Chapter 33: Irritant Poisons
Irritant poison — mainly produce inflammation on the site of contact, especially in the gastrointestinal tract, respiratory tract, and skin.
When a poison has a systemic effect and death ensues because of it, then it is classified as a poison affecting that system most, for example, cardiac poison or cerebral poison, or a spinal poison.
Inorganic Irritants
Nonmetallic: Phosphorus, halogens, formaldehyde, etc.
Metallic: Arsenic, mercury, lead, copper, iron, etc.
Organic Irritants
Vegetable: Abrus, castor, croton, calatropis, semicarpus, capsicum, ergot, etc.
Animal: Snakes and other poisonous insects.
Mechanical Irritants
Nails, hair, glass pieces, diamond dust, etc.
Burning pain in mouth, throat, esophagus, stomach, etc. which radiates all over the abdomen.
Intense thirst, but dysphagic due to painful deglutition. So, cannot take water or food which leads to dehydration and starvation.
Continuous painful vomiting. Vomitus shows normal contents initially, but later turns bilious or contains altered blood.
Continuous severe diarrhea and tenesmus.
Collapse due to shock with a rapid, feeble pulse, pale anxious face, cold clammy skin, sighing respiration, cramps in leg muscles, etc.
Convulsions, loss of consciousness, coma, extreme exhaustion, and death when not treated properly.
Cough
Feeling of constriction of chest
Breathlessness
Suffocation
Pulmonary oedema
Hemoptysis
Pain
Irritation
Itching
Redness
Vesication and blisters
It acts as a protoplasmic poison due to which normal metabolism is disturbed and cellular oxidation is severely affected.
Garlicky taste, and severe burning sensation in the mouth, throat, retrosternal area, and epigastrium, followed by nausea, vomiting, and diarrhea.
Breath and vomitus have a garlicky odor.
Fatal Dose:
White/Yellow Phosporous Dose: 1mg/kg
A yellowish-green gas with an irritating pungent odor.
It acts as a direct irritant of the mucous membrane of the respiratory tract by locally forming hydrochloric acid as it comes in contact with moisture.
Fatal dose: 400 ppm for few minutes (inhalation) or 1 part of chlorine in 1000 parts of air exposed for 5 minutes.
Fatal period: 24 hours of inhalation of pure chlorine gas.
It is a reddish-brown liquid, volatilizing to red fumes at room temperature and emitting an unpleasant odor.
It is more often n use as medicine and act as a sedative and cough elixir.
Fatal period: Uncertain. The maximum permissible level of vapor in the air is 0.1 ppm.
A volatile crystalline substance with purple glittering color, a characteristic odor, and an acrid taste. It gives violet fumes/vapors at room temperature.
It acts as an antiseptic. It is a powerful irritant and vesicant.
Fatal dose: 2-4 gm of iodine or 30-60 ml (1-2 ounces) of tincture iodine.
Fatal period: Average 24 hours
Toxicity rating: 3-5
A colorless gas with a pungent odor. Commercially it is available as formalin, which is a 40 percent aqueous solution of formaldehyde gas.
A disinfectant, antiseptic, deodorant, tissue fixative, and embalming agent.
Fatal dose: 30-90mL
Fatal period: 24-48 hrs.
Toxicity rating: 3
It is not poisonous as it is insoluble in water and cannot be absorbed from the gastrointestinal tract.
Arsenious oxide or arsenic trioxide (sankhyal or somalkar) is poisonous.
Arsenic compounds act by inactivating the sulfhydryl enzymes, which in turn interfere with the cellular metabolism, in the liver, lungs, intestinal wall, and spleen.
Arsenic can replace phosphorus in the bones where it may remain for years. It also gets deposited in the hairs.
Fatal dose: 100 to 200 mg of arsenious oxide.
Fatal period: 2 to 3 days.
Toxicity rating: 5 for all arsenic salts, except arsenic trioxide, which has a toxicity rating of 6.
Metallic mercury is a heavy, silvery liquid and is nonpoisonous. But it volatilizes at room temperature and inhalation of vapors is toxic.
A potential source of elemental mercury is at home, which includes mercury switches, and mercury-containing devices such as thermometers, thermostats, and barometers.
Absorption is possible through all routes.
The pure metallic form is nontoxic. The mercurial compounds can act by inactivating sulfhydryl enzymes, which in turn interfere with cellular metabolism.
Fatal dose: 100-400 mg of mercuric chloride.
Fatal period: Few hours 1 to 2 weeks.
Toxicity rating: 5 or 6 for most of the salts.
Absorption is possible through all routes.
Pure metallic forms are nontoxic is a steel-grey metal.
Lead compounds can act by producing spasms of the capillaries and arterioles or by fixation of the poison in the tissues such as brain, bones, etc.
It can also combine with sulfhydryl enzymes and interfere with its action.
Lead can decrease the synthesis of heme leading to anemia and can bring about hemolysis as well as release immature RBCs into circulation (reticulocytosis and basophilic stippling of RBCs).
Lead can destroy nerve cells, myelin sheaths in CNS and also produce cerebral edema. It also exerts toxic effects on kidneys (nephritis) and reproductive system (infertility).
Fatal dose: depends on toxic compound (20 gm of lead acetate).
Fatal period: 1 to 2 days.
Toxicity rating: 3 or 4 for most of lead salts.
Copper sulfate is a crystalline salt with blue color and has a metallic taste. In small dose of 0.5 gm it acts as an emetic, but in large doses it acts as an irritant poison.
Poisoning is usually accidental or suicidal. Homicidal use is rare because of its metallic taste and striking blue color.
Copper subacetate is a bluish-green salt.
It is formed by the action of vegetable acids while cooking in copper cooking utensils, which have been not properly tin lined.
