The rate of obstetric anal sphincter injury (OASIS) is approximately 4.4% of vaginal deliveries, with 3.3% 3rd-degree tears and 1.1% 4th-degree tears.¹ In the United States in 2019 there were 3,745,540 births—a 31.7% rate of cesarean delivery (CD) and a 68.3% rate of vaginal delivery—resulting in approximately 112,600 births with OASIS.² A meta-analysis reported that, among 716,031 vaginal births, the risk factors for OASIS included: forceps delivery (relative risk [RR], 3.15), midline episiotomy (RR, 2.88), occiput posterior fetal position (RR, 2.73), vacuum delivery (RR, 2.60), Asian race (RR, 1.87), primiparity (RR, 1.59), mediolateral episiotomy (RR, 1.55), augmentation of labor (RR, 1.46), and epidural anesthesia (RR, 1.21).³ OASIS is associated with an increased risk for developing postpartum perineal pain, anal incontinence, dyspareunia, and wound breakdown.⁴ Complications following OASIS repair can trigger many follow-up appointments to assess wound healing and provide physical therapy.

This editorial review focuses on evolving recommendations for preventing and repairing OASIS.

The optimal cutting angle for a mediolateral episiotomy is 60 degrees from the midline

For spontaneous vaginal delivery, a policy of restricted episiotomy reduces the risk of OASIS by approximately 30%.⁵ With an operative vaginal delivery, especially forceps delivery of a large fetus in the occiput posterior position, a mediolateral episiotomy may help to reduce the risk of OASIS, although there are minimal data from clinical trials to support this practice. In one clinical trial, 407 women were randomly assigned to either a mediolateral or midline episiotomy.⁶ Approximately 25% of the births in both groups were operative deliveries. The mediolateral episiotomy began in the posterior midline of the vaginal introitus and was carried to the right side of the anal sphincter for 3 cm to 4 cm. The midline episiotomy began in the posterior midline of the vagina and was carried 2 cm to 3 cm into the midline perineal tissue. In the women having a midline or mediolateral episiotomy, a 4th-degree tear occurred in 5.5% and 0.4% of births, respectively. For the midline or mediolateral episiotomy, a third-degree tear occurred in 18.4% and 8.6%, respectively. In a prospective cohort study of 1,302 women with an episiotomy and vaginal birth, the rate of OASIS associated with midline or mediolateral episiotomy was 14.8% and 7%, respectively (P<.05).⁷ In this study, the operative vaginal delivery rate was 11.6% and 15.2% for the women in the midline and mediolateral groups, respectively.

The angle of the mediolateral episiotomy may influence the rate of OASIS and persistent postpartum perineal pain. In one study, 330 nulliparous women who were assessed to need a mediolateral episiotomy at delivery were randomized to an incision with a 40- or 60-degree angle from the midline.⁸ Prior to incision, a line was drawn on the skin to mark the course of the incision and then infiltrated with 10 mL of lignocaine. The fetal head was delivered with a Ritgen maneuver. The length of the episiotomy averaged 4 cm in both groups. After delivery, the angle of the episiotomy incision was reassessed. The episiotomy incision cut 60 degrees from the midline was measured on average to be 44 degrees from the midline after delivery of the newborn. Similarly, the incision cut at a 40-degree angle was measured to be 24 degrees from the midline after delivery. The rates of OASIS in the women who had a 40- and 60-degree angle incision were 5.5% and 2.4%, respectively (P = .16).

Continue to: Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair...

Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair

Many experts recommend one dose of a prophylactic antibiotic prior to, or during, OASIS repair in order to reduce the risk of wound complications. In a trial 147 women with OASIS were randomly assigned to receive one dose of a second-generation cephalosporin (cefotetan or cefoxitin) with extended anaerobic coverage or a placebo just before repair of the laceration.⁹ At 2 weeks postpartum, perineal wound complications were significantly lower in women receiving one dose of prophylactic antibiotic with extended anaerobe coverage compared with placebo—8.2% and 24.1%, respectively (P = .037). Additionally, at 2 weeks postpartum, purulent wound discharge was significantly lower in women receiving antibiotic versus placebo, 4% and 17%, respectively (P = .036). Experts writing for the Society of Obstetricians and Gynaecologists of Canada also recommend one dose of cefotetan or cefoxitin.¹⁰ Extended anaerobic coverage also can be achieved by administering a single dose of BOTH cefazolin 2 g by intravenous (IV) infusion PLUS metronidazole 500 mg by IV infusion or oral medication.¹¹ For women with severe penicillin allergy, a recommended regimen is gentamicin 5 mg/kg plus clindamycin 900 mg by IV infusion.¹¹ There is evidence that for colorectal or hysterectomy surgery, expanding prophylactic antibiotic coverage of anaerobes with cefazolin PLUS metronidazole significantly reduces postoperative surgical site infection.^12,13 Following an OASIS repair, wound breakdown is a catastrophic problem that may take many months to resolve. Administration of a prophylactic antibiotic with extended coverage of anaerobes may help to prevent wound breakdown.

Prioritize identifying and separately repairing the internal anal sphincter

The internal anal sphincter is a smooth muscle that runs along the outside of the rectal wall and thickens into a sphincter toward the anal canal. The internal anal sphincter is thin and grey-white in appearance, like a veil. By contrast, the external anal sphincter is a thick band of red striated muscle tissue. In one study of 3,333 primiparous women with OASIS, an internal anal sphincter injury was detected in 33% of cases.¹⁴ In this large cohort, the rate of internal anal sphincter injury with a 3A tear, a 3B tear, a complete tear of the external sphincter and a 4th-degree perineal tear was 22%, 23%, 42%, and 71%, respectively. The internal anal sphincter is important for maintaining rectal continence and is estimated to contribute 50% to 85% of resting anal tone.¹⁵ If injury to the internal anal sphincter is detected at a birth with an OASIS, it is important to separately repair the internal anal sphincter to reduce the risk of postpartum rectal incontinence.¹⁶

Polyglactin 910 vs Polydioxanone (PDS) Suture—Is PDS the winner?

Polyglactin 910 (Vicryl) is a braided suture that is absorbed within 56 to 70 days. Polydioxanone suture is a long-lasting monofilament suture that is absorbed within 200 days. Many colorectal surgeons and urogynecologists prefer PDS suture for the repair of both the internal and external anal sphincters.¹⁶ Authors of one randomized trial of OASIS repair with Vicryl or PDS suture did not report significant differences in most clinical outcomes.¹⁷ However, in this study, anal endosonographic imaging of the internal and external anal sphincter demonstrated more internal sphincter defects but not external sphincter defects when the repair was performed with Vicryl rather than PDS. The investigators concluded that comprehensive training of the surgeon, not choice of suture, is probably the most important factor in achieving a good OASIS repair. However, because many subspecialists favor PDS suture for sphincter repair, specialists in obstetrics and gynecology should consider this option.

Continue to: Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

The breakdown of an OASIS repair is an obstetric catastrophe with complications that can last many months and sometimes stretch into years. The best approach to a perineal laceration wound breakdown remains controversial. It is optimal if all patients with a wound breakdown can be offered an early secondary repair or healing by secondary intention, permitting the patient to select the best approach for their specific situation.

As noted by the pioneers of early repair of episiotomy dehiscence, Drs. Hankins, Haugh, Gilstrap, Ramin, and others,^18-20 conventional doctrine is that an episiotomy repair dehiscence should be managed expectantly, allowing healing by secondary intention and delaying repair of the sphincters for a minimum of 3 to 4 months.²¹ However, many small case-series report that early secondary repair of a perineal laceration wound breakdown is possible following multiple days of wound preparation prior to the repair, good surgical technique and diligent postoperative follow-up care. One large case series reported on 72 women with complete perineal wound dehiscence who had early secondary repair.²² The median time to complete wound healing following early repair was 28 days. About 36% of the patients had one or more complications, including skin dehiscence, granuloma formation, perineal pain, and sinus formation. A pilot randomized trial reported that, compared with expectant management of a wound breakdown, early repair resulted in a shorter time to wound healing.²³

