Physicians wear white coats. In many medical centers, the length of one's coat grows with seniority; medical students, interns, and residents wear short white coats, while attending staff graduate to long white coats with their names embroidered on the front. This traditional uniform serves a similar role to the stripes on a military sleeve. That is, by examining the length of a person's coat, a nurse or other hospital employee can rapidly determine the seniority, and theoretically the increased medical knowledge, of the person inside.

Of course, it isn't quite this simple. In many places, all residents wear long coats (with embroidered names). In other hospitals, attending staff wear short coats. The problem of distinguishing between a medical student, resident, and attending physician can be quite vexing, particularly after the summer months when the anxiety visible on the faces of new house staff and third‐year medical students fades away into the more seasoned look of fatigue and malaise. As hospital‐based practitioners, what are we to do?

To be certain there are clues one can use to identify one's rank in the medical profession. Often medical students wear a medical school pin bestowed upon them at a robing ceremony or other coming‐of‐age festivity to mark the transition to the clinical training years.1 (Little do they know that the primary utility of such adornments is to mark them, as though with a scarlet letter, for easy identification when one wishes to pimp the medical team.)2 Similarly, one can look for an arm patch. Just as a mother hen has the need to identify her own chicks, so too is it helpful for the residency director to have each of his or her own residents easily identifiable by the residency patch emblazoned upon the arm of their (long) white coat. The patch test can fail, though, for too often the residency emblem is merely a simple modification of the hospital or medical center logo, and thus not easily distinguishable.

When all else fails, of course, you can look to the pockets. As one's medical knowledge and training rank increases, the number of papers, pens, and instruments in the pockets of the white coat decreases. This inverse relationship provides some increased ability to identify medical students and junior house staff. For example, a short white coat, busting with oversized index cards held together by a large metal ring, several tattered and folded journal articles, and a worn spiral‐bound text suggests a medical student or intern. If they have an electrocardiogram (ECG), calipers, and tuning fork visible, safe bet is you've found a medical student. Conversely, if the white coat sports several free pens (with medication logos embossed on their stems) and has more than a few stains, chances are you've spotted an intern.

Unfortunately, none of this is of much utility in identifying a physician, as the initial premise that physicians wear white coats may be false. The problem is 2‐fold. First of all, not all physicians wear white coats (or any coat for that matter), and, many nonphysicians wear white coats. Commonly, phlebotomists, pharmacists, and respiratory technicians wear white coats; long white coats, in fact. So do nutritionists, speech pathologists, the clerk at the radiology file room, and even the cashiers in the cafeteria. And why not? Each of these persons has an important role to play in the operation of a modern medical center. The long white coat serves as professional uniform to identify the wearer as contributing to the mission of the medical center. It engenders confidence and suggests cleanliness and purity.

The problem remains, however, what should I, as an attending physician wear? You see, patients encounter so many persons in their visits to the hospital that it is not clear who their doctor is. (It's not statistically likely to be the man in a long white coat.) Being able to identify the attending physician is important. The attending physician is ultimately responsible for the patient's care.

There are many guidelines for how to dress. For example, don't wear white after Labor Day. The pleats on a cummerbund point so that the folds open pointing up (apparently it was originally meant to serve as a ticket holder, perhaps in the days before pockets?). Match your belt to your shoes. The list goes on. However, physicians are not commonly associated with natty attire, so fashion help for the MD is hard to find, though nonetheless necessary.

Even wearing white is questionable. White robes have been associated with purity and sanctity for centuries. Religious leaders have donned white for spiritual cleansing of their communities on the most holy of days. I like the idea of appearing pure and holy. Of course, I don't want to mislead anybody, either.

Brides have traditionally worn white dresses. But, while many believe this is to convey a sense of premarital purity, more likely the tradition stems from an ancient Roman practice of wearing white as a symbol of joyous celebration. Interestingly, in some parts of Asia, people at a funeral wear white while the deceased is dressed in red.

In some environments, the culture of the medical center prescribes appropriate apparel. The Mayo Clinic in Minnesota, for example, has had a tradition of having their physician staff dress in business attire. By this, they mean conservative sport coats or suits with ties for men, and similar appropriate women's business clothing. As noted by Leonard L. Berry and Neeli Bendapudi in their article Why Docs Don't Wear White Coats or Polo Shirts at the Mayo Clinic3 in the Harvard Business School publication Working Knowledge for Business Leaders, while some may consider this semiformal business dress pretentious, it should be considered no more pretentious than, say, the dress code for airline pilots. Airline passengers don't want to see their pilot in a polo shirt, and patients feel the same way about their doctors. The business attire is a uniform; it's a visible clue that communicates respect to patients and their families. But, isn't a white coat a uniform that conveys respect? Perhaps a white coat isn't safe if the physician wants to stand out to oncoming traffic in his snowy Minnesota environs.

Besides, is it true that patients don't want their physician to wear a polo shirt? Perhaps casual dress will break down 1 of the patient‐doctor barriers to communication and allow for improved comfort with greater honesty in patientphysician interactions? Prior to designing a prospective controlled randomized trial to answer this question myself, I reviewed the available literature.

It turns out, that an evaluation of polo‐shirt‐wearing physicians has been carried out. Drs. Barrett and Booth4 from the Birmingham Maternity Hospital in England questioned 203 groups of parents and children (406 individuals) about various levels of physician dress. Seventy percent of participants thought that how the doctor dressed was important. Among children, a male physician in a polo shirt was considered more friendly and gentle than the male physician in a white coat (who did get points for being more competent and more concerned). Women physicians in T‐shirts were also though to be friendlier than if in a white coat, but similarly less competent. Parents were more likely to prefer casually‐dressed physicians and were poor at predicting what their children would want.

So, a polo shirt makes me look friendly, gentle, and less competent? What about a polo shirt under a white coatis that the whole package? What about business attire, as per the Mayo Clinic requirements? These questions remain unanswered. So, back to the literature.

In the Journal of the American Medical Association, in 1987, Dunn et al.5 evaluated 200 medical patients in Boston and San Francisco regarding their preference for physician dress. Sixty‐five percent believed physicians should wear a white coat, 27% said no tennis shoes, one‐half said no blue jeans, and about one‐third thought male physicians should wear ties and female physicians should be in a skirt or dress. I suppose the conclusion here is to wear a white coat with or without jeans and most of the time without a tie, though almost always with proper shoes, or at least without tennis shoes. (I practice in Boston and trained partly in San Francisco so this advice seems particularly valid for me.)

It may be more obvious what to do in Japan. Ikusaka et al.6 evaluated the experience of patients at a university clinic seen by a consulting physician in either a white coat, or private clothes. To me, private clothes imply pajamas and a bathrobe, but we must assume this means some form of professional dress lacking a white coat. It turns out that 71% of the Japanese patients seeing a doctor in a white coat preferred a white coat, though more patients seeing a physician in a white coat (vs. private clothes) felt tense during their consultation. The researchers stress that the presence of a white coat did not increase satisfaction with the consultation. They conclude, that while patients may say they prefer a white coat, maybe it would be better not to wear one since it makes patients feel tense.

In addition to feeling tense, white coats may cause hypertension. The phenomenon of elevated blood pressure when in the presence of the physician (or other hospital staff in a white coat) has been long documented. This white coat hypertension can be found in more than 15% of the population who have a measured blood pressure in the office of over 140/90 mmHg with normal daytime mean ambulatory blood pressure readings (when not around a white‐coat‐wearing stress‐inducing medical worker).7 Older adults, females, and nonsmokers were more likely to have white coat hypertension than other persons.

And yet, older adults prefer white coats. The Japanese study (Ikusaka et al.6) concluded that elderly patients prefer a white coat to other attire. Similarly, a study from the Royal Free Hospital, London, showed that white coats were twice as popular with patients as they were with physicians.8 Specifically, patients found the white coats made doctors easier to identify. In an article by the British Broadcasting Corporation (BBC) on the subject, it was noted that the elderly largely preferred physicians in white coats, while children preferred physicians without white coats. British children must prefer a friendly doctor to a competent one.

The article further suggests that only 1 in 8 physicians wears a white coat, complaining that they are too hot and uncomfortable, and may carry the risk of transmitting infections. The white coat, the symbol of cleanliness and purity, a source of infection? To add hypocrisy to the equation, one‐half of physicians who thought white coats should be worn admitted to never actually wearing a white coat. In fact, only 7 of 86 physicians surveyed wore their white coat on a daily basis. The BBC goes on to note that in Australia, the white coat is gaining momentum as there seems to be a movement towards rediscovering the white coat as a symbol of purpose and pride as a profession.8

Really? Let's consult the literature! According to Dr. D.A. Watson,9 White coats have largely disappeared from Australian teaching hospitals and the majority of junior doctors in Australia oppose the wearing of white coats. In a survey of 337 junior medical officers, only 16% preferred to wear a white coat. Peer pressure seems to have something to do with this, as 70% say they don't wear a white coat because nobody else wears a white coat. This is indeed a compelling argument.

Of course, a better argument against wearing a white coat may be that it causes tension (at least in Japanese patients) and may cause white‐coat‐hypertension, resulting in the inappropriate diagnosis and treatment of elevated blood pressure. In Australia, however, it seems that wearing a white coat may make patients too relaxed. Wing et al.10 noted that in 21% to 45% of elderly patients, blood pressure was atypically low when checked in the physician's office as compared to mean ambulatory blood pressure. This reverse‐white‐coat‐hypertension could result in the omission of necessary blood pressure treatment.

In the United States, residentsour own version of the Australian junior medical officercommonly wear scrubs covered by a white coat. Scrub clothes are typically available without charge from the hospital, limit the amount of laundry a busy resident needs to do, and can be put on with little concern as to pressed pleats or matching colors. The overlying white coat adds a moderate degree of formality to what could otherwise be mistaken as pajamas, while providing convenient pockets for the aforementioned papers and miscellaneous equipment and souvenirs. This outfit is likely one of practicality rather than a desire to be most appealing to patients. But, what do you know? It seems that patients prefer their resident physicians to dress this way. Dr. A. Cha et al.11 at the Northeastern Ohio College of Medicine found that patients in an obstetrics and gynecology clinic overall felt that resident physicians dressed in surgical scrubs with a white coat made them feel more comfortable and confident than if dressed otherwise. On the question of a white coat specifically, the majority had no preference that their physician wear one.

So, it's very much unclear whether a white coat is a tension‐causing, blood‐pressure‐elevating, infection risk or a competence‐implying blood‐pressure‐lowering way to identify a physician. As a result, the jury is still out on whether physicians should wear white.

One thing I do know, however, is that patients shouldn't wear white. But they do. As an OtolaryngologistHead and Neck Surgeon, my clinical practice is split between surgical procedures and office visits. Commonly, patients with sinus or nasal surgery will require some form of cotton gauze or foam material within the nose in order to tamponade bleeding. Similarly, patients presenting to the emergency department or urgent care center with epistaxis may have their noses packed and then be told to see an otolaryngologist (eg, me) in 3 or 4 days to have the packing removed. I also commonly remove facial skin lesions, biopsy tongue masses, reduce nasal fractures, and otherwise engage in activities with an above average propensity to result in a mess. More often than happenstance will allow, patients come to see me for such visits in their white Sunday best. I truly care for my patients. I respect them as individuals and desire to do no harm. This includes not staining their shirts, ties, or pants. However, there is no amount of blue towels or gauze pads than can keep a white shirt clean when you have that first sneeze after removal of your nasal packing.12

So what is it that makes so many patients come to the office in a white shirt? Perhaps patients subconsciously associate healthcare with the color white since their doctors wear white coats and the nurses wear starched white dresses with tight white folded caps on top of their head. I've never seen a nurse in a white dress and hat, but believe television programs have shown this in the past.

Maybe the answer lies in an adaptation of data from another Australian study. In a survey of 180 oncology patients about white coats on physicians, the most common argument against wearing the white coat was that it represented a barrier between the physician and the patient.13 However, it is indeed the sane patient who desires to have a barrier between their physician and the removal of nasal packing, a skin lesion, or a tongue mass. Another possibility is that as fewer and fewer physicians wear white, patients are gravitating toward this color as a way of distinguishing themselves from the medical staff. Perhaps a person dressed in white is less likely to be grabbed in the hallway with a Doctor come quick! and more likely to be allowed to just sit peacefully in the waiting room with a 1997 issue of Ladies Home Journal or Senior Fisherman magazine.

Of course, perhaps patients believe the fashion experts who expound that white goes with everything. If so, they soon learn that white doesn't go so well with blotchy splattered red.

The truth is, I don't want my patients to wear white. Between making certain I project myself as approachable and easy to speak with, remembering to cover all the appropriate irrelevant parts of the history and physical to comply with billing requirements, entering data in our easy‐to‐navigate electronic medical record, and attempting to both diagnose the problem and discern an acceptable and effective treatment, the last thing I need is to worry about staining patient shirts! I believe that this phenomenon is widespread among medical practitioners and should be called white‐shirt‐hypertension.

Conclusion

After reviewing the available literature, I've determined that patients should not wear white. However, I'm still not certain how I should dress. For now, I'll stick with whatever is clean and professional and make sure my belt and shoes match. I may or may not wear a tie, since another study showed that 30% of patients believed their physician wore a tie even if they didn't.14 Of course, I'll put on the white coat for the semiannual meeting with the chairman, or if I'm having something messy for lunch and wore a tie that day.

I'll also wear my name badge. It says I'm an attending physician and not a resident. It opens doors around the hospital. Literally. It's got a magnetic stripe.

Physicians wear white coats. In many medical centers, the length of one's coat grows with seniority; medical students, interns, and residents wear short white coats, while attending staff graduate to long white coats with their names embroidered on the front. This traditional uniform serves a similar role to the stripes on a military sleeve. That is, by examining the length of a person's coat, a nurse or other hospital employee can rapidly determine the seniority, and theoretically the increased medical knowledge, of the person inside.

Of course, it isn't quite this simple. In many places, all residents wear long coats (with embroidered names). In other hospitals, attending staff wear short coats. The problem of distinguishing between a medical student, resident, and attending physician can be quite vexing, particularly after the summer months when the anxiety visible on the faces of new house staff and third‐year medical students fades away into the more seasoned look of fatigue and malaise. As hospital‐based practitioners, what are we to do?

To be certain there are clues one can use to identify one's rank in the medical profession. Often medical students wear a medical school pin bestowed upon them at a robing ceremony or other coming‐of‐age festivity to mark the transition to the clinical training years.1 (Little do they know that the primary utility of such adornments is to mark them, as though with a scarlet letter, for easy identification when one wishes to pimp the medical team.)2 Similarly, one can look for an arm patch. Just as a mother hen has the need to identify her own chicks, so too is it helpful for the residency director to have each of his or her own residents easily identifiable by the residency patch emblazoned upon the arm of their (long) white coat. The patch test can fail, though, for too often the residency emblem is merely a simple modification of the hospital or medical center logo, and thus not easily distinguishable.

When all else fails, of course, you can look to the pockets. As one's medical knowledge and training rank increases, the number of papers, pens, and instruments in the pockets of the white coat decreases. This inverse relationship provides some increased ability to identify medical students and junior house staff. For example, a short white coat, busting with oversized index cards held together by a large metal ring, several tattered and folded journal articles, and a worn spiral‐bound text suggests a medical student or intern. If they have an electrocardiogram (ECG), calipers, and tuning fork visible, safe bet is you've found a medical student. Conversely, if the white coat sports several free pens (with medication logos embossed on their stems) and has more than a few stains, chances are you've spotted an intern.

Unfortunately, none of this is of much utility in identifying a physician, as the initial premise that physicians wear white coats may be false. The problem is 2‐fold. First of all, not all physicians wear white coats (or any coat for that matter), and, many nonphysicians wear white coats. Commonly, phlebotomists, pharmacists, and respiratory technicians wear white coats; long white coats, in fact. So do nutritionists, speech pathologists, the clerk at the radiology file room, and even the cashiers in the cafeteria. And why not? Each of these persons has an important role to play in the operation of a modern medical center. The long white coat serves as professional uniform to identify the wearer as contributing to the mission of the medical center. It engenders confidence and suggests cleanliness and purity.

The problem remains, however, what should I, as an attending physician wear? You see, patients encounter so many persons in their visits to the hospital that it is not clear who their doctor is. (It's not statistically likely to be the man in a long white coat.) Being able to identify the attending physician is important. The attending physician is ultimately responsible for the patient's care.

There are many guidelines for how to dress. For example, don't wear white after Labor Day. The pleats on a cummerbund point so that the folds open pointing up (apparently it was originally meant to serve as a ticket holder, perhaps in the days before pockets?). Match your belt to your shoes. The list goes on. However, physicians are not commonly associated with natty attire, so fashion help for the MD is hard to find, though nonetheless necessary.

Even wearing white is questionable. White robes have been associated with purity and sanctity for centuries. Religious leaders have donned white for spiritual cleansing of their communities on the most holy of days. I like the idea of appearing pure and holy. Of course, I don't want to mislead anybody, either.

Brides have traditionally worn white dresses. But, while many believe this is to convey a sense of premarital purity, more likely the tradition stems from an ancient Roman practice of wearing white as a symbol of joyous celebration. Interestingly, in some parts of Asia, people at a funeral wear white while the deceased is dressed in red.

In some environments, the culture of the medical center prescribes appropriate apparel. The Mayo Clinic in Minnesota, for example, has had a tradition of having their physician staff dress in business attire. By this, they mean conservative sport coats or suits with ties for men, and similar appropriate women's business clothing. As noted by Leonard L. Berry and Neeli Bendapudi in their article Why Docs Don't Wear White Coats or Polo Shirts at the Mayo Clinic3 in the Harvard Business School publication Working Knowledge for Business Leaders, while some may consider this semiformal business dress pretentious, it should be considered no more pretentious than, say, the dress code for airline pilots. Airline passengers don't want to see their pilot in a polo shirt, and patients feel the same way about their doctors. The business attire is a uniform; it's a visible clue that communicates respect to patients and their families. But, isn't a white coat a uniform that conveys respect? Perhaps a white coat isn't safe if the physician wants to stand out to oncoming traffic in his snowy Minnesota environs.

Besides, is it true that patients don't want their physician to wear a polo shirt? Perhaps casual dress will break down 1 of the patient‐doctor barriers to communication and allow for improved comfort with greater honesty in patientphysician interactions? Prior to designing a prospective controlled randomized trial to answer this question myself, I reviewed the available literature.

