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Diabetic Ketoacidosis (DKA) - BMJ Best Practice 2025 Summary

What is DKA?

DKA is an acute, potentially fatal metabolic complication of diabetes defined by a triad of:
  • Hyperglycaemia (blood glucose usually ≥11.1 mmol/L; 10% present with "euglycaemic DKA" <11.1)
  • Ketonaemia (beta-hydroxybutyrate ≥3 mmol/L)
  • Metabolic acidosis (arterial pH <7.3, bicarbonate <18 mmol/L)
Symptoms develop rapidly, usually within 24 hours or less.

Pathophysiology

Insulin deficiency + excess counter-regulatory hormones (glucagon, catecholamines, cortisol, GH) causes:
  1. Increased gluconeogenesis and glycogenolysis → hyperglycaemia
  2. Lipolysis → free fatty acids → hepatic ketone production → ketonaemia and acidosis
  3. Osmotic diuresis → volume depletion and electrolyte loss

Causes / Triggers

  • Most common: Missed/inadequate insulin, infection (UTI, pneumonia)
  • Others: MI, stroke, pancreatitis, surgery, trauma
  • Drugs: Corticosteroids, SGLT2 inhibitors (can cause euglycaemic DKA), atypical antipsychotics, immune checkpoint inhibitors, cocaine
  • New-onset type 1 DM presents with DKA in 6-25% of cases

Clinical Features

CategoryFeatures
SymptomsPolyuria, polydipsia, polyphagia, weakness, weight loss, nausea, vomiting, abdominal pain
SignsDry mucous membranes, poor skin turgor, tachycardia, hypotension, Kussmaul breathing, acetone breath
SevereAltered consciousness, stupor, coma

Investigations

  • Blood glucose - typically elevated (sometimes normal in euglycaemic DKA)
  • ABG/VBG - metabolic acidosis (pH <7.3, bicarb <18)
  • Beta-hydroxybutyrate - preferred ketone marker (≥3 mmol/L confirms DKA)
  • Electrolytes - K+ often normal/high on admission despite total body depletion; Na+ often low
  • Anion gap - >12 (high anion gap metabolic acidosis)
  • Urinalysis, FBC, ECG, cultures - to identify precipitant

Severity Classification

MildModerateSevere
pH 7.25-7.30pH 7.00-7.24pH <7.00
Bicarb 15-18Bicarb 10-14Bicarb <10
AlertDrowsyStupor/Coma

Management (The 5 Pillars)

1. Fluid Replacement

  • Start with 0.9% normal saline (isotonic)
  • Titrate based on haemodynamic status; switch to 0.45% NaCl if corrected sodium is normal/elevated

2. Insulin

  • Continuous IV infusion of short-acting insulin is preferred
  • Do NOT start insulin until K+ >3.5 mmol/L (risk of fatal hypokalaemia)
  • Subcutaneous rapid-acting insulin analogues may be used for mild/moderate uncomplicated DKA as an alternative

3. Potassium

  • Replace K+ to keep levels 4-5 mmol/L
  • Start replacement when K+ <5.0 mmol/L (once insulin is running)
  • If K+ <3.5 mmol/L: hold insulin, replace K+ first

4. Bicarbonate

  • Not routinely recommended
  • Consider only if arterial pH <7.0 with severe haemodynamic compromise

5. Phosphate

  • Not routinely replaced unless <1 mmol/L with respiratory/cardiac compromise

Resolution Criteria

DKA is resolved when ALL of:
  • Capillary/plasma ketones <0.6 mmol/L
  • Venous pH ≥7.3 or bicarbonate ≥18 mmol/L
  • Blood glucose <11.1 mmol/L (ideally)
Transition to subcutaneous insulin with a 1-2 hour overlap before stopping IV insulin.

Complications of Treatment

  • Hypokalaemia (most common, potentially fatal)
  • Hypoglycaemia
  • Cerebral oedema (rare but life-threatening - avoid overly rapid fluid replacement)
  • Pulmonary oedema, hypoxaemia

Prognosis

  • In-hospital mortality in the US: ~0.4% (improved from 1.1% in 2000)
  • Much higher in low/middle-income countries (up to 30-41%)
  • Mortality increases with age, comorbidities, and severe acidosis
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