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Acute Renal Failure due to Paraphenylenediamine Intoxication (Hair Colouring Dye): Report of A Case and Discussion of Management Guidelines Based on A Review of the Literature

Author(s): Rahat Kumar, Baljeet Singh, Sita R Sharma, Narinder Singh and Jaswinder Singh

Vol. 6, No. 2 (2006-03 - 2006-06)

Rahat Kumar, Baljeet Singh, Sita R Sharma, Narinder Singh and Jaswinder Singh
SGRDIMSAR, Amritsar

Abstract

Paraphenylenediamine (PPD) poisoning has been known for many years. Accidental or deliberate ingestion of Paraphenylenediamine has rarely been reported, but is potentially severe. We report a case of systemic poisoning with paraphenylenediamine (PPD) presenting with characteristic features of severe angioneurotic edema, rhabdomyolysis and intravascular hemolysis with hemoglobinuria culminating in acute renal failure. There is no specific antidote available but some guidelines for management of such a case are reviewed which includes therapy with gastric lavage, IV fluid infusion, mechanical ventilation, alkalinization of urine, corticosteroids, vasopressors and renal replacement therapy.

Introduction

A 20 year-old male was brought to the emergency room because of drowsiness, shivering, confusion and severe vomiting.. His family members mentioned that he has consumed more than 10 tablets of Paraphenylenediamine lumps 20 gm, the empty bottle of which was also brought by the relatives in suicide attempt. Within one and half hour of ingestion he had developed vomiting of bluish blackish discoloration and diffuse abdominal pain. During the next few hours he developed dizziness and was irritable. His urinary output started declining 24 h later (200 ml/day) with hemoglobin urea 3 + and with increase in blood urea and S. creatinine persisting over coming days. Physical examination revealed a stuporous patient, with a blood pressure of 100/80 mmHg, a heart rate of 114/min, a respiratory rate of 38/min, and a temperature of 36°C. Face of the patient was puffy with bilateral edema feet. A strong uraemic fetor and marked distension of the jugular veins were noted. Pulmonary auscultation revealed diffuse coarse crackles. Patient complained of severe pain in lower limbs. Neurological examination revealed decreased muscle strength, absent ankle and triceps reflexes, normal perception of vibration, but diminished touch and pinprick sensation in stocking and glove distribution. The laboratory data on admission were: hemoglobin 10.7 g/dl, haematocrit 23%, WBC count was 15 000 /ml, with 95% neutrophils count, platelet count was 101 000/ml, Serum sodium = 120 mmol/l, Potassium = 5.6 mmol/l, Blood urea = 128 mg/dl and Serum creatinine = 6.3 mg/dl . The presence of schistocytes on a peripheral blood film, a low haptoglobin, and elevated lactate dehydrogenase suggested intravascular haemolysis. Urinalysis revealed trace proteinuria but 3+ hemoglobinuria. Blood sugar was normal and G6PD enzyme was not deficient. A chest X-ray showed bilateral alveolar edema. On ultrasound, increased echogenicity of the kidneys was the only abnormal finding. Patient was managed on basic life support management as intravenous fluids, Inj. Lasix (Furosemide) and Respiratory support. Urine output increased, but renal function parameters remained elevated. Haemodialysis was performed daily initially. Six days after admission urea was 210 mg/dl and serum creatinine 7.1 mg/dl with increase in urinary output ( 700ml/day). The patient therefore was maintenance on dialysis three times a week. Renal biopsy was advised 7 days after admission and showed normal glomeruli, severe fibrosis of the interstitium with inflammatory changes. Audiometry revealed no sins and symptoms of sensorineural hearing loss. Inspite of all the measures to revive the patient the patient was taken to Private Hospital against medical advice (LAMA) after 17 days. The patient was reported to expire after 4 weeks.

