DESCRIPTION

Caustic alkaline chemicals are typically used in a wide array of cleaning products.

FORMS AND USES

• Caustic alkaline (basic) substances include ammonia, borax, calcium carbide, calcium hydroxide, calcium oxide, caustic potash, caustic soda, Clinitest tablets, diethanolamine, diethylenetriamine, isopropylamine, isopropyl amino-ethanol, lime, lye, Portland cement, potassium carbonate, potassium hydroxide, potassium nitrate, potassium oxide, sodium carbonate, sodium hydroxide, sodium metasilicate, sodium oxide, sodium silicate, sodium tripolyphosphate, tetraethylenepentamine, triethylenetetramine, and trisodium phosphate.
• Corrosive alkaline chemicals are used in drain and pipeline cleaners; oven cleaners; denture cleaners; bathroom, household, and industrial cleaners; hair relaxers; electric dishwasher soaps and low-phosphate detergents; fertilizers; Portland cement; automobile air bags; and Clinitest tablets.

TOXIC DOSE

Just a few milliliters of highly caustic alkali (e.g., sodium hydroxide) can cause severe injury.

PATHOPHYSIOLOGY

• Alkaline corrosives saponify the fat in cell membranes, destroying the cell and causing liquefaction necrosis.
• These substances may be simply irritating or truly corrosive, depending on the molarity, concentration, amount ingested, and other factors.
• In general, significant gastrointestinal injury is not associated with alkaline products with a pH of less than 11.5.

EPIDEMIOLOGY

• Poisoning is common.
• Toxic effects following exposure are typically mild after inadvertent "taste" exposures of a household product in children.
• Severe injury or death occur more often after suicidal ingestion or industrial accidents.

CAUSES

• Toxic ingestion is usually accidental.
• Child neglect or abuse should be considered if the patient is less than 1 year of age, suicide attempt if the patient is over 6 years of age.

RISK FACTORS

Underlying pulmonary disease confers greater risk after inhalation.

WORKPLACE STANDARDS

Sodium hydroxide

• ACGIH. TLV TWA is 2 mg/m³.
• OSHA. PEL TWA is 2 mg/m³.
• NIOSH. IDLH is 10 mg/m³.

Section Outline:

• DESCRIPTION
• FORMS AND USES
• TOXIC DOSE
• PATHOPHYSIOLOGY
• EPIDEMIOLOGY
• CAUSES
• RISK FACTORS
• WORKPLACE STANDARDS

DIFFERENTIAL DIAGNOSIS

• Toxicologic causes of caustic injury include ingestion of iron, acids, button batteries, phenol, copper sulfate, hydrogen peroxide, silver nitrate, zinc chloride, ethylene dichloride, mercuric chloride, formaldehyde, and other compounds.
• Nontoxicologic causes of caustic injury depend on the route of injury.
  • After ingestion, caustic injury should be differentiated from esophagitis, gastritis, peptic or duodenal ulcers, or perforated ulcer.
  • After inhalation exposure, caustic injury should be differentiated from reactive airway disease, epiglottitis, adult respiratory distress syndrome, pulmonary edema, and upper airway edema of other etiologies.

SIGNS AND SYMPTOMS

• Caustic burns of the mouth and esophagus are most common, but gastric or intestinal burns may occur with large ingestion; the presence or absence of oral burns does not correlate with the presence of esophageal burns.
• Inhalation exposure can cause wheezing, upper airway edema, and, in severe cases, pulmonary edema.
• Shock, metabolic acidosis, and renal failure are rare complications seen with severe gastrointestinal burns.

Vital Signs

Tachycardia is common; hypotension may develop in severe cases.

HEENT

• Ocular exposure may result in corneal burns, opacification, visual loss, and/or perforated globe.
• Oropharyngeal burns may develop.

Dermatologic

Dermal contact may cause irritation or chemical burns.

Pulmonary

• Inhalation may cause bronchospasm, upper airway edema or obstruction, laryngospasm, or adult respiratory distress syndrome.
• Young children are at greater risk of severe upper airway edema after ingestion.

Gastrointestinal

• Gastrointestinal burns may develop after ingestion.
• Esophageal burns are most common, occurring in 5% to 35% of patients.
• Gastric burns are less common, and intestinal burns are unusual except after large ingestions.
• Most patients with significant gastrointestinal burns develop vomiting, drooling, and stridor.
• Peritoneal signs may be present if perforation occurs.

Renal

Renal failure is a rare complication of severe burns, accompanied by shock and gastrointestinal bleeding.

Fluids and Electrolytes

Metabolic acidosis may develop in patients with severe gastrointestinal bleeding or massive tissue necrosis after corrosive ingestion.

PROCEDURES AND LABORATORY TESTS

Essential Tests

No tests may be needed after a minor "sip" ingestion of a household product.

Recommended Tests

• Complete blood count, serum electrolytes, BUN, and creatinine should be assayed in patients with gastrointestinal symptoms; anemia, metabolic acidosis, and renal failure are usually the result of complications (bleeding, shock, and massive tissue necrosis) and are associated with a poorer prognosis.
• Arterial blood gases should be measured in patients with pulmonary symptoms; hypoxia generally occurs only after severe inhalation exposure.
• Chest radiography should be undertaken in patients with pulmonary symptoms; upright chest and abdominal radiographs should be taken when perforation is suspected.
• Barium swallow imaging may be needed to detect gastrointestinal strictures and obstruction in the weeks after ingestion.
• Gastrointestinal endoscopy should be performed within 24 hours of ingestion in patients at risk for significant burns; indications include stridor, drooling, or vomiting, and adults with suicidal or large ingestions (the absence of oropharyngeal burns does not reliably exclude esophageal or gastric burns).
  • Grade I. Mucosal hyperemia AND superficial epithelial desquamation with intact mucous membranes
  • Grade II. Superficial blisters, ulcers, and hyperemia; patchy membranous mucosal exudates.
  • Grade III. Necrosis and total loss of esophageal epithelium.

