Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 125. Alkalis and Acids

William J.  Lewander

Alfred  Aleguas

HIGH-YIELD FACTS

• Asymptomatic children with a history of alkali or acid ingestion should be observed for a few hours and may be discharged from the emergency department if oral intake without discomfort is demonstrated.

• All symptomatic children should be admitted to hospital.

• Eye exposures require urgent and copious irrigation and referral to an ophthalmologist if injury is present.

Alkalis and acids damage or destroy living tissue on direct contact. This process is generically referred to as corrosion. A caustic is an alkali. Consumer product examples of alkalis and acids include drain cleaners, automatic dishwasher detergents, hair relaxer products, toilet bowl cleaners, and bathroom tile cleaners. Improvements in safety packaging, child-resistant closures, and federal regulations lowering the maximum concentration for many household alkalis and acids have decreased the overall incidence of unintentional corrosive exposures in children. Despite this success, thousands of accidental and intentional exposures occur annually1 and continue to result in a significant burden on health care resources.2

Exposures in small children are usually limited by pain on contact and generally involve small amounts. Most exposures occur in children younger than 6 years, but this group accounts for only 1.7% of the fatalities.1 In contrast, intentional ingestion by adolescents and adults may involve larger quantities, which generally have a worse outcome. Long-term survivors of moderate and severe esophageal caustic injuries have a 1000-fold increased risk of esophageal carcinomas.3

PATHOPHYSIOLOGY

Alkalis and acids cause tissue damage by different mechanisms. Alkalis cause liquefaction necrosis by a process involving saponification of fatty acids within cell membranes and protein disruption. This produces a rapid, penetrating injury associated with a pronounced exothermic reaction, which can occur in seconds. Ingestions of household bleach containing dilute sodium hypochlorite rarely cause serious injury.4 Higher concentrations found in industrial strength products and lye products containing sodium or potassium hydroxide can cause severe esophageal injuries.5

Acids cause tissue damage by a process known as coagulation necrosis. Hydrogen ions are released when acids come in contact with water and cause tissue damage. A coagulum or eschar may form in some cases and limits the extent and depth of injury. Toilet bowl cleaners and anticorrosive cleaners containing higher concentrations of hydrochloric acid can cause serious injuries.

Acids and alkalis can cause both esophageal and gastric injuries. Clinical experience has demonstrated that multiple sites are often affected.6 Following the initial tissue contact, the acid or alkali undergoes a process of neutralization resulting in an exothermic reaction, which may worsen the injury.7

The initial acute inflammatory reaction proceeds on to necrosis. The necrotic tissue is sloughed resulting in ulceration or perforation. After a few days and during the next few weeks granulation tissue develops. Because this tissue is weak, perforation may occur during this period. This is followed by cicatrization producing variable degrees of scarring contracture and stricture formation.

The severity of injury is modulated by several factors (Table 125-1). Solids such as crystals or granules can produce intense localized oral, pharyngeal, or upper esophageal injury while liquids, especially strong bases, tend to produce circumferential lesions in the esophagus, which often form strictures. Products with a pH less than 2 or with a pH of 12.5 or greater are likely to cause significant esophageal injury.8 Increasing volume, concentration, and the titratable alkaline or acidic reserve of the agent correlates with esophageal injury.9

TABLE 125-1

Factors Modulating the Severity of Corrosive Injury

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The presence of stomach contents may decrease tissue injury by exerting a buffering effect. Pylorospasm prevents gastric emptying, which increases contact time of the corrosive within the stomach and results in more severe gastric injury. Any reflux of ingested material back into the esophagus re-exposes the tissue to further corrosive damage.

Caustic burns are graded first, second, and third degree based on their endoscopic appearance.10 Grade I injuries are superficial, involve the mucosa and resemble a sunburn. Strictures would not be expected to develop following this type of injury.

