MD & DO I/NF CASE #9 (Triple Stack Bacon Burger)

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sozme

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I/NF CASE #9
(Emergency medicine, surgery, internal medicine)

The expert for this case will be @Instatewaiter
====================================================================
Links to previous cases:
Case 1 Case 2 Case 3
Case 4 Case 5 Case 6
Case 7 Case 8
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59-year old morbidly obese female with type II diabetes (on insulin) and a 40-pack-year smoking history presents to the ED with nausea and severe RUQ pain that began right after eating a triple-stack bacon burger at Wendy's. She is brought to the ED by her husband, who states that the patient has been "under the weather" recently, stating that she'd been diagnosed with an URI about a month ago by her primary NP. Her medications include metformin, allopurinol, albuterol inhaler, and Levaquin (which patient was switched after finishing Z-pak for her URI). She is also on Lantus QHS. Her other medical problems include obstructive sleep apnea (non-complaint with CPAP), and asthma.

In the ED, patient is in AF with RVR, and the treating PA orders IV Lopressor. One of the EM interns on his ultrasound rotation performs a bedside hepatobiliary U/S, noting several opacites inside the gallbladder as well as moderately thickened gallbladder wall.

CBC:
  • Shows mild leukocytosis (12.4) with left-shift
CMP:
  • Na+: 133
  • K+: 5.3
  • Cr: 1.6
  • BUN: 54
  • AST: 100
  • ALT: 95
  • ALKP: 285
Bilirubin: 1.7
Lipase/amylase: Negative
POC troponin: Negative
EKG: Atrial fibrillation with RVR

EXAM:

VITALS: BP 99/67; HR 116; Temp 98.6 F; SpO2 95% on 2 L LFNC;
GENERAL: Adult obese female appearing older than stated age, poorly dressed in ripped T-shirt and undersized shorts, smells strongly of tobacco smoke.
LUNGS/CHEST: Limited due to body habitus. Diffuse crackles.
HEART: Limited by body habits. Mildly tachycardic. Soft heart sounds but not distant. S1. S2. Cannot palpate PMI in the setting of body habitus.
ABDOMEN: Protuberant. Exam limited secondary to morbid obesity. Tender to palpation in epigastrium and RUQ.
EXTREMITIES: No obvious joint swelling or deformity of distal extremities.
INTEGUMENT: No rash. No lower extremity edema. Skin cool to the touch.
NEUROLOGIC: Patient somewhat somnolent.

PA calls Surgical resident for "obvious cases of cholecystitis." Patient is admitted to Step-Down unit where she is given fluids and IV antibiotics to be temporized for surgery.

Overnight, She converts to NSR. A serum procalcitonin is negative in the StepDown unit. Patient is taken to surgery after midnight, a couple hours after your shift begins.

At 0234, patient is transported from the PACU back to the Step-Down Unit. You are called by the Step-Down nurse stating the patient is "acting strange." You hurry over to the room, hearing the telemetry alarm bleeping from the end of the hall. When you get there, 2 nurses are in the room, yelling out questions to the patient who is pale-faced and blabbering incomprehensibly. You look up at the telemetry monitor while the BP cuff inflates - HR is 143 and irregular.

"What do you wanna do, Buck?" the nurse asks.

You look-up at her suddenly. "Uh..."

The crisp sound of the BP cuff deflating interrupts your thinking: 84/43.

The other nurse turns from the patient, scowling openly at you. "Well?????"

====================================================================

1. What is going on?
2. What do you do?
3. What is the likely diagnosis?

====================================================================

UPDATE #1
UPDATE #2
RESOLUTION

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I'm assuming this is a narrow complex irregular rhythm (atrial fibrillation with rapid ventricular rate). The patient is unstable.

Get those pacer pads on and do synchronized cardioversion. Afterwards, time for a 12 lead EKG, some fluids (she probably already has this going), and something like a dilt drip.

Diagnosis? Sick middle aged lady who's a crap surgical candidate. She likely has Afib secondary to pulmonary hypertension due to her COPD.
 
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Just a 2nd year med student with really no clue about anything clinical but always good to just throw something out there to see if I've learned anything. I don't really have a great understanding about exactly how much time you have to get stuff done in these situations but I can imagine not much.

I would do a quick physical exam - vitals, heart, lungs, abdomen, extremities
Draw labs - CBC w/ diff, cmp, coag studies

In addition to what was suggested in the post above i want to check for septic shock 2ndary to perfed gall bladder. checking for peritoneal signs, clammy (edit: warm flushed!!!) extremities, repeat RUQ ultrasound. Call the ICU, get lactic acid and draw cultures. start empiric abx, pressors, fluids, (insulin? not sure what to do for glycemic + electrolyte control in a crashing diabetic)

Also would think about hypoglycemic shock as she is diabetic and had been on a beta blocker for her afib

(edit: just to save face i want to point out that i wrote this post before the op included the information that the patients decompensation occurred after surgery which obviously changes a lot)

please rip into me if this post was entirely dumb, i feel pretty clueless about actual clinical medicine and welcome anything as I start 3rd year in a few months..
 
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I'm assuming this is a narrow complex irregular rhythm (atrial fibrillation with rapid ventricular rate). The patient is unstable.

Get those pacer pads on and do synchronized cardioversion. Afterwards, time for a 12 lead EKG, some fluids (she probably already has this going), and something like a dilt drip.

