scholarly journals Determinants affecting the prognosis of decompressive craniectomy for traumatic brain injury

2020 ◽  
Vol 36 (4) ◽  
Author(s):  
Haitao Jiang ◽  
Guangshan Hao ◽  
Rui Zhang ◽  
Qi Pang

Objective: This research was designed to investigate the prognostic determinants of patients with traumatic brain injury (TBI) undergoing decompressive craniectomy (DC). Methods: The present study was a retrospective single center research including a total of 112 patients undergoing DC for TBI in Liaocheng People’s Hospital between January 2017 and December 2018. The results were measured by Extended Glasgow Outcome Sale (GOSE). The prognostic determinants were identified by univariate and binary logistic regression analysis between the deaths and survivors or favorable and unfavorable outcomes. Results: At the six-month follow-up, the mortality was 45.5% including 37 (33.0%) patients died within 30 days. The independent prognostic factors of 30-day mortality were age (p=0.033), D-dimer level at admission (p=0.032) and postoperative hypernatremia (p=0.014). Seventy five patients survived more than 30 days after DC, among which 27 (36.0%) patients had unfavorable prognosis (GOSE 1-4) and 48 (64.0%) patients presented favorable prognosis (GOSE 5-8). After 30 days from DC, the occurrence of post-traumatic hydrocephalus(PTH) (p= 0.008) was associated with unfavorable prognosis. Conclusions: Although DC is an effective treatment for TBI patients, the mortality and morbidity risk remain high. A combination of age, D-dimer level at admission and postoperative hypernatremia may be a good prognostic factor for 30-day mortality. Developing an accurate therapy strategy to prevent and control PTH may be beneficial to the 6-month prognosis for TBI patients undergoing DC. doi: https://doi.org/10.12669/pjms.36.4.2045 How to cite this:Jiang H, Hao G, Zhang R, Pang Q. Determinants affecting the prognosis of decompressive craniectomy for traumatic brain injury. Pak J Med Sci. 2020;36(4):---------. doi: https://doi.org/10.12669/pjms.36.4.2045 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

2019 ◽  
Author(s):  
Katrin Rauen ◽  
Lara Reichelt ◽  
Philipp Probst ◽  
Barbara Schäpers ◽  
Friedemann Müller ◽  
...  

2018 ◽  
Vol 17 (9) ◽  
pp. 689-695 ◽  
Author(s):  
Nidhi Khatri ◽  
Manisha Thakur ◽  
Vikas Pareek ◽  
Sandeep Kumar ◽  
Sunil Sharma ◽  
...  

Background & Objective: Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. Conclusion: In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI.


Author(s):  
Gopal Krishna ◽  
Varun Aggarwal ◽  
Ishwar Singh

Abstract Introduction Traumatic brain injury (TBI) affects the coagulation pathway in a distinct way than does extracranial trauma. The extent of coagulation abnormalities varies from bleeding diathesis to disseminated thrombosis. Design Prospective study. Methods The study included 50 patients of isolated TBI with cohorts of moderate (MHI) and severe head injury (SHI). Coagulopathy was graded according to the values of parameters in single laboratory. The incidence of coagulopathy according to the severity of TBI and correlation with disseminated intravascular coagulation (DIC) score, platelets, prothrombin time (PT), activated partial thromboplastin time (APTT), D-dimer, and fibrinogen was observed. The comparison was also made between expired and discharged patients within each group. It also compared coagulation derailments with clinical presentation (Glasgow Coma Scale [GCS]) and outcome (Glasgow Outcome Scale [GOS]). Results Road traffic accident was the primary (72%) mode of injury. Fifty-two percent had MHI and rest had SHI. Eighty-four percent of cases were managed conservatively. The mean GCS was 12.23 and 5.75 in MHI and SHI, respectively. Sixty-two percent of MHI and 96% of the patients with SHI had coagulation abnormalities. On statistical analysis, DIC score (p < 0.001) strongly correlated with the severity of head injury and GOS. PT and APTT were also significantly associated with the severity of TBI. In patients with moderate TBI, D-dimer and platelet counts showed association with clinical outcome. Fibrinogen levels did not show any statistical significance. The mean platelet counts remained normal in both the groups of TBI. The mean GOS was 1.54 and 4.62 in SHI and MHI, respectively. Conclusion Coagulopathy is common in isolated TBI. The basic laboratory parameters are reliable predictors of coagulation abnormalities in TBI. Coagulopathy is directly associated with the severity of TBI, GCS, and poor outcome.


Trauma ◽  
2020 ◽  
pp. 146040862093576
Author(s):  
Nida Fatima ◽  
Mujeeb-Ur-Rehman ◽  
Samia Shaukat ◽  
Ashfaq Shuaib ◽  
Ali Raza ◽  
...  

Objectives Decompressive craniectomy is a last-tier therapy in the treatment of raised intracranial pressure after traumatic brain injury. We report the association of demographic, radiographic, and injury characteristics with outcome parameters in early (<24 h) and late (≥24 h) decompressive craniectomy following traumatic brain injury. Methods We retrospectively identified 204 patients (158 (early decompressive craniectomy) and 46 (late decompressive craniectomy)), with a median age of 34 years (range 2–78 years) between 2015 and 2018. The primary endpoint was Glasgow Outcome Scale Extended (GOSE) at 60 days, while secondary endpoints included Glasgow Coma Score (GCS) at discharge, mortality at 30 days, and length of hospital stay. Regression analysis was used to assess the independent predictive variables of functional outcome. Results With a clinical follow-up of 60 days, the good functional outcome (GOSE = 5–8) was 73.5% versus 74.1% (p = 0.75) in early and late decompressive craniectomy, respectively. GCS ≥ 9 at discharge was 82.2% versus 91.3% (p = 0.21), mortality at 30 days was 10.8% versus 8.7% (p = 0.39), and length of stay in the hospital was 21 days versus 28 days (p = 0.20), respectively, in early and late decompressive craniectomy groups. Univariate analysis identified that GCS at admission (0.07 (0.32–0.18; < 0.05)) and indication for decompressive craniectomy (3.7 (1.3–11.01; 0.01)) are significantly associated with good functional outcome. Multivariate regression analysis revealed that GCS at admission (<9/≥9) (0.07 (0.03–0.16; <0.05)) and indication for decompressive craniectomy (extradural alone/ other hematoma) (1.75 (1.09–3.25; 0.02)) were significant independent predictors of good functional outcome irrespective of the timing of surgery. Conclusions Our results corroborate that the timing of surgery does not affect the outcome parameters. Furthermore, GCS ≥ 9 and/or extra dural hematoma are associated with relatively good clinical outcome after decompressive craniectomy.


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.


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