Grade II partial thickness injuries involve the mucosa and submucosa and demonstrate ulcers and hemorrhage. Overall they have a 20% risk of stricture formation, which increases to 75% when they are circumferential.11

Grade III burns are full thickness, demonstrate deep ulcers and areas of necrosis and are at risk to perforate. Ninety percent of survivors develop strictures.12

PRESENTATION

The signs and symptoms of caustic ingestion depend on the location and severity of the injury. The clinical presentation may range from asymptomatic to fulminant respiratory distress or shock. The gastrointestinal tract, respiratory tract, eyes, and skin are potential sites for injury. Common complaints include oral or abdominal pain, vomiting, and drooling.13 Dysphagia, crying, hematemesis, wheezing, coughing, and chest pain may also be seen. Laryngeal edema with accompanying upper airway compromise may present with stridor, dyspnea, and dysphonia and develop over minutes to hours. Peritoneal signs in conjunction with systemic toxicity and shock may be seen in cases of esophageal or gastric perforation.

Several studies indicate that the clinical manifestations of caustic ingestion injuries are poor predictors of the severity of injuries. The relationship between symptoms or the presence or absence of oral burns with the presence of esophageal or gastric injuries is not strong.1416 If two of the three symptoms of vomiting, drooling, or stridor are present, the likelihood of gastrointestinal burns is high. Of the three, vomiting is the most powerful predictor of esophageal injury.15

The most significant long-term complications of caustic ingestions are stricture formation and esophageal carcinoma. The majority of esophageal and gastric strictures occur 2 weeks to 2 months from the time of initial exposure. The risk increases (15–90%) with more severe burns.11,16 Symptoms of stricture formation range from dysphagia and food impaction to gastric outlet obstruction with vomiting.

Long-term survivors of moderate and severe esophageal caustic injuries have a 1000-fold increased risk of esophageal carcinoma. Patients require lifelong surveillance because the latent period between caustic exposure and the development of cancer may be as long as 50 years.3

EVALUATION AND MANAGEMENT

The patient typically presents with a history of ingestion. If the container is available, the label, by regulation, will indicate if the product is a corrosive by warning text and by the presence of a hazardous product symbol. If the container is not available, attempts should be made for telephone identification either by reading the label or by sending a photograph by email. The poison control center can assist with identifying the ingredients of a brand name product or chemical compound and with its potential for corrosive effect. The universal number in the United States is 1-800-222-1222.

Evaluation of the patient for airway compromise and signs of esophageal or gastric perforation is the initial priority. Oropharyngeal and laryngeal edema may develop rapidly. Patients with stridor, dyspnea, or dysphonia should be intubated under direct visualization; severe edema precluding oral intubation may require a surgical airway. Blind nasotracheal intubation is contraindicated. Immediate surgical consultation is indicated if there are signs of perforation: peritonitis, worsening chest and abdominal pain, or the presence of free air. In these critically ill patients, chest and abdominal x-rays should be obtained to assess for mediastinal or peritoneal free air indicative of perforation. Fluid resuscitation should be initiated, and pain control should be provided. The patient should be carefully examined for ocular or dermal exposure and receive copious irrigation if detected.

Patients without immediate airway issues should be observed for excessive crying, vomiting, drooling, or refusal to eat or drink, all of which may indicate a significant injury. The oral cavity should be evaluated for evidence of intraoral burns. The chest should be visualized for retractions and auscultated for wheezes or rhonchi indicating aspiration. The abdomen should be examined for distention, tenderness, or rigidity, which suggests the possibility of gastrointestinal tract perforation. All symptomatic patients should remain NPO. Diluents and buffers are not recommended because they may result in emesis and further injury of the esophagus.

Gut decontamination procedures, such as the administration of activated charcoal, syrup of ipecac, and gastric lavage, are contraindicated. Activated charcoal poorly absorbs caustics, may increase the risk of emesis, and will obscure endoscopic visualization.

Following evaluation and stabilization of the patient, the clinician must determine the need for upper gastrointestinal endoscopy. Endoscopy helps determine the extent of injury and the potential for complications.17

Patients who present without symptoms and are able to drink fluids without discomfort can be assumed to have no significant injury.16 They may be discharged from the emergency department after a 2–4-hour period of observation and a successful trial of oral fluids. Symptomatic patients require admission to hospital for investigation and management.

