STRYCHNOS NUX VOMICA Strychnine (kuchila) is a powerful alkaloid obtained from the seeds of strychnos nux vomica, and other species of strychnos, which are found in the jungles in India. Fruit is round, hard, slightly rough, glossy-orange, 4 to 5 cm. wide, with jelly-like white or pale yellow pulp. It has 3 to 5 seeds Fig. (34-1). Strychnine occurs as colourless, odourless, rhombic prisms, having an intensely bitter taste. The bark contains only brucine. The fruit pulp has very low strychnine content. All parts of the tree are toxic. Seeds: The seeds are flat, circular dises or slightly convex on one side, concave on the other, two-and-half cm. in diameter, 6 mm. in thickness Figs. (34-2 and 34-3). They are ash-grey or light-brown in colour, have a shining surface and covered with radiating silky fibres. They are very hard, tough and difficult to pulverize. The seeds of nux vomica contained in the ripe fruit are poisonous. The seeds contain two principal alkaloids; strychnine and brucine one-and-half percent each. The seeds also contain a glucoside, loganin. The bark, wood and leaves contain brucine but no strychnine. Brucine is allied to strychnine in composition and action. Strychnine is 10 to Surface covered with silky fibers Albumin and emovo Fig. (34-2). Nux vomica seeds. Central cavity Fig. (34-3). Nux vomica. 20 times more poisonous than brucine. Strychnine is used as a respiratory stimulant, as a rodenticide and for killing stray dogs. Absorption and Excretion: All mucous membranes absorb strychnine. Much is taken up by the liver and muscles to be either released again to blood stream or to be destroyed. The release of strychnine from the liver and muscles produces convulsions on second or third day of poisoning, after sedation is discontinued. About 80% is oxidised mainly in the liver. It is excreted slowly by the kidneys and traces in bile, milk and saliva. It may be found in the cadaver up to four years. Action: It competitively blocks ventral horn motor neurone postganglionic receptor sites in the spinal cord and brainstem and prevents the effects of glycine (the presumed inhibitory transmitter). Widespread inhibition in the spinal cord results in 'release' excitation. The action is particularly

Make simplified notes from this text STRYCHNOS NUX VOMICA Strychnine (kuchila) is a powerful alkaloid obtained from the seeds of strychnos nux vomica, and other species of strychnos, which are found in the jungles in India. Fruit is round, hard, slightly rough, glossy-orange, 4 to 5 cm. wide, with jelly-like white or pale yellow pulp. It has 3 to 5 seeds Fig. (34-1). Strychnine occurs as colourless, odourless, rhombic prisms, having an intensely bitter taste. The bark contains only brucine. The fruit pulp has very low strychnine content. All parts of the tree are toxic. Seeds: The seeds are flat, circular dises or slightly convex on one side, concave on the other, two-and-half cm. in diameter, 6 mm. in thickness Figs. (34-2 and 34-3). They are ash-grey or light-brown in colour, have a shining surface and covered with radiating silky fibres. They are very hard, tough and difficult to pulverize. The seeds of nux vomica contained in the ripe fruit are poisonous. The seeds contain two principal alkaloids; strychnine and brucine one-and-half percent each. The seeds also contain a glucoside, loganin. The bark, wood and leaves contain brucine but no strychnine. Brucine is allied to strychnine in composition and action. Strychnine is 10 to Surface covered with silky fibers Albumin and emovo Fig. (34-2). Nux vomica seeds. Central cavity Fig. (34-3). Nux vomica. 20 times more poisonous than brucine. Strychnine is used as a respiratory stimulant, as a rodenticide and for killing stray dogs. Absorption and Excretion: All mucous membranes absorb strychnine. Much is taken up by the liver and muscles to be either released again to blood stream or to be destroyed. The release of strychnine from the liver and muscles produces convulsions on second or third day of poisoning, after sedation is discontinued. About 80% is oxidised mainly in the liver. It is excreted slowly by the kidneys and traces in bile, milk and saliva. It may be found in the cadaver up to four years. Action: It competitively blocks ventral horn motor neurone postganglionic receptor sites in the spinal cord and brainstem and prevents the effects of glycine (the presumed inhibitory transmitter). Widespread inhibition in the spinal cord results in 'release' excitation. The action is particularly Table (34-1). Difference between strychnine poisoning and tetanus Strychnine poisoning No history of injury. Sudden. All muscles of the body are affected at a time. Does not start in, nor especially affects the jaw. Between fits, muscles are completely relaxed. 1-2 hours. Chemical analysis: Strychnine found. Chapter 34: Spinal Poisons 467 History of injury present. Gradual. All muscles are not affected at a time. Usually starts in, and especialle afeets lower iaw. Between fits, muscles are slightly rigid. More than 24 hours. No poison found. die the anterior horn cells. It stimulates the cerebral contex. intervals between the convulsions become longer and the spasm Poste neurotransmitter for presynaptic inhibitory neurons less, until these entirely stop within 12 to 24 hours, and recovery signs and Symptoms nous alive unryshed, the seeds of takes place in a day or two Table (34-1). mica have no poisonous action, as they are not dissolved Fatal Dose: 50to 100 mg.; one crushed seed. are When crushed seeds are taken, the symptoms are delayed he castrointestinal tract, and are passed entire in the Fatal Period: 1 to 2 hours. Treatment: (1) The first step is the effective control of sia bour or more. IF the alkaloid is swallowed, the symptoms convulsions, ie the symptoms treated before the disease a very rapidly, usually within five to fiteen minutes. Bitter The patient should bekept in a dark room, free from noise and ara h mouth, sense of unting i swallotesness, feling disturbance. Convulsions may be controlled initially with diazepam 0.1 to 0.5 mg/kg. i.v. slowly, and then phenobarbital -focation and fear, and difficulty in swallowing occur. The i.v. If these prove ineffective consider general anaesthesia and/or mukions are preceded by such prodromal symptoms as muscle relaxation immediately by using succinylcholine, curare, erased cuity of perception, increased rigidity of muscles, gallamine or pancuronium bromide. Inhalation anaesthetics muscular twitchings. Convulsions are produced due to et action on the reflex centres of spinal cord, and affect all are of little value during convulsion, because of fixation of respiratory muscles and therefore failure of absorption of muscles at a time. These are at first clonic, but eventually me tonic. During the convulsions, the face is cyanosed vapour. Between convulsions, ether may be administered to has anxious look, eyes are staring, eyeballs prominent and the point of unconsciousness. (2) Short-acting barbiturates like pentobarbital sodium, or sodium amytal are antidotes - are dilated. Risus sardonicus results from contraction to strychnine and should be given in dose of 0.3 to 0.6 g. i.v. the jaws and facial muscles in which the corners of the (3) Wash the stomach with warm water and dilute solution ath are drawn back. The mouth is covered with froth. of potassium permanganate, and then introduce a suspension gently bloodstained. The convulsions are most marked of activated charcoal to adsorb strychnine, which should a aat-gravity muscles, so that the body typically arches in be removed later. Tannic acid may be used if charcoal is not hiperestension (opisthotonus). In supine position, the body available. (4) Acidifying the urine will increase excretion of Supported by the heels and head. The legs are adducted and strychnine. (5) Treat the symptoms on general lines. etended, the arms are flexed over the chest or rigidly extended, Postmortem Appearances: They are not characteristic. Rigor ed the hands are tightly clenched. The head is bent backwards, and the whole of the body becomes rigid, often assuming a mortis appears early but is not necessarily prolonged. There may be signs of asphyxia. Extravasated blood may be found in the on-like form. Sometimes, the spasm of the abdominal muscles muscles. Haemorrhages are sometimes found under the peritoneal ay bend the body forward (emprosthotonus), or to the side coat of the stomach. The mucosa of the stomach and duodenum pleurosthotonus). Consciousness is not lost and the mind may show patches of ecchymoses or congestion. The lungs, liver, emains clear till death. The suffering during the spasm is severe, kidneys, brain and spinal cord are congested. the patient is conscious of impending danger of death. The Physiological Test: Injection of an aqueous solution of duration of convulsion varies from half to two minutes. In the suspected material into the dorsal lymph sac of a frog, will etween the convulsions the muscles are completely relaxed, ud the patient looks well though somewhat exhausted, produce tetanic convulsions in a few minutes if strychnine is present. Later stimulation of the frog will produce convulsions. and the breathing is resumed. The cyanosis lessens, cold perspirations cover the skin; dilated pupils may contract. After 5 The Circumstances of Poisoning: (1) It is sometimes used for homicide in the form of alkaloid, or as powdered nux vomica • 5 minutes or on slightest impulse, e.g. a sudden noise, a current fair, or gently touching the patient, another convulsion occurs. seeds, in spite of bitter taste. (2) Suicide is rare because of the la fatal cases, the convulsions rapidly succeed one another, and painful death. (3) Accidental deaths are more common, due to rease in severity and in duration, and death usually occurs an overdose of medicinal preparation, or the poison being given aler four to five convulsions. The patient cannot breathe because by mistake, or in children by eating the seeds. (4) Sometimes, se diaphragm and thoracic muscles are fully contracted. Hypoxia the seeds are used for killing the cattle, and as arrow poison. (5) cases medullary paralysis and death. in non-fatal cases the Sometimes, it is taken as an aphrodisiac.

