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.

What inflammation looks like up close and personal, part II

February 6, 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. The action picks up at the point where you, the reader, have taken your microscopic voyage to reach the smallest blood vessels in the body — the capillaries.

Before you reach the site of the action itself, though, you pause to look around at what is floating along with you in the bloodstream. It is a crowded thoroughfare because the diameter of the tube has become narrower with each branching of the way. When you were in the aorta and the larger arteries, things were simply shooting along too fast to see anything, but now the flow is more sluggish, and you can easily see your fellow travelers, the blood cells, out the window. Several of these cells are key to understanding how healing works, so this is a good time to look them over and learn a little about what they do.

You easily see there are two principal categories of cells. The vast majority, by a thousand-fold or more, are red disks with a dimple in the middle of each side. These are the red blood cells, and their only job is to carry oxygen. They accomplish this by being stuffed full, nearly to the exclusion of everything else, of a carrier substance called hemoglobin. When hemoglobin is loaded with oxygen it is bright red; when unloaded, it is darker in color. This is why oxygen-rich blood from the arteries is so red, whereas oxygen-depleted blood from the veins is a darker, reddish blue. The red blood cells go endlessly round and round the circulation, picking up fresh oxygen as they pass through the lungs and delivering it to the rest of the body. Healing body parts, such as injured fingers, require lots of oxygen.

Mixed in among the hordes of red blood cells, you see an occasional larger cell float by the window. Some of these are little spheres; others look more like jellyfish. Now that you are traveling slowly enough, you see that there is an especially large number of the jellyfish-type cells drifting languidly along the walls of the tube. Both the small spheres and the jellyfish are members of a family of cells called white blood cells. They are not really white, being more translucent in quality. They got their name mainly because they are not red and, when clumped together in a large mass, look whitish.

The jellyfish cells are called neutrophils. These creatures are moving along with you in particularly large numbers to your son’s sore finger, because they are key actors in the cellular drama of inflammation. Although their walls are translucent, like a real ocean jellyfish, you see that they are filled with dark, granular pellets.

You and the blood cells have now entered the narrowest portion of the capillary meshwork. The passageway here is very tight, being the same diameter of the blood cells or even less, which must squeeze through in places by deforming and squishing their elastic sides. Now that the walls are pressing upon your craft, you can see that, as was the case further back up in the artery, these walls are also made up of cells stretched flat and stitched together along their edges like a quilt. Unlike in the arteries, however, here there are substantial gaps along the seams between the cells. These gaps are small enough that the cells cannot slip though, but some of the fluid part of the blood, the river you are moving in, does seep out.

Then you spy just ahead a strange thing: a neutrophil, one of the jellyfish cells, has attached itself to the wall and is squeezing itself through one of the gaps. Neutrophils can slither and crawl along a surface, scrunching themselves between the tiniest of cracks between cells.

Finally you approach the scene. Your first sign of this is that the passageway walls have swollen back out, enlarged in size. This has created huge gaps in them. In fact, it is now difficult to tell if you are inside the capillary or outside it. The gaps are so big that quite a few red blood cells have floated out through the gaps into the surrounding tissue. There seems to be little distinction between the inside and the outside of the vessel. Since the walls are now as porous as cheesecloth, an even larger amount of the surrounding river of blood passes from the capillary.

What you are seeing from your microscopic window is the cellular basis of why an inflamed finger is red and swollen. Normal tissue does not have any red blood cells in it; they stay in the capillary network. The red cells function like long lines of boxcars laden with oxygen that pass through the capillary bed. As the train lumbers along it unloads its cargo of oxygen, which diffuses the short distance into the surrounding tissues to meet the energy needs of the cells there. Your son’s finger is intensely red on the tip because so many red blood cells have leaked out, leaving their usual track.

The leaky capillaries also show you why his finger is swollen and painful—all that fluid leaving the blood vessels stretches the tissues tight as a drumhead. The pressure inside his fingertip becomes dramatically higher than normal, and the increased pressure pushes on the exquisitely sensitive nerve endings there. The result is pain.

More about what happens next in a later post.

Where does fever come from?

February 4, 2011  |  General  |  No Comments

Here is an excerpt from my recent book, How Your Child Heals. It’s about fever, from the chapter about symptoms and signs.

