Forensic medicine and toxicology 3rd

Review of Forensic Medicine and Toxicology Review of Forensic Medicine and Toxicology Including Clinical and Pathological Aspects MCQs of Previous Years PG Entrance Examinations Included Third Edition Gautam Biswas MD (UCMS) Professor and Head Department of Forensic Medicine and Toxicology Dayanand Medical College and Hospital Ludhiana, Punjab, India Forewords George Paul Satish K Verma The Health Sciences Publisher New Delhi | London | Philadelphia | Panama Jaypee Brothers Medical Publishers (P) Ltd Headquarters Jaypee Brothers Medical Publishers (P) Ltd 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 Email: jaypee@jaypeebrothers.com 2YHUVHDV2I¿FHV J.P Medical Ltd 83 Victoria Street, London SW1H 0HW (UK) Phone: +44 20 3170 8910 Fax: +44 (0)20 3008 6180 Email: info@jpmedpub.com Jaypee-Highlights Medical Publishers Inc City of Knowledge, Bld 237, Clayton Panama City, Panama Phone: +1 507-301-0496 Fax: +1 507-301-0499 Email: cservice@jphmedical.com Jaypee Brothers Medical Publishers (P) Ltd 17/1-B Babar Road, Block-B, Shaymali Mohammadpur, Dhaka-1207 Bangladesh Mobile: +08801912003485 Email: jaypeedhaka@gmail.com Jaypee Brothers Medical Publishers (P) Ltd Bhotahity, Kathmandu, Nepal Phone +977-9741283608 Email: kathmandu@jaypeebrothers.com Jaypee Medical Inc The Bourse 111 South Independence Mall East Suite 835, Philadelphia, PA 19106, USA Phone: +1 267-519-9789 Email: jpmed.us@gmail.com Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2015, Jaypee Brothers Medical Publishers The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and not necessarily represent those of editor(s) of the book All rights reserved No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners The publisher is not associated with any product or vendor mentioned in this book Medical knowledge and practice change constantly This book is designed to provide accurate, authoritative information about the subject matter in question However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications It is the responsibility of the practitioner to take all appropriate safety precautions Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book This book is sold on the understanding that the publisher is not engaged in providing professional medical services If such advice or services are required, the services of a competent medical professional should be sought Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material If any have EHHQLQDGYHUWHQWO\RYHUORRNHGWKHSXEOLVKHUZLOOEHSOHDVHGWRPDNHWKHQHFHVVDU\DUUDQJHPHQWVDWWKH¿UVWRSSRUWXQLW\ Inquiries for bulk sales may be solicited at: jaypee@jaypeebrothers.com Review of Forensic Medicine and Toxicology First Edition: 2010 Second Edition: 2012 Third Edition: 2015 ISBN 978-93-5152-864-7 Printed at With lots of love to my son Gaurav & All my students—past, present and future Foreword This textbook, aimed for the medical undergraduate for preparing him/her for the various long and short questions on the subject of Forensic Medicine and Toxicology as taught to medical undergraduates all over India, as well as MCQs of nearly all the various entrance test exams for postgraduation, is an extensive labor of love, in an attempt to present the subject in a most systematic and organized manner The approach is to make mining FQYP VQ ſPG FGVCKNUōGKVJGT HQT C NQPI GUUC[ SWGUVKQP QT VQ QTICPK\G QPGŏU CPUYGT HQT C short text answer, easier, and in that sense it has well succeeded All the various headings coming under the broad chapter of Forensic Medicine and Toxicology have been broken down very clearly into sub-topics and subheadings Where the subject leads to some important questions and answers often required of the medical witness, they are presented in addition, at the end of the chapter, as question and answers The author has also put in a lot of effort to cull from all possible sources, MCQs that have been made in the past on the various subjects – itemized them with their source reference listed (i.e the various entrance exams they have been used in), and given the most appropriate answer to the question, based on the construction of the sentences, or the stem or statement However this book, being primarily a resource book for undergraduates and those graduates appearing in XCTKQWU RQUVITCFWCVG CPF TGETWKVKPI EQOOKUUKQPŏU GZCOU KU VCKNQTGF VQ YJCV KU GZRGEVGF QH VJG UVWFGPV HTQO the current set of forensic examiners, rather than updating all users of the textbook to the current concepts and recent advances and norms in practice, of some of these topics And one can hardly blame the author for this, because, looking at the current MCQs listed at the end of chapters of toxicology and other sections, some of VJGUG GZCO UGVVGTU CTG UVKNN KP VJG RTCEVKEG QH HQTGPUKE OGFKEKPG CPF VJG MPQYNGFIG QH KV VJGTGQH QH VJG ŏU CPF ŏU TCVJGT VJCP VJG PGY OKNNGPPKWO #PVKFQVGU CTG UVKNN GPVTGPEJGF KP QWVFCVGF ENKPKECN EQPEGRVU QH ŎWPKXGTUCN CPVKFQVGŏ CPF DWTPV VQCUV HQT CEVKXCVGF EJCTEQCN CPF QPG ECPPQV DNCOG VJG CWVJQT HQT KV HQT VJGUG XCTKQWU entrance exams extensively feature knowledge of this in their selection MCQs While the chapters on sexual abuse cover the legal and medical features well, the emphasis in the chapter on detection of seminal stains for establishing sexual intercourse with the victim is still stuck with outdated tests, which have been given up in modern countries and replaced by their DNA and forensic labs test such as screening with PSA and Seminogelin jointly and then progress to DNA markers using single-locus-probes or multi-loci probes 6GEJPQNQI[JCUCFXCPEGFCPFUQOGQHKVJCUHQWPFVJGKTRNCEGKP(QTGPUKE/GFKEKPG(QTGPUKETCFKQNQI[ōWUG QHTCFKQNQIKECNVGEJPKSWGU PQVVJGWDKSWKVQWUŎXKTVQRU[ŏKPCUUKUVKPIHQTGPUKEYQTMJCUTGUWNVGFKPCSWKVGCHGY clinical radiologists taking special interest and training in forensic radiology, as there are vast differences between imaging and techniques possible in the living and dead At an undergraduate level, textbooks of quality such as these should incorporate key features where its techniques are now baseline for diagnosis or investigations KP UQOG HQTOU QH UWFFGP FGCVJ KFGPVKſECVKQP RCTCOGVGTU FGCVJU HTQO DCTQVTCWOCUōGURGEKCNN[ FKXKPI FGCVJU etc But I would not be surprised if the inclusion of these would get the candidates into trouble during their exams, as many of the examiners are still anachronistic in their understanding of many of these topics, and have never put any of them to use /QFGTPEQPEGRVUUWEJCUDTCKPFGCVJōTGNCVGFVQQTICPJCTXGUVKPIKUCPKORQTVCPVEQPEGRVYJKEJYKNNHGCVWTG quite a bit in clinical practice, as it is doing overseas The young medical graduate should be brought onto a sound basis on these by textbooks such as this 5QOG QH VJG YGNNRTGUGPVGF EJCRVGTU FGUGTXG OGPVKQPKPI 6JWU VJG EJCRVGT QP LWTKURTWFGPEG KPLWTKGUōVJGKT OGFKEQNGICN KORQTVCPEG ſTGCTOU VJGTOCN KPLWTKGU KFGPVKſECVKQP GURGEKCNN[ VJG OGFKEQNGICN KORQTVCPEG QH CIG YJKEJ ſPFU ITGCV UKIPKſECPEG KP VJG /%3UōVJQWIJ KP HCEV KU LWUV C NGICN KPVGTRTGVCVKXG RCTV RTGIPCPE[ viii Review of Forensic Medicine and Toxicology and delivery, sexual offences, forensic psychiatry, toxicological chapters such as mercury, cannabis, cocaine, belladonna, cardiac poisons, carbon monoxide, agricultural poisons, aluminum phosphide, kerosene poisoning and food poisoning are quite adequate for an undergraduate level and are well presented with good coverage for even answering MCQs There are good coverage of general concepts in the chapters on explosions and falls HTQO JGKIJV UVCTXCVKQP FGCVJU VQTVWTG FGEQORTGUUKQP UKEMPGUU KPHCPVKEKFG