Quantitative assessment of retinochoroidal microvasculature in patients with carotid artery stenosis using OCT angiography.

PURPOSE: To investigate the alterations in retinochoroidal parameters measured by optical coherence tomography (OCT) and OCT angiography (OCTA) in patients with carotid artery stenosis (CAS) and assess their associations with digital subtraction angiography (DSA) data. METHOD: This study enrolled patients diagnosed with CAS and age-matched healthy controls. Both groups underwent OCT and OCTA examinations. DSA and assessment of carotid artery stenosis were performed only in the CAS group. The study evaluated various retinochoroidal parameters from OCT and OCTA, including linear vessel density (LVD), foveal avascular zone (FAZ), choroidal thickness (ChT), and retinal nerve fiber layer (RNFL) thickness. DSA-derived measures included cervical segment (C1) diameter, cavernous segment (C4) diameter, stenosis percentage, ophthalmic artery (OA) filling time, C1-OA filling time, and residual stenosis. RESULTS: A total of 42 eyes from 30 CAS patients and 60 eyes from 30 healthy controls were included. Patients with CAS displayed significantly decreased LVD compared to controls (p < 0.001). Additionally, the CAS group had thinner choroid and RNFL (p = 0.047 and p < 0.001, respectively). Macular LVD negatively correlated with both stenosis percentage and C1-OA filling time (p = 0.010 and p = 0.014, respectively). In patients who underwent carotid artery stenting, preoperative ChT significantly correlated with residual stenosis (Pearson r = -0.480, p = 0.020). CONCLUSION: OCT and OCTA provide a quantitative assessment of retinochoroidal microstructural changes associated with CAS, suggesting potential for noninvasive evaluation of the disease. This might contribute to the prevention of irreversible ocular complications and early detection of CAS. Furthermore, ChT may not only aid in diagnosing CAS more reliably but also offer prognostic information.

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.

Tim-3 facilitates immune escape in benzene-induced acute myeloid leukemia mouse model by promoting macrophage M2 polarization.

Benzene poisoning can cause acute myeloid leukemia (AML) through a variety of passways. Tim-3 has gained prominence as a potential candidate in mediating immunosuppression in tumor microenvironments. The macrophage polarization is also related to immune escape. Herein, we reported that Tim-3 and macrophage M2 polarization play a vital role in benzene-induced AML. First, the benzene-induced AML C3H/He mouse model was constructed by subcutaneously injecting 250 mg/kg of benzene. After six months, macrophage phenotype, cytokines, and Tim-3 expression levels were investigated. Flow cytometry assay revealed that the T-cell inhibitory receptor Tim-3 was significantly upregulated in both bone marrow and spleen of the benzene-induced AML mouse model. Elisa's results displayed a decreased serum level of IL-12 while increased TGF-ß1. Mechanistically, changes in cytokine secretion promote the growth of M2-type macrophages in the bone marrow and spleen, as determined by immunofluorescence assay. The increased levels of PI3K, AKT, and mTOR in the benzene-exposure group further proved the crucial role of Tim-3 in regulating the functional status of macrophages in the AML microenvironment. These results demonstrate that Tim-3 and macrophage polarization may play a vital role during the immune escape of the benzene-induced AML. This study provides a new potential intervention site for immune checkpoint-based AML therapeutic strategy.

Case report: Reversible splenial lesion syndrome caused by diquat poisoning.

Diquat (DQ), chemically known as 1,1 '-ethylene-2,2' -bipyridine, is a non-selective herbicide for leaf removal and drying. It has toxic effects on central nervous system cells, and toxic neurological lesions include axonal degeneration and pontine myelolysis. At the same time, DQ can also affect the activity of dopaminergic nerve cells through oxidative stress, causing degeneration and reducing dopamine uptake. With the increasing application of DQ in agricultural production, the clinical reports of neurotoxicity caused by acute DQ poisoning are also increasing. At present, DQ rapid-phase-related toxic encephalopathy mainly involves the pons, midbrain, basal ganglia, thalamus and other brain regions. However, this case is unusual in that the lesion mainly involved the splenium of the corpus callosum. It is also the first time to be reported.

