Clinical Review

Office hysteroscopy offers many benefits and is becoming more acceptable among patients and gynecologists for both diagnostic and operative procedures (TABLE 1). Despite its clear advantages, however, many gynecologists remain hesitant to perform in-office procedures out of fear that the patient, who is generally awake, will experience significant discomfort.

Certainly, pain and low patient tolerance of discomfort have been the primary limitations to widespread use of office hysteroscopy without anesthesia.¹ Data on the use of anesthesia for office hysteroscopy—especially diagnostic procedures—historically have been inconsistent in regard to the reduction of patient discomfort.²

Bettocchi and Selvaggi first reported a vaginoscopic approach to diagnostic hysteroscopy to reduce the discomfort of the procedure, compared with the conventional approach. They did not place a vaginal speculum or tenaculum and, therefore, avoided placing local anesthetic into the cervix.³

A randomized controlled trial by Sagiv and colleagues found reduced pain during diagnostic hysteroscopy with vaginoscopy (VIDEO).⁴

Vidyard Video

In 2004, Bettocchi and colleagues reported nearly 5,000 operative hysteroscopic procedures performed with this technique (the “no-touch” technique) in an outpatient setting, demonstrating very high patient tolerance and a low degree of procedural pain. More than 90% of patients experienced little to no pain, except for those undergoing ­polypectomy when the polyps were larger than the diameter of the cervical os, as well as those who had anatomic abnormalities, with moderate discomfort reported by 33.2% and 12.7% of these women, respectively.⁵ These few patients may have benefited from anesthetic intervention for the procedure.

In a 2010 review of the literature on hysteroscopy without anesthesia, Cicinelli found that diagnostic hysteroscopy was more successful, with less patient discomfort, when smaller hysteroscopes were used (3.5 mm or smaller, including flexible lenses) and when the approach was vaginoscopic.¹ Reduced pain with operative procedures was associated with a number of variables, including:

Variables associated with increased pain during operative procedures included:

In the review, Cicinelli noted that not all patients are likely to have a successful hysteroscopic procedure without the use of anesthesia or analgesia, regardless of the approach used.¹

Only 1 randomized controlled trial explored the use of anesthesia (versus placebo) during operative hysteroscopy, and the authors found a benefit for preprocedural paracervical block using local anesthetic to reduce cervical pain.⁶

The success of diagnostic and operative hysteroscopic procedures with minimal and acceptable levels of patient discomfort in the office depends, therefore, on multiple factors. Procedural factors affecting the outcome of hysteroscopy include the size of the instrument used, the type and length of the procedure, the use of preprocedure anesthesia or analgesia, and a vaginoscopic approach. The skill of the surgeon also affects the hysteroscopic experience and outcome. In addition, patient variables such as menopausal status, anatomic distortion (eg, cervical stenosis), and anxiety may adversely affect the patient’s experience.

In summary, it is possible for the gynecologist to appropriately accommodate any given patient and clinical scenario, keeping in mind that many patients will require a customized approach for ultimate success. In this article, I review 3 recent studies on office hysteroscopy, focusing on the reduction of procedural pain and anxiety. Because of the protective effect of a high degree of surgeon experience, it is important that we offer adequate education in hysteroscopy during residency and postgraduate courses.

Placement of local anesthetic at multiple anatomic sites facilitates patient comfort during hysteroscopy

Keyhan S, Munro MG. Office diagnostic and operative hysteroscopy using local anesthesia only: an analysis of patient reported pain and other procedural outcomes. J Minim Invasive Gynecol. 2014;21(5):791–798.

In a 2010 review of randomized controlled trials of the use of local anesthesia versus placebo during hysteroscopy, data from several studies indicated a significant decrease in procedural pain when local anesthesia was given, while other studies found no difference.² Most of the studies in that review evaluated a single site of anesthesia placement and focused on diagnostic hysteroscopy. The findings of that review, as well as the differential innervation of the uterine cervix and fundus (FIGURE), prompted Keyhan and Munro to evaluate the efficacy of multimodal local anesthetic for office diagnostic and operative hysteroscopy without the use of any systemic agents except for preprocedural cyclooxygenase (COX) inhibitors (TABLE 2).  Accordingly, they placed local anesthetic at multiple anatomic sites to alleviate patient pain and improve procedural success in a spectrum of office-based hysteroscopic procedures.

Details of the trial
Procedures generally were performed using a continuous-flow sheath with an outside diameter of 5.5 mm and a 5 French operative channel for placement of operative instruments such as scissors, graspers, and sterilization microinserts. Normal saline or sterile water was used as the uterine distention medium, with gravity inflow assisted by pressure cuff, when necessary. Occasionally, a sheath system with an outside diameter of 6.5 mm was used, or an outside diameter of 9 mm for resectoscopic procedures using a bipolar radiofrequency resectoscope. When needed, cervical dilation was performed to accommodate the specific instrument used.

The impact of the multimodal, multisite anesthetic protocol was evaluated using contemporaneous patient reporting of numeric pain scores (worst pain experienced) that included anesthesia-related pain, procedure-related pain, and overall pain.

A total of 478 women underwent 535 procedures. A patient verbal response scale (range, 0–10) was used to assess the worst pain experienced. The overall mean (SD) procedure pain score was 3.7 (2.5). The mean score for patients undergoing diagnostic hysteroscopy was 3.2 (2.5), and it was 4.1 (2.5) for operative hysteroscopy (P<.001).

TABLE 3 shows the procedures performed under the anesthetic protocol. Pain associated with placement of anesthesia was similar for diagnostic and operative procedures (mean score, 2.7), but the mean overall pain scores for diagnostic procedures were about 1 unit less than for operative procedures, regardless of age or delivery history.

Complications were limited to 3 transient vasovagal episodes. Five procedures could not be completed because of intolerable pain or inability to access the uterine cavity. There was no difference in pain scores between menopausal and premeno-pausal women.

Malcolm G. Munro, MD, offers a protocol for pain relief during hysteroscopy

 

In this video, Malcolm G. Munro, MD, makes use of both topical and injectable lidocaine at 5 anatomic sites

Dr. Munro is Professor of Obstetrics and Gynecology at the David Geffen School of Medicine at UCLA and Director of Gynecologic Services at Kaiser Permanente, Los Angeles Medical Center, in Los Angeles, California.
 

When placing anesthesia at multiple sites, allow time for onset of action
Keyhan and Munro demonstrated that ­successful completion of hysteroscopic procedures in the office environment can be achieved with acceptable levels of patient discomfort using a multimodal, multisite approach for preemptive placement of local anesthetic in the vagina, cervix, and endometrial cavity. They emphasize that the waiting time allotted for the onset of anesthesia is critical to the success of this approach. They also stress that no preprocedure oral sedative or narcotic is used with their approach. In addition, they note that the minimal discomfort experienced during placement of local anesthetic was overshadowed by general comfort during the wide spectrum of procedures performed.

What this EVIDENCE means for practice
The placement of preemptive local anesthesia at multiple anatomic sites facilitates diagnostic and operative hysteroscopy with an acceptable degree of patient comfort and successful completion of office procedures.

Music may reduce patient anxiety during hysteroscopy

Angioli R, De Cicco Nardone C, Plotti F, et al. Use of music to reduce anxiety during office hysteroscopy: prospective randomized trial. J Minim Invasive Gynecol. 2014;21(3):454–459.

Angioli and colleagues set out to address another factor that can impede patient comfort during office hysteroscopy—anxiety. Their randomized prospective trial is the only such trial evaluating the use of music to establish a calm and relaxing environment prior to office hysteroscopy for patients who are awake. Music supports an environment that “stimulates and maintains relaxation, well-being, and comfort and can be used as a self-management technique to reduce or control distress,” Angioli and colleagues write. The theory is that music distracts the patient by drawing her attention away from negative stimuli, thereby reducing pain, anxiety, and stress.

Details of the trial
A standardized visual analog scale (range, 0–10) was used to assess patient discomfort, and a State-Trait Anxiety Inventory (STAI; range, 20–80) also was given. Both tools were administered at baseline. The visual analog scale was measured again during the procedure, and the STAI was administered again after the procedure.

A hysteroscopic sheath with an outside diameter of 5 mm was used with a 5 French operative channel, and a vaginoscopic approach was used for each hysteroscopic procedure. A total of 372 women were enrolled and randomly allocated to either:

The surgical procedure was not completed in 15 patients (9 in the music group and 6 in the no-music group) because of stenosis of the cervix and/or excessive pain.

Women in the music group were allowed to select a playlist of classical, pop, jazz, or rock music that was played through a speaker system in the room. Of these patients, 50% preferred classical, 45% preferred pop, 5% chose jazz, and none selected rock music.

There were no statistically significant differences between the 2 groups in terms of preprocedure wait time, preprocedure scores on the visual analog scale or STAI, preprocedure vital signs, patient characteristics, type of procedure, or duration of the procedure. However, the music group had a lower visual analog score during the procedure and a lower postoperative STAI for diagnostic hysteroscopy than the no-music group did. The music group also had a statistically significant lower visual analog score for operative hysteroscopy than the no-music group did. In addition, the music group had a lower postoperative STAI score than the no-music group, but this difference was not statistically significant (TABLE 4).

Interestingly, in the music group, the STAI scores were lower after both diagnostic and operative hysteroscopy when classical music was selected rather than pop music.

Anxiety and pain are highly correlated
Angioli and colleagues found that patients who listened to music intraoperatively had a lower perception of pain and less anxiety. In addition, systolic blood pressure and heart rate were significantly lower in the music group than the no-music group, implying that patients who listened to music experienced less physical stress during the procedure.

Angioli and colleagues also noted that the level of anxiety and perception of pain were highly correlated. Pain is not an emotionally neutral experience but is almost always accompanied by distress. Investigators concluded that “anxiety can enhance painful sensations at all levels of the nervous system, from the peripheral receptors to the cortical level.”

What this EVIDENCE means for practice
Music is a useful complementary method to control patient anxiety and reduce the perception of pain during office hysteroscopy by creating a more relaxed and comfortable environment.

What are the risk factors for pain and discomfort during office hysteroscopy?

De Freitas FM, Sessa FV, Resende AD Jr, et al. Identifying predictors of unacceptable pain at office hysteroscopy. J Minim Invasive Gynecol. 2014;21(4):586–591.

De Freitas and colleagues conducted their prospective observational study to identify predictors of unacceptable pain during diagnostic office hysteroscopy (with or without directed or curette endometrial biopsy) and at the time of discharge. They hoped that any identifiable causes of unacceptable pain could be addressed individually in future patients undergoing office hysteroscopy to reduce their level of discomfort.

Details of the trial
A total of 558 procedures were evaluated. Hysteroscopists had varying levels of experience, with some having performed fewer than 50 procedures and others having performed more than 500.

A verbal response scale (range, 0–10) was used to assess pain at the end of each procedure and at the time of discharge. Investigators considered a score of 7 or more at the time of the procedure and a score of 4 or more at the time of discharge to be unacceptable.

A diagnostic, single-channel hysteroscope with an outside diameter of 3.5 mm was used with normal saline (at room temperature), along with a gravity system with pressure established to maintain intrauterine pressure at approximately 110 mm Hg. All hysteroscopic procedures were performed using a vaginoscopic approach, and biopsies were obtained as clinically indicated. Any patients who reported cramping at discharge (ie, a verbal response scale score of 4 or more) were offered an oral nonsteroidal anti-inflammatory drug.

Overall, the prevalence of unacceptable pain during office hysteroscopy was 32.3%. Experience of the hysteroscopist had a ­significant protective effect against pain. Longer procedures were significantly associated with unacceptable procedural pain.

The prevalence of unacceptable cramping at discharge was 28.6%. The risk of discomfort at discharge was significantly higher for women who reported dyspareunia or dysmenorrhea. Surgeon experience was significantly protective against unacceptable pain at discharge, and longer procedures were significantly associated with increased discomfort at discharge.

Dysmenorrhea and dyspareunia were significant predictors of pain at discharge
In this study, dysmenorrhea was a significant predictor of unacceptable pain at discharge, increasing the risk of unacceptable cramps by approximately threefold. Women who reported dyspareunia were nearly twice as likely to report unacceptable cramping at ­discharge.

Although a high level of expertise is not a prerequisite for office hysteroscopy, the skill and experience of the hysteroscopist, as well as shorter procedures, proved to be protective against procedural pain and discomfort at discharge but did not eliminate them altogether. Therefore, De Freitas and colleagues recommend that patients who can be identified as high-risk for procedural or discharge pain, such as women with dysmenorrhea or dyspareunia, should be offered preprocedure analgesia and/or anesthesia to reduce overall discomfort.

What this EVIDENCE means for practice
If a patient reports dysmenorrhea or dyspareunia preoperatively, she may benefit from preprocedure anesthesia or analgesia, or both, in an office setting.

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

Office hysteroscopy offers many benefits and is becoming more acceptable among patients and gynecologists for both diagnostic and operative procedures (TABLE 1). Despite its clear advantages, however, many gynecologists remain hesitant to perform in-office procedures out of fear that the patient, who is generally awake, will experience significant discomfort.

Certainly, pain and low patient tolerance of discomfort have been the primary limitations to widespread use of office hysteroscopy without anesthesia.¹ Data on the use of anesthesia for office hysteroscopy—especially diagnostic procedures—historically have been inconsistent in regard to the reduction of patient discomfort.²

Bettocchi and Selvaggi first reported a vaginoscopic approach to diagnostic hysteroscopy to reduce the discomfort of the procedure, compared with the conventional approach. They did not place a vaginal speculum or tenaculum and, therefore, avoided placing local anesthetic into the cervix.³

A randomized controlled trial by Sagiv and colleagues found reduced pain during diagnostic hysteroscopy with vaginoscopy (VIDEO).⁴

Vidyard Video

In 2004, Bettocchi and colleagues reported nearly 5,000 operative hysteroscopic procedures performed with this technique (the “no-touch” technique) in an outpatient setting, demonstrating very high patient tolerance and a low degree of procedural pain. More than 90% of patients experienced little to no pain, except for those undergoing ­polypectomy when the polyps were larger than the diameter of the cervical os, as well as those who had anatomic abnormalities, with moderate discomfort reported by 33.2% and 12.7% of these women, respectively.⁵ These few patients may have benefited from anesthetic intervention for the procedure.

In a 2010 review of the literature on hysteroscopy without anesthesia, Cicinelli found that diagnostic hysteroscopy was more successful, with less patient discomfort, when smaller hysteroscopes were used (3.5 mm or smaller, including flexible lenses) and when the approach was vaginoscopic.¹ Reduced pain with operative procedures was associated with a number of variables, including:

Variables associated with increased pain during operative procedures included:

In the review, Cicinelli noted that not all patients are likely to have a successful hysteroscopic procedure without the use of anesthesia or analgesia, regardless of the approach used.¹

Only 1 randomized controlled trial explored the use of anesthesia (versus placebo) during operative hysteroscopy, and the authors found a benefit for preprocedural paracervical block using local anesthetic to reduce cervical pain.⁶

The success of diagnostic and operative hysteroscopic procedures with minimal and acceptable levels of patient discomfort in the office depends, therefore, on multiple factors. Procedural factors affecting the outcome of hysteroscopy include the size of the instrument used, the type and length of the procedure, the use of preprocedure anesthesia or analgesia, and a vaginoscopic approach. The skill of the surgeon also affects the hysteroscopic experience and outcome. In addition, patient variables such as menopausal status, anatomic distortion (eg, cervical stenosis), and anxiety may adversely affect the patient’s experience.

In summary, it is possible for the gynecologist to appropriately accommodate any given patient and clinical scenario, keeping in mind that many patients will require a customized approach for ultimate success. In this article, I review 3 recent studies on office hysteroscopy, focusing on the reduction of procedural pain and anxiety. Because of the protective effect of a high degree of surgeon experience, it is important that we offer adequate education in hysteroscopy during residency and postgraduate courses.

Placement of local anesthetic at multiple anatomic sites facilitates patient comfort during hysteroscopy

Keyhan S, Munro MG. Office diagnostic and operative hysteroscopy using local anesthesia only: an analysis of patient reported pain and other procedural outcomes. J Minim Invasive Gynecol. 2014;21(5):791–798.

In a 2010 review of randomized controlled trials of the use of local anesthesia versus placebo during hysteroscopy, data from several studies indicated a significant decrease in procedural pain when local anesthesia was given, while other studies found no difference.² Most of the studies in that review evaluated a single site of anesthesia placement and focused on diagnostic hysteroscopy. The findings of that review, as well as the differential innervation of the uterine cervix and fundus (FIGURE), prompted Keyhan and Munro to evaluate the efficacy of multimodal local anesthetic for office diagnostic and operative hysteroscopy without the use of any systemic agents except for preprocedural cyclooxygenase (COX) inhibitors (TABLE 2).  Accordingly, they placed local anesthetic at multiple anatomic sites to alleviate patient pain and improve procedural success in a spectrum of office-based hysteroscopic procedures.

Details of the trial
Procedures generally were performed using a continuous-flow sheath with an outside diameter of 5.5 mm and a 5 French operative channel for placement of operative instruments such as scissors, graspers, and sterilization microinserts. Normal saline or sterile water was used as the uterine distention medium, with gravity inflow assisted by pressure cuff, when necessary. Occasionally, a sheath system with an outside diameter of 6.5 mm was used, or an outside diameter of 9 mm for resectoscopic procedures using a bipolar radiofrequency resectoscope. When needed, cervical dilation was performed to accommodate the specific instrument used.

The impact of the multimodal, multisite anesthetic protocol was evaluated using contemporaneous patient reporting of numeric pain scores (worst pain experienced) that included anesthesia-related pain, procedure-related pain, and overall pain.

A total of 478 women underwent 535 procedures. A patient verbal response scale (range, 0–10) was used to assess the worst pain experienced. The overall mean (SD) procedure pain score was 3.7 (2.5). The mean score for patients undergoing diagnostic hysteroscopy was 3.2 (2.5), and it was 4.1 (2.5) for operative hysteroscopy (P<.001).

TABLE 3 shows the procedures performed under the anesthetic protocol. Pain associated with placement of anesthesia was similar for diagnostic and operative procedures (mean score, 2.7), but the mean overall pain scores for diagnostic procedures were about 1 unit less than for operative procedures, regardless of age or delivery history.

Complications were limited to 3 transient vasovagal episodes. Five procedures could not be completed because of intolerable pain or inability to access the uterine cavity. There was no difference in pain scores between menopausal and premeno-pausal women.

Malcolm G. Munro, MD, offers a protocol for pain relief during hysteroscopy

 

In this video, Malcolm G. Munro, MD, makes use of both topical and injectable lidocaine at 5 anatomic sites

Dr. Munro is Professor of Obstetrics and Gynecology at the David Geffen School of Medicine at UCLA and Director of Gynecologic Services at Kaiser Permanente, Los Angeles Medical Center, in Los Angeles, California.
 

When placing anesthesia at multiple sites, allow time for onset of action
Keyhan and Munro demonstrated that ­successful completion of hysteroscopic procedures in the office environment can be achieved with acceptable levels of patient discomfort using a multimodal, multisite approach for preemptive placement of local anesthetic in the vagina, cervix, and endometrial cavity. They emphasize that the waiting time allotted for the onset of anesthesia is critical to the success of this approach. They also stress that no preprocedure oral sedative or narcotic is used with their approach. In addition, they note that the minimal discomfort experienced during placement of local anesthetic was overshadowed by general comfort during the wide spectrum of procedures performed.

What this EVIDENCE means for practice
The placement of preemptive local anesthesia at multiple anatomic sites facilitates diagnostic and operative hysteroscopy with an acceptable degree of patient comfort and successful completion of office procedures.

Music may reduce patient anxiety during hysteroscopy

Angioli R, De Cicco Nardone C, Plotti F, et al. Use of music to reduce anxiety during office hysteroscopy: prospective randomized trial. J Minim Invasive Gynecol. 2014;21(3):454–459.

Angioli and colleagues set out to address another factor that can impede patient comfort during office hysteroscopy—anxiety. Their randomized prospective trial is the only such trial evaluating the use of music to establish a calm and relaxing environment prior to office hysteroscopy for patients who are awake. Music supports an environment that “stimulates and maintains relaxation, well-being, and comfort and can be used as a self-management technique to reduce or control distress,” Angioli and colleagues write. The theory is that music distracts the patient by drawing her attention away from negative stimuli, thereby reducing pain, anxiety, and stress.

Details of the trial
A standardized visual analog scale (range, 0–10) was used to assess patient discomfort, and a State-Trait Anxiety Inventory (STAI; range, 20–80) also was given. Both tools were administered at baseline. The visual analog scale was measured again during the procedure, and the STAI was administered again after the procedure.

A hysteroscopic sheath with an outside diameter of 5 mm was used with a 5 French operative channel, and a vaginoscopic approach was used for each hysteroscopic procedure. A total of 372 women were enrolled and randomly allocated to either:

The surgical procedure was not completed in 15 patients (9 in the music group and 6 in the no-music group) because of stenosis of the cervix and/or excessive pain.

Women in the music group were allowed to select a playlist of classical, pop, jazz, or rock music that was played through a speaker system in the room. Of these patients, 50% preferred classical, 45% preferred pop, 5% chose jazz, and none selected rock music.

There were no statistically significant differences between the 2 groups in terms of preprocedure wait time, preprocedure scores on the visual analog scale or STAI, preprocedure vital signs, patient characteristics, type of procedure, or duration of the procedure. However, the music group had a lower visual analog score during the procedure and a lower postoperative STAI for diagnostic hysteroscopy than the no-music group did. The music group also had a statistically significant lower visual analog score for operative hysteroscopy than the no-music group did. In addition, the music group had a lower postoperative STAI score than the no-music group, but this difference was not statistically significant (TABLE 4).

Interestingly, in the music group, the STAI scores were lower after both diagnostic and operative hysteroscopy when classical music was selected rather than pop music.

Anxiety and pain are highly correlated
Angioli and colleagues found that patients who listened to music intraoperatively had a lower perception of pain and less anxiety. In addition, systolic blood pressure and heart rate were significantly lower in the music group than the no-music group, implying that patients who listened to music experienced less physical stress during the procedure.

Angioli and colleagues also noted that the level of anxiety and perception of pain were highly correlated. Pain is not an emotionally neutral experience but is almost always accompanied by distress. Investigators concluded that “anxiety can enhance painful sensations at all levels of the nervous system, from the peripheral receptors to the cortical level.”

What this EVIDENCE means for practice
Music is a useful complementary method to control patient anxiety and reduce the perception of pain during office hysteroscopy by creating a more relaxed and comfortable environment.

What are the risk factors for pain and discomfort during office hysteroscopy?

De Freitas FM, Sessa FV, Resende AD Jr, et al. Identifying predictors of unacceptable pain at office hysteroscopy. J Minim Invasive Gynecol. 2014;21(4):586–591.

De Freitas and colleagues conducted their prospective observational study to identify predictors of unacceptable pain during diagnostic office hysteroscopy (with or without directed or curette endometrial biopsy) and at the time of discharge. They hoped that any identifiable causes of unacceptable pain could be addressed individually in future patients undergoing office hysteroscopy to reduce their level of discomfort.

Details of the trial
A total of 558 procedures were evaluated. Hysteroscopists had varying levels of experience, with some having performed fewer than 50 procedures and others having performed more than 500.

A verbal response scale (range, 0–10) was used to assess pain at the end of each procedure and at the time of discharge. Investigators considered a score of 7 or more at the time of the procedure and a score of 4 or more at the time of discharge to be unacceptable.

A diagnostic, single-channel hysteroscope with an outside diameter of 3.5 mm was used with normal saline (at room temperature), along with a gravity system with pressure established to maintain intrauterine pressure at approximately 110 mm Hg. All hysteroscopic procedures were performed using a vaginoscopic approach, and biopsies were obtained as clinically indicated. Any patients who reported cramping at discharge (ie, a verbal response scale score of 4 or more) were offered an oral nonsteroidal anti-inflammatory drug.

Overall, the prevalence of unacceptable pain during office hysteroscopy was 32.3%. Experience of the hysteroscopist had a ­significant protective effect against pain. Longer procedures were significantly associated with unacceptable procedural pain.

The prevalence of unacceptable cramping at discharge was 28.6%. The risk of discomfort at discharge was significantly higher for women who reported dyspareunia or dysmenorrhea. Surgeon experience was significantly protective against unacceptable pain at discharge, and longer procedures were significantly associated with increased discomfort at discharge.

Dysmenorrhea and dyspareunia were significant predictors of pain at discharge
In this study, dysmenorrhea was a significant predictor of unacceptable pain at discharge, increasing the risk of unacceptable cramps by approximately threefold. Women who reported dyspareunia were nearly twice as likely to report unacceptable cramping at ­discharge.

Although a high level of expertise is not a prerequisite for office hysteroscopy, the skill and experience of the hysteroscopist, as well as shorter procedures, proved to be protective against procedural pain and discomfort at discharge but did not eliminate them altogether. Therefore, De Freitas and colleagues recommend that patients who can be identified as high-risk for procedural or discharge pain, such as women with dysmenorrhea or dyspareunia, should be offered preprocedure analgesia and/or anesthesia to reduce overall discomfort.

What this EVIDENCE means for practice
If a patient reports dysmenorrhea or dyspareunia preoperatively, she may benefit from preprocedure anesthesia or analgesia, or both, in an office setting.

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

Office hysteroscopy offers many benefits and is becoming more acceptable among patients and gynecologists for both diagnostic and operative procedures (TABLE 1). Despite its clear advantages, however, many gynecologists remain hesitant to perform in-office procedures out of fear that the patient, who is generally awake, will experience significant discomfort.

Certainly, pain and low patient tolerance of discomfort have been the primary limitations to widespread use of office hysteroscopy without anesthesia.¹ Data on the use of anesthesia for office hysteroscopy—especially diagnostic procedures—historically have been inconsistent in regard to the reduction of patient discomfort.²

Bettocchi and Selvaggi first reported a vaginoscopic approach to diagnostic hysteroscopy to reduce the discomfort of the procedure, compared with the conventional approach. They did not place a vaginal speculum or tenaculum and, therefore, avoided placing local anesthetic into the cervix.³

A randomized controlled trial by Sagiv and colleagues found reduced pain during diagnostic hysteroscopy with vaginoscopy (VIDEO).⁴

Vidyard Video

In 2004, Bettocchi and colleagues reported nearly 5,000 operative hysteroscopic procedures performed with this technique (the “no-touch” technique) in an outpatient setting, demonstrating very high patient tolerance and a low degree of procedural pain. More than 90% of patients experienced little to no pain, except for those undergoing ­polypectomy when the polyps were larger than the diameter of the cervical os, as well as those who had anatomic abnormalities, with moderate discomfort reported by 33.2% and 12.7% of these women, respectively.⁵ These few patients may have benefited from anesthetic intervention for the procedure.