CPF EJKNF CDWUG URGEKſE VQRKEU KP toxicology such as corrosives, alcohol, opioids, medicinal drugs, snakebite, cyanide, drug dependence and war gases, such that the candidate has a good overview of these topics All in all, this textbook is well organized The layout makes breaking up and assimilating the various diverse topics that come under its ambit – easy, and systematic, with an approach which makes it easy and effective KP QTICPK\KPI QPGŏU MPQYNGFIG CPF VJQWIJVU QP GCEJ UWDLGEV (QT QPEG DCUGF QP VJG EJCRVGTU TGXKGYGF + would recommend this book as a good basic reference book for undergraduates, to prepare them both for their university exams and entrance tests I look forward to further amendments which would raise this textbook to QPG QH ITGCV EWTTGPV TGNGXCPEG VJTQWIJ TGXKUKQPU QP UQOG QH VJG UOCNN FGſEKGPEKGU VJCV JCXG DGGP QDUGTXGF  +YKUJ2TQH)CWVCO$KUYCUITGCVUWEEGUUKPVJKUTFGFKVKQPQHVJG4GXKGYQH(QTGPUKE/GFKEKPGCPF6QZKEQNQI[ō Including Clinical and Pathological Aspects, and congratulate him for single-handedly maintaining great standards and depth of knowledge, as well as keeping up-to-date with the needs of the medical undergraduates all over +PFKC HQT RTGRCTKPI VJGO HQT VJGKT TGURGEVKXG WPKXGTUKV[ŏU WPFGTITCFWCVG CPF XCTKQWU RQUVITCFWCVG GPVTCPEG examinations George Paul Senior Consultant Forensic Pathologist and Branch Director-Technical Capabilities Forensic Medicine Division, Applied Sciences Group, Health Sciences Authority, 11 Outram Road, Singapore 169078 and Senior Lecturer-Yong Loo Lin School of Medicine National University of Singapore Foreword It is indeed a moment of immense pleasure and sense of pride to write a foreword for a book authored by one of my most sincere, hardworking and brightest students to whom fortunately I introduced the art and science of the specialty of Forensic Medicine and Toxicology, both as undergraduate and postgraduate at UCMS # VGCEJGT QT C IWKFG HGGNU URGEKCN CPF RTKXKNGIGF YJGP JKU UVWFGPVU GZEGN KP VJG ſGNF initiated by him, the words are too timid to describe this feeling The current book is 3rd edition in the series of this title, Review of Forensic Medicine and Toxicology I have no iota of doubt about the success of this title and this will be rather loved more than the earlier versions The current title contains 63 chapters covering the entire MCI undergraduate curriculum, presented in a student friendly fashion I have gone through, some of the chapters of this title and found them even more informative and attractive than previous ones with lots of new information being added Major changes and updates have been provided in chapters such as: Medical jurisprudence and ethics (MCI, Declarations of WMA, informed consent, euthanasia), Acts (POCSO Act, Sexual Harassment of Women at Workplace Act, Protection QH 9QOGP HTQO &QOGUVKE 8KQNGPEG #EV CPF +FGPVKſECVKQP GVE A special feature of the book is MCQs drawn from various PG entrance and other competitive examinations at the end of each chapter making it more relevant to undergraduates even after passing 2nd Professional MBBS examination $[ PQY )CWVCO + WUWCNN[ ECNN JKO D[ JKU ſTUV PCOG FWG VQ O[ URGEKCN NQXG JCU GUVCDNKUJGF JKOUGNH CU C RTQNKſE CWVJQT CPF + CO UWTG VJCV VJKU GFKVKQP YKNN CFF CPQVJGT HGCVJGT KP JKU UWEEGUU UVQT[ May God bless him… Satish K Verma Professor Department of Forensic Medicine and Toxicology University College of Medical Sciences Former Head Department of Forensic Medicine (University of Delhi) 535 Organic Irritans—Animal Systemic reactions occur due to multiple stinging YKVJ UKIPU QH )+6 FKUVWTDCPEG PCWUGC XQOKVKPI CPF FKCTTJGCUYGCVKPIDTQPEJQURCUOJ[RQVGPUKQPUJQEM and unconsciousness Immediate anaphylactic reactionsOC[DGUGGPKPUQOG ECUGU 0CWUGC XQOKVKPI FKCTTJGC WTVKECTKC UYGNNKPI VCEJ[ECTFKCJ[RQVGPUKQPTGURKTCVQT[FKUVTGUUHCKPVPGUU CPF WPEQPUEKQWUPGUU OC[ DG UGGP &GCVJ OC[ QEEWT KP Ō OKP 6TGCVOGPV i Tourniquet is applied proximal to the site of the sting and incision is given The sting is located CPF TGOQXGF D[ UETCRKPI QT WUKPI VYGG\GTU +EG or cold packs are applied  KK 6JG CTGC KU VJGP ENGCPGF YKVJ UQCR CPF YCVGT and tincture of iodine or local application QH CPVKJKUVCOKPG QT J[FTQEQTVKUQPG ETGCO KU useful  KKK #FTGPCNKPG KU IKXGP VQ EQODCV U[UVGOKE TGCE tions  KX %CNEKWO INWEQPCVG Ō I +8 v Glucocorticoids are useful for urticaria  XK #TVKſEKCN TGURKTCVKQP CPF 1 inhalation is given XKK 6GVCPWU KOOWPK\CVKQP KU TGEQOOGPFGF MULTIPLE CHOICE QUESTIONS Cobras belong to: NEET A Viperidae B Elapidae C Colubriadae D Crotalidae All are true about poisonous snakes, H[FHSW: PGI A Nocturnal in habit B. *CXG EQORTGUUGF VCKN C. *CXG UQNKF CPF UVQWV HCPIU D. *CXG NCTIG UECNGU QP JGCF True of poisonous snakes are all, H[FHSW: Delhi A. (CPIU RTGUGPV B. $GNN[ UECNGU CTG UOCNN C Small head scales D Grooved teeth Snake that causes paralysis with convulsions: NEET A Vipers B Sea snakes C Cobra D Krait Cobra poison is: Kerala 09; FMGE10; Bihar A Neurotoxic B. /[QVQZKE C Cardiotoxic D Vasculotoxic Neurotoxin in which snake: NEET A Viper B Krait C Sea snake D None Viper venom is: AIIMS A Neurotoxic B Vasculotoxic C. /[QVQZKE D Cardiotoxic Snakebite causing hematologic abnormalities: NEET A Cobra B Krait C Viper D Sea snake Cholinesterase is seen in venom of: DNB A Elapids B Vipers C Sea snakes D. #NN 13 14 06 14 12 13 14 13 08 B C & D B C A 11 A 12 B 13 D 14 C 15 A 10 Lethal dose of krait venom: AP 11 A.  OI B  OI C.  OI D.  OI 11 Ophitoxemia is: BHU 12 A Snakebite poisoning B. 2JGPQN RQKUQPKPI C Chronic lead poisoning D Opium poisoning 12 Most characteristic feature of elapidae snake envenomation: UPSC 09 A Bleeding manifestation B 0GWTQRCTCN[VKE U[ORVQOU C 4JCDFQO[QN[UKU D %CTFKQVQZKEKV[ 13 A patient presented with history of snakebite along with ptosis, paralysis and external ophthalmoplegia Most probable species implicated: CMC (Vellore) 13, 14 A Sea snake B Krait C Viper D Cobra 14 A girl, otherwise healthy, sleeping on the floor suddenly develops nausea, vomiting, abdominal pain, quadriplegia at night Diagnosis is: NIMS 11 A )WKNNCKP $CTTG U[PFTQOG B 2QNKQO[GNKVKU C Krait bite D 2GTKQFKE RCTCN[UKU 15 Muscle paralysis is caused by bite of: Kerala 11 A Sea snake B Krait C /CODC D 2[VJQP B B C A 10 B 536 Review of Forensic Medicine and Toxicology 16 Treatment of snakebite all, H[FHSW: AFMC 11 A (KTO DCPFCIG VQ QEENWFG N[ORJCVKE B +PEKUKQP QXGT YQWPF C Reassure the patient D +OOQDKNK\CVKQP QH DKVVGP RCTV 17 Following is/are recommended primary management of a patient with snake bite, H[FHSW: PGI 11; NEET 13 A 5RNKPVKPI CPF KOOQDKNK\CVKQP B -GGR VJG UKVG QH DKVG DGNQY JGCTV C 9CUJ YKVJ UQCR CPF YCVGT D Reassure the patient 18 Ligature pressure that should be used to resist spread of poison in elapidae poisoning: WB 11; MAHE 12 A   OO *I B Ō OO *I C Ō OO *I D   OO *I 19 Polyvalent snake vaccines contains immunoglobins against all, H[FHSW: PGI 11 A Ophiophagus hannah B Naja naja C Daboia rusellii D Bungarus caeruleus 20 In a snake envenomation, antivenom is started by giving a dose of: NEET 14 A  XKCNU B vials C  XKCNU D  XKCNU 21 Antisnake venom may cause: CMC (Vellore) 13 A 6[RG ++ J[RGTUGPUKVKXKV[ TGCEVKQPU B 6[RG +++ J[RGTUGPUKVKXKV[ TGCEVKQPU 16 B 26 D 17 C 18 C 19 A 20 C 22 23 24 25 26 C. 6[RG +8 J[RGTUGPUKVKXKV[ TGCEVKQPU D. 6[RG 8 J[RGTUGPUKVKXKV[ TGCEVKQPU Drug used for muscarinic symptoms seen in cobra envenomation: CMC (Vellore) 13 A Neostigmine B. 2TCNKFQZKOG C. 2TC\QEKP D Naloxone Priapism occurs in: AIIMS 06; 13 A Snake bite B Rati poisoning C Cantharide poisoning D. #TUGPKE RQKUQPKPI Scorpion venom resembles venom of: NEET 14 A Cobra B Viper