A 57‐year‐old woman developed a pruritic rash 6 hours after undergoing coronary angiography. On exam, symmetrical, eczematous plaques were noted in her bilateral groin (Figure 1), buttocks, axillae (Figure 2), and the intertriginous folds of her breasts. No palmar, plantar, or mucosal lesions were noted and laboratory tests were normal. This patient presents with symmetrical drug‐related intertriginous and flexural exanthema (SDRIFE) secondary to iodine‐based contrast dye. It is a type IV hypersensitivity reaction most often reported to nickel, mercury, and systemic antibiotics, although previous sensitization is often unknown. Also called baboon syndrome because its distribution mimics the pink bottom of a baboon, SDRIFE appears hours to days after exposure to the offending agent. The unusual distribution may be explained by high concentrations of the allergen in sweat. Resolution is typical with discontinuation of the offending drug, although antihistamines, topical steroids, and possibly oral steroids may be useful adjuncts.

Figure 1

Figure 2

A 57‐year‐old woman developed a pruritic rash 6 hours after undergoing coronary angiography. On exam, symmetrical, eczematous plaques were noted in her bilateral groin (Figure 1), buttocks, axillae (Figure 2), and the intertriginous folds of her breasts. No palmar, plantar, or mucosal lesions were noted and laboratory tests were normal. This patient presents with symmetrical drug‐related intertriginous and flexural exanthema (SDRIFE) secondary to iodine‐based contrast dye. It is a type IV hypersensitivity reaction most often reported to nickel, mercury, and systemic antibiotics, although previous sensitization is often unknown. Also called baboon syndrome because its distribution mimics the pink bottom of a baboon, SDRIFE appears hours to days after exposure to the offending agent. The unusual distribution may be explained by high concentrations of the allergen in sweat. Resolution is typical with discontinuation of the offending drug, although antihistamines, topical steroids, and possibly oral steroids may be useful adjuncts.

Figure 1

Figure 2

A 57‐year‐old woman developed a pruritic rash 6 hours after undergoing coronary angiography. On exam, symmetrical, eczematous plaques were noted in her bilateral groin (Figure 1), buttocks, axillae (Figure 2), and the intertriginous folds of her breasts. No palmar, plantar, or mucosal lesions were noted and laboratory tests were normal. This patient presents with symmetrical drug‐related intertriginous and flexural exanthema (SDRIFE) secondary to iodine‐based contrast dye. It is a type IV hypersensitivity reaction most often reported to nickel, mercury, and systemic antibiotics, although previous sensitization is often unknown. Also called baboon syndrome because its distribution mimics the pink bottom of a baboon, SDRIFE appears hours to days after exposure to the offending agent. The unusual distribution may be explained by high concentrations of the allergen in sweat. Resolution is typical with discontinuation of the offending drug, although antihistamines, topical steroids, and possibly oral steroids may be useful adjuncts.

Figure 1

Figure 2

I knew that he was going to die. I do not remember when it became evident to me, and I was not sure how to tell the family. I thought that I could arrange a family meeting and inform them of the sad reality in a calm, sympathetic manner. The patient had chronic lymphocytic leukemia, and his case was advanced. The only medication available to him was chlorambucil. As the days passed, I could not bring myself to call the family meeting because they had so much hope. Every day as we got results and I shared them, I would sandwich the bad news with some optimism to ease their pain. Well, his white blood cell count has come down, but his platelet count and red blood cell counts are very low, and this puts him in danger of bleeding. The medicine is bringing the white cell count down but has not yet brought the other cell counts up. What we can do is give him some blood. I tried not to allow despair to creep into my thoughts or my voice. I knew that the blood bank had no platelets or packed red blood cells. He was not eating or drinking, and we had placed a nasogastric tube through which his family fed him wheat or millet porridge (manufactured tube feeds are not widely available in Uganda). I tried not to think about the time that he had almost died a few weeks before.

I had been called to the bedside because the patient was in respiratory distress. The doctor on call was in his office when I arrived, and I wondered why he was not at the bedside. I took one look at the patient and had to step away for a moment to compose myself. I felt the tears threatening to come, but I had to stop them. This was not the time for emotions. I had to assess the patient and make some quick decisions. The doctor on call seemed to have given up. He was a young trainee in a system in which you treat when you can and, if the situation is hopeless, you move on to the next patient. There are no resources for perpetuating hope. This is so different from my practice in the United States, where if a patient wants everything done, we will do it. We are not taught when to give up hope, and futility does not figure into the allocation of resources. I looked at the patient struggling to breathe and felt that I had to do all that I could for him. I asked the doctor on call to place the patient on oxygen and hoped that the tanks were not empty. I was worried about a lot of things, such as pulmonary embolus, myocardial infarction, and pneumonia. Diagnosing any of these would not be easy (the hospital did not have a computed tomography scanner, and obtaining cardiac enzymes was not as simple as clicking a button on a computer). First things first: the chest X‐ray. I thanked God that we were in a private hospital, one of the best in the city of Kampala, so we were able to get a chest X‐ray right away. As we transported the patient (portable X‐rays are nonexistent), the resident told me that he had called the consultant (the equivalent of an attending physician in the United States), who happened to be out of town. The consultant instructed us to transfer the patient to Mulago Hospital (the largest tertiary center in Uganda with well over 1000 beds and some of the equipment that you might find in an American hospital). I wondered how an attending physician could be out of town and leave a resident in charge. The thought was disturbing, but I had no time to ponder it. I later learned that physicians are so poorly paid that many have their own private clinics. My patient got the X‐ray, and I reviewed it with the resident. Tuberculosis, he said. Tuberculosis was this resident's reality. Many patients who need chest X‐rays in Uganda have tuberculosis. As I reviewed the X‐ray, though, I was certain that this was congestive heart failure. However, in Uganda, congestive heart failure is rarely diagnosed in the hospital. Patients with an ejection fraction low enough to cause congestion generally die before they get to a hospital. I knew that some furosemide would work for this patient, but I could not get the resident to listen to me. He had orders from the consultant to transfer the patient immediately, and the ambulance was ready. I tried to convince the resident to administer furosemide before transferring the patient, but he feared administering a drug not approved by his superior. As the patient was loaded onto the ambulance, I reflected for a second on how different things would be if we were in the United States. We arrived at Mulago in record time, and I tried to get the intake doctors to understand what the problem was; however, they did not want to hear from the US doctor. I stared in frustration as they wasted valuable time. I wondered how long the patient would survive in respiratory distress with nothing being done. I called the patient's son and asked him to come to Mulago immediately. Miraculously, he had already been on his way. As I held the patient's hand, sure that he would die right then and there in a waiting area as nobody did anything, I saw the patient's son. I knew that he was a pharmacist, and I asked him to go to the pharmacy and buy furosemide and some syringes. In Uganda, one can buy any medication without a prescription. Luckily, the hospital pharmacy had the drug. We treated the patient, and in no time, his breathing had returned to normal.

I was jolted back to reality. He was dying, and I knew it. He had had many close calls. There was the time that he got the wrong blood during a blood transfusion. I informed the doctor on call as the blood was being administered that I thought the patient was getting a transfusion reaction because he had rigors. The physician on call suggested covering him in blankets, and I suggested stopping the infusion and administering steroids. The pack of blood showed that he was getting his blood type. The patient was typed and crossed again, and to our surprise, we got a different result. I went to the laboratory to perform a third, tie‐breaking cross match and was surprised to note that the reagents had passed their expiration date. However, I knew that these were small battles we were winning and that there was no winning the war.

I recognized that the challenges of practicing medicine in the developing world were many. I wondered how the patients of families with fewer resources survived. The answer was obvious: they didn't. I personally picked up blood when it was available from the blood bank and vividly remember walking from the blood bank at night to the private hospital with units of blood in each hand. Once we arrived at the hospital, I had to warm the blood to room temperature by holding it close to my own skin. Many tests that we perform routinely on a hospitalized patient in the United States are not available.

There was still the problem of breaking the news to the family. Despite everything that had been done and the many near misses that the patient had survived, he was still going to die. It turns out that the family was more intuitive than I thought. One day, the son came to me and asked how long his dad had. Not long, I said quietly. I thought about all that I could potentially do if I had the patient in the hospital at which I worked in the United States. Would it have made a difference? I do not know. It was impossible doctoring this patient, and I suspect doing it in a resource‐rich environment would not have made it any easier. You see this patient, perhaps the most important patient of my life, certainly a patient that I will never forget, was my father.

It had been 15 years since I had traveled to the United States for an education. I knew that my father was so incredibly proud of me. I think that he was the happiest I had ever seen him when he attended my graduation from medical school in Minnesota. I had been looking forward to this visit back home because it had been 3 years since I had last seen my family. I was somewhat concerned because my father had told me a week before I traveled that he was not feeling well. When I arrived, there seemed to be relief on my brother's face when he met me at the airport. We drove straight to the hospital, and along with the joy of seeing me, I could sense that my father was glad that I was home at this particular point in time. They had just received the diagnosis. He had leukemia, and they were glad that their doctor was home. They had particular faith in the daughter (sister) sent abroad for an education. Things would now be okay. Initially, I never got to choose the role of doctor that I played in the final chapter of my father's life. The decision was made for me out of my family's desperation to make sure that they had left no stone unturned to help my father, and I accepted it out of necessity. As my father became my father when I entered this world, I became his doctor when he was leaving it; there was never any question in my mind, as there never was in his. As it became clear that my father would not survive, I chose to continue the role of doctor. I have watched many patients die as a physician and have done my best to make sure that their passing is comfortable, peaceful, and dignified. The doctor could help this patient die, but the daughter could not watch her father go. When it was evident that he had only days to live and did not need this doctor or know his daughter, I flew back to the United States. Three days later my father died. I was not physically at his bedside, but my spirit was. I have no regrets. Although the head knows that he passed on, in my mind's eye, he is laughing and has a twinkle in his eye. I could not bear to see him without life. A piece of my heart is buried with him, and for this reason, I will never be out of Africa.

I knew that he was going to die. I do not remember when it became evident to me, and I was not sure how to tell the family. I thought that I could arrange a family meeting and inform them of the sad reality in a calm, sympathetic manner. The patient had chronic lymphocytic leukemia, and his case was advanced. The only medication available to him was chlorambucil. As the days passed, I could not bring myself to call the family meeting because they had so much hope. Every day as we got results and I shared them, I would sandwich the bad news with some optimism to ease their pain. Well, his white blood cell count has come down, but his platelet count and red blood cell counts are very low, and this puts him in danger of bleeding. The medicine is bringing the white cell count down but has not yet brought the other cell counts up. What we can do is give him some blood. I tried not to allow despair to creep into my thoughts or my voice. I knew that the blood bank had no platelets or packed red blood cells. He was not eating or drinking, and we had placed a nasogastric tube through which his family fed him wheat or millet porridge (manufactured tube feeds are not widely available in Uganda). I tried not to think about the time that he had almost died a few weeks before.

