Staying in Place: Compensation and Endpoints

Man’s leaning against a wall. He doesn’t move for hours. Just stands there not moving. Finally, someone says, “You been here all day — don’t you have anything to do?”

“I’m doing it,” he answers.

“Doing what?”

“Holding up the wall.”

And who’s to say he’s not? Maybe he’s working as hard as he can to make sure that wall doesn’t fall down.

In this situation, the man is a compensating mechanism. He is struggling to prevent changes in the wall; keeping that wall upright is an endpoint he cares to maintain, to sustain, to keep intact.

How do we know that the wall isn’t holding up the man? Because we don’t care about the man. Whether he leans or falls doesn’t matter much to anybody. But it would be a terrible thing if the wall collapsed. So we’ll let the man lean or shift in order to prop up the wall when it starts to totter — we’ll use him, adjust him, to compensate for any wall-changes. That’s why he’s there.

If the wall gets weak enough or tilts too far, though, he won’t be able to keep it up. He’ll try, but he’s not infinitely strong, and then maybe the wall begins to tilt or collapses completely. Since we know that under normal circumstances, he’s doing his best to prevent this, if we walk in and see that the wall is tilting, that is not a good sign. It may mean that despite his best efforts, the man has exhausted his strength and is no longer able to resist further wall-changes; or it may mean that, for some reason, the man isn’t doing his job properly. Either way, any further tilting will be unopposed, and will probably happen rapidly and uncontrollably.

Compensators and endpoints

This same dynamic plays out within the human body. As we know, living organisms seek to maintain a certain homeostatic equilibrium. We put our vital metabolic processes in motion and we don’t want them to halt or change, despite any insults or fluctuations imposed upon us by our surrounding environment. So our bodies struggle to keep all of our complex systems at an even keel, using a diverse and powerful array of knobs, dials, and other regulatory tools. Not too hot or too cool, not too acid or too basic, not too fast or too slow. Just right.

The kicker is this, however. Some of our physical parameters are more important than others. In other words, while some parameters have room to adjust, others aren’t negotiable, can’t change much, without derailing our basic ability to function and survive. Things like blood pressure (or at least tissue perfusion, for which blood pressure is a pretty good surrogate measure) are essential to life; your pressure can fluctuate a little, but if it drops too low, you are unquestionably going to suffer organ damage and then die. And yet there are many insults that could potentially lower our blood pressure if we let them: if we bleed a little, or pee a little, or don’t drink enough water, or sweat, or even just stand up instead of sitting down. How do we preserve this vital parameter despite such influences?

By compensating, of course. Our body gladly modulates certain processes in order to preserve other, more important parameters. So in order to maintain blood pressure, perhaps we accelerate our heartrate. In an ideal world, it might be nice if the heart were thumping along at — let’s say — a mellow 80 beats per minute. It’ll use little less energy and less oxygen than if it were beating faster. But it’s really important to keep our blood pressure up, and speeding up the heart can increase the pressure, so we gladly make that trade and induce tachycardia. (Many of these compensatory systems are linked to the sympathetic nervous system, our body’s standard “all hands on deck” response to stress and crisis.)

So imagine we find a patient who’s bleeding and notice that he’s tachycardic, with a normal blood pressure. This suggests a compensated shock; the body is using tachycardia to maintain that normal pressure we see; although his volume is lower than usual, the critical endpoint of adequate blood pressure is still intact.

But what if instead, we found him tachycardic and hypotensive? Well, that’s not good. We see that the body is trying to compensate, but we also see that the important endpoint — blood pressure — is falling nonetheless. The body would never intentionally allow that; BP is too important. So we recognize this as decompensated shock. The hypovolemia has progressed so far, and volume is now so low, that he can’t make up the difference anymore — the compensatory slack has run out — and any further decreases in volume will probably lead to an immediate and unopposed drop in pressure. There’s nothing more the body can do on its own; it’s out of rope.

The skilled clinician — or “homeostatic technician” as Jeff Guy says — uses this predictable progression to understand what’s happening in almost any crisis. Because primary insults are initially covered up by compensatory mechanisms, they may not be immediately apparent, and the earliest and most detectable signs of physical insult are usually nothing more than the footprints of the answering compensation. Thus, when when we encounter those, we know to suspect the underlying problem even if it’s not obvious yet. It’s like seeing brakelights flash from cars on the road ahead; even if you can’t see an obstacle yet, you know people are slowing down for something.

Obvious signs of decompensation usually show up late. Once the primary, underlying problem is revealed by failure of the corrective mechanisms, it’s often progressed so far that it’s too late to address. If you wait to brake until you can see the wreck itself, you might not be able to stop in time.

Two signposts for decompensation

There are two great ways to recognize which signs and symptoms connote decompensation.

The first is to understand which physical parameters are endpoints — which functions the body tries to preserve at all costs. These processes are only compromised as a last resort, so if you see them deteriorate, things are in the end-game; the body doesn’t intentionally sacrifice these for the benefit of anything else.

The second clue is more subtle. In this case, you observe a compensatory mechanism (not an endpoint), but find that it’s no longer successfully compensating — it’s failing, and starting to unwind and scale back, rather than doing its job. The changes in the compensatory system are inappropriate, resulting in less of what we need, not more. This happens when our systems are so damaged that they can’t even fix problems and pursue homeostasis anymore; our infrastructure, maintenance, and repair systems are breaking down. Consider this: we saw how tachycardia could be compensatory, but could bradycardia ever be beneficial in shock? Probably not. So if we found a shocked patient with bradycardia (and likely hypotension, the failing endpoint), we should be very alarmed indeed. There’s nothing helpful, compensatory, or beneficial about bradycardia in the setting of shock, so we recognize that the body would never go there on purpose. It’ll only happen when the machinery itself is falling apart.

Consider, for instance, Cushing’s Triad, the collection of signs often encountered after severe traumatic brain injury, when intracranial pressure has increased enough to squeeze the brain out from the skull like toothpaste. The triad includes hypertension, bradycardia, and irregular or slow respirations. What’s interesting is that, while all are a result of increased ICP, one of these is compensatory, while the others are merely the result of damage. Hypertension is the body’s compensatory attempt to force blood into the brain despite the elevated pressure in the skull. But bradycardia and bradypnea simply result from pressure upon the regulatory centers of the brain tasked with maintaining breathing and heart-rate. That’s why hypertension may be seen earlier, while the other two signs won’t usually manifest until the brain is actively herniating. One signals compensation, the other two decompensation.

Of course, there can be other reasons why compensatory mechanisms might fail, or at least exhibit lackluster performance. Some medications or other aspects of a medical history (potentially unrelated to the current complaint) might throw a wrench in the system. For instance, beta blockers (such as metoprolol and other -olol drugs) limit heart-rate as part of their basic mechanism, so patients with beta blockade often have trouble mustering compensatory tachycardia during shock states. That doesn’t mean they’re any less shocked; in fact, it means they’re more susceptible to hypotension, and that you must be especially on the lookout, because you won’t see one of the red flags (a rapid heart-rate) you might usually expect. Elderly patients with many comorbidities are generally not able to muster up effective compensation for anything, so they can deteriorate quickly, and without much fanfare. Ironically, healthy pediatric patients are the opposite: since they’re so “springy” and smoothly functioning, they compensate very well, with few changes in observable endpoints, until suddenly running out of slack and crashing hard because they’re already so far from shore.

Here are a few important compensatory signs, breakdowns of compensatory systems, and vital physical endpoints:

Appropriate signs of compensation

Tachycardia — increases cardiac output
Vasoconstriction (cool, pale skin) — raises blood pressure
Diaphoresis (sweatiness) — decreases temperature when necessary, but is often just a side effect of sympathetic stimulation
Tachypnea — increases oxygenation, CO2 blowoff, and cardiac preload
Fever — part of the immune system’s response to infection
Shivering — warms a hypothermic body

Inappropriate changes in compensatory mechanisms

Bradycardia — reduces cardiac output, rarely useful in illness; as a chronic finding may be the result of high levels of cardiovascular fitness (in healthy young patients) or medications (in sick old patients); but acutely, it is an ominous finding
Bradypnea — reduces oxygenation, CO2 blowoff, and cardiac preload
Hypothermia (or normothermia when a fever is expected) — suggests a failure of temperature regulation

Inviolable endpoints

Blood pressure — can elevate in stress states, but should not drop below resting levels
Mental status — except in the presence of a drug or similar agent directly affecting cognition, maintaining appropriate alertness and mentation are always a top priority for the body
Blood glucose — kept at normal levels in almost all situations, except when the regulatory systems fail, as in diabetes mellitus
pH — most of the cellular machinery fall apart if significant acidosis or alkalosis occurs
Low O2 saturation or cyanosis — although oxygen saturation can dip briefly without harm, and in some patients (particularly those with COPD, or long-time smokers) it may run low at baseline, a significant acute drop — or the clinical equivalent, which is frank cyanosis — is always inappropriate.

Glucometry: Clinical Interpretation

Continued from Glucometry: Introduction and Glucometry: How to Do it

Implementing glucometry into your overall assessment means understanding three things: when to use it, what the results mean, and when it fails.

Indications

First of all, by and large the only people with derangements of their blood sugar should be diabetics. The rest of us are generally able to maintain euglycemia through our homeostatic mechanisms, except perhaps in critical illness causing organ failure and similar abnormal states. Now, if someone injected you — a non-diabetic — with a syringe of insulin, you’d become terribly hypoglycemic, since it would overwhelm your body’s ability to compensate for the loss of glucose. But nobody’s likely to do that if you’re not a diabetic, unless it’s meant for somebody else and a drug error occurs, or I suppose if they’re trying to assassinate you.

With that said, people walk around who are diabetic and don’t know it. I’ve lost track of the patients I’ve transported who presented with signs suggestive of a diabetic emergency, denied a history of diabetes, and came back with a BGL of 600. Well, my friend, I have some bad news for you. “Everybody is diabetic, even if they’re not” is my attitude. Almost a fifth of older Americans are diagnosed, and the older and sicker they are, the more common it is.

Which brings us back to: who needs a BGL?

The most correct answer is anybody with clinical indications of either hypo- or hyperglycemia. As we saw, diabetes itself is really associated with hyperglycemia, which is why the classic signs of hyperglycemia are usually used to diagnose diabetes: polyuria (excessive urination, as extra glucose is excreted by the kidneys and brings water along with it osmotically), polydipsia (excessive thirst and water consumption, to replace the fluids urinated out), and polyphagia (constant hunger, since despite all the sugar floating around it’s not reaching the cells very easily). If your patient is complaining of those, you might be the first one to discover their condition. The diagnosis doesn’t require elaborate tests and imaging; a fasting glucose over 126 BGL tested on multiple occasions, or just once in combination with clinical symptoms, or a post-prandial (after eating) glucose exceeding 200, is the definition of type II DM. (With that said, I wouldn’t go around diagnosing your patients; that’s not your job, and you’re not quite that good.)

Once the glucose gets higher than the “renal threshold” — usually around 180 in average folks — the body starts to excrete it into the urine. This can actually be detectable by chemical dip-stick, or even by odor and texture at very high levels.

