Short and long-term outcomes of multidimensional physiotherapy in cases with acute compartment syndrome secondary to carbon monoxide poisoning with prolonged forearm compression.

BACKGROUND: Compartment syndrome following carbon monoxide (CO) poisoning and compression, can have a devastating impact on neuromuscular structures, depending on a time-based dosage. PURPOSE: To investigate multidimensional physiotherapy's short-term and long-term outcomes in identical twin cases who developed compartment syndrome due to CO poisoning and prolonged compression. STUDY DESIGN: Case report. METHODS: This study was conducted with two male cases, a 21-year-old identical twin. The loss of consciousness due to CO poisoning lasted for 15 hours. Case one had compartment syndrome that caused damage to the median and ulnar nerves in the right forearm, while Case two had compartment syndrome that caused damage to the radial nerve in the left forearm. No surgical intervention was performed (Fasciotomy etc). RESULTS: The disability, dexterity, hand health status, sensory-motor function, and edema were evaluated. Initial evaluations showed severe sensory and motor dysfunction, disability, and edema. Treatment included Complex decongestive physiotherapy, electrical stimulation, therapeutic ultrasound, orthotics, and exercises. On the 144th day (discharge day), both cases still exhibited weakness in functional strength and sensory loss compared to the uninjured side. At the ninth month, all parameters except strength were similar to the uninjured side in both cases. By the 53rd month, strength also reached normal values. CONCLUSIONS: Multidimensional physiotherapy effectively manages edema, improves sensory-motor function, and enhances hand function in the short and long term.

Sex differences among patients with intentional poisoning presenting to the emergency Department at a Tertiary Care Centre in Beirut, Lebanon.

Poisoning poses a worldwide public health challenge and recent data from Lebanon in 2020 revealed that over half patients presenting with acute toxicological exposure intentionally poisoned themselves, primarily with suspected suicidal intent. This study aims to assess sex disparities in intentional toxicological exposures among patients presenting to the Emergency Department, at a tertiary care centre in Lebanon. This was a secondary analysis of an existing toxicological database, including patients aged 6 years and older admitted due to acute overdose from March 2015 to August 2022. A total of 444 cases of intentional poisoning were analysed, with 302 (68.0%) women. The primary cause of intentional poisoning was suspected suicide in both sexes, significantly more common in women (85.1% versus 65.5%, P < 0.001). Specific agents exposed to patients varied by sex; sedatives/hypnotics/antipsychotics, antihistamines, and melitracen/flupentixol were significantly more prevalent in women (P < 0.001) while men showed higher prevalence for ethanol (P = 0.02), stimulants, street drugs and opioids (P < 0.001). Our study underscores substantial sex differences in intentional poisoning cases in Lebanon. Women exhibited a higher likelihood of exposures to sedatives/hypnotics/antipsychotics, antihistamines and melitracen/flupentixol, while stimulant drugs, ethanol, and opioids were prevalent in men. Developing proper and effective sex-specific measures may mitigate potential physical and psychological consequences.

An autopsy case of intoxication caused by drug interaction with multiple psychotropic drugs, fluvoxamine, levomepromazine, and trihexyphenidyl.

A case of death due to combined use of multiple drugs is reported, and the pharmacokinetic interactions are discussed. A woman in her thirties was found dead in her home. A medico-legal autopsy found no findings suggestive of injury or natural disease. Toxicological analysis using liquid chromatography tandem mass spectrometry (LC-MS/MS) identified a toxic level of fluvoxamine (0.947 µg/mL), and concentrations greater than the therapeutic levels of levomepromazine (0.238 µg/mL) and trihexyphenidyl (0.225 µg/mL) were present, while bromazepam, haloperidol, sulpiride, and 7-aminoflunitrazepam were within or below their therapeutic ranges. Fluvoxamine is mainly metabolized by cytochrome P450 2D6 (CYP2D6), and levomepromazine is a potent CYP2D6 inhibitor. A high concentration of levomepromazine may increase the blood fluvoxamine level. Since the combined use of levomepromazine and fluvoxamine induces seizures, it may have been involved in causing the subject's death. In addition, combined use of trihexyphenidyl may potentiate anticholinergic effects of fluvoxamine overdose, including convulsions and coma. It was concluded that the cause of the subject's death was the interaction of multiple drugs.

Review of the lethal mechanism of insulin poisoning and the characteristic of forensic identification.

