Toxicology – Caustics—Acidic

Core concept

Strong acids cause immediate chemical injury to skin, eyes, respiratory mucosa, and the gastrointestinal tract.

The major acute hazards are:

Airway edema + esophageal/gastric necrosis + hemorrhage + perforation + shock

A useful sequence is:

Strong-acid contact → protein denaturation/coagulative necrosis → mucosal ulceration/necrosis → edema/bleeding → perforation or later stricture

However, the traditional statement that acids cause only superficial coagulation necrosis while alkalis cause deep liquefaction is an oversimplification.

Concentrated acids can produce profound transmural esophageal and gastric necrosis.

Modern management centers on:

Airway protection + resuscitation + early assessment of injury depth with endoscopy and/or contrast-enhanced CT

There is no specific antidote.

Important terminology

Simply having a:

pH <7

does not make a substance clinically “caustic.”

Many weak acids encountered in foods are harmless.

The potential for corrosive injury depends on:

• Concentration
• pH
• Titratable acidity
• Volume ingested
• Contact time
• Viscosity
• Chemical composition
• Solid vs liquid formulation

Thus:

Concentrated strong acid ≠ ordinary acidic liquid

Important acidic caustics

Examples include:

• Hydrochloric acid
• Sulfuric acid
• Nitric acid
• Phosphoric acid
• Concentrated acetic acid / glacial acetic acid
• Formic acid
• Oxalic acid

Special acids with important systemic toxicities are often managed separately, particularly:

• Hydrofluoric acid
• Chromic acid
• Boric acid
• Selenium-containing acids

Common sources

Household and industrial products include:

• Toilet-bowl cleaners
• Metal cleaners
• Rust removers
• Descaling agents
• Battery acid
• Industrial cleaning solutions
• Laboratory reagents
• Metal-pickling solutions
• Fertilizer/chemical manufacturing
• Etching and engraving products

The exact commercial formulation matters because products may contain:

• Additional corrosives
• Oxidizers
• Metals
• Surfactants
• Solvents

Toxic dose

There is no useful universal toxic dose.

Severity depends much more on:

Agent × concentration × volume × contact time

than on a simple number of milliliters.

A small amount of a highly concentrated industrial acid may produce devastating injury, while a larger exposure to a weakly acidic household solution may produce little damage.

Intentional ingestions generally carry much higher risk because they involve:

• Larger volumes
• Higher concentrations
• Longer contact

Pathophysiology

Gastrointestinal injury

Strong acids cause:

H⁺-mediated protein denaturation → coagulative necrosis

with:

• Edema
• Erosion
• Ulceration
• Thrombosis of small vessels
• Eschar formation

Classically, acids were thought to injure the stomach more than the esophagus because:

• Liquids transit the esophagus rapidly
• Pylorospasm may retain acid in the stomach

However:

Severe esophageal injury absolutely can occur after acid ingestion.

Do not use the acid-vs-alkali distinction to determine whether endoscopy is needed.

Tissue evolution

Caustic injury evolves over time.

Early:

• Edema
• Hyperemia
• Thrombosis
• Necrosis

Over subsequent days:

• Mucosal sloughing
• Inflammation
• Bacterial invasion
• Granulation tissue

The damaged GI wall becomes mechanically weak during the healing phase, increasing concern for perforation after instrumentation.

Later:

Fibrosis → esophageal stricture and/or gastric outlet obstruction

Respiratory injury

Acid fumes or aspiration can cause:

Upper-airway irritation → laryngeal edema

and:

Lower-airway irritation → bronchospasm → chemical pneumonitis → ARDS

Nitric acid exposure deserves particular caution because associated nitrogen oxides can cause significant delayed pulmonary injury.

Clinical features

HEENT / Oropharyngeal

Possible findings include:

• Oral pain
• Lip/tongue burns
• Oral ulceration
• Drooling
• Dysphonia
• Hoarseness
• Dysphagia
• Odynophagia
• Stridor

Critical pitfall

Absence of visible oral burns does not exclude severe esophageal or gastric injury.

Oropharyngeal examination cannot reliably grade distal injury.

