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Alkali Toxicity

Editor: Arlene V. McTeer Updated: 6/21/2022 12:48:47 AM

Alkali toxicity, though rare, can lead to significant medical problems. In developed nations, alkaline ingestions are more predominant when compared to acidic ingestions.[1] Worldwide caustic ingestions occurring amongst children are usually accidental and therefore benign given the small amounts ingested. In contrast, adult caustic ingestions are usually intentional, involving larger amounts, and have more significant sequelae. Patients with intentional ingestions require more involved medical management and long term treatment.


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Caustic ingestions can cause functional and histological damage to any surface in which they come in contact.  Any alkaline agent with a pH greater than 7.0 is considered caustic. Some household cleaning compounds contain strong alkalis. Alkali substances can cause liquefactive necrosis and can be especially corrosive at high pH values as the necrosis continues until the alkali becomes neutralized.[2] This chemical pathway is especially damaging to human tissue within the esophagus. 

There are many products, both household and industrial, that contain chemicals with caustic potential. Bleach is the most common household alkali, which has a pH of 11 and is 3% to 6% sodium hypochlorite solution. Household caustics are usually less concentrated; therefore, they are usually benign. On the other hand, industrial strength bleach has a greater concentration of sodium hypochlorite, thus may cause more extensive damage, including gastric and esophageal necrosis.

In developed countries, there is less morbidity and mortality related to caustic ingestion secondary to better product regulations and education about alkali products. Exposure to caustics is still a problem in underdeveloped nations.[2] Caustic ingestions are either intentional usually amongst adolescents and adults with suicidal ideation, unintentional mostly toddlers and children that gain access to the substance and are curious about it, or incidental often associated with occupational or industrial exposures. The majority of reported exposures are unintentional; however, the majority of serious injuries occur after intentional ingestions.[3] 

Developed countries have more effective exposure preventions, such as childproof containers, regulation of highly corrosive substances, better access to emergency care, healthier nutrition status, and better follow up. As opposed to underdeveloped nations where lack of regulations, delay of care, malnutrition, and cultural-specific propensities to the use of caustic agents during attempted suicides pose a more significant challenge with increased morbidity and mortality.[3]

Many physiologic characteristics determine the degree of damage that alkali ingestion may cause.  These properties include the pH of the material, the duration of time in which the substance is in contact with the surface, the amount or volume ingested, as well as the amount of acid required to neutralize the substance.[3] Other physical properties that influence the degree of damage caused by caustic ingestions have to do with its formulation. Examples include solid, granular, gel, liquid, or gaseous forms. Liquid and gaseous forms can travel further throughout the GI and airway tract, thus causing more extensive esophageal or gastric injury. Ingestions of solid alkali materials, like lye, will mostly cause oropharyngeal and proximal esophageal injury as opposed to distal GI tract damage caused by liquid caustics.

The pH of the substance determines the type of damage in a caustic ingestion. Acids or substances with very low pH values cause coagulative necrosis resulting in an eschar formation. Alkalis or substances with high pH values will cause liquefactive necrosis. Alkalis with a pH above 11 tend to cause more significant injury. While the pH, concentration, and duration of contact with human tissue influence the extent of damage directly to GI tissue, irritation of the pulmonary tract may also occur. When a caustic agent mixes with other contents in the stomach, chlorine gas forms.[4] This gas then causes pulmonary irritation, which can lead to respiratory distress.[5]

Once a body surface is exposed to an alkali substance, hydrogen ions penetrate the tissue leading to protein denaturation and lipid saponification. Thrombosis of microvasculature also occurs during this process, leading to further tissue necrosis and deep tissue injury called liquefaction necrosis. This process can lead to gastric and esophageal necrosis, emesis secondary to gastric irritations, pneumonitis after aspiration, and pulmonary irritation from chlorine gas production in the stomach.[6][7] 

