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Caustic Esophageal Injury Revision Notes [SKF 47]

Introduction

  • Caustic esophageal ingestion involves damage to the esophageal wall due to direct contact with acids or bases.
  • Leads to a significant inflammatory response.
  • Understanding the pathophysiology is crucial for guiding complex management decisions.

Epidemiology

Etiologies

  • Accidental Ingestion: Predominantly in children under 5 years.
  • Intentional Ingestion: Occurs in adolescents and adults as an act of self-harm.

Risk Factors for Accidental Ingestion

  • Low socioeconomic status.
  • Low parental education.
  • Living in low-income countries.
  • Crowded living conditions.
  • Poor compliance with safety measures (e.g., lack of safety caps).

Common Substances Ingested

  • Alkaline substances are more commonly ingested, especially household cleaning agents.
  • Often stored in unlabeled containers.

Pathophysiology

Chemical Factors Affecting Severity

  • pH level of the substance (significant damage at pH <2 or >12).
  • Viscosity and concentration of the substance.
  • Amount ingested and contact time with the esophageal mucosa.
  • Presence of comorbidities.

Substances Commonly Ingested

  • Alkali Agents:
    • Drain cleaners (e.g., Liquid Plumr, Drano containing sodium hydroxide).
    • Oven cleaners.
    • Dishwasher detergents (contain phosphates).
    • Hair relaxers (contain sodium, calcium, or ammonium hydroxide).
    • Bleach (pH varies by brand).
  • Acid Agents:
    • Toilet cleaners (e.g., Lysol).
    • Swimming pool cleaners.

Inflammatory Response

Acid Ingestion

  • Causes coagulation necrosis.
  • Results in a protective eschar formation.
  • Less quantity ingested due to instant burning sensation.
  • More injury to the stomach due to gastric retention.

Alkali Ingestion

  • Causes liquefaction necrosis.
  • Leads to deeper tissue penetration and more severe injuries.

Phases of Injury

  1. Acute Necrotic Phase (First 72 hours)
    • Cell death via protein coagulation.
    • Intense inflammation and thrombosis of vessels.
    • Infiltration with hemorrhage and bacteria.
    • Risk of transmural necrosis and perforation.
  2. Ulcerative/Granular Phase (3 days to 3 weeks)
    • Sloughing of necrotic tissue leading to ulcers.
    • Infiltration of fibroblasts and new blood vessel formation.
    • Formation of granulation tissue.
    • Esophagus is weakest; high risk of hemorrhage or perforation.
  3. Cicatrization and Stricture Formation Phase (3 weeks to 3 months)
    • Replacement of inflammatory cells with dense fibrotic tissue.
    • Re-epithelialization with squamous cells.
    • Development of esophageal strictures due to fibrosis.

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Clinical Features

History and Symptoms

  • Substance details: Name, type (solid/liquid), quantity, and time of ingestion.
  • Symptoms indicating esophageal injury:
    • Dysphagia (difficulty swallowing).
    • Odynophagia (painful swallowing).
    • Refusal to drink (especially in children).
    • Chest pain.
  • Symptoms indicating gastric injury:
    • Epigastric pain.
  • Vomiting: Risk of re-exposure and aspiration.

Physical Examination Findings

  • Vital Signs: Assess for instability or signs of shock.
  • Oral Examination:
    • Presence of mucosal burns or ulcers.
    • Drooling.
    • Hoarseness or stridor indicating airway involvement.
  • Abdominal Examination:
    • Tenderness suggesting gastric injury or perforation.

Clinical Phases

  1. Acute Phase: Immediate management focusing on stabilization and assessment for necrosis or perforation.
  2. Intermediate Phase: Monitoring for delayed complications like perforation.
  3. Chronic Phase: Management of long-term complications such as strictures, dysmotility, and potential cancer development.

Initial Investigations and Management

Laboratory Studies

  • Complete Blood Count (CBC):
    • Elevated white blood cell count (>20,000) may predict severe injury or mortality.
  • Serum Electrolytes and Renal Function Tests.
  • Acid-Base Status:
    • Serum pH <7.22 or base excess <12 may indicate severe injury requiring surgical intervention.

