irritant poison final #poisoning # irritants #

Poisoning

1. Irritant Poisons Dr Muhammad Wasif

2. Irritant poison T hey mainly produce inflammation on the site of contact, especially in the gastrointestinal tract, respiratory tract and the skin.  Corrosives in dilute solutions act as irritants They can cause symptoms of gastroenteritis and also produces a marked depressant action after absorption.

3. Classification

4. COPPER Pure metallic copper is not poisonous but many salts of copper are poisonous. Uses Insecticide Fungicide Algaecide (to kill algae in water) Used in alloys Used as pigments

5. Absorption, Metabolism and Excretion Copper is normal constituent of body and normal content is 150 mg. It is present in two forms – bound with albumin and other form bound with copper enzyme ceruloplsmin. Copper is absorbed through skin, GIT, lungs and mucous membrane It is excreted through bile and traces are found in saliva and milk.

6. Clinical features Acute poisoning Ingestion: Metallic taste Increased salivation Colicky abdominal pain Nausea and vomiting Diarrhea Myalgia Pancreatitis Hemolysis Jaundice Oliguria and renal failure Convulsions Delirium Coma.

7. Chronic poisoning Abdominal pain Greenish line on dental margins of gum ( Clapton’s line ) Vineyard Sprayer’s lung disease : Greenish hair discolouration Wilson’s disease.

8. Management Gastric lavage with potassium ferrocyanide. Ferrocyanide converts copper salts into insoluble cupric ferrocyanide. Chelation – initially with dimercaprol (BAL) 2.5 mg/kg four hourly IM followed by oral penicillamine 2 g/day Symptomatic.

9. Fatal Dose Copper sulphate – 30 gm Copper subacetate – 15 gm Fatal Period 1 to 3 days

10. Autopsy findings Jaundice Greenish-blue froth at mouth Bluish line on gums Greenish or bluish stomach contents and gastric mucosa Hemolysis Kidneys – tubular necrosis, edema of medulla and appearance of eosinophilic cast Muscle atrophy Liver – soft and fatty. Microscopy shows centrilobular necrosis.

11. Medicolegal Importance Suicidal poisoning – common Accidental poisoning may occur in children. Chronic poisoning – industrial hazard. Use to procure criminal abortion. Cattle poison.

12. Arsenic Arsenic is a metalloid is not very toxic, however, arsenic salts are toxic. The arsenic has inorganic and organic compounds

13. Organic compounds of arsenic are: Cacodylic acid Sodium cacodylate Atoxyl Stovarsol Inorganic compounds Arsenic oxide Arsenic sulphide Arsenic chloride

14. Uses Rodenticide Weed killer In alloys Depletory Coloring agent

15. Sources Rocks and soil Hot spring mineral water Drinking water Sea water Vegetable, fruits and grains Sea food Industrial sources

16. Absorption, Excretion and Metabolism Arsenic is absorbed through all routes viz . through skin, inhalation, and GIT mucosa. The inorganic pentavalent forms are absorbed at higher rate than bivalent forms. The absorbed inorganic arsenic undergoes methylation mainly in liver excreted in urine. After absorption, arsenic is redistributed to the liver, lungs, intestinal wall, spleen, and kidneys. It has minimal penetration in blood-brain-barrier

17. Mechanism of Action Arsenic reversibly combines with sulphydrl enzymes. It blocks Krebs cycle and interrupts oxidative phosphorylation causing depletion of ATP and death of cell. It also inhibits transformation of thiamine into acetyl CoA and Succinyl –CoA resulting in thiamine deficiency. It replaces the phosphorus in the bones Arsenic is incorporated into hair, nails and skin. It causes increased permeability of small blood vessels with inflammation and necrosis of intestinal mucosa thus causing manifestation of hemorrhagic gastroenteritis.

