Forensic Medicine (Resp) PDF

FORENSIC MEDICINE RESPIRATORY MODULE ASPHYXIA 1 Definition: physiologic and chemical state in a living organism in which acute lack of o2 available for cell metabolism is associated with inability to eliminate excess co2. (hypoxia and hypercapnia) Mechanical asphyxia: airway is...

FORENSIC MEDICINE RESPIRATORY MODULE ASPHYXIA 1 Definition: physiologic and chemical state in a living organism in which acute lack of o2 available for cell metabolism is associated with inability to eliminate excess co2. (hypoxia and hypercapnia) Mechanical asphyxia: airway is blocked in an unnatural way either from within or without. eg) smothering, gagging, choking, throttling, hanging, strangulation. Toxic asphyxia: uptake of O2 prevented by poisonous gasses/ fumes eg) industrial leakage, incineration of plastic and foams Environmental asphyxia: insufficient o2 in inspired air or breathing in vitiated atmosphere eg) high altitude, deep sea diving, death in deep unused wells, death in sewer gasses Iatrogenic asphyxia: resulting due to doctors negligence eg) anesthetic deaths. Positioned asphyxia: Body’s position prevents entry of o2. eg) forcible flexion of neck on chest by weight of body, entangling of body (neck) Postictal: falling of tongue backwards against post pharyngeal wall. eg) unconscious patient, epileptics AIRWAY OBSTRUCTION: caused due to mechanical obstruction of oronasal passage. Force directed cephalad, pharynx and tongue root are elevated and forced back resulting in obstruction of laryngeal entrance. Resulting in compressive narrowing of laryngeal and tracheal lumina. JUGULAR VENOUS SYSTEM OBSTRUCTION: anterior, external, internal jugular vein. External force on the neck sufficient to cause airway obstruction compresses the great veins. EFFECTS:1) hyperemia distal to cervical compression 2) overdistension of intracranial venous sinuses, cerebral veins and capillaries. 3) cervical back pressure 4) punctuate hemorrhage (brain, subconjunctival region) 5) bleeding from external auditory meatus rare 6) skin and surrounding areas become deeply congested. CAROTID ARTERIAL FLOW OBSTRUCTION: common carotid arteries from the level of cricoid cartilage to upper border of thyroid cartilage rest on transverse processes of 4th,5th,6th cervical vertebrae BONES AND CARTILAGES: 1) hyoid bone (bilateral fracture cause fracture) 2) laryngeal cartilages (vulnerable to compressive trauma) 3) thyroid and cricoid cartilages 4) cervical vertebrae and its content compression CAROTID SINUS STIMULATION: initiate inhibitory vagal nerve impulses causing instantaneous stoppage of heart. VAGUS NERVE STIMULATION: causes cardiac arrest. ??? Physiology of Asphyxia: STAGE 1 STAGE 2 STAGE 3 Obstruction Expiratory Dysponea Exhaustion Reduction of o2 Struggle to breath coma cyanosis Expiratory breathing Irregular breathing Accumulation of co2 Deep cyanosis Slow resp rate with long intervals Stimulation of Neck veins engorged Resp fails but heart respiratory center continues to beat for sometime Increased rate and Congestion of face and Pupils dilate, amplitude of respiration other visceral organs conjunctiva becomes unresponsive BP and pulse rate confusion Diastolic BP falls unchanged unconsciousness Unconsciousness: 2-3 min Death: 4-5 min BIOCHEMISTRY OF ASPHYXIA: Reduction of o2 Inc in co2 conc Lowering pH to acidic side Blood sugar level increase Exchange of Na with K ions across cell membrane Effects on Cells: cells most susceptible to o2 insult Brain cells, Capillary Endothelial cells Pathology of asphyxia: 1) Cyanosis. Color of blood changes from normal pink to purple/blue.  For cyanosis the value is 5gm of reduced blood/per 100 ml of blood. Cyanosis made within a few hrs of death. Cyanosis is masked in: a) congestion of face due to constriction of face. b) post mortem changes (PM lividity) c) body kept in cold environment assumes pink color. d) terminal cyanosis is common in many forms of death. 2) Congestion: hypoxia/anoxia causes dilatation of capillary endothelium. Dilatation causes stasis of blood in capillaries and venules, displayed as redenning. Congestion of face/organs. 3) Edema(Pulmonary): Injury to capillary wall causes increased capillary permeability. Transudation of plasma in tissue spaces. Edema is predominantly appreciated in lungs. 4) Petechial Haemorrhage: also called Tardieu’s Spots. These are small, punctuate, pinpoint hemorrhages of venular origin seen on certain particular sites. (tissues like skin, eyelids, sclera, conjunctivae, pleura, pericardium) Size varies form 1/10th of mm to 2mm. Mechanism of formation: Acute rise in venous pressure that causes overdistension and rupture of thin walled peripheral venules especially in lax tissues. Petechial Haemorrhages in conditions other than asphyxial deaths: i) sudden death due to coronary artery diseases. ii) meningococcemia iii) blood dyscrasias scurvy, purpura hemophilia. iv) sub bacterial endocarditis Absence of Petechial Haemorrhages in Asphyxial Deaths: i) Immersion (drowning) ii) hanging when body is completely suspended iii) suffocation in plastic bags iv) co poisoning inert gas breathing 5) Fluidity of Blood (Persistent): Postmortem clotting of blood is significantly delayed or completely inhibited in obstruction to external respiratory exchange. 6) Dilation (Engorgement) of Right Sided Heart: terminal engorgement of right sided heart and ventricle due to generalized rise in venous and intracardiac pressure. GARDON’S CLASSIFICATION OF ANOXIA:  1) Anoxic anoxia: when sufficient o2 cannot reach the pulmonary alveoli. eg) breathing in a low o2 content environment, occlusion of nasal and oral orifices. 2) Anemic anoxia: results from deficiency in the quantity of Hb available to combine with o2 present in normal conc in pulmonary alveoli. eg) formation of carboxyhemoglobin and methemoglobin, Anemia. 3) Stagnant Anoxia: when normally oxygenated Hb is not transported efficiently to its destination- individual cells. eg) shock with resultant cardiac stagnation, cardiac failure. 