Corrosive Ingestion 🔥

Pathophysiology of Corrosive Ingestion

• Corrosive substances are frequently reported agents of accidental poisoning in toddlers and young children, often due to the inappropriate storage of these chemicals in unlabeled containers or drinking glasses.
• Corrosives are broadly classified into acids and alkalis, each possessing a distinct pathophysiological mechanism of tissue injury.
• Acids (commonly found in toilet bowl cleaners, battery fluids, and industrial agents) rapidly cause coagulation necrosis upon contact with tissues.
• This coagulative process forms a protective eschar that generally limits deeper tissue penetration, although severe cases can still result in perforation; the healing phase is characterized by intense fibrosis and stricture formation.
• Alkalis (commonly found in bleaching agents, paint removers, sodium hydroxide, and household soaps) induce liquefaction necrosis.
• Liquefaction necrosis results in the saponification of fats and solubilization of proteins, allowing the alkaline substance to penetrate deeply into the tissues, which dramatically increases the risk of transmural injury and hollow viscus perforation.
• The overall severity of a corrosive injury is directly proportional to the potential of hydrogen ($pH$), particularly when the $pH<2$ or $pH>12$, as well as the concentration of the ingested agent and the duration of mucosal contact.

Clinical Manifestations

Immediate Local and Gastrointestinal Effects

• Immediate symptoms include intense, burning pain at the site of the spill, the lips, and the oral cavity.
• Oropharyngeal injury commonly presents with excessive salivation, drooling, dysphagia, and odynophagia.
• Esophageal and gastric involvement manifests as hematemesis, severe epigastric pain, and refusal to feed.
• Patients with full-thickness necrosis may develop perforation of the stomach or esophagus, leading to peritonitis or mediastinitis, characterized by a rigid abdomen, rebound tenderness, and hemodynamic collapse.

Respiratory and Systemic Effects

• Respiratory involvement is a critical emergency, manifesting as hoarseness of voice, dyspnea, and stridor secondary to rapidly progressing laryngeal edema.
• Aspiration of the corrosive agent can result in chemical pneumonitis, pulmonary edema, and acute respiratory distress syndrome (ARDS).
• Severe systemic absorption of specific agents can lead to metabolic acidosis, hepatic dysfunction, and renal failure.

Delayed Complications

• The most significant delayed complication is the formation of strictures in the esophagus or larynx, typically manifesting weeks after the initial injury.
• Systemic delayed effects can also include pulmonary fibrosis, particularly if significant aspiration occurred.
• Long-term follow-up is necessary due to an increased risk of neoplastic changes (squamous cell carcinoma) in the scarred esophageal tissue during adulthood.

Emergency Management and Resuscitation

Airway and Hemodynamic Stabilization

• Airway protection is the absolute priority; laryngeal edema can progress over minutes to hours, causing complete airway obstruction and death.
• Elective endotracheal intubation must be performed early in the presence of respiratory distress, stridor, or hoarseness.
• Surgical airway expertise (emergency tracheostomy or cricothyrotomy) should be immediately available during intubation attempts, due to the high risk of distorted airway anatomy.
• Intravenous access must be established with two large-bore cannulae, and aggressive fluid resuscitation with isotonic crystalloids ($20$ $ml/kg$ boluses) should be initiated if the patient exhibits tachycardia, hypotension, or other signs of shock.
• Adequate pain control is essential and should be achieved using intravenous opioids (e.g., morphine or fentanyl) to alleviate severe distress.

Decontamination: Absolute Contraindications

• Gastric Lavage: Blind insertion of a nasogastric tube and gastric lavage are strictly contraindicated as they significantly increase the risk of esophageal or gastric perforation.
• Induced Emesis: The use of syrup of ipecac or any emetic agent is contraindicated, as vomiting re-exposes the vulnerable esophageal mucosa to the corrosive agent and drastically increases the risk of aspiration.
• Activated Charcoal: Charcoal administration is contraindicated because it does not bind to corrosive agents, obscures the mucosal view for subsequent endoscopy, and predisposes the child to vomiting.
• Neutralization: Attempting to neutralize an acid with a base (or vice versa) is contraindicated, as the resulting exothermic chemical reaction generates heat that causes superimposed thermal burns.

Medical Therapy

• Patients should be kept strictly nil per os (NPO) during the initial evaluation phase.
• Intravenous proton pump inhibitors (PPIs) should be initiated to suppress gastric acid secretion, raise gastric $pH$, and prevent superimposed peptic injury to the damaged mucosa.
• The routine use of prophylactic antibiotics or intravenous/nebulized corticosteroids is not recommended, as evidence shows they do not prevent stricture formation or reduce the need for intubation.
• Surface decontamination should be performed if dermal or ocular exposure occurred, utilizing copious irrigation with tepid water or normal saline for a minimum of $15-20$ minutes.

Diagnostic Evaluation

• Chest and abdominal radiographs (erect or cross-table lateral views) are mandatory to screen for free air under the diaphragm or in the mediastinum, which indicates gastrointestinal perforation.
• Computed Tomography (CT) scans of the chest and abdomen may be utilized to assess transmural injury and extra-luminal complications if perforation is suspected but not visible on plain radiographs.
• In the event of suspected perforation based on clinical signs (persistent acidosis, abdominal rigidity) or radiological evidence, immediate surgical consultation for laparotomy and repair is mandated.

Upper Gastrointestinal Endoscopy

• Upper gastrointestinal endoscopy is the diagnostic gold standard and should be performed within $12$ to $24$ hours of ingestion to assess the extent and severity of the esophageal and gastric mucosal injury.
• Endoscopy is contraindicated in patients with hemodynamic compromise, clinical signs of peritonitis or mediastinitis, severe oropharyngeal burns precluding safe scope passage, and in entirely asymptomatic children with a history of mild, doubtful ingestion.

Zargar Classification of Corrosive Injury

• The Zargar classification is utilized during endoscopy to objectively grade the severity of the corrosive burn, which directly dictates the subsequent nutritional strategy and prognosticates stricture risk.

Long-Term Management of Complications

• Stricture formation is the most prominent complication, primarily occurring in patients with Grade 2b or Grade 3 injuries.
• Dilatation therapy is the first-line treatment for the prevention and management of established strictures, typically initiated $3$ to $6$ weeks following the initial injury.
• Dilatation is performed by progressively increasing the size of bougies passed over endoscopically placed guidewires to gently stretch the fibrotic tissue.
• Because the risk of mechanical perforation during dilatation is high, the procedure must be performed with extreme caution by an experienced pediatric gastroenterologist.
• In cases of complex, long, or refractory esophageal strictures that fail to respond to repeated endoscopic dilatation, surgical correction via esophageal resection and bowel interposition (esophageal bypass) is required.