DESCRIPTION

Acids are caustic substances with a pH of less than 7.

FORMS AND USES

• Acidic caustic substances include phosphoric acid, sulfuric acid, oxalic acid, acetic acid, hydrochloric acid, formic acid, and nitric acid. Hydrofluoric acid, boric acid, chromic acid, selenious acids are included in separate chapters.
• Acids are used in a variety of household products: toilet bowl cleaners, descalers, metal cleaners, antirust compounds, battery fluid, and pool sanitizers.
• Industrial uses of concentrated acids include plating, photography, cement manufacturing, leather tanning, bleaching, metal refining, plumbing, engraving, metal cleaning, rustproofing, chemicals, munitions and fertilizer manufacturing, hat making, printing, dyeing, rayon manufacturing, hair-wave neutralizing, airplane glue manufacturing, blueprint paper production, cellulose formate manufacturing, and many other areas of production.

TOXIC DOSE

The toxic dose varies tremendously by type and concentration of acid.

PATHOPHYSIOLOGY

• Acids cause coagulation necrosis on contact with mucosal surfaces, destroying submucosal structures.
• Fumes may cause airway irritation, bronchospasm, and adult respiratory distress syndrome in severe cases.

EPIDEMIOLOGY

• Poisoning is common.
• Toxic effects following exposure are typically mild.
• Death occurs after ingestion of a large amount of dilute solution or a smaller amount of concentrated, highly acidic compounds.
• Occupational exposure to acid mists is associated with laryngeal cancer.

CAUSES

• Toxic ingestion is usually accidental in children.
• Adult toxicity is most likely to result from suicidal or occupational exposure.
• Child neglect or abuse should be considered if the patient is less than 1 year of age, suicide attempt if the patient is older than 6 years of age.

WORKPLACE STANDARDS

Hydrochloric Acid

• ACGIH. TLV ceiling is 5 ppm (7 mg/m³).
• OSHA. PEL ceiling is 5 ppm (7 mg/m³).
• NIOSH
  • REL ceiling is 5 ppm (7mg/m³).
  • IDLH is 50 ppm.

Nitric Acid

• OSHA
  • PEL TWA is 2 ppm (5 mg/m³).
  • STEL is 4 ppm (10 mg/m³).
• NIOSH. IDLH is 25 ppm.

Section Outline:

• DESCRIPTION
• FORMS AND USES
• TOXIC DOSE
• PATHOPHYSIOLOGY
• EPIDEMIOLOGY
• CAUSES
• WORKPLACE STANDARDS
  • Hydrochloric Acid
  • Nitric Acid

DIFFERENTIAL DIAGNOSIS

• Other toxicologic causes of gastrointestinal injury include ingestion of alkaline caustic agents or massive ingestion of hypochlorite or other gastrointestinal irritant.
• Nontoxicologic causes of acute gastrointestinal pain and bleeding include peptic ulcer disease and perforated viscus.

SIGNS AND SYMPTOMS

• Ingestion may produce gastrointestinal burns, most commonly in the stomach, but oral and esophageal burns may occur as well; perforation is a rare complication.
• Metabolic acidosis, shock, gastrointestinal hemorrhage, and renal failure are rare complications of serious ingestion.

Vital Signs

Tachypnea is common after inhalation.

HEENT

• Ocular exposure effects range from corneal burns to opacification, blindness, and perforated globe.
• Oral burns may develop.

Dermatologic

Dermal toxicity ranges from irritation to full-thickness burns.

Cardiovascular

Cardiovascular collapse is a rare complication of severe exposure.

Pulmonary

• Bronchospasm may occur after inhalation.
• In severe cases adult respiratory distress syndrome may develop.
• Upper airway edema may develop after inhalation or aspiration.

Gastrointestinal

• Injuries are more common after deliberate ingestion of strong acids.
• Esophageal injury is usually maximal in the middle and lower thirds of the esophagus; gastric burns are more common.
• Gastrointestinal bleeding or perforation may occur acutely after grade III (full-thickness) injury.

Renal

Acute renal failure occurs rarely, generally caused by hypotension.

Hematologic

• Hemolysis has occurred after severe formic, acetic, or sulfuric acid exposure.
• Disseminated intravascular coagulation is a rare complication in severe cases.

Fluids and Electrolytes

• Metabolic acidosis may develop in cases complicated by shock.
• Extensive gastrointestinal injury may result in massive fluid loss.
• Hyperkalemia may develop secondary to hemolysis.
• Hyperphosphatemia has occurred after phosphoric acid ingestion.

PROCEDURES AND LABORATORY TESTS

Essential Tests

• Complete blood count should be obtained to detect hemolysis or gastrointestinal bleeding.
• Electrolytes, BUN, and creatinine should be obtained to evaluate for metabolic acidosis or renal failure associated with severe injury and shock.

Recommended Tests

• Coagulation studies (prothrombin time/partial thromboplastin time or international normalized ratio, fibrinogen, fibrin degradation products) should be obtained in patients with severe effects.
• Chest radiograph should be obtained for pulmonary symptoms or if gastrointestinal perforation is expected.
• A barium swallow and small-bowel follow-through should be obtained several weeks after ingestion to assess delayed gastrointestinal complications, such as strictures, that may develop after grade II or III injury (burn extends deeper than mucosa of gastrointestinal tract).
• Endoscopy is recommended after deliberate or large ingestion and in patients who are symptomatic or have oral burns; the likelihood of complications (strictures, obstruction, bleeding, and perforation) is related to the severity of the injury.
  • 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
  • Cardiovascular
  • Pulmonary
  • Gastrointestinal
  • Renal
  • Hematologic
  • Fluids and Electrolytes
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests

• Treatment should focus on hemodynamic support and evaluating the injury.
• Aggressive airway management after aspiration or inhalation exposure is indicated because airway edema may develop rapidly.
• Dose and time of exposure should be determined for all substances involved.

