Sometimes an interesting thing happens on patient rounds. Rounds are a traditional exercise in hospitals going back at least a century. In the old days, this meant the physician going from patient to patient. He (it was nearly always he back then) went over the patient’s progress with the bedside nurse, examined the patient, reviewed pertinent test results, made an assessment, decided on a plan for the day, and gave orders to implement the plan. He also explained things to the patient. That traditional system worked fine when there was only one physician running things. These days there are many caregivers involved, and intensive care units pioneered the practice of multidisciplinary rounds. What those amount to is an often fairly large group of people going together from patient to patient. Typically in the group are the bedside nurse(s), physician(s), which at an academic center includes residents, fellows and medical students, pharmacists, dieticians, physical therapists, and assorted other people involved in the patient’s care. It can be a large group, so large that some ICUs I know of hold these “rounds” sitting down around a table in a conference room.
I am often struck by the language people use at these rounds. In particular, there is an intriguing lack of assigning agency to what is going on. This is accomplished by extensive use of both the passive voice and strange sentence constructions in the third person: “The patient was thought to have pulmonary edema,” for example. Who thought this? “The patient was given furosemide (a medication to induce water loss).” Who gave this? They did — you know, them. Or you’ll hear something like this: “The patient was thought to have decreased cardiac function so an echocardiogram was ordered.” Who thought this and who ordered the test? Why did whoever it was think this?
In today’s ICUs there’s a lot of shift work. Nurses typically work 12 hour shifts. Resident physicians now also work shifts, since limits have been placed on how much time they can work without relief. Often the only person who has been caring for the patient on successive days is the attending physician, the leader of the care team. A nurse or resident, someone who has not been caring for the patient consistently (or ever before) may only know what other people have told them. There is also the medical record, of course, but in these days of the electronic medical record there typically is a huge amount of extraneous stuff in the computer that obscures one’s ability to figure things out. (I’ve written about this issue before.) This can make for some amusing — or discouraging — exchanges on rounds. “They were thinking the patient might be in heart failure so they got an echocardiogram.” At which point I need raise my hand and point out “they” was me.
The old game of telephone (also known as the Chinese whispering game) is where people explain the same incident to a successive chain of listeners. The story unavoidably gets altered a bit with each retelling such that after a few rounds key details get left out, wrong ones get added, and it can transform itself into a completely different tale. I have seen that happen many times in the ICU setting. Now and then I have to rummage through the medical record to track down the source of whatever it is and call that person to get the story. You know, the old fashioned technique of one colleague talking to another, one who has first hand knowledge of events. These days that often seems a quaint old practice.
In today’s complex hospital environment, especially at academic centers with resident physicians, it is uncommon for the same physician to admit a patient, care for him throughout his hospital stay, and then dismiss him. At one of the smaller hospitals where I work I actually do this frequently because I cover the PICU for a week-long chunk of time all by myself. The nurses change, though. So now and then I hear from one of them at morning bedside report about the mysterious “they” doing this or that when “they” is really just me.
The telephone game illustrates the problem with handoffs, times when care of a patient is transferred from one individual to another. Handoffs happen at both the nursing and the physician level. They are made necessary by the way shift work happens, but they are known to be fraught with danger. Many standardized communication tools are now available to reduce the risk of things getting missed or misrepresented but none of them are perfect. My advice is, when things are murky, to take a big breath and dive down the rabbit hole of the electronic record and identify when and why the thing started. Then if necessary call the person involved. Of course that takes time, precious minutes we often don’t have. That’s another problem for another day.
The following is from this recent study. It’s from Pediatrics, official journal of the American Academy of Pediatrics. That’s a medical journal, but the introduction to the paper is so clearly written as to be understandable by anyone that I’m quoting it pretty much as written.
Approximately 1.6 to 3.8 million sport/recreation-related concussions (SRCs) occur annually in the United States. In 2007, there were 250 000 emergency departments visits for SRC, more than double the rate in 1997. Concussions result in symptoms (eg, headache, dizziness, nausea), impairment (eg, cognitive, vestibular, visual), academic and/or psychosocial problems, and recovery times ranging from days to months. Adolescents are at greatest risk for SRC and experience longer recovery than adult athletes due to maturation or other unknown etiology. Clinical guidelines recommend immediate removal from play if an athlete has a suspected SRC. These guidelines are based on . . . research indicating compromised neurometabolic function during the first 10 days’ postinjury that increases the risk of a subsequent SRC. These guidelines are also intended to reduce the risk of second impact syndrome, a rare but catastrophic condition that involves the loss of cerebrovascular autoregulation and brain herniation, and is often fatal among adolescent athletes who sustain brain injuries in short succession.
