The reversed De Ritis ratio for predicting in-hospital mortality among intensive care patients with organophosphate poisoning.

INTRODUCTION: The uncontrolled use of pesticides signifies a substantial health hazard. This study was designed to explore the prognostic role of on-admission hepatic aminotransferases [alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and the reversed De Ritis ratio (ALT/AST)] in the prediction of in-hospital mortality among patients with acute organophosphate (OP) poisoning. PATIENTS AND METHODS: We conducted a retrospective study based on extracting the required information from the specific medical records for acutely OP-intoxicated patients admitted to the intensive care unit. RESULTS: A total of 49 acutely malathion-intoxicated patients were enrolled in the study. The in-hospital mortality rate was 32.7%. Patients were stratified into survivors and non-survivors. Compared to the survivors, the non-survivors had significantly lower Glasgow coma scale scores, mean arterial blood pressure, significantly higher reversed De Ritis ratio (ALT/AST), and ALT and AST activities. The reversed De Ritis ratio (ALT/AST) and ALT demonstrated good discrimination between the survivors and the non-survivors with an area under the curve (AUC) of 0.708 vs 0.781, respectively, however, AST showed satisfactory discrimination, AUC of 0.694. CONCLUSION: Hepatic aminotransferases are useful in predicting in-hospital mortality in acute OP poisoning. ALT is the most specific biomarker. However, the reversed De Ritis ratio (ALT/AST) is the most sensitive one.

Conjugates of nucleobases with triazole-hydroxamic acids for the reactivation of acetylcholinesterase and treatment of delayed neurodegeneration induced by organophosphate poisoning.

A series of new uncharged conjugates of adenine, 3,6-dimetyl-, 1,6-dimethyl- and 6-methyluracil with 1,2,4-triazole-3-hydroxamic and 1,2,3-triazole-4-hydroxamic acid moieties were synthesized and studied as reactivators of organophosphate-inhibited cholinesterase. It is shown that triazole-hydroxamic acids can reactivate acetylcholinesterase (AChE) inhibited by paraoxon (POX) in vitro, offering reactivation constants comparable to those of pralidoxime (2-PAM). However, in contrast to 2-PAM, triazole-hydroxamic acids demonstrated the ability to reactivate AChE in the brain of rats poisoned with POX. At a dose of 200 mg/kg (i.v.), the lead compound 3e reactivated 22.6 ± 7.3% of brain AChE in rats poisoned with POX. In a rat model of POX-induced delayed neurodegeneration, compound 3e reduced the neuronal injury labeled with FJB upon double administration 1 and 3 h after poisoning. Compound 3e was also shown to prevent memory impairment of POX-poisoned rats as tested in a Morris water maze.

Tuning the Envelope Structure of Enzyme Nanoreactors for In Vivo Detoxification of Organophosphates.

Encapsulated phosphotriesterase nanoreactors show their efficacy in the prophylaxis and post-exposure treatment of poisoning by paraoxon. A new enzyme nanoreactor (E-nRs) containing an evolved multiple mutant (L72C/Y97F/Y99F/W263V/I280T) of Saccharolobus solfataricus phosphotriesterase (PTE) for in vivo detoxification of organophosphorous compounds (OP) was made. A comparison of nanoreactors made of three- and di-block copolymers was carried out. Two types of morphology nanoreactors made of di-block copolymers were prepared and characterized as spherical micelles and polymersomes with sizes of 40 nm and 100 nm, respectively. The polymer concentrations were varied from 0.1 to 0.5% (w/w) and enzyme concentrations were varied from 2.5 to 12.5 µM. In vivo experiments using E-nRs of diameter 106 nm, polydispersity 0.17, zeta-potential -8.3 mV, and loading capacity 15% showed that the detoxification efficacy against paraoxon was improved: the LD50 shift was 23.7xLD50 for prophylaxis and 8xLD50 for post-exposure treatment without behavioral alteration or functional physiological changes up to one month after injection. The pharmacokinetic profiles of i.v.-injected E-nRs made of three- and di-block copolymers were similar to the profiles of the injected free enzyme, suggesting partial enzyme encapsulation. Indeed, ELISA and Western blot analyses showed that animals developed an immune response against the enzyme. However, animals that received several injections did not develop iatrogenic symptoms.

