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 Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 2  |  Issue : 2  |  Page : 156-159

Cardiogenic shock with 1° heart block after organophosphorus poisoning: A case report and review of cardiac complication in organophosphorus poisoning


Department of Medicine, Sampurnanand Medical College, Jodhpur, Rajasthan, India

Date of Web Publication16-Mar-2015

Correspondence Address:
Hans Raj Pahadiya
Room No 15, PG Hostel, MG Hospital, Railway Station Road, Jodhpur - 342 001, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2348-3334.153264

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  Abstract 

Organophosphorus (OP) compounds have been widely used as pesticide in India. Because of wide use and easy availability, it is the most common poisoning. OP compound poisoning can lead to cardiac complications. Here we report a case of 26-year-old female who presented after ingestion of unknown quantity of chlorpyrifos. She had cardiogenic shock, 1° heart block with prolonged QTc interval, and sinus bradycardia. She recovered completely after treatment with atropine and pralidoxime.

Keywords: Electrocardiographical abnormalities, heart block, organophosphorus poisoning, shock


How to cite this article:
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;2:156-9

How to cite this URL:
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 [serial online] 2015 [cited 2019 Oct 21];2:156-9. Available from: http://www.cjhr.org/text.asp?2015/2/2/156/153264


  Introduction Top


Organophosphates and carbamates are the commonly used agricultural insecticides throughout the world. The poisoning with these compounds result due to the occupational exposure or accidental or suicidal ingestion. Organophosphorus (OP) poisoning can lead to acute and chronic effects. The common presenting symptoms are hypersalivation, diaphoresis, urination, decreased respiratory effort, abdominal pain, depressed level of consciousness, and muscle fasciculation. Cardiac complications often accompany poisoning with OP compound poisoning, which may be serious and often fatal. Cardiac complications include electrocardiographic (ECG) abnormalities, such as sinus tachycardia, sinus bradycardia, prolonged Q-Tc interval, prolong PR interval, ST-T changes, and conduction defects. Cardiac arrhythmia, pulmonary edema, hypertension, hypotension, and noncardiogenic pulmonary edema are the life-threatening complications. [1],[2] Here we report a case of chlorpyrifos ingestion who presented with vomiting, salivation, urination, and respiratory distress which is complicated by shock, 1° heart block with prolonged QTc interval, and sinus bradycardia.


  Case Report Top


A 26-year-old female presented to the hospital 3 h after accidental ingestion of unknown quantity of chlorpyrifos. She did not have any chronic medical and psychiatric illness and no addiction to any drug. She had a history of five to six episodes of vomiting. She also had excessive sweating, cooling of the body, salivation, and two episodes of urination on the bed. On examination, patient was drowsy and poorly responsive to verbal and motor stimuli with constricted pupil. The blood pressure was 80/60 mmHg, pulse rate 55 beats/min regular, the respiratory rate 14 breaths/min, and axillary temperature was 35.5°C. Cardiac auscultation was normal. On chest auscultation, bilateral crept was present. Electrocardiograph (ECG) had sinus bradycardia with a rate of 55/min, a normal axis, a PR interval of 300 ms, QRS duration of 80 ms, and a QTc interval of 465 ms [Figure 1]. The arterial blood gas analysis (ABG) showed pH 7.39, oxygen saturation (SpO 2 ) 98.5%, on room air, bicarbonate 17.8 meq/L, PaO 2 119.5 mmHg, and PaCO 2 was 32 mmHg. In the emergency department, gastric lavage was done and treatment in the form of atropine and pralidoxime was started.
Figure 1: ECG showing prolong PR interval (first degree heart block), prolong QTc and sinus bradycardia

