Images in acute diquat poisoning, including hepatic portal venous gas and gastrointestinal pneumatosis on computed tomography.

INTRODUCTION: Severe diquat poisoning often leads to acute kidney injury, gastrointestinal injury, paralytic ileus, rhabdomyolysis, respiratory failure, refractory circulatory failure, and brainstem damage. CASE SUMMARY: A previously healthy 38-year-old man was admitted to our hospital with anuria, mild abdominal distension, and calf pain after ingesting diquat (200 g/L) 100 mL approximately 13 h before presentation. His blood diquat concentration was 8.14 µg/L on admission. Gastrointestinal catharsis, haemoperfusion, and haemodiafiltration were performed. Subsequently, he developed marked abdominal distention, impaired consciousness, hypotension, and respiratory failure, leading to death. IMAGES: Computed tomography revealed gas accumulation in the portal venous system and mesenteric vessels. Moreover, gastrointestinal pneumatosis was present. Computed tomography also revealed changes in the lung, brainstem, and calf muscles. CONCLUSION: Diquat poisoning can result in acute kidney injury, hepatic injury, gastrointestinal injury, paralytic ileus, rhabdomyolysis, refractory circulatory failure, brainstem damage, and hepatic portal venous gas, all observed in this patient.

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.

A mass event of paraquat poisoning via inhalation.

Objective: In January 2023, a rare event of collective inhalation paraquat poisoning occurred in Shandong, China. To analyze the clinical characteristics of an event of respiratory tract paraquat poisoning through inhalation. Methods: Clinical data from eight patients with paraquat inhalation poisoning were retrospectively analyzed. Results: The patients were mainly exposed to paraquat via the respiratory tract. The main clinical manifestations were ocular and respiratory irritation. Lung computed tomography (CT) showed that all eight patients had varying degrees of lung injury, mainly manifesting as exudative lesions. Laboratory tests revealed arterial blood gas hypoxemia, abnormal white blood cell count, and increased neutrophil ratio. Sufficient glucocorticoid impact therapy was effective, and all eight patients survived. Conclusion: Eight patients experienced chest tightness, shortness of breath, and varying degrees of lung injury due to inhalation of paraquat through the respiratory tract. The early use of glucocorticoids and other comprehensive treatment measures, active prevention and treatment of lung infections, and protection of organ function have beneficial effects in such cases.

Multiorgan failure caused by Chinese herbal medicine Xanthii Fructus poisoning: a case report.

BACKGROUND: Xanthii Fructus was used in the treatment of rhinitis and related nasal disease. It is the most commonly used chemically active component in compounds formulated for the treatment of rhinitis. However, poisoning, resulting in serious consequences, can easily occur owing to cocklebur overdose, improper processing, or usage without processing. CASE PRESENTATION: We reported on a 55-year-old man who experienced allergic rhinitis for 2.5 years. He ingested unprocessed Xanthii Fructus for 2 months as treatment. However, he developed anorexia; nausea; abdominal pain; general weakness; hiccups; oliguria and anuria; significantly elevated serum alanine aminotransferase, aspartate aminotransferase, and creatinine levels; and abnormalities in blood coagulation series. Nutritional support; daily drugs for liver protection, gastric protection, inflammation reduction; fresh plasma; and cryoprecipitate infusion were administered. Continuous venovenous hemodialysis (Prismaflex ST100) was also administered. However, the patient's multiple organ failure gradually worsened, ultimately leading to death. CONCLUSION: Xanthii Fructus poisoning affects multiple systems, and its clinical manifestations are complex. Therefore, it is easily misdiagnosed and missed. Along with careful inquiry of medical and medication history, early diagnosis and intervention are vital for a successful treatment. It is also important to educate people and create awareness about this poisoning. Therefore, this intractable case has great clinical significance.

Current situation and influencing factors for suicidal intent in patients with intentional acute pesticide poisoning.