Insulin, as the only hypoglycemic hormone in the body, plays a key role in blood sugar control. However, excessive insulin intake can lead to insulin poisoning and even death, which often occurs in clinical and forensic work. At present, some researches on insulin poisoning have been carried out at home and abroad, however, it seems that the mechanism and forensic characteristics of insulin poisoning are not clear and complete. Therefore, in this paper, we reviewed the potential mechanism of insulin poisoning, the methods of insulin detection and the forensic identification of poisoning cases, aiming at providing services for the forensic identification of insulin poisoning.

Exposure to anticoagulant rodenticides in steppe polecat (Mustela eversmanii) and European polecat (Mustela putorius) in central Europe.

Poisoning caused by coumarin-type anticoagulant rodenticides (ARs) stands as the predominant method for controlling rodents globally. ARs, through secondary poisoning, pose a significant threat to predators due to their lethal and sublethal effects. We examined the concentration of accumulated ARs in liver samples of mostly road-killed steppe polecats (Mustela eversmanii) and European polecats (M. putorius) collected throughout Hungary between 2005 and 2021. The steppe polecat samples were found mainly from Eastern Hungary, while European polecats from Western Hungary. We measured the concentration of six residues by HPLC-FLD. Our analysis revealed the presence of one first-generation and four second-generation ARs in 53 % of the steppe polecat (36) and 39 % of the European polecat (26) samples. In 17 samples we detected the presence of at least two AR compounds. Although we did not find significant variance in AR accumulation between the two species, steppe polecats displayed greater prevalence and maximum concentration of ARs, whereas European polecat samples exhibited a more diverse accumulation of these compounds. Brodifacoum and bromadiolone were the most prevalent ARs; the highest concentrations were 0.57 mg/kg and 0.33 mg/kg, respectively. The accumulation of ARs was positively correlated with human population density and negatively correlated with the extent of the more natural habitats in both species. To the best of our knowledge, this is the first study to demonstrate anticoagulant rodenticide exposure in steppe polecats globally, and for European polecats in Central European region. Although the extent of AR accumulation in European polecat in Hungary appears comparatively lower than in many other European countries, the issue of secondary poisoning remains a serious problem as these ARs intrude into food webs. Reduced and more prudent usage of pesticides would provide several benefits for wildlife, included humans. However, we advocate a prioritization of ecosystem services through the complete prohibition of the toxicants.

Liver injury in paraquat poisoning: A retrospective cohort study.

BACKGROUND AND AIMS: Liver injury is one of the common complications of paraquat (PQ) poisoning, but whether the degree of liver injury is related to patient prognosis is still controversial. This study aimed to investigate whether liver injury was a risk factor for death in PQ-poisoned patients. METHODS: We conducted a retrospective cohort study of PQ-poisoned patients from the past 10 years (2011-2020) from a large tertiary academic medical centre in China. PQ-poisoned patients were divided into a normal liver function group (n = 580) and a liver injury group (n = 60). Propensity score matching (PSM) analysis was then performed. RESULTS: A total of 640 patients with PQ poisoning were included in this study. To reduce the impact of bias, dose of PQ, urinary PQ concentration and time from poisoning to hospital admission were matched between the two groups. A 3:1 PSM analysis was performed, ultimately including 240 patients. Compared with the normal liver function group, patients in the liver injury group were older, had a higher R value ([ALT/ULN]/[ALP/ULN]) (p < .001) and had a higher mortality rate. Cox regression analysis showed that there was no significant association between alanine aminotransferase, alkaline phosphatase, total bilirubin levels and hazard of death, but age, PQ dose, creatine kinase isoenzyme, creatine kinase, white blood cell count, neutrophil percentage and lymphocyte percentage were associated with mortality in patients with PQ poisoning. CONCLUSIONS: The occurrence of liver injury within 48 h after PQ poisoning was a risk factor for mortality, and such liver injury was likely of a hepatocellular nature. Age, PQ dose, creatine kinase isoenzyme and white blood cell count were positively correlated with mortality, while creatine kinase, percentage of neutrophils and lymphocytes were inversely correlated.

A clinical study and laboratory evaluation of the cardiac and hepatic toxic effects of paraphenylenediamine.