Early repair of perineal wound dehiscence often involves a course of care that extends over multiple weeks. As an example, following a vaginal birth with OASIS and immediate repair, the patient is often discharged from the hospital to home on postpartum day 3. The wound breakdown often is detected between postpartum days 6 to 10. If early secondary repair is selected as the best treatment, 1 to 6 days of daily debridement of the wound is needed to prepare the wound for early secondary repair. The daily debridement required to prepare the wound for early repair is often performed in the hospital, potentially disrupting early mother-newborn bonding. Following the repair, the patient is observed in the hospital for 1 to 3 days and then discharged home with daily wound care and multiple follow-up visits to monitor wound healing. Pelvic floor physical therapy may be initiated when the wound is healed. The prolonged process required for early secondary repair may be best undertaken by a subspecialty practice.²⁴

The surgical repair and postpartum care of OASIS continues to evolve. In your practice you should consider:

• performing a mediolateral episiotomy at a 60-degree angle to reduce the risk of OASIS in situations where there is a high risk of anal sphincter injury, such as in forceps delivery
• using one dose of a prophylactic antibiotic with extended anaerobic coverage, such as cefotetan or cefoxitin
• focus on identifying and separately repairing an internal anal sphincter injury
• using a long-lasting absorbable suture, such as PDS, to repair the internal and external anal sphincters
• ensuring that the patient with a dehiscence following an episiotomy or anal sphincter injury has access to early secondary repair. Standardizing your approach to the prevention and repair of anal sphincter injury will benefit the approximately 112,600 US women who experience OASIS each year. ●

The rate of obstetric anal sphincter injury (OASIS) is approximately 4.4% of vaginal deliveries, with 3.3% 3rd-degree tears and 1.1% 4th-degree tears.¹ In the United States in 2019 there were 3,745,540 births—a 31.7% rate of cesarean delivery (CD) and a 68.3% rate of vaginal delivery—resulting in approximately 112,600 births with OASIS.² A meta-analysis reported that, among 716,031 vaginal births, the risk factors for OASIS included: forceps delivery (relative risk [RR], 3.15), midline episiotomy (RR, 2.88), occiput posterior fetal position (RR, 2.73), vacuum delivery (RR, 2.60), Asian race (RR, 1.87), primiparity (RR, 1.59), mediolateral episiotomy (RR, 1.55), augmentation of labor (RR, 1.46), and epidural anesthesia (RR, 1.21).³ OASIS is associated with an increased risk for developing postpartum perineal pain, anal incontinence, dyspareunia, and wound breakdown.⁴ Complications following OASIS repair can trigger many follow-up appointments to assess wound healing and provide physical therapy.

This editorial review focuses on evolving recommendations for preventing and repairing OASIS.

The optimal cutting angle for a mediolateral episiotomy is 60 degrees from the midline

For spontaneous vaginal delivery, a policy of restricted episiotomy reduces the risk of OASIS by approximately 30%.⁵ With an operative vaginal delivery, especially forceps delivery of a large fetus in the occiput posterior position, a mediolateral episiotomy may help to reduce the risk of OASIS, although there are minimal data from clinical trials to support this practice. In one clinical trial, 407 women were randomly assigned to either a mediolateral or midline episiotomy.⁶ Approximately 25% of the births in both groups were operative deliveries. The mediolateral episiotomy began in the posterior midline of the vaginal introitus and was carried to the right side of the anal sphincter for 3 cm to 4 cm. The midline episiotomy began in the posterior midline of the vagina and was carried 2 cm to 3 cm into the midline perineal tissue. In the women having a midline or mediolateral episiotomy, a 4th-degree tear occurred in 5.5% and 0.4% of births, respectively. For the midline or mediolateral episiotomy, a third-degree tear occurred in 18.4% and 8.6%, respectively. In a prospective cohort study of 1,302 women with an episiotomy and vaginal birth, the rate of OASIS associated with midline or mediolateral episiotomy was 14.8% and 7%, respectively (P<.05).⁷ In this study, the operative vaginal delivery rate was 11.6% and 15.2% for the women in the midline and mediolateral groups, respectively.

