Someone post a case or something, please. I don't have any good ones.

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luxatio erecta, hyperabduction? honestly have forgotten the classic mechanism. reduction is two step vs just yanking on it (in-line).

had a decent one this week, this is more for medical students, residents:

0400 on a weekday night:

EMS calls in: ~40 y/o M intoxicated, found in the back of his car with an empty handle of vodka. Hx ETOH, DM, BG 250 en route.

Pt arrives with a GCS of ~12, with a strong odor of EtOH, only VS abnormality is a RR of 28.

Police officer is present and says, "Just let me know when you've medically cleared him so I can take him to jail."

I do a pretty vigorous sternal rub and he opens his eyes and slurs his name and birthday. Seems a little too intoxicated to just DC to jail, even though it is very tempting because I'm single coverage and there's an impressive uvulitis, a GI bleeder, a 60 y/o CP, and a 60 y/o mildly hypoxic COPDer who all decided to check in at the same time.

First orders are IVF, thiamine, CMP, Mg, EtOH lvl, and venous pH on a hunch.

pH is an istat and comes back first : 6.6

The CMP took ~30 minutes to result and by that time many decisions in management were made based on VS, exam and pH so I'm not going to give it yet. Accucheck was ~275

What is the likely diagnosis? How does the Emergent management of the two possible diagnoses differ?

How do you correct his acid base status? What do you replace even though the lab may be normal?

How do you minimize peri-procedural complications that are likely to occur if the patient is intubated?
 
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***Let the students and junior rezzies answer first, please***

Single coverage = admit to ICU, next patient.

Sorry, you did said let the med studs and interns play....
 
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Single coverage = admit to ICU, next patient.

Sorry, you did said let the med studs and interns play....

I said residents. Also, the patient has not yet been stabilized and a direct admit to the ICU (where hospitalists cover w/ CC consults) would likely result in a rapid response = bad press for yours truly.

Also, I'm at a single coverage community ED, no ICU. I am the only MD in the hospital overnight (although this will soon change as the hospital expands.) If I wanted to be a chicken-$hit I would give him IVF, NRB, pray, call emergent transport to the tertiary ED (wait 30 min for EMS, 10 minute transfer time) but then the patient just gets stabilized by one of my partners downtown who then call me out on it later.
 
Alcoholic ketoacidosis.

Lactic acidosis could be caused by MI, PE, metformin, positional asphyxiation, aspiration, ethanol.

Ethylene glycol ingestion also on list.

Without ABG could get etco2 quicker might help? What were other labs from the VBG? EKG for MI and could possibly indicate further PE workup. Any other physical exam or chart findings like DVT, hx of PE? Any physical exam findings besides RR consistent with sepsis?

With relatively stable VS and GCS of 12 I think I might consider adding insulin and potassium to what he is getting and wait on other labs. His elevated RR should be compensating some for his acidosis?
 
Toxic alcOhio, methanol vs ethylene.


Fomepizole, bicarbonate, check an ecg and potentially give calcium empirically. Call nephrology. Hyperventilate
 
What is the most likely outcome if nothing is done aside from letting him sober up and nature take its course?
 
Toxic alcOhio, methanol vs ethylene.


Fomepizole, bicarbonate, check an ecg and potentially give calcium empirically. Call nephrology. Hyperventilate

Less likely toxic alcohol. History cw ethanol usage, (ethanol came back 250). Fomepizole not in ED pyxis, pharmacy not available at 0400. Methanol/ethylene levels are send outs and take ~3 hours to come back. Why calcium? Narrow complex NSR on cardiac monitor, EKG w/o acute changes. Ca normal on CMP, Cr was 2.4 but emergently this patient does not need dialysis.

What is the most likely outcome if nothing is done aside from letting him sober up and nature take its course?

Impending death.

A pH of 6.6 is generally not compatible with life. FWIW the patient deteriorated.
 
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With life threatening acidosis, would you not administer insulin?

http://www.ncbi.nlm.nih.gov/pubmed/6828000

Yes.

Despite a history more consistent with alcoholic ketoacidosis than DKA, based on a ph of 6.6 and BG of 275 I ordered 1L NS, followed by an insulin drip at 0.1u/kg with D5/0.5NS w/ 20 meq K at 250/hr along with a bunch more labs/ekg/cxr/hct/bloodcx/empriricabx/etc.

K was 3.6 but needed replacement with ongoing resuscitation due to metabolic acidosis.

I then informed staff that the patient was critically ill, had him transferred to a resuscitation room, took 15 sec to read the EKG and review pmh and put in some generic cardiac orders for the 60 y/o w/ CP, reviewed the GI bleeders chart, gave the original patient a shot at avoiding intubation due to inherent risks of that procedure (some would have intubated him on the spot), and went to see the swollen uvula patient and the COPDer.
 
Toxic alcOhio, methanol vs ethylene.