History and Physical

If possible, a thorough history should be obtained to determine the amount, type of substance, and other substances taken. It is also essential to establish whether or not the ingestion was intentional or unintentional. A cardinal sign of alkali ingestion is chemical burns on the mucosa of the oral cavity.[8] Symptoms associated with caustic ingestions include pain, drooling, nausea, vomiting, abdominal pain, burning sensation in the upper GI tract, odynophagia and shortness of breath secondary to an edematous airway, aspiration, or fume inhalation.[2] The physical exam may reveal signs suggestive of mucosal and skin damage such as edema, erythema, desquamation, as well as tachycardia, tachypnea, abdominal tenderness, hematemesis, and bloody stools.[2]

When caustic ingestions occur, splashing can expose other parts of the body to these substances. For example, caustic materials that come into contact with the conjunctiva may cause ocular burns, which are very painful and can cause visual damage to structures in the anterior portion of the eye.  Another physical finding associated with caustic ingestion is “dribble burns,” which are streaks of burns on the chest and face.


The mainstay of treatment when initially evaluating a patient after a caustic ingestion is airway assessment, recognition & management of circulatory shock, and stabilization. Signs suggestive of airway compromise and serious esophageal injuries are stridor, drooling, and vomiting.[9]  The presence of oral burns is not always present with serious esophageal damage, and pain is an unreliable predictor of injury severity.  It is also important to assess the circulatory status of the patient as hemodynamic instability may be secondary to GI perforation and/or GI bleeding. For patients that have peritonitis, general surgery should be consulted immediately while simultaneously fluid resuscitating the patient. Coingestants should always be considered, especially for patients that are hemodynamically unstable with a benign abdominal exam and no signs of upper or lower GI bleeding. Clinicians should also evaluate for injury to the mediastinum by palpating the chest and neck for subcutaneous emphysema.

Laboratory testing is important mostly for evaluating intentional ingestions or any ingestion where significant injury is suspected. Useful labs include blood gas to assess for acidosis; comprehensive metabolic panel to assess for hepatic function abnormality, electrolyte disturbances, and renal failure; complete blood count to evaluate for anemia and hemolysis; coagulation profile to assess for coagulopathy; blood type and screen in case surgery or blood transfusion are necessary; acetaminophen and salicylate levels to evaluate for possible co-ingestions. In caustic ingestions tissue injury and shock lead to lactate production, thus reflect an anion gap acidosis. ECG is also prudent to assess signs of ischemia, arrhythmia, or interval abnormalities.

Radiographs of the chest and abdomen may be obtained to assess for signs of perforation or the presence of alkali-containing products, such as disk batteries.[4] For cases related to battery explosion (i.e., electronic cigarette batteries), practitioners should assess for alkali pH using litmus testing before irrigating burns.[5] CT of chest and abdomen may be useful in stable patients with suspected intra-abdominal perforated viscus. The gold standard is endoscopy. Endoscopy should occur between 12 and 24 hours post-ingestion to have the lowest risk for iatrogenic perforation.[10] Endoscopy is used to visualize and grade the esophageal mucosal burn. Grade 1 is the classification given when tissue edema and hyperemia are visible during endoscopy. Ulcerations, blisters, and whitish exudates classify as grade 2 (grade 2a if noncircumferential and grade 2b if circumferential). Grade 3 burns classify by necrotic lesions and deep ulcerations. If endoscopy is not available or risk for esophageal perforation from endoscopy outweigh the benefits, CT of the abdomen and chest with contrast may be used to evaluate the extent of GI injuries.

Treatment / Management

The first priority while treating caustic ingestions is airway management. If there are any signs suggestive of respiratory distress, intubation may be required. The airway after a caustic ingestion is considered a problematic airway secondary to oropharyngeal edema, friable tissue, and bleeding. Thus it is ideal to evaluate the airway with a fiberoptic device when possible. Direct laryngoscopy is the first line for a definitive airway. Blind nasotracheal intubations is an absolute contraindication. Laryngeal mask airways, combination tubes, retrograde intubation, and bougies are relatively contraindicated given the risk of perforation.

