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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 7  |  Issue : 4  |  Page : 198-201

A true killer among us: A case series of yellow phosphorus poisoning in children at a tertiary care center in South India


Department of Pediatrics, Mazumdar Shaw Medical Centre, Paediatric Intensive Care Unit, Narayana Hrudayalaya, Bengaluru, Karnataka, India

Date of Submission05-Mar-2020
Date of Decision03-May-2020
Date of Acceptance14-May-2020
Date of Web Publication13-Jul-2020

Correspondence Address:
Dr. Hiremath Sagar
Department of Pediatrics, Mauzumdar Shaw Medical Centre, Narayana Hrudayalaya, Bengaluru, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JPCC.JPCC_31_20

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  Abstract 


Rodenticides constitute 7%–11% of total poisonings in children. The rodenticide commonly available in South India is a paste made of yellow phosphorus, which causes a spectrum of clinical manifestations from gastrointestinal irritation to multiorgan dysfunction for which there is no antidote or specific treatment. There are scanty reports of this poisoning in children worldwide. Hence, we did a retrospective chart review of eight patients admitted in our unit from July 2017 to January 2019, and the demographic data, mode of poisoning, clinical manifestations, treatment modalities, and outcome of poisoning were collected from the hospital records and documented in the prestructured pro forma and analyzed. Majority of our patients were adolescent males, who had ingested the poison as an act of deliberate self-harm. The most common feature seen was acute liver failure. Clinical outcomes were better in those who received plasmapheresis for acute liver failure. However, this requires further studies for a proven benefit.

Keywords: Plasmapheresis, rodenticide, yellow phosphorus poisoning


How to cite this article:
Jeyapal S, Sagar H. A true killer among us: A case series of yellow phosphorus poisoning in children at a tertiary care center in South India. J Pediatr Crit Care 2020;7:198-201

How to cite this URL:
Jeyapal S, Sagar H. A true killer among us: A case series of yellow phosphorus poisoning in children at a tertiary care center in South India. J Pediatr Crit Care [serial online] 2020 [cited 2020 Aug 13];7:198-201. Available from: http://www.jpcc.org.in/text.asp?2020/7/4/198/289519




  Introduction Top


Acute poisoning in children has become a common problem that is being encountered in the pediatric intensive care unit today. Pediatric poisonings constituted 0.23%–3.3% of the total poisoning.[1] Of these, rodenticides constitute 7%–11% of total poisonings in children.[2],[3] The rodenticide commonly available in South India is a paste made of yellow phosphorus which contains 2%–5% of elemental phosphorus. The immediately dangerous to life or health concentration of yellow phosphorus in humans is 5 mg/m3 according to Centers for Disease Control (CDC).[4] Yellow phosphorus poisoning causes a spectrum of clinical manifestations from the gastrointestinal (GI) irritation to multiorgan dysfunction. There are scanty reports of yellow phosphorus poisoning in the Western literature due to the lack of availability of the poison there. However, in India, yellow phosphorus poisoning has been well reported in adults.[5] The incidence has been on the rise in children, especially adolescents, and it is commonly intentional. There is no specific antidote or treatment modality for yellow phosphorus poisoning. It is highly fatal with a reported mortality of approximately 27%.[6] We report a case series of eight patients admitted in our unit from July 2017–January 2019 with yellow phosphorus poisoning and the possibility of plasmapheresis as a treatment modality.


  Materials and Methods Top


A retrospective chart review of eight patients admitted in our unit from July 2017 to January 2019 with yellow phosphorus poisoning was done.

Data regarding the age, sex, mode of poisoning, clinical manifestations, treatment modalities, and outcome of poisoning were collected from the hospital records and documented in the prestructured pro forma and analyzed using a descriptive statistical method.


  Results Top


During the study period, we identified eight patients with yellow phosphorus poisoning [details in [Table 1] and [Table 2]. The median age of our eight patients was 16 years, the youngest being 1 year and oldest being 18 years. Majority of them were males, 6 (75%) and females were 2 (25%). Deliberate self-harm was the cause of poisoning in 7 (87.5%) patients and only 1 (12.5%) patient had accidental poisoning. The exact amount of poison ingested could not be ascertained due to the retrospective nature of the study. Out of the eight patients, 2 were mildly symptomatic (Case 1 and 4), 5 developed acute liver failure with encephalopathy, and one developed cardiotoxicity leading to cardiogenic shock (Case 7). Out of the five patients that developed acute liver failure (Case 2, 3, 5, 7, 8), 3 of them also had bone marrow suppression (Case 2, 3, and 5) and 2 of them also had renal failure (Case 2 and 8).
Table 1: Demography, clinical manifestations, and Investigations of cases

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Table 2: Treatment and outcome of cases

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The median time between the ingestion of poison to admission in our unit was 4 days (1–6 days). The two patients who were mildly symptomatic recovered with minimal supportive therapy. Out of the five patients with hepatic encephalopathy, 2 of them had a moderate derangement of international normalized ratio (INR) (mean 2.9) at admission and they improved with supportive treatment including injection Vitamin K, N-acetyl cysteine infusion. The remaining three patients had a mean INR of 8 on admission and were considered for plasmapheresis and renal replacement therapy. One patient survived with two cycles of plasmapheresis and 4 days of continuous renal replacement therapy, 1 patient survived with three cycles of plasmapheresis, 1 patient succumbed on treatment with sustained low efficiency daily diafiltration for 6 h without plasmapheresis. Time to discharge with plasmapheresis was 15–18 days and without plasmapheresis was 12–14 days. The mortality rate in our case series was 2 (25%); of which 1 patient died due to cardiotoixcity leading to refractory cardiogenic shock and 1 patient due to hepatic encephalopathy.


