#euglycemic DKA

[liebermintz]

a peculiar comorbidity, part three

And to close this off, I want healthcare providers to do a few things. There are going to be a lot more cases like me. There are people out there who are fucking struggling. In fact, I'm sure most of the diabetes-related suicides out there were from late-in-life diabetics with an autism comorbidity. this shit isn't easy to deal with, especially when your comforts are now lethal. and it's not like you can just say "well, don't do it." do you have any idea how super-ingrained these comforts, these stims, these safe foods are to an autistic person? they run deep. and they run deep even when you're a kid. it's the main reason why applied behavior analysis is straight-up considered psychological torture in the autistic community - people suggest that just to rip an autistic person away from bad actions, only to realize way too late they're making them miserable. and right now, I'm going through one hell of an ABA session, only that it's my fucking pancreas that's playing pretend-psychiatrist. combine that with the "gotta keep you alive no matter what" mindset of every type 1 resource, endocrinologists, diabetes educators, and PCPs and you have yourself a system that is designed to kill neurodivergent late-in-life diabetics in a short amount of time. in a way, it's genocide. you're getting rid of one group of people in order to not have to deal with them down the line. in another way, it's a form of eugenics since it's designed to weed out the undesirables from the health pool, so they can take their time delaying closed artificial pancreas loops, fool-proof insertion kits that can't be ripped out during sleep or strenuous activity, 10/20-minute-peak insulins with two-hour total lifespan, seven-day patch pumps, stuff that doesn't exactly benefit a neurotypical diabetic at the moment since they're easily adaptable (plus there's this dogged "can't teach an old dog new tricks" mindset you see a lot in diabetic circles) but benefits a neurodivergent diabetic who has way more to worry about than high and low blood sugars. the healthcare industry doesn't give a shit about me. in fact, i'm pretty sure it wants me to die either by my own hand or by theirs.

but here I am, asshole. and here's my final demand: I want Tzield to be approved for honeymooning patients NOW.

I want late-in-life diabetics (priority going to those with neurodivergences) to automatically be added to pancreas and islet cell transplant lists upon diagnosis. you will see significantly less suicides, less deaths, less eugenics, less murder, less mistakes, less meltdowns, less burnout - if you let them on those lists and not just relegated those to life-long diabetics whose organs are starting to crap out on them.

I want all next-gen ultra-rapid-acting insulins to be released now. again, they're just Humalog with more shit.

I want insulin to be totally free. Forever.

I want, upon diagnosis, all diabetics to receive lifelong healthcare from the government, even after remission and surgical intervention. In fact, I want all healthcare to be free.

I want all clinicals for stem-cell effective-cures to widen their criteria to include cases like mine that are way more susceptible to early-onset DKA and euglycemic DKA. those are as lethal as severe hypoglycemic events, but you just wanna blame DKA on not having enough insulin in your system. that way, you can see if stuff like VX-880 and VX-264 have an Awakenings effect (works for a bit before it stops working) or if manages to stick around for longer. I want all clinicals for immunotherapies to have their ages expanded to 35.

And I want Beyond Type 1 to publish all three of my posts - uncensored - on their website if they ever run into it. No edits save for some basic proofreading.

Anything else is genocide.

[mcatmemoranda]

You expect to see ketonuria in someone who has been vomiting and not eating for days, but not glucosuria. So a urinalysis alone can clue you into DKA.

You have to have a diagnosis of diabetes, high blood sugar, and bicarbonate less than 15 (acidosis) to diagnose DKA.

If bicarbonate is below 15, start insulin gtt. Give lots of IV fluids. You will need insulin for the rest of your life whether it's type 1 or 2 diabetes. DKA is a risk factor for brain edema, electrolyte imbalance (hypokalemia), lactic acidosis.

VBG is as good as ABG if VBG oxygenation is greater than 75%.

