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Toxicology

Corrosives (Caustics)

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Common Corrosives (Caustics)

  • Acids
    • Inorganic:- Sulphuric, Nitric, Hydrochloric, Chromic,Phosphoric, Boric
    • Organic:- Carbolic, Oxalic, Acetic, Formic, Citric
  • Alkalis:- Sod./ Pot./ Cal. Hydroxide; Sod./Pot. Carbonate, Ammonia
  • Others:- H2O2’ Iodine, Pot.permanganate, Quat.ammo. Comp.

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Inorganic Acids

  • Act on site of application Causing
    • Desiccation- Extract water from tissue and liberate heat
    • Precipitate protein and coagulation necrosis
    • Fix, destroy, and erode tissue
    • Convert haemoglobin to haematin
    • Formation of eschar

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Clinical Effect

  • Local application – Chemical burn
  • Ingestion
    • Chemical burn of lips and area around
    • Mucosa of mouth - coagulation necrosis
    • Pain in mouth, throat & abdomen
    • Features of shock, unable to speak may vomit blood, may be constant retching and eructation

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Management

  • Do not give alkali to neutralize acid
  • Give milk, egg-white, Boiled rice water
  • Supportive measures
  • Combat shock
  • Parenteral pain killers

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Causes of Death

  • Early
    • Shock, & haemorrhage
    • Perforation of stomach & peritonitis
    • Oedema of larynx or laryngeal spasm
    • Toxaemia
  • Delayed
    • Renal failure
    • Secondary infection & Aspiration pneumonia
    • Pyloric stenosis & malnutrition

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Medico-legal aspect

  • Accidental- taken in mistake of medicine or alcoholic drink
  • Suicidal poisoning- orally taken by people who professionally in contact with acids.
  • Homicidal- Vitriolage (By Sulphuric acid)- concentrated acid thrown on face and body to kill or to disfigure especially in sexual jealousy.

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Post- Mortem Findings

  • Most severe corrosive effect in sulphuric acid followed by nitric acid and mild in hydrochloric acid.
  • Teeth may be chalky white in sulphuric a
  • Yellowish discolouration in nitric a due to xanthoproteic reaction is distinctive
  • Effect on respiratory system more in hydrochloric a as fuming

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Individual Acids

  • Sulphuric acid (Oil of Vitriol)
    • Oily, colourless, heavy, no fumes, Carbonizes blackish eschar. Fatal dose- 5-10 ml
  • Nitric acid (Aqua fortis/ Red Spirit of Nitre
    • Fuming, causes yellowish discolouration Fatal dose 10-15 ml
  • Hydrochloric acid (Muriatic acid, spirit of Salts)
    • Yellowish,volatile, fuming, less corrosive, brownish fatal dose 15-20 ml

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Organic Acids- Carbolic Acid

  • Also called phenol or phenyl or hydroxy-benzene; the group includes Lysol & dettol
  • Used to be very important antiseptic in surgery even now used as disinfectant
  • Colourless prismatic needle like crystal turning pink & liquid on exposure to air
  • Fatal dose 2 gm crystal or 25-50 ml liquid
  • Fatal Period- 3-4 hrs, delayed some days

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Clinical Picture

  • Poisoning called Carbolism
  • Local effect on application to skin
    • Burning pain, numbness, tingling, corrosion & anaesthesia. Eschar (Scab) falls off in a few days leaving brown stained area.
  • Systemic effect on oral ingestion
    • GIT-
      • Nausea, vomiting, burning pain, in chest and abdomen followed by tingling, numbness.

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Clinical Picture

  • Systemic effect
    • Respiration- Slow and laboured
    • CNS- Headache, giddiness, convulsion, Coma
    • Oliguria & Hepatic faillure
    • Hydroquinone & pyrocatechol causes pigmentation of cornea and cartilages - ochronosis
    • Carboluria-
      • Fresh urine colourless but on exposure to air turns green due to oxidation of metabolites of phenol (hydroquinone & pyrocatechol)

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Management

  • Oxygen/ Ventilatory Support
  • Blood pressure management
  • Management of cardiac arrhythmias
  • Management of convulsion
  • Skin- Wash with undiluted polyethylene Glycol
  • Gastric lavage with Mag.sulph/ sod. Sulph
  • Treat methaemoglobinaemia by Methylene blue 1-2mg/kg. Exchange transfusion may be needed

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Autopsy Findings

  • Smell of Carbolic acid is found in viscera
  • Mucosa of stomach is tough grey, corrugated in longitudinal folds & leathery
  • Mucosa of mouth, lips, throat, sodden, and ash grey.
  • May show corrosion of skin which is initially white but later turns brown
  • Urine on exposure to air turns green

