Continuing Education Activity

Caustic ingestions pose a substantial challenge in clinical practice due to their potential for severe morbidity and mortality. Although the upper digestive tract sustains primary injury, understanding the complex anatomy—from the oral cavity through the esophagus, stomach, and duodenum—is pivotal in diagnosis and management. The intricate nature of this region, the varying tissue compositions, and the different functions and vulnerabilities across sections require a nuanced approach for better patient outcomes. Patient care involves every level of the medical team, from poison control outreach and medical toxicologists to the surgeons on the floor.

This activity is designed to equip healthcare professionals with comprehensive knowledge and practical skills in managing caustic ingestions. Focused on the complexities of the upper digestive tract anatomy and the diverse manifestations of caustic injuries, this program discusses diagnostic strategies, evidence-based guidelines, and optimal treatment modalities. Through case-based discussions and interactive sessions, participants will enhance their competence in promptly assessing, triaging, and treating caustic ingestion cases, ultimately improving patient care and outcomes.

Objectives:

• Differentiate severity levels, distinguishing between mild, moderate, and severe cases based on tissue damage and symptoms.
• Implement immediate management, initiating emergency measures for airway protection, stabilization, and symptomatic treatment.
• Apply treatment strategies tailored to the injury's severity, including supportive care, endoscopic interventions, or surgery.
• Collaborate with an interprofessional team to enhance outcomes for patients with caustic ingestion. 

Introduction

The upper digestive tract is the primary site of tissue damage due to caustic ingestion. This part of the gut runs from the head, neck, mediastinum, and epigastric area. The oral region, pharynx, esophagus, stomach, and duodenum comprise the upper gastrointestinal tract (see Image. Digestive and Respiratory Anatomical Structures Connected to the Esophagus). 

The oral region (mouth) is the entryway to the digestive system, composed of the oral cavity, gingivae, teeth, tongue, palate, and palatine tonsil area. Mechanical and some enzymatic food digestion take place in the oral cavity. Nonkeratinized stratified squamous epithelium lines most oral mucosal surfaces. Masticatory areas like the gingivae and hard palate have keratinized or parakeratinized stratified squamous epithelium.[69] Mastication muscles surround the oral region.

The pharynx passes from the cranial base to the C6 vertebra level. This upper gut area is divided into the nasopharynx, oropharynx, and laryngopharynx. The nasopharynx and oropharynx have sensory functions during eating. The oropharynx and laryngopharynx help in the transit of food boluses from the oral cavity to the esophagus.

Head and neck structures surrounding the pharynx include the upper respiratory tract, salivary glands, thyroid and parathyroid glands, vagus nerve and its branches, cervical nerves, carotid arteries and its branches, external and internal jugular veins, deglutition muscles, and lymph nodes. Nonkeratinized stratified squamous epithelium lines the pharyngeal mucosal surfaces.

The esophagus is a long muscular tube where food passes from the mouth and pharynx to the stomach. This part of the gut has cervical, thoracic, and abdominal regions. In the neck, the esophagus lies posterior to the larynx and trachea. The thoracic esophagus runs in the mediastinum anterior to the vertebral column, posterior to the trachea, and to the right of the aorta. The abdominal esophagus begins at the T11 vertebral level, where the muscular tube opens to the stomach.

The following are the 3 esophageal constrictions:

• Cervical constriction: located 15 cm from the incisors and formed by the cricopharyngeus muscle; also known as the upper esophageal sphincter (UES)
• Broncho-aortic constriction: a compound constriction; the aortic arch crosses the esophagus 22.5 cm from the incisors, while the left main bronchus crosses the tube 27.5 cm from the incisors
• Diaphragmatic constriction: located 40 cm from the incisors; the area passing through the esophageal hiatus of the diaphragm, also known as the lower esophageal sphincter (LES)

These constrictions are important landmarks during esophagogastroduodenoscopy (EGD) and radiologic evaluation of esophageal lesions.

The esophageal mucosa is lined by nonkeratinized stratified squamous epithelium. The upper third of the esophagus has striated muscles. The lower third has smooth muscles. The middle third has mixed striated and smooth muscles. The esophagus has no serosa, so infections and tumors can quickly spread from this muscular tube to the neighboring regions.

