Escalating Mean Arterial Pressure in Severe Traumatic Brain Injury: A Prospective, Observational Study

Kow, Chien Yew; Harley, Benjamin; Li, Charles; Romo, Phillip; Gkolia, Panagiota; Lu, Kuan-Ying; Bell, Catherine; Jithoo, Rondhir; Tee, Jin; Cooper, DJ; Rosenfeld, Jeffrey V.; Lewis, Philip; Udy, Andrew; Hunn, Martin

doi:10.1089/neu.2020.7289

Cited by 6 publications

(8 citation statements)

References 27 publications

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“…Acute intracranial hypertension (AICH) is one of the most common causes for death and disability of patients suffering from traumatic brain injury (TBI) and hypertensive cerebral hemorrhage. The persistent high cranial pressure has been reported to be associated with poor prognosis and especially high mortality in adults with severe TBI [ 1 , 2 ].…”

Section: Introductionmentioning

confidence: 99%

Controlled Decompression Alleviates Brain Injury via Attenuating Oxidative Damage and Neuroinflammation in Acute Intracranial Hypertension

Zhang

Qian

Zheng

et al. 2022

BioMed Research International

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Background. The benefits of controlled decompression (CDC) for patients with acute intracranial hypertension especially in terms of alleviating the complications caused by rapid decompression (RDC) have been confirmed by clinical studies. This study is aimed at evaluating the therapeutic potency of CDC with ubiquitin C-terminal hydrolase-L1 (UCH-L1) and glial fibrillary acidic protein (GFAP) by investigating the potential molecular mechanism in the acute intracranial hypertension (AICH) rabbit model. Methods. Male New Zealand white rabbits were randomly subdivided into the sham-operated (SH) group, CDC group, and RDC group. Blood plasma samples and brain tissue were collected 2 days before operation (baseline) and at 3, 6, 24, and 72 hours after operation to measure the levels of UCH-L1, GFAP, oxidative stress indicators, and inflammatory cytokines by performing ELISA or Western blot. The neurological score of the rabbits and brain water content was graded 24 h after surgery. qPCR, immunofluorescence, and FJ-C staining were conducted. Results. CDC improved neurological function, lowered brain water content, ameliorated neuronal degeneration, attenuated oxidative damage, and inflammatory responses to a greater extent than RDC. Plasma UCH-L1 level was significantly lower in the CDC group at 3 h postoperatively than in the RDC group. CDC reduced plasma GFAP levels to various degrees at 3 h, 6 h, and 24 h postoperatively compared with RDC. Immunofluorescence confirmed that the expression of UCH-L1 and GFAP in the cortex of the CDC group was lower than that of the RDC group. Conclusions. Our data collectively demonstrate that CDC could attenuate oxidative damage and inflammatory responses, downregulate UCH-L1 and GFAP levels, and contribute to an improved neuroprotective effect compared with RDC.

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Section: Introductionmentioning

confidence: 99%

Controlled Decompression Alleviates Brain Injury via Attenuating Oxidative Damage and Neuroinflammation in Acute Intracranial Hypertension

Zhang

Qian

Zheng

et al. 2022

BioMed Research International

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“…In recent years, ICP monitoring technology has significantly improved the treatment of TBI patients ( 3 , 24 , 25 ). By accurately and continuously measuring the ICP throughout the treatment process, calculating the cerebral perfusion pressure, and adjusting the MAP to control the cerebral perfusion pressure at 60–70 mmHg, blood perfusion and compliance of cerebral tissue can be ensured, and the aggravation of ischemia and hypoxia can be avoided ( 26 ). At the same time, this also guides clinical precision medicine ( 27 ), and plays an important guiding role in the treatment of PTCI and cerebral herniation.…”

Section: Discussionmentioning

confidence: 99%

Predictive role of shock index in the early formation of cerebral infarction in patients with TBI and cerebral herniation

Hu¹,

Tian²,

Xie³

et al. 2022

Front. Neurol.

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Background and purposeTraumatic brain injury (TBI) with brain herniation predisposes to posttraumatic cerebral infarction (PTCI), which in turn seriously affects the prognosis of patients. At present, there is a lack of effective indicators that can accurately predict the occurrence of PTCI. We aimed to find possible risk factors for the development of PTCI by comparing the preoperative and postoperative clinical data of TBI patients with brain herniation.MethodsThe clinical data of 120 patients with craniocerebral trauma and brain herniation were retrospectively analyzed. Among them, 54 patients had cerebral infarction within 3–7 days after injury. The two groups of patients were compared through univariate and multivariate logistic regression analysis, and a classification tree model and a nomogram model were constructed. Finally, receiver operating characteristic curve analysis and decision curve analysis were conducted to analyze the clinical utility of the prediction model.ResultsLogistic regression analysis showed that factors like the Glasgow Coma Scale (GCS) score (P = 0.002), subarachnoid hemorrhage (SAH) (P = 0.005), aspiration pneumonia (P < 0.001), decompressive craniectomy (P < 0.05), intracranial pressure (ICP) monitoring (P = 0.006), the shock index (SI) (P < 0.001), the mean arterial pressure (MAP) (P = 0.005), and blood glucose (GLU) (P < 0.011) appeared to show a significant statistical correlation with the occurrence of infarction (P < 0.05), while age, sex, body temperature (T), D-dimer levels, and coagulation tests were not significantly correlated with PTCI after cerebral herniation. Combined with the above factors, Classification and Regression Tree was established, and the recognition accuracy rate reached 76.67%.ConclusionsGCS score at admission, no decompressive craniectomy, no ICP monitoring, combined SAH, combined aspiration pneumonia, SI, MAP, and high GLU were risk factors for infarction, of which SI was the primary predictor of PTCI in TBI with an area under the curve of 0.775 (95% CI = 0.689–0.861). Further large-scale studies are needed to confirm these results.