When hyperglycemia becomes severe and prolonged enough, we start to worry about diabetic ketoacidosis. Although burning fat and protein is not necessarily dangerous (some popular diets actually put you into a mild ketogenic state intentionally), extensive accumulation of ketones caused by a total lack of insulin (as in type I diabetics — DKA is rarely seen in type II) creates a metabolic acidosis in the body. This is when the long-term harm of hyperglycemia becomes a short-term hazard. DKA causes altered mental status, usually elevated states of confusion and disorientation, and combative behavior isn’t uncommon. Combined with the acetone odor that sometimes presents on the patient’s breath — which can smell like alcohol — DKA patients can seem suspiciously like drunks, and treating them like drunks is a great way to go down a bad path. (A word of wisdom: not only is everybody diabetic, but drunks are definitely diabetic.) DKA also frequently presents with symptoms of dehydration, due to the osmotic water loss in the urine; nausea and vomiting; and deep, rapid Kussmaul breathing to blow off the acidic CO2.

A few situations can cause short-term hyperglycemia, including stressors of any kind (there’s even “white coat hyperglycemia,” where patients tend to produce elevated sugars at the doctor’s office), but these typically won’t produce anything like the massive levels leading to DKA.

With all of that said, you need to really build up some glucose before hyperglycemia becomes symptomatic, and even more than that before it becomes acutely dangerous and unstable. That’s why as a rule, we’re more concerned with hypoglycemia, usually due to medication administration, physical exertion, or metabolic demand exceeding what was expected. Hypoglycemia again presents as altered mental status, in this case more often an inhibited rather than an elevated state: confusion, lethargy, disorientation, inability to focus or follow commands, weakness, headache, seizures, and eventually coma and death. The fun part is that the impairments can present as focal as well as generalized deficits: unilateral weakness of the limbs or face, speech slurring, poor gait, vision abnormalities, and more. In fact, hypoglycemia is a neurological chameleon, and can look like almost anything; it’s particularly notorious for imitating strokes, and for causing (not imitating) seizures. Interestingly, kids are particularly prone to hypoglycemia due to their gigantic heads, full of glucose-hungry brain.

Despite all this, the primary manifestations of early hypoglycemia are actually not symptoms of hypoglycemia. Rather, they’re caused by catecholamines — by the body releasing stress hormones, primarily epinephrine, in a response to the emergency. (This is not an irrational move: epinephrine helps us release and retain glucose.) As a result, we often seen the same signs we’d expect in anybody with a profound sympathetic stimulus: pale and diaphoretic skin, anxiety and shakiness, tachycardia and hypertension, even dilated pupils. Wise diabetics recognize the early signs of this sympathetic response and drink some Pepsi. As levels keep dropping, these symptoms combine with the neurological effects of glucose starvation to produce a confused, sweaty, increasingly stuporous individual. If left untreated, finally the sugar drops until we’re looking at the picture of impaired and diminished consciousness caused by true hypoglycemia. So just like always, the signs of compensation are our early warning system; once the body decompensates, it’s already late in the game.

To make a long story short, anybody with altered mental status, or any kind of general systemic complaint (weakness, fatigue, anxiety, nausea, etc.) should probably get their glucose tested, whether or not they have a known history of diabetes. This is true even if you suspect another cause, such as stroke. Not only can diabetic emergencies look like anything, they can also be comorbid; it is extremely common for patients to have another problem, yet also to bring a high or low sugar along for the ride, due to the illness throwing a wrench in their normal intrinsic and extrinsic glycemic homeostatic systems.

A number of years ago, there was some limited but compelling research that suggested poorly-controlled blood glucose (meaning not severe derangements but merely small deviations from the ideal range) was associated with increased mortality among an inpatient population with a wide variety of conditions. In other words, if you were hospitalized with something like sepsis, you were more likely to end up dying if your sugar tended to float around 160 instead of 110. As a result, it become trendy to practice extremely tight and aggressive glucose management for virtually everybody; diabetic patients were being tested every few hours and ping-ponged around using medication to keep their numbers textbook-perfect. More recently a number of studies have suggested that this may be less important than was thought, and in fact that excessive paranoia leads to a lot of iatrogenic harm from accidental insulin overdoses. This battle is still being fought in the hospitals, but for our purposes a reasonable take-away would be: when managing acute illness, from sepsis to head injury to cardiac arrest, once everything else is done it’s not a bad idea to check the patient’s sugar.

What’s the Number Mean?

So you’ve taken a blood glucose, either by capillary finger-stick or from a venous sample. Now what?

We mentioned that the “normal” range is something like 70–140. Diabetics seeking to control their condition and not have their toes falling off in a few years usually strive for tighter control of their BGL than is needed for acute care; a sugar of 175 is a little on the high side for a routine check, but a pretty meaningless elevation for our purposes.

All things are also relative, in that a given BGL must be compared to the patient’s baseline to predict its effects. In other words, poorly-controlled diabetics who are routinely sitting at 200 may become symptomatic of hypoglycemia at relatively high levels, whereas very well-controlled diabetics who usually run lower may be able to drop very low indeed without noticing it. However, a few rules-of-thumb are useful:

Non-diabetics usually become noticeably symptomatic below a sugar of, on average, about 53. (Diabetics, particularly those who are usually poorly-controlled, are more variable — their average symptomatic threshold is more like 78.)

After a recent meal, diabetics may demonstrate hyperglycemia to various degrees depending on whether they ate a Cobb salad or an entire chocolate cake. Non-diabetics should not exceed 200 or so. A few people can exhibit hypoglycemia after meals, due to alcohol consumption, “dumping syndrome,” or some other phenomena, but far more often they’ll exhibit similar symptoms without any true hypoglycemia; some people get shaky and sick due to postprandial epinephrine release.

After an unusual period of fasting (“haven’t eaten since yesterday”), non-diabetics should still have a largely unremarkable sugar. For diabetics, it will depend mainly on how much and what type of medication they’re using.

There’s usually a gap of 10–20 mg/dL between hypoglycemia that’s noticeable to the patient (i.e. sympathetic effects) and hypoglycemia that causes cognitive impairment (i.e. neurological changes). This is their safety margin, when they’re taught to eat or drink some fast carbs; if it keeps dropping they may no longer be able to take care of themselves.

But here’s the problem: the sympathetic “warning signs” can be mediated or impaired for various reasons. For one thing, if your body has to flip that switch often, you become numbed to it, and your hypoglycemic thresholds becomes lower and lower. And many patients with various metabolic and endocrine failures simply can’t muster much of a stress response — the same reason why the elderly may not produce tachycardia and other shock signs when they become hypovolemic. Finally, drugs like beta blockers that directly block sympathetic activity can seriously obscure hypoglycemia. Grab your nearest bottle of beta blockers and read the list of adverse effects: one will be hypoglycemic unawareness, a five-dollar term that means beta blockade can make it difficult to know when your sugar drops low.

Another important consideration in evaluating glucose levels is the expected trend. For instance, a BGL of 70 in a diabetic patient might not excite anybody. However, if you’re testing her because her nurse said that she just accidentally received four times her normal insulin dose, then a BGL of 70 should be alarming, because it’s probably going to keep dropping, and she doesn’t have very far to go.

To make a long story short, the clinical effects of both hypo- and hyperglycemia can vary substantially. What to do? It’s simple: assess the patient physically, obtain a history of their oral intake, medications, and metabolic demands (such as exercise), test their sugar if there’s any possibility of glucose derangement, and compare all those data against each other. A low number in the setting of obvious clinical symptoms is bad. A low number in an asymptomatic patient, or a normal number in a patient with highly suggestive signs and symptoms, should force you to bring out your thinking cap and weigh the odds.

What about treatment? Severe hypoglycemia needs ALS or the hospital — they’ll receive IV dextrose. Severe hyperglycemia needs the hospital only, where they’ll receive carefully-dosed insulin; this is generally considered too dangerous to administer in the field (although patients may have their own), so paramedics are reduced to giving fluid boluses, which may help dilute high glucose concentrations (not a very elegant solution) and is probably needed by a patient in DKA anyway, but isn’t really a fix.

What about oral glucose, in the cute little tubes we carry? Typically these are gels containing 15g of glucose, taken orally (either swallowed or held in the mouth — against the cheek or under the tongue — until it’s absorbed). Do they work? Sure. But it’s not much sugar and it’s not very fast. I found one source that suggests 15g of oral glucose should raise the BGL by 50 mg/dL within 15 minutes of administration — but I’ve never found it to be nearly that effective. In my experience, a bump of about 10 mg/dL per tube is about the best you can hope for in the short-term. If you need more than that, go with the medics and the IV syrup.

Testing Errors

When is a tested capillary or venous glucose unreliable? Usually it’s your fault.

Well over 90% of BGLs that test outside the maximum error range (remember, around 15%) are due to user error. Some of the main ones:

Your meter requires lot coding, and you failed to do so or used strips from the wrong lot.
You failed to clean the skin before lancing, contaminating the sample (not to mention creating an infection risk), or you had some D50 on your glove and it got mixed in there.
Rather than gently wicking the sample into the strip, you “smeared” the two together with mechanical pressure, interfering with the expected reaction process.
You drew blood from an arm with an IV infusion of D50, TPN, or other meds distal to it. Particularly when peripheral perfusion is poor, always try to sample at a different limb from any running drips.
You tried to reuse a non-reusable strip (gross).

Okay, okay, so nobody’s perfect. Factors that may not be as obvious include:

Temperature. The test reaction is designed to function within a specific temperature range, which is broad (often around 40–104 degrees) but not limitless, so don’t use them in freezing weather, and try not to leave your equipment ungaraged without climate control when it’s very hot or cold out.
Altitude. Just in case you’re an Everest expedition doctor.
Humidity. The strips have trouble when it gets very humid.
Air. The reagents in the strips will actually degrade if exposed to air for sufficient periods of time, so make sure that you keep them in their tightly-sealed case, and follow their printed expiration dates.
Time. If you draw whole blood and leave it around (much more likely to happen in the laboratory than in the ambulance), the erythrocytes will metabolize glucose at about 5-7% per hour.

The good news is that in many of these situations, internal error-checking within the glucometer will recognize the problem, and flash an error rather than a reading. Errors messages are usually numbered and can be informative, but each manufacturer uses different codes, so read the manual if you want to know what “ER2” means. (Hint: not enough blood in the sample is by far the most common.) Many of the other problems can be caught if you regularly check the meter using a known-value test solution, which you should be doing anyway according to most drug and safety agreements. (By the way, both the test strips and those vials of solution are usually meant to expire a few months after opening — the printed date is for an unopened bottle — so if they’ve around forever it’s probably time to retire them.)

