The association between the neutrophil lymphocyte ratio and local edema after viper snake envenomation in South Korea.

The role of the inflammatory process in the pathogenesis of local edema-related envenomation has not been explored with endemic venomous snakebites in Korea. Gloydius species are responsible for most snakebites in South Korea. In this study we aimed to investigate whether the neutrophil-lymphocyte ratio is relevant to snake envenomation-induced local edema in South Korea. This retrospective study divided 126 patients into two groups according to local edema severity at presentation. Logistic regression models were used to investigate the association between the neutrophil-lymphocyte ratio and local edema. Sixty-one (48.4%) patients had grade 2 or higher local edema at presentation despite 21 of them being given antivenom before presentation. During hospitalization, local edema progressed in 61 patients 48 (11.5-48) hours after presentation, and 54 patients demonstrated grade 3 or higher local edema. A higher neutrophil-lymphocyte ratio at presentation after adjustment for factors related to envenomation and antivenom administration and factors influencing the neutrophil-lymphocyte ratio were associated with both a higher grade of local edema at presentation and a higher peak local edema grade during hospitalization. The delta neutrophil-lymphocyte ratio during the first 24 h after presentation was related to the local edema progression after presentation. The neutrophil-lymphocyte ratio at presentation is associated with the severity of local edema-related envenomation. Furthermore, the change in the neutrophil-lymphocyte ratio during the first 24 h is related to the risk of local edema progression. Further clinical and experimental research aimed at investigating the role of inflammation on the pathogenesis of local edema should be conducted. This study may suggest the introduction of short-term anti-inflammatory agents considering the failure of antivenom to curb local edema.

Coagulopathy after snake envenomation in South Korea.

OBJECTIVE: This retrospective study investigated the nature and severity of venom-induced consumption coagulopathy (VICC) and determined the clotting factors involved in VICC in patients after envenomation by South Korea's snakes. Additionally, we studied the effectiveness of antivenom for the treatment of VICC after envenomation. METHODS: Included patients were divided into three groups according to the severity of VICC (no VICC, partial VICC, and complete VICC). Data, including changes in coagulation parameters during hospitalization and clotting factors at presentation, were collected and analyzed. RESULTS: One hundred nineteen patients who presented at our emergency department within 3 h after snake envenomation were included. VICC developed in 34 patients (27 patients with partial VICC and 7 patients with complete VICC). Two of 34 patients with VICC required blood transfusions. Five patients with complete VICC had an undetectable fibrinogen concentration at presentation. Three patients with complete VICC had an unmeasurable INR and aPTT within 24 h. The median times of the most extreme values were 10 h for INR, 12 h for aPTT, and 16 h for fibrinogen after presentation in the VICC group. The D-dimer concentration peaked at a median of 63.5 h after presentation. The activities of factors II and X were significantly reduced in the complete VICC group (factor II: 88 (84-99.3)% in the non-VICC group vs. 69 (49.5-83.5)% in the complete VICC group; factor X:94 (83-102) in the non-VICC group vs. 70 (66.5-79.8)% in the complete VICC group), while there was no difference in factor V activity at presentation. The time from bite to first antivenom administration did not correlate with the time course and most extreme concentrations for fibrinogen and D-dimer within the VICC groups. DISCUSSION AND CONCLUSION: VICC occurs in approximately one-quarter of snakebite patients in South Korea; however, VICC itself does not appear to lead to clinical deterioration. Fibrinogen is an early diagnostic maker for complete VICC. Clotting factors II and X are involved in VICC. Future investigations should explore the mechanism of VICC from Korean snakebites and the effect of antivenom on VICC.

The effect of myocardial injury on the clinical course of snake envenomation in South Korea.

