Fun "intern/night float" case 2

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sozme

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I/NF CASE #2

Case 1 (link)

Wanted to create another thread to discuss a case. I guess I will just call these threads "intern/night float" cases. Probably a lame name, but whatever. The reason I am doing these is because a.) I think they are interesting and doing these exercises collaboratively is fun and b.) Because Allopathic forums are kind of quiet right now save for the regular troll thread or pre-allo intrusion. The first one I made had some good responses (it is linked at the bottom).
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Case 2

72-year-old man with no known pulmonary history admitted to the hospital with E. coli sepsis due to cholecystitis. He receives antibiotics, fluids, and narcotic analgesia. On hospital day 3, he gets out of bed to go to the bathroom and becomes “winded.” When you arrive to see him, he is sitting on the edge of the bed with his elbows on his knees, with a RR of 30 breaths/min. He states he cannot catch his breath. His pulse ox registers an SpO2 of 87%.

1. What is the differential diagnosis of this patient’s acute respiratory failure?

2. Detail your immediate and short-term management (i.e. orders including immediate interventions, treatments, and tests).

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This is easy. Consult pulm for respiratory distress. In the mean time, put patient on 100% NIV. Get a CXR, place bilateral pigtails, get another CXR to assess proper placement of pigtails, consider possible need for intubation. Consult ID for sepsis. In the meantime, IV meropenem, vanc, flagyl, micafungin. Culture everything. Blood from every access line, blood from venipuncture, candida T2 panel, urine via straight cath, then place new foley cath for close I/O, culture sputum, C diff of stool, culture stool, call IR, decompress with perc cholecystostomy, send bile for culture, call IR again, parecentesis, send peritoneal fluid for culture/cytology. D/c ID consult, you've done what they would want you to do. Better get a central line in 4 hours ago for the massive fluid resuscitation and IV antibiotics you need to tx sepsis, also start pt on bumex drip and high dose lasix for volume overload because you treated sepsis. Consider cardiovascular insult. EKG, serial Tn, CKMB, Echo, emergent cardio consult.

Just an MS5 here so I may be off the mark, but that's my strategy.
 
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This is easy. Consult pulm for respiratory distress. In the mean time, put patient on 100% NIV. Get a CXR, place bilateral pigtails, get another CXR to assess proper placement of pigtails, consider possible need for intubation. Consult ID for sepsis. In the meantime, IV meropenem, vanc, flagyl, micafungin. Culture everything. Blood from every access line, blood from venipuncture, candida T2 panel, urine via straight cath, then place new foley cath for close I/O, culture sputum, C diff of stool, culture stool, call IR, decompress with perc cholecystostomy, send bile for culture, call IR again, parecentesis, send peritoneal fluid for culture/cytology. D/c ID consult, you've done what they would want you to do. Better get a central line in 4 hours ago for the massive fluid resuscitation and IV antibiotics you need to tx sepsis, also start pt on bumex drip and high dose lasix for volume overload because you treated sepsis. Consider cardiovascular insult. EKG, serial Tn, CKMB, Echo, emergent cardio consult.

Just an MS5 here so I may be off the mark, but that's my strategy.

Just an M2 here. Isn't meropenem like the last resort because of it being the last line of defense and the fact that it can cause seizures? I'm not saying I know anything, just didn't know it was given empirically.


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Just an M2 here. Isn't meropenem like the last resort because of it being the last line of defense and the fact that it can cause seizures? I'm not saying I know anything, just didn't know it was given empirically.


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Meropenem is used quite frequently as a broad-spectrum to cover pretty much everything except MRSA.
 
Just an M2 here. Isn't meropenem like the last resort because of it being the last line of defense and the fact that it can cause seizures? I'm not saying I know anything, just didn't know it was given empirically.


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You're right. The meropenem was overkill. Zosyn should be fine gram negative coverage. All the rest stands though as appropriate management.
 
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I would get the vitals (T, BP, Pulse, RR). Do quick physical exam. I will consider calling rapid response for back up.

Patient received narcotic analgesia, however RR are >20 so unlikely to be opioid-induced toxicity. DDx are pulmonary embolism, pneumothorax (no idea why this would happen given history but I would want to rule it out); less likely but will consider: MI, arrhythmia, tamponade/pericardial effusion.

I will give O2 in the meantime via NC, and upgrade to BiPAP, CPAP, etc if needed.

Tests: continuous pulse ox, stat (ABG, C-xray, EKG, BMP, CBC, lactate, PTT/INRblood ctx). PTX will show on portable xray which will indicate need for chest tube or needle thoracostomy. Test results will guide further management.

With clear Cxray and if vitals show tachycardia, will consider starting heparin pending coag results and doing CTA. Patient just had surgery, so not too sure about starting heparin. I would defer to my senior.
 
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This is easy. Consult pulm for respiratory distress. In the mean time, put patient on 100% NIV. Get a CXR, place bilateral pigtails, get another CXR to assess proper placement of pigtails, consider possible need for intubation. Consult ID for sepsis. In the meantime, IV meropenem, vanc, flagyl, micafungin. Culture everything. Blood from every access line, blood from venipuncture, candida T2 panel, urine via straight cath, then place new foley cath for close I/O, culture sputum, C diff of stool, culture stool, call IR, decompress with perc cholecystostomy, send bile for culture, call IR again, parecentesis, send peritoneal fluid for culture/cytology. D/c ID consult, you've done what they would want you to do. Better get a central line in 4 hours ago for the massive fluid resuscitation and IV antibiotics you need to tx sepsis, also start pt on bumex drip and high dose lasix for volume overload because you treated sepsis. Consider cardiovascular insult. EKG, serial Tn, CKMB, Echo, emergent cardio consult.

Just an MS5 here so I may be off the mark, but that's my strategy.

A peripheral IV is much better for fluid resuscitation than a central line. Short with wide-bore is what you want. A 16 Fr peripheral has a flow rate of about 13 liters/hr, where the shortest central line has a flow rate of about 3. Anyways.

He's in for cholecystitis sepsis, so probably already has broad cover. Day 3 is too soon for a fungemia from lines. And the main acute medical issue isn't sepsis but acute respiratory failure with the potential for intubation. Sure, sepsis can cause respiratory failure, but so can a lot of things (like septic cardiomyopathy, ARDS, PE, pneumothorax, MI, tachydysrhythmias etc.) This patient is unstable. No point in chasing etiology right now.

Immediate management would include a brief but systematic cardiopulmonary exam, stat CXR, EKG, ABG, CBC, BMP, serial troponins, and getting help. I'd have a low threshold for intubation, especially with RR of 30. Not easy to sustain. I'd start him on NIV right away. Cultures can wait until help arrives.

Too many branch points based on the results of the initial assessment.
 
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I've caught more than my fair share of PEs in real life. Surprisingly, in neurosurgery, it's pretty low on the differential.
They certainly happen, but my comment was based on my experience as a radiology resident that 2-5% of "suspect PE" cases are positive for PE.

More commonly are the incidental ones on asymptomatic cancer pts.
 
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A peripheral IV is much better for fluid resuscitation than a central line. Short with wide-bore is what you want. A 16 Fr peripheral has a flow rate of about 13 liters/hr, where the shortest central line has a flow rate of about 3. Anyways.

