Does stage of labor at time of cesarean affect the risk of subsequent preterm birth?

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Does stage of labor at time of cesarean affect the risk of subsequent preterm birth?

Recent policy changes in the United States have led to a modest reduction in the incidence of late PTB (34–37 weeks), but the rate of PTB before 34 weeks’ gestation has changed little over the past 40 years. One reason: It has taken us more than 30 years to recognize that uterine contractions are a downstream consequence—not a cause—of preterm labor. By the time a woman presents to labor and delivery with regular phasic uterine contractions and cervical change, it is too late to alter the course of events; the pathogenic processes leading to this clinical presentation have been active for weeks—probably months. Efforts to suppress myometrial contractility at this point using standard tocolytic medications have little or no effect. At best, they delay delivery for 24 to 48 hours, just time enough to transfer the patient to a tertiary care center, administer antenatal corticosteroids, and, possibly, administer magnesium sulfate for neuroprotection.

There is mounting evidence that the cervix plays a central role in spontaneous PTB pathogenesis. The task of the cervix is to remain functionally intact (long and closed) throughout gestation even as the fetus grows and the uterus expands, and then to efface and dilate in the days and hours before labor. PTB ensues if this process of cervical remodeling occurs prematurely.

In support of this hypothesis, cervical shortening on transvaginal ultrasound in the mid second trimester is a major risk factor for spontaneous PTB that is independent of parity and obstetric history.1 This risk can be abrogated by interventions that artificially “strengthen” the cervix (such as placement of a cervical cerclage or pessary) or interfere with the biochemical changes within the cervical stroma that promote cervical effacement (by progesterone supplementation). This analysis by Levine and colleagues provides additional evidence in support of the role of the cervix in spontaneous PTB.

As the investigators themselves hypothesize: “… there may be an inherent biologic risk in achieving complete dilation, regardless of mode of delivery, or perhaps something protective about not achieving complete dilation. This could be attributed to changes in cervical stroma that occur with complete dilation that causes the cervix to be more susceptible to premature dilation in a future pregnancy.”

Although compelling, the “cervical trauma” hypothesis remains to be confirmed. Additional studies are needed to confirm these observations, and it would be preferable to limit these studies to the risk of subsequent spontaneous PTB with intact membranes only, rather than including women with preterm premature rupture of membranes, as in the current study.

What this evidence means for practice
This study suggests that the attainment of full dilation during the course of labor may damage the fibrous tissues that make up the cervical stroma, leading to a persistent functional defect that manifests as spontaneous PTB in a future pregnancy. If that is true, could it also be true that a normal vaginal delivery at term is a “risk factor” for spontaneous PTB in a future pregnancy? There is one clinical variable that could account for this apparent contradiction—the interpregnancy interval. It is well known that a short interval (<6 months) is a risk factor for adverse pregnancy outcomes, including PTB. It is possible that, having been injured at the time of delivery, the cervical stroma needs time to heal. Similar observations have been made when investigating the association between cervical conization and PTB.2 This is a testable hypothesis that I hope these investigators will pursue. In the meantime, we should continue to advise our patients to allow for an appropriate interval between pregnancies.
Errol R. Norwitz, MD, PHD

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

References

1. Iams JD, Goldenberg RL, Meis PJ, et al. The length of the cervix and the risk of spontaneous premature delivery. N Engl J Med. 1996;334(9):567–572.
2.Himes KP, Simhan HN. Time from cervical conization to pregnancy and preterm birth. Obstet Gynecol. 2007;109(2 pt 1):314–319.

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Errol R. Norwitz, MD, PhD, Louis E. Phaneuf Professor of Obstetrics and Gynecology, Tufts University School of Medicine, and Chair of the Department of Obstetrics and Gynecology, Tufts Medical Center, Boston, Massachusetts. Dr. Norwitz serves on the OBG Management Board of Editors.

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Recent policy changes in the United States have led to a modest reduction in the incidence of late PTB (34–37 weeks), but the rate of PTB before 34 weeks’ gestation has changed little over the past 40 years. One reason: It has taken us more than 30 years to recognize that uterine contractions are a downstream consequence—not a cause—of preterm labor. By the time a woman presents to labor and delivery with regular phasic uterine contractions and cervical change, it is too late to alter the course of events; the pathogenic processes leading to this clinical presentation have been active for weeks—probably months. Efforts to suppress myometrial contractility at this point using standard tocolytic medications have little or no effect. At best, they delay delivery for 24 to 48 hours, just time enough to transfer the patient to a tertiary care center, administer antenatal corticosteroids, and, possibly, administer magnesium sulfate for neuroprotection.

There is mounting evidence that the cervix plays a central role in spontaneous PTB pathogenesis. The task of the cervix is to remain functionally intact (long and closed) throughout gestation even as the fetus grows and the uterus expands, and then to efface and dilate in the days and hours before labor. PTB ensues if this process of cervical remodeling occurs prematurely.

In support of this hypothesis, cervical shortening on transvaginal ultrasound in the mid second trimester is a major risk factor for spontaneous PTB that is independent of parity and obstetric history.1 This risk can be abrogated by interventions that artificially “strengthen” the cervix (such as placement of a cervical cerclage or pessary) or interfere with the biochemical changes within the cervical stroma that promote cervical effacement (by progesterone supplementation). This analysis by Levine and colleagues provides additional evidence in support of the role of the cervix in spontaneous PTB.

As the investigators themselves hypothesize: “… there may be an inherent biologic risk in achieving complete dilation, regardless of mode of delivery, or perhaps something protective about not achieving complete dilation. This could be attributed to changes in cervical stroma that occur with complete dilation that causes the cervix to be more susceptible to premature dilation in a future pregnancy.”

Although compelling, the “cervical trauma” hypothesis remains to be confirmed. Additional studies are needed to confirm these observations, and it would be preferable to limit these studies to the risk of subsequent spontaneous PTB with intact membranes only, rather than including women with preterm premature rupture of membranes, as in the current study.

What this evidence means for practice
This study suggests that the attainment of full dilation during the course of labor may damage the fibrous tissues that make up the cervical stroma, leading to a persistent functional defect that manifests as spontaneous PTB in a future pregnancy. If that is true, could it also be true that a normal vaginal delivery at term is a “risk factor” for spontaneous PTB in a future pregnancy? There is one clinical variable that could account for this apparent contradiction—the interpregnancy interval. It is well known that a short interval (<6 months) is a risk factor for adverse pregnancy outcomes, including PTB. It is possible that, having been injured at the time of delivery, the cervical stroma needs time to heal. Similar observations have been made when investigating the association between cervical conization and PTB.2 This is a testable hypothesis that I hope these investigators will pursue. In the meantime, we should continue to advise our patients to allow for an appropriate interval between pregnancies.
Errol R. Norwitz, MD, PHD

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

Recent policy changes in the United States have led to a modest reduction in the incidence of late PTB (34–37 weeks), but the rate of PTB before 34 weeks’ gestation has changed little over the past 40 years. One reason: It has taken us more than 30 years to recognize that uterine contractions are a downstream consequence—not a cause—of preterm labor. By the time a woman presents to labor and delivery with regular phasic uterine contractions and cervical change, it is too late to alter the course of events; the pathogenic processes leading to this clinical presentation have been active for weeks—probably months. Efforts to suppress myometrial contractility at this point using standard tocolytic medications have little or no effect. At best, they delay delivery for 24 to 48 hours, just time enough to transfer the patient to a tertiary care center, administer antenatal corticosteroids, and, possibly, administer magnesium sulfate for neuroprotection.

