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Recovering From Military Sexual Trauma
Military sexual trauma (MST) refers to experiences of sexual assault or repeated, threatening sexual harassment experienced while on federal active duty or active duty for training. About 1 in 4 women and 1 in 100 men have reported MST to their VA doctors. However, these numbers do not account for those who have not sought health care for their MST experience or who have sought care for MST outside the VA.
Military sexual trauma is:
Military sexual trauma is the term VA uses to refer to sexual assault or sexual harassment that occurred while the veteran was in the military. A victim of MST may have been:
- Involved in sexual activity against his or her will, by physical force or nonphysical pressure. Nonphysical pressure includes threats of negative consequences for refusing to be sexually cooperative, or indirect promises of faster promotions or better treatment in exchange for sex.
- Unable to consent to sexual activities. This includes intoxication by alcohol or other substances.
Other experiences include sexual touching or grabbing, threatening or offensive remarks about a person’s body or sexual activities, as well as threatening and unwelcome sexual advances.
How do I know if I’m at risk?
Military sexual trauma can occur on or off base and while a service member—man or woman—is on or off duty. Those who commit sexual assault or sexual harassment can be men or women, military personnel or civilians, commanding officers or subordinates, strangers, friends, spouses, or intimate partners.
When do I need medical attention?
The VA reports sexual assault is more likely to result in symptoms of PTSD (posttraumatic stress disorder) than are most other types of trauma, including combat. You should seek medical attention from your primary care doctor, a mental health professional, or your VA facility’s MST Coordinator following a MST experience, especially if you experience any of the following symptoms:
- Depression
- Suicidal thoughts
- Feeling angry or irritable most of the time
- Strong emotional reactions
- Feeling emotionally numb
- Trouble falling or staying asleep
- Nightmares
- Trouble focusing
- Difficulty remembering things
- Substance abuse
- Trouble feeling safe or trusting others
- Feeling isolated or disconnected from others
- Headaches
- Gastrointestinal difficulties
- Sexual dysfunction
- Chronic pain
- Chronic fatigue
- Weight or eating problems
Survivors who are not formally diagnosed may still struggle in certain situations with emotional reactions, memories related to their experiences of MST, or other interpersonal issues.
How is MST treated?
Because MST is an experience, not a diagnosis, treatment needs may vary from patient to patient. However, VA provides free, confidential counseling and treatment to male and female veterans for mental and physical health conditions related to experiences of MST. It is important to note that treatment is available even if the MST incident was not reported at the time it happened.
Your doctor may recommend individual therapy, group therapy, or medication, depending on your symptoms. Therapies that may be used to treat MST include:
- Cognitive behavioral therapy. The main goal of this therapy is to help you change your thought patterns, which will help you change the emotions and behavior connected with the MST experience. A counselor might encourage you to reimagine your trauma repeatedly under controlled conditions—an approach called exposure therapy—as a way of learning to cope.
- Stress inoculation (in-ock-you-lay-shun) training. This therapy involves combining stress management strategies with stress-relieving techniques, such as muscle relaxation, breathing retraining, self-dialogue, and thought stopping.
- Group therapy. This therapy enables you to discuss your trauma with others who have had similar experiences.
- Inpatient therapy. Nationwide, there are programs that offer specialized sexual trauma treatment for veterans who need more intense treatment and support, including that for severe depression or substance abuse.
- Medication. If your MST experience resulted in PTSD, your doctor may prescribe medication to help control symptoms of anxiety or to help you sleep. Your doctor will monitor you closely for any possible adverse effects of these medications. It is also possible that an STD (sexually transmitted disease) was passed during the trauma, so your doctor may choose to screen you for an STD. If the test comes back positive, your doctor will prescribe the appropriate drug for treatment.
Services are designed to help veterans at all stages of their recovery, whether that is focusing on strategies for coping with emotions and memories or, for veterans who are ready, talking about their MST experiences in depth.
What can I do to cope?
When trauma survivors take direct action to cope with their stress reactions, they put themselves in a position of power. This is called active coping, which involves accepting the impact the trauma had on your life and taking direct action to make improvements.
It is important to remember that recovery is a process and takes time. Healing from trauma, including MST, does not happen all at once, and healing does not mean that you must forget the experience. Instead, it means you have less pain and fewer bad feelings when you think about the experience, and any associated symptoms will over time bother you less.
Discussing your trauma with other survivors in a controlled setting can help you learn that you are not alone or weak. In addition, surrounding yourself with people you can talk to about your MST experience may help you feel more understood. You may even choose to distract yourself with positive recreational or work activities.
When you experience unwanted or distressing memories, remind yourself that they are just memories, and talk about them with someone you trust. If you feel that the trauma is happening again, which is known as a flashback, keep your eyes open and remind yourself where you presently are and that the trauma happened in the past.
Although VA and DoD are working to put an end to MST, it is an ongoing problem that affects a large percentage of women and men who proudly serve in the armed forces. For information on how to access free VA services and to determine your eligibility in MST benefits, visit http://www.mentalhealth.va.gov/msthome.asp.
Military sexual trauma (MST) refers to experiences of sexual assault or repeated, threatening sexual harassment experienced while on federal active duty or active duty for training. About 1 in 4 women and 1 in 100 men have reported MST to their VA doctors. However, these numbers do not account for those who have not sought health care for their MST experience or who have sought care for MST outside the VA.
Military sexual trauma is:
Military sexual trauma is the term VA uses to refer to sexual assault or sexual harassment that occurred while the veteran was in the military. A victim of MST may have been:
- Involved in sexual activity against his or her will, by physical force or nonphysical pressure. Nonphysical pressure includes threats of negative consequences for refusing to be sexually cooperative, or indirect promises of faster promotions or better treatment in exchange for sex.
- Unable to consent to sexual activities. This includes intoxication by alcohol or other substances.
Other experiences include sexual touching or grabbing, threatening or offensive remarks about a person’s body or sexual activities, as well as threatening and unwelcome sexual advances.
How do I know if I’m at risk?
Military sexual trauma can occur on or off base and while a service member—man or woman—is on or off duty. Those who commit sexual assault or sexual harassment can be men or women, military personnel or civilians, commanding officers or subordinates, strangers, friends, spouses, or intimate partners.
When do I need medical attention?
The VA reports sexual assault is more likely to result in symptoms of PTSD (posttraumatic stress disorder) than are most other types of trauma, including combat. You should seek medical attention from your primary care doctor, a mental health professional, or your VA facility’s MST Coordinator following a MST experience, especially if you experience any of the following symptoms:
- Depression
- Suicidal thoughts
- Feeling angry or irritable most of the time
- Strong emotional reactions
- Feeling emotionally numb
- Trouble falling or staying asleep
- Nightmares
- Trouble focusing
- Difficulty remembering things
- Substance abuse
- Trouble feeling safe or trusting others
- Feeling isolated or disconnected from others
- Headaches
- Gastrointestinal difficulties
- Sexual dysfunction
- Chronic pain
- Chronic fatigue
- Weight or eating problems
Survivors who are not formally diagnosed may still struggle in certain situations with emotional reactions, memories related to their experiences of MST, or other interpersonal issues.
How is MST treated?
Because MST is an experience, not a diagnosis, treatment needs may vary from patient to patient. However, VA provides free, confidential counseling and treatment to male and female veterans for mental and physical health conditions related to experiences of MST. It is important to note that treatment is available even if the MST incident was not reported at the time it happened.
Your doctor may recommend individual therapy, group therapy, or medication, depending on your symptoms. Therapies that may be used to treat MST include:
- Cognitive behavioral therapy. The main goal of this therapy is to help you change your thought patterns, which will help you change the emotions and behavior connected with the MST experience. A counselor might encourage you to reimagine your trauma repeatedly under controlled conditions—an approach called exposure therapy—as a way of learning to cope.
- Stress inoculation (in-ock-you-lay-shun) training. This therapy involves combining stress management strategies with stress-relieving techniques, such as muscle relaxation, breathing retraining, self-dialogue, and thought stopping.
- Group therapy. This therapy enables you to discuss your trauma with others who have had similar experiences.
- Inpatient therapy. Nationwide, there are programs that offer specialized sexual trauma treatment for veterans who need more intense treatment and support, including that for severe depression or substance abuse.
- Medication. If your MST experience resulted in PTSD, your doctor may prescribe medication to help control symptoms of anxiety or to help you sleep. Your doctor will monitor you closely for any possible adverse effects of these medications. It is also possible that an STD (sexually transmitted disease) was passed during the trauma, so your doctor may choose to screen you for an STD. If the test comes back positive, your doctor will prescribe the appropriate drug for treatment.
Services are designed to help veterans at all stages of their recovery, whether that is focusing on strategies for coping with emotions and memories or, for veterans who are ready, talking about their MST experiences in depth.
What can I do to cope?
When trauma survivors take direct action to cope with their stress reactions, they put themselves in a position of power. This is called active coping, which involves accepting the impact the trauma had on your life and taking direct action to make improvements.
It is important to remember that recovery is a process and takes time. Healing from trauma, including MST, does not happen all at once, and healing does not mean that you must forget the experience. Instead, it means you have less pain and fewer bad feelings when you think about the experience, and any associated symptoms will over time bother you less.
Discussing your trauma with other survivors in a controlled setting can help you learn that you are not alone or weak. In addition, surrounding yourself with people you can talk to about your MST experience may help you feel more understood. You may even choose to distract yourself with positive recreational or work activities.
When you experience unwanted or distressing memories, remind yourself that they are just memories, and talk about them with someone you trust. If you feel that the trauma is happening again, which is known as a flashback, keep your eyes open and remind yourself where you presently are and that the trauma happened in the past.
Although VA and DoD are working to put an end to MST, it is an ongoing problem that affects a large percentage of women and men who proudly serve in the armed forces. For information on how to access free VA services and to determine your eligibility in MST benefits, visit http://www.mentalhealth.va.gov/msthome.asp.
Military sexual trauma (MST) refers to experiences of sexual assault or repeated, threatening sexual harassment experienced while on federal active duty or active duty for training. About 1 in 4 women and 1 in 100 men have reported MST to their VA doctors. However, these numbers do not account for those who have not sought health care for their MST experience or who have sought care for MST outside the VA.
Military sexual trauma is:
Military sexual trauma is the term VA uses to refer to sexual assault or sexual harassment that occurred while the veteran was in the military. A victim of MST may have been:
- Involved in sexual activity against his or her will, by physical force or nonphysical pressure. Nonphysical pressure includes threats of negative consequences for refusing to be sexually cooperative, or indirect promises of faster promotions or better treatment in exchange for sex.
- Unable to consent to sexual activities. This includes intoxication by alcohol or other substances.
Other experiences include sexual touching or grabbing, threatening or offensive remarks about a person’s body or sexual activities, as well as threatening and unwelcome sexual advances.
How do I know if I’m at risk?
Military sexual trauma can occur on or off base and while a service member—man or woman—is on or off duty. Those who commit sexual assault or sexual harassment can be men or women, military personnel or civilians, commanding officers or subordinates, strangers, friends, spouses, or intimate partners.
When do I need medical attention?
The VA reports sexual assault is more likely to result in symptoms of PTSD (posttraumatic stress disorder) than are most other types of trauma, including combat. You should seek medical attention from your primary care doctor, a mental health professional, or your VA facility’s MST Coordinator following a MST experience, especially if you experience any of the following symptoms:
- Depression
- Suicidal thoughts
- Feeling angry or irritable most of the time
- Strong emotional reactions
- Feeling emotionally numb
- Trouble falling or staying asleep
- Nightmares
- Trouble focusing
- Difficulty remembering things
- Substance abuse
- Trouble feeling safe or trusting others
- Feeling isolated or disconnected from others
- Headaches
- Gastrointestinal difficulties
- Sexual dysfunction
- Chronic pain
- Chronic fatigue
- Weight or eating problems
Survivors who are not formally diagnosed may still struggle in certain situations with emotional reactions, memories related to their experiences of MST, or other interpersonal issues.
How is MST treated?
Because MST is an experience, not a diagnosis, treatment needs may vary from patient to patient. However, VA provides free, confidential counseling and treatment to male and female veterans for mental and physical health conditions related to experiences of MST. It is important to note that treatment is available even if the MST incident was not reported at the time it happened.
Your doctor may recommend individual therapy, group therapy, or medication, depending on your symptoms. Therapies that may be used to treat MST include:
- Cognitive behavioral therapy. The main goal of this therapy is to help you change your thought patterns, which will help you change the emotions and behavior connected with the MST experience. A counselor might encourage you to reimagine your trauma repeatedly under controlled conditions—an approach called exposure therapy—as a way of learning to cope.
- Stress inoculation (in-ock-you-lay-shun) training. This therapy involves combining stress management strategies with stress-relieving techniques, such as muscle relaxation, breathing retraining, self-dialogue, and thought stopping.
- Group therapy. This therapy enables you to discuss your trauma with others who have had similar experiences.
- Inpatient therapy. Nationwide, there are programs that offer specialized sexual trauma treatment for veterans who need more intense treatment and support, including that for severe depression or substance abuse.
- Medication. If your MST experience resulted in PTSD, your doctor may prescribe medication to help control symptoms of anxiety or to help you sleep. Your doctor will monitor you closely for any possible adverse effects of these medications. It is also possible that an STD (sexually transmitted disease) was passed during the trauma, so your doctor may choose to screen you for an STD. If the test comes back positive, your doctor will prescribe the appropriate drug for treatment.
Services are designed to help veterans at all stages of their recovery, whether that is focusing on strategies for coping with emotions and memories or, for veterans who are ready, talking about their MST experiences in depth.
What can I do to cope?
When trauma survivors take direct action to cope with their stress reactions, they put themselves in a position of power. This is called active coping, which involves accepting the impact the trauma had on your life and taking direct action to make improvements.
It is important to remember that recovery is a process and takes time. Healing from trauma, including MST, does not happen all at once, and healing does not mean that you must forget the experience. Instead, it means you have less pain and fewer bad feelings when you think about the experience, and any associated symptoms will over time bother you less.
Discussing your trauma with other survivors in a controlled setting can help you learn that you are not alone or weak. In addition, surrounding yourself with people you can talk to about your MST experience may help you feel more understood. You may even choose to distract yourself with positive recreational or work activities.
When you experience unwanted or distressing memories, remind yourself that they are just memories, and talk about them with someone you trust. If you feel that the trauma is happening again, which is known as a flashback, keep your eyes open and remind yourself where you presently are and that the trauma happened in the past.
Although VA and DoD are working to put an end to MST, it is an ongoing problem that affects a large percentage of women and men who proudly serve in the armed forces. For information on how to access free VA services and to determine your eligibility in MST benefits, visit http://www.mentalhealth.va.gov/msthome.asp.
Potential treatment method induces severe side effects
Previous studies have shown that inhibiting the activity of the Malt1 protein can kill lymphoma cells.
Now, research published in Cell Reports has revealed that it also causes the immune system to malfunction.
Malt1 carries out a variety of tasks in lymphocytes, including acting as a protease that breaks down messenger substances and controls their quantity.
Until now, researchers were unsure about the role the protease function plays in immune cell development.
Several years ago, Jürgen Ruland, PhD, of Technische Universität München in Germany, and his colleagues turned their attention to this question.
Via cell culture experiments, the researchers found that blocking the protease function of Malt1 kills lymphoma cells. The team decided to test this strategy in an animal model to shed light on the exact function of Malt1 protease.
“It’s only possible to study complex interactions in the immune system, which comprises a finely orchestrated interplay of various cell types, in an intact organism, not in cell cultures,” Dr Ruland noted. “The processes are too complex to recreate in cells outside the body.”
The mice the researchers used were genetically modified so their Malt1 protein could no longer act as a protease but was still able to carry out all of its other functions.
The team was surprised to find that these mice developed severe signs of inflammation. Moreover, the immune system attacked and destroyed key neurons that coordinate movements.
The researchers were able to explain how this serious malfunction occurred and, in doing so, discovered an unexpected function of Malt1.
They found that, in the absence of the protease function, the mice were unable to produce regulatory T cells, and this caused their immune responses to spin
out of control.
The team also found that normal lymphocytes can be activated without the protease function of Malt1, but they release messenger substances uncontrollably, which causes inflammation.
“Our study showed that Malt1 protease is surprisingly important for the development of regulatory T cells and for damping the immune response in general,” Dr Ruland said. “Since the blockade of the protease function in the organism produces undesirable effects, new alternatives should urgently be sought for the treatment of lymphoma.”
Previous studies have shown that inhibiting the activity of the Malt1 protein can kill lymphoma cells.
Now, research published in Cell Reports has revealed that it also causes the immune system to malfunction.
Malt1 carries out a variety of tasks in lymphocytes, including acting as a protease that breaks down messenger substances and controls their quantity.
Until now, researchers were unsure about the role the protease function plays in immune cell development.
Several years ago, Jürgen Ruland, PhD, of Technische Universität München in Germany, and his colleagues turned their attention to this question.
Via cell culture experiments, the researchers found that blocking the protease function of Malt1 kills lymphoma cells. The team decided to test this strategy in an animal model to shed light on the exact function of Malt1 protease.
“It’s only possible to study complex interactions in the immune system, which comprises a finely orchestrated interplay of various cell types, in an intact organism, not in cell cultures,” Dr Ruland noted. “The processes are too complex to recreate in cells outside the body.”
The mice the researchers used were genetically modified so their Malt1 protein could no longer act as a protease but was still able to carry out all of its other functions.
The team was surprised to find that these mice developed severe signs of inflammation. Moreover, the immune system attacked and destroyed key neurons that coordinate movements.
The researchers were able to explain how this serious malfunction occurred and, in doing so, discovered an unexpected function of Malt1.
They found that, in the absence of the protease function, the mice were unable to produce regulatory T cells, and this caused their immune responses to spin
out of control.
The team also found that normal lymphocytes can be activated without the protease function of Malt1, but they release messenger substances uncontrollably, which causes inflammation.
“Our study showed that Malt1 protease is surprisingly important for the development of regulatory T cells and for damping the immune response in general,” Dr Ruland said. “Since the blockade of the protease function in the organism produces undesirable effects, new alternatives should urgently be sought for the treatment of lymphoma.”
Previous studies have shown that inhibiting the activity of the Malt1 protein can kill lymphoma cells.
Now, research published in Cell Reports has revealed that it also causes the immune system to malfunction.
Malt1 carries out a variety of tasks in lymphocytes, including acting as a protease that breaks down messenger substances and controls their quantity.
Until now, researchers were unsure about the role the protease function plays in immune cell development.
Several years ago, Jürgen Ruland, PhD, of Technische Universität München in Germany, and his colleagues turned their attention to this question.
Via cell culture experiments, the researchers found that blocking the protease function of Malt1 kills lymphoma cells. The team decided to test this strategy in an animal model to shed light on the exact function of Malt1 protease.
“It’s only possible to study complex interactions in the immune system, which comprises a finely orchestrated interplay of various cell types, in an intact organism, not in cell cultures,” Dr Ruland noted. “The processes are too complex to recreate in cells outside the body.”
The mice the researchers used were genetically modified so their Malt1 protein could no longer act as a protease but was still able to carry out all of its other functions.
The team was surprised to find that these mice developed severe signs of inflammation. Moreover, the immune system attacked and destroyed key neurons that coordinate movements.
The researchers were able to explain how this serious malfunction occurred and, in doing so, discovered an unexpected function of Malt1.
They found that, in the absence of the protease function, the mice were unable to produce regulatory T cells, and this caused their immune responses to spin
out of control.
The team also found that normal lymphocytes can be activated without the protease function of Malt1, but they release messenger substances uncontrollably, which causes inflammation.
“Our study showed that Malt1 protease is surprisingly important for the development of regulatory T cells and for damping the immune response in general,” Dr Ruland said. “Since the blockade of the protease function in the organism produces undesirable effects, new alternatives should urgently be sought for the treatment of lymphoma.”
Reintroducing heparin in patients with a history of HIT
Two tests used to measure antibodies in patients with a history of heparin-induced thrombocytopenia (HIT) can produce radically different results, new research shows.
The anti-PF4/heparin IgG-specific enzyme-immunoassay can show that HIT antibody levels are high, while the functional platelet serotonin-release assay indicates that levels are low.
And researchers said the functional assay’s results may be the better indicator of a patient’s readiness for re-exposure to heparin.
Theodore Warkentin, MD, of McMaster University in Hamilton, Ontario, Canada, and his colleagues expressed this viewpoint and detailed the research supporting it in Blood.
When patients with a history of HIT require urgent heart surgery, physicians must test for the presence of HIT antibodies to determine whether the patient can be re-exposed to heparin during the procedure.