INTRODUCTION: Paraphenylenediamine is the main component in many commercial hair dyes, and can produce severe local and systemic toxicity reactions after acute ingestion or dermal absorption. The aim of this study was to assess the factors contributing to morbidity and mortality in cases of acute paraphenylenediamine poisoning, with a focus on evaluating the resultant hepatic and cardiac toxicity. METHODS: This observational study was conducted on patients with acute paraphenylenediamine poisoning presenting to Sohag University Hospitals, and included a retrospective part from February 2021 to January 2022 and a prospective part from February 2022 to July 2022. Clinical data were extracted and receiver operating characteristic curves created to identify prognostic markers. RESULTS: Among 50 eligible patients 39 (78 percent) recovered, and 11 (22 percent) died or had permanent complications. Angioedema and anuria were the most frequent features in complicated cases. By receiver operating characteristic analysis, either an increase in aspartate aminotransferase activity greater than 644 IU/L or alanine aminotransferase activity greater than 798 IU/L, a time delay to presentation of greater than 4.5 hours, and a pH of less than 7.32 were associated with a significant increase in morbidity and mortality. While cardiac enzyme activities, and concentrations of blood urea nitrogen and creatinine increased in most cases, they were not associated with mortality. DISCUSSION: Management of patients with paraphenylenediamine poisoning is mainly supportive, as there is no specific antidote. Respiratory failure and kidney failure are the most life threatening complications. Hepatoxicity and cardiotoxicity also occur. The ability to predict the events can help guide patient disposition and care. CONCLUSION: Elevated liver enzyme activities, increased time delay to admission, decreased pH, and the presence of angioedema and anuria can be used as predictors of morbidity and mortality in patients with acute paraphenylenediamine poisoning.

Risk of lung diseases in patients with previous carbon monoxide poisoning: a nationwide population-based cohort study in the Republic of Korea.

INTRODUCTION: Carbon monoxide poisoning is associated with severe damage to various organs. In this study, we aimed to determine if previous carbon monoxide poisoning was associated with an increased risk of lung diseases. METHODS: The study population was derived from the National Health Insurance Service database of Korea between 1 January 2002 and 31 December 2021. Adults with carbon monoxide poisoning, with at least one visit to medical facilities between 2002 and 2021, were included. For comparison, an equal number of matched controls with the same index date were selected from the database. RESULTS: A total of 28,618 patients with carbon monoxide poisoning and 28,618 matched controls were included in this study. Approximately 42.8 per cent of the patient and control groups were female, with a mean age of 51.3 years. In patients with carbon monoxide poisoning, there was a significant increase in the risk of lung cancer (adjusted hazard ratio, 1.84; 95 per cent confidence interval, 1.42-2.39; P < 0.001), chronic obstructive pulmonary disease (adjusted hazard ratio, 1.60; 95 per cent confidence interval, 1.36-1.89; P < 0.001), pulmonary tuberculosis (adjusted hazard ratio, 1.46; 95 per cent confidence interval, 1.13-1.88; P = 0.003), and non-tuberculous mycobacterial infection (adjusted hazard ratio, 1.54; 95 per cent confidence interval, 1.01-2.36; P = 0.047). DISCUSSION: In this retrospective cohort study, previous carbon monoxide poisoning was associated with an increased risk of lung cancer, chronic obstructive pulmonary disease, pulmonary tuberculosis, and non-tuberculous mycobacterial infection. Further studies are needed to confirm such an association in other populations and the risk of lung diseases due to the toxic effect of carbon monoxide from different sources. CONCLUSIONS: Previous carbon monoxide poisoning was associated with an increased risk of lung diseases, but the relative importance of the causes and sources of exposure was not known. The long-term management of survivors of acute carbon monoxide poisoning should include monitoring for lung cancer, chronic obstructive pulmonary disease, pulmonary tuberculosis, and non-tuberculous mycobacterial infection.

Tralopyril poisoning due to respiratory exposure.

