Alkali toxicity, though rare, can lead to serious medical problems.

Adult caustic ingestions are

usually intentional, involving more substantial amounts, and may result in significant medical
sequelae. This activity describes the evaluation and management of alkali ingestions and
highlights the role of the interprofessional team in managing patient post alkali ingestions.

Objectives:

●Identify the etiology of alkali ingestion medical conditions and emergencies.

●Describe the history and physical findings expected during an examination for alkali toxicity
secondary to ingestion.
●Outline the treatment and management options available for alkali toxicity secondary to
ingestion.
●Explain some interprofessional team strategies for improving care coordination and
communication to advance alkali toxicity management and improve outcomes.

Access free multiple choice questions on this topic. Go to:

Introduction
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.

Go to:

Etiology
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.
Go to:

Epidemiology
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]

Go to:

Pathophysiology
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]

Go to:

Histopathology
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]

Go to:

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.

Go to:

Evaluation
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.

Go to:

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.

Go to:

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.

Go to:

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.

Go to:

Prognosis
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]

Go to:

Complications
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]

Go to:

Consultations
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.

Go to:

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.

Go to:

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]