Posts Tagged ‘asthma’

Asthma rates in children may finally be abating . . . somewhat

July 19, 2016  |  General  |  2 Comments

Asthma is by far the most common chronic lung problem in children, affecting nearly 10% of all children. It may even be the most common chronic health problem of any sort if you exclude obesity. What is it?

Here is a schematic drawing of what a normal lung looks like:

You can think of the lungs as being composed of two parts. The first is a system of conducting tubes that begin at the nose and mouth, move through the trachea (windpipe), split into ever smaller tubes, called bronchi, and end with tiny tubes called bronchioles. The job of this system is to get the air to the business portion of the lungs, which are the alveolar sacs. This second part of the lung brings the air right next to tiny blood vessels, or lung capillaries. Entering capillary blood is depleted in oxygen and loaded with carbon dioxide, one of the waste products of the body’s metabolism. What happens next is gas exchange: as the blood moves through the capillaries, oxygen from the air we breathe in goes into the blood, and carbon dioxide leaves the blood and goes into the air we breathe out. The newly recharged blood then leaves the lungs in an ever enlarging system of pulmonary veins and then goes out to the body.

The main problem in asthma is that the conducting airway system gets blocked in several ways, so the oxygen can’t get in and the carbon dioxide can’t leave. Although both are a problem in a severe asthma attack, getting the air out is usually a bigger issue than getting it in because it is easier for us to generate more force sucking in air than blowing it out. So the hallmark of asthma is not getting the air out — called air trapping. Why does this happen? There are two principal reasons: for one, the small airways, the bronchioles, constrict, get smaller; for another, the walls of the airways swell and the airways themselves fill with excess mucous, blocking air flow. Here’s another schematic drawing of what that looks like.

Thus during an asthma attack these things happen, all of which act together to narrow the airways and reduce air flow:

  1. The smooth muscle bands around the tiny airways tighten
  2. The linings of the airways get inflamed and swell
  3. The mucous glands in the airways release too much mucous, filling the airways

The medicines that we use to treat asthma work by reducing (or even preventing) one or more of these things.

Between 1980 and 1995 the prevalence of asthma in children doubled. Then from 1995 to 2010 the number continued to increase, but more slowly. Where are we now? A recent report in Pediatrics, the journal of the American Academy of Pediatrics, gives some answers. The authors looked at the time period from 2000-2013. They separated patients by gender, race, geographical location, and socioeconomic group.

The investigators found that across all groups asthma prevalence steadily increased from 2000-2009, although the rate of rise had slackened compared with the previous 2 decades. The year 2009 was the peak. After that there was a plateau, and since then the rates have actually fallen a bit for the total group. Among poor children, however, asthma rates have continued to rise steadily. This is concerning. The reasons for these changes in asthma prevalence are complex and experts think it is most likely an interplay of several things. If you are interested you can find more information in the article linked above. But it does appear that, on balance, the “asthma epidemic” is abating.

The Benefits of Standardized Asthma Care

December 20, 2015  |  General  |  No Comments

 

 

Asthma is a common childhood condition. Some estimates are that around 10% of all children have it. The incidence has been steadily increasing for many years, but some recent data suggest the burden of the disease in children may have leveled off over the past couple of years. That’s encouraging, but the number of children with asthma is still huge. The best way to think of asthma is that of an exaggerated reaction of the small airways in the lungs to common irritants, making them constrict and reduce airflow. These include viral infections, environmental triggers, and poorly understood things intrinsic to the individual. There is a strong familial tendency to developing asthma. Additionally, some things predispose to it, including sedentary lifestyle and obesity.

A big push in pediatric practice over the past decade or so has been to try to keep kids with asthma out of the hospital. This can be accomplished by a good asthma care plan for the family to use when a child’s symptoms get worse. Another key component is a team approach to managing this chronic disease. Asthma is the most common preventable reason for a child to be admitted to the hospital. A recent report from the American Academy of Pediatrics shows how effective these care plans can be.

The investigators looked at 3,510 children with asthma treated over the years at Primary Children’s Hospital in Utah. The notion was to see if increased compliance with asthma control measures by the family would reduce the number of hospital admissions. That turned out to be the case, significantly so. Interestingly, one of the biggest problems for the research project was to get physicians to accept and go along with the best current evidence-based information about how to manage asthma. I’m actually not surprised by this. Asthma management has changed over the years and current best practice is not what I was taught years ago. Things change, but many physicians don’t.

The key for any parent who has a child with asthma is to have a clear understanding of exactly what to do if your child has worse breathing problems. Many visits to the hospital could be headed off if all parents had such a plan, as well as a resource person to call if the plan is not working.