INTRODUCTION: Tralopyril is a metabolite of the pesticide chlorfenapyr. Direct toxicity by tralopyril has not been described. We report two cases of tralopyril poisoning via inhalation. CASE PRESENTATIONS: Two workers developed heat intolerance, diaphoresis, and weight loss after occupational inhalational exposure to tralopyril. Patient 1: The exposure was due to the absence of respiratory protection. Magnetic resonance imaging showed abnormal signals in the bilateral periventricular white matter, corpus callosum, basal ganglia, brainstem, and spinal cord. The patient's blood tralopyril concentrations on days 1, 3, 5, 8, and 11 post-admission were 1.09 mg/L, 1.04 mg/L, 1.01 mg/L, 0.71 mg/L, and 0.313 mg/L, respectively. Haemoperfusion (HA330), haemoperfusion (HA380), and haemodiafiltration were performed on days 1-3, 5-8, and 9-10, respectively. Patient 2: The patient's symptoms followed inappropriate use of respiratory protection. His blood tralopyril concentrations on days 1, 4, 5, and 6 were 0.592 mg/L, 0.482 mg/L, 0.370 mg/L, and 0.228 mg/L, respectively. DISCUSSION: The patients presented with features typical of chlorfenapyr poisoning, which suggests that tralopyril is the main toxic metabolite of chlorfenapyr. CONCLUSION: Tralopyril can be absorbed by inhalation, leading to delayed clinical symptoms and organ damage, including toxic encephalopathy and spinal cord damage.

CARDIOGENIC SHOCK AND GLOBUS PALLIDUS INJURY AS A PRESENTATION OF CARBON MONOXIDE POISONING.

Carbon monoxide poisoning is one of the leading causes of mortality and morbidity by poisoning in the world. Signs and symptoms are nonspecific and related to impaired oxygen delivery to tissues, with the brain being the most affected organ due to its high oxygen demand. CO-Hb is a poor indicator of severity and long-term outcome, with clinicians relying more on clinical features such as level of consciousness and need for intubation, organ dysfunction and shock and also pH level. A 45-year-old female was found unconscious in her home with the fireplace lit and smoke all over the house. She was last seen well 18 hours before. She was brought to the emergency department and was admitted to the ICU in coma and cardiogenic shock, with a metabolic acidosis with hyperlactacidemia and a CO-Hb level of 15.5%. Laboratorial investigation revealed hepatic cytolysis, acute renal failure, rhabdomyolysis and a troponin I level of 338 ng/L. ECG showed no acute myocardial ischemia. Echocardiogram revealed diffuse hypokinesia with an ejection fraction of 25%. Head CT scan showed bilateral and symmetrical hypodensities of the globus pallidus. The patient underwent hyperbaric oxygen treatment with full neurological and cardiac recovery, allowing extubation 48 hours after admission. This rare severe case of coma due to carbon monoxide intoxication with globus pallidus injury and cardiogenic shock was successfully treated with hyperbaric oxygen, showing that it can be the right treatment choice in these cases, with an excellent impact on neurological and cardiac outcome.

L'intoxication au CO est une des causes principales de décès par empoisonnement dans le monde. Les signes, non spécifiques, sont dus à l'hypoxie cellulaire et le cerveau est le plus souvent atteint en raison de sa consommation d'oxygène élevée. Le taux d'HbCO est un indice peu fiable de la gravité initiale et du risque de séquelles si bien que l'on préfère se baser sur la clinique (conscience, nécessité d'intubation, dysfonctions d'organe, choc) et le pH sanguin. Une femme de 45 ans a été trouvée inconsciente à son domicile entièrement enfumé, cheminée allumée. Le dernier contact remontait à 18 heures. Elle a été hospitalisée en réanimation en coma et choc cardiogénique, avec une acidose lactique et une HbCO à 15,5%. La biologie retrouvait une cytolyse hépatique, une insuffisance rénale aiguë, une rhabdomyolyse et une troponine I à 338 ng/L. L'ECG ne trouvait pas d'ischémie, l'échocardiographie objectivait une hypokinésie globale et évaluait la fraction d'éjection à 25%. La TDM cérébrale montrait une hypodensité pallidale bilatérale. L'oxygénothérapie hyperbare (OHB) a permis une récupération neurologique et cardiaque complètes, permettant l'extubation à h48. Cette récupération complète après OHB confirme qu'il peut s'agir du traitement idoine des intoxications graves au CO, avec un excellent impact sur les devenirs cardiaque et neurologique.

Alocasia odora poisoning due to calcium oxalate needle crystals in Japan.

