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The roles of childhood abuse and interleukin (IL)-1β levels, a representative pro-inflammatory cytokine, in suicidal behavior are unclear. This study investigated the main and interactive effects of childhood abuse and IL-1β levels on suicidal behavior in patients with a depressive disorder before and after pharmacological treatment.At baseline, exposure to self-reported childhood abuse, including emotional, physical, and sexual abuse, before the age of 16 years, and IL-1β levels, were measured in 1,094 outpatients with a depressive disorder, 884 of whom were followed for 1 year. Suicidal behavior was evaluated, including previous suicide attempts (at baseline), suicidal ideation (at baseline and follow-up), and fatal/non-fatal suicide attempts (at follow-up). The main and interaction effects of self-reported childhood abuse and IL-1β level on the four types of suicidal behavior were analyzed using logistic regression after adjusting for covariates.Individual associations of self-reported childhood abuse were significant only with previous suicidal attempt but not with other suicidal behaviors. There was no significant association of plasma IL-1β level with any suicidal behavior. There were significant interactive associations of self-reported childhood abuse and a high IL-1β level on previous suicide attempts, baseline suicidal ideation, and fatal/non-fatal suicidal attempts during follow-up.Suicidal behavior in patients with a depressive disorder could be influenced by considering the interactive effect of childhood abuse and IL-1β levels. Our study suggests that childhood trauma and biochemical factors play roles in the pathology of suicide in depressed patients.

Neurotoxicity related to glufosinate ammonium is known to occur after a latent period of 4-60 hr following ingestion of this herbicide. However, neurotoxicity is difficult to predict in the emergency department (ED) and only a few parameters are known to be useful to indicate development of neurotoxicity. Determination of a systemic inflammation parameter such as the neutrophil to lymphocyte ratio (NLR), is a rapid and simple method which was found to be a prognostic marker in various clinical conditions such as sepsis, cardiac disorders, stroke, and cancer. Therefore, the aim of this study was to determine whether the NLR might predict neurotoxicity and be used at ED to detect neurotoxicity induced following glufosinate ammonium poisoning in admitted patients. This retrospective observational study collected data from consecutive patients diagnosed with acute glufosinate ammonium poisoning between January 2005 and December 2020. The primary outcome was development of neurotoxicity following acute glufosinate ammonium poisoning. Out of the 72 patients selected 44 patients (61.1%) exhibited neurotoxic symptoms. Neurotoxicity appeared with an approximate latent period of 12 hr. The NLR was significantly higher in the group displaying neurotoxicity. Multivariable analysis showed that the NLR was significant in predicting neurotoxicity. The NLR was independently associated with neurotoxicity initiated by glufosinate ammonium. Therefore, the use of the NLR might help clinically to readily and rapidly predict development of neurotoxicity associated with glufosinate ammonium at the ED.

Since glufosinate irreversibly inhibits glutamine synthetase, leading to intracellular accumulation of ammonia, hyperammonemia is considered one of the main mechanisms of glufosinate ammonium toxicity in humans. However, whether hyperammonemia causes neurotoxicity has not yet been studied. Therefore, the purpose of this study was to determine whether the serum ammonia level is elevated before the development of neurotoxicity. In this retrospective observational study, we analyzed data from consecutive patients diagnosed with acute glufosinate ammonium poisoning. The primary outcome was the development of neurotoxicity following the poisoning. Patients who developed neurotoxicity were characterized by higher initial ammonia levels compared to patients without neurotoxicity (121.0 µg/dL [87.0; 141.0] vs 83.0 µg/dL [65.0; 119.0], p 0.01). However, there was no increase in ammonia levels over time in both the asymptomatic and neurotoxicity groups when serial serum ammonia levels were examined from emergency department admission to hospital discharge. In addition, there was no statistically significant difference between the peak ammonia levels in the asymptomatic group and the peak ammonia levels before symptom onset in the neurotoxicity group (135.0 µg/dL [109.0; 158.0] vs 144.0 µg/dL [120.0; 189.0], p = 0.15). Following the onset of neurotoxicity, the serum ammonia level increased significantly (125.0 [111.0; 151.0] µg/dL to 148.0 [118.0; 183.0] µg/dL, p 0.01). In conclusion, hyperammonemia cannot be assumed as the cause of neurotoxicity in glufosinate ammonium poisoning and further research is needed to examine the exact mechanism of GA poisoning.

The objective was to describe the prevalence of derangement of the partial pressure of arterial carbon dioxide (PaCO2) and to determine the association between PaCO2 and adverse cardiovascular events (ACVEs) in carbon monoxide (CO)-poisoned patients. Additionally, we evaluated whether the derangement of PaCO2 was simply secondary to metabolic changes. This retrospective study included 194 self-breathing patients after CO poisoning with an indication for hyperbaric oxygen therapy and available arterial blood gas analysis at presentation and 6 h later. The incidence rate of hypocapnia at presentation after acute CO poisoning was 67.5%, and the mean PaCO2 during the first 6 h was 33 (31–36.7) mmHg. The most common acid–base imbalance in 131 patients with hypocapnia was primary respiratory alkalosis. The incidence rate of ACVEs during hospitalization was 50.5%. A significant linear trend in the incidence of ACVEs was observed across the total range of PaCO2 variables. In multivariate regression analysis, mean PaCO2 was independently associated with ACVEs (odds ratio 0.051; 95% confidence interval 0.004–0.632). PaCO2 derangements were common after acute CO poisoning and were not explainable as a mere secondary response to metabolic changes. The mean PaCO2 during the first 6 h was associated with ACVEs. Given the high incidence of ACVEs and PaCO2 derangement and the observed association between the mean PaCO2 and ACVEs, this study suggests that (1) PaCO2 should be monitored in the acute stage to predict and/or prevent ACVEs and (2) further investigation is needed to validate this result and explore the early manipulation of PaCO2 as a treatment strategy.

