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Results for “Brain Hemorrhage, Traumatic”

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At least 19 recordsLinked to original sources
PubMed2000

Infratentorial traumatic brain hemorrhage: may outcome be predicted by initial GCS?

BACKGROUND: Overall prognosis of nonpenetrating traumatic brain hemorrhage may be predicted by neurologic function days after insult. The relationship between immediate function and outcome has not been examined for infratentorial traumatic brain hemmorhage (iTBH) identified on computed tomographic (CT) scan. Given the severity of brain stem injury, it is conceivable that immediate function may be predictive. METHODS: A retrospective review of 1,500 brain injuries occurring at our institution identified 18 patients (1.2%) with iTBH on CT scan (eight brain stem, five cerebellum, five both). Demographics, supratentorial injuries, and outcome at 6 months (Glasgow Outcome Scale) were recorded. RESULTS: Initial Glasgow Coma Scale (GCS) in 11 patients was less than 5 (group I). Seven patients had GCS scores greater than or equal to 6 (group II). Nine patients in group I either died or were vegetative. In group II, one died; none were vegetative (p < 0.02). Regression analysis demonstrated a strong correlation between initial GCS and Glasgow Outcome Scale scores at 6 months for all patients (p < 0.001). CONCLUSION: We conclude that initial GCS score may be predictive of long-term outcome in patients with CT scan evidence of iTBH-a relationship to be explored further for prognostic information.

Adolescent↗
PubMed1997

Effects of nalmefene, CG3703, tirilazad, or dopamine on cerebral blood flow, oxygen delivery, and electroencephalographic activity after traumatic brain injury and hemorrhage.

Hemorrhage after traumatic brain injury (TBI) in cats produces significant decreases in cerebral oxygen delivery (DcereO2) and electroencephalographic (EEG) activity. To determine whether effective treatments for the separate insults of TBI and hemorrhagic shock would also prove effective after the clinically relevant combination of the two, we measured the effects of a kappa-opiate antagonist (nalmefene), an inhibitor of lipid peroxidation (tirilazad), a thyrotropin-releasing hormone analog (CG3703), a clinically useful pressor agent (dopamine) or a saline placebo on cerebral blood flow (CBF), and EEG activity after TBI and mild hemorrhagic hypotension. Cats (n = 40, 8 per group) were anesthetized with 1.6% isoflurane in N2O:O2 (70:30) and prepared for fluid-percussion TBI and microsphere measurements of CBF. Cats were randomized to receive nalmefene (1 mg/kg), tirilazad (5 mg/kg), CG3703 (2 mg/kg), dopamine (20 microg x kg(-1) x min[-1]) or a saline placebo (2 ml, 0.9% NaCl). Animals were injured (2.2 atm), hemorrhaged to 70% of preinjury blood volume, treated as just described and resuscitated with a volume of 10% hydroxyethyl starch equal to shed blood. CBF was determined and EEG activity recorded before injury, after hemorrhage, and 0, 60, and 120 min after resuscitation (R0, R60, and R120). CBF increased significantly after resuscitation (R0) in the nalmefene- and CG3703-treated groups. CBF did not differ significantly from baseline in any group at R60 or R120. DcereO2 was significantly less than baseline in the saline-, dopamine-, and tirilazad-treated groups at R60 and in the dopamine-, tirilazad-, and CG3703-treated groups at R120. EEG activity remained unchanged in the nalmefene-treated group but deteriorated significantly at R60 or R120 compared to baseline in the other groups. Nalmefene and CG3703 preserved the hyperemic response to hemodilution (otherwise antagonized by TBI), and nalmefene prevented the deterioration in DcereO2 and EEG activity that occurs after TBI and hemorrhage.

Animals↗
PubMed1993

Traumatic brain injury, hemorrhagic shock, and fluid resuscitation: effects on intracranial pressure and brain compliance.

