Complications
This iatrogenic complication can occur with excessive high-dose insulin therapy and bicarbonate therapy due to intracellular shift of potassium. In one study, hypokalaemia (serum potassium <3.5 mmol/L) occurred in 54% of patients admitted to hospital with diabetic ketoacidosis (DKA).[169] Severe hypokalaemia ≤2.5 mmol/L was independently associated with almost fivefold-higher odds for death in a combined cohort of patients treated for DKA and hyperosmolar hyperglycaemic state.[169] Hypokalaemia can be prevented by following treatment protocols, ensuring frequent monitoring of potassium levels and appropriate replacement.[1][170][171]
This iatrogenic complication can occur with excessive high-dose insulin therapy. In studies of diabetic ketoacidosis treatment, the risk of hypoglycaemia (blood glucose <3.9 mmol/L) varied between 16% and 28%, with severe hypoglycaemia (blood glucose <2.2 mmol/L) occurring in 2% of cases.[158][169] Hypoglycaemia during treatment was associated with a 4.8-fold increase in mortality.[169] Hypoglycaemia can be prevented by following current treatment protocols with frequent monitoring of plasma glucose (every 1-2 hours) and use of glucose-containing intravenous fluids.[1]
Diabetic ketoacidosis causes a hypercoagulable state with increased risk of thrombosis. Risk of thrombosis is increased when central venous catheters are used to gain intravenous access (if peripheral access was not possible owing to severe dehydration).[11] Prophylactic low molecular weight heparin should be used to mitigate the risk of thrombosis.[1][2] Consult your local protocol.
Risk factors for cerebral injury include severe acidaemia and severe deficits in circulatory volume.[11] It can exist at the time of presentation, but is more common during the first 12 hours of treatment.[11] The underlying cause is not fully understood but may reflect osmotic changes, hypoperfusion and/or inflammatory responses.[1] It occurs most commonly in children and adolescents, and is rare over the age of 28 years. It is the most common cause of mortality in diabetic ketoacidosis.[2][63][79]
Pulmonary oedema and ARDS are rare but significant complications of treatment for diabetic ketoacidosis and present with fluid overload and low oxygen saturations.[163] Pulmonary oedema typically occurs several hours after treatment is started and can occur even in patients with normal cardiac function.[2][20]
Pulmonary oedema and ARDS are more common in patients who are severely dehydrated or with higher glucose levels on arrival.
Look for an increased alveolar to oxygen gradient (AaO2) and auscultate for lung crepitations.
Request a chest x-ray if oxygen saturations fall. Consider performing an arterial blood gas.
This occurs due to urinary loss of ketoanions needed for bicarbonate regeneration, and also increased reabsorption of chloride secondary to intensive administration of chloride-containing fluids. It may be observed during the recovery phase of diabetic ketoacidosis. This acidosis usually resolves and should not affect the treatment.[1] There is some evidence that hyperchloraemic acidosis occurs less frequently with balanced electrolyte solutions and when slower saline infusion is administered.[1]
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