Objective: To elucidate the actual circumstances of damage caused by Japanese Alocasia (A) odora. Materials and Methods: We investigated cases in Japan from our own hospital in the eastern part of Shizuoka Prefecture as well as published reports. Results: A. dorais found in western Japan, and plants of the Alocasia genus are cultivated often. A. odora is frequently associated with food poisoning because its aboveground parts resemble those of Satoimo (Colocasia esculenta). Moreover, A. odora contains insoluble calcium oxalate crystals, which cause poisoning symptoms, such as oral pain, nausea, vomiting, and laryngeal edema, resulting in near asphyxia, diarrhea following shock, and skin dermatitis. Calcium oxalate crystals are abundant in Araceae family plants, and cases of health damage owing to the accidental ingestion of Araceae plants have been reported worldwide. Conclusion: Due to the strong irritation felt in the mouth upon contact with the plant, it is advisable to immediately spit out the plant and rinse the mouth. In addition to drug administration, ensuring a secure airway may be necessary if there is a risk of asphyxiation.

Age- and gender-specific acute poisoning with drugs and medications affecting nervous system.

BACKGROUND: We investigated acute poisonings resulting from medications affecting the nervous system and illicit substances at Loghman Hakim Hospital in Tehran. METHODS: We retrospectively reviewed patient records at Iran's largest tertiary toxicology referral center between January 2010 and December 2015. We analyzed the prevalence, trend, age and gender distribution of acute poisoning caused by nervous system agents. RESULTS: The present study included 16,657 (57.27%) males and 12,426 (42.73%) females, resulting in 29,083 patients. The median age of men and women was 29 and 26 years, respectively (p < 0.0001). There were 12,071 (72.47%) men and 10,326 (83.10%) women under the age of 40 (p < 0.001). Most cases were intentional (69.38% in men and 79.00% in women, p < 0.001) and 44.10% had a history of poisoning. The proportions of men and women varied significantly between different age groups and nervous system agents. For women, the most common agent was alprazolam, whereas for men, methadone. The overall trend of acute poisoning with drug used in addictive disorders, opioids and alcohol was increasing but decreasing with benzodiazepines and antidepressants. Acute poisoning by nervous system agents led to more deaths in men (1.95% vs. 0.56%; p < 0.001). CONCLUSIONS: Methadone intoxication was common especially among young men and most of these intoxications were intentional. Women and men aged 20-29 most frequently suffer poisoning from alprazolam and clonazepam, respectively. Women over 60 and men over 30 used opium. Illicit drugs caused more than half of the deaths, and opium dominated. This study may create awareness and develop educational and preventive gender and age-specific local programs.

Electrocardiogram Abnormality in Poisoned Patients with Tricyclic Antidepressant.

Background: A wide variety of electrocardiogram (ECG) changes can manifest with antidepressant drugs, occurring at both therapeutic doses and toxic levels. Notably, ECG abnormalities like wide QRS and QT prolongation may be observed in poisoned patients with tricyclic antidepressants (TCAs), indicating severe conditions that necessitate the implementation of cardiac monitoring systems. This study aimed to investigate ECG Abnormality in poisoned patients with tricyclic antidepressants. Methods: This retrospective patient record study was conducted at Razi Hospital in Ahvaz, Iran, from 2006 to 2009. Patient information was extracted from hospital medical records after the established protocol. The chi-square test was employed for initial analysis; subsequently, logistic regression was applied to identify risk factors associated with abnormal ECG findings. We analyzed the data using SPSS (Version 19; IBM) statistical software. P < 0.05 was defined as statistically significant. Results: Among the 210 poisoned patients, comprising 88 men (41.9%) and 122 women (58.1%), the majority fell within the age range of 15 to 25 years. In our study, the most commonly ingested drugs by poisoned patients were amitriptyline in 134 patients (63.8%) and nortriptyline in 42 patients (20%). A significant portion of 137 patients (65.2%) exhibited poisoning symptoms within ˂ 6 hours, while 73 patients (34.8%) showed symptoms between 6 and 24 hours. Our findings indicated that the initial symptoms in poisoned patients included a decreased level of consciousness in 168 patients (80%), nausea and vomiting in 20 patients (9.5%), and various other symptoms. Notably, our results revealed ECG changes in 70 patients, with 32 patients (15.2%) showing a QRS widening (> 0.1sec), 5 patients (2.4%) displaying a tall R wave in aVR, 5 patients (2.4%) exhibiting right axis deviation, and other observed changes. Conclusion: QRS widening in poisoned patients with tricyclic antidepressants is more frequently observed in symptomatic patients, highlighting the importance of ECG screening in these patients.

Association of the OPRM1 variant rs1799971 (A118G) and clinical manifestations in tramadol poisoned patients: a cross-sectional study.

