1. When you are suspicious for DKA do you get a VBG or an ABG? How good is a VBG for determining acid/base status? 
2. Do you use serum or urine ketones to guide your diagnosis and treatment of DKA?
3. Do you use IV bicarbonate for the treatment of severe acidosis in DKA? If so, when?
4. When do you start an insulin infusion in patients with hypokalemia? Bolus or no bolus?
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EM Lyceum 
Venous blood gases are perfectly sufficient for the determination of acid-base status; if I see a high anion gap metabolic acidosis with hyperglycemia I have a diagnosis of DKA and won’t need to check for ketones; if I want to check for them, I check serum ketones; I don’t use bicarb for DKA, ever, and I don’t give a bolus of insulin, just start the infusion. Mind you, this is for my patients (dogs and cats) only. I am a veterinarian.
VBG always. Rarely check serum acetone and just rely on anion gap. No bicarb and no bolus. Usually just 2L of NS then start drip. Replace potassium early if hypokalmia or even low normal. I routinely see insulin boluses and early drips prior to rehydration and K check though. Curious if others are using LR with push to stop using NS in acidodic patients (literature recently on sepsis/acidosis). Have just used NS for last 10 years and do it out of habit/comfort…..
I never use NS for these, only Normosol R (similar to Plamalyte A), which is a more balanced crystalloid. I learned this from my ED mentor and this has become common practice now in veterinary medicine for DKA.
1. the Ph is virtually the same (0.03 difference) see below
Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Anthony L Byrne1, Michael Bennett2,3, Robindro Chatterji3, Rebecca Symons3, Nathan L Pace5 andPaul S Thomas1,4,*
Article first published online: 3 JAN 2014
Abstract
Peripheral venous blood gas (PVBG) analysis is increasingly being used as a substitute for arterial blood sampling; however, comparability has not been clearly established. To determine if the pH, PCO2 and PO2 obtained from PVBG analysis is comparable with arterial blood gas (ABG) analysis. A search was conducted of electronic databases as well as hand-searching of journals and reference lists through December 2012 to identify studies comparing PVBG with ABG analysis in adult subjects. A systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement. A meta-analysis using a random effects model was used to calculate the average difference (bias) and the limits of agreement for the venous and arterial pH, PCO2 and PO2. A total of 18 studies comprising 1768 subjects were included in the meta-analysis. There was considerable heterogeneity between studies with I2 approaching 100%. There was little difference between the pH obtained from the PVBG and the ABG, with the arterial pH typically 0.03 higher than the venous pH (95% confidence interval 0.029–0.038). The venous and arterial PCO2 were not comparable because the 95% prediction interval of the bias for venous PCO2 was unacceptably wide, extending from −10.7 mm Hg to +2.4 mm Hg. The PO2 values compared poorly, the arterial PO2 typically 36.9 mm Hg greater than the venous with significant variability (95% confidence interval from 27.2 to 46.6 mm Hg). PVBG analysis compares well with ABG analysis for pH estimations in adults but not to the PCO2 or PO2. These differences are sufficiently large to be of clinical significance.
2. There are only 3 lab abnormalities that are liseted as part of the diagnostic criteria for DKA. According to the American Diabetes Association the presence of ketones in the blood OR the urine is one of the diagnostic criteria. They say “the presence” of ketone so the actual level is meaningless. You can do a quick bedside urine dip to confirm ketones. see below from Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2006;29:2739-2748..
“diagnostic criteria for DKA are plasma glucose >250 mg/dL and arterial pH <7.3 and presence of ketonemia and/or ketonuria"
3. I never use Bicarb in DKA, ESPECIALLY IN KIDS!!!!!!! see below
Bicarbonate in diabetic ketoacidosis – a systematic review
Horng Ruey Chua,1 Antoine Schneider,1 and Rinaldo Bellomo1,2
Ann Intensive Care. 2011; 1: 23. Published online Jul 6, 2011
Results
From 508 potentially relevant articles, 44 were included in the systematic review, including three adult randomized controlled trials (RCT) on bicarbonate administration versus no bicarbonate in DKA. We observed a marked heterogeneity in pH threshold, concentration, amount, and timing for bicarbonate administration in various studies. Two RCTs demonstrated transient improvement in metabolic acidosis with bicarbonate treatment within the initial 2 hours. There was no evidence of improved glycemic control or clinical efficacy. There was retrospective evidence of increased risk for cerebral edema and prolonged hospitalization in children who received bicarbonate, and weak evidence of transient paradoxical worsening of ketosis, and increased need for potassium supplementation. No studies involved patients with an initial pH < 6.85.
