AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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. 

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.

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

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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.

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

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Airway obstruction may occur secondary to edema, bleeding, and the presence of necrotic material. Because this can develop rapidly, airway protection is paramount following caustic ingestions.

Esophageal gastric, bowel, airway, or vascular perforation may occur.

Fluid losses from vomiting, third spacing, and gastrointestinal bleeding may lead to hypovolemia and shock. This is particularly true after ingestion of metallic chlorides.

After significant acidic ingestions, the patient may develop metabolic acidosis, hemolysis, and multiorgan failure including acute renal failure.

Hypocalcemia develops precipitously after ingestion of significant amounts of hydrogen fluoride.

In patients who survive the initial phases of injury, late-developing problems include strictures, fistula, hypomotility disorders, and an increased risk of gastrointestinal cancers.

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

• pH testing of product  
• • A pH less than 2 or greater than 12.5 indicates greater potential for severe tissue damage.
  • A pH outside of this range does not preclude significant injury.
• pH testing of saliva: Unexpected high or low values may confirm ingestion in questionable cases; however, a neutral pH cannot rule out a caustic ingestion.
• Complete blood count (CBC), electrolyte levels, BUN levels, creatinine level, and ABG levels may all be helpful as baseline values and as indications of systemic toxicity.
• Liver function tests and DIC panel may also be helpful to establish baselines or, if abnormal, confirm severe injury following acid ingestions.
• Urinalysis and urine output may help guide fluid replacement.
• Type and cross are indicated for any potential surgical candidates or those with the potential for gastrointestinal bleeding.
• Obtain aspirin and acetaminophen levels as well as an ECG in any patient whose intent may have been suicidal.
• In cases of hydrofluoric acid (HF) ingestion, precipitous falls in calcium level may lead to sudden cardiac arrest. Although ionized calcium levels are likely to have too long a turnaround to be clinically useful, cardiac monitoring and serial ECGs may help anticipate this event.

Imaging Studies

• Chest radiography: Obtain an upright chest radiograph in all cases of caustic ingestion. Findings may include mediastinitis, pleural effusions, pneumoperitoneum, aspiration pneumonitis, or a button battery. However, the absence of findings does not preclude perforation or other significant injury.
• Abdominal radiography: Findings may include pneumoperitoneum, ascites, or an ingested button battery.
• If contrast studies are obtained, water-soluble contrast agents are recommended because they are less irritating to the tissues in cases of perforation.
• CT can sometimes delineate small amounts of extraluminal air.

Procedures

• Airway protection is critical following caustic ingestion if there is any indication of airway compromise. This can develop rapidly and be complicated by multiple factors. See Emergency Department Care.
• Cardiac monitoring is indicated for any patient with a caustic ingestion.
• Large-bore intravenous access allows administration of fluids and medications as needed.
• Endoscopy is generally indicated for the following patients:  
• • Small children
  • Symptomatic older children and adults
  • Patients with abnormal mental status
  • Those with intentional ingestions
  • Patients in whom injury is suspected for other reasons (eg, ingestion or large volumes or concentrated products)
• However, because of the risk of increased injury, esophagoscopy should not be performed in patients with evidence of esophageal or gastrointestinal perforation, significant airway edema, or necrosis and in those who are hemodynamically unstable.
• Obtaining meaningful information from endoscopy after treatment with activated charcoal is very difficult.
• Endoscopic ultrasonography has been shown to more accurately show the depth of lesions than endoscopy alone. Further studies will be necessary to determine the utility of this procedure in aiding in diagnosis and treatment.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Prehospital Care

• Attempt to identify the specific product, concentration of active ingredients, and estimated volume and amount ingested. Obtain MSDS sheets when possible. The product container or labels may be available. Avoid exposure to health care workers.
• Do not induce emesis or attempt to neutralize the substance by using a weak acid or base. This induces an exothermic reaction, which can compound the chemical injury with a thermal injury. It may also induce emesis.
• Small amounts of a diluent, although controversial, may be beneficial if administered as soon as possible after a solid or granular alkaline ingestion, to remove any adhering particles to the oral or esophageal mucosa. Water or milk may be administered in small amounts. It is very unlikely to be of any benefit after more than 30 minutes.  
• • Some authors discourage the use of diluents because of the concern of inducing emesis.
  • Diluents should not be used with any acid ingestion or liquid alkaline ingestion. The risk of vomiting with reexposure of the oral or esophageal mucosa to the offending substance can result in worsening injury or perforation.