Fever means an abnormal elevation of body temperature. But what is abnormal? Most of us have heard or read that “normal” is 98.6 degrees Fahrenheit, which is 37 degrees centigrade. In fact, normal temperature varies throughout the day. It is as much as one degree lower in the morning than in the afternoon, and exertion of any kind raises it. Where you measure it also matters. Internal temperature, such as taken on a child with a rectal thermometer, is usually a degree or so higher than a simultaneous measurement taken in the mouth or under the arm pit.

There is also a range of what is normal for each individual — not all people are the same. So what is a fever in me may not be a fever in you. As a practical matter, most doctors stay clear of this controversy by choosing a number to label as fever that is high enough so this individual variability does not matter. Most choose a value of 100.4 degrees Fahrenheit, or 38 degrees centigrade, as the definition of fever. It is not a perfect answer, but it is a number that has stood the test of time in practice.

We maintain our normal body temperature in several ways. Chief among them is our blood circulation. Heat radiates from our body surface, so by directing blood toward or away from our skin we can unload or conserve heat. We can also control body temperature by sweating — evaporation of sweat cools us down. We know how important a mechanism this is because the rare person who cannot sweat, or who is taking a medicine that interferes with sweating, has trouble keeping his body temperature regulated when he gets sick. If a swing in blood flow inwards to raise temperature happens very fast, we respond by shivering. This is also why we shiver if we go outside without a coat in the winter; our bodies are redirecting blood flow from our skin to our core in order to maintain temperature.

All parents know that a common cause of fever in children is infection. A more precise way to think about it is that a common cause of fever is actually inflammation. Since in children infection is the most common cause of inflammation, we generally assume a child with a fever has an infection somewhere in her body unless we can prove otherwise.

Our brains have a kind of thermostat built into them. Like the thermostat in a house, it senses the temperature of the blood passing by it and uses a series of controlling valves in the blood circulation to fine-tune the temperature. Also like your house thermostat, it continues to sense the temperature, and adjust it as necessary, until it has reached the value for which the thermostat is set. Fever happens when the thermostat is reset, just as happens when you twist the dial on the wall for your furnace — the body reacts to bring itself to the new setting. What twists the knob on the brain’s thermostat to cause fever are substances in the blood.

These fever-inducing substances belong to a family of inflammatory molecules that are released from body cells. Mostly they come from a cell called a macrophage, but germs themselves can also release things that have the same effect. The sudden rises and falls a parent often sees in their child’s temperature when they have an infection reflect the usually brief time these substances are in the blood. Sustained fever for many hours can happen if these materials are steadily present.

Opinions vary among doctors about when fever needs treatment. Fever itself virtually never causes harm on its own. The only times it can do harm is when it gets very, very high — 106 degrees or more — for a sustained period. That only happens in highly unusual situations; ordinary childhood infections never get it that high. It is true fever can make a child uncomfortable, although children generally tolerate it much better than adults. For that reason alone many doctors advise treatment.

There is another reason to treat fever. Toddlers may experience brief convulsions – seizures — when their body temperature rises very fast. These so-called febrile seizures cause no harm to the brain itself, and often run in families, but fever treatment makes good sense for a child who has had them in the past.

We have two effective drugs to treat fever — acetaminophen (Tylenol) and ibuprofen (Motrin). Both work the same way: they reset the brain thermostat back down to a lower lever. Both only last a few of hours or so in their effect, which is why you will see your child’s fever go back up again when they wear off if there are still any of those fever-causing substances from the inflamed site still in the circulation.

Just what is wheezing, anyway?

February 1, 2011  |  General  |  No Comments

The traffic analysis of this blog tells me that wheezing — what causes it and what we do about it — is one of the most common search terms that bring people here. It’s a common problem, and I’ve written some about it before. The fact that so many people are searching for information about it tells me that doctors may not be doing a great job in explaining what it is. This post will tell you what a doctor means by the word.

“Wheezing” is one of those words which, when commonly used by non-physicians means one thing (noisy breathing), but which means something else when doctors use it. So, when a doctor tells you your child is wheezing, what is she telling you? To understand that you need to know a little about the anatomy of the lungs.

