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Year : 2021  |  Volume : 8  |  Issue : 5  |  Page : 246-248

Acute pulmonary edema in an adolescent female with zinc phosphide poisoning: A case report

Department of Pediatrics, Government Medical College, Jammu, Jammu and Kashmir, India

Date of Submission11-Jun-2021
Date of Decision18-Aug-2021
Date of Acceptance23-Aug-2021
Date of Web Publication28-Sep-2021

Correspondence Address:
Dr. Mohammad Irfan Dar
Department of Pediatrics, Government Medical College, Jammu - 180 001, Jammu and Kashmir
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcc.jpcc_45_21

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Zinc phosphide is a commonly used rodenticide in India. Intoxication is associated with multiorgan failure and high mortality. We present a case of 17-year-old adolescent female with suicidal zinc phosphide poisoning, complicated to acute pulmonary edema and refractory shock. The patient responded well to supportive management and intravenous magnesium sulfate. As there is no specific antidote for zinc phosphide, the parenteral magnesium sulfate can be used as adjunct therapy.

Keywords: Intoxication, rat poison, rodenticide

How to cite this article:
Dar MI, Raina S, Bhat V. Acute pulmonary edema in an adolescent female with zinc phosphide poisoning: A case report. J Pediatr Crit Care 2021;8:246-8

How to cite this URL:
Dar MI, Raina S, Bhat V. Acute pulmonary edema in an adolescent female with zinc phosphide poisoning: A case report. J Pediatr Crit Care [serial online] 2021 [cited 2021 Oct 26];8:246-8. Available from: http://www.jpcc.org.in/text.asp?2021/8/5/246/326864

  Introduction Top

Zinc phosphide is a rodenticide commonly used against small mammals such as mice, rats, and field mice.[1] Intoxication may lead to severe complications and multiorgan failure, resulting in high mortality.[2] Symptoms start almost instantaneously and involve almost all systems primarily the cardiovascular system, leading to palpitation, tachycardia, and marked hypotension with signs of cardiac failure. The gastrointestinal (GI) systems include vomiting, abdominal pain, and loose stools. Dyspnea, cyanosis, and pulmonary edema followed by respiratory failure are the respiratory complications.[3] Lethal dose of zinc phosphide is 4–5 g (55–70 mg/kg) with a high mortality rate between 37% and 100%.[4] To date, there is no known antidote for metal phosphide poisoning. Adequate supportive therapy, often provided within an intensive care unit, is needed for recovery.[2],[5]

  Case Report Top

A 17-year-old adolescent female presented with pain abdomen associated with multiple episodes of nonbilious and nonprojectile vomiting and 5–6 episodes of loose stools. There was a preceding history of ingestion of one teaspoonful (5 mg) of zinc phosphide with one cup of water (16 h back) with suicidal intent. The patient did not have a history of bleeding from any site, loss of consciousness, frothing from mouth, or any abnormal body movement. Medical and family histories were unremarkable.

On examination, the patient was conscious, Glasgow coma score was 14/15, and she was oriented to time, place, and person with respiratory rate of 32/min and blood pressure (BP) of 89/56 mmHg (<50th percentile). The patient was pale looking with low volumic pulses with a pulse rate of 124/min, and peripheries were cold and clammy. SpO2 was 94% without oxygen. On auscultation, breath sounds and heart sounds were normal. The abdomen had diffuse tenderness on palpation.

The patient was administered oxygen via nonrebreathing mask at 6 L/min. The gastric lavage was not done as 16 h had already elapsed since ingestion. Two wide bored cannulas were secured, and intravenous (IV) bolus of NS at 20 mL/kg was administered. Injection Vitamin K 10 mg IV was given in view of possible coagulopathy. Two subsequent fluid boluses were administered (total of 60 mL/kg) over the 1st h of admission after which injection dopamine at 10 mcg/kg/min was added for fluid refractory shock. At 11 h of admission, inotropic support was increased to 15 mcg/kg/min of dopamine with the addition of injection adrenaline at 0.3 μg/kg/min in view of persistent shock. The patient had upper GI bleed on the 2nd day of admission, and second dose of injection vitamin K 10 mg and injection pantoprazole was administered intravenously. Pro-time was 18/12 s, with INR 1.6.