4) Histotoxic Anoxia: An intracellular abnormality resulting in defect in intracellular oxidative system. Prevents the cell from either accepting or utilizing the o2 brought to it in adequate supply. Divided into 4 categories: EXTRACELLULAR PERICELLULAR METABOLIC SUBSTRATE HISTOTOXIC HISTOTOXIC HISTOTOXIC HISTOTOXIC Tissue oxygen Decrease in cell End products of There is enzyme system membrane cellular insufficient food of the body is permeability. respiration stuff for efficient poisoned. eg) Prevent access cannot be metabolism by cyanide of o2. eg) removed, cell. eg) poisoning, halogenated preventing hypoglycemia, hypnotic and hydrocarbon, further cerebral sedatives, chloroform, metabolism. eg) ischemia. opiates ether. uremia and co2 poisoning MECHANICAL/VIOLENT ASPHYXIAL DEATHS: Classification: 1) External opening Suffocation (plastic bag/ adhesive tape) Gagging (cloth in mouth)  Smothering (by hands/pillow) Overlaying 2) Upper respiratory passage Glottis choking 3) larynx/trachea Hanging Strangulation (garotting/throttling) 4) Lower respiratory Foreign body impaction passage(trachea/bronchi) 5) Chest wall (respiratory Traumatic asphyxia muscles) HANGING/SUSPENSION Death caused by suspension of a body by a ligature encircling the neck where the force is derived from the gravitational drag of weight of body/ parts of body. TYPES: complete (typical/atypical) Incomplete complete incomplete typical atypical Feet doesn't All other When the point When the point touch the situations where of suspension is of suspension is ground. Weight feet touch the placed centrally another position of the whole ground. over the on the body act as Eg) kneeling occipital. The neck/scalp constricting force position, ligature runs reclining position symmetrically on both sides of the neck. AUTOPSY FINDING: External a) General (body) b) Locus (neck) Internal EXTERNAL GENERAL (BODY) Lividity marked on the skin of dependant parts Head declined to side opposite to knot If asphyxial death: face and neck above ligature maybe congested If death instantaneous: arteries occluded, pale face Tongue protruded out with saliva dribbling External neck region Appearance: depressed grooved area showing pattern of material used Color: early- pale late- dry, hard, yellowish brown parchment like Number: single Location: upper part of neck above the level of thyroid cartilage Course/Direction: inverted v shaped mark or unmarked area near the knot In case of running noose:- Mark horizontally running with an addition vertical mark caused by suspending ligature Knot area:-Thickened broader depression on the scalp or on the contact area Surrounding:- Abrasions & Bruising in the depth of ligature mark. Edges may show hyperemia and few ecchymoses Character of impression: a)Thin rope (string, wire) deep & narrow b)Broad fold soft peace of cloth wide shallow c)Well defined mark if body is heavy & suspended for longer time INTERNAL FINDINGS I. Long drop (Judicial hanging) Injury (Bruising, rupture, Laceration of neck's soft structures) Transverse intimal tear of carotid with extravasations of blood in the surrounding tissue Fracture + dislocation of C1,C2,C3 cervical vertebrae Pons and medulla may show injury I. Usual form of hanging Fibers of platysma and S.c mastoid may be torn Posterior horn of thyroid may be fractured due to pressure exerted on thyrohyoid ligament Hyoid bone rarely fractured Certain amount of hyperemia of trachea, epiglottis and lymphoid nodes Area below the ligature mark shows a dry, glisting, white band with few ecchymosis. Caution:- Don't undo the knot, photograph it, cut from the sides of ligature MEDICO-LEGAL ASPECTS Two major issues: 1) Whether ante mortem or post mortem 2)Manner of death suicidal / homicidal / accidental. Following points can guide an examiner: -Presence of some other cause of death /injuries that can not be attribute to self infliction/ suspension -An unacceptable distribution of hypostasis provided it is fixed -The anchorage used for suspension may show evidence of rope movement from below upward -Absence of dribbling marks of saliva -Absence of congestion and hemorrhage in the lymph nodes above and below the ligature -Suspension from higher area without presence of support or approach Manner of death I. Suicidal hanging -One of the commonest method in illiterate/poor class -Mostly male young - middle age -Selection of secluded place -Undisturbed surroundings -Election of readily available material -Fare well notes -Psychological autopsy, marital, social, financial problems KNOT:-Tied on back of neck (Nape) GAG:-In mouth LIMBS:- Tied Tightly INJURIES:- On body due to struggle / resistance. III. Accident: -Auto erotic activity -Infant lying in a crib may slide between side bars of crib -Kite flying accident -In industrial set up belts, rope and part of clothing caught in rooters, wheels, or chains -Clothes (Dopatta) caught in bike's wheel ASPHYXIA 2 Anything that interferes with oxygen transfer can be called 'asphyxia Strangulation: It's a form of asphyxial death caused by the constriction of the neck by ligature or by any means without suspending the body. 1. Ligature 2. Manual strangulation/ Throttling 3. Mugging 4. Garroting 5. Bansdola Causes of death Coma Congestion Asphyxia Vagal inhibition Classic signs of Asphyxia Petechial hemorrhages Congestion and Edema Cyanosis Engorgement of right heart and Fluidity of blood Congestion Petechiae Caused by an acute rise in venous pressure (pressure on jugular) Rupture of overdistended thin walled peripheral venules Size varies from 1/10th - 2 mm Specially found in lax tissues, such as the eyelid, face, and in unsupported serous membranes, such as the pleura and epicardium (Tradieu spots) Cyanosis >5 g of reduced hemoglobin per 100 ml blood is necessary before cyanosis becomes evident. Classical features of strangulation when cardiac arrest is delayed -Petechiae -Ear bleed -Nose bleed -Ligature mark -Congestion -Bruises, abrasions and fingernail marks -Paler skin below neck -Congested and cyanosed face -Sub-conjunctival hemorrhage -nail marks -Tardieu's spots -Protruded tongue -Horizontal ligature Mark Ligature Mark -well defined, slightly depressed, transverse -Oblique-if victim is sitting & assailant is standing -Usually at the level of thyroid cartilage or below -More prominently at the front of neck -Bruises and abrasions around it show antemortem nature -May be interrupted by clothing or victims finger or ornaments -Examination of ligature-for blood, fragments of epidermis, hair or other substances. -Sign of struggle. PSEUDO STRANGULATION GROOVE: Seen in infants and children with short necks. Tight collars may produce a mark similar. Hanging Ligature furrow elevates to the Back&sides of the neck behind the ears