Diagnosis? Sick middle aged lady who's a crap surgical candidate. She likely has Afib secondary to pulmonary hypertension due to her COPD.

She likely has afib due to her systemic infection aka sepsis.

Afib rarely causes hypotension on its own. Your first thought for this lady shouldn't be cardiovert. It should be resuscitate. Give her a liter and watch her BP.

Now I'm not saying you shouldn't think about cardioverting. You won't be wrong doing it. But for this lady it's likely a temporary fix.
 
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Sorry to above - had to edit case a little to make it clear she had surgery the night she was admitted, and is in the SDICU after being transferred from PACU.
 
Just a 2nd year med student with really no clue about anything clinical but always good to just throw something out there to see if I've learned anything. I don't really have a great understanding about exactly how much time you have to get stuff done in these situations but I can imagine not much.

I would do a quick physical exam - vitals, heart, lungs, abdomen, extremities
Draw labs - CBC w/ diff, cmp, coag studies

In addition to what was suggested in the post above i want to check for septic shock 2ndary to perfed gall bladder. checking for peritoneal signs, clammy extremities, repeat RUQ ultrasound. Call the ICU, get lactic acid and draw cultures. start empiric abx, pressors, fluids, (insulin? not sure what to do for glycemic + electrolyte control in a diabetic)

Also would think about hypoglycemic shock as she is diabetic and had been on a beta blocker for her afib


please rip into me if this post was entirely dumb, i feel pretty clueless about actual clinical medicine and welcome anything as I start 3rd year in a few months..
Not bad for a second year except you completely ignored the unstable a fib w rvr. You shock (cardiovert) unstable rvr before you do anything else. Along with fluids, etc. Sure she got a brief hit of beta blocker, but the hr is 143 so she is clearly not rate controlled at this time and will probably go on a drip of dilt or amio in addition to the cardio version.

Not sure what you mean by clammy but remember if you are thinking about sepsis that is classically a warm and well perfumed shock.

If you can't control blood sugar in a sick as **** patient put them on an insulin drip. If you are doing an infectious/sepsis work up in this lady don't forget the cxr, urinalysis w reflex culture along with your blood cultures x2. You mentioned pressors, it's good to know that first line in sepsis is norepi. Repeat ruq probably won't buy you anything. If anything after stabilization and if they have worsening abdominal exam maybe a ct.

I'd put this patient on oxygen as well (never a bad idea with someone who is crashing for unknown cause) and get an abg to check hypoxia and hypercarbia.
 
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Bedside us
Trop bnp
Ekg

This fatty with tachycardia hypotension ?hypoxemia ruq pain could be having a massive pe
 
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She got admitted yesterday? Call me if things get worse and I'm responsible for floor codes, airways, lines, etc. I was only up here looking for the cafeteria. I heard it's taco day.

But before I go, can someone get an ECG?
 
How much blood did she loose?
Is she bleeding post op and the BP is due to hypovolemia?
Sepsis?
Pancreatitis?

Fluid bolous , EKG , troponins,cultures, Abdominal CT call the surgical resident and my attending. Start thinking about possible intubation because she is going to be hard to intubate.

Not a doctor or a medical student. But these are fun.
 
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Get full set of vitals
Do my exam/abcs, gives fluids (less if she has crackles) and likely O2, watch bp response
Stat ekg and management of possible unstable afib
Follow with stat draw of glucose, CBC, bmp, troponins, ddimer, bcx
Likely needs cta at some point
Bed side us is also a good idea
 
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Not bad for a second year except you completely ignored the unstable a fib w rvr. You shock (cardiovert) unstable rvr before you do anything else. Along with fluids, etc. Sure she got a brief hit of beta blocker, but the hr is 143 so she is clearly not rate controlled at this time and will probably go on a drip of dilt or amio in addition to the cardio version.

Not sure what you mean by clammy but remember if you are thinking about sepsis that is classically a warm and well perfumed shock.

If you can't control blood sugar in a sick as **** patient put them on an insulin drip. If you are doing an infectious/sepsis work up in this lady don't forget the cxr, urinalysis w reflex culture along with your blood cultures x2. You mentioned pressors, it's good to know that first line in sepsis is norepi. Repeat ruq probably won't buy you anything. If anything after stabilization and if they have worsening abdominal exam maybe a ct.

I'd put this patient on oxygen as well (never a bad idea with someone who is crashing for unknown cause) and get an abg to check hypoxia and hypercarbia.
She's relatively unstable, but I certainly don't cardiovert before I do anything else. I evaluate the patient, confirm the blood pressure with a manual check (morbidly obese lady with an automated blood pressure cuff has a lot of possible points for error), and give some mild-moderate fluid resuscitation first. If the BP improves and the HR comes down, then give some additional resuscitation and consider medical rate control with your poison of choice. Dilt or metoprolol if their pressure can tolerate it, potentially digoxin if the renal function is OK, or even amiodarone (which can do both rate and rhythm control without affecting the blood pressure), all while treating the underlying condition.

There's possible morbidity to cardioverting a patient, especially if you have no clue how long they've been in atrial fib. Why do a potentially unnecessary procedure that risks triggering a stroke if you don't have to? Obviously if the patient remains relatively hypotensive or worsens you can seriously consider it, but that's not yet apparent.
 