I’ve seen a death from second impact syndrome. The second head injury that produced it was a trivial tumble down 2 carpeted steps.
The Centers for Disease Control’s Heads Up concussion education program states, “It is better to miss one game than the whole season.” However, due to many factors, including the culture of sports (ie, play through injury), poor awareness of the signs and symptoms, and limited access to medical professionals, an estimated 50% to 70% of concussions go unreported/undetected. In fact, in 2013, the Institute of Medicine and National Research Council stated that the culture of sports negatively influences SRC reporting and that athletes, coaches, and parents do not fully acknowledge the risks of playing while injured.
There is immense social pressure to ignore the symptoms and keep playing.
Researchers suggest that exposure to physical activity immediately after concussion decreases neuroplasticity and cognitive performance and increases neuroinflammation. The physical exertion required for an athlete to remain in play after SRC may increase energy demand at a time when the brain is metabolically compromised and lead to similar outcomes reported in animal models. Axonal injury, astrocytic reactivity [two kinds of brain cells], and memory impairment are also exacerbated following a second injury 24 hours after an initial injury. The potential effects of continuing to play with an SRC have yet to be examined in adolescent and young adult athletes at risk for these adverse outcomes. The present study compared recovery time and related outcomes between athletes with an SRC who were immediately removed from play and athletes who continued to play with an SRC.
Understand this: a concussion, defined as a transient interruption in brain function, is brain damage. Just because we don’t yet have a specific scan or test to document the damage doesn’t mean it’s not there. The symptoms described above are proof enough. The good news is that the damage generally heals if allowed to do so. But if we don’t allow the brain to heal, repetitive injury leaves lasting damage. The recent recognition among professional football players of what is currently termed chronic traumatic encephalopathy is chilling evidence of what can happen. We don’t know what the lower threshold for causing this entity is — how much recurrent injury is required to produce it — but it has recently been identified in college football players.
So if your child suffers a concussion follow the rules, no matter what the coach or your overeager child wants. We’re talking about the brain here. This article well demonstrates that we’re not protecting our children well.
A manifesto has been making the rounds on Twitter (and other places) over the past year. It has been attributed to Dr. Mike Ginsberg, a California pediatrician. It reportedly was originally a Facebook post that has since been taken down, perhaps because of the controversy it generated. I can understand why — vaccines are a hot button topic and anyone who writes about them attracts attention, some of it unpleasant. I know that’s happened to me. Anyway, here’s the quotation attributed to Dr. Ginsberg:
In my practice you will vaccinate and you will vaccinate on time. You will not get your own “spaced-out” schedule that increases your child’s risk of illness or adverse event. I will not have measles-shedding children sitting in my waiting room. I will answer all your questions about vaccine and present you with facts, but if you will not vaccinate then you will leave my practice. . . . .
I have patients who are premature infants with weak lungs and hearts. I have kids with complex congenital heart disease. I have kids who are on chemotherapy for acute lymphoblastic leukemia who cannot get all of their vaccines. In short, I have patients who have true special needs and true health issues who could suffer severe injury or death because of your magical belief that your kid is somehow more special than other children and that what’s good for other children is not good for yours. This pediatrician is not putting up with it.
Never have, never will.
These are strong words indeed, and they came out of the context of the recent measles epidemic experienced by California that was driven by unvaccinated children. I’ve seen it percolate around social media and wondered how common his (assuming it’s his) stance is. Of interest is that California recently passed legislation severely restricting the ability of parents who send their children to public schools to opt out of vaccinations. A recent article in the journal Pediatrics, the official journal of the American Academy of Pediatrics, gives us some answers about how widespread Dr. Ginsberg’s viewpoint is. The title of the article was “Vaccine delays, refusals, and patient dismissals: A survey of pediatricians.”
