DKA Diagnostic Triad (ALL THREE required): Hyperglycaemia >11 mmol/L + Ketonaemia >3 mmol/L (or 2+ urine ketones) + Acidosis pH <7.3 or bicarbonate <15 mmol/L
| Severity | Mild | Moderate | Severe |
|---|---|---|---|
| pH | 7.25–7.30 | 7.00–7.24 | <7.00 |
| Bicarbonate | 15–18 mmol/L | 10–14 mmol/L | <10 mmol/L |
| Anion gap | >10 | >12 | >12 |
| Mental status | Alert | Alert/drowsy | Stupor/coma |
| Parameter | DKA | HHS |
|---|---|---|
| Glucose | >11 mmol/L | >30 mmol/L |
| pH | <7.3 | Normal (≥7.3) |
| Ketones | Strongly positive | Absent/trace |
| Osmolality | Variable | >320 mOsm/kg |
| Bicarbonate | <15 mmol/L | Normal/raised |
| Onset | Hours (T1DM) | Days–weeks (T2DM) |
| VTE risk | Moderate | Very High |
Infection accounts for up to 40% of DKA cases. Always investigate for source — urine culture, CXR, blood cultures if febrile.
SGLT2 inhibitors (empagliflozin, dapagliflozin) cause Euglycaemic DKA — glucose may be normal or near-normal.
In GCC context: Ramadan fasting — missed insulin, altered meal timing, and dehydration significantly increase DKA risk in T1DM patients.
Critical awareness: EDKA presents with normal or near-normal glucose (typically 8–14 mmol/L) but positive ketones and acidosis — easily missed.
Always ask about SGLT2 inhibitor use (gliflozins) in any patient with ketoacidosis — even if glucose appears normal.
JBDS Protocol Order: (1) IV fluids first → (2) Check K+ → (3) Start insulin only if K+ >3.5 → (4) Potassium replacement → (5) Monitor hourly
Target glucose during DKA: 10–14 mmol/L. Do NOT aim for euglycaemia — too rapid correction risks cerebral oedema.
0.1 units/kg/hr of soluble insulin
NEVER start insulin if K+ <3.5 mmol/L. Replace potassium first. Insulin drives K+ intracellularly and can cause fatal arrhythmias.
Hypokalaemia is the most common cause of death in DKA treatment. Insulin + rehydration both shift K+ intracellularly — mandatory monitoring and replacement.
| Serum K+ level | Potassium in IV bag | Insulin action | Notes |
|---|---|---|---|
| <3.5 mmol/L | 40 mmol/L — URGENT replacement | STOP INSULIN — call senior | Give KCl via central/large vein; ECG monitoring; repeat K+ in 1h |
| 3.5–5.5 mmol/L | 40 mmol/L in each litre | Continue FRIII | Target K+ 4.0–5.0 mmol/L during DKA treatment |
| >5.5 mmol/L | No potassium in bag | Continue FRIII | Recheck K+ in 2h; do not add potassium until <5.5 |
ALL of the following must be met before stopping IV insulin:
2-hour overlap rule: Give subcutaneous insulin dose and wait 2 hours BEFORE stopping IV insulin infusion.
HHS key principle: Slower is safer. Avoid rapid fluid or osmolality correction. Target osmolality reduction of 3–8 mOsm/kg/hr only.
>30 mmol/L
Typically much higher than DKA. Extreme hyperglycaemia drives hyperosmolality.
>320 mOsm/kg
Formula: 2(Na) + glucose + urea (all in mmol/L). Often 350–400+ in HHS.
Absent / Trace
No significant ketonaemia. pH normal (>7.3). This distinguishes HHS from DKA.
Target: replace fluid deficit over 24–48 hours — NOT rapidly.
Do NOT start insulin immediately in HHS. Fluids alone will lower glucose. Premature insulin risks hypoglycaemia and rapid osmolality shift.
HHS carries very high VTE risk due to extreme hyperviscosity, dehydration, and immobility. DVT/PE is a major cause of HHS mortality.
