Archives for July 2011

Pediatric Infectious Airway Emergencies

Most of us in EMS are pretty good with the typical adult respiratory illnesses — your asthmas, your COPDs, your CHF exacerbations. Maybe the occasional pneumonia. But upper airway illnesses can be harder to keep straight, and two of them are known for occurring especially in pediatrics.



Croup is an infectious disease, usually caused by viral infection of the upper airway. Once upon a time, it was typically caused by diptheria; with the widespread adoption of diptheria vaccination in the US, this has become rare, and the most common cause is now the parainfluenza virus.

Croup is typically seen in children from 6 months to 6 years of age; approximately 15% of all children will contract it at some point.

Its characteristic finding is a coarse, barking, “seal-like” cough. High-pitched stridor is also often present, as is hoarseness of voice, and dyspnea at late stages. All are caused by narrowing of the upper airway due to inflammation from the infection.

This inflammation is normally at the level of the trachea, possibly stretching down into the large bronchi and up into the larynx, but below the level of the glottis.

The onset is usually gradual, lasting from several days to two weeks. Often, there will be fever or coryzal (cold-type) symptoms, such as congestion or headache. A sudden onset is uncommon; usually there will be a day or two of cold symptoms prior to the onset of cough or hoarseness. The upper airway symptoms are often worse at night. (Occasionally, croup may have a spasmodic cause, sometimes triggered by an allergic reaction [akin to asthma]; in these cases coryzal symptoms are rarely present.)

The main differential here should be croup vs. epiglottitis vs. an aspirated foreign body or anaphylaxis. In most cases, these last can be ruled out by a thorough history. As for epiglottitis, it can best be revealed by the severity of symptoms. In almost all cases, croup does not cause significant airway obstruction leading to major dyspnea or hypoxia. A poor general impression (“big sick”), diminished responsiveness, or respiratory failure should point you towards epiglottitis instead. Drooling is not normal. Death is possible but very rare.

Other signs and symptoms are as typical for respiratory difficult in children, including tachypnea, tachycardia, hypotonia (weak or flaccid muscle tone in the exhausted child), chest retractions, and potentially low O2 saturation. In severe cases, as respirations become shallow and weak, stridor and coughing may not be audible.

Treatment is generally supportive. Keep the child comfortable and reassured, if possible with their mother or other caretaker — panic will increase their oxygen demand and may increase stridor. Provide supplemental oxygen as tolerated; blow-by may be most appropriate. Nebulized racemic epinephrine is appropriate field care for significant cases, and most will receive steroids in the hospital. Steam or humidified oxygen is an old standby, and is anecdotally popular, but research suggests it has no benefit.



Epiglottitis is similar in presentation to croup. Its cause is also infectious, but bacterial instead of viral, and historically the microbial agent was almost always hemophilus influenza type B, a bacterium unrelated to the flu except by name. Effective HIB vaccine became widespread in in the late 1980s; as a result, epiglottitis in the US today is actually more common in adults than in vaccinated children. When it does occur in pediatrics, it is typically between the ages of 3 and 7.

Like croup, epiglottitis is a narrowing of the upper airway. However, it occurs higher, above the glottis, and primarily involving the epiglottis and surrounding tissue. Due to inflammation of this flap at the gate of the airway, a sore throat and difficulty swallowing are almost always present. Fever, stridor, and hoarseness of voice are common, as is a muffled speaking voice and tenderness of the larynx, which may present as severe pain provoked by even gentle external palpation. Typically in children there are no other prodromal symptoms such as congestion; adults often do experience coryzal symptoms.

The chief distinction between epiglottitis and croup is the severity. Although far less common, epiglottitis should be considered an acute emergency, and the narrowing of the airway can lead to significant or total obstruction and resultant respiratory failure. The classical late clinical presentation is the young child found in a “sniffing” position, tripodding or sitting upright, with audible stridor (or quiet respirations as failure approaches), drooling and close to exhaustion. (Drooling results from the inability to easily swallow.) Symptoms can be insidious in onset, but usually progress very rapidly. Mortality in adults with epiglottitis is around 7%, although less than 1% in children.

Treatment may involve supplemental oxygen, but maintaining a patent airway should be your main concern. Intubation may be necessary, sometimes suddenly, so prepare for a difficult airway even if the situation seems relatively controlled. Cricothyrotomy is appropriate as a last resort. Direct manipulation can provoke further inflammation, so the use of basic airways (OPA/NPA) is unhelpful and unwise. Although laryngoscopy can help confirm the diagnosis of epiglottitis (the epiglottis and arytenoids will be cherry red and swollen), it can also provoke spasm and further inflammation, so it is discouraged in the field unless immediate and unhesitating intubation is intended.