The authors compared two surveys done on a random sample of pediatricians who belong to the American Academy of Pediatrics (nearly all do). The first was from 2006, the second from 2013. It found the percentage of pediatricians dealing with families that refuse standard vaccination schedules has risen from 75% to 87%; in other words, most practicing pediatricians encounter this. The survey also asked what reasons the parents gave for declining to vaccinate. The pediatricians perceived that, although most parents declined out of fear of vaccine toxicity, a rising number — 73% in 2013 — did so because they believed they are not necessary. What has changed significantly is what pediatricians do in this situation. The percentage of pediatricians who will dismiss from their practice families who do not vaccinate has doubled, from 6% to 12%.
This is a complicated issue. Dismissing a patient from one’s practice is a formalized process that may take several months. Common reasons include nonpayment of bills or repeated failure to follow treatment advice, vaccinations in this case. There is a legal process for doing this that involves written notification. That’s the legal part. Ethically, physicians have a duty to care for their patients. When you “fire” a patient from your practice, you have a duty to help them locate another physician. Meanwhile you should continue to care for them. The fallout from this varies significantly depending where you are. As near as I can tell, Dr. Ginsberg practices in Northern California near a large metropolitan area. He is also part of a large group. So there should be plenty of other pediatricians in the area. But what if there aren’t? And what if what the patient wants is so far outside the mainstream that no physician will accept them? Are the physician and the patient stuck with each other?
It appears to me some pediatricians are handling the issue by refusing to accept new patients who won’t vaccinate. This approach gets around the problem because in that case the physician has no duty to care for the prospective patient. That’s not good enough for pediatricians like Dr. Ginsberg and, apparently, now 12% of all America’s pediatricians. We will have to see if this trend continues.
You should not have to guess my own view on vaccines. I trained in the subspecialty of pediatric infectious diseases before I trained in pediatric critical care. I well recall the severely damaged or dead children from, for example, H. influenza infection. The current HIB vaccine has eliminated this scourge. I also have an advanced degree in history of medicine, and have studied epidemics over time. Vaccines have had an enormously beneficial effect. Recall the famous line of Santayana: “Those who cannot remember the past are condemned to repeat it.”
Asthma is a complex, chronic lung problem that now affects nearly 10% of all children. Both the incidence of new cases and the prevalence of ongoing cases in the pediatric population have been rising steadily for years, although there are hints these increases may have leveled off. A wealth of research suggests a huge part of asthma causation comes from the environment the child lives in, things like air quality and exposure to various agents. Some children have clear-cut allergies as a contributing factor, but the majority don’t. Genetic factors also play a role, probably because the way the lung responds to these various things is a tendency we inherit. Exactly what might be triggering the rise in asthma has been debated for many years. Candidate causes include a more sedentary lifestyle in children, increasing childhood obesity, and increasing urbanization of our country. A century ago most people lived on farms; now most don’t. This possibility is the subject of a recently published and fascinating study in the New England Journal of Medicine. The authors were curious about asthma rates and causation in children who live in the traditional, rural setting typical many years ago. There are some data children raised on traditional dairy farms with early exposure to farm animals have a reduced risk of asthma. The investigators used a clever comparison between two groups of children: Amish children in Indiana and Hutterite children in South Dakota. Both of these are religious groups descended from seventeenth century Pietistic sects originating in Europe.
I have had many Amish patients in my career, but not any Hutterites. They are similar in lifestyle but there are some key differences that the authors of the study used to get at studying asthma. The Amish are predominately farmers, although I have known many who are not. Amish farming practice is straight out of the 19th century. They use no power machinery. They use horses to plow, they manure their fields as their great-great grandparents did, and they use horse-drawn implements to harvest their crops. If they have dairy cows, they milk them by hand into a bucket. The religious practices of Hutterites are very close to those of the Amish, but their farming practices definitely are not. The Hutterites live communally and use modern machinery on highly industrialized modern farms. The comparison between the two groups is useful because in other respects they have very similar lifestyles in things believed to be important for asthma risk. These include large families, minimal exposure to urban air, prolonged breast feeding, no indoor pets, minimal exposure to tobacco smoke, and low rates of obesity. They also have very similar diets and similar genetic backgrounds. Going into the study the authors already knew the prevalence of asthma for Hutterite children was 21% (a high rate) versus only 5% in Amish children. Why the difference?
The investigators measured many things, but key among them were studies on dust samples collected from the children’s environments. They analyzed the microbial makeup of these samples, as well as used them to challenge the lungs of mice in an experimental asthma model. They also looked at several markers of immune function in the blood cells of the two groups of children. What did they find?
