Children in the PICU without health insurance have higher mortality

March 25, 2011  |  General  |  No Comments

I’ve written before about how poor children and children without health insurance are far more likely to need PICU care than are more affluent children. For example, although children on Medicaid account for 20 – 25% (depending upon the state) of children in America, about half of all children in America’s PICUs are on Medicaid. Once in the PICU, though, do the poorer kids have worse outcomes than the richer kids? Does their chronically disadvantaged situation set them up for being more difficult to treat and cure?

I’ve been looking for information about this crucial question for some time and recently found some disturbing data about it, in the form of an article in the journal Pediatric Critical Care Medicine (volume 7, pages 2-6, 2006). You need a subscription to the journal to get the article, but I’ll summarize its important findings for you.

First, the study confirmed that children without insurance are far more likely to suffer critical illness: ” . . . far more serious illness and injuries were associated with uninsured children admitted to the PICU.” But did that make it more likely that these children would suffer worse outcomes, or even make it more likely for them to die?

Unfortunately, uninsured children did have poorer chances of survival. In fact, they were three to four times more likely to die in the PICU. Why was that? The answer was not that they received different care in the PICU once they got there; the answer was that they were much sicker to start with. Compared to children with either private insurance or public assistance (Medicaid), the uninsured children came into the PICU in much worse shape, with far worse derangements in their physiological state. Most likely their parents, fearful of the cost, delayed bringing them to the hospital until sometimes it was too late to save them.

What can we learn from this? Lack of health insurance kills children. That is both a tragedy and a terrible indictment of how we presently care for America’s children.

How large should a PICU be to give good care?

March 21, 2011  |  General  |  No Comments

I’ve worked in several PICUs over the years. Some were as large as 36 beds (which counts as pretty large in the PICU world), and some were as small as 4 beds. Inevitably, larger PICUs can offer services that smaller ones cannot. This is particularly the case with more specialized services, like some kinds of surgery and access to super-specialists. When I’ve been in a smaller unit, there have been times when I’ve needed to transfer children to a larger one so they could get these more esoteric services. When I’ve been in a larger unit, I’ve received transfers of kids like that. Would these children who needed transfer have been better off going to the larger PICU in the first place?

The dilemma for smaller PICUs is that they can never become as experienced in caring for children with rare conditions, and it is hard for someone working in one of the smaller units to keep their skill levels up. Research has shown, not surprisingly, that physicians who do the same thing a lot are better at doing it than physicians who don’t do it so often. On the other hand, transferring a child from a local, smaller PICU to a bigger one is often hard on families, since often the larger unit is in another city — sometimes in another state. And many PICU problems can be handled just fine in a smaller place, nearer to home.

The process of transferring a critically ill child — by ambulance, helicopter, or airplane — carries risks, too. These risks are not just those inherent in traffic or flight. I can tell you from personal experience that no matter how much supplies and equipment you bring on the transport, you still can’t recreate a PICU. And the simple working environment of a transport vehicle, especially a helicopter, is cramped and noisy — far from optimal. So sometimes a critically ill child is safer staying where they are, at least until they can be made more stable.

What to do? As pediatric intensivists, we are sort of feeling our way as we figure this out. Most smaller PICUs have formal or informal relationships with larger units to which they can send children they cannot handle. But these relationships are a patchwork across the nation — we simply don’t know the ideal size for a PICU. When PICUs began several decades ago they were rare, found only in large children’s hospitals. In those days people’s expectations were different about what smaller community hospitals needed to provide. In today’s world, we believe all children should have access to the same life-saving PICU care. So smaller hospitals began to open PICUs to provide that care as best they could. Someday PICU care may be truly regionalized, with formal relationships between big and small units in the region, complete with standardized criteria for appropriate care at one unit or the other. We don’t have anything like that yet.

What parents should realize is that there are differences between what a smaller and a larger PICU can do. If your child has a particularly unusual or difficult problem, it is never inappropriate to ask your child’s doctor if transfer to a larger unit makes sense.