In a 2010 review of the literature on hysteroscopy without anesthesia, Cicinelli found that diagnostic hysteroscopy was more successful, with less patient discomfort, when smaller hysteroscopes were used (3.5 mm or smaller, including flexible lenses) and when the approach was vaginoscopic.¹ Reduced pain with operative procedures was associated with a number of variables, including:

Variables associated with increased pain during operative procedures included:

In the review, Cicinelli noted that not all patients are likely to have a successful hysteroscopic procedure without the use of anesthesia or analgesia, regardless of the approach used.¹

Only 1 randomized controlled trial explored the use of anesthesia (versus placebo) during operative hysteroscopy, and the authors found a benefit for preprocedural paracervical block using local anesthetic to reduce cervical pain.⁶

The success of diagnostic and operative hysteroscopic procedures with minimal and acceptable levels of patient discomfort in the office depends, therefore, on multiple factors. Procedural factors affecting the outcome of hysteroscopy include the size of the instrument used, the type and length of the procedure, the use of preprocedure anesthesia or analgesia, and a vaginoscopic approach. The skill of the surgeon also affects the hysteroscopic experience and outcome. In addition, patient variables such as menopausal status, anatomic distortion (eg, cervical stenosis), and anxiety may adversely affect the patient’s experience.

In summary, it is possible for the gynecologist to appropriately accommodate any given patient and clinical scenario, keeping in mind that many patients will require a customized approach for ultimate success. In this article, I review 3 recent studies on office hysteroscopy, focusing on the reduction of procedural pain and anxiety. Because of the protective effect of a high degree of surgeon experience, it is important that we offer adequate education in hysteroscopy during residency and postgraduate courses.

Placement of local anesthetic at multiple anatomic sites facilitates patient comfort during hysteroscopy

Keyhan S, Munro MG. Office diagnostic and operative hysteroscopy using local anesthesia only: an analysis of patient reported pain and other procedural outcomes. J Minim Invasive Gynecol. 2014;21(5):791–798.

In a 2010 review of randomized controlled trials of the use of local anesthesia versus placebo during hysteroscopy, data from several studies indicated a significant decrease in procedural pain when local anesthesia was given, while other studies found no difference.² Most of the studies in that review evaluated a single site of anesthesia placement and focused on diagnostic hysteroscopy. The findings of that review, as well as the differential innervation of the uterine cervix and fundus (FIGURE), prompted Keyhan and Munro to evaluate the efficacy of multimodal local anesthetic for office diagnostic and operative hysteroscopy without the use of any systemic agents except for preprocedural cyclooxygenase (COX) inhibitors (TABLE 2).  Accordingly, they placed local anesthetic at multiple anatomic sites to alleviate patient pain and improve procedural success in a spectrum of office-based hysteroscopic procedures.

Details of the trial
Procedures generally were performed using a continuous-flow sheath with an outside diameter of 5.5 mm and a 5 French operative channel for placement of operative instruments such as scissors, graspers, and sterilization microinserts. Normal saline or sterile water was used as the uterine distention medium, with gravity inflow assisted by pressure cuff, when necessary. Occasionally, a sheath system with an outside diameter of 6.5 mm was used, or an outside diameter of 9 mm for resectoscopic procedures using a bipolar radiofrequency resectoscope. When needed, cervical dilation was performed to accommodate the specific instrument used.

The impact of the multimodal, multisite anesthetic protocol was evaluated using contemporaneous patient reporting of numeric pain scores (worst pain experienced) that included anesthesia-related pain, procedure-related pain, and overall pain.

A total of 478 women underwent 535 procedures. A patient verbal response scale (range, 0–10) was used to assess the worst pain experienced. The overall mean (SD) procedure pain score was 3.7 (2.5). The mean score for patients undergoing diagnostic hysteroscopy was 3.2 (2.5), and it was 4.1 (2.5) for operative hysteroscopy (P<.001).

TABLE 3 shows the procedures performed under the anesthetic protocol. Pain associated with placement of anesthesia was similar for diagnostic and operative procedures (mean score, 2.7), but the mean overall pain scores for diagnostic procedures were about 1 unit less than for operative procedures, regardless of age or delivery history.

Complications were limited to 3 transient vasovagal episodes. Five procedures could not be completed because of intolerable pain or inability to access the uterine cavity. There was no difference in pain scores between menopausal and premeno-pausal women.

Malcolm G. Munro, MD, offers a protocol for pain relief during hysteroscopy

 

In this video, Malcolm G. Munro, MD, makes use of both topical and injectable lidocaine at 5 anatomic sites

Dr. Munro is Professor of Obstetrics and Gynecology at the David Geffen School of Medicine at UCLA and Director of Gynecologic Services at Kaiser Permanente, Los Angeles Medical Center, in Los Angeles, California.
 

When placing anesthesia at multiple sites, allow time for onset of action
Keyhan and Munro demonstrated that ­successful completion of hysteroscopic procedures in the office environment can be achieved with acceptable levels of patient discomfort using a multimodal, multisite approach for preemptive placement of local anesthetic in the vagina, cervix, and endometrial cavity. They emphasize that the waiting time allotted for the onset of anesthesia is critical to the success of this approach. They also stress that no preprocedure oral sedative or narcotic is used with their approach. In addition, they note that the minimal discomfort experienced during placement of local anesthetic was overshadowed by general comfort during the wide spectrum of procedures performed.

What this EVIDENCE means for practice
The placement of preemptive local anesthesia at multiple anatomic sites facilitates diagnostic and operative hysteroscopy with an acceptable degree of patient comfort and successful completion of office procedures.

Music may reduce patient anxiety during hysteroscopy

Angioli R, De Cicco Nardone C, Plotti F, et al. Use of music to reduce anxiety during office hysteroscopy: prospective randomized trial. J Minim Invasive Gynecol. 2014;21(3):454–459.

Angioli and colleagues set out to address another factor that can impede patient comfort during office hysteroscopy—anxiety. Their randomized prospective trial is the only such trial evaluating the use of music to establish a calm and relaxing environment prior to office hysteroscopy for patients who are awake. Music supports an environment that “stimulates and maintains relaxation, well-being, and comfort and can be used as a self-management technique to reduce or control distress,” Angioli and colleagues write. The theory is that music distracts the patient by drawing her attention away from negative stimuli, thereby reducing pain, anxiety, and stress.

Details of the trial
A standardized visual analog scale (range, 0–10) was used to assess patient discomfort, and a State-Trait Anxiety Inventory (STAI; range, 20–80) also was given. Both tools were administered at baseline. The visual analog scale was measured again during the procedure, and the STAI was administered again after the procedure.

A hysteroscopic sheath with an outside diameter of 5 mm was used with a 5 French operative channel, and a vaginoscopic approach was used for each hysteroscopic procedure. A total of 372 women were enrolled and randomly allocated to either:

The surgical procedure was not completed in 15 patients (9 in the music group and 6 in the no-music group) because of stenosis of the cervix and/or excessive pain.

Women in the music group were allowed to select a playlist of classical, pop, jazz, or rock music that was played through a speaker system in the room. Of these patients, 50% preferred classical, 45% preferred pop, 5% chose jazz, and none selected rock music.

There were no statistically significant differences between the 2 groups in terms of preprocedure wait time, preprocedure scores on the visual analog scale or STAI, preprocedure vital signs, patient characteristics, type of procedure, or duration of the procedure. However, the music group had a lower visual analog score during the procedure and a lower postoperative STAI for diagnostic hysteroscopy than the no-music group did. The music group also had a statistically significant lower visual analog score for operative hysteroscopy than the no-music group did. In addition, the music group had a lower postoperative STAI score than the no-music group, but this difference was not statistically significant (TABLE 4).

Interestingly, in the music group, the STAI scores were lower after both diagnostic and operative hysteroscopy when classical music was selected rather than pop music.

Anxiety and pain are highly correlated
Angioli and colleagues found that patients who listened to music intraoperatively had a lower perception of pain and less anxiety. In addition, systolic blood pressure and heart rate were significantly lower in the music group than the no-music group, implying that patients who listened to music experienced less physical stress during the procedure.

Angioli and colleagues also noted that the level of anxiety and perception of pain were highly correlated. Pain is not an emotionally neutral experience but is almost always accompanied by distress. Investigators concluded that “anxiety can enhance painful sensations at all levels of the nervous system, from the peripheral receptors to the cortical level.”

What this EVIDENCE means for practice
Music is a useful complementary method to control patient anxiety and reduce the perception of pain during office hysteroscopy by creating a more relaxed and comfortable environment.

What are the risk factors for pain and discomfort during office hysteroscopy?

De Freitas FM, Sessa FV, Resende AD Jr, et al. Identifying predictors of unacceptable pain at office hysteroscopy. J Minim Invasive Gynecol. 2014;21(4):586–591.

De Freitas and colleagues conducted their prospective observational study to identify predictors of unacceptable pain during diagnostic office hysteroscopy (with or without directed or curette endometrial biopsy) and at the time of discharge. They hoped that any identifiable causes of unacceptable pain could be addressed individually in future patients undergoing office hysteroscopy to reduce their level of discomfort.

Details of the trial
A total of 558 procedures were evaluated. Hysteroscopists had varying levels of experience, with some having performed fewer than 50 procedures and others having performed more than 500.

A verbal response scale (range, 0–10) was used to assess pain at the end of each procedure and at the time of discharge. Investigators considered a score of 7 or more at the time of the procedure and a score of 4 or more at the time of discharge to be unacceptable.

A diagnostic, single-channel hysteroscope with an outside diameter of 3.5 mm was used with normal saline (at room temperature), along with a gravity system with pressure established to maintain intrauterine pressure at approximately 110 mm Hg. All hysteroscopic procedures were performed using a vaginoscopic approach, and biopsies were obtained as clinically indicated. Any patients who reported cramping at discharge (ie, a verbal response scale score of 4 or more) were offered an oral nonsteroidal anti-inflammatory drug.

Overall, the prevalence of unacceptable pain during office hysteroscopy was 32.3%. Experience of the hysteroscopist had a ­significant protective effect against pain. Longer procedures were significantly associated with unacceptable procedural pain.

The prevalence of unacceptable cramping at discharge was 28.6%. The risk of discomfort at discharge was significantly higher for women who reported dyspareunia or dysmenorrhea. Surgeon experience was significantly protective against unacceptable pain at discharge, and longer procedures were significantly associated with increased discomfort at discharge.

Dysmenorrhea and dyspareunia were significant predictors of pain at discharge
In this study, dysmenorrhea was a significant predictor of unacceptable pain at discharge, increasing the risk of unacceptable cramps by approximately threefold. Women who reported dyspareunia were nearly twice as likely to report unacceptable cramping at ­discharge.

Although a high level of expertise is not a prerequisite for office hysteroscopy, the skill and experience of the hysteroscopist, as well as shorter procedures, proved to be protective against procedural pain and discomfort at discharge but did not eliminate them altogether. Therefore, De Freitas and colleagues recommend that patients who can be identified as high-risk for procedural or discharge pain, such as women with dysmenorrhea or dyspareunia, should be offered preprocedure analgesia and/or anesthesia to reduce overall discomfort.

What this EVIDENCE means for practice
If a patient reports dysmenorrhea or dyspareunia preoperatively, she may benefit from preprocedure anesthesia or analgesia, or both, in an office setting.

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

It can be expensive, but multidisciplinary rehabilitation may be more cost-effective for treating chronic low back pain in the long-term, according to researchers from the University of Sydney in Australia; VU University Medical Centre in Amsterdam and Maastricht University Medical Centre, both in the Netherlands; and University of British Columbia in Vancouver, Canada. After analyzing 41 trials comparing a variety of biopsychosocial interventions with usual care and physical treatment, researchers found benefits in reduced pain and disability and a greater likelihood of returning to work (odds ratio 1.04, .73-1.47) that lasted beyond 1 year.

Related: Establishing and Evaluating an Acupuncture Clinic in a VA Medical Center

The multidisciplinary approach involved a physical component and a psychological component and/or a social/work-targeted component. The interventions were of any intensity and rehabilitation approach and could be provided in inpatient or outpatient settings. The control interventions were classified as usual care, physical treatment, surgery, and waiting list.

The researchers found moderate-quality evidence that multidisciplinary rehabilitation programs are more effective than is usual care (95% confidence interval, .04-.37) for reducing pain and disability from chronic low back pain. They also found no difference between the effects of surgery compared with multidisciplinary treatment on pain (standardized mean difference [SMD] .72, 0.24-1.22); disability (SMD .49, 0.22-0.76); and work (SMD .67, 0.31-1.45). The researchers also noted that surgery comes with a greater risk of adverse events.

Related: Development of a Multidisciplinary Stroke Program

The modest results should be weighed against the monetary costs and time commitments associated with multidisciplinary rehabilitation, the researchers caution. They suggest referring only those patients for whom low back pain has major physical and psychological effects.

Source
Kamper SJ, Apeldoorn AT, Chiarotto A, et al. BMJ. 2015;350:h444.
doi: 10.1136/bmj.h444.

It can be expensive, but multidisciplinary rehabilitation may be more cost-effective for treating chronic low back pain in the long-term, according to researchers from the University of Sydney in Australia; VU University Medical Centre in Amsterdam and Maastricht University Medical Centre, both in the Netherlands; and University of British Columbia in Vancouver, Canada. After analyzing 41 trials comparing a variety of biopsychosocial interventions with usual care and physical treatment, researchers found benefits in reduced pain and disability and a greater likelihood of returning to work (odds ratio 1.04, .73-1.47) that lasted beyond 1 year.

Related: Establishing and Evaluating an Acupuncture Clinic in a VA Medical Center

The multidisciplinary approach involved a physical component and a psychological component and/or a social/work-targeted component. The interventions were of any intensity and rehabilitation approach and could be provided in inpatient or outpatient settings. The control interventions were classified as usual care, physical treatment, surgery, and waiting list.

The researchers found moderate-quality evidence that multidisciplinary rehabilitation programs are more effective than is usual care (95% confidence interval, .04-.37) for reducing pain and disability from chronic low back pain. They also found no difference between the effects of surgery compared with multidisciplinary treatment on pain (standardized mean difference [SMD] .72, 0.24-1.22); disability (SMD .49, 0.22-0.76); and work (SMD .67, 0.31-1.45). The researchers also noted that surgery comes with a greater risk of adverse events.

Related: Development of a Multidisciplinary Stroke Program

The modest results should be weighed against the monetary costs and time commitments associated with multidisciplinary rehabilitation, the researchers caution. They suggest referring only those patients for whom low back pain has major physical and psychological effects.

Source
Kamper SJ, Apeldoorn AT, Chiarotto A, et al. BMJ. 2015;350:h444.
doi: 10.1136/bmj.h444.

It can be expensive, but multidisciplinary rehabilitation may be more cost-effective for treating chronic low back pain in the long-term, according to researchers from the University of Sydney in Australia; VU University Medical Centre in Amsterdam and Maastricht University Medical Centre, both in the Netherlands; and University of British Columbia in Vancouver, Canada. After analyzing 41 trials comparing a variety of biopsychosocial interventions with usual care and physical treatment, researchers found benefits in reduced pain and disability and a greater likelihood of returning to work (odds ratio 1.04, .73-1.47) that lasted beyond 1 year.

Related: Establishing and Evaluating an Acupuncture Clinic in a VA Medical Center

The multidisciplinary approach involved a physical component and a psychological component and/or a social/work-targeted component. The interventions were of any intensity and rehabilitation approach and could be provided in inpatient or outpatient settings. The control interventions were classified as usual care, physical treatment, surgery, and waiting list.

The researchers found moderate-quality evidence that multidisciplinary rehabilitation programs are more effective than is usual care (95% confidence interval, .04-.37) for reducing pain and disability from chronic low back pain. They also found no difference between the effects of surgery compared with multidisciplinary treatment on pain (standardized mean difference [SMD] .72, 0.24-1.22); disability (SMD .49, 0.22-0.76); and work (SMD .67, 0.31-1.45). The researchers also noted that surgery comes with a greater risk of adverse events.

Related: Development of a Multidisciplinary Stroke Program

The modest results should be weighed against the monetary costs and time commitments associated with multidisciplinary rehabilitation, the researchers caution. They suggest referring only those patients for whom low back pain has major physical and psychological effects.

Source
Kamper SJ, Apeldoorn AT, Chiarotto A, et al. BMJ. 2015;350:h444.
doi: 10.1136/bmj.h444.

Alzheimer disease (AD), the most common form of dementia, affects more than 5 million Americans.¹ Estimates suggest that by 2050, the prevalence could triple, reaching 13 to 16 million.¹ To effectively care for patients with AD and their families, primary care providers need to be familiar with the latest evidence on all facets of care, from initial detection to patient management and end-of-life care.

This evidence-based review will help you toward that end by answering common questions regarding Alzheimer care, including whether routine screening is advisable, what tests should be ordered, which interventions (including nonpharmacologic options) are worth considering, and how best to counsel patients and families about end-of-life care.

ROUTINE SCREENING? STILL SUBJECT TO DEBATE
The key question regarding routine dementia screening in primary care is whether it improves outcomes. Advocates note that individuals with dementia may appear unimpaired during office visits and may not report symptoms due to lack of insight; they point out, too, that waiting for an event that makes cognitive impairment obvious (eg, driving mishap) is risky.² Those who advocate routine screening also note that only about half of those who have dementia are ever diagnosed.³

Others, including the US Preventive Services Task Force (USPSTF), disagree. In its 2014 evidence review, the USPSTF indicated that there is “insufficient evidence to assess the balance of benefits and harms of screening for cognitive impairment in older adults.”⁴

Mixed messages
The dearth of evidence is also reflected in the conflicting recommendations of the Affordable Care Act (ACA) and the Centers for Medicare and Medicaid Services (CMS). The ACA requires clinicians to assess cognitive function during Medicare patients’ annual wellness visits. CMS, however, instructs providers to screen for dementia only if observation or concerns raised by the patient or family suggest the possibility of impairment and does not recommend any particular test.⁵

Cost-effectiveness analyses also raise questions about the value of routine screening. Evidence suggests that screening 300 older patients will yield 39 positive results. But only about half of those will agree to a diagnostic evaluation, and no more than nine will ultimately be diagnosed with dementia. The estimated cost of identifying nine cases is nearly $40,000—all in the absence of a treatment to cure or stop the progression of the disorder.⁶

The bottom line: Evidence does not support routine dementia screening of older adults. When cognitive impairment is suspected, however, clinicians should conduct a diagnostic evaluation—and consider educating patients and families about the Alzheimer’s Association (AA)’s 10 Warning Signs of AD (see box, above).⁷ A longer version (www.alz.org/national/documents/checklist_10signs.pdf) outlines the cognitive changes that are characteristic of healthy aging and compares them to changes suggestive of early dementia.⁷

Next: How to proceed when you suspect AD >>

Continue for mild cognitive impairment >>

Progression: Less likely than you might think
Patients with MCI are at risk for progression to overt dementia, with an overall annual conversion rate from MCI to dementia estimated at 10% to 15%.^15,16 This estimate must be interpreted with caution, however, because most studies were conducted prior to the 2011 guidelines, when different diagnostic criteria were used. Observers have noted, too, that the numbers largely reflect data collected in specialty clinics and that community-based studies reveal substantially lower conversion rates (3% to 6% per year).¹⁶ In addition, evidence suggests that many patients with MCI demonstrate long-term stability or even reversal of deficits.¹⁷

While there is some consideration of the use of biomarkers and amyloid imaging tests to help determine which patients with MCI will progress to AD, practice guidelines do not currently recommend such testing and it is not covered by Medicare.

WHEN EVIDENCE INDICATES AN AD DIAGNOSIS
When faced with the need to communicate an AD diagnosis, follow the general recommendations for delivering any bad news or discouraging prognosis.

Prioritize and limit the information you provide, determining not only what the patient and family want to hear but also how much they are able to comprehend.

Confirm that the patient and family understand the information you’ve provided.

Offer emotional support and recommend additional resources (see Table 2).¹⁸

Given the progressive cognitive decline that characterizes AD, it is important to address the primary caregiver’s understanding of, and ability to cope with, the disease. It is also important to explore beliefs and attitudes regarding AD. Keep in mind that cultural groups tend to differ in their beliefs about the nature, cause, and appropriate management of AD, as well as the role of spirituality, help-seeking, and stigma.^19,20

The progressive and ultimately fatal nature of AD also makes planning for the future a priority. Ideally, patients should be engaged in discussions regarding end-of-life care as early as possible, while they are still able to make informed decisions and express their preferences. Discussing end-of-life care can be overwhelming for newly diagnosed patients and their families, however, so it is important that you address issues—medical, financial, and legal planning, for example—that families should be considering.

Next: Medication for cognitive and behaviorial function >>

Drugs address cognitive and behavioral function
No currently available treatments can cure or significantly alter the progression of AD, but two classes of medications are used in an attempt to improve cognitive function. One is cholinesterase inhibitors (ChEIs), which potentiate acetylcholine synaptic transmission. The other is N-methyl-D-aspartate (NMDA) glutamate receptor blockers. Other classes of drugs are sometimes used to treat behavioral symptoms, such as agitation, aggression, mood disorders, and psychosis (eg, delusions, hallucinations).

Cognitive function. Results from studies of pharmacologic management of MCI vary widely, but recent reviews have found no convincing evidence that either ChEIs or NMDA receptor blockers have an effect on progression from MCI to dementia.^21,22 Neither class is FDA-approved for treatment of MCI.

In patients with dementia, the effects of ChEIs and NMDA receptor blockers on cognition are statistically significant but modest and often of questionable clinical relevance.²³ Nonetheless, among ChEIs, donepezil is approved by the FDA for mild, moderate, and severe dementia, and galantamine and rivastigmine are approved for mild and moderate dementia. There is no evidence that one ChEI is more effective than another,²⁴ and the choice is often guided by cost, adverse effects, and health plan formularies. Memantine, the only FDA-approved NMDA receptor blocker, is approved for moderate to severe dementia and can be used alone or in combination with a ChEI.

If these drugs are used in an attempt to improve cognition in AD, guidelines recommend the following approach for initial therapy: Prescribe a ChEI for the mild stage, a ChEI plus memantine for the moderate stage, and memantine (with or without a ChEI) for the severe stage.²⁵ The recommendations also include monitoring every six months.

There is no consensus about when to discontinue medication. Various published recommendations call for continuing treatment until the patient has “lost all cognitive and functional abilities;”²² until the patient’s MMSE score falls below 10 and there is no indication that the drug is having a “worthwhile effect;”²¹ or until he or she has reached stage 7 on the Reisberg Functional Assessment Staging scale, indicating nonambulatory status with speech limited to one to five words a day.¹⁰

Behavioral function. A variety of drugs are used to treat behavioral symptoms in AD. While not FDA-­approved for this use, the most widely prescribed agents are second-generation antipsychotics (aripiprazole, olanzapine, quetiapine, and risperidone). The main effect of these drugs is often nothing more than sedation, and one large multi­site clinical trial concluded that the adverse effects offset the benefits for patients with AD.²⁶ Indeed, the FDA has issued an advisory on the use of second-generation antipsychotics in AD patients, stating that they are associated with increased mortality risk.²⁷ The recently updated Beers Criteria strongly recommend avoiding these drugs for treatment of behavioral disturbances in AD unless nonpharmacologic options have failed and the patient is a threat to self or others.²⁸

Because of the black-box warning that antipsychotics increase the risk for death, some clinicians have advocated obtaining informed consent prior to prescribing such medications.²⁹ At the very least, when family or guardians are involved, a conversation about risks versus benefits should take place and be documented in the medical record.

Other drug classes are also sometimes used in an attempt to improve behavioral function, including antiseizure medications (valproic acid, carbamazepine), antidepressants (trazodone and selective serotonin reuptake inhibitors), and anxiolytics (benzodiazepines and buspirone). Other than their sedating effects, there is no strong evidence that these drugs are effective for treating dementia-related behavioral disorders. If used, caution is required due to potential adverse effects.

NONPHARMACOLOGIC MANAGEMENT IS "PROMISING"
A recent systematic review of nonpharmacologic interventions for MCI evaluated exercise, training in compensatory strategies, and engagement in cognitively stimulating activities and found “promising but inconclusive” results. The researchers found that studies show mostly positive effects on cognition but have significant methodologic limitations.³⁰ Importantly, there is no evidence of delayed or reduced conversion to dementia.

For patients who already have mild-to-moderate dementia, cognitive stimulation seems to help in the short term.³¹ There is also some evidence that exercise and occupational therapy may slow functional decline,³² but the effects are small to modest and their actual clinical significance (eg, the ability to delay institutionalization) is unclear. There is promising but preliminary evidence that cognitive rehabilitation (helping patients devise strategies to complete daily activities) may improve functioning in everyday life.³³

While behavioral symptoms are often due to the dementia itself, it is important to identify and treat medical and environmental causes that may be ­contributing, such as infection, pain, and loud or unsafe environments. As noted before, nonpharmacologic treatments are generally preferred for behavioral problems and should be considered prior to drug therapy. Approaches that identify and modify both the antecedents and consequences of problem behaviors and increase pleasant events have empiric support for the management of behavioral symptoms.³⁴ Interventions including massage therapy, aromatherapy, exercise, and music therapy may also be effective in the short term for agitated behavior.³⁵

Caregivers should be encouraged to receive training in these strategies through organizations such as AA. Caregiver education and support can reduce caregivers’ distress and increase their self-efficacy and coping skills.³⁶

Continue: Is it time for hospice? >>

Next page: Prevention >>

FINALLY, A WORD ABOUT PREVENTION
Numerous risk factors have been associated with an increased risk for AD (see Table 4).^2,3 Some, like age and genetics, are nonmodifiable, while others—particularly cardiovascular risk factors—can be modified.¹ There are also factors associated with decreased risks—most notably, physical exercise and participation in cognitively stimulating activities.³ Identification of these factors has led to the hope that addressing them can prevent AD.

But association does not equal causation. In 2010, a report from the National Institutes of Health concluded that, although there are modifiable factors associated with AD, there is insufficient evidence that addressing any of them will actually prevent AD.⁴³ In fact, there is good evidence that some of these factors (eg, statin therapy) are not effective in reducing the incidence of dementia and that others (eg, vitamin E and estrogen therapy) are potentially harmful.⁴⁴

The absence of empirically supported preventive interventions does not mean, however, that we should disregard these risks and protective factors. Encouraging social engagement, for example, may improve both emotional health and quality of life. Addressing cardiovascular risk factors can reduce the rate of coronary and cerebrovascular disease, potentially including vascular dementia, even if it does not reduce the rate of AD.