 

 

http://www.aappublications.org/news/2015/11/12/Asthma111215

How placebo and nocebo effects work

July 18, 2015  |  General  |  No Comments

All physicians are familiar with what is called the placebo effect: the improvement in a patient’s symptoms after receiving a treatment that has no known effect on the particular disease. I was taught that statement could be further refined to state: improvement in a patient’s symptoms after receiving a treatment that has no known biological effect on the particular disease. The standard example is a “sugar pill.” That’s an important distinction, but it’s also clearly wrong; improvement in symptoms is obviously a biological effect, no matter the mechanism. The placebo effect is evidence of the complex interactions between mind and body because symptoms, by definition, are things perceived by the brain and cannot be specifically measured. Placebo effects are perception. They do not, for example, shrink tumors, cure asthma, or control diabetes.

The placebo effect is a key reason why, as much as possible (sometimes it isn’t), we study patient response to new treatments using a placebo arm in randomized, controlled trials. These are studies in which a patient is randomly chosen to receive either the new drug or something presumed biologically to have no effect on the particular disease. Neither the patient nor the investigator knows which one the patient is getting until after the trial is over. (Some trials compare a new treatment with an existing one — that’s a different topic.) The placebo effect is when a patient receiving the inert substance, the sugar pill, experiences an improvement. How big is the effect? Sometimes it can be as high as 30% of patients. This is why a placebo group is so important for studying disorders in which subjective symptoms are the essence of the disease, such as migraine headaches. There is no objective test one can do to assess improvement; it is all patient-reported.

How does the placebo effect work? There is a wonderful and highly understandable discussion of this in a recent edition of The New England Journal of Medicine. The article is only a couple of pages long and well worth a read. There is also a good podcast accompanying the piece. The bottom line is that clearly the placebo is not really an inert substance in the sense of doing nothing. It is doing something to the patient’s perception of symptoms, often by using known pathways of neurotransmitters in the brain. From the article:

Moreover, recent clinical research into placebo effects has provided compelling evidence that these effects are genuine biopsychosocial phenomena that represent more than simply spontaneous remission, normal symptom fluctuations, and regression to the mean.

The authors describe a fascinating example of how the placebo effect can play a role in a complex disorder like asthma. In asthma we can measure air flow as the patient breathes; that is, we can get an objective measure of how severe a patient’s problem is. The patient typically feels short of breath, and the degree of reduction of airflow correlates with that symptom. But feeling short of breath is a subjective thing. It comes from the brain. I have seen both patients in severe subjective distress with only modest reduction in airflow and patients surprisingly comfortable with very decreased objective numbers. There is a significant subjective component to asthma. This has been demonstrated by giving an placebo breathing treatment to an asthmatic and then showing that, as expected, there is no improvement in airflow. Yet the patient may experience an impressive improvement in perceived breathing symptoms.

There is also another side to the coin, what is called the nocebo effect.

 . . . the psychosocial factors that promote therapeutic placebo effects also have the potential to cause adverse consequences, known as nocebo effects. Not infrequently, patients perceive side effects of medications that are actually caused by anticipation of negative effects or heightened attentiveness to normal background discomforts of daily life in the context of a new therapeutic regimen.

Here is an example. Patients in randomized controlled trials do not know if they are receiving the placebo or not. But just in case they are receiving the real drug they are informed of possible side effects. Interestingly, 4 – 26% of patients in the placebo groups in such trials stop their participation because of these perceived adverse effects. This is the nocebo effect.

One of the most fascinating aspects of this is that there appear to be genetic predispositions among people for experiencing a placebo effect. This is an area of active research. The authors’ conclusion is a good one, I think:

Of course, placebo effects are modest as compared with the impressive results achieved by lifesaving surgery and powerful, well-targeted medications. Yet we believe such effects are at the core of what makes medicine a healing profession.

The placebo effect has always been a part of medicine. Patient’s perceptions of their physician’s compassion have long been known to be important. Really, until quite recently in medicine the placebo effect was all physicians had to offer. And it’s not a bad thing. I think it explains the modest improvements reported by some patients receiving a wide variety of what we call these days alternative therapies, such as homeopathy.

Anyway, the essay is a good review of this fascinating subject, and I recommend it to you.

Has Obamacare made it easier or harder to get a doctor’s appointment?

April 23, 2015  |  General  |  No Comments

One of the goals of the Affordable Care Act (aka Obamacare) was to increase access to primary care physicians. The notion is that if people have insurance it would be easier for them to get appointments with primary care physicians. This is because many physicians are unwilling to accept new patients who are uninsured. Further, a key component of the ACA was to increase physician reimbursement for Medicaid because this program was a major mechanism for expanding insurance coverage. Medicaid reimbursement has always been low — significantly lower than Medicare pays for the same encounter — so many physicians would not take it. The ACA drafters hoped higher reimbursement would entice these physicians to accept Medicaid. We don’t know if any of these assumptions are correct, but a recent study published in The New England Journal of Medicine suggests a positive impact.

The authors’ method was a bit sneaky, I suppose. They had trained field staff call physicians’ offices posing as potential patients asking for new appointments. They were divided into two groups; one group said they had private insurance, the other said they had Medicaid. The authors compared two time periods — before and after the early implementation of the ACA. A sample of states were compared to see if the rates of acceptance of new Medicaid patients was associated with a particular state increasing physician Medicaid reimbursement.