The structures surrounding the esophagus include the following:

• In the neck: trachea, aortic and carotid artery branches, vagal and cervical nerve branches, thyroid and parathyroid glands, and thoracic duct
• In the trunk: thoracic duct, trachea, main bronchi, heart, the great blood vessels, pericardium, vagus nerve and branches, esophageal plexus, and azygos vein
• In the abdomen: posterior aspect of the liver, vagus nerve, esophageal plexus, diaphragm, abdominal aorta and branches, stomach fundus

The stomach starts at the esophagogastric junction (EGJ), where the mucosal lining transitions from squamous to simple columnar epithelium. Gastric secretions, characterized by high acidity, serve dual roles as digestive agents and potent defense mechanisms against pathogens due to their antimicrobial properties. The mucus protects the stomach from its secretions.

The duodenum is the proximal part of the small intestine, neutralizing acidic chyme and accomplishing most of the digestive process. Bicarbonate secretions raise the duodenal pH. This part of the upper gastrointestinal tract has microvilli and simple columnar epithelium, as it is specialized for food digestion and absorption.

Caustic ingestions can injure any part of the upper digestive tract. The esophagus is most vulnerable to alkaline damage, while the stomach is most prone to acidic injury. Severe cases can cause overspills or gut perforation that can spread the damage to neighboring structures.

Caustic ingestions are severe causes of morbidity and mortality and can affect all age groups. About 80% of caustic ingestion cases in the United States occur in children. For the best outcomes, critical ingestions require coordination between surgical and medical teams.[1]

Etiology

Caustic exposure can be accidental or intentional. Accidental exposures are most common in young children, often termed "exploratory ingestions." Accidental caustic ingestion often occurs in small amounts and typically involves household cleaners with low concentrations of chemicals like bleach and ammonia. Meanwhile, intentional exposures often result from self-harm attempts and involve large amounts of highly concentrated caustic chemicals.

Most caustic exposures involve oral ingestion (76%) and occur at home (93%). More than 80% of cases are unintentional. Substances ingested are either highly acidic or highly alkaline, requiring different treatment approaches.[1][2]

Epidemiology

The American Association of Poison Control Centers reported that 180,000 caustic exposure incidents were documented in the United States in 2019. Most cases involved pediatric accidental ingestion of household cleaning products. The rest were comprised of intentional caustic ingestion cases among adults. The alkaline substance lye is the most frequently reported component in caustic ingestions.

Pathophysiology

Generally, the pathophysiology underscoring tissue damage depends on the ingested agent's pH. Substances with pH over 7.0 are alkaline, and below 7.0 are acidic. Extremes of pH—specifically below 3.0 and above 11.0—are of greatest concern in human exposures. Strong alkalis and acids can damage tissues by different mechanisms.

Alkalis are classically associated with liquefactive necrosis. The process involves saponification and subsequent disruption of the lipid-rich cell membranes. Cell lysis releases digestive enzymes, dissolving the surrounding tissues. Strong alkalis can penetrate tissues more deeply than acids and cause more extensive tissue damage.[3]

In contrast, acids are classically associated with coagulative necrosis. Acid-related tissue injury is more superficial due to eschar formation, which limits acid penetration into the underlying tissues.[4] Acid ingestions are associated with "skip lesions," where the esophagus sustains discontinuous areas of damage.

However, distinguishing liquefactive from coagulative necrosis is less important in clinical practice. Strong alkalis and acids are equally capable of severe, full-thickness injury to the gastrointestinal tract.[5]

The titrable acid or alkali reserve (TAR) predicts tissue damage potential more accurately than pH. TAR is estimated by the amount of acid or alkali required to bring a substance's pH to 8.00. The higher the TAR, the more corrosive the agent. Still, pH is more often used in practice than TAR, as pH is more readily available and can approximate TAR in many cases. However, substances like zinc chloride and phenol require TAR values for predicting the potential for tissue damage, as these chemicals have near-physiologic pH but very high TAR.[6]

Other factors that will influence the extent and severity of damage include the physical state of the caustic substance (solid, liquid, or gel), tissue contact time, and quantity and concentration of the offending agent.[7]

Histopathology

Initial contact with a caustic substance produces eosinophilic necrosis and hemorrhagic congestion. A fibrinous layer forms over ulcerated areas in the first few days post-injury. Around the 5th day, an esophageal mold, comprised of dead cells, secretions, and food remnants, forms over the lesion.

Tissue repair commences around the 10th day, although edema and lymphatic ectasia can persist for weeks. Fibrosis, scarring, and stenosis can arise in the gastrointestinal mucosa and submucosa. Depending on the injury depth, the muscular layer may become sclerotic, and the esophageal plexus may be permanently damaged. Vascular injury can delay epithelial healing or produce recurrent ulcers.[3]

History and Physical

Individuals with caustic injuries may present unresponsive, breathless, and pulseless. After a quick primary survey, resuscitation must be administered promptly for patients with signs of cardiorespiratory arrest, regardless of the cause. Airway, breathing, and circulation must be stabilized. Patients should be monitored continuously on telemetry, with frequent assessments of vital signs. Once stabilized, the secondary survey may be initiated.

