Corrosive Poisons PDF

Chapter 34 Corrosive Poisons It hurts to be on the cutting edge. - Proverb Corro...

Chapter 34 Corrosive Poisons It hurts to be on the cutting edge. - Proverb Corrosive poisons are the substances which are caustic i.e. Converts hemoglobin to hematin capable of burning the tissue when applied. The local injury There is formation of eschar, which has self-limiting inflicted may be of varying degree and severity ranging from effect, and formation of eschar minimizes the further superficial burns to charring. Corrosive substances include damage of tissue. Thus, due to precipitation of proteins acids, alkalis and some metallic salts and non-metallic com- and formation of eschar, the acids do not penetrate tissue pounds. They are mentioned in Table 34.1. much deeper and causes less damage than alkalis. Acids cause more damage to the stomach than that of Inorganic Acids esophagus.1 It is thought that squamous epithelium of esophagus is more resistant to acids but vulnerable for Mechanism of Action alkalis. Columnar epithelium of stomach is susceptible for acids and causes gastric outlet obstruction. The pyloric In concentrated form, inorganic acids acts as corrosive spasm induced by the presence of acid in stomach results and in dilute form, they act as irritant poison. in maximum damage to pylorus and pyloric antrum.2 In These acids act mainly at local site of application with rare cases duodenal obstruction may be seen.3 However, minimal remote or systemic action in rare cases, acids may also produce esophageal injury.4 Inorganic acids are powerful desiccants. When these agents come in contact with body, they extract water Pathophysiology from the tissue and liberate heat. The acid precipitates the protein and causes coagulation necrosis of the tissue Following phases have been identified after ingestion of cor- in contact. They fix, destroy and erode the tissue. rosive agent:5 1. Inflammatory stage: It occurs during the first 4 days. edema and erythema develops first followed by throm- Table 34.1 Showing corrosive substances bosis of vessels and tissue necrosis. Compound Examples 2. Granulation stage: It starts at about day 4 and ends approx- Inorganic acids Sulfuric acid, hydrochloric acid etc imately 7 days after ingestion. Fibroplasia results in the formation of granulation tissue with the laying down of collagen over the denuded areas of mucosal sloughing. Organic acids Acetic acid, carbolic acid etc 3. Perforation: Most often occur between day 7 and 21. Alkali Sodium hydroxide, potassium During this period the tissues are week and the risk of hydroxide etc perforation is high. Metal salts Ferric chloride, zinc chloride, 4. Cicatrization stage: Starts at 3 weeks and may persist for chromate etc years. Dense fibrous tissue formation occurs at variable Non-metal Iodine, potassium permanganate, rates. Overproduction of scar tissue results in stricture compound hydrogen peroxide etc formation and obstruction.  438 Principles of Forensic Medicine and Toxicology Clinical Features B) Delayed 1. Aspiration pneumonia Local application: produces chemical burns. 2. Secondary infection 3. Renal failure Ingestion: 4. Malnutrition Pain in mouth, throat and abdomen Dribbling of saliva Preservation of Viscera Eructation In case of inorganic acid poisoning deaths, viscera should Retching be preserved in rectified spirit. Vomiting Hematemesis Medicolegal Importance Dysphagia Dysarthria 1. Accidental poisoning – common (mistaken for medicine, Dyspnea and dysphonia due to regurgitation or fumes. industrial, etc).8 2. May be thrown over face or body with malicious inten- Management tion (vitriolage). 3. Suicide – rare.8 Dilution of acid by milk or water Demulcent – starch, egg white, milk Supportive measures Sulfuric Acid H2SO4 Contraindication. 1. Gastric lavage Synonyms: Oil of Vitriol 2. Emesis 3. Neutralization with alkali as it may cause exothermic Properties reaction and increases the risk of perforation Heavy, oily, colourless, odourless and non-fuming liquid 4. Carbonated alkali – may react with acid and produces Hygroscopic carbon dioxide gas that may distend the stomach and Carbonizes organic substances. increases risk of perforation. Fatal dose: 5 to 10 ml Fatal period: 12 to 18 hours. Complication of Inorganic Acid Poisoning A) Acute:6, 7 Autopsy Findings 1. Massive gastric hemorrhage Corrosion of chin, angle of mouth, lips, oral mucosa, 2. Bronchopneumonia tongue, throat. 3. Perforation of stomach Corrosion over hands may be noted 4. Perforation peritonitis Teeth chalky white 5. Transient laryngeal edema The corroded area of skin or mucous membrane appear 6. Infection/sepsis brownish or blackish (due to chemical charring of the 7. Renal failure affected tissue) 8. Shock. Perforation of stomach may be seen. B) Delayed (Chronic) 1. Gastric outlet obstruction/pyloric stenosis Nitric Acid Toxicology 2. Malnutrition. Synonyms: Aqua Fortis, Red Spirit of Nitre Cause of Death A) Early Properties B 1. Shock Clear, colourless, fuming liquid 2. Spasm or edema of larynx Pungent odour Section 3. Perforation peritonitis With organic substances, it causes yellowish discoloura- 4. Toxemia tion due to xanthoproteic reaction.  Corrosive Poisons 439 Fatal dose: 10 to 15 ml 5. Citric acid Fatal period: 12 to 24 hours. 