Organophosphorus agents are easily absorbed via respiratory, gastrointestinal, and dermal routes, and inhibit the acetylcholine transferase enzyme, which is responsible for the majority of toxicity caused by organophosphates in the body. A comprehensive search was conducted across three prominent databases (Google Scholar, PubMed, and Science Direct) to identify relevant articles. The search focused on the keywords “MgSO4” or “magnesium sulfate” in conjunction with “organophosphate” or “organophosphate poisoning.” Inhibition of acetylcholine transferase enzyme results in the accumulation of acetylcholine in synapses and the stimulation of cholinergic receptors. As several studies have shown that magnesium sulfate (MgSO4) can inhibit the release of acetylcholine in the central and peripheral sympathetic and parasympathetic synapses, this study reviews the role of MgSO4 in the treatment of organophosphorus poisoning. The intravenous administration of MgSO4 exhibits favorable tolerability and clinical efficacy in alleviating cardiac toxicity associated with organophosphorus poisoning.
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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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Horse chestnut (Aesculus hippocastanum) is a common tree found on roads and parks. The shape of the fruit is very similar to that of the edible Korean chestnut (Castanea crenata); thus, people can eat it by mistake. However, reports of the side effects and toxicity from ingestion are very rare. A 46-year-old male who had no unusual findings in the past had eaten horse chestnut seed which he had mistaken to be Korean chestnut. He visited the emergency department (ED) with complaints of epigastric pain, nausea, and sweating. Blood tests showed a slight increase in the levels of liver enzymes, serum amylase, and pancreatic amylase. During the monitoring, he complained of palpitations, and electrocardiogram showed atrial fibrillation. On the following day after conservative treatment, blood testing and electrocardiogram showed normal findings. He was discharged from the ED as he did not complain of any further symptoms. When a patient who has eaten horse chestnut visits the ED, blood examination and electrocardiogram monitoring are needed, and conservative treatment is required.
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Objective The number of deaths due to acute poisoning (AP) is on the increase. It is crucial to predict AP patient mortality to identify those requiring intensive care for providing appropriate patient care as well as preserving medical resources. The aim of this study is to predict the risk of in-hospital mortality associated with AP using an artificial neural network (ANN) model.
Methods In this multicenter retrospective study, ANN and logistic regression models were constructed using the clinical and laboratory data of 1,304 patients seeking emergency treatment for AP. The ANN model was first trained on 912/1,304 (70%) randomly selected patients and then tested on the remaining 392/1,304 (30%). Receiver operating characteristic curve analysis was used to evaluate the mortality prediction of the two models.
Results Age, endotracheal intubation status, and intensive care unit admission were significant predictors of mortality in patients with AP in the multivariate logistic regression model. The ANN model indicated age, Glasgow Coma Scale, intensive care unit admission, and endotracheal intubation status were critical factors among the 12 independent variables related to in-hospital mortality. The area under the receiver operating characteristic curve for mortality prediction was significantly higher in the ANN model compared to the logistic regression model.
Conclusion This study establishes that the ANN model could be a valuable tool for predicting the risk of death following AP. Thus, it may facilitate effective patient triage and improve the outcomes.
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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 This study aimed to compare the diagnostic performance of cardiac biomarkers and to evaluate the optimal cut-off values for echocardiographic cardiac injury prediction in patients with carbon monoxide (CO) poisoning.
Methods This retrospective observational cohort study included adult patients with acute CO poisoning. Patients who did not undergo transthoracic echocardiography, which was used to define patients with cardiac injury (ejection fraction <55%), were excluded. The area under the curve was used to evaluate diagnostic performance for cardiac injury prediction. Mann-Whitney U, chi-square, and Fisher exact tests were used to analyze data.
Results After excluding the 27 patients who did not undergo echocardiography, 114 patients were included in the study. Fifteen (13.2%) patients had cardiac injury. The area under the curve values for the B-type natriuretic peptide, creatine kinase-myocardial band, and troponin I were 0.711 (95% confidence interval [CI], 0.527–0.895; P=0.011), 0.766 (95% CI, 0.607–0.926; P=0.001), and 0.801 (95% CI, 0.647–0.955; P<0.001), respectively, with optimal cut-off values of 330 pg/mL, 10.1 ng/mL, and 0.455 ng/mL, respectively. The sensitivity, specificity, and positive and negative predictive values of troponin I were 67%, 91%, 53%, and 95%, respectively.
