ELEVATED INTRACRANIAL-PRESSURE MASKS HEMORRHAGIC HYPOTENSION IN A CANINE MODEL

Previous clinical studies of blunt trauma patients with severe brain i njuries have demonstrated that emergency department vital signs failed to consistently identify life-threatening abdominal injury. One hypot hesis to explain this is that bradycardia and systemic hypertension fr om brainstem injury (the Gushing response) may mask the tachycardia an d hypotension ordinarily manifested by hemorrhagic hypovolemia. This m ould result in inappropriately normal or near-normal emergency departm ent vital signs for otherwise clinically apparent hypovolemia. To test this hypothesis, splenectomized dogs (n = 9) were phlebotomized to a systolic blood pressure (SEP) of 60 mm Hg. Subsequently, intracranial pressure (ICP) was artificially elevated in a controlled, incremental fashion. From a mean SEP of 58.4 +/- 3.9 mm Hg at a baseline ICP of 8. 1 +/- 4.2 mm Hg, increases in ICP of only 20 mm Hg significantly raise d SEP (in some animals). When ICP reached 70 mm Hg, mean SEP reached 9 5.1 +/- 8.7 mm Hg (p < 0.001) in spite of profound hemorrhagic hypovol emia. In all subjects, the tachycardia that accompanied hypovolemia tr ended towards normal with incremental increases in ICP. However, this did not reach statistical significance. In response to elevations in I CP, this hypovolemic canine model displayed normalization of SEP with variable changes in heart rate. These changes could mask hemorrhagic h ypotension in humans sustaining multiple system trauma, These experime ntal data support clinical studies advocating immediate definitive abd ominal evaluation in unconscious blunt trauma patients, regardless of vital signs.