a) List the features which distinguish diabetic ketoacidosis (DKA) from the hyperosmolar hyperglycaemic state (HHS).
b) Describe your specific treatment for a 62-year-old female presenting with a decreased conscious state secondary to HHS.
a)
1. History
i. Known type 1 DM; discontinuation of insulin therapy
ii. Presentation: DKA evolves rapidly (24 hours); HHS typically days-weeks with polydipsia, polyuria and weight loss.
2. Clinical features
i. Neurological symptoms more common in HHS.
ii. Abdominal pain and hyperventilation more common in DKA.
3. Laboratory features
i. Degree of hyperglycaemia (HHS typical higher, exceeding 56 mmol/l; DKA usually < 44 mmol/L)
ii. Degree of acidosis: severe in DKA, mild in HHS
iii. Anion gap acidosis present in DKA; absent (or mild in case of concomitant lactic acidosis) in HHS
iv. Ketones: HHS small ketonuria, absent to low ketonaemia [there is sufficient basal insulin secretion to prevent ketogenesis]; both high in DKA
v. Hyperosmolality more severe in HHS, typically > 320 mosm/L
4. NOTE: Significant overlap can occur in 30% of patients – represent part of a spectrum
b)
1. Fluid replacement
i. Expect fluid replacement of up to 10 litres, but GO SLOW (replace over 48 hours)
ii. Start with isotonic crystalloids (boluses if in shock, infusion rate up to 1L/hour). Need justification for choice of fluid, while recognising there is substantial controversy in this area.
iii. Continue isotonic if serum Na+ low; change to 0.45% NaCl if serum Na+ is normal or elevated.
iv. Change to 5% dextrose with 0.45% NaCl when serum glucose reaches 15 mmol/L or below
v. Individual tailoring based on heart rate, blood pressure, peripheral perfusion, urine output
2. Insulin infusion 0.05 U/kg/hr. initially following adequate fluid resuscitation aiming for steady but slow reduction in blood sugar levels (e.g. 5 mmol/hr)
3. Electrolyte replacement
i. Expect potassium deficit even if level appears normal
ii. Give 20 - 30 mmol K+ in each Litre of fluid or use separate infusion; aim for serum K+ 4 – 5 mmol/L
iii. Phosphate depletion only requires treatment if levels are very low (e.g. < 0.3 mmol/L) or symptomatic (Ref: BMJ best practice)
4. Treat possible precipitating cause (infection? need for broad spectrum antibiotics? Think about underlying precipitant in this case – there is a long list of possible causes (e.g. pancreatitis). What about drugs [both β blockers and HMGCo-A reductase inhibitors have been associated with HHS. Other common precipitating drugs e.g. antipsychotics, steroids…] Does she even have diabetes? [Check HbA1C].
5. Thromboprophylaxis mandatory – consider risks and benefits of heparin infusion.
6. Monitor
i. Haemodynamic situation
ii. Mental state
iii. Urine output
iv. Levels of glucose and electrolytes every 1 – 4 hours
v. Levels of ketones in DKA
7. Consider CT brain scan (possibility of ischaemic stroke).
a)
In summary:
Domain |
Features suggestive of DKA |
Features suggestive of HONK |
History |
|
|
Examination |
|
|
Biochemistry |
|
|
b)
A stereotypical approach to management is offered below:
Key issues of "specific therapy:
UpToDate has a nice summary of this topic for the paying customer.
Oh's Intensive Care manual: Chapter 58 (pp. 629) Diabetic emergencies by Richard Keays
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