Endocrinology · PANCE / PANRE

Diabetic Ketoacidosis (DKA)

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 (>250 mg/dL, or near-normal in euglycemic DKA), ketonemia/ketonuria, and high anion-gap metabolic acidosis (pH <7.30, 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?
  • ASodium bicarbonate infusion
  • BIntravenous insulin drip
  • COral electrolyte replacement
  • DIV saline and potassium check
Reveal answer & full explanation
Correct answer: D — IV saline and potassium check
  • ASodium bicarbonate infusion
  • BIntravenous insulin drip
  • COral electrolyte replacement
  • DIV 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: if K+ below 3.5 — hold insulin and give K+ replacement first; if K+ 3.5–5.5 — start KCl 20–40 mEq/hour concurrent with insulin; if K+ above 5.5 — hold potassium and start insulin.

Why the others are wrong

  • A) Sodium bicarbonate infusion — indicated only if pH is below 6.9; this patient's pH is 7.18, so bicarbonate is not appropriate.
  • B) Intravenous insulin drip — must be deferred until K+ is confirmed above 3.5 to prevent life-threatening hypokalemia.
  • C) Oral electrolyte replacement — inadequate in severe DKA with altered mental status and nausea; IV route is required.

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 when the anion gap closes 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?
  • AOral fluids and subcutaneous insulin
  • BIV insulin bolus
  • CSodium bicarbonate infusion
  • DIV normal saline fluid resuscitation
Reveal answer & full explanation
Correct answer: D — IV normal saline fluid resuscitation
  • AOral fluids and subcutaneous insulin
  • BIV insulin bolus
  • CSodium bicarbonate infusion
  • DIV 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 (1–2 L per hour initially) 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

  • A) Oral fluids and subcutaneous insulin — Oral fluids are insufficient given the severity of dehydration in DKA; IV fluids and IV insulin are required.
  • B) IV insulin bolus — An insulin bolus without fluids can worsen hemodynamics; fluids must be initiated first.
  • C) Sodium bicarbonate infusion — Bicarbonate is not routinely given in DKA; it is reserved only for pH below 6.9.
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Risk factors

  • Insulin omission or pump failure (most common precipitant in established T1DM)
  • Infection (UTI, pneumonia, sepsis) — accounts for ~30-40% of cases
  • New-onset T1DM (initial presentation in ~30% of pediatric cases)
  • Acute illness: MI, stroke, pancreatitis, trauma
  • Drugs: SGLT2 inhibitors (euglycemic DKA), glucocorticoids, atypical antipsychotics, cocaine
  • Pregnancy (can develop at lower glucose levels)

Pathophysiology

Absolute or relative insulin deficiency combined with counter-regulatory hormone excess (glucagon, cortisol, catecholamines, growth hormone) drives unrestrained hepatic gluconeogenesis and glycogenolysis (hyperglycemia), lipolysis (free fatty acids), and hepatic ketogenesis (β-hydroxybutyrate, acetoacetate). Osmotic diuresis causes dehydration, potassium and phosphate depletion. Ketoacids generate a high anion-gap metabolic acidosis.

Clinical presentation

Symptoms

  • Polyuria, polydipsia, fatigue progressing over hours to days
  • Nausea, vomiting, diffuse abdominal pain (mimics surgical abdomen, especially in children)
  • Altered mental status from drowsiness to coma (correlates with osmolarity, not pH)
  • Weight loss, weakness

Signs / physical exam

  • Kussmaul respirations — deep, rapid, sighing breathing as respiratory compensation
  • Fruity (acetone) breath odor
  • Signs of dehydration: tachycardia, hypotension, dry mucous membranes, poor skin turgor
  • Hypothermia or normothermia even with underlying infection (peripheral vasodilation from acidosis)

Classic findings

Young T1DM patient with Kussmaul respirations, fruity breath, abdominal pain, and altered sensorium after missing insulin doses.

