scholarly journals Temporal effects of barbiturate coma on intracranial pressure and compensatory reserve in children with traumatic brain injury

2020 ◽  
Author(s):  
Fartein Velle ◽  
Anders Lewén ◽  
Timothy Howells ◽  
Pelle Nilsson ◽  
Per Enblad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
High Resolution ◽  
Bolus Injection ◽  
Perfusion Pressure ◽  
Good Recovery ◽  
Barbiturate Coma ◽  
High Resolution Data ◽  
Compensatory Reserve

Abstract Background The aim was to study the effects of barbiturate coma treatment (BCT) on intracranial pressure (ICP) and intracranial compensatory reserve (RAP index) in children (< 17 years of age) with traumatic brain injury (TBI) and refractory intracranial hypertension (RICH). Methods High-resolution monitoring data were used to study the effects of BCT on ICP, mean arterial pressure (MAP), cerebral perfusion pressure (CPP), and RAP index. Four half hour long periods were studied: before bolus injection and at 5, 10, and 24 hours thereafter, respectively, and a fifth tapering period with S-thiopental between < 100 and < 30 μmol/L. S-thiopental concentrations and administered doses were registered. Results Seventeen children treated with BCT 2007–2017 with high-resolution data were included; median age 15 (range 6–17) and median Glasgow coma score 7 (range 3–8). Median time from trauma to start of BCT was 44.5 h (range 2.5–197.5) and from start to stop 99.0 h (range 21.0–329.0). Median ICP was 22 (IQR 20–25) in the half hour period before onset of BCT and 16 (IQR 11–20) in the half hour period 5 h later (p = 0.011). The corresponding figures for CPP were 65 (IQR 62–71) and 63 (57–71) (p > 0.05). The RAP index was in the half hour period before onset of BCT 0.6 (IQR 0.1–0.7), in the half hour period 5 h later 0.3 (IQR 0.1–0.7) (p = 0.331), and in the whole BCT period 0.3 (IQR 0.2–0.4) (p = 0.004). Eighty-two percent (14/17) had favorable outcome (good recovery = 8 patients and moderate disability = 6 patients). Conclusion BCT significantly reduced ICP and RAP index with preserved CPP. BCT should be considered in case of RICH.

Severe Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Kee D. Kim ◽  
Marike Zwienenberg ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Traumatic Brain Injury ◽  
Neurocritical Care ◽  
Secondary Brain Injury ◽  
Brain Oxygenation ◽  
Barbiturate Coma ◽  
Blast Traumatic Brain Injury ◽  
Penetrating Traumatic Brain Injury

Traumatic brain injury remains a leading cause of death and disability worldwide. Patients with severe traumatic brain injury are best treated with a multidisciplinary, evidence-based, protocol-directed approach, which has been shown to decrease mortality and improve functional outcomes. Therapy is directed at the prevention of secondary brain injury through optimizing cerebral blood flow and the delivery of metabolic fuel (ie, oxygen and glucose). This is accomplished through the measurement and treatment of elevated intracranial pressure (ICP), the strict avoidance of hypotension and hypoxemia, and in some instances, surgical management. The treatment of elevated ICP is approached in a protocolized, tiered manner, with escalation of care occurring in the setting of refractory intracranial hypertension, culminating in either decompressive surgery or barbiturate coma. With such an approach, the rates of mortality secondary to traumatic brain injury are declining despite an increasing incidence of traumatic brain injury. This review contains 3 figures, 5 tables and 69 reference Key Words: blast traumatic brain injury, brain oxygenation, cerebral perfusion pressure, decompressive craniectomy, hyperosmolar therapy, intracranial pressure, neurocritical care, penetrating traumatic brain injury, severe traumatic brain injury

scholarly journals Brain Temperature Influences Intracranial Pressure and Cerebral Perfusion Pressure After Traumatic Brain Injury: A CENTER TBI Study

2020 ◽  
Author(s):  
Tatiana Birg ◽  
Fabrizio Ortolano ◽  
Eveline J.A. Wiegers ◽  
Peter Smielewski ◽  
Yan Savchenko ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Brain Temperature ◽  
Mixed Effects ◽  
Wilcoxon Test ◽  
Brain Physiology

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

scholarly journals Intracranial pressure–based barbiturate coma treatment in children with refractory intracranial hypertension due to traumatic brain injury

2020 ◽  
Vol 25 (4) ◽  
pp. 375-383 ◽  
Author(s):  
Fartein Velle ◽  
Anders Lewén ◽  
Timothy Howells ◽  
Per Enblad ◽  
Pelle Nilsson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Scale Score ◽  
Effective Means ◽  
Physiological Data ◽  
Barbiturate Coma ◽  
Severe Condition ◽  
Long Term Outcome

OBJECTIVERefractory intracranial pressure (ICP) hypertension following traumatic brain injury (TBI) is a severe condition that requires potentially harmful treatment strategies such as barbiturate coma. However, the use of barbiturates may be restricted due to concerns about inducing multiorgan system complications related to the therapy. The purpose of this study was to evaluate the outcome and occurrence of treatment-related complications to barbiturate coma treatment in children with refractory intracranial hypertension (RICH) due to TBI in a modern multimodality neurointensive care unit (NICU).METHODSThe authors conducted a retrospective cohort study of 21 children ≤ 16 years old who were treated in their NICU between 2005 and 2015 with barbiturate coma for RICH following TBI. Demographic and clinical data were acquired from patient records and physiological data from digital monitoring system files.RESULTSThe median age of these 21 children was 14 years (range 2–16 years) and at admission the median Glasgow Coma Scale score was 7 (range 4–8). Barbiturate coma treatment was added due to RICH at a median of 46 hours from trauma and had a median duration of 107 hours. The onset of barbiturate coma resulted in lower ICP values, lower pulse amplitudes on the ICP curve, and decreased amount of A-waves. No major disturbances in blood gases, liver and kidney function, or secondary insults were observed during this period. Outcome 1 year later revealed a median Glasgow Outcome Scale score of 5 (good recovery), however on the King’s Outcome Scale for Childhood Head Injury, the median was 4a (moderate disability).CONCLUSIONSThe results of this study indicate that barbiturate coma, when used in a modern NICU, is an effective means of lowering ICP without causing concomitant severe side effects in children with RICH and was compatible with good long-term outcome.

