I had an interesting case the other day – and one that I thought would make for a good medical quiz.
58 y/o male with history of HTN, DM and High cholesterol who came in with progressive SOB since the night before. In the morning it was severe and accompanied by chest tightness. He admits to drinking heavy ETOH the evening before at a BBQ but denies regular heavy drinking.
He called EMS due to severe SOB and chest pain – he was found tachypnoeic (RR 30) with b/l lower lung field rales. He had +1 peripheral edema and was quite tachycardic. EKG showed sinus tach with no acute ST changes. He was normotenisve. They gave him a SL NTG with no improvement and put him on 100% NRB since his pulse ox was 90% on RA.
When he came to me, he remained tachypoeic and tachycardic but was afebrile and satting 100% on the NRB. He had b/l rales and JVD at 6o degrees and was in moderate distress. His BP was 123/86
I gave him 60mg of Lasix and he started to diurese but still felt terrible and his HR and RR did not improve. His CXR showed mild cardiomegaly and very mild vascular congestion and no focal infiltrate.
His WBC was 15, His chemistries were significant for slightly elevated BUN and CR, Sodium of 130, and a HCO3- of 8. His cardiac enzymes were normal as was his urinalysis. His LFT’s were nonspecifically slightly elevated.
What do you order next? What treatment do you institute? What is your differential?
Ask me some questions in the comments section and I will provide what I knew during his three hours in the ER.
Answer tomorrow.
DD: pulmonary embolus, ARDS, aspiration, pneumonia, pericarditis, Mallory-Weis (Boerhaave) – perhaps still MI (despite normal enzymes and no response on nitro).
Next:
* Any vomiting after the binge drinking? (aspiration, Marrolry-Weis, Boerhaave)
* Any prior leg pain, discolouration? (embolus)
* Previous deep vein thrombosis or pulmonary embolism
* Any known thrombophilia, antithrombin deficiency, protein C or S deficiency, factor V Leiden, etc.?
* Lab: LDH, D-dimer, V/Q-scan, CT-chest (embolus)
Treatment:
LMWH, oral anticoagulants (for long term use)
Considering streptokinase
Note: medical student on holiday with hangover after lost World Cup final ;)
PE vs. Boerhaave’s syndrome vs. aspiration PNA
Workup: D-dimer, or straight to CTA if he has hx making him high risk. Chest CT to rule out boerhaave’s. Troponins and CKMB because everyone in the ED seems to get those.
Anyone want to explain the gap acidosis and the hyponatremia? (oooo– electrolytes are HARD!)
Hyponatremia could be from thiazide use, beer potomania, or just dehydration (sweating and/ or vomiting) with volume replacement with hypotonic fluids.
Gap acidosis is pretty easy– barring a history of other toxin ingestions I’ll take ketones or lactate:
alcoholic ketoacidosis (tachycardia– even if it’s just SVT– can be a cause of CHF; acidosis causes decreased inotropy and tachycardia not to mention the increased WOB from the tachypnea as a response to the acidosis). DKA is unlikely as this is probably a type 2 diabetic but is not impossible.
Lactic acidosis from another cause– everyone’s pointing at boerhaaves but likely ruled out by CXR; pancreatitis also unlikely given normal LFT’s and chest pain rather than abdominal pain.
Less likely is lactic acidosis from the metformin they’re handing out to all the diabetics these days– decreased renal function from dehydration could be a precipitant; tachycardia, CHF and tachypnea from the same mechanism.
Blood for lactate, urine and blood for ketones (esp.hydroxybutyrate); rule out other toxins associated with gap acidosis by history and labwork as necessary.
dextrose (with thiamine) +/- insulin for AKA (follow blood glucose, gap acidosis, and ketones)
My first thought is congestive heart failure (left sided). Is the hyponatremia seen after the lasix administration, or was it noted before?
Testing – repeat the chemistries and cardiac enzymes. Repeat the 12-lead EKG to r/o MI that is possibly progressing. V/Q scan to r/o PE.
Prophylactic tx for MI with ASA. Small dose of morphine IV to help with pulmonary edema (reduction of preload).
What medications does he take for HTN, DM, and hyperlipidemia? What are his normal glucose readings? Probably do hourly glucose checks while in the ER, and potentially start an insulin drip if indicated.
Differential dx: CHF vs MI vs PE
And remember, I’m the L&D nurse. So I may be way off on this. Cardiac drugs are NOT my specialty!
Intern weighing in:
Overall picture is CHF exacerbation in a DMII patient after a single day of binge drinking (yeah right) and eating cookout food. High gap met acidosis is probably due to a mix of his sugar being elevated and alcoholic ketosis. Sodium is going to be falsely low in someone with a super high sugar anyway, so we’ll have to get the fingerstick and correct it. Leukocytosis is acute phase reactant and probably non-specific. Elevated BUN/Cr probably already elevated due to his DMII. DMII means atypical presentations of everything. JVD at 60 and tachycardia/tachypnea- could be CHF, CXR cardiomegally could be due to CHF but could also be a rapidly accumulated tamponade. Transaminitis with the gap acidosis gets me a little worried for toxic alcohols, salicylates. As above- if he’s on metforamin the lactic acidosis.
