With so many fires in the last few days (weeks) and forecast over this coming month, I though it might be time to review smoke inhalation injury as a presentation.
The reality is that inhalation of smoke causes more deaths in fires than the burns. It has been estimated that greater than half, and up to 80% of fire related deaths are due to toxic exposure to products of combustion and or asphyxia. When stuff burns it releases gases and particulate matter (smoke). The gases are toxic, colourless and often odourless. When you smell or see smoke, this is aerosolised ash, and incomplete or unburned product.
It’s what you can’t see or smell that is actually the killer. Let’s look at these:
Carbon dioxide (CO2) is produced in all carbon fuelled fires (wood, paper, oils, petrochemicals and any products manufactured from these). When inhaled, CO2 displaces oxygen in the lungs, reducing gas exchange (less oxygen into blood, and dramatically less CO2 out) = profound hypoxaemia and hypercapnic acidosis (Respiratory acidosis).
Carbon monoxide (CO) is present in any incomplete carbon fuel combustion. Like CO2 it’s odourless, colourless and deadly poisonous. When inhaled, it binds to haemoglobin in red blood cells with such high bonding affinity, that it displaces oxygen. This means that red blood cells can’t carry oxygen, so the patient is not just hypoxaemic, but globally hypoxic. Headaches, confusion, chest pain and altered consciousness. When measuring Sats on these patients, the sats probe can’t differentiate between oxygen rich blood and carbon monoxide poisoned blood. They often look pink, perfused and in severe poisoning, their sats are 100%. The probe is just looking at blood colour, and CO causes blood to turn bright red just like oxygen. Think exposure to car fumes, bush fires.
Cyanide gas - Cyanide is a cellular toxin. It is released from burning synthetics and wool. Once breathed in, it diffuses into plasma where it off gases into cells. It is a deadly cytotoxic that shuts down cellular metabolism and energy production. Death is quick when cyanide (the blue death) is involved. Think of caravan, tent, building and car fires, where synthetic textiles are abundant.
Inhalation of other pneumotoxic particles/ash that can be super heated, causes burns and inflammation in the delicate lung tissues. This rapidly leads to acute lung injury (ALI) and surfactant decrease (pneumonia) resulting in two presentations - atelectasis (lung collapse and consolidation) and pulmonary oedema, as damaged lung swells and leaks fluid into the spaces between the alveoli and the capillaries. In technical terms, this leads to a VQ (ventilation/Perfusion (Q)) mismatch which reduces oxygen gas exchange.
Finally asphyxia - Asphyxia is caused when there is a lack of oxygen in the air you breathe. In a poorly ventilated area, fire is consuming oxygen, reducing that which is available. As you breathe poorly oxygenated air, you asphyxiate. Fresh air has 21% oxygen, and as the fire burns, it consumes this oxygen just like you and I. As oxygen levels in the air drops to around 15%, the concentration of oxygen still supports burning, but is too low to maintain consciousness. So when these situations occur, like in a building fire, or in a bush when you are surrounded by dense smoke and smouldering trees, you’d collapse and go unconscious before you got burned. In a home fire, the reality is, they never wake up to smell the smoke or fire or even to respond to the smoke alarm (as controversial as that last bit may sound). They were unconsciousness, and never felt a thing.
So.... the patients you see with smoke inhalation are actually the lucky ones.
Any way you look at smoke inhalation, asphyxia, cyanide or CO poisoning; these conditions all represent an injury due to poor oxygenation.... this is quite simply, shock.
Management - Oxygen is the first line treatment. In smoke inhalation we can not rely on pulse oximetry to assess oxygen status because the probes can’t differentiate between carbon monoxide and oxygen. Formal arterial blood gases must be used. The benefit of arterial blood gas analysis, is that a carbon monoxide reading called a carboxyhaemoglobin can also measure the CO in the red blood cells. Normal is less than 3% for non smokers. Anything over COHb 15% is cause for concern and high flow O2 (aiming for 100% oxygen via a tight fitting mask), is recommended until COHb drops below 4-5%.
Secondary management of smoke inhalation is symptomatic. If pulmonary oedema is manifest, then non-invasive positive pressure ventilation (Ni-PPV), Lasith and or nitrates (GTN infusion or patches) might be useful.
Acute lung injuries have high mortality and poor prognosis, so management often requires ICU admission and steroids to stem inflammation.