Organophosphorus Poisoning: Acute Respiratory Distress Syndrome (ARDS) and Cardiac Failure as Cause of Death in Hospitalized Patients.

Industrial production of food for animals and humans needs increasing amounts of pesticides, especially of organophosphates, which are now easily available worldwide. More than 3 million cases of acute severe poisoning are estimated to occur worldwide every year, and even more cases remain unreported, while 200,000-350,000 incidentally or intentionally poisoned people die every year. Diagnostic and therapeutic procedures in organophosphate poisoning have, however, remained unchanged. In addition to several neurologic symptoms (miosis, fasciculations), hypersecretion of salivary, bronchial, and sweat glands, vomiting, diarrhea, and loss of urine rapidly induce dehydration, hypovolemia, loss of conscience and respiratory distress. Within hours, signs of acidosis due to systemic hypoxia can be observed at first laboratory investigation after hospitalization. While determination of serum-cholinesterase does not have any diagnostic value, it has been established that hypoalbuminemia alone or accompanied by an increase in creatinine, lactate, or C-reactive protein serum levels has negative prognostic value. Increased serum levels of C-reactive protein are a sign of systemic ischemia. Protective mechanical ventilation should be avoided, if possible. In fact, acute respiratory distress syndrome characterized by congestion and increased weight of the lung, accompanied by heart failure, may become the cause of death. As the excess of acetylcholine at the neuronal level can persist for weeks until enough newly, locally synthesized acetylcholinesterase becomes available (the value of oximes in reducing this time is still under debate), after atropine administration, intravenous albumin and fluid infusion should be the first therapeutic interventions to reestablish normal blood volume and normal tissue oxygenation, avoiding death by cardiac arrest.

Pro: Oximes should be used routinely in organophosphate poisoning.

In poisoning with organophosphorus compounds (OP), patients can only profit from the regeneration of acetylcholinesterase, when the poison load has dropped below a toxic level. Every measure that allows an increase of synaptic acetylcholinesterase (AChE) activity at the earliest is essential for timely termination of the cholinergic crisis. Only drug-induced reactivation allows fast restoration of the inhibited AChE. Obidoxime and pralidoxime have proved to be able to reactivate inhibited cholinesterase thereby saving life of poisoned animals. A plasma level of obidoxime or pralidoxime allowing reactivation in humans poisoned by OP can be adjusted. There is no doubt that obidoxime and pralidoxime are able to reactivate OP-inhibited AChE activity in poisoned patients, thereby increasing AChE activity and contributing substantially to terminate cholinergic crisis. Hence, a benefit may be expected when substantial reactivation is achieved. A test system allowing determination of red blood cell AChE activity, reactivatability, inhibitory equivalents and butyrylcholinesterase activity is available for relatively low cost. If any reactivation is possible while inhibiting equivalents are present, oxime therapy should be maintained. In particular, when balancing the benefit risk assessment, obidoxime or palidoxime should be given as soon as possible and as long as a substantial reactivation may be expected.

Chemical, biological, radiological, and nuclear mass casualty medicine: a review of lessons from the Salisbury and Amesbury Novichok nerve agent incidents.

On March 4, 2018, two casualties collapsed on a park bench in Salisbury, Wiltshire, UK. They were later discovered to have been the victims of an attempted murder using the Soviet-era Novichok class of nerve agent. The casualties, along with three further critically ill patients, were cared for in Salisbury District Hospital's Intensive Care Unit. Before the COVID-19 pandemic, the Salisbury and Amesbury incidents were the longest-running major incidents in the history of the UK National Health Service. This narrative review seeks to reflect on the lessons learned from these chemical incidents, with a particular focus on hospital and local organisational responses.

Factors associated with time to successful weaning in mechanically ventilated organophosphate poisoned patients.