Airway

Warning signs include:

• Hoarse voice
• Stridor
• Drooling
• Progressive swelling
• Respiratory distress
• Hypoxemia
• Inability to handle secretions

Airway edema can progress rapidly.

Therefore:

Secure a threatened airway early rather than waiting until intubation becomes impossible.

Gastrointestinal

Possible manifestations include:

• Severe mouth/throat burning
• Retrosternal pain
• Epigastric pain
• Dysphagia
• Odynophagia
• Vomiting
• Hematemesis
• Abdominal tenderness

Severe injury may progress to:

• GI hemorrhage
• Mediastinitis
• Peritonitis
• Perforation
• Shock

Perforation

Suspect esophageal or gastric perforation with:

• Sudden severe chest/abdominal pain
• Peritoneal signs
• Subcutaneous emphysema
• Pneumomediastinum
• Free intraperitoneal air
• Fever/sepsis
• Hemodynamic collapse

This requires:

Immediate surgical evaluation

Cardiovascular

Severe exposures may cause:

• Tachycardia
• Hypotension
• Hemorrhagic shock
• Distributive/inflammatory shock
• Cardiovascular collapse

Shock may result from:

• GI hemorrhage
• Third-spacing
• Tissue necrosis
• Perforation/sepsis

Metabolic

Severe poisoning may cause:

• Lactic acidosis
• High anion-gap metabolic acidosis
• Hyperkalemia
• Acute kidney injury

Some specific acids produce additional systemic metabolic abnormalities.

Acid-specific systemic toxicities

Concentrated acetic acid

Severe ingestion may cause:

• Intravascular hemolysis
• Hemoglobinuria
• AKI
• DIC
• Hepatic injury

Formic acid

May cause:

• Severe metabolic acidosis
• Hemolysis
• Multiorgan injury

Oxalic acid

Can bind calcium and produce:

• Hypocalcemia
• Tetany
• Dysrhythmias
• Calcium oxalate nephropathy
• AKI

Phosphoric acid

Large systemic exposures may produce:

• Hyperphosphatemia
• Secondary hypocalcemia

Thus:

Not every acidic caustic is merely a local burn.

Identify the precise acid whenever possible.

Dermatologic exposure

Acid skin exposure may range from:

• Erythema
• Pain
• Superficial chemical burn

to:

• Deep dermal necrosis
• Full-thickness injury

Concentrated acids can continue to cause injury while chemical remains on the skin or clothing.

Ocular exposure

The eye is particularly vulnerable.

Possible injury includes:

• Conjunctivitis
• Corneal epithelial defects
• Corneal ulceration
• Stromal damage
• Corneal opacification
• Perforation
• Permanent blindness

This is an ocular emergency.

Diagnosis

Diagnosis is based on:

Known/suspected corrosive exposure + clinical evaluation + assessment of tissue injury

Do not rely on:

• Oral appearance alone
• pH of the product alone
• Amount reported alone

Initial investigations

For a minor asymptomatic exposure, laboratory testing may not be necessary.

For significant or symptomatic exposure consider:

• CBC
• Electrolytes
• Bicarbonate
• BUN/creatinine
• Glucose

For severe poisoning:

• Blood gas
• Lactate
• PT/INR
• aPTT
• Fibrinogen
• Liver enzymes
• Type and crossmatch

Agent-specific testing may include:

• Calcium
• Phosphate
• Hemolysis profile

depending on the acid involved.

Imaging

Plain radiographs

Chest/abdominal radiographs may demonstrate:

• Pneumomediastinum
• Pneumoperitoneum
• Pleural abnormalities

but a normal radiograph does not exclude serious injury.

Contrast-enhanced CT

Modern management increasingly uses:

Contrast-enhanced CT of the neck/chest/abdomen

in severe caustic ingestion.

CT can evaluate:

• Esophageal wall enhancement
• Transmural necrosis
• Gastric necrosis
• Mediastinal injury
• Perforation
• Adjacent-organ injury

A particularly concerning finding is:

Loss of mural enhancement → possible full-thickness necrosis

which may indicate a need for emergency surgery. WSES guidance supports CT-based emergency assessment, particularly for identifying transmural injury.

Current nuance

There is still debate over whether CT should completely replace endoscopy.