Studies are evaluating the use of monoclonal antibodies with anti-amyloid properties for prevention of AD in individuals who have APOE ε⁴ genotypes or high amyloid loads on neuroimaging.⁴⁵ It will be several years before results are available, however, and the outcome of these studies is uncertain, as the use of anti-amyloid agents for treating established dementia has not been effective.^46,47   

REFERENCES
1. Alzheimer’s Association. 2013 Alzheimer’s disease facts and figures. www.alz.org/downloads/facts_figures_2013.pdf. Accessed March 21, 2015.
2. Román GC, Nash DT, Fillit H. Translating current knowledge into dementia prevention. Alzheimer Dis Assoc Disord. 2012;26:295-299.
3. Jak AJ. The impact of physical and mental activity on cognitive aging. Curr Top Behav Neurosci. 2012;10:273-291.
4. US Preventive Services Task Force. Cognitive impairment in older adults: screening. www.uspreventiveservicestaskforce.org/Page/Topic/recommendation-summary/cognitive-impairment-in-older-adults-screening. Accessed March 21, 2015.
5. Centers for Medicare & Medicaid Services. The Guide to Medicare Preventive Services. 4th ed. 2011. www.curemd.com/fqhc/The%20Guide%20to%20Medicare%20Preventative%20Services%20for%20Physicans,%20Providers%20and%20Suppliers.pdf. Accessed March 21, 2015.
6. Boustani M. Dementia screening in primary care: not too fast! J Amer Geriatr Soc. 2013;61:1205-1207.
7. Alzheimer’s Association. Know the 10 signs: early detection matters. www.alz.org/national/documents/checklist_10signs.pdf. Accessed March 21, 2015.
8. Cordell CB, Borson S, Boustani M, et al; Medicare Detection of Cognitive Impairment Workgroup. Alzheimer’s Association recommendations for operationalizing the detection of cognitive impairment during the Medicare Annual Wellness Visit in a primary care setting. Alzheimers Dement. 2013;9:141-150.
9. McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:263-269.
10. The American Geriatrics Society. A guide to dementia diagnosis and treatment. http://dementia.americangeriatrics.org/documents/AGS_PC_Dementia_Sheet_2010v2.pdf. Accessed March 21, 2015.
11. Jack CR, Knopman DS, Jagust WJ, et al. Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol. 2013;12:207-216.
12. Johnson KA, Minoshima S, Bohnen NI, et al; Alzheimer’s Association; Society of Nuclear Medicine and Molecular Imaging; Amyloid Imaging Taskforce. Appropriate use criteria for amyloid PET: a report of the Amyloid Imaging Task Force, the Society of Nuclear Medicine and Molecular Imaging, and the Alzheimer’s Association. Alzheimers Dement. 2013;9:e1-e16.
13. Centers for Medicare and Medicaid Services. National coverage determination (NCD) for FDG PET for dementia and neurodegenerative diseases (220.6.13). www.cms.gov/medicare-coverage-database/details/ncd-details.aspx?NCDId=288&ncdver=3&bc=BAABAAAAAAAA&. Accessed March 21, 2015.
14. Albert MS, DeKosky ST, Ruckson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:270-179.
15. Mitchell AJ, Shiri-Feshki M. Rate of progression of mild cognitive impairment to dementia—meta-analysis of 41 robust inception studies. Acta Psychiatr Scand. 2009;119:252-265.
16. Farias ST, Mungas D, Reed BR, et al. Progression of mild cognitive impairment to dementia in clinic- vs community-based cohorts. Arch Neurol. 2009;66:1151-1157.
17. Bensadon BA, Odenheimer GL. Current management decisions in mild cognitive impairment. Clin Geriatr Med. 2013;29:847-871.
18. Ngo-Metzger Q, August KJ, Srinivasan M, et al. End-of-life care: guidelines for patient-centered communication. Am Fam Physician. 2008;77: 167-174.
19. Sayegh P, Knight BG. Cross-cultural differences in dementia: the Sociocultural Health Belief Model. Int Psychogeriatr. 2013;25:517-530.
20. McDaniel SH, Campbell TL, Hepworth J, et al. Family-Oriented Primary Care. 2nd ed. New York, NY: Springer; 2005.
21. Bensadon BA, Odenheimer GL. Current management decisions in mild cognitive impairment. Clin Geriatr Med. 2013:29;847-871.
22. Russ TC, Morling JR. Cholinesterase inhibitors for mild cognitive impairment. Cochrane Database Syst Rev. 2012;9:CD009132.
23. Sadowsky CH, Galvin JE. Guidelines for the management of cognitive and behavioral problems in dementia. J Am Board Fam Med. 2012;25: 350-366.
24. Birks J. Cholinesterase inhibitors for Alzheimer’s disease. Cochrane Database Syst Rev. 2006;(1):CD005593.
25. Fillit HM, Doody RS, Binaso K, et al. Recommendations for best practices in the treatment of Alzheimer’s disease in managed care. Am J Geriatr Pharmacother. 2006;4(suppl A):S9-S24;quiz S25-S28.
26. Schneider LS, Tariot PN, Dagerman KS, et al; CATIE-AD Study Group. Effectiveness of atypical antipsychotic drugs in patients with Alzheimer’s disease. N Engl J Med. 2006;355:1525-1538.
27. FDA. Public health advisory: Deaths with antipsychotics in elderly patients with behavioral disturbances. www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm053171.htm. Updated August 16, 2013. Accessed March 21, 2015.
28. The American Geriatrics Society 2012 Beers Criteria Update Expert Panel. American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2012;60: 616-631.
29. Brummel-Smith K. It’s time to require written informed consent when using antipsychotics in dementia. Br J Med Pract. 2008;1:4-6.
30. Huckans M, Hutson L, Twamley E, et al. Efficacy of cognitive rehabilitation therapies for mild cognitive impairment (MCI) in older adults: working toward a theoretical model and evidence-based interventions. Neuropsychol Rev. 2013;23:63-80.
31. Woods B, Aguirre E, Spector AE, et al. Cognitive stimulation to improve cognitive functioning in people with dementia. Cochrane Database Syst Rev. 2012;2:CD005562.
32. McLaren AN, Lamantia MA, Callahan CM. Systematic review of non-pharmacologic interventions to delay functional decline in community-dwelling patients with dementia. Aging Ment Health. 2013;17:655-666.
33. Bahar-Fuchs A, Clare L, Woods B. Cognitive training and cognitive rehabilitation for mild to moderate Alzheimer’s disease and vascular dementia. Cochrane Database Syst Rev. 2013;6:CD003260.
34. Logsdon RG, McCurry SM, Teri L. Evidence-based psychological treatments for disruptive behaviors in individuals with dementia. Psychol Aging. 2007;22:28-36.
35. Raetz J. A nondrug approach to dementia. J Fam Pract. 2013;62:548-557.
36. Gallagher-Thompson D, Coon DW. Evidence-based psychological treatments for distress in family caregivers of older adults. Psychol Aging. 2007;22:37-51.
37. Mitchell SL, Teno JM, Kiely DK, et al. The clinical course of advanced dementia. N Engl J Med. 2009:361:1529-1538.
38. Parsons C, Hughes CM, Passmore AP, et al. Withholding, discontinuing and withdrawing medications in dementia patients at the end of life: a neglected problem in the disadvantaged dying? Drugs Aging. 2010; 27:435-449.
39. The American Geriatrics Society. Feeding tubes in advanced dementia position statement. www.americangeriatrics.org/files/documents/feeding.tubes.advanced.dementia.pdf. Accessed March 21, 2015.
40. Goodman C, Evans C, Wilcock J, et al. End of life care for community dwelling older people with dementia: an integrated review. Int J Geriatr Psychiatry. 2010;25:329-337.
41. Storey CP. A quick-reference guide to the hospice and palliative care training for physicians: UNIPAC self-study program. American Academy of Hospice and Palliative Medicine. Chicago; 2009.
42. Kaszniak AW, Kligman EW. Hospice care for patients with dementia. Elder Care. 2013. http://azalz.org/wp-content/uploads/2013/07/Hospice-Care-for-Pts-with-Dementia.pdf. Accessed March 21, 2015.
43. Daviglus ML, Bell CC, Berrettini W, et al. NIH state-of-the-science conference statement: Preventing Alzheimer’s disease and cognitive decline. NIH Consens State Sci Statements. 2010;27:1-30.
44. Patterson C, Feightner JW, Garcia A, et al. Diagnosis and treatment of dementia: 1. Risk assessment and primary prevention of Alzheimer disease. CMAJ. 2008;178:548-556.
45. Carrillo MC, Brashear HR, Logovinsky V, et al. Can we prevent Alzheimer’s disease? Secondary “prevention” trials in Alzheimer’s disease. Alzheimers Dement. 2013;9:123-131.e1.
46. Salloway S, Sperling R, Fox NC, et al; Bapineuzumab 301 and 302 Clinical Trial Investigators. Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer’s Disease. N Engl J Med. 2014;370:322-333.
47. Doody RS, Thomas RG, Farlow M, et al; Alheimer’s Disease Cooperative Study Steering Committee; Solanezumab Study Group. Phase 3 trials of solanezumab for mild-to-moderate Alzheimer’s Disease. N Engl J Med. 2014;370:311-321.

Alzheimer disease (AD), the most common form of dementia, affects more than 5 million Americans.¹ Estimates suggest that by 2050, the prevalence could triple, reaching 13 to 16 million.¹ To effectively care for patients with AD and their families, primary care providers need to be familiar with the latest evidence on all facets of care, from initial detection to patient management and end-of-life care.

This evidence-based review will help you toward that end by answering common questions regarding Alzheimer care, including whether routine screening is advisable, what tests should be ordered, which interventions (including nonpharmacologic options) are worth considering, and how best to counsel patients and families about end-of-life care.

ROUTINE SCREENING? STILL SUBJECT TO DEBATE
The key question regarding routine dementia screening in primary care is whether it improves outcomes. Advocates note that individuals with dementia may appear unimpaired during office visits and may not report symptoms due to lack of insight; they point out, too, that waiting for an event that makes cognitive impairment obvious (eg, driving mishap) is risky.² Those who advocate routine screening also note that only about half of those who have dementia are ever diagnosed.³

Others, including the US Preventive Services Task Force (USPSTF), disagree. In its 2014 evidence review, the USPSTF indicated that there is “insufficient evidence to assess the balance of benefits and harms of screening for cognitive impairment in older adults.”⁴

Mixed messages
The dearth of evidence is also reflected in the conflicting recommendations of the Affordable Care Act (ACA) and the Centers for Medicare and Medicaid Services (CMS). The ACA requires clinicians to assess cognitive function during Medicare patients’ annual wellness visits. CMS, however, instructs providers to screen for dementia only if observation or concerns raised by the patient or family suggest the possibility of impairment and does not recommend any particular test.⁵

Cost-effectiveness analyses also raise questions about the value of routine screening. Evidence suggests that screening 300 older patients will yield 39 positive results. But only about half of those will agree to a diagnostic evaluation, and no more than nine will ultimately be diagnosed with dementia. The estimated cost of identifying nine cases is nearly $40,000—all in the absence of a treatment to cure or stop the progression of the disorder.⁶

The bottom line: Evidence does not support routine dementia screening of older adults. When cognitive impairment is suspected, however, clinicians should conduct a diagnostic evaluation—and consider educating patients and families about the Alzheimer’s Association (AA)’s 10 Warning Signs of AD (see box, above).⁷ A longer version (www.alz.org/national/documents/checklist_10signs.pdf) outlines the cognitive changes that are characteristic of healthy aging and compares them to changes suggestive of early dementia.⁷

Next: How to proceed when you suspect AD >>

Continue for mild cognitive impairment >>

Progression: Less likely than you might think
Patients with MCI are at risk for progression to overt dementia, with an overall annual conversion rate from MCI to dementia estimated at 10% to 15%.^15,16 This estimate must be interpreted with caution, however, because most studies were conducted prior to the 2011 guidelines, when different diagnostic criteria were used. Observers have noted, too, that the numbers largely reflect data collected in specialty clinics and that community-based studies reveal substantially lower conversion rates (3% to 6% per year).¹⁶ In addition, evidence suggests that many patients with MCI demonstrate long-term stability or even reversal of deficits.¹⁷

While there is some consideration of the use of biomarkers and amyloid imaging tests to help determine which patients with MCI will progress to AD, practice guidelines do not currently recommend such testing and it is not covered by Medicare.

WHEN EVIDENCE INDICATES AN AD DIAGNOSIS
When faced with the need to communicate an AD diagnosis, follow the general recommendations for delivering any bad news or discouraging prognosis.

Prioritize and limit the information you provide, determining not only what the patient and family want to hear but also how much they are able to comprehend.

Confirm that the patient and family understand the information you’ve provided.

Offer emotional support and recommend additional resources (see Table 2).¹⁸

Given the progressive cognitive decline that characterizes AD, it is important to address the primary caregiver’s understanding of, and ability to cope with, the disease. It is also important to explore beliefs and attitudes regarding AD. Keep in mind that cultural groups tend to differ in their beliefs about the nature, cause, and appropriate management of AD, as well as the role of spirituality, help-seeking, and stigma.^19,20

The progressive and ultimately fatal nature of AD also makes planning for the future a priority. Ideally, patients should be engaged in discussions regarding end-of-life care as early as possible, while they are still able to make informed decisions and express their preferences. Discussing end-of-life care can be overwhelming for newly diagnosed patients and their families, however, so it is important that you address issues—medical, financial, and legal planning, for example—that families should be considering.

Next: Medication for cognitive and behaviorial function >>

Drugs address cognitive and behavioral function
No currently available treatments can cure or significantly alter the progression of AD, but two classes of medications are used in an attempt to improve cognitive function. One is cholinesterase inhibitors (ChEIs), which potentiate acetylcholine synaptic transmission. The other is N-methyl-D-aspartate (NMDA) glutamate receptor blockers. Other classes of drugs are sometimes used to treat behavioral symptoms, such as agitation, aggression, mood disorders, and psychosis (eg, delusions, hallucinations).

Cognitive function. Results from studies of pharmacologic management of MCI vary widely, but recent reviews have found no convincing evidence that either ChEIs or NMDA receptor blockers have an effect on progression from MCI to dementia.^21,22 Neither class is FDA-approved for treatment of MCI.

In patients with dementia, the effects of ChEIs and NMDA receptor blockers on cognition are statistically significant but modest and often of questionable clinical relevance.²³ Nonetheless, among ChEIs, donepezil is approved by the FDA for mild, moderate, and severe dementia, and galantamine and rivastigmine are approved for mild and moderate dementia. There is no evidence that one ChEI is more effective than another,²⁴ and the choice is often guided by cost, adverse effects, and health plan formularies. Memantine, the only FDA-approved NMDA receptor blocker, is approved for moderate to severe dementia and can be used alone or in combination with a ChEI.

If these drugs are used in an attempt to improve cognition in AD, guidelines recommend the following approach for initial therapy: Prescribe a ChEI for the mild stage, a ChEI plus memantine for the moderate stage, and memantine (with or without a ChEI) for the severe stage.²⁵ The recommendations also include monitoring every six months.

There is no consensus about when to discontinue medication. Various published recommendations call for continuing treatment until the patient has “lost all cognitive and functional abilities;”²² until the patient’s MMSE score falls below 10 and there is no indication that the drug is having a “worthwhile effect;”²¹ or until he or she has reached stage 7 on the Reisberg Functional Assessment Staging scale, indicating nonambulatory status with speech limited to one to five words a day.¹⁰

Behavioral function. A variety of drugs are used to treat behavioral symptoms in AD. While not FDA-­approved for this use, the most widely prescribed agents are second-generation antipsychotics (aripiprazole, olanzapine, quetiapine, and risperidone). The main effect of these drugs is often nothing more than sedation, and one large multi­site clinical trial concluded that the adverse effects offset the benefits for patients with AD.²⁶ Indeed, the FDA has issued an advisory on the use of second-generation antipsychotics in AD patients, stating that they are associated with increased mortality risk.²⁷ The recently updated Beers Criteria strongly recommend avoiding these drugs for treatment of behavioral disturbances in AD unless nonpharmacologic options have failed and the patient is a threat to self or others.²⁸

Because of the black-box warning that antipsychotics increase the risk for death, some clinicians have advocated obtaining informed consent prior to prescribing such medications.²⁹ At the very least, when family or guardians are involved, a conversation about risks versus benefits should take place and be documented in the medical record.

Other drug classes are also sometimes used in an attempt to improve behavioral function, including antiseizure medications (valproic acid, carbamazepine), antidepressants (trazodone and selective serotonin reuptake inhibitors), and anxiolytics (benzodiazepines and buspirone). Other than their sedating effects, there is no strong evidence that these drugs are effective for treating dementia-related behavioral disorders. If used, caution is required due to potential adverse effects.

NONPHARMACOLOGIC MANAGEMENT IS "PROMISING"
A recent systematic review of nonpharmacologic interventions for MCI evaluated exercise, training in compensatory strategies, and engagement in cognitively stimulating activities and found “promising but inconclusive” results. The researchers found that studies show mostly positive effects on cognition but have significant methodologic limitations.³⁰ Importantly, there is no evidence of delayed or reduced conversion to dementia.

For patients who already have mild-to-moderate dementia, cognitive stimulation seems to help in the short term.³¹ There is also some evidence that exercise and occupational therapy may slow functional decline,³² but the effects are small to modest and their actual clinical significance (eg, the ability to delay institutionalization) is unclear. There is promising but preliminary evidence that cognitive rehabilitation (helping patients devise strategies to complete daily activities) may improve functioning in everyday life.³³

While behavioral symptoms are often due to the dementia itself, it is important to identify and treat medical and environmental causes that may be ­contributing, such as infection, pain, and loud or unsafe environments. As noted before, nonpharmacologic treatments are generally preferred for behavioral problems and should be considered prior to drug therapy. Approaches that identify and modify both the antecedents and consequences of problem behaviors and increase pleasant events have empiric support for the management of behavioral symptoms.³⁴ Interventions including massage therapy, aromatherapy, exercise, and music therapy may also be effective in the short term for agitated behavior.³⁵

Caregivers should be encouraged to receive training in these strategies through organizations such as AA. Caregiver education and support can reduce caregivers’ distress and increase their self-efficacy and coping skills.³⁶

Continue: Is it time for hospice? >>

Next page: Prevention >>

FINALLY, A WORD ABOUT PREVENTION
Numerous risk factors have been associated with an increased risk for AD (see Table 4).^2,3 Some, like age and genetics, are nonmodifiable, while others—particularly cardiovascular risk factors—can be modified.¹ There are also factors associated with decreased risks—most notably, physical exercise and participation in cognitively stimulating activities.³ Identification of these factors has led to the hope that addressing them can prevent AD.

But association does not equal causation. In 2010, a report from the National Institutes of Health concluded that, although there are modifiable factors associated with AD, there is insufficient evidence that addressing any of them will actually prevent AD.⁴³ In fact, there is good evidence that some of these factors (eg, statin therapy) are not effective in reducing the incidence of dementia and that others (eg, vitamin E and estrogen therapy) are potentially harmful.⁴⁴

The absence of empirically supported preventive interventions does not mean, however, that we should disregard these risks and protective factors. Encouraging social engagement, for example, may improve both emotional health and quality of life. Addressing cardiovascular risk factors can reduce the rate of coronary and cerebrovascular disease, potentially including vascular dementia, even if it does not reduce the rate of AD.

Studies are evaluating the use of monoclonal antibodies with anti-amyloid properties for prevention of AD in individuals who have APOE ε⁴ genotypes or high amyloid loads on neuroimaging.⁴⁵ It will be several years before results are available, however, and the outcome of these studies is uncertain, as the use of anti-amyloid agents for treating established dementia has not been effective.^46,47   

REFERENCES
1. Alzheimer’s Association. 2013 Alzheimer’s disease facts and figures. www.alz.org/downloads/facts_figures_2013.pdf. Accessed March 21, 2015.
2. Román GC, Nash DT, Fillit H. Translating current knowledge into dementia prevention. Alzheimer Dis Assoc Disord. 2012;26:295-299.
3. Jak AJ. The impact of physical and mental activity on cognitive aging. Curr Top Behav Neurosci. 2012;10:273-291.
4. US Preventive Services Task Force. Cognitive impairment in older adults: screening. www.uspreventiveservicestaskforce.org/Page/Topic/recommendation-summary/cognitive-impairment-in-older-adults-screening. Accessed March 21, 2015.
5. Centers for Medicare & Medicaid Services. The Guide to Medicare Preventive Services. 4th ed. 2011. www.curemd.com/fqhc/The%20Guide%20to%20Medicare%20Preventative%20Services%20for%20Physicans,%20Providers%20and%20Suppliers.pdf. Accessed March 21, 2015.
6. Boustani M. Dementia screening in primary care: not too fast! J Amer Geriatr Soc. 2013;61:1205-1207.
7. Alzheimer’s Association. Know the 10 signs: early detection matters. www.alz.org/national/documents/checklist_10signs.pdf. Accessed March 21, 2015.
8. Cordell CB, Borson S, Boustani M, et al; Medicare Detection of Cognitive Impairment Workgroup. Alzheimer’s Association recommendations for operationalizing the detection of cognitive impairment during the Medicare Annual Wellness Visit in a primary care setting. Alzheimers Dement. 2013;9:141-150.
9. McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:263-269.
10. The American Geriatrics Society. A guide to dementia diagnosis and treatment. http://dementia.americangeriatrics.org/documents/AGS_PC_Dementia_Sheet_2010v2.pdf. Accessed March 21, 2015.
11. Jack CR, Knopman DS, Jagust WJ, et al. Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol. 2013;12:207-216.
12. Johnson KA, Minoshima S, Bohnen NI, et al; Alzheimer’s Association; Society of Nuclear Medicine and Molecular Imaging; Amyloid Imaging Taskforce. Appropriate use criteria for amyloid PET: a report of the Amyloid Imaging Task Force, the Society of Nuclear Medicine and Molecular Imaging, and the Alzheimer’s Association. Alzheimers Dement. 2013;9:e1-e16.
13. Centers for Medicare and Medicaid Services. National coverage determination (NCD) for FDG PET for dementia and neurodegenerative diseases (220.6.13). www.cms.gov/medicare-coverage-database/details/ncd-details.aspx?NCDId=288&ncdver=3&bc=BAABAAAAAAAA&. Accessed March 21, 2015.
14. Albert MS, DeKosky ST, Ruckson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:270-179.
15. Mitchell AJ, Shiri-Feshki M. Rate of progression of mild cognitive impairment to dementia—meta-analysis of 41 robust inception studies. Acta Psychiatr Scand. 2009;119:252-265.
16. Farias ST, Mungas D, Reed BR, et al. Progression of mild cognitive impairment to dementia in clinic- vs community-based cohorts. Arch Neurol. 2009;66:1151-1157.
17. Bensadon BA, Odenheimer GL. Current management decisions in mild cognitive impairment. Clin Geriatr Med. 2013;29:847-871.
18. Ngo-Metzger Q, August KJ, Srinivasan M, et al. End-of-life care: guidelines for patient-centered communication. Am Fam Physician. 2008;77: 167-174.
19. Sayegh P, Knight BG. Cross-cultural differences in dementia: the Sociocultural Health Belief Model. Int Psychogeriatr. 2013;25:517-530.
20. McDaniel SH, Campbell TL, Hepworth J, et al. Family-Oriented Primary Care. 2nd ed. New York, NY: Springer; 2005.
21. Bensadon BA, Odenheimer GL. Current management decisions in mild cognitive impairment. Clin Geriatr Med. 2013:29;847-871.
22. Russ TC, Morling JR. Cholinesterase inhibitors for mild cognitive impairment. Cochrane Database Syst Rev. 2012;9:CD009132.
23. Sadowsky CH, Galvin JE. Guidelines for the management of cognitive and behavioral problems in dementia. J Am Board Fam Med. 2012;25: 350-366.
24. Birks J. Cholinesterase inhibitors for Alzheimer’s disease. Cochrane Database Syst Rev. 2006;(1):CD005593.
25. Fillit HM, Doody RS, Binaso K, et al. Recommendations for best practices in the treatment of Alzheimer’s disease in managed care. Am J Geriatr Pharmacother. 2006;4(suppl A):S9-S24;quiz S25-S28.
26. Schneider LS, Tariot PN, Dagerman KS, et al; CATIE-AD Study Group. Effectiveness of atypical antipsychotic drugs in patients with Alzheimer’s disease. N Engl J Med. 2006;355:1525-1538.
27. FDA. Public health advisory: Deaths with antipsychotics in elderly patients with behavioral disturbances. www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm053171.htm. Updated August 16, 2013. Accessed March 21, 2015.
28. The American Geriatrics Society 2012 Beers Criteria Update Expert Panel. American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2012;60: 616-631.
29. Brummel-Smith K. It’s time to require written informed consent when using antipsychotics in dementia. Br J Med Pract. 2008;1:4-6.
30. Huckans M, Hutson L, Twamley E, et al. Efficacy of cognitive rehabilitation therapies for mild cognitive impairment (MCI) in older adults: working toward a theoretical model and evidence-based interventions. Neuropsychol Rev. 2013;23:63-80.
31. Woods B, Aguirre E, Spector AE, et al. Cognitive stimulation to improve cognitive functioning in people with dementia. Cochrane Database Syst Rev. 2012;2:CD005562.
32. McLaren AN, Lamantia MA, Callahan CM. Systematic review of non-pharmacologic interventions to delay functional decline in community-dwelling patients with dementia. Aging Ment Health. 2013;17:655-666.
33. Bahar-Fuchs A, Clare L, Woods B. Cognitive training and cognitive rehabilitation for mild to moderate Alzheimer’s disease and vascular dementia. Cochrane Database Syst Rev. 2013;6:CD003260.
34. Logsdon RG, McCurry SM, Teri L. Evidence-based psychological treatments for disruptive behaviors in individuals with dementia. Psychol Aging. 2007;22:28-36.
35. Raetz J. A nondrug approach to dementia. J Fam Pract. 2013;62:548-557.
36. Gallagher-Thompson D, Coon DW. Evidence-based psychological treatments for distress in family caregivers of older adults. Psychol Aging. 2007;22:37-51.
37. Mitchell SL, Teno JM, Kiely DK, et al. The clinical course of advanced dementia. N Engl J Med. 2009:361:1529-1538.
38. Parsons C, Hughes CM, Passmore AP, et al. Withholding, discontinuing and withdrawing medications in dementia patients at the end of life: a neglected problem in the disadvantaged dying? Drugs Aging. 2010; 27:435-449.
39. The American Geriatrics Society. Feeding tubes in advanced dementia position statement. www.americangeriatrics.org/files/documents/feeding.tubes.advanced.dementia.pdf. Accessed March 21, 2015.
40. Goodman C, Evans C, Wilcock J, et al. End of life care for community dwelling older people with dementia: an integrated review. Int J Geriatr Psychiatry. 2010;25:329-337.
41. Storey CP. A quick-reference guide to the hospice and palliative care training for physicians: UNIPAC self-study program. American Academy of Hospice and Palliative Medicine. Chicago; 2009.
42. Kaszniak AW, Kligman EW. Hospice care for patients with dementia. Elder Care. 2013. http://azalz.org/wp-content/uploads/2013/07/Hospice-Care-for-Pts-with-Dementia.pdf. Accessed March 21, 2015.
43. Daviglus ML, Bell CC, Berrettini W, et al. NIH state-of-the-science conference statement: Preventing Alzheimer’s disease and cognitive decline. NIH Consens State Sci Statements. 2010;27:1-30.
44. Patterson C, Feightner JW, Garcia A, et al. Diagnosis and treatment of dementia: 1. Risk assessment and primary prevention of Alzheimer disease. CMAJ. 2008;178:548-556.
45. Carrillo MC, Brashear HR, Logovinsky V, et al. Can we prevent Alzheimer’s disease? Secondary “prevention” trials in Alzheimer’s disease. Alzheimers Dement. 2013;9:123-131.e1.
46. Salloway S, Sperling R, Fox NC, et al; Bapineuzumab 301 and 302 Clinical Trial Investigators. Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer’s Disease. N Engl J Med. 2014;370:322-333.
47. Doody RS, Thomas RG, Farlow M, et al; Alheimer’s Disease Cooperative Study Steering Committee; Solanezumab Study Group. Phase 3 trials of solanezumab for mild-to-moderate Alzheimer’s Disease. N Engl J Med. 2014;370:311-321.

Alzheimer disease (AD), the most common form of dementia, affects more than 5 million Americans.¹ Estimates suggest that by 2050, the prevalence could triple, reaching 13 to 16 million.¹ To effectively care for patients with AD and their families, primary care providers need to be familiar with the latest evidence on all facets of care, from initial detection to patient management and end-of-life care.