It turns out, that an evaluation of polo‐shirt‐wearing physicians has been carried out. Drs. Barrett and Booth4 from the Birmingham Maternity Hospital in England questioned 203 groups of parents and children (406 individuals) about various levels of physician dress. Seventy percent of participants thought that how the doctor dressed was important. Among children, a male physician in a polo shirt was considered more friendly and gentle than the male physician in a white coat (who did get points for being more competent and more concerned). Women physicians in T‐shirts were also though to be friendlier than if in a white coat, but similarly less competent. Parents were more likely to prefer casually‐dressed physicians and were poor at predicting what their children would want.

So, a polo shirt makes me look friendly, gentle, and less competent? What about a polo shirt under a white coatis that the whole package? What about business attire, as per the Mayo Clinic requirements? These questions remain unanswered. So, back to the literature.

In the Journal of the American Medical Association, in 1987, Dunn et al.5 evaluated 200 medical patients in Boston and San Francisco regarding their preference for physician dress. Sixty‐five percent believed physicians should wear a white coat, 27% said no tennis shoes, one‐half said no blue jeans, and about one‐third thought male physicians should wear ties and female physicians should be in a skirt or dress. I suppose the conclusion here is to wear a white coat with or without jeans and most of the time without a tie, though almost always with proper shoes, or at least without tennis shoes. (I practice in Boston and trained partly in San Francisco so this advice seems particularly valid for me.)

It may be more obvious what to do in Japan. Ikusaka et al.6 evaluated the experience of patients at a university clinic seen by a consulting physician in either a white coat, or private clothes. To me, private clothes imply pajamas and a bathrobe, but we must assume this means some form of professional dress lacking a white coat. It turns out that 71% of the Japanese patients seeing a doctor in a white coat preferred a white coat, though more patients seeing a physician in a white coat (vs. private clothes) felt tense during their consultation. The researchers stress that the presence of a white coat did not increase satisfaction with the consultation. They conclude, that while patients may say they prefer a white coat, maybe it would be better not to wear one since it makes patients feel tense.

In addition to feeling tense, white coats may cause hypertension. The phenomenon of elevated blood pressure when in the presence of the physician (or other hospital staff in a white coat) has been long documented. This white coat hypertension can be found in more than 15% of the population who have a measured blood pressure in the office of over 140/90 mmHg with normal daytime mean ambulatory blood pressure readings (when not around a white‐coat‐wearing stress‐inducing medical worker).7 Older adults, females, and nonsmokers were more likely to have white coat hypertension than other persons.

And yet, older adults prefer white coats. The Japanese study (Ikusaka et al.6) concluded that elderly patients prefer a white coat to other attire. Similarly, a study from the Royal Free Hospital, London, showed that white coats were twice as popular with patients as they were with physicians.8 Specifically, patients found the white coats made doctors easier to identify. In an article by the British Broadcasting Corporation (BBC) on the subject, it was noted that the elderly largely preferred physicians in white coats, while children preferred physicians without white coats. British children must prefer a friendly doctor to a competent one.

The article further suggests that only 1 in 8 physicians wears a white coat, complaining that they are too hot and uncomfortable, and may carry the risk of transmitting infections. The white coat, the symbol of cleanliness and purity, a source of infection? To add hypocrisy to the equation, one‐half of physicians who thought white coats should be worn admitted to never actually wearing a white coat. In fact, only 7 of 86 physicians surveyed wore their white coat on a daily basis. The BBC goes on to note that in Australia, the white coat is gaining momentum as there seems to be a movement towards rediscovering the white coat as a symbol of purpose and pride as a profession.8

Really? Let's consult the literature! According to Dr. D.A. Watson,9 White coats have largely disappeared from Australian teaching hospitals and the majority of junior doctors in Australia oppose the wearing of white coats. In a survey of 337 junior medical officers, only 16% preferred to wear a white coat. Peer pressure seems to have something to do with this, as 70% say they don't wear a white coat because nobody else wears a white coat. This is indeed a compelling argument.

Of course, a better argument against wearing a white coat may be that it causes tension (at least in Japanese patients) and may cause white‐coat‐hypertension, resulting in the inappropriate diagnosis and treatment of elevated blood pressure. In Australia, however, it seems that wearing a white coat may make patients too relaxed. Wing et al.10 noted that in 21% to 45% of elderly patients, blood pressure was atypically low when checked in the physician's office as compared to mean ambulatory blood pressure. This reverse‐white‐coat‐hypertension could result in the omission of necessary blood pressure treatment.

In the United States, residentsour own version of the Australian junior medical officercommonly wear scrubs covered by a white coat. Scrub clothes are typically available without charge from the hospital, limit the amount of laundry a busy resident needs to do, and can be put on with little concern as to pressed pleats or matching colors. The overlying white coat adds a moderate degree of formality to what could otherwise be mistaken as pajamas, while providing convenient pockets for the aforementioned papers and miscellaneous equipment and souvenirs. This outfit is likely one of practicality rather than a desire to be most appealing to patients. But, what do you know? It seems that patients prefer their resident physicians to dress this way. Dr. A. Cha et al.11 at the Northeastern Ohio College of Medicine found that patients in an obstetrics and gynecology clinic overall felt that resident physicians dressed in surgical scrubs with a white coat made them feel more comfortable and confident than if dressed otherwise. On the question of a white coat specifically, the majority had no preference that their physician wear one.

So, it's very much unclear whether a white coat is a tension‐causing, blood‐pressure‐elevating, infection risk or a competence‐implying blood‐pressure‐lowering way to identify a physician. As a result, the jury is still out on whether physicians should wear white.

One thing I do know, however, is that patients shouldn't wear white. But they do. As an OtolaryngologistHead and Neck Surgeon, my clinical practice is split between surgical procedures and office visits. Commonly, patients with sinus or nasal surgery will require some form of cotton gauze or foam material within the nose in order to tamponade bleeding. Similarly, patients presenting to the emergency department or urgent care center with epistaxis may have their noses packed and then be told to see an otolaryngologist (eg, me) in 3 or 4 days to have the packing removed. I also commonly remove facial skin lesions, biopsy tongue masses, reduce nasal fractures, and otherwise engage in activities with an above average propensity to result in a mess. More often than happenstance will allow, patients come to see me for such visits in their white Sunday best. I truly care for my patients. I respect them as individuals and desire to do no harm. This includes not staining their shirts, ties, or pants. However, there is no amount of blue towels or gauze pads than can keep a white shirt clean when you have that first sneeze after removal of your nasal packing.12

So what is it that makes so many patients come to the office in a white shirt? Perhaps patients subconsciously associate healthcare with the color white since their doctors wear white coats and the nurses wear starched white dresses with tight white folded caps on top of their head. I've never seen a nurse in a white dress and hat, but believe television programs have shown this in the past.

Maybe the answer lies in an adaptation of data from another Australian study. In a survey of 180 oncology patients about white coats on physicians, the most common argument against wearing the white coat was that it represented a barrier between the physician and the patient.13 However, it is indeed the sane patient who desires to have a barrier between their physician and the removal of nasal packing, a skin lesion, or a tongue mass. Another possibility is that as fewer and fewer physicians wear white, patients are gravitating toward this color as a way of distinguishing themselves from the medical staff. Perhaps a person dressed in white is less likely to be grabbed in the hallway with a Doctor come quick! and more likely to be allowed to just sit peacefully in the waiting room with a 1997 issue of Ladies Home Journal or Senior Fisherman magazine.

Of course, perhaps patients believe the fashion experts who expound that white goes with everything. If so, they soon learn that white doesn't go so well with blotchy splattered red.

The truth is, I don't want my patients to wear white. Between making certain I project myself as approachable and easy to speak with, remembering to cover all the appropriate irrelevant parts of the history and physical to comply with billing requirements, entering data in our easy‐to‐navigate electronic medical record, and attempting to both diagnose the problem and discern an acceptable and effective treatment, the last thing I need is to worry about staining patient shirts! I believe that this phenomenon is widespread among medical practitioners and should be called white‐shirt‐hypertension.

Conclusion

After reviewing the available literature, I've determined that patients should not wear white. However, I'm still not certain how I should dress. For now, I'll stick with whatever is clean and professional and make sure my belt and shoes match. I may or may not wear a tie, since another study showed that 30% of patients believed their physician wore a tie even if they didn't.14 Of course, I'll put on the white coat for the semiannual meeting with the chairman, or if I'm having something messy for lunch and wore a tie that day.

I'll also wear my name badge. It says I'm an attending physician and not a resident. It opens doors around the hospital. Literally. It's got a magnetic stripe.

Physicians wear white coats. In many medical centers, the length of one's coat grows with seniority; medical students, interns, and residents wear short white coats, while attending staff graduate to long white coats with their names embroidered on the front. This traditional uniform serves a similar role to the stripes on a military sleeve. That is, by examining the length of a person's coat, a nurse or other hospital employee can rapidly determine the seniority, and theoretically the increased medical knowledge, of the person inside.

Of course, it isn't quite this simple. In many places, all residents wear long coats (with embroidered names). In other hospitals, attending staff wear short coats. The problem of distinguishing between a medical student, resident, and attending physician can be quite vexing, particularly after the summer months when the anxiety visible on the faces of new house staff and third‐year medical students fades away into the more seasoned look of fatigue and malaise. As hospital‐based practitioners, what are we to do?

To be certain there are clues one can use to identify one's rank in the medical profession. Often medical students wear a medical school pin bestowed upon them at a robing ceremony or other coming‐of‐age festivity to mark the transition to the clinical training years.1 (Little do they know that the primary utility of such adornments is to mark them, as though with a scarlet letter, for easy identification when one wishes to pimp the medical team.)2 Similarly, one can look for an arm patch. Just as a mother hen has the need to identify her own chicks, so too is it helpful for the residency director to have each of his or her own residents easily identifiable by the residency patch emblazoned upon the arm of their (long) white coat. The patch test can fail, though, for too often the residency emblem is merely a simple modification of the hospital or medical center logo, and thus not easily distinguishable.

When all else fails, of course, you can look to the pockets. As one's medical knowledge and training rank increases, the number of papers, pens, and instruments in the pockets of the white coat decreases. This inverse relationship provides some increased ability to identify medical students and junior house staff. For example, a short white coat, busting with oversized index cards held together by a large metal ring, several tattered and folded journal articles, and a worn spiral‐bound text suggests a medical student or intern. If they have an electrocardiogram (ECG), calipers, and tuning fork visible, safe bet is you've found a medical student. Conversely, if the white coat sports several free pens (with medication logos embossed on their stems) and has more than a few stains, chances are you've spotted an intern.

Unfortunately, none of this is of much utility in identifying a physician, as the initial premise that physicians wear white coats may be false. The problem is 2‐fold. First of all, not all physicians wear white coats (or any coat for that matter), and, many nonphysicians wear white coats. Commonly, phlebotomists, pharmacists, and respiratory technicians wear white coats; long white coats, in fact. So do nutritionists, speech pathologists, the clerk at the radiology file room, and even the cashiers in the cafeteria. And why not? Each of these persons has an important role to play in the operation of a modern medical center. The long white coat serves as professional uniform to identify the wearer as contributing to the mission of the medical center. It engenders confidence and suggests cleanliness and purity.

The problem remains, however, what should I, as an attending physician wear? You see, patients encounter so many persons in their visits to the hospital that it is not clear who their doctor is. (It's not statistically likely to be the man in a long white coat.) Being able to identify the attending physician is important. The attending physician is ultimately responsible for the patient's care.

There are many guidelines for how to dress. For example, don't wear white after Labor Day. The pleats on a cummerbund point so that the folds open pointing up (apparently it was originally meant to serve as a ticket holder, perhaps in the days before pockets?). Match your belt to your shoes. The list goes on. However, physicians are not commonly associated with natty attire, so fashion help for the MD is hard to find, though nonetheless necessary.

Even wearing white is questionable. White robes have been associated with purity and sanctity for centuries. Religious leaders have donned white for spiritual cleansing of their communities on the most holy of days. I like the idea of appearing pure and holy. Of course, I don't want to mislead anybody, either.

Brides have traditionally worn white dresses. But, while many believe this is to convey a sense of premarital purity, more likely the tradition stems from an ancient Roman practice of wearing white as a symbol of joyous celebration. Interestingly, in some parts of Asia, people at a funeral wear white while the deceased is dressed in red.

In some environments, the culture of the medical center prescribes appropriate apparel. The Mayo Clinic in Minnesota, for example, has had a tradition of having their physician staff dress in business attire. By this, they mean conservative sport coats or suits with ties for men, and similar appropriate women's business clothing. As noted by Leonard L. Berry and Neeli Bendapudi in their article Why Docs Don't Wear White Coats or Polo Shirts at the Mayo Clinic3 in the Harvard Business School publication Working Knowledge for Business Leaders, while some may consider this semiformal business dress pretentious, it should be considered no more pretentious than, say, the dress code for airline pilots. Airline passengers don't want to see their pilot in a polo shirt, and patients feel the same way about their doctors. The business attire is a uniform; it's a visible clue that communicates respect to patients and their families. But, isn't a white coat a uniform that conveys respect? Perhaps a white coat isn't safe if the physician wants to stand out to oncoming traffic in his snowy Minnesota environs.

Besides, is it true that patients don't want their physician to wear a polo shirt? Perhaps casual dress will break down 1 of the patient‐doctor barriers to communication and allow for improved comfort with greater honesty in patientphysician interactions? Prior to designing a prospective controlled randomized trial to answer this question myself, I reviewed the available literature.

It turns out, that an evaluation of polo‐shirt‐wearing physicians has been carried out. Drs. Barrett and Booth4 from the Birmingham Maternity Hospital in England questioned 203 groups of parents and children (406 individuals) about various levels of physician dress. Seventy percent of participants thought that how the doctor dressed was important. Among children, a male physician in a polo shirt was considered more friendly and gentle than the male physician in a white coat (who did get points for being more competent and more concerned). Women physicians in T‐shirts were also though to be friendlier than if in a white coat, but similarly less competent. Parents were more likely to prefer casually‐dressed physicians and were poor at predicting what their children would want.

So, a polo shirt makes me look friendly, gentle, and less competent? What about a polo shirt under a white coatis that the whole package? What about business attire, as per the Mayo Clinic requirements? These questions remain unanswered. So, back to the literature.

In the Journal of the American Medical Association, in 1987, Dunn et al.5 evaluated 200 medical patients in Boston and San Francisco regarding their preference for physician dress. Sixty‐five percent believed physicians should wear a white coat, 27% said no tennis shoes, one‐half said no blue jeans, and about one‐third thought male physicians should wear ties and female physicians should be in a skirt or dress. I suppose the conclusion here is to wear a white coat with or without jeans and most of the time without a tie, though almost always with proper shoes, or at least without tennis shoes. (I practice in Boston and trained partly in San Francisco so this advice seems particularly valid for me.)

It may be more obvious what to do in Japan. Ikusaka et al.6 evaluated the experience of patients at a university clinic seen by a consulting physician in either a white coat, or private clothes. To me, private clothes imply pajamas and a bathrobe, but we must assume this means some form of professional dress lacking a white coat. It turns out that 71% of the Japanese patients seeing a doctor in a white coat preferred a white coat, though more patients seeing a physician in a white coat (vs. private clothes) felt tense during their consultation. The researchers stress that the presence of a white coat did not increase satisfaction with the consultation. They conclude, that while patients may say they prefer a white coat, maybe it would be better not to wear one since it makes patients feel tense.

In addition to feeling tense, white coats may cause hypertension. The phenomenon of elevated blood pressure when in the presence of the physician (or other hospital staff in a white coat) has been long documented. This white coat hypertension can be found in more than 15% of the population who have a measured blood pressure in the office of over 140/90 mmHg with normal daytime mean ambulatory blood pressure readings (when not around a white‐coat‐wearing stress‐inducing medical worker).7 Older adults, females, and nonsmokers were more likely to have white coat hypertension than other persons.

And yet, older adults prefer white coats. The Japanese study (Ikusaka et al.6) concluded that elderly patients prefer a white coat to other attire. Similarly, a study from the Royal Free Hospital, London, showed that white coats were twice as popular with patients as they were with physicians.8 Specifically, patients found the white coats made doctors easier to identify. In an article by the British Broadcasting Corporation (BBC) on the subject, it was noted that the elderly largely preferred physicians in white coats, while children preferred physicians without white coats. British children must prefer a friendly doctor to a competent one.

The article further suggests that only 1 in 8 physicians wears a white coat, complaining that they are too hot and uncomfortable, and may carry the risk of transmitting infections. The white coat, the symbol of cleanliness and purity, a source of infection? To add hypocrisy to the equation, one‐half of physicians who thought white coats should be worn admitted to never actually wearing a white coat. In fact, only 7 of 86 physicians surveyed wore their white coat on a daily basis. The BBC goes on to note that in Australia, the white coat is gaining momentum as there seems to be a movement towards rediscovering the white coat as a symbol of purpose and pride as a profession.8

Really? Let's consult the literature! According to Dr. D.A. Watson,9 White coats have largely disappeared from Australian teaching hospitals and the majority of junior doctors in Australia oppose the wearing of white coats. In a survey of 337 junior medical officers, only 16% preferred to wear a white coat. Peer pressure seems to have something to do with this, as 70% say they don't wear a white coat because nobody else wears a white coat. This is indeed a compelling argument.

Of course, a better argument against wearing a white coat may be that it causes tension (at least in Japanese patients) and may cause white‐coat‐hypertension, resulting in the inappropriate diagnosis and treatment of elevated blood pressure. In Australia, however, it seems that wearing a white coat may make patients too relaxed. Wing et al.10 noted that in 21% to 45% of elderly patients, blood pressure was atypically low when checked in the physician's office as compared to mean ambulatory blood pressure. This reverse‐white‐coat‐hypertension could result in the omission of necessary blood pressure treatment.

In the United States, residentsour own version of the Australian junior medical officercommonly wear scrubs covered by a white coat. Scrub clothes are typically available without charge from the hospital, limit the amount of laundry a busy resident needs to do, and can be put on with little concern as to pressed pleats or matching colors. The overlying white coat adds a moderate degree of formality to what could otherwise be mistaken as pajamas, while providing convenient pockets for the aforementioned papers and miscellaneous equipment and souvenirs. This outfit is likely one of practicality rather than a desire to be most appealing to patients. But, what do you know? It seems that patients prefer their resident physicians to dress this way. Dr. A. Cha et al.11 at the Northeastern Ohio College of Medicine found that patients in an obstetrics and gynecology clinic overall felt that resident physicians dressed in surgical scrubs with a white coat made them feel more comfortable and confident than if dressed otherwise. On the question of a white coat specifically, the majority had no preference that their physician wear one.

