Should We Discuss A Case?

[Tipsy McStagger]

I've been sitting on this case for awhile, but it's a good one and I thought you all may be interested. I admitted this patient to the ICU from the ED. Let's roll:

HPI:-
Mid 50s patient presents to small ED complaining of shortness of breath. History of HTN, T2DM, Hypothyroidism. Recent tibia/fibula fracture s/p ORIF. Of note the patient had to be readmitted to the hospital for intractable pain and spent 4 days inpatient until an effective pain regimen was obtained. At that time compartment syndrome was ruled out. They are now presenting 3 days after discharge with worsening shortness of breath and per spouse, alteration of mental status.

Small ED notes the patient had tachycardia, tachypnea and somnolence. CT scanner is down and no ability for VQ. After discussion with mothership ED they initiate an ED ➔ ED transfer. Patient arrives in mothership ED with the following vitals, labs obtained in the ED are found in the images I've attached.

Temp: 98.4 F
HR: 128
BP: 99/61 (MAP 73)
RR: 28
O2: 97% on 2L nasal cannula

Physical Exam as performed & documented by ED physician:
HENT: PERRL, moist mucous membranes
CV: tachycardia, regular rhythm, no m/g/r
Pulm: CTAB, tachypnea
Abd: Obese, soft, no tenderness
Neuro: GCS 8 (E2 V2 M4)
Extrem: No edema, 2+ peripheral pulses

More Patient History (obtained from spouse):
- Medical history as above
- Surgical history as above, +lap cholecystectomy (8 years prior)
- Current Everyday smoker, 1ppd x30 years
- occasional EtOH

Med List (spouse brought it in!)
- Aspirin 81mg daily
- Methocarbamol
- Dulaglutide
- Venlafaxine
- Empaglifozin
- D3
- Rosuvastatin
- Pantoprazole
- Metformin
- Lisinopril
- Glipizide


ED physician obtained a CT PE. There was significant motion artifact, but no clear PE in the Left/Right main pulmonary artery, segmental likely clear. Subsegmental cannot be evaluated.

At this point the patient was admitted to the ICU with diagnosis of respiratory failure, possibly PE. A DVT study was ordered by ED but not completed prior to transfer. So this is what I know when the patient comes to the ICU. Think about what your differential is for this patient, what other workup you think you'd want. I'll start post #2 now, so more info coming.

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[Tipsy McStagger]

So think about your differential at this point. Is there anything that jumps out in the labs to you? Anything else you'd like to add to the workup, or other labs you would have obtained in the ED if this patient was in front of you?

Working diagnosis from the ED was possible PE, but truth be told an inability to evaluate the sub segmental pulmonary arteries doesn't scream hemodynamically significant PE, and surely not one that would cause an alteration in mental status.

I had originally typed out the rest of our workup and treatment, but decided to delete it to see what discussion could be generated.

 

[oldtown]

So think about your differential at this point. Is there anything that jumps out in the labs to you? Anything else you'd like to add to the workup, or other labs you would have obtained in the ED if this patient was in front of you?

Working diagnosis from the ED was possible PE, but truth be told an inability to evaluate the sub segmental pulmonary arteries doesn't scream hemodynamically significant PE, and surely not one that would cause an alteration in mental status.

I had originally typed out the rest of our workup and treatment, but decided to delete it to see what discussion could be generated.

Salicylate toxicity? Did ABG show a pH of 7.33 with a pCO2 of 10?

 

[RustedFox]

Something has chewed all his bicarb away.

Add:

ABG.
Tox panel.
UA & U tox.

 

[ShockIndex]

Euglycemic DKA from their SGLT2 inhibitor.

At the very least, they need a VBG (I’d prefer an ABG since they’re altered), POCUS TTE/RUSH since they’re hypotensive, ASA, ACET, B-hydroxybutyrate, serum Osm, UA, cultures, ECG, etc.