This evidence-based review will help you toward that end by answering common questions regarding Alzheimer care, including whether routine screening is advisable, what tests should be ordered, which interventions (including nonpharmacologic options) are worth considering, and how best to counsel patients and families about end-of-life care.

ROUTINE SCREENING? STILL SUBJECT TO DEBATE
The key question regarding routine dementia screening in primary care is whether it improves outcomes. Advocates note that individuals with dementia may appear unimpaired during office visits and may not report symptoms due to lack of insight; they point out, too, that waiting for an event that makes cognitive impairment obvious (eg, driving mishap) is risky.² Those who advocate routine screening also note that only about half of those who have dementia are ever diagnosed.³

Others, including the US Preventive Services Task Force (USPSTF), disagree. In its 2014 evidence review, the USPSTF indicated that there is “insufficient evidence to assess the balance of benefits and harms of screening for cognitive impairment in older adults.”⁴

Mixed messages
The dearth of evidence is also reflected in the conflicting recommendations of the Affordable Care Act (ACA) and the Centers for Medicare and Medicaid Services (CMS). The ACA requires clinicians to assess cognitive function during Medicare patients’ annual wellness visits. CMS, however, instructs providers to screen for dementia only if observation or concerns raised by the patient or family suggest the possibility of impairment and does not recommend any particular test.⁵

Cost-effectiveness analyses also raise questions about the value of routine screening. Evidence suggests that screening 300 older patients will yield 39 positive results. But only about half of those will agree to a diagnostic evaluation, and no more than nine will ultimately be diagnosed with dementia. The estimated cost of identifying nine cases is nearly $40,000—all in the absence of a treatment to cure or stop the progression of the disorder.⁶

The bottom line: Evidence does not support routine dementia screening of older adults. When cognitive impairment is suspected, however, clinicians should conduct a diagnostic evaluation—and consider educating patients and families about the Alzheimer’s Association (AA)’s 10 Warning Signs of AD (see box, above).⁷ A longer version (www.alz.org/national/documents/checklist_10signs.pdf) outlines the cognitive changes that are characteristic of healthy aging and compares them to changes suggestive of early dementia.⁷

Next: How to proceed when you suspect AD >>

Continue for mild cognitive impairment >>

Progression: Less likely than you might think
Patients with MCI are at risk for progression to overt dementia, with an overall annual conversion rate from MCI to dementia estimated at 10% to 15%.^15,16 This estimate must be interpreted with caution, however, because most studies were conducted prior to the 2011 guidelines, when different diagnostic criteria were used. Observers have noted, too, that the numbers largely reflect data collected in specialty clinics and that community-based studies reveal substantially lower conversion rates (3% to 6% per year).¹⁶ In addition, evidence suggests that many patients with MCI demonstrate long-term stability or even reversal of deficits.¹⁷

While there is some consideration of the use of biomarkers and amyloid imaging tests to help determine which patients with MCI will progress to AD, practice guidelines do not currently recommend such testing and it is not covered by Medicare.

WHEN EVIDENCE INDICATES AN AD DIAGNOSIS
When faced with the need to communicate an AD diagnosis, follow the general recommendations for delivering any bad news or discouraging prognosis.

Prioritize and limit the information you provide, determining not only what the patient and family want to hear but also how much they are able to comprehend.

Confirm that the patient and family understand the information you’ve provided.

Offer emotional support and recommend additional resources (see Table 2).¹⁸

Given the progressive cognitive decline that characterizes AD, it is important to address the primary caregiver’s understanding of, and ability to cope with, the disease. It is also important to explore beliefs and attitudes regarding AD. Keep in mind that cultural groups tend to differ in their beliefs about the nature, cause, and appropriate management of AD, as well as the role of spirituality, help-seeking, and stigma.^19,20

The progressive and ultimately fatal nature of AD also makes planning for the future a priority. Ideally, patients should be engaged in discussions regarding end-of-life care as early as possible, while they are still able to make informed decisions and express their preferences. Discussing end-of-life care can be overwhelming for newly diagnosed patients and their families, however, so it is important that you address issues—medical, financial, and legal planning, for example—that families should be considering.

Next: Medication for cognitive and behaviorial function >>

Drugs address cognitive and behavioral function
No currently available treatments can cure or significantly alter the progression of AD, but two classes of medications are used in an attempt to improve cognitive function. One is cholinesterase inhibitors (ChEIs), which potentiate acetylcholine synaptic transmission. The other is N-methyl-D-aspartate (NMDA) glutamate receptor blockers. Other classes of drugs are sometimes used to treat behavioral symptoms, such as agitation, aggression, mood disorders, and psychosis (eg, delusions, hallucinations).

Cognitive function. Results from studies of pharmacologic management of MCI vary widely, but recent reviews have found no convincing evidence that either ChEIs or NMDA receptor blockers have an effect on progression from MCI to dementia.^21,22 Neither class is FDA-approved for treatment of MCI.

In patients with dementia, the effects of ChEIs and NMDA receptor blockers on cognition are statistically significant but modest and often of questionable clinical relevance.²³ Nonetheless, among ChEIs, donepezil is approved by the FDA for mild, moderate, and severe dementia, and galantamine and rivastigmine are approved for mild and moderate dementia. There is no evidence that one ChEI is more effective than another,²⁴ and the choice is often guided by cost, adverse effects, and health plan formularies. Memantine, the only FDA-approved NMDA receptor blocker, is approved for moderate to severe dementia and can be used alone or in combination with a ChEI.

If these drugs are used in an attempt to improve cognition in AD, guidelines recommend the following approach for initial therapy: Prescribe a ChEI for the mild stage, a ChEI plus memantine for the moderate stage, and memantine (with or without a ChEI) for the severe stage.²⁵ The recommendations also include monitoring every six months.

There is no consensus about when to discontinue medication. Various published recommendations call for continuing treatment until the patient has “lost all cognitive and functional abilities;”²² until the patient’s MMSE score falls below 10 and there is no indication that the drug is having a “worthwhile effect;”²¹ or until he or she has reached stage 7 on the Reisberg Functional Assessment Staging scale, indicating nonambulatory status with speech limited to one to five words a day.¹⁰

Behavioral function. A variety of drugs are used to treat behavioral symptoms in AD. While not FDA-­approved for this use, the most widely prescribed agents are second-generation antipsychotics (aripiprazole, olanzapine, quetiapine, and risperidone). The main effect of these drugs is often nothing more than sedation, and one large multi­site clinical trial concluded that the adverse effects offset the benefits for patients with AD.²⁶ Indeed, the FDA has issued an advisory on the use of second-generation antipsychotics in AD patients, stating that they are associated with increased mortality risk.²⁷ The recently updated Beers Criteria strongly recommend avoiding these drugs for treatment of behavioral disturbances in AD unless nonpharmacologic options have failed and the patient is a threat to self or others.²⁸

Because of the black-box warning that antipsychotics increase the risk for death, some clinicians have advocated obtaining informed consent prior to prescribing such medications.²⁹ At the very least, when family or guardians are involved, a conversation about risks versus benefits should take place and be documented in the medical record.

Other drug classes are also sometimes used in an attempt to improve behavioral function, including antiseizure medications (valproic acid, carbamazepine), antidepressants (trazodone and selective serotonin reuptake inhibitors), and anxiolytics (benzodiazepines and buspirone). Other than their sedating effects, there is no strong evidence that these drugs are effective for treating dementia-related behavioral disorders. If used, caution is required due to potential adverse effects.

NONPHARMACOLOGIC MANAGEMENT IS "PROMISING"
A recent systematic review of nonpharmacologic interventions for MCI evaluated exercise, training in compensatory strategies, and engagement in cognitively stimulating activities and found “promising but inconclusive” results. The researchers found that studies show mostly positive effects on cognition but have significant methodologic limitations.³⁰ Importantly, there is no evidence of delayed or reduced conversion to dementia.

For patients who already have mild-to-moderate dementia, cognitive stimulation seems to help in the short term.³¹ There is also some evidence that exercise and occupational therapy may slow functional decline,³² but the effects are small to modest and their actual clinical significance (eg, the ability to delay institutionalization) is unclear. There is promising but preliminary evidence that cognitive rehabilitation (helping patients devise strategies to complete daily activities) may improve functioning in everyday life.³³

While behavioral symptoms are often due to the dementia itself, it is important to identify and treat medical and environmental causes that may be ­contributing, such as infection, pain, and loud or unsafe environments. As noted before, nonpharmacologic treatments are generally preferred for behavioral problems and should be considered prior to drug therapy. Approaches that identify and modify both the antecedents and consequences of problem behaviors and increase pleasant events have empiric support for the management of behavioral symptoms.³⁴ Interventions including massage therapy, aromatherapy, exercise, and music therapy may also be effective in the short term for agitated behavior.³⁵

Caregivers should be encouraged to receive training in these strategies through organizations such as AA. Caregiver education and support can reduce caregivers’ distress and increase their self-efficacy and coping skills.³⁶

Continue: Is it time for hospice? >>

Next page: Prevention >>

FINALLY, A WORD ABOUT PREVENTION
Numerous risk factors have been associated with an increased risk for AD (see Table 4).^2,3 Some, like age and genetics, are nonmodifiable, while others—particularly cardiovascular risk factors—can be modified.¹ There are also factors associated with decreased risks—most notably, physical exercise and participation in cognitively stimulating activities.³ Identification of these factors has led to the hope that addressing them can prevent AD.

But association does not equal causation. In 2010, a report from the National Institutes of Health concluded that, although there are modifiable factors associated with AD, there is insufficient evidence that addressing any of them will actually prevent AD.⁴³ In fact, there is good evidence that some of these factors (eg, statin therapy) are not effective in reducing the incidence of dementia and that others (eg, vitamin E and estrogen therapy) are potentially harmful.⁴⁴

The absence of empirically supported preventive interventions does not mean, however, that we should disregard these risks and protective factors. Encouraging social engagement, for example, may improve both emotional health and quality of life. Addressing cardiovascular risk factors can reduce the rate of coronary and cerebrovascular disease, potentially including vascular dementia, even if it does not reduce the rate of AD.

Studies are evaluating the use of monoclonal antibodies with anti-amyloid properties for prevention of AD in individuals who have APOE ε⁴ genotypes or high amyloid loads on neuroimaging.⁴⁵ It will be several years before results are available, however, and the outcome of these studies is uncertain, as the use of anti-amyloid agents for treating established dementia has not been effective.^46,47   

REFERENCES
1. Alzheimer’s Association. 2013 Alzheimer’s disease facts and figures. www.alz.org/downloads/facts_figures_2013.pdf. Accessed March 21, 2015.
2. Román GC, Nash DT, Fillit H. Translating current knowledge into dementia prevention. Alzheimer Dis Assoc Disord. 2012;26:295-299.
3. Jak AJ. The impact of physical and mental activity on cognitive aging. Curr Top Behav Neurosci. 2012;10:273-291.
4. US Preventive Services Task Force. Cognitive impairment in older adults: screening. www.uspreventiveservicestaskforce.org/Page/Topic/recommendation-summary/cognitive-impairment-in-older-adults-screening. Accessed March 21, 2015.
5. Centers for Medicare & Medicaid Services. The Guide to Medicare Preventive Services. 4th ed. 2011. www.curemd.com/fqhc/The%20Guide%20to%20Medicare%20Preventative%20Services%20for%20Physicans,%20Providers%20and%20Suppliers.pdf. Accessed March 21, 2015.
6. Boustani M. Dementia screening in primary care: not too fast! J Amer Geriatr Soc. 2013;61:1205-1207.
7. Alzheimer’s Association. Know the 10 signs: early detection matters. www.alz.org/national/documents/checklist_10signs.pdf. Accessed March 21, 2015.
8. Cordell CB, Borson S, Boustani M, et al; Medicare Detection of Cognitive Impairment Workgroup. Alzheimer’s Association recommendations for operationalizing the detection of cognitive impairment during the Medicare Annual Wellness Visit in a primary care setting. Alzheimers Dement. 2013;9:141-150.
9. McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:263-269.
10. The American Geriatrics Society. A guide to dementia diagnosis and treatment. http://dementia.americangeriatrics.org/documents/AGS_PC_Dementia_Sheet_2010v2.pdf. Accessed March 21, 2015.
11. Jack CR, Knopman DS, Jagust WJ, et al. Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers. Lancet Neurol. 2013;12:207-216.
12. Johnson KA, Minoshima S, Bohnen NI, et al; Alzheimer’s Association; Society of Nuclear Medicine and Molecular Imaging; Amyloid Imaging Taskforce. Appropriate use criteria for amyloid PET: a report of the Amyloid Imaging Task Force, the Society of Nuclear Medicine and Molecular Imaging, and the Alzheimer’s Association. Alzheimers Dement. 2013;9:e1-e16.
13. Centers for Medicare and Medicaid Services. National coverage determination (NCD) for FDG PET for dementia and neurodegenerative diseases (220.6.13). www.cms.gov/medicare-coverage-database/details/ncd-details.aspx?NCDId=288&ncdver=3&bc=BAABAAAAAAAA&. Accessed March 21, 2015.
14. Albert MS, DeKosky ST, Ruckson D, et al. The diagnosis of mild cognitive impairment due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement. 2011;7:270-179.
15. Mitchell AJ, Shiri-Feshki M. Rate of progression of mild cognitive impairment to dementia—meta-analysis of 41 robust inception studies. Acta Psychiatr Scand. 2009;119:252-265.
16. Farias ST, Mungas D, Reed BR, et al. Progression of mild cognitive impairment to dementia in clinic- vs community-based cohorts. Arch Neurol. 2009;66:1151-1157.
17. Bensadon BA, Odenheimer GL. Current management decisions in mild cognitive impairment. Clin Geriatr Med. 2013;29:847-871.
18. Ngo-Metzger Q, August KJ, Srinivasan M, et al. End-of-life care: guidelines for patient-centered communication. Am Fam Physician. 2008;77: 167-174.
19. Sayegh P, Knight BG. Cross-cultural differences in dementia: the Sociocultural Health Belief Model. Int Psychogeriatr. 2013;25:517-530.
20. McDaniel SH, Campbell TL, Hepworth J, et al. Family-Oriented Primary Care. 2nd ed. New York, NY: Springer; 2005.
21. Bensadon BA, Odenheimer GL. Current management decisions in mild cognitive impairment. Clin Geriatr Med. 2013:29;847-871.
22. Russ TC, Morling JR. Cholinesterase inhibitors for mild cognitive impairment. Cochrane Database Syst Rev. 2012;9:CD009132.
23. Sadowsky CH, Galvin JE. Guidelines for the management of cognitive and behavioral problems in dementia. J Am Board Fam Med. 2012;25: 350-366.
24. Birks J. Cholinesterase inhibitors for Alzheimer’s disease. Cochrane Database Syst Rev. 2006;(1):CD005593.
25. Fillit HM, Doody RS, Binaso K, et al. Recommendations for best practices in the treatment of Alzheimer’s disease in managed care. Am J Geriatr Pharmacother. 2006;4(suppl A):S9-S24;quiz S25-S28.
26. Schneider LS, Tariot PN, Dagerman KS, et al; CATIE-AD Study Group. Effectiveness of atypical antipsychotic drugs in patients with Alzheimer’s disease. N Engl J Med. 2006;355:1525-1538.
27. FDA. Public health advisory: Deaths with antipsychotics in elderly patients with behavioral disturbances. www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm053171.htm. Updated August 16, 2013. Accessed March 21, 2015.
28. The American Geriatrics Society 2012 Beers Criteria Update Expert Panel. American Geriatrics Society updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2012;60: 616-631.
29. Brummel-Smith K. It’s time to require written informed consent when using antipsychotics in dementia. Br J Med Pract. 2008;1:4-6.
30. Huckans M, Hutson L, Twamley E, et al. Efficacy of cognitive rehabilitation therapies for mild cognitive impairment (MCI) in older adults: working toward a theoretical model and evidence-based interventions. Neuropsychol Rev. 2013;23:63-80.
31. Woods B, Aguirre E, Spector AE, et al. Cognitive stimulation to improve cognitive functioning in people with dementia. Cochrane Database Syst Rev. 2012;2:CD005562.
32. McLaren AN, Lamantia MA, Callahan CM. Systematic review of non-pharmacologic interventions to delay functional decline in community-dwelling patients with dementia. Aging Ment Health. 2013;17:655-666.
33. Bahar-Fuchs A, Clare L, Woods B. Cognitive training and cognitive rehabilitation for mild to moderate Alzheimer’s disease and vascular dementia. Cochrane Database Syst Rev. 2013;6:CD003260.
34. Logsdon RG, McCurry SM, Teri L. Evidence-based psychological treatments for disruptive behaviors in individuals with dementia. Psychol Aging. 2007;22:28-36.
35. Raetz J. A nondrug approach to dementia. J Fam Pract. 2013;62:548-557.
36. Gallagher-Thompson D, Coon DW. Evidence-based psychological treatments for distress in family caregivers of older adults. Psychol Aging. 2007;22:37-51.
37. Mitchell SL, Teno JM, Kiely DK, et al. The clinical course of advanced dementia. N Engl J Med. 2009:361:1529-1538.
38. Parsons C, Hughes CM, Passmore AP, et al. Withholding, discontinuing and withdrawing medications in dementia patients at the end of life: a neglected problem in the disadvantaged dying? Drugs Aging. 2010; 27:435-449.
39. The American Geriatrics Society. Feeding tubes in advanced dementia position statement. www.americangeriatrics.org/files/documents/feeding.tubes.advanced.dementia.pdf. Accessed March 21, 2015.
40. Goodman C, Evans C, Wilcock J, et al. End of life care for community dwelling older people with dementia: an integrated review. Int J Geriatr Psychiatry. 2010;25:329-337.
41. Storey CP. A quick-reference guide to the hospice and palliative care training for physicians: UNIPAC self-study program. American Academy of Hospice and Palliative Medicine. Chicago; 2009.
42. Kaszniak AW, Kligman EW. Hospice care for patients with dementia. Elder Care. 2013. http://azalz.org/wp-content/uploads/2013/07/Hospice-Care-for-Pts-with-Dementia.pdf. Accessed March 21, 2015.
43. Daviglus ML, Bell CC, Berrettini W, et al. NIH state-of-the-science conference statement: Preventing Alzheimer’s disease and cognitive decline. NIH Consens State Sci Statements. 2010;27:1-30.
44. Patterson C, Feightner JW, Garcia A, et al. Diagnosis and treatment of dementia: 1. Risk assessment and primary prevention of Alzheimer disease. CMAJ. 2008;178:548-556.
45. Carrillo MC, Brashear HR, Logovinsky V, et al. Can we prevent Alzheimer’s disease? Secondary “prevention” trials in Alzheimer’s disease. Alzheimers Dement. 2013;9:123-131.e1.
46. Salloway S, Sperling R, Fox NC, et al; Bapineuzumab 301 and 302 Clinical Trial Investigators. Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer’s Disease. N Engl J Med. 2014;370:322-333.
47. Doody RS, Thomas RG, Farlow M, et al; Alheimer’s Disease Cooperative Study Steering Committee; Solanezumab Study Group. Phase 3 trials of solanezumab for mild-to-moderate Alzheimer’s Disease. N Engl J Med. 2014;370:311-321.

Cirrhosis and its complications are among the top 10 causes of death in the United States.^1,2 One of the most common complications of cirrhosis is ascites, an abnormal accumulation of fluid in the peritoneal cavity.³ Although ascites can be of nonhepatic origin, in approximately 85% of cases, the cause is cirrhosis.^2,4

Developing in some 60% of cirrhosis patients within 10 years,³ ascites indicates disease progression from compensated to decompensated cirrhosis.⁵ Mortality from ascites is approximately 15% in the first year and 44% by the fifth year, so referral for liver transplant evaluation is often indicated.²

Frequently, however, patients do not meet the criteria for transplantation because of comorbidities such as morbid obesity, severe cardiac or pulmonary disease, severe malignancy, chemical dependency, or lack of caregiver support.⁶ Primary care clinicians need to know about the management of ascites in chronic liver disease in order to meet the significant ongoing health care needs of these patients.

This article reviews the diagnosis and treatment of cirrhosis-related ascites and discusses one particularly life-threatening infection—spontaneous bacterial peritonitis (SBP)—to which these patients are susceptible.

CASE A 52-year-old African-American man presented to the emergency department (ED) with complaints of severe diffuse abdominal pain, worsening over the past few days, as well as nausea and vomiting. History was significant for hepatitis C–related cirrhosis, unresponsive to antiviral treatment, and liver disease complications that included hepatic encephalopathy; portal hypertension; ascites requiring large-volume paracentesis every one to two weeks (most recently, six days earlier); esophageal varices (status postbanding by esophagogastroduodenoscopy); portal hypertensive gastropathy; and gastric varices.

Due to decompensated cirrhosis, the patient had previously undergone extensive screening, radiologic imaging, and laboratory testing, and was found by a multidisciplinary selection committee to be an acceptable liver transplant candidate. He was actively listed for transplantation.

Other significant history included hypertension; sleep apnea; gastroesophageal reflux; osteopenia; zinc, vitamin A, and vitamin D deficiencies; thrombocytopenia; and anemia of chronic disease (liver disease–related). Surgical history was negative. The patient reported no known drug allergies and was taking spironolactone (50 mg/d) and furosemide (20 mg/d).

Physical exam was notable for a low-grade fever of 99.1ºF; blood pressure, 132/81 mm Hg; heart rate, 84 beats/min; icteric sclerae; and moderate distress related to the patient’s abdominal pain, which worsened with deep palpation. The abdomen was distended, with ascites present as indicated by a positive fluid wave test. Bowel sounds were hypoactive. The patient was alert and oriented without asterixis; mental state was within normal limits.

Continue for pathophysiology of ascites >>

Continue for SBP >>

SBP
Approximately 87% of patients with SBP will have signs or symptoms of infection,³ but symptoms can be very vague, so careful attention to detail and thorough assessment are necessary (see Table 1).^2,4,7,12 An elevated absolute polymorphonuclear (PMN) leukocyte cell count of ≥ 250 cells/µL and a positive ascitic culture, with no other apparent source of intra-abdominal infection, are diagnostic for SBP.²

Any cirrhotic patient with ascites who presents with two or more of the following criteria for systemic inflammatory response syndrome should be evaluated for an infectious cause:¹³
• Temperature > 100.4°F or < 96.8°F
• Heart rate > 90 beats/min
• Tachypnea (respiratory rate > 20 breaths/min) or hyperventilation (arterial carbon dioxide tension [PaCO₂] < 32 mm Hg)
• Abnormal white blood cell count (> 12,000/µL or < 4,000/µL or > 10% immature neutrophils [band forms])

CASE Abdominal x-ray, CT, and laboratory testing were ordered in the ED (see Table 2 for laboratory test results). Imaging revealed multiple loops of small bowel in the midabdomen, with several air-fluid levels and a paucity of gas in the rectum. These findings were consistent with small bowel obstruction. In addition, laboratory data were significant for leukocytosis (higher than the patient’s usual level), worsening hyperbilirubinemia and hypoalbuminemia, elevated serum creatinine level indicating acute kidney injury (AKI), and lactic acidosis. The patient was admitted to the hospital for further management.

Because of his severe abdominal pain and leukocytosis, bedside paracentesis was performed. He was found to have an absolute PMN cell count of approximately 1,273 cells/µL, suggesting a diagnosis of SBP. The patient’s status on the transplant list was changed to inactive due to the infection.

Next page: Treatment >>

Refractory ascites
Approximately 10% of patients develop refractory ascites when the condition becomes unresponsive to diuretics or when adverse effects preclude the use of diuretics.⁵ In such cases, large-volume paracentesis (> 5 L removed) is the standard treatment. The patient should be monitored closely during the procedure; blood pressure can decrease drastically due to the large fluid loss. Vital signs should be checked every 15 min to 30 min for the first hour postprocedure, and then hourly if signs remain stable. Albumin should be administered (6-8 g/L of fluid removed) to increase circulating fluid volume.² The patient’s renal function (ie, serum creatinine level and urinary output) should also be monitored closely, as dehydration and/or AKI can occur.⁴ Complications of paracentesis are uncommon but may include bleeding, infection, and bowel perforation. No data support the routine administration of blood products before paracentesis.²

Treatment of SBP
Broad-spectrum antibiotics, particularly cefotaxime, are effective against approximately 94% of the bacterial flora associated with SBP. Initial treatment with cefotaxime (or ceftriaxone, if cefotaxime is unavailable) at a dose of 2 g IV q8h for seven days is recommended, unless or until culture results identify susceptibility to a specific narrow-spectrum antibiotic.^2,4,7,9 After completion of a total of seven days of IV antibiotics, it is cost effective and safe to transition clinically improved patients to an oral antibiotic for SBP prophylaxis (see discussion below).⁹

A repeat paracentesis performed 48 hours after treatment is initiated is useful in assessing response to treatment, defined as a ≥ 25% decrease in ascitic fluid PMN count.⁷

Even if the infection is successfully treated, one-third of patients who have an episode of SBP develop renal failure; those who experience a recurrence of SBP within one year have a 50% to 60% mortality rate.^4,7,9,14 This is because infection causes vasodilation, with a concomitant decrease in blood volume and compensatory activation of renal vasoconstrictors, so renal function worsens.

A randomized controlled trial found that patients treated with IV cefotaxime with albumin in doses of 1.5 g/kg on day 1 and 1 g/kg on day 3 had significantly lower rates of AKI and mortality than patients who received cefotaxime alone.¹⁵ An albumin infusion, given in conjunction with antibiotics, improves blood volume, enhances renal perfusion, and has been shown to decrease mortality from SBP from 29% to 10%.^2,12,16

CASE For small bowel obstruction, the patient was made NPO and a nasogastric tube was placed for 36 hours. During this time, he had a bowel movement, diet was advanced, and the obstruction resolved.

At the same time, the patient was started on IV cefotaxime 2 g q8h for treatment of SBP, along with IV albumin and fluids. Diuretics were withheld because of impaired kidney function.

Ascitic fluid was cultured, and Streptococcus viridans was identified. After consultation with the infectious disease service, broader-spectrum vancomycin was added to the patient’s IV antibiotic regimen 24 hours after admission while culture results finalized. Cultures were analyzed after three days and found to be susceptible to ceftriaxone, which was administered 2 g IV q24h for three days, for a total of seven days of IV antibiotics.

The patient’s AKI improved after treatment with IV antibiotics, fluids, and albumin. Seventy-two hours after admission, repeat paracentesis revealed a significant decrease in white blood cells; cultures were negative for infection.

Neutrocytic ascites
In some cases, the bacteria count in ascitic fluid is so low that cultures may be negative.⁴ This is termed neutrocytic ascites, characterized by an elevated PMN cell count with negative cultures. Patients with neutrocytic ascites should be treated as though they have SBP.^2,7

Prophylactic antibiotics
Of patients successfully treated for SBP, 69% will experience another episode within one year; many of these cases can be prevented with the use of prophylactic antibiotics. Historically, quinolones were used for SBP prophylaxis, and they are cost-effective. However, multiorganism drug resistance hasoccurred after quinolone prophylaxis, especially if given long-term.^2,4,7
 
Alternatives to quinolones include trimethoprim/sulfamethoxazole double strength or ciprofloxacin 500 mg/d.² Renal dose adjustment is necessary for patients with acute or chronic kidney disease and can usually be guided by a pharmacist. One study found norfloxacin and trimethoprim-sulfamethoxazole to be similarly effective for SBP prevention, but trimethoprim-sulfamethoxazole was noted to be more cost-effective.¹⁰

In patients with active gastrointestinal bleeding, IV ceftriaxone 1 g/d for seven days can be given for SBP prevention. In patients with low ascitic protein and/or history of prior SBP, norfloxacin 400 mg/d is an option.

