Pediatric Asthma Case

[MediRounds]

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A 5 year-old boy with a past medical history of asthma with 3 prior asthma-related hospitalizations (including 1 prior ICU admission where he was intubated for status asthmaticus) presents to your ER with another asthma exacerbation. His home medication regiment is budesonide nebulized treatment BID with albuterl nebulized treatment BID. Over the last 24 hours, he has had increased difficulty of breathing and his peak flow measurements have been < 50% of his baseline normal measurements. His parents have been giving him the albuterol nebulized treatments every 4 hours during the last 24 hour without improvement. His presenting respiratory rate is 32 and his oxygen saturations are 92-95% on room air. His other vital signs are: temperature = 37.8 C, heart rate = 123, and blood pressure = 91/56.

1. What else would you like to know about the encounter?

2. What is your treatment / management plan?

 

[OveractiveBrain]

A 5 year-old boy with a past medical history of asthma with 3 prior asthma-related hospitalizations (including 1 prior ICU admission where he was intubated for status asthmaticus) presents to your ER with another asthma exacerbation. His home medication regiment is budesonide nebulized treatment BID with albuterl nebulized treatment BID. Over the last 24 hours, he has had increased difficulty of breathing and his peak flow measurements have been < 50% of his baseline normal measurements. His parents have been giving him the albuterol nebulized treatments every 4 hours during the last 24 hour without improvement. His presenting respiratory rate is 32 and his oxygen saturations are 92-95% on room air. His other vital signs are: temperature = 37.8 C, heart rate = 123, and blood pressure = 91/56.

1. What else would you like to know about the encounter?

2. What is your treatment / management plan?

Oh Reggie! He was part of the 85th airborne REGIMENT!

Don't you think these would be better suited in the Pediatric forum? You know, since they are peds specific?

 

[duckie99]

1. What else would you like to know about the encounter?

2. What is your treatment / management plan?

clearly he has pulmonary histoplasmosis, often misdiagnosed as asthma:
http://www.foxnews.com/health/2012/09/17/common-fungus-killed-minnesota-teen/

 

[Rendar5]

Oh Reggie! He was part of the 85th airborne REGIMENT!

Don't you think these would be better suited in the Pediatric forum? You know, since they are peds specific?

Yeah, but they're also well-suited for med students in the clinical years and the work-up/treatment is the same for adults until you get into subtleties of end-stage management. At this point, the only peds specific thing you need to know are age appropriate vital signs.

 

[loveoforganic2]

Wish there were more case discussions, good random reading. Carry on!

 

[MediRounds]

Anybody interested in taking a stab at this? It's all for learning...no judgement! 🙂

 

[caveat87]

Well in the acute setting I would probably give duonebs and oxygen. Consider prednisone/Mag if tachypnea does not resolve. This may drop the saturation a bit, but stay the course with high flow oxygen. I am not that concerned with his current O2 saturation since he remains above 92%. Intubation as a last resort because it is not fun to intubate asthmatics.

But we have to dive a little more into history when he is stable. What provoked the attack? Where there new sick contacts, seasonal allergy symptoms, etc. Is the kid compliant with his pulmicort at home? I am also interested in classifying the severity of asthma as this will guide medication choices and the need for an asthma specialist if we are looking at moderate to severe asthma.

From there it is a matter of treating symptoms and lots of parent/patient education, putting into place an asthma control plan, providing access to appointment with providers. Even after all this stuff there is a darn good chance the kid will be back in a few months because his parents will stop giving him the control medication (or so I have seen three times already on my only 5 week Peds rotation).

 

[MediRounds]

Great start!

The key thing to be aware of is that this child has been intubated previously which raises a red flag for me in how sick he can get. I tell residents and fellows to "hit them hard" with medication up front and be aggressive because you can always remove medications once the asthma is under control. So, the medication list that I would pull from would include:

Oxygen.

Some form of inhaled beta-agonist (ie. albuterol) and an anticholinergic (ie. ipratropium bromide) x 3 back-to-back and then reassess to see if the child needs a continuous treatment of albuterol.

As that is being instituted, I would start IV steroids (ie. solumedrol) and IV fluid hydration.

IV magnesium is an option, but if the patient continued to be having respiratory distress I would start a beta-agonist infusion (ie. terbutaline) and likely an aminophyline infusion as well.

I would obtain a blood gas (ABG being the gold standard).

You thought correctly about obtaining a sick contact history or recent illnesses because the asthma attack may have been triggered by an illness (may consider antimicrobial treatment, if high index of suspicion, such as an atypical pneumonia like mycoplasma) or noncompliance. Of course, you will see if there are any other comorbid conditions or exposures at home (ie. parents smoking).

What signs and symptoms would make you more concerned about this patient getting worse?

What would an initial ABG look like in this child and what would be a concerning trend, if you obtained another ABG a couple hours later?

 

[loveoforganic2]

ABG showing increasing respiratory acidosis/hypoxia on the way to decreased respiratory effort with altered consciousness -> intubate?

 

[Rendar5]

ABG showing increasing respiratory acidosis/hypoxia on the way to decreased respiratory effort with altered consciousness -> intubate?