If there is no RV failure on the my bedside TTE, I treat’em with IVF/LR, insulin, electrolyte replacement just like any other DKA with the caveat that they will need D5 or D10 up front. I may also put them on a non-bolus heparin gtt until the VTE issue can be further addressed with LE compression US.

If they start to tire, I’d put them on BiPAP so that any genius who plans on intubating them can ponder the 20+ L of minute ventilation that is probably being pulled before rushing into that mistake...

 

[Jabbed]

Euglycemic DKA from their SGLT2 inhibitor.

Beat me to it.

Would check BHB, start insulin gtt, D10 gtt.

Big risk factor is recent surgery.

 

[Make Or Break]

White count of 22, tachycardic, tachypnec, recent surg, was no one at least thinking sepsis? I get all these zebras but consider the big stuff too.

 

[Tipsy McStagger]

You guys are solid. It's honestly a fairly tough diagnosis when you're in the trenches and things are flying by you. But it's critical to make the diagnosis because this will be fatal if left untreated. I'll throw some additional labs up and then some thoughts at the end.

Salicylate toxicity? Did ABG show a pH of 7.33 with a pCO2 of 10?

I love where your head is at. One of the first things I noticed is the anion gap, significant depletion of their bicarb. So I talk to the spouse: so I understand pain has been a problem, have they been taking aspirin. Spouse tells me (and I literally quote): "... has been eating it like candy"

And in my mind I'm thinking maybe we just nailed it. So I ask about GI symptoms? Yep. Nausea, Vomiting? Yep. Stomach pain? Yep. Headache? Yep. Confusion? Obviously. Ringing in the ears? Hmmm, nooo, not that they mention.

Well, that's ok, they don't need ringing in the ears I say to myself. So I order the lab and a few others. I also decide to treat empirically. So I bolus them HCO3 and started a drip until the salicylate came back negative at which point I discontinued them.

Something has chewed all his bicarb away.

Add:

ABG.
Tox panel.
UA & U tox.

Yeah man. Was surprised that they didn't draw a gas of any sort. When I did my residency there was like an aversion to Utox orders. Expensive, doesn't change management etc. But I must say that it's been fun to see what the medicine folks discuss on ED admissions. It makes me chuckle. I'll talk more on this later, but they do order Utox like water.

Euglycemic DKA from their SGLT2 inhibitor.

At the very least, they need a VBG (I’d prefer an ABG since they’re altered), POCUS TTE/RUSH since they’re hypotensive, ASA, ACET, B-hydroxybuterate, serum Osm, UA, cultures, ECG, etc.

If there is no RV failure on the my bedside TTE, I treat’em with IVF/LR, insulin, electrolyte replacement just like any other DKA with the caveat that they will need D5 or D10 up front. I may also put them on a non-bolus heparin gtt until the VTE issue can be further addressed with LE compression US.

If they start to tire, I’d put them on BiPAP so that any genius who plans on intubating them can ponder the 20+ L of minute ventilation that is probably being pulled before rushing into that mistake...

I like everything about this. It was on my differential as well. I'll cut to the chase and just say that you nailed it.

White count of 22, tachycardic, tachypnec, recent surg, was no one at least thinking sepsis? I get all these zebras but consider the big stuff too.

Common things are common. They got a dose of Vanc/Zosyn at the first ED. I did continue their antibiotics, also drew cultures.



So right off the bat the HCO3 rang alarm bells. Immediately sent a VBG which results you'll see posted below. Also added a UDS, UA, serum ketones, serum asa/acetaminophen levels.

 

[Tipsy McStagger]

As a brief aside, I will mention how interesting it's been to see what the medicine folk discuss on an ED admission. I recall being criticized for pretty much anything I did or did not do. But secretly, the medical team is quite interested in what you've chosen to do/not do.

The patient was admitted without CT? Prepare to hear an hour long discussion on if they should be scanned or not, and "dang, I wish they had just scanned them."