The angle of the mediolateral episiotomy may influence the rate of OASIS and persistent postpartum perineal pain. In one study, 330 nulliparous women who were assessed to need a mediolateral episiotomy at delivery were randomized to an incision with a 40- or 60-degree angle from the midline.⁸ Prior to incision, a line was drawn on the skin to mark the course of the incision and then infiltrated with 10 mL of lignocaine. The fetal head was delivered with a Ritgen maneuver. The length of the episiotomy averaged 4 cm in both groups. After delivery, the angle of the episiotomy incision was reassessed. The episiotomy incision cut 60 degrees from the midline was measured on average to be 44 degrees from the midline after delivery of the newborn. Similarly, the incision cut at a 40-degree angle was measured to be 24 degrees from the midline after delivery. The rates of OASIS in the women who had a 40- and 60-degree angle incision were 5.5% and 2.4%, respectively (P = .16).

Continue to: Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair...

Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair

Many experts recommend one dose of a prophylactic antibiotic prior to, or during, OASIS repair in order to reduce the risk of wound complications. In a trial 147 women with OASIS were randomly assigned to receive one dose of a second-generation cephalosporin (cefotetan or cefoxitin) with extended anaerobic coverage or a placebo just before repair of the laceration.⁹ At 2 weeks postpartum, perineal wound complications were significantly lower in women receiving one dose of prophylactic antibiotic with extended anaerobe coverage compared with placebo—8.2% and 24.1%, respectively (P = .037). Additionally, at 2 weeks postpartum, purulent wound discharge was significantly lower in women receiving antibiotic versus placebo, 4% and 17%, respectively (P = .036). Experts writing for the Society of Obstetricians and Gynaecologists of Canada also recommend one dose of cefotetan or cefoxitin.¹⁰ Extended anaerobic coverage also can be achieved by administering a single dose of BOTH cefazolin 2 g by intravenous (IV) infusion PLUS metronidazole 500 mg by IV infusion or oral medication.¹¹ For women with severe penicillin allergy, a recommended regimen is gentamicin 5 mg/kg plus clindamycin 900 mg by IV infusion.¹¹ There is evidence that for colorectal or hysterectomy surgery, expanding prophylactic antibiotic coverage of anaerobes with cefazolin PLUS metronidazole significantly reduces postoperative surgical site infection.^12,13 Following an OASIS repair, wound breakdown is a catastrophic problem that may take many months to resolve. Administration of a prophylactic antibiotic with extended coverage of anaerobes may help to prevent wound breakdown.

Prioritize identifying and separately repairing the internal anal sphincter

The internal anal sphincter is a smooth muscle that runs along the outside of the rectal wall and thickens into a sphincter toward the anal canal. The internal anal sphincter is thin and grey-white in appearance, like a veil. By contrast, the external anal sphincter is a thick band of red striated muscle tissue. In one study of 3,333 primiparous women with OASIS, an internal anal sphincter injury was detected in 33% of cases.¹⁴ In this large cohort, the rate of internal anal sphincter injury with a 3A tear, a 3B tear, a complete tear of the external sphincter and a 4th-degree perineal tear was 22%, 23%, 42%, and 71%, respectively. The internal anal sphincter is important for maintaining rectal continence and is estimated to contribute 50% to 85% of resting anal tone.¹⁵ If injury to the internal anal sphincter is detected at a birth with an OASIS, it is important to separately repair the internal anal sphincter to reduce the risk of postpartum rectal incontinence.¹⁶

Polyglactin 910 vs Polydioxanone (PDS) Suture—Is PDS the winner?

Polyglactin 910 (Vicryl) is a braided suture that is absorbed within 56 to 70 days. Polydioxanone suture is a long-lasting monofilament suture that is absorbed within 200 days. Many colorectal surgeons and urogynecologists prefer PDS suture for the repair of both the internal and external anal sphincters.¹⁶ Authors of one randomized trial of OASIS repair with Vicryl or PDS suture did not report significant differences in most clinical outcomes.¹⁷ However, in this study, anal endosonographic imaging of the internal and external anal sphincter demonstrated more internal sphincter defects but not external sphincter defects when the repair was performed with Vicryl rather than PDS. The investigators concluded that comprehensive training of the surgeon, not choice of suture, is probably the most important factor in achieving a good OASIS repair. However, because many subspecialists favor PDS suture for sphincter repair, specialists in obstetrics and gynecology should consider this option.

