Why I love rural EM

[EMEDPA]

not a lot of pcp here. saw a lot in philly but not much on the west coast.

best pcp o.d. ever was at a pink floyd concert I was doing a standby at. guy had it in some kind of oil form and wiped it all over his body and began seizing. intubated after acute resp. failure.

[medic25]

not a lot of pcp here. saw a lot in philly but not much on the west coast.

best pcp o.d. ever was at a pink floyd concert I was doing a standby at. guy had it in some kind of oil form and wiped it all over his body and began seizing. intubated after acute resp. failure.

 

On the bright side, we don't see any meth in this part of the country!  The nice thing about PCP is that you can sometimes make the diagnosis before the patient rolls through the ambulance door.  If the chief complaint is "found running naked down Whalley Avenue through traffic" and it's 10 degrees outside in January, you can pretty much guarantee they've been smoking some illy!

[EMEDPA]

I see multiple meth addicts/day and not just teens/20s but folks up to 60. my 2 icu admissions last shift both over 55 and both freebase meth. one with a hx of bad copd and the other with poorly controlled afib.

[primadonna22274]

I was worried about seizing too--grateful she didn't (at least not on my watch). Thanks for the info about the PCP. I'm also a bit (just a bit) skeptical about the cocaine but haven't researched cross-reactivity with other drugs. Wonder if that much tramadol could do it.

Also, we did not believe this was an intentional OD--just a case of an uninformed patient with a long history of rx drug dependence being switched to tramadol, which she may have thought harmless, and in her usual fashion she took more than prescribed.

[skyblu]

Our urine drug assay does not test for PCP, so I am not sure if I've seen it. The only "classic" PCP-type patient I had ended up being bath salts. He was cuh-razy! The drugs of choice in my area are crack and heroin, plus a gazillion rx opiate abusers.

 

I've never sen a tramadol OD, how interesting. And how very, very interesting that people get on Suboxone to get off it! Does that even work?

 

I may have missed this info, but primadonna, do we know how much tramadol it took to OD on it?

 

I've never used romazicon for benzo OD. I've intubated a few, but mostly they maintain their airway and we just approach with supportive care. I'd use it, as someone else said, to reverse a benzo I (or EMS) had given, but otherwise, I don't want to kick someone into hard benzo withdrawal.

 

What substances do your urine tox panels test for? Ours is: cocaine, amphetamines, benzos, cannabinoids, opiates, and barbiturates. Everything else is a serum fox that gets sent out to the state lab, so useless in the ED.

[primadonna22274]

She had a new bottle filled the day before (after her 2pm appt per her brother) of #60, 50 mg tabs. There were 27 remaining in the bottle. She came in about 10am the next day. Doing the math that's 1,650 mg tramadol in less than 20 hr (and probably less than that if she more likely got the script about 4pm). 400 mg/day max (epocrates), so she had more than 4x that.

[EMEDPA]

I see. I know he's in good hands with you E. This may be his easy exit, you know? Comfort care is always appropriate.

actually doing better this am. off bipap. on o2  nc at 4l with nl resp. rate now.

[EMEDPA]

What substances do your urine tox panels test for? Ours is: cocaine, amphetamines, benzos, cannabinoids, opiates, and barbiturates. Everything else is a serum fox that gets sent out to the state lab, so useless in the ED.

we also get TCAs.

[skyblu]

Cool, I wish we got TCA's! 

[EMEDPA]

another cool rural case:

50 yr old nonsmoking male brought in by ems for syncope.

hx of migraine only. awoke with typical h/a this am and then passed out. spouse called 911. noted by spouse and ems to have mild facial droop and slurred speech. cbg nl in field. neg trauma exam per medics.

by arrival @ ed facial droop has resolved, word finding difficulty present but resolved within minutes of arrival. straight to ct.

VS and exam nl

standard labs nl(cbc, cmp, coags, tsh, ua).

head ct ? old lacunar infarcts, nothing acute

ekg: afib at 95, presumably new

b/l carotid u/s neg

 

so atypical migraine with incidental afib or new afib with TIA? MRI with contrast being done now. echo pending. anticoagulated.  I love cases like this that require some thought. great opportunities to learn.