C Krait D. #NN QH VJG CDQXG A 3-year-old child sleeping in a hut woke up in the middle of the night screaming Her mother thought the child had a nightmare and tried to pacify her After sometime, she noticed that the child was sweating profusely and the hands were becoming cold She vomited a couple of times The mother immediately rushed her to the emergency services Her pulse was 150/minute and her BP 90/60 mmHg This child is likely to have: COMEDK 14 A Snake bite B Scorpion bite C Septic shock D. (QQF RQKUQPKPI Drug used in scorpion bite: CMC (Vellore) 13, 14; COMEDK 14 A. '&6# B Neostigmine C. 0CEGV[NE[UVGKPG D. 2TC\QUKP 21 B 22 A 23 C 24 D 25 B CHAPTER 47 Somniferous Poisons (Narcotic Poisons) &GſPKVKQPU „ „ „ „ Narcotic: It refers to a sleep inducing agent, and initially used to mean the opioids Currently, the term is used by law enforcement agencies to indicate any illicit psychoactive substance Opiate: It refers to natural alkaloids derived directly from the poppy plant Opioids: They are broader class of agents that are capable of producing opium-like effects on binding to opioid receptors Endogenous neural polypeptides such as endorphins and enkephalins are natural opioids Toxidrome: A constellation of clinical examination ſPFKPIU VJCV CUUKUVU KP VJG FKCIPQUKU CPF VTGCVOGPV of the patient who presents with an exposure to an unknown agent 1RKWO Introduction: Opium (poppy, afim, kasoomba or madak chandu) is derived from Papaver somniferum, an CPPWCN RNCPV YKVJ YJKVG QT TGF ƀQYGTU ITQYKPI QP C central bulbous pod (Fig 47.1) Crude opium has a characteristic odor and bitter taste Distribution: Worldwide Toxic part: Unripe fruit capsule, latex juice.1 „ Latex is obtained by lacerating (‘scoring’) the immature seed pods; the latex leaks out and dries Fig 47.1: Papaver somniferum „ to a sticky brown residue (Fig 47.1) This is scraped off the fruit Seeds are non-poisonous and are called ‘khaskhas’ which constitutes a condiment in cooking (Fig 47.2) #EVKXG 2TKPEKRNGU The latex juice of opium has about 25 alkaloids, divided into two groups a Phenanthrene derivatives (main narcotic constituents) i Natural alkaloids z Morphine (10%): White powder/crystals, bitter taste and alkaline in reaction z Codeine (0.5%) z Thebaine (0.3%) ii Semi-synthetic opioids: They are produced by EJGOKECN OQFKſECVKQP QH CP QRKCVG CPF KPENWFG hydromorphone, diacetylmorphine (heroin, brown sugar or smack), oxymorphone and oxycodone iii Synthetic opioids: These compounds are not derived from an opiate, but binds to an opioid receptor and produce opioid effects clinically It includes methadone, fentanyl, pentazocine, tramadol and meperidine (pethidine).2 b Benzyl-isoquinolone derivatives PQUKIPKſECPV%05 effects)3 i Papaverine (1%)  KK 0QUECRKPG  Fig 47.2: Poppy seeds (Non-poisonous) 538 Review of Forensic Medicine and Toxicology   Alkaloids are complex substance having nitrogenous base, and is found in various plants Chemically, it behaves like an alkali as it unites with acids to form salts Its basic quality depends on the pyridine nucleus In nature, they are usually combined with certain acids to from salts They act mainly on the CNS, each compound having its own individual action Important alkaloids: Atropine, hyoscine, morphine, quinine, strychnine, cocaine and codeine Some synthetic substances, such as amphetamine, heroin, pethidine and methadone also behave chemically like alkaloids.4 „ „ /GVCDQNKUO „ „ Most opioids are metabolized by hepatic conjugation to inactive compounds that are excreted readily in the urine Certain opioids (e.g propoxyphene, fentanyl and buprenorphine) are more soluble in lipids and can be stored in the fatty tissues of the body %.+0+%#. 61:+&41/' #EVKQP „ be mixed with cocaine (known as speed balling) and then taken by addicts.5 Opioids act by binding to opioid receptors on neurons distributed throughout the nervous system and immune system Four major types of opioid receptors have been identified: mu, kappa, delta and the recently TGEQIPK\GF1(306JGUGTGEGRVQTUCTGVJGDKPFKPI sites for endogenous peptides Activation of opioid receptors results in inhibition QH U[PCRVKE PGWTQVTCPUOKUUKQP KP VJG %05 CPF 205 Routes of administration: It can be taken by snorting, smoking or chasing (chasing the dragon), intravenously (mainlining) and subcutaneously (skin popping) It can Some poisons may produce a collection of symptoms (toxidromes) that can assist in making diagnosis and are also useful for anticipating other symptoms that may occur (Table 47.1) The symptoms of an opiate/ narcotic toxidrome include the classic triad of respiratory depression, pin-point pupils and impairment of sensorium 5KIPU CPF 5[ORVQOU Peak effects are seen in 10 minutes (min) with IV route, Ō OKP CHVGT PCUCN KPUWHƀCVKQPU Ō OKP YKVJ +/  OKP CHVGT VCMKPI QTCNN[ CPF Ō JQWTU J CHVGT dermal application i Stage of Excitement: It is of short duration There is euphoria, increased sense of well-being, freedom Table 47.1: Clinical toxidromes Toxidrome Clinical features Common poisons Treatment Site of action Opiate Respiratory depression and oxygen desaturations, miosis, decreased GI motility, bradycardia, hypothermia and coma Morphine, codeine, oxycodone, fentanyl Naloxone Opioid receptor Anticholinergic Tachycardia, hyperthermia (mild to severe), agitation, delirium, seizures, mydriasis, dry, flushed skin, urinary retention, decreased intestinal motility Datura, atropine, scopolamine, antihistamines Physostigmine Muscarinic acetylcholine receptors Sympathomimetic Hypertension, tachycardia, pyrexia, pupillary dilatation, diaphoresis, altered mental status Cocaine, amphetamines Benzodiazepines α and β adrenergic receptors Cholinergic Bradycardia, respiratory depression, (Organophosphate and miosis, SLUDGE (salivation, carbamates) lacrimation, urination, defecation, GIT distress, emesis) CNS: Seizures, coma Muscle: Fasiculations, paralysis DDT, parathion, malathion, diazinon Atropine Pralidoxime (for OP insecticides) Nicotinic and muscarinic acetylcholine receptors Sedative hypnotic (Benzodiazepines) Alprazolam, flunitrazepam, oxazepam Flumazenil b-aminobutyric acid receptors Sedation or coma, normal vital signs, diplopia, ataxia, impaired motor function, slurred speech, anterograde amnesia, anxiety, hallucinations, delirium ^ŽŵŶŝĨĞƌŽƵƐWŽŝƐŽŶƐ;EĂƌĐŽƟĐWŽŝƐŽŶƐͿ from anxiety, talkativeness and laughter HalluciPCVKQPUƀWUJKPIQHHCEGEQPLWPEVKXCNKPLGEVKQPCPF rapid heart rate are seen ii Stage of Stupor: Headache, nausea, vomiting, weakness, heaviness in limbs, giddiness, drowsiness, diminished sensibility and strong tendency to sleep from which the patient can be aroused by painful stimuli z Pupils are contracted, and face and lips are cyanosed z Pulse and respiration: Almost normal iii Stage of Narcosis/Coma: Patient passes into deep coma from which he cannot be aroused In this stage: z Muscles: Flaccid and relaxed z Face: Pale z 4GƀGZGU #DUGPV z Conjunctiva: Congested z Skin: Cold with profuse perspiration, all other secretions are suspended z Pupils: Constricted to pin-point (Fig 47.3), nonreacting8,9 z Blood pressure: Hypotension z Temperature: Hypothermia z Pulse: Weak, feeble z 4GURKTCVKQP 5NQY UVGCVQTQWU Ō DTGCVJU min)10 z Sphincter tone: Increased (can lead to urinary retention) During the terminal stages, pink froth comes from the mouth, pulse is slow, irregular and imperceptible, respiration becomes Cheyne-Stokes, and ultimately deep coma and death due to respiratory depression and cardiorespiratory arrest Fatal dose „ Opium: g 11 „ Morphine: 200 mg „ Codeine: 50 mg &KHHGTGPVKCN &KCIPQUKU „ „ „ „ „ Intracranial hemorrhage: Cerebrovascular accidents or brain trauma Poisoning: Alcohol, barbiturates, benzodiazepine, carbolic acid, carbon monoxide or organophosphorus Metabolic conditions: Diabetic and uremic coma CNS infections: Meningitis, encephalitis, encephalopathy or cerebral malaria Others: Epileptic or hysterical coma, or heat hyperpyrexia 6TGCVOGPV i Support vitals through respirator and other emergency procedures ii Decontamination: Stomach wash frequently with 1:5000 KMnO leaving some solution in stomach to oxidize the alkaloid that might be secreted in stomach after absorption Lavage should be carried out even after IV/IM injection of drug, as it is secreted in the stomach iii Administer activated charcoal—method of choice for decontamination following ingestion iv Enema with 30 g of sodium sulfate twice daily v Whole-bowel irrigation in body packers vi Antidote:0CTEQVKECPVCIQPKUVnaloxone in an initial FQUGQHŌOIIV/IM repeated every 2–3 upto 10 mg, if no response occurs.12 If there is little response to naloxone alone, possibility of an overdose with a benzodiazepine should be considered, and a challenge with IV ƀWOC\GPKN  OIOKP WRVQ OCZKOWO QH  OI in an hour might be used &GVGEVKQP Marquis test: It is a simple spot-test to presumptively identify alkaloids It can be used to test cocaine, opiates and phenethylamines.13 Three ml of concentrated H2SO + drops of formalin are added to the suspected sample Purple-red color is observed which gradually changes to violet Fatal period: Ō J 2QUVOQTVGO (KPFKPIU A B Figs 47.3: (A) Normal pupil, (B) Pinpoint pupil External i Smell of opium ii Face/body is bluish, deeply cyanosed or blackish iii Postmortem staining is purple or blackish iv Froth at the nostrils v Pupils are constricted, can be dilated also 539 540 Review of Forensic Medicine and Toxicology vi Allergic reactions to IV heroin may be seen XKK 0GGFNG VTCEMU CTG HQWPF QEECUKQPCNN[ FGRGPFKPI on the route of intake  Internal i Diffuse cerebral edema ii All organs are congested, trachea contains frothy secretions KKK $NQQF KU FCTM CPF ƀWKF iv Stomach may show presence of small, soft brownish lumps of opium, and smell of drug may be perceived /GFKEQNGICN #URGEVU „ „ „ „ „ „ „ „ „ „ „   0GINKIGPEG OC[ DG CNNGIGF KP ECUGU QH RTGJQURKVCN discharge-on-scene after naloxone treatment followed in most western countries, since this practice is sometimes associated with risk of death due to rebound toxicity after such episodes Opioid poisoning nowadays is from street drugs which not only have brown sugar, but also therapeutic opioids like hydrocodone or oxycodone, codeine taken with glutethemide, and abuse of Subutex (buprenorphine hydrochloride) It is a poison of choice to commit suicide (ideal suicidal poison) Homicide is rare, because of bitter taste and characteristic odor Infanticide by breastfeeding an infant by a woman who had smeared her nipple with tincture opium Accidental opium poisoning is also common Drugging of children by opium to keep them quiet, and overdose of medicines may result in accidental poisoning.* Various nonproprietary formulations, folk remedies, and herbs may contain opium, and administration of these results in unintentional poisoning Sometimes, opium is used for doping racehorses It is said to increase libido, hence used as an aphrodisiac Some criminals take opium to build courage before committing a crime Opium disappears with putrefaction, so it may not DG FGVGEVGF KP RWVTGſGF DQFKGU It should be noted that opioid exposure does not always result in pupillary constriction, and respiratory depression is the most specific sign.10 Other important presenting signs are ventricular arrhythmias, acute mental status changes and seizures Acute lung injury is known sequelae of heroin, propoxyphene and methadone overdose, and present in fatal cases of opioid overdose The findings are cyanosis, dyspnea, pink frothy sputum, rales, tachypnea and tachycardia  Earlier opioid overdose was treated with analeptics In 1950s, specific antidotes were introduced: nalorphine and levallorphan which were capable of reversing the respiratory effects by blocking the opioid receptors However, they have a mixed agonist-antagonist properties that significantly limited their usefulness Naloxone with its pure opioid antagonistic properties completely replaced nalorphine and levallorphan in the treatment of opioid overdose Nalmefene and naltrexone are newer opioid antagonists that have longer half-lives than naloxone (4–8 h and 8–12 h vs h) The routine use of a long-acting antagonist in the patient who is unconscious for unknown reasons is not recommended $QF[ 2CEMGTU „ „ „ „ Multiple-wrapped packets of illicit drugs (cocaine or heroin) may be ingested or inserted into body cavities by ‘swallowers,’ ‘internal carriers,’ ‘couriers,’ or ‘mules’ to intentionally transport drugs from one country to another After they arrive at their destination, cathartics are administered so that the packets can be passed and delivered When the authorities discover such individuals or when individuals in custody become ill, they may be brought to a nearby hospital for evaluation and management Although, these patients generally are asymptomatic on arrival, they are at risk for delayed, prolonged or lethal poisoning as a consequence of packet rupture If there is a suspicion of body packing or body UVWHſPI ECTGHWN ECXKV[ UGCTEJGU QH VJG TGEVWO CPF XCIKPC CTG FQPG #P CDFQOKPCN :TC[ ECP EQPſTO the diagnosis Ultrasonography and CT are other recommended diagnostic modalities Polyethylene glycol electrolyte lavage solution is WUGF VQ ƀWUJ QWV VJG RCEMGVU +PVGUVKPCN RGTHQTCVKQP or obstruction by the packets may require surgical intervention %JCUKPI VJG &TCIQP „ „ +PVTCXGPQWUKPLGEVKQPCPFKPUWHƀCVKQPCTGVJGRTGHGTTGF means of heroin self-administration in the US In the QVJGT EQWPVTKGU KPENWFKPI VJG 0GVJGTNCPFU 7- CPF Spain, the prevalent method is ‘chasing the dragon’ In this, users inhale a thick, white pyrolyste that is generated by heating heroin base on aluminum HQKNWUKPICJCPFJQNFƀCOG6JKUOGCPUQHCFOKPK stration produces heroin concentration similar to those observed following IV administration * In the early 18th century in the UK, with industrial revolution, 18 h workdays, extra cost in feeding and loss of sleep due to infant’s ETKGU XCTKQWU EQPEQEVKQPU QH QRKWO YGTG URGEKſECNN[ FGUKIPGF HQT VJG RWTRQUG QH SWKGVKPI WPTWN[ EJKNFTGP ^ŽŵŶŝĨĞƌŽƵƐWŽŝƐŽŶƐ;EĂƌĐŽƟĐWŽŝƐŽŶƐͿ „ Chasing the dragon is not a new phenomenon, but it has gained acceptance recently among both IV heroin users and non-addict individuals %JTQPKE /QTRJKPG 2QKUQPKPI /QTRJKPKUO „ „ „ Opioid dependence is seen among patients with chronic pain syndromes, and the physicians, nurses and pharmacists because of its easy access The most important dependence producing derivatives are morphine and heroin Heroin is more addicting than morphine and can cause dependence after a short period of exposure Tolerance to heroin occurs rapidly and can be increased to more than  VKOGU VJG ſTUV FQUG PGGFGF The important complications of chronic opioid use may include one or more of the following: 541 i Due to illicit drug (contaminants): Peripheral neuropathy, amblyopia, degeneration of globus pallidus, Parkinsonism and transverse myelitis ii Due to intravenous use: Skin infections, thrombophlebitis, AIDS, hepatitis, pulmonary embolism, endocarditis, osteomyelitis, pneumonia, septicemia and tetanus (GPVCP[N Fentanyl is 50–l00 times more potent than morphine It is the preferred drug of abuse of anesthesiologists It is available both in hospitals