Hyperosmolar hyperglycaemia (HH) is generally the fulminant result of poorly treated type 2 diabetes or delayed diagnosis of previously unknown type 2 diabetes. HH is less frequent than DKA, but mortality is higher and remains close to 15% in many centres [1,20]. As implied hyperosmolality is the primary clinical problem and there will be hyperglycaemia of >35-40 mmol/L and an effective serum osmolality of >320 mOsm/kg (Table 1). HH most often occurs in frail patients in combination with other potentially fatal conditions. Strict differentiation between DKA and HH can be difficult, because some degree of ketosis may be present in HH and because, for example, lactic acidosis, respiratory and renal failure may also be present. In practise this dilemma is mainly ornamental, since diagnostic and therapeutic efforts follow the same principles.
In line with DKA, HH is most often precipitated by infectious diseases or cardiovascular events and symptoms of hyperglycaemia usually have been present for some days. Hyperglycaemia is caused by a vicious cycle, in which relative insulin deficiency and high levels of stress hormones lead to increased endogenous glucose production and decreased peripheral glucose utilisation; hyperglycaemia in turn induces hyper-osmolality and dehydration, which amplifies the stress hormone response and further impairs insulin secretion and vice versa.
At presentation the clinical condition is poor and the patient is very dehydrated with poor skin turgor and often exhibits altered level of consciousness (ranging from drowsiness to coma) and signs of hypovolaemic shock. In general the diagnostic procedures are similar to DKA. Typically, there will be a water deficit of 10-20% of body weight together with sodium, chloride and potassium deficits between 5 and 10 mmol/kg body weight.
Treatment of HH also follows the same guidelines as for DKA, the main aim being a controlled correction of hyperglycaemia, hyperosmolality and water and electrolyte deficits over 24 h. Patients are generally more sensitive to insulin and an infusion of 0.1 IU/kg BW/h is more than adequate in most cases. Repeated hourly boluses of 0.15 IU/kg BW (or 10 IU) may also be used. As with DKA dosage should be adjusted according to normal daily insulin needs and depending on therapeutic response. Usually 1L of isotonic saline is infused in the first hour but after that slower rehydration is advisable. Haemodynamic performance should be monitored carefully and it should be borne in mind that many of the patients have pre- or coexisting cardiac disease. The use of a central venous pressure line is helpful. It should be noted that a significant proportion of HH patients are hyperna-traemic. In this case hypotonic saline can be used but more slowly. Potassium is administered along the same lines as with DKA and it is often wise to monitor the patient in the intensive care unit.
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