Skip to main content

Advertising Disclaimer »

Main menu

  • Journals
    • Pediatrics
    • Hospital Pediatrics
    • Pediatrics in Review
    • NeoReviews
    • AAP Grand Rounds
    • AAP News
  • Authors/Reviewers
    • Submit Manuscript
    • Author Guidelines
    • Reviewer Guidelines
    • Editorial Policies
  • Content
    • Current Issue
    • Online First
    • Archive
    • Topic/Program Collections
    • Blog
  • Subscribe
  • Alerts
  • Careers
  • Other Publications
    • American Academy of Pediatrics

User menu

  • Log in

Search

  • Advanced search
American Academy of Pediatrics

AAP Gateway

Advanced Search

AAP Logo

  • Log in
  • Journals
    • Pediatrics
    • Hospital Pediatrics
    • Pediatrics in Review
    • NeoReviews
    • AAP Grand Rounds
    • AAP News
  • Authors/Reviewers
    • Submit Manuscript
    • Author Guidelines
    • Reviewer Guidelines
    • Editorial Policies
  • Content
    • Current Issue
    • Online First
    • Archive
    • Topic/Program Collections
    • Blog
  • Subscribe
  • Alerts
  • Careers
American Academy of Pediatrics
Illustrative Case

Pediatric Pesticide Poisoning: A Clinical Challenge

Stefani Samples, Alexander Eason and Henry Wiles
Hospital Pediatrics March 2016, 6 (3) 183-186; DOI: https://doi.org/10.1542/hpeds.2014-0218
Stefani Samples
aDepartment of Pediatric Cardiology, Georgia Regents University, Augusta, Georgia; and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Alexander Eason
bMedical College of Georgia at Georgia Regents University, Augusta, Georgia
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Henry Wiles
aDepartment of Pediatric Cardiology, Georgia Regents University, Augusta, Georgia; and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • Comments
Loading
Download PDF

Case

The patient in this case was an otherwise healthy 12-year-old boy who presented to our hospital for monitoring after exposure to a pesticide. His medical history was significant only for attention-deficit/hyperactivity disorder, for which he took daily stimulant therapy. In the trailer he shared with his grandmother, an unknown amount of the pesticide tablets were accidentally spilled indoors. In an attempt to clean it up, they vacuumed up the substance, which reportedly caused the vacuum to explode, dispersing the pesticide in the air. When both the patient and his grandmother began vomiting a few hours later, they were taken to a local emergency department by family members. The grandmother experienced cardiac arrest and expired in the local emergency department within 12 hours of exposure. The patient was then transferred to our tertiary medical center for additional monitoring because of his pesticide exposure. He was initially monitored with no concerning symptoms. His heart rate was mildly elevated at rest, averaging 110 to 130 beats per minute, but his blood pressure was normal for age and height. Less than 48 hours after initial pesticide exposure, he developed a new, prominent gallop rhythm on physical examination. An echocardiogram was performed, which demonstrated a mildly dilated left ventricle with severely diminished left ventricular systolic function. The fractional shortening was 22%, and the ejection fraction was 36%. The electrocardiogram (ECG) was also abnormal, demonstrating sinus tachycardia, left axis deviation, poor R-wave progression, and diffuse T-wave flattening (Fig 1). All intervals, including QRS duration (88 msec) and QTc (444 msec), were within normal limits.

FIGURE 1
  • Download figure
  • Open in new tab
  • Download powerpoint
FIGURE 1

Electrocardiogram obtained at initial cardiology evaluation demonstrating sinus tachycardia, left axis deviation, poor R-wave progressive, and diffuse T-wave flattening.

Question What are the findings in dilated cardiomyopathy?

