Acute metabolic emergency of insulin deficiency producing hyperglycemia, ketonemia, and anion-gap acidosis.
Also known as: DKA, diabetic ketoacidosis, ketoacidosis, euglycemic DKA
Overview
Life-threatening complication of insulin deficiency defined by the triad of hyperglycemia (glucose ≥200 mg/dL) or known diabetes (euglycemic DKA if glucose <200), ketonemia (β-hydroxybutyrate ≥3.0 mmol/L), and high anion-gap metabolic acidosis (venous pH <7.30 and/or bicarbonate <18 mEq/L).
Epidemiology
Annual incidence ~8 per 1,000 patients with diabetes. Most common in T1DM but increasingly seen in T2DM (~10-30% of DKA admissions), particularly with SGLT2 inhibitors. In-hospital mortality <1% with modern care; higher in elderly and those with comorbid sepsis.
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Question 1EndocrineEasy
A 45-year-old male presents to the ED with altered mental status, severe abdominal pain, and nausea. He is a known type 1 diabetes mellitus (T1DM) patient on insulin but has been ill for 3 days and unable to keep food down. Labs: glucose 480, pH 7.18, bicarbonate 11, anion gap 28, beta-hydroxybutyrate 6.2 mmol/L, K+ 5.9. Which of the following is the most critical initial intervention before starting insulin?
AIV potassium repletion
BEmpiric IV antibiotics and blood cultures
CIV phosphate repletion
DSodium bicarbonate infusion
EIV saline and potassium check
Reveal answer & full explanation
Correct answer: E — IV saline and potassium check
AIV potassium repletion
BEmpiric IV antibiotics and blood cultures
CIV phosphate repletion
DSodium bicarbonate infusion
EIV saline and potassium check✓
Why IV saline and potassium check is correct
Diabetic ketoacidosis (DKA) management priority: IV fluids first — normal saline (NS) 1 L/hour for the first hour to correct dehydration and hypoperfusion.
Potassium must be checked before starting insulin: insulin drives K+ into cells and can cause fatal hypokalemia if given when K+ is already low.
Algorithm (2024 ADA/EASD consensus): if K+ below 3.5 — hold insulin and give K+ replacement (about 10 mEq/hour) first; if K+ 3.5–5.0 — add 20–30 mEq KCl per liter of IV fluid alongside insulin, targeting K+ 4–5; if K+ above 5.0 — withhold potassium, start insulin, and recheck K+ within 2 hours.
Why the others are wrong
Sodium bicarbonate infusion — considered only if pH is below 7.0 (2024 consensus); this patient's pH is 7.18, so bicarbonate is not appropriate.
IV phosphate repletion — phosphate is given only for a level below 1.0 mg/dL or symptomatic hypophosphatemia, never ahead of volume resuscitation; routine repletion has no outcome benefit in DKA.
Empiric IV antibiotics and blood cultures — infection is the most common DKA precipitant and cultures are reasonable, but no fever, leukocytosis, or infectious source is described, and antibiotics do nothing about the volume depletion and potassium shift that make insulin dangerous.
IV potassium repletion — tempting because DKA causes a large total-body potassium deficit, but with K+ 5.9 (above 5.0) the 2024 consensus algorithm withholds potassium and rechecks K+ within 2 hours, starting KCl in the IV fluids once K+ falls to 5.0 or below.
Additional high-yield points
Insulin: regular insulin 0.1 units/kg/hour IV drip once K+ confirmed above 3.5.
Phosphate: replace if below 1.0 or symptomatic.
Monitor electrolytes, glucose, and anion gap (AG) every 1–2 hours.
Switch to subcutaneous insulin once DKA has resolved (beta-hydroxybutyrate below 0.6 mmol/L with pH 7.30 or higher or bicarbonate 18 or higher) and the patient is tolerating PO.
Question 2EndocrineMedium
A 29-year-old woman with type 1 diabetes presents with nausea, vomiting, and abdominal pain. She ran out of insulin 2 days ago. Labs: glucose 520 mg/dL, pH 7.18, bicarbonate 10 mEq/L, anion gap 24, ketones positive in blood and urine. What is the most important initial treatment?
