A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

A recent Agency for Healthcare Research and Quality (AHRQ) report, “Making Health Care Safer II: An Updated Critical Analysis of the Evidence for Patient Safety Practices,” holds nearly 1,000 pages of practice-management tips for improving outcomes. But where does a hospitalist begin when reviewing such a massive playbook for progress?

Jim Battles, PhD, an AHRQ social science analyst for patient safety who worked on the report, says the best place to start is by asking yourself: “What keeps you up at night? … What scares the heck out of you?”

The report, a follow-up to the influential and controversial 2001 report “Making Health Care Safer: A Critical Analysis of Patient Safety Practices,” is viewed by its authors as the next step in the continuum of improving patient outcomes. The latest research culled a list of more than 100 patient-safety practices (PSPs) down to 10 that should be “strongly encouraged” and another dozen that are “encouraged.” Battles looks at the 2001 report as more about pushing physicians to think about PSPs, with the updated version as a guidebook on how to think about it.

Listen to AHRQ analyst Jim Battles, PhD, talk about how hospitalists and others should view the new report

Paul Shekelle, MD, PhD, director of the Southern California Evidence-Based Practice Center site of RAND Corp., which AHRQ commissioned to produce the report, says that some might look at safety initiatives since the landmark Institute of Medicine report “To Err is Human” in 1999 and question whether enough progress has been made. But all progress is meaningful to individual patients, and the improvements of the past decade and a half have been important, he adds.

“What I believe is that we’ve made a lot of progress in certain areas,” Dr. Shekelle says, “but this can't be seen when we look at aggregate data, because the improvements we have seen don't account for a sufficiently large proportion in aggregate of the overall patient safety problem.”

Dr. Shekelle—one of three co-principal investigators on the report, along with Peter Pronovost, MD, PhD, FCCM, of Johns Hopkins School of Medicine in Baltimore and HM pioneer Robert Wachter, MD, MHM, chief of the division of hospital medicine at the University of California at San Francisco—says he hopes physicians realize that while the report’s recommendations are evidence-based, they’re not a magic bullet.

“One of the main messages of our report is this is not like writing a prescription for a statin,” Dr. Shekelle says. “This is going to take work. It’s going to take local adaptation, and it’s going to take talking to your front-line clinicians to try and find out how to make this thing work.”

Dr. Wachter, who helped craft both the 2001 and 2013 reports, says patient safety “can be one of those things that is so compelling and so dramatic that you develop a little bit of Nike syndrome—let’s just do it, let’s just computerize, let’s just do teamwork training, let’s do simulation.” However, the healthcare system has a much better, deeper understanding of patient safety and “the role of context, the role of the setting, the role of collateral interventions. It’s generally not going to be one thing that’s the magic bullet, but it’s going to be one thing embedded in a series of other activities that are designed to make sure that you have the right design and the right culture.”

Drs. Wachter and Shekelle and Battles agree that much of the difficulty with patient safety practices is rooted in healthcare system cultures. Each uses different terms to describe the roadblock, as Dr. Wachter discusses implementation science and Battles highlights the difference between the technical work of PSPs and their “social adoption.” But all concur that unless PSPs are committed for the long haul, implementation might be little more than lip service.

“It’s a responsibility of the CEO, the CMO, the CNO, and environmental services, all the way down,” Battles says. “You have to develop around these practices the shared ownership of the risk you’re trying to mitigate. Otherwise, this list of practices, OK, it’s a nice list. But you’ve got to say, ‘What are the risks and hazards to my organization, and how can I apply these evidence practices to the problem?’” TH

Richard Quinn is a freelance writer in New Jersey.

Click here to listen to Dr. Agarwal-Antal

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Click here to listen to Dr. Agarwal-Antal

Click here to listen to Paul Stander

Click here to listen to Paul Stander

Click here to listen to Paul Stander

In July 2010, 443-bed Mary Washington Hospital in Fredericksburg, Va., decided to end its contract for hospitalist services with a local private practice, the Fredericksburg Hospitalist Group (FGH), and to contract instead with national management company HMG (now Cogent HMG).

“We thought the local group might fold and leave, even though they retained a contract with our smaller affiliated hospital,” the 100-bed Stafford Hospital in nearby Stafford, Va., says Rebecca Bigoney, MD, vice president of medical affairs at Mary Washington Hospital. But FHG chose to stay and started aggressively marketing its services to local physicians.

“Today, we have two hospitalist groups that are similar in size, with an almost identical number of patients. They are both competitive and collegial, and it works far better than we thought it would,” Dr. Bigoney says. “We have seen many benefits from having two hospitalist groups; it makes both of them try harder. They have good leaders and aligned incentives.”

The groups also work together on such projects as developing order sets, managing lengths of hospital stay, and implementing computerized physician order entry.

Both groups are represented on hospital committees and within the recently formed division of hospital medicine. Rules of engagement were negotiated with the leadership of the two groups, including a policy on hospitalist admissions and transfers, protocols for handling unassigned patients, a process for local medical groups and physicians to designate their preference for hospitalist coverage, and what to do if the patient is admitted to the wrong group because the primary-care physician is not known at time of admission. If no preference for hospitalist group is given by the primary-care physician, the referral goes to Cogent HMG.

Dr. Bigoney acknowledges FHG physicians had some hard feelings at first. That sentiment is confirmed by FHG founder and hospitalist Feroz Tamana, MD.

“Of course, there was some confusion and anxiety [over the transfer],” Dr. Tamana says. “But from Day One, it has worked pretty well.”