When taking the history of individuals with suspected caustic ingestion, 5 signficant details (the "5 Ws") must be elicited:

• Who - patient's personal information, including age and weight; details about accompanying family, friends, or witnesses are also important
• What - characteristics of the substances ingested
• When - time and date of ingestion
• Where - route of poisoning and geographic location of the incident 
• Why - determines if the caustic ingestion is intentional

Environmental factors may contribute to the pathology. Thus, the geographic location should be noted. Meanwhile, intentionality must be established, as the final disposition, eg, whether psychiatric referral is required, depends on this information. If caustic ingestion is nonaccidental, overdosing with other substances, such as acetaminophen, salicylates, cocaine, alcohol, and opioids, must also be considered.

Patients with caustic ingestion may be asymptomatic in one extreme or develop severe manifestations in another. Vomiting, drooling, chest pain, abdominal pain, and breathing and swallowing difficulty may be reported. Hematemesis may be caused by blood vessel erosion.

Physical examination may reveal oral and tongue edema and drooling. Upper airway edema may lead to vocal changes, stridor, and respiratory distress. Esophageal perforation can cause mediastinitis and peritonitis. Mediastinitis typically presents with nonspecific signs like tachycardia and fever. Occasionally, it may produce the Hamman sign—a systolic precordial crunching sound heard on auscultation. Peritonitis presents with abdominal tenderness and rigidity.[8] A complete exam should be performed to assess for other injuries, particularly oral and orbital burns.

Evaluation

Initial lab studies may include a complete blood count (CBC), coagulation studies, complete metabolic profile (CMP), and arterial or venous blood gas. The CBC may show inflammation-associated neutrophilia. Dehydration may falsely elevate the hemoglobin and hematocrit. Hematemesis may reduce hemoglobin to abnormal levels if severe.

The CMP can help detect electrolyte imbalances in patients with repeated vomiting. This test can also provide baseline renal and liver function information, which is crucial if surgery is contemplated. Blood gases help examine the severity of respiratory damage.

A comprehensive drug panel may be contemplated if multiple drug ingestion is also suspected.

Plain chest and abdominal radiography may identify free air in the mediastinum (pneumomediastinum) or peritoneum (pneumoperitoneum). Caustic substance aspiration may produce infiltrates on chest x-ray. An upper gastrointestinal series with a water-soluble contrast medium may confirm esophageal perforation but is not required if EGD is available (see Image. Esophageal Radiography With Contrast).

EGD is currently the gold standard in evaluating injuries from caustic ingestion (see Image. Esophagus Examination on Esophagogastroduodenoscopy).[9] The prognosis and stricture formation risk may be predicted based on the injury grade found on EGD (see under Staging below). However, a major decision point involves which patients should get an EGD. Some expert groups suggest that all patients with caustic exposure, regardless of severity, should receive an EGD, as asymptomatic patients can still have significant injury.[10][11] However, others report that accidental or unintentional ingestion has a low risk of clinically significant esophageal damage.[12][13]

EGD should be strongly considered in symptomatic patients, especially if they have posterior pharyngeal burns, stridor, respiratory distress, chest or abdominal pain, or inability to tolerate oral liquids.[14][15] The procedure must also be recommended for any patient who intentionally ingests a caustic substance, regardless of their symptomatology.[16] However, in asymptomatic patients without oral or mucosal burns, EGD may be deferred on physical examination.

Early endoscopy shows favorable results. However, a personalized approach is recommended for caustic ingestions, as some individuals may have a greater need for immediate surgical intervention and hemodynamic stabilization.[17] The most common injury found on early endoscopy is a grade I injury. Early endoscopy helps guide treatment if evidence of severe manifestations like mediastinitis is lacking.[18][19] The general consensus is to obtain EGD within 24 hours. Literature suggests that EGD may be safe up to 96 hours post-ingestion if performed with gentle insufflation.[20]If the procedure is delayed longer, iatrogenic perforation from damaging friable tissue may occur.

Alternative or adjunctive modalities for evaluating caustic ingestion-related injuries include endoscopic ultrasound (EUS) and contrast-enhanced computed tomography (CECT).[21] EUS remains under investigation for use in the treatment of caustic injuries. One study showed that, as an adjunct test, EUS does not increase the accuracy of EGD in predicting complications from caustic ingestion.[22] However, other studies suggest that EUS may be useful in determining prognosis, specifically stricture formation when used with an appropriate grading system. Overall, the evidence is insufficient to recommend EUS as part of the standard caustic ingestion evaluation protocol.