CARDIAC POISONS NICOTIANA TABACUM All parts are poisonous except the ripe seeds. The dried leaves unlala) contain 1 to 8% of nicotine and are used in the Ma redestor deed, the nes conti act real, mich, Boricotine (less foxic. Nicotine is a colourless, volatile, bitter, ABSORPTION AND EXCRETION: Each cigarette contains about 15 to 20 mg of nicotine of which 1 to 2 mg. is absorbed by smoking; exc dar contains 15 to 40 mg. Nicotine is rapidly absorbed from all sacos membranes, lungs and the skin. 80 to 90 percent is metabolised by deliver, bat some may be metabolised in the kidneys and the lungs. tis excreted by the kidneys. ACTION: It acts on the autonomic ganglia which are stimulated aal, bet are depressed and blocked at later stage. It also acts on ibe somatic neuromuscular junction, and afferent fibres from sensory ACUTE POISONING: G.I.T. Burning acid sensation, nausea, eating, abdominal pain, hypersalivation. CARDIOPULMONARY: Tacbycardia, hypertension, tachypnoea (carly); bradycardia, Sypoteasion, respiratory depression (late). Cardiac arrhythmias may screr. C.N.S.: Miosis, confusion, headache, sweating, ataxia, agitation, redesess, hyperthermia (early); mydriasis, lethargy, convulsions, sou (late). Death may occur from respiratory failure. CHRONIC POISONING: Symptoms are cough, wheezing, eypaoca, anorexia, vomiting, diarrhoca, anaemia, faintness, tremors, Inpaired memory, amblyopia, blindness, irregularity of the heart with estrasstoles and occasionally attacks of pain suggesting angina pectoris. WITHDRAWAL SYMPTOMS: Intense urge to smoke, anxiety, spaired concentration and memory, depression or hostility, headache, ascle cramps, sicep disturbances, increased appetite and weight gain, dapboresis and rapid respirations. A short period (6 to 12 weeks) of malatenance often followed by a gradual reduction in 6 to 12 weeks is Nicotine replacement therapy (NRT) includes use of nicotine reducts including gum, transdermal patch, nasal spray, lozenge and Labaler. Bupropion can be used in those who are motivated to quit. Clonidine and nortryptyline can be used as second line of treatment. FATAL DOSE: 50 to 100 mg. of nicotine. It rivals cyanide as a poison capable of producing rapid death; 15 to 30g. of crude tobacco. FATAL PERIOD: 5 to 15 minutes. TREATMENT: (1 Wash the stomach with warm water containing charcoal, tannin or potassium permanganate. (2) A purge and colonic wash-out. (3) Mccamvlamine (Inversine) Is a specific antidote giver rally. (4) Protect airway. In mild to moderate poisoning, atropine sulphate 1 to 2 mg. i.m. and hexamethonium chloride 25 to 50 mg. s.c. to counteract peripheral autonomic disturbances and as respiratory stimulant. (5) Vasodilators can be given. (6) Oxygen. (7) Symptomatic. THE CIRCUMSTANCES OF POISONING: (I) Accidental poisoning results due to ingestion, excessive smoking and application of Icaves or juice to wound or skin. (2) For malingering tobacco leaves are soaked in water for some hours and placed in axillae at bed time, which is held in position by a bandage. Poisonous symptoms are seen the next morning. (3) Suicidal and homicidal poisoning is rare. DIGITALIS PURPUREA Entire plant is toxic, containing over thirty cardiac and steroidal glucosides Fig. (35-1). The root, leaves and seeds of digitalis contain digitoxin, digoxin, digitalin and digitonin (glycosides). SIGNS AND SYMPTOMS: GIT: Anorexia, nausea, vomiting, diarrhoea. CARDIAC: Arrhythmias: extrasystoles, ventricular tachycardia and fibrillation, atrial flutter and fibrillation, SA block, AV block. ENDOCRINE: Gynaecomastia. VISUAL: Transient amblyopia, photophobia, diplopia, blurring, scotomata, colour aberration, halos. SKIN: Urticaria. CNS: Headache, fatigue, muscle weakness, neuro-psychiatrie disorders, confusion, anxiety, depression, disorientation, drowsiness, delirium, hallucinations, trigeminal neuralgia. Death occurs from cardiovascular collapse. FATALDOSE: 15 to 30 mg. of digitalin: 4 mg. of digitoxin; digoxin FATAL PERIOD: 1 to 24 hours. TREATMENT: (I) Stomach wash with a solution of tannie acid. (2) The bowels should be evacuated. (3) Activated charcoal in repeated doses. (4) Digoxin-specific antibody fragments (Fab) one vial İ.v. in 30 minutes. Each vial, contains 38 mg Fab fragments. Total 10 to 20 vials. (5) In the absence of Fab fragments, ventricular irritability can be treated with phenytoin 50 mg/min. i.v. up to 1 g, followed by 300 to 400 mg. daily. Specific antidote for digitalis induced cardiac arrhythmias are: 100 mg. lignocaine i.v. or dilantin or propranolol. (6) Trisodium EDTA may help to lower the serum calcium. (7) Potassium salts to reduce extrasystoles and tachyarrhythmias. (8) Bradycardia should be treated with atropine sulphate 0.6 mg. i.v. repeated as necessary up to four days. (9) Symptomatic. Poisoning is accidental, due to therapeutic overdose. NERIUM ODORUM Characteristies: Nerium odorum (white oleander, kaner) grows wild in India. Flowers usually fragrant, are borne in terminal clusters. They are white, pink, dark-red or rarely pale-yellow. They are two-and-half to five cm. wide and have five petals or in double blooms, many petals. The leaves are narrow, lanceolate, leathery, dark-green on upper surface, lighter beneath, and 10 to 25 cm. long. Seed pod is slim, cylindrical, ribbed, up to 15 cm. long, turns brown, dries and splits, releasing small seeds tipped with brown hairs Fig. (35-2). Active Principles: All parts of the plant, including nectar are poisonous, containing several cardiac glycosides, primarily oleandroside (oleandrin), and nerioside (nerin), which resemble digitalis in action and folinerin and rosagenin. The nector yields poisonous honey. Signs and Symptoms: The plant is occasionally a source of contact dermatitis. Emanations from flowers, especially when fading cause headache, dizziness, respiratory difficulty and nausea. Ingestion causes difficulty in swallowing and articulation, abdominal pain, vomiting, profuse frothy salivation and diarrhoea. Pulse is first slow and later rapid and weak, blood pressure falls, fibrillation, AV block, respirations are increased, pupils are dilated, muscular twitchings, tetanic spasms, lock-jaw, drowsiness, coma, respiratory paralysis and death occurs. Death usually results from cardiac failure. Fatal Dose: 15 to 20 g. of the root; 5 to 15 leaves. 8 to 10 seeds. Fatal Period: 20 to 36 hours. Treatment: (1) Stomach wash. Activated charcoal. (2) Digoxin immune Fab. Postmortem Appearances: They are not characteristic. Congestion of organs is seen. It can be detected long after death. The Circumstances of Poisoning: (1) The root, leaves or fruit are often used as a paste or decoction for suicidal purposes. (2) Homicide is rare. (3) As an abortifacient, root is used either locally or taken internally. (4) Root is taken internally for treating venereal diseases. (5) Root is used for treating cancers and ulcers in the form of paste. (6) The decoction of leaves is applied externally to reduce swelling. (7) As a cattle poison, the juice of root is applied on piece of cloth and inserted into the anus of the animal. (8) Smoke from the burning plant is toxic. When plant material is used to roast food over a fire, the poisonous sap transferred to the food may be lethal. CERBERA THEVETIA CHARACTERISTICS: All parts of cerbera thevetia (yellow oleander; pila kaner) are poisonous. The Rowers are large, bell-shaped and yellow, to to cm. long and five cm. wide, the five lobes spirally twisted and spreading, and the leaves are lanceolate. The fruit is globular, light-green, about 4 to 5cm. in diameter and contains a single nut which is triangular with a deep groove along the edge. Each nut contains five pale yellow seeds Figs. (35-3 and 35-4). Active Principles: The seeds contain 4% of the cardiac glycoside thevetin, which is one-eighth as potent as ouabain and similar to digitalis in action; thevetoxin is similar to but less toxic than thevetin; nerifolin (more potent than thevetin); peruvoside, me orberin and also a bitter principle that acts on the androduces tetanoid convulsions. All active principles are within three hours of ingestion. There is bitter taste, nausca, severe ads. Milky juice exudes from all parts of the plant. retching, vomiting, abdominal pain and in few cases diarrhoea, Spar and Symptoms: The sap of the plant may cause general weakness, blurring of vision, sinus bradycardia, irregular Armaice in sensitive individuals. Chewing the bark or seed respiration, collapse and death from heart failure. ECG may show sinus bradycardia, S-A block, atrial fibrillation and other belues a slight numbing sensation and feeling of heat in the such ad purging. Ingestion causes burning pain in the mouth, arrhythmias. Hyperkalaemia and depression of transaminase year ef troat, tingling and numbness of tongue, vomiting, activity are chief biochemical changes. doc, adache, giddiness, dilated pupils, loss of muscular Fatal Dose: Kernel of one fruit. yet and fainting. Pulse is rapid, weak and irregular, blood Fatal Period: 1 to 2 days or more. rasure lo: Heart block, collapse and death from peripheral POSTMORTEM APPEARANCES: They are those of asphyxia. Eyes are congested. Lungs are congested and oedematous. Subepicardial, saltrey failure occurs. subendecardiat and sebpleural petechial haemorrhages are found. Fital Dose: S to 10 sceds; 15 to 20 g. of root; 5 to 10 leaves. Stomach mucosa is congested with submacous haemorrhages and Fatal Period: 2 to 3 hours. gastritis. The internal organs are congested. Treatmeat: (1) Wash out the stomach. (2) Digoxin immune Treatment: (I) Stomach wash. (2) Digoxin immune Fab is (a (prise) is effective in poisoning from digitalis, cerbera the specifie antidote. Atropine 0.5 mg. i.v. and repeated every bei, cerera dallam, nerium odorum, etc. Each vial contains 15 to 30 minutes to keep heart rate above 50 per minute. (3) sag Fab which should be dissolved in 4 ml of sterile water and Correct hyperkalaemia. fit i 101020 vials can be given through a membrane filter i.vi Circumstances of Poisoning: (1) For suicide, the kernels xa prisoning. Sodium molar lactate transfusion with glucose are taken as such, or after grinding it with jaggery or adlag atropine, 2 ml. adrenaline and 2 mg. noradrenaline is molasses or by preparing a curry with it. (2) For homicide, ericial (3) Symptomatic. the powdered kernel is added to alcohol. (3) Bark, leaves and Pestmortem Appearances: They are not specific. milky juice are used as emetic and as purgative. The Circumstances of Polsoning: (I) The root and seeds are ACONITE set seetimes for suicide or homicide. (2) Root and seeds are There are several varieties of aconite (monk's hood, blue sla for criminal abortion. (3) For cattle poisoning, the seeds rocket, meetha zeher, bish, bikh), but the roots of Aconitum a crashed and fed to the animal with com or bread napellus and Aconitum ferox are commonly used. It grows in the CERBERA ODALLAM /Pilkber Himalayas. All varieties and all parts of the plant are poisonous; CHARACTERISTICS: This plant is closely allied botanically to least when young, more so when seeds ripen and most when bloom. artera tbevetia. It is a small plant or a shrub that grows wild all over bin The leaves are dark-green, fleshy and lanccolate, 20 to 30 cm. Active Principles: The root and seeds are most potent; leg and 4 to 6 cm. broad. The flowers are white, like these of jasmine. contain aconitine and ten or more other alkaloids, such as De frait resembles a mango, is globular and dark-green and has a sik Shras mesocarp which encloses usually a single seed. The seed pseudo-aconitine, indaconitine, bikhaconitine, picraconitine, Astroid and oseid and contains twe kernels which are pearly-white aconine, mesaconitine, jesaconitine, etc. Aconitine stimulates inite dry it may have a bluish tinge or it may become gelatinous. and then depresses CNS. Gly acrid juice (toxic) exudes from all parts of the plant. The active redpies are cerberin, cerberoside, odollia, odolotoxin, theyetin and Dried roots: The dry root is conical or tapering, and shows arapaía (glycosides) Fig. (35-5). scars or bases of broken rootlets, and is arched or shrivelled with longitudinal wrinkles Fig. (35-6). It is usually 5 to 10 cm. Sipes and Symptoms: They appear within one hour. The long, and 1½ to 2 cm. thick at the upper end. The external colour unil symptoms are gastrointestinal. Cardiac toxicity may occur is dark-brown, and when freshly cut the internal colour is white.. which becomes pink on exposure to air. It is odourless but the taste is sweet, then acrid. When dried and soaked in oil the root is black, heavy, hard and brittle with a strong offensive odour. The root is mistaken for horse-radish root which is long, cylindrical, yellowish-white externally and whitish internally, does not change on exposure to air and the taste is pungent. Action:

Make simplified notes

Make simplified notes CARDIAC POISONS NICOTIANA TABACUM All parts are poisonous except the ripe seeds. The dried leaves unlala) contain 1 to 8% of nicotine and are used in the Ma redestor deed, the nes conti act real, mich, Boricotine (less foxic. Nicotine is a colourless, volatile, bitter, ABSORPTION AND EXCRETION: Each cigarette contains about 15 to 20 mg of nicotine of which 1 to 2 mg. is absorbed by smoking; exc dar contains 15 to 40 mg. Nicotine is rapidly absorbed from all sacos membranes, lungs and the skin. 80 to 90 percent is metabolised by deliver, bat some may be metabolised in the kidneys and the lungs. tis excreted by the kidneys. ACTION: It acts on the autonomic ganglia which are stimulated aal, bet are depressed and blocked at later stage. It also acts on ibe somatic neuromuscular junction, and afferent fibres from sensory ACUTE POISONING: G.I.T. Burning acid sensation, nausea, eating, abdominal pain, hypersalivation. CARDIOPULMONARY: Tacbycardia, hypertension, tachypnoea (carly); bradycardia, Sypoteasion, respiratory depression (late). Cardiac arrhythmias may screr. C.N.S.: Miosis, confusion, headache, sweating, ataxia, agitation, redesess, hyperthermia (early); mydriasis, lethargy, convulsions, sou (late). Death may occur from respiratory failure. CHRONIC POISONING: Symptoms are cough, wheezing, eypaoca, anorexia, vomiting, diarrhoca, anaemia, faintness, tremors, Inpaired memory, amblyopia, blindness, irregularity of the heart with estrasstoles and occasionally attacks of pain suggesting angina pectoris. WITHDRAWAL SYMPTOMS: Intense urge to smoke, anxiety, spaired concentration and memory, depression or hostility, headache, ascle cramps, sicep disturbances, increased appetite and weight gain, dapboresis and rapid respirations. A short period (6 to 12 weeks) of malatenance often followed by a gradual reduction in 6 to 12 weeks is Nicotine replacement therapy (NRT) includes use of nicotine reducts including gum, transdermal patch, nasal spray, lozenge and Labaler. Bupropion can be used in those who are motivated to quit. Clonidine and nortryptyline can be used as second line of treatment. FATAL DOSE: 50 to 100 mg. of nicotine. It rivals cyanide as a poison capable of producing rapid death; 15 to 30g. of crude tobacco. FATAL PERIOD: 5 to 15 minutes. TREATMENT: (1 Wash the stomach with warm water containing charcoal, tannin or potassium permanganate. (2) A purge and colonic wash-out. (3) Mccamvlamine (Inversine) Is a specific antidote giver rally. (4) Protect airway. In mild to moderate poisoning, atropine sulphate 1 to 2 mg. i.m. and hexamethonium chloride 25 to 50 mg. s.c. to counteract peripheral autonomic disturbances and as respiratory stimulant. (5) Vasodilators can be given. (6) Oxygen. (7) Symptomatic. THE CIRCUMSTANCES OF POISONING: (I) Accidental poisoning results due to ingestion, excessive smoking and application of Icaves or juice to wound or skin. (2) For malingering tobacco leaves are soaked in water for some hours and placed in axillae at bed time, which is held in position by a bandage. Poisonous symptoms are seen the next morning. (3) Suicidal and homicidal poisoning is rare. DIGITALIS PURPUREA Entire plant is toxic, containing over thirty cardiac and steroidal glucosides Fig. (35-1). The root, leaves and seeds of digitalis contain digitoxin, digoxin, digitalin and digitonin (glycosides). SIGNS AND SYMPTOMS: GIT: Anorexia, nausea, vomiting, diarrhoea. CARDIAC: Arrhythmias: extrasystoles, ventricular tachycardia and fibrillation, atrial flutter and fibrillation, SA block, AV block. ENDOCRINE: Gynaecomastia. VISUAL: Transient amblyopia, photophobia, diplopia, blurring, scotomata, colour aberration, halos. SKIN: Urticaria. CNS: Headache, fatigue, muscle weakness, neuro-psychiatrie disorders, confusion, anxiety, depression, disorientation, drowsiness, delirium, hallucinations, trigeminal neuralgia. Death occurs from cardiovascular collapse. FATALDOSE: 15 to 30 mg. of digitalin: 4 mg. of digitoxin; digoxin FATAL PERIOD: 1 to 24 hours. TREATMENT: (I) Stomach wash with a solution of tannie acid. (2) The bowels should be evacuated. (3) Activated charcoal in repeated doses. (4) Digoxin-specific antibody fragments (Fab) one vial İ.v. in 30 minutes. Each vial, contains 38 mg Fab fragments. Total 10 to 20 vials. (5) In the absence of Fab fragments, ventricular irritability can be treated with phenytoin 50 mg/min. i.v. up to 1 g, followed by 300 to 400 mg. daily. Specific antidote for digitalis induced cardiac arrhythmias are: 100 mg. lignocaine i.v. or dilantin or propranolol. (6) Trisodium EDTA may help to lower the serum calcium. (7) Potassium salts to reduce extrasystoles and tachyarrhythmias. (8) Bradycardia should be treated with atropine sulphate 0.6 mg. i.v. repeated as necessary up to four days. (9) Symptomatic. Poisoning is accidental, due to therapeutic overdose. NERIUM ODORUM Characteristies: Nerium odorum (white oleander, kaner) grows wild in India. Flowers usually fragrant, are borne in terminal clusters. They are white, pink, dark-red or rarely pale-yellow. They are two-and-half to five cm. wide and have five petals or in double blooms, many petals. The leaves are narrow, lanceolate, leathery, dark-green on upper surface, lighter beneath, and 10 to 25 cm. long. Seed pod is slim, cylindrical, ribbed, up to 15 cm. long, turns brown, dries and splits, releasing small seeds tipped with brown hairs Fig. (35-2). Active Principles: All parts of the plant, including nectar are poisonous, containing several cardiac glycosides, primarily oleandroside (oleandrin), and nerioside (nerin), which resemble digitalis in action and folinerin and rosagenin. The nector yields poisonous honey. Signs and Symptoms: The plant is occasionally a source of contact dermatitis. Emanations from flowers, especially when fading cause headache, dizziness, respiratory difficulty and nausea. Ingestion causes difficulty in swallowing and articulation, abdominal pain, vomiting, profuse frothy salivation and diarrhoea. Pulse is first slow and later rapid and weak, blood pressure falls, fibrillation, AV block, respirations are increased, pupils are dilated, muscular twitchings, tetanic spasms, lock-jaw, drowsiness, coma, respiratory paralysis and death occurs. Death usually results from cardiac failure. Fatal Dose: 15 to 20 g. of the root; 5 to 15 leaves. 8 to 10 seeds. Fatal Period: 20 to 36 hours. Treatment: (1) Stomach wash. Activated charcoal. (2) Digoxin immune Fab. Postmortem Appearances: They are not characteristic. Congestion of organs is seen. It can be detected long after death. The Circumstances of Poisoning: (1) The root, leaves or fruit are often used as a paste or decoction for suicidal purposes. (2) Homicide is rare. (3) As an abortifacient, root is used either locally or taken internally. (4) Root is taken internally for treating venereal diseases. (5) Root is used for treating cancers and ulcers in the form of paste. (6) The decoction of leaves is applied externally to reduce swelling. (7) As a cattle poison, the juice of root is applied on piece of cloth and inserted into the anus of the animal. (8) Smoke from the burning plant is toxic. When plant material is used to roast food over a fire, the poisonous sap transferred to the food may be lethal. CERBERA THEVETIA CHARACTERISTICS: All parts of cerbera thevetia (yellow oleander; pila kaner) are poisonous. The Rowers are large, bell-shaped and yellow, to to cm. long and five cm. wide, the five lobes spirally twisted and spreading, and the leaves are lanceolate. The fruit is globular, light-green, about 4 to 5cm. in diameter and contains a single nut which is triangular with a deep groove along the edge. Each nut contains five pale yellow seeds Figs. (35-3 and 35-4). Active Principles: The seeds contain 4% of the cardiac glycoside thevetin, which is one-eighth as potent as ouabain and similar to digitalis in action; thevetoxin is similar to but less toxic than thevetin; nerifolin (more potent than thevetin); peruvoside, ruvoside, cerberin and also a bitter principle that acts on the (AS, and produces tetanoid convulsions. All active principles are masides. Milky juice exudes from all parts of the plant. Signs and Symptoms: The sap of the plant may cause mation in sensitive individuals. Chewing the bark or seed nelcanses aslight numbing sensation and feeling of heat in the muth and purging. Ingestion causes burning pain in the mouth, toss of throat, tingling and numbness of tongue, vomiting, bartoc, headache, giddiness, dilated pupils, loss of muscular par and fainting. Pulse is rapid, weak and irregular, blood mure ow. Heart block, collapse and death from peripheral arculatory failure occurs. Fatal Dose: 8 to 10 seeds; 15 to 20 g. of root; 5 to 10 leaves. Fatal Period: 2 to 3 hours. Treatment: (1) Wash out the stomach. (2) Digoxin immune Eb (vine) is effective in poisoning from digitalis, cerbera beretia, erbera odallam, nerium odorum, etc. Each vial contains Ng Fab which should be dissolved in 4 ml of sterile water and frien . 10 to 20 vials can be given through a membrane filter i.v. naute poisoning. Sodium molar lactate transfusion with glucose sd1 mg. atropine, 2 ml. adrenaline and 2 mg. noradrenaline is beeficial. (3) Symptomatic. Postmortem Appearances: They are not specific. The Circumstances of Poisoning: (1) The root and seeds are sed sometimes for suicide or homicide. (2) Root and seeds are aken for criminal abortion. (3) For cattle poisoning, the seeds are crushed and fed to the animal with corn or bread.