Decontamination and dilution are other vital steps in the treatment of caustic ingestions. Medical staff must take precautions to prevent self-exposure of the suspected caustic agent by utilizing gowns, gloves, and mask with face shields. Patients should also undergo decontamination by removal of soiled garments and copious irrigation.

For alkali injuries caused by ingestion, immediate dilution with drinking a glass of water is the recommendation in the prehospital setting. Charcoal and ipecac syrup are contraindicated; charcoal will prevent adequate visualization during endoscopy and vomiting, which will re-expose upper GI tissue to the caustic agent. The one exception for the use of charcoal is when co-ingestion is suspected, and the healthcare provider has concern for severe toxicity.[11]

Fluid resuscitation if often indicated. Central venous access may be necessary for refractory shock and accurate blood pressure monitoring. Steroids are not indicated in caustic ingestions as there has yet to be any proven benefits for its use. [12] If the caustic ingestion causes GI perforation, then surgical repair and antibiotics are required. 

Prompt endoscopy is necessary for grading the extent of a caustic injury in symptomatic patients.  Also, if an ingested disk battery appears on radiographic studies, immediate endoscopy is warranted for removal. [2] If there is esophageal perforation, free intraperitoneal air, or peritoneal signs, then emergent laparotomy is indicated. Surgical exploration should also be a consideration in the setting of signs of shock, ingestion of more than 150 mL of a caustic substance, respiratory distress, and persistent lactic acidosis.[13]

All patients with symptomatic ingestions should be admitted to a monitored setting. Grade 1 injury patients can usually be discharged once they can tolerate oral intake. Grade 2a injury patients rewquire observation for injury progression and symptomatic treatment. Grade 2b and 3a injury patients require intensive care unit admission for enteral or parenteral nutrition, continuous monitoring, and symptomatic treatment.

Differential Diagnosis

It is crucial to determine the substance ingested, as well as the amount, duration of time of exposure, and the type of substance (i.e., solid, liquid). The treatment for the ingestion of acidic substances differs from the treatment for the ingestion of alkali substances. For ingestion injuries that are intentional, it is also extremely important to assess for polysubstance ingestions.[7] Patients that are attempting to hurt themselves may take aspirin, acetaminophen, alcohol, cocaine, amphetamines, etc. Clinicians must address and rule out any coingestions while managing the alkali toxicity. 

Toxicity and Adverse Effect Management

In systemic toxicity, the goal is to maximize the patient's hemodynamics and maintain their airway. Oral intubation using direct laryngoscopy is the first choice to establish the patient’s airway. If there is co-ingestion, a patient may experience third spacing, bleeding, metabolic abnormalities, or shock. Patients should have resuscitation with crystalloids. Central venous access may be necessary for aggressive resuscitation.


In grade 1 and some grade 2a burns, the function of the esophagus usually recovers over time. Grade 2b and grade 3 burns may result in dense scar tissue leading to stricture formation. Strictures require long-term management, including dilations, stenting, and sometimes surgery. Poor prognosis is associated with grade 3 esophageal injury, systemic complications, or age greater than 65.[14]  


Alkali ingestions may lead to stricture formation. Esophageal strictures can cause odynophagia and dysphagia with subsequent malnutrition. Squamous cell carcinoma of the esophagus is a complication of grade 3 esophageal caustic injuries.[15] Cancer can present decades after the initial exposure. Hence total removal of the esophagus is recommended if reconstructive surgery for strictures is necessary.[10]


A gastroenterologist should be consulted for esophagogastroduodenoscopy within 12 to 24 hours of ingestion to assess the extent of the damage. A regional poison control center should render consultation to guide clinicians on treatment options and the duration of observation.  If the ingested substance has several known ingredients, then poison control can also advise in the management of the additional ingredients.

