Most educators, and plenty of parents, think children these days spend too much time in front of a screen — computer screen, video game screen, or television screen. It is the last of these that has particularly interested physicians who care for children because increased TV time is associated with some health problems. For example, there is a correlation between time spent watching TV and the propensity to develop asthma. It’s not that TV causes asthma, but that children who spend hours each day watching it are more likely not to have less healthy lifestyles overall — like the kid in the picture.
Several things are associated with children spending more time in front of the tube. Not surprisingly, having a TV in a child’s bedroom is one. The American Academy of Pediatrics is particularly concerned about TV use in children under two years of age — here is their policy statement about that.
A new study, whose author one could easily call Captain Obvious, demonstrates that the highest correlation regarding how much TV a child watches is with how much his or her parents watch. Still, it’s helpful to have research confirm common sense.
So, if you want your child to watch less TV, watch less yourself.
Imagine this scenario. Your two-year-old son has had a runny nose for a day or two and an occasional cough, but seemed no worse to you that everyone else in his preschool class. Two hours after you put him to bed you hear him coughing, only this cough is like none you have ever heard from him before. It sounds like a barking seal at the circus–a brassy, honking noise. In between coughs he his making a strange crowing-like noise. When you snap on the light you see him sitting up in his crib, leaning forward, and coughing that strange cough. You also notice the part of his chest below his ribcage is sinking inwards with each breath, backwards from the way it should go. Your little boy has a scared look in his eyes, and you are more than a little scared yourself. He has croup.
What is croup?
Croup is a disorder caused by inflammation of the trachea, the main breathing tube in the neck, just below the vocal cords, in an area called the subglottic region. Some say it gets its name for the old Anglo-Saxon word kropan, which means to croak or cry out. If true, such venerable terminology tells us this common childhood ailment has been recognized as a distinct entity by parents for a very long time. Physicians sometimes give it a much fancier name, laryngotracheobronchitis. This learned construction merely describes what croup is: inflammation (hence the “itis”) of the breathing tubes extending from the vocal cords (the larynx), through the trachea, and often down to the lower breathing tubes (the bronchi). Even though the inflammation can stretch up and down the airway, it is in the subglottic region where the symptoms happen. Why this is so is because of a simple law of physics–that is where the airway of a toddler is at its narrowest. The symptoms of croup come from blockage of airflow.
The inflammation of the subglottic region makes the lining of the trachea swell. Since the trachea is more or less round, this swelling makes the diameter of the airway smaller. Sometimes the swelling of the tissues gets so bad the size of the child’s airway is narrowed to that of a small straw. What happens next is simple physics, and is analogous to what happens in cold water pipes if they have their diameter narrowed by mineral deposits in them: flow through a tube is proportional to the fourth power of the radius of the tube. This may sound esoteric, but the principle has important practical implications for small children with croup.
Imagine an adult whose airway has a diameter of twelve millimeters. Then imagine the lining of this tube develops one millimeter of swelling all around its lining, thereby reducing its diameter to ten millimeters. If one does the calculations, this slight reduction in size reduces airflow by about half. Now consider a toddler with a five millimeter airway who has the same one millimeter of swelling all the way around it, reducing it to three millimeters in diameter. The adult in this example loses about half the airflow, something easily compensated for by just breathing a little harder. In contrast, the toddler has his airflow reduced to only thirteen percent of what it was. This reduction is too much to compensate for, although the child tries. His trying causes the symptoms of croup.
It is air rushing turbulently through a newly tiny airway that causes the crowing sound characteristic of the breathing of a child with croup. It is called stridor, and an experienced person can often make the diagnosis of croup based upon that sound alone, even over the telephone. Additionally, the front portion of a toddler’s ribcage is not yet solid bone–it is still partly cartilage. This means that, since a child’s chest is not yet firm in the scaffolding of the ribs, the increased effort of breathing makes the chest cave in the wrong way with each breath. These are called retractions. They are not specific to croup, but happen in a child with respiratory distress from a variety of causes. The final characteristic finding of croup, the seal-like barking cough, is from irritation of the vocal cords.
One of the characteristic attributes of croup is how sudden the onset of the stridor, the sign of upper airway, often is. For some reason croup tends to be worse at night; most visits to emergency departments for croup occur between ten in the evening and four in the morning. A typical story is that parents put their child to bed with just a mild cough only to awaken in the middle of the night to the sound of severe stridor. This is a predictable result of the place where the inflammation is happening. Since airflow is dependent upon the fourth power of the radius of the child’s trachea, he may not have much distress during the early stages of the illness. But as the airway gets smaller, subsequent reduction in size becomes critical. The analogy to water pipes is a good one: loss of half the space inside the pipe from mineral deposits causes only slight reduction in water flow when one turns on the tap, but just a little more blockage severely cuts down flow.
