Understanding Shock IX: Assessment and Recognition

To wrap up our story on shock, let’s discuss how to recognize it.

We all have some idea what shock looks like. Like many pathologies, its loudest early markers are actually indirect — we’ll often recognize the body’s reactions to shock rather than the shock itself.

Although there are a few ways to classify the stages of shock, let’s just use three categories here.

Early or Insignificant

Shock that is very early or minimal in effect may have no particular manifestations. One situation where significant or late shock may also be “hidden” is in the elderly patient, or anyone with significant comorbidities; if their body’s ability to mobilize its compensatory mechanisms is poor, then the red flags won’t be as obvious. This doesn’t mean the shock isn’t as bad; in fact, it means that it’s worse, because their body can’t do as much to mitigate it.

The way to recognize shock at this stage is from the history. If we see an obvious bullet hole in the patient’s chest, and three liters of blood pooling on the ground beside him, then it doesn’t matter how the patient presents otherwise; we’re going to assume that shock is a concern. Blood volume is proportional to bodyweight, but for a typical adult, a fair rule of thumb is to assume about 5-7 liters of total volume. (Not sure what a liter looks like? The bags of saline the medics usually carry are a liter; so are those Nalgene water bottles many people drink from. “Party size” soda bottles are two liters.) Losing more than a liter or two rapidly is difficult to compensate for.

Remember, of course, that blood can also be lost internally, and aside from the occasional pelvic fracture or hemothorax, the best environment for this is the abdomen. Always examine and palpate the abdomen of the trauma patient, looking for rigidity, tenderness, or distention. Remember also that the GI tract is a great place to lose blood; be sure to ask your medical patients about blood or “coffee grounds” (old blood) in the vomit or stool.

Fluid enters and leaves the body continuously, and any disruption in this should be recognized. If a patient complains “I haven’t been able to eat or drink anything in two days,” they’re telling you that they haven’t taken in any fluid for 48 hours. If they tell you they’ve been vomiting or experiencing profuse diarrhea, that’s fluid leaving their body in significant volumes. What about the man who just ran a marathon and sweated out a gallon? Did he drink a gallon to replace it?

Compensated Shock

Significant shock will result in the body attempting to compensate for the low blood volume. Much of this work is done by the sympathetic system, and there are two primary effects: vasoconstriction and cardiac stimulation.

By constricting the blood vessels, we can maintain a reasonable blood pressure and adequate flow even with a smaller circulating volume. We normally vasoconstrict in the periphery — particularly the outer extremities and skin — “stealing” blood from those less-important tissues and retaining it in the vital core. This causes pallor (paleness) and coolness of the external skin. The sympathetic stimulation may also cause diaphoresis (sweating), which is not compensatory, but simply a side effect of the adrenergic release.

The heart also kicks into overdrive, trying to keep the remaining volume moving faster to make up for the loss. It beats faster (chronotropy) and harder (inotropy), resulting in tachycardia. Note that patients who use beta blockers (such as metoprolol) may not be able to muster much, if any, compensatory tachycardia.

A narrowing pulse pressure (the difference between the systolic and diastolic numbers) may be noted; since the diastolic reflects baseline pressure and the systolic reflects the added pressure created by the pumping of the heart, a narrow pulse pressure suggests that cardiac output is diminishing (due to loss of preload), and that more and more of the pressure we’re seeing is simply produced by shrinking the vasculature.

Tachypnea (rapid respirations) are also typically seen. In some cases, this may be due to emotional excitement, and there is also a longstanding belief that it reflects the body’s attempts to “blow off” carbon dioxide and reduce the acidosis created by anaerobic metabolism. (Interestingly, lactate — a byproduct of anaerobic metabolism — can be measured by lab tests, and is also a sign of shock, particularly useful in sepsis.) Additionally, it ensures that all remaining blood has the greatest possible oxygenation. However, it is also plausible that this tachypnea serves to assist the circulatory system: by creating negative pressure in the thorax (the “suction” you make in your chest whenever you inhale) and positive pressure in the abdomen (due to the diaphragm dropping down), you “milk” the vena cava upward during inspiration, improving venous return to the heart and allowing greater cardiac output. This “bellows” effect helps the heart fill more and expel more with each beat.

The more functional the patient’s body is — such as the young, strong, healthy victim — the more effective these compensatory systems will be. Hence the old truism that pediatric patients “fall off a cliff” — they may look great even up through quite profound levels of shock, due to their excellent ability to compensate, then when they finally run out of room they’re already so far in the hole that they become rapidly unhinged. It’s great that these people can compensate well, but it does mean we need to have a high index of suspicion, looking closely for signs of compensation (such as tachycardia) rather than outright signs of shock — because by the time the latter appears, it may be very late indeed.

Patients in compensated shock may become orthostatic; their bodies are capable of perfusing well in more horizontal postures, but when gravity pulls their remaining blood away from the core, this added challenge makes the hypovolemia noticeable. Less acute shock due to causes like dehydration may result in dry skin (particularly the mucus membranes; try examining the inside of the lower eyelid) with poor turgor (pinch a “tent” out of their skin and release it; does it snap back quickly or sluggishly?), and potentially with complaints of thirst. Urine output will usually be minimal. Generally, the more gradually the hypovolemia sets in, the more gradually it can be safely corrected; it’s the sudden, acute losses from causes like bleeding that we’re most worried about.