Albuterol is not indicated, and epinephrine has no benefit. In-hospital care includes antibiotics to clear the infection, and possibly the use of steroids to manage swelling.

Acceptable Risk

Following up on our previous post where we discussed patient refusals, it behooves us to say a few things about risk.

The culture of “everyone goes to the ED” is not writ in stone, and in some places, efforts are underway to expand it into a more sophisticated system. For instance, some patients might be transported directly to detox programs, homeless shelters, urgent care facilities, or psych treatment. Some, of course, don’t need to be transported at all, and can stay home, perhaps with instructions to follow up with their PCP. A few areas are experimenting with, or at least moving towards, the concept of an “Advanced Practice Paramedic” or “Advanced Paramedic Practitioner” who could sensibly and intelligently perform this assessment and triage, determining whether patients need immediate definitive care, or (in essence) “clearing” them of acute high-risk pathologies. Ideas like this may prove central to solving the many problems of healthcare in general and EMS in particular, such as ED overcrowding and the inefficient use of available resources.

However, just like the issue of patient refusals, to even discuss the possibility of such a system requires a fundamental shift in our thinking. At the moment, the approach is, “Try to recognize and treat Sick People — but if you don’t, that’s okay, because they’ll recognize them at the hospital.” Obviously, this practice is based firmly on the presumption that most or all of our patients do end up being evaluated in a full-fledged emergency department. Even the very notion that a patient can refuse to be transported ends up as a grudging allowance — we reluctantly acknowledge that we can’t actually kidnap people, but we still make them jump through hoops to make it entirely clear that we wanted them to go all along.

What if we started to accept that some of these patients don’t need an emergency room? Realistically, and retrospectively, it’s obvious that many of them don’t. Other destinations are more appropriate, and in some cases, no transport at all is necessary. But in order to make decisions like that, we need to be able to accept the assessment, clinical decision-making, and risk stratification of our field providers.

It goes without saying that instituting such a practice would require additional training, and providers (such as this mythical APP) practicing at a higher level than our current EMTs and medics. But it’s bigger than that. We have to be willing to let go of the safety net of everyone filtering through the ED. We have to be willing to accept the field workup as final — or at least, good enough that no further evaluation is immediately needed.

Closely wedded with the prehospital culture that treats patient refusals as bogeymen is the in-hospital culture that says every patient needs a comprehensive workup to rule out every possible killer. It doesn’t matter if the odds are 1,000,000 to 1 that the problem is benign rather than a massive MI or hidden PE; that 1/1,000,000 chance of missing the Badness is still unacceptable, so the patient gets the works.

We have the mindset that any miss is one miss too many.

This costs a lot of money. It puts patients through a lot of hell. But most of all, if we’re going to imagine a world where not every patient ends up even going to the emergency department, we have to accept a world where the ones who don’t will not receive that exhaustive workup.

Certainly, this triage process be handled sensibly, and conservatively, because we’re here to help people, not let them die at reasonable rates. So where do we draw the line? Is one miss in a thousand acceptable? One in a million? One in a billion?

We can draw the line wherever we want, but no matter where, there’s going to be a qualitative difference between a reasonable risk and “we did everything.” Because eventually, we’re going to miss one. A well-trained and conscientious clinician is going to assess a patient in their home, and appropriately conclude that their complaint is not dangerous, and that patient is going to die.

Because it happens — because flukes are inevitable. If we throw the kitchen sink at them, and we still lose, then at least we can hold ourselves blameless. But if we take a more reasonable approach, then we have to accept in advance that occasionally, the chips will fall against us. And that has to be okay.

The prevailing belief today is that anytime something goes wrong, something was done wrong. Adverse outcomes are an indicator of error, either an individual error or a flaw in policy or protocol. If I follow our procedures to the letter, and a patient slips through the cracks, it means we need to change the procedure.

Can we get to the point where we understand that if a situation is correctly evaluated, and the risks are correctly balanced, and we simply happen to get unlucky, that the decision was still right? Where we can stop spending ever-increasing amounts of time and money in the pursuit of ever-more-infinitesimal risk?

I don’t know. But if we can’t, then we’re never going to be able to solve some of these problems. Because perfection doesn’t exist, and chasing it is a good way to get very tired.

But it’s Just a Broken Nail!

