ARDS and Proning
CCP Podcast 140: Proning from bench to bedside.
I am joined by Yogesh Apte, a doctor based in Australia, who recently went through a plan, do, study, act cycle with his team in critical care to ensure they prone well and safely. The article this is based on is below.
What is ARDS?
This was first defined in 1994 by the America-European Consensus Conference, but due to issues with reliability and validity of this tool, it was then redefined in a collaboration with the European Society of Intensive Care Medicine endorsed by the American Thoracic Society and the Society of Critical Care Medicine and is known as the Berlin definition.
So ARDS is non cardiogenic pulmonary oedema., with fluid in the alveolar space.
It has three defining criteria:
- Acute onset of bilateral opacities on the chest x ray
- Low oxygen levels
- Pulmonary oedema is not due to heart failure.
- It further defined mild moderate and severe ARDS using the P:F ratio which have increasing levels of mortality. I will go on to discuss the P:F ratio later.
It can develop after direct lung injury such as in pneumonia or aspiration of gastric contents, when the alveoli are subjected to damage directly, or because of indirect lung injury such as in sepsis, pancreatitis, or severe trauma, in which case inflammatory mediators in the circulation will make their way to the lung vasculature.
On the left side of this illustration, you can see that the normal alveoli have a thin epithelial layer, and the inside is coated with surfactant. The gas exchange, therefore, can take place very easily across this area by diffusion.
The epithelial layer is normally tight and prevents any fluid from crossing over into the alveoli.
The type II cells are where the surfactant is produced.
On the right side of the illustration, we can see the damaged alveoli where the inside has filled with this protein rich pulmonary oedema fluid.
This is filled with inflammatory cells. These inflammatory cells are releasing chemicals which can make the process worse. The alveolar macrophages recruit neutrophils and circulating macrophages to the site of injury.
This then goes on to encourage proteases and cytokines amongst others which perpetuate the inflammatory response.
The border between the epithelial and the endothelial layers is swollen, creating a bigger gap for the gases to diffuse across making that process harder.
The basement layer is a thin, pliable sheet-like type of extracellular matrix, that provides cell and tissue support, and protects the alveoli from stress. This is now denuded or stripped of its covering, and necrotic.
The capillary endothelium is also involved. As the endothelium is acted upon by a range of stimuli it itself becomes dysregulated leading to the endothelial surface becoming abnormal and having larger gaps for fluid and other substances to move through.
Neutrophils can cross over into the interstitium and there is greater platelet activation. These neutrophils will release proteases which can break down the elastic tissue around the alveoli affecting the compliance.
The overwhelming activation of neutrophils contributes to surrounding tissue damage and even lung dysfunction. In COVID-19 ARDS patients, higher counts of neutrophil are observed and represent a predictor of poor outcome.
The worsening inflammation and injury will damage the type II endothelial cells reducing the production of surfactant causing a decreased compliance. Type II cells also have a role in managing lung fluid.
Activated fibroblasts secrete several extracellular matrix proteins within the interstitium but also migrate into the alveolar space where they form attachments to damaged basement membranes and contribute to the intra-alveolar fibrosis which can predominate in some cases.
This can lead to established fibrosis and the obliteration of alveolar spaces with a dense irregular matrix. Over time scarring will occur which will go on to reduce diffusion across the membranes.
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Why do we prone?
The physiology of why we prone is key to its understanding and, I think, gives a greater appreciation of its efficacy.
There are three terms that play a key part in the understanding of why we prone- Ventilation, Perfusion and Gravity.
The first part to understand is the shape matching of the lung and the effect that has on the patient’s ability to ventilate well.
Let us start with a simple diagram of the lung which we will gradually add to, to aid understanding.
Imagine that the patient is now lying on their back and that we have taken a slice through their lungs. We are now looking at that slice from the position of the feet up.
We represent each lung in an enclosed box, which represents the pleura and the chest wall, giving the lung some limitations as to how it can expand.
You can see the individual alveoli represented by the circles within the box. In this diagram they are all an equal shape and size.
However, our lungs are subject to the force of gravity, just like everything else and when we add that, as above, you can see that the picture changes.
Now, the alveoli at the top of the image, or the ventral part of the lung are pressing down on the alveoli in the lower part of the lung or the dorsal part.
So, due to this compression effect we have larger alveoli higher up and more compressed alveoli lower down.
We now consider the true shape of the lung and I represent this by the tear shaped lung I have illustrated below. This is an exaggeration of the true shape but helps illustrate the principles we need to understand.
This shape means that, when the patient is on their back, or supine, there is slightly less room at the top then the bottom. Consequently, with the added gravity much of the lung tends to drop into the lower part where it is compressed by the lung above it.
The key point here is that there is a lot of room for this compressed lung to fall into.