The results were not striking, but they suggest a significant positive trend. This is what the results showed, in the authors’ words:

The availability of primary care appointments in the Medicaid group increased by 7.7 percentage points, from 58.7% to 66.4%, between the two time periods. The states with the largest increases in availability tended to be those with the largest increases in reimbursements, with an estimated increase of 1.25 percentage points in availability per 10% increase in Medicaid reimbursements (P=0.03). No such association was observed in the private-insurance group.

Again, these are data from the early days of ACA implementation. But they are encouraging. One of the most important components of slowing the seemingly inexorable rise in healthcare costs is getting people good primary and preventative care. This keeps people with a chronic, manageable condition out of the emergency room and, one hopes, out of the hospital. This is particularly the case with common conditions like diabetes and asthma. For both of those disorders regular care by a primary care physician can spare patients much suffering and save many thousands of dollars.

I hope this kind of research continues as the ACA matures. It’s a good way to see if the overall goals are being met. Of course it raises a new challenge: making sure we have enough primary care physicians. Right now we don’t.

Pediatric Newsletter #15: Food Allergies, Gluten, and Pizza

March 29, 2015  |  General  |  No Comments

Welcome to the latest edition of my newsletter for parents about pediatric topics. In it I highlight and comment on new research, news stories, or anything else about children’s health I think will interest parents. In this particular issue I tell you about a couple of new findings about allergies in children, as well as some new information about gluten sensitivity. I have over 30 years of experience practicing pediatrics, pediatric critical care (intensive care), and pediatric emergency room care. So sometimes I’ll use examples from that experience to make a point I think is worth talking about. If you would like to subscribe, there is a sign-up form on the home page.

Big News About Peanut Allergies

This one made a big splash both in the medical news sites and in the general media. Peanut allergy is common. It has doubled in the past decade, now affecting between 1 and 3% of all children. And it can be a big deal for children who have it, even life-threatening. For years we recommended that children not be given peanut products early in life, especially if they are at risk (based on their other medical issues) for developing allergy. Unfortunately, avoiding peanuts in the first year of life doesn’t make a child less likely to develop the allergy. So what, if anything, can?

This recent, very well done study published in the prestigious New England Journal of Medicine is really ground-breaking. It took 4 to 11-month-old children at high risk for developing peanut allergy and divided them into 2 groups. One group got the “standard” approach — being told to avoid peanut exposure. The other group was fed peanuts 3 times per week. It was done in the form of either a peanut snack or peanut butter.

At age 5 years (the long follow-up time is a particularly strong feature of the study) the children who had been fed the peanuts had nearly a 90% reduction in the development of peanut allergy. This is a huge difference.

The study also was able to provide a scientific explanation for the difference. The children fed the peanuts developed protective antibodies that cancel out the ones that provoke the allergic response.

Washing Dishes by Hand May Reduce the Risk of Food Allergies

This report comes from Pediatrics, the journal of the American Academy of Pediatrics. There has been a long-standing theory about how allergies develop in children called the “hygiene hypothesis.”

The notion is that children, particularly in Western countries, are more prone to allergies (and asthma) because their exposure to microbes is delayed by our more sanitized environment.

In this study from Sweden, children in households that washed dishes by hand rather than using a dishwasher experienced a lower risk of subsequent allergies. The authors speculated that there was a causal association. They couldn’t prove that, but they also noted that early exposure to fermented foods and if the family bought food directly from farms also correlated with less allergies. I’m not totally convinced, but it is an interesting study worth thinking about. I expect to see more on the topic.

Does the Age at Which You Introduce Gluten Into Your Child’s Diet Affect Future Risk of Gluten Sensitivity?

Gluten sensitivity is in the news, with signs everywhere advertising “gluten free” as if this is always a good thing. I hear a lot of misconceptions about gluten sensitivity. Gluten is a protein found in grains such as wheat and barley. There is a condition, called celiac disease or sprue, in which a person can develop moderate or severe intestinal symptoms triggered by gluten. It is one of the eighty or so autoimmune diseases. The incidence of celiac disease in the US is about 0.7%. The risk of developing celiac disease is closely linked to a genetic predisposition to getting it. Importantly, if you don’t have the disorder, there is no benefit to eliminating gluten from your diet. In fact, the great majority of people who think they have sensitivity to gluten . . . don’t.

But for those children who do have a higher risk for developing celiac disease because of their genetic makeup it has long been a question if delaying gluten exposure will affect their chances of actually getting the disease. A good recent study gives an answer to that question, and the answer is no. There is no correlation.

If you think your child (or you) have problems with gluten there is a useful blood test that looks for a specific antibody. However, many people who have the antibody never get symptoms of celiac disease. The ultimate test is an intestinal biopsy.

My take-away conclusion is that all this gluten-free stuff you see in, for example, restaurants, is just the latest dietary fad. For over 99% of us there is no health benefit to avoiding gluten.

So How Much Pizza Do Teenagers Eat?

