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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 2  |  Issue : 2  |  Page : 91-93

Aluminum phosphide toxicity: A rare cause of multiorgan dysfunction syndrome


1 Department of Pediatrics, Division of Pediatric Intensive Care, Sanliurfa Training and Research Hospital, Sanliurfa, Turkey
2 Department of Pediatrics, Sanliurfa Training and Research Hospital, Sanliurfa, Turkey
3 Department of Medical Biochemistry, Aydin Adnan Menderes University Health Sciences Institute, Aydin, Turkey

Date of Submission06-Jan-2022
Date of Decision26-Mar-2022
Date of Acceptance26-Apr-2022
Date of Web Publication30-May-2022

Correspondence Address:
Dr. Hatice Feray Ari
Sanliurfa Training and Research Hospital, Pediatric Intensive Care Unit, Sanliurfa
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ipcares.ipcares_3_22

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  Abstract 

Background: Aluminum phosphides (ALPs) are still being used in developing countries as a pesticide despite the fact that ingestion and/or inhalation can cause significant morbidity and mortality. The generation of phosphine when ALP comes in contact with water leads to the blockade of electron transfer, which inhibits oxidative phosphorylation and in turn, cellular respiration in multiple organ systems. Clinical Description: A 3-year-old Turkish girl and her family were inadvertently exposed to overnight inhalation intoxication after a tablet of ALP was dissolved in water and used as a pesticide for Isot pepper, a local spice used in their household. The child presented with rapidly progressive respiratory distress and coma. The other members displayed mild respiratory symptoms. Management: At the time of admission, she was in altered sensorium, tachycardic, tachypneic, hypoxic, and in shock. She was immediately intubated and intermittent positive pressure ventilation started. Shock was managed as per the standard protocol. The child emanated garlic odor breath, had sluggishly reactive bilateral mitotic pupils. She had cardiorespiratory arrest within 30 min of intubation and could be revived. Despite supportive treatment, multiorgan dysfunction syndrome developed cardiac, pulmonary, renal, hepatic, coagulopathy, hyperglycemia, and metabolic acidosis. She succumbed to another cardiorespiratory arrest before plasmapheresis and continuous renal replacement therapy could be started in an attempt to eliminate the toxins. Consent for autopsy was not given. Conclusions: ALPs poisoning still occurs in developing countries and is a leading cause of mortality. The most common cause of death within the first 24 h is cardiovascular collapse.

Keywords: Aluminum phosphide, cardiac failure, inhalation, intoxication, MODS


How to cite this article:
Ari HF, Turhan M, Baspinar H, Kirhan B, Ari M. Aluminum phosphide toxicity: A rare cause of multiorgan dysfunction syndrome. Indian Pediatr Case Rep 2022;2:91-3

How to cite this URL:
Ari HF, Turhan M, Baspinar H, Kirhan B, Ari M. Aluminum phosphide toxicity: A rare cause of multiorgan dysfunction syndrome. Indian Pediatr Case Rep [serial online] 2022 [cited 2022 Jul 4];2:91-3. Available from: http://www.ipcares.org/text.asp?2022/2/2/91/346253

The treatment of agricultural products with pesticides such as aluminum phosphides (ALP) is high in low- and middle-income countries (LMICs). Ingestion or inhalation of ALP may cause severe cases of acute and/or chronic poisoning. Once consumed, ALP combines with water and the hydrochloric acid present in the stomach to form phosphine gas. This gets rapidly absorbed from the gastrointestinal tract to enter the systemic circulation and results in multiple organ failure.[1] ALP toxicity has been widely reported since the 1980s. Most intoxications are due to accidental ingestion followed by suicidal ingestion.[1] Around 300,000 deaths occur per year globally, mostly from LMIC.[2] An Indian study of autopsies performed on cases of poisoning over 25 years reported of mortality causes. ALP was detected the most common cause after 1982, with an incidence of 65%.[3] Metal phosphides such as aluminum, magnesium, and calcium phosphides are popular in LMIC because of their potency, cheapness, and minimal adverse effects in crop protection the storage of cereals, animal feed, and tobacco leaves, despite the high risk of human mortality.[4] The ALP tablets are sold without restriction in Turkey and India, even though they are potentially toxic.[5] Their use in high-income countries is minimal. Even almost a decade ago (1983–2003), only 188 cases of ALP poisoning were reported from Germany (65% accidental).[6]

In this case, we report the circumstances and death of a Turkish child due to multiorgan failure within 24 h of inhalation of ALP that was being for the preservation of local Isot pepper. The aim of reporting this case is to sensitize the pediatricians to also enquire about the use of ALP as a pesticide or preservative in households when one encounters a child presenting with sudden onset, inexplicable cardiorespiratory failure.


  Clinical Description Top


A previously healthy 3-year-old girl was brought to our pediatric emergency department with sudden onset altered sensorium and breathing difficulty overnight. She had been apparently well on going to bed and was noticed to have difficulty in breathing on awakening which rapidly worsened till she lapsed into altered sensorium. The labored breathing involved chest retraction.