Discussion

As a whole, cardiomyopathy is a diverse class of cardiac diseases. Dilated cardiomyopathy is characterized by the development of dilated, poorly functional ventricles with normal wall thickness not precipitated by an abnormal cardiac preload or afterload.1,2 Dilated cardiomyopathy can be accompanied by cardiac arrhythmias and symptoms of heart failure. The ECGs of patients with dilated cardiomyopathy may be normal but may also demonstrate varying types of heart block, atrial fibrillation, or even ventricular arrhythmias.1,2 Echocardiography demonstrates increased ventricular dimensions, ventricular hypokinesia, and a decreased fractional shortening. Symptomatic relief can often be achieved through the use of diuretics to decrease the volume load placed on the heart. Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone antagonists, vasodilators, and β-blockers are all associated with increased survival and are used in almost all patients with dilated cardiomyopathy, from those with severe heart failure to those with asymptomatic left ventricular systolic dysfunction.2

Case Continuation

After an extensive literature review and discussion with several national toxicologists, we determined that this was a documented effect of exposure to aluminum phosphide pesticides. This was also supported by review of the patient’s admission laboratory values, which demonstrated a metabolic acidosis (bicarbonate 15 mEq/L) and mild hyperglycemia (glucose 147 mg/dL), both of which quickly resolved on subsequent testing. To ensure this was not a coincidental finding of cardiomyopathy of another cause, a cardiomyopathy evaluation was undertaken. Acute viral titers, including herpes simplex virus, Epstein-Barr virus, echovirus, cytomegalovirus, coxsackievirus, and adenovirus, as well as convalescent titers obtained 20 days later, were negative with the exception of a positive mumps immunoglobulin G, thus indicating an appropriate immune response to vaccines without any additional evidence of acute infection. The patient’s erythrocyte sedimentation rate at diagnosis was normal (8 mm/hr). C-reactive protein was only mildly elevated (1.063 mg/dL). Thyroid studies were normal, as were profiles of amino acids, acylcarnitines, and carnitines. An initial troponin was elevated (1.308 ng/mL), but this quickly normalized.

Supportive treatment was then initiated. Several national toxicologists recommended placing the patient on intravenous (IV) fluids, which could aid in pesticide excretion. Although asymptomatic, he was also started on afterload reduction using lisinopril due to his diminished left ventricular systolic function. A 24-hour Holter monitor returned with normal findings, and a follow-up echocardiogram performed 3 days later demonstrated normal left ventricular systolic function with an improvement of his fractional shortening (32%) and ejection fraction (61.3%). Another echocardiogram done during his outpatient follow-up 20 days later continued to demonstrate normal left ventricular systolic function.

Question How frequently does aluminum phosphide exposure occur, and what are its biological effects?

Discussion

Aluminum phosphide poisoning is a rarely reported entity in the United States. Most reports are due to job-related exposure or suicidal attempts occurring outside the United States.3–6 Childhood exposure is even less common, with the exception of older teenagers who ingest aluminum phosphide containing pesticide pellets with suicidal intent.4 The national poison control centers data from 2013 reported that 3.27% of reported exposures were due to pesticides in general, and only 0.006% were due to aluminum phosphide exposure, the majority of which occurred in adults.7 There have been rare case reports of unintentional aluminum phosphide poisoning of entire families that have reported fatalities due to acute cardiopulmonary collapse in children aged 15 months up to 6 years.8,9 Both of these reports demonstrated that the cardiac deterioration could occur far removed from the initial exposure. These reported families had repeated exposure to the aluminum phosphide-containing pesticides before the poisoning symptoms were recognized, which differs from our case.

Aluminum phosphide is an inorganic compound commercially available as pesticides that are used to protect crops from insects and rodents.10 Commercial names for aluminum phosphide include Fumtoxin, L-Fume, Tri-Tox, Fumiphos, Phostoxin, Fumex, Gastoxin, and Quik-Fume. It is manufactured in dust, granular, and pellet forms. These readily react to form phosphine gas (PH3) after coming into contact with water, moisture, or the acidic content in the human stomach.3,10 Once inhaled or ingested, phosphine gas leads to the production and accumulation of reactive oxygen species (ROS) at the cellular level and subsequent lipid peroxidation. It is this extensive ROS generation that is believed to be responsible for the wide systemic toxicities of phosphine gas exposure. Specifically, these effects cause alterations in the cardiac transmembrane action potentials, which lead to dysrhythmias.3 They may also cause ischemic effects that can induce focal areas of necrosis as well as cardiac failure.3

Phosphide exposure is known to rapidly affect multiple organ systems including the respiratory, cardiovascular, hepatic, renal, hematologic, and gastrointestinal systems. Early symptoms of acute exposure can vary on the exposure route and dose, but typically include fatigue, dyspnea, nausea, vomiting, abdominal pain, hypotension, and tachycardia.11–13 Progression of illness can be rapid and may lead to organ failure of any of the affected organs systems, but the most common effects include acute respiratory failure and cardiac shock.11–13 Other potential systemic results of exposure include acute hepatitis, acute renal failure, and disseminated intravascular coagulation. Multiple metabolic derangements have also been described including abnormalities in sodium, potassium, and/or magnesium levels, lactic acidosis, and hypo- or hyperglycemia.11–13

Question What are the cardiac effects of aluminum phosphide exposure?