18. Clinical Features Acute poisoning Fulminant type: collapse and circulatory failure Gastroenteritis type Metallic taste Garlicky odour Nausea and vomiting Colicky abdominal pain Profuse diarrhea resembling rice water stool of cholera. Circulatory failure Intense thirst Oliguria Uremia Ventricular tachycardia Headache Vertigo Tremors Convulsions

19. Chronic poisoning The features are exhibited in four stages 1. First stage GIT symptoms dominate Malaise, loss of appetite and salivation Colicky abdominal pain Constipation (sometimes diarrhea) ,Vomiting Gums – red Periorbital edema 2. Second stage Cutaneous eruptions Voice – hoarse and husky • Rhinorrhea Rain drop pigmentation Epithelial hyperplasia with keratosis – mostly on sole and palms

20. Nails – become brittle and show Mees’ line . A lopecia Arsenic dust – painless perforation of nasal septum . Liver enlarged (hepatomegaly) and cirrhotic Melanosis of neck, eyelids and nipples Bowen’s disease. 3. Third stage Headache Tingling and numbness of extremities Hyperasthesia of skin Cramps in muscle and tenderness Arthralgia Knee jerk lost Impotence Bone marrow depression with aplstic anemia Hematological abnormalities

21. 4 . Fourth stage Peripheral neuropathy • Neuropathy Wrist drop Foot drop Ataxia Tremors Emaciation Anemia Dysuria Delusion Encephalopathy Death.

22. Management Acute poisoning Gastric lavage Administer activated charcoal Aggressive fluid resuscitation and cardiovascular support remains the mainstay of initial management. Chelation – BAL, Succimer (DMSA), or DMPS. Every 50 mg BAL binds 30 mg of arsenic. Exchange transfusion Continuous venovenous hemodiafiltration. Disadvantage of BAL • Have to give as an intramuscular injection • Unpredictable bioavailability. BAL is Contraindicated in: Patients with glucose-6-phosphate dehydrogenase deficiency, because BAL may cause hemolysis.

23. Autopsy Findings • Rigor mortis last for longer duration Jaundice GIT – mucosa is congested and edematous. The mucosa may be reddened or show hemorrhagic gastroenteritis. The focal hemorrhages give rise to flea bitten appear ance and this appearance is considered as characteristic. Subendocardial hemorrhages in heart with fatty degeneration Liver – fatty degeneration.

24. Medicolegal Importance

25. Mercury Synonyms: Quick silver. Para Features Only metal, which is liquid at room temperature Metallic mercury is having bright silvery luster and is volatile at room temperature. The fumes are odourless and invisible It is 13.5 denser than water Metallic mercury is not poisonous if taken by mouth, as it is not absorbed. However, if vapours are inhaled, may exert toxic effects. Mercury exists in three forms : 1. Elemental mercury – Hgo – vapours are toxic 2. Inorganic mercury 3. Organic mercury. • Inorganic salts are of two types as: Mercuric (bivalent Hg++) – more poisonous Mercurous (monovalent Hg+) – less poisonous.

26. Toxic Compounds Inorganic compounds oxides, chlorides, sulphides and Organic compounds of mercury are more toxic than inorganic compounds and are: 1. Ethyl mercury 2. Methyl mercury 3. Mercurochrome.

27. Uses Barometers, thermometers Ceramics Dry cell batteries Antiseptic and disinfectant Embalming Fingerprint powder Grain preservative Pesticide Paints

28. Absorption, Metabolism and Excretion • Elemental mercury is readily absorbed through alveolar membrane and enters the blood. Mercury salts are absorbed through skin, GIT mucosa, vaginal mucosa and bladder. Organic compounds can pass placental barrier and cause fetal toxicity. In blood mercury is converted into mercuric ions and causes tubular damage during excretion. In CNS, mercury acts on cerebellum, temporal lobe, basal ganglia and corpus callosum. Mercury gets deposited in liver, kidneys, spleen and bone. Mercury is excreted in urine, feces and bile with eneterohepatic circulation.

