Caustic Ingestions 

Updated: Oct 27, 2018
Author: Eric M Kardon, MD, FACEP; Chief Editor: David Vearrier, MD, MPH 



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

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

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.

Toxicity, caustic ingestions. Endoscopic view of t 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.
Toxicity, caustic ingestions. Endoscopic view of t 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 t 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.

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]




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 the possibility of significant internal injury (although 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 caustic agents.


Common acid-containing sources include the following:

  • 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 include the following:

  • Drain-cleaning products
  • Ammonia-containing products
  • Oven-cleaning products
  • Swimming pool–cleaning products
  • Automatic dishwasher detergent
  • Hair relaxers
  • Clinitest tablets
  • Bleaches
  • Cement

Physical Examination

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 in the absence of oropharyngeal lesions

  • Drooling

  • Subcutaneous air

  • Acute peritonitis – Abdominal guarding, rebound tenderness, and diminished bowel sounds

  • Hematemesis

Indications of severe injury include the following:

  • Altered mental status

  • Peritoneal signs

  • Evidence of viscous perforation

  • Stridor

  • Hypotension

  • Shock



Diagnostic Considerations

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. Delays in securing a definitive airway can result in increased difficulty due to progressive airway edema.

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 the following:

  • Strictures
  • Fistula
  • Hypomotility disorders
  • Increased risk of gastrointestinal cancers

Differential Diagnoses



Laboratory Studies

Laboratory studies may include the following:

  • pH testing of product: A pH less than 2 or greater than 12.5 indicates greater potential for severe tissue damage,[10] but 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) and electrolyte, blood urea nitrogen (BUN), creatinine, and arterial blood gas (ABG) levels may all be helpful as baseline values and as indications of systemic toxicity

  • Liver function tests and a disseminated intravascular coagulation (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

  • Blood type and crossmatch are indicated for any potential surgical candidates or those with the potential for gastrointestinal bleeding

  • Obtain aspirin and acetaminophen levels as well as an electrocardiogram (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

Obtain an upright chest radiograph in all cases of caustic ingestion. Findings may include pneumomediastinum or other findings suggestive of mediastinitis, pleural effusions, pneumoperitoneum, aspiration pneumonitis, or a button battery (metallic foreign body). However, the absence of findings does not preclude perforation or other significant injury.

Abdominal radiographic findings may include pneumoperitoneum, ascites, or an ingested button battery (metallic foreign body). If contrast studies are obtained, water-soluble contrast agents are recommended because they are less irritating to the tissues in cases of perforation.

Computed tomography (CT) scans will often be able to delineate small amounts of extraluminal air, not seen on plain radiographs.

Chirica et al cite CT as CT scan superior to traditional endoscopy for helping to decide whether patients require emergency resection or observation.[1]  Similarly, Bruzzi et al reported that emergency CT outperforms endoscopy in predicting esophageal stricture formation after caustic ingestion.[11]

On the other hand, Lurie et al evaluated the role of chest and abdominal CT in assessing the severity of acute corrosive ingestion and concluded that CT should not be the only basis for surgical decisions during the initial phase of acute corrosive ingestions. They noted that CT can underestimate the severity of corrosive ingestion as compared with endoscopy. In their retrospective study of 23 patients, endoscopy findings were graded as 0, 1, 2a, 2b, 3a, and 3b (Zargar criteria); and CT findings were graded as 0, 1, 2, and 3. Endoscopy grading was found to be higher than CT grading in 14 patients (66%).[12]


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 who are not tolerating liquids or with complaints of pain

  • 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 of 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. Endoscopy is typically avoided when more than 24 hours have elapsed after the ingestion due to decreased wound strength and an increased risk of iatrogenic perforation. 

Obtaining meaningful information from endoscopy after treatment with activated charcoal is very difficult. Routine use of activated charcoal is not recommended in caustic ingestions.

Endoscopic ultrasonography has been shown to more accurately show the depth of lesions than endoscopy alone.[13] Further studies will be necessary to determine the utility of this procedure in aiding in diagnosis and treatment.