Section Outline:

• DIFFERENTIAL DIAGNOSIS
• SIGNS AND SYMPTOMS
  • Vital Signs
  • HEENT
  • Dermatologic
  • Pulmonary
  • Gastrointestinal
  • Renal
  • Fluids and Electrolytes
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests

• Treatment should focus on airway control, support of hemodynamic function, and assessment of burn severity.
• Intubation can be extremely difficult; crico-thyrotomy or tracheostomy may be necessary.
• Dose and time of exposure should be determined for all substances involved.
• Surgical evaluation must be considered for any patient with Grade III esophageal injury to assess the extent of gastric or duodenal burns.
• Any patient with a suspected perforation is a surgical emergency; the absence of free air on abdominal or chest radiographs does not reliably exclude perforation.

DIRECTING PATIENT COURSE

The health-care professional should call the poison control center when:

• Serious effects (Grade I or Grade II burns or complications of hypotension, acidosis, hypoxia, gastrointestinal bleeding, or perforation) are present.
• Toxic effects are not consistent with alkaline corrosive poisoning.
• Coingestant or underlying disease presents an unusual problem.

The patient should be referred to a health-care facility when:

• Attempted suicide or homicide is possible.
• Patient or caregiver seems unreliable.
• Toxic effects are present.
• Coingestant or underlying disease presents an unusual problem.

Admission Considerations

Inpatient management is warranted if the patient exhibits Grade II or III burns, bleeding, hypotension, respiratory distress, wheezing, hypoxia, of upper airway injury, or if endoscopy is needed.

DECONTAMINATION

• Decontamination is not recommended after caustic ingestion.
• Emesis should not be induced with ipecac.
• Neutralization with an acidic solution should not be attempted because it may cause thermal burns.
• Ingestion may be diluted with a small amount (4 ounces) of milk or water; nothing else should be taken orally until injury is evaluated.
• Gastric lavage should not be performed because this may worsen gastrointestinal injury.
• Activated charcoal should not be administered unless a coingestant is suspected because it may induce vomiting and obscure endoscopy findings.
• Exposed eyes should be irrigated with sterile water or saline for at least 20 minutes; irrigation should continue until the pH of the cul de sac has returned to normal.

ANTIDOTES

There is no specific antidote for alkaline corrosive poisoning.

ADJUNCTIVE TREATMENT

• Steroid administration is recommended in certain cases to reduce stricture formation after alkaline-induced esophageal burns.
  • Steroids should be considered in patients with Grade II burns.
  • They are not indicated with Grade I burns because strictures are unlikely to develop.
  • Steroids also should be avoided with Grade III burns because the risk of perforation is greater and strictures often form regardless of therapy.
  • The adult or pediatric dose is 0.1 mg/kg of dexamethasone or prednisone 1 to 2.5 mg/kg for 3 weeks then taper off.
• Prophylactic use of antibiotics has not shown any benefit.
• Hypotension is treated in the standard manner, beginning with infusion of 0.9% saline, 10 to 20 ml/kg. Further management is described in SECTION II, Hypotension chapter.

Section Outline:

• DIRECTING PATIENT COURSE
  • Admission Considerations
• DECONTAMINATION
• ANTIDOTES
• ADJUNCTIVE TREATMENT

PATIENT MONITORING

• Airway must be monitored carefully in patients with inhalation or significant oral exposure.
• Blood pressure and temperature should be monitored, and serial abdominal examinations should be performed in patients with Grade III burns.

EXPECTED COURSE AND PROGNOSIS

• Children generally do well after taste ingestion.
• Adults with deliberate ingestion or industrial exposures are most likely to sustain complications or death.
• Delayed sequelae of gastrointestinal burns may include stricture formation, gastrointestinal bleeding, pyloric stenosis, perforation, and tracheoesophageal or aortotracheal fistula formation.
• Patients who develop esophageal burns and stricture are at increased risk for esophageal cancer (1,000-fold increase in risk; latency 12-40 years).

DISCHARGE CRITERIA/INSTRUCTIONS

• From the emergency department. Patients who are asymptomatic after taste ingestion and patients with Grade I burns or documented absence of gastrointestinal burns who are tolerating oral intake may be discharged after 6 hours of observation and psychiatric evaluation, if needed.
• From the hospital. Patients with documented Grade II or III burns may be discharged when they are tolerating a soft diet (or parenteral nutrition), with follow-up endoscopy or upper gastrointestinal series to detect stricture formation.

Section Outline:

• PATIENT MONITORING
• EXPECTED COURSE AND PROGNOSIS
• DISCHARGE CRITERIA/INSTRUCTIONS

DIAGNOSIS

The absence of oropharyngeal burns does not reliably exclude esophageal or gastric burns.

TREATMENT

Children less than 1 year of age are at increased risk for developing upper airway edema requiring intubation after minor alkaline corrosive ingestion.

FOLLOW-UP

Patients with stricture formation require periodic evaluation for esophageal carcinoma.

Section Outline:

• DIAGNOSIS
• TREATMENT
• FOLLOW-UP

Toxic effect of corrosive aromatics, acids, and caustic alkalis: caustic alkalis.

See Also: SECTION II, Hypotension chapter.

RECOMMENDED READING

Hoffman RS. Caustics and batteries. In: Goldfrank LR, Flomenbaum NE, Lewin NA, et al., eds. Goldfrank's toxicologic emergencies, 6th ed. Norwalk, CT: Appleton & Lange, 1998.

Author: Katherine M. Hurlbut

Reviewer: Richard C. Dart