So, it's very much unclear whether a white coat is a tension‐causing, blood‐pressure‐elevating, infection risk or a competence‐implying blood‐pressure‐lowering way to identify a physician. As a result, the jury is still out on whether physicians should wear white.

One thing I do know, however, is that patients shouldn't wear white. But they do. As an OtolaryngologistHead and Neck Surgeon, my clinical practice is split between surgical procedures and office visits. Commonly, patients with sinus or nasal surgery will require some form of cotton gauze or foam material within the nose in order to tamponade bleeding. Similarly, patients presenting to the emergency department or urgent care center with epistaxis may have their noses packed and then be told to see an otolaryngologist (eg, me) in 3 or 4 days to have the packing removed. I also commonly remove facial skin lesions, biopsy tongue masses, reduce nasal fractures, and otherwise engage in activities with an above average propensity to result in a mess. More often than happenstance will allow, patients come to see me for such visits in their white Sunday best. I truly care for my patients. I respect them as individuals and desire to do no harm. This includes not staining their shirts, ties, or pants. However, there is no amount of blue towels or gauze pads than can keep a white shirt clean when you have that first sneeze after removal of your nasal packing.12

So what is it that makes so many patients come to the office in a white shirt? Perhaps patients subconsciously associate healthcare with the color white since their doctors wear white coats and the nurses wear starched white dresses with tight white folded caps on top of their head. I've never seen a nurse in a white dress and hat, but believe television programs have shown this in the past.

Maybe the answer lies in an adaptation of data from another Australian study. In a survey of 180 oncology patients about white coats on physicians, the most common argument against wearing the white coat was that it represented a barrier between the physician and the patient.13 However, it is indeed the sane patient who desires to have a barrier between their physician and the removal of nasal packing, a skin lesion, or a tongue mass. Another possibility is that as fewer and fewer physicians wear white, patients are gravitating toward this color as a way of distinguishing themselves from the medical staff. Perhaps a person dressed in white is less likely to be grabbed in the hallway with a Doctor come quick! and more likely to be allowed to just sit peacefully in the waiting room with a 1997 issue of Ladies Home Journal or Senior Fisherman magazine.

Of course, perhaps patients believe the fashion experts who expound that white goes with everything. If so, they soon learn that white doesn't go so well with blotchy splattered red.

The truth is, I don't want my patients to wear white. Between making certain I project myself as approachable and easy to speak with, remembering to cover all the appropriate irrelevant parts of the history and physical to comply with billing requirements, entering data in our easy‐to‐navigate electronic medical record, and attempting to both diagnose the problem and discern an acceptable and effective treatment, the last thing I need is to worry about staining patient shirts! I believe that this phenomenon is widespread among medical practitioners and should be called white‐shirt‐hypertension.

Conclusion

After reviewing the available literature, I've determined that patients should not wear white. However, I'm still not certain how I should dress. For now, I'll stick with whatever is clean and professional and make sure my belt and shoes match. I may or may not wear a tie, since another study showed that 30% of patients believed their physician wore a tie even if they didn't.14 Of course, I'll put on the white coat for the semiannual meeting with the chairman, or if I'm having something messy for lunch and wore a tie that day.

I'll also wear my name badge. It says I'm an attending physician and not a resident. It opens doors around the hospital. Literally. It's got a magnetic stripe.

A 59‐year‐old white female, with a 3‐year history of Port‐A‐Cath (PAC) placement for abdominal mesothelioma, presented with 2 episodes of cardiac palpitations. The onset of palpitations occurred 2 days prior to admission, following 15 minutes of vigorous but failed attempts to access the PAC with normal saline and tissue plasminogen activator at her oncologist's office. Although asymptomatic at the time of manipulation, each episode was triggered by subsequent exertion, lasting for about 1 minute, and not associated with chest pain. Electrocardiogram showed normal sinus rhythm and occasional premature ventricular contractions. A chest x‐ray showed a catheter fragment spanning the right atrium and ventricle (Figure 1). Computed tomography (CT) scan confirmed a 10‐cm dislodged catheter (Figure 2). Following emergent catheter retrieval via right‐sided heart catheterization, the patient's symptoms resolved. At least 42 cases of catheter embolization have been reported in the recent literature.1 Of these cases, only 7% had palpitations. Although rare, catheter fracture should be considered in patients with palpitations and history of indwelling venous catheter.

Figure 1

Figure 2

A 59‐year‐old white female, with a 3‐year history of Port‐A‐Cath (PAC) placement for abdominal mesothelioma, presented with 2 episodes of cardiac palpitations. The onset of palpitations occurred 2 days prior to admission, following 15 minutes of vigorous but failed attempts to access the PAC with normal saline and tissue plasminogen activator at her oncologist's office. Although asymptomatic at the time of manipulation, each episode was triggered by subsequent exertion, lasting for about 1 minute, and not associated with chest pain. Electrocardiogram showed normal sinus rhythm and occasional premature ventricular contractions. A chest x‐ray showed a catheter fragment spanning the right atrium and ventricle (Figure 1). Computed tomography (CT) scan confirmed a 10‐cm dislodged catheter (Figure 2). Following emergent catheter retrieval via right‐sided heart catheterization, the patient's symptoms resolved. At least 42 cases of catheter embolization have been reported in the recent literature.1 Of these cases, only 7% had palpitations. Although rare, catheter fracture should be considered in patients with palpitations and history of indwelling venous catheter.

Figure 1

Figure 2

A 59‐year‐old white female, with a 3‐year history of Port‐A‐Cath (PAC) placement for abdominal mesothelioma, presented with 2 episodes of cardiac palpitations. The onset of palpitations occurred 2 days prior to admission, following 15 minutes of vigorous but failed attempts to access the PAC with normal saline and tissue plasminogen activator at her oncologist's office. Although asymptomatic at the time of manipulation, each episode was triggered by subsequent exertion, lasting for about 1 minute, and not associated with chest pain. Electrocardiogram showed normal sinus rhythm and occasional premature ventricular contractions. A chest x‐ray showed a catheter fragment spanning the right atrium and ventricle (Figure 1). Computed tomography (CT) scan confirmed a 10‐cm dislodged catheter (Figure 2). Following emergent catheter retrieval via right‐sided heart catheterization, the patient's symptoms resolved. At least 42 cases of catheter embolization have been reported in the recent literature.1 Of these cases, only 7% had palpitations. Although rare, catheter fracture should be considered in patients with palpitations and history of indwelling venous catheter.

Figure 1

Figure 2

Focal bacterial infections (FBIs), including otitis media (OM), cellulitis, and lymphadenitis, can occur at any age and are usually treated with oral antibiotics. When patients with focal infections present as a young infant, healthcare providers often worry about the risk of coexisting or concomitant systemic infections (CSIs), often termed serious bacterial infections (SBIs) in the published literature.1, 2 Risk of CSI becomes more worrisome when young infants have fever as part of their presentation, especially within the traditional rule‐out sepsis age range of less than 2 months. Often, these patients are well‐appearing and lack prenatal and neonatal risk factors for systemic infections, but are assumed to be at high risk for CSI based on the presence of focal bacterial infection.1, 3, 4

FBIs have been the subject of multiple studies, especially OM and cellulitis. However, few investigations have looked specifically at infants less than 60 days of age, lending uncertainty to medical decision‐making for both community and emergency physicians. Therefore, no standardized evidence‐based practice exists for treating young infants with FBIs. While some clinicians treat these infections using systemic antibiotics without performing laboratory tests, others opt for a full diagnostic evaluation for CSI; including serum blood counts, blood cultures, lumbar punctures (LPs), and bladder catheterizations. Also, some clinicians opt for treatment with oral antibiotics at home, while others choose intravenous (IV) antibiotics and hospitalization.

These decisions are likely due to studies of febrile infants under 60 days of age who present to an emergency department (ED), appear well, and have no focal source of infection on exam, yet are known to have a risk of systemic or occult bacterial infection of roughly 10%.310 There are no such studies documenting the risk of CSI in well‐appearing, afebrile patients, as fever is regarded as the main risk factor for CSI in this age.

Based on our clinical experience and review of the literature, we felt that afebrile, well‐appearing infants less than 60 days of age with an FBI on exam would have a very low risk of CSI. The primary objectives of this study were to determine the risk of CSI when presented with a well‐appearing infant who has an FBI on exam and to examine that risk in relation to the presence of fever. Other objectives were to describe the clinical presentation of FBIs in well‐appearing infants in this age group and to describe the current management and resource utilization of such infections in the ED.

Patients and Methods

Results

Secondary Study OutcomeCurrent Management of FBI in the ED: Resource Utilization

Febrile patients underwent significantly more diagnostic testing procedures than afebrile infants. Specifically, CBCs, peripheral blood cultures, urine analyses with cultures, LPs, and radiographic imaging were performed more often in infants with fever (Figure 1). Fifty‐seven infants had urine cultures performed: 32 of 158 afebrile infants and 25 of 39 febrile infants. Among these selected infants, again 3 UTIs occurred: 1 of 32 tested (3.1%) in the afebrile group and 2 of 25 tested (8%) in the febrile group. A total of 115 infants had blood cultures performed: 82 of the 158 afebrile infants and 33 of the 39 febrile infants. Among these selected infants, again 1 positive blood culture occurred: 0 of 82 tested (0%) in the afebrile group and 1 of 33 tested (3%) in the febrile group. Fifty‐five infants had LP performed: 35 of 158 afebrile infants and 30 of 39 febrile infants. No case of meningitis occurred in these selected infants. Twenty infants had diagnostic radiographs performed, 10 in the febrile group and 10 in the afebrile group. None of the radiographs showed signs of pneumonia on final radiology attending reading.

Figure 1

Overall, 33 of 39 febrile infants had cultures drawn and/or radiographs performed, with 3 CSIs discovered, and 87 of 158 afebrile infants had cultures drawn and/or radiographs performed, with 1 CSI discovered (Table 3). This means that 77 infants diagnosed with FBIs did not have any diagnostic testing for CSI performed while in the ED. The overall risk of CSI in patients who were tested was 3.3%. Comparing febrile and afebrile patients who had diagnostic workups performed, febrile infants had a trend toward increased risk of CSI (OR, 8.6; 95% CI, 0.8613‐85.8686).

Table 3.Presence of CSI in Patients Who Underwent Diagnostic Workups

	CSI	No CSI	Risk (%)
Abbreviation: CSI, concomitant systemic infection.
Febrile (n = 33)	3	30	9.1
Afebrile (n = 87)	1	86	1.1
Totals (n = 120)	4	116	3.3

No significant differences existed in the use of consultants, use of IV antibiotics, or admission rate. Sixty‐six (42%) of the 158 afebrile infants were admitted. The average length of stay for these infants was 2.59 days (range, 1‐22 days). This included a 22‐day‐old female with mastitis who required multiple surgeries and a protracted hospital course. Sixteen (41%) of the febrile infants were admitted and had an average stay of 2.87 days (range, 1‐6 days).

Discussion

This study is the first to investigate the risk of CSI specifically in well‐appearing infants under 60 days of age presenting with FBI. Inclusion criteria were not limited to 1 specific infection, ie, OM, but included all FBI. This study demonstrated that the risk of CSI in afebrile infants is small (0.6%), which is similar to what has been shown in the OM literature.19, 20 However, the risk of CSI among febrile infants is not negligible (7.7%), and is similar to the risk of SBIs among young infants presenting with a fever of unknown source.57

Limitations

The main limitation of our study was the retrospective design. A research assistant utilizing a computerized database program of ED patients performed the initial query based upon search criteria. A local expert using an established list of International Statistical Classification of Diseases and Related Health Problems (ICD) codes for any and all of the FBIs performed the chart review. Secondary diagnoses may have been omitted as a result of limited physician charting, which could have resulted in missed patients. CCHMC is currently transitioning from paper records to electronic medical records, which may explain why 12 charts were not found, despite exhaustive searches for them. Ultimately, 94% of all the eligible patients were found. Yet, with so few CSI diagnosed, 1 or 2 could conceivably change our results. As noted above, focal infections in infants under 2 months of age seem to be uncommon, not only in the ED setting, but also in a large cohort of primary care patients.35 With only a small number FBIs present over 6 years and so few having CSIs, we were limited to a univariate analysis, which limited our potential results and conclusions. Performing this study prospectively would have addressed these limitations, but would have required years of recruitment or multicenter collaboration.

Another potential limitation was the search strategy to identify eligible infants. Specifically, we did not search the records for infants diagnosed with UTI, bacteremia, or meningitis. Infants with these more serious conditions may have been coded as the primary or only problem, even if other problems such as OM were also present. Therefore, we may have underestimated the occurrence of systemic bacterial complications in a systematic way. This form of spectrum bias was a potential limitation. We approached this clinical question from the eye of the emergency department practitioner and thus used a search strategy based on the discharge diagnosis from the ED. If we were to look back to see if any patients discharged from the hospital with CSI also had FBI, we doubt our retrospective design would have allowed identification of patients with FBIs.

Other limitations may be our definition of CSI and the potential for missed CSIs. We defined meningitis, bacteremia, and UTI as a positive CSF, blood, or urine culture, respectively. Many studies are now defining culture‐negative meningitis or UTI based on WBC findings on a screening cell count or urine microscopy. However, because no patients were pretreated with antibiotics, we felt that a positive culture from a sterile site was a reasonable definition. Also, not all of the enrolled patients received full diagnostic workups to screen for CSI. In the smaller cohort of infants who received diagnostic testing, febrile infants still seemed to be at higher risk for CSI. To capture all possible CSIs, one would have needed to perform blood culture, suprapubic bladder aspiration, or catheterization for urine culture, LP, and chest radiograph on all patients with an FBI. Given the low risk of CSI in the United States, the previous literature's hinting at low risk for CSI in afebrile patients, and the presence of multiple clinical trials defining low risk characteristics for CSI, such a protocol would not receive support as being standard clinical practice and have difficulty being permitted by an institutional review board.

Another limitation of our study was follow‐up. Ideally, every patient would have been contacted to ensure reliable outcomes measurement. Patients may have been seen after their initial evaluation at their primary care provider's office or at another healthcare facility and had more diagnostic studies performed. However, because our institution is the sole admitting pediatric center in the area, particularly in infants, and most CSIs in this age group require admission; we feel that a reasonable degree of reliability for the outcomes of interest was maintained.

Last, we could not establish the rationale of clinical decision making, as our study was retrospective. For example, staff physicians may have foregone diagnostic testing if they had committed to a therapeutic course of antibiotics and felt diagnostic cultures would not change management. Also, we cannot ensure that interpretation of culture results was consistent with national standards. As described previously, 1 afebrile infant in our study potentially had a CSI that was clinically felt to be a contaminant by the inpatient healthcare team. This 11‐day‐old female was admitted with mastitis and had a negative urinalysis, but grew E. coli on urine culture. This was treated as a contaminant by the ward team, despite her age.

Conclusions

CSI is very uncommon in afebrile, well‐appearing infants under 2 months of age with an FBI. However, febrile infants have a greater risk of CSI. UTI is the most common CSI in well‐appearing infants less than 2 months of age with an FBI found on examination. Prospective, multicentered studies need to be performed to determine whether diagnostic evaluation should change the management of well‐appearing infants with an FBI found on examination.

Focal bacterial infections (FBIs), including otitis media (OM), cellulitis, and lymphadenitis, can occur at any age and are usually treated with oral antibiotics. When patients with focal infections present as a young infant, healthcare providers often worry about the risk of coexisting or concomitant systemic infections (CSIs), often termed serious bacterial infections (SBIs) in the published literature.1, 2 Risk of CSI becomes more worrisome when young infants have fever as part of their presentation, especially within the traditional rule‐out sepsis age range of less than 2 months. Often, these patients are well‐appearing and lack prenatal and neonatal risk factors for systemic infections, but are assumed to be at high risk for CSI based on the presence of focal bacterial infection.1, 3, 4

FBIs have been the subject of multiple studies, especially OM and cellulitis. However, few investigations have looked specifically at infants less than 60 days of age, lending uncertainty to medical decision‐making for both community and emergency physicians. Therefore, no standardized evidence‐based practice exists for treating young infants with FBIs. While some clinicians treat these infections using systemic antibiotics without performing laboratory tests, others opt for a full diagnostic evaluation for CSI; including serum blood counts, blood cultures, lumbar punctures (LPs), and bladder catheterizations. Also, some clinicians opt for treatment with oral antibiotics at home, while others choose intravenous (IV) antibiotics and hospitalization.

These decisions are likely due to studies of febrile infants under 60 days of age who present to an emergency department (ED), appear well, and have no focal source of infection on exam, yet are known to have a risk of systemic or occult bacterial infection of roughly 10%.310 There are no such studies documenting the risk of CSI in well‐appearing, afebrile patients, as fever is regarded as the main risk factor for CSI in this age.

Based on our clinical experience and review of the literature, we felt that afebrile, well‐appearing infants less than 60 days of age with an FBI on exam would have a very low risk of CSI. The primary objectives of this study were to determine the risk of CSI when presented with a well‐appearing infant who has an FBI on exam and to examine that risk in relation to the presence of fever. Other objectives were to describe the clinical presentation of FBIs in well‐appearing infants in this age group and to describe the current management and resource utilization of such infections in the ED.

Patients and Methods

Results

Secondary Study OutcomeCurrent Management of FBI in the ED: Resource Utilization

Febrile patients underwent significantly more diagnostic testing procedures than afebrile infants. Specifically, CBCs, peripheral blood cultures, urine analyses with cultures, LPs, and radiographic imaging were performed more often in infants with fever (Figure 1). Fifty‐seven infants had urine cultures performed: 32 of 158 afebrile infants and 25 of 39 febrile infants. Among these selected infants, again 3 UTIs occurred: 1 of 32 tested (3.1%) in the afebrile group and 2 of 25 tested (8%) in the febrile group. A total of 115 infants had blood cultures performed: 82 of the 158 afebrile infants and 33 of the 39 febrile infants. Among these selected infants, again 1 positive blood culture occurred: 0 of 82 tested (0%) in the afebrile group and 1 of 33 tested (3%) in the febrile group. Fifty‐five infants had LP performed: 35 of 158 afebrile infants and 30 of 39 febrile infants. No case of meningitis occurred in these selected infants. Twenty infants had diagnostic radiographs performed, 10 in the febrile group and 10 in the afebrile group. None of the radiographs showed signs of pneumonia on final radiology attending reading.