Admit with a normal CT? "Obviously this CT was unnecessary". haha, I love it. I chuckle through my residents' presentation as I soak in their indecision about whether to order one or not.

Medicine is tough. We should laugh at ourselves more. But honestly my resident saw this patient and determined they had a PE and started them on heparin while completely glossing over the HCO3 of 5 and their first declaration was "this patient needs emergent intubation" which I argued would probably kill the patient.

The ED has enormous influence whether it's realized or not. The presumed diagnosis of PE was followed from 2 ED physicians, the ICU resident and also an ED PA.

 

[southerndoc]

The euglycemic DKA from SGLT2 inhibitors has been in my experience to be more profoundly acidotic than type 1 DKA's. I've only seen a handful of cases, so my n=5 or so is not statistically significant. However, all of them have had pH's <7 and all have presented with shortness of breath as their primary complaint.

 

[ShockIndex]

The ED has enormous influence whether it's realized or not. The presumed diagnosis of PE was followed from 2 ED physicians, the ICU resident and also an ED PA.

Anchoring bias. It is endemic among a generation doctors who don’t know how to get off their ass, away from a computer, and go see a damn patient without first seeing what someone else thinks.

 

[Radetzky]

great case

residents need to be taught physiology more in depth- this would avoid believing that a, non-proven, subsegmental pe could cause such a presentation

 

[Dr Mantis Toboggan]

great case

residents need to be taught physiology more in depth- this would avoid believing that a, non-proven, subsegmental pe could cause such a presentation

MUDPILES baby. The basics are still important.

 

[RustedFox]

So, forgive me for perhaps being the dense one; but I'm gonna ask.

"Euglycemic DKA."

How is this different from simply the metabolic acidosis that we all learned can happen from [Metformin, any drug]?

 

[Radetzky]

So, forgive me for perhaps being the dense one; but I'm gonna ask.

"Euglycemic DKA."

How is this different from simply the metabolic acidosis that we all learned can happen from [Metformin, any drug]?

There’s a production of Ketoacids being the driver of acidosis as opposed to lactate for metformin [or whatever other anion for whatever other drug].

 

[southerndoc]

So, forgive me for perhaps being the dense one; but I'm gonna ask.

"Euglycemic DKA."

How is this different from simply the metabolic acidosis that we all learned can happen from [Metformin, any drug]?

Metformin causes lactic acidosis in the setting of renal failure.

SGLT2 inhibitors can cause euglycemic DKA (euDKA). They lower blood glucose levels by excreting glucose. The low glucose causes lower insulin levels, which triggers increased glucagon release (insulin inhibits glucagon release). Low insulin/high glucagon leads to increased fat metabolism and generation of ketones. There is some evidence that SGLT2 inhibitors actually stimulate glucagon release by having a direct effect on pancreatic alpha-cells.

Also, during starvation renal reabsorption of ketones occurs. SGLT2 inhibitors are thought to cause the kidneys to do this independently of a starvation state. This may occur as a secondary consequence of lowering the glucose excretion threshold from 180-240 to the low 80-100's.

EuDKA usually starts with an injury (including surgery), dehydration, physical activity (i.e., beginning a new exercise regimen), low carb diets, intoxication, and possibly changes in altitude.

 

[RustedFox]

Thanks guys.
I knew I was forgetting some critical detail.

 

[southerndoc]

Thanks guys.
I knew I was forgetting some critical detail.

I only know this crap because I have diabetes and have researched the meds pretty extensively.

 

[RustedFox]

I only know this crap because I have diabetes and have researched the meds pretty extensively.

Honestly; I was missing the distinction between lactic acidosis and ketoacidosis.
I'm beat tired.

 

[DrDrummer]

Cool case. Thanks for posting. Would love to see more of this content on this board, the discussion tends to be pretty good.