INTRODUCTION: The opioid receptor mu1 is a protein coding gene that can have different codes for a protein and may have variations (polymorphisms) affecting how opioids work. The aim of this study was to investigate the prevalence of the most common opioid receptor mu1 polymorphism (A118G) and any relationship between this polymorphism and features following tramadol overdose. MATERIALS AND METHODS: This was a cross-sectional study of patients admitted with tramadol poisoning to an Iranian hospital. These patients were not taking any other drugs or medications and had no history of seizures. RESULTS: The results showed that among the 83 patients included in the study, 57 (69 per cent) had the AA genotype, 25 (30 per cent) had the AG genotype, and one (1 per cent) had the GG genotype for the opioid receptor mu1 A118G polymorphism. Nausea and/or vomiting occurred in nine (11 per cent) patients and dizziness in 38 (46 per cent) patients. Serious adverse events included seizures in 51 (60 per cent) patients and respiratory failure requiring mechanical ventilation in 21 (25 per cent) patients. However, there was no significant association between the opioid receptor mu1 A118G polymorphism and these adverse events. DISCUSSION: In our study, the frequency of the A allele was greater than the G allele, and the AA genotype was more prevalent than AG. The GG genotype was the least common among the polymorphisms of opioid receptor mu1 rs1799971. There was no significant association between the opioid receptor mu1 A118G polymorphism and symptoms in tramadol-poisoned patients. Although these allele proportions are similar to the results reported in other Caucasian populations, they are dissimilar to the findings in Chinese and Singaporean populations. In these Asian studies, the predominant allele was the G allele. It has been suggested that a mutated G allele will decrease the production of opioid receptor mu1-related messenger ribonucleic acid and related proteins, leading to fewer mu-opioid receptors in the brain. CONCLUSIONS: This study found no significant association between the opioid receptor mu1 A118G polymorphism and adverse outcomes in tramadol-poisoned patients. However, more research is needed to draw more definitive conclusions due to the limited evidence and variability of opioid receptor mu1 polymorphisms in different populations.

Toxicokinetics of α- and ß-amanitin in mice following single and combined administrations: Simulating in vivo amatoxins processes in clinical cases.

α-Amanitin and ß-amanitin, two of the most toxic amatoxin compounds, typically coexist in the majority of Amanita mushrooms. The aim of this study was to use a newly developed ultra-performance liquid chromatography-mass spectrometry (UPLC-MS/MS) method to determine the toxicokinetics and tissue distribution of α- and ß-amanitin following single or combined oral (po) administration in mice. α-Amanitin and ß-amanitin administered at 2 or 10 mg/kg doses showed similar toxicokinetic profiles, except for peak concentration (Cmax). The elimination half-life (t1/2) values of α-amanitin and ß-amanitin in mice were 2.4-2.8 h and 2.5-2.7 h, respectively. Both α- and ß-amanitin were rapidly absorbed into the body, with times to reach peak concentration (Tmax) between 1.0 and 1.5 h. Following single oral administration at 10 mg/kg, the Cmax was significantly lower for α-amanitin (91.1 µg/L) than for ß-amanitin (143.1 µg/L) (p < 0.05). The toxicokinetic parameters of α-amanitin, such as t1/2, mean residence time (MRT), and volume of distribution (Vz/F) and of ß-amanitin, such as Vz/F, were significantly different (p < 0.05) when combined administration was compared to single administration. Tissues collected at 24 h after po administration revealed decreasing tissue distributions for α- and ß-amanitin of intestine > stomach > kidney > lung > spleen > liver > heart. The substantial distribution of toxins in the kidney corresponds to the known target organs of amatoxin poisoning. The content in the stomach, liver, and kidney was significantly higher for of ß-amanitin than for α-amanitin at 24 h following oral administration of a 10 mg/kg dose. No significant difference was detected in the tissue distribution of either amatoxin following single or combined administration. After po administration, both amatoxins were primarily excreted through the feces. Our data suggest the possibility of differences in the toxicokinetics in patients poisoned by mushrooms containing both α- and ß-amanitin than containing a single amatoxin. Continuous monitoring of toxin concentrations in patients' blood and urine samples is necessary in clinical practice.

Evaluation of the Protective Effects of Lugol's Solution in Rats Poisoned with Aluminum Phosphide (Rice Tablets).