CONTENT: This study investigated the incidence, progression and clinical course of myocardial injury-related snake envenomation in South Korea. In addition, this study evaluated whether antivenom guidelines are appropriate to control envenomation in patients with myocardial injury. METHODS: The study included 198 patients who received antivenom after a snakebite, and they were divided into two groups according to evidence of myocardial injury (defined as elevated troponin I or ischemic change on electrocardiogram) at presentation. Data including serial troponin I, echocardiogram/coronary angiogram findings, the clinical course, and treatment were collected and analyzed. RESULTS: The incidence of myocardial injury at presentation was 15.2%. The troponin I level was 0.11 (0.07-0.56) ng/ml at presentation and tended to decrease over 24 h. Echocardiograms revealed neither regional wall motion abnormalities nor left ventricular dysfunction in 15 of 17 patients, while two patients showed signs of coronary artery stenosis on echocardiograms and coronary angiograms. However, compared with patients without myocardial injury, patients with myocardial injury had a higher frequency of systemic envenomation complications, including bleeding, respiratory failure, hypotension, acute kidney injury, thrombocytopenia and venom-induced consumption coagulopathy (VICC). The patients with myocardial injury at presentation needed significantly more frequent and larger doses of antivenom than indicated by the initial severity of envenomation. Multivariate analysis showed that myocardial injury was associated with the need for additional antivenom administration after initial administration. DISCUSSION AND CONCLUSION: Myocardial injury is not uncommon after snake envenomation in Korea. Although myocardial injury itself seems to be benign, the clinical course of patients with myocardial injury is complicated, and myocardial injury is associated with the need for additional antivenom administration. The optimal use of antivenom to control envenomation in patents with myocardial injury after snake envenomation in South Korea should be established.

Derangement of PaCO2 requires physician attention in acute carbon monoxide 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.

Predictive value of plasma neutrophil gelatinase-associated lipocalin in acute charcoal-burning carbon monoxide poisoning.

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.

Diagnostic Value of Parameters Related to White Blood Cell Counts for Troponin I Elevation in CO Poisoning.

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.

The impact of hyperthermia after acute carbon monoxide poisoning on neurological sequelae.

This study investigated whether hyperthermia within the first 24 h after presentation was associated with long-term neurological outcomes after acute carbon monoxide (CO) poisoning. This retrospective study included 200 patients with acute severe CO poisoning. Hyperthermia (≥ 37.5°C) developed during the first 24 h after presentation in 55 (27.5%) patients, and poor long-term neurological sequelae assessed at 23 months after acute CO poisoning developed in 19.5% of the patients. The incidence of poor long-term neurological outcomes was significantly higher in the hyperthermia group than in the normothermia group. Patients with poor long-term neurological outcomes had higher maximum temperatures than patients with good outcomes. No significant difference was found in the time of hyperthermia onset within the first day according to the neurological outcomes. Hyperthermia (adjusted odds ratio (aOR) 5.009 (95% confidence interval (CI) 1.556-16.126)) and maximum temperature (aOR 2.581 (95% CI 1.098-6.063)) within the first 24 h after presentation to the emergency department were independently associated with poor long-term neurological outcomes. Body temperature measurements, which are easily and noninvasively recorded at the bedside in any facility, help to predict the risk for poor long-term neurological outcomes. This study carefully emphasizes fastidious control of pyrexia, particularly during the early period after acute CO poisoning.

Initial diffusion-weighted MRI and long-term neurologic outcomes in charcoal-burning carbon monoxide poisoning.

CONTEXT: This study assessed the results of diffusion-weighted imaging (DWI) at presentation for acute charcoal-burning carbon monoxide (CO) poisoning and investigated whether the initial DWI results can predict long-term neurologic outcomes. METHODS: The study included 128 patients who suffered from CO poisoning after burning charcoal and underwent DWI. These patients were divided into two groups based on imaging results: a normal DWI group and an abnormal DWI group. Data regarding clinical courses and long-term neurologic outcomes (persistent severe neurologic sequelae) were collected and compared. RESULTS: The rate of abnormal DWI findings at presentation was 23.4%, and the most common site of abnormalities was the globus pallidus. All lesions in abnormal DWI had decreased apparent diffusion coefficient (ADC) values. The long-term neurologic state was assessed at a median follow-up of 19.5 months, and the frequency of poor long-term neurologic outcome was significantly higher in the abnormal DWI group (40.0% in the abnormal DWI group vs. 1.0% in the normal DWI group; p < .001). Abnormal DWI (odds ratio [OR]): 31.3, 95% confidence interval [CI]: 2.5-397) and old age (OR 1.1, 95% CI: 1.001-1.13) were independent factors for poor long-term neurologic outcomes, whereas the Glasgow Coma Scale score at presentation (OR: 0.7, 95% CI: 0.6-0.9) was negatively associated with the risk of poor long-term neurologic outcome. CONCLUSIONS: In cases involving CO poisoning due to charcoal burning, DWI at presentation may help predict the long-term neurological outcome after discharge.

Serum neuron-specific enolase levels at presentation and long-term neurological sequelae after acute charcoal burning-induced carbon monoxide poisoning.