Cerebral oedema is more common in children with DKA but can occur in HHS with rapid osmolality correction. The brain adapts to hyperosmolality — rapid correction causes osmotic water movement into brain cells.
| Parameter | Frequency | Target / Action |
|---|---|---|
| Blood glucose (CBG) | Hourly | DKA: 10–14 mmol/L; add dextrose if <14 mmol/L |
| Blood ketones | Hourly | Target fall ≥0.5 mmol/L/hr; resolution <0.6 |
| Serum potassium | 2-hourly (1h if <3.5) | Target 4.0–5.0 mmol/L; adjust replacement accordingly |
| Venous blood gas (pH/HCO₃) | 2-hourly | Target pH >7.3; bicarbonate rising |
| Urine output | Hourly | Target ≥0.5 mL/kg/hr — catheterise if oliguric |
| Fluid balance | Hourly | Document all inputs/outputs; cumulative total q4h |
| Vital signs (HR, BP, SpO₂, RR, Temp) | Hourly | NEWS2 scoring; escalate if deteriorating |
| GCS / neurological status | Hourly | Deteriorating GCS — consider cerebral oedema |
| Osmolality (HHS) | 2-hourly | Target reduction 3–8 mOsm/kg/hr |
| U&E, Mg, Phosphate | 4-hourly | Replace electrolytes as per protocol |
Continuous ECG monitoring mandatory if K+ <3.0 mmol/L or patient has cardiac history.
Glucose can fall rapidly with IV insulin. Do NOT stop insulin — switch fluid to prevent hypoglycaemia while maintaining insulinaemia to clear ketones.
Never stop insulin to treat hypoglycaemia in DKA — give dextrose instead. Stopping insulin allows ketogenesis to continue.
DKA causes gastroparesis — gastric stasis increases vomiting risk even if patient appears alert. Consider NG early if vomiting uncontrolled.
Premature transition to subcutaneous insulin leads to rebound ketoacidosis. Strict criteria must be met.
In patients without known insulin regimen — use T1DM starter regimen or endocrinology review before discharge.
Extra sugar-free fluids (water, diluted juice). If vomiting, sip small amounts frequently. Aim 3L/day minimum.
Reduce activity. Stress hormones (cortisol, adrenaline) raise blood glucose further.
Check blood glucose every 2–4 hours when unwell. If consistently >14 mmol/L, check ketones.
Check blood ketones every 2–4 hours if glucose >14 mmol/L. Blood meter preferred over urine strips.
Even if not eating, continue long-acting insulin. Short-acting may need increasing by 10–20% during illness. Call diabetes team if unsure.
Treat underlying infection. Antibiotics if confirmed bacterial source. Paracetamol for fever — avoid NSAIDs if dehydrated.
Pump users are at higher DKA risk. No subcutaneous long-acting insulin — pump failure means total insulin deficiency within 4–8 hours.
All pump users should have a backup pen and long-acting insulin prescription. Education on recognising pump failure symptoms is essential.
T1DM fasting during Ramadan carries high DKA risk. Structured pre-Ramadan education and individualised insulin adjustment plan is mandatory. Many Islamic scholars advise T1DM patients are exempt from fasting.
| Criterion | Value |
|---|---|
| Blood glucose | >11 mmol/L (200 mg/dL) |
| Blood ketones | >3.0 mmol/L |
| Urine ketones (alternative) | 2+ or more |
| pH | <7.3 |
| Bicarbonate | <15 mmol/L |
| Anion gap | >10 (corrected) |
Potassium (K+). Insulin drives K+ into cells, causing dangerous hypokalaemia. The biggest DKA killer.
DHA/DOH/SCFHS commonly test the K+ protocol. Never start insulin if K+ <3.5 mmol/L.
0.1 units/kg/hr of soluble insulin as a fixed rate infusion — not a sliding scale.
SGLT2 inhibitors (gliflozins — empagliflozin, dapagliflozin, canagliflozin). Glucose may appear normal but ketones are elevated.
Fluids alone will lower glucose in HHS. Premature insulin risks hypoglycaemia and rapid osmolality shift causing cerebral oedema.
When transitioning from IV to SC insulin in DKA resolution: give the subcutaneous dose and continue IV insulin for 2 more hours before stopping the infusion.
LMWH thromboprophylaxis (e.g. enoxaparin) must be started immediately in HHS unless contraindicated. HHS has very high hyperviscosity and VTE mortality.
pH >7.3 AND blood ketones <0.6 mmol/L AND glucose <14 mmol/L AND patient eating and drinking.