He's in for cholecystitis sepsis, so probably already has broad cover. Day 3 is too soon for a fungemia from lines. And the main acute medical issue isn't sepsis but acute respiratory failure with the potential for intubation. Sure, sepsis can cause respiratory failure, but so can a lot of things (like septic cardiomyopathy, ARDS, PE, pneumothorax, MI, tachydysrhythmias etc.) This patient is unstable. No point in chasing etiology right now.

Immediate management would include a brief but systematic cardiopulmonary exam, stat CXR, EKG, ABG, CBC, BMP, serial troponins, and getting help. I'd have a low threshold for intubation, especially with RR of 30. Not easy to sustain. I'd start him on NIV right away. Cultures can wait until help arrives.

Too many branch points based on the results of the initial assessment.
Mero, vanc, Flagyl, mica? Wtf. This is why ID rolls their eyes at everyone.

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Man, I thought my post was so overly ridiculous people would know it was a joke.
 
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Man, I thought my post was so overly ridiculous people would know it was a joke.

I just spilled my coffee from laughing. 10/10.

You can't just be such a quality poster and pull something like that. I was nodding my head, like, yeah, bilateral pigtails totally make sense here.
 
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I would get the vitals (T, BP, Pulse, RR). Do quick physical exam. I will consider calling rapid response for back up.

Patient received narcotic analgesia, however RR are >20 so unlikely to be opioid-induced toxicity. DDx are pulmonary embolism, pneumothorax (no idea why this would happen given history but I would want to rule it out); less likely but will consider: MI, arrhythmia, tamponade/pericardial effusion.

I will give O2 in the meantime via NC, and upgrade to BiPAP, CPAP, etc if needed.

Tests: continuous pulse ox, stat (ABG, C-xray, EKG, BMP, CBC, lactate, PTT/INRblood ctx). PTX will show on portable xray which will indicate need for chest tube or needle thoracostomy. Test results will guide further management.

With clear Cxray and if vitals show tachycardia, will consider starting heparin pending coag results and doing CTA. Patient just had surgery, so not too sure about starting heparin. I would defer to my senior.
I think high pretest prob for PE.
Agree w that approach, but would think CTA has to be done now, + bilateral LE U/S, bedside echo to (have someone) eyeball RV, and TTE. BNP.



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One thing @Cyal said: call for help. Call an RRT.

Often the most important step, often overlooked until things have really hit the fan.

There are all kinds of people in the hospital available to help. Extra nurses to draw and send labs, hang meds and fluids, call radiology etc, respiratory therapists to draw ABGs and manage supplemental oxygenation/ventilation like NRB or CPAP, etc.

You don't have to wait until the pulse is lost or the patient can't oxygenate/ventilate to call a code.

Medicine is a lot like sailing. It's really exciting if you don't know what you're doing because you're just reacting to events. If you stay ahead of the weather and anticipate badness before it happens, it should be boring. Medicine should be boring.
 
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I think high pretest prob for PE.
Agree w that approach, but would think CTA has to be done now, + bilateral LE U/S, bedside echo to (have someone) eyeball RV, and TTE. BNP.



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Agree with Duplex, and he might be a candidate for IVC filter or IR if anticoagulation is a no go. What does a BNP get you that a high pretest probability and a CTA doesn't?

I'm not entirely convinced of the PE. I want the ABG, CXR, and EKG. Is this type 1 or type 2 failure? And I would intubate much sooner rather than later. He's going to keep deteriorating from a work of breathing point of view. Better to intubate when things aren't quite emergent.

@sozme: You gotta do some follow-up!
 
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This is easy. Consult pulm for respiratory distress. In the mean time, put patient on 100% NIV. Get a CXR, place bilateral pigtails, get another CXR to assess proper placement of pigtails, consider possible need for intubation. Consult ID for sepsis. In the meantime, IV meropenem, vanc, flagyl, micafungin. Culture everything. Blood from every access line, blood from venipuncture, candida T2 panel, urine via straight cath, then place new foley cath for close I/O, culture sputum, C diff of stool, culture stool, call IR, decompress with perc cholecystostomy, send bile for culture, call IR again, parecentesis, send peritoneal fluid for culture/cytology. D/c ID consult, you've done what they would want you to do. Better get a central line in 4 hours ago for the massive fluid resuscitation and IV antibiotics you need to tx sepsis, also start pt on bumex drip and high dose lasix for volume overload because you treated sepsis. Consider cardiovascular insult. EKG, serial Tn, CKMB, Echo, emergent cardio consult.

Just an MS5 here so I may be off the mark, but that's my strategy.

This is incredible.
 
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So here is what I have... (critique any of it)

1. VTE/Pulmonary embolism, cardiogenic pulmonary edema, acute coronary syndrome, sepsis-related pulmonary vasodilation/shunting, peritonitis (decreased chest wall compliance/increased elastic work), pneumonia, pneumothorax, electrolyte disturbance.
2. Management:
  • Start with 2-4 L/min LFNC or 4-8 L/min via Venturi mask (approx. 24-40% FiO2)
    • If no improvement from this…? Then….? BiPAP?
  • Call for assistance/have other personnel call for assistance. Call for crash cart.
  • Quick re-check of vital signs and physical exam, noting:
    • Signs of respiratory failure (tachypnea, tachycardia/bradycardia, use of accessory muscles, perioral cyanosis, acrocyanosis, altered mental status, hypertension, tremor, restlessness/agitation, papilledema, asterixis, conjunctival hyperemia, etc).
    • Wheezes, rhonchi, prolonged expiratory phase, diminished breath sounds (airway etiology).
    • Stridor (anaphylaxis, foreign body aspiration)
    • S3 gallop, bibasilar crackles, jugulovenous distention, bilateral 2-4+ pitting edema of distal LE (heart failure)
  • Tests to order:
    • Critical care panel/ABG (immediately) and 1-2 hours following supplemental oxygen (or ~20 minutes post-intubation)
    • Secure 2 large-bore IV sites
    • BMP
    • Serum Magnesium
    • CBC with differential
    • Serum lactate (if not already part of critical care panel)
    • CK-MB
    • Troponin T
    • PT/INR
    • aPTT
    • 2-site blood cultures
    • Portable CXR
    • EKG
    • Duplex U/S of bilateral lower extremities
    • TTE
    • +/- bedside echo (if you have U/S at hand and are proficient enough at noting RV strain)
    • nT-BNP (even if this sub-massive or massive PE, this can be used as a surrogate for RV strain in the absence of quick echo)
Contingencies:
  • What if patient is not temporized with supplemental O2? What is your next immediate step?
  • What if your exam reveals marked peripheral edema, bibasilar crackles and your quick check of the EMR show I/O of +11,025 L? (And the saline is still running).
    • Do you turn it off?
    • Lasix?
    • Wait for CXR?
    • Etc.
Point is think about what you would do with the little info you have right there in the first 5-10 minutes at the bedside by yourself, and assuming you are the only physician available in the interim between now and when the senior resident or outside service resident/attending arrives.

Especially looking for comments on red colored text items.
 
