Mechanisms of injury

1. Heat (oedema, erythema and oedema of the mucosa)
2. Toxins (e.g. sulphur dioxide, chlorine) cause pH-related or free-radical-related damage
3. Hypoxia due to environmental oxygen consumption

Pathophysiology

There is a similar pattern to other forms of lung injury:

Exudative phase: Neutrophil influx, macrophage activation, increased permeability, type 2 pneumocyte dysfunction (surfactant production)

Fibrotic phase: Fibrosing alveolitis, collagen deposition

Specific toxins

 

 

 

 

 

Carbon monoxide

Binds to haemoglobin with 250x the affinity of oxygen

The oxy-haemoglobin dissociation curve is shifted to the left

Results in tissue hypoxia

COHb levels >10% are potentially dangerous

Management is with oxygen therapy

• COHb >10%: High concentration oxygen therapy
• COHb >25%: Oxygen therapy +/- ventilation
• COHb >40% and comatose, pregnancy or not responding to conventional therapy – consider hyperbaric therapy

Cyanide

Binds to the ferric ion on cytochrome oxidase

This blocks aerobic cellular metabolism