Continue for conclusion >>

REFERENCES
1. Asrani SK, Larson JJ, Yawn B, Therneau TM, Kim WR. Underestimation of liver-related mortality in the United States. Gastroenterology. 2013;145(2):375-382.
2. Runyon BA. American Association for the Study of Liver Diseases practice guideline. Management of adult patients with ascites due to cirrhosis: update 2012. www.aasld.org/sites/default/files/guideline_documents/adultascitesenhanced.pdf. Accessed March 24, 2015.
3. European Association for the Study of the Liver (EASL). EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol. 2010;53(3):397-417.
4. Sargent S. The management and nursing care of cirrhotic ascites. Br J Nurs. 2006;15(4):212-219.
5. Sargent S. Management of patients with advanced liver cirrhosis. Nurs Stand. 2006;21(11):48-56.
6. Martin P, DiMartini A, Feng S, Brown R Jr, Fallon M. American Association for the Study of Liver Diseases and the American Society of Transplantation. Evaluation for liver transplantation in adults: 2013 practice guideline. Hepatology. 2014;59(3):1144-65.
7. Loo NM, Souza FF, Garcia-Tsao G. Non-hemorrhagic acute complications associated with cirrhosis and portal hypertension. Best Pract Res Clin Gastroenterol. 2013;27(5):665-678.
8. Orman ES, Hayashi PH, Bataller R, Barritt AS. Paracentesis is associated with reduced mortality in patients hospitalized with cirrhosis and ascites. Clin Gastroenterol Hepatol. 2014;12(3):496-503.
9. Ghassemi S, Garcia-Tsao G. Prevention and treatment of infections in patients with cirrhosis. Best Pract Res Clin Gastroenterol. 2007;21(1):
77-93.
10. Lontos S, Gow PJ, Vaughan RB, Angus PW. Norfloxacin and trimethoprim-sulfamethoxazole therapy have similar efficacy in prevention of spontaneous bacterial peritonitis. J Gastroenterol Hepatol. 2008;23(2): 252-255.
11. Desai AP, Satoskar R, Appannagari A, et al. Co-management between hospitalist and hepatologist improves the quality of care of inpatients with chronic liver disease. J Clin Gastroenterol. 2014;48(4):e30-e36.
12. Moore CM, Van Thiel DH. Cirrhotic ascites review: pathophysiology, diagnosis and management. World J Hepatol. 2013;5(5):251-263.
13. Bone RC, Balk RA, Cerra FB, et al; ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest. 1992;101(6):1644-1655.
14. Wong F, O’Leary JG, Reddy KR, et al; North American Consortium for Study of End-Stage Liver Disease. New consensus definition of acute kidney injury accurately predicts 30-day mortality in patients with cirrhosis and infection. Gastroenterology. 2013;145(6):1280-1288.
15. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999;341(6):403-409.
16. Rozga J, Piatek T, Malkowski P. Human albumin: old, new, and emerging applications. Ann Transplant. 2013;18:205-217.

Cirrhosis and its complications are among the top 10 causes of death in the United States.^1,2 One of the most common complications of cirrhosis is ascites, an abnormal accumulation of fluid in the peritoneal cavity.³ Although ascites can be of nonhepatic origin, in approximately 85% of cases, the cause is cirrhosis.^2,4

Developing in some 60% of cirrhosis patients within 10 years,³ ascites indicates disease progression from compensated to decompensated cirrhosis.⁵ Mortality from ascites is approximately 15% in the first year and 44% by the fifth year, so referral for liver transplant evaluation is often indicated.²

Frequently, however, patients do not meet the criteria for transplantation because of comorbidities such as morbid obesity, severe cardiac or pulmonary disease, severe malignancy, chemical dependency, or lack of caregiver support.⁶ Primary care clinicians need to know about the management of ascites in chronic liver disease in order to meet the significant ongoing health care needs of these patients.

This article reviews the diagnosis and treatment of cirrhosis-related ascites and discusses one particularly life-threatening infection—spontaneous bacterial peritonitis (SBP)—to which these patients are susceptible.

CASE A 52-year-old African-American man presented to the emergency department (ED) with complaints of severe diffuse abdominal pain, worsening over the past few days, as well as nausea and vomiting. History was significant for hepatitis C–related cirrhosis, unresponsive to antiviral treatment, and liver disease complications that included hepatic encephalopathy; portal hypertension; ascites requiring large-volume paracentesis every one to two weeks (most recently, six days earlier); esophageal varices (status postbanding by esophagogastroduodenoscopy); portal hypertensive gastropathy; and gastric varices.

Due to decompensated cirrhosis, the patient had previously undergone extensive screening, radiologic imaging, and laboratory testing, and was found by a multidisciplinary selection committee to be an acceptable liver transplant candidate. He was actively listed for transplantation.

Other significant history included hypertension; sleep apnea; gastroesophageal reflux; osteopenia; zinc, vitamin A, and vitamin D deficiencies; thrombocytopenia; and anemia of chronic disease (liver disease–related). Surgical history was negative. The patient reported no known drug allergies and was taking spironolactone (50 mg/d) and furosemide (20 mg/d).

Physical exam was notable for a low-grade fever of 99.1ºF; blood pressure, 132/81 mm Hg; heart rate, 84 beats/min; icteric sclerae; and moderate distress related to the patient’s abdominal pain, which worsened with deep palpation. The abdomen was distended, with ascites present as indicated by a positive fluid wave test. Bowel sounds were hypoactive. The patient was alert and oriented without asterixis; mental state was within normal limits.

Continue for pathophysiology of ascites >>

Continue for SBP >>

SBP
Approximately 87% of patients with SBP will have signs or symptoms of infection,³ but symptoms can be very vague, so careful attention to detail and thorough assessment are necessary (see Table 1).^2,4,7,12 An elevated absolute polymorphonuclear (PMN) leukocyte cell count of ≥ 250 cells/µL and a positive ascitic culture, with no other apparent source of intra-abdominal infection, are diagnostic for SBP.²

Any cirrhotic patient with ascites who presents with two or more of the following criteria for systemic inflammatory response syndrome should be evaluated for an infectious cause:¹³
• Temperature > 100.4°F or < 96.8°F
• Heart rate > 90 beats/min
• Tachypnea (respiratory rate > 20 breaths/min) or hyperventilation (arterial carbon dioxide tension [PaCO₂] < 32 mm Hg)
• Abnormal white blood cell count (> 12,000/µL or < 4,000/µL or > 10% immature neutrophils [band forms])

CASE Abdominal x-ray, CT, and laboratory testing were ordered in the ED (see Table 2 for laboratory test results). Imaging revealed multiple loops of small bowel in the midabdomen, with several air-fluid levels and a paucity of gas in the rectum. These findings were consistent with small bowel obstruction. In addition, laboratory data were significant for leukocytosis (higher than the patient’s usual level), worsening hyperbilirubinemia and hypoalbuminemia, elevated serum creatinine level indicating acute kidney injury (AKI), and lactic acidosis. The patient was admitted to the hospital for further management.

Because of his severe abdominal pain and leukocytosis, bedside paracentesis was performed. He was found to have an absolute PMN cell count of approximately 1,273 cells/µL, suggesting a diagnosis of SBP. The patient’s status on the transplant list was changed to inactive due to the infection.

Next page: Treatment >>

Refractory ascites
Approximately 10% of patients develop refractory ascites when the condition becomes unresponsive to diuretics or when adverse effects preclude the use of diuretics.⁵ In such cases, large-volume paracentesis (> 5 L removed) is the standard treatment. The patient should be monitored closely during the procedure; blood pressure can decrease drastically due to the large fluid loss. Vital signs should be checked every 15 min to 30 min for the first hour postprocedure, and then hourly if signs remain stable. Albumin should be administered (6-8 g/L of fluid removed) to increase circulating fluid volume.² The patient’s renal function (ie, serum creatinine level and urinary output) should also be monitored closely, as dehydration and/or AKI can occur.⁴ Complications of paracentesis are uncommon but may include bleeding, infection, and bowel perforation. No data support the routine administration of blood products before paracentesis.²

Treatment of SBP
Broad-spectrum antibiotics, particularly cefotaxime, are effective against approximately 94% of the bacterial flora associated with SBP. Initial treatment with cefotaxime (or ceftriaxone, if cefotaxime is unavailable) at a dose of 2 g IV q8h for seven days is recommended, unless or until culture results identify susceptibility to a specific narrow-spectrum antibiotic.^2,4,7,9 After completion of a total of seven days of IV antibiotics, it is cost effective and safe to transition clinically improved patients to an oral antibiotic for SBP prophylaxis (see discussion below).⁹

A repeat paracentesis performed 48 hours after treatment is initiated is useful in assessing response to treatment, defined as a ≥ 25% decrease in ascitic fluid PMN count.⁷

Even if the infection is successfully treated, one-third of patients who have an episode of SBP develop renal failure; those who experience a recurrence of SBP within one year have a 50% to 60% mortality rate.^4,7,9,14 This is because infection causes vasodilation, with a concomitant decrease in blood volume and compensatory activation of renal vasoconstrictors, so renal function worsens.

A randomized controlled trial found that patients treated with IV cefotaxime with albumin in doses of 1.5 g/kg on day 1 and 1 g/kg on day 3 had significantly lower rates of AKI and mortality than patients who received cefotaxime alone.¹⁵ An albumin infusion, given in conjunction with antibiotics, improves blood volume, enhances renal perfusion, and has been shown to decrease mortality from SBP from 29% to 10%.^2,12,16

CASE For small bowel obstruction, the patient was made NPO and a nasogastric tube was placed for 36 hours. During this time, he had a bowel movement, diet was advanced, and the obstruction resolved.

At the same time, the patient was started on IV cefotaxime 2 g q8h for treatment of SBP, along with IV albumin and fluids. Diuretics were withheld because of impaired kidney function.

Ascitic fluid was cultured, and Streptococcus viridans was identified. After consultation with the infectious disease service, broader-spectrum vancomycin was added to the patient’s IV antibiotic regimen 24 hours after admission while culture results finalized. Cultures were analyzed after three days and found to be susceptible to ceftriaxone, which was administered 2 g IV q24h for three days, for a total of seven days of IV antibiotics.

The patient’s AKI improved after treatment with IV antibiotics, fluids, and albumin. Seventy-two hours after admission, repeat paracentesis revealed a significant decrease in white blood cells; cultures were negative for infection.

Neutrocytic ascites
In some cases, the bacteria count in ascitic fluid is so low that cultures may be negative.⁴ This is termed neutrocytic ascites, characterized by an elevated PMN cell count with negative cultures. Patients with neutrocytic ascites should be treated as though they have SBP.^2,7

Prophylactic antibiotics
Of patients successfully treated for SBP, 69% will experience another episode within one year; many of these cases can be prevented with the use of prophylactic antibiotics. Historically, quinolones were used for SBP prophylaxis, and they are cost-effective. However, multiorganism drug resistance hasoccurred after quinolone prophylaxis, especially if given long-term.^2,4,7
 
Alternatives to quinolones include trimethoprim/sulfamethoxazole double strength or ciprofloxacin 500 mg/d.² Renal dose adjustment is necessary for patients with acute or chronic kidney disease and can usually be guided by a pharmacist. One study found norfloxacin and trimethoprim-sulfamethoxazole to be similarly effective for SBP prevention, but trimethoprim-sulfamethoxazole was noted to be more cost-effective.¹⁰

In patients with active gastrointestinal bleeding, IV ceftriaxone 1 g/d for seven days can be given for SBP prevention. In patients with low ascitic protein and/or history of prior SBP, norfloxacin 400 mg/d is an option.

Continue for conclusion >>

REFERENCES
1. Asrani SK, Larson JJ, Yawn B, Therneau TM, Kim WR. Underestimation of liver-related mortality in the United States. Gastroenterology. 2013;145(2):375-382.
2. Runyon BA. American Association for the Study of Liver Diseases practice guideline. Management of adult patients with ascites due to cirrhosis: update 2012. www.aasld.org/sites/default/files/guideline_documents/adultascitesenhanced.pdf. Accessed March 24, 2015.
3. European Association for the Study of the Liver (EASL). EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol. 2010;53(3):397-417.
4. Sargent S. The management and nursing care of cirrhotic ascites. Br J Nurs. 2006;15(4):212-219.
5. Sargent S. Management of patients with advanced liver cirrhosis. Nurs Stand. 2006;21(11):48-56.
6. Martin P, DiMartini A, Feng S, Brown R Jr, Fallon M. American Association for the Study of Liver Diseases and the American Society of Transplantation. Evaluation for liver transplantation in adults: 2013 practice guideline. Hepatology. 2014;59(3):1144-65.
7. Loo NM, Souza FF, Garcia-Tsao G. Non-hemorrhagic acute complications associated with cirrhosis and portal hypertension. Best Pract Res Clin Gastroenterol. 2013;27(5):665-678.
8. Orman ES, Hayashi PH, Bataller R, Barritt AS. Paracentesis is associated with reduced mortality in patients hospitalized with cirrhosis and ascites. Clin Gastroenterol Hepatol. 2014;12(3):496-503.
9. Ghassemi S, Garcia-Tsao G. Prevention and treatment of infections in patients with cirrhosis. Best Pract Res Clin Gastroenterol. 2007;21(1):
77-93.
10. Lontos S, Gow PJ, Vaughan RB, Angus PW. Norfloxacin and trimethoprim-sulfamethoxazole therapy have similar efficacy in prevention of spontaneous bacterial peritonitis. J Gastroenterol Hepatol. 2008;23(2): 252-255.
11. Desai AP, Satoskar R, Appannagari A, et al. Co-management between hospitalist and hepatologist improves the quality of care of inpatients with chronic liver disease. J Clin Gastroenterol. 2014;48(4):e30-e36.
12. Moore CM, Van Thiel DH. Cirrhotic ascites review: pathophysiology, diagnosis and management. World J Hepatol. 2013;5(5):251-263.
13. Bone RC, Balk RA, Cerra FB, et al; ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest. 1992;101(6):1644-1655.
14. Wong F, O’Leary JG, Reddy KR, et al; North American Consortium for Study of End-Stage Liver Disease. New consensus definition of acute kidney injury accurately predicts 30-day mortality in patients with cirrhosis and infection. Gastroenterology. 2013;145(6):1280-1288.
15. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999;341(6):403-409.
16. Rozga J, Piatek T, Malkowski P. Human albumin: old, new, and emerging applications. Ann Transplant. 2013;18:205-217.

Cirrhosis and its complications are among the top 10 causes of death in the United States.^1,2 One of the most common complications of cirrhosis is ascites, an abnormal accumulation of fluid in the peritoneal cavity.³ Although ascites can be of nonhepatic origin, in approximately 85% of cases, the cause is cirrhosis.^2,4

Developing in some 60% of cirrhosis patients within 10 years,³ ascites indicates disease progression from compensated to decompensated cirrhosis.⁵ Mortality from ascites is approximately 15% in the first year and 44% by the fifth year, so referral for liver transplant evaluation is often indicated.²

Frequently, however, patients do not meet the criteria for transplantation because of comorbidities such as morbid obesity, severe cardiac or pulmonary disease, severe malignancy, chemical dependency, or lack of caregiver support.⁶ Primary care clinicians need to know about the management of ascites in chronic liver disease in order to meet the significant ongoing health care needs of these patients.

This article reviews the diagnosis and treatment of cirrhosis-related ascites and discusses one particularly life-threatening infection—spontaneous bacterial peritonitis (SBP)—to which these patients are susceptible.

CASE A 52-year-old African-American man presented to the emergency department (ED) with complaints of severe diffuse abdominal pain, worsening over the past few days, as well as nausea and vomiting. History was significant for hepatitis C–related cirrhosis, unresponsive to antiviral treatment, and liver disease complications that included hepatic encephalopathy; portal hypertension; ascites requiring large-volume paracentesis every one to two weeks (most recently, six days earlier); esophageal varices (status postbanding by esophagogastroduodenoscopy); portal hypertensive gastropathy; and gastric varices.

Due to decompensated cirrhosis, the patient had previously undergone extensive screening, radiologic imaging, and laboratory testing, and was found by a multidisciplinary selection committee to be an acceptable liver transplant candidate. He was actively listed for transplantation.

Other significant history included hypertension; sleep apnea; gastroesophageal reflux; osteopenia; zinc, vitamin A, and vitamin D deficiencies; thrombocytopenia; and anemia of chronic disease (liver disease–related). Surgical history was negative. The patient reported no known drug allergies and was taking spironolactone (50 mg/d) and furosemide (20 mg/d).

Physical exam was notable for a low-grade fever of 99.1ºF; blood pressure, 132/81 mm Hg; heart rate, 84 beats/min; icteric sclerae; and moderate distress related to the patient’s abdominal pain, which worsened with deep palpation. The abdomen was distended, with ascites present as indicated by a positive fluid wave test. Bowel sounds were hypoactive. The patient was alert and oriented without asterixis; mental state was within normal limits.

Continue for pathophysiology of ascites >>

Continue for SBP >>

SBP
Approximately 87% of patients with SBP will have signs or symptoms of infection,³ but symptoms can be very vague, so careful attention to detail and thorough assessment are necessary (see Table 1).^2,4,7,12 An elevated absolute polymorphonuclear (PMN) leukocyte cell count of ≥ 250 cells/µL and a positive ascitic culture, with no other apparent source of intra-abdominal infection, are diagnostic for SBP.²

Any cirrhotic patient with ascites who presents with two or more of the following criteria for systemic inflammatory response syndrome should be evaluated for an infectious cause:¹³
• Temperature > 100.4°F or < 96.8°F
• Heart rate > 90 beats/min
• Tachypnea (respiratory rate > 20 breaths/min) or hyperventilation (arterial carbon dioxide tension [PaCO₂] < 32 mm Hg)
• Abnormal white blood cell count (> 12,000/µL or < 4,000/µL or > 10% immature neutrophils [band forms])

CASE Abdominal x-ray, CT, and laboratory testing were ordered in the ED (see Table 2 for laboratory test results). Imaging revealed multiple loops of small bowel in the midabdomen, with several air-fluid levels and a paucity of gas in the rectum. These findings were consistent with small bowel obstruction. In addition, laboratory data were significant for leukocytosis (higher than the patient’s usual level), worsening hyperbilirubinemia and hypoalbuminemia, elevated serum creatinine level indicating acute kidney injury (AKI), and lactic acidosis. The patient was admitted to the hospital for further management.

Because of his severe abdominal pain and leukocytosis, bedside paracentesis was performed. He was found to have an absolute PMN cell count of approximately 1,273 cells/µL, suggesting a diagnosis of SBP. The patient’s status on the transplant list was changed to inactive due to the infection.

Next page: Treatment >>

Refractory ascites
Approximately 10% of patients develop refractory ascites when the condition becomes unresponsive to diuretics or when adverse effects preclude the use of diuretics.⁵ In such cases, large-volume paracentesis (> 5 L removed) is the standard treatment. The patient should be monitored closely during the procedure; blood pressure can decrease drastically due to the large fluid loss. Vital signs should be checked every 15 min to 30 min for the first hour postprocedure, and then hourly if signs remain stable. Albumin should be administered (6-8 g/L of fluid removed) to increase circulating fluid volume.² The patient’s renal function (ie, serum creatinine level and urinary output) should also be monitored closely, as dehydration and/or AKI can occur.⁴ Complications of paracentesis are uncommon but may include bleeding, infection, and bowel perforation. No data support the routine administration of blood products before paracentesis.²

Treatment of SBP
Broad-spectrum antibiotics, particularly cefotaxime, are effective against approximately 94% of the bacterial flora associated with SBP. Initial treatment with cefotaxime (or ceftriaxone, if cefotaxime is unavailable) at a dose of 2 g IV q8h for seven days is recommended, unless or until culture results identify susceptibility to a specific narrow-spectrum antibiotic.^2,4,7,9 After completion of a total of seven days of IV antibiotics, it is cost effective and safe to transition clinically improved patients to an oral antibiotic for SBP prophylaxis (see discussion below).⁹

A repeat paracentesis performed 48 hours after treatment is initiated is useful in assessing response to treatment, defined as a ≥ 25% decrease in ascitic fluid PMN count.⁷

Even if the infection is successfully treated, one-third of patients who have an episode of SBP develop renal failure; those who experience a recurrence of SBP within one year have a 50% to 60% mortality rate.^4,7,9,14 This is because infection causes vasodilation, with a concomitant decrease in blood volume and compensatory activation of renal vasoconstrictors, so renal function worsens.

A randomized controlled trial found that patients treated with IV cefotaxime with albumin in doses of 1.5 g/kg on day 1 and 1 g/kg on day 3 had significantly lower rates of AKI and mortality than patients who received cefotaxime alone.¹⁵ An albumin infusion, given in conjunction with antibiotics, improves blood volume, enhances renal perfusion, and has been shown to decrease mortality from SBP from 29% to 10%.^2,12,16

CASE For small bowel obstruction, the patient was made NPO and a nasogastric tube was placed for 36 hours. During this time, he had a bowel movement, diet was advanced, and the obstruction resolved.

At the same time, the patient was started on IV cefotaxime 2 g q8h for treatment of SBP, along with IV albumin and fluids. Diuretics were withheld because of impaired kidney function.

Ascitic fluid was cultured, and Streptococcus viridans was identified. After consultation with the infectious disease service, broader-spectrum vancomycin was added to the patient’s IV antibiotic regimen 24 hours after admission while culture results finalized. Cultures were analyzed after three days and found to be susceptible to ceftriaxone, which was administered 2 g IV q24h for three days, for a total of seven days of IV antibiotics.

The patient’s AKI improved after treatment with IV antibiotics, fluids, and albumin. Seventy-two hours after admission, repeat paracentesis revealed a significant decrease in white blood cells; cultures were negative for infection.

Neutrocytic ascites
In some cases, the bacteria count in ascitic fluid is so low that cultures may be negative.⁴ This is termed neutrocytic ascites, characterized by an elevated PMN cell count with negative cultures. Patients with neutrocytic ascites should be treated as though they have SBP.^2,7

Prophylactic antibiotics
Of patients successfully treated for SBP, 69% will experience another episode within one year; many of these cases can be prevented with the use of prophylactic antibiotics. Historically, quinolones were used for SBP prophylaxis, and they are cost-effective. However, multiorganism drug resistance hasoccurred after quinolone prophylaxis, especially if given long-term.^2,4,7
 
Alternatives to quinolones include trimethoprim/sulfamethoxazole double strength or ciprofloxacin 500 mg/d.² Renal dose adjustment is necessary for patients with acute or chronic kidney disease and can usually be guided by a pharmacist. One study found norfloxacin and trimethoprim-sulfamethoxazole to be similarly effective for SBP prevention, but trimethoprim-sulfamethoxazole was noted to be more cost-effective.¹⁰

In patients with active gastrointestinal bleeding, IV ceftriaxone 1 g/d for seven days can be given for SBP prevention. In patients with low ascitic protein and/or history of prior SBP, norfloxacin 400 mg/d is an option.

Continue for conclusion >>

REFERENCES
1. Asrani SK, Larson JJ, Yawn B, Therneau TM, Kim WR. Underestimation of liver-related mortality in the United States. Gastroenterology. 2013;145(2):375-382.
2. Runyon BA. American Association for the Study of Liver Diseases practice guideline. Management of adult patients with ascites due to cirrhosis: update 2012. www.aasld.org/sites/default/files/guideline_documents/adultascitesenhanced.pdf. Accessed March 24, 2015.
3. European Association for the Study of the Liver (EASL). EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis. J Hepatol. 2010;53(3):397-417.
4. Sargent S. The management and nursing care of cirrhotic ascites. Br J Nurs. 2006;15(4):212-219.
5. Sargent S. Management of patients with advanced liver cirrhosis. Nurs Stand. 2006;21(11):48-56.
6. Martin P, DiMartini A, Feng S, Brown R Jr, Fallon M. American Association for the Study of Liver Diseases and the American Society of Transplantation. Evaluation for liver transplantation in adults: 2013 practice guideline. Hepatology. 2014;59(3):1144-65.
7. Loo NM, Souza FF, Garcia-Tsao G. Non-hemorrhagic acute complications associated with cirrhosis and portal hypertension. Best Pract Res Clin Gastroenterol. 2013;27(5):665-678.
8. Orman ES, Hayashi PH, Bataller R, Barritt AS. Paracentesis is associated with reduced mortality in patients hospitalized with cirrhosis and ascites. Clin Gastroenterol Hepatol. 2014;12(3):496-503.
9. Ghassemi S, Garcia-Tsao G. Prevention and treatment of infections in patients with cirrhosis. Best Pract Res Clin Gastroenterol. 2007;21(1):
77-93.
10. Lontos S, Gow PJ, Vaughan RB, Angus PW. Norfloxacin and trimethoprim-sulfamethoxazole therapy have similar efficacy in prevention of spontaneous bacterial peritonitis. J Gastroenterol Hepatol. 2008;23(2): 252-255.
11. Desai AP, Satoskar R, Appannagari A, et al. Co-management between hospitalist and hepatologist improves the quality of care of inpatients with chronic liver disease. J Clin Gastroenterol. 2014;48(4):e30-e36.
12. Moore CM, Van Thiel DH. Cirrhotic ascites review: pathophysiology, diagnosis and management. World J Hepatol. 2013;5(5):251-263.
13. Bone RC, Balk RA, Cerra FB, et al; ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest. 1992;101(6):1644-1655.
14. Wong F, O’Leary JG, Reddy KR, et al; North American Consortium for Study of End-Stage Liver Disease. New consensus definition of acute kidney injury accurately predicts 30-day mortality in patients with cirrhosis and infection. Gastroenterology. 2013;145(6):1280-1288.
15. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999;341(6):403-409.
16. Rozga J, Piatek T, Malkowski P. Human albumin: old, new, and emerging applications. Ann Transplant. 2013;18:205-217.

Safe and efficient advanced surgical skill training is of tremendous importance. With the recent increase in Internet use for medical education, there has been a concomitant increase in video recording of surgical procedures and techniques. Surgical recordings have been used in a variety of ways—as live webcasts for remote participants, as “coaching” opportunities for surgeons evaluating their own performance in the operating room, and even as informational resources for patients about to undergo the same surgery.

Surgical multimedia is being delivered through several different outlets. Many academic conferences and meetings showcase videos of different procedures, and several subspecialty societies (eg, Arthroscopy Association of North America) house archives of technical videos for viewing by members. In addition, the VuMedi website offers videos and allows members to comment on them and interact with the videographers. Surgeons are even posting technique videos on YouTube and other public websites.

A large proportion of surgical multimedia is recorded with conventional high-definition video cameras.¹ Besides being able to experience a case at any time and from outside the operating room, the audience can watch from numerous vantage points, angles, and zoom levels. Also, surgeons’ narration can be valuable in helping the audience follow along with the case.

Recording surgical multimedia historically required tight coordination and precise planning by surgeon and videographer. However, innovations in wearable technology now allow surgeons to literally wear video cameras and record procedures as they perform them, in real time—to act as both surgeon and videographer.

