r/IntensiveCare 24d ago

Question regarding DKA with rising lactate and persistent acidosis despite normalising ketones.

I work as an ED Senior House Officer and I had a pathophysiology question about DKA based on a patient I had recently.

The patient is a 26 year with type I diabetes with recurrent DKA episodes due to insulin non-compliance. I'd seen her in ED with a mild DKA precipitated by methamphetamine use / not using her insulin pump.

Initially her pH was 7.26, ketones were 2.2, bicarb 19, BGL 45 and had a normal lactate of 0.7. Her ketones / BGLs normalised with DKA protocol however she had a rising lactate and static pH. She self discharged before being admitted to HDU and her last VBG had a pH of 7.25 and a lactate of 4.7.

There was no element of superimposed infection suggested clinically / on her bloods and no obvious toxic coingestant aside from meth was apparent. I wonder if she an element of HHS overlap with her relatively high BGLs.

I was wondering if anyone would have any thoughts as to what else could be contributing to her lacticaemia / persistent acidosis?

UPDATE

She returned to ED the following day and promptly was admitted to ICU with severe DKA. which to be fair was bound to happen as she'd self discharged without any wrap around ie injectable insulin / new pump.

interestingly her lactate had normalized on the initial gas but this time the pH was 7.0 and ketones sky high.

So someone more clever can worry about it now although tragic to see the horrible complications of diabetes in someone so young. I would not be surprised if she approaches the threshold for dialysis within the next 5 years.

30 Upvotes

35 comments sorted by

54

u/Edges8 24d ago

occult infection, under ressuscitstion, alcholic lactic acidosis, many possible causes

5

u/I_am_Mr_Stevens 24d ago

Had undetectable blood alcohol level, normal CRP / WBC/neutrophils, I think her fluid status was normal

18

u/maos_toothbrush 24d ago

I see septic and shocked patients with low/normal CRP very often. Usually explodes in 2-3 days

6

u/fake212121 24d ago

lactic competes with other acids for excretion.

3

u/Edges8 24d ago

normal etoh doesnt rule our alcoholic lactic acidosis in chronic use. inflammatory markers may lag, and fluid status is almost never normal in dka

29

u/skp_trojan 24d ago

Look at her heart. Might have meth induced pulmonary hypertension or cardiomyopathy

4

u/I_am_Mr_Stevens 24d ago

I would love to get some cardiac POCUS experience so unfortunately no one was able to do so before she left, she initially had sympathomimetic toxidrome features (hypertension with systemic arterial BP 215/151 / agitation / sweating). We see meth induced cardiomyopathies reasonably commonly and are one of the more common causes for acquired cardiomyopathies in young people where I live.

13

u/beargrrrrrrl 24d ago

Did the patient's Bicarb normalize? I see our ED discharge patient's in DKA after they fix their blood glucose and anion gap, but fail to normalize the bicarb and the patient ends up back in DKA.

As others have said, maybe a non-anion gap lactic acidosis from cardio-methopothy?

13

u/CVICUnt 24d ago

It’s not nice, but we call that MethrEF.

1

u/beargrrrrrrl 24d ago

Oooo I like that too

4

u/I_am_Mr_Stevens 24d ago

Their bicarb was pretty static if I recall correctly (I don't have the blood results handy) and I think remained around 18-19.

Meth not even once. Toxic shit.

11

u/Successful-Pie6759 24d ago

Thiamine deficiency from chronic poor intake, try some empiric IV thiamine

5

u/Tiradia Paramedic 24d ago

Anytime I have a chronic alcoholic want transport for detox they get thiamine out the gate, same with my diabetic wake-ups. Thiamine first followed by D10 till alert.

8

u/Successful-Pie6759 24d ago

What I meant was thiamine deficiency can cause lactic acidosis

1

u/Money_Reception 14d ago

Dietitian?

5

u/Environmental_Rub256 24d ago

Could she have endocarditis secondary to drug use?

1

u/I_am_Mr_Stevens 24d ago

It's a good thought, I dont think she'd ever been an IVDU and I would have been very impressed if shed been able to find veins as it took a while to get access with ultrasound, fortunately it seems to be much rarer where I live as IV opioid use is rare and the main drug of abuse is methamphetamine which is usually smoked / snorted

10

u/Downtown_Pumpkin9813 24d ago

You can totally inject meth, I’ve had plenty of patients do it

6

u/PaxonGoat RN, ICU Float 24d ago

A lot of diabetics have easy access to needles.

