Description
- Triad: hyperglycaemia + ketosis + metabolic acidosis
- Absolute (or near-absolute) insulin deficiency
- Contrast HHS: enough insulin to suppress ketogenesis, not enough to prevent extreme hyperglycaemia
2024 diagnostic criteria - all 3 required
| D | Glucose >=11.1 mmol/L OR known diabetes at any glucose |
| K | beta-hydroxybutyrate >=3.0 mmol/L (or urine ketones >=2+) |
| A | pH <7.3 and/or HCO3 <18 mmol/L |
- Anion gap dropped as a primary criterion - too many confounders of acid-base
- "Known diabetes at any glucose" exists to capture euglycaemic DKA
Euglycaemic DKA
- Glucose <11 (may be normal), full ketoacidosis
- SGLT2i (dominant cause), pregnancy, starvation, EtOH, hepatic glycogen depletion
- Missed if you screen on glucose - measure ketones on the gas in any acidotic diabetic
HHS - for contrast
- Glucose >=33.3 mmol/L
- Effective osmolality >300 (or total >320) mOsm/kg
- BOHB <3.0, pH >=7.3, HCO3 >=15
- Altered mental state no longer required for diagnosis
- Overlap DKA/HHS in ~1/3 - treat the ketoacidosis
Epidemiology
- ~4-9 per 1000 person-years in T1DM
- Presenting feature of T1DM in ~25-30% of new diagnoses
- Increasingly in T2DM - ketosis-prone, and SGLT2i-associated
- Mortality <1% in Australian centres (>5% in elderly, HHS, comorbid)
- Recurrent DKA: young, socioeconomic disadvantage, insulin omission, mental health comorbidity
- Aboriginal and Torres Strait Islander: higher DKA admission rates, younger age
Aetiopathogenesis
Mechanism
- Insulin deficiency + counter-regulatory excess (glucagon, catecholamines, cortisol, GH)
- inc gluconeogenesis + glycogenolysis -> hyperglycaemia
- dec peripheral glucose uptake
- -> osmotic diuresis -> profound total-body water, Na, K, Mg, PO4 depletion
- Unrestrained lipolysis -> FFA to liver
- Glucagon inc carnitine palmitoyltransferase-1 -> beta-oxidation
- -> acetoacetate + beta-hydroxybutyrate (the dominant ketone, ~3:1)
- -> high anion gap metabolic acidosis
- Urine nitroprusside detects acetoacetate only -> can appear to "worsen" during treatment as BOHB converts back
Potassium paradox
- Total body K deficit 3-5 mmol/kg
- Measured K normal or high: acidosis + insulin deficiency + hypertonicity drive K extracellular
- Insulin will drop it fast - the single commonest lethal error
Precipitants - always name one
- Infection (~30-40%)
- Insulin omission / pump failure (commonest in young)
- New-onset diabetes
- MI, stroke, pancreatitis, trauma, surgery
- Drugs: SGLT2i, glucocorticoids, atypical antipsychotics, checkpoint inhibitors (autoimmune T1DM), thiazides
- Pregnancy (DKA at lower glucose, faster)
Diagnosis1 exam ›
Bedside
- Polyuria, polydipsia, weight loss, vomiting, abdominal pain
- Kussmaul respiration, ketotic fetor, dehydration
- Abdominal pain is often the acidosis itself - but do not miss a surgical precipitant
Bloods
- VBG - pH, HCO3, K (venous adequate; arterial adds nothing)
- Capillary/serum beta-hydroxybutyrate - diagnosis, severity and resolution
- BGL, UEC, Mg, PO4, FBE, CRP, lipase, septic screen, ECG, troponin if indicated
- Osmolality if mixed picture
Severity
| BOHB | pH | HCO3 | Mental state | |
|---|---|---|---|---|
| Mild | <=6 | >7.25 | >=15 | Normal |
| Moderate | <=6 | 7.0-7.25 | 10-<15 | Normal/drowsy |
| Severe | >6 | <7.0 | <10 | Stupor/coma |
Traps
- Leucocytosis is usual in DKA - only >25 or left shift suggests infection
- Na: correct for glucose (add ~2.4 mmol/L per 5.5 above normal). A high measured Na = severe water deficit
- Amylase/lipase often raised without pancreatitis
- Normal or low HCO3 with normal pH -> mixed picture (vomiting alkalosis)
- Creatinine falsely raised by acetoacetate on some assays
Management
Fluid, then potassium, then insulin - in that order of priority.