Approach Considerations

In patients with caustic ingestion, airway monitoring and control is the first priority. When airway compromise is present, a definitive airway must be established. In patients with a stable airway and no clinical or radiological sign of perforation, medical therapy should be initiated.[14, 15, 16, 17]

Arrangements should be made for urgent esophagogastroduodenoscopy (EGD) to grade the degree of injury and establish long-term prognosis, In asymptomatic patients, however, EGD may be withheld in favor of observation. Pediatric patients who remain asymptomatic for several hours (2 - 4 hours) after an exploratory ingestion and who are tolerating a normal diet may be discharged with appropriate follow-up and return precautions. Surgical consultation is indicated for suspected perforation. Because of the risk of late complications—most commonly, esophageal stricture formation—arrangements for follow-up need to be made.[14, 15, 16]



Prehospital Care

Attempt to identify the specific product, concentration of active ingredients, and estimated volume and amount ingested. Obtain MSDS sheets when possible for workplace exposures. 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, re-exposing tissue to the caustic agent.

Small amounts of a diluent may be beneficial if administered as soon as possible after a solid or granular alkaline ingestion, to remove any particles that are adhering 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. This practice is controversial: Some of the literature available on this topic discourages the use of diluents because of the concern of inducing emesis resulting in re-exposure of tissue to caustic agent.

Diluents should not be used with any acid ingestion or liquid alkaline ingestion. The risk of vomiting with re-exposure 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. Intravenous fluids and blood products may be required in the event of significant bleeding, vomiting, or third spacing.

Airway control

Because of the risk of rapidly developing airway edema, the patient’s airway and mental status should be immediately assessed and continually monitored. Equipment for endotracheal intubation and cricothyrotomy should be readily available. Gentle orotracheal intubation or fiberoptic-assisted intubation is preferred. Blind nasotracheal intubation should be avoided due to 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. If a difficult airway is anticipated, IV ketamine can be used to provide enough sedation to obtain a direct look at the airway.

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 re-exposure 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.

In large-volume liquid acid ingestions, nasogastric tube (NGT) suction may be beneficial 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, unless signs of perforation are present. This should be done after consulting with a regional poison control center.

Activated charcoal is relatively contraindicated in caustic ingestions because of poor adsorption and endoscopic interference.


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; this would result in excessive heat production.


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.


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)

Consultation with the local poison control center may be helpful, particularly if unfamiliar or unique agents are involved. These may include industrial strength detergents, button batteries, zinc chloride, mercuric chloride, hydrogen fluoride, phenol, and Clinitest tablets.

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



Guidelines Summary

Guidelines on pediatric gastrointestinal endoscopy from the European Society of Gastrointestinal Endoscopy (ESGE) and European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) include the following suggestions and recommendations for management of corrosive ingestion in pediatric patients[18] :

  • Suggestion: Every child who has ingested a corrosive substance should have a thorough follow-up, with endoscopy dictated only by symptoms; depending on the symptoms, endoscopy should be performed within 24 hours. (Strong recommendation, high quality evidence.)
  • Recommendation: Every child with a suspected caustic ingestion and symptoms or signs (eg, oral lesions, vomiting, drooling, dysphagia, hematemesis, dyspnea, abdominal pain) should undergo esophagogastroduodenoscopy (EGD) to identify all consequent digestive tract lesions. (Strong recommendation, high quality evidence.)
  • Suggestion: In cases of suspected corrosive ingestion where the child is asymptomatic (no drooling of saliva/other symptoms, no mouth lesions) and adequate follow-up is assured, EGD may be withheld. (Weak recommendation, moderate quality evidence.)
  • Recommendation: In patients with grade IIb esophagitis after corrosive ingestion, high doses of intravenous dexamethasone (1 g/1.73 m 2 per day) should be administered for a short period (3 days), to prevent the development of esophageal stricture. No evidence of benefit exists for the use of corticosteroids in other grades of esophagitis (I, IIa, III). (Strong recommendation, moderate quality evidence.)