Meanwhile, CECT has gained significant attention as a potential alternative to EGD. This modality is non-invasive, fast, and able to assess deep structures. The study of choice is a CECT of the neck, chest, abdomen, and pelvis.

Several studies compared the ability of CECT with EGD to grade tissue damage, guide surgical intervention, and predict the risk of stricture formation.[23][24][25] CECT has been shown to have high specificity but low sensitivity in predicting stricture formation. Additionally, CECT findings may not correlate well with endoscopic grading.[26][27] Evidence is insufficient to support CECT as a replacement for EGD in evaluating upper gastrointestinal injury. However, this modality remains a useful EGD adjunct when managing caustic ingestion.

Treatment / Management

The airway should be secured in patients with signs of impending respiratory failure, including drooling, hypoxia, and vocal changes. One study showed that 50% of adults with caustic ingestions required intubation. Multi-site large-bore intravenous access should be promptly obtained and intravenous fluids administered for patients who display signs of shock. Vasopressors should be initiated for patients who remain hypotensive despite adequate fluid challenge.

Early interventions that have been described for caustic ingestion include pH neutralization and dilution with water or milk. The pH may be neutralized by giving a weak acid or base. Animal studies suggest that, if performed correctly, pH neutralization can decrease esophageal injury.[28] However, this practice is limited by titration challenges and the potential for exothermic injury. Additionally, no human data supports the benefit of pH neutralization in managing caustic ingestion. Thus, it is not a recommended treatment for this condition.

Dilution with milk or water was once proposed to help reduce alkali injury.[29] However, this intervention may only be beneficial within the first few minutes. Little clinical data supports the effectiveness of dilution with milk or water in caustic ingestion, and the treatment may even cause distention-related injury. Dilution with milk or water is currently not recommended in clinical practice.

Activated charcoal administration should be considered if the caustic agent is zinc or mercuric chloride. Heavy metals can damage mucosal surfaces and be absorbed systemically, causing severe multi-organ toxicity. Activated charcoal can absorb metals in the gut, prevent their enterohepatic recirculation, and hasten their clearance.[30][31][32]

The role of H2-blockers and proton pump inhibitors is yet to be defined. One study suggests that omeprazole may improve EGD grading after 72 hours.[33] Emesis induction should not be used in managing caustic ingestion.

Nasogastric (NG) tube insertion is controversial. Multiple studies suggest that early NG tube placement may help maintain esophageal patency and reduce stricture formation.[34][35][36] Despite this evidence, blind NG tube placement in the emergency department risks bacterial infection and esophageal perforation.[35] Therefore, NG tube placement should only be considered if performed with direct endoscopic visualization.[37]

Besides acute injury management, the long-term sequelae of caustic ingestion must also be addressed. The most concerning complication is stricture formation. Corticosteroid treatment can theoretically attenuate inflammation and reduce granulation and fibrous tissue formation.[38] Several studies suggest that steroids do not prevent esophageal stenosis, regardless of the injury grade.[39][40][41] However, high-dose methylprednisolone may prevent stenosis in patients with grade 2b injury.[42][43]

Procedural interventions in the treatment of strictures include bougienage,[44] esophageal stent placement,[45][46][47] and endoscopic dilatation. Other potential interventions include administration of vitamin E,[48] ketotifen,[49] phosphatidylcholine,[50] halofunginone,[51] 5-fluorouracil,[52] octreotide, and interferon-α2b.[53] These modalities are still under investigation, and their use is currently not recommended in clinical practice.

Individuals with suspected mediastinitis, peritonitis, or hemodynamic instability require emergent surgical consultation. Patients with large ingestions and are in shock, acidotic, or coagulopathic may have more severe findings on surgical exploration.[54] Surgical consultation may also be required for patients with high-grade injuries on EGD, CECT, or both.

The goal of emergency surgery is to remove all necrotic tissue. Exploratory laparotomy is the standard approach. The size of the resected area depends on the extent of damage. Small fragments may be removed in some cases. A pancreaticoduodenectomy may be necessary if pancreatic and duodenal injuries are extensive.

Differential Diagnosis

The differential diagnosis of caustic ingestion includes the following:

• Trauma
• Congenital abnormalities
• Direct burns
• Multiple drug ingestion

A complete evaluation can help distinguish between these conditions. 

