Hyperglycaemic hyperosmolic state (HHS) Flashcards
Pathophysiology of HHS
Hyperglycaemia - high serum osmolality - osmotic diuresis - severe volume depression
Marked dehydration and glucose >30mmol/L
There are no precise diagnostic criteria but the following are typically seen:
hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
- can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 – acidosis can occur due to lactic acidosis or renal impairment)
Why is there no significant hyperketonaemia?
There is no seitch to ketone metabolism so ketonaemia stays <3mmol/L and pH<7.3
What is the main danger + complication of HHS?
Occlusive events
Vascular complications due to hyperviscosity such as MI or stoke
give LMWH prophylaxis to all unless CI
Management of HHS
fluid replacement
- fluid losses in HHS are estimated to be between 100 - 220 ml/kg
- IV 0.9% sodium chloride solution
- typically given at 0.5 - 1 L/hour depending on clinical assessment
- potassium levels should be monitored and added to fluids depending on the level
Insulin
- should not be given unless blood glucose stops falling while giving IV fluids
Venous thromboembolism prophylaxis
- patients are at risk of thrombosis due to hyperviscosity (give LMWH unless CI)
Keep blood glucose at least 10-15mmol/L for first 24 hours of management to avoid?
cerebral oedema
Clinical presentation of HHS
whilst DKA presents within hours of onset, HHS comes on over many days, and consequently, the dehydration and metabolic disturbances may be more extreme
consequences of volume loss
- clinical signs of dehydration
- polyuria
- polydipsia
systemic
- lethargy
- nausea and vomiting
neurological
- altered level of consciousness
- focal neurological deficits
haematological
- hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