Fomepizole, bicarbonate, check an ecg and potentially give calcium empirically. Call nephrology. Hyperventilate
Where? To accept the transfer? Where I am, where I am the only doc in the hospital from 5pm to 6am, there isn't a renal doc in 75 miles in any direction. I have exactly zero medical subspecialists on staff. However, ironically, one of my two surgeons is colorectal fellowship trained, and my ortho guy is fellowship-trained hand surgery. He's only on-call from M-F, and only in town from 10am Monday to approx 1pm Friday.

Whoever said it, it's right - this is where the rubber meets the road.
 
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Pretty impressive ph for aka. Pco2 bicarb, anion gap, ua with microscopic. Intubate no doubt... Transfer


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Bicarb was 3, + AG, UA shows ketones, glucose. BG on CMP 325.

Likely AKA +/- DKA w/ ETOH intox.

Guy was surprisingly able to say his name/date on initial eval, but was obviously altered. Smelled of EtOH along with ketones. After moving him to the resus room on reeval he was a little less tachypneic and a little more altered, so he was intubated.

Primary concern intubating these people is ventilatory failure during peri-intubation dropping their pH even further causing dysrhythmias and death. This guy was maybe 6' 250lbs but otherwise his airway anatomy looked OK. You can put these people on NIV/hyperventilate while setting up for intubation but in this case we just did everything at once; essentially the moment he went apneic post sux he was tubed. Did have some s.tach in 160s post intubation which resolved after a few minutes. vent settings RR 25 tv 700 10/5 etc, gas rechecked etc. I'm sure there is a more optimal vent setting but in this case he improved with treatment and was transferred directly to ICU..

Next case?
 
Intern question coming up...

So what's the deal with intubating people with this low of a pH? I'm assuming it's one of those things where if you have to do it, you do it, but even the transient apnea from RSI could cause the pH to fall even further, precipitating a cardiac arrest.

Do you give bicarbonate first? Do you just say f*&# it and intubate? Do you attempt a crash airway without meds?

Rather than google I figured I would ask you fine folks
 
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Alcoholic ketoacidosis.

Lactic acidosis could be caused by MI, PE, metformin, positional asphyxiation, aspiration, ethanol.

Ethylene glycol ingestion also on list.

Without ABG could get etco2 quicker might help? What were other labs from the VBG? EKG for MI and could possibly indicate further PE workup. Any other physical exam or chart findings like DVT, hx of PE? Any physical exam findings besides RR consistent with sepsis?

With relatively stable VS and GCS of 12 I think I might consider adding insulin and potassium to what he is getting and wait on other labs. His elevated RR should be compensating some for his acidosis?

Correct me if I'm wrong, but hasn't this been shown to be false? I thought I heard something about this recently...
 
I said residents. Also, the patient has not yet been stabilized and a direct admit to the ICU (where hospitalists cover w/ CC consults) would likely result in a rapid response = bad press for yours truly.

Also, I'm at a single coverage community ED, no ICU. I am the only MD in the hospital overnight (although this will soon change as the hospital expands.) If I wanted to be a chicken-$hit I would give him IVF, NRB, pray, call emergent transport to the tertiary ED (wait 30 min for EMS, 10 minute transfer time) but then the patient just gets stabilized by one of my partners downtown who then call me out on it later.

I was kidding. Sarcasm doesn't always come across.
 
Bicarb was 3, + AG, UA shows ketones, glucose. BG on CMP 325.

Likely AKA +/- DKA w/ ETOH intox.

Guy was surprisingly able to say his name/date on initial eval, but was obviously altered. Smelled of EtOH along with ketones. After moving him to the resus room on reeval he was a little less tachypneic and a little more altered, so he was intubated.

Primary concern intubating these people is ventilatory failure during peri-intubation dropping their pH even further causing dysrhythmias and death. This guy was maybe 6' 250lbs but otherwise his airway anatomy looked OK. You can put these people on NIV/hyperventilate while setting up for intubation but in this case we just did everything at once; essentially the moment he went apneic post sux he was tubed. Did have some s.tach in 160s post intubation which resolved after a few minutes. vent settings RR 25 tv 700 10/5 etc, gas rechecked etc. I'm sure there is a more optimal vent setting but in this case he improved with treatment and was transferred directly to ICU..

Next case?
Any chance you sent an ASA level on this guy and know what the result was?

HH
 
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Correct me if I'm wrong, but hasn't this been shown to be false? I thought I heard something about this recently...
It's not false, just not fully understood and likely multifactorial.

The biguanides are well known for hyperlactatemia, and is why phenformin was pulled. Metformin, at normal renal function with normal dosing has little effect on [lactate] which is why it's still on market.

That said, we know little of the true toxicokinetics of MALA, other than associations with renal insufficiency & the like... but it's truly a chicken/egg problem.

As there are multiple case reports of MALA in isolated overdose, I'd argue it's a real entity we just don't fully understand.