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Medico-legal aspect

  • Occupational hazard and skin of hands usually were affected in surgeons using carbolic acid as antiseptic
  • Poisoning is generally accidental, sometimes suicidal and rarely homicidal due to its strong smell

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Oxalic Acid (Ethanedioic Acid, Salt of Sorrel)

  • Physical Property:- Colourless, odourless, prismatic crystals with a sour and slightly bitter taste
  • Uses:-Bleaching & cleaning agents, ink remover,rust remover, metal polishing
  • Industry:- Ceramic, leather, metallurgic, paper, pharmaceutical, & rubber industry

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Mechanism of Action

  • Local- Corrosive action
    • Prolonged contact may cause cyanosis or even gangrene
  • Systemic
    • Shock
    • Hypocalcaemia
    • Nephrotoxicity

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Clinical Picture

  • Fulminating poisoning caused by orally taking of large dose death within minutes
  • Acute Poisoning characterized by survival for a few hours in which clinical picture of hypocalcemia manifested.
  • Delayed Poisoning due to injury to kidney causing oliguria, haematuria, oxaluria albuminuria & uraemia

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Clinical Features

  • Yellowish/ whitish corrosion of mucosa with surrounding tissue congestion
  • Vomiting mixed with blood (Coffee grounds)
  • Signs & symptoms of hypocalcaemia (tetany) as oxalic acid combines with calcium ions.
      • Tonic muscle spasms, cramps, & Accoucher’s hand
      • +ve Trousseau & Chvostek’s sign
      • Pupils usually dilated,
      • Metabolic acidosis, renal failure & vent. fibrillation

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Diagnosis

  • Demonstration of oxalates in Urine
  • Low serum calcium but raised oxalates
  • Fatal Dose:- 15 to 30 gm of oxalic acid
  • Mode of action:- Corrosive action & combining property with serum calcium causing hypocalcaemia & precipitation of oxalates in Liver, Kidneys, heart, lungs and blood
  • Fatal period – 1 to 2 hours

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Treatment

  • Stomach wash with Calcium gluconate or lactate solution also to be left in stomach
  • Calcium gluconate I.V. (10 ml 10% soln.) to be repeated
  • Dialysis or exchange transfusion for renal failure
  • Affected part should be washed with copious water

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Autopsy Findings

  • Whitish or yellowish corroded areas in GI Tract if taken orally.
  • Underlying tissue congested and may be brownish or black
  • Crystals of oxalate may be demonstrated in mucosal scrapping
  • Altered blood may be present in GI tract

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Medico - Legal Importance.

  • Majority of cases are accidental and in children
  • Poisoning may occur from over eating of plants containing oxalates like- rhubarb leaves, sorrel etc.
  • Less frequently used as suicidal poison
  • It is rarely used as homicidal poison

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Caustic Alkalis

  • Ammonia Gas- Smelling Salt
  • Ammonium hydroxide- Paint, oil and dirt remover. Refrigerant
  • Sod.hydroxide(caustic soda)- Drain cleaner, oven cleaner
  • Pot. Hydroxide(caustic potash)- drain cleaner, hearing aid batteries
  • Sod. Carbonate- (washing soda)- Household cleaning agent, detergent
  • Pot. Carbonate- Household cleaning Agent
  • Sod. Hypochlorite- Household bleach

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Clinical Features

  • Greyish soapy necrosis of affected skin / mucosa of mouth GI tract due to liquefactive necrosis
  • Pain, abdominal ache, tenderness,diarrhoea, tenesmus haematemesis
  • Oedema of the pharynx/larynx, glottis requiring emergency tracheostomy
  • Injury to eye and respiratory embarrassment and pulmonary oedema in ammonia poisoning

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Management

  • Removal of the residual poison-washing
  • 1-2 glass of milk/ water to dilute
  • Watch for complications especially respiratory and manage- Corticosteroid
  • Fluid & electrolyte balance
  • Endoscopic examination of upper GI tract
  • Surgical intervention to prevent/ repair perforation
  • Emesis, gastric lavage & acid to neutralise alkali absolutely contraindicated

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Medico- Legal points

  • Death from caustic alkali is rarely seen
  • PM findings are similar but milder than by acids
  • Poisoning is mostly accidental and in children in domestic setting
  • 10-15 gm/ 15-20 ml Fatal
  • Industrial accidental poisoning specially by ammonia often reported

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