This is kind of a quirky item. If nothing else, it demonstrates how weird the medical literature can be sometimes. Every parent knows kids, teenagers in particular, mostly love pizza. A recent article in Pediatrics, a fairly respected journal, used food surveys to find how much pizza kids eat and the percentage of their daily calories they get on average from pizza.

The answer? The authors claim that in 2010 21% of kids ages 12-19 reported eating pizza sometime in the past 24 hours. That number is actually down from a similar survey in 2003. What about calories? For those kids who reported eating pizza, it accounted for about 25% of their daily calories, and that hasn’t changed. The authors primly suggest that we should make pizza more nutritious. I wish them luck with that. And I’m 63 years old and still like pizza.

New recommendations for the treatment of bronchiolitis: we should do less because it doesn’t help

December 2, 2014  |  General  |  No Comments

Every fall I write about bronchiolitis because it is one of the most common respiratory ailments affecting infants and children under about two years of age. It is the most common reason infants end up in the hospital during the winter and early spring months. Every year we get severe cases in the PICU. Pediatricians have struggled for decades to figure out how to treat bronchiolitis but we don’t have any specific therapies that work very well. (We have some promising treatments on the horizon, though, as I wrote about here.) Recognizing this, the American Academy of Pediatrics has significantly revised its recommendations of what we should and should not do for children with bronchiolitis. Before I describe these new recommendations, however, I should review what bronchiolitis is and why it can make small children, particularly infants, so sick.

Bronchiolitis is caused by a viral infection of the small airways, the bronchioles. By far the most common virus to do this is one we call respiratory syncytial virus, or RSV. To scientists, RSV is a fascinating virus with several unique properties. One of these is its behavior in the population. When it’s present, RSV is everywhere. Then it suddenly vanishes. There are exceptions to everything in medicine — I have seen sporadic cases during the off-months — but generally RSV arrives with a bang in mid-winter and then leaves suddenly in the spring. It’s the only virus that consistently and reliably causes an epidemic every year, although it often alternates more severe with milder visitations. RSV epidemics often have some regional variability. For example, often one city will have a much more severe epidemic than do others in other regions of the country.

Another aspect of RSV that interests medical scientists is how poor a job our immune systems do in fighting it off. Virtually all children are infected with RSV during the first few years of life. Not only that, all of us are reinfected multiple times during our lives. Attempts at devising a vaccine for RSV have all been unsuccessful. In fact, early versions of an experimental vaccine seemed to make the disease worse in some infants, raising the possibility that some aspect of our immune response to the virus actually contributes to the symptoms.

RSV has a high attack rate — the term scientists use for the chances that a susceptible person will get the infection if exposed to it. That, plus our generally poor defenses against it, explain the frequent epidemics. Every year a new crop of susceptible infants enters the population.

So what is bronchiolitis? What does it look like? In medical terminology, adding the ending “itis” to a word means that whatever comes before is inflamed. Thus tonsillitis is an inflammation of the tonsils and appendicitis means an inflamed appendix. So bronchiolitis is an inflammation of the bronchioles, the final part of the system of air-conducting tubes that connect the lungs with the outside world. Beyond the bronchioles are the aveoli, the grape-like clusters of air sacs where the business of the lungs — getting oxygen into our bodies and carbon dioxide out — takes place.

Bronchiolitis is a disorder of blocked small airways. This prevents air from getting in and out normally, primarily out.  The principal source of the blockage is that the bronchiole tubes are blocked from swelling of the walls and from debris caused by the RSV infection — bits of broken airway cells and mucous plugs. This picture shows what it looks like:

Infants are the ones who have the most trouble breathing with bronchiolitis. There are several reasons for this, but a key one is the construction of an infant’s chest. When small airways get blocked, we use our chest muscles — tightening them — to force air in and out of our lungs. We are helped in doing this by the fact that our lungs are encased in a fairly rigid rib cage; when we use our muscles to squeeze or expand our chest the system works like a bellows. Infants can’t do this well because the ribs across the entire front half of their chest are not yet solid bone — they are still soft cartilage.  So when a small infant tries to move air against anything that is restricting airflow, like clogged bronchioles, his chest tends to sink inwards, causing what we call retractions. These are easiest to see just below the last ribs. They especially have trouble forcing air out, so their chests become hyperexpanded with air, making it look as if their chests are puffed out a little. The other reason infants have so much trouble handling debris in their bronchioles is that these tubes are already much smaller to start with, so they get more easily clogged up than do the larger airways of older children.

How does a child with bronchiolitis look? Typically they are breathing faster than the normal respiratory rate of 25-35; often they are puffing along at 60-70 breaths per minute. They also will show those chest retractions and have a cough. Fever is uncommon. They may look a bit dusky from not having enough oxygen in the blood. They often have trouble feeding because they are breathing so fast. The fast breathing, along with the poor feeding, often makes them become dehydrated. Our breath is completely humidified, so when we breathe fast we lose more water.