-d

PS - @Hamhock I was wondering the same thing about ASA. d=)

Semper Brunneis Pallium
 
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Less likely toxic alcohol. History cw ethanol usage, (ethanol came back 250). Fomepizole not in ED pyxis, pharmacy not available at 0400. Methanol/ethylene levels are send outs and take ~3 hours to come back. Why calcium? Narrow complex NSR on cardiac monitor, EKG w/o acute changes. Ca normal on CMP, Cr was 2.4 but emergently this patient does not need dialysis.



Impending death.

A pH of 6.6 is generally not compatible with life. FWIW the patient deteriorated.



Dialysis to help with the pH. Indications include pH less than 7.25 in a toxic alcohol, and calcium empirically because they often become hypocalcemic as calcium oxalate crystals form.

I know you said it wasn't a toxic alcohol but just supporting my reasoning.


Why would it be aka? It's not like he stopped drinking, plus I Never see severe acidosis with aka.
 
Intern question coming up...

So what's the deal with intubating people with this low of a pH? I'm assuming it's one of those things where if you have to do it, you do it, but even the transient apnea from RSI could cause the pH to fall even further, precipitating a cardiac arrest.

Do you give bicarbonate first? Do you just say f*&# it and intubate? Do you attempt a crash airway without meds?

Rather than google I figured I would ask you fine folks
Patients like this are compensating as best they can with massive minute ventilation. When you turn off their breathing, bad things can happen.

I would give a couple amps of bicarb peri-intubation in the hope that it would ever so transiently help.

I guess you could consider an awake Intubation with a scope, but they're probably going to need some type of medication (ketamine) for it. The respiratory drive will probably be preserved during this, but I don't want to be stuck with a scope in front of an upright patient as their drive drops and now I need to drop them, push paralytic, move to the head, etc.

Better to just stick with old, reliable RSI, then bag with some enthusiasm while someone dials in high minute ventilation settings.
 
I then informed staff that the patient was critically ill.

I love this part.

"Hey, team...you know the patient whose EtOH level you're all taking bets on? Mmmm yeah, he's about to die, so can we maybe get him a room?"

Response: [collective eye roll]
 
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I was kidding. Sarcasm doesn't always come across.

Haha, yeah that makes more sense.

Any chance you sent an ASA level on this guy and know what the result was?

HH

I did send an ASA and it was negative.

Dialysis to help with the pH. Indications include pH less than 7.25 in a toxic alcohol, and calcium empirically because they often become hypocalcemic as calcium oxalate crystals form.

I know you said it wasn't a toxic alcohol but just supporting my reasoning.


Why would it be aka? It's not like he stopped drinking, plus I Never see severe acidosis with aka.

Good ideas. FWIW the patient did go on dialysis about 24 hrs afterwards, for failure to improve pH and worsened Cr. Probably institution specific, in my hospital system nephrology does not admit new renal failure or accept transfers, so hospitalist/medicine accepts and immediately consults, etc.

My reasoning for aka along with dka and shock would be: hx of alcoholism, found next to those plastic bottles of vodka that people who consume nothing but alcohol are fond of buying, vomit on clothes and dry membranes indicating dehydration, strong smell of ketones on exam, BG relatively low for DKA, ketones in UA. Ended up having beta hydroxybuterate in his urine (which can also happen in DKA).

Also his lactate was 20 which probably greatly contributed to his low pH. So he probably went on a long binger, didn't control his DM, didn't eat anything, kept drinking, went into shock causing hypoperfusion and worsened acidosis. His acidosis was not caused entirely by AKA but a combination of metabolic acidoses..

I did give 2 amps of bicarp prior to intubation and despite our efforts to match his MV he still initially got more acidotic on the vent.

I love this part.

"Hey, team...you know the patient whose EtOH level you're all taking bets on? Mmmm yeah, he's about to die, so can we maybe get him a room?"

Response: [collective eye roll]

Very funny because this is exactly how it happened. I guessed EtOH of 450 and was wrong.. the exact quote from the RN (after the eye-roll) was, "Why do you keep adding orders to this guy?".
 
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Very funny because this is exactly how it happened. I guessed EtOH of 450 and was wrong.. the exact quote from the RN (after the eye-roll) was, "Why do you keep adding orders to this guy?".

Piecemealing orders? Bad Doctor! BAD DOCTOR!

This case points out that tachypnea is almost always important to note... sometimes its just "anxiety" but RR = 26 means the patient is sick, and you better figure it out and fast. Similar to real diaphoresis... almost always something going on...
 
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I love this part.

"Hey, team...you know the patient whose EtOH level you're all taking bets on? Mmmm yeah, he's about to die, so can we maybe get him a room?"

Response: [collective eye roll]
been there. people look at you like youre mentally challeneged. then ****bhits the fan and then they get it.

Sent from my VS986 using Tapatalk
 
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