There is mounting evidence that the cervix plays a central role in spontaneous PTB pathogenesis. The task of the cervix is to remain functionally intact (long and closed) throughout gestation even as the fetus grows and the uterus expands, and then to efface and dilate in the days and hours before labor. PTB ensues if this process of cervical remodeling occurs prematurely.

In support of this hypothesis, cervical shortening on transvaginal ultrasound in the mid second trimester is a major risk factor for spontaneous PTB that is independent of parity and obstetric history.1 This risk can be abrogated by interventions that artificially “strengthen” the cervix (such as placement of a cervical cerclage or pessary) or interfere with the biochemical changes within the cervical stroma that promote cervical effacement (by progesterone supplementation). This analysis by Levine and colleagues provides additional evidence in support of the role of the cervix in spontaneous PTB.

As the investigators themselves hypothesize: “… there may be an inherent biologic risk in achieving complete dilation, regardless of mode of delivery, or perhaps something protective about not achieving complete dilation. This could be attributed to changes in cervical stroma that occur with complete dilation that causes the cervix to be more susceptible to premature dilation in a future pregnancy.”

Although compelling, the “cervical trauma” hypothesis remains to be confirmed. Additional studies are needed to confirm these observations, and it would be preferable to limit these studies to the risk of subsequent spontaneous PTB with intact membranes only, rather than including women with preterm premature rupture of membranes, as in the current study.

What this evidence means for practice
This study suggests that the attainment of full dilation during the course of labor may damage the fibrous tissues that make up the cervical stroma, leading to a persistent functional defect that manifests as spontaneous PTB in a future pregnancy. If that is true, could it also be true that a normal vaginal delivery at term is a “risk factor” for spontaneous PTB in a future pregnancy? There is one clinical variable that could account for this apparent contradiction—the interpregnancy interval. It is well known that a short interval (<6 months) is a risk factor for adverse pregnancy outcomes, including PTB. It is possible that, having been injured at the time of delivery, the cervical stroma needs time to heal. Similar observations have been made when investigating the association between cervical conization and PTB.2 This is a testable hypothesis that I hope these investigators will pursue. In the meantime, we should continue to advise our patients to allow for an appropriate interval between pregnancies.
Errol R. Norwitz, MD, PHD

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

References

1. Iams JD, Goldenberg RL, Meis PJ, et al. The length of the cervix and the risk of spontaneous premature delivery. N Engl J Med. 1996;334(9):567–572.
2.Himes KP, Simhan HN. Time from cervical conization to pregnancy and preterm birth. Obstet Gynecol. 2007;109(2 pt 1):314–319.

References

1. Iams JD, Goldenberg RL, Meis PJ, et al. The length of the cervix and the risk of spontaneous premature delivery. N Engl J Med. 1996;334(9):567–572.
2.Himes KP, Simhan HN. Time from cervical conization to pregnancy and preterm birth. Obstet Gynecol. 2007;109(2 pt 1):314–319.

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Avoid misdiagnosing pediatric viral myocarditis

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SAN DIEGO– Pediatricians are at risk of misdiagnosing myocarditis despite its severity. That’s because children tend to present with abdominal symptoms and a history of a recent viral illness that lacked signs of cardiac involvement, Dr. Kevin Shannon said.

“Typically, they have a bout of flu, they seem to be getting better, and then they start vomiting or having stomach pain again,” he said at the annual meeting of the American Academy of Pediatrics.

Viruses ranging from adenovirus to varicella have been implicated in myocarditis in children (J. Clin. Microbiol. 2010;48:642-5; Pediatr. Cardiol. 2011;32:1241-3). Pediatricians should watch for patients who were recently ill and are now presenting with an apparent relapse and tachycardia that is worse than how they appear overall, said Dr. Shannon, a pediatric cardiologist at the University of California, Los Angeles, Medical Center. “A lot of these children will seem more ill than their vomiting will suggest,” he added. “They’ll have a heart rate of 180 [beats per minute] that is out proportion to how they look.”

Fluid therapy does not improve tachycardia and may even worsen it, indicating that dehydration is not the underlying cause, said Dr. Shannon. Children with viral myocarditis also often have acute upper-right quadrant pain as a result of hepatic distension, he said.

Laboratory findings can be very helpful. Cardiac troponin T is almost always elevated in children with myocarditis (Pediatr. Emerg. Care 2012;28:1173-8), and erythrocyte sedimentation rate also may be high. Electrocardiography can show a variety of focal or diffuse abnormalities, none of which are pathognomonic for the condition, Dr. Shannon said. Focal abnormalities can mimic an ST segment elevation myocardial infarction (STEMI), he added.

On chest x-ray, the heart margins also are often normal because the heart has not yet enlarged to compensate for impaired function, said Dr. Shannon. “This is a poorly functioning, normal-sized heart,” he added. Chest films often will reveal interstitial edema that might be misinterpreted as interstitial pneumonia, in keeping with the child’s recent illness.

Treatment of acquired myocarditis is based on supportive care, said Dr. Shannon, adding that use of immunomodulators in children with myocarditis is controversial. “If they have low blood pressure, they need volume, even if their heart rate gets higher,” he added. “If they don’t tolerate fluid therapy, they need inotropes and sometimes intubation.”

Dr. Shannon reported no conflicts of interest.

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SAN DIEGO– Pediatricians are at risk of misdiagnosing myocarditis despite its severity. That’s because children tend to present with abdominal symptoms and a history of a recent viral illness that lacked signs of cardiac involvement, Dr. Kevin Shannon said.

“Typically, they have a bout of flu, they seem to be getting better, and then they start vomiting or having stomach pain again,” he said at the annual meeting of the American Academy of Pediatrics.

Viruses ranging from adenovirus to varicella have been implicated in myocarditis in children (J. Clin. Microbiol. 2010;48:642-5; Pediatr. Cardiol. 2011;32:1241-3). Pediatricians should watch for patients who were recently ill and are now presenting with an apparent relapse and tachycardia that is worse than how they appear overall, said Dr. Shannon, a pediatric cardiologist at the University of California, Los Angeles, Medical Center. “A lot of these children will seem more ill than their vomiting will suggest,” he added. “They’ll have a heart rate of 180 [beats per minute] that is out proportion to how they look.”

