ISSN 0971-0973 J Indian Acad Forensic Med, <strong>32</strong>(2)Results:Sr. Biochemical Parameter Percentage of casesNo.shown derangement1 Raised total Leucocyte 78.125counts2 Raised Liver enzymes: 62.5SGPT, SGOT3 Raised serum creatinine 46.884 Hypocalcemia 37.55 Raised Bilirubin 68.756 Reduced Hemoglobin 31.257 Prolonged BT and CT 18.758 Thrombocytopenia 31.259 Blood urea 46.810 ABG Derangement 46.811 Albuminuria 50Discussion:Hair dye containing PPD is used for haircolouration and is added to Henna to accentuate thecolour when used on the skin. Over-doses with thischemical is common, and can be fatal if taken inlarge quantities.Death is usually caused by angioneuroticedema or arrhythmias due to direct cardiotoxicity ofPPD cases of poisoning of PPD which develops renalfailure require dialysis. The cause of renal injury isprobably direct nephrotoxicity of compound.Rhabdomyolysis caused by PPD is also a cause ofARF in these patients.The lethal dose of PPD is not known;estimates vary from 7-10 grams. The characteristicchocolate brown colour of the urine could beconfirmative evidence of hair dye poisioning inindividual with the poisioning of PPD (Presence ofhair dye in urine can be confirmed by this layerchromatography in the lab). First case of systemictoxicity with PPD was described by the Nott in 1924in the owner of a hair saloon. [7] A report fromSudan described a series of 18 cases of acute hair dyepoisoning. Sood et al and Chug et al have reportedhair dye poisoning from India. [8, 9]Clinical studies were also done by Ansory etal 1983, [1] Fathi et al 1995, [2] Kamil and Devidson1996, [3]Yagi et al 1996, [5] Ababou et al 1995,Ayuoub Filali, Llham Semlali 2006. [4] All ourpatient took poison intentionally with a suicidalintent. In the study of Ayoub et al & Yagi et al fewcases were accidental but most of the cases were seenwith suicidal intent. [4, 6]In our study entire poisioning was byIngestion. The toxic effects of PPD are many. Themost explainable in the combined effect to kidneyresulting from hypoxia, dehydration, intravascularhemolysis, methemoglobinea and a direct toxic effectof the chemical or its by products on the renaltubules. Rhabdomyolysis may also contribute to renalfailure. [10, 11] In our study total leucocutes countwas raised in 78.125 percent cases 62.5 cases wereraised liver enzymes, S. creatinine and blood ureawas raised in 46.88 percent cases, these patients alsohave deranged ABG. Albumunaria seen in 50percent case prolonged BT, CT in 18.75 percentcases, thrombocytopenia in 31.25 percent cases. 6cases were Refered for dialysis were expired,mortality was 18.75%. mortality was 21.1% is studyby Ayoub et al [4, 6] and 41.9 in study by M, SirHasim et al and 22% in study by Yagi et al. [6] Themortality was less in our study probably because ofingestion of low amount of dye, and early treatmentof patient.Conclusion:The systemic effects of PPD poisoning haveserious consequences which may eventually lead todeath. The Lethal dose of PPD is not known;estimates from 7-10 grams. The mechanisms of acutetubular necrosis are many. The most of the injuriesresulting from hypoxia dehydration, intravascularhaemolysis, Methaemoglobinaemia and direct toxicactions of chemical or it‟s by products on the renaltubules.This study showed that PPD poisoning wasfatal in about 18.75 percent cases. The poisoning ofPPD was not more common in this region previously.Previously cases of Celphos poisoning weremore but due to the strict control of sale of Celphos,poisoning of hair dye (PPD) is more common thesedays. The controlled supervision over selling of hairdye is necessary to stop PPD poisoning. Werecommend that the selling of hair dye containingPPD should be banned and public educationprogramme should be initiated in this regard so thatmortality from PPD may be prevented, becauseavailability of PPD in home causes easy accessibilityof this poison.References:1. El. Ansary, E.H., Ahmed, M.K., Clague H.W., (1983).Systemic toxicity of paraphyelendiamine. Lancet, I, 1341.2. Fatihi, E., Laraki, M., Zaid, D., Benaguida, M., (1995).Toxicite systemique de la paraphenylene diamine a propos de13 cas. Rea Urg 4, 671-673.3. Kamil A., A.A. Davidson. N.m., (1996). A woman whocollapsed after painting her soles. Lancet B: 658.4. Ayoub Filali, Llham Semlali et al. A retrospective study ofacute systemic poisoning of paraphenylendediamine inMorocco. African Journal 2006. Vol-3, Num, 1, 2006, pp.142-149.5. Yagi H.I., El Hindi, A.M., Diab, A., Elshikh, A.A., (1996).Paraphenylendediamine induced optic atrophy following hairdye poisoning. Hum exp Toxicol 15:617-618.6. Yagi H.I., El Hindi, A.M., Khalil, S.I. (1991). Acutepoisoning from hair dye. East Afr. Med. J. 68: 404-411.7. Nott HW. Systemic poisoning by hair dye. The Br Med J1924; 1:421-2.8. Sood AK, Yadav SP, Sood S et al. Hair dye poisoning. JAssoc Physicians lnd 1996; 44 (1):69.9. Chugh KS, Malik GH, Singhal PC. Acute renal failurefollowing paraphenylenediamine (hair dye) poisoning.Report of 2 cases. Journal of Medicine 1982; 131-7.10. Gabow PH, Kachny WD, Kelleher SP. The spectrum ofrhabdomyolysis. Medicine 1982; 61:14-52.11. Suliman SM, Homedia M Aboval Ol.Paraphenylenediamine induced acute tubular necrosisfollowing hair dye ingestion Human Toxicol 1983; 2:633-5.164