Hematologists use two types of tests to measure HIT antibodies—a functional platelet serotonin-release assay and an anti-PF4/heparin IgG-specific enzyme-immunoassay. If the more widely used immunoassay indicates the presence of HIT antibodies in a patient, surgery is usually delayed or plasma exchange is performed to lower the antibodies.
Practitioners have historically understood the two assays to provide similar conclusions, but a case report suggested otherwise.
A 76-year-old female with kidney cancer and previous HIT required urgent cardiac surgery to remove a tumor that had spread to her heart. After both her initial functional and immunoassays indicated the presence of HIT antibodies, her doctors deemed her ineligible for surgery.
But after repeated plasma exchange, the researchers performed both the functional and immunoassays on the patient again, and, this time, they observed strikingly different results.
“We were surprised to see that levels of HIT antibodies in this patient fell very quickly according to the functional assay, yet the antibodies detected by the immunoassay remained high,” Dr Warkentin said.
“This suggested to us that, while physicians in many situations may be waiting for the immunoassay to indicate lower antibody levels, patients in urgent need of heart surgery may be ready much earlier than the results suggest.”
To better understand the dissociation between the results of the two tests, Dr Warkentin’s team developed a model comparing functional and immunoassay results among 15 HIT blood samples. The samples were sequentially diluted and tested with both assays to mimic the effects of repeated plasma exchange.
The researchers observed that HIT antibody levels as measured by the functional assay decreased rather quickly, while the immunoassay continued to indicate high levels.
This suggests the sensitivity of the immunoassay may provide an overly conservative estimate of HIT antibody levels and their clinical relevance. The analysis illustrates how quickly platelet-activating properties can decline in a patient, either naturally or by using plasma exchange.
The observations also support the use of repeated plasma exchange as a therapeutic strategy prior to planned heparin re-exposure among patients with a recent HIT episode who require urgent cardiac surgery.
“Based on these findings, physicians should consider utilizing both of these tests when preparing a patient with a history of HIT for urgent heart surgery, considering the functional assay result as the stronger indicator of a patient’s readiness,” Dr Warkentin said.
“For these patients, [plasma exchange] can be a useful option to help rapidly reduce their remaining HIT antibody levels, minimize their risk of developing clots, and get them into the operating room sooner.”
Two tests used to measure antibodies in patients with a history of heparin-induced thrombocytopenia (HIT) can produce radically different results, new research shows.
The anti-PF4/heparin IgG-specific enzyme-immunoassay can show that HIT antibody levels are high, while the functional platelet serotonin-release assay indicates that levels are low.
And researchers said the functional assay’s results may be the better indicator of a patient’s readiness for re-exposure to heparin.
Theodore Warkentin, MD, of McMaster University in Hamilton, Ontario, Canada, and his colleagues expressed this viewpoint and detailed the research supporting it in Blood.
When patients with a history of HIT require urgent heart surgery, physicians must test for the presence of HIT antibodies to determine whether the patient can be re-exposed to heparin during the procedure.
Hematologists use two types of tests to measure HIT antibodies—a functional platelet serotonin-release assay and an anti-PF4/heparin IgG-specific enzyme-immunoassay. If the more widely used immunoassay indicates the presence of HIT antibodies in a patient, surgery is usually delayed or plasma exchange is performed to lower the antibodies.
Practitioners have historically understood the two assays to provide similar conclusions, but a case report suggested otherwise.
A 76-year-old female with kidney cancer and previous HIT required urgent cardiac surgery to remove a tumor that had spread to her heart. After both her initial functional and immunoassays indicated the presence of HIT antibodies, her doctors deemed her ineligible for surgery.
But after repeated plasma exchange, the researchers performed both the functional and immunoassays on the patient again, and, this time, they observed strikingly different results.
“We were surprised to see that levels of HIT antibodies in this patient fell very quickly according to the functional assay, yet the antibodies detected by the immunoassay remained high,” Dr Warkentin said.
“This suggested to us that, while physicians in many situations may be waiting for the immunoassay to indicate lower antibody levels, patients in urgent need of heart surgery may be ready much earlier than the results suggest.”
To better understand the dissociation between the results of the two tests, Dr Warkentin’s team developed a model comparing functional and immunoassay results among 15 HIT blood samples. The samples were sequentially diluted and tested with both assays to mimic the effects of repeated plasma exchange.
The researchers observed that HIT antibody levels as measured by the functional assay decreased rather quickly, while the immunoassay continued to indicate high levels.
This suggests the sensitivity of the immunoassay may provide an overly conservative estimate of HIT antibody levels and their clinical relevance. The analysis illustrates how quickly platelet-activating properties can decline in a patient, either naturally or by using plasma exchange.
The observations also support the use of repeated plasma exchange as a therapeutic strategy prior to planned heparin re-exposure among patients with a recent HIT episode who require urgent cardiac surgery.
“Based on these findings, physicians should consider utilizing both of these tests when preparing a patient with a history of HIT for urgent heart surgery, considering the functional assay result as the stronger indicator of a patient’s readiness,” Dr Warkentin said.
“For these patients, [plasma exchange] can be a useful option to help rapidly reduce their remaining HIT antibody levels, minimize their risk of developing clots, and get them into the operating room sooner.”
Two tests used to measure antibodies in patients with a history of heparin-induced thrombocytopenia (HIT) can produce radically different results, new research shows.
The anti-PF4/heparin IgG-specific enzyme-immunoassay can show that HIT antibody levels are high, while the functional platelet serotonin-release assay indicates that levels are low.
And researchers said the functional assay’s results may be the better indicator of a patient’s readiness for re-exposure to heparin.
Theodore Warkentin, MD, of McMaster University in Hamilton, Ontario, Canada, and his colleagues expressed this viewpoint and detailed the research supporting it in Blood.
When patients with a history of HIT require urgent heart surgery, physicians must test for the presence of HIT antibodies to determine whether the patient can be re-exposed to heparin during the procedure.
Hematologists use two types of tests to measure HIT antibodies—a functional platelet serotonin-release assay and an anti-PF4/heparin IgG-specific enzyme-immunoassay. If the more widely used immunoassay indicates the presence of HIT antibodies in a patient, surgery is usually delayed or plasma exchange is performed to lower the antibodies.
Practitioners have historically understood the two assays to provide similar conclusions, but a case report suggested otherwise.
A 76-year-old female with kidney cancer and previous HIT required urgent cardiac surgery to remove a tumor that had spread to her heart. After both her initial functional and immunoassays indicated the presence of HIT antibodies, her doctors deemed her ineligible for surgery.
But after repeated plasma exchange, the researchers performed both the functional and immunoassays on the patient again, and, this time, they observed strikingly different results.
“We were surprised to see that levels of HIT antibodies in this patient fell very quickly according to the functional assay, yet the antibodies detected by the immunoassay remained high,” Dr Warkentin said.
“This suggested to us that, while physicians in many situations may be waiting for the immunoassay to indicate lower antibody levels, patients in urgent need of heart surgery may be ready much earlier than the results suggest.”
To better understand the dissociation between the results of the two tests, Dr Warkentin’s team developed a model comparing functional and immunoassay results among 15 HIT blood samples. The samples were sequentially diluted and tested with both assays to mimic the effects of repeated plasma exchange.
The researchers observed that HIT antibody levels as measured by the functional assay decreased rather quickly, while the immunoassay continued to indicate high levels.
This suggests the sensitivity of the immunoassay may provide an overly conservative estimate of HIT antibody levels and their clinical relevance. The analysis illustrates how quickly platelet-activating properties can decline in a patient, either naturally or by using plasma exchange.
The observations also support the use of repeated plasma exchange as a therapeutic strategy prior to planned heparin re-exposure among patients with a recent HIT episode who require urgent cardiac surgery.
“Based on these findings, physicians should consider utilizing both of these tests when preparing a patient with a history of HIT for urgent heart surgery, considering the functional assay result as the stronger indicator of a patient’s readiness,” Dr Warkentin said.
“For these patients, [plasma exchange] can be a useful option to help rapidly reduce their remaining HIT antibody levels, minimize their risk of developing clots, and get them into the operating room sooner.”
FDA grants CAR T-cell therapy orphan designation
The US Food and Drug Administration (FDA) has granted orphan drug designation for the chimeric antigen receptor (CAR) T-cell therapy JCAR015 to treat acute lymphoblastic leukemia (ALL).
The designation will provide the product’s developer, Juno Therapeutics, with multiple benefits, including the availability of grant money, certain tax credits, and 7 years of market exclusivity, as well as the possibility of an expedited regulatory process.
JCAR015 consists of autologous T cells expressing a CD19-specific, CD28/CD3z CAR. The treatment has shown promise in an ongoing phase 1 trial of patients with B-cell ALL.
Initial results from this study were published in Science Translational Medicine last year and in February. Updated results were presented at the AACR Annual Meeting in April.
At that point, the researchers had enrolled 22 adult patients with relapsed or refractory B-ALL who were minimal residual disease-positive or were in first complete remission at enrollment. Patients in complete remission were monitored and only received JCAR015 if they relapsed.
The remaining patients received re-induction chemotherapy (physician’s choice), followed by an infusion of JCAR015. After treatment, patients could receive allogeneic transplant, a different salvage therapy, or monitoring.
Eighty-two percent of patients achieved a complete response to JCAR015. The average time to complete response was about 24.5 days.
Twelve of the responders were eligible for transplant. Of the 8 patients who ultimately underwent transplant and survived, 1 relapsed, but the rest remained in remission.
Ten patients had died at the time of the AACR presentation. Six deaths were a result of disease relapse or progression, and 2 patients died of complications from stem cell transplant.
The 2 remaining deaths prompted a temporary suspension of enrollment in this trial.
Those deaths were related to complications from cytokine release syndrome. One patient died of cardiovascular disease, and the other died following “persistent seizure activity.”
So researchers at the Memorial Sloan-Kettering Cancer Center, where the trial is being conducted, reviewed these cases.
The results prompted them to amend trial enrollment criteria and dosing recommendations. Now, patients with cardiac disease are ineligible to receive JCAR015.
And the T-cell dose a patient receives will depend on the extent of his or her disease. The hope is that this will reduce the risk of cytokine release syndrome and any resulting seizures.
The researchers also noted that the monoclonal antibody tocilizumab has proven effective in treating cytokine release syndrome.
In addition to this trial, JCAR015 is under investigation in another phase 1 trial of patients with relapsed and refractory non-Hodgkin lymphoma.
The US Food and Drug Administration (FDA) has granted orphan drug designation for the chimeric antigen receptor (CAR) T-cell therapy JCAR015 to treat acute lymphoblastic leukemia (ALL).
The designation will provide the product’s developer, Juno Therapeutics, with multiple benefits, including the availability of grant money, certain tax credits, and 7 years of market exclusivity, as well as the possibility of an expedited regulatory process.
JCAR015 consists of autologous T cells expressing a CD19-specific, CD28/CD3z CAR. The treatment has shown promise in an ongoing phase 1 trial of patients with B-cell ALL.
Initial results from this study were published in Science Translational Medicine last year and in February. Updated results were presented at the AACR Annual Meeting in April.
At that point, the researchers had enrolled 22 adult patients with relapsed or refractory B-ALL who were minimal residual disease-positive or were in first complete remission at enrollment. Patients in complete remission were monitored and only received JCAR015 if they relapsed.
The remaining patients received re-induction chemotherapy (physician’s choice), followed by an infusion of JCAR015. After treatment, patients could receive allogeneic transplant, a different salvage therapy, or monitoring.
Eighty-two percent of patients achieved a complete response to JCAR015. The average time to complete response was about 24.5 days.
Twelve of the responders were eligible for transplant. Of the 8 patients who ultimately underwent transplant and survived, 1 relapsed, but the rest remained in remission.
Ten patients had died at the time of the AACR presentation. Six deaths were a result of disease relapse or progression, and 2 patients died of complications from stem cell transplant.
The 2 remaining deaths prompted a temporary suspension of enrollment in this trial.
Those deaths were related to complications from cytokine release syndrome. One patient died of cardiovascular disease, and the other died following “persistent seizure activity.”
So researchers at the Memorial Sloan-Kettering Cancer Center, where the trial is being conducted, reviewed these cases.
The results prompted them to amend trial enrollment criteria and dosing recommendations. Now, patients with cardiac disease are ineligible to receive JCAR015.
And the T-cell dose a patient receives will depend on the extent of his or her disease. The hope is that this will reduce the risk of cytokine release syndrome and any resulting seizures.
The researchers also noted that the monoclonal antibody tocilizumab has proven effective in treating cytokine release syndrome.
In addition to this trial, JCAR015 is under investigation in another phase 1 trial of patients with relapsed and refractory non-Hodgkin lymphoma.
The US Food and Drug Administration (FDA) has granted orphan drug designation for the chimeric antigen receptor (CAR) T-cell therapy JCAR015 to treat acute lymphoblastic leukemia (ALL).
The designation will provide the product’s developer, Juno Therapeutics, with multiple benefits, including the availability of grant money, certain tax credits, and 7 years of market exclusivity, as well as the possibility of an expedited regulatory process.
JCAR015 consists of autologous T cells expressing a CD19-specific, CD28/CD3z CAR. The treatment has shown promise in an ongoing phase 1 trial of patients with B-cell ALL.
Initial results from this study were published in Science Translational Medicine last year and in February. Updated results were presented at the AACR Annual Meeting in April.
At that point, the researchers had enrolled 22 adult patients with relapsed or refractory B-ALL who were minimal residual disease-positive or were in first complete remission at enrollment. Patients in complete remission were monitored and only received JCAR015 if they relapsed.
The remaining patients received re-induction chemotherapy (physician’s choice), followed by an infusion of JCAR015. After treatment, patients could receive allogeneic transplant, a different salvage therapy, or monitoring.
Eighty-two percent of patients achieved a complete response to JCAR015. The average time to complete response was about 24.5 days.
Twelve of the responders were eligible for transplant. Of the 8 patients who ultimately underwent transplant and survived, 1 relapsed, but the rest remained in remission.
Ten patients had died at the time of the AACR presentation. Six deaths were a result of disease relapse or progression, and 2 patients died of complications from stem cell transplant.
The 2 remaining deaths prompted a temporary suspension of enrollment in this trial.
Those deaths were related to complications from cytokine release syndrome. One patient died of cardiovascular disease, and the other died following “persistent seizure activity.”
So researchers at the Memorial Sloan-Kettering Cancer Center, where the trial is being conducted, reviewed these cases.
The results prompted them to amend trial enrollment criteria and dosing recommendations. Now, patients with cardiac disease are ineligible to receive JCAR015.
And the T-cell dose a patient receives will depend on the extent of his or her disease. The hope is that this will reduce the risk of cytokine release syndrome and any resulting seizures.
The researchers also noted that the monoclonal antibody tocilizumab has proven effective in treating cytokine release syndrome.
In addition to this trial, JCAR015 is under investigation in another phase 1 trial of patients with relapsed and refractory non-Hodgkin lymphoma.
Early Warning System Boosts Sepsis Detection, Care
A recent study published in the Journal of Hospital Medicine reports on an early warning and response system (EWRS) for sepsis used in all three hospitals within the Philadelphia-based University of Pennsylvania Health System (UPHS) for three-month spans in 2012 and 2013. The system integrates laboratory values and vital signs into patients EHRs and establishes a threshold for triggering the alert.
After implementing the EWRS, at-risk patients received faster care for sepsis and/or were transferred to the ICU more quickly, says lead author Craig A. Umscheid, MD, MSCE, director of the Center for Evidence-Based Practice at the University of Pennsylvania in Philadelphia. Study authors also note that quicker care suggested reduced mortality from sepsis as well.
"Whenever a patient triggered the alert, their probability of mortality was much higher than patients who didn't trigger the alert," Dr. Umscheid says. "I think what makes our study unique compared to other studies that have tried to predict sepsis is that beyond just creating a prediction rule for sepsis, we actually implemented it into a clinical care setting, alerted providers in real time, and then those providers changed their care based on the prediction."
More than 90% of care teams arrived at the bedside when they received an alert. "Meaning that they saw some value in the alert, and the infrastructure that we put in place was able to mobilize the team and get them to the bedside within 30 minutes," Dr. Umscheid adds. "We saw an increase in sepsis antibiotics used, and we saw an increase in fluid boluses within six hours.”
As many as 3 million cases of severe sepsis occur in the U.S. annually, and 750,000 result in deaths, according to the study. The high number of cases has led to several efforts to create better clinical practices for sepsis patients.
"Sepsis is arguably one of the most, if not the most important, causes of preventable mortality in the inpatient setting," Dr. Umscheid says. "One thing that we thought we could do better was identify sepsis cases earlier so that we could provide early antibiotics and fluids."
Visit our website for more information on identifying and treating sepsis.
A recent study published in the Journal of Hospital Medicine reports on an early warning and response system (EWRS) for sepsis used in all three hospitals within the Philadelphia-based University of Pennsylvania Health System (UPHS) for three-month spans in 2012 and 2013. The system integrates laboratory values and vital signs into patients EHRs and establishes a threshold for triggering the alert.
After implementing the EWRS, at-risk patients received faster care for sepsis and/or were transferred to the ICU more quickly, says lead author Craig A. Umscheid, MD, MSCE, director of the Center for Evidence-Based Practice at the University of Pennsylvania in Philadelphia. Study authors also note that quicker care suggested reduced mortality from sepsis as well.
"Whenever a patient triggered the alert, their probability of mortality was much higher than patients who didn't trigger the alert," Dr. Umscheid says. "I think what makes our study unique compared to other studies that have tried to predict sepsis is that beyond just creating a prediction rule for sepsis, we actually implemented it into a clinical care setting, alerted providers in real time, and then those providers changed their care based on the prediction."
More than 90% of care teams arrived at the bedside when they received an alert. "Meaning that they saw some value in the alert, and the infrastructure that we put in place was able to mobilize the team and get them to the bedside within 30 minutes," Dr. Umscheid adds. "We saw an increase in sepsis antibiotics used, and we saw an increase in fluid boluses within six hours.”
As many as 3 million cases of severe sepsis occur in the U.S. annually, and 750,000 result in deaths, according to the study. The high number of cases has led to several efforts to create better clinical practices for sepsis patients.
"Sepsis is arguably one of the most, if not the most important, causes of preventable mortality in the inpatient setting," Dr. Umscheid says. "One thing that we thought we could do better was identify sepsis cases earlier so that we could provide early antibiotics and fluids."
Visit our website for more information on identifying and treating sepsis.
A recent study published in the Journal of Hospital Medicine reports on an early warning and response system (EWRS) for sepsis used in all three hospitals within the Philadelphia-based University of Pennsylvania Health System (UPHS) for three-month spans in 2012 and 2013. The system integrates laboratory values and vital signs into patients EHRs and establishes a threshold for triggering the alert.
After implementing the EWRS, at-risk patients received faster care for sepsis and/or were transferred to the ICU more quickly, says lead author Craig A. Umscheid, MD, MSCE, director of the Center for Evidence-Based Practice at the University of Pennsylvania in Philadelphia. Study authors also note that quicker care suggested reduced mortality from sepsis as well.
"Whenever a patient triggered the alert, their probability of mortality was much higher than patients who didn't trigger the alert," Dr. Umscheid says. "I think what makes our study unique compared to other studies that have tried to predict sepsis is that beyond just creating a prediction rule for sepsis, we actually implemented it into a clinical care setting, alerted providers in real time, and then those providers changed their care based on the prediction."
More than 90% of care teams arrived at the bedside when they received an alert. "Meaning that they saw some value in the alert, and the infrastructure that we put in place was able to mobilize the team and get them to the bedside within 30 minutes," Dr. Umscheid adds. "We saw an increase in sepsis antibiotics used, and we saw an increase in fluid boluses within six hours.”
As many as 3 million cases of severe sepsis occur in the U.S. annually, and 750,000 result in deaths, according to the study. The high number of cases has led to several efforts to create better clinical practices for sepsis patients.
"Sepsis is arguably one of the most, if not the most important, causes of preventable mortality in the inpatient setting," Dr. Umscheid says. "One thing that we thought we could do better was identify sepsis cases earlier so that we could provide early antibiotics and fluids."
Visit our website for more information on identifying and treating sepsis.
Hospitalist Adds County Coroner to His Résumé
Hospitalists have taken positions in every corner of healthcare: the C-suite, hospital administration, and even nominee for U.S. surgeon general.
Now, add county coroner to the list.
This month, hospitalist Adam Duckett, MD, was elected coroner for Cayuga County, N.Y., whose county seat of Auburn is about 30 miles west of Syracuse. Dr. Duckett, who had never run for public office, is a hospitalist at Auburn Community Hospital and serves as a board member for Hospice of the Finger Lakes.
The Hospitalist spoke with him about his new post, which might make him the only hospitalist/coroner in the country.
Question: HM is a time-consuming job. Why take time out for public service?
