Diabetic Emergencies
Diabetic emergencies include DKA and HHS. DKA requires insulin infusion, fluid resuscitation, and potassium replacement following the JBDS guidelines. HHS requires cautious rehydration over 48 hours with low-dose insulin.
Key Facts
DKA diagnostic criteria: Blood glucose >11 mmol/L (or known DM), ketones >3 mmol/L (or ketonuria ≥2+), pH <7.3 and/or bicarbonate <15 mmol/L DKA treatment: 0.9% NaCl fluid resuscitation (per JBDS protocol) + fixed-rate insulin infusion (FRII) 0.1 units/kg/hr + potassium replacement HHS diagnostic criteria: Blood glucose >30 mmol/L, serum osmolality >320 mOsm/kg, no significant ketonaemia/acidosis HHS treatment: Cautious fluid replacement over 48 hours (aim 50% deficit replacement in first 12h); insulin ONLY if ketones >1 or glucose not falling with fluids Potassium management in DKA: Replace if K⁺ <5.5; hold if K⁺ >5.5 — insulin drives K⁺ intracellularly; hypokalaemia is a major cause of death Cerebral oedema is the most serious complication of DKA treatment in children — occurs in ~1%; high mortality Fixed-rate insulin infusion (FRII): 50 units Actrapid in 50mL 0.9% NaCl at 0.1 units/kg/hr; do NOT bolus insulin JBDS (Joint British Diabetes Societies) guidelines are the UK standard for DKA and HHS management
Overview
Key Facts
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are the two major hyperglycaemic emergencies. Both are potentially fatal without treatment. DKA predominantly affects type 1 diabetes (but can occur in type 2), while HHS occurs in type 2 diabetes.
Epidemiology
DKA accounts for approximately 8,000-10,000 admissions per year in England. In-hospital mortality for DKA is approximately 0.5-2% (higher in elderly and those with significant comorbidity). HHS has a higher mortality of approximately 15-20% despite being less common. DKA is the most common cause of death in young people with type 1 diabetes.
Aetiology
DKA triggers:
- Infection (most common precipitant ~40%)
- Non-adherence to insulin (especially in young people)
- New diagnosis of type 1 diabetes
- Acute illness, surgery, trauma
- Drugs: Corticosteroids, SGLT2 inhibitors (can cause euglycaemic DKA)
HHS triggers:
- Infection (most common)
- MI, stroke
- Non-adherence to medications
- New diagnosis of type 2 diabetes
Pathophysiology
DKA: Insulin deficiency + counter-regulatory hormone excess → hyperglycaemia + lipolysis → ketogenesis (acetoacetate, beta-hydroxybutyrate, acetone) → metabolic acidosis. Osmotic diuresis causes dehydration (average 5-8L deficit).
HHS: Relative insulin deficiency (enough to suppress ketogenesis but not hyperglycaemia) → profound hyperglycaemia → severe osmotic diuresis → extreme dehydration (average 8-12L deficit) → hyperosmolality → altered consciousness.
Clinical Presentation
DKA Presentation
- Polyuria, polydipsia, weight loss
- Nausea, vomiting, abdominal pain (may mimic surgical abdomen)
- Kussmaul breathing (deep, sighing respirations — compensatory for acidosis)
- Ketotic breath (pear drops/acetone smell)
- Dehydration (dry mucous membranes, reduced skin turgor, tachycardia)
- Altered consciousness (10-15% present with GCS <12)
HHS Presentation
- Insidious onset over days to weeks
- Profound dehydration (often more severe than DKA)
- Altered consciousness, confusion, drowsiness, coma
- Focal neurological signs (may mimic stroke)
- NO significant ketoacidosis
- Often elderly with multiple comorbidities
Red Flags
- pH <7.1 — severe DKA, requires critical care
- Potassium <3.5 or >6.0 — life-threatening; correct before/during insulin therapy
- Osmolality >350 — severe HHS; high mortality
- New confusion or GCS deterioration in DKA — cerebral oedema (especially children)
- Euglycaemic DKA (glucose <14 with ketoacidosis) — SGLT2 inhibitor use
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| DKA | High glucose, ketones, acidosis | Glucose, ketones, VBG, U&Es |
| HHS | Very high glucose (>30), high osmolality, no acidosis | Glucose, osmolality, U&Es |
| Alcoholic ketoacidosis | Alcohol history, ketoacidosis, glucose may be low/normal | Clinical, ketones, glucose |
