Purpose: Cardiovascular or respiratory complications of acute intoxication are the most common causes of mortality. Advanced cardiac life support (ACLS) or specific antidotes help manage these cardiac or respiratory complications in acute intoxication. On the other hand, some cases do not respond to ACLS or antidotes and they require some special treatment, such as extracorporeal life support (ECLS). ECLS will provide the chance of recovery from acute intoxication. This study examined the optimal timing of ECLS in acute intoxication cases. Methods: This paper is a brief report of a case series about ECLS in acute poisoning. The cases of ECLS were reviewed and the effects of ECLS on the blood pressure and serum lactate level of the patients were analyzed. Results: A total of four cases were reviewed; three of them were antihypertensive agent-induced shock, and one was respiratory failure after the inhalation of acid. The time range of ECLS application was 4.8-23.5 hours after toxic exposure. The causes of ECLS implementation were one for recurrent cardiac arrest, two for shock that did not respond to ACLS, and one for respiratory failure that did not respond to mechanical ventilator support. Three patients showed an improvement in blood pressure and serum lactate level and were discharged alive. In case 1, ECLS was stared at 23.5 hours post toxic exposure; the patient died due to refractory shock and multiple organ failure. Conclusion: The specific management of ECLS should be considered when a patient with acute intoxication does not recovery from shock or respiratory failure despite ACLS, antidote therapies, or mechanical ventilator support. ECLS improved the hemodynamic and ventilator condition in complicated poisoned patients. The early application of ECLS may improve the tissue perfusion state and outcomes of these patients before the toxic damage becomes irreversible.
Purpose: This study was conducted to describe the characteristics of patients with carbon monoxide (CO) poisoning. Methods: We retrospectively surveyed data from the Emergency Department based Injury In-depth Surveillance of 20 hospitals (2011-2014). We included patients whose mechanism of injury was acute CO poisoning caused by inhalation of gases from charcoal or briquettes. We surveyed the annual frequency, gender, age, result of emergency treatment, rate of intensive care unit (ICU) admission, result of admission, association with alcohol, and place of accident. We also surveyed the cause and experience of past suicide attempts by intentional poisoning. Results: A total of 3,405 patients were included (2,015 (59.2%) and 1,390 (40.8%) males and females, respectively) with a mean age of $39.83{pm}18.51$ year old. The results revealed that the annual frequency of CO poisoning had increased and the frequency of unintentional CO poisoning was higher than that of intentional CO poisoning in January, February and December. The mean age of intentional CO poisoning was younger than that of unintentional CO poisoning ($38.41{pm}13.03$ vs $40.95{pm}21.83$) (p<0.001). The rates of discharge against medical advice (DAMA), ICU care and alcohol association for intentional CO poisoning were higher than for unintentional CO poisoning (36.4% vs 14.0%, 17.8% vs 4.7%, 45.2% vs 5.6%) (p<0.001). The most common place of CO poisoning was in one's residence. Conclusion: The annual frequency of total CO poisoning has increased, and unintentional CO poisoning showed seasonal variation. DAMA, ICU care, and alcohol association of intentional CO poisoning were higher than those of unintentional CO poisoning.
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Prevalence of Carbon Monoxide Poisoning and Hyperbaric Oxygen Therapy in Korea: Analysis of National Claims Data in 2010–2019 Eunah Han, Gina Yu, Hye Sun Lee, Goeun Park, Sung Phil Chung Journal of Korean Medical Science.2023;[Epub] CrossRef
A 24 year-old man attempted suicide by injection of 1 cc of thinner into his left antecubital vein; 3 hours later, he visited our emergency room because of left chest pain. We suspected a chemical pneumonitis based on the abnormal findings of his chest X-ray and computed tomography. On the 3rd day after admission, a cellulitis also occurred at the injection area. His symptoms were relieved after supportive care for 2 weeks. There is significant experience with intoxication of thinner inhalation, whereas intoxication of intravenous thinner is rare.
Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. Following are brief statements describing the motor peripheral neuropathy involved bilateral lower extremities of a patient who recovered following acute carbon monoxide poisoning. After inhalation of smoke from a fire, a 60-year-old woman experienced bilateral leg weakness without edema or injury. Neurological examination showed diplegia and deep tendon areflexia in lower limbs. There was no sensory deficit in lower extremities, and no cognitive disturbances were detected. Creatine kinase was normal. Electroneuromyogram patterns were compatible with the diagnosis of bilateral axonal injury. Clinical course after normobaric oxygen and rehabilitation therapy was marked by complete recovery of neurological disorders. Peripheral neuropathy is an unusual complication of CO intoxication. Motor peripheral neuropathy involvement of bilateral lower extremities is exceptional. Various mechanisms have been implicated, including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia, and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without sequelae. Emergency physicians should understand the possible-neurologic presentations of CO intoxication and make a proper decision regarding treatment.
Purpose: The purpose of this systematic review was to evaluate the evidence regarding injury and poisoning associated with the clinical mercury thermometer. Methods: Electronic literature searches were conducted for identification of relevant studies and case reports of injury and poisoning associated with the clinical mercury thermometer. The search outcomes were limited to literature with English and Korean languages published from 1966. Studies related to occupational mercury exposure, or mercury exposure from sphygmomanometer, barometer, and fluorescent light were excluded. Results: A total of 60 reports, including 59 case reports, were finally included. Of those, nine cases pertained to an intact thermometer as a foreign body, 25 injuries were related to a thermometer, and 26 cases involved exposures to mercury from a broken thermometer. Case reports were classified according to severity into 16 mild, 41 moderate, and two severe cases. Two cases of mortality were reported, one was deliberate intravenous injection of mercury and the other was acute vapor inhalation of mercury from broken thermometers. Conclusion: Findings of this systematic review suggested that the mercury thermometer could cause various forms of poisoning and injury. In particular, inhalation of mercury vapor from a broken thermometer can lead to systemic toxicity requiring chelating therapy.
Trichloroethylene (TCE, $C_2HCl_3$), which was introduced as a gas for general anesthesia and analgesia in early 1900's has been widely used in industry as an organic solvent. Occupational exposure to TCE is an important medical problem. Manifestations of acute exposure to TCE include mucocutaneous irritation, hepatotoxicity, cognitive impairment, sleep, headache, respiratory insufficiency and death. We report a 38-year-old man who was admitted to a department of emergency medicine after occupational inhalation exposure to TCE. He rapidly developed semicoma and respiratory depression. After mechanical ventilation, hypercapnea and hypoxemia disappeared and his mental state again became alert. Careful evaluation and proper respiratory support are important for respiratory failure after occupational TCE inhalation.
Purpose: Surveys on poisoning usually involves intoxication rather than inhalation, skin contact, etc. Therefore, we examined the characteristics of patients who visited the emergency department in an industrial complex after acute industrial exposure to toxic materials. Methods: Medical records of patients exposed to toxic materials in the work places from April, 2006, to March, 2008, were analyzed retrospectively. Inhalation patients due to fire were excluded. Results: Subjects included 66 patients, with a mean age of $35.4{pm}10.9$ years, mostly men (91%). Toxicity occurred in 51 patients (77%) by contact, 15 patients (23%) by inhalation, and none by oral ingestion. For toxic materials, 10 patients were exposed to hydrofluoric acid, 8 to hydrochloric acid, 7 to sodium hydroxide, 7 to metals, and others. The face and hands were the most frequent exposure site by contact. Most exposures were caused by accidents, with 29 cases (42%) exposed because of carelessness or not wearing protective equipment. Most complaints were pain on exposure site, but 7 of the inhalation patients complained of dyspnea. The majority of patients with contact exposure were discharged after wound care or observation. After inhalation exposure, 1 patient died and 5 patients were admitted to the intensive care unit. Conclusion: Major causes of workplace exposure were not wearing protective equipment or carelessness. Although contact exposures are usually benign, cautious observation and management are required in patients with inhalation exposure.
