Hospitalists sometimes come across skin problems in pediatric patients, and some of these issues fall outside the scope of their expertise.

“I find lesions incidentally that I recommend be referred to dermatologists for evaluation on an outpatient basis” more often than in inpatient dermatologic situations, says Logan Murray, MD, a pediatric hospitalist at the Barbara Bush Children’s Hospital at Maine Medical Center in Portland. “I recently managed a newborn with a 6 cm diameter brown patch in the lumbar area with fine, dark, vellus hair, which I suspect is a congenital giant melanocytic nevus,” he says. To properly evaluate the birthmark, he referred the patient’s parents to a dermatologist.

In these instances, it makes sense for a hospitalist to request that a dermatologist see the child and talk with the parents during hospitalization.

“We get many consults [that] are appropriate,” says Susan Bayliss, MD, a pediatric dermatologist at St. Louis Children’s Hospital. If a hospitalist can’t identify a particular skin issue and reassure parents, it’s time to call a dermatologist.

Distinguishing between acute and chronic dermatologic conditions is important. “The skin is often overlooked among hospitalists,” who are managing sicker patients nowadays, says Neera Agarwal-Antal, MD, head of the division of dermatology at Akron Children’s Hospital in Akron, Ohio.

One of the most dangerous and potentially fatal dermatologic emergencies is Stevens-Johnson syndrome, known in later stages as toxic epidermal necrolysis. Usually triggered by a drug-related reaction, the disease can cause large areas of skin to detach and lesions to develop in the mucous membranes. However, “the good news is most skin conditions are not acute or deadly,” Dr. Agarwal-Antal says.

Warts are very common and often can wait for examination in an outpatient setting. If an adolescent has significant acne, a hospitalist may ask gently, “Are you interested in doing something about your complexion?” To a patient who answers “yes,” a hospitalist could suggest over-the-counter benzoyl peroxide, says Dr. Bayliss, who is also professor of dermatology and pediatrics at Washington University School of Medicine in St. Louis.

“Pediatric dermatology is basically an outpatient specialty,” she adds. “Many kids have skin issues, but most of them do not need to be addressed by a hospitalist.” TH

Susan Kreimer is a freelance writer in New York.

Hospitalists sometimes come across skin problems in pediatric patients, and some of these issues fall outside the scope of their expertise.

“I find lesions incidentally that I recommend be referred to dermatologists for evaluation on an outpatient basis” more often than in inpatient dermatologic situations, says Logan Murray, MD, a pediatric hospitalist at the Barbara Bush Children’s Hospital at Maine Medical Center in Portland. “I recently managed a newborn with a 6 cm diameter brown patch in the lumbar area with fine, dark, vellus hair, which I suspect is a congenital giant melanocytic nevus,” he says. To properly evaluate the birthmark, he referred the patient’s parents to a dermatologist.

In these instances, it makes sense for a hospitalist to request that a dermatologist see the child and talk with the parents during hospitalization.

“We get many consults [that] are appropriate,” says Susan Bayliss, MD, a pediatric dermatologist at St. Louis Children’s Hospital. If a hospitalist can’t identify a particular skin issue and reassure parents, it’s time to call a dermatologist.

Distinguishing between acute and chronic dermatologic conditions is important. “The skin is often overlooked among hospitalists,” who are managing sicker patients nowadays, says Neera Agarwal-Antal, MD, head of the division of dermatology at Akron Children’s Hospital in Akron, Ohio.

One of the most dangerous and potentially fatal dermatologic emergencies is Stevens-Johnson syndrome, known in later stages as toxic epidermal necrolysis. Usually triggered by a drug-related reaction, the disease can cause large areas of skin to detach and lesions to develop in the mucous membranes. However, “the good news is most skin conditions are not acute or deadly,” Dr. Agarwal-Antal says.

Warts are very common and often can wait for examination in an outpatient setting. If an adolescent has significant acne, a hospitalist may ask gently, “Are you interested in doing something about your complexion?” To a patient who answers “yes,” a hospitalist could suggest over-the-counter benzoyl peroxide, says Dr. Bayliss, who is also professor of dermatology and pediatrics at Washington University School of Medicine in St. Louis.

“Pediatric dermatology is basically an outpatient specialty,” she adds. “Many kids have skin issues, but most of them do not need to be addressed by a hospitalist.” TH

Susan Kreimer is a freelance writer in New York.

Hospitalists sometimes come across skin problems in pediatric patients, and some of these issues fall outside the scope of their expertise.

“I find lesions incidentally that I recommend be referred to dermatologists for evaluation on an outpatient basis” more often than in inpatient dermatologic situations, says Logan Murray, MD, a pediatric hospitalist at the Barbara Bush Children’s Hospital at Maine Medical Center in Portland. “I recently managed a newborn with a 6 cm diameter brown patch in the lumbar area with fine, dark, vellus hair, which I suspect is a congenital giant melanocytic nevus,” he says. To properly evaluate the birthmark, he referred the patient’s parents to a dermatologist.

In these instances, it makes sense for a hospitalist to request that a dermatologist see the child and talk with the parents during hospitalization.

“We get many consults [that] are appropriate,” says Susan Bayliss, MD, a pediatric dermatologist at St. Louis Children’s Hospital. If a hospitalist can’t identify a particular skin issue and reassure parents, it’s time to call a dermatologist.

Distinguishing between acute and chronic dermatologic conditions is important. “The skin is often overlooked among hospitalists,” who are managing sicker patients nowadays, says Neera Agarwal-Antal, MD, head of the division of dermatology at Akron Children’s Hospital in Akron, Ohio.

One of the most dangerous and potentially fatal dermatologic emergencies is Stevens-Johnson syndrome, known in later stages as toxic epidermal necrolysis. Usually triggered by a drug-related reaction, the disease can cause large areas of skin to detach and lesions to develop in the mucous membranes. However, “the good news is most skin conditions are not acute or deadly,” Dr. Agarwal-Antal says.

Warts are very common and often can wait for examination in an outpatient setting. If an adolescent has significant acne, a hospitalist may ask gently, “Are you interested in doing something about your complexion?” To a patient who answers “yes,” a hospitalist could suggest over-the-counter benzoyl peroxide, says Dr. Bayliss, who is also professor of dermatology and pediatrics at Washington University School of Medicine in St. Louis.

“Pediatric dermatology is basically an outpatient specialty,” she adds. “Many kids have skin issues, but most of them do not need to be addressed by a hospitalist.” TH

Susan Kreimer is a freelance writer in New York.

Not infrequently, less than 90 day old infants have fever and irritability and are more sleepy than usual, but have no apparent focus of infection. The sepsis evaluation is usually negative. It is frustrating for parents and providers when we report that we don’t really know what caused the febrile illness.

In summer/autumn season, some infants have enterovirus, with the predominate serotypes varying year to year. The enterovirus genus has several species, i.e., polio, enterovirus, echovirus, and Coxsackie A and Coxsackie B viruses. Echovirus is an acronym for enteric, cytopathic, human, orphan virus. Coxsackie is named from the city where it was first reported. Recently discovered enteroviruses have numbers starting at 68, and include a strain causing severe disease in Asia, enterovirus 71.

Sometimes clinicians can tell that enterovirus is in the community without laboratory tests because children present with hand, foot, and mouth (and sometimes buttock) disease. or herpangina. Enteroviruses also cause pericarditis, myocarditis, or pleurodynia (a.k.a. the "devil’s grippe").

But enteroviruses also cause aseptic meningitis. A modest pleocytosis with a mononuclear predominance and near-normal CSF glucose/protein values, plus negative bacterial cultures, is commonly called "aseptic meningitis."

Enteroviruses cause modest CSF pleocytosis (50-400 WBC), usually with mononuclear predominance and relatively normal CSF chemistries. While there can initially be a CSF neutrophil predominance, the differential usually shifts to mostly mononuclear cells less than 24 hours later. In the 1970s and 1980s (before polymerase chain reaction [PCR]), we used a "double tap" strategy to allow early discontinuation of antibiotics and hospital discharge. If the second CSF obtained within 24 hours of the first CSF had reasonably normal chemistries plus fewer WBCs or shifted to almost all mononuclear cells, children were discharged before final culture results. While hypoglycorrhachia is seen rarely with enterovirus (as low as 10 mg/dL), low CSF glucose values are usually due to bacterial or tuberculous meningitis. CSF protein concentrations with enteroviral meningitis are rarely greater than 80 mg/dL, the usual values for bacterial meningitis.

But consider this caveat: When "aseptic meningitis" seems present but CSF chemistries are abnormal (elevated protein or low glucose), check for tuberculosis risk factors and/or indolent neurological findings that could indicate tuberculous meningitis. In infants less than 2 months of age, consider neonatal herpes simplex virus (HSV) disease, particularly if the CSF protein is elevated.

These days "double taps" are not routine. Instead, CSF PCR is used. HSV and enterovirus PCR on CSF is available at most institutions with results available before bacteria cultures are final. A positive CSF enterovirus PCR (J. Pediatr. 1997;131:393-7) allows discontinuing antibacterials and acyclovir, if it was started empirically, plus early discharge. A positive HSV PCR also clarifies management: Continue acyclovir but discontinue antibacterial drugs. Keep in mind that enteroviral meningitis outbreaks are quite seasonal, with the majority of disease noted in the summer and early fall.