Dehydration in children

March 16, 2011  |  General  |  No Comments

Our bodies are mostly water — about 60% water, in fact. This varies a little with age and sex, but it is a good rough estimate. Of that 60% water, about a third of it is outside the body’s cells, so-called extracellular fluid, and two thirds of it is inside the body’s cells, so-called intracellular fluid. The easiest way to remember this is the “60/40/20” rule: total body water is 60% of our weight, intracellular water is 40% of total body weight, and 20% is extracellular water. Water can move back and forth between these compartments as needed. Dehydration is a relative deficit of body water, and children are especially prone to developing it.

Dehydration results from loss of body water being greater than replacement of it. Our bodies lose fluid constantly: our kidneys must make a minimum amount of urine to stay functional; we lose water as sweat; and our breath, being fully humidified (saturated with water) takes water from our bodies. These are called obligatory, or insensible water losses. Children have a proportionately higher insensible losses than do adults because their ratio of surface area to body mass is higher. So, compared with adults, children need to take in a relatively larger amount of water to keep all those body compartments full.

What causes dehydration in children? The most common causes are those that increase losses, such as diarrhea, vomiting, or rapid breathing from some respiratory problem. Sick children also tend to take in less fluid, so decreased intake of fluids also contributes.

How can we tell if a child is dehydrated? The most common early sign is decreased urine production, since the kidneys respond to the problem by conserving water. The urine also becomes more concentrated because there is less water in it. As a rule of thumb, the kidneys of a child weighing 10 pounds normally puts into her bladder about 1-2 teaspoons of urine per hour. What a parent can tell, for infants, is if the baby is wetting diapers at the rate she usually does.

As dehydration becomes more advanced, there are other signs we look for. These include a decrease in weight (because so much of our body is water), listlessness, poor color with a doughy feel to the skin, and a more rapid heart rate.

Most cases of dehydration can be treated with increased oral fluids, but sometimes, particularly if the child is too listless to drink, we use intravenous fluids for a day or so until the child is better. We have a good rough guide, based on body weight, about how much fluid a child needs to keep from becoming dehydrated when they are sick.

A common version of the formula divides children into three categories: less than twenty-five pounds, twenty-five to fifty pounds, and over fifty pounds. The first group needs about a half teaspoon of fluid each hour for each pound of body weight. This means a ten-pound child needs five teaspoons an hour, which is a little more than two- thirds of an ounce, or roughly about two ounces every three hours. A twenty-pound child then needs twice that—about four ounces every three hours.

The second group of children, those weighing twenty-five to fifty pounds, need about four to six ounces every three hours. Children weighing over fifty ponds need about six to eight ounces every three hours.

A cup of juice is usually about four ounces and a large glass closer to eight ounces. So offering you child something to drink every three to four hours should keep them well hydrated.

You can read an excellent discussion about dehydration in children here.

High tech meets low tech: the role of watchful waiting in the PICU

March 11, 2011  |  General  |  No Comments

Offhand you would not think a child with severe viral pneumonia and one with a major head injury are much alike, but they are. Together they illustrate a great truth of pediatric intensive care medicine, which is much of what we do is not specific treatment for the child’s problem; rather, it is what we term “supportive care,” because it supports the continued functioning of the child’s vital organs and systems while the problem runs its course and the child heals.

Both of these children often require very sophisticated technology to provide that organ support, things like mechanical ventilators and devices for measuring pressures inside the brain, but that technology doesn’t actually cure anything. But if it doesn’t cure anything, what does it do?

One of the most important principles of supportive care in the pediatric intensive care unit is that we make sure what we are doing does not make the problem worse. A good example of that is the child with a severe head injury. Although there are a few things we do to help the situation, a key aspect of what we do is the maneuvers we go through to make sure the brain is given a chance to heal without further stresses. For the child with severe pneumonia, the sort of child who is often on a mechanical ventilator machine, we do a similar thing — we use the machinery in such a way to minimize the chances that the ventilator itself does no harm, although this is not always possible.

This kind of watchful waiting at a sick child’s bedside is something parents have done for millennia. What the PICU often offers is simply an updated version of that time-honored vigil.

On croup

March 8, 2011  |  General  |  No Comments

It’s that time of the year in the PICU for more respiratory illnesses, one of them being croup. This is an ancient illness — its very name comes from the Anglo-Saxon word to croak, which is what children with croup can sound like. The characteristic brassy cough sounds more like a seal to our modern ears, though. Also characteristic is a sound we call stridor, the sound of air rushing through a narrowed tube, in this case the child’s airway.