I had been called to the bedside because the patient was in respiratory distress. The doctor on call was in his office when I arrived, and I wondered why he was not at the bedside. I took one look at the patient and had to step away for a moment to compose myself. I felt the tears threatening to come, but I had to stop them. This was not the time for emotions. I had to assess the patient and make some quick decisions. The doctor on call seemed to have given up. He was a young trainee in a system in which you treat when you can and, if the situation is hopeless, you move on to the next patient. There are no resources for perpetuating hope. This is so different from my practice in the United States, where if a patient wants everything done, we will do it. We are not taught when to give up hope, and futility does not figure into the allocation of resources. I looked at the patient struggling to breathe and felt that I had to do all that I could for him. I asked the doctor on call to place the patient on oxygen and hoped that the tanks were not empty. I was worried about a lot of things, such as pulmonary embolus, myocardial infarction, and pneumonia. Diagnosing any of these would not be easy (the hospital did not have a computed tomography scanner, and obtaining cardiac enzymes was not as simple as clicking a button on a computer). First things first: the chest X‐ray. I thanked God that we were in a private hospital, one of the best in the city of Kampala, so we were able to get a chest X‐ray right away. As we transported the patient (portable X‐rays are nonexistent), the resident told me that he had called the consultant (the equivalent of an attending physician in the United States), who happened to be out of town. The consultant instructed us to transfer the patient to Mulago Hospital (the largest tertiary center in Uganda with well over 1000 beds and some of the equipment that you might find in an American hospital). I wondered how an attending physician could be out of town and leave a resident in charge. The thought was disturbing, but I had no time to ponder it. I later learned that physicians are so poorly paid that many have their own private clinics. My patient got the X‐ray, and I reviewed it with the resident. Tuberculosis, he said. Tuberculosis was this resident's reality. Many patients who need chest X‐rays in Uganda have tuberculosis. As I reviewed the X‐ray, though, I was certain that this was congestive heart failure. However, in Uganda, congestive heart failure is rarely diagnosed in the hospital. Patients with an ejection fraction low enough to cause congestion generally die before they get to a hospital. I knew that some furosemide would work for this patient, but I could not get the resident to listen to me. He had orders from the consultant to transfer the patient immediately, and the ambulance was ready. I tried to convince the resident to administer furosemide before transferring the patient, but he feared administering a drug not approved by his superior. As the patient was loaded onto the ambulance, I reflected for a second on how different things would be if we were in the United States. We arrived at Mulago in record time, and I tried to get the intake doctors to understand what the problem was; however, they did not want to hear from the US doctor. I stared in frustration as they wasted valuable time. I wondered how long the patient would survive in respiratory distress with nothing being done. I called the patient's son and asked him to come to Mulago immediately. Miraculously, he had already been on his way. As I held the patient's hand, sure that he would die right then and there in a waiting area as nobody did anything, I saw the patient's son. I knew that he was a pharmacist, and I asked him to go to the pharmacy and buy furosemide and some syringes. In Uganda, one can buy any medication without a prescription. Luckily, the hospital pharmacy had the drug. We treated the patient, and in no time, his breathing had returned to normal.

I was jolted back to reality. He was dying, and I knew it. He had had many close calls. There was the time that he got the wrong blood during a blood transfusion. I informed the doctor on call as the blood was being administered that I thought the patient was getting a transfusion reaction because he had rigors. The physician on call suggested covering him in blankets, and I suggested stopping the infusion and administering steroids. The pack of blood showed that he was getting his blood type. The patient was typed and crossed again, and to our surprise, we got a different result. I went to the laboratory to perform a third, tie‐breaking cross match and was surprised to note that the reagents had passed their expiration date. However, I knew that these were small battles we were winning and that there was no winning the war.

I recognized that the challenges of practicing medicine in the developing world were many. I wondered how the patients of families with fewer resources survived. The answer was obvious: they didn't. I personally picked up blood when it was available from the blood bank and vividly remember walking from the blood bank at night to the private hospital with units of blood in each hand. Once we arrived at the hospital, I had to warm the blood to room temperature by holding it close to my own skin. Many tests that we perform routinely on a hospitalized patient in the United States are not available.

There was still the problem of breaking the news to the family. Despite everything that had been done and the many near misses that the patient had survived, he was still going to die. It turns out that the family was more intuitive than I thought. One day, the son came to me and asked how long his dad had. Not long, I said quietly. I thought about all that I could potentially do if I had the patient in the hospital at which I worked in the United States. Would it have made a difference? I do not know. It was impossible doctoring this patient, and I suspect doing it in a resource‐rich environment would not have made it any easier. You see this patient, perhaps the most important patient of my life, certainly a patient that I will never forget, was my father.

It had been 15 years since I had traveled to the United States for an education. I knew that my father was so incredibly proud of me. I think that he was the happiest I had ever seen him when he attended my graduation from medical school in Minnesota. I had been looking forward to this visit back home because it had been 3 years since I had last seen my family. I was somewhat concerned because my father had told me a week before I traveled that he was not feeling well. When I arrived, there seemed to be relief on my brother's face when he met me at the airport. We drove straight to the hospital, and along with the joy of seeing me, I could sense that my father was glad that I was home at this particular point in time. They had just received the diagnosis. He had leukemia, and they were glad that their doctor was home. They had particular faith in the daughter (sister) sent abroad for an education. Things would now be okay. Initially, I never got to choose the role of doctor that I played in the final chapter of my father's life. The decision was made for me out of my family's desperation to make sure that they had left no stone unturned to help my father, and I accepted it out of necessity. As my father became my father when I entered this world, I became his doctor when he was leaving it; there was never any question in my mind, as there never was in his. As it became clear that my father would not survive, I chose to continue the role of doctor. I have watched many patients die as a physician and have done my best to make sure that their passing is comfortable, peaceful, and dignified. The doctor could help this patient die, but the daughter could not watch her father go. When it was evident that he had only days to live and did not need this doctor or know his daughter, I flew back to the United States. Three days later my father died. I was not physically at his bedside, but my spirit was. I have no regrets. Although the head knows that he passed on, in my mind's eye, he is laughing and has a twinkle in his eye. I could not bear to see him without life. A piece of my heart is buried with him, and for this reason, I will never be out of Africa.

I knew that he was going to die. I do not remember when it became evident to me, and I was not sure how to tell the family. I thought that I could arrange a family meeting and inform them of the sad reality in a calm, sympathetic manner. The patient had chronic lymphocytic leukemia, and his case was advanced. The only medication available to him was chlorambucil. As the days passed, I could not bring myself to call the family meeting because they had so much hope. Every day as we got results and I shared them, I would sandwich the bad news with some optimism to ease their pain. Well, his white blood cell count has come down, but his platelet count and red blood cell counts are very low, and this puts him in danger of bleeding. The medicine is bringing the white cell count down but has not yet brought the other cell counts up. What we can do is give him some blood. I tried not to allow despair to creep into my thoughts or my voice. I knew that the blood bank had no platelets or packed red blood cells. He was not eating or drinking, and we had placed a nasogastric tube through which his family fed him wheat or millet porridge (manufactured tube feeds are not widely available in Uganda). I tried not to think about the time that he had almost died a few weeks before.

I had been called to the bedside because the patient was in respiratory distress. The doctor on call was in his office when I arrived, and I wondered why he was not at the bedside. I took one look at the patient and had to step away for a moment to compose myself. I felt the tears threatening to come, but I had to stop them. This was not the time for emotions. I had to assess the patient and make some quick decisions. The doctor on call seemed to have given up. He was a young trainee in a system in which you treat when you can and, if the situation is hopeless, you move on to the next patient. There are no resources for perpetuating hope. This is so different from my practice in the United States, where if a patient wants everything done, we will do it. We are not taught when to give up hope, and futility does not figure into the allocation of resources. I looked at the patient struggling to breathe and felt that I had to do all that I could for him. I asked the doctor on call to place the patient on oxygen and hoped that the tanks were not empty. I was worried about a lot of things, such as pulmonary embolus, myocardial infarction, and pneumonia. Diagnosing any of these would not be easy (the hospital did not have a computed tomography scanner, and obtaining cardiac enzymes was not as simple as clicking a button on a computer). First things first: the chest X‐ray. I thanked God that we were in a private hospital, one of the best in the city of Kampala, so we were able to get a chest X‐ray right away. As we transported the patient (portable X‐rays are nonexistent), the resident told me that he had called the consultant (the equivalent of an attending physician in the United States), who happened to be out of town. The consultant instructed us to transfer the patient to Mulago Hospital (the largest tertiary center in Uganda with well over 1000 beds and some of the equipment that you might find in an American hospital). I wondered how an attending physician could be out of town and leave a resident in charge. The thought was disturbing, but I had no time to ponder it. I later learned that physicians are so poorly paid that many have their own private clinics. My patient got the X‐ray, and I reviewed it with the resident. Tuberculosis, he said. Tuberculosis was this resident's reality. Many patients who need chest X‐rays in Uganda have tuberculosis. As I reviewed the X‐ray, though, I was certain that this was congestive heart failure. However, in Uganda, congestive heart failure is rarely diagnosed in the hospital. Patients with an ejection fraction low enough to cause congestion generally die before they get to a hospital. I knew that some furosemide would work for this patient, but I could not get the resident to listen to me. He had orders from the consultant to transfer the patient immediately, and the ambulance was ready. I tried to convince the resident to administer furosemide before transferring the patient, but he feared administering a drug not approved by his superior. As the patient was loaded onto the ambulance, I reflected for a second on how different things would be if we were in the United States. We arrived at Mulago in record time, and I tried to get the intake doctors to understand what the problem was; however, they did not want to hear from the US doctor. I stared in frustration as they wasted valuable time. I wondered how long the patient would survive in respiratory distress with nothing being done. I called the patient's son and asked him to come to Mulago immediately. Miraculously, he had already been on his way. As I held the patient's hand, sure that he would die right then and there in a waiting area as nobody did anything, I saw the patient's son. I knew that he was a pharmacist, and I asked him to go to the pharmacy and buy furosemide and some syringes. In Uganda, one can buy any medication without a prescription. Luckily, the hospital pharmacy had the drug. We treated the patient, and in no time, his breathing had returned to normal.

I was jolted back to reality. He was dying, and I knew it. He had had many close calls. There was the time that he got the wrong blood during a blood transfusion. I informed the doctor on call as the blood was being administered that I thought the patient was getting a transfusion reaction because he had rigors. The physician on call suggested covering him in blankets, and I suggested stopping the infusion and administering steroids. The pack of blood showed that he was getting his blood type. The patient was typed and crossed again, and to our surprise, we got a different result. I went to the laboratory to perform a third, tie‐breaking cross match and was surprised to note that the reagents had passed their expiration date. However, I knew that these were small battles we were winning and that there was no winning the war.

I recognized that the challenges of practicing medicine in the developing world were many. I wondered how the patients of families with fewer resources survived. The answer was obvious: they didn't. I personally picked up blood when it was available from the blood bank and vividly remember walking from the blood bank at night to the private hospital with units of blood in each hand. Once we arrived at the hospital, I had to warm the blood to room temperature by holding it close to my own skin. Many tests that we perform routinely on a hospitalized patient in the United States are not available.

There was still the problem of breaking the news to the family. Despite everything that had been done and the many near misses that the patient had survived, he was still going to die. It turns out that the family was more intuitive than I thought. One day, the son came to me and asked how long his dad had. Not long, I said quietly. I thought about all that I could potentially do if I had the patient in the hospital at which I worked in the United States. Would it have made a difference? I do not know. It was impossible doctoring this patient, and I suspect doing it in a resource‐rich environment would not have made it any easier. You see this patient, perhaps the most important patient of my life, certainly a patient that I will never forget, was my father.

It had been 15 years since I had traveled to the United States for an education. I knew that my father was so incredibly proud of me. I think that he was the happiest I had ever seen him when he attended my graduation from medical school in Minnesota. I had been looking forward to this visit back home because it had been 3 years since I had last seen my family. I was somewhat concerned because my father had told me a week before I traveled that he was not feeling well. When I arrived, there seemed to be relief on my brother's face when he met me at the airport. We drove straight to the hospital, and along with the joy of seeing me, I could sense that my father was glad that I was home at this particular point in time. They had just received the diagnosis. He had leukemia, and they were glad that their doctor was home. They had particular faith in the daughter (sister) sent abroad for an education. Things would now be okay. Initially, I never got to choose the role of doctor that I played in the final chapter of my father's life. The decision was made for me out of my family's desperation to make sure that they had left no stone unturned to help my father, and I accepted it out of necessity. As my father became my father when I entered this world, I became his doctor when he was leaving it; there was never any question in my mind, as there never was in his. As it became clear that my father would not survive, I chose to continue the role of doctor. I have watched many patients die as a physician and have done my best to make sure that their passing is comfortable, peaceful, and dignified. The doctor could help this patient die, but the daughter could not watch her father go. When it was evident that he had only days to live and did not need this doctor or know his daughter, I flew back to the United States. Three days later my father died. I was not physically at his bedside, but my spirit was. I have no regrets. Although the head knows that he passed on, in my mind's eye, he is laughing and has a twinkle in his eye. I could not bear to see him without life. A piece of my heart is buried with him, and for this reason, I will never be out of Africa.

There has been marked recent growth in the employment and utilization of both pediatric and adult hospitalists. Recent data demonstrate that approximately 25% of current pediatric hospitalist programs are less than 2 years old.1 Some have posited that this growth is due to increasing pressure from the public and payors to deliver cost‐effective and high‐quality care.2 However, little is known about the mechanisms by which those who deliver care in this framework are trained, nor the scope of clinical practice they provide.37 One study has shown that among those who direct pediatric hospitalist services there is a great degree of variability in the description of the roles, work patterns, and employment characteristics of hospitalists.1 That study provided only 1 perspective on the roles and career trajectories of those in the field. To better understand both the range and frequency of experiences, clinical and nonclinical roles, training, work expectations, and career plans, we conducted a national survey study of practicing pediatric hospitalists.

