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Diabetic ketoacidosis: Diabetic ketoacidosis – a clinical update a clinical update
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Read this article and complete the quiz to earn 1 iFolio hour Diabetic ketoacidosis (DKA) is a serious and potentially life-threatening complication of diabetes mellitus.1 DKA more commonly occurs in patients with type 1 diabetes, however it can also affect patients with type 2 diabetes.1 DKA is a complex metabolic disturbance characterised by hyperglycaemia, ketonaemia, and metabolic acidosis.2 It occurs as a result of insulin deficiency accompanied by an elevation of counterregulatory hormones, such as catecholamines, adrenaline, cortisol, and glucagon.2 Insulin deficiency may be absolute (during lapses in the administration of exogenous insulin) or relative (when usual insulin doses do not meet metabolic needs during physiologic stress).2,3 The annual incidence of DKA is 4-8 episodes per 1000 patient admissions with diabetes.4 Rates of admissions are increasing due to the increasing incidence of diabetes in the population.5 Diabetes is the fastest growing chronic condition in Australia; 280 Australians develop diabetes every day.6 While mortality from DKA remains relatively low in developed countries, less than 1%, it is the leading cause of death in patients with type 1 diabetes under 58 years of age.7 DKA is a medical emergency, it should be diagnosed promptly and managed intensively.7
PATHOPHYSIOLOGY Insulin reduces blood glucose levels by increasing the uptake of glucose from the bloodstream into the cells and decreasing hepatic glucose production by inhibiting glycogenolysis and gluconeogenesis.1,5 In DKA insulin deficiency leads to impaired glucose uptake and utilisation, increased gluconeogenesis, and accelerated glycogenolysis, resulting in hyperglycaemia.1,8 The increased concentrations of counterregulatory hormones activates hormone-sensitive lipase in adipose tissue, and the resulting enhanced lipolysis releases large quantities of free fatty acids and glycerol into the circulation.1,8 The free fatty acids are oxidised in the hepatic mitochondria to form ketone bodies (acetone, beta-hydroxybutyrate Concurrent with and acetoacetate).1,8 the increased production of ketones, the clearance of ketoacids β-hydroxybutyrate and acetoacetate is reduced, resulting in an accumulation of in ketoacids in the blood, a decrease in serum bicarbonate concentration, and the development of metabolic acidosis.8 The severity of hyperglycaemia and the high concentrations of ketoacids cause osmotic diuresis leading to hypovolaemia, which leads to further increases in counterregulatory hormone levels, further aggravating hyperglycaemia.8
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As insulin also maintains potassium concentrations within the intracellular fluid, insulin deficiency causes potassium to move into the extracellular space leading to electrolyte imbalance.8
CAUSES AND RISK FACTORS The most common precipitating factors for DKA are inadequate or inappropriate insulin therapy and infection.1,2 Inadequate or inappropriate insulin therapy may occur due to missing or inadequate insulin doses, recent medicine titration, or undiagnosed or recently diagnosed diabetes.2,5 The physiologic stress associated with infection stimulates the release of counterregulatory hormones, causing insulin resistance, increased lipolysis, ketogenesis, and volume depletion, which may contribute to hyperglycaemic crises.2,5 Other precipitating factors for developing DKA include:1,2 • Acute illnesses, such as myocardial infarction, stroke, pancreatitis, acromegaly, Cushing’s syndrome, and hyperthyroidism • Bariatric surgery • Medications, such as corticosteroids, thiazide diuretics, second-generation antipsychotics, immune checkpoint inhibitor therapy, and sodium-glucose cotransporter-2 (SGLT-2) inhibitors • Eating disorders • Alcohol and illicit drug use.
SIGNS AND SYMPTOMS Common signs and symptoms of DKA include (see Illustration 1):2,9 • Increased thirst • Abdominal pain • Polyuria • Weight loss • Excessive tiredness • Nausea • Vomiting • Ketone breath (breath smells like sweet acetone) • Dehydration • Confusion • Reduced consciousness. Increasing acidosis is associated with Kussmaul respiration (rapid, deep, laboured breathing).1,2 Severe and prolonged DKA is also associated with hypothermia as a result of peripheral vasodilation.5
DIAGNOSIS The varied presentations of DKA can make diagnosis difficult.1 It is important to exclude other causes of ketoacidosis, such as alcohol ketoacidosis, lactic acidosis, uraemic acidosis, and starvation ketosis.1,2,7 DKA is generally diagnosed using a combination of preliminary clinical assessment and serological tests to measure glucose levels, ketone levels, and venous blood gas.1,2 Diagnosing DKA requires the presence of all of the following:2,7 Glucose: blood glucose level greater than 11mmol/L or known diabetes. Ketones: blood ketones greater than 3mmol/L or ketonuria on a standard urine dipstick. Acidosis: venous pH less than 7.3 and/or bicarbonate level less than 15mmol/L. Rarely, some patients may present with euglycaemic DKA and have a normal blood glucose level.2 Patients treated with SGLT-2 inhibitors are at increased risk of developing euglycaemic DKA.1 The presence of one or more of the following criteria may indicate severe DKA:2,7 • Blood ketones greater than 6mmol/L • Bicarbonate level less than 5.0mmol/L • Venous pH less than 7.0 • Hypokalaemia • Glasgow Coma Scale (GCS) score of less than 12 • Oxygen saturation below 92% on air (assuming normal baseline respiratory function) • Systolic blood pressure below 90mmHg • Pulse over 100 or below 60 beats per minute.
TREATMENT Treatment of DKA consists of fluid resuscitation and maintenance, insulin therapy, electrolyte replacement, and supportive care (see Table 1 for treatment pathway).1 The most urgent goals of treatment are rapid intravascular volume repletion, correction of hyperglycaemia and acidosis, suppression of ketogenesis, and prevention of hypokalaemia.3,7 Identifying and treating precipitating factors is also important.3 Ketonaemia and acidosis should resolve within 24 hours.7 Biochemical markers, ketones, bicarbonate, pH, glucose, and potassium, should be regularly monitored.2 The recommended metabolic treatment targets are:7 • Reduction of blood ketone concentration by 0.5mmol/L/hour • Increase in venous bicarbonate by 3.0mmol/L/hour