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if you are pouring fluids in him for suspected sepsis i would probably consider an acute exacerbation of an undiagnosed CHF if no prior echo or anything, in that case i would just give him some lasix
 
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So here is what I have... (critique any of it)

  • What if patient is not temporized with supplemental O2? What is your next immediate step?
  • What if your exam reveals marked peripheral edema, bibasilar crackles and your quick check of the EMR show I/O of +11,025 L? (And the saline is still running).
    • Do you turn it off?
    • Lasix?
    • Wait for CXR?
    • Etc.
Especially looking for comments on red colored text items.

that patient is clearly volume overloaded. turn off IVF and shoot him up with some lasix. you shouldn't need a cxr to make the call
 
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This is pulmonary edema or early ards until proven otherwise imo. Much more likely the former, hx of heart failure or not. Get vitals and hook up to face mask otw there, stat abg and cxr, exam and likely call a rapid depending on your impression in the room. Quick chart check and after confirming the almost certainly +++fluid balance gets a lasix slug if pressures look like they'll tolerate it. Consider caval US if unclear fluid status, and probably before lasix regardless. If he looks euvolemic or dry and chest is clear, I'd chase other etiologies at that point, PE would get bumped up. Stabilize, assess risk factors, and likely go to CT at that point. Not going to fiddle with ddimers and compression US if I think they're really acutely hypoxic from a PE
 
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Atalectasis. Just have him walk around the floor with a nurse. And get an acapella.
 
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This is pulmonary edema or early ards until proven otherwise imo. Much more likely the former, hx of heart failure or not. Get vitals and hook up to face mask otw there, stat abg and cxr, exam and likely call a rapid depending on your impression in the room. Quick chart check and after confirming the almost certainly +++fluid balance gets a lasix slug if pressures look like they'll tolerate it. Consider caval US if unclear fluid status, and probably before lasix regardless. If he looks euvolemic or dry and chest is clear, I'd chase other etiologies at that point, PE would get bumped up. Stabilize, assess risk factors, and likely go to CT at that point. Not going to fiddle with ddimers and compression US if I think they're really acutely hypoxic from a PE

Yes! A resident! Can I throw potentially dumb ideas at you? Better dumb now than next year.

I'm thinking BP, work of breathing, and SpO2 guide management here, since this person can crump from a respiratory or cardiac point of view.

Before CT, supposing clinically euvolemic with a wet chest and SBP > 120 (as OP seems to be asking about with the follow-up post):

2-5 mg morphine
40 mg furosemide IV STAT
CPAP, but I'm getting really worried about work of breathing, so I'm following his mentation and resp effort as well as SpO2 carefully. Regardless, call the airway team now. Much better to intubate early in a controlled fashion, especially if suspecting ARDS, septic cardiomyopathy, or PE.
Nitro drip starting at 10 mcg/min titrate up with an eye on SBP. Preload reduction seems like the aim here with a wet chest, likely RV dysfunction, and huge positive fluid balance. Might just start with S/L as things are getting set up.
High index of suspicion for PE makes me want to therapeutically anticoagulate now, before CT (after checking the ECG to see if there isn't something obviously cardiogenic like tachydysrhythmia or MI or hypertensive exacerbation--those would all change management, and I might be more in favour of IV ACE-i instead of furosemide if hypertensive to get at after-load reduction)

Thoughts? The intern is not making most of these calls, and the first step is always to call for help, but these case discussions are really fun.
 
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Yes! A resident! Can I throw potentially dumb ideas at you? Better to be dumb now than next year.

I'm thinking BP, work of breathing, and SpO2 guide management here, since this person can crump from a respiratory or cardiac point of view.

Before CT, supposing clinically euvolemic with a wet chest and SBP > 120 (as OP seems to be asking about with the follow-up post):

2-5 mg morphine
40 mg furosemide IV STAT
CPAP, but I'm getting really worried about work of breathing, so I'm following his mentation and resp effort as well as SpO2 carefully. Regardless, call the airway team now. Much better to intubate early in a controlled fashion, especially if suspecting ARDS, septic cardiomyopathy, or PE.
Nitro drip starting at 10 mcg/min titrate up with an eye on SBP. Preload reduction seems like the aim here with a wet chest, likely RV dysfunction, and huge positive fluid balance. Might just start with S/L as things are getting set up.
High index of suspicion for PE makes me want to therapeutically anticoagulate now, before CT (after checking the ECG to see if there isn't something obviously cardiogenic like tachydysrythmia or MI or hypertensive exacerbation--those would all change management, and I might be more in favour of IV ACE-i instead of furosemide if hypertensive to get at after-load reduction)

Thoughts? The intern is not making most of these calls, and the first step is always to call for help, but these case discussions are really fun.

I'm a med peds intern starting on the peds side, so I'm functionally more or less a medicine subI at this point. Regardless, my thoughts would be... An ekg should be in the initial work up, easy, fast, and decent for picking up ultrabadness, 100% something I should've mentioned. The other things I think are hard to comment on without more feel for the scenario. NPPV I'd be inclined to start early. I'd really ideally like to try to skate by on supportive care + diuresis if the patient can tolerate the time it takes. Can try a soft preload reduction with repositioning, tripod on the edge of the bed, let them third space into their legs and let fluids work against gravity. The guy is old and sick but I feel like he has some reserve to see how more conservative therapy goes. I'd lean away from an ace regardless though due to concern for the kidneys in a septic patient; regardless of what volume status seemed to be the renovasculature could still be tight, and AKI increases M&M dramatically. As I said before though, take all with a grain of salt. Not really coming from a different knowledge base from you in this arena
 
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I'm a med peds intern starting on the peds side, so I'm functionally more or less a medicine subI at this point. Regardless, my thoughts would be... An ekg should be in the initial work up, easy, fast, and decent for picking up ultrabadness, 100% something I should've mentioned. The other things I think are hard to comment on without more feel for the scenario. NPPV I'd be inclined to start early. I'd really ideally like to try to skate by on supportive care + diuresis if the patient can tolerate the time it takes. Can try a soft preload reduction with repositioning, tripod on the edge of the bed, let them third space into their legs and let fluids work against gravity. The guy is old and sick but I feel like he has some reserve to see how more conservative therapy goes. I'd lean away from an ace regardless though due to concern for the kidneys in a septic patient; regardless of what volume status seemed to be the renovasculature could still be tight, and AKI increases M&M dramatically. As I said before though, take all with a grain of salt. Not really coming from a different knowledge base from you in this arena

I didn't even think about repositioning. More tricks to use as an intern.
 
I like this exercise. Good to think through some things before being called on in the middle of the night, alone.

Alright. Just to clear up some thought processes.

If this guy is hypoxic from acute decompensated heart failure aka "flash" Pulm edema. You are describing someone who is likely tachypneic, hypoxic, volume overloaded, and possibly hypertensive. A term used for this (by Scott weingart, a EM/crit care guru - search EMCRIT) is "sympathetic crashing acute pulmonary edema" or SCAPE. This helps describe what's going on, and helps describe why this patient is likely hypertensive. The hypertension is a combo of Liley baseline essential hypertension or poor vascular compliance coupled with a crazy sympathetic surge.

The treatment for this is much more than oxygen and lasix. I know lasix seems like a great idea, and over the next few days it is. But that's not what this patient needs RIGHT NOW. Right now, he needs a few things (assuming you've declared this guys as Pulm edema - which you can by vitals, physical exam, maybe a quick BSUS if you want to be fancy looking at thoracic b-lines diffusely and a huge IVC).

-for lords sake, stop fluids

- PPV - he needs bipap like now. Like 2 hours ago now. This hastily idle beneficial effects, but essentially increased LVEF by reducing after load, which stops the accumulation of Pulm edema

- BP control - slap some nitroglycerin paste on (ordered as 1/2 or 1 inch, depending on the BP)

- you can give sublingual nitro in the meantime. This comes as 400 mcg. This is a fairly immediate absorption over 5 minutes.