What about physiological states that can interfere with the reading? We’ve discussed a few, but briefly:

Hematocrit. Anemia from any cause, including cancer or blood loss, causes falsely high readings. High crit, common in neonates, causes falsely low readings.
PaO2. Oxygen interferes with the electrochemical redox reaction; thus high concentrations of dissolved oxygen cause falsely low readings, and low PaO2 (i.e. hypoxia) cause falsely high readings, potentially masking a true hypoglycemia.
pH. Primarily in meters using the glucose oxidase enzyme, alkalosis will cause falsely elevated readings, while acidosis causes falsely low readings. The acidosis of DKA can therefore cause falsely low readings, masking the profound underlying hyperglycemia, so if the clinical picture screams DKA, don’t necessarily let the glucometer tell you different.
Macronutrients. High levels of circulating proteins or fats can cause falsely low readings due to dilution.
Hypoperfusion and inadequate circulation. See our previous remarks on this, and remember that venous sources will be more accurate than capillary.

Finally, are there medications that can interfere with glucometer accuracy? There sure are. These in particularly are highly device-dependent, with the glucose oxidase-type meters most often affected. Generally, the effects are not profound, but occasionally they may be clinically relevant.

Ascorbic acid. Better known as Vitamin C, some people take megadoses of this stuff, thinking it’ll cure their cold or flu. Depending on the meter it can cause falsely high or low readings, usually a minimal change, but at “megadose” levels the effect can be significant.
Acetaminophen. Also known as Tylenol. The effect is similar to ascorbic acid, but even more modest; it should only be considered in major overdoses, and even then the difference is unlikely to break 35.
Dopamine. Massive doses, such as might be used for intensive inotropic support, can modestly influence glucose dehydrogenase-based meters.
Mannitol. High doses can elevated the measured BGL by around 35.
Icodextrin. This is a dialysate solution used for peritoneal dialysis (not hemodialysis — this is where they pump fluid into the abdomen, let it sit, then drain it out), mainly in patients with diabetes. It metabolizes to maltose, which can cause falsely elevated readings in certain meters. There’s at least one tragic and unfortunate case report of a patient death resulting from massive insulin overdose due to this effect, not noticed until the true BGL was obtained by laboratory analysis. If your patient undergoes peritoneal dialysis, try to find out what dialysate is used, and if that’s not possible, it may be safest to assume their sugar is lower than you’re measuring.

Conclusions

After all this you’re probably thinking glucometry is so convoluted and rife with pitfalls that you’re better off just eyeballing how sweet your patients are. But don’t let me turn you off! This remains one of the best assessment aids we have, because diabetic emergencies remain some of the most common, most treatable, and most easily confused disorders that we encounter. We can’t perform exploratory surgery, and we may never see prehospital CT scans, but this is a diagnostic test that’s so cheap and simple, with such real potential to affect your decisions, that it should be available everywhere. If you maintain your equipment, learn how to do it right, and keep a few basic confounders in mind, it’ll serve you well as one of your most reliable tools.

Glucometry: How to Do it

Read part one at Glucometry: Introduction

So we want to know how much glucose is in our blood. How can we determine this?

Most modern systems involve a handheld electronic meter, which accepts disposable test strips. The general method:

Insert a strip into the meter; this usually turns it on automatically, and the screen will indicate when it’s ready for a sample.
Clean the patient’s fingertip with an alcohol swab.
Using an automatic lancet (a spring-loaded needle), prick their finger-tip, drawing out a droplet of blood. You may need to push or massage the skin toward the puncture site in order to “milk” blood out, particularly if there’s poor circulation.
[Optional] Many services recommend wiping away the first drop of blood and drawing out a second for your sample.
Once you have a sizable, “hanging” drop of blood, apply it directly to the sample site on the test strip. It will wick inside and be absorbed.
The meter will usually display some kind of count-down. Once it’s finished analyzing, it will show the blood glucose concentration (BGL) in mg/dL or mmol/L.
Apply a band-aid to the site, and dispose of the test strip, lancet, and other bloody bits as appropriate.

What magic happens when you apply blood to the strip? There are a few methods.

(Skip this paragraph if chemistry wasn’t your favorite class.) As a general rule, the glucose in the sample is broken down by an enzyme (often glucose oxidase, or a version of glucose dehydrogenase). This reaction is proportional to the glucose concentration, and can be visualized by the accumulation of an indicator; the more glucose that reacts, the more color develops, and this is measured by a photometric transmission sensor. Alternately, in most current sensors, a more modern and somewhat more robust electrochemical method is used; here glucose is selectively oxidized, and electrons are pulled across a mediator to an electrode, which measures the current generated — either average, peak, or total depending on the type of analysis.

Results

Across the US, blood glucose is measured in the units mg/dL (milligrams per deciliter). In much of the rest of the world, the unit is mmol/L (millimoles per liter). This means that if your paramedic buddy from the UK is telling you about a diabetic he treated, the numbers may seem peculiarly low. Since we’re mostly Yanks here, we’ll be working in mg/dL, but if you ever need to convert to mmol/L, you can simply divide it by 18 (or multiply by 18 to get from mmol/L back to mg/dL).

Much like vital signs, textbook ranges for “normal” blood glucose levels vary. A loose range for practical purposes would be around 70–140, although ideally we should be under 100 most of the time, and routinely testing over 125 is not a great indicator for your health. Numbers will be elevated after eating, but non-diabetics still shouldn’t break 200 or so.

Although we’ll talk more about clinical interpretation later, in general it’s safe to say that the lower the number, the more each point matters. The difference between 70 to 50 can be profound, while the difference between 200 and 180 may be totally undetectable.

Accuracy and Precision

Glucometers have evolved through quite a few generations by now, and they continue to improve in robustness and reliability. Most diabetics use them regularly to track their sugar and thereby guide their diet and medications.

How accurate are they? Depends on who you ask. The American Diabetes Association says that at a minimum, they should give readings within 15% of the true value, and ideally manufacturers should shoot for an error of under 5%, at all concentrations. But percentages can be a confusing way to measure it, because as we observed, a 15% difference at a sugar of 500 (a possible range of 425–575) may mean little, while a 15% difference at a sugar of 60 (a range from 59, which is low, to 69, which is about normal) can be rather important. So the FDA says this instead: 95% of the time, for values below 100, meters should be within 20 points of the true value, while for values above 100, they only need to be within 20 percent.

Whatever the case, every meter varies, but generally they can be relied upon to fall within about 15% of reality, as long as no user errors or confounding factors (we’ll talk about those) are present.

Blood Source

Traditionally, capillary blood for glucometry is taken from the fingertips. This is painful, so most modern glucometers have been evaluated to determine their accuracy when blood is drawn from alternate sites. Any location with lean, vascular muscle close to the surface (i.e. not too much fat overlying, which you may not be able to penetrate with a lancet) can be usable — the forearm is the most common site. The research has shown that this practice is generally fairly accurate for routine purposes, but the danger is that BGL from the forearm lags behind that from the fingertips. It takes longer for these readings to approach reality — about 30 minutes, in fact, before you’ll read the same from the forearm as you’d read at the fingertip, and until then the numbers may be radically wrong (for instance, a reading of 145 when it’s really 50). So glucometer manufacturers recommend that diabetics always use the fingertip when there’s any question of hypoglycemia, when they’ve recently eaten, or any time when it’s important to have the most current and accurate figure. Obviously, this is always important for EMS, so we should generally stick to fingers.

On the other hand, in many areas it’s common for paramedics to start IVs and then use a drop of blood from the catheter’s flash chamber for glucometry. Briefly, like so:

The rubber stopper behind the flash chamber

Press on the rubber until a usable drop of blood comes out the end

This method works, saves you the trouble of lancing a finger, and spares the patient some extra pain. But it’s usually considered technically incorrect, because the blood in the catheter is venous, whereas glucometers are calibrated for capillary blood. See, since venous blood has already given up glucose to the tissues whereas capillary blood is still in the process of doing so, venous BGL is lower than from capillary sources — usually about 5–10 mg/dL. (If by chance you have a source of arterial blood, then that should be higher still.) However, after eating, particularly carb-rich foods, capillary sugar may be as much as 25% higher than venous, because of the extra glucose sequestered in the muscular tissue. (Stockpiling this fuel is why marathon runners like to “carbo load” before events.)

With that said, I’m going to make a controversial recommendation: in most cases, whenever it’s available, venous blood should be used instead of capillary blood. If someone has started an IV, then you should be using that instead of a fingerstick. Why? Despite the small and usually predictable difference, in sick people, it’s actually a more accurate result.

In sick people, circulation is often impaired; this is particularly true in situations like shock, sepsis, and the mother of all shock states, cardiac arrest. When perfusion is poor, the first thing we lose is the peripheral circulation, and it doesn’t get more peripheral than the capillaries of the fingertips. What does this mean? It means that in many acute patients, when it’s important to have accurate diagnostics, capillary blood sugars can be utterly, totally inaccurate. Since blood is no longer moving actively through the periphery, it tends to “pool” there stagnantly, letting the tissues chew through its glucose supply without resupplying it. This results in a falsely depressed capillary BGL even when the venous BGL is normal. Conversely, it’s also possible that in poor circulation, the distal capillaries are the “last to hear” about a drop in sugar, resulting in a falsely elevated BGL. But high or low — usually low — it’s not reliable. Anybody with impaired circulation should get a venous glucose if there’s a chance of it affecting care. (And if there’s no chance of it affecting care, then why do it?) By the way, this includes impaired local circulation, such as patients with PVD. Not that a diabetic would ever have PVD…

(Edited 6/12/12: A few commenters have pointed out that the practice of drawing blood samples from used IV catheters can present a safety risk; although modern safety catheters usually retract or obscure the needle, this is not a fail-proof mechanism, and pushing on the plunger can potentially lead to an accidental stick. We should all be sensible about this sort of thing, so be cautious and give a moment of serious thought to the conditions, equipment, and your technique before trying such a move — and of course be aware of any policies your service has on the subject.)

Coding and Calibration

The important business during glucometry is taking place in the test strip, where the actual chemical reaction occurs. Since this is a rather minute organic event, individual test strips tend to vary a little in their performance.

Traditionally, this is handled by lot coding. Each batch of strips (they come in packs of so-many) would usually include an electronic coding strip, which looks like a regular test strip, with some extra electronics attached. You insert it into the meter, and it automatically calibrates it for the current lot. If your device works this way, it is essential that you code your meter for the lot you’re using, and do not mix your strips with those from other lots; your results can be off by over 30% due to using the wrong code. However, many current glucometers no longer require coding, either by automatically self-calibrating using information in the strip itself, or by controlling manufacturing tolerances so that all strips are the same. Read the manual or check your policy!

Now, is a rose a rose, or are there different BGLs out there? Really, there are two that matter. When we prick the finger and sample capillary blood, we’re measuring the glucose concentration in whole blood — the raw, unmodified stuff running through your veins. We could also take that blood, centrifuge out all the big cells (particularly red blood cells), and measure the glucose in the plasma that remains. This latter method is how it’s done in the laboratory, and this is the gold standard for this type of test. (In the handheld glucometer, the test strip usually uses a filter to either absorb or lyse the red cells, but their presence still affects the measured concentration.)

