Complications
Hypoglycemia is a common complication encountered in the treatment of HHS.
In studies of diabetic ketoacidosis (DKA) and HHS treatment, the risk of hypoglycemia varies between 13% and 30% (<70 g/dL [3.9 mmol/L]) with severe hypoglycemia (<40 g/dL [2.2 mmol/L]) occurring in 2% of cases.[6]
Hypoglycemia (<40 mg/dL [<2.2 mmol/L]) during treatment was associated with a 4.8-fold increase in mortality (adjusted odd's ratio [OR] 4; 95% confidence interval [CI] 1.4 to 16.8).[6]
It can be prevented by following treatment protocols with frequent monitoring of plasma glucose and use of glucose-containing intravenous fluids.[2][68] Frequent blood glucose monitoring (every 1-2 hours) is mandatory to recognize hypoglycemia.
When glucose levels are reduced to <250 mg/dL (<13.9 mmol/L), it is advised to reduce the insulin infusion rate to 0.05 units/hour and replacement fluids should be modified to contain 5% to 10% dextrose to prevent hypoglycemia.
Hypokalemia is a common complication owing to intracellular shift of potassium following insulin treatment. In one study, hypokalemia (<3.5 mEq/L) occurred in ~51% of HHS patients.[6]
Severe hypokalemia ≤2.5 mEq/L associated with increased inpatient mortality (adjusted OR 4.9; 95% CI 1.3 to 18.8).[6]
Careful potassium monitoring every 4 hours is mandatory during treatment and potassium replacement should be added to fluid resuscitation to prevent hypokalemia.
Reported as a complication of HHS. Predisposing factors include volume depletion with increased viscosity, hyperfibrinogenemia, and elevated levels of plasma plasminogen activator inhibitor (PAI-1).[19][69]
Aggressive early hydration is helpful in reducing the incidence of thromboembolic complication.[19] There is no evidence for full anticoagulation, though everyone with HHS should receive prophylactic low-molecular-weight heparin for the entirety of their hospital admission, unless there are contraindications.[3]
Reported as a complication of HHS. Predisposing factors include volume depletion with increased viscosity, hyperfibrinogenemia, and elevated levels of plasma PAI-1.[19][69]
Aggressive early hydration is helpful in reducing the incidence of thromboembolic complication.[19] There is no evidence for full anticoagulation, though everyone with HHS should receive prophylactic low-molecular-weight heparin for the entirety of their hospital admission, unless there are contraindications.[3]
Reported as a complication of HHS.[19][69]
Aggressive early hydration is helpful in reducing the incidence of thromboembolic complication.[19] There is no evidence for full anticoagulation, though everyone with HHS should receive prophylactic low-molecular-weight heparin for the entirety of their hospital admission, unless there are contraindications.[3]
Cerebral edema is rare in adults. The underlying cause is not fully understood but may reflect osmotic changes, hypoperfusion, and/or inflammatory responses.
Mannitol infusion and mechanical ventilation should be used. Cerebral edema can be prevented by avoiding a rapid and aggressive reduction in plasma osmolality of more than 3 mOsm/kg/hour. This can be achieved by monitoring plasma osmolality, adding dextrose to intravenous fluids once plasma glucose falls below 250 to 300 mg/dL, and selecting the correct concentration of intravenous saline.[44]
In adults with HHS, a slow rate of correction of hyperosmolarity is indicated.
Usually associated with total serum osmolality levels >330 to 340 mOsm/kg and is most often more hypernatremic than hyperglycemic in nature.[9][13]
Intensive care unit admission, close monitoring, and aggressive fluid and insulin therapy are necessary. Many patients may require airway protection and mechanical ventilation.
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