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CASE REPORT
Year : 2022  |  Volume : 20  |  Issue : 3  |  Page : 187-190

Dimethoate self-poisoning–Induced severe hypotension


Department of Neurointensive Care and Trauma Unit, Ruby Hall Clinic, Pune, Maharashtra, India

Date of Submission21-Jan-2022
Date of Decision12-Mar-2022
Date of Acceptance25-Mar-2022
Date of Web Publication01-Aug-2022

Correspondence Address:
Dr. Anand M Tiwari
Department of Neurointensive Care and Trauma Unit, Ruby Hall Clinic, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_12_22

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  Abstract 


Intentional ingestion of organophosphorus compound (OP) poisoning continues to be a frequent reason for critical care admission in India. For the past 6 decades, the OP compounds used in India for the poisoning had effects on cholinergic and neurogenic fibers producing the respiratory and neurologic presentation. Recently, a less frequent OP poison has appeared which acts on cardiac sympathetic fibers with bradycardia and hypotension as presenting features. The shock which was nonresponsive to dopamine/dobutamine was identified as a major cause of death in patients with dimethoate poisoning in a large prospective cohort study. Severe dimethoate poisoning in contrast to other OP compounds has a high case fatality rate. There have been case reports from outside India. We report the first two cases with successful treatment of this toxicity in India.

Keywords: Case report, dimethoate, hypotension, norepinephrine, poisoning


How to cite this article:
Tiwari AM, Zirpe KG, Wadia RS, Gurav SK, Deshmukh AM. Dimethoate self-poisoning–Induced severe hypotension. Curr Med Issues 2022;20:187-90

How to cite this URL:
Tiwari AM, Zirpe KG, Wadia RS, Gurav SK, Deshmukh AM. Dimethoate self-poisoning–Induced severe hypotension. Curr Med Issues [serial online] 2022 [cited 2022 Aug 10];20:187-90. Available from: https://www.cmijournal.org/text.asp?2022/20/3/187/352966




  Introduction Top


Accidental exposure or self-poisoning with the organophosphorus (OP) pesticide dimethoate has been reported in the literature for a high case fatality rate compared with chlorpyrifos.[1],[2] Unlike the other organophosphorus insecticides, dimethoate poisoning results in a clinical syndrome characterized by severe hypotension at the time of admission and death from hypotensive shock while being ventilated.[3] We report novel adjuvant use of norepinephrine for treatment in two patients with dimethoate poisoning with persistent hypotension with success. We also highlight the need of a specific management protocol based on the OP compound ingested.


  Case Reports Top


Case 1

A 44-year-old male presented with increased secretions, respiratory distress, pinpoint pupil, found obtunded with a history of an unknown amount of consumption of Anugor (Dimethoate 30%) with suicidal intent. He was admitted within 2 h of ingestion.

Case 2

A 49-year-old male presented after about 6 h after intentionally ingesting an unknown amount of Rogor (dimethoate 30% with solvent) in depression due to economic burden. No other agent or alcohol was co-ingested in either cases.

Clinical parameters and course of both cases are illustrated in [Table 1].
Table 1: Clinical parameters at presentation and course in hospital

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Case 1 – On arrival, pulse rate was 60/min, systolic blood pressure (SBP) 90 systolic with poor respiratory effort, and was intubated and ventilated in emergency department.

Case 2 – On arrival, he was obtunded with (Glasgow Coma Scale <8), increased secretions with garlicky odor, respiratory distress, profound hypotension with SBP 70 systolic and heart rate 54/min, pinpoint pupil, and was immediately intubated and ventilated.

Hemodynamic variables of both cases are illustrated in [Table 2].
Table 2: Hemodynamic monitoring and resuscitation

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Both cases received a fluid challenge of crystalloid (Plasma-Lyte) 1.5 l initially and a bolus dose of atropine 5 mg followed by infusion with hemodynamic monitoring.

Both cases were assessed with the point of care ultrasound examination, electrocardiographic (ECG), and 2D echocardiography bedside for hemodynamic stabilization. Norepinephrine was used initiated in view of persistent hypotension despite fluid challenge and atropinization. Both cases shock was with warm peripheries pointing clinically toward vasodilatory shock. However, we preferred noninvasive hemodynamic monitoring as mentioned above and did not measure systemic vascular resistance (SVR). Requirement and duration of norepinephrine are depicted in [Figure 1].
Figure 1: Duration of treatment with norepinephrine in Cases 1 and 2. Time 0 in X-axis denotes norepinephrine initiation after fluid challenge and atropinization started at 1 h for persistent hypotension. Note atropine infusion was continued in both cases.