Fluid therapy does not improve tachycardia and may even worsen it, indicating that dehydration is not the underlying cause, said Dr. Shannon. Children with viral myocarditis also often have acute upper-right quadrant pain as a result of hepatic distension, he said.

Laboratory findings can be very helpful. Cardiac troponin T is almost always elevated in children with myocarditis (Pediatr. Emerg. Care 2012;28:1173-8), and erythrocyte sedimentation rate also may be high. Electrocardiography can show a variety of focal or diffuse abnormalities, none of which are pathognomonic for the condition, Dr. Shannon said. Focal abnormalities can mimic an ST segment elevation myocardial infarction (STEMI), he added.

On chest x-ray, the heart margins also are often normal because the heart has not yet enlarged to compensate for impaired function, said Dr. Shannon. “This is a poorly functioning, normal-sized heart,” he added. Chest films often will reveal interstitial edema that might be misinterpreted as interstitial pneumonia, in keeping with the child’s recent illness.

Treatment of acquired myocarditis is based on supportive care, said Dr. Shannon, adding that use of immunomodulators in children with myocarditis is controversial. “If they have low blood pressure, they need volume, even if their heart rate gets higher,” he added. “If they don’t tolerate fluid therapy, they need inotropes and sometimes intubation.”

Dr. Shannon reported no conflicts of interest.

SAN DIEGO– Pediatricians are at risk of misdiagnosing myocarditis despite its severity. That’s because children tend to present with abdominal symptoms and a history of a recent viral illness that lacked signs of cardiac involvement, Dr. Kevin Shannon said.

“Typically, they have a bout of flu, they seem to be getting better, and then they start vomiting or having stomach pain again,” he said at the annual meeting of the American Academy of Pediatrics.

Viruses ranging from adenovirus to varicella have been implicated in myocarditis in children (J. Clin. Microbiol. 2010;48:642-5; Pediatr. Cardiol. 2011;32:1241-3). Pediatricians should watch for patients who were recently ill and are now presenting with an apparent relapse and tachycardia that is worse than how they appear overall, said Dr. Shannon, a pediatric cardiologist at the University of California, Los Angeles, Medical Center. “A lot of these children will seem more ill than their vomiting will suggest,” he added. “They’ll have a heart rate of 180 [beats per minute] that is out proportion to how they look.”

Fluid therapy does not improve tachycardia and may even worsen it, indicating that dehydration is not the underlying cause, said Dr. Shannon. Children with viral myocarditis also often have acute upper-right quadrant pain as a result of hepatic distension, he said.

Laboratory findings can be very helpful. Cardiac troponin T is almost always elevated in children with myocarditis (Pediatr. Emerg. Care 2012;28:1173-8), and erythrocyte sedimentation rate also may be high. Electrocardiography can show a variety of focal or diffuse abnormalities, none of which are pathognomonic for the condition, Dr. Shannon said. Focal abnormalities can mimic an ST segment elevation myocardial infarction (STEMI), he added.

On chest x-ray, the heart margins also are often normal because the heart has not yet enlarged to compensate for impaired function, said Dr. Shannon. “This is a poorly functioning, normal-sized heart,” he added. Chest films often will reveal interstitial edema that might be misinterpreted as interstitial pneumonia, in keeping with the child’s recent illness.

Treatment of acquired myocarditis is based on supportive care, said Dr. Shannon, adding that use of immunomodulators in children with myocarditis is controversial. “If they have low blood pressure, they need volume, even if their heart rate gets higher,” he added. “If they don’t tolerate fluid therapy, they need inotropes and sometimes intubation.”

Dr. Shannon reported no conflicts of interest.

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VIDEO: How U.S. health providers can contain Ebola

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AUSTIN, TEX. – Why would travel restrictions make the Ebola epidemic worse in West Africa and expand its spread to U.S. shores? What can American intensive care units do to prepare, even if they aren’t designated Ebola centers? And are there lessons medical professionals and policymakers can apply from the successes and failures of the AIDS epidemic 30 years ago?

In a video interview at the annual meeting of the American College of Chest Physicians, Dr. Lewis Rubinson offered answers to those questions and perspectives on the current American response to the Ebola outbreak. Dr. Rubinson recently returned from treating more than 300 Ebola patients in Sierra Leone as a consulting physician for the World Health Organization.

“Honestly, I think if we don’t get it under control in the next few months in West Africa, there will be sporadic cases coming back [to the United States] for as long as we can think of,” cautioned Dr. Rubinson, director of the R. Adams Cowley Trauma Shock Center at the University of Maryland, Baltimore.

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AUSTIN, TEX. – Why would travel restrictions make the Ebola epidemic worse in West Africa and expand its spread to U.S. shores? What can American intensive care units do to prepare, even if they aren’t designated Ebola centers? And are there lessons medical professionals and policymakers can apply from the successes and failures of the AIDS epidemic 30 years ago?

In a video interview at the annual meeting of the American College of Chest Physicians, Dr. Lewis Rubinson offered answers to those questions and perspectives on the current American response to the Ebola outbreak. Dr. Rubinson recently returned from treating more than 300 Ebola patients in Sierra Leone as a consulting physician for the World Health Organization.

“Honestly, I think if we don’t get it under control in the next few months in West Africa, there will be sporadic cases coming back [to the United States] for as long as we can think of,” cautioned Dr. Rubinson, director of the R. Adams Cowley Trauma Shock Center at the University of Maryland, Baltimore.

[email protected]

On Twitter @whitneymcknight

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

AUSTIN, TEX. – Why would travel restrictions make the Ebola epidemic worse in West Africa and expand its spread to U.S. shores? What can American intensive care units do to prepare, even if they aren’t designated Ebola centers? And are there lessons medical professionals and policymakers can apply from the successes and failures of the AIDS epidemic 30 years ago?

In a video interview at the annual meeting of the American College of Chest Physicians, Dr. Lewis Rubinson offered answers to those questions and perspectives on the current American response to the Ebola outbreak. Dr. Rubinson recently returned from treating more than 300 Ebola patients in Sierra Leone as a consulting physician for the World Health Organization.

“Honestly, I think if we don’t get it under control in the next few months in West Africa, there will be sporadic cases coming back [to the United States] for as long as we can think of,” cautioned Dr. Rubinson, director of the R. Adams Cowley Trauma Shock Center at the University of Maryland, Baltimore.

[email protected]

On Twitter @whitneymcknight

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
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Dengue, West Nile threaten to set up housekeeping in U.S.A.

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BALTIMORE – Two imported mosquito-borne illnesses continue to push into the United States, threatening to take up residence in areas with a favorable environment.

