Hyperosmolar Hyperglycaemia Syndrome

Question 1

What is hyperosmolar hyperglycaemia syndrome (HSS)?

Answer 1

Characterised by profound hyperglycaemia (glucose >30 mmol/L [>540 mg/dL]), hyperosmolality (effective serum osmolality >320 mOsm/kg [>320 mmol/kg]), and volume depletion in the absence of significant ketoacidosis (pH >7.3 and bicarbonate >15 mmol/L [>15 mEq/L]), and is a serious complication of diabetes.

Question 2

What are the risk factors of HSS?

Answer 2

• Infection
  
  • Pneumonia, UTI and always consider diabetic foot infection
• Inadequate insulin or oral antidiabetic therapy
  
  • In practice, look out for patients with worsening glycaemic control
• Risk factors for hyperglycaemia
  
  • Corticosteroids or antipsychotic drugs
• Acute illness
  
  • Myocardial infarction, sepsis and stroke

Question 3

What are the signs of HSS?

Answer 3

• Acute cognitive impairment (GCS or APVU)
• Dry mucous membranes
• Poor skin turgor
• Tachycardia
• Hypotension

Question 4

What are the syptoms of HSS?

Answer 4

• Polyuria
• Polydipsia
• Weight loss
• Nausea and vomiting
• Weakness

Question 5

What investigations should be ordered for HSS?

Answer 5

• Blood glucose
• Blood ketones
• Venous blood gas
• Serum osmolality
• Urea, electrolyes and creatinine
• FBC
• ECG

Question 6

Why investigate blood glucose? And what may this show?

Answer 6

• Blood glucose is high; usually >30 mmol/L (>540 mg/dL)

Question 7

Why investigate blood ketones? And what may this show?

Answer 7

• Use the blood ketone concentration to help distinguish HHS from diabetic ketoacidosis (DKA)
• Negative or low (usually <3 mmol/L)

Question 8

Why investigate venous blood gas? And what may this show?

Answer 8

• Check the lactate level and pH:
  
  • A mild acidosis (pH >7.3, bicarbonate >15 mmol/L [>15 mEq/L]) may be present due to renal impairment secondary to dehydration
  • Lactic acidosis may be present due to sepsis or treatment with metformin
• Mild acidosis (pH >7.3, bicarbonate >15 mmol/L [>15 mEq/L]); lactic acidosis

Question 9

Why investigate serum osmolality? And what may this show?

Answer 9

• Calculate the serum osmolality; this is >320 mOsm/kg (>320 mmol/kg) in patients with HHS

Question 10

Why investigate urea, electrolyes and creatinine? And what may this show?

Answer 10

• Co-existing renal failure is common
• May show:
  
  • Renal impairment
  • Hypo/hyperkalaemia
  • Hypo/hypernatraemia
  • Hypophosphataemia
  • Hypomagnesaemia

Question 11

Why investigate FBC? And what may this show?

Answer 11

• Leukocytosis is common in HHS and correlates with blood ketone levels

Question 12

Why investigate using ECG? And what may this show?

Answer 12

• Can be used to look for:
  
  • Cardiac precipitants of HHS such as myocardial infarction
  • Cardiac effects of electrolyte abnormalities
• Abnormal T or Q waves or ST segment changes in myocardial infarction; evidence of hypokalaemia (U waves) or hyperkalaemia (tall ‘peaked’ T waves)

Question 13

Briefly describe the treatment for HSS

Answer 13

• Fluid replacement and fixed-rate intravenous insulin
• Correction of serum osmolality, electrolytes, and blood glucose
• Prevention of venous thromboembolism, complications of treatment, and foot ulceration
• Treatment of the underlying cause

Question 14

Why do IV fluids need to be given before insulin?

Answer 14

Insulin treatment prior to adequate fluid replacement may cause cardiovascular collapse

Question 15

What IV fluid is used to treat HSS?

Answer 15

Give 1 L of 0.9% sodium chloride (normal saline) over 1 hour

Question 16

What are the complciations of HSS?

Answer 16

• Insulin-related hyperglycaemia
• Treatment-related hypokalaemia

Question 17

Why is insulin-related hyperglycaemia a complication of HSS?

Answer 17

This iatrogenic complication can occur with excessive high-dose insulin therapy.

It can be prevented by following treatment protocols with frequent monitoring of plasma glucose and use of glucose-containing intravenous fluids.

Question 18

Why is treatment-related hypokalaemia a complication of HSS?

Answer 18

This iatrogenic complication can occur with excessive high-dose insulin therapy, inadequate potassium replacement, and bicarbonate therapy.

It can be prevented by following treatment protocols with frequent monitoring of potassium levels and appropriate replacement.

Question 19

What differentials should be considered for HSS?

Answer 19

• Diabetic ketoacidosis (DKA)
• Lactic acidosis
• Alcohol ketoacidosis

Question 20

How does HSS and diabetic ketoacidosis (DKA) differ?

Answer 20

• Differentiating signs and symptoms: patients are often younger and leaner; usually with type 1 diabetes. Abdominal pain is uncommon in hyperosmolar hyperglycaemic state (HHS) but frequently seen (>50%) in patients in DKA.
• Differentiating investigations:
  
  • Venous pH <7.3
  • Bicarbonate <15 mmol/L; raised anion gap
  • Ketonaemia (ketones ≥3.0 mmol/L) or ketonuria (more than 2+ on standard urine sticks)

Question 21

How does HSS and lactic acidosis differ?

Answer 21

• Differentiating signs and symptoms: may be clinically indistinguishable from HHS and DKA, although most patients do not have a history of diabetes.
• Differentiating investigations:
  
  • Venous pH <7.3.
  • Bicarbonate <15 mmol/L ; anion gap >12 mmol/L
  • Lactic acid >5 mmol/L
  • Serum glucose and ketones are normal

Question 22

How does HSS and alcohol ketoacidosis differ?

Answer 22

• Differentiating signs and symptoms: a history of chronic alcohol abuse is present. Produced by starvation due to poor food intake. Peripheral signs of chronic liver disease, such as spider naevi, leukonychia, palmar erythema, bruising, jaundice, scratch marks, and hepatomegaly, are present.
• Differentiating investigations:
  
  • Venous pH is variable and can be normal
  • Bicarbonate <15 mmol/L; anion gap >12 mmol/L
  • Serum glucose is low or normal but serum ketones or beta-hydroxybutyrate is elevated