Make simplified notes from this text CERBERA ODALLAM (Pilikirbir) CHARACTERISTICS: This plant is closely allied botanically to abera thevetia. It is a small plant or a shrub that grows wild all over dia. The leaves are dark-green, fleshy and lanceolate, 20 to 30 cm. eng, and 4 to 6 cm. broad. The flowers are white, like those of jasmine. The fruit resembles a mango, is globular and dark-green and has a tick fibrous mesocarp which encloses usually a single seed. The seed i tattened and ovoid and contains two kernels which are pearly-white hat when dry it may have a bluish tinge or it may become gelatinous. Milky acrid juice (toxic) exudes from all parts of the plant. The active oraciples are cerberin, cerberoside, odollin, odolotoxin, thevetin and urapain (glycosides) Fig. (35-5). Signs and Symptoms: They appear within one hour. The ital symptoms are gastrointestinal. Cardiac toxicity may occur Chapter 35: Cardiac Poisons 471 within three hours of ingestion. There is bitter taste, nausca, severe retching, vomiting, abdominal pain and in few cases diarrhoea, general weakness, blurring of vision, sinus bradycardia, irregular respiration, collapse and death from heart failure. ECG may show sinus bradycardia, S-A block, atrial fibrillation and other arrhythmias. Hyperkalaemia and depression of transaminase activity are chief biochemical changes. Fatal Dose: Kernel of one fruit. Fatal Period: 1 to 2 days or more. POSTMORTEM APPEARANCES: They are those of asphyxia. Eyes are congested. Lungs are congested and oedematous. Subepicardial, subendocardial and subpleural petechial haemorrhages are found. Stomach mucosa is congested with submucous haemorrhages and gastritis. The internal organs are congested. Treatment: (1) Stomach wash. (2) Digoxin immune Fab is the specific antidote. Atropine 0.5 mg. i.v. and repeated every 15 to 30 minutes to keep heart rate above 50 per minute. (3) Correct hyperkalaemia. Circumstances of Poisoning: (1) For suicide, the kernels are taken as such, or after grinding it with jaggery or molasses or by preparing a curry with it. (2) For homicide, the powdered kernel is added to alcohol. (3) Bark, leaves and milky juice are used as emetic and as purgative. There are several varieties of aconite (monk's hood, blue rocket, meetha zeher, bish, bikh), but the roots of Aconitum napellus and Aconitum ferox are commonly used. It grows in the Himalayas. All varieties and all parts of the plant are poisonous; least when young, more so when seeds ripen and most when bloom. Active Principles: The root and seeds are most potent; contain aconitine and ten or more other alkaloids, such as pseudo-aconitine, indaconitine, bikhaconitine, picraconitine, aconine, mesaconitine, jesaconitine, etc. Aconitine stimulates and then depresses CNS. Dried roots: The dry root is conical or tapering, and shows scars or bases of broken rootlets, and is arched or shrivelled with longitudinal wrinkles Fig. (35-6). It is usually 5 to 10 cm. long, and 1½ to 2cm. thick at the upper end. The external colour is dark-brown, and when freshly cut the internal colour is white, which becomes pink on exposure to air. It is odourless but the taste is sweet, then acrid. When dried and soaked in oil the root is black, heavy, hard and brittle with a strong offensive odour. The root is mistaken for horse-radish root which is long, cylindrical, yellowish-white externally and whitish internally, does not change on exposure to air and the taste is pungent. Action: It first simulates sensory nerves. The motor ganglia of heart are paralysed and respiratory centre is slowed. Signs and Symptoms: Leaves handled or rubbed on the skin, produce tingling and numbness; so also the root if held for a long time in the hand. The odour of the plant has a narcotic effect. The pollen causes pain and swelling in the eyes. The symptoms occur immediately or within a few minutes. There is a burning sensation from the mouth to the stomach and tingling and numbness in the mouth, tongue and pharynx. This is followed by salivation, nausea, vomiting and diarrhoea. Later the mouth is dry and patient suffers from thirst and is unable to swallow. Tingling and numbness are then felt all over the body. There is headache, giddiness, pallor, profuse sweating, subnormal temperature, the limbs become weak and the patient is unable to walk or stand. Paraesthesias, ataxia and slurred speech occur. There may be twitching of the muscles with darting pains, and cramps and convulsions may occur. The pupils alternately contract and dilate (hippus), but remain dilated in the later stages. The vision becomes dim and there may be diplopia. Hypotension, cardiac arrhythmia with AV block occurs. At first there is tachycardia, but in later stages bradycardia occurs due to AV block. The mind usually remains clear, although there may be hallucinations. There is marked general muscular weakness, oppression in the chest, and death occurs from paralysis of heart or respiratory centres or both. It is eliminated by all routes but mainly in the urine. Fatal Dose: One g. root; 2 to 5 mg. of aconitine; 250 mg. extract; 10 to 30 ml. tincture. Fatal Period: Two to six hours. Treatment: (1) Gastric lavage with warm water, and weak solution of iodine in potassium iodide or tannic acid to precipitate alkaloid, or animal charcoal. (2) Multiple-dose activated charcoal. (3) Cathartic. (4) Atropine half to one mg. is useful. (5) Symptomatic. Postmortem Appearances: They are not characteristic, but are those of asphyxia. The mucosa of the stomach and duodenum show congestion and occasionally ecchymosis. The lungs, Kidneys and brain are congested. Aconitine is extremely unstable and is destroyed by putretaction. The Circumstances of Poisoning: (1) Accidental poisoning is due to eating the roots in mistake for horseradish root, by the use of quack remedies containing it, or from taking liquor to which aconite is added to increase intoxication. (2) Suicidal cases often occur. (3) It is given with betel leaf to conceal its taste for homicide. (4) Root is used as an abortifacient. (5) Cattle poison. (6) Arrow poison.

Make simplified notes from this text CERBERA ODALLAM (Pilikirbir) CHARACTERISTICS: This plant is closely allied botanically to abera thevetia. It is a small plant or a shrub that grows wild all over dia. The leaves are dark-green, fleshy and lanceolate, 20 to 30 cm. eng, and 4 to 6 cm. broad. The flowers are white, like those of jasmine. The fruit resembles a mango, is globular and dark-green and has a tick fibrous mesocarp which encloses usually a single seed. The seed i tattened and ovoid and contains two kernels which are pearly-white hat when dry it may have a bluish tinge or it may become gelatinous. Milky acrid juice (toxic) exudes from all parts of the plant. The active oraciples are cerberin, cerberoside, odollin, odolotoxin, thevetin and urapain (glycosides) Fig. (35-5). Signs and Symptoms: They appear within one hour. The ital symptoms are gastrointestinal. Cardiac toxicity may occur Chapter 35: Cardiac Poisons 471 within three hours of ingestion. There is bitter taste, nausca, severe retching, vomiting, abdominal pain and in few cases diarrhoea, general weakness, blurring of vision, sinus bradycardia, irregular respiration, collapse and death from heart failure. ECG may show sinus bradycardia, S-A block, atrial fibrillation and other arrhythmias. Hyperkalaemia and depression of transaminase activity are chief biochemical changes. Fatal Dose: Kernel of one fruit. Fatal Period: 1 to 2 days or more. POSTMORTEM APPEARANCES: They are those of asphyxia. Eyes are congested. Lungs are congested and oedematous. Subepicardial, subendocardial and subpleural petechial haemorrhages are found. Stomach mucosa is congested with submucous haemorrhages and gastritis. The internal organs are congested. Treatment: (1) Stomach wash. (2) Digoxin immune Fab is the specific antidote. Atropine 0.5 mg. i.v. and repeated every 15 to 30 minutes to keep heart rate above 50 per minute. (3) Correct hyperkalaemia. Circumstances of Poisoning: (1) For suicide, the kernels are taken as such, or after grinding it with jaggery or molasses or by preparing a curry with it. (2) For homicide, the powdered kernel is added to alcohol. (3) Bark, leaves and milky juice are used as emetic and as purgative. There are several varieties of aconite (monk's hood, blue rocket, meetha zeher, bish, bikh), but the roots of Aconitum napellus and Aconitum ferox are commonly used. It grows in the Himalayas. All varieties and all parts of the plant are poisonous; least when young, more so when seeds ripen and most when bloom. Active Principles: The root and seeds are most potent; contain aconitine and ten or more other alkaloids, such as pseudo-aconitine, indaconitine, bikhaconitine, picraconitine, aconine, mesaconitine, jesaconitine, etc. Aconitine stimulates and then depresses CNS. Dried roots: The dry root is conical or tapering, and shows scars or bases of broken rootlets, and is arched or shrivelled with longitudinal wrinkles Fig. (35-6). It is usually 5 to 10 cm. long, and 1½ to 2cm. thick at the upper end. The external colour is dark-brown, and when freshly cut the internal colour is white, which becomes pink on exposure to air. It is odourless but the taste is sweet, then acrid. When dried and soaked in oil the root is black, heavy, hard and brittle with a strong offensive odour. The root is mistaken for horse-radish root which is long, cylindrical, yellowish-white externally and whitish internally, does not change on exposure to air and the taste is pungent. Action: It first simulates sensory nerves. The motor ganglia of heart are paralysed and respiratory centre is slowed. Signs and Symptoms: Leaves handled or rubbed on the skin, produce tingling and numbness; so also the root if held for a long time in the hand. The odour of the plant has a narcotic effect. The pollen causes pain and swelling in the eyes. The symptoms occur immediately or within a few minutes. There is a burning sensation from the mouth to the stomach and tingling and numbness in the mouth, tongue and pharynx. This is followed by salivation, nausea, vomiting and diarrhoea. Later the mouth is dry and patient suffers from thirst and is unable to swallow. Tingling and numbness are then felt all over the body. There is headache, giddiness, pallor, profuse sweating, subnormal temperature, the limbs become weak and the patient is unable to walk or stand. Paraesthesias, ataxia and slurred speech occur. There may be twitching of the muscles with darting pains, and cramps and convulsions may occur. The pupils alternately contract and dilate (hippus), but remain dilated in the later stages. The vision becomes dim and there may be diplopia. Hypotension, cardiac arrhythmia with AV block occurs. At first there is tachycardia, but in later stages bradycardia occurs due to AV block. The mind usually remains clear, although there may be hallucinations. There is marked general muscular weakness, oppression in the chest, and death occurs from paralysis of heart or respiratory centres or both. It is eliminated by all routes but mainly in the urine. Fatal Dose: One g. root; 2 to 5 mg. of aconitine; 250 mg. extract; 10 to 30 ml. tincture. Fatal Period: Two to six hours. Treatment: (1) Gastric lavage with warm water, and weak solution of iodine in potassium iodide or tannic acid to precipitate alkaloid, or animal charcoal. (2) Multiple-dose activated charcoal. (3) Cathartic. (4) Atropine half to one mg. is useful. (5) Symptomatic. Postmortem Appearances: They are not characteristic, but are those of asphyxia. The mucosa of the stomach and duodenum show congestion and occasionally ecchymosis. The lungs, Kidneys and brain are congested. Aconitine is extremely unstable and is destroyed by putretaction. The Circumstances of Poisoning: (1) Accidental poisoning is due to eating the roots in mistake for horseradish root, by the use of quack remedies containing it, or from taking liquor to which aconite is added to increase intoxication. (2) Suicidal cases often occur. (3) It is given with betel leaf to conceal its taste for homicide. (4) Root is used as an abortifacient. (5) Cattle poison. (6) Arrow poison.