- the SLN is just temporizing. Get a nitro drip going. someone mentioned a nitro drip at 10 mcg/min. That is honestly a homeopathic and pathetic dose. Multiple papers mention slamming 400-600 mcg in as a bolus, and starting ~50-100 mcg/min. That's akin to giving 1-2 sublingual a over 20 min then starting the drip. If you do this, you have to be IN THE ROOM to titrate that drip. Nitro is nearly immediate on, immediate off so it's quick to titrate. And once the Pulm edema/sympathetic part of the equation starts fixing itself, the nitro will likely be coming off

-in the middle of all this - give lasix. If they are naive, give 20-40 IV. You really just need the amount that will get the guy increasing his UOP. Those who take 40 PO daily - give him AT LEAST that much IV. Likely more.
- of course, if this guys starts becoming somnolent, more hypoxic, or appears to be tiring out via exam or ABG's (hyper apnea, etc) then he needs to be intubated. Positive pressure can be NIPPV or by ETT. Whatever.

Ok, just to answer some misconceptions I saw on the Pulm edema aspect, hopefully this was helpful.

- also, to the poster above who said a normal IVC would increase suspicion of a PE - not necessarily. A PE big enough to cause this guy to look this sh*tty could cause RV strain and a bulky IVC.

*wrote on phone, sorry for typos.

Nice. Great tip about GTN. And thanks for the reference. I had no idea that was his first ever podcast: http://emcrit.org/podcasts/scape/

Thoughts on IV ACE-i vs furosemide if hypertensive? And what about CPAP at 10 mm Hg over BiPAP for hypertensive pulmonary edema? My understanding is that CPAP is probably better since it gets afterload reduction in the hypertensive situation.
 
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This is meant to elicit more thinking, so feel free to respond whenever.

Yes! A resident! Can I throw potentially dumb ideas at you? Better dumb now than next year.

I'm thinking BP, work of breathing, and SpO2 guide management here, since this person can crump from a respiratory or cardiac point of view.

Before CT, supposing clinically euvolemic with a wet chest and SBP > 120 (as OP seems to be asking about with the follow-up post):

The vitals and your clinical exam/abbreviated history should guide your decision-making here. If the patient is "clinically euvolemic", why are you going down the path of getting fluid off of them?

2-5 mg morphine

Why morphine? I would not give this patient morphine. The only people in respiratory distress that I would give morphine to are comfort care patients with air hunger.

40 mg furosemide IV STAT

Goes back to what I previously said. If the patient's clinically euvolemic, it doesn't make sense to give diuretics. If the patient is genuinely in flash pulm edema, IV 40 of Lasix isn't that huge of a dose. Regardless of whether or not they're Lasix-naive, I'd give them 160 IV and deal with the kidneys later. Regardless, the most important thing you can do for this patient after giving Lasix is checking to make sure they're actually producing urine.

CPAP, but I'm getting really worried about work of breathing, so I'm following his mentation and resp effort as well as SpO2 carefully. Regardless, call the airway team now. Much better to intubate early in a controlled fashion, especially if suspecting ARDS, septic cardiomyopathy, or PE.

Sure, you can call an RRT. No one will ever fault you for calling for help too early. Apart from the tachypnea, what makes you worried this guy's going to decompensate in front of you? If you're going into IM, you'll frequently be called to bedside for dyspneic patients who are satting (briefly) in the mid-to-upper 80s. As you gain experience, you'll get a better sense of when to call for help early and when you know you have time to figure things out.

In this case, you have time to figure out what's going on. Unless they've been super tachypneic for a good bit of time (and I have clinical/ABG findings supporting that), I'm not worried about them tiring out right in front of me.

Regarding CPAP vs. BiPAP, which scenarios would you choose one over the other? I don't necessarily think BiPAP is a bad choice if you had to choose it here, but if someone was flashing on me, I'd generally use CPAP.

Additionally, what does PPV do RV preload and RV afterload? Does that change whether or not you'd place them on PPV if you're worried about RV dysfunction?

Nitro drip starting at 10 mcg/min titrate up with an eye on SBP. Preload reduction seems like the aim here with a wet chest, likely RV dysfunction, and huge positive fluid balance. Might just start with S/L as things are getting set up.

NTG is fair if you genuinely think someone's flashing on you (though I wouldn't start it as a drip when the SL gives a whopping 400 mcg dose right off the bat -- assuming they don't have critical AS or pulm HTN or RV dysfunction).

The problem here is that you're worried about this guy maybe having submassive vs. massive PE and RV dysfunction. What's your rationale for dropping the preload on a failing right heart?

High index of suspicion for PE makes me want to therapeutically anticoagulate now, before CT (after checking the ECG to see if there isn't something obviously cardiogenic like tachydysrhythmia or MI or hypertensive exacerbation--those would all change management, and I might be more in favour of IV ACE-i instead of furosemide if hypertensive to get at after-load reduction)

Several questions here:

1. How does an EKG tell you someone's having a "hypertensive exacerbation"?

2. IV ACEi? Why'd you pick that one? There are far, far better go-to's for IV drips in the case of HTN emergency. I cannot imagine a single scenario where I'm choosing IV ACEi. Not only that, even if you really wanted to, good luck convincing the pharmacy to let you use that.

Thoughts? The intern is not making most of these calls, and the first step is always to call for help, but these case discussions are really fun.

Depends where you're training.
 
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Lots of good responses.

Are you going to start with LFNC or Venturi mask or are you going to go right to CPAP or BPAP? What are your BPAP settings going to be? Lets assume your exam and the CXR on the radiology tech's screen leads you strongly in the direction of hydrostatic pulmonary edema as cause?

Are you going to give him Lasix?
  • What if his Cr (taken a few hours prior) was 1.0, more or less what's its been everyday?
  • What if his Cr came back at 1.7 (has been 1.0 pretty much everyday since admission)?
Now lets assume he is clinically euvolemic and CXR is clear, EKG sinus tachycardia but no acute changes compared to admission EKG. The NC or CPAP/BPAP or w/e has improved the numbers on the monitor, which temporarily relieves the nurse standing next to you. He looks a little better, and is now speaking in full sentences, but diaphoretic with RR 18, complaining of mild chest pain. He's anxious but overall mental status unchanged. What now?

What if his EKG shows STEs in the inferior leads big enough to drive a truck through? Then what? (Try to just focus on what you would do in the 10 minutes or so after your handed the EKG. Yes, someone more senior/cardiologist is coming to the rescue, but assume that you are calling the shots in the 10-15 minutes it takes to get ahold of them, give them enough of the story to take over).

What if EKG shows new-onset A Fib with RVR?
  • What are you going to do in this scenario if his vitals are all otherwise essentially stable?
  • What are you going to do in this scenario if he is fighting the BPAP and becomes agitated/confused (or even more or less unchanged from the initial prompt)?
 
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This is meant to elicit more thinking, so feel free to respond whenever.

The vitals and your clinical exam/abbreviated history should guide your decision-making here. If the patient is "clinically euvolemic", why are you going down the path of getting fluid off of them?

Why morphine? I would not give this patient morphine. The only people in respiratory distress that I would give morphine to are comfort care patients with air hunger.

Goes back to what I previously said. If the patient's clinically euvolemic, it doesn't make sense to give diuretics. If the patient is genuinely in flash pulm edema, IV 40 of Lasix isn't that huge of a dose. Regardless of whether or not they're Lasix-naive, I'd give them 160 IV and deal with the kidneys later. Regardless, the most important thing you can do for this patient after giving Lasix is checking to make sure they're actually producing urine.