Construction of a clinical nursing pathway for acute paraquat poisoning: Evidence-based research.

Aim: This study used the Delphi method and clinical expert discussions to develop an acute paraquat poisoning clinical nursing pathway to standardize acute paraquat poisoning nursing care. Background: In clinical practice, especially in basic-level hospitals, there is no unified standard pattern of treatment and nursing care for patients with paraquat poisoning. Methods: An extensive literature search was used to gather current clinical guidelines for treating paraquat poisoning which were then compiled into a Delphi expert letter of inquiry questionnaire which was sent to a panel of 12 experts. Results: A preliminary draft of the clinical nursing pathway table for acute paraquat poisoning with a standard hospitalization period of 21 days was established, with 6, 23, and 152 classes and I, II, and III indicators determined. The clinical nursing pathway table reduced the randomness of work, avoided nursing interruptions or omissions caused by negligence, and simplified the writing of nursing documents. Conclusions: The clinical nursing pathway can promote and improve the nursing care quality and management efficiency and has good clinical application value.

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 report: Methemoglobinemia caused by nitrobenzene poisoning.

Nitrobenzene poisoning is uncommon, with most cases occurring in the dye, paint, and other chemical industries. Nitrobenzene enters the body mainly through the skin, respiratory tract, and oral cavity. Nitrobenzene poisoning symptoms include hypermethemoglobinemia, hemolytic anemia, liver and kidney dysfunction, cardiogenic pulmonary edema, and toxic encephalopathy, which endanger people's lives. Therefore, we present a case of nitrobenzene poisoning caused by skin absorption, focusing on its clinical characteristics and treatment outcomes. A 58 years-old man presented to our department with confusion and cyanosis. He has a history of hypertension and cerebral infarction. The patient was diagnosed with moderate occupational acute benzene poisoning with nitro compounds. Symptomatic support, methylene blue, and other antioxidant treatments were commenced after diagnosis. After treatment, the patient's condition gradually improved, and he was discharged.

Comparing the application of three thrombosis risk assessment models in patients with acute poisoning: A cross-sectional survey.

Background: Patients with acute toxic hemoperfusion are prone to deep vein thrombosis. However, there is no risk assessment model for thrombosis in patients with acute toxic hemoperfusion. Therefore, we compared three commonly used risk assessment models for deep vein thrombosis to determine the model most suitable for assessment of deep vein thrombosis in patients with acute toxic hemoperfusion. Methods: Caprini, Autar, and Padua thrombosis risk assessment models were used to assess the risk of deep vein thrombosis in patients with acute poisoning and hemoperfusion admitted to a grade A hospital in Shandong province from October 2017 to February 2019. The predictive values of the three models were compared using receiver operating characteristic (ROC) curve analysis. Results: The risk assessment model scores of Caprini, Autar, and Padua were 7.55 ± 1.76, 8.63 ± 2.36, and 3.92 ± 0.55, respectively. The Caprini risk assessment model was significantly different (p < 0.05) in high-risk patients in the thrombus and non-thrombotic groups; the difference between the other two models was not significant (p > 0.05). The areas under the ROC curve of the Caprini, Autar, and Padua risk assessment models were 0.673, 0.585, and 0.535, respectively. The difference in areas under the ROC curve between the Caprini risk assessment model and the Autar risk assessment model as well as the Padua risk assessment model was significant (p < 0.05), but the areas under the ROC curve of the Autar risk assessment model and the Padua risk assessment model were not statistically significant (p > 0.05). The Caprini risk assessment model had a sensitivity of 91.9%, specificity of 33.1%, and a Youden index of 0.249. The sensitivity and specificity of Autar's risk assessment model were 37.0 and 77.2%, respectively, and the Youden index was 0.141. The Padua risk assessment model had a sensitivity of 91.3%, specificity of 15.0%, and a Youden index of 0.063. Conclusion: The three thrombosis risk assessment models were not suitable for patients with acute poisoning and hemoperfusion.

