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Year : 2013  |  Volume : 16  |  Issue : 2  |  Page : 258-259

Paraphenylenediamine poisoning

Department of Medicine, C. S. M. Medical University and AH, Lucknow, UP, India

Date of Web Publication6-Apr-2013

Correspondence Address:
S C Chaudhary
Department of Medicine, C. S. M. Medical University and AH, Lucknow, UP
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1119-3077.110138

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Hair dye containing paraphenylenediamine (PPD) is widely used in India because of its free availability and low cost. PPD produces local as well as systemic toxic effects when applied topically and/or ingested. It is highly toxic when taken by mouth and the outcome depends mainly on the dose taken. Important clinical manifestations are angioedema leading to dysphasia and respiratory distress, rhabdomyolysis, intravascular hemolysis, acute renal failure and hepatic necrosis. Myocarditis or fatal arrhythmia may also occur in PPD poisoning. Mainstay of management is early recognition and supportive measures as there is no specific antidote. We hereby report a young female who presented to us with features of angioedema, cardiac manifestation and hepatic dysfunction after ingesting PPD, which was treated successfully. In the absence of laboratory facilities, clinical features like angioedema and chocolate brown-colored urine could be suggestive of PPD poisoning.

Keywords: Angioneurotic edema, myocarditis, paraphenylenediamine

How to cite this article:
Chaudhary S C, Sawlani K K, Singh K. Paraphenylenediamine poisoning. Niger J Clin Pract 2013;16:258-9

How to cite this URL:
Chaudhary S C, Sawlani K K, Singh K. Paraphenylenediamine poisoning. Niger J Clin Pract [serial online] 2013 [cited 2022 Jan 22];16:258-9. Available from:

   Introduction Top

Paraphenylenediamine (PPD), a derivative of p-nitroanaline is widely used as an oxidizable hair dye. It is commonly mixed with henna in Africa, Middle East and Indian subcontinent, which is traditionally applied to color palms of hands, soles and feet, and to dye hair a dark red shade. [1] PPD produces local as well as systemic toxic effects when applied topically and/or ingested. It is highly toxic when taken by mouth and the outcome depends mainly on the dose taken. The lethal dose of PPD is not known; estimates vary from 7-10 g [2] (our patient had ingested 10 g). A large dose will cause death within the first 6-24 hours of ingestion from angioneurotic edema or cardiotoxicity (fatal arrhythmias). Smaller doses, or if the patient vomits most of the dye, will usually present as angioneurotic edema with no further sequelae. A moderate dose will cause acute renal failure within the first week. We are presenting this case to highlight the importance of adequate history taking, early recognition of the drug poison symptoms and prompt management of toxicities.

   Case Report Top

A 15-year-old female presented to us after consuming about 10 g of PPD with swelling of face, lips and neck, and dysphasia suggestive of angioedema within 4 hours of ingestion. She also had recurrent vomiting for the previous 2 hours. On admission, she had tachypnea (respiratory rate 28/min), blood pressure of 110/70 mm Hg and pulse rate of 86/min, but there was no cyanosis. Other general and systemic clinical examinations were within normal limits. Routine investigations, including hemogram, urine examination and kidney function tests, along with serum electrolyte and serum CPK levels were within normal limits at the time of admission and during hospital stay. Serial liver function tests revealed progressive elevation of aspartate and alanine aminotransferases up to maximum levels of 925 and 1122 μ/L, respectively on the fifth day with normal bilirubin. Her serial electrocardiograms showed T wave inversion in V1-V4 chest leads. Chest radiograph, cardiac enzymes including troponin-T and echocardiography were normal. She was put on conservative management in the form of oxygen inhalation, intravenous fluids, methyl prednisolone (125 mg × 6 hourly), pantoprazole and antibiotics to which she showed gradual improvement. Her urine output, repeated renal function tests and hemogram were normal, and there was no evidence of intravascular hemolysis during the hospital stay. Her ECG changes reverted to normal on the seventh day of admission.

