Young-Gi Min

The usefulness of the serum s100b protein for predicting delayed neurological sequelae in acute carbon monoxide poisoning

Context. Some patients with acute carbon monoxide poisoning will experience delayed neurological sequelae. Several factors associated with delayed neurological sequelae have been reported, but these factors are unsatisfactory for the assessment of unconscious patients. Objective. The aim of this study was to assess the usefulness of the serum S100B protein as a biochemical marker for predicting delayed neurological sequelae. Materials and methods. In this retrospective study, we evaluated the data for patients who visited an emergency medical center once during a period of 7 months. The enrollment criteria were the diagnosis of acute carbon monoxide poisoning and the measurement of the serum S100B level. A standardized extraction using medical records was performed. Result. A total of 71 patients were enrolled, and 10 patients (14.1%) presented delayed neurological sequelae. The delayed neurological sequelae group had a longer duration of carbon monoxide exposure, a longer duration of loss of consciousness, and a worse mental status (p-value < 0.001). In addition, the S100B protein levels were higher in the delayed neurological sequelae group (0.891 vs. 0.063, p-value < 0.001). Multiple logistic regression analysis showed that only the serum S100B protein level was independently associated with the development of delayed neurological sequelae (OR, 120.594; 95% CI, 4.194–3467.220), and a serum S100B protein level of more than 0.165 μg/L predicted the development of delayed neurological sequelae (sensitivity 90%, specificity 87%). Discussion and conclusion. In the present study, the level of serum S100B protein was found to be useful for evaluating acute CO poisoning patients and was found to be an independent predictor of the development of DNS after acute CO poisoning.

Prediction of prognosis in acute paraquat poisoning using severity scoring system in emergency department.

Objective. The aim of this study was to validate and compare the performance of serum paraquat level, severity index of paraquat poisoning (SIPP), Acute Physiology And Chronic Health Evaluation II (APACHE II), modified Simplified Acute Physiology Score II (MSAPS II), and modified Expanded Simplified Acute Physiology Score II (MSAPS IIe) calculated immediately after arrival on emergency department (ED) for assessing the mortality of acute paraquat poisoning. Methods. A retrospective study design was employed with the main outcome measure being mortality from year 2001 to 2010. MSAPS II and MSAPS IIe were employed in that assessment of the 24-hour urine output were not included. The performance of APACHE II, MSAPS II, MSAPS IIe, serum paraquat level and SIPP for prediction of mortality in acute paraquat poisoning were compared. Results. A total of 102 patients were enrolled in the study. The area under the ROC curve for APACHE II (0.800) was statistically lower than those for MSAPS II, MSAPS IIe, SIPP and serum paraquat (0.879, 0.893, 0.924,and 0.951, respectively). The Hosmer-Lemeshow goodness-of-fit test C statistic revealed that APACHE II, MSAPS II, MSAPS IIe and serum paraquat level showed good calibrations (chi-square 8.477 and p = 0.388, chi-square 4.614 and p = 0.798, chi-squared 5.301 and p = 0.725, chi-squared 1.009 and p = 0.985 respectively), but poor calibration for SIPP (chi-square 21.293 and p = 0.006). Conclusion. Serum paraquat level is still the most reliable prognosis factor in acute paraquat poisoning. But MSAPS II or MSAPS IIe calculated immediately after arrival on ED may be helpful to predict mortality in acute paraquat poisoning especially when hospital has no facility to measure serum paraquat level.

Pathophysiology of brain injuries in acute carbon monoxide poisoning: A novel hypothesis

Acute carbon monoxide (CO) poisoning causes the neurologic symptoms and brain lesions during both acute and delayed phase. We propose that catecholamine crises in globus pallidus and deep white matter are the key pathophysiological factors causing acute and delayed brain injuries respectively. Increased sympathetic activities due to acute CO poisoning is followed by increases of catecholamine levels in synapses or nerve terminals in organs including the brain, especially, limbic system. A dopamine excess in the synaptic cleft of the mesolimbic system, including globus pallidus, may cause the destruction of synapses and nuclei in the globus pallidus. Consequently, the striatal lesion is affected in the acute phase of CO intoxication. Moreover, an increase of catecholamine levels in synapses of deep white matter can persist after the acute stage of CO intoxication. A dopamine excess could lead to oxidative metabolism of dopamine, serotonergic axonal injury, or secondary myelin damage.

Treatment of acute carbon monoxide poisoning with induced hypothermia

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.