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Standard care management for OP inclusive of atropine and pralidoxime was followed in both cases.


  Discussion Top


In developing countries, organophosphate (OP) poisoning is still a common cause for admission to hospitals and the intensive care unit (ICU). In terms of clinically important medical outcomes, patients admitted with dimethyl organophosphate poisoning have a poorer outcome than those admitted with diethyl organophosphate poisoning.[4]

Salivation, lacrimation, urination, defecation, gastric cramps, and emesis symptoms are common in organophosphate (OP) poisoning. Several other manifestations, however, are identified.[5]

Pesticides containing organophosphates, such as dimethoate, are used to control household pests as well as those found in agriculture and forestry.[6]

It differs from other OP compounds in that it is lipophobic, has a limited distribution volume, and has a high serum concentration.[7] Dimethoate poisoning with blood pressure <80 systolic has an 80% case fatality rate.[4] In patients mechanically ventilated in the ICU, a SBP of <100 mmHg and the need for a FiO2 >40% to maintain sufficient oxygenation are predictors of poor outcomes.[8]

We report successful management of two cases of self-ingestion with 30% dimethoate compound a as Anugor and Rogor, respectively. Anugor contains the active ingredient dimethoate alone, while Rogor contains dimethoate and cyclohexanone as solvents. We observed that case 1 presented with hypotension with SBP 90 systolic on presentation which reverted in 12 h whereas case 2 had severe hypotension with blood pressure 70 systolic on admission and required a higher dose of inotropic norepinephrine for a prolonged period around 72 h [Figure 1]. These observations are in agreement with an experimental study that showed more mammalian cardiotoxicity with dimethoate formulation containing solvent as cyclohexanone versus dimethoate active ingredient alone.[9]

Cardiac abnormalities have only been identified in a few cases of pesticide poisoning, and even fewer cases of organophosphorus poisoning. The mechanism of these compounds' cardiotoxicity is still unclear. Previous studies on the cardiac effects of OP poisoning have primarily concentrated on arrhythmias,[10],[11] and hypertension,[12] with hypotensive effects being much less commonly described.[13]

Both dimethoate self-poisoning cases reported here presented as hypotension with warm peripheries and were clinically suggestive of reduced SVR. Direct cardiotoxic effects (cardiogenic shock) and peripheral vasodilation (distributive shock) are common side effects of dimethoate, which may have led to refractory hypotension. We tailored the treatment to the patient's needs, with an emphasis on hemodynamic parameters. In both cases, 2D echocardiography was performed, allowing for a complete evaluation of cardiac function. Fluid resuscitation was accomplished with crystalloid fluid (Plasma-Lyte).

After initial fluid resuscitation, we used norepinephrine as the vasopressor of choice in both cases. There have been past reports of similar cases with a high case fatality rate. In a case series of three deaths, Davies J et al. reported mortality in all three cases due to dimethoate poisoning.[3]

The variation in treatment reported in current case report is that both patients received norepinephrine as vasopressor of choice,as opposed to Davies J et al. were authors used dopamine. Dopamine is known to induce an arrhythmogenic effect and might contribute to cardiac toxicity. We highlight the need for the evaluation of cardiac abnormalities by physical examination, ECG, and ECHO bedside. ECG disorders such as sinus tachycardia, sinus bradycardia, prolonged Q-Tc interval, prolonged PR interval, ST-T modifications, and conduction defects are examples of cardiac complications.[14] In OP poisoning apart from usual respiratory failure, one of the causes of mortality is cardiovascular collapse, so ECG and ECHO can be regarded as a mandatory tool in severe dimethoate poisoning cases and to be performed periodically. In treating and resuscitating patients in shock, bedside assessment of the inferior vena cava is well recognized.[15] Vasodilatory shock responded to norepinephrine which was gradually tapered off in both cases of severe dimethoate poisoning after hemodynamic stabilization was achieved.