Our objective was to determine how much PaO2 levels increase after normobaric oxygen (NBO) therapy and whether NBO therapy exerts therapeutic effects regardless of the PaO2 level. We suggest the optimal PaO2 level to use during NBO therapy for the acute treatment of carbon monoxide (CO) poisoning. This retrospective study included 311 patients who received oxygen administration after CO poisoning and had a measurable PaO2 level upon arrival. Baseline characteristics, clinical courses and long-term neurological outcome were collected and compared. The PaO2 level upon arrival was 192 (161-225) mm Hg, and 272 (87.5%) of the patients presented with hyperoxia. The incidence of poor long-term neurological outcome was 11.3% at a median follow-up period of 35 months. PaO2 levels upon arrival were higher in patients with good long-term neurological outcome than in those with poor outcome. The incidence of poor long-term neurological outcome was significantly dependent on the PaO2 level when patients were stratified at 100-mm Hg increments. A multivariate regression analysis showed that PaO2 levels, when considered a continuous, interval or ordinal variable, were associated with long-term neurological outcome in separate models. According to the three models, a PaO2 level of 200-300 mm Hg has the lowest risk of poor long-term neurological outcome. The results of the analysis of the predicted probability of poor long-term outcome according to the PaO2 level exhibited a U-shaped curve. Further large-scale studies are needed to confirm the association between 200-300 mm Hg of PaO2 and long-term neurological outcome and evaluate the impact of PaO2 levels above 300 mm Hg on acute CO poisoning outcome.

Background: The effects of serum folate levels on suicidal behavior, strongly associated with depression, have not been investigated. Therefore, this study investigated the associations between serum folate levels and suicidal behavior in patients with depressive disorders.Methods: Serum folate levels were measured at baseline in 1,094 patients with depressive disorder, 884 of whom were followed during a 12-month period of stepwise pharmacotherapy. Suicidal behaviors evaluated at baseline were (i) previous suicide attempt and (ii) baseline suicidal severity; behaviors evaluated at follow-up were (iii) increased suicidal severity and iv) fatal/non-fatal suicide attempt. Associations of serum folate levels with four types of suicidal behaviors were analyzed using logistic regression models after adjustment for relevant covariates; they were also examined using area under receiver operating characteristic (AUROC) curve analyses.Results: Reduced serum folate levels (Conclusions: Serum folate levels could serve as a biomarker of suicidal behavior in depressive patients. However, it should be used as an adjunct rather than a substitute for prediction of suicidal behavior considering its low prognostic values. Further replication studies are needed for its clinical utilization.

This study aimed to assess the feasibility of using the plasma neutrophil gelatinase-associated lipocalin (NGAL) level at the time of presentation in the emergency department (ED) to predict acute kidney injury (AKI) and the long-term neurological outcomes of acute charcoal-burning carbon monoxide (CO) poisoning. This retrospective study included 260 patients who suffered acute charcoal-burning CO poisoning. The median plasma NGAL concentration at the time of presentation in the ED after acute charcoal-burning CO poisoning was 78 (54–115) ng/ml. The NGAL level was an independent predictor of AKI development and could be used to stratify the severity of AKI. However, the area under the receiver operating characteristic curve (AUC) of the predictive model for AKI that included both the plasma NGAL level and clinical parameters was comparable to that of the predictive model including only the clinical parameters. The plasma NGAL level at the time of presentation in the ED was an independent factor predicting long-term neurological outcomes in patients who did not develop AKI. In these patients, the plasma NGAL level significantly improved the predictive accuracy of the model when used in combination with clinical parameters. In contrast, the plasma NGAL level was not associated with long-term neurological outcomes in patients who developed AKI. Measurement of the plasma NGAL level at the time ED presentation might improve the prediction of long-term neurological outcomes in patients who do not develop AKI after acute charcoal-burning CO poisoning. However, it might not offer additional benefit for AKI prediction compared to previously used markers.

AIM This study aimed to identify whether quick sequential organ failure assessment (qSOFA) performed immediately upon arrival can predict the outcome of patients with glyphosate surfactant herbicide (GlySH) poisoning. METHODS Adult patients with GlySH poisoning between January 2006 and April 2017 were included in this retrospective observational study. The qSOFA score (respiratory rate ≥22 breaths per minute, systolic blood pressure

Growing evidence indicates that inflammation is associated with neurological sequelae after CO poisoning. Several scores incorporating the peripheral complete blood cell (CBC) count have been introduced as indicators of systemic inflammation. This study investigated whether these scores can improve the predictive accuracy for long-term neurological outcome of acute carbon monoxide (CO) poisoning. Two hundred seventy-nine patients who suffered from acute CO poisoning were included. Data on the demographic details, serial peripheral CBC counts and scores based on peripheral CBC counts (neutrophil-lymphocyte ratio (NLR), monocyte-lymphocyte ratio (MLR), platelet-lymphocyte ratio (PLR), systemic immune inflammation index [SII]) over the first 12 hours after presentation together with the clinical course during hospitalization and long-term neurological outcome were collected. Both a multivariate logistic regression model with only significant univariate predictors and a model with univariate predictors plus each score for long-term neurological outcome were constructed. Patients with a poor long-term neurological outcome had higher neutrophil and monocyte counts and lower lymphocyte counts over the first 12 hours after admission than patients with a good outcome. The diagnostic performance of the NLR, MLR and SII over the first 12 hours for predicting long-term neurological outcome was acceptable. These scores at presentation were independently associated with the long-term neurological outcome. Among these scores, only the SII at presentation significantly improved the predictive accuracy of the model when combined with clinical parameters (AUC 0.949, 95% CI 0.916-0.972 vs AUC 0.923, 95% CI 0.884-0.952 for the model with clinical parameters only, P = 0.0476). The optimal cut-off value for SII at presentation was 1012.2, resulting in a sensitivity of 97% (84.2%-99.9%) and specificity of 64.6% (58.2%-70.6%). The SII at presentation could significantly improve the prognostic accuracy for predicting the long-term neurological outcome in patients with acute CO poisoning. Because the SII is an inexpensive and easily measurable parameter, it might be used as a prognostic tool in clinical fields.