Conclusion Troponin I showed the best diagnostic performance for predicting cardiac injury in patients with CO poisoning. A cut-off value of 0.455 ng/mL appeared optimal for cardiac injury prediction. However, further studies on cardiac biomarkers and other diagnostic tools in CO poisoning are needed given the low sensitivity of troponin I.
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Carbon dioxide is widely used for a variety of purposes. As it is a normal constituent of air, the public generally regards it as safe. Although low concentrations of carbon dioxide are not harmful to human beings, high concentrations are toxic, and can cause serious harm, including cardiac arrest. Only a limited number of cases of carbon dioxide intoxication have been reported in Korea, and they have all been mild, with no cases of cardiac arrest following acute exposure to high concentrations of carbon dioxide, reported previously. We describe a case of carbon dioxide poisoning following an explosion of a carbon dioxide tank, which led to cardiac arrest in a 66-yearold patient. This cardiac arrest could have been avoided if the patient was fully aware of the hazardous effects and serious consequences of exposure to high concentrations of carbon dioxide.
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Objective We aimed to analyze the differences in epidemiological aspects and clinical courses of acute poisonings in each region of the Gyeonggi-do province in Korea.
Methods This retrospective study analyzed data from the National Emergency Department Information System of Korea. We retrospectively reviewed cases of acute poisonings between April 2006 and March 2015 recorded at 13 emergency departments in eight different cities of Gyeonggi-do province in Korea. The differences in the incidence, age distribution, causative agent, and clinical course of poisonings among regions were the main outcomes measured.
Results The proportion of poisonings in the ≤9 age group was high in Yongin (17.44%) and that in ≥65 age group was high in Gwangmyeong (21.76%). The proportion of cases involving carbon monoxide was high in Ansan (8.82%) in patients hospitalized and the proportion of cases involving pesticides was high in Pyeongtaek (52.78%) in patients admitted to the intensive care unit. The admission rate of poisoned patients was high in Osan (36.02%).
Conclusion In this study, differences in the characteristics of poisoned patients between 8 cities were noted. Therefore, hospitals need to arrange treatment resources for poisoned patients according to the characteristics of the specific region. The results of this study may serve as evidence for new strategies to prepare for the acute poisonings in hospitals.
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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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Objective The effect of induced hypothermia on severe acute carbon monoxide (CO) poisoning remains to be addressed further. We investigated the effect of induced hypothermia on severe acute CO poisoning.
Methods Retrospective chart review was conducted for patients who diagnosed as severe acute CO poisoning in emergency department and underwent induced hypothermia from May 2013 to May 2014. Hospital courses with critical medication and major laboratory results were investigated through the chart review.
Results Among total 227 patients with acute CO poisoning during the period of study, patients with severe acute CO poisoning were 15. All patients underwent induced hypothermia with a temperature goal 33°C. Initial and follow-up levels of S100B protein after induced hypothermia were 0.47 μg/L (interquartile range, 0.11 to 0.71) and 0.10 μg/L (interquartile range, 0.06 to 0.37), respectively (P = 0.01). The mean Glasgow Coma Scales at emergency department admission was 6.87 ± 3.36. Except 1 patient who expired after cardiopulmonary resuscitation, Glasgow Coma Scales at 30-day of hospital discharge were 15 in 10 patients (71.4%), 14 in 1 patient (7.1%), 13 in 1 patient (7.1%), and 6 in 2 patients (14.2%). Seven patients (46.7%) developed delayed neurologic sequelae. Four patients showed mild types of delayed neurologic sequelae and 3 showed moderate to severe types of delayed neurologic sequelae.
Conclusion Most of patients underwent induced hypothermia had a good recovery from severe acute CO poisoning. Therefore, induced hypothermia may be considered as a possible treatment in severe acute CO poisoning.
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