A fatal case of flufenoxuron-containing insecticide poisoning complicated by lactic acidosis, shock, abdominal compartment syndrome.

Flufenoxuron is a newly developed benzoylurea insecticide. The Cascade TM formulation is composed of flufenoxuron (5.3%), polyoxyethylene nonylphenol (8.0%), N-methyl-2-pyrrolidone (20.0%), ethoxylated nonylphenol phosphate (10.0%) and cyclohexanone (56.7%). Its toxicity on human still remains uncertain. Until now, only one case of human poisoning with a flufenoxuron-containing insecticide was reported which was successfully managed. 1 We report a fatal case of flufenoxuron-containing insecticide poisoning complicated by lactic acidosis, shock and abdominal compartment syndrome. A 66-year-old male presented to emergency department 1 h after self-poisoning with 100 mL of Cascade TM . On arrival, Glasgow coma scale was 5/15 and initial vital signs were: blood pressure 121/50 mmHg, pulse rate 120 beats/min, respiratory rate 24 breaths/min, and temperature 36.5° C. Endotracheal intubation was performed, and he was mechanically ventillated. Blood Laboratory results revealed lactic acidosis (pH 7.11, PaO 2 284.9 mmHg, PaCO 2 35.8 mmHg, base excess 19.8 mmol/L, HCO 3 11.0 mmol/L, lactic acid level 9.12 mmol/L and methemoglobin 0.3%. The patient was admitted to the intensive care unit 3 h after ingestion. By 4 h after ingestion, blood pressure was 84/47 mmHg, despite fl uid resuscitation. Cardiac index (CI) and systemic vascular resistance index (SVRI) were measured at 2.7 L/min/m 2 and 980 dynes-sec/ m 2 /cm 5 , respectively. Administration of norepinephrine was initiated at the rate of 4 microgram/min and titrated up to 10 microgram/min. Blood pressure returned to normal with this therapy. Lactic acidosis deteriorated (lactic acid 13.56 mmol/L, pH 6.98) despite sodium bicarbonate infusion. Continuous venovenous hemodiafi ltration (CVVHDF) was initiated to reverse metabolic acidosis. Metabolic acidosis gradually improved after initiation of CVVHDF and blood pressure stabilized. On hospital day (HD) 7, urine output decreased to less than 10 mL/h and serum creatinine increased to 2.7 mg/dL. A tense and distended abdomen was also observed. Intra-abdominal pressure monitoring (IAP) was initiated with a fi rst reading of 24 mmHg. Subsequently, a non-enhanced abdominal CT scan showed ascites in the abdominal cavity and diffuse bowel wall swelling (Fig. 1). In spite of conservative management, IAP remained more than 20 mmHg with oliguria, hypercapnea and increased peak airway pressure. Decompressive surgery could not be performed because the patient ’ s family refused surgical intervention. His condition deteriorated, and he died of multiple organ failure on HD 19. To our best knowledge, this is the fi rst documented case report of a lethal human poisoning with fl ufenoxuroncontaining insecticide. Our case showed three features. First was severe lactic acidosis, which was fi rst reported in fl ufenoxuron-containing insecticide poisoning by Jeong et al. 1 In their case, lactic acidosis returned to a near-normal state with conservative care. Unlike their case, in this patient lactic acidosis could not be reversed by sodium bicarbonate, and CVVHDF was needed to reverse lactic acidosis. The mechanisms of toxicity leading to lactic acidosis is uncertain, but inhibition of the oxygen utilization at the cellular level might contribute. Second was profound shock. Shock might be caused by vasodilation and might also relate in part to cardiogenic failure. While severe metabolic acidosis developed without evidence of hypotension in a previous report, 1 profound shock followed the onset of lactic acidosis in our case. As oral ingestion of cyclohexanone, used as solvent in Cascade TM , can cause circulatory shock and metabolic acidosis, 2 this may have contributed to the development of circulatory shock and metabolic acidosis in our case. However, the pathophysiology of fl ufenoxuroncontaining insecticide poisoning remains to be elucidated. A third problem was the development of an abdominal Clinical Toxicology (2011), 49, 876–877 Copyright