The lungs are made up of two main components: tiny air sacs (called aveoli), where the business of getting oxygen into the blood stream happens, and the pipes that conduct the air down to the air sacs. This system of pipes begins with the largest of them – the windpipe (called the trachea) – in the throat. It ends with the tiniest of them – called the bronchioles – which are just before the air sacs. Think of the system as an immense tree: the trunk, branches, and twigs are the pipes, and the leaves are the air sacs. Here is a picture.

Wheezing is the noise that happens when the small airways have something blocking them. The blockage most commonly comes from constriction of the airways, but sometimes it may be from debris, such as mucus, obstructing the passage. The sound of air flowing past these choke points in the small airways makes a whistling sound – that is a wheeze. Most of the time it is a sound heard when a child breathes out, not in, because it’s more difficult to get air out than in so that’s when the problem is obvious.

We can hear wheezes with a stethoscope, but sometimes they are so obvious we don’t need one. A more subtle sign of wheezing is when a child takes more time to get air out with each breath than he does to breathe air in.

How do we treat wheezing? Since the most common cause is constriction of the small airways, we typically give inhaled medications to reverse the constriction.

Bottom line: when a doctor uses the word wheeze, we aren’t just describing noisy breathing. We mean a specific thing that has a specific treatment.

Respiratory syncytial virus (RSV): here today, gone tomorrow

January 28, 2011  |  General  |  No Comments

I’ve written before (here, here, and here) about RSV, one of the most common causes of respiratory illness in infants and toddlers, and the most common cause of illness severe enough to land them in the hospital. It’s so common that virtually 100% of children have gotten the infection by the time they’re two years old. RSV generally causes an illness called bronchiolitis. In this post I’ll tell you about why it causes such sudden and explosive epidemics.

I’ve hardly seen any RSV yet this year. But all of us know it will come; generally we see a few cases, quickly followed by an explosion of cases. The way RSV behaves in the population is fascinating. It’s also utterly predictable, based upon what we know about the properties of the virus and our immune response to it.

The first thing to know is that RSV is highly contagious — one of the most contagious of all viruses. It’s spread by droplets of respiratory secretions, and it can survive for several hours at least on objects, such as shared toys or cookies. Its attack rate, the number of people who are susceptible to the infection and who get it if exposed — is well over 90%. So once cases appear, if there is a large population of people susceptible to it, we would predict a lot of infections.

The second thing to know is that there is always a large number of susceptible people. This is because our immunity to RSV is not good; most of us, especially if we are exposed to small children, get the infection every few years. For some reason RSV doesn’t induce a very good immune response, so when we get it we don’t develop very good protective antibodies to it. This is why we haven’t been able to develop a vaccine against it.

It also explains why infants get it so easily. Babies are born with a dose of antibodies they get from their mothers, protection that lasts a couple of months or so. In the case of RSV, though, mothers can’t give them this protection. So they’re all susceptible, and it’s generally the infants, especially those born early, who have the most trouble from it. (Adults generally get only mild to moderate cold symptoms.)

So why do we have the explosive epidemics from RSV? The answer is that each year a whole new crop of susceptible infants are born for the virus to infect. That, plus the high attack rate, causes RSV to rampage through the population once a few cases appear.

Although all children will eventually get RSV, there are a few things you can do to reduce the chances of your infant getting it during the typical epidemic of mid to late winter and early spring. Simply postponing infection until your child gets out of infancy is very helpful, because older children rarely need to come into the hospital for treatment. Avoid close exposure of your infant to anybody who has cold symptoms, and have everybody wash their hands before handling your baby.

In sum, although RSV infection is a rite of passage in childhood, there are a few practical things you can do to keep your child out of the hospital.

Medical ethics, patient autonomy, and futile care

January 25, 2011  |  General  |  No Comments

A while back the New England Journal of Medicine carried an excellent editorial by Dr. Robert Truog, a highly-respected medical ethicist at Harvard. It is about futility of care. Recently I had occasion to read it again, and it’s still an excellent summary of the issues.

