Strangulation Injuries in Children. Part 2. Cerebrovascular Hemodynamics

Abstract

The cerebrovascular hemodynamics were recorded in two children with comparable hypoxic-ischemic injuries after strangulation. Monitoring was initiated within 13 hours of injury and continued for at least 38 hours. The profile included continuous measurements of cortical regional cerebral blood flow (rCBF) with a subdural thermal diffusion probe, intracranial pressure, mean arterial pressure, and expired CO2 tension. Data sets were obtained every 15 minutes or every 5 minutes during epochs of hyperventilation and inotropic support. Arterial CO2 and oxygen content and pH and, in the second patient, cardiac output (and cardiac index) were determined every 3 to 6 hours. Both children showed cortical hyperemia with a gradual rise of rCBF during the study; neither child showed elevated intracranial pressure. Mean CO2 reactivities were 1.8 and 2.1 mL/100 g/minute/mm Hg, with gradual elevations during the study. Mean cerebrovascular resistances were 0.7 and 0.9 mL/100 g/minute/mm Hg, respectively. Dissociative vasoparalysis with loss of autoregulation and preservation of CO2 reactivity was observed in both children. In the second child, during two periods of hyperventilation, an inverse steal occurred with rCBF indirectly related to expired CO2 tension; the rCBF was not related to changes in cardiac output or cardiac index. Neurologic outcome was not related to mean levels of rCBF, CPP, and CO2 reactivity, or clinical dissociative vasoparalysis. Lower initial and mean values of rCBF and an inverse steal after hyperventilation were associated with a poor outcome in the second patient.

Anoxic Injury-Associated Cerebral Hyperperfusion Identified with Arterial Spin-Labeled MR Imaging

“…Previous studies have shown up to a 200% increase in CBF as PCO 2 increases to values similar to case 6 (PCO 2 , 54). [18][19][20][21][22][23][24][25][26] We believe that the global hyperperfusion in case 6 is a result of hypercapnia rather than anoxia.…”

“…17,18,20,[27][28][29] Autoregulation of CBF maintains the relationship CBF ϭ CPP/CVR, where CPP is cerebral perfusion pressure and CVR is cerebral vascular resistance. As long as the cerebral arterioles can constrict and dilate to modulate CVR, they can accommodate a range of cerebral perfusion pressures and maintain constant CBF.…”

“…17,27,28 Little human research exists regarding the effect of global anoxia on autoregulation. 4,20,[29][30][31][32][33][34][35][36][37] Animal models have shown a loss of cerebral vascular resistance in the postanoxic state resulting in uncontrolled hyperperfusion. [38][39][40][41][42] Cerebral blood volume has been shown to increase with loss of autoregulation secondary to ischemia, but no large studies have demonstrated a similar relationship for CBF.…”

“…We believe that a similar loss of autoregulation accounts for the cerebral hyperperfusion seen in our ASL patient series. 20,36,38 Xenon-CT perfusion has been used to evaluate CBF after cardiac resuscitation. A study by Cohan et al 4 showed an increase in global whole-brain CBF by up to 300% in nonsurviving patients.…”

“…Currently the finding of global hyperperfusion associated with anoxic injury is an ominous sign and portends a poor outcome. 2,4,20,50 The superphysiologic perfusion shown on ASL may open a door to further research opportunities aimed to improve outcome and establish treatment guidelines for global anoxic injuries. 51 …”