Modification of acute cardiovascular homeostatic responses to hemorrhage following mild to moderate traumatic brain injury

McMahon, Colm J.; Kenny, RoseAnne; Bennett, Kathleen; Kirkman, Emrys

doi:10.1097/01.ccm.0000295425.41831.85

Cited by 27 publications

(14 citation statements)

References 39 publications

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“…26,27 McMahon et al, also found a similar association between brain-specific injury and cardiovascular response to hemorrhage in rats where heart rate remained elevated longer and there was a delayed hypotensive response to graded fixed-volume hemorrhage with TBI. 28 However, other investigators have found impaired vascular responses similar to our witnessed response during hemorrhage and resuscitation in a rat model where vascular compensation was blunted in the setting of TBI. 29 Our data agrees with an immediate attenuation of initial tachycardia and impaired peripheral vasoactivity during hemorrhage and fluid resuscitation in the setting of brain injury.…”

Section: Discussionsupporting

confidence: 65%

Fluid Resuscitation of Uncontrolled Hemorrhage Using a Hemoglobin-Based Oxygen Carrier

White¹,

Wang²,

Bradbury³

et al. 2013

Shock

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Objective Animal models of combined TBI and hemorrhagic shock (HS) suggest a benefit of HBOC-based resuscitation, but their use remains controversial and little is known of the specific effects of TBI and high-pressure (large arterial injury) bleeding on resuscitation. We examine the effect of TBI and aortic tear injury on low volume HBOC resuscitation in a swine polytrauma model and hypothesize that HBOC-based resuscitation will improve survival in the setting of aortic tear regardless of the presence of TBI. Methods Anesthetized swine subjected to HS with aortic tear +/− fluid percussion TBI underwent equivalent limited resuscitation with HBOC, LR, or HBOC+nitroglycerine (NTG) (vasoattenuated HBOC) and were observed for 6 hours. Results There was no independent effect of TBI on survival time after adjustment for fluid type and there was no interaction between TBI and resuscitation fluid type. However, total catheter hemorrhage volume required to reach target shock blood pressure was less with TBI (14.0 ml/kg [12.4, 15.6]) vs. HS-only (21.0 ml/kg [19.5, 22.5]), with equivalent lactate accumulation. Conclusion TBI did not affect survival in this polytrauma model, but less hemorrhage was required in the presence of TBI to achieve an equivalent degree of shock suggesting globally impaired cardiovascular response to hemorrhage in the presence of TBI. There was also no benefit of HBOC-based fluid resuscitation over LR, contrary to models using liver injury as the source of hemorrhage. Considering wound location is of paramount importance when choosing resuscitation strategy.

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Section: Discussionsupporting

confidence: 65%

Fluid Resuscitation of Uncontrolled Hemorrhage Using a Hemoglobin-Based Oxygen Carrier

White¹,

Wang²,

Bradbury³

et al. 2013

Shock

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“…Previous work with rodent TBI models collectively supports the premise that TBI causes loss of hemodynamic resilience (i.e., the ability to regulate vascular tone during hemorrhagic shock), and in so doing alters the resuscitative needs (Yuan et al, 1991;Yuan and Wade, 1992;Law et al, 1996;McMahon et al, 2008). Airblast also acutely disrupted cardiovascular compensatory responses to hemorrhage; we observed a significant reduction in PSBV and time to PSBV (i.e., cardiovascular decompensation), as well as the survival time with sustained reduction in MAP (Fig.…”

Section: Blast Overpressure In Ratsmentioning

confidence: 86%

“…Fluid percussion injury data from several laboratories indicate that TBI adversely affects cardiovascular homeostatic responses to blood loss and resuscitation (Yuan et al, 1991;Yuan and Wade, 1992;Law et al, 1996;McMahon et al, 2008). It is very likely that the blast-induced brain trauma also substantially alters fluid resuscitation requirements, particularly when one considers that it occurs in combination with deleterious effects on other organ systems.…”

Section: Introductionmentioning

confidence: 95%

“…Not surprisingly, these data clearly reinforce the perspective that in addition to all the other medical challenges they create, blast injuries also clearly complicate far-forward resuscitation following hemorrhage. Acute TBI has been noted to yield an unexpectedly high mortality rate when included as a component of multisystem trauma (McMahon et al, 1999;McMahon et al, 2008;Patel et al, 2005;Chesnut, 2007). Blast injury is likely to do so as well.…”

mentioning

confidence: 96%

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Blast Overpressure in Rats: Recreating a Battlefield Injury in the Laboratory

