Corrosive poisons

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Corrosive Poisons

Definition and Terminology

A caustic or corrosive is a dry or liquid chemical agent that is immediately dangerous to living tissue upon contact. In contrast, a poison exerts a systemic toxic effect that requires time to become apparent. Some agents are both corrosives and poisons. The word "corrosive" is derived from the Latin corrodere — "to gnaw" through flesh. "Caustic" is often used synonymously with "corrosive" but strictly refers to strong bases/alkalis; however, medical literature groups both acids and alkalis under "caustic." — Cummings Otolaryngology, p. 3984

Classification of Corrosive Agents

Class	pH	Examples	Common Products
Alkali (bases)	>7	Sodium hydroxide (NaOH/lye), potassium hydroxide (KOH), ammonia	Drain cleaners (Drano, Liquid Plumbr), oven cleaners, hair relaxers, dish detergents
Acids	<7	Sulfuric acid, hydrochloric acid, nitric acid, formic acid, acetic acid	Toilet bowl cleaners, swimming pool cleaners, rust removers, battery fluid
Bleaches/Oxidants	~7	Sodium hypochlorite	Mildew removers, household bleach

Mechanisms of Tissue Injury

Alkalis → Liquefaction Necrosis

Strong alkalis cause liquefaction necrosis — rapid disintegration of mucosa with deep penetration into tissues. The process involves:

Intense inflammatory reaction and edema
Hemorrhagic congestion and eosinophilic necrosis
Bacterial invasion and saponification (tissue fats + lye form a viscous, soap-like mass)
Thrombosis → further compromise of blood supply → necrosis and perforation

Because there is no coagulum barrier, alkalis penetrate full thickness and cause the most severe esophageal injuries (60–80% of serious cases). NaOH (lye) at pH 13–14 (drain cleaners) is the most dangerous.

Acids → Coagulation Necrosis

Acids cause coagulation necrosis — denaturation of proteins forming a gel-like coagulum on the mucosa. This coagulum limits deep penetration in the esophagus. However:

Acids cause greater injury to the stomach, where the higher pH may allow deeper penetration
Gastric complications: pyloric stenosis, gastric outlet obstruction, perforation with peritonitis

Severity Factors

The severity of tissue injury depends on:

pH — the more extreme, the more severe
Concentration of the agent
Contact time — solid/crystal forms adhere longer; liquids cause more circumferential burns
Volume ingested

Timeline of Tissue Injury (Alkali)

Time	Pathological Event
First 24 hr	Epithelial degeneration, lymphocytic submucosa infiltration
Day 4	Fibroblasts and new blood vessels emerge
Day 7	Necrosis complete
Week 2	Granulation tissue predominates, contractile (stricture) stage begins
3–4 weeks	Established strictures

Endoscopic Grading (Zargar Classification)

Grade	Findings
0	No injury
1	Mucosal edema and hyperemia
IIa	Superficial, non-circumferential whitish membranes, shallow ulcers, hemorrhage
IIb	Deep, circumferential lesions with stricture formation
IIIa	Small, scattered areas of necrosis
IIIb	Extensive necrosis
IV	Perforation

Circumferential injuries have an extremely high likelihood of stricture formation. — Cummings Otolaryngology, p. 3985

Clinical Presentation

Common symptoms:

Vomiting (most common), dysphagia, drooling
Oral pain, odynophagia
Chest pain, abdominal pain

Danger signs (perforation):

Fever + chest/abdominal pain + hypotension

Laryngeal injury (especially with powders): hoarseness, stridor, nasal flaring, retractions — onset within hours

Severe complications: hemolysis, DIC, renal failure, peritonitis, mediastinitis, metabolic acidosis, CNS depression, death — Cummings Otolaryngology, p. 3985–3986

Important: The presence/absence of oral lesions does not predict esophageal injury. In one series of 473 cases, 61% of patients without oral lesions had esophageal injuries. Conversely, 82% of symptomatic children had no esophageal injury. — Cummings Otolaryngology, p. 3986

Management Algorithm

Fig. 211.13 — Caustic ingestion management algorithm (Cummings Otolaryngology)

Immediate Steps

Secure airway if emergency (flexible fiberoptic intubation preferred to avoid emergency cricothyrotomy)
Do NOT induce vomiting — re-exposes the esophagus/larynx to corrosive
Do NOT give activated charcoal — does not adsorb caustic agents
Oral dilution — limited to ≤15 mL/kg of water or milk (may reduce injury, but evidence in humans is weak; excessive amounts may trigger vomiting)
Blind NG tube placement is contraindicated — risk of perforation
IV fluids + NPO if admitted
Chest/abdominal X-ray — rule out free air (mediastinum or peritoneum)

Neutralization (Schwartz's Surgery):

Alkali → neutralize with half-strength vinegar, lemon juice, or orange juice (within 1 hour)
Acid → neutralize with milk, egg white, or antacids
Sodium bicarbonate is avoided (generates CO₂ → risk of perforation)

Endoscopy

Optimal window: 12–48 hours after ingestion
<12 hours: evolving lesion may be missed
48 hours: necrotic tissue sloughs, esophageal wall too weak → risk of perforation
Do not advance scope beyond the first level of burn to avoid perforation
If presenting >48 hours: barium esophagogram instead

Stage-Based Management

Stage	Management
0–I	Discharge, follow-up as needed
II	Feeding tube; steroids (controversial)
III	Feeding tube or stent, IV antibiotics
IV/V	Esophageal replacement, IV antibiotics

Stricture Management

60% of strictures develop within 1 month; 80% within 2 months
Fluoroscopically guided balloon dilation (with concurrent esophagoscopy)
Retrograde dilation via gastrostomy + transesophageal string technique for severe cases
If strictures do not develop within 8 months, unlikely to occur — Schwartz's Surgery, p. 1113

Special Agents

Hydrofluoric Acid (HFA)

Although corrosive, the hydrogen ion plays a relatively minor role in HFA injury. The fluoride ion is the primary culprit — a protoplasmic poison that causes systemic toxicity including hypocalcemia and cardiac arrhythmias, requiring systemic calcium treatment. — Roberts & Hedges' Clinical Procedures in Emergency Medicine

Bleach (Sodium Hypochlorite, pH ~7)

Acts as a mild irritant, not a true caustic
Rarely causes deep penetration or stricture formation
Common misconception that bleach causes severe injury

Location of Caustic Injury (Distribution)

Location	Frequency
Esophagus (overall)	70%
— Middle third	65%
— Upper	15%
— Lower	2%
— Whole esophagus	18%
Stomach	20%
Pharynx	10%
Both esophagus and stomach	14%

— Schwartz's Principles of Surgery, p. 1114

Long-term Complications

Esophageal stricture (most common late complication)
Gastric outlet obstruction / pyloric stenosis (acid ingestion)
Tracheoesophageal fistula
Increased risk of esophageal carcinoma (squamous cell carcinoma — risk rises 1,000-fold decades after lye ingestion)
Mediastinitis, peritonitis

Sources: Cummings Otolaryngology Head and Neck Surgery | Schwartz's Principles of Surgery, 11th ed. | K.J. Lee's Essential Otolaryngology | Roberts and Hedges' Clinical Procedures in Emergency Medicine

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