6. Picric acid. Autopsy Findings Acetic Acid Corrosion of skin, angle of mouth, lips, mucosa with yellowish discolouration Synonyms: Ethanoic Acid, Ethylic Acid Stomach wall is soft and friable, ulcerated. Perforation is less common. Properties Colourless, volatile liquid with pungent odour Hydrochloric Acid Pure acetic acid is an ice-like solid below 16°C, hence it often described as glacial acetic acid. Above this tem- Synonyms: Muriatic Acid, Spirit of Salts perature, it is colourless liquid. The dilute form of acid is called as vinegar (vinegar is Properties about 4-5% solution).10 Fatal dose: 50 to 100 ml (concentrated) Colorless, odourless, volatile, fuming liquid Fatal period: about 48 hours. May acquire yellowish tinge when exposed to air. Fatal dose: 15 to 20 ml Mechanism of Action Fatal period: 18 to 30 hours. In concentrated form it acts as corrosive Autopsy Findings In dilute form it acts as an irritant Systemic absorption causes hemolysis, hemoglobinuria, The skin or mucous membrane shows corrosion. renal failure, disseminated intravascular coagulation, However, corrosion is less severe. metabolic acidosis and liver dysfunction.11 The skin may be brownish discolored and parchment like Coagulation of the surface of the tongue and the mucosa Autopsy Findings11 of pharynx and esophagus is seen9 Stomach is soft, edematous, congested, and desquamated Massive geographic liver necrosis or may be ulcerated Degeneration and swelling of renal tubular epithelium. Perforations is less common Stomach contents – mixed altered blood with mucus Carbolic Acid Inflammation and edema of respiratory passage. Synonyms: Phenol, Hydroxy-Benzene Vitriolage Properties Vitriolage means throwing of acid on the face or body Colourless, prismatic, needle-like crystals that turns pink of a person with a malicious intention to cause bodily and liquefies when exposed to air (Fig. 34.1) harm or disfigurement or to cause blindness. Has sweetish burning taste and phenol like smell The term is derived from the practice of throwing sul- Concentrated phenol is a dark brown liquid and contains furic acid (oil of vitriol). However, it is broadly used impurities like cresol (Fig. 34.2). to denote injury caused by throwing any corrosive sub- Lysol is 50% solution of cresol in saponified vegetable Toxicology stance such as acid or alkali. oil. However, phenol is 8 times more toxic than Lysol Dettol is chlorinated phenol with turpineol Organic Acid Household phenol (sold as phenyle) contains five percent Examples are: phenol in water. 1. Acetic acid Derivatives of phenol B 1. Cresol Section 2. Carbolic acid 3. Oxalic acid 2. Thymol 4. Formic acid 3. Creosate (coal tar)  440 Principles of Forensic Medicine and Toxicology 4. Menthol 5. Tannic acid 6. Napthol 7. Resorcinol. Uses 1. Antiseptic and disinfectant 2. Manufacture of plastic Absorption, Metabolism and Excretion Phenol is absorbed from skin, gastric mucosa, per rec- tum, per vagina and respiratory tract Phenol is converted into hydroquinone and pyrocatechol and excreted in urine. Traces are excreted by lungs, sali- vary glands, and skin. Fig. 34.2: Carbolic acid in liquid form Fatal dose: 2 gm crystals 25 to 50 ml of household phenol Clinical Features Fatal period: 3 to 4 hours. Local: When applied to skin or mucosa, it causes burning pain, numbness, tingling and anesthesia. It causes corrosion Mechanism of Action12,13 and produce white eschar (scar), which falls off in few days Phenol has local as well as systemic action leaving brown stained area. Locally it acts as corrosive agent and when absorbed, Systemic: it causes CNS depression, metabolic acidosis and renal 1. GIT: Burning pain followed by tingling numbness and failure. anesthesia. Nausea and vomiting. Carbolic acid has great penetrating power and it coagu- 2. RS: Respiration is slow and labored. lates protein. 3. CNS: Headache, giddiness, unconsciousness, convul- Phenols have a powerful antipyretic effect similar to that sions, coma. of salicylates. 4. Oliguria and hepatic failure. Phenols and derivatives of phenols cause methemoglo- 5. Urine: May be colorless but on exposure to air turns binemia. green due to oxidation of phenol metabolites (hydroqui- none and pyrocatechol). It is known as carboluria. 6. The hydroquinone and pyrocatechol may cause pigmen- tation in the cornea and various cartilages, a condition known as oochronosis. Management13 Skin: Wash with undiluted polyethylene glycol. Oxygen/ventilatory support Intravenous fluids and vasopressors to support blood Toxicology pressure Ingestion: Cautious stomach wash with sodium or mag- nesium sulfate solution Lidocaine for ventricular arrhythmias B Benzodiazepines for seizures Section Treat methemoglobinemia – if methemoglobinemia is > 30%, ingest Methylene blue (1-2 mg/kg). Exchange trans- Fig. 34.1: Carbolic acid crystals fusion may be needed if methemoglobinemia is > 70%.  Corrosive Poisons 441 Autopsy Findings Phenol smell Corrosion of skin, at angle of mouth, chin. Corrosions are initially white but turns brown in colour Splashing may be noted Tongue – white and swollen Mucosa of stomach is tough, white or gray, corrugated and arranged in longitudinal folds and looks leathery. Mucous membrane of mouth, throat, lips are sodden whitened or ash gray Urine on exposure to air turns green. Medicolegal Importance 1. Accidental poisoning. 2. Suicidal ingestion. Fig. 34.3: Oxalic acid 3. Homicide – not possible. Oxalic Acid 5. Cleaning brass and copper articles Fatal dose: 15 to 20 gm Synonyms: Salts of Sorrel, Acid of Sugar Fatal period: 1 to 2 hours Properties (Fig. 34.3) Mechanism of Action Colourless, transparent, odourless, prismatic crystals Local: It acts as corrosive when used in concentrated resembling the crystals of magnesium sulphate and zinc form and act as irritants when used in dilute form sulphate (differences are mentioned in Table 34.2). Systemic: After absorption, oxalic acid combines with It has sour and slightly bitter acidic taste calcium ion and causes hypocalcemia. It also causes It is present in rhubarb leaves, beets and many other tubular necrosis and renal failure. vegetables. Potassium oxalate, sodium oxalate and ammonium Clinical Features oxalate are toxic salts of oxalic acid. Local: Corrosion of mucosa with underlying congestion. The corroded area is referred as “scalded” in appearance. Uses Systemic 1. Bleaching and