Figure 1

Overall, 33 of 39 febrile infants had cultures drawn and/or radiographs performed, with 3 CSIs discovered, and 87 of 158 afebrile infants had cultures drawn and/or radiographs performed, with 1 CSI discovered (Table 3). This means that 77 infants diagnosed with FBIs did not have any diagnostic testing for CSI performed while in the ED. The overall risk of CSI in patients who were tested was 3.3%. Comparing febrile and afebrile patients who had diagnostic workups performed, febrile infants had a trend toward increased risk of CSI (OR, 8.6; 95% CI, 0.8613‐85.8686).

Table 3.Presence of CSI in Patients Who Underwent Diagnostic Workups

	CSI	No CSI	Risk (%)
Abbreviation: CSI, concomitant systemic infection.
Febrile (n = 33)	3	30	9.1
Afebrile (n = 87)	1	86	1.1
Totals (n = 120)	4	116	3.3

No significant differences existed in the use of consultants, use of IV antibiotics, or admission rate. Sixty‐six (42%) of the 158 afebrile infants were admitted. The average length of stay for these infants was 2.59 days (range, 1‐22 days). This included a 22‐day‐old female with mastitis who required multiple surgeries and a protracted hospital course. Sixteen (41%) of the febrile infants were admitted and had an average stay of 2.87 days (range, 1‐6 days).

Discussion

This study is the first to investigate the risk of CSI specifically in well‐appearing infants under 60 days of age presenting with FBI. Inclusion criteria were not limited to 1 specific infection, ie, OM, but included all FBI. This study demonstrated that the risk of CSI in afebrile infants is small (0.6%), which is similar to what has been shown in the OM literature.19, 20 However, the risk of CSI among febrile infants is not negligible (7.7%), and is similar to the risk of SBIs among young infants presenting with a fever of unknown source.57

Limitations

The main limitation of our study was the retrospective design. A research assistant utilizing a computerized database program of ED patients performed the initial query based upon search criteria. A local expert using an established list of International Statistical Classification of Diseases and Related Health Problems (ICD) codes for any and all of the FBIs performed the chart review. Secondary diagnoses may have been omitted as a result of limited physician charting, which could have resulted in missed patients. CCHMC is currently transitioning from paper records to electronic medical records, which may explain why 12 charts were not found, despite exhaustive searches for them. Ultimately, 94% of all the eligible patients were found. Yet, with so few CSI diagnosed, 1 or 2 could conceivably change our results. As noted above, focal infections in infants under 2 months of age seem to be uncommon, not only in the ED setting, but also in a large cohort of primary care patients.35 With only a small number FBIs present over 6 years and so few having CSIs, we were limited to a univariate analysis, which limited our potential results and conclusions. Performing this study prospectively would have addressed these limitations, but would have required years of recruitment or multicenter collaboration.

Another potential limitation was the search strategy to identify eligible infants. Specifically, we did not search the records for infants diagnosed with UTI, bacteremia, or meningitis. Infants with these more serious conditions may have been coded as the primary or only problem, even if other problems such as OM were also present. Therefore, we may have underestimated the occurrence of systemic bacterial complications in a systematic way. This form of spectrum bias was a potential limitation. We approached this clinical question from the eye of the emergency department practitioner and thus used a search strategy based on the discharge diagnosis from the ED. If we were to look back to see if any patients discharged from the hospital with CSI also had FBI, we doubt our retrospective design would have allowed identification of patients with FBIs.

Other limitations may be our definition of CSI and the potential for missed CSIs. We defined meningitis, bacteremia, and UTI as a positive CSF, blood, or urine culture, respectively. Many studies are now defining culture‐negative meningitis or UTI based on WBC findings on a screening cell count or urine microscopy. However, because no patients were pretreated with antibiotics, we felt that a positive culture from a sterile site was a reasonable definition. Also, not all of the enrolled patients received full diagnostic workups to screen for CSI. In the smaller cohort of infants who received diagnostic testing, febrile infants still seemed to be at higher risk for CSI. To capture all possible CSIs, one would have needed to perform blood culture, suprapubic bladder aspiration, or catheterization for urine culture, LP, and chest radiograph on all patients with an FBI. Given the low risk of CSI in the United States, the previous literature's hinting at low risk for CSI in afebrile patients, and the presence of multiple clinical trials defining low risk characteristics for CSI, such a protocol would not receive support as being standard clinical practice and have difficulty being permitted by an institutional review board.

Another limitation of our study was follow‐up. Ideally, every patient would have been contacted to ensure reliable outcomes measurement. Patients may have been seen after their initial evaluation at their primary care provider's office or at another healthcare facility and had more diagnostic studies performed. However, because our institution is the sole admitting pediatric center in the area, particularly in infants, and most CSIs in this age group require admission; we feel that a reasonable degree of reliability for the outcomes of interest was maintained.

Last, we could not establish the rationale of clinical decision making, as our study was retrospective. For example, staff physicians may have foregone diagnostic testing if they had committed to a therapeutic course of antibiotics and felt diagnostic cultures would not change management. Also, we cannot ensure that interpretation of culture results was consistent with national standards. As described previously, 1 afebrile infant in our study potentially had a CSI that was clinically felt to be a contaminant by the inpatient healthcare team. This 11‐day‐old female was admitted with mastitis and had a negative urinalysis, but grew E. coli on urine culture. This was treated as a contaminant by the ward team, despite her age.

Conclusions

CSI is very uncommon in afebrile, well‐appearing infants under 2 months of age with an FBI. However, febrile infants have a greater risk of CSI. UTI is the most common CSI in well‐appearing infants less than 2 months of age with an FBI found on examination. Prospective, multicentered studies need to be performed to determine whether diagnostic evaluation should change the management of well‐appearing infants with an FBI found on examination.

Focal bacterial infections (FBIs), including otitis media (OM), cellulitis, and lymphadenitis, can occur at any age and are usually treated with oral antibiotics. When patients with focal infections present as a young infant, healthcare providers often worry about the risk of coexisting or concomitant systemic infections (CSIs), often termed serious bacterial infections (SBIs) in the published literature.1, 2 Risk of CSI becomes more worrisome when young infants have fever as part of their presentation, especially within the traditional rule‐out sepsis age range of less than 2 months. Often, these patients are well‐appearing and lack prenatal and neonatal risk factors for systemic infections, but are assumed to be at high risk for CSI based on the presence of focal bacterial infection.1, 3, 4

FBIs have been the subject of multiple studies, especially OM and cellulitis. However, few investigations have looked specifically at infants less than 60 days of age, lending uncertainty to medical decision‐making for both community and emergency physicians. Therefore, no standardized evidence‐based practice exists for treating young infants with FBIs. While some clinicians treat these infections using systemic antibiotics without performing laboratory tests, others opt for a full diagnostic evaluation for CSI; including serum blood counts, blood cultures, lumbar punctures (LPs), and bladder catheterizations. Also, some clinicians opt for treatment with oral antibiotics at home, while others choose intravenous (IV) antibiotics and hospitalization.

These decisions are likely due to studies of febrile infants under 60 days of age who present to an emergency department (ED), appear well, and have no focal source of infection on exam, yet are known to have a risk of systemic or occult bacterial infection of roughly 10%.310 There are no such studies documenting the risk of CSI in well‐appearing, afebrile patients, as fever is regarded as the main risk factor for CSI in this age.

Based on our clinical experience and review of the literature, we felt that afebrile, well‐appearing infants less than 60 days of age with an FBI on exam would have a very low risk of CSI. The primary objectives of this study were to determine the risk of CSI when presented with a well‐appearing infant who has an FBI on exam and to examine that risk in relation to the presence of fever. Other objectives were to describe the clinical presentation of FBIs in well‐appearing infants in this age group and to describe the current management and resource utilization of such infections in the ED.

Patients and Methods

Results

Secondary Study OutcomeCurrent Management of FBI in the ED: Resource Utilization

Febrile patients underwent significantly more diagnostic testing procedures than afebrile infants. Specifically, CBCs, peripheral blood cultures, urine analyses with cultures, LPs, and radiographic imaging were performed more often in infants with fever (Figure 1). Fifty‐seven infants had urine cultures performed: 32 of 158 afebrile infants and 25 of 39 febrile infants. Among these selected infants, again 3 UTIs occurred: 1 of 32 tested (3.1%) in the afebrile group and 2 of 25 tested (8%) in the febrile group. A total of 115 infants had blood cultures performed: 82 of the 158 afebrile infants and 33 of the 39 febrile infants. Among these selected infants, again 1 positive blood culture occurred: 0 of 82 tested (0%) in the afebrile group and 1 of 33 tested (3%) in the febrile group. Fifty‐five infants had LP performed: 35 of 158 afebrile infants and 30 of 39 febrile infants. No case of meningitis occurred in these selected infants. Twenty infants had diagnostic radiographs performed, 10 in the febrile group and 10 in the afebrile group. None of the radiographs showed signs of pneumonia on final radiology attending reading.

Figure 1

Overall, 33 of 39 febrile infants had cultures drawn and/or radiographs performed, with 3 CSIs discovered, and 87 of 158 afebrile infants had cultures drawn and/or radiographs performed, with 1 CSI discovered (Table 3). This means that 77 infants diagnosed with FBIs did not have any diagnostic testing for CSI performed while in the ED. The overall risk of CSI in patients who were tested was 3.3%. Comparing febrile and afebrile patients who had diagnostic workups performed, febrile infants had a trend toward increased risk of CSI (OR, 8.6; 95% CI, 0.8613‐85.8686).

Table 3.Presence of CSI in Patients Who Underwent Diagnostic Workups

	CSI	No CSI	Risk (%)
Abbreviation: CSI, concomitant systemic infection.
Febrile (n = 33)	3	30	9.1
Afebrile (n = 87)	1	86	1.1
Totals (n = 120)	4	116	3.3

No significant differences existed in the use of consultants, use of IV antibiotics, or admission rate. Sixty‐six (42%) of the 158 afebrile infants were admitted. The average length of stay for these infants was 2.59 days (range, 1‐22 days). This included a 22‐day‐old female with mastitis who required multiple surgeries and a protracted hospital course. Sixteen (41%) of the febrile infants were admitted and had an average stay of 2.87 days (range, 1‐6 days).

Discussion

This study is the first to investigate the risk of CSI specifically in well‐appearing infants under 60 days of age presenting with FBI. Inclusion criteria were not limited to 1 specific infection, ie, OM, but included all FBI. This study demonstrated that the risk of CSI in afebrile infants is small (0.6%), which is similar to what has been shown in the OM literature.19, 20 However, the risk of CSI among febrile infants is not negligible (7.7%), and is similar to the risk of SBIs among young infants presenting with a fever of unknown source.57

Limitations

The main limitation of our study was the retrospective design. A research assistant utilizing a computerized database program of ED patients performed the initial query based upon search criteria. A local expert using an established list of International Statistical Classification of Diseases and Related Health Problems (ICD) codes for any and all of the FBIs performed the chart review. Secondary diagnoses may have been omitted as a result of limited physician charting, which could have resulted in missed patients. CCHMC is currently transitioning from paper records to electronic medical records, which may explain why 12 charts were not found, despite exhaustive searches for them. Ultimately, 94% of all the eligible patients were found. Yet, with so few CSI diagnosed, 1 or 2 could conceivably change our results. As noted above, focal infections in infants under 2 months of age seem to be uncommon, not only in the ED setting, but also in a large cohort of primary care patients.35 With only a small number FBIs present over 6 years and so few having CSIs, we were limited to a univariate analysis, which limited our potential results and conclusions. Performing this study prospectively would have addressed these limitations, but would have required years of recruitment or multicenter collaboration.

Another potential limitation was the search strategy to identify eligible infants. Specifically, we did not search the records for infants diagnosed with UTI, bacteremia, or meningitis. Infants with these more serious conditions may have been coded as the primary or only problem, even if other problems such as OM were also present. Therefore, we may have underestimated the occurrence of systemic bacterial complications in a systematic way. This form of spectrum bias was a potential limitation. We approached this clinical question from the eye of the emergency department practitioner and thus used a search strategy based on the discharge diagnosis from the ED. If we were to look back to see if any patients discharged from the hospital with CSI also had FBI, we doubt our retrospective design would have allowed identification of patients with FBIs.

Other limitations may be our definition of CSI and the potential for missed CSIs. We defined meningitis, bacteremia, and UTI as a positive CSF, blood, or urine culture, respectively. Many studies are now defining culture‐negative meningitis or UTI based on WBC findings on a screening cell count or urine microscopy. However, because no patients were pretreated with antibiotics, we felt that a positive culture from a sterile site was a reasonable definition. Also, not all of the enrolled patients received full diagnostic workups to screen for CSI. In the smaller cohort of infants who received diagnostic testing, febrile infants still seemed to be at higher risk for CSI. To capture all possible CSIs, one would have needed to perform blood culture, suprapubic bladder aspiration, or catheterization for urine culture, LP, and chest radiograph on all patients with an FBI. Given the low risk of CSI in the United States, the previous literature's hinting at low risk for CSI in afebrile patients, and the presence of multiple clinical trials defining low risk characteristics for CSI, such a protocol would not receive support as being standard clinical practice and have difficulty being permitted by an institutional review board.

Another limitation of our study was follow‐up. Ideally, every patient would have been contacted to ensure reliable outcomes measurement. Patients may have been seen after their initial evaluation at their primary care provider's office or at another healthcare facility and had more diagnostic studies performed. However, because our institution is the sole admitting pediatric center in the area, particularly in infants, and most CSIs in this age group require admission; we feel that a reasonable degree of reliability for the outcomes of interest was maintained.

Last, we could not establish the rationale of clinical decision making, as our study was retrospective. For example, staff physicians may have foregone diagnostic testing if they had committed to a therapeutic course of antibiotics and felt diagnostic cultures would not change management. Also, we cannot ensure that interpretation of culture results was consistent with national standards. As described previously, 1 afebrile infant in our study potentially had a CSI that was clinically felt to be a contaminant by the inpatient healthcare team. This 11‐day‐old female was admitted with mastitis and had a negative urinalysis, but grew E. coli on urine culture. This was treated as a contaminant by the ward team, despite her age.

Conclusions

CSI is very uncommon in afebrile, well‐appearing infants under 2 months of age with an FBI. However, febrile infants have a greater risk of CSI. UTI is the most common CSI in well‐appearing infants less than 2 months of age with an FBI found on examination. Prospective, multicentered studies need to be performed to determine whether diagnostic evaluation should change the management of well‐appearing infants with an FBI found on examination.

If you wish to receive credit for this activity, which beginson the next page, please refer to the website: www.blackwellpublishing.com/cme.

Accreditation and Designation Statement

Blackwell Futura Media Services designates this educational activity for a 1 AMA PRA Category 1 Credit. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Blackwell Futura Media Services is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Educational Objectives

Continuous participation in the Journal of Hospital Medicine CME program will enable learners to be better able to:

• Interpret clinical guidelines and their applications for higher quality and more efficient care for all hospitalized patients.

• Describe the standard of care for common illnesses and conditions treated in the hospital; such as pneumonia, COPD exacerbation, acute coronary syndrome, HF exacerbation, glycemic control, venous thromboembolic disease, stroke, etc.

• Discuss evidence‐based recommendations involving transitions of care, including the hospital discharge process.

• Gain insights into the roles of hospitalists as medical educators, researchers, medical ethicists, palliative care providers, and hospital‐based geriatricians.

• Incorporate best practices for hospitalist administration, including quality improvement, patient safety, practice management, leadership, and demonstrating hospitalist value.

• Identify evidence‐based best practices and trends for both adult and pediatric hospital medicine.

Instructions on Receiving Credit

For information on applicability and acceptance of continuing medical education credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity during the valid credit period that is noted on the title page.

Follow these steps to earn credit:

• Log on to www.blackwellpublishing.com/cme.

• Read the target audience, learning objectives, and author disclosures.

• Read the article in print or online format.

• Reflect on the article.

• Access the CME Exam, and choose the best answer to each question.

• Complete the required evaluation component of the activity.

If you wish to receive credit for this activity, which beginson the next page, please refer to the website: www.blackwellpublishing.com/cme.

Accreditation and Designation Statement

Blackwell Futura Media Services designates this educational activity for a 1 AMA PRA Category 1 Credit. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Blackwell Futura Media Services is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Educational Objectives

Continuous participation in the Journal of Hospital Medicine CME program will enable learners to be better able to:

• Interpret clinical guidelines and their applications for higher quality and more efficient care for all hospitalized patients.

• Describe the standard of care for common illnesses and conditions treated in the hospital; such as pneumonia, COPD exacerbation, acute coronary syndrome, HF exacerbation, glycemic control, venous thromboembolic disease, stroke, etc.

• Discuss evidence‐based recommendations involving transitions of care, including the hospital discharge process.

• Gain insights into the roles of hospitalists as medical educators, researchers, medical ethicists, palliative care providers, and hospital‐based geriatricians.

• Incorporate best practices for hospitalist administration, including quality improvement, patient safety, practice management, leadership, and demonstrating hospitalist value.

• Identify evidence‐based best practices and trends for both adult and pediatric hospital medicine.

Instructions on Receiving Credit

For information on applicability and acceptance of continuing medical education credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity during the valid credit period that is noted on the title page.

Follow these steps to earn credit:

• Log on to www.blackwellpublishing.com/cme.

• Read the target audience, learning objectives, and author disclosures.

• Read the article in print or online format.

• Reflect on the article.

• Access the CME Exam, and choose the best answer to each question.

• Complete the required evaluation component of the activity.

If you wish to receive credit for this activity, which beginson the next page, please refer to the website: www.blackwellpublishing.com/cme.

Accreditation and Designation Statement

Blackwell Futura Media Services designates this educational activity for a 1 AMA PRA Category 1 Credit. Physicians should only claim credit commensurate with the extent of their participation in the activity.

Blackwell Futura Media Services is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

Educational Objectives

Continuous participation in the Journal of Hospital Medicine CME program will enable learners to be better able to:

• Interpret clinical guidelines and their applications for higher quality and more efficient care for all hospitalized patients.

• Describe the standard of care for common illnesses and conditions treated in the hospital; such as pneumonia, COPD exacerbation, acute coronary syndrome, HF exacerbation, glycemic control, venous thromboembolic disease, stroke, etc.