Imaging

Chest Radiography

  • Assess for signs of mediastinal air, pleural effusions, or pneumothorax indicating perforation.

Computed Tomography (CT) Scans

  • Used to assess the extent of injury and guide management.
  • CT Grading helps predict the risk of stricture formation and need for surgery.
  • Especially useful in grade 3b injuries to reduce unnecessary surgeries without increasing mortality.

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Endoscopy

  • Gold standard for assessing esophageal injury.

  • Should be performed within the first 12-24 hours if the patient is stable.

  • Zargar Classification for grading injuries:

    • Grade 0: Normal mucosa.
    • Grade 1: Edema and hyperemia.
    • Grade 2a: Superficial ulcers, erosions, blisters.
    • Grade 2b: Deep or circumferential ulcers.
    • Grade 3a: Focal necrosis.
    • Grade 3b: Extensive necrosis.

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Key Points on Endoscopy

  • All patients with suspected caustic ingestion should undergo endoscopy, regardless of symptoms.
  • Flexible endoscopy is preferred due to lower risk of perforation.
  • A complete examination is important for accurate grading and management planning.
  • Avoids unnecessary surgeries and aids in early prognosis and discharge planning.

Treatment in Acute Phase

General Management

  • Secure airway and begin intravenous resuscitation.
  • Initiate investigations promptly to grade the injury and guide management:
    • Grade 1 & 2a: Trial of oral intake and observation for 1-2 days.
    • Grade 2b & 3a: Nil per os (NPO), monitor in intensive care unit (ICU), follow-up endoscopy in 5-7 days before starting oral intake.
    • Grade 3b & 4: Urgent operative intervention.

Medical Management

  • Goals: Prevent acute perforation and chronic strictures.
  • Contraindicated Interventions:
    • Agents to induce emesis: Reexposes esophagus to caustic substance.
    • Neutralizing agents: Risk of exothermic reactions.
    • Milk and activated charcoal: No proven benefit; can inhibit endoscopic examination.
  • Antibiotics:
    • Controversial; some use in higher-grade injuries to address bacterial infiltration.
    • Broad-spectrum antibiotics often administered despite mixed evidence.
  • Proton Pump Inhibitors (PPIs):
    • Utility unclear; no routine recommendation.
    • Some studies suggest potential benefits, but evidence is inconclusive.
  • Steroids:
    • Not beneficial; may increase risk of perforation and infection.
    • Recommended against for grades 1 to 3 injuries.

Surgical Management

  • Grades 3b or 4 Injuries:
    • Require operative intervention.
    • Principles of Damage Control Surgery:
      • Assess esophagus and stomach.
      • Remove necrotic/nonviable tissue.
      • Preserve hemostasis.
      • Defer definitive reconstruction.
    • Esophagectomy with cervical esophagostomy if esophagus is nonviable.
    • Feeding Jejunostomy for grade 3a injuries.
    • Second Look: Scheduled 12-24 hours post-operation if tissue viability is uncertain.

Treatment in Intermediate Phase

Nutritional Support

  • Grade-Based Protocol:
    • Grade 0 & 1: Normal diet, discharge after 1 day observation.
    • Grade 2 to 3a:
      • Total Parenteral Nutrition (TPN).
      • Repeat endoscopy at 1 week.
      • Trial of oral intake if improved/healed; otherwise continue TPN with repeat endoscopy at 3 weeks.
      • Feeding Jejunostomy for prolonged oral intake needs in grade 3a.
    • Grade 3b & 4: Operative exploration.
  • Nasogastric (NG) Tubes:
    • Not routinely recommended.
    • Risks: Perforation, erosion, exacerbated reflux.
    • Alternative: Endoscopically placed NG tubes over a wire into the duodenum showed no difference in stricture rate compared to jejunostomy feeds.