Triggers for DKA: infection, menstruation increases risk

Fluids, insulin, electrolytes. Isotonic NS or 0.45 NS with other added electrolytes like K+. Start with LR or NS. Then can decrease to 0.45 NS as you add K+. Give fluids as if pt is 10% dehydrated over 48 hours. Start by giving fluids before insulin. Bolus fluids will help decrease glucose. Insulin gtt: 0.1 units per Kg per hour.

You give insulin until the anion gap closes. Can stop insulin gtt when bicarbonate is above 15. At that point, you need to start subQ insulin. You can give basal insulin at time of presentation. Lantus for example; 0.2 per kilogram. Can give SubQ insulin 1 hour before stopping the gtt.

If glucose drops more than 100 mg/dL/hour, you may need to add dextrose to the fluids. If blood glucose is 250 to 300 mg/dL, you can add glucose to fluids. This is to prevent dropping osmolarity too fast and prevent brain edema. Capillary leak can cause brain edema.

Bicarbonate can be given if you're worried about other organs shutting down due to the acidosis. pH below 6.9, can give Bicarbonate. Check bmp at least q4 hours. Insulin moves K+ into cells. Could check BMP q2 hours if you didn't give K+. Don't give K+ if there is EKG abnormality or no urine output.

Type 2 DM can also have DKA. Their phosphorus can be low, which can cause rhabdomyolysis. Check for evidence of rhabdomyolysis.

SGLT2 inhibitor can cause euglycemic DKA. They lower blood glucose by making you eliminate it. People with DM1 took SGLT2 inhibitor, which lowered their blood glucose. Then since they had lower blood glucose levels, they lowered the amount of insulin they took. So basically, they lowered their blood glucose, but then also were not getting glucose into cells. This then lead to DKA where the blood glucose level was normal, but they had ketone production. So these pts need treatment with insulin gtt and dextrose-containing fluid.

To get CME credit, go to:

This is from the post-test for this episode:

While both DKA itself and treatment of DKA have been associated with the development of cerebral edema, many RCTs have shown no difference in neuro outcomes when comparing 0.9% NaCl, 0.45% NaCl, and LR.   Key Point: The sodium chloride content (0.9% vs 0.45% vs LR) of intravenous fluids does not significantly influence the neurologic outcomes in children with diabetic ketoacidosis.  

Citation: Wolfsdorf JI, Glaser N, Agus M, Fritsch M, Hanas R, Rewers A, Sperling MA, Codner E. ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatr Diabetes. 2018 Oct;19 Suppl 27:155-177. doi: 10.1111/pedi.12701. PMID: 29900641.

Resolution of DKA: pH is greater than 7.3, bicarbonate is greater than 15, blood ketone level less than 0.6 mmol/L.

Blood glucose level does not play a role in determining whether a patient is in DKA or not. A patient is considered no longer in DKA when their pH is >7.3, bicarbonate is >15, and blood ketone level is <0.6 mmol/L.  

Key Point: While patients in DKA often present with hyperglycemia, it is not required for a diagnosis of DKA. Additionally, glucose levels play no role in determining the resolution of DKA.  

Citation: Evans K. Diabetic ketoacidosis: update on management. Clin Med (Lond). 2019;19(5):396-398. doi:10.7861/clinmed.2019-0284

Insulin has a short half-life (7-10 minutes), so when stopping an insulin drip, subcutaneous basal insulin should be given before the insulin drip is stopped or at the time of stopping the drip. This is due to the high likelihood of ketosis returning promptly without insulin on board. Additionally, there is a movement starting of giving basal insulin at the time of presentation along with the insulin drip. This gives a safety level of insulin, so there is less worry when stopping the insulin drip.

Key Point: Due to the risk of opening the anion gap back up without any insulin on board, basal insulin should either be administered at the time of presentation along with the insulin drip or immediately after stopping the insulin drip.  

