46. Diabetic hyperosmolar syndrome (HHS) and coma

Page created on March 30, 2019. Last updated on April 4, 2019 at 12:49

Hyperosmolar hyperglycaemic state

Also called HHS, this complication primarily affects elderly people with type 2 diabetes and not type 1. It can be thought of as the 2DM variant of DKA. Like DKA it’s a potentially life-threatening complication with approx. 15% death rate. Symptoms are mostly similar to those of DKA:

  • Vomiting
  • Polyuria
  • Polydipsia
  • Dehydration
  • Altered mental state, potentially coma

There is no ketoacidosis (and therefore no hyperventilation) and no abdominal pain. It has a slow onset, usually in the course of days.

HHS is caused by relative insulin deficiency. It can develop due to:

  • Stress
    • Infections
    • Surgeries
    • Trauma
    • Myocardial infarction
  • Incorrect administration of insulin
  • Cortisol therapy

The causes are the same as for DKA. These etiologies increase production of insulin-antagonist hormones, causing a relative insulin deficiency that causes severe hyperglycaemia. The hyperglycaemia in HHS is usually more severe than in DKA; here it can reach even 50 – 60 mmol/L.

The reason that the blood glucose level is usually higher in HHS compared to DKA is that in DKA symptoms are caused by both hyperglycaemia and ketoacidosis, while in HHS there is no ketoacidosis. This means that the blood glucose level must be higher to produce equally severe symptoms as in DKA. 

The slow development of this disease has two consequences: Firstly, the patient has time to realize that something is wrong and contact help. Secondly, any decline in mental function may not be as easily noticed by others as it develops so slowly. These two factors together mean that HHS usually only occurs in institutionalized, elderly patients who receive poor care and cannot replace fluids themselves. Elderly people also have reduced feeling of thirst. It rarely occurs in people who have no deficiency of fluid intake.

Many of the pathomechanisms of HHS are similar to those of DKA. The major difference is that the small amount of insulin that is present in patients with 2DM is enough to prevent lipolysis by inhibiting hormone sensitive lipase, preventing ketosis and metabolic acidosis.

Hyperglycaemia: As the hyperglycaemia is more severe in HHS than in DKA is the osmotic diuresis, pseudohypoxia (due to polyol pathway), hyperosmolarity and hypovolaemia also more severe. Up to 10L of body fluids may be lost! These factors cause even stronger non-specific enzyme inhibition than in DKA.

Lactic acidosis may develop as the hypovolaemia causes disordered microcirculation and therefore disordered tissue metabolism. This acidosis is much less severe than that in DKA. The pH may be normal or just slightly on the acidic side.

Potassium: There is total body K+ deficit, similar as in DKA. Insulin deficiency causes K+ to shift out of cells, which is lost with the urine.

Coma develops in 20% of patients. It occurs when the glucose level reaches around 60 mmol/L. The mechanism is mostly the same as for DKA; decreased cerebral blood flow due to hypovolaemia, and lots of non-specific enzyme inhibition and pseudohypoxia. Hyperosmolarity increases the permeability of the blood-brain barrier, allowing toxins to cross. Patients who develop HHS are usually also affected by atherosclerosis, which further decreases cerebral blood flow.

There is no increased osmotic gap in HHS compared to DKA because no ketone bodies are produced in HHS.


Treatment is similar to that of DKA, except no bicarbonate is usually needed. Fluid replacement and insulin infusion should be performed very slowly. K+ should be replaced and all electrolytes should be monitored.

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