Emergency Department Care

• In the treatment area, patients suspected of ingesting a caustic substance should be triaged to a high priority for prompt evaluation and treatment. This includes prompt evaluation of airway and vital signs as well as immediate cardiac monitoring and intravenous access.
• Airway control   
• • Because of the risk of rapidly developing airway edema, immediate assessment of the patient’s airway and mental status should be performed and carefully monitored. Equipment for endotracheal intubation and cricothyrotomy should be readily available. Gentle orotracheal intubation or fiberoptic-assisted intubation is preferred over blind nasotracheal intubation to avoid the increased risk of soft-tissue perforation.
  • If possible, it is best to avoid inducing paralysis for intubation because of the risk of anatomical distortion from bleeding and necrosis.
  • Cricothyrotomy or percutaneous needle cricothyrotomy may be necessary in the presence of extreme tissue friability or significant edema.
• Gastric emptying and decontamination  
• • Do not administer emetics because of risks of reexposure of the vulnerable mucosa to the caustic agent. This may result in further injury or perforation.
  • Gastric lavage by traditional methods using large-bore orogastric Ewald tubes are contraindicated in both acidic and alkaline ingestions because of risk of esophageal perforation and tracheal aspiration of stomach contents.
  • Large-volume liquid acid ingestions may benefit from nasogastric tube (NGT) suction if performed rapidly after ingestion. Pyloric sphincter spasm may prolong contact time of the agent to the gastric mucosa for up to 90 minutes. NGT suction may prevent small intestine exposure. Esophageal perforation is rare. NGT suction may be of particular value following ingestion of zinc chloride, mercuric chloride, or hydrogen fluoride.
  • Activated charcoal is relatively contraindicated in caustic ingestions because of poor adsorption and endoscopic interference.
• Dilution: Dilution may be beneficial for ingestion of solid or granular alkaline material if performed within 30 minutes after ingestion using small volumes of water. Because of the risk of emesis, carefully consider the risks versus benefits of dilution.
• Do not dilute acids with water because of excessive heat production.
• Neutralization: Do not administer a weak acid in alkaline ingestions or a weak alkaline agent in acid ingestions. There is a risk of heat production resulting from this exothermic reaction. In addition, the risk of emesis makes this a hazardous intervention.
• Intravenous fluids and blood products may be required in the event of significant bleeding, vomiting, or third spacing.

Consultations

Airway management can be a multifaceted problem and may be best approached with the availability of a wide array of visualization techniques, and, if time allows, a team of experts. However, the rapid development of airway edema may prompt the need for rapid airway management with the best immediately available visualization approach.

• Obtain a surgical consultation when the following are expected or observed:  
• • Perforation
  • Mediastinitis
  • Peritonitis
• Obtain an endoscopic consultation for the following patients:  
• • Small children
  • Symptomatic older children and adults
  • Patients with altered mental status
  • Patients with intentional ingestions
  • Others with a potential for significant injury (eg, ingestion or large volumes or concentrated products)

Once a patient is stabilized, obtain a psychiatric consultation for any patients with a history of an intentional ingestion.

MEDICATION

Section 7 of 12  

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• Introduction
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• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Supportive care, rather than specific antidotes, are the mainstay of management following caustic ingestions. A significant exception to this would be the aggressive administration of intravenous calcium for dysrhythmias precipitated by hypocalcemia from hydrogen fluoride ingestion. Such therapy is best performed with the guidance of the toxicologist at the local poison center.

The use of corticosteroids, previously proposed to be beneficial, should be discouraged. Studies have shown that stricture formation is based on the depth of the tissue damage.

The following agents may be of value in supportive care.

Drug Category: Antibiotic, Cephalosporin (Third Generation)

These agents should be administered if evidence of perforation exists. A third-generation cephalosporin or ampicillin/sulbactam may be considered.

Drug Category: Antibiotic, Penicillin and Beta-lactamase Inhibitor

These agents should be administered if evidence of perforation exists. A third-generation cephalosporin or ampicillin/sulbactam may be considered.

Drug Category: Proton Pump Inhibitor

Proton pump inhibitors reduce exposure of injured esophagus to gastric acid, which may result in decreased stricture formation.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Further Inpatient Care

• Admit all small children, symptomatic patients, those with altered mental status, and those whose ingestions are worrisome for other reasons such as large volumes, high concentrations, or unique issues such as those posed by hydrogen fluoride or phenol for observation and possible endoscopy. Admit all symptomatic patients to the ICU to closely monitor their airway status and to watch for signs of perforation.
• Ensure that all patients take nothing per mouth (NPO) until the extent of injury has been determined.
• Begin an intravenous line to administer fluids and medications.
• Administer parenteral analgesics as needed for pain. Monitor for signs of sedation and respiratory depression.