Make simplified notes on this text

Make simplified notes on this text ASPHYXIANTS 2502 e% Recribe general principles and basic methodalegies in treatment of poisonina: decontamination, supportive thora sto pery, procedures of enhanced elimination with regard to ammonia, carbon monoxide, hydrogen caride and derivatives, methyl scynate, tear (riot control) gases. CLASSIFICATION: Henderson and Haggard divided noxious pes into five groups. (g) IRRITANTS: The gases ingure the air passages or lungs or soti, ormaldehyde, chlorine, phosgene, nitrogen dioxide, sulphur ( CHEMICAL ASPHYXIANTS: These are gases which by saing with haemoglobin, or by acting on some tissue constituent rat ogen from reaching tissue or the isues from usin, ct. The gumpis are carbon monoxide, hydrogen sulphide, arsine, carbon daphide, and cyanide. ()SIMPLE ASPHYXIANTS: These are inert gases, which when frated in high concentration act mechanically by excluding oxygen. They are carbon dioxide, methane, helium, nitrogen and nitrous oxide. Saptoms appear when these gases exceed 20 to 30% of inspired air. When the inspired air contains less than 10% oxygen death may result from slight exertion. (9) VOLATILE DRUGS: These are gases with little or no irritant Mat upon the air-passages, which act after absorption into the blood, iber as an anaesthetic, or as agents toxic to the liver, kidneys or other ryans including the nervous system. They are aliphatic hydrocarbons, bagenated hydrocarbons and aromatic hydrocarbons. (5) SYSTEMIC POISONS: These are insecticides, arsine, stibine. CARBON MONOXIDE Features: It is a colourless, tasteless, non-irritative gas mich is produced due to incomplete combustion of carbon. lis insoluble in water. It burns with a blue flame producing CO? it is lighter than air and significant quantities are present only in the upper reaches in the vicinity of a fire. Ina closed environment, greater concentration is present at 1.5 to 2 metres above the ground. CO seeps through openings around doors or large cracks in walls. It may also ne through a ceiling crack into an attic or from a tight confined spec, trough plaster board or dry wall, into an adjacent area. In this ay it may spread through an entire house and even upstair coms. A mixture of CO with 2½ times of its volume of air is righly explosive in the presence of a flame. SOURCES: The common sources of CO include coal gas, smoke from firs and the fumes from defective heating appliances, e.g., furnace, sore, waer heater, fire places, burning oil lamps. A yellow name strates CO, while a blue flame burns completely with no byproducts. lial ond as a component of the fumes of coke kilns, lime kilns, eplain in mines (after damp), choke damp (improperly ventilated collieries at the dead ends), detonation of explosives, and the exhaust fumes of internal combustion engines. Industry accounts for about 20%. In a person smoking one pack of cigarettes per day, CO levels are about 5 to 6% and in a heavy smoker 15 to 20%. Traffic policemen may have up to 10% saturation. The exhaust gas of motor cars contain 1 to 7% of CO, which causes the air of a small garage poisonous in 5 to 10 minutes. "Petrol (gasoline) engines produce up to 5-7% CO in their exhaust fumes and more if engine is idling". Emissions like CO, HC, and smoke opacity depend on both fuel and engine type. Gasoline and CNG engines have 15 to 20 times higher CO emissions as compared to diesel engines. During haemoglobin catabolism 0.4 to 0.7% COH is produced in the body endogenously. In haemolytic anaemia, СОН levels may reach 8%. In females CO is twice as great during the progesterone phase of the menstrual cycle as during Action: CO is readily absorbed across the alveolus and combines with haemoglobin. Normal blood contains 21% of oxygen, with 18 to 19% bound to haemoglobin and 2% dissolved in plasma. About 10 to 21% CO is present in extracellular tissues combined with myoglobin and haemoproteins. CO affinity to myoglobin is about 40 times greater than oxygen, which may cause direct myocardial depression. CO has 200 to 300 times greater affinity for haemoglobin than that of oxygen. It displaces oxygen from its combination with haemoglobin and forms a relatively stable compound known as carboxyhaemoglobin. It thus reduces the oxygen content of the blood, and hence that of the tissues. It acts as a chemical asphyxiant and produces death due to anaemic anoxia. CO is a potent cellular toxin. It effectively and firmly binds to haemoglobin and myoglobin. It inhibits the electron transport by blocking cytochrome A, oxidase and cytochrome P-450, and therefore intracellular respiration. It interferes with other ferroproteins such as myoglobin and various enzymes. The presence of COb in the circulation alters the oxygen affinity of the haemoglobin by shifting oxyhaemoglobin dissociation curve to the left, decreasing the release of oxygen to the tissues. This results in a hypoxia of the tissue greater than what would be produced by an equivalent degree of anaemia. Normally, after somatic death, the cells near the capillaries continue to function, extract oxygen from oxyhaemoglobin and cause blue staining. In CO poisoning this cannot occur, because the cells cannot break the COb compound. Potent cellular poisons, c.g.. cyanide, fluoroacetate and freezing, block the metabolism of the cells so fast and completely that they cannot extract oxygen from oxyhaemoglobin. In these cases, the blood under the skin and in the tissues will be cherry-red due to oxyhaemoglobin. Platelet aggregation is inhibited. ELIMINATION: It is eliminated through lungs; about 1% is metabolised to CO,. Half-life of CO in a healthy adult breathing 21% oxygen (room air) is 4 to 5 hours. It is not metabolised and is not lost through the skin, bile, perspiration, urine or faces. CO is not absorbed by a body after death. Signs and Symptoms: The brain and heart extract the greatest percentage of oxygen, 6.1 and Il vol%. Therefore, these organs are the carliest and most greatly affected by a reduction in oxygen delivery. The symptoms of poisoning are often mistaken for symptoms of influenza or illness caused by eating contaminated food. The development of symptoms has a progression, roughly parallel to the rise in the saturation of the blood by CO Table (36-I). Similarly, regression of symptoms corresponds with the clearance of CO from the blood. Victims may not notice anything, except a headache, until they lapse into coma and die. The effects of CO are simply those of suboxia. As most deaths are relatively rapid, blisters are rare. Bullae tend to be separate and isolated lesions. The bullous fluid is usually thick and cellular and there is often an inflammatory reaction in the surrounding skin. These bullae are localised by external pressure and are seen in the regions of the calves, buttocks, wrists and knees. They are caused due to skin hypoxia which can be mistaken for second degree burns. They rarely involve fingers and toes. There is a tendency of the dying victim to wild, erratic swinging movements inside the room, disturbing clothing and furniture which gives an impression of violent struggle (CO automatism). The saturation required СОНЬЯ 0-10 10-20 20-30 30-40 40-50 50-60 60-70 70-80 > 80 Table (36-1). Symptoms of CO poisoning Symptoms No appreciable symptoms. Breathlessness on moderate exertion, mild headache, weakness. Throbbing headache, irritability, emotional instability, disturbed judgement, defective memory and rapid fatigue. Severe headache, nausea, vomiting, dizziness, dimness of vision, confusion. cherry-red colour. Increasing confusion, sometimes hallucinations, severe ataxia, rapid respirations and collapse with attempts at exertion. Symptoms resemble alcoholic intoxication. Syncope or coma with intermittent convulsions, rapid respirations, tachycardia with a weak pulse and pink or red discolouration of the skin. Increasing depth of coma with incontinence of urine and faeces. Profound coma with depressed or absent reflexes, a weak thready pulse, shallow and irregular respirations and death. Rapid death from respiratory arrest. to cause death varies with the age and health of the person. Death usually occurs when eighty percent of haemoglobin is saturated with CO. Senility, any disease or the co-existence of any respiratory or circulatory deficiency, or of anaemia or in association with hypnotic drugs and alcohol result in a significant reduction of maximum lethal saturation, and death can occur from as little as thirty percent saturation. CO can pass from the maternal to the foetal blood, and COb concentrations are 10 to 15% higher than maternal levels, and can produce intrauterine death, even though the mother survives. The rate of CO combining with haemoglobin depends on the atmospheric concentration and rate of respiratory exchange. Physical activity during exposure increases rate of saturation of blood. Children saturate their blood more rapidly than adults because of their relatively high rates of respiratory exchange. Patients recovering from CO poisoning may suffer neurological sequelae including tremors, personality changes, memory impairment, monoplegia, hemiplegia, psychosis, peripheral neuropathy, visual loss, inability to concentrate and Parkinsonism within 2 to 4 weeks. These effects may be temporary or permanent. Complete recovery after serious poisoning may take many weeks. Sometimes, people become ill again up to 4 weeks after recovery. Chronic Poisoning: Symptoms include headache, confusion. weakness, paraesthesias, visual disturbances, hypertension. hyperthermia, palpitations, atrial fibrillation, bundle branch blocks, AV block, abnormal left ventricular function, decreased cognitive ability, mental retardation, psychosis, Parkinsonism and incontinence. Delayed Deaths: Coma is accompanied by degenerative changes in brain and capillaries. Individuals with long term survival following significant exposure may have a Parkinsonian syndrome or may develop even neurological states. The Effect of Different Air Concentrations of CO Table (36-1): Humidity, high environmental temperature, and physical activity increase the respiratory rate and thus, the absorption of CO. The upper limit of safety is 0.01% CO in air. If a person breathes CO in low concentration for a considerable length of time, especially during sleep, he will be poisoned just as effectively as though he were exposed to a high concentration for a shorter period. When low concentrations of gas are inhaled, coma does not occur immediately, but often cause severe muscular incoordination, weakness and confusion, due to which the victim is unable to escape and dies of asphyxia, the body being burnt after death. A concentration of 0.5 to 1% of CO in the atmosphere can produce carboxyhaemoglobin saturation levels of 75% in 2 to 15 minutes. Exposure to atmosphere containing 0.2% of gas will cause death in about four hours, 0.4% in one hour, and 10% in 20 to 30 minutes. If production of CO ceases after the onset of irreversible coma, individual will gradually eliminate CO from the body, even through irreversible injury has occurred. In such cases, low carboxyhaemoglobin will be seen. Treatment: (1) Remove the patient to fresh air immediately. If he is conscious and breathing, no treatment is required. (2) Any patient with COH level greater than 25% should be treated. (3) The most widely accepted treatment is 100% oxygen provided *adcht-fitting mask preferably with rubber seals and scheal intubation for patients with a depressed mental antil COb falls to 15 to 20%. (4) CO, should not be (s) Hyperbaric oxygen (HBO) therapy has several duatages, such as vomiting, convulsions, agitation, ripare neunic membranes, blocked sinuses, etc. (6) Gastric Hae carty in the course of treatment may prevent aspiration nis (7) A whole blood transfusion is useful. (8) The should be kept at complete rest for at least 48 hours. (9) a stimulant drugs. (10) Give antibiotics as a prophylaxis net ung fiction. (11) Cerebral oedema should be treated a fid restriction, steroids, and mannitol. Postmortem Appearances: A cherry-red colouration of de sin, mucous membranes, conjunctivac, nail-beds, areas Whostasis, blood, tissues and internal organs is seen in 15 * 3% of cases only, it is associated with 30 to 40% CH He semic person, the colour may be faint or absent. In dark-alured victims, the colour may be masked, but may be seen in He iser aspect of lips, nail-beds, tongue, palms and soles, inside teyelids, but rarely in the sclera. The colour will not be changed yealming or preservation by formalin. Cyanide poisoning nd exposure of the dead body to the cold may cause redness gilan to that due to CO. The

Postmortem Appearances: A cherry-red colouration of heskin, mucous membranes, conjunctivae, nail-beds, areas (lypostasis, blood, tissues and internal organs is seen in 15 * 20% of cases only. It is associated with 30 to 40% COHb. hun anaemic person, the colour may be faint or absent. In dark-oloured victims, the colour may be masked, but may be seen in te in aspect of lips, nail-beds, tongue, palms and soles, inside te eyelids, but rarely in the sclera. The colour will not be changed byebalming or preservation by formalin. Cyanide poisoning and exposure of the dead body to the cold may cause redness similar to that due to CO. The cherry-red discolouration changes in dark- gren, then to brown with the onset of decomposition. The blood is fluid, hyperaemia is general and serous effusions are common. There may be blistering of the skin of dependent areas, such as buttocks, calves, wrists and knees, due to cutaneous oedema. Congestion of the lungs with pink fluid blood, and if the victim survived for some time, pulmonary oedema with congestion are found. The lungs may show bronchopneumonic consolidation. In delayed deaths, tiny focal necroses occur in the myocardium. Frank myocardial infarction has been reported after severe exposure and relative hypoxia, usually in the presence of pre-existing coronary disease. Within five days histological changes occur here. Pleural and pericardial anoxial haemorrhages are common. In persons surviving after severe CO exposure and in delayed deaths bilateral, symmetrical necrosis and cavitation of the basal ganglia in the brain, especially the putamen and globus pallidus is the most characteristic lesion, though the cerebral cortex, hippocampus, cerebellum and substantia nigra of brainstem may be affected. Punctiform and ring-shaped haemorrhages in the white matter of the brain with widespread odema are common. Haemorrhages in the meninges and cortex, and selective cellular necrobiosis of ganglion cells in the cortex may be seen. After death, small quantities of CO are produced due to decomposition of haemoglobin and myoglobin.