Two such products are Google Glass (Google, Mountain View, California) and GoPro Hero (GoPro, San Mateo, California), both of which allow surgeons to record exactly what they see during procedures (Figure 1). Using a wearable technology for surgical multimedia creation requires a deep familiarity with its capabilities and limitations. In this article, we summarize these products’ similarities and differences and provide a technical overview for using wearable technologies in surgical multimedia creation.

1. Choosing a device

When purchasing either wearable device, several factors must be considered, including budget, possible uses outside the operating room, and possible limitations of the technology (Table 1). At this time, Google Glass is significantly more expensive than GoPro Hero. The Google Glass base unit costs $1500, and the GoPro Hero 3 model costs approximately $200 (higher-priced Hero models are available). Both devices require accessories (eg, portable battery unit, dedicated hard drive).

Device capabilities must also be considered (Table 2). Google Glass consists of both hardware and software. Users can record what is seen and heard through the lens and then use apps to create text and e-mail portals to online gaming, social media, and even golf-course GPS. The app market for Google Glass is nascent but undoubtedly will increase in volume and scope as more users adopt the technology (Google Glass comes with both Bluetooth and Wi-Fi and can function tethered through a smartphone). GoPro is mainly a hardware unit that can record in various settings (it is popular with athletes who want to capture and broadcast their participation in action sports). Newer GoPro Hero versions offer Wi-Fi, which allows streaming of video content to a smartphone or tablet through an app. Having clearly defined goals for a device—‌‌as they pertain to use outside the operating room, such as outdoor activities and underwater recording—‌may help the surgeon decide which product is more suitable. Last, it is important to consider limitations. Google Glass resolution is 720p (1280×720) for video and 5 MP for still images, and GoPro resolution can reach 1080p (1920×1080) for video and 5 MP for stills.

Both devices require purchase of accessories. An external USB battery pack is useful for both devices, as is a password-encrypted hard drive for media storage. Lenswear does not come with the base version of Google Glass and is purchased separately from the company. GoPro users buy micro SD cards (~$50 per 64-GB high-speed transfer card) for storage on the device and may buy lithium-ion batteries as an alternative to the external USB battery pack.

Author Update

In January 2015, Google announced that it was temporarily suspending its “Explorer” program, which allowed individual users to buy and test the device for personal use. However, Google is continuing its development of Glass with health care technology, among other areas of growth and development.^2,3

2. Recording a successful surgical video

Unlike a camcorder, which typically is set on a tripod for conventional video recording of surgery, Google Glass and GoPro are intricately linked to the operator. Surgeons must be constantly aware of where they are during surgery and try not to let anything obstruct the camera’s view.

Before starting a case, the surgeon using either device must ensure that its battery is fully charged, as a full charge typically supports 1 hour of continuous recording (the Google Glass battery is a lithium-ion 670-mAh internal unit). A full charge should be enough to capture a short case. Newer GoPro models, with a battery listed at 1050 mAh, provide 1 to 2 hours of recording. When more than 1 hour is needed, an external USB battery pack can be used. This pack allows the device to remain plugged in throughout the case (the pack is kept in the surgeon’s back pocket). We recommend having an external battery pack that is at least 10,000 mAh (~$30 online retail), which easily provides 3+ hours of recording. Unfortunately, this arrangement can be cumbersome. Alternatively, with GoPro, additional batteries may be purchased, but the user needs to dismount the device in order to swap them in (may be difficult during surgery). With both units, partitioning a video into shorter segments conserves battery power and minimizes the risk of file corruption, which may occur if the battery dies or the device overheats.

Google Glass users can bypass manual operation of the device by giving it voice commands (eg, start video, take still image). The exception is for recording video for more than 10 seconds (current default setting). Unfortunately, the surgeon must touch the device to start this recording, which means using extra gloves to preserve operating field sterility. Still images can be made through a combination of voice and head gestures and without manual intervention (Figure 2). Last, users must ensure that the device is not actively connected through Bluetooth to a mobile phone, as incoming calls, text messages, and e-mails may disrupt active recording and become a distraction. The connection can be deactivated by disabling Bluetooth on the host smartphone or by placing the phone into airplane mode and turning off Wi-Fi.

Google Glass users can see what is being recorded through the viewfinder prism, whereas GoPro requires precise framing of the video before recording. Framing is done by grossly aiming the device in the desired direction. However, there is no way to ensure exact aim during recording. If at any point during a case there is slight repositioning of the GoPro, there is a risk of recording the case out of the center of view. An important advantage to newer GoPro versions is the ability to control the device through a wireless remote that can be placed under the surgeon’s gown. The remote can be used to pause and resume recording, without changing gloves, as is done with Google Glass. Last, because the minimum viewing distance from the surgical field is usually 18 inches or more, typically there is no loss of focus or blurring of the image from short-distance recording on either device.

3. File management and playback

Before using wearable technology in the operating room, surgeons must become aware of its limitations with respect to file storage and playback. Google Glass has a usable memory of about 12 GB (1 hour of video may require 1.5-2.0 GB). Conversely, GoPro’s capacity is defined by the micro SD card used. Therefore, the Google Glass hard drive must be regularly maintained well before being brought into the operating room, whereas recording can be extended (with respect to memory) for the GoPro if the media card is large enough.

Both devices allow for wired file transfer, which may be done with Windows Explorer (PC) or iPhoto (Macintosh). However, Google Glass also allows for wireless transfer, through portable storage supported by Google. Although this type of file transfer may be convenient for short, everyday clips made outside the operating room, it is prohibitive for surgical media, mainly because of patient privacy concerns. With wireless transfer to a nonsecure cloud platform, there is a risk of breach of patient confidentiality. We therefore recommend against using wireless upload when producing surgical multimedia, as patient identifiers are likely to be included in the recorded audio or video contents. Conversely, with GoPro, the micro SD card can be used as a portable hard drive to transfer files to a laptop or media reader, obviating the need for wired or wireless transmission. Last, when using traditional wire transfer or memory card to upload to a hard drive, users must ensure that the drive complies with patient privacy laws and regulations.

 4. Privacy and patient consent

As mentioned, great care must be taken to ensure that patient privacy laws are followed. This is especially relevant with content uploaded to online cloud storage, as with Google Glass. The upload may occur automatically if the unit is connected to a Wi-Fi hotspot. In addition, when using surgical media for a real-time webcast for education or demonstration purposes, surgeons must ensure that no protected health information is broadcast and that the patient and the surgical team are aware of the webcast and its purposes.

Before using wearable technology during patient care, patient consent must be obtained. Surgeons should ask the patient to consent to video recording of surgery or an encounter (eg, clinic visit) for education purposes. Our institution’s consent form includes a section for this particular type of consent. If an institution’s form lacks such a section, surgeons should consult their risk management department to ensure there is a proper avenue for obtaining patient consent to record the procedure or encounter. A separate, dedicated media consent form may be required. Last, whoever operates a wearable device should be careful to use the device only during encounters that have received explicit recording consent—as opposed to wearing the device in the hallways or elsewhere in the hospital, where protected health information might be inadvertently recorded.⁴

 5. Putting it all to use

After successful recording of surgery, an effort should be made to produce a high-quality video for education or demonstration purposes. Unfortunately, there is no built-in optical zooming with Google Glass or GoPro, and recording segments in which surgeons focus on detailed anatomy (with high-quality zoom) may prove difficult. Online descriptions of do-it-yourself modifications to place zoom capability on GoPro devices may be useful in surgical video recording, particularly for small surgical fields (hand or foot surgery). In addition, footage may be zoomed in on during postprocessing (Figure 3), though some resolution will be lost in the editing.

There is no practical way to incorporate Google Glass or GoPro while using surgical loupes or a surgical microscope. As a result, videos recorded with wearable technology may not reach the minimum resolution needed for useful surgical technique videos, as these traditionally are produced on high-definition camcorders with optical zoom, allowing detailed viewing of anatomical structures without resolution loss through digital zoom or postprocessing editing.

There has been tremendous benefit in incorporating wearable technology into our practice. Videos made with Google Glass and GoPro have been successfully used for surgical preparation and training, allowing orthopedic surgical residents to rehearse surgery before participating in it. Alternatively, having used Google Glass or GoPro to record a case, residents have then been able to review each surgical step on video—thereby reinforcing their knowledge of the steps, techniques, pearls, and pitfalls before performing the surgery again. Footage from surgeries recorded with Google Glass and GoPro has also been shown at weekly technique-focused conferences, allowing surgeons to analyze particular steps and highlight applicable learning points. Last, attending surgeons in our practice have used wearable technology in “coaching” mode, either reviewing case footage to identify areas for improvement or sharing footage with senior surgeons in order to elicit feedback and suggestions for possible improvement.

As new iterations of wearable video technology come to market, with advancements in both hardware and software, surgeons may be able to enhance education and teaching through seamless recording of surgical procedures. Use of wearable technology may also begin to extend beyond the operating room—to outpatient settings, such as preoperative and postoperative physical examinations. The latest versions of Google Glass and GoPro Hero allow surgeons to record surgical procedures with relative ease, without the personnel, equipment, and coordination required for traditional surgical videography.

Video 1. Coracoid harvest for transfer during Latarjet procedure performed and filmed by Dr. Jobin using GoPro Hero 3.

Video 2. Distal biceps repair performed by Dr. Makhni and Dr. Jobin, filmed by Dr. Makhni using Google Glass.

Safe and efficient advanced surgical skill training is of tremendous importance. With the recent increase in Internet use for medical education, there has been a concomitant increase in video recording of surgical procedures and techniques. Surgical recordings have been used in a variety of ways—as live webcasts for remote participants, as “coaching” opportunities for surgeons evaluating their own performance in the operating room, and even as informational resources for patients about to undergo the same surgery.

Surgical multimedia is being delivered through several different outlets. Many academic conferences and meetings showcase videos of different procedures, and several subspecialty societies (eg, Arthroscopy Association of North America) house archives of technical videos for viewing by members. In addition, the VuMedi website offers videos and allows members to comment on them and interact with the videographers. Surgeons are even posting technique videos on YouTube and other public websites.

A large proportion of surgical multimedia is recorded with conventional high-definition video cameras.¹ Besides being able to experience a case at any time and from outside the operating room, the audience can watch from numerous vantage points, angles, and zoom levels. Also, surgeons’ narration can be valuable in helping the audience follow along with the case.

Recording surgical multimedia historically required tight coordination and precise planning by surgeon and videographer. However, innovations in wearable technology now allow surgeons to literally wear video cameras and record procedures as they perform them, in real time—to act as both surgeon and videographer.

Two such products are Google Glass (Google, Mountain View, California) and GoPro Hero (GoPro, San Mateo, California), both of which allow surgeons to record exactly what they see during procedures (Figure 1). Using a wearable technology for surgical multimedia creation requires a deep familiarity with its capabilities and limitations. In this article, we summarize these products’ similarities and differences and provide a technical overview for using wearable technologies in surgical multimedia creation.

1. Choosing a device

When purchasing either wearable device, several factors must be considered, including budget, possible uses outside the operating room, and possible limitations of the technology (Table 1). At this time, Google Glass is significantly more expensive than GoPro Hero. The Google Glass base unit costs $1500, and the GoPro Hero 3 model costs approximately $200 (higher-priced Hero models are available). Both devices require accessories (eg, portable battery unit, dedicated hard drive).

Device capabilities must also be considered (Table 2). Google Glass consists of both hardware and software. Users can record what is seen and heard through the lens and then use apps to create text and e-mail portals to online gaming, social media, and even golf-course GPS. The app market for Google Glass is nascent but undoubtedly will increase in volume and scope as more users adopt the technology (Google Glass comes with both Bluetooth and Wi-Fi and can function tethered through a smartphone). GoPro is mainly a hardware unit that can record in various settings (it is popular with athletes who want to capture and broadcast their participation in action sports). Newer GoPro Hero versions offer Wi-Fi, which allows streaming of video content to a smartphone or tablet through an app. Having clearly defined goals for a device—‌‌as they pertain to use outside the operating room, such as outdoor activities and underwater recording—‌may help the surgeon decide which product is more suitable. Last, it is important to consider limitations. Google Glass resolution is 720p (1280×720) for video and 5 MP for still images, and GoPro resolution can reach 1080p (1920×1080) for video and 5 MP for stills.

Both devices require purchase of accessories. An external USB battery pack is useful for both devices, as is a password-encrypted hard drive for media storage. Lenswear does not come with the base version of Google Glass and is purchased separately from the company. GoPro users buy micro SD cards (~$50 per 64-GB high-speed transfer card) for storage on the device and may buy lithium-ion batteries as an alternative to the external USB battery pack.

Author Update

In January 2015, Google announced that it was temporarily suspending its “Explorer” program, which allowed individual users to buy and test the device for personal use. However, Google is continuing its development of Glass with health care technology, among other areas of growth and development.^2,3

2. Recording a successful surgical video

Unlike a camcorder, which typically is set on a tripod for conventional video recording of surgery, Google Glass and GoPro are intricately linked to the operator. Surgeons must be constantly aware of where they are during surgery and try not to let anything obstruct the camera’s view.

Before starting a case, the surgeon using either device must ensure that its battery is fully charged, as a full charge typically supports 1 hour of continuous recording (the Google Glass battery is a lithium-ion 670-mAh internal unit). A full charge should be enough to capture a short case. Newer GoPro models, with a battery listed at 1050 mAh, provide 1 to 2 hours of recording. When more than 1 hour is needed, an external USB battery pack can be used. This pack allows the device to remain plugged in throughout the case (the pack is kept in the surgeon’s back pocket). We recommend having an external battery pack that is at least 10,000 mAh (~$30 online retail), which easily provides 3+ hours of recording. Unfortunately, this arrangement can be cumbersome. Alternatively, with GoPro, additional batteries may be purchased, but the user needs to dismount the device in order to swap them in (may be difficult during surgery). With both units, partitioning a video into shorter segments conserves battery power and minimizes the risk of file corruption, which may occur if the battery dies or the device overheats.

Google Glass users can bypass manual operation of the device by giving it voice commands (eg, start video, take still image). The exception is for recording video for more than 10 seconds (current default setting). Unfortunately, the surgeon must touch the device to start this recording, which means using extra gloves to preserve operating field sterility. Still images can be made through a combination of voice and head gestures and without manual intervention (Figure 2). Last, users must ensure that the device is not actively connected through Bluetooth to a mobile phone, as incoming calls, text messages, and e-mails may disrupt active recording and become a distraction. The connection can be deactivated by disabling Bluetooth on the host smartphone or by placing the phone into airplane mode and turning off Wi-Fi.

Google Glass users can see what is being recorded through the viewfinder prism, whereas GoPro requires precise framing of the video before recording. Framing is done by grossly aiming the device in the desired direction. However, there is no way to ensure exact aim during recording. If at any point during a case there is slight repositioning of the GoPro, there is a risk of recording the case out of the center of view. An important advantage to newer GoPro versions is the ability to control the device through a wireless remote that can be placed under the surgeon’s gown. The remote can be used to pause and resume recording, without changing gloves, as is done with Google Glass. Last, because the minimum viewing distance from the surgical field is usually 18 inches or more, typically there is no loss of focus or blurring of the image from short-distance recording on either device.

3. File management and playback

Before using wearable technology in the operating room, surgeons must become aware of its limitations with respect to file storage and playback. Google Glass has a usable memory of about 12 GB (1 hour of video may require 1.5-2.0 GB). Conversely, GoPro’s capacity is defined by the micro SD card used. Therefore, the Google Glass hard drive must be regularly maintained well before being brought into the operating room, whereas recording can be extended (with respect to memory) for the GoPro if the media card is large enough.

Both devices allow for wired file transfer, which may be done with Windows Explorer (PC) or iPhoto (Macintosh). However, Google Glass also allows for wireless transfer, through portable storage supported by Google. Although this type of file transfer may be convenient for short, everyday clips made outside the operating room, it is prohibitive for surgical media, mainly because of patient privacy concerns. With wireless transfer to a nonsecure cloud platform, there is a risk of breach of patient confidentiality. We therefore recommend against using wireless upload when producing surgical multimedia, as patient identifiers are likely to be included in the recorded audio or video contents. Conversely, with GoPro, the micro SD card can be used as a portable hard drive to transfer files to a laptop or media reader, obviating the need for wired or wireless transmission. Last, when using traditional wire transfer or memory card to upload to a hard drive, users must ensure that the drive complies with patient privacy laws and regulations.

 4. Privacy and patient consent

As mentioned, great care must be taken to ensure that patient privacy laws are followed. This is especially relevant with content uploaded to online cloud storage, as with Google Glass. The upload may occur automatically if the unit is connected to a Wi-Fi hotspot. In addition, when using surgical media for a real-time webcast for education or demonstration purposes, surgeons must ensure that no protected health information is broadcast and that the patient and the surgical team are aware of the webcast and its purposes.

Before using wearable technology during patient care, patient consent must be obtained. Surgeons should ask the patient to consent to video recording of surgery or an encounter (eg, clinic visit) for education purposes. Our institution’s consent form includes a section for this particular type of consent. If an institution’s form lacks such a section, surgeons should consult their risk management department to ensure there is a proper avenue for obtaining patient consent to record the procedure or encounter. A separate, dedicated media consent form may be required. Last, whoever operates a wearable device should be careful to use the device only during encounters that have received explicit recording consent—as opposed to wearing the device in the hallways or elsewhere in the hospital, where protected health information might be inadvertently recorded.⁴

 5. Putting it all to use

After successful recording of surgery, an effort should be made to produce a high-quality video for education or demonstration purposes. Unfortunately, there is no built-in optical zooming with Google Glass or GoPro, and recording segments in which surgeons focus on detailed anatomy (with high-quality zoom) may prove difficult. Online descriptions of do-it-yourself modifications to place zoom capability on GoPro devices may be useful in surgical video recording, particularly for small surgical fields (hand or foot surgery). In addition, footage may be zoomed in on during postprocessing (Figure 3), though some resolution will be lost in the editing.

There is no practical way to incorporate Google Glass or GoPro while using surgical loupes or a surgical microscope. As a result, videos recorded with wearable technology may not reach the minimum resolution needed for useful surgical technique videos, as these traditionally are produced on high-definition camcorders with optical zoom, allowing detailed viewing of anatomical structures without resolution loss through digital zoom or postprocessing editing.

There has been tremendous benefit in incorporating wearable technology into our practice. Videos made with Google Glass and GoPro have been successfully used for surgical preparation and training, allowing orthopedic surgical residents to rehearse surgery before participating in it. Alternatively, having used Google Glass or GoPro to record a case, residents have then been able to review each surgical step on video—thereby reinforcing their knowledge of the steps, techniques, pearls, and pitfalls before performing the surgery again. Footage from surgeries recorded with Google Glass and GoPro has also been shown at weekly technique-focused conferences, allowing surgeons to analyze particular steps and highlight applicable learning points. Last, attending surgeons in our practice have used wearable technology in “coaching” mode, either reviewing case footage to identify areas for improvement or sharing footage with senior surgeons in order to elicit feedback and suggestions for possible improvement.

As new iterations of wearable video technology come to market, with advancements in both hardware and software, surgeons may be able to enhance education and teaching through seamless recording of surgical procedures. Use of wearable technology may also begin to extend beyond the operating room—to outpatient settings, such as preoperative and postoperative physical examinations. The latest versions of Google Glass and GoPro Hero allow surgeons to record surgical procedures with relative ease, without the personnel, equipment, and coordination required for traditional surgical videography.

Video 1. Coracoid harvest for transfer during Latarjet procedure performed and filmed by Dr. Jobin using GoPro Hero 3.

Video 2. Distal biceps repair performed by Dr. Makhni and Dr. Jobin, filmed by Dr. Makhni using Google Glass.

Safe and efficient advanced surgical skill training is of tremendous importance. With the recent increase in Internet use for medical education, there has been a concomitant increase in video recording of surgical procedures and techniques. Surgical recordings have been used in a variety of ways—as live webcasts for remote participants, as “coaching” opportunities for surgeons evaluating their own performance in the operating room, and even as informational resources for patients about to undergo the same surgery.

Surgical multimedia is being delivered through several different outlets. Many academic conferences and meetings showcase videos of different procedures, and several subspecialty societies (eg, Arthroscopy Association of North America) house archives of technical videos for viewing by members. In addition, the VuMedi website offers videos and allows members to comment on them and interact with the videographers. Surgeons are even posting technique videos on YouTube and other public websites.

A large proportion of surgical multimedia is recorded with conventional high-definition video cameras.¹ Besides being able to experience a case at any time and from outside the operating room, the audience can watch from numerous vantage points, angles, and zoom levels. Also, surgeons’ narration can be valuable in helping the audience follow along with the case.

Recording surgical multimedia historically required tight coordination and precise planning by surgeon and videographer. However, innovations in wearable technology now allow surgeons to literally wear video cameras and record procedures as they perform them, in real time—to act as both surgeon and videographer.

Two such products are Google Glass (Google, Mountain View, California) and GoPro Hero (GoPro, San Mateo, California), both of which allow surgeons to record exactly what they see during procedures (Figure 1). Using a wearable technology for surgical multimedia creation requires a deep familiarity with its capabilities and limitations. In this article, we summarize these products’ similarities and differences and provide a technical overview for using wearable technologies in surgical multimedia creation.

1. Choosing a device

When purchasing either wearable device, several factors must be considered, including budget, possible uses outside the operating room, and possible limitations of the technology (Table 1). At this time, Google Glass is significantly more expensive than GoPro Hero. The Google Glass base unit costs $1500, and the GoPro Hero 3 model costs approximately $200 (higher-priced Hero models are available). Both devices require accessories (eg, portable battery unit, dedicated hard drive).

Device capabilities must also be considered (Table 2). Google Glass consists of both hardware and software. Users can record what is seen and heard through the lens and then use apps to create text and e-mail portals to online gaming, social media, and even golf-course GPS. The app market for Google Glass is nascent but undoubtedly will increase in volume and scope as more users adopt the technology (Google Glass comes with both Bluetooth and Wi-Fi and can function tethered through a smartphone). GoPro is mainly a hardware unit that can record in various settings (it is popular with athletes who want to capture and broadcast their participation in action sports). Newer GoPro Hero versions offer Wi-Fi, which allows streaming of video content to a smartphone or tablet through an app. Having clearly defined goals for a device—‌‌as they pertain to use outside the operating room, such as outdoor activities and underwater recording—‌may help the surgeon decide which product is more suitable. Last, it is important to consider limitations. Google Glass resolution is 720p (1280×720) for video and 5 MP for still images, and GoPro resolution can reach 1080p (1920×1080) for video and 5 MP for stills.

Both devices require purchase of accessories. An external USB battery pack is useful for both devices, as is a password-encrypted hard drive for media storage. Lenswear does not come with the base version of Google Glass and is purchased separately from the company. GoPro users buy micro SD cards (~$50 per 64-GB high-speed transfer card) for storage on the device and may buy lithium-ion batteries as an alternative to the external USB battery pack.

Author Update

In January 2015, Google announced that it was temporarily suspending its “Explorer” program, which allowed individual users to buy and test the device for personal use. However, Google is continuing its development of Glass with health care technology, among other areas of growth and development.^2,3

2. Recording a successful surgical video

Unlike a camcorder, which typically is set on a tripod for conventional video recording of surgery, Google Glass and GoPro are intricately linked to the operator. Surgeons must be constantly aware of where they are during surgery and try not to let anything obstruct the camera’s view.

Before starting a case, the surgeon using either device must ensure that its battery is fully charged, as a full charge typically supports 1 hour of continuous recording (the Google Glass battery is a lithium-ion 670-mAh internal unit). A full charge should be enough to capture a short case. Newer GoPro models, with a battery listed at 1050 mAh, provide 1 to 2 hours of recording. When more than 1 hour is needed, an external USB battery pack can be used. This pack allows the device to remain plugged in throughout the case (the pack is kept in the surgeon’s back pocket). We recommend having an external battery pack that is at least 10,000 mAh (~$30 online retail), which easily provides 3+ hours of recording. Unfortunately, this arrangement can be cumbersome. Alternatively, with GoPro, additional batteries may be purchased, but the user needs to dismount the device in order to swap them in (may be difficult during surgery). With both units, partitioning a video into shorter segments conserves battery power and minimizes the risk of file corruption, which may occur if the battery dies or the device overheats.

Google Glass users can bypass manual operation of the device by giving it voice commands (eg, start video, take still image). The exception is for recording video for more than 10 seconds (current default setting). Unfortunately, the surgeon must touch the device to start this recording, which means using extra gloves to preserve operating field sterility. Still images can be made through a combination of voice and head gestures and without manual intervention (Figure 2). Last, users must ensure that the device is not actively connected through Bluetooth to a mobile phone, as incoming calls, text messages, and e-mails may disrupt active recording and become a distraction. The connection can be deactivated by disabling Bluetooth on the host smartphone or by placing the phone into airplane mode and turning off Wi-Fi.

Google Glass users can see what is being recorded through the viewfinder prism, whereas GoPro requires precise framing of the video before recording. Framing is done by grossly aiming the device in the desired direction. However, there is no way to ensure exact aim during recording. If at any point during a case there is slight repositioning of the GoPro, there is a risk of recording the case out of the center of view. An important advantage to newer GoPro versions is the ability to control the device through a wireless remote that can be placed under the surgeon’s gown. The remote can be used to pause and resume recording, without changing gloves, as is done with Google Glass. Last, because the minimum viewing distance from the surgical field is usually 18 inches or more, typically there is no loss of focus or blurring of the image from short-distance recording on either device.

3. File management and playback

Before using wearable technology in the operating room, surgeons must become aware of its limitations with respect to file storage and playback. Google Glass has a usable memory of about 12 GB (1 hour of video may require 1.5-2.0 GB). Conversely, GoPro’s capacity is defined by the micro SD card used. Therefore, the Google Glass hard drive must be regularly maintained well before being brought into the operating room, whereas recording can be extended (with respect to memory) for the GoPro if the media card is large enough.

Both devices allow for wired file transfer, which may be done with Windows Explorer (PC) or iPhoto (Macintosh). However, Google Glass also allows for wireless transfer, through portable storage supported by Google. Although this type of file transfer may be convenient for short, everyday clips made outside the operating room, it is prohibitive for surgical media, mainly because of patient privacy concerns. With wireless transfer to a nonsecure cloud platform, there is a risk of breach of patient confidentiality. We therefore recommend against using wireless upload when producing surgical multimedia, as patient identifiers are likely to be included in the recorded audio or video contents. Conversely, with GoPro, the micro SD card can be used as a portable hard drive to transfer files to a laptop or media reader, obviating the need for wired or wireless transmission. Last, when using traditional wire transfer or memory card to upload to a hard drive, users must ensure that the drive complies with patient privacy laws and regulations.

 4. Privacy and patient consent

As mentioned, great care must be taken to ensure that patient privacy laws are followed. This is especially relevant with content uploaded to online cloud storage, as with Google Glass. The upload may occur automatically if the unit is connected to a Wi-Fi hotspot. In addition, when using surgical media for a real-time webcast for education or demonstration purposes, surgeons must ensure that no protected health information is broadcast and that the patient and the surgical team are aware of the webcast and its purposes.

