Student Challenge Case: "Nausea and vomiting, and she does NOT look good!"

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Sorry for the delay folks - I had a few busy shifts last few days but now I can jump back in to update you all.  I'll share my answers to these questions (not saying they are the only right answers by any means) and then share the rest of the labs.  

 

- the electrolyte derangements you are seeing - what do you think is the unifying cause that would explain all of these electrolyte derangements?   This is the classic hypokalemic hypochloremic metabolic alkalosis with a likely unifying cause of significant nausea/vomiting GI losses.  Remember vomiting up stomach acid (HCl) causes the loss of acid and Chloride with resultant increase in bicarb/HCO3- .  This explains the low Cl and the high CO2 on the BMP (remember the CO2 on the BMP represents bicarb/HCO3- and not carbon dioxide that you'd see on a blood gas).  What is the mechanism for the low K with vomiting?  There is small amounts of K in gastric secretions but the bigger mechanism is actually renal losses of K in the setting of the acid base issues going on.  So, a part of fixing the low K is fixing the acid base problems and the underlying cause (nausea and vomiting).

 

-what is the suspected acid base status and why? ( give me your best guess for the most likely scenario given that we don't have a blood gas yet - it ties in with the above electrolyte prompt).  We see from the high bicarb and NV that they likely have a metabolic alkalosis (ddx would include a primary respiratory acidosis like COPD CO2 retention and metabolic alkalosis as compensation, but that seems much less likely here).  However we notice that there is a high anion gap suggests concomitant metabolic acidosis thus it is a mixed process.

 

-You notice there is a HAGMA as well - practically speaking while working in the ED, what do you do when you notice a high anion gap on the BMP?  

You try to find the cause of the HAGMA and treat that underlying cause.  It's often clinically apparent.   I go through the ddx "KULT".  You were likely taught the ddx MUDPILES, which is a great and comprehensive list.   KULT is a shortened form of MUDPILES that is much easier to remember and will identify 95+% of the causes of HAGMAs.

 

• K = ketone elevation. DKA, AKA (alcoholic ketoacidosis), or starvation ketosis. This is easy to check for by looking at the blood sugar or clinical picture.

• U = uremia or a high BUN and low GFR (also easy to check on the metabolic panel).

• L = lactate elevation. (Easy to check for when it makes sense clinically.)

• T = toxins Ask the patient if they drank alcohol or any other type of toxin, as well as if there was suicidal ideation, etc.

If you can’t find the cause for the AGMA after reviewing KULT, then go through your “MUDPILES” and dive deeper through this ddx. 

In our case, she has multiple potential causes in the KULT ddx - it could be ketosis from AKA or starvation - we checked ketones and they were only mildly elevated.  Uremia was not present per BMP.  Lactate was sent and you'll see result shortly.  Toxins - patient denied toxic alcohol ingestion.  You can send a serum osmol and compare that to the calculated osmol, and if there is an osmol gap have a higher suspicion for a toxic alcohol ingestion.  In this case we had an alternative explanation in the lactate elevation you will soon see.  

 

How do we make progress on figuring out the main issue going on for this patient?  A helpful exercise is to reflect on which of the obtained data is the most unique/specific.  A lot of that data that we have seen are somewhat nonspecific, like the nausea vomiting or even the shock state which could be from many potential causes.  

One of the more specific findings that we've seen that can help to anchor us and give us a center to focus on is the profound bilirubin elevation / jaundice.  You won't see that very often and the ddx is limited.  Reflect on how you'd approach the jaundiced patient in general, and in this case given how sick the patient is, we need to first and foremost focus on the life threatening causes of jaundice.  What are the most acutely life threatening causes jaundice?  How do we address/workup/consider these here?   Some of you have started mentioning ideas here but I'd like you to collate / summarize them.  I am looking for a ddx of at least 3 life threatening conditions.

EMEDPA got all of the most critical ones, but here they are again for your review.  Any time you see a patient with jaundice/elevated bilirubin who looks sick, always consider these!