So we know the answer if the enterovirus or HSV PCR is positive. But what if these PCRs and bacterial cultures are negative in a child not pretreated with antibiotics? Well, the new kid on the block for aseptic meningitis is human parechovirus (HPeV). The first viruses classified as HPeV (HPeV1 and HPeV2) were previously called echovirus 22 and echovirus 23. But clinical and genome differences from enteroviruses led to reclassification as HPeVs. Now there are 16 HPeV serotypes. So why do we care?

In the past 6 years, HPeV3 emerged as the most common definable cause of sepsis-like syndrome in young infants with negative bacterial cultures (J. Clin. Virol. 2011;52:187-91; Pediatr. Infect. Dis. J. 2013;32:213-6). Interestingly, HPeV3-infected infants have more frequent peripheral leukopenia and lymphopenia plus more febrile days and higher fevers than those with enteroviruses. HPeV3 has a nearly every-other-year cycle (May-November). HPeV was as frequent or more frequent than all enteroviruses combined.

HPEV is not detected by enterovirus PCR, but is confirmed by HPeV-specific PCR. Like enteroviruses, PCR of blood is usually positive in HPeV-infected infants.

An important difference from HSV or enteroviruses is that almost no HPeV3 CNS-infected infants have CSF pleocytosis. That’s right. CSF in HPeV CNS infection is like HHV-6 (minimal CSF WBCs despite CNS infection). At our institution, HPeV3 PCR is performed routinely on CSF from all infants less than 90 days of age undergoing sepsis evaluations in summer/autumn.

If cultures and PCRs are negative in young infants with sepsis-like syndrome, your laboratory can likely perform or send out HPeV3 PCR. When HPeV3 CSF PCRs are positive, antibacterials can be stopped and patients discharged. Clinicians may be reluctant to discharge before final negative bacterial cultures because these infants can still "look ill," and providers are just learning about HPeV3. But based on our multiyear experience, it appears safe. We saw only three concurrent bacterial infections when HPeV3 was detected in CSF – all urinary tract infections that were easily detected during the sepsis evaluation and treated as such.

There have been no defined sequelae of HPeV CNS infection to date in the United States, although long-term follow-up is lacking for this emerging pathogen. There have been rare CNS sequelae, including white matter changes or seizures outside the United States, but these were apparent during the acute illness. We recommend outpatient follow-up soon after discharge, particularly if fever persists at discharge.

If we add HPeV3 PCR to our testing for infant sepsis-like syndrome during summer/fall, particularly when there is no or minimal CSF pleocytosis plus peripheral leuko/lymphopenia, there will fewer times when we lack a confirmed cause.

Dr. Harrison is a professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. Dr. Harrison said he has no relevant financial disclosures.

Not infrequently, less than 90 day old infants have fever and irritability and are more sleepy than usual, but have no apparent focus of infection. The sepsis evaluation is usually negative. It is frustrating for parents and providers when we report that we don’t really know what caused the febrile illness.

In summer/autumn season, some infants have enterovirus, with the predominate serotypes varying year to year. The enterovirus genus has several species, i.e., polio, enterovirus, echovirus, and Coxsackie A and Coxsackie B viruses. Echovirus is an acronym for enteric, cytopathic, human, orphan virus. Coxsackie is named from the city where it was first reported. Recently discovered enteroviruses have numbers starting at 68, and include a strain causing severe disease in Asia, enterovirus 71.

Sometimes clinicians can tell that enterovirus is in the community without laboratory tests because children present with hand, foot, and mouth (and sometimes buttock) disease. or herpangina. Enteroviruses also cause pericarditis, myocarditis, or pleurodynia (a.k.a. the "devil’s grippe").

But enteroviruses also cause aseptic meningitis. A modest pleocytosis with a mononuclear predominance and near-normal CSF glucose/protein values, plus negative bacterial cultures, is commonly called "aseptic meningitis."

Enteroviruses cause modest CSF pleocytosis (50-400 WBC), usually with mononuclear predominance and relatively normal CSF chemistries. While there can initially be a CSF neutrophil predominance, the differential usually shifts to mostly mononuclear cells less than 24 hours later. In the 1970s and 1980s (before polymerase chain reaction [PCR]), we used a "double tap" strategy to allow early discontinuation of antibiotics and hospital discharge. If the second CSF obtained within 24 hours of the first CSF had reasonably normal chemistries plus fewer WBCs or shifted to almost all mononuclear cells, children were discharged before final culture results. While hypoglycorrhachia is seen rarely with enterovirus (as low as 10 mg/dL), low CSF glucose values are usually due to bacterial or tuberculous meningitis. CSF protein concentrations with enteroviral meningitis are rarely greater than 80 mg/dL, the usual values for bacterial meningitis.

But consider this caveat: When "aseptic meningitis" seems present but CSF chemistries are abnormal (elevated protein or low glucose), check for tuberculosis risk factors and/or indolent neurological findings that could indicate tuberculous meningitis. In infants less than 2 months of age, consider neonatal herpes simplex virus (HSV) disease, particularly if the CSF protein is elevated.

These days "double taps" are not routine. Instead, CSF PCR is used. HSV and enterovirus PCR on CSF is available at most institutions with results available before bacteria cultures are final. A positive CSF enterovirus PCR (J. Pediatr. 1997;131:393-7) allows discontinuing antibacterials and acyclovir, if it was started empirically, plus early discharge. A positive HSV PCR also clarifies management: Continue acyclovir but discontinue antibacterial drugs. Keep in mind that enteroviral meningitis outbreaks are quite seasonal, with the majority of disease noted in the summer and early fall.

So we know the answer if the enterovirus or HSV PCR is positive. But what if these PCRs and bacterial cultures are negative in a child not pretreated with antibiotics? Well, the new kid on the block for aseptic meningitis is human parechovirus (HPeV). The first viruses classified as HPeV (HPeV1 and HPeV2) were previously called echovirus 22 and echovirus 23. But clinical and genome differences from enteroviruses led to reclassification as HPeVs. Now there are 16 HPeV serotypes. So why do we care?

In the past 6 years, HPeV3 emerged as the most common definable cause of sepsis-like syndrome in young infants with negative bacterial cultures (J. Clin. Virol. 2011;52:187-91; Pediatr. Infect. Dis. J. 2013;32:213-6). Interestingly, HPeV3-infected infants have more frequent peripheral leukopenia and lymphopenia plus more febrile days and higher fevers than those with enteroviruses. HPeV3 has a nearly every-other-year cycle (May-November). HPeV was as frequent or more frequent than all enteroviruses combined.

HPEV is not detected by enterovirus PCR, but is confirmed by HPeV-specific PCR. Like enteroviruses, PCR of blood is usually positive in HPeV-infected infants.

An important difference from HSV or enteroviruses is that almost no HPeV3 CNS-infected infants have CSF pleocytosis. That’s right. CSF in HPeV CNS infection is like HHV-6 (minimal CSF WBCs despite CNS infection). At our institution, HPeV3 PCR is performed routinely on CSF from all infants less than 90 days of age undergoing sepsis evaluations in summer/autumn.

If cultures and PCRs are negative in young infants with sepsis-like syndrome, your laboratory can likely perform or send out HPeV3 PCR. When HPeV3 CSF PCRs are positive, antibacterials can be stopped and patients discharged. Clinicians may be reluctant to discharge before final negative bacterial cultures because these infants can still "look ill," and providers are just learning about HPeV3. But based on our multiyear experience, it appears safe. We saw only three concurrent bacterial infections when HPeV3 was detected in CSF – all urinary tract infections that were easily detected during the sepsis evaluation and treated as such.

There have been no defined sequelae of HPeV CNS infection to date in the United States, although long-term follow-up is lacking for this emerging pathogen. There have been rare CNS sequelae, including white matter changes or seizures outside the United States, but these were apparent during the acute illness. We recommend outpatient follow-up soon after discharge, particularly if fever persists at discharge.

If we add HPeV3 PCR to our testing for infant sepsis-like syndrome during summer/fall, particularly when there is no or minimal CSF pleocytosis plus peripheral leuko/lymphopenia, there will fewer times when we lack a confirmed cause.

Dr. Harrison is a professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. Dr. Harrison said he has no relevant financial disclosures.

Not infrequently, less than 90 day old infants have fever and irritability and are more sleepy than usual, but have no apparent focus of infection. The sepsis evaluation is usually negative. It is frustrating for parents and providers when we report that we don’t really know what caused the febrile illness.

In summer/autumn season, some infants have enterovirus, with the predominate serotypes varying year to year. The enterovirus genus has several species, i.e., polio, enterovirus, echovirus, and Coxsackie A and Coxsackie B viruses. Echovirus is an acronym for enteric, cytopathic, human, orphan virus. Coxsackie is named from the city where it was first reported. Recently discovered enteroviruses have numbers starting at 68, and include a strain causing severe disease in Asia, enterovirus 71.

Sometimes clinicians can tell that enterovirus is in the community without laboratory tests because children present with hand, foot, and mouth (and sometimes buttock) disease. or herpangina. Enteroviruses also cause pericarditis, myocarditis, or pleurodynia (a.k.a. the "devil’s grippe").

But enteroviruses also cause aseptic meningitis. A modest pleocytosis with a mononuclear predominance and near-normal CSF glucose/protein values, plus negative bacterial cultures, is commonly called "aseptic meningitis."