OBJECTIVE: This study aimed to investigate whether clinical parameters and serum neuron-specific enolase (NSE) levels measured at emergency department (ED) presentation help stratify the risk of acute or delayed persistent severe neurological sequelae after acute carbon monoxide (CO) poisoning induced by charcoal burning. METHODS: This retrospective study included 236 patients who suffered from CO poisoning. Demographic information, serum NSE levels measured in the ED, treatment, clinical course, and long-term neurological outcomes were recorded. RESULTS: The median serum NSE level at presentation was 15.5 (10.9-22.7) ng/mL. No differences were observed in the duration of CO exposure; the initial Glasgow Coma Scale (GCS) score; the levels of arterial HCO3-, white blood cells (WBCs), C-reactive protein (CRP) or troponin I; or the frequency of abnormal diffusion-weighted imaging finding at presentation among the groups with different serum NSE levels at presentation. The incidences of acute and delayed persistent neurologic sequelae assessed at 22.3 months after acute charcoal CO poisoning were 5.1% and 8.5%, respectively. No difference in the NSE level was observed between patients stratified according to long-term neurological status. According to the multinomial logistic regression analysis, age, serum CRP levels and the initial GCS score were risk factors for the two types of persistent severe neurological sequelae, whereas troponin I levels were associated only with the acute persistent severe neurological sequelae. However, the adjusted NSE level was not a risk factor for any persistent neurological sequelae. CONCLUSIONS: Serum NSE levels at presentation were not correlated with the risk of acute or delayed persistent neurological sequelae. Further studies with blood sampling at optimal time points and serial measurements should be conducted. Age, initial GCS score, and CRP levels may be risk factors for persistent severe neurological sequelae.

In-hospital outcomes and delayed neurologic sequelae of seizure-related endosulfan poisoning.

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.

Serial ammonia measurement in patients poisoned with glufosinate ammonium herbicide.

This study investigated whether ammonia concentrations can predict delayed neurotoxicity development and neurotoxicity latency in glufosinate ammonium (GLA) herbicide-poisoned patients presenting with an alert mental state and stable hemodynamics. This retrospective observational case study included 26 patients divided into 2 groups: neurotoxicity during hospitalization (complicated group) and without neurotoxicity (noncomplicated group). Thirteen patients (50.0%) experienced neurotoxicity at 16 h post-ingestion. Although ammonia concentrations at presentation did not differ significantly between the two groups, the ammonia level in the complicated group increased significantly at the next measurement and remained significantly higher than that in the noncomplicated group until 48 h after ingestion. The peak ammonia concentration before neurotoxicity development was an independent predictor of neurotoxicity (odds ratio: 1.047, 95% confidence interval: 1.010-1.087, p value = 0.014), and the optimal cutoff value of peak ammonia concentration for predicting neurotoxicity was 101.5 µg/dL. The rate of ammonia increase was not associated with the time latency from ingestion to neurotoxicity development. This study showed that serial ammonia measurements in GLA-poisoned patients may identify those who are at high risk of developing neurotoxicity. However, as this study enrolled few patients, further qualified trials are required to confirm our results and to reveal the etiology of hyperammonemia and its causality in neurotoxicity.

Clinical characteristics of patients after dicamba herbicide ingestion.

OBJECTIVE: 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. MATERIAL AND METHOD: 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. RESULT: The most common symptom was altered mental state (Glasgow Coma Scale ≤ 14). Laboratory abnormalities were elevations in lactate, and creatine kinase, metabolic acidosis (pH < 7.35, 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. DISCUSSION AND CONCLUSION: 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.

Predicting the complicated neutropenic fever in the emergency department.

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 x 10(3) cells/mm(3)) <50 000 cells/mm(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.

Spontaneous intercostal artery bleeding.

We present a patient who complained of right flank pain resulting from spontaneous intercostal artery rupture while sleeping. He did not have symptoms or a history to suggest other diseases or trauma except hypertension. Arteriography revealed a rupture of the right 10th and 11th intercostal artery, and transcatheter arterial embolisation was successfully done. The patient was discharged without any sequelae. To our knowledge, this is the second report in the literature documenting spontaneous intercostal artery rupture without associated illness or injury. Through comparison with the first reported case, we discuss the cause, the vulnerable site, and the treatment of spontaneous intercostal bleeding.

Lipid-mediated delivery of brain-specific angiogenesis inhibitor 1 gene reduces corneal neovascularization in an in vivo rabbit model.

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.