METHODS

RESULTS

RESULTS BY ACADEMIC STATUS

Only significant differences between academic and nonacademic hospitalists are presented.

RESULTS BY HOSPITAL CHARACTERISTICS

For each hospital characteristic, only significant differences between dichotomized groups are presented.

DISCUSSION

This study provides the most comprehensive information available regarding the clinical and nonclinical roles, training, work expectations, and career plans of pediatric hospitalists. Among the most important of our findings is the distribution of the length of time that pediatric hospitalists had served in their roles. While over one‐third (37%) reported having been practicing as hospitalists for over 5 years, 45% of our respondents had been in practice for fewer than 3 years. This is consistent with both the perceptions of rapid growth of the field and with significant turnover of hospitalists.1, 8 It is important to note that our findings may actually overestimate the proportion of hospitalists with longer durations of employment as our sampling strategy would have been less likely to include those who left the field within the first 12 to 18 months of practice. Nevertheless, over half (61%) of our respondents expected to remain a hospitalist for the duration of their career and few reported choosing to become a hospitalist as a short‐term employment option. This finding has important implications for the future stability of the hospitalist workforce and the potential development of specific expertise among this cadre of clinicians.6

The demographic profile of pediatric hospitalists was also consistent with these findings. The mean age of 39 years for our respondents is indicative of a significant proportion of this group of physicians recently having completed their residency training. Further, the gender distribution approximates that of current pediatric residency graduates, thus indicating that that this is not a clinical choice for which there would be a skewed distribution as is the case in some pediatric subspecialties.9

Our findings were similar to the 2004 Ottolini et al.10 findings on the roles of pediatric hospitalists. Respondents in our study reported spending less time providing inpatient care (61% versus 75%), providing clinical teaching or supervising residents (16% versus 26%), performing administrative duties (8% versus 19%), and conducting research (3% versus 9%) compared with the respondents in the Ottolini et al.10 survey.

At this point in time, fewer than half of our respondents reported any hospitalist‐specific training, including workshops at professional meetings or CME coursework. As there are a paucity of fellowships offering postresidency training in pediatric hospital medicine, and most of the existing programs are newly established, few in practice have completed such programs.11 In addition, most respondents reported that current CME offerings do not meet their needs, and that they could have used additional QI training to prepare them for their role as pediatric hospitalists. However, almost three‐quarters of respondents (73%) do not believe any additional training beyond residency should be required. As such, it is unclear if a defined, unique body of knowledge specific to hospitalists is either needed or desired by those currently in the field.

Although there are a broad range of potential clinical roles within hospital medicine, and this clinical variety influenced most respondents' decisions to become hospitalists, the current scope of an individual hospitalist tends to become somewhat focused.12, 13 While we found almost all provided service on the pediatric inpatient unit, many fewer provided inpatient consultation and normal newborn care, or were involved in interhospital transport or as part of an emergency response team. There is also wide variation in the types of procedures performed or supervised by hospitalists at different institutions. More than half never perform or supervise infusion services, PICC or central line placement, or circumcision. The variation seen among hospitalists practicing in different hospital settings likely is a result, at least in part, of different needs in teaching hospitals for both service and for clinical experience of trainees. For example, our results demonstrate that pediatric hospitalists in nonteaching and non‐children's hospitals are more likely to have a broader scope of clinical care provision. Another potential issue is that some hospitalists may be employed by institutions which have no pediatric ICU, neonatal ICU, or other specialty unit. As such, these hospitalists would not have the opportunity to work in such settings.

Further, those without academic appointments are also more likely to have expanded clinical roles compared with their academic counterparts. This may be due to the fact that there is likely a greater number of subspecialty‐trained pediatric providers in academic centers and thus the need for hospitalists to cover specific services or perform specific procedures is lessened. There may also be a desire to prevent competition among care providers within the same institution. In contrast, hospitalists with academic appointments are more likely (though still uncommonly) to have taken leadership roles in hospital administration and QI initiatives. Thus, the nature of their efforts appears to expand into nonclinical delivery areas.

Clearly, hospitalists report they have assumed a significant role in the clinical teaching of trainees at all levels, with 94% of our respondents maintaining at least some involvement in education. On average, they spend 16% of their time in educational efforts. However, there are few data on the impact of their work in this area.5, 13 Studies in pediatrics to date have been limited to a few institutions,3, 5 and have not addressed the issue from the perspective of residency program directors or those who are in charge of inpatient curricula.

This study, like the majority of studies related to pediatric hospitalists, is hampered by the difficulty of identifying pediatric hospitalists. Rather than utilizing a hospital medicine membership list, which would be potentially biased by self‐selection, we attempted to obtain a more representative sample through utilization of the AHA database.

CONCLUSIONS

Findings from this study provide an additional perspective regarding pediatric hospitalists to add to our previous study of hospitalist program directors.1 However, the field is currently a moving target. Our data demonstrate that there is significant flux in the hospitalist workforce, uncertainty regarding turnover, and variation in the roles of these professionals in their clinical and nonclinical work environment. Moreover, additional studies of the educational impact of hospitalists on residency and medical student education are needed. Questions regarding the nature and degree of resident autonomy and experience conducting procedures in the hospitalist environment have been raised. These must be assessed through studies of residency program directors, their expectations of residents, and the curricula they have developed.

As with any new phenomenon, it will take time to understand the impact of hospitalists in a variety of domains. Additional research will be helpful in following the development of this field and the manner in which it will interface with existing medical practice and educational programs.

There has been marked recent growth in the employment and utilization of both pediatric and adult hospitalists. Recent data demonstrate that approximately 25% of current pediatric hospitalist programs are less than 2 years old.1 Some have posited that this growth is due to increasing pressure from the public and payors to deliver cost‐effective and high‐quality care.2 However, little is known about the mechanisms by which those who deliver care in this framework are trained, nor the scope of clinical practice they provide.37 One study has shown that among those who direct pediatric hospitalist services there is a great degree of variability in the description of the roles, work patterns, and employment characteristics of hospitalists.1 That study provided only 1 perspective on the roles and career trajectories of those in the field. To better understand both the range and frequency of experiences, clinical and nonclinical roles, training, work expectations, and career plans, we conducted a national survey study of practicing pediatric hospitalists.

METHODS

RESULTS

RESULTS BY ACADEMIC STATUS

Only significant differences between academic and nonacademic hospitalists are presented.

RESULTS BY HOSPITAL CHARACTERISTICS

For each hospital characteristic, only significant differences between dichotomized groups are presented.

DISCUSSION

This study provides the most comprehensive information available regarding the clinical and nonclinical roles, training, work expectations, and career plans of pediatric hospitalists. Among the most important of our findings is the distribution of the length of time that pediatric hospitalists had served in their roles. While over one‐third (37%) reported having been practicing as hospitalists for over 5 years, 45% of our respondents had been in practice for fewer than 3 years. This is consistent with both the perceptions of rapid growth of the field and with significant turnover of hospitalists.1, 8 It is important to note that our findings may actually overestimate the proportion of hospitalists with longer durations of employment as our sampling strategy would have been less likely to include those who left the field within the first 12 to 18 months of practice. Nevertheless, over half (61%) of our respondents expected to remain a hospitalist for the duration of their career and few reported choosing to become a hospitalist as a short‐term employment option. This finding has important implications for the future stability of the hospitalist workforce and the potential development of specific expertise among this cadre of clinicians.6

The demographic profile of pediatric hospitalists was also consistent with these findings. The mean age of 39 years for our respondents is indicative of a significant proportion of this group of physicians recently having completed their residency training. Further, the gender distribution approximates that of current pediatric residency graduates, thus indicating that that this is not a clinical choice for which there would be a skewed distribution as is the case in some pediatric subspecialties.9

Our findings were similar to the 2004 Ottolini et al.10 findings on the roles of pediatric hospitalists. Respondents in our study reported spending less time providing inpatient care (61% versus 75%), providing clinical teaching or supervising residents (16% versus 26%), performing administrative duties (8% versus 19%), and conducting research (3% versus 9%) compared with the respondents in the Ottolini et al.10 survey.

At this point in time, fewer than half of our respondents reported any hospitalist‐specific training, including workshops at professional meetings or CME coursework. As there are a paucity of fellowships offering postresidency training in pediatric hospital medicine, and most of the existing programs are newly established, few in practice have completed such programs.11 In addition, most respondents reported that current CME offerings do not meet their needs, and that they could have used additional QI training to prepare them for their role as pediatric hospitalists. However, almost three‐quarters of respondents (73%) do not believe any additional training beyond residency should be required. As such, it is unclear if a defined, unique body of knowledge specific to hospitalists is either needed or desired by those currently in the field.

Although there are a broad range of potential clinical roles within hospital medicine, and this clinical variety influenced most respondents' decisions to become hospitalists, the current scope of an individual hospitalist tends to become somewhat focused.12, 13 While we found almost all provided service on the pediatric inpatient unit, many fewer provided inpatient consultation and normal newborn care, or were involved in interhospital transport or as part of an emergency response team. There is also wide variation in the types of procedures performed or supervised by hospitalists at different institutions. More than half never perform or supervise infusion services, PICC or central line placement, or circumcision. The variation seen among hospitalists practicing in different hospital settings likely is a result, at least in part, of different needs in teaching hospitals for both service and for clinical experience of trainees. For example, our results demonstrate that pediatric hospitalists in nonteaching and non‐children's hospitals are more likely to have a broader scope of clinical care provision. Another potential issue is that some hospitalists may be employed by institutions which have no pediatric ICU, neonatal ICU, or other specialty unit. As such, these hospitalists would not have the opportunity to work in such settings.

Further, those without academic appointments are also more likely to have expanded clinical roles compared with their academic counterparts. This may be due to the fact that there is likely a greater number of subspecialty‐trained pediatric providers in academic centers and thus the need for hospitalists to cover specific services or perform specific procedures is lessened. There may also be a desire to prevent competition among care providers within the same institution. In contrast, hospitalists with academic appointments are more likely (though still uncommonly) to have taken leadership roles in hospital administration and QI initiatives. Thus, the nature of their efforts appears to expand into nonclinical delivery areas.

Clearly, hospitalists report they have assumed a significant role in the clinical teaching of trainees at all levels, with 94% of our respondents maintaining at least some involvement in education. On average, they spend 16% of their time in educational efforts. However, there are few data on the impact of their work in this area.5, 13 Studies in pediatrics to date have been limited to a few institutions,3, 5 and have not addressed the issue from the perspective of residency program directors or those who are in charge of inpatient curricula.

This study, like the majority of studies related to pediatric hospitalists, is hampered by the difficulty of identifying pediatric hospitalists. Rather than utilizing a hospital medicine membership list, which would be potentially biased by self‐selection, we attempted to obtain a more representative sample through utilization of the AHA database.

CONCLUSIONS

Findings from this study provide an additional perspective regarding pediatric hospitalists to add to our previous study of hospitalist program directors.1 However, the field is currently a moving target. Our data demonstrate that there is significant flux in the hospitalist workforce, uncertainty regarding turnover, and variation in the roles of these professionals in their clinical and nonclinical work environment. Moreover, additional studies of the educational impact of hospitalists on residency and medical student education are needed. Questions regarding the nature and degree of resident autonomy and experience conducting procedures in the hospitalist environment have been raised. These must be assessed through studies of residency program directors, their expectations of residents, and the curricula they have developed.

As with any new phenomenon, it will take time to understand the impact of hospitalists in a variety of domains. Additional research will be helpful in following the development of this field and the manner in which it will interface with existing medical practice and educational programs.

There has been marked recent growth in the employment and utilization of both pediatric and adult hospitalists. Recent data demonstrate that approximately 25% of current pediatric hospitalist programs are less than 2 years old.1 Some have posited that this growth is due to increasing pressure from the public and payors to deliver cost‐effective and high‐quality care.2 However, little is known about the mechanisms by which those who deliver care in this framework are trained, nor the scope of clinical practice they provide.37 One study has shown that among those who direct pediatric hospitalist services there is a great degree of variability in the description of the roles, work patterns, and employment characteristics of hospitalists.1 That study provided only 1 perspective on the roles and career trajectories of those in the field. To better understand both the range and frequency of experiences, clinical and nonclinical roles, training, work expectations, and career plans, we conducted a national survey study of practicing pediatric hospitalists.

