ◽  
...  
2020 ◽  
Author(s):  
Tatiana Birg ◽  
Fabrizio Ortolano ◽  
Eveline J.A. Wiegers ◽  
Peter Smielewski ◽  
Yan Savchenko ◽  
...  

Abstract BackgroundAfter Traumatic Brain Injury (TBI) fever is frequent. Brain temperature, which is directly linked to body temperature, may influence brain physiology. Increased body and/or brain temperature may cause secondary brain damage, with deleterious effects on intracranial pressure (ICP), cerebral perfusion pressure (CPP) and outcome. MethodsCENTER-TBI, a prospective, multicenter, longitudinal study on TBI in Europe and Israel, includes a high resolution (HR) cohort of patients with data sampled at high-frequency (from 100 Hz to 500 Hz). In this study, simultaneous BT, ICP and CPP recordings were investigated. A mixed effects linear model was used to examine the association between different BT levels and ICP. We additionally focused on changes of ICP and CPP during the episodes of BT changes (delta BT ≥0.5 °C, lasting from 15 minutes to 3 hours) up or down-wards. The significance of ICP and CPP variations was estimated with the paired samples Wilcoxon test. Results Twenty-one patients with 2435 hours of simultaneous BT and ICP monitoring were studied. All patients reached a BT of 38° and experienced at least one episode of ICP above 20 mmHg. The linear mixed effects model revealed an association between BT above 37.5°C and higher ICP levels that was not confirmed for lower BT. We identified 149 episodes of BT changes. During BT elevations (n=79) ICP increased while CPP was reduced; opposite ICP and CPP variations occurred during episodes of BT reduction (n=70). All these changes were of moderate clinical relevance, even if statistically significant (p<0.0001). It has to be noted, however, that a number of therapeutic interventions against intracranial hypertension was documented during those episodes.ConclusionPatients after TBI usually develop BT> 38° soon after the injury. Brain temperature may influence brain physiology, as reflected by ICP and CPP. An association between BT exceeding 37.5°C and a higher ICP was identified. The relationship between BT, ICP and CPP become clearer during rapid temperature changes.Trial registration: The core study was registered with ClinicalTrials.gov, number NCT02210221, registered on July 29, 2014


Author(s):  
Tatiana Birg ◽  
Fabrizio Ortolano ◽  
Eveline J. A. Wiegers ◽  
Peter Smielewski ◽  
Yan Savchenko ◽  
...  

Abstract Background After traumatic brain injury (TBI), fever is frequent. Brain temperature (BT), which is directly linked to body temperature, may influence brain physiology. Increased body and/or BT may cause secondary brain damage, with deleterious effects on intracranial pressure (ICP), cerebral perfusion pressure (CPP), and outcome. Methods Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI), a prospective multicenter longitudinal study on TBI in Europe and Israel, includes a high resolution cohort of patients with data sampled at a high frequency (from 100 to 500 Hz). In this study, simultaneous BT, ICP, and CPP recordings were investigated. A mixed-effects linear model was used to examine the association between different BT levels and ICP. We additionally focused on changes in ICP and CPP during the episodes of BT changes (Δ BT ≥ 0.5 °C lasting from 15 min to 3 h) up or downward. The significance of ICP and CPP variations was estimated with the paired samples Wilcoxon test (also known as Wilcoxon signed-rank test). Results Twenty-one patients with 2,435 h of simultaneous BT and ICP monitoring were studied. All patients reached a BT of 38 °C and experienced at least one episode of ICP above 20 mm Hg. The linear mixed-effects model revealed an association between BT above 37.5 °C and higher ICP levels that was not confirmed for lower BT. We identified 149 episodes of BT changes. During BT elevations (n = 79) ICP increased, whereas CPP was reduced; opposite ICP and CPP variations occurred during episodes of BT reduction (n = 70). All these changes were of moderate clinical relevance (increase of ICP of 4.5 and CPP decrease of 7.5 mm Hg for BT rise, and ICP reduction of 1.7 and CPP elevation of 3.7 mm Hg during BT defervescence), even if statistically significant (p < 0.0001). It has to be noted, however, that a number of therapeutic interventions against intracranial hypertension was documented during those episodes. Conclusions Patients after TBI usually develop BT > 38 °C soon after the injury. BT may influence brain physiology, as reflected by ICP and CPP. An association between BT exceeding 37.5 °C and a higher ICP was identified but not confirmed for lower BT ranges. The relationship between BT, ICP, and CPP become clearer during rapid temperature changes. During episodes of temperature elevation, BT seems to have a significant impact on ICP and CPP.


2012 ◽  
Vol 117 (3) ◽  
pp. 589-596 ◽  
Author(s):  
Edson Bor-Seng-Shu ◽  
Eberval G. Figueiredo ◽  
Robson L. O. Amorim ◽  
Manoel Jacobsen Teixeira ◽  
Juliana Spelta Valbuza ◽  
...  

Object In recent years, the role of decompressive craniectomy for the treatment of traumatic brain injury (TBI) in patients with refractory intracranial hypertension has been the subject of several studies. The purpose of this review was to evaluate the contribution of decompressive craniectomy in reducing intracranial pressure (ICP) and increasing cerebral perfusion pressure (CPP) in these patients. Methods Comprehensive literature searches were performed for articles related to the effects of decompressive craniectomy on ICP and CPP in patients with TBI. Inclusion criteria were as follows: 1) published manuscripts, 2) original articles of any study design except case reports, 3) patients with refractory elevated ICP due to traumatic brain swelling, 4) decompressive craniectomy as a type of intervention, and 5) availability of pre- and postoperative ICP and/or CPP data. Primary outcomes were ICP decrease and/or CPP increase for assessing the efficacy of decompressive craniectomy. The secondary outcome was the persistence of reduced ICP 24 and 48 hours after the operation. Results Postoperative ICP values were significantly lower than preoperative values immediately after decompressive craniectomy (weighted mean difference [WMD] −17.59 mm Hg, 95% CI −23.45 to −11.73, p < 0.00001), 24 hours after (WMD −14.27 mm Hg, 95% CI −24.13 to −4.41, p < 0.00001), and 48 hours after (WMD −12.69 mm Hg, 95% CI −22.99 to −2.39, p < 0.0001). Postoperative CPP was significantly higher than preoperative values (WMD 7.37 mm Hg, 95% CI 2.32 to 12.42, p < 0.0001). Conclusions Decompressive craniectomy can effectively decrease ICP and increase CPP in patients with TBI and refractory elevated ICP. Further studies are necessary to define the group of patients that can benefit most from this procedure.


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