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She's relatively unstable, but I certainly don't cardiovert before I do anything else. I evaluate the patient, confirm the blood pressure with a manual check (morbidly obese lady with an automated blood pressure cuff has a lot of possible points for error), and give some mild-moderate fluid resuscitation first. If the BP improves and the HR comes down, then give some additional resuscitation and consider medical rate control with your poison of choice. Dilt or metoprolol if their pressure can tolerate it, potentially digoxin if the renal function is OK, or even amiodarone (which can do both rate and rhythm control without affecting the blood pressure), all while treating the underlying condition.

There's possible morbidity to cardioverting a patient, especially if you have no clue how long they've been in atrial fib. Why do a potentially unnecessary procedure that risks triggering a stroke if you don't have to? Obviously if the patient remains relatively hypotensive or worsens you can seriously consider it, but that's not yet apparent.
The question of stable/unstable is interesting, and I like to ask attendings what they're using to categorize people beyond BP. In preclinical learning BP<90 is "always unstable", but after a few weeks on the wards it's clear that magnitude of BP in isolation is not useful. In this case, the patient is acutely altered. Although there are a few reasons she could be altered (hypercarbia, PE as mentioned above, post-op sepsis seems a bit early, delirium in context of analgesia post-op...) change in mental status with low BP and taccharhythmia would lead me to think electricity should be considered sooner rather than later. Bolus first seem appropriate though. Playing odds, afib post-op is due to volume loss.
As a side note, re: concern for complications of cardioversion - would you be that worried without a history of afib and a record of NSR less than 12 hours prior to this event? I would think that risk of throwing a clot would be pretty low for her.

Other things I would be interested in getting - SpO2, ECG, I&O's since admission, current medications, ABG for concern of hypercarbia, troponin, bedside TTE, maybe blood cx if they hadn't been drawn prior to surgery
Things I would not be interested in - ddimer (she's not low risk given her history and, she just had some endothelial injury)
 
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I thought sepsis in the context of URI and feeling under the weather for the past month.
 
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The question of stable/unstable is interesting, and I like to ask attendings what they're using to categorize people beyond BP. In preclinical learning BP<90 is "always unstable", but after a few weeks on the wards it's clear that magnitude of BP in isolation is not useful. In this case, the patient is acutely altered. Although there are a few reasons she could be altered (hypercarbia, PE as mentioned above, post-op sepsis seems a bit early, delirium in context of analgesia post-op...) change in mental status with low BP and taccharhythmia would lead me to think electricity should be considered sooner rather than later. Bolus first seem appropriate though. Playing odds, afib post-op is due to volume loss.
As a side note, re: concern for complications of cardioversion - would you be that worried without a history of afib and a record of NSR less than 12 hours prior to this event? I would think that risk of throwing a clot would be pretty low for her.

Other things I would be interested in getting - SpO2, ECG, I&O's since admission, current medications, ABG for concern of hypercarbia, troponin, bedside TTE, maybe blood cx if they hadn't been drawn prior to surgery
Things I would not be interested in - ddimer (she's not low risk given her history and, she just had some endothelial injury)

She came in afib before going to nsr so I would think we would have no idea how long she was previously in afib and that she maybe at risk for throwing a clot. I definitely agree that you need to look at her pulse ox, rr and WOB with abg (and probably cxr) if she had abnormalities. Definitely fluids.

Side question: with a patient who is acutely hypotensive with crackles and you aren't sure if you are dealing with decompensated heart failure due to whatever reason or sepsis with ARDS, do you still slam with fluids? If they do end up being the heart failure I would think a large fluid boils would make things worse.

I love thinking through these things even though I don't know much
 
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Meh, probably not. With the information we have, her primary issue on presentation was cholecystitis (RUQ tenderness, leukocytosis, stones and GB wall thickening on US). If you're a fan of sepsis2, she qualified when in the ED. The prior URI was not something I was thinking about, to be honest.
My thinking is that sepsis due to post-op infection would be less , given the temporal proximity to her intervention.

She came in afib before going to nsr so I would think we would have no idea how long she was previously in afib and that she maybe at risk for throwing a clot. I definitely agree that you need to look at her pulse ox, rr and WOB with abg (and probably cxr) if she had abnormalities. Definitely fluids.
Fair.
 
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The question of stable/unstable is interesting, and I like to ask attendings what they're using to categorize people beyond BP. In preclinical learning BP<90 is "always unstable", but after a few weeks on the wards it's clear that magnitude of BP in isolation is not useful. In this case, the patient is acutely altered. Although there are a few reasons she could be altered (hypercarbia, PE as mentioned above, post-op sepsis seems a bit early, delirium in context of analgesia post-op...) change in mental status with low BP and taccharhythmia would lead me to think electricity should be considered sooner rather than later. Bolus first seem appropriate though. Playing odds, afib post-op is due to volume loss.
As a side note, re: concern for complications of cardioversion - would you be that worried without a history of afib and a record of NSR less than 12 hours prior to this event? I would think that risk of throwing a clot would be pretty low for her.

Other things I would be interested in getting - SpO2, ECG, I&O's since admission, current medications, ABG for concern of hypercarbia, troponin, bedside TTE, maybe blood cx if they hadn't been drawn prior to surgery
Things I would not be interested in - ddimer (she's not low risk given her history and, she just had some endothelial injury)
You never know if patients are in and out of afib all the time at home. Most people can't tell. Unless the patient has been anticoagulated for >1 month, there's always a chance she has a clot in the left atrial appendage.