Sure, you can call an RRT. No one will ever fault you for calling for help too early. Apart from the tachypnea, what makes you worried this guy's going to decompensate in front of you? If you're going into IM, you'll frequently be called to bedside for dyspneic patients who are satting (briefly) in the mid-to-upper 80s. As you gain experience, you'll get a better sense of when to call for help early and when you know you have time to figure things out.

NTG is fair if you genuinely think someone's flashing on you (though I wouldn't start it as a drip when the SL gives a whopping 400 mcg dose right off the bat -- assuming they don't have critical AS or pulm HTN or RV dysfunction).

The problem here is that you're worried about this guy maybe having submassive vs. massive PE and RV dysfunction. What's your rationale for dropping the preload on a failing right heart?

Several questions here:

1. How does an EKG tell you someone's having a "hypertensive exacerbation"?

2. IV ACEi? Why'd you pick that one? There are far, far better go-to's for IV drips in the case of HTN emergency. I cannot imagine a single scenario where I'm choosing IV ACEi. Not only that, even if you really wanted to, good luck convincing the pharmacy to let you use that.

Depends where you're training.

Awesome. Thank you for this. I don't need much time to respond. Point by point.

1. My mistake. I meant not clinically hypovolemic. Clearly he's hypervolemic +11 L with a wet chest. Was posting on my phone.

2. Morphine has some evidence for preload reduction, but mostly it reduces anxiety associated with dyspnea. It's the standard cock-tail for acute decompensated HF, but I looked into it, and its use turns out to be an independent predictor of mortality and intubation from the ADHERE registry. It's also associated with increased RV filling pressure and negative inotropy. For me, morphine seems out for acute decompensated heart failure. If I really need anxiolysis, I'd rather reach for a small dose benzo, which doesn't seem to have the same haemodynamic consequences. Thank you for making me look into this. And acute decompensated heart failure is just one of my differentials pending CXR, ABG, EKG, etc.

3. I'm worried that he might deteriorate because OP specifically asked, "what if he fails supplemental oxygen"? Need to move on to 10 mg Hg CPAP and anticipate for failure. My differentials includes submassive PE, ARDS, or septic cardiomyopathy (in addition to acute decompensated HF)--happy to trial NIV, but "intubate early" is not an unreasonable thought. Watch for excessive WOB or AMS closely and let someone know earlier rather than later.

4. I'm dropping preload on a guy + 11 L, SBP > 120, and a wet chest with a GTN spray. What's the cost/benefit here? Dropping preload on a failing ventricle is not a bad thing, since it often repositions you on the Frank-Starling curve. This is the same rationale that's new being convincingly argued to run septic patients dry. It's also consistent with the evidence on acute decompensated HF, which is high on the differentials.

5. My point was to pay close attention for any cardiac etiologies that might change management. But LVH and evidence of old infarcts on EKG suggests structural cardiac lesions consistent with hypertensive exacerbation of underlying CHF (and of course you look at the BP and physical exam).

6. One off IV ACE-i actually has great evidence for this clinical situation, even though it's not a common practice. Key is after-load reduction. I think both furosemide and enalapril are worth pushing if hypertensive.

7. Really? The intern is pushing therapeutic anticoagulation on this patient before getting a CTA? Okay. Are you throwing on thrombolytics? Do you feel confident interpreting MOPETT vs TOPCAT vs PEITHO vs ULTIMA? I don't. Some decisions are okay for an intern to make. Some I would want a resident's input (that just might be my hospital though). And I'm still not convinced this is a PE, but since it's really high on my differentials... would you push anticoagulation?


Annane D, Bellissat E, Pussare E, et al. Placebo-controlled, randomized, double-blind study of intravenous enalapril efficacy and safety in acute cardiogenic pulmonary edema. Circulation 1996;94:1316–24.

Amsterdam EA, Zelis R, Kohfeld DB, et al. Effect of morphine on myocardial contractility: negative inotropic action during hypoxia and reversal by isoproterenol. Circulation 1971; 43–4(Suppl II):135.

Lappas DG, Geha D, Fischer JE, et al. Filling pressures of the heart and pulmonary circulation of the patient with coronary artery disease after large intravenous doses of morphine. Anesthesiology 1975;42:153–9.

Sacchetti A, Ramoska E, Moakes ME, et al. Effect of ED management on ICU use in acute pulmonary edema. Am J Emerg Med 1999;17:571–4.

Southall JC, Bissell DM, Burton JH, et al. ACE inhibitors in acutely decompensated congestive heart failure. Acad Emerg Med 2004;11:503.
 
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1. My mistake. I meant not clinically hypovolemic. Clearly he's hypervolemic +11 L with a wet chest.

My understanding was that this was a "what if..." mentioned on a subsequent post. If we're sticking with volume overload, that's fine. However, throughout your post, you also seemed worried about PE and said that it was high on your differential. It's important to make this branch-point decision early, since if you're really worried about PE, some of the interventions would not be ideal in that situation.

3. I'm worried that he might deteriorate because OP specifically asked, "what if he fails supplemental oxygen"? Need to move on to 10 mg Hg CPAP and anticipate for failure. My differentials includes submassive PE, ARDS, or septic cardiomyopathy--happy to trial NIV, but "intubate early" is not an unreasonable thought. Watch for excessive WOB or AMS closely and let someone know earlier rather than later.

That's fine.

In the case of RV dysfunction though, be very careful with PPV because you'll be dropping RV preload and increasing RV afterload.

4. I'm dropping preload on a guy + 11 L, SBP > 120, and a wet chest with a GTN spray. What's the cost/benefit here? Dropping preload on a failing ventricle is not a bad thing, since it often repositions you on the Frank-Starling curve. This is the same rationale that's new being convincingly argued to run septic patients dry. It's also consistent with the evidence on acute decompensated HF, which is high on the differentials.

Again, if you're worried about flash pulm edema in a volume-overloaded patient, that's fine.

Just keep in mind that if you're really worried about PE to the point of worrying about RV dysfunction (ie. categorizing it as submassive in the case of normal BPs), dropping preload is not ideal.

5. My point was to pay close attention for any cardiac etiologies that might change management. But LVH and evidence of old infarcts on EKG suggests structural cardiac lesions consistent with hypertensive exacerbation of underlying CHF (and of course you look at the BP and physical exam).

I'm still unclear how the EKG tells you whether they're currently in a hypertensive exacerbation. The BP check should tell you whether they're hypertensive or not. LVH is a chronic issue and doesn't tell you if they're currently hypertensive or not.

6. One off IV ACE-i actually has great evidence for this clinical situation, even though it's not a common practice. Key is after-load reduction. I think both furosemide and enalapril are worth pushing.

In someone flashing, I would not give IV ACEi. Ever. FYI, if someone is flashing because of HTN, that's technically HTN emergency (flashing implies it's acute-onset). There are much better ways to reduce afterload. I would be reaching for nicardipine gtt, most likely. In the case of someone slowly building up fluid over several days, that's not flash pulm edema anymore and I would approach that similarly to any other ADHF patient I take care of.

Edit: That Annane study you're quoting is not "great evidence". I would avoid using an n=20 study to guide your decision-making when there's much better evidence for other meds.