DIRECTING PATIENT COURSE

• Emergency surgical evaluation is needed for patients with signs of perforation.
• Laparoscopic evaluation should be considered in patients with third-degree injury because transmucosal gastric burns or perforation may be present.

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

• Hypotension, gastrointestinal bleeding, perforation, metabolic acidosis, or other severe effects are present.
• Toxic effects are not consistent with acid exposure.
• Coingestant, drug interaction, 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.
• Any symptoms develop.
• Coingestant, drug interaction, or underlying disease presents an unusual problem.

Admission Considerations

Inpatient management is warranted if:

• Patients have oral burns or symptoms (drooling, dysphagia, and stridor), unless endoscopy is immediately available and excludes grade II or III injury.
• Patients have grade II or III gastrointestinal injury noted on endoscopy.
• Patients exhibit dyspnea, wheezing, stridor, upper airway edema or burns, or any degree of respiratory distress.

DECONTAMINATION

Out of Hospital

• Emesis should not be induced.
• Neutralization with a basic solution should not be attempted because it may cause thermal injury.
• Ingestion should be diluted with 4 to 8 ounces of milk or water.
• Exposed mouth, skin, and eyes should be irrigated copiously with water.
• Patients with inhalation injury should be removed from further exposure.

In Hospital

• Oxygen should be administered to all patients with pulmonary symptoms.
• Following an ingestion, gastric lavage should not be performed because of the potential for perforation.
• Ingestion that occurred within the preceding 30 minutes should be diluted with 4 to 8 ounces of milk or water; neutralization with an alkaline solution is not recommended.
• Activated charcoal should not be administered unless a toxic coingestant is involved.
• 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.
• Exposed skin should be irrigated with copious amounts of water.

ANTIDOTES

There is no specific antidote for caustic acid poisoning.

ADJUNCTIVE TREATMENT

• Intravenous crystalloid (10 to 20 ml/kg) should be administered for hypotension.
• Steroids should be considered for patients showing second-degree burns under endoscopy. The decision to administer steroids should involve a toxicologist, gastroenterologist, or surgeon experienced in managing these injuries.
  • Steroids are not indicated for first-degree burns because stricture formation is unlikely.
  • They are generally not indicated for third-degree burns because steroids increase the risk of perforation.
• Antibiotics are used only for suspected infection or perforation.
• Packed red blood cells and fresh frozen plasma may be needed if severe hemorrhage or hemolysis develops.

Section Outline:

• DIRECTING PATIENT COURSE
  • Admission Considerations
• DECONTAMINATION
  • Out of Hospital
  • In Hospital
• ANTIDOTES
• ADJUNCTIVE TREATMENT

PATIENT MONITORING

Patients with grade II or III gastrointestinal injury, those awaiting endoscopic evaluation, and those with significant inhalation exposure should be monitored in an intensive care setting.

EXPECTED COURSE AND PROGNOSIS

• Patients with first-degree injuries generally recover uneventfully.
• Patients with second-degree injuries may develop fistulas, strictures, or gastric outlet obstruction, but generally survive.
• Acute third-degree injuries are often complicated by gastrointestinal bleeding, shock, perforation, stricture, renal failure, and high mortality rate.

DISCHARGE CRITERIA/INSTRUCTIONS

• From the emergency department. Patients who are asymptomatic after taste ingestion and patients with no visible gastrointestinal injury or those with documented grade I gastrointestinal injury and tolerating oral intake may be discharged after a 6-hour observation period and psychiatric evaluation, if needed.
• From the hospital.
  • Patients with documented grade II injuries may be discharged when they are tolerating a soft diet, with follow-up endoscopy or upper gastrointestinal series to detect sequelae.
  • Patients with grade III injuries may be discharged when complications have resolved and adequate nutrition (enteral or parenteral) is achieved.

Section Outline:

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

DIAGNOSIS

• Oral burns may not adequately reflect the severity of distal gastrointestinal injury.
• Upper airway edema may develop abruptly after inhalation or aspiration.

FOLLOW-UP

Patients with grade II esophageal injury are at risk for stricture formation, gastric outlet obstruction, and possibly carcinoma; periodic follow-up and possibly dilation or surgery may be required.

Section Outline:

• DIAGNOSIS
• FOLLOW-UP

Toxic effect of acids.

See Also: SECTION II, Hypotension chapter; SECTION IV, Ammonia, Boric Acid and Borates, Caustics—Basic, Chromium, Hydrofluoric Acid, and Selenium chapters.

RECOMMENDED READING

Dilawari JB, Singh S, Rao PN, et al. Corrosive acid ingestion in man: a clinical and endoscopic study. Gut 1984;25:183-187.

Wu M, Lai W. Surgical management of extensive corrosive injuries of the alimentary tract. Surg Gynecol Obstet 1993;177:12-16.

Zarger SA, Kochhar R, Nagi B, et al. Ingestion of corrosive acids: spectrum of injury to upper gastrointestinal tract and natural history. Gastroenterol 1989;97:702-707.

Author: Katherine M. Hurlbut

Reviewer: Richard C. Dart