Mind you, cardioversion should still be done if acutely indicated, but you still need to consider if there's any other options before pulling the trigger. Fluids is still my first reflex.
 
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A layperson question. Are step 1 questions like this with multiple choice answers?
 
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Oh, this is post-op. I misunderstood in my first post.

I'll point out that the real world is far more grey than board exam world. I would just like to say for anybody who has a scenario like this on a standardized exam, a systolic BP <90 and altered mental status with AFIB w/RVR is unstable and requires cardioversion.

In the real world, we think about things like throwing off a clot and patients are usually "questionably altered" and blood pressures are more like "well I got 80 and then we got a 99 and then we got an 89" and you're left with your gestalt to see if you can throw on some more fluids/meds to save a shock.

So yes, recheck the BP manually and make sure you have a documented number you can stand behind. That goes for all the vitals (in this case a temperature and pulse ox would be nice). Also, don't underestimate with a respiratory rate can tell you. This patient likely has very recent labs so a lot of things probably aren't going to be high yield but in an acute decompensation you're going to get the CBC, CMP, POC glucose, and do a pretty good physical exam (is POCUS available? that's part of a thorough physical exam). You're going to look pretty dumb if you miss a dehiscing surgical site.

This patient is screaming afib w/RVR causing her decompensation. I need more physical exam findings/vitals changes before I start going down the Sepsis route. Besides, she's on antibiotics and fluids already so considering other diagnoses isn't exactly going to delay her care. PE? Sure it's possible but I'd be more concerned if she were decompensating in sinus tachycardia, not an irregular one. The good news is that if she really does have a clinically significant PE, it should be relatively apparent when you slap an ultrasound probe down on her chest and see a big ol RV, as opposed to the hyperdynamic heart you'd see in afib w/RVR. I adore POCUS in hypotensive patients for this very reason; scanning the heart can give you very actionable information.
 
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The question of stable/unstable is interesting, and I like to ask attendings what they're using to categorize people beyond BP. In preclinical learning BP<90 is "always unstable", but after a few weeks on the wards it's clear that magnitude of BP in isolation is not useful. In this case, the patient is acutely altered. Although there are a few reasons she could be altered (hypercarbia, PE as mentioned above, post-op sepsis seems a bit early, delirium in context of analgesia post-op...) change in mental status with low BP and taccharhythmia would lead me to think electricity should be considered sooner rather than later. Bolus first seem appropriate though. Playing odds, afib post-op is due to volume loss.
As a side note, re: concern for complications of cardioversion - would you be that worried without a history of afib and a record of NSR less than 12 hours prior to this event? I would think that risk of throwing a clot would be pretty low for her.

Other things I would be interested in getting - SpO2, ECG, I&O's since admission, current medications, ABG for concern of hypercarbia, troponin, bedside TTE, maybe blood cx if they hadn't been drawn prior to surgery
Things I would not be interested in - ddimer (she's not low risk given her history and, she just had some endothelial injury)
Get a VBG. It will give you the information you want without the need to stab an artery (a painful procedure that is not without risk of complications).
 
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She came in afib before going to nsr so I would think we would have no idea how long she was previously in afib and that she maybe at risk for throwing a clot. I definitely agree that you need to look at her pulse ox, rr and WOB with abg (and probably cxr) if she had abnormalities. Definitely fluids.

Side question: with a patient who is acutely hypotensive with crackles and you aren't sure if you are dealing with decompensated heart failure due to whatever reason or sepsis with ARDS, do you still slam with fluids? If they do end up being the heart failure I would think a large fluid boils would make things worse.

I love thinking through these things even though I don't know much
Give the hypotensive undifferentiated patient at least some fluid and see how they respond while you come up with other ideas.
 
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She's relatively unstable, but I certainly don't cardiovert before I do anything else. I evaluate the patient, confirm the blood pressure with a manual check (morbidly obese lady with an automated blood pressure cuff has a lot of possible points for error), and give some mild-moderate fluid resuscitation first. If the BP improves and the HR comes down, then give some additional resuscitation and consider medical rate control with your poison of choice. Dilt or metoprolol if their pressure can tolerate it, potentially digoxin if the renal function is OK, or even amiodarone (which can do both rate and rhythm control without affecting the blood pressure), all while treating the underlying condition.

There's possible morbidity to cardioverting a patient, especially if you have no clue how long they've been in atrial fib. Why do a potentially unnecessary procedure that risks triggering a stroke if you don't have to? Obviously if the patient remains relatively hypotensive or worsens you can seriously consider it, but that's not yet apparent.
Glad to see you in this thread @Raryn I always appreciate your comments. I'll admit I was typing on my phone and not really talking through the nuances of the case in my response. @FindMeOnTheLinks had written a pretty reasonable post for a second year and I was certainly painting with some broad strokes to get across the point that as important as the eventual 19 point work up will be (labs, cultures, etc), the first thing you need to care about when a patient is crashing in front of you is why they are crashing. In this case, I think 9/10 times it is unstable a fib, so that needs to be the first thing in your mind when you start managing this patient. Sure maybe you don't cardiovert right away, but my #1 step is putting pads on this patient just in case, and the whole time I am monitoring for decompensation and ready to shock while I am rechecking blood pressure, giving fluids, etc. I also interpreted this patient in my head as someone I see whose blood pressure is still dropping and getting more and more altered (the issue with these scenarios is so much has to be left to interpretation given the text medium), while I fully admit if the scenario is different than I was imagining and their blood pressure is stable or starts to improve slightly that a shock would be premature.