Why does this matter? Only because whole blood BGL differs slightly from plasma BGL. Since the number is a concentration, and the presence of hemoglobin slightly dilutes the blood, plasma values are typically 5-15% higher than than whole blood values. In most of us it’ll be about 11%, but the exact difference depends on how much space your red blood cells are filling up, aka your hematocrit, so that estimate only works for people with a normal “crit” (around 45). The higher your crit, the larger the difference (and the levels of other circulating lipids and proteins can be relevant as well). The good news? In order to make home BGL readings comparable to laboratory readings, most glucometers report results as a “plasma equivalent,” either by assuming a normal crit and performing a quick mathematical adjustment, or by actually measuring the hematocrit. Some meters can be set to display either whole-blood or plasma equivalents, and ideally we should know which we’re looking at, but plasma is usually the default.

Ketones?

We know that when hyperglycemia becomes severe, the body often develops high levels of ketones in the blood and urine. (These are involved in a secondary metabolism that cells can use as an alternative to directly consuming glucose.) Lots of ketones in a diabetic is a corroborating sign of a highly elevated sugar, and suggests deterioration to diabetic ketoacidosis, a dangerous state involving a deranged pH.

There are handheld meters that can measure ketone levels, but simple glucometers can’t. However, many models have a feature where, if BGL is found to be over a certain level (often around 300), an indicator will light up with a warning like: ketones?

This is not indicating that ketone bodies are present, which the meter can’t know, but is merely a reminder that at these glucose levels, we should consider the possibility of their presence. Which, as clinical wizards, we already knew, so it doesn’t tell us much. (In fact, it’s more intended for patients, who may have the specialized strips with which to measure their ketone levels.)

Takeaway points:

Glucometry can vary by around 15% even when it’s working correctly.
Use venous blood (e.g. from an IV) rather than capillary blood (from a fingerstick) whenever possible.
If using capillary blood, use a finger rather than alternate sites like the forearm.
If your meter needs coding, make sure you do it.
Remember that many conditions (such as shock, PVD, and a recent meal) can alter capillary BGL, and some (such as anemia or hyperlipidemia) can even alter a venous reading.
Ordinary glucometers don’t measure ketones.

Tune in next time for a discussion of more clinical phenomena that can influence blood glucose readings, as well as interpreting and applying the results in real patients.

Editor’s note: Remember that although we often don’t cite specific references for our figures and data, if you ever want to know what studies or evidence we’re using to support our claims… just ask! We’re happy to oblige. This applies to all of our posts, but may be particularly germane for this one, where some specific and possibly controversial points have been made.

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.

Diabetes

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

Thoughts from WMEMS

This past weekend, I was able to attend the Western Massachusetts EMS Conference alongside such luminaries as Scott Kier and Kyle David Bates (of the extraordinary Pedi-U podcast). We sat through two days of outstanding lectures on various EMS-related topics, and walked away with some ideas and information I haven’t found anywhere else. Here are just a few of the unique pearls from the conference. Thanks to everyone for the great time!

Kyle David Bates on Mechanism of Injury

In an MVC, ejected (that is, fully ejected) victims have a 1/3 chance of a cervical spine fracture.
They also have around 25 times higher chance of mortality than an equivalent non-ejected patient.
Is “another death in the same vehicle” a legitimate concern when considering mechanism? Yes, but make sure that death wasn’t from an localized cause—for instance, a girder in the face, or they had a heart attack before they crashed.
How about “intrusion”? Over twelve inches into the patient compartment where your patient is found (meaning, visible from inside—not from the outside, which includes the buffer space of the walls), not including areas like the hood, trunk, etc. Alternately, over 18 inches into the patient compartment in areas where your patient is not found—for instance, the rear seating area, when you’re treating the solo driver.
“Distracting injuries” can mean painful injuries that distract the patient, but also gross stuff that distracts the provider. Consider a head-to-toe on virtually everyone, even when the funky arm fracture is drawing your attention.
Many “trauma” patients are no longer being treated with surgery anyway, so sending everything to the trauma centers overloads them for no reason.
One more reason why the sternal rub is not a great diagnostic: if they do clutch at their chest in response, is that localizing—or an abnormal, decorticate flexion response? Different GCS scores, but you can’t tell.
Are extremity injuries significant mechanisms? Penetrating injury proximal to the elbows or knees should be considered threatening to the torso, so yes. Pelvic fractures? For sure. (“How much blood can you lose into your pelvis? All of it!”)
With the automobile safety technology available today, you can crash fast, turn your car into a paperweight, but walk away unharmed. We no longer care about “high-speed,” only “high-risk,” which has many factors (see the Rogue Medic’s recent post on this).
Auto vs. pedestrians: kids get upper body injuries; adults get lateral trauma as we turn and try to get out of the way. Both can get run over.
Motorcycles. Harley-type riders seem to have more head injuries: they get hit by cars, due to low profile and dark clothing, and they wear partial helmets. Sports bikes get more extremity injuries: they wear good protection, are higher visibility, but they ride fast and run into things, breaking any and every bone they have.
Rollovers: no longer trauma criteria. You can roll and do great if you’re restrained. Number of rolls, final position, even roof intrusion have no correlation to injury severity.
Extrication time >20 minutes: no longer trauma criteria. Sometimes it just takes a while due to weather, access, etc, and newer vehicles are supposed to crumple more anyway.
Are burns trauma criteria? No. If they need specialized care, it’s a burn center, but this is not that time-sensitive—more a long-term management thing—so someone with burns and trauma should go to the trauma center instead, can be transferred later for burn care.
Helicopter transport: costs can range from $2,000 to $20,000 depending on distance, and insurers are refusing to pay many of these bills due to lack of necessity. Also consider the possibility of everyone dying in a fiery crash. Weigh cost vs. benefit.

Kyle David Bates on Shortness of Breath

Anxiety is caused by hypoxia; the cure for this is supplemental oxygen.
Sleepiness is caused by hypercapnia; the cure for this is bagging.
OPA or NPA? Testing the gag reflex may create a bigger airway problem (vomit). Better yet, check the mouth for pooled saliva; if present, there is no gag, use an OPA. If absent, they have a gag and are managing their own secretions, use an NPA.
Respiratory distress means there’s a problem, but they’re compensating (compensatory signs like tachypnea).
Respiratory failure means they’re decompensating (hypoxic/hypercarbic signs like altered mental status, cyanosis, falling sats)
Respiratory arrest means they’re not breathing.
Normal inspiration:expiration cycle about 1:2. Obstructive pulmonary problems impede expiration first, because that’s the passive process—it’s easier to inhale past obstructions because it’s an active process. So asthmatics have ratios like 1:4 or 1:5, they’re using active exhalation, and using auto-PEEP maneuvers. (Pursed lips in adults, grunting in kids.)
In adults, look for retractions intercostal (between the ribs) and sternal notch (between the clavicles); in kids, look substernal (below the ribs).
40% of patients hospitalized with asthma have a pneumothorax! (Not necessarily clinically significant, though.)
Pulsus paradoxus/paradoxical pulses are a useful early sign of significant pulmonary dysfunction.
90% of asthma attacks linked with an allergic reaction; however, rhinovirus (the common cold) may now be a contender. Others include: exercise (not sure why; maybe the temperature differential), active menstruation (asthma very common in young post-pubescent women—maybe the hormones), psychological (stress, panic), aspirin use.
Kids compensate great, so cyanosis (a decompensation sign) in kids is very late and very bad.
Risk-stratify these patients, because high risk patients can decompensate fast even if they look okay now. Previous hospitalizations? ICU admits? Intubations?
Cough asthma: no dyspnea, just dry coughing. It happens.
Smokers: measured in pack-years. 1 pack a day for 20 years is 20 pack-years, 2 packs a day for 5 years is 10 pack-years; 30–35 pack-years is where we start to see bad dysfunction.
Best place to check skin? Under the lower eyelid—lift it and check the mucus membranes. Dry for dehydration, pale for shock, blue for cyanosis, the whole gamut.
Ascites is a sign of fluid overload; try the fluid wave test. (Scroll down to “Examining for a fluid wave” here.)
Nebulized ipratropium/Atrovent: its role is mainly to reduce mucus and secretions (cf. atropine). Tachycardia etc. is not a contraindication, because it’s not absorbed systemically; it remains in the lungs.
Give nebs by hand-held mask or T-piece instead of strapping it to their face; that way you have a warning of deterioration when they can no longer hold it to their face.
Bronchodilators may not work great in beta-blocked patients.
Steroids take hours to have an effect, but the earlier they’re given the better the outcomes; give ’em if you have ’em.
If they need RSI, ketamine is nice because it also bronchodilates.
“Facilitated intubation” (i.e. snow ’em with a ton of benzos/narcs)? Be careful, because if you don’t get that tube, it’ll take forever to wear off; these aren’t short-duration drugs.

Kyle David Bates on Pediatrics

Use the Pediatric Assessment Triangle! Appearance, Work of Breathing, Circulation.
Appearance: General activity level and impression. Muscle tone, interactivity and engagement, look/gaze, crying. Appropriate appearance depends on age. Indicates a CNS/metabolic problem. (Make sure to check their sugar.)
Work of Breathing: Flaring, retractions, audible sounds, positioning. Remember they’re belly breathers.
Circulation: mostly skin. Cyanosis (bad), pallor, mottling (pallor + patchy cyanosis), marbling (in newborns—bright red skin with visible blood vessels, maybe some white areas—this is normal). Check cap refill on bottom of foot in little kids.
Shock in kids is most often from dehydration.
Airway: crying is a great sign. Remember to pad under the shoulders when lying flat, their huge heads can tip them forward and block the airway. Avoid NPAs in infants. In very small kids, breath sounds can transmit, so you may hear upper sounds in the chest or chest sounds in the trachea.
Under 2 months: peripheral cyanosis is normal, central cyanosis is bad. Limited behavior, often won’t visually track. Ask parents if their behavior is normal. Ask about obstetric history, it’s still relevant. They have no immune system really, so any infection (temp over 100.4) is a serious emergency.
2–6 months: social smile, will track visually, recognize mom, strong cry and can roll/sit with support. May still be okay with strangers, but try to keep them with parents; if parents like you, they’ll like you
6–12 months: stranger anxiety (unless they’re raised very communally). Very mobile and explore with their mouth, so always think about foreign body airway obstructions, especially up the nose, especially for dyspnea with sudden onset. Separation anxiety, so keep with parent. Offer distractions (toys, etc.). Do exam from toe to head so they get used to you before you reach their face.
1–3 yrs (toddlers, “terrible 2s”): mobile, curious, opinionated, ego-centric, can’t abstractly connect cause-and-effect but learn from experience. Keep with the parents, distract them, assess painful part last (or everything you touch afterwards will hurt). May talk a lot or not much, it’s all normal, but they always understand more than they let on, so be careful what you say.
3–5 yrs (preschool): magical thinkers, misconceptions (“silly” ideas like if they leak too much they’ll run out of blood), many fears (death/darkness/mutilation/aloneness), short attention span. Explain things in simple terms, relate to them (any cartoons or toys in the house you recognize?), use toys, involve them (here hold this, which arm should I use, etc). Don’t ever negotiate, just tell them what to do; praise them often; never ridicule.
6–12 yrs (school aged): talkative, mobile, may not get cause and effect, want reassurance, involvement, praise. Live in present, may not think about danger or risk. Peer involvement. Speak directly to them, anticipate questions (will this hurt? am I going to die?), give simple explanations, don’t ever lie, respect privacy. If you need to do something painful (IVs, etc.) don’t tell them until just before, or they’ll dwell on it. Head-to-toe okay.
13–18 (adolescents): regress when hurt or sick—act like big toddlers. Can understand and theoretically have common sense, but still take risks. Peer support. Speak directly, give concrete explanations, respect privacy, have patience.
Under 21 usually considered “pediatric.”
Degree of fever temp not associated with severity. No actual danger to brain until 106–107 degrees F or so.