Intracranial hypertension following traumatic brain injury is associated with considerable morbidity and mortality. Hemorrhagic hypovolemia commonly coexists with head injury in this population of patients. Therapy directed at correcting hypovolemic shock includes vigorous volume expansion with crystalloid solutions. It is hypothesized that, following traumatic brain injury, cerebrovascular dysfunction results in rapid loss of brain compliance, resulting in increased sensitivity to cerebrovascular venous pressure. Increased central venous pressure (CVP) occurring with vigorous crystalloid resuscitation may therefore contribute to the loss of brain compliance and the development of intracranial hypertension. The authors tested this hypothesis in miniature swine subjected to traumatic brain injury, hemorrhage, and resuscitation. Elevated CVP following resuscitation from hemorrhage to a high CVP significantly worsened intracranial hypertension in animals with concurrent traumatic brain injury, as compared to animals subjected to traumatic brain injury alone (mean +/- standard error of the mean: 33.0 +/- 2.0 vs. 20.0 +/- 2.0 mm Hg, p < 0.05) or to animals subjected to the combination of traumatic brain injury, hemorrhage, and resuscitation to a low CVP (33.0 +/- 2.0 vs. 24.0 +/- 2.0 mm Hg, p < 0.05). These data support the hypothesis that reduction in brain compliance can occur secondary to elevation of CVP following resuscitation from hemorrhagic shock. This may worsen intracranial hypertension in patients with traumatic brain injury and hemorrhagic shock.

Animals↗
PubMed2005

IL-1RN and IL-1B gene polymorphisms and cerebral hemorrhagic events after traumatic brain injury.

OBJECTIVE: To investigate the association of (variable number tandem repeat) interleukin (IL) 1RN and (-511) IL-1B gene polymorphisms with brain hemorrhagic events after traumatic brain injury (TBI). METHODS: Data from brain CT, Glasgow Coma Scale (GCS) at admission, and 6-month Glasgow Outcome Scale (GOS) and modified Rankin Scale (mRS) were collected for 151 prospectively recruited patients with TBI. IL-1RN and IL-1B genotypes were determined using standard methods. Presence vs absence of any type of brain hemorrhage was the main outcome. Type of brain hemorrhage, GCS at admission, and 6-month GOS and mRS were secondary outcomes. Odd ratios (ORs) and corresponding 95% CI were calculated using logistic regression analyses. In adjusted models, the associations were controlled for age, gender, diffuse brain edema, volume of intracranial hematoma, neurosurgical intervention, and GCS at admission. p values less than 0.01 were considered significant. RESULTS: Compared with noncarriers, IL-1RN allele 2 carriers had higher odds of having cerebral hemorrhages after TBI (adjusted OR = 4.57; 95% CI = 1.67 to 12.96; p = 0.004). The associations for (-511) IL-1B polymorphism were not significant. CONCLUSION: There is an association between the presence of interleukin-1RN allele 2 and posttraumatic brain hemorrhage.

Adult↗
PubMed2005

Analysis of the brain bioavailability of peripherally administered magnesium sulfate: A study in humans with acute brain injury undergoing prolonged induced hypermagnesemia.

OBJECTIVE: Based on preclinical investigations, magnesium sulfate (MgSO4) has gained interest as a neuroprotective agent. However, the ability of peripherally administered MgSO4 to penetrate the blood-brain barrier is limited in normal brain. The current study measured the passage of intravenously administered Mg into cerebrospinal fluid in patients with brain injury requiring ventricular drainage. DESIGN: A prospective evaluation of the cerebrospinal fluid total and ionized magnesium concentration, [Mg], during sustained hypermagnesemia was performed. SETTING: Neurosciences intensive care unit at a major teaching institution. PATIENTS: Thirty patients with acute brain injury secondary to subarachnoid hemorrhage, traumatic brain injury, primary intracerebral hemorrhage, subdural hematoma, brain tumor, central nervous system infection, or ischemic stroke were studied. INTERVENTIONS: Patients underwent 24 hrs of induced hypermagnesemia during which total and ionized cerebrospinal fluid [Mg] was measured. Serum [Mg] was adjusted to 2.1-2.5 mmol/L. Cerebrospinal fluid [Mg] was measured at baseline, at 12 and 24 hrs after onset of infusion, and at 12 hrs following infusion termination. MEASUREMENTS AND MAIN RESULTS: At baseline, total (1.25 +/- 0.14 mmol/L) and ionized (0.80 +/- 0.10 mmol/L) cerebrospinal fluid [Mg] was greater than serum total (0.92 +/- 0.18 mmol/L) and ionized (0.63 +/- 0.07 mmol/L) [Mg] (p < .05). Total (1.43 +/- 0.13 mmol/L) and ionized (0.89 +/- 0.12 mmol/L) cerebrospinal fluid [Mg] was maximally increased by 15% and 11% relative to baseline, respectively, during induced hypermagnesemia (p < .05). CONCLUSIONS: Hypermagnesemia produced only marginal increases in total and ionized cerebrospinal fluid [Mg]. Regulation of cerebrospinal fluid [Mg] is largely maintained following acute brain injury and limits the brain bioavailability of MgSO4.