Enteroviruses cause modest CSF pleocytosis (50-400 WBC), usually with mononuclear predominance and relatively normal CSF chemistries. While there can initially be a CSF neutrophil predominance, the differential usually shifts to mostly mononuclear cells less than 24 hours later. In the 1970s and 1980s (before polymerase chain reaction [PCR]), we used a "double tap" strategy to allow early discontinuation of antibiotics and hospital discharge. If the second CSF obtained within 24 hours of the first CSF had reasonably normal chemistries plus fewer WBCs or shifted to almost all mononuclear cells, children were discharged before final culture results. While hypoglycorrhachia is seen rarely with enterovirus (as low as 10 mg/dL), low CSF glucose values are usually due to bacterial or tuberculous meningitis. CSF protein concentrations with enteroviral meningitis are rarely greater than 80 mg/dL, the usual values for bacterial meningitis.

But consider this caveat: When "aseptic meningitis" seems present but CSF chemistries are abnormal (elevated protein or low glucose), check for tuberculosis risk factors and/or indolent neurological findings that could indicate tuberculous meningitis. In infants less than 2 months of age, consider neonatal herpes simplex virus (HSV) disease, particularly if the CSF protein is elevated.

These days "double taps" are not routine. Instead, CSF PCR is used. HSV and enterovirus PCR on CSF is available at most institutions with results available before bacteria cultures are final. A positive CSF enterovirus PCR (J. Pediatr. 1997;131:393-7) allows discontinuing antibacterials and acyclovir, if it was started empirically, plus early discharge. A positive HSV PCR also clarifies management: Continue acyclovir but discontinue antibacterial drugs. Keep in mind that enteroviral meningitis outbreaks are quite seasonal, with the majority of disease noted in the summer and early fall.

So we know the answer if the enterovirus or HSV PCR is positive. But what if these PCRs and bacterial cultures are negative in a child not pretreated with antibiotics? Well, the new kid on the block for aseptic meningitis is human parechovirus (HPeV). The first viruses classified as HPeV (HPeV1 and HPeV2) were previously called echovirus 22 and echovirus 23. But clinical and genome differences from enteroviruses led to reclassification as HPeVs. Now there are 16 HPeV serotypes. So why do we care?

In the past 6 years, HPeV3 emerged as the most common definable cause of sepsis-like syndrome in young infants with negative bacterial cultures (J. Clin. Virol. 2011;52:187-91; Pediatr. Infect. Dis. J. 2013;32:213-6). Interestingly, HPeV3-infected infants have more frequent peripheral leukopenia and lymphopenia plus more febrile days and higher fevers than those with enteroviruses. HPeV3 has a nearly every-other-year cycle (May-November). HPeV was as frequent or more frequent than all enteroviruses combined.

HPEV is not detected by enterovirus PCR, but is confirmed by HPeV-specific PCR. Like enteroviruses, PCR of blood is usually positive in HPeV-infected infants.

An important difference from HSV or enteroviruses is that almost no HPeV3 CNS-infected infants have CSF pleocytosis. That’s right. CSF in HPeV CNS infection is like HHV-6 (minimal CSF WBCs despite CNS infection). At our institution, HPeV3 PCR is performed routinely on CSF from all infants less than 90 days of age undergoing sepsis evaluations in summer/autumn.

If cultures and PCRs are negative in young infants with sepsis-like syndrome, your laboratory can likely perform or send out HPeV3 PCR. When HPeV3 CSF PCRs are positive, antibacterials can be stopped and patients discharged. Clinicians may be reluctant to discharge before final negative bacterial cultures because these infants can still "look ill," and providers are just learning about HPeV3. But based on our multiyear experience, it appears safe. We saw only three concurrent bacterial infections when HPeV3 was detected in CSF – all urinary tract infections that were easily detected during the sepsis evaluation and treated as such.

There have been no defined sequelae of HPeV CNS infection to date in the United States, although long-term follow-up is lacking for this emerging pathogen. There have been rare CNS sequelae, including white matter changes or seizures outside the United States, but these were apparent during the acute illness. We recommend outpatient follow-up soon after discharge, particularly if fever persists at discharge.

If we add HPeV3 PCR to our testing for infant sepsis-like syndrome during summer/fall, particularly when there is no or minimal CSF pleocytosis plus peripheral leuko/lymphopenia, there will fewer times when we lack a confirmed cause.

Dr. Harrison is a professor of pediatrics and pediatric infectious diseases at Children’s Mercy Hospitals and Clinics, Kansas City, Mo. Dr. Harrison said he has no relevant financial disclosures.

A57-year-old Caucasian man with a 32 pack-year history of smoking presented to the prime care clinic with a 2-week history of left index finger pain, redness, and swelling after sustaining a minor injury while closing his car door. Physical examination revealed a blackish discoloration of the skin. An X-ray of his left hand showed complete demineralization of the distal phalanx of the left index finger (Figure 1). The pain did not respond to NSAIDS, narcotics, and antibiotics. He subsequently underwent partial amputation of the finger. Pathology from the surgical specimen revealed a “poorly differentiated metastatic small-cell carcinoma” (Figure 2). He denied any dyspnea, cough, fever, night sweats, or loss of weight or appetite. The results of a computerized tomography scan of his thorax (Figure 3), abdomen, and pelvis revealed a large right lower lobe lung mass of 6.2 cm
4.2 cm adjacent to the right lower lobe bronchus that was consistent with lung cancer associated with pulmonary, hepatic, nodal, and skeletal metastasis. Magnetic resonance imaging of the brain showed multiple metastatic lesions throughout the brain, including the cerebellum. An MRI of the spine showed extensive metastatic lesions involving the thoracic vertebrae, T4 –T12, and the lumbar vertebra, L2. Given the extensive metastases and poor prognosis, the patient chose hospice care and palliative services. Discussion Digital acrometastases represent only 0.1% of all skeletal metastases.1 They have been described with various malignancies, including breast, gastrointestinal tract, head and neck, and small-cell and non–small-cell lung carcinomas.1,2 Metastases to the hand are most commonly caused by bronchogenic carcinomas,1-7 whereas foot metastases are seen with tumors originating in the gastrointestinal or genitourinary tracts.6,7 The most commonly involved bones are the phalanges in the hand and the tarsal bones in the foot.7,8 Acrometastases account for about 1 out of 500 lung cancers that present with bony metastases.2 Prognosis is grim, with a mean survival of 3– 6 months after presentation.1,2 Although acrometastasis from lung cancer itself is rare, occult lung cancer presenting as metastasis to the finger is even more unusual.

A57-year-old Caucasian man with a 32 pack-year history of smoking presented to the prime care clinic with a 2-week history of left index finger pain, redness, and swelling after sustaining a minor injury while closing his car door. Physical examination revealed a blackish discoloration of the skin. An X-ray of his left hand showed complete demineralization of the distal phalanx of the left index finger (Figure 1). The pain did not respond to NSAIDS, narcotics, and antibiotics. He subsequently underwent partial amputation of the finger. Pathology from the surgical specimen revealed a “poorly differentiated metastatic small-cell carcinoma” (Figure 2). He denied any dyspnea, cough, fever, night sweats, or loss of weight or appetite. The results of a computerized tomography scan of his thorax (Figure 3), abdomen, and pelvis revealed a large right lower lobe lung mass of 6.2 cm
4.2 cm adjacent to the right lower lobe bronchus that was consistent with lung cancer associated with pulmonary, hepatic, nodal, and skeletal metastasis. Magnetic resonance imaging of the brain showed multiple metastatic lesions throughout the brain, including the cerebellum. An MRI of the spine showed extensive metastatic lesions involving the thoracic vertebrae, T4 –T12, and the lumbar vertebra, L2. Given the extensive metastases and poor prognosis, the patient chose hospice care and palliative services. Discussion Digital acrometastases represent only 0.1% of all skeletal metastases.1 They have been described with various malignancies, including breast, gastrointestinal tract, head and neck, and small-cell and non–small-cell lung carcinomas.1,2 Metastases to the hand are most commonly caused by bronchogenic carcinomas,1-7 whereas foot metastases are seen with tumors originating in the gastrointestinal or genitourinary tracts.6,7 The most commonly involved bones are the phalanges in the hand and the tarsal bones in the foot.7,8 Acrometastases account for about 1 out of 500 lung cancers that present with bony metastases.2 Prognosis is grim, with a mean survival of 3– 6 months after presentation.1,2 Although acrometastasis from lung cancer itself is rare, occult lung cancer presenting as metastasis to the finger is even more unusual.