Introduction: Since pesticides have been widely used in agricultural production, acute pesticide poisoning (APP) has gradually become a worldwide public health problem. Recently, the number of APP cases has been high in China, and the intentional self-administration of pesticides is the main cause of APP. However, there is a lack of relevant studies on the factors influencing suicidal intent in patients with intentional APP. This study aimed to explore the current situation and influencing factors for suicidal intent among patients with intentional APP. Methods: In this cross-sectional study, we enrolled a total of 225 patients with intentional APP admitted to the emergency department of our Grade A comprehensive hospital in Shandong Province between June 2019 and January 2021. Patients were investigated using a health status interview questionnaire, Beck Suicidal Intent Scale, Duke Social Support Index, psychological stress scale, Dickman Impulsivity Inventory, Trait Anxiety Inventory, Center for Epidemiologic Studies Depression Scale, and Beck Hopelessness Scale. Descriptive statistics, single-factor analysis, and multiple linear regression were used for data analysis. Results: Suicidal intent scores were collected and averaged (14.23 ± 6.22). Multiple linear regression analysis revealed that marital status, residential area, impulsivity, hopelessness, depression, psychological strain, and social support impact suicidal intent. Conclusion: Patients with intentional APP have high suicidal intent. Therefore, different interventions should be tailored to different patients.

Case Report: Acute Intoxication from Phosphine Inhalation.

Aluminum phosphide is a highly effective insecticide for fumigation in granaries and is often used in rural grain storage. However, people's awareness of its toxicity is not strong. A case of acute inhalation toxicity of phosphine caused by the use of aluminum phosphide to fumigate a granary is reported here. The case presented with aspiration pneumonia and acute left heart failure. The patient was cured using comprehensive life support treatment, including respiratory support, antiarrhythmic treatment, and blood pressure maintenance with vasoactive drugs. There is no specific antidote for phosphine poisoning at present, and the comprehensive application of restricted fluid resuscitation, high-dose glucocorticoid shock, vasoactive drugs and bedside hemofiltration is significant in improving the prognosis of patients. It is also important to remind people to pay attention to their own protection in the process of using aluminum phosphide.

Case series: Diquat poisoning with acute kidney failure, myocardial damage, and rhabdomyolysis.

Diquat is a herbicide that can have deleterious effects on the kidneys, liver, heart, lungs, and central nervous system on ingestion. Diquat poisoning-associated rhabdomyolysis has rarely been reported. We describe two cases of diquat poisoning with acute renal failure, myocardial damage, and rhabdomyolysis. Case 1: A 17-year-old man experienced anuria after ingesting ~200 mL of diquat 16 h prior. On admission, his creatinine (400 µmol/L), urea (11.7 mmol/L), creatine kinase (2,534 IU/L), and myohemoglobin (4,425 ng/mL) concentrations were elevated. Case 2: An 18-year-old woman who ingested ~200 mL of diquat 5.5 h prior to admission had normal creatinine, urea, and creatine kinase concentrations. Eleven hours after ingestion, she developed anuria with elevated creatinine (169 µmol/L) concentration; her creatine kinase (13,617 IU/L) and myohemoglobin (>3,811 ng/mL) concentrations were remarkably elevated 24 h after ingestion. Both patients also had elevated aminotransferase and myocardial enzyme concentrations. After undergoing hemoperfusion and hemofiltration, blood diquat concentrations in cases 1 and 2 on admission (16/6 h after ingestion), after hemoperfusion (20/11 h after ingestion), and after 8 h of hemofiltration/8 h of hemofiltration and 2 h of hemoperfusion (29/21 h after ingestion) were 4.9/9.1, 3.4/5.4, and 1.5/1.2 µg/mL, respectively. Severe diquat poisoning can cause acute kidney failure and rhabdomyolysis. Rhabdomyolysis may induce myocardial injury, aggravating kidney damage, and also increase transaminase concentration. Hemoperfusion and hemofiltration could be effective treatments for eliminating diquat in the blood.

Clinical analysis of pipeline dredging agent poisoning: A case report.

BACKGROUND: Pipeline dredging agents are new household deep cleaning products used to dredge blockages in kitchen and bathroom pipeline caused by grease, hair, vegetable residue, paper cotton fibre, and other organic substances. Pipeline dredging agents are corrosive chemicals that can cause poisoning through corrosive damage to the digestive tract; however, this has not been reported clinically. Therefore, this report emphasises that oral pipeline dredging agent poisoning can cause corrosive damage to the digestive tract and may have serious health consequences. CASE SUMMARY: A 68-year-old man consumed liquor (200 mL) at approximately 13:00 on April 22, 2021. At approximately 16:00, his family found him unresponsive with blackened lips, blood spots in the corners of the mouth, and blood stains on the ground, as well as an empty bottle of a pipeline dredging agent. One hour later, he was admitted to the emergency department of a local hospital. Considering the empty bottle, he was suspected to have sustained severe corrosive damage to the digestive tract and was transferred to our department at 23:15 on April 22, 2021. He developed dysphagia and intermittent fever and experienced difficulty in opening his mouth throughout his hospital stay. The patient's condition gradually stabilised. However, he suddenly developed respiratory failure on day 12, and endotracheal intubation and ventilator-assisted ventilation were performed. However, the patient died after 1.5 h despite emergency rescue efforts. CONCLUSION: Pipeline dredging agents are highly corrosive and may cause corrosive damage to the digestive tract and asphyxia upon consumption.

