Question 6

A 21-year-old 50kg patient with insulin-dependent diabetes presents to the emergency department with a 3-day history of vomiting. The diagnosis of diabetic ketoacidosis is confirmed. This is the arterial blood gas on air at presentation:

Parameter

Patient value

Adult normal range

pH

6.93*

7.35-7.45

Bicarbonate                

2 mmol/L*

22-26

Base excess

-28 mmol/L*

-2-+2

Lactate

2.8 mmol/L*

0.5-1.6

Sodium

127 mmol/L*

135-145

Potassium

5.5 mmol/L*

3.5-5

Chloride

98 mmol/L

95-105

Glucose

22 mmol/L*

3.5-6

Urine analysis:    Ketones 4+
Blood ketones:    2 mmol/l
a)    Outline your management of fluid replacement, electrolyte replacement and insulin therapy in the  next 24-hours. (8 marks)
b)    Briefly outline the pathophysiology of euglycaemic ketoacidosis in a patient taking dapagliflozin (a sodium-glucose co-transporter 2 inhibitor). (2 marks)
 

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College Answer

Syllabus topic/section:

2.1.9    Endocrine Intensive Care – L1.
2.1.21 Applied Pharmacology in Intensive Care.

Aim:

To demonstrate a detailed understanding of the practical management of diabetic ketoacidosis and to demonstrate knowledge of the pathogenesis of the most important complications of these drugs.

Discussion:

Part (A) – This question tests recall of how to manage DKA and explores the application of these management principles to the clinical scenario given. Candidates scored well if: They detailed a standard approach to DKA specifically addressing 24hrs management of fluids, electrolytes, and insulin for the patient scenario provided with clearly mentioned endpoints. Candidates scored poorly if they did not mention management of these domains and failed to write clear endpoints or inaccurate doses of insulin and inadequate fluids were administered.
Strategies to improve: Address the question asked by reading and understanding the question, do not waste time in writing things not asked e.g. resuscitation issues other than those of volume status. Mentioning management plan/goals with reference to standard guidelines are rewarded.

Part (B) – Candidates scored if well if they mentioned: as the SGLT2 inhibitors block the sodium-glucose co- transporter 2, the resulting glucosuria leads to decreased plasma glucose levels and decreased insulin release. Carbohydrate deficit, insulinopenia, and increased glucagon release lead to upregulation of lipolysis and ketogenesis resulting in ketoacidosis. Candidates scored poorly if they were unable to demonstrate the pathophysiology of euglycaemic ketogenesis.
 

Discussion

a)  

These management strategies are derived from the 2022 JBDSIC guidelines 

  • Fluid replacement
    • 20ml/kg of IV fluid (saline or balanced crystalloid) in the first hour
    • 4-14 ml/kg/hr in the next two hours
    • Aim for total replacement of up to 100ml/kg (total water deficit in DKA)
    • Endpoints:
      • Restoration of circulating volume: haemodynamic goals, eg. SBP 90 mmHg, as well as clinical features such as urine output and peripheral perfusion
  • Electrolyte replacement
    • Replace potassium (ideally as potassium acetate)
    • Replace phosphate (as potassium dihydrogen phosphate)
    • Ideally via central line, to allow concentrated electrolyte infusion
    • Expect to replace about 3-5 mmol/kg of potassium and 1 mmol/kg of phosphate, in total
    • Endpoints:
      • maintain normal potassium concentration (4.0-5.0 mmol/L)
      • maintain normal phosphate and magnesium concentration
  • Insulin therapy
    • Insulin infusion at 0.1u/kg/hr
    • Hourly monitoring of BSLK and ketones
    • Endpoints:
      • Increase the HCO3- by 3mmol/L every hour
      • Decrease the BSL by 3mmol/L every hour
      • Decrease the blood ketone concentration by 0.5mmol/L every hour
    • Continued until BSL is reduced to below 14mmol/L
    • Then, continued together with IV dextrose (5% or 10%) until ketone levels <1.5


b)  Pathophysiology of euglycaemic ketoacidosis, for 2 marks, would literally have to be something in about forty words. Thus:

  • Reduced glucose availability due to glycosuria produced by the SGLT2 inhibitor
  • Thus, reduced insulin secretion and increased glucagon secretion
  • Thus, lipolysis and ketogenesis
  • Plus, glycosuria produced by the SGLT2 inhibitor adds to the problem by producing volume depletion

References

Long, Brit, et al. "Euglycemic diabetic ketoacidosis: etiologies, evaluation, and management." The American Journal of Emergency Medicine 44 (2021): 157-160.

Dhatariya, Ketan K., and Joint British Diabetes Societies for Inpatient Care. "The management of diabetic ketoacidosis in adults—An updated guideline from the Joint British Diabetes Society for Inpatient Care." Diabetic Medicine 39.6 (2022): e14788.