cleansing agent Vomiting and diarrhea 2. Ink remover Hypocalcemia (tetany) 3. Rust remover Muscle irritability, tenderness, cramps 4. Metal polishing Convulsions Table 34.2 Showing difference between oxalic acid, magnesium sulphate and zinc sulphate Toxicology Features Oxalic acid Magnesium sulphate Zinc sulphate Taste Sour and acid Bitter Metallic Reaction Strongly acid Neutral Slightly acid Heat Sublimes Fixed Fixed B Sodium carbonate Effervescence and no No effervescence and white No effervescence and white Section precipitate precipitate precipitate Stains (ink) Disappears No action No action  442 Principles of Forensic Medicine and Toxicology Accoucher’s hand due to carpopedal spasm Table 34.3 Showing corrosive alkalis Chavostek’s sign positive. When tapping is done over Alkali Common name Uses facial nerve area, there is spasm of facial muscles. Metabolic acidosis Ammonium Ammonia, Fertilizer, hydroxide Hartshorn refrigerant, pant Renal failure remover, oil Uremia. remover Ammonium Sal volatile Top job Management carbonate Local exposure: Wash the affected skin with copious Sodium Washing soda Household carbonate cleaning agent, water detergent Gastric lavage with calcium gluconate or calcium lactate Calcium gluconate intravenously Potassium Pearl ash, salt Household Symptomatic. carbonate of tartar cleaning agent, detergent Autopsy Findings Sodium Caustic soda Drain cleaner Scalded mucosa of GIT hydroxide Mucous membrane of mouth, tongue, pharynx, esopha- Potassium Caustic potash Drain cleaner gus may be bleached and has scalded appearance hydroxide Kidneys show edema, congestion with oxalate crystals Calcium Slaked lime Paint, industrial in renal tubules with necrosis of proximal convoluted hydroxide tubule. Medicolegal Importance Production of ulcers are more common 1. Accidental poisoning – common Esophagus is more commonly affected than stomach 2. Suicidal ingestion – rare resulting in stricture formation or perforation. 3. Homicide – not possible. Type of material ingested may result in varying degree and location of injury, details are mentioned in Table 34.4. Corrosive Alkalis Fatal Dose Properties (Figs 34.4 and 34.5) Sodium carbonate – 30 gm Common corrosive alkalis are given in Table 34.3 Potassium carbonate – 15 gm Ammonia is a colourless gas with pungent odour. It con- Sodium hydroxide – 5 gm denses to a liquid at –33.4°C. The chemical formula is Potassium hydroxide – 5 gm NH3. Ammonia – 30 ml Ammonium hydroxide is a liquid containing about Fatal period: 24 hours. 30 percent ammonia Other corrosive alkalis occur as white powder or colour- Clinical Features less solution. Local: Application causes chemical burns of the skin with Toxicology Mechanism of Action skin showing grayish, soapy, necrotic areas without charring. In concentrated form, alkali acts as corrosive and in Inhalation dilute form they act as irritant B Strong alkali produces liquefaction necrosis and causes Irritation of eyes and watering Cough, breathlessness saponification of fats and dissolves proteins thus caus- Section ing deep penetration in the tissue resulting in extensive Respiratory tract – edematous and inflamed tissue destruction.5 Laryngeal edema or spasm may occur causing death.  Corrosive Poisons 443 Fig. 34.4: Washing soda Fig. 34.5: Potassium carbonate Ingestion Ingestion Caustic taste and burning pain Milk or water may be given to dilute the alkali Abdominal pain Contraindications: Vomiting and vomitus is alkaline in reaction 1. Gastric lavage Diarrhea and tenesmus 2. Emesis The lips, mucous membrane of oral cavity, and the 3. Neutralization with acid as it may cause exothermic tongue appears soft, swollen, bleached and bogy. reaction and increases the risk of perforation. The mucosa of GIT is swollen, soft, grayish or bleached Assess the injury of esophagus by esophagoscopy and sloughs easily Symptomatic. Esophagus is affected commonly than stomach and results in dysphagia, drooling and hematemesis. Autopsy Findings Alkali induced injury of esophagus is classified by Hawkins et al.14 It is determined at esophagoscopy. Ammonia like odour may be perceived Alkali induced injury of esophagus is mentioned in Mucosa of mouth, tongue, esophagus and stomach is Table 34.5. bleached and sodden with areas of necrosis Esophagus may show esophagitis or perforation Pulmonary edema Management Inhalation – laryngeal edema Local: Wash the affected area with copious water. Skin application – chemical burns Table 34.4 Showing type alkali ingested and lesion produced Toxicology Type of alkali Ingestion Location of injury Degree of injury preparation Powder/solid/ Not swallowed, Mouth, pharynx, upper Injury localized, less severe, granules spit out esophagus penetrating B Liquid Swallowed Distal esophagus, stomach, Injury generalized, deep, Section duodenum circumferential, more severe  444 Principles of Forensic Medicine and Toxicology 4. Gaudreault P, Parent M, McGuigan MA, Chicoine L, Lovejoy Table 34.5 Displays esophageal injury FH Jr. Predictability of esophageal injury from signs and symp- (on esophagoscopy) toms: A study of caustic ingestion in 378 children. Pediatrics Grade of Features 1983; 71: 767-70. esophageal 5. Homan CS. Acids and alkalis. In: Viccellio P (ed) Handbook injury of Medical Toxicology, 1st edn. 1993. Little, Brown and 0 No visible lesion Company, Boston. 249-63. 1 Burns limited to mucosa 6. Eamir O, Hod G, Lernau OZ, Mogle P, Nissan J. Corrosive characterized by the presence of injury to the stomach due to acid ingestion. Am Surg 1985; edema and/or erythema 51: 170-2. 7. Dilawari JB, Singh S, Rao PN, Anand BS. Corrosive acid 2 Burns penetrating beyond the ingestion in man – a clinical and endoscopic study. Gut 1984; mucosa characterized by presence of 25: 183-7. ulceration and/or whitish membrane 8. Arevalo –silva C, Eliashar R, Woblqeternter J, Elidan J, Gross M. Ingestion of caustic substances: a 15 year experience. 