Strangulation Strangulation Ligature furrow low horizontal, completely encircles the neck. back of neck has trauma HANGING STRANGULATION Suicidal usually Homicidal usually Face usually pale Face congested Bleeding from nose and mouth rare Bleeding from nose and mouth common Injury to muscles of neck rare Injury to muscles of neck common Neck usually stretched Neck not stretched No signs of struggle Signs of struggle present Limitation of classic features Petechiae: Highly unreliable indicators of an asphyxial process. Congestion and edema: Caused by of obstructed venous return Cyanosis: Caused by diseases of the heart or lungs or by abnormal haemoglobin types like methemoglobin etc. Internal Examination Findings Autopsy technique (v shaped incision, eviscerate cranial, throacic and abdmoninal viscera) Severe congestion and hemorrhage Fracture of Thyroid cartilage Laceration of muscles Injury to Laryngeal cartilages, tracheal rings and carotid arteries Fracture of hyoid-Outward Death occurs due to hypoxia (anoxic) Cerebral ischemia / venous congestion Asphyxia and venous congestion combined Shock due to reflex cardiac arrest -Pale face would indicate a rapid death from reflex cardiac arrest while a cyanosed face with petechiae would suggest a delayed death. Look like ligature marks -Decomposed bodies present as swollen necks and exaggerated fold of skin -Creases on necks of elderly people who have less amount of fat -When body is placed in a mortuary refrigerator with head propped on block -In children, skin crease followed by refrigeration with the head raised on adult sized block Homicidal strangulation -Knot is tied at back of neck -Hands are tied, mouth is gagged -Signs of struggle present Infanticide-by strangulation with umbilical cord accidental strangling In newborns when umbilical cord is tightly twisted around the neck Children restrained in their cots by harness When neck tie/scarf caught in moving machinery. Throttling Asphyxia produced by compression of neck by hands. Internal findings -Hemorrhages, from pinpoint to extensive in mucous membrane of larynx, epiglottis, pharynx -Inward compression fracture of hyoid bone (Inward, anteroposterior, avulsion) External findings -Bruises produced by tips of fingers -Pressure of nails produce crescentic marks Garrotting Compression of neck by a ligature which is quickly tightened by twisting it with a lever Results in sudden loss of consciousness and collapse Mugging Strangulation by holding the neck in the bend of the elbow/knee. Bansadola Strangulation practiced in North India using Bamboo (sticks) A foot or knee may be placed across the front of the throat and pressed while the victim is lying on the ground. Suffocation It is a general term used to indicate death from deprivation of oxygen, either from lack of the gas in the breathable environment or from obstruction of the external air passages. Classification External air passages (smothering, overlaying) Internally- nasopharynx, larynx (gagging, choking) Chest (traumatic asphyxia) Combination of two (burking) Smothering It's a form of asphyxia caused by closure of external respiratory passage either by hand or other means, or introduction of foreign materials like cloth or paper etc. Plastic bag asphyxia Children may suffocate accidentally Means of comitting suicide by elderly Addictive habit of glue-sniffing may lead to death by suffocation, as the solvent is sometimes put in a plastic bag. Overlaying Also called compression suffocation It results from compression of the chest, nose and mouth May happen accidentally when a mother, sharing a bed with her child who may roll over during sleep and occlude the air passages. Choking It is a form of asphyxia caused by an obstruction within the air-passages by a foreign object, like coin, fruit seed, toffees, candies, fish or any other material. Café coronary Accidental choking when a bolus of food produces complete obstruction of the larynx mimics a heart attack usually seen in an intoxicated restaurant person Laryngeal irritation causes vagus stimulation causing sudden death due to cardiac arrest. Gagging Asphyxia which results from pushing a gag (rolled up cloth or paper balls) into the mouth, sufficiently deep to block the pharynx. Suffocation- Causes of death Asphyxia Vagal inhibition Laryngeal spasm Infection Traumatic asphyxia Post-mortem appearances: Intense deep purple red color of the head, neck and upper part of the chest above the level of constriction. Respiratory arrest due to mechanical fixation of chest so that the respiratory movements are prevented. E.g. Stampede in a theater or in places where crowded gatherings are there. Fall of earth-coal mines, tunneling accidents etc. Burking Method of homicidal smothering+Traumatic asphyxia. ASPHYXIA 3 Drowning: Death resulting from defective oxygenation of blood in the lungs due to presence of fluid in air passages after interning through mouth or nose. Fatal period (Typical): Fresh Water: 3-5 minutes Salt water: 8-12 minutes Classification: Whether fluids blocks the air passages to cause death Typical (Wet Drowning) Fresh Water Salt Water A Typical (Dry Drowning) Immersion Syndrome Submersion of unconsciousness Post immersion syndrome (secondary drowning) Causes/mode of death 1. Asphyxia/hypoxic Hypoxia: Obstruction by inhalation of fluid. Laryngeal spasm. 2. Syncope: Ventricular fibrillation - In Fresh Water. Cardiac standstill- in Salt Water 3. Vagal Inhibition: Dry drowning. 4. Hypothermia: Chilling by immersion in cold water 5. Injuries during fall: Concussion (Head and Vitalorgans) Mechanism of death 1. Typical drowning (Wet Drowning) in Fresh Water: Large quantity of water crosses alveolar membrane reaches circulation produces marked hypervolemia, red cell swell and burst (lysis) causes liberation of K* results in biochemical insult to myocardium giving rise to ventricular fibrillation and death. Aggravating factors: -Extreme myocardial anoxia -Overloaded circulation (Hemodilution) -Plasma K+ excess Na+ less -Cerebral anoxia. in Salt water: Hyper tonicity of inhaled water causes hemo concentration causing withdrawal of water from circulation into the lungs producing massive pulmonary edema and death. Aggravating factors  Exchange of electrolytes Increasing viscosity of blood causes weakening of the heart. Atypical drowning: 1) Dry Drowning :- 20% falls in this category Mechanism: Water entering the nasopharynx or larynx triggers intense laryngeal spasm and death (Anoxic anoxia), but no water enters the lower respiratory tract. 