Myocardial infarction in organophosphorus poisoning: Association or just chance?

Kumar, Sunil; Diwan, Sanjay; Dubey, Sameeksha

doi:10.4103/0974-2700.130885

Cited by 10 publications

(9 citation statements)

References 4 publications

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“…[27][28][29] The bradycardia in the early cholinergic phase of the poisoning was less frequently observed whereas the hypertension and sinus tachycardia seen in organophosphate and carbamate poisoning due to nicotinic effects was found in our study. Administration of atropine in high doses has been implicated in the development of ventricular arrhythmias.…”

Section: Discussionmentioning

confidence: 51%

Study of clinical profile of organophosphorus poisoning with special reference to electrocardiographic changes and electrolyte derangement

et al. 2018

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Background: Organophosphorus Compounds (OPC) are main cause of accidental and suicidal poisoning in agrarian countries like India. Aim was to study the clinical profile of OPC-Poisoning and correlate it with the electrocardiographic (ECG) changes and electrolyte abnormalities.Methods: Hundred consecutive cases admitted to Medicine Department underwent clinical examination, ECG, electrolytes, Acetyl Choline Esterase (AChE) estimation from time to time and Paradeniya Organophosphorus Poisoning (POP) score at the time of admission. All these parameter with duration of hospital stay and outcome were statistically analysed using X2 test, Fisher exact test, and inference was drawn.Results: In hundred OPC-Poisoning patients [Male (n=48), Female (n=52), M: F ratio 0.92:1] with mean age of 37.78±12.95 years, commonest poison was cholropyrifos+cypermethrin and was mostly suicidal (96%). Common symptoms were sweating (48%), salivation, blurring of vision, breathlessness and signs were smell of poison (90%), tachypnea, altered sensorium, miosis and fasciculation. POP scoring found 41% of patients in mild, 26% in moderate and 33% in sever grade of poisoning. Hospital stay ranged from 4-18 days. Complications were pulmonary Edema (PE) in 28%, Respiratory Failure (RF) 18%, Aspiration Pneumonia (AP) 15% and Intermediate Syndrome (IS) 4%. 10 died out of 42 patients who had complications and the cause of death was RF in 4, Ventricular Fibrillation (VF) 2 and IS in 2. ECG finding showed sinus tachycardia (31%), prolonged corrected QT (QTc) interval (28%), sinus bradycardia (25%), ST-T changes (17%) and Premature Ventricular Contraction (PVC) in 4% which degenerated to VF in 2%. 24 patients were Hypokalemic from which 16 developed complications.Conclusions: Similar to earlier studies we observed poisoning which was suicidal. QTc prolongation and Hypokalemia are associated with high morbidity and mortality in OPC-Poisoning.

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Section: Discussionmentioning

confidence: 51%

Study of clinical profile of organophosphorus poisoning with special reference to electrocardiographic changes and electrolyte derangement

et al. 2018

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“…Pesticides can increase the amount of catecholamines and other vasoactive amines, which can cause coronary thrombosis or spasm and eventually lead to myocardial infarction ( 16 ). Ischaemic ECG changes that followed (new ST-segment elevation by ≥1 mm and T wave inversion), a rise in cTnI, regional wall motion abnormality, and normal epicardial coronary arteries on angiography reinforced our initial diagnosis of a type 2 MI.…”

Section: Discussionmentioning

confidence: 99%

“…Our search of articles published over the last 15 years and indexed in PubMed, Oxford Journals, Scopus, Google Academic, Science Direct, Springerlink, and Web of Science resulted in only 11 case reports of MI following OP poisoning (see Table 1 ), which confirms that this is a rare occurrence. MI can occur within hours ( 4 , 19 , 20 ) or days after acute OP exposure ( 16 , 23 , 24 ). Two articles ( 6 , 25 ) report type 1 MI early after OP exposure.…”

Section: Discussionmentioning

confidence: 99%

Unusual aetiology of a type 2 myocardial infarction: a case-based review

Toma

Toma²,

Bologa

et al. 2021

Archives of Industrial Hygiene and Toxicology

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Organophosphate pesticide (OP) poisoning is quite common and can cause cardiovascular complications and even direct myocardial injury. However, no guideline has included an acute poisoning as a potential cause for a type 2 myocardial infarction (MI) so far. Here we present a case of a 61-year-old woman brought by ambulance to emergency department one hour after accidental ingestion of an unknown quantity of a solution she used against flea infestation. The patient presented with dizziness, myosis, excessive sweating, hypersalivation, sphincteric incontinence, muscle fasciculation, tremor of the extremities, pale skin, alcoholic and pesticide breath odour. Even though we had no guidelines to fall back on, we successfully treated the patient with low-molecular-weight heparin, antiplatelets, statin, diltiazem, antidote therapy, and supportive care. Physicians should be aware that OP poisoning can induce type 2 MI as a complication within a few hours since exposure, and emergency management should always include close cardiac monitoring.

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“…Recently, thrombotic preconditioning has been shown in patients without comorbidites, who had been treated for acute OP poisoning; they presented a” 1.55-fold increased risk for developing DVT compared with the general population” in a one year follow up after the index date (acute OP poisoning); developing pulmonary thromboembolism (PTE) after surviving acute OP poisonings was significantly higher in patients with a history of comorbidites [9]. Also, thrombotic events during acute OP poisoning have been illustrated in several studies; there was a case report that showed upper limb deep vein thrombosis (DVT) as result of a complication of acute suicidal OP poisoning [11] and several cases of acute myocardial infarction, one resolved with fibrinolytic therapy [10]. Mural thrombosis was found at an autopsy in severe OP poisoning [14].…”

Section: Discussionmentioning

confidence: 99%

“…Lately, a nationwide prospective cohort study pointed out increased prothrombotic diathesis in patients who survived acute OP intoxication [9]. Thrombotic complications associated with non-target tissues of ACh receptor overstimulation were also described, such as myocardial infarction [10] and “upper limb venous thrombosis” [11]. In the published cases so far, there was no reported thrombosis of pulmonary circulation developed during subacute phase of OP (Organophosphate) poisoning.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary thrombosis in acute organophosphate poisoning—Case report and literature overview of prothrombotic preconditioning in organophosphate toxicity

et al. 2019

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Highlights Acute OP poisoning complicated with pulmonary thrombosis during the first week of poisoning. Antidote treatment included atropine, whereas diazepam was administered in the first 48 h. There was no administration of oximes due to unavailability. Prolonged hypoxemia in acute OP intoxication indicates exclusion of thrombotic pulmonary event.

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Myocardial infarction in organophosphorus poisoning: Association or just chance?

Cited by 10 publications

References 4 publications

Study of clinical profile of organophosphorus poisoning with special reference to electrocardiographic changes and electrolyte derangement

Study of clinical profile of organophosphorus poisoning with special reference to electrocardiographic changes and electrolyte derangement

Unusual aetiology of a type 2 myocardial infarction: a case-based review

Pulmonary thrombosis in acute organophosphate poisoning—Case report and literature overview of prothrombotic preconditioning in organophosphate toxicity

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