Definitely a consideration on the road to intubation.

1. Back to medi's question, what would the CO2 on the initial asthmatic typically and what's the CO2 on the end stage asthmatic? And how is the patient acting as you reach end-stage asthma that might clue you in on those CO2 measurements? Loveoforganic's already there with his answer, but just needs to explain this last part of the ABG.

2. Why give steroids before seeing the effect of the albuterol/atrovent?

3. Why not intubate early on while they're still moving some air? Why the desire to try so many things before securing the airway?

4. Last question to think about is why is medi giving IV fluids? that's not a typical maneuver on an adult patient.

 

[MediRounds]

Good questions, Rendar5!

 

[loveoforganic2]

Definitely a consideration on the road to intubation.

1. Back to medi's question, what would the CO2 on the initial asthmatic typically and what's the CO2 on the end stage asthmatic? And how is the patient acting as you reach end-stage asthma that might clue you in on those CO2 measurements? Loveoforganic's already there with his answer, but just needs to explain this last part of the ABG.

Progression from normocapnic/hypocapnic early on due to anxiety-related hyperventillation to hypercapnic when obstruction worsens and the patient still has hurried expiration exacerbating the air trapping

2. Why give steroids before seeing the effect of the albuterol/atrovent?

It seems like based on the time course (past 24 hours?) the asthma would already be in the inflammation stage, so I guess to limit further eicosanoid production as much as possible?

3. Why not intubate early on while they're still moving some air? Why the desire to try so many things before securing the airway?

I'm just a 2nd year, and I think this is starting to get above what I can reasonably guess at. I'm not sure why you would intubate a patient that may resolve without it - seems like a last resort in any patient. In asthma in particular, I assume you'd have to keep an undesirably high PEEP to avoid bronchiolar collapse (risk pleural effusion and tamponade?), but with that in mind, I'm not sure why you couldn't use some kind of combo of calcium channel blockers and and antimuscarinics to prevent that from being too much of an issue?

4. Last question to think about is why is medi giving IV fluids? that's not a typical maneuver on an adult patient.

I can't think of anything that would be peds specific

Edit: I'll bow out of venturing guesses if someone who knows more about what they're talking about wants to chime in

 

[Khaos]

I was trolling around forums and thought I'd chime in since we see a bunch of these in the emergency department. First question I would ask in this scenario is how does the kid look when you walk in the room. I've seen plenty of 5 year olds that look wonderful with those vital signs, they just are breathing a little faster. I would say 75 to 85% of the time I send those kids home. I've also seen kids that look like total crap with those vital signs...so it definitely would make a difference.

ABG - I don't give a crap what the ABG shows. Is the patient awake, alert, talking or is he progressing and in significant distress and maybe even altered? In an adult a VBG or ABG can be used to determine intubation (very rarely since usually the same signs for intubation occur with both). In a child who has great reserves and a nice young heart and lungs that can keep a heart rate of 160 without problems and a respiratory rate of 50 for quite a while, I don't ever get an ABG unless they are intubated.

Steroids - they don't work right away. It has been shown over and over that they kick in 3 to 5 hours after administration. I'm not giving them steroids for now, I'm giving them for later. If you are able to get them through the acute distress with 5mg albuterol x 3 and 0.5 atrovent x 3 you are talking about doses of albuterol that is 60 times that of an inhaler...(80mcg/puff) x 3 doses. That is why 90% of your asthma patients end up improving with neb instead of MDI. However, after that gigantic dose of albuterol and atrovent start wearing off you want something else to start kicking in so that MDI actually works.

Intubation - two things you don't want to intubate because we have not been able to figure out the best way to oxygenate them with a machine. We can't replicate the lung mechanisms of an asthma or COPD patients that actually protect them the best. We do a horrible job simulating the exhalation pattern in COPD and asthma. So, I will try everything before intubating. For Asthma patients --> albuterol/atrovent, IV steroids then IV mag, then IM epi, then if still in significant distress (these initial vital signs shown are far from distress) the next meds will be ketamine and succinyl choline for RSI. The difference in COPD would be before intubation try bipap if they aren't too confused yet.

IV fluids - I have never seen this in practice and have no idea what good this would be for a straight forward asthma or COPD. Plus in adults you risk misdiagnosing COPD for the CHF they truly have and you just made things worse.

 

[Rendar5]

Progression from normocapnic/hypocapnic early on due to anxiety-related hyperventillation to hypercapnic when obstruction worsens and the patient still has hurried expiration exacerbating the air trapping

Exactly. To get more in details, hypercapnia causes a progressive alteration of mental status from lethargy to obtundation to coma. This is why when patients start to tire, they get sleepy, which leads into a vicious cycle. As khaos mentioned, you don't always need the ABG, particularly in adult patients who you can accurately gauge a mental status on. But on a kid, it's sometimes hard to appreciate the degree of hypercapnia.

It seems like based on the time course (past 24 hours?) the asthma would already be in the inflammation stage, so I guess to limit further eicosanoid production as much as possible?