We designed this study to identify the factors associated with time to successful weaning in mechanically ventilated organophosphate (OP)-poisoned patients as the primary outcomes while duration of mechanical ventilation (MV) support, intensive care unit (ICU), and hospital length of stay (LOS) and in-hospital mortality as the secondary outcomes. We conducted a retrospective study of mechanically ventilated OP-poisoned patients admitted to the ICU of Poison Control Center of Ain Shams, Cairo, Egypt, starting from January 2019 to December 2019. Weaning was considered successful if the patient succeeded in the first spontaneous breathing trial of weaning and did not need reinstitution of MV. We used Cox proportional hazards regression models to identify factors associated with time to successful weaning in the studied patients. A total of 55 patients were enrolled in the study. Thirty-eight patients were weaned successfully. Lower initial red cell distribution width (RDW) levels [adjusted hazard ratio (HR), 0.299, 95% confidence interval (CI) (0.184-0.486)] and lower initial doses of atropine [adjusted HR, 0.97, 95% CI (0.935-0.999)] were independently associated with shorter time to achieve successful weaning. Successfully weaned patients had significantly longer hospital LOS (p = 0.019) and no reported in-hospital mortality (p < 0.001) compared with patients who failed to wean. We concluded that initial RDW and initial doses of atropine were found to be the strongest factors associated with time to successful weaning in mechanically ventilated OP-poisoned patients. RDW and atropine can be used as simple risk assessment tools in OP poisoning.

Ingestion poisoning related lung injury- a pictorial review.

Poison ingestion is a medical emergency requiring immediate care in the emergency department. Respiratory symptoms with ingested poisons can occur due to aspiration, cardiopulmonary effects, or direct lung toxicity due to injury of the alveolar epithelium. Chest imaging (chest radiographs/CT) is usually performed in the emergency setting to evaluate such symptoms. It is often impossible to elicit the nature of the poison ingested by the patients due to their unconscious state. Identification of the culprit poison can expedite the patient's management towards a specific antidote or help understand the underlying mechanism causing the pulmonary symptoms. The imaging manifestations depend on the underlying mechanisms, varying for each ingested poison, forming an imaging signature which has not been adequately discussed in existing literature. Poisons like paraquat and organophosphate are important to differentiate as indiscriminate use of oxygen therapy in the former can exacerbate the lung injury caused by redox cycling. In this pictorial assay, we present the chest imaging spectrum of commonly ingested poisons, and further suggest algorithmic approach towards identification of common poisons based on their chest imaging.

Microglia Remodelling and Neuroinflammation Parallel Neuronal Hyperactivation Following Acute Organophosphate Poisoning.

Organophosphate (OP) compounds include highly toxic chemicals widely used both as pesticides and as warfare nerve agents. Existing countermeasures are lifesaving, but do not alleviate all long-term neurological sequelae, making OP poisoning a public health concern worldwide and the search for fully efficient antidotes an urgent need. OPs cause irreversible acetylcholinesterase (AChE) inhibition, inducing the so-called cholinergic syndrome characterized by peripheral manifestations and seizures associated with permanent psychomotor deficits. Besides immediate neurotoxicity, recent data have also identified neuroinflammation and microglia activation as two processes that likely play an important, albeit poorly understood, role in the physiopathology of OP intoxication and its long-term consequences. To gain insight into the response of microglia to OP poisoning, we used a previously described model of diisopropylfluorophosphate (DFP) intoxication of zebrafish larvae. This model reproduces almost all the defects seen in poisoned humans and preclinical models, including AChE inhibition, neuronal epileptiform hyperexcitation, and increased neuronal death. Here, we investigated in vivo the consequences of acute DFP exposure on microglia morphology and behaviour, and on the expression of a set of pro- and anti-inflammatory cytokines. We also used a genetic method of microglial ablation to evaluate the role in the OP-induced neuropathology. We first showed that DFP intoxication rapidly induced deep microglial phenotypic remodelling resembling that seen in M1-type activated macrophages and characterized by an amoeboid morphology, reduced branching, and increased mobility. DFP intoxication also caused massive expression of genes encoding pro-inflammatory cytokines Il1ß, Tnfα, Il8, and to a lesser extent, immuno-modulatory cytokine Il4, suggesting complex microglial reprogramming that included neuroinflammatory activities. Finally, microglia-depleted larvae were instrumental in showing that microglia were major actors in DFP-induced neuroinflammation and, more importantly, that OP-induced neuronal hyperactivation was markedly reduced in larvae fully devoid of microglia. DFP poisoning rapidly triggered massive microglia-mediated neuroinflammation, probably as a result of DFP-induced neuronal hyperexcitation, which in turn further exacerbated neuronal activation. Microglia are thus a relevant therapeutic target, and identifying substances reducing microglial activation could add efficacy to existing OP antidote cocktails.

Transdermal Delivery of 2-PAM as a Tool to Increase the Effectiveness of Traditional Treatment of Organophosphate Poisoning.