Medication Summary

Supportive care, rather than specific antidotes, is the mainstay of management following caustic ingestions. A systematic review and meta-analysis by Katibe et al concluded that the available evidence does not support the use of corticosteroids for the prevention of esophageal strictures following caustic ingestion, but noted that the overall quality of the evidence is limited.[19]

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 following agents may be of value in supportive care.

Antibiotic, Cephalosporin (Third Generation)

Class Summary

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

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.

Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations < 25 mcg/mL to 85% bound at 300 mcg/mL.

Antibiotic, Penicillin and Beta-lactamase Inhibitor

Class Summary

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

Ampicillin and sulbactam (Unasyn)

Drug combination of beta-lactamase inhibitor with ampicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.

Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.

Proton Pump Inhibitor

Class Summary

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

Pantoprazole (Protonix)

Indicated for short-term treatment of GERD associated with erosive esophagitis. Also effective in treating gastric ulcers, including those caused by H pylori.

Analgesic, Narcotic

Class Summary

Narcotic analgesics should be used to reduce the pain associated with these ingestions.


DOC for analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone.

Various IV doses are used; commonly titrated until desired effect obtained.



Further Outpatient Care

Adult patients with an unintentional exposure may be discharged after a 2- to 4-hour observation period if the clinician has no unique concerns regarding the ingested substance (eg, large volume, high concentration, agent with potential for systemic toxicity) and the patient meets all the following criteria:

  • Asymptomatic
  • Clear sensorium
  • Able to ingest oral fluids without difficulty
  • Demonstrate easy speech
  • Reliable
  • Familiar with delayed symptoms and able to return if any occur

Postdischarge arrangements may include the following:

  • Psychiatric evaluation for all patients with intentional ingestion
  • Follow-up esophagram 3-4 weeks postingestion

Treatment of esophageal stricture

Esophageal stricture can develop as early as 3 weeks after caustic ingestion, but typically occurs 8 weeks or longer afterwards. Strictures can be treated with esophageal dilatation, using bougies (usually Savary) or balloon catheters. Savary bougies are considered more reliable for treatment of consolidated and fibrotic strictures or long, tortuous ones, and bougie dilatation may pose lower risk of perforation, with rates as high as 30% reported with balloon dilatation of caustic strictures.[16]

However, in a study by Uygun et al, fluoroscopically guided esophageal balloon dilatation (EBD) was found to be a safe procedure, with a low rate of complications; and it had a 100% success rate. In their review of of 369 EBD sessions in 38 children (aged 14 months to 14 years, median 3.5 years) with caustic esophageal strictures, six (1.6%) esophageal perforations occurred in five patients (13.2%).[20]

Ugyun et al recommend that in children, dilatation should be performed gently with balloons of gradually increasing appropriate diameters over consecutive sessions. In addition, the study findings showed that EBD treatment was significantly faster and shorter in patients who began EBD earlier (mean, 15 days) after caustic ingestion than in those who began it later (mean, 34 days).[20]

When esophageal dilatation is not possible or fails to provide an adequate esophageal caliber in the long-term, esophageal replacement by retrosternal stomach or, preferably, right colonic interposition should be considered. Arguments can be made for either bypass or resection of the native esophagus.[16]

Esophageal cancer

Patients who have experienced caustic injury are at increased risk for esophageal cancer (both adenocarcinoma and squamous cell carcinoma), typically developing 1 to 3 decades after ingestion. Consequently, long-term endoscopic screening is recommended for these patients.[16]

Further Inpatient Care

Admit, for observation and possible endoscopy, 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. 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.

Rollin et al have proposed an algorithm for surgical management of caustic ingestion injuries in adult patients.[6]


If an ICU bed is not available or if endoscopy is not available when indicated, transfer is advised.


In the home, caustic substances should be kept in their original labeled containers to avoid accidental ingestion. They should be stored out of reach of toddler-aged children.

In the workplace, policies and procedures need to be developed and disseminated, so that employee exposures can be treated quickly and effectively.


