Posts Tagged ‘book’

Medical ethics: a brief primer

April 4, 2011  |  General  |  1 Comment

Medical ethics is something we deal with frequently in the PICU. It may sound esoteric, but generally it isn’t. Even so, it can be complicated. Complicated or not, it’s also something all of us should know a little about. This is because, in fact, many of us will encounter its issues quite suddenly and unexpectedly with our loved ones, or even ourselves.

So what are the accepted principles of medical ethics? There are four main principles, which on the surface are quite simple. They are these:

1. Beneficence (or, only do good things)
2. Nonmaleficence (or, don’t do bad things)
3. Autonomy (or, the patient decides important things)
4. Justice (or, be fair to everyone)

The first of these principles, beneficence, is the straightforward imperative that whatever we do should, before all else, benefit the patient. At first glance this seems an obvious statement. Why would we do anything that does not help the patient? In reality, we in the PICU are frequently tempted to do (or asked to do by families or other physicians) things that are of marginal or even no benefit to the patient. Common examples include a treatment or a test we think is unlikely to help, but just might.

There is a long tradition in medicine, one encapsulated in the Latin phrase primum non nocere (“first do no harm”), which admonishes physicians to avoid harming our patients. This is the principle of nonmaleficence. Again, this seems obvious. Why would we do anything to harm our patients? But let’s consider the example of tests or treatments we consider long shots — those which probably won’t help, but possibly could. It is one thing when someone asks us to mix an innocuous herbal remedy into a child’s feeding formula. It is quite another when we’re considering giving a child with advanced cancer a highly toxic drug that might treat the cancer, but will certainly cause the child pain and suffering.

Our daily discussions in the PICU about the proper action to take, and particularly about who should decide, often lead us directly to the third key principle of medical ethics, which is autonomy. Autonomy means physicians should respect a patient’s wishes regarding what medical care he or she wants to receive. Years ago patients tended to believe, along with their physicians, that the doctor always knew best. The world has changed since that time, and today patients have become much more involved in decisions regarding their care. This is a good thing. Recent legal decisions have emphasized the principle that patients who are fully competent mentally may choose to ignore medical advice and do (or not do) to their own bodies as they wish.

The issue of autonomy becomes much more complicated for children, or in the situation of an adult who is not able to decide things for himself. Who decides what to do? In the PICU, the principle of autonomy generally applies to the wishes of the family for their child. But what if they want something the doctors believe is wrong or dangerous? What if the family cannot decide what they want for their child? Finally, what if the child does not want what his or her parents want — at what age and to what extent should we honor the child’s wishes? As you can see, the simple issue of autonomy is often not simple at all.

The fourth key principle of medical ethics, justice, stands somewhat apart from the other three. Justice means physicians are obligated to treat every patient the same, irrespective of age, race, sex, personality, income, or insurance status.

You can see how these ethical principles, at first glance so seemingly straightforward, can weave themselves together into a tangled knot of conflicting opinions and desires. The devil is often in the details. For example, as a practical matter, we often encounter a sort of tug-of-war between the ethical principles of beneficence and nonmaleficence — the imperative to do only helpful things and not do unhelpful ones. This is because everything we do carries some risk. We have different ways of describing the interaction between them, but we often speak of the “risk benefit ratio.” Simply put: Is the expected or potential benefit to the child worth the risk the contemplated test, treatment, or procedure will carry?

The difficult situations, of course, are those painted in shades of grey, and this includes a good number of them. In spite of that, thinking about how these four principles relate to each other is an excellent way of framing your thought process.

If you are interested in medical ethics, there are many good sites where you can read more. Here is a good site from the University of Washington, here is a link to the President’s Council on Bioethics (which discusses many specific issues), and here is an excellent blog specifically about the issues of end of life care maintained by Thaddeus Pope, a law professor who is expert in the legal ramifications. If you want a really detailed discussion, an excellent standard book is Principles of Biomedical Ethics, by Beauchamp and Childress.

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.

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.

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.

Removing infant cold medicines from the market has reduced untoward events from them

December 1, 2010  |  General  |  No Comments

No pediatrician I know has ever liked any of the many over-the-counter cough and cold remedies very much, especially for very young children. There never has been any evidence that they help cold symptoms, and what’s in them (typically a decongestant and an antihistamine) can cause actual harm to children. Risking harm for dubious benefit is never a good trade-off in medical practice. I’ve seen more than a few kids over the years need to be admitted to the PICU because they have overdosed on these medications, either because they got into the meds and took them themselves or because their parents miscalculated the dose and gave too much.