Decompensated Shock

As shock continues, compensatory systems will struggle harder and harder to maintain perfusion and pressure. Eventually they will fail; further vasoconstriction will reduce rather than improve organ perfusion, beating the heart faster will expel less rather than more blood, and the blood pressure will start to drop.

The hallmark of this stage of shock is the normal functioning of the body beginning to fail. The measured blood pressure will decrease and eventually become unobtainable. Pulses will weaken until they cannot be palpated. As perfusion to the brain decreases, the patient’s mental status will deteriorate. Heart rate and respirations, previously rapid, will begin to slow as the body loses the ability to drive them; like a government office that can’t pay its workers, the regulatory systems that should be fighting the problem begin to shutter their own operations. As the heart continues to “brady down,” eventually it may lose coherence (ventricular fibrillation), or keep stoically trying to contract until the last, but lose all effective output due to the lack of available blood (PEA). Cardiac arrest ensues, with dismal chances for resuscitation.

Alternative Forms of Shock

Although we have focused so far on hypovolemic shock, particularly of traumatic etiology, there are other possibilities. A wide range of shock types exist, but speaking broadly, there are only two other categories important to us: distributive, and cardiogenic/obstructive.

Distributive shocks include anaphylactic, septic, and neurogenic. The essential difference here is that rather than any loss of fluid, the vasculature has simply expanded. Rather than squeezing down on the blood volume to maintain an appropriate pressure, the veins and arteries have gone “slack,” and control of the circulating volume has been lost; it’s simply puddled, like standing water in a sewer pipe. (Depending on the type of shock there may also be some true fluid losses due to edema and third-spacing.) Imagine tying your shoes: in order to stay securely on your feet, the laces need to be pulled snugly (not too tight, not too loose). If the knot comes undone and the laces lose their tension, the shoe will likely slip right off. Your foot hasn’t gotten smaller, but the shoe needs to be hugging it properly to stay in place, and it’s no longer doing its job.

The hallmark of distributive shock is hyperemic (flush or highly perfused) rather than constricted peripheral circulation. The visible skin is warm (or hot) and pink (or red), and the patient may be profoundly orthostatic. Septic shock is associated with infection; anaphylactic with an allergic trigger; and neurogenic with an injury to the spinal cord.

Cardiogenic and obstructive shocks are a different story. In this case, there’s nothing wrong with the circulating volume, or with the vasculature it flows within; instead, there’s a problem with the pump. Cardiogenic shock typically refers to situations like a post-MI heart that’s no longer pumping effectively. Obstructive shock refers to the special cases of pericardial tamponade, massive pulmonary embolism, or tension pneumothorax: physical forces are preventing the heart from expanding or blood from entering it, and hence (despite an otherwise functional myocardium) it’s unable to pump anything out. In either case, we can expect a clinical picture generally similar to hypovolemic shock, but likely with cardiac irregularities — such as ischemic changes or loss of QRS amplitude on the ECG, irregularity or slowing of the pulse, or changes in heart tone (such as muffling) upon auscultation. Pulsus paradoxus (a drop in blood pressure — usually detected by the strength of the palpable pulses — during the inspiratory phase of breathing), electrical alternans (alternating QRS amplitudes on the ECG), and jugular vein distention also may be present in the case of tamponade or severe tension pneumothorax.

In sum, remember these general points:

The history and clinical context should be enough to make you suspect shock even without other signs or symptoms.
The faster the onset, the more urgent the situation; acute shock needs acute care.
Look both for signs of compensation (such as tachycardia) and for signs of decompensation (such as falling blood pressure). However, remember that due to confounding factors (such as particularly effective or ineffective compensatory ability, or pharmacological beta blockade), any or all of these may be absent.
Distributive shocks are mainly characterized by well-perfused peripheral skin; cardiogenic/obstructive shocks are characterized by cardiac irregularities.

Interested parties can stay tuned for a brief appendix discussing fluid choices for resuscitation — otherwise, this journey through shock is finally finished!

Go to Part X (appendix) or back to Part VIII

Understanding Shock VIII: Prehospital Course of Care

Now that we have a pretty good idea of how shock works, what does it all mean for our treatment in the field?

Much like cardiac arrest and some of the other “big sick” emergencies, there are really a couple essential interventions we need to execute, maybe a couple others that aren’t a bad idea, and beyond that, our main job is to ensure that we don’t kill our patient by wasting time doing anything else.

Step 1: Control the bleeding

As we emphasized ad nauseam, the number one goal with the bleeding patient is to stop the bleeding. No need to beat this to death, but just remember: if you can control the bleeding, yet don’t get much of anything else done, you’re doing absolutely fine.

Step 2: Transport to surgery

In most significant cases of hemorrhage, definitively controlling the bleeding will require surgical intervention. We don’t do surgery, but we do set the stage, which is why it’s essential for us to know what we’re doing. Get thee to a trauma center, and quickly!