1. Fluid
- Isotonic saline or balanced crystalloid 500-1000 mL/hr for first 2-4 hr
- Balanced crystalloid preferred - faster resolution, less hyperchloraemic acidosis
- 250 mL aliquots if elderly, HF or CKD
- Then maintenance + ongoing deficit; typical total deficit 5-7 L
2. Potassium - before or with insulin
- K <3.5: replace at 10 mmol/hr and HOLD insulin until >3.5
- K 3.5-5.0: replace with fluids, target 4-5
- K >5.0: no replacement, recheck in 2 hr
- Measure at baseline, 2 hr after insulin, then 4-hourly
3. Insulin
- Fixed-rate IV infusion 0.1 units/kg/hr
- No bolus needed
- Mild/moderate uncomplicated DKA may be managed with 1-2 hourly SC rapid-acting insulin
- Continue usual basal insulin through the infusion
- Add dextrose 5-10% once glucose <14 mmol/L, keep glucose ~11 - insulin continues until the ketosis clears, not the glucose
- Aim BOHB fall >=0.5 mmol/L/hr; if not, increase the infusion rate
4. Resolution and transition
- Resolved when: BOHB <3.0 (preferred marker), pH >=7.3, HCO3 >=15
- SC basal-bolus, total daily 0.3-0.6 units/kg if insulin-naive
- Overlap basal insulin >=1-2 hr before stopping the infusion (rebound DKA otherwise)
- Patient eating before transition
Not routine
- Bicarbonate - only pH <7.0, and evidence is poor (paradoxical CSF acidosis, hypokalaemia, delayed ketone clearance)
- Phosphate - only if <0.3 mmol/L or cardiac/respiratory/haemolytic compromise
Before discharge
- Name and treat the precipitant
- Sick-day plan, ketone meter, diabetes educator, endocrine follow-up
- If SGLT2i-associated: cease the SGLT2i; withhold 3 days pre-operatively
- Review for insulin omission and psychosocial drivers if recurrent
Associations
- T1DM; ketosis-prone T2DM
- SGLT2i therapy
- Pregnancy - euglycaemic, lower threshold, fetal risk
- Checkpoint-inhibitor diabetes (fulminant, presents in DKA, C-peptide flat)
- Other autoimmune disease: coeliac, thyroid, Addison's
- Eating disorder / insulin restriction ("diabulimia")
- Pancreatic disease, cystic fibrosis-related diabetes
- Alcohol and starvation ketosis (overlapping biochemistry, different treatment)
Natural history & complications
- Corrects within 12-24 hr with adequate therapy
- Mortality driven by the precipitant, not the acidosis
Complications
- Hypokalaemia - commonest preventable death
- Cerebral oedema
- Mostly children/young adults; mortality ~20-25%, morbidity high
- Risk: rapid osmolar shift, excess fluid, severe acidosis, high urea, bicarbonate use
- Headache, falling GCS, bradycardia + hypertension after initial improvement
- -> mannitol or hypertonic saline, do not delay for imaging
- Hypoglycaemia (inadequate dextrose cover)
- Rebound ketosis from premature infusion cessation
- Hyperchloraemic metabolic acidosis from saline (benign, resolves)
- VTE (esp. HHS), aspiration, ARDS, AKI
- Recurrent DKA -> excess mortality; treat as a red flag for psychosocial need
7 of 7 sections written · drafted 2026-09-12