Differential diagnosis

  • Hyperosmolar hyperglycemic state (HHS) — Older T2DM patients; profound hyperglycemia (>600), marked hyperosmolarity (>320), minimal ketosis, pH >7.30; more profound dehydration and altered mental status
  • Starvation ketosis — Mild ketosis with normal/low glucose, bicarbonate >18, no significant acidosis
  • Alcoholic ketoacidosis — Chronic alcohol use, recent binge with poor intake, vomiting; low/normal glucose; positive ketones; responds to glucose + thiamine
  • Lactic acidosis — Elevated lactate (sepsis, shock, metformin); no ketones; high anion gap
  • Toxic alcohol ingestion (methanol, ethylene glycol) — High anion + osmolar gap, no ketones, visual changes (methanol) or oxalate crystals (ethylene glycol)
  • Salicylate toxicity — Mixed respiratory alkalosis + anion-gap acidosis, tinnitus, hyperthermia; elevated salicylate level
  • Uremic acidosis — Advanced CKD with elevated BUN/creatinine; non-ketotic anion gap acidosis

Diagnostic workup

Diagnostic criteria

ADA criteria: glucose >250 mg/dL (or <250 in euglycemic DKA), arterial pH <7.30, bicarbonate <18, anion gap >12, positive serum/urine ketones. Severity: mild (pH 7.25-7.30), moderate (7.00-7.24), severe (<7.00).

Labs

  • POC glucose, then serum glucose (>250 mg/dL; may be normal in euglycemic DKA)
  • VBG or ABG: pH <7.30, HCO3 <18 mEq/L
  • Anion gap >12 (calculate: Na − [Cl + HCO3])
  • Serum or urine ketones; β-hydroxybutyrate is the preferred quantitative marker
  • 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

ParameterDKAHHS
Typical populationT1DM (any age)Elderly T2DM
Glucose>250 mg/dL (may be normal in euglycemic DKA)>600 mg/dL
pH<7.30>7.30
Bicarbonate<18 mEq/L>18 mEq/L
Anion gap>12 (high)Variable, usually normal
Ketones (serum/urine)Strongly positiveMild or absent
Effective osmolarityVariable>320 mOsm/kg
Mental statusAlert → drowsy → comaOften profoundly altered
OnsetHours to 1-2 daysDays to weeks
Mortality<1%5-20%
Comparison of DKA vs HHS — overlap exists; mixed presentations occur.

Treatment

First-line

  • IV fluids — 0.9% NaCl 15-20 mL/kg in the first hour, then transition to 0.45% NaCl if corrected serum Na normal/elevated; switch to D5-0.45% NaCl when glucose <200-250 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
  • Potassium — check before insulin: if K <3.3, HOLD insulin and replace K (10-40 mEq/hr) first; if 3.3-5.2, add 20-30 mEq KCl per liter of fluid; if >5.2, no K replacement initially but recheck q2h
  • Bicarbonate — only if pH <6.9 (controversial; consider 100 mEq in 400 mL 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
  • Acute kidney injury from volume depletion
  • Venous thromboembolism (hyperosmolar, dehydrated state)
  • Aspiration pneumonia if obtunded
  • Mucormycosis (rhinocerebral) — rare but devastating; consider in immunocompromised DKA patient with facial pain or black eschar

PANCE pearls

  • Euglycemic DKA (glucose <250) — increasingly common with SGLT2 inhibitors; hold SGLT2i during illness and 3-4 days before surgery.
  • Pseudohyponatremia: each 100 mg/dL of glucose above normal lowers measured Na by ~1.6 mEq/L; corrected Na guides fluid choice.
  • Total-body potassium is depleted even when serum K is normal/high — insulin will rapidly drive K intracellularly causing dangerous hypokalemia.
  • Anion gap closure (not bicarbonate normalization) is the marker of resolution; bicarbonate may lag due to hyperchloremic acidosis from saline.
  • Always overlap subcutaneous insulin BEFORE stopping the infusion — failing to overlap is the most common cause of rebound DKA.

References

  • ADA 2025 — American Diabetes Association Standards of Care in Diabetes—2025: Diabetes Technology and Hyperglycemic Crises (Diabetes Care 2025; 48 Suppl 1)
  • 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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