Purpose: Pyrethroid is an insecticide that produces moderate intoxication in mammals, with neither exposure to skin nor inhalation resulting in severe systemic manifestations. In 2005 we made a nationwide survey of agrichemical human intoxication. The object of this study is to analyze pyrethroid intoxications based on the 2005 survey. Methods: We prospectively collected data from 1 August 2005 to 31 July 2006 by a standard investigation protocol. We analyzed demographic data, exposure data (cause, amount, ingredients), clinical features, and courses. Results: A total of 125 cases of pyrethroid intoxication were surveyed. The mean patient age was $56.78{pm}16.158$ years old, and the mean amount ingested was $121.85{pm}110.732ml$. Patients were classified into four severity groups according to symptoms and mental status: the asymptomatic group (27 patients, 21.6%), the mild symptom group (48, 38.4%), the moderate symptom group (21, 16.8%), and the severe symptom group (7, 5.6%). There were statistically significant differences in mental status, severity, and mean ICU days between two groups. Admission days by severity grade for the asymptomatic, mild, moderate, and severe symptom groups were $5.49{pm}16.051,;3.65{pm}4.143,;4.59{pm}3.335,;and;8.14{pm}7.199days$, respectively (p=0.047). Conclusion: Nationwide surveillance was extremely telling in uncovering a high frequency of agrichemical intoxication in Korea. In pyrethroid intoxication, severity grading can be a useful prognostic tool.
The carbamates are a group of insecticides derived from carbamic acid, with a broad spectrum of uses as agricultural and household garden insecticides. Carbamate insecticides are reversible cholinesterase inhibitors. Their inhibitory action is mediated by reversible carbamylation of acetylcholine, as with the organophosphate insecticides. Carbamates are absorbed by the body through multiple routes, including inhalation, ingestion, and dermal absorption. Although poisoning can result from occupational exposure or accidental ingestion, in most cases there is suicidal intent. This is particularly true in developing countries, where the highest incidence of morbidity and mortality from this cause occurs. Cardiac complications often accompany poisoning by carbamate compounds, which may be serious and often fatal. The extent, frequency, and pathogenesis of cardiac toxicity from carbamate compounds has not been clearly defined. Possible mechanismsinclude sympathetic and parasymphatetic overactivity, hypoxemia, acidosis, electrolyte derangements, and a direct toxic effect of the compounds on the myocardium. Patients with carbamate poisoning should immediately be transferred to an intensive or coronary care unit where appropriate monitoring and resuscitative facilities are available. We here report a case of acute coronary syndrome resulting from acute carbamate ingestionthat resulted in a healthy discharge.
Organophosphate insecticides, commonly used in agriculture, are a gradually increasing cause of accidental and suicidal poisoning. Intoxication can occur by ingestion, inhalation or dermal contact. Exposure to organophosphorus agents causes a sequentially triphasic illness consisting of the cholinergic phase, the intermediate syndrome, and organophosphate-induced delayed polyneuropathy. Acute pancreatitis as a rare complication of organophosphate intoxication has also been infrequently observed. We report a case of intoxication with organophosphate (phos-phamidon) by parenteral exposure (inhalation and/or dermal contact). A 34-year-old male patient was transferred to our Emergency Medical Center and was intubated due to a progressive respiratory failure. He presented with meiotic pupils, cranial nerve palsies, weak respiration, and proximal limb motor weaknesses without sensory changes. He had been employed in filling syringes with phosphamidon during the previous month. Because the patient's history and symptoms suggested organophosphate intoxication with intermediate syndrome, he was mechanically ventilated for 18 days with continuous infusion of atropine and pralidoxime (total amounts of 159 mg and 216 g, respectively). During his admission, hyperamylasemia and hyperli-pasemia were detected, and his abdominal CT scan showed a finding compatible with acute pancreatitis. He was administered a conservative treatment with NPO and nasogastric drainage. The patient was discharged and showed neither gastrointestinal nor neurologic sequelae upon follow up at one week and three months.
Cyanides and Hydrogen cyanide are used in production of chemicals, electroplating, photographic development, making plastics, fumigating ships, and some mining processes. We experienced of Hydrogen cyanide inhalation injury. A 45-year-old man worked at electroplating. As soon as he mixed sodium cyanide with acid, cyanide produced hydrogen cyanide, occasionally he inhaled Hydrogen cyanide and he lost his consciousness. He was moved to near hospital and took emergency treatment and then was transferred to our hospital. On arrival he had severe dyspnea, metabolic acidosis, and tachycardia. After he was treated with supportive method he recovered his consciousness in 20 hours at emergency room.
