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Toxicity, Caustic Ingestions
Updated: Nov 4, 2008
Introduction
Background
Caustics and corrosives cause tissue injury by a chemical reaction. The vast majority of caustic chemicals are acidic or alkaline substances that damage tissue by accepting a proton (alkaline substance) or donating a proton (acidic substance) in an aqueous solution.
Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the extensive thrombosis of the esophageal submucosal vessels giving the appearance similar to chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD.
The pH of a chemical is a measure of how easily the chemical accepts or donates a proton; these terms are a measure of the strength or likelihood of serious damage upon tissue contact. Substances with a pH less than 2 are considered to be strong acids; those with a pH greater than 12 are considered to be strong bases. The severity of tissue injury from acidic and alkaline substances is determined by the duration of contact; the amount and state (liquid, solid) of the substance involved; and the substance's physical properties, such as its pH, concentration, ability to penetrate tissue, and its titratable reserve. The latter reflects the amount of tissue required to neutralize a given amount of the involved substance and is particularly useful for measuring the amount of damage that can be caused by caustics, such as phenol, which have a near-neutral pH.
Pathophysiology
Caustic chemicals produce tissue injury by altering the ionized state and structure of molecules and disrupting covalent bonds. In aqueous solutions, the hydrogen ion (H+) produces the principle toxic effects for the majority of acids, whereas the hydroxide ion (OH-) produces such effects for alkaline substances.
Alkaline ingestions
Alkaline ingestions cause tissue injury by liquefactive necrosis, a process that involves saponification of fats and solubilization of proteins. Cell death occurs from emulsification and disruption of cellular membranes. The hydroxide ion of the alkaline agent reacts with tissue collagen and causes it to swell and shorten. Small vessel thrombosis and heat production occurs.
Severe injury occurs rapidly after alkaline ingestion, within minutes of contact The most severely injured tissues are those that first contact the alkali, that is the squamous epithelial cells of the oropharynx, hypopharynx, and esophagus. The esophagus is the most commonly involved organ with the stomach much less frequently involved after alkaline ingestions. Tissue edema occurs immediately, may persist for 48 hours, and may eventually progress sufficiently to create airway obstruction. Over time, if the injury was severe enough, granulation tissue starts to replace necrotic tissue.
Over the next 2-4 weeks, any scar tissue formed initially remodels and may thicken and contract enough to form strictures. The likelihood of stricture formation primarily depends upon burn depth. Superficial burns result in strictures in fewer than 1% of cases, whereas full-thickness burns result in strictures in nearly 100% of cases. The most severe burns also may be associated with esophageal perforation.
Acid ingestions
Acid ingestions cause tissue injury by coagulation necrosis, which causes desiccation or denaturation of superficial tissue proteins, often resulting in the formation of an eschar or coagulum. This eschar may protect the underlying tissue from further damage. Unlike alkali ingestions, the stomach is the most commonly involved organ following an acid ingestion. Small bowel exposure also occurs in about 20% of cases. Emesis may be induced by pyloric and antral spasm.
The eschar sloughs in 3-4 days and granulation tissue fills the defect. Perforation may then occur after the third or fourth day as the eschar sloughs. A gastric outlet obstruction may develop as the scar tissue contracts over a 2- to 4-week period. Acute complications include gastric and intestinal perforation and upper gastrointestinal hemorrhage.
Significant exposures may also result in absorption of the acidic substances leading to significant metabolic acidosis, hemolysis, acute renal failure, and death.
Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the appearance of the thrombosed esophageal submucosal vessels giving the appearance of chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD.
Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the extensive burn and thrombosis of the submucosal esophageal vessels, which gives the appearance of chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD.
Frequency
United States
Ingestions of caustic substances accounted for more toxic exposures than any other class of agents. Cleaning substances, many of which contain potentially caustic agents, account for more than 200,000 exposures per year reported to US poison control centers.1
Mortality/Morbidity
The alkali drain cleaners and acidic toilet bowl cleaners are responsible for the most fatalities from corrosive agents.
- Approximately 10% of caustic ingestions result in severe injury requiring treatment.
- Between 1% and 2% of caustic ingestions results in stricture formation.
Race
No race predilection exists.
Sex
No sex predilection exists.
Age
- Childhood ingestions: Approximately 80% of caustic ingestions occur in children younger than 5 years. Critical solid ingestions are rare because children generally do not swallow the burning particles that adhere to their oropharynx. Liquid ingestions, however, can be quite serious.
- Adult ingestions: Most intentional ingestions occur in adults. Adult exposures have increased morbidity than childhood exposures because of the often higher volume of the exposure and the presence of possible co-ingestants. Occupational exposures often are more severe than other exposures because industrial products are more concentrated.
Clinical
History
The physician should try to identify the specific agent ingested, as well as the concentration, pH, and amount of substance ingested. The time, nature of exposure, duration of contact, and any immediate on-scene treatment are important in determining management of toxicity.
The presence or absence of the following symptoms should be determined since the presence of any of these symptoms suggests significant internal injury. However, their absence does not preclude significant injury.