Answer: I believe everyone owes a debt of service to their community, and I felt that this was one that I would enjoy.
Q: What skills from HM apply to your new position?
A: The majority of unattended deaths in our county are related to long-standing medical illness. Because of this, I feel that in order to understand how somebody may have died, you must first know how they lived. I believe my role as a hospitalist enables me to review medical records and determine if the medical history provides enough information to determine a cause of death.
Q: What skills from your hospice care experience apply?
A: My role as a hospitalist has given me valuable insight in helping families cope with the loss of a loved one by providing explanations as to why somebody might have passed. It’s very important for a family to understand why a loved one died before they can accept it, and it’s very rewarding to help families through this process.
Get involved in public policy via SHM's advocacy home page. TH
Visit our website for more information about community involvement.
Hospitalists have taken positions in every corner of healthcare: the C-suite, hospital administration, and even nominee for U.S. surgeon general.
Now, add county coroner to the list.
This month, hospitalist Adam Duckett, MD, was elected coroner for Cayuga County, N.Y., whose county seat of Auburn is about 30 miles west of Syracuse. Dr. Duckett, who had never run for public office, is a hospitalist at Auburn Community Hospital and serves as a board member for Hospice of the Finger Lakes.
The Hospitalist spoke with him about his new post, which might make him the only hospitalist/coroner in the country.
Question: HM is a time-consuming job. Why take time out for public service?
Answer: I believe everyone owes a debt of service to their community, and I felt that this was one that I would enjoy.
Q: What skills from HM apply to your new position?
A: The majority of unattended deaths in our county are related to long-standing medical illness. Because of this, I feel that in order to understand how somebody may have died, you must first know how they lived. I believe my role as a hospitalist enables me to review medical records and determine if the medical history provides enough information to determine a cause of death.
Q: What skills from your hospice care experience apply?
A: My role as a hospitalist has given me valuable insight in helping families cope with the loss of a loved one by providing explanations as to why somebody might have passed. It’s very important for a family to understand why a loved one died before they can accept it, and it’s very rewarding to help families through this process.
Get involved in public policy via SHM's advocacy home page. TH
Visit our website for more information about community involvement.
Hospitalists have taken positions in every corner of healthcare: the C-suite, hospital administration, and even nominee for U.S. surgeon general.
Now, add county coroner to the list.
This month, hospitalist Adam Duckett, MD, was elected coroner for Cayuga County, N.Y., whose county seat of Auburn is about 30 miles west of Syracuse. Dr. Duckett, who had never run for public office, is a hospitalist at Auburn Community Hospital and serves as a board member for Hospice of the Finger Lakes.
The Hospitalist spoke with him about his new post, which might make him the only hospitalist/coroner in the country.
Question: HM is a time-consuming job. Why take time out for public service?
Answer: I believe everyone owes a debt of service to their community, and I felt that this was one that I would enjoy.
Q: What skills from HM apply to your new position?
A: The majority of unattended deaths in our county are related to long-standing medical illness. Because of this, I feel that in order to understand how somebody may have died, you must first know how they lived. I believe my role as a hospitalist enables me to review medical records and determine if the medical history provides enough information to determine a cause of death.
Q: What skills from your hospice care experience apply?
A: My role as a hospitalist has given me valuable insight in helping families cope with the loss of a loved one by providing explanations as to why somebody might have passed. It’s very important for a family to understand why a loved one died before they can accept it, and it’s very rewarding to help families through this process.
Get involved in public policy via SHM's advocacy home page. TH
Visit our website for more information about community involvement.
PoCUS for Hospitalists
Similar to the physical exam, diagnostic point‐of‐care ultrasound exams are performed at the bedside in real time by hospitalists who are seeking a diagnosis. In contrast, referral ultrasound exams involve multiple providers and several steps. Typically, an ultrasound technologist acquires images, a radiologist or cardiologist interprets the images, a report is prepared, and results are sent to the referring hospitalist (Figure 1). Another important difference is that although referral ultrasound exams are usually comprehensive evaluations of entire organs or anatomic spaces, often without specific diagnoses in mind, point‐of‐care ultrasound exams are aimed at making specific diagnoses for well‐defined clinical scenarios.[1]

The American Medical Association has reassured providers that ultrasound imaging is within the scope of practice of appropriately trained physicians.[2] A growing body of literature demonstrates that point‐of‐care ultrasound is increasingly used by hospitalists for more than just bedside procedures. Incited by ongoing miniaturization of ultrasound devices, hospitalists are beginning to use point‐of‐care ultrasound for diagnosis, treatment, monitoring, and screening of patients (Figure 2). Our aim was to review the current literature for point‐of‐care ultrasound applications most relevant to hospitalists and highlight gaps in the current literature.

ABDOMEN
Ascites
Ultrasound is the gold standard for diagnosing ascites and can detect as little as 100 mL of ascitic fluid.[3] When ascites is not immediately evident, hospitalists can apply the principles of the FAST (Focused Assessment with Sonography in Trauma) examination to detect small amounts of ascites by evaluating the most dependent areas of the abdominopelvic cavity, the hepatorenal, left subdiaphragmatic, and rectovesicular or rectouterine spaces.[1] When ascites is identified and paracentesis is indicated, ultrasound guidance for site selection reduces bleeding complications.[4]
Aortic Aneurysm
Novice providers with limited ultrasound training can accurately screen patients for abdominal aortic aneurysm (AAA). Multiple studies from emergency departments have shown that point‐of‐care ultrasound can be used to accurately detect AAA, and a recent meta‐analysis of 7 high‐quality studies demonstrated a sensitivity of 99% (95% confidence interval [CI]: 96%‐100%) and a specificity of 98% (95% CI: 97%‐99%).[5] Hospitalists could use ultrasound to rapidly detect AAA in patients with acute abdominal pain, monitor the size in patients with known AAA, and possibly screen high‐risk patients.[6]
Hydronephrosis
Once detected, relief of postrenal obstruction usually results in rapid reversal of acute kidney injury. Although diagnostic accuracy studies of detection of hydronephrosis have yet to be conducted with hospitalists, studies of other frontline providers with limited training in renal ultrasonography have revealed sensitivities of 72% to 87% and specificities of 73% to 82% in patients with renal colic.[7, 8]
HEART
Studies of point‐of‐care cardiac ultrasound have focused most on detection of left ventricular systolic dysfunction. Yet studies among hospitalists have yielded high diagnostic accuracy for an array of abnormalities.[9, 10, 11] Lucas et al. evaluated the diagnostic accuracy of 9 hospitalists for 5 cardiac abnormalities including left ventricular systolic dysfunction after a 27‐hour, structured training program. Positive and negative likelihood ratios for point‐of‐care cardiac ultrasound increased and decreased, respectively, the prior odds by 5‐fold or more for left ventricular systolic dysfunction, severe mitral regurgitation, and moderate or large pericardial effusion. Likelihood ratios changed the prior odds by 2‐fold or more for moderate or severe left atrial enlargement, and moderate or severe left ventricle hypertrophy.[9] Martin et al. found that after a brief training program, hospitalists' image acquisition and interpretation skills were respectively below echocardiography technicians' and senior cardiology fellows' skills.[10] Yet in a follow‐up study, they found that bedside diagnosis of left ventricle systolic dysfunction, cardiomegaly, and pericardial effusion improved when point‐of‐care cardiac ultrasound supplemented hospitalists' physical examination.[11]
In 1 of the few experimental studies of the impact of point‐of‐care ultrasound on clinical care, Lucas et al. randomized general medicine patients who were referred by hospitalists for standard echocardiography to care guided by point‐of‐care cardiac ultrasound versus care guided by the referral echocardiography (usual care). Point‐of‐care cardiac ultrasound changed hospitalists' management for 37% of patients, and a post hoc subgroup analysis of heart failure patients demonstrated a statistically significant 15% reduction in length of stay.[12]
LUNGS
Pneumonia
Normally aerated lung parenchyma generates A‐lines, horizontal hyperechoic lines that are artifacts due to repeated reflections, or reverberations, between the highly reflective pleura and transducer.[1] These normal A‐lines disappear with pneumonia due to accumulation of interstitial fluid and cellular exudate in consolidated alveoli. A meta‐analysis of 9 studies of lung ultrasound to diagnose pneumonia reported pooled sensitivity of 97% (95% CI: 93%‐99%) with specificity of 94% (95% CI: 85%‐98%).[13]
Pleural Effusion
Half of patients with community‐acquired pneumonia have a pleural effusion, yet chest x‐ray often cannot differentiate pneumonia from pleural effusion, especially along the lower lung fields. Ultrasound can accurately differentiate consolidated lung from pleural effusion and is more sensitive than a chest x‐ray for detecting small pleural fluid volumes (100% vs 71%).[14] Serial monitoring of size and character of a pleural effusion can distinguish free flowing from loculated pleural effusions. Drainage of pleural effusions with ultrasound guidance is associated with a lower rate of postprocedure pneumothorax and lower total hospital costs.[15]
Pneumothorax
Lung ultrasound can accurately and rapidly detect pneumothorax after lung and pleural procedures, including thoracentesis, bronchoscopy, and transthoracic biopsy.[2] Multiple studies have demonstrated that lung ultrasound is superior to chest x‐ray. Three recent meta‐analyses reported near‐perfect specificity for both ultrasound and x‐ray. But the sensitivity of ultrasound (79%95%) was far better than that of x‐ray (40%52%) to detect pneumothorax.[16, 17]
The hallmark ultrasound findings of pneumothorax include absence of lung sliding, absence of B‐lines, and a stratified pattern using M‐mode ultrasonography (stratosphere sign). Both lung sliding and B‐lines rule out pneumothorax with a negative predictive value of 100%.[18] Absence of either finding, however, does not rule in pneumothorax with similar strength. Absent lung sliding is seen in other conditions, such as pleurodesis, mainstem intubation, and massive atelectasis; absent B‐lines are most suggestive of the normal lung (see below).[1]
Pulmonary Edema
The classic ultrasound finding of acute pulmonary edema is bilateral anterior B‐lines. In contrast to horizontal A‐lines, B‐lines are vertical, laser‐like reverberations that originate from the pleura and are due to interlobular septal edema. A linear correlation has been shown between the quantity of B‐lines and radiographic lung water score (r=0.78; P<0.01).[19] Yet B‐lines are not specific for high pulmonary capillary wedge pressure because interstitial edema can be caused by a variety of etiologies. Nonetheless, visualization of multiple B‐lines in a single intercostal space corresponds with a sensitivity of 86% to 100% and specificity of 92% to 98% for either high‐ or low‐pressure pulmonary edema.[20, 21]
VEINS
Central Venous Volume
The physiologic relationship between central venous volume and central venous pressure (CVP) is complex. Initially, there is upward stepwise progression to the stressed volume threshold, and then the relationship becomes curvilinear with the steepness of the slope dependent on the stiffness or tone of the central veins.[22]
The complexity of this relationship may explain the variable diagnostic accuracy of inferior vena cava (IVC) measurements to determine CVP, with measurements best reflecting CVP at extreme values. An IVC maximal diameter >2.0 cm predicted CVP >10 mm Hg (sensitivity 82% and specificity 84%) and pulmonary capillary wedge pressure >16 mm Hg (sensitivity 75% and specificity 83%) in 1 study.[23] Adding measurement of the collapsibility of the IVC with respiration may improve diagnostic accuracy, particularly with intermediate ranges of CVP and is recommended by current echocardiography guidelines.[24]
Nonetheless, in patients with acute dyspnea, a dilated, noncollapsing IVC may differentiate acute decompensated heart failure (ADHF) from primary pulmonary disease.[25, 26] IVC measurements may guide fluid removal in hemodialysis and heart failure patients.[27, 28] In 2 studies of patients hospitalized with ADHF, lack of improvement of IVC collapsibility index at the time of discharge was associated with higher rates of readmission.[29, 30] A follow‐up study comparing diuresis guided by IVC collapsibility to usual care in patients hospitalized with ADHF showed a reduction in hospital readmission rates (4% vs 30%, P=0.03) without an increase in hospital length of stay or renal dysfunction.[31] Patients with small, collapsed IVCs can be administered intravenous fluids safely, particularly in the setting of hypovolemic or septic shock, and the response to this fluid resuscitation can be assessed by serially measuring the change in IVC diameter.[32]
Thromboembolism
Multiple studies have shown that point‐of‐care ultrasound can accurately diagnose deep venous thrombosis (DVT) with a pooled sensitivity of 96% and specificity of 96% based on a recent meta‐analysis of 19 studies.[33] In symptomatic patients with a lung ultrasound pattern showing A‐lines, positive and negative predictive values of DVT in predicting pulmonary embolism (PE) were 94% and 98%, respectively.[34] A diagnostic accuracy study to diagnose PE using lung ultrasound to detect pleural‐ or subpleural‐based lesions yielded a sensitivity of 90%, specificity of 60%, positive predictive value of 80%, and negative predictive value of 78%.[35] In a study of 96 patients with suspected PE who underwent computed tomography pulmonary angiogram (CTPA), a focused ultrasound exam of the heart, lungs, and lower extremity veins was able to detect DVT (2.1%) or an alternative diagnosis (56.2%) in the majority of these patients, potentially obviating the need for CTPA in 58.4% of patients.[36] In addition, point‐of‐care cardiac ultrasound may reveal direct findings, such as free‐floating thrombus in the pulmonary artery, or indirect findings, such as right ventricular dilation and systolic dysfunction, septal bowing, McConnell's sign, or IVC dilation.[1] Cardiac abnormalities are more specific (88%94%) than sensitive (31%77%), and absence of cardiac abnormalities rules out massive PE, justifying withholding thrombolytic medications in most patients.[37]
RESEARCH GAPS
Most point‐of‐care ultrasound research has focused on diagnostic accuracy. Yet the training required for hospitalists to attain diagnostic competency remains controversial.[38] Evidence from cardiac point‐of‐care ultrasound training suggests that the number of supervised studies is a key determinate in competency.[39] For example, training programs based on 30 supervised studies[11, 15, 40] outperformed those based on only 5 supervised studies.[11] Nevertheless, the real value of point‐of‐care ultrasound will be in leading hospitalists to more appropriate treatment decisions that result in better outcomes for patients.[41] We believe that there are 4 important clinical areas where future research ought to focus.
First, can point‐of‐care ultrasound guide hospitalists' decision making during cardiac arrest? Current advanced cardiac life support (ACLS) guidelines recommend ruling out potentially reversible causes of cardiac arrest, including tension pneumothorax, cardiac tamponade, and massive pulmonary embolism, but traditional physical examination techniques are impractical to perform during cardiopulmonary resuscitation. Point‐of‐care ultrasound may be able to detect these conditions and facilitate emergent interventions, such as pericardiocentesis or needle decompression.[1] Identifying the absence of cardiac contractility is importantly associated with a significantly low likelihood of return of spontaneous circulation.[1, 42] Whether or not point‐of‐care ultrasound should be added to either crash carts or ACLS guideline recommendations will depend on further evidence demonstrating its value.
Second, should hospitalists seize the opportunity to screen inpatients for abdominal aortic aneurysm and asymptomatic left ventricular systolic dysfunction? Although such screening has been successfully carried out,[6, 43] widespread screening applications have been slow to develop. Ultrasound waves, themselves, impart no harm, but further research is needed to weigh the benefits of early detection against the harms of false‐positive findings.
Third, how can hospitalists best utilize bedside ultrasound to perform serial examinations of patients? Unlike referral ultrasound examinations that take single snapshots of patients at 1 point in time, point‐of‐care ultrasound allows hospitalists to iteratively monitor patients. Promising and needed applications include serial examinations of the IVC as a surrogate for central venous volume[44] during both fluid resuscitation and removal, left ventricular contraction in response to inotrope initiation, and resolution or worsening of a pneumothorax or pneumonia.
Fourth, how should hospitalists integrate point‐of‐care ultrasound into their workflow for common conditions? Recognized protocols most relevant to hospital medicine include RUSH (Rapid Ultrasound for Shock and Hypotension),[45] FALLS (Fluid Administration Limited by Lung Sonography),[46] BLUE (Bedside Lung Ultrasound in Emergency),[34] CLUE (Cardiovascular Limited Ultrasound Exam),[47] and intensive care unit‐sound.[48] Several small single‐institution studies have demonstrated that bedside ultrasound may benefit clinical decision making by differentiating cardiac versus pulmonary causes of acute dyspnea.[49, 50] However, large, validating, multicenter trials are needed. In addition, outcomes that better reflect both the patients' and payers' perspectives ought to be considered. For example, how are doctor‐patient relationships affected? Is shared decision making and patient (or physician) satisfaction improved? How are resources utilized and healthcare costs affected?
CONCLUSIONS
Hospitalists are striving to provide high‐quality, cost‐effective healthcare, and point‐of‐care ultrasound may contribute to achieving these goals by expediting diagnoses and decreasing costly ancillary testing that utilizes ionizing radiation. Hospitalists are uniquely poised to advance the field by studying how point‐of‐care ultrasound is best incorporated into patient care algorithms.
Disclosure: Nothing to report.
1. Soni NJ, Arntfield R, Kory P. Point-of-Care Ultrasound. 1st ed. Philadelphia,
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2. American Medical Association. House of Delegates. H-230.960 Privileging
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https://ssl3.ama-assn.org/apps/ecomm/PolicyFinderForm.pl?site5www.
ama-assn.org&uri5%2fresources%2fhtml%2fPolicyFinder%2fpolicy
files%2fHnE%2fH-230.960.HTM. Accessed October 2, 2014.
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distinction between pulmonary edema and COPD: the comet-tail artifact.
Intensive Care Med. 1998;24(12):1331–1334.
21. Volpicelli G, Mussa A, Garofalo G, et al. Bedside lung ultrasound in
the assessment of alveolar-interstitial syndrome. Am J Emerg Med.
2006;24(6):689–696.
22. Rothe CF. Reflex control of veins and vascular capacitance. Physiol
Rev. 1983;63(4):1281–1342.
23. Blair JE, Brennan JM, Goonewardena SN, Shah D, Vasaiwala S,
Spencer KT. Usefulness of hand-carried ultrasound to predict elevated
left ventricular filling pressure. Am J Cardiol. 2009;103(2):246–247.
24. Beigel R, Cercek B, Luo H, Siegel RJ. Noninvasive evaluation of right
atrial pressure. J Am Soc Echocardiogr. 2013;26(9):1033–1042.
25. Miller JB, Sen A, Strote SR, et al. Inferior vena cava assessment in the
bedside diagnosis of acute heart failure. Am J Emerg Med. 2012;
30(5):778–783.
26. Blehar DJ, Dickman E, Gaspari R. Identification of congestive heart
failure via respiratory variation of inferior vena cava diameter. Am J
Emerg Med. 2009;27(1):71–75.
27. Goonewardena SN, Spencer KT. Handcarried echocardiography to
assess hemodynamics in acute decompensated heart failure. Curr
Heart Fail Rep. 2010;7(4):219–227.
28. Guiotto G, Masarone M, Paladino F, et al. Inferior vena cava collapsibility
to guide fluid removal in slow continuous ultrafiltration: a pilot
study. Intensive Care Med. 2010;36(4):692–696.
29. Carbone F, Bovio M, Rosa GM, et al. Inferior vena cava parameters
predict readmission in ischemic heart failure. Eur J Clin Invest. 2014;
44(4):341–349.
30. Goonewardena SN, Gemignani A, Ronan A, et al. Comparison of
hand-carried ultrasound assessment of the inferior vena cava and Nterminal
pro-brain natriuretic peptide for predicting readmission after
hospitalization for acute decompensated heart failure. JACC Cardiovasc
Imaging. 2008;1(5):595–601.
31. Laffin L, Patel AR, Saha N, et al. Inferior vena cava measurement by
focused cardiac ultrasound in acute decompensated heart failure prevents
hospital readmissions. J Am Coll Cardiol. 2014;63(12 suppl):
A542.
32. Zhang Z, Xu X, Ye S, Xu L. Ultrasonographic measurement of the
respiratory variation in the inferior vena cava diameter is predictive of
fluid responsiveness in critically ill patients: systematic review and
meta-analysis. Ultrasound Med Biol. 2014;40(5):845–853.
33. Pomero F, Dentali F, Borretta V, et al. Accuracy of emergency
physician-performed ultrasonography in the diagnosis of deep-vein
thrombosis: a systematic review and meta-analysis. Thromb Haemost.
2013;109(1):137–145.
34. Lichtenstein DA, Meziere GA. Relevance of lung ultrasound in the
diagnosis of acute respiratory failure: the BLUE protocol. Chest.
2008;134(1):117–125.
35. Comert SS, Caglayan B, Akturk U, et al. The role of thoracic ultrasonography
in the diagnosis of pulmonary embolism. Ann Thorac Med.
