Acute Asthma.

[Blakes Username]

Hi,

have been a member for a while (post study even) and now I feel I can actually contribute to the forums!

- Appologies for my absence btw, I have been focusing on tech 100% (and I have a 9mth old kid which makes it a mission)

So, I am currently doing a case study and need to look at a medicine for the situation of respiratory arrest.secondary to asthma (when initial treatments such as salbutamol [b2 agonist] and ipratropium [choinergic antagonist] have had no effect)

As far as I have read adrenaline [epinephrine] is a good next step to take in this situation, but some sources have mentioned that the effect is little more than the other sympathomemetic and therefore the best option is a corticosteroid (we have hydrocortisone in NZ).

So just wondering, in a situation of respiratory arrest where IPPV is being given and we are on route to hospital - what is the most important thing to focus on, and is it perhaps worth considering intubation or even starting induction with ketamine and calling the helicopter?

I can look at any medicine at any skill level used in paramedicine anywhere that is appropriate for this situation, oh and pt has a chest infection - so I am thinking maybe steroids are contra-indicated?

Anyway, just looking for an opinion - or possibly a bit of direction to focus my referencing in;

let me know what you think,

Thanks for your time,

- Blake.

[chbare]

Did you talk about early and late phase inflammatory response in school? If not, basically, you have two broad periods of time associated with asthma triggering and the inflammatory response. You have the early phase where you have mast cell degranulation, release of inflammatory mediators and so on. Next, you have the late phase response that is associated with the metabolism of a substance from ruptured cell membranes known as arachidonic acid. This phase can take several hours to develop and is one of the reasons why you can treat initial signs and symptoms, only to have them return hours later. My point being, steriods are good at preventing the early phase and preventing the late phase issues; however, not as good at dealing with an acutely deteriorating patient. However, the long term benefits of early steriod use cannot be ignored.

Unfortunately, treating a severe, refractory asthma attack (status) will be difficult and quite complicated as the patient you have described will likely be moribund.

Ketamine, magnesium sulfate and inhaled anaesthetics are potential options with varying degrees of evidence to support their use. Ketamine and magnesium are probably realistic options. I would also be very careful about ventilator management. You will need to allow for a prolonged expiratory phase. You may even do this at the cost of allowing the CO2 to rise and initiate permissive hypercapnea. IM epinephrine and terbutaline are options along with in line inhaled Beta agonists with an anticholinergic agent. Also, a fluid bolus is probably a good idea for many acute asthma patients. In the hospital, you can even look at heliox therapy.

[Blakes Username]

Hey chbare,

Thanks for the clarification, have only had a very brief look at bronchospasm and inflammatory stages at school, l wonder if the bronchspasm stage is where mast cell degranuation occurs and inflammatory mediators are released - and if so, the spasm is a manifestation related to the inflammatory cascade?

I will have a look at magnesium some more and have got a few articles on ketamine - will check terbutaline out too, although I am not familiar with fluid bolus - does that mean a drink? or IV fluids?

Interesting about the ventilation, by allowing permissive hypercapnia do you mean attaching high flow O2 to the BVM and maintaining a slower resp. rate? Interestingly, I had recently read that it was the expiration stifled by asthma and have been discussing/debating with class collegues weather in a cardiac arrest secondary to asthma; an altered ratio (such as 30:2) would be more appropriate than the 15:2 suggested by the guidelines for a cardiac arrest secondary to a respiratory arrest, what do you think?

Thanks again.

[Kiwiology]

Adrenaline is a high priority, put 1mg in a one litre bag of 0.9% NaCl, shake well and label and give as an infusion starting at 2gtt/s

I am not sure but unless things have changed in the last week we do not have hydrocortisone in New Zealand; and yes an immunosupressant is relatively contraindicated in somebody who has an active infection however you need to balance it with the therapeutic effect.

Permissive hypercaponea is critically important, ventilate the patient at a very slow rate (6/min) to prevent dynamic hyperinflation

Do not waste time calling for RSI qualified R50; asthma is not an indication for RSI and Tony Smith has said he doesn't want it used in an asthmatic patient but as an aside ketamine is a brilliant induction agent for an asthmatic patient because it is a bronchodilator

Helicopter eh? where are you? Northland or something?

Have you talked to one of the Clinical Standards Officers at all?

Edited September 15, 2012 by Kiwiology

[HarryM]

WFA uses both magnesium and IV steroids for treatment of severe asthama Kiwi.

[Blakes Username]

Awesome,

Yeah - have been doing a bit more research on Adrenaline, just at this point determining why it is not used instead of Salbutamol 'exactly' as far as I can tell its to be used is Salbutamol has no effect because it has a greater affinity for b2 receptors and is something like 95x more effective at binding (am still in the process of researching though, feel free to correct me on that one).

Helicopter = next step for RSI (my logic was they are the peeps with the suxamethonium), the main reason I am even looking at things like RSI is that its a pharmacology assignment and is only loosely based on things like qualification level and regional protocol - its more about analysing an effective agent for the situation used by paramedics.

Yeah, was looking at the WFA guidelines when I mentioned the corticosteroids, seems like they would do more harm though - depending on the bacteria it could even speed up the process of something like meningitis (is what I now understand), actually I was wondering about the use of Ceftriaxone in such a situation... I think I will stick to the basics and look at Adrenaline some more.

Thanks for the Tips!

[Kiwiology]

There is much conjecture about which is more effective between IV salbutamol or IV adrenaline but at any rate IV adrenaline is pretty badass; I have only had one life threatening asthma she was a 19yof who later complained "the adrenaline that got put in my drip made me so high!" lolz

RSI in an asthmatic patient is a dubious thing AFAIK and it is best left to the hospital for now, in the future this may change. RSI is road based now as well, calling for RSI for an asthmatic patient is pointless tho, Tony Smith has specifically said he does not want it used in asthmatic patients.

To answer your question more completely tho your game plan should be nebulised salbutamol and ipratropium; if the patient is status one or two give them some adrenaline. Magnesium and steroids probably confer benefit but I am not aware of randomised trials which support this hypothesis but I know they are popular in hospital and in many US ambulance services' for asthma.

Now as ... hang on, *takes a squiz at pager, hmm, R50 required, be back later

[Arctickat]

KIWI!!!!!!!!!!!!!!!!!!!!!!!!!

Welcome back buddy!!

[Kiwiology]

KIWI!!!!!!!!!!!!!!!!!!!!!!!!!

Welcome back buddy!!

Hey settle down, lets not be getting any ideas that I am back, I just couldn't bare to see a fellow Kiwi needing help ...

[rock_shoes]

Hey settle down, lets not be getting any ideas that I am back, I just couldn't bare to see a fellow Kiwi needing help ...

Well it's good to see your post regardless.

Back on topic, I've seen all the usual suspects mentioned (epi, salbutamol, Atrovent, corticosteroids, mag, etc.), but I haven't seen any mention of CPAP.

CPAP is another option which falls squarely on the, potentially effective but controversial, end of the spectrum. One of our resident RT's can probably explain it better than I, but the general idea involves using pressure levels that exceed the pressure of the tapped air. This allows a kind of waterfall type effect (can't remember the correct term off hand) to take place which essentially "releases" the trapped air from the alveoli. It also "splints" bronchi open from the inside (kind of like using positive pressure ventilation for a patient with a flail segment). The obvious downside is that obtaining these effects involves experimenting with high airway pressures (pneumothorax potential).

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