  Discussion Top


Yellow phosphorus is a compound widely used in India in the manufacture of rodenticides and fireworks. The easily available and cheap rodenticides contain a concentration of 2%–5% of yellow phosphorus. It's acute intake affects the liver, kidneys, hematopoietic system, brain, GIT, and the myocardium (arrhythmias).[7] It is rapidly absorbed and is mainly incorporated into the liver where it reaches its maximum (69%–73% of the given dose) concentration within 2–3 h.[8] It causes damage to the rough and smooth endoplasmic reticulum and disaggregation of the polyribosomes leading to impairment in protein synthesis. It causes a decrease in the production of very-low-density lipoprotein, increased accumulation of triglycerides in liver, leading to fatty liver. A similar process occurs in the other organ systems also.

The clinical manifestation of intoxication has three Stages.[9] Stage I (GI symptoms): appears in the first 24 h of ingestion as epigastric pain, profuse diarrhea, nausea, vomiting, and in some cases fever. The breath, vomit, and burps may have garlicky odour. Phosphorescence of the stool and vomitus has also been described.[10] The laboratory tests in this stage are normal. Stage II (asymptomatic): occurs between 24 and 72 h after ingestion. However, the histology of the liver in this stage demonstrates the early changes of toxic hepatitis with mild elevation of serum aminotransferases and bilirubin. Stage III (advanced): after 72 h of ingestion until either the resolution of the symptoms or death. This stage is characterized by the multisystem organ failure.

Our patients commonly presented to us with GI symptoms. However, the median time to hospitalization to our unit was 4 days which falls in the 3rd clinical stage. This could be due to the apparent resolution of symptoms during the 2nd Stage or due to delayed referral from the first point of contact of medical facility. A case series by Mishra et al. found that the median delay to the presentation to their unit was 5 days which was similar to ours.[5] Another case series by Venugopal et al.[11] and Jothimani et al.[12] also depicted a delay in seeking medical help.

On admission, majority of our patients had deranged liver parameters with encephalopathy and coagulopathy which lead to a significant morbidity. Few of our patients also had associated bone marrow suppression and renal failure. A similar case profile was demonstrated by Mishra et al.[5] and Nalabothu et al.[6]

Yellow phosphorus poisoning is highly lethal, and currently, there is no antidote for it. Routine decontamination measures have to be initiated within 2 h of the exposure to the poison. In our case series, only 37% of the patients received decontamination due to the late presentation to the hospital. This is significant as the mortality increases with the delay in seeking treatment as reported by Nalabothu et al.[6] The use of N-acetylcysteine in yellow phosphorus poisoning is based on anecdotal evidence, with studies showing mixed results. Improved survival was seen by Bhat and Kenchetty[13] and Venugopal et al.,[11] however, Fernandez and Canizares reported no significant improvement in the outcome.[14] Despite the mixed evidence to support this practice, we initiated the treatment with N-acetylcysteine, Vitamin K, and neuroprotection in all our patients with acute liver failure in encephalopathy.

Plasmapheresis is an upcoming treatment modality in the management of acute liver failure due to yellow phosphorus poisoning with very few case reports outlining the benefits of the same. In our case series, we had five patients with acute liver failure with encephalopathy (Grade 2–3). We planned to initiate plasmapheresis in those patients (n = 3) who were in encephalopathy Grade II and above with an admission INR of >3.5. Out of the three patients, 1 patient died even before plasmapheresis was carried out. The other two patients did receive plasmapheresis and had improvement in liver function and then discharged. The blood counts, renal function, and the ammonia levels were not significantly different between the patients. Currently, there are no guidelines as to the number of cycles required. Hence, we serially monitored INR levels and clinical status and used the normalization of INR and improvement in sensorium to normal as therapeutic endpoints for plasmapheresis. A study done by Banjan et al. in 11 adults has suggested that plasmapheresis is a viable treatment option with good clinical outcomes and that plasmapheresis worked only with INR ratios between 1.17–2.93 above which deaths were shown even with plasmapheresis.[15] However, we have seen that plasmapheresis provides good outcomes in those with INR >3.5, provided it is initiated early. An open randomized control study of high-volume plasma exchange in acute liver failure showed increased liver transplant-free survival in patients with acute liver failure[16] A retrospective analysis by Sardar et al. pointed to high von Willebrand factor levels may predispose to platelet microthrombi and multiorgan failure in phosphorus poisoning-induced hepatotoxicity and plasma exchange as one of the modalities to improve the survival in these patients.[17] Our time to discharge with plasmapheresis was 15–18 days and without plasmapheresis was 12–14 days. This probably due to the late presentation to our unit and the patients were sicker than the ones who did not require plasmapheresis. The mortality rate in our case series was 25% which is similar to those reported worldwide.[6],[14]