One of the most common topics of debate in this business is something that should be simple. When is it okay for a patient to refuse transport to the hospital?

On the face of it this is a strange dilemma. When is it “okay”? What does that even mean? When is it okay to have Milano cookies and a bottle of Scotch for dinner? I don’t know. Leave me alone.

The chain of reasoning goes something like this. People call 911 because they have problems, and they don’t know how bad those problems are. By and large, we — the EMTs and paramedics on the ambulance — don’t know either. We don’t have the training or the tools to truly rule out major problems. So the only safe thing is to take the patient to the hospital. There, tall men with white coats, eight years of medical training, large expensive machines, and extensive liability insurance can decide if the patient is dying or not.

Okay. In some ways, that makes sense.

In other ways, it’s absurd. We all experience symptoms or incur injuries from time to time, and for the most part, we do not feel the need to visit the hospital to rule out deadly causes. Although it’s always a remote possibility that something is horribly wrong, in most cases it’s extremely unlikely, and it’s senseless to make an emergency out of every ache or sniffle. As we recently discussed, although it is possible to be very sick without looking like it, it is uncommon. If I woke up today with a minor headache, I wouldn’t want to spend hours of my time and hundreds of dollars at the emergency room “just in case.” So why does that suddenly become a reasonable course of action just because an EMS crew is standing in front of me?

There’s one good answer to this, which is that normally, I wouldn’t call 911 for a headache. So if there’s an ambulance here, it already means that for some reason, I had some special concern about this episode. Perhaps it was unusually bad, or prolonged, or I have medical history which makes me worried about what a headache might entail. Alternately, perhaps a friend or family member called on my behalf, but even then, presumably it’s because they had some reason to be worried.

This is all true. People who call for an ambulance are self-selected to be a higher-risk group than the general population. The headache patient who does dial 911 is more likely to be sick than the headache patient who doesn’t.

However, this isn’t always the case, and even when it is, it isn’t always significant. Some patients, or friends and family of patients, have a very low threshold for concern. Sometimes people misinterpret warning signs. Sometimes things just happen. Consider the hundreds of calls we take each year for minor MVCs. Someone dents their fender in traffic, a concerned passerby calls 911, and we show up to evaluate the occupants. There are no noteworthy injuries, and it wasn’t even the people involved who called for us. Is there a chance they have head bleeds, spinal fractures, pulmonary contusions? There’s always a chance. But do they need to go to the hospital? Or, put another way: they didn’t plan on going to the hospital before we arrived. We performed our medical assessment and found nothing alarming. Does the simple fact that we’re here mean there’s any better reason for them to go to the hospital than before we arrived?

Obviously, the answer is no. But we still tend to default to transporting them.

A cynic might suggest that this is because in most areas, ambulance providers can only bill for transports, not for refusals. In fairness, I don’t think this is usually the main reason.

A bigger reason is liability. There is a real concern on the part of providers, and on the part of the services employing us, that anytime we fail to transport a patient to definitive care, we might be “missing” something bad. As a result, they might later sue us for missing this. Would they have a case? Maybe, maybe not; it would depend on whether we followed the standard of care, and whether we implied to them that we “knew” they were okay with any greater certainty than we truly had. That’s the underlying issue, after all. It’s up to the patient whether they want to go, but we are medical professionals, with impressive uniforms and stethoscopes around our necks, and patients are therefore inclined to think that we know things they don’t. They’re inclined to do what we recommend. But even if we think they’re okay, we don’t know they’re okay, so our “recommendation” is usually to see the doctor, because that’s the only truly “safe” choice from our point of view.

Fair enough. But there’s a small problem with this. We’re lying.

Or at least deceiving. We are trained to assess patients, look for abnormalities, and identify findings that point to the possibility of injury or pathology. If we perform this task, and find nothing alarming or even suspicious, we are going to be thinking, “they’re probably okay. I’m not worried.” Why, then, do we turn to the patient and say, “You should really go to the hospital. I’m worried.”? One major national ambulance company has a policy that you should never ask, “Do you want to go to the hospital?” as it implies a choice — but instead, “Which hospital do you want to go to?” Railroading at its finest.

Certainly, it would be just as misleading to tell a patient, “You’re definitely okay.” We don’t know that, because as we already agreed, we lack the training and resources to diagnose anything for sure. But we do have enough tools to make medical decisions, which we do all the time — what’s the best transport destination? which medication is indicated? — and here, too, we can make an analysis of the risk factors. It’s not the same analysis that would be made by a team of doctors with a hospital at their backs, but as long as we don’t pretend that it is, that shouldn’t be a problem.