Deterrence and Patient Education

It is crucial that household cleaning products are stored in a safe childproof location to prevent accidental ingestions. If caustic ingestion is suspected, it is contraindicated to induce vomiting as this re-exposes the gastrointestinal tract to the substance. Milk or water are options within a few minutes of accidental ingestion.

Enhancing Healthcare Team Outcomes

Managing patients with alkali toxicity requires an interprofessional team comprised of emergency physicians, nurses, pharmacist, gastroenterologist, and possibly general surgeons. If the ingestion was intentional, then psychological help is also necessary. Another important step in the management of caustic ingestion is staging and assessing the extent of injury to establish the appropriate treatment course. The Zagar modified endoscopic classification scheme is used to stage caustic ingestion injuries.[14]  A retrospective medical chart review at the Chang Gung Memorial Hospital in Tao-Yuan, Taiwan between June 1999 and July 2006 looked at the outcomes of 273 patients admitted for caustic ingestion. Of the 273 patients, 82 had grade 3b injuries.  The second most common injury was grade 2b (n = 62). The most common complication was strictures (n = 66), followed by aspiration pneumonia (n = 31), and respiratory failure (n = 21).[14] Understanding that grade 3b injuries are the most common is important, as these patients usually require longer hospital stays and ICU admission, with higher rates of morbidity requiring close follow up with gastroenterology every 6 months. 

Alkali toxicity requires a comprehensive, interprofessional healthcare team effort for assessment and subsequent management.  Initial contact will often be in the ED and the clinician there will need to assess as to the severity and whether it was intentional or accidental. A triage nurse can be of great help at this stage of the evaluation. Both physicians and nurses will work together in rendering immediate supportive care, intubation, and engaging poison control resources. Pharmacists can offer help with preparing colloids and other necessary medications, as well as performing medication reconciliation in conjunction with nursing. If the toxicity is the result of an intentional event, then psychological resources can be brought in as soon as the patient is stable. Nursing can continue to monitor vital signs and report back to the team any unusual or abnormal findings. As can be seen, a collaborative interprofessional team effort is needed in alkali toxicity cases to direct outcomes to a positive result. [Level 5]



Riffat F, Cheng A. Pediatric caustic ingestion: 50 consecutive cases and a review of the literature. Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus. 2009:22(1):89-94. doi: 10.1111/j.1442-2050.2008.00867.x. Epub 2008 Oct 1     [PubMed PMID: 18847446]

Level 3 (low-level) evidence


Brent J. Water-based solutions are the best decontaminating fluids for dermal corrosive exposures: a mini review. Clinical toxicology (Philadelphia, Pa.). 2013 Sep-Oct:51(8):731-6. doi: 10.3109/15563650.2013.838628. Epub 2013 Sep 5     [PubMed PMID: 24003912]


Contini S, Swarray-Deen A, Scarpignato C. Oesophageal corrosive injuries in children: a forgotten social and health challenge in developing countries. Bulletin of the World Health Organization. 2009 Dec:87(12):950-4. doi: 10.2471/BLT.08.058065. Epub     [PubMed PMID: 20454486]


Karnak I, Tanyel FC, Büyükpamukçu N, Hiçsönmez A. Pulmonary effects of household bleach ingestion in children. Clinical pediatrics. 1996 Sep:35(9):471-2     [PubMed PMID: 8877246]


Turner A, Robinson P. Respiratory and gastrointestinal complications of caustic ingestion in children. Emergency medicine journal : EMJ. 2005 May:22(5):359-61     [PubMed PMID: 15843706]


Contini S, Scarpignato C, Rossi A, Strada G. Features and management of esophageal corrosive lesions in children in Sierra Leone: lessons learned from 175 consecutive patients. Journal of pediatric surgery. 2011 Sep:46(9):1739-45. doi: 10.1016/j.jpedsurg.2011.03.017. Epub     [PubMed PMID: 21929983]