• Discuss evidence‐based recommendations involving transitions of care, including the hospital discharge process.

• Gain insights into the roles of hospitalists as medical educators, researchers, medical ethicists, palliative care providers, and hospital‐based geriatricians.

• Incorporate best practices for hospitalist administration, including quality improvement, patient safety, practice management, leadership, and demonstrating hospitalist value.

• Identify evidence‐based best practices and trends for both adult and pediatric hospital medicine.

Instructions on Receiving Credit

For information on applicability and acceptance of continuing medical education credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity during the valid credit period that is noted on the title page.

Follow these steps to earn credit:

• Log on to www.blackwellpublishing.com/cme.

• Read the target audience, learning objectives, and author disclosures.

• Read the article in print or online format.

• Reflect on the article.

• Access the CME Exam, and choose the best answer to each question.

• Complete the required evaluation component of the activity.

Historically, the milk‐alkali syndrome developed as an adverse reaction to the Sippy regimen of frequent feedings of milk, cream, and alkaline powders as treatment for peptic ulcer disease.1 The classic description includes hypercalcemia, metabolic alkalosis, and renal failure. This syndrome seemingly disappeared when modern acid suppression therapies such as histamine‐2 blockers and proton pump inhibitors improved dyspepsia treatment. Over the past 20 years, milk‐alkali syndrome has had a resurgence, as consumption of supplements containing calcium has increased.2 Calcium carbonate supplements are a popular over‐the‐counter treatment for osteoporosis, dyspepsia, hypocalcemia, and hyperphosphatemia; these supplements provide both the calcium and alkali required for the development of milk‐alkali syndrome.

A 46‐year‐old man presented to the emergency department after his physician ordered outpatient laboratory tests to evaluate his fatigue. The patient was found to have acute renal failure and hypercalcemia. His serum creatinine was 3.6 mg/dL, increased from his baseline of 1.1 mg/dL several months prior, and his serum calcium was 14.9 mg/dL. Ten days prior to admission he developed increasing fatigue, decreased appetite, and decreased urine output, which he attributed to recent manual labor during summer. He reported taking an occasional calcium carbonate (Tums) for dyspepsia. He did not report pain or other complaints.

His medical history included hypertension and hyperlipidemia. He had a colonoscopy 1 year prior to presentation that was significant for a high‐grade dysplastic polyp and was currently due for repeat colonoscopy. His medications included clonidine, lisinopril, and aspirin. He had no recent medication changes. He had a 30 pack/year history of cigarette smoking and drank occasionally.

On physical exam, his temperature was 99.8F, blood pressure 97/48 mmHg, heart rate 89 beats per minute, respirations 20 breaths per minute, with a room air saturation of 97%. He had dry mucus membranes and the remainder of the physical exam was unremarkable.

In the emergency department laboratory testing revealed a creatinine of 4.6 mg/dL, serum total calcium of 15.9 mg/dL, serum bicarbonate level of 26 mmol/L, phosphate of 3.9 mg/dL, albumin of 4.4 gm/dL, and alkaline phosphatase of 92 IU/L. The urine specific gravity was 1.019 gm/mL (see Table 1 for the patient's complete admission laboratory values).

His intact parathyroid (PTH) hormone was 18.8 pg/mL (normal, 15‐65). PTH hormone‐related peptide (PTHrP) was <2.5 pmol/L. After reviewing these laboratory test results, we proceeded with further questioning, during which he admitted to taking approximately 15 to 20 Tums (>7.5 gm of calcium carbonate) daily for dyspepsia rather than the occasional Tums he had originally reported. Over the next 3 days, his calcium decreased to 8.4 mg/dL and his creatinine decreased to 1.6 mg/dL with intravenous hydration. His fatigue improved. His 25‐hydroxy vitamin D (25‐OH‐Vitamin D) level was 23 ng/mL (normal, 16‐74 ng/mL).

At his 1 week follow‐up, his calcium was 8.1 mg/dL, and his creatinine had returned to normal at 0.9 mg/dL. His intact PTH level was elevated at 240 pg/mL.

Discussion

Milk‐alkali syndrome is now believed to be the third most common reason for hypercalcemia hospital admission.2, 3 Malignancy and primary hyperparathyroidism are the only 2 causes of hypercalcemia more common than milk‐alkali syndrome in hospitalized patients; these must be excluded before making a definitive diagnosis of milk‐alkali syndrome. The differential diagnosis for hypercalcemia also includes other less common etiologies such as medications (hydrochlorothiazide and lithium), as well as familial hypocalciuric hypercalcemia, hyperthyroidism, Addison's disease, acromegaly, tertiary hyperparathyroidism, and vitamin D intoxication. Physicians often discover hypercalcemia incidentally on routine laboratory tests, and diagnostic workup should include a thorough history and physical examination, as well as further laboratory evaluation.

The diagnosis of milk‐alkali syndrome requires a history of increased calcium and alkali intake, but is otherwise a diagnosis of exclusion. Given the increasing consumption of nonprescribed calcium supplements, one should have a high index of suspicion for the diagnosis of milk‐alkali syndrome, as patients may not consider calcium carbonate to be hazardous or even a medication and thus may not report calcium carbonate consumption. Patients often view calcium carbonate as a benign treatment for dyspepsia. Its over‐the‐counter availability and economical price make it a common self‐treatment for minor dyspepsia or as prevention of osteoporosis. Calcium supplementation is increasingly added to many products, making it easy for patients to consume large quantities of calcium unknowingly. Of note, without the absorbable alkali supplied by the carbonate in calcium carbonate (Tums), milk‐alkali syndrome does not occur. The amount of calcium carbonate necessary to cause milk‐alkali syndrome is not well known, though it is speculated to be as little as 5 to 10 g of calcium in the form of calcium carbonate, especially in those with other risk factors for hypercalcemia such as chronic renal insufficiency or vomiting.2 Workup of hypercalcemia should entail careful questioning about medications, as well as over‐the‐counter supplements, vitamins, and foods.

Manifestations of the milk‐alkali syndrome include renal failure, metabolic alkalosis, and volume contraction. Normally, the kidneys prevent hypercalcemia by excretion of excess calcium. Hypercalcemia can cause tubular damage and vasoconstriction of the renal afferent arteriole leading to acute renal failure.2, 4 Hypercalcemia can also cause nephrogenic diabetes insipidus, causing impaired renal concentrating ability, leading to increased sodium excretion and volume contraction.2 In addition, alkalosis further impairs calciuresis.2 Laboratory values usually reveal suppressed PTH and vitamin D levels due to hypercalcemia caused by exogenous intake of calcium.5 Hypercalcemia causes suppression of PTH, which can lead to hyperphosphatemia, as well as decreased conversion of vitamin D to the active 1,25‐dihyroxyvitamin‐D form.

The management of hypercalcemia due to milk‐alkali syndrome is supportive and includes saline hydration as well as withholding calcium carbonate. Management of hypercalcemia due to malignancy and hyperparathyroidism includes bisphosphonates with the addition of calcitonin if symptoms are severe.6, 7 There is no evidence that supports the use of bisphosphonates in the treatment of milk‐alkali syndrome. Loop diuretics are sometimes used to promote calciuresis, though evidence is lacking to support this, and it may worsen renal failure.6

In this case, a middle‐aged man took greater than the recommended dose of calcium carbonate for dyspepsia, which led to the development of acute renal failure and hypercalcemia. At first, the patient did not provide an accurate history of the extent of his calcium carbonate ingestion, leading us to focus on hyperparathyroidism or malignancy. With aggressive hydration and cessation of calcium carbonate, his renal function and serum calcium returned to baseline. Because we initially assumed occult malignancy as the most likely diagnosis, we gave the patient pamidronate. The patient did not have a significant alkalemia (serum bicarbonate level was normal). This was thought to be due to the patient's degree of renal failure causing a concomitant metabolic acidosis. The patient's follow‐up elevated PTH level may be explained by bisphosphonate administration or underlying primary hyperparathyroidism. Of note, decreasing calcium levels have also been speculated to be a cause of high PTH levels.8

In conclusion, physicians should have a high index of suspicion for milk‐alkali syndrome in patients with hypercalcemia. Calcium carbonate is responsible for most cases of milk‐alkali syndrome, and clinicians should inquire about the use of this supplement in all patients with hypercalcemia. Milk‐alkali syndrome is no longer a merely a historical curiosity; it is currently the third most common cause of hospital admissions for hypercalcemia.

Historically, the milk‐alkali syndrome developed as an adverse reaction to the Sippy regimen of frequent feedings of milk, cream, and alkaline powders as treatment for peptic ulcer disease.1 The classic description includes hypercalcemia, metabolic alkalosis, and renal failure. This syndrome seemingly disappeared when modern acid suppression therapies such as histamine‐2 blockers and proton pump inhibitors improved dyspepsia treatment. Over the past 20 years, milk‐alkali syndrome has had a resurgence, as consumption of supplements containing calcium has increased.2 Calcium carbonate supplements are a popular over‐the‐counter treatment for osteoporosis, dyspepsia, hypocalcemia, and hyperphosphatemia; these supplements provide both the calcium and alkali required for the development of milk‐alkali syndrome.

A 46‐year‐old man presented to the emergency department after his physician ordered outpatient laboratory tests to evaluate his fatigue. The patient was found to have acute renal failure and hypercalcemia. His serum creatinine was 3.6 mg/dL, increased from his baseline of 1.1 mg/dL several months prior, and his serum calcium was 14.9 mg/dL. Ten days prior to admission he developed increasing fatigue, decreased appetite, and decreased urine output, which he attributed to recent manual labor during summer. He reported taking an occasional calcium carbonate (Tums) for dyspepsia. He did not report pain or other complaints.

His medical history included hypertension and hyperlipidemia. He had a colonoscopy 1 year prior to presentation that was significant for a high‐grade dysplastic polyp and was currently due for repeat colonoscopy. His medications included clonidine, lisinopril, and aspirin. He had no recent medication changes. He had a 30 pack/year history of cigarette smoking and drank occasionally.

On physical exam, his temperature was 99.8F, blood pressure 97/48 mmHg, heart rate 89 beats per minute, respirations 20 breaths per minute, with a room air saturation of 97%. He had dry mucus membranes and the remainder of the physical exam was unremarkable.

In the emergency department laboratory testing revealed a creatinine of 4.6 mg/dL, serum total calcium of 15.9 mg/dL, serum bicarbonate level of 26 mmol/L, phosphate of 3.9 mg/dL, albumin of 4.4 gm/dL, and alkaline phosphatase of 92 IU/L. The urine specific gravity was 1.019 gm/mL (see Table 1 for the patient's complete admission laboratory values).

His intact parathyroid (PTH) hormone was 18.8 pg/mL (normal, 15‐65). PTH hormone‐related peptide (PTHrP) was <2.5 pmol/L. After reviewing these laboratory test results, we proceeded with further questioning, during which he admitted to taking approximately 15 to 20 Tums (>7.5 gm of calcium carbonate) daily for dyspepsia rather than the occasional Tums he had originally reported. Over the next 3 days, his calcium decreased to 8.4 mg/dL and his creatinine decreased to 1.6 mg/dL with intravenous hydration. His fatigue improved. His 25‐hydroxy vitamin D (25‐OH‐Vitamin D) level was 23 ng/mL (normal, 16‐74 ng/mL).

At his 1 week follow‐up, his calcium was 8.1 mg/dL, and his creatinine had returned to normal at 0.9 mg/dL. His intact PTH level was elevated at 240 pg/mL.

Discussion

Milk‐alkali syndrome is now believed to be the third most common reason for hypercalcemia hospital admission.2, 3 Malignancy and primary hyperparathyroidism are the only 2 causes of hypercalcemia more common than milk‐alkali syndrome in hospitalized patients; these must be excluded before making a definitive diagnosis of milk‐alkali syndrome. The differential diagnosis for hypercalcemia also includes other less common etiologies such as medications (hydrochlorothiazide and lithium), as well as familial hypocalciuric hypercalcemia, hyperthyroidism, Addison's disease, acromegaly, tertiary hyperparathyroidism, and vitamin D intoxication. Physicians often discover hypercalcemia incidentally on routine laboratory tests, and diagnostic workup should include a thorough history and physical examination, as well as further laboratory evaluation.

The diagnosis of milk‐alkali syndrome requires a history of increased calcium and alkali intake, but is otherwise a diagnosis of exclusion. Given the increasing consumption of nonprescribed calcium supplements, one should have a high index of suspicion for the diagnosis of milk‐alkali syndrome, as patients may not consider calcium carbonate to be hazardous or even a medication and thus may not report calcium carbonate consumption. Patients often view calcium carbonate as a benign treatment for dyspepsia. Its over‐the‐counter availability and economical price make it a common self‐treatment for minor dyspepsia or as prevention of osteoporosis. Calcium supplementation is increasingly added to many products, making it easy for patients to consume large quantities of calcium unknowingly. Of note, without the absorbable alkali supplied by the carbonate in calcium carbonate (Tums), milk‐alkali syndrome does not occur. The amount of calcium carbonate necessary to cause milk‐alkali syndrome is not well known, though it is speculated to be as little as 5 to 10 g of calcium in the form of calcium carbonate, especially in those with other risk factors for hypercalcemia such as chronic renal insufficiency or vomiting.2 Workup of hypercalcemia should entail careful questioning about medications, as well as over‐the‐counter supplements, vitamins, and foods.

Manifestations of the milk‐alkali syndrome include renal failure, metabolic alkalosis, and volume contraction. Normally, the kidneys prevent hypercalcemia by excretion of excess calcium. Hypercalcemia can cause tubular damage and vasoconstriction of the renal afferent arteriole leading to acute renal failure.2, 4 Hypercalcemia can also cause nephrogenic diabetes insipidus, causing impaired renal concentrating ability, leading to increased sodium excretion and volume contraction.2 In addition, alkalosis further impairs calciuresis.2 Laboratory values usually reveal suppressed PTH and vitamin D levels due to hypercalcemia caused by exogenous intake of calcium.5 Hypercalcemia causes suppression of PTH, which can lead to hyperphosphatemia, as well as decreased conversion of vitamin D to the active 1,25‐dihyroxyvitamin‐D form.

The management of hypercalcemia due to milk‐alkali syndrome is supportive and includes saline hydration as well as withholding calcium carbonate. Management of hypercalcemia due to malignancy and hyperparathyroidism includes bisphosphonates with the addition of calcitonin if symptoms are severe.6, 7 There is no evidence that supports the use of bisphosphonates in the treatment of milk‐alkali syndrome. Loop diuretics are sometimes used to promote calciuresis, though evidence is lacking to support this, and it may worsen renal failure.6

In this case, a middle‐aged man took greater than the recommended dose of calcium carbonate for dyspepsia, which led to the development of acute renal failure and hypercalcemia. At first, the patient did not provide an accurate history of the extent of his calcium carbonate ingestion, leading us to focus on hyperparathyroidism or malignancy. With aggressive hydration and cessation of calcium carbonate, his renal function and serum calcium returned to baseline. Because we initially assumed occult malignancy as the most likely diagnosis, we gave the patient pamidronate. The patient did not have a significant alkalemia (serum bicarbonate level was normal). This was thought to be due to the patient's degree of renal failure causing a concomitant metabolic acidosis. The patient's follow‐up elevated PTH level may be explained by bisphosphonate administration or underlying primary hyperparathyroidism. Of note, decreasing calcium levels have also been speculated to be a cause of high PTH levels.8

In conclusion, physicians should have a high index of suspicion for milk‐alkali syndrome in patients with hypercalcemia. Calcium carbonate is responsible for most cases of milk‐alkali syndrome, and clinicians should inquire about the use of this supplement in all patients with hypercalcemia. Milk‐alkali syndrome is no longer a merely a historical curiosity; it is currently the third most common cause of hospital admissions for hypercalcemia.

Historically, the milk‐alkali syndrome developed as an adverse reaction to the Sippy regimen of frequent feedings of milk, cream, and alkaline powders as treatment for peptic ulcer disease.1 The classic description includes hypercalcemia, metabolic alkalosis, and renal failure. This syndrome seemingly disappeared when modern acid suppression therapies such as histamine‐2 blockers and proton pump inhibitors improved dyspepsia treatment. Over the past 20 years, milk‐alkali syndrome has had a resurgence, as consumption of supplements containing calcium has increased.2 Calcium carbonate supplements are a popular over‐the‐counter treatment for osteoporosis, dyspepsia, hypocalcemia, and hyperphosphatemia; these supplements provide both the calcium and alkali required for the development of milk‐alkali syndrome.

A 46‐year‐old man presented to the emergency department after his physician ordered outpatient laboratory tests to evaluate his fatigue. The patient was found to have acute renal failure and hypercalcemia. His serum creatinine was 3.6 mg/dL, increased from his baseline of 1.1 mg/dL several months prior, and his serum calcium was 14.9 mg/dL. Ten days prior to admission he developed increasing fatigue, decreased appetite, and decreased urine output, which he attributed to recent manual labor during summer. He reported taking an occasional calcium carbonate (Tums) for dyspepsia. He did not report pain or other complaints.

His medical history included hypertension and hyperlipidemia. He had a colonoscopy 1 year prior to presentation that was significant for a high‐grade dysplastic polyp and was currently due for repeat colonoscopy. His medications included clonidine, lisinopril, and aspirin. He had no recent medication changes. He had a 30 pack/year history of cigarette smoking and drank occasionally.

On physical exam, his temperature was 99.8F, blood pressure 97/48 mmHg, heart rate 89 beats per minute, respirations 20 breaths per minute, with a room air saturation of 97%. He had dry mucus membranes and the remainder of the physical exam was unremarkable.

In the emergency department laboratory testing revealed a creatinine of 4.6 mg/dL, serum total calcium of 15.9 mg/dL, serum bicarbonate level of 26 mmol/L, phosphate of 3.9 mg/dL, albumin of 4.4 gm/dL, and alkaline phosphatase of 92 IU/L. The urine specific gravity was 1.019 gm/mL (see Table 1 for the patient's complete admission laboratory values).

His intact parathyroid (PTH) hormone was 18.8 pg/mL (normal, 15‐65). PTH hormone‐related peptide (PTHrP) was <2.5 pmol/L. After reviewing these laboratory test results, we proceeded with further questioning, during which he admitted to taking approximately 15 to 20 Tums (>7.5 gm of calcium carbonate) daily for dyspepsia rather than the occasional Tums he had originally reported. Over the next 3 days, his calcium decreased to 8.4 mg/dL and his creatinine decreased to 1.6 mg/dL with intravenous hydration. His fatigue improved. His 25‐hydroxy vitamin D (25‐OH‐Vitamin D) level was 23 ng/mL (normal, 16‐74 ng/mL).

