How to manage Redux II

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Paseo Del Norte

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You are called to transport a 15 year old patient from a rural facility to a paediatric subspecialty centre. You can expect just over an hour long transport time not including packaging, hand over, and report.


HPI:

Male patient presents to ER with a several day history of generalised weakness, polyuria, polydipsia, and nausea.

PMH:

No medical or surgical Hx. reported, no family history reported, NKA.

Initial impression and rapid ROS:

You arrive to find a 15 year old male patient (60 kg ) sitting in high fowlers on the ER stretcher. The patient is tachypneic and tachycardic and is lethargic (responds to painful stimuli with a moan). ER staff report the patient has become increasing fatigued and lethargic and you also note use of accessory muscles.

Current vital signs and Rapid Physical exam:

P- 130 weak and regular at the radial = to apical (S1S2 tachy per prior information) This matches a narrow complex sinus tachycardia without any other conduction abnormalities on the monitor in lead I, II, & III.

RR- 40 deep and regular with accessory muscle use, lungs are clear
throughout all lobes anterior and posterior.

SPO2: 100 % on nasal cannula at 2 LPM.

B/P: 88/70

Temp: 99.9 F

Dry mucus membranes and delayed capillary refill noted with an unremarkable physical exam with the exception of the abnormalities noted above.

Diagnostics are as follows:

NA+: 128
K+: 5.9
Cl-: 91
BUN: 65
Creat: 3
Glucose: 718
Serum Acetone +
Hb: 14
HCt: 59%

ABG:

PH- 7.28
PaCO2- 22
PaO2- 110
HCO3-: 10

PA Chest Film:

Normal

Assessment:

The current Dx is new onset DKA.

Plan so far:

Bilateral 20 ga IV's (AC) have been placed along with a foley catheter that is draining scant, concentrated urine. The RN is administering an initial bolus of insulin and an insulin infusion is ordered at 6 units of regular insulin per hour. In addition, a fluid bolus of 1,000 ml 0.9% saline is ordered. You will transport this patient as described above. You work for a progressive system and can assume your crew is well versed in critical care transport.

Take it from here...

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I'm not quite sure what kind of an answer you are looking for here. Is this scenario from the CCEMTP course? My priority would obviously be to get the Pt to the specialty center alive and stable; that being said, I would probably have the equipment necessary to RSI the Pt if he took a turn for the worse during transport. You did not mention if it was ground or air transport. If ground, I would probably try to find a helicopter to significantly cut down on the transport time. But again, I am not quite sure what kind of answer you are looking for here...
 
This is a fairly open ended scenario. If you saw this kid with the information given, what interventions would you consider? Do you have any questions or concerns? Think of it as part scenario and part discussion as we will most likely have different concerns and considerations; however, this patient has interesting pathophysiology and as the scenario progresses I will force you down a pathway to emphasize some of the implications of this pathophysiology.

This can be either an air or ground transport; however, the transport time will not change.
 
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Gas:
Partially compensated metabolic acidosis, with hyperoxemia.

I'd tube him for the ride. How long has he been keeping up this Kussmauls? He's rapidly fatiguing while compensating for that metabolic acidosis (in this case DKA). At the least some NIPPV may reduce his WOB, but I suspect he's beyond that point. Why is he on O2? Were there prior gasses run? Why is his end tidal not being monitored? I bet his PaCO2 is trending upwards.
The dehydration may explain the tacycardia, low BP, lytes, and the crit. However, if I'm not mistaken the elevated BUN and Creatinine may indicate moderate to severe renal failure.......he may need a diuretic as well.
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Then again, maybe not.
 
This type of situation is common in CCT EMS. It really boils down to that the transferring facility wants the patient to go NOW but the best thing would be to stabilize the patient better before transport. I'm an assistant medical director for the CCT program here so I get these calls from the crews when they get nervous. In this case I'd advise them to not transport and I'd ask the transferring doc to try to tune the patient up some.

In this particular sceanario we're not talking about some Zebra. This sounds like pretty typical DKA. I'd like to see the transferring facility hit this kid with at least 2 L of NS and give some insulin (gtt or not, just to try to stop the ketosis). Give the kid some time to either improve or, if he doesn't, tube him in the ED rather than in the back of the ambulance. RSI will be tricky. I wouldn't use Sux due to the hyperK so it'd be Roc and that will keep him paralyzed for ~40 min. Consequently problem getting the airway could be a real disaster. All things considered though, I'd like to avoid tubing this kid. He should improve with some basic interventions.

This does illustrate one thing I've seen both in ERs I've worked in and from the field end. When an ER gets a patient they are definitely going to have to transfer they frequently start persuing the transfer more than treating the patient.
 
Awesome replies!

Poresofkohn, absolutely correct on the ABG. In addition, would you expect an elevated anion gap with this patient? You are on the right direction with the BUN/Creat, in this case (The BUN/Creat ratio should be elevated, I hope.) giving fluids may help more than anything.