Citation: Barski L, Brandstaetter E, Sagy I, Jotkowitz A. Basal insulin for the management of diabetic ketoacidosis. Eur J Intern Med. 2018 Jan;47:14-16. doi: 10.1016/j.ejim.2017.08.025. Epub 2017 Aug 31. PMID: 28864157.  

[brynnmclean]

Just read a message board post and learned that Euglycemic DKA is a thing. The poster got it because of medication, but it apparently can happen because of low caloric intake / fasting. :/

[step2ckmap]

Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors

Canagliflozin, Dapagliflozin, and Empagliflozin

Reduces reabsorption of glucose in the kidney in proximal convoluted tubule

Side effects:

Euglycemic DKA-> Ketones in urine, though BG usually <250 due to increased release of glucose in urine.

Hyperkalemia

Hyperlipidemia 

Vulvovaginal candidiasis (due to increased glucose in urine)

Fluid loss -> symptomatic hypotension or AKI

[type2diabetestreatments-blog]

UK doctor calls for DKA guidelines revision in bid to improve diagnosis

New Post has been published on http://type2diabetestreatment.net/diabetes-news/uk-doctor-calls-for-dka-guidelines-revision-in-bid-to-improve-diagnosis/

UK doctor calls for DKA guidelines revision in bid to improve diagnosis

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A UK doctor has called for an overhaul of guidance related to the diagnosis and management of diabetic ketoacidosis (DKA) in adults. DKA is a complication of type 1 diabetes and, in some cases, latent autoimmune diabetes of adults (LADA), characterised by a lack of insulin aggravated by high blood sugar levels and the build-up of ketone bodies in the blood. In a new editorial written in The Lancet, Dr Ketan Dhatariya, a diabetes and endocrinology consultant based at the Norfolk and Norwich University Hospitals NHS Trust, argues that our national guidance is laconic. He believes that the international recommendations we resort to are largely outdated, and that a number of modifications should be made, highlighting new evidence that has emerged since the American Diabetes Association's (ADA) last position statement on DKA in 2009. Dhatariya's proposed changes include the use of more criteria to define DKA and different management options for short-term complications of DKA. The problem with the diagnosis of DKA, as seen by Dhatariya, is twofold: the blood sugar cut-off point of 13.9 mmol/L to identify DKA is set too high, and DKA is too often diagnosed based on a single risk factor like the disruption of insulin treatment or elevated ketone levels. Drawing from accumulated professional experience, Dhatariya knows that many patients vulnerable to DKA can present with smaller increases in blood sugar levels than this cut-off point after lowering their insulin dose, reducing their food intake, or when ill. By referring to the standardised cut off score of 13.9 mmol/mol, euglycemic DKA (defined as DKA without marked hyperglycemia) seen in patients with gestational diabetes or those treated with SGLT2 inhibitors, can go amiss too. Euglycemic DKA is thought to occur when blood sugar levels are as low as 11.1 mmol/L. Dhatariya would also like to see introduced an alternate ketone testing method in the guidelines. Urine methods for the early diagnosis of DKA test for the ketone body acetoacetate, but do not usually detect for a separate ketone body known as beta-hydroxybutyrate (BHA). Recent studies have found BHA to be the predominant ketone body at the onset of DKA and suggest that the measurement of blood BHA is a more accurate predictor of ketosis than is the detection of acetoacetate through the urine. In terms of in-hospital care, Dhatariya urged simplified DKA management, similar to the Emergency Valuable Approach and Diabetes Education (EVADE) protocol used in US emergency rooms, to treat patients with mild and moderate DKA. Dhatariya concluded by calling for either new national guidelines or revised DKA international guidance that is evidence-based, practical, and easy to follow to be used by healthcare staff managing DKA in the UK.Type 2 Diabetes Treatment Type 2 Diabetes Diet Diabetes Destroyer Reviews Original Article