Continue to: Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

The breakdown of an OASIS repair is an obstetric catastrophe with complications that can last many months and sometimes stretch into years. The best approach to a perineal laceration wound breakdown remains controversial. It is optimal if all patients with a wound breakdown can be offered an early secondary repair or healing by secondary intention, permitting the patient to select the best approach for their specific situation.

As noted by the pioneers of early repair of episiotomy dehiscence, Drs. Hankins, Haugh, Gilstrap, Ramin, and others,^18-20 conventional doctrine is that an episiotomy repair dehiscence should be managed expectantly, allowing healing by secondary intention and delaying repair of the sphincters for a minimum of 3 to 4 months.²¹ However, many small case-series report that early secondary repair of a perineal laceration wound breakdown is possible following multiple days of wound preparation prior to the repair, good surgical technique and diligent postoperative follow-up care. One large case series reported on 72 women with complete perineal wound dehiscence who had early secondary repair.²² The median time to complete wound healing following early repair was 28 days. About 36% of the patients had one or more complications, including skin dehiscence, granuloma formation, perineal pain, and sinus formation. A pilot randomized trial reported that, compared with expectant management of a wound breakdown, early repair resulted in a shorter time to wound healing.²³

Early repair of perineal wound dehiscence often involves a course of care that extends over multiple weeks. As an example, following a vaginal birth with OASIS and immediate repair, the patient is often discharged from the hospital to home on postpartum day 3. The wound breakdown often is detected between postpartum days 6 to 10. If early secondary repair is selected as the best treatment, 1 to 6 days of daily debridement of the wound is needed to prepare the wound for early secondary repair. The daily debridement required to prepare the wound for early repair is often performed in the hospital, potentially disrupting early mother-newborn bonding. Following the repair, the patient is observed in the hospital for 1 to 3 days and then discharged home with daily wound care and multiple follow-up visits to monitor wound healing. Pelvic floor physical therapy may be initiated when the wound is healed. The prolonged process required for early secondary repair may be best undertaken by a subspecialty practice.²⁴

The surgical repair and postpartum care of OASIS continues to evolve. In your practice you should consider:

• performing a mediolateral episiotomy at a 60-degree angle to reduce the risk of OASIS in situations where there is a high risk of anal sphincter injury, such as in forceps delivery
• using one dose of a prophylactic antibiotic with extended anaerobic coverage, such as cefotetan or cefoxitin
• focus on identifying and separately repairing an internal anal sphincter injury
• using a long-lasting absorbable suture, such as PDS, to repair the internal and external anal sphincters
• ensuring that the patient with a dehiscence following an episiotomy or anal sphincter injury has access to early secondary repair. Standardizing your approach to the prevention and repair of anal sphincter injury will benefit the approximately 112,600 US women who experience OASIS each year. ●

The rate of obstetric anal sphincter injury (OASIS) is approximately 4.4% of vaginal deliveries, with 3.3% 3rd-degree tears and 1.1% 4th-degree tears.¹ In the United States in 2019 there were 3,745,540 births—a 31.7% rate of cesarean delivery (CD) and a 68.3% rate of vaginal delivery—resulting in approximately 112,600 births with OASIS.² A meta-analysis reported that, among 716,031 vaginal births, the risk factors for OASIS included: forceps delivery (relative risk [RR], 3.15), midline episiotomy (RR, 2.88), occiput posterior fetal position (RR, 2.73), vacuum delivery (RR, 2.60), Asian race (RR, 1.87), primiparity (RR, 1.59), mediolateral episiotomy (RR, 1.55), augmentation of labor (RR, 1.46), and epidural anesthesia (RR, 1.21).³ OASIS is associated with an increased risk for developing postpartum perineal pain, anal incontinence, dyspareunia, and wound breakdown.⁴ Complications following OASIS repair can trigger many follow-up appointments to assess wound healing and provide physical therapy.