2) Immersion syndrome: -Sudden impact with very cold water -Falling or diving with feet first. -Horizontal entry into water causing a blow on abdomen. -Vagal stimulation leading to instantaneous death 3) Submersion of unconscious: Victim may be suffering from Epilepsy Pre-existing cardiac disease Dizziness due to essential hypertension Drunk 4) Secondary drowning syndrome: (Near drowning) Defined as immediate survival after asphyxia due to submersion. 5) Post immersion syndrome: Resuscitated after drowning and survives for 24 hours. May develop hypoxemia resulting in brain damage, cerebral edema, pulmonary edema, pneumonitis, myocardial anoxia, cardiac arrhythmias, electrolyte imbalance, metabolic acidosis, hemoglobinuria, fever and sepsis. Autopsy findings (external) A) General changes occurring after death 1. Cooling. Rate twice that of the environment. usually cool when recovered 2. Hypostasis. Depends upon the state of water whether running or stagnant In stagnant water i. Distribution = Head, neck & chest area, legs ii. Colour= Pink 3. Rigor Mortis: Struggling for survival, muscular Exhaustion so Rigor Mortis Sets early. 4. Putrefaction: purification sets early and it is usually advanced. B) Due to contact with water: 1. Body wet. 2. Clothes wet (findings of medium). 3. Goose flesh (cutis anserina). 4. Washer Woman feet. Goose flesh (cutis anserina): Feature:- Skin appears granular puckered with hair standing out (pimpling of skin) Mechanism:-Spasm of erector pilae muscles due to exposure to cold water. Value:- Not a sure sign of death due to drowning Washer Woman feet: Feature:- Skin of palms and soles, sodden, wrinkled and bleached Mechanism:-Action of water on thickened epidermis, loss of skin tone & vascular contraction Value:- Not a sure sign of death due to drowning Cadaveric spasm: Features:- Aquatic vegetation, contents of water or floating objects are tightly clenched in the hands Mechanism:- Person may make terminal attempts to grasp the things for support. Usual objects:- weeds, grass Value:- One of the surest signs of death due to drowning. C) Due to inhalation of water Oro-nasal fine froth (Foam) -Colour: Whitish or Pinkish (Blood tinged). -Quality: Fine, tenacious, persistent. -Quantity: Abundant, if wiped away, reappears. -Shape: Small balloon, mushroom like, sometimes resembling a protruded tongue -Mechanism: Fluid entering the air passages provokes the lining membrane to produce mucus. The mucous + surfactant + water vigorously produces fine froth. -Value:- Vital phenomenon indicates ante mortem drowning. Differential diagnosis: Oro-nasal secretion resembling froth is seen in the following cases i. Strangulation (Ligature, Manual) ii. Cardiac disease death iii. Pulmonary edema iv. Epileptic shock v. Poisoning Insecticide Narcotic, hypnotic, sedatives, opium, cocaine, barbiturates. vi. Putrefaction Autopsy findings (internal findings): i) Fine froth in air passages ii) Lungs (Emphysema aquosum) : lungs feel heavy, pale, spongy and caught in water. Essential sign of antemortem drowning. Size:-Large, voluminous Shape:- Ballooned Colour:- Pink Location:- Overlapping the heart Contents:- Froth, visible at hilar region, grass, weed or sand indicates the medium Sectioning:- Crepitus sound, froth extrudes  iii) Diatoms: Algae (Plant) -Body composition:- Unicellular. -Size:- Microscopic 10-80 microns. -Inhabitant:- All type of salt & fresh water where photosynthesis is possible. -Shape:- Variable. -Constitution:- Exo skeleton made of silica. -No of species:- More than 15000, every water have its own. -Properties:-Thick silica wall, resist to acid digestion and putrefaction Medico-legal value a) There presence in stomach and lung is of no importance. Finding in the brain, kidney, liver indicates ante mortem drowning. b) Comparative study of diatoms found in the body and river area give idea about the site where drowning occurred. iv) Haemmorhage in middle eur cavity is indicative of drowning when the tympanic membrane is intact. Medico-legal value: controversial Gettler's Chemical test: It is the estimation of the chloride content of blood from both sides of the heart. In fresh water drowning---> chloride content of the left side of heart is diminished. In salt water drowning-> chloride content of the left side of heart increases. Water cannot enter the left side of the heart if a dead body is thrown in water Medico-legal value: controversial Medico-legal aspects: "Suicide" Prevalence 1/3 of total cases 1. Some clothes and personal articles are left at the scene, spectacles, cap, gloves, overcoat, umbrella, shoes.  2. Farewell note 3. Psychological autopsy "Homicide" Children, Female, Old debilitate person and intoxicated Person "Accidental" Prevalence 2/3 of all deaths due to drowning Major catastrophe:- tsunami, cyclones, Floods, Boat capsized, overturn, shipwrecks, automobile falling in river Minor/ Individuals: -while Boating, Bathing, Fall water games -epilepsy, Cardiac disease, intoxication -children Sexual Asphyxias: An asphyxial death in which the fatal condition is self induced during course of solitary erotic behavior Alternate Terms: -Auto erotic exercise (some self-hazardous exercises) -Masochistic practices (sexual gratification from one's own pain or humiliation) -Sex hanging (asphyxial death by hanging) Characteristic features: Bizarre picture showing a composite trait of -Erotic -Asphyxial -Masochism -Transexualism Death scene: Choice: Quiet secluded place, where nobody can disturb or discover the deceased A. Usual Place:- Home: Toilet, Bed room  Outside: Garden, Garage Paraphernalia: Presence of miscellaneous articles, (especially the equipment needed for a particular activity) Mirror ensure visibility during the exercise. Pornographic pictures, book or films. Lubricants, condoms. Personal factors: Peak age: 13-17 years Sex:-Always male but female cases are reported. Social Class:- No social class is exempted. Professional, white collared, artistic class more vulnerable. Clothing:- Invariably naked, scantily dressed or dressed in bizarre fashion opposite sex's attire. Genitalia:- Enclosed/ wrapped in cloth, handkerchief, tissue papers to avoid soiling of other clothing during ejaculation. Reason for death: When cerebral hypoxia occurs with erotic sensations, it may lead to progressive loss of voluntary control, consciousness fades and allowing the constrictive device to slacken (tightens). Manner of death: Death from a failure of the safety precautions of equipment usually practiced by the deceased classified as an: Accident Misadventure Suicide gesture Psycho-analysis:  A complicated/composite picture of sexual perversions like, -Masochism: (sexual gratification from one's own pain or humiliation), -Transvestism: Cross-dressing (practice of wearing the clothes of the opposite sex) -Narcissism: (mental health condition in which people have an unreasonably high sense of their own importance) CHLORINATED INSECTICIDES (DDT) Chlorinated insecticides: These insecticides contain chlorine in their molecular structure. Some of them include. 