When
glucose utilisation is impaired due to decreased
insulin effect,
ketones are produced by the liver from
free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe
metabolic acidosis and tends to occur in patients with type I (
insulin-dependent) diabetes mellitus. In addition,
hypovolemia is an almost invariable finding with marked
hypoglycemia and is primarily induced by the associated glucosuria.
Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar
hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of
acetone on the patient's breath sometimes suggests that
ketoacidosis is present. The classical triad of symptoms associated with
hyperglycemia are
polyuria,
polydipsia, and
weight loss. Circulatory insufficiency with
hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including
lethargy,
seizures or
coma. Some patients also have marked
vomiting and
abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled
diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma
glucose concentration. Glucosuria and
ketonuria can be semiquantitatively detected with
reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the
metabolic acidosis.
Therapy must be directed toward each of the metabolic disturbances: hyperosmolality,
ketoacidosis,
hypovolemia and
potassium, and
phosphate depletion. The mainstays of
therapy are the administration of low-dose
insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)