and illicitly It can be taken IV, orally, smoked, snorted or by way of skin patches, with the IV route the most common Therapeutic levels are low (1–3 ng/ml) Fatalities are seen at levels beginning at ng/ml MULTIPLE CHOICE QUESTIONS Opium is derived from: NEET 13 A Leaf B Root C Poppy seed D Unripe capsule Which of these is not an opioid agonist: AIIMS 10 A Heroin B Ketamine C Methadone D Fentanyl Which of the following is least narcotic: AIIMS 09 A Morphine B Codeine C Thebane D Papaverine All are alkaloids, H[FHSW: BHU 10 A Morphine B Physostigmine C Atropine D Abrine Route not used by addicts for morphine: WB 07 A Intravenous B Intramuscular C Subcutaneous D Oral A 28-year-old male patient is brought to casualty in comatose state with pin-point pupils, reduced respiratory rate and bradycardia Most likely diagnosis: UPSC 09; CMC (Vellore) 14 A Tricyclic antidepressant poisoning B Opioid poisoning C Benzodiazepine poisoning D Organophosphorus poisoning D B D 11 B 12 A 13 C D D All are features of acute morphine poisoning, H[FHSW: Kerala 11; MAHE 12 A Pin-point pupil B Hyperpyrexia C Fall in blood pressure D Slow labored breathing Pin-point pupils are seen in: Kerala 09; Punjab 09; UP 10 A OPC poisoning B Opium poisoning C Alphos poisoning D Dhatura poisoning Pupil condition in opium poisoning: NEET 13 A Miosis B Mydriasis C. +TTGIWNCT & 0Q EJCPIG 10 Most common feature of opiate poisoning: NIMHANS 11 A Respiratory depression B Hypotension C Bradycardia D Hypothermia 11 Fatal dose morphine is: BHU 12 A 100 mg B 200 mg C 300 mg D 500 mg 12 Opium poisoning is treated with: MAHE 06; Bihar 12; UPSC 13 A. 0CNQZQPG B Atropine C. 0GQUVKIOKPG D Physostigmine 13 Marquis test is done for: BHU 08 A Mercury poisoning B Arsenic poisoning C Morphine poisoning D Cyanide poisoning B B B A 10 A 542 CHAPTER 48 Inebriants—Alcohol Introduction Ethanol (ethyl alcohol) is a transparent, colorless, volatile liquid having a characteristic odor and a DWTPKPI VCUVG YKVJ C URGEKſE ITCXKV[ QH  'VJCPQN KU RTQFWEGF D[ VJG GP\[OCVKE CEVKQP QH [GCUVU QP XGIGVCDNG UWDUVTCVG EQPVCKPKPI UWICTU &KTGEV HGTOGPVCVKQP ECPPQV TCKUG VJG EQPEGPVTCVKQP to tŌCUVJG[GCUVKUMKNNGFDWVFKUVKNNCVKQPQH RTKOCT[HGTOGPVCVKQPECPEQPEGPVTCVGVJGCNEQJQNVQ Ō UVTGPIVJ &KHHGTGPV V[RGU QH DGXGTCIGU YKVJ RGTEGPVCIG QH CNEQJQN CTG IKXGP KP Table 48.1 #V NQY FQUGU CNEQJQN KU UCKF VQ JCXG DGPGſEKCN GHHGEVU UWEJ CU FGETGCUGF TCVGU QH O[QECTFKCN KPHCTEVKQPFKCDGVGUUVTQMGICNNUVQPGUCPFRQUUKDN[ #N\JGKOGTŏU FGOGPVKC DWV EQPUWORVKQP QH VYQ UVCPFCTF FTKPMU RGT FC[ KPETGCUGU VJG TKUM QH JGCNVJ RTQDNGOU KP OCP[ QTICP U[UVGOU 4GIWNCT EQPUWORVKQP QH Ō IFC[ HQT OGP CPF Ō IFC[ HQT YQOGP CTG EQPUKFGTGF CU UCHG NKOKVU HQT FTKPMKPIKHNKXGTFCOCIGKUVQDGCXQKFGF FKHHGTGPEG between the sexes was due to the lower weight and YCVGTVQDQF[OCUU TCVKQ QH YQOGP „ „ „     Earlier, weekly safe limit was recommended [168–210 g/week (d 21 units) of alcohol for men and 98–140 g for women (d 14 units)].1 This is not advised, since a study showed that many people were in effect ‘saving up’ their units and using them at the end of the week for binge drinking where the primary intention is to become intoxicated by heavy consumption of alcohol over a short period of time An international study found that persons who reported drinking > units/day had an increased risk of fractures compared to non-drinkers Units of alcohol are a measure of the volume of pure alcohol in alcoholic beverages used as a guideline in some countries One unit of alcohol is defined as 10 ml in the UK and as 10 g (12.7 ml) in Australia A standard drink is 30 ml of spirits; 330 ml can of beer or 100 ml glass of wine To calculate standard drinks, the following formula is used: Volume of container (liters) × % alcohol by volume (ml/100 ml) × 0.789 = Number of standard drinks Commercial Preparations of Alcohol „ Absolute alcohol EQPVCKPU  GVJCPQN Table 48.1: Approximate percentage of alcohol by volume in beverages Beverage Spirits (whisky, brandy, rum, gin, vodka) Alcohol by volume 35–50% Port (fortified with brandy), sherry 17–21% Wine 10–15% Champagne 10–13% Beers, stout, cider „ „ „ 4–8% Mineralized methylated spiritEQPUKUVUQHGVJCPQN  YQQF PCRJVJC OGVJCPQN CPF  R[TKFKPG CPF KU EQNQTGF RKPM HQT GCU[ KFGPVKſECVKQP Industrial methylated spirit EQPVCKPUGVJCPQNCPF  OGVJCPQN YKVJ PQ EQNQTKPI CIGPV Surgical spirit EQPUKUVU QH  QH GVJCPQN CPF  OGVJCPQNYKVJQKNQHYKPVGTITGGPVQIKXGKVCUYGGVKUJ ƀCXQT Proof of spiritKPFKECVGUCOKZVWTGEQPVCKPKPID[ XQNWOGQTD[YGKIJVQHCDUQNWVGCNEQJQN+PVJG 75 VJG VGTO RTQQH TGHGTU VQ VYKEG VJG RGTEGPVCIG QH CNEQJQN D[ XQNWOG 5Q VJG EQOOQP RTQQH YJKUM[ UQNF KP VJG 75 EQPVCKPU  CNEQJQN D[ XQNWOG +P +PFKC VJG URKTKV YJKUM[ TWO QT DTCPF[ KU WUWCNN[  D[ XQNWOG CPF RTQQH 6JG EQPEGPVTCVKQP YTKVVGP QP VJG NCDGNU QH OQUV DQVVNGU KU XX KG XQNWOG QH CNEQJQN RGT XQNWOG QH FTKPM Various country liquors  Mahua: Traditional tribal drink in central and eastern India It is made from dried flower of mahua tree (Madhuca longifolia) and chhowa gud (granular mollasses)  Toddy (palm wine) is made from sap of various species of palm tree It is common across Asia and Africa  Feni: Goan spirit, made from coconut or juice of cashew apple  Arrack (Arabic araq—sweet liquor usually made from raisins in those regions) is distilled from coco-palm, rice, sugar or jaggery and has strength of 40–50% It may be mixed with chloral hydrate or potassium bromide  Tharra is made by fermenting the mash of sugarcane juice/ pulp in ceramic containers and distilling to high alcohol content 543 Inebriants—Alcohol     Chhaang (Tibetan: ‘nectar of gods’) is a Tibetan/Sherpa rice beer, also popular in parts of eastern Himalayas It can be brewed from barley and millet stuffed in a barrel of bamboo, over which water is poured Handia: It is made by fermenting boiled rice mixed with herbs Commonly seen in Bihar, Jharkhand, Odisha, MP and Chhatisgarh Chuak is made by fermenting rice in water, common in Tripura Sonti is similar to wine in its alcohol content It is made by steaming rice A mold, Rhizopus sonti, is used, followed by fermentation Action 'VJCPQNCEVUOCKPN[QPVJG%05+VCEVUCUCFGRTGUUCPV QH URGEKCNK\GF CPF UGPUKVKXG EGNNU QH EGTGDTCN EQTVGZ EGPVGTUTGIWNCVKPIEQPFWEVLWFIOGPVCPFUGNHETKVKEKUO YKVJTGNGCUGQHKPJKDKVQT[VQPGNGCFKPIVQWPTGUVTCKPGF DGJCXKQT6JKUKUHQNNQYGFD[FGRTGUUKQPQHXKVCNEGPVGTU QH OGFWNNC RTQFWEKPI EQOC CPF FGCVJ Alcohol also acts a hypnotic, diaphoretic, and in UOCNN FQUGU CU CP CRRGVK\GT Metabolism (QNNQYKPI CDUQTRVKQP VJG EQPEGPVTCVKQP QH CNEQJQN KP VJGDNQQFTGCEJGUCOCZKOWOKPCDQWVŌOKPWVGU OKPCHVGTKPIGUVKQP6JGblood alcohol concentration (BAC) KU QHVGP TGRTGUGPVGF D[ C ITCRJ 6JG OCLQT FGVGTOKPCPVU QH VJG VKOKPI CPF RGCM QH VJG $#% KPENWFGDQF[UK\GIGPFGTCOQWPVCPFV[RGQHDGXGTCIG KPIGUVGF FWTCVKQP QH FTKPMKPI CPF VJG RTGUGPEG CPF V[RG QH HQQF (Table 48.2) „ With an empty stomach, there is a rapid rise and slow decline (Fig 48.1) „ 9KVJ FKNWVGF FTKPMU QT C HWNN UVQOCEJ VJG TKUG KU UNQYGTCPFVJGOCZKOWORGCMKUNQYGTYKVJCƀCVVGT Table 48.2: Factors affecting rate of absorption of alcohol Factors enhancing absorption Factors decreasing absorption Femaleness Maleness Empty stomach Full stomach Drugs: Cholinergic agents, parasympathomimetic agents, aspirin, erythromycin, metoclopramide, H2-receptor antagonists Drugs: Anticholinergic agents, sympathomimetic agents, nicotine or caffeine, tricyclic antidepressants, amphetamines, opiates Gastric resection, gastric ulcers, Malignant gastric neoplasm, gastritis pyloric stenosis Carbonated drinks Fatty foods $#%EWTXG+HUWDUGSWGPVFTKPMUCTGVCMGPVJGPGY CNEQJQN KU UWRGTCFFGF VQ VJG GZKUVKPI