Risk Factors for Early Hemorrhagic Progression after Traumatic Brain Injury: A Focus on Lipid Profile

Kim, Hoon; Jin, Seon Tak; Kim, Young Woo; Kim, Seong Rim; Park, Ik Seong; Jo, Kwang Wook

doi:10.1089/neu.2014.3697

Cited by 18 publications

(17 citation statements)

References 33 publications

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“…7,32,42 However, in a 2015 study by Kim et al, patients with HPC had a mean SBP of 134.5 mm Hg, which was significantly higher than the mean SBP in patients without HPC (119.6 mm Hg). 21 As discussed by Oertel et al, it is possible that the management of hypotension with fluid resuscitation could in itself lead to increased bleeding or hemorrhagic progression. 32 Given the findings of this study as well as the conflicting findings from prior studies, blood pressure may not independently predict HPC or the expansion rate, but it seems to play a role in more severe outcomes as determined by disposition.…”

Section: Systolic Blood Pressurementioning

confidence: 99%

Blossoming contusions: identifying factors contributing to the expansion of traumatic intracerebral hemorrhage

Carnevale

Segar

Powers

et al. 2018

Journal of Neurosurgery

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OBJECTIVE Traumatic brain injury (TBI) remains a significant cause of neurological morbidity and mortality. Each year, more than 1.7 million patients present to the emergency department with TBI. The goal of this study was to evaluate the prognosis of traumatic cerebral intraparenchymal hemorrhage (tIPH), to develop subclassifications of these injuries that relate to prognosis, and to provide a more comprehensive assessment of hemorrhagic progression contusion (HPC) by analyzing the rate at which tIPH "blossom" (i.e., expansion), depending on a variety of intrinsic and modifiable factors. METHODS In this retrospective study, 726 patients (age range 0-100 years) were admitted to a level 1 trauma center with tIPH during an 8-year period (2005-2013). Of these patients, 491 underwent both admission and follow-up head CT (HCT) within 72 hours. The change in tIPH volume over time, the expansion rate, was recorded for all 491 patients. Effects of prehospital and in-hospital variables were examined using ordinal response logistic regression analyses. These variables were further examined using multivariate linear regression analysis to accurately predict the extent to which a hemorrhage will progress. RESULTS Of the 491 (67.6%) patients who underwent both admission and follow-up HCT, 368 (74.9%) patients experienced HPC. These hemorrhages expanded on average by 61.6% (4.76 ml) with an average expansion rate of 0.71 ml per hour. On univariate analysis, certain patient characteristics were significantly (p < 0.05) related to HPC, including age (> 60 years), admission Glasgow Coma Scale score, blood alcohol level, international normalized ratio, absolute platelet count, transfusion of platelets, concomitant anticoagulation and antiplatelet medication, the initial tIPH volume on admission HCT, and ventriculostomy. Increased expansion rate was significantly associated with patient disposition to hospice or death (p < 0.001). To determine which factors most accurately predict overall patient disposition, an ordinal-response logistic regression identified systolic blood pressure, Injury Severity Score, admission Glasgow Coma Scale score, follow-up scan volume, transfusion of platelets, and ventriculostomy as predictors of patient discharge disposition following tIPH. A multivariate logistic regression identified several prehospital and in-hospital variables (age, Injury Severity Score, blood alcohol level, initial scan volume, concomitant epidural hematoma, presence of subarachnoid hemorrhage, transfusion of platelets, and ventriculostomy) that predicted the volumetric expansion of tIPH. Among these variables, the admission tIPH volume by HCT proved to be the factor most predictive of HPC. CONCLUSIONS Several factors contribute to the rate at which traumatic cerebral contusions blossom in the acute posttraumatic period. Identifying the intrinsic and modifiable aspects of cerebral contusions can help predict the rate of expansion and highlight potential therapeutic interventions to improve TBI-associated morbidity and mortality.

