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CDHB

Hyperglycaemic Hyperosmolar Non Ketotic State

Differentiated from patients with DKA by:

• Absence of significant ketosis (there may be a lactic acidosis).
• High blood glucose and plasma osmolality, for example a measured serum osmolality of >320 mosm/kg and a serum glucose of >33 mmol/L.
• Profound dehydration.

These patients are often drowsy, confused or comatose, due to cerebral intracellular dehydration. This syndrome tends to occur in older patients with Type 2 diabetes. Precipitating causes include infection, diuretic therapy and myocardial infarction. It is associated with mortality rates of up to 40%.

Investigations

As for DKA but include plasma osmolality.

Management

• General Principles
  • The key to adequate management is appropriate fluid replacement.
  • The correct choice of fluid replacement and speed of administration are critical.
  • The management plan should be tailored to the individual patient, and will depend on factors such as degree of dehydration, urine output, serial serum sodium readings and concomitant medical problems such as underlying cardiac disease.
  • If management does not result in a steady improvement in the level of consciousness, serum sodium and osmolality, urgent Specialist review is indicated.
  • If severely unwell (measured serum osmolality >340 mosm/kg, glucose >50 mmol/L, significant intercurrent illness or comorbidities), consider admission to ICU. Many patients will benefit from monitoring of CVP. (This is likely to be of particular benefit in patients with congestive cardiac failure or renal insufficiency).
  • Flow chart; plotting fluid replacement, urine output and serum glucose and electrolytes. Venous blood samples should be taken two hourly for the first four hours then at least every four hours thereafter.
  • The flow chart should also document level of consciousness. With adequate fluid and electrolyte replacement, this should gradually improve.
• Fluid and electrolyte replacement
  • Total body sodium will be low, however serum sodium is often elevated secondary to dehydration.
  • Initial therapy is 1 L sodium chloride 0.9% over 30-60 minutes.
  • Subsequent therapy will be dependent on the patient's clinical state but is likely to be 2-3 L sodium chloride 0.9% or sodium chloride 0.45% at 500 mL/hr. Serum sodium may rise during treatment, however this is unlikely to be of major concern if effective osmolarity is falling (see Treatment for an explanation of effective osmolarity), level of consciousness is improving, and IV therapy is producing a slow but steady improvement in metabolic status.
  • Aim for slow metabolic correction, i.e., over >24 hours for less severely unwell patients and up to 72 hours for more severely affected patients.
  • Run 5% glucose in addition to sodium chloride 0.9% or sodium chloride 0.45% when the blood glucose is <15 mmol/L and sodium <150 mmol/L. If glucose is <15 mmol/L but sodium >150 mmol/L, change to 4% glucose and sodium chloride 0.18% or 5% glucose only.
  • Potassium replacement will probably not be needed initially, but, after a few hours rehydration, potassium may be needed at a rate averaging 10-20 mmol/hr. (Total body potassium deficiency will be less marked than in diabetic ketoacidosis). For safety reasons, potassium infusions of >30 mmol potassium chloride/L need to be given via an infusion pump.
• IV insulin replacement
  • Infuse at a rate of 5 units/hr, initially.
  • Once the glucose has reached 15 mmol/L, decrease the rate to 1-2 units/hr.
  • Once the patient is fully rehydrated (which may take >36 hours), consider instituting subcut insulin, as for the management of diabetic ketoacidosis.
  • Longer term, the patient may manage on diet or diet plus oral agents. Discuss this with the Diabetes Physician or Registrar.
• Prevention of venous thrombosis
  • These severely dehydrated comatose patients are at high risk of DVT. Consider prophylactic low molecular weight heparin.

Topic Code: 1372