1. DDT (Di Chloro Di Phenyl Tri Chloro Ethane) 2. Gammaxine 3. Hexaphane Endrin 4. Aldrin 5. Dialdrin DDT 1) DDT is the most commonly used ChLoro group of insecticide. 2) Powered DOT is a white crystalline solid which is readily soluble in kerosene oil. 3) It is used to kill flies, mosquitoes, lice, fleas, and bed bugs. Mode of action: (i) it first stimulates then depress the cerebellum and motor cortex (ii) It sensitizes the myocardium to the action of catecholamine, so that injection of epinephrine may induce ventricular fibrillation. (ii) It depresses the adrenal cortex causing irritation and sensitization of the skin. (iv) Locally it acts as an irritant, when swallowed (v) Chronic exposure causes liver necrosis, degeneration of renal tubules, myocardium and voluntary muscles. Portal of entry 1) Oral (ingestion) 2) local (dermal contacts) 3) Inhalation Routes of absorption: insoluble in water In pure solid form, it does not get absorbed through skin but when it is dissolved in kerosene oil or other solvents, it gets easily absorbed through the gastrointestinal tract, skin and lungs. A 2% solution of D.D.T. acts as poison to human beings and its solution in fatty acids increases the toxicity. Fatal Dose: D.D.T: 30 gm or 0.5 gm/kg. Lindane: 15 gm. Chlordane: 30 gm. Methoxychlor: 350 gm Fatal period: ranges from half to four hours General symptoms: 1. Nausea and Vomiting 2. Coughing 3. Excitability 4. Vertigo 5. Weakness 6. Muscular tremors 7. Convulsions 8. Tingling in arms and legs 9. Paralysis of legs 10. Pulmonary edema 11. Unconsciousness and coma 12. Death from respiratory failure Acute poisoning The signs and symptoms develop within half hour of ingestion of the poison (1)Salivation, nausea, vomiting and abdominal pain. (2)Apprehension, hyper excitability, restlessness, Nervousness (3)Tinnitus and vertigo (4) Blurred vision with twitching of eyelids that is followed by tremors, first affecting the head and neck then involving the extremities: (5) Tonic Clonic convulsion are characteristic of D.D.T Aldrin, dieldrin and lindane poisoning (6) Generalized epileptiform convulsions occur in toxaphene poisoning (7) Rarely muscular weakness, ataxia, incoordination numbness, and paralysis may occur Chronic poisoning: After absorption, these insecticides accumulate in body fat and concentration gradually falls over several months. The workers with a history of many months of exposure having more than 648 ppm of D.D.T. in their fat suffer from chronic poisoning. DDT can be transferred to babies through breast milk Signs and symptoms: (i) Anorexia, nausea and vomiting (ii) Cachexia, loss of weight anemia (iii) Anxiety, headache hyperirritability (iv) Blurred vision (v) Tremors, convulsion and coma (vi) Liver is moderately enlarged Treatment: (i) Immediate gastric lavage with 2% potassium permanganate (ii) Emetics should be given (iii) There is no known antidote of DDT (iv) Cathartic fats, or oils should be avoided as they promote absorption. (v) Atropine sulfate, should be administered (vi) Oxygen inhalation and artificial respiration is given (vii) To control muscular twitching, tremors and convulsion, Thiopentone sodium 100-250 mg IV. followed by I.M. injection of 100 mg of Phenobarbital sodium also diazepam and barbiturates viii) Calcium gluconate 10 ml of 10% with glucose IV and calcium lactate orally beneficial (ix) Adrenaline, epinephrine should not be used; they induce ventricular fibrillation. Morphine is also avoided (x) For skin contamination, through washing with soap and water (xi) In chronic poisonings, the patient should be removed from the site of exposure and given a low fat, high protein and carbohydrate diet. The treatment is symptomatic. Postmortem findings: Stomach contents may smell of kerosene and are bloodstained (ii) Mucosa of stomach and intestines is congested and petechial hemorrhagic fatty changes in heart (iii) Liver is enlarged with fatty degeneration (iv) Lungs are congested and edematous (v) Spleen, brain and kidneys are congested. Medico legal importance 1. Used for suicidal purpose 2. Accidental poisoning ORGANOPHOSPHATE INSECTICIDE POISONING INSECTICIDES: Chemical substances used for killing, control or eradication of unwanted pests, insects and worms. Some of the most commonly used insecticides compounds are * ORGANO PHOSPHORUS GROUP (OPC) * CARBAMATES * CHLORINATED GROUP DDT, endrin * NAPHTHALENE coal tar product ORGANO PHOSPHATES & CARBAMATES * Diverse group of synthetic organic poisons. * Used as insecticides, herbicides, & nerve gas in chemical warfare. TYPES OF POISONING IN PAKISTAN * Chemical/gas (43.8%) * Drug/medicine (27%) * Alcohol (16.7%) * Food/plant (6%) CLASSIFICATION OF ORGANOPHOSPHATES 1) Alkyl group Hexa Ethyl Tetra Phosphate (HETP) Tetra Ethyl Pyro Phosphate (TEPP) Octa Methyl Pyro Phosphate (OMPP) Malathion Dipterex 2) Aryl group Parathion Paraoxon Chlorothion Diazinon Eketox Organophosphates inhibit acetylcholinesterase. Acetylcholine accumulates in the BRAIN: Post synaptic neurons SPINAL CORD: Autonomic synapses Endings of the postganglionic parasympathetic nerves Skeletal muscle junction/efferent nerves. Toxic effects resemble Physostigmine and Neostigmine but may be much more persistent. Accumulation of acetylcholine causes hyper excitation of voluntary and involuntary muscles with increased secretions all together resulting in toxic symptoms. CARBAMATE GROUP Lack of phosphate group unlike organophosphates. Carbamate group substituted instead of alkyl or aryl groups in the hydrocarbon chain. Reversible inhibitors of cholinesterase Commonly used