medic25 Posted November 2, 2012 Share Posted November 2, 2012 Since EMED was good enough to revive the interesting case discussions this week, I thought I'd add one of my one from a recent shift. Female in her 80's, PMH of HTN, DM, CHF, hyperlipidemia. In usual state of health until waking that morning feeling mildly short of breath. This persisted throughout the day until that evening she developed a light-headed sensation while using the bathroom. VS: afebrile, RR-16, HR-80's, BP- 114/82, SaO2 98% on 3lpm NC from EMS Exam: Pleasant, slightly anxious appearing. Lungs clear, Cor: no r/m/g, no S3/S4, abd: obese, soft, NT. Ext: 1+ pitting edema bilaterally. Neuro:Alert and oriented, although slightly somnolent. Meds: diovan, lasix, omeprazole, amlodipine, albuterol. Recently stopped ASA due to GI upset. EKG is a sinus tach with old Q waves in the inferior leads, but nothing acute. As you're thinking it's a fairly stable sounding patient, the nurse lets you know that her BP is now 82/58. What's the next step? What else do you want (interventions, imaging, labs, etc)? Anything else you want to know about the patient? Link to comment Share on other sites More sharing options...
Moderator EMEDPA Posted November 2, 2012 Moderator Share Posted November 2, 2012 cbc, cmp, blood gas, bnp, d-dimer, ua micro, troponin, Pcxr for starters. gentle hydration should be ok. old person with dizzyness and recent asa use gotta think occult gi bleed. rectal done? any prior gi bleeds? any prior dvt/pe? risk factors for same? she's on 3 meds that affect her bp. recent addition of new med or change in dose? it's new england. does she have an oil furnace? get a carboxyhemoglobin level if risks for CO poisoning. slightly somnolent? check tox screen for accidental ingestion. Link to comment Share on other sites More sharing options...
medic25 Posted November 3, 2012 Author Share Posted November 3, 2012 Good start E; here are the initial results: 13 6>----<125 42 140 105 56 4.4 14 2.6 <120 gap of 23, creatinine is double the previous. portable CXR: negative foley: minimal urine output istat troponin: 0.1 (slightly elevated) proBNP: pending (add a little mystery) Didn't run a d-dimer or a CO level. No hx of DVT/PE or obvious risk factors. CO is a good thought, especially given the fact that half of the state was running on generator power. No hx of GI bleed, heme negative on rectal. Patient states that this feels just like her last CHF exacerbation, so her initial fluids were gentle. Within 30 minutes or so, BP has dropped into the 70's; HR still 80-90, unable to get a reliable pleth on the pulse oximetry. We open up the fluids while monitoring closely for signs of pulmonary edema, but her lungs remain clear. SBP temporarily bumps up to the 90's after 1 liter, but soon starts trending down again into the 60-70's SBP. Given the patients body habitus, the best peripheral access is a 20 gauge. So what's your next step? PA students/new grads, any thoughts? Link to comment Share on other sites More sharing options...
Moderator EMEDPA Posted November 3, 2012 Moderator Share Posted November 3, 2012 Blood gas?(arterial or venous) pretty acidotic based on cmp... Acidotic with renal failure...interesting i'll let some others play.... Link to comment Share on other sites More sharing options...
medic25 Posted November 3, 2012 Author Share Posted November 3, 2012 ABG on 100% FiO2: 7.26 / 36 / 321 / 99 / 16 / -10 Link to comment Share on other sites More sharing options...
flyingsquirrel Posted November 3, 2012 Share Posted November 3, 2012 The AKI looks pre-renal so can we push fluids (LR) aggressively but carefully to see if that increases urine output (while watching cardiopulmonary status of course)? Maybe take a look at her IVC with US to assess her current volume status to see how far we need to go (and a full RUSH exam would be great). I'd like to see the BNP, lactate, UA…and start thinking seriously about a vasopressor/inotrope once she has some fluid on board. The PaO2/FiO2 ratio does not bode well for things to come. Link to comment Share on other sites More sharing options...
Moderator EMEDPA Posted November 3, 2012 Moderator Share Posted November 3, 2012 Just how much aspirin was she taking..... Link to comment Share on other sites More sharing options...
sk732 Posted November 3, 2012 Share Posted November 3, 2012 Just how much aspirin was she taking..... Was wondering the same thing.... Link to comment Share on other sites More sharing options...
Moderator ventana Posted November 3, 2012 Moderator Share Posted November 3, 2012 abd exam? petal pulses when first arrived? Adb bruit? acid, MS depression, BUN/CR elevation central line? crumping....... Link to comment Share on other sites More sharing options...
medic25 Posted November 4, 2012 Author Share Posted November 4, 2012 Crumping is the word.... A little more info.... Aspirin had been stopped several weeks before, so not an issue. Lactate of 3.5 ProBNP of 750 Finally a little urine output after the first liter, looks infected. Broad spectrum Abx started. Started dopamine via peripheral while setting up for central access; became very tachycardic, and switched to levophed after putting in an IJ. Didn't specifically look at the IVC, but the IJ was massively plump when placing the central line, so it was probably safe to assume she was not completely volume depleted. Levophed brought the BP up to the 90's-100's SBP, and the patient became more alert and avoided the impending intubation. Once access was squared away, we did a bedside echo, which gave us our presumptive diagnosis... I don't have the actual images at home, but this is a pretty similar shot. So what's our culprit? Link to comment Share on other sites More sharing options...