How common is croup and what causes it?
Croup is an extremely common childhood illness. Estimates vary, but studies suggest as many as fifteen percent of all children have croup at least once, and five percent have it more than once. Some have estimated croup accounts for fifteen percent of all respiratory tract disease seen in pediatric practice. The peak time for croup is fall and early winter, but it can occur any time of year, even summer. The peak risk age for children to get croup is eighteen months, and boys are one-and-one-half times more likely to get it than are girls.
Croup is caused by infection with a respiratory virus. Although there are a few ailments that resemble croup and are caused by something else (more on them below), standard croup symptoms are brought on by viral infection. There are multiple viruses that can do it, but nearly three-quarters of all cases stem from infection from a single family of three closely-related viruses–the parainfluenza viruses, which are cousins of true influenza. Less commonly croup is caused by the true influenza virus, respiratory syncytial virus (RSV), or a few others.
All these viruses are spread from child to child in the manner of most respiratory viruses–tiny droplets of infected mucous or saliva. These droplets can fly through the air after a cough or sneeze and be inhaled by someone nearby. Alternatively, virus-laden mucous gets deposited on a child’s hands when she puts them in her mouth or nose and the virus then moves on to someone else when the child touches them.
Either way, the first step is for the virus to infect the back of the throat, causing cold-like symptoms of nasal congestion, cough, and low-grade fever. For reasons we do not understand, some children get no more than that. Often, however, and especially with the parainfluenza viruses, the infection moves to the subglottic area of the trachea. There it causes the local irritation and inflammation that leads to the airway swelling and subsequent symptoms of obstructed airflow.
How is croup diagnosed?
Croup is entirely a clinical diagnosis; there is no specific test for it. This means the doctor decides it is croup based upon a typical story (cough, congestion, stridor, and mild fever). Sometimes, though, a doctor will get an x-ray of the child’s neck, which often shows some narrowing of the airway. The figure below is an example of this. Air on an x-ray appears black, bones are white, and tissue is grey. The central black column of this child’s trachea is narrowed abnormally at the point of the arrowhead. (The bones stacked like coins in the neck are part of the spinal column.) Doctors do not always get such an x-ray, especially if everything points to croup. If the story is atypical, a common reason for getting the x-ray is to make sure the child’s symptoms are not from something else. Those other possibilities are divided into infectious ones and non-infectious ones.
There are other infections besides viral ones that can infect a child’s airway and block airflow. Serious bacterial infection can do this also. The principal one of these is epiglottitis, a severe and rapid swelling of the epiglottis, a structure that sits just above the opening of the trachea at the back of the throat. The epiglottis is what keeps food from going into the trachea during swallowing. When it becomes severely swollen, which is what happens with epiglottitis, it can completely block the airway and cause a life-threatening emergency. Another infection that can mimic croup is bacterial tracheitis, a severe infection of the entire trachea that causes so much infected pus that a child’s airway can become obstructed. It, too, can be life-threatening.
Fortunately, both epiglottis and bacterial tracheitis are extremely rare. Epiglottis was once not uncommon, but near universal vaccination of children against the bacterium Hemophilus influenzae, the main causative organism, has dramatically reduced the incidence of the disorder. Both these serious conditions usually behave quite differently from croup. The main difference is that both cause high fever (croup’s fever is nearly always low-grade) and the children appear quite ill. The key distinction between croup and epiglottis is that the latter not only makes breathing difficult but also makes swallowing painful or even impossible for the child. Thus a child with epiglottis will not only have stridor, but will sit hunched forward and drool, unable to swallow.
An x-ray of the neck can help distinguish croup from these more serious infections. However, if the doctor thinks epiglottis is possible the standard way to proceed is for the child to be given a sedative and have his airway directly inspected using a procedure called laryngoscopy. If this is necessary, it is usually done by an airway specialist, such as an otolaryngologist, commonly called an ENT specialist.
There also are non-infectious things that can cause upper airway obstruction and stridor, since anything blocking the airway gives the same symptoms. Overall, what distinguishes these non-infectious causes of upper airway obstruction from the infectious ones is the lack of any other evidence of infection, such as nasal congestion, fever, or malaise.