Before using wearable technology during patient care, patient consent must be obtained. Surgeons should ask the patient to consent to video recording of surgery or an encounter (eg, clinic visit) for education purposes. Our institution’s consent form includes a section for this particular type of consent. If an institution’s form lacks such a section, surgeons should consult their risk management department to ensure there is a proper avenue for obtaining patient consent to record the procedure or encounter. A separate, dedicated media consent form may be required. Last, whoever operates a wearable device should be careful to use the device only during encounters that have received explicit recording consent—as opposed to wearing the device in the hallways or elsewhere in the hospital, where protected health information might be inadvertently recorded.⁴

 5. Putting it all to use

After successful recording of surgery, an effort should be made to produce a high-quality video for education or demonstration purposes. Unfortunately, there is no built-in optical zooming with Google Glass or GoPro, and recording segments in which surgeons focus on detailed anatomy (with high-quality zoom) may prove difficult. Online descriptions of do-it-yourself modifications to place zoom capability on GoPro devices may be useful in surgical video recording, particularly for small surgical fields (hand or foot surgery). In addition, footage may be zoomed in on during postprocessing (Figure 3), though some resolution will be lost in the editing.

There is no practical way to incorporate Google Glass or GoPro while using surgical loupes or a surgical microscope. As a result, videos recorded with wearable technology may not reach the minimum resolution needed for useful surgical technique videos, as these traditionally are produced on high-definition camcorders with optical zoom, allowing detailed viewing of anatomical structures without resolution loss through digital zoom or postprocessing editing.

There has been tremendous benefit in incorporating wearable technology into our practice. Videos made with Google Glass and GoPro have been successfully used for surgical preparation and training, allowing orthopedic surgical residents to rehearse surgery before participating in it. Alternatively, having used Google Glass or GoPro to record a case, residents have then been able to review each surgical step on video—thereby reinforcing their knowledge of the steps, techniques, pearls, and pitfalls before performing the surgery again. Footage from surgeries recorded with Google Glass and GoPro has also been shown at weekly technique-focused conferences, allowing surgeons to analyze particular steps and highlight applicable learning points. Last, attending surgeons in our practice have used wearable technology in “coaching” mode, either reviewing case footage to identify areas for improvement or sharing footage with senior surgeons in order to elicit feedback and suggestions for possible improvement.

As new iterations of wearable video technology come to market, with advancements in both hardware and software, surgeons may be able to enhance education and teaching through seamless recording of surgical procedures. Use of wearable technology may also begin to extend beyond the operating room—to outpatient settings, such as preoperative and postoperative physical examinations. The latest versions of Google Glass and GoPro Hero allow surgeons to record surgical procedures with relative ease, without the personnel, equipment, and coordination required for traditional surgical videography.

Video 1. Coracoid harvest for transfer during Latarjet procedure performed and filmed by Dr. Jobin using GoPro Hero 3.

Video 2. Distal biceps repair performed by Dr. Makhni and Dr. Jobin, filmed by Dr. Makhni using Google Glass.

Acute cholecystitis, an inflammatory disease of the gallbladder, is a known risk factor for gastrointestinal cancers, say researchers from Taipei Veterans General Hospital in Taiwan. Many studies have shown that the risk rises with cholelithiasis or after cholecystectomy. But they note that most studies have had limited adjustment for the potential risk factors for each specific cancer. Until their study, they say, no other study had focused on the general and specific cancer risks in patients with cholecystitis.

Related: Do Age and Gender Matter in Colorectal Cancer?

In their retrospective study of 20,431 patients with cholecystitis, the researchers documented 1,541 cancers (mostly liver, colorectal, lung, extrahepatic biliary, and gastric) over a follow-up period of a median 5.4 years. Significantly higher hazard ratios (HRs) were found among patients with cholecystitis in liver cancer (95% confidence interval [CI], 1.73-2.34), biliary tract cancer (95% CI, 2.23-4.18), and pancreatic cancer (95% CI, 1.38-2.88). But after adjusting for other demographic characteristics and comorbidities, cholecystitis was an independent risk factor for biliary tract cancer, which doubled the risk for extrahepatic biliary cancer. Men aged < 60 years had the greatest risk of developing cancer. The increased risk of cancer persisted after 5 years of follow-up.

Related: Bisphosphonates and Gastrointestinal Cancer: Is There a Link?

Though the study findings supported the elevated risk for biliary tract cancer in patients who had had cholecystectomy, that risk was reduced after the researchers controlled for other risk factors. Their results suggested that, in fact, cholecystectomy markedly lowered the risk (HR dropped from 2.34 to 1.28), perhaps because it alleviated inflammation.

Source
Lee P-C, Hu Y-W, Hu L-Y, et al. Am J Med. 2015;128(2):185-191.
doi: 10.1016/j.amjmed.2014.08.036.

Acute cholecystitis, an inflammatory disease of the gallbladder, is a known risk factor for gastrointestinal cancers, say researchers from Taipei Veterans General Hospital in Taiwan. Many studies have shown that the risk rises with cholelithiasis or after cholecystectomy. But they note that most studies have had limited adjustment for the potential risk factors for each specific cancer. Until their study, they say, no other study had focused on the general and specific cancer risks in patients with cholecystitis.

Related: Do Age and Gender Matter in Colorectal Cancer?

In their retrospective study of 20,431 patients with cholecystitis, the researchers documented 1,541 cancers (mostly liver, colorectal, lung, extrahepatic biliary, and gastric) over a follow-up period of a median 5.4 years. Significantly higher hazard ratios (HRs) were found among patients with cholecystitis in liver cancer (95% confidence interval [CI], 1.73-2.34), biliary tract cancer (95% CI, 2.23-4.18), and pancreatic cancer (95% CI, 1.38-2.88). But after adjusting for other demographic characteristics and comorbidities, cholecystitis was an independent risk factor for biliary tract cancer, which doubled the risk for extrahepatic biliary cancer. Men aged < 60 years had the greatest risk of developing cancer. The increased risk of cancer persisted after 5 years of follow-up.

Related: Bisphosphonates and Gastrointestinal Cancer: Is There a Link?

Though the study findings supported the elevated risk for biliary tract cancer in patients who had had cholecystectomy, that risk was reduced after the researchers controlled for other risk factors. Their results suggested that, in fact, cholecystectomy markedly lowered the risk (HR dropped from 2.34 to 1.28), perhaps because it alleviated inflammation.

Source
Lee P-C, Hu Y-W, Hu L-Y, et al. Am J Med. 2015;128(2):185-191.
doi: 10.1016/j.amjmed.2014.08.036.

Acute cholecystitis, an inflammatory disease of the gallbladder, is a known risk factor for gastrointestinal cancers, say researchers from Taipei Veterans General Hospital in Taiwan. Many studies have shown that the risk rises with cholelithiasis or after cholecystectomy. But they note that most studies have had limited adjustment for the potential risk factors for each specific cancer. Until their study, they say, no other study had focused on the general and specific cancer risks in patients with cholecystitis.

Related: Do Age and Gender Matter in Colorectal Cancer?

In their retrospective study of 20,431 patients with cholecystitis, the researchers documented 1,541 cancers (mostly liver, colorectal, lung, extrahepatic biliary, and gastric) over a follow-up period of a median 5.4 years. Significantly higher hazard ratios (HRs) were found among patients with cholecystitis in liver cancer (95% confidence interval [CI], 1.73-2.34), biliary tract cancer (95% CI, 2.23-4.18), and pancreatic cancer (95% CI, 1.38-2.88). But after adjusting for other demographic characteristics and comorbidities, cholecystitis was an independent risk factor for biliary tract cancer, which doubled the risk for extrahepatic biliary cancer. Men aged < 60 years had the greatest risk of developing cancer. The increased risk of cancer persisted after 5 years of follow-up.

Related: Bisphosphonates and Gastrointestinal Cancer: Is There a Link?

Though the study findings supported the elevated risk for biliary tract cancer in patients who had had cholecystectomy, that risk was reduced after the researchers controlled for other risk factors. Their results suggested that, in fact, cholecystectomy markedly lowered the risk (HR dropped from 2.34 to 1.28), perhaps because it alleviated inflammation.

Source
Lee P-C, Hu Y-W, Hu L-Y, et al. Am J Med. 2015;128(2):185-191.
doi: 10.1016/j.amjmed.2014.08.036.

Femoroacetabular impingement (FAI), a recently described hip condition in adolescents and young adults, results from abnormal physical contact between the proximal femur and the acetabulum.¹ FAI is usually characterized by the site of the predominant morphologic abnormality—proximal femur (cam-type FAI), acetabulum (pincer-type FAI), or both (mixed impingement). Cam-type FAI is typified by the aspherical extension of the articular surface at the anterosuperior head–neck junction of the proximal femur with loss of the normal offset. With hip motion, especially in the maximal ranges of flexion and internal rotation, the aspherical proximal femur repeatedly contacts the anterosuperior acetabulum, damaging the chondrolabral junction and ultimately the labrum itself. In pincer-type impingement, femoral head overcoverage caused by acetabular retroversion and/or coxa profunda directly damages the anterior labrum when the acetabular rim contacts the proximal femur during physiologic motion. “Contrecoup” injury of the posterior-inferior acetabular cartilage may also occur. Over time, recurrent microtrauma to the acetabular cartilage and/or labrum may lead to degenerative changes of the hip and ultimately to premature osteoarthritis.^1,2

Patients with FAI typically present with groin pain that may be activity-related or that may occur with prolonged sitting with the hip in a flexed position. Physical examination findings suggestive of FAI include decreased passive internal hip rotation and reproducible pain with adduction and internal rotation of the flexed hip—the impingement sign, or the flexion, adduction, and internal rotation (FADIR) test.³ Diagnostic imaging evaluation initially includes radiographs of the pelvis and hips. These radiographs may show a “pistol-grip” deformity and/or decreased head–neck offset (as determined by increased alpha angle) in the setting of cam-type impingement (Figure 1).⁴ Pincer-type impingement may be associated with a crossover sign, coxa profunda, and an increased center-edge angle (CEA). Advanced imaging studies, such as computed tomography (CT), magnetic resonance imaging (MRI) arthrogram, and delayed gadolinium-enhanced MRI of cartilage (dGEMRIC), are commonly used to better delineate bony deformity and concomitant injuries of the labrum and cartilage (Figure 2).

Treatment for FAI often consists initially of activity modification, use of anti-inflammatory medications, and physical therapy. Intra-articular corticosteroid injections may be used both diagnostically and therapeutically. When nonsurgical measures fail to adequately relieve symptoms, surgery may be warranted. Whether performed open or arthroscopically, surgery is directed first at correcting the underlying osseous abnormality—performing an osteoplasty of the proximal femur to remove the cam lesion, performing an acetabular osteoplasty (“rim-trimming”) to address a focal pincer lesion, and/or performing a periacetabular osteotomy to decrease global acetabular overcoverage (Figure 3).⁵

Sex-Based Differences in FAI Incidence

Traditionally, it was thought that cam-type impingement occurred predominantly in young, athletic males, whereas pincer-type impingement resulting from acetabular overcoverage occurred primarily in females during their fourth decade. However, our understanding of the sex-based differences in the incidence and presentation of FAI has evolved, and it is now clear that the interplay of sex, radiographic signs of impingement, and development of symptoms requiring treatment is more complex.

In recent large population-based studies, investigators have attempted to better characterize the sex-based differences in the incidence of osseous FAI deformity. Gosvig and colleagues² examined radiographic and questionnaire outcomes of 3620 patients (age range, 21-90 years) and found that males were more likely than females to have a pistol-grip deformity of the hip (19.6% vs 5.2%); that deep acetabular sockets were common in both sexes (15.2% vs 19.4%); and that the presence of pistol-grip deformity or deep socket was significantly associated with development of osteoarthritis, independent of sex.

In a study of 2081 asymptomatic patients (mean age, 18.6 years), Laborie and colleagues⁴ reported similar radiographic findings. Males were significantly more likely than females to have a cam-type deformity, as evidenced by pistol-grip deformity, focal prominence of the femoral neck, and/or flattening of the lateral aspect of the femoral head. Males were also more likely than females to have a pincer deformity, though radiographic signs of pincer deformity—a crossover sign, excessive acetabular coverage (defined by increased CEA), and a posterior wall sign—were common in both sexes, occurring in 16.6% of females and 34.3% of males. Bilateral findings of FAI-associated deformity were also more common in males than in females, both for cam-type deformity (24.7% vs 6.3%) and pincer-type deformity (21.7% vs 9.7%).

Sex-Based Differences in FAI Presentation

In males and females, the clinical presentation of FAI is similar—insidious onset of deep groin pain, often exacerbated with activity, and physical examination findings of decreased hip motion (particularly internal rotation) and a positive impingement test.³ Nevertheless, the sexes’ clinical presentation differs in several ways. Specifically, in a study using 3-dimensional CT to assess bony deformity in both symptomatic and asymptomatic patients, Beaulé and colleagues⁶ reported that alpha angles were significantly higher in symptomatic males than in symptomatic females (73.3° vs 58.7°). Hetsroni and colleagues⁷ recently reported similar results in a study of 217 symptomatic young adults treated arthroscopically for hip pain. Preoperative CT showed that alpha angles were significantly larger in males than in females (63.6° vs 47.8°). The authors postulated that females may be more likely to be symptomatic in the setting of smaller cam lesions because of the increased peak hip flexion and frontal plane motion commonly demonstrated by females during drop landings in sport. The authors further hypothesized that sex differences in muscle mass (which contributes to dynamic hip stability) and ligamentous laxity (a component of static hip stability) may result in larger physiologic ranges of motion for many females. As a result, bony impingement may occur in the setting of smaller anatomical lesions in females. The authors further noted that, compared with their male counterparts, females being treated for symptomatic FAI had significantly more femoral and acetabular anteversion.

Another male–female presentation difference involves symptom bilaterality. Specifically, males are significantly more likely than females to have symptomatic FAI involving both hips. In a recent study of 646 patients who underwent hip arthroscopy for symptomatic FAI during a 2-year period, Klingenstein and colleagues⁸ found that females constituted 48.2% of unilateral arthroscopy patients but only 34.8% of bilateral arthroscopy patients. The odds ratio of males treated for both hips, compared with females, was 1.7 (95% confidence interval, 1.16–2.54).

Last, it has been reported that, on clinical presentation, hip function scores are significantly lower in females than in males. In a recent study of 612 cases of symptomatic FAI treated with hip arthroscopy, Malviya and colleagues⁹ found that females had significantly lower quality-of-life scores both before and after surgery. Hetsroni and colleagues⁷ reported similar findings, with females having significantly lower preoperative modified Harris Hip Scores and lower Hip Outcome Scores in the domains of Activities of Daily Living and Sports.

Sex-Based Differences in FAI Treatment
and Outcomes

Surgical treatment of FAI is focused on identifying the source of hip pain and dysfunction—be it osseous lesion, labral tearing, chondral injury, or iliopsoas tendonitis—and treating it accordingly, regardless of sex. Most studies of this approach find consistent improvement in the short-term and midterm outcome scores for a majority of patients. However, relatively few studies have focused specifically on sex in determining the percentage of patients who require surgical treatment, in deciding the type of surgery that should be performed, or in measuring surgical outcomes in patients with symptomatic FAI.

In their review of 23 studies of FAI surgery, Ng and colleagues¹⁰ found that, of 970 patients, 608 (62.7%) were male and 362 (37.3%) were female. Similarly higher rates for males were previously published.^5,11 More recently, Clohisy and colleagues¹² reported on the descriptive epidemiology of patients having surgery for FAI at 8 different medical centers in North America. Fifty-five percent of the hips surgically treated for symptomatic FAI were females’. The authors speculated that this unexpectedly high rate could have resulted from US and Canadian female athletes’ increasingly higher level of sports participation. The results of this study, one of the largest examining the rate of surgery for males and females with FAI, suggest that females are more likely to have surgery for symptomatic FAI despite being less likely to have radiographic evidence of impingement. Our understanding of this phenomenon continues to advance.

In a recent prospective study, Krych and colleagues¹³ evaluated the clinical outcomes of FAI surgeries (labral débridement, labral repair) in an all-female patient cohort. Female patients with symptomatic FAI were randomized to undergo either labral débridement or labral repair. There were clinical improvements in both groups, but, compared with labral débridement patients, labral repair patients had more significantly improved Hip Outcome Scores in the domains of Activities of Daily Living and Sports, as well as better subjective outcomes. Although the study did not compare female patients with male patients, it does provide evidence that female patients specifically may benefit more from labral repair than from labral débridement alone.

With respect to different surgical treatments for male and female patients, Hetsroni and colleagues⁷ introduced the idea of sex-specific treatment when they noted more hip anteversion in their study’s female patients than in its male patients. They suggested that, because the anterosuperior acetabulum is subjected to a high amount of stress during weight-bearing and gait, this area in females with suspected pincer lesions should be rim-trimmed judiciously to avoid increasing the stress and perhaps even hastening the development of degenerative disease. Last, though several authors have noted that hip function scores are lower in females than in males on presentation, it has also been reported that females demonstrate more improvement in functional scores after surgery.⁹ This may be important information to discuss during preoperative counseling about expected goals and outcomes.

Conclusion

Femoroacetabular impingement is a common clinical entity that affects both males and females. However, sexual dimorphism in FAI incidence, presentation, treatment, and outcomes has recently been described in the literature (Table). Being aware of these sex-based differences and tailoring patient evaluation and management accordingly will likely result in optimal outcomes for each person who presents with symptomatic FAI.

Femoroacetabular impingement (FAI), a recently described hip condition in adolescents and young adults, results from abnormal physical contact between the proximal femur and the acetabulum.¹ FAI is usually characterized by the site of the predominant morphologic abnormality—proximal femur (cam-type FAI), acetabulum (pincer-type FAI), or both (mixed impingement). Cam-type FAI is typified by the aspherical extension of the articular surface at the anterosuperior head–neck junction of the proximal femur with loss of the normal offset. With hip motion, especially in the maximal ranges of flexion and internal rotation, the aspherical proximal femur repeatedly contacts the anterosuperior acetabulum, damaging the chondrolabral junction and ultimately the labrum itself. In pincer-type impingement, femoral head overcoverage caused by acetabular retroversion and/or coxa profunda directly damages the anterior labrum when the acetabular rim contacts the proximal femur during physiologic motion. “Contrecoup” injury of the posterior-inferior acetabular cartilage may also occur. Over time, recurrent microtrauma to the acetabular cartilage and/or labrum may lead to degenerative changes of the hip and ultimately to premature osteoarthritis.^1,2

Patients with FAI typically present with groin pain that may be activity-related or that may occur with prolonged sitting with the hip in a flexed position. Physical examination findings suggestive of FAI include decreased passive internal hip rotation and reproducible pain with adduction and internal rotation of the flexed hip—the impingement sign, or the flexion, adduction, and internal rotation (FADIR) test.³ Diagnostic imaging evaluation initially includes radiographs of the pelvis and hips. These radiographs may show a “pistol-grip” deformity and/or decreased head–neck offset (as determined by increased alpha angle) in the setting of cam-type impingement (Figure 1).⁴ Pincer-type impingement may be associated with a crossover sign, coxa profunda, and an increased center-edge angle (CEA). Advanced imaging studies, such as computed tomography (CT), magnetic resonance imaging (MRI) arthrogram, and delayed gadolinium-enhanced MRI of cartilage (dGEMRIC), are commonly used to better delineate bony deformity and concomitant injuries of the labrum and cartilage (Figure 2).

Treatment for FAI often consists initially of activity modification, use of anti-inflammatory medications, and physical therapy. Intra-articular corticosteroid injections may be used both diagnostically and therapeutically. When nonsurgical measures fail to adequately relieve symptoms, surgery may be warranted. Whether performed open or arthroscopically, surgery is directed first at correcting the underlying osseous abnormality—performing an osteoplasty of the proximal femur to remove the cam lesion, performing an acetabular osteoplasty (“rim-trimming”) to address a focal pincer lesion, and/or performing a periacetabular osteotomy to decrease global acetabular overcoverage (Figure 3).⁵

Sex-Based Differences in FAI Incidence

Traditionally, it was thought that cam-type impingement occurred predominantly in young, athletic males, whereas pincer-type impingement resulting from acetabular overcoverage occurred primarily in females during their fourth decade. However, our understanding of the sex-based differences in the incidence and presentation of FAI has evolved, and it is now clear that the interplay of sex, radiographic signs of impingement, and development of symptoms requiring treatment is more complex.

In recent large population-based studies, investigators have attempted to better characterize the sex-based differences in the incidence of osseous FAI deformity. Gosvig and colleagues² examined radiographic and questionnaire outcomes of 3620 patients (age range, 21-90 years) and found that males were more likely than females to have a pistol-grip deformity of the hip (19.6% vs 5.2%); that deep acetabular sockets were common in both sexes (15.2% vs 19.4%); and that the presence of pistol-grip deformity or deep socket was significantly associated with development of osteoarthritis, independent of sex.

In a study of 2081 asymptomatic patients (mean age, 18.6 years), Laborie and colleagues⁴ reported similar radiographic findings. Males were significantly more likely than females to have a cam-type deformity, as evidenced by pistol-grip deformity, focal prominence of the femoral neck, and/or flattening of the lateral aspect of the femoral head. Males were also more likely than females to have a pincer deformity, though radiographic signs of pincer deformity—a crossover sign, excessive acetabular coverage (defined by increased CEA), and a posterior wall sign—were common in both sexes, occurring in 16.6% of females and 34.3% of males. Bilateral findings of FAI-associated deformity were also more common in males than in females, both for cam-type deformity (24.7% vs 6.3%) and pincer-type deformity (21.7% vs 9.7%).

Sex-Based Differences in FAI Presentation

In males and females, the clinical presentation of FAI is similar—insidious onset of deep groin pain, often exacerbated with activity, and physical examination findings of decreased hip motion (particularly internal rotation) and a positive impingement test.³ Nevertheless, the sexes’ clinical presentation differs in several ways. Specifically, in a study using 3-dimensional CT to assess bony deformity in both symptomatic and asymptomatic patients, Beaulé and colleagues⁶ reported that alpha angles were significantly higher in symptomatic males than in symptomatic females (73.3° vs 58.7°). Hetsroni and colleagues⁷ recently reported similar results in a study of 217 symptomatic young adults treated arthroscopically for hip pain. Preoperative CT showed that alpha angles were significantly larger in males than in females (63.6° vs 47.8°). The authors postulated that females may be more likely to be symptomatic in the setting of smaller cam lesions because of the increased peak hip flexion and frontal plane motion commonly demonstrated by females during drop landings in sport. The authors further hypothesized that sex differences in muscle mass (which contributes to dynamic hip stability) and ligamentous laxity (a component of static hip stability) may result in larger physiologic ranges of motion for many females. As a result, bony impingement may occur in the setting of smaller anatomical lesions in females. The authors further noted that, compared with their male counterparts, females being treated for symptomatic FAI had significantly more femoral and acetabular anteversion.

Another male–female presentation difference involves symptom bilaterality. Specifically, males are significantly more likely than females to have symptomatic FAI involving both hips. In a recent study of 646 patients who underwent hip arthroscopy for symptomatic FAI during a 2-year period, Klingenstein and colleagues⁸ found that females constituted 48.2% of unilateral arthroscopy patients but only 34.8% of bilateral arthroscopy patients. The odds ratio of males treated for both hips, compared with females, was 1.7 (95% confidence interval, 1.16–2.54).

Last, it has been reported that, on clinical presentation, hip function scores are significantly lower in females than in males. In a recent study of 612 cases of symptomatic FAI treated with hip arthroscopy, Malviya and colleagues⁹ found that females had significantly lower quality-of-life scores both before and after surgery. Hetsroni and colleagues⁷ reported similar findings, with females having significantly lower preoperative modified Harris Hip Scores and lower Hip Outcome Scores in the domains of Activities of Daily Living and Sports.

Sex-Based Differences in FAI Treatment
and Outcomes

Surgical treatment of FAI is focused on identifying the source of hip pain and dysfunction—be it osseous lesion, labral tearing, chondral injury, or iliopsoas tendonitis—and treating it accordingly, regardless of sex. Most studies of this approach find consistent improvement in the short-term and midterm outcome scores for a majority of patients. However, relatively few studies have focused specifically on sex in determining the percentage of patients who require surgical treatment, in deciding the type of surgery that should be performed, or in measuring surgical outcomes in patients with symptomatic FAI.

In their review of 23 studies of FAI surgery, Ng and colleagues¹⁰ found that, of 970 patients, 608 (62.7%) were male and 362 (37.3%) were female. Similarly higher rates for males were previously published.^5,11 More recently, Clohisy and colleagues¹² reported on the descriptive epidemiology of patients having surgery for FAI at 8 different medical centers in North America. Fifty-five percent of the hips surgically treated for symptomatic FAI were females’. The authors speculated that this unexpectedly high rate could have resulted from US and Canadian female athletes’ increasingly higher level of sports participation. The results of this study, one of the largest examining the rate of surgery for males and females with FAI, suggest that females are more likely to have surgery for symptomatic FAI despite being less likely to have radiographic evidence of impingement. Our understanding of this phenomenon continues to advance.

In a recent prospective study, Krych and colleagues¹³ evaluated the clinical outcomes of FAI surgeries (labral débridement, labral repair) in an all-female patient cohort. Female patients with symptomatic FAI were randomized to undergo either labral débridement or labral repair. There were clinical improvements in both groups, but, compared with labral débridement patients, labral repair patients had more significantly improved Hip Outcome Scores in the domains of Activities of Daily Living and Sports, as well as better subjective outcomes. Although the study did not compare female patients with male patients, it does provide evidence that female patients specifically may benefit more from labral repair than from labral débridement alone.

With respect to different surgical treatments for male and female patients, Hetsroni and colleagues⁷ introduced the idea of sex-specific treatment when they noted more hip anteversion in their study’s female patients than in its male patients. They suggested that, because the anterosuperior acetabulum is subjected to a high amount of stress during weight-bearing and gait, this area in females with suspected pincer lesions should be rim-trimmed judiciously to avoid increasing the stress and perhaps even hastening the development of degenerative disease. Last, though several authors have noted that hip function scores are lower in females than in males on presentation, it has also been reported that females demonstrate more improvement in functional scores after surgery.⁹ This may be important information to discuss during preoperative counseling about expected goals and outcomes.

Conclusion

Femoroacetabular impingement is a common clinical entity that affects both males and females. However, sexual dimorphism in FAI incidence, presentation, treatment, and outcomes has recently been described in the literature (Table). Being aware of these sex-based differences and tailoring patient evaluation and management accordingly will likely result in optimal outcomes for each person who presents with symptomatic FAI.