The results are a bit complicated, and if you want the details look at the article. There’s also a good editorial accompanying it. The bottom line is that the innate immune response of the Amish children was profoundly different from that of the Hutterite children, and this difference appeared to be shaped by exposure to very different microbial agents in the environment as measured in the dust samples. More than that, the dust samples from the Amish farms actually protected the mice in the animal model from an asthma attack. That’s amazing. Maybe we should be treating asthma with Amish farm dust? I’m not serious, of course, but the study does suggest some reasons why the change from a traditional farming way of life to the way we live now may be part of why asthma is now so common. Early and sustained exposure to certain microbes may be a good thing, a notion that was proposed many years ago — the so-called hygiene hypothesis.
The bacterium Neisseria Meningititis, also known as meningococcus, is a horrible pathogen. It can cause rapidly lethal infection. The infection comes in two forms. It can cause meningitis, inflammation of the surface of the brain, or it can just circulate in the bloodstream, a condition called meningococcemia. Some patients have evidence of both. You might think the brain infection is the worse of the two, but actually meningococcemia without meningitis has a far worse outcome. When the bacteria circulate in the bloodstream they cause profound shock, which can itself be fatal. They also activate the blood clotting system so the patient clots off blood vessels, leading to loss of limbs and worse. I’ve cared for more than a few patients with this infection, and it’s a dreadful one. The bacterium itself is actually quite commonly carried in the throat of well, normal people. It gets passed around by respiratory secretions. Invasion of the body is rare, and we don’t know why it happens in a few people and not everybody. We do know once the percentage of people in a confined area, such as an army camp or a college dormitory, who carry the organism reaches a certain point the risk of invasive infection rises quickly. There are many reports of epidemics in such settings.
Vaccines are designed to neutralize whatever pathogen they’re directed against. The immune system has several components that work in concert to accomplish this. Vaccines cause the body to produce antibodies, proteins that specifically bind to the surface of the microorganism. Antibodies call down other cells and blood proteins that recognize the red flag of the bound antibody and which destroy the bug. So the effectiveness of a vaccine depends on its ability to do this. Researchers typically measure blood levels of the relevant antibody as a proxy for effectiveness because it has been shown to neutralize the bug. You can verify that by what is known as a bactericidal test, in which blood components including antibody and other things are mixed with bacteria in a tube to see if it kills them.
Meningococcus comes in several related but distinct strains, as do most bacteria. We have an FDA-licensed, effective vaccine for all the strains except one, termed type B. These vaccines induce antibodies directed against the sugar coating (polysaccharide) on the bacteria. But type B has a surface polysaccharide similar to those on our own cells, and we don’t want antibodies against those things or they could also attack our own tissues. There is a vaccine, licensed in Europe, against type B meningococcus that chemists made by purifying six of the unique protein components on the bacterial wall and mixing them together in a vaccine. When injected into a person, that person makes antibody aimed at the components. But is that enough to kill the bacteria? That’s the bottom line. The answer turns out to be: more often than not, but not all the time. The safety of the vaccine has been shown, but its effectiveness leaves something to be desired. A recent paper and editorial in the New England Journal of Medicine is instructive. If you want to dive into the details of how vaccines are made and work it’s a good article to look at, especially the editorial.
There have been 7 outbreaks of type B disease during the past 6 years at US universities. The investigators studied the vaccine when it was used (with FDA approval) during a recent outbreak of type B meningococcal disease in New Jersey that caused 9 cases and 1 death. The vaccine was offered to 6,000 students, and this paper reports results from 607 of them. Of note, the strain causing this particular epidemic was shown to have 2 of the protein components contained in the vaccine. How well did it work?
Sixty-six percent of the students developed the ability to neutralize the strain of meningococcus that caused the outbreak. That’s not very good, really. When tested against the reference strain, the one used to make the vaccine, nearly 100% had neutralizing ability. Recall that the outbreak strain had at least 2 of the six protein components included in the vaccine strain. So one way to look at it is that yes, the vaccine induced immunity to the reference strain, but not so much to the strain that actually caused the outbreak. In the authors’ words:
Our results indicate that knowledge of [bacterial killing] immunity against the vaccine reference strains is not sufficient to predict individual-level immunity against an outbreak strain, even when the [outbreak] strain expresses one or more antigens that are closely related to the vaccine antigens.