Neither dengue fever nor West Nile virus are naturally endemic to any part of the United States, Dr. Larry Davis said at the annual meeting of the American Neurological Association. But both diseases show some indications of establishing a local infective reservoir.

Dr. Larry Davis

Dengue remains a rare disease here, with about 650 cases reported in 2013. The majority of those occurred in patients who had just returned from endemic countries. But since 2009, local transmission appears to be occurring in three hot spots: Hawaii, Texas, and south Florida, including Key West and Miami, said Dr. Davis, a professor of neurology at the University of New Mexico, Albuquerque.

Locally acquired disease first popped up during 2009-2010 in Key West, Fla. During that time, 29 residents developed clinical dengue. Many more probably carried the virus, however, since a robust immune response usually tamps down about 80% of first infections. But those asymptomatic carriers provide a potent reservoir for hungry mosquitoes, and dengue is one virus that doesn’t need an intermediate host. Instead, Dr. Davis said, any mosquito that bites an infected person passes the agent directly into the bloodstream of his next meal.

During the Key West outbreak, the Centers for Disease Control and Prevention (CDC) estimated that about 5% of those living on the small island had been infected at some point.

Last year, 53 clinical cases were identified in south Texas. About half of these were locally acquired, which is another sign that the virus may be taking up residence, Dr. Davis said. And, so far this year, four residents of Miami-Dade County, Fla. have been diagnosed with locally acquired disease. The outbreak recently prompted local health officials to issue an alert for mosquito-borne disease, and remind residents to take precautions against being bitten.

In addition to its direct transmissibility, dengue has another neat infective trick, Dr. Davis noted. There are four serotypes, each with their own unique immunogenic profile. Thus, infection with any one confers no protection against any of the others. Any vaccine, therefore, would have to protect against all four serotypes.

 

 

In fact, such a tetravalent vaccine is in clinical trials, he said. Last month, Sanofi-Pasteur reported that its candidate vaccine, tested in almost 21,000 children in Latin America and the Caribbean, reduced the risk of disease by more than 60%, and the risk of dengue-related hospitalization by 80%. The results mirror those seen in an earlier Asian trial, the drug company noted.There has been no such progress on a human vaccine against West Nile virus, Dr. Davis said. So far this year, 1,585 cases in 47 states have been reported to the CDC, with the majority occurring in California (563), Colorado (108), and Texas (207). Of these, 917 (58%) were classified as neuroinvasive disease (such as meningitis or encephalitis). Thus far, 54 patients have died; 20 of these in California alone.

The California Department of Public Health has identified 3,282 positive mosquito samples as of Oct. 27. Director Dr. Ron Chapman said in a press statement that the state has never experienced such a severe outbreak.

“The proportion of mosquitoes infected with West Nile virus is at the highest level ever detected in California,” Dr. Chapman said. “We expect to see more people become infected as this is the time of year when the risk of infection is the highest.”

Like dengue, the majority of West Nile cases are asymptomatic, Dr. Davis noted. But in the absence of a robust immune response, the virus can cross the blood-brain barrier and initiate a devastating neuroinvasive illness than can cause a flaccid paralysis, seizures, and death.

Neuroinvasive West Nile carries many clinical and diagnostic similarities to polio, he said. Like polio, the limb weakness has a sudden onset and can be accompanied by pain, although the sensory neurons aren’t apparently involved. Imaging studies show the virus attacking at the anterior horns of the spinal cord; nerve conduction studies show a motor axonopathy, but without much demyelination. Survivors have a variable course of recovery; some may regain full strength of the affected limbs, but many retain persistent weakness.

There is no vaccine against the disease, although several are in early-stage development, including a live, attenuated chimeric vaccine that did well in a phase II, placebo-controlled trial. Within 28 days of vaccination, 98% of subjects experienced seroconversion.

Dr. Davis had no relevant conflicts of interest.

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BALTIMORE – Two imported mosquito-borne illnesses continue to push into the United States, threatening to take up residence in areas with a favorable environment.

Neither dengue fever nor West Nile virus are naturally endemic to any part of the United States, Dr. Larry Davis said at the annual meeting of the American Neurological Association. But both diseases show some indications of establishing a local infective reservoir.

Dr. Larry Davis

Dengue remains a rare disease here, with about 650 cases reported in 2013. The majority of those occurred in patients who had just returned from endemic countries. But since 2009, local transmission appears to be occurring in three hot spots: Hawaii, Texas, and south Florida, including Key West and Miami, said Dr. Davis, a professor of neurology at the University of New Mexico, Albuquerque.

Locally acquired disease first popped up during 2009-2010 in Key West, Fla. During that time, 29 residents developed clinical dengue. Many more probably carried the virus, however, since a robust immune response usually tamps down about 80% of first infections. But those asymptomatic carriers provide a potent reservoir for hungry mosquitoes, and dengue is one virus that doesn’t need an intermediate host. Instead, Dr. Davis said, any mosquito that bites an infected person passes the agent directly into the bloodstream of his next meal.

During the Key West outbreak, the Centers for Disease Control and Prevention (CDC) estimated that about 5% of those living on the small island had been infected at some point.

Last year, 53 clinical cases were identified in south Texas. About half of these were locally acquired, which is another sign that the virus may be taking up residence, Dr. Davis said. And, so far this year, four residents of Miami-Dade County, Fla. have been diagnosed with locally acquired disease. The outbreak recently prompted local health officials to issue an alert for mosquito-borne disease, and remind residents to take precautions against being bitten.

In addition to its direct transmissibility, dengue has another neat infective trick, Dr. Davis noted. There are four serotypes, each with their own unique immunogenic profile. Thus, infection with any one confers no protection against any of the others. Any vaccine, therefore, would have to protect against all four serotypes.

 

 

In fact, such a tetravalent vaccine is in clinical trials, he said. Last month, Sanofi-Pasteur reported that its candidate vaccine, tested in almost 21,000 children in Latin America and the Caribbean, reduced the risk of disease by more than 60%, and the risk of dengue-related hospitalization by 80%. The results mirror those seen in an earlier Asian trial, the drug company noted.There has been no such progress on a human vaccine against West Nile virus, Dr. Davis said. So far this year, 1,585 cases in 47 states have been reported to the CDC, with the majority occurring in California (563), Colorado (108), and Texas (207). Of these, 917 (58%) were classified as neuroinvasive disease (such as meningitis or encephalitis). Thus far, 54 patients have died; 20 of these in California alone.

The California Department of Public Health has identified 3,282 positive mosquito samples as of Oct. 27. Director Dr. Ron Chapman said in a press statement that the state has never experienced such a severe outbreak.

“The proportion of mosquitoes infected with West Nile virus is at the highest level ever detected in California,” Dr. Chapman said. “We expect to see more people become infected as this is the time of year when the risk of infection is the highest.”

