What is the management of acute corrosive poisoning?

Management of Acute Corrosive Poisoning

Immediate Resuscitation and Stabilization

The first priority in acute corrosive poisoning is to secure the airway, establish breathing support, and stabilize circulation—airway compromise from laryngeal edema or aspiration can develop rapidly and is a leading cause of early mortality. 1, 2

• Assess airway patency immediately and prepare for early intubation if stridor, hoarseness, drooling, or respiratory distress are present, as vapor inhalation (ammonia, formaldehyde) can cause severe airway burns 1
• Establish IV access and begin fluid resuscitation, particularly if signs of perforation or shock are present 3
• Obtain vital signs and continuous cardiac monitoring, as systemic toxicity can cause electrolyte disturbances including hypocalcemia, hyponatremia, hypokalemia, and metabolic acidosis 1

Critical "Do Not" Actions

Never induce vomiting, perform gastric lavage, administer activated charcoal, or attempt neutralization with antacids or any other agents—these interventions are explicitly contraindicated and cause additional harm through re-exposure of tissues, exothermic reactions, and increased perforation risk. 2, 4

• Do not give anything by mouth including water or milk unless specifically directed by Poison Control Center 2
• Neutralization with acids, alkalis, or antacids provides no clinical benefit and generates heat that worsens tissue injury 2
• Activated charcoal is ineffective for corrosive substances and may obscure endoscopic visualization 4

Poison Control Center Consultation

Contact the Poison Control Center immediately to evaluate systemic toxicity of the specific ingested agent and receive guidance on management. 1, 2

• Identify the nature (acid vs. alkali), physical form (solid vs. liquid), quantity, and concentration of the corrosive substance 1
• Determine whether ingestion was accidental or intentional, as massive suicidal ingestions in adults typically cause more severe injury than accidental pediatric exposures 1
• Strong acids and alkalis cause the most severe injuries; oxidants like bleach usually cause mild injury but can occasionally require emergency resection 1

Initial Laboratory and Imaging Evaluation

Obtain complete blood count, electrolytes (sodium, potassium, chloride, magnesium, calcium), renal function (urea, creatinine), liver enzymes, arterial blood gas, and lactate level to assess for systemic toxicity and metabolic derangements. 1

• Hypocalcemia suggests phosphoric or hydrofluoric acid ingestion 1
• Severe metabolic acidosis and elevated lactate indicate extensive tissue necrosis and predict poor outcomes 5
• Obtain chest and abdominal radiographs to evaluate for free air indicating perforation 1

Endoscopic Assessment

Perform urgent esophagogastroduodenoscopy within 12-24 hours of ingestion to assess the extent and severity of injury—clinical symptoms and oral lesions do NOT correlate reliably with gastrointestinal damage, and absence of oral burns does not rule out life-threatening esophageal or gastric injury. 1, 6, 4

• Endoscopy can be safely performed in most cases; procedure-related perforation is rare 6
• Use the Zargar classification system to grade injuries: Grade 0 (normal), Grade 1 (mucosal edema/hyperemia), Grade 2A (superficial ulcers), Grade 2B (deep ulcers), Grade 3A (focal necrosis), Grade 3B (extensive necrosis) 5
• Do not advance the endoscope beyond areas of Grade 3 injury to avoid perforation 1
• Endoscopic findings predict complications: Grade 2B and 3 injuries have high rates of stricture formation (up to 70-90%) and perforation 6, 5

Medical Management

Initiate broad-spectrum antibiotics, proton pump inhibitors, and nutritional support; maintain NPO status until the extent of injury is determined. 4, 7

• Administer IV antibiotics to prevent secondary infection and sepsis 7
• Use high-dose proton pump inhibitors to reduce gastric acid secretion 7
• Establish enteral nutrition via nasojejunal tube or jejunostomy if prolonged NPO status is anticipated 8, 7
• Monitor fluid and electrolyte balance carefully, particularly in patients with extensive injuries 4

Corticosteroid Controversy

The role of corticosteroids remains controversial; some evidence suggests they may reduce stricture formation in Grade 2B injuries, but they are not universally recommended and should not be used in Grade 3 injuries due to infection risk. 6, 7

• If used, initiate within 48 hours of ingestion 7
• Do not use corticosteroids if perforation or Grade 3 necrosis is present 7

Surgical Indications and Timing

Immediate surgical consultation is mandatory; upfront emergency surgery should be performed for esophageal or gastric perforation with extensive pleural or mediastinal contamination, signs of peritonitis, or hemodynamic instability despite resuscitation. 1

• Indications for surgery include: perforation, extensive transmural necrosis (Grade 3B), uncontrolled bleeding, mediastinitis, pleural empyema, or peritonitis 1
• Surgical approach depends on location and extent of injury: cervical esophagotomy for cervical injuries, thoracotomy or thoracoscopy for thoracic esophageal injuries, laparotomy for gastric injuries 1
• Esophagectomy with delayed reconstruction may be necessary for extensive esophageal necrosis 1
• Gastrectomy may be required for extensive gastric necrosis 7

Special Considerations

Ammonia Ingestion

Ammonia causes superficial hemorrhagic gastritis that may progress during the first 24-48 hours and requires specific surveillance with repeat endoscopy. 1

Acetic Acid Ingestion

Concentrated acetic acid ingestion frequently causes acute renal failure requiring hemodialysis; monitor renal function closely and prepare for dialysis if creatinine rises or oliguria develops. 5

• Acute renal failure develops in approximately 60% of concentrated acetic acid poisonings 5
• Recovery of renal function occurs in over 90% of cases with appropriate dialysis support 5

Follow-Up and Long-Term Management

All patients with Grade 2B or 3 injuries require serial endoscopic evaluation at 15 and 25 days post-ingestion to assess for stricture formation, followed by contrast esophagography at 25-30 days. 4, 5

• Stricture formation occurs in 70-90% of patients with Grade 2B and 3 injuries 5, 7
• Esophageal dilation and stent placement may be necessary for stricture management 8, 7
• Reconstructive surgery may be required for severe strictures refractory to dilation 8
• Long-term cancer surveillance is essential: esophageal and gastric carcinoma risk increases beginning 30-40 years after injury 6, 7

Psychiatric Follow-Up

All patients with intentional ingestion require mandatory psychiatric evaluation and follow-up, as these patients have underlying psychiatric disease and high risk of repeat suicide attempts. 1, 8

Prognosis

Despite advances in management, mortality remains 1-5% in the acute phase, with perforation, sepsis, and multiorgan failure being the leading causes of death; long-term morbidity from strictures and dysphagia significantly impairs quality of life. 5, 7

• Mortality was historically 20% but has decreased to 1-5% with modern intensive care 7
• Up to 20% of survivors develop esophageal or gastric stenosis requiring long-term management 5
• The economic burden is substantial due to prolonged hospitalization, multiple procedures, and permanent disability 5