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Section: Systolic Blood Pressurementioning

confidence: 99%

Blossoming contusions: identifying factors contributing to the expansion of traumatic intracerebral hemorrhage

Carnevale

Segar

Powers

et al. 2018

Journal of Neurosurgery

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“…Neuroimaging studies demonstrated a reduced pericontusional cerebral blood flow following METH administration in patients prior to sustaining TBI, 140 while cigarette smoking has been associated with a significant risk factor for hemorrhage and microvascular bleeding after TBI. 141 It was previously shown that METH-induced neurotoxicity and conditions such as traumatic brain injury (TBI) share common cellular and molecular neuropathological substrates. 142 In fact, compelling evidence from clinical and preclinical studies suggest that BBB dysfunction is an important neurovascular complication following TBI that involves the activation of oxidative and inflammatory stress signaling cascades.…”

Section: Smoking and Cerebrovascular Complications: Does Nicotine Havmentioning

confidence: 99%

Drugs of abuse and blood-brain barrier endothelial dysfunction: A focus on the role of oxidative stress

Sajja

Rahman

Cucullo

2015

J Cereb Blood Flow Metab

112

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Psychostimulants and nicotine are the most widely abused drugs with a detrimental impact on public health globally. While the long-term neurobehavioral deficits and synaptic perturbations are well documented with chronic use of methamphetamine, cocaine, and nicotine, emerging human and experimental studies also suggest an increasing incidence of neurovascular complications associated with drug abuse. Short-or long-term administration of psychostimulants or nicotine is known to disrupt blood-brain barrier (BBB) integrity/function, thus leading to an increased risk of brain edema and neuroinflammation. Various pathophysiological mechanisms have been proposed to underlie drug abuse-induced BBB dysfunction suggesting a central and unifying role for oxidative stress in BBB endothelium and perivascular cells. This review discusses drug-specific effects of methamphetamine, cocaine, and tobacco smoking on brain microvascular crisis and provides critical assessment of oxidative stress-dependent molecular pathways focal to the global compromise of BBB. Additionally, given the increased risk of human immunodeficiency virus (HIV) encephalitis in drug abusers, we have summarized the synergistic pathological impact of psychostimulants and HIV infection on BBB integrity with an emphasis on unifying role of endothelial oxidative stress. This mechanistic framework would guide further investigations on specific molecular pathways to accelerate therapeutic approaches for the prevention of neurovascular deficits by drugs of abuse.

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“…These terms include delayed traumatic intracerebral hematoma (DTICH), progressive hemorrhagic injury, hemorrhagic progression of contusion (HPC) and hemorrhage progression (HP). 1 , 5 , 6 , 7 , 8 , 9 Each definition focus on different molecular mechanisms and progression process. In this review, we use the term PHI to emphasize and clarify: (1) progressive focus on the progression process of hemorrhage in TBI patients, and (2) the new hemorrhage site which is not continuum to the original contusion.…”

Section: Phi Definition and Incidencementioning

confidence: 99%

“…Progressive hemorrhagic injury (PHI) is demonstrated to have a high risk of poor outcomes in traumatic brain injury (TBI) patients, including immediate consequences such as death and morbidity, and long-term health disorders. 1 , 2 To date, A series of studies on the mechanisms of PHI have been made, especially in coagulopathy-related ones. Meanwhile, trauma-induced coagulopathy (TIC) has been discussed in many recent studies, which showed some association with PHI.…”

Section: Introductionmentioning

confidence: 99%

Relationship between trauma-induced coagulopathy and progressive hemorrhagic injury in patients with traumatic brain injury

Liu

Huang

2016

Chinese Journal of Traumatology

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Progressive hemorrhagic injury (PHI) can be divided into coagulopathy-related PHI and normal coagulation PHI. Coagulation disorders after traumatic brain injuries can be included in trauma-induced coagulopathy (TIC). Some studies showed that TIC is associated with PHI and increases the rates of disability and mortality. In this review, we discussed some mechanisms in TIC, which is of great importance in the development of PHI, including tissue factor (TF) hypothesis, protein C pathway and thrombocytopenia. The main mechanism in the relation of TIC to PHI is hypocoagulability. We also reviewed some coagulopathy parameters and proposed some possible risk factors, predictors and therapies.

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Risk Factors for Early Hemorrhagic Progression after Traumatic Brain Injury: A Focus on Lipid Profile

Cited by 18 publications

References 33 publications

Blossoming contusions: identifying factors contributing to the expansion of traumatic intracerebral hemorrhage

Blossoming contusions: identifying factors contributing to the expansion of traumatic intracerebral hemorrhage

Drugs of abuse and blood-brain barrier endothelial dysfunction: A focus on the role of oxidative stress

Relationship between trauma-induced coagulopathy and progressive hemorrhagic injury in patients with traumatic brain injury

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