Accidental verdigris poisoning from contamination of food cooked in such utensils, are often reported.
Fatal dose:
Copper sulphate — 30 gm
Verdigris — 15 gm
Toxicity rating: 4 for copper salts
Iron salts are used for the treatment of prophylaxis from iron deficiency anemia.
The early features of iron poisoning are due to the corrosive effects of iron, while later effects are largely due to the disruption of the cellular processes.
Iron tablets may adhere to the stomach and duodenum causing irritation and in severe cases hemorrhagic necrosis and perforation.
Absorbed iron is rapidly cleared from extracellular spaces by uptake into parenchymal cells, particularly in the liver.
It causes mitochondrial damage and cellular dysfunction resulting in metabolic acidosis and necrosis.
Widespread organ damage becomes apparent, hepatic failure with hypoglycemia and coagulopathy may develop and this is often fatal.
Fatal dose: 20-40 gm of ferrous sulfate/> 150 mg of elemental iron.
Fatal Period: Uncertain
Toxicity Rating: 3
It is a slender vine and climber, with compound leaves having 10-15 pairs of narrow leaves, small pinkish flowers with seedpods which split open when ripe exposing 4-6 seeds within.
These seeds are bright red in color with black spot in one pole and weigh about 105 mg.
Toxic Principles: N-methyltryptophan, Glycyrrhizin, Abrin, Abrine, Abralin & Abric Acid.
Usual Fatal Dose: 60-120 mg of abrin (1-2 crushed seeds)
Fatal Period: 3-5 days
Toxicity Rating: 5 to 6 (Super toxic)
Also known as Castor Oil Plant.
It is a large shrub with greenish-red leaves.
Fruits are borne in clusters and are soft-spined greenish/ brownish capsules with seeds.
Seed oil are toxic.
Active principle: Riconoleic Acid & Ricin
Fatal dose: 1 mg/kg body weight or 6 mg of ricin (about 8- 10 seeds).
Fatal period: Several days.
Toxicity rating: Ricin 6 (Super toxic), castor oil 2 (Slightly toxic).
It is an evergreen tree with smooth ash-colored bark.
The leaves of the tree are ovate-lanceolate.
Flowers are small, and oblong.
Fruits are three lobed containing oval, dark brown seeds, with brownish black color and longitudinal striations.
Toxic part: Seed and oil extracted from the seeds is extremely toxic. Seed oil is commented to have tumor promoting phorbol diesters.
Active principles: Crotin & Crotonoside
Fatal dose: 1 to 2 ml of oil or 4 to 6 crushed seeds
Fatal period: 4 to 6 hours to 3-6 days
Toxicity rating: 5 (croton oil)
It is a tall shrub with yellowish-white bark, and oblong thick leaves and purplish or white flowers.
When the stem, branches and leaves are cut, crushed or incised, it yields milky white latex, which is an acrid juice called madar juice.
Toxic part: Stem, branches, leaves and the milky white latex (madar juice).
Active principles: Uscharin, Calotoxin, Calotropin, & Gigantin.
Fatal dose: Uncertain.
Fatal period: 12 hours
It is a small tree of East Indian origin. Its flower is dull/greenish yellow in color.
Fruit is black, heart- shaped with hard rind within which is a thick fleshy pericarp which yields brown oily resinous fluid.
This turns black on exposure to air.
This fluid is often used as ‘marking ink’, on linen and cotton clothes by the washer men (Dhobis).
Active principles: Semicarpol & Bhilawanol.
Fatal dose: Uncertain.
Fatal period: 12 to 24 hours.
It is a small herb bearing somewhat long, tapering fruits, which become red when ripe, and possess a pungent odor and taste.
The fruit (chilly) contains a number of small, flat, yellowish seeds, which bear a superficial resemblance to datura seeds.
Toxic part: Fruit and the seeds
Active principles: Capsicin (crystalline) and capsaicin are both acrid, volatile, alkaloid substances.
Usual Fatal Dose: Can cause serious toxicity.
Fatal Period: Fatality unlikely.
It is a tall tree with smooth bark, long curved leaves, and large flowers. Eucalyptus oil obtained by steam distillation of the extract derived from the leaves.
Active principle: Eucalyptole
Usual fatal dose: 5 to 10 ml can cause serious toxicity.
Fatal period: Fatality is unlikely.
It is a tree. Seed grown in the tree yields a yellowish oil (margosa oil), which has a disagreeable odour and bitter taste.
Active principles: Azadirachtin, Meliantriol, Nimbin, Salanmin, & Nimbidin
Usual fatal dose: Can cause serious toxicity
Fatal period: Fatality is unlikely.
Perennial herb (Category: Bulbs)
Height: 15-30 cm, with basal, slender leaves; and long, tubular, 6-parted, flowers which are pink, violet/ lavender or white in colour.
Poisonous part: All parts of plant are highly poisonous,and may be fatal if eaten.
Active principle: Alkaloid colchicines and demecolcin.
Usual fatal dose: Can cause serious toxicity.
Fatal period: Fatality unlikely.
Ergot is an alkaloid.
It is the sclerotium (mycelium) of a fungus Claviceps purpura, which grows on many cereals like rye, barley, wheat, oat, etc. fungus gradually replaces the whole grain to a dark purple mass, which on drying yields ergot.
Active Principles: Ergotamine, Ergotoxin, & Ergometrine.
Fatal dose and period: Both uncertain.
Toxicity rating: 4 to 5
Snakes are ectothermic (cold-blooded) limbless vertebrates of the Class Reptilia.
There are at least 3,000 species of snakes, but only 400 are poisonous, which means most of them is non-venomous.
Some snakes have evolved specialized glands, which produce venom, mostly derived from salivary glands.