2013;8(2):99–104.
36. Koenig S, Chandra S, Alaverdian A, Dibello C, Mayo PH,
Narasimhan M. Ultrasound assessment of pulmonary embolism in
patients receiving computerized tomography pulmonary angiography.
Chest. 2014;145(4):818–823.
37. Mookadam F, Jiamsripong P, Goel R, Warsame TA, Emani UR,
Khandheria BK. Critical appraisal on the utility of echocardiography
in the management of acute pulmonary embolism. Cardiol Rev. 2010;
18(1):29–37.
38. Gesensway D. Making the case for portable ultrasound. Todays Hospitalist.
2012;10:32–36.
39. Spencer KT, Kimura BJ, Korcarz CE, Pellikka PA, Rahko PS, Siegel
RJ. Focused cardiac ultrasound: recommendations from the American
Society of Echocardiography. J Am Soc Echocardiogr. 2013;26(6):
567–581.
40. Hellmann DB, Whiting-O’Keefe Q, Shapiro EP, Martin LD, Martire
C, Ziegelstein RC. The rate at which residents learn to use hand-held
echocardiography at the bedside. Am J Med. 2005;118(9):1010–
1018.
41. Redberg RF, Walsch J. Pay now, benefits may follow—the case of cardiac
computed tomographic angiography. N Engl J Med. 2008;359:
2309–2311.
42. Blyth L, Atkinson P, Gadd K, Lang E. Bedside focused echocardiography
as predictor of survival in cardiac arrest patients: a systematic
review. Acad Emerg Med. 2012;19(10):1119–1126.
43. Martin LD, Mathews S, Ziegelstein RC, et al. Prevalence of asymptomatic
left ventricular systolic dysfunction in at-risk medical inpatients.
Am J Med. 2013;126(1):68–73.
44. Low D, Vlasschaert M, Novak K, Chee A, Ma IWY. An argument for
using additional bedside tools, such as bedside ultrasound, for volume
status assessment in hospitalized medical patients: a needs assessment
survey. J Hosp Med. 2014;9:727–730.
45. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid
Ultrasound in SHock in the evaluation of the critically lll. Emerg Med
Clin North Am. 2010;28(1):29–56, vii.
46. Lichtenstein D. FALLS-protocol: lung ultrasound in hemodynamic
assessment of shock. Heart Lung Vessel. 2013;5(3):142–147.
47. Kimura BJ, Yogo N, O’Connell CW, Phan JN, Showalter BK,
Wolfson T. Cardiopulmonary limited ultrasound examination for
“quick-look” bedside application. Am J Cardiol. 2011;108(4):586–
590.
48. Manno E, Navarra M, Faccio L, et al. Deep impact of ultrasound in
the intensive care unit: the “ICU-sound” protocol. Anesthesiology.
2012;117(4):801–809.
49. Cibinel GA, Casoli G, Elia F, et al. Diagnostic accuracy and reproducibility
of pleural and lung ultrasound in discriminating cardiogenic
causes of acute dyspnea in the emergency department. Intern Emerg
Med. 2012;7(1):65–70.
50. Anderson KL, Jenq KY, Fields JM, Panebianco NL, Dean AJ. Diagnosing
heart failure among acutely dyspneic patients with cardiac,
inferior vena cava, and lung ultrasonography. Am J Emerg Med.
2013;31(8):1208–1214.
Similar to the physical exam, diagnostic point‐of‐care ultrasound exams are performed at the bedside in real time by hospitalists who are seeking a diagnosis. In contrast, referral ultrasound exams involve multiple providers and several steps. Typically, an ultrasound technologist acquires images, a radiologist or cardiologist interprets the images, a report is prepared, and results are sent to the referring hospitalist (Figure 1). Another important difference is that although referral ultrasound exams are usually comprehensive evaluations of entire organs or anatomic spaces, often without specific diagnoses in mind, point‐of‐care ultrasound exams are aimed at making specific diagnoses for well‐defined clinical scenarios.[1]

The American Medical Association has reassured providers that ultrasound imaging is within the scope of practice of appropriately trained physicians.[2] A growing body of literature demonstrates that point‐of‐care ultrasound is increasingly used by hospitalists for more than just bedside procedures. Incited by ongoing miniaturization of ultrasound devices, hospitalists are beginning to use point‐of‐care ultrasound for diagnosis, treatment, monitoring, and screening of patients (Figure 2). Our aim was to review the current literature for point‐of‐care ultrasound applications most relevant to hospitalists and highlight gaps in the current literature.

ABDOMEN
Ascites
Ultrasound is the gold standard for diagnosing ascites and can detect as little as 100 mL of ascitic fluid.[3] When ascites is not immediately evident, hospitalists can apply the principles of the FAST (Focused Assessment with Sonography in Trauma) examination to detect small amounts of ascites by evaluating the most dependent areas of the abdominopelvic cavity, the hepatorenal, left subdiaphragmatic, and rectovesicular or rectouterine spaces.[1] When ascites is identified and paracentesis is indicated, ultrasound guidance for site selection reduces bleeding complications.[4]
Aortic Aneurysm
Novice providers with limited ultrasound training can accurately screen patients for abdominal aortic aneurysm (AAA). Multiple studies from emergency departments have shown that point‐of‐care ultrasound can be used to accurately detect AAA, and a recent meta‐analysis of 7 high‐quality studies demonstrated a sensitivity of 99% (95% confidence interval [CI]: 96%‐100%) and a specificity of 98% (95% CI: 97%‐99%).[5] Hospitalists could use ultrasound to rapidly detect AAA in patients with acute abdominal pain, monitor the size in patients with known AAA, and possibly screen high‐risk patients.[6]
Hydronephrosis
Once detected, relief of postrenal obstruction usually results in rapid reversal of acute kidney injury. Although diagnostic accuracy studies of detection of hydronephrosis have yet to be conducted with hospitalists, studies of other frontline providers with limited training in renal ultrasonography have revealed sensitivities of 72% to 87% and specificities of 73% to 82% in patients with renal colic.[7, 8]
HEART
Studies of point‐of‐care cardiac ultrasound have focused most on detection of left ventricular systolic dysfunction. Yet studies among hospitalists have yielded high diagnostic accuracy for an array of abnormalities.[9, 10, 11] Lucas et al. evaluated the diagnostic accuracy of 9 hospitalists for 5 cardiac abnormalities including left ventricular systolic dysfunction after a 27‐hour, structured training program. Positive and negative likelihood ratios for point‐of‐care cardiac ultrasound increased and decreased, respectively, the prior odds by 5‐fold or more for left ventricular systolic dysfunction, severe mitral regurgitation, and moderate or large pericardial effusion. Likelihood ratios changed the prior odds by 2‐fold or more for moderate or severe left atrial enlargement, and moderate or severe left ventricle hypertrophy.[9] Martin et al. found that after a brief training program, hospitalists' image acquisition and interpretation skills were respectively below echocardiography technicians' and senior cardiology fellows' skills.[10] Yet in a follow‐up study, they found that bedside diagnosis of left ventricle systolic dysfunction, cardiomegaly, and pericardial effusion improved when point‐of‐care cardiac ultrasound supplemented hospitalists' physical examination.[11]
In 1 of the few experimental studies of the impact of point‐of‐care ultrasound on clinical care, Lucas et al. randomized general medicine patients who were referred by hospitalists for standard echocardiography to care guided by point‐of‐care cardiac ultrasound versus care guided by the referral echocardiography (usual care). Point‐of‐care cardiac ultrasound changed hospitalists' management for 37% of patients, and a post hoc subgroup analysis of heart failure patients demonstrated a statistically significant 15% reduction in length of stay.[12]
LUNGS
Pneumonia
Normally aerated lung parenchyma generates A‐lines, horizontal hyperechoic lines that are artifacts due to repeated reflections, or reverberations, between the highly reflective pleura and transducer.[1] These normal A‐lines disappear with pneumonia due to accumulation of interstitial fluid and cellular exudate in consolidated alveoli. A meta‐analysis of 9 studies of lung ultrasound to diagnose pneumonia reported pooled sensitivity of 97% (95% CI: 93%‐99%) with specificity of 94% (95% CI: 85%‐98%).[13]
Pleural Effusion
Half of patients with community‐acquired pneumonia have a pleural effusion, yet chest x‐ray often cannot differentiate pneumonia from pleural effusion, especially along the lower lung fields. Ultrasound can accurately differentiate consolidated lung from pleural effusion and is more sensitive than a chest x‐ray for detecting small pleural fluid volumes (100% vs 71%).[14] Serial monitoring of size and character of a pleural effusion can distinguish free flowing from loculated pleural effusions. Drainage of pleural effusions with ultrasound guidance is associated with a lower rate of postprocedure pneumothorax and lower total hospital costs.[15]
Pneumothorax
Lung ultrasound can accurately and rapidly detect pneumothorax after lung and pleural procedures, including thoracentesis, bronchoscopy, and transthoracic biopsy.[2] Multiple studies have demonstrated that lung ultrasound is superior to chest x‐ray. Three recent meta‐analyses reported near‐perfect specificity for both ultrasound and x‐ray. But the sensitivity of ultrasound (79%95%) was far better than that of x‐ray (40%52%) to detect pneumothorax.[16, 17]
The hallmark ultrasound findings of pneumothorax include absence of lung sliding, absence of B‐lines, and a stratified pattern using M‐mode ultrasonography (stratosphere sign). Both lung sliding and B‐lines rule out pneumothorax with a negative predictive value of 100%.[18] Absence of either finding, however, does not rule in pneumothorax with similar strength. Absent lung sliding is seen in other conditions, such as pleurodesis, mainstem intubation, and massive atelectasis; absent B‐lines are most suggestive of the normal lung (see below).[1]
Pulmonary Edema
The classic ultrasound finding of acute pulmonary edema is bilateral anterior B‐lines. In contrast to horizontal A‐lines, B‐lines are vertical, laser‐like reverberations that originate from the pleura and are due to interlobular septal edema. A linear correlation has been shown between the quantity of B‐lines and radiographic lung water score (r=0.78; P<0.01).[19] Yet B‐lines are not specific for high pulmonary capillary wedge pressure because interstitial edema can be caused by a variety of etiologies. Nonetheless, visualization of multiple B‐lines in a single intercostal space corresponds with a sensitivity of 86% to 100% and specificity of 92% to 98% for either high‐ or low‐pressure pulmonary edema.[20, 21]
VEINS
Central Venous Volume
The physiologic relationship between central venous volume and central venous pressure (CVP) is complex. Initially, there is upward stepwise progression to the stressed volume threshold, and then the relationship becomes curvilinear with the steepness of the slope dependent on the stiffness or tone of the central veins.[22]
The complexity of this relationship may explain the variable diagnostic accuracy of inferior vena cava (IVC) measurements to determine CVP, with measurements best reflecting CVP at extreme values. An IVC maximal diameter >2.0 cm predicted CVP >10 mm Hg (sensitivity 82% and specificity 84%) and pulmonary capillary wedge pressure >16 mm Hg (sensitivity 75% and specificity 83%) in 1 study.[23] Adding measurement of the collapsibility of the IVC with respiration may improve diagnostic accuracy, particularly with intermediate ranges of CVP and is recommended by current echocardiography guidelines.[24]
Nonetheless, in patients with acute dyspnea, a dilated, noncollapsing IVC may differentiate acute decompensated heart failure (ADHF) from primary pulmonary disease.[25, 26] IVC measurements may guide fluid removal in hemodialysis and heart failure patients.[27, 28] In 2 studies of patients hospitalized with ADHF, lack of improvement of IVC collapsibility index at the time of discharge was associated with higher rates of readmission.[29, 30] A follow‐up study comparing diuresis guided by IVC collapsibility to usual care in patients hospitalized with ADHF showed a reduction in hospital readmission rates (4% vs 30%, P=0.03) without an increase in hospital length of stay or renal dysfunction.[31] Patients with small, collapsed IVCs can be administered intravenous fluids safely, particularly in the setting of hypovolemic or septic shock, and the response to this fluid resuscitation can be assessed by serially measuring the change in IVC diameter.[32]
Thromboembolism
Multiple studies have shown that point‐of‐care ultrasound can accurately diagnose deep venous thrombosis (DVT) with a pooled sensitivity of 96% and specificity of 96% based on a recent meta‐analysis of 19 studies.[33] In symptomatic patients with a lung ultrasound pattern showing A‐lines, positive and negative predictive values of DVT in predicting pulmonary embolism (PE) were 94% and 98%, respectively.[34] A diagnostic accuracy study to diagnose PE using lung ultrasound to detect pleural‐ or subpleural‐based lesions yielded a sensitivity of 90%, specificity of 60%, positive predictive value of 80%, and negative predictive value of 78%.[35] In a study of 96 patients with suspected PE who underwent computed tomography pulmonary angiogram (CTPA), a focused ultrasound exam of the heart, lungs, and lower extremity veins was able to detect DVT (2.1%) or an alternative diagnosis (56.2%) in the majority of these patients, potentially obviating the need for CTPA in 58.4% of patients.[36] In addition, point‐of‐care cardiac ultrasound may reveal direct findings, such as free‐floating thrombus in the pulmonary artery, or indirect findings, such as right ventricular dilation and systolic dysfunction, septal bowing, McConnell's sign, or IVC dilation.[1] Cardiac abnormalities are more specific (88%94%) than sensitive (31%77%), and absence of cardiac abnormalities rules out massive PE, justifying withholding thrombolytic medications in most patients.[37]
RESEARCH GAPS
Most point‐of‐care ultrasound research has focused on diagnostic accuracy. Yet the training required for hospitalists to attain diagnostic competency remains controversial.[38] Evidence from cardiac point‐of‐care ultrasound training suggests that the number of supervised studies is a key determinate in competency.[39] For example, training programs based on 30 supervised studies[11, 15, 40] outperformed those based on only 5 supervised studies.[11] Nevertheless, the real value of point‐of‐care ultrasound will be in leading hospitalists to more appropriate treatment decisions that result in better outcomes for patients.[41] We believe that there are 4 important clinical areas where future research ought to focus.
First, can point‐of‐care ultrasound guide hospitalists' decision making during cardiac arrest? Current advanced cardiac life support (ACLS) guidelines recommend ruling out potentially reversible causes of cardiac arrest, including tension pneumothorax, cardiac tamponade, and massive pulmonary embolism, but traditional physical examination techniques are impractical to perform during cardiopulmonary resuscitation. Point‐of‐care ultrasound may be able to detect these conditions and facilitate emergent interventions, such as pericardiocentesis or needle decompression.[1] Identifying the absence of cardiac contractility is importantly associated with a significantly low likelihood of return of spontaneous circulation.[1, 42] Whether or not point‐of‐care ultrasound should be added to either crash carts or ACLS guideline recommendations will depend on further evidence demonstrating its value.
Second, should hospitalists seize the opportunity to screen inpatients for abdominal aortic aneurysm and asymptomatic left ventricular systolic dysfunction? Although such screening has been successfully carried out,[6, 43] widespread screening applications have been slow to develop. Ultrasound waves, themselves, impart no harm, but further research is needed to weigh the benefits of early detection against the harms of false‐positive findings.
Third, how can hospitalists best utilize bedside ultrasound to perform serial examinations of patients? Unlike referral ultrasound examinations that take single snapshots of patients at 1 point in time, point‐of‐care ultrasound allows hospitalists to iteratively monitor patients. Promising and needed applications include serial examinations of the IVC as a surrogate for central venous volume[44] during both fluid resuscitation and removal, left ventricular contraction in response to inotrope initiation, and resolution or worsening of a pneumothorax or pneumonia.
Fourth, how should hospitalists integrate point‐of‐care ultrasound into their workflow for common conditions? Recognized protocols most relevant to hospital medicine include RUSH (Rapid Ultrasound for Shock and Hypotension),[45] FALLS (Fluid Administration Limited by Lung Sonography),[46] BLUE (Bedside Lung Ultrasound in Emergency),[34] CLUE (Cardiovascular Limited Ultrasound Exam),[47] and intensive care unit‐sound.[48] Several small single‐institution studies have demonstrated that bedside ultrasound may benefit clinical decision making by differentiating cardiac versus pulmonary causes of acute dyspnea.[49, 50] However, large, validating, multicenter trials are needed. In addition, outcomes that better reflect both the patients' and payers' perspectives ought to be considered. For example, how are doctor‐patient relationships affected? Is shared decision making and patient (or physician) satisfaction improved? How are resources utilized and healthcare costs affected?
CONCLUSIONS
Hospitalists are striving to provide high‐quality, cost‐effective healthcare, and point‐of‐care ultrasound may contribute to achieving these goals by expediting diagnoses and decreasing costly ancillary testing that utilizes ionizing radiation. Hospitalists are uniquely poised to advance the field by studying how point‐of‐care ultrasound is best incorporated into patient care algorithms.
Disclosure: Nothing to report.
Similar to the physical exam, diagnostic point‐of‐care ultrasound exams are performed at the bedside in real time by hospitalists who are seeking a diagnosis. In contrast, referral ultrasound exams involve multiple providers and several steps. Typically, an ultrasound technologist acquires images, a radiologist or cardiologist interprets the images, a report is prepared, and results are sent to the referring hospitalist (Figure 1). Another important difference is that although referral ultrasound exams are usually comprehensive evaluations of entire organs or anatomic spaces, often without specific diagnoses in mind, point‐of‐care ultrasound exams are aimed at making specific diagnoses for well‐defined clinical scenarios.[1]

The American Medical Association has reassured providers that ultrasound imaging is within the scope of practice of appropriately trained physicians.[2] A growing body of literature demonstrates that point‐of‐care ultrasound is increasingly used by hospitalists for more than just bedside procedures. Incited by ongoing miniaturization of ultrasound devices, hospitalists are beginning to use point‐of‐care ultrasound for diagnosis, treatment, monitoring, and screening of patients (Figure 2). Our aim was to review the current literature for point‐of‐care ultrasound applications most relevant to hospitalists and highlight gaps in the current literature.

