Notes · Medicine · 3 November 2026

Diabetic ketoacidosis

Definition

• Diabetic ketoacidosis (DKA) is an acute, life‑threatening metabolic emergency characterized by hyperglycaemia, metabolic acidosis due to accumulation of ketone bodies, and a high anion‑gap. It results from absolute or relative insulin deficiency combined with increased counter‑regulatory hormones (glucagon, catecholamines, cortisol, growth hormone).

Epidemiology

• DKA accounts for 4–9 % of all hospital admissions in people with diabetes and is the most common cause of death in newly diagnosed type 1 diabetes.
• Incidence is higher in adolescents and young adults with type 1 diabetes (≈30–80 episodes per 1 000 patient‑years) and in patients with type 2 diabetes during periods of severe stress or infection.
• Mortality in high‑income countries is <1 % but rises to 5–10 % in low‑resource settings.

Aetiology (Common precipitating factors)

• Infection – urinary tract infection, pneumonia, skin/soft‑tissue infection.
• Insulin omission – missed doses, pump failure, or inadequate insulin therapy.
• New‑onset diabetes – especially type 1, where diagnosis is delayed.
• Acute illness or stress – myocardial infarction, stroke, pancreatitis, trauma, surgery.
• Medications – glucocorticoids, thiazide diuretics, atypical antipsychotics, SGLT2 inhibitors (can cause euglycaemic DKA).
• Substance abuse – alcohol binge, cocaine, amphetamines.
• Pregnancy – increased insulin resistance and vomiting.

Pathophysiology (Step‑by‑step)

1. Insulin deficiency → reduced glucose uptake in peripheral tissues → hyperglycaemia.
2. Unopposed glucagon (and other counter‑regulatory hormones) → hepatic glycogenolysis and gluconeogenesis → further rise in blood glucose.
3. Lipolysis – insulin normally inhibits hormone‑sensitive lipase; its deficiency allows triglyceride breakdown → free fatty acids (FFAs) released into circulation.
4. Ketogenesis – the liver converts FFAs to ketone bodies (β‑hydroxybutyrate, acetoacetate, acetone).
5. Metabolic acidosis – accumulation of β‑hydroxybutyrate and acetoacetate lowers serum bicarbonate, producing a high anion‑gap metabolic acidosis.
6. Osmotic diuresis – hyperglycaemia exceeds renal reabsorption threshold (~180 mg/dL) → glucose spills into urine, pulling water and electrolytes → polyuria, dehydration, and loss of Na⁺, K⁺, Mg²⁺, PO₄³⁻.
7. Electrolyte shifts – insulin deficiency and acidosis cause potassium to move out of cells; total body potassium is depleted despite normal or high serum K⁺ initially.

Clinical Features (Typical presentation)

• General: polyuria, polydipsia, weight loss, fatigue, nausea, vomiting, abdominal pain.
• Dehydration signs: dry mucous membranes, decreased skin turgor, tachycardia, hypotension, orthostatic drop.
• Respiratory: Kussmaul respirations (deep, rapid breathing) as a compensatory response to metabolic acidosis.
• Neurological: altered mental status ranging from lethargy to coma; may have a fruity (acetone) odor on breath.
• Cardiovascular: tachyarrhythmias due to electrolyte disturbances, especially hyper‑ or hypokalaemia.
• Physical exam: may reveal signs of underlying precipitant (e.g., lung crackles in pneumonia).

Investigations (Key laboratory and bedside tests)

• Capillary blood glucose: usually >250 mg/dL (13.9 mmol/L).
• Arterial blood gas (ABG): pH <7.30, bicarbonate ≤18 mmol/L, PaCO₂ low (respiratory compensation).
• Serum electrolytes: Na⁺ (often low‑normal), K⁺ (may be normal/high but total body deficit), Cl⁻, Mg²⁺, PO₄³⁻.
• Serum ketones: β‑hydroxybutyrate >3 mmol/L; urine dipstick for acetoacetate (may be falsely low if β‑hydroxybutyrate predominates).
• Anion gap: calculated as Na⁺ – (Cl⁻ + HCO₃⁻); >12 mmol/L indicates high‑gap acidosis.
• Renal function: BUN and creatinine to assess dehydration severity.
• Complete blood count (CBC): leukocytosis may suggest infection.
• Serum osmolality: useful in mixed hyperosmolar‑hyperglycaemic state.
• ECG: look for peaked T waves (hyperkalaemia) or arrhythmias.
• Additional tests based on precipitant: chest X‑ray, urine culture, blood cultures, COVID‑19 PCR, etc.

Management (ADA 2024 guideline – 3‑phase approach)

1. Initial Resuscitation (First hour)

• Airway, Breathing, Circulation – give supplemental O₂ if SpO₂ <94 %.
• Fluid replacement – start isotonic saline (0.9 % NaCl) at 15–20 mL/kg (≈1 L) over the first hour.
• Assess volume status – if signs of severe hypovolaemia, consider adding 5 % dextrose after the initial 2 L of saline if glucose falls <250 mg/dL.