29. Mechanism of Action Mercury compounds act by inactivating sulphydril enzymes causing interference with cellular metabolism.

30. Fatal Dose Mercuric chloride – 1 gm Mercuric cyanide – 0.6 to 1.3 gm Mercuric nitrate – 4 gm Mercurous chloride (calomel) – 1.5 to 2 gm Fatal period: 3 to 5 days.

31. Clinical features Inhalation: Breathlessness Cough Fever, chills (metal fume fever) Headache Blurring of vision Non-cardiogenic pulmonary edema Convulsions Ataxia Delirium.

32. Management Gastric lavage with egg white or albumin or milk to bind the mercury • Demulcents • Laxative • X-ray follow up • Chelation with BAL, DMPS • Supportive B. Poisoning by organic compounds • Dysarthria • Ataxia • Paraesthesia • Neuropathy • Diminished visual and auditory activity • Mental deterioration • Chorea • Minimata disease

33. Chronic poisoning • Also called as hydrargyrism , mercurialism Excessive salivation (Ptyalism, Sialorrhea) Metallic taste Anorexia Insomnia Headache Gingivitis Halitosis Blue line on gums Lassitude Visual blurring Concentric constriction of visual field ( tunnel vision ) Mercuria lentis – opacities of the anterior capsule of the lens of eye due to deposition of mercury Ataxia – reeling gait Tremors

34. Autopsy Findings Emaciated body Mouth, throat, stomach appear grayish with softening and corrosion with hemorrhagic areas Colitis Liver and heart – fatty degeneration Kidneys – pale, swollen with edema of renal cortex with necrosis of renal tubules. Medicolegal Importance Poisoning occur due to accidental consumption of mercury as Folk medicine/indigenous medicine Toothpaste Industrial exposure Food poisoning – consumption of contaminated fish with methyl mercury Dry cell battery Homicide and suicide – rare

35. lead Properties Lead is heavy, soft, steel-gray metal which gives off toxic fumes when it is melted Lead and its compounds are toxic. Sources Automobile exhaust Battery makingGlass manufacture Plastic manufacture House paints Steel welding and cutting. Uses Paint Glazing of pottery and enamel ware Anti-knock for petrol Lead-acid batteries Projectiles for firearms Glass.

36. Mechanism of Action Combines with sulphhydryl enzymes and inhibit cell metabolism. It also inhibits following enzymes required for heme synthesis and causes anemia. 1. Aminolaevulinic acid dehydratase 2. Aminolaevulinic acid synthetase 3. Coproporphyrinogen oxidase 4. Ferrchelatase It causes hemolysis.

37. Absorption, Metabolism and Excretion Absorbed from all routes viz . skin, GIT mucosa, inhalationAfter absorption, it is stored in bones as phosphate and carbonate. It is also deposited in liver and kidney Lead is a cumulative poison and its rate of excretion is less than absorption. It is excreted in urine and bile. Fatal Dose • Lead acetate – 20 gm • Lead carbonate – 40 gm • Lead tetra-ethyl – 100 mg/kg Fatal period: 2 to 3 days.

38. Clinical Features Acute poisoning • Metallic taste Colicky abdominal pain • Constipation • Ataxia • Apathy • Headache • Insomnia • Paraesthesia • Lethargy • Drowsiness • Acute lead encephalopathy • Convulsions • Coma.

39. Chronic Poisoning • Called as plumbisim , saturnism • Myalgia • Paraesthesia • Fatigue • Irritability • Abdominal discomfort/pain • Arthralgia • Tremor • Headache • Anorexia • Vomiting • Weight loss • Facial pallor – Anemia Basophillic stippling Lead line Colic and constipation Lead palsy

40. Management Chelation: The use of calcium chelate of disodium EDTA act as an ion exchanger in which the Ca++ is exchanged or the heavy metal ion and a soluble and stable chelate of lead is formed. This lead chelate is excreted by kidneys as a ring complex Diazepam for convulsions Thiamine Calcium gluconate.