METHODS

RESULTS

RESULTS BY ACADEMIC STATUS

Only significant differences between academic and nonacademic hospitalists are presented.

RESULTS BY HOSPITAL CHARACTERISTICS

For each hospital characteristic, only significant differences between dichotomized groups are presented.

DISCUSSION

This study provides the most comprehensive information available regarding the clinical and nonclinical roles, training, work expectations, and career plans of pediatric hospitalists. Among the most important of our findings is the distribution of the length of time that pediatric hospitalists had served in their roles. While over one‐third (37%) reported having been practicing as hospitalists for over 5 years, 45% of our respondents had been in practice for fewer than 3 years. This is consistent with both the perceptions of rapid growth of the field and with significant turnover of hospitalists.1, 8 It is important to note that our findings may actually overestimate the proportion of hospitalists with longer durations of employment as our sampling strategy would have been less likely to include those who left the field within the first 12 to 18 months of practice. Nevertheless, over half (61%) of our respondents expected to remain a hospitalist for the duration of their career and few reported choosing to become a hospitalist as a short‐term employment option. This finding has important implications for the future stability of the hospitalist workforce and the potential development of specific expertise among this cadre of clinicians.6

The demographic profile of pediatric hospitalists was also consistent with these findings. The mean age of 39 years for our respondents is indicative of a significant proportion of this group of physicians recently having completed their residency training. Further, the gender distribution approximates that of current pediatric residency graduates, thus indicating that that this is not a clinical choice for which there would be a skewed distribution as is the case in some pediatric subspecialties.9

Our findings were similar to the 2004 Ottolini et al.10 findings on the roles of pediatric hospitalists. Respondents in our study reported spending less time providing inpatient care (61% versus 75%), providing clinical teaching or supervising residents (16% versus 26%), performing administrative duties (8% versus 19%), and conducting research (3% versus 9%) compared with the respondents in the Ottolini et al.10 survey.

At this point in time, fewer than half of our respondents reported any hospitalist‐specific training, including workshops at professional meetings or CME coursework. As there are a paucity of fellowships offering postresidency training in pediatric hospital medicine, and most of the existing programs are newly established, few in practice have completed such programs.11 In addition, most respondents reported that current CME offerings do not meet their needs, and that they could have used additional QI training to prepare them for their role as pediatric hospitalists. However, almost three‐quarters of respondents (73%) do not believe any additional training beyond residency should be required. As such, it is unclear if a defined, unique body of knowledge specific to hospitalists is either needed or desired by those currently in the field.

Although there are a broad range of potential clinical roles within hospital medicine, and this clinical variety influenced most respondents' decisions to become hospitalists, the current scope of an individual hospitalist tends to become somewhat focused.12, 13 While we found almost all provided service on the pediatric inpatient unit, many fewer provided inpatient consultation and normal newborn care, or were involved in interhospital transport or as part of an emergency response team. There is also wide variation in the types of procedures performed or supervised by hospitalists at different institutions. More than half never perform or supervise infusion services, PICC or central line placement, or circumcision. The variation seen among hospitalists practicing in different hospital settings likely is a result, at least in part, of different needs in teaching hospitals for both service and for clinical experience of trainees. For example, our results demonstrate that pediatric hospitalists in nonteaching and non‐children's hospitals are more likely to have a broader scope of clinical care provision. Another potential issue is that some hospitalists may be employed by institutions which have no pediatric ICU, neonatal ICU, or other specialty unit. As such, these hospitalists would not have the opportunity to work in such settings.

Further, those without academic appointments are also more likely to have expanded clinical roles compared with their academic counterparts. This may be due to the fact that there is likely a greater number of subspecialty‐trained pediatric providers in academic centers and thus the need for hospitalists to cover specific services or perform specific procedures is lessened. There may also be a desire to prevent competition among care providers within the same institution. In contrast, hospitalists with academic appointments are more likely (though still uncommonly) to have taken leadership roles in hospital administration and QI initiatives. Thus, the nature of their efforts appears to expand into nonclinical delivery areas.

Clearly, hospitalists report they have assumed a significant role in the clinical teaching of trainees at all levels, with 94% of our respondents maintaining at least some involvement in education. On average, they spend 16% of their time in educational efforts. However, there are few data on the impact of their work in this area.5, 13 Studies in pediatrics to date have been limited to a few institutions,3, 5 and have not addressed the issue from the perspective of residency program directors or those who are in charge of inpatient curricula.

This study, like the majority of studies related to pediatric hospitalists, is hampered by the difficulty of identifying pediatric hospitalists. Rather than utilizing a hospital medicine membership list, which would be potentially biased by self‐selection, we attempted to obtain a more representative sample through utilization of the AHA database.

CONCLUSIONS

Findings from this study provide an additional perspective regarding pediatric hospitalists to add to our previous study of hospitalist program directors.1 However, the field is currently a moving target. Our data demonstrate that there is significant flux in the hospitalist workforce, uncertainty regarding turnover, and variation in the roles of these professionals in their clinical and nonclinical work environment. Moreover, additional studies of the educational impact of hospitalists on residency and medical student education are needed. Questions regarding the nature and degree of resident autonomy and experience conducting procedures in the hospitalist environment have been raised. These must be assessed through studies of residency program directors, their expectations of residents, and the curricula they have developed.

As with any new phenomenon, it will take time to understand the impact of hospitalists in a variety of domains. Additional research will be helpful in following the development of this field and the manner in which it will interface with existing medical practice and educational programs.

Takotsubo cardiomyopathy, also known as transient left ventricular apical ballooning, stress cardiomyopathy, and broken heart syndrome, is a condition that mimics acute myocardial infarction. Patients typically present with chest pain, electrocardiographic changes consistent with acute ischemia or infarct, and elevated cardiac enzymes in the absence of significant coronary artery disease. Left ventriculography demonstrates a characteristic pattern of dysfunction: dyskinesis of the cardiac apex and hyperkinesis of the base. This resulting appearance of apical ballooning is reminiscent of the takotsubo, a Japanese octopus pot with a wide base and narrow top. The syndrome occurs almost exclusively in postmenopausal women and demonstrates a distinct temporal association with extreme emotional or physiological stress. The pathophysiology is poorly understood, but one theory suggests that the transient cardiomyopathy reflects myocardial stunning due to excessive sympathetic output.1 Treatment is supportive, and most patients rapidly recover normal systolic function.

A 57‐year‐old African American female with a past medical history significant only for chronic obstructive pulmonary disease presented with severe dyspnea that was progressive over several hours following the unexpected death of her son. She denied chest pain, palpitations, cough, or fever. On examination, she was afebrile with a blood pressure of 145/82 mm Hg, a pulse of 90 beats per minute, and a respiratory rate of 24 breaths per minute with oxygen saturations of 88% on room air. Lung examination revealed coarse breath sounds with a slightly prolonged expiration phase, but it was otherwise clear. Cardiac examination was unremarkable. Chest radiograph showed only emphysematous changes. Initial electrocardiogram and serial cardiac enzymes were negative. A computed tomography pulmonary angiogram showed no evidence of pulmonary embolism. The patient was admitted with the diagnosis of chronic obstructive pulmonary disease exacerbation and treated with supplemental oxygen, bronchodilators, and corticosteroids.

On the following day, the patient developed worsening dyspnea, hypoxia, and diffuse crackles on examination. Electrocardiogram at that time demonstrated ST‐segment elevations in leads V1 and V2 as well as T‐wave inversions in all precordial leads (Figure 1). The troponin‐I concentration was 1.92 ng/mL (<0.05 nL), and the brain natriuretic peptide concentration was 1425 pg/mL. The patient underwent urgent cardiac catheterization with no evidence of coronary artery obstruction. Left ventriculogram revealed a hyperdynamic base and akinetic apex extending into the mid‐heart (Figure 2). Left ventricular systolic function was severely reduced, with an estimated ejection fraction of 10% to 15%. The normal diastolic ventriculogram image is shown for comparison (Figure 3). These findings were felt to be consistent with takotsubo syndrome. The patient required inotropic support briefly but experienced full clinical recovery by the sixth hospital day.

Figure 1

Figure 2

Figure 3

DISCUSSION

Takotsubo cardiomyopathy was first described in Japan in 1991.2 Although the condition made a relatively recent debut in the United States, with the first case series published in 2003, subsequent reports have suggested that the condition is not rare.3 Recent analyses of Western populations estimate the prevalence to be approximately 2% among patients with acute coronary syndrome.1, 4, 5 Because women compose the majority of patients with takotsubo cardiomyopathy, the prevalence among women as a subset of patients with acute coronary syndrome is likely much higher. The syndrome has been described as a clinical entity in Japanese, European, Caucasian, and African American patients.2, 3 Interesting differences appear to exist among different ethnic groups. For example, evidence suggests that the condition is more likely to be precipitated by emotional stress in Caucasians, whereas physiological stress is a more frequent trigger in Asians.6

Although chest pain is described as a cardinal feature in takotsubo cardiomyopathy, existing data suggest that African American patients may lack this typical symptom. The first African American female reported with takotsubo syndrome presented with heart failure and hypotension in the absence of chest pain.1 Subsequently, Patel et al.7 reported 5 African American women with takotsubo syndrome. Three patients presented with dyspnea, and 2 presented with nausea: none of the patients experienced chest pain. Our case adds to this evidence by describing an African American woman with takotsubo syndrome whose presenting symptom was severe dyspnea without chest pain. Unlike the majority of reported cases, electrocardiographic and biomarker abnormalities were not present in our patient at admission. As with our patient, the diagnosis of takotsubo cardiomyopathy may initially be overlooked in African Americans because of the atypical presentation. As takotsubo syndrome becomes increasingly recognized in the United States, clinicians are encouraged to consider the diagnosis in African American women who present with severe dyspnea in the setting of extreme emotional or physiological stress. Further research on the pathophysiology of takotsubo cardiomyopathy is needed to explain why such differences in presenting symptoms may exist.

Takotsubo cardiomyopathy, also known as transient left ventricular apical ballooning, stress cardiomyopathy, and broken heart syndrome, is a condition that mimics acute myocardial infarction. Patients typically present with chest pain, electrocardiographic changes consistent with acute ischemia or infarct, and elevated cardiac enzymes in the absence of significant coronary artery disease. Left ventriculography demonstrates a characteristic pattern of dysfunction: dyskinesis of the cardiac apex and hyperkinesis of the base. This resulting appearance of apical ballooning is reminiscent of the takotsubo, a Japanese octopus pot with a wide base and narrow top. The syndrome occurs almost exclusively in postmenopausal women and demonstrates a distinct temporal association with extreme emotional or physiological stress. The pathophysiology is poorly understood, but one theory suggests that the transient cardiomyopathy reflects myocardial stunning due to excessive sympathetic output.1 Treatment is supportive, and most patients rapidly recover normal systolic function.

A 57‐year‐old African American female with a past medical history significant only for chronic obstructive pulmonary disease presented with severe dyspnea that was progressive over several hours following the unexpected death of her son. She denied chest pain, palpitations, cough, or fever. On examination, she was afebrile with a blood pressure of 145/82 mm Hg, a pulse of 90 beats per minute, and a respiratory rate of 24 breaths per minute with oxygen saturations of 88% on room air. Lung examination revealed coarse breath sounds with a slightly prolonged expiration phase, but it was otherwise clear. Cardiac examination was unremarkable. Chest radiograph showed only emphysematous changes. Initial electrocardiogram and serial cardiac enzymes were negative. A computed tomography pulmonary angiogram showed no evidence of pulmonary embolism. The patient was admitted with the diagnosis of chronic obstructive pulmonary disease exacerbation and treated with supplemental oxygen, bronchodilators, and corticosteroids.

On the following day, the patient developed worsening dyspnea, hypoxia, and diffuse crackles on examination. Electrocardiogram at that time demonstrated ST‐segment elevations in leads V1 and V2 as well as T‐wave inversions in all precordial leads (Figure 1). The troponin‐I concentration was 1.92 ng/mL (<0.05 nL), and the brain natriuretic peptide concentration was 1425 pg/mL. The patient underwent urgent cardiac catheterization with no evidence of coronary artery obstruction. Left ventriculogram revealed a hyperdynamic base and akinetic apex extending into the mid‐heart (Figure 2). Left ventricular systolic function was severely reduced, with an estimated ejection fraction of 10% to 15%. The normal diastolic ventriculogram image is shown for comparison (Figure 3). These findings were felt to be consistent with takotsubo syndrome. The patient required inotropic support briefly but experienced full clinical recovery by the sixth hospital day.