Dr. Lisa Patterson on Trauma and Field Triage

RR <20 in infants is trauma center criteria since this is the one easily-measurable vital sign for them.
Crushed/degloved/mangled extremities: although not life-threatening, still worth the divert, because usually needs multi-specialty care (plastic surgery, orthopedics, hand specialists, etc.) to maximize function.
Calling in “altered mental status” or “unresponsive” is not super helpful—give a GCS or otherwise specify what you mean, there’s a big range here.
Trauma activations here are typically three tiers: category 1 (life threat), category 2 (no immediate emergency, but some concern or suspicion due to mechanism or presentation), consult (no concern on initial presentation, but later decision to admit, trauma paged down to consult).
Activation may alert/standby numerous parties including radiology, OR, pharm, blood bank, lab, ICU, respiratory, anesthesiology, social workers, etc. Not a small thing.

Sean Dorr on OEMS investigations

[This is Massachusetts-specific information; local providers can contact me directly if they want to hear about some of this material.— ed.]

Ginnie Teed on Organ and Tissue Donation

Donation is hugely hugely valuable and lifesaving, but there’s not nearly enough. About 60-70% of Americans are registered donors, around 100 million people, but only 1% end up as usable donors and we need far more. Low rates aren’t from consent, they’re from the logistics of getting viable candidates.
Uniform Anatomical Gift Act (UAGA) is federal regulation providing basic requirements for process; states use this standard to form their own systems. Registered donors must be recognized and organ procurement agencies are required to advocate for them even against wishes of family, etc. Driver’s license “opt-in” now considered legal consent in some but not all states.
National Organ Transplant Act establishes the rules of the registry, blinds the entire process, prevents manipulation or line-jumping; the database is centralized and controlled; you can’t legally buy or otherwise get around the system. Manipulation is taken very very seriously and massively investigated, because it’s not only unethical, the pall it casts over the process makes others decide not to donate—the result is many lives lost.
Referrals (i.e. calling procurement organization to say, “we have a potential donor”) come from hospitals, nursing homes, clinics, whomever. This process is exempt from HIPAA.
Tissues tested more heavily than organs, because if an infection is carried through transplanted (i.e. nonliving) tissue, it’s almost impossible to eradicate.
Organs used: vital organs. Heart, lungs, kidneys and livers (most common), pancreas, sometimes small bowel. Max 9 organs per donor.
Tissues used: not living, usually good for about 24 hours after death. Bones (not marrow, which is living), although we try to not obviously mutilate people (for their family’s sake), skin (hugely beneficial), corneas, vessels, heart valves, pericardium, connective tissue (for orthopedic repairs).
Three ways to declare death: neurological (no brain activity; body only alive due to our mechanical support; recovery team responds to site and performs planned recovery); cardiac death (heart stops; not planned); planned extubation/cardiac death (patient is mechanically supported, determination made that there is no possibility to survive on their own; vent is pulled, if heart stops within 59 minutes they can take some organs; usually just the durable liver and kidneys unless bypass is available).
Live organs can only be taken from perfused patients. Someone “dead” (i.e. no pulses) can be a tissue donor but not an organ donor unless you get ROSC. No point in continuing CPR to “maintain the organs” if there’s no possibility of getting return of circulation.
EMS documentation absolutely critical for determining donor eligibility. Need to know downtime in arrests, how much CPR, any ROSC no matter how brief, events/mechanism leading to arrest. There are hard limits on fluid/blood/colloids received, so they must know how much fluid you gave (reasonable estimate is fine). Must document all needlesticks, number and location; if they find any holes that aren’t accounted for they’ll have to assume they’re a drug user or that additional lines were started and extra liters given. If you don’t want to document something at least tell the receiving staff.
If blood is drawn, label must be placed so that expiration date of tube is still readable (FDA requirement).
Every donor can save up to 200 people; failure to document can kill just as many.

UMass Memorial LifeFlight on Air Ambulance Transport

Consider: how do you want the helicopter used? Need their higher level of care? Rapid transport to trauma center? Transport multiple patients in an MCI to more distant hospitals to reduce burden on closest facilities? Can even split the crew to provide higher level of care for multiple ground ambulances.
Many services simply will not fly into a hazmat situation.
Best makeshift landing zones are schools—big open areas, everyone knows where it is.
Wires are a major hazard, make sure to warn pilot—you can see them but he can’t.
Need about 100 x 100 ft for an LZ, or 35–40 big-ish strides per side. Secure the area against bystanders.
Hazards to clear, alert the pilot to, or just pick another spot: poles, antennas, trees, bushes, livestock, stumps, holes, rocks, logs, mile markers, debris. Tall grass can hide hazards. Close all vehicle doors, put your chinstraps on, secure loose items. Don’t stare at the bird landing, turn your back and watch for hazards.
Bad surfaces are dust, dirt, snow, ice, hay. Snow should ideally be very fluffy or very packed. If they land and get iced they may not be able to take off again. Don’t wash down a dusty LZ unless pilot requests it. Paved areas are simplest and best. Large clear roadways can land multiple choppers in a row.
Lighting options: orange traffic cone at each corner, with a handlight placed in each at nighttime. Or, flashing ministrobe at each corner. Or, vehicle headlights crossing the LZ. Don’t shine anything up at the helo, don’t mark with loose material, don’t use flares.
Designate one person as LZ Command (not the IC). Nobody else communicates with the helicopter. Your portable radio probably won’t reach them; use the mobile in the truck. If there’s any hazard on final approach, say one word—”STOP”—and pilot will abort.
Most crashes are pilot error, and most pilot error is due to fatigue. There should be hour limits for a pilot, and this is a valid reason to refuse to fly.

Detective John LeClair, EMT-P, on Opiates and Prescription Pills

Heroin is still big, but pills are a huge player now too. You get an easy prescription from a walk-in clinic or ED, pay maybe a couple bucks with Medicare/Medicaid, and can not only sell them for easy cash but can crush and snort/shoot it for the same effect as heroin. Then if money or access runs low, you end up on heroin anyway to chase that high.
Oxycontin/oxycodone best selling narcotic in the nation ten years ago, but now on the wane. You scrape off the time-release coating, crush it and snort or chew it. “Hillybilly heroin,” “blue,” “oxycotton,” “kicker,” etc. Street price about $1/mg (40mg, 80mg, 160mg common), so many turned to crime. In Aug 2010, manufacturer (Purdue) added a “geling” agent which turns it to gel when it contacts water, making it difficult to snort. Try to snort this Oxycontin OP and it turns into a ball in your nose. Some people are sticking straws/tubes up in there to try and get it deeper and deeper, so airway obstructions are happening.
Percocet: oxy plus acetaminophen. For years the most common analgesic for sports injuries, so common among youth. Kids shared ’em, put out bowls of them at parties, girls prostituted themselves for pills. Taken with alcohol the APAP/Tylenol kills your liver. “Littles,” “little babies,” “little dogs.”
Opana/oxymorphone: getting popular after Oxy OP started ruining everyone’s fun. Same idea but you can still snort it. Twice as strong, and costs twice as much ($2/mg)
How to grind? Take a hose clamp, cut it, straighten it, tape it down, run the pill across the holes to grind it. Or use a Pedi-Egg, which collects the powder for you. The finer, the better high.
Heroin: snort, “skin pop” (subcutaneous), mainline. Must be pretty pure to snort, which it now tends to be, so popularity grew (people were afraid of needles due to HIV). However now some HIV/Hep is spreading through bloody noses and sharing straws anyway.
Smack, horse, china white, chiva, junk, H, tar, black, fix, dope, brown, dog, food, negra, nod, white horse, stuff. Dealers have their own “brand names.”
Heroin addicts are creatures of habit; get high same place, same way. Any change in their routine (e.g. different location) can get them amped up, changing their sensitivity and leading to OD even with their usual dose. Consider this if you find an OD somewhere like a car or alley.
“Cotton fever”: they pluck out wads of cotton from cigarette filters and drop it in the heroin to help filter it. Sometimes when they draw out the liquid they get a bit of cotton, and when they shoot it they get a sort of phlebitis/infection/sepsis.

Drug Families: Anticoagulants and Antiplatelets

One of the most common drugs we encounter in the field are various forms of anticoagulant and antiplatelet medications. These are relevant to our care both in their therapeutic role as well as in their adverse reactions and potential for harm.

Unfortunately, coagulation is a miserably complex process, and it has to be understood at least generally in order to understand these drugs. In the hope of making this less confusing, rather than throw a wall of text at you, the worker gnomes at EMS Basics have put together an illustrated video. View this, then read on — the drugs won’t make any sense if you don’t start with the physiology.

This form of teaching is a new frontier here, so any input or feedback is welcome. Due to both personal and technical failings, it didn’t turn out exactly how I’d hoped, but hopefully things will continue to improve in the future.

Now that we understand the process, we should talk about the drugs.

There are two major categories here: anticoagulants and antiplatelets. Antiplatelet drugs inhibit the initial step of platelet aggregation and adhesion, where they collect at the wound site in activated form and create a loose plug. Anticoagulants have no effect on this, but instead interfere with the production of fibrin, and therefore prevent a solid clot from growing.

As a general rule, the anticoagulants are rather more clinically significant, as far as their effects on bleeding.

Anticoagulants

First off, to be clear: tPA (tissue plasminogen activator) is not an anticoagulant of any shade. It is a thrombolytic; it attacks and degrades existing clots, dissolving their fibrin bonds. It has no role as a protective agent, and would be far too hazardous in such a role anyway; even its emergency use for acute events like ischemic stroke always requires careful weighing of benefit vs. risk — because the risks are significant.

With that said, there are two main anticoagulants we see frequently in the field.

Warfarin (Coumadin)

Coumadin is an old drug with an interesting backstory; one of its original uses was for rat poison. It’s given orally.

Nowadays, it’s mainly used for chronic anticoagulation of patients at high risk for embolic events. For instance, if you’re in atrial fibrillation at baseline, the blood in your atria isn’t being pumped downstream effectively, and tends to pool. We saw that brisk movement of the blood is one of the main ways we prevent clotting; A-fib is therefore a risk factor for hazardous clots. So when possible, these patients are covered by Coumadin or similar drugs.

The mechanism is interesting. Recall that for the activation of several factors, primarily in the extrinsic and common pathways (including thrombin and Xa), Vitamin K needs to be present. (For some factors, Vitamin K is also needed for the initial production of their inactive forms.) The process looks like this: in order for the factors to be activated, a second background process must also occur, where Vitamin K is changed into a form called Vitamin K epoxide. Once this is done, Vitamin K epoxide can be cycled back into Vitamin K, allowing it to be reused again for the next activation.