EWTXG Factors that interfere with absorption are (Table 48.2): 2TGUGPEG QH HQQF GURGEKCNN[ HCVU CPF RTQVGKPU KP UVQOCEJ TGVCTFU CDUQTRVKQP „ 5VTGPIVJ QH CNEQJQNKE DGXGTCIGU VCMGPōJKIJGT VJG UVTGPIVJ OQTG TCRKF YKNN DG VJG TCVG QH CDUQTRVKQP „ Diluted drinks, such as beer may take double the VKOG VQ CDUQTD EQORCTGF VQ UVTQPIGT FTKPMU „ Carbonated drinks hasten absorption as the bubbles ITGCVN[ KPETGCUG VJG UWTHCEG CTGC ECTT[KPI CNEQJQN „ Warm alcoholic drinks which dilate gastric mucosal capillaries are more quickly absorbed than iced drinks QH UCOG UVTGPIVJ „ Distribution Ethanol is distributed evenly throughout the body, RCUUKPIVJGDNQQFDTCKPDCTTKGTGCUKN[VQCHHGEVEGTGDTCN HWPEVKQP *QYGXGT KV KU RQQTN[ UQNWDNG KP DQF[ HCV HGOCNGU QH UCOG DQF[ UK\G CU OCNGU YKNN RTQFWEG C JKIJGT $#% HQT VJG UCOG COQWPV QH FTKPM CU VJGKT CSWGQWU EQORCTVOGPV KU UOCNNGT +VCVVCKPUGSWKNKDTKWOYKVJCEQPUVCPVDNQQFCNEQJQN EQPEGPVTCVKQP CPF EQPEGPVTCVKQP QH CNEQJQN KP QVJGT DQF[ ƀWKFU VJG TCVKQ DGKPI „ $NQQF 7TKPG   „ $NQQF 'ZJCNGF CKT DTGCVJ   „ $NQQF 5CNKXC   „ $NQQF %5(   &GVQZKſECVKQP Fig 48.1: Blood alcohol concentration in relation to presence of food 0KPGV[ RGTEGPV QH GVJCPQN KU OGVCDQNK\GF KP VJG NKXGT while the kidneys and lungs help to excrete about  QPN[ +P VJG NKXGT CNEQJQN KU QZKFK\GF D[ CNEQJQN dehydrogenase (Flow chart 48.1) „ Non-habituated persons metabolize ethanol at  OIFNJ +P CNEQJQNKEU VJKU TCVG KPETGCUGU VQ ŌOIFNJ$GECWUGQHVQNGTCPEG$#%UOWUVDG 544 Review of Forensic Medicine and Toxicology Flow chart 48.1: Metabolism of ethanol in liver [(A) causes increased blood acetaldehyde levels and (B) causes increased dopamine levels] A B „ interpreted in conjunction with history and clinical RTGUGPVCVKQP 'ZETGVKQP QH CNEQJQN KU OCKPN[ D[ VJG MKFPG[U lungs and skin through urine, breath and sweat TGURGEVKXGN[ +H KU CNUQ UGETGVGF KP UCNKXC CPF OKNM A number of metabolic effects from alcohol are directly linked to the production of an excess of both NADH and acetaldehyde  NADH is utilized in the conversion of pyruvic acid (intended for conversion into glucose by gluconeogenesis) to lactic acid The final result may be acidosis from lactic acid build-up and hypoglycemia from lack of glucose synthesis  Excess NADH may be used as a reducing agent in two pathways— one to synthesize glycerol (from a glycolysis intermediate) and the other to synthesis fatty acids As a result, heavy drinkers may initially be overweight (‘beer belly’)  The accumulated acetaldehyde acts by inhibiting the mitochondrial reactions and functions There is a vicious cycle—high acetaldehyde level impairs mitochondria function, metabolism of acetaldehyde to acetic acid decreases, more acetaldehyde accumulates and causes further liver damage— hepatitis and cirrhosis  Acetaldehyde may be responsible for the development of alcohol addiction Signs and Symptoms (Acute Poisoning) K Stage of Excitement (Blood level: 50–150 mg%) z 2GTUQP YKNN DG GWRJQTKE UGPUG QH YGNNDGKPI Actions, speech and emotions are less restrained FWG VQ NQYGTKPI QH VJG KPJKDKVKQP PQTOCNN[ GZGTEKUGF D[ VJG JKIJGT EGPVGTU QH VJG DTCKP +V CNVGTU VKOG CPF URCEG RGTEGRVKQP z *G OC[ RGTHQTO FCPEKPI VJTKNNKPI UJQYU ECTGNGUUN[ CPF HGCTNGUUN[ z *G OKIJV FKUENQUG UGETGVU ‘in vino veritas’ōKP YKPG VJGTG KU VTWVJ 2GTUQP OKIJV UJQY KPETGCUG KP EQPſFGPEG DWV NCEM QH UGNHEQPVTQN z 6JGTG KU NQYGTKPI QH XKUWCN CEWKV[ 0[UVCIOWU RTGUGPV z Mental concentration is poor and judgment KORCKTGF z (CEWNV[ QH CVVGPVKQP FGVGTKQTCVGU z 4GECNN OGOQT[ KU FKUVWTDGF RGTUQP ECPPQV CEEWTCVGN[ TGECNN EGTVCKP UKVWCVKQPU QT PCOGU QH KPFKXKFWCNU z +V KPETGCUGU VJG FGUKTG HQT UGZ DWV OCTMGFN[ KORCKTU RGTHQTOCPEG TGUWNVKPI KP RTQNQPIGF KPVGTEQWTUG YKVJQWV GLCEWNCVKQP KK Stage of In-coordination (Blood level: 150–250 mg%) z &WG VQ HWTVJGT FGRTGUUKQP QH JKIJGT EGPVGTU VJG RGTUQP OC[ DG OQTQUGEJGGTHWNKTTKVCDNG KNNVGORGTGFGZEKVCDNGUNGGR[ FGRGPFKPI QP VJG FQOKPCPV KORWNUGU TGNGCUGF z %GPVGTUQHRGTEGRVKQPCPFUMKNNGFOQXGOGPVUCTG KPXQNXGFōVJGTG KU ENWOUKPGUU KPEQQTFKPCVKQP QH ſPG CPF UMKNNGF OQXGOGPVU CPF CNVGTCVKQPU KP URGGEJ CPF ſPG ſPIGT OQXGOGPVU z 0CWUGC CPF XQOKVKPI z (CEG (NWUJGF z 2WNUG 4CRKF z 5GPUG QH VQWEJ VCUVG UOGNN CPF JGCTKPI CTG FKOKPKUJGF z *[RQVJGTOKC z $TGCVJ UOGNNU QH CNEQJQN z 2WRKNUCTGFKNCVGFCPFTGCEVUNWIIKUJN[VQNKIJV  KKK Stage of Coma (Blood level > 250 mg%) z 6JKEM UNWTTGF URGGEJ z %QQTFKPCVKQP KU OCTMGFN[ CHHGEVGFōDGEQOGU IKFF[ UVCIIGT CPF HCNN z 2WNUG KU TCRKF z *[RQVJGTOKC z Inebriants—Alcohol z z 2WRKNUCTGEQPVTCEVGFDWVQPUVKOWNCVKQPQHVJG RGTUQPGID[RKPEJKPIQTUNCRRKPIECWUGUVJGO to dilate with slow return (McEwan’s sign) Patient passes into coma with steatorous DTGCVJKPI 6JG RJ[UKQNQIKE GHHGEVU QH CNEQJQN CTG OQTG pronounced when the blood level is rising, as compared to levels attained at peak or plateau, or when the level KUHCNNKPI6JKUKUMPQYPCUVJGMellanby effect and is DGNKGXGF VQ TGUWNV HTQO CP CEWVG VQNGTCPEG VQ CNEQJQN VJCV FGXGNQRU FWTKPI KPVQZKECVKQP Recovery: 7PNGUU C NCTIG SWCPVKV[ QH CNEQJQN KU EQPUWOGF KP C UJQTV VKOG TGEQXGT[ KU VJG TWNG „ #DQWV  QH FTKPMGTU OC[ GZRGTKGPEG C blackout, CP GRKUQFG QH VGORQTCT[ CPVGTQITCFG COPGUKC KP YJKEJVJGRGTUQPHQTIGVUCNNQTRCTVQHYJCVQEEWTTGF FWTKPI C FTKPMKPI UGUUKQP2 „ #VVKOGUCUOCNNFQUGQHCNEQJQNOC[RTQFWEGCEWVG intoxication in some persons which is known as pathological intoxication With recovery, coma gradually lightens into deep UNGGR2GTUQPYKNNYCMGWRKPŌJQWTU JYKVJCEWVG FGRTGUUKQP QH OQQF PCWUGC CPF JGCFCEJGōalcohol hangover Death: +HVJGXKEVKOFQGUPQVTGEQXGTHTQOEQOCYKVJKP h, prognosis is bad and may result in death due to UJQEM FGRTGUUKQP QH TGURKTCVQT[ EGPVGT QT CURKTCVKQP QH XQOKV Fatal dose (non-addict) Ō ON QH CDUQNWVG CNEQJQN EQPUWOGF KP  J „ 4KUM QH FGCVJ KU KPETGCUGF KH $#%   OIFN CPF FGCVJ KU V[RKECN KH VJG $#% KU DGVYGGP   OIFN „ Fatal period: Ō J Diagnosis6JGFKUVKPEVKXGCTQOCQHCNEQJQNOC[CUUKUV KPFKCIPQUKU%QPſTOCVKQPKUFQPGD[CPCN[UKUQHDNQQF UGTWO INWEQUG NGXGN UJQWNF DG FQPG CNQPI YKVJ KV 2QUUKDKNKV[ QH KPVQZKECVKQP YKVJ QVJGT FTWIU UJQWNF DG considered and a blood or urine sample is indicated VQ UETGGP HQT QRKQKF CPF QVJGT %05 FGRTGUUCPVU RCTVKEWNCTN[ DGP\QFKC\GRKPGU CPF DCTDKVWTCVGU Treatment 1WVNKPG QH OCPCIGOGPV KU IKXGP KP Flow chart 48.2  K 2CVKGPVOWUVDGMGRVYCTOCPFRNCEGFKPC SWKGV environment, and made to lie on the side to OKPKOK\G TKUM QH CURKTCVKQP  KK )CUVTKE NCXCIG YKVJ CNMCNKPG UQNWVKQP YKVJKP  J QH KPIGUVKQP  KKK 1PG NKVGT QH PQTOCN UCNKPG YKVJ  INWEQUG CPF WPKVUQHKPUWNKPQTFGZVTQUG KPON KU IKXGP +8  KX 6JKCOKPG  OI KP  ON INWEQUG UQNWVKQP +8  X 4GURKTCVQT[ UWRRQTV CPF 12 VJGTCR[  XK *GOQFKCN[UKU CPF RGTKVQPGCN FKCN[UKU OC[ DG WUGF Flow chart 48.2: Management of an intoxicated patient 545 546 Review of Forensic Medicine and Toxicology XKK +PECUGQHCIITGUUKXGDGJCXKQTPQPVJTGCVGPKPIHQTEG by intervention team or short-acting benzodiazepine, UWEJ CU NQTC\GRCO  OI QTCNN[ OC[ DG WUGF Complications Patient may exhibit holiday heart syndrome in which ECTFKCE F[UTJ[VJOKCU GURGEKCNN[ CVTKCN ſDTKNNCVKQP CPF XGPVTKEWNCT CTTJ[VJOKCU CTG QHVGP QDUGTXGF CHVGT C JGCX[ FTKPMKPI GRKUQFG 4 *[RQIN[EGOKC ICUVTKVKU RCPETGCVKVKU CPF VQZKE RU[EJQUKU OC[ CNUQ QEEWT +P teenagers, it may lead to anemia, macrocytosis, and GNGXCVKQP QH GP\[OGU DKNKTWDKP CPF WTKE CEKF Postmortem Findings  K 1FQT QH CNEQJQN CTQWPF VJG OQWVJ CPF PQUG  KK %QPIGUVKQP QH EQPLWPEVKXC  KKK 4KIQT OQTVKU KU RTQNQPIGF CPF FGEQORQUKVKQP KU TGVCTFGF  KX #EWVG KPƀCOOCVKQP QH VJG UVQOCEJ YKVJ EQCVKPI QH OWEWU  X #NN XKUEGTC CTG EQPIGUVGF CPF UOGNNU QH CNEQJQN  XK $NQQF KU ƀWKF CPF FCTM Medico-legal Aspects „ „ „ „ 4QWVKPG WUG QH $#% KU EQPVTQXGTUKCN DGECWUG KV KU