a) Outline the distinguishing features that differentiate between diabetic ketoacidosis (OKA) and
hyperosmolar hyperglycaemic state (HHS). (70% marks)

b) List six possible complications seen during treatment of HHS. (30% marks)

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College answer

a) 

  1. History
    1. Known type 1 DM; discontinuation of or inadequate insulin therapy in DKA
    2. HHS – history of type 2 DM +/- non-compliance
    3. Age – DKA usually younger, HHS usually older
    4. Presentation: DKA evolves rapidly (24 hours); HHS typically days-weeks with polydipsia, polyuria and weight loss.
    5. Abdominal pain may be a presenting symptom in DKA
  2. Clinical features
    1. Neurological symptoms more common in HHS. ii. Abdominal pain more common in DKA.
    2. Kussmaul respiration / hyperventilation in DKA
    3. Ketotic breath
  3. Laboratory features
    1. Degree of hyperglycemia (HHS typical higher, exceeding 56 mmol/l; DHA usually< 44 mmol/l)
    2. i. Degree of acidosis: severe in DKA, mild in HHS
    3. Anion gap acidosis present in DKA; absent (or mild in case of concomitant lactic acidosis) in HHS
    4. Ketones: HHS small ketonuria, absent to low ketonaemia [there is sufficient basal insulin secretion to prevent ketogenesis]; both high in DKA
    5. Hyperosmolality more severe in HHS, typically > 320 mosm/l
  4. NOTE: Significant overlap can occur in 30% of patients

 b) 

  1. Hypoglycaemia
  2. Hypokalaemia
  3. Hypophosphataemia
  4. Hypo or Hypernatremia
  5. Cerebral oedema (more common in DKA, has been reported in HHS), may result in decreased LOC, seizures, bradycardia and respiratory arrest
  6. Pulmonary oedema
  7. Deep venous thrombosis and pulmonary embolism
  8. Hyperchloraemic acidosis (usually not clinically significant)

Additional Examiners‟ Comments:

There was a lack of reference to clinical features. Surprisingly few candidates mentioned the presence of ketones and ketoacidosis as a distinguishing feature.

Discussion

Most intelligent people would view the presence of ketones and acidosis in ketoacidosis to be so obvious that it does not merit a mention in a serious discussion. However, it appears to have been one of the tickboxes for the marking examiners. Let that be a lesson to all us candidates. Next time in an exam answer regarding lactic acidosis, be sure to strongly stress the fact that lactate and acidaemia are cardinal features.

a)

This question closely resembles the first part of Question 17 from the first paper of 2014.

In summary:

  • DKA presents with acidosis as the major feature
  • HONK presents with hyperglycaemia as the major feature
Discriminating Between HONK and DKA
Domain

Features suggestive of DKA

Features suggestive of HONK

Demographic
  • Young
  • Known Type 1 diabetic
  • Elderly
  • Known Type 2 diabetic
History
  • Rapid clinical course
  • History of noncompliance with insulin
  • Abdominal pain
  • Shortness of breath
  • Prolonged course
  • History of noncompliance with oral antihyperglycaemic agents and insulin
  • Polydipsia, polyuria, weight loss
  • Neurological symptoms
Examination
  • Tachypnoea
  • Normal level of consciousness, or only slightly decreased
  • Coma
  • Seizures
Biochemistry
  • Severe acidosis
  • Severe ketosis
  • Mild hyperglycaemia
  • Renal function normalises rapidly
  • Mild acidosis
  • Little ketosis; mainly lactate is raised
  • Severe hyperglycaemia
  • Established renal failure

b)

The following list of complications of HHS is a combination of several sources, including local resources as well as the college answers to Question 18.1 from the second paper of 2008 and Question 13 from the first paper of 2002.

  • HHS-specific physiological abnormalities
    • Hypotension and shock
    • Metabolic acidosis
    • Coma
  • Complications arising from the HHS disease state:
    • Cardiac arrest
    • Cardiovascular collapse
    • Myocardial infarction
    • Pulmonray oedema
    • Stroke
    • Cerebral oedema and brain injury
    • Venous thrombosis (DVT, PE)
    • Aspiration
  • Complications of therapy for HHS:
    • Dysnatraemia
    • Hyperchloremia from saline administration
    • Phosphate depletion
    • Hypokalemia
    • Hypoglycaemia
    • Osmotic demyelination (Hegazi et al, 2013)

References

References

Hyperglycemic Comas by P. VERNON VAN HEERDEN from Vincent, Jean-Louis, et al. Textbook of Critical Care: Expert Consult Premium. Elsevier Health Sciences, 2011.

Oh's Intensive Care manual: Chapter 58  (pp. 629) Diabetic  emergencies  by Richard  Keays

Gerich, John E., Malcolm M. Martin, and Lillian Recant. "Clinical and metabolic characteristics of yperosmolar nonketotic coma." Diabetes 20.4 (1971): 228-238.

Kitabchi, Abbas E., et al. "Hyperglycemic crises in adult patients with diabetes." Diabetes care 32.7 (2009): 1335-1343.

Kitabchi, Abbas E., et al. "Hyperglycemic crises in adult patients with diabetes a consensus statement from the American Diabetes Association." Diabetes care 29.12 (2006): 2739-2748.

Hegazi, Mohamed Osama, and Anant Mashankar. "Central pontine myelinolysis in the hyperosmolar hyperglycaemic state." Medical Principles and Practice 22.1 (2013): 96-99.