A57-year-old Caucasian man with a 32 pack-year history of smoking presented to the prime care clinic with a 2-week history of left index finger pain, redness, and swelling after sustaining a minor injury while closing his car door. Physical examination revealed a blackish discoloration of the skin. An X-ray of his left hand showed complete demineralization of the distal phalanx of the left index finger (Figure 1). The pain did not respond to NSAIDS, narcotics, and antibiotics. He subsequently underwent partial amputation of the finger. Pathology from the surgical specimen revealed a “poorly differentiated metastatic small-cell carcinoma” (Figure 2). He denied any dyspnea, cough, fever, night sweats, or loss of weight or appetite. The results of a computerized tomography scan of his thorax (Figure 3), abdomen, and pelvis revealed a large right lower lobe lung mass of 6.2 cm
4.2 cm adjacent to the right lower lobe bronchus that was consistent with lung cancer associated with pulmonary, hepatic, nodal, and skeletal metastasis. Magnetic resonance imaging of the brain showed multiple metastatic lesions throughout the brain, including the cerebellum. An MRI of the spine showed extensive metastatic lesions involving the thoracic vertebrae, T4 –T12, and the lumbar vertebra, L2. Given the extensive metastases and poor prognosis, the patient chose hospice care and palliative services. Discussion Digital acrometastases represent only 0.1% of all skeletal metastases.1 They have been described with various malignancies, including breast, gastrointestinal tract, head and neck, and small-cell and non–small-cell lung carcinomas.1,2 Metastases to the hand are most commonly caused by bronchogenic carcinomas,1-7 whereas foot metastases are seen with tumors originating in the gastrointestinal or genitourinary tracts.6,7 The most commonly involved bones are the phalanges in the hand and the tarsal bones in the foot.7,8 Acrometastases account for about 1 out of 500 lung cancers that present with bony metastases.2 Prognosis is grim, with a mean survival of 3– 6 months after presentation.1,2 Although acrometastasis from lung cancer itself is rare, occult lung cancer presenting as metastasis to the finger is even more unusual.

Enthusiasm continues in the medical community anxious for effective agents for men with metastatic castration-resistant prostate cancer (mCRPC). Most prostate cancer patients who develop metastatic disease are initially treated with readily available luteinizing hormone-releasing hormone (LHRH) agonists or antagonists, with or without an anti-androgen. The rationale here is to decrease androgen levels and/or block androgen receptor (AR) binding. In patients whose disease becomes refractory to this front-line hormonal deprivation, the molecular mechanisms involved in androgen independence include androgen receptor gene amplification, AR mutations that allow stimulation by a variety of weak androgens, and AR activation by autocrine production of androgens from tumor cells. Patients with metastatic castration-resistant prostate cancer (mCRPC) who biochemically recur after androgendeprivation therapy with significant prostate-specific antigen (PSA) elevations and/or who develop radiographic or symptomatic metastases are then usually considered for cytotoxic chemotherapy. The only approved initial cytotoxic chemotherapeutic agent that has demonstrated improved survival for patients with mCRPC is docetaxel. For patients who fail docetaxel, cabazitaxel with prednisone is an approved second-line treatment. Similarly, another approved second-line treatment (albeit, hormonal) for patients who have failed docetaxel therapy is abiraterone acetate, which attacks the adrenal and extragonadal synthesis of androgen. The magnitude of this effect was not appreciated until it was recognized that the androgen receptor and ligand-dependent androgen receptor signaling remain active and upregulated in men with castrate levels of testosterone (
50 ng/dL).1 Recognition of the importance of the signaling of the androgen receptor and its seemingly independent behavior in a milieu of little or no androgen is now appreciated.

Enthusiasm continues in the medical community anxious for effective agents for men with metastatic castration-resistant prostate cancer (mCRPC). Most prostate cancer patients who develop metastatic disease are initially treated with readily available luteinizing hormone-releasing hormone (LHRH) agonists or antagonists, with or without an anti-androgen. The rationale here is to decrease androgen levels and/or block androgen receptor (AR) binding. In patients whose disease becomes refractory to this front-line hormonal deprivation, the molecular mechanisms involved in androgen independence include androgen receptor gene amplification, AR mutations that allow stimulation by a variety of weak androgens, and AR activation by autocrine production of androgens from tumor cells. Patients with metastatic castration-resistant prostate cancer (mCRPC) who biochemically recur after androgendeprivation therapy with significant prostate-specific antigen (PSA) elevations and/or who develop radiographic or symptomatic metastases are then usually considered for cytotoxic chemotherapy. The only approved initial cytotoxic chemotherapeutic agent that has demonstrated improved survival for patients with mCRPC is docetaxel. For patients who fail docetaxel, cabazitaxel with prednisone is an approved second-line treatment. Similarly, another approved second-line treatment (albeit, hormonal) for patients who have failed docetaxel therapy is abiraterone acetate, which attacks the adrenal and extragonadal synthesis of androgen. The magnitude of this effect was not appreciated until it was recognized that the androgen receptor and ligand-dependent androgen receptor signaling remain active and upregulated in men with castrate levels of testosterone (
50 ng/dL).1 Recognition of the importance of the signaling of the androgen receptor and its seemingly independent behavior in a milieu of little or no androgen is now appreciated.

Enthusiasm continues in the medical community anxious for effective agents for men with metastatic castration-resistant prostate cancer (mCRPC). Most prostate cancer patients who develop metastatic disease are initially treated with readily available luteinizing hormone-releasing hormone (LHRH) agonists or antagonists, with or without an anti-androgen. The rationale here is to decrease androgen levels and/or block androgen receptor (AR) binding. In patients whose disease becomes refractory to this front-line hormonal deprivation, the molecular mechanisms involved in androgen independence include androgen receptor gene amplification, AR mutations that allow stimulation by a variety of weak androgens, and AR activation by autocrine production of androgens from tumor cells. Patients with metastatic castration-resistant prostate cancer (mCRPC) who biochemically recur after androgendeprivation therapy with significant prostate-specific antigen (PSA) elevations and/or who develop radiographic or symptomatic metastases are then usually considered for cytotoxic chemotherapy. The only approved initial cytotoxic chemotherapeutic agent that has demonstrated improved survival for patients with mCRPC is docetaxel. For patients who fail docetaxel, cabazitaxel with prednisone is an approved second-line treatment. Similarly, another approved second-line treatment (albeit, hormonal) for patients who have failed docetaxel therapy is abiraterone acetate, which attacks the adrenal and extragonadal synthesis of androgen. The magnitude of this effect was not appreciated until it was recognized that the androgen receptor and ligand-dependent androgen receptor signaling remain active and upregulated in men with castrate levels of testosterone (
50 ng/dL).1 Recognition of the importance of the signaling of the androgen receptor and its seemingly independent behavior in a milieu of little or no androgen is now appreciated.

The effects of sequestration-related cuts on oncology practices have kicked in. In early April, Sarah Kliff, a blogger at The Washington Post, reported that cancer clinics had already started turning away Medicare patients because the funding cuts would make it impossible for them to continue treating their chemotherapy patients and avoid financial ruin.1 In early May, a month after the April 1 cuts took effect, we already had 2 separate survey reports, one from the American Society of Clinical Oncology (ASCO), the other from the Community Oncology Alliance (COA), that showed that the 2% cut in Medicare reimbursement had caused oncology practices “to make signifi- cant shifts in how they do business and care for patients.”2 ASCO surveyed 500 of its members (41% in suburban settings; 41%, in urban; 16%, in rural). In all, 80% of respondents said sequestration was affecting their practices, and about 75% said they were having trouble paying for chemotherapy drugs. Half of the respondents said they could care only for patients who had other sources of income independent of Medicare, 14% had stopped seeing Medicare patients, and half said they were sending their Medicare patients to outpatient infusion centers for their chemotherapy. ASCO president Sandra Swain expressed concern that some patients’ care was being disrupted and compromised, which could be detrimental to the clinical outcomes and emotional well-being of these fragile individuals, and she warned in a statement that the society’s initial findings “may just be the tip of the iceberg.”³ The fact that a quarter of respondents reported that they were planning to close satellite clinics should also raise concerns about the impact such closures might have on research and participation in clinical trials.

The effects of sequestration-related cuts on oncology practices have kicked in. In early April, Sarah Kliff, a blogger at The Washington Post, reported that cancer clinics had already started turning away Medicare patients because the funding cuts would make it impossible for them to continue treating their chemotherapy patients and avoid financial ruin.1 In early May, a month after the April 1 cuts took effect, we already had 2 separate survey reports, one from the American Society of Clinical Oncology (ASCO), the other from the Community Oncology Alliance (COA), that showed that the 2% cut in Medicare reimbursement had caused oncology practices “to make signifi- cant shifts in how they do business and care for patients.”2 ASCO surveyed 500 of its members (41% in suburban settings; 41%, in urban; 16%, in rural). In all, 80% of respondents said sequestration was affecting their practices, and about 75% said they were having trouble paying for chemotherapy drugs. Half of the respondents said they could care only for patients who had other sources of income independent of Medicare, 14% had stopped seeing Medicare patients, and half said they were sending their Medicare patients to outpatient infusion centers for their chemotherapy. ASCO president Sandra Swain expressed concern that some patients’ care was being disrupted and compromised, which could be detrimental to the clinical outcomes and emotional well-being of these fragile individuals, and she warned in a statement that the society’s initial findings “may just be the tip of the iceberg.”³ The fact that a quarter of respondents reported that they were planning to close satellite clinics should also raise concerns about the impact such closures might have on research and participation in clinical trials.

The effects of sequestration-related cuts on oncology practices have kicked in. In early April, Sarah Kliff, a blogger at The Washington Post, reported that cancer clinics had already started turning away Medicare patients because the funding cuts would make it impossible for them to continue treating their chemotherapy patients and avoid financial ruin.1 In early May, a month after the April 1 cuts took effect, we already had 2 separate survey reports, one from the American Society of Clinical Oncology (ASCO), the other from the Community Oncology Alliance (COA), that showed that the 2% cut in Medicare reimbursement had caused oncology practices “to make signifi- cant shifts in how they do business and care for patients.”2 ASCO surveyed 500 of its members (41% in suburban settings; 41%, in urban; 16%, in rural). In all, 80% of respondents said sequestration was affecting their practices, and about 75% said they were having trouble paying for chemotherapy drugs. Half of the respondents said they could care only for patients who had other sources of income independent of Medicare, 14% had stopped seeing Medicare patients, and half said they were sending their Medicare patients to outpatient infusion centers for their chemotherapy. ASCO president Sandra Swain expressed concern that some patients’ care was being disrupted and compromised, which could be detrimental to the clinical outcomes and emotional well-being of these fragile individuals, and she warned in a statement that the society’s initial findings “may just be the tip of the iceberg.”³ The fact that a quarter of respondents reported that they were planning to close satellite clinics should also raise concerns about the impact such closures might have on research and participation in clinical trials.

