Decompressive craniectomy or medical management for refractory intracranial hypertension

Nirula, Ram; Millar, D.; Greene, Tom; McFadden, Molly; Shah, Lubdha M.; Scalea, Thomas M.; Stein, Deborah M.; Magnotti, Louis J.; Jurkovich, Gregory J.; Vercruysse, Gary; Δημητριάδης, Δημήτριος; Scherer, Lynette A.; Peitzman, Andrew; Sperry, Jason L.; Beauchamp, Kathryn M.; Bell, Scott E.; Feiz-Erfan, Iman; O’Neill, Patrick J.; Coimbra, Raúl

doi:10.1097/ta.0000000000000194

Cited by 38 publications

(40 citation statements)

References 24 publications

(7 reference statements)

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“…The morbidity and mortality of TBI is intimately linked with the increased ICP, hemorrhagic contusions, and cerebral edema . Thus, prevention of these secondary brain injuries is crucial.…”

Section: Mechanisms and Complications Of Injurymentioning

confidence: 99%

“…The morbidity and mortality of TBI is intimately linked with the increased ICP, hemorrhagic contusions, and cerebral edema. 26,27 Thus, prevention of these secondary brain injuries is crucial. Malignant cerebral edema is especially difficult to manage, as it is usually refractory to medical therapy and causes irreversible injury, with mortality approaching 100% when untreated.…”

Section: Morbidity and Mortalitymentioning

confidence: 99%

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Management of moderate and severe traumatic brain injury

2019

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Traumatic brain injury (TBI) is a common disorder with high morbidity and mortality, accounting for one in every three deaths due to injury. Older adults are especially vulnerable. They have the highest rates of TBI‐related hospitalization and death. There are about 2.5 to 6.5 million US citizens living with TBI‐related disabilities. The cost of care is very high. Aside from prevention, little can be done for the initial primary injury of neurotrauma. The tissue damage incurred directly from the inciting event, for example, a blow to the head or bullet penetration, is largely complete by the time medical care can be instituted. However, this event will give rise to secondary injury, which consists of a cascade of changes on a cellular and molecular level, including cellular swelling, loss of membrane gradients, influx of immune and inflammatory mediators, excitotoxic transmitter release, and changes in calcium dynamics. Clinicians can intercede with interventions to improve outcome in the mitigating secondary injury. The fundamental concepts in critical care management of moderate and severe TBI focus on alleviating intracranial pressure and avoiding hypotension and hypoxia. In addition to these important considerations, mechanical ventilation, appropriate transfusion of blood products, management of paroxysmal sympathetic hyperactivity, using nutrition as a therapy, and, of course, venous thromboembolism and seizure prevention are all essential in the management of moderate to severe TBI patients. These concepts will be reviewed using the recent 2016 Brain Trauma Foundation Guidelines to discuss best practices and identify future research priorities.

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“…The morbidity and mortality of TBI is intimately linked with the increased ICP, hemorrhagic contusions, and cerebral edema . Thus, prevention of these secondary brain injuries is crucial.…”

Section: Mechanisms and Complications Of Injurymentioning

confidence: 99%

Section: Morbidity and Mortalitymentioning

confidence: 99%

Management of moderate and severe traumatic brain injury

2019

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“…14 Inclusion criteria were age 16 years or older, evidence of blunt TBI on admission head CT, and admission Glascow Coma Score (GCS) of 13 or less. Patient demographics, pre-existing comorbidities, clinical and laboratory data, and admission CT scans were collected utilizing an online web-portal data entry system developed in conjunction with the American Association for the Surgery of Trauma (AAST) and Acute Care Surgery (ACS).…”

