Endocrine Emergencies

C.M. Elwood MA VetMB CertSAC MSc PhD MRCVS DACVIM DECVIM
Davies Veterinary Specialists

Diabetic ketoacidosis (DKA)

Aetiology

Absolute or relative lack of insulin alone is not considered sufficient for generation of ketoacidosis in a diabetic. An excess of diabetogenic and ketogenic hormone is also considered necessary, these hormones include corticosteroids, growth hormone, glucagon and catecholamines, and are increased in circumstances of stress or intercurent illness. Thus a diabetic that is restricted of food or fluid, or develops an infection, is a risk of developing DKA.

Insulin deficiency and diabetogenic hormone excess leads to cellular starvation, lipolysis and protein catabolism. The absence of insulin prevents effective hepatic lipogenesis and leads to ketone body production (acetoacetic acid, acetone, acetone, beta hydroxybutyrate). This is enhanced by diabetogenic hormone excess and fasting or dehydration.

Hyperglycamia leads to glycosuria and obligate osmotic diuresis with loss of water, potassium, sodium and phosphate. Ketonaemia leads to a high anion gap acidosis, cellular potassium loss, ketonuria (with obligate loss of anions such as sodium and potassium) and nausea/vomiting (worsening loss of water and anions and preventing rehydration). The pathophysiological cascade leads to further dehydration, pre-renal azotaemia, hyperkalaemia (in the face of cellular deficiency) and acidosis. This worsens insulin resistance and further increases diabetogenic hormones. Ultimately severe acidosis and cardiovascular collapse can ensue.