Give simplified notes on this text There are more than 3500 species of snakes, but only about 250 are venomous. In India about 216 species are found, of which 52 are venomous. According to WHO, there are more than 2.5 million venomous snake bites world-wide each year with more than 1,25,000 deaths. In India only five of them are dangerously poisonous to man, i.e., king cobra, common cobra, common krait, Russell's viper and saw-scaled viper. The most common venomous snake is common krait. Classification: The venomous snake may be divided into five families. (1) (A) Viperidae: Russell's viper, gaboon viper, saw scaled viper, puff adder. They are found in all parts of the world except the Americas. (B) Crotalidae: Rattlesnakes, pigmy rattlesnakes, copperheads, cottonmouths (water moccasins), pit viper, and the massasaugas, bushmaster. They are found in Asia and the Americas. The water moccasin is found in swampy areas or along the banks of streams. It is a strong swimmer and can bite under water. (2) Elapidae: Cobras, kraits, mambas, tiger snake, taipan, death adder, copperhead snakes, coral snakes. They are found in all parts of the world except Europe. (3) Hydrophidae Fig. (29-8). Cobra: (1) Binocellate, (2) Black, (3) Monocellate. or sea snakes: All sea snakes are poisonous but they seldom bite. (4) Colubridae: Boomslangs, bird snake of the African continent. (5) Atractaspididae: Airan and Middle Eastern burrowing asps or stilleto snakes also known as burrowing or mole vipers or adders, or false vipers. COMMON VENOMOUS SNAKES: (1) THE COBRA (nag, naja tripudians, naja naja, kala samp) has a hood, which on dorsal side often bears a double or single spectacle mark, but it has sometimes an oval spot surrounded by an ellipse. Head scales are large and the third labial touches the eye and the nasal shield. The portion of the neck surrounding the spectacle mark is darker than the rest of the back, and is often speckled with small golden spots. The hood cannot be seen in a dead cobra, as the joints and neck become stiff. There are two black spots, and three black bands on the underside of the hood. The caudal scales are double. There is a white band in the region where the hood touches the body region. The colour is brown or dark Fig. (29-8). It grows to a length of about two metres. Maxillary bone extends beyond palate. Poison fangs are followed by one or two small teeth. The neck is dilatable. It is found throughout India. The monocled cobra (N. Kaouthia) is found in Bengal, Orissa, Madhya Pradesh, Uttar Pradesh and Sikkim. A third variety, the central Asian or black cobra (NOxiano) is found in J&K, Punjab, Rajasthan and Madhya Pradesh. Difference between cobra and viper is given in Table (29-1). (2) THE KING COBRA (rajnag, nagraj, naja bungarus, humadryad), has a hood but no mark on it, and the length is about three to four metres. The colour may be yellow, green, brown or black and has yellowish or white cross-bands in the body. The tail scales are entirely present in their proximal ends, but divided in the distal ends. It is confined to the Western Ghats and it rarely bites humans. (3) THE COMMON KRAIT (karayat, bungarus caerulus, manyar, kalotaro, kawriya) is steel-blue, often shining and has single or double white bands Table (29-1). Difference between cobra and viper Fe (29-9), Common krait (Bung Trait Cobra Viper (1) Body: Long and cylindrical. Short, narrow neck. (2) Head: Small; seldom broader than body; covered by large scales or shields of special forms. Large; broader than body; triangular and covered by numerous small scales. (3) Pupil: Round. Vertical. (4) Maxillary bone: Carries poison fangs and other teeth. (5) Fangs: Grooved, short, fine. Carries only poison fangs. (6) Venom: Neurotoxic. Canalised, long. (7) Tail: Round. Haemotoxic. (8) Eggs: Lay eggs. Tapering. Give birth to young ones. Asian or black on Not ud Madhya Prost Mee ble (29-1, 0 THE T eat in their pru he Westera Gut alim a 4JT (ars apor asi lae, often shining as he Fig. (29-10). Banded krait. across the back, and a creamy-white belly. Its length is one to one-and-half metres. The stripes are not very distinct in the anterior region. The bead is covered with large shields. Four shields are found on either side of the lower lip. The scales in the central row down the back are large and beagonal. The tail is round. The plates under the tail like those on the belly are entire and not divided Fig. (29-9). These snakes are nocturnal la habit. They are seen throughout India. (4) THE BANDED KRAIT (ahirej, raj sanp, bungarus fasciatus, koelea krait is one-and-half to two metres in length. The tail ends bluntly and is swollen at the tip. It has a jet black five cm. wide cross-band alternating with a deep yellow band of the same size on its back. There is a black mark on the neck which is spread up to the eyes. The scales are hexagonal Fig. (29-10). They are found in Bengal, Orissa, Madhya Pradesh, Andra, Assam. The newer kraits are Sind krait (B. Sindanus) found in Rajasthan; Wall's Sind krait (B Sindanus Walli) found in Maharashtra, Bengal, Uttar Pradesh and Bibar and black krait (B. niger) found in North-East States, Sikkim, Bengal and Assam. These kraits have either no markings in the case of lack krait or have less obviously paired, equally placed white bands, after with a large spot on the hexagonal scale. The hexagonal scale is a constant key identification throughout the krait species. It is usually found in North-Eastern States. (5) RUSSELL'S VIPER OR DABOIA (kander, charn viper, khadchitro) has a flat, heavy and triangular head mith a white V-shaped mark, the angle of the V pointing forwards. It tar three rows of diamond-shaped black or brown spots along the back, te outer two rows consisting of spots ringed with white edges. Its body a whitish with dark semilunar spots. It narrows towards its tail, which i short. It can be identified by the entire broad plates on the belly, the small scales on the head, and the shield beneath the tail divided into two rows Fig. (29-11). It is heard to hiss loudly and continuously. It is found throughout India. (6) THE SAW-SCALED VIPER (afai, echis carinate) is brown, half metre in length, and has wavy white line on each flank of the back with diamond-shaped areas between these two lines. It has a triangular head, the upper surface of which is covered with a white mark resembling a bird's foot-print or an arrow. The tail is short and tapering. The broad belly plates with brown or dark spots, small scales on the head, and entire shields beneath the tail are the distinguishing features Fig. (29-12). It is found in most parts of India. The northern sawscaled viper (Echis Sochureki) is found in Rajasthan, Gujarat and J&K. In the Western Ghats, the hump-nosed pit viper (Hypnale hypnale) is found which is poisonous. (7) PIT VIPERS have a pit located between the nostrils and the eyes. Banded krait and common green pit viper (bamboo snake) are also venomous. Rat snake is not venomous. Common krait, cobra, Russell's viper, and saw-scaled viper are seen all over India. Banded krait is seen mainly in East India, and King cobra in Western Ghats. Sea Snakes: Twenty types are seen in Indian waters, all of them being venomous. They have small eyes, prominent nostrils on the top of the head, broad ventrals, small tuberculated dorsal scales and paddle-shaped flat tails. They are black, greenish-black or bluish-black with or without bands. They can be found is estuaries, rivers and even fresh Table (29-2), Difference between venomous and non-venomous snakes Non-venomous snakes (Fig. 29-3) Venomous snakes Trail (1) Head scales: (1) Small (vipers). (2) Large, and (a) if there is an opening or pit between the eye and nostril Large with the exceptions as mentioned, under the poisonous snakes. (pit viper). (b) Third labial touches the eye and nasal shields (cobra or coral snake). (e) No pit and third labial does not touch the nose and eye and central row of seales on back enlarged; undersurface of the mouth has only four infralabials, the fourth being the largest (kraits). (2) Belly scales: Large and cover entire breadth. (3) (6) Fangs: Teeth: Tail: Habits: Hollow like hypodermic needles. Two long fangs. Compressed. Usually nocturnal. Round pupil Anal plate No fangs Double row of subcaudal plates Fig. (29-13), Nonvenomous snake. Poison Venom Glands: They are the salivary glands of the snake and are situated behind the eyes, one on each side of the head above the upper jaw. FANGS: All venomous snakes have two fangs. These are curved teeth situated on the maxillary bones and are attached to parotid salivary glands situated behind both eyes and lie along the jaws, and are covered by a flap of mucous membrane. When the snake is about to bite, they become erect and point directly forward. They are bigger than the other teeth and are grooved or canalised in venomous snakes, and are solid in non-venomous snakes. When a venomous snake bites, it normally leaves two deep faint impressions, the distance between them being 8 mm to 4cm. A side swipe may produce a single puncture and also small marks of other teeth. Many venomous species have more than one set of fangs and can produce multiple puncture marks. Many non-venomous species have two enlarged teeth that can produce two puncture marks. Non-venomous snake bites leave a number of small impressions in a row Table (29-2) and Fig. (29-13). The discharge orifice of a viper fang is usually well above its tip. The fang can penetrate deeply, but part or most of the venom may be ejected superficially or externally without entering the wound. As such, even a thin layer of clothing may afford great protection. As the venom is injected superficially by vipers, and also by elapids and hydrophids, about 20% of patients bitten by venomous snakes do not show evidence of poisoning, even though the fangs have penetrated the skin, "dry bites". In sea snake bites, symptoms are not produced in about 80% of bites. The exact number of fang marks vary because of glancing blows, multiple fangs, multiple strikes, or from protection of clothing or shoes. Snake Venom: Venom is the saliva of the snake. Cobra venom is faint transparent yellow and is slightly viscous. When exposed to sun, it becomes slightly turbid. Russell's viper venom is white or yellow. Venoms of different species of poisonous snakes vary in toxicity, composition and antigenic structure. It Small, like those on the back or moderately large, but do not cover the entire breadth. Short and solid. Several small teeth. Not much compressed. Not so. is basically a mixture of toxalbumins and enzymes in varying proportions. The enzymatic components cause local and systemic effects and the kon-enzymatic compounds provide lethality. Venon is water and alcohol soluble. CONSTITUENTS: (1) Proteolytic enzymes liberate histamine from damaged endothelium leading to dissolution of blood vessel walls with extravasation of blood. They cause digestion of tissue proteins and peptides and produce marked tissue changes, oedema, blistering, bruising and necrosis. They may contribute to hypersensitive action. (2) Fibrin ferments enhance coagulation process. (3) Neurotoxins are found in elapid, hydrophid, vipirid and cortalid venoms. They are neuromuscular non-depolarising blocking agents, which produce a curare-like effect and paralysis, especially of respiratory centre. (4) Cholinesterase is rich in venom of cobra and krait. It causes hydrolysis of acetylcholine to choline and acetic acid leading to impairment of neuromuscular transmission. (5) Haemolysins (mainly in viper venom) cause disruption of endothelial cell functions and alveolar septa and cause pulmonary congestion and increased lung weight. These effects also occur locally at the site of bite, causing haemorrhagic oedema and systemic bleeding leading to shock. (6) Cardiotoxin found particularly in cobra venom is toxic to the heart. It also affects skeletal and smooth muscle membranes and neuromuscular junction. (7)