Severe Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Kee D. Kim ◽  
Marike Zwienenberg ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Traumatic Brain Injury ◽  
Neurocritical Care ◽  
Secondary Brain Injury ◽  
Brain Oxygenation ◽  
Barbiturate Coma ◽  
Blast Traumatic Brain Injury ◽  
Penetrating Traumatic Brain Injury

Traumatic brain injury remains a leading cause of death and disability worldwide. Patients with severe traumatic brain injury are best treated with a multidisciplinary, evidence-based, protocol-directed approach, which has been shown to decrease mortality and improve functional outcomes. Therapy is directed at the prevention of secondary brain injury through optimizing cerebral blood flow and the delivery of metabolic fuel (ie, oxygen and glucose). This is accomplished through the measurement and treatment of elevated intracranial pressure (ICP), the strict avoidance of hypotension and hypoxemia, and in some instances, surgical management. The treatment of elevated ICP is approached in a protocolized, tiered manner, with escalation of care occurring in the setting of refractory intracranial hypertension, culminating in either decompressive surgery or barbiturate coma. With such an approach, the rates of mortality secondary to traumatic brain injury are declining despite an increasing incidence of traumatic brain injury. This review contains 3 figures, 5 tables and 69 reference Key Words: blast traumatic brain injury, brain oxygenation, cerebral perfusion pressure, decompressive craniectomy, hyperosmolar therapy, intracranial pressure, neurocritical care, penetrating traumatic brain injury, severe traumatic brain injury

Central Nervous System Injury

2017 ◽  
Author(s):  
Brandon R Bruns ◽  
Deborah M Stein
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Intracranial Pressure Monitoring ◽  
Pressure Monitoring ◽  
Cerebral Contusion ◽  
Different Types ◽  
Hospital Visits

Traumatic brain injury (TBI) accounts for 2.5 million hospital visits annually and is the leading cause of death and disability in patients age 1 to 44 years. Evaluation of patients with suspected TBI requires prompt physical examination with a focus on calculation of the Glasgow Coma Score and pupillary examination as early treatments can be initiated at this stage in patient management. Diagnostic studies include basic laboratory parameters and prompt evaluation with brain computed tomography to identify space-occupying lesions (blood) within the rigid calvarium. Distinction between the different types of traumatic intracerebral hemorrhage is imperative and enables prompt neurosurgical consultation, as well as initiation of appropriate medical therapies to treat elevated intracranial pressure and maintain cerebral perfusion pressure. Paramount in managing patients with suspected TBI is the avoidance of hypotension and hypoxia. Intracranial pressure monitoring remains controversial but is a cornerstone in TBI management. Patients with TBI may have lifelong complications and require careful follow-up. Many new prognostic tools are currently available. This review contains 4 figures, 4 tables, and 47 references. Key words: cerebral contusion, epidural hematoma, intracranial pressure monitoring, subdural hematoma, traumatic brain injury 

scholarly journals Moderately Elevated Intracranial Pressure after Diffuse Traumatic Brain Injury is Associated with Exacerbated Neuronal Pathology and Behavioral Morbidity in the Rat

2014 ◽  
Vol 34 (10) ◽  
pp. 1628-1636 ◽  
Author(s):  
Audrey D Lafrenaye ◽  
Thomas E Krahe ◽  
John T Povlishock
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Neuronal Damage ◽  
Neuronal Loss ◽  
Global Ischemia ◽  
Neuronal Membrane ◽  
Elevated Intracranial Pressure ◽  
Membrane Perturbation

Traumatic brain injury (TBI)-induced elevated intracranial pressure (ICP) is correlated with ensuing morbidity/mortality in humans. This relationship is assumed to rely mostly on the recognition that extremely elevated ICP either indicates hematoma/contusions capable of precipitating herniation or alters cerebral perfusion pressure (CPP), which precipitates global ischemia. However, whether subischemic levels of elevated ICP without hematoma/contusion contribute to increased morbidity/mortality remains unknown. To address this knowledge gap, we utilized a model of moderate diffuse TBI in rats followed by either intraventricular ICP monitoring or manual ICP elevation to 20 mm Hg, in which CPP was above ischemic levels. The effects of ICP elevation after TBI on acute and chronic histopathology, as well as on behavioral morbidity, were evaluated. ICP elevation after TBI resulted in increased acute neuronal membrane perturbation and was also associated with reduced neuronal density at 4 weeks after injury. Somatosensory hypersensitivity was exacerbated by ICP elevation and was correlated to the observed neuronal loss. In conclusion, this study indicates that morbidity and increased neuronal damage/death associated with elevated ICP can occur without concurrent global ischemia. Therefore, understanding the pathologies associated with subischemic levels of elevated ICP could lead to the development of better therapeutic strategies for the treatment and management of TBI patients.

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