For the first time, the efficacy of post-exposure treatment of organophosphate (OP) poisoning was increased by transdermal delivery of acetylcholinesterase (AChE) reactivator pyridine-2-aldoxime methochloride (2-PAM) as a preventive countermeasure. By selecting the optimal ratio of components, classical transfersomes (based on soybean phosphatidylcholine and Tween 20) and modified transfersomes (based on soybean phosphatidylcholine, Tween 20 and pyrrolidinium cationic surfactants with different hydrocarbon tail lengths) were obtained for 2-PAM encapsulation. Transfersomes modified with tetradecylpyrrolidinium bromide showed the best results in encapsulation efficiency and sustained release of 2-PAM from vesicles. Using Franz cells, it was found that the incorporation of surfactants into PC liposomes results in a more prolonged release of 2-PAM through the rat skin. Transfersomes containing 2-PAM, after exhaustive physical and chemical characterization, were embedded in a gel based on Carbopol® 940. A significantly high degree of erythrocyte AChE reactivation (23 ± 7%) was shown for 2-PAM in unmodified transfersomes in vivo. Preliminary transdermal administration of 2-PAM 24 h before emergency post-exposure treatment of OP poisoning leads to an increase in the survival rate of rats from 55% to 90%.

Frequency of Acute Kidney Injury (AKI) among patients presenting with Organophosphate Poisoning at National Poison Control Centre, Karachi: A prospective cross-sectional survey.

Background and Objective: Organophosphates poisoning is among the most prevalent forms of intentional and unintentional poisoning in Pakistan. However, the actual burden of AKI secondary to organophosphate poisoning in Pakistani population is still not known. This study aimed to determine the actual burden of AKI among patients admitted at National Poison Control Centre, Karachi. Methods: A cross-sectional survey was conducted at National Poison Control Centre, Karachi November, 2013 to April, 2014. A sample of 300 patients of age 18 years and above, presenting with organophosphate poisoning within 24 of exposure or ingestion were included in the study. Frequency of acute kidney injury was calculated using the diagnostic criteria of serum creatinine level of >1.4 mg/dL. Data was analyzed using SPSS version 19. Results: The frequency of AKI which was defined as creatinine level >1.4 mg/dL was 22.3% (n=67). However, there was no statistically significant difference was found in frequency of AKI on the basis of age, sex, amount of organophosphates ingested and BMI. This study found statistically significant differences in the AKI frequency on the basis of lag time. Those who presented earlier after poisoning had relatively low frequency of AKI. Conclusion: This study concludes that AKI is a common complication among patients presenting with organophosphate poisoning at National Poison Control Center, Karachi. Lag time is a key determinant of AKI among patients with organophosphate poisoning. Timely treatment can prevent this critical complication among patients with organophosphate poisoning.

[One case of rhabdomyolysis caused by acute phoxim poisoning].

Patients with organophosphate poisoning usually die from respiratory depression and respiratory failure. The incidence of rhabdomyolysis is relatively low, but the mortality rate is extremely high once it occurs. In this paper, the treatment of a patient with acute phoxim poisoning was analyzed. The patient developed severe rhabdomyolysis syndrome on the 3rd day of treatment, the creatine kinase exceeded the normal value by more than 300 times (up to 103510.65 U/L) , and renal failure occurred. Clinical treatment included active detoxification, blood purification, organ support, and internal environment maintenance. The patient's rhabdomyolysis continued, and the condition worsened. Finally, the family gave up the treatment and the patient died. It is suggested that attention should be paid to the occurrence of rhabdomyolysis syndrome during the treatment of organophosphorus poisoning, and timely blood purification technology may be the key to treatment.

A case report of delayed lower intestinal bleeding after organophosphate poisoning.