A 2025 review found that although CT is increasingly valuable—especially for detecting deep necrosis—EGD remains the predominant first-line assessment in many centers, and evidence is not yet sufficient to universally replace endoscopy with CT.

Thus:

EGD and CT are complementary tools, with local expertise determining the exact algorithm.

Upper GI endoscopy

EGD remains a central method for grading mucosal injury.

Strongly consider EGD after:

• Intentional ingestion
• Significant deliberate exposure
• Drooling
• Dysphagia/odynophagia
• Vomiting
• Oral/pharyngeal burns
• Chest or abdominal pain
• Inability to tolerate liquids
• Other concerning symptoms

Current reviews generally recommend performing EGD:

Within approximately 24 hours

when indicated.

When endoscopy may be deferred

An asymptomatic patient after a clearly:

• Accidental
• Small-volume
• Low-concentration

exposure, with:

• No oral injury
• Normal examination
• Ability to swallow normally

may not require routine EGD.

This decision should consider the actual agent and exposure reliability.

Endoscopy cautions

Endoscopy requires particular caution when there is:

• Suspected perforation
• Hemodynamic instability
• Severe airway compromise
• Extensive necrosis

In these situations:

Resuscitation and CT/surgical evaluation take priority.

Zargar endoscopic classification

Grade 0

Normal mucosa

Grade I

• Edema
• Hyperemia

Generally low risk of late stricture.

Grade IIa

• Friability
• Hemorrhage
• Erosions
• Blisters
• Superficial ulcers
• Exudates

Stricture risk is usually low.

Grade IIb

Grade IIa findings plus:

Deep or circumferential ulceration

High risk of stricture.

Grade IIIa

Focal areas of necrosis

High risk of stricture and perforation.

Grade IIIb

Extensive necrosis

Very high risk of:

• Perforation
• Systemic complications
• Death

These grades remain useful for prognosis, although CT may better assess whether injury is actually transmural.

Treatment

1. Airway first

Assess immediately for:

• Stridor
• Hoarseness
• Drooling
• Oropharyngeal edema
• Progressive respiratory distress

When airway compromise is anticipated:

Intubate early

Ideally use:

• Experienced airway personnel
• Video or fiberoptic techniques as appropriate
• Surgical-airway backup

because edema and distorted anatomy can make later airway control very difficult.

2. Circulation

Establish IV access.

For shock:

• Give isotonic crystalloid when appropriate
• Transfuse blood products for significant hemorrhage

Persistent hypotension despite adequate resuscitation generally warrants:

Norepinephrine

rather than the older routine preference for dopamine.

3. Do NOT induce vomiting

Never induce emesis.

Re-exposure of the esophagus can:

• Worsen injury
• Increase aspiration risk

Ipecac has no role.

4. Do NOT neutralize

Do not give:

• Sodium bicarbonate after acid ingestion
• Other alkaline neutralizing agents

Neutralization can produce:

Exothermic reaction → additional thermal injury

and unpredictable gas generation.

Modern guidance does not support therapeutic neutralization.

5. Routine milk/water dilution is no longer recommended

The older recommendation:

“Give 4–8 oz milk or water within 30 minutes”

is no longer standard clinical practice.

Possible problems include:

• Vomiting
• Gastric distention
• Aspiration
• Lack of demonstrated human benefit

Current toxicology guidance states that dilution might theoretically help only within the first few minutes but lacks evidence and is not routinely recommended.

Thus:

Do not routinely force oral dilution after significant caustic ingestion.

6. No activated charcoal

Activated charcoal is generally not indicated for isolated acid ingestion because:

• Acids are poorly adsorbed
• Charcoal can provoke vomiting
• Aspiration is dangerous
• It may obscure subsequent endoscopy

Modern charcoal guidance specifically lists acids and alkalis among substances not meaningfully adsorbed by activated charcoal.

Use charcoal only for a clinically important separate coingestant when its benefits clearly outweigh the risks.

7. No gastric lavage

Gastric lavage is contraindicated/routinely avoided.

It can:

• Re-expose the esophagus
• Cause perforation
• Cause aspiration

There is no routine role for lavage after caustic acid ingestion.

8. Avoid blind NG/OG tube insertion

Blind insertion may:

• Perforate injured tissue
• Increase bleeding

If enteral access is required:

Placement should generally be performed under endoscopic or surgical guidance.

