This afternoon Dr Cara Levin brought us on an exciting journey of a middle aged man with a significant cardiovascular history (prior CABG, DES, TAVR) who was transferred to OHSU for ongoing management of shock initially felt secondary to acute GIB and acute hypoxic respiratory failure, who, when presenting to our institution, demonstrated difficult to explain labs: significant mixed AG and non-AG metabolic acidosis with respiratory acidosis, profound neutrophil predominant leukocytosis (to the 50,000s), mildly elevated lactate and then stable Hg.
What was the cause of his shock if we now couldn’t blame it on hypovolemia from his GIB bleed? Could it be cardiogenic? Was he septic? Were his new vent settings causes obstruction?
We turned to the lab abnormalities we did observe in search of other clues for our unifying diagnosis, namely… his acid base status!
In true internal medicine form, we broke down those labs in a step-wise fashion. Find below a helpful diagram courtesy of Dr Joel Topf (@kidney_boy), as featured on the hit IM podcast, “The Curbsiders”.
Through these steps we arrived at our multifactorial mixed AG and non-AG metabolic acidosis with respiratory acidosis and grew our differential through expoloring causes for a MAGA (metabolic anion gap acidosis) with the helpful mnemonic “Goldmark”.
In this case, it turns out that our patient had been on Empagliflozin, an SGLT-2 inhibitor agent used in management of type 2 diabetes. While the SLGT-2 inhibitors have shown great promise in terms of reducing important cardiovascular outcomes in patients at high risk fo CV events (like our patient!), they unfortunately have a known side effect of increased risk of euglycemic DKA.
Euglycemic DKA can present with an MAGA, leukomoid reaction, and elevated lactate, like this patient. More so, acidosis is a direct cause of hypotension and shock. Per one source " Cardiac contractility and cardiac output are reduced and arterial vasodilatation develops, which contributes to the development of hypotension". (source below) After appropriate treatment with insulin and glucose, this patient’s gap closed.
In full disclosure about this case, although his labs have improved, the etiology of his initial hypotension and shock picture is not yet clear. This is, however, often the case in medicine, and shock in particular, that a single, clear, elegant explanation doesn’t exist. And as such, we again thank Dr Levin for this honest and exciting case that allowed us to walk down the often confusing paths of shock and its attedant management in a real “choose your own adventure” fashion.
Citations: -https://img.ma-shops.com/hild/pic/image01646.jpg -https://ai2-s2-public.s3.amazonaws.com/figures/2017-08-08/4eb58c5284bc04a8a9c4325f003add3d36b4e18a/7-Table2-1.png -https://thecurbsiders.com/show-notes/88-acid-base-boy-bands-grandfather-clocks-joel-topf-md -https://www.medscape.org/viewarticle/718583_6