carbamate insecticides include: 1. Aldicarb 2. Premicarb 3. Carboryl (highly toxic) 4. Propoxur 5. Methiocarb 6. Thiofanox 7. Methomyl 8. Oxamyl SYMPTOMS OF ORGANOPHOSPHORUS AND CARBAMATE POISONING Illness first affects involuntary muscles and secretory glands, then voluntary muscles, and finally vital brain centres A) Muscarinic effects 1. Bronchial Tree (Asthma-like) This symptom complex is Spasm sometimes called SLUD, the prominent Increases secretions symptoms being salivation, lacrimation, urination, and defecation. Chest pain Dyspnea Cough Edema Cyanosis 2. Gastrointestinal Tract Increased salivation Nausea Anorexia Cramps Sub-sternal tightness/cardio spasm Tenesmus Involuntary defecation 3. Heart: Bradycardia 4. Eyes Red tears (Chromogenic tears) due to porphyrins Meiosis Blurred vision 5. Skin  Excessive sweating 6. Urinary bladder Incontinence Cholinergic Toxidrome Mnemonic DUMBELS D: Diarrhea U: Urination M: Miosis, Muscle fasciculations and weakness B: Bronchospasm, Bronchorrhea, Bradycardia , Blurring of vision (d/t miosis) E: Emesis L: Lacrimation (red tears) S: Salivation, Sweating B) Nicotine like effects 1. Striated Muscles' Weakness, twitching/ fasciculation and cramps 2. Cardiovascular effect: remember from Mon=Mydriasis, Tues= Tachycardia, Wed= Hypertension bradycardia Weakness of muscles, Thurs= hyperTension, Fri= Fasiculations more Tachycardia pronounced 3. Eyes: Mydriasis miosis i.e. muscarinic effect more pronounced OTHER: Diaphragmatic failure, paralysis, areflexia and respiratory failure. Central Nervous System Side effects: Irritability, drowsiness, confusion, tremors of hands, lips, face or tongue, slurred speech, ataxia, generalized weakness Cheyne-Stokes respiration, delirium, Areflexia, coma, convulsions, respiratory and circulatory depression, psychosis and death Garlic or kerosene like odor Skin becomes red and blistered LAB DIAGNOSIS Death is generally caused by paralysis of 1. Depression of CHOLINESTERASE ACTIVITY musculature but may result from * In acute poisoning, signs and symptoms occur respiratory failure, circulatory arrest, oedema of lungs or brain when > 50% of cholinesterase is inhibited.  RBC cholinesterase is therefore called true while plasma one is called pseudo cholinesterase RBC cholinesterase is considered more accurate as Plasma cholinesterase declines more rapidly so it is less reliable. 2. P-nitrophenol test more helpful in parathion poisoning P-nitrophenol is a metabolite of some OPCs and is excreted in the urine. It can also be performed on vomitus or gastric contents. 3. Quantitative methods: Spectrophotometry TREATMENT Treatment may be summarized in the following order 1. Decontamination 2. Care of Airway 3. Administration of antidote 4. Administration of cholinesterase reactivators 5.General measures Decontamination 1. Remove the person from the source of poison. 2. Strip off all contaminated clothes 3. Flush the skin and mucous membrane thoroughly with water. 4. Gastric lavage with water/ KMnO4. Activated charcoal (1 g/kg) 5. Irrigate eyes with NS or ringer lactate ADMINISTRATION OF ANTIDOTE Preservative free atropine is the drug of choice Atropine blocks the muscarinic manifestations MANIFESTATION OF ATROPINIZATION: Drying of secretions Tachycardia Flushing Dry mouth Dilated pupils (early sign, does not mean endpoint)  -Initial dose of I mg I/V (check for adverse effects) -Repeat dose 2 mg every 15 minutes until atropinization is achieved. -Average patients requires 40 mg/day. CHOLINESTERASE REACTIVATORS 1. Oxime compounds which reactivate the phosphorylated acetyl cholinesterase enzyme. must be given as early as possible. After 24 hours efficacy comes down 2. Use of Cholinesterase reactivator in carbamate poisoning may worsen symptoms. 3. Ineffective in reversing the CNS effects of organophosphate because it cannot enter into the CNS. 4. 2 PAM (Pralidoxime chloride) is given in a dose of 1 to 2gm diluted in 5% isotonic saline and may be repeated 12 hourly. 5. OR Continuous Infusion 400 mg IV DIAZEPAM For convulsions Improves survival (must not be used with other CNS depressants). Decreases the cardiac and brain morphologic damage resulting from OPC seizures. Dose: 0.5-2 mg IV every 15 min. SUPPORTIVE CARE -Diuretics like lasix -Coramine or Dextrose Saline for collapse. -Bronchodilators to improve respiration. -Tracheostomy or Mechanical ventilation if necessary. Postmortem findings: The changes are suggestive of asphyxia. Externally, the face is cyanosed. There is froth, usually bloodstained, at the nose and mouth. A kerosene-like smell may be perceived. Internal: Contents of the stomach are blood-stained, the mucosa is congested, and submucous petechial haemorrhages are seen. The other postmortem findings are: pulmonary oedema, capillary dilatation, petechial haemorrhages, and hyperaemia of lungs, brain and other organs In delayed paralysis of the extremities induced by parathion, malathion, and other compounds, the findings are demyelination of ascending and descending spinal tracts with degeneration of motor horn cells THERAPEUTIC POISONS 1 (BARBITURATES, DIAZEPAM, AND TRANQUILIZERS) Barbiturates are used as sedatives, hypnotics, anticonvulsants, anesthetics and tranquilizers. Barbituric acid (Malonyl Urea) is a combination of Urea and Malonic acid. MODE OF ACTION They have a depressant effect on the C.N.S. and affect the Cardiac and Respiratory centers and death usually occurs due to respiratory failure i.e. Asphyxia. ROUTES OF EXCRETION -Detoxicated and excreted by LIVER. -By Kidneys. (So contraindicated in cases of impairment of Liver or Kidneys) MILD INTOXICATION-GRADE I * The patient is drowsy or asleep, a state from which he is readily aroused by calling his name loudly or by shaking him. The patient thinks slowly, mild disorientation, variation of mood, impairment of judgment, slurred speech, ataxic gait and Nystagmus. Reflex activity and vital signs are not affected. MODERATE INTOXICATION - GRADE II This follows 5-10 times the oral hypnotic dose. Here state of consciousness is more severely depressed, and is usually associated by depressd or absent deep reflexes and slow but not shallow respiration. Corneal reflexes are retained with occasional exceptions. At times patients can be aroused by vigorous manual stimulation, when awakened, he is confused and dysarthric and after a few moments he drifts back into unconsciousness. SEVERE