The purpose of this study was to identify the demographic and clinical characteristics of suicide attempts in adolescents who visit the emergency department compared to those of adults. This study included 149 children under the age of 18, and 1427 people in the age of 19–65 who came to the emergency department with suicide attempt from 2009 to 2015. We compare sociodemographic, clinical, and suicide attempt-related characteristics through Chi-square test and logistic regression analysis to evaluate the difference between two groups. In adolescents, suicide attempters had more number of previous suicide attempt history than adults. Adolescents used more non-lethal method such as poisoning of over the counter drugs and had about 5 times higher odds ratio in suicide attempts with analgesics. The motivation of suicide attempt among adolescents was more related with interpersonal problems but less with financial or illness-related problems. The intention of suicide attempt in adolescents was less serious and lethal compared to adults. Suicide attempts among adolescents had showed different from adults in method, motivation and intention. Considering the characteristics of suicide attempt among adolescent, it is necessary to keep close attention to adolescent’s suicide attempters and develop the customized intervention program to prevent the suicide attempt in this groups.

Objectives: Sustained myocardial injury is a significant predictor of mortality in carbon monoxide (CO) poisoning. There are few reports in the literature regarding the presence of CO-induced cardiomyopathy from early stages in the emergency department (ED). We prospectively investigated the early incidence of CO-induced cardiomyopathy and its patterns in patients with cardiomyopathy. Materials and methods: During a 10-month period, transthoracic echocardiography (TTE) was performed in 43 consecutive patients with CO poisoning and myocardial injury, which was defined as elevated high-sensitive troponin I within 24 h after ED arrival. Measurements of left ventricular ejection fraction and wall motion abnormalities were performed to evaluate cardiac function. If a patient had CO-induced cardiomyopathy, we measured cardiac function at the time of patient admission, day 1, day 2, and once within seven days of hospitalization. Results: The incidence of cardiomyopathy was as high as 74.4% (32 of 43 patients) in CO-poisoned patients with myocardial injury based on initial ED results. Echocardiographic patterns included non-cardiomyopathy (25.6%), global dysfunction (51.2%), and Takotsubo-like cardiomyopathy (23.2%). Patients in the global dysfunction group had significantly more normalized cardiac dysfunction within 72 h than did those in the Takotsubo-like cardiomyopathy group (81.8% vs. 22.2%, p = 0.001). Discussion and conclusion: Patients with CO poisoning and myocardial injury experienced cardiomyopathy, including reversible global dysfunction and a Takotsubo-like pattern. Investigation of cardiomyopathy needs to be considered in patients with CO poisoning and myocardial injury.

Background. In organophosphate (OP) poisoning cardiac complications may occur. However, the current body of knowledge largely consists of limited studies, and case reports are mainly on electrocardiogram (ECG) abnormalities. As definite myocardial injury is difficult to assess through ECG, we investigated the prevalence of myocardial injury through cardiac biochemical markers such as troponin I (TnI) in severe OP poisoning. Methods. We conducted a retrospective review of 99 consecutive OP insecticide poisoning cases that were diagnosed and treated at the emergency department of the Wonju Severance Christian Hospital between March 2008 and December 2013. Results. Based on Namba classification for OP poisoning, there were no patients with mild toxicity, 9 patients (9.1%) with moderate toxicity and 90 patients (90.9%) with severe toxicity. On ECG, normal sinus rhythm was most common, and ST depression and elevation were seen in 11 patients (11.1%). Elevation of TnI within 48 h was seen in 34 patients (34.3%). The median peak level and peak time of TnI were 0.305 (IQR, 0.078–2.335) ng/mL and 15 (IQR 6.9–34.4) hours, respectively. There were differences between patients with normal TnI and elevated TnI in terms of age (yrs), number of patients who were exposed to OP via the oral route, and initial Glasgow Coma Scale (GCS; 58 ± 17 vs. 66 ± 16, p = 0.015, 56 [87.5%] vs. 33 [97.1%], p = 0.048 and 12.0 [IQR, 8.0–15.0] vs. 9.0 [IQR, 5.8–12.0], p = 0.019). Conclusions. OP can cause direct myocardial injury during the acute early phase in severe OP poisoning. Monitoring of TnI may be needed in severe OP poisoning.

Glufosinate ammonium poisoning can cause neurological complications even after a symptom-free period. We prospectively investigated the predictors of neurologic complications in acute glufosinate ammonium poisoning and the change of serum ammonia level as a predictor of patient’s presence and recovery of neurologic complication. This prospective observational study collected data from consecutive patients diagnosed with acute glufosinate ammonium poisoning between September 2014 and June 2016. Serum ammonia was serially measured. The patients were divided into two groups: the neurologic complication group and the nonneurologic complication group. We also defined 25 other insecticide- or herbicide-poisoned patients as controls. The neurologic complication group included 18 patients (72.0%). The latency period for neurologic complications was within 48-h postingestion. The peak ammonia level was statistically higher in the neurologic complication group than in the control group (p < 0.001) and the nonneurologic complication groups (p = 0.001). There was a statistical difference between the nonneurologic complication group and the neurologic complication group (p = 0.0085) in terms of ingested amount. The peak ammonia was the only predictor for the development of neurologic complications (the optimal cutoff: 90 μg/dL). In patients with mental changes, the mean serum ammonia levels before and after recovery of the mental changes were statistically different (p = 0.0019). In acute glufosinate ammonium poisoning, serial serum ammonia level measurements are needed and a serum peak ammonia level greater than 90 μg/dL is a predictor of neurologic complications. Also, it is important to treat the hyperammonemia in acute glufosinate ammonium poisoning.

Kim YW, et al. J Korean Med Sci. 2015 Jun;30(6):802-807. https://doi.org/10.3346/jkms.2015.30.6.802