Diabetic ketoacidosis (DKA) and Hyperosmolar Hyperglycaemic State (HHS)

E10.0-1/E11.0-1/E12.0-1/E13.0-1/E14.0-1

Diabetic comas – recognition and clinical profiles

DKA often occurs in younger patients and develops over hours to days. There may be vomiting, abdominal pain and acidotic breathing.

  • blood glucose usually <40 mmol/L
  • blood ketones are positive
  • serum osmolality <350 mOsm/L

Hyperosmolar hyperglycaemic state (HHS) is a syndrome characterised by impaired consciousness, sometimes accompanied by seizures, extreme dehydration and severe hyperglycaemia, that is not accompanied by severe ketoacidosis (pH usually >7.2). It usually occurs in elderly type 2 diabetic patients and develops over days to weeks.

  • Blood glucose usually >40 mmol/L.
  • Blood ketones usually negative to moderately elevated.
  • Urine ketones may be positive.
  • Serum osmolality is >320 mOsm/L.

Anion gap = Na – (CI + HCO3) (Normal = ± 12: DKA >20).

Calculated serum osmolarity = 2 (Na + K) + glucose + urea.

GENERAL MEASURES

All patients:

  • Set up an intravenous line.
  • Protect airway and insert a nasogastric tube, if unconscious.
  • Monitor urine output.
  • Monitor plasma glucose, ketones, urine, electrolytes and venous blood gas.
  • Look for precipitating causes, e.g. infection or MI.

MEDICINE TREATMENT

Fluids

Average deficit 6 L, may be as much as 12 L.

If renal or cardiac disease is present, monitor with central venous pressure.

In the absence of renal or cardiac compromise:

  • Sodium chloride 0.9%, IV, 15–20 mL/kg in the first hour.
    • Patients <20 years of age: initial volume of 10–20 mL/kg in the 1st hour.
    • Subsequent infusion rate varies from 5–15 mL/kg/hour depending on the clinical condition.
    • Correction of estimated deficits should take place over 24 hours.
    • The volume infused in the first 4 hours should not exceed 50 mL/kg.
    • Fluid therapy thereafter is calculated to replace the estimated deficit in 48 hours, ± 5 mL/kg/hour.
    • Reduction in serum osmolality should not exceed 3 mOsm/kg/hour.

Correct plasma sodium value for blood glucose.

[Rough guide: divide glucose by 3 and add to sodium value.]

If plasma Na⁺ >140 mmol/L:

  • Sodium chloride 0.45%, IV.

If plasma Na⁺ ≤140 mmol/L:

  • Sodium chloride 0.9%, IV.

If plasma glucose <15 mmol/L, but ketones still present:

  • Dextrose 5% or dextrose 10% in sodium chloride 0.9%, IV.

LoEIII [22]

Note:

  • Adjust fluid volumes according to clinical criteria.
  • Cerebral oedema may occur with over-aggressive fluid replacement or rapid sodium change.

Potassium

Potassium will fall on insulin treatment and patients with DKA have potassium depletion even if initial potassium is normal or high.

It is therefore essential to monitor and replace potassium.

Total body deficit 300–1 000 mmol.

(1 ampoule = 20 mmol = 10 mL)

  • Potassium chloride, IV, added to 1 L of fluid.
    • potassium <3.5 mmol/L: add 40 mmol (2 ampoules).
    • potassium 3.5–5.5 mmol/L: add 20 mmol (1 ampoule).
    • potassium >5.5 mmol/L: do not add any potassium.

Maximum potassium dose: 40 mmol/hour.

Monitor potassium hourly initially, then 2 hourly when stabilised.

LoEIII

If serum potassium results are not readily available:

  • Potassium chloride, IV, 20 mmol (1 ampoule) added to 1 L of fluid as soon as the patient has established adequate urinary output.

Bicarbonate

There is no proven role for the use of intravenous sodium bicarbonate and it could potentially cause harm.

Insulin therapy

Patients should be preferentially managed with continuous intravenous infusions or hourly intramuscular injections (see below) in a high care ward, with appropriate monitoring.

Note:

  • Ketonaemia takes longer to clear than hyperglycaemia and combined insulin and glucose (and K+) are needed to ensure clearance of ketonaemia.
  • Avoid focusing on glucose control alone!
  • Continue insulin until acidosis and ketosis have resolved.

Continuous intravenous infusion:

  • Insulin, short-acting, IV infusion, 50 units in 200 mL sodium chloride 0.9%.
    • 4 mL solution = 1 unit insulin.
    • Initial infusion: 0.1 unit/kg/hour.
    • Usually 5–7 units/hour: 20–28 mL/hour.
    • If plasma glucose does not fall by 3 mmol/L in the 1st hour, double the insulin infusion (hourly) until a steady reduction of plasma glucose is achieved, i.e. at least 3–4 mmol/L per hour.
    • If plasma glucose <14 mmol/L, reduce insulin infusion rate to 1–2 units/hour and adjust subsequently according to hourly bedside capillary glucose level measured with glucose test strips.

Hourly intramuscular bolus injections:

Where intravenous infusion cannot be safely administered:

  • Insulin, short-acting
    • Dilute 100 units with sodium chloride 0.9% to 10 mL i.e. 10 units/mL.
    • Loading dose: 0.5 units/kg body weight.
    • Administer half the dose as an intravenous bolus injection and the other half IM. Do not administer with an insulin syringe and needle.
    • Subsequent hourly doses: ± 5–10 units IM every hour (i.e. 0.1 units/kg/hour) and titrated against the bedside capillary glucose level.

Progress management

Continue insulin therapy until the acidosis has resolved and:

  • the patient is able to eat, and
  • subcutaneous insulin therapy is instituted either at previous doses or, for newly diagnosed diabetes at 0.5–1 unit/kg total daily dose divided into at least 2 doses with mixed short- and long-acting insulin (biphasic insulin ⅔ in the morning and ⅓ at night).

Infusion must overlap with subcutaneous regimen for 1–2 hour to avoid reversion to keto-acidosis.

Heparin.

For all patients:

  • Low molecular weight heparin, e.g.:
  • Enoxaparin, SC, 40 mg daily.

LoEI [23]

OR

  • Unfractionated heparin, SC, 5 000 units 12 hourly.