Nitrogen dioxide ($NO_2$), which produced during the process of silage, metal etching, explosives, rocket fuels, welding, and by-product of burning of fossil fuels, is one of major components of air pollutant. Accidental exposure of high level of $NO_2$ produces cough, dyspnea, pulmonary edema which may be delayed $4~12$ hours and, in $2~6$weeks, bronchiolitis obliterans. We experienced a case of acute pulmonary injuny induced by industrial exposure to high level of $NO_2$ during repair of $NO_2$ pipeline in a refinery. A 55-year-old man experienced nausea and severe dyspnea in 6 hours after $NO_2$ inhalation. Initial blood gas examination revealed severe hypoxemia accompanying increased alveolar-arterial O2 difference. Radiological examination showed diffuse ground glass opacities in both lung fields. Clinical symptoms and laboratory findings, including radiological study and pulmonary function test were improved with conservative treatment using inhaled oxygen and bronchodilator. and there was no evidence of bronchial fibrosis and bronchiolitis obliterance in chest high resolution computed tomography performed 6 weeks after exposure. Here, we report a case of $NO_2$ induced acute pulmonary injuny with a brief review of the relevant literature.
Purpose: Paraquat is the most commonly used herbicide in Korea. Exposure to paraquat through the skin has resulted in local irritation or inflammation of varying degree, sometimes severe. The purpose of this study was to review the patients with paraquat poisoning by skin absorption. Methods: We analysed retrospectively the clinical and laboratory findings of 45 patients with paraquat poisoning after dermal exposure, who were admitted to Soonchunhyang University Cheonan Hospital from January 1999 to December 2003. Results: Among 870 cases of paraquat poisoning, 45 cases were exposed to paraquat through the skin. The peak incidence was the fifth decade($40\%$). The clinical symptoms were pain, pruritus, nausea, and vomiting. The major skin lesions were generalized vesicobullae and necrotic erosion in face, scrotum, trunk, upper and lower extremities and etc. All patients were survived after skin contact or inhalation of paraquat. Conclusion: This study illustrates the extreme toxicity of paraquat and demonstrates that lethal quantities of paraquat may be absorbed if repeated exposure to it. Stricter precautions, including the mandatory use of protective clothing, should be recommended whenever this material is used.
Purpose: In recent review of physician suicides] the relative risk of physicians is higher than the general population. The majority of physician suicide were by poisoning. The purpose of this study was to analyse the medical personnels with suicide by poisoning compared with the general population. Methods: We reviewed medical records of 15 medical related personnels with suicide by poisoning who visited the emergency medical centers of St. Mary's and Kangnam St. Mary's hospitals from March 1998 to Aug 2004. For the comparison with general population in analysis] the collected data was acquired from medical records of 677 intoxicated patients in St. Mary's Hospital during the same period. Results: Fifteen suicides of physicians (n=7), nurses (n=4), medical students (n=2), pharmacist (n=1) and medical assistant technician (n=1) was evaluated with regard to the method of poisoning. Preferred methods were ingestion of medications orally ($54\%$) and by infusion/injection ($46\%$). The results were compared with the general population group (n=677: oral ingestion of medications $98\%$, inhalation $1.6\%$). Intoxications by infusion/injection predominated more clearly in physicians than in the total collective. Conclusion: Comparing with the general population, the tendency to a method of suicidal poisoning being typical of the profession rises among physicians and related occupations with the degree of specialization, caused by increasing knowledge, easier access to appropriate drugs and methods.
Arsenic poisoning has three types of poisoning. First, acute arsenic poisoning is usually caused by oral intake of large amount of arsenic compound with purpose of homicide or suicide. Second, chronic arsenic poisoning is caused by inhalation of arsenic in the occupational setting or by long-term oral intake of arsenic-contaminated well water. Third, arsine poisoning occurs acutely when impurities of arsenic in non-ferrous metal react with acid. Clinical manifestation of acute arsenic poisoning is mainly gastrointestinal symptoms and cardiovascular collapse. Those of chronic poisoning are skin disorder and cancer. Arsine poisoning shows massive intravascular hemolysis and hemoglobinuria with acute renal failure. Exposure evaluation is done by analysis of arsenic in urine, blood, hair and nail. Species analysis of arsenic is very important to evaluate inorganic arsenic acid and mono methyl arsenic acid (MMA) separated from dimethyl arsenic acid (DMA) and trimethyl arsenic acid (TMA) which originate from sea weed and sea food. Treatment with dimercaprol (BAL) is effective in acute arsenic poisoning only.