Background In the absence of ST-segment elevation (STE) in post-return of spontaneous circulation (ROSC) electrocardiogram (ECG), coronary angiography (CAG) is required in patients with suspected coronary artery disease (CAD). However, it is a challenge to identify patients with CAD after cardiac arrest (CA). Recent European Society of Cardiology guidelines recommends transthoracic echocardiography in patients presenting with cardiac arrest. We aimed to assess the diagnostic value of regional wall motion abnormalities (RWMAs) on transthoracic echocardiography (TTE) compared to ECG in diagnosing significant coronary artery stenosis in CA patients. Methods This is a retrospective, observational study of adult CA patients with presumed cardiac etiology who underwent CAG from a single tertiary care hospital. We compared the predictive value of RWMA on TTE and STE on ECG in significant stenosis of ≥70% of the coronary artery diameter. The primary outcome was significant stenosis on CAG. Results There were 145 patients included in this study and CAG revealed significant stenosis in 76 (52.4%) patients. Among the 76 patients with significant stenosis, 68 (89.5%) had RWMA on TTE and 41 (54.0%) had STE. RWMA on TTE (OR 3.67; 95% CI 1.52–8.85) was independently associated with significant stenosis. Combining both RWMA on TTE and STE on ECG improved performance in the receiver operating characteristic curve analysis (area under the curve 0.722) for predicting significant stenosis compared to using only ECG alone (p = 0.001). Conclusions RWMAs on TTE was independently associated with significant stenosis. The RWMA and STE combination had better predictive performance than using only STE on ECG to predict significant stenosis.

This retrospective study investigated whether the serum albumin (SA) concentration at presentation is associated with mortality and the mechanism underlying the association. This study enrolled 217 patients poisoned with organophosphate (OP). Hypoalbuminemia (albumin

Aconitine belongs to the Aconitum alkaloids and is a natural toxic substance. Aconitine has been used as a traditional medicine in East Asian culture. Today, aconitine is still in use with or without a prescription, in the Republic of Korea. Here we present a case report of accidental death due to acute aconitine poisoning. An 81-year-old woman ingested liquid that had been heat extracted from the root of the Aconitum plant; she presented to the emergency room 1 h after ingestion. Her electrocardiogram showed irregular ventricular arrhythmias including ventricular tachycardia; she progressed to cardiac arrest. Cardiopulmonary resuscitation and anti-arrhythmic drugs were administered, but the patient did not survive. An autopsy was performed 2 days postmortem. Toxicological analysis was performed, and aconitine was detected by liquid chromatography tandem mass spectrometry. The antemortem blood concentration of aconitine was 39.1 ng/ml and the concentrations of aconitine in the postmortem cardiac blood, peripheral blood, cerebrospinal fluid (CSF), pericardial fluid, and urine were 21.1 ng/ml, 28.6 ng/ml, 6.8 ng/ml, 24.1 ng/ml, and 67.4 ng/ml, respectively. This is the first forensic case report of an aconitine poisoning death in the Republic of Korea with quantitative measurement of aconitine in the antemortem blood and various postmortem body fluids. To the best of our knowledge, this is the first report of the detection of aconitine in the CSF. These data about the distribution of aconitine in the antemortem blood and various postmortem body fluids is helpful for future aconitine poisoning death cases.

Purpose This study investigated the predictive factors for progression from seizure-related endosulfan poisoning to status epilepticus (SE) and refractory SE (RSE). This study also investigated delayed neurologic sequelae in seizure-related endosulfan poisoning. Methods This retrospective, observational case series consisted of 73 patients who developed at least one seizure after endosulfan ingestion. Results The progression rates from seizure-related endosulfan poisoning to SE and from SE-related endosulfan poisoning to RSE were 78.1% and 54.4%, respectively. The SE and RSE fatality rates were 19.2% and 41.9%, respectively. No patients reported the development of delayed neurological sequelae at least six months after discharge. Glasgow coma scale (GCS) score were identified as an independent factor for progression from seizure-related endosulfan poisoning to SE and from SE-related endosulfan poisoning to RSE. Lorazepam administration was independently associated with preventing progression from SE-related endosulfan poisoning to RSE. Conclusion Seizure-related endosulfan poisoning had higher progression rates to SE and RSE and higher fatality rates than other drug-induced seizures. However, delayed neurologic sequelae after discharge were not demonstrated. Due to the high progression rates from seizure-related endosulfan poisoning to SE and RSE and the absence of an established treatment for SE-related endosulfan poisoning, physicians should aggressively treat patients who experience a seizure after endosulfan poisoning and who present with decreased GCS score. Lorazepam should be considered a first-line anti-epileptic drug for controlling seizures in patients with endosulfan poisoning.

Objectives: This study investigated whether alcohol influences the predictive value of initial blood lactate concentration and Glasgow Coma Scale (GCS) score at presentation for the severity of acu...