We observed the beneficial effect of norepinephrine in a patient with persistent hypotension with dimethoate poisoning, however, to conclusively evaluate the efficiency of vasopressor in dimethoate-induced persistent hypotension larger studies with more data including direct assessment of cardiac output and SVR are required.


  Conclusion Top


Patients can benefit from management protocols established for specific organophosphorus insecticides. OP compounds should be treated as individual poison. Severe dimethoate poisoning-induced hypotension needs careful evaluation of composition of the dimethoate compound consumed. In patients with severe dimethoate poisoning, hemodynamic monitoring is needed, and norepinephrine is the preferred vasopressor. Thus, individualized treatment as per type and chemical composition of OP compound is just as critical as regular atropine and pralidoxime therapy to avert mortality

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Wadia RS, Sadagopan C, Amin RB, Sardesai HV. Neurological manifestations of organophosphorous insecticide poisoning. J Neurol Neurosurg Psychiatry 1974;37:841-7.  Back to cited text no. 1
    
2.
Eddleston M, Eyer P, Worek F, Mohamed F, Senarathna L, von Meyer L, et al. Differences between organophosphorus insecticides in human self-poisoning: A prospective cohort study. Lancet 2005;366:1452-9.  Back to cited text no. 2
    
3.
Davies J, Roberts D, Eyer P, Buckley N, Eddleston M. Hypotension in severe dimethoate self-poisoning. Clin Toxicol (Phila) 2008;46:880-4.  Back to cited text no. 3
    
4.
Peter JV, Jerobin J, Nair A, Bennett A, Samuel P, Chrispal A, et al. Clinical profile and outcome of patients hospitalized with dimethyl and diethyl organophosphate poisoning. Clin Toxicol (Phila) 2010;48:916-23.  Back to cited text no. 4
    
5.
Peter JV, Sudarsan TI, Moran JL. Clinical features of organophosphate poisoning: A review of different classification systems and approaches. Indian J Crit Care Med 2014;18:735-45.  Back to cited text no. 5
  [Full text]  
6.
Paudyal BP. Organophosphorus poisoning. JNMA J Nepal Med Assoc 2008;47:251-8.  Back to cited text no. 6
    
7.
Tarbah FA, Shaheen AM, Benomran FA, Hassan AI, Daldrup T. Distribution of dimethoate in the body after a fatal organophosphate intoxication. Forensic Sci Int 2007;170:129-32.  Back to cited text no. 7
    
8.
Munidasa UA, Gawarammana IB, Kularatne SA, Kumarasiri PV, Goonasekera CD. Survival pattern in patients with acute organophosphate poisoning receiving intensive care. J Toxicol Clin Toxicol 2004;42:343-7.  Back to cited text no. 8
    
9.
Eddleston M, Street JM, Self I, Thompson A, King T, Williams N, et al. A role for solvents in the toxicity of agricultural organophosphorus pesticides. Toxicology 2012;294:94-103.  Back to cited text no. 9
    
10.
Kiss Z, Fazekas T. Arrhythmias in organophosphate poisonings. Acta Cardiol 1979;34:323-30.  Back to cited text no. 10
    
11.
Dalvi CP, Abraham P, Iyer SS. Correlation of electrocardiographic changes with prognosis in organophosphorus poisoning. J Postgrad Med 1986;32:115-9.  Back to cited text no. 11
[PUBMED]  [Full text]  
12.
Petroianu G, Toomes LM, Petroianu A, Bergler W, Rüfer R. Control of blood pressure, heart rate and haematocrit during high-dose intravenous paraoxon exposure in mini pigs. J Appl Toxicol 1998;18:293-8.  Back to cited text no. 12
    
13.
Asari Y, Kamijyo Y, Soma K. Changes in the hemodynamic state of patients with acute lethal organophosphate poisoning. Vet Hum Toxicol 2004;46:5-9.  Back to cited text no. 13
    
14.
Lakhotia M, Pahadiya HR, Kumar H, Jainapur SR, Choudhary A. Cardiogenic shock with 1 heart block after organophosphorus poisoning: A case report and review of cardiac complication in organophosphorus poisoning. CHRISMED J Health Res 2015;2:156.  Back to cited text no. 14
  [Full text]  
15.
Abu-Zidan FM. Optimizing the value of measuring inferior vena cava diameter in shocked patients. World J Crit Care Med 2016;5:7-11.  Back to cited text no. 15
    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2]



 

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