At admission, she was noted to be cyanosed. Her temperature was 36.5°C, heart rate 172 beats per minute (min), regular, but with low volume, respiratory rate 68/min with severe respiratory distress, SpO2 80% in room air, capillary refill time 4 s, and blood pressure 69/32 mm Hg (<3rd percentile). The weight was 15 kg (normal for age). Other anthropometric parameters were not taken. The Modified Glasgow Coma Scale was 6; E1M3V2. She was immediately intubated and started on intermittent positive pressure ventilation (IPPV) and fluid management for shock was initiated with 0.9% normal saline (NS) intravenous (IV) fluid as per the standard protocol. On the spot testing revealed hyperglycemia that was out of range. The arterial blood gas (ABG) analysis was consistent with metabolic acidosis; pH 6.67 (normal 7.35–7.45), pCO2 29.9 mm Hg (normal 35–45 mm/Hg), HCO3 9 mmol/L (normal 18–22 mmol/L), and lactate 16.8 mmol/L (normal 0–2 mmol/L). The patient was immediately shifted to the pediatric intensive care unit where she was started on mechanical ventilation. The random blood sugar (RBS) confirmed hyperglycemia of 450 mg/dl (normal 60–110 mg/dl), but urinary ketones were negative. Serum sodium (Na+) was 129 mEq/l (normal 35–145 mEq/l) and serum potassium (K+) 5.9 mEq/l (normal 3.5–5.5 mEq/l). Fluid management comprised of 0.9% NS (1000 cc/m2) with insulin (0.01 IU/kg/h), IV NaHCO3 (1 cc/kg), and empirical IV antibiotics (cephtriaxone). Subsequently, we initiated a detailed history and examination to ascertain the cause of sudden deterioration in a previously healthy child.


  Management and Outcome Top


There was no preceding history of any fever, cough, coryza, change in the voice, rashes, or sore throat. The child did not have any diarrhea, vomiting, hematemesis or abdominal pain. The child did not have any seizures, fall or trauma to the head. There was no history of redness of eyes, swelling of face or lips, itchy rash, or wheezing immediately following ingestion of any food or exposure to any substance at home. History of a bout of sudden coughing and choking associated with bluish discoloration, following play with a small toy or consumption of any small food items suggestive of foreign-body inhalation was not forthcoming. There was no history of preceding injury to the chest, past allergies, or recurrent wheezing. The parents were not related and the family history was not contributory. The child was immunized and developmental milestones were age appropriate. The family belonged to a low socioeconomic strata and lived together in a single room. A significant history of isolated respiratory symptoms (without fever, cough, or coryza) in multiple family members was present, and an unknown poisoning was suspected. On further probing, her mother disclosed that ALP tablets had been used as an preservative in the local Isot pepper pot in the evening.

The child's nutritional status appeared good. The cyanosis had resolved post-IPPV. A strong “garlic” odor was present. There was no pallor, jaundice, rashes, petechiae, purpurae, or ecchymosis. Both pupils were mitotic and sluggishly reacting to light. Tone and power assessment were inconclusive due to medications given for respiratory paralysis in lieu of IPPV. The deep-tendon reflexes were normal and plantars downgoing. The cardiovascular, respiratory, and abdominal systems were normal. Based on circumstantial history and clinical phenotype, a provisional diagnosis of ALP poisoning was kept, and her clothes were removed. Diabetic ketoacidosis was also considered, although there was no history of increased frequency of urination, hunger, thirst, or recent weight loss, or family history of diabetes mellitus. Since there is no specific antidote, supportive therapy was started. In this situation, calcium infusion and magnesium sulfate were used for membrane stabilization.

She had a cardiorespiratory arrest within 30 min of intubation and required cardiorespiratory resuscitation, following which she was continued on the management of shock as per standard protocol; initially for fluid refractory shock, followed by adrenaline for fluid refractory-dopamine resistant shock. [Table 1] gives the results of the preliminary hemogram and biochemical tests. These indicated renal and hepatic dysfunction. Fresh-frozen plasma was administered for the coagulopathy. The electrocardiogram showed sinus tachycardia of 168 beats/min, with regular RR interval, normal PR interval, QRS duration, and an isoelectric ST segment. Troponin-T levels were elevated; 36.6 pg/ml, normal 0–14 pg/ml. An echocardiogram detected a systolic ejection fraction of 32% (normal >55%). The chest X-ray showed bilateral diffuse opacities suggestive of pulmonary edema. The child continued to deteriorate progressing rapidly from catecholamine-resistant shock to persistent catecholamaine-resistant shock, despite the escalation of established medical algorithmic approach, but without any evidence of improvement.
Table 1: Reports of the child with aluminum phosphides poisoning at admission and after 12 h

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We repeated her investigations after 12 h [Table 1] which reflected the deteriorating clinical status. The worsening ABG parameters (pH 7.07, pCO2 23 mm Hg, HCO3 10.2 mmol/L, and lactate 9.8 mmol/L), hyperkalemia, hyponatremia, hyperglycemia (RBS 643 mg/dl), coagulopathy, and cardiac failure (Troponin-T 36.6 pg/ml) reflected the rapidly progressive and severe cardiac, renal, central nervous system, hepatic and pulmonary involvement, signaling multiorgan dysfunction syndrome. Before we could initiate plasmapheresis and continuous renal replacement therapy, the child had another cardiorespiratory arrest and succumbed. The family did not consent to an autopsy.