Coumadin prevents this second step. It allows the inital activation and conversion, but it blocks Vitamin K epoxide from being recycled to Vitamin K. So over time, as you use up available Vitamin K, it doesn’t get replaced, and you end up with less and less of it available. Less available Vitamin K means less activation of thrombin and its precursors, which means less fibrin, which means less clotting.

Obviously this process takes time. Since Coumadin has no effect on the active factors already present, if we start you on Coumadin today, it won’t have any effect for several days. We need to wait for currently circulating factors to degrade. So for newly anticoagulated patients, a more fast-acting drug is usually used to cover this loading period; heparin is common.

Other than its widespread use, warfarin is also famous for frequent misdosing. It has a narrow therapeutic index, where it’s very easy to give too much or too little, and depending on diet and other drugs, the appropriate dose can change daily. It therefore requires regular monitoring of the patient’s actual anticoagulation, which is done through a test called the prothrombin time (PT). This is a lab test that measures clotting time with an emphasis on the extrinsic and common pathways, and gives a result in seconds. Due to different PT tests available, a standardized result has been devised called the INR (or International Normalized Ratio). This is essentially a ratio of your clotting time over the standard clotting time; a normal result is therefore close to 1.0. Obviously, anticoagulated patients should have a longer clotting time, so 2.0–3.0 is more typical. Much higher than this puts one at high risk of bleeding — into the GI tract, into the lungs, into the nose and mouth, and if trauma occurs, the chance of significant bleeding is magnified. A too-low INR, of course, simply removes the benefits of protective anticoagulation.

In the event of overdoses that need reversal, patients can receive supplemental Vitamin K, as well as plasma (or concentrates) to replace the missing factors directly.

Heparin

Heparin is another old drug. It’s actually a biological substance naturally present in the blood, one of the body’s own anticoagulants, and when extracted for pharmacological use it’s derived from sources like pig intestines. Lovely. You can’t take it orally, so as a rule it’s given by IV.

Compared to warfarin, heparin has a more direct mechanism. Recall that one of the antagonistic factors that works to deactivate thrombin (as well as a few other factors) is antithrombin. Heparin, when taken in therapeutic doses, multiplies the effects of antithrombin by several thousand times. It therefore deactivates far more factors, which are then unable to produce fibrin. Thrombin and factor Xa are two of the factors most affected.

You can already imagine that heparin will probably work much faster than Coumadin. Aside from being given intravenously, it’s not simply stopping the influx of new Vitamin K and waiting for the old factors to degrade; it’s actually going in and deactivating them directly. In fact, heparin takes effect within half an hour or so. However, its half-life is short, so it’s often given as a continuous drip. Obviously, its usage is typically for acute events, such as acute coronary syndromes, or the bridging to Coumadin we mentioned.

However, there is another version of heparin that’s available. To briefly describe the chemical structure of heparin, it’s a polysaccharide, or a repeating chain. When we cook this stuff from pig parts, we end up with a collection of heparin chains in widely varying lengths. The problem is that only chains of a relatively long length will deactivate thrombin. So depending on the actual size of our heparin molecules, unaltered heparin — known as unfractionated heparin — can be fairly unpredictable in its effectiveness as an anticoagulant.

Even very short chains, however, will deactivate factor Xa, and since Xa is a necessary precursor for thrombin, this has the same effect. So if we can produce an artificial product that only includes short heparin chains, then it will mostly affect Xa rather than thrombin, and its effects will be more predictable. This is called low molecular weight heparin, and it has several advantages. It’s easier to manage, it requires less close monitoring, and it has a longer half-life. In fact, it can be given once a day by subcutaneous injection; for instance, post-operative patients can be taught to inject themselves and sent home with the ability to manage their own anticoagulation. Most of these LMWHs end in -arin: enoxaparin (Lovenox), dalteparin (Fragmin), and tinzaparin (Innohep) are common. Fondaparinux (Arixtra) is also used; although technically not a LMWH, it’s very similar in all respects.

Heparin can be monitored by testing the partial thromboplastin time (PTT), which focuses on the intrinsic and common pathways. LWMH can, if necessary, be monitored by testing levels of factor Xa. Overdose leads to bleeding complications, and in a few cases heparin can induce a disorder called heparin-induced thrombocytopenia (HIT), causing a paradoxically elevated chance of clotting. Super-therapeutic levels can be reversed by protamine sulfate, which binds to heparin and prevents its utilization.

Dabigatran (Pradaxa)

A few brief words on this relatively new drug, only made available over the past year or so.

Dabigatran is an anticoagulant from a wholly different class known as direct thrombin inhibitors. Unlike the somewhat roundabout pathways of warfarin and heparin, these drugs inhibit thrombin directly, and may therefore be somewhat more predictable and easily managed.

In the case of dabigatran, it’s being marketed as a replacement for Coumadin. Although supposedly just as effective for chronic anticoagulation, its claim to fame is that it requires no monitoring of INR, which would be a huge burden lifted from patients and caregivers.

Still very new, it remains to be seen how widely it will be adopted. The main concerns about it are: 1. Cost, and 2. Reversal. Unlike warfarin, which in the case of hazardous events (the proverbial bonk-to-the-head with an epidural bleed) can be readily reversed by Vitamin K and fresh frozen plasma, there is no easy or clear method of reversing dabigatran. Some ideas are out there, but clinical experience remains scarce at this point. In any case, this drug isn’t too common yet, but you may start to see it more often.

Antiplatelets

Aspirin

Aspirin is probably in your medicine cabinet somewhere. It has widespread uses from analgesia to antipyretic effects, but also plays a role in platelet adhesion. It’s taken orally, although IV aspirin does exist, and is used both for chronic risk-reduction and acute treatment of coronary syndromes. This stuff is good enough that nearly everybody you know with wrinkles on their face probably takes it every day.

As platelets are activated and degranulate, one of the chemicals they release is thromboxane A2. It has several effects, including vasoconstriction of the immediate area and stimulating further platelet activation. However, it also promotes platelet adhesion by a pretty neat mechanism.

Remember fibrinogen? The inactive precursor of fibrin? Unlike some of the other inactive factors, this one has its own chance to be the star of the show. Fibrinogen can form a bond between activated platelets, attaching at their glycoprotein IIB/IIIA receptors and creating a link. This isn’t anywhere near as strong as a fibrin bond, but it’s enough to make platelets stick together and clump. Thromboxane activates glycoprotein IIB/IIIA receptors and allows the formation of these fibrinogen bridges.

Aspirin inhibits thromboxane release. Fewer fibrinogen bonds are formed, and less platelets adhere. Coagulation itself proceeds unimpeded, but there are fewer platelets in the clot to be married by fibrin.

Due to the widespread effects of aspirin, overdose is a complex subject. Altered mental status, neurological and cardiovascular signs, sensory disturbances (blurred vision or ringing of the ears), and GI problems are all possible. However, there are typically no obvious bleeding abnormalities. Treatment of acute toxicity can include attempts to limit the dosage (such as gastric lavage and activated charcoal), bicarb, supportive care, and if necessary hemodialysis.

Glycoprotein IIB/IIIA inhibitors

This mouthful of a name is another class of drugs from the antiplatelet family. They’re typically not used chronically like aspirin; one reason is because they’re given intravenously, with oral forms rarely seen. (Another reason is because they’re simply stronger drugs). We see these most often used during and after known coronary “events,” such as a STEMI, NSTEMI, or a coronary catheterization, at which times they can help prevent reocclusions.

Their mechanism is similar to aspirin. As we saw, fibrinogen binding to glycoprotein IIB/IIIA receptors helps bind together platelets and allows them to adhere and aggregate. GBIIB/IIIA inhibitors block these receptors by competitive binding, and hence prevent the fibrinogen bonds.

We rarely see these in the field, but common ones include: abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Adverse effects mainly involve bleeding.

Thienopyridines

Although there are a few drugs in this class, by far the most common is clopidogrel (Plavix). Think of these as an alternative, somewhat more powerful aspirin; they work similarly, have similar effects, and are used for similar purposes. Like aspirin, some people use it chronically and it can be given in acute events as well. It can “stack” with aspirin for a synergistic effect, or be used in its place for those who cannot tolerate aspirin.

Once again, the mechanism will sound familiar. One of the pathways that activates glycoprotein IIB/IIIA receptors requires the binding of adenosine diphosphate, or ADP. (ADP is more famous as the product of ATP once energy is released, but it has its fingers in a lot of cellular pies.) The thienopyridines block ADP binding and hence discourage platelet aggregation. Prasugrel (Effient) is another drug in this class.

Adverse effects generally involve bleeding diatheses.

More Drug Families: Stimulants and Depressants; Steroids and Antibiotics; ACE Inhibitors and ARBs

Drug Families: ACE Inhibitors and ARBs

Understanding the renin-angiotensin-aldosterone system is like following one of those dotted-line Family Circus cartoons — not just long and tortuous, but seemingly designed just to be obnoxious.

Here’s the basic idea. The RAAS is the basic system your body uses to control blood pressure, as well as related values like fluid volume and sodium levels. The most important thing to understand is that the activation of this system causes an increase in blood pressure. Following the trail:

First, renin is released by the kidneys. Renin attacks circulating angiotensinogen, turning it into angiotensin I. Angiotensin I is attacked by circulating angiotensin converting enzyme (or ACE), which turns it into angiotensin II. Angiotensin II has various effects, one of which is to stimulate the release of aldosterone.

Whew.

But this isn’t as complicated as it looks. Renin has no real effect. Angiotensinogen just makes angiotensin I. Angiotensin I’s main role is to make angiotensin II. The real money here is in angiotensin II, as well as aldosterone.

Angiotensin II has the primary effect of vasoconstriction. It tightens up the vasculature, increasing blood pressure and systemic resistance. It also produces vasopressin (aka ADH, or anti-diuretic hormone) and aldosterone, which cause the kidneys to downregulate urine production — more fluid will be returned to the circulation rather than discarded into the bladder. Vasopressin also helps angiotensin II to induce further vasoconstriction.

To make a long story short, the activation of the RAAS system causes an increase in blood pressure via both vasoconstriction and a decrease in kidney output. It is always active, playing a key role in maintaining homeostasis; if you sweat out a liter of water running a marathon, or bleed out a liter from a gunshot wound, the system simply upregulates itself to maintain your blood pressure using the remaining volume. (Unlike the sympathetic and parasympathetic systems, which also play a major role in regulating blood pressure, regulation via the RAAS is captained mainly at the kidneys, where low pressure and throughput induces increased renin production.)

Cool? Cool.

Okay, so the role of ACE, or angiotensin-converting enzyme, was to transform the useless angiotensin I into the powerful angiotensin II. What do you think a drug called an ACE inhibitor would do? Indeed: it inhibits the activity of ACE, thus reducing the production of angiotensin II, which then causes reduced production of aldosterone and vasopressin.