3 Presence of perforation Laryngoscope 2006; 116: 1422-6. 9. Yoshitome K, Miyaishi S, Ishikawa T, Yamamoto Y, Ishizu H. Distribution of orally ingested hydrochloric acid in Medicolegal Importance thoracoabdominal cavity after death. J Anal Toxicol 2006; 1. Accidental poisoning – common (mistaken for medicine, 30: 278-80. 10. Rentoul E, Smith H. Toxic materials. In: Glaister’s Medical industrial etc.) Jurisprudence and Toxicology, 13th edn. 1973. Churchill 2. May be thrown over face or body with malicious inten- Livingstone, Edinburgh. 517-709. tion (vitriolage) 11. Yashito K, Kazui S, Keiichi I, Takashi O. Massive non- 3. Suicide – rare. inflammatory periportal liver necrosis following concen- trated acetic acid ingestion. Arch Pathol Lab Med 2000; 124: 127-9. References 12. Lo Dico C, Caplan YH, Levine B, Smyth DE, Smialek JE. 1. Mills SW, Okoye MI. Sulfuric acid poisoning. Am J Forensic Phenol: tissue distribution in a fatality. J Forensic Sci 1989; Med Pathol 1987; 8: 252-5. 34: 1013-5. 2. Sharma J, Debnath PR, Agrawal LD, Gupta V. Gastric outlet 13. Barclay PJ. Phenols. In: Viccellio P (ed) Handbook of Medical obstruction without esophageal involvement: A late sequlae of Toxicology, 1st edn. 1993. Little, Brown and Company, acid ingestion in children. J Indian Assoc Pediatr Surg 2007; Boston. 264-70. 12: 47-9. 14. Hawkins DB, Demeter MJ, Barnett TE. Caustic inges- 3. Tamisanis AM, Di Noto C, Di Rovasenda E. A rare complication tion: Controversies in management: A review of 264 cases. due to sulfuric acid ingestion. Eur J Pediatr Surg 1992; 2: 162-4. Laryngoscope 1980; 90: 98-109. Toxicology B Section  Chapter 35 Inorganic Irritants: Non-metallic Poisons All people have the right to stupidity but some abuse the privilege. - Anonymous Examples are: Uses 1. Phosphorus Used in antiseptic preparations such as Lugol’s iodine, 2. Iodine tincture of iodine etc. 3. Chlorine Therapeutic purpose – radioactive iodine is used in treat- 4. Bromine ment of goiter. 5. Fluorine Mechanism of Action Iodine It is a protoplasmic poison fixing proteins and causing Features necrosis. Locally, strong iodine solution may cause an intense Bluish-black, soft and scaly crystals with metallic luster irritation. (Fig. 35.1) Systemic toxicity is due to combination of free iodine It has unpleasant taste with serum bicarbonate causing metabolic acidosis. It It gives off violet colored vapour with iodine like odour is also associated with hyperchloremia, hypernatremia, hyperosmolarity and renal failure. Iodine vapours are irritant to respiratory passage. Absorption, Metabolism and Excretion Elemental iodine is absorbed quickly from gastrointes- tinal 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. Clinical Features Fig. 35.1: Iodine Crystals Iodine may cause acute or chronic poisoning.  446 Principles of Forensic Medicine and Toxicology Acute Poisoning Chronic Poisoning 1. Inhalation: Vapors of iodine causes irritation of respi- Stop iodine intake ratory tract, rhinorrhea and produces cough, pulmonary Increase intake of sodium chloride. Sodium chloride will edema and glottic edema. compete with iodide at the level of renal tubules and thus 2. Local: Application may cause irritation, inflammation, promotes excretion of iodides. and necrosis with yellowish-brown staining of skin. 3. Ingestion: When ingested, iodine act as corrosive with Autopsy Findings pain extending from mouth to abdomen, increased saliva- Clothes will have yellow stains tion, metallic taste, vomiting and diarrhea. The vomitus The skin, lips, angle of mouth and mucosa will be stained may be dark brown or blue in colour with iodine odour. yellowish brown Iodine may cause nephritis, renal failure with suppressed Gastric mucosa may be yellowish-brown stained. urine or scanty urine. Urine is red-brown in color and However, it may appear blue if starch is present in stom- contains albumin. ach or starch solution is used to treat the patient. 4. Iodine induced acute sialadenitis (iodide mumps), Iodine like odour consisting of diffuse submandibular and parotid gland Congestion of organs. enlargement. It has been identified as a complication of using iodide in contrast radiography.1,2 Medicolegal Importance Chronic Poisoning 1. Accidental poisoning may occur due to therapeutic expo- sure Also called as iodism 2. Iodinated radiologic contrast media or agents are known It causes metallic taste, anorexia, insomnia, lymphaden- to produce anaphylactic reactions. opathy, and emaciation. Parotid swelling (iodine mumps) Stomatitis Phosphorus Conjunctivitis There are two verities of phosphorus Rhinorrhea 1. White or yellow phosphorus Skin manifestations in form of erythema, urticaria and 2. Red phosphorus acne together referred as “ioderma”. Differences are mentioned in Table 35.1. Management Table 35.1: Showing difference between yellow Acute Poisoning and red phosphorus Decontamination Features Yellow Red phosphorus Skin exposure: Wash with copious water or 20 percent phosphorus alcohol Colour and White, waxy, Violet-red, Eye exposure: copious irrigation with running water appearance crystalline amorphous mass GIT: Gastric lavage can be attempted if no esopha- translucent soft geal injury is present or suspected. Gastric lavage cylinders. On exposure to air can be done with becomes yellow 1. Starch solution or Toxicology Taste and Garlicky odour Odourless and 2. Five percent solution of sodium thiosulfate odour and taste tasteless (thiosulfate converts iodine to iodide) Luminosity in Luminous Not luminous 3. Administer activated charcoal dark Sodium bicarbonate for metabolic acidosis B Hemodialysis followed by continuous venovenous hemo- Exposure to Phosphorescence Not air Phosphorescence diafiltration3 Section Toxicity Highly toxic Non-toxic Supportive measures.  