Croup is caused by viral infection of the region just below the vocal cords. One of several viruses can do it, but the usual offenders are members of the parainfluenza group. The infection causes swelling, and the swelling causes narrowing of the airway. This makes it more difficult for the child to breath — in some ways it is like breathing through a straw — and the child has to work harder to get air in. This can make the child’s chest cave in the wrong way with each breath, something called retractions. Fever, if present, is usually mild.

As with most viral illnesses, there is no specific treatment for croup — what treatment we have is directed at relieving the symptoms of throat pain and difficulty breathing. We do have several effective ways of doing this. Simple mist, as from a steamy bathroom, is a time-honored therapy to help a child breath. Inhaling a mist of the drug epinephrine shrinks the swollen tissues, although it only lasts for an hour or two. The drug dexamethasone, either orally or by injection, has become a standard therapy for moderately severe croup and it is quite effective. Acetaminophen or ibuprofen can treat fever and throat pain.

When should you bring your child to the doctor for croup? A good rule of thumb is if your child has stridor when sitting quietly or if there are any retractions present — both of these are indications for therapy with epinephrine or dexamethasone.

We always see a few children in the PICU with severe croup, usually those who need repeated doses of epinephrine or are working very hard to breath. On very rare occasions we need to use a breathing tube and a mechanical ventilator for these children. Nearly all children, however, recover from croup with no complications.

I’ve written a more detailed discussion of croup, which includes an x-ray of what it looks like and some uncommon causes of airway obstruction, in a Google Knol here. (A glitch in the Google software refuses to list my name as the author; I’ve given up trying to fix it.)

Can an adolescent decide for himself to forgo medical care?

March 4, 2011  |  General  |  No Comments

One of the four key principles of standard medical ethics is the principle of autonomy, which I’ve written about here. Autonomy means that patients are in control of their own bodies and make the key decisions about what sort of medical care they will (or will not) receive. For children, this principle means that the child’s parents make these decisions.

There are exceptions, as with all things in medicine. For example, if a child’s physicians believe that the parent’s choice will harm the child, the physician can ask a court to intervene. This is a very rare occurrence, but it happens sometimes. I have been involved in a few of those cases. But that’s not what I’m writing about now — I’m writing about nearly-adults, those children who are almost independent, but not quite.

The law generally defines the age of majority, the point at which a child is no longer a child and may decide these things for herself, at age eighteen, although there are variations between states. (The situation is different for so-called emancipated minors — those rare children who are entirely self-supporting.) What should we do when such a near-adult and her parents disagree about the treatment the child should get? There have been several recent examples of the variety of things that can happen then.

One case is that of Dennis Lindberg, a fourteen-year-old boy who died from leukemia in 2007. Dennis was a Jehovah’s Witness and, like others in his faith, rejected blood transfusions, even in life-saving situations. It is common for the courts to mandate transfusions in very small children over the objections of Jehovah’s Witness parents. The rationale for this is that a small child is too young to decide himself if he agrees with his parents. Dennis’s doctors went to court to get such an order.

But this case was different — Dennis was not a toddler or small child. He was an aware, articulate, young man who understood the meaning of both his illness and the consequences of not getting the transfusion. The court ruled that Dennis had the right to make his own choice, which he did.

His case dramatized a very grey area in medical ethics — when ought a young person be able to make these decisions on his own? In my own career I have had several occasions when an adolescent disagreed with the doctors, his parents, or both about what to do. In all those situations everyone eventually came to an understanding. That’s the best outcome, of course, but these will always be ambiguous situations because children mature at differing rates. Some thirteen-year-olds are wiser than seventeen-year-olds. For that matter, some young adolescents are wiser than others who have already attained the magic age beyond which we give them the right to make all these decisions.

If you are interested in these kinds of ethical questions as they relate to children, here is an excellent site from the ethics program at Seattle Children’s Hospital with a good list of further readings. And here is another example of a teen (with the support of his parents) going to court to assert his right to refuse standard therapy for cancer.

What inflammation looks like up close and personal, part IV

February 23, 2011  |  General  |  No Comments

Here’s another snippet from the first chapter of my new book, How Your Child Heals. It’s from the chapter about inflammation, and follows from here. You’re at the battlefield of inflammation, a sore finger, and are positioned to observe the conclusion of the struggle.