| Starvation ketosis | Fasting, mild ketosis, no significant acidosis | Clinical, ketones |
| Lactic acidosis | Acidosis without ketones, high lactate | ABG, lactate |
| Sepsis | Fever, source, organ dysfunction | Blood cultures, CRP, lactate |
Diagnosis / Investigation
Bedside
- Capillary blood glucose: Immediately
- Capillary/blood ketones: β-hydroxybutyrate — >3 mmol/L diagnostic for DKA
- VBG/ABG: pH, bicarbonate, lactate, potassium
- Urine dipstick: Ketonuria, UTI
- ECG: Hyperkalaemia/hypokalaemia changes
- Weight: For insulin infusion calculation
Bloods
- U&Es: Potassium (CRITICAL — guide replacement), sodium (corrected), creatinine, urea
- FBC: WCC (infection trigger — note WCC may be elevated in DKA without infection)
- CRP: If infection suspected
- Serum osmolality: Calculated: 2(Na⁺) + glucose + urea (all in mmol/L) — >320 = HHS
- Blood cultures: If febrile
- HbA1c: If new diagnosis
- Amylase/lipase: May be elevated in DKA (not always pancreatitis)
Imaging
- CXR: If pneumonia suspected as trigger
- CT head: If focal neurology in HHS (exclude stroke)
Special Tests
- Hourly capillary glucose and ketones: Guide insulin adjustment
- VBG at 1h, 2h, 4h, 6h, 12h, 24h: Monitor resolution
Management
DKA Management (JBDS Protocol)
Fluid resuscitation:
- 0.9% NaCl: 1L over 1h, 1L over 2h, 1L over 2h, 1L over 4h, 1L over 4h, 1L over 6h
- Switch to 10% glucose (125mL/hr) when glucose <14 mmol/L (continue insulin to clear ketones)
Fixed-rate insulin infusion (FRII):
- 0.1 units/kg/hr (e.g., 7 units/hr for 70kg patient)
- Continue patient's background long-acting insulin (prevent rebound DKA)
- Do NOT bolus insulin
Potassium replacement:
- K⁺ >5.5: No potassium added
- K⁺ 3.5-5.5: 40mmol KCl per litre of fluid
- K⁺ <3.5: Senior review; aggressive replacement before insulin
Resolution targets (within first 24h):
- Ketones falling by ≥0.5 mmol/L/hr
- Bicarbonate rising by ≥3 mmol/L/hr
- Glucose falling by ≥3 mmol/L/hr
- If not achieving targets → increase FRII by 1 unit/hr
HHS Management (JBDS Protocol)
- Cautious rehydration: 0.9% NaCl — aim to replace 50% of estimated fluid deficit in first 12h, remainder over next 12-24h
- Insulin: Only start if ketones >1 mmol/L or glucose not falling with fluids alone; low rate 0.05 units/kg/hr
- Aim: Glucose fall ≤5 mmol/L/hr; osmolality fall ≤3-8 mOsm/kg/hr (too rapid correction risks osmotic demyelination and cerebral oedema)
- VTE prophylaxis: LMWH — high thromboembolic risk
- Potassium replacement: As per DKA protocol
Referral Criteria
- Severe DKA (pH <7.1, K⁺ <3.5, GCS <12) — critical care
- HHS — HDU/critical care recommended
- Children with DKA — paediatric protocol; cerebral oedema risk
- New diagnosis diabetes — diabetes specialist nurse and endocrinology review
- Recurrent DKA — diabetes psychology review for adherence support
Prognosis
- DKA mortality: ~0.5-2% (higher in elderly and those with comorbidity)
- HHS mortality: ~15-20% (largely due to older age, comorbidity, and thrombotic complications)
- Cerebral oedema (paediatric DKA): ~1% incidence; ~25% mortality; risk factors include young age, new diagnosis, excessive fluid rate, rapid glucose fall
- Recurrent DKA: Strong predictor of future complications and premature mortality in type 1 diabetes
- Post-discharge: All patients need diabetes specialist review within 24-48h; insulin dose optimisation
Other Relevant Information
DKA vs HHS Comparison
| Feature | DKA | HHS |
|---|---|---|
| Glucose | >11 mmol/L | >30 mmol/L |
| Ketones | >3 mmol/L | <1 mmol/L |
| pH | <7.3 | >7.3 |
| Bicarbonate | <15 mmol/L | >15 mmol/L |
| Osmolality | Variable | >320 mOsm/kg |
| Dehydration | 5-8L | 8-12L |
| Onset | Hours | Days to weeks |
| Mortality | 0.5-2% | 15-20% |
| Insulin | FRII 0.1 u/kg/hr | Low dose or none initially |
JBDS DKA Treatment Targets
| Parameter | Target |
|---|---|
| Ketones | Fall by ≥0.5 mmol/L/hr |
| Bicarbonate | Rise by ≥3 mmol/L/hr |
| Glucose | Fall by ≥3 mmol/L/hr |
| K⁺ | 4.0-5.5 mmol/L |
| pH | Normalising (>7.3) |