Serum phosphate is not an early predictor of neurocognitive outcomes in acute carbon monoxide poisoning patients

Abstract

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. MethodsWe 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. ResultsData 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). ConclusionSerum phosphate level measured in the ED did not predict poor neurocognitive outcomes 1 month after CO poisoning.

Correlation between Carboxyhemoglobin Levels Measured by Blood Gas Analysis and by Multiwave Pulse Oximetry

“…In laboratory tests, the median COHb level in blood gas analysis was 10.1% (IQR, 4.6-19.5). The median COHb level in multiwave pulse oximetry was 11% (IQR, [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19]. The median Troponin I level was 0.01 ng/mdL (IQR, 1-3.1).…”

“…Additionally, it initiates the generation of free radicals, leading to acute tissue damage in the brain, heart, and other organs [4,8,18]. Although there is no well-defined diagnostic criteria, survivors of severe acute poisoning have reported delayed neuropsychiatric sequelae characterized by symptoms such as memory loss, impaired concentration or language abilities, mood changes including depression, and symptoms resembling Parkinson's disease [4,5,8,12,[18][19][20][21]. These sequelae are reported to arise 3 to 240 days after apparent recovery, generally occurring within 20 days of CO poisoning [22][23][24].…”

Predicting acute brain lesions on magnetic resonance imaging in acute carbon monoxide poisoning: a multicenter prospective observational study

“…Therefore, preventing DNS occurrence has become a major goal of CO poisoning treatment. The search for predictive factors of DNS occurrence have yielded inconsistent results across studies, with varying degrees of accuracy 13 , 14 . A recent study suggested that the presence of an acute brain lesion (ABL) on magnetic resonance imaging (MRI) is strongly associated with an increased risk of DNS occurrence, with patients who exhibit ABLs on MRI having a 14-fold greater risk of DNS occurrence compared to those without ABLs 15 .…”