J Indian Acad Forensic Med, <strong>32</strong>(2) ISSN 0971-0973Case reportAcute Myocardial Infarction related to blunt Thoracic Trauma:Review of literature with two case reports*Dr Amit Sharma, MDAbstractCardiac injury occasionally occurs as a result of blunt chest trauma. Most cardiac complications in chesttrauma are due to myocardial contusion rather than direct damage to the coronary arteries. Coronary artery injuryrarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequentlyoverlooked. However, traumatic coronary injury has been reported, and a variety of underlying pathophysiologicalmechanisms have been proposed. For young adults, blunt chest trauma is one of the non-atherosclerotic mechanismsleading to acute myocardial infarction. Not only a severe trauma, but also a mild trauma such as sports trauma cancause acute myocardial infarction. Myocardial infarction after blunt chest trauma, however, is an extremely rareentity with most cases received conservative therapy. Here two cases of acute myocardial infarction due to bluntthoracic trauma are described in patients who were previously healthy and had no symptoms suggestive of coronaryartery disease.Key Words: Blunt Thoracic Trauma; Traumatic Coronary Injury; Acute Myocardial InfarctionIntroduction:In blunt chest trauma patients, it is importantto consider myocardial injury, which is mostly theresult of myocardial contusion. The consequences ofcontusion include ECG-changes, arrhythmia andnecrotic damage of the heart muscle. Direct damageto the coronary arteries however is a rare finding.Acute myocardial infarction (AMI) is described as arare complication of blunt thoracic trauma (BTT),although there is no accurate data available regardingthe true incidence of this condition.Early diagnosis is difficult due to thenonspecific post-trauma clinical picture presented bypatients. BTT may cause damage to the myocardium,cardiac valves, coronary arteries and pericardium,leading to serious complications such as arrhythmiasand sudden death. [1, 2, 3] In promoting acceleration,deceleration or direct compression of the chest, thetrauma can cause acute myocardial infarction throughthe following proposed mechanisms: dissection ofcoronary arteries, coronary thrombosis, vasospasmand rupture of atherosclerotic plaque. [4]This paper deals with two case reports ofpatients who evolved with AMI after a BTT, as wellas a review of literature.Corresponding Author:*Dr Amit Sharma,Senior Resident,Department of Forensic Medicine,Maulana Azad Medical College, New DelhiEmail: dr_amitsharma@hotmail.comCase Reports:Case 1:A 25 yrs old auto rickshaw (private threewheeler taxi) driver was rushed to the emergencyblock in unconscious state with history that hisvehicle overturned while negotiating a sharp turn. Hewas declared dead on arrival. During autopsyexamination it was noted that the deceased was ofaverage built and multiple contused grazed abrasionswere present over front of chest and abdominalregion, the largest being of size 5cmX4cm. Oninternal examination, effusion of blood present overthe thoracic and intercostal muscles. The thoraciccage was intact. Heart weighs 284gm. Onexamination of coronaries, the left anteriordescending artery lumen shows 85% block. All otherfindings were insignificant.Case 2:A 55 yrs old male was assaulted by hisneighbors over an issue of parking the car. Heallegedly received blows over his chest as stated byeyewitnesses. The person becomes unconscious aftersuffering the assault and was taken to the nearbyhospital where he was declared dead on arrival. OnPostmortem examination, he was of average built andwas wearing four layers of clothing‟s over his upperpart of the body, out of which one was a thick woolensweater and other is a leather jacket. On externalexamination minor abrasions were noted to bepresent over both elbow and knee regions. No otherinjuries present. During internal examination, thethoracic cage was intact and no internal contusions165