  Discussion Top


Isot pepper is a traditional hot pepper that is produced in Şanlıurfa, the south-eastern region of Turkey.[5] Turkish people use it as a spice in their meal preparation. In Turkey, various commercial tablet preparations are available that are dissolved in water. This particular household was using a 500 mg tablet dissolved in water as a pesticide to protect their Isot pepper. Since the entire family slept in the same room, and other family members were also symptomatic and did not give a history of ingestion, it was presumed that poisoning was inhalation. When ALP comes in contact with moisture, phosphine gas is released and a dose of 1400 mg/m3 for 30 min can be fatal.[7],[8] This family was presumably exposed overnight.

The underlying pathophysiology is the blockade of electron transfer, particularly of cytochrome c oxidase, which inhibits oxidative phosphorylation and, in turn, affects cellular respiration and results in the activation of peroxide radicals. Phosphine also inhibits catalase and depletes glutathione, which may result in the cell wall and cell ion channel dysfunction as well.[7] When poisoning is due to ingestion, manifestations occur within 10 − 15 min and progress rapidly. Early symptoms may be gastrointestinal (nausea, vomiting, hematemesis, and epigastric pain) or respiratory. An odor of garlic may emanate from the patients' breath.[7] Inhalation of high amounts of phosphine lead to cardiac failure, dysrhythmias (ventricular/atrial tachycardia, ventricular/atrial fibrillation, torsades de pointes, etc.), acute respiratory distress syndrome, and hepatic/kidney failure.[7],[8] Central nervous system manifestations include seizures, ataxia, paraesthesias, tremors, and coma.[7] Various dyselectrolytemias occur hypo/hypernatremia, hypo/hyperkalemia, or hypo/hypermagnesemia. Both hypo/hyperglycemia may be seen.

Symptomatic patients should be closely monitored. Medical personnel who come in close contact with victims of intoxication should wear rubber gloves and a full-face mask. It is recommended that the patient's contaminated clothes should be removed and the skin and eyes are washed. Treatment is supportive. Calcium is added for the stabilization of the cell membranes. Magnesium and N-acetylcysteine may act as antioxidants. Other modalities such as Vitamin E, melatonin, glutathione, betacarotene, steroid, and hyperbaric oxygen have been tried, but their efficacy is unclear.[7],[8] Renal replacement therapies can be applied in addition to bicarbonate support in patients with persistent metabolic acidosis.[5] Treatment of acidosis and removal of high-molecular-weight cytokines by hemodiafiltration may be helpful if initiated in time.[8] We were unable to initiate plasmapheresis in this case.



Declaration of patient consent

The authors certify that they had obtained the appropriate consent from the parent. The legal guardian has given his consent for the images and other clinical information to be reported in the journal. The guardian understands that the name and initials will not be published, and due efforts have been made to conceal the same, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Hassanian-Moghaddam H, Pajoumand A. Two years epidemiological survey of aluminum phosphide poisoning in Tehran. Iran J Toxicol 2007;1:35-9.  Back to cited text no. 1
    
2.
Gunnell D, Eddleston M. Suicide by intentional ingestion of pesticides: A continuing tragedy in developing countries. Int J Epidemiol 2003;32:902-9.  Back to cited text no. 2
    
3.
Singh D, Jit I, Tyagi S. Changing trends in acute poisoning in Chandigarh zone: A 25-year autopsy experience from a tertiary care hospital in northern India. Am J Forensic Med Pathol 1999;20:203-10.  Back to cited text no. 3
    
4.
Tolunay O, Celik T, Yücel G, et al. A rare but potentially fatal poisoning; aluminum phosphide poisoning. J Pediatr Emerg Intensive Care Med 2017;4:27-9.  Back to cited text no. 4
    
5.
Aydogdu MH, Atasoy AF, Eren ME, et al. The evaluation of the producers' view towards a local agricultural food product for marketing; ısot pepper of sanliurfa-GAP, Turkey. IOSR J Environ Sci, Toxicol and F Techno 2016;10:59-64.  Back to cited text no. 5
    
6.
Lauterbach M, Solak E, Kaes J, et al. Epidemiology of hydrogen phosphide exposures in humans reported to the poison center in Mainz, Germany, 1983-2003. Clin Toxicol (Phila) 2005;43:575-81.  Back to cited text no. 6
    
7.
Bogle RG, Theron P, Brooks P, et al. Aluminium phosphide poisoning. Emerg Med J 2006;23:e3.  Back to cited text no. 7
    
8.
German Jørgensen JR, Rössel PR. Poisoning with aluminumphosphide can be life-threatening for patients as well as health professionals. Ugeskr Laeger 2013;175:1706-7.  Back to cited text no. 8
    



 
 
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