Moderator EMEDPA Posted November 4, 2012 Moderator Share Posted November 4, 2012 Quick question- did you consider bipap/cpap? Link to comment Share on other sites More sharing options...
deborah212 Posted November 4, 2012 Share Posted November 4, 2012 The RV is dilated... could be right hear failure causing cardio-renal sydnrome. The symptomatic SOB could be explained by compensating respiratory alkalosis for her met acidosis. BNP, though, isn't terribly high. Is there a clot in the LA? I can't tell. The MV and TV are hard to make out. Link to comment Share on other sites More sharing options...
medic25 Posted November 4, 2012 Author Share Posted November 4, 2012 Quick question- did you consider bipap/cpap? Not really. The intubation was going to be more for deteriorating mental status, especially if we were going to be giving a lot of IV fluids to a CHF patient. She was never visibly in respiratory distress; just reported feeling short of breath. Link to comment Share on other sites More sharing options...
medic25 Posted November 4, 2012 Author Share Posted November 4, 2012 The RV is dilated... could be right hear failure causing cardio-renal sydnrome. The symptomatic SOB could be explained by compensating respiratory alkalosis for her met acidosis. BNP, though, isn't terribly high. Is there a clot in the LA? I can't tell. The MV and TV are hard to make out. Sorry, not a great still image. The patient had massive RV dilation with hypokinetic wall motion; we actually called it a McConnell's Sign; significant RV dysfunction with mid-wall akinesia and preserved apical motion. Here's a better example: Heparin was started, and we ordered tPA to the bedside. Her hemodynamics improved so we held off on lytics, but after dropping her BP again in the ICU the tPA was pushed; last I checked she was doing very well. We were unable to CT her chest given the renal function, but lower extremity ultrasounds showed multiple DVT's. Definitely a case where ED ultrasound made a huge difference in management; as Flyingsquirrel suggested, I'll definitely be trying to make more use of the RUSH exam for hypotensive patients. Link to comment Share on other sites More sharing options...
Moderator EMEDPA Posted November 4, 2012 Moderator Share Posted November 4, 2012 Thanks for posting this cool case! Link to comment Share on other sites More sharing options...
flyingsquirrel Posted November 4, 2012 Share Posted November 4, 2012 Yes, very cool case. Thank you! Link to comment Share on other sites More sharing options...
medic25 Posted November 4, 2012 Author Share Posted November 4, 2012 Definitely an interesting shift that night. She came just as we were intubating a combative subdural bleed, and right after her was a trauma with a pelvic fracture/hip dislocation/ angulated wrist fracture (2 for 1 deal on his conscious sedation; one person popping the hip back, and another reducing the wrist)! Link to comment Share on other sites More sharing options...
rcdavis Posted November 4, 2012 Share Posted November 4, 2012 I have a couple questions... Did you attribute the metabolic acidosis all to the acute cardio renal insufficiency? Why was there not a compensatory tachycardia to either the rhf or the pulmonary hypertension? Was a sepsis syndrome considered? It seems to me that her numbers are not explained by the coagulopathy.. Infact, I would posit that the coagulopathy occured as a result of a sepsis... Good case, but would you complete the package? What were the cultures? Did you consider a v/q scan? Did that lactic acidosis imporove with fluid! Any consideration of mesenteric ischemia? As always, thanks.. Just a few random questions Link to comment Share on other sites More sharing options...
medic25 Posted November 5, 2012 Author Share Posted November 5, 2012 Good questions RC; in true ED fashion, we got her upstairs to the ICU before having the answers to some of them :) We considered sepsis and gave her antibiotics empirically, although she was afebrile, had a normal WBC count, and was in her usual state of health until the day of presentation. Last I checked her blood cultures were negative, although she grew klebsiella out of the urine. The lactate cleared and renal function improved in the ICU, although I'm not sure if this is from the IV fluids or the improved circulation after thrombolysis. I'm also a little puzzled about the relative lack of tachycardia. There was a period when the HR was in the 110-140's, although it seemed to coincide with the dopamine starting. The patient wasn't the best of historians, so I suppose it's possible that she forgot to mention a beta blocker. We didn't really give much consideration to a VQ scan; clinically she was too unstable to ship out of the department to nuclear medicine at 2am. Given the echo and the profound hypotension massive PE seemed to be the most logical diagnosis. Link to comment Share on other sites More sharing options...
chiaroscuro27 Posted November 5, 2012 Share Posted November 5, 2012 Very cool case, indeed! Link to comment Share on other sites More sharing options...
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