At his 1 week follow‐up, his calcium was 8.1 mg/dL, and his creatinine had returned to normal at 0.9 mg/dL. His intact PTH level was elevated at 240 pg/mL.

Discussion

Milk‐alkali syndrome is now believed to be the third most common reason for hypercalcemia hospital admission.2, 3 Malignancy and primary hyperparathyroidism are the only 2 causes of hypercalcemia more common than milk‐alkali syndrome in hospitalized patients; these must be excluded before making a definitive diagnosis of milk‐alkali syndrome. The differential diagnosis for hypercalcemia also includes other less common etiologies such as medications (hydrochlorothiazide and lithium), as well as familial hypocalciuric hypercalcemia, hyperthyroidism, Addison's disease, acromegaly, tertiary hyperparathyroidism, and vitamin D intoxication. Physicians often discover hypercalcemia incidentally on routine laboratory tests, and diagnostic workup should include a thorough history and physical examination, as well as further laboratory evaluation.

The diagnosis of milk‐alkali syndrome requires a history of increased calcium and alkali intake, but is otherwise a diagnosis of exclusion. Given the increasing consumption of nonprescribed calcium supplements, one should have a high index of suspicion for the diagnosis of milk‐alkali syndrome, as patients may not consider calcium carbonate to be hazardous or even a medication and thus may not report calcium carbonate consumption. Patients often view calcium carbonate as a benign treatment for dyspepsia. Its over‐the‐counter availability and economical price make it a common self‐treatment for minor dyspepsia or as prevention of osteoporosis. Calcium supplementation is increasingly added to many products, making it easy for patients to consume large quantities of calcium unknowingly. Of note, without the absorbable alkali supplied by the carbonate in calcium carbonate (Tums), milk‐alkali syndrome does not occur. The amount of calcium carbonate necessary to cause milk‐alkali syndrome is not well known, though it is speculated to be as little as 5 to 10 g of calcium in the form of calcium carbonate, especially in those with other risk factors for hypercalcemia such as chronic renal insufficiency or vomiting.2 Workup of hypercalcemia should entail careful questioning about medications, as well as over‐the‐counter supplements, vitamins, and foods.

Manifestations of the milk‐alkali syndrome include renal failure, metabolic alkalosis, and volume contraction. Normally, the kidneys prevent hypercalcemia by excretion of excess calcium. Hypercalcemia can cause tubular damage and vasoconstriction of the renal afferent arteriole leading to acute renal failure.2, 4 Hypercalcemia can also cause nephrogenic diabetes insipidus, causing impaired renal concentrating ability, leading to increased sodium excretion and volume contraction.2 In addition, alkalosis further impairs calciuresis.2 Laboratory values usually reveal suppressed PTH and vitamin D levels due to hypercalcemia caused by exogenous intake of calcium.5 Hypercalcemia causes suppression of PTH, which can lead to hyperphosphatemia, as well as decreased conversion of vitamin D to the active 1,25‐dihyroxyvitamin‐D form.

The management of hypercalcemia due to milk‐alkali syndrome is supportive and includes saline hydration as well as withholding calcium carbonate. Management of hypercalcemia due to malignancy and hyperparathyroidism includes bisphosphonates with the addition of calcitonin if symptoms are severe.6, 7 There is no evidence that supports the use of bisphosphonates in the treatment of milk‐alkali syndrome. Loop diuretics are sometimes used to promote calciuresis, though evidence is lacking to support this, and it may worsen renal failure.6

In this case, a middle‐aged man took greater than the recommended dose of calcium carbonate for dyspepsia, which led to the development of acute renal failure and hypercalcemia. At first, the patient did not provide an accurate history of the extent of his calcium carbonate ingestion, leading us to focus on hyperparathyroidism or malignancy. With aggressive hydration and cessation of calcium carbonate, his renal function and serum calcium returned to baseline. Because we initially assumed occult malignancy as the most likely diagnosis, we gave the patient pamidronate. The patient did not have a significant alkalemia (serum bicarbonate level was normal). This was thought to be due to the patient's degree of renal failure causing a concomitant metabolic acidosis. The patient's follow‐up elevated PTH level may be explained by bisphosphonate administration or underlying primary hyperparathyroidism. Of note, decreasing calcium levels have also been speculated to be a cause of high PTH levels.8

In conclusion, physicians should have a high index of suspicion for milk‐alkali syndrome in patients with hypercalcemia. Calcium carbonate is responsible for most cases of milk‐alkali syndrome, and clinicians should inquire about the use of this supplement in all patients with hypercalcemia. Milk‐alkali syndrome is no longer a merely a historical curiosity; it is currently the third most common cause of hospital admissions for hypercalcemia.

The current state of our profession is that the US population is aging rapidly, requiring ever more healthcare, and there is a stagnant number of physicians to care for them. The question of who will care for our aging population has been raised over and over in the past decade but the question is worth repeating. As our country continues to deliver state‐of‐the‐art medical care, it is slow to embrace the notion that in order for it to continue, it will need to incorporate the professions of advanced practice nurses and physician assistants. Without these nonphysician providers our medical community will not be able to reach the patients we have sworn to treat.

The percent of the US population age >65 years is projected to increase from 12.4% in 2000 to 19.6% in 2030. The number of persons age >65 years is expected to increase from approximately 35 million in 2000 to an estimated 71 million in 2030, and the number of persons age >80 years is expected to increase from 9.3 million in 2000 to 19.5 million in 2030.1 Our aging America is also coupled with a growing physician shortage. In its report entitled Physician Workforce Policy Guidelines for the United States, 2000‐2020, the Council on Graduate Medical Education recommended increasing the number of medical school graduates by 3000 per year by the year 2015 to meet the increasing need.2 Given the current trend of decreasing physician reimbursement coupled with the average medical school debt of $139,517,3 it is doubtful that the extra 3000 physicians needed to graduate in 2015 will actually ever do so. Despite this possible additional physician workforce, there still stands to be enormous need for the nonphysician provider with our rapidly expanding senior population.

Our nation's hospitals are by no means spared from our aging population or physician shortage. In fact, they are likely to be the hardest hit. Hospitalists are already feeling the pressure of an overstressed workforce coupled with increasing patient volume.4 There is a growing body of evidence supporting the successful collaboration between hospitalists and nurse practitioners (NPs)/physician assistants (PAs) (collectively, nonphysician providers [NPPs]). No longer are NPPs only working in outpatient practices or in the operating room, but they are actively involved with inpatient medical units improving our Hospital Medicine (HM) specialty. According to Myers et al.,5 the hospitalist NP model improved program finances and increased physician and resident satisfaction. In order for Hospital Medicine to create increasing value for its parent hospital or to the community it serves, NPPs will need increased integration into our care model for improved overall efficiency. We focus herein on the advantages and potential benefits of NPPs relating to their varied roles within HM.

Scope of Practice

The scope of practice of NPPs is regulated by each individual state board of registration. However, differences from state to state are usually minor and general statements on the practice scope of PAs and NPs can be made.

Potential Benefits of NPPs

Models of Care

There are many models for NPP roles in hospital medicine groups. Some groups use NPPs in the same role as physicians. They perform admissions, rounding, and discharges with varying degrees of oversight by physicians. Other groups use NPPs for a more limited role, such as exclusively performing histories and physicals in the emergency department or handling discharges on the wards. It is important to take into account the preferences and expectations of NPPs when designing job descriptions. While some NPPs may like the fast pace and quick turnover of admissions and discharges, others may prefer to follow patients throughout their hospital stay. The quality of handoffs is crucial if the former model is used, just as it is with physicians in this more truncated role. An NPP who works in a nonacademic model will likely have more autonomy and control over patient care decisions. An NPP role in the teaching service of an academic hospital is likely to be more collaborative and focus more on quality initiatives, patient teaching, and communication. It is crucial to design an NPP model that is sustainable with very strong support of management once the NPP is hired and orientated.

Registered Nurses And Hospital Medicine

Patient handoffs and communication are one of the most challenging aspects of an HMG. There is an increasing movement, throughout the country, to incorporate registered nurses (RNs) into daily workflow. The RN on the HM team can serve to augment the communication and workflow process. A highly motivated and organized registered nurse can help to improve overall provider's workflow efficiency. Communication to primary care physician and collecting ancillary medical information can allow the provider to treat more patients in a given shift and decrease the liability risk from lack of information. As HM organizations and hospitals become more financially bound, HMGs will need to become more efficient at time management and a dedicated RN can help smooth that process.

Potential Unintended Side Effects

Obviously, integration of NPPs can be a disaster for an HMG if not handled properly. Most hospitalists have heard of an integration of NPP into a group that was an unqualified failure. NPPs can feel unsupported, poorly oriented to the job, or thrown into a situation that is over their heads. Before an NPP is hired into an HMG, there needs to be a thorough examination of the rationale behind the decision and assessment of the hospital culture that will be the host of the new NPP. What does the HMG need for support? Are they looking for a short‐term fix for increased volume or a long‐term strategy to build a multidisciplinary team? Does the hospital culture see NPPs as poorly qualified to act as hospitalists or uniquely qualified to address shortcomings of the program? A clear job description should be the first step in determining what the NPP is expected to do. This can then be shared with the hospital leadership in advance to promote buy‐in. The second step is finding an NPP that fits the goals of the program. A new NPP, by virtue of the fact that they have less clinical hours in training than a physician hospitalist, will need more support and a longer orientation. NPPs who have experience in hospital medicine will have a much shorter orientation. A stepwise approach to orientation can be helpful in assessing skill level of new hires. These NPPs can be initially paired with an enthusiastic physician to provide support and assessment of existing skills. A gradual increase in independence can provide assurance that the NPP is qualified to provide care and gives many opportunities for reevaluation of the NPP. Clear expectations and constructive feedback should ultimately lead to a degree of comfort within the HMG, hospital, and the NPPs themselves.

Conclusions

It is clear that our healthcare system will need a very different approach to the economic problems it is facing. Standardization of care, integrated medical records, and expanded and universal resource utilization will drive the next generation of healthcare providers. The model of a private physician working alone under the direction of only his or her own medical knowledge is a thing of the past. Just as the HM specialty has grown from 300 in 1996 to more than 20,000 in 2008, so shall the integration of NPPs grow into our healthcare fabric.

The current state of our profession is that the US population is aging rapidly, requiring ever more healthcare, and there is a stagnant number of physicians to care for them. The question of who will care for our aging population has been raised over and over in the past decade but the question is worth repeating. As our country continues to deliver state‐of‐the‐art medical care, it is slow to embrace the notion that in order for it to continue, it will need to incorporate the professions of advanced practice nurses and physician assistants. Without these nonphysician providers our medical community will not be able to reach the patients we have sworn to treat.

The percent of the US population age >65 years is projected to increase from 12.4% in 2000 to 19.6% in 2030. The number of persons age >65 years is expected to increase from approximately 35 million in 2000 to an estimated 71 million in 2030, and the number of persons age >80 years is expected to increase from 9.3 million in 2000 to 19.5 million in 2030.1 Our aging America is also coupled with a growing physician shortage. In its report entitled Physician Workforce Policy Guidelines for the United States, 2000‐2020, the Council on Graduate Medical Education recommended increasing the number of medical school graduates by 3000 per year by the year 2015 to meet the increasing need.2 Given the current trend of decreasing physician reimbursement coupled with the average medical school debt of $139,517,3 it is doubtful that the extra 3000 physicians needed to graduate in 2015 will actually ever do so. Despite this possible additional physician workforce, there still stands to be enormous need for the nonphysician provider with our rapidly expanding senior population.

Our nation's hospitals are by no means spared from our aging population or physician shortage. In fact, they are likely to be the hardest hit. Hospitalists are already feeling the pressure of an overstressed workforce coupled with increasing patient volume.4 There is a growing body of evidence supporting the successful collaboration between hospitalists and nurse practitioners (NPs)/physician assistants (PAs) (collectively, nonphysician providers [NPPs]). No longer are NPPs only working in outpatient practices or in the operating room, but they are actively involved with inpatient medical units improving our Hospital Medicine (HM) specialty. According to Myers et al.,5 the hospitalist NP model improved program finances and increased physician and resident satisfaction. In order for Hospital Medicine to create increasing value for its parent hospital or to the community it serves, NPPs will need increased integration into our care model for improved overall efficiency. We focus herein on the advantages and potential benefits of NPPs relating to their varied roles within HM.

Scope of Practice

The scope of practice of NPPs is regulated by each individual state board of registration. However, differences from state to state are usually minor and general statements on the practice scope of PAs and NPs can be made.

Potential Benefits of NPPs

Models of Care

There are many models for NPP roles in hospital medicine groups. Some groups use NPPs in the same role as physicians. They perform admissions, rounding, and discharges with varying degrees of oversight by physicians. Other groups use NPPs for a more limited role, such as exclusively performing histories and physicals in the emergency department or handling discharges on the wards. It is important to take into account the preferences and expectations of NPPs when designing job descriptions. While some NPPs may like the fast pace and quick turnover of admissions and discharges, others may prefer to follow patients throughout their hospital stay. The quality of handoffs is crucial if the former model is used, just as it is with physicians in this more truncated role. An NPP who works in a nonacademic model will likely have more autonomy and control over patient care decisions. An NPP role in the teaching service of an academic hospital is likely to be more collaborative and focus more on quality initiatives, patient teaching, and communication. It is crucial to design an NPP model that is sustainable with very strong support of management once the NPP is hired and orientated.

Registered Nurses And Hospital Medicine

Patient handoffs and communication are one of the most challenging aspects of an HMG. There is an increasing movement, throughout the country, to incorporate registered nurses (RNs) into daily workflow. The RN on the HM team can serve to augment the communication and workflow process. A highly motivated and organized registered nurse can help to improve overall provider's workflow efficiency. Communication to primary care physician and collecting ancillary medical information can allow the provider to treat more patients in a given shift and decrease the liability risk from lack of information. As HM organizations and hospitals become more financially bound, HMGs will need to become more efficient at time management and a dedicated RN can help smooth that process.

Potential Unintended Side Effects

Obviously, integration of NPPs can be a disaster for an HMG if not handled properly. Most hospitalists have heard of an integration of NPP into a group that was an unqualified failure. NPPs can feel unsupported, poorly oriented to the job, or thrown into a situation that is over their heads. Before an NPP is hired into an HMG, there needs to be a thorough examination of the rationale behind the decision and assessment of the hospital culture that will be the host of the new NPP. What does the HMG need for support? Are they looking for a short‐term fix for increased volume or a long‐term strategy to build a multidisciplinary team? Does the hospital culture see NPPs as poorly qualified to act as hospitalists or uniquely qualified to address shortcomings of the program? A clear job description should be the first step in determining what the NPP is expected to do. This can then be shared with the hospital leadership in advance to promote buy‐in. The second step is finding an NPP that fits the goals of the program. A new NPP, by virtue of the fact that they have less clinical hours in training than a physician hospitalist, will need more support and a longer orientation. NPPs who have experience in hospital medicine will have a much shorter orientation. A stepwise approach to orientation can be helpful in assessing skill level of new hires. These NPPs can be initially paired with an enthusiastic physician to provide support and assessment of existing skills. A gradual increase in independence can provide assurance that the NPP is qualified to provide care and gives many opportunities for reevaluation of the NPP. Clear expectations and constructive feedback should ultimately lead to a degree of comfort within the HMG, hospital, and the NPPs themselves.

Conclusions

It is clear that our healthcare system will need a very different approach to the economic problems it is facing. Standardization of care, integrated medical records, and expanded and universal resource utilization will drive the next generation of healthcare providers. The model of a private physician working alone under the direction of only his or her own medical knowledge is a thing of the past. Just as the HM specialty has grown from 300 in 1996 to more than 20,000 in 2008, so shall the integration of NPPs grow into our healthcare fabric.

The current state of our profession is that the US population is aging rapidly, requiring ever more healthcare, and there is a stagnant number of physicians to care for them. The question of who will care for our aging population has been raised over and over in the past decade but the question is worth repeating. As our country continues to deliver state‐of‐the‐art medical care, it is slow to embrace the notion that in order for it to continue, it will need to incorporate the professions of advanced practice nurses and physician assistants. Without these nonphysician providers our medical community will not be able to reach the patients we have sworn to treat.

The percent of the US population age >65 years is projected to increase from 12.4% in 2000 to 19.6% in 2030. The number of persons age >65 years is expected to increase from approximately 35 million in 2000 to an estimated 71 million in 2030, and the number of persons age >80 years is expected to increase from 9.3 million in 2000 to 19.5 million in 2030.1 Our aging America is also coupled with a growing physician shortage. In its report entitled Physician Workforce Policy Guidelines for the United States, 2000‐2020, the Council on Graduate Medical Education recommended increasing the number of medical school graduates by 3000 per year by the year 2015 to meet the increasing need.2 Given the current trend of decreasing physician reimbursement coupled with the average medical school debt of $139,517,3 it is doubtful that the extra 3000 physicians needed to graduate in 2015 will actually ever do so. Despite this possible additional physician workforce, there still stands to be enormous need for the nonphysician provider with our rapidly expanding senior population.

Our nation's hospitals are by no means spared from our aging population or physician shortage. In fact, they are likely to be the hardest hit. Hospitalists are already feeling the pressure of an overstressed workforce coupled with increasing patient volume.4 There is a growing body of evidence supporting the successful collaboration between hospitalists and nurse practitioners (NPs)/physician assistants (PAs) (collectively, nonphysician providers [NPPs]). No longer are NPPs only working in outpatient practices or in the operating room, but they are actively involved with inpatient medical units improving our Hospital Medicine (HM) specialty. According to Myers et al.,5 the hospitalist NP model improved program finances and increased physician and resident satisfaction. In order for Hospital Medicine to create increasing value for its parent hospital or to the community it serves, NPPs will need increased integration into our care model for improved overall efficiency. We focus herein on the advantages and potential benefits of NPPs relating to their varied roles within HM.

Scope of Practice

The scope of practice of NPPs is regulated by each individual state board of registration. However, differences from state to state are usually minor and general statements on the practice scope of PAs and NPs can be made.

