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Year : 2017  |  Volume : 15  |  Issue : 2  |  Page : 136-138

Early use of intravenous N-acetylcysteine in treatment of acute yellow phosphorus poisoning

Department of Internal Medicine, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication18-May-2017

Correspondence Address:
Meban Aibor Kharkongor
Department of Internal Medicine, Christian Medical College, Vellore - 632 004, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-4651.206530

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Rodenticides remain an important cause of morbidity and mortality among patients with deliberate self-harm. Yellow phosphorus is an important class of rodenticide due to its high toxic nature and is associated with a high mortality rate. The absence of any specific antidote is an important factor for poor prognosis among those who consume this poison. We report a case of acute liver injury secondary to yellow phosphorus poisoning which was successfully managed with intravenous N-acetylcysteine.

Keywords: N-acetylcysteine, rodenticide, yellow phosphorus

How to cite this article:
Kharkongor MA, Mishra AK, Ninan K F, Iyadurai R. Early use of intravenous N-acetylcysteine in treatment of acute yellow phosphorus poisoning. Curr Med Issues 2017;15:136-8

How to cite this URL:
Kharkongor MA, Mishra AK, Ninan K F, Iyadurai R. Early use of intravenous N-acetylcysteine in treatment of acute yellow phosphorus poisoning. Curr Med Issues [serial online] 2017 [cited 2023 Mar 21];15:136-8. Available from: https://www.cmijournal.org/text.asp?2017/15/2/136/206530

  Introduction Top

Rodenticides for many years have been an important cause of significant morbidity and mortality in patients who present to an emergency room with deliberate self harm. An annual incidence of 500,000 cases has been reported.[1] The easy availability of these compounds has made this a problem almost impossible to control. Of the different classes of rodenticides available, yellow phosphorus is considered a highly toxic compound and it can cause hepatocellular necrosis and fulminant hepatic failure in up to 50% of patients.[2] Treatment, however, has continued to be difficult as no specific antidote has been identified so far. Supportive management is the mainstay of therapy.[3] The possible benefits of N-acetylcysteine (NAC) in improving the prognosis of patients with yellow phosphorus poisoning have been noticed in recent case series, with the best results seen among patients in whom NAC was started early in the course of illness.[4],[5]

We present a case of yellow phosphorus poisoning [Box 1] which was successfully managed with early intravenous NAC.

  Case Report Top

A 20-year-old male, a daily wage laborer, was brought to the emergency department after he had allegedly consumed five packets of ratol, a rodenticide containing 3% of yellow phosphorus, equivalent to a total cumulative dose of 15 g of yellow phosphorus. There was no history of consumption of any other poison. He was initially taken to a local hospital where he had two episodes of vomiting and was given a gastric lavage with normal saline at approximately 2 h following consumption of the above poison. He was then referred to a higher center for further management. The patient reached the hospital 5 h after the incident. He had no further episodes of vomiting and was otherwise asymptomatic.

On examination, he was conscious, oriented and in no apparent distress. General and systemic examinations were normal. There were no bleeding manifestations, jaundice, or other signs of liver failure.

Laboratory evaluation revealed deranged liver function tests with elevated liver enzymes, aspartate transaminase (AST), and alanine transaminase (ALT) (serum AST and ALT were 283 μ/L and 143 μ/L, respectively). Bleeding parameters, blood counts, and other laboratory investigations did not reveal significant abnormalities [Table 1]. Electrocardiogram was within normal limits, and chest roentgenogram showed no abnormalities.
Table 1: Laboratory investigations

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Supportive management with intravenous fluids, proton pump inhibitors, and anti-emetics was initiated. He was also immediately initiated on intravenous NAC within 1 h of admission into the emergency room. The dose of intravenous NAC that was administered was according to the recommended clinical practice guidelines for the treatment of acetaminophen overdose - 150 mg/kg of NAC in 200 mL of 5% dextrose over 15–60 min and then 50 mg/kg in 500 mL of 5% dextrose over 4 h followed by 100 mg/kg in 1000 mL of 5% dextrose over 16 h. A cumulative dose of 300 mg/kg of injection NAC was administered over 21 h.[6] He was placed under continuous monitoring of vital parameters in an intensive care setting. Clinical and laboratory parameters for liver function were monitored daily.

Serum AST and ALT decreased to 113 μ/L and 99 μ/L, respectively, by day 2 and improved to 39 μ/L and 60 μ/L, respectively, by day 5 [Figure 1]. He received psychiatric evaluation and was discharged in a stable condition after 5 days of admission.
Figure 1: Serum alanine transaminase aspartate transaminase levels - serial measurements over 3 days.