Less angiotensin II means less vasoconstriction; the systemic circulation opens up, reducing blood pressure. Less aldosterone means less fluid is retained at the kidneys, so urine output is increased, reducing circulating volume, and again, reducing blood pressure. Handy!

A secondary role of ACE is to degrade, or break down, bradykinin. Bradykinin is basically just another vasodilator. If ACE is inhibited, then less bradykinin will be broken down, hence more bradykinin will be available. The result is more vasodilation — once again, reducing blood pressure.

Readers who can recognize patterns will probably have deduced that ACE inhibitors are used primarily to reduce blood pressure. Obviously, this includes the typical patient with primary hypertension that needs to be managed to reduce long-term morbidity. But it also means other things:

Reduced afterload — the resistance the heart has to push against when it pumps blood — means less work for the heart. This is beneficial for patients with heart failure, whose hearts aren’t pumping very well to begin with; or with coronary artery disease, whose hearts need to manage their workload to match the oxygen they’re able to bring in. It reduces “remodelling,” where the heart and the arteries thicken and change shape to better pump hypertensive volumes, with harmful results. And it reduces the damage following myocardial infarction.
Reduced preload — the amount of blood that passively fills the heart during diastole — — also means less work for the heart. Greater preload causes greater filling and hence greater contraction, which all means more work, more oxygen demand, and more remodelling. In heart failure, where the heart is unable to fully expel its contents, reduced preload also means less “extra” fluid to back up into the lungs and circulation, and therefore less edema.
Better renal function. This is a desirable effect in patients with various forms of kidney disease.

Angiotensin receptor blockers (ARBs) are a closely related family of drugs. Instead of interfering with the conversion of angiotensin I to angiotensin II, they simply prevent angiotensin II from binding with its receptors. The effects are therefore largely the same: vasodilation; reduced aldosterone production, with corresponding greater urine output; and reduction in hypertension with less work for the heart.

The main difference between ACE inhibitors and ARBs goes back to bradykinin. If you remember, ACE plays two roles: converting angiotensin I to angiotensin II, and degrading bradykinin, a vasodilator. Since ARBs have no effect on ACE, bradykinin is broken down normally. This may result in slightly less vasodilation, but it also reduces the side effects of elevated bradykinin, which can include edema and a nasty cough. ARBs are most often used in patients who can’t tolerate ACE inhibitors.

Overdose on ACE inhibitors is generally unremarkable. The main effect is hypotension, but it is rarely severe.

Examples

Generic names of ACE inhibitors and ARBs are very, very easy. Trade names are harder, but do have some common elements.

ACE inhibitors

Drugs ending in -pril are invariably ACE inhibitors (enalapril, ramipril, captopril, lisinopril, etc.)
Drugs ending in -ace are often trade names of ACE inhibitors (Altace, Tritace)
Drugs ending in -tec are often trade names of ACE inhibitors (Vasotec, Renitec, Novatec)

ARBs

Drugs ending in -sartan are invariably ARBs (losartan, valsartan, candesartan, etc.)

More Drug Families: Stimulants and Depressants; Steroids and Antibiotics; Anticoagulants and Antiplatelets

Polypharmacy in the Elderly

A tremendously valuable Educational Pearl from the wonderful UMEM mailing list, courtesy of Amal Mattu, emergency physician extraordinaire.

We already know that polypharmacy is a big issue in the elderly, but here are a few key points to keep in mind:

Adverse drug effects are responsible for 11% of ED visits in the elderly.

Almost 50% of all adverse drug effects in the elderly are accounted for by only 3 drug classes:
a. oral anticoagulant or antiplatelet agents
b. antidiabetic agents
c. agents with narrow therapeutic index (e.g. digoxin and phenytoin)

1/3 of all adverse-effect-induced ED visits are accounted for by warfarin, insulin, and digoxin.

Up to 20% of new prescriptions given to elderly ED patients represents a potential drug interaction.

The bottom line here is very simple–scrutinize that medication list and any new prescriptions in the elderly patient!

References
Samaras N, Chevalley T, Samaras D, et al. Older patients in the emergency department: a review. Ann Emerg Med 2010;56:261-269.
[Source]

The value of this is inestimable. We know that polypharmacy is a big deal, but it’s such a big deal that it can be hard to shrink down the problem enough to really consider it when an elderly patient presents themselves. Could their problem involve something on this med list that’s as long as your arm? Certainly, but where to start?

Start with the above. Over half of your problems will involve anticoagulants, antidiabetics, and easily misdosed drugs. Those are the usual suspects; they should jump out at you from the list. But we can do even better, because nearly half of those will involve one of three particular serial offenders: insulin, warfarin (aka Coumadin), and digoxin. And let’s add a fourth one: any new or recently modified prescriptions. If any of these are present in a patient with an appropriate complaint or presentation, it should be strongly considered as being part of the problem if not the actual smoking gun.

Insulin is easy, especially if you have access to finger-stick glucometry; diabetic emergencies (especially hypoglycemia), including iatrogenic ones, are so common that you might as well assume anybody with an altered mental status is diabetic — even if they aren’t. Definitive treatment is obviously oral glucose or IV dextrose, as appropriate.

Warfarin is still an extremely common anticoagulant, although a couple new alternatives are now available, and it requires close and frequent monitoring of levels in order to maintain a therapeutic dose. (The usual standard is a measure of clotting speed called INR; the test can be performed in the lab, but nowadays can also be done right at the bedside.) Various medication interactions and even dietary changes can shift this range. Overdose is associated with, no surprise, bleeding — in all forms. If necessary, supertherapeutic warfarin levels can be antagonized with Vitamin K or IV clotting factors.

Digoxin is seen less today than in yesteryear, but once upon a time everybody and their mother was on “dig,” and it’s still used with some regularity. Its most common application is for rate control of atrial fibrillation patients. Although other antiarrhythmics are now more common, dig has the peculiar magic of reducing cardiac rate while actually increasing contractility (negative chronotropic but positive inotropic effects). However, its therapeutic range is narrow and is easily shifted by pharmacological, renal, and other issues; as a result, dig toxicity is famously common. Overdose symptoms include GI problems and neurological complaints such as visual disturbances and changes in mood or energy level. It can also present prominently on the ECG, with the most classic sign being degradation of AV conduction with an increase in atrial and ventricular ectopy — for instance, slow A-fib or atrial tachycardia, a third-degree AV block, and a junctional escape with PVCs. (As a result, the atrial fibrillation patient controlled on dig may present with an unexpected “regularization” of his pulses, due to a junctional or ventricular escape taking over from the usual A-fib. This is a clue even the BLS guys can catch.) Treatment is supportive for arrhythmias and heart failure; severe cases can be managed with Digoxin Immune Fab (aka Digibind or Digifab).

Drug Families: Steroids and Antibiotics

When things go wrong
as they usually do —
Inflammation!

Inflammation

There are a lot of bad things that can happen to your body. Homeostasis, as we like to call it, is that smooth state when all your bits and pieces behave just as they ought to; and “bad things” are anything that knock this out of whack.

And what’s funny is that, no matter what that insult is, you can pretty much count on the body to respond with inflammation. Other, more specific things too, but inflammation will be there. It’s physiological duct tape: your basic, one-size-fits-all solution for any physical calamity.

Inflammation is caused by a complex blend of chemical mediators, but physically, the result is usually some combination of five classic signs.

Heat [calor]
Redness [rubor]
Swelling [tumor]
Pain [dolor]
And sometimes included, a general loss of function [functio laesa]

Try the Latin if you’re trying to impress someone at the bar.

Suppose you fall and bang your elbow, causing minor soft tissue damage. The body reacts immediately by activating a local inflammatory cascade, whereby numerous processes swing into gear. Local vasodilation occurs, bringing more blood into the area, to support faster healing; this increased bloodflow (hyperemia) produces the redness and warmth associated with injury. Vascular permeability is also increased, allowing fluid to leak into the surrounding tissue, which results in edematous swelling; this not only conveys healing factors into the damaged area, it also physically limits movement around the affected joint by “self-splinting.” Other chemical mediators increase your local sensitivity to pain, which further discourages you from movement; a decrease in the joint’s function is the result.

All of which is part of the inflammatory package. Neat!

The inflammatory cascade in soft tissue damage

Now suppose you catch a cold. Viral particles enter your mouth or nose, whether by direct contact or by inhaling them as an aerosol, and lodge somewhere in your oronasopharynx. Our response: inflammation! Your immune system recognizes the intrusion and responds with an influx of infection-fighting white blood cells, such as neutrophils and monocytes, along with the same cocktail of general inflammatory mediators (bradykinin, cytokines, etc.) that we saw with the injured elbow. The result? Swelling; excess mucus production; pain (as in sore throat); a general discomfort and sense of crumminess; and in more systemic cases, a fever to make the environment less hospitable for the virus.

It’s all the same story. When things go wrong, the body responds in various ways, but it’s almost always accompanied by some sort of inflammatory response to facilitate and assist the repairs.

Sometimes, however, this process becomes maladaptive. Whether it’s an immune response to infection or a local response to injury, short, appropriate, and effective inflammatory activity is a valuable part of our defenses — but if becomes too severe, lasts too long, or serves no purpose, then it can become part of the problem. For our bumped elbow, inflammation will promote healing, but if after a few days we find that the area is still swollen, this is no longer valuable; it’s impeding our ability to use the joint, which is what we need to do in order to circulate blood and encourage further healing. Our body’s response was excessive. So we apply ice to vasoconstrict the area, elevate the extremity, and take anti-inflammatory drugs, all to reduce that local edema and tamp down our inflammatory freak-out.

Numerous illnesses and injuries exhibit this sort of excessive, harmful inflammatory response. For example:

Traumatic brain injury is deadly because swelling within the cranium has nowhere to go, resulting in a self-feeding cycle of increased pressure and increased damage.
Sepsis occurs when an infection becomes widespread enough that it causes a system-wide inflammatory response, resulting in organ damage and vascular disruption — this cascade is self-feeding and can quickly become more harmful than the infection itself, even causing death long after the initial infection has been eradicated.
COPD and asthma are caused, in part, by inflammation of the lower airway (due to prior damage or various dysfunctions).
Shock kills early by hypoperfusion, but if that is survived, it kills later by an uncontrolled inflammatory cascade resulting from that hypoperfusion. If not managed early, this cascade can continue to spread independently of the original shock state.
The entire spectrum of autoimmune diseases is characterized by an inappropriate immune response to the body’s own tissues.
Allergic reactions, including lethal anaphylaxis, are hypersensitive immune responses to benign foreign agents like dust or foods.

To make a long story short, sometimes, inflammation sucks.

Steroids

Steroids are modern medicine’s answer. Steroids are a large class of molecule, including the anabolic steroids that “pump you up” and sex steroids like testosterone and estrogen, but what we’re interested in are glucocorticoids (sometimes called corticosteroids, which is actually a broader category, but the terms are often confused). Glucocorticoids are interesting hormones with numerous effects; as a matter of fact, they’re part of the “fight or flight” stress response we talked about before. (Put simply, catecholamines like adrenaline give you a boost to help deal with danger right now; glucocorticoids, on the other hand, give you a slightly more delayed “second wind,” so you’ll still have some juice a few hours later.) And fighting infections and healing injuries is a real waste of energy when we’re running from wild tigers. The result? Glucocorticoids inhibit the inflammatory response.

