Question 25

College answer

Syllabus topic/section:

2.1.9 Endocrine Intensive Care / Diabetes Mellitus: L1

Discussion:  

In general candidates were familiar with the calculations, were able to recognise HHS/ DKA and describe management. It is helpful to show formulae that are being used (so if the calculations are incorrect, marks can be allocated for the principles), provide specifics in answers to management questions, and provide lists relevant to the scenario and explaining why. For instance, specifics of fluid resuscitation, the role and dosage of insulin use, resuscitation and metabolic targets to achieve were outlined in the more successful answers.

Discussion

a)

To go through these results systematically:

• There is acidaemia.
• The CO2 is appropriately depressed;  for a HCO3 of 4, it should be something like (1.5 × 4) + 8 = 14. 
• The anion gap is (145 - 108 - 4) =  33
• Assuming the albumin is normal, the delta ratio is (33-12)/(24-4) = 1.05; i.e. a pure HAGMA.
• The lactate is raised, but only by 7 mmol/L, which means it does not account for all of the anion gap. 

So:

• this is HHS
• the pH is depressed by the combined lactic acidosis and ketoacidosis
• There is a good earnest attempt at compensation
• The renal failure is due to dehydration (as revealed by the urea:creatinine ratio, which, using an online calculator to cheat,  is 13.1  - i.e. there is no intrinsic renal damage, and this is all pre-renal).

b) 

The corrected sodium and the osmolar gap:

• The corrected sodium, using the classical equation, is (55/5.6) × 1.6 + [measured Na], which ends up being 160.6.
• The calculated osmolality, (145 × 2) + 55 + 46, = 391. 
• This leaves us with an osmolar gap of 406-391 = 15, which is slightly abnormal (it is supposed to be no greater than 10)

c) "List the likely etiologies" sounds a lot like "explain the abnormalities", but okey:

• Again, this is HHS
• The hyperglycaemia acted as an osmotic diuretic, producing the volume loss, renal failure, urea accumulation, and lactic acidosis. The vom,citing surely did not help.
• The insulin resistance has resulted in the ketoacidosis

d)  For every decrease of 10 g/L i albumin, the anion gap will decrease by 2.5; i.e. the expected normal anion gap of a hypalbuminaemic patient is smaller.

e) The "management of blood glucose and osmolality" here sounds like a hint that the examiners wanted to see a slow deliberate strategy that prevents cerebral oedema. Thus:

• Start fluid resuscitation:
  • 15-20ml/kg in the first hour
  • 4-14ml/kg in the second hour (of 0.45% NaCl)
  • 4-14ml/kg again in the third hour (use 0.9% NaCl if the sodium is low)
  • Then, when glucose is under 15mmol/L, can add some 5% dextrose
• Insulin may be required to address the ketosis, and would be used at a constant rate of 0.1 U/kg/hr 
• Aim for a decrease in osmolality by about 3–8 mOsm/kg/h, as a safe rate (Diabetes UK Position Statement - Scott et al, 2015) - this can often be achieved with fluid resuscitation alone
• Remember to replace electrolytes such as phosphate and potassium