Conclusions
The evidence to date does not justify the administration of bicarbonate for the emergent treatment of DKA, especially in the pediatric population, in view of possible clinical harm and lack of sustained benefits.
4. In my opinion management of potassium for DKA patients in the ER is an important part of treatment and almost always overlooked. see below from the ADA.
Hyperglycemic Crises in Adult Patients With Diabetes
A consensus statement from the American Diabetes Association
Abbas E. Kitabchi, PHD, MD1, Guillermo E. Umpierrez, MD2, Mary Beth Murphy, RN, MS, CDE, MBA1 and Robert A. Kreisberg, MD3
Potassium
Despite total-body potassium depletion (40,57), mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises. Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration. To prevent hypokalemia, potassium replacement is initiated after serum levels decrease to 3.3 mEq/l to avoid arrhythmias or cardiac arrest and respiratory muscle weakness (57–58).
K 3.3
K = 3.3-5.3 – add 20-30 mEq of K in each liter of fluid
K > 5.3 – do not give K



sorry, i messed up the quotation for point #4
Hyperglycemic Crises in Adult Patients With Diabetes
A consensus statement from the American Diabetes Association
Abbas E. Kitabchi, PHD, MD1, Guillermo E. Umpierrez, MD2, Mary Beth Murphy, RN, MS, CDE, MBA1 and Robert A. Kreisberg, MD
Potassium
Despite total-body potassium depletion (40,57), mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises. Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration. To prevent hypokalemia, potassium replacement is initiated after serum levels decrease to 3.3 mEq/l to avoid arrhythmias or cardiac arrest and respiratory muscle weakness (57–58).
K 3.3
K = 3.3-5.3 – add 20-30 mEq of K in each liter of fluid
K > 5.3 – do not give K
one more time. i guess the images from the figure do not paste right so here is full text.
Potassium
Despite total-body potassium depletion (40,57), mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises. Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration. To prevent hypokalemia, potassium replacement is initiated after serum levels decrease to less then 5.3 mEq/l, assuming the presence of adequate urine output at 50 ml/h). Generally, 20–30 mEq potassium in each liter of infusion fluid is sufficient to maintain a serum potassium concentration within the normal range of 4–5 mEq/l. Rarely, DKA patients may present with significant hypokalemia. In such cases, potassium replacement should begin with fluid therapy, and insulin treatment should be delayed until potassium concentration is restored to 3.3 mEq/l to avoid arrhythmias or cardiac arrest and respiratory muscle weakness (57–58).
-VBGs correlate well. I think ALIEM has a PV card on this.
-think our institute likes serum, but to guide dx and tx, I use AG, UA, and VBG. If they feel awful or are vomiting everywhere and spilling ketones in their urine, my argument for LR over NS gets more winnable at our shop I this instance.
– no on bicarb, unless ICU specifically asks for it, which tends to be infrequent.
– if hypokalemic, hmmm. It’s going to take awhile to fix this pt, and going slow is probably a good idea. I try to avoid IV bolus of insulin either way. If super low K, like under 2.5, I would probably replete PO / IV if they can tolerate PO. I’d empirically give IV magnesium unless I was smart & lucky enough to order a mag level it off the bat. Once over k 3, I’d start insulin drip without bolus and continue K repletion. Probably q1-2hr k check while in ED, watch for arrhythmia, etc.
I use vbg and anion gap. The vbg fudge factor is 0.036. In the clinical setting the Abg=Vbg but I need to know the 0.036 number because I teach residents. I very rarely use bicarb. I use bicarb for people who have a ph < 7(although doing so in kids makes me very nervous and I hold off on this if possible) and are showing signs of hemodynamic instability. Any use of IV insulin essentially a waste of time and potentially dangerous therefore no bolus for me