Further history ?: Did he use a ton of bengay or attempt to kill himself with anything, drink moonshine at the bbq (even though you’re in the northeast)? What meds is he on…did he take them?
Physical exam ?s: crepitus of neck/chest? Clonus? radial pulses equal b/l?
Ddx: five I’s of hyperglycemia (Ischemia, intoxication, infection, iatrogenic and idiot forgot his insulin). ACS looks unlikely at this point with negative TnI 24 hours into it, PE, tamponade first before going onto other diagnoses. Another cause of hyponatremia not mentioned by mir is SIADH which has a billion causes including his probable psych meds…or maybe he has a tumor.
Workup: bedside echo would be my next step (gives you EF, volume status, tamponade, aorta and volume status if you can peek at the IVC), continue the ACS rule-out (repeat trops and CK/CK-MB, posterior lead EKG as well), CTA chest PE protocol (d-dimer will be worthless at this point), lactate, blood Cx, salicylate level, urine OSM from the pre-lasix sample if available, urine microscopy for oxalate crystals.
Treatment: ntg, morphine, and supportive treatment until diagnostics arrive.
If this ends up being gastrointestinal, I’m going to be really disappointed.
OK, well after about 20 minutes of me seeing him, and just as the first blood tests came back, the RN told me his BP was 80/50. I ordered some fluids and then ordered a serum Osm, a lactate level, and ETOH level, and an acetone level. I also did an ABG.
The results were
Osm 330 (normal up to 300), ETOH 52, Acetone negative, and Lactate 15.8! ABG showed a Ph of 7.1 and a PO2 of 70. PCO2 (I think) was about 30.
The CXR was also officially read as negative.
Now what do you do?
Can we have, as a first piece of information, the lactate and the results of the bedside ultrasound; ie, is there tamponade/effusion, or signs of RV dilitation/PE?
I just gave you the lactate, 15.8. The only sign of RV dilation was JVD. I did not do an US at this point.
What were his home meds?? Because of the DM dx I’m leaning toward Metformin-induced lactic acidosis brought on by a day of binge drinking. I would keep the supportive care & hydrate him. Keep an eye on the kidney function. Refer to a DM educator!!
Guess what I do for a living?! Ha!!
The WBCs, Lactate, tachypnea/tachycardia, elevated BUN/Creat and hypotension all point to severe sepsis/SIRS. Careful fluid resuscitation, antibiotics immediately, a central line to measure CVP and keep tabs on ScVO2 and for pressors if needed. Tox screen to see if he was snorting coke or something else at his party.
I would say give that drunk a shot of thiamine and get some blood cultures.
“Osm 330 (normal up to 300), ETOH 52, Acetone negative, and Lactate 15.8! ABG showed a Ph of 7.1 and a PO2 of 70. PCO2 (I think) was about 30.”
From what recall for the ABG results, he’s retaining too much CO2, and blowing off too much O2, plus his pH is 7.1 = some kind of acidosis. High lactate plus acidosis = lactic acidosis, respiratory cause by his history. Although, with his DM, it could be a mixed metabolic and respiratory acidosis.
Beyond that, I have no clue.
I have no idea what is wrong with this dude, but I just wanted to say that, as someone whose only degree is actually in sociology, I am proud of myself for knowing what the hell most of the abbreviations in your post were.
Don’t mind me, carry on.
OK, I did a CT of the chest to r/o PE. I will post the image tomorrow and tell me what you think it looks like.
His lungs have to be just full of vomit.
Dear TK,
I vote bigass PE. Lactate is insanely high due to being “really sick” and “trying to die”. Heart be failing, gas exchange be sucking, lactate be rising…
Intubation and central line then worry about thinking about underlying cause, Happy Hospitalist. Rock the levophed like a mofo.
If the patient codes, push tPA.
Love,
Nurse K
Zebra’s or Horses…..I wanna see that CT of the chest.
PE vs isopropyl alcohol vs right sided heart failure
He’s faking it!
But have the TPA vs enoxaparin ready if i’m wrong, saddle emboli can ruin your day.
Next on my ddx is malignant fibromyalgia
…I am mostly with Nurse K (miss you, btw!) except here in the south we call it “Fixin’ to die”.
Beyond that, I have no medical words of wisdom, except those of the fictional Gregory House, MD…
“Patients lie”.
my only comment is “Circling the drain”.
dunno I dont read ER jargon- ERP NOT all of your readers a re med students or practitioners!
Right with you Dreamgazer. I’m a third year nursing student with all of a week of MedSurge under my belt. I wouldn’t have had a clue what the hell was going on a week ago(or when all this went down for that matter)but I’m actually following most of what’s going on. Not bad, eh? Props to my prof!