Caustics

Principles of Toxicity

Some household products, such as liquid drain cleaners, continue to have high concentrations of alkali (30% KOH) or acid (93% H ₂ SO ₄ ) ( Table 143.1 ). These products often do not have concentration or content information available on the label, making it difficult for clinicians to determine the severity of exposure. Industrial, agricultural (dairy pipeline cleaners containing liquid NaOH and KOH in concentrations of 8% to 25%), and swimming pool chemicals also contain caustics in high concentrations.

Crystals and solid particles can have prolonged tissue adherence, causing more severe injury. Household detergents such as laundry powders and detergent pods (LDPs) and dishwasher detergents containing silicates, carbonates, and phosphates have the potential to induce caustic burns and strictures, even when ingested unintentionally. These ingestions are limited by immediate oral pain, usually causing them to be spit out sooner than a liquid agent. The ingestion of granular automatic dishwashing detergents or brightly colored laundry detergent capsules or “pods” can be associated with devastating injuries. Compared to children with traditional non-LDP exposures, LDP exposures are associated with a higher incidence of toxicity including central nervous system depression and respiratory compromise with failure. Whether the toxicity observed with LDP exposures is due to other ingredients in the products, pH, concentration, tensile strength, or the delivery vehicle remains unclear.

Crystal drain cleaners have lye concentrations as high as 74% NaOH and may cause proximal esophageal injury. Liquid dishwashing detergents and laundry detergents have a pH higher than 12, but because the titratable alkaline reserve is low, tissue equilibration occurs quickly, and there is less risk of injury after ingestion.

Liquid household bleach typically contains dilute (3% to 5%) sodium hypochlorite (NaOCl), and ingestion rarely causes consequential injury. Industrial-strength bleach, however, contains significantly higher concentrations of NaOCl, which are more likely to cause esophageal necrosis. Toilet bowl cleaners contain HCl concentrations as high as 26%. General-purpose anticorrosive cleaners, such as 31% hydrochloride acid (HCl), are sold in gallon containers for home use and as swimming pool cleaners.

The alkali powder in air bags can cause ocular burns. Perfume unintentionally sprayed in the eyes can be caustic. Cement is alkaline and causes topical burns, typically on the knees and hands. Although hair relaxer creams contain NaOH and have a pH of 11.2 to 11.9, injuries after ingestion are usually mild.

Caustic ingestions may occur when methamphetamine is produced from over-the-counter medications and household chemicals. H ₂ SO ₄ , HCl, NaOH, ammonium hydroxide, anhydrous ammonia, and metallic lithium are all used in the clandestine production of methamphetamine. Severe caustic injuries occurring from ingestion of these agents can cause stricture formation, esophageal resection, and the need for colonic interposition.

Many medication pills can cause injury when they come in contact with the esophageal mucosa for prolonged periods. Patients who take medications in the supine position or who take pills without water are at higher risk of pill esophagitis. The pills most likely to adhere are doxycycline, tetracycline, potassium chloride, antimalarials, and aspirin. Although uncommon, potassium chloride is particularly dangerous and can cause esophageal perforation with devastating communication with the aorta, left atrium, and bronchial artery.

Pathophysiology

Factors that influence the extent of injury from a caustic exposure include type of agent, concentration of solution, volume, viscosity, duration of contact, pH, and presence or absence of food in the stomach. The titratable acid/alkaline reserve of an alkali or acid correlates with the ability to produce tissue damage. Concentrated forms of acids and bases generate heat, resulting in superimposed thermal injury.

Acidic compounds desiccate epithelial cells and cause coagulation necrosis. An eschar is formed that limits further penetration. Because acids tend to have a strong odor and cause immediate pain on contact, the quantity ingested is usually limited. Because of resistance of squamous epithelium to coagulation necrosis , acids are thought to be less likely to cause esophageal and pharyngeal injury, although severe esophageal and laryngeal injury still occur, particularly with intentional ingestions. In many case series, acid ingestion results in equal esophageal and gastric mucosal injury. Acids can also be absorbed systemically, causing metabolic acidosis as well as damage to the spleen, liver, biliary tract, pancreas, and kidneys from perforation and direct local contact.

Alkaline contact, in contrast to acids, causes liquefaction necrosis , fat saponification, and protein disruption, allowing further penetration of the alkaline substance into the tissue. The depth of the necrosis depends on the concentration of the agent. A concentration of 30% NaOH in contact with tissue for one second results in a full-thickness burn. Alkalis are colorless and odorless, and unlike acids, they do not cause immediate pain on contact. Alkaline ingestions typically involve the squamous epithelial cells of the oropharynx, hypopharynx, and esophagus. The narrow portions of the esophagus, where pooling of secretions can occur, are also commonly involved. Alkalis may also cause gastric necrosis ( Figs. 143.1 and 143.2 ), intestinal necrosis, and perforation. The esophagus can also be injured ( Fig. 143.3 ). Burns below the pylorus carry a 50% mortality compared with 9% for burns above the pylorus.

Caustic damage occurs in four phases. Initially, necrosis occurs, with invasion by bacteria and polymorphonuclear leukocytes. Vascular thrombosis follows, increasing the damage. During the next two to five days, superficial layers of injured tissue begin to slough. The tensile strength of the healing tissue may be low for up to three weeks after the caustic exposure, greatly increasing the chance of delayed perforation in some cases. Between one week and several months, granulation tissue forms, collagen is deposited, and reepithelialization occurs in the burn area. Esophageal strictures may form during a period of weeks to years from contraction of the scar.

Caustic injury is categorized as first, second, and third degree, similar to a thermal burn, by appearance on endoscopy. The initial depth of injury found on esophagoscopy correlates with the risk of stricture formation. Grade I injury consists of edema and hyperemia. Grade II injury can be further divided into grade IIa, which is non-circumferential, and grade IIb, which is nearly circumferential. Overall, grade II injuries are characterized by superficial ulcers, whitish membranes, exudates, friability, and hemorrhage. Grade III injury is associated with transmural involvement with deep injury, necrotic mucosa, or perforation of the stomach or esophagus. Although grade I injuries do not progress to stricture, 15% to 30% of all grade IIa injuries and up to 75% of circumferential grade IIb injuries of the esophagus develop strictures. With grade III injury, up to 90% result in stricture. Recently, the formation of strictures is decreasing for both grade II and grade III injury, possibly because of the type and caustic intensity of the substance ingested.