Drugs: Corticosteroids, SGLT2 inhibitors (euglycaemic DKA — glucose may be normal/mildly elevated)
Pregnancy: Increased insulin requirements; higher DKA risk even at lower glucose levels
Investigations
Bedside / Point-of-Care
Blood glucose: Glucometer (confirm with lab)
Blood ketones: Beta-hydroxybutyrate meter (Abbott Optium or similar) — most important monitoring parameter during treatment
Capillary/venous blood gas: pH, bicarbonate, pCO₂, potassium (VBG acceptable; arterial only if respiratory concern)
ECG: Hypokalaemia (flat T waves, U waves) or hyperkalaemia (peaked T waves) on presentation
Laboratory Investigations
Test
Expected Finding
Purpose
Serum glucose
Usually 14–40 mmol/L
Confirm; guide dextrose addition
Serum potassium
May be high, normal or low initially — total body K⁺ always DEPLETED
Critical — guide replacement
Sodium
Often low (pseudohyponatraemia) or high; correct for glucose
Hydration monitoring
Urea/creatinine
Elevated — pre-renal AKI from dehydration
Renal function baseline
FBC
Leucocytosis (DKA itself; not always infection)
Infection screen
Urinalysis
Glycosuria, ketonuria
Infection screen — MSU for culture
Blood cultures
Positive if bacteraemia/sepsis precipitant
If febrile or suspected infection
HbA1c
Elevated (chronic poor control)
Chronic glycaemic assessment
Lipase/amylase
May be elevated (acute pancreatitis precipitant)
If abdominal pain prominent
Potassium paradox: Serum K⁺ may be HIGH at presentation (acidosis shifts K⁺ extracellular) but total body K⁺ is severely depleted. As insulin is given and acidosis corrects, K⁺ shifts intracellular → rapid hypokalaemia. Monitor 1–2 hourly and replace aggressively.
DKA Treatment Protocol (JBDS/NICE-Based)
Step 1 — IV Fluid Resuscitation
0.9% NaCl (normal saline) is the standard first-line fluid. Avoid Hartmann's (lactate may worsen acidosis in theory — though recent trials show equivalence). Use 0.45% NaCl only in hyperosmolar/hypernatraemic DKA.
Time
Volume
Rate
0–30 min (initial resuscitation)
500 mL–1000 mL 0.9% NaCl
Over 15–30 min (shock bolus if haemodynamically compromised)
0–1 hr
1000 mL 0.9% NaCl
1 L/hr
1–3 hrs
2000 mL 0.9% NaCl
1 L over 2 hrs
3–6 hrs
2000 mL 0.9% NaCl
1 L over 2 hrs
6–12 hrs
2000 mL 0.9% NaCl
1 L over 4 hrs
When blood glucose falls to <14 mmol/L → ADD 10% dextrose at 125 mL/hr alongside 0.9% NaCl to prevent hypoglycaemia whilst continuing insulin to clear ketones.
Step 2 — Fixed-Rate IV Insulin Infusion (FRIII)
Rate: 0.1 units/kg/hr of Actrapid (soluble insulin) in 0.9% NaCl (50 units in 50 mL = 1 unit/mL)
DO NOT give IV bolus of insulin — increases risk of hypokalaemia and cerebral oedema
Withhold long-acting insulin? NO — continue background (basal) insulin at usual dose; this prevents rebound ketosis
Do NOT reduce insulin rate if blood glucose falls — instead add 10% dextrose to maintain glucose 10–14 mmol/L while keeping insulin running
Insulin target: Ketones fall at ≥0.5 mmol/L/hr; bicarbonate rise ≥3 mmol/L/hr
If ketones not falling at expected rate after 1 hour: check infusion pump, line, and consider increasing insulin rate to 0.15 or 0.2 units/kg/hr — escalate to senior.
Step 3 — Resolution Criteria (JBDS)
Parameter
Target
Blood ketones
<0.6 mmol/L
Venous pH
>7.3
Bicarbonate
>18 mmol/L
Blood glucose
<14 mmol/L (not needed if other criteria met)
When resolution criteria met AND patient eating + drinking → switch to subcutaneous insulin. Continue IV insulin for 30–60 min after first SC dose to prevent rebound ketosis.
Potassium Replacement — Critical Protocol
NEVER start insulin if serum K⁺ <3.5 mmol/L. Insulin drives K⁺ into cells — hypokalaemia before insulin risks fatal cardiac arrhythmia. Correct K⁺ first.