They can therefore play a role in the management of all the problems we just mentioned. Maintenance-type inhalers for asthma and COPD are often steroids. Anti-allergy nasal sprays too. Appropriate steroid use can be complex, because we must be careful not to over-inhibit our inflammatory system; for instance, although they would seem like an obvious answer to sepsis, their use for those patients is unclear and has long been controversial. Or how about using steroids to treat epiglottitis, an infectious swelling of the epiglottis that can obstruct the airway? We would expect the steroids to combat the swelling, but also to impair our ability to fight the underlying infection. So finding the balance can be difficult.

Corticosteroids can be administered locally, when a local effect is desired, such as via metered-dose inhaler for asthma. Or they can be administered globally for systemic conditions, such as by IV or oral routes for autoimmune conditions.

Antibiotics

Of course, sometimes the body is fighting for a reason.

As we’ve seen, the body responds with inflammation to a wide range of insults, but one of the most common is infection. And in the many cases of infection when our primary goal is simply to eradicate the source, pharmacological support can be beneficial.

Antibiotics are generally well-recognized as agents that kill bacteria. The terminology has become somewhat clouded nowadays, as the word “antibiotics” is sometimes used to strictly mean anti-bacterial agents, and sometimes to mean all anti-microbials, including anti-fungals and anti-virals. But the general idea of immunosupport is the same.

These agents generally work in one of two ways: either by directly killing the microbe, or by impeding its ability to replicate. They’re tuned so that they affect the bad guys without harming (not too badly anyway) our body’s own cells.

It’s therefore natural to think of antibiotic therapy as the natural opposite of steroids, and this has some truth to it. In the case of infection — which, remember, is not the only cause of inflammation — steroids do inhibit the immune response. But bear in mind that antibiotics do not, as a general rule, actually support or promote the body’s inflammatory response; rather, they work independently by attacking the infection directly along their own pathways. The result is that some pathologies (such as the contentious cases of sepsis and epiglottitis) may respond both to steroids — to manage the excessive inflammatory response — and antibiotics — to help eliminate the source infection.

Examples

Once again, remember that common drug suffixes are usually only applicable to generic drug names. Trade names tend to be unique.

Steroids

Drugs ending in -one (prednisone, hydrocortisone, clocortolone, etc.)
Drugs ending in -ide (fluocinonide, budesonide, desonide, etc.)
Drugs with pred in the name (prednisolone, loteprednol, prednicarbate, etc.)
Drugs with cort in the name (fluocortin, Cyclocort, Entocort)

Antimicrobials

Drugs beginning with ceph- or cef- are antibiotics of the cephalosporin type (cefixime, cephalexin, cefepime, etc)
Drugs ending in -illin are antibiotics of the pencillin type (penicillin, methicillin, nafcillin, etc.)
Drugs ending in -cycline are antibiotics of the tetracycline type (doxycycline, methacycline, etc.); not to be confused with the -tyline of tricyclic antidepressants.
Drugs ending in -azole are generally from a large family that can have antibiotic, anti-fungal, and anthelmintic (anti-parasitic) effects (metronidazole, fluconazole, miconazole, etc.). However, this does not include the -prazole drugs (omeprazole, pantoprazole, and others) which are actually proton pump inhibitors, with no antimicrobial effects.
Drugs ending in -floxacin are antibiotics of the quinolone type (levofloxacin, ciprofloxacin, etc.).
Drugs ending in -mycin are antibiotics of the macrolide type (azithromycin, erythromycin, etc.)
Drugs beginning with sulf- are antibiotics of the sulphonamide type (sulfamethoxazole, etc.)
Drugs ending with -adine are antivirals of the adamantane type (amantadine, rimantadine)
Drugs containing vir are generally antivirals (acyclovir, oseltamivir, ribavirin, efavirenz), including antiretrovirals for HIV treatment
Drugs ending with -vudine are antivirals (lamivudine, telbivudine, etc.)

More Drug Families: Stimulants and Depressants; ACE Inhibitors and ARBs; Anticoagulants and Antiplatelets

Drug Families: Stimulants and Depressants

There are many, many, many, many, many, many drugs.

And I think it’s noble and wise for a sharp EMT-B to learn as much as he can about as many of them as he can. General mechanism, typical routes, notable adverse effects and contraindications. The most common meds are encountered so frequently that you can’t help but become familiar with them.

But what about all the rest? (You remember those — many, many, many, etc.) Memorize them all? Maybe, but that’s a task on par with memorizing the map of London. I’ll freely admit that my own mental encyclopedia of pharmacology is weaker than it should be.

Use a reference? These are certainly handy; printed quick-books are available, as are digital versions you can access with a smartphone (Epocrates and Medscape are a couple good ones — see the Droid Medic for guidance). But we really ought to have at least a surface recognition of most drugs we come across, without having to consult an Ouija board.

Fortunately, 80-90% of the drugs you’ll encounter can be broadly categorized into a few major types. If you understand these types, and their basic physiological behavior, you’ll understand most of what’s relevant to your care; and it’s easy business to memorize which type a drug belongs to. So let’s go over some of these categories.

Some of these groups seem to fall naturally into matched opposites. So today, let’s discuss…

Stimulants and Depressants

Basically, it’s all about speeding up, or slowing down.

Most of us have heard of the “fight or flight” response, our body’s instinctive ability to step on the gas in times of need — an acute stress response that lets us climb trees, hunt mammoths, and escape from tigers. It’s the get-up-and-go state, and its physiological trigger is known to laymen as adrenaline. This is partly correct; in actuality, your body creates this high-output condition through a variety of hormonal mediators (including adrenaline, more commonly known in the US as epinephrine, but also dopamine and norepinephrine). Overall, this functionality of your autonomic nervous system is known as the sympathetic system.

Some of us have also heard of the reverse state of fight-or-flight, often called “rest and digest” (or sometimes “breed and feed”). This is the slow down, recover, repair, rebuild, and relax state; this is the brake to the sympathetic’s gas. Although slowing down is the last thing you want when escaping from sabre-toothed tigers, it’s just the ticket when you’re enjoying supper or having a snooze. This side of things is known as the parasympathetic system.

(How to keep these two straight? Try this mnemonic: the s in sympathetic is for “stress,” because this is your fight-or-flight stress response. The p in parasympathetic is for “peace,” because this is your peaceful, resting state. Thanks to Mark O’Brien for this one.)

Together, these two systems keep your body tuned like a guitar string. It’s a mistake to think that when one is active, the other is switched off; actually, they’re both active at all times, merely to different degrees. Although their combined results are directly antagonistic, they’re independent systems, which means that you can have a mixture of a little sympathetic, a lot of parasympathetic, vice versa, a lot of both, or any combination thereof.

Think of it like the hot and cold knobs on your sink. You adjust them separately, but the result is a single water temperature. A little hot and a little cold will give you warm water, but so will a lot of hot and a lot of cold. And if you want to cool it down, you can either turn up the cold, or turn down the hot. Simple.

Well, the secret is that many of the drugs we use in medicine function primarily by adjusting this balance.

A drug that turns up the sympathetic system (thus “speeding you up”) is known as a sympathomimetic. A drug that turns down the sympathetic system is known as a sympatholytic.

A drug that turns up the parasympathetic system (thus “slowing you down”) is known as a parasympathomimetic. A drug that turns down the parasympathetic system is known as a parasympatholytic.

Okay, so those are mouthfuls. But the important thing to remember is that, while they’re not identical, the result of both a sympathomimetic and a parasympatholytic will be to support your fight-or-fight responses (run from the lion!), and the result of both a parasympathomimetic and a sympatholytic will be to support your rest-and-digest behavior (take a nap!). So whichever end you approach it from, there are still only two important end results here — up and down.

Virtually the entire body is controlled by these systems. If you can keep track of how each organ system is affected when you nudge this balance one way or the other, you’ll be able to understand a great deal of how drugs do their work.

For instance, consider epinephrine itself, which we use in auto-injectors to treat severe anaphylaxis. The life-threatening effects of an allergic reaction are primarily shock, due to vascular dilation, and respiratory distress, due to bronchial constriction. Epinephrine is a sympathomimetic (okay, “mimetic” means “mimick,” and epinephrine is actually one of the body’s own sympathetic hormones, so it’s not really mimicking anything — but bear with me here). So it produces a fight or flight response. What is the sympathetic effect on the skin and peripheral vascular system? Vasoconstriction (to pull blood away from the periphery into the core). What is the sympathetic effect on the lungs? Bronchodilation (to allow for greater air exchange during exertion). So the entire cocktail of epi’s beneficial results in anaphylaxis comes from stimulating sympathetic tone.

What if I shoot some heroin? My breathing will become slower and weaker. My level of consciousness will decrease. I will become generally slowwww, because heroin (like all opiates) is fundamentally a depressant. And my pupils, pleasantly parasympathetic, will constrict — the third hallmark sign of opiate use. Who needs light when we’re relaxing?

Subtypes

Now, not all drugs from the same neck of the woods are identical, of course. The effects of the same neurotransmitters can be radically different depending on where they bind. An important distinction should be made between non-selective drugs like epinephrine, which binds with all of the primary adrenergic receptor sites (alpha-1, beta-1, and beta-2), and selective agonists like albuterol, which primarily binds only at certain receptors (beta-2 in that case). In brief:

Alpha-1 (properly styled, α₁) receptors are mainly in the blood vessels, and cause systemic vasoconstriction. Alpha-1 blockers, or antagonists, therefore cause systemic vasodilation.
Beta-1 (β₁) receptors are mainly in the heart, and increase heart rate and contractility. Beta-1 antagonists therefore slow and reduce cardiac output. (Mnemonic: you have 1 heart.)
Beta-2 (β₂) receptors are mainly in the lungs, and cause bronchodilation. Beta-2 antagonists therefore cause bronchoconstriction. (Mnemonic: you have 2 lungs.)

Naturally, none of these categories tell the whole story of a drug. (If they did, we wouldn’t need so many different ones.) Caffeine, atropine, and crystal meth are all very different drugs, even though they all fall roughly into the category of stimulants. But you can keep track of a good deal of their shared effects by understanding their common nature.

Examples

Drugs ending in -zepam (or sometimes -zolam — eg. diazepam, triazolam) are benzodiazepines, which have broad sedative effects.
Drugs ending in -alol (or -ilol, -olol — eg. atenolol, labetalol) are beta blockers, which have a sedative effect, usually localized to the heart via beta-1 antagonism.
Drugs ending in -erol (e.g. albuterol, clenbuterol) are beta-2 agonists, or bronchodilators; they are stimulants that primarily cause bronchodilation via beta-2 receptors.

Most pain killers, sedatives, and anesthetic agents are depressants.

Note: most common suffixes are only applicable to generic drug names. Trade names are usually unique.

More Drug Families: Steroids and Antibiotics; ACE Inhibitors and ARBs; Anticoagulants and Antiplatelets