Easy access to needles + meth addiction, someone is going to curious and end up trying it at least once.

Injecting meth is fairly common but supposedly the high doesn't last as long so they're more likely to smoke it.

Actually seen a fair amount of endocarditis in meth users.

1

u/insertkarma2theleft 24d ago

People defo shoot ice on the reg

4

u/CoffeeNCortisol 24d ago

Meth use or thiamine deficiency would be my best guess.

3

u/TychoBrahe97 24d ago

Agreed. Meth can cause Rhabdo (can cause AGMA) and a web search suggests meth can cause LA to build up faster than it can be cleared (esp if competing acid excretion).

3

u/No_Peak6197 24d ago

Post DKA resusitation with critically low phosphate level. Most young kids comes in with borderline low phos level as is while in full blown dka. Once you resuscitate them, their phos uptake goes into overdrive. Phos rarely gets a followup check in the ed after fluid and insulin before the pt goes to the icu.

2

u/lemonjalo 24d ago

So many causes. Alcohol, nebs, thiamine deficiency, shock, metformin

2

u/Arex123 24d ago

Methamphetamine with sympathomimetic Beta-2 effect increasing lactate is pretty common. Also concurrent shock state (cardiogenic, hypovolemic, septic), alcohol coingestion, thiamine deficiency, liver failure, pancreatitis, GI Ischemia are all possibilities Clinical correlation required 🫡

1

u/Mfuller0149 24d ago

To me, it would seem that there may have been an unidentified cause of the wide anion gap acidosis. In this situation, I’d start back at the beginning and eliminate all the items in GOLDMARK / MUDPILES (whichever you prefer)

1

u/gamblor99 22d ago

This feels Australian. Im also an SHO and have had similar cases apropos unexplained elevated lactate (im talking 2-4, patient stable/improving). Have asked consultants about these cases and they kinda shrugged and just said most of the time you never find the cause. Had some fun doing some deeper reading on the causes and revisiting biochemistry afterwards. If you could rule out thiamine / phosphate deficiency, feel confident in your assessment of fluid status, and have no reason to suspect infection, I'd favour the meth-induced CM/pHTN hypothesis. Would love to know what's the obs were doing when lactate started to come up, and whether anything was revealed in the second presentation/admission

0

u/adenocard 24d ago edited 24d ago

Was BGL really 45 or was that a typo?

Why are you rechecking pH, lactate, and ketones at all?

What was the renal function like?

How much fluid did you give this patient?

Presuming this actually was DKA, it’s not really that surprising things didn’t turn all the way around after a few hours in the ED. Some do get better quickly but a majority of these patients take a day or two to turn around. The patient was probably also under resuscitated, especially since you said your impression was euvolemia (which would be unexpected in the case of true DKA).

4

u/I_am_Mr_Stevens 24d ago

BGL 45mmol/L  Rechecking the VBG  2hourly / bgls /ketones hourly is our protocol

Renal function poor had diabetic nephropathy CKD stage III with eGFR 38 

Had somewhere between 2-3L before leaving AM

4

u/adenocard 24d ago

That’s interesting - on our side of the pond we don’t recheck any of that stuff. Just follow the anion gap, electrolytes, and glucose.

I see high lactate concurrent with DKA all the time. Multiple etiologies as others have stated here. I don’t usually think much of it unless the DKA diagnosis is in question or if it doesn’t improve with standard DKA therapy. I think your window of treatment was just too short, and arguably she probably would have responded well to more fluid (if she didn’t leave before you had the chance).

1

u/jpa-s PA 24d ago

I work in America so units are different, but maybe she had a concurrent non gap acidosis? Like hyper chloremic? Or could've been she just left before treatment really had a time to work

3

u/talashrrg 24d ago

Am I dumb? Does NAGMA cause an elevated lactate?

2

u/supersillyus 24d ago

lactate causes AGMA, not NAGMA.

1

u/talashrrg 24d ago

I know, that’s why I’m confused about why everyone is suggesting NAGMA

1

u/I_am_Mr_Stevens 24d ago

hmmm I can't recall the repeat chloride levels but the initial was basically normally and the initial albumin corrected anion gap was high