BACKGROUND: Organophosphate poisoning is a serious issue and it results in significant casualties in developing countries. Since agriculture remains an important and necessary sector of human society and organophosphate are commonly used in agriculture, it is difficult to prevent organophosphate poisoning. Gastrointestinal bleeding is not a common but life threatening symptom of organophosphate poisoning. We report a rare case of gastrointestine bleeding due to organophosphate poisoning. CASE PRESENTATION: A 78-year-old woman presented to our hospital approximately 12 h after ingesting a mouthful of organophosphate and benzodiazepines in a suicide attempt. Six weeks after successful medical treatment for respiratory failure, she developed recurring melena. Colonoscopy and esophagogastroduodenoscopy findings were negative for ulcers or bleeding. Enteroscopy revealed severe circumferential ulcers with luminal narrowing 10 cm proximal to the ileocecal valve. The patient underwent a 100-cm ileum resection after failed medical treatment and recovered uneventfully. The resected terminal ileum demonstrated severe inflammation and a sharp transitional zone between the healthy and injured mucosa approximately 50 cm proximal to the ileocecal valve. Pathological examination revealed an injured mucosa with inflammatory cell infiltration and structural damage. This case highlights a rare event of OP poisoning with late-onset lower gastrointestinal bleeding, which prolonged the patient's recovery course and parenteral alimentation period. CONCLUSION: We report a rare case of a patient with organophosphate poisoning, with late-onset lower GI tract bleeding, which raised clinical awareness regarding the organophosphate poisoning that induce intestinal symptoms.

[Forensic characteristics of the cardio-toxic effect of organophosphorus compounds]. / Sudebno-meditsinskaya kharakteristika kardiotoksicheskogo deistviya fosfororganicheskikh soedinenii.

Objective - to identify the morphological equivalents of the cardiotoxic action of organophosphate poisoning. It was studied 110 fatal organophosphate poisonings in toxicogenic and somatogenic stages. The study of the heart was a comprehensive in term of clinical, biochemical, histological, micromorphometric, histochemical and histoenzymological approaches. We have identified a complex of deep metabolic disorders and necrobiotic changes in the heart muscle and the level of cholinesterase activity inhibition in the cholinergic structures of the heart in the toxicogenic and somatogenic stages of fatal organophosphate poisoning.

Efficacy of fresh frozen plasma transfusion in comparison with conventional regimen in organophosphate poisoning treatment: a meta-analysis study.

OBJECTIVE: To evaluating the efficacy of fresh frozen plasma (FFP) in comparison with conventional regimen in the treatment of organophosphate (OP) poisoning. METHODS: PubMed, ScopeMed, Cochrane, Scopus, and Google Scholar databases were searched. The search strategy used the following key words "organophosphate" and "poisoning or toxicity", "(atropine and oxime)", "fresh frozen plasma", "clinical trial", "outcome". The treatment with atropine or/and oxime was considered conventional therapy. The length of hospitalization, the length of ICU admission, need for mechanical ventilation and its duration, clinical recovery point, choline esterase level, mortality rate, and intermediate syndrome (IMS) occurrence were the key outcomes of interest. Databases were searched during the period of 2003-2019. Five studies were included in the analysis. RESULTS: Pooling of data showed that the relative risk (RR) of mortality in OP poisoning for five included trials comparing FFP-treated group with conventional regimen therapy was [0.563 (95% CI (0.252, 1.255)]. The summary of RR for IMS in two studies was [RR: 1.34, 95% CI (0.655, 2.742)]. In addition, there was a non-significant mean difference (MD) in hospital stay [MD: -0.106, 95% CI (-0.434, 0.223)] in three included trials. A significant MD was observed in the length of ICU admission in two trials between FFP-treated group compared to the conventional treatment group [MD: -2.672, 95% CI (-4.189, -1.154)], but after random effects meta-analysis, the changes were not significant [MD: -2.015, 95% CI (-6.308, 2.277)]. The summary of fixed-effect meta-analysis for choline esterase level in three trails was [MD: -0.117, 95% CI (-0.468, 0.234)]. The RR of ventilation requirement for two included trials in the FFP-treated group comparing to the conventional regimen therapy was [0.84, 95% CI (0.691, 1.022)] while for ventilation duration in two studies was [MD: -0.183, 95% CI (-0.567, 0.201)]. CONCLUSION: The addition of FFP to conventional therapy did not improve the outcomes of mortality, IMS, hospital length of stay, cholinesterase levels, need or duration of mechanical ventilation, and only the length of ICU stay could affect in the treated group.

Development of a practical prediction scoring system for severe acute organophosphate poisoning.

