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Introduction

A wide variety of chemical and physical agents may cause caustic or corrosive injury. They include mineral and organic acids, alkalis, oxidizing agents, denaturants, some hydrocarbons, and agents that cause exothermic reactions. Although the mechanism and the severity of injury vary, the consequences of mucosal damage and permanent scarring are shared by all these agents.

Button batteries are small disk-shaped batteries used in electronic devices such as watches, toys, and LED lights. Ingestion requires special consideration due to the potential for severe injury. They can generate an electric current across a mucosal surface and contain caustic metal salts such as mercuric chloride that may cause corrosive injury.

Mechanism of Toxicity

  1. Acids cause an immediate coagulation-type necrosis, creating an eschar that may limit deep tissue injury.
  2. In contrast, alkalis cause a liquefactive necrosis with saponification and penetration into deeper tissues, resulting in extensive damage.
  3. Other agents may act by alkylating, oxidizing, reducing, or denaturing cellular proteins or by defatting surface tissues.
  4. Button batteries cause injury by leakage of the caustic metal salts and burns from local discharge of electric current at the site of impaction.

Toxic Dose

There is no specific toxic dose or level because the concentration of products and the potency of caustic effects vary widely. For example, whereas the acetic acid concentration in most household vinegar is 5-10%, that of “Russian vinegar” may be as high as 70%. The pH or concentration of the solution may indicate the potential for serious injury. A pH lower than 2 or higher than 12 increases the risk for injury. For alkalis, the titratable alkalinity (concentration of the base) is a better predictor of caustic effect than is the pH. Injury is also related to the volume ingested and duration of exposure.

Clinical Presentation

  1. Inhalation of corrosive gases (eg, chlorine and ammonia) may cause upper respiratory tract injury, with stridor, hoarseness, wheezing, and noncardiogenic pulmonary edema. Pulmonary symptoms may be delayed after exposure to gases with low water solubility (eg, nitrogen dioxide and phosgene).
  2. Eye or skin exposure usually results in immediate pain and redness, followed by blistering. Conjunctivitis and lacrimation are common. Serious full-thickness burns and blindness can occur.
  3. Ingestion can cause dysphagia, drooling, and pain in the mouth, throat, chest, or abdomen. Esophageal or gastric perforation can occur, accompanied by severe chest or abdominal pain and signs of peritonitis. Hematemesis and shock can occur. Free air may be visible on radiographs of the mediastinum or abdomen. Systemic acidosis has been reported after acid ingestion and may be caused partly by absorption of hydrogen ions. Scarring of the esophagus or stomach can result in permanent stricture formation and chronic dysphagia. Long-term complications also include an increased risk of esophageal malignancy.
  4. Systemic toxicity can occur after inhalation, skin exposure, or ingestion of a variety of agents (Table II-20).
  5. Button batteries can cause serious injury if they become impacted or adherent in the esophagus, leading to perforation into the aorta or mediastinum. Most such cases involve larger (25-mm-diameter) batteries. If button batteries reach the stomach without impaction in the esophagus, they often pass uneventfully via the stools within several days, but case series suggest there is still a risk of injury.
TABLE II-20. CAUSTIC AGENTS WITH SYSTEMIC EFFECTS (SELECTED CAUSES)a
AgentSystemic Symptoms
FormaldehydeMetabolic acidosis, formate poisoning
Hydrofluoric acidHypocalcemia, hyperkalemia
Methylene chlorideCNS depression, cardiac dysrhythmias, converted to carbon monoxide
Oxalic acidHypocalcemia, renal injury
ParaquatPulmonary fibrosis
PermanganateMethemoglobinemia
PhenolSeizures, coma, hepatic and renal injury
PhosphorusHepatic and renal injury
Picric acidRenal injury
Silver nitrateMethemoglobinemia
Tannic acidHepatic injury

aReproduced with permission from Edelman PA. Chemical and electrical burns. In: Achauer BM, ed. Management of the Burned Patient, New York; Appleton & Lange (McGraw Hill); 1987.

Diagnosis

Is based on a history of exposure to a corrosive agent and characteristic findings of skin, eye, or mucosal irritation or redness and the presence of injury to the GI tract. Victims with oral or esophageal injury nearly always have drooling or pain on swallowing.

  1. Endoscopy. Esophageal or gastric injury is unlikely after ingestion if the patient is completely asymptomatic, but studies have shown repeatedly that a small number of patients will have injury in the absence of oral burns or obvious dysphagia. For this reason, some authorities recommend endoscopy for all patients regardless of symptoms.
  2. Radiographs of the chest and abdomen usually reveal impacted button batteries. Plain radiographs and CT scans may also demonstrate air in the mediastinum from esophageal perforation or free abdominal air from GI perforation.
  3. Specific levels. See the specific chemical. Urine mercury levels have been reported to be slightly elevated after some 15-mm mercuric oxide button battery ingestions.
  4. Other useful laboratory studies include CBC, electrolytes, glucose, arterial blood gases, and radiographic imaging.

Treatment

  1. Emergency and supportive measures
    1. Inhalation. Give supplemental oxygen and observe closely for signs of progressive airway obstruction or noncardiogenic pulmonary edema.
    2. Ingestion
      1. Assessment of the airway is paramount. Early intubation should be considered to avoid progressive airway obstruction from oropharyngeal edema.
      2. Otherwise, if tolerated, immediately give water or milk to drink. Provide antiemetics (eg, ondansetron, 8 mg IV in adults or 0.15 mg/kg in children to prevent additional esophageal injury from emesis.
      3. If esophageal or gastric perforation is suspected, obtain immediate surgical or endoscopic consultation.
      4. Patients with mediastinitis or peritonitis need broad-spectrum antibiotics and aggressive management of hemorrhage and septic shock.
  2. Specific drugs and antidotes. For most agents, there is no specific antidote (see for hydrofluoric acid burns and for phenol burns). The use of corticosteroids is controversial. While prolonged courses of steroids are associated with esophageal perforation and serious infection, recent studies indicate that a short course of steroids may benefit select patient populations (Grade 2B alkaline injuries).
  3. Decontamination. Caution: Rescuers should use appropriate respiratory and skin-protective equipment.
    1. Inhalation. Remove from exposure. Give supplemental oxygen as needed.
    2. Skin and eyes. Remove all clothing. Wash skin and irrigate eyes with copious water or saline.
    3. Ingestion
      1. Prehospital. If tolerated, immediately give water or milk to drink. Do not induce vomiting or give pH-neutralizing solutions (eg, dilute vinegar or bicarbonate).
      2. Hospital. Aspiration of gastric liquid contents with a nasogastric tube to remove the corrosive material is controversial but possibly beneficial in acute liquid corrosive ingestion, and it would otherwise be required before endoscopy. Use a soft, flexible tube and lavage with repeated aliquots of water or saline, frequently checking the pH of the washings.
      3. In general, do not give activated charcoal, as it may interfere with visibility at endoscopy. Charcoal may be appropriate if the ingested agent can cause significant systemic toxicity.
      4. Button batteries lodged in the esophagus require immediate endoscopic removal to prevent rapid perforation. Batteries located in the stomach can also cause significant mucosal damage; strongly consider prompt endoscopic removal especially in symptomatic patients (even if minor). If endoscopy is not performed, ensure complete passage through the GI tract with serial radiographs.
  4. Enhanced elimination. In general, there is no role for any of these procedures (see specific chemical).