Potential Benefits of NPPs

Models of Care

There are many models for NPP roles in hospital medicine groups. Some groups use NPPs in the same role as physicians. They perform admissions, rounding, and discharges with varying degrees of oversight by physicians. Other groups use NPPs for a more limited role, such as exclusively performing histories and physicals in the emergency department or handling discharges on the wards. It is important to take into account the preferences and expectations of NPPs when designing job descriptions. While some NPPs may like the fast pace and quick turnover of admissions and discharges, others may prefer to follow patients throughout their hospital stay. The quality of handoffs is crucial if the former model is used, just as it is with physicians in this more truncated role. An NPP who works in a nonacademic model will likely have more autonomy and control over patient care decisions. An NPP role in the teaching service of an academic hospital is likely to be more collaborative and focus more on quality initiatives, patient teaching, and communication. It is crucial to design an NPP model that is sustainable with very strong support of management once the NPP is hired and orientated.

Registered Nurses And Hospital Medicine

Patient handoffs and communication are one of the most challenging aspects of an HMG. There is an increasing movement, throughout the country, to incorporate registered nurses (RNs) into daily workflow. The RN on the HM team can serve to augment the communication and workflow process. A highly motivated and organized registered nurse can help to improve overall provider's workflow efficiency. Communication to primary care physician and collecting ancillary medical information can allow the provider to treat more patients in a given shift and decrease the liability risk from lack of information. As HM organizations and hospitals become more financially bound, HMGs will need to become more efficient at time management and a dedicated RN can help smooth that process.

Potential Unintended Side Effects

Obviously, integration of NPPs can be a disaster for an HMG if not handled properly. Most hospitalists have heard of an integration of NPP into a group that was an unqualified failure. NPPs can feel unsupported, poorly oriented to the job, or thrown into a situation that is over their heads. Before an NPP is hired into an HMG, there needs to be a thorough examination of the rationale behind the decision and assessment of the hospital culture that will be the host of the new NPP. What does the HMG need for support? Are they looking for a short‐term fix for increased volume or a long‐term strategy to build a multidisciplinary team? Does the hospital culture see NPPs as poorly qualified to act as hospitalists or uniquely qualified to address shortcomings of the program? A clear job description should be the first step in determining what the NPP is expected to do. This can then be shared with the hospital leadership in advance to promote buy‐in. The second step is finding an NPP that fits the goals of the program. A new NPP, by virtue of the fact that they have less clinical hours in training than a physician hospitalist, will need more support and a longer orientation. NPPs who have experience in hospital medicine will have a much shorter orientation. A stepwise approach to orientation can be helpful in assessing skill level of new hires. These NPPs can be initially paired with an enthusiastic physician to provide support and assessment of existing skills. A gradual increase in independence can provide assurance that the NPP is qualified to provide care and gives many opportunities for reevaluation of the NPP. Clear expectations and constructive feedback should ultimately lead to a degree of comfort within the HMG, hospital, and the NPPs themselves.

Conclusions

It is clear that our healthcare system will need a very different approach to the economic problems it is facing. Standardization of care, integrated medical records, and expanded and universal resource utilization will drive the next generation of healthcare providers. The model of a private physician working alone under the direction of only his or her own medical knowledge is a thing of the past. Just as the HM specialty has grown from 300 in 1996 to more than 20,000 in 2008, so shall the integration of NPPs grow into our healthcare fabric.

An association between hypertension and operative risk has been reported in small studies since the early 1970s. In two studies, Prys‐Roberts et al.1, 2 found that subjects with uncontrolled hypertension were more likely to have myocardial ischemic changes on electrocardiography with episodes of hypotension during induction of anesthesia. Subjects without hypertension or with hypertension controlled by medication were less likely to have episodes of hypotension, regardless of the type of anesthetic.

Hypertension increases the risk of developing perioperative heart failure (HF), renal failure, myocardial ischemia, or stroke. The level of risk is dependent upon the blood pressure (BP) level. It has been shown that a BP of <180/110 mm Hg without target‐organ damage (TOD) is not an independent risk factor for perioperative cardiovascular (CV) complications, suggesting this level of BP does not need to be reduced rapidly to normal.3, 4

The Joint National Committee defines hypertensive emergency as severe elevations in BP (usually >180/120 mm Hg) that produce evidence of TOD.5 Patients with this level of BP who are asymptomatic and have no signs of TOD are considered to have hypertensive urgency. As patients with this level of BP are at higher risk perioperatively, pharmacotherapy is indicated. When oral medications cannot be administered, hypertensive urgency can be managed with a parenteral medication. The agent should be easily and predictably titrated, safe, and convenient (Table 1). This article reviews the management of perioperative hypertensive urgency with parenteral medications. The management of hypertensive emergencies, aortic dissection, and hypertension of pregnancy is outside the scope of this review.

Preoperative Considerations

In normotensive patients the induction of anesthesia can cause an acute elevation in BP (2030 mm Hg) and heart rate (HR) (1520 bpm).6 In patients with preexisting hypertension these changes are often greater, with elevations up to 90 mm Hg and 40 bpm. As anesthesia progresses systolic BP starts to fall (30 mm Hg), as a direct effect of both the anesthetic and the inhibition of the sympathetic nervous system (SNS). Patients with uncontrolled hypertension can have more severe reductions (60 mm Hg).6 This can result in intraoperative hypotension and shock. In a study of over 650 patients, marked intraoperative hypotension (<50% of preoperative BP or a 33% reduction for more than 10 minutes) was an independent risk factor for perioperative CV complications (cardiac arrhythmia, ischemia, HF, or renal failure).7

Therefore, when BP is mildly elevated at the time of surgery (<180/110 mm Hg), rapid reduction in BP is not necessary, and studies have been unable to demonstrate a benefit to delaying surgery.8 However, when BP is 180/110 mm Hg preoperatively, antihypertensive medications should be administered and intraoperative blood pressure monitored closely. There is a lack of data to support delay of surgery.9

Postoperative Considerations

The postoperative period is also associated with elevations in BP. In the immediate recovery phase from anesthesia, there is a mild elevation in BP within 10 to 15 mm Hg, but there are larger fluctuations in patients with preexisting hypertension.6 Otherwise postoperative hypertension can be seen from a variety of causes such as pain, excitement on emergence from anesthesia, and hypercarbia.10 Less common causes include agitation, hypoxemia, and hypervolemia. These secondary causes should be identified and treated before any antihypertensive medications are administered.

Discussion

Nitroprusside, nitroglycerin, nicardipine, and fenoldopam are all effective antihypertensive medications. However, their availability only as continuous infusions requires ICU monitoring and an intraarterial catheter, and they are therefore unnecessary in the management of hypertensive urgency. The parenteral medications that do not require a continuous infusion are diltiazem, verapamil, metoprolol, labetalol, enalaprilat, hydralazine, and transdermal clonidine.

As stated, the intravenous formulations of diltiazem and verapamil are indicated only for certain arrhythmias. Because the onset of action of transdermal clonidine is about 2 days and the offset is 8 hours, it has limited usefulness in the treatment of perioperative hypertension. Therefore, only metoprolol, labetalol, enalaprilat, and hydralazine have a major role in the treatment of hypertensive urgency when oral medications cannot be used.

When given intravenously, enalaprilat and hydralazine are safe, effective, widely available, and inexpensive. When deciding between these 2 agents, a few other considerations may be of importance. Even though ACE inhibitors have well‐recognized benefits in the management of HF50 and diabetic nephropathy,51 these characteristics are not relevant in the short‐term use of enalaprilat to treat perioperative hypertension. However, enalaprilat may be preferred over hydralazine when activation of the SNS and reflex tachycardia is to be avoided (cardiac ischemia, aortic dissection, increased intracranial pressure). Hydralazine may be preferred in the setting of hyperkalemia and acute renal failure. It must be preferred in pregnancy or bilateral renal artery stenosis.

Although the weight of the evidence of perioperative ‐blocker use to reduce CV events in noncardiac surgery suggests a benefit, there are significant limitations. Few studies have compared different ‐blockers. Studies to determine the ideal target population, duration of therapy, and route of administration are lacking. Additionally, using perioperative ‐blockers may cause harm in low‐risk patients.52 Care should be taken when using labetalol and metoprolol in combination as they can induce a dangerous reduction in HR. The role of acute administration of intravenous ‐blockers in the setting of myocardial ischemia is debatable, and probably dangerous in the setting of hypotension, bradycardia, HB, pulmonary edema, or bronchospasm.53

Therefore, generalizing the perioperative ‐blocker data to all patients with perioperative hypertension seems unlikely to have significant benefit, and may possibly pose harm.29 However, it seems reasonable to use ‐blockers in those in whom it would be indicated otherwise, and to continue parenteral therapy in those already taking a ‐blocker preoperatively in order to avoid withdrawal.54

When deciding between metoprolol and labetalol, a few considerations may be of importance. First, there is much more evidence documenting the safety and efficacy of labetalol in perioperative hypertension. Second, even though metoprolol has proven benefit in patients with chronic HF, coronary artery disease (CAD), and MI, these long‐term studies investigated oral metoprolol, not the intravenous formulation.55 Most importantly, labetalol is more effective at lowering BP due to its additional blockade of alpha₁ adrenoreceptors. Neither drug should be used in acute HF, bradycardia or greater than first‐degree HB, or bronchospasm. In conclusion, intravenous labetalol should be preferred over intravenous metoprolol for the management of perioperative hypertension.

Conclusions

Perioperative hypertension ideally should be evaluated well before the operative time period, when there is adequate time to initiate medications. Secondary causes such as pain, agitation, hypercarbia, hypoxemia, and hypervolemia should be treated directly prior to the administration of antihypertensive medications. It is uncertain whether patients with a BP of <180/110 mm Hg benefit from any specific parenteral medication, as there is little evidence from several studies that this level of BP without TOD leads to an increase in perioperative morbidity or mortality.3, 4, 7, 56 However, patients with hypertensive urgency are at higher risk for perioperative complications; therefore, their BP should be managed gradually to <160/110 mm Hg with the outlined recommended parenteral regimen (Figure 1).

Figure 1

When selecting a parenteral medication, we suggest first to exclude any contraindications, or see if an indication exists for a specific agent. Hydralazine, enalaprilat, metoprolol, or labetalol can be used as first‐line agents. Due to the scarcity of comparative trials looking at clinically significant outcomes (length of hospital stay, morbidity, mortality), decisions for the management of perioperative hypertension should be made based on comorbidity, efficacy, toxicity, and cost (Table 1).

An association between hypertension and operative risk has been reported in small studies since the early 1970s. In two studies, Prys‐Roberts et al.1, 2 found that subjects with uncontrolled hypertension were more likely to have myocardial ischemic changes on electrocardiography with episodes of hypotension during induction of anesthesia. Subjects without hypertension or with hypertension controlled by medication were less likely to have episodes of hypotension, regardless of the type of anesthetic.

Hypertension increases the risk of developing perioperative heart failure (HF), renal failure, myocardial ischemia, or stroke. The level of risk is dependent upon the blood pressure (BP) level. It has been shown that a BP of <180/110 mm Hg without target‐organ damage (TOD) is not an independent risk factor for perioperative cardiovascular (CV) complications, suggesting this level of BP does not need to be reduced rapidly to normal.3, 4

The Joint National Committee defines hypertensive emergency as severe elevations in BP (usually >180/120 mm Hg) that produce evidence of TOD.5 Patients with this level of BP who are asymptomatic and have no signs of TOD are considered to have hypertensive urgency. As patients with this level of BP are at higher risk perioperatively, pharmacotherapy is indicated. When oral medications cannot be administered, hypertensive urgency can be managed with a parenteral medication. The agent should be easily and predictably titrated, safe, and convenient (Table 1). This article reviews the management of perioperative hypertensive urgency with parenteral medications. The management of hypertensive emergencies, aortic dissection, and hypertension of pregnancy is outside the scope of this review.

Preoperative Considerations

In normotensive patients the induction of anesthesia can cause an acute elevation in BP (2030 mm Hg) and heart rate (HR) (1520 bpm).6 In patients with preexisting hypertension these changes are often greater, with elevations up to 90 mm Hg and 40 bpm. As anesthesia progresses systolic BP starts to fall (30 mm Hg), as a direct effect of both the anesthetic and the inhibition of the sympathetic nervous system (SNS). Patients with uncontrolled hypertension can have more severe reductions (60 mm Hg).6 This can result in intraoperative hypotension and shock. In a study of over 650 patients, marked intraoperative hypotension (<50% of preoperative BP or a 33% reduction for more than 10 minutes) was an independent risk factor for perioperative CV complications (cardiac arrhythmia, ischemia, HF, or renal failure).7

Therefore, when BP is mildly elevated at the time of surgery (<180/110 mm Hg), rapid reduction in BP is not necessary, and studies have been unable to demonstrate a benefit to delaying surgery.8 However, when BP is 180/110 mm Hg preoperatively, antihypertensive medications should be administered and intraoperative blood pressure monitored closely. There is a lack of data to support delay of surgery.9

Postoperative Considerations

The postoperative period is also associated with elevations in BP. In the immediate recovery phase from anesthesia, there is a mild elevation in BP within 10 to 15 mm Hg, but there are larger fluctuations in patients with preexisting hypertension.6 Otherwise postoperative hypertension can be seen from a variety of causes such as pain, excitement on emergence from anesthesia, and hypercarbia.10 Less common causes include agitation, hypoxemia, and hypervolemia. These secondary causes should be identified and treated before any antihypertensive medications are administered.

Discussion

Nitroprusside, nitroglycerin, nicardipine, and fenoldopam are all effective antihypertensive medications. However, their availability only as continuous infusions requires ICU monitoring and an intraarterial catheter, and they are therefore unnecessary in the management of hypertensive urgency. The parenteral medications that do not require a continuous infusion are diltiazem, verapamil, metoprolol, labetalol, enalaprilat, hydralazine, and transdermal clonidine.

As stated, the intravenous formulations of diltiazem and verapamil are indicated only for certain arrhythmias. Because the onset of action of transdermal clonidine is about 2 days and the offset is 8 hours, it has limited usefulness in the treatment of perioperative hypertension. Therefore, only metoprolol, labetalol, enalaprilat, and hydralazine have a major role in the treatment of hypertensive urgency when oral medications cannot be used.

When given intravenously, enalaprilat and hydralazine are safe, effective, widely available, and inexpensive. When deciding between these 2 agents, a few other considerations may be of importance. Even though ACE inhibitors have well‐recognized benefits in the management of HF50 and diabetic nephropathy,51 these characteristics are not relevant in the short‐term use of enalaprilat to treat perioperative hypertension. However, enalaprilat may be preferred over hydralazine when activation of the SNS and reflex tachycardia is to be avoided (cardiac ischemia, aortic dissection, increased intracranial pressure). Hydralazine may be preferred in the setting of hyperkalemia and acute renal failure. It must be preferred in pregnancy or bilateral renal artery stenosis.

Although the weight of the evidence of perioperative ‐blocker use to reduce CV events in noncardiac surgery suggests a benefit, there are significant limitations. Few studies have compared different ‐blockers. Studies to determine the ideal target population, duration of therapy, and route of administration are lacking. Additionally, using perioperative ‐blockers may cause harm in low‐risk patients.52 Care should be taken when using labetalol and metoprolol in combination as they can induce a dangerous reduction in HR. The role of acute administration of intravenous ‐blockers in the setting of myocardial ischemia is debatable, and probably dangerous in the setting of hypotension, bradycardia, HB, pulmonary edema, or bronchospasm.53

Therefore, generalizing the perioperative ‐blocker data to all patients with perioperative hypertension seems unlikely to have significant benefit, and may possibly pose harm.29 However, it seems reasonable to use ‐blockers in those in whom it would be indicated otherwise, and to continue parenteral therapy in those already taking a ‐blocker preoperatively in order to avoid withdrawal.54

When deciding between metoprolol and labetalol, a few considerations may be of importance. First, there is much more evidence documenting the safety and efficacy of labetalol in perioperative hypertension. Second, even though metoprolol has proven benefit in patients with chronic HF, coronary artery disease (CAD), and MI, these long‐term studies investigated oral metoprolol, not the intravenous formulation.55 Most importantly, labetalol is more effective at lowering BP due to its additional blockade of alpha₁ adrenoreceptors. Neither drug should be used in acute HF, bradycardia or greater than first‐degree HB, or bronchospasm. In conclusion, intravenous labetalol should be preferred over intravenous metoprolol for the management of perioperative hypertension.

Conclusions

Perioperative hypertension ideally should be evaluated well before the operative time period, when there is adequate time to initiate medications. Secondary causes such as pain, agitation, hypercarbia, hypoxemia, and hypervolemia should be treated directly prior to the administration of antihypertensive medications. It is uncertain whether patients with a BP of <180/110 mm Hg benefit from any specific parenteral medication, as there is little evidence from several studies that this level of BP without TOD leads to an increase in perioperative morbidity or mortality.3, 4, 7, 56 However, patients with hypertensive urgency are at higher risk for perioperative complications; therefore, their BP should be managed gradually to <160/110 mm Hg with the outlined recommended parenteral regimen (Figure 1).

Figure 1

When selecting a parenteral medication, we suggest first to exclude any contraindications, or see if an indication exists for a specific agent. Hydralazine, enalaprilat, metoprolol, or labetalol can be used as first‐line agents. Due to the scarcity of comparative trials looking at clinically significant outcomes (length of hospital stay, morbidity, mortality), decisions for the management of perioperative hypertension should be made based on comorbidity, efficacy, toxicity, and cost (Table 1).

An association between hypertension and operative risk has been reported in small studies since the early 1970s. In two studies, Prys‐Roberts et al.1, 2 found that subjects with uncontrolled hypertension were more likely to have myocardial ischemic changes on electrocardiography with episodes of hypotension during induction of anesthesia. Subjects without hypertension or with hypertension controlled by medication were less likely to have episodes of hypotension, regardless of the type of anesthetic.

Hypertension increases the risk of developing perioperative heart failure (HF), renal failure, myocardial ischemia, or stroke. The level of risk is dependent upon the blood pressure (BP) level. It has been shown that a BP of <180/110 mm Hg without target‐organ damage (TOD) is not an independent risk factor for perioperative cardiovascular (CV) complications, suggesting this level of BP does not need to be reduced rapidly to normal.3, 4

The Joint National Committee defines hypertensive emergency as severe elevations in BP (usually >180/120 mm Hg) that produce evidence of TOD.5 Patients with this level of BP who are asymptomatic and have no signs of TOD are considered to have hypertensive urgency. As patients with this level of BP are at higher risk perioperatively, pharmacotherapy is indicated. When oral medications cannot be administered, hypertensive urgency can be managed with a parenteral medication. The agent should be easily and predictably titrated, safe, and convenient (Table 1). This article reviews the management of perioperative hypertensive urgency with parenteral medications. The management of hypertensive emergencies, aortic dissection, and hypertension of pregnancy is outside the scope of this review.