Discussion

From a cardiac perspective, phosphide exposure can present with a variety of complications, including peripheral circulatory collapse, dysrhythmias, and, rarely, acute cardiomyopathy.3,4,8,14 One study following 20 patients with aluminum phosphide exposure reported cardiac manifestations occurring within 12 hours in all patients, although there are case reports with presentation delayed up to 48 hours after exposure.4,5,9 Cardiac dysrhythmias have been reported at a rate of 50% in 1 study and may include atrial fibrillation or flutter, junctional rhythms, supraventricular tachycardia, ventricular tachycardia or fibrillation, QT prolongation, and varying degrees of heart block.4,5,15 Additional ECG findings of ST-segment elevation or depression and significant T-wave inversions may be seen.4,9 Direct cardiac toxicity and myocardial dysfunction may present as ventricular hypokinesia, cardiomyopathy, myocarditis, or pericarditis.4,13,16 One patient reportedly had prolonged ECG abnormalities attributed to subendocardial ischemia.4

Question What are the available treatments for aluminum phosphide exposure?

Discussion

Perhaps because of the wide range of cytotoxic effects that phosphide exposure has, no antidote has yet been identified. If exposure occurs, the Centers for Disease Control recommends decontamination as soon as possible by experienced personnel.17 Treatment remains largely supportive, and several therapeutic strategies have been proposed to aid in the management of acute exposure. Maintaining renal perfusion with IV fluids may aid in phosphine elimination.5,18 Digoxin and other inotropic agents have had some effect in treating cardiovascular collapse and ventricular dysfunction in these cases.19 In 1 case report, calcium gluconate and magnesium sulfate were used for cardiac membrane stabilization.11 In 1 study of children after ingestion of aluminum phosphide pesticides, magnesium sulfate was associated with better survival.20 Other proposed treatments include high doses of vitamin C as an antioxidant or IV magnesium and/or N-acetylcysteine to replenish intracellular glutathione stores and reduce systemic ROS levels; however, none of these methods have as yet demonstrated themselves to be particularly effective.5,6,21 There is a report of using of an intra-aortic balloon pump successfully for a patient with myocarditis and cardiac shock whose clinical condition initially worsened despite inotropic support.22 Our patient received only minimal supportive treatment with IV fluids and lisinopril therapy before recovery. Several patients with phosphide-induced cardiomyopathy have reportedly experienced improvements of their left ventricular function over the course of their hospital stay, as our patient did.23 It is likely that this rapid recovery is due to clearance of phosphide from the patient’s system.

Conclusions

Although aluminum phosphide exposure is rare in the United States, it presents a treatment dilemma given the paucity of definitive information available in the literature, especially in relation to children. Although there are no current consensus statements, supportive treatment appears to be the best choice for now. However, the best treatment is always the prevention of exposure by limiting usage of these pesticides, especially in the presence of children, and appropriately storing and disposing of them. If a pesticide spill occurs in the home or workplace, families should contact the national poison control hotline (1-800-222-1222) for instructions on appropriate cleanup and treatment as needed.

Footnotes

  • FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.

  • FUNDING: No external funding.

  • POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.