Venom may have several functions for the snake such as rapid immobilization and predigestion of prey.
Body is elongated and covered with horny epidermal scales, which are shed/molted off several times a year.
Snakes usually move on the tips of their ribs.
Eyelids are fused so appear to be absent.
There are no visible external ears, and hence there is a great controversy on whether snakes can hear sound.
Skull bones are movably articulated.
Tongue is forked at the tip and serves as a sense organ and can be protruded out even when the mouth is closed through a gap in the upper jaw.
Jacobson’s organ — a cavity in the roof of the mouth with olfactory cells in which the snake inserts the tips of the forked tongue.
They have got a paired copulatory organ and the cloacal aperture is transverse.
Colubridae
They rely instead on the trauma caused by other teeth to provide an entry track for their “venom”.
A few of these may cause some effects in humans, though are not expected to be lethal.
Elapidae
Include “cobra” type snakes, common in Asia and Africa.
They have small to moderate-sized fangs at the front of the mouth, possibly the “true fangs”.
Cobra venoms are quite toxic and they are a major cause of human envenoming morbidity and mortality.
Viperidae
All species have well-developed, longer fangs on hinged maxillae, allowing rotation (elevation) when biting, than in any other groups of venomous snakes.
Venom glands are also typically larger than in other groups.
They have heat-sensing pit organs at the front of the head, giving some degree of infrared or heat-sensitive “vision”.
Hydrophidae
These are sea snakes and are closely related to the cobras, with similar fang structure, but live most or all of their lives in an aquatic, usually marine environment.
They are a significant cause of envenoming amongst fishermen in the Indian and Pacific oceans.
Atractaspidae
These are side fanged viper like snakes confined to Africa and the Middle East. They have unusual fang structure and venoms, which contain endothelin-like compounds called sarafotoxins, causing potent smooth muscle contraction.
Snake venom is the poisonous secretion ejected from the poison apparatus (modified parotid gland) of a poisonous snake, during the act of biting.
Snake venoms are usually clear and amber-colored fluid when fresh.
They are poisonous only when injected by a needle or by bite of a snake.
The venom is non-poisonous when taken orally.
Neurotoxic Venom
Common in Elapidae Snakes.
Acts like Curare.
Convulsions may be seen with Cobra venom.
Hemotoxic Venom
Common in Viperidae snakes
Acts by cytolysis of endothelium of blood vessels, lysis of red cells and other tissue cells, and coagulation disorders.
It can lead to:
Severe swelling with oozing of blood and spreading cellulitis at the bite site. Blood from such patients fails to clot even on adding thrombin, because of a very low levels of fibrin.
Necrosis of renal tubules; and
Functional disturbances like convulsions, due to intracerebral hemorrhage.
Myotoxic Venom
Common in hydrophidae or sea snakes.
Produces generalized muscular pain, followed by:
Myoglobinuria within 3 to 5 hours.
Death usually occurs due to respiratory failure.
They have no poison apparatus.
They possess 4 longitudinal rows of teeth in upper jaw and 2 rows in lower jaw.
Tail is not compressed.
Ventral shields are small/moderately large.
Head scales are usually larger and without any special features.
Fangs are short and solid.
These are not nocturnal.
The bite marks show more than two teeth markings
Snakebites are usually accidental. Rarely it can also be homicidal or suicidal.
Venom is inoculated into the body. Snakes like cobra can inject/ emit venom by spitting
Degree of toxicity depends on three factors:
Toxic principle in the venom.
Quantity of venom injected.
Type of fang:
Channeled (viperine) fangs — complete transfer of venom.
Grooved (elapid) fangs — less transfer of venom.
Neurotoxic Venomous Snake Bite
Severe burning at bite site, rapid edema and inflammatory changes followed by oozing of serum.
Found within 15-30 minutes or 2 hours of biting.
Hemotoxic Venomous Snake Bite
Severe pain at bite site, followed by swelling, ecchymosis, cellulitis and severe hemorrhage.
It is due to hemolytic effect on heart and blood vessels resulting in cardiovascular collapse and death.
If the patient survives suppuration, sloughing with infection at the site of bite, hemorrhage from the mucosa of rectum, other natural orifice, etc. and gangrene of the parts involved can occur.
Myotoxic Venomous Snake Bite
Minimal swelling and pain
Myalgia, muscle stiffness, myoglobinuria, renal tubular necrosis.
Allaying of the Anxiety and Fear
Prevention of the Spread of Venom
First Aid
Reassurance of the victim.
Do not tamper with the bite wound, except wipe with a damp cloth to remove the venom lying on the skin surface.
Immobilization of the bitten limb.
Transport the patient to a medical facility immediately.
Identify the snake if possible but not necessary.
Better to take along the dead snake for identification. Be sure it is dead. Severed snakeheads, both fresh and preserved, have inflicted severe and even fatal bites.
Avoid potentially harmful traditional first aid measures.
Do not apply tourniquets, ligatures, or constricting bands unless the snake is a neurotoxic envenomating.
Dangers of Tourniquets, Compression Bandages and Other Occlusive Methods
Ischemia and gangrene.
Damage to superficial peripheral nerves, especially the lateral poplitial nerve at the neck of fibula.
Increased fibrinolytic activity in the occluded limb.
Congestion, swelling, and increased bleeding from the occluded limb.
Shock on releasing a tight tourniquet.
Intensification of local effects of venom in the occluded limb.
Do not use antivenom treatment routinely and indiscriminately because of reasons:
All commercial antivenoms carry a risk of potentially serous serum reaction.
Antivenom is not always necessary; many patients are bitten by nonvenomous snakes, and a large portion of those bitten by venomous snakes are not envenomated.
Antivenoms have a range of specific and para-specific neutralizing activity and are useless for venoms outside that range. Specific antivenoms are not available for treatment of envenomation by some species.