AIV potassium chloride infusion
BSodium bicarbonate infusion
CIntravenous half-normal saline bolus
DIV insulin bolus
EIV normal saline fluid resuscitation
Reveal answer & full explanation
Correct answer: E — IV normal saline fluid resuscitation
AIV potassium chloride infusion
BSodium bicarbonate infusion
CIntravenous half-normal saline bolus
DIV insulin bolus
EIV normal saline fluid resuscitation✓
Why IV normal saline fluid resuscitation is correct
In diabetic ketoacidosis (DKA) management, the first step is aggressive IV fluid resuscitation with isotonic saline (500-1,000 mL per hour for the first 2-4 hours in adults without cardiac or kidney compromise) to restore intravascular volume.
Insulin is started after fluids and only after potassium is 3.5 mEq/L or higher, because insulin drives K+ intracellularly and hypokalemia must be corrected first.
Why the others are wrong
Intravenous half-normal saline bolus — hypotonic fluid is the wrong choice for initial volume expansion; 0.9% saline is given first to refill the intravascular space, and 0.45% saline belongs to the later replacement phase once perfusion is restored and the corrected sodium is normal or high.
IV insulin bolus — An insulin bolus without fluids can worsen hemodynamics; fluids must be initiated first.
Sodium bicarbonate infusion — Bicarbonate is not routinely given in DKA; it is considered only for severe acidosis with pH below 7.0 (2024 ADA/EASD consensus), and this patient's pH is 7.18.
IV potassium chloride infusion — potassium is a real priority, since total-body K+ is depleted and insulin will drive it into cells, but the serum level is often normal or even high at presentation and has not been reported here; potassium is added to the fluids once the level and urine output are known, so restoring intravascular volume with isotonic saline still comes first.
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Uremic acidosis — Advanced CKD with elevated BUN/creatinine; non-ketotic anion gap acidosis
Diagnostic workup
Diagnostic criteria
2024 ADA/EASD/JBDS/AACE/DTS consensus (D-K-A): D = glucose ≥200 mg/dL or known diabetes regardless of glucose; K = β-hydroxybutyrate ≥3.0 mmol/L (or urine ketones ≥2+); A = venous pH <7.30 and/or bicarbonate <18 mEq/L. Euglycemic DKA = glucose <200 with the ketone and acid criteria. An anion gap >12 supports the diagnosis but is no longer a first-line criterion (older 2009 criteria used glucose >250 and the anion gap). Severity: mild (pH 7.25-7.30 or HCO3 15-18, alert), moderate (pH 7.00-7.24 or HCO3 10 to <15, alert or drowsy), severe (pH <7.00 or HCO3 <10, stupor or coma).
Labs
POC glucose, then serum glucose (≥200 mg/dL, or any value with known diabetes; <200 in euglycemic DKA)
VBG or ABG: pH <7.30, HCO3 <18 mEq/L
Anion gap >12 (calculate: Na − [Cl + HCO3])
Serum or urine ketones; serum β-hydroxybutyrate is the preferred marker (≥3.0 mmol/L supports DKA; urine ketones ≥2+ if unavailable)
BMP: serum K may be normal or elevated initially despite total-body depletion; phosphate, magnesium often low
CBC (leukocytosis common even without infection), lipase, urinalysis, blood/urine cultures if infection suspected
ECG to assess for hyperkalemia and ischemic precipitants
Pregnancy test in women of reproductive age
Imaging
CXR if infection suspected
CT head only if focal deficits or persistent altered mentation despite metabolic correction (cerebral edema risk in pediatrics)
Diagnostic algorithm
Parameter
DKA
HHS
Typical population
T1DM (any age)
Elderly T2DM
Glucose
≥200 mg/dL or known diabetes (<200 in euglycemic DKA)
≥600 mg/dL
pH
<7.30
≥7.30
Bicarbonate
<18 mEq/L
≥15 mEq/L (usually ≥18)
Anion gap
>12 (high)
Variable, usually normal
Ketones (serum/urine)
Strongly positive (β-hydroxybutyrate ≥3.0 mmol/L)
Mild or absent (β-hydroxybutyrate <3.0 mmol/L)
Effective osmolarity
Variable
>300 mOsm/kg effective (or >320 total)
Mental status
Alert → drowsy → coma
Often profoundly altered
Onset
Hours to 1-2 days
Days to weeks
Mortality
<1%
5-20%
Comparison of DKA vs HHS — overlap exists; mixed presentations occur.