Generally, if someone goes to the ER for asthma, it means that albuterol alone is not cutting it. Otherwise, they'd just stay at home treating themselves. So you're right that there's a lot of airway inflammation acting up at that point. Doesn't matter if the nebs make em feel better because they're just a temporizing measure until steroids begin to exert their effectiveness as Khaos mentioned.

In asthma in particular, I assume you'd have to keep an undesirably high PEEP to avoid bronchiolar collapse (risk pleural effusion and tamponade?), but with that in mind, I'm not sure why you couldn't use some kind of combo of calcium channel blockers and and antimuscarinics to prevent that from being too much of an issue?

Usually you can avoid intubation being an issue, but even with correct treatment, things don't always go as planned. Some people respond well to treatment, but others are either too far gone or don't respond as well as everyone else.
I'll let a couple other people weigh in on the problems intubating these patients in particular, though khaos hit most of the salient points.

As for IV fluids, also gonna see if anyone else wants to wager a guess. As Khaos mentioned, not something for use really in adults, especially because you get into a COPD vs. CHF situation fairly often (and anyone who's worked the wards knows that these two disease entities are very tricky to distinguish between)

 

[loveoforganic2]

Found something for IV fluids, but it wasn't peds specific, so when you give the reason, if you could give why it's peds only indication I would appreciate it!

 

[J-Rad]

COPD is going to be a pretty non-existent entity in peds.

1. Kids in the midst of an asthma exacerbation tend to be fluid down, especially if they've been ill leading up to it (often a URI)

2. Diastolic hypotension in a known side effect of beta agonists, especially in high doses-which they are going to get in the ED. Fluids are a pretty good first line treatment for that.

3. MIVF with D5NS+K is probably in order for a patient who gets admitted to the general peds ward as they aren't going to want to hydrate all that well until they are recuperating.

I was trained that a fluid bolus was a good thing for a kid with an asthma exacerbation. It isn't a hard and fast rule or "standard of care" (to my knowledge), but I think it makes clinical sense.

 

[J-Rad]

ABG - I don't give a crap what the ABG shows. Is the patient awake, alert, talking or is he progressing and in significant distress and maybe even altered? In an adult a VBG or ABG can be used to determine intubation (very rarely since usually the same signs for intubation occur with both). In a child who has great reserves and a nice young heart and lungs that can keep a heart rate of 160 without problems and a respiratory rate of 50 for quite a while, I don't ever get an ABG unless they are intubated.

👍👍

 

[OveractiveBrain]

Yeah, but they're also well-suited for med students in the clinical years and the work-up/treatment is the same for adults until you get into subtleties of end-stage management. At this point, the only peds specific thing you need to know are age appropriate vital signs.

Is THAT why more than 75% of the posts have been me or... attendings... Awesome.

 

[Rendar5]

Is THAT why more than 75% of the posts have been me or... attendings... Awesome.

lol, ok they're interesting questions os quickly bump up to the resident level 🙂 But I still think they're good discussions for clinical years med students to see and think about.

 

[MediRounds]

You guys have really done a great job with this discussion. I want to emphasize what J-Rad said about the IV fluids. Usually, children are somewhat dehydrated with status asthmaticus, which was where this patient was headed. Also, part of the physiology of asthma includes not only bronchiole muscle constriction and inflammation, but also mucous plugging. Preventing further dehydration with IV hydration will prevent thick mucous plugs from developing (theoretically). I've heard of intensivists lavaging the airways via bronchoscopy to wash out mucous plugs to improve ventilation after intubation. Obviously, there is not much evidence to support placing bronchoscopy into standard of care therapy for this condition, but it just emphasizes the point that mucous plugging plays a role in this pathology.

Next, the point about the ABG is well taken. You never need an ABG to decide whether or not to intubate a patient. The point of the question was to emphasize that the initial ABG will actually show a respiratory alkalosis due to the hypoxemia that initially develops. As the patient's lower airway obstruction continues, causing increased dead space, and the patient begins to fatigue, the respiratory alkalosis begins to reverse and the patient develops a respiratory acidosis moving towards respiratory failure, A relatively normocapneic ABG is actually a little concerning because the patient is starting to fatigue and lose the ability to compensate (assuming the patient still has significant respiratory distress.

Ok, now for a physiology question:

What is the significance of pulsus paradoxus in status asthmaticus? How does it change with improvement and worsening of the patient's clinical condition?

Any takers? Prefer residents or medical students to think this through... 🙂

 

[VenusinFurs]

Well, pulsus paradoxus in this case could be due to the increased oxygen demand to the diaphragm (need to take deeper breaths, use more accessory muscles, tachypnea) during inspiration which means blood flow to that area would probably increase, resulting in a lowering of systolic pressure/ maybe a decrease in venous return to the left atrium, which might also be due to lowered alveolar pressure. Then you're probably somewhat hypovolemic. Then you're tachycardic so have decreased stroke volume?

 

[loveoforganic2]

That should be compensated for by an increase in inotropy I would think, as it would be a gradual process (and would be constant once it was there, not varying much with each inspiration/expiration cycle)