So now what? I assume researchers just need to keep trying, although it’s a daunting task because there is quite a bit of variability among the proteins in type B organisms. Clearly hitting 2 out of 6 was not enough in this case. Should the vaccine be licensed in the US even though it’s not as effective as we would like? The editorialist puts things this way:
The regulatory approval and clinical use of vaccines for pathogens that cause outbreaks will remain challenging.
Yeah, I’d say so.
I found this study to be absolutely fascinating. The link is to the abstract — the complete article is behind a paywall but I can get it for anybody who’s interested in reading the whole study in detail. Its title is “Fundamental frequency variation in crying of Mandarin and German neonates.” I have always assumed, like most people I suspect, that babies cry the same the world over. When they’re uncomfortable or hungry they let us know by crying. It turns out this may not be the case. If so, then language development is pushed to the very first days of life — even before that, perhaps.
Some languages are tonal. This means the pitch of the speaker’s voice affects the meaning of the words; the same sound can mean something entirely different depending upon the pitch. Mandarin Chinese, spoken by over a billion people, is such a language. There are four pitches that must be mastered to speak Mandarin. I have a friend who spent three years in China and really struggled with this. I don’t recall the details, but as I recall she told me, as one example, the word for “fish” means something entirely different when uttered in a different pitch. There is a language spoken in Cameroon that is even more complicated, sound-wise. This language has eight different pitches that affect word meaning, and there are further modulations in pitch that complicate things even more.
This study was a collaboration between investigators in China and Germany. German is not a tonal language, of course. They recorded the vocalizations of 102 newborn infants, examining in particular pitch, fluctuation, and range. The results, in the words of the lead author, were clear:
The crying of neonates whose mothers speak a tonal language is characterized by a significantly higher melodic variation as compared to – for example – German neonates.
It’s even more interesting when you consider that these are newborns. They’ve only been out of the womb a couple of days. So the implication is that they heard their mothers speaking while still in utero and acquired patterns of vocalization that they begin to use immediately after they were born. That’s quite amazing, I think. It has implications even for those mothers who don’t speak tonal languages: that is, your baby can hear what you’re saying, sense your tone. So maybe if you are angry and yell a lot your infant may actually be impacted by that. Something to think about.
I’m being sarcastic, of course, but that’s often how it seems some days. Those are days when I’ve been busy at patients’ bedsides all day and then struggle to get my documentation done later, typically many hours later. I jot notes to myself as I go along, but it can be hard to recall at 5 PM just what I did and why at 8 AM.
It used to be very much the other way, and that wasn’t always a good thing either. Years ago I spent months going through patient charts from the era of 1920-1950. They were all paper, of course, and the hospital charts were remarkably thin, even for complicated patients. I recall one chart in particular. It was for a young child who was clearly deathly ill. The physician progress notes for her already prolonged stay in the hospital consisted of maybe 2 sheets of paper. Most of the daily notes were a single line. I could tell from the graphs of the child’s vital signs — temperature, pulse, breathing rates, and blood pressure — that one night in particular was nearly fatal. The note the next morning was written by a very famous and distinguished physician. I knew him in his retirement and he was a very loquacious man in person. His note after the child’s bad night was this: “mustard plaster did not work.” If I were caring for a patient like that today there would be just for that day and night multiple entries probably totally several pages on the computer screen.
Patient charts are burdened with several purposes that don’t always work together. The modern medical record as we know it was invented by Dr. Henry Plummer of the Mayo Clinic in the first decade of the twentieth century. Up until that time each physician kept his (only rarely her) case notes really as notes to themselves. When the multi-specialty group appeared, and Mayo was among the first, the notion of each physician have separate records for the same patient made no sense; it was far more logical to have a single record that traveled from physician to physician with the patient. That concept meant the medical record now was a means for one physician to communicate with another. So progress notes were sort of letters to your colleagues. You needed to explain what you were thinking and why. Even today’s electronic medical records are intended to do this, although they do it less and less well.
Now, however, the record is also the principal way physicians document what they did so they can get paid for it. Patient care is not at all part of that consideration. The record is also the main source for defending what you did, say in court, if you are challenged or sued. The result is that documentation, doctors entering things in the record, has eaten more and more of our time. Patients and families know this well and the chorus of complaints over it is rising. Doctors may only rarely make eye contact these days as they stare at a computer screen and type or click boxes. But we don’t have much choice if we are to get the crucial documentation done. That’s how we (and our hospitals) are paid and payers are demanding more and more complex and arcane documentation. I don’t know what the answer is, but I do think we are approaching a breaking point. We are supposed to see as many patients as we can. But the rate-limiting step is documentation.