To assess myocardial injury related to acute carbon monoxide (CO) poisoning, serial troponin I is measured in patients not presenting with troponin I elevation. This retrospective study investigated whether parameters related to white blood cell (WBC) counts (total and differential WBC counts, neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio) improved predictive accuracy for troponin I elevation (> 0.04 ng/ml) in patients not presenting with evidence of myocardial injury. Serial parameters, troponin I values, and clinical courses were collected in 241 patients. Troponin I was elevated in 33 (13.7%) patients after hospitalization. The median lag times to troponin I elevation in patients with undetectable and detectable troponin I (0.015 ng/ml ≤ troponin I ≤ 0.04 ng/ml) at presentation were 5.9 h and 3.0 h, respectively. Patients with troponin I elevation after presentation had higher total WBC and neutrophil counts and NLRs and a lower lymphocyte count during the first 4 h after presentation than patients without troponin I elevation during hospitalization. Total WBC count, neutrophil count, and log NLR at presentation were selected as independent predictive factors for troponin I elevation after presentation. However, only the neutrophil count and log NLR at presentation improved the predictive accuracy in combination with clinical parameters compared with that achieved with a predictive model including only clinical parameters. The optimal cut-off neutrophil count and NLR were 5.21 × 103 /uL and 4.02, respectively. The total neutrophil count and NLR, which are widely available and inexpensive parameters obtained in the emergency department (ED), are promising screening tools for predicting the risk of troponin I elevation in patients without evidence of myocardial injury-related acute CO poisoning at presentation.

Background This report describes a patient who developed coagulopathy after ingesting snake wine, which is an alcoholic libation containing an entire venomous snake. Case Report A 68-year-old man was admitted to the hospital 19 h after ingesting snake wine. The laboratory features upon admission included unmeasurable activated partial thromboplastin (aPTT) values, prolonged prothrombin time (PT) values, increased fibrinogen levels, modestly elevated fibrin degradation product and D-dimer values, uncorrected aPTT and PT values after a mixing test, and normal levels of aspartate transaminase and alanine transaminase. No pesticides, warfarin, or superwarfarin in the patient's blood or urine were detected. His coagulation profile normalized on the 6th day after admission after antivenom treatment. He was discharged 10 days later without sequelae. Why Should an Emergency Physician Be Aware of This? The physician should be aware that ingesting snake wine may lead to systemic envenomation. As for coagulopathy, which may develop by ingesting snake venom, related laboratory findings may differ from the features observed after direct envenomation by snakebite.

Objective This study aims to help set domestic guidelines for administration of antivenom to envenomated patients after snakebites. Methods This retrospective observational case series comprised 128 patients with snake envenomation. The patients were divided into two groups according to the need for additional antivenom after the initial treatment based on the traditional snakebite severity grading scale. One group successfully recovered after the initial treatment and did not need any additional antivenom (n=85) and the other needed an additional administration of antivenom (n=43). Results The group requiring additional administration of antivenom showed a higher local effect score and a traditional snakebite severity grade at presentation, a shorter prothrombin and activated partial prothrombin time, a higher frequency of rhabdomyolysis and disseminated intravascular coagulopathy, and longer hospitalization than the group that did not need additional antivenom. The most common cause for additional administration was the progression of local symptoms. The independent factor that was associated with the need for additional antivenom was the local effect pain score (odds ratio, 2.477; 95% confidence interval, 1.309 to 4.689). The optimal cut-off value of the local effect pain score was 1.5 with 62.8% sensitivity and 71.8% specificity. Conclusion When treating patients who are envenomated by a snake, and when using the traditional snakebite severity scale, the local effect pain score should be taken into account. If the score is more than 2, additional antivenom should be considered and the patient should be frequently assessed.

This study aimed to investigate whether the quick Sequential Organ Failure Assessment (qSOFA) score at emergency department (ED) presentation can help improve the risk assessment of glyphosate-surfactant herbicide (GlySH) poisoning complications. A total of 150 patients presenting with acute glyphosate herbicide ingestion were enrolled in this retrospective observational study. The qSOFA scores at presentation, ΔqSOFA (calculated by subtracting the worst qSOFA score from 1 hr after admission from the qSOFA score at presentation), baseline characteristics, clinical courses and outcome were collected and analysed. A total of 41 patients had life-threatening complications (27.3%), and 14 patients died (9.3%). Patients with a qSOFA score of 0 at presentation had a 1.5% incidence rate of complications. As the qSOFA score at presentation increased from 1 to 3, the rate of life-threatening complications significantly increased from 29.6% to 100%. Patients with a ΔqSOFA of 1 had a higher frequency of complications than did patients with a ΔqSOFA of 0. The qSOFA score (OR: 8.39, 95% CI: 3.51-26.67) and ΔqSOFA (OR: 27.60, 95% CI: 3.87-575.67) were associated with the development of life-threatening complications in the multivariate analysis. The qSOFA score showed high sensitivity (97.56%), and the ΔqSOFA score showed high specificity (99.08%). The values of area under the curve were significantly higher in the models using the qSOFA and ΔqSOFA than they were in the models using previously known prognostic factors (p < 0.01). The clinician should pay more attention to patients with high qSOFA scores at presentation or an increase in the qSOFA score 1 hr after admission.