This editorial review focuses on evolving recommendations for preventing and repairing OASIS.

The optimal cutting angle for a mediolateral episiotomy is 60 degrees from the midline

For spontaneous vaginal delivery, a policy of restricted episiotomy reduces the risk of OASIS by approximately 30%.⁵ With an operative vaginal delivery, especially forceps delivery of a large fetus in the occiput posterior position, a mediolateral episiotomy may help to reduce the risk of OASIS, although there are minimal data from clinical trials to support this practice. In one clinical trial, 407 women were randomly assigned to either a mediolateral or midline episiotomy.⁶ Approximately 25% of the births in both groups were operative deliveries. The mediolateral episiotomy began in the posterior midline of the vaginal introitus and was carried to the right side of the anal sphincter for 3 cm to 4 cm. The midline episiotomy began in the posterior midline of the vagina and was carried 2 cm to 3 cm into the midline perineal tissue. In the women having a midline or mediolateral episiotomy, a 4th-degree tear occurred in 5.5% and 0.4% of births, respectively. For the midline or mediolateral episiotomy, a third-degree tear occurred in 18.4% and 8.6%, respectively. In a prospective cohort study of 1,302 women with an episiotomy and vaginal birth, the rate of OASIS associated with midline or mediolateral episiotomy was 14.8% and 7%, respectively (P<.05).⁷ In this study, the operative vaginal delivery rate was 11.6% and 15.2% for the women in the midline and mediolateral groups, respectively.

The angle of the mediolateral episiotomy may influence the rate of OASIS and persistent postpartum perineal pain. In one study, 330 nulliparous women who were assessed to need a mediolateral episiotomy at delivery were randomized to an incision with a 40- or 60-degree angle from the midline.⁸ Prior to incision, a line was drawn on the skin to mark the course of the incision and then infiltrated with 10 mL of lignocaine. The fetal head was delivered with a Ritgen maneuver. The length of the episiotomy averaged 4 cm in both groups. After delivery, the angle of the episiotomy incision was reassessed. The episiotomy incision cut 60 degrees from the midline was measured on average to be 44 degrees from the midline after delivery of the newborn. Similarly, the incision cut at a 40-degree angle was measured to be 24 degrees from the midline after delivery. The rates of OASIS in the women who had a 40- and 60-degree angle incision were 5.5% and 2.4%, respectively (P = .16).

Continue to: Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair...

Use a prophylactic antibiotic with extended coverage for anaerobes prior to or during your anal sphincter repair

Many experts recommend one dose of a prophylactic antibiotic prior to, or during, OASIS repair in order to reduce the risk of wound complications. In a trial 147 women with OASIS were randomly assigned to receive one dose of a second-generation cephalosporin (cefotetan or cefoxitin) with extended anaerobic coverage or a placebo just before repair of the laceration.⁹ At 2 weeks postpartum, perineal wound complications were significantly lower in women receiving one dose of prophylactic antibiotic with extended anaerobe coverage compared with placebo—8.2% and 24.1%, respectively (P = .037). Additionally, at 2 weeks postpartum, purulent wound discharge was significantly lower in women receiving antibiotic versus placebo, 4% and 17%, respectively (P = .036). Experts writing for the Society of Obstetricians and Gynaecologists of Canada also recommend one dose of cefotetan or cefoxitin.¹⁰ Extended anaerobic coverage also can be achieved by administering a single dose of BOTH cefazolin 2 g by intravenous (IV) infusion PLUS metronidazole 500 mg by IV infusion or oral medication.¹¹ For women with severe penicillin allergy, a recommended regimen is gentamicin 5 mg/kg plus clindamycin 900 mg by IV infusion.¹¹ There is evidence that for colorectal or hysterectomy surgery, expanding prophylactic antibiotic coverage of anaerobes with cefazolin PLUS metronidazole significantly reduces postoperative surgical site infection.^12,13 Following an OASIS repair, wound breakdown is a catastrophic problem that may take many months to resolve. Administration of a prophylactic antibiotic with extended coverage of anaerobes may help to prevent wound breakdown.