Hanging-associated left ventricular systolic dysfunction

BACKGROUNDS Although hanging injury is infrequent, its clinical course is usually devastating. Hanging patients usually need cardiopulmonary resuscitation (CPR). However, hanging-associated cardiovascular damage has not been fully established. The aim of this study was to evaluate echocardiographic findings in patients with hanging injury. METHODS We enrolled 25 patients (nine males and 16 females with mean age of 33±15 years) with hanging injury. Echocardiography was performed within 2 weeks after admission. Clinical, demographic, and laboratory data as well as transthoracic echocardiographic findings were analyzed. RESULTS Of the 25 patients, eight (two males and six females with mean age of 34±13 years) showed left ventricular systolic dysfunction (LVSD). Mean LV ejection fraction was 34±16%. Global hypokinesia was present in one patient. Apical ballooning with sparing of the basal segment was present in two patients. Basal akinesia and apical hyperkinesia were present in one patient. Four patients showed regional wall motion abnormalities unmatched with coronary territories. The duration of suspension or CPR was not significantly different according to the presence of LVSD. CONCLUSION This study showed the echocardiographic findings in considerable numbers of patients with hanging injury for the first time. Variable patterns of LVSD were present in patients with hanging injury.

A quantitative analysis of the relation between the clavicular tilt angle and subclavian central venous catheter misplacement

Objective The aim of the present study was to investigate the relation between shoulder position and subclavian central venous (SCV) catheter misplacement. The shoulder position was estimated using clavicular tilt angle (CTA) values observed on anteroposterior chest X-ray images. Methods A retrospective case-control study was conducted on all adult patients who underwent SCV catheterization in the emergency department during a 12-month period. Collected data included patient age, sex, diagnosis, catheterization side, catheter misplacement, and physician’s level of experience in catheterization. The CTA and other radiological variables such as the ipsilateral transverse length of the thorax and thickness of the clavicle were investigated. Results Among all central venous catheterizations (n=1,599), the subclavian route was used 981 times (61.4%). There were 51 misplacements of SCV catheters (5.2%) during the study period. There were no differences in the sex, age, blood pressure, and diagnosis between the two groups. The CTA values were 28.5°±7.3° and 22.6°±6.3° in the misplacement group and control group, respectively (95% confidence interval, 3.6 to 8.1; P<0.001). Conclusion In this study, the CTA was found to be 5.9° larger in the misplacement group than in the control group. Assuming that CTA indicates the shoulder position, our findings suggest that the chance of SCV catheter misplacement may be reduced by avoiding the shoulder elevated.

Injuries associated with the 580 km university student grand voluntary road march: focus on foot injuries.

College student volunteers (n = 142) completed a 580 km road march for 21 consecutive days. Each volunteer carried a backpack that weighed 14.1 ± 1.4 kg on the average. We investigated the incidence and location of blisters associated with the road march using a foot map along with other injuries. Overall, 95.1% of the subjects (135 of 142) sustained one or more injuries. All injured subjects had foot blisters, and 18% had other foot injuries. The most common locations of blister development were the right 5th toe (61%) and the left 5th toe (57%). The little toes seem to have been subjected to the greatest friction and shearing forces. March-related injuries, excluding foot injuries, were ankle pain (12.7%), knee pain (12.7%) and Achilles tendon pain (7.7%). Six subjects (4.2%) needed extra medical treatment for more than 2 weeks prior to returning to their daily lives after completion of the march due to associated injuries. The present study observed a very high incidence rate of injuries (95.1%) associated with the 580 km university students grand road march. These injuries posed an obstacle against completion of the road march and against returning to daily life. Active preventive interventions such as physical therapy and customized reinforced shoes and education program are recommended for reducing incidence rate and severity of injuries.

The Emerging Method of Suicide by Electronic Cigarette Liquid: a Case Report.

Electronic cigarettes (ECs) are a device that aerosolize liquid nicotine by heating a solution of nicotine, glycerol and flavoring agents. The awareness and the usage of ECs has increased in many countries. Due to the online sales and the absence of EC regulations, the prevalence of EC usage is especially high in adolescents and young adults. Due to the large amount and the high nicotine concentration of EC liquid, the ingestion for suicide can lead to cardiac death. We had two patients, a 27-year-old male who ingested about 23 mg/kg of nicotine and a 17-year-old female who ingested about 30 mg/kg of nicotine. Both patients presented seizure-like movement and cardiac arrest. They had metabolic acidosis and transient cardiomyopathy. They were ultimately discharged with a cerebral performance category of 2 and 4, respectively. Increasing EC use may produce more cases of medical problems or suicide by nicotine intoxication.

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

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.