No abstract available.
Emergency Medicine*

Serotonin syndrome is a drug-induced clinical syndrome caused by increased serotonin activity in the central nervous system. It occurs when starting a serotonergic drug, increasing its dose (including overdoses) or using a serotonergic drug in combination with other drugs. It manifests along a broad spectrum, ranging from mild side effects to life-threatening conditions. This condition should be suspected if patients have altered mental states, autonomic dysfunction, or neuromuscular symptoms such as clonus and tremor after using serotonergic drugs. Although the Hunter criteria have been widely used, new diagnostic criteria have recently been proposed to screen severe serotonin toxicity. It is necessary to differentiate it from neuroleptic malignant syndrome, which is associated with taking antipsychotic drugs that exert dopamine-antagonistic effects. If serotonin syndrome is suspected, the relevant drug should be stopped, and the patient should be treated with benzodiazepines. Severely ill patients with hyperthermia or neuromuscular symptoms require aggressive treatment. Serotonin receptor antagonists such as cyproheptadine or chlorpromazine have been tried as antidotes, but the level of evidence for their therapeutic effectiveness is very low.

Serotonin syndrome is a drug-induced clinical syndrome caused by increased serotonin activity in the central nervous system. It occurs when starting a serotonergic drug, increasing its dose (including overdoses) or using a serotonergic drug in combination with other drugs. It manifests along a broad spectrum, ranging from mild side effects to life-threatening conditions. This condition should be suspected if patients have altered mental states, autonomic dysfunction, or neuromuscular symptoms such as clonus and tremor after using serotonergic drugs. Although the Hunter criteria have been widely used, new diagnostic criteria have recently been proposed to screen severe serotonin toxicity. It is necessary to differentiate it from neuroleptic malignant syndrome, which is associated with taking antipsychotic drugs that exert dopamine-antagonistic effects. If serotonin syndrome is suspected, the relevant drug should be stopped, and the patient should be treated with benzodiazepines. Severely ill patients with hyperthermia or neuromuscular symptoms require aggressive treatment. Serotonin receptor antagonists such as cyproheptadine or chlorpromazine have been tried as antidotes, but the level of evidence for their therapeutic effectiveness is very low.

Serotonin syndrome is a drug-induced clinical syndrome caused by increased serotonin activity in the central nervous system. It occurs when starting a serotonergic drug, increasing its dose (including overdoses) or using a serotonergic drug in combination with other drugs. It manifests along a broad spectrum, ranging from mild side effects to life-threatening conditions. This condition should be suspected if patients have altered mental states, autonomic dysfunction, or neuromuscular symptoms such as clonus and tremor after using serotonergic drugs. Although the Hunter criteria have been widely used, new diagnostic criteria have recently been proposed to screen severe serotonin toxicity. It is necessary to differentiate it from neuroleptic malignant syndrome, which is associated with taking antipsychotic drugs that exert dopamine-antagonistic effects. If serotonin syndrome is suspected, the relevant drug should be stopped, and the patient should be treated with benzodiazepines. Severely ill patients with hyperthermia or neuromuscular symptoms require aggressive treatment. Serotonin receptor antagonists such as cyproheptadine or chlorpromazine have been tried as antidotes, but the level of evidence for their therapeutic effectiveness is very low.

No abstract available.
Humans ; Urinalysis*

Acute organophosphate (OP) poisoning produces cholinergic symptoms resulting from the inhibition of cholinesterase, and the overstimulation of muscarinic and nicotinic receptors in the synapses. The dominant clinical features of acute cholinergic toxicity include bradycardia, miosis, lacrimation, salivation, bronchorrhea, and bronchospasm. All symptomatic patients should receive therapy with oxygen, atropine, and pralidoxime. Atropine works as a physiologic antidote by competitively occupying muscarinic receptor sites, reducing the effects of excessive acetylcholine. Atropine should be immediately administered, and the dose can be titrated according to the severity of OP poisoning. A large dose may be necessary to overcome the excessive cholinergic state in case of severe poisoning. Pralidoxime is a biochemical antidote that reactivates acetylcholinesterase by removing OP from it. It is effective in treating both muscarinic and nicotinic symptoms. After some period of time, the acetylcholinesterase-OP compound undergoes a conformational change, known as aging, which renders the enzyme irreversibly resistant to reactivation by a pralidoxime. There has been a great deal of controversy over the effectiveness of pralidoxime in acute OP poisoning. However, it may be beneficial to administer pralidoxime for a sufficient period in case of severe poisoning with a large quantity of OP, which is common in Korea.
Acetylcholine ; Acetylcholinesterase ; Aging ; Atropine* ; Bradycardia ; Bronchial Spasm ; Cholinesterases ; Humans ; Korea ; Miosis ; Oxygen ; Poisoning* ; Pralidoxime Compounds ; Receptors, Muscarinic ; Receptors, Nicotinic ; Salivation ; Synapses