Figure 1

Figure 2

Figure 3

DISCUSSION

Takotsubo cardiomyopathy was first described in Japan in 1991.2 Although the condition made a relatively recent debut in the United States, with the first case series published in 2003, subsequent reports have suggested that the condition is not rare.3 Recent analyses of Western populations estimate the prevalence to be approximately 2% among patients with acute coronary syndrome.1, 4, 5 Because women compose the majority of patients with takotsubo cardiomyopathy, the prevalence among women as a subset of patients with acute coronary syndrome is likely much higher. The syndrome has been described as a clinical entity in Japanese, European, Caucasian, and African American patients.2, 3 Interesting differences appear to exist among different ethnic groups. For example, evidence suggests that the condition is more likely to be precipitated by emotional stress in Caucasians, whereas physiological stress is a more frequent trigger in Asians.6

Although chest pain is described as a cardinal feature in takotsubo cardiomyopathy, existing data suggest that African American patients may lack this typical symptom. The first African American female reported with takotsubo syndrome presented with heart failure and hypotension in the absence of chest pain.1 Subsequently, Patel et al.7 reported 5 African American women with takotsubo syndrome. Three patients presented with dyspnea, and 2 presented with nausea: none of the patients experienced chest pain. Our case adds to this evidence by describing an African American woman with takotsubo syndrome whose presenting symptom was severe dyspnea without chest pain. Unlike the majority of reported cases, electrocardiographic and biomarker abnormalities were not present in our patient at admission. As with our patient, the diagnosis of takotsubo cardiomyopathy may initially be overlooked in African Americans because of the atypical presentation. As takotsubo syndrome becomes increasingly recognized in the United States, clinicians are encouraged to consider the diagnosis in African American women who present with severe dyspnea in the setting of extreme emotional or physiological stress. Further research on the pathophysiology of takotsubo cardiomyopathy is needed to explain why such differences in presenting symptoms may exist.

Takotsubo cardiomyopathy, also known as transient left ventricular apical ballooning, stress cardiomyopathy, and broken heart syndrome, is a condition that mimics acute myocardial infarction. Patients typically present with chest pain, electrocardiographic changes consistent with acute ischemia or infarct, and elevated cardiac enzymes in the absence of significant coronary artery disease. Left ventriculography demonstrates a characteristic pattern of dysfunction: dyskinesis of the cardiac apex and hyperkinesis of the base. This resulting appearance of apical ballooning is reminiscent of the takotsubo, a Japanese octopus pot with a wide base and narrow top. The syndrome occurs almost exclusively in postmenopausal women and demonstrates a distinct temporal association with extreme emotional or physiological stress. The pathophysiology is poorly understood, but one theory suggests that the transient cardiomyopathy reflects myocardial stunning due to excessive sympathetic output.1 Treatment is supportive, and most patients rapidly recover normal systolic function.

A 57‐year‐old African American female with a past medical history significant only for chronic obstructive pulmonary disease presented with severe dyspnea that was progressive over several hours following the unexpected death of her son. She denied chest pain, palpitations, cough, or fever. On examination, she was afebrile with a blood pressure of 145/82 mm Hg, a pulse of 90 beats per minute, and a respiratory rate of 24 breaths per minute with oxygen saturations of 88% on room air. Lung examination revealed coarse breath sounds with a slightly prolonged expiration phase, but it was otherwise clear. Cardiac examination was unremarkable. Chest radiograph showed only emphysematous changes. Initial electrocardiogram and serial cardiac enzymes were negative. A computed tomography pulmonary angiogram showed no evidence of pulmonary embolism. The patient was admitted with the diagnosis of chronic obstructive pulmonary disease exacerbation and treated with supplemental oxygen, bronchodilators, and corticosteroids.

On the following day, the patient developed worsening dyspnea, hypoxia, and diffuse crackles on examination. Electrocardiogram at that time demonstrated ST‐segment elevations in leads V1 and V2 as well as T‐wave inversions in all precordial leads (Figure 1). The troponin‐I concentration was 1.92 ng/mL (<0.05 nL), and the brain natriuretic peptide concentration was 1425 pg/mL. The patient underwent urgent cardiac catheterization with no evidence of coronary artery obstruction. Left ventriculogram revealed a hyperdynamic base and akinetic apex extending into the mid‐heart (Figure 2). Left ventricular systolic function was severely reduced, with an estimated ejection fraction of 10% to 15%. The normal diastolic ventriculogram image is shown for comparison (Figure 3). These findings were felt to be consistent with takotsubo syndrome. The patient required inotropic support briefly but experienced full clinical recovery by the sixth hospital day.

Figure 1

Figure 2

Figure 3

DISCUSSION

Takotsubo cardiomyopathy was first described in Japan in 1991.2 Although the condition made a relatively recent debut in the United States, with the first case series published in 2003, subsequent reports have suggested that the condition is not rare.3 Recent analyses of Western populations estimate the prevalence to be approximately 2% among patients with acute coronary syndrome.1, 4, 5 Because women compose the majority of patients with takotsubo cardiomyopathy, the prevalence among women as a subset of patients with acute coronary syndrome is likely much higher. The syndrome has been described as a clinical entity in Japanese, European, Caucasian, and African American patients.2, 3 Interesting differences appear to exist among different ethnic groups. For example, evidence suggests that the condition is more likely to be precipitated by emotional stress in Caucasians, whereas physiological stress is a more frequent trigger in Asians.6

Although chest pain is described as a cardinal feature in takotsubo cardiomyopathy, existing data suggest that African American patients may lack this typical symptom. The first African American female reported with takotsubo syndrome presented with heart failure and hypotension in the absence of chest pain.1 Subsequently, Patel et al.7 reported 5 African American women with takotsubo syndrome. Three patients presented with dyspnea, and 2 presented with nausea: none of the patients experienced chest pain. Our case adds to this evidence by describing an African American woman with takotsubo syndrome whose presenting symptom was severe dyspnea without chest pain. Unlike the majority of reported cases, electrocardiographic and biomarker abnormalities were not present in our patient at admission. As with our patient, the diagnosis of takotsubo cardiomyopathy may initially be overlooked in African Americans because of the atypical presentation. As takotsubo syndrome becomes increasingly recognized in the United States, clinicians are encouraged to consider the diagnosis in African American women who present with severe dyspnea in the setting of extreme emotional or physiological stress. Further research on the pathophysiology of takotsubo cardiomyopathy is needed to explain why such differences in presenting symptoms may exist.

A 33‐year‐old Caucasian woman presented to an outside hospital with a 10‐day history of fever, cough, and progressive dyspnea on exertion. Ten days prior to the onset of symptoms, she had traveled to Calgary, Alberta, Canada. Her niece and nephew had recently suffered upper respiratory symptoms. Additional review of systems was negative for joint pain, rash, diarrhea, or bloody stools. She had a history of ulcerative colitis, primary sclerosing cholangitis, and juvenile rheumatoid arthritis. Her outpatient medications included prednisone 10 mg daily, methotrexate 7.5 mg weekly, and ursodiol 200 mg 3 times daily. She was employed at a local hospital and her annual purified protein derivative (PPD) test had been negative. Computed tomography angiography demonstrated bilateral patchy consolidation. Vancomycin, levofloxacin, piperacillin/tazobactam, and fluconazole were initiated and she was transferred to our hospital for further evaluation.

On arrival, her vital signs were within normal limits. She was breathing comfortably but on auscultation had crackles at the right‐mid lung field. A complete blood cell count demonstrated a white blood cell count of 7000/L with left shift, hemoglobin 10.7 g/dL, and platelet count 156,000/L. Liver function tests showed albumin 2.6 g/dL, total bilirubin 9.0 mg/dL with conjugated fraction 6.6 mg/dL, alkaline phosphatase 586 U/L, aspartate aminotransferase 104 U/L, and alanine aminotransferase 72 U/L; these were all near her baseline. The basic metabolic panel was within normal limits. A chest X‐ray showed dense areas of consolidation in the lingula and left upper lobe. All antibiotics from the outside hospital were discontinued and empiric moxifloxacin was initiated.

On hospital day 1, she underwent bronchoscopy, which yielded cloudy fluid from the bronchoalveolar lavage (BAL). Initial BAL gram stain showed moderate white blood cells but no organisms; fungal smears and stains for acid fast bacilli were negative. Blood cultures and Legionella and Streptococcus urinary antigen tests were negative. The remainder of her hospital course was uneventful. Her shortness of breath improved and she remained afebrile. She was discharged home on a 10‐day course of moxifloxacin with close follow‐up. Six days after the BAL specimen was collected, the culture grew Legionella micdadei. Repeat chest film 2 weeks later demonstrated resolution of the original findings.

DISCUSSION

Legionella is responsible for 8000 to 18,000 hospitalizations for pneumonia annually.1 It is associated with community‐acquired, hospital‐acquired, and travel‐associated pneumonia. Twenty‐five Legionella species have been identified and 8 species are associated with pneumonia in humans.2 Community‐acquired and travel‐acquired Legionella pneumonia is most commonly caused by Legionella pneumophila; the second most common cause is L. micdadei.2, 3 It was initially identified in 1977 at the University of Pittsburgh in renal transplant patients with acute pneumonitis and is known as the Pittsburgh pneumonia agent. Similar cases were identified in a group of immunocompromised patients in Virginia, all of whom were receiving steroids and cytotoxic chemotherapy. It is unclear why L. micdadei predominates in this population, but is likely related to its decreased virulence compared to L. pneumophila. The definitive mode of transmission of L. micdadei is not known; it may be from contaminated water supplies but infections from inhalation of respiratory secretions have also been documented.2 While L. micdadei is not commonly seen in travel‐associated Legionella pneumonia, the patient's immunocompromised status secondary to the treatment of her underlying medical conditions made her particularly vulnerable. Given the temporal association with her trip, she was most likely exposed during her travels but her hospital employment should also be considered.

Legionella pneumonia is underdiagnosed because of difficulty distinguishing it from other types of pneumonia, failure to order diagnostic tests, and variable sensitivity of available diagnostic tests.4 Culture is considered the gold standard and is ideally performed from lower respiratory secretions, but variable sensitivity due to interlaboratory variation (range, 10%‐80%) limits its use.3, 4 Direct immunofluorescence assay (DFA) testing of respiratory secretions is available but also limited by poor sensitivity. Both culture and DFA have specificities approaching 100%. A newer test, the Legionella urinary antigen test, is an immunochromatographic assay. It is less technically difficult and results are available in less than 1 hour. The assay can detect the antigen in the urine starting 1 day after the onset of symptoms, and can remain positive for days or weeks following treatment.4

With the introduction and wide availability of the Legionella urinary antigen test, it is important to consider its limitations. While the test carries a high specificity, it detects only the soluble antigen of Legionella pneumophila serogroup 1. Thus, as in this case, the urinary test can be negative when infection is caused by other species such as L. micdadei. In the literature, the urine assay's sensitivity is variously reported at 45% to 100% with lower sensitivities in circumstances such as hospital‐acquired disease, where the association with other species is higher than in the community setting.3, 4 For instance, in nosocomial infections, the reported sensitivity is 45%.3 False‐positive results have also been seen in patients with serum sickness.4

The Legionella urinary antigen test has improved detection of Legionella pneumonia. Given its limitations, it is likely to be most accurate in community‐acquired and travel‐acquired cases.3 The Centers for Disease Control and Prevention recommend testing for Legionella in pneumonia patients requiring admission to the intensive care unit (ICU), immunocompromised patients, patients who traveled within 2 weeks of presentation, and those who have failed treatment with beta‐lactams or cephalosporins. A negative test does not rule out Legionella infection and additional testing with bronchoscopy may be indicated, especially in immunocompromised hosts.4

A 33‐year‐old Caucasian woman presented to an outside hospital with a 10‐day history of fever, cough, and progressive dyspnea on exertion. Ten days prior to the onset of symptoms, she had traveled to Calgary, Alberta, Canada. Her niece and nephew had recently suffered upper respiratory symptoms. Additional review of systems was negative for joint pain, rash, diarrhea, or bloody stools. She had a history of ulcerative colitis, primary sclerosing cholangitis, and juvenile rheumatoid arthritis. Her outpatient medications included prednisone 10 mg daily, methotrexate 7.5 mg weekly, and ursodiol 200 mg 3 times daily. She was employed at a local hospital and her annual purified protein derivative (PPD) test had been negative. Computed tomography angiography demonstrated bilateral patchy consolidation. Vancomycin, levofloxacin, piperacillin/tazobactam, and fluconazole were initiated and she was transferred to our hospital for further evaluation.