7. Really? The intern is pushing therapeutic anticoagulation on this patient before getting a CTA? Okay. Are you throwing on thrombolytics? Catheter-directed or otherwise? Do you feel confident interpreting MOPETT vs TOPCAT vs PEITHO vs ULTIMA? I don't. Some decisions are okay for an intern to make. Some I would want a resident's input (that just might be my hospital though). And I'm still not convinced this is a PE, but since it's really high on my differentials... would you push anticoagulation?

Yes, really. Intern autonomy is very program-dependent. As an intern, I routinely started patients on systemic AC by myself, whether it's for ACS or PE or a whole host of other reasons. So did my co-interns. This is expected at my program. Regarding thrombolytics for submassive vs. massive PE, we activate a team that includes IR before a decision is made. That's fine that you don't feel confident interpreting the studies you listed; I wouldn't expect a medical student to feel comfortable with them when experienced clinicians don't. I'm familiar with them as well as what their limitations are. Regarding this particular case, it depends on what the OP says is the next step of the "choose your own adventure". If the patient's dry and I have high suspicion for PE, I have no problem starting systemic AC (assuming no absolute contraindications). If the patient's grossly overloaded, I'll give time for the Lasix to kick in, put them in a sitting up position, and +/- PPV.
 
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My understanding was that this was a "what if..." mentioned on a subsequent post. If we're sticking with volume overload, that's fine. However, throughout your post, you also seemed worried about PE and said that it was high on your differential. It's important to make this branch-point decision early, since if you're really worried about PE, some of the interventions would not be ideal in that situation.



That's fine.

In the case of RV dysfunction though, be very careful with PPV because you'll be dropping RV preload and increasing RV afterload.



Again, if you're worried about flash pulm edema in a volume-overloaded patient, that's fine.

Just keep in mind that if you're really worried about PE to the point of worrying about RV dysfunction (ie. categorizing it as submassive in the case of normal BPs), dropping preload is not ideal.



I'm still unclear how the EKG tells you whether they're currently in a hypertensive exacerbation. The BP check should tell you whether they're hypertensive or not. LVH is a chronic issue and doesn't tell you if they're currently hypertensive or not.



In someone flashing, I would not give IV ACEi.

Regarding thrombolytics for submassive vs. massive PE, we activate a team that includes IR before a decision is made. That's fine that you don't feel confident interpreting the studies you listed -- I wouldn't expect a medical student to feel comfortable with them when experienced clinicians don't. I'm familiar with them as well as what their limitations are. Regarding this particular case, it depends on what the OP says is the next step of the "choose your own adventure". If the patient's dry and I have high suspicion for PE, I have no problem starting systemic AC (assuming no absolute contraindications). If the patient's grossly overloaded, I'll give time for the Lasix to kick in, put them in a sitting up position, and +/- PPV.

From way back when I started, my differentials were submassive PE, ARDS, septic cardiomyopathy, acute decompensated HF (secondary to MI or tachydysrhythmia). I agree with making the branch point early and treating accordingly. @cbrons took us down the PE path, and I didn't think that was unreasonable (even though I wasn't at all convinced). But the follow-up post suggested something else entirely. I'm still voting for aggressive preload reduction on this hypervolemic patient with SBP > 120. Good point about positive pressure ventilation if suspecting RV dysfunction. But I'm still pushing for CPAP at 10mm Hg on this patient who seems to perfusing just fine.

Look, fair enough. I don't think interns should be pushing therapeutic AC for suspected submassive PE without some input. (That's not the same as asking for permission--but engaging in a clinical dialogue with somebody who has more experience.) Why? Because many of the studies I cited suggest the timing of fibrinolytics in relation to AC matter. Like PEITHO. You can't just add it on later. Or can you? It's a complicated decision.

Of course you would look at the BP. No argument there. I thought that was obvious. But elevated BP shouldn't make you leap to hypertensive acute decompensated HF. BP can be elevated for many reasons. You have to look at the whole clinical picture, and that includes looking at the EKG for other cardiac etiologies (or factors supporting decompensated HF). Nobody should be going on BP alone, even with a wet (sounding) chest.

I will say this: you wouldn't use IV ACE-i--"ever"--but why? I cited studies supporting their use in this population. What would change your practice? I'm happy to post more.

Anyways. I really appreciate the discussion. Thank you. I'm crawling out of the hot seat for now so others can jump in.
 
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Lots of good responses.

Are you going to start with LFNC or Venturi mask or are you going to go right to CPAP or BPAP? What are your BPAP settings going to be? Lets assume your exam and the CXR on the radiology tech's screen leads you strongly in the direction of hydrostatic pulmonary edema as cause?
CPAP if theres strong immediate evidence of congestion.

Are you going to give him Lasix?
Yes.

  • What if his Cr (taken a few hours prior) was 1.0, more or less what's its been everyday?
    80mg x1.
    What if his Cr came back at 1.7 (has been 1.0 pretty much everyday since admission)?
    Higher than 80...
Now lets assume he is clinically euvolemic and CXR is clear, EKG sinus tachycardia but no acute changes compared to admission EKG. The NC or CPAP/BPAP or w/e has improved the numbers on the monitor, which temporarily relieves the nurse standing next to you. He looks a little better, and is now speaking in full sentences, but diaphoretic with RR 18, complaining of mild chest pain. He's anxious but overall mental status unchanged. What now?
CTA

What if his EKG shows STEs in the inferior leads big enough to drive a truck through? Then what? (Try to just focus on what you would do in the 10 minutes or so after your handed the EKG.
No NTG or Lopressor right away. Other than that aspirin and Plavix and stuff. Some morphine but going to be careful. Await rescue.

What if EKG shows new-onset A Fib with RVR?
  • What are you going to do in this scenario if his vitals are all otherwise essentially stable?
  • What are you going to do in this scenario if he is fighting the BPAP and becomes agitated/confused (or even more or less unchanged from the initial prompt)?
Start diltiazem or Lopressor. Hope that there isnt something immediately disastrous causing it. Await rescue.


Sent from my SM-N910P using SDN mobile
 
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Edit: That Annane study you're quoting is not "great evidence". I would avoid using an n=20 study to guide your decision-making when there's much better evidence for other meds.

As an intern, I routinely started patients on systemic AC by myself,

That's fine that you don't feel confident interpreting the studies you listed
; I wouldn't expect a medical student to feel comfortable with them when experienced clinicians don't.

I'm familiar with them as well as what their limitations are. Regarding this particular case, it depends on what the OP says is the next step of the "choose your own adventure".

Did you look at the Southall paper too? I just cited what I had available in EndNote at the time. Maybe a good thread to have in the ED or CC forum so attendings can join in? I think I have a good argument based on my reading of the literature.

Thank you for a lot of good ideas and stuff to think about.
 
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Edited to clean up the format, but not change the initial plan. Hoping for a resident to rip it apart.

Lots of good responses.

Are you going to start with LFNC or Venturi mask or are you going to go right to CPAP or BPAP? What are your BPAP settings going to be? Lets assume your exam and the CXR on the radiology tech's screen leads you strongly in the direction of hydrostatic pulmonary edema as cause?

CPAP at 10mg high FiO2 on this person who is perfusing just fine.

Are you going to give him Lasix?
  • What if his Cr (taken a few hours prior) was 1.0, more or less what's its been everyday?
  • What if his Cr came back at 1.7 (has been 1.0 pretty much everyday since admission)?