Staging

EGD findings are graded based on the Zargar classification:

• Grade 0 - The esophagus is normal.
• Grade 1 - Mucosal edema and hyperemia are present.
• Grade 2a - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates, and superficial ulcerations may be found.
• Grade 2b - Deep or circumferential ulceration besides 2a lesions may be present.
• Grade 3a - Small and scattered areas of necrosis are seen.
• Grade 3b - Extensive necrosis is present.

For CECT, the following is the grading scale proposed by Bruzzi et al:[24]

• Grade I - The esophageal wall is clearly delineated. Homogenous postcontrast enhancement is appreciated but not edema or fat stranding.
• Grade IIa - Internal esophageal mucosal enhancement is seen. Significant esophageal wall edema appears hypodense. The “target” aspect may be seen. Mediastinal fat stranding is present.
• Grade IIb - A fine rim of esophageal enhancement is present, but the mucosa does not enhance. The esophageal lumen is dilated. Mediastinal fat stranding is seen.
• Grade III - Transmural necrosis is present, as shown by the absence of postcontrast wall enhancement.

Meanwhile, Ryu et al proposed the following CECT-based grading system:[55]

• Grade I - The esophagus wall has no definitive swelling (less than 3 mm, within normal limits).
• Grade II - Edematous wall thickening (greater than 3 mm) is seen without peri-esophageal soft tissue infiltration.
• Grade III - Edematous wall thickening is accompanied by peri-esophageal soft tissue infiltration. A well-demarcated tissue interface is also visible.
• Grade IV - Edematous wall thickening is accompanied by peri-esophageal soft tissue infiltration. Tissue interface blurring or localized fluid collection around the esophagus or descending aorta may also be seen.

Currently, no studies have compared these CECT grading systems. Thus, we have no information on which system is superior. 

Prognosis

The prognosis of caustic ingestion depends mostly on the initial injury's extent. Mild-to-moderate ingestions have the most favorable prognosis, while severe ingestions requiring emergency surgery have the worst outcomes. Grade 3 injuries necessitate emergency surgery and significant follow-up care. Mediastinitis is often associated with high-grade injury and also has a poor prognosis.[56][57]

Patients and their families must be primed about the likelihood of complications after surgery. Individuals who survive high-grade caustic injuries experience a significant decline in quality-of-life scores. Surgical teams must consider possible posttreatment outcomes when making the operative plan.[58]

Complications

The most common early sequelae of caustic ingestion are mediastinitis and bleeding-related hemodynamic instability. These complications require emergency surgery. Meanwhile, gastrointestinal stricture is the most common late sequela of caustic ingestion, with the esophagus being the most frequently involved region. Esophageal dilatation is often enough to relieve this condition. However, surgical resection with bypass or replacement may be performed if esophageal dilatation fails or is infeasible. Bowel or gastric tissue may be used in surgical bypass, depending on the stricture's severity.

Stenosis prevention is a controversial topic. Early oral feedings are thought to prevent stricture in patients with a superficial injury. Stent placement has limited success (less than 50%) and high migration rates (up to 25%). No pharmacologic agents have been effective in preventing gastrointestinal stenosis after caustic ingestion.

Postoperative and Rehabilitation Care

Surgical care for esophagectomy and severe caustic ingestion-related injuries requires intensive care, as patients may need airway management, hemodynamic support, and parenteral nutrition. Patients' altered eating habits and wound healing needs will require the services of nutritionists. Mental health practitioners must monitor patients' mental status in cases of intentional ingestion.[59][60]

Deterrence and Patient Education

Caustic ingestion prevention requires a community-wide effort due to the heavy social burden it can create. Robust legislation is recommended to regulate packaging practices and ensure children cannot easily access caustic chemicals. Parents must be reminded to keep harmful substances away from children's reach and use properly labeled containers for storing chemicals.

Since most adult ingestions are intentional, access to mental health services must be ensured. Social support systems must be instituted widely to reduce the risk of suicide attempts.[61]

Enhancing Healthcare Team Outcomes

Patients with caustic ingestions are best managed with an interprofessional team approach. Besides emergency clinicians and surgeons, the multidisciplinary team may also include intensivists, nurses, nutrition services, and mental health practitioners. These team members are critical in ensuring that a patient gets the appropriate care in the acute setting and on follow-up. Smooth coordination between these health professionals has been shown to improve outcomes in patients with this condition.[62][63][64][65]

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Disclosure: Joseph Bielecki declares no relevant financial relationships with ineligible companies.

Disclosure: Richard Chen declares no relevant financial relationships with ineligible companies.

Disclosure: Vikas Gupta declares no relevant financial relationships with ineligible companies.