Severe methyl bromide poisoning causing early acute renal failure and anuria: a case report.

Methyl bromide is a pre-plant soil fumigant that is widely used to control nematodes, insects, and fungi in farmlands. Methyl bromide enters the human body through dermal absorption or inhalation and can damage the respiratory, nervous, circulatory, urinary, and other systems. A 62-year-old man who had inhaled a large amount of methyl bromide was admitted to our department. He presented with respiratory failure and pink foamy sputum. He was started on dexamethasone, alanyl glutamine, sulbactam, furosemide, vitamin B1, mouse nerve growth factor, and other treatments, and mechanical ventilation and continuous venovenous hemodiafiltration (CVVHF) were performed daily. He subsequently developed coagulopathy because of the CVVHF, for which protamine, recombinant human brain natriuretic peptide, and albumin were administered intravenously. Notably, the patient developed sustained anuria and eventually died owing to multiple organ failure; specifically, failure of the brain, heart, lungs, and kidneys. This report presents the diagnosis, clinical course, management, and prognosis of a patient who was treated at our hospital for severe methyl bromide poisoning.

Diagnosis and treatment of acquired factor VIII deficiency: a case report and literature review.

Acquired haemophilia A (AHA) is a rare haemorrhagic disease characterized by spontaneous extensive subcutaneous haemorrhage and soft tissue haematoma. The activated partial thromboplastin time is significantly prolonged and cannot be corrected by normal plasma. Approximately 50% of AHA patients lack a specific aetiology, so this can easily result in a misdiagnosis. This current case report describes a 27-year-old male that presented with gingival bleeding, haematuria and haematochezia with no obvious cause. At first, it was thought that he might have experienced anticoagulant rodenticide poisoning, but the subsequent anticoagulant rodenticide test was negative. At the same time, the patient was screened for mutations associated with bleeding and coagulation diseases. Two mutations were identified: a p.Y471H mutation the plasminogen activator, tissue type (PLAT) gene; and a p.Y244Y mutation the serpin family E member 1 (SERPINE1) gene. It should be noted that patient had no previous history of thrombosis or haemorrhagic disease, which confused the diagnosis. A professional haemophilia research centre provided clarification of the diagnosis when anti-factor VIII antibodies were detected. The patient was treated with 30 mg/day prednisone orally. Multiple follow-up examinations showed continuous complete remission. No factor VIII antibodies were detected in his blood and coagulation factor VIII increased significantly.

The toxicokinetics of acute paraquat poisoning in specific patients: a case series.

Paraquat is a non-selective contact herbicide that is absorbed through the digestive tract and skin and can cause multiple organ damage. The toxicokinetics of paraquat poisoning in specific patients are rarely reported. Case 1 was a 76-year-old man who intermittently immersed his perineum in diluted paraquat solution for 3 consecutive days because of eczema of the perineal skin. On admission, the patient's scrotal skin was severely corroded and his blood paraquat concentration was 0.5 µg/mL. He developed severe kidney and lung damage after admission and died on Day 6 of admission. Case 2 was a 23-year-old woman who ingested paraquat during gestational week 36. Her initial blood paraquat concentration was 0.81 µg/mL. The patient refused hemoperfusion and a cesarean section. She birthed a baby girl 83 hours after ingesting paraquat. Paraquat concentrations in postnatal maternal blood, fetal blood, umbilical cord blood, and amniotic fluid were 0.19 µg/mL, 0.23 µg/mL, 0.20 µg/mL, and 0.47 µg/mL, respectively. The baby died within hours of birth and the mother died of refractory respiratory failure 2 days after delivery. This paper provides clues about paraquat toxicokinetics in specific patient types and indicates that paraquat can be absorbed through the scrotal skin and the placental barrier.

Methemoglobinemia and Delayed Encephalopathy After 5-Bromo-2-Nitropyridine Poisoning: A Rare Case Report.

