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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:

Increased gluconeogenesis and glycogenolysis → hyperglycaemia
Lipolysis → free fatty acids → hepatic ketone production → ketonaemia and acidosis
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

Category	Features
Symptoms	Polyuria, polydipsia, polyphagia, weakness, weight loss, nausea, vomiting, abdominal pain
Signs	Dry mucous membranes, poor skin turgor, tachycardia, hypotension, Kussmaul breathing, acetone breath
Severe	Altered 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

Mild	Moderate	Severe
pH 7.25-7.30	pH 7.00-7.24	pH <7.00
Bicarb 15-18	Bicarb 10-14	Bicarb <10
Alert	Drowsy	Stupor/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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