BUENA VISTA, FLA – The cups and ribbons that young athletes bring home sometimes come with a price – injuries that can sideline them for a few games or haunt them for the rest of their lives.

Teenagers are more likely than adults to sustain sports injuries, Dr. Ilene Claudius said at a meeting sponsored by the American College of Emergency Physicians and the American Academy of Pediatrics. Immature bones, strong tendons, and a general tendency to brush off aches and pains all conspire to increase the risk.

Open epiphyseal plates are always points of weakness on a growing bone, said Dr. Claudius of the University of Southern California, Los Angeles. "During periods of rapid growth, the epiphyses are incredibly weak, so boys in their early teens get a lot of sports injuries. They also have strong tendons that insert there and set those kids up for inflammation."

Most of these stress injuries occur in runners, jumpers, and dancers, she said – but they can be seen in those who play other sports. The risk is highest in two periods during a young athlete’s career – just as they delve enthusiastically into their sport and when they reach an elite level, during which time physical efforts grow even more demanding.

"Think about what that person has been doing that might predispose him to an injury: the couch potato who has been doing nothing for 12 years and then starts running every day, the elite athlete who excels in a sport and never deviates from that sport, or the athlete who has played a single sport for years and then takes up a new one, which uses an entirely different set of muscles and bones."

Muscles and bones grow rapidly to accommodate new activities, Dr. Claudius said. Muscles increase in mass and pull on bones, increasing bone mass. It takes a full 14 months for skeletal remodeling. But, in the meantime, when bone absorption outstrips bone repair, stress fractures can occur.

With some ice, rest, and NSAIDs, most of these injuries will heal within 8 weeks. Occasionally, stress fractures appear in more concerning places, like the navicular bone, femur, or femoral neck "These have a higher risk of complete fracture, so they need more aggressive treatment."

Gymnastics, football, and wrestling predispose athletes to hyperextension injuries. Symptoms include lower back pain that radiates to the buttocks and gets worse with exercise. Affected teens can present with paresthesia. These patients usually respond to a few months of activity modification and some physical therapy.

Repetitive hyperextension injuries can leave a lasting effect in the form of traction apophysitis, impingement of the spinous processes, or pseudoarthrosis of the transitional vertebrae.

Concussion is probably the most-feared sports injury. Every time an athlete sustains a concussion, the chances of getting another are increased and the time it takes to recover is extended.

Repeated head trauma can lead to a chronic traumatic encephalopathy. The latency period is 6-10 years, after which the athlete may begin to express emotional disorders, paranoia, memory problems, and even suicidal ideation. "Pathologically, it looks a lot like Alzheimer’s," Dr. Claudius said.

Concussion isn’t always easy to identify on the field or in the emergency department. Preseason neurocognitive testing can make diagnosis easier. "This gives you a baseline; if a concussion is present, the score typically decreases by 10% or more."

While adults typically return to normal in 4 or 5 days, research shows that young people have a much longer recovery time. For a teenager, up to 3 weeks or recovery is not unusual. Any kind of return to full play is absolutely contraindicated during recovery, and resting the brain is just as important as resting other parts of the body.

Cognitive rest can be a difficult concept for the teen to grasp. Dr. Claudius said. "We always need to tailor our message to the audience, and in this case, our audience is an adolescent. A week of cognitive rest means more than just a few days off school. It means not staying up late; it means no texting or video games. It means no sex."

When symptoms recede to mild – for example, sustained attention for 30 minutes without the return of somatic symptoms- the teen can take on a limited amount of school work. It’s important to get up out of bed and start returning to regular activities, with the exception of sports.

"They should avoid aerobic activity until they’re completely asymptomatic," Dr. Claudius said. "Then there can be a careful program that includes light aerobic exercise."

This should be followed by sport-specific training, then noncontact training, followed by full contact practice and, finally, returning to the game.

"Athletes should stay at each level until are completely asymptomatic for 24 hours. If they become symptomatic, they need to drop back to the prior level and stay there until they are."

Dr. Claudius had no financial disclosures.

[email protected]

BUENA VISTA, FLA – The cups and ribbons that young athletes bring home sometimes come with a price – injuries that can sideline them for a few games or haunt them for the rest of their lives.

Teenagers are more likely than adults to sustain sports injuries, Dr. Ilene Claudius said at a meeting sponsored by the American College of Emergency Physicians and the American Academy of Pediatrics. Immature bones, strong tendons, and a general tendency to brush off aches and pains all conspire to increase the risk.

Open epiphyseal plates are always points of weakness on a growing bone, said Dr. Claudius of the University of Southern California, Los Angeles. "During periods of rapid growth, the epiphyses are incredibly weak, so boys in their early teens get a lot of sports injuries. They also have strong tendons that insert there and set those kids up for inflammation."

Most of these stress injuries occur in runners, jumpers, and dancers, she said – but they can be seen in those who play other sports. The risk is highest in two periods during a young athlete’s career – just as they delve enthusiastically into their sport and when they reach an elite level, during which time physical efforts grow even more demanding.

"Think about what that person has been doing that might predispose him to an injury: the couch potato who has been doing nothing for 12 years and then starts running every day, the elite athlete who excels in a sport and never deviates from that sport, or the athlete who has played a single sport for years and then takes up a new one, which uses an entirely different set of muscles and bones."

Muscles and bones grow rapidly to accommodate new activities, Dr. Claudius said. Muscles increase in mass and pull on bones, increasing bone mass. It takes a full 14 months for skeletal remodeling. But, in the meantime, when bone absorption outstrips bone repair, stress fractures can occur.

With some ice, rest, and NSAIDs, most of these injuries will heal within 8 weeks. Occasionally, stress fractures appear in more concerning places, like the navicular bone, femur, or femoral neck "These have a higher risk of complete fracture, so they need more aggressive treatment."

Gymnastics, football, and wrestling predispose athletes to hyperextension injuries. Symptoms include lower back pain that radiates to the buttocks and gets worse with exercise. Affected teens can present with paresthesia. These patients usually respond to a few months of activity modification and some physical therapy.

Repetitive hyperextension injuries can leave a lasting effect in the form of traction apophysitis, impingement of the spinous processes, or pseudoarthrosis of the transitional vertebrae.

Concussion is probably the most-feared sports injury. Every time an athlete sustains a concussion, the chances of getting another are increased and the time it takes to recover is extended.

Repeated head trauma can lead to a chronic traumatic encephalopathy. The latency period is 6-10 years, after which the athlete may begin to express emotional disorders, paranoia, memory problems, and even suicidal ideation. "Pathologically, it looks a lot like Alzheimer’s," Dr. Claudius said.

Concussion isn’t always easy to identify on the field or in the emergency department. Preseason neurocognitive testing can make diagnosis easier. "This gives you a baseline; if a concussion is present, the score typically decreases by 10% or more."

While adults typically return to normal in 4 or 5 days, research shows that young people have a much longer recovery time. For a teenager, up to 3 weeks or recovery is not unusual. Any kind of return to full play is absolutely contraindicated during recovery, and resting the brain is just as important as resting other parts of the body.

Cognitive rest can be a difficult concept for the teen to grasp. Dr. Claudius said. "We always need to tailor our message to the audience, and in this case, our audience is an adolescent. A week of cognitive rest means more than just a few days off school. It means not staying up late; it means no texting or video games. It means no sex."

When symptoms recede to mild – for example, sustained attention for 30 minutes without the return of somatic symptoms- the teen can take on a limited amount of school work. It’s important to get up out of bed and start returning to regular activities, with the exception of sports.

"They should avoid aerobic activity until they’re completely asymptomatic," Dr. Claudius said. "Then there can be a careful program that includes light aerobic exercise."

This should be followed by sport-specific training, then noncontact training, followed by full contact practice and, finally, returning to the game.

"Athletes should stay at each level until are completely asymptomatic for 24 hours. If they become symptomatic, they need to drop back to the prior level and stay there until they are."

Dr. Claudius had no financial disclosures.

[email protected]

BUENA VISTA, FLA – The cups and ribbons that young athletes bring home sometimes come with a price – injuries that can sideline them for a few games or haunt them for the rest of their lives.

Teenagers are more likely than adults to sustain sports injuries, Dr. Ilene Claudius said at a meeting sponsored by the American College of Emergency Physicians and the American Academy of Pediatrics. Immature bones, strong tendons, and a general tendency to brush off aches and pains all conspire to increase the risk.

Open epiphyseal plates are always points of weakness on a growing bone, said Dr. Claudius of the University of Southern California, Los Angeles. "During periods of rapid growth, the epiphyses are incredibly weak, so boys in their early teens get a lot of sports injuries. They also have strong tendons that insert there and set those kids up for inflammation."