Add to this the fluid that will also be affected by gravity and you can see that now we have compressed alveoli surrounded by the fluid- making diffusion in these alveoli much harder.
The perfusion to the dorsal part of the lung is a little better than the perfusion to the ventral part- and the key here is that does not change significantly when the patient is proned.
So, you can see in the illustration above, where the patient is supine, we have the better perfusion where there is the poorest ventilation and the better ventilation with the slightly less good perfusion- in other words a V/Q mismatch.
In the illustration below, we have proned our patient so, because of the shape matching, and the effects of gravity on the fluid in the patient’s lungs we now have the better perfusion taking place where there is the better ventilation- improving the V/Q balance.
The other effect to be considered is the way the abdominal contents can add pressure to the diaphragm when it is moving up and down.
In these illustrations we are looking at the patient from the side.
The arrows indicate the pressure from the abdomen on the diaphragm. Remember that there is already a V/Q mismatch in this region when the patient is supine, and this added pressure contributes to make it worse.
If we then turn our patient onto their front, as in the second illustration the pressure remains the same but is now pressing on the front of the diaphragm and no longer the back.
Again, remember that the back of the lung, when proned, is where we have the improved V/Q matching, so now we have also relieved some of that pressure also.
The final point is about the position of the heart within the chest cavity.
The heart is nearer to the front of the chest than the back. This means that, when the patient is lying on their back the weight of the heart, gravity in action again, is lying on top of much of the lung, thereby adding to the compression.
You can see here that, when we lie the patient on their front there is less lung for the heart to lie on top of and much of it is supported by the sternum.
This again reduces some of the compression on the alveoli and certainly takes some of the weight off that area of the lung with the best V/Q match.
When do we prone?
The definition of the severity of ARDS is what leads us to the action of proning.
This relies on the P:F ratio. So, ask yourself two questions. First what is the patients FiO2. Is it 0.3, 0.5 or 0.7 for example?
Then divide that into the latest PO2 from your blood gas analysis.
Now depending on whether you use kilopascals or millimetres of mercury you will have a value which will tell you how severe that ARDS is.
If the value is less than 300 mm Hg or 40kPa then it is considered mild. If less than 200 mm Hg or 27 kPa then moderate, and finally if less than 100 mm Hg or 13 kPa then it is severe.
The Intensive Care Society recommends proning the patient with moderate to severe ARDS.
Does it work?
One of the latest studies, the PROSEVA study, showed a significantly decreased 28 day and 90-day mortality. In 28 day mortality it was 16% proned and 32.8% supine.
There are several criticisms of this study where again blinding is an issue and the fact that all the centres involved in the study were considered experienced with greater than 5 years of regular proning.
In this meta-analysis of 11 randomised controlled trials which included 2,200 patients they found that proning significantly reduced overall mortality and the effects were more marked in the sub group which was proned for more than 10 hours
A meta-analysis in 2015 also found it to be a safe strategy, which reduces oxygenation in patients with severely impaired oxygenation. It went on to add that it should be started early, for prolonged periods and combined with a lung protective strategy.
What is new?
Perhaps one of the key changes to have come about from the COVID-19 pandemic is that more proning is now occurring in the awake, non-ventilated patient, or self proning.
The studies on this practice are limited now but early signs are encouraging that this practice is a useful one in reducing the number of patients who then go on to be mechanically ventilated.
This Italian study of 44 patients proned awake patients for a minimum of three hours with the main study outcome being the variation in oxygenation, the P:F ratio, between baseline and resupination. They found that oxygenation substantially improved from supine to prone positioning and there was some improvement when the patient was supined although this was not significant.
Interestingly those patients who did respond had higher CRP and platelet levels than those who did not.
Some interesting points are raised in this discussion paper. They note that Gattinoni et al postulate that there may be two phases of COVID-19 pneumonitis, an early compliant lung stage when awake proning will prove beneficial and a later non-compliant stage when it may not.
The minimum duration of awake proning may also need to be more defined. Expecting an awake patient to stay prone for similar times to the sedated patient is impractical for many reasons.
The longest duration in any study so far was eight hours and I suspect most patients would not achieve any where near this. It would seem sensible then to base studies on what patients can achieve rather than on what we think they should.
It is also noted that the prone position, because of its effects on the ventilation may lead to increased secretion clearance which could further lead to greater aerosolization. Greater care would need to be taken to ensure that adequate PPE is provided in those areas for the healthcare staff.
It may be then that there is a place for awake proning and could certainly have a place in the low resource economies which may have limited access to mechanical ventilation.
What is clear is that more studies are needed.
Prone positioning in patients with acute respiratory distress syndrome, translating research and implementing practice change from bench to bedside in the era of coronavirus disease 2019 AUSTRALIAN CRITICAL CARE 2021
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