Acute organophosphorus poisoning (AOPP) is a serious public health issue, especially in the rural areas. This study was designed to establish a scoring system to assess the risk of cases with severe AOPP. A retrospective cohort study was conducted at two independent hospitals. The derivation cohort included 444 patients with AOPP and the validation cohort included 274 patients. A risk score for patients with severe AOPP was developed. The rates of severe AOPP cases were 20.7% and 20.1% in the derivation and validation cohorts, respectively. A scoring system for severe AOPP risk was developed that included: (1) age >50 years, (2) white blood cell count of >15 × 109 /L, (3) plasma cholinesterase of <360 U/L, (4) plasma albumin of <35 g/L, (5) blood pH <7.3, and (6) lactic acid >3.0 mmol/L. The predicted score in severe cases of AOPP had good accuracy in both the derivation (area under the receiver operating characteristic curve [AUC] 0.88, 95% confidence interval [CI], 0.85-0.92) and validation cohorts (AUC 0.83, 95% CI, 0.77-0.90). A practical bedside prediction scoring system was developed for patients with severe AOPP. The routine use of this scoring system could rapidly assist in identifying patients at higher risk who require more intensive care or transfer to a larger better-equipped hospital.

[The role of noninvasive hemodynamic monitoring in the evaluation of acute and severe pesticide poisoning].

Objective: To explore the method of noninvasive hemodynamic monitoring system (NICaS) in monitoring the hemodynamics of patients with acute pesticide poisoning, and to analyze the clinical guiding value of NICaS in hemodynamics of patients with severe pesticide poisoning. Methods: In August 2019, 200 patients with severe acute organophosphorus pesticide poisoning (AOPP) or moderate severe acute paraquat pesticide poisoning (APP) admitted to Harrison international peace hospital from January 2017 to August 2019 were randomly divided into NICaS group (n=68) , transpulmonary thermodilution method (n=67) and empirical treatment group (n=65) . The relationship between acute physiology and chronic health score (APACHE Ⅱ) , heart rate, hemodynamic indexes, survival rate and complications were analyzed. Results: There were no significant differences in age, sex ratio, body mass index, heart rate, systolic blood pressure, no treatment period and admission APACHE II score between NICaS group, Picco group and experience group (P>0.05) ; Compared with the experience group, the mortality of AOPP and app in NICaS group and Picco group were lower, and the differences were statistically significant (P<0.05) .The cardiac output (CO) had a significant correlation in the interval of 2.8-6.7 L·min(-1) (r=0.738, r(2)=0.545, P<0.01) , and peripheral vascular resistance index (SVRI) had a significant correlation in the interval of 410-1 950 d·s·cm(-5)·m(2) (r=0.792, r(2)=0.627, P<0.01) . Bland Altman analysis showed that CO and SVRI measured by Picco and NICaS had 97.01% and 95.52% consistency, respectively. Compared with the experience group, the average daily infusion volume and daily colloid infusion volume of NICaS group and Picco group were lower, the differences were statistically significant (P<0.05) . Conclusion: NICaS can effectively monitor the hemodynamic indexes of patients with acute pesticide poisoning.

[Predictive value of early detection of hs-cTnI and sST2 for secondary cardiac damage in severe acute organophosphorus pesticide poisoning].

Objective: To investigate the value of high-sensitivity cardiac troponin I (hs-cTnI) and soluble suppression of tumorigenicity 2 (sST2) in predicting cardiac complications of severe acute organophosphorus pesticide poisoning (SAOPP) . Methods: All 274 SAOPP patients from September 2014 to February 2019 were selected. According to the results of hs-cTnI detection, the patients were divided into non-elevated troponin group (78 cases) and troponin elevation group (196 cases) at 1 hour after admission. 3 days after admission, there were 109 cases of complication and 165 cases of non-complication according to the presence or absence of cardiac complications. The changes of hs-cTnI, sST2, N-terminal B-type brain natriuretic peptide (NT proBNP) , acute physiology and chronic health (APACHE-Ⅱ) , cholinesterase activity, left ventricular ejection fraction (LVEF) , short axis shortening rate (FS) were observed and analyzed. The predictive value of hs-cTnI and sST2 were evaluated by receiver operating characteristic curve (ROC) analysis. Results: The sST2 level in patients with troponin elevation group was significantly higher than that in non-elevated troponin group (P<0.05) . Compared with the non-complication and non-elevated troponin group, the patients with non-complication and troponin elevation group had elevated hs-cTnI, sST2 and decreased cholinesterase (P<0.05) . Compared with other groups, the hs-cTnI, sST2, NT-proBNP, and APACHE-Ⅱ scores in the complication and troponin elevation group were significantly increased, and cholinesterase was significantly reduced (P<0.05) . In the non-complication group, LVEF and FS were in the normal range, and there was no significant difference between the groups (P>0.05) . Compared with other groups, the LVEF and FS of patients with elevated troponin in the complications group were significantly decreased (P<0.05) . Correlation analysis showed that hs-cTnI and sST2 were positively correlated in patients with SAOPP complications (r=0.725, P<0.01) . hs-cTnI, sST2 and APACHE-Ⅱ scores were positively correlated in the complications group (r=0.846, 0.885, P<0.01) . ROC results showed that the areas under the curve for predicting SAOPP secondary heart damage of hs-cTnI (1 hour after admission) and sST2 (3 days after admission) were 0.945 and 0.833, respectively. Conclusion: hs-cTnI and sST2 may have important clinical value in the early diagnosis and prognosis evaluation of patients with SAOPP secondary cardiac damage.