Can other hospitals perform surgical intervention? Sometimes. Maybe. A world-class trauma surgeon might happen to be in the building for a conference. Maybe the operating room is between scheduled procedures and happens to be clean and available. But the point to a trauma center is that it’s guaranteed to have certain resources available, and that’s the kind of place we want to bring these patients. 9 times out of 10, if we transport them elsewhere, they’ll simply end up being transferred back out to the trauma center anyway, making the whole exercise essentially one very long transport. Can a small community hospital help stabilize the patient before surgery? Sure — but as we know, everything else is a distant second priority to bleeding control. Even transfusing blood may need to be done sparingly until the leak has been corked.

What about ALS? Do these patients need paramedics? Now, if they acutely decompensate and need airway management or other interventions you can’t provide (or have other issues like pneumothorax), then ALS-level care would be valuable. But outside of that, and even granting that to a certain extent, a medic unit is not going to stitch up the bleeding, and meeting them will certainly delay transport to surgery at least by a few minutes. True, they’ll be able to initiate IV access that can be used for blood later, but in most cases this takes mere seconds at the ED (where there’s plenty of room, good lighting, and ample personnel) — and prehospital IVs will sometimes be replaced anyway.

Step 3: Promote oxygen delivery

Okay, you shock technician, now what?

Can we talk about coagulopathy of trauma — aka the “deadly triad”?

Bleeding control is the priority, right? And bleeding control requires clotting. But there’s a set of conditions guaranteed to obstruct clotting, and three of them are almost always present during hemorrhagic shock.

One is hemodilution. When we top off our bleeding patients with non-blood fluids, as we’re so fond of doing, it dilutes both oxygen-carrying capacity (since we’re not adding red blood cells) and clotting speed (since we’re not adding platelets or clotting factors). So this one’s our fault, and can be readily avoided by simply resisting the urge to replace blood with salty water.

One is acidosis. If you’ve been paying attention, you know that acidosis tends to develop in shock due to anaerobic cellular activity, and can be further encouraged by overzealous fluid administration. Is this the end of the world? (After all, a little acidosis might even improve oxygen delivery by shifting the oxyhemoglobin dissociation curve.) Well, the trouble is that acidosis also leads to coagulopathy. According to some in vitro studies, in fact, even mild acidosis can precipitously decrease platelet aggregation, and in significant acidosis platelets won’t activate at all. Zero.

The last is hypothermia. Not only do cold patients have poor oxygen delivery and other problems, they clot poorly; low temperatures cause coagulopathy too.

Now, we can’t do much about the initial trauma. We can discourage acidosis by limiting fluid use, and ensuring that ventilations remain adequate. What about hypothermia? Do our trauma patients get cold? What would you expect when you take someone who’s bleeding, strip them naked on a cold sidewalk, pump cold saline into their veins, and chuck them into an ambulance carefully heated to your comfort?

Keep your trauma patients warm. This is not about human kindness or TLC, this is a serious and important intervention for shock. Hypothermia is great for cardiac arrest, it may be beneficial in some other scenarios, but it is not good for bleeding people.

How about supplemental oxygen? Well, I suppose so. In the patient with adequate respirations, it is doubtful that “topping off” their PaO2 will affect them appreciably; but as they begin to decompensate, they’ll need all the help they can get.

Positioning? Remember how big a deal they made about the Trendelenburg position in school — how it pulls blood from the lower extremities into the core? And ever noticed how it’s not exactly our number one emphasis in the field? Trendelenburg has little real evidence supporting it, and the bulk of what does exist suggests its effect is fairly minimal — it moves only a little blood, the effect is transient, and the body’s compensation can actually cause a paradoxical reduction in core perfusion. Mostly these studies were done in healthy people, so it’s possible that our shocky patients do get a little benefit — and one supposes that if things are dire enough to need every last cc of blood, you can give it a shot. But typically it won’t do you too many favors. (I certainly wouldn’t advise propping the patient bolt upright, though!)

Step 4: Supportive care

Supportive care means battling secondary problems as they arise. It doesn’t mean waffling over nonsense while your patient bleeds out.

If the patient’s airway is compromised, or you have legitimate reason to think that it may become compromised, then it should be managed. If they’re breathing inadequately, they’ll need assistance. Beyond that, any other care should only occur after you’ve stuck a cork in the bleeding and started rolling toward the guys with knives. Cardiac fiddling, pain management, splinting or minor bandaging — these should take place en route or simultaneous to other care, if at all. Shock kills people; is a nice sling-and-swath going to save them?

Spinal immobilization? It’s been pretty definitively shown to hurt rather than help in penetrating trauma. What about combined blunt and penetrating? There’s no evidence that it helps and some evidence that it’s harmful. We have no reason to think that tying people to boards does anything good, but we do know that wasting time here does everything bad. So if your local protocols demand immobilizing these patients, I won’t tell you otherwise — but please, at least, try and hurry.

That’s it, folks. Let’s wrap it all up next time by talking about recognizing the beast.

Key points:

Stop the bleeding to the greatest extent possible in the field.
Immediately and without delay transport to a facility capable of emergency surgery.
Provide other supportive care as necessary, without delaying #1 and #2.
Maximize oxygen delivery with supplemental O2, keeping the patient warm, and consider the Trendelenburg position.
Minimize delays created by any and all non-essential care.

Go to Part IX or back to Part VII

Understanding Shock VII: Negatives of Fluid Resuscitation

The last time we talked, we learned about the arguments in favor of non-blood fluid resuscitation. What are the arguments against it?

