Glucometry: Introduction


Glucometry — i.e. bedside measurement of blood glucose levels, usually from a capillary finger-stick — is an ALS skill almost everywhere, and in some systems it’s available to BLS providers as well. Even in places where it isn’t technically permitted for BLS, it’s often still widely allowed on a “wink and nod” basis, especially on mixed-staffing units where the paramedic has better things to do than apply droplets to test strips.

In other words, it’s something we do. Moreover, it’s something very valuable that we do. I work in a system that allows BLS glucometry along with various other “extras,” and if I had to give up all of it (nebulized albuterol, nasal naloxone, and more) to keep the glucometer, I’d do it in a heartbeat. It serves an invaluable and often irreplaceable role in patient assessment, and it’s used often, not sometimes.

As with any tool, though (such as pulse oximetry), intelligently using the device requires understanding how it works, how its results should be clinically applied, and when it fails. Unfortunately, this is rarely taught in depth, beyond perhaps a brief “How’s how you press the buttons” in-service. So let’s talk about glucometry. And talking about glucometry means starting with glucose.


Glucose Physiology

Practically speaking, glucose is the fuel of human life.

What’s a fuel? Imagine I’m starting a campfire. I build a pile of wood, I light it with a match, and it begins to merrily burn. As any firefighter (or Boy Scout) knows, a fire needs certain things. It won’t burn without a supply of oxygen. It won’t light without a heat source. And, of course, it needs something to actually burn — a fuel.

Although humans have a few different metabolic processes that allow us to survive in difficult circumstances, for the most part, we work the same way as the campfire, except our fuel isn’t wood: it’s glucose. We make a pile of glucose, mix it with oxygen, “light” it with some excess energy, and we’re rewarded with an outpouring of energy far greater than we put in. It’s called aerobic respiration, and almost all of the energy we need to live (sing, dance, hunt the mammoth, think about cellular metabolism, buy cheeseburgers) is generated in this way.

Glucose comes from food; in other words, we eat it. Glucose itself is a very simple sugar, and generally, we don’t literally spoon glucose into our mouths; instead, we eat more complex foods (like cheeseburgers), and our bodies break them down or transform them — either directly into glucose for immediate use, or into a form we can store (like fat), which can be readily broken down to burn later.

Remember, folks: the basic “fire” of life burns glucose and oxygen. We know that without oxygen, we quickly die. For the exact same reason, without glucose — we die. This is not optional stuff, and the only reason we survive longer without cheeseburgers than without air is because our bodies can store substantial amounts of fuel for later use, whereas we can only retain a few minute’s worth of oxygen. (We can also generate some energy through anaerobic metabolism, an “oxygenless fire,” but only very little; it’s a short-term reserve that burns out fast.) Every cell in the body therefore needs a constant supply of fuel to keep its machinery running, and this is supplied by glucose circulating in the bloodstream. Since this stuff is so important, our bodies are very good at monitoring the amount of circulating glucose, replenishing it from reserves when it’s low, and dumping it off when it’s high.

One of the main ways that this fine-tuning is done is using a hormone called insulin. Glucose needs to enter cells in order to be burned, but we want tight control on how much of it enters at any given time (since we need to keep enough circulating for the rest of the cells), so access is managed by a “lock-and-key” mechanism. To pass into most cells, glucose needs to “unlock the door” using an insulin “key.” Without insulin, we can have all the glucose in the world circulating through the blood, but it won’t be able to enter the cells hungry for it, any more than you can get into your house to feed your cat if you’ve lost your keys.



Now, let’s say that I have glucose in my blood. And I’m releasing insulin to let it access my cells. But my cells aren’t listening. It’s like somebody changed all the locks on me; we still have the key, but suddenly, it’s no longer opening the doors.

Why would this happen? There are various reasons, including genetics, certain medications, and a few diseases. But often, a key factor is habituation. If we keep our glucose levels elevated all the time (say, by eating a lot of rapidly-digested sugars), then our insulin levels will also be elevated all the time, and eventually, the insulin receptors on the cell membranes will say: “Boy, it seems like there’s a ton of this stuff around; I must be too sensitive to it. I’ll start ignoring some of it.” This is called insulin resistance, and it can range from mild (only some receptors of some cells are a little resistant) to severe (most cells are practically ignoring insulin). Unfortunately, this problem tends to exacerbate itself, because when our control centers see that releasing insulin isn’t lowering the circulating blood glucose as much as it should, we release more insulin, which encourages further insulin resistance… and so on.

The result of this is that more glucose tends to remain in our blood than we need: hyperglycemia. This isn’t a good thing; all that extra sugar zooming through our veins has a habit of piling up in the wrong places, which leads to strokes, heart attacks, pulmonary embolisms, DVTs, peripheral vascular disease, kidney failure, and more. It sucks, and it’s called type II diabetes mellitus. (Mellitus refers to sugar, and it distinguishes DM from diabetes insipidus, a totally unrelated disease.)

On the other hand, what if we can’t make insulin at all? Usually, this happens when our body’s immune system attacks the emitters that produce insulin, for unclear but unfortunate reasons. It usually begins when we’re young, and although it can be precipitated by various triggers, it generally happens more or less on its own. Whatever the case, if we can’t produce insulin, we’ve lost the key, and glucose can’t enter our cells. Without glucose, the fire doesn’t burn, and we die. It’s called type I diabetes mellitus, and without treatment, it’s always fatal.

Nowadays, type I diabetics survive by taking exogenous insulin — since they can’t make their own, we synthesize it for them, and they simply inject it. (They still make their own insulin, so most type II diabetics don’t need to inject the stuff; they manage their blood sugar through careful control of how much they eat. In some cases, however, particularly in the elderly or anyone who is less able to tightly manage their diet, type IIs will also use insulin to help adjust their levels.) How do they know how much to take?

There are ways to estimate insulin doses by, for instance, measuring how much food you’re eating, or from past experience. However, it’s also incredibly easy to misdose. Insulin is a powerful, powerful drug, and a small change in dose can mean the difference between bringing you to a normal, healthy blood sugar, and sucking every last glucose molecule out of your blood until you’re dangerously low — hypoglycemic.

Although hyperglycemia is unhealthy in the long run, and massive hyperglycemia can be an acute danger, even brief periods of modest hypoglycemia can be deadly, so it’s something to avoid. As a rule, the problem in diabetes is too much sugar, not too little, so left on their own, almost no diabetic would become hypoglycemic. However, since all type I and some type II diabetics take exogenous insulin, hypoglycemia happens all the time due to overdosing. In other words, we do it to ourselves — or to our patients — accidentally. (Even when type IIs don’t take insulin, they almost always take other drugs that help mitigate glucose levels or sensitize their insulin receptors, and some of these meds can also cause hypoglycemia.) Getting it right isn’t as easy as it sounds, because numerous factors can cause changes in your blood glucose and/or your insulin sensitivity; for instance, exercise depletes glucose (the hotter fire needs that fuel), so if you hit the gym and forget to eat more or to reduce your dose to compensate, you can easily deplete your available sugar and collapse.

The best way to get the right insulin dose is to accurately track your current blood sugar, and nowadays, this is done easily and quickly using a hand-held glucometer. Tune in next time, and we’ll talk about how they work and how to use them.

Continued in Glucometry: How to Do It and Glucometry: Clinical Interpretation


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