If the onset of a child’s breathing problems is quite sudden, the doctor might consider the possibility of a foreign body stuck in the airway. Toddlers put anything into their mouths–toys and bits of food are frequent offenders when this happens. On the other hand, if the progression of a child’s symptoms is progressive over days or weeks, the doctor might think about several kinds of tissue growths that can occur within the airway. If either of these possibilities is likely, the child usually needs laryngoscopy or bronchoscopy, inspection of the trachea and lower airway, for diagnosis.
A few children have recurrent, sudden episodes of croup symptoms without any other evidence of viral infection. These attacks from what is called spasmodic croup also generally happen at night. The cause is unknown, but it may be related to allergies. It is generally treated the same way as viral croup (see below).
The walls of the trachea are stiffened with bands of cartilage; this is what holds them open and keeps them that way. Some children have an airway that is intrinsically less stiffened with cartilage than most, causing it to collapse a bit when the child breathes, causing stridor that can sound like croup. In this condition, called tracheomalacia, the symptoms are chronic and are often worse when the child is lying on his back because the weight of the tissue in the neck compresses the airway more. It requires bronchoscopy to diagnose for certain.
Croup ranges in severity from quite mild to the rare case of near total obstruction of the airway. To help categorize this severity doctors have devised various scoring systems to rate the child’s symptoms. One commonly used of these “croup scores” is the Westley scale. The scale assigns points for various symptoms and groups children into “mild,” (less than three points), “moderate,” (three to six points), and “severe” (more than six points). It uses five criteria to do this: severity of retractions, degree of stridor, how well the air is getting into the child’s lungs as assessed with the examiner’s stethoscope, if the child is dusky-colored from insufficient air, and if the child is becoming poorly responsive from lack of oxygen. Generally mild croup can be treated at home; moderate and severe croup require medical attention, and usually the more ill children will be admitted to the hospital.
How is croup treated?
Once a doctor decides a child has croup, it is fairly well-accepted how to treat it. Therapy is directed at two things: making the child feel better and reducing the airway inflammation to improve airflow. Mist has been a mainstay of treatment for mild croup for many years.
Most physicians believe steam often gives a child significant relief from the pain and raspy, dry feeling in the throat, although whether it actually helps reduce the inflammation of the airway itself and improves air flow is doubtful. Mist may also help loosen airway mucous and allow the child to cough it up easier. Throat pain and fever are helped by treatment with acetaminophen or ibuprofen.
The traditional home remedy for mild croup is to close the bathroom door and run a tap until the room is completely steamy, then turn it off and sit with the child in the mist. A parent needs to be careful with this, of course; children have been burned from scalding water. Exposure to cool night air (since croup happens mostly at night) is also a traditional remedy. Although widely practiced and certainly benign, it, too, has never been validated.
Doctors typically use one or both of two ways to reduce the inflammation and swelling in the child’s airway. Direct application of the drug epinephrine (adrenaline) to the swollen tissues shrinks them by constricting the tiny blood vessels under their surface; it is the virus-induced engorgement of these vessels and leakage of fluid out of them that causes the swelling in the first place. The drug is given by nebulization, blowing high-flow air or a mixture of air and oxygen through the liquid epinephrine and thereby dispersing it into a fine mist, which the child then breathes to carry the drug to the subglottic area. Epinephrine works within minutes and usually gives a child prompt relief from the stridor and retractions. Unfortunately the effects of epinephrine only last a few hours at most. It can then be repeated, although dose after dose of epinephrine can rarely lead to worse swelling when the drug wears off.
The subglottic swelling of croup is from inflammation in the area, so standard treatment of moderate or severe croup also consists of using a drug to reduce the inflammation–a steroid. Steroids are also being used increasingly for mild croup, both to make the child feel better and to interrupt in its early stages progression of the swelling. Steroids can be given orally, by intramuscular injection, or even nebulization like the epinephrine. A commonly used steroid for croup is dexamethasone (Decadron), a single dose of which is usually sufficient to reduce the inflammation. Unfortunately, steroids do not act immediately like inhaled epinephrine–they take four to six hours at least to work.
A typical treatment scenario for a child coming to the emergency department with croup would be to have him breathe some cool mist, followed by a nebulized epinephrine treatment. Usually the best way to do this is to have the child sit in a parent’s lap, since he is most comfortable there and agitation makes the stridor and retractions worse. Then the child receives a dose of steroids. Often by then the child’s symptoms are much better, but it is important to keep the child in the emergency department for at least an hour or two more to make sure the symptoms do not recur after the epinephrine wears off and the child needs more treatment. A child who has continues to have symptoms after epinephrine or who needs repeated doses of epinephrine needs admission to the hospital. What doctors particularly look for is continued stridor when the child is completely calm; called “stridor at rest,” it is a standard indication for hospital admission.