WPNKMGN[VQCHHGEVOCPCIGOGPVKPCRCVKGPVYJQKUCYCMG CPF CNGTV +V KU UCHG VQ FKUEJCTIG VJG RCVKGPV QPEG JG UJGKUENKPKECNN[ PQVPWOGTKECNN[PQNQPIGTKPVQZKECVGF Patients with alcohol intoxication should be evaluated HQT EQGZKUVKPI KPLWTKGU CPF OGVCDQNKE FKUQTFGTU A patient with altered mental status is simply EQPUKFGTGF KPVQZKECVGF YKVJQWV EQPUKFGTCVKQP QH QVJGTRQUUKDNGECWUGU*[RQIN[EGOKCUJQWNFCNYC[U DG UQWIJV KP UWEJ ECUGU *GOQFKCN[UKU UJQWNF DG WUGF GURGEKCNN[ KP VJG RTGUGPEG QH OGVCDQNKE CDPQTOCNKVKGU 6JGTG UJQWNF PQV DG CP[ FGNC[ KP YCKVKPI HQT NCDQTCVQT[VGUVU VQEQPſTOVJGRTGUGPEGQHCNEQJQN DGHQTG UVCTVKPI VJG VTGCVOGPV Chronic Alcoholism (Systemic Effects) +V KU EJCTCEVGTK\GF D[ C ITCFWCN RJ[UKECN OGPVCN CPF OQTCN FGVGTKQTCVKQP  Physical: 6JGTG KU NCEM QH RGTUQPCN J[IKGPG NQUU QH appetite, chronic gastroenteritis, wasting, peripheral PGWTQRCVJKGU KORQVGPEG UVGTKNKV[ HCVV[ EJCPIGU KP liver and heart, cirrhosis, tremors, insomnia, red eyes CPF KPVGTOKVVGPV KPHGEVKQPU  Mental: 6JGTG KU NQUU QH OGOQT[ KORCKTGF RQYGT QH LWFIOGPV CPF FGOGPVKC Clinical syndromes associated with chronic alcoholism5  Delirium tremens  Alcoholic hallucinosis  -QTUCMQHHŏU RU[EJQUKU  Wernicke’s encephalopathy  /CTEJKCHCXC$KIPCOK U[PFTQOG  Alcoholic paranoia  Alcoholic seizures  Moral: +V OCPKHGUVU CU ETKOGU YJKEJ VJG CFFKEV EQOOKVU VQ IGV JKU FTKPM *G DGEQOGU OQTDKFN[ LGCNQWUCPFUWURKEKQWUQHJKUYKHGŏUſFGNKV[CPFOC[ CUUCWNV JGT Treatment  K 5WFFGP YKVJFTCYCN QH CNEQJQNKE FTKPMU  KK Antabuse (disulfiram) is given as an aversion VGEJPKSWG5&KUWNſTCO VGVTCGVJ[NVJKWTCOFKUWNſFG DNQEMU OGVCDQNKUO QH CNEQJQN CV VJG CEGVCNFGJ[FG stage (see Flow chart 48.1  Acetaldehyde CEEWOWNCVGU KP DNQQF ECWUKPI FKUWNſTCOGVJCPQN reaction (aldehyde syndrome z Symptoms: Flushing, palpitation, nausea, XQOKVKPICPZKGV[VKIJVPGUUQHEJGUVJ[RQVGPUKQP sweating, throbbing headache, giddiness, sense QH KORGPFKPI FQQO CPF CDFQOKPCN ETCORU CRRGCT FWG VQ YJKEJ RCVKGPV FKUNKMGU CNEQJQN &WTCVKQP QH VJG U[PFTQOG Ō J FGRGPFU QP VJG COQWPV QH CNEQJQN EQPUWOGF z Dose: 6JG KPKVKCN FQUG KU Ō OI HQT Ō YGGMU VCMGP DGHQTG DGFVKOG HQNNQYGF D[ C OCKPVGPCPEGFQUGQHOIFC[ TCPIGŌ OI 6JG VQVCN FCKN[ FQUCIG UJQWNF PQV GZEGGF  OI z Contraindications: Coronary artery disease, NKXGT HCKNWTG EJTQPKE TGPCN HCKNWTG RGTKRJGTCN PGWTQRCVJ[ OWUEWNCT FKUGCUG JKUVQT[ QH RU[EJQUKU CPF RTGIPCPE[ UV VTKOGUVGT  KKK %KVTCVGF ECNEKWO ECTDKOKFG Temposil  OI FC[ KP  FKXKFGF FQUGU KPUVGCF QH CPVCDWUG OC[ DG IKXGP  KX /GVTQPKFC\QNGPKVTCHG\QNGCPFOGVJ[NVGVTC\QNGVJKQN CTG QVJGT CNVGTPCVKXGU  X 0WVTKGPVUXKVCOKPUCPFITCFWCNTGVWTPVQCPQTOCN DCNCPEGF FKGV  XK 5[ORVQOCVKE VTGCVOGPV Inebriants—Alcohol Withdrawal Symptoms Signs and Symptoms11 Tremulousness or shakes or jitters (most common sign), YGCMPGUURCKPKPOWUENGEQNFUYGCVKPUQOPKCNQUUQH appetite, vomiting, diarrhea, restlessness, exaggerated TGƀGZGUTCKUGFVGORGTCVWTGƀWEVWCVKPI$2JCNNWEKPC VKQPU NQUU QH OGOQT[ CPF FGNKTKWO VTGOGPU Many alcoholics experience ‘the shakes’ approximately Ō J CHVGT VJGKT NCUV FTKPM 6JG UJCMGU CTG VTGOQTU ECWUGF D[ QXGT GZEKVCVKQP QH VJG %05 6TGOQTU OC[ be accompanied by tachycardia, diaphoresis, anorexia, CPF KPUQOPKC #HVGT Ō J VJG CNEQJQNKE OC[ JCXG ‘rum fitsŏ KG IGPGTCNK\GF UGK\WTGU There is an acute attack of insanity in which there is:  K %NQWFKPI QH EQPUEKQWUPGUU YKVJ FKUQTKGPVCVKQP KP VKOG CPF URCEG  KK %QCTUGOWUEWNCTVTGOQTUQHHCEGVQPIWGCPFJCPFU  KKK +PUQOPKC YKVJ TGXGTUCN QH UNGGRYCMG E[ENG CPF NQUU QH OGOQT[  KX 2U[EJQOQVQTCIKVCVKQPCVCZKCWPEQPVTQNNCDNGHGCT CPFVGPFGPE[VQEQOOKVUWKEKFGJQOKEKFGXKQNGPV CUUCWNV QT ECWUG FCOCIG VQ RTQRGTV[  X /CTMGFCWVQPQOKEFKUVWTDCPEGUYKVJVCEJ[ECTFKC HGXGT UYGCVKPI J[RGTVGPUKQP CPF RWRKNNCT[ FKNCVCVKQP  XK 2GEWNKCT V[RG QH delirium of horrors due to halluciPCVKQPU QH UKIJV CPF JGCTKPI Tactile hallucinations QHKPUGEVUCPFCPVUETCYNKPIWPFGTVJGUMKPQTQP VJG DGFU OC[ QEEWT    Disulfiram action was discovered accidentally, as the substance was intended to provide a remedy for parasitic infestations However, workers testing the substance on themselves reported severe symptoms after alcohol consumption It is also being studied as a treatment for cocaine dependence, as it prevents the breakdown of dopamine (neurotransmitter whose release is stimulated by cocaine), the excess dopamine results in increased anxiety, higher blood pressure, restlessness and other unpleasant symptoms (Flow chart 48.1) Animal charcoal, fungus (Coprinus atramentarius), sulfonylureas and certain cephalosporins also cause a disulfirum-like action CAGE questionnaire: Developed by Dr John Ewing, CAGE is an internationally used assessment instrument for identifying alcoholics.9 i Have you ever felt you should Cut down on your drinking? ii Have people Annoyed you, by criticizing your drinking? iii Have you ever felt bad or Guilty about your drinking? iv Have you ever had a drink, first thing in the morning, to steady your nerves or to get rid of a hangover (Eye opener)? Scoring: Item responses on the CAGE are scored or 1, with a higher score an indication of alcohol problems A total score of or greater is considered clinically significant Delirium Tremens This is an acute organic brain syndrome, usually seen YKVJKPŌFC[UQHEQORNGVGCDUGPEGHTQOJGCX[CNEQJQN drinking in chronic alcoholics, and most severe alcohol YKVJFTCYCN U[PFTQOG Treatment (For both withdrawal symptoms and delirium tremens)  K &KC\GRCO ŌOIFC[KPFKXKFGFFQUGUKUWUGF12  KK 1TCNOWNVK$XKVCOKPUKPENWFKPIVJKCOKPGŌ OI KU IKXGP FCKN[ HQT C YGGM QT OQTG  KKK %JNQTFKC\GRQZKFG Ō OIFC[ KP FKXKFGF FQUGUQTJCNQRGTKFQNOIQTOQTGFC[OC[DG WUGF  KX +PVTCXGPQWU ƀWKFU CTG CXQKFGF WPNGUU VJGTG KU GXKFGPEG QH DNGGFKPI XQOKVKPI QT FKCTTJGC  X +P UQOG YKVJFTCYCN U[ORVQO ECUGU QPN[ TGUVQTCVKQP QH CNEQJQNKE FTKPMU JGNRU  XK +PECUGUQHWTIGPVUGFCVKQPCUKPFGNKTKWOVTGOGPUō phenobarbitone or chlorpromazine injection can be IKXGPCPFVJGPFGVQZKſECVKQPCPFOCKPVGPCPEGQH nutrition is carried on with 5% dextrose solution +8 CPF VJKCOKPG XKK 5[ORVQOCVKE VTGCVOGPV Medico-legal Aspects „ „ Causes „ „ „ „ 5WFFGP GZEGUU QT UWFFGP YKVJFTCYCN QH CNEQJQN QPI EQPVKPWCN KPIGUVKQP QH CNEQJQN 5JQEMFWGVQUGXGTGVTCWOCGIHTCEVWTGKPCEJTQPKE CNEQJQNKE #EWVG KPHGEVKQPU NKMG RPGWOQPKC QT KPƀWGP\C KP C EJTQPKE CNEQJQNKE +VKUCOGFKECNGOGTIGPE[CPFUJQWNFDGVTGCVGFQP CP KPRCVKGPV DCUKU When a person in delirium tremens commits any illegal act, he is not held responsible by the reason VJCV JGUJG KU EQPUKFGTGF VQ DG OGPVCNN[ WPUQWPF during this state (Sec 84 IPC) Alcoholic Hallucinosis „ +V KU C UVCVG QH JCNNWEKPCVKQP OCKPN[ CWFKVQT[ YKVJ systematized delusions of persecution NCUVKPI HTQO YGGMU VQ OQPVJU 547 548 Review of Forensic Medicine and Toxicology „ „ „ „ 1EEWTU FWTKPI CDUVKPGPEG KP  QH RCVKGPVU YJQ JCXG DGGP QP TGIWNCT CNEQJQN VKNN VJGP +VKUCRU[EJKCVTKEGOGTIGPE[TGSWKTKPIJQURKVCNK\CVKQP UGFCVKQP CPF ENQUG OQPKVQTKPI 7UWCNN[ TGEQXGT[ QEEWTU KP C OQPVJ Patient may become homicidal or suicidal in response VQ JKU JCNNWEKPCVKQP Treatment: 5COG CU FGNKTKWO VTGOGPU Treatment  K +PVTCXGPQWUVJKCOKPG KPVJGHQTOQHPabrinex, two XKCNU  JQWTN[ HQT  J KPKVKCNN[ HQNNQYGF D[ QTCN  OI  JQWTN[  KK 5WRRNGOGPVCVKQPQHGNGEVTQN[VGURCTVKEWNCTN[OCI nesium and potassium, may be required in addition VQ VJKCOKPG Alcoholic peripheral neuropathy: 5[ORVQOU QH alcoholic polyneuritis are weakness, pain in extremities, YTKUVCPFHQQVFTQRWPUVGCF[ICKVNQUUQHFGGRTGƀGZGU CPF VGPFGTPGUU QH OWUENGU QH CTOU CPF NGIU Alcoholic paranoia:+PVJKUVJGTGKUCſZGFFGNWUKQP DWV PQ JCNNWEKPCVKQPU Patient becomes suspicious QHVJGOQVKXGUCPFCEVKQPUQHVJQUGJGOGGVUCPFQH JKU HCOKN[ OGODGTU Marchiafava-Bignami syndrome: This is a rare disorder characterized by