How did those germs get through the barrier of your son’s skin to cause infection? As you approach the epicenter of the action, you discover the answer. Sometimes germs can simply crawl through the skin via a small break, but other times they have an accessory to aid their attack. Up ahead you now can see that the bacteria gained entry to his finger through a break in his skin caused by a small wood splinter. The tip of the splinter stands in the center of the cellular fray, marking the spot where it began.

Like most battles, the outcome of this one can go either way. If the body’s defenses win, the immediate result is what we call an abscess, a walled-off pocket containing dead phagocytes and dead bacteria. This is the whitish pus we have all seen beneath the skin of an infected area, such as a skin boil. Usually, there are also some living bacteria remaining in the pus, the relative amount of which depends upon how many were there at the beginning—generally, the phagocytes cannot kill them all. But any remaining living bacteria are now at least cordoned off, contained within the protective barrier walls of the abscess.

If the germ attackers win the initial battle, no abscess forms. Rather, the bacteria breach the body’s initial defenses and spread through the body, sometimes by using the bloodstream, but other times just by marching through the tissues. When that happens, the child is generally quite obviously ill with fever and other symptoms, such as chills, muscle aches, and a general malaise. These symptoms come from all of those substances that got the inflammatory response going at the site of invasion—the signals calling the phagocytes and the auxiliary cells. Only now these substances are not just in one spot and exerting their effects there; they are circulating throughout the child’s entire system. When that happens, it is usually a sign the child’s body will need help dealing with the infection, such as antibiotic treatment.

The formation of an abscess is an immediate victory for the body, but it still represents a kind of standoff between the attacking bacteria and the body’s defensive systems. The residual bacteria can still cause problems. For one thing, the toxins they release leak out into the regions surrounding the abscess and inflame those areas, too. Plus, the dead and dying phagocytes also give off substances that keep the fire of inflammation burning. For these reasons the area surrounding the abscess usually continues to be at least a little inflamed—red, swollen, and painful.

The bacteria remaining in an abscess can cause further problems, even though they failed in their first attempt to invade further. If they are still very numerous, they continue to reproduce, and they can do so very quickly—doubling their numbers every hour or less. Reinforced by all these new recruits, they can overwhelm the local defenses, break through the abscess walls, and spread throughout the body. One important thing that can aid bacterial growth is the presence of a bit of material foreign to the body, such as the splinter that is still in your son’s finger. Phagocytes have a much more difficult time searching down and eradicating bacteria if there is something like that in the wound that gives the bacteria a place to hide.

You have now witnessed close up the complicated drama of what happens during what you may previously have thought was a simple matter—your child getting a small infection at the end of his finger. What you have seen are the early and middle stages of inflammation, the principal way our bodies fight off infections like the one on your son’s finger. The same sequence of events happens on a larger scale when the initial injury and bacterial invasion is much larger. The larger the battlefield, the higher the stakes. For even the smallest abscess, a child’s body usually benefits from a little help to handle the problem or at least to make it heal more quickly. Larger, more serious infections nearly always require help. So, having seen enough, you finally turn your craft around and leave the area. After all, you have to call the doctor’s office to find out what to do about all of this.

You can read about how the battlefield of inflammation heals in a later post.

Do drug ads in medical journals affect physician practice?

February 18, 2011  |  General  |  No Comments

Open any medical journal, including the most prestigious of them, such as the New England Journal of Medicine, and you will see page upon page of glossy advertisements from drug companies for their products. This has been going on for many decades. Do these ads affect physician behavior? Are we more likely to prescribe ones we read about?

There has always been a concern that advertising, not science, can affect doctors’ prescribing practices. Surely the drug companies think so, or they wouldn’t spend all the money on the ads. Now one medical journal, Emergency Medicine Australasia, has taken a stand against the practice; they’ve banned drug company advertising from their pages. In a recent editorial, they explained why.