Objective: This study aimed to investigate whether the serum N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin I levels at emergency department (ED) presentation predict long-term neurologic outcomes after acute charcoal-burning carbon monoxide (CO) poisoning. Methods: This retrospective study included 220 patients suffering from charcoal-burning CO poisoning. The demographics, serum NT-proBNP and troponin I levels at ED presentation, treatment, clinical course during hospitalization, and long-term neurologic outcomes were collected. Results: The median serum NT-proBNP level at presentation was 48.8 (16.5–259) pg/mL, and 78 patients (35.5%) had elevated troponin I (>0.04 ng/mL) after acute charcoal-burning CO poisoning. The upper NT-proBNP and elevated troponin I groups had higher prevalences of respiratory failure, hypotension, and myocardial injury during hospitalization and altered mentality (GCS ≤14) at discharge than the lower NT-proBNP and normal troponin I groups. The incidence of persistent severe neurologic sequelae at 25 months after acute CO poisoning was 10.9%. The upper NT-proBNP and elevated troponin I groups had a higher incidence of poor long-term neurologic outcome than the counterpart groups. Log-transformed NT-proBNP and elevated troponin I were associated with poor long-term neurologic outcome in the univariate analysis, but only the adjusted log-transformed NT-proBNP remained an independent factor in the multivariate analysis. Compared with a predictive model including previously proposed predictors, the addition of log NT-proBNP improved the diagnostic accuracy for predicting poor long-term neurologic outcome. The serum NT-proBNP values for predicting poor long-term neurologic outcome were 74.6 and 32.7 pg/mL at fixed sensitivities of 95 and 99%, respectively. Conclusions: Elevated serum NT-proBNP at ED presentation is correlated with a risk of poor long-term neurologic outcome after discharge in cases of acute charcoal-burning CO poisoning. NT-proBNP could significantly improve the risk stratification of patients who will experience poor long-term neurologic outcome after CO poisoning. This potentially valuable marker should be further validated.

This study aimed to compare adverse cardiovascular events and fatalities and to identify the risk factors for fatalities associated with the glyphosate salt herbicide formulation. Additionally, we examined whether glyphosate ammonium salt herbicides increased serum ammonia levels. One hundred forty-seven patients were divided into an ammonium group (glyphosate ammonium salt herbicide) and an isopropylamine (IPA) group (glyphosate IPA salt herbicide) according to the type of glyphosate salt formulation ingested. Although no differences in the variables were observed between the groups, the IPA group had more fatalities, a higher incidence of QTc prolongation and a higher tendency for PR prolongation than the ammonium group. Additionally, the IPA group required a longer duration of vasopressor administration. PR prolongation and age were independently associated with fatalities in glyphosate IPA salt poisoning cases in the multivariate regression. Serum ammonia levels were higher at presentation and decreased continuously during the first 48 h after presentation in the ammonium group. This study is the first to suggest potentially different toxicities, especially cardiovascular effects, of glyphosate herbicide poisoning in humans based on the glyphosate salt herbicide formulation and to determine the association between PR prolongation and fatality in glyphosate IPA salt herbicide poisoning cases.

Despite a widespread use of dicamba herbicide and numerous animal model studies, there had not been studies on acute toxicity of this chemical compound in human subjects following ingestion. Therefore, this study was conducted to investigate clinical characteristics of dicamba poisoning and to guide physicians treating patients intoxicated with dicamba herbicide.A retrospective observational case series was conducted for 14 patients with history of dicamba herbicide ingestion. Data were collected for clinical manifestation, patient management, and final outcome.The most common symptom was altered mental state (Glasgow Coma Scale ≤ 14). Laboratory abnormalities were elevations in lactate, and creatine kinase, metabolic acidosis (pH7.35, and HCO3(-)20 mmol/L), and elevated lipase. QTc prolongation was commonly observed. These abnormal clinical findings had normalized within two days of supportive treatment after dicamba ingestion. One patient did demonstrate corrosive esophagitis.Acute toxicity of dicamba herbicide in human following oral exposure was manageable with supportive treatment. However, physician should take into account for corrosive effect on GI tract, rhabdomyolysis, or acute pancreatitis.

This study evaluated whether the initial venous glucose level at presentation is associated with fatality in organophosphate (OP)-poisoned patients without diabetes mellitus (DM) and whether the association between glucose and outcome differs depending on the chemical formulation of the OP ingested.This retrospective observational case series consisted of 184 patients without DM who had a history of OP poisoning. Initial glucose level at presentation, outcome and general clinical data were recorded. The patients were categorized into the following groups according to their glucose level at presentation: group 1 (140 mg/dl, n = 63), group 2 (140-200 mg/dl, n = 58), group 3 (200-300 mg/dl, n = 41), and group 4 (≥300 mg/dl, n = 22). The most commonly ingested OPs were dichlorvos (n = 33), fenitrothion (n = 25), and ethyl p-nitrophenol thio-benzene phosphonate (EPN) (n = 24). The primary outcome was case fatality.Group 4 had a higher case fatality than groups 1 (p = 0.003) and 2 (p = 0.015), and group 3 had a higher case fatality than group 1 (p = 0.040). Multivariate analysis revealed that age [odds ratio (OR) 1.065, 95% confidence interval (CI) 1.020-1.112, p = 0.001], being in group 3 (OR 6.997, 95% CI 1.063-46.066, p = 0.043) and being in group 4 (OR 9.101, 95% CI 1.380-60.044, p = 0.022) were associated with case fatality. When using the glucose level at presentation 233 mg/dl, the dichlorvos group had a higher sensitivity (66.7% vs. 50.0%), specificity (90.0% vs. 86.4%), and positive (40.0% vs. 25.0%) and negative (96.4% vs. 95.0%) predictive values for predicting case fatality than the EPN group. No patient died of fenitrothion poisoning (mean glucose level at presentation = 169.4 ± 39.6 mg/dl).The case fatality risk independently increases as the initial venous glucose level at presentation increases in OP-poisoned patients without DM. However, because the association between the venous glucose level at presentation and case fatality varies according to the type of OP ingested, the chemical identity of the OP should be considered.