Preoperative Considerations

In normotensive patients the induction of anesthesia can cause an acute elevation in BP (2030 mm Hg) and heart rate (HR) (1520 bpm).6 In patients with preexisting hypertension these changes are often greater, with elevations up to 90 mm Hg and 40 bpm. As anesthesia progresses systolic BP starts to fall (30 mm Hg), as a direct effect of both the anesthetic and the inhibition of the sympathetic nervous system (SNS). Patients with uncontrolled hypertension can have more severe reductions (60 mm Hg).6 This can result in intraoperative hypotension and shock. In a study of over 650 patients, marked intraoperative hypotension (<50% of preoperative BP or a 33% reduction for more than 10 minutes) was an independent risk factor for perioperative CV complications (cardiac arrhythmia, ischemia, HF, or renal failure).7

Therefore, when BP is mildly elevated at the time of surgery (<180/110 mm Hg), rapid reduction in BP is not necessary, and studies have been unable to demonstrate a benefit to delaying surgery.8 However, when BP is 180/110 mm Hg preoperatively, antihypertensive medications should be administered and intraoperative blood pressure monitored closely. There is a lack of data to support delay of surgery.9

Postoperative Considerations

The postoperative period is also associated with elevations in BP. In the immediate recovery phase from anesthesia, there is a mild elevation in BP within 10 to 15 mm Hg, but there are larger fluctuations in patients with preexisting hypertension.6 Otherwise postoperative hypertension can be seen from a variety of causes such as pain, excitement on emergence from anesthesia, and hypercarbia.10 Less common causes include agitation, hypoxemia, and hypervolemia. These secondary causes should be identified and treated before any antihypertensive medications are administered.

Discussion

Nitroprusside, nitroglycerin, nicardipine, and fenoldopam are all effective antihypertensive medications. However, their availability only as continuous infusions requires ICU monitoring and an intraarterial catheter, and they are therefore unnecessary in the management of hypertensive urgency. The parenteral medications that do not require a continuous infusion are diltiazem, verapamil, metoprolol, labetalol, enalaprilat, hydralazine, and transdermal clonidine.

As stated, the intravenous formulations of diltiazem and verapamil are indicated only for certain arrhythmias. Because the onset of action of transdermal clonidine is about 2 days and the offset is 8 hours, it has limited usefulness in the treatment of perioperative hypertension. Therefore, only metoprolol, labetalol, enalaprilat, and hydralazine have a major role in the treatment of hypertensive urgency when oral medications cannot be used.

When given intravenously, enalaprilat and hydralazine are safe, effective, widely available, and inexpensive. When deciding between these 2 agents, a few other considerations may be of importance. Even though ACE inhibitors have well‐recognized benefits in the management of HF50 and diabetic nephropathy,51 these characteristics are not relevant in the short‐term use of enalaprilat to treat perioperative hypertension. However, enalaprilat may be preferred over hydralazine when activation of the SNS and reflex tachycardia is to be avoided (cardiac ischemia, aortic dissection, increased intracranial pressure). Hydralazine may be preferred in the setting of hyperkalemia and acute renal failure. It must be preferred in pregnancy or bilateral renal artery stenosis.

Although the weight of the evidence of perioperative ‐blocker use to reduce CV events in noncardiac surgery suggests a benefit, there are significant limitations. Few studies have compared different ‐blockers. Studies to determine the ideal target population, duration of therapy, and route of administration are lacking. Additionally, using perioperative ‐blockers may cause harm in low‐risk patients.52 Care should be taken when using labetalol and metoprolol in combination as they can induce a dangerous reduction in HR. The role of acute administration of intravenous ‐blockers in the setting of myocardial ischemia is debatable, and probably dangerous in the setting of hypotension, bradycardia, HB, pulmonary edema, or bronchospasm.53

Therefore, generalizing the perioperative ‐blocker data to all patients with perioperative hypertension seems unlikely to have significant benefit, and may possibly pose harm.29 However, it seems reasonable to use ‐blockers in those in whom it would be indicated otherwise, and to continue parenteral therapy in those already taking a ‐blocker preoperatively in order to avoid withdrawal.54

When deciding between metoprolol and labetalol, a few considerations may be of importance. First, there is much more evidence documenting the safety and efficacy of labetalol in perioperative hypertension. Second, even though metoprolol has proven benefit in patients with chronic HF, coronary artery disease (CAD), and MI, these long‐term studies investigated oral metoprolol, not the intravenous formulation.55 Most importantly, labetalol is more effective at lowering BP due to its additional blockade of alpha₁ adrenoreceptors. Neither drug should be used in acute HF, bradycardia or greater than first‐degree HB, or bronchospasm. In conclusion, intravenous labetalol should be preferred over intravenous metoprolol for the management of perioperative hypertension.

Conclusions

Perioperative hypertension ideally should be evaluated well before the operative time period, when there is adequate time to initiate medications. Secondary causes such as pain, agitation, hypercarbia, hypoxemia, and hypervolemia should be treated directly prior to the administration of antihypertensive medications. It is uncertain whether patients with a BP of <180/110 mm Hg benefit from any specific parenteral medication, as there is little evidence from several studies that this level of BP without TOD leads to an increase in perioperative morbidity or mortality.3, 4, 7, 56 However, patients with hypertensive urgency are at higher risk for perioperative complications; therefore, their BP should be managed gradually to <160/110 mm Hg with the outlined recommended parenteral regimen (Figure 1).

Figure 1

When selecting a parenteral medication, we suggest first to exclude any contraindications, or see if an indication exists for a specific agent. Hydralazine, enalaprilat, metoprolol, or labetalol can be used as first‐line agents. Due to the scarcity of comparative trials looking at clinically significant outcomes (length of hospital stay, morbidity, mortality), decisions for the management of perioperative hypertension should be made based on comorbidity, efficacy, toxicity, and cost (Table 1).

In recent years, the demand for hospitalists has outstripped the supply, creating a national shortage.1, 2 A recent Society of Hospital Medicine (SHM) survey found that in the last 2 years there has been a 31% mean growth increase in the number of hospitalist groups.3 As hospitalists are becoming more difficult to recruit, many practices are utilizing physician assistants (PAs) and nurse practitioners (NPs), collectively referred to as nonphysician providers (NPPs) to help offset the workload.4 The SHM survey also noted that the number of hospitalist groups utilizing NPPs increased from 29% to 38%.3 The exact number of NPPs working for hospitalist groups is unknown.

Hospitalist NPPs are in demand for reasons other than just physician shortages. NPPs have been utilized to fill the gap in many institutions where the workforce was impacted by the 2002 Accreditation Council for Graduate Medical Education (ACGME) ruling to restrict resident work hours. Several studies have documented NPPs' ability to assist with the compliance of ACCGME resident work‐hour restrictions while maintaining patient continuity of care, improving length of stays, and reducing health care costs on various hospital services.59 Dresselhaus et al.10 found that 56% of medical resident's time on service was delegated to tasks not related to direct patient care. They proposed that these tasks can be delegated to the NPPs, leaving more time for the residents to focus on direct patient care. In a recent study performed at a Pennsylvania hospital, patients presenting to the emergency department with low‐risk chest pain (based upon thrombolysis in myocardial infarction [TIMI] risk score) were admitted to a nonteaching service staffed with NPPs and attending physicians. Simultaneously, a similar group of low‐risk chest pain patients were admitted to a traditional internal medicine resident service. The results demonstrated lower median length of stay and hospital charges on the nonteaching service. This study suggested that NPPs can offset the workload volume for medical residents, allowing them to focus on patients with higher acuity and greater learning value.11

Barriers to Finding Experienced NPPs in Hospital Medicine

Although many hospitalist groups are interested in hiring NPPs, there can be significant obstacles to recruitment. For example, most experienced PAs and NPs have clinical backgrounds in either surgical or medical subspecialties and therefore typically need extensive on‐the‐job training in hospital medicine, which can often take at least 6 to 12 months to acquire the basic skill set.12 Hiring new graduates may require even longer training periods.

The inexperience of new graduates has become an even more pertinent issue due to recent changes in PA education. Traditionally, PA programs attracted older students with prior healthcare experience, who wished to return to school for additional training. However, in 2005 a major shift occurred in PA education: programs began transitioning from graduating trainees with a bachelor's degree to now requiring a master's level degree for completion of the PA program.13 The acquisition of more advanced degrees has changed the demographics of the students matriculating into PA programs, attracting younger students, straight from undergraduate institutions, with less prior healthcare experience.14 As a result, not only are new PA graduates less experienced overall, but they are particularly lacking in exposure to hospital medicine. After PA students complete their first 12 months of PA school in the basic sciences and didactic coursework, they embark on 12 to 15 months of clinical rotations, which are largely rooted in primary care. In fact, many PA programs find it difficult to offer hospital‐based rotations while fulfilling the required rotations in primary care. These factors have resulted in the need for more extensive on‐the‐job training particularly for those new graduates interested in hospital medicine. In light of these challenges, our institution created a 12‐month postgraduate PA fellowship program in Hospital Medicine.

Postgraduate PA Training Programs

Postgraduate PA fellowships, interchangeably called residencies, are voluntary 1‐year training programs that provide both didactic instruction and clinical experience in a medical or surgical subspecialty, thereby lessening the need for on‐the‐job training. These programs are recognized by the Association of Postgraduate Physician Assistant Programs.15 Currently, there are 44 postgraduate training programs in the United States, in a wide range of medical and surgical specialties. At the end of these 1‐year postgraduate PA programs, most graduates receive a certificate of completion. Until now, the only postgraduate education option for PAs interested in Hospital Medicine was a master's completion program only available to PAs who were already employed by a hospitalist group.15 This work reviews the first reported postgraduate hospitalist training program for PAs. Specifically, the program's background, curriculum, anticipated program outcomes, and future plans are discussed.

Background for A Hospitalist Postgraduate PA Fellowship

Mayo Clinic Arizona is a multispecialty private group comprised of both outpatient services and a tertiary care hospital medical center, located in the metropolitan Phoenix, AZ, area. The Mayo Clinic Hospital is a 7‐story facility with 244 licensed beds, 18 operating rooms, and a Level II emergency department. The Mayo Hospitalist group is composed of 15 full time hospitalists and 6 part‐time hospitalists, all of whom are salaried Mayo employees. The group provides 24‐hour in‐house staffing, covering both resident services (teams composed of interns and residents supervised by a staff hospitalist) and nonresident services (staff hospitalists). Over the years there has been steady growth in the number of nonresident services, in part due to resident work‐hour restrictions. To support the physicians working on these nonresident services, the first PA was hired in 2001. Since then, the number of NPPs in our Hospitalist group has increased to 9.35 full‐time equivalents (FTEs), including 1 nurse practitioner. However, one of the greatest challenges in expanding the NPP service was the difficulty finding candidates with experience in hospital internal medicine. This need inspired the creation of a PA fellowship in Hospital Medicine. At the time, there were 2 other postgraduate PA training programs at the Mayo Clinic Arizona in Hepatology and Otolaryngology/Ear, Nose, and Throat (ENT) Surgery.

Program Description

The Mayo Clinic Arizona PA fellowship in Hospital Medicine began in October 2007 and currently accepts 1 fellow per year. Applicants must be graduates of an Accreditation Review Commission in Education for the Physician Assistant (ARC‐PA)‐accredited PA program and be certified through the National Commission on Certification of Physician Assistants (NCCPA). Furthermore, they must be licensed to work as a PA in the state of Arizona. The program is 12 months in duration, and is comprised of both didactic and clinical components. Upon graduation, the fellow earns a certificate of completion from the Mayo Clinic College of Medicine. The program has received recognition with the Association of Postgraduate Physician Assistant Programs (APPAP).

Two physician assistants act as co‐program directors of the PA fellowship in hospital medicine. They are given 0.10 full‐time equivalent (FTE) for management of the program, which includes day‐to‐day operations, curriculum development, and candidate selection. The program also has 2 volunteer physician medical directors, both of whom have previous medical residency experience. The physicians and NPPs in our hospitalist group volunteer their time to serve as faculty for the program, assisting with much of the didactic and clinical education. The program receives a budget of $99,500 per year, which is funded by the organization's foundation through the department of education. This includes the fellow stipend of $44,000 per 12 months and institutional malpractice insurance coverage. The fellow also receives health and dental insurance, 2 weeks of paid vacation, and $500 stipend toward attendance of a continuing medical education (CME) conference.

CURRICULUM

The PA fellowship curriculum is designed in a diverse unique format that strives to accommodate all types of learners. It includes clinical rotations in various medicine/surgical subspecialties, didactic instruction, and teaching modules (Figure 1). The curriculum is based upon the SHM Core Competencies.15

Figure 1

Clinical Rotations

The PA fellow completes 12 to 14 general hospital medicine and medical specialty rotations, each 2 to 4 weeks in duration. The rotation calendar for the current fellow is given in Figure 2. These rotations are all inpatient‐based and are supervised by either the hospitalist or the respective inpatient subspecialists. The PA fellow's specific clinical responsibilities vary from rotation to rotation, and are designed to maximize the fellow's exposure to that particular specialty. Each rotation has specific written objectives created by the program directors and reviewed by the rotation's preceptor(s) (Figure 2). During the clinical rotations, complementary didactic lectures, coursework, and readings are provided to ensure the PA fellow receives a strong foundation. Didactic instruction is designed by the program directors, physician preceptors and staff NPPs, and is coordinated with the clinical rotation specialty. At the end of each rotation the fellow is evaluated by the preceptor and given direct feedback on their performance.

Figure 2

Teaching Modules

One component of the Hospital Medicine PA fellowship curriculum that may be unique is the concept of teaching modules. While receiving regular didactic instruction and completing their clinical rotations, the PA is also expected to complete self‐directed teaching module assignments. These modules serve to educate the PA fellow on the hospital as a systemthe true essence of hospital medicine. The modules cover a variety of topics not directly addressed during their rotations. These topics are outlined in Figure 3. Each teaching module consists of a didactic component, clinical application, and assessment (Figure 4) and has its own specific objectives and goals. Teaching modules are often taught by the local expert in the hospital in that particular area. For example, for the infectious control teaching module, the PA fellow will rotate with the infection control nursing staff learning about the isolation and infection control policies of the institution.

Figure 3

Figure 4

Assessment Tools

There are several tools utilized to assess both the PA fellow and the fellowship program itself (Figure 5). The assessment tools used include both ongoing and summative assessments. To fulfill the ongoing assessment, each rotation and teaching module contains assessment tools provided by the preceptor, which are reviewed by the program directors. Additionally, during the clinical rotations, skills are assessed using competency checklists that require the preceptor to directly observe the PA fellow perform a specific task or skill‐set and sign off on its successful completion (Supplementary Figures 6, 7).

Figure 5

There are 2 forms of summative assessment for the PA fellow. First, to assess the PA fellow's knowledge, comprehensive mid‐year and end‐year examinations are utilized. These multiple‐choice examinations are comprised of questions which align with the didactic lectures/objectives provided by the Hospital Medicine faculty throughout the year. The second form of summative evaluation of the fellow is project‐based and divided into 2 parts. First, the fellow is expected to write a publication‐quality manuscript on a hospital medicine topic by the end of the year. Second, the PA fellow is expected to create a professional portfolio, which is comprised of a collection of all of the rotation/module assessments, the formal program assessments, and documentation of all of the skills obtained by the fellow throughout year (competency checklists). This portfolio can be used by the graduate to demonstrate to future employers what skills they possess and provide documentation of knowledge gained during the fellowship.

The program itself is evaluated by several measures. First, the fellow provides formal feedback during the mid‐year and end‐of‐the‐year assessments, which are used to enhance the experience of future fellows. Second, there is ongoing review by both the division of Hospital Medicine and the institution's Allied Health Education Committee, which ensures that the program maintains the appropriate standards and goals.

Future Goals for the PA Fellowship

The program graduated its first fellow at the end of October 2008 and has enjoyed early success. Integrating the PA fellow onto the hospitalist services augmented the present mid‐level and physician teams. There has been excellent institutional support for the program with extremely positive feedback from the rotation preceptors. There are several futures plans for the program. Our first goal is to seek accreditation from the Accreditation Review Commission for Physician Assistants (ARC‐PA), the organization that accredits entry level PA programs and which began formal, voluntary accreditation of postgraduate programs in early 2008. We plan to begin this process within the next academic year.

Our second long‐term goal for the program is to include NPs in the training program. Because of the desire to seek accreditation, the program directors felt temporarily limiting the fellowship to PAs would aide in the rigorous accreditation process, which can take approximately 1 year to complete. There is an NP on our faculty and the program has received interest from NPs. Once we obtain accreditation, expand the program enrollment, and develop an NP curriculum, we plan to open the fellowship to either PA or NP applicants.

Our third goal is to substantiate our PA Fellowship validity with outcome measures and ultimately publishable data. Thus far, the success of the PA fellowship is qualitative, and with small numbers of graduates it is difficult to quantify. After graduation of many subsequent PA fellows, our goal is to obtain quantifiable data that can be used to improve the quality of the PA fellowship and demonstrate the value of postgraduate training for physician assistants.

Perhaps the most important goal of the program is to eventually accept additional PA/NP fellows per year. While 1 program does not meet the demands of a national shortage of hospitalist providers, it may serve as a model that other institutions can adapt to their own needs. Since the program is based upon the SHM Core Competencies, the curriculum can be applied to a variety of hospitalist programs, and its relatively low operating cost makes it feasible for both academic‐based and community‐based institutions. Importantly, since recruitment and retention of employees is such a challenge for most hospitalist groups, this PA fellowship program may serve as a vehicle for recruitment and long‐term retention of well‐trained employees. This precedent has been set, as our division has hired our first PA fellow, whose transition from PA fellow to PA staff was seamless.

In conclusion, our PA fellowship in Hospital Medicine represents the first reported postgraduate PA program of this kind in the United States offering a certificate of completion. As the need for hospitalists increase so will the need for NPPs, particularly those with additional training in hospital medicine. This program serves as an example of 1 type of training tool for physician assistants looking to work in hospital medicine.