Most of these stress injuries occur in runners, jumpers, and dancers, she said – but they can be seen in those who play other sports. The risk is highest in two periods during a young athlete’s career – just as they delve enthusiastically into their sport and when they reach an elite level, during which time physical efforts grow even more demanding.

"Think about what that person has been doing that might predispose him to an injury: the couch potato who has been doing nothing for 12 years and then starts running every day, the elite athlete who excels in a sport and never deviates from that sport, or the athlete who has played a single sport for years and then takes up a new one, which uses an entirely different set of muscles and bones."

Muscles and bones grow rapidly to accommodate new activities, Dr. Claudius said. Muscles increase in mass and pull on bones, increasing bone mass. It takes a full 14 months for skeletal remodeling. But, in the meantime, when bone absorption outstrips bone repair, stress fractures can occur.

With some ice, rest, and NSAIDs, most of these injuries will heal within 8 weeks. Occasionally, stress fractures appear in more concerning places, like the navicular bone, femur, or femoral neck "These have a higher risk of complete fracture, so they need more aggressive treatment."

Gymnastics, football, and wrestling predispose athletes to hyperextension injuries. Symptoms include lower back pain that radiates to the buttocks and gets worse with exercise. Affected teens can present with paresthesia. These patients usually respond to a few months of activity modification and some physical therapy.

Repetitive hyperextension injuries can leave a lasting effect in the form of traction apophysitis, impingement of the spinous processes, or pseudoarthrosis of the transitional vertebrae.

Concussion is probably the most-feared sports injury. Every time an athlete sustains a concussion, the chances of getting another are increased and the time it takes to recover is extended.

Repeated head trauma can lead to a chronic traumatic encephalopathy. The latency period is 6-10 years, after which the athlete may begin to express emotional disorders, paranoia, memory problems, and even suicidal ideation. "Pathologically, it looks a lot like Alzheimer’s," Dr. Claudius said.

Concussion isn’t always easy to identify on the field or in the emergency department. Preseason neurocognitive testing can make diagnosis easier. "This gives you a baseline; if a concussion is present, the score typically decreases by 10% or more."

While adults typically return to normal in 4 or 5 days, research shows that young people have a much longer recovery time. For a teenager, up to 3 weeks or recovery is not unusual. Any kind of return to full play is absolutely contraindicated during recovery, and resting the brain is just as important as resting other parts of the body.

Cognitive rest can be a difficult concept for the teen to grasp. Dr. Claudius said. "We always need to tailor our message to the audience, and in this case, our audience is an adolescent. A week of cognitive rest means more than just a few days off school. It means not staying up late; it means no texting or video games. It means no sex."

When symptoms recede to mild – for example, sustained attention for 30 minutes without the return of somatic symptoms- the teen can take on a limited amount of school work. It’s important to get up out of bed and start returning to regular activities, with the exception of sports.

"They should avoid aerobic activity until they’re completely asymptomatic," Dr. Claudius said. "Then there can be a careful program that includes light aerobic exercise."

This should be followed by sport-specific training, then noncontact training, followed by full contact practice and, finally, returning to the game.

"Athletes should stay at each level until are completely asymptomatic for 24 hours. If they become symptomatic, they need to drop back to the prior level and stay there until they are."

Dr. Claudius had no financial disclosures.

[email protected]

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Dr. Flanders

SHM has named its 2013-2014 board of directors and three new Masters in Hospital Medicine, the highest designation in the HM specialty.

The Master in Hospital Medicine (MHM) designation is reserved for hospitalists who have distinguished themselves in the specialty through the excellence and significance of their contributions to hospital medicine and health care as a whole. Nominations were reviewed by SHM’s Masters Selection Committee and the board of directors. The MHM designation was introduced in 2010; this year’s designees bring the total number of MHMs to 13.

The 2013 Masters in Hospital Medicine are:

Dr. Flanders

Scott A. Flanders, MD, MHM, professor in the division of general internal medicine at the University of Michigan in Ann Arbor, where he serves as associate division chief of general medicine for inpatient programs and associate director of inpatient programs for the department of internal medicine. He is also the director of the University of Michigan’s hospitalist program.

Dr. Meltzer

David O. Meltzer, MD, PhD, MHM, chief of the section of hospital medicine, director of the Center for Health and the Social Sciences, associate professor in the medicine and economics departments and the Harris School of Public Policy Studies, at the University of Chicago.

Dr. Wiese

Jeffrey G. Wiese, MD, MHM, professor of medicine and associate dean for graduate medical education at the Tulane University Health Sciences Center, as well as associate chair of medicine and the chief of the charity medical service. He is also the director of Tulane’s internal-medicine residency program.

The new MHMs will take the stage to officially be inducted, along with more than 200 Fellows and Senior Fellows, on May 18 at HM13, SHM’s annual meeting (www.hospitalmedicine2013.org) at the Gaylord National Resort and Conference Center in National Harbor, Md.

“SHM’s Masters in Hospital Medicine are truly the hall of fame of the hospital medicine specialty,” says SHM President Shaun Frost, MD, SFHM. “It is an honor to recognize their contributions to hospitalists and patients alike.”

Nominations for all three levels of SHM’s Fellows program are accepted throughout the year. For details, visit www.hospitalmedicine.org/fellows.

SHM also announced the election of three new board members; each will serve a three-year term beginning this month. The new board members are:

Dr. Epstein

Howard Epstein, MD, FHM, chief health systems officer at the Institute for Clinical Systems Improvement in Bloomington, Minn.

Dr. Sharpe

Bradley Sharpe, MD, FACP, SFHM, professor of medicine at the University of California at San Francisco’s department of medicine, associate program director for UCSF’s internal medicine residency program and associate division chief in the division of hospital medicine.

Dr. Torcson

Patrick J. Torcson, MD, MMM, SFHM, vice president and chief integration officer, and director of hospital medicine for St. Tammany Parish Hospital, Covington, La.

“We welcome these new faces to the SHM board of directors and appreciate the commitment of their time and expertise to the goals of SHM, hospitalists, and hospitalized patients everywhere,” Dr. Frost says.

For more information about SHM’s leadership and nomination process, visit www.hospitalmedicine.org.

Brendon Shank is SHM’s associate vice president of communications.

Dr. Flanders

SHM has named its 2013-2014 board of directors and three new Masters in Hospital Medicine, the highest designation in the HM specialty.

The Master in Hospital Medicine (MHM) designation is reserved for hospitalists who have distinguished themselves in the specialty through the excellence and significance of their contributions to hospital medicine and health care as a whole. Nominations were reviewed by SHM’s Masters Selection Committee and the board of directors. The MHM designation was introduced in 2010; this year’s designees bring the total number of MHMs to 13.

The 2013 Masters in Hospital Medicine are:

Dr. Flanders

Scott A. Flanders, MD, MHM, professor in the division of general internal medicine at the University of Michigan in Ann Arbor, where he serves as associate division chief of general medicine for inpatient programs and associate director of inpatient programs for the department of internal medicine. He is also the director of the University of Michigan’s hospitalist program.

Dr. Meltzer

David O. Meltzer, MD, PhD, MHM, chief of the section of hospital medicine, director of the Center for Health and the Social Sciences, associate professor in the medicine and economics departments and the Harris School of Public Policy Studies, at the University of Chicago.

Dr. Wiese

Jeffrey G. Wiese, MD, MHM, professor of medicine and associate dean for graduate medical education at the Tulane University Health Sciences Center, as well as associate chair of medicine and the chief of the charity medical service. He is also the director of Tulane’s internal-medicine residency program.

The new MHMs will take the stage to officially be inducted, along with more than 200 Fellows and Senior Fellows, on May 18 at HM13, SHM’s annual meeting (www.hospitalmedicine2013.org) at the Gaylord National Resort and Conference Center in National Harbor, Md.

“SHM’s Masters in Hospital Medicine are truly the hall of fame of the hospital medicine specialty,” says SHM President Shaun Frost, MD, SFHM. “It is an honor to recognize their contributions to hospitalists and patients alike.”

Nominations for all three levels of SHM’s Fellows program are accepted throughout the year. For details, visit www.hospitalmedicine.org/fellows.

SHM also announced the election of three new board members; each will serve a three-year term beginning this month. The new board members are:

Dr. Epstein

Howard Epstein, MD, FHM, chief health systems officer at the Institute for Clinical Systems Improvement in Bloomington, Minn.

Dr. Sharpe

Bradley Sharpe, MD, FACP, SFHM, professor of medicine at the University of California at San Francisco’s department of medicine, associate program director for UCSF’s internal medicine residency program and associate division chief in the division of hospital medicine.

Dr. Torcson

Patrick J. Torcson, MD, MMM, SFHM, vice president and chief integration officer, and director of hospital medicine for St. Tammany Parish Hospital, Covington, La.

“We welcome these new faces to the SHM board of directors and appreciate the commitment of their time and expertise to the goals of SHM, hospitalists, and hospitalized patients everywhere,” Dr. Frost says.

For more information about SHM’s leadership and nomination process, visit www.hospitalmedicine.org.

Brendon Shank is SHM’s associate vice president of communications.

Dr. Flanders

SHM has named its 2013-2014 board of directors and three new Masters in Hospital Medicine, the highest designation in the HM specialty.