5-bromo-2-nitropyridine, an intermediate in the synthesis of pharmaceutical and pesticide products, is toxic to the human body. However, 5-bromo-2-nitropyridine poisoning has not been previously reported. Here, we report the case of a 40-year-old man who suffered skin and respiratory tract exposure to leaked 5-Bromo-2-nitropyridine at work. After exposure, the patient rapidly developed dizziness, fatigue, nausea, vomiting, chest distress, diffuse cyanosis, and coma. Methemoglobinemia, hemolytic anemia, rhabdomyolysis, and acute renal failure were observed after admission. He improved markedly after treatment, but delayed encephalopathy was confirmed 82 days after the exposure. This case highlights that 5-bromo-2-nitropyridine can be absorbed through the skin and respiratory tract, resulting in methemoglobinemia and delayed encephalopathy.

Clinical Analysis of Acute Organophosphorus Pesticide Poisoning and Successful Cardiopulmonary Resuscitation: A Case Series.

Acute organophosphorus pesticide poisoning (AOPP) with cardiac arrest has an extremely high mortality rate, and corresponding therapeutic strategies have rarely been reported. Therefore, this study aimed to explore the prognostic factors and effective treatments of AOPP-related cardiac arrest. This retrospective study was conducted in our department in the years 2018-2021. We conducted a descriptive analysis of the clinical manifestations, rescue strategies, and prognosis of patients with AOPP who had experienced cardiac arrest and successful cardiopulmonary resuscitation. This study included six cases of patients with AOPP in addition to cardiac arrest; in four cases, cardiac arrest occurred <12 h after ingestion, and in two, cardiac arrest occurred more than 48 h after ingestion. Five patients had not undergone hemoperfusion therapy before cardiac arrest, and all six were treated with atropine during cardiopulmonary resuscitation and subsequent pralidoxine. Four patients recovered and were discharged from the hospital, one died in our department, and one was transferred to a local hospital and died there 2 h later. The last two patients had severe pancreatic injuries and disseminated intravascular coagulation. This, along with their death, might have been related to their prognosis. Cardiac arrest can occur in patients with severe AOPP for whom antidote administration was insufficient or not timely. Application of atropine and pralidoxine in a timely manner after cardiac arrest following AOPP is the key to successful treatment. This study provides useful guidelines for the treatment of similar cases in the future.

Two cases of methaemoglobinaemia and haemolysis due to poisoning after skin absorption of 4-chloro-1-nitrobenzene.

INTRODUCTION: While 4-chloro-1-nitrobenzene has oxidising properties and can lead to methaemoglobinaemia and haemolysis, such reports are rare. We herein describe two cases of 4-chloro-1-nitrobenzene poisoning after skin exposure and detail relevant clinical characteristics and treatment outcomes. CASE PRESENTATION: A 45-year-old man and his 32-year-old male co-worker presented at our department shortly after skin exposure to 4-chloro-1-nitrobenzene. They developed similar symptoms, including dizziness, dyspnoea, excessive fatigue, and coma. Patients' chest inspection yielded normal findings. Despite maximal oxygen supplementation, neither patient exhibited improvements in the following clinical parameters: diffuse cyanosis, chocolate-coloured blood, and decreased pulse oximetry. For patients 1 and 2, methaemoglobin levels at admission were 78.6% and 63.6%, and 4-chloro-1-nitrobenzene concentrations were 4.12 µg/mL and 2.89 µg/mL, respectively. Their symptoms and methaemoglobin levels improved after we cautiously administered methylene blue; we subsequently detected oxidative haemolysis (confirmed by peripheral blood smears) that later resolved without further aggravation. No further episodes of anaemia were documented via telephone follow-up for eight months after hospital discharge for either patient. DISCUSSION: Typical features of methaemoglobinaemia included diffuse cyanosis, dark chocolate-coloured blood, elevated partial pressure of oxygen, and decreased pulse oximetry saturation. Haemolysis likely occurred secondary to the toxic effects of 4-chloro-1-nitrobenzene.

A rare form of intoxication: acute methyl ethyl ketone peroxide poisoning.