Modern reviews recommend avoiding blind NG placement because of perforation risk.

Skin decontamination

Immediately:

• Remove contaminated clothing/jewelry
• Brush away dry chemical if applicable
• Irrigate skin with copious water

Continue irrigation until all residual chemical is removed.

Exception

Agent-specific exceptions may exist—for example hydrofluoric acid has additional specific treatment—and should be managed separately.

Ocular decontamination

Immediately irrigate with:

• Water
• Normal saline

Do not delay irrigation while searching for a special solution.

Continue copiously and reassess:

Conjunctival-sac pH

after irrigation, allowing a brief pause before measurement to avoid falsely measuring the irrigant.

Continue until physiologic pH is restored and remains stable.

Significant ocular burns require urgent:

Ophthalmology evaluation

Inhalational exposure

Move patient to fresh air.

Provide:

• Oxygen for hypoxemia
• Bronchodilator for bronchospasm

Patients with:

• Stridor
• Progressive edema
• Hypoxemia
• Significant respiratory distress

require aggressive airway/respiratory management.

Chemical pneumonitis or ARDS is treated supportively with lung-protective ventilation when required.

Proton-pump inhibitors

PPIs are commonly given after significant upper GI caustic injury.

However:

Evidence that PPIs change major outcomes such as stricture formation is limited.

They may be reasonable for:

• Significant mucosal injury
• Stress-ulcer/acid suppression

but should not be described as an antidote.

Current literature regards their definitive role as uncertain.

Corticosteroids

Major modernization

The older text suggests steroids should be considered for second-degree burns.

Routine systemic corticosteroids are now:

NOT recommended for prevention of caustic esophageal strictures

A systematic review/meta-analysis of randomized trials found no significant reduction in stricture formation with corticosteroid therapy.

A broader pooled analysis likewise failed to support routine steroids in grade II burns.

Nuance

Some pediatric/selected protocols have investigated high-dose steroids for grade IIb injury, but this remains controversial.

Therefore:

Do not routinely prescribe steroids solely to prevent strictures.

Any selected use should involve:

• Gastroenterology
• Toxicology
• Surgery/pediatric GI as appropriate

Antibiotics

Routine prophylactic antibiotics are not indicated for uncomplicated caustic injury.

Use antibiotics when there is:

• Perforation
• Mediastinitis
• Peritonitis
• Aspiration pneumonia
• Documented/suspected infection
• Selected severe necrotic injury according to surgical protocol

Do not give antibiotics simply because a caustic agent was swallowed.

Nutrition

Nutrition should be individualized according to injury severity.

Mild injury

Patients with:

• Grade 0/I or selected IIa injury
• Ability to swallow normally
• No significant pain/vomiting

may resume oral intake as clinically appropriate.

Severe injury

Grade IIb/III injury may require:

• NPO initially
• Enteral feeding through carefully placed access
• Jejunal feeding
• Occasionally parenteral nutrition

The modern goal is:

Use the gut when safely possible rather than prolonged unnecessary starvation.

Emergency surgery

Immediate surgical consultation is required for evidence of:

• Perforation
• Peritonitis
• Mediastinitis
• Uncontrolled hemorrhage
• Extensive transmural necrosis
• Progressive abdominal catastrophe
• Refractory shock attributable to GI necrosis

Contrast CT evidence of:

Absent esophageal/gastric wall enhancement

is a major sign suggesting full-thickness necrosis and can guide urgent surgical management.

Acid-specific treatment

Individual acids may require additional management.

For example:

Oxalic acid

Monitor/treat:

• Hypocalcemia
• Dysrhythmias
• AKI

Concentrated acetic/formic acid

Monitor:

• Hemolysis
• Hemoglobin
• LDH
• Haptoglobin
• Bilirubin
• Renal function
• Coagulation

Phosphoric acid

Monitor:

• Phosphate
• Calcium
• Renal function

Hydrofluoric acid

Requires its own emergency management because:

Fluoride toxicity → hypocalcemia/hypomagnesemia + dysrhythmias

and calcium therapy may be lifesaving.

Antidote

There is no general antidote for strong-acid caustic injury.