The Master in Hospital Medicine (MHM) designation is reserved for hospitalists who have distinguished themselves in the specialty through the excellence and significance of their contributions to hospital medicine and health care as a whole. Nominations were reviewed by SHM’s Masters Selection Committee and the board of directors. The MHM designation was introduced in 2010; this year’s designees bring the total number of MHMs to 13.

The 2013 Masters in Hospital Medicine are:

Dr. Flanders

Scott A. Flanders, MD, MHM, professor in the division of general internal medicine at the University of Michigan in Ann Arbor, where he serves as associate division chief of general medicine for inpatient programs and associate director of inpatient programs for the department of internal medicine. He is also the director of the University of Michigan’s hospitalist program.

Dr. Meltzer

David O. Meltzer, MD, PhD, MHM, chief of the section of hospital medicine, director of the Center for Health and the Social Sciences, associate professor in the medicine and economics departments and the Harris School of Public Policy Studies, at the University of Chicago.

Dr. Wiese

Jeffrey G. Wiese, MD, MHM, professor of medicine and associate dean for graduate medical education at the Tulane University Health Sciences Center, as well as associate chair of medicine and the chief of the charity medical service. He is also the director of Tulane’s internal-medicine residency program.

The new MHMs will take the stage to officially be inducted, along with more than 200 Fellows and Senior Fellows, on May 18 at HM13, SHM’s annual meeting (www.hospitalmedicine2013.org) at the Gaylord National Resort and Conference Center in National Harbor, Md.

“SHM’s Masters in Hospital Medicine are truly the hall of fame of the hospital medicine specialty,” says SHM President Shaun Frost, MD, SFHM. “It is an honor to recognize their contributions to hospitalists and patients alike.”

Nominations for all three levels of SHM’s Fellows program are accepted throughout the year. For details, visit www.hospitalmedicine.org/fellows.

SHM also announced the election of three new board members; each will serve a three-year term beginning this month. The new board members are:

Dr. Epstein

Howard Epstein, MD, FHM, chief health systems officer at the Institute for Clinical Systems Improvement in Bloomington, Minn.

Dr. Sharpe

Bradley Sharpe, MD, FACP, SFHM, professor of medicine at the University of California at San Francisco’s department of medicine, associate program director for UCSF’s internal medicine residency program and associate division chief in the division of hospital medicine.

Dr. Torcson

Patrick J. Torcson, MD, MMM, SFHM, vice president and chief integration officer, and director of hospital medicine for St. Tammany Parish Hospital, Covington, La.

“We welcome these new faces to the SHM board of directors and appreciate the commitment of their time and expertise to the goals of SHM, hospitalists, and hospitalized patients everywhere,” Dr. Frost says.

For more information about SHM’s leadership and nomination process, visit www.hospitalmedicine.org.

Brendon Shank is SHM’s associate vice president of communications.

Dr. Bryan Huang, MD

Dr. Bryan Huang, MD

Dr. Grace Huang

In July 2011, the Accreditation Council for Graduate Medical Education (ACGME) implemented new duty-hour restrictions on resident physicians. Among other changes, interns were restricted to a maximum of 16 hours of continuous duty. New rules also limited second-year residents and above to 24 hours of continuous duty, plus up to four additional hours for transition and educational activities. Recommendations were made for strategic napping, greater supervision requirements, and a minimum of eight to 10 hours off between shifts.

The 2012 State of Hospital Medicine report, which is based on 2011 data encompassing the period of these duty-hour changes, takes a systematic look at how academic HM practices have adjusted to the new resident rules. The most notable changes have been the addition of physician FTEs (51.3% of adult academic HM practices have done so) and nurse practitioners or physician assistants (23%). Additional common responses to resident work-hour limitations are listed in Table 1.

Dr. Bryan Huang, MD

These data underscore the immensity of changes academic HM groups have faced as a result of new work-hour limitations, as the majority of internal-medicine residents work with hospitalist attendings on inpatient medicine rotations. House staff no longer can be used as an inexpensive source of labor, given limitations on service and new expectations for resident education and supervision.

As others have commented on this topic in The Hospitalist, the role of the academic hospitalist is being redefined. No longer is academic HM synonymous with teaching alone; the clinical duties of many academic hospitalists now include a combination of teaching and non-teaching services, often with some night coverage. At our hospitals in San Diego and Boston, for instance, changes incurred due to work-hour restrictions include elimination of house staff coverage from one of the medical center’s hospitals and a significant increase in nonteaching service responsibilities across all hospitalists. An alternative approach that some programs have embraced is the recruitment of separate cadres of teaching and nonteaching hospitalists, which might result in markedly different professional expectations within the same group or institution.

Trends shifting clinical work from residents to hospitalists are likely to continue, no doubt increasing demand for hospitalists and physician extenders. In the past, the combination of less expensive resident labor and lower salaries in academia was financially favorable for hospitals. Due to resident duty-hour limitations, academic hospitalist groups have had to negotiate not only for additional hires, but, in many instances, also higher salaries commensurate with nonteaching work.

Given the impact on a hospital’s finances, academic HM practices have had to look more closely at clinical volumes and productivity, making protected time for nonclinical pursuits more difficult to come by. Alignment of hospitalists’ interests with those of hospital administrators through performance-improvement projects (e.g. reducing length of stay, readmissions, or nosocomial infections) will be crucial to the financial viability of the academic HM practice, and leadership in these areas will define and differentiate academic hospitalists in the future.

Dr. Bryan Huang, who works in Boston, and Dr. Grace Huang, who works in San Diego, both are members of SHM’s Practice Analysis Committee.

Dr. Bryan Huang, MD

Dr. Bryan Huang, MD

Dr. Grace Huang

In July 2011, the Accreditation Council for Graduate Medical Education (ACGME) implemented new duty-hour restrictions on resident physicians. Among other changes, interns were restricted to a maximum of 16 hours of continuous duty. New rules also limited second-year residents and above to 24 hours of continuous duty, plus up to four additional hours for transition and educational activities. Recommendations were made for strategic napping, greater supervision requirements, and a minimum of eight to 10 hours off between shifts.

The 2012 State of Hospital Medicine report, which is based on 2011 data encompassing the period of these duty-hour changes, takes a systematic look at how academic HM practices have adjusted to the new resident rules. The most notable changes have been the addition of physician FTEs (51.3% of adult academic HM practices have done so) and nurse practitioners or physician assistants (23%). Additional common responses to resident work-hour limitations are listed in Table 1.

Dr. Bryan Huang, MD

These data underscore the immensity of changes academic HM groups have faced as a result of new work-hour limitations, as the majority of internal-medicine residents work with hospitalist attendings on inpatient medicine rotations. House staff no longer can be used as an inexpensive source of labor, given limitations on service and new expectations for resident education and supervision.

As others have commented on this topic in The Hospitalist, the role of the academic hospitalist is being redefined. No longer is academic HM synonymous with teaching alone; the clinical duties of many academic hospitalists now include a combination of teaching and non-teaching services, often with some night coverage. At our hospitals in San Diego and Boston, for instance, changes incurred due to work-hour restrictions include elimination of house staff coverage from one of the medical center’s hospitals and a significant increase in nonteaching service responsibilities across all hospitalists. An alternative approach that some programs have embraced is the recruitment of separate cadres of teaching and nonteaching hospitalists, which might result in markedly different professional expectations within the same group or institution.

Trends shifting clinical work from residents to hospitalists are likely to continue, no doubt increasing demand for hospitalists and physician extenders. In the past, the combination of less expensive resident labor and lower salaries in academia was financially favorable for hospitals. Due to resident duty-hour limitations, academic hospitalist groups have had to negotiate not only for additional hires, but, in many instances, also higher salaries commensurate with nonteaching work.

Given the impact on a hospital’s finances, academic HM practices have had to look more closely at clinical volumes and productivity, making protected time for nonclinical pursuits more difficult to come by. Alignment of hospitalists’ interests with those of hospital administrators through performance-improvement projects (e.g. reducing length of stay, readmissions, or nosocomial infections) will be crucial to the financial viability of the academic HM practice, and leadership in these areas will define and differentiate academic hospitalists in the future.

Dr. Bryan Huang, who works in Boston, and Dr. Grace Huang, who works in San Diego, both are members of SHM’s Practice Analysis Committee.

Dr. Bryan Huang, MD

Dr. Bryan Huang, MD

Dr. Grace Huang

In July 2011, the Accreditation Council for Graduate Medical Education (ACGME) implemented new duty-hour restrictions on resident physicians. Among other changes, interns were restricted to a maximum of 16 hours of continuous duty. New rules also limited second-year residents and above to 24 hours of continuous duty, plus up to four additional hours for transition and educational activities. Recommendations were made for strategic napping, greater supervision requirements, and a minimum of eight to 10 hours off between shifts.

The 2012 State of Hospital Medicine report, which is based on 2011 data encompassing the period of these duty-hour changes, takes a systematic look at how academic HM practices have adjusted to the new resident rules. The most notable changes have been the addition of physician FTEs (51.3% of adult academic HM practices have done so) and nurse practitioners or physician assistants (23%). Additional common responses to resident work-hour limitations are listed in Table 1.

Dr. Bryan Huang, MD

These data underscore the immensity of changes academic HM groups have faced as a result of new work-hour limitations, as the majority of internal-medicine residents work with hospitalist attendings on inpatient medicine rotations. House staff no longer can be used as an inexpensive source of labor, given limitations on service and new expectations for resident education and supervision.