Carbamate is a widely used insecticide, and fatality due to carbamate insecticide intoxication has been reported. However, no studies have addressed the factors associated with outcome of patients poisoned by carbamate insecticide. The present study sought to identify the independent factors that could help predict the development of medical complications as a result of carbamate intoxication.Fifty two patients presenting with acute carbamate insecticide ingestion at Chonnam National University Hospital were enrolled in this retrospective observational case series. The morbidities that needed intensive treatment such as hypotension, respiratory failure, and death were regarded as complications. To identify the associated factors to these complications, objective variables that are easily assessed at presentation, such as age, initial Glasgow coma scale (GSC) and corrected QT (QTc) prolongation, were analyzed by univariate and multivariate stepwise logistic regression analyses.Of the 52 patients, 35 (67.3%) had medical complications within 24 hours after carbamate insecticide intoxication and seven (13.5%) died. Respiratory failure was the most common medical complication. The significant factors determined by univariate analysis were initial GCS, elevated lactate, and QTc prolongation. However, initial GCS (≤13) was the only independent factor determined by multivariate analysis that was associated with serious complications requiring intensive medical treatment.Carbamate insecticide intoxication is not a mild disease, as previously thought, having a mortality rate of 13.8% and a morbidity rate of 67.3%. Initial GCS ≤ 13 can be used as a significant factor to identify carbamate insecticide-intoxicated patients who will experience complications.

Fentanyl has an analgesic effect 100 times greater than that of morphine; therefore, transdermal administration of fentanyl has been widely used to control pain. Due to misconceptions regarding the proper use of fentanyl, its simple method of administration, and the absence of regulatory rules regarding its use, both medical providers and non-medical providers have abused fentanyl. We report on three cases of fentanyl intoxication and suggest solutions to prevent its abuse in the future. Three patients were intoxicated by transdermal fentanyl, which resulted in respiratory depression. Two of these cases were attributed to non-medical use of the drug and the other occurred while using fentanyl as directed by medical personnel. Physicians should use transdermal fentanyl only to control chronic pain, and rules should be established to prevent abuse of fentanyl that occurs due to its ease of use and the absence of any established policy regarding the prescription and disposal of this drug.

Alocasia, the Araceae family, is a genus of more than 100 species of perennial, herbaceous, diminutive to extremely large, usually robust herbs with a clear-to-milky latex. They are distributed throughout subtropical and tropical Asia and in the tropical western pacific as well as eastern Australia. Despite easy access to A odora, there have been no published reports in English regarding the toxic symptoms following the ingestion of raw A odora. Here, the clinical manifestations of 2 patients that ingested raw A odora are described. Two patients experienced oral numbness and intractable tongue pain, and 1 patient required endotracheal intubation because of upper respiratory tract obstruction. Although conservative treatment is the primary approach to A odora poisoning, physicians should be aware of the potential for upper respiratory obstruction in patients exposed to A odora, as well as the need for controlling tongue pain.

Paraquat (PQ) poisoning is an extremely difficult condition to manage clinically because of the lack of effective treatments. The purpose of this study was to assess the effect of high doses of vitamin C in combination with anti-inflammatory and immunosuppressant therapy in patients with PQ poisoning. The medical records of 134 patients who presented to the emergency department within 24 hours after PQ poisoning were reviewed retrospectively. The 57 patients presented between January 2004 and September 2005 were group 1; they received pulse therapy, which included cyclophosphamide and methylprednisolone, followed by the administration of dexamethasone over 2 weeks. The 77 patients that presented between October 2005 and January 2008 were group 2; they received the above-mentioned therapy and high-dose vitamin C for 2 weeks. There was no difference in the distribution of baseline variables between the 2 groups. However, group 2 showed a significant reduction in acute kidney injury related to PQ. Furthermore, a multivariate logistic regression analysis showed that the addition of vitamin C to the treatment was significantly associated with an increased survival of the patients. Larger trials will be needed to verify the effect of high-dose vitamin C on survival in patients with PQ poisoning.

Patients with carbon monoxide (CO) poisoning have been found to have a correlation between initial clinical severity on admission and blood lactate levels. Recently, it is suggested that the lactate level may be a useful prognostic factor in cases study. The purpose of this study was to determine whether lactate levels were associated with the short-term outcome of patients with CO poisoning and identify the characteristics of patients with high initial lactate levels. Eighty patients that presented to the Chonnam National University Hospital after CO poisoning, over 5 years, were enrolled in this retrospective study. Fifty-six (70.0%) patients had high lactate (>2.1 mmo/L) on admission. Thirty-three (41.3%) patients had medical complications and one patient (1.3%) died. The patients with high initial lactate had an altered mental status more frequently, higher WBC, glucose and carboxyhemoglobin (COHb), and lower base deficit on admission. The multivariate analysis showed that lactate was an independent factor associated with serious complications and the need for intensive medical treatment, along with advanced age, WBC, and altered mental status on admission. The results of this study show that the initial lactate was useful for patient prognosis after CO poisoning.

Reversible posterior leukoencephalopathy syndrome (RPLS) is a neurological disorder characterized by signs of posterior cerebral edema upon radiographic examination. RPLS has been strongly associated with abrupt and significant elevations in blood pressure or the administration of immunosuppressive drugs. Here, we report a case of RPLS occurring in a 30-year-old-mother with a presumed amniotic fluid embolism subsequent to delivery by cesarean section. On the fifth day after the initial successful resuscitation from the cardiorespiratory collapse, she manifested generalized seizure activity and abnormal radiological findings, which were found to be consistent with RPLS. Through our experience, we have suggested that RPLS might occur more easily at lower blood pressures than has been previously recognized. It is important to consider the lower limit at which blood pressure is controlled, especially if accompanied with fever.

A 44-year-old woman intentionally ingested a solution of copper sulphate. She had minimal intravascular haemolysis and methemoglobinaemia but developed acute respiratory distress syndrome (ARDS) 4 hours after acute copper sulphate poisoning. This required extracorporeal membrane oxygenation (ECMO) management in the intensive care unit. Subsequently, she improved clinically and was successfully weaned from ECMO. Acute copper sulphate poisoning can cause severe pulmonary toxicity even in the absence of other serious symptoms. Therefore, a physician treating acute copper sulphate poisoning should look out for respiratory symptoms even in the absence of other common symptoms. We suggest early initiation of venovenous ECMO in those with ARDS following copper sulphate poisoning.