Treatment is:

• Immediate decontamination
• Airway management
• Hemodynamic support
• Assessment of injury depth
• Surgical treatment when required
• Management of acid-specific systemic toxicity

Stricture formation

The most important delayed GI complication is:

Esophageal stricture

Risk is greatest after:

• Grade IIb injury
• Grade III injury

Symptoms may appear approximately:

3 weeks or later

after ingestion.

Symptoms include:

• Progressive dysphagia
• Food sticking
• Regurgitation
• Weight loss

Gastric outlet obstruction

Deep gastric injury may heal with fibrosis producing:

• Early satiety
• Postprandial vomiting
• Weight loss
• Gastric retention

This may develop within several weeks; older series commonly describe onset around 5–6 weeks after severe injury.

Stricture treatment

Established esophageal strictures are generally managed with:

Endoscopic dilation

using:

• Balloon dilators
• Bougie dilation

Repeat procedures are often required.

Complex/refractory strictures may require:

• Advanced endoscopic therapy
• Feeding access
• Surgical reconstruction

Routine prophylactic esophageal stenting solely to prevent strictures is not standard practice.

Long-term cancer risk

Severe caustic injury is associated with an increased long-term risk of:

Esophageal squamous cell carcinoma

often decades after the original exposure.

Expert reviews describe cancer developing typically around:

10–40 years later

although the exact magnitude of risk is uncertain.

Some experts suggest surveillance endoscopy beginning approximately:

10–20 years after severe caustic injury

with repeat examinations every few years, but:

There is no universally validated surveillance schedule.

Occupational carcinogenicity

The old text broadly states:

“Acid mists are associated with laryngeal cancer.”

The more precise modern statement is:

Occupational exposure to strong inorganic acid mists is carcinogenic to humans (IARC Group 1), with sufficient evidence for laryngeal cancer.

Historically this classification was strongly associated with sulfuric-acid–containing mists.

This does not mean every brief exposure to any household acid carries a meaningful cancer risk.

Occupational limits – Hydrochloric Acid

Current NIOSH/OSHA limits:

NIOSH REL ceiling: 5 ppm (7 mg/m³)

OSHA PEL ceiling: 5 ppm (7 mg/m³)

NIOSH IDLH: 50 ppm

The old numerical HCl workplace limits remain broadly accurate.

Occupational limits – Nitric Acid

Current values:

NIOSH REL TWA: 2 ppm (5 mg/m³)

NIOSH STEL: 4 ppm (10 mg/m³)

OSHA PEL TWA: 2 ppm (5 mg/m³)

NIOSH IDLH: 25 ppm

Correction to the old text

The 4-ppm STEL is a NIOSH recommendation, not part of the current federal OSHA PEL.

Monitoring

Patients with significant injury require monitoring for:

• Airway edema
• Respiratory failure
• Hemorrhage
• Perforation
• Shock
• Electrolyte abnormalities
• AKI

Severe injury generally warrants:

• ICU-level monitoring
• Gastroenterology consultation
• Surgical consultation

depending on findings.

Admission

Admit patients with:

• Significant intentional ingestion
• Drooling
• Dysphagia/odynophagia
• Oral/pharyngeal burns plus concerning exposure
• Stridor
• Respiratory symptoms
• Significant chest/abdominal pain
• Hematemesis
• Hemodynamic instability
• Abnormal CT/EGD
• Grade IIb or III injury

ICU care is appropriate for:

• Threatened airway
• Respiratory failure
• Shock
• Severe bleeding
• Full-thickness necrosis
• Perforation

Disposition

Patients with a clearly trivial accidental exposure may be discharged when:

• Completely asymptomatic
• Able to eat/drink normally
• Normal examination
• No concerning product characteristics
• Reliable observation is available

For significant exposure:

Do not use an arbitrary fixed observation period as a substitute for risk assessment.

Intentional ingestions generally deserve formal GI injury assessment even when symptoms initially appear mild.

Prognosis

Grade 0–I

Usually excellent.

Grade IIa

Generally favorable, with low stricture risk.