To some extent we brought this on ourselves. In our fee-for-service system physicians once more or less said to payers: “We did this — trust us, we did it — now pay us for it.” I can’t think of a formula more guaranteed to cause over-utilization or even outright fraud. But there is only so much time in the day. In my world an ever smaller proportion of it is spent actually with the patient.
Asthma is by far the most common chronic lung problem in children, affecting nearly 10% of all children. It may even be the most common chronic health problem of any sort if you exclude obesity. What is it?
Here is a schematic drawing of what a normal lung looks like:
You can think of the lungs as being composed of two parts. The first is a system of conducting tubes that begin at the nose and mouth, move through the trachea (windpipe), split into ever smaller tubes, called bronchi, and end with tiny tubes called bronchioles. The job of this system is to get the air to the business portion of the lungs, which are the alveolar sacs. This second part of the lung brings the air right next to tiny blood vessels, or lung capillaries. Entering capillary blood is depleted in oxygen and loaded with carbon dioxide, one of the waste products of the body’s metabolism. What happens next is gas exchange: as the blood moves through the capillaries, oxygen from the air we breathe in goes into the blood, and carbon dioxide leaves the blood and goes into the air we breathe out. The newly recharged blood then leaves the lungs in an ever enlarging system of pulmonary veins and then goes out to the body.
The main problem in asthma is that the conducting airway system gets blocked in several ways, so the oxygen can’t get in and the carbon dioxide can’t leave. Although both are a problem in a severe asthma attack, getting the air out is usually a bigger issue than getting it in because it is easier for us to generate more force sucking in air than blowing it out. So the hallmark of asthma is not getting the air out — called air trapping. Why does this happen? There are two principal reasons: for one, the small airways, the bronchioles, constrict, get smaller; for another, the walls of the airways swell and the airways themselves fill with excess mucous, blocking air flow. Here’s another schematic drawing of what that looks like.
Thus during an asthma attack these things happen, all of which act together to narrow the airways and reduce air flow:
- The smooth muscle bands around the tiny airways tighten
- The linings of the airways get inflamed and swell
- The mucous glands in the airways release too much mucous, filling the airways
The medicines that we use to treat asthma work by reducing (or even preventing) one or more of these things.
Between 1980 and 1995 the prevalence of asthma in children doubled. Then from 1995 to 2010 the number continued to increase, but more slowly. Where are we now? A recent report in Pediatrics, the journal of the American Academy of Pediatrics, gives some answers. The authors looked at the time period from 2000-2013. They separated patients by gender, race, geographical location, and socioeconomic group.
The investigators found that across all groups asthma prevalence steadily increased from 2000-2009, although the rate of rise had slackened compared with the previous 2 decades. The year 2009 was the peak. After that there was a plateau, and since then the rates have actually fallen a bit for the total group. Among poor children, however, asthma rates have continued to rise steadily. This is concerning. The reasons for these changes in asthma prevalence are complex and experts think it is most likely an interplay of several things. If you are interested you can find more information in the article linked above. But it does appear that, on balance, the “asthma epidemic” is abating.
It’s common sense that language and thought are closely related. For example, any politician knows the words one uses to describe something can profoundly affect how listeners understand and react to what they hear. Some think it goes deeper than that. An old theory of linguistics, the Sapir-Whorf hypothesis, has been batted around since the mid-20th century. This notion, named for Edward Sapir and his student, Benjamin Whorf, proposed that language actually controls thought, how we regard the world. Their argument was that we think using language, and thus the idiosyncrasies of our language determine how we think. The theory implies there are some things two native speakers of different languages cannot fully explain to each other or even completely understand. In its purer form the hypothesis is not that highly regarded these days among experts, but in its more rudimentary form the notion makes considerable sense to me. You can read more about the linguistic pros and cons of Sapir-Whorf many places, such as here, here, and here. Here is a nice PowerPoint presentation of its basic tenets. George Orwell’s 1984 is a powerful expression of the way whoever controls language can control thought. Today’s seemingly endless debates about “political correctness,” which generally seem silly to me, are getting at the same notion.