[GetMeOuttaThisMess]

ETOH hx. (ETOH->CM->AFib) or known pulm. hx.? My brother, 50 y/o w/ hx of hypothyroidism, recently found on annual exam to have asx AF w/o other known risk factors. Successful CV following TEE.

[EMEDPA]

_{Wine daily. not in excess. nl tsh. nonsmoker, no pulmonary dz}

[GetMeOuttaThisMess]

As you already know, treat worst case scenario. Needs anticoagulation, echo (preferably TEE), cardioversion, which the first two have been accomplished, at least a transthoracic echo. Now here's the million dollar question. Does the patient need admission? Pt. has already had primary w/u, both acute and non-acute and sx have resolved, at least the presumed TIA (remember new folks, migraines can have focal neuro sx as well which resolve). Risk of CVA greatest over next week but with anti-coagulation the risk of event is same regardless of of in/out pt. Time to access stroke center from his residential location in the low risk event he has the CVA (TIA's now considered CVA's for us old schoolers)? The other consideration is if it was an embolic event and the echo is negative, do you quit looking for sources?

[EMEDPA]

mri unremarkable. admitted for further workup of afib with echo pending.

[MedicinePower]

same shift. next pt: 87 yrs old with chest pain via ems. chronic afib now @ 150. on dialysis. dialyzed today. pain 4/10. bp 110/p. no ready IV access ( L arm fx in cast, R arm has shunt and edematous, both legs edematous). pt really in nad so hesitated to IO. not sick enough for cardioversion. thought about PE workup but can't give IV contrast and can't get VQ scan here. will let accepting hospitalist at transfer facility r/o that ddx.

tiny 22 g IV started R hand, minimal blood drawn from IV, lab tech attempts x 2 for a bit more blood. Trop #1 surprisingly <.02 even with renal failure on dialysis. given fentanyl 25 mcg and metoprolol 5 mg iv x 2. rate controlled to 110, pain free. transfered as we have no dialysis capability and pt needs second set of enzymes, etc.

at same time relatively spry 85 yr old with gastroenteritis and n/v/d x 4 days. k=2.8, bun 30, cr 1.6. tuned up and admitted.

have only seen 7 pts so far in 13 hrs but admitted 1 to icu, 1 to tele, and transfered 1. 11 hrs to go. hope to get some sleep.

 

Any idea what her Mg++ and K+ levels were? I know a-fib patients can become unstable with just minor drops in their magnesium and potassium levels.

[GetMeOuttaThisMess]

Getting back to Mr. 50 y/o for a moment, what would be the justification for admission for those naysayers who would bring up the point that I mentioned earlier which was do you admit (common sense says yes but literature shows that a traditional "TIA" w/o evidence of bleed on imaging can be evaluated OP just as effectively while initiating/maintaining anti-coagulation since risk of frank CVA is same regardless of where patient is located which is why I brought up the question of how far from a stroke center is pt. located)?  It would be a hard sale to a pt./family but from a medical/cost perspective I can see the point of those who would argue that they can be discharged and followed up the next day or so as an OP.  I'm not arguing for or against, I just find the question interesting.

[EMEDPA]

Any idea what her Mg++ and K+ levels were? I know a-fib patients can become unstable with just minor drops in their magnesium and potassium levels.

they were both fine.

[EMEDPA]

Getting back to Mr. 50 y/o for a moment, what would be the justification for admission for those naysayers who would bring up the point that I mentioned earlier which was do you admit (common sense says yes but literature shows that a traditional "TIA" w/o evidence of bleed on imaging can be evaluated OP just as effectively while initiating/maintaining anti-coagulation since risk of frank CVA is same regardless of where patient is located which is why I brought up the question of how far from a stroke center is pt. located)?  It would be a hard sale to a pt./family but from a medical/cost perspective I can see the point of those who would argue that they can be discharged and followed up the next day or so as an OP.  I'm not arguing for or against, I just find the question interesting.