[liebermintz]

a peculiar comorbidity, part one

okay, so over the past few months, i've been dealing with this relatively new diagnosis of what the doctors think is type 1 diabetes, but what I hope is just some sort of weird insulin processing disorder (I had the A1C of a type 2 diabetic; the antibody reaction and the DKA admission of a type 1 diabetic; the C-peptide of a type 2 diabetic; the fat and protein bump of a nondiabetic) that might be LADA, might just be my body's way of doing type 1, might be something entirely new. either way, it's a pain in the ass not just in the expected ways (my grandparents refuse to recognize that my medical costs have gone up exponentially and think that the insurance company just automatically covers insulin and that it's the fault of the CVS for charging me $120 for 90 days of pen needles and $150 for insulin without coupon; they're part of that "fend for yourself" crowd; I've run head-first into how absolutely fucked up and monstrous the American healthcare system is, especially with the fact that no person on the executive branch has proposed a total end of the insulin pricing wars; I've run into the health food and wellness industry going full steam ahead, fucking up the minds of diabetics into thinking they need to chug laxative bread and laxative soda just to keep their blood sugar down; I've run into the FDA dragging their feet for approving life-altering treatments for people like me, like way-faster insulins that can close the loop for artificial pancreas systems AND Tzield - there's no reason those should take 10-30 years to make it to market, especially if all the next-gen ultra-rapid-acting insulins are just Novolog/Humalog with added shit), but it's a pain in the ass in ways nobody even really considers. I am autistic. I was autistic way before I was diabetic. I've been autistic all my life. that means I have a set variety of safe foods. a lot of weirdly-textured foods are what I like to call "danger foods," stuff like beans, most legumes, cheese by itself, most game meat, soup/hot liquid, etc. these foods scare me. and a lot of my safe foods are more snack food-based stuff - stuff like rice cakes, peanut butter sandwiches, Cheez-Its (I don't think that's real cheese in the Cheez-It), even the occasional dessert. stuff I can snack on easily. so imagine having a food-processing disorder that requires me to inject outside insulin every time I want to eat something that's not a free food. i'm not just experiencing the traditional onset of diabetes burnout and diabetes distress - no, i'm experiencing something entirely new, something that Nick Jonas and Priyanka Chopra (yes, I know Beyond Type 1 scours Tumblr and Social Media for posts - they are ultimately a content aggregator since they foolishly push keto diets to T!D patients, which most government and medical resources refuse to push due to the risk of developing euglycemic ketoacidosis) have never considered in their life. something that friends of mine who are on-the-spectrum and diabetic (they were diagnosed really early on) have never even considered.

[step2ckmap]

Diabetes Mellitus Type 2

More common (90%), adult, obese body type, rare DKA, strong polygenetic predisposition, treated with lifestyle oral agents or insulin

Initial treatment:

Lifestyle modification (diet, weight loss, exercise) 25% respond to this alone

DM2 Medical Management:

Metformin best initial medical therapy

Second add Sufonylurea if not controlled with metformin

Metformin: Inhibits gluconeogenesis

No risk of hypoglycemia, does not worsen obesity

Conraindicated in renal disease (lactic acidosis), liver disease

Sulfonylureas: Increase insulin secretion and insulin sensitivity

Glyburide, Glimepiride, Glipizide

Can cause hypoglycemia, weight gain, SIADH

DPP-IV Inhibitors: Block metabolism of incretins, increase post prandial glucose utilization

Sitagliptin, Linagliptin, Saxagliptin, Alogliptin

Thiazolidinediones: Increase peripheral insulin sensitivity

Rosiglitazone, Pioglitazone

Can worsen CHF, cause hepatocellular injury 

Alpha-glucosidase inhibitors: Block glucose absorption at intestinal lining

Acarbose, Miglitol

Flatulence, GI disturbance, diarrhea (think lactose intolerance)

SGLT2 Inhibitors: Decrease renal glucose absorption

Canagliflozin, Dapagliflozin, and Empagliflozin

UTI, hypoglycemia, euglycemic DKA

*If agents fail to control glucose, may use insulin. Long acting, plus short acting at mealtime