Antivenom is expensive, always in short supply, and has a limited shelf life.
Systematic Envenomation
Hemostatic disturbances; spontaneous systemic bleeding.
Cardiovascular abnormalities: shock, hypotension, abnormal electrocardiogram, arrhythmia, cardiac failure, pulmonary edema.
Neurotoxicity.
Generalized rhabdomyolysis.
Impaired consciousness of any cause.
In patients with definite signs of local envenomation, the following indicate significant systemic envenomation:
Neutrophil leukocytosis
Elevated creatine phosphokinase and aminotransferases,
Hemoconcentration, uremia, hypercreatininemia, oliguria, hypoxemia, acidosis and vomiting.
Severe Local Envenoming
Local swelling involving more than half of the bitten limb, or associated with extensive blistering or bruising, especially in patients bitten by species whose venoms are known to cause local neurosis. Bites on digits carry a high risk of necrosis.
There is no absolute contraindication to antivenom in patients with life-threatening systemic envenomation.
Patients with an atopic history and those who had reactions to equine antiserum on previous occasions have an increased risk of severe reactions.
In case of pretreatment with subcutaneous adrenaline and intravenous antihistamine and corticosteroids may prevent or diminish the reaction.
Rapid desensitization is not recommended.
Local Envenomation
Secondary infection: Prevention with penicillin or erythromycin and booster dose of tetanus toxoid.
Clean wound with antiseptic.
Bullae can be aspirated to dryness with a fine sterile needle.
Nurse limbs in most comfortable position.
Examine the wound frequently for evidence of necrosis.
Polyspecific/Polyvalent Antivenom
Haffkin’s Institute, Mumbai and Central Research Institute Kasauli, Himachal Pradesh, King’s Institute, Chennai, Serum Institute, Pune prepares this. It is available as a lyophilized powder in an ampoule, with potency for nearly 10 years.
It can neutralize the venom of cobra, common krait, Russel’s viper and Echis carinata.
It is effective when given within four hours of biting.
It is to be dissolved in distilled water or normal saline before use.
Use only if the solution prepared is clear, if it is opaque, it is considered as not potent.
Always perform serum sensitivity test (test dose) before giving it.
The skin test procedure
Inject 0.02 to 0.03 ml of the antivenin in 1:10 dilution, intradermally.
If there is a hypersensitivity reaction (urticarial wheal with erythema within 15 minutes) the patient should be desensitized.
The desensitization procedure
Inject 0.1, 0.2 and 0.5 ml of the antivenin in 1:100 dilutions at an interval of 15 minutes.
A 1:10 dilution is given in the same manner, followed by undiluted antivenin. If no severe reaction occurs, the usual dose is given intravenously.
According to another view, skin testing is not necessary, but adrenaline should be injected subcutaneously as premedication with a dose of a systemic corticosteroid.
Spanish Fly, Blister Beetle, Lytta
It is a winged insect, which has a body of: length 2 cm and breadth 0.6 cm and greenish black colour with shiny wings of same color.
The insect as such or the powder of dried body has the toxic (active) principle.
Active principle: Cantharidin.
Fatal dose — 15 to 30 mg of cantharidin 1.5 gm of powdered cantharides.
Toxicity rating — For cantharidin 6.
Treatment — Stomach wash, demulcents, symptomatic.
Mouth, stomach and intestines may show inflammation and vesication. Particles of insect may be found in the stomach contents.
Heart, lungs, kidneys are also found to be inflamed and hemorrhagic.
Used often as an aphrodisiac
Poisoning is reported very rarely (accidental/homicidal)
Used also as stimulant for scalp hair growth (hair oil).
They belong to Myriapoda (under class Arthropods) and are organic animal irritants.
They have a long segmented dark to brownish black colored body with a pairs of legs in each segment.
Usually centipedes can inflict painful bites with erythema, oedema, and local lymphangitis.
Treatment is by washing the bite site with soap and water and administering analgesics.
Scorpion: A poisonous arthropod with a crab like body with eight legs and a segmented tail having a bulbous expansion and a sting in the last segment which has a clear, colorless venom having two components, a hemolytic and a neurotoxic fractions.
Fatality is rare as dose in sting is not lethal.
Hemolytic factors can mimic viperine snakebite. Diagnosis is by locating only one deep punctured wound with red surrounding area, edema, severe burning pain, etc.
Neurotoxic factor can mimic strychnine poisoning. Victim presents with nausea, vomiting, restlessness, fever followed by convulsions, paralysis, coma and death.
Measures to reduce the rate of absorption of the venom by:
Tourniquet above the level of stinging.
Ice packing, incision and suction (first aid).
Wash with solution of ammonia.
Local anesthetics can also be helpful to reduce the pain.
Intravenous administration of calcium gluconate may reduce swelling.
Giving barbiturate can alleviate anxiety.
Atropine may be given to reduce the pulmonary edema (do not use morphine).
Venom of bees, wasps, hornets, ants, etc. is a complex mixture of biomedical compounds ranging from simple amines to complicated proteins or enzymes.
It may be rarely fatal if venom is histamine. It can result in laryngeal edema leading to asphyxia and deat, when not treated immediately.
When there are multiple stings, it can lead to severe systemic reactions, resulting in gastrointestinal disturbances, shock, unconsciousness and death.
Measures to reduce the rate of absorption of venom by:
Tourniquet above the level of stinging or incision and suction.
Adrenaline is also useful.
Apply tincture iodine/antihistaminic (to reduce inflammation).
Adrenocorticotrophic hormone (ACTH) 25 mg in 1000 ml normal saline given as an intravenous drip can help in prevention of severe allergic reactions.
Calcium gluconate given intravenously can reduce edema/ rash.
