Archives for December 2011

Understanding Shock IV: Bleeding Control

December 30, 2011 by 2 Comments

 

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:

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

Go to Part V or back to Part III

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Understanding Shock III: Pathophysiology

December 27, 2011 by Leave a Comment

An example of the shock cascade

Another model

Yet another model

 

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:

  1. The processes of shock are multiple and self-reinforcing.
  2. Inflammation plays a major role.
  3. 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

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Understanding Shock II: What the What?

December 22, 2011 by 1 Comment

. . . 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:

  1. Shock is characterized by inadequate oxygen delivery to the cells.
  2. This is typically caused by inadequate bloodflow to the tissues.
  3. 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

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Understanding Shock: Introduction

December 14, 2011 by 7 Comments

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

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Unique, Just Like Everyone Else

December 5, 2011 by 1 Comment

A few years back, a video of a lecture by Carnegie Mellon professor Randy Pausch made the YouTube rounds, becoming enormously popular; you’ve probably seen it. He later wrote a book discussing and unpacking many of the points he brought up in the lecture. If you haven’t watched or read them, I highly recommend both.

In any case, in the book Pausch describes the birth of his first child, how a complicated birth (a placental abruption) forced him to rush his wife to the Magee-Womens Hospital at the University of Pittsburgh Medical Center, and how his newborn child was brought into their neonatal ICU. He writes,

At Magee, they did a wonderful job of simultaneously communicating two dissonant things. In so many words, they told parents that 1) Your child is special and we understand that his medical needs are unique, and 2) Don’t worry, we’ve had a million babies like yours come through here. (91–92)

This is an elegant account of the demeanor we should all be trying to strike with the families of patients, and indeed with our patients themselves.

Many beginning providers, understandably unsure, will approach each patient like an antique porcelain vase: precious, delicate, and prone to breakage. This is the right attitude as far as priorities — we should take our care seriously — but that doubt is communicated in our body language and tone, and it’s not what sick and scared people want to hear. Imagine being the patient whose doctor says, “Man, look at that! I’ve never seen anything like that! Can we publish you?” or “Okay, I’m not going to lie, I’ve never done this in my life. But I did stay at a Holiday Inn Express last night…”

On the other hand, it can be very few moons indeed until you’re a “veteran” in the worst sense of the word, dragging your technically skilled but burned-out husk from patient to patient, seeing nothing but a stack of paperwork and a routine litany of tests and treatments. Her? Oh, just another abominal pain. Yawn. Her name? Search me. Is it lunchtime yet?

See, people want to be treated like people, and people are unique, precious (at least in their own eyes), scared, and need to be engaged with on the same human level as when you say “thank you” to your barista or read a bedtime story to your son. But people are also machines, and the trick to fixing broken machines is to fix a lot of them, and treat them all the same. We need to be able to reconcile these paired, antagonistic traits, because otherwise we can’t do what they called us to do. It’s not a matter of nailing one goal but missing the other: you miss both. You can’t reassure anyone if you don’t competently address their actual problem, and you can’t practice sound medicine if you don’t engage with patients as people.

That’s the trick that the obstetrics and neonatal teams at Magee pulled off, and it’s all the more important for us, who have to approach patients without the comforting backdrop (that is, comforting to them and to us) of a bright beeping hospital. It’s the trick of quiet confidence, of demonstrating without words that you know exactly what you’re doing, that you bring tremendous skill and experience to the table — but that those tools are being brought to bear for your patient, for the scared individual you’re kneeling beside. The “all the kings horses” response by fire and EMS, the loud and alarming transport to the hospital, the wires and tubes and countless gloved hands — it’s overwhelming and frightening if you’re thrown into it as an unknown environment, but if you understand that it’s all being done for you, then it’s comforting. It’s like calling for help and getting the Wolf. That’s exactly what you wanted in your time of need.

You may not want to date a cocky lawyer. But he’s the one you’d want at trial.

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