On arrival, her vital signs were within normal limits. She was breathing comfortably but on auscultation had crackles at the right‐mid lung field. A complete blood cell count demonstrated a white blood cell count of 7000/L with left shift, hemoglobin 10.7 g/dL, and platelet count 156,000/L. Liver function tests showed albumin 2.6 g/dL, total bilirubin 9.0 mg/dL with conjugated fraction 6.6 mg/dL, alkaline phosphatase 586 U/L, aspartate aminotransferase 104 U/L, and alanine aminotransferase 72 U/L; these were all near her baseline. The basic metabolic panel was within normal limits. A chest X‐ray showed dense areas of consolidation in the lingula and left upper lobe. All antibiotics from the outside hospital were discontinued and empiric moxifloxacin was initiated.

On hospital day 1, she underwent bronchoscopy, which yielded cloudy fluid from the bronchoalveolar lavage (BAL). Initial BAL gram stain showed moderate white blood cells but no organisms; fungal smears and stains for acid fast bacilli were negative. Blood cultures and Legionella and Streptococcus urinary antigen tests were negative. The remainder of her hospital course was uneventful. Her shortness of breath improved and she remained afebrile. She was discharged home on a 10‐day course of moxifloxacin with close follow‐up. Six days after the BAL specimen was collected, the culture grew Legionella micdadei. Repeat chest film 2 weeks later demonstrated resolution of the original findings.

DISCUSSION

Legionella is responsible for 8000 to 18,000 hospitalizations for pneumonia annually.1 It is associated with community‐acquired, hospital‐acquired, and travel‐associated pneumonia. Twenty‐five Legionella species have been identified and 8 species are associated with pneumonia in humans.2 Community‐acquired and travel‐acquired Legionella pneumonia is most commonly caused by Legionella pneumophila; the second most common cause is L. micdadei.2, 3 It was initially identified in 1977 at the University of Pittsburgh in renal transplant patients with acute pneumonitis and is known as the Pittsburgh pneumonia agent. Similar cases were identified in a group of immunocompromised patients in Virginia, all of whom were receiving steroids and cytotoxic chemotherapy. It is unclear why L. micdadei predominates in this population, but is likely related to its decreased virulence compared to L. pneumophila. The definitive mode of transmission of L. micdadei is not known; it may be from contaminated water supplies but infections from inhalation of respiratory secretions have also been documented.2 While L. micdadei is not commonly seen in travel‐associated Legionella pneumonia, the patient's immunocompromised status secondary to the treatment of her underlying medical conditions made her particularly vulnerable. Given the temporal association with her trip, she was most likely exposed during her travels but her hospital employment should also be considered.

Legionella pneumonia is underdiagnosed because of difficulty distinguishing it from other types of pneumonia, failure to order diagnostic tests, and variable sensitivity of available diagnostic tests.4 Culture is considered the gold standard and is ideally performed from lower respiratory secretions, but variable sensitivity due to interlaboratory variation (range, 10%‐80%) limits its use.3, 4 Direct immunofluorescence assay (DFA) testing of respiratory secretions is available but also limited by poor sensitivity. Both culture and DFA have specificities approaching 100%. A newer test, the Legionella urinary antigen test, is an immunochromatographic assay. It is less technically difficult and results are available in less than 1 hour. The assay can detect the antigen in the urine starting 1 day after the onset of symptoms, and can remain positive for days or weeks following treatment.4

With the introduction and wide availability of the Legionella urinary antigen test, it is important to consider its limitations. While the test carries a high specificity, it detects only the soluble antigen of Legionella pneumophila serogroup 1. Thus, as in this case, the urinary test can be negative when infection is caused by other species such as L. micdadei. In the literature, the urine assay's sensitivity is variously reported at 45% to 100% with lower sensitivities in circumstances such as hospital‐acquired disease, where the association with other species is higher than in the community setting.3, 4 For instance, in nosocomial infections, the reported sensitivity is 45%.3 False‐positive results have also been seen in patients with serum sickness.4

The Legionella urinary antigen test has improved detection of Legionella pneumonia. Given its limitations, it is likely to be most accurate in community‐acquired and travel‐acquired cases.3 The Centers for Disease Control and Prevention recommend testing for Legionella in pneumonia patients requiring admission to the intensive care unit (ICU), immunocompromised patients, patients who traveled within 2 weeks of presentation, and those who have failed treatment with beta‐lactams or cephalosporins. A negative test does not rule out Legionella infection and additional testing with bronchoscopy may be indicated, especially in immunocompromised hosts.4

A 33‐year‐old Caucasian woman presented to an outside hospital with a 10‐day history of fever, cough, and progressive dyspnea on exertion. Ten days prior to the onset of symptoms, she had traveled to Calgary, Alberta, Canada. Her niece and nephew had recently suffered upper respiratory symptoms. Additional review of systems was negative for joint pain, rash, diarrhea, or bloody stools. She had a history of ulcerative colitis, primary sclerosing cholangitis, and juvenile rheumatoid arthritis. Her outpatient medications included prednisone 10 mg daily, methotrexate 7.5 mg weekly, and ursodiol 200 mg 3 times daily. She was employed at a local hospital and her annual purified protein derivative (PPD) test had been negative. Computed tomography angiography demonstrated bilateral patchy consolidation. Vancomycin, levofloxacin, piperacillin/tazobactam, and fluconazole were initiated and she was transferred to our hospital for further evaluation.

On arrival, her vital signs were within normal limits. She was breathing comfortably but on auscultation had crackles at the right‐mid lung field. A complete blood cell count demonstrated a white blood cell count of 7000/L with left shift, hemoglobin 10.7 g/dL, and platelet count 156,000/L. Liver function tests showed albumin 2.6 g/dL, total bilirubin 9.0 mg/dL with conjugated fraction 6.6 mg/dL, alkaline phosphatase 586 U/L, aspartate aminotransferase 104 U/L, and alanine aminotransferase 72 U/L; these were all near her baseline. The basic metabolic panel was within normal limits. A chest X‐ray showed dense areas of consolidation in the lingula and left upper lobe. All antibiotics from the outside hospital were discontinued and empiric moxifloxacin was initiated.

On hospital day 1, she underwent bronchoscopy, which yielded cloudy fluid from the bronchoalveolar lavage (BAL). Initial BAL gram stain showed moderate white blood cells but no organisms; fungal smears and stains for acid fast bacilli were negative. Blood cultures and Legionella and Streptococcus urinary antigen tests were negative. The remainder of her hospital course was uneventful. Her shortness of breath improved and she remained afebrile. She was discharged home on a 10‐day course of moxifloxacin with close follow‐up. Six days after the BAL specimen was collected, the culture grew Legionella micdadei. Repeat chest film 2 weeks later demonstrated resolution of the original findings.

DISCUSSION

Legionella is responsible for 8000 to 18,000 hospitalizations for pneumonia annually.1 It is associated with community‐acquired, hospital‐acquired, and travel‐associated pneumonia. Twenty‐five Legionella species have been identified and 8 species are associated with pneumonia in humans.2 Community‐acquired and travel‐acquired Legionella pneumonia is most commonly caused by Legionella pneumophila; the second most common cause is L. micdadei.2, 3 It was initially identified in 1977 at the University of Pittsburgh in renal transplant patients with acute pneumonitis and is known as the Pittsburgh pneumonia agent. Similar cases were identified in a group of immunocompromised patients in Virginia, all of whom were receiving steroids and cytotoxic chemotherapy. It is unclear why L. micdadei predominates in this population, but is likely related to its decreased virulence compared to L. pneumophila. The definitive mode of transmission of L. micdadei is not known; it may be from contaminated water supplies but infections from inhalation of respiratory secretions have also been documented.2 While L. micdadei is not commonly seen in travel‐associated Legionella pneumonia, the patient's immunocompromised status secondary to the treatment of her underlying medical conditions made her particularly vulnerable. Given the temporal association with her trip, she was most likely exposed during her travels but her hospital employment should also be considered.

Legionella pneumonia is underdiagnosed because of difficulty distinguishing it from other types of pneumonia, failure to order diagnostic tests, and variable sensitivity of available diagnostic tests.4 Culture is considered the gold standard and is ideally performed from lower respiratory secretions, but variable sensitivity due to interlaboratory variation (range, 10%‐80%) limits its use.3, 4 Direct immunofluorescence assay (DFA) testing of respiratory secretions is available but also limited by poor sensitivity. Both culture and DFA have specificities approaching 100%. A newer test, the Legionella urinary antigen test, is an immunochromatographic assay. It is less technically difficult and results are available in less than 1 hour. The assay can detect the antigen in the urine starting 1 day after the onset of symptoms, and can remain positive for days or weeks following treatment.4

With the introduction and wide availability of the Legionella urinary antigen test, it is important to consider its limitations. While the test carries a high specificity, it detects only the soluble antigen of Legionella pneumophila serogroup 1. Thus, as in this case, the urinary test can be negative when infection is caused by other species such as L. micdadei. In the literature, the urine assay's sensitivity is variously reported at 45% to 100% with lower sensitivities in circumstances such as hospital‐acquired disease, where the association with other species is higher than in the community setting.3, 4 For instance, in nosocomial infections, the reported sensitivity is 45%.3 False‐positive results have also been seen in patients with serum sickness.4

The Legionella urinary antigen test has improved detection of Legionella pneumonia. Given its limitations, it is likely to be most accurate in community‐acquired and travel‐acquired cases.3 The Centers for Disease Control and Prevention recommend testing for Legionella in pneumonia patients requiring admission to the intensive care unit (ICU), immunocompromised patients, patients who traveled within 2 weeks of presentation, and those who have failed treatment with beta‐lactams or cephalosporins. A negative test does not rule out Legionella infection and additional testing with bronchoscopy may be indicated, especially in immunocompromised hosts.4

The field of pediatric hospital medicine is undergoing rapid growth. In 2002, there were approximately 600 pediatric hospitalists1 and in 2006 this number was estimated to be approximately 1000.2 A recent study found that approximately 25% of pediatric hospitalist practices are less than 2 years old.3 As such, there are many new physicians entering the field and most do so without specific training in hospital medicine prior to beginning their employment.4 There is also significant variability in the roles, work patterns, and scope of practice across institutions,3 and hospitalists are engaged in a wide variety of clinical, educational, and administrative functions.

A survey of pediatric department chairs in 2001 found that very few believed that any additional training beyond a pediatric residency was required to perform hospitalist medicine.5 However, since then the field has undergone significant growth. A more recent survey of practicing hospitalists found that 92% believed there was a need for additional training in a variety of domains.6 Specifically, respondents were most interested in achieving greater skill in performing critical care procedures and academic training. These hospitalists regarded pediatric hospitalist fellowships as the best way to gain the additional skills in teaching, research, and administration needed for their positions.

Nonetheless, for a variety of reasons, not the least of which is perhaps the paucity of hospitalist fellowship training programs, few hospitalists in practice today have completed a fellowship in hospital medicine. Over the past several years, a number of pediatric‐specific hospitalist fellowship programs have been initiated, yet little is known of their requirements or curricula. We conducted a study to explore the structure, components, and training goals of the pediatric hospitalist fellowship programs in North America.

MATERIALS AND METHODS

RESULTS

DISCUSSION

There appear to be 2 distinct tracks for pediatric hospitalist training programs: clinical or academic specialization. However, this is not surprising, as most programs are relatively new and there are no standards or requirements for fellowship training from an external accrediting body. As such, the curriculum for these programs is likely driven by a combination of service requirements and local speculation on the needs of a future generation of pediatric hospitalists. Most programs also reported that they provide significant flexibility for each fellow based on their self‐perceived training needs and background.

Although there has been considerable emphasis on the potential educational role of hospitalists, formal coursework in teaching and education is not a part of the curriculum for half of the existing fellowship programs. Recent reports have demonstrated that hospitalists have received better teaching evaluations than traditional subspecialty attendings.7 However, this is in the absence of additional training in education and may reflect greater time that hospitalists might devote to their clinical trainees. The opportunity to further improve the educational training of hospitalists could be an important part of the fellowship experience.