The number of times I have seen critically low bicarbs ignored is growing quickly. I've seen at least two for euglycemic DKA or ASA toxicity this year. I think people often forget about metabolic acidosis driving respiratory compensation once they no longer have to do ABG interpretation in med school or on ICU rotations. Maybe the lab should consider calling people for acidemia rather than hemoglobins or blood glucoses with a "hey dummy pay attention" robocall.

 

[Tipsy McStagger]

Metformin causes lactic acidosis in the setting of renal failure.

SGLT2 inhibitors can cause euglycemic DKA (euDKA). They lower blood glucose levels by excreting glucose. The low glucose causes lower insulin levels, which triggers increased glucagon release (insulin inhibits glucagon release). Low insulin/high glucagon leads to increased fat metabolism and generation of ketones. There is some evidence that SGLT2 inhibitors actually stimulate glucagon release by having a direct effect on pancreatic alpha-cells.

Also, during starvation renal reabsorption of ketones occurs. SGLT2 inhibitors are thought to cause the kidneys to do this independently of a starvation state. This may occur as a secondary consequence of lowering the glucose excretion threshold from 180-240 to the low 80-100's.

EuDKA usually starts with an injury (including surgery), dehydration, physical activity (i.e., beginning a new exercise regimen), low carb diets, intoxication, and possibly changes in altitude.

Dynamite write up man. I didn't know that they also cause renal reabsorption of ketones in a non-starvation state. Thank you for this.

 

[gamerEMdoc]

Good case. My first thought was methanol with the AMS, severe acidosis, but normal renal function (as opposed to EG).

 

[bravotwozero]

Euglycemic DKA from their SGLT2 inhibitor.

At the very least, they need a VBG (I’d prefer an ABG since they’re altered), POCUS TTE/RUSH since they’re hypotensive, ASA, ACET, B-hydroxybutyrate, serum Osm, UA, cultures, ECG, etc.

If there is no RV failure on the my bedside TTE, I treat’em with IVF/LR, insulin, electrolyte replacement just like any other DKA with the caveat that they will need D5 or D10 up front. I may also put them on a non-bolus heparin gtt until the VTE issue can be further addressed with LE compression US.

If they start to tire, I’d put them on BiPAP so that any genius who plans on intubating them can ponder the 20+ L of minute ventilation that is probably being pulled before rushing into that mistake...

Welcome back!

 

[d2305]

Wonder why anyone Rx TGLT2s? I did when they first came out because they were free (didn't last long).

 

[Rendar5]

Reminds me of a recent case of a 60 something year old woman no hx of DM coming in for just dyspnea which was how their acidosis and new onset diabetes presented

 

[InternistDO]

Wonder why anyone Rx TGLT2s? I did when they first came out because they were free (didn't last long).

As far as oral antihyperglycemics go they're pretty good--they have a benefit for heart failure possibly independent of DM, and they have better patient centered outcomes (mortality, kidney failure, cardioprotection) than almost every other oral diabetes medication except metformin. Current guidelines usually say you go metformin-->GLP-1-->SGLT-2.

 

[d2305]

Glycosuria can't be good either. GLP1s and SGLT2s are expensive while metformin is free here.

 

[southerndoc]

Glycosuria can't be good either. GLP1s and SGLT2s are expensive while metformin is free here.

Glycosuria has been associated with increased infections -- particularly Fournier.

 

[Apollyon]

Glycosuria has been associated with increased infections -- particularly Fournier.

Now that's a REAL pain in the balls!

 

[VA Hopeful Dr]

Glycosuria can't be good either. GLP1s and SGLT2s are expensive while metformin is free here.

Which is why metformin is still first line.

But the newer, more expensive medications have significant benefits beyond their glucose lowering abilities. A previous post fleshed out that for SGLT-2s. The GLP1s are also cardioprotective, cause weight loss, and have an overall mortality benefit.

Its odd, when the SGLT-2s first came out 8 years ago I figured the glycosuria would be a much bigger problem than it is. I have maybe 1 patient in 20 that has to stop because of recurrent candida/jock itch but the rest don't seem to have any problems from that.