GTN before furosemide. Dropping preload is the priority for me. Still, give. Is this guy naive or not? Some are resistant and might need a thiazide like one-off 5mg metolazone PO to maximize diuresis. Assuming not, I'd push 40mg IV furosemide. With renal insufficiency, I'd push 100mg. Watch for diuresis. Double the dose on the hour if <1 liter UO. Failure to respond still, and I'm throwing on the thiazide. I'm not sure about the evidence for higher doses of furosemide.

Now lets assume he is clinically euvolemic and CXR is clear, EKG sinus tachycardia but no acute changes compared to admission EKG. The NC or CPAP/BPAP or w/e has improved the numbers on the monitor, which temporarily relieves the nurse standing next to you. He looks a little better, and is now speaking in full sentences, but diaphoretic with RR 18, complaining of mild chest pain. He's anxious but overall mental status unchanged. What now

Sinus tachy, chest pain, diaphoresis and tachypnea. Screams PE. Still. Don't want to lose sight of easy to miss differentials, like ACS. Ask about the chest pain. Give aspirin and be sure to get a repeat EKG. I want to push empiric AC before the CTA. STAT Echo is going to tell me if this is submassive or not. RV dysfunction, and I need to call about thrombolysis. No dysfunction, what's this guy's weight and CrCl again? Generally, 1mg/kg enoxaparin and get him started on warfarin 2.5mg. Any contraindications, and I want to look at the LL U/S to see if this guy could benefit from IVC filter. Call the resident. Of course, you're thinking about relevant contraindications throughout all of this (as well as all the relevant labs for monitoring.) But all things equal, since this is how the case is presented.

What if his EKG shows STEs in the inferior leads big enough to drive a truck through? Then what? (Try to just focus on what you would do in the 10 minutes or so after your handed the EKG. Yes, someone more senior/cardiologist is coming to the rescue, but assume that you are calling the shots in the 10-15 minutes it takes to get ahold of them, give them enough of the story to take over).

STEMI cocktail and ABC's keeping in mind that he's preload sensitive so not for nitro or BB (at least not now for the BB). Risk is cardiogenic shock. Needs constant reassessment. If he goes hypotensive with a wet chest (so no fluid bolus), signs of poor perfusion (including AMS), and help is far away, what about dobutamine drip 5 mcg/kg/minute? You can give it perhiperhally, and it's mostly beta-1. Titrate up. No morphine since he's preload sensitive. Low dose benzo for anxiolysis.

What if EKG shows new-onset A Fib with RVR?
  • What are you going to do in this scenario if his vitals are all otherwise essentially stable?
  • What are you going to do in this scenario if he is fighting the BPAP and becomes agitated/confused (or even more or less unchanged from the initial prompt)?

Metoprolol is the obvious answer, but what's the clinical situation? Wet chest with stable vitals, so what about amiodarone? Seems better for AF with signs of HF. 150mg IV over 10 minutes then 1 mg/min.

Strongly disagree with above about pharmacological rate control in the second situation. ACLS. AMS is a sign of poor perfusion in the context of tachydysrhythmia. He needs synchronised cardioversion. 200J biphasic. Light him up. (Minding the airway. RSI might be appropriate here.)
 
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Rushing to get ready for work, but re Cr 1 -> 1.7, you have to know when the last Cr was. If it was yesterday / that morning, you might be looking at RRT
 
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Good responses. Going to try to post another case later...
 
Rushing to get ready for work, but re Cr 1 -> 1.7, you have to know when the last Cr was. If it was yesterday / that morning, you might be looking at RRT
You'd still try to diurese him first. Remember, an AKI tells you jack-diddly squat about the patient's fluid status. He could have an elevated Cr because of cardio-renal syndrome (super, super common), and the first go-to is to try to diurese. There's no evidence for empiric use of ultrafiltration via RRT (CRRT or IHD or otherwise) to get fluid off if the patient is peeing.

And the lasix dosing discussion up above is funny. Whether you give 40 or 160 or any other number doesn't matter at all, at least when they've bothered studying it and looked at hard outcomes. What *does* matter is following up whatever dose you gave: If the patient peed after 40, then the dose was right. If he didn't make urine within the first 30-40 minutes, double it and try again.
 
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You'd still try to diurese him first. Remember, an AKI tells you jack-diddly squat about the patient's fluid status. He could have an elevated Cr because of cardio-renal syndrome (super, super common), and the first go-to is to try to diurese. There's no evidence for empiric use of ultrafiltration via RRT (CRRT or IHD or otherwise) to get fluid off if the patient is peeing.

And the lasix dosing discussion up above is funny. Whether you give 40 or 160 or any other number doesn't matter at all, at least when they've bothered studying it and looked at hard outcomes. What *does* matter is following up whatever dose you gave: If the patient peed after 40, then the dose was right. If he didn't make urine within the first 30-40 minutes, double it and try again.

Lz6AOnm.jpg


I'm fine with trialing diuresis, but I also think you can use that observation time while you wait to see if they respond to start prepping for access if it doesn't pan out, at least for patients you can make an educated guess aren't going to respond appropriately. Granted, i was a bit off on the numbers and 0.7 in 12 probably wouldn't put you in that range
 
Too much in this thread to reply to (without writing a 30 page post), but I will say as the person who is going to be receiving this patient, I'm glad to see the thought process going into the differentials.
With that said, many patients are better managed by not doing anything. Ok, sure, put some oyxgen on them. But the average person who needs to be moved from the floor to the ICU doesn't need a lot of emergent interventions. I've had to reverse a lot of well-intentioned (and even well-thought out) interventions because they didn't actually have the problem the floor team thought they did. And it's ok to be wrong. Heck it's even ok to give a wrong intervention for the right reasons. TBH, there isn't a lot you can do to the patient on the floor that I can't fix. Except wait too long to call me.
It's great to think through what might be going on with this person, but you also want to think "do I absolutely need to do this intervention in the uncontrolled environment of the floor or can it wait until they're in the unit". The ED deals with stabilization of the undifferentiated person all the time, but they're also equipped to handle everything when they're wrong and the interventions make the patient worse.

With that said (I picked these two because they were recent comments)...

In someone flashing, I would not give IV ACEi. Ever. FYI, if someone is flashing because of HTN, that's technically HTN emergency (flashing implies it's acute-onset). There are much better ways to reduce afterload. I would be reaching for nicardipine gtt, most likely. In the case of someone slowly building up fluid over several days, that's not flash pulm edema anymore and I would approach that similarly to any other ADHF patient I take care of.
I use IV enalapril often for undifferentiated flash pulm edema and true, it's usually because of BP spikes. I can get nicardipine from the pyxis in the ICU; in the ED it takes an act of Congress. YMMV

I want to push empiric AC before the CTA. STAT Echo is going to tell me if this is submassive or not. RV dysfunction, and I need to call about thrombolysis. No dysfunction, what's this guy's weight and CrCl again? Generally, 1mg/kg enoxaparin and get him started on warfarin 2.5mg. Any contraindications, and I want to look at the LL U/S to see if this guy could benefit from IVC filter. Call the resident. Of course, you're thinking about relevant contraindications throughout all of this (as well as all the relevant labs for monitoring.) But all things equal, since this is how the case is presented.
If their only dysfunction is hypoxemia, I'm not sure I'd rush to anticoagulate before CTA. If they're hypoxemic and hypotensive, and I had ruled out tension, then sure, my TPA finger starts getting itchy. If there's no dysfunction on bedside US, and there's no BP abnormality, then I'm going to hold off on anticoag until after the CTA.
 