Like dengue, the majority of West Nile cases are asymptomatic, Dr. Davis noted. But in the absence of a robust immune response, the virus can cross the blood-brain barrier and initiate a devastating neuroinvasive illness than can cause a flaccid paralysis, seizures, and death.

Neuroinvasive West Nile carries many clinical and diagnostic similarities to polio, he said. Like polio, the limb weakness has a sudden onset and can be accompanied by pain, although the sensory neurons aren’t apparently involved. Imaging studies show the virus attacking at the anterior horns of the spinal cord; nerve conduction studies show a motor axonopathy, but without much demyelination. Survivors have a variable course of recovery; some may regain full strength of the affected limbs, but many retain persistent weakness.

There is no vaccine against the disease, although several are in early-stage development, including a live, attenuated chimeric vaccine that did well in a phase II, placebo-controlled trial. Within 28 days of vaccination, 98% of subjects experienced seroconversion.

Dr. Davis had no relevant conflicts of interest.

[email protected]

On Twitter @alz_gal

BALTIMORE – Two imported mosquito-borne illnesses continue to push into the United States, threatening to take up residence in areas with a favorable environment.

Neither dengue fever nor West Nile virus are naturally endemic to any part of the United States, Dr. Larry Davis said at the annual meeting of the American Neurological Association. But both diseases show some indications of establishing a local infective reservoir.

Dr. Larry Davis

Dengue remains a rare disease here, with about 650 cases reported in 2013. The majority of those occurred in patients who had just returned from endemic countries. But since 2009, local transmission appears to be occurring in three hot spots: Hawaii, Texas, and south Florida, including Key West and Miami, said Dr. Davis, a professor of neurology at the University of New Mexico, Albuquerque.

Locally acquired disease first popped up during 2009-2010 in Key West, Fla. During that time, 29 residents developed clinical dengue. Many more probably carried the virus, however, since a robust immune response usually tamps down about 80% of first infections. But those asymptomatic carriers provide a potent reservoir for hungry mosquitoes, and dengue is one virus that doesn’t need an intermediate host. Instead, Dr. Davis said, any mosquito that bites an infected person passes the agent directly into the bloodstream of his next meal.

During the Key West outbreak, the Centers for Disease Control and Prevention (CDC) estimated that about 5% of those living on the small island had been infected at some point.

Last year, 53 clinical cases were identified in south Texas. About half of these were locally acquired, which is another sign that the virus may be taking up residence, Dr. Davis said. And, so far this year, four residents of Miami-Dade County, Fla. have been diagnosed with locally acquired disease. The outbreak recently prompted local health officials to issue an alert for mosquito-borne disease, and remind residents to take precautions against being bitten.

In addition to its direct transmissibility, dengue has another neat infective trick, Dr. Davis noted. There are four serotypes, each with their own unique immunogenic profile. Thus, infection with any one confers no protection against any of the others. Any vaccine, therefore, would have to protect against all four serotypes.

 

 

In fact, such a tetravalent vaccine is in clinical trials, he said. Last month, Sanofi-Pasteur reported that its candidate vaccine, tested in almost 21,000 children in Latin America and the Caribbean, reduced the risk of disease by more than 60%, and the risk of dengue-related hospitalization by 80%. The results mirror those seen in an earlier Asian trial, the drug company noted.There has been no such progress on a human vaccine against West Nile virus, Dr. Davis said. So far this year, 1,585 cases in 47 states have been reported to the CDC, with the majority occurring in California (563), Colorado (108), and Texas (207). Of these, 917 (58%) were classified as neuroinvasive disease (such as meningitis or encephalitis). Thus far, 54 patients have died; 20 of these in California alone.

The California Department of Public Health has identified 3,282 positive mosquito samples as of Oct. 27. Director Dr. Ron Chapman said in a press statement that the state has never experienced such a severe outbreak.

“The proportion of mosquitoes infected with West Nile virus is at the highest level ever detected in California,” Dr. Chapman said. “We expect to see more people become infected as this is the time of year when the risk of infection is the highest.”

Like dengue, the majority of West Nile cases are asymptomatic, Dr. Davis noted. But in the absence of a robust immune response, the virus can cross the blood-brain barrier and initiate a devastating neuroinvasive illness than can cause a flaccid paralysis, seizures, and death.

Neuroinvasive West Nile carries many clinical and diagnostic similarities to polio, he said. Like polio, the limb weakness has a sudden onset and can be accompanied by pain, although the sensory neurons aren’t apparently involved. Imaging studies show the virus attacking at the anterior horns of the spinal cord; nerve conduction studies show a motor axonopathy, but without much demyelination. Survivors have a variable course of recovery; some may regain full strength of the affected limbs, but many retain persistent weakness.

There is no vaccine against the disease, although several are in early-stage development, including a live, attenuated chimeric vaccine that did well in a phase II, placebo-controlled trial. Within 28 days of vaccination, 98% of subjects experienced seroconversion.

Dr. Davis had no relevant conflicts of interest.

[email protected]

On Twitter @alz_gal

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Female sexual dysfunction: Is pharmacologic treatment a future reality or just wishful thinking?

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MenoPro: An app from NAMS for you and your menopausal patient

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Ideal patient selection for this new approach to HT

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Dr. Moore and Dr. Pinkerton focus on a new estrogen therapy: the combination conjugated estrogen and bazedoxifene (CE/BZA) for the treatment of moderate to severe hot flashes due to menopause and the prevention of menopausal osteoporosis.

Which patients can benefit most? What is CE/BZA’s safety profile? How do traditional estrogen-progestin therapies compare with CE/BZA therapy? Tune in for answers to these questions and more.

 

 

Read Cases in Menopause: Conjugated estrogen plus bazedoxifene—a new approach to estrogen therapy, from Dr. Anne Moore and Dr. JoAnn Pinkerton (October 2014).

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Dr. Moore and Dr. Pinkerton focus on a new estrogen therapy: the combination conjugated estrogen and bazedoxifene (CE/BZA) for the treatment of moderate to severe hot flashes due to menopause and the prevention of menopausal osteoporosis.

Which patients can benefit most? What is CE/BZA’s safety profile? How do traditional estrogen-progestin therapies compare with CE/BZA therapy? Tune in for answers to these questions and more.

 

 

Read Cases in Menopause: Conjugated estrogen plus bazedoxifene—a new approach to estrogen therapy, from Dr. Anne Moore and Dr. JoAnn Pinkerton (October 2014).

Dr. Moore and Dr. Pinkerton focus on a new estrogen therapy: the combination conjugated estrogen and bazedoxifene (CE/BZA) for the treatment of moderate to severe hot flashes due to menopause and the prevention of menopausal osteoporosis.

Which patients can benefit most? What is CE/BZA’s safety profile? How do traditional estrogen-progestin therapies compare with CE/BZA therapy? Tune in for answers to these questions and more.