Recognizing the problem, the makers of these products agreed voluntarily three years ago to take the ones intended for children less than two years of age off the market. These were usually various kinds of drops. Did this new policy have any effect? A recent study in the journal Pediatrics, the official journal of the American Academy of Pediatrics, suggests that it did.

The authors looked at emergency room visits before and after the product withdrawal went into effect. They sampled sixty-three representative pediatric emergency rooms across the country. What they found is that the number of trips to the ER for untoward effects from these medications — overdoses or just funny reactions — dropped by half. Such ER visits for children older than two did not change. Of course, as we say, correlation doesn’t prove causation, so it may have been a coincidence. But I don’t think so — I think the new policy helped.

It’s good that ER visits from the ill effects of over-the-counter cold remedies dropped for young children, but there still were too many of them — 1,248 in the sample hospitals. That’s a lot of risk for no benefit at all. For children over two years of age, there were nearly ten thousand ER visits for this problems. That concerns me just as much. Roughly two-thirds of the cases were ones in which unsupervised children took the medicine themselves, but fully a third of them were because parents gave the children the medication. My advice — don’t use these agents unless your doctor suggests them, and never in children less than four.

Every parent should know where to find the number of their local poison control center — it’s generally in the front pages of the telephone book. Call them if you have any questions about drug effects — they are always very helpful and you might save yourself and your child a trip to the emergency department.

Reminders: another simple, low-tech way to reduce hospital infections

August 20, 2010  |  General  |  2 Comments

There’s a best-selling book out about how simple checklists can prevent complications of medical treatments. It’s simple, the lowest of low tech, requires no expensive equipment, and it works. It seems a bit sad that we need research to confirm common sense. Now a new study describes how yet another very simple thing can reduced complications — simple, automated reminders.

Medical care in the PICU is quite complicated at times and the pace is often hectic. When we are going from patient to patient we focus on the major stuff — the mechanical ventilator, for example. It’s easy to overlook smaller items; smaller items which, in the longer term, can become much bigger things. Urinary catheters are an example of this.

We use these tubes to drain urine out of the bladder of a patient who is unable to urinate themselves. They’re useful and handy. But urinary catheters do carry some risk of infection, especially if they are left in for a long time.

A recent study showed that simply asking the doctor — prompting them with a small reminder each day — if the catheter was still needed led to a 50% drop in catheter-associated infections. It’s simple, easy, and cheap. It’s something I now have on my daily checklist for each patient.

Patient safety: when doctors are the problem

July 31, 2010  |  General  |  No Comments

We’ve always know that hospitals can be dangerous places for patients. In a landmark study some years ago, the Institute of Medicine, a part of the National Academy of Sciences, demonstrated just how dangerous they can be; anywhere from 50,000 to 100,000 people die annually from preventable errors. How are we doing at reducing that grim statistic? The answer is that we are making some progress, but there remain serious roadblocks.

The deaths studied by the Institute of Medicine came from a whole host of causes, and many of these causes are complex and difficult to address. But it turns out that one cause — serious infections from central venous catheters — can be easily improved. We can’t prevent all of these infections, but we can dramatically reduce them. The way to do this is absurdly simple and the lowest of low-tech: use a checklist that ensures basic procedural steps are followed in the correct order. Hospital safety guru Peter Pronovost demonstrated this some years ago. Checklists for all sorts of procedures are useful. Well-known medical author and surgeon Atul Gawande had even written a best-selling book about them. So what’s the problem? The answer is that the problem is often doctors and our medical culture. A recent editorial by Dr. Pronovost helps explain why. (The editorial is from the Journal of the American Medical Association, which requires a subscription. If anybody wants a copy, let me know.) Here’s the crux of the problem, as described by Dr. Pronovost:

“Although most physicians and hospital leaders genuinely want to prevent harming patients, and many physicians practice good teamwork, this view of not questioning physicians is pervasive. Physicians are often rushed, sleep deprived, and overworked and are offered limited training about teamwork and conflict resolution. The practice setting is not always conducive to completing recommended practice and anything that takes extra time for one patient (eg, searching for supplies) detracts from the care of others. Physicians also may not receive feedback on individual performance or hospital infection rates. Social, cultural, educational, and financial differences between physicians and nurses also may inhibit some nurses from speaking up, even when physicians may welcome such feedback.