Hospitalists have also been hypothesized to be in a prime position to either lead or have meaningful participation in quality improvement and cost‐saving efforts in the hospital setting. However, only half of programs provide formal coursework in QI and even fewer in areas of hospital economics.

Interestingly, most programs provide coursework in research methods, epidemiology, and grant writing. Requirements regarding clinical duties ranged from a minimum of 17% to a maximum of 67% of program time. It is unclear what the long‐term expectations in career achievement with regard to research will be for those physicians who spend the majority of their training time providing clinical care rather than in research. Previous authors have described the fallacy of expecting brief periods of coursework to prepare individuals for independent research careers.8 However, such coursework can certainly assist graduates of such programs to meaningfully participate in research projects and to put to valuable use their knowledge in both the educational and clinical aspects of their work. Though trainees enrolled in 1‐year programs will spend a larger proportion of their time providing clinical care based on program requirements, trainees in multiyear programs can choose to spend additional time performing clinical duties. Thus, 1 of the possible advantages of a 2‐year or 3‐year program may simply be the flexibility that the fellow has to tailor the program to his or her individual career goals.

Although previous studies have demonstrated that pediatric hospitalists may provide clinical service in a variety of hospital settings,2, 3, 911 most of the current fellowship programs do not provide extensive clinical experiences beyond the general pediatric ward. If hospitalists are to play a more comprehensive role in the care of the pediatric hospitalized patient, programs should consider expanding the scope of clinical training and exposure they provide.

The financial viability of hospitalist fellowship programs is also an important issue. If the additional training provided by these programs is felt to be of value to individual hospitals, it is likely that there will be an increase in the proportion of hospitals who wish to fund such training. A likely incentive for hospitals would be to position themselves to attract and retain hospitalists who possess a unique skill set for which they ascribe value for their patients and/or their bottom line.

Currently, in contrast to traditional, subspecialty‐based fellowships, half of the existing hospitalist fellowship programs allow hospitalist fellows to bill independently. This will have important implications both from an economic perspective, as well as relative to the perceptions of the degree of supervision provided by the respective training programs. This finding may also raise questions as to whether the need for additional clinical training after residency is really necessary to practice hospital medicine.

Whether the training and experience provided by these programs will be seen as a necessary precursor for careers in hospital medicine remains unknown. However, currently there appears to be a mismatch between what some hospitalists have identified as potential clinical educational needs6 with more than 50% desiring additional training in intensive care unit settings, and what is provided through the existing programs. In 2001, a survey of pediatric department chairs found that most did not believe additional formal training beyond residency was necessary to take on the role of a pediatric hospitalist.5 The value of pediatric hospitalist training programs may lie in their provision of or exposure to academic skill sets and the provision of administrative opportunities, in addition to targeted clinical training.

CONCLUSIONS

Pediatric hospitalist fellowship training programs are in the very early stages of their development. In time, greater structure across institutions will need to be put in place if they are to succeed in becoming a necessary prerequisite to the practice of hospital medicine. As the roles of hospitalists become more defined, the nature and extent of their advanced training needs will do so as well.

The field of pediatric hospital medicine is undergoing rapid growth. In 2002, there were approximately 600 pediatric hospitalists1 and in 2006 this number was estimated to be approximately 1000.2 A recent study found that approximately 25% of pediatric hospitalist practices are less than 2 years old.3 As such, there are many new physicians entering the field and most do so without specific training in hospital medicine prior to beginning their employment.4 There is also significant variability in the roles, work patterns, and scope of practice across institutions,3 and hospitalists are engaged in a wide variety of clinical, educational, and administrative functions.

A survey of pediatric department chairs in 2001 found that very few believed that any additional training beyond a pediatric residency was required to perform hospitalist medicine.5 However, since then the field has undergone significant growth. A more recent survey of practicing hospitalists found that 92% believed there was a need for additional training in a variety of domains.6 Specifically, respondents were most interested in achieving greater skill in performing critical care procedures and academic training. These hospitalists regarded pediatric hospitalist fellowships as the best way to gain the additional skills in teaching, research, and administration needed for their positions.

Nonetheless, for a variety of reasons, not the least of which is perhaps the paucity of hospitalist fellowship training programs, few hospitalists in practice today have completed a fellowship in hospital medicine. Over the past several years, a number of pediatric‐specific hospitalist fellowship programs have been initiated, yet little is known of their requirements or curricula. We conducted a study to explore the structure, components, and training goals of the pediatric hospitalist fellowship programs in North America.

MATERIALS AND METHODS

RESULTS

DISCUSSION

There appear to be 2 distinct tracks for pediatric hospitalist training programs: clinical or academic specialization. However, this is not surprising, as most programs are relatively new and there are no standards or requirements for fellowship training from an external accrediting body. As such, the curriculum for these programs is likely driven by a combination of service requirements and local speculation on the needs of a future generation of pediatric hospitalists. Most programs also reported that they provide significant flexibility for each fellow based on their self‐perceived training needs and background.

Although there has been considerable emphasis on the potential educational role of hospitalists, formal coursework in teaching and education is not a part of the curriculum for half of the existing fellowship programs. Recent reports have demonstrated that hospitalists have received better teaching evaluations than traditional subspecialty attendings.7 However, this is in the absence of additional training in education and may reflect greater time that hospitalists might devote to their clinical trainees. The opportunity to further improve the educational training of hospitalists could be an important part of the fellowship experience.

Hospitalists have also been hypothesized to be in a prime position to either lead or have meaningful participation in quality improvement and cost‐saving efforts in the hospital setting. However, only half of programs provide formal coursework in QI and even fewer in areas of hospital economics.

Interestingly, most programs provide coursework in research methods, epidemiology, and grant writing. Requirements regarding clinical duties ranged from a minimum of 17% to a maximum of 67% of program time. It is unclear what the long‐term expectations in career achievement with regard to research will be for those physicians who spend the majority of their training time providing clinical care rather than in research. Previous authors have described the fallacy of expecting brief periods of coursework to prepare individuals for independent research careers.8 However, such coursework can certainly assist graduates of such programs to meaningfully participate in research projects and to put to valuable use their knowledge in both the educational and clinical aspects of their work. Though trainees enrolled in 1‐year programs will spend a larger proportion of their time providing clinical care based on program requirements, trainees in multiyear programs can choose to spend additional time performing clinical duties. Thus, 1 of the possible advantages of a 2‐year or 3‐year program may simply be the flexibility that the fellow has to tailor the program to his or her individual career goals.

Although previous studies have demonstrated that pediatric hospitalists may provide clinical service in a variety of hospital settings,2, 3, 911 most of the current fellowship programs do not provide extensive clinical experiences beyond the general pediatric ward. If hospitalists are to play a more comprehensive role in the care of the pediatric hospitalized patient, programs should consider expanding the scope of clinical training and exposure they provide.

The financial viability of hospitalist fellowship programs is also an important issue. If the additional training provided by these programs is felt to be of value to individual hospitals, it is likely that there will be an increase in the proportion of hospitals who wish to fund such training. A likely incentive for hospitals would be to position themselves to attract and retain hospitalists who possess a unique skill set for which they ascribe value for their patients and/or their bottom line.

Currently, in contrast to traditional, subspecialty‐based fellowships, half of the existing hospitalist fellowship programs allow hospitalist fellows to bill independently. This will have important implications both from an economic perspective, as well as relative to the perceptions of the degree of supervision provided by the respective training programs. This finding may also raise questions as to whether the need for additional clinical training after residency is really necessary to practice hospital medicine.

Whether the training and experience provided by these programs will be seen as a necessary precursor for careers in hospital medicine remains unknown. However, currently there appears to be a mismatch between what some hospitalists have identified as potential clinical educational needs6 with more than 50% desiring additional training in intensive care unit settings, and what is provided through the existing programs. In 2001, a survey of pediatric department chairs found that most did not believe additional formal training beyond residency was necessary to take on the role of a pediatric hospitalist.5 The value of pediatric hospitalist training programs may lie in their provision of or exposure to academic skill sets and the provision of administrative opportunities, in addition to targeted clinical training.

CONCLUSIONS

Pediatric hospitalist fellowship training programs are in the very early stages of their development. In time, greater structure across institutions will need to be put in place if they are to succeed in becoming a necessary prerequisite to the practice of hospital medicine. As the roles of hospitalists become more defined, the nature and extent of their advanced training needs will do so as well.

The field of pediatric hospital medicine is undergoing rapid growth. In 2002, there were approximately 600 pediatric hospitalists1 and in 2006 this number was estimated to be approximately 1000.2 A recent study found that approximately 25% of pediatric hospitalist practices are less than 2 years old.3 As such, there are many new physicians entering the field and most do so without specific training in hospital medicine prior to beginning their employment.4 There is also significant variability in the roles, work patterns, and scope of practice across institutions,3 and hospitalists are engaged in a wide variety of clinical, educational, and administrative functions.

A survey of pediatric department chairs in 2001 found that very few believed that any additional training beyond a pediatric residency was required to perform hospitalist medicine.5 However, since then the field has undergone significant growth. A more recent survey of practicing hospitalists found that 92% believed there was a need for additional training in a variety of domains.6 Specifically, respondents were most interested in achieving greater skill in performing critical care procedures and academic training. These hospitalists regarded pediatric hospitalist fellowships as the best way to gain the additional skills in teaching, research, and administration needed for their positions.

Nonetheless, for a variety of reasons, not the least of which is perhaps the paucity of hospitalist fellowship training programs, few hospitalists in practice today have completed a fellowship in hospital medicine. Over the past several years, a number of pediatric‐specific hospitalist fellowship programs have been initiated, yet little is known of their requirements or curricula. We conducted a study to explore the structure, components, and training goals of the pediatric hospitalist fellowship programs in North America.

MATERIALS AND METHODS

RESULTS

DISCUSSION

There appear to be 2 distinct tracks for pediatric hospitalist training programs: clinical or academic specialization. However, this is not surprising, as most programs are relatively new and there are no standards or requirements for fellowship training from an external accrediting body. As such, the curriculum for these programs is likely driven by a combination of service requirements and local speculation on the needs of a future generation of pediatric hospitalists. Most programs also reported that they provide significant flexibility for each fellow based on their self‐perceived training needs and background.

Although there has been considerable emphasis on the potential educational role of hospitalists, formal coursework in teaching and education is not a part of the curriculum for half of the existing fellowship programs. Recent reports have demonstrated that hospitalists have received better teaching evaluations than traditional subspecialty attendings.7 However, this is in the absence of additional training in education and may reflect greater time that hospitalists might devote to their clinical trainees. The opportunity to further improve the educational training of hospitalists could be an important part of the fellowship experience.

Hospitalists have also been hypothesized to be in a prime position to either lead or have meaningful participation in quality improvement and cost‐saving efforts in the hospital setting. However, only half of programs provide formal coursework in QI and even fewer in areas of hospital economics.

Interestingly, most programs provide coursework in research methods, epidemiology, and grant writing. Requirements regarding clinical duties ranged from a minimum of 17% to a maximum of 67% of program time. It is unclear what the long‐term expectations in career achievement with regard to research will be for those physicians who spend the majority of their training time providing clinical care rather than in research. Previous authors have described the fallacy of expecting brief periods of coursework to prepare individuals for independent research careers.8 However, such coursework can certainly assist graduates of such programs to meaningfully participate in research projects and to put to valuable use their knowledge in both the educational and clinical aspects of their work. Though trainees enrolled in 1‐year programs will spend a larger proportion of their time providing clinical care based on program requirements, trainees in multiyear programs can choose to spend additional time performing clinical duties. Thus, 1 of the possible advantages of a 2‐year or 3‐year program may simply be the flexibility that the fellow has to tailor the program to his or her individual career goals.

Although previous studies have demonstrated that pediatric hospitalists may provide clinical service in a variety of hospital settings,2, 3, 911 most of the current fellowship programs do not provide extensive clinical experiences beyond the general pediatric ward. If hospitalists are to play a more comprehensive role in the care of the pediatric hospitalized patient, programs should consider expanding the scope of clinical training and exposure they provide.

The financial viability of hospitalist fellowship programs is also an important issue. If the additional training provided by these programs is felt to be of value to individual hospitals, it is likely that there will be an increase in the proportion of hospitals who wish to fund such training. A likely incentive for hospitals would be to position themselves to attract and retain hospitalists who possess a unique skill set for which they ascribe value for their patients and/or their bottom line.

