Unreliable Early Neuroprognostication After Severe Carbon Monoxide Poisoning Is Likely Due to Cytopathic Hypoxia: A Case Report and Discussion

Abstract

A 17-year-old girl was found unconscious in a running vehicle. She developed very severe acute respiratory distress syndrome (which was treated with rescue high-frequency oscillation), hemodynamic instability, acute kidney injury, rhabdomyolysis, and remained comatose with a Glasgow Coma Scale score of 3 and gasping respirations for 67 hours (when the Glasgow Coma Scale score improved to 6, with tachypnea to Paco 2 28 and pH 7.5). By 92 hours, she was obeying commands, and she was extubated at 96 hours, shortly after which she was conversing with family and texting on her phone. A magnetic resonance imaging (MRI) scan 6 days after being found showed subacute infarctions affecting the medial aspect of the globus pallidus bilaterally as well as a small cortical/subcortical infarction in the right parietal lobe. At a 7-week follow-up, she had no delayed-onset signs of brain injury. This case demonstrated that neurologic prognostication after carbon monoxide poisoning may be unreliable for more than 72 hours after injury. We discuss that it is possible that the mitochondrial dysfunction induced by carbon monoxide was responsible for a functional coma without irreversible brain injury, similar to the mechanism of cytopathic hypoxia in multiple-organ dysfunction that allows some other organ recovery without necrosis in survivors.

Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response

“…Even high oxygen content has toxic effects (Shykoff and Lee, 2019). One can envision respiratory and metabolic acidosis under low oxygen partial pressure (Epstein and Singh, 2001;Kao and Nañagas, 2005;Cho et al, 2008;Swenson, 2016;Kuniavsky et al, 2018;Joffe et al, 2020). It is known that hypoxia (and low pH) would lead to a shift of Hb from its high-affinity R state to the low-affinity T state.…”

Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response

“…Even high oxygen content has toxic effects (Shykoff and Lee, 2019). One can envision respiratory and metabolic acidosis under low oxygen partial pressure (Epstein and Singh, 2001;Kao and Nañagas, 2005;Cho et al, 2008;Swenson, 2016;Kuniavsky et al, 2018;Joffe et al, 2020). It is known that hypoxia (and low pH) would lead to a shift of Hb from its high-affinity R state to the low-affinity T state.…”

Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response

“…Even high oxygen content has toxic effects (Shykoff and Lee, 2019). One can envision respiratory and metabolic acidosis under low oxygen partial pressure (Epstein and Singh, 2001;Kao and Nañagas, 2005;Cho et al, 2008;Swenson, 2016;Kuniavsky et al, 2018;Joffe et al, 2020). It is known that hypoxia (and low pH) would lead to a shift of Hb from its high-affinity R state to the low-affinity T state.…”

Carbon Monoxide Signaling: Examining Its Engagement with Various Molecular Targets in the Context of Binding Affinity, Concentration, and Biologic Response

“…Even high oxygen content has toxic effects (Shykoff and Lee, 2019). One can envision respiratory and metabolic acidosis under low oxygen partial pressure (Epstein and Singh, 2001;Kao and Nañagas, 2005;Cho et al, 2008;Swenson, 2016;Kuniavsky et al, 2018;Joffe et al, 2020). It is known that hypoxia (and low pH) would lead to a shift of Hb from its high-affinity R state to the low-affinity T state.…”