Adolescent↗
PubMed2003

The role of thrombin and thrombin receptors in ischemic, hemorrhagic and traumatic brain injury: deleterious or protective?

In the last two decades it has become apparent that thrombin has many extravascular effects that are mediated by a family of protease-activated receptors (PARs). PAR-1, -3 and -4 are activated via cleavage by thrombin. The importance of extravascular thrombin in modulating ischemic, hemorrhagic and traumatic injury in brain has recently become clear. Thus, in vitro, thrombin at low concentration protects neurons and astrocytes from cell death caused by a number of different insults. In vivo, pretreating the brain with a low dose of thrombin (thrombin preconditioning), attenuates the brain injury induced by a large dose of thrombin, an intracerebral hemorrhage or by focal cerebral ischemia. Thrombin may also be an important mediator of ischemic preconditioning. In contrast, high doses of thrombin kill neurons and astrocytes in vitro and cause disruption of the blood-brain barrier, brain edema and seizures in vivo. This review examines the role of thrombin in brain injury and the molecular mechanisms and signaling cascades involved.

Animals↗
PubMed2006

Increased lactate levels impair the coagulation system--a potential contributing factor to progressive hemorrhage after traumatic brain injury.

Progressive intracerebral contusions are a major problem in the management of patients with severe traumatic brain injury that is also linked to worse outcome. Microdialysis studies have revealed that lactate levels are very high inside contusions, corresponding to significant acidosis. The current study was performed in an effort to investigate whether the lactate accumulation inside cerebral contusions may be a contributing factor to the prolonged bleeding inside contusions. We have investigated the effects of lactic acidosis on the coagulation system with rotational thromboelastometry. It was a laboratory study involving 6 healthy volunteers. Blood was drawn and the pH was adjusted by addition of lactic acid in vitro. The pH levels studied were 7.4, 7.2, 7.0, and 6.8. The pH was also readjusted to 7.4 by addition the buffer THAM to blood initially adjusted to a pH of 6.8 to study the reversibility of potential adverse effects induced by the lactic acidosis. We found the coagulation to be significantly impaired by lactic acidosis (P = 0.000l). The impairment found was reversible after correction of the acidosis by a buffer. In conclusion, we found that lactic acidosis impaired the coagulation system. The impairment caused by lactic acidosis may be one factor causing the progressive hemorrhage in posttraumatic cerebral contusions, known to have high levels of lactate and correspondingly low pH. It may also be important to consider in bleeding trauma patients.

Acidosis↗
PubMed1999

Effects of ethanol on brain lactate in experimental traumatic brain injury with hemorrhagic shock.

OBJECTIVE: Previous studies of traumatic brain injury (TBI) and hemorrhagic shock (HS) models, have shown cardiorespiratory depression in ethanol-treated animals. This study investigated the effects of ethanol (ET) on brain lactate concentrations and acidosis in a TBI/HS model. METHODS: Anesthetized swine were instrumented and subjected to injury (INJ) consisting of fluid percussion TBI of 3 atm with concurrent 30 ml/kg graded hemorrhage over 30 min. Three groups were studied: Sham, INJ and INJ/ET. ET was given preinjury as a 2-g/kg i.v. bolus over 30 min, and an infusion of 0.4 g kg(-1) h(-1). Cardiorespiratory and cerebral physiologic data were monitored continuously for 150 min postinjury. Cerebral and renal blood flow was measured with colored microspheres. Brains were frozen in situ with liquid nitrogen. Lactate was measured with an enzymatic method. RESULTS: ET levels at injury were 219+/-24 mg/dl. The INJ/ET group had increased mortality, impaired ventilation, and reduced renal blood flow. Brain (cortical) lactate levels were significantly higher and cerebral venous lactate concentrations were increased in the INJ/ET group during the postinjury period. Cerebral venous glucose was significantly higher in the INJ/ET group, and cerebral venous pH was significantly lower. CONCLUSION: In this TBI/HS model, ethanol-induced increases in lactate concentrations in brain tissue and cerebral venous blood are associated with respiratory depression and reduced organ blood flow.