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The investigations revealed hemoglobin 11.7 g/dL (12-16); total leukocyte count 14,500/mm 3 (4,000-11,000) with differential leukocyte count of neutrophils 69%, lymphocytes 21%, and eosinophils 2.8%; and platelet count 151,000/mm 3 . Blood urea was 25 mg/dL (14-40), serum creatinine 0.87 mg/dL (0.5-1.2), serum sodium 141.4 meq/L (135-145), serum potassium 3.5 meq/L (3.5-5.0), serum calcium 8.8 mg/dL (8.5-10.2), and blood sugar 84 mg/dL (70-110). Serum bilirubin was 1.14 mg/dL (0.3-1.3) with direct 0.75 mg/dL (0.1-0.4), serum glutamic-pyruvic transaminase (SGPT) 31 U/L (8-40 U/L), and serum glutamic oxaloacetic transaminase (SGOT) 19 U/L (10-38). Cardiac enzymes were creatine phosphokinase (CPK-MB) 78 U/L (0-24), and troponin-I <0.03 mg/dL. Two-dimensional echocardiography was done which revealed no abnormality in the heart. Chest X-ray and ultrasonography was normal. Electrocardiograph was reverted in normal sinus rhythm with pulse rate of 90/min after 48 h of treatment. At that time the blood pressure (BP) was 112/76 mmHg. She had been treated with atropine and pralidoxime for 5 days with complete recovery.


  Discussion Top


OP compounds act as irreversible cholinesterase inhibitors. Toxicity of these compounds leads to cholinergic excess symptoms through the muscarinic, nicotinic, and central nervous system (CNS) receptors.

Cardiac complications may vary from asymptomatic electrocardiographic abnormalities such as sinus tachycardia, sinus bradycardia, prolonged Q-Tc interval, prolong PR interval, and ST-T changes to life-threatening complications like cardiac arrhythmias, pulmonary edema, hypertension, hypotension, myocardial ischemia, and noncardiogenic pulmonary edema. [1],[2] The mechanism of the cardiotoxic effect of OP compounds is very complex.

Ludomirsky et al., [3] described the mechanism in three phases. First phase is a brief period of sympathetic overactivity which causes tachycardia and hypertension. These are considered nicotinic effects and may be due to excessive release of catecholamines. In practice, tachycardia is usually observed as a result of fear and anxiety. In the second phase, parasympathetic overactivity predominates for a more prolong period which is characterized by cholinergic excess and causes bradycardia, hypotension along with ST-T changes, and life-threatening arrhythmias. The last and third phase is longer, usually associated with a prolonged QT interval and polymorphic ventricular tachycardia (torsades de pointes) that can result in sudden death. These toxic compounds can also directly damage the myocardium and vascular system.

Study conducted by Paul and Bhattacharyya [4] and Yurumez et al., [5] showed prolonged Q-Tc interval as the commonest electrocardiographic abnormality, followed by sinus tachycardia and sinus bradycardia, elevation of ST segment, T wave inversion, 1° heart block (P-R interval >0.20 s), atrial fibrillation, ventricular tachycardia, and ventricular premature complexes. Ventricular fibrillation was found as a common cardiac cause of death. [4],[5] Anand et al., [6] found sinus tachycardia as the most common electrocardiographic abnormality. Corrected QT interval prolongation, ST-T changes, U waves, and ventricular premature contractions were also found. They showed patchy myocardial involvement responsible for cardiac complications.

Other effects of OP poisoning are hyperglycemias, hypokalemia, leukocytosis, hypoxemia, and metabolic acidosis. These factors can also precipitate cardiac toxicity in OP poisoning. [2],[7] There are few reported case of acute myocardial infarction (MI) [8],[9] and complete heart block [10] after OP poisoning in the literature. The mechanism of coronary vasospasm in acute MI is probably due to parasympathetic overactivity. [9] Vasospasm in myocardial angina or infarction is triggered by release of inflammatory mediator like histamines, neutral proteases, arachidonic acid products, platelet activating factors, and various cytokines and chemokines release secondary to pesticide. [11]

The exact mechanism of QT prolongation in OP poisoning is not clear. Most of the congenital long QT syndromes (LQTS) have abnormal functioning of ion channels. Metabolic abnormalities (hypokalemia, hypocalcemia, or hypomagnesemia) also precipitate the QT prolongation. Other theories for QT prolongation are vagal overstimulation due to incomplete reactivation of the acetylcholinesterase (AChE), an abnormal regulation of potassium channels by the muscarinic receptor, local damage to autonomic innervation of the heart, and coronary vasospasm due to cholinergic excess. [12]

