What is the management approach for a patient with ammonia ingestion?

Management of Ammonia Ingestion

Immediate Stabilization and Airway Management

For ammonia ingestion, immediately stabilize the patient's airway, breathing, and circulation—intubate if there is any sign of respiratory distress, altered mental status, or visible airway injury, as ammonia causes liquefactive necrosis and can rapidly progress to airway edema and respiratory failure. 1

• Secure the airway with intubation and mechanical ventilation if the patient shows declining consciousness, respiratory distress, hoarseness, copious oral secretions, or visible mucosal injury 1, 2
• Establish intravenous access immediately for fluid resuscitation and medication administration 1, 2
• Begin high-rate infusion of dextrose-containing fluids (8-10 mg/kg/min glucose infusion rate) to prevent catabolism and provide hemodynamic support 1, 2
• Assess neurological status continuously, as ammonia exposure can cause lethargy, disorientation, and coma 2

Gastrointestinal and Pulmonary Assessment

Contact Poison Control Centers to evaluate systemic toxicity and obtain specific guidance on the ingested ammonia formulation. 1

• Perform urgent upper endoscopy to assess for caustic injury to the esophagus and stomach, as ammonia ingestion results in superficial hemorrhagic gastritis that may progress during the first 24-48 hours 1
• Obtain chest radiography and consider chest/abdominal CT to evaluate for pneumonitis, pulmonary edema, pneumothorax, or gastrointestinal perforation 1
• Perform bronchoscopy if inhalational exposure occurred or if respiratory symptoms are present, as ammonia vapor can cause severe laryngeal edema and mucosal injury to the segmental bronchial level 3, 4

Nutritional and Metabolic Management

Temporarily stop all protein intake to reduce nitrogen load, but provide aggressive caloric support (≥100 kcal/kg/day) through IV dextrose and lipids to prevent catabolism. 2

• Maintain glucose infusion rate of 8-10 mg/kg/min 2
• Administer IV lipids starting at 0.5 g/kg/day, titrating up to 3 g/kg/day for additional caloric support 2
• Crucially, reintroduce protein within 48 hours once the patient stabilizes to avoid catabolism-induced hyperammonemia 2

Laboratory Monitoring

Check plasma ammonia levels every 3-4 hours using proper technique: free-flowing venous or arterial blood in lithium heparin or EDTA tube, transported on ice, and processed within 15 minutes. 2

• Obtain initial labs including CBC, comprehensive metabolic panel (sodium, potassium, chloride, magnesium, calcium, urea, creatinine), liver function tests, pH, serum lactate, and blood alcohol levels 1
• Monitor for severe acidosis, elevated lactate, deranged liver function, leukocytosis, elevated CRP, renal failure, and thrombocytopenia—these predict transmural necrosis and poor outcomes 1

Pharmacological Treatment

Administer nitrogen-scavenging agents (sodium benzoate and sodium phenylacetate) if plasma ammonia levels exceed 150 μmol/L. 2

• Sodium benzoate dosing: 250 mg/kg (weight <20 kg) or 5.5 g/m² (weight >20 kg) given over 90 minutes as bolus, then as maintenance over 24 hours 1
• Sodium phenylacetate dosing: same as sodium benzoate 1
• L-carnitine: 50 mg/kg loading dose over 90 minutes, then 100-300 mg/kg daily (particularly important if organic acidemia is suspected) 1, 2
• Consider broad-spectrum antibiotics if aspiration pneumonia or secondary infection develops 5, 6
• Consider systemic corticosteroids and inhaled bronchodilators for significant inhalational exposure to prevent late pulmonary complications 6

Kidney Replacement Therapy Decision Algorithm

Initiate hemodialysis or continuous kidney replacement therapy (CKRT) immediately if ammonia levels exceed 300-400 μmol/L despite medical therapy, or if there is rapidly deteriorating neurological status or coma. 7, 2

• Hemodialysis is first-line when available, achieving 95-96% ammonia filtration fraction and reducing ammonia by 50% within 1-3 hours 7
• CKRT is preferred for hemodynamically unstable patients 7
• Continue nitrogen scavengers during dialysis despite being dialyzed, as they remain effective 8

Prognostic Factors and Critical Timing

The duration of hyperammonemic coma (not the rate of ammonia clearance) is the most important prognostic factor—coma lasting >3 days predicts poor neurological outcome. 7

• Peak ammonia levels >1,000 μmol/L are associated with severe irreversible brain damage 7
• Delayed recognition and treatment leads to irreversible neurological damage, seizures, and death 7, 2

Common Pitfalls to Avoid

• Do not delay endoscopy—ammonia causes progressive injury over 24-48 hours, and early assessment guides management 1
• Do not prolong protein restriction beyond 48 hours—this causes catabolism and paradoxically worsens hyperammonemia 2
• Do not rely on absence of oral lesions—clinical symptoms do not correlate reliably with extent of gastrointestinal damage 1
• Do not use improper ammonia sampling technique—false elevations are common and lead to inappropriate interventions 2