5% of folks who have suffered a TIA will go on to have a stroke in the next 24-48 hrs if not appropriately risk stratified and anticoagulated if I am remembering correctly.

this facility is a 2 hr drive to nearest stroke ctr or 30 min by air.

[MedicinePower]

they were both fine.

I learned by shadowing UGoLong that Mg++ and K+ levels even slightly low might allow for A-Fib. Mag really needs to be 2.0 and Potassium at 4. The "normal" reference range may still allow for A-fib if it is on the low side.

[skyblu]

The 50 yo with neuro sxs: I would admit, at least for observation. He has a history of migraines, and the headache was typical but the neuro sxs were not, correct? I don't feel qualified to say for sure his sxs were just a new manifestation of his old migraines, so I would admit to obs, neuro consult, serial exams.

[EMEDPA]

The 50 yo with neuro sxs: I would admit, at least for observation. He has a history of migraines, and the headache was typical but the neuro sxs were not, correct? I don't feel qualified to say for sure his sxs were just a new manifestation of his old migraines, so I would admit to obs, neuro consult, serial exams.

yup, done. I'm still not convinced it wasn't a TIA but the stroke team neuro guy seems to be...

[True Anomaly]

Okay, here's an interesting case I had the other day- I wasn't exactly in a rural setting, but it wasn't our main inner-city hospital setting.

 

32 y/o female came in from outpatient testing for palpitations and nausea/vomiting. She was getting set up in a room that I had my back to, but I look up at the tele monitor when she was put on it and it was going at about 150, so I head over to the room. Monitor appeared very regular and narrow-complex, and the EKG confirmed it- SVT. I asked her if she had a history of the same- she said yes, many times before, and she had had adenosine before which would break it. After vagal maneuver didn't work, the first 6 mg adenosine was given without any slowdown. 1st dose of 12- slowed down into the 70's with definite P waves, but immediately returned to 140's. 2nd 12 mg did the same. She still had normal BP and was awake and alert. During this time when we're pulling adenosine, I notice the port in her R chest wall- she states that she has a rare disorder called "Gitelman's Syndrome" and she self-infuses potassium nightly through the port. I also notice that now her HR isn't as high as before- now it's between 110-130, which some discernable P waves- so, no longer in SVT, but something isn't right.

 

So I grab the doc I'm working with that day, explain the situation and show the EKG's- we decide to call cardiology to bedside. When the cardiologist comes down, as soon as I say the word "Gitelman's", she immediately knows who the patient is, looks at the EKGs and tells me "This is her baseline- send her home. She doesn't need to be admitted". Whoa.

 

So if you've read this far, and had googled "Gitelman's" by now and briefly read it, you know it's a kidney-based disorder- and of course, she has a nephrologist who is quite familiar with her. Her nephrologist was thankfully in the hospital and came to bedside- she explained that the pt ALWAYS has tachycardia to some degree, frequently mimicking SVT but it isn't, and nausea/vomiting is common for her. She was at her baseline per the nephrologist too. Since Gitelman's is a defect of distal tubule transport cells causing salt wasting and subsequently chronic low electrolytes, it turns out the patient takes UPWARDS OF 200 MEQ OF POTASSIUM DAILY. She runs an IV infusion of K riders all night- 10 mEq an hour, all night, plus the additional PO she takes during the day. Her K runs an average of 2.0. Its damn incredible.

 

She did fine- thankfully, we all took a step back before the ED doc wanted to do amiodarone for her dysrhythmia and just called cardiology first- what stopped us is her HR had slowed down to a level where SVT was unlikely.

 

Cool case!

[primadonna22274]

And now you know about Gitelman's!