Grade IIb

Substantial risk of:

• Esophageal stricture
• Nutritional complications

Grade III

High risk of:

• Hemorrhage
• Perforation
• Mediastinitis/peritonitis
• Shock
• Stricture
• Death

Outcome depends heavily on recognizing transmural necrosis before perforation occurs.

Important Pitfalls

1. Defining a caustic simply as “pH <7”

Acidity alone does not determine corrosive potential.

Concentration and titratable acidity matter greatly.

2. Assuming acids only injure the stomach

Acids may produce:

Severe esophageal as well as gastric injury.

3. Using oral burns to rule injury in or out

The mouth may look normal despite serious distal injury.

4. Waiting too long to secure the airway

Progressive laryngeal edema can make later intubation extremely difficult.

Hoarseness + stridor + progressive swelling → early airway intervention.

5. Inducing vomiting

Never induce emesis.

6. Neutralizing acid with alkali

Never routinely neutralize.

The reaction may generate heat and worsen injury.

7. Automatically giving milk or water

The old 4–8 oz dilution recommendation is no longer routine modern practice.

Benefit is unproven and adverse effects are possible.

8. Giving activated charcoal

Charcoal poorly adsorbs acids and can interfere with endoscopy.

Routine charcoal is contraindicated/not useful.

9. Performing gastric lavage

Caustic injury + instrumentation = increased perforation risk.

Routine lavage has no role.

10. Blindly inserting an NG tube

Use endoscopic/surgical guidance when GI access is necessary.

11. Giving routine steroids for grade II injury

Modern evidence does not demonstrate consistent prevention of strictures.

12. Giving prophylactic antibiotics to everyone

Antibiotics are for:

• Infection
• Perforation
• Selected severe necrosis

not routine uncomplicated exposure.

13. Treating EGD and CT as competitors

Modern severe-ingestion assessment often uses them complementarily:

EGD → luminal/mucosal grading

Contrast CT → depth/transmural necrosis + adjacent structures

14. Missing acid-specific systemic effects

Think beyond the burn:

• Oxalic → hypocalcemia/renal injury
• Acetic/formic → hemolysis/systemic toxicity
• Phosphoric → hyperphosphatemia
• HF → life-threatening fluoride toxicity

15. Forgetting long-term follow-up

Deep injuries can produce:

• Strictures
• Gastric outlet obstruction
• Long-term esophageal cancer risk

even after the acute episode resolves.

High-Yield Toxicology Pearls

Acid caustic ingestion = airway + GI necrosis problem

Think:

Drooling/dysphagia + chest/abdominal pain after strong acid → significant corrosive injury until assessed

Key points:

• “pH <7” alone does not define a dangerous caustic
• Strong acids classically cause coagulative necrosis
• Concentrated acids can still cause deep transmural injury
• Gastric injury is common, but severe esophageal injury also occurs
• Normal mouth does not exclude severe esophageal/gastric burns
• Threatened airway → early intubation
• Do not induce vomiting
• Do not neutralize with alkali
• Routine milk/water dilution is no longer recommended
• Activated charcoal is not useful for acids
• Gastric lavage is contraindicated/not routine
• Avoid blind NG placement
• Significant symptomatic or intentional ingestion → early GI injury assessment
• EGD is generally performed within ~24 h when indicated
• Contrast-enhanced CT is especially valuable for:
• 
  
• Suspected deep necrosis
• Perforation
• Surgical decision-making
• CT finding of absent wall enhancement suggests transmural necrosis
• Zargar IIb/III injury → high stricture risk
• Emergency surgery for:
• 
  
• Perforation
• Peritonitis/mediastinitis
• Full-thickness necrosis
• Uncontrolled hemorrhage
• Routine corticosteroids do not reliably prevent strictures
• Routine prophylactic antibiotics are not indicated
• Strictures may become symptomatic ~3 weeks or later
• Established strictures → endoscopic dilation
• Severe previous caustic injury carries increased long-term esophageal SCC risk
• Occupational strong inorganic acid mists are IARC Group 1 carcinogens
• HCl:
• 
  
• OSHA/NIOSH ceiling 5 ppm
• IDLH 50 ppm
• Nitric acid:
• 
  
• OSHA/NIOSH TWA 2 ppm
• NIOSH STEL 4 ppm
• IDLH 25 ppm
• There is no general antidote