concentration of venom shows diurnal and seasons Chapter 29: Organic Irritant Poisons 427 Bites inficted at nights and immediately after biternation are the most severe. Venom travels in the body absent. Systemic symptoms appear after about 30 minutes. The bronth subcutancous arcolar space. through lymphatics and superficial veins and spreads rapid! patient feels sleepy, slightly intoxicated, weakness of legs, and is reluctant to stand or move. Nausea and vomiting are sometimes the Crotalidae venoms are rich in proteolytic enzyme activity. carly symptoms. Cyanosis is very marked. Ptosis is the earliest The viperidae venoms have lesser amounts and the elapidae neuroparalytic manifestation followed by ophthalmoplegia. ophidae venoms have little or no proteolytic activity. There may be extraocular muscle weakness and strabismus. Aaluronidase is found in every snake venom. L-aminoacic Weakness of the muscles increases, and develops into paralysis exidase is found mainly in the viperoid and crotalid venoms. It of the lower limbs. The paralysis then spreads to the trunk, not found in sea snake venoms. Cholinesterase is rich in elapic and affects the head which falls forward. The eyelids also hang viperid and crotalid venoms. oms wale it is absent or found only in small amounts in down. After half to one hour, there is excessive salivation and even vomiting, headache, vertigo, paraesthesia around the mouth and Tones of Venom: The colubrine and elapidae venom myalgia. This is followed by paralysis of the facial muscles, a mainly neurotoxic, and has a primary toxicity for the palate, jaws, tongue, vocal cords, neck muscles. Muscles of moiratory and cardiac centres. Neurotoxic features are due deglutition become progressively flaccidly paralysed due to a selective d-tubocurarin-like neuromuscular blockade which Which there is difficulty in speech and swallowing. After about results in flaceid paralysis of muscles. It can produce marked two hours, the paralysis is complete. Respiratory arrest may occur due to obstruction of upper airway by the paralysed tongue cardiac or vascular changes, or have a direct effect on the or inhaled vomitus, or due to paralysis of intercostal muscles and Food. The vinerine venom is mainly haemolytic and causes diaphragm. A basic means of assessing imminent respiratory jaravascular haemolysis and depression of the coagulation failure is inability to raise the head in supine position. Though mechanism. It can produce changes in the nervous system or in the patient is conscious, he is not able to speak. Coma sets in vascular dynamics. Russell's viper venom contains two proteases and finally the respirations stop with or without convulsions and which activate the blood clotting cascade. As a rule, one of the the heart stops. In cases of recovery, the skin and cellular tissues modes of action far exceeds the other. The sea snake venom surrounding the bite mark undergo necrosis. is myotoxic. Krait bite: Symptoms resemble those of cobra bite, but The venom of rattlesnakes, cotton mouth and copperhead contain there is no swelling or burning pain at the site of the bite, and cymes that possess cytotoxic, haemorrhagic and neurotoxic properties. the convulsions are milder, while the feeling of drowsiness and Coral snake venom is neurotoxic causing curare-like effects on the intoxication is more intense. Albumin appears in urine. neuromuscular junctions and neurologic symptoms. Russell's Viper and Echis Carinate Bite: A viperid snake Venom may not be detected in dry bite, washing of the merely strikes, discharging the venom the moment the fangs area, bite through thick layers of clothing, leakage from penetrate the skin and then immediately leaves it. More than superficial bite in mobile parts of body. 50% of the victims have minimal or no poisoning, as little Signs and Symptoms: Ophitoxaemia is poisoning by or no venom is injected. About 25% will develop serious stake venom. Most of the snake bites are from non-venomous generalised poisoning, but death is rare. When venom snakes. In venomous snake bites, inadequate snake venom is injected, the spot develops a severe pain within eight is injected in more than half of the cases, producing mild minutes. The area around the bite is red and painful. Small symptoms. The most common symptom following snake bite clots maybe present in vicinity of fang marks and blood (venomous or non-venomous) is fright, especially the fear vessels. The onset of swelling starts within 15 minutes and of rapid and unpleasant death. Due to fright, the victim may there is often blood-stained discharge from the wound. become semiconscious with cold clammy skin, hypotension, Persistent bleeding from bite site is a constant feature. feeble pulse and rapid breathing. These emotional symptoms Blisters begin to appear in about 12 hours in and around appear within few minutes of the bite. Sometimes, it produces the bitesite, progressing subsequently to involve the entire psychological shock and even death. It may also give rise to limb. When the amount of venom injected is less, pain and swelling restricted to below the elbow or knee, and tetanus or gas gangrene. some nausea disappear within one to two days. In moderate The signs and symptoms depend upon: (1) the nature, poisoning, there is a marked feeling of intense pain, vomiting, location, depth and number of bites; 98% of the snake bites occur giddiness, sweating, abdominal pain, dilatation of the pupils, over the extremities; (2) the length of time the snake holds on; getting insensitive to light and in about one to two hours, there (3) the extent of anger or fear that motivates the snake; (4) the is marked collapse and often complete loss of consciousness. amount of venom injected; (5) the species and size of the snake; Skin temperature is raised. Tingling and numbness over the (6) the condition of its fangs and venom glands; (7) the age and tongue and mouth or scalp and paraesthesia around the size of the victim; (8) the victim's sensitivity to the venom; (9) the wound occur. These symptoms usually subside within the pathogens in the snake; and (10) the first aid and medical care. next few hours. There is local extravasation of blood, and Cobra bite: In cobra bite, the transfer of venom is not swelling spreads as far as the trunk in one to two days, complete. Local symptoms start within 6 to 8 minutes. A small without further generalised symptoms. Though the limb reddish-bluish coloured wheal develops at the site of bite. The is swollen and red, it is usually not tender. Haematuria may bitten area is tender with slight radiating burning pain and be seen within a few hours of the bite. The local swelling oozing of bloodstained fluid. Swelling may be minimal or even and discolouration, and sometimes a few blisters heal without 428 Section 2: Toxicology Fatal Dose: Cobra 12 mg; Russell's viper 15 mg; echis 8 mg; necrosis within one to four weeks. In about 10 to 15% of the cases, extensive necrosis of skin, s.c. tissues and muscles krait 6 mg; of dried venom. The approximate yield in one bite in terms of dry weight of lyophilised venom is: cobra 170 to 325 may occur followed by epistaxis, haemoptysis, ecchymoses, mg; Russell's viper 130 to 250 mg; krait 20 mg; and echis 20 to intracranial and subconjunctival haemorrhages, and bleeding into the floor of the mouth, tympanic membrane, G.l and G-U tract, retroperitoneum and intraperitoneum. In severe cases, Diagnosis: (1) Snake specific venom antigens have been Fatal Period: Cobra half to six hours; viper one to two days. the main feature is the persisting shock. Blood may show detected in wound swabs, aspirates or biopsies, serum, CSF, haemoconcentration early, then a decrease in red cells and urine and other body fluids. As such, skin and underlying platelets, and urine contains blood, sugar and protein. Bleeding tissue surrounding the fang punctures, wound and blister and clotting time are usually prolonged. A haemorrhagic aspirates, serum and urine should be collected. Bitten area syndrome with blood-stained sputum, haemorrhages from should be preserved in normal saline. Urinary venom may the gums, rectum, the site of bite, etc., occur due to the remain detectable even though the victim is treated with increased coagulation time. Intravascular haemolysis may antivenom. (2) Radioimmunoassay (RIA) is most sensitive lead to haemoglobinuria. In the case of Russell's viper and and specific which can detect venom levels of 0.4 ug/1. Bitten hump-nosed viper, renal failure is a frequent complication. area of skin should be preserved. (3) Enzyme immunoassay Petechial haemorrhages are common. In systemic poisoning, (EIA) is commonly used as it is simple and can detect venom the blood becomes defibrinated and therefore will not clot. levels of 5 ug/1. (4) Cholinesterase and thromboplastin may be Increasing respiratory depression, blurring of vision, headache, detectable in bitten area of skin if there is no bacterial infection dizziness and weakness often occur. Towards the end, there is an or putrefaction, by radioimmunoassay method. (5) Immunological extensive suppuration and sloughing, followed by a malignant detection of small amounts of venom antigens in body fluids oedema of the bitten area. Paralysis does not occur. Death is can be done by ELISA. Fang marks tissues should be sent to usually due to shock and haemorrhage. In the case of echis, microbiology department. (6) A swab taken from the wound site death may not occur, but the secondary symptoms continue for or extract from the skin is injected into a frog for evidence of days, and the haemorrhages are severe and the wound shows mild necrosis. The patient should be observed for 12 to 24 hours toxicity. First Aid: (1) Assure the patient. (2) Apply firm pressure Table (29-3). Sea Snake Bites: Bites cause little or no local reaction. over the bitten area, which delays absorption of venom. (3) After