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Too much in this thread to reply to (without writing a 30 page post), but I will say as the person who is going to be receiving this patient, I'm glad to see the thought process going into the differentials.
With that said, many patients are better managed by not doing anything. Ok, sure, put some oyxgen on them. But the average person who needs to be moved from the floor to the ICU doesn't need a lot of emergent interventions. I've had to reverse a lot of well-intentioned (and even well-thought out) interventions because they didn't actually have the problem the floor team thought they did. And it's ok to be wrong. Heck it's even ok to give a wrong intervention for the right reasons. TBH, there isn't a lot you can do to the patient on the floor that I can't fix. Except wait too long to call me.
It's great to think through what might be going on with this person, but you also want to think "do I absolutely need to do this intervention in the uncontrolled environment of the floor or can it wait until they're in the unit". The ED deals with stabilization of the undifferentiated person all the time, but they're also equipped to handle everything when they're wrong and the interventions make the patient worse.

With that said (I picked these two because they were recent comments)...


I use IV enalapril often for undifferentiated flash pulm edema and true, it's usually because of BP spikes. I can get nicardipine from the pyxis in the ICU; in the ED it takes an act of Congress. YMMV


If their only dysfunction is hypoxemia, I'm not sure I'd rush to anticoagulate before CTA. If they're hypoxemic and hypotensive, and I had ruled out tension, then sure, my TPA finger starts getting itchy. If there's no dysfunction on bedside US, and there's no BP abnormality, then I'm going to hold off on anticoag until after the CTA.

Doctor Bob!! Yes! I really hope you pop your head in the other case discussions too!

Two questions I'm unclear about:

1. Inferior STEMI, wet chest, goes hypotensive with clinical signs of hypoperfusion, and help is far away. Would you consider dobutamine? You can give it peripherally, but it's beta-1 so you might exacerbate ischemia. And this guy isn't winning with fluids either. Not sure what's in my bag of tricks here.

2. New onset A-fib with RVR and confusion fighting BiPAP. I think he needs synchronised cardioversion but RSI too? Not sure how to manage on the airway front (other than waiting for the airway team--and waiting might be the best answer if otherwise haemodynamically stable). Any thoughts would be appreciated.
 
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Doctor Bob!! Yes! I really hope you pop your head in the other case discussions too!

Two questions I'm unclear about:

1. Inferior STEMI, wet chest, goes hypotensive with clinical signs of hypoperfusion, and help is far away. On the wards. Would you consider dobutamine? You can give it peripherally, but it's beta-1 so you might exacerbate ischemia. And this guy isn't winning with fluids either. Not sure what's in my bag of tricks here.

2. New onset A-fib with RVR and confusion fighting BiPAP. I think he needs synchronised cardioversion but RSI too? Not sure how to manage on the airway front (other than waiting for the airway team--and waiting might be the best answer if otherwise haemodynamically stable). Any thoughts would be appreciated.

#2 I'd call a code and prep for RSI + cardiovert, if we're assuming the AMS is cardiopulmonary etiology. If they're altered due to hypercarbia/hypoxia or not perfusing brain, theyre not "otherwise HD stable", theyre sick
 
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Doctor Bob!! Yes! I really hope you pop your head in the other case discussions too!

Two questions I'm unclear about:

1. Inferior STEMI, wet chest, goes hypotensive with clinical signs of hypoperfusion, and help is far away. Would you consider dobutamine? You can give it peripherally, but it's beta-1 so you might exacerbate ischemia. And this guy isn't winning with fluids either. Not sure what's in my bag of tricks here.

2. New onset A-fib with RVR and confusion fighting BiPAP. I think he needs synchronised cardioversion but RSI too? Not sure how to manage on the airway front (other than waiting for the airway team--and waiting might be the best answer if otherwise haemodynamically stable). Any thoughts would be appreciated.

1. Its a tricky situation but essentially you're giving fluid boluses while also titrating inotropes (dobutamine) and pressors (norepinephrine). Many people will also go ahead and insert an IABP or LVAD to improve cardiac output but there's never been any mortality benefit. The bottom line is that this patient needs the cath lab or lytics ASAP.

2. First try to sedate the patient with Ketamine. Oftentimes that will help patients who aren't tolerating BiPAP.
 
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I would get the vitals (T, BP, Pulse, RR). Do quick physical exam. I will consider calling rapid response for back up.

With clear Cxray and if vitals show tachycardia, will consider starting heparin pending coag results and doing CTA. Patient just had surgery, so not too sure about starting heparin. I would defer to my senior.

Just pointing out that he hasn't had surgery yet as far as I can glean from prompt.
 
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This is easy. Consult pulm for respiratory distress. In the mean time, put patient on 100% NIV. Get a CXR, place bilateral pigtails, get another CXR to assess proper placement of pigtails, consider possible need for intubation. Consult ID for sepsis. In the meantime, IV meropenem, vanc, flagyl, micafungin. Culture everything. Blood from every access line, blood from venipuncture, candida T2 panel, urine via straight cath, then place new foley cath for close I/O, culture sputum, C diff of stool, culture stool, call IR, decompress with perc cholecystostomy, send bile for culture, call IR again, parecentesis, send peritoneal fluid for culture/cytology. D/c ID consult, you've done what they would want you to do. Better get a central line in 4 hours ago for the massive fluid resuscitation and IV antibiotics you need to tx sepsis, also start pt on bumex drip and high dose lasix for volume overload because you treated sepsis. Consider cardiovascular insult. EKG, serial Tn, CKMB, Echo, emergent cardio consult.

Just an MS5 here so I may be off the mark, but that's my strategy.

i knew they wouldn't get the joke
 
I think high pretest prob for PE.
Agree w that approach, but would think CTA has to be done now, + bilateral LE U/S, bedside echo to (have someone) eyeball RV, and TTE. BNP.



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If you are doing the CTA you don't need the bilateral LE U/S, it doesn't change management of what you see on CTA. Even with LE exam findings you wouldn't need it because if the CTA comes back positive PE, in the setting of LE findings c/w DVT you still don't need to see it because it won't change management of the PE.

Some will argue that if you show that there was a DVT you would feel more comfortable calling this a provoked DVT/PE, which can change what tests you order in a coag workup, and how long to extend dosing and if a patient can use estrogen BCs, etc, as "unprovoked" PEs/DVTs are treated differently.

However, +/- DVT isn't going to going to change which you label this as, because they meet criteria for for this being a provoked PE on the basis of how long they have been in the hospital and not running around.

The point of ddimers and LE dopplers is to help risk stratify who is going to get a CTA to find a PE, but if your suspicion is quite high, as it is in this case, you go straight for CTA the rest be damned.

I know this is the case, as I embarrassed a senior resident over this in front of everyone at AM report. Oops.

I recommend the EMRA clinical prediction card. I have embarrassed more than one doc above me with the following that are on it:
Ottawa Ankle, Foot, Knee
Nexus Criteria/C-Spine
Canaidan C-Spine
Centor Criteria Pharygitis
Canadian CT Head

and the main ones that apply here:
Wells Criteria for PE and DVT
PE Rule out criteria

Really understanding what the point of ddimer and DVT doppler has in dx of PE can avoid a lot of tests.
 
Now, if there are other scores that have become the gold standard let me know.

I will say that even though the above is an EMRA card, still useful for gen med practitioners to have the score models I mentioned.
Easy way to practice EBM and save your brain.
 
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