Discussion

We report a case of systemic poisoning with Para-phenylenediamine (PPD) presenting with characteristic features of edema, rhabdomyolysis and intravascular hemolysis with hemoglobinuria culminating in acute renal failure. Though rare in western countries, such poisoning is not uncommon in East Africa, Indian subcontinent and Middle East countries1. We discuss here the clinical features and key management issues of systemic PPD poisoning. Hair colors are either permanent or semi permanent. The permanent agents contain oxidizing agents that interact with the dye to cause color molecule to fix on to hair shaft and most common being the Hydrogen Peroxide. Common dye intermediates used in 1:1 concentration with Hydrogen Peroxide are Paraphenylenediamine, Resorcinol or Aminophenols2. The remaining ingradients are soaps and synthetic detergents. Paraphenylenediamine is a type of permanent hair color used as a component of permanent waving kits in hair styling. So far only few case reports have been described about Paraphenylenediamine poisoning. In a series 3 of 18 cases of acute hair dye (paraphenylenediamine) poisoning the characteristic features of swollen face and the chocolate brown color of the urine were diagnostic. For patients presenting with asphyxia, Tracheostomy and intensive medical treatment with hydrocortisone and chlorpheniramine maleate (antihistaminic drug) and penicillin cover were life savings. The mild cases were successfully treated with hydrocortisone and chlorpheniramine maleate and penicillin without tracheostomy. The dye was detected in the urine by thin layer chromatography on silica gel and proved to be paraphenylenediamine. Early prompt diagnosis and clinical management proved to be life saving in both serious and mild hair dye poisoning. In another case report of rhabdomyolysis following homicidal intoxication of paraphenylenediamine has been described4. The case was of a 44 years healthy male, drinking a beverage containing PPD, prepared for a homicidal use. Total intake of PPD was about 3 g (63 mg/kg). Presentations of the patient was muscle rigor with tenderness, initially developed in the lower extremities and subsequently extending to all over the skeletal muscles. Laboratory examinations disclosed high CPK (137,600), LDH (3895), GOT (3400) and GPT (545), and leukocytosis (26600), indicating massive skeletal muscle necrosis. ECG revealed mild depression of ST junction in the II and aVF leads. Urine showed dark brownish discoloration and subsequently oliguria. Scattered necrosis of muscular fibers was observed in a biopsy of the femoral muscles. The patient collapsed suddenly and soon died in the course of about 30 hours. Clinically, the cause of death was thought to be acute renal failure due to rhabdomyolysis. Afterwards PPD was detected in the urine obtained in the hospital. Autopsy confirmed the clinical diagnosis. Histopathology of the cadaveric kidney showed Renal collecting ductules and distal tubules occluded by dark brownish myoglobin casts and its epithelium massively necrotized; Skeletal muscles showed scatteredly coagulation necrosis partially associated with inflammatory cell infiltration. In other case reports multiple cause of death were reported as cardiogenic shock secondary to myocardial rhabdomyolysis confirmed by a postmortem biopsy as a cause of death5, severe angioneurotic edema, rhabdomyolysis and intravascular hemolysis with hemoglobinuria culminating in acute renal failure in another report1, a suicidal report6 of four cases by drinking varying amounts of that hair dye in women aged 18 to 35 years, seen in the nephrology department the initial symptom was acute asphyxia which required emergency tracheotomy in 3 cases. Thereafter, the most important visceral damage was acute renal failure, usually with oliguria or anuria, for which haemodialysis was performed in 2 cases. In these patients treated at an early stage the midand long-term prognosis was satisfactory. Rhabdomyolysis was the principal mechanism underlying PPD systemic toxicity was particular, responsible for the renal failure observed. Systemic poisoning with paraphenylenediamine (PPD) is rare in western countries, and therefore a high degree of awareness and circumstantial evidence is required to make an early diagnosis. The classical and other less commonly reported features of this poisoning are show Rhabdomyolysis as the principal mechanism underlying PPD systemic toxicity; it is, in particular, responsible for the renal failure. Proposed mechanisms for the renal damage include direct tubular toxicity due to induction of active oxygen radicals and reduced renal perfusion resulting from intravascular volume depletion and possibly decreased vasomotor tone.

