Saturday, 9 November 2019

Smoke inhalation

Smoke inhalation
#KYJ #KnowingYourJargon

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.

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.

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Sunday, 15 September 2019


Originally published in social media in Nov 2018...

That bite of summer has well and truly come early this year and with that heat, comes snakes.
Our neighbors (Toowoomba region) have reported many sightings.
3000 bites are reported annually.
300-500 hospitalisations
2-3 deaths annually.
Average time to death is 12 hours  (many references cite between 4 - 24 hours). The point is that the urban myth that you are bitten in the yard and die before you can walk from your chook pen back to the house is a load of rubbish.  It can happen but it is an epic case of rare!!
While not new, the management of snake bite (like a flood/fire evacuation plan or CPR) should be refreshed each season.
Let’s start with a
Basic overview.
There are five genus of snakes that will harm us (seriously)  (Disclaimer:  these are the ones for which there is antivenin.  Other snakes eg copperheads and whips , small eyed etc still make us sick)
Browns, Blacks, Adders, Tigers and Taipans.
All snake venom is made up of huge proteins (like egg white). When bitten, a snake injects some venom into the meat of your limb  (NOT into your blood).
This venom can not be absorbed into the blood stream from the bite site directly.  
It travels in a fluid transport system in your body called the lymphatic system (not the blood stream).
Now this fluid (lymph) is moved differently to blood.
Your heart pumps blood around, so even when you are lying dead still, your blood still circulates around the body. Lymph fluid is different. It moves around with physical muscle movement like bending your arm, bending knees, wriggling fingers and toes, walking/exercise etc.
Now here is the thing. Lymph fluid becomes blood after these lymph vessels converge to form one of two large vessels (lymphatic trunks)which are connected to veins at the base of the neck.
Back to the snake bite site.
When bitten, the venom has been injected into this lymph fluid (which makes up the bulk of the water in your tissues).
The only way that the venom can get into your blood stream is to be moved from the bite site in the lymphatic vessels. The only way to do this is to physically move the limbs that were bitten.
Stay still!!! Venom can’t move if the victim doesn’t move.  (disclaimer - gravity plays a role, and some lymph can very slowly move...but super slow)
Stay still!!
Remember people are not bitten into their blood stream.
In the 1980s a technique called Pressure immobilisation bandaging was developed to further retard venom movement. It completely stops venom /lymph transport toward the blood stream.
A firm roll bandage is applied directly over the bite site (don’t wash the area).
Three steps: keep them still
Step 1
Apply a bandage over the bite site, to an area about 10cm above and below the bite.
Step 2:
Then using another elastic roller bandage, apply a firm wrap from Fingers/toes all the way to the armpit/groin.
The bandage needs to be firm, but not so tight that it causes fingers or toes to turn purple or white. About the tension of a sprain bandage.
Step 3:
Splint the limb so the patient can’t walk or bend the limb.
Do nots:
Do not cut, incise or suck the venom.
Do not EVER use a tourniquet
Don’t remove the shirt or pants - just bandage over the top of clothing.
Remember movement (like wriggling out of a shirt or pants) causes venom movement.
DO NOT try to catch, kill or identify the snake!!! This is important.
In hospital we NO LONGER NEED to know the type of snake; it doesn’t change treatment.
5 years ago we would routinely do a test on the bite, blood or urine to identify the snake so the correct anti venom can be used.
we don’t do this as often. Our newer Antivenom neutralises the venoms of all the 5 listed snake genus, so it doesn’t matter what snake bit the patient.
Read that again- one injection for all snakes!
Polyvalent is our one shot wonder, stocked in almost all hospitals, so many hospitals no longer stock specific Antivenins. Regional differences (Tassie, Victoria, south of Perth, outer islands)use region specific antivenins.
Australian snakes tend to have 3 main effects in differing degrees.
Bleeding - internally and bruising.
Muscles paralysed causing difficulty talking, moving & breathing.
In some snakes severe muscle pain in the limb, and days later the bite site can break down forming a nasty wound.
Allergy to snakes is rarer than winning lotto twice.
Final tips: not all bitten people are envenomated and only those starting to show symptoms above are given antivenom.
Did I mention to stay still.
Call help (000 or 112)
You need hospital!!!
Rob Is a writer and teacher for ECT4Health. This snake /spider envenomation material is included in our Emergency courses called #whatMergency and found