In it he describes a situation in which parents of an 18-month-old boy with a rapidly progressive, fatal neurological problem disagreed with the doctors over what to do. In his editorial, Dr. Truog examines the various ethical aspects of futile medical care: pain and suffering, patient (and family) autonomy, and healthcare costs. I recommend the essay to anybody interested in these issues, especially after all the talk of “death panels” last year during the healthcare debate.

Most experienced pediatric intensivists, myself included, have encountered situations in which we, the doctors, believe continuing to support a child is unethical because it is not saving the life but prolonging the dying, whereas the child’s parents believe the opposite—that it is unethical to withdraw life support because all life is sacred, no matter the circumstances. Sometimes these situations arise because poor communication causes families to distrust the doctors. But sometimes both sides understand each other clearly, but still disagree profoundly about the proper thing to do. What happens then?

Doctors often make the argument that we should not prolong suffering. Establishing if a patient is actually in pain can be difficult, and anyway we virtually always have the means to relieve pain in these situations. More telling to me is the argument that families cannot compel physicians to act unethically, and most of us regard futile care as unethical. Yet even then the physician can simply withdraw from the case, although from experience I can tell you it is difficult to find another physician to take on cases like this, and abandoning our patient without finding them another physician is clearly unethical (and illegal).

What to do? I have been involved in several cases like the one Dr. Truog describes. Thankfully, in all but one the family and the doctors were ultimately able to reach an understanding both sides accepted. In the one case in which we could not agree, nature ultimately decided things for us, as she often does.

Stories like these remind me that the pediatric intensive care unit is a place where, if we pay attention, we can learn a great deal both about life and about ourselves.

Disparities in payments to providers for Medicaid vs Medicare: a legacy of racism

January 20, 2011  |  General  |  10 Comments

In all the noise of our current debate over government funding of healthcare, most people seem unaware that the government — federal and state — already pay half of our nation’s healthcare bills. Although some of this funding comes through the Veteran’s Administration system, the bulk of it is in the form of two government programs — Medicare and Medicaid. Again, most people lump them together in their minds. Physicians and hospitals, however, realize that, although the two programs were begun at the same time in the mid-1960s, they are very, very different.

Medicare is the federally funded program that cares for the elderly. We pay into the program with a payroll tax and are generally eligible for coverage under it when we reach age 65. Everybody is eligible, regardless of income. In contrast, Medicaid is a program jointly funded by the federal government and the states. It is for children of low-income families, pregnant women, and the disabled. (This is slated to change with implementation of the Affordable Care Act, aka Obamacare, with low-income adults also eligible.) The ratio of federal money to state money in Medicaid varies — the federal contribution is higher for poorer states — but for most states the number is about fifty-fifty.

That’s the funding side. Looking at the payment side, the money paid out to hospitals and doctors shows a huge disparity between Medicare and Medicaid that few people outside healthcare know about. Medicare typically pays much more to the provider than Medicaid does FOR THE EXACT SAME SERVICE. You can read more about the details of this disparity, which the Affordable Care Act also aims to change, here. As with all things about Medicaid, it does vary from state to state. But it is not unusual for a physician to be paid ten times as much by Medicare for the same thing. Why is this?

The fundamental reason is that, when Medicaid was established, the Congress needed to compromise to get it passed. That compromise needed to accommodate Congressmen who were frank racists, mostly Southern Democrats. As Timothy Jost wrote:

The fact that Medicaid is a federal-state cooperative program, rather than a national program like Medicare, is an artifact of a history of which we should not be proud. It is in part the history of trying to keep poor people on relief under the thumb of local government, where their lives could be managed more closely. It is also in part the history of racism, with which President Roosevelt had to come to terms to get his New Deal programs past Southern Democratics in Congress who insisted on control over who got welfare and how much.

A huge proportion of poor people in the South during the 1960s were black. And Congress wanted to make sure of two things: not as much money would be spent on them; and the individual states could keep the medical care the poor received worse than that of more affluent people by the simple expedient of paying doctors and hospitals less money to deliver it.

The effects of this huge disparity in reimbursement has had predictable effects on physicians, who frequently lose money with every Medicaid patient they see. Not surprisingly, six times as many physicians refuse to see Medicaid patients as refuse to see Medicare patients.

It’s all a sorry legacy, and its correction is a key component of the Affordable Care Act.