ABDOMEN
Ascites
Ultrasound is the gold standard for diagnosing ascites and can detect as little as 100 mL of ascitic fluid.[3] When ascites is not immediately evident, hospitalists can apply the principles of the FAST (Focused Assessment with Sonography in Trauma) examination to detect small amounts of ascites by evaluating the most dependent areas of the abdominopelvic cavity, the hepatorenal, left subdiaphragmatic, and rectovesicular or rectouterine spaces.[1] When ascites is identified and paracentesis is indicated, ultrasound guidance for site selection reduces bleeding complications.[4]
Aortic Aneurysm
Novice providers with limited ultrasound training can accurately screen patients for abdominal aortic aneurysm (AAA). Multiple studies from emergency departments have shown that point‐of‐care ultrasound can be used to accurately detect AAA, and a recent meta‐analysis of 7 high‐quality studies demonstrated a sensitivity of 99% (95% confidence interval [CI]: 96%‐100%) and a specificity of 98% (95% CI: 97%‐99%).[5] Hospitalists could use ultrasound to rapidly detect AAA in patients with acute abdominal pain, monitor the size in patients with known AAA, and possibly screen high‐risk patients.[6]
Hydronephrosis
Once detected, relief of postrenal obstruction usually results in rapid reversal of acute kidney injury. Although diagnostic accuracy studies of detection of hydronephrosis have yet to be conducted with hospitalists, studies of other frontline providers with limited training in renal ultrasonography have revealed sensitivities of 72% to 87% and specificities of 73% to 82% in patients with renal colic.[7, 8]
HEART
Studies of point‐of‐care cardiac ultrasound have focused most on detection of left ventricular systolic dysfunction. Yet studies among hospitalists have yielded high diagnostic accuracy for an array of abnormalities.[9, 10, 11] Lucas et al. evaluated the diagnostic accuracy of 9 hospitalists for 5 cardiac abnormalities including left ventricular systolic dysfunction after a 27‐hour, structured training program. Positive and negative likelihood ratios for point‐of‐care cardiac ultrasound increased and decreased, respectively, the prior odds by 5‐fold or more for left ventricular systolic dysfunction, severe mitral regurgitation, and moderate or large pericardial effusion. Likelihood ratios changed the prior odds by 2‐fold or more for moderate or severe left atrial enlargement, and moderate or severe left ventricle hypertrophy.[9] Martin et al. found that after a brief training program, hospitalists' image acquisition and interpretation skills were respectively below echocardiography technicians' and senior cardiology fellows' skills.[10] Yet in a follow‐up study, they found that bedside diagnosis of left ventricle systolic dysfunction, cardiomegaly, and pericardial effusion improved when point‐of‐care cardiac ultrasound supplemented hospitalists' physical examination.[11]
In 1 of the few experimental studies of the impact of point‐of‐care ultrasound on clinical care, Lucas et al. randomized general medicine patients who were referred by hospitalists for standard echocardiography to care guided by point‐of‐care cardiac ultrasound versus care guided by the referral echocardiography (usual care). Point‐of‐care cardiac ultrasound changed hospitalists' management for 37% of patients, and a post hoc subgroup analysis of heart failure patients demonstrated a statistically significant 15% reduction in length of stay.[12]
LUNGS
Pneumonia
Normally aerated lung parenchyma generates A‐lines, horizontal hyperechoic lines that are artifacts due to repeated reflections, or reverberations, between the highly reflective pleura and transducer.[1] These normal A‐lines disappear with pneumonia due to accumulation of interstitial fluid and cellular exudate in consolidated alveoli. A meta‐analysis of 9 studies of lung ultrasound to diagnose pneumonia reported pooled sensitivity of 97% (95% CI: 93%‐99%) with specificity of 94% (95% CI: 85%‐98%).[13]
Pleural Effusion
Half of patients with community‐acquired pneumonia have a pleural effusion, yet chest x‐ray often cannot differentiate pneumonia from pleural effusion, especially along the lower lung fields. Ultrasound can accurately differentiate consolidated lung from pleural effusion and is more sensitive than a chest x‐ray for detecting small pleural fluid volumes (100% vs 71%).[14] Serial monitoring of size and character of a pleural effusion can distinguish free flowing from loculated pleural effusions. Drainage of pleural effusions with ultrasound guidance is associated with a lower rate of postprocedure pneumothorax and lower total hospital costs.[15]
Pneumothorax
Lung ultrasound can accurately and rapidly detect pneumothorax after lung and pleural procedures, including thoracentesis, bronchoscopy, and transthoracic biopsy.[2] Multiple studies have demonstrated that lung ultrasound is superior to chest x‐ray. Three recent meta‐analyses reported near‐perfect specificity for both ultrasound and x‐ray. But the sensitivity of ultrasound (79%95%) was far better than that of x‐ray (40%52%) to detect pneumothorax.[16, 17]
The hallmark ultrasound findings of pneumothorax include absence of lung sliding, absence of B‐lines, and a stratified pattern using M‐mode ultrasonography (stratosphere sign). Both lung sliding and B‐lines rule out pneumothorax with a negative predictive value of 100%.[18] Absence of either finding, however, does not rule in pneumothorax with similar strength. Absent lung sliding is seen in other conditions, such as pleurodesis, mainstem intubation, and massive atelectasis; absent B‐lines are most suggestive of the normal lung (see below).[1]
Pulmonary Edema
The classic ultrasound finding of acute pulmonary edema is bilateral anterior B‐lines. In contrast to horizontal A‐lines, B‐lines are vertical, laser‐like reverberations that originate from the pleura and are due to interlobular septal edema. A linear correlation has been shown between the quantity of B‐lines and radiographic lung water score (r=0.78; P<0.01).[19] Yet B‐lines are not specific for high pulmonary capillary wedge pressure because interstitial edema can be caused by a variety of etiologies. Nonetheless, visualization of multiple B‐lines in a single intercostal space corresponds with a sensitivity of 86% to 100% and specificity of 92% to 98% for either high‐ or low‐pressure pulmonary edema.[20, 21]
VEINS
Central Venous Volume
The physiologic relationship between central venous volume and central venous pressure (CVP) is complex. Initially, there is upward stepwise progression to the stressed volume threshold, and then the relationship becomes curvilinear with the steepness of the slope dependent on the stiffness or tone of the central veins.[22]
The complexity of this relationship may explain the variable diagnostic accuracy of inferior vena cava (IVC) measurements to determine CVP, with measurements best reflecting CVP at extreme values. An IVC maximal diameter >2.0 cm predicted CVP >10 mm Hg (sensitivity 82% and specificity 84%) and pulmonary capillary wedge pressure >16 mm Hg (sensitivity 75% and specificity 83%) in 1 study.[23] Adding measurement of the collapsibility of the IVC with respiration may improve diagnostic accuracy, particularly with intermediate ranges of CVP and is recommended by current echocardiography guidelines.[24]
Nonetheless, in patients with acute dyspnea, a dilated, noncollapsing IVC may differentiate acute decompensated heart failure (ADHF) from primary pulmonary disease.[25, 26] IVC measurements may guide fluid removal in hemodialysis and heart failure patients.[27, 28] In 2 studies of patients hospitalized with ADHF, lack of improvement of IVC collapsibility index at the time of discharge was associated with higher rates of readmission.[29, 30] A follow‐up study comparing diuresis guided by IVC collapsibility to usual care in patients hospitalized with ADHF showed a reduction in hospital readmission rates (4% vs 30%, P=0.03) without an increase in hospital length of stay or renal dysfunction.[31] Patients with small, collapsed IVCs can be administered intravenous fluids safely, particularly in the setting of hypovolemic or septic shock, and the response to this fluid resuscitation can be assessed by serially measuring the change in IVC diameter.[32]
Thromboembolism
Multiple studies have shown that point‐of‐care ultrasound can accurately diagnose deep venous thrombosis (DVT) with a pooled sensitivity of 96% and specificity of 96% based on a recent meta‐analysis of 19 studies.[33] In symptomatic patients with a lung ultrasound pattern showing A‐lines, positive and negative predictive values of DVT in predicting pulmonary embolism (PE) were 94% and 98%, respectively.[34] A diagnostic accuracy study to diagnose PE using lung ultrasound to detect pleural‐ or subpleural‐based lesions yielded a sensitivity of 90%, specificity of 60%, positive predictive value of 80%, and negative predictive value of 78%.[35] In a study of 96 patients with suspected PE who underwent computed tomography pulmonary angiogram (CTPA), a focused ultrasound exam of the heart, lungs, and lower extremity veins was able to detect DVT (2.1%) or an alternative diagnosis (56.2%) in the majority of these patients, potentially obviating the need for CTPA in 58.4% of patients.[36] In addition, point‐of‐care cardiac ultrasound may reveal direct findings, such as free‐floating thrombus in the pulmonary artery, or indirect findings, such as right ventricular dilation and systolic dysfunction, septal bowing, McConnell's sign, or IVC dilation.[1] Cardiac abnormalities are more specific (88%94%) than sensitive (31%77%), and absence of cardiac abnormalities rules out massive PE, justifying withholding thrombolytic medications in most patients.[37]
RESEARCH GAPS
Most point‐of‐care ultrasound research has focused on diagnostic accuracy. Yet the training required for hospitalists to attain diagnostic competency remains controversial.[38] Evidence from cardiac point‐of‐care ultrasound training suggests that the number of supervised studies is a key determinate in competency.[39] For example, training programs based on 30 supervised studies[11, 15, 40] outperformed those based on only 5 supervised studies.[11] Nevertheless, the real value of point‐of‐care ultrasound will be in leading hospitalists to more appropriate treatment decisions that result in better outcomes for patients.[41] We believe that there are 4 important clinical areas where future research ought to focus.
First, can point‐of‐care ultrasound guide hospitalists' decision making during cardiac arrest? Current advanced cardiac life support (ACLS) guidelines recommend ruling out potentially reversible causes of cardiac arrest, including tension pneumothorax, cardiac tamponade, and massive pulmonary embolism, but traditional physical examination techniques are impractical to perform during cardiopulmonary resuscitation. Point‐of‐care ultrasound may be able to detect these conditions and facilitate emergent interventions, such as pericardiocentesis or needle decompression.[1] Identifying the absence of cardiac contractility is importantly associated with a significantly low likelihood of return of spontaneous circulation.[1, 42] Whether or not point‐of‐care ultrasound should be added to either crash carts or ACLS guideline recommendations will depend on further evidence demonstrating its value.
Second, should hospitalists seize the opportunity to screen inpatients for abdominal aortic aneurysm and asymptomatic left ventricular systolic dysfunction? Although such screening has been successfully carried out,[6, 43] widespread screening applications have been slow to develop. Ultrasound waves, themselves, impart no harm, but further research is needed to weigh the benefits of early detection against the harms of false‐positive findings.
Third, how can hospitalists best utilize bedside ultrasound to perform serial examinations of patients? Unlike referral ultrasound examinations that take single snapshots of patients at 1 point in time, point‐of‐care ultrasound allows hospitalists to iteratively monitor patients. Promising and needed applications include serial examinations of the IVC as a surrogate for central venous volume[44] during both fluid resuscitation and removal, left ventricular contraction in response to inotrope initiation, and resolution or worsening of a pneumothorax or pneumonia.
Fourth, how should hospitalists integrate point‐of‐care ultrasound into their workflow for common conditions? Recognized protocols most relevant to hospital medicine include RUSH (Rapid Ultrasound for Shock and Hypotension),[45] FALLS (Fluid Administration Limited by Lung Sonography),[46] BLUE (Bedside Lung Ultrasound in Emergency),[34] CLUE (Cardiovascular Limited Ultrasound Exam),[47] and intensive care unit‐sound.[48] Several small single‐institution studies have demonstrated that bedside ultrasound may benefit clinical decision making by differentiating cardiac versus pulmonary causes of acute dyspnea.[49, 50] However, large, validating, multicenter trials are needed. In addition, outcomes that better reflect both the patients' and payers' perspectives ought to be considered. For example, how are doctor‐patient relationships affected? Is shared decision making and patient (or physician) satisfaction improved? How are resources utilized and healthcare costs affected?
CONCLUSIONS
Hospitalists are striving to provide high‐quality, cost‐effective healthcare, and point‐of‐care ultrasound may contribute to achieving these goals by expediting diagnoses and decreasing costly ancillary testing that utilizes ionizing radiation. Hospitalists are uniquely poised to advance the field by studying how point‐of‐care ultrasound is best incorporated into patient care algorithms.
Disclosure: Nothing to report.
1. Soni NJ, Arntfield R, Kory P. Point-of-Care Ultrasound. 1st ed. Philadelphia,
PA: Saunders; 2014.
2. American Medical Association. House of Delegates. H-230.960 Privileging
for ultrasound imaging. Policy finder website. Available at:
https://ssl3.ama-assn.org/apps/ecomm/PolicyFinderForm.pl?site5www.
ama-assn.org&uri5%2fresources%2fhtml%2fPolicyFinder%2fpolicy
files%2fHnE%2fH-230.960.HTM. Accessed October 2, 2014.
3. Goldberg BB, Goodman GA, Clearfield HR. Evaluation of ascites by
ultrasound. Radiology. 1970;96(1):15–22.
4. Mercaldi CJ, Lanes SF. Ultrasound guidance decreases complications
and improves the cost of care among patients undergoing thoracentesis
and paracentesis. Chest. 2013;143(2):532–538.
5. Rubano E, Mehta N, Caputo W, Paladino L, Sinert R. Systematic
review: emergency department bedside ultrasonography for diagnosing
suspected abdominal aortic aneurysm. Acad Emerg Med. 2013;
20(2):128–138.
6. Dijos M, Pucheux Y, Lafitte M, et al. Fast track echo of abdominal
aortic aneurysm using a real pocket-ultrasound device at bedside.
Echocardiography. 2012;29(3):285–290.
7. Rosen CL, Brown DF, Sagarin MJ, Chang Y, McCabe CJ, Wolfe RE.
Ultrasonography by emergency physicians in patients with suspected
ureteral colic. J Emerg Med. 1998;16(6):865–870.
8. Gaspari RJ, Horst K. Emergency ultrasound and urinalysis in the evaluation
of flank pain. Acad Emerg Med. 2005;12(12):1180–1184.
9. Lucas BP, Candotti C, Margeta B, et al. Diagnostic accuracy of
hospitalist-performed hand-carried ultrasound echocardiography after
a brief training program. J Hosp Med. 2009;4(6):340–349.
10. Martin LD, Howell EE, Ziegelstein RC, Martire C, Shapiro EP,
Hellmann DB. Hospitalist performance of cardiac hand-carried ultrasound
after focused training. Am J Med. 2007;120(11):1000–1004.
11. Martin LD, Howell EE, Ziegelstein RC, et al. Hand-carried ultrasound
performed by hospitalists: does it improve the cardiac physical
examination? Am J Med. 2009;122(1):35–41.
PoCUS for Hospitalists | Soni and Lucas
An Official Publication of the Society of Hospital Medicine Journal of Hospital Medicine Vol 10 | No 2 | February 2015 123
12. Lucas BP, Candotti C, Margeta B, et al. Hand-carried echocardiography
by hospitalists: a randomized trial. Am J Med. 2011;124(8):766–
774.
13. Hu QJ, Shen YC, Jia LQ, et al. Diagnostic performance of lung ultrasound
in the diagnosis of pneumonia: a bivariate meta-analysis. Int J
Clin Exp Med. 2014;7(1):115–121.
14. Reissig A, Gramegna A, Aliberti S. The role of lung ultrasound in the
diagnosis and follow-up of community-acquired pneumonia. Eur J
Intern Med. 2012;23(5):391–397.
15. Patel PA, Ernst FR, Gunnarsson CL. Ultrasonography guidance
reduces complications and costs associated with thoracentesis procedures.
J Clin Ultrasound. 2012;40(3):135–141.
16. Ding W, Shen Y, Yang J, He X, Zhang M. Diagnosis of pneumothorax
by radiography and ultrasonography: a meta-analysis. Chest.
2011;140(4):859–866.
17. Alrajab S, Youssef AM, Akkus NI, Caldito G. Pleural ultrasonography
versus chest radiography for the diagnosis of pneumothorax: review
of the literature and meta-analysis. Crit Care. 2013;17(5):R208.
18. Lichtenstein D, Meziere G, Biderman P, Gepner A. The comet-tail
artifact: an ultrasound sign ruling out pneumothorax. Intensive Care
Med. 1999;25(4):383–388.
19. Picano E, Frassi F, Agricola E, Gligorova S, Gargani L, Mottola G.
Ultrasound lung comets: a clinically useful sign of extravascular lung
water. J Am Soc Echocardiogr. 2006;19(3):356–363.
20. Lichtenstein D, Meziere G. A lung ultrasound sign allowing bedside
distinction between pulmonary edema and COPD: the comet-tail artifact.
Intensive Care Med. 1998;24(12):1331–1334.
21. Volpicelli G, Mussa A, Garofalo G, et al. Bedside lung ultrasound in
the assessment of alveolar-interstitial syndrome. Am J Emerg Med.
2006;24(6):689–696.
22. Rothe CF. Reflex control of veins and vascular capacitance. Physiol
Rev. 1983;63(4):1281–1342.
23. Blair JE, Brennan JM, Goonewardena SN, Shah D, Vasaiwala S,
Spencer KT. Usefulness of hand-carried ultrasound to predict elevated
left ventricular filling pressure. Am J Cardiol. 2009;103(2):246–247.
24. Beigel R, Cercek B, Luo H, Siegel RJ. Noninvasive evaluation of right
atrial pressure. J Am Soc Echocardiogr. 2013;26(9):1033–1042.
25. Miller JB, Sen A, Strote SR, et al. Inferior vena cava assessment in the
bedside diagnosis of acute heart failure. Am J Emerg Med. 2012;
30(5):778–783.
26. Blehar DJ, Dickman E, Gaspari R. Identification of congestive heart
failure via respiratory variation of inferior vena cava diameter. Am J
Emerg Med. 2009;27(1):71–75.
27. Goonewardena SN, Spencer KT. Handcarried echocardiography to
assess hemodynamics in acute decompensated heart failure. Curr
Heart Fail Rep. 2010;7(4):219–227.
28. Guiotto G, Masarone M, Paladino F, et al. Inferior vena cava collapsibility
to guide fluid removal in slow continuous ultrafiltration: a pilot
study. Intensive Care Med. 2010;36(4):692–696.
29. Carbone F, Bovio M, Rosa GM, et al. Inferior vena cava parameters
predict readmission in ischemic heart failure. Eur J Clin Invest. 2014;
44(4):341–349.
30. Goonewardena SN, Gemignani A, Ronan A, et al. Comparison of
hand-carried ultrasound assessment of the inferior vena cava and Nterminal
pro-brain natriuretic peptide for predicting readmission after
hospitalization for acute decompensated heart failure. JACC Cardiovasc
Imaging. 2008;1(5):595–601.
31. Laffin L, Patel AR, Saha N, et al. Inferior vena cava measurement by
focused cardiac ultrasound in acute decompensated heart failure prevents
hospital readmissions. J Am Coll Cardiol. 2014;63(12 suppl):
A542.
32. Zhang Z, Xu X, Ye S, Xu L. Ultrasonographic measurement of the
respiratory variation in the inferior vena cava diameter is predictive of
fluid responsiveness in critically ill patients: systematic review and
meta-analysis. Ultrasound Med Biol. 2014;40(5):845–853.
33. Pomero F, Dentali F, Borretta V, et al. Accuracy of emergency
physician-performed ultrasonography in the diagnosis of deep-vein
thrombosis: a systematic review and meta-analysis. Thromb Haemost.
2013;109(1):137–145.
34. Lichtenstein DA, Meziere GA. Relevance of lung ultrasound in the
diagnosis of acute respiratory failure: the BLUE protocol. Chest.
2008;134(1):117–125.
35. Comert SS, Caglayan B, Akturk U, et al. The role of thoracic ultrasonography
in the diagnosis of pulmonary embolism. Ann Thorac Med.
2013;8(2):99–104.
36. Koenig S, Chandra S, Alaverdian A, Dibello C, Mayo PH,
Narasimhan M. Ultrasound assessment of pulmonary embolism in
patients receiving computerized tomography pulmonary angiography.
Chest. 2014;145(4):818–823.
37. Mookadam F, Jiamsripong P, Goel R, Warsame TA, Emani UR,
Khandheria BK. Critical appraisal on the utility of echocardiography
in the management of acute pulmonary embolism. Cardiol Rev. 2010;
18(1):29–37.
38. Gesensway D. Making the case for portable ultrasound. Todays Hospitalist.
2012;10:32–36.
39. Spencer KT, Kimura BJ, Korcarz CE, Pellikka PA, Rahko PS, Siegel
RJ. Focused cardiac ultrasound: recommendations from the American
Society of Echocardiography. J Am Soc Echocardiogr. 2013;26(6):
567–581.
40. Hellmann DB, Whiting-O’Keefe Q, Shapiro EP, Martin LD, Martire
C, Ziegelstein RC. The rate at which residents learn to use hand-held
echocardiography at the bedside. Am J Med. 2005;118(9):1010–
1018.
41. Redberg RF, Walsch J. Pay now, benefits may follow—the case of cardiac
computed tomographic angiography. N Engl J Med. 2008;359:
2309–2311.
42. Blyth L, Atkinson P, Gadd K, Lang E. Bedside focused echocardiography
as predictor of survival in cardiac arrest patients: a systematic
review. Acad Emerg Med. 2012;19(10):1119–1126.
43. Martin LD, Mathews S, Ziegelstein RC, et al. Prevalence of asymptomatic
left ventricular systolic dysfunction in at-risk medical inpatients.
Am J Med. 2013;126(1):68–73.
44. Low D, Vlasschaert M, Novak K, Chee A, Ma IWY. An argument for
using additional bedside tools, such as bedside ultrasound, for volume
status assessment in hospitalized medical patients: a needs assessment
survey. J Hosp Med. 2014;9:727–730.
45. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid
Ultrasound in SHock in the evaluation of the critically lll. Emerg Med
Clin North Am. 2010;28(1):29–56, vii.
46. Lichtenstein D. FALLS-protocol: lung ultrasound in hemodynamic
assessment of shock. Heart Lung Vessel. 2013;5(3):142–147.
47. Kimura BJ, Yogo N, O’Connell CW, Phan JN, Showalter BK,
Wolfson T. Cardiopulmonary limited ultrasound examination for
“quick-look” bedside application. Am J Cardiol. 2011;108(4):586–
590.
48. Manno E, Navarra M, Faccio L, et al. Deep impact of ultrasound in
the intensive care unit: the “ICU-sound” protocol. Anesthesiology.
2012;117(4):801–809.
49. Cibinel GA, Casoli G, Elia F, et al. Diagnostic accuracy and reproducibility
of pleural and lung ultrasound in discriminating cardiogenic
causes of acute dyspnea in the emergency department. Intern Emerg
Med. 2012;7(1):65–70.
50. Anderson KL, Jenq KY, Fields JM, Panebianco NL, Dean AJ. Diagnosing
heart failure among acutely dyspneic patients with cardiac,
inferior vena cava, and lung ultrasonography. Am J Emerg Med.
2013;31(8):1208–1214.
1. Soni NJ, Arntfield R, Kory P. Point-of-Care Ultrasound. 1st ed. Philadelphia,
PA: Saunders; 2014.
