SEPT 10 Built from the handwritten pages you uploaded on 10 September 2026.

DKA & HHS

The two hyperglycaemic emergencies side by side — diagnosis, the numbers, and where they are treated differently.

Side by side

	DKA	HHS
Diabetes type	Type 1	Type 2
Glucose	> 11 mmol/L (often 14–30)	> 33 mmol/L (600 mg/dL)
pH	< 7.3	> 7.3
Bicarbonate	< 15 mmol/L	> 15 mmol/L
Ketones	Present — ketonaemia > 3 mmol/L or ketonuria	Absent or minimal
Anion gap	Raised (HAGMA)	Normal (NAGMA)
Osmolality	Normal or mildly raised	> 320–330 mOsm/kg
Sodium	125–135 (often low)	Pseudohyponatraemia, then high
Volume state	Dehydrated	Profoundly volume depleted — deficit often 8–10 L
Onset	Hours	Days
Mortality	Lower	Higher

The sodium correction

Hyperglycaemia draws water out of cells, diluting the measured sodium — a pseudohyponatraemia.
Corrected Na⁺ rises by about 1.5–2 mmol/L for every 5.5 mmol/L (100 mg/dL) that glucose falls.
So a "normal" sodium in a patient with a glucose of 40 mmol/L conceals a substantial true hypernatraemia — and the sodium will rise as you treat.
A rising corrected sodium during treatment is expected. A falling one means you are giving free water too fast, and risks cerebral oedema.

Treatment targets

Fluid first

Fluid resuscitation takes priority over insulin. Insulin without volume worsens hypotension by driving glucose and water intracellularly.
0.9% sodium chloride; the deficit is typically 5–7 L in DKA and greater in HHS.

Insulin

Fixed rate 0.1 units/kg/h, continuing the patient's usual long-acting basal insulin.
Targets: glucose should fall by 3 mmol/L/h (about 50–70 mg/dL/h) and ketones by 0.5 mmol/L/h, with bicarbonate rising by 3 mmol/L/h.
If targets are not met, increase the insulin rate by 1 unit/h.
When glucose falls below about 14 mmol/L (250 mg/dL), add glucose 10% alongside — the insulin is being run to clear ketones, not to normalise glucose, so it must not be stopped.

Potassium — the one that kills

Total body potassium is always depleted, however the initial figure looks. Acidosis and insulin deficiency have driven potassium out of cells.
As soon as insulin starts, potassium crashes. Replace early and measure hourly.
If K⁺ < 3.5 mmol/L, do not start insulin until replacement is under way.

When to stop the insulin infusion

pH > 7.3, bicarbonate > 18, and no ketones — and the patient is eating and drinking with subcutaneous insulin overlapped before stopping.
Do not use glucose alone as the endpoint — glucose normalises long before ketosis resolves.

Cerebral oedema — the commonest cause of death in DKA

Particularly in children and young adults, and typically 4–12 hours into treatment.
Warning signs: falling GCS · headache · cranial nerve palsy · rising BP with bradycardia (Cushing response) · irritability then drowsiness.
Treatment: hypertonic saline 3% at 3–5 ml/kg, or mannitol 0.5–1 g/kg; head up, secure the airway, and slow the fluid.
Prevention: correct slowly, avoid overzealous fluid, and do not let the corrected sodium fall.

Anaesthetic implications

Both are medical emergencies. Where surgery is the precipitant (sepsis, ischaemic limb, abscess), resuscitate while arranging source control — do not wait for perfect biochemistry, and do not operate on an unresuscitated patient either.
Expect gastroparesis, a full stomach and aspiration risk; consider rapid sequence induction.
Kussmaul breathing is compensating for the acidosis — if you paralyse and ventilate, match their minute ventilation or the pH will plummet.
Watch for hypothermia, hypophosphataemia and hypomagnesaemia, and recheck ketones and potassium frequently.

Quick recall

DKA type 1 · ketones · HAGMA

HHS type 2 · osm >320 · no ketones

Fluid before insulin

0.1 u/kg/h fixed rate

K <3.5 hold insulin

Glucose <14 add 10% dextrose

Na ↑1.5–2 per 100 mg/dL glucose fall

Cerebral oedema commonest death

Built from your DKA/HHS page. Your note gives the DKA glucose threshold as >14 mmol/L (250–300 mg/dL); most current guidance uses >11 mmol/L — and DKA can occur at normal glucose in a patient on an SGLT2 inhibitor.