Think of it this way. If you were in the patient’s situation, would you want to go to the hospital?

Bear in mind that this isn’t a small thing. Depending on your circumstances, this may involve missing work (even losing a job), arrangements needing to be made for babysitting, housesitting, or pet care, cars retrieved, plans cancelled, and oh yes — a bill ranging from a few dollars to many thousands. Can’t pay that? Now your credit is on the line. You can also look forward to hours of sitting on a series of stretchers, wheelchairs, and beds, while busy people wearing scrubs stick sharp things into your flesh, capture your bodily excreta in plastic cups, and ask you an endless series of the same questions over and over and over. You will miss sleep, get behind on projects or errands, and in the end you will have to find a way to get yourself home and clean up from all this chaos. Possibly with a new infection that you picked up in the waiting room.

If we are responsible, we should view transportation to the hospital as a medical intervention in the same category as medications, invasive procedures, and diagnostic tests. It has certain indications and benefits, but also certain risks and harms associated with it, and we should consider both sides in balance before making a recommendation on the best choice. Certainly, that decision will have to be made by the patient, not by us, because it’s the patient who is undergoing these risks and benefits, so it’s they who get to decide how to weigh them. But they also don’t have the medical understanding of the situation that we do. So that’s our job: to transmit to them what we’ve found in our assessment of their complaint. The risk factors, the positive or negative findings on their physical, any alarming vital signs, and the salient features of their history. In many cases, this process is why they called us — because although they’re experiencing something abnormal, they don’t know if they should be worried or not. We won’t have all the answers, but we can give them more information than they had before, and they can use that information to better inform their decision on whether to seek further care. (Remember, this might include scheduling an appointment with their PCP, visiting an urgent care clinic, getting a ride to the ED or driving themselves, and of course the old “wait-and-see” approach. Even when more care is needed, the ambulance isn’t the only answer.)

For the reasons of liability, and policy, and the general fear-mongering attitude that has swept over the healthcare industry in recent years, this is a very difficult line to walk, and in many cases to preserve your job and license you may need to err on the side of “encouraging” a patient to be transported. However, I find it ethically troubling when we mindlessly push everyone towards the ED, no matter what common sense or their medical situation tell us. When we visit someone with a complaint that we’d ignore in ourselves, our partner, or our mother, and convince them to climb into the ambulance anyway, whose best interest are we looking out for?

Are we hurting the patient to help ourselves?

Are we okay with that?

The Art of the Transfer (part 3)

Continued from part 2

There’s another benefit of patient transfers beyond the merely educational. You get to meet the people.

Oh, you meet people on emergencies. Depending on the nature. Dead people don’t talk much. (You get a look at their houses, maybe.) And really sick people, well, you’re pretty focused on the medical stuff then. Patch this, pump that, push the magic potion. When did it start? Have you felt this way before? What Russ Reina calls the business of being a “flesh mechanic.”

But on a routine transfer, and to a lesser extent on the non-emergent “emergencies” (when you have little to do and no hurry to do it), you get to actually chat with the human being upon your stretcher. Imagine that! They don’t just have a name and date of birth — they have a trade, a family, a history, a life.

Everyone has a story. Some of them are more interesting than others on the surface, such as the retired spy or the film star, but everyone has a story, and they’re all worth hearing, if you care.

Most of these people are old. If you’re not old, you may think this means they have less to say to you, but really, it’s the opposite. You’re 25 and they’re 90; all of the problems you’ve got, all the changes in the world you think are new, every dilemma you’ve ever faced, they’ve seen it and heard it and done it. They’ve been alive for several of you. Do you think people live that long without knowing their way around?

I once heard it suggested that you don’t really grow any wiser as you age, because although you learn from your mistakes, there are still an infinite number of future mistakes to be made. You never “run out” of new errors.

Perhaps that’s true. But even if the 90-year-old benefits little from his wisdom, that doesn’t mean you can’t borrow some of it. And even if his experiences or decisions differ from yours, they were just as important to him as yours are to you, and you can bet the stories are worth hearing.

Where else can you meet such a range of people? And not just meet, but find yourself forced into spending one-on-one time with them? If you’re a misanthrope, this is not a good career for you. Multiple times a day you’ll be placed in a small box with a stranger for a period lasting minutes to hours. It’s like speed dating.

But if you like people — enjoy meeting them, appreciate their company, take pleasure in their lives — then there’s no better job to have.

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.


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.



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)


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

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