 

 

Read Cases in Menopause: Conjugated estrogen plus bazedoxifene—a new approach to estrogen therapy, from Dr. Anne Moore and Dr. JoAnn Pinkerton (October 2014).

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Homecare Will Help You Achieve the Triple Aim

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Where there is variation, there is room for improvement. The Institute of Medicine’s report on geographic variation in Medicare spending concluded that the largest contributor to overall spending variation is spending for post-acute care services.1 Furthermore, we know that a significant amount of overall spending is devoted to post-acute care. For example, for patients hospitalized with a flare-up of a chronic condition like COPD or heart failure, Medicare spends nearly as much on post-acute care and readmissions in the first 30 days after discharge as it does on the initial admission.1

What does this mean for hospitalists?

Numerous research articles and quality improvement projects have focused on what makes a good hospital discharge or hand off to the ‘next provider of care’; however, hospitalists are increasingly participating in value-based payment programs like accountable care organizations (ACOs), risk contracts, and bundled payments. This means they must begin to pay attention to the cost side of the value equation (quality divided by cost) as it relates to hospital discharge.

A day of home care represents a more cost-effective alternative than a day of care in a skilled nursing facility (SNF). Hospitalists who can identify those patients who are appropriate to send home with home health services—and who otherwise would have gone to a SNF—will serve the dual goals of improving patient experience and decreasing costs.

Hospitalists will need to develop a decision-making process that determines the appropriate level of care for the patient after discharge. The decision-making process should address questions like:

  • What skilled services lead a patient to go to a SNF instead of home with home health?
  • Which patients go to a SNF instead of home simply because they don’t have family or a caregiver to help them with activities of daily living?
  • Are there services requiring a nurse or a therapist that can’t be delivered in the home?

Hospitalists also will need to develop a more intimate understanding of the following levels of care:

  • Skilled nursing includes management of a nursing care plan, assessment of a patient’s changing condition, and services like wound care, infusion therapy, and management of medications, feeding or drainage tubes, and pain.
  • Skilled rehabilitation refers to the array of services provided by physical, occupational, speech, and respiratory therapists.
  • Custodial care, usually supplied by a home health aid or family member, includes help with activities of daily living (feeding, dressing, bathing, grooming, personal hygiene, and toileting).

Even though home care has been around for a while, there is a sizeable group of patients, especially in geographic areas of high SNF spending, who might be better served in the home environment.

It should be noted that most skilled nursing or therapy services can be delivered in the home setting if the patient’s custodial care needs are met—a big ‘if’ in some cases. Some patients go to a SNF because they require three or more skilled nursing or therapy services, and it is therefore impractical for them to go home.

Here are my suggestions to hospitalists seeking to reengineer the discharge process with the goals of “right-sizing” the number of patients who go to SNFs and optimizing the utilization of home healthcare services:

  • Become familiar with the range of post-acute care providers and care coordination services in your community.
  • Refer any patient who wishes to go home, either directly or after a SNF stay, for a home care evaluation. Home care agencies are experts in determining if and how patients can return home.
  • If a need for help with activities of daily living is the major barrier to having a patient discharged to home, create a system in which case management develops a custodial care plan with the patient and caregivers during the inpatient stay. Currently, this step is delayed until well into the SNF stay and may prolong that stay. Such a plan includes a financial analysis, screening for Medicaid eligibility, and evaluating whether a family member can assume some or all of the custodial care needs.
  • If a patient is being discharged to a SNF, review the list of needed services leading to the SNF transfer. Ask the case manager if these services can be provided in the home. If not, then why?
  • Bed capacity permitting, consider keeping patients who are functionally improving in the hospital an extra day so they can be discharged directly home instead of to a SNF.2
 

 

In his seminal work, The Innovator’s Dilemma, Clayton Christensen describes “disruptive innovation” as that which gives rise to products or services that are cheaper, simpler, and more convenient to use. Even though home care has been around for a while, there is a sizeable group of patients, especially in geographic areas of high SNF spending, who might be better served in the home environment. As we create better systems under value-based payment, we should see an increase in the use of home healthcare as a disruptive innovation when applied to appropriate patients transitioning out of the hospital or a SNF.


Dr. Whitcomb is Chief Medical Officer of Remedy Partners. He is co-founder and past president of SHM. Email him at [email protected].

 

 

References

  1. Newhouse JP, Garber AM. Geographic variation in Medicare services. N Engl J Med. 2013;368:1465-1468.
  2. Mechanic R. Post-acute care—The next frontier for controlling Medicare spending. N Engl J Med. 2014;370(8):692-694.
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Where there is variation, there is room for improvement. The Institute of Medicine’s report on geographic variation in Medicare spending concluded that the largest contributor to overall spending variation is spending for post-acute care services.1 Furthermore, we know that a significant amount of overall spending is devoted to post-acute care. For example, for patients hospitalized with a flare-up of a chronic condition like COPD or heart failure, Medicare spends nearly as much on post-acute care and readmissions in the first 30 days after discharge as it does on the initial admission.1

What does this mean for hospitalists?

Numerous research articles and quality improvement projects have focused on what makes a good hospital discharge or hand off to the ‘next provider of care’; however, hospitalists are increasingly participating in value-based payment programs like accountable care organizations (ACOs), risk contracts, and bundled payments. This means they must begin to pay attention to the cost side of the value equation (quality divided by cost) as it relates to hospital discharge.

A day of home care represents a more cost-effective alternative than a day of care in a skilled nursing facility (SNF). Hospitalists who can identify those patients who are appropriate to send home with home health services—and who otherwise would have gone to a SNF—will serve the dual goals of improving patient experience and decreasing costs.

Hospitalists will need to develop a decision-making process that determines the appropriate level of care for the patient after discharge. The decision-making process should address questions like:

  • What skilled services lead a patient to go to a SNF instead of home with home health?
  • Which patients go to a SNF instead of home simply because they don’t have family or a caregiver to help them with activities of daily living?
  • Are there services requiring a nurse or a therapist that can’t be delivered in the home?

Hospitalists also will need to develop a more intimate understanding of the following levels of care:

  • Skilled nursing includes management of a nursing care plan, assessment of a patient’s changing condition, and services like wound care, infusion therapy, and management of medications, feeding or drainage tubes, and pain.
  • Skilled rehabilitation refers to the array of services provided by physical, occupational, speech, and respiratory therapists.
  • Custodial care, usually supplied by a home health aid or family member, includes help with activities of daily living (feeding, dressing, bathing, grooming, personal hygiene, and toileting).

Even though home care has been around for a while, there is a sizeable group of patients, especially in geographic areas of high SNF spending, who might be better served in the home environment.

