Hyperosmolar Hyperglycaemic State

Epidemiology and Risk Factors

Pathophysiology

Similar to DKA, there is an alteration in normal carbohydrate metabolism due to insulin deficiency. However, unlike DKA there is still some insulin, such that:

  • Hyperglycaemia still occurs
    • Due to:
      • ↑ Gluconeogenesis
      • ↓ Peripheral uptake of glucose
    • Leads to polyuria (and subsequently, polydipsia) due to the high filtered load
      • Water deficit in HHS is about twice that of DKA
  • There is no ↑ in lipolysis
    Therefore, there is no ↑ free fatty acid oxidation and so generally no ketones.

Aetiology

Clinical Manifestations

Develops over days-weeks with:

  • Polyuria
  • Polydipsia
  • Weakness
  • Weight loss

Other symptoms include:

  • Neurological symptoms
    More common in HHS than DKA, as it occurs secondary to a hyperosmolar state. Include:
    • Confusion
    • Seizures
    • Coma

Diagnostic Approach and DDx

Features include:

  • Hypovolaemia
  • Severe ↑ BSL (usually >30mmol/L)
    • Without ketosis (<3mmol/L)
    • Without acidosis (pH >7.3)
  • ↑ Osmoles (>320mOsmol/kg)

Investigations

Bedside:

  • ABG
    • ↑ BSL

Laboratory:

  • Osmolality

Imaging:

Other:

Management

  • Slow correction of metabolic abnormalities
    Management is similar to DKA, but should occur slowly to prevent overcorrection.
  • Fluid resuscitation
    Water repletion and volume resuscitation should ↑ Na+, ↓ BSL, and ↓ osmolality.
  • Insulin infusion
  • Electrolyte correction

Resuscitation:

  • C
    • Gradual volume resuscitation and water repletion
      • Balanced crystalloid preferred
      • Change to 0.45% saline if osmolality is ↑, despite appropriately positive fluid balance
  • D
    • Insulin
      • Ideally delay insulin until volume resuscitation commenced and potassium is corrected
        Glucose will by diluted by water repletion.
      • Otherwise fixed rate intravenous insulin infusion at 0.02-0.1 unit/kg/hr
      • Commence insulin at 0.02-0.05 unit/kg/hr, targeting 10-15mmol/L in the initial setting
  • F
    • Electrolyte correction
      • Potassium
        • Begin correction of total body deficit once serum potassium is <5.5mmol/L
        • Consider only initiating insulin when potassium is >3.3mmol/L to avoid precipitating severe hypokalaemia

Supportive care:

  • F
    • Magnesium
      Often deplete, PRN replenishment is sufficient.
    • Phosphate

Free water deficit can be crudely estimated as: \(Free \ Water \ Deficit = 0.6 \times Weight \times (1 - {Na_{ideal} \over Na_{serum}})\)

Where:

  • Free water deficit is in litres
  • Weight is in kg
  • Serum sodium is in mmol/L

Disposition:

  • ICU admission for:
    • Neurological symptoms
      • GCS <12
    • Severe electrolyte derangements

Preventative:

  • Appropriate insulin administration
    • Baseline maintenance
    • ↑ Dosing in times of physiologic stress

Marginal and Ineffective Therapies

Anaesthetic Considerations

Complications

  • Aspiration
  • D
    • ↓ BSL
    • CVA
    • Cerebral oedema
  • F
    • ↓ K+
  • H
    • DVT

Hypoglycaemia and hypokalaemia are the most common serious complication, due to excessive insulin replacement with inadequate potassium supplementation.

Prognosis

Key Studies

References

  1. Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.