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  Discussion Top

A recent study conducted in South India showed that yellow phosphorus was the most common rodenticide used in suicide attempts in the region and carried a 30% mortality despite maximal supportive therapy.[4] The LD50 dose in yellow phosphorus poisoning is 10 mg/kg body weight; however, ingestion of a dose as low as 100 mg has been seen to result in death.[7] Indicators for poor outcome included early elevation of liver transaminases and alkaline phosphatase, more than 10-fold increase in alanine aminotransferase, derangement in prothrombin time, metabolic acidosis, and hypoglycemia.[2] These individuals usually demonstrate only minimal gastrointestinal symptoms during the first 48–72 h but subsequently develop acute liver failure, progressing to multi-organ failure and death in severe cases.[8],[9]

The mechanism of toxicity of yellow phosphorus is by means of an exothermic reaction producing phosphoric acid that causes direct tissue damage due to the production of free radicals against organic molecules. This, in turn, will bring about changes in ribosomal function and protein synthesis, failure of regulation of blood glucose, and fatty degeneration of multiple organs.[5] The reason for an increased predilection to cause liver toxicity is, however, not fully understood.

Management of this condition is purely supportive as there is no specific antidote available to date. NAC, a glutathione precursor, has been shown to neutralize the active metabolite of acetaminophen by replenishing the glutathione stores in the liver, resulting in improved prognosis in acetaminophen overdose. The possibility of similar effects of NAC in yellow phosphorus has been evaluated in recent studies with limited success. A meta-analysis involving 616 patients, conducted to assess the role of NAC in nonacetaminophen-related acute liver failure, showed no significant difference in overall survival of the patients.[10],[11] Other studies that specifically looked at the role of NAC in the treatment of liver injury in yellow phosphorus overdose have yielded mixed results.[4],[5] However, it was noted that survival was greater among patients who received NAC early, compared to those who received it later during the course of illness.

The individual in this report had consumed a large dose of yellow phosphorus (15 g) and had elevation of liver enzymes within the first 6 h of consumption, both of which were indicators of a poor prognosis. He was initiated on NAC at an appropriate dose within 6 h of consumption of yellow phosphorus with which he showed a complete resolution of liver injury. He developed no side effects or complications.

  Conclusion Top

When high mortality results from the lack of a specific antidote, our case report emphasizes the possible survival benefit of early intravenous NAC in yellow phosphorus poisoning. More research is required to determine the efficacy, dosage, and side effects of the same.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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. 1
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. 2
Singh S, Bhalla A. Aluminum Phosphide Poisoning. Available from: http://www.jmgims.co.in/article.asp?issn=0971-9903;year=2015;volume= 20;issue=1;spage=15;epage=19;aulast=Singh#ref1. [Last cited on 2016 Dec 20].  Back to cited text no. 3
Nalabothu M, Monigari N, Acharya R. Clinical profi le and outcomes of rodenticide poisoning in tertiary care hospital. Int J Sci Res Publ 2015; 5:1-12. Available from: http://www.ijsrp.org/research-paper-0815/ijsrp-p4442.pdf. [Last accessed on 2016 Jan 05].  Back to cited text no. 4
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 2016. pii: 0049475516668986.  Back to cited text no. 5
Clinical Practice Guidelines: Paracetamol Poisoning. Available from: http://www.rch.org.au/clinicalguide/guideline_index/paracetamol_poisoning/. [Last cited on 2016 Dec 22].  Back to cited text no. 6
Fletcher GF, Galambos JT. Phosphorus poisoning in humans. Arch Intern Med 1963;112:846-52.  Back to cited text no. 7
Mauskar A, Mehta K, Nagotkar L, Shanbag P. Acute hepatic failure due to yellow phosphorus ingestion. Indian J Pharmacol 2011;43:355-6.  Back to cited text no. 8
[PUBMED]  [Full text]  
Karanth S, Nayyar V. Rodenticide-induced hepatotoxicity. J Assoc Physicians India 2003;51:816-7.  Back to cited text no. 9
Lee WM, Hynan LS, Rossaro L, Fontana RJ, Stravitz RT, Larson AM, et al. Intravenous N-acetylcysteine improves transplant-free survival in early stage non-acetaminophen acute liver failure. Gastroenterology 2009;137:856-64.e1.  Back to cited text no. 10
Hu J, Zhang Q, Ren X, Sun Z, Quan Q. Efficacy and safety of acetylcysteine in “non-acetaminophen” acute liver failure: A meta-analysis of prospective clinical trials. Clin Res Hepatol Gastroenterol 2015;39:594-9.  Back to cited text no. 11


  [Figure 1]

  [Table 1]

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