Please let me know if I am totally off base, but I just wanted to point out that I was (in the words of onlinemeded) substituting clarity for truth in the hope of making a teaching point.
 
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Should I be more impressed by the AFRVR than I am? I've seen far brittler patients tolerate AFRVR to the 160/170's essentially without symptoms / HD compromise. 140's in a 50 yo w/o known cardiac disease just doesn't strike me as being causative for this presentation. It could certainly be contributory, and I'd think why the extra hit to her CI tipped her over, but at least in my experience I'd definitely think there's more to it
 
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Glad to see you in this thread @Raryn I always appreciate your comments. I'll admit I was typing on my phone and not really talking through the nuances of the case in my response. @FindMeOnTheLinks had written a pretty reasonable post for a second year and I was certainly painting with some broad strokes to get across the point that as important as the eventual 19 point work up will be (labs, cultures, etc), the first thing you need to care about when a patient is crashing in front of you is why they are crashing. In this case, I think 9/10 times it is unstable a fib, so that needs to be the first thing in your mind when you start managing this patient. Sure maybe you don't cardiovert right away, but my #1 step is putting pads on this patient just in case, and the whole time I am monitoring for decompensation and ready to shock while I am rechecking blood pressure, giving fluids, etc. I also interpreted this patient in my head as someone I see whose blood pressure is still dropping and getting more and more altered (the issue with these scenarios is so much has to be left to interpretation given the text medium), while I fully admit if the scenario is different than I was imagining and their blood pressure is stable or starts to improve slightly that a shock would be premature.

Please let me know if I am totally off base, but I just wanted to point out that I was (in the words of onlinemeded) substituting clarity for truth in the hope of making a teaching point.
Basically, you're on the right track.

Just the general question you can try to ask with afib is *why* are they suddenly in RVR. It can happen randomly, absolutely, but it can also happen due to a different underlying etiology. If the patient is relatively hypovolemic (quite common after an abdominal surgery if they third-space some fluids), that can lead to hypotension which will decompensate the atrial fib. Treating the underlying hypovolemia fixes the problem.

Or if someone is in RVR with a decent blood pressure but they report significant pain. Well, pain can worsen tachyarrhythmias. Try treating that first before you jump on just treating the heartrate.

If the patient is stable enough that you can stop and think about the underlying condition, that is almost always the right answer. And I consider a patient who is breathing on her own with a MAP of 56 to be stable enough that I don't need to jump to electricity without trying something else first. Obviously putting the pads on the pt is absolutely reasonable, but I wouldn't personally shock the described situation *as a first measure*.
 
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Basically, you're on the right track.

Just the general question you can try to ask with afib is *why* are they suddenly in RVR. It can happen randomly, absolutely, but it can also happen due to a different underlying etiology. If the patient is relatively hypovolemic (quite common after an abdominal surgery if they third-space some fluids), that can lead to hypotension which will decompensate the atrial fib. Treating the underlying hypovolemia fixes the problem.

Or if someone is in RVR with a decent blood pressure but they report significant pain. Well, pain can worsen tachyarrhythmias. Try treating that first before you jump on just treating the heartrate.

If the patient is stable enough that you can stop and think about the underlying condition, that is almost always the right answer. And I consider a patient who is breathing on her own with a MAP of 56 to be stable enough that I don't need to jump to electricity without trying something else first. Obviously putting the pads on the pt is absolutely reasonable, but I wouldn't personally shock the described situation *as a first measure*.

Well Raryn, I'll be a surgery intern in a few short months and all my experience with a fib and RVR is in surgical critical care, so I don't know what this "thinking" thing all you internal medicine doctors talk about is. :p

Our differential for a fib is typically, they had surgery, they got too many or too few fluids and now their old heart can't handle it. Turn up their fluids, Metop 5 if their BP can handle it, otherwise amio bolus and drip. Shock if their BP tanks (along with AMS) and we can't bring it back up. We also always had them on tele so I know they weren't in a fib prior (didn't catch that they came in in a fib in the prompt), so complications of cardioversion are less of a concern.

(This is all tongue-in-cheek of course, I'm actually married to an internist. I always try to learn as much from you all as I can, thanks for the extra variables to think about.)

Question for you: say this patient is on the floor. They are altered and the bp (MAP 56) is stable to slowly decreasing. Are they stable enough for a trip to the ICU? Or do you temporize them first, and if so, to what general threshold?
 
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Conferring with Expert.

Update coming soon.

Someone here is on the right track. Look into her history a little more closely - try to come up with a hypothesis of what the big picture is here. Hint - don't trust everyone with a stethoscope and prescription pad.
 
Im gonna go with missing an original underlying infection like cholangitis (missed dilated CBD by em resident doing US, she has leukcytosis and increased bili) which caused her afib and has now progressed to full blown sepsis.

After sozme's comment I just don't trust this "viral URI", something is definitely getting missed there
 
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Im gonna go with missing an original underlying infection like cholangitis (missed dilated CBD by em resident doing US, she has leukcytosis and increased bili) which caused her afib and has now progressed to full blown sepsis.