Irritant poison — mainly produce inflammation on the site of contact, especially in the gastrointestinal tract, respiratory tract, and skin.
When a poison has a systemic effect and death ensues because of it, then it is classified as a poison affecting that system most, for example, cardiac poison or cerebral poison, or a spinal poison.
Inorganic Irritants
Nonmetallic: Phosphorus, halogens, formaldehyde, etc.
Metallic: Arsenic, mercury, lead, copper, iron, etc.
Organic Irritants
Vegetable: Abrus, castor, croton, calatropis, semicarpus, capsicum, ergot, etc.
Animal: Snakes and other poisonous insects.
Mechanical Irritants
Nails, hair, glass pieces, diamond dust, etc.
Burning pain in mouth, throat, esophagus, stomach, etc. which radiates all over the abdomen.
Intense thirst, but dysphagic due to painful deglutition. So, cannot take water or food which leads to dehydration and starvation.
Continuous painful vomiting. Vomitus shows normal contents initially, but later turns bilious or contains altered blood.
Continuous severe diarrhea and tenesmus.
Collapse due to shock with a rapid, feeble pulse, pale anxious face, cold clammy skin, sighing respiration, cramps in leg muscles, etc.
Convulsions, loss of consciousness, coma, extreme exhaustion, and death when not treated properly.
Cough
Feeling of constriction of chest
Breathlessness
Suffocation
Pulmonary oedema
Hemoptysis
Pain
Irritation
Itching
Redness
Vesication and blisters
It acts as a protoplasmic poison due to which normal metabolism is disturbed and cellular oxidation is severely affected.
Garlicky taste, and severe burning sensation in the mouth, throat, retrosternal area, and epigastrium, followed by nausea, vomiting, and diarrhea.
Breath and vomitus have a garlicky odor.
Fatal Dose:
White/Yellow Phosporous Dose: 1mg/kg
A yellowish-green gas with an irritating pungent odor.
It acts as a direct irritant of the mucous membrane of the respiratory tract by locally forming hydrochloric acid as it comes in contact with moisture.
Fatal dose: 400 ppm for few minutes (inhalation) or 1 part of chlorine in 1000 parts of air exposed for 5 minutes.
Fatal period: 24 hours of inhalation of pure chlorine gas.
It is a reddish-brown liquid, volatilizing to red fumes at room temperature and emitting an unpleasant odor.
It is more often n use as medicine and act as a sedative and cough elixir.
Fatal period: Uncertain. The maximum permissible level of vapor in the air is 0.1 ppm.
A volatile crystalline substance with purple glittering color, a characteristic odor, and an acrid taste. It gives violet fumes/vapors at room temperature.
It acts as an antiseptic. It is a powerful irritant and vesicant.
Fatal dose: 2-4 gm of iodine or 30-60 ml (1-2 ounces) of tincture iodine.
Fatal period: Average 24 hours
Toxicity rating: 3-5
A colorless gas with a pungent odor. Commercially it is available as formalin, which is a 40 percent aqueous solution of formaldehyde gas.
A disinfectant, antiseptic, deodorant, tissue fixative, and embalming agent.
Fatal dose: 30-90mL
Fatal period: 24-48 hrs.
Toxicity rating: 3
It is not poisonous as it is insoluble in water and cannot be absorbed from the gastrointestinal tract.
Arsenious oxide or arsenic trioxide (sankhyal or somalkar) is poisonous.
Arsenic compounds act by inactivating the sulfhydryl enzymes, which in turn interfere with the cellular metabolism, in the liver, lungs, intestinal wall, and spleen.
Arsenic can replace phosphorus in the bones where it may remain for years. It also gets deposited in the hairs.
Fatal dose: 100 to 200 mg of arsenious oxide.
Fatal period: 2 to 3 days.
Toxicity rating: 5 for all arsenic salts, except arsenic trioxide, which has a toxicity rating of 6.
Metallic mercury is a heavy, silvery liquid and is nonpoisonous. But it volatilizes at room temperature and inhalation of vapors is toxic.
A potential source of elemental mercury is at home, which includes mercury switches, and mercury-containing devices such as thermometers, thermostats, and barometers.
Absorption is possible through all routes.
The pure metallic form is nontoxic. The mercurial compounds can act by inactivating sulfhydryl enzymes, which in turn interfere with cellular metabolism.
Fatal dose: 100-400 mg of mercuric chloride.
Fatal period: Few hours 1 to 2 weeks.
Toxicity rating: 5 or 6 for most of the salts.
Absorption is possible through all routes.
Pure metallic forms are nontoxic is a steel-grey metal.
Lead compounds can act by producing spasms of the capillaries and arterioles or by fixation of the poison in the tissues such as brain, bones, etc.
It can also combine with sulfhydryl enzymes and interfere with its action.
Lead can decrease the synthesis of heme leading to anemia and can bring about hemolysis as well as release immature RBCs into circulation (reticulocytosis and basophilic stippling of RBCs).
Lead can destroy nerve cells, myelin sheaths in CNS and also produce cerebral edema. It also exerts toxic effects on kidneys (nephritis) and reproductive system (infertility).
Fatal dose: depends on toxic compound (20 gm of lead acetate).
Fatal period: 1 to 2 days.
Toxicity rating: 3 or 4 for most of lead salts.
Copper sulfate is a crystalline salt with blue color and has a metallic taste. In small dose of 0.5 gm it acts as an emetic, but in large doses it acts as an irritant poison.
Poisoning is usually accidental or suicidal. Homicidal use is rare because of its metallic taste and striking blue color.
Copper subacetate is a bluish-green salt.
It is formed by the action of vegetable acids while cooking in copper cooking utensils, which have been not properly tin lined.