Prioritize identifying and separately repairing the internal anal sphincter

The internal anal sphincter is a smooth muscle that runs along the outside of the rectal wall and thickens into a sphincter toward the anal canal. The internal anal sphincter is thin and grey-white in appearance, like a veil. By contrast, the external anal sphincter is a thick band of red striated muscle tissue. In one study of 3,333 primiparous women with OASIS, an internal anal sphincter injury was detected in 33% of cases.¹⁴ In this large cohort, the rate of internal anal sphincter injury with a 3A tear, a 3B tear, a complete tear of the external sphincter and a 4th-degree perineal tear was 22%, 23%, 42%, and 71%, respectively. The internal anal sphincter is important for maintaining rectal continence and is estimated to contribute 50% to 85% of resting anal tone.¹⁵ If injury to the internal anal sphincter is detected at a birth with an OASIS, it is important to separately repair the internal anal sphincter to reduce the risk of postpartum rectal incontinence.¹⁶

Polyglactin 910 vs Polydioxanone (PDS) Suture—Is PDS the winner?

Polyglactin 910 (Vicryl) is a braided suture that is absorbed within 56 to 70 days. Polydioxanone suture is a long-lasting monofilament suture that is absorbed within 200 days. Many colorectal surgeons and urogynecologists prefer PDS suture for the repair of both the internal and external anal sphincters.¹⁶ Authors of one randomized trial of OASIS repair with Vicryl or PDS suture did not report significant differences in most clinical outcomes.¹⁷ However, in this study, anal endosonographic imaging of the internal and external anal sphincter demonstrated more internal sphincter defects but not external sphincter defects when the repair was performed with Vicryl rather than PDS. The investigators concluded that comprehensive training of the surgeon, not choice of suture, is probably the most important factor in achieving a good OASIS repair. However, because many subspecialists favor PDS suture for sphincter repair, specialists in obstetrics and gynecology should consider this option.

Continue to: Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

Can your patient access early secondary repair if they develop a perineal laceration wound breakdown?

The breakdown of an OASIS repair is an obstetric catastrophe with complications that can last many months and sometimes stretch into years. The best approach to a perineal laceration wound breakdown remains controversial. It is optimal if all patients with a wound breakdown can be offered an early secondary repair or healing by secondary intention, permitting the patient to select the best approach for their specific situation.

As noted by the pioneers of early repair of episiotomy dehiscence, Drs. Hankins, Haugh, Gilstrap, Ramin, and others,^18-20 conventional doctrine is that an episiotomy repair dehiscence should be managed expectantly, allowing healing by secondary intention and delaying repair of the sphincters for a minimum of 3 to 4 months.²¹ However, many small case-series report that early secondary repair of a perineal laceration wound breakdown is possible following multiple days of wound preparation prior to the repair, good surgical technique and diligent postoperative follow-up care. One large case series reported on 72 women with complete perineal wound dehiscence who had early secondary repair.²² The median time to complete wound healing following early repair was 28 days. About 36% of the patients had one or more complications, including skin dehiscence, granuloma formation, perineal pain, and sinus formation. A pilot randomized trial reported that, compared with expectant management of a wound breakdown, early repair resulted in a shorter time to wound healing.²³

Early repair of perineal wound dehiscence often involves a course of care that extends over multiple weeks. As an example, following a vaginal birth with OASIS and immediate repair, the patient is often discharged from the hospital to home on postpartum day 3. The wound breakdown often is detected between postpartum days 6 to 10. If early secondary repair is selected as the best treatment, 1 to 6 days of daily debridement of the wound is needed to prepare the wound for early secondary repair. The daily debridement required to prepare the wound for early repair is often performed in the hospital, potentially disrupting early mother-newborn bonding. Following the repair, the patient is observed in the hospital for 1 to 3 days and then discharged home with daily wound care and multiple follow-up visits to monitor wound healing. Pelvic floor physical therapy may be initiated when the wound is healed. The prolonged process required for early secondary repair may be best undertaken by a subspecialty practice.²⁴