FHG initially downsized from 24 physicians to eight, but has since grown back to 14.

Kerry Lecky, MD, joined Mary Washington in November 2011 to lead the contracting Cogent HMG practice. Everyone was in agreement as to the rules of engagement at that time “and how to align with the hospital’s goals,” said Dr. Lecky, who has since moved on to another position. “The competition has been an opportunity to improve quality. It could be a problem if there were too many hospitalist groups. But two is a very manageable number.”

Is this approach sustainable for the long haul?

“With two groups, we keep each other on our toes,” she says. And the ability to offer a choice of hospitalists to primary-care physicians has been a plus. TH

Larry Beresford is a freelance writer in Oakland, Calif.

In July 2010, 443-bed Mary Washington Hospital in Fredericksburg, Va., decided to end its contract for hospitalist services with a local private practice, the Fredericksburg Hospitalist Group (FGH), and to contract instead with national management company HMG (now Cogent HMG).

“We thought the local group might fold and leave, even though they retained a contract with our smaller affiliated hospital,” the 100-bed Stafford Hospital in nearby Stafford, Va., says Rebecca Bigoney, MD, vice president of medical affairs at Mary Washington Hospital. But FHG chose to stay and started aggressively marketing its services to local physicians.

“Today, we have two hospitalist groups that are similar in size, with an almost identical number of patients. They are both competitive and collegial, and it works far better than we thought it would,” Dr. Bigoney says. “We have seen many benefits from having two hospitalist groups; it makes both of them try harder. They have good leaders and aligned incentives.”

The groups also work together on such projects as developing order sets, managing lengths of hospital stay, and implementing computerized physician order entry.

Both groups are represented on hospital committees and within the recently formed division of hospital medicine. Rules of engagement were negotiated with the leadership of the two groups, including a policy on hospitalist admissions and transfers, protocols for handling unassigned patients, a process for local medical groups and physicians to designate their preference for hospitalist coverage, and what to do if the patient is admitted to the wrong group because the primary-care physician is not known at time of admission. If no preference for hospitalist group is given by the primary-care physician, the referral goes to Cogent HMG.

Dr. Bigoney acknowledges FHG physicians had some hard feelings at first. That sentiment is confirmed by FHG founder and hospitalist Feroz Tamana, MD.

“Of course, there was some confusion and anxiety [over the transfer],” Dr. Tamana says. “But from Day One, it has worked pretty well.”

FHG initially downsized from 24 physicians to eight, but has since grown back to 14.

Kerry Lecky, MD, joined Mary Washington in November 2011 to lead the contracting Cogent HMG practice. Everyone was in agreement as to the rules of engagement at that time “and how to align with the hospital’s goals,” said Dr. Lecky, who has since moved on to another position. “The competition has been an opportunity to improve quality. It could be a problem if there were too many hospitalist groups. But two is a very manageable number.”

Is this approach sustainable for the long haul?

“With two groups, we keep each other on our toes,” she says. And the ability to offer a choice of hospitalists to primary-care physicians has been a plus. TH

Larry Beresford is a freelance writer in Oakland, Calif.

In July 2010, 443-bed Mary Washington Hospital in Fredericksburg, Va., decided to end its contract for hospitalist services with a local private practice, the Fredericksburg Hospitalist Group (FGH), and to contract instead with national management company HMG (now Cogent HMG).

“We thought the local group might fold and leave, even though they retained a contract with our smaller affiliated hospital,” the 100-bed Stafford Hospital in nearby Stafford, Va., says Rebecca Bigoney, MD, vice president of medical affairs at Mary Washington Hospital. But FHG chose to stay and started aggressively marketing its services to local physicians.

“Today, we have two hospitalist groups that are similar in size, with an almost identical number of patients. They are both competitive and collegial, and it works far better than we thought it would,” Dr. Bigoney says. “We have seen many benefits from having two hospitalist groups; it makes both of them try harder. They have good leaders and aligned incentives.”

The groups also work together on such projects as developing order sets, managing lengths of hospital stay, and implementing computerized physician order entry.

Both groups are represented on hospital committees and within the recently formed division of hospital medicine. Rules of engagement were negotiated with the leadership of the two groups, including a policy on hospitalist admissions and transfers, protocols for handling unassigned patients, a process for local medical groups and physicians to designate their preference for hospitalist coverage, and what to do if the patient is admitted to the wrong group because the primary-care physician is not known at time of admission. If no preference for hospitalist group is given by the primary-care physician, the referral goes to Cogent HMG.

Dr. Bigoney acknowledges FHG physicians had some hard feelings at first. That sentiment is confirmed by FHG founder and hospitalist Feroz Tamana, MD.

“Of course, there was some confusion and anxiety [over the transfer],” Dr. Tamana says. “But from Day One, it has worked pretty well.”

FHG initially downsized from 24 physicians to eight, but has since grown back to 14.

Kerry Lecky, MD, joined Mary Washington in November 2011 to lead the contracting Cogent HMG practice. Everyone was in agreement as to the rules of engagement at that time “and how to align with the hospital’s goals,” said Dr. Lecky, who has since moved on to another position. “The competition has been an opportunity to improve quality. It could be a problem if there were too many hospitalist groups. But two is a very manageable number.”

Is this approach sustainable for the long haul?

“With two groups, we keep each other on our toes,” she says. And the ability to offer a choice of hospitalists to primary-care physicians has been a plus. TH

Larry Beresford is a freelance writer in Oakland, Calif.

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]