32 yo Male - general illness

[SpecialK]

Easy as pie. Simply based on his unrelenting tachypnoea and tachycardia and the fact has says he took an unknown quantity of insulin means I cannot leave him in the community or send him on down to the GP or local A&M .. the GP or A&M doc would run a mile at the sight of this bloke.

Now, as to what treatment I'd give him? I can't see anything specific, maybe a dribble of IV fluid if hospital was ages away.

 

[Akulahawk]

Easy as pie. Simply based on his unrelenting tachypnoea and tachycardia and the fact has says he took an unknown quantity of insulin means I cannot leave him in the community or send him on down to the GP or local A&M .. the GP or A&M doc would run a mile at the sight of this bloke.

Now, as to what treatment I'd give him? I can't see anything specific, maybe a dribble of IV fluid if hospital was ages away.

Given that his BGL reads "HI" after taking some unknown amount of insulin, you really shouldn't leave him there. The tachypnea and tachycardia tell me that he's probably quite dehydrated. The CAH I worked at could easily stabilize him and get things rolling for a transfer to a more capable facility. We got these patients a few times per week and I got reasonably decently good at initial stabilization.

My treatment en-route would have been bilat IV lines (because I know he's going to need them), and probably 1L wide open to start. Since our ambulances aren't allowed to carry insulin, I can't give it... 2nd liter will go up once the first one is done. I'd leave the 2nd line as a saline lock.

As to destination decision-making, I probably would have gone to the tertiary facility because of the drug use as it could be messing with his head too, making him a DKA with possible OD (or at least intoxicated) because of the stuff he's known to take. It's only another 30 minutes and it gives me time to really reassess him as he's getting rehydrated. If he develops coarsening lung sounds, I'm not going to suspect fluid overload as I doubt I can overload him in 30 minutes using 1 liter of fluid, given his present state. I might start thinking aspiration pneumonia is developing. He did vomit and he's wiped-out. Aspiration could have happened.

 

[NomadicMedic]

This is another of the ALS "bread and butter" calls. We all run these at least a couple of times a year. Its right up there with chest pain, diff breathers, abdominal pain of unknown origin and general malaise.

Thanks for all the input.

 

[SpecialK]

Given that his BGL reads "HI" after taking some unknown amount of insulin, you really shouldn't leave him there. The tachypnea and tachycardia tell me that he's probably quite dehydrated.

Hence why I said I would not. I'd leave him at home or send him down to the A&M if he hadn't taken the insulin and unknown other medicines. If he just needed a bit of IV fluid and somebody to give him a lookey loo for a couple hours then the A&M could do it fine. Most patient's don't want to go though because they have to pay whereas the hospital is free. And I don't bloody blame them, rubbish idea charging people for healthcare ... criminal.

My treatment en-route would have been bilat IV lines (because I know he's going to need them), and probably 1L wide open to start. Since our ambulances aren't allowed to carry insulin, I can't give it... 2nd liter will go up once the first one is done. I'd leave the 2nd line as a saline lock.

Oh good heavens no! If you pour IV fluid into him aren't you worried about upsetting his sodium osmoality and potentially causing cerebral oedema?

 

[E tank]

Oh good heavens no! If you pour IV fluid into him aren't you worried about upsetting his sodium osmoality and potentially causing cerebral oedema?

With a balanced salt solution? Besides, that's a rare pediatric complication. 20-30 kg of crystalloid will definitely not hurt this guy. He needs the fluid.

 

[medichopeful]

Clearly he's in a metabolic acidosis---probably compensated, or a mixed disturbance, at this point---and cannot R/O HHNK based off of your glucometers reading. I'd head for the critical access, reassess en route, if he remaines agitated transport to the closest; if he perks up, divert to the city.

He needs an insulin gtt, a full set of lab work, and quite possibly potassium; that's all I got for now. Can we get a temp en route, and/ or is he abnormally hot to the touch?

What's your thinking on HHNK as complared to DKA Vent? If you're thinking that he's in metabolic acidosis, I'd lean more towards DKA than HHNK.

Any idea what the EtCO2 was? And do we have access to an iStat by any chance?

 

[VentMonkey]

What's your thinking on HHNK as complared to DKA Vent?

Aside from an extremely high BGL, which can hardly be confirmed via accucheck alone, not much. It's merely something I could not, or would not rule out.

This kind of patient made for a good learning experience with interns I've had, as I would throw HHNK at them just to get their wheels turning.

Will it change our treatment modalities? Hardly, but nonetheless, these are the sought after interesting medical cases in my book.