The “blow out the clots” argument

The vascular system is a pressurized circuit. Bleeding means poking an opening in this circuit, and we know that repairing this hole is our number one priority.

The body is pretty good at fixing leaks in its vasculature. But it’s not magic. It’s going to try to form a stable clot that covers and seals the hole, just like wrapping tape around a leaky pipe fitting.

What’s a good way to make this task harder? Increase the pressure inside the pipe. The faster that blood wants to rush out of the hole, the tougher it’s going to be to get a clot to stick there.

Imagine your inflatable raft has a pinhole in it, so you cover it with a piece of tape. It seals well. Then you drop a cooler of beer onto the raft, increasing the internal pressure. The tape blows off. Simple.

Many providers have therefore moved towards the practice of permissive hypotension — resuscitating only to a lower than normal blood pressure — and/or delayed resuscitation — waiting for substantial fluid replacement until bleeding has been controlled. Permissive may mean a pressure of 80, 90, or 100; it may mean giving crystalloids sparingly and only until blood becomes available; or it may mean giving nothing at all except the good stuff. Or you can take a page from the military, which says to resuscitate until a radial pulse is palpable, and the patient’s mental status is restored — then stop.

The dilution argument

There’s another reason why filling the patient with salt water might make it harder to control their bleeding.

Their body is trying to build clots at the location of injury. We want to encourage this process. In order to occur, it requires the activity of circulating platelets and clotting factors.

Mixing the patient’s blood with saline increases its volume but doesn’t increase the number of these clotting precursors. In other words, we’re diluting their blood, just like a bartender watering down your drink. There’s more volume in your cup, but there’s no more of the stuff we care about. And since the ability to form clots is closely related to the concentration of the clotting components, diluting the blood means slower clotting.

Together, these two arguments form a compelling case against the “volume for the sake of volume” theory. The patient’s ability to form clots and stop the bleeding isn’t a small thing; in a way, it’s the only thing. In fact, INR (a measure of clotting speed) has been shown to be a key predictor of whether a trauma patient will survive their injuries.

The proinflammatory argument

One of the key forces in the shock cascade is inflammation. So it seems like promoting more inflammation is the last thing we’d want.

But surprise: infusing fluids can do exactly this. It’s not entirely clear why this happens, but it’s unquestionably true; fluids encourage the inappropriate immune response and increase inflammation and tissue dysfunction. Suffice to say that this is bad.

Back in Vietnam, when aggressive fluid resuscitation really became trendy, doctors were perplexed to find many of their volume-resuscitated patients with a severe condition called “Da Nang lung” (nowadays Acute Respiratory Distress Syndrome) — wet, failing, edematous lungs with no cardiac cause. The combination of increased fluid volume plus increased inflammation means failing lungs. Or check your nearest ICU to see some abdominal compartment syndrome, where fluid fills the abdomen until the organs fail. What were you were saying about fluids being harmless?

The acidosis argument

The pH of our bodies is a hair over 7. Pick up the nearest bag of normal saline and read the label. What’s its pH?

Is it 7? No? More like between 5.0 and 6.0? Interesting. Remember that pH is a logarithmic scale, so we’re talking a difference of 10–100 here. So that nice “normal” fluid can promote significant acidosis.

Is this bad? Only if you like clotting. Acidosis is detrimental to coagulation (among other things), for reasons we’ll get into later. Clotting is good!

The what’s-the-point? argument

In the end, the most compelling argument against pouring what amounts to water into trauma patients is this: fundamentally it is not what they need. Their problem is not a lack of normal saline. “When I find a patient who’s bleeding crystalloid,” some providers are fond of saying, “I’ll give them crystalloid. But usually, the puddle on the ground is blood.”

Now, in some patients, crystalloid may indeed be what’s missing; we’ll touch upon situations like sepsis and dehydration later. But if they’re bleeding, it seems like — at best — playing with any fluid except those that can restore oxygen-carrying capacity or promote clotting is a waste of time that could be spent patching the hole and rushing toward surgery. And at worst, it may be exacerbating the problem.

For a long time, paramedics were taught to fill the hypotensive patient with fluid until their blood pressure was normal. The jury is still out on the best practices for fluid resuscitation, but there is fairly widespread agreement now that this is a bad idea. Many progressive systems have gone the route of giving no crystalloid whatsoever for hemorrhagic shock, or at least giving it very sparingly. Seeing the numbers 120/80 on the monitor seems like a good thing, but shock is not a blood pressure, raising the blood pressure is not necessarily beneficial, and we’re supposed to be making the patient feel better, not ourselves.

So, stop the bleeding, and restore the stuff that matters. Since we rarely give blood in the field, the first one is the main business of EMS. And oddly enough, it’s very much a BLS skill.

Summary:

Increasing the blood pressure interferes with bleeding control.
Diluting the blood discourages clotting while doing nothing for oxygen transport.
Aggressive fluid resuscitation promotes inflammation, edema, and organ dysfunction.
Current best practices are unclear, but likely involve a minor role for crystalloid resuscitation, in favor of bleeding control, blood products, and early surgical intervention.

Next time: mastering the field treatment of hemorrhagic shock.

Go to Part VIII or back to Part VI

Understanding Shock VI: Fluid Resuscitation

So we know now that in any hemorrhagic shock, controlling the bleeding is step one, and restoring the supply of something resembling blood is step two. Should we also consider infusing some other fluids, even those that don’t help carry any oxygen?