Scombroid fish poisoning (SFP) is a form of histamine food poisoning caused by the ingestion of improperly stored fish. The term “scombroid” derives from the family name of the fish family first implicated, such as tuna and mackerel. On the other hand, non-scombroid fish species, such as sardine and herring, can also cause histamine poisoning. The histamine is converted from histidine by a bacterial enzyme in the causative fish. Because the symptoms of SFP can easily be confused with food allergies, it is believed to have been significantly under-reported. In 2016, an outbreak of SFP occurred among primary school students who had eaten yellowtail steak in Korea. The most common findings consisted of a rapid onset of flushing of the face and trunk, erythematous and urticarial rash, diarrhea, and headache occurring soon after consuming the spoiled fish. Usually, the course is self-limiting and antihistamines can be used successfully to relieve symptoms, but several life-threatening SFP cases have been reported. Clinical toxicologists should be familiar with SFP and have competency to make a differential diagnosis between fish allergy and histamine poisoning. SFP is a histamine-induced reaction caused by the ingestion of histamine-contaminated fish, whereas a fish allergy is an IgE-mediated reaction. This review discusses the epidemiology, pathophysiology, diagnosis, treatment, and preventive measures of SFP.
Diagnosis ; Diagnosis, Differential ; Diarrhea ; Eating ; Epidemiology ; Exanthema ; Flushing ; Food Hypersensitivity ; Foodborne Diseases ; Hand ; Headache ; Histamine Antagonists ; Histamine ; Histidine ; Humans ; Hypersensitivity ; Korea ; Perciformes ; Poisoning ; Tuna

N-Acetylcysteine (NAC) is the standard antidote treatment for preventing hepatotoxicity caused by acetaminophen (AAP) poisoning. This review summarizes the recent evidence for the treatment of AAP poisoning. Several alternative intravenous regimens of NAC have been suggested to improve patient safety by reducing adverse drug reactions and medication errors. A two-bag NAC infusion regimen (200 mg/kg over 4 h, followed by 100 mg/kg over 16 h) is reported to have similar efficacy with significantly reduced adverse reactions compared to the traditional 3-bag regimen. Massive AAP poisoning due to high concentrations (more than 300-lines in the nomogram) needs to be managed with an increased maintenance dose of NAC. In addition to NAC, the combination therapy of hemodialysis and fomepizole is advocated for severe AAP poisoning cases. In the case of a patient presenting with an altered mental status, metabolic acidosis, elevated lactate, and an AAP concentration greater than 900 mg/L, hemodialysis is recommended even if NAC is used. Fomepizole decreases the generation of toxic metabolites by inhibiting CYP2E1 and may be considered an off-label use by experienced clinicians. Since the nomogram cannot be applied to sustained-release AAP formulations, all potentially toxic sustained-release AAP overdoses should receive a full course of NAC regimen. In case of ingesting less than the toxic dose, the AAP concentration is tested twice at an interval of 4 h or more; NAC should be administered if either value is above the 150-line of the nomogram.

PURPOSE: Despite the clinical and socio-economic impact of acute poisoned patients, many of the treatments are not standardized in Korea. Moreover, no formal training that is specifically focused on clinical toxicology exists. Rather, training and education are conducted case by case in various institutions. This study was conducted to develop a standardized simulation-based clinical toxicology training curriculum for healthcare providers. This program will focus on specific assessment and treatment of critical toxicology patients, specifically those who have been poisoned with organophosphate. METHODS: The study was performed using a pre- and post-design to determine the effects of implementation of this program. The study was conducted at eight different urban teaching hospitals in a simulated room in the clinical area. The study was targeted to 19 groups composed of emergency residents and nurses. Simulation-based learning was conducted for each group. RESULTS: All 19 groups achieved the minimum passing score of 75%. Implementation of the program led to improved performance rates for overall management and cooperative moods competency (p<0.01). Inter-rater agreement between the two evaluators was excellent. In general, the participants thought the program was realistic and were able to recognize and improve the competencies needed to care for organophosphate poisoned patients. CONCLUSION: Simulation-based learning is an effective educational strategy that can be applied to improving and understanding proper care for rare but critical patients. This program was effective at improving team performance and cooperative moods when managing an organophosphate poisoned patient in the Emergency Department.
Critical Illness* ; Curriculum ; Education ; Emergencies ; Emergency Service, Hospital ; Health Personnel ; Hospitals, Teaching ; Humans ; Korea ; Learning* ; Organophosphate Poisoning ; Practice Guidelines as Topic* ; Simulation Training ; Toxicology

Pulmonary embolism is a serious complication, which is well known in patients undergoing total hip or total knee arthroplasty or lower extremity fracture surgery. But, there are few literatures concerning pulmonary embolism after upper extremity surgery. Pulmonary embolism after minor upper extremity fracture surgery is extremely rare. We report a case of 66-year-old female patient that developed pulmonary embolism after percutaneous cannulated screw fixation for a greater tubercle fracture of the proximal humerus with literature review.
Aged ; Arthroplasty ; Female ; Fracture Fixation ; Hip ; Humans ; Humerus* ; Knee ; Lower Extremity ; Pulmonary Embolism* ; Shoulder Fractures ; Upper Extremity