If ingested the oxidizing agents (permanent hair colors) can be fairly toxic. Vomiting is a common presentation as the free ammonia and ethanolamine present in these products is highly emetogenic7. There is no specific antidote available but some guidelines for management of such a case are reviewed. Rinsing the mouth with water and drinking milk alleviate the gastric symptoms2. Besides supportive treatment and renal replacement therapy, specific therapy involves prompt removal of unabsorbed poison from the gastrointestinal tract, and elimination of the unreacted Paraphenylenediamine from the circulation. Immediate gastric lavage should be performed, preferentially with 2% sodium bicarbonate. No explicit recommendations on the use of oral activated charcoal can be made. The hydrophilic nature and low molecular weight of PPD would suggest a low adsorbability. On the other hand, charcoal therapy is simple, inexpensive, well tolerated and non-toxic. The mild cases can be successfully treated with hydrocortisone and chlorpheniramine maleate and penicillin without tracheostomy3. In an another retrospective case report8 conducted over 6 yrs in a medical intensive care unit of a university hospital on 19 patients hospitalized for systemic PPD intoxication reported that the major clinical symptoms of presentation was cervicofacial edema followed by upper airway tract edema, oliguria, renal failure and shock. Rhabdomyolysis and metabolic acidosis was seen in all the patients and acute renal failure in half of the patients. 13 out of 19 patients were managed successfully with gastric lavage, IV fluid infusion, and mechanical ventilation, alkalinization of urine, corticosteroids, vasopressors and renal replacement therapy. Out of six patients died cause of death in five was due to acute renal failure.

Conclusion

Clinical manifestations of systemic PPD intoxication were associated with respiratory, muscular, renal and hemodynamic syndromes. Acute renal failure signifies the severity of intoxication. There is no specific antidote available but some guidelines for management of such a case can be made as Rinsing the mouth with water and drinking milk alleviate the gastric symptoms, Immediate gastric lavage should be performed, preferentially with 2% sodium bicarbonate. The mild cases can be successfully treated with IV fluid infusion, hydrocortisone and chlorpheniramine maleate. But in event of presentation with cervicofacial edema, upper airway tract edema, oliguria, renal failure or shock aggressive therapy with gastric lavage, IV fluid infusion, mechanical ventilation, alkalinization of urine, corticosteroids, vasopressors and renal replacement therapy should be done as early as possible.

References:

  1. Anuradha S, Arora S, Mehrotra S, Arora A, Kar P. Acute renal failure following para-phenylenediamine (PPD) poisoning: a case report and review. Ren Fail. 2004 May;26(3):329-32.
  2. Judith KL. Cosmatics and Toilet Articles. In: Haddad LM, Shannon MW and Winchester JF, editors. Clinical management of poisoning. WB Saunders Company; 1998. p.1169-74.
  3. Yagi H, Hind AM, Khalil SI. Acute poisoning from hair dye. East Afr Med J. 1991 Jun;68(6):404-11.
  4. Saito K, Murai T, Yabe K, Hara M, Watanabe H, Hurukawa T. [Rhabdomyolysis due to paraphenylenediamine (hair dye)–report of an autopsy case] [Article in Japanese]. Nippon Hoigaku Zasshi. 1990 Dec;44(5-6):469-74.
  5. Ababou A, Ababou K, Mosadik A, Lazreq C, Sbihi A. [Myocardial rhabdomyolysis following paraphenylene diamine poisoning] [Article in French]. Ann Fr Anesth Reanim. 2000 Feb;19(2):105-7.
  6. Bourquia A, Jabrane AJ, Ramdani B, Zaid D. [Systemic toxicity of paraphenylenediamine. 4 cases][Article in French]. Presse Med. 1988 Oct 15;17(35):1798-800.
  7. Gosselin Re, Hodge HD, Smith RP el al: Clinical toxicology of commercial products, 4th ed, Baltomore, Wiliams and Wilkins, 1976.
  8. Kallei H, Chelly H, Dammak H, Bahloul M, Ksibi H, Hamida CB et al. Clinical manifestation of systemic paraphenylene diamine intoxication. J Nephrol 2005 May-Jun;18(3):308-11.

Reprint request: Rahat Kumar
Associate Prof. Department of Pharmacology
& Toxicology, SGRDIMSAR, Amritsar
E-mail: [email protected],
[email protected]

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