Why would we even consider such a thing? It would make sense if “fluid” is what we’re missing, which is the case when shock is caused by something like dehydration. But in hemorrhage, we’re missing blood, not water. Still, there are a few reasons this might be worthwhile. Let’s discuss the “pro” arguments first, then come back around and talk about the “cons.”

The hydraulic argument

Fundamentally, the human vascular system is a hydraulic circuit.

In other words, it’s a giant circle of stretchy elastic tubes, like those long circus balloons. It’s all filled with fluid, which stretches out those tubes and pressurizes the whole system. Then a central pump pushes all the fluid in the system around in an endless loop.

One of the properties of such a system is that, without adequate internal pressure, it won’t work. It’s not that it works badly; it just fails altogether. And although pumping harder and faster can help elevate the pressure a little, and squeezing down on the tubes to make them smaller can help more, in the end if there’s not enough fluid in the system, nothing’s moving anywhere. If the heart isn’t filling with a certain amount of blood during diastole, it won’t push it forward during systole; it can’t pump out what it doesn’t take in.

So maybe there’s a certain logic for maintaining an adequate blood pressure, no matter what sort of fluid we’re actually circulating. Although pressure alone doesn’t carry oxygen, maintaining some pressure is certainly a prerequisite for carrying anything. To put it dryly, although BP isn’t everything, people with no BP are dead.

Moreover, some of the pathways in the shock cascade are, perhaps, initiated by low intravascular volume as much as by actual inadequate oxygen delivery. If we can keep the circulating volume pretty decent, maybe we can convince the body that all’s well — no need for a freak-out today.

The extravascular resuscitation argument

Flip back the calendar to the era of the Vietnam War, a landmark time in trauma care. Researchers like Dr. Tom Shires were experimenting on dogs.

They’d do things like drain from them a fixed volume of blood, then clamp off the bleeding and wait for a bit. Then they’d put back every drop of blood they’d removed. Most of the dogs died nonetheless, a phenomenon you and I now understand, since we’re totally experts in the self-sufficiency of the shock process.

But then they’d repeat the experiment. Only this time, rather than just giving the dogs back their blood, they’d also give them some crystalloid fluid. Just water with some stuff like electrolytes in it. This time, more of the dogs survived.

The theory explaining this goes something like so: where is most of the fluid in your body? We know that a high percentage of our bodyweight is water, but does that flow mostly in the blood? Anatomists talk about three different fluid “spaces”: the intravascular space (inside the vessels, where the blood circulates); the intracellular space (the interior of our actual cells); and the interstitial space (the “sea” of fluid permeating the tissue beds but outside the cells, bathing and nourishing them). Fluid moves between these spaces as needed, but at any given time, the majority of your body’s fluid is actually in the interstitial and intracellular (the extravascular) spaces — that is to say, not in the blood at all.

Shock causes increased permeability of the tissues and of the vascular tree, while simultaneously dropping intravascular (hydrostatic) pressure. So when the dogs entered shock, after a short while fluid began to “leak” from the interstitial and intracellular spaces back into the intravascular space. In essence, the dogs’ tissues were returning some of their retained fluid back into the bloodstream — and human tissues do this too. This shift actually increases the vascular volume, which is nice in a sense, and can be seen as a method of compensation: the body is tapping some of its reserve fluid to restore what was lost. However, it does leave the tissues dry. By infusing some saline along with the blood, Shires was helping his test subjects resuscitate both spaces. The intravascular space needed blood, but the extravascular spaces just needed fluid. (Of course, if we replace the blood, eventually the extravascular tissues will be rehydrated and the loaner fluid returned; but if we didn’t provide any extra fluid, that would once again leave the intravascular compartment a little light. Also, some of it — which leaked into neither the intravascular nor extravascular spaces, but the “third space,” areas such as the abdomen where it doesn’t belong — won’t be readily returned at all.)

Some combination of these two arguments became the foundation for a decades-long practice whereby hemorrhaging patients are given a certain amount of crystalloid (usually saline, or a modified form of saline like Lactated Ringer’s), often prior or in addition to giving blood products. In many cases this fluid is titrated to maintain a desired blood pressure, and this practice is still widespread today, especially in the prehospital world. In some cases, colloidal fluids (which contain large molecules such as proteins) are also used and have generally similar effects.

Key points:

Bleeding control and restoring actual oxygen-carrying capacity are the main priorities in hemorrhagic shock, but there may also be value in non-blood fluid resuscitation.
One argument for this is the maintenance of adequate blood pressure in order for the circulatory system to function.
Another argument is the replenishment of the fluid lost from extravascular spaces.

Next episode we’ll discuss the dark side of crystalloid resuscitation.

Go to Part VII or back to Part V

Understanding Shock V: Blood Transfusion

So let’s say we’ve stopped the bleeding as best we can. Now what?

The patient is still low on blood, and we know about all the problems this will cause. So shouldn’t we try and give them some back?

Well, maybe.

It makes sense that someone who loses blood should get some blood replaced. And this is a very old concept. Once upon a time, we simply drew blood from one person and gave it to another — a process that was greatly improved when we learned how to screen and test blood for compatibility and disease. This method is still used in some settings, such as the military, which treats its entire force as a “walking blood bank.” If Pvt. Joe needs blood, they check the registries to find a match, then call up Pvt. James and have him swing by to donate a few bags.

