The patient is drowsy and the pulse rate is counted as 110. The respiration is fast at 25 deep and sighing breaths per minute, acetone on breath and keto-acidosis has been made.
Type I diabetes can occur in patients of any age and is characterised by the inability of the pancreas to secrete the hormone insulin due to autoimmune destruction of the beta cells. It occurs in children quite abruptly, though new antibody tests have been developed to detect new onset adult form of type I diabetes mellitus known as LADA (latent Auto-immune Diabetes of Adults). What distinguishes them from other diabetic patients is the fact that if insulin is withdrawn, they develop ketosis and eventually ketoacidosis. Hence such patients are always dependent on exogenous insulin.
Many of the pathophysiological disturbances in a patient with DKA can be measured by a clinician and should be monitored on a real-time basis throughout the course of the treatment. Attention to clinical laboratory data can help the clinician to track and prevent the onset of secondary lethal complications such as hypoglycemia and hyponatremia and hypokalemia.
In the absence of insulin, the primary anabolic hormone, muscles and fats as well as the liver do not take up glucose. Counter regulatory hormones such as glucagons, GH and catecholamines enhance triglyceride breakdown into free fatty acids and gluconeogenesis causing an upshot in the level of serum glucose levels in DKA while there is no insulin. Betaoxidation of these free fatty acids then lead to increased ketone body formations. Metabolism in DKA shifts from the normal fed state to the fasting state characterised by fat metabolism.
Secondary complications of primary metabolic derangement include an ensuing metabolic acidosis as ketone bodies deplete extra-cellular and cellular acid buffers. The hyperglycaemia induced osmotic diuresis depletes phosphates, potassium, sodium and water together with glucose and ketones. Most commonly, it depletes 10% of body water and 5mEq per kg of body mass of potassium. The total body potassium may be masked by acidosis by sustaining an increased serum potassium level. The levels can fall precipitously once the rehydration and insulin treatments start. Loss of ketoanions in urine with brisk diuresis and intact renal function may also lead to hyperchloremic metabolic acidosis.
In the USA, DKA is seen in patients with type I diabetes. The incidence is grossly 2% patient years of diabetes and almost 3% of diabetes patients initially presenting with DKA. It can occur in type 2 diabetic patients as well though not as a rule. The mortality rate of DKA is nearly 2% per episode. Before the discovery of insulin in 1922, the mortality rate was almost 100 percent. Though patients less than 19 years of age are more prone to DKA, it can occur to a person of any age.
History of patients and symptoms at presentation.
Clinicians should look out for the classical symptoms of hyperglycemia such as thirst, polyuria, polydispisia and nocturia. Other symptoms include:
Increased appetite and Anorexia
Clinicians should also be on the