Values for sodium and potassium in DKA and HHS are mean (standard deviation). Source: adapted from Chiasson etal. 2003.1

Patients with DKA tend to produce larger increases in some counter-regulatory hormones—catecholamines, growth hormones and cortisol—but not glucagon, inducing a greater degree of insulin resistance compared with patients with HHS.

The treatment goals for HHS are improving circulatory volume and tissue perfusion, reducing serum glucose and plasma osmolality and correcting electrolyte imbalances, as well as identifying and treating precipitating factors (Figure 8.1). The choice of initial replacement fluid in patients with HHS remains debated. Some authorities advocate the use of hypotonic fluid (e.g. 0.45% saline) from the outset, whereas others advocate the initial use of isotonic fluid (0.9% saline) in the first hour followed by the use of 0.45% or 0.9% saline, depending on corrected plasma sodium and the haemodynamic status of the patient. In the absence of clear evidence, it would be reasonable to firstly correct extracellular fluid depletion by infusing isotonic saline at a rate of 15-20 ml/kg/h (which is hypotonic to the patient's extracellular fluid and remains restricted to the extracellular fluid

Fig. 8.1 Management of HHS. CVP = central venous pressure; U+E = urea and electrolytes.

compartment) in the first one to two hours until vital signs are stabilized, followed by the administration of hypotonic saline at a rate of 4-14 ml/kg/h with the aim of restoring deficits in both intracellular and extracellular compartments as well as ongoing fluid losses.2 Dextrose should be added to replacement fluids when plasma glucose is around 14 mmol/l, with administration of 5% or even 10% dextrose depending on the patient's sodium level. Correction of the patient's dehydration and hyperglycaemic state may result in a transient false elevation of the observed plasma sodium, but when serum sodium is corrected for glucose levels—calculated as ([observed sodium] + 1.6 X [(plasma glucose -5.5)/5.5])—the level of serum sodium may, in fact, be stable or gradually improving. It is also important that changes in plasma osmolality do not exceed 3 mOsm/kg/h. In patients with renal or cardiac dysfunction, it is important to maintain close monitoring of fluid balance, occasionally by central venous pressure and/or pulmonary artery pressure monitoring, in order to avoid iatrogenic fluid overload.

Insulin treatment should be initiated while the patient is being rehydrated with an initial bolus of 0.15 unit/kg (or 10 units soluble insulin) followed by continuous intravenous insulin infusion at a rate of 0.1 unit/kg/h. Failure to reduce plasma glucose level by 3-4 mmol/l/h is often due to inadequate hydration. The appropriate level of hydration reduces the amount of counter-regulatory hormones such as cortisol, growth hormones, glucagon and catecholamines, produced in response to stress, making cells more responsive to insulin. If hydration status is acceptable, insulin rate should be increased hourly until a decrease in plasma glucose of 3-4 mmol/l/h is achieved. Patients are considered to have recovered from HHS if effective osmolality is <315 mOsm/kg and the patient is alert, at which time intravenous insulin treatment can be discontinued. Some patients with HHS may not require long-term subcutaneous insulin treatment, with some requiring only dietary treatment at follow-up.

Treatment with insulin and fluid typically results in a decline in plasma potassium levels, particularly in the first five hours of therapy. Potassium levels should therefore be monitored two-hourly in the first six hours and less frequently thereafter, with appropriate correction (see Chapter 7). High osmolality, dehydration, contracted vascular volume and increased blood viscosity associated with HHS increase the risk of thrombosis. Low-molecular-weight heparin should therefore be administered for prophylaxis in all patients with HHS. Physicians should also be aware of other potential treatment-related complications of HHS. Cerebral oedema can be prevented by correcting sodium and water deficits gradually and avoiding rapid decline in plasma glucose. A reduction in the partial pressure of oxygen caused by increased water in the lungs and reduced lung compliance may lead to adult respiratory distress syndrome. Finally, preventing, identifying and treating the underlying precipitant to HHS are paramount in order to reduce the incidence of HHS and to improve clinical outcomes of patients with this condition.

Recent Developments

While preliminary evidence supports the safety of subcutaneous insulin treatment in patients with mild to moderate DKA, the evidence for this mode of insulin replacement in patients with HHS is not available. Given the greater risks of drowsiness in patients with HHS, only the intravenous route of insulin replacement is recommended.

Hypophosphataemia is seen regularly in patients with HHS. The theoretical benefit of phosphate replacement includes the prevention of respiratory depression, skeletal muscle weakness and risks of cardiac dysfunction. Conversely, excessive phosphate replacement can lead to tetanus, hypocalcaemia and soft-tissue calcification. There are currently no studies on the use of phosphate therapy for HHS.

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