Femoroacetabular impingement (FAI), a recently described hip condition in adolescents and young adults, results from abnormal physical contact between the proximal femur and the acetabulum.¹ FAI is usually characterized by the site of the predominant morphologic abnormality—proximal femur (cam-type FAI), acetabulum (pincer-type FAI), or both (mixed impingement). Cam-type FAI is typified by the aspherical extension of the articular surface at the anterosuperior head–neck junction of the proximal femur with loss of the normal offset. With hip motion, especially in the maximal ranges of flexion and internal rotation, the aspherical proximal femur repeatedly contacts the anterosuperior acetabulum, damaging the chondrolabral junction and ultimately the labrum itself. In pincer-type impingement, femoral head overcoverage caused by acetabular retroversion and/or coxa profunda directly damages the anterior labrum when the acetabular rim contacts the proximal femur during physiologic motion. “Contrecoup” injury of the posterior-inferior acetabular cartilage may also occur. Over time, recurrent microtrauma to the acetabular cartilage and/or labrum may lead to degenerative changes of the hip and ultimately to premature osteoarthritis.^1,2

Patients with FAI typically present with groin pain that may be activity-related or that may occur with prolonged sitting with the hip in a flexed position. Physical examination findings suggestive of FAI include decreased passive internal hip rotation and reproducible pain with adduction and internal rotation of the flexed hip—the impingement sign, or the flexion, adduction, and internal rotation (FADIR) test.³ Diagnostic imaging evaluation initially includes radiographs of the pelvis and hips. These radiographs may show a “pistol-grip” deformity and/or decreased head–neck offset (as determined by increased alpha angle) in the setting of cam-type impingement (Figure 1).⁴ Pincer-type impingement may be associated with a crossover sign, coxa profunda, and an increased center-edge angle (CEA). Advanced imaging studies, such as computed tomography (CT), magnetic resonance imaging (MRI) arthrogram, and delayed gadolinium-enhanced MRI of cartilage (dGEMRIC), are commonly used to better delineate bony deformity and concomitant injuries of the labrum and cartilage (Figure 2).

Treatment for FAI often consists initially of activity modification, use of anti-inflammatory medications, and physical therapy. Intra-articular corticosteroid injections may be used both diagnostically and therapeutically. When nonsurgical measures fail to adequately relieve symptoms, surgery may be warranted. Whether performed open or arthroscopically, surgery is directed first at correcting the underlying osseous abnormality—performing an osteoplasty of the proximal femur to remove the cam lesion, performing an acetabular osteoplasty (“rim-trimming”) to address a focal pincer lesion, and/or performing a periacetabular osteotomy to decrease global acetabular overcoverage (Figure 3).⁵

Sex-Based Differences in FAI Incidence

Traditionally, it was thought that cam-type impingement occurred predominantly in young, athletic males, whereas pincer-type impingement resulting from acetabular overcoverage occurred primarily in females during their fourth decade. However, our understanding of the sex-based differences in the incidence and presentation of FAI has evolved, and it is now clear that the interplay of sex, radiographic signs of impingement, and development of symptoms requiring treatment is more complex.

In recent large population-based studies, investigators have attempted to better characterize the sex-based differences in the incidence of osseous FAI deformity. Gosvig and colleagues² examined radiographic and questionnaire outcomes of 3620 patients (age range, 21-90 years) and found that males were more likely than females to have a pistol-grip deformity of the hip (19.6% vs 5.2%); that deep acetabular sockets were common in both sexes (15.2% vs 19.4%); and that the presence of pistol-grip deformity or deep socket was significantly associated with development of osteoarthritis, independent of sex.

In a study of 2081 asymptomatic patients (mean age, 18.6 years), Laborie and colleagues⁴ reported similar radiographic findings. Males were significantly more likely than females to have a cam-type deformity, as evidenced by pistol-grip deformity, focal prominence of the femoral neck, and/or flattening of the lateral aspect of the femoral head. Males were also more likely than females to have a pincer deformity, though radiographic signs of pincer deformity—a crossover sign, excessive acetabular coverage (defined by increased CEA), and a posterior wall sign—were common in both sexes, occurring in 16.6% of females and 34.3% of males. Bilateral findings of FAI-associated deformity were also more common in males than in females, both for cam-type deformity (24.7% vs 6.3%) and pincer-type deformity (21.7% vs 9.7%).

Sex-Based Differences in FAI Presentation

In males and females, the clinical presentation of FAI is similar—insidious onset of deep groin pain, often exacerbated with activity, and physical examination findings of decreased hip motion (particularly internal rotation) and a positive impingement test.³ Nevertheless, the sexes’ clinical presentation differs in several ways. Specifically, in a study using 3-dimensional CT to assess bony deformity in both symptomatic and asymptomatic patients, Beaulé and colleagues⁶ reported that alpha angles were significantly higher in symptomatic males than in symptomatic females (73.3° vs 58.7°). Hetsroni and colleagues⁷ recently reported similar results in a study of 217 symptomatic young adults treated arthroscopically for hip pain. Preoperative CT showed that alpha angles were significantly larger in males than in females (63.6° vs 47.8°). The authors postulated that females may be more likely to be symptomatic in the setting of smaller cam lesions because of the increased peak hip flexion and frontal plane motion commonly demonstrated by females during drop landings in sport. The authors further hypothesized that sex differences in muscle mass (which contributes to dynamic hip stability) and ligamentous laxity (a component of static hip stability) may result in larger physiologic ranges of motion for many females. As a result, bony impingement may occur in the setting of smaller anatomical lesions in females. The authors further noted that, compared with their male counterparts, females being treated for symptomatic FAI had significantly more femoral and acetabular anteversion.

Another male–female presentation difference involves symptom bilaterality. Specifically, males are significantly more likely than females to have symptomatic FAI involving both hips. In a recent study of 646 patients who underwent hip arthroscopy for symptomatic FAI during a 2-year period, Klingenstein and colleagues⁸ found that females constituted 48.2% of unilateral arthroscopy patients but only 34.8% of bilateral arthroscopy patients. The odds ratio of males treated for both hips, compared with females, was 1.7 (95% confidence interval, 1.16–2.54).

Last, it has been reported that, on clinical presentation, hip function scores are significantly lower in females than in males. In a recent study of 612 cases of symptomatic FAI treated with hip arthroscopy, Malviya and colleagues⁹ found that females had significantly lower quality-of-life scores both before and after surgery. Hetsroni and colleagues⁷ reported similar findings, with females having significantly lower preoperative modified Harris Hip Scores and lower Hip Outcome Scores in the domains of Activities of Daily Living and Sports.

Sex-Based Differences in FAI Treatment
and Outcomes

Surgical treatment of FAI is focused on identifying the source of hip pain and dysfunction—be it osseous lesion, labral tearing, chondral injury, or iliopsoas tendonitis—and treating it accordingly, regardless of sex. Most studies of this approach find consistent improvement in the short-term and midterm outcome scores for a majority of patients. However, relatively few studies have focused specifically on sex in determining the percentage of patients who require surgical treatment, in deciding the type of surgery that should be performed, or in measuring surgical outcomes in patients with symptomatic FAI.

In their review of 23 studies of FAI surgery, Ng and colleagues¹⁰ found that, of 970 patients, 608 (62.7%) were male and 362 (37.3%) were female. Similarly higher rates for males were previously published.^5,11 More recently, Clohisy and colleagues¹² reported on the descriptive epidemiology of patients having surgery for FAI at 8 different medical centers in North America. Fifty-five percent of the hips surgically treated for symptomatic FAI were females’. The authors speculated that this unexpectedly high rate could have resulted from US and Canadian female athletes’ increasingly higher level of sports participation. The results of this study, one of the largest examining the rate of surgery for males and females with FAI, suggest that females are more likely to have surgery for symptomatic FAI despite being less likely to have radiographic evidence of impingement. Our understanding of this phenomenon continues to advance.

In a recent prospective study, Krych and colleagues¹³ evaluated the clinical outcomes of FAI surgeries (labral débridement, labral repair) in an all-female patient cohort. Female patients with symptomatic FAI were randomized to undergo either labral débridement or labral repair. There were clinical improvements in both groups, but, compared with labral débridement patients, labral repair patients had more significantly improved Hip Outcome Scores in the domains of Activities of Daily Living and Sports, as well as better subjective outcomes. Although the study did not compare female patients with male patients, it does provide evidence that female patients specifically may benefit more from labral repair than from labral débridement alone.

With respect to different surgical treatments for male and female patients, Hetsroni and colleagues⁷ introduced the idea of sex-specific treatment when they noted more hip anteversion in their study’s female patients than in its male patients. They suggested that, because the anterosuperior acetabulum is subjected to a high amount of stress during weight-bearing and gait, this area in females with suspected pincer lesions should be rim-trimmed judiciously to avoid increasing the stress and perhaps even hastening the development of degenerative disease. Last, though several authors have noted that hip function scores are lower in females than in males on presentation, it has also been reported that females demonstrate more improvement in functional scores after surgery.⁹ This may be important information to discuss during preoperative counseling about expected goals and outcomes.

Conclusion

Femoroacetabular impingement is a common clinical entity that affects both males and females. However, sexual dimorphism in FAI incidence, presentation, treatment, and outcomes has recently been described in the literature (Table). Being aware of these sex-based differences and tailoring patient evaluation and management accordingly will likely result in optimal outcomes for each person who presents with symptomatic FAI.

Hepatitis C virus (HCV) infection is reported in 0.05% to 0.36% of children in developed nations.1 Since improved screening of donor blood and blood products began in the 1990s, vertical transmission has become the primary cause of HCV infection in children.1-5 As many as 4,000 new cases of pediatric HCV infection may develop each year in the United States.6

At present, no clear interventions exist to prevent mother-to-child transmission (MTCT) of HCV.^4,7 No HCV vaccine is yet available, and most current antiviral therapies are not considered safe for pregnant patients: ribavirin and interferon α, for example, are in pregnancy categories X and C, respectively.^3,7 (See “Safer HCV Treatment Options in Pregnancy?”^8,9) Some might argue that HCV infection is reported in only 1% to 2% of pregnant women in industrialized countries⁷ and that the rate of MTCT is low at 2% to 10%.^3-5 Nevertheless, researchers maintain that HCV during pregnancy is a “neglected condition” and call for substantial improvements in public health response to affected patients.^3,4 Awareness of risk factors for MTCT is essential.

Vertical transmission is believed to be limited to women with detectable viral load,^3,4,10 and the risk grows with increasing maternal viremia (ie, HCV RNA > 10⁵ copies/mL¹). Risk for MTCT is heightened in women who are coinfected with HIV,^3,11 with one systematic review showing a 10.8% vertical transmission risk among coinfected women, versus 5.8% among those with HCV infection alone.² Transmission risk is increased in mothers with a history of IV drug use or a sexual partner infected with HCV.¹⁰ Perinatal procedures that expose the infant to HCV-infected maternal blood (eg, episiotomy, internal fetal monitoring) also elevate MTCT risk.^3,7,1011

In an effort to identify strategies to reduce vertical transmission of HCV, researchers for the US Preventive Services Task Force (USPSTF)⁶ performed a review of studies on the impact of mode of delivery, breastfeeding practices, and other factors on MTCT. No difference in HCV transmission was found in vaginal vs cesarean deliveries; however, in one good-quality study, a higher MTCT rate was found among cases involving prolonged duration of ruptured membranes (> 6 h before delivery).

Continue for association between breastfeeding and HCV >>

The USPSTF researchers found no association between breastfeeding and HCV transmission,⁶ although the CDC recommends against the practice in HCV-infected women whose nipples are cracked or bleeding.⁵ Of note, both breastfeeding and cesarean delivery are associated with increased transmission risk among HCV/HIV coinfected women.⁷ HCV genotype is reported to have little impact on MTCT.^1,10

Until the development of an effective HCV vaccine and safe, effective HCV treatment for pregnant patients,^1,3 strategies to interrupt MTCT represent our best hope to protect children against HCV infection.

REFERENCES
1. Yeung CY, Lee HC, Chan WT, et al. Vertical transmission of hepatitis C virus: current knowledge and perspectives. World J Hepatol. 2014;6(9):643-651.

2. Benova L, Mohamoud YA, Calvert C, Abu-Raddad LJ. Vertical transmission of hepatitis C virus: systematic review and meta-analysis. Clin Infect Dis. 2014;59(6):765-773.

3. Prasad MR, Honegger JR. Hepatitis C virus in pregnancy. Am J Perinatol. 2013;30(2):149-159.

4. Arshad M, El-Kamary SS, Jhaveri R. Hepatitis C virus infection during pregnancy and the newborn period: are they opportunities for treatment? J Viral Hepat. 2011;18(4):229-236.

5. CDC. Hepatitis C FAQs for health professionals. www.cdc.gov/hepatitis/HCV/HCVfaq.htm. Accessed February 9, 2015.

6. Cottrell EB, Chou R, Wasson N, et al. Reducing risk for mother-to-infant transmission of hepatitis C virus: a systematic review for the US Preventive Services Task Force. Ann Intern Med. 2013;158(2):109-113.

7. Tosone G, Maraolo AE, Mascolo S, et al. Vertical hepatitis C virus transmission: main questions and answers. World J Hepatol. 2014;6(8):538-548.

8. Harvoni^®: highlights of prescribing information. www.gilead.com/~/media/Files/pdfs/medicines/liver-disease/harvoni/harvoni_pi.pdf. Accessed February 15, 2015.

9. Viekira Pak^™: highlights of prescribing information. www.rxabbvie.com/pdf/viekirapak_pi.pdf. Accessed February 15, 2015.

10. Indolfi G, Resti M. Perinatal transmission of hepatitis C virus infection. J Med Virol. 2009;81(5):8836-843.

11. Mast EE, Hwang LY, Seto DS, et al. Risk factors for perinatal transmission of hepatitis C virus (HCV) and the natural history of HCV infection acquired in infancy. J Infect Dis. 2005;192:1880-1889. 

Hepatitis C virus (HCV) infection is reported in 0.05% to 0.36% of children in developed nations.1 Since improved screening of donor blood and blood products began in the 1990s, vertical transmission has become the primary cause of HCV infection in children.1-5 As many as 4,000 new cases of pediatric HCV infection may develop each year in the United States.6

At present, no clear interventions exist to prevent mother-to-child transmission (MTCT) of HCV.^4,7 No HCV vaccine is yet available, and most current antiviral therapies are not considered safe for pregnant patients: ribavirin and interferon α, for example, are in pregnancy categories X and C, respectively.^3,7 (See “Safer HCV Treatment Options in Pregnancy?”^8,9) Some might argue that HCV infection is reported in only 1% to 2% of pregnant women in industrialized countries⁷ and that the rate of MTCT is low at 2% to 10%.^3-5 Nevertheless, researchers maintain that HCV during pregnancy is a “neglected condition” and call for substantial improvements in public health response to affected patients.^3,4 Awareness of risk factors for MTCT is essential.

Vertical transmission is believed to be limited to women with detectable viral load,^3,4,10 and the risk grows with increasing maternal viremia (ie, HCV RNA > 10⁵ copies/mL¹). Risk for MTCT is heightened in women who are coinfected with HIV,^3,11 with one systematic review showing a 10.8% vertical transmission risk among coinfected women, versus 5.8% among those with HCV infection alone.² Transmission risk is increased in mothers with a history of IV drug use or a sexual partner infected with HCV.¹⁰ Perinatal procedures that expose the infant to HCV-infected maternal blood (eg, episiotomy, internal fetal monitoring) also elevate MTCT risk.^3,7,1011

In an effort to identify strategies to reduce vertical transmission of HCV, researchers for the US Preventive Services Task Force (USPSTF)⁶ performed a review of studies on the impact of mode of delivery, breastfeeding practices, and other factors on MTCT. No difference in HCV transmission was found in vaginal vs cesarean deliveries; however, in one good-quality study, a higher MTCT rate was found among cases involving prolonged duration of ruptured membranes (> 6 h before delivery).

Continue for association between breastfeeding and HCV >>

The USPSTF researchers found no association between breastfeeding and HCV transmission,⁶ although the CDC recommends against the practice in HCV-infected women whose nipples are cracked or bleeding.⁵ Of note, both breastfeeding and cesarean delivery are associated with increased transmission risk among HCV/HIV coinfected women.⁷ HCV genotype is reported to have little impact on MTCT.^1,10

Until the development of an effective HCV vaccine and safe, effective HCV treatment for pregnant patients,^1,3 strategies to interrupt MTCT represent our best hope to protect children against HCV infection.

REFERENCES
1. Yeung CY, Lee HC, Chan WT, et al. Vertical transmission of hepatitis C virus: current knowledge and perspectives. World J Hepatol. 2014;6(9):643-651.

2. Benova L, Mohamoud YA, Calvert C, Abu-Raddad LJ. Vertical transmission of hepatitis C virus: systematic review and meta-analysis. Clin Infect Dis. 2014;59(6):765-773.

3. Prasad MR, Honegger JR. Hepatitis C virus in pregnancy. Am J Perinatol. 2013;30(2):149-159.

4. Arshad M, El-Kamary SS, Jhaveri R. Hepatitis C virus infection during pregnancy and the newborn period: are they opportunities for treatment? J Viral Hepat. 2011;18(4):229-236.

5. CDC. Hepatitis C FAQs for health professionals. www.cdc.gov/hepatitis/HCV/HCVfaq.htm. Accessed February 9, 2015.

6. Cottrell EB, Chou R, Wasson N, et al. Reducing risk for mother-to-infant transmission of hepatitis C virus: a systematic review for the US Preventive Services Task Force. Ann Intern Med. 2013;158(2):109-113.

7. Tosone G, Maraolo AE, Mascolo S, et al. Vertical hepatitis C virus transmission: main questions and answers. World J Hepatol. 2014;6(8):538-548.

8. Harvoni^®: highlights of prescribing information. www.gilead.com/~/media/Files/pdfs/medicines/liver-disease/harvoni/harvoni_pi.pdf. Accessed February 15, 2015.

9. Viekira Pak^™: highlights of prescribing information. www.rxabbvie.com/pdf/viekirapak_pi.pdf. Accessed February 15, 2015.

10. Indolfi G, Resti M. Perinatal transmission of hepatitis C virus infection. J Med Virol. 2009;81(5):8836-843.

11. Mast EE, Hwang LY, Seto DS, et al. Risk factors for perinatal transmission of hepatitis C virus (HCV) and the natural history of HCV infection acquired in infancy. J Infect Dis. 2005;192:1880-1889. 

Hepatitis C virus (HCV) infection is reported in 0.05% to 0.36% of children in developed nations.1 Since improved screening of donor blood and blood products began in the 1990s, vertical transmission has become the primary cause of HCV infection in children.1-5 As many as 4,000 new cases of pediatric HCV infection may develop each year in the United States.6

At present, no clear interventions exist to prevent mother-to-child transmission (MTCT) of HCV.^4,7 No HCV vaccine is yet available, and most current antiviral therapies are not considered safe for pregnant patients: ribavirin and interferon α, for example, are in pregnancy categories X and C, respectively.^3,7 (See “Safer HCV Treatment Options in Pregnancy?”^8,9) Some might argue that HCV infection is reported in only 1% to 2% of pregnant women in industrialized countries⁷ and that the rate of MTCT is low at 2% to 10%.^3-5 Nevertheless, researchers maintain that HCV during pregnancy is a “neglected condition” and call for substantial improvements in public health response to affected patients.^3,4 Awareness of risk factors for MTCT is essential.

Vertical transmission is believed to be limited to women with detectable viral load,^3,4,10 and the risk grows with increasing maternal viremia (ie, HCV RNA > 10⁵ copies/mL¹). Risk for MTCT is heightened in women who are coinfected with HIV,^3,11 with one systematic review showing a 10.8% vertical transmission risk among coinfected women, versus 5.8% among those with HCV infection alone.² Transmission risk is increased in mothers with a history of IV drug use or a sexual partner infected with HCV.¹⁰ Perinatal procedures that expose the infant to HCV-infected maternal blood (eg, episiotomy, internal fetal monitoring) also elevate MTCT risk.^3,7,1011

In an effort to identify strategies to reduce vertical transmission of HCV, researchers for the US Preventive Services Task Force (USPSTF)⁶ performed a review of studies on the impact of mode of delivery, breastfeeding practices, and other factors on MTCT. No difference in HCV transmission was found in vaginal vs cesarean deliveries; however, in one good-quality study, a higher MTCT rate was found among cases involving prolonged duration of ruptured membranes (> 6 h before delivery).

Continue for association between breastfeeding and HCV >>

The USPSTF researchers found no association between breastfeeding and HCV transmission,⁶ although the CDC recommends against the practice in HCV-infected women whose nipples are cracked or bleeding.⁵ Of note, both breastfeeding and cesarean delivery are associated with increased transmission risk among HCV/HIV coinfected women.⁷ HCV genotype is reported to have little impact on MTCT.^1,10

Until the development of an effective HCV vaccine and safe, effective HCV treatment for pregnant patients,^1,3 strategies to interrupt MTCT represent our best hope to protect children against HCV infection.

REFERENCES
1. Yeung CY, Lee HC, Chan WT, et al. Vertical transmission of hepatitis C virus: current knowledge and perspectives. World J Hepatol. 2014;6(9):643-651.

2. Benova L, Mohamoud YA, Calvert C, Abu-Raddad LJ. Vertical transmission of hepatitis C virus: systematic review and meta-analysis. Clin Infect Dis. 2014;59(6):765-773.

3. Prasad MR, Honegger JR. Hepatitis C virus in pregnancy. Am J Perinatol. 2013;30(2):149-159.

4. Arshad M, El-Kamary SS, Jhaveri R. Hepatitis C virus infection during pregnancy and the newborn period: are they opportunities for treatment? J Viral Hepat. 2011;18(4):229-236.

5. CDC. Hepatitis C FAQs for health professionals. www.cdc.gov/hepatitis/HCV/HCVfaq.htm. Accessed February 9, 2015.

6. Cottrell EB, Chou R, Wasson N, et al. Reducing risk for mother-to-infant transmission of hepatitis C virus: a systematic review for the US Preventive Services Task Force. Ann Intern Med. 2013;158(2):109-113.

7. Tosone G, Maraolo AE, Mascolo S, et al. Vertical hepatitis C virus transmission: main questions and answers. World J Hepatol. 2014;6(8):538-548.

8. Harvoni^®: highlights of prescribing information. www.gilead.com/~/media/Files/pdfs/medicines/liver-disease/harvoni/harvoni_pi.pdf. Accessed February 15, 2015.

9. Viekira Pak^™: highlights of prescribing information. www.rxabbvie.com/pdf/viekirapak_pi.pdf. Accessed February 15, 2015.

10. Indolfi G, Resti M. Perinatal transmission of hepatitis C virus infection. J Med Virol. 2009;81(5):8836-843.

11. Mast EE, Hwang LY, Seto DS, et al. Risk factors for perinatal transmission of hepatitis C virus (HCV) and the natural history of HCV infection acquired in infancy. J Infect Dis. 2005;192:1880-1889. 

The highest risk for readmission and death after pneumonia is in the early days following discharge, but although the risk diminishes after that time, it doesn’t disappear, say researchers from Columbia University in New York City; Yale-New Haven Hospital and Yale University, both in New Haven, Connecticut; and Harvard School of Public Health in Boston, Massachusetts. Findings from their study of > 3 million patients aged ≥ 65 years with heart failure, acute myocardial infarction (AMI), and pneumonia suggest that patients “should remain vigilant for deterioration in health well beyond the first month after hospital discharge.”

Related: HIV-Negative Patients at Risk for Pneumocystosis

Their study was designed to define trajectories of risk for a full year after hospitalization. Those risks varied according to diagnosis. For instance, for the risk of first readmission to decline 50% for pneumonia took 25 days and for risk of death to decline 50% took 10 days. By contrast, risk of readmission declined 50% by day 38 for heart failure and by day 13 for AMI. The number of days required for the daily change in risk of first readmission to decline 95% from its maximum daily decline was 45 days for pneumonia, 38 for AMI, and 45 for heart failure.

Related: Special Operations Flight Training: An Atypical Presentation of Aspiration Pneumonia

Daily risks of first readmission and death reached plateaus of minimal day-to-day change by 7 weeks after hospitalization for all 3 conditions. A key finding, the researchers say, is the fact that patients remain at increased risk of acute health events for much longer than the amount of time for which they are at highest risk of death. Depending on the diagnosis, the risk of readmission declined 50% within 13 to 39 days, whereas a similar decline in risk of death required only 6 to 12 days. Such information, the researchers note, can help hospitals better align preventive interventions with the periods of greatest risk.

Source
Dharmarajan K, Hsieh AF, Kulkarni VT, et al. BMJ. 2015;350:h411.
doi: 10.1136/bmj.h411.

The highest risk for readmission and death after pneumonia is in the early days following discharge, but although the risk diminishes after that time, it doesn’t disappear, say researchers from Columbia University in New York City; Yale-New Haven Hospital and Yale University, both in New Haven, Connecticut; and Harvard School of Public Health in Boston, Massachusetts. Findings from their study of > 3 million patients aged ≥ 65 years with heart failure, acute myocardial infarction (AMI), and pneumonia suggest that patients “should remain vigilant for deterioration in health well beyond the first month after hospital discharge.”

Related: HIV-Negative Patients at Risk for Pneumocystosis

Their study was designed to define trajectories of risk for a full year after hospitalization. Those risks varied according to diagnosis. For instance, for the risk of first readmission to decline 50% for pneumonia took 25 days and for risk of death to decline 50% took 10 days. By contrast, risk of readmission declined 50% by day 38 for heart failure and by day 13 for AMI. The number of days required for the daily change in risk of first readmission to decline 95% from its maximum daily decline was 45 days for pneumonia, 38 for AMI, and 45 for heart failure.

Related: Special Operations Flight Training: An Atypical Presentation of Aspiration Pneumonia

Daily risks of first readmission and death reached plateaus of minimal day-to-day change by 7 weeks after hospitalization for all 3 conditions. A key finding, the researchers say, is the fact that patients remain at increased risk of acute health events for much longer than the amount of time for which they are at highest risk of death. Depending on the diagnosis, the risk of readmission declined 50% within 13 to 39 days, whereas a similar decline in risk of death required only 6 to 12 days. Such information, the researchers note, can help hospitals better align preventive interventions with the periods of greatest risk.

Source
Dharmarajan K, Hsieh AF, Kulkarni VT, et al. BMJ. 2015;350:h411.
doi: 10.1136/bmj.h411.

The highest risk for readmission and death after pneumonia is in the early days following discharge, but although the risk diminishes after that time, it doesn’t disappear, say researchers from Columbia University in New York City; Yale-New Haven Hospital and Yale University, both in New Haven, Connecticut; and Harvard School of Public Health in Boston, Massachusetts. Findings from their study of > 3 million patients aged ≥ 65 years with heart failure, acute myocardial infarction (AMI), and pneumonia suggest that patients “should remain vigilant for deterioration in health well beyond the first month after hospital discharge.”

Related: HIV-Negative Patients at Risk for Pneumocystosis

Their study was designed to define trajectories of risk for a full year after hospitalization. Those risks varied according to diagnosis. For instance, for the risk of first readmission to decline 50% for pneumonia took 25 days and for risk of death to decline 50% took 10 days. By contrast, risk of readmission declined 50% by day 38 for heart failure and by day 13 for AMI. The number of days required for the daily change in risk of first readmission to decline 95% from its maximum daily decline was 45 days for pneumonia, 38 for AMI, and 45 for heart failure.

Related: Special Operations Flight Training: An Atypical Presentation of Aspiration Pneumonia

Daily risks of first readmission and death reached plateaus of minimal day-to-day change by 7 weeks after hospitalization for all 3 conditions. A key finding, the researchers say, is the fact that patients remain at increased risk of acute health events for much longer than the amount of time for which they are at highest risk of death. Depending on the diagnosis, the risk of readmission declined 50% within 13 to 39 days, whereas a similar decline in risk of death required only 6 to 12 days. Such information, the researchers note, can help hospitals better align preventive interventions with the periods of greatest risk.

Source
Dharmarajan K, Hsieh AF, Kulkarni VT, et al. BMJ. 2015;350:h411.
doi: 10.1136/bmj.h411.