Accidental verdigris poisoning from contamination of food cooked in such utensils, are often reported.
Fatal dose:
Copper sulphate — 30 gm
Verdigris — 15 gm
Toxicity rating: 4 for copper salts
Iron salts are used for the treatment of prophylaxis from iron deficiency anemia.
The early features of iron poisoning are due to the corrosive effects of iron, while later effects are largely due to the disruption of the cellular processes.
Iron tablets may adhere to the stomach and duodenum causing irritation and in severe cases hemorrhagic necrosis and perforation.
Absorbed iron is rapidly cleared from extracellular spaces by uptake into parenchymal cells, particularly in the liver.
It causes mitochondrial damage and cellular dysfunction resulting in metabolic acidosis and necrosis.
Widespread organ damage becomes apparent, hepatic failure with hypoglycemia and coagulopathy may develop and this is often fatal.
Fatal dose: 20-40 gm of ferrous sulfate/> 150 mg of elemental iron.
Fatal Period: Uncertain
Toxicity Rating: 3
It is a slender vine and climber, with compound leaves having 10-15 pairs of narrow leaves, small pinkish flowers with seedpods which split open when ripe exposing 4-6 seeds within.
These seeds are bright red in color with black spot in one pole and weigh about 105 mg.
Toxic Principles: N-methyltryptophan, Glycyrrhizin, Abrin, Abrine, Abralin & Abric Acid.
Usual Fatal Dose: 60-120 mg of abrin (1-2 crushed seeds)
Fatal Period: 3-5 days
Toxicity Rating: 5 to 6 (Super toxic)
Also known as Castor Oil Plant.
It is a large shrub with greenish-red leaves.
Fruits are borne in clusters and are soft-spined greenish/ brownish capsules with seeds.
Seed oil are toxic.
Active principle: Riconoleic Acid & Ricin
Fatal dose: 1 mg/kg body weight or 6 mg of ricin (about 8- 10 seeds).
Fatal period: Several days.
Toxicity rating: Ricin 6 (Super toxic), castor oil 2 (Slightly toxic).
It is an evergreen tree with smooth ash-colored bark.
The leaves of the tree are ovate-lanceolate.
Flowers are small, and oblong.
Fruits are three lobed containing oval, dark brown seeds, with brownish black color and longitudinal striations.
Toxic part: Seed and oil extracted from the seeds is extremely toxic. Seed oil is commented to have tumor promoting phorbol diesters.
Active principles: Crotin & Crotonoside
Fatal dose: 1 to 2 ml of oil or 4 to 6 crushed seeds
Fatal period: 4 to 6 hours to 3-6 days
Toxicity rating: 5 (croton oil)
It is a tall shrub with yellowish-white bark, and oblong thick leaves and purplish or white flowers.
When the stem, branches and leaves are cut, crushed or incised, it yields milky white latex, which is an acrid juice called madar juice.
Toxic part: Stem, branches, leaves and the milky white latex (madar juice).
Active principles: Uscharin, Calotoxin, Calotropin, & Gigantin.
Fatal dose: Uncertain.
Fatal period: 12 hours
It is a small tree of East Indian origin. Its flower is dull/greenish yellow in color.
Fruit is black, heart- shaped with hard rind within which is a thick fleshy pericarp which yields brown oily resinous fluid.
This turns black on exposure to air.
This fluid is often used as ‘marking ink’, on linen and cotton clothes by the washer men (Dhobis).
Active principles: Semicarpol & Bhilawanol.
Fatal dose: Uncertain.
Fatal period: 12 to 24 hours.
It is a small herb bearing somewhat long, tapering fruits, which become red when ripe, and possess a pungent odor and taste.
The fruit (chilly) contains a number of small, flat, yellowish seeds, which bear a superficial resemblance to datura seeds.
Toxic part: Fruit and the seeds
Active principles: Capsicin (crystalline) and capsaicin are both acrid, volatile, alkaloid substances.
Usual Fatal Dose: Can cause serious toxicity.
Fatal Period: Fatality unlikely.
It is a tall tree with smooth bark, long curved leaves, and large flowers. Eucalyptus oil obtained by steam distillation of the extract derived from the leaves.
Active principle: Eucalyptole
Usual fatal dose: 5 to 10 ml can cause serious toxicity.
Fatal period: Fatality is unlikely.
It is a tree. Seed grown in the tree yields a yellowish oil (margosa oil), which has a disagreeable odour and bitter taste.
Active principles: Azadirachtin, Meliantriol, Nimbin, Salanmin, & Nimbidin
Usual fatal dose: Can cause serious toxicity
Fatal period: Fatality is unlikely.
Perennial herb (Category: Bulbs)
Height: 15-30 cm, with basal, slender leaves; and long, tubular, 6-parted, flowers which are pink, violet/ lavender or white in colour.
Poisonous part: All parts of plant are highly poisonous,and may be fatal if eaten.
Active principle: Alkaloid colchicines and demecolcin.
Usual fatal dose: Can cause serious toxicity.
Fatal period: Fatality unlikely.
Ergot is an alkaloid.
It is the sclerotium (mycelium) of a fungus Claviceps purpura, which grows on many cereals like rye, barley, wheat, oat, etc. fungus gradually replaces the whole grain to a dark purple mass, which on drying yields ergot.
Active Principles: Ergotamine, Ergotoxin, & Ergometrine.
Fatal dose and period: Both uncertain.
Toxicity rating: 4 to 5
Snakes are ectothermic (cold-blooded) limbless vertebrates of the Class Reptilia.
There are at least 3,000 species of snakes, but only 400 are poisonous, which means most of them is non-venomous.
Some snakes have evolved specialized glands, which produce venom, mostly derived from salivary glands.
Venom may have several functions for the snake such as rapid immobilization and predigestion of prey.