References

  1. ↵
    1. Elliott P
    . Cardiomyopathy. Diagnosis and management of dilated cardiomyopathy. Heart. 2000;84(1):106–112
    OpenUrlFREE Full Text
  2. ↵
    1. Lakdawala NK,
    2. Winterfield JR,
    3. Funke BH
    . Dilated cardiomyopathy. Circ Arrhythm Electrophysiol. 2013;6(1):228–237
    OpenUrlFREE Full Text
  3. ↵
    1. Soltaninejad K,
    2. Beyranvand MR,
    3. Momenzadeh SA,
    4. Shadnia S
    . Electrocardiographic findings and cardiac manifestations in acute aluminum phosphide poisoning. J Forensic Leg Med. 2012;19(5):291–293
    OpenUrlCrossRefPubMed
  4. ↵
    1. Kaushik RM,
    2. Kaushik R,
    3. Mahajan SK
    . Subendocardial infarction in a young survivor of aluminium phosphide poisoning. Hum Exp Toxicol. 2007;26(5):457–460
    OpenUrlAbstract/FREE Full Text
  5. ↵
    1. Taromsari MR,
    2. Shad B,
    3. Aghajani Nargesi D,
    4. Akhoundzadeh N,
    5. Fallah Karkan M
    . The study of various cardiac arrhythmias in patients poisoned with phosphine (rice tablet). Iran J Toxicol. 2011;5(1–2):448–453
    OpenUrl
  6. ↵
    1. Sudakin DL
    . Occupational exposure to aluminium phosphide and phosphine gas? A suspected case report and review of the literature. Hum Exp Toxicol. 2005;24(1):27–33
    OpenUrlAbstract/FREE Full Text
  7. ↵
    1. Mowry JB,
    2. Spyker DA,
    3. Cantilena LR Jr.,
    4. McMillan N,
    5. Ford M
    . 2013 Annual report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st annual report. Clin Toxicol (Phila). 2014;52(10):1032–1283
    OpenUrlCrossRefPubMed
  8. ↵
    1. Shadnia S,
    2. Mehrpour O,
    3. Abdollahi M
    . Unintentional poisoning by phosphine released from aluminum phosphide. Hum Exp Toxicol. 2008;27(1):87–89
    OpenUrlAbstract/FREE Full Text
  9. ↵
    1. Lemoine TJ,
    2. Schoolman K,
    3. Jackman G,
    4. Vernon DD
    . Unintentional fatal phosphine gas poisoning of a family. Pediatr Emerg Care. 2011;27(9):869–871
    OpenUrlCrossRefPubMed
  10. ↵
    Environmental Protection Agency. Aluminum and magnesium phosphide. December 1998. Available at: http://www.epa.gov/oppsrrd1/reregistration/alphosphide (accessed January 27, 2015)
  11. ↵
    1. Moghadamnia AA
    . An update on toxicology of aluminum phosphide. Daru. 2012;20(1):25
    OpenUrlCrossRefPubMed
    1. Gurjar M,
    2. Baronia AK,
    3. Azim A,
    4. Sharma K
    . Managing aluminum phosphide poisonings. J Emerg Trauma Shock. 2011;4(3):378–384
    OpenUrlCrossRefPubMed
  12. ↵
    1. Mehrpour O,
    2. Jafarzadeh M,
    3. Abdollahi M
    . A systematic review of aluminium phosphide poisoning. Arh Hig Rada Toksikol. 2012;63(1):61–73
    OpenUrlPubMed
  13. ↵
    1. Khosla SN,
    2. Nand N,
    3. Kumar P
    . Cardiovascular complications of aluminum phosphide poisoning. Angiology. 1988;39(4):355–359
    OpenUrlAbstract/FREE Full Text
  14. ↵
    1. Louriz M,
    2. Dendane T,
    3. Abidi K,
    4. Madani N,
    5. Abouqal R,
    6. Zeggwagh AA
    . Prognostic factors of acute aluminum phosphide poisoning. Indian J Med Sci. 2009;63(6):227–234
    OpenUrlCrossRefPubMed
  15. ↵
    1. Shah V,
    2. Baxi S,
    3. Vyas T
    . Severe myocardial depression in a patient with aluminium phosphide poisoning: a clinical, electrocardiographical and histopathological correlation. Indian J Crit Care Med. 2009;13(1):41–43
    OpenUrlCrossRefPubMed
  16. ↵
    Centers for Disease Control and Prevention. Phosphine: lung damaging agent. Available at: http://www.cdc.gov/niosh/ershdb/EmergencyResponseCard_29750035.html (January 27, 2015)
  17. ↵
    International Programme on Chemical Safety. Environmental health criteria 73: phosphine and selected metal phosphides. Geneva, Switzerland: World Health Organization; 1998
  18. ↵
    1. Mehrpour O,
    2. Farzaneh E,
    3. Abdollahi M
    . Successful treatment of phosphine poisoning with digoxin: a case report and review of literature. Int J Pharmacol. 2011;7:761–764
    OpenUrlCrossRef
  19. ↵
    1. Sharma A,
    2. Dishant,
    3. Gupta V,
    4. Kaushik JS,
    5. Mittal K
    . Aluminum phosphide (celphos) poisoning in children: a 5-year experience in a tertiary care hospital from northern India. Indian J Crit Care Med. 2014;18(1):33–36
    OpenUrlCrossRefPubMed
  20. ↵
    1. Azad A,
    2. Lall SB,
    3. Mittra S
    . Effect of N-acetylcysteine and L-NAME on aluminium phosphide induced cardiovascular toxicity in rats. Acta Pharmacol Sin. 2001;22(4):298–304
    OpenUrlPubMed
  21. ↵
    1. Siddaiah L,
    2. Adhyapak S,
    3. Jaydev S,
    4. et al
    . Intra-aortic balloon pump in toxic myocarditis due to aluminum phosphide poisoning. J Med Toxicol. 2009;5(2):80–83
    OpenUrlCrossRefPubMed
  22. ↵
    1. Akkaoui M,
    2. Achour S,
    3. Abidi K,
    4. et al
    . Reversible myocardial injury associated with aluminum phosphide poisoning. Clin Toxicol (Phila). 2007;45(6):728–731
    OpenUrlCrossRefPubMed
  • Copyright © 2016 by the American Academy of Pediatrics
View Abstract
PreviousNext
Back to top