Historically, corticosteroids were routinely used with the intent of preventing stricture formation. However, prospective studies and literature review demonstrate no benefit.16,1821

SPECIAL CONCERNS

image CORROSIVE EYE INJURIES

Corrosive eye injuries can have devastating consequences, including blindness. The alkaline by-products of sodium azide released in automobile air bags can cause ophthalmic injury. The cornerstone of management of ophthalmologic exposure is immediate irrigation of the eye for a minimum of 15–20 minutes with 0.9% saline, lactated Ringer’s solution, or tap water. Irrigation is intended to dilute and remove the corrosive, remove any foreign bodies, and normalize the pH. Delays of just a few minutes can affect outcome dramatically. After exposure to acids or alkalis, normalization of the conjunctival pH is often suggested as a useful end point. Full extent of injury may not be evident for 48–72 hours. Ophthalmologist evaluation is recommended for all corrosive eye injuries.

REFERENCES

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2. Christopher MJ, Matthew TB. The public health impact of pediatric caustic ingestion injuries. Arch Otolaryngol Head Neck Surg. 2012; 138(12):1111–1115.

3. Isolauri JM. Ingestion and carcinoma of the esophagus. Acta Chir Scand. 1989;155–269.

4. Caravati EM. Caustics. In: Dart RC, ed. Medical Toxicology. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004:1294–1309.

5. Kirsch MM, Ritter F. Caustic ingestion and subsequent damage to the oropharyngeal and digestive passages. Ann Thorac Surg. 1976;21:74.

6. Thompson J: Corrosive esophageal strictures. I. A study of nine cases of concurrent accidental caustic ingestion. Laryngoscope. 1987;97:1060.

7. Fulton JA, Rao RB, Flomenbaum NE, et al. Caustics. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS, eds. Goldfranks’ Toxicologic Emergencies. 8th ed. New York, NY: McGraw Hill;2006:1405–1416.

8. Vancura EM, Clinton JE, Ruiz E, et al. Toxicity of alkaline solutions. Ann Emerg Med. 1980;9:118.

9. Hoffman RH, Kamerow HN, Goldfrank LR. Comparison of titratable acid/alkaline reserve and PH in potentially caustic household products. J Toxicol Clin Toxicol. 1989;27:241.

10. Zargar SA. Ingestion of corrosive acids. Gastroenterology. 1989; 97:702.

11. Christesen H. Prediction of complications following unintentional caustic ingestions in children. Is endoscopy always necessary? Acta Paediatr Scand. 1995;84:1177.

12. Haddad LM, Shannon MW, Borron SW, et al. Clinical management of poisoning and drug overdose. Chapter 98Corrosives. Philadelphia, PA: Saunders/Elsevier; 2007:1407–1414.

13. Gorman RK, Khin-Maung-Gyi MT, Klein-Schwartz W, et al. Initial symptoms as predictors of esophageal injury in alkaline corrosive ingestions. Am J Emerg Med. 1992;10:189.

14. Crain EF, Gershel JC, Mezey AP. Caustic ingestions: symptoms as predictors of esophageal injury. Am J Dis Child. 1984;138: 863–865.

15. Dogan Y, Erkan T, Cokugras FC. Caustic gastroesophageal lesions in childhood: an analysis of 473 cases. Clin Pediatr (Phila). 2006; 45(5):435–438.

16. Gaudreault P, Parent M. Predictability of esophageal injury from signs and symptoms: a study of caustic ingestions in 378 children. Pediatrics. 1983;71:767–770.

17. Lamireau T, Rebouissoux I, Denis D, Lancelin F, Vergnes P, Fayon M. Accidental caustic ingestion in children: is endoscopy always mandatory? J Pediatr Gastroenterol Nutr. 2001;33:81.

18. Anderson KR, Randolph JG A controlled trial of corticosteroids in children with corrosive Injury of the esophagus. N Engl J Med. 1990;323:637.

19. Boukthir S, Fetni I, Mrad SM, Mongalgi MA, Debbabi A, Barsaoui S. High doses of steroids in the management of caustic esophageal burns in children. Arch Pediatr. 2004;11:13.

20. Peclova D, Navratil T. Do corticosteroids prevent esophageal stricture after corrosive ingestion? Toxicol Rev. 2005;24:125–129.

21. Fulton JA, Hoffman RS. Steroids in second degree caustic burns of the esophagus: a systematic pooled analysis of fifty years of human data: 1956-2006. Clin Toxicol. 2007;45:402–408.