Inorganic Irritants: Non-metallic Poisons 447 Uses B. Chronic poisoning Occurs due to long term exposure 1. Matches Nausea, vomiting, diarrhea, eructation and abdominal 2. Fire works discomfort 3. Military use (incendiary bombs, gun powders etc.) Wasting and weakness of muscle 4. Insecticide and rodenticide Anemia, 5. Fertilizers. Jaundice Fatal dose: 60 to 120 mg (roughly 1 mg/kg body weight) Phossy jaw or glass jaw develops. It is osteomyelitis Fatal period: 4 to 10 hours. of jawbone (lower jaw) due to chronic phosphorus poisoning. Initially there is toothache in caries tooth Mechanism of Action with swelling of gums. There is loosening of teeth, Yellow phosphorus is a protoplasmic poison and affects sloughing of gums followed by necrosis, sequestra- cellular oxidation. tion and osteomyelitis of mandible. It is also hepatotoxic and cardiotoxic The epiphysis of children become compact and in It causes fatty infiltration and necrosis of liver and kidney adults, the Haversian canals and marrow spaces are Locally it produces severe irritation or burn injuries of filled with dense bone. skin and mucosa. Management Absorption, Metabolism and Excretion Do not give milk or oily or fatty food/drink because it Phosphorus is absorbed quickly when stomach contains will enhance the absorption of phosphorus. fatty food. Gastric lavage with potassium permanganate (1:5000). After absorption, it is distributed to all organs where it Potassium permanganate oxidizes phosphorus into less is retained and metabolized to hypophosphate. The hypo- toxic phosphoric acid and phosphate. phosphate is excreted through urine and small part is Intravenous fluid support excreted unchanged through feces and expired air. Vitamin K for hypoprothrombinemia Blood/products for correction of coagulation cascade Clinical Features Glucose for hypoglycemia Calcium gluconate for hypocalcemia A. Acute poisoning4 Benzodiazepines for convulsions. Three stages are usually recognized in acute phosphorus poi- soning extending over a period of 8 to 10 days. Autopsy Findings6 1. First stage: It is one of acute irritation of GIT with vomiting, diarrhea and abdominal pain. There is Petechial hemorrhages may be noted over skin garlicky odour. Vomitus and stool may be luminous Jaundice in the dark. Fumes may evolve from the stools and Garlicky odour called as smoky stool syndrome. Gastric mucosa is yellowish or greenish-white in colour 2. Second stage: If patient survives, the acuteness of symp- and is softened toms may subside and condition appears to improve. Gastric contents emits garlicky odour and luminous in dark 3. Third stage: The symptoms of first stage re-appear Liver shows necrobiosis. Liver is enlarged, doughy in with increased severity. Manifestation of hepatic fail- consistency, uniformly yellow and contains many hemor- ure in form of tender and enlarged liver, jaundice, rhagic areas in parenchyma Toxicology pruritis and encephalopathy. There are purpuric hem- Heart, kidneys and voluntary muscle fibers shows fatty orrhagic areas and cramps. Convulsions may appear degeneration at later stage. Renal failure develops with oliguria, On microscopy, hepatocellular necrosis and cholestasis are seen. hematuria, and albuminuria. Decrease in granulocyte count noted5 B Bone marrow depression. Biopsy reveals decreased Medicolegal Importance Section cellular mass with degenerative changes5 Accidental poisoning – few Local application causes corrosive burns. Suicidal or homicidal poisoning – rare  448 Principles of Forensic Medicine and Toxicology Yellow phosphorus rolled up in wet cloth was employed continuous venovenous hemodiafiltration. Am J Kidney Dis to set fire to postal letterboxes during the Indian civil 2003; 41: 702-8. disobedience movement7 in 1932. 4. McCarron MM, Gaddis GP, Trotter AT. Acute yellow phos- phorus poisoning from pesticide pastes. Clin Toxicol 1981; 18: 693-711. References 5. Tafur AJ, Zapatier JA, Idrovo LA, Oliveros JW, Garces JC. 1. Nakadar AS, Harris-Jones JN. Sialadenitis after intravenous Bone marrow toxicity after yellow phosphorus ingestion. pyelography. BMJ 1971; 3: 351-2. Emerg Med J 2004; 21: 259-60. 2. Kalaria VG, Porsche R, Ong LS. Iodide mumps: acute sialad- 6. Fernandez OU, Conizares LL. Acute hepatotoxicity from enitis after contrast administration for angiography. Circulation ingestion of yellow phosphorus containing fire works. J Clin 2001; 104: 2384. Gastroenterol 1995; 21: 139-42. 3. Kanakiriya S, De Chazal I, Nath KA, Haugen EN, Albright 7. Pande TK, Pandey S. White phosphorus poisoning – explosive RC, Juncos LA. Iodine toxicity treated with Hemodialysis and encounter. J Assoc Phys Ind 2004; 52: 249-50. Toxicology B Section  Chapter 36 Inorganic Irritants: Metallic Poisons The only medicine for suffering, crime and all other woes of mankind, is wisdom. - Thomas Huxley Even at present times, many metals and their salts causes Table 36.1: Showing salts of copper morbidity and mortality. This chapter deals with poisoning Chemical name Common name Features of arsenic, mercury, lead, copper, zinc, iron, thallium and antimony compounds. Copper sulphate Blue vitriol, Crystalline blue (See Fig. 36.2) Nila tutia (Hindi) powder Copper Copper Verdigris Crystalline subacetate Zangal green powder Pure metallic copper is not poisonous but many salts of cop- Copper Paris green Crystalline per are poisonous (Fig. 36.1). The copper salts are presented acetoarsenite Emerald green green powder in Table 36.1. Copper arsenite Scheele’s green Crystalline Uses green powder Copper Mountain green Crystalline 1. Insecticide carbonate green powder 2. Fungicide 3. Algaecide (to kill algae in water) 4. Used in alloys 5. Used as pigments. Absorption, Metabolism and Excretion Copper is normal constituent of body and normal con- tent is 150 mg. It is present in two forms – bound with albumin and other form bound with copper enzyme ceru- loplsmin. Copper is absorbed through skin, GIT, lungs and mucous membrane It is excreted through bile and traces are found in saliva and milk. Clinical Features Acute Poisoning Ingestion: Fig. 36.1: Copper metal Metallic taste  450 Principles of Forensic Medicine and Toxicology Management Gastric lavage with potassium ferrocyanide. Ferrocyanide converts copper salts into insoluble cupric ferrocyanide. Chelation – initially with dimercaprol 2.5 mg/kg four hourly IM followed by oral penicillamine 2 g/day Symptomatic. Fatal Dose Copper sulphate – 30 gm Copper subacetate – 15 gm Fatal period: 1 to 3 days Autopsy Findings Jaundice Fig. 36.2: Copper sulphate Greenish-blue froth at mouth Bluish line on gums Greenish or bluish stomach contents and gastric mucosa Increased salivation (Fig. 36.3) Colicky abdominal pain Hemolysis Nausea and vomiting. Vomitus is bluish or greenish in Kidneys – tubular necrosis, edema of medulla and color appearance of eosinophilic cast2 Diarrhea Muscle atrophy Myalgia Liver – soft and fatty. Microscopy shows centrilobular Pancreatitis necrosis.2 Methemoglobinemia Hemolysis Medicolegal Importance Jaundice 1. Suicidal poisoning – common Oliguria and renal failure Convulsions Delirium Coma. Inhalation of Copper Fumes or Dust Causes Respiratory tract irritation Cough Conjunctivitis Metal fume fever. Chronic Poisoning Toxicology Abdominal pain Greenish line on dental margins of gum (Clapton’s line) 1 Vineyard Sprayer’s lung disease: Copper sulphate is used as an insecticide spray in vineyards. During spray- B ing, chronic inhalation of copper sulphate causes this Section disease. Greenish hair discolouration Fig. 36.3: Gastric mucosa in copper sulphate Wilson’s disease. poisoning  Inorganic Irritants: Metallic Poisons 451 2. Accidental poisoning may occur in children. Convulsions 3. Chronic poisoning – industrial hazard. Retrobulbar neuritis 4. Use to procure criminal abortion. Ophthalmoplegia 5. Cattle poison. Peripheral neuropathy. Thallium Chronic Poisoning Alopecia - falling of hairs from head, eyebrows and Properties axilla are common Thallium is soft and pliable metal Skin rash Have tin-white colour but tarnishes the surface on expo- Acneform eruptions sure to air due to formation of black thallous oxide Dystrophy of nails Thallium sulfate is odourless and tasteless. Ascending sensorimotor neuropathy Ataxia Toxic Compounds of Thallium Optic neuropathy Encephalopathy 1. Thallium sulfate Ptosis 2. Thallium acetate Nystagmus 3. Thallium iodide Combination of alopecia and skin rash, painful peripheral 4. Thallium nitrate neuropathy and mental confusion with lethargy is called 5. Thallium carbonate. as thallium triad.1 Uses Management5 1. Dye industry Gastric lavage with ferric ferrocyanide (Prussian blue). 2. Optical glass Prussian blue binds thallium in the intestine and enhances 3. Imitation jewelry its fecal excretion. 4. Rodenticide Hemodialysis 5. Depilatory agent Forced diuresis 6. Fire works. Supportive measures. Mechanism3 Autopsy Findings Exact mechanism is unclear but postulated that thallium There may be alopecia results in ligand formation with protein sulphydryl group Stomatitis of enzymes and inhibits cellular respiration. Fatty degeneration of liver and heart It disrupts calcium homeostasis Tubular necrosis Interaction with riboflavin and riboflavin based cofactors. Pulmonary edema Cerebral edema Clinical Features Fatal dose: 12 mg/kg body weight6 Fatal period: 24 to 30 hours Acute Poisoning4 Medicolegal Importance Toxicology Pain in abdomen Features of gastroenteritis 1. Popular as ideal homicidal agent. Hematemesis 2. Also consumed as suicidal agent. Hematochezia Headache Confusion Arsenic B Section Disorientation Arsenic is a metalloid and per se is not very toxic, however, Paraesthesia arsenic salts are toxic.7 The arsenic has inorganic and organic Hallucinations compounds. Inorganic compounds are mentioned in Table 36.2.  452 Principles of Forensic Medicine and Toxicology Table 36.2: Showing inorganic compounds of arsenic Compound Common name Properties Arsenious oxide Sankhya White crystalline (Arsenic Somakhar powder trioxide) White arsenic Arsenic Manseel Red powder disulphide Red arsenic Arsenic Hartal Yellow powder trisulphide Yellow arsenic (Fig. 36.4) Orpiment Sodium - White or grayish arsenates powder Potassium - arsenates Arsenic acid Arsenic White crystalline pentoxide powder Fig. 36.4: Arsenic trisulphide (Courtesy: Dr Vaibhav Arsenic Sonar Lecturer, Forensic Medicine, GMS, Miraj) anhydride Arsenic - Colourless fuming Sources trichloride liquid Arsenic triodide Arsenious Orange colour 1. Rocks and soil iodide crystals (Fig. 36.5) 2. Hot spring mineral water Arsine Arseniuretted Colourless and hydrogen inflammable gas, 3. Drinking water Arsenic Garlicky odour 4. Sea water hydride 5. Vegetable, fruits and grains Sodium arsenite - White powder 6. Sea food Potassium - White powder 7. Industrial sources arsenite Copper arsenite Scheele’s Greenish crystalline Absorption, Excretion and Metabolism (Fig. 36.6) green powder Copper Paris green Greenish crystalline Arsenic is absorbed through all routes viz. through skin, acetoarsenite powder inhalation, and GIT mucosa. However, cutaneous absorp- tion is low except in cases of damaged skin. The inor- ganic pentavalent forms are absorbed at higher rate than Organic compounds of arsenic are: bivalent forms.8 1. Cacodylic acid The absorbed inorganic arsenic undergoes methylation 2. Sodium cacodylate mainly in liver to monomethylarsonic acid and dimethy- 3. Atoxyl larsinic acid and excreted in urine.9 Toxicology 4. Stovarsol After absorption, arsenic is redistributed to the liver, lungs, intestinal wall, spleen, and kidneys. It has mini- Uses mal penetration in blood-brain-barrier. 