Aluminum phosphide (AlP) is the main component of rice tablets (a pesticide), which produces phosphine gas (PH3) when exposed to stomach acid. The most important symptoms of PH3 toxicity include, lethargy, tachycardia, hypotension, and cardiac shock. It was shown that Iodine can chemically react with PH3, and the purpose of this study is to investigate the protective effects of Lugol solution in poisoning with rice tablets. Five doses (12, 15, 21, 23, and 25 mg/kg) of AlP were selected, for calculating its lethal dose (LD50). Then, the rats were divided into 4 groups: AlP, Lugol, AlP + Lugol, and Almond oil (as a control). After 4 h, the blood pressure and electrocardiogram (ECG) were recorded, and blood samples were obtained for biochemical tests, then liver, lung, kidney, heart, and brain tissues were removed for histopathological examination. The results of the blood pressure showed no significant changes (P > 0.05). In ECG, the PR interval showed a significant decrease in the AlP + Lugol group (P < 0.05). In biochemical tests, LDH, Ca2+, Creatinine, ALP, Mg2+, and K+ represented significant decreases in AlP + Lugol compared to the AlP group (P < 0.05). Also, the administration of Lugol's solution to AlP-poisoned rats resulted in a significant decrease in malondialdehyde levels and a significant increase in catalase activity (P < 0.05). Histopathological evaluation indicates that Lugol improves changes in the lungs, kidneys, brain, and heart. Our results showed that the Lugol solution could reduce tissue damage and oxidative stress in AlP-poisoned rats. We assume that the positive effects of Lugol on pulmonary and cardiac tissues are due to its ability to react directly with PH3.

Development of a risk prediction nomogram for delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning.

OBJECTIVES: Delayed neuropsychiatric sequelae (DNS) are critical complications following acute carbon monoxide (CO) poisoning that can substantially affect the patient's life. Identifying high-risk patients for developing DNS may improve the quality of follow-up care. To date, the predictive DNS determinants are still controversial. Consequently, this study aimed to construct a practical nomogram for predicting DNS in acute CO-poisoned patients. METHODS: This retrospective study was conducted on patients with acute CO poisoning admitted to the Tanta University Poison Control Center (TUPCC) from December 2018 to December 2022. Demographic, toxicological, and initial clinical characteristics data, as well as laboratory investigation results, were recorded for the included patients. After acute recovery, patients were followed up for six months and categorized into patients with and without DNS. RESULTS: Out of 174 enrolled patients, 38 (21.8%) developed DNS. The initial Glasgow Coma Scale (GCS), carboxyhemoglobin (COHb) level, CO exposure duration, oxygen saturation, PaCO2, and pulse rate were significantly associated with DNS development by univariate analysis. However, the constructed nomogram based on the multivariable regression analysis included three parameters: duration of CO exposure, COHb level, and GCS with adjusted odd ratios of 1.453 (95% CI: 1.116-1.892), 1.262 (95% CI: 1.126-1.415), and 0.619 (95% CI: 0.486-0.787), respectively. The internal validation of the nomogram exhibited excellent discrimination (area under the curve [AUC] = 0.962), good calibration, and satisfactory decision curve analysis for predicting the DNS probability. CONCLUSIONS: The proposed nomogram could be considered a simple, precise, and applicable tool to predict DNS development in acute CO-poisoned patients.

Chlorfenapyr poisoning: a systematic review.