Treatment
First-line
IV fluids — 0.9% NaCl or a balanced crystalloid (lactated Ringer's, Plasma-Lyte) 15-20 mL/kg in the first hour, then transition to 0.45% NaCl if corrected serum Na normal/elevated; add 5-10% dextrose when glucose falls below 250 (from the start in euglycemic DKA) to allow continued insulin infusion
Insulin — IV regular insulin 0.1 unit/kg bolus then 0.1 unit/kg/hr infusion (omit bolus in pediatrics); titrate to lower glucose 50-75 mg/dL/hr; reduce to 0.05 unit/kg/hr once dextrose is added and continue until ketoacidosis resolves; SC rapid-acting insulin every 1-2 h is an alternative for uncomplicated mild-moderate DKA
Potassium — check before insulin: if K <3.5, HOLD insulin and replace K (about 10 mEq/hr) until K >3.5; if 3.5-5.0, add 20-30 mEq KCl per liter of fluid to keep K 4-5; if >5.0, no K replacement initially but recheck within 2 h (2024 consensus; older 2009 protocols used 3.3 and 5.2)
Bicarbonate — consider only if pH <7.0 in adults (2024 consensus; older adult protocols and ISPAD pediatric guidance use 6.9): 100 mEq in 400 mL sterile water over 2 h
Identify and treat precipitating cause (infection, MI, missed insulin)
Complications
Cerebral edema — feared complication in pediatric DKA (mortality up to 25%); presents 4-12 h into treatment with headache, bradycardia, altered mental status; treat with mannitol or hypertonic saline; avoid overly rapid fluid resuscitation
Hypokalemia, hypophosphatemia, hypomagnesemia during insulin therapy
Hypoglycemia from prolonged insulin infusion without dextrose
Mucormycosis (rhinocerebral) — rare but devastating; consider in immunocompromised DKA patient with facial pain or black eschar
PANCE pearls
Euglycemic DKA (glucose <200 mg/dL by 2024 criteria) — increasingly common with SGLT2 inhibitors: stop the SGLT2 inhibitor and start the insulin infusion with 5-10% dextrose from the outset, titrating to ketone and acid clearance rather than glucose. Prevent it by holding SGLT2 inhibitors during acute illness and 3-4 days before surgery.
Hyperglycemia causes true translocational (dilutional) hyponatremia, not pseudohyponatremia: add ~1.6 mEq/L to the measured Na for each 100 mg/dL of glucose above normal (some references use 2.4); corrected Na guides fluid choice. True pseudohyponatremia is a lab artifact, e.g., from severe hypertriglyceridemia.
Total-body potassium is depleted even when serum K is normal/high — insulin will rapidly drive K intracellularly causing dangerous hypokalemia.
Resolution is defined by ketone clearance (β-hydroxybutyrate <0.6 mmol/L) plus venous pH ≥7.30 or bicarbonate ≥18; bicarbonate can lag and the anion gap can mislead because saline causes a hyperchloremic non-gap acidosis during recovery.
Always overlap subcutaneous insulin BEFORE stopping the infusion — failing to overlap is the most common cause of rebound DKA.
References
ADA 2026 — American Diabetes Association Professional Practice Committee. 6. Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises: Standards of Care in Diabetes—2026 (Diabetes Care 2026;49 Suppl 1:S132-S149)
ADA Consensus 2024 — Hyperglycemic Crises in Adults With Diabetes: A Consensus Report (Umpierrez et al., Diabetes Care 2024)
ISPAD 2022 — ISPAD Clinical Practice Consensus Guidelines 2022: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State
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