In most other settings, however, whole blood transfusion has largely become a thing of the past. Instead, when blood is donated, it’s immediately reduced to its constituent parts. The red blood cells are pulled out and stored as packed red blood cells (PRBCs); the platelets are pulled out and stored as condensed platelet concentrate; and everything that’s left — the plasma itself, including electrolyte-rich water, clotting factors, immune factors, and other ingredients — is frozen and stored as fresh frozen plasma (FFP). One unit of blood (around a pint) yields one unit of each component. Since most patients only need one or two of these components, we can divvy them out as indicated, and the same blood supply can benefit up to three people.

So for years it’s been standard to transfuse traumatic shock patients red blood cells. As we know, the key problem of shock is inadequate oxygen delivery, and red blood cells are how we deliver oxygen. So drop in a few extra hemoglobin, perhaps top them off with a bit of fluid to keep things moving, and we should be set, right?

Maybe. But this leaves out a number of factors.

First of all, remember our prime directive. Stopping the bleeding is more important than topping off the tanks. How does our body control bleeding? Platelet aggregation and coagulation. And remember that platelets, the bricks of this process, are not reusable; if we have a lot of trauma, and we lose a lot of blood, we can easily run out of them. Does transfusing red blood cells alone provide any platelets? Nope.

So maybe we should throw in some platelets too. But wait — we know that to actually bind the platelets into a cohesive clot, we need a host of backup players, the numerous coagulation factors that live in the plasma. Does a platelet pack provide these? Nope. (Okay, platelets are usually stored in a small amount of plasma, so there’s a few, but not enough.) So maybe we should give the patient some plasma too (or even isolated concentrates of clotting factors to really supercharge the process).

The result of all this is the recent movement towards so-called 1:1:1 therapy, where trauma patients receive equal proportions of red blood cells, plasma, and platelets. In other words, they end up getting all the individual components of whole blood; we just don’t often have whole blood available, or we might give that. This is still an area of active research, and the exact ideal ratios are up for debate; the ratio of red blood cells to plasma is often either 1:1 or very close to it (1:2, 1:3, etc.), and platelets are usually given in somewhat lower quantities, but should not be neglected. The best ratio, as well as the actual quantity of blood to ultimately give, remains to be seen.

Logistics can stand in the way of some of these efforts. For instance, plasma is typically stored frozen (as FFP), and therefore needs to be thawed before use, a process that takes some time. Very large trauma centers may be able to keep a rotating supply of thawed plasma on hand for emergency use, but many facilities won’t be able to have plasma immediately available in this way. And although transfusing in the field seems tempting, the practical challenges of carrying blood products on an ambulance are daunting.

Furthermore, banked blood is not “as good” as the patient’s own blood no matter how it’s given. Even a 1:1:1 transfusion, properly typed, screened, and cross-matched, has real risks of transmitting infection or causing an adverse reaction, carries less oxygen than fresh blood, has reduced hemoglobin pliability (the little disks “stiffen,” becoming less able to squeeze down capillaries to reach the hungry cells), and reduced numbers of labile clotting factors (particularly V and VII). It carries less 2,3-DPG, its pH is lower, and due to the anticoagulants and preservatives added for storage, it’s literally larger and more dilute than the whole blood it started as. Since transfusions are generally not our problem in the field, the applicable moral here is simply that “top ’em up” is not a simple or easy answer to shock, and the only intervention that truly keeps the patient out of trouble is to stop the bleeding!

From the Trauma Professional’s Blog at http://regionstraumapro.com/

In brief:

Blood transfusion is an important step in treating traumatic shock, secondary only to controlling the source of hemorrhage.
Modern “component” blood banking allows for the administration of almost any ratio of red blood cells, plasma, and platelets.
Transfusing primarily red blood cells is the traditional approach, but a movement has recently developed toward more balanced ratios.

Next time: the legacy of crystalloids.

Go to Part VI or back to Part IV

Understanding Shock IV: Bleeding Control

The first, the last, and always the most important answer to the shock progression is to fix the underlying cause.

To illustrate the principles, let’s focus for the moment on traumatic shock caused by hemorrhage — you were injured, began to bleed, and now you’ve got less intravascular blood. What should we do about that? Stop the bleeding? Give you more blood?

If you’re caught in a sudden rainstorm, should your first reaction be toweling yourself off, or getting under shelter?

Both will be needed, but one will be futile without the other.

Shock caused by bleeding is cured by stopping the bleeding. The body will try to do this on its own, but definitively, in significant trauma, this is almost always accomplished through surgery. Trauma is a surgical disease; its medicine is an operating room, sutures, and cautery.

Prior to that, just about anything we can do to stop or slow the bleeding is worth doing. Direct pressure on an injury is often very effective. Pressure slows the flow of blood and promotes the clotting process (by creating stasis and degranulating platelets). It most often fails when it can’t be properly applied — such as when the bleeding is internal, as with a lacerated abdominal organ.

Tourniquets for extremity injuries are perhaps the most definitive pre-surgical intervention of all, and despite years of demonization they have been shown to be generally effective in most cases, with relatively minor risks. More discussion of tourniquets will come another day.