What can we do to treat bronchiolitis? You read above that we have no specific medicine that will kill the virus. What we have to offer is what we call supportive care: treating the symptoms until the infection clears. Some of that supportive care has been based on how we treat asthma, another condition where air has trouble getting into and out of the lungs. Some years ago we learned that these asthma treatments, such as albuterol breathing treatments and steroids, helped very few children. Even though we knew that fact, a common thing was to try the asthma drugs and see if they helped an individual child, then continue them if it appeared they did.

The new recommendations come down strongly on the side of not even trying these asthma drugs because compelling research argues against it. More than that, the new recommendations say not to take a chest x-ray because it doesn’t help the child and may cause more risk; taking a chest x-ray often leads to physicians over-diagnosing pneumonia and giving antibiotics when they aren’t called for. The new recommendations even suggest we stop testing for the RSV virus, which has been commonly done, because it doesn’t affect anything we do. One thing the recommendations continue from the past is providing good hydration, as well as oxygen if the child needs it — some do, but many do not.

One important point to make, especially for me as a pediatric intensivist, is that these recommendations only apply to children with milder disease. Some children with bronchiolitis become extremely ill and require help with their breathing, either with soft plastic prongs in their nose that deliver oxygen and air pressure or with a mechanical breathing machine. For those children we do what it takes to keep their blood oxygen levels in the safe range.

Old ways die hard, and it will be interesting to see if physicians follow these new recommendations. My guess is that, over time, we will. More and more we are learning that therapies that add risk and cost, without adding any benefit, are not the way to go.

Finally, an effective treatment for respiratory syncytial virus (RSV)?

September 22, 2014  |  General  |  1 Comment

Respiratory syncytial virus infection, aka RSV, is a common infection in children. A key aspect of RSV is how poor a job our immune systems do in fighting it off. Virtually all children are infected with RSV during the first few years of life. Not only that, all of us are reinfected multiple times during our lives. Attempts at devising a vaccine for RSV have all been unsuccessful. In fact, early versions of an experimental vaccine seemed to make the disease worse in some infants, raising the possibility that some aspect of our immune response to the virus actually contributes to the symptoms.

RSV has a high attack rate — the term scientists use for the chances that a susceptible person will get the infection if exposed to it. That, plus our generally poor defenses against it, explain the frequent epidemics. Every year a new crop of susceptible infants enters the population.

The most common form of RSV infection is called bronchiolitis. In medical terminology, adding the ending “itis” to a word means that whatever comes before is inflamed. Thus tonsillitis is an inflammation of the tonsils and appendicitis means an inflamed appendix. So bronchiolitis is an inflammation of the bronchioles, the final part of the system of air-conducting tubes that connect the lungs with the outside world. Beyond the bronchioles are the aveoli, the grape-like clusters of air sacs where the business of the lungs — getting oxygen into our bodies and carbon dioxide out — takes place.

Bronchiolitis is a disorder of blocked small airways. This prevents air from getting in and out normally, primarily out. In bronchiolitis, the main problem is that the bronchiole tubes are blocked from swelling of the walls and from debris caused by the RSV infection — bits of broken airway cells and mucous plugs. It looks like this, with the arrows showing air movement.

Infants are the ones who have the most trouble breathing with bronchiolitis. There are several reasons for this, but a key one is the construction of an infant’s chest. When small airways get blocked, we use our chest muscles — tightening them — to force air in and out of our lungs. We are helped in doing this by the fact that our lungs are encased in a fairly rigid rib cage; when we use our muscles to squeeze or expand our chest the system works like a bellows. Infants can’t do this well because the ribs across the entire front half of their chest are not yet solid bone — they are still soft cartilage.  So when a small infant tries to suck air in against anything that is restricting airflow, like clogged bronchioles, his chest tends to sink inwards, causing what we call retractions. These are easiest to see just below the last ribs. They also have trouble forcing air out, so their chests become hyperexpanded with air, making it look as if their chests are puffed out a little. The other reason infants have so much trouble handling debris in their bronchioles is that these tubes are already much smaller to start with, so they get more easily clogged up than do the larger airways of older children.

We have never had any specific treatment that works for RSV bronchiolitis. All we can do is what we call supportive care — oxygen, some breathing treatments (which usually don’t help much), IV fluids if the child is too sick to eat, and a few things we can do to help with mucus clearance. But now that may be changing. A recent study looked at a new drug to kill the RSV virus directly, something we’ve never had before.

The drug, which can be given orally, was tested on adults, not children — yet. The results were very encouraging. One of the issues with other anti-viral drugs has been that they only work well if they are given very early in the course of the illness or even before symptoms start. This new anti-RSV drug works even after people are sick with the virus. It greatly reduced the amount of virus in respiratory mucus, where we usually find the virus. Perhaps more importantly for sick infants, it also caused rapid improvement in symptoms.

Dr. Peter Wright, an RSV expert, is excited about the possibilities of the drug. Dr. Wright has worked on RSV for many, many years — so many that he was one of my teachers at Vanderbilt Hospital way back in 1978. I can recall that he does not get excited easily. I’m excited, too, because severe RSV bronchiolitis is a real scourge we see frequently in the PICU. Some infants even die from it. I was also pleased to read that Dr. Wright is still on the RSV case after all these years.