After sozme's comment I just don't trust this "viral URI", something is definitely getting missed there
Good point, bumped AST/ALT fit better with cholangitis on presentation. I wonder, if CBD dilation was missed on US early in the course, would the surgical team have noticed something abnormal during the chole to suggest cholangitis (inflammation out of proportion to simple cholecystitis, purulent drainage during resection)? I guess at this point she does fit Reynold's pentad. Given the severity of her current picture, broadening to metronidazole with pip-tazo or cefepime could be useful. Interestingly, levofloxicin is an option for severe cholangitis according to the 2011 IDSA guidelines.

I still can't connect the URI to her admission though.
 
UPDATE #1

Immediate management:
  • Airway:
    • No obstruction.
    • Patient is altered right now, so she cannot be trusted to protect her airway.
    • The best way to protect her airway is through ET intubation.
      • But you decide that because she is hypotensive, and the use of sedatives and PPV may further hemodynamic collapse.
      • Furthermore, you decide that depending on the etiology, this may be reversible with less invasive support methods.
  • Breathing:
    • SpO2 is 90%; RR 18 on 4 L/min LFNC
    • You remove low-flow NC and place her on BiPAP
    • You order a Venous blood gas
    • LUNGS: Diffuse crackles. No use of accessory muscles,
  • Circulation:
    • SKIN: Cool and clammy.
      • This signifies an element of hypoperfusion.
    • You run 1 L 0.90% NS wide-open
    • You see Type & Screen was performed prior to surgery, so you order up 2 units of blood just to be ready
  • Other decisions:
    • In the context of suspected infection plus postoperative status, the differential includes postoperative hemorrhage or distributive shock due to septicemia.
    • You order her placed on IV broad spectrum antibiotics.

  • You order:
    • CMP
    • Serum Mg2+
    • CBC
    • VBG
    • Serum lactate
    • 2-site blood cultures
    • Plasma nT-pro BNP
    • Troponin T
    • EKG
    • Stat TT echo
  • You call ICU fellow and arrange transfer to the ICU
==========================================================
  1. Which of these decisions is incorrect? (hint: color code) And why?
 
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UPDATE #2

  • CMP
    • Na+ 136
    • K+ 5.6
    • Cr 2.1
    • BUN: 64
    • AST: 103
    • ALT: 96
    • ALKP: 289
  • Mg2+: Mildly low
  • CBC
  • WCT 13.3 with left-shift
  • Lactacte: 2.6
  • NT proBNP: 12,103
  • EKG: AF RVR
ECHO (interpreted by cards fellow):
  • Dilated left ventricle with a LV diastolic dimension of 6.5.
  • EF 25-30%
  • RV is mildly dilated with moderate RV dysfunction
  • There is 2-3+ functional mitral regurgitation caused by angular dilation
  • There is 2+ tricuspid regurgitation
  • RVSP is 60mmHg. The IVC is dilated and does not collapse with inspiration.

=================================================================
  1. What is the diagnosis? Thinking back to the initial history from the E.D., what do you think happened here?
  2. Since you (the intern) have already completed your initial management and passed it along to the ICU team, you won't be making any more decisions. However, if you were the one still in-charge, what would be your approach here? [Answer coming in Update #3 from our expert]
 
Cardiogenic shock....

IVFs wrong because you cold & clammy profile = hypoperfusion with congestion. That fluid will run from the bag directly into the interstitium.
 
UPDATE #1

Immediate management:
  • Airway:
    • No obstruction.
    • Patient is altered right now, so she cannot be trusted to protect her airway.
    • The best way to protect her airway is through ET intubation.
      • But you decide that because she is hypotensive, and the use of sedatives and PPV may further hemodynamic collapse.
      • Furthermore, you decide that depending on the etiology, this may be reversible with less invasive support methods.
  • Breathing:
    • SpO2 is 90%; RR 18 on 4 L/min LFNC
    • You remove low-flow NC and place her on BiPAP
    • You order a Venous blood gas
    • LUNGS: Diffuse crackles. No use of accessory muscles,
  • Circulation:
    • SKIN: Cool and clammy.
      • This signifies an element of hypoperfusion.
    • You run 1 L 0.90% NS wide-open
    • You see Type & Screen was performed prior to surgery, so you order up 2 units of blood just to be ready
  • Other decisions:
    • In the context of suspected infection plus postoperative status, the differential includes postoperative hemorrhage or distributive shock due to septicemia.
    • You order her placed on IV broad spectrum antibiotics.

  • You order:
    • CMP
    • Serum Mg2+
    • CBC
    • VBG
    • Serum lactate
    • 2-site blood cultures
    • Plasma nT-pro BNP
    • Troponin T
    • EKG
    • Stat TT echo
  • You call ICU fellow and arrange transfer to the ICU
==========================================================
  1. Which of these decisions is incorrect? (hint: color code) And why?
I'd argue putting the obtunded hypotensive patient on bipap is more wrong than a fluid trial, but that's just me. Especially with no evidence of hypoxia or hypoventilation yet.

Yes, the later update points more at a cardiogenic picture, but at this point? I see risks and not that many benefits.
 
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I'd argue putting the obtunded hypotensive patient on bipap is more wrong than a fluid trial, but that's just me. Especially with no evidence of hypoxia or hypoventilation yet.

Yes, the later update points more at a cardiogenic picture, but at this point? I see risks and not that many benefits.
You can blow some water out of the lungs.
But you can also drop preload.
And risk aspiration.
But you can get good preoxygenation while fixing the BP.
 