Let's say you try BiPAP; however, the patient "poops out" and you need to consider more aggressive management. I agree that staying away from intubation is the best way to go, but we have to go that route in this case.

Doc B, good call on the Roc. For those who are not as familiar, what is the potassium relationship with Sux and why is potassium a potential concern with this patient? (Can apply to many cases of acidosis actually.) In addition, let's say following two litres of fluid the doc orders maintenance fluids with 20 of K+. The ER nurse refuses to hang the fluid quoting the elevated serum K+, what do you think? Does elevated serum K+ always mean the total reserve of K+ in the body is elevated? What will happen when the kidneys come on line and the acidosis corrects, what has been occurring in the days leading up to hospitalisation? (Think polydipsia.)

Who wants to take a swing at the ventilator settings?
 
poreofkohn, just wondering, why would you tube the kid prior to transport with pulse ox of 100% at 2 lpm via NC? docB makes a good point about the Succs/hyperkalemia that I must admit that I didn't fully consider prior to my suggestion of RSI if Pt goes downhill during transport. I think it is important to consider what the receiving facility/physician wants. Has anybody considered sepsis?
 
Numbers can lie in some cases. While this kid is oxygenating and ventilating quite well, he has been breathing fast and deep. He is using accessory muscles and has become lethargic. While avoiding intubation Is a good thing, we need to at least consider the possible clinical course with this kid. As he becomes more pooped out from all the WOB, are we going to chance an hour long transport without airway protection?

I agree we need to see if the receiving doc has any special orders; however, as DocB stated, this patient is still the sending doc's problem.
 
if it was me I would like better access than 2 20 g IV's. either a lg bore IV(or 2) or an IO(or 2).
this kid needs way more than 2 L of fluid before being switched to maint. fluids.
also his intracellular K is low at this point and he should be getting K not having it restricted....and defintely no diuretic...
if we take out his contribution from blowing off co2 down to 22 his uncorrected ph is around 7.12
this kid is obviously icu material(duh).
I wouldn't intubate this kid yet but would be ready to do so as needed. I have sent sicker kids than this to the unit before without a tube.
 
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You manage to place an 18 ga peripheral IV and happen to look up at the patient and note he is unresponsive and breathing rather shallow at about 10 times a minute.

Good call on the K+. Serum K+ is elevated due to shifts but he has been peeing K+ out like a big dog and will continue to do so as the kindeys come back on line with fluids. In addition, serum K+ will likely decrease as you correct the acidosis.
 
kid just bought himself a tube. his rhythm is still sinus tach with pulses(and a palpable pressure?)?
by the way, any idea what his mag. level is?
also did they do an etoh, uds and tox. screen with asa and apap levels before transfer(he is 15 after all and did have an altered level of consciousness.........)
 
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Lets say 1.3 and the UDS is negative along with serum ETOH, ASA, & APAP. Sinus tach with pulses that match what you see on the monitor.

Yeah, sorry it was inevitable. So, what about ventilator management?
 
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I don't do a lot (ok I don''t do any) vent management so this is a guess.
put him down with roc(as discussed above) then start a propofol drip at 0.2-0.3 mcg/kg/min to keep him down with adjustments as needed.
we need to maintain his prior hyperventilation so a rate of at least say 32 on full control setting(CMV) and a tidal volume of 5-10ml/kg so let's split the difference and say 7.5ml/kg with peep set at 5 to start. then recheck abg's q 15 min for the first hr and make adjustments as needed.
the only vents I have ever used are basic transport vents with 2 settings; tidal volume and rate and only 1 mode setting(cmv)..it definitely beats manual bagging looking at a watch for an hr...
in my current job I intubate the pt then hand them off to RT and they whisk them off to the icu.
I'll be honest. I learn enough about vents to pass the course every few yrs in fccs then promptly forget all the info because I don't use it. what I need is a month or two working in the icu....or a critical care residency....I keep thinking about it but the 75% pay cut keeps getting in the way....
 
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Sounds like a good plan. You nail a key point about maintaining respiratory compensation. I agree that a healthy 15 year old would be just fine with a volume controlled ventilation modality.

The specific mode is debatable I am sure; however, here are my thoughts:

-Somebody breathing in a compensatory pattern may do well in assist control. We can essentially let them rest while assisting them when they take a breath. Because DKA patients may poop out from hard and fast breathing, assist control may be a helpful consideration in giving the patient a rest while maintaining respiratory compensation.

-Many people like SIMV (Really common in transport.); however, SIMV can lead to increased distress in some patients. A way to help patients in SIMV can be the addition of pressure support to help the patient initiate a breath and overcome circuit resistance. A ghetto rule of thumb for pressure support is to take the difference between the PIP and Pplat. This number can be your starting point for PS; however, I find many people simply default to a PS of 10.

We have had a few cases of DKA where I work and the management was questioned, so I thought about making a case to emphasize a few key points:

1) These patients are quite dehydrated and initial therapy will typically be isotonic volume replacement.

2) Acidosis is commonly associated with a shift of potassium to the extracellular environment; however, DKA patients will typically be potassium depleted. Depletion of other lytes such as magnesium are common as well.

