Caustic Ingestions

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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. ^[1]

The pH of a chemical is a measure of how easily the chemical accepts or donates a proton. This relates to the strength of the acidic or alkaline substance, and provides some, but not precise, correlation with the likelihood of injury. 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.

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 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, which 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 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. This may due to some natural protection of the esophageal squamous epithelium. 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 occur at this time. 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.

Endoscopic view of the esophagus after ingestion of an acid is shown in the images below.

Significant exposures may also result in gastrointestinal absorption of the acidic substances leading to significant metabolic acidosis, hemolysis, acute renal failure, and death.

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. ^{[2, 3, 4, 5]}

The alkali drain cleaners and acidic toilet bowl cleaners are responsible for the most fatalities from corrosive agents. In adults, 10% of caustic ingestions result in death. ^[6]

Approximately 10% of caustic ingestions result in severe injury requiring treatment. Approximately 1-2% of caustic ingestions result in stricture formation. ^[6]

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. ^{[7, 8]}

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 than those found in the home. ^[9]

Chirica M, Bonavina L, Kelly MD, Sarfati E, Cattan P. Caustic ingestion. Lancet. 2017 May 20. 389 (10083):2041-2052. [Medline].

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Rollin M, Jaulim A, Vaz F, Sandhu G, Wood S, Birchall M, et al. Caustic ingestion injury of the upper aerodigestive tract in adults. Ann R Coll Surg Engl. 2015 May. 97 (4):304-7. [Medline]. [Full Text].

Denney W, Ahmad N, Dillard B, Nowicki MJ. Children will eat the strangest things: a 10-year retrospective analysis of foreign body and caustic ingestions from a single academic center. Pediatr Emerg Care. 2012 Aug. 28(8):731-4. [Medline].

Elshabrawi M, A-Kader HH. Caustic ingestion in children. Expert Rev Gastroenterol Hepatol. 2011 Oct. 5(5):637-45. [Medline].

Chang JM, Liu NJ, Pai BC, Liu YH, Tsai MH, Lee CS, et al. The role of age in predicting the outcome of caustic ingestion in adults: a retrospective analysis. BMC Gastroenterol. 2011 Jun 14. 11:72. [Medline]. [Full Text].

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Bruzzi M, Chirica M, Resche-Rigon M, Corte H, Voron T, Sarfati E, et al. Emergency Computed Tomography Predicts Caustic Esophageal Stricture Formation. Ann Surg. 2018 Mar 12. 22 (10):1659-1664. [Medline].

Lurie Y, Slotky M, Fischer D, Shreter R, Bentur Y. The role of chest and abdominal computed tomography in assessing the severity of acute corrosive ingestion. Clin Toxicol (Phila). 2013 Nov. 51(9):834-7. [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].

Bird JH, Kumar S, Paul C, Ramsden JD. Controversies in the management of caustic ingestion injury: an evidence-based review. Clin Otolaryngol. 2017 Jun. 42 (3):701-708. [Medline].

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Contini S, Scarpignato C. Caustic injury of the upper gastrointestinal tract: a comprehensive review. World J Gastroenterol. 2013 Jul 7. 19 (25):3918-30. [Medline]. [Full Text].

Bird JH, Kumar S, Paul C, Ramsden JD. Controversies in the management of caustic ingestion injury: an evidence-based review. Clin Otolaryngol. 2017 Jun. 42 (3):701-708. [Medline].

[Guideline] Tringali A, Thomson M, Dumonceau JM, Tavares M, Tabbers MM, et al. Pediatric gastrointestinal endoscopy: European Society of Gastrointestinal Endoscopy (ESGE) and European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) Guideline Executive summary. Endoscopy. 2017 Jan. 49 (1):83-91. [Medline]. [Full Text].

Katibe R, Abdelgadir I, McGrogan P, Akobeng AK. Corticosteroids for Preventing Caustic Esophageal Strictures: Systematic Review and Meta-analysis. J Pediatr Gastroenterol Nutr. 2018 Jun. 66 (6):898-902. [Medline].

Uygun I, Arslan MS, Aydogdu B, Okur MH, Otcu S. Fluoroscopic balloon dilatation for caustic esophageal stricture in children: an 8-year experience. J Pediatr Surg. 2013 Nov. 48(11):2230-4. [Medline].

Eric M Kardon, MD, FACEP Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center

Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Medical Association of Georgia

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph’s Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Michael J Burns, MD Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David Vearrier, MD, MPH Associate Professor, Medical Toxicology Fellowship Director, Department of Emergency Medicine, Drexel University College of Medicine

David Vearrier, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Lance W Kreplick, MD, FAAEM, MMM, UHM Staff Physician for Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC

Lance W Kreplick, MD, FAAEM, MMM, UHM is a member of the following medical societies: American Academy of Emergency Medicine, American Association for Physician Leadership

Disclosure: Nothing to disclose.

Caustic Ingestions

Research & References of Caustic Ingestions|A&C Accounting And Tax Services
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