Isolated Brain Trauma in Cats Triggers Rapid Onset of Hypovolemia

Abstract

BackgroundHemodynamic instability responsive to fluid resuscitation is common after a traumatic brain injury (TBI), also in the absence of systemic hemorrhage. The present study tests if an isolated severe TBI induces a decrease in plasma volume (PV).MethodsThe study was performed in three groups of anesthetized and tracheostomized male cats (n = 21). In one group (n = 8), the cats were prepared with a cranial borehole (10 mm i.d) used to expose the brain to a fluid percussion brain injury (FPI) (1.90–2.20 bar), and two smaller cranial boreholes (4 mm i.d) for insertion of an intracranial pressure (ICP) and a microdialysis catheter. To differentiate the effect of FPI from that of the surgical preparation, a sham group was exposed to the same surgical preparation but no FPI trauma (n = 8). A control group had no brain trauma and no surgical preparation (n = 5). PV was determined by a 125I-albumin dilution technique. PV, electrolytes, pH, BE (base excess), hematocrit (Hct), PaO2, and PaCO2 were measured at baseline and after 3 h. Mean arterial pressure (MAP) was measured continuously. ICP was measured in the FPI and the sham group.ResultsIn the FPI group, PV decreased by 11.2 mL/kg from 31.7 mL/kg (p < 0.01) with a simultaneous increase in Hct and decrease in pH. In the sham group, PV decreased by 5.7 mL/kg from 32.7 mL/kg (p < 0.01). The control group showed no PV reduction.ConclusionsThe results support that an isolated severe head trauma triggers a significant and rapid reduction in PV, most likely due to vascular leak.

Association between vasopressor use and mortality in patients with severe traumatic brain injury: a nationwide retrospective cohort study in Japan

“…In this study, which focused on isolated TBI, hypotension in the emergent phase would be caused by transcapillary leakage-induced hypovolemia in the hyperadrenergic state after TBI, following removal of the potential confounding variable of non-brain injury-related fatal conditions. 29 Arterial BP could be conversely increased in the hyperadrenergic state, where the BP value would be an unreliable parameter for the evaluation of hypovolemia. In both situations, unless there is adequate fluid resuscitation, the use of vasopressors would exacerbate cerebral ischemia caused by reduced cerebral perfusion flow, due to the contraction of arterial vessels.…”

“…Although most guidelines target systolic BP, there are some problems. In this study, which focused on isolated TBI, hypotension in the emergent phase would be caused by transcapillary leakage‐induced hypovolemia in the hyperadrenergic state after TBI, following removal of the potential confounding variable of non‐brain injury‐related fatal conditions 29 . Arterial BP could be conversely increased in the hyperadrenergic state, where the BP value would be an unreliable parameter for the evaluation of hypovolemia.…”

Critical Evaluation of the Lund Concept for Treatment of Severe Traumatic Head Injury, 25 Years after Its Introduction

“…In this study, cats were exposed to a standardized fluid percussion brain trauma. The brain trauma resulted in 15% reduction in plasma volume, as measured 3 h after the trauma ( 86 ). In spite of the reduction in plasma volume, there was an increase in arterial blood pressure, most likely due to a trauma-induced hyperadrenergic state, showing that blood pressure is an unreliable parameter for evaluation of hypovolemia after a brain trauma.…”

“…Optimal fluid substitution is important for s-TBI patients, to prevent hypovolemia. As mentioned above, there is a risk that s-TBI patients develop hypovolemia very soon after the trauma, even if there is no extracranial bleeding ( 86 ). Isotonic crystalloids (e.g., saline or ringer lactate) and albumin are currently the only plasma volume expanders that can be recommended for s-TBI patients.…”