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“…Secondary brain injury can result from impaired cerebral blood flow, impairment of autoregulation, disruption of tissue oxygenation and brain metabolism, tissue inflammation and necrosis, edema, oxidative stress, and vasospasm, and from hematoma expansion due to factors such as hypertension [5,6,[9][10][11][12]. On the other hand, any episode of hypotension, defined as SBP<90, has been associated with increased mortality and worsened neurological outcomes in severe TBI [1][2][3][4][5][6][7][8]17]. This could be due to the critical importance of maintaining optimal cerebral perfusion pressure, which can mitigate the detrimental effects of cerebrovascular autoregulation impairment in TBI patients, thus reducing ischemic and hyperemic brain damage [2][3][4][17][18][19][20].…”

Section: Discussionmentioning

confidence: 99%

“…There is debate over optimal systolic blood pressure (SBP) after traumatic subdural hematoma (SDH) [1]. While hypotension, defined as SBP<90mmHg, is predictive of increased mortality in traumatic brain injury (TBI) patients [1][2][3][4][5][6][7][8], hypertension is associated with an increased risk of hematoma expansion [9][10][11], or the cause of the hematoma itself [12]. While Brain Trauma Foundation (BTF) fourth edition guidelines and expert opinion suggest SBP>100 for patients aged 50-69, SBP>110 for patients aged 15-49 or >70 years, and mean arterial pressure (MAP) >70 [2], Seattle International Brain Injury Consensus Conference recommendations are for SBP>90 and goal cerebral perfusion pressure (CPP) of 70 [5].…”

Section: Introductionmentioning

confidence: 99%

Blood Pressure Control in Traumatic Subdural Hematomas

Hallan¹

2022

Cureus

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BackgroundThere is debate over optimal systolic blood pressure (SBP) after traumatic subdural hematoma. Increased SBP has the benefit of increasing cerebral perfusion pressure and limiting the detrimental secondary effects of traumatic brain injury but poses a risk of hematoma expansion. While prior studies have shown that SBP<90mmHg is associated with worsened morbidity and mortality in subdural hematoma patients, clinical guidelines and expert opinion have differing initial SBP goals. The aim of this study is to leverage a large database to determine the effects of two such goals, namely SBP 100-150mmHg versus SBP<180mmHg in this patient population. MethodsA de-identified database network (TriNetX Research Network) was used to retrospectively query all patients with a first instance diagnosis of acute traumatic SDH, who also had a recorded GCS, with maintenance of SBP 100-150 within the first 24 hours (cohort 1) versus patients with an SBP<180 (cohort 2). Data came from 68 health care organizations (HCOs) with a total of 105,897,964 patients on 9/1/2022. The primary outcome of interest was mortality within 30 days. Secondary outcomes include gastrostomy tube placement, craniotomy/craniectomy/burr hole drainage, venous thromboembolism, ischemic stroke, myocardial infarction, seizure, falls, cardiac arrest, and acute kidney injury within 30 days. Cohorts were propensityscore matched for confounders. ResultsAfter propensity score matching, 1,243 patients were identified in each cohort. Age at index was 57.97+/-23.21 years and 58.28+/-22.35 years for cohorts 1 and 2, respectively. Mortality was seen in 243 patients (19.756%) vs. 209 (16.992%) (OR 1.203, 95% CI (0.98,1.476), p=0.0767) in cohorts 1 and 2, respectively. There was no statistical difference in secondary outcomes. ConclusionThe results of this study demonstrate that the primary outcome of mortality at 30 days is not statistically different in acute traumatic SDH patients, whether their SBP is kept at 100-150 or below 180. Likewise, it shows no statistical difference in the subsequent incidence of gastrostomy tube placement, craniotomy/craniectomy/burr holes, venous thromboembolism, ischemic stroke, myocardial infarction, seizure, falls, or acute kidney injury.

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Escalating Mean Arterial Pressure in Severe Traumatic Brain Injury: A Prospective, Observational Study

Cited by 6 publications

References 27 publications

Controlled Decompression Alleviates Brain Injury via Attenuating Oxidative Damage and Neuroinflammation in Acute Intracranial Hypertension

Controlled Decompression Alleviates Brain Injury via Attenuating Oxidative Damage and Neuroinflammation in Acute Intracranial Hypertension

Predictive role of shock index in the early formation of cerebral infarction in patients with TBI and cerebral herniation

Blood Pressure Control in Traumatic Subdural Hematomas

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