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.

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.

Case Report: Toxic encephalopathy caused by repeated inhalation of liquid sealant.

Short-term exposure to high levels of organic solvents, as well as long-term exposure to small doses, can damage the central nervous system, thereby leading to toxic encephalopathy. However, toxic encephalopathy caused by long-term inhalation of liquid sealant is rarely reported. This study describes the clinical data of a case of toxic encephalopathy caused by repeated inhalation of liquid sealants and discusses the pathophysiological characteristics and treatment of organic solvent toxic encephalopathy. This report aims to strengthen the understanding of this disease among clinical staff.

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.

Development and validation of a prediction model of deep venous thrombosis for patients with acute poisoning following hemoperfusion: a retrospective analysis.

OBJECTIVE: To develop and confirm an individualized predictive model to ascertain the probability of deep venous thrombosis in patients with acute poisoning after undergoing hemoperfusion. METHODS: Three hundred eleven patients with acute poisoning who were admitted to a hospital in China between October 2017 and February 2019 were included in the development group. Eighty patients with acute poisoning who were admitted between February and May 2019 were included in the validation group. The independent risk factors for deep venous thrombosis were examined. An individualized predictive model was developed using regression coefficients. RESULTS: The number of catheter indwelling days, having a catheter while being transported, elevated serum homocysteine concentrations, and dyslipidemia were independent risk factors for deep venous thrombosis following hemoperfusion in patients with acute poisoning. The areas under the receiver operating characteristic curve of the development and validation groups were 0.713 and 0.702, respectively, which suggested that the prediction model had good discrimination capacity. The calibration belts of the two groups were ideal. CONCLUSIONS: Our prediction model has a moderate predictive effect for the occurrence of deep venous thrombosis in patients with acute poisoning. In clinical practice, this model could be combined with a common thrombosis risk assessment model.

Kidney and lung injury in rats following acute diquat exposure.

Diquat (1,1'-ethylene-2,2'-bipyridylium) is a type of widely used agricultural chemical, whose toxicity results in damage to numerous tissues, including the lung, liver, kidney and brain. The aim of the present study was to establish a rat model of acute diquat exposure and explore the relationship between diquat concentration, and kidney and lung injury, in order to provide an experimental basis for clinical treatment. A total of 140 healthy adult male Wistar rats were randomly divided into control and exposure groups. The diquat solution was administered intragastrically to the exposure group at 1/2 of the lethal dose (140 mg/kg). An equal volume of water was administered to the control group. The dynamic changes in the plasma and tissue diquat levels were quantitatively determined at 0.5, 1, 2, 4, 8, 16 and 24 h following exposure using liquid chromatography mass spectrometry. The content of hydroxyproline (HYP) in the lung tissues, as well as the levels of blood urea nitrogen (BUN), creatinine (Cr), uric acid (UA), kidney injury molecule-1 (KIM-1) and tumor growth factor (TGF)-ß1, were detected using western blot analysis at every time point. Lung and kidney morphology were also assessed. Electron microscopy showed that the degree of renal damage gradually increased with time. Vacuolation gradually increased, some mitochondrial bilayer membrane structures disappeared and lysosomes increased. The lung tissue damage was mild, and the cell membrane integrity and organelles were damaged to varying degrees. The plasma and organ levels of diquat peaked at ~2 h, followed by a steady decrease, depending on the excretion rate. Over time, the serum concentrations of UA, BUN, Cr and KIM-1 were all significantly increased (P<0.05). Serum KIM-1 in rats was increased after 0.5 h, and was significantly increased after 4 h, suggesting that KIM-1 is an effective predictor of early renal injury. Early TGF-ß1 expression was clearly observed in renal tissue, while no clear TGF-ß1 expression was observed in the lung tissue. In conclusion, the concentration of diquat in the serum and tissue of rats with acute diquat poisoning peaked at an early stage and then rapidly decreased. The renal function damage and pathological changes persisted, the lung tissue was slightly damaged with inflammatory cell infiltration, and early pulmonary fibrosis injury was not obvious.

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.