1. Rodenticide B 2. Weed killer Mechanism of Action 3. In alloys Section Arsenic reversibly combines with sulphydrl enzymes. It 4. Depletory blocks Krebs cycle and interrupts oxidative phosphoryla- 5. Coloring agent tion causing depletion of ATP and death of cell.  Inorganic Irritants: Metallic Poisons 453 Fig. 36.5: Arsenic triodide Fig. 36.6: Copper arsenite 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. Table 36.3: Showing difference between arsenic poisoning and cholera Clinical Features Features Arsenic poisoning Cholera Pain in throat Before vomiting After vomiting Acute poisoning Conjunctiva Inflamed Not inflamed A patient with acute arsenic consumption may present in Vomitus Contains mucus, It is watery or 1. Fulminant type: collapse and circulatory failure bile and streaks of whey like blood 2. Gastroenteritis type Purging Follows vomiting Usually precedes 3. Narcotic form vomiting Metallic taste Garlicky odour Stools Rice watery in Rice water early stages, later liquid, Nausea and vomiting becomes bloody, involuntary jet Colicky abdominal pain discharged with Profuse diarrhea resembling rice water stool of chol- straining and era. Difference between arsenic poisoning and chol- tenesmus era is summarized in Table 36.3 Laboratory 1. Radio-opaque Vibrio cholera Circulatory failure examination shadow on X-ray detected on Toxicology Intense thirst of abdomen in microscopic Oliguria arsenic trioxide examination Uremia poisoning Ventricular tachycardia 2. Coproporphyrin Headache in urine B Vertigo 3. Arsenic Section detected in Tremors chemical analysis Convulsions  454 Principles of Forensic Medicine and Toxicology Formication Nails – become brittle and show Mees’ line. Mees’ Delirium line are white transverse lines over nails Tenderness in muscle Hairs – dry and may fall off; patchy or diffuse alopecia Paralysis Arsenic dust – flexor eczema, painless perforation Hyperpyrexia of nasal septum. QT prolongation, tachyarrhythmia including torsades Liver enlarged (hepatomegaly) and cirrhotic de pointes may develop within first 24 hours after Melanosis of neck, eyelids and nipples ingestion.10 Bowen’s disease. 3. Third stage Subacute Poisoning Headache Tingling and numbness of extremities This results when arsenic is given in small doses at frequent Hyperasthesia of skin intervals. The features are: Cramps in muscle and tenderness Dyspepsia Arthralgia Cough Knee jerk lost Tingling in throat followed by vomiting Impotence Diarrhea with tenesmus and abdominal pain Bone marrow depression with aplstic anemia Cramps in muscle Interference with folic acid metabolism with defi- Restlessness. ciency Hematological abnormalities (Table 36.5). Chronic Poisoning 4. Fourth stage The features are exhibited in four stages6 Peripheral neuropathy 1. First stage Neuropathy is hallmark of arsenic poisoning. It is GIT symptoms dominate usually symmetrical sensorimotor polyneuropathy Malaise resembling Guillain-Barre syndrome Loss of appetite Weakness of muscle and atrophy – extensor muscles Salivation more commonly affected resulting in wrist drop and Colicky abdominal pain foot drop Constipation (sometimes diarrhea) Ataxia Vomiting Tremors Gums – red and soft Emaciation Circumscribed edema of ankle Anemia Periorbital edema Dysuria 2. Second stage Delusion Cutaneous eruptions Encephalopathy Voice – hoarse and husky Death. Rhinorrhea Skin – generalized or localized fine mottled pigmenta- tion of skin (Rain drop pigmentation, see Table 36.4) Table 36.5: Showing hematological abnormalities Epithelial hyperplasia with keratosis – mostly on sole in arsenic poisoning and palms Hematological abnormalities Toxicology Leukopenia Table 36.4: Displaying differential diagnosis of Thrombocytopenia raindrop pigmentation of arsenic Mild eosinophilia B Rain drop pigmentation may be mistaken for Karyorrhexis – manifested by bizarre nuclear forms 1. Addison’s disease Megaloblastic anemia Section 2. Secondary syphilis Basophilic stippling  Inorganic Irritants: Metallic Poisons 455 Differential Diagnosis 4. Muscle 5. Skin 1. Acute poisoning resembles cholera 6. Nails. 2. Alcoholic neuritis 3. Guillain-Barre syndrome. Medicolegal Importance 10,11 Management 1. Homicidal poison – in past it is considered as ideal homi- cidal poison. The arsenic is administered in chronic way Acute poisoning to a person and the clinical features is manifested for Gastric lavage natural disease Administer activated charcoal 2. Used as cattle poison13 Aggressive fluid resuscitation and cardiovascular support 3. Accidental poisoning: due to remains the mainstay of initial management. Used in indigenous medicine – chronic poisoning Chelation – BAL, Succimer (DMSA), or DMPS. Every Well water (tube well water) 7 50 mg BAL binds 30 mg of arsenic. Adulteration with alcohol drink Exchange transfusion Mistaken for medicine Continuous venovenous hemodiafiltration. Arsenophagist – some people take arsenic daily as an aphrodisiac and are habituated for arsenic. Disadvantage of BAL Have to give as an intramuscular injection Mercury Unpredictable bioavailability. Synonyms: Quick silver. Para BAL is Contraindicated in: Features Patients with glucose-6-phosphate dehydrogenase deficiency because BAL may cause hemolysis. Only metal, which is liquid at room temperature Metallic mercury is having bright silvery luster and is Chemical Test for Arsenic Detection volatile at room temperature. The fumes are odourless and invisible (Fig. 36.7). 1. Reinsch’s test It is 13.5 denser than water 2. Marsh’s test Metallic mercury is not poisonous if taken by mouth, as 3. Gutzeit test. it is not absorbed. However, if vapours are inhaled, may Fatal dose: Arsenious oxide – 180 mg exert toxic effects. Fatal period: 12 to 48 hours. Mercury exists in three forms:14 1. Elemental mercury – Hgo – vapours are toxic Autopsy Findings 2. Inorganic mercury Rigor mortis last for longer duration 3. Organic mercury. Jaundice Inorganic salts are of two types as: GIT – mucosa is congested and edematous. The mucosa 4. Mercuric (bivalent Hg++) – more poisonous may be reddened or show hemorrhagic gastroenteritis. 