If you're thinking that he's in metabolic acidosis, I'd lean more towards DKA than HHNK.

Generally agreed, though I'd argue a patient in HHNK would present as metabolically acidotic in their own right in the absence of ketone production.

And again, the similarities in the prehospital setting are often too close to discern (though I suppose one could argue the rapid respiratory rate would favor more of a compensatory mechanism seen with a ketone byproduct over one with a "non-ketotic" presentation), nor should it matter with respect to prehospital therapies.

 

[medichopeful]

Aside from an extremely high BGL, which can hardly be confirmed via accucheck alone, not much. It's merely something I could not, or would not rule out.

This kind of patient made for a good learning experience with interns I've had, as I would throw HHNK at them just to get their wheels turning.

Will it change our treatment modalities? Hardly, but nonetheless, these are the sought after interesting medical cases in my book.

Generally agreed, though I'd argue a patient in HHNK would present as metabolically acidotic in their own right in the absence of ketone production.

And again, the similarities in the prehospital setting are often too close to discern (though I suppose one could argue the rapid respiratory rate would favor more of a compensatory mechanism seen with a ketone byproduct over one with a "non-ketotic" presentation), nor should it matter with respect to prehospital therapies.

I definitely agree that with prehospital therapies it wouldn't matter (unless we had more info, like labs and ABGs). The RR is borderline, so I don't think there's anyway to tell without lab work like you said. I was just curious if I had missed something that you had picked up on!

 

[VentMonkey]

@medichopeful not at all, I just like to keep my wheels turning. Also, here's a fairly straightforward question I pose to others on here:

If you had to intubate this patient, how would you go about managing their airways post ETI? What would your vent management goals be, and why?

@SpecialK the amount of crystalloids we'd typically infuse in these (adult) patients prehospital isn't enough to warrant cerebral edema. That said, the pediatric DKA population seems much more prone to this a lot sooner.

 

[E tank]

Just for the sake of the conversation, as this guy is clearly a Type I diabetic, the odds of this not being DKA were pretty low.

 

[StCEMT]

@VentMonkey standard tidal volume, higher rate of maybe 25 since increases RR is to compensate for the acidosis. Don't want to take his compensatory mechanism away.

If NS leads to worsening acidosis and we are dumping fluids, would there not be a role for bicarb mixed with fluid administration? I remember some mention of cerebral edema regarding this, but I don't know how prevalent that is in an adult. I'll look it up when I get home.

 

[medichopeful]

@medichopeful not at all, I just like to keep my wheels turning. Also, here's a fairly straightforward question I pose to others on here:

If you had to intubate this patient, how would you go about managing their airways post ETI? What would your vent management goals be, and why?

@SpecialK the amount of crystalloids we'd typically infuse in these (adult) patients prehospital isn't enough to warrant cerebral edema. That said, the pediatric DKA population seems much more prone to this a lot sooner.

I'll be 100% honest, vent management is a weak point of mine and I'm currently studying up on it to improve my knowledge regarding them (at my current job, we only mess with FiO2 in emergencies and the alarm silence button, the most important button there is).

With that being said, I do know that for this type of patient, one of the things that can kill them or cause serious issues is underventilating them (thus completely eliminating or screwing up their ability to compensate for their metabolic acidosis through hyperventilation, leading to decreasing pH/increasing acidosis and then cardiac arrest). Trying to at least match their pre-intubation minute volume would be extremely important, and EtCO2 would be important to make sure they are not becoming even more acidotic through CO2 retention (though ABGs in addition would be better). A quick intubation would be necessary, too: you don't want to have any lengthy periods of apnea (again due to taking aware their compensatory breathing). It's all about controlling their airway, while allowing the (now mechanical) breathing to continue to blow off CO2. I also know that placing someone on a vent can also raise PaCO2, so that's something we'd have to consider, and we might need to even increase their minute volume to cancel this out.

 

[VentMonkey]

@VentMonkey standard tidal volume, higher rate of maybe 25 since increases RR is to compensate for the acidosis. Don't want to take his compensatory mechanism away.
You don't want to arbitrarily guesstimate these patients RR, though you're on the right path by increasing their rate (f).

I'll let others chime in if they so wish.

 

[Handsome Robb]

Get a pre-intubation EtCO2 and titrate your RR to target that number. That's the number their body is happy at and has gotten itself to. Ultimately we need serial ABGs to truly managed him on a vent for any extended periods of time.


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[VentMonkey]

Ultimately we need serial ABGs to truly managed him on a vent for any extended periods of time.

While true, a most accurate and up to date ABG would yield our target Ve, we can still calculate this patients RR in the field without POC ABG fairly accurately utilizing another formula.