Currently, in contrast to traditional, subspecialty‐based fellowships, half of the existing hospitalist fellowship programs allow hospitalist fellows to bill independently. This will have important implications both from an economic perspective, as well as relative to the perceptions of the degree of supervision provided by the respective training programs. This finding may also raise questions as to whether the need for additional clinical training after residency is really necessary to practice hospital medicine.

Whether the training and experience provided by these programs will be seen as a necessary precursor for careers in hospital medicine remains unknown. However, currently there appears to be a mismatch between what some hospitalists have identified as potential clinical educational needs6 with more than 50% desiring additional training in intensive care unit settings, and what is provided through the existing programs. In 2001, a survey of pediatric department chairs found that most did not believe additional formal training beyond residency was necessary to take on the role of a pediatric hospitalist.5 The value of pediatric hospitalist training programs may lie in their provision of or exposure to academic skill sets and the provision of administrative opportunities, in addition to targeted clinical training.

CONCLUSIONS

Pediatric hospitalist fellowship training programs are in the very early stages of their development. In time, greater structure across institutions will need to be put in place if they are to succeed in becoming a necessary prerequisite to the practice of hospital medicine. As the roles of hospitalists become more defined, the nature and extent of their advanced training needs will do so as well.

Influenza is a common cause of acute respiratory illness in children, resulting in hospitalization of both healthy and chronically ill children due to influenza‐related complications.1, 2 Currently, amantadine, rimantadine, oseltamivir, and zanamivir are approved for use in children to treat influenza. In early 2006, more than 90% of influenza isolates tested in the US were found to be resistant to the adamantanes, suggesting that these medications might be of limited benefit during future influenza seasons.3 To date, most isolates of influenza remain susceptible to neuraminidase inhibitors, zanamivir and oseltamivir. Zanamivir has not been used extensively in pediatrics because it is delivered by aerosolization, and is only approved by the US Food and Drug Administration (FDA) for children 7 years of age. Oseltamivir is administered orally and is FDA‐approved for use in children 1 year of age within 48 hours of onset of symptoms of influenza virus infection.

Studies performed in outpatient settings have shown that oseltamivir can lessen the severity and reduce the length of influenza illness by 36 hours when therapy is initiated within 2 days of the onset of symptoms.4 Treatment also reduced the frequency of new diagnoses of otitis media and decreased physician‐prescribed antibiotics.4

To date, there are limited data evaluating the use of oseltamivir in either adult or pediatric patients hospitalized with influenza. We sought to describe the use of antiviral medications among children hospitalized with community‐acquired laboratory‐confirmed influenza (CA‐LCI) and to evaluate the effect of a computer‐based electronic reminder to increase the rate of on‐label use of oseltamivir among hospitalized children.

PATIENTS AND METHODS

We performed a retrospective cohort study of patients 21 years of age who were hospitalized with CA‐LCI during 5 consecutive seasons from July 2000 through June 2005 (seasons 1‐5) at the Children's Hospital of Philadelphia (CHOP). CHOP is a 418‐bed tertiary care hospital with about 24,000 hospital admissions each year. Viral diagnostic studies are performed routinely on children hospitalized with acute respiratory symptoms of unknown etiology, which aids in assigning patients to cohorts. Patients who had laboratory confirmation of influenza performed at an outside institution were excluded from this analysis.

From June 2005 through May 2006 (season 6), an observational trial of an electronic clinical decision reminder was performed to assess a mechanism to increase the proportion of eligible children treated with oseltamivir. Patients were included in this analysis if they were 21 years of age and had a diagnostic specimen for influenza obtained less than 72 hours after admission. The CHOP Institutional Review Board approved this study with a waiver of informed consent.

RESULTS

Use of Antiviral Medications in Children Hospitalized with Influenza, 2000‐2005

From July 2000 to June 2005, 1,058 patients were admitted with laboratory confirmed influenza; 8 were excluded because confirmatory testing was done at an outside institution, 24 were repeat hospitalizations, 89 nosocomial cases, and 8 cases were in patients >21 years. Thus, 929 patients had CA‐LCI and were eligible for inclusion in this study. Most children were infected with influenza A and were 1 year of age (Table 1). During this study period, only 9.3% of study subjects were treated with antiviral medications, most of whom (91%) received oseltamivir. Eight patients received amantadine over all seasons studied.

Table 1.Characteristics of Patients Hospitalized with CA‐LCI and Oseltamivir Eligibility During Five Influenza Seasons, 2000‐2001 to 2004‐2005

Characteristics	Patients Hospitalized with CA‐LCI (n = 929)*	Eligible to Receive Oseltamivir (n = 305)*
* Values are number of patients (%).
Age (years)
<1	342 (37)	0
1	587 (63)	305 (100)
Season
2000‐2001	107 (11.5)	32 (10)
2001‐2002	252 (27)	78 (26)
2002‐2003	135 (14.5)	31 (10)
2003‐2004	243 (26)	86 (28)
2004‐2005	192 (21)	78 (26)
Influenza type
A	692 (75)
B	237 (25)

Overall, one‐third of patients (305/929; 33%) were eligible for treatment with oseltamivir. Among patients 1 year of age, approximately one‐half (305/587; 52%) were oseltamivir‐eligible. The additional 282 patients 1 year were ineligible because test results were returned to the clinician >48 hours after hospital admission. Only 49 (16.1%) of oseltamivir‐eligible patients were prescribed oseltamivir during hospitalization (Figure 1). The rate of prescription of oseltamivir increased over all seasons from 0% in 2000‐2001 to 20% in 2004‐2005. On‐label prescription rates increased from 0% in 2000‐2001 to 37.2% in 2004‐2005 (P < 0.0001; Figure 2).

Figure 1

Figure 2

Evaluation of a Computer‐Based Electronic Reminder Designed to Enhance the On‐Label Prescription of Oseltamivir

During season 6, an electronic reminder about the labeled use of oseltamivir was evaluated to determine its ability to increase the rate of prescription of oseltamivir among eligible children hospitalized with CA‐LCI. During season 6, most patients (226/311; 73%) were 1 year of age. A total of 84 patients were determined to be oseltamivir‐eligible (age 1 year and test results back to the clinician within 48 hours of symptom onset).

During the initial 10 weeks of local influenza activity, 20 oseltamivir‐eligible patients were admitted to our institution, and 8 received oseltamivir (40% prescription rate) (Table 2). In addition, 2 of 54 (3.7%) oseltamivir‐ineligible patients were also treated. The computer‐based electronic reminder was initiated in week 11 of the influenza season. After initiation of the reminder, 237 additional children with CA‐LCI were hospitalized, of whom 64 (27%) were determined to be oseltamivir‐eligible. The rate of on‐label prescription of oseltamivir was similar to that observed prior to initiation of the reminder: 16 of 64 patients eligible for antiviral therapy received oseltamivir (25% prescription rate) (Figure 3). An additional 8 patients were prescribed oseltamivir off‐label. The rate of oseltamivir prescription did not change significantly for either oseltamivir‐eligible (40‐25%) or oseltamivir‐ineligible (3.7‐4.6%) (Figure 4).

Figure 3

Figure 4

Table 2.Oseltamivir Eligibility and Use Among Patients Hospitalized with CA‐LCI During the Intervention Season, 2005‐2006

Prompt Active?	Oseltamivir Use		Total
	Yes*	No
NOTE: No significant difference found in prescription of oseltamivir for those eligible and ineligible before and after the prompt was active, by Fisher's exact tests (P > 0.5). * Values are number of patients (%). Values are number of patients.
No
Eligible	8 (40)	12	20
Ineligible	2 (3.7)	52	54
Yes
Eligible	16 (25)	48	64
Ineligible	8 (4.6)	165	173
Total	34	277	311

DISCUSSION AND CONCLUSION

In this report, we describe the use of oseltamivir over 6 seasons in a cohort of children hospitalized with CA‐LCI at 1 tertiary care pediatric hospital and examine the impact of a mechanism designed to increase prescription among those eligible for oseltamivir. We found that only one‐third of patients hospitalized at our institution were eligible for oseltamivir treatment based on FDA‐approved indications. Of the eligible patients, few were prescribed oseltamivir during their hospitalization. During the sixth season, we employed a computer reminder system for oseltamivir prescription, which had no appreciable effect upon prescription rates. Despite the lack of effect of the electronic reminder system, we observed an increase of on‐label oseltamivir prescriptions over the entire study period. Finally, we identified 11 patients <1 year of age (3%) who were treated with oseltamivir. There were no adverse events identified in this group.

Although previous studies have addressed prescription rates of oseltamivir in children with influenza, few, if any, have looked at how these prescriptions correspond with FDA label criteria. In our cohort, only one‐third of hospitalized children were eligible for treatment with oseltamivir based upon their age and symptom duration at the time the results of rapid laboratory testing became available. Of those patients in our cohort eligible for oseltamivir, few were treated. The prescription of oseltamivir in seasons falls within the ranges found by Schrag et al.7 in their multistate review of pediatric influenza hospitalizations in 2003‐2004. They noted that use of antiviral medications varied by location of surveillance ranging from 3% in Connecticut to 34% in Colorado, indicating significant regional differences in prescription practices.7 Potential causes of low rates of appropriate use of oseltamivir include the observation that many physicians remain unaware of the potential severity of influenza infection in children.8 Additionally, physicians may differ on how to define the onset of influenza infection in children. A recent study published by Ohmit and Monto9 indicated that a fever and cough predicted 83% of children 5 to 12 years old who were determined to be influenza‐positive. Finally, many physicians who do not prescribe antiviral therapy may believe that their patients present too late for appropriate initiation of therapy.10

We identified 29 patients who received oseltamivir although they did not meet the FDA label criteria, of whom 72% had a chronic underlying condition. Moore et al.11 in their surveillance of influenza admissions in Canada found a similar trend. They described 26 of 29 (90%) hospitalized patients receiving antiinfluenza drugs had an underlying disease, and of those without a chronic condition, all had severe influenza‐related complications such as encephalopathy.11

Implementation of a computerized reminder to improve use of oseltamivir had no statistically significant effect on prescribing practice. Our sample size calculation was based on detecting a 40% difference in prescription rates, which limited our power to detect a smaller difference in prescription rates. A systematic review by Garg et al.12 identified barriers to the success of computer‐based decision support systems (CDS), which included failure of practitioners to use the system, poor integration of the system to the physician's workflow, and disagreement with what was recommended. Future enhancements to our inpatient electronic hospital record may allow for more targeted and robust CDS interventions.

We observed an increase in on‐label prescription rates of oseltamivir over the entire study period. We hypothesize that increased use of oseltamivir might be associated with growing concerns of pandemic influenza and attention to fatal influenza in children,13 as evidenced by the recent addition of influenza‐associated deaths in children to the list of nationally notifiable conditions in 2004.14

There has been considerable focus upon potential adverse events associated with treatment with oseltamivir in children. Reports have emerged, primarily from Japan, of neuropsychiatric and dermatologic adverse events of oseltamivir treatment.15 In the fall of 2006, the FDA added a precaution to the labeling of oseltamivir due to these neuropsychiatric events.16 In our treated cohort, no neurologic, neuropsychiatric, or dermatologic adverse events were identified. However, this finding is not surprising given the rarity of these adverse events and the limited number of children treated with oseltamivir in this study.

The strengths of this current study include a large cohort of laboratory‐confirmed influenza in hospitalized children over multiple influenza seasons. In addition, this is the first study of which we are aware that has assessed the number of children eligible for oseltamivir but not treated. The limitations of this study include misclassification bias related to the retrospective study design. Because of this design, onset of influenza symptoms was collected through chart review, and the time of receipt of influenza results from virology was based upon known laboratory turnover time, rather than actual knowledge of time of physician awareness of the result. To address this issue we used a conservative estimate of the time of receipt of influenza test results. In addition, the retrospective design prevented us from assessing the clinical decision‐making process, which led some patients to be treated with oseltamivir and others not. Our evaluation of the electronic reminder was designed to show a large change in prescription practices (ie, 40%), so it had insufficient power to detect a smaller impact. Finally, ascertainment bias may have limited our ability to identify adverse effects.

This study demonstrates that oseltamivir is prescribed infrequently among hospitalized children. Future studies are needed to determine whether appropriate use of oseltamivir improves outcomes among hospitalized children. Additional study of the safety and efficacy of oseltamivir in children aged <1 year is also needed given the large burden of disease in this age group.