diabetic ketoacidosis — management

diagnosis

criterion	threshold
glucose	>14 mmol/L (can be normal in euglycaemic DKA)
pH	≤7.3
bicarbonate	≤15 mmol/L
anion gap	>12 mmol/L
ketones	serum BHB >3.0 mmol/L or urine ketones ≥2+

severity

	mild	moderate	severe
pH	7.25–7.30	7.00–7.24	<7.00
HCO₃⁻	15–18	10–15	<10
sensorium	alert	alert/drowsy	obtunded

vs HHS

HHS: glucose typically ≥34 mmol/L, osmolality >320 mOsm/kg, minimal/no acidosis, greater volume depletion, more altered LOC and seizures. Mixed DKA/HHS occurs.

initial workup

• glucose, VBG (arterial not needed), serum BHB
• electrolytes (Na⁺, K⁺, Cl⁻, Ca²⁺, Mg²⁺, PO₄³⁻), creatinine, urea
• anion gap calculation
• urinalysis, CBC, HbA1c
• ECG
• directed precipitant workup: cultures, CXR, troponin, lipase as indicated

search for the cause — the “5 I”s

Infection | Insulin deficiency (missed doses) | Infarction (MI, stroke) | Intoxication | Iatrogenic (steroids, SGLT2i, antipsychotics)

management — the three pillars

pillar 1: fluids first

Restores perfusion, damps counter-regulatory hormone drive, improves renal glucose/ketone clearance.

phase	fluid	rate
first hour	isotonic crystalloid	1 L over 1 hour (15–20 mL/kg)
ongoing (corrected Na⁺ normal/high)	0.45% NaCl	250–500 mL/hr
ongoing (corrected Na⁺ low)	0.9% NaCl	250–500 mL/hr
glucose <14 mmol/L	add dextrose 5–10%	continue insulin — you are treating acidosis, not glucose

Two-bag system: one bag crystalloid, one bag crystalloid + dextrose — allows rapid titration of dextrose without changing the line. Shortened time to AG closure by ~4 hours in implementation studies.

pillar 2: potassium — the one that kills

See diabetic ketoacidosis — pathophysiology for why serum K⁺ is misleading (total body is always depleted despite normal/high serum level).

serum K⁺	action
<3.3 mmol/L	hold insulin; aggressive KCl replacement (40 mmol/hr IV via central line or split peripherals); recheck hourly
3.3–5.3 mmol/L	add 20–30 mmol KCl per litre of IV fluid; start insulin
>5.3 mmol/L	hold K⁺ replacement; start insulin; recheck in 2 hours

Potassium acetate or citrate instead of KCl reduces chloride load → less hyperchloraemic acidosis.

pillar 3: insulin — treating the acidosis

protocol	dose
IV insulin (standard)	0.1 U/kg/hr fixed rate (no bolus — bolus ↑ hypokalaemia/hypoglycaemia without faster AG closure)
glucose <14 mmol/L	reduce to 0.05 U/kg/hr + add D5–D10W to IV fluids
SC insulin (mild-moderate DKA)	0.3 U/kg bolus then 0.1 U/kg/hr or 0.2 U/kg q2h — non-inferior to IV in selected patients

Early basal insulin: glargine (0.25 U/kg new diagnosis; full home dose if known) given early during IV infusion → ~4 hours faster DKA resolution (meta-analysis of 8 RCTs). JBDS-UK recommends this; ADA/Diabetes Canada more conservative.

Bicarbonate: no routine role. No mortality benefit. Consider only if pH <6.9 (even this is debated). Risks: worsening intracellular acidosis, hypokalaemia, delayed ketone clearance.

monitoring

parameter	frequency	rationale
capillary glucose	hourly	detect hypoglycaemia, guide insulin/dextrose
serum K⁺	q2h (q1h if abnormal)	prevent fatal arrhythmia
electrolytes (Na⁺, Cl⁻)	q2–4h	guide fluid choice, detect hyperchloraemia
VBG (pH, HCO₃⁻)	q2–4h	track acidosis resolution
anion gap	q2–4h (with lytes)	the resolution marker — close the gap
serum BHB	q2–4h if available	direct ketone monitoring; <0.6 mmol/L = resolved
telemetry	continuous	arrhythmia from K⁺ shifts

closing the gap — when is DKA resolved?

All of:

• anion gap ≤12 mmol/L
• pH >7.3
• bicarbonate ≥18 mmol/L
• BHB <0.6 mmol/L (if available)
• patient alert and tolerating PO

transition to subcutaneous insulin

1. confirm AG closure + above criteria met
2. give SC basal insulin (glargine 0.3 U/kg if insulin-naïve; home dose if known) 2–4 hours before stopping IV insulin
3. overlap IV and SC insulin for ≥2 hours (pharmacokinetic delay of SC absorption)
4. resume or initiate basal-bolus regimen (0.5–0.8 U/kg/day total, split ~50/50 basal:prandial for insulin-naïve)
5. ensure patient is eating before stopping IV insulin

euglycaemic DKA

Glucose may be <14 mmol/L at presentation (especially with SGLT2 inhibitors). Full acidosis and ketosis despite near-normal glucose.

• start D10W early (75–125 mL/hr) so insulin can keep running
• do not reduce insulin for “normal” glucose — ketosis is the problem
• discontinue SGLT2i; do not restart after DKA episode

Mechanism: diabetic ketoacidosis — pathophysiology.

what NOT to do

• start insulin before checking K⁺ (or before repleting if K⁺ <3.3)
• give an insulin bolus (no benefit, ↑ hypoglycaemia/hypokalaemia)
• reduce insulin when glucose normalises without checking the AG — glucose is not the target
• give bicarbonate routinely (no benefit, real harms)
• use only urine ketones to monitor — nitroprusside misses BHB and can paradoxically increase during recovery
• stop IV insulin before SC insulin has had time to absorb (≥2 hr overlap)
• diagnose “resolved DKA” based on glucose alone
• intubate without extreme caution — loss of compensatory hyperventilation → rapid pH collapse; if absolutely required, match the patient’s pre-intubation minute ventilation

special populations

pregnancy

• lower glucose thresholds for diagnosis (glucose may be >11 mmol/L)
• foetal distress common but usually resolves with maternal resuscitation — avoid emergency C-section during acute DKA
• continuous foetal monitoring once viable

renal failure / dialysis

• AG may never fully normalise — use BHB <1.0 mmol/L as resolution target
• cautious with fluids and K⁺ (no osmotic diuresis → volume overload risk)
• may need dialysis for refractory acidosis or volume management

SGLT2i-associated

• see euglycaemic DKA above
• any patient on SGLT2i with nausea, vomiting, malaise — check BHB even if glucose is normal