Double Whammy Asthma

( updated 2-2014)
I often find it frustrating that here I am, a life long asthmatic, a Respiratory therapist and an asthma educator, yet still unable in normal conversation, to describe what makes my type of asthma so different from others. When asked to define asthma in general, I usually give the spiel about how asthma is an inflammatory disease of the airways, and blah.. blah.. blah .
But lately it’s hit me that the explanation Ive been giving for so long, though medically correct and easier for lay people to understand, doesn’t really paint an accurate picture of what’s actually happening with MY own asthma. So, I’d like to take this opportunity to explain more in depth why my type of asthma is so different. I hope I can do this without boring you, or worse, loosing you.

What makes my asthma so different from others, is that are actually TWO distinct processes going on in my lungs. A “double whammy” if you will. Both of these components are related to, and caused by asthma, but they are uniquely separate medical entities. One of them I have control over, the other I don’t . Let’s break these components down;

The first and primary component of my asthma, is pretty much the same one that all asthmatics have to some degree, and that is, hypersensitive, mucus producing-inflamed airways. When you have an asthma flare up, it’s the swelling of the lining of the airways, and/or the excessive mucus production, and/or the tightening of the muscle bands that attach to the outside of the airway, and/or ALL all of the above, that causes you to wheeze and feel short of breath. No one really knows why this happens, but luckily, most of these symptoms are treatable, and even preventable, when following an asthma action plan and taking the proper asthma medications. So, as with most asthmatics, this is the part of my asthma that I some control over.

My Bronchioles( sorry, it’s the best illustration I could find)

In addition to having sensitive and inflamed airways however , I also have a 2nd component which is more commonly seen in people with COPD,but is now showing up more and more in severe asthmatics. This component involves scarring and/or the loss of what they call “alveolar attachments” (essentially, elastic fibers which help pull the alveoli open from the outside).
Years and years of unchecked asthma exacerbations and multiple intubations, has left the inside of my airways severely damaged and scarred (what they call remodeling). The tissue that lines the inside of my breathing passages is literally scarred over, causing permanent narrowing ( see illustration above). Scarring of the airways looks just the way you would imagine any scar tissue to look. It’s thick, fibrous and pale looking. ( Click here to view the inside of my actual airways). Because of this scarring, my lung function and expiratory flow rates(Spirometry) are severely diminished. The combination of a loss of elastic recoil and a loss of alveolar attachments, makes it hard for me to empty my lungs completely (air trapping), which results in chronic breathlessness, sometimes severe. Additionally, I have what they call bronchial malacia, a condition where my airways tend to narrow and/or collapse when I exhale, compounding the other problems. ( maybe I should call this post “Triple Whammy Asthma”). Because the malacia involves my smaller airways, it’s not treatable with stent placement. We are however, looking to see if nighttime bipap therapy might help.

The damage caused by lung scarring, cannot be reversed. Hence, this is the part of my asthma that I cannot control. Short of lung transplant, there’s not really a lot that can be done for me. All I can do is try and prevent the deterioration from getting worse. Ironically, it’s thought by some asthma researchers, that this kind of scarring might actually have a protective effect on the weaker airways and alveoli by preventing them from collapsing in on themselves. This might explain why Ive been able to bounce back so quickly from some really severe exacerbations.

So anyway, because of this double whammy effect on my lungs, what might be considered a minor flare up for some asthmatics, can turn into some pretty nasty ones for me. Essentially, I have no reserve left. The inside of my air passages are so narrowed from the scarring, that even the slightest bronchospasm or inflammation of those airways can cause them to completely close off.

The message here is simple, if you wanna maintain some control over your asthma, take your disease seriously from day one. Do everything you can to keep your symptoms in check, so that you can minimize your chances of developing “Double Whammy” asthma. If you find that you have “difficult- to- control” asthma, try to get evaluated by a Pulmonologist who specializes in severe asthma . I can’t tell you how many general practitioners Ive seen over the years who claimed they knew everything there was to know about treating asthma ( but that’s another post).

Addendum : There is a small glimmer of hope out there, that at least some forms of severe asthma might actually be treatable someday. The key, is asthma research and finding out why scarring occurs in some asthmatics and not in others. This is why the phenotyping of asthma and the work of people like Dr Sally Wenzel, is so crucial.
If you have asthma, please consider being a volunteer for SARP. Help the researchers find the answer, so that we can all breath better. If you’d like to read more about my flavor of asthma, check the “About my Asthma” section

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Most frequently asked question

"Can you have an asthma attack with a normal sat reading"?
The answer is..YES!
While it's a little unusual to see a person with a perfect O2 sat of a 100% during a severe exacerbation, its pretty typical to see sats in the 94-97% range. The reason for this, is that asthma is a disease of the airways , not the alveoli where gas exchange takes place. Most asthmatics dont desaturate during the early stages of an attack,unless theres a secondary problem such as pneumonia. You have to be extremely ill with asthma if your sats are low.

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