It's bronchiolitis time again: all about respiratory syncytial virus (RSV)

It’s bronchiolitis time again: all about respiratory syncytial virus (RSV)

January 25, 2014  |  General  |  2 Comments

It’s time again for bronchiolitis, which usually comes in winter through spring. In some ways this problem is similar to asthma, but in other important ways it is very different. With winter upon us it’s time to reacquaint ourselves with this common entity. There is a reliable seasonal arrival of the virus we call RSV, the chief cause of bronchiolitis. The letters stand for respiratory syncytial virus, a description of what it looks like when it grows in the laboratory.

To scientists, RSV is a fascinating virus with several unique properties. One of these is its behavior in the population. When it’s present, RSV is everywhere. Then it suddenly vanishes. There are exceptions to everything in medicine — I have seen sporadic cases during the off-months — but generally RSV arrives with a bang in mid-winter and then leaves suddenly in the spring. It’s the only virus that consistently and reliably causes an epidemic every year, although it often alternates more severe with milder visitations. RSV epidemics often have some regional variability. For example, often one city will have a much more severe epidemic than do others in other regions of the country. Right now my colleagues on the East Coast tell me there is quite a lot of it; I haven’t seen so much yet.

Another aspect of RSV that interests medical scientists is how poor a job our immune systems do in fighting it off. Virtually all children are infected with RSV during the first few years of life. Not only that, all of us are reinfected multiple times during our lives. Attempts at devising a vaccine for RSV have all been unsuccessful. In fact, early versions of an experimental vaccine seemed to make the disease worse in some infants, raising the possibility that some aspect of our immune response to the virus actually contributes to the symptoms.

RSV has a high attack rate — the term scientists use for the chances that a susceptible person will get the infection if exposed to it. That, plus our generally poor defenses against it, explain the frequent epidemics. Every year a new crop of susceptible infants enters the population.

So what is bronchiolitis? What does it look like? In medical terminology, adding the ending “itis” to a word means that whatever comes before is inflamed. Thus tonsillitis is an inflammation of the tonsils and appendicitis means an inflamed appendix. So bronchiolitis is an inflammation of the bronchioles, the final part of the system of air-conducting tubes that connect the lungs with the outside world. Beyond the bronchioles are the aveoli, the grape-like clusters of air sacs where the business of the lungs — getting oxygen into our bodies and carbon dioxide out — takes place.

Bronchiolitis, like asthma, is a disorder of blocked small airways. This prevents air from getting in and out normally, primarily out.  But the principal source of that blockage differs between the two lung problems. In bronchiolitis, the main problem is that the bronchiole tubes are blocked from swelling of the walls and from debris caused by the RSV infection — bits of broken airway cells and mucous plugs. The picture above shows what it looks like.

Infants are the ones who have the most trouble breathing with bronchiolitis. There are several reasons for this, but a key one is the construction of an infant’s chest. When small airways get blocked, we use our chest muscles — tightening them — to force air in and out of our lungs. We are helped in doing this by the fact that our lungs are encased in a fairly rigid rib cage; when we use our muscles to squeeze or expand our chest the system works like a bellows. Infants can’t do this well because the ribs across the entire front half of their chest are not yet solid bone — they are still soft cartilage.  So when a small infant tries to suck air in against anything that is restricting airflow, like clogged bronchioles, his chest tends to sink inwards, causing what we call retractions. These are easiest to see just below the last ribs. They also have trouble forcing air out, so their chests become hyperexpanded with air, making it look as if their chests are puffed out a little. The other reason infants have so much trouble handling debris in their bronchioles is that these tubes are already much smaller to start with, so they get more easily clogged up than do the larger airways of older children.

How does a child with bronchiolitis look? Typically they are breathing faster than the normal respiratory rate of 25-35; often they are puffing along at 60-70 breaths per minute. They also will show those chest retractions and have a cough. Fever is uncommon. They may look a bit dusky from not having enough oxygen in the blood. They often have trouble feeding because they are breathing so fast. The fast breathing, along with the poor feeding, often makes them become dehydrated. Our breath is completely humidified, so when we breathe fast we lose more water.

Can we do anything to treat this illness, make the symptoms better, make it go away faster? Sadly, the answer is that our toolkit is pretty unsatisfactory. I’ve been taking care of children with RSV for over 30 years, and I’ve seen a long list of things tried — breathing treatments, anti-viral medicines, steroids, medicines intended to open up the small airways. None of them work very well, if at all. Even though the symptoms resemble asthma in some ways, none of the asthma medicines work very well, although often we try them just to see because the occasional child will get just a little better with them. The research over the past few years is conclusive — the best we can do is to use what we call supportive care and wait for the infection to pass, meanwhile helping breathing as needed with oxygen, clearing the lungs of mucous, and sometimes a mechanical breathing machine, a ventilator, in severe cases.