As others have commented on this topic in The Hospitalist, the role of the academic hospitalist is being redefined. No longer is academic HM synonymous with teaching alone; the clinical duties of many academic hospitalists now include a combination of teaching and non-teaching services, often with some night coverage. At our hospitals in San Diego and Boston, for instance, changes incurred due to work-hour restrictions include elimination of house staff coverage from one of the medical center’s hospitals and a significant increase in nonteaching service responsibilities across all hospitalists. An alternative approach that some programs have embraced is the recruitment of separate cadres of teaching and nonteaching hospitalists, which might result in markedly different professional expectations within the same group or institution.

Trends shifting clinical work from residents to hospitalists are likely to continue, no doubt increasing demand for hospitalists and physician extenders. In the past, the combination of less expensive resident labor and lower salaries in academia was financially favorable for hospitals. Due to resident duty-hour limitations, academic hospitalist groups have had to negotiate not only for additional hires, but, in many instances, also higher salaries commensurate with nonteaching work.

Given the impact on a hospital’s finances, academic HM practices have had to look more closely at clinical volumes and productivity, making protected time for nonclinical pursuits more difficult to come by. Alignment of hospitalists’ interests with those of hospital administrators through performance-improvement projects (e.g. reducing length of stay, readmissions, or nosocomial infections) will be crucial to the financial viability of the academic HM practice, and leadership in these areas will define and differentiate academic hospitalists in the future.

Dr. Bryan Huang, who works in Boston, and Dr. Grace Huang, who works in San Diego, both are members of SHM’s Practice Analysis Committee.

Medicare requires beneficiaries to have at least three consecutive days as a hospital inpatient to qualify for Medicare-covered skilled nursing facility (SNF) care. As the use and duration of observation status continues to rise throughout the nation, patients have been getting caught more frequently within a policy trap: Even though they are physically within the hospital and generally receive care that is indistinguishable from the care received by other inpatients, Medicare is not covering their subsequent SNF stays.

Why? Observation status is considered “outpatient” by both the hospital and Medicare and, therefore, is not counted toward Medicare’s three-day rule.

This leaves seniors on the hook for their skilled nursing care costs, which often exceed their ability to pay. Further, this shortsighted policy might actually result in a net greater cost to Medicare and the health-care system. Faced with mounting costs, many seniors truncate or opt out of SNF care altogether, leaving them vulnerable to added health issues (e.g. dehydration, falls). With new conditions that were not present at the time of the original hospital stay, many of these seniors are at risk to return to the hospital and become another readmission statistic.

As key players in hospitals and, increasingly, in skilled nursing facilities, hospitalists are caught squarely in the middle of this policy. Transitions of care both in and out of these institutions should be guided by sound medical decision-making, not whether Medicare will cover the costs incurred. Although the three-day rule—and, indeed, observation status itself—was originally cast as a cost-containment policy, such policies should incorporate broader care process and delivery reforms that do not add burden to patients when they are at their most vulnerable.

SHM affirms that it is sensible for Medicare to provide coverage for skilled nursing care if a clinician recommends it as part of a treatment plan. Coverage determination should not be beholden to a patient status subject to other systemic pressures, but should reflect the best interest of the patient and the care ordered by providers.

The Improving Access to Medicare Coverage Act, sponsored by Rep. Joe Courtney (D-Conn.), Rep. Tom Latham (R-Iowa), and Sen. Sherrod Brown (D-Ohio), would clarify the law to indicate that Medicare beneficiaries in observation status are deemed inpatients in the hospital for the purposes of the three-day requirement for SNF coverage. This simple adjustment would ensure that patients are able to access the skilled nursing care they need and that providers do not have to worry about this systemic barrier to patient care.

SHM is actively supporting this legislation. A letter of support was sent to Courtney and Brown earlier this year, and membership was mobilized to take action through our Legislative Action Center (www.hospitalmedicine.org/advocacy). Hospitalists also plan to voice their support for the legislation during Hospitalists on the Hill, to be held this month in conjunction with HM13.

As one of only a few specialty medical societies that are active on this issue, SHM stands out as a leader on health-care-system reforms that improve access to care for patients and reduce administrative barriers to medically appropriate care.

Joshua Lapps is SHM’s government relations specialist.

Medicare requires beneficiaries to have at least three consecutive days as a hospital inpatient to qualify for Medicare-covered skilled nursing facility (SNF) care. As the use and duration of observation status continues to rise throughout the nation, patients have been getting caught more frequently within a policy trap: Even though they are physically within the hospital and generally receive care that is indistinguishable from the care received by other inpatients, Medicare is not covering their subsequent SNF stays.

Why? Observation status is considered “outpatient” by both the hospital and Medicare and, therefore, is not counted toward Medicare’s three-day rule.

This leaves seniors on the hook for their skilled nursing care costs, which often exceed their ability to pay. Further, this shortsighted policy might actually result in a net greater cost to Medicare and the health-care system. Faced with mounting costs, many seniors truncate or opt out of SNF care altogether, leaving them vulnerable to added health issues (e.g. dehydration, falls). With new conditions that were not present at the time of the original hospital stay, many of these seniors are at risk to return to the hospital and become another readmission statistic.

As key players in hospitals and, increasingly, in skilled nursing facilities, hospitalists are caught squarely in the middle of this policy. Transitions of care both in and out of these institutions should be guided by sound medical decision-making, not whether Medicare will cover the costs incurred. Although the three-day rule—and, indeed, observation status itself—was originally cast as a cost-containment policy, such policies should incorporate broader care process and delivery reforms that do not add burden to patients when they are at their most vulnerable.

SHM affirms that it is sensible for Medicare to provide coverage for skilled nursing care if a clinician recommends it as part of a treatment plan. Coverage determination should not be beholden to a patient status subject to other systemic pressures, but should reflect the best interest of the patient and the care ordered by providers.

The Improving Access to Medicare Coverage Act, sponsored by Rep. Joe Courtney (D-Conn.), Rep. Tom Latham (R-Iowa), and Sen. Sherrod Brown (D-Ohio), would clarify the law to indicate that Medicare beneficiaries in observation status are deemed inpatients in the hospital for the purposes of the three-day requirement for SNF coverage. This simple adjustment would ensure that patients are able to access the skilled nursing care they need and that providers do not have to worry about this systemic barrier to patient care.

SHM is actively supporting this legislation. A letter of support was sent to Courtney and Brown earlier this year, and membership was mobilized to take action through our Legislative Action Center (www.hospitalmedicine.org/advocacy). Hospitalists also plan to voice their support for the legislation during Hospitalists on the Hill, to be held this month in conjunction with HM13.

As one of only a few specialty medical societies that are active on this issue, SHM stands out as a leader on health-care-system reforms that improve access to care for patients and reduce administrative barriers to medically appropriate care.

Joshua Lapps is SHM’s government relations specialist.

Medicare requires beneficiaries to have at least three consecutive days as a hospital inpatient to qualify for Medicare-covered skilled nursing facility (SNF) care. As the use and duration of observation status continues to rise throughout the nation, patients have been getting caught more frequently within a policy trap: Even though they are physically within the hospital and generally receive care that is indistinguishable from the care received by other inpatients, Medicare is not covering their subsequent SNF stays.

Why? Observation status is considered “outpatient” by both the hospital and Medicare and, therefore, is not counted toward Medicare’s three-day rule.

This leaves seniors on the hook for their skilled nursing care costs, which often exceed their ability to pay. Further, this shortsighted policy might actually result in a net greater cost to Medicare and the health-care system. Faced with mounting costs, many seniors truncate or opt out of SNF care altogether, leaving them vulnerable to added health issues (e.g. dehydration, falls). With new conditions that were not present at the time of the original hospital stay, many of these seniors are at risk to return to the hospital and become another readmission statistic.

As key players in hospitals and, increasingly, in skilled nursing facilities, hospitalists are caught squarely in the middle of this policy. Transitions of care both in and out of these institutions should be guided by sound medical decision-making, not whether Medicare will cover the costs incurred. Although the three-day rule—and, indeed, observation status itself—was originally cast as a cost-containment policy, such policies should incorporate broader care process and delivery reforms that do not add burden to patients when they are at their most vulnerable.

SHM affirms that it is sensible for Medicare to provide coverage for skilled nursing care if a clinician recommends it as part of a treatment plan. Coverage determination should not be beholden to a patient status subject to other systemic pressures, but should reflect the best interest of the patient and the care ordered by providers.

The Improving Access to Medicare Coverage Act, sponsored by Rep. Joe Courtney (D-Conn.), Rep. Tom Latham (R-Iowa), and Sen. Sherrod Brown (D-Ohio), would clarify the law to indicate that Medicare beneficiaries in observation status are deemed inpatients in the hospital for the purposes of the three-day requirement for SNF coverage. This simple adjustment would ensure that patients are able to access the skilled nursing care they need and that providers do not have to worry about this systemic barrier to patient care.

SHM is actively supporting this legislation. A letter of support was sent to Courtney and Brown earlier this year, and membership was mobilized to take action through our Legislative Action Center (www.hospitalmedicine.org/advocacy). Hospitalists also plan to voice their support for the legislation during Hospitalists on the Hill, to be held this month in conjunction with HM13.

As one of only a few specialty medical societies that are active on this issue, SHM stands out as a leader on health-care-system reforms that improve access to care for patients and reduce administrative barriers to medically appropriate care.

Joshua Lapps is SHM’s government relations specialist.