This term is used to describe patients with recurrent ketoacidosis and/or recurrent hypoglycaemic coma. Of these, the largest group is made up of those who experience recurrent severe hypoglycaemia.
Recurrent severe hypoglycaemia
This affects 1-3% of insulin-dependent patients. Most are adults who have had diabetes for more than 10 years. By this stage, endogenous insulin secretion is negligible in the great majority of patients. Pancreatic alpha -cells are still present in undiminished numbers, but the glucagon response (Opposite action of insulin) to hypoglycaemia is virtually absent. Long term patients are thus subject to fluctuating hyperinsulinaemia owing to erratic absorption of insulin from injection sites, and lack a major component of the hormonal defense against hypoglycaemia. In this situation adrenaline (epinephrine) secretion becomes vital, but this too may become impaired in the course of diabetes. Loss of adrenaline (epinephrine) secretion has been attributed to autonomic neuropathy, but this is unlikely to be the sole cause; central adaptation to recurrent hypoglycaemia may also be a factor.
The following factors may also predispose to recurrent hypoglycaemia:
Overtreatment with insulin. Frequent biochemical hypoglycaemia lowers the glucose level at which symptoms develop. Symptoms often reappear when overall
glucose control is relaxed.
An unrecognized low renal threshold for glucose. Attempts to render the urine sugar -free will inevitably produce hypoglycaemia.
Excessive insulin doses. A common error is to increase the dose when a patient needs more frequent injections to overcome a problem of timing.
Endocrine causes. These include pituitary insufficiency, adrenal insufficiency and premenstrual insulin sensitivity.
Alimentary causes. These include exocrine pancreatic failure and diabetic gastroparesis.
Renal failure. Clearance of insulin is diminished.
Patient causes. Patient s may be unintelligent, uncooperative or may manipulate their therapy.
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