2. American Medical Association. House of Delegates. H-230.960 Privileging
for ultrasound imaging. Policy finder website. Available at:
https://ssl3.ama-assn.org/apps/ecomm/PolicyFinderForm.pl?site5www.
ama-assn.org&uri5%2fresources%2fhtml%2fPolicyFinder%2fpolicy
files%2fHnE%2fH-230.960.HTM. Accessed October 2, 2014.
3. Goldberg BB, Goodman GA, Clearfield HR. Evaluation of ascites by
ultrasound. Radiology. 1970;96(1):15–22.
4. Mercaldi CJ, Lanes SF. Ultrasound guidance decreases complications
and improves the cost of care among patients undergoing thoracentesis
and paracentesis. Chest. 2013;143(2):532–538.
5. Rubano E, Mehta N, Caputo W, Paladino L, Sinert R. Systematic
review: emergency department bedside ultrasonography for diagnosing
suspected abdominal aortic aneurysm. Acad Emerg Med. 2013;
20(2):128–138.
6. Dijos M, Pucheux Y, Lafitte M, et al. Fast track echo of abdominal
aortic aneurysm using a real pocket-ultrasound device at bedside.
Echocardiography. 2012;29(3):285–290.
7. Rosen CL, Brown DF, Sagarin MJ, Chang Y, McCabe CJ, Wolfe RE.
Ultrasonography by emergency physicians in patients with suspected
ureteral colic. J Emerg Med. 1998;16(6):865–870.
8. Gaspari RJ, Horst K. Emergency ultrasound and urinalysis in the evaluation
of flank pain. Acad Emerg Med. 2005;12(12):1180–1184.
9. Lucas BP, Candotti C, Margeta B, et al. Diagnostic accuracy of
hospitalist-performed hand-carried ultrasound echocardiography after
a brief training program. J Hosp Med. 2009;4(6):340–349.
10. Martin LD, Howell EE, Ziegelstein RC, Martire C, Shapiro EP,
Hellmann DB. Hospitalist performance of cardiac hand-carried ultrasound
after focused training. Am J Med. 2007;120(11):1000–1004.
11. Martin LD, Howell EE, Ziegelstein RC, et al. Hand-carried ultrasound
performed by hospitalists: does it improve the cardiac physical
examination? Am J Med. 2009;122(1):35–41.
PoCUS for Hospitalists | Soni and Lucas
An Official Publication of the Society of Hospital Medicine Journal of Hospital Medicine Vol 10 | No 2 | February 2015 123
12. Lucas BP, Candotti C, Margeta B, et al. Hand-carried echocardiography
by hospitalists: a randomized trial. Am J Med. 2011;124(8):766–
774.
13. Hu QJ, Shen YC, Jia LQ, et al. Diagnostic performance of lung ultrasound
in the diagnosis of pneumonia: a bivariate meta-analysis. Int J
Clin Exp Med. 2014;7(1):115–121.
14. Reissig A, Gramegna A, Aliberti S. The role of lung ultrasound in the
diagnosis and follow-up of community-acquired pneumonia. Eur J
Intern Med. 2012;23(5):391–397.
15. Patel PA, Ernst FR, Gunnarsson CL. Ultrasonography guidance
reduces complications and costs associated with thoracentesis procedures.
J Clin Ultrasound. 2012;40(3):135–141.
16. Ding W, Shen Y, Yang J, He X, Zhang M. Diagnosis of pneumothorax
by radiography and ultrasonography: a meta-analysis. Chest.
2011;140(4):859–866.
17. Alrajab S, Youssef AM, Akkus NI, Caldito G. Pleural ultrasonography
versus chest radiography for the diagnosis of pneumothorax: review
of the literature and meta-analysis. Crit Care. 2013;17(5):R208.
18. Lichtenstein D, Meziere G, Biderman P, Gepner A. The comet-tail
artifact: an ultrasound sign ruling out pneumothorax. Intensive Care
Med. 1999;25(4):383–388.
19. Picano E, Frassi F, Agricola E, Gligorova S, Gargani L, Mottola G.
Ultrasound lung comets: a clinically useful sign of extravascular lung
water. J Am Soc Echocardiogr. 2006;19(3):356–363.
20. Lichtenstein D, Meziere G. A lung ultrasound sign allowing bedside
distinction between pulmonary edema and COPD: the comet-tail artifact.
Intensive Care Med. 1998;24(12):1331–1334.
21. Volpicelli G, Mussa A, Garofalo G, et al. Bedside lung ultrasound in
the assessment of alveolar-interstitial syndrome. Am J Emerg Med.
2006;24(6):689–696.
22. Rothe CF. Reflex control of veins and vascular capacitance. Physiol
Rev. 1983;63(4):1281–1342.
23. Blair JE, Brennan JM, Goonewardena SN, Shah D, Vasaiwala S,
Spencer KT. Usefulness of hand-carried ultrasound to predict elevated
left ventricular filling pressure. Am J Cardiol. 2009;103(2):246–247.
24. Beigel R, Cercek B, Luo H, Siegel RJ. Noninvasive evaluation of right
atrial pressure. J Am Soc Echocardiogr. 2013;26(9):1033–1042.
25. Miller JB, Sen A, Strote SR, et al. Inferior vena cava assessment in the
bedside diagnosis of acute heart failure. Am J Emerg Med. 2012;
30(5):778–783.
26. Blehar DJ, Dickman E, Gaspari R. Identification of congestive heart
failure via respiratory variation of inferior vena cava diameter. Am J
Emerg Med. 2009;27(1):71–75.
27. Goonewardena SN, Spencer KT. Handcarried echocardiography to
assess hemodynamics in acute decompensated heart failure. Curr
Heart Fail Rep. 2010;7(4):219–227.
28. Guiotto G, Masarone M, Paladino F, et al. Inferior vena cava collapsibility
to guide fluid removal in slow continuous ultrafiltration: a pilot
study. Intensive Care Med. 2010;36(4):692–696.
29. Carbone F, Bovio M, Rosa GM, et al. Inferior vena cava parameters
predict readmission in ischemic heart failure. Eur J Clin Invest. 2014;
44(4):341–349.
30. Goonewardena SN, Gemignani A, Ronan A, et al. Comparison of
hand-carried ultrasound assessment of the inferior vena cava and Nterminal
pro-brain natriuretic peptide for predicting readmission after
hospitalization for acute decompensated heart failure. JACC Cardiovasc
Imaging. 2008;1(5):595–601.
31. Laffin L, Patel AR, Saha N, et al. Inferior vena cava measurement by
focused cardiac ultrasound in acute decompensated heart failure prevents
hospital readmissions. J Am Coll Cardiol. 2014;63(12 suppl):
A542.
32. Zhang Z, Xu X, Ye S, Xu L. Ultrasonographic measurement of the
respiratory variation in the inferior vena cava diameter is predictive of
fluid responsiveness in critically ill patients: systematic review and
meta-analysis. Ultrasound Med Biol. 2014;40(5):845–853.
33. Pomero F, Dentali F, Borretta V, et al. Accuracy of emergency
physician-performed ultrasonography in the diagnosis of deep-vein
thrombosis: a systematic review and meta-analysis. Thromb Haemost.
2013;109(1):137–145.
34. Lichtenstein DA, Meziere GA. Relevance of lung ultrasound in the
diagnosis of acute respiratory failure: the BLUE protocol. Chest.
2008;134(1):117–125.
35. Comert SS, Caglayan B, Akturk U, et al. The role of thoracic ultrasonography
in the diagnosis of pulmonary embolism. Ann Thorac Med.
2013;8(2):99–104.
36. Koenig S, Chandra S, Alaverdian A, Dibello C, Mayo PH,
Narasimhan M. Ultrasound assessment of pulmonary embolism in
patients receiving computerized tomography pulmonary angiography.
Chest. 2014;145(4):818–823.
37. Mookadam F, Jiamsripong P, Goel R, Warsame TA, Emani UR,
Khandheria BK. Critical appraisal on the utility of echocardiography
in the management of acute pulmonary embolism. Cardiol Rev. 2010;
18(1):29–37.
38. Gesensway D. Making the case for portable ultrasound. Todays Hospitalist.
2012;10:32–36.
39. Spencer KT, Kimura BJ, Korcarz CE, Pellikka PA, Rahko PS, Siegel
RJ. Focused cardiac ultrasound: recommendations from the American
Society of Echocardiography. J Am Soc Echocardiogr. 2013;26(6):
567–581.
40. Hellmann DB, Whiting-O’Keefe Q, Shapiro EP, Martin LD, Martire
C, Ziegelstein RC. The rate at which residents learn to use hand-held
echocardiography at the bedside. Am J Med. 2005;118(9):1010–
1018.
41. Redberg RF, Walsch J. Pay now, benefits may follow—the case of cardiac
computed tomographic angiography. N Engl J Med. 2008;359:
2309–2311.
42. Blyth L, Atkinson P, Gadd K, Lang E. Bedside focused echocardiography
as predictor of survival in cardiac arrest patients: a systematic
review. Acad Emerg Med. 2012;19(10):1119–1126.
43. Martin LD, Mathews S, Ziegelstein RC, et al. Prevalence of asymptomatic
left ventricular systolic dysfunction in at-risk medical inpatients.
Am J Med. 2013;126(1):68–73.
44. Low D, Vlasschaert M, Novak K, Chee A, Ma IWY. An argument for
using additional bedside tools, such as bedside ultrasound, for volume
status assessment in hospitalized medical patients: a needs assessment
survey. J Hosp Med. 2014;9:727–730.
45. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid
Ultrasound in SHock in the evaluation of the critically lll. Emerg Med
Clin North Am. 2010;28(1):29–56, vii.
46. Lichtenstein D. FALLS-protocol: lung ultrasound in hemodynamic
assessment of shock. Heart Lung Vessel. 2013;5(3):142–147.
47. Kimura BJ, Yogo N, O’Connell CW, Phan JN, Showalter BK,
Wolfson T. Cardiopulmonary limited ultrasound examination for
“quick-look” bedside application. Am J Cardiol. 2011;108(4):586–
590.
48. Manno E, Navarra M, Faccio L, et al. Deep impact of ultrasound in
the intensive care unit: the “ICU-sound” protocol. Anesthesiology.
2012;117(4):801–809.
49. Cibinel GA, Casoli G, Elia F, et al. Diagnostic accuracy and reproducibility
of pleural and lung ultrasound in discriminating cardiogenic
causes of acute dyspnea in the emergency department. Intern Emerg
Med. 2012;7(1):65–70.
50. Anderson KL, Jenq KY, Fields JM, Panebianco NL, Dean AJ. Diagnosing
heart failure among acutely dyspneic patients with cardiac,
inferior vena cava, and lung ultrasonography. Am J Emerg Med.
2013;31(8):1208–1214.
© 2014 Society of Hospital Medicine
Medication Reconciliation Perspectives
Medication reconciliation, when performed well, effectively identifies discrepancies and reduces medication errors in the hospital setting.[1, 2, 3] This process involves 4 major steps: (1) obtain and document a comprehensive medication history on admission, (2) compare the medication history to medication orders in the hospital and identify and resolve discrepancies, (3) provide the patient with a written list of discharge medications, and (4) educate the patient about their discharge medication regimen.[4, 5, 6]
However, medication reconciliation has been challenging to implement given difficulties with accurate medication information, patients' ability to communicate or remember, and clinician's not having enough time, motivation, or clear roles.[5, 7, 8, 9, 10, 11] Lack of role clarity is generally a barrier to quality improvement; therefore, we studied the perceptions of physicians, nurses, and pharmacists about their roles and responsibilities in completing inpatient medication reconciliation.
METHODS
We independently surveyed attending and resident physicians, nurses, and pharmacists at the University of California San Francisco (UCSF) Medical Center via email who were actively caring for hospitalized patients in April 2010. We collected data on demographics, roles on specific tasks in the medication reconciliation process from admission through discharge, and attitudes and barriers toward medication reconciliation and health information technology systems. Responses to questions used a 4‐point Likert scale. We calculated frequencies and proportions, and used the Fisher exact test to evaluate differences in role agreement for specific medication reconciliation tasks.
RESULTS
Of 256 active clinicians, 78 completed the survey (30.5% overall response rate) providing care in various hospital services (medicine, surgery, cardiology, neurology, pediatrics, obstetrics/gynecology). We received responses from 7 attending physicians (16% response rate), 14 resident physicians (19% response rate), 35 nurses (43% response rate), and 22 pharmacists (43% response rate). Most clinicians worked more than 5 years at UCSF, except residents (14 years).
Overall agreement was poor to fair on whose primary role it was for specific medication reconciliation tasks from admission through discharge (Table 1). Clinicians mainly agreed that it was a physician's responsibility to decide which medications should be continued or discontinued on admission and discharge, although agreement between attending and resident physicians varied. Fisher exact test revealed significant differences in agreement among attending and resident physicians, nurses, and pharmacists to obtain and document a medication history on admission (P=0.001), provide a list of the discharge medications (P<0.001), or educate patients on the postdischarge medication regimen (P<0.001). For these tasks, the physician, nurse, pharmacist or a combination of these clinicians (multiple category) were each identified to be responsible.
Response to who is responsible | |||||
---|---|---|---|---|---|
Clinician | Attending | Resident | Nurse | Pharmacist | Multiple* |
| |||||
A. On admission, obtaining and documenting the patient's medication history (P=0.001) | |||||
Attending | 1 (14%) | 6 (86%) | 0 | 0 | 0 |
Resident | 0 | 14 (100%) | 0 | 0 | 0 |
Nurse | 6 (17%) | 20 (57%) | 5 (14%) | 2 (6%) | 2 (6%) |
Pharmacist | 1 (5%) | 9 (41%) | 0 | 10 (45%) | 2 (9%) |
B. On admission, deciding which medications will be continued or discontinued (P=0.027) | |||||
Attending | 6 (86%) | 1 (14%) | 0 | 0 | 0 |
Resident | 3 (21%) | 11 (79%) | 0 | 0 | 0 |
Nurse | 12 (34%) | 22 (63%) | 0 | 0 | 1 (3%) |
Pharmacist | 4 (18%) | 15 (68%) | 0 | 2 (9%) | 1 (5%) |
C. On discharge, deciding which medications will be continued or discontinued (P=0.123) | |||||
Attending | 6 (86%) | 1 (14%) | 0 | 0 | 0 |
Resident | 5 (36%) | 9 (64%) | 0 | 0 | 0 |
Nurse | 10 (29%) | 15 (43%) | 1 (3%) | 1 (3%) | 8 (23%) |
Pharmacist | 5 (23%) | 12 (55%) | 1 (5%) | 0 | 4 (18%) |
D. On discharge, providing a list of the discharge medications to the patient (P<0.001) | |||||
Attending | 1 (14%) | 6 (86%) | 0 | 0 | 0 |
Resident | 0 | 13 (93%) | 0 | 1 (7%) | 0 |
Nurse | 2 (6%) | 22 (63%) | 3 (11%) | 6 (17%) | 2 (6%) |
Pharmacist | 0 | 4 (18%) | 2 (9%) | 14 (64%) | 2 (9%) |
E. On discharge, educating the patient on the postdischarge medication regimen (P<0.001) | |||||
Attending | 1 (14%) | 4 (57%) | 1 (14%) | 1 (14%) | 0 |
Resident | 0 | 4 (29%) | 8 (57%) | 2 (14%) | 0 |
Nurse | 0 | 2 (6%) | 23 (66%) | 8 (23%) | 2 (6%) |
Pharmacist | 0 | 0 | 3 (14%) | 14 (64%) | 5 (23%) |
Most clinicians believed that maintaining a patient's list of medications improves patient care (94%100% agreement). However, when asked whether clinicians other than yourself should be responsible for an accurate medication list, most nurses (73%) and pharmacists (52%) agreed with this statement compared to resident (50%) and attending physicians (29%). Most clinicians agreed that information technology systems for reconciling medications were complicated, and that patients who do not know their medications, accessing outside medical records, working with inaccurate lists, or nonEnglish‐speaking patients are barriers to reconciliation.
DISCUSSION
We found fair agreement among clinicians that physicians were responsible for reconciling medications on admission and discharge. However, attending and resident physicians each believed it was their primary responsibility, respectively, suggesting the need for better communication between each other. We found poor agreement among clinicians about whose primary role it was to perform the other main steps of medication reconciliation including obtaining and documenting a medication history, and providing a medication list and educating the patient at discharge. For these tasks, there was more confusion among physicians, nurses, and pharmacists. Our findings highlight the need for better role clarity and good communication among team members, particularly at discharge.
Nearly all clinicians agreed that updating patients' medication lists improves patient care. However, most nurses and pharmacists preferred that physicians be responsible for updating information and reconciling medications. They also noted a number of patient‐related and information system barriers to effective reconciliation as others have identified.[7, 8, 9, 10, 11] Although standardizing medication information reporting and implementing technology that can integrate medical records to create, update, and share information between patients and providers can help streamline the medication reconciliation process,[4, 5, 7, 8, 12] these procedures are unlikely to be effective unless good interprofessional communication, role clarity, and clinician understanding of how the system works are in place.
When this study was conducted, our institution's policy required that medication reconciliation be completed, but no specific roles or standard work documents existed. Since then, we have clarified the role of the physician to be responsible for completing medication reconciliation with ancillary help from nurses, pharmacists, and other clinicians, particularly when obtaining a medication history and preparing the patient for discharge. This role clarity has led to focused training and standard work guide documents as guidance to clinicians in different hospital settings about expectations and how to complete medication reconciliation. Clearly, no single reconciliation workflow process will meet the needs of all hospitals. However, it is crucial that interprofessional teams are established with clearly defined roles and responsibilities, and how these roles and responsibilities may change in various situations or services.[8]
Our study had several limitations. We surveyed 1 academic medical center, thus limiting the generalizability of our findings to other organizations or settings. Our small sample size and low response rate could be susceptible to selection bias. However, our findings are similar to other studies.[7, 10, 11] Finally, we included clinicians practicing on various services throughout our hospital, and the local medication reconciliation process could have contributed to the poor agreement. Nonetheless, differences in perceived roles and attitudes for completing medication reconciliation were observed.
In conclusion, lack of agreement among clinicians about their specific roles and responsibilities in the medication reconciliation process exists, and this may result in incomplete reconciliation, inefficiency, duplication of work, and possibly more confusion about a patient's medication regimen. Clinically meaningful and efficient medication reconciliation requires interprofessional teamwork with clear roles and responsibilities, good communication and better information reporting, and tracking systems to successfully combine the steps of medication reconciliation and ensure patient safety.[8, 12]
Disclosures: Funded by research grant NHLBI R01 HL086473 to Dr. Auerbach, and through UCSF‐ CTSI grant number KL2 RR024130 to Dr. Lee from the National Center for Research Resources, the National Center for Advancing Translational Sciences, and the Office of the Director, National Institutes of Health. The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health. Dr. Lee had full access to all study data and takes responsibility for data integrity and data analysis accuracy. The authors report no conflicts of interest.
- Medication reconciliation: a practical tool to reduce the risk of medication errors. J Crit Care. 2003;18(4):201–205. , , , et al.
- Hospital‐based medication reconciliation practices: a systematic review. Arch Intern Med. 2012;172(14):1057–1069. , , , .
- Results of the Medications at Transitions and Clinical Handoffs (MATCH) study: an analysis of medication reconciliation errors and risk factors at hospital admission. J Gen Intern Med. 2010;25(5):441–447. , , , et al.
- Institute for Healthcare Improvement. How‐to Guide: Prevent Adverse Drug Events (Medication Reconciliation). Available at: www.ihi.org/knowledge/Pages/Tools/HowtoGuidePreventAdverseDrugEvents.aspx. Accessed March 22, 2014.
- The Joint Commission. National patient safety goals effective January 1, 2014. Hospital Accreditation Program. Available at: http://www.jointcommission.org/assets/1/6/HAP_NPSG_Chapter_2014.pdf. Accessed March 22, 2014.
- Agency for Healthcare Research and Quality. Introduction: medications at transitions and clinical handoffs (MATCH) toolkit for medication reconciliation. Available at: http://www.ahrq.gov/professionals/quality‐patient‐safety/patient‐safety‐resources/resources/match/matchintro.html. Updated August 2012. Accessed March 22, 2014.
- Results of a medication reconciliation survey from the 2006 Society of Hospital Medicine national meeting. J Hosp Med. 2008;3(6):465–472. , , , , .
- Making inpatient medication reconciliation patient centered, clinically relevant and implementable: a consensus statement on key principles and necessary first steps. J Hosp Med. 2010;5(8):477–485. , , , et al.
- How reliable are patient‐completed medication reconciliation forms compared with pharmacy lists? Am J Emerg Med. 2012;30(7):1048–1054. , , , , .