It should be noted that most skilled nursing or therapy services can be delivered in the home setting if the patient’s custodial care needs are met—a big ‘if’ in some cases. Some patients go to a SNF because they require three or more skilled nursing or therapy services, and it is therefore impractical for them to go home.

Here are my suggestions to hospitalists seeking to reengineer the discharge process with the goals of “right-sizing” the number of patients who go to SNFs and optimizing the utilization of home healthcare services:

  • Become familiar with the range of post-acute care providers and care coordination services in your community.
  • Refer any patient who wishes to go home, either directly or after a SNF stay, for a home care evaluation. Home care agencies are experts in determining if and how patients can return home.
  • If a need for help with activities of daily living is the major barrier to having a patient discharged to home, create a system in which case management develops a custodial care plan with the patient and caregivers during the inpatient stay. Currently, this step is delayed until well into the SNF stay and may prolong that stay. Such a plan includes a financial analysis, screening for Medicaid eligibility, and evaluating whether a family member can assume some or all of the custodial care needs.
  • If a patient is being discharged to a SNF, review the list of needed services leading to the SNF transfer. Ask the case manager if these services can be provided in the home. If not, then why?
  • Bed capacity permitting, consider keeping patients who are functionally improving in the hospital an extra day so they can be discharged directly home instead of to a SNF.2
 

 

In his seminal work, The Innovator’s Dilemma, Clayton Christensen describes “disruptive innovation” as that which gives rise to products or services that are cheaper, simpler, and more convenient to use. Even though home care has been around for a while, there is a sizeable group of patients, especially in geographic areas of high SNF spending, who might be better served in the home environment. As we create better systems under value-based payment, we should see an increase in the use of home healthcare as a disruptive innovation when applied to appropriate patients transitioning out of the hospital or a SNF.


Dr. Whitcomb is Chief Medical Officer of Remedy Partners. He is co-founder and past president of SHM. Email him at [email protected].

 

 

References

  1. Newhouse JP, Garber AM. Geographic variation in Medicare services. N Engl J Med. 2013;368:1465-1468.
  2. Mechanic R. Post-acute care—The next frontier for controlling Medicare spending. N Engl J Med. 2014;370(8):692-694.

Where there is variation, there is room for improvement. The Institute of Medicine’s report on geographic variation in Medicare spending concluded that the largest contributor to overall spending variation is spending for post-acute care services.1 Furthermore, we know that a significant amount of overall spending is devoted to post-acute care. For example, for patients hospitalized with a flare-up of a chronic condition like COPD or heart failure, Medicare spends nearly as much on post-acute care and readmissions in the first 30 days after discharge as it does on the initial admission.1

What does this mean for hospitalists?

Numerous research articles and quality improvement projects have focused on what makes a good hospital discharge or hand off to the ‘next provider of care’; however, hospitalists are increasingly participating in value-based payment programs like accountable care organizations (ACOs), risk contracts, and bundled payments. This means they must begin to pay attention to the cost side of the value equation (quality divided by cost) as it relates to hospital discharge.

A day of home care represents a more cost-effective alternative than a day of care in a skilled nursing facility (SNF). Hospitalists who can identify those patients who are appropriate to send home with home health services—and who otherwise would have gone to a SNF—will serve the dual goals of improving patient experience and decreasing costs.

Hospitalists will need to develop a decision-making process that determines the appropriate level of care for the patient after discharge. The decision-making process should address questions like:

  • What skilled services lead a patient to go to a SNF instead of home with home health?
  • Which patients go to a SNF instead of home simply because they don’t have family or a caregiver to help them with activities of daily living?
  • Are there services requiring a nurse or a therapist that can’t be delivered in the home?

Hospitalists also will need to develop a more intimate understanding of the following levels of care:

  • Skilled nursing includes management of a nursing care plan, assessment of a patient’s changing condition, and services like wound care, infusion therapy, and management of medications, feeding or drainage tubes, and pain.
  • Skilled rehabilitation refers to the array of services provided by physical, occupational, speech, and respiratory therapists.
  • Custodial care, usually supplied by a home health aid or family member, includes help with activities of daily living (feeding, dressing, bathing, grooming, personal hygiene, and toileting).

Even though home care has been around for a while, there is a sizeable group of patients, especially in geographic areas of high SNF spending, who might be better served in the home environment.

It should be noted that most skilled nursing or therapy services can be delivered in the home setting if the patient’s custodial care needs are met—a big ‘if’ in some cases. Some patients go to a SNF because they require three or more skilled nursing or therapy services, and it is therefore impractical for them to go home.

Here are my suggestions to hospitalists seeking to reengineer the discharge process with the goals of “right-sizing” the number of patients who go to SNFs and optimizing the utilization of home healthcare services:

  • Become familiar with the range of post-acute care providers and care coordination services in your community.
  • Refer any patient who wishes to go home, either directly or after a SNF stay, for a home care evaluation. Home care agencies are experts in determining if and how patients can return home.
  • If a need for help with activities of daily living is the major barrier to having a patient discharged to home, create a system in which case management develops a custodial care plan with the patient and caregivers during the inpatient stay. Currently, this step is delayed until well into the SNF stay and may prolong that stay. Such a plan includes a financial analysis, screening for Medicaid eligibility, and evaluating whether a family member can assume some or all of the custodial care needs.
  • If a patient is being discharged to a SNF, review the list of needed services leading to the SNF transfer. Ask the case manager if these services can be provided in the home. If not, then why?
  • Bed capacity permitting, consider keeping patients who are functionally improving in the hospital an extra day so they can be discharged directly home instead of to a SNF.2
 

 

In his seminal work, The Innovator’s Dilemma, Clayton Christensen describes “disruptive innovation” as that which gives rise to products or services that are cheaper, simpler, and more convenient to use. Even though home care has been around for a while, there is a sizeable group of patients, especially in geographic areas of high SNF spending, who might be better served in the home environment. As we create better systems under value-based payment, we should see an increase in the use of home healthcare as a disruptive innovation when applied to appropriate patients transitioning out of the hospital or a SNF.


Dr. Whitcomb is Chief Medical Officer of Remedy Partners. He is co-founder and past president of SHM. Email him at [email protected].

 

 

References

  1. Newhouse JP, Garber AM. Geographic variation in Medicare services. N Engl J Med. 2013;368:1465-1468.
  2. Mechanic R. Post-acute care—The next frontier for controlling Medicare spending. N Engl J Med. 2014;370(8):692-694.
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How useful is random biopsy when no colposcopic lesions are seen?

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When performing colposcopy for abnormal cytology results or high-risk human papillomavirus (HPV), clinicians often are faced with an absence of visible lesions. This situation raises the following question in his or her mind: “Should I perform a random biopsy?”