Body is elongated and covered with horny epidermal scales, which are shed/molted off several times a year.
Snakes usually move on the tips of their ribs.
Eyelids are fused so appear to be absent.
There are no visible external ears, and hence there is a great controversy on whether snakes can hear sound.
Skull bones are movably articulated.
Tongue is forked at the tip and serves as a sense organ and can be protruded out even when the mouth is closed through a gap in the upper jaw.
Jacobson’s organ — a cavity in the roof of the mouth with olfactory cells in which the snake inserts the tips of the forked tongue.
They have got a paired copulatory organ and the cloacal aperture is transverse.
Colubridae
They rely instead on the trauma caused by other teeth to provide an entry track for their “venom”.
A few of these may cause some effects in humans, though are not expected to be lethal.
Elapidae
Include “cobra” type snakes, common in Asia and Africa.
They have small to moderate-sized fangs at the front of the mouth, possibly the “true fangs”.
Cobra venoms are quite toxic and they are a major cause of human envenoming morbidity and mortality.
Viperidae
All species have well-developed, longer fangs on hinged maxillae, allowing rotation (elevation) when biting, than in any other groups of venomous snakes.
Venom glands are also typically larger than in other groups.
They have heat-sensing pit organs at the front of the head, giving some degree of infrared or heat-sensitive “vision”.
Hydrophidae
These are sea snakes and are closely related to the cobras, with similar fang structure, but live most or all of their lives in an aquatic, usually marine environment.
They are a significant cause of envenoming amongst fishermen in the Indian and Pacific oceans.
Atractaspidae
These are side fanged viper like snakes confined to Africa and the Middle East. They have unusual fang structure and venoms, which contain endothelin-like compounds called sarafotoxins, causing potent smooth muscle contraction.
Snake venom is the poisonous secretion ejected from the poison apparatus (modified parotid gland) of a poisonous snake, during the act of biting.
Snake venoms are usually clear and amber-colored fluid when fresh.
They are poisonous only when injected by a needle or by bite of a snake.
The venom is non-poisonous when taken orally.
Neurotoxic Venom
Common in Elapidae Snakes.
Acts like Curare.
Convulsions may be seen with Cobra venom.
Hemotoxic Venom
Common in Viperidae snakes
Acts by cytolysis of endothelium of blood vessels, lysis of red cells and other tissue cells, and coagulation disorders.
It can lead to:
Severe swelling with oozing of blood and spreading cellulitis at the bite site. Blood from such patients fails to clot even on adding thrombin, because of a very low levels of fibrin.
Necrosis of renal tubules; and
Functional disturbances like convulsions, due to intracerebral hemorrhage.
Myotoxic Venom
Common in hydrophidae or sea snakes.
Produces generalized muscular pain, followed by:
Myoglobinuria within 3 to 5 hours.
Death usually occurs due to respiratory failure.
They have no poison apparatus.
They possess 4 longitudinal rows of teeth in upper jaw and 2 rows in lower jaw.
Tail is not compressed.
Ventral shields are small/moderately large.
Head scales are usually larger and without any special features.
Fangs are short and solid.
These are not nocturnal.
The bite marks show more than two teeth markings
Snakebites are usually accidental. Rarely it can also be homicidal or suicidal.
Venom is inoculated into the body. Snakes like cobra can inject/ emit venom by spitting
Degree of toxicity depends on three factors:
Toxic principle in the venom.
Quantity of venom injected.
Type of fang:
Channeled (viperine) fangs — complete transfer of venom.
Grooved (elapid) fangs — less transfer of venom.
Neurotoxic Venomous Snake Bite
Severe burning at bite site, rapid edema and inflammatory changes followed by oozing of serum.
Found within 15-30 minutes or 2 hours of biting.
Hemotoxic Venomous Snake Bite
Severe pain at bite site, followed by swelling, ecchymosis, cellulitis and severe hemorrhage.
It is due to hemolytic effect on heart and blood vessels resulting in cardiovascular collapse and death.
If the patient survives suppuration, sloughing with infection at the site of bite, hemorrhage from the mucosa of rectum, other natural orifice, etc. and gangrene of the parts involved can occur.
Myotoxic Venomous Snake Bite
Minimal swelling and pain
Myalgia, muscle stiffness, myoglobinuria, renal tubular necrosis.
Allaying of the Anxiety and Fear
Prevention of the Spread of Venom
First Aid
Reassurance of the victim.
Do not tamper with the bite wound, except wipe with a damp cloth to remove the venom lying on the skin surface.
Immobilization of the bitten limb.
Transport the patient to a medical facility immediately.
Identify the snake if possible but not necessary.
Better to take along the dead snake for identification. Be sure it is dead. Severed snakeheads, both fresh and preserved, have inflicted severe and even fatal bites.
Avoid potentially harmful traditional first aid measures.
Do not apply tourniquets, ligatures, or constricting bands unless the snake is a neurotoxic envenomating.
Dangers of Tourniquets, Compression Bandages and Other Occlusive Methods
Ischemia and gangrene.
Damage to superficial peripheral nerves, especially the lateral poplitial nerve at the neck of fibula.
Increased fibrinolytic activity in the occluded limb.
Congestion, swelling, and increased bleeding from the occluded limb.
Shock on releasing a tight tourniquet.
Intensification of local effects of venom in the occluded limb.
Do not use antivenom treatment routinely and indiscriminately because of reasons:
All commercial antivenoms carry a risk of potentially serous serum reaction.
Antivenom is not always necessary; many patients are bitten by nonvenomous snakes, and a large portion of those bitten by venomous snakes are not envenomated.
Antivenoms have a range of specific and para-specific neutralizing activity and are useless for venoms outside that range. Specific antivenoms are not available for treatment of envenomation by some species.