- Medication reconciliation: barriers and facilitators from the perspectives of resident physicians and pharmacists. J Hosp Med. 2011;6(6):329–337. , , , , .
- Medication reconciliation: a qualitative analysis of clinicians' perceptions. Res Social Adm Pharm. 2013;9(4):419–430. , , , .
- Improving care transitions: optimizing medication reconciliation. J Am Pharm Assoc (2003). 2012;52(4):e43–e52. , .
Medication reconciliation, when performed well, effectively identifies discrepancies and reduces medication errors in the hospital setting.[1, 2, 3] This process involves 4 major steps: (1) obtain and document a comprehensive medication history on admission, (2) compare the medication history to medication orders in the hospital and identify and resolve discrepancies, (3) provide the patient with a written list of discharge medications, and (4) educate the patient about their discharge medication regimen.[4, 5, 6]
However, medication reconciliation has been challenging to implement given difficulties with accurate medication information, patients' ability to communicate or remember, and clinician's not having enough time, motivation, or clear roles.[5, 7, 8, 9, 10, 11] Lack of role clarity is generally a barrier to quality improvement; therefore, we studied the perceptions of physicians, nurses, and pharmacists about their roles and responsibilities in completing inpatient medication reconciliation.
METHODS
We independently surveyed attending and resident physicians, nurses, and pharmacists at the University of California San Francisco (UCSF) Medical Center via email who were actively caring for hospitalized patients in April 2010. We collected data on demographics, roles on specific tasks in the medication reconciliation process from admission through discharge, and attitudes and barriers toward medication reconciliation and health information technology systems. Responses to questions used a 4‐point Likert scale. We calculated frequencies and proportions, and used the Fisher exact test to evaluate differences in role agreement for specific medication reconciliation tasks.
RESULTS
Of 256 active clinicians, 78 completed the survey (30.5% overall response rate) providing care in various hospital services (medicine, surgery, cardiology, neurology, pediatrics, obstetrics/gynecology). We received responses from 7 attending physicians (16% response rate), 14 resident physicians (19% response rate), 35 nurses (43% response rate), and 22 pharmacists (43% response rate). Most clinicians worked more than 5 years at UCSF, except residents (14 years).
Overall agreement was poor to fair on whose primary role it was for specific medication reconciliation tasks from admission through discharge (Table 1). Clinicians mainly agreed that it was a physician's responsibility to decide which medications should be continued or discontinued on admission and discharge, although agreement between attending and resident physicians varied. Fisher exact test revealed significant differences in agreement among attending and resident physicians, nurses, and pharmacists to obtain and document a medication history on admission (P=0.001), provide a list of the discharge medications (P<0.001), or educate patients on the postdischarge medication regimen (P<0.001). For these tasks, the physician, nurse, pharmacist or a combination of these clinicians (multiple category) were each identified to be responsible.
Response to who is responsible | |||||
---|---|---|---|---|---|
Clinician | Attending | Resident | Nurse | Pharmacist | Multiple* |
| |||||
A. On admission, obtaining and documenting the patient's medication history (P=0.001) | |||||
Attending | 1 (14%) | 6 (86%) | 0 | 0 | 0 |
Resident | 0 | 14 (100%) | 0 | 0 | 0 |
Nurse | 6 (17%) | 20 (57%) | 5 (14%) | 2 (6%) | 2 (6%) |
Pharmacist | 1 (5%) | 9 (41%) | 0 | 10 (45%) | 2 (9%) |
B. On admission, deciding which medications will be continued or discontinued (P=0.027) | |||||
Attending | 6 (86%) | 1 (14%) | 0 | 0 | 0 |
Resident | 3 (21%) | 11 (79%) | 0 | 0 | 0 |
Nurse | 12 (34%) | 22 (63%) | 0 | 0 | 1 (3%) |
Pharmacist | 4 (18%) | 15 (68%) | 0 | 2 (9%) | 1 (5%) |
C. On discharge, deciding which medications will be continued or discontinued (P=0.123) | |||||
Attending | 6 (86%) | 1 (14%) | 0 | 0 | 0 |
Resident | 5 (36%) | 9 (64%) | 0 | 0 | 0 |
Nurse | 10 (29%) | 15 (43%) | 1 (3%) | 1 (3%) | 8 (23%) |
Pharmacist | 5 (23%) | 12 (55%) | 1 (5%) | 0 | 4 (18%) |
D. On discharge, providing a list of the discharge medications to the patient (P<0.001) | |||||
Attending | 1 (14%) | 6 (86%) | 0 | 0 | 0 |
Resident | 0 | 13 (93%) | 0 | 1 (7%) | 0 |
Nurse | 2 (6%) | 22 (63%) | 3 (11%) | 6 (17%) | 2 (6%) |
Pharmacist | 0 | 4 (18%) | 2 (9%) | 14 (64%) | 2 (9%) |
E. On discharge, educating the patient on the postdischarge medication regimen (P<0.001) | |||||
Attending | 1 (14%) | 4 (57%) | 1 (14%) | 1 (14%) | 0 |
Resident | 0 | 4 (29%) | 8 (57%) | 2 (14%) | 0 |
Nurse | 0 | 2 (6%) | 23 (66%) | 8 (23%) | 2 (6%) |
Pharmacist | 0 | 0 | 3 (14%) | 14 (64%) | 5 (23%) |
Most clinicians believed that maintaining a patient's list of medications improves patient care (94%100% agreement). However, when asked whether clinicians other than yourself should be responsible for an accurate medication list, most nurses (73%) and pharmacists (52%) agreed with this statement compared to resident (50%) and attending physicians (29%). Most clinicians agreed that information technology systems for reconciling medications were complicated, and that patients who do not know their medications, accessing outside medical records, working with inaccurate lists, or nonEnglish‐speaking patients are barriers to reconciliation.
DISCUSSION
We found fair agreement among clinicians that physicians were responsible for reconciling medications on admission and discharge. However, attending and resident physicians each believed it was their primary responsibility, respectively, suggesting the need for better communication between each other. We found poor agreement among clinicians about whose primary role it was to perform the other main steps of medication reconciliation including obtaining and documenting a medication history, and providing a medication list and educating the patient at discharge. For these tasks, there was more confusion among physicians, nurses, and pharmacists. Our findings highlight the need for better role clarity and good communication among team members, particularly at discharge.
Nearly all clinicians agreed that updating patients' medication lists improves patient care. However, most nurses and pharmacists preferred that physicians be responsible for updating information and reconciling medications. They also noted a number of patient‐related and information system barriers to effective reconciliation as others have identified.[7, 8, 9, 10, 11] Although standardizing medication information reporting and implementing technology that can integrate medical records to create, update, and share information between patients and providers can help streamline the medication reconciliation process,[4, 5, 7, 8, 12] these procedures are unlikely to be effective unless good interprofessional communication, role clarity, and clinician understanding of how the system works are in place.
When this study was conducted, our institution's policy required that medication reconciliation be completed, but no specific roles or standard work documents existed. Since then, we have clarified the role of the physician to be responsible for completing medication reconciliation with ancillary help from nurses, pharmacists, and other clinicians, particularly when obtaining a medication history and preparing the patient for discharge. This role clarity has led to focused training and standard work guide documents as guidance to clinicians in different hospital settings about expectations and how to complete medication reconciliation. Clearly, no single reconciliation workflow process will meet the needs of all hospitals. However, it is crucial that interprofessional teams are established with clearly defined roles and responsibilities, and how these roles and responsibilities may change in various situations or services.[8]
Our study had several limitations. We surveyed 1 academic medical center, thus limiting the generalizability of our findings to other organizations or settings. Our small sample size and low response rate could be susceptible to selection bias. However, our findings are similar to other studies.[7, 10, 11] Finally, we included clinicians practicing on various services throughout our hospital, and the local medication reconciliation process could have contributed to the poor agreement. Nonetheless, differences in perceived roles and attitudes for completing medication reconciliation were observed.
In conclusion, lack of agreement among clinicians about their specific roles and responsibilities in the medication reconciliation process exists, and this may result in incomplete reconciliation, inefficiency, duplication of work, and possibly more confusion about a patient's medication regimen. Clinically meaningful and efficient medication reconciliation requires interprofessional teamwork with clear roles and responsibilities, good communication and better information reporting, and tracking systems to successfully combine the steps of medication reconciliation and ensure patient safety.[8, 12]
Disclosures: Funded by research grant NHLBI R01 HL086473 to Dr. Auerbach, and through UCSF‐ CTSI grant number KL2 RR024130 to Dr. Lee from the National Center for Research Resources, the National Center for Advancing Translational Sciences, and the Office of the Director, National Institutes of Health. The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health. Dr. Lee had full access to all study data and takes responsibility for data integrity and data analysis accuracy. The authors report no conflicts of interest.
Medication reconciliation, when performed well, effectively identifies discrepancies and reduces medication errors in the hospital setting.[1, 2, 3] This process involves 4 major steps: (1) obtain and document a comprehensive medication history on admission, (2) compare the medication history to medication orders in the hospital and identify and resolve discrepancies, (3) provide the patient with a written list of discharge medications, and (4) educate the patient about their discharge medication regimen.[4, 5, 6]
However, medication reconciliation has been challenging to implement given difficulties with accurate medication information, patients' ability to communicate or remember, and clinician's not having enough time, motivation, or clear roles.[5, 7, 8, 9, 10, 11] Lack of role clarity is generally a barrier to quality improvement; therefore, we studied the perceptions of physicians, nurses, and pharmacists about their roles and responsibilities in completing inpatient medication reconciliation.
METHODS
We independently surveyed attending and resident physicians, nurses, and pharmacists at the University of California San Francisco (UCSF) Medical Center via email who were actively caring for hospitalized patients in April 2010. We collected data on demographics, roles on specific tasks in the medication reconciliation process from admission through discharge, and attitudes and barriers toward medication reconciliation and health information technology systems. Responses to questions used a 4‐point Likert scale. We calculated frequencies and proportions, and used the Fisher exact test to evaluate differences in role agreement for specific medication reconciliation tasks.
RESULTS
Of 256 active clinicians, 78 completed the survey (30.5% overall response rate) providing care in various hospital services (medicine, surgery, cardiology, neurology, pediatrics, obstetrics/gynecology). We received responses from 7 attending physicians (16% response rate), 14 resident physicians (19% response rate), 35 nurses (43% response rate), and 22 pharmacists (43% response rate). Most clinicians worked more than 5 years at UCSF, except residents (14 years).
Overall agreement was poor to fair on whose primary role it was for specific medication reconciliation tasks from admission through discharge (Table 1). Clinicians mainly agreed that it was a physician's responsibility to decide which medications should be continued or discontinued on admission and discharge, although agreement between attending and resident physicians varied. Fisher exact test revealed significant differences in agreement among attending and resident physicians, nurses, and pharmacists to obtain and document a medication history on admission (P=0.001), provide a list of the discharge medications (P<0.001), or educate patients on the postdischarge medication regimen (P<0.001). For these tasks, the physician, nurse, pharmacist or a combination of these clinicians (multiple category) were each identified to be responsible.
Response to who is responsible | |||||
---|---|---|---|---|---|
Clinician | Attending | Resident | Nurse | Pharmacist | Multiple* |
| |||||
A. On admission, obtaining and documenting the patient's medication history (P=0.001) | |||||
Attending | 1 (14%) | 6 (86%) | 0 | 0 | 0 |
Resident | 0 | 14 (100%) | 0 | 0 | 0 |
Nurse | 6 (17%) | 20 (57%) | 5 (14%) | 2 (6%) | 2 (6%) |
Pharmacist | 1 (5%) | 9 (41%) | 0 | 10 (45%) | 2 (9%) |
B. On admission, deciding which medications will be continued or discontinued (P=0.027) | |||||
Attending | 6 (86%) | 1 (14%) | 0 | 0 | 0 |
Resident | 3 (21%) | 11 (79%) | 0 | 0 | 0 |
Nurse | 12 (34%) | 22 (63%) | 0 | 0 | 1 (3%) |
Pharmacist | 4 (18%) | 15 (68%) | 0 | 2 (9%) | 1 (5%) |
C. On discharge, deciding which medications will be continued or discontinued (P=0.123) | |||||
Attending | 6 (86%) | 1 (14%) | 0 | 0 | 0 |
Resident | 5 (36%) | 9 (64%) | 0 | 0 | 0 |
Nurse | 10 (29%) | 15 (43%) | 1 (3%) | 1 (3%) | 8 (23%) |
Pharmacist | 5 (23%) | 12 (55%) | 1 (5%) | 0 | 4 (18%) |
D. On discharge, providing a list of the discharge medications to the patient (P<0.001) | |||||
Attending | 1 (14%) | 6 (86%) | 0 | 0 | 0 |
Resident | 0 | 13 (93%) | 0 | 1 (7%) | 0 |
Nurse | 2 (6%) | 22 (63%) | 3 (11%) | 6 (17%) | 2 (6%) |
Pharmacist | 0 | 4 (18%) | 2 (9%) | 14 (64%) | 2 (9%) |
E. On discharge, educating the patient on the postdischarge medication regimen (P<0.001) | |||||
Attending | 1 (14%) | 4 (57%) | 1 (14%) | 1 (14%) | 0 |
Resident | 0 | 4 (29%) | 8 (57%) | 2 (14%) | 0 |
Nurse | 0 | 2 (6%) | 23 (66%) | 8 (23%) | 2 (6%) |
Pharmacist | 0 | 0 | 3 (14%) | 14 (64%) | 5 (23%) |
Most clinicians believed that maintaining a patient's list of medications improves patient care (94%100% agreement). However, when asked whether clinicians other than yourself should be responsible for an accurate medication list, most nurses (73%) and pharmacists (52%) agreed with this statement compared to resident (50%) and attending physicians (29%). Most clinicians agreed that information technology systems for reconciling medications were complicated, and that patients who do not know their medications, accessing outside medical records, working with inaccurate lists, or nonEnglish‐speaking patients are barriers to reconciliation.
DISCUSSION
We found fair agreement among clinicians that physicians were responsible for reconciling medications on admission and discharge. However, attending and resident physicians each believed it was their primary responsibility, respectively, suggesting the need for better communication between each other. We found poor agreement among clinicians about whose primary role it was to perform the other main steps of medication reconciliation including obtaining and documenting a medication history, and providing a medication list and educating the patient at discharge. For these tasks, there was more confusion among physicians, nurses, and pharmacists. Our findings highlight the need for better role clarity and good communication among team members, particularly at discharge.
Nearly all clinicians agreed that updating patients' medication lists improves patient care. However, most nurses and pharmacists preferred that physicians be responsible for updating information and reconciling medications. They also noted a number of patient‐related and information system barriers to effective reconciliation as others have identified.[7, 8, 9, 10, 11] Although standardizing medication information reporting and implementing technology that can integrate medical records to create, update, and share information between patients and providers can help streamline the medication reconciliation process,[4, 5, 7, 8, 12] these procedures are unlikely to be effective unless good interprofessional communication, role clarity, and clinician understanding of how the system works are in place.
When this study was conducted, our institution's policy required that medication reconciliation be completed, but no specific roles or standard work documents existed. Since then, we have clarified the role of the physician to be responsible for completing medication reconciliation with ancillary help from nurses, pharmacists, and other clinicians, particularly when obtaining a medication history and preparing the patient for discharge. This role clarity has led to focused training and standard work guide documents as guidance to clinicians in different hospital settings about expectations and how to complete medication reconciliation. Clearly, no single reconciliation workflow process will meet the needs of all hospitals. However, it is crucial that interprofessional teams are established with clearly defined roles and responsibilities, and how these roles and responsibilities may change in various situations or services.[8]
Our study had several limitations. We surveyed 1 academic medical center, thus limiting the generalizability of our findings to other organizations or settings. Our small sample size and low response rate could be susceptible to selection bias. However, our findings are similar to other studies.[7, 10, 11] Finally, we included clinicians practicing on various services throughout our hospital, and the local medication reconciliation process could have contributed to the poor agreement. Nonetheless, differences in perceived roles and attitudes for completing medication reconciliation were observed.
In conclusion, lack of agreement among clinicians about their specific roles and responsibilities in the medication reconciliation process exists, and this may result in incomplete reconciliation, inefficiency, duplication of work, and possibly more confusion about a patient's medication regimen. Clinically meaningful and efficient medication reconciliation requires interprofessional teamwork with clear roles and responsibilities, good communication and better information reporting, and tracking systems to successfully combine the steps of medication reconciliation and ensure patient safety.[8, 12]
Disclosures: Funded by research grant NHLBI R01 HL086473 to Dr. Auerbach, and through UCSF‐ CTSI grant number KL2 RR024130 to Dr. Lee from the National Center for Research Resources, the National Center for Advancing Translational Sciences, and the Office of the Director, National Institutes of Health. The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health. Dr. Lee had full access to all study data and takes responsibility for data integrity and data analysis accuracy. The authors report no conflicts of interest.
- Medication reconciliation: a practical tool to reduce the risk of medication errors. J Crit Care. 2003;18(4):201–205. , , , et al.
- Hospital‐based medication reconciliation practices: a systematic review. Arch Intern Med. 2012;172(14):1057–1069. , , , .
- Results of the Medications at Transitions and Clinical Handoffs (MATCH) study: an analysis of medication reconciliation errors and risk factors at hospital admission. J Gen Intern Med. 2010;25(5):441–447. , , , et al.
- Institute for Healthcare Improvement. How‐to Guide: Prevent Adverse Drug Events (Medication Reconciliation). Available at: www.ihi.org/knowledge/Pages/Tools/HowtoGuidePreventAdverseDrugEvents.aspx. Accessed March 22, 2014.
- The Joint Commission. National patient safety goals effective January 1, 2014. Hospital Accreditation Program. Available at: http://www.jointcommission.org/assets/1/6/HAP_NPSG_Chapter_2014.pdf. Accessed March 22, 2014.
- Agency for Healthcare Research and Quality. Introduction: medications at transitions and clinical handoffs (MATCH) toolkit for medication reconciliation. Available at: http://www.ahrq.gov/professionals/quality‐patient‐safety/patient‐safety‐resources/resources/match/matchintro.html. Updated August 2012. Accessed March 22, 2014.
- Results of a medication reconciliation survey from the 2006 Society of Hospital Medicine national meeting. J Hosp Med. 2008;3(6):465–472. , , , , .
- Making inpatient medication reconciliation patient centered, clinically relevant and implementable: a consensus statement on key principles and necessary first steps. J Hosp Med. 2010;5(8):477–485. , , , et al.
- How reliable are patient‐completed medication reconciliation forms compared with pharmacy lists? Am J Emerg Med. 2012;30(7):1048–1054. , , , , .
- Medication reconciliation: barriers and facilitators from the perspectives of resident physicians and pharmacists. J Hosp Med. 2011;6(6):329–337. , , , , .
- Medication reconciliation: a qualitative analysis of clinicians' perceptions. Res Social Adm Pharm. 2013;9(4):419–430. , , , .
- Improving care transitions: optimizing medication reconciliation. J Am Pharm Assoc (2003). 2012;52(4):e43–e52. , .
- Medication reconciliation: a practical tool to reduce the risk of medication errors. J Crit Care. 2003;18(4):201–205. , , , et al.
- Hospital‐based medication reconciliation practices: a systematic review. Arch Intern Med. 2012;172(14):1057–1069. , , , .
- Results of the Medications at Transitions and Clinical Handoffs (MATCH) study: an analysis of medication reconciliation errors and risk factors at hospital admission. J Gen Intern Med. 2010;25(5):441–447. , , , et al.
- Institute for Healthcare Improvement. How‐to Guide: Prevent Adverse Drug Events (Medication Reconciliation). Available at: www.ihi.org/knowledge/Pages/Tools/HowtoGuidePreventAdverseDrugEvents.aspx. Accessed March 22, 2014.
- The Joint Commission. National patient safety goals effective January 1, 2014. Hospital Accreditation Program. Available at: http://www.jointcommission.org/assets/1/6/HAP_NPSG_Chapter_2014.pdf. Accessed March 22, 2014.
- Agency for Healthcare Research and Quality. Introduction: medications at transitions and clinical handoffs (MATCH) toolkit for medication reconciliation. Available at: http://www.ahrq.gov/professionals/quality‐patient‐safety/patient‐safety‐resources/resources/match/matchintro.html. Updated August 2012. Accessed March 22, 2014.
- Results of a medication reconciliation survey from the 2006 Society of Hospital Medicine national meeting. J Hosp Med. 2008;3(6):465–472. , , , , .
- Making inpatient medication reconciliation patient centered, clinically relevant and implementable: a consensus statement on key principles and necessary first steps. J Hosp Med. 2010;5(8):477–485. , , , et al.
- How reliable are patient‐completed medication reconciliation forms compared with pharmacy lists? Am J Emerg Med. 2012;30(7):1048–1054. , , , , .
