DOI: 10.1097/PCC.0b013e3181a0dfb0
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PMID: 19584639
Issn Print: 1529-7535
Publication Date: 2009/07/01
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Excerpt
The hemodynamic deterioration associated with CA and subsequent conventional cardiopulmonary resuscitation (C-CPR) follows four distinct phases: prearrest, no flow or untreated CA, low flow during C-CPR, and return of spontaneous circulation and the postresuscitation period (6). The low-flow phase of C-CPR can be converted into a period of improved and restored blood flow with the use of extracorporeal membrane oxygenation to support circulation and respiration, so-called extracorporeal cardiopulmonary resuscitation (E-CPR). The intervention could act as a “bridge” to effective return of spontaneous circulation in a child who would otherwise die immediately. E-CPR extends the time limit of C-CPR by providing an interval, of up to days, during which the myocardium or process that led to CA can hopefully recover. To date, a number of case series of E-CPR in children have shown survival rates above 35% (7–14). On the basis of these reports, Topjian and Nadkarni (15) concluded in a recent editorial “E-CPR (in children) has reached a ‘tipping-point’ for rapid deployment rescue of selected patients with presumed reversible underlying disease processes.” In the clinical setting the key issue, although, is the basis of our presumption for reversible pathology and, presumably, for brain recovery.
In this issue of Pediatric Critical Care Medicine, Barrett et al (16) have extended the analysis in their previously reported series and provided useful information that helps to describe the limits of reversibility and recovery in E-CPR. In a large series of children undergoing E-CPR during CA (registered on the Extracorporeal Life Support Organization registry between 1992 and 2005), they determined the prevalence and risk factors for neurologic injury. Their definition of “neurologic injury” was brain death, and brain infarction or hemorrhage. In the context of hypoxia-ischemia–related acute patterns of neurotoxicity (i.e., brain swelling, watershed infarction ± hemorrhagic conversion), the following markers of pathophysiology might occur after CA. Some patients will develop cerebral edema and progress to brain death while maintained on E-CPR, most likely those with severe hypoxia and metabolic acidosis in the prearrest phase. Some patients may have regional cerebral infarction attributable to low flow or hypoxia. Last, infarcted watershed areas may become hemorrhagic because of heparin-induced alteration in coagulation during extracorporeal membrane oxygenation. In both of these latter groups, there may be progression to brain death. In the series of 682 cases analyzed by Barrett et al, 245 patients (36%) survived to hospital discharge with no evidence of acute neurotoxicity as defined earlier. A further 16 patients (2%) survived with evidence of hypoxia-related or low-flow phase pathology, i.e., cerebral infarction or hemorrhage. There were 421 deaths (62%). Almost 70% of these deaths were, most likely, related to the lack of reversibility of the cardiopulmonary injury resulting in CA, since none had “neurologic injury.
