Cerebral Extraction of Oxygen and Intracranial Hypertension in Severe, Acute, Pediatric Brain Trauma: Preliminary Novel Management Strategies

Abstract

In severe, acute, non-missile pediatric brain trauma, phasic physiological patterns demonstrated an association between the development of intracranial hypertension and relative cerebral hyperperfusion (decreased global CEO(2)), especially after postinjury Day 1. Unfavorable clinical outcomes were significantly related to more pronounced intracranial hypertension and more profound concomitant decreases in CEO(2), indicating hyperoxic uncoupling between global cerebral consumption of oxygen and cerebral blood flow.

Practical and comprehensive guidelines for bedside cerebral hemometabolic multitherapeutic optimization

“…In our experience, ICP, CPP, and CEO 2 monitoring and management have lasted approximately 7-10 days for both adults 2,4,9,11 and children 12 17 first demonstrated that, immediately following intravenous bolus injections of barbiturates for the treatment of elevated ICP refractory to ongoing optimized mannitol and optimized hyperventilation, blood pressure may fall, along with SjO 2 decreases (CEO 2 increases) in some patients. Therefore, caution should be exercised whenever intravenous barbiturate boluses are administered for ICP control, and the use of vasopressor drugs should be immediately instituted if necessary.…”

“…As a humanitarian alternative to those 1996 "guidelines" 1 , the present practical and comprehensive guidelines address not only treatment of intracranial pressure (ICP) and CPP but also cerebral ex-traction of oxygen (CEO 2 ) 2,4,[7][8][9][10][11][12] . The latter represents the ratio of global cerebral consumption of oxygen (CCO 2 ) to cerebral blood flow (CBF) 8 , and thus provides accurate bedside information regarding coupling or uncoupling between CBF and CCO 2 .…”

“…This original animal study thus suggested that artificially maintaining high CPP levels (as proposed in the 1996 "guidelines" 1 ) may, in fact, lead to catastrophic consequences when managing brain-injured patients with decreased cerebrospinal fluid spaces and elevated ICP. CEO CEO 2 2 2 2 2 , CCO , CCO , CCO , CCO , CCO 2 2 2 2 2 , and CBF , and CBF , and CBF , and CBF , and CBF CEO 2 is simply the arteriojugular oxyhemoglobin saturation difference, and represents one of several novel parameters that we have previously proposed for bedside assessment of cerebral hemometabolism 2,4,[7][8][9][10][11][12] . Because CEO 2 is the ratio of CCO 2 to CBF, it then becames clear that CCO 2 and CBF need not be measured, because CEO 2 alone accurately informs about coupling or uncoupling between CBF and CCO 2 8,9 .…”

“…Because CEO 2 is the ratio of CCO 2 to CBF, it then becames clear that CCO 2 and CBF need not be measured, because CEO 2 alone accurately informs about coupling or uncoupling between CBF and CCO 2 8,9 . The normal CEO 2 ranges are 17-35% and 24-42% for children and adults, respectively 2,4,[8][9][10][11][12] . For therapeutic purposes, the target values are the normal means of 26% and 33%, respectively.…”

“…The latter is usually accomplished by decreasing the infusion dose by 50% at intervals of approximately 6 hours. Discontinuing the cumulative treatment protocol [9][10][11][12] should be considered no earlier than at least 4-5 days after the start of treatment. When instituting barbiturate therapy if necessary, it is obvious that the first step of the protocol (nonbarbiturate intravenous sedation) should be discontinued.…”