Section: Methodsmentioning

confidence: 99%

Neuro, trauma, or med/surg intensive care unit

Lombardo

Scalea

Sperry

et al. 2017

Journal of Trauma and Acute Care Surgery

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Introduction Patients with non-traumatic acute intracranial pathology benefit from neurointensivist care. Similarly, trauma patients with and without TBI fare better when treated by a dedicated trauma team. No study has yet evaluated the role of specialized neurocritical (NICU) and trauma intensive care units (TICU) in the management of TBI patients, and it remains unclear which TBI patients are best served in NICU, TICU, or general (Med/Surg) ICU. Methods This study is a secondary analysis of The American Association for the Surgery of Trauma Multi-Institutional Trials Committee (AAST-MITC) decompressive craniectomy study. Twelve Level 1 trauma centers provided clinical data and head CT scans of patients with Glasgow Coma Scale (GCS) ≤13 and CT evidence of TBI. Non-ICU admissions were excluded. Multivariate logistic regression was performed to measure the association between ICU-type and survival and calculate the probability of death for increasing ISS. Polytrauma patients (ISS > 15) with TBI and isolated TBI patients (other AIS < 3) were analyzed separately. Results There were 3641 patients with CT evidence of TBI with 2951 admitted to an ICU. Prior to adjustment, patient demographics, injury severity, and survival differed significantly by unit type. After adjustment, unit-type, age and ISS remained independent predictors of death. Unit-type modified the effect of ISS on mortality. TBI-polytrauma patients admitted to a TICU had improved survival across increasing ISS (Fig1). Survival for isolated TBI patients was similar between TICU and NICU. Med/Surg ICU carried the greatest probability of death. Conclusion Polytrauma patients with TBI have lower mortality risk when admitted to a Trauma ICU. This survival benefit increases with increasing injury severity. Isolated TBI patients have similar mortality risk when admitted to a Neuro ICU compared to a Trauma ICU. Med/Surg ICU admission carries the highest mortality risk.

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“…Brain edema following TBI can cause serious complications by limiting brain oxygen delivery and increasing intracranial pressure (124). The pressure increase is more common in children experiencing TBI than adults (48) Hounsfield unit values from brain CT mapped across an intracranial area can be used to accurately predict brain edema following TBI in children (82).…”

Section: Vasospasms Subarachnoid Hemorrhage Edema and Ischemic Hypoxiamentioning

confidence: 99%

“…Ulinastatin, a serine protease inhibitor, is currently being investigated for reduction of edema in rodents following TBI (35). Decompressive craniectomies are common in clinical practice (124). Decompressive craniectomies can prevent the intracranial pressure rise and potential herniation associated with edema (22).…”

Section: Vasospasms Subarachnoid Hemorrhage Edema and Ischemic Hypoxiamentioning

confidence: 99%

Role of Microvascular Disruption in Brain Damage from Traumatic Brain Injury

Logsdon

Lucke‐Wold

Turner

et al. 2015

Comprehensive Physiology

125

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Traumatic brain injury (TBI) is acquired from an external force, which can inflict devastating effects to the brain vasculature and neighboring neuronal cells. Disruption of vasculature is a primary effect that can lead to a host of secondary injury cascades. The primary effects of TBI are rapidly occurring while secondary effects can be activated at later time points and may be more amenable to targeting. Primary effects of TBI include diffuse axonal shearing, changes in blood brain barrier (BBB) permeability, and brain contusions. These mechanical events, especially changes to the BBB, can induce calcium perturbations within brain cells producing secondary effects, which include cellular stress, inflammation, and apoptosis. These secondary effects can be potentially targeted to preserve the tissue surviving the initial impact of TBI. In the past, TBI research had focused on neurons without any regard for glial cells and the cerebrovasculature. Now a greater emphasis is being placed on the vasculature and the neurovascular unit following TBI. A paradigm shift in the importance of the vascular response to injury has opened new avenues of drug treatment strategies for TBI. However, a connection between the vascular response to TBI and the development of chronic disease has yet to be elucidated. Long-term cognitive deficits are common amongst those sustaining severe or multiple mild TBIs. Understanding the mechanisms of cellular responses following TBI is important to prevent the development of neuropsychiatric symptoms. With appropriate intervention following TBI, the vascular network can perhaps be maintained and the cellular repair process possibly improved to aid in the recovery of cellular homeostasis.

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Decompressive craniectomy or medical management for refractory intracranial hypertension

Abstract: Therapeutic care/management, level III.

Cited by 38 publications

References 24 publications

Management of moderate and severe traumatic brain injury

Management of moderate and severe traumatic brain injury

Neuro, trauma, or med/surg intensive care unit

Role of Microvascular Disruption in Brain Damage from Traumatic Brain Injury

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