41. Autopsy Findings • Pale skin • Blue line on gums • Emaciation • Lead line on X-ray GIT – ulceration, hemorrhage with contracted wall • Renal tubular degeneration • Bone marrow hyperplasia • Segmental demyelination of peripheral nerves • Paralyzed muscles are flaccid and show fatty infiltration • blood.19

42. Iodine

43. Uses Used in antiseptic preparations such as Lugol’s iodine, tincture of iodine etc. Therapeutic purpose – radioactive iodine is used in treatment of goiter. Mechanism of Action It is a protoplasmic poison fixing proteins and causing necrosis. Locally, strong iodine solution may cause an intense irritation. Systemic toxicity is due to combination of free iodine with serum bicarbonate causing metabolic acidosis. It is also associated with hyperchloremia, hypernatremia, hyperosmolarity and renal failure. Iodine vapours are irritant to respiratory passage.

44. Absorption, Metabolism and Excretion Elemental iodine is absorbed quickly from gastrointestinal tract. Small doses of iodine are usually changed to iodide and iodate in the bowel. Large doses are absorbed unchanged and reacts with body proteins. They are changed largely to iodide and iodate before being excreted by all glands of the body. Fatal dose • 2 to 4 gm of iodine • 30 to 60 ml of tincture Fatal period: 24 hours.

45. Acute Poisoning 1. Inhalation : Vapors of iodine causes irritation of respiratory tract, rhinorrhea and produces cough, pulmonary edema and glottic edema. 2. Local : Application may cause irritation, inflammation, and necrosis with yellowish-brown staining of skin. 3 . Ingestion: When ingested, iodine act as corrosive with pain extending from mouth to abdomen, increased salivation, metallic taste, vomiting and diarrhea. The vomitus may be dark brown or blue in colour with iodine odour . Iodine may cause nephritis, renal failure with suppressed urine or scanty urine. Urine is red-brown in color and contains albumin. 4 . Iodine induced acute sialadenitis ( iodide mumps ), consisting of diffuse submandibular and parotid gland enlargement. It has been identified as a complication of using iodide in contrast radiography.1,2

46. Chronic Poisoning • Also called as iodism • It causes metallic taste, anorexia, insomnia, lymphadenopathy, and emaciation. • Parotid swelling ( iodine mumps ) • Stomatitis • Conjunctivitis • Rhinorrhea • Skin manifestations in form of erythema, urticaria and acne together referred as “ ioderma ”

47. Management Acute Poisoning • Decontamination • Skin exposure: Wash with copious water or 20 percent alcohol • Eye exposure: copious irrigation with running water • GIT: Gastric lavage can be attempted if no esophageal injury is present or suspected. Gastric lavage can be done with 1. Starch solution or 2. Five percent solution of sodium thiosulfate (thiosulfate converts iodine to iodide) 3. Administer activated charcoal • Sodium bicarbonate for metabolic acidosis • Hemodialysis followed by continuous venovenous hemo diafiltration 3 • Supportive measures.

48. Chronic Poisoning • Stop iodine intake • Increase intake of sodium chloride. Sodium chloride will compete with iodide at the level of renal tubules and thus promotes excretion of iodides.

49. Autopsy Findings • Clothes will have yellow stains • The skin, lips, angle of mouth and mucosa will be stained yellowish brown • Gastric mucosa may be yellowish-brown stained. However, it may appear blue if starch is present in stomach or starch solution is used to treat the patient. • Iodine like odour • Congestion of organs. Medicolegal Importance 1. Accidental poisoning may occur due to therapeutic exposure 2. Iodinated radiologic contrast media or agents are known to produce anaphylactic reactions.