Gastric lavage should be considered only if the patient is stable and arrives within 1 h of ingesting poison. There is no evidence suggesting that patients with pesticide poisoning benefit from treatment with activated charcoal. [13]

In the treatment of QT prolongation, immediate cardioversion should be performed when torsades de pointes does not terminate spontaneously and results in hemodynamic compromise. Sometime temporary transvenous cardiac pacing and intravenous isoproterenol is required. After treating the underlying cause, QT interval becomes normal. The patients with sick sinus syndrome or AV blocks with a pause or bradycardia which can precipitate torsades, require permanent pacemaker implantation. [12]

Atropine is the mainstay in the treatment of OP poisoning. It is the antimuscarinic agent of choice, the aim of early therapy is to reverse cholinergic features and to improve cardiac and respiratory function as quickly as possible. The role of oximes is not completely clear. Pralidoxime reactivates AChE inhibited by oganophosphorus. [14] In a controlled trial, the high-dose regimen (2 g loading dose, then 1 g either every hour or every 4 h for 48 h, then 1 g every 4 h until recovery) in 200 patients with moderate OP poisoning (excluding severely ill patients with aspiration pneumonia or hypoxic brain injury before treatment) was associated with reduced case fatality. [15] Acutely agitated patient benefits from treatment with diazepam. [13]

Alternative therapies in the management of OP poisoning include use of magnesium sulfate, clonidine, and sodium bicarbonate. [13] Magnesium sulfate acts by blocking the ligand-gated calcium channels at neuromuscular junctions which leads to decrease acetylcholine release from presynaptic terminals and thus improving function and reduced CNS overstimulation mediated via N-methyl-D-aspartate (NMDA) receptor activation. [16] Clonidine is an alpha-2-adrenergic receptor agonist which also reduces acetylcholine synthesis and release from presynaptic terminals. [17] Clonidine showed benefits in animal studies when it is given with atropine. In human beings, effect is uncertain. Sodium bicarbonate is sometimes used for treatment of OP poisoning. Infusion of high doses of NaHCO 3 (5 mEq/kg over 1 h, followed by 5-6 mEq/kg daily until recovery or death to maintain the arterial pH between 7.45 and 7.55) appears to be beneficial in treatment of patients with OP poisoning. [18]

The roles of hemodialysis and hemofiltration are not yet clear for removing OP from the blood. Bioscavengers such as fresh frozen plasma (FFP) or albumin has been recently suggested as a useful therapy through clearing of free organophosphates. [19]

Our patient presented in shock with 1° heart block. She also had prolonged QTc interval and sinus bradycardia. It was due to exaggerated cholinergic stimulation which increases the vagal nerve influence on heart rate and induces bradycardia and slowed cardiac conduction, leading to a decrease in cardiac output. Shock and heart block recovered completely after anticholinergic treatment.

Conclusively, it should be mandatory to monitor ECG in a case of OP poisoning regularly. Patient should be discharged after normalization of QT interval. So these life-threatening preventable complications can be avoided by early recognition, early treatment, and proper monitoring of the patients.


  Acknowledgment Top


Special thanks to Dr. Prakash choudhary and Dr. Shashank.

 
  References Top

1.
Saadeh AM, Farsakh NA, al-Ali MK. Cardiac manifestations of acute carbamate and organophosphate poisoning. Heart 1997;77:461-4.  Back to cited text no. 1
    
2.
Karki P, Ansari J, Bhandary S, Koirala S. Cardiac and electrocardiographical manifestations of acute organophosphate poisoning. Singapore Med J 2004;45:385-9.  Back to cited text no. 2
    
3.
Ludomirsky A, Klein HO, Sarelli P, Becker B, Hoffman S, Taitelman U, et al. Q-T prolongation and polymorphous ("torsade de pointes") ventricular arrhythmias associated with organophosphorus insecticide poisoning. Am J Cardiol 1982;49:1654-8.  Back to cited text no. 3
    