3) If you have to intubate a DKA patient, you need to ensure you continue respiratory compensation. I have seen charts where intubated patients were ventilated to the generic normal 35-45 mm/Hg. Clearly, substantial alterations in PH were reported at the receiving facilities.

4) Number can be misleading. While the ABG was not the typical respiratory failure ABG, occasionally these patient can fatigue from the WOB and require intubation.

Thank you for the replies, I hope people found this case study worth while.
 
if it was me I would like better access than 2 20 g IV's. either a lg bore IV(or 2) or an IO(or 2).
this kid needs way more than 2 L of fluid before being switched to maint. fluids.
also his intracellular K is low at this point and he should be getting K not having it restricted....and defintely no diuretic...
if we take out his contribution from blowing off co2 down to 22 his uncorrected ph is around 7.12
this kid is obviously icu material(duh).
I wouldn't intubate this kid yet but would be ready to do so as needed. I have sent sicker kids than this to the unit before without a tube.

I was approaching this more from the point of view of what do I want to see done before I let my CCT guys put this on the rig for an hour transport. I didn't mean that 2 L was definitive management. I just think that would be enough to see the kid either get better and be more likely to make the trip without a tube or get worse and get tubed prior to transport.

HyperK with DKA is pretty tricky. They are generally depleted in their whole body K but if their serum K gets too high due to the acidosis they can fibrillate. There's also often some degree of renal impairmant with the severe dehydration that can make fluid and K managment difficult.

We had a pretty good discussion of this on the EM board some time ago:
http://forums.studentdoctor.net/showthread.php?t=682266
 
Was a tox screen done? Also, a bit of an unrelated question: can Succs and ROC be administered IO? Situation came up a couple years ago on a job for a Pt. with Dx of DKA; family had watched her "sleep" on couch for 3 days before trying to awaken her (she was unconscious but WITH gag reflex). Respiratory rate was something like 6-8 and she was in a sinus tach if I remember correctly. Peripheral IV access was unattainable so we went for IO. When it came to RSI, we were unsure if we could push the Succs through the IO; called up the doc and he also was unsure. Eneded up tubing her with just sedation and no Succs. Has anybody had any situation where they were able to successfully push the Succs IO?
 
Was a tox screen done? Also, a bit of an unrelated question: can Succs and ROC be administered IO? Situation came up a couple years ago on a job for a Pt. with Dx of DKA; family had watched her "sleep" on couch for 3 days before trying to awaken her (she was unconscious but WITH gag reflex). Respiratory rate was something like 6-8 and she was in a sinus tach if I remember correctly. Peripheral IV access was unattainable so we went for IO. When it came to RSI, we were unsure if we could push the Succs through the IO; called up the doc and he also was unsure. Eneded up tubing her with just sedation and no Succs. Has anybody had any situation where they were able to successfully push the Succs IO?

If I remember the marketing literature for the EZIO correctly, one of the case studies was a flight crew using an IO for RSI in this way. Never did it myself so can't give you first-hand knowledge.

The only IV medication I've heard of that shouldn't be given IO is hypertonic saline, because it can cause cell death in the bone marrow. Dr. Jeff Guy mentions this in one of his critical care podcasts discussing IO's... link to the abstract of the (2002) paper that found this:
http://journals.lww.com/jtrauma/Abs...c_Saline__Intraosseous_Infusion_Causes.6.aspx

Is anyone aware of more recent research?
 
Tox screen was negative as above.

You can give virtually any medication including blood products through IO access. Of the recent RSI's I have done in the HEMS environment, one was an RSI through the sternal FAST and one was a crash airway that required sux through a FAST. (Not a true RSI.) In both cases, IO delivery was effective.

I am not aware of HTS being a contraindication. Typically, I do not give anything beyond 3%. The study states 7.5% was utilised. I have never used HTS in the transport environment by the IO route.
 
Hopefuly IO would be unnecessary. If you're in an ER and really need additional access the ER doc could place a central line before transport. I know that sometimes they are reluctant but then it sometimes helps to explain that IO is your option to motivate them. Knowing that the patient could wind up with osteomyelitis because they didn't place a line for a forseeable problem enroute should make them think. Remember that they are certifying on their COBRA form that the benefits of transfer outweigh the risks. They are obligated to stabilize the patient sufficiently within their capabilities to make that true.

It might help frame this discussion if we knew what type of ER the transferring place is. A glorified urgent care with a non-EM doc who hasn't put in a central line or treated a DKA in 20 years and is hiding in the bathroom until you take the patient away is a different story than a real ED with an EP.
 
The typical ER's we deal with are smaller and have non-EM physicians; however, the care delivered can vary. So, it's not always a bad situation. I took liberties with this scenario and the patient and labs were totally manufactured. The real scenarios that this was based upon had patients who were already intubated. I wanted to add a few more concepts for EMS providers to think about. (Labs, respiratory distress with a "good" ABG, and management post intubation) Hope that clears up any confusion.
 
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