Moreover, many physicians have not accepted that fallibilities are part of the human condition. Thus, when a nurse questions them, it causes embarrassment or shame. Clinicians are sometimes arrogant, believing they have all the answers, dismissing team input, responding aggressively when questioned. The line between autonomy and arrogance is fine and nuanced. Society has benefited tremendously from physician autonomy and innovation, producing new drugs, devices, therapies, operations, and anesthetics. Therefore, autonomy and innovation must be continued. However, autonomy becomes arrogance when actions are mindless and not mindful, when something is done simply because a physician demands it, when a clinician does not learn from mistakes, and when experimentation occurs without a clear rationale or testable hypothesis. Too often autonomy is mindless and driven by arrogance. When placing a catheter, reliability not autonomy is needed.

As Pogo said many years ago: “We have met the problem, and he is us.”

What inflammation looks like up close and personal, part I

July 29, 2010  |  General  |  No Comments

Here’s a snippet from the first chapter of my new book, How Your Child Heals. It picks up at the point where you, the reader, have begun a microscopic voyage to see what an infected splinter looks like from the perspective of inside your child’s body.

Now that you have had the full-sized, outside view of what happened to your son’s finger, it is time for you to go inside to places where the ancient physicians could not go. It is time to take a seat in the audience of the microscopic drama. You are about to make the first of several trips you will make throughout this book in a tiny, imaginary, high-tech vessel. Think of it as a cross between a submarine and an all-terrain vehicle; it can swim in the blood stream or leave the circulation to crawl around between the cells of the body. It is well-equipped with spotlights and spacious windows, allowing you to see what is happening all around you. The dramatic setting for your first foray is the time just before you called the doctor’s office to ask what to do about it.

The blood vessels in the body form an immense, self-contained system that is divided into two halves. We need oxygen to live, and one half of the circulation, the arteries, carries oxygen-rich blood out to all the parts of the body, down to the tiniest places. The other half, the veins, brings oxygen-depleted and carbon dioxide-laden blood back to the lungs to get more oxygen, which we breathe in, and dump the carbon dioxide waste, which we breathe out. The two halves of the circulation join in a microscopic meshwork of vessels called the capillaries. This is where the true business of circulation happens, where oxygen and other important nutrients get delivered to the body’s cells.

The capillary bed of your son’s throbbing finger is the key place to visit as you investigate what is causing all the problems, but to get there you must first get inside his circulation. You need a location where the tiniest of blood vessels are accessible, close to the surface. The lining of the eye is such a place.

Imagine you begin by poising your craft at the base of one of his lower eyelashes. You look over the edge into the wet, shiny world below. Your son momentarily pulls down his lower lid, revealing the pink inner lining of his lower lid, called the conjunctiva. You seize your chance, zip over the edge, and find yourself motoring about in the clear liquid of his tears, nature’s way of keeping our eyeballs moist. Here there are blood vessels close at hand, just below the surface. You slide your craft into the nearest one and then drift along with the stream, ever faster, as it takes you toward the heart.

You do not stay in his heart long, though, because nothing does. The blood rockets out of the heart like a fire hose because the heart pumps an enormous amount of blood very quickly. A typical adult heart, for example, sends out about a gallon and a half of blood every minute, proportionately less in a child. The effect on your vessel is the equivalent of taking a trip over Niagara Falls. You get bounced around, but soon find yourself in the aorta, the large vessel exiting from his heart.

The aorta is wide and fast, but it soon divides, then subdivides, into multiple rounds of ever smaller vessels. As this branching happens, the velocity of the stream in each of them slows down dramatically. Within seconds after leaving his heart you are scooting down one of these tributaries, headed for his painful index finger.

Things were moving so fast in the aorta and the first couple of branchings that you could not see any details in the surrounding walls of the blood vessels. Although you are going slower now, your pace is still a brisk one, and the flow still pulses along–now faster, now slower–in rhythm with your son’s heartbeat. Soon the stream slows down enough for you to get some idea of just what kind of pipe you are traveling through. The first thing you see when you shine a light at the walls is that the surface is covered by a bumpy layer of cobblestone-appearing cells. The junctions between these cells make a completely watertight barrier; no blood can leave this sealed pipe, and thus you cannot see what is going on in the tissues outside of it.