half to one hour, the patient develops pain, stiffness Pressure immobilisation is recommended for elapid and and weakness of the skeletal muscles. Sea snake bites result sea-snake bites, but not for viper bites as it may cause local in marked polymyositis with a limb-girdle distribution. necrosis. Immediately apply a broad firm bandage (Sutherland Trismus occurs in early stage. Later, flaccid paralysis develops, wrap) on the bitten area and around the limb. As much of beginning with ptosis. Muscle enzymes and plasma potassium the limb should be bandaged as is possible. It should be tight levels are increased and myoglobinuria with renal failure may enough to occlude the superficial venous and lymphatic return, occur. Marked weakness of muscles persists for several months. but not the arterial or deep venous flow. A pressure of 50 to 70 Death may occur due to cardiac arrest or paralysis of mm Hg is maintained. In bites on the trunk, head or neck, apply respiratory muscles. firm pressure over the bitten area. (4) Immobilise the limb, as Pythons and boas kill by constricting chest causing traumatic movement can accelerate the spread of venom. Avoid elevation of asphyxia. an extremity, as it may hasten systemic absorption of venom. (5) (1) Trait Area bitten : Table (29-3). Difference between Colubrine and Viperine bites Colubrine bite Reddish wheal; tender with slight burning pain; oozing of bloodstained fluid less. Minimal or absent in bitten area. Neurotoxic. Appear after 30 minutes or more. Difficult. iperine bite (2) (3) (4) Swelling: Symptoms : Speech and deglutition : (5) (6) (7) (8) (9) Paralysis: Salivation : Pupils: Blood pressure: Bleeding and clotting time: (10) Haemorrhagic manifestations: 11) Cause of death : Pain and oozing of bloodstained fluid are more. Involves limb and spreads up to trunk. Haemotoxic. Appear immediately to 15 minutes. Normal. Of lower limbs spreading to trunk and head. Present. Normal. Normal. Normal. Not present. Absent. Dilated; do not react to light. Hypotension. Prolonged. Not present. Prominent feature. Respiratory failure. Circulatory failure due to a haemolysis and haemorrhage, shin and suction should not we and nerve injury. (6) Do no St do not use chemicals or 1 mund should not be cauteris thin the tissues. (8) Cryother Hy wound with soap and water; yam. (10) Make patient lie o that the airway is clear, in patient is brought after few i local swelling and no sy ander observation for 24

tal bleeding and nerve injury. (6) Do not suck venom out of the Local incision and suction should not be done as it can cause wound, and do not use chemicals or medicines on the wound in The wound should not be cauterised as it actually seals the clean the wound with soap and water, or iodine and cover with s poison within the tissues. (8) Cryotherapy is not of much use. (9) erile dressing. (10) Make patient lie on one side in the recovery position so that the airway is clear, in case of vomiting or fainting. If a patient is brought after few hours (4 to 6) of snake bite with mild local swelling and no systemic symptoms, he should he kept under observation for 24 hours, closely monitored for taxoid and discharged al signs, cardiac system and oxygen saturation, given tetanus Treatment: Polyvalent antisnake venon (PAVJIS prepared viper and sawscaled viper. common poisonous snakes, i.e., cobra, common krait Russell's by hyperimmunising horses against the venom of the four specifically neutralising the venom Antisnake venom (polyvalent): Each ml has capacity of (1) 0.60 mg of dried Indian Cobra (Najanaja) venom (2) 0.45 mg of dried common Krait (Bungarus Cacruleus) venom (3) 0.60 mg of dried Russell's viper (Daboiarusselii) venom (4) 0.45 mg of dried Saw-Scaled viper (Echiscarinatus) venom (Dilute vial with 10 ml liquid or distilled water given with This is mixed with normal saline 5 ml/kg and infused Plasma obtained from the hyperimmunised horses is concentrated and purified. The serum 1S lyophilised by drying it from the frozen state under high vacuum. It is prepared in the Hafkine Institute, Mumbai, King Institute, Chennai, Serum Institute, Pune, and at Kasauli in India, and is availabie in the form of lyophilised powder in an ampoule, which retains potency for about five years. It is useful when given within four hours of bite, It is of less value if delayed for eight hours, and is of doubtful value after twenty-four hours. Each vial of PAV will neutralise about 6 to 8 mg of venom. Its half-ife is about 90 hours. Test dose of PAV should not be administered as it is a poor predictor of carly anaphylactoid reactions and may presensitie the patient 1o PAV. If the swelling involves at least half of the bitten limb within a few hours of bite in the absence of a tourniquet, or if the swelling rapidly continues or if swelling has crossed a joint within first one or two hours of its starting, it indicates envenomation. Swelling that is several hours old is not good evidence of current envenomation. In case of viper bites, incoagulable blood or evidence of spontaneous bleeding from the gums will indicate envenomation. Dose: (1) Minimal symptoms: Local swelling but no systemic reactions, 5 vials. (2) Moderate: Swelling progressing beyond site of bite with systemic reaction, 10 vials (3) Severe: Marked local reaction, severe symptoms, 10 to 15 vials. Children require the same dose as in adults. The lyophilised powder is diluted in 500 ml of distilled water or normal saline and infused over a period of one hour. In neurotoxic poisoning, a second dose of ten vials should be given after one hour. In the case of haemotoxic patients the initial dose of antiserum will be neutralising unbound, free flowing venom. The liver requires six hours to restore clotting factors, as such patient will not require further PAV for six hours after the first dose. Chapter 29: Organic Irritant Poisons 429 20 minutes blood clotting test: Few ml. of fresh venous blood is put in a clean dry glass tube and left undisturbed for 20 minuies and then genily tilted. fe the blood is still liquid, it indicates viper bite. This test is repeated every 6 hours for determining repeat dose requirement. Normalisation of clotting time is taken as endpoint of therapy. After that the test is done at 12 hour intervals for at least 48 hours to detect recurring envenoming. Repeat dosing is required for recurrence of systemic signs. Other measures: At the first sign of any of the following. c.g. urticaria, itching, shivering, chills, nausea or vomiting, hypotension, bronchospasm, angio-oedema: (1) (A) Stop PAV infusion. (B) Administer 0.5 mg. 1:1000 adrenaline i.m. for adults (0.01 mg/kg for children). (C) Give hydrocortisone and antihistamine to provide longer term protection. (D) If there is no improvement after 10 to 15 minutes give a second dose of adrenaline. (E) Once the condition has improved start antiserum infusion. (2) If the antisnake venom is not available, 40 ml. of antivenene is given i.v. and repeated as required. It is effective for cobra and Russell's viper bites. (3) When treating viper bite a watch should be kept on prothrombin time. (4) If there are signs of neuroparalysis, give 1.5 mg neostigmine for adults paediatric dose 0.04 mg/kg) i.m. with 0.6 mg atropine i.v. (paediatric dose 0.05 mg/kg) to counteract the muscarinic effects of neostigmine. It is repeated twice at ten minutes interval. If the victim shows improvement give 0.5 mg neostigmine half hourly with atropine. In cases of presynaptic envenoming such as kraits or Russell's viper a positive response does not occur. Before every injection, half mg. atropine should be given to block muscarinic side effects. (5) Heparin 1000 to 5000 i.u. may be given i.v. if there are clotting abnormalities. (6) Inject tetanus antitoxin or a booster dose of tetanus toxoid. (7) A broadspectrum antibiotic should be given if there is severe tissue involvement. (8) In viper poisons, sedatives may be given to relieve pain and nervousness. (9) In case of collapse, general stimulants are of value. (10) Mechanical ventilatory support is necessary in respiratory failure. (11) In severe poisoning, infusion of normal saline or transfusion of blood or plasma are very useful. (12) Haemodialysis may be necessary. Peritoneal dialysis is better. (13) Give paracetamol for pain, but aspirin should not be given, as it may make the patient bleed. (14) Surgical debridement of the blebs, bloody vesicles, and superficial necrosis may be necessary. Postmortem Appearances: Clothing shows amber-coloured fluid, which becomes yellowish needles on drying. Venom over skin will be present as yellow crystals. Venomous snakes leave two or occasionally one fang mark. Non-venomous snakes leave a semicircular set of tooth-marks. The punctures are one-and-half cm. deep in colubrine and two-and-half cm. deep in viperine bites. Sometimes, the bite marks may not be visible. In colubrine bite, the site of bite contains fluid and haemolysed blood causing staining of vessels. In viperine bite, there is discolouration, swelling and cellulitis about the mark and haemorrhages occur from the puncture and mucous membranes. Haemorrhages into the bowel, purpuric spots on pericardium, and haemorrhages in the lungs and in many tissues may be seen. Kidneys are inflamed and show tubular necrosis, cortical necrosis and interstitial nephritis and marked congestion. Subcapsular pinpoint haemorrhages are seen in most cases of viperine bite. Acute renal failure is the leading cause of death in viper bite. Regional lymph nodes are swollen and haemorrhagic. Internal organs are congested. Washing from the bite area may contain cholinesterase or thromboplastin. The skin and underlying tissue surrounding fang marks should be removed for analysis. ELISA (enzyme-linked immunosorbent assay) can identify the nature of venom from the bite site. Absorption and Excretion: Snake venom is poisonous only when injected, and is harmless when taken by the mouth, as it will be digested by enzymes in intestinal tract and absorbed as amino acids. It is excreted by kidneys, milk and probably by salivary glands and the mucous membranes. The Circumstances of Poisoning: (1) Poisoning is as a rule accidental. (2) Occasionally, a murder is committed by throwing a venomous snake on the bed of sleeping person. (3) It is very rarely used for suicide. (4) Cattle are sometimes poisoned by snake venom. For this, a cobra is shut up in an earthen vessel containing a banana and heat is applied to the vessel. The snake being irritated, bites the fruit and the venom is injected to the pulp, which is crushed and smeared on a rag. The rag is thrust into the animal's rectum by means of a split bamboo. (5) The bodies of animals killed by snake poisoning may be eaten without ill-effects, but their blood is poisonous and is fatal if injected into the human body. CASE: Queen Cleopatra is reputed to have committed suicide by getting her self-bitten by a venomous snake.