   Discussion Top

PPD, a coal-tar derivative, on oxidation produces Bandrowski's base, which is allergic, mutagenic and highly toxic. Early manifestations of oral PPD intake (usually within 4 to 6 hours of ingestion) are numbness and burning of mouth and throat, vomiting, swelling of upper GI tract leading to dysphagia, and respiratory distress due to swelling of upper airway and angioedema. If the patient survives this acute phase, a late phase sets in usually after 12 hours of ingestion. It may last from few days to several weeks. Rhabdomyolysis, intravascular hemolysis, oliguria/anuria, and acute tubular necrosis/acute renal failure are delayed complications in some patients who survive the late phase. Rhabdomyolysis is the main cause of renal failure, morbidity and mortality. [3] Although our patient had ingested the lethal dose, she luckily did not develop renal failure probably because of early recognition of the poison and proper conservative management.

Cardiotoxicity and hepatic necrosis due to PPD have also been described, but very few reports in the literature have mentioned myocarditis, [4],[5],[6] myocardial infarction, [7] ventricular thrombus formation [6] and cardiac arrhythmias. [3] Clinical manifestations can vary from asymptomatic myocarditis to fatal arrhythmia. Electrocardiographic manifestations include ventricular and supraventricular ectopics, bundle branch block and ST-T changes. Increased serum levels of cardiac troponin-T provides evidence of myocyte injury in patients with clinically suspected myocarditis more sensitively than does conventional determination of cardiac enzyme levels. [5] Our patient had cardiac involvement as evidenced by ECG changes, which reverted to normal on the seventh day of admission. Myocardial involvement as evidenced by ECG changes is a rare manifestation of PPD poisoning mentioned in the literature.

PPD poisoning is a medical emergency and has high mortality if not recognized and intervened early. There is no specific antidote but the most important aspect of management is early recognition and supportive measures that include gastric lavage, normal saline and sodium bicarbonate infusion. Respiratory distress, myocarditis and cardiac arrhythmias are the major early challenges, which require vigilant monitoring to prevent early deaths. Intubation and ventilator support may be required for asphyxia and all modalities of dialysis have been found useful in renal failure. [3]

During emergency particularly when patient history and good laboratory facilities are lacking, the characteristic angioedema of the face and neck with difficulty in breathing and acute renal failure manifesting as chocolate brown-colored urine could be suggestive of PPD poisoning. Vigilance must be maintained regarding cardiac manifestations and other late complications of PPD poisoning for at least 1 month in all cases.

   References Top

1.Ashar A. Acute angioedema in paraphenylenediamine poisoning. J Pak Med Assoc 2003;53:120-2.  Back to cited text no. 1
2.Singla S, Miglani S, Lal AK, Gupta P, Agarwal AK. Para-penylenediamine (PPD) Poisoning. Journal, Indian Academy of Clinical Medicine 2005;6:236-8.  Back to cited text no. 2
3.Sampathkumar K, Yesudas S. Hair dye poisoning and the developing world. J Emerg Trauma Shock 2009;2:129-31.  Back to cited text no. 3
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4.Singh N, Jatav OP, Gupta RK, Tailor MK. Myocardial damage in hair dye poisoning - An uncommon presentation. J Assoc Physicians India 2008;56:463-4.  Back to cited text no. 4
5.Lauer B, Niedraic C, Schanhwell M, Pauschinger M, Strauer BE, Schultheiss HP. Cardiac Troponin-T in patients with clinically suspected myocarditis. J Am Coll Cardiol 1997;30:1354-9.  Back to cited text no. 5
6.Zeggwagh AA, Abouqcal R, Abidi K, Madani K, Zekraoui A, Karkeb O. Left ventricular thrombus and myocarditis induced by PPD poisoning. Ann Fr Anesth Reanim 2003;22:639-41.  Back to cited text no. 6
7.Brahmi N, Kouraichi N, Blel Y, Mourali S, Thabet H, Mechmeche R, et al. Acute Myocarditis and Myocardial Infarction induced by paraphenylene diamine interest of angiocoronarygraphy. Int J Cardiol 2006;113:E93-5.  Back to cited text no. 7

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