Diabetic ketoacidosis (DKA) is one of the most commonly encountered endocrine emergencies in small animal practice. DKA is
typically seen in previously undiagnosed diabetics and less commonly occurs in patients that are on inadequate amounts of
insulin. In patients currently receiving insulin, DKA is typically seen in those with a concurrent illness leading to insulin
resistance. The pathogenesis of DKA is multifactorial; the four underlying causes include insulin deficiency, diabetogenic
hormone excess (catecholamines, cortisol, glucagons, growth hormone), fasting, and dehydration. The interplay between these
factors further antagonizes the situation.
Clinical Findings Patients with DKA are divided into those that are "healthy" and those that are sick. Healthy DKAs only
display clinical signs typical of diabetes (pu-pd, polyphagia, weight loss) and present without a history of vomiting, anorexia,
or lethargy. Typically these patients have only trace-to-small amounts of ketonuria noted. Healthy DKA's can be treated like
Sick DKA patients have other systemic signs such as vomiting and lethargy. Physical exam findings may include depression,
dehydration, weakness, tachypnea – this may progress to Kussmaul respiration (slow, deep breathing) due to acidosis and an
acetone odor to the breath. It is not uncommon for patients in DKA to be presented semicomatose. These patients are true
EMERGENCIES!!! Signs may reflect concurrent illnesses as well.
Diagnosis DKA can be rapidly and easily diagnosed. The criteria for establishing this diagnosis include hyperglycemia, glucosuria,
ketonuria, and metabolic acidosis. The presence of hyperglycemia which can be documented using a portable glucometer or point-of-care
analyzer in combination with glucosuria and ketonuria (detected using urine reagent strips) in a patient with appropriate
clinical signs is usually sufficient to establish the diagnosis and begin treatment. Whenever you suspect that a patient
may be suffering from DKA, immediately check urine for the presence of both glucose and ketones! Metabolic acidosis can be
documented by doing a venous or arterial blood gas. For the purpose of analyzing pH, a venous blood gas is sufficient. Normal
pH is 7.35-7.45. Bicarbonate (tCO2) is often included on biochemistry profiles and will be decreased in acidotic patients.
A minimum database (CBC, biochemistry profile, complete UA with culture) is crucial to thoroughly rule out any concurrent
disorders such as pancreatitis. It may be difficult to initially assess renal function due to the presence of pre-renal azotemia
and an osmotic diuresis secondary to the glucosuria.