You soon find you are slowing down even further as you come closer to the sore on his finger, and you notice a dramatic change in the walls of the blood-filled passage you are passing down. For one thing, the wall of the tube is now translucent; you can shine your light right through and get a hazy view of what lies beyond. There are now some small gaps between the pavement of flat cells that makes up the walls, but the cells still mostly touch one another along their edges.

You have reached the capillaries. In real life there would be millions upon millions of options for you to have chosen on your trip from the aorta as the tubes branched into ever smaller pathways, but for our purposes we assume your miniature craft has the proper instruments to sense the correct path among the myriad of choices to lead you to the sore spot on your son’s finger.

What causes diarrhea in children?

July 10, 2010  |  General  |  1 Comment

Here’s another excerpt from my new book, How Your Child Heals. It’s from the chapter on symptoms, and it’s about what causes diarrhea.

Diarrhea, the frequent passage of watery stools, is something with which most parents of small children are well acquainted. It is a common symptom because its most common causes, intestinal viruses, are all around us. There are many of these for a child’s immune system to meet as it matures. Each new encounter usually causes illness, but subsequent exposures often cause few or no problems. These viruses are highly infectious, so they spread easily wherever toddlers gather to share toys and cookies. The result is what doctors call gastroenteritis, a fancy term for an inflamed stomach and intestines.

Other things besides viruses can cause diarrhea, but most of these cause it in the same way intestinal viruses do — injuring the cells lining the intestines so they cannot do their job of absorbing the nutrients passing by them. A wide variety of food intolerances can also lead to diarrhea, often because the absorbing cells, though present in the intestine, are in some individuals unable to deal with a particular food properly. Common examples of this include a deficiency of the absorbing cells that process lactose, a type of sugar in dairy products, or a sensitivity to the proteins present in cow’s milk. Whatever the cause of the poor functioning of the absorbing cell lining, the result is often diarrhea. If there is significant stretching and squeezing going on in the intestine the child will often have cramping pain, too.

When the intestinal lining is injured, it cannot do its job of absorbing food. If a large amount of unabsorbed food makes it to the lower reaches of the small intestine, it draws water out of the intestinal wall. It also becomes excellent food for all the bacteria living there, and the action of the germs gorging themselves on this sudden feast produces even more substances that draw water into the intestine. When this mixture is dumped into the large intestine, the enormous mass of bacteria normally living there magnifies the effect. The large intestine can absorb quite a bit of water, but it can become overwhelmed by the volume of what it is being asked to take in. Plus, its lining cells may themselves be injured by the infection and be less able to do their job.

These things makes the stools watery. Diarrhea also means more frequent stools. The simple increase in the amount of material the intestines must deal with is one cause of the more frequent stools. Another is that most causes of diarrhea also speed up the transit time, the length of time it takes what a child swallows to pass all the way through.

There is another kind of diarrhea, one less common in children. This disorder is of the large intestine, the colon, and is called colitis because that word means an inflamed colon. It is typically caused by one of several varieties of infectious bacteria. Since the colon can become quite irritated and inflamed, the diarrhea of colitis often has blood in it from oozing off the intestinal wall. It is usually a more serious illness than simple gastroenteritis of the upper reaches of the intestine. This is why seeing blood in your child’s stools is a reason to visit or call the doctor, especially if your child has fever as well.

We have several ways to deal with diarrhea, the first of which is to do nothing other than make sure your child is getting enough fluid to replace that lost in the stools. This is how doctors usually handle the situation, because typical gastroenteritis is quite self-limited and will pass soon. When it does, the damaged absorbing cells very rapidly replace themselves on the villi and all is well. If it persists for many days, that is a reason to suspect something else is causing it.

Simple common sense teaches us we should not challenge the intestines of a child with diarrhea with large meals full of complex, difficult to absorb foods, because the poorer the absorption, the worse the diarrhea potential. Parents have known this for generations. This is the rationale for using smaller, more frequent meals of simple starches like rice and bread, or even of eliminating all solids for a day or so. There are several ways of approaching this issue, but many parents find out by trial and error which dietary manipulations work for their children and which ones do not.

We do have several drugs to treat diarrhea, most of which work by slowing down the transit time through the intestines. Lomotil is the brand-name of a commonly used one. These drugs affect the intestinal nerves that control how fast the intestines squeeze the food along, slowing down the process. They work well in adults, although you can easily see how it is possible to overshoot and end up with constipation. However, doctors rarely recommend these drugs for small children because, as with the nausea and vomiting medicines, the potential side effects outweigh any benefit of using them for a condition that usually quickly passes without treatment.