Stricture Prophylaxis

  • Systemic Therapies:
    • Antibiotics and PPIs: No evidence for stricture prevention.
    • Steroids: Not beneficial, potentially harmful.
  • Experimental Treatments:
    • Triamcinolone: Injected into strictures to prevent progression.
    • Mitomycin C: Topical application or injection reduces strictures in pediatric trials.
    • 5-Fluorouracil (5-FU): Intraluminal application in animal models reduces strictures.
    • Antioxidants: Various agents (e.g., pirfenidone, tamoxifen) tested in animal models.
    • Mesenchymal Stem Cells: Attempted to prevent strictures in animal studies.
  • Mechanical Management:
    • Dilatation:
      • Savary Dilators: Safer than balloon dilatation; operator can feel resistance.
      • Timing: Avoid between 7-21 days post-injury to reduce perforation risk.
      • Complications: Perforation rate 5-32% based on operator expertise.
    • Stenting:
      • Intraluminal Stents: Avoid serial dilations; variable success rates (50-72%).
      • Complications: Migration (~10%), tracheoesophageal fistula.
      • Patient Selection: Must be individualized; no clear superiority over dilation.

Treatment in Chronic Phase

Objectives

  • Restore functional gastrointestinal continuity.
  • Manage long-term complications:
    • Strictures.
    • Dysmotility.
    • Gastroesophageal Reflux Disease (GERD).
    • Malignancy risk.

Stricture Management

  • Endoscopic Dilation: First-line therapy.
  • Stenting: Consider to avoid serial dilations; requires careful timing and selection.
  • Surgical Intervention:
    • Resection vs. Bypass:
      • Resection: Prevents mucoceles and cancer development; risks include operating in inflamed fields.
      • Bypass: Gastric conduit or colonic interposition graft.
  • Reconstruction Options:
    • Gastric Conduit: Single anastomosis; risk of reflux and aspiration.
    • Colonic Interposition Graft: More complex; better functional outcomes but higher operative time.
    • Jejunal Interposition Graft: Technically challenging; requires microvascular anastomosis.
    • Reverse Gastric Tubes: Technically difficult.
    • Pedicled Skin Flaps: Alternative options.
    • Supercharged Reverse Gastric Tube: Anastomosis to superior thyroid vessels for diffuse injuries.

Long-Term Considerations

  • Malignancy:
    • Adenocarcinoma and Squamous Cell Carcinoma: 2-8% incidence; latency 15-40 years.
    • Surveillance: Individualized based on risk factors.
  • Tracheoesophageal Fistula:
    • Requires resection and airway repair.
  • GERD:
    • 63.5% incidence in pediatric patients post-injury.
    • Associated with stricture length and Barrett Esophagus risk.
  • Other Complications:
    • Dysmotility.
    • Recurrent Aspiration.

Summary

  • Epidemiology: Majority of caustic injuries are accidental ingestions in children; intentional ingestions in adolescents and adults are less common.
  • Pathophysiology: Well-described through animal models; involves distinct phases of injury and inflammatory responses based on substance type.
  • Assessment: Endoscopy is essential to grade injuries and guide management. Clinical assessment, blood work, and CT imaging are important adjuncts.
  • Management:
    • Grade 1 & 2a: Managed with a trial of oral intake.
    • Grade 2b & 3a: Require close monitoring in hospital with follow-up endoscopy.
    • Grade 3b & 4: Necessitate urgent surgical intervention.
  • Medical Treatments: Steroids are not beneficial and may be harmful; antibiotics may be used in higher-grade injuries; PPIs have unclear benefits.
  • Surgical Treatments: Necessary for severe injuries; options include esophagectomy, gastric conduit, and colonic interposition grafts.
  • Long-Term Complications: Include malignancy, strictures, dysmotility, and GERD. Requires ongoing surveillance and management.
  • Overall: Caustic injuries require multidisciplinary care involving gastroenterologists, surgeons, and critical care specialists to optimize outcomes.

Note: Early and accurate assessment combined with appropriate management is critical in improving outcomes for patients with caustic esophageal injuries. Always consider the potential for rapid deterioration and the need for multidisciplinary care.