INTOXICATION-GRADE III Occur with ingestion of 15-20 times the oral hypnotic dose. The patient can not be roused by any means indicated. Respiration is slow and shallow or irregular and pulmonary edema and cyanosis may be present. The deep tendon reflexes are absent. Usually patients show no response to plantar stimulation. Corneal reflex is absent, but may be present unless the patient is severely asphyxiated. (In early hours of Coma, there may be a phase of rigidity of limbs, hyperactive reflexes, ankle clonus extensor plantar signs, the temperature is subnormal the pulse thready and rapid and blood pressure at shock levels i.e. decreased.) LONG ACTING BARBITURATES - Effect lasts from 1 to 8-10 hours. F.D. 2-4 GMS. Barbitone (Veronal) (Gardenal) Phenobarbitone (Luminol) INTERMEDIATE ACTING BARBITURATES - Effects last from ½ hour to 5-6 hours F.D. 1.5-2GMS Amylobarbitone (Amytal) Butobarbitone (Soneryl) ULTRA SHORT ACTING BARBITURATES - Immediate Anesthesia up to few minutes. F.D. 1gm (15 grains) Thiopentane (Pentothal) Methohexitone (Brevital ) SIGNS & SYMPTOMS OF ACUTE BARBITURATE POISONING Giddiness. Ataxic gait Occasional nausea. Diplopia  Stupor Coma Rapid and shallow or slow and labored respiration. Cold and Clammy skin. The pupils are contracted, but light reflex is present unless the patient is severely asphyxiated. Plantars are extensors. In severe asphyxia due to advance poisoning pupils are dilated and light reflex is -ve. Face tends to become progressively cyanotic. Oliguria may be present. Bullous lesions may be present over pressure points especially legs. Coma may continue for one or two days, but the period of survival is much shorter. Death occurs from Cardiac failure due to lung edema or aspiration broncho- pneumonia. Slowing of pulse rate TREATMENT OF ACUTE BARBITURATE POISONING -In Mild cases the patient is allowed to sleep off the actions of barbiturates under careful observation. While moderate and severe cases are treated on following basic principles:- 1. Removal of unabsorbed poison. 2. Maintain respiration. 3. Stimulate circulation. 4. General measures. 1. REMOVAL OF UNABSORBED POISON -By Gastric lavage with Warm Water, normal saline or weak KMno4 sol. -No emetics may be used when patient is unconscious -FORCED diuresis for rapid elimination of Poison. (The Patient should be catheterized so as to keep an accurate account of urinary output) (Diuresis is induced by giving 5% Dextrose saline + 40 mg Lasix + 20 m eq of Potassium chloride IV) (500 ml of Mannitol 20% may also be given to increase diuresis) -As the alkaline reaction of Urine increases diuresis, we can give about 150 ml of 7.5% Sodium Bicarbonate. (After correcting the initial emergency state, the fluids should be administered at a rate to ensure an output of 500 ml/hr) -Serum Electrolytes, especially Potassium should be determined every 2 hours until the clinical state of the patient has stabilized. 2. MAINTAIN RESPIRATION The routine administration of oxygen is contraindicated in cases of severe respiratory depression. Antibiotics be given to prevent Pneuminitis. If there is severe respiratory depression with cyanosis pupillary dilatation, give artificial respiration with intermittent positive pressure respirator. 3.STIMULATE CIRCULATION If patient is in shock: We raise the foot end of the bed. Give D/S drip. Forced Diuresis Peritoneal dialysis Haemodialysis BARBITURATE AUTOMATISM: When a person becomes addicted to barbiturates, he forgets that he has taken a tablet and so takes one more; this is repeated till intoxication occurs. POST MORTEM APPEARANCES: EXTERNAL -CYANOSIS. INTERNAL: -Mucous membranes of G.I.T. are congested. -Kidney shows degeneration of tubules. -Lung are congested and edematous -The brain is also congested. BENZODIAZEPINES These agents depress mental and respiratory function when taken in overdose. Flunitrazepam intoxication has emerged as an increasing problem. Ten times as potent as diazepam. It is mixed with low-quality heroin and used to soften the effects of cocaine. It is also mixed with alcohol as date rape drug. It may cause hallucination, and mixing with alcohol increases respiratory depression. It often is not detected on standard toxicology screens. Symptoms: Include drowsiness, dysarthria, ataxia. Slurred speech, and confusion. Treatment: -Do not induce emesis. Consider gastric lavage if presentation is within 1 hour of ingestion. -administer activated charcoal. -Provide general supportive measures for hypotension and bradycardia. -Rarely, respiratory depression may require intubation. -Flumazenil, a benzodiazepine antagonist, reverses toxicity without causing respiratory depression(can be given IV/ intratracheal tube) If mixed overdose with cyclic antidepressants is suspected or the patient has a known history of seizure disorder, Flumazenil should not be used. Gamma-Hydroxybutyrate: It is often sold to participants at large dance parties and has been responsible for mass intoxication It has also been used as a date rape drug. Synonyms include "liquid Ecstasy," "liquid E," "grievous bodily harm," "Georgia home boy," "soap," "salty water" SYMPTOMS: Include ataxia, nystagmus, somnolence progressing to coma, vomiting, and random clonic movements of the face and extremities. Respiratory depression may progress to apnea. Treatment: -NO gastric lavage, NO emetics, NO charcoal -Administer oxygen and protect the airway; monitor oxygenation -Give atropine for persistent symptomatic bradycardia. -Treat hypotension with IV fluids; pressors are rarely necessary. -Obtain an ECG and monitor the cardiac rhythm continuously. -Intoxication is usually short lived; coma typically lasts for 1-2 hours, and full recovery often occurs within 8 hours. NEUROLEPTICS Chlorpromazine, thioridazine, prochlorperazine, haloperidol (a butyrophenone), and thiothixene are the most commonly used phenothiazines. OVERDOSE: Are characterized by agitation or delirium, which may progress rapidly to coma. Pupils may be mydriatic Deep tendon reflexes are depressed. Seizures and disorders of thermoregulation, particularly hyperthermia, may occur. Frank neuroleptic malignant syndrome may complicate use of these agents. Hypotension tachycardia, arrhythmias, and depressed cardiac conduction occur. Radiographs may reveal pill concentrations present in the stomach despite apparently effective gastric emptying. TREATMENT -Includes