A child with severe croup needs more complicated management, although this is very uncommon. If the child is clearly not getting enough air to stay alert and keep his blood oxygen levels up he needs immediate placement of a breathing tube, called an endotracheal tube. It is placed by a procedure known as intubation. A child with less severe croup, but who remains in significant distress and begins to tire from the effort of breathing also needs intubation.
What is the typical course of a child with croup?
Croup usually runs its course in five to seven days, typically with one day of worst symptoms and several more of cough and hoarseness. Since the symptoms characteristically get better in the day, it is common during the middle of the illness for a child to have minimal symptoms during the day but several nights of worse cough.
What is the risk of a child getting croup again and are there any long-lasting effects?
There is no clear-cut evidence that children who have one episode of croup are more likely to get it again. There is some evidence children who have group are more at risk later to develop reactive airways disease–asthma–than children who never have croup. However, if true, this may not be a cause-and-effect association; the propensity for a child to get croup when infected by a respiratory virus may reflect the same innate tendency to develop asthma. They may be different manifestations of the same thing. There are no long-term after-effects of typical viral croup.
It’s pretty well known that emergency room use is on the increase. This recent study summarized the trend over the past decade (the complete article is behind a paywall — let me know if anybody wants a complete copy). The authors compared 1997 with 2007, looking at the number of ED visits per 1000 population. They found that the total number of visits had increased from 353 per 1000 persons in 1997 to 390 per 1000 persons. The total increase in number of visits was about double what you would predict just from population growth. So more folks have been going to the ED over the past decade. How many of these were children?
It turns out that the rate among children has not changed significantly over the past decade — it’s stable at 362 per 1000 population. So the past decade’s growth in ED use has come from other age groups. The study found all adults between 18 and 64 years of age increased their rate of use. Interestingly, older people, those over 65, did not.
ED use by insurance status confirmed what all of us have known for quite some time: the uninsured and those with Medicaid have the highest rate of ED use. A patient with Medicaid was roughly twice likely as a patient with insurance to go to the ED for care, and someone with no insurance was half again as likely to go to the ED as an insured person. The reason for this is most likely little or no access to regular primary care, care which would keep them out of the ED. It’s getting harder and harder for kids on Medicaid to find a doctor, largely because the reimbursement rate is so bad. In my state, for example, a pediatrician gets paid less to see a child with complicated health problems than it costs to change the oil in your car.
Another recent study, this one just involving children, examines the issue of inappropriate ED use. After all, if children can get care from a regular doctor, they are less likely to use the ED to get routine care. (Unfortunately there’s a paywall on this article, too.)
The authors examined the characteristics of what they called “inappropriate” use of the ED — essentially things for which, if the child had a regular doctor, they would not have come to the ED. Their findings also confirmed what we would have suspected: poor kids, kids on Medicaid, and uninsured kids — those who had trouble finding a regular doctor — were more likely to use the ED for routine care. ED care is extremely expensive care: the same visit for asthma, for example, is far cheaper in the office than in the ED. But if you’re a parent whose child is without regular healthcare, where are you supposed to go, if not the ED? From the article:
“Specifically, patients identified access barriers in the primary care clinic as the major reason for choosing the ED instead of the clinic. They reported a cumbersome scheduling system, long waiting times for appointments, and no availability of walk-in care.”
All this seems obvious. But sometimes we need actual research studies to confirm the intuitively obvious. And excessive ED use is one of the engines in our ever-increasing healthcare bills.
My last post was about asthma. This one is about another very common breathing problem in children — bronchiolitis. In some ways it is similar to asthma, but in other important ways it is very different. With winter nearly upon us it’s time to reacquaint ourselves with this common entity.
I’ve written before (here and here) about the reliable seasonal arrival of the virus we call RSV, the chief cause of bronchiolitis. To scientists, RSV is a fascinating virus with several unique properties.
One of these is its behavior in the population. When it is 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 is the only virus that consistently and reliably causes an epidemic every year, although it often alternates more severe with milder visitations. However, RSV epidemics may still 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 year 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.
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, which are 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. Here’s 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. They also have trouble forcing air out, so their chests become hyperexpanded with air. The other reason infants have so much trouble handling debris in their bronchioles is that they are already narrow to start with, so they get more easily clogged up than do larger, adult-sized airways.
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, although 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 no. I’ve been taking care of children with RSV for 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 of 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 in severe cases.
RSV is generally not a serious illness, but for some children it can be life-threatening. 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 this is not ideal.
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.
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:
- The smooth muscle bands around the tiny airways tighten
- The linings of the airways get inflamed and swell
- 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.
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.