Also, just a personal note:

I would not bother intubating this patient prehospital unless there was some inherent reason to such as evidence of aspiration, or impending aspiration.

They're compensating on their own, and this is one patient where an overzealous and aggressive airway management approach can be extremely detrimental. Their ultimate cure is not ETI, it is Insulin.

 

[StCEMT]

@VentMonkey, it's not entirely arbitrary. All I know is I don't want to cut their rate in half. 25 is simply a starting place. Adjust their tidal volume from the generic male volume to something more appropriate, then adjust the rate to maintain their EtCO2 within a few points of what it was initially. Same concept as my dopamine shortcut, just trying to start close then dial it in.

ETI seems like it isn't often needed, at least never in the DKA cases I've come across. I'd rather avoid messing with them all together and let the docs do all the lab work ups.

 

[VentMonkey]

@VentMonkey, it's not entirely arbitrary. All I know is I don't want to cut their rate in half. 25 is simply a starting place. Adjust their tidal volume from the generic male volume to something more appropriate, then adjust the rate to maintain their EtCO2 within a few points of what it was initially. Same concept as my dopamine shortcut, just trying to start close then dial it in.

ETI seems like it isn't often needed, at least never in the DKA cases I've come across. I'd rather avoid messing with them all together and let the docs do all the lab work ups.

Right, but for the sake of continued conversation this patient has already vomited once. What if you did elect to divert to the tertiary hospital 40 minutes away, and they vomited again?

SGA's certainly have their place, however, this would not be one of them. What if the combativeness did not resolve as well? What if your service doesn't carry in-line ETCO2 NC's? Where would you come up with a starting point for goal directed ETCO2? How would you manage this patient once you realized it was "too late" to turn back, or not worth it to re-route to the CAH?

 

[ERDoc]

One thing to remember with DKA is there is often some sort of precipitating cause. Sure, medication noncompliance is common but infections are another pretty common cause.

 

[Akulahawk]

Oh good heavens no! If you pour IV fluid into him aren't you worried about upsetting his sodium osmoality and potentially causing cerebral oedema?

Actually no. What this patient needs is fluids. NS will do this just fine. He's going to need a LOT more than that. Chances are pretty good that his sodium level is low and 0.9% Saline will start bringing that up. In the short run I'm actually more worried about K+ loss. While an initial lab draw may show a relatively normal K+ level, as he's rehydrated, an underlying hypokalemia will likely begin to show. Sure the CAH can start doing K+ replacement but their ED may not think about doing that during their initial eval and tx of this patient. They'll be concentrating pretty closely upon getting the blood glucose level lower while they arrange for a transfer to that same "big" hospital that's 30 minutes away. Once the patient is there, their ICU will likely do a huge eye-roll, start doing K+ replacement, continuing insulin replacement while considering when to change over to something like 1/2 NS or D5 mixed in. They may take a few DAYS to fine-tune the patient, getting the sodium level, chloride level, K+ level, and even phosphorus all back to normal while maintaining relatively tight glycemic control. Catch the patient early enough and the K+ and phos derangements may not even occur...

Now if the patient was, say, fairly young (early teens or younger) then I'd be quite worried about cerebral edema but even then initial resus with NS isn't likely to kick-off cerebral edema. Continued use of it may. Repeat stat labs should help keep them from correcting the sodium levels too quickly.

 

[StCEMT]

Right, but for the sake of continued conversation this patient has already vomited once. What if you did elect to divert to the tertiary hospital 40 minutes away, and they vomited again?

SGA's certainly have their place, however, this would not be one of them. What if the combativeness did not resolve as well? What if your service doesn't carry in-line ETCO2 NC's? Where would you come up with a starting point for goal directed ETCO2? How would you manage this patient once you realized it was "too late" to turn back, or not worth it to re-route to the CAH?

Suppose it depends on his mental status and ability to maintain his own airway.

An SGA wouldn't be my preference here, I'd rather not take the airway unless necessary and if so then SGA will just remain the backup. My service actually doesn't (for a while longer) have them, it is something I have wondered myself recently. Off topic, but I've been curious about the accuracy of having someone just blow on a ET end tidal adapter, but I have never actually tried this. Not that this is of any use in the case of ALOC.

Assuming I had no baseline to work with? Doctors recommendation, along with anything else I would want to know. While I've seen a few DKA cases, I haven't seen any at this level of severity where intubation and long term management was required on my end. Knowing when that time has come would be unfamiliar territory and 40 minutes gives me plenty of time to consult and proceed from there.