You can blow some water out of the lungs.
But you can also drop preload.
And risk aspiration.
But you can get good preoxygenation while fixing the BP.
But the patient is oxygenating.

What are you treating with your BiPAP?

Yes, it does help the preload, but do you know that then.
 
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But the patient is oxygenating.

Honestly, I'd argue that she's not oxygenating all that well. She came in at 95% on 2L, and is now at 90% on 4L. She's not grossly hypoxemic at this point, but she's right at the drop-off point of the O2-sat curve and not trending in a good direction.

One thing that strikes me is she came into the ED with euvolemic pre-renal dysfunction that wasn't really addressed. BUN:Cr of >30 with no signs of volume depletion would make me want an echo before I surgerize her.
 
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Cardiogenic shock....

IVFs wrong because you cold & clammy profile = hypoperfusion with congestion. That fluid will run from the bag directly into the interstitium.

Cardiogenic shock was always the answer.

The patient never had cholecystitis.

They presented to the ED with right heart failure with volume overload, leading to hepatic congestion/hepatopathy. This can cause right upper quadrant pain and GB wall thickening/pericholecystic fluid. It's a known masquerader and can easily be misdiagnosed as cholecystitis.

------

A couple of points that have been missed:

1. Look, I don't mean to downplay cholecystitis, but it rarely makes you floridly septic. Especially not AFTER source control has been obtained and antibiosis given. This doesn't mean a GB patient can't get sick, but if someone is tanking in septic shock that's typically more a cholangitic picture if anything and always makes me take a step back and rethink my diagnosis.

2. Regarding the post-op management and whether to give fluids to this hypotensive patient: Again, you've gotten source control in the OR already. Sepsis should be on the wane. The usual cause of afib with RVR in a postop patient is volume overload/atrial stretch. The hypotension is secondary to the poorly perfusing rhythm. Giving fluid doesn't fix it. Rate control or shocks fix it. Diuresis too in the less acute patient who can handle it.
 
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Traction pins and bone patellar tendon bone autograft reconstruction.

Did someone call?
 
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Cardiogenic shock was always the answer.

The patient never had cholecystitis.

They presented to the ED with right heart failure with volume overload, leading to hepatic congestion/hepatopathy. This can cause right upper quadrant pain and GB wall thickening/pericholecystic fluid. It's a known masquerader and can easily be misdiagnosed as cholecystitis.

------

A couple of points that have been missed:

1. Look, I don't mean to downplay cholecystitis, but it rarely makes you floridly septic. Especially not AFTER source control has been obtained and antibiosis given. This doesn't mean a GB patient can't get sick, but if someone is tanking in septic shock that's typically more a cholangitic picture if anything and always makes me take a step back and rethink my diagnosis.

2. Regarding the post-op management and whether to give fluids to this hypotensive patient: Again, you've gotten source control in the OR already. Sepsis should be on the wane. The usual cause of afib with RVR in a postop patient is volume overload/atrial stretch. The hypotension is secondary to the poorly perfusing rhythm. Giving fluid doesn't fix it. Rate control or shocks fix it. Diuresis too in the less acute patient who can handle it.

So would you try fluids at all or just go straight down the unstable afib approach?
 
RESOLUTION

This is a case of acute decompensated heart failure which was misdiagnosed twice (one in the outpatient setting as a URI... the hint is the switch in the antibiotics) and again in the E.D. as cholecystitis. The patient was inappropriately taken to the OR and wound up in cardiogenic shock. Please see the post by @SouthernSurgeon regarding oft confused HF for cholecystitis diagnosis - this point is also repeated in an excellent lecture by Dr. Dmitry Abramov, a HF cardiologist at the University of Louisville (I highly recommend it - its a gold mine of information and a lot of the HF pathophysiology taught in medical school is wrong or emphasizes super rare presentations):



Some important points:
  • Physical examination alone is insensitive for determining ECF volume excess. Good history-taking should elucidate mild congestive symptoms, which can indicate volume excess.
  • Patients presenting with nausea and elevated liver enzymes are often misdiagnosed with cholecystitis (they often undergo RUQ U/S and possibly hepatobiliary (HIDA) scan which are often abnormal). Such patients may then undergo cholecystectomy, which can precipitate cardiogenic shock.
  • In the context of HF, elevated bilirubin and liver enzymes signify both congestion and hypoperfusion. It is a particularly ominous sign and is itself an indication for emergent cardiology consultation.
  • Remember the warm vs. cold / dry vs. wet "profiles" of heart failure presentations:
upload_2017-2-28_14-16-33.png


Advanced management

This from @Instatewaiter who graciously agreed to be the expert on this case:

Initial management should be acute afterload reduction. The patient is very clamped down so provided there is adequate blood pressure (which is somewhat subjective but as long as the MAP is ~70) you often see the blood pressure either stay steady or improve by using something like sodium nitroprusside. Others will recommend an inotrope like milrnone or dobutamine. People will probably worry that the BP will drop but if done carefully, it rarely does.

Skin: cool and clammy signifies peripheral constriction. NO FLUIDS! this is a relative contraindication. Blood is +/- but isn't the primary treatment which really should be afterload reduction and diuresis.

Should get aggressive diuretics probably after starting either NTP or milrinone/dobutamine.​

I want to also point out that in the lecture I linked, he talks about aggressive diuresis in the presence of the rising creatinine and why it is sometimes the correct approach.