:)

We had a lady on my OB rotation with this disorder. G6P5...and despite everybody else's anxiety about her chronic K+ of 2.7 she was well-acclimated to it. Still kinda freaked me out lol

[GetMeOuttaThisMess]

Here's a question from "Bevo" to "Reveille" (he'll know).  If this is her "norm", what was different to warrant her coming to the ED?  These types of cases always drive me nuts when specialists "assume" that this is the norm.  Case in point was a patient decades ago who went in/out of stable VT....until the last case when it wasn't quite so stable and the patient died.

 

skyblu, put down the Mai-tai that you're having on the beach at Hanalei Bay on Kauai (same beach as the G. Clooney movie "The Descendants") and ponder what would you being doing for the TIA male that you just put in as opposed to sending him home, ASSUMING that the working diagnosis of TIA is correct?  Just raising that all important  "are we getting our bang for our buck" question.  This presumes that the echo came back clean, that you have the individual with an appropriate INR, and the individual/family have been instructed to return at the sign of any recurrent symptoms with a reasonable time to presentation, which is why I asked EMEDPA how far away they were and the distance to the stroke center (During the summer I saw a female who had been diagnosed with a "TIA" and had been evaluated by the neurologist and given these instructions as above.  She had recurrent sx.'s, presented to a level I trauma center/ED in a large metro area, and was promptly put in "timeout" in the waiting room for several hours.  I know this because I was renewing a certification and was playing the role of lowly triage person and heard her CC.  No one ever assessed her neuro status until she was brought back to an exam area hours later.).  I'm just raising the question that so many others are now of why do we do some of the things that we've done for ages (classic example are pre-op evaluations when in only a minuscule number of instances does it impact the impending surgery per studies looked at by others)?

 

OK, you two can resume your "Gig 'em" cheers (I'm still disowning a nephew in the band) and Mai-tai, though skyblu, I'm a little concerned about you since it is 7:50 a.m. their local time.  BTW, can you order me one as well?  They taste much better with fresh, local pineapple wedges.

[True Anomaly]

Here's a question from "Bevo" to "Reveille" (he'll know).  If this is her "norm", what was different to warrant her coming to the ED?  These types of cases always drive me nuts when specialists "assume" that this is the norm.  Case in point was a patient decades ago who went in/out of stable VT....until the last case when it wasn't quite so stable and the patient died.

She underwent some outpatient testing for her parathyroid that morning as ordered by the nephrologist referenced earlier- started becoming symptomatic from her tachycardia. The nephrologist said that this will happen with slight stresses to her system- whether viral illnesses, testing or the like. The cardiologist had seen her multiple times at a neighboring facility, so they both were quite familiar with her course of illness. Believe me, it all stunned us who weren't familiar with her- we ended up admitting her overnight, as the nephrologist thought she looked "a little less than punky" and wanted cultures done on her because, oh by the way, her WBCs were 28K. Regardless, there was little chance I or my attending were going to send her home directly from the ED. By the time she went upstairs, her HR was in the 110's, she was still awake and alert, no longer vomiting and still had a non-focal abd exam and was afebrile.

 

I hear you- specialists can be a little too cavalier with their recommendations. Case in point- 32 year old IVDA woman who had a hot, swollen R knee that she couldn't walk on came in at night to one of our satellite facilities- obvious, right? Only problem was she had a nasty looking abscess overlying the knee joint that was hot and swollen all around too. I call ortho- he asked why I didn't tap it. I explain why I'm not going through the hugely obvious abcess overlying the joint. He tries to tell me that "ER literature allows for arthrocentesis through cellulitis/abscess". I said, "Uh, no, we're not doing that. You need to come in. Period." Just to make sure I wasn't missing something obvious as a change in practice patterns in the ER, I grabbed Roberts and Hedges and scanned the arthrocentesis chapter- of course it confirmed what we thought (I didn't even realize that chapter was written by the director of that particular ER). Ortho did come in- did the joint aspiration anyway (it was negative for gram stain or WBCs), but I&D'd the abscess at bedside- it was so large and nasty, he ended up transferring the patient down to our main campus so she could go to the OR for washout.

 

PS- Now that we're no longer in the same conference, I hope you have a "Strong" showing this coming year :)