Complications
This iatrogenic complication can occur with excessive high-dose insulin therapy. In studies of diabetic ketoacidosis treatment, the risk of hypoglycemia (<70 mg/dL [<3.9 mmol/L]) varied between 16% and 28%, with severe hypoglycemia (<40 mg/dL [<2.2 mmol/L]) occurring in 2% of cases.[103][104] Hypoglycemia during treatment was associated with a 4.8-fold increase in mortality.[104] It 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]
This iatrogenic complication can occur with excessive high-dose insulin therapy and bicarbonate therapy due to intracellular shift of potassium. In one study, hypokalemia (serum potassium <3.5 mEq/L [<3.5 mmol/L]) occurred in 54% of patients admitted to hospital with diabetic ketoacidosis (DKA).[104] Severe hypokalemia ≤2.5 mEq/L (≤2.5 mmol/L) was independently associated with almost fivefold-higher odds for death in a combined cohort of patients treated for DKA or hyperosmolar hyperglycemic state.[104] Hypokalemia can be prevented by following current treatment protocols with frequent monitoring of potassium levels (every 4 hours) and appropriate replacement.[1][105][106]
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).[9] Prophylactic low molecular weight heparin should be used to mitigate the risk of thrombosis.[1]
This occurs due to urinary loss of ketoanions that are 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 hyperchloremic acidosis occurs less frequently with balanced electrolyte solutions and when slower saline infusion is administered.[1]
Rare in adults, more commonly occurs in children; severe cerebral injury occurs in 0.3% to 0.9% of diabetic ketoacidosis episodes in children.[9] Risk factors for cerebral injury include severe acidemia and severe deficits in circulatory volume.[9] The underlying cause is not fully understood but may reflect osmotic changes, hypoperfusion and/or inflammatory responses.[1] Cerebral injury can exist at the time of presentation, but is more common during the first 12 hours of treatment.[9] Symptoms include headache, lethargy, changes in mental status, recurrence of vomiting during treatment, and seizures.[9] Cerebral edema is a serious complication with a reported mortality of approximately 30% compared with those without edema.[1] Cerebral edema may be found on imaging studies, but many patients have no detectable imaging abnormalities at the time of neurologic deterioration.[107] Thus, treatment should not be delayed while awaiting imaging studies.[9] Treatment involves administration of mannitol or hypertonic saline, both of which induce osmotic shifts of fluid from within the intracellular space into the vascular compartment, and mechanical ventilation.[1][9]
Pulmonary edema and ARDS are rare but significant complications of treatment for diabetic ketoacidosis and present with fluid overload and low oxygen saturations.[9][108] They occur when excess fluid is given, even in patients with normal cardiac function. They are more common in patients who are severely dehydrated or with higher glucose levels on arrival. Treatment-related reduction in colloid osmotic pressure may lead to accumulation of water in the lungs, decreased lung compliance and possibly hypoxemia. Pulmonary edema typically occurs several hours after treatment is started and can occur even in patients with normal cardiac function.[66] Simultaneous development of cerebral edema and ARDS has been reported, suggesting a shared pathophysiologic process.[109]
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