50. Phosphorus There are two verities of phosphorus 1. White or yellow phosphorus 2. Red phosphorus

51. Uses 1. Matches 2. Fire works 3. Military use (incendiary bombs, gun powders etc.) 4. Insecticide and rodenticide 5. Fertilizers. Fatal dose: 60 to 120 mg (roughly 1 mg/kg body weight) Fatal period: 4 to 10 hours. Mechanism of Action • Yellow phosphorus is a protoplasmic poison and affects cellular oxidation. • It is also hepatotoxic and cardiotoxic • It causes fatty infiltration and necrosis of liver and kidney • Locally it produces severe irritation or burn injuries of skin and mucosa.

52. Absorption, Metabolism and Excretion • Phosphorus is absorbed quickly when stomach contains fatty food. • After absorption, it is distributed to all organs where it is retained and metabolized to hypophosphate. The hypophosphate is excreted through urine and small part is excreted unchanged through feces and expired air.

53. A. Acute poisoning Three stages are usually recognized in acute phosphorus poisoning extending over a period of 8 to 10 days. 1. First stage: It is one of acute irritation of GIT with: vomiting, diarrhea and abdominal pain. There is garlicky odour . Vomitus and stool may be luminous in the dark. Fumes may evolve from the stools and called as smoky stool syndrome . burns.

54. 2. Second stage : If patient survives, the acuteness of symptoms may subside and condition appears to improve. 3. Third stage: The symptoms of first stage re-appear with increased severity. Manifestation of hepatic failure in form of tender and enlarged liver, jaundice, pruritis and encephalopathy. There are purpuric hemorrhagic areas and cramps. Convulsions may appear

55. B. Chronic poisoning • Occurs due to long term exposure • Nausea, vomiting, diarrhea, eructation and abdominal discomfort • Wasting and weakness of muscle • Anemia, • Jaundice • Phossy jaw or glass jaw develops. It is osteomyelitis of jawbone (lower jaw) due to chronic phosphorus poisoning. Initially there is toothache in caries tooth with swelling of gums. There is loosening of teeth, sloughing of gums followed by necrosis, sequestration and osteomyelitis of mandible. • The epiphysis of children become compact and in adults, the Haversian canals and marrow spaces are filled with dense bone.

56. Management • Do not give milk or oily or fatty food/drink because it will enhance the absorption of phosphorus. • Gastric lavage with potassium permanganate (1:5000). Potassium permanganate oxidizes phosphorus into less toxic phosphoric acid and phosphate. • Intravenous fluid support • Vitamin K for hypoprothrombinemia • Blood/products for correction of coagulation cascade • Glucose for hypoglycemia • Calcium gluconate for hypocalcemia • Benzodiazepines for convulsions

57. Autopsy Findings • Petechial hemorrhages may be noted over skin • Jaundice • Garlicky odour • Gastric mucosa is yellowish or greenish-white in colour and is softened • Gastric contents emits garlicky odour and luminous in dark • Liver shows necrobiosis. Liver is enlarged, doughy in consistency, uniformly yellow and contains many hemorrhagic areas in parenchyma • Heart, kidneys and voluntary muscle fibers shows fatty degeneration • On microscopy, hepatocellular necrosis and cholestasis are seen.

58. Medicolegal Importance Accidental poisoning – few Suicidal or homicidal poisoning – rare Yellow phosphorus rolled up in wet cloth was employed to set fire to postal letterboxes during the Indian civil disobedience movement in 1932.