To contrast, consider the counter-example of septic shock. The initial insult there is an infection. How do we treat infection? Antibiotics. Early antibiotic therapy is so important for the sepsis patient that the time from hospital arrival to administration of antibiotics is recorded, and measured in minutes.

The takeaway:

The prime directive in correcting shock is reversing the original cause; this takes precedence over any other treatment.
In trauma, this means stopping the bleeding; that usually means surgery, and before that, direct pressure or tourniquets.
Achieving this control is absolutely essential and absolutely time-critical.

Go to Part V or back to Part III

Understanding Shock III: Pathophysiology

The common thread that defines the shock process is inflammation.

As we know, inflammation is the body’s response to damage. When things go wrong, when trouble calls, we ring the bell for inflammation to make it right. Often this serves us well, but like any militia, if left unchecked it can be worse than the problem it came to fix.

The many twists and turns of the pathology of shock are still not fully understood, but here are some of the important stepping stones along the way:

Shock occurs, and many of the body’s systems are left without adequate oxygen. Although oxygen supplies our primary method of generating energy — the aerobic metabolism — we do have secondary systems in place that can produce energy without oxygen, the anaerobic cycles. In the setting of shock, these take over.

But they’re not great. They provide far less energy than aerobic metabolism, and they produce by-products that accumulate in the body. Among other things, this includes the accumulation of hydrogen ions, creating a widespread acidosis. Think about running sprints or lifting heavy weights; think about that burning feeling, and the eventual failure of your muscles. Operating in an anearobic mode causes trouble and is shortlived at best.

Sooner or later, this isn’t enough to keep things working, and cells begin to accumulate toxic products and eventually shut down. They’re not quite dead yet; they’re hurting, but they can still recover. Like a business that shuts its doors in the off-season, there simply isn’t enough inflow for them to operate right now.

The trouble is, we need those cells. They make up the tissues that form the heart, the brain, the lungs, the kidneys, the liver, and so forth. When the cells close up shop, the organs begin to fail. When organs fail, they cease to provide their essential functions. Let’s consider just one, the heart.

The heart pumps blood. When it loses its effectiveness, it pumps less blood. This means less circulation of oxygen, which means hypoxia is exacerbated. Look at that — we just magnified the problem. If the shock gets worse, is that going to help the heart pump any better? Dream on. The vicious cycle accelerates further.

As hypoxic damage to the cells progresses, the body responds with widespread inflammation to repair it. The trouble is, there’s no real hope of repairing anything without restoring the oxygen supply — but that never stopped Old Man Inflammation. One of his brute-force tactics is to increase capillary permeability, the “tightness” of tissues; everything becomes more susceptible to leakage. The fluid that runs throughout your body begins to ooze everywhere. Generalized edema occurs. In some cases, this is just gross; look at the bloated extremities of the recently dead for an example. But what happens when there’s edema and inflammation of the vital organs? They fail. Fluid in the lungs impairs respiration. Fluid in the brain causes increased intracranial pressure. Another blind response of the inflammatory system is apoptosis, where hypoxic cells — sensing that they’re done for — trigger self-destruct mechanisms and tear themselves apart. Unfortunately, you need those cells.

And hey, what about that acidosis? Our cells (including the ligand-receptor complexes that trigger our sympathetic processes) are designed to function at a specific pH. Placing them in an acidotic environment impairs their function. Combo attack!

But what about our compensatory systems? When our body sees shock, it does things like vasoconstricting, increasing heart rate and contractility, and attempting to maximize the availability of oxygen. That’s great when it works. But when things progress, it’s not so great. Vasoconstriction can choke off the organs, giving them even less oxygenated blood. Tachycardia increases the heart’s demand for oxygen.

And oh, by the way, none of this is adds much to the body’s ability to combat the original cause of the shock, whether that was traumatic injury, a septic infection, or something else.

Key points:

The processes of shock are multiple and self-reinforcing.
Inflammation plays a major role.
Multi-organ dysfunction and failure also plays a major role.

Next time: so what do we do about it?

Go to Part IV or back to Part II

Understanding Shock II: What the What?

. . . the rude unhinging of the machinery of life.

Samuel Gross

When we say shock, what do we mean?

First, to be clear, we’re not talking about “shock” as in “I’m shocked by all this,” or as in “shell shock,” or as in “tasers give an electric shock.” Shock is a formal medical term with a specific meaning.

Here’s the simple definition: shock is what happens when your body runs low on oxygen.

Your entire body, from the top of your horns to the bottom of your hooves, is made of cells. Your cells do various things to keep you alive. In order to do those things, they need a supply of oxygen. Just like your car runs on gasoline or your computer draws electricity, if your cells don’t have oxygen, they don’t work. Essentially, every death, no matter what started the trouble, is caused in the end by insufficient oxygen delivered to the cells.

Without oxygen, eventually your cells die, and then, so do you. However, before that happens, you enter shock.

Mind you that we’re not talking about localized tissue hypoxia. If you tie a tourniquet around your arm, your hand will run out of oxygen and have problems. If a clot blocks an artery in your brain, parts of your noodle will die. These are problems, but they aren’t shock. Shock is a generalized situation; shock happens when hypoxia is widespread and systemic.