Complications may include the following:

  • Airway edema or obstruction may occur immediately or up to 48 hours following an alkaline exposure.
  • Gastroesophageal perforation may occur acutely.
  • Upper gastrointestinal hemorrhage may occur acutely in caustic exposure

  • 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.

  • Delayed upper GI bleeding may occur in acid burns 3-4 days after exposure as the eschar sloughs.

  • 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.

  • Though many button batteries may pass through the GI tract without causing damage, they can result in perforation at any time during their course through the gastrointestinal system, particularly if they are 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 calcium chloride.

  • Long-term risks include squamous cell carcinoma, which occurs in 1-4% of all significant exposures and may occur as late as 40 years after exposure.


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 the following:

  • Phenol
  • Zinc chloride
  • Mercuric chloride
  • Hydrogen fluoride

Patient Education

See the list below:

  • 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 patient education information, see the First Aid and Injuries Center, as well as Battery Ingestion.


Questions & Answers


What are caustic ingestions?

What is the pathophysiology of caustic alkaline ingestions?

What is the pathophysiology of caustic ingestions?

What is the pathophysiology of caustic acid ingestions?

What is the incidence of caustic ingestions in the US?

What are the mortality rates from caustic ingestions?

What is the frequency of severe injury from caustic ingestions?

How does the incidence of caustic ingestions vary by age?


What is the clinical history of caustic ingestions?

What are the signs and symptoms of caustic ingestions?

What is the focus of clinical history in suspected caustic ingestions?

What are the common sources of caustic acid ingestions?

What are the common sources of caustic alkaline ingestions?

What are the signs and symptoms of impending airway obstruction of caustic ingestions?

Which physical signs of injury suggest caustic ingestions?

What are indications of severe injury in patients with caustic ingestions?


What are the initial complications of caustic ingestions?

What are the late-developing complications of caustic ingestions?

What are the differential diagnoses for Caustic Ingestions?


Which lab tests are performed in the workup of caustic ingestions?

Which imaging studies are performed in the workup of caustic ingestions?

Which initial procedures are performed following a caustic ingestion?

What is the role of endoscopy in the workup of caustic ingestions?

What is the role of activated charcoal in the treatment of caustic ingestions?

What is the role of endoscopic ultrasonography in the evaluation of caustic ingestions?


What is the focus of treatment for caustic ingestions?

What is the prehospital care for caustic ingestions?

How are patients with caustic ingestions triaged in the emergency department (ED)?

What are the steps in the emergency department to ensure airway control in patients with caustic ingestions?

What is the role of gastric emptying and decontamination in the emergency department care of caustic ingestions?

What is the role of dilution in the emergency department care of caustic ingestions?

What is the role of neutralization in the emergency department care of caustic ingestions?

Which visualization technique is used for airway management in patients with caustic ingestions?

When is surgical consultation indicated for the treatment of caustic ingestions?

When is endoscopic consultation indicated for the management of caustic ingestions?

Which specialist consultations are beneficial for patients with caustic ingestion?


What are the ESGE-ESPGHAN treatment guidelines for caustic ingestions in pediatric patients?


What is the focus of management for caustic ingestions?

Which medications in the drug class Analgesic, Narcotic are used in the treatment of Caustic Ingestions?

Which medications in the drug class Proton Pump Inhibitor are used in the treatment of Caustic Ingestions?

Which medications in the drug class Antibiotic, Penicillin and Beta-lactamase Inhibitor are used in the treatment of Caustic Ingestions?

Which medications in the drug class Antibiotic, Cephalosporin (Third Generation) are used in the treatment of Caustic Ingestions?


What are the criteria for discharge following treatment for a caustic ingestion?

What should be included in followup treatment after a caustic ingestion?

How are esophageal strictures treated following a caustic ingestion?

Why is long-term endoscopic screening required for patients following a caustic ingestion?

When is inpatient care indicated for caustic ingestions?

When is patient transfer needed following caustic ingestions?

How are caustic ingestions prevented?

What are complications of caustic ingestions?

What is the prognosis of caustic ingestions?

What information should patients be given about preventing caustic ingestions?