Antivenom is expensive, always in short supply, and has a limited shelf life.
Systematic Envenomation
Hemostatic disturbances; spontaneous systemic bleeding.
Cardiovascular abnormalities: shock, hypotension, abnormal electrocardiogram, arrhythmia, cardiac failure, pulmonary edema.
Neurotoxicity.
Generalized rhabdomyolysis.
Impaired consciousness of any cause.
In patients with definite signs of local envenomation, the following indicate significant systemic envenomation:
Neutrophil leukocytosis
Elevated creatine phosphokinase and aminotransferases,
Hemoconcentration, uremia, hypercreatininemia, oliguria, hypoxemia, acidosis and vomiting.
Severe Local Envenoming
Local swelling involving more than half of the bitten limb, or associated with extensive blistering or bruising, especially in patients bitten by species whose venoms are known to cause local neurosis. Bites on digits carry a high risk of necrosis.
There is no absolute contraindication to antivenom in patients with life-threatening systemic envenomation.
Patients with an atopic history and those who had reactions to equine antiserum on previous occasions have an increased risk of severe reactions.
In case of pretreatment with subcutaneous adrenaline and intravenous antihistamine and corticosteroids may prevent or diminish the reaction.
Rapid desensitization is not recommended.
Local Envenomation
Secondary infection: Prevention with penicillin or erythromycin and booster dose of tetanus toxoid.
Clean wound with antiseptic.
Bullae can be aspirated to dryness with a fine sterile needle.
Nurse limbs in most comfortable position.
Examine the wound frequently for evidence of necrosis.
Polyspecific/Polyvalent Antivenom
Haffkin’s Institute, Mumbai and Central Research Institute Kasauli, Himachal Pradesh, King’s Institute, Chennai, Serum Institute, Pune prepares this. It is available as a lyophilized powder in an ampoule, with potency for nearly 10 years.
It can neutralize the venom of cobra, common krait, Russel’s viper and Echis carinata.
It is effective when given within four hours of biting.
It is to be dissolved in distilled water or normal saline before use.
Use only if the solution prepared is clear, if it is opaque, it is considered as not potent.
Always perform serum sensitivity test (test dose) before giving it.
The skin test procedure
Inject 0.02 to 0.03 ml of the antivenin in 1:10 dilution, intradermally.
If there is a hypersensitivity reaction (urticarial wheal with erythema within 15 minutes) the patient should be desensitized.
The desensitization procedure
Inject 0.1, 0.2 and 0.5 ml of the antivenin in 1:100 dilutions at an interval of 15 minutes.
A 1:10 dilution is given in the same manner, followed by undiluted antivenin. If no severe reaction occurs, the usual dose is given intravenously.
According to another view, skin testing is not necessary, but adrenaline should be injected subcutaneously as premedication with a dose of a systemic corticosteroid.
Spanish Fly, Blister Beetle, Lytta
It is a winged insect, which has a body of: length 2 cm and breadth 0.6 cm and greenish black colour with shiny wings of same color.
The insect as such or the powder of dried body has the toxic (active) principle.
Active principle: Cantharidin.
Fatal dose — 15 to 30 mg of cantharidin 1.5 gm of powdered cantharides.
Toxicity rating — For cantharidin 6.
Treatment — Stomach wash, demulcents, symptomatic.
Mouth, stomach and intestines may show inflammation and vesication. Particles of insect may be found in the stomach contents.
Heart, lungs, kidneys are also found to be inflamed and hemorrhagic.
Used often as an aphrodisiac
Poisoning is reported very rarely (accidental/homicidal)
Used also as stimulant for scalp hair growth (hair oil).
They belong to Myriapoda (under class Arthropods) and are organic animal irritants.
They have a long segmented dark to brownish black colored body with a pairs of legs in each segment.
Usually centipedes can inflict painful bites with erythema, oedema, and local lymphangitis.
Treatment is by washing the bite site with soap and water and administering analgesics.
Scorpion: A poisonous arthropod with a crab like body with eight legs and a segmented tail having a bulbous expansion and a sting in the last segment which has a clear, colorless venom having two components, a hemolytic and a neurotoxic fractions.
Fatality is rare as dose in sting is not lethal.
Hemolytic factors can mimic viperine snakebite. Diagnosis is by locating only one deep punctured wound with red surrounding area, edema, severe burning pain, etc.
Neurotoxic factor can mimic strychnine poisoning. Victim presents with nausea, vomiting, restlessness, fever followed by convulsions, paralysis, coma and death.
Measures to reduce the rate of absorption of the venom by:
Tourniquet above the level of stinging.
Ice packing, incision and suction (first aid).
Wash with solution of ammonia.
Local anesthetics can also be helpful to reduce the pain.
Intravenous administration of calcium gluconate may reduce swelling.
Giving barbiturate can alleviate anxiety.
Atropine may be given to reduce the pulmonary edema (do not use morphine).
Venom of bees, wasps, hornets, ants, etc. is a complex mixture of biomedical compounds ranging from simple amines to complicated proteins or enzymes.
It may be rarely fatal if venom is histamine. It can result in laryngeal edema leading to asphyxia and deat, when not treated immediately.
When there are multiple stings, it can lead to severe systemic reactions, resulting in gastrointestinal disturbances, shock, unconsciousness and death.
Measures to reduce the rate of absorption of venom by:
Tourniquet above the level of stinging or incision and suction.
Adrenaline is also useful.
Apply tincture iodine/antihistaminic (to reduce inflammation).
Adrenocorticotrophic hormone (ACTH) 25 mg in 1000 ml normal saline given as an intravenous drip can help in prevention of severe allergic reactions.
Calcium gluconate given intravenously can reduce edema/ rash.