College Answer

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).

Discussion

a)

In summary:

• DKA presents with acidosis as the major feature
• HONK presents with hyperglycaemia as the major feature

b)

A stereotypical approach to management is offered below:

1. Assess airway patency. Intubate to protect the airway if comatose.
2. Ventilate with mandatory mode initially; aim for normocapnea if the metabolic acidosis is not particularly severe.
3. Insert arterial line for frequent sampling and haemodynamic monitoring.
   Insert central line to manage electrolyte and fluid infusions.
   Check ECG/serial enzymes  for MI (common complication)
   Expect a 200ml/kg total water deficit
   Commence fluid resuscitation:
   1. 15-20ml/kg in the first hour
   2. 4-14ml/kg in the second hour (of 0.45% NaCl)
   3. 4-14ml/kg again in the third hour (use 0.9% NaCl if the sodium is low)
   4. When glucose is under 15mmol/L, start 5% dextrose 100-250ml/hr
4. May require benzodiazepines or anticonvulsants if the presentation history included seizures.
   May require a head CT venogram to rule out dural sinus thrombosis / venous infarction
5. Watch for a precipitous drop in serum osmolality.
   A safe drop is 3–8 mOsm/kg/h
   Correct electrolyte deficit:
   1. Sodium deficit: 5-13mmol/kg
   2. Potassium deficit: 5-15mmol/kg
   3. Chloride deficit: 3-7mmol/kg
   4. Phosphate deficit: 1-2mmol/kg
   5. Magneisum deficit: 1-1.5mmol/Kg
   6. Calcium deficit: 1-2mmol/Kg 
6. Monitor renal function and consider dialysis
7. Insulin therapy may not be required, and may even be dangerous.
   BSL may decrease at a satisfactory rate with fluid resuscitation alone.
8. May require anticoagulation for dural sinus thrombosis.
9. May require antibiotics, given that infection is a common precipitant.
   A septic screen should be sent.

Key issues of "specific therapy:

• Fluid resuscitation
• Electrolyte replacement
• Careful slow reduction of serum osmolality
• Investigation for complications:
  • Myocardial infarction
  • Stroke
  • Cerebral oedema and brain injury
  • Venous thrombosis
• Management of other possible precipitating causes:
  • Infection, systemic inflammatory response
  • Intracranial haemorrhage
  • Hepatic encephalopathy
  • Drugs, including illicit substances, steroids, phenytoin, diuretics, TPN, lithium