STUDY DESIGN.: A case report and review of the literature. OBJECTIVE.: To discuss the significance of identifying symptomatic epidural pneumorrhachis associated with an occult pneumomediastinum in the absence of pneumothorax and subcutaneous emphysema after minor trauma. SUMMARY OF BACKGROUND DATA.: Pneumorrhachis is defined as the presence of air in the epidural space or subarachnoid space. Previous reports have suggested that traumatic epidural pneumorrhachis was usually asymptomatic and a combination of pneumothorax, pneumomediastinum, and subcutaneous emphysema following major trauma and managed by conservative treatment. METHODS.: A 53-year-old man was admitted to the emergency department after the traffic collision. He presented with diffuse pain ranging from the neck to back, and complained of radiating shoulder pain. RESULTS.: The lateral cervical spine radiograph revealed an air shadow in the anterior cervical space. Axial image of cervical spine computed tomography (CT) revealed epidural pneumorrhachis. The sagittal reconstruction image of neck CT showed a small amount of air in the posterior mediastinum, and scattered air in the anterior cervical spinal canal. Our patient was treated conservatively and had a complete and uneventful recovery. CONCLUSION.: To our knowledge, this is the first case in which symptomatic traumatic epidural pneumorrhachis was associated with an occult pneumomediastinum in the absence of pneumothorax and subcutaneous emphysema. These findings may be useful in alerting trauma specialists to carefully evaluate the associated pathologies leading to pneumorrhachis enabling adequate therapy.

Objectives: The purpose of this study was to identify independent factors that can be used to predict whether febrile neutropenic patients who appear healthy at presentation will develop subsequent complications, using variables that are readily available in the emergency department (ED). Method: The medical records of 192 episodes in which the patients presented to the ED with neutropenic fever resulting from chemotherapy, with an alert mental state and haemodynamic stability were retrospectively reviewed. Endpoints examined were fever response to administered antibiotics, death or severe medical complications during hospitalisation. Results: Thirty-eight episodes of neutropenic fever with complicated outcomes were identified from among a total of 192 episodes. Three parameters emerged as independent factors for the prediction of neutropenic fever with complications in the multivariate regression analysis: platelet count (130−450 × 10 3 cells/mm 3 ) 3 , serum C-reactive protein (CRP, 0.1–1 mg/dl) >10 mg/dl and pulmonary infiltration on chest x ray. Conclusions: Platelet count, CRP and pulmonary infiltration on chest x ray at presentation could be used to identify febrile neutropenic patients who will develop complications, and these factors may be useful in making treatment-related decisions in the ED.

The ingestion of small amounts of glyphosate herbicide usually causes only mild symptoms. However, when large volumes of concentrates are ingested intentionally, it can generate potentially fatal symptoms that are refractory to treatment. It also is well known that the treatment for glyphosate poisoning is primarily of a supportive nature. We report two patients who intentionally ingested glyphosate herbicide, and both exhibited cardiovascular collapse and complicated renal failure despite the use of aggressive supportive therapy. Hemodialysis was conducted and the results were satisfactory; both patients were discharged without any sequelae. After analyzing these cases, we suggest that hemodialysis might have contributed to the favorable outcomes of our patients, and that there are several mechanisms that might justify the use of hemodialysis in these patients. In conclusion, physicians may wish to consider the early use of hemodialysis to improve the prognosis of patients exhibiting refractory hypotension and oliguria, despite vigorous supportive treatment in glyphosate herbicide intoxication.

Corneal neovascularization, which occurs in many pathologic states of the cornea, reduces the visual acuity. Recently, we found that the extracellular region of brain-specific angiogenesis inhibitor 1 (BAI1-ECR) has antiproliferative activity through functional blocking of alpha(v)beta(5) integrin in endothelial cells. In this study, we investigated the effects of lipid-mediated subconjunctival injection of the BAI1-ECR gene on corneal angiogenesis induced by epithelial debridement by heptanol in the rabbit. When a pEGFP-BAI1-ECR plasmid was given subconjunctivally 1 week after epithelial debridement, green fluorescence was detected in the corneal stroma with expression persisting for 7 days. To test the effect of BAI1-ECR on neovascularization, rabbits were injected with the BAI1-ECR gene or empty vector two or three times at 1-week intervals beginning 1 week after debridement. When measured with biomicroscopy at 1 or 2 weeks after two weekly injections, BAI1-delivered eyes had significantly less neovascularized corneal area than vector-injected ones in both time periods. Similar microscopic results were obtained after three weekly injections of BAI1-ECR. In quantitative histological examination, the BAI1-receiving eyes showed significantly less neovascular area and number of vessels than vector-injected ones. Also, after two weekly injections, BAI1-delivered eyes had decreased neovascularized corneal area equivalent to that of anti-VEGF antibody-injected ones. These results indicate that BAI1-ECR gene delivery effectively reduces experimental corneal neovascularization and suggest that the BAI1-ECR protein can be used as an angiogenesis suppressor in the eye.

Restricting transgene expression to specific cell types and maintaining long-term expression are major goals for gene therapy. Previously, we cloned brain-specific angiogenesis inhibitor 1-associated protein 4 (BAI1-AP4), a novel brain-specific protein that interacts with BAI1, and found that it was developmentally upregulated in the adult brain. In this report, we isolated 5 kb of the 5′ upstream sequence of the mouse BAI1-AP4 gene and analyzed its promoter activity. Functional analyses demonstrated that an Sp1 site was the enhancer, and the region containing the transcription initiation site and an AP2-binding site was the basal promoter. We examined the ability of the BAI1-AP4 promoter to drive adult brain-specific expression by using it to drive lacZ expression in transgenic (TG) mice. Northern blot analyses showed a unique pattern of β-galactosidase expression in TG brain, peaking at 1 month after birth, like endogenous BAI1-AP4. Histological analyses demonstrated the same localization and developmental expression of β-galactosidase and BAI1-AP4 in most neurons of the cerebral cortex and hippocampus. Our data indicate that TG mice carrying the BAI1-AP4 promoter could be a valuable model system for region-specific brain diseases.