airway protection. Respiratory and hemodynamic support -administration of activated charcoal. -Emesis is contraindicated. Consider gastric lavage, which may be effective hours later owing to delayed gastric emptying caused by the phenothiazines. -Monitor the cardiac rhythm and treat ventricular arrhythmias with lidocaine and phenytoin;. -Treat hypotension with IV fluid administration and a- adrenergic vasopressors (norepinephrine). Dopamine is an acceptable alternative. -treat seizures with diazepam and phenytoin. -Treat hyperthermia with cooling CLOZAPINE is an atypical neuroleptic OVERDOSE -altered mental status, ranging from somnolence to coma. -Anticholinergic effects occur, including blurred vision, dry mouth (although hypersalivation may occur in overdose), lethargy, delirium, and constipation. -Seizures occur in a minority of overdoses. Coma may occur -physical manifestations include hypotension, tachycardia, fasciculations, tremor, and myoclonus. -Agranulocytosis may result. -atrioventricular block may occur. TREATMENT -Monitor BP and respiratory status, including ABGS if respiratory depression occurs. -Obtain an ECG and monitor the cardiac rhythm continuously. -Obtain WBC and liver function tests. -Induction of emesis is contraindicated. -Perform gastric lavage if the patient presents within I hour of ingestion. -Treat seizures with benzodiazepines and phenytoin. -Provide ventilatory support for respiratory failure. OLANZAPINE Is an atypical antipsychotic that is similar to clozapine. OVERDOSE Similar to clozapine TREATMENT -Induction of emesis is contraindicated. -Consider gastric lavage if presentation is within 1 hour of Ingestion. -Give activated charcoal. -Treat hypotension with fluids and, if ineffective, norepinephrine or dopamine. -Give benzodiazepines and phenytoin for seizures. -Provide ventilatory support for the unusual manifestation of respiratory failure SPINAL POISONS This group of poisons acts mainly on the spinal cord, ether as 1)Stimulants: resulting in spasms eg. Strychnine or, 2)Depressants: resulting in paralysis and loss of sensations eg Gelsemium STRYCHNINE Strychnine is the principal alkaloid in the seeds of strychnos plant. It is a powerful spinal stimulant. Botanical Name: Strychnos nux Vomica Other Names: Dog button, Kuchila, Poison nut POISONOUS PARTS: Seeds Bark, wood and leaves(mild, 5-10% strychnine like) Active Principles: 1) Alkaloids: Strychnine (present in seeds) and Brucime 2) Glucoside: Loganun MOA: motor Stimulates all parts of CNS, particularly the anterior horn cells of the spinal cord. Strychnine competitively antagonizes the inhibitory neurotransmitter GLYCINE by binding noncovalently to the same receptor. blocks inhibitory neurotransmitter - leading to excitatory / stimulatory effects SYMPTOMS AND SIGNS Intensely bitter taste, when chewed Symptoms appear within 15 minutes to 1 hour Patient becomes anxious and restless, muscles stiffen Face: Cyanosed, look is anxious, eyes are staring, eyeballs are prominent and the pupils are dilated. Mouth is filled with blood stained froth. Convulsions Conscious' seizure, last about half to 2 min clonic- intermittent Initially, clonic but eventually become tonic tonic- sustained Affect the flexors and extensors simultaneously Convulsions are most marked in antigravity muscles resulting in hyperextension Risas sardonicus (Latin, scornful laughter) a facial expression characterized by raised eyebrows and grinning distortion of the face resulting from spasm of facial muscles.  Opisthotonus Spasm of the muscles causing severe hyperextension resulting in backward arching of the head, neck, and spine, with only head and heels touching the ground. Emprosthotonus due to the spasm of the abdominal muscles, bending the body forward OR Pleurosthotonus Sideways Convulsions (General features): Increased muscle tone, hyperreflexia, agitation, restlessness Causes of death Cause lactic acidosis, rhabdomyolysis and hyperthermia, myoglobinuria, renal failure Death occurs within 4-5 convulsions as the patient cannot breathe. At the time of death, the body 'freezes' even in the middle of convulsions resulting in 'cadaveric spasm Death is extremely painful DIFFERENTIAL DIAGNOSIS Tetanus Epilepsy (patient is depressed with obtunded mental status) Hysteria Hypocalcemia Neuroleptic malignant syndrome, malignant hyperthermia and stimulant use DIAGNOSIS -Urine or gastric aspirate analysis utilizing a qualitative test such as thin layer chromatography (TLC) -GC-MS and high-performance liquid chromatography are also sensitive methods to detect strychnine. Cause of death: ASPHYXIA due to: Medullary paralysis Spasm of respiratory muscles Exhaustion from convulsions FAILURE OF RESP CENTRE FAILURE OF RESP MUSCLES antidepressants Neuromuscular blocking agents antipsychotics nicotine ethanol organophosphates opiates Shellfish poisoning sedatives Snake bite (cobra) strychnine Fatal Dose 1 crushed seed Strychnine: 15-50 mg (1-2 mg/kg body wt) gastric lavage can provoke convulsions but can be done with tannic acid if needed TREATMENT (after convulsion have stopped) -Gastric lavage with KMnO4 may be done cautiously, if there are no convulsions. -Activated charcoal is recommended as it adsorbs strychnine and may reduce its absorption if given 1 h of ingestion. Control of convulsions: -Dark room, free from noise and disturbance -Barbiturates, like pentobarbital sodium or sodium amytal are antidotes -Dose: 300-600 mg IV. -Diazepam 0.1-0.5 mg/kg IV slowly. (If ineffective, general anesthetics and muscle relaxants like gallamine should be given) -Maintain clear airway and ventilation with endotracheal intubation -Hyperthermia is treated by active cooling with ice water immersion, cooling blanket or mist and fan. -Intravenous fluid to maintain a urine output of 1 ml/kg/h. since metabolic acidosis and renal failure may occur. AUTOPSY FINDINGS Postmortem caloricity i.e increase in temperature after death instead of Asphyxial features usual fall Rigor mortis starts and ends quickly Unabsorbed poison/seeds may be found in the stomach. MEDICOLEGAL IMPORTANCE -Accidental due to overdose, exposure to rodenticide, quack remedies and poison mistaken for some other harmless drug, or in children eating the seeds. -Intentional self harm has also been reported -However, homicide is rare, because of its bitter taste, hence it is impossible to disguise in food and beverages