Yet language really does matter. I think that, over time, the words we physicians use to describe patients to each other, to interview patients and their families, and to explain treatments and therapies have importance far beyond the particular encounter. Our words have a cumulative impact on us, on our own attitudes and feelings. It is important to be empathetic and respectful not just because that is the correct way to behave to our patients, but also because it is the most caring way to nurture ourselves.
The intensive care unit is a place that can harden you. You hear it all around you in the language people use to describe patients and families. There can be a compulsion to sound hard-boiled and savvy. This easily degenerates into cynicism. Much has been written about the burn-out rate of people who work in the ICU environment. I think a portion of the burn-out relates to the language we use. After practicing critical care for 35 years I don’t think I’m in any danger anymore of experiencing burn-out. I also think one way we can at least partially inoculate ourselves against that possibility is to be careful of how we speak to each other, to our patients, and to their families.
There is a troubling entity in pediatrics. Sometimes infants appear to have suffered some catastrophic problem, only to recover within minutes. Forty years ago these were termed “near miss sudden infant death syndrome events.” The notion was that they represented part of the spectrum of SIDS — sudden infant death syndrome — that had, for some reason, been averted. In the mid-1980s researchers realized these spells weren’t really related to SIDS because infants who experienced them were not at higher risk for having a real SIDS event later. A new term was coined: “Apparent life threatening event (ALTE).” The working definition was this:
An episode that is frightening to the observer and that is characterized by some combination of apnea [pause or cessation of breathing], color change (usually cyanotic [blue] or pallid but occasionally erythematous [red, flushed] or plethoric), marked change in muscle tone (usually marked limpness), choking, or gagging. In some cases the observer fears that the infant has died.
ALTE events are not only terrifying to parents; physicians are also worried and uncertain about what to do. I know — I’ve cared for many infants over the years who fit this description. It’s easy to know what to do if the infant looks abnormal when you examine him because whatever abnormality you find guides your course of action. But typically these babies look fine by the time the physician sees them. If the parents called 911, the paramedics also find a normal-appearing baby. Usually we admit such babies to the hospital and place them on heart and breathing monitors to see if they do whatever it was again. In my experience, they typically don’t. So now what? In at most half the cases we identify a probable cause, the most common of which is reflux of feedings from the stomach to the mouth, after which a small amount gets in the airway. When that happens a common infant reflex is to stop breathing — stimulating them gets them to start again. Respiratory infections (particularly RSV) and convulsions are also potential causes. But at least half the time we have no idea what happened.
What is the risk of an ALTE recurring? It turns out we have no idea about that, either. A recent review of nearly 37 research articles spanning 40 years concluded such a prediction can’t be made, largely because the definitions used for what is or is not an ALTE have been quite variable in spite of the above consensus statement. A huge issue is that infants who are clearly abnormal, but who arrive for evaluation with an ALTE, are often lumped in with children who appear normal after the event. Those are very different groups.
To try to analyze this troubling condition the American Academy of Pediatrics has just issued a clinical practice guideline about what to call these events and what to do about them. They did add to the alphabet soup by coining a new term: “Brief, resolved, unexplained event (BRUE).” I’m not sure how useful that term will be, but the intent is to separate out those children in which a detailed conversation with the parents and a thorough physical examination do not identify any potential cause. For those infants the committee (and it was a committee, with all the problems that can bring) recommends not doing so many tests. One thing is clear; a home apnea monitor does not at all reduce the risk of future harm, and so using one is not recommended. A BRUE (or ALTE) is not associated with risk for SIDS — that’s a key observation that has stood the test of time. We do know one thing that is clearly associated with SIDS: putting babies to sleep on their stomachs. Ever since the introduction of the “back to sleep program,” of instructing parents to put their babies to sleep lying on their backs, the incidence of SIDS has dropped remarkably, although it still happens.
What do I think? We don’t know what causes these spells. However, premature infants are at higher risk for them and we know such infants often have disordered breathing and heart reflexes. I have no data at all about it, but my guesswork opinion is these spells represent immaturity of infants’ brains such that they respond to a variety of stimuli by pausing or stopping breathing or slowing their heart rate. The tendency goes away with growing older because we only see this problem in infants. I hope this new categorization leads to useful research about what is really happening during these mysterious events.