4.
Paul UK, Bhattacharyya AK. ECG manifestations in acute organophosphorus poisoning. J Indian Med Assoc 2012;110:98, 107-8.  Back to cited text no. 4
    
5.
Yurumez Y, Yavuz Y, Saglam H, Durukan P, Ozkan S, Akdur O, et al. Electrocardiographic findings of acute organophosphate poisoning. J Emerg Med 2009;36:39-42.  Back to cited text no. 5
    
6.
Anand S, Singh S, Nahar Saikia U, Bhalla A, Paul Sharma Y, Singh D. Cardiac abnormalities in acute organophosphate poisoning. Clin Toxicol (Phila) 2009;47:230-5.  Back to cited text no. 6
    
7.
Taira K, Aoyama Y, Kawamata M. Long QT and ST-T change associated with organophosphate exposure by aerial spray. Environ Toxicol Pharmacol 2006;22:40-5.  Back to cited text no. 7
    
8.
Pankaj M, Krishna K. Acute organophosphorus poisoning complicated by acute coronary syndrome. J Assoc Physicians India 2014;62:614-6.  Back to cited text no. 8
    
9.
Kumar S, Diwan SK, Dubey S. Myocardial infarction in organophosphorus poisoning: Association or just chance? J Emerg Trauma Shock 2014;7:131-2.  Back to cited text no. 9
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10.
Siegal D, Kotowycz MA, Methot M, Baranchuk A. Complete heart block following intentional carbamate ingestion. Can J Cardiol 2009;25:e288-90.  Back to cited text no. 10
    
11.
Gázquez V, Dalmau G, Gaig P, Gómez C, Navarro S, Mercé J. Kounis syndrome: Report of 5 cases. J Investig Allergol Clin Immunol 2010;20:162-5.  Back to cited text no. 11
    
12.
Bar-Meir E, Schein O, Eisenkraft A, Rubinshtein R, Grubstein A, Militianu A, et al. CBRN Medical Branch, Medical Corps, Israel Defense Forces. Guidelines for treating cardiac manifestations of organophosphates poisoning with special emphasis on long QT and Torsades De Pointes. Crit Rev Toxicol 2007;37:279-85.  Back to cited text no. 12
    
13.
Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet 2008;371:597-607.  Back to cited text no. 13
    
14.
Eyer P. The role of oximes in the management of organophosphorus pesticide poisoning. Toxicol Rev 2003;22:165-90.  Back to cited text no. 14
    
15.
Pawar KS, Bhoite RR, Pillay CP, Chavan SC, Malshikare DS, Garad SG. Continuous pralidoxime infusion versus repeated bolus injection to treat organophosphorus pesticide poisoning: A randomised controlled trial. Lancet 2006;368:2136-41.  Back to cited text no. 15
    
16.
Singh G, Avasthi G, Khurana D, Whig J, Mahajan R. Neurophysiological monitoring of pharmacological manipulation in acute organophosphate poisoning. The effects of pralidoxime, magnesium sulphate and pancuronium. Electroencephalogr Clin Neurophysiol 1998;107:140-8.  Back to cited text no. 16
    
17.
Liu WF. A symptomatological assessment of organophosphate-induced lethality in mice: Comparison of atropine and clonidine protection. Toxicol Lett 1991;56:19-32.  Back to cited text no. 17
    
18.
Balali-Mood M, Ayati MH, Ali-Akbarian H. Effect of high doses of sodium bicarbonate in acute organophosphorous pesticide poisoning. Clin Toxicol (Phila) 2005;43:571-4.  Back to cited text no. 18
    
19.
Güven M, Sungur M, Eser B, Sari I, Altuntaº F. The effects of fresh frozen plasma on cholinesterase levels and outcomes in patients with organophosphate poisoning. J Toxicol Clin Toxicol 2004;42:617-23.  Back to cited text no. 19
    


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