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Diabetes Mellitus

To begin with, the talk of diabetes, I want to give you a definition, a working definition the sort of phenotype of the child - or adult for that matter - with type I or insulin-dependent diabetes. Such patients are insulinopenic by definition. That is to say, they are absolutely dependent on exogenous insulin for survival. Without insulin they are prone to ketoacidosis. They typically, without insulin, would be lean and complain of recent weight loss.

A word about the pathogenesis. Again there’s probably a three-part explanation to this. It’s not absolute gospel but it’s the working hypothesis; there is a genetic predisposition linked to the HLA locus. That alone does not give you diabetes, or in identical twin pairs when the first one got it the second one would get it, and that only happens 35% of the time. But there appears to be necessary, atop that genetic predisposition, an environmental trigger such as an infection and Coxsackie viral infection has been purported as one of those.

The clinical presentation; polyuria is present in about 75%, weight loss 35%, actual DKA 25% and actual coma 5%. What does this say? This says that patients are not nearly as sick as they used to be when I first started out in this business.

Now, when the patient actually gets to the acidosis, which again is much less common than in the past, one of the key metabolic events responsible for that - well, everybody knows about insulin deficiency and without insulin of course there will a failure of peripheral tissues to utilize glucose normally and that will result in hyperglycemia, there will also be a breakdown of tissue fat leading to overproduction of fatty acids and ketoacids. Now what’s probably less well appreciated is that when there is insulin deficiency there will also be overproduction of glucagon. Now glucagon comes from the pancreatic alpha cells which have a connection to the beta cells.

Now, with all that said, in the last nine years 90% of our newly diagnosed patients with type I diabetes above the age of two have not required most all of that. But rather they come in and go home the same day with no IV and just being educated and taught survival skills related to diabetes. So again, they are not that sick and just because a patient is newly diagnosed with diabetes does not mean any IV’s, blood gases or even hospitalization. If only I could convince my emergency room colleagues of that point.

If the patient, however, is sick and does require all nine yards, so to speak, I will outline to you my approach to that. The first thing you are likely to do to such a patient is give them intravenous fluids, and you determine how much based on the percent dehydration, and always be aware that unlike other forms of dehydration there will be significant ongoing losses, in most cases, again, because of the glucose drive. If shock is present, personally I would get help. But you do things like boluses of normal saline, Foley catheters, NG tubes, etc. Now the usual fluid approach that I employ in this scenario would be to calculate a figure.

Now what about insulin? If the patient is sick enough to come into the hospital they usually need IV and we usually use either Humalog, which is the ultra short-acting insulin analog, also known as lispro, or human regular insulin and we give that by continuous infusion, and this is sort of a standard cookbook; 1/10 of a unit per kilo per hour, which is a rate studied and proven to lower plasma glucose concentration by about 100 mg/dl per hour and you don’t want to lower it any faster than that because of the osmolality situation. Now in the old days we used to precede this with a bolus of 1/10 of a unit per kilo but this turns out not to make any difference.

Now more on insulin. We typically mix the insulin solution. Something like half a unit per milliliter, or 250 units in a 500 mg bag of normal saline and then you piggy-back it into the system. But you must remember that before piggy-backing it that you have to flush the catheter tubing, or the nurse should, with 50 ml of insulin saline solution to saturate the insulin binding sites in the plastic tubing. If you don’t do that, based on the slow infusion rates that the pumps will deliver of this solution, the patient won’t get insulin for seven hours; until you fill up all the dead space in the tubing. You’ll wonder why the patient is not getting better. As I mentioned previously, as the glucose falls you have to add dextrose to the IV fluids rather than lowering the insulin, so as to continue to prevent further lipolysis. The advantages of this IV insulin regime.

What is conventional insulin treatment as we use it in the clinic setting? Well, that typically can be defined as a split dose, or two injections, containing mixtures in each dose of short and intermediate acting insulin, such as regular NPH or Humalog and NPH. An intensive regimen would be a three-shot regimen which would include a pre-breakfast dose, similar to this, with a mixture of short and intermediate acting insulin and typically at dinner, only short acting insulin.

Glucose monitoring that we recommend; the conventional way is to do like three tests a day, before the two injections, and at bedtime. The more intensive program would involved this pattern plus testing before lunch and even during the night on occasion. Glycosylated hemoglobin we tend to get every three months. Some people do it a little more often. I don’t think it is particularly valuable that way. Just to remind you that glycosylated is a name that is inclusive of various moieties including hemoglobin A1C.