Objective Carbon monoxide (CO) poisoning causes brain injury by hypoxia and inflammatory mechanisms. Hypoxic conditions result in increased serum phosphate concentration due to loss of polarity of the cell membrane, changes in membrane fluidity, and consequent destruction of phospholipids in the cell membrane. This study aimed to evaluate whether serum phosphate measured in the emergency department (ED) can serve as an early predictor of neurocognitive sequelae 1 month after acute CO poisoning.
Methods We included patients ≥16 years with acute CO poisoning from a cohort who were treated at a single tertiary academic hospital in Wonju, Korea, between January 2006 and May 2021. Neurocognitive outcome was assessed using the Global Deterioration Scale score; patients were classified into favorable (1–3 points) or poor (4–7 points) neurocognitive outcome groups based on this score. These two groups were compared before and after propensity score matching.
Results Data from 888 patients were analyzed. Seven hundred seventy-one patients (86.8%) were assigned to the favorable outcome group and 117 patients (13.2%) to the poor outcome group. Patients with a poor outcome had a higher mean serum phosphate level than those with a favorable outcome (3.9 mg/dL vs. 3.5 mg/dL, P=0.001). Propensity score matching yielded 85 matched patient pairs. After matching, serum phosphate level in the ED was not significantly different between the favorable and poor outcome groups (3.9 vs. 3.7 mg/dL, P=0.349).
Conclusion Serum phosphate level measured in the ED did not predict poor neurocognitive outcomes 1 month after CO poisoning.
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Objective Carbon monoxide (CO) activates intravascular neutrophils through platelet-neutrophil aggregates, which cause neutrophil degranulation. This process causes the release of myeloperoxidase (MPO), proteases, and reactive oxygen species. The MPO index (MPXI) is a newly reported inflammatory marker that reflects the MPO level within neutrophils. The MPXI in conditions associated with neutrophil activation depends on the net effect of azurophil degranulation. This study aimed to determine whether the MPXI can predict neurocognitive prognosis 1 month after acute CO poisoning.
Methods We included patients aged ≥16 years with acute CO poisoning from a cohort at a single tertiary academic hospital in Wonju, Korea, between January 2010 and May 2021. Data from 699 patients were analyzed. The neurocognitive outcome was assessed using Global Deterioration Scale scores and classified as favorable (score, 1–3 points) or poor (score, 4–7 points). The MPXI was determined within 1 hour of arrival to the emergency department.
Results Among the 699 patients, 52 (7.4%) showed poor outcomes. The median MPXI of the patients in the poor outcome group was higher than that of the favorable outcome group (0.85 vs. 0.2, P=0.189). However, a significant difference was not found between the favorable and poor outcome groups, and MPXI was not a significant variable in multivariate logistic regression.
Conclusion The MPXI evaluated in the emergency department did not differ based on neurocognitive outcome at 1 month after acute CO poisoning.
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Objective To analyze the incidence patterns of nervous system diseases in survivors of carbon monoxide (CO) poisoning using nationwide claims data from South Korea.
Methods A national cohort was abstracted from a database that includes patients diagnosed with CO poisoning between January 2012 and December 2018. For all nervous system diseases, we investigated the frequency, pattern of incidence, effect of intensive care unit admission, and the standardized incidence ratios (SIRs) to estimate the risk of nervous system disease after CO poisoning.
Results Of 26,778 patients, 18,720 (69.9%) were diagnosed with nervous system diseases after CO poisoning. The most common disease was disorders of sleep initiation and maintenance (n=701, 3.74%), followed by tension-type headache (n=477, 2.55%) and anoxic brain injury (n=406, 2.17%). Over half of the nervous system diseases occurred within the first year after CO poisoning. The cumulative hazard ratio for nervous system diseases in patients admitted to the intensive care unit was 2.25 (95% confidence interval [CI], 2.07–2.44). Among the frequent nervous system diseases after CO poisoning, patients had a higher risk of disorders of initiating and maintaining sleep (SIR, 1.61; 95% CI, 1.52–1.71), tension-type headache (SIR, 2.41; 95% CI, 2.23–2.61), anoxic brain injury (SIR, 58.76; 95% CI, 53.95–63.88), and post-zoster neuralgia (SIR, 1.94; 95% CI, 1.70–2.20).
Conclusion Patients who experience CO poisoning are at higher risk for several nervous system diseases. Therefore, monitoring for specific nervous system diseases is important after CO poisoning within the first year.
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Objective Reliable biomarkers of delayed neuropsychological sequelae (DNS) after acute carbon monoxide (CO) poisoning are lacking. This study investigated the associations between potential serum markers and the development of DNS after acute CO poisoning.
Methods Retrospective chart reviews were conducted for patients diagnosed with acute CO poisoning during a 28-month period. The patients were divided into two groups according to the presence or absence of having developed DNS. Multivariate analysis was performed to identify predictors of DNS after CO poisoning.
Results Of a total of 102 patients, 10 (9.8%) developed DNS. The levels of serum osmolarity, S100B protein, and serum lactate, as well as serum anion gap, were statistically significant in univariate analysis. Multiple logistic regression analysis showed that anion gap (adjusted odds ratio [AOR], 1.36; 95% confidence interval [CI], 1.11 to 1.88), serum lactate level (AOR, 1.74; 95% CI, 1.26 to 2.75), and serum S100B protein level ([AOR, 7.02×105; 95% CI, 4.56×102 to 9.00×1010] in model 1, [AOR, 3.69×105; 95% CI, 2.49×102 to 2.71×1011] in model 2) were independently associated with DNS development.
Conclusion Based on our preliminary results, serum lactate level, serum anion gap, and serum S100B protein level in the emergency department could be informative predictors of DNS development in patients with acute CO poisoning. These markers might have the potential to improve early recognition of DNS in patients with acute CO poisoning.
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