59. arbus Botanical name: Abrus precatorius Common name: Rati, gunja, jequirity Features • Abrus is green, slender, climbing vine bearing compound leaves. Flowers are pinkish and seeds are present in seed pots. • Each seed pot contains 3 to 5 seeds. Seeds are egg shaped with 5 mm in diameter and having weight of 105 mg. Seed has an attractive hard glossy outer shell. The seeds are of three types: 1. Scarlet red seeds with a black spot at one end (Fig. 37.1). 2. Black seeds with a white spot at one end (Fig. 37.2). 3. White seeds with a black spot at one end

60. Toxic Part of Plant • Seed • Root • Leaves Toxic Principle • Abrin Present in seed and is toxalbumin • Abrin is similar to viper snake venom

61. Mechanism of Action1, 2, 3 • Abrin is composed of two polypeptide chains (A and B). These chains are connected by a disulfide bond • Chewing or crushing of seed releases abrin. The “B” polypeptide chain (called as heptomer ) binds to the intestinal cell membrane while “A” polypeptide chain (called as effectomer ) enters the cytoplasm. In cytoplasm, “A” polypeptide chain act on 60S ribosomal subunit and prevents binding of elongation factor EF-2 thus inhibiting protein syntheses, thereby causing cell death.

62. Clinical Features 1. Dermal manifestations: When abrin is injected in skin, there will be inflammation, swelling, ecchymoses and necrosis at the site. Similarly there will be faintness, vertigo, vomiting, dyspnoea and convulsion occurs before death. The symptoms resemble those of viper snakebite. 2. Ocular exposure: Causes redness, chemosis, swelling and conjunctivitis. 3. Oral ingestion: Causes pain in abdomen, vomiting, diarrhoea , bleeding per rectum, cardiac arrhythmias, convulsions and CNS depression.

63. Management • Gastric lavage • Supportive measures • Convulsions can be controlled by diazepam/lorazepam • Local exposure should be treated with copious irrigation with plain water

64. Fatal Dose • 1 to 2 crushed seeds • 90 to 120 mg of abrin Fatal period: 3 to 5 days

65. Autopsy Findings • Local-fragments of needle or sui may be found in the skin along with oedema, inflammation, local necrosis and ecchymoses • GIT-shows edematous bowel with hemorrhage 4 Cerebral edema • Liver, spleen, kidneys — congested

66. Medicolegal Importance 1. Accidental poisoning may occur in children while explor ing the seeds. 2. Homicide by sui prepared with abrin (sui is needle or spike made with crushed seed alone or mixed with onion paste. Then the needle is dried under sun. The sui is kept between two fingers and is pushed into skin of other person). 3. Cattle poison. 4. Malingerers use powder of abrus seed to produce con junctivitis. 5. When intact seeds are swallowed or when seeds are boiled or cooked, they are not poisonous

67. Mechanical irritants Powdered glass Clinical Features • Powdered glass, diamond powder, needles, etc. may cause pain in abdomen, nausea and vomiting, may injure tissue and causes bleeding. If bleeding is considerable and acute, death may occur due to hemorrhagic shock. If bleeding is gradual and concealed, e.g. malena may induce anemia, weakness, general debility, etc. • Similarly death may occur if the agents cause perforation of stomach or intestine • Pieces of chopped hairs cause nausea, vomiting and irri tation. GIT mucosa may be inflamed. Fatal dose and fatal period: Uncertain Mechanical Irritants Take calculated risks. That is quite different from being rash - George S Patton Chapter 39 Fig. 39.1:

68. Complication1 • Bowel/esophagus perforation • Mechanical intestinal obstruction • GIT hemorrhage • Perforation peritonitis. Management • Bulky food and then purgatives to pass the irritants in stools • Ice pieces to reduce thirst • Analgesics to relieve pain. Autopsy Findings • Erosions may be noted in mouth, pharynx, esophagus, stomach and intestine • Fragments of glass, stone, hairs, etc. may be found in GIT adhered to mucosa • Mucosa of GIT may be inflamed.

69. Medicolegal Importance 1. Accidental ingestion may occur with jam, jelly or food, etc. 2. Show-men may swallow glass particles while showing the show 3. These agents may be used with an evil intention to cause ill health and death 4. Occasionally used as cattle poisons 5. These agents are considered as “unwholesome drugs” under section 328 of IPC 6. Children having access to these substances may accidentally ingest them or may inhale in respiratory tract causing respiratory obstruction.2