disorientation, epilepsy, ataxia, dysarthria, hallucinations, spastic limb paralysis, and RGTUQPCNKV[ CPF KPVGNNGEVWCN FGVGTKQTCVKQP 6JGTG KU C YKFGURTGCFFGO[GNKPCVKQPQHEQTRWUECNNQUWOQRVKE VTCEVUCPFEGTGDGNNCTRGFWPENGU6JGECWUGKURTQDCDN[ UQOG CNEQJQNTGNCVGF PWVTKVKQPCN FGſEKGPE[ #NEQJQNKEUGK\WTGU ŎTWOſVUŏ+PCNEQJQNFGRGPFGPEG persons, generalized tonic clonic seizure may occur CHVGT Ō J QH JGCX[ DQWV QH FTKPMKPI CNEQJQN Multiple seizures are more common than single UGK\WTG 5QOGVKOGU UVCVWU GRKNGRVKEWU CPF FGNKTKWO VTGOGPU OC[ DG RTGEKRKVCVGF „ Wernicke’s Encephalopathy This is an acute reaction due to severe thiamine FGſEKGPE[ 8KV$VJGEQOOQPGUVECWUGDGKPIEJTQPKE CNEQJQNCDWUG%JCTCEVGTKUVKECNN[VJGQPUGVQEEWTUCHVGT C RGTKQF QH RGTUKUVGPV XQOKVKPI „ Signs and Symptoms14 K Ocular: Coarse nystagmus and opthalmoparesis WUWCNN[ VJG 8+VJ ETCPKCN PGTXG KU KPXQNXGF Pupillary irregularity, retinal hemorrhages, RCRKNNGFGOC CPF KORCKTOGPV QH XKUKQP KK CNS: &KUQTKGPVCVKQP EQPHWUKQP TGEGPV OGOQT[ disturbances, poor attention span and distractiDKNKV[ #RCVJ[ CPF CVCZKC CTG GCTN[ U[ORVQOU KKK 2GTKRJGTCN PGWTQRCVJ[ CPF UGTKQWU OCNPWVTKVKQP CTG QHVGP EQGZKUVGPV „ „ Pathologically, neuronal degeneration and hemorrhage is seen in the thalamus, hypothalamus (mammillary DQFKGU CPF OKFDTCKP Korsakoff’s Psychosis -QTUCMQHH HKTUV KFGPVKHKGF VJKU EQPFKVKQP KP  -QTUCMQHHŏURU[EJQUKUQHVGPHQNNQYU9GTPKEMGŏUGPEGRJC NQRCVJ[ UQ VJG[ CTG TGHGTTGF VQ CU Wernicke-Korsakoff syndrome   Cause:5GXGTGWPVTGCVGFVJKCOKPGFGſEKGPE[UGEQPFCT[ VQ EJTQPKE CNEQJQN CDWUG Signs and Symptoms +VRTGUGPVUCUCPorganic amnestic syndrome, characterized D[ KPCDKNKV[ VQ NGCTP PGY KPHQTOCVKQP KORCKTOGPV QH UJQTVVGTO OGOQT[ CPF EQORGPUCVQT[ EQPHCDWNCVKQP +PUKIJV KU QHVGP KORCKTGF The pathological lesion is usually widespread, but EJCPIGU CTG UGGP KP DKNCVGTCN FQTUQOGFKCN PWENGK QH VJCNCOWU CPF OCOOKNNCT[ DQFKGU 6JG EJCPIGU CTG also seen in periventricular and periaqueductal gray OCVVGT EGTGDGNNWO CPF RCTVU QH DTCKPUVGO Sometimes, alcohol dementia may be associated YKVJ9GTPKEMG-QTUCMQHHU[PFTQOGYJKEJKUECWUGFD[ long-term or excessive drinking resulting in neurological FCOCIG CPF KORCKTOGPV QH OGOQT[  Thiamine is absorbed from the duodenum; alcohol interferes with its active transport, and chronic liver disease causes decreased capacity of the liver to store thiamine Thiamine is converted to its active form thiamine pyrophosphate in neuronal and glial cells which serves as a cofactor for several enzymes (transketolase, pyruvate dehydrogenase and alpha ketoglutarate) The main function of these enzymes in the brain is lipid (myelin sheath) and carbohydrate metabolism, production of amino acids and production of glucose-derived neurotransmitters Within 2–3 weeks of decreased intake and thiamine depletion, areas of the brain with the highest thiamine content and turnover (thalamus and the mammillary bodies) will demonstrate cellular impairment and injury Drunkenness &GſPKVKQP+VKUCEQPFKVKQPYJKEJTGUWNVUHTQOGZEGUUKXG KPVCMGQHCNEQJQN6JGRGTUQPWPFGTKVUKPƀWGPEGUJQYU VJG HQNNQYKPI  K QUU QH EQPVTQN QXGT JKU OGPVCN HCEWNVKGU  KK +PCDKNKV[ VQ RGTHQTO VJG FWVKGU KP YJKEJ JG KU GPICIGF  KKK &CPIGTQWU VQ JKOUGNH QT VQ QVJGTU Inebriants—Alcohol Consent for Examination „ „ „ The detained person should not be examined and blood, urine or breath should not be collected without JKU YTKVVGP EQPUGPV +H VJG RGTUQP DGEQOGU WPEQPUEKQWU QT KPECRCDNG QH giving consent, examination and treatment can be carried out, but the doctor should not disclose any KPHQTOCVKQP QDVCKPGF FWTKPI GZCOKPCVKQP CPF YCKV HQT JKU EQPUGPV VKNN JG TGICKPU EQPUEKQWUPGUU Under Sec 53 (1) CrPCGZCOKPCVKQPQHCPCEEWUGF ECP DG ECTTKGF QWV D[ C FQEVQT CV VJG TGSWGUV QH VJG RQNKEGGXGPYKVJQWVJKUEQPUGPVCPFD[WUGQHHQTEG KH PGEGUUCT[ 5WEJ GZCOKPCVKQP OC[ KPENWFG VCMKPI QH DQF[ ƀWKFU KP ECUGU QH UWURGEVGF KPVQZKECVKQP Diagnosing a Case of Drunkenness Preliminary data such as name, age, sex, address, time QH GZCOKPCVKQP VYQ KFGPVKſECVKQP OCTMU CPF RGTUQP GUEQTVKPI VJG RCVKGPV UJQWNF DG PQVGF History: 6JG JKUVQT[ QH TGNGXCPV GXGPVU UJQWNF DG QDVCKPGFHTQOVJGRGTUQPYJKNGQDUGTXKPIJKO'PSWKTG CDQWV RCUV KNNPGUUGU CPF FTWI VTGCVOGPV 0QVG KH JG CFOKVUJCXKPIVCMGPCNEQJQNKEFTKPMU+HUQVJGPCVWTG SWCPVKV[CPFVKOGQHEQPUWORVKQPUJQWNFDGTGEQTFGF Exclusion of Injuries and Pathological Conditions $GHQTGFKCIPQUKPIVJGECUGCUFTWPMGPPGUUKVKUDGVVGT VQ TWNG QWV VJG HQNNQYKPI EQPFKVKQPU YJKEJ UKOWNCVG alcoholic intoxication: „ *GCF KPLWT[ „ Metabolic disorders: *[RQIN[EGOKCFKCDGVKERTGEQOC WTGOKC CPF J[RGTVJ[TQKFKUO „ Neurological conditions: +PVTCETCPKCNVWOQTUGRKNGRU[ 2CTMKPUQPKUO CPF FKUUGOKPCVGF UENGTQUKU „ Drug overdose: +PUWNKP DCTDKVWTCVGU CPVKJKUVCOKPGU EQECKPGOQTRJKPGCVTQRKPGJ[QUEKPGCPFVTCPSWKNK\GTU „ Psychological disorders: *[RQOCPKC CPF IGPGTCN RCTGUKU „ (GDTKNG KNNPGUUGU „ 'ZRQUWTG VQ ECTDQP OQPQZKFG Clinical Examination General appearance /CPPGT QH FTGUUKPIōRTQRGTN[ FTGUUGF QT PQV CPF UQKNKPI QH ENQVJGU „ 2QUVWTGōYJGVJGT QXGTGTGEV CPF QXGT UOCTV ECP UVCPFUVGCF[QTPQVNGCPUVQCUKFGQTUVQQRUHQTYCTF CPF ECP UVCPF YKVJQWV UWRRQTV QT PQV „ General Examination 6JGUECNRUJQWNFDGKPURGEVGFCPFRCNRCVGFHQTGXKFGPEG QHCP[JGCFKPLWT[#P[QVJGTKPLWT[RTGUGPVKUPQVGF +PLWTKGU EQWNF JCXG DGGP UWUVCKPGF KP C OQVQT XGJKENG CEEKFGPV QT CU C TGUWNV QH TGUKUVCPEG VQ CTTGUV %CTGHWN FQEWOGPVCVKQP QH VJGUG KPLWTKGU PGGFU VQ DG FQPG 5RGEKſE Physical Examination  K GaitKUQDUGTXGFHQTCP[WPUVGCFKPGUUUVCIIGTKPI DWORKPI KPVQ RGQRNG QT HWTPKVWTG 6JG DGUV YC[ is to watch him approaching the examination HCEKNKV[QTVQCUMVJGRGTUQPVQIQVQVJGYGKIJKPI OCEJKPGCPFYJKNGFQKPIUQYCVEJVJGICKV)CKV on turning (normal, unsteady, stumbling) is also PQVGF  KK Orientation and memory: Ask him about KPEKFGPVUYJKEJJCXGQEEWTTGFHGYJQWTURTKQTVQ examination to check his memory (clear, vague or EQPHWUGFCPFOGPVCNCNGTVPGUU#UMJKOCDQWVVJG date, time and place where he is at present (good, OQFGTCVG DCF QT KPFGſPKVG  KKK Behavior: 9JGVJGT PQKU[ LQXKCN DQCUVHWN rude, emotional, talkative, excited, nervous or WPEQPVTQNNCDNG +H VJG UWDLGEV KU EQQRGTCVKXG UVCVG KV  KX Face: 0QVG JKU HCEG YJGVJGT PQTOCN ƀWUJGF QT RCNG#NEQJQNKUXCUQFKNCVCVQT[CPFTGFPGUUQHVJG HCEG KU KPFKECVKXG QH VJKU  X Speech:4GEQTFYJGVJGTVJGRCVKGPVECPWPFGTUVCPF and whether his speech is normal, thick and UNWTTGF UVWVVGTKPI QT EQPHWUGF 5RGGEJ KU CNUQ QDUGTXGFHQTKPEQJGTGPEGWPKPVGNNKIKDNGCIITGUUKXG QHHGPUKXG QT QXGT RTGEKUG  XK Tongue: Examine the tongue, whether dry, moist CPF ENGCP QT HWTTGF &T[ VQPIWG KU UGGP KP VJKTUV CPF YCPKPI RJCUG QH $#% /QKUV VQPIWG OC[ DG KPFKECVKXG QH JCXKPI VCMGP CP[ FTKPM KPENWFKPI YCVGT XKK Signs of vomiting and salivation: As soon as the CNEQJQN TGCEJGU C EQPEGPVTCVKQP QH CDQWV  KP VJGKPVGUVKPGUCPKNGWUHQNNQYUYJKEJKUTGURQPUKDNG HQT XQOKVKPI 0CWUGC KU TGURQPUKDNG HQT CDPQTOCN UCNKXCVKQP5CNKXCVKQPCPFFTQQNKPIOC[CNUQDGVJG TGUWNV QH UWRRTGUUKQP QH UYCNNQYKPI TGƀGZ +V KU VJGTGHQTG QPN[ HQWPF KP VJG UGXGTGN[ KPVQZKECVGF XKKK Smell of alcohol:5VTQPIOQFGTCVGHCKPVQTPQPG 6JG UOGNN KU FGRGPFGPV QP VJG ECRCDKNKVKGU QH VJG GZCOKPGTCPFUOGNNCEWKV[FKHHGTUHTQORGTUQPVQ RGTUQP6JGUOGNNQHVJGDTGCVJ OC[EQPſTOVJCV 549 ...Review of Forensic Medicine and Toxicology Review of Forensic Medicine and Toxicology Including Clinical and Pathological Aspects MCQs of Previous Years... of Forensic Medicine and Toxicology in the year 2009, there has been considerable attention, and gradual recognition and liking by the students and faculty both This book has now become a standard... sincere, hardworking and brightest students to whom fortunately I introduced the art and science of the specialty of Forensic Medicine and Toxicology, both as undergraduate and postgraduate at