inpatient / endocrinology
Diabetic Ketoacidosis (DKA)
# *** Diabetic Ketoacidosis
# Type *** Diabetes
DKA if glucose >250, BHB >2, pH <7.3 OR Bicarb <18
Checklist
-- ABCs: intubate if AMS and not protecting airway
-- Chart Check: prior DKA, insulin regimen, issues with adherence
-- HPI Intake: symptoms, insulin use and adherence, infectious symptoms
-- Can't Miss: sepsis, need to be intubated
-- Admission Orders: glucose q2-4 hours, BHB, UA, lactate, trop and EKG, infectious workup, lipase, tox screen if concern,
-- Initial Treatment to Consider: fluids --> electrolyte repletion --> insulin drip; consider bicarb if severe acidosis; treat underlying etiology - abx, ACS pathway, etc
Assessment:
-- History: *** insulin use and adherence/access, infectious symptoms, sick contacts
-- Clinical: *** dehydration, polyuria, weight loss, N/V, abd pain, AMS
-- Exam: *** general appearance, AMS, volume status (mucous membrane, skin tugro, JVP, JVC), Kussmaul breathing (deep breaths to blow off CO2)
-- Data: *** glucose, bicarb, BHB, anion gap, VBG/lactate
-- Etiology/DDx: *** infection (PNA and UTI most common), insulin non-adherence, inflammatory state (pancreatitis), infarction, intoxication, medications (steroids, thiazides, SGLT2i)
The patient's HPI is notable for ***. Exam showed ***. Labwork and data were notable for ***. Taken together, the patient's presentation is most concerning for ***, with a differential including ***.
Plan:
Workup
-- f/u BHB, UA, lactate; consider trop, lipase, UDS
-- q hour glucose checks
-- q 2-4 VBG and BHB
Treatment
-- Fluids: *** Initial bolus LR ~1-2L, then hourly until resuscitated (usually 5-8L); switch to D5LR based on glucose levels; now s/p *** L of fluids
-- Electrolytes: *** q2 BMP, Mg, Phos until the gap closes, then q4 until K normalizes; replete PRN (K>3.3, Phos>1, Mag >1.2)
-- Potassium *** (<3.3 - 60 IV, hold insulin; 3.3-3.5 - 40mEq; 3.6-5.1 - 20mEq; >5.1 - none)
-- Insulin: *** bolus, then drip (both 0.1U/kg); maintain rate if >10% reduction or >50 drop (goal 50-100cc hour); hold for K<3.3 or glucose <70; basal-bolus with SSI upon resolution - basal to be given 2 hours before stopping IV drip; basal-bolus units based on home dose, or precipitant and weight
-- if pH <6.9, severe AMS, or severe kidney disease - can give 50mEq sodium bicarbonate, repeat q30-60minutes until pH >7
-- NPO - progress as tolerated
DKA Resolution:
-- Glucose 100-200
-- Tolerate Clear Liquid Diet
-- Alert, or Baseline Mental Status
AND 2 of 3:
-- Bicarb >18
-- pH >7.3
-- Anion gap <12
PDF coming soon!
If You Remember Nothing Else
DKA is the complex constellation of various physiological pathways that happen when the body is without insulin. The end result of low insulin is hypovolemia 2/2 osmotic diuresis and metabolic acidosis from ketones. Initially, ABCs and volume should be prioritized (patients usually present with a 5-8L deficit) followed closely by managing electrolyte disturbances, most notably hypokalemia. Hypokalemia and acidosis can be life-threatening (arrythmia, decreased cardiac contractility, diminished response to catecholamines/pressors, etc). Patients may present with hyperkalemia (in blood), but in actuality they are likely hypokalemic which will be exacerbated once insulin is added. After acidosis and electrolytes are addressed, then you can focus on the patient's glucose and insulin. The goal of insulin is to stop ketogenesis (acidosis) and close the anion gap. Once the patient is out of DKA, you can begin to switch back to a basal-bolus regimen.
Clinical Pearls
- Prioritize ABCs, volume, etiology THEN electrolytes (K+) THEN glucose/insulin; glucose won’t kill you, but hypokalemia and acidosis might (decreased cardiac contractility, diminished response to catecholamines, predisposition to arrhythmias)
- DKA usually has a 5-8 L deficit - resusciate with LR
- May present with hyperkalemia, but likely has low total body K; once insulin is in, serum K will tank - hypokalemia will limit the timing of insulin drip - get out ahead of it (same idea with Phos, but less life-threatening)
- Low insulin → hyperglycemia → osmotic diuresis → hypovolemia
- Low insulin → ketones (BHB) → metabolic acidosis → anion gap and bicarb taken up
- The goal of insulin is to stop ketogenesis (acidosis) and close the gap
- When you stop insulin drip, insulin is out of your system within minutes - the reason we need to overlap with long-acting by ~2 hours
- For every 1g/dL of albumin below 4, you should add 2.5 to the gap (albumin is an anion that is not included in the calculation of the gap)
- In general, the bicarb decrease should equal the increase in the anion gap (assuming euvolemia, so you can only tell when the patient is resuscitated), this is the basis of the delta-delta calculation
- Lipase, transaminases, and WBC may all be elevated with hyperglycemia and DKA in the absence of a specific infectious or intraabdominal pathology - might be red herring
- Don’t forget Sodium Correction when assessing hyponatremia and volume (add 0.02 * glucose-100) MD Calc Sodium Correction
- Kussmaul Respirations are deep breaths to blow off CO2 due to acidosis
- Vomiting may be a way for the body to correct acidosis by expelling gastric acid
- Acidosis can lead to peritoneal irritation which may be why patients sometimes have abd pain
- Urine Dip Ketone does not include BHB which is the main ketone in DKA
- Euglycemic DKA Causes - SGLT2i, EtOH liver disease, pregnancy
- Scary complications of DKA and treatment - mucormycosis, cerebral edema, arrhythmia, hypoglycemia
- Severe acidosis not correcting on its own is an indication for dialysis
- HHS same general principles, but no ketosis due to some insulin present, more dehydration, AMS, seizures, higher glucose
Trials and Literature
- Balanced Crystalloids (LR) vs Saline (NS) in adults with DKA - Subgroup analysis of pooled patients from SALT-ED (ED) and SMART (ICU) trials done at Vanderbilt that presented with DKA; Balanced crystalloids (LR or Plasma-Lyte) vs. saline - noting that it was like 90+% LR; Believed saline can cause hyperchloremic metabolic acidosis, which can also cause kidney injury (main finding of the above trials); LR also has more potassium which needs to be repleted in DKA; Outcomes - primary: time from ED presentation and DKA resolution AND secondary: time between initiation and discontinuation of insulin infusion; 94 patients received LR, 78 saline; DKA resolution - 13 vs. 16.9 hours (p=0.004); Insulin discontinued - 9.8 vs. 13.4 hours (p=0.03) (JAMA, 2020)
- Systematic review of bicarb in DKA - Essentially no good trials to support better outcomesMight be useful if pH<6.9, AMS, or severe kidney disease - use on an individual basisIf anything, more likely to cause cerebral edema in pediatric populationsBicarb would help by turning more acid (H+) to CO2 to be blown off, but likely already breathing at the maximal rate as compensation, so RR is limiting factor (Ann Intensive Care, 2011)
- Review of Acid-Base Disturbances in DKA (NEJM, 2015)
Other Resources
- The Cubsiders Podcast - DKA
- Core EM - DKA Episode
- Run the List - DKA Episode