Further Outpatient Care

• Adult asymptomatic patients with an unintentional exposure, a clear sensorium, and no unique concerns in the history (eg, large volume, high concentration, agent with potential for systemic toxicity) and no physical abnormalities may be discharged after a 2- to 4-hour observation period. Discharged patients should be able to ingest oral fluids without difficulty, demonstrate easy speech, be reliable, and be familiar with and able to return should any delayed symptoms occur.
• Obtain a psychiatric evaluation for all patients with intentional ingestion.
• Arrange for an esophagram 3-4 weeks postingestion.

Complications

• Airway edema or obstruction may occur immediately or up to 48 hours following an alkaline exposure.
• Gastroesophageal perforation may occur acutely.   
• • Secondary complications include mediastinitis, pericarditis, pleuritis, tracheoesophageal fistula formation, esophageal-aortic fistula formation, and peritonitis.
  • Delayed perforation may occur as many as 4 days after an acid exposure.
  • Deep circumferential or deep focal burns may result in strictures in more than 70% of patients; these strictures typically develop 2-4 weeks postingestion.
  • Gastric outlet obstruction may develop 3-4 weeks after an acid exposure.
  • Upper gastrointestinal hemorrhage may occur acutely in caustic exposures.
  • Delayed upper GI bleeding may occur in acid burns 3-4 days after exposure as the eschar sloughs.
  • Though many pass through without causing damage, batteries can cause perforation at any time during their course through the gastrointestinal system, particularly if damaged.
  • Zinc chloride, mercuric chloride, and phenol can all cause significant systemic toxicity.
  • Cardiac arrest from sudden hypocalcemia may occur in patients who have ingested hydrogen fluoride–containing substances. Patients have been successfully resuscitated with aggressive use of intravenous CaCl₂.
• Long-term risks include squamous cell carcinoma, which occurs in 1-4% of all significant exposures and may occur as many as 40 years after exposure.

Prognosis

• The prognosis is directly proportional to the degree of tissue damage, which is primarily a function of the duration of exposure and the physical properties of the agent involved. These include the pH, the volume, and concentration of the agent; its ability to penetrate tissues; and its titratable reserve. The titratable reserve is a term that reflects the amount tissue required to neutralize a given amount of agent.
• Some agents have the ability to cause systemic toxicity that affects the prognosis in addition to their caustic properties. These include phenol, zinc chloride, mercuric chloride, and hydrogen fluoride.

Patient Education

• Caustic agents should be stored in their original child-resistant containers. Many accidental childhood ingestions occur as a result of caustic substances being placed in easily accessed containers, such as milk cartons or soda bottles.
• The reduced concentration of household products compared with their industrial strength counterparts has also been helpful in mitigating the severity of childhood exposures to agents such as household cleaners.
• For excellent patient education resources, visit eMedicine's Poisoning Center. Also, see eMedicine's patient education article Battery Ingestion.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to evaluate and aggressively manage the airway in patients with respiratory distress, significant laryngeal involvement, or an altered mental status
• Attempting to neutralize the ingested caustic agent with a weak acid or alkaline agent
• Inducing emesis
• Assuming that the absence of oropharyngeal burns precludes the presence of significant distal injuries
• Failing to consult a gastroenterologist or surgeon for evaluation of all symptomatic patients
• Failure to recognize and prepare for the possibility of cardiac arrest following ingestion of a hydrogen fluoride–containing agent, or, if arrest occurs, failing to treat it aggressively enough with CaCl₂
• Failure to recognize that some substances, such as phenol, can be caustic despite a near-neutral pH
• Failure to obtain sufficient information on the involved substance to make good treatment decisions - Examples include failing to confirm an agent’s key physical properties, such as concentration, or failing to appreciate the unique issues involving ingestions of some caustics such as button batteries, metallic chlorides, phenols, and hydrogen chloride.
• Lack of recognition of the unique issues involved in the management of special patient populations such as pediatrics and intentional ingestions

Special Concerns

• Although most childhood ingestions are accidental, be sure to consider child abuse in these instances.

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the medical review of this article by Lada Kokan, MD.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  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.
	View Full Size Image
Media type:  Photo

Media file 2:  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.
	View Full Size Image
Media type:  Photo

Media file 3:  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.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol. Dec 2007;45(8):815-917. [Medline].
2. 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].
3. 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].
4. 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].
5. 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].
6. 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].
7. 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].
8. Pelclová D, Navrátil T. Do corticosteroids prevent oesophageal stricture after corrosive ingestion?. Toxicol Rev. 2005;24(2):125-9. [Medline].
9. 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].
10. 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].
11. Turner A, Robinson P. Respiratory and gastrointestinal complications of caustic ingestion in children. Emerg Med J. May 2005;22(5):359-61. [Medline].

Article Last Updated: Nov 4, 2008