Why would such a thing happen? Usually, it happens because there isn’t enough blood flowing to supply oxygen to your organs. Blood is the expressway for oxygen delivery; without enough blood moving at the right speed to all the nooks and crannies of your body, the oxygen won’t get there, and your cells will start to lose their little minds. Blood plays a lot of roles, but this is by far the most important. So although hypoxia is the problem, inadequate perfusion is typically the cause, and we often talk about blood supply as a shorthand for talking about oxygen delivery. There are different types of shock with different underlying causes, but this is the common element that unites them.

Everyone on board so far? If you made it past page 2 of your EMT textbook, you probably knew all of this. But there’s a twist coming, and it’s important. To illustrate it, consider this parable.

You’re shot in the belly, and you bleed out a large portion of your blood onto the ground. We bring you to the hospital, where surgeons repair every inch of damage; you are made as good as new. We replace every drop of blood you’ve lost. At this point, your tissues are repaired, your blood supply is restored, and you’re alive.

But a week later, you die in the ICU.

Why?

The key to understanding shock is this:

Shock is caused by inadequate perfusion, but shock is far more than that.

Say what?

Okay, put another way: no matter what causes the shock, shock leads to more shock.

The shock cascade

When cells become hypoxic, what happens next?

What happens is that they start to do their jobs badly, and this leads to all sorts of systemic problems. When the organs stop working properly, it leads to worsening shock and decreased perfusion, which in turn worsens the original hypoxia, which causes further dysfunction. This process feeds itself.

Dr. Jeff Guy uses this metaphor: suppose you drop a lit match in a dry forest. At this moment, what is the problem? Simple: a burning match. Correcting the problem is equally simple: extinguish it.

But then, the match catches some leaves, and the leaves ignite some dry twigs, and there’s a small fire. What’s the problem? Well, now it’s a little fire going. We can correct it, but we’ll need some blankets or water or well-placed dirt.

What about two minutes from now? The flame has grown, and now it’s a bonfire. We can put it out, but it’ll take some real effort, and it’s going to leave damage.

What about an hour from now? The entire forest is ablaze. The only hope of stopping it will be a massive effort by helicopters and tanker trucks, and even then, most of the trees are probably a lost cause. Maybe we won’t be able to beat a fire that size no matter what we do.

Question: even if we can find that original match in the forest fire, will putting it out extinguish the blaze?

Of course not. The fire has spread.

Shock is a forest fire. The initial hypoperfusion is one thing, and we should try and correct it. But if we don’t, and it starts to cause damage, then that process will start to run away on its own. It will start to cascade, and expand, and feed itself; a new monster is born. Once this has happened, guess what?

We can completely fix the initial hypoperfusion, and still lose the patient.

This happens all the time. Shock occurs, for whatever reason, and we recognize and treat it. But we got there too late. The fire spread. We extinguished the match, but we couldn’t put out the blaze before the damage was too profound to survive. The complications of shock affect nearly every organ system, disrupt nearly every physiological parameter, and undermine the very homeostatic mechanisms that exist to help “fight the fire.” Once this process gets past a certain point, there’s no beating it; the essential fabric of the body is corrupted, and its ability to repair and maintain itself is destroyed. Days or weeks later, despite our best medical care, the patient dies from general, widespread complications. “The operation was successful,” as the surgeons say, “but the patient died.”

That doesn’t mean that we shouldn’t try to fix the initial shock state. That means we should try to fix it immediately. It means it’s a time-critical, every-second-counts priority — because it’s not the kind of thing we can handle at the last minute. If we don’t nip it in the bud, we’ll go down paths that we can’t come back from.

So, the lessons for today:

Shock is characterized by inadequate oxygen delivery to the cells.
This is typically caused by inadequate bloodflow to the tissues.
Once initiated, shock involves numerous pathological processes that range far beyond the initial hypoxic injury. These complications can persist long after the underlying trigger is corrected.

Next time: a deeper look into some of the “unhingings” that characterize the evolution of shock.

Go to Part III or back to Part I

Understanding Shock: Introduction

Ladies and gentlemen, it is time to crack the door to a vast and terrible realm.

It won’t be a short journey, and it won’t be an easy one. But it is our destiny.

What am I talking about? I’m talking about shock, of course.

Prehospital providers don’t understand shock. That’s understandable — because shock is complicated. It’s as complicated as disease processes get.

But we need to understand it. Shock is quite literally in our blood. Since the very birth of EMS, reducing the harm associated with shock states has been one of our main reasons for existing. It kills many, it debilitates many more, it spares no age, race, or gender, and its physical effects are exhaustively widespread. Yet when properly managed, many of those patients can be saved.

We should all be experts. To work in EMS is to be, among other things, a shock technician. This is our wheelhouse.

So, although it will take more than a few posts to walk through the different facets of this Very Big Topic, let’s talk about shock.

Sharpen your pencils, gird your loins, and stand by for further.

Understanding Shock II: What the What?

Understanding Shock III: Pathophysiology

Understanding Shock IV: Bleeding Control

Understanding Shock V: Blood Transfusion

Understanding Shock VI: Fluid Resuscitation

Understanding Shock VII: Negatives of Fluid Resuscitation

Understanding Shock VIII: Prehospital Course of Care

Understanding Shock IX: Assessment and Recognition

Understanding Shock X (supplement): Fluid Choices

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.