Long

Bentley

Wessner

et al. 2009

Journal of Neurotrauma

312

283

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Blast injury to the brain is the predominant cause of neurotrauma in current military conflicts, and its etiology is largely undefined. Using a compression-driven shock tube to simulate blast effects, we assessed the physiological, neuropathological, and neurobehavioral consequences of airblast exposure, and also evaluated the effect of a Kevlar protective vest on acute mortality in rats and on the occurrence of traumatic brain injury (TBI) in those that survived. This approach provides survivable blast conditions under which TBI can be studied. Striking neuropathological changes were caused by both 126- and 147-kPa airblast exposures. The Kevlar vest, which encased the thorax and part of the abdomen, greatly reduced airblast mortality, and also ameliorated the widespread fiber degeneration that was prominent in brains of rats not protected by a vest during exposure to a 126-kPa airblast. This finding points to a significant contribution of the systemic effects of airblast to its brain injury pathophysiology. Airblast of this intensity also disrupted neurologic and neurobehavioral performance (e.g., beam walking and spatial navigation acquisition in the Morris water maze). When immediately followed by hemorrhagic hypotension, with MAP maintained at 30 mm Hg, airblast disrupted cardiocompensatory resilience, as reflected by reduced peak shed blood volume, time to peak shed blood volume, and time to death. These findings demonstrate that shock tube-generated airblast can cause TBI in rats, in part through systemic mediation, and that the resulting brain injury significantly impacts acute cardiovascular homeostatic mechanisms as well as neurobehavioral function.

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“…Several studies have shown that TBI may impair cardiovascular compensation to acute blood loss [12-16]. In detail, it has been demonstrated that the autonomic response to haemorrhage is disturbed in the presence of TBI and the physiological response to acute blood loss, like hypotension or the modification of vascular tone may be impaired or delayed [14,15,17]. Yuan and colleagues even demonstrated that TBI may suppress spontaneous hemodynamic recovery from hemorrhage and also impede the efficacy of fluid resuscitation [12,18].…”

Section: Introductionmentioning

confidence: 99%

The impact of severe traumatic brain injury on a novel base deficit- based classification of hypovolemic shock

Mutschler

Nienaber²,

Wafaisade

et al. 2014

Scand J Trauma Resusc Emerg Med

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BackgroundRecently, our group has proposed a new classification of hypovolemic shock based on the physiological shock marker base deficit (BD). The classification consists of four groups of worsening BD and correlates with the extent of hypovolemic shock in severely injured patients. The aim of this study was to test the applicability of our recently proposed classification of hypovolemic shock in the context of severe traumatic brain injury (TBI).MethodsBetween 2002 and 2011, patients ≥16 years in age with an AIShead ≥ 3 have been retrieved from the German TraumaRegister DGU® database. Patients were classified into four strata of worsening BD [(class I (BD ≤ 2 mmol/l), class II (BD > 2.0 to 6.0 mmol/l), class III (BD > 6.0 to 10 mmol/l) and class IV (BD > 10 mmol/l)] and assessed for demographic and injury characteristics as well as blood product transfusions and outcomes. The cohort of severely injured patients with TBI was compared to a population of all trauma patients to assess possible differences in the applicability of the BD based classification of hypovolemic shock.ResultsFrom a total of 23,496 patients, 10,201 multiply injured patients with TBI (AIShead ≥ 3) could be identified. With worsening of BD, a consecutive increase of mortality rate from 15.9% in class I to 61.4% in class IV patients was observed. Simultaneously, injury severity scores increased from 20.8 (±11.9) to 41.6 (±17). Increments in BD paralleled decreasing hemoglobin, platelet counts and Quick’s values. The number of blood units transfused correlated with worsening of BD. Massive transfusion rates increased from 5% in class I to 47% in class IV. Between multiply injured patients with TBI and all trauma patients, no clinically relevant differences in transfusion requirement or massive transfusion rates were observed.ConclusionThe presence of TBI has no relevant impact on the applicability of the recently proposed BD-based classification of hypovolemic shock. This study underlines the role of BD as a relevant clinical indicator of hypovolaemic shock during the initial assessment in respect to haemostatic resuscitation and transfusion requirements.

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Modification of acute cardiovascular homeostatic responses to hemorrhage following mild to moderate traumatic brain injury

Abstract: Acute mild and moderate traumatic brain injury disrupts cardiovascular homeostatic responses to extracranial hemorrhage; this disruption is graded according to the severity of traumatic brain injury. Severe disruption is associated with an increase in early mortality.

Cited by 27 publications

References 39 publications

Fluid Resuscitation of Uncontrolled Hemorrhage Using a Hemoglobin-Based Oxygen Carrier

Fluid Resuscitation of Uncontrolled Hemorrhage Using a Hemoglobin-Based Oxygen Carrier

Blast Overpressure in Rats: Recreating a Battlefield Injury in the Laboratory

The impact of severe traumatic brain injury on a novel base deficit- based classification of hypovolemic shock

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