Thanks again to everyone who participated.
 
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Giving fluid is literally the exact opposite of what you need to do here

Yes obviously once you know they are in cardiogenic shock. I just picture myself in the room doing my abcs and not being able to tell right then and there if this is cardiogenic vs distributive (history does sound like possible cholangitis to me) and I would try something like 10cc/kg and see how they respond?
 
Yes obviously once you know they are in cardiogenic shock. I just picture myself in the room doing my abcs and not being able to tell right then and there if this is cardiogenic vs distributive (history does sound like possible cholangitis to me) and I would try something like 10cc/kg and see how they respond?

I mean my hope would be that I wouldn't have misdiagnosed it in the first place. I've run across literally this exact scenario in the ED a few times. It's easy when they are a known HF patient- then you just get to brag that you're smart and the ED docs are dumb. It's hard when it's occult HF. I almost took out a GB last year in this type of scenario last year - however the patient was kind enough to throw himself into a fib with RVR in the PACU and we wised up and cancelled the case and got the diagnosis right.

But in general, this case aside, for postop fib w/ RVR, no I would not be giving fluids. Overwhelming majority of the time they need diuresis, not fluids. This case was obviously a little confusing setup because you're wondering about multiple things going on at once (i.e. is it ongoing septic shock, is it hypovolemic shock from surgery, etc).
 
I mean my hope would be that I wouldn't have misdiagnosed it in the first place. I've run across literally this exact scenario in the ED a few times. It's easy when they are a known HF patient- then you just get to brag that you're smart and the ED docs are dumb. It's hard when it's occult HF. I almost took out a GB last year in this type of scenario last year - however the patient was kind enough to throw himself into a fib with RVR in the PACU and we wised up and cancelled the case and got the diagnosis right.

But in general, this case aside, for postop fib w/ RVR, no I would not be giving fluids. Overwhelming majority of the time they need diuresis, not fluids. This case was obviously a little confusing setup because you're wondering about multiple things going on at once (i.e. is it ongoing septic shock, is it hypovolemic shock from surgery, etc).

Thanks, very informative
 
Well too bad it's done but yea I would have :

#1 Intubate Jabba
#2 Bolus Ringer & Voluven
#3 VBG
#4 Call cardio
#5 Have the PA executed at dawn
#6 Echo

IMHO a chest and abdomen CT should have been performed before yanking out the gall bladder + echo cord , you know since morbidly obese patients usually have shot hearts.
 
This case was intentionally misleading. However it is a great learning case and there were a lot of subtle cues.

I see a lot of heart failure and in the outpatient we often see that these people are diagnosed with a URI that just won't go away until someone gets an echo. Similarly, rights sided failure very commonly presents with abdominal pain and fullness. The abdominal pain is due to elevated venous pressure causing hepatic congestion. So, you often see RUQ discomfort. The fluid overload can occasionally mimic fluid around the GB. The hepatic congestion also leads to elevated liver enzymes. The elevated LFTs are often overlooked. We will talk more about this below with regard to perfusion status.

For the med studs: There are two concerns when evaluatting heart failure.
1) Volume status (Wet or dry)- this is trickier than it seems especially in true cardiomyopaths. Sure lower extremity edema is an easy finding to see but in those with chronic overload, they often present overloaded from redistribution of fluid. These patients have no LE edema. Their sign is massive jugular venous dilation. This is also going to be the patient population that is at higher risk of cardiogenic shock. So, it is vital to learn to do a good JVP exam for the surgeon and internist alike. On a similar ilk, the pulmonary findings in chronic heart failure patients are absent because they create increased lymphatic drainage.

The liver is often overlooked. A pulsatile liver is very commonly found in the setting of 3 or 4+ TR. I feel it is tough to use the liver size to gauge congestion just because a lot of these people are going to have NAFL.

2) Perfusion status- (Cold vs warm)
On exam things like mental status, heart rate, and most importantly skin temperature will give you clues about perfusion status. Heart rate elevates in compensation when the cardiac ouput (and namely the SV) is insufficient to meet the metabolic demands of the body. In cardiogenic shock, as the vital organs are hypoperfused, the body will redistribute blood by constricting blood flow to the skin. So the skin, especially in the legs, becomes cold.
End organ perfusion will also be evident by labs; labs will show a pre-renal kidney injury, elevated lactate, elevated LFTs and often hyponatremia.

Treatment is directed at two things that you need to figure out by examination: are they wet or dry and are they cold or warm.

Warm and wet is the run of the mill heart failure and needs just diuresis

Cold and wet needs something more than just diuresis. Afterload reduction (nitroprusside, ISDN/hydral, ACEi/ARB) will often improve the perfusion status enough on its own. However, if it doesn't inotropes or mechanical circulatory support should be the next choice IMO.

In this case, she was moving toward being cold on presentation and underwent surgery and fluids which would only make this worse and take a minimally compensated ventricle to a completely uncompensated patient. In the case presented, both metoprolol and diltiazem would have made things worse and decreased contractillity in a ventricle that was already struggling. Here either cardioversion, dig or amio would have been the right treatments One thing that wasn't mentioned is that someone with new AF RVR after surgery you need to think ischemia. Surgery is often the insult that leads to an MI, and an MI/ischemia is one of the common triggers of new AF.
 
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