Complications
This iatrogenic complication can occur with excessive high-dose insulin therapy.[11] Treatment-related severe hypoglycaemia is associated with increased mortality.[5]
It can be prevented by following treatment protocols with frequent monitoring of plasma glucose and use of glucose-containing intravenous fluids.[1][13]
If blood glucose falls below 14 mmol/L (252 mg/dL), start 5% or 10% glucose at 125 mL/hour in addition to 0.9% sodium chloride (normal saline).[6]
This iatrogenic complication can occur with excessive high-dose insulin therapy, inadequate potassium replacement, and bicarbonate therapy.[11] Treatment-related severe hypokalaemia is associated with increased mortality.[5]
It can be prevented by following treatment protocols with frequent monitoring of potassium levels and appropriate replacement.[13]
Reported as a complication of HHS. Predisposing factors include volume depletion with increased viscosity, hyperfibrinogenaemia, and elevated levels of plasma plasminogen activator inhibitor (PAI-1).[16][68]
Aggressive early hydration is helpful in reducing the incidence of thromboembolic complications to approximately 2%.[16] 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.[13]
Reported as a complication of HHS. Predisposing factors include volume depletion with increased viscosity, hyperfibrinogenaemia, and elevated levels of plasma PAI-1.[16][68]
Aggressive early hydration is helpful in reducing the incidence of thromboembolic complications to approximately 2%.[16] 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.[13]
Reported as a complication of HHS. Predisposing factors include volume depletion with increased viscosity, hyperfibrinogenaemia, and elevated levels of plasma PAI-1.[16][68]
Aggressive early hydration is helpful in reducing the incidence of thromboembolic complications to approximately 2%.[16] 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.[13]
This is rare in adults with HHS. It presents with headache, lethargy, pupillary changes, and seizure. Mortality is high.
Mannitol infusion and mechanical ventilation should be used. Cerebral oedema can be prevented by avoiding a reduction in plasma osmolality of more than 3 mOsm/kg/hour (3 mmol/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.[13]
Presents with a deteriorating conscious level; seek immediate senior and critical care support.
Consider ordering a CT head if the Glasgow Coma Scale score is deteriorating or the patient has a new or worsening headache.[67]
Usually associated with serum osmolality levels >330 to 340 mmol/kg (>330-340 mOsm/kg) and is most often more hypernatraemic than hyperglycaemic in nature.[10]
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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