Organophosphorus nerve agent poisoning: managing the poisoned patient.

Organophosphorus (OP) nerve agent poisoning made the headlines in 2018 with the nerve agent 'Novichok' poisonings in Salisbury, England. This event highlighted a gap in the knowledge of most clinicians in the UK. In response, this special article aims to enlighten and signpost anaesthetists and intensivists towards the general management of OP nerve agent poisoned patients. Drawing on a broad range of sources, we will discuss what OP nerve agents are, how they work, and how to recognise and treat OP nerve agent poisoning. OP nerve agents primarily act by inhibiting the enzyme acetylcholinesterase, causing an acute cholinergic crisis; death usually occurs through respiratory failure. The antimuscarinic agent atropine, oximes (to reactivate acetylcholinesterase), neuroprotective drugs, and critical care remain the mainstays of treatment. The risk to medical staff from OP poisoned patients appears low, especially if there is a thorough decontamination of the poisoned patient and staff wear appropriate personal protective equipment. The events in Salisbury in the past year were shocking, and the staff at Salisbury District General Hospital performed admirably in treating those affected by Novichok nerve agent poisoning. We eagerly anticipate their future clinical publications so that the medical community might learn from their valuable experiences.

Efficacy and outcomes of lipid resuscitation on organophosphate poisoning patients: A systematic review and meta-analysis.

OBJECTIVE: Organophosphate (OP) pesticides are still widely available in developing countries, leading to numerous accidental or suicidal poisonings every year. Lipid emulsion treatments are commonly used in resuscitating OP poisoning patients but few studies regarding their use have been reported. Our meta-analysis aimed to analyze the efficacy and outcomes of lipid resuscitation on OP poisoning patients. METHODS: A systematic search for associated studies was conducted in Pubmed, EMBASE, MEDLINE, the Cochrane Library and the Chinese National Knowledge Infrastructure. Collected data was pooled using Revman v5.3. Outcomes included prognosis (cured vs. mortality rates), hepatic function (serum ALT, AST, Total Bilirubin (TBIL) level), serum acetylcholinesterase (AchE) level and respiratory function (rate of respiratory muscular paralysis). RESULTS: Seven randomized controlled studies consisting of 630 patients meeting inclusion criteria were identified. Lipid emulsion helped to improve the cure rate [OR = 2.54, 95% CI (1.33, 4.86), p = 0.005] and lower the mortality rate [OR = 0.31, 95% CI (0.13, 0.74), p = 0.009]. Serum ALT, AST and TBIL in patients undergoing lipid resuscitation were lower than those in the control groups [ALT, SMD = -1.52, 95% CI (-2.64, 0.40), p = 0.008; AST, SMD = -1.66, 95% CI (-3.15, 0.16), p = 0.03; TBIL, SMD = -1.26, 95% CI (-2.32, 0.20), p = 0.02]. Serum AchE level were increased in patients treated with lipid emulsion [SMD = 2.15, 95% CI (1.60, 2.71), p < 0.00001]. Rate of respiratory muscular paralysis was lower in patients undergoing lipid resuscitation than those in the control groups [OR = 0.19, 95% CI (0.05, 0.71), p = 0.01]. CONCLUSION: Based on our meta-analysis of included RCT reports, lipid resuscitation seems likely to help improve prognosis and liver function of OP poisoning patients. However, larger multi-center RCTs are still recommended.