2. Insulin Therapy (Start after initial fluids)

• Continuous IV regular insulin: 0.1 U/kg/h (≈0.14 U/kg/h for rapid‑acting analogues) without a loading bolus (bolus not recommended in 2024 ADA).
• Goal: reduce glucose by 50–70 mg/dL (2.8–3.9 mmol/L) in the first hour, then 100 mg/dL per hour thereafter.
• Transition to subcutaneous insulin once DKA is resolved (pH >7.30, bicarbonate >15 mmol/L, anion gap closed) and patient can eat; give subQ rapid‑acting insulin 0.05–0.1 U/kg plus basal insulin, overlapping IV insulin for 1–2 h.

3. Electrolyte Management

• Potassium: if serum K⁺ <3.3 mmol/L, hold insulin and give 20–30 mmol KCl in 1 L saline; if K⁺ 3.3–5.0 mmol/L, add 20–30 mmol KCl/L of fluid; if K⁺ >5.0 mmol/L, give K⁺‑free fluids but monitor closely.
• Phosphate: replace if PO₄³⁻ <1.0 mg/dL and patient is symptomatic or has cardiac dysfunction (0.08–0.16 mmol/kg phosphate).
• Magnesium: replace if Mg²⁺ <1.5 mg/dL (1–2 g MgSO₄ over 24 h).

4. Ongoing Monitoring (Every 1–2 h)

• Vitals: blood pressure, heart rate, respiratory rate, temperature.
• Glucose: bedside capillary every hour until stable, then every 2–4 h.
• Electrolytes & ABG: every 2–4 h until anion gap closes.
• Fluid balance: input‑output chart; aim for net negative balance of 2–3 L over first 24 h.

5. Treat Underlying Cause

• Start appropriate antibiotics for infection, discontinue offending drugs (e.g., SGLT2 inhibitors), manage myocardial infarction, etc.

6. Prevention of Recurrence

• Patient education on sick‑day rules, insulin dose adjustment, glucose monitoring, and when to seek care.

Complications (Potential adverse events)

• Cerebral oedema – rare but most feared; presents with headache, altered mental status, seizures; risk higher in children, rapid correction of hyperglycaemia, or excessive fluid administration.
• Hypokalaemia – can precipitate arrhythmias; occurs after insulin shifts K⁺ intracellularly.
• Hypoglycaemia – from over‑insulinisation or rapid glucose fall; monitor glucose closely.
• Acute kidney injury – due to severe dehydration and prerenal azotemia.
• Thromboembolism – hypercoagulable state in DKA; consider prophylactic low‑molecular‑weight heparin in high‑risk patients.
• Infection – both a precipitant and a possible consequence of immune dysfunction.

High‑Yield Exam Points

• Diagnostic triad: hyperglycaemia >250 mg/dL, metabolic acidosis (pH <7.30 or HCO₃⁻ ≤18 mmol/L), and ketonaemia/ketonuria.
• Anion gap formula: Na⁺ – (Cl⁻ + HCO₃⁻); >12 mmol/L indicates high‑gap acidosis.
• Fluid choice: start with 0.9 % NaCl; switch to 0.45 % NaCl or add dextrose when glucose <250 mg/dL to avoid hypoglycaemia.
• Insulin without loading dose is current recommendation (ADA 2024).
• Potassium rule: never start insulin if K⁺ <3.3 mmol/L; replace first.
• Cerebral oedema risk: children, rapid ↓ glucose (>100 mg/dL/h), excessive fluids >3–4 L in 24 h.
• Euglycaemic DKA: can occur with SGLT2 inhibitors; glucose may be <250 mg/dL, so ketones are essential to check.
• Resolution criteria: pH >7.30, HCO₃⁻ >15 mmol/L, anion gap ≤12 mmol/L, and glucose <200 mg/dL.

Practice questions

1. A 22‑year‑old man with newly diagnosed type 1 diabetes presents with polyuria, vomiting, Kussmaul respirations, and a blood glucose of 480 mg/dL. ABG shows pH 7.20, HCO₃⁻ 14 mmol/L, and serum β‑hydroxybutyrate 5 mmol/L. Which of the following is the most appropriate initial fluid therapy?
A. 0.45 % NaCl 500 mL over 30 min
B. 0.9 % NaCl 1 L over the first hour
C. 5 % dextrose in 0.9 % NaCl 1 L over the first hour
D. Lactated Ringer’s solution 1 L over the first hour

Answer: B — start isotonic saline 0.9 % NaCl 15–20 mL/kg (≈1 L) in the first hour to restore intravascular volume.

2. In a patient with DKA, the serum potassium is 3.0 mmol/L. What is the correct next step?
A. Begin insulin infusion immediately
B. Give 20 mmol KCl in 1 L saline and re‑check potassium before insulin
C. Give 40 mmol KCl in 500 mL saline and start insulin simultaneously
D. No potassium replacement needed; insulin will correct it

Answer: B — insulin should be withheld until K⁺ is ≥3.3 mmol/L; give potassium replacement first.

3. Which of the following statements about cerebral oedema in DKA is true?
A. It is more common in adults than in children.
B. Rapid reduction of serum glucose by >150 mg/dL in the first hour decreases risk.
C. Early signs include headache, vomiting, and decreasing level of consciousness.
D. Treatment consists of high‑dose insulin bolus.

Answer: C — early cerebral oedema presents with headache, vomiting, and altered mental status; prompt recognition is essential.

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AI-assisted study material for exam revision. Always confirm with standard textbooks and current guidelines; not medical advice.