Analysis of Variance↗
PubMed2006

Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury.

OBJECTIVE: Two series of experiments were designed to evaluate whether early arginine vasopressin improves acute outcome following resuscitation from traumatic brain injury and severe hemorrhagic hypotension. DESIGN: Prospective randomized, blinded animal study. SETTING: University laboratory. SUBJECTS: Thirty-three swine. INTERVENTIONS: In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure approximately 20 mm Hg), survivors (n = 16) were initially resuscitated with 10 mL/kg crystalloid. After 30 mins, crystalloid and blood with either 0.1 unit x kg(-1) x hr(-1) arginine vasopressin or placebo was titrated to a mean arterial pressure target >or=60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure >or=60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO2 was administered periodically. In series 2 (n = 14), the identical protocol was followed except the shock period was 20 mins and survivors (n = 10) received a bolus of either arginine vasopressin (0.2 units/kg) or placebo during the initial fluid resuscitation. MEASUREMENTS AND MAIN RESULTS: In series 1, by 300 mins after traumatic brain injury with arginine vasopressin (n = 8) vs. placebo (n = 8), the fluid and transfusion requirements were reduced (both p < .01), intracranial pressure was improved (11 +/- 1 vs. 23 +/- 2 mmHg; p < .0001), and the CO2-evoked intracranial pressure elevation was reduced (7 +/- 2 vs. 26 +/- 3 mm Hg, p < .001), suggesting improved compliance. In series 2, with arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (p < .05). With arginine vasopressin, five of five animals survived 300 mins, whereas three of five placebo animals died. The survival time with placebo was 54 +/- 4 mins (p < .05 vs. arginine vasopressin). CONCLUSIONS: Early supplemental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury.

Animals↗
PubMed2000

Management of hydrocephalus with programmable valves after traumatic brain injury and subarachnoid hemorrhage.

Programmable shunt valves are a recent technological advance that enhance the management of most patients with hydrocephalus secondary to subarachnoid hemorrhage or traumatic brain injury. An improved understanding of the intracranial pressure dynamics occurring both before and after a cerebrospinal fluid diversionary shunt has provided a more scientific basis for the application of these valves.

Animals↗
PubMed2005

Traumatic brain injury and hemorrhagic hypotension suppress neuroprotective gene expression in injured hippocampal neurons.

BACKGROUND: After traumatic brain injury, memory dysfunction is due in part to damage to the hippocampus. To study the molecular mechanisms of this selective vulnerability, the authors used laser capture microdissection of neurons stained with Fluoro-Jade to directly compare gene expression in injured (Fluoro-Jade-positive) and adjacent uninjured (Fluoro-Jade-negative) rat hippocampal neurons after traumatic brain injury and traumatic brain injury plus hemorrhagic hypotension. METHODS: Twelve isoflurane-anesthetized Sprague-Dawley rats underwent moderate (2.0 atm) fluid percussion traumatic brain injury followed by either normotension or hemorrhagic hypotension. Animals were killed 24 h after injury. Frozen brain sections were double stained with 1% cresyl violet and 0.001% Fluoro-Jade. RNA from 10 Fluoro-Jade-positive neurons and 10 Fluoro-Jade-negative neurons, obtained from the hippocampal CA1, CA3, and dentate gyrus subfields using laser capture microdissection, was linearly amplified and analyzed by quantitative ribonuclease protection assay for nine neuroprotective and apoptosis-related genes. RESULTS: In injured CA3 neurons, expression of the neuroprotective genes glutathione peroxidase 1, heme oxygenase 1, and brain-derived neurotrophic factor was significantly decreased compared with that of adjacent uninjured neurons. Superimposition of hemorrhagic hypotension was associated with down-regulation of neuroprotective genes in both injured and uninjured neurons of all subregions. Expression of apoptosis-related genes did not vary between injured and uninjured neurons, with or without superimposed hemorrhage. CONCLUSIONS: The authors show, in the first direct comparison of messenger RNA levels in injured and uninjured hippocampal neurons, that injured neurons express lower levels of neuroprotective genes than adjacent uninjured neurons.

Animals↗