The systolic dysfunction was noted on two-dimensional (2D) echocardiography. Injection dobutamine was added for in view of poor ejection fraction of 40%. At 30 hours of admission shock was persistent and refractory to catecholamines .Patient was intubated and put on mechanical ventilation with lung protective strategies (volume control pressure support SIMV mode, with PEEP of 7cm water, Tidal Volume @6ml/kg, FiO2 100%). Blood gas shown: pH 7.26 mmHg, PCO2 59 mmHg, PO2 74 mm of Hg just after intubation. Chest X-ray was suggestive of pulmonary edema [Figure 1]. Injection magnesium sulfate (1 g IV infusion over 30 min) was also administered in view of refractory shock. After 12 h of mechanical ventilation and first dose injection magnesium sulfate, the patient started to show signs of improvement in hemodynamic parameters (BP 98/68, FiO2 0.8), and PEEP requirement decreased progressively and SpO2 also improved. On day 2nd of mechanical ventilation, the patient had persistent systolic dysfunction on 2D echocardiography; hence, second dose of injection magnesium sulfate was administered with injection dexamethasone and injection calcium gluconate to which the patient responded well. Hemodynamic parameters improved progressively. Inotropic support was subsequently tapered, and on day 4 of mechanical ventilation, dopamine infusion was stopped, dobutamine was tapered to 50% of initial (7.5 μg/kg/min), and adrenaline was also tapered to 50% of initial dose. The patient was extubated after 78 h of mechanical ventilation and was tapered to oxygen via nonrebreathing mask. On day 8 of admission, oxygen and inotropes were stopped and Ryle's tube feeding was started. The patient had asymptomatic hypokalemia (3.1 mEq/L) detected on routine biochemistry on the same day which was corrected by the administration of oral potassium chloride syrup given. Renal function tests and liver function tests were within normal range. The patient was shifted from PICU to step-down ward on the 9th day of admission. Injection dexamethasone was tapered and stopped after 5 days. Antibiotics were administered for a total of 7 days. No purgative was given to the patient in view of multiple episodes of loose motions during hospitalization. The patient was successfully discharged on 13th day of admission and attached to the child counselor and the psychiatry OPD.
Figure 1: (a) Chest X-ray (anteroposterior view) in spine position taken 3 h before intubation showing diffuse homogenous opacities on the bilateral peripheral lung fields, suggestive of noncardiogenic pulmonary edema. (b) Chest X-ray (anteroposterior) in spine position on mechanical ventilation 40 h after previous film showing decreased white shadowing of lung fields, suggestive of resolving pulmonary edema

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  Discussion Top

Suicidal or accidental intoxication of zinc phosphide is quite fatal.[2] The mortality due to zinc phosphide ranges anywhere between 37% and 100%.[4] Zinc phosphide liberates phosphine gas, when it comes in contact with gastric hydrochloric acid causing cellular hypoxia by inhibiting the mitochondrial cytochrome oxidase C and generating oxygen free radicals.[3] Manifestations of phosphide toxicity appear rapidly, usually presenting within 30 min following exposure. Early features include nausea, vomiting, and epigastric pain due to the corrosive nature of phosphides. These features are rapidly followed by circulatory collapse, hypotension, myocarditis, pericarditis, acute pulmonary edema, and congestive heart failure.

Echocardiography often reveals global hypokinesia of the left ventricle and depressed ejection fraction. Acute renal failure, jaundice, transaminitis progressing to acute liver failure, and disseminated intravascular coagulation are also common. Following inhalation, chest tightness, headache, giddiness, lethargy, convulsions, and delirium may be seen. Circulatory failure is an important cause of death.[6]

Hypokalemia and hypoglycemia can also occur frequently postpoisoning.[7] Diagnosis of phosphide poisoning is based mainly on history and clinical features. There is no specific antidote; hence, the management remains primarily supportive. Due to radiopacity of zinc, abdominal X-ray in zinc phosphide-poisoned patients has prognostic significance and is helpful in determining treatment protocol. Most important step of successful treatment is the management of shock by fluid resuscitation and judicious use of inotropes.[8] Vitamin K (phytomenadione) can be given if the prothrombin time is prolonged.[9] Endotracheal intubation and need for mechanical ventilation depend upon respiratory involvement. IV magnesium sulfate as a treatment option has been described in various studies on poisoning with metal phosphides.[10] This antiarrhythmic action could probably result in improvement in myocardial functioning among children with shock.[10]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/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


Conflicts of interest

There are no conflicts of interest.

  References Top

Doğan E, Güzel A, Çiftçi T, Aycan İ, Çelik F, Çetin B, et al. Zinc phosphide poisoning. Case Rep Crit Care 2014;2014:1-3.  Back to cited text no. 1
Bilics G, Héger J, Pozsgai É, Bajzik G, Nagy C, Somoskövi C, et al. successful management of zinc phosphide poisoning –A Hungarian case. Int J Emerg Med 2020;13:48.  Back to cited text no. 2
Satapathy AK, John J. Insecticide and pesticide poisonings. In: Bagga A, Chugh K, Ramji S, Lodha R, Gupta P, editors. Principles of Pediatric & Neonatal Emergencies. 4th ed. New Delhi: Jaypee Brothers; 2020. p. 628-33.  Back to cited text no. 3
Zinc Phosphide – National Library of Medicine HSDB Database; 2017. Available from: https://toxnet.nlm.nih.gov/cgi-bin/sis/search/a? [Last accessed on 2021 Apr 22].  Back to cited text no. 4
Shakoori V, Agahi M, Vasheghani-Farahani M, Marashi SM. Successful management of zinc phosphide poisoning. Indian J Crit Care Med 2016;20:368-70.  Back to cited text no. 5
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D'Silva C, Krishna B. Rodenticide poisoning. Indian J Crit Care Med 2019;23:S272-7.  Back to cited text no. 6
Yogendranathan N, Herath HM, Sivasundaram T, Constantine R, Kulatunga A. A case report of zinc phosphide poisoning: Complicated by acute renal failure and tubulo interstitial nephritis. BMC Pharmacol Toxicol 2017;18:37.  Back to cited text no. 7
Satapathy A K , John J. insecticide and pesticide poisonings. In principles of pediatric and neonatal emergencies, Gupta P, 4rd ed. New Delhi: Jaypee Brothers; 2020.p.628 -633.  Back to cited text no. 8
Mahesh M, Jain S, Madhumitha M. A case of zinc phosphide poisoning with ST segment elevation ECG changes. IP Int J Forensic Med Toxicol Sci 2017;2:60-2.  Back to cited text no. 9
Sharma A, Dishant, Gupta V, Kaushik JS, 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;18:33-36. doi:10.4103/0972-5229.125434.  Back to cited text no. 10


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