Advertising Disclaimer »

In this issue

Hospital Pediatrics: 6 (3)
Hospital Pediatrics
Vol. 6, Issue 3
1 Mar 2016
  • Table of Contents
  • Table of Contents (PDF)
  • Index by author
View this article with LENS
PreviousNext
Email Article

Thank you for your interest in spreading the word on American Academy of Pediatrics.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Pediatric Pesticide Poisoning: A Clinical Challenge
(Your Name) has sent you a message from American Academy of Pediatrics
(Your Name) thought you would like to see the American Academy of Pediatrics web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Request Permissions
Article Alerts
Log in
You will be redirected to aap.org to login or to create your account.
Or Sign In to Email Alerts with your Email Address
Citation Tools
Pediatric Pesticide Poisoning: A Clinical Challenge
Stefani Samples, Alexander Eason, Henry Wiles
Hospital Pediatrics Mar 2016, 6 (3) 183-186; DOI: 10.1542/hpeds.2014-0218

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Share
Pediatric Pesticide Poisoning: A Clinical Challenge
Stefani Samples, Alexander Eason, Henry Wiles
Hospital Pediatrics Mar 2016, 6 (3) 183-186; DOI: 10.1542/hpeds.2014-0218
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
Print
Download PDF
Insight Alerts
  • Table of Contents

Jump to section

  • Article
    • Case
    • Conclusions
    • Footnotes
    • References
  • Figures & Data
  • Info & Metrics
  • Comments

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Cited By...

  • No citing articles found.
  • Google Scholar

More in this TOC Section

  • Not All Aseptic Meningitis Is Created Equal
  • Cardiac Tamponade in a Child With Fever of Unknown Origin
  • Atypical Altered Mental Status in a Toddler
Show more Illustrative Case

Similar Articles

Subjects

  • Injury, Violence & Poison Prevention
    • Injury, Violence & Poison Prevention
    • Hazardous Exposure
  • Cardiology
    • Cardiology
  • Journal Info
  • Editorial Board
  • Editorial Policies
  • Overview
  • Licensing Information
  • Authors/Reviewers
  • Author Guidelines
  • Reviewer Guidelines
  • Submit My Manuscript
  • Librarians
  • Institutional Subscriptions
  • Usage Stats
  • Support
  • Subscribe
  • Contact Us
  • Resources
  • Media Kit
  • About
  • International Access
  • Terms of Use
  • Privacy Statement
  • FAQ
  • RSS Feeds
  • shopAAP
  • AAP.org
  • Follow American Academy of Pediatrics on Instagram
  • Visit American Academy of Pediatrics on Facebook
  • Follow American Academy of Pediatrics on Twitter
  • Follow American Academy of Pediatrics on Youtube
American Academy of Pediatrics

© 2021 American Academy of Pediatrics