This followed extensive debate on the growing evidence about the detrimental effects of the drug industry in medicine. Among the issues discussed were that the industry, one of the most profitable in the world, distorts research findings, such that drug company sponsored research is approximately four times as likely to be favourable to its product than independently funded research; authors of company-sponsored research are far more likely to recommend a company’s drug than independent researchers, and researchers with industry connections are more likely to publish data favourable to a company’s product than those without; selective reporting of results by industry is likely to inflate our views of the efficacy of company products; the drug industry has been shown to engage in dubious and unethical publishing practices, including guest and ghost authorship, and to apply pressure to academics to withhold negative findings; and the industry spends enormous amounts of money on advertising, which has been shown to change the prescribing practices of doctors, increasing sales in a dose-related manner to the volume of advertising.

Doctors, for their part, claim that such advertising has no effect at all on their prescribing practices. I know I would deny it. But really, how would I know? Advertisers put enormous effort into sending subliminal messages that work beneath the surface of our conscious radar. I could be manipulated as much as the next physician.

Drug companies value drug advertising in medical journals because it works. It is regarded as highly effective by pharmaceutical marketers, generating at least US$2-5 in revenue per dollar spent, with returns growing in the long term.

Not taking drug company ads has large financial consequences for journals, especially the second and third-rank ones; they more or less run on advertising revenue. The top ranking journals can depend upon high subscription fees; the lesser ones can’t. There are also many journals sent out to doctors that are actually free. We call them “throw-aways.” Trash cans next to the mailboxes in doctors’ lounges are stuffed with them. These can have a useful bit of information in them here and there, but mostly they are massive advertisements for the pharmaceutical industry. Doctors recognize this. But I think we’re less aware of the huge number of ads that appear in highly-ranked journals.

Emergency Medicine Australasia is a foreign journal, based in Australia, and has small impact on American physicians. But the principle they are arguing may well become a trend. I think the internet will help this, since the high costs of printing and mailing medical journals could be dramatically reduced by having the journals online only. Only a small paid editorial staff would be required, since the folks who review and decide on publication are nearly all unpaid as it is. (I used to do that a lot; you get an annual thank-you note for your efforts.)

I think it’s something to watch closely.

What inflammation looks like up close and personal, part III

February 9, 2011  |  General  |  No Comments

Here’s another snippet from the first chapter of my new book, How Your Child Heals. It’s from the chapter about inflammation, and follows from here. You’re finally arrived at the battlefield of inflammation, a sore finger, and are starting to observe what is happening there.

But why did those capillary walls open up and allow all those gaps to form? What could possibly be the usefulness of having all the contents of the blood vessel leak out into the surrounding tissue? You drive on, hoping to find the answer.

There are still many red blood cells passing by your window, but by now there is a vast number of neutrophils, too. There are so many of these and they are all moving along with you toward the end of the finger that it is clear that these amoeba-like creatures are traveling along in response to a signal, a sort of bugle call, which is summoning them to the battleground that is the inflamed fingertip. The summons takes several forms: one comes in the form of substances given off by the germs invading your son’s fingertip; another consists of substances that act as distress calls that are released by the cells living at the point of the enemy invasion; yet another comes from normal blood substances that are activated by all the cellular commotion.

The neutrophils are the foot soldiers in the inflammation wars. Most of the time they are called to fight outside invaders, like bacteria. They pick up the call for help, those released message substances, from the inflamed tissue and follow them exactly as a bloodhound follows a scent; like a bloodhound, the neutrophils can detect the concentration of these substances and keep going in the direction in which the concentration gets higher and higher, until at last they reach their target—the invading bacteria.

You are now moving toward the front lines of the battle, and as you get closer you pass many dead combatants. Bloated neutrophils are stuffed to overflowing with germs, bacteria which look like tiny round clusters of grapes. The neutrophils have engulfed them, eaten them. When they do that they are called phagocytes, a word that even derives from the Greek word “to eat.” There are other cells besides neutrophils that can be phagocytes, but neutrophils are the principal ones. Many of these cells are so full after their bacterial meal that they have broken apart and are merely drifting, dead after sacrificing themselves to destroy the invaders. The liquid around you is a murky soup made up of bits and pieces of cells and bacteria.

Those granular pellets you noticed earlier in the neutrophils are the bullets they use to kill the bacteria when they function as phagocytes. But as they fire off these bullets, the phagocytes themselves are injured beyond repair. Thus, a phagocyte is a sort of suicide cell that sacrifices itself for the good of our bodies. Fortunately, when needed, our bodies can pump out billions upon billions of these cellular soldiers in a very short time. This is why one of the most useful signs of an infection anywhere in our bodies is a increase in the number of neutrophils in our circulation. It is a test physicians use frequently.

