GRAND ROUNDS 05 · DISEASE EDUCATION

DKA

Diabetic ketoacidosis — starving in a sea of sugar
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DKA = absolute (or relative) insulin deficiency → the triad of hyperglycemia + ketosis + anion-gap metabolic acidosis. Without insulin, glucose can't enter cells — the body burns fat, the liver floods with ketones, and the blood turns acidic while sugar spills into the urine. Triggers: infection · missed/insufficient insulin · new-onset diabetes · MI / stroke / pancreatitis / stress (the 5 I's).
1Pathophysiologyno insulin → cascade
1Insulin deficiency — absolute (type 1) or relative + counter-regulatory surge (glucagon, cortisol, catecholamines).
2Hyperglycemia — glucose can't enter cells + hepatic gluconeogenesis & glycogenolysis pour more out.
3Cell starvation — no intracellular glucose → switch to fat breakdown (lipolysis) → free fatty acids.
4Ketogenesis — liver converts FFAs to ketoacids (β-hydroxybutyrate, acetoacetate) → anion-gap acidosis.
5Osmotic diuresis — glucosuria drags water + Na/K/PO₄ out → dehydration, electrolyte loss, hypovolemia.
2Presentation

Osmotic: polyuria, polydipsia, weight loss, fatigue, blurred vision — often over hours to a day or two.

Acidosis & volume: Kussmaul breathing (deep, sighing), fruity / acetone breath, tachycardia, dry mucosa, hypotension, poor turgor.

The mimic: abdominal pain, nausea, vomiting — can look surgical. Altered mentation tracks osmolality & acidosis; frank coma is a red flag.

SSeveritygrade the acidosis
GRADEpHHCO₃⁻MENTAL
Mild7.25–7.3015–18alert
Moderate7.00–7.2410–<15alert / drowsy
Severe<7.00<10stupor / coma
HHS>7.30>18Glu>600, osm>320

Grade by pH / HCO₃ / mentation, not the glucose number. Euglycemic DKA (SGLT2 inhibitors, pregnancy, starvation) hides at glucose <250.

TTriggersthe 5 I's — find & treat
Infection (#1)Insulin missedIschemia / MI New-onset (Initial)Infarct / strokePancreatitis SGLT2 inhibitorPregnancySteroids · drugs
6Differentialhigh anion-gap · MUDPILES
  • HHS (little/no ketosis)
  • Alcoholic ketoacidosis
  • Starvation ketosis
  • Lactic acidosis / sepsis
  • Uremia (renal failure)
  • Toxic alcohols (MeOH, EG)
  • Salicylate toxicity
  • Isoniazid · iron
PSpecial Populations
PEDSHighest cerebral-edema risk. Correct slowly; avoid fluid boluses beyond volume needs; watch for headache/↓GCS.
SGLT2Euglycemic DKA — acidotic with near-normal glucose. Check ketones/gas if symptomatic; hold the drug.
PREGDKA at lower glucose, develops fast, threatens fetus. Treat aggressively, monitor closely.
▲The Mechanismno insulin → starve → ketones → acid
starving in a sea of sugar
WHY THE CELL STARVES WHILE SUGAR RISES glucose · fat · ketones · acid
▉ A SEA OF GLUCOSE (gold hexagons) — but it can't get in ▉ STARVING CELL no fuel inside GLUT channel LOCKED — no insulin key ① NO INSULIN → glucose locked out → cell starves FAT broken down ② lipolysis ③ free fatty acids LIVER makes ketones ④ KETONES β-OHB · acetoacetate ⑤ ACIDOSIS anion gap ↑, pH ↓ hyperglycemia → osmotic diuresis dehydration + Na/K/PO₄ loss
Hyperglycemia
Glu ≥ 200
sugar spills → osmotic diuresis
Ketosis
β-OHB ↑
fat → ketoacids from the liver
Acidosis
pH < 7.3 · gap ↑
HCO₃ < 18, high anion gap
⚠ The Potassium Paradox

Osmotic diuresis + acidosis shift K⁺ out of cells → serum K may look normal or HIGH while total-body K is severely depleted. Insulin drives K back into cells — serum K falls fast. Verify & replace K before/with insulin; never start insulin if K < 3.5.

4Diagnosticsthe triad + the math

The diagnostic TRIAD: hyperglycemia (glucose ≥200 or known DM) · anion-gap metabolic acidosis (pH <7.3, HCO₃ <18) · ketonemia / ketonuria (measure β-hydroxybutyrate — the dominant ketone; urine dipstick underreads it).

Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻)   (>12 = high)

Corrected Na⁺ = measured + 1.6 × (glucose − 100)/100   — glucose falsely lowers Na

Effective osm = 2×Na⁺ + glucose/18   — >320 & altered → HHS overlap

Corrected K⁺ — acidosis masks depletion; recheck as pH corrects.

DKA vs HHS: DKA = ketoacidosis, glucose often 350–800, hours-to-days, type 1>2. HHS = little/no ketosis, glucose >600, osm >320, profound dehydration, days-to-weeks, elderly type 2. Overlap exists.

▲Treat the Gapglucose falls first — the gap lags
CLOSE THE GAP, NOT JUST THE GLUCOSE two curves over time
time on insulin infusion → GLUCOSE — falls fast ↓ glu < 250 → add D5 ANION GAP — closes slower gap closed = resolved
Continue the insulin infusion until the anion gap closes (HCO₃/pH normalize, β-OHB clears) — not when glucose alone is normal. Add dextrose when glucose < 250 (hold ~200) so you can keep insulin running.
5TreatmentFLUIDS → K → INSULIN · per protocol
Fluids first isotonic crystalloid 0.9% NaCl / balanced, ~1 L bolus — restore volume before/alongside insulin.
Check potassium — K < 3.5 → hold insulin, replace K first. K 3.5–5.0 → give insulin + add K to fluids.
Insulin infusion ~0.1 U/kg/hr IV (± bolus) — closes the gap. Don't start if K low.
Add dextrose (D5/D10) when glucose < 250 — keep insulin running until the gap closes.
Potassium to fluids to keep K 4–5; replace phosphate/Mg if very low.
Find the trigger — infection, MI, missed insulin, pancreatitis. Treat it or DKA won't clear.
Avoid bicarbonate routinely — reserve for severe acidemia (pH < 7.0) per protocol.
CResolution & Transitionwhen it's over
CRITERIONTARGET
Anion gapclosed (≤12)
HCO₃⁻ / pH≥15–18 · >7.30
β-OHBcleared / <0.6
Patientalert & eating

Transition to SC insulin only when gap closed & eating — overlap the SC basal dose 1–2 h before stopping the drip or the gap reopens.

7Critical Proceduressequencing is the skill
⚠ Order & safety rules
  • Fluids before insulin — insulin into an empty tank drops BP & worsens perfusion.
  • K before/with insulin — never start insulin if K < 3.5; insulin will crash it further.
  • Never stop the insulin drip for hyperglycemia alone — add dextrose and keep it running until the gap closes.
  • Watch cerebral edema (esp. peds): headache, ↓GCS, bradycardia, vomiting after initial improvement → treat, slow correction.
  • Skip routine bicarbonate — no outcome benefit; risks hypokalemia, paradoxical CNS acidosis, edema.
PPitfalls & Pearls
  • Treat the GAP, not the glucose. Normal sugar + open gap = still in DKA.
  • K before insulin. A "normal" serum K hides total-body depletion.
  • Cerebral edema in kids — correct slowly; new headache/↓GCS is an emergency.
  • Euglycemic DKA (SGLT2, pregnancy) — check ketones/gas even if glucose is normal.
  • Kussmaul ≠ primary lung problem — it's respiratory compensation for the acidosis.
REMEMBER — Fluids → Potassium → Insulin. Treat the GAP not the glucose. K before insulin (never if <3.5). Add D5 at <250. Find the trigger. Slow in kids — watch for cerebral edema.
DDisposition
ICU / STEP-DOWN
  • Severe (pH <7.0, HCO₃ <10)
  • ↓GCS, hemodynamic instability
  • Peds / cerebral-edema risk
  • Frequent labs & drip titration
FLOOR / HOME
  • Mild & gap closing on Rx
  • Tolerating PO, trigger treated
  • SC insulin transition done
  • Education + follow-up
Sheet
DKA
Series / No.
GRAND ROUNDS 05
Part No.
CC-GR-05
Rev
A
Status
EDUCATION REFERENCE — NOT A PROTOCOL. VERIFY LOCALLY.

SOURCES: ADA/EASD/JBDS/AACE/DTS, Hyperglycemic Crises in Adults: A Consensus Report (Diabetes Care 2024) · ADA Standards of Care in Diabetes · Marino, The ICU Book; Tintinalli, Emergency Medicine (DKA management). Doses & thresholds educational — not medical advice & not a protocol; reference for trained clinicians only. Verify all drugs, doses & treatments against local protocol & current guidelines. Full disclaimer: crashcard.co/legal. © 2026 Claustrum LLC d/b/a Crash Card · crashcard.co · Printed in Minnesota.