Serum markers and development of delayed neuropsychological sequelae after acute carbon monoxide poisoning: anion gap, lactate, osmolarity, S100B protein, and interleukin-6

Abstract

ObjectiveReliable 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.MethodsRetrospective 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.ResultsOf 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.ConclusionBased 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.

S-100β in predicting the need of hyperbaric oxygen in CO-induced delayed neurological sequels

“…57 Follow-up of our patients for 6 months after discharge showed that DNS manifestations were reported by six patients (12%), which is nearly similar to the rates (14-16.5%) reported by previous studies. 46,47,58,59 However, both higher rates (24.1-26%) 21,60 and lower rates of DNS (9.8%) 23 were also found in other studies. These discrepancies in the incidence of DNS among the studies may be due to various factors such as the age of the studied patients, the duration of exposure to CO, the delay before receiving medical care, and the concentration of the gas.…”

“…Also, Di et al 67 and Hassan et al 46 reported that serum S-100b levels were significantly higher in patients with DNS. Kim et al 23 found that serum S-100b protein level was independently associated with DNS. However, Ide et al 45 and Rasmussen et al 44 argued that serum measurements of S-100b protein could not be used for predicting CO-induced DNS as the blood-brain barrier is not compromised.…”

“…Therefore, prevention of this complication is a target goal in the treatment of CO poisoning. [21][22][23] Brain hypoxia that ensues due to CO poisoning results in oxidative stress, necrosis, apoptosis, 24 lipid peroxidation, and reversible CNS demyelination. 25 Further damage to the CNS is produced by COactivated neutrophils that produce reactive oxygen species.…”

“…Moreover, hyperbaric oxygen (HBO) therapy was recommended in patients with severe CO poisoning due to its beneficial effect in preventing inflammatory changes in the brain and lipid peroxidation, consequently reducing the DNS rates. 5,23,31 A meta-analysis showed that there was no significant difference in neurologic sequels in four out of six randomized controlled trials that investigated the use of HBO for the treatment of CO exposures. 32 The indications for HBO therapy in acute CO poisoning comprise various clinical manifestations and laboratory tests, including loss of consciousness, neurological deficits, significant metabolic acidosis, and COHb level above 25%.…”

“…S-100b, glial fibrillary acidic protein, and neuron-specific enolase) for the prediction of DNS occurrence. 23,34 The S-100b protein is a calciumbinding protein found in high concentrations in astroglial cells. It regulates calcium-dependent signaling in neuronal differentiation, outgrowth, and apoptosis.…”