5. Mercurous (monovalent Hg+) – less poisonous. The focal hemorrhages give rise to flea bitten appear- ance and this appearance is considered as characteristic. Toxic Compounds The mucosal appearance is described as red velvet like12 Toxicology Subendocardial hemorrhages in heart with fatty degen- Inorganic compounds are mentioned in Table 36.6. eration Liver – fatty degeneration. Organic Compounds B Organic compounds of mercury are more toxic than inor- Preserved for Chemical Analysis ganic compounds and are: Section 1. Routine viscera 1. Ethyl mercury 2. Long bone – femur 2. Methyl mercury 3. Scalp hairs 3. Mercurochrome.  456 Principles of Forensic Medicine and Toxicology Uses 1. Barometers, thermometers 2. Ceramics 3. Dry cell batteries 4. Felt hat 5. Antiseptic and disinfectant 6. Embalming 7. Fingerprint powder 8. Grain preservative 9. Pesticide 10. Paints Absorption, Metabolism and Excretion Elemental mercury is readily absorbed through alveo- Fig. 36.7: Mercury (Courtesy: Dr PG Dixit, Prof and lar membrane and enters the blood. Mercury slats are Head, Forensic Medicine, GMCH, Nagpur) 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, mer- Table 36.6: Displaying inorganic compounds of cury acts on cerebellum, temporal lobe, basal ganglia mercury and corpus callosum.1 Mercury gets deposited in liver, Compound Common name Features kidneys, spleen and bone. Mercuric oxide Sipichand Brick-red crystalline Mercury is excreted in urine, feces and bile with enetero- powder (Fig. 36.8) hepatic circulation.14 Mercuric Perchloride of Heavy colourless chloride mercury prismatic crystals Mechanism of Action Corrosive sublimate Mercury compounds act by inactivating sulphydril Mercuric Red iodide Scarlet red powder enzymes causing interference with cellular metabo- iodide (Fig. 36.9) lism.15 Mercuric - White prismatic cyanide crystals Mercuric - Deliquescent nitrate crystalline Mercuric Cinnabar, Red crystalline sulphide Hingul powder (Fig. 36.10) Ras sindoor, Cheena sindoor Pigment vermillion Toxicology Mercuric - White crystalline sulphate powder Mercurous Calmol, Fibrous, heavy, dirty chloride raskapoor white mass B Subchloride of (Fig. 36.11) mercury Section Mercurous - Colorless crystalline nitrate powder Fig. 36.8: Mercuric oxide  Inorganic Irritants: Metallic Poisons 457 Fig. 36.9: Mercuric iodide Fig. 36.10: Mercuric sulphide Fatal Dose Fever, chills (metal fume fever) Headache Mercuric chloride – 1 gm Blurring of vision Mercuric cyanide – 0.6 to 1.3 gm Non-cardiogenic pulmonary edema Mercuric nitrate – 4 gm Convulsions Mercurous chloride (calomel) – 1.5 to 2 gm Ataxia Fatal period: 3 to 5 days. Delirium. Clinical Features Injection A. Acute poisoning with inorganic compounds Subcutaneous or intramuscular injection of mercury Inhalation: causes abscess formation with ulceration Breathlessness Intravenous administration results in thrombophlebitis, Cough granuloma formation and pulmonary embolism Intra-arterial administration results in peripheral embo- lism with ischemia and gangrene. Ingestion Metallic taste Abdominal pain Vomiting Shock Corrosion of mouth and tongue Toxicology Hematemesis Renal failure Pulmonary edema Urine – pinkish in colour Glossitis and ulcerative gingivitis Loosening of teeth B Section Necrosis of jaw Fig. 36.11: Mercurous chloride Membranous colitis  458 Principles of Forensic Medicine and Toxicology Management personality, abnormal shyness, timidity, loss of self confidence, insomnia, excitability, progressing later Gastric lavage with egg white or albumin or milk to into delirium with hallucinations (Mad as hatter). bind the mercury Colitis Demulcents Melanosis coli Laxative Mercury dermatitis – from mercuric sulphide (cin- X-ray follow up nabar) as red areas of tattoo has been reported. Also Chelation with BAL, DMPS contact dermatitis as occupational hazard had been Supportive noted.16 B. Poisoning by organic compounds Dementia Dysarthria Renal failure Ataxia Acrodynia (Pink disease): Paraesthesia Seen mostly in children and caused by chronic Neuropathy mercury exposure. It causes anorexia, insomnia, Diminished visual and auditory activity profuse sweating, skin rash, redness, vesication Mental deterioration and desquamation (peeling) of palm, finger, sole Chorea and photophobia. Minimata disease The hands and feet becomes – puffy, pinkish, C. Chronic poisoning painful, paraesthetic, perspiring and peeling Also called as hydrargyrism, mercurialism (remember 6 P’s) 1 Excessive salivation (Ptyalism, Sialorrhea) Shedding of teeth and ulceration of gums. Metallic taste Anorexia Autopsy Findings Insomnia Headache Emaciated body Gingivitis Mouth, throat, stomach appear grayish with softening Halitosis and corrosion with hemorrhagic areas Blue line on gums Colitis12 Lassitude Liver and heart – fatty degeneration Visual blurring Kidneys – pale, swollen with edema of renal cortex with Concentric constriction of visual field (tunnel vision) necrosis of renal tubules. Mercuria lentis – opacities of the anterior capsule of the lens of eye due to deposition of mercury Medicolegal Importance Ataxia – reeling gait 1. Poisoning occur due to accidental consumption of mer- Tremors – classical manifestation of chronic mercury cury as poisoning and is referred as “Danbury tremor”. The Folk medicine/indigenous medicine tremors are coarse, intentional type, interspersed with Toothpaste jerky movements, initially involving hands. Later it Industrial exposure involves lip, tongue, arms and legs. The advanced condition of tremors is called as “Hatter’s shakes” (because the condition was first described am