Chibishev A, Pereska Z, Chibisheva V, Simonovska N. Corrosive poisonings in adults. Materia socio-medica. 2012:24(2):125-30. doi: 10.5455/msm.2012.24.125-130. Epub     [PubMed PMID: 23678319]


Cowan D, Ho B, Sykes KJ, Wei JL. Pediatric oral burns: a ten-year review of patient characteristics, etiologies and treatment outcomes. International journal of pediatric otorhinolaryngology. 2013 Aug:77(8):1325-8. doi: 10.1016/j.ijporl.2013.05.026. Epub 2013 Jun 17     [PubMed PMID: 23786788]


Crain EF, Gershel JC, Mezey AP. Caustic ingestions. Symptoms as predictors of esophageal injury. American journal of diseases of children (1960). 1984 Sep:138(9):863-5     [PubMed PMID: 6475876]


Cheng HT, Cheng CL, Lin CH, Tang JH, Chu YY, Liu NJ, Chen PC. Caustic ingestion in adults: the role of endoscopic classification in predicting outcome. BMC gastroenterology. 2008 Jul 25:8():31. doi: 10.1186/1471-230X-8-31. Epub 2008 Jul 25     [PubMed PMID: 18655708]


Chyka PA, Seger D, Krenzelok EP, Vale JA, American Academy of Clinical Toxicology, European Association of Poisons Centres and Clinical Toxicologists. Position paper: Single-dose activated charcoal. Clinical toxicology (Philadelphia, Pa.). 2005:43(2):61-87     [PubMed PMID: 15822758]


Anderson KD, Rouse TM, Randolph JG. A controlled trial of corticosteroids in children with corrosive injury of the esophagus. The New England journal of medicine. 1990 Sep 6:323(10):637-40     [PubMed PMID: 2200966]


Wu MH, Lai WW. Surgical management of extensive corrosive injuries of the alimentary tract. Surgery, gynecology & obstetrics. 1993 Jul:177(1):12-6     [PubMed PMID: 8322144]


Zhang X, Wang M, Han H, Xu Y, Shi Z, Ma G. Corrosive induced carcinoma of esophagus after 58 years. The Annals of thoracic surgery. 2012 Dec:94(6):2103-5. doi: 10.1016/j.athoracsur.2012.03.110. Epub     [PubMed PMID: 23176921]


Uygun I, Aydogdu B, Okur MH, Arayici Y, Celik Y, Ozturk H, Otcu S. Clinico-epidemiological study of caustic substance ingestion accidents in children in Anatolia: the DROOL score as a new prognostic tool. Acta chirurgica Belgica. 2012 Sep-Oct:112(5):346-54     [PubMed PMID: 23175922]

Level 2 (mid-level) evidence


Gummin DD, Mowry JB, Beuhler MC, Spyker DA, Brooks DE, Dibert KW, Rivers LJ, Pham NPT, Ryan ML. 2019 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 37th Annual Report. Clinical toxicology (Philadelphia, Pa.). 2020 Dec:58(12):1360-1541. doi: 10.1080/15563650.2020.1834219. Epub     [PubMed PMID: 33305966]


Hoffman RS, Howland MA, Kamerow HN, Goldfrank LR. Comparison of titratable acid/alkaline reserve and pH in potentially caustic household products. Journal of toxicology. Clinical toxicology. 1989:27(4-5):241-6     [PubMed PMID: 2600988]


Lupa M, Magne J, Guarisco JL, Amedee R. Update on the diagnosis and treatment of caustic ingestion. The Ochsner journal. 2009 Summer:9(2):54-9     [PubMed PMID: 21603414]


Mamede RC, de Mello Filho FV. Ingestion of caustic substances and its complications. Sao Paulo medical journal = Revista paulista de medicina. 2001 Jan 4:119(1):10-5     [PubMed PMID: 11175619]