Details of the study
In a multicenter US study of more than 47,000 women, performed to assess HPV diagnostics between May 2008 and August 2009, colposcopy was performed in nonpregnant women aged 25 or older with an intact uterus due to atypical squamous cells of undetermined significance or greater cytology results or high-risk HPV. The study participants and the colposcopists were blinded to the test results. In women with satisfactory colposcopy results but in whom no colposcopic lesions were noted, one random biopsy of the squamocolumnar junction was performed.

Among 2,796 women (mean age, 39.5 years) with a random biopsy performed, the findings were: normal, cervical intraepithelial neoplasia (CIN)−1, CIN2, and CIN3 in 90.0%, 5.7%, 1.3%, and 1.4%, respectively. Among all participants aged 25 and older, random biopsies accounted for 20.9% and 18.9% of the CIN2 or worse and CIN3 or worse cases, respectively. Among women positive for HPV 16 or 18, the likelihood of the random biopsy detecting CIN2 or worse was 24.7% and 8.6% for those with abnormal cytology or normal cytology, respectively.

What this evidence means for your practice
Consistent with other reports, the results of this post hoc analysis underscore the limitations of colposcopy. Just as results of a prior study indicated that taking two or more biopsies increases diagnostic yield,1 this large study points out the substantial benefit gained from performing a random biopsy of the squamocolumnar junction when no colposcopic lesions are identified.
                                                                    —Andrew M. Kaunitz, MD

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

References

Reference

  1. Gage JC, Hanson VW, Abbey K, et al; SCUS LSIL Triage Study (ALTS) Group. Number of cervical biopsies and sensitivity of colposcopy. Obstet Gynecol. 2006;108(2):264–272.
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Andrew M. Kaunitz, MD, is University of Florida Research Foundation Professor and Associate Chairman, Department of Obstetrics and Gynecology, University of Florida College of Medicine-Jacksonville, and Director, Menopause and Gynecologic Ultrasound Services, University of Florida Women’s Health Specialists-Emerson, in Jacksonville, Florida.

Dr. Kaunitz reports that he receives grant or research support from Bayer and Teva, and is a consultant to Actavis, Bayer, and Teva.

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When performing colposcopy for abnormal cytology results or high-risk human papillomavirus (HPV), clinicians often are faced with an absence of visible lesions. This situation raises the following question in his or her mind: “Should I perform a random biopsy?”

Details of the study
In a multicenter US study of more than 47,000 women, performed to assess HPV diagnostics between May 2008 and August 2009, colposcopy was performed in nonpregnant women aged 25 or older with an intact uterus due to atypical squamous cells of undetermined significance or greater cytology results or high-risk HPV. The study participants and the colposcopists were blinded to the test results. In women with satisfactory colposcopy results but in whom no colposcopic lesions were noted, one random biopsy of the squamocolumnar junction was performed.

Among 2,796 women (mean age, 39.5 years) with a random biopsy performed, the findings were: normal, cervical intraepithelial neoplasia (CIN)−1, CIN2, and CIN3 in 90.0%, 5.7%, 1.3%, and 1.4%, respectively. Among all participants aged 25 and older, random biopsies accounted for 20.9% and 18.9% of the CIN2 or worse and CIN3 or worse cases, respectively. Among women positive for HPV 16 or 18, the likelihood of the random biopsy detecting CIN2 or worse was 24.7% and 8.6% for those with abnormal cytology or normal cytology, respectively.

What this evidence means for your practice
Consistent with other reports, the results of this post hoc analysis underscore the limitations of colposcopy. Just as results of a prior study indicated that taking two or more biopsies increases diagnostic yield,1 this large study points out the substantial benefit gained from performing a random biopsy of the squamocolumnar junction when no colposcopic lesions are identified.
                                                                    —Andrew M. Kaunitz, MD

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

When performing colposcopy for abnormal cytology results or high-risk human papillomavirus (HPV), clinicians often are faced with an absence of visible lesions. This situation raises the following question in his or her mind: “Should I perform a random biopsy?”

Details of the study
In a multicenter US study of more than 47,000 women, performed to assess HPV diagnostics between May 2008 and August 2009, colposcopy was performed in nonpregnant women aged 25 or older with an intact uterus due to atypical squamous cells of undetermined significance or greater cytology results or high-risk HPV. The study participants and the colposcopists were blinded to the test results. In women with satisfactory colposcopy results but in whom no colposcopic lesions were noted, one random biopsy of the squamocolumnar junction was performed.

Among 2,796 women (mean age, 39.5 years) with a random biopsy performed, the findings were: normal, cervical intraepithelial neoplasia (CIN)−1, CIN2, and CIN3 in 90.0%, 5.7%, 1.3%, and 1.4%, respectively. Among all participants aged 25 and older, random biopsies accounted for 20.9% and 18.9% of the CIN2 or worse and CIN3 or worse cases, respectively. Among women positive for HPV 16 or 18, the likelihood of the random biopsy detecting CIN2 or worse was 24.7% and 8.6% for those with abnormal cytology or normal cytology, respectively.

What this evidence means for your practice
Consistent with other reports, the results of this post hoc analysis underscore the limitations of colposcopy. Just as results of a prior study indicated that taking two or more biopsies increases diagnostic yield,1 this large study points out the substantial benefit gained from performing a random biopsy of the squamocolumnar junction when no colposcopic lesions are identified.
                                                                    —Andrew M. Kaunitz, MD

Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.

References

Reference

  1. Gage JC, Hanson VW, Abbey K, et al; SCUS LSIL Triage Study (ALTS) Group. Number of cervical biopsies and sensitivity of colposcopy. Obstet Gynecol. 2006;108(2):264–272.
References

Reference

  1. Gage JC, Hanson VW, Abbey K, et al; SCUS LSIL Triage Study (ALTS) Group. Number of cervical biopsies and sensitivity of colposcopy. Obstet Gynecol. 2006;108(2):264–272.
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PHILADELPHIA – How would your hospital handle an Ebola patient? Ask Dr. Bruce Ribner.

At ID Week 2014 in Philadelphia, Dr. Ribner, medical director of Emory University Hospital’s serious communicable diseases unit in Atlanta, gave a detailed account of his hospital’s management of the first two American patients treated at Emory after contracting the disease while working in Africa.

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PHILADELPHIA – How would your hospital handle an Ebola patient? Ask Dr. Bruce Ribner.

At ID Week 2014 in Philadelphia, Dr. Ribner, medical director of Emory University Hospital’s serious communicable diseases unit in Atlanta, gave a detailed account of his hospital’s management of the first two American patients treated at Emory after contracting the disease while working in Africa.

[email protected]

PHILADELPHIA – How would your hospital handle an Ebola patient? Ask Dr. Bruce Ribner.

At ID Week 2014 in Philadelphia, Dr. Ribner, medical director of Emory University Hospital’s serious communicable diseases unit in Atlanta, gave a detailed account of his hospital’s management of the first two American patients treated at Emory after contracting the disease while working in Africa.

[email protected]

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