- Medication reconciliation: barriers and facilitators from the perspectives of resident physicians and pharmacists. J Hosp Med. 2011;6(6):329–337. , , , , .
- Medication reconciliation: a qualitative analysis of clinicians' perceptions. Res Social Adm Pharm. 2013;9(4):419–430. , , , .
- Improving care transitions: optimizing medication reconciliation. J Am Pharm Assoc (2003). 2012;52(4):e43–e52. , .
Repeat BMD screening not helpful for women under 65
Postmenopausal women without osteoporosis on their first bone mineral density test are unlikely to fracture before age 65, and are therefore unlikely to benefit from regular or repeated screening before that age, according to an analysis of results from a large cohort study.
“Our data can help inform a BMD testing interval for postmenopausal women who are screened before age 65 years. Using the more conservative time estimates for major osteoporotic fracture, clinicians might allow women aged 50 to 54 years without osteoporosis on their first BMD test to wait 10 years for their next test. Similarly, women aged 60 to 64 years without osteoporosis on their first BMD test might wait until after age 65 years for their next test,” Dr. Margaret Lee Gourlay of the University of North Carolina, Chapel Hill, and her associates wrote in their analysis.
Dr. Gourlay and her coinvestigators on the larger Women’s Health Initiative cohort study looked at data from 4,068 postmenopausal women between the ages of 50 and 64 years. None of the women had prior hip or vertebral fractures or received antifracture treatment; they underwent baseline bone mineral density testing between 1993 and 2005. Fracture follow-up continued through 2012 (Menopause 2014 [doi: 10.1097/gme.0000000000000356]).
Among women with a normal BMD on first screening, the estimated time for 1% of those aged 50-54 years to have a hip or clinical vertebral fracture was 12.8 years. Among women aged 60-64 years, the time to fracture was 7.6 years, Dr. Gourlay and her colleagues found.
For the 8.5% of women in the cohort (all ages) with osteoporosis at baseline (n = 344), the age-adjusted time to hip or vertebral fracture was only 3 years.
Dr. Gourlay and her colleagues also estimated times to major osteoporotic fracture for 3% of the cohort, finding that it took 11.5 years for women aged 50-54 years to sustain a hip, clinical vertebral, proximal humerus, or wrist fracture, compared with 8.6 years for women who were 60-64 years at baseline. For women who had osteoporosis at baseline, the age-adjusted time for 3% to have an osteoporotic fracture was 2.5 years.
The researchers acknowledged as limitations of the study the fact that time estimates were based only on transitions to major fracture; that the full benefits and risks of screening, including cost-effectiveness, were not analyzed; and that the study was not powered to determine fracture risk in subgroups defined by individual risk factors.
Nonetheless, the results suggest that deferred repeat screening can be safe for postmenopausal women aged 50 years and older with normal BMD results at baseline, Dr. Gourlay and her coauthors wrote.
The study was funded by the National Institutes of Health. One of Dr. Gourlay’s coauthors is a consultant for MSD, and another reported receiving recent funding from Bone Ultrasound Finland.
This post hoc analysis of the Women’s Health Initiative cohort pursues the question of how frequently we should repeat BMD assessment on women under age 65 with normal baseline BMD. The study offers meaningful insight into how minuscule the fracture and osteoporosis risks are for women younger than 65 who have normal BMD at baseline. The younger cohort in this large study did not fracture or develop osteoporosis under surveillance to any significant extent.
While guidelines advise that women 65 and older be screened, as should younger postmenopausal women with risk factors, in clinical practice this often means that younger postmenopausal women with normal baseline BMD will enter into “autopilot” and undergo testing every 2 years. For young postmenopausal women with healthy BMD, we don’t need to fall into this default of biannual assessment. Clinicians could consider safely deferring a follow-up BMD test for young postmenopausal women with documented normal BMD for a few years, and for some even until age 65.
Nonetheless, clinicians should be mindful that this observational study was carried out in an asymptomatic group of women, and that the clinical picture should always guide the decision-making process on when and how often to screen.
Importantly, this study does not provide us any guidance regarding a young postmenopausal patient who has had a change in health status, such as a newly diagnosed autoimmune disease necessitating treatment with oral steroids, or after discontinuation of systemic menopausal hormone therapy, for whom repeating BMD assessment within 2 years or even 1 year of the initial study can be clinically justified despite evidence of normal BMD on her baseline scan.
Lubna Pal, M.D., is an associate director of obstetrics, gynecology, and reproductive sciences as well as director of the Menopause Program at Yale University in New Haven, Conn.
This post hoc analysis of the Women’s Health Initiative cohort pursues the question of how frequently we should repeat BMD assessment on women under age 65 with normal baseline BMD. The study offers meaningful insight into how minuscule the fracture and osteoporosis risks are for women younger than 65 who have normal BMD at baseline. The younger cohort in this large study did not fracture or develop osteoporosis under surveillance to any significant extent.
While guidelines advise that women 65 and older be screened, as should younger postmenopausal women with risk factors, in clinical practice this often means that younger postmenopausal women with normal baseline BMD will enter into “autopilot” and undergo testing every 2 years. For young postmenopausal women with healthy BMD, we don’t need to fall into this default of biannual assessment. Clinicians could consider safely deferring a follow-up BMD test for young postmenopausal women with documented normal BMD for a few years, and for some even until age 65.
Nonetheless, clinicians should be mindful that this observational study was carried out in an asymptomatic group of women, and that the clinical picture should always guide the decision-making process on when and how often to screen.
Importantly, this study does not provide us any guidance regarding a young postmenopausal patient who has had a change in health status, such as a newly diagnosed autoimmune disease necessitating treatment with oral steroids, or after discontinuation of systemic menopausal hormone therapy, for whom repeating BMD assessment within 2 years or even 1 year of the initial study can be clinically justified despite evidence of normal BMD on her baseline scan.
Lubna Pal, M.D., is an associate director of obstetrics, gynecology, and reproductive sciences as well as director of the Menopause Program at Yale University in New Haven, Conn.
This post hoc analysis of the Women’s Health Initiative cohort pursues the question of how frequently we should repeat BMD assessment on women under age 65 with normal baseline BMD. The study offers meaningful insight into how minuscule the fracture and osteoporosis risks are for women younger than 65 who have normal BMD at baseline. The younger cohort in this large study did not fracture or develop osteoporosis under surveillance to any significant extent.
While guidelines advise that women 65 and older be screened, as should younger postmenopausal women with risk factors, in clinical practice this often means that younger postmenopausal women with normal baseline BMD will enter into “autopilot” and undergo testing every 2 years. For young postmenopausal women with healthy BMD, we don’t need to fall into this default of biannual assessment. Clinicians could consider safely deferring a follow-up BMD test for young postmenopausal women with documented normal BMD for a few years, and for some even until age 65.
Nonetheless, clinicians should be mindful that this observational study was carried out in an asymptomatic group of women, and that the clinical picture should always guide the decision-making process on when and how often to screen.
Importantly, this study does not provide us any guidance regarding a young postmenopausal patient who has had a change in health status, such as a newly diagnosed autoimmune disease necessitating treatment with oral steroids, or after discontinuation of systemic menopausal hormone therapy, for whom repeating BMD assessment within 2 years or even 1 year of the initial study can be clinically justified despite evidence of normal BMD on her baseline scan.
Lubna Pal, M.D., is an associate director of obstetrics, gynecology, and reproductive sciences as well as director of the Menopause Program at Yale University in New Haven, Conn.
Postmenopausal women without osteoporosis on their first bone mineral density test are unlikely to fracture before age 65, and are therefore unlikely to benefit from regular or repeated screening before that age, according to an analysis of results from a large cohort study.
“Our data can help inform a BMD testing interval for postmenopausal women who are screened before age 65 years. Using the more conservative time estimates for major osteoporotic fracture, clinicians might allow women aged 50 to 54 years without osteoporosis on their first BMD test to wait 10 years for their next test. Similarly, women aged 60 to 64 years without osteoporosis on their first BMD test might wait until after age 65 years for their next test,” Dr. Margaret Lee Gourlay of the University of North Carolina, Chapel Hill, and her associates wrote in their analysis.
Dr. Gourlay and her coinvestigators on the larger Women’s Health Initiative cohort study looked at data from 4,068 postmenopausal women between the ages of 50 and 64 years. None of the women had prior hip or vertebral fractures or received antifracture treatment; they underwent baseline bone mineral density testing between 1993 and 2005. Fracture follow-up continued through 2012 (Menopause 2014 [doi: 10.1097/gme.0000000000000356]).
Among women with a normal BMD on first screening, the estimated time for 1% of those aged 50-54 years to have a hip or clinical vertebral fracture was 12.8 years. Among women aged 60-64 years, the time to fracture was 7.6 years, Dr. Gourlay and her colleagues found.
For the 8.5% of women in the cohort (all ages) with osteoporosis at baseline (n = 344), the age-adjusted time to hip or vertebral fracture was only 3 years.
Dr. Gourlay and her colleagues also estimated times to major osteoporotic fracture for 3% of the cohort, finding that it took 11.5 years for women aged 50-54 years to sustain a hip, clinical vertebral, proximal humerus, or wrist fracture, compared with 8.6 years for women who were 60-64 years at baseline. For women who had osteoporosis at baseline, the age-adjusted time for 3% to have an osteoporotic fracture was 2.5 years.
The researchers acknowledged as limitations of the study the fact that time estimates were based only on transitions to major fracture; that the full benefits and risks of screening, including cost-effectiveness, were not analyzed; and that the study was not powered to determine fracture risk in subgroups defined by individual risk factors.
Nonetheless, the results suggest that deferred repeat screening can be safe for postmenopausal women aged 50 years and older with normal BMD results at baseline, Dr. Gourlay and her coauthors wrote.
The study was funded by the National Institutes of Health. One of Dr. Gourlay’s coauthors is a consultant for MSD, and another reported receiving recent funding from Bone Ultrasound Finland.
Postmenopausal women without osteoporosis on their first bone mineral density test are unlikely to fracture before age 65, and are therefore unlikely to benefit from regular or repeated screening before that age, according to an analysis of results from a large cohort study.
“Our data can help inform a BMD testing interval for postmenopausal women who are screened before age 65 years. Using the more conservative time estimates for major osteoporotic fracture, clinicians might allow women aged 50 to 54 years without osteoporosis on their first BMD test to wait 10 years for their next test. Similarly, women aged 60 to 64 years without osteoporosis on their first BMD test might wait until after age 65 years for their next test,” Dr. Margaret Lee Gourlay of the University of North Carolina, Chapel Hill, and her associates wrote in their analysis.
Dr. Gourlay and her coinvestigators on the larger Women’s Health Initiative cohort study looked at data from 4,068 postmenopausal women between the ages of 50 and 64 years. None of the women had prior hip or vertebral fractures or received antifracture treatment; they underwent baseline bone mineral density testing between 1993 and 2005. Fracture follow-up continued through 2012 (Menopause 2014 [doi: 10.1097/gme.0000000000000356]).
Among women with a normal BMD on first screening, the estimated time for 1% of those aged 50-54 years to have a hip or clinical vertebral fracture was 12.8 years. Among women aged 60-64 years, the time to fracture was 7.6 years, Dr. Gourlay and her colleagues found.
For the 8.5% of women in the cohort (all ages) with osteoporosis at baseline (n = 344), the age-adjusted time to hip or vertebral fracture was only 3 years.
Dr. Gourlay and her colleagues also estimated times to major osteoporotic fracture for 3% of the cohort, finding that it took 11.5 years for women aged 50-54 years to sustain a hip, clinical vertebral, proximal humerus, or wrist fracture, compared with 8.6 years for women who were 60-64 years at baseline. For women who had osteoporosis at baseline, the age-adjusted time for 3% to have an osteoporotic fracture was 2.5 years.
The researchers acknowledged as limitations of the study the fact that time estimates were based only on transitions to major fracture; that the full benefits and risks of screening, including cost-effectiveness, were not analyzed; and that the study was not powered to determine fracture risk in subgroups defined by individual risk factors.
Nonetheless, the results suggest that deferred repeat screening can be safe for postmenopausal women aged 50 years and older with normal BMD results at baseline, Dr. Gourlay and her coauthors wrote.
The study was funded by the National Institutes of Health. One of Dr. Gourlay’s coauthors is a consultant for MSD, and another reported receiving recent funding from Bone Ultrasound Finland.
FROM MENOPAUSE
Key clinical point: Women under age 65 without risk factors whose first BMD screen is normal are not likely to benefit from repeat screening.
Major finding: Time to hip or vertebral fracture for 1% of women aged 50-54 years with normal BMD at baseline was 12.8 years, and 7.6 years for women aged 60-64 years, compared with 3 years for women aged 50-64 years with baseline osteoporosis.
Data source: An observational cohort of 4,068 women recruited as part of a larger trial cohort of postmenopausal women (n = 161,808) in the Women’s Health Initiative study.
Disclosures: The study was funded by the National Institutes of Health. One of Dr. Gourlay’s coauthors is a consultant for MSD, and another reported receiving recent funding from Bone Ultrasound Finland.
Up to 90% of gout hospitalizations might be preventable
BOSTON – Nearly all hospitalizations of people who were discharged with a primary diagnosis of gout were likely preventable, based on the results of a retrospective analysis of 79 cases at a single institution.
Because most of these patients presented to the emergency department rather than their doctor’s office, and were in pain and had other comorbidities, admission seemed the correct medical care decision, said Dr. Thomas Olenginski of the Geisinger Health System and one of the study’s lead authors. If the ED had gotten a rheumatology consult during the patients’ observation periods, however, the diagnosis could have been confirmed and most of these admissions would likely have been avoided, with a potential savings of over $200,000 in total hospitalization-related costs, Dr. Olenginski said at the annual meeting of the American College of Rheumatology.
Further, most of these patients were not adherent to their prescribed gout medications. Better clinical care and compliance with gout therapy might prevent most gout flareups that result in hospitalization, he added.
As a result of these findings, Geisinger has reassessed its approach to gout patients, especially those who present to the ED. For identified gout patients, they have ramped up efforts to make sure patients are adhering to therapy and are at goal, as well as educating them about their disease and how it can worsen without adherence. Rheumatologists are available to the ED by pager, encouraging arthrocentesis and crystal confirmation, thereby allowing the ED to focus on treating any associated skin infections and comorbidities, Dr. Olenginski said.
Of 56 gout-related admissions to their hospital, the Geisinger researchers found that 50 (89%) met the study’s definition of a preventable admission. A preventable admission was defined as one with a primary admitting diagnosis of mono- or polyarthritis subsequently diagnosed as gout and without any concomitant illness warranting admission on presentation.
The clinical diagnoses included 76% septic arthritis, 14% inflammatory polyarthritis, and 8% cellulitis.
Of the 50 preventable admissions, 33 patients underwent arthrocentesis, 24 of which were performed in the ED where the diagnosis could have been made based on crystal-confirmed diagnosis, he said.
Among the 35 patients with a prior history of gout, there were 23 patients whose serum uric acid levels were recorded within 1 year of their hospitalization, and 18 (78%) did not reach the goal of less than 6 mg/dL. Of 15 patients on long-term gout treatment, 5 (33%) were noncompliant with their treatment plans.
The total additive length of stay for the preventable gout admissions was 171 days with a mean stay of 3.42 days. Total hospitalization-related costs of these admissions were $208,000, with an average cost per admission of $4,160.
The study was performed as a quality initiative at Geisinger Health System. Dr. Olenginski had no relevant financial disclosures.
BOSTON – Nearly all hospitalizations of people who were discharged with a primary diagnosis of gout were likely preventable, based on the results of a retrospective analysis of 79 cases at a single institution.
Because most of these patients presented to the emergency department rather than their doctor’s office, and were in pain and had other comorbidities, admission seemed the correct medical care decision, said Dr. Thomas Olenginski of the Geisinger Health System and one of the study’s lead authors. If the ED had gotten a rheumatology consult during the patients’ observation periods, however, the diagnosis could have been confirmed and most of these admissions would likely have been avoided, with a potential savings of over $200,000 in total hospitalization-related costs, Dr. Olenginski said at the annual meeting of the American College of Rheumatology.
Further, most of these patients were not adherent to their prescribed gout medications. Better clinical care and compliance with gout therapy might prevent most gout flareups that result in hospitalization, he added.
As a result of these findings, Geisinger has reassessed its approach to gout patients, especially those who present to the ED. For identified gout patients, they have ramped up efforts to make sure patients are adhering to therapy and are at goal, as well as educating them about their disease and how it can worsen without adherence. Rheumatologists are available to the ED by pager, encouraging arthrocentesis and crystal confirmation, thereby allowing the ED to focus on treating any associated skin infections and comorbidities, Dr. Olenginski said.
Of 56 gout-related admissions to their hospital, the Geisinger researchers found that 50 (89%) met the study’s definition of a preventable admission. A preventable admission was defined as one with a primary admitting diagnosis of mono- or polyarthritis subsequently diagnosed as gout and without any concomitant illness warranting admission on presentation.
The clinical diagnoses included 76% septic arthritis, 14% inflammatory polyarthritis, and 8% cellulitis.
Of the 50 preventable admissions, 33 patients underwent arthrocentesis, 24 of which were performed in the ED where the diagnosis could have been made based on crystal-confirmed diagnosis, he said.
Among the 35 patients with a prior history of gout, there were 23 patients whose serum uric acid levels were recorded within 1 year of their hospitalization, and 18 (78%) did not reach the goal of less than 6 mg/dL. Of 15 patients on long-term gout treatment, 5 (33%) were noncompliant with their treatment plans.
The total additive length of stay for the preventable gout admissions was 171 days with a mean stay of 3.42 days. Total hospitalization-related costs of these admissions were $208,000, with an average cost per admission of $4,160.
The study was performed as a quality initiative at Geisinger Health System. Dr. Olenginski had no relevant financial disclosures.
BOSTON – Nearly all hospitalizations of people who were discharged with a primary diagnosis of gout were likely preventable, based on the results of a retrospective analysis of 79 cases at a single institution.
Because most of these patients presented to the emergency department rather than their doctor’s office, and were in pain and had other comorbidities, admission seemed the correct medical care decision, said Dr. Thomas Olenginski of the Geisinger Health System and one of the study’s lead authors. If the ED had gotten a rheumatology consult during the patients’ observation periods, however, the diagnosis could have been confirmed and most of these admissions would likely have been avoided, with a potential savings of over $200,000 in total hospitalization-related costs, Dr. Olenginski said at the annual meeting of the American College of Rheumatology.
Further, most of these patients were not adherent to their prescribed gout medications. Better clinical care and compliance with gout therapy might prevent most gout flareups that result in hospitalization, he added.
As a result of these findings, Geisinger has reassessed its approach to gout patients, especially those who present to the ED. For identified gout patients, they have ramped up efforts to make sure patients are adhering to therapy and are at goal, as well as educating them about their disease and how it can worsen without adherence. Rheumatologists are available to the ED by pager, encouraging arthrocentesis and crystal confirmation, thereby allowing the ED to focus on treating any associated skin infections and comorbidities, Dr. Olenginski said.
Of 56 gout-related admissions to their hospital, the Geisinger researchers found that 50 (89%) met the study’s definition of a preventable admission. A preventable admission was defined as one with a primary admitting diagnosis of mono- or polyarthritis subsequently diagnosed as gout and without any concomitant illness warranting admission on presentation.
The clinical diagnoses included 76% septic arthritis, 14% inflammatory polyarthritis, and 8% cellulitis.
Of the 50 preventable admissions, 33 patients underwent arthrocentesis, 24 of which were performed in the ED where the diagnosis could have been made based on crystal-confirmed diagnosis, he said.
Among the 35 patients with a prior history of gout, there were 23 patients whose serum uric acid levels were recorded within 1 year of their hospitalization, and 18 (78%) did not reach the goal of less than 6 mg/dL. Of 15 patients on long-term gout treatment, 5 (33%) were noncompliant with their treatment plans.
The total additive length of stay for the preventable gout admissions was 171 days with a mean stay of 3.42 days. Total hospitalization-related costs of these admissions were $208,000, with an average cost per admission of $4,160.
The study was performed as a quality initiative at Geisinger Health System. Dr. Olenginski had no relevant financial disclosures.
AT THE ACR ANNUAL MEETING
Key clinical point: Gout patients are often admitted to the hospital via the emergency department; most of these admissions could be avoidable.
Major finding: Of 56 gout-related admissions to their hospital, the Geisinger researchers found that 50 (89%) met the study’s definition of a preventable admission.
Data source: A retrospective analysis of 79 cases of gout at a single institution.
Disclosures: The study was performed as a quality initiative at Geisinger Health System. Dr. Olenginski had no relevant financial disclosures.