RSV is generally not a serious illness, but for some children it can be life-threatening. Usually these children are very small infants, especially those born prematurely, and those with underlying problems with their lungs or their hearts. For those infants we have a monthly shot (called Synagis) that helps reduce the severity of RSV when they get it, and may even prevent a few cases, but it is not an ideal treatment. But older and otherwise normal children, such as toddlers, can get severe cases. We have no idea why that is.

Since RSV cannot be prevented, the best thing a parent can do is try to postpone it. That is, if you have a newborn infant in the height of RSV season, try to minimize exposure of your child to people with cold symptoms, especially toddlers. And for those who do handle your infant, have them wash their hands first. If your child gets bronchiolitis it is a good idea to take them to the doctor for an evaluation unless the symptoms are very mild. The usual course of the illness is a week or so.

Tests and procedures on hospitalized kids: first, do no harm

December 27, 2013  |  General  |  No Comments

There are ample data in adult medicine than up to a third of the treatments and interventions we do in adults are useless at best, maybe harmful. Nobody knows if a similar percentage applies to children, but it is certainly true we do too many tests on kids in the hospital. I have to say that intensivists like me are frequent offenders with all the “routine” blood tests and chest x-rays we do. It is true intensive care requires more intensive testing, but every time I order a test these days I’m much more aware of these questions when I do so than I was in the past: Do I really need it? What will I do differently depending upon the test result? Now a new initiative from the professional organization of pediatric hospital doctors addresses this problem directly. It’s called Choosing Wisely. It’s patterned after a similar program by pediatric radiologists aimed at reducing radiation exposure, the Image Gently program.

The program recommendations starts small with 5 simple, concrete guidelines. All of these have been or are common practices of dubious or no benefit.

  1. Do not order chest x-rays on children with straightforward asthma or bronchiolitis.
  2. Do not use steroids in children less than 2 years of age with pneumonia
  3. Do not use bronchodilators (like albuterol) in children with bronchiolitis
  4. Do not routinely treat gastro-esophageal reflux in infants with acid suppression therapy (like Zantac or Prilosec)
  5. Do not use a pulse oximeter machine on children who are not receiving oxygen therapy. (This is a device that goes on a finger or a toe and measures oxygen in the blood continuously.)

These are all very sensible guidelines, but they’re only a beginning. The idea is not to forbid doctors from doing these things, but rather to make us think twice about ordering them to make sure they make sense for a particular patient. We don’t want to add cost, and certainly not risk, without adding any benefit.

What is asthma and how do we treat it?

November 11, 2013  |  General  |  No Comments

Asthma is a common problem in children — nearly 10% now have it — and the number is increasing. Researchers are not sure of the reasons for this steady increase (more here), but decreased air quality, lower activity levels among children, and an increase childhood obesity have all been implicated. Whatever the cause, it means that millions of American children take medicine for asthma. A significant number of these children end up in the PICU for a severe asthma attack. As I speak to their parents, it is clear that more than a few parents have only vague ideas of how the different types of asthma medicines we use work in their child’s body. This is an important subject, since using the medicines correctly is the best way to keep your child out of breathing trouble, and to use them correctly it very much helps to understand how they work.

The first thing to understand is what is taking place inside the lung during an asthma attack. Once you know that, you can see how the different asthma medicines relieve the symptoms. Here is a schematic drawing of what a normal lung looks like:

You can think of the lungs as being composed of two parts. The first is a system of conducting tubes that begin at the nose and mouth, move through the trachea (windpipe), split into ever smaller tubes, called bronchi, and end with tiny tubes called bronchioles. The job of this system is to get the air to the business portion of the lungs, which are the alveolar sacs. This second part of the lung brings the air right next to tiny blood vessels, or lung capillaries. Entering capillary blood is depleted in oxygen and loaded with carbon dioxide, one of the waste products of the body’s metabolism. What happens next is gas exchange: as the blood moves through the capillaries, oxygen from the air we breathe in goes into the blood, and carbon dioxide leaves the blood and goes into the air we breathe out. The newly recharged blood then leaves the lungs in an ever enlarging system of pulmonary veins and then goes out to the body.

The main problem in asthma is that the conducting airway system gets blocked in several ways, so the oxygen can’t get in and the carbon dioxide can’t leave. Although both are a problem in a severe asthma attack, getting the air out is usually a bigger issue than getting it in because it is easier for us to generate more force sucking in air than blowing it out. So the hallmark of asthma is not getting the air out — called air trapping. Why does this happen? There are two principal reasons: for one, the small airways, the bronchioles, constrict, get smaller; for another, the walls of the airways swell and the airways themselves fill with excess mucous, blocking air flow. Here’s another schematic drawing of what that looks like.

Thus during an asthma attack these things happen, all of which act together to narrow the airways and reduce air flow:

  1. The smooth muscle bands around the tiny airways tighten
  2. The linings of the airways get inflamed and swell
  3. The mucous glands in the airways release too much mucous, filling the airways

The medicines that we use to treat asthma work by reducing (or even preventing) one or more of these things. But before we get to them, an obvious question is why are our lungs are constructed in this way, especially if it can cause trouble? Why are those smooth muscle bands there? Why does there need to be mucous in our airways?