  Conclusion Top


Acute liver failure is the major cause or mortality and morbidity in those with acute ingestion of yellow phosphorus. We have found that the early initiation of plasmapheresis in patients with encephalopathy with INR >3.5 can lead to improved survival and better outcomes. It can also be tried in patients where liver transplant is not a feasible option. However, there is very limited data to support this, and further randomized control trials have to be conducted to recommend plasmapheresis as a standard of care for the same.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Dutta AK, Seth A, Goyal PK, Aggarwal V, Mittal SK, Sharma R, et al. Poisoning in children: Indian scenario. Indian J Pediatr 1998;65:365-70.  Back to cited text no. 1
    
2.
Roy MP, Gupta R, Bhatt M, Aggarwal KC. Profile of children hospitalized with acute poisoning in New Delhi. Indian Pediatr 2017;54:246-7.  Back to cited text no. 2
    
3.
Gupta SK, Peshin SS, Srivastava A, Kaleekal T. A study of childhood poisoning at National Poisons Information Centre, All India Institute of Medical Sciences, New Delhi. J Occup Health 2003;45:191-6.  Back to cited text no. 3
    
4.
Sollman T. A Manual of Pharmacology and its Applications to Therapeutics and Toxicology. 6th ed. Philadelphia: Saunders; 1942. p. 884-9.  Back to cited text no. 4
    
5.
Mishra AK, Devakiruba NS, Jasmine S, Sathyendra S, Zachariah A, Iyadurai R. Clinical spectrum of yellow phosphorous poisoning in a tertiary care centre in South India: A case series. Trop Doct 2017;47:245-9.  Back to cited text no. 5
    
6.
Nalabothu M, Monigari N, Acharya R. Clinical profile and outcomes of rodenticide poisoning in tertiary care hospital. Int J Sci Res Publ 2015;5:1-12.  Back to cited text no. 6
    
7.
Phosphorus MAK Value Documentation, 2007. MAK Collection Occup Health Saf 2015;2007:1-20.  Back to cited text no. 7
    
8.
Ghoshal AK, Porta EA, Stanley Hartroft W. Isotopic studies on the absorption and tissue distribution of white phosphorus in rats. Exp Mol Pathol 1971;14:212-9.  Back to cited text no. 8
    
9.
Santos O, Restrepo JC, Velásquez L, Castaño J, Correa G, Sepúlveda E, et al. Acute liver failure due to white phosphorus ingestion. Ann Hepatol 2009;8:162-5.  Back to cited text no. 9
    
10.
Simon FA, Pickering LK. Acute yellow phosphorus poisoning. “Smoking stool syndrome.” JAMA 1976;235:1343-4.  Back to cited text no. 10
    
11.
Venugopal R, Narayanasamy K, Chezhian A, Kumar RS, Jasmine JJ. Rat killer poisoning vs. liver damage: A view in South Indian patients of tertiary care center. J Gastrointest Dig Syst 2018;8:569. Available from: https://www.omicsonline.org/open-access/rat-killer-poisoning-vs-liver-damage-a-view-in-south-indian-patients-of-terti ary-care- center-2161-069X-1000569-102595.html. [Last accessed on 2019 Dec 19].  Back to cited text no. 11
    
12.
Jothimani D, Venkatraman J, Srinivasan V, Muthamizh G, Olithselvan A, Vargese J, et al. Acute liver failure (ALF) due to yellow phosphorous poisoning. J Clin Exp Hepatol 2014;4:S1.  Back to cited text no. 12
    
13.
Bhat S, Kenchetty KP. N-Acetyl cysteine in the management of rodenticide consumption — Life saving? J Clin Diagn Res 2015;9:OC10-3.  Back to cited text no. 13
    
14.
Fernandez OU, Canizares LL. Acute hepatotoxicity from ingestion of yellow phosphorus-containing fireworks. J Clin Gastroenterol 1995;21:139-42.  Back to cited text no. 14
    
15.
Banjan D, Sane K, Wattamvar S, More M. Predictable factors for intervention with heparin free plasmapheresis in impending liver cell failure due to consumption of phosphorus rodenticide. Int J Res Med Sci 2019;7:3026.  Back to cited text no. 15
    
16.
Larsen FS, Schmidt LE. High-volume plasma exchange in patients with acute liver failure: An open randomised controlled trial. J Hepatol 2016;64:69-78.  Back to cited text no. 16
    
17.
Indian Society of Gastroenterology. Indian J Gastroenterol 2018;37:1-37.  Back to cited text no. 17
    



 
 
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