Moving on, you explore the war zone a bit further. You suspect this is not a random fight, because there appears to be a method to the phagocytes’ operations. Although as far as you can tell there is no overall, guiding hand—no single commanding general—this army clearly has a coordinated plan. The effect is very much like watching an anthill: at first glance, the ants seem to be scurrying around to no purpose, but if you observe them long enough, you can discern an organized pattern. By converging from all directions on the zone where the bacteria managed to get through your son’s skin, the phagocyte soldiers surround and cordon off the danger area. A glance around the perimeter shows you how that happens. It is a marvel to see.

This battle, like any battle, has its front lines and its rear echelons. As the fight has been raging up front, you see that at the rear of the battle zone other participants have been busy. Behind the phagocytes there is a developing palisade—a stout wall—composed of tough, interlocking ropes. This material is called fibrin. It is also the stuff from which blood clots and scabs are made.

Fibrin is a solid material, but its building blocks are always circulating in the bloodstream, ready for use when needed. Several things can initiate the cascade of events that make the building blocks come together when needed to weave fibrin strands into a barrier. One of these is the debris of the fight, the bits of broken cells. Another is an impressive array of auxiliary cells—support troops—which answer the same call along with the phagocytes and join the scene of action. As the phagocyte soldiers battle the invading bacteria, these supporting cells in the rear erect a defensive barrier to wall off and contain the battle.

You can read about the battle’s conclusion and its aftermath in a later post.

Infant feeding practices and obesity study: an example of how people react to scientific data

February 8, 2011  |  General  |  No Comments

I read an interesting news report today by Liz Szabo in USA Today. It was about a recent article in Pediatrics, the official journal of the American Academy of Pediatrics. The article described an apparent association the authors found between early feeding of solid food (age younger than 4 months) and obesity at age 3 years. The association was only present in children who were formula-fed and not breast-fed. To restate: the authors found that, in formula-fed babies, early introduction of solid food was associated with being overweight at age 3. Early introduction of solid food in breast-fed babies had no effect.

What I found most interesting about Ms. Szabo’s article, although it was quite good, was the comment trail; it showed how most folks really don’t understand how to interpret medical studies. Some of the commentators denied the possibility of such an association because of their own experience with their children. Other commentators immediately leaped to the conclusion that the study authors were claiming feeding solids before the age of 4 months to your formula-fed infant would make them all fat. Still other commentators decried the “breast-feeding Nazis” who insist mothers who choose not to breast feed are negligent and try to make them feel guilty. If any of the commentators took the time to read the full study (it’s available free online here), they would have found that the authors make no such sweeping claims.

First of all, the study is observational. That means that the authors merely collected information about mothers and babies. There was no intervention, such as convincing mothers who chose not to breast-feed to nurse their babies, or vice-versa; the mothers chose, and the investigators merely watched what happened over the next 3 years. This approach leaves any study like this wide open to selection bias — the possibility that the 2 groups of mothers differed in some other way than feeding choice, possibly in a way that would influence that choice and future obesity in the children. The authors did examine a few possible confounders like this, education and family income, but there are many other possible ones.

What did the authors find, really? Well, they studied a total of 847 infants — 568 breast-fed, 279 formula-fed. Within those groups, 43 of the breast-fed babies started on some solids before 4 months (7.5%). In contrast, 91 of the formula-fed infants had started solids before 4 months (33%). So clearly mothers of formula-fed babies were more likely to start solids sooner, for whatever reason. That might matter for the ultimate results or it might not — there’s no way to tell.

At 3 years of age, 3 of the 43 breast-fed babies who had early solids were obese — 7%. In contrast, 23 of the 91 formula-fed babies were obese — 25%. To a statistician, that’s a significant number. It means there’s an association between 2 things. But it does not prove causation of anything. And note that 75% of the formula-fed babies were not obese at age 3, so personal anecdotes from commentators don’t mean much.

The bottom line to me is that this is an intriguing study, but it is far from the last word on it. And most of the irate commentators to the USA Today article complained about things that the authors of the article didn’t claim. So, whenever possible, it is good to read the original study before you decide anything — or get upset about it.