What is the medical management for inhalation of peroxyacetic acid?

Medical Management of Peroxyacetic Acid Inhalation

Immediately remove the patient from exposure, administer high-flow oxygen to maintain SpO2 >92%, and treat any resulting bronchospasm with nebulized beta-agonists as you would for acute severe asthma, while monitoring closely for delayed pulmonary edema up to 72 hours post-exposure. 1, 2

Immediate Actions

Remove from Exposure and Assess Severity

• Immediately evacuate the patient from the contaminated area to prevent continued exposure to peroxyacetic acid (PAA) vapors 1
• Assess for signs of severe respiratory distress including:
  • Respiratory rate >30 breaths/min in adults or >50 breaths/min in children 3
  • Oxygen saturation <92% 3, 4
  • Inability to speak in full sentences, confusion, or altered mental status 3, 5
  • Silent chest, cyanosis, or feeble respiratory effort 3, 5

Oxygen Therapy

• Start high-flow oxygen immediately (40-60% via face mask or 15 L/min via reservoir mask) to maintain SpO2 >92% 3, 4
• PAA inhalation can cause severe mucous membrane irritation and bronchospasm similar to acute asthma; oxygen therapy is critical and does not aggravate CO2 retention in this setting 3
• Use continuous pulse oximetry monitoring throughout treatment 4, 6

Bronchodilator Therapy

For Significant Bronchospasm or Wheezing

• Administer nebulized salbutamol 5-10 mg (or terbutaline 5-10 mg) via oxygen-driven nebulizer at flow rate >6 L/min 3, 4
• Repeat every 15-30 minutes if patient is not improving 3
• Add ipratropium 0.5 mg to nebulizer and repeat every 6 hours until improvement occurs 3
• PAA exposure can cause occupational asthma with late asthmatic responses, so aggressive bronchodilator therapy is warranted 2

Corticosteroids

• Give systemic corticosteroids early: prednisolone 30-60 mg orally or hydrocortisone 200 mg IV if significant bronchospasm or respiratory distress is present 3
• High-dose corticosteroids have been recommended for laryngeal and pulmonary edema, though their value is unproven 1

Monitoring and Observation

Critical Monitoring Parameters

• Monitor for delayed pulmonary edema, which may occur 24-72 hours post-exposure to concentrated PAA vapors 1
• Repeat arterial blood gas measurements within 2 hours if:
  • Initial PaO2 <8 kPa (60 mmHg) 3, 4
  • Initial PaCO2 is normal or elevated (paradoxical finding indicating inability to compensate) 3, 5
  • Patient deteriorates clinically 3, 4
• Serial peak expiratory flow measurements should be obtained before and after bronchodilator administration 3, 2

Hospital Admission Criteria

• Admit patients with:
  • Persistent hypoxemia (SpO2 <92%) despite oxygen therapy 3, 6
  • Significant bronchospasm requiring repeated nebulizer treatments 3
  • Any evidence of pulmonary edema or severe mucous membrane inflammation 1
  • Symptoms not resolving within 4-6 hours of treatment 3

Advanced Airway Management

Indications for ICU Transfer and Intubation Preparation

• Transfer to ICU with physician prepared to intubate if: 3, 5
  • Deteriorating peak expiratory flow despite aggressive treatment
  • Persistent or worsening hypoxia (PaO2 <8 kPa/60 mmHg)
  • Rising hypercapnia (PaCO2 >6 kPa/45 mmHg)
  • Exhaustion, confusion, coma, or respiratory arrest
• Life-threatening laryngeal edema may require endotracheal intubation or rarely tracheostomy 1
• Do not attempt intubation until the most experienced physician (ideally an anesthesiologist) is present 3

Decontamination and Supportive Care

Mucous Membrane Exposure

• Irrigate eyes immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes if ocular exposure occurred 1
• Instillation of local anesthetic may reduce discomfort and assist decontamination 1
• Assess for corneal injury with concentrated exposures 1

Skin Decontamination

• Wash contaminated skin with copious amounts of water 1
• Treat any skin lesions as thermal burns 1

Important Clinical Considerations

Sensitization Risk

• PAA-hydrogen peroxide mixtures can cause respiratory sensitization and occupational asthma through an IgE-mediated mechanism 2
• Patients may develop late asthmatic responses (occurring hours after exposure) even after initial improvement 2
• Consider serial peak flow monitoring for 24-48 hours to detect delayed bronchospasm 2

Toxicity Mechanism

• PAA is a potent oxidizing agent with RD50 (concentration causing 50% decrease in respiratory rate) of only 5.4 ppm, making it approximately 42 times more irritating than acetic acid and 21 times more irritating than hydrogen peroxide 7
• The threshold limit value for short-term exposure should not exceed 0.5 ppm 7
• Severe mucous membrane irritation with coughing, dyspnoea, and potential for shock and convulsions can occur with highly concentrated exposures 1

Pitfalls to Avoid

• Do not delay oxygen therapy; hypoxemia increases mortality risk 6
• Do not discharge patients prematurely; observe for at least 24 hours for delayed pulmonary edema 1
• Do not underestimate the severity based on initial presentation; late asthmatic responses may occur 2
• Do not use chlorhexidine for disinfection of equipment, as PAA is not inactivated by it (use 75% ethanol or chlorine-containing disinfectants instead) 3