The smooth muscle bands are there for a good reason. The lungs need a way to direct the air we breathe in to the best spots, which are those regions of the lung with the best blood flow, and that changes from minute to minute from such things as changes in our position — lying down to standing up, for example. Those muscle bands function like the head gates of an irrigation system, opening and closing to direct air to the best places. The mucous is important because it is one of the chief defenses our lungs have against harmful or irritating things we breathe in. The mucous traps debris and steadily moves it up and out of our lungs. In asthma, both of these natural systems become deranged. The so-called triggers for this derangement vary from person to person, but the results are similar. The medicines we use are similar, too, no matter what started the asthma attack.

One of the mainstays of asthma treatment is a member of a class of medicines we call selective beta agonists. The generic name for the one we use most commonly is albuterol. Common brand names for albuterol are Ventolin and Proventil. Albuterol comes as a liquid, which we blow into a mist either with a device called a nebulizer or with what’s called a metered dose inhaler (“puffer”). The second of these is more convenient to carry around, but it can be more difficult to use with small children, although adding a special chamber to the device can help. The patient inhales the mist of albuterol. It works by soaking into the smooth muscle bands, making them relax, and in that way making the airway tubes bigger to allow more air flow. (There is also an oral form of albuterol, but for a variety of reasons it is not a good choice for children with asthma.) For many patients with asthma, inhaled albuterol alone is adequate treatment for their symptoms. A key thing to know about albuterol is that it goes to work right away, generally within minutes, so it is a good medicine for an acute asthma attack.

Another class of medicines long used in the treatment of asthma is corticosteroids, or steroids for short. These medicines work by being powerful blockers of inflammation. If you have ever had a poison ivy rash, for example, you are familiar with inflammation: redness, swelling, and seepage of fluid from the tissue (we can use steroids to treat poison ivy, too). A similar inflammation around the small airways is characteristic of asthma. It makes the linings of the airways swell, weep fluid, and increase mucous production. For a severe attack, we give steroids by mouth or intravenously (IV, directly into the bloodstream). They are very effective when given that way. But they do not go to work right away — several hours are needed at least. So although we may start them during an acute attack, we don’t expect them to help for a while.

Steroids are powerful drugs. When you take them by mouth they affect your entire body, not just your asthma, and that can cause problems. This is why we only use systemic steroids — those by vein or by mouth — for as short a time as possible, typically five days or so. We have other forms of steroids that are inhaled. This allows them to work directly on the airways without affecting the entire body. Common brand names of inhaled steroids are Pulmicort and Flovent. The inhaled steroids, like the systemic ones, don’t go to work right away. So they are intended primarily as a medicine to maintain control of the asthma. It is a common mistake for parents to give their child multiple doses of inhaled steroids when they have worsening breathing troubles — steroids are not intended to be used that way. The proper so-called “rescue medication” for worsening symptoms is albuterol or drugs like it.

These days we have hybrid medications that combine a long-acting albuterol type drug with an inhaled steroid. This combination is intended as something to be taken for chronic control of patients with moderate or worse asthma, and these agents are quite effective at doing that. Common brand names are Advair and Symbicort.

So albuterol (and beta-agonists like it) and steroids are mainstay medicines for treating asthma. In combination they make a good team because they attack the asthma via two different modes of action. We have some other medications that work by still other mechanisms. Montelukast (brand name Singulair) blocks airway inflammation by another mechanism than do steroids. Unlike systemic steroids, the action of montelukast is more selective and this medication is safe to take for prolonged periods. For some patients, montelukast and an occasional puff of albuterol is sufficient to keep them out of trouble. Finally, an inhaled drug called ipratropium (brand name Atrovent) blocks excessive mucous production by another method than blocking inflammation; it is often helpful as an adjunct to the other medicines. A couple of medications (brand names Combivent and DuoNeb) combine ipratropium and albuterol together so they can be inhaled at the same time.

So how do doctors decide what asthma medicines to use? One obvious principle is that it makes little sense to use more than one medication of the same category: combinations ought to work in different ways so they can work together. But beyond that obvious principle, how do we decide? The usual approach is to classify patients with asthma according to their severity and then add medicines in a logical, step-wise way until we get control of the symptoms. There are guidelines to help us do this. A good, recent summary is here, published by the National Institutes of Health. If you or your child has asthma it is a good place to find information. It is also useful to look at the actual decision tree doctors use to decide what medicines to use and in what order. You can find it here. One key principle is that we divide medicines into maintenance medications — those the child takes every day — and “rescue” medications, ones the child takes for worsening symptoms.

Asthma is common and is getting more common every year. Certainly speak with your child’s doctor about doing some good detective work to figure out what your child’s asthma triggers are. Then take steps to modify exposure to them or avoid them. Common sense tells us that if we can reduce symptoms by reducing exposure to common triggers, such as tobacco smoke, we should do everything we can to reduce the need for asthma medications. But for many children, this will not be enough; their parents should understand how these medicines work in order to make the best use of them.