The adjuvant for Gramoxone INTEON is composed of 20% methanol, 20% sodium lingo sulphonate, 10% alkylaryl polyoxyethylene ether, and 50% water. Although the adjuvant is a potential source of intoxication due to the widespread use of Gramoxone INTEON, there has been no prior report characterizing the acute toxicity of this adjuvant. This study evaluated the acute toxicity of adjuvant ingestion. Seven patients presenting with acute adjuvant intoxication at Chonnam National University Hospital were enrolled in this retrospective study. The patients had intentionally or accidentally ingested 20-150 mL of adjuvant. Gastrointestinal symptoms such as nausea and vomiting were most common, and no ocular symptoms were reported. Cardiovascular symptoms were limited to electrocardiogram changes such as corrected QT interval (QTc) prolongation (71.4%) and sinus tachycardia (28.6%). All patients had an elevated serum osmolar gap and lactate levels. One patient had metabolic acidosis with a high anion gap that required administration of sodium bicarbonate. These clinical symptoms were resolved within 3 days with supportive treatment without any sequelae. There were no life-threatening symptoms and no deaths. However, the physician should keep in mind the possibility of methanol intoxication in patients poisoned with this adjuvant.

Glyphosate herbicide intoxication results in a range of mortality and morbidity, depending on patients' factors. Predicting which patient will need intensive medical treatment might help reduce mortality by providing prompt treatment, as well as triage those patients not likely to develop complications. Thus, we sought to identify independent factors that could predict which patient will develop subsequent medical complications.Seventy-six patients presenting with acute glyphosate herbicide ingestion at Chonnam National University Hospital were enrolled in this retrospective study. To identify the predictive factors for complications, objective variables easily assessed at presentation including previously reported predictive factors for mortality, such as age, vital signs, X-ray abnormalities, and laboratory findings, were analyzed by univariate and multivariate stepwise logistic regression analyses.Of the 76 patients, 32 (42.1%) had medical complications and 2 (2.6%) died. Metabolic acidosis was the most common medical complication. Whereas metabolic acidosis, respiratory failure, hypotension, acute kidney injury, hyperkalemia, and seizures developed within 24 h, acute pancreatitis occurred a few days after the ingestion. The univariate analysis showed that an advanced age, amount ingested100 mL, X-ray abnormalities, elevated amylase, alanine aminotransferase (ALT), and blood nitrogen urea were significant factors. However, the multivariate analysis showed that advanced age, elevated ALT, and X-ray abnormalities were independent factors associated with serious complications and the need for intensive medical treatment.The results of this study showed that age50 years, X-ray abnormalities, and ALT40 U/L were significant predictive factors for complications in patients with glyphosate surfactant herbicide poisoning; patients with these findings might require admission to the intensive care unit.

Localization of protein kinase A (PKA) via A-kinase-anchoring proteins (AKAPs) is important for cAMP responsiveness in many cellular systems, and evidence suggests that AKAPs play an important role in cardiac signaling. To test the importance of AKAP-mediated targeting of PKA on cardiac function, we designed a cell-permeable peptide, which we termed trans-activator of transcription (TAT)-AKAD for TAT-conjugated A-kinase-anchoring disruptor, using the PKA binding region of AKAP10 and tested the effects of this peptide in isolated cardiac myocytes and in Langendorff-perfused mouse hearts. We initially validated TAT-AKAD as a PKA localization inhibitor in cardiac myocytes by the use of confocal microscopy and cellular fractionation to show that treatment with the peptide disrupts type I and type II PKA regulatory subunits. Knockdown of PKA activity was demonstrated by decrease in phosphorylation of phospholamban and troponin I after beta-adrenergic stimulation in isolated myocytes. Treatment with TAT-AKAD reduced myocyte shortening and rates of contraction and relaxation. Injection of TAT-AKAD (1 microM), but not scrambled control peptide, into the coronary circulation of isolated perfused hearts rapidly (1 min) and reversibly decreased heart rate and peak left ventricular developed pressure. TAT-AKAD also had a pronounced effect on developed pressure (-dP/dt), consistent with a delayed relaxation of the heart. The effects of TAT-AKAD on heart rate and contractility persisted in hearts pretreated with isoproterenol. Disruption of PKA localization with TAT-AKAD thus had negative effects on chronotropy, inotropy, and lusitropy, thereby indicating a key role for AKAP-targeted PKA in control of heart rate and contractile function.

Endosulfan is a widely used insecticide that is associated with a high fatality rate in humans when ingested accidentally or with the aim of suicide. However, the literature concerning human endosulfan exposure is limited to case reports. Thus, we sought to 1) describe the clinical features of patients with acute endosulfan poisoning and 2) identify independent factors to predict patients’ outcome. Fifty-two patients who presented with acute endosulfan poisoning between January 2001 and January 2007 were enrolled in this retrospective study. Sixteen (30.7%) of the 52 patients died, and 48 patients experienced seizures. Endosulfan poisoning caused the hypotension and the abnormalities on electrocardiogram at presentation. Over half of the patients developed complications, such as rhabdomyolysis, hepatic toxicity, and hypotension. These complications resolved without sequelae in the survival group. Refractory status epilepticus was the most common cause of death in this series (75.0%). Amount ingested being greater than 35 g of endosulfan was the most found to be an independent variable that predicted patient mortality. Patients with this risk factor must be treated aggressively during the early stage of endosulfan poisoning.