#1 ascending cholangitis - RUQ US or CT would note dilated CBD.

#2 acute liver failure - how do you make the diagnosis of acute liver failure? 

Liver insult + coagulopathy (INR >1.5) + encephalopathy.  If you suspect acute liver failure or injury, you must consider the causes (tylenol, shock liver/ischemic, infection, etc)

#3 Hemolysis ddx like MAHA (TTP, DIC, HELLP, etc) - an easy one to forget but the lab derangement pattern can have a lot of overlap with liver disease (anemia, low platelets, elevated bilirubin).  Always send a direct/conjugated bilirubin and if you notice that it is low, that suggests the elevated bili is mostly unconjugated, at which point you should send hemolysis labs (LDH, haptoglobin, peripheral smear, etc).

 

 

Okay!  More labs incoming shortly...

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Platelets 130k

 

 

There might have been more labs requested but I apologize these were the only screenshots I took at the time of the case.

 

So at this point, how would you summarize the case into a succinct "problem representation"?  What is your leading suspicion and next steps?  

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Hello all - I apologize for the gap in posting as I've been on a stretch of busy shifts!  I think it is time to wrap this up.

 

Problem representation / summary statement: This is a 45 year old alcoholic presenting jaundiced, hypotensive, borderline febrile, and with complaints of vomiting with RUQ pain.  Workup is suggestive of shock state with high lactate, and imaging shows gallstones with enlarged CBD.  With this in mind, our top concern was ascending cholangitis and patient required emergent ERCP.  

 

Much to everyone's surprise, the ERCP actually ended up coming back negative.  The patient responded very well to general resuscitation / treatment and the eventual discharge diagnosis from the primary and specialists involved in the case was ETOH hepatitis with decompensated cirrhosis!  It was definitely a great case that brought together so many important medical concepts.

 

Here is a summary of a few key learning points from this case:

-When you notice an EKG with a particularly long QT, you should have a high suspicion for electrolyte abnormality, most commonly hypoK and hypoMag, which would make sense in the picture of extensive vomiting.  Be very careful to avoid QT prolongers!

-Have a systematic approach to working up and empirically treating "sick" or unstable patients, using ABCDE or whatever format you'd like.  

-Recognize the patterns for clinically relevant lab abnormalities and the risks associated with them.

-Remember the 3 fastest killers of patients presenting with jaundice who are acutely ill: ascending cholangitis, acute liver injury/failure, and don't forget about MAHA/TMA.

 

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When I was a student I definitely struggled with cases like this, as is expected.  This is not your typical "fast track case" with one simple chief complaint and all of the data fitting snuggly within the standard workup for that chief complaint.  Even for middle acuity/complexity patients, they have numerous comorbidities, several chief complaints or positive ROS, and most of the test results come back abnormal in some way or form.  Knowing how to effectively sort through data and synthesize is a skill that takes years to hone.  Add in the factor of the patient being sick / unstable with management being time-critical, and it makes for high stress situations for those who are not prepared.  

This is in part why I chose to do a residency program.  My program integrated me into the high acuity main ED from day one where I was managing cases like this with excellent support, mentorship and supervision.  I recognize that there are PAs who are not fans of residency programs, and that is fine!  It is definitely not for everyone.  But for me, the benefits were huge and well worth the sacrifice!

That is in part why I have went on to write a book for PA students who want to learn more about residency programs and what they offer.  For those who are interested in pursuing these programs, it also details how to optimize your chances getting accepted and succeeding while in the program.  

I had alluded to this project in the beginning of this case, and now I am excited to share it all with you! (link below).  I also wrote a blog here on the forums sharing my experience as I went through each rotation of my residency program and the medical lessons learned each step of the way.  Check it out if interested!   

Link: The Ultimate Guide to PA & NP Residency & Fellowship Programs - available on Amazon.  

I'm happy to answer any questions about the case, the book, or anything else!
Best,

-SN