INTRODUCTION: Chlorfenapyr, a N-substituted halogenated pyrrole, is a broad-spectrum insecticide. The insecticidal activity of chlorfenapyr depends on its biotransformation by hepatic cytochrome P450 monooxygenases to tralopyril, which uncouples mitochondrial oxidative phosphorylation and disrupts adenosine triphosphate production. Neither the metabolism of chlorfenapyr nor the mechanism of tralopyril is completely elucidated. Acute human chlorfenapyr poisoning is not well characterized, and best practice in management following acute exposure is unclear. The purpose of this review is to characterize acute human chlorfenapyr poisoning by its clinical course, laboratory investigations, and imaging findings and propose a management plan for acute human chlorfenapyr exposure. METHODS: We systematically searched PubMed, Web of Science, Google Scholar, and EMBASE from inception to April 2024 across all languages for human chlorfenapyr and tralopyril cases, with descriptions of exposure, clinical manifestations, and clinical course included. Only manuscripts and abstracts from scientific conferences with sufficient clinical data following acute human exposures were included. In vitro studies, animal studies, agricultural studies, environmental impact studies, and non-clinical human studies were excluded. We then reviewed citations of included studies for additional eligible publications. Non-English publications were translated using Google Translate or primarily translated by our authors. The study adhered to Preferred Reporting for Systematic Reviews and Meta-analyses (PRISMA) guidelines for systematic reviews. RESULTS: We identified 3,376 publications of which 48 met study inclusion criteria, describing 75 unique cases of human poisoning from ingestion, inhalation, dermal exposure, and intra-abdominal injection of chlorfenapyr. No cases of tralopyril exposure were identified. The median time from exposure to symptom onset was six hours (interquartile range 1-48 hours). The most frequent initial or presenting signs/symptoms included diaphoresis, nausea and/or vomiting, and altered mental status. While hyperthermia (≥38 degrees centigrade) was less common at presentation, hyperthermia developed in 61 percent of all patients and was temporally associated with clinical deterioration and death. Most common laboratory abnormalities included elevated blood creatine kinase activity, hepatic aminotransferase activities, and lactate concentration. Imaging studies of the central nervous system often showed extensive symmetrical white matter abnormalities with swelling. Case fatality was 76 percent, and survivors commonly experienced sustained neurological sequelae. Management strategies were highly varied, and the effectiveness of specific medical interventions was unclear. DISCUSSION: Acute human chlorfenapyr poisoning is characterized by a latent period as long as 14 days, deterioration over hours to days, and can result in serious morbidity and mortality. Development of hyperthermia, likely driven by oxidative phosphorylation uncoupling by tralopyril, is an ominous clinical sign and is temporally associated with clinical decompensation and death. Laboratory abnormalities, particularly elevated creatine kinase activity, hepatic aminotransferase activities, and lactate concentration, were common, but only creatine kinase activity differed amongst survivors and fatalities. Best clinical practice in the management of patients exposed to chlorfenapyr is unclear, and we opine that a conservative approach with close clinical monitoring and supportive care is prudent. LIMITATIONS: The limitations of all reviews include their inherent retrospective and observational nature as well as publication bias that emphasizes severe outcomes, thus impacting the spectrum of illness and skewing mortality percentage. In addition, we interrogated a finite number of databases for publications on human chlorfenapyr exposure and there were limited cases with laboratory testing to confirm chlorfenapyr poisoning. Analysis of our systematic review was not powered to detect differences between groups, comparative statistics were not performed, and significance is not reported. CONCLUSIONS: Acute human chlorfenapyr toxicity is characterized by a latent period following exposure, development of new or progression of established signs/symptoms, potential for critical illness, rapid deterioration, serious morbidity, and mortality. A conservative approach to patient management is prudent.

Colchicine poisoning: Case report of three homicides in a family.

Background: Colchicine is a common therapeutic agent for inflammatory conditions such as gout, yet its narrow therapeutic range frequently results in cases of overdose and subsequent poisoning. Acute colchicine poisoning can be difficult to identify due to its nonspecific clinical manifestations, posing a diagnostic challenge for emergency physicians without a clear history of colchicine ingestion. Case presentation: This report describes a tragic case of acute colchicine poisoning that resulted in three familial homicides. The patients presented with fever, abdominal pain, and diarrhea, which rapidly escalated to shock during their emergency department visits. Laboratory tests revealed a marked leukocytosis, mild elevation in procalcitonin (PCT), significantly elevated creatine kinase (CK) and CK-MB levels, and liver function abnormalities. Despite treatment with carbapenem antibiotics and aggressive fluid resuscitation, the patients' condition deteriorated, marked by a progressive decline in leukocytes and neutrophils. Initially misdiagnosed as septic shock, the ineffectiveness of the standard treatment protocols led to a fatal outcome for all three individuals. Conclusion: Emergency physicians should consider acute colchicine poisoning as a differential diagnosis in patients presenting with shock and the following clinical indicators: (1) pronounced increase in peripheral leukocytes with a disproportionate rise in neutrophils; (2) discordance between the level of serum procalcitonin and the severity of presumed septic shock; (3) early increase in serum creatine kinase (CK) and CK-MB; (4) poor response to antibiotics and resuscitative efforts, accompanied by a continuous decrease in white blood cells and neutrophils. This case underscores the critical need for awareness of colchicine toxicity in the emergency setting, particularly when the clinical presentation mimics septic shock but fails to respond to standard treatments.