We report two suicidal cases of acute methyl ethyl ketone peroxide (MEKP) poisoning. A woman in her late 60s suffered from oral mucosal erosion, functional impairment of the heart, liver and other organs, pulmonary inflammation, elevated inflammatory markers, pleural effusion, hypoproteinemia and metabolic acidosis after oral administration of approximately 50 mL of MEKP. After admission, the patient was administered hemoperfusion four times, 8 mg of betamethasone for 6 days and symptomatic support. Hemoperfusion had an obvious effect on the treatment of oral MEKP poisoning. After discharge, the patient developed progressive dysphagia and secondary esophageal stenosis. Supplementary feeding was administered with a gastrostomy tube after the patient was completely unable to eat. A man in his mid-40s developed oropharyngeal mucosal erosion, bronchitis and esophageal wall thickening after oral administration of 40 ml MEKP. After receiving total gastrointestinal dispersal, 80 mg of methylprednisolone was administered for 7 days, and symptomatic supportive treatment was provided. Slight dysphagia was observed after discharge, and there was no major effect on the quality of life. Patients with acute oral MEKP poisoning should be followed up regularly to observe its long-term effects on digestive tract corrosion and stenosis.

Acute diquat poisoning resulting in toxic encephalopathy: a report of three cases.

INTRODUCTION: Diquat-related acute kidney injury is well-known. However, neurological disorders caused by diquat are often underestimated, and changes in the imaging findings are rarely reported. We present three cases of acute diquat poisoning resulting in toxic encephalopathy. CASE REPORT: In the first case, a 20-year-old previously healthy man ingested approximately 80-100 mL of diquat. He developed acute renal failure, neurological disorders, and respiratory failure. Central pontine myelinolysis was considered by magnetic resonance imaging (MRI), 18 days after ingestion. In the second case, a 20-year-old man ingested approximately 100 mL of diquat. Toxic encephalopathy was confirmed by MRI, 13 days after ingestion. Unfortunately, he experienced cardiac arrest and died 18 days after ingestion. In the third case, a 31-year-old previously healthy man ingested approximately 50 mL of diquat. The imaging features of toxic encephalopathy mainly involved the medulla oblongata, pons, midbrain, bilateral brachium pontis, cerebellum, and pedunculus cerebri. He demonstrated significant recovery. DISCUSSION: Ingestion of diquat can cause acute renal failure, neurological disorders, and respiratory failure. The pons, midbrain, pedunculus cerebri may be the most commonly impaired locations of diquat-related toxic encephalopathy.

Gluteal muscle damage and rhabdomyolysis after olanzapine poisoning: a case report.

Olanzapine is a widely adopted atypical antipsychotic medication used to manage schizophrenia. Reports show that the incidence rate of adverse reactions to olanzapine is significantly lower than those of other classic antipsychotic medications. However, olanzapine overdose may be associated with severe consequences. Herein, we report a 21-year-old female patient who had taken nearly 700 mg (70 tablets) of olanzapine; she was found after 30 hours. As her condition progressed, she presented with rhabdomyolysis, swelling in the thighs and hips, paralytic ileus, digestive tract hemorrhage, and elevated serum amylase and lipase levels; notably, she recovered after treatment. This intractable case is of great clinical significance and suggests that early-phase hemoperfusion plays a critical role in olanzapine poisoning-related rhabdomyolysis.

Esophagitis dissecans superficialis associated with acute transoral paraquat poisoning: Clinical study of 15 cases.

To analyze the clinical characteristics and therapeutic effects of transoral paraquat poisoning combined with Esophagitis dissecans superficialis (EDS). A retrospective observational study was conducted on paraquat poisoning patients between January 1, 2011 and August 30, 2016 in Qilu hospital. Fifteen patients with EDS were enrolled in this study. The clinical characteristics, prognosis, and pathological features of esophageal necrosis mucosa of these patients were retrospectively analyzed and summarized. Esophageal mucosal dissection occurs mainly within 3-8 days after transoral paraquat poisoning in 15 patients. Dosage of paraquat is range from 50 to 100 ml. Most patients have physical problems with swallowing before the intramural esophageal dissection occurred. And there are other symptoms, including sore throat or dysphagia (100%), nausea and vomiting (86.7%), heartburn or upper abdominal pain (73.3%), hematemesis (60%), abdominal distension (20%) and cough frequently (6.7%). In death group, most patients demonstrate features of the multiple organ failure when the esophageal mucosal stripping happened, including lung injury, renal failure, and hepatic failure. The shape of esophageal dissection was tubular in 60%, irregular in 40%, and they vary in size. Pathological examination showed extensive injury, necrosis and hemorrhage of digestive tract epithelium, and obvious inflammatory reaction of epithelial tissue. Transoral paraquat poisoning has certain damage to the patient's esophageal mucosa, and some may be complicated with EDS, and the prognosis is poor, especially when combined with multiple organ dysfunction. Esophageal damage is mainly located in the esophageal mucosa and have different degrees. Special attention should be paid on such patients.