Potassium Replacement Protocol
Serum K⁺
Action
<3.5 mmol/L
HOLD insulin. Replace K⁺ (40 mmol/hr via central line) until K⁺ ≥3.5, then start insulin
3.5–5.5 mmol/L
Add 40 mmol KCl to each litre of IV fluid (0.9% NaCl bag); start insulin
>5.5 mmol/L
No K⁺ in IV fluid initially; recheck in 1 hour; monitor ECG
Monitoring Frequency
Parameter
Frequency
Blood glucose (BGL)
Hourly
Blood ketones
Hourly (or 2-hourly if ketones <3)
Venous blood gas (pH, HCO₃, K⁺)
Every 2 hours
Electrolytes (U&E)
Every 2–4 hours
Fluid balance
Hourly urine output; IDC in severe DKA or unconscious patient
Neurological observations
Every 1–2 hours — cerebral oedema watch
Cerebral Oedema — Most Feared Complication
Predominantly in children and young adults. Warning signs: sudden headache, confusion, change in behaviour, bradycardia, pupillary changes, deteriorating GCS during treatment.
Prevention: Avoid rapid fluid replacement; replace deficit over 24–48 hours in children; do not let glucose fall too quickly
Treatment: Mannitol 0.5–1 g/kg IV over 20 min (or hypertonic saline if no mannitol); restrict IV fluids; neurosurgery consult; consider intubation
Risk factors: Very young, new-onset DM, severe acidosis, very high BUN, bicarbonate administration (avoid routine NaHCO₃)
GCC-Specific Context
DKA in the GCC
Highest rates globally: GCC has among the world's highest rates of DKA admission — driven by high T1DM/T2DM prevalence, poor glycaemic control and late presentations
Presentation at DM diagnosis: 40–50% of new T1DM in GCC children present in DKA — reflects delayed recognition of early symptoms in primary care
Ramadan fasting: DKA risk increases during Ramadan in T1DM patients who attempt fasting — insulin omission, dehydration, altered eating schedules. Saudi ADA guidelines provide specific Ramadan DKA management protocols
SGLT2 inhibitors (gliflozins): Increasingly used in GCC for T2DM — cause euglycaemic DKA where blood glucose may only be 11–14 mmol/L. High index of suspicion required; check ketones in any unwell diabetic on gliflozins
Heat and dehydration: Summer heat exacerbates fluid losses; DKA presentations increase in summer months across the GCC
SGLT2 inhibitors → euglycaemic DKA — important GCC exam topic
Exam MCQs — DHA / SCFHS / QCHP
Q1. A patient with DKA has serum potassium of 3.1 mmol/L. The fixed-rate insulin infusion is about to be started. What is the CORRECT action?
✅ B — Never start insulin when K⁺ <3.5 mmol/L. Insulin drives potassium intracellularly. Starting insulin with an already low K⁺ risks life-threatening hypokalaemia and cardiac arrhythmia. Correct K⁺ first (IV replacement via central or large peripheral line), then start insulin when K⁺ ≥3.5.
Q2. After 4 hours of DKA treatment with fixed-rate insulin, a patient's blood glucose has fallen from 28 mmol/L to 11 mmol/L. Ketones are still 3.8 mmol/L and pH is 7.18. What is the APPROPRIATE action?
✅ C — DKA resolution requires ketone clearance (target <0.6 mmol/L) AND pH >7.3. Ketones are still high. Do NOT stop or reduce insulin. Add 10% dextrose infusion to maintain glucose 10–14 mmol/L whilst continuing insulin to clear ketones. Stopping insulin prematurely leads to rebound ketosis.
Q3. A child with DKA develops sudden headache, confusion and bradycardia after 6 hours of treatment. What complication should be suspected and what is the IMMEDIATE treatment?
✅ B — Cerebral oedema is the most feared complication of DKA in children and young adults. Warning signs: headache, confusion, behaviour change, bradycardia, pupillary changes. Immediate treatment: mannitol 0.5–1 g/kg IV over 20 minutes OR hypertonic saline. Restrict IV fluids. Urgent CT head and critical care team.
Q4. Which finding CONFIRMS DKA resolution and allows transition to subcutaneous insulin?
✅ C — The JBDS criteria for DKA resolution: blood ketones <0.6 mmol/L AND venous pH >7.3 AND bicarbonate >18 mmol/L, plus patient clinically stable and eating/drinking. Urine ketones lag behind blood ketones and should not be used as the primary resolution marker.