Title: HAIR DYE POISONING:

Biography:

Abstract

An estimated 1 million people worldwide die by suicide every year. According to W.H.O, 381 suicide cases are reported daily in India. In India most of the suicide is committed by poison mainly pesticide. Nowadays Hair dye poisoning is also emerging mainly among the female. Age group of 15 to 45yrs. One of the widely chosen means of suicide is Poisoning in south India mainly among middle class people in our country. Trend of Consuming hair dyes for suicide has increased. It is less costly and widely available.
Case Study:
A 20 -year-old female presented to ED with Alleged H/o intentional consumption of hair dye poisoning (content of para phenylene diamine, propylene glycol, resorcinol, sodium lauryl sulphate liquid, light liquid paraffin, herbal extracts along with preservatives and perfumes) about 100 ml at her residence around 12p.m. She had facial swelling with edema of lips, swelling of neck and tongue; stridor was present and difficulty in speaking.
Report:
No H/o Altered sensorium/ Seizure/ Decreased urine output/ Dark color urine/ vomiting/ Blurring vision. On receiving BP: 110/80 mmHg PR: 100/min Temp: 98.2°F, Spo2: 98 % with oxygen by mask, CBG: 146mg/dl, GCS: E4 M6 V4 14/15.
General Examination:
Patient was conscious, oriented and afebrile, on exposure facial swelling with edema of lips, swollen neck and tongue. No external injury.
Systemic Examination:
CVS: S1S2 (+), No added sounds RS: B/L AE (+), No added sounds CNS: B/L PERL, NFND, P/A: Soft, mild epigastric tenderness with no organomegaly P/R: Normal, P/V: Normal.
Comorbities: Nil; Previous Medical/Surgical History: NIL
Investigations:
ABG, Beta-HCG, CBG, ECG, USG, Complete metabolic panel, Sr. Calcium, CPK Total, urine.
Myoglobin, LFT, RFT, Peripheral smears, Chest X-ray was ordered.
Airway & Breathing : In order to protect the airway, patient was intubated and put her on mechanical ventilator.
Circulation: IV line is secured, and hypotension is corrected by IV fluid bolus.
Decontamination: Gastric lavage was done to the patient with activated charcoal
Laryngeal edema and ARDS: she was treated with injection hydrocortisone 200 mg stat and Neb. Adrenaline inhalation and antihistamines for angioneurotic edema.
Enhanced Elimination: Forced Diuresis by giving isotonic saline + sodium bicarbonate+ Lasix.
Initial ABG SHOWED SEVERE METABOLIC ACIDOSIS for which she was treated with Inj. Sodium
Bicarbonate stat dose followed by sodium bicarbonate infusion pump.
Dispatch:
Patient was shifted to ICU.
On the 2nd day, the patient developed dark coloured urine with a decreased urine output and pedal edema.
Laboratory investigations revealed:
Blood urea of 180 mg/dl (7 – 30 mg/dl) | Serum creatinine of 5.6 mg/dl (0.7 – 1.2 mg/dl) | Serum creatinine phosphokinase (CPK)1750 U/L(Male: 39 – 308U/L & Female: 26- 192U/L).
Urine Myoglobin was positive.The liver function tests were normal and the peripheral smear did not revea evidence of hemolysis
Ultrasonography of the abdomen showed normal size and echo texture of both kidneys.The chest x-ray and electrocardiogram were also normal.
Patient was treated with Inj. Hydrocortisone and anti-histamine in view of stridor and respiratory distress which resolved after 2 days of treatment.
On the 3rd day, she developed rhabdomyolysis and ARF. Her Blood urea and creatinine levels were elevated and ABG shows severe metabolic acidosis. She was managed initially with forced alkaline diuresis and in view of severe metabolic acidosis and hyperkalaemia she received 3 sittings of haemodialysis. Acute renal failure resolved over 6 days with dialysis.
She was clinically improved and extubated and put on NIV to prevent further atelectasis of both lungs and transferred on High Flow Mask and graded clinically and discharged home on 9th day of admission after obtaining counselling.
PARAPHENYLENE DIAMINE (PPD) (C6H4(NH2)2:
Main component aromatic amine not found in nature a toxic substance since 1924.PPD is banned in certain countries like Germany, France, Sweden, Sudan, etc. Derivative of para nitro Aniline (coal-tar derivative).White in colour which turns brown when exposed to air. On Oxidation it produces- Bandrowski’s base – Anaphylactic, Mutagenic and Toxic Properties. Severity of the poisoning is directly proportional to the Concentration of PPD.
PPD – Severe Angioneurotic Edema, Rhabdomyolysis and Intravascular Hemolysis.
Lethal Dose:
Severity of the poisoning Increases with the Dose (7 to 10 gms), 3gms sufficient to cause systemic complication
Resorcinol:
Phenolic Derivative, Corrosive | Seizure, Lethargy, Coma, Death
Nausea, Dyspnea, Hypotension, Diaphoresis, Salivation, Methemoglobinemia, Pulmonary edema
Propyelene Glycol:
Metabolic Acidosis, CNS depression, Arrhythmia, Renal dysfunction
EDTA Ethylene diamine tetra acetic acid Sodium - Hypocalcaemia ( due to rhabdomyolysis) NEPHROTOXIC COCTAIL
PPD + Resorcinol + Propylene Glycol.
Pathophysiology:
Para phenylene diamine: Severe Angioneurotic Edema, Rhabdomyolysis and Intravascular Hemolysis.
Rhabdomyolysis:
Leakage of calcium ions from Smooth ER, followed by continuous contraction and irreversible change in muscle structure. Rhabdomyolysis along with Hypervolemia and PPD metabolites causes Acute Renal Failure.
Propylene glycol:
Hyperosmolarity, increased anion gap, metabolic acidosis, CNS depression, Arrhythmia and Renal dysfunction.
Resorcinol: 
Eye, skin, oral and gastrointestinal injuries, renal toxicity.
Phase 1:
Vomiting | Gastritis | Hypertension| Vertigo| Severe Edema of Face, Neck, Tongue, Pharynx and Larynx with Respiratory Distress –Stridor | Convulsions 
Phase 2:
Hemolysis | Rhabdomyolysis: Chocolate brown colour of the urine | ARF | Hypocalcaemia
Phase 3:
Muscular Edema | Multi organ Failure | Shock
Stages of  Angioedema:
Cricopharyngeal edema + Laryngeal edema Asphyxia            Respiratory distress and Hypoxia Respiratory failure
Cause of death:
Respiratory Obstruction | Renal Failure | Arrhythmia | ARDS
ECG shows non-specific changes with frequent premature ventricular complex suggesting myocarditis after hair dye ingestion.
ECG shows ventricular tachycardia suggesting myocarditis after hair dye ingestion.  
Diagnosis:
History of consumption or materials got from the scene | Clinical Features | RFT | CPK | Serum Calcium | Urine dip stick | Thin layer chromatography
PPD can be diagnosed by thin layer chromatography on silica gel ( solvent system benzene, ethyl acetate or hexane acetate) and sprayed with 0.2% solution of potassium dichromate as chromogenic reagent to give a pinkish brown spot.
Myoglobinuria: urine dip stick or urine color change
Treatment:
No specific Antidote | Treat the complications | Gastric Lavage is useful within 1 hour of presentation | Activated Charcoal (1g/kg) | Mainly Symptomatic and Supportive | Emergency – Airway protection : Intubation or Tracheostomy
Conclusion:
In Pediatric also accidental ingestion of Hair dye poisoning the management is the same. Mortality depends on the amount of hair dye ingested, the time interval between consumption and intervention, hyperkalaemia, hypocalcaemia, and hypophosphatemia; and mortality rates varied between 0.03% and 60%. Whenever Stridor due to upper airway oedema, Rhabdomyolysis, Haemoglobinuria.
Myoglobinuria, ARF develops in a poisoning Hair dye poisoning should be considered. Early Diagnosis & Intervention will save a life. In addition, Community awareness & Health education. Remembering the fact that there is no specific antidote for PPD, the patient must be managed by watching like a hawk. In conclusion, hair dye poisoning is a life-threatening emergency which requires life-saving emergency resuscitation and early management of anaphylaxis. Early recognition of rhabdomyolysis, early prevention of acidosis and early initiation of forced alkaline diuresis prevent ARF minimizing the need for dialysis.
We are uncertain of the time of development of Renal Failure following ingestion of PPD and hence all patients should be monitored in the hospital for development of renal and other complications.Hair Dye Poisoning: Kills the kidney, hits the heart, cuffs the trachea.