Sulfuric acid poisoning in fmt

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Sulfuric Acid Poisoning (H₂SO₄)

The Essentials of Forensic Medicine and Toxicology, 36th edition (2026)

Characteristics

  • Pure sulfuric acid = oil of vitriol (H₂SO₄)
  • Heavy, odorless, colorless, nonfuming, hygroscopic, oily liquid
  • Strong tendency to carbonize organic substances
  • Commercial form is brown or dark in color
  • Causes superficial burns after 1 second and full-thickness burns after 30 seconds of contact

Signs and Symptoms

FeatureDescription
LipsSwollen, excoriated; brown/black streaks from mouth angles to chin/neck
Mouth/throatCorrosion of mucous membranes; immediate burning pain
TeethChalky-white
TongueSwollen, sodden, black
VoiceHoarse and husky
AirwaysStridor, drooling; edema of glottis may cause asphyxia
SwallowingOdynophagia, dysphagia; pharyngeal pain is the most common presenting symptom
GIEpigastric pain spreading to abdomen and thorax; eructation, nausea, vomiting
VomitBrown or black, mucoid, strongly acid, may contain charred shreds of stomach wall
ThirstIntense; any attempt to drink causes vomiting
AbdomenDistended, very tender; severe constipation; tenesmus
EyesSunken; pupils usually dilated
SensoriumMind remains clear until death
Late sequelaeEsophageal, gastric, and pyloric strictures/stenoses; permanent scars in skin and oropharynx

Fatal Dose and Period

  • Fatal Dose: 10-5 mL
  • Fatal Period: 12-24 hours

Causes of Death

  1. Circulatory collapse
  2. Spasm or edema of glottis
  3. Collapse due to perforation of stomach
  4. Toxemia
  5. Delayed death - hypostatic pneumonia, secondary infection, renal failure, or starvation from esophageal stricture

Complications

Acute:
  1. Upper airway obstruction and injury
  2. GI hemorrhage
  3. Esophageal and gastric perforation
  4. Sepsis
  5. Tracheobronchial necrosis, atelectasis, obstructive lung injury
Chronic:
  1. Esophageal obstruction
  2. Pyloric stenosis
  3. Vocal cord paralysis with airway obstruction

Treatment

  1. NO gastric lavage or emetics (contraindicated - risk of re-exposure and perforation)
  2. Dilute and neutralize in situ - give 1/4 litre of water, milk, milk of magnesia, lime water, soap suds, or aluminium hydroxide gel within 30 minutes
    • Do NOT use alkaline carbonates/bicarbonates (liberate CO₂ → gastric distension → rupture)
  3. Demulcents - olive oil, milk, egg whites, starch water, mineral oil, melted butter
  4. Prednisolone 60 mg/day in divided doses to prevent esophageal stricture and for shock (generally not recommended due to increased perforation risk)
  5. 4 cm diameter mercury-filled bougie passed daily if stricture develops
  6. Flexible fiber optic endoscopy within first 24-48 hours to assess damage; if circumferential 2nd/3rd-degree burns → exploratory laparotomy; if gastric necrosis → esophagogastrostomy
  7. Tracheostomy if there is edema of glottis
  8. NPO - IV nutrition for ~1 week, then liquids → soft food → regular diet
  9. Skin burns - wash with large amounts of water; apply paste of magnesium oxide or sodium bicarbonate
  10. Eye burns - irrigate with water or sodium bicarbonate solution for 10-15 minutes (suspended IV bag for low-pressure irrigation is ideal)
  11. Symptomatic treatment

Postmortem Appearances

External

  • Corrosion of mucous membranes of lips, mouth, throat
  • Corrosion of skin over chin, angles of mouth, and hands
  • Necrotic areas initially grayish-white, then become brown or black and leathery
  • Examine clothing for burns and stains

Internal

  • Upper digestive tract inflamed and swollen with edema and severe interstitial hemorrhage
  • Acids mainly affect columnar epithelium of the stomach (squamous esophageal epithelium is relatively resistant) - superficial erosion, coagulation, eschar formation
  • Perforation of esophagus is rare
  • Greater part of stomach may be converted into a soft, spongy, black mass that readily disintegrates on touch
  • Sometimes only the pyloric region is involved (fluid pathway along lesser curvature to pylorus; initial acid exposure causes pyloric spasm, promoting injury there)
  • Mucosal ridges more damaged than intervening furrows
  • Stomach contains altered blood, dark brown/black from acid hematin; wall studded with acute erosions
  • Calcium oxalate crystals may be seen in stomach contents or mucosal scrapings
  • Perforation → chemical peritonitis and corrosion of adjacent organs
  • Perforation of diaphragm may occur
  • Duodenum: similar but less intense changes; small intestine: signs of irritation
  • Little to no free acid may be found if victim survived 2+ days (acid converted to normal body substances)
  • Larynx and trachea: corrosion or severe inflammation
  • Liver and kidney: secondary toxic swelling if survival is prolonged
  • Renal tubules: necrosis, primarily in proximal convoluted tubules
Stomach in sulfuric acid poisoning showing extensive dark brown/black discoloration and mucosal destruction
Fig. 26.1: Stomach in sulfuric acid poisoning - note the extensive dark discoloration and necrotic changes

Time Course of Injury

StageTimeFeatures
Acute inflammatoryDays 1-7Perforation and acidosis may occur
GranulationDays 4-7
Perforation most likelyDays 7-21Tissue is weakest at this stage
CicatrizationFrom ~3rd weekMay persist for years; excessive scar → stricture

Tests / Chemical Analysis

  • Only the stomach contents are suitable for analysis (mineral acids decompose rapidly)
  1. Strong acid chars organic matter
  2. Barium nitrate or chloride solution produces a white precipitate of barium sulphate (confirmatory for sulfate)

Circumstances of Poisoning

  • Accidental - mistaking it for glycerin or castor oil; inhalation of vapors in chemical factories
  • Suicidal - most common mode
  • Homicide - rare/not used (acid taste, immediate local action, visible physical changes in food make it impractical)
  • Also used as an abortifacient (injected into vagina) or out of vengeance

Vitriolage (Vitriol Throwing)

  • Throwing of sulfuric acid on another individual
  • Done by jealous or disgruntled persons to disfigure and harm enemies
  • Burns are penetrating, devitalize tissues, predispose to infection
  • Burns initially described as painless
  • Repair is slow; scar tissue causes contracture
  • Blindness if eyes are involved
  • Death from shock or toxemia if extensive area involved
  • Other agents also used for vitriolage: nitric acid, carbolic acid, corrosive alkali, juice of marking nut or calotropis
Vitriolage - acid burns on skin
Fig. 26.2: Vitriolage

Source: The Essentials of Forensic Medicine and Toxicology, 36th edition (2026), Chapter 26
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