- Dyspnea
- Dysphagia
- Oral pain and odynophagia
- Chest pain
- Abdominal pain
- Nausea and vomiting
Rapidly obtaining reliable information on the particular agent involved is vital. This is particularly true of uncommon caustic agents, some of which have important toxic concerns beyond those of a simple caustic ingestion.
A good example of this is the potential for abrupt, life-threatening hypocalcemia following ingestion of hydrogen fluoride, even in a relatively dilute form such as that found in some rust removers. Case reports of patients surviving such suicidal ingestions underline the value of being able to anticipate and aggressively manage the systemic hypocalcemia, which is unique to hydrogen fluoride, with intravenous calcium. Other examples of caustic agents with unique toxicities include phenol, zinc chloride, and mercuric chloride, all of which can cause significant systemic toxicity and which may require significant changes in management.Material Safety Data Sheets (MSDS), online databases, and consultations with the local poison center are all ways for a clinician to rapidly familiarize themselves with unfamiliar caustics agents.
Physical
As with the history, physical examination findings may be deceptively unremarkable after a significant caustic ingestion, despite the presence of significant tissue necrosis.
- Signs of impending airway obstruction may include the following:
- Stridor
- Hoarseness
- Dysphonia or aphonia
- Respiratory distress, tachypnea, hyperpnea
- Cough
- Other signs of injury may include the following:
- Tachycardia
- Oropharyngeal burns - These are important when identified; however, significant esophageal involvement may occur without the presence of oropharyngeal lesions.
- Drooling
- Subcutaneous air
- Acute peritonitis
- Abdominal guarding
- Rebound tenderness
- Diminished bowel sounds
- Hematemesis
- Indications if severe injury - Altered mental status, peritoneal signs, other indications of viscous perforation, stridor, hypotension, and shock
Causes
- Common acid-containing sources
- Toilet bowl cleaning products
- Automotive battery liquid
- Rust removal products
- Metal cleaning products
- Cement cleaning products
- Drain cleaning products
- Soldering flux containing zinc chloride
- Common alkaline-containing sources
- Drain cleaning products
- Ammonia-containing products
- Oven cleaning products
- Swimming pool cleaning products
- Automatic dishwasher detergent
- Hair relaxers
- Clinitest tablets
- Bleaches
- Cement
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References
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Gorman RL, Khin-Maung-Gyi MT, Klein-Schwartz W, Oderda GM, Benson B, Litovitz T, et al. Initial symptoms as predictors of esophageal injury in alkaline corrosive ingestions. Am J Emerg Med. May 1992;10(3):189-94. [Medline].
Havanond C, Havanond P. Initial signs and symptoms as prognostic indicators of severe gastrointestinal tract injury due to corrosive ingestion. J Emerg Med. Nov 2007;33(4):349-53. [Medline].
Homan CS, Maitra SR, Lane BP, Thode HC Jr, Finkelshteyn J, Davidson L. Effective treatment for acute alkali injury to the esophagus using weak-acid neutralization therapy: an ex-vivo study. Acad Emerg Med. Nov 1995;2(11):952-8. [Medline].
Homan CS, Maitra SR, Lane BP, Thode HC, Sable M. Therapeutic effects of water and milk for acute alkali injury of the esophagus. Ann Emerg Med. Jul 1994;24(1):14-20. [Medline].
Kamijo Y, Kondo I, Watanabe M, Kan'o T, Ide A, Soma K. Gastric stenosis in severe corrosive gastritis: prognostic evaluation by endoscopic ultrasonography. Clin Toxicol. 2007;45(3):284-6. [Medline].
Kim SJ, Cho SB, Cho JM, et al. CT imaging of gastric and hepatic complications after ingestion of glacial acetic acid. J Comput Assist Tomogr. Jul-Aug 2007;31(4):564-8. [Medline].
Pelclová D, Navrátil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion?. Toxicol Rev. 2005;24(2):125-9. [Medline].
Poley JW, Steyerberg EW, Kuipers EJ, Dees J, Hartmans R, Tilanus HW, et al. Ingestion of acid and alkaline agents: outcome and prognostic value of early upper endoscopy. Gastrointest Endosc. Sep 2004;60(3):372-7. [Medline].
Salzman M, O'Malley RN. Updates on the evaluation and management of caustic exposures. Emerg Med Clin North Am. May 2007;25(2):459-76. [Medline].
Turner A, Robinson P. Respiratory and gastrointestinal complications of caustic ingestion in children. Emerg Med J. May 2005;22(5):359-61. [Medline].
Further Reading
Keywords
caustic ingestion, poisoning, alkaline ingestion, acid ingestion, corrosive agent toxicity, acidic or alkaline substance toxicity, toilet bowl cleaning product ingestion, automotive battery liquid ingestion, rust removal product ingestion, metal cleaning product ingestion, cement cleaning product ingestion, drain cleaning product ingestion, soldering flux-containing zinc chloride ingestion, ammonia-containing product ingestion, oven cleaning product ingestion, swimming pool cleaning product ingestion, automatic dishwasher detergent ingestion, hair relaxer ingestion, Clinitest tablet ingestion, bleach ingestion, cement ingestion, hydrogen fluoride exposure phenol exposure, disk battery ingestion