The surgical repair and postpartum care of OASIS continues to evolve. In your practice you should consider:

• performing a mediolateral episiotomy at a 60-degree angle to reduce the risk of OASIS in situations where there is a high risk of anal sphincter injury, such as in forceps delivery
• using one dose of a prophylactic antibiotic with extended anaerobic coverage, such as cefotetan or cefoxitin
• focus on identifying and separately repairing an internal anal sphincter injury
• using a long-lasting absorbable suture, such as PDS, to repair the internal and external anal sphincters
• ensuring that the patient with a dehiscence following an episiotomy or anal sphincter injury has access to early secondary repair. Standardizing your approach to the prevention and repair of anal sphincter injury will benefit the approximately 112,600 US women who experience OASIS each year. ●

Cerebral palsy (CP) is the most common cause of severe neurodisability in children, and it occurs in about 2 to 3 per 1,000 births worldwide.¹ This nonprogressive disorder is characterized by symptoms that include spasticity, dystonia, choreoathetosis, and/or ataxia that are evident in the first few years of life. While many perinatal variables have been associated with CP, in most cases a specific cause is not identified.

Other neurodevelopmental disorders, such as intellectual disability, epilepsy, and autism spectrum disorder, are often associated with CP.² These other neurodevelopmental disorders are often genetic, and this has raised the question as to whether CP also might have a substantial genetic component, although this has not been investigated in any significant way until recently. This topic is of great interest to the obstetric community, given that CP often is attributed to obstetric events, including mismanagement of labor and delivery.

Emerging evidence of a genetic-CP association

In an article published recently in JAMA, Moreno-De-Luca and colleagues sought to determine the diagnostic yield of exome sequencing for CP.³ This large cross-sectional study included results of exome sequencing performed in 2 settings. The first setting was a commercial laboratory in which samples were sent for analysis due to a diagnosis of CP, primarily in children (n = 1,345) with a median age of 8.8 years. A second cohort, recruited from a neurodevelopmental disorders clinic at Geisinger, included primarily adults (n = 181) with a median age of 41.9 years.

As is standard in exome sequencing, results were considered likely causative if they were classified as pathogenic or likely pathogenic based on criteria of the American College of Genetics and Genomics. In the laboratory group, 32.7% (440 of 1,345) had a genetic cause of the CP identified, while in the clinic group, 10.5% (19 of 181) had a genetic etiology found. Although most of the identified genetic variants were de novo (that is, they arose in the affected individual and were not clearly inherited), some were inherited from carrier parents.³

A number of other recent studies also have investigated genetic causes of CP and similarly have reported that a substantial number of cases are genetic. Several studies that performed chromosomal microarray analysis in individuals with CP found deleterious copy number variants in 10% to 31% of cases.^4-6 Genomic variants detectable by exome sequencing have been reported in 15% to 20% of cases.³ In a recent study in Nature Genetics, researchers performed exome sequencing on 250 parent-child “trios” in which the child had CP, and they found that 14% of cases had an associated genetic variant that was thought to be causative.⁴ These studies all provide consistent evidence that a substantial proportion of CP cases are due to genetic causes.

Contributors to CP risk

Historically, CP was considered to occur largely as a result of perinatal anoxia. In 1862, the British orthopedic surgeon William John Little first reported an association between prematurity, asphyxia, difficult delivery, and CP in a paper presented to the Obstetrical Society of London.⁷ Subsequently, much effort has gone into the prevention of perinatal asphyxia and birth injury, although our ability to monitor fetal well-being remains limited. Nonreassuring fetal heart rate patterns are nonspecific and can occur for many reasons other than fetal asphyxia. Studies of electronic fetal monitoring have found that continuous monitoring primarily leads to an increase in cesarean delivery with no decrease in CP or infant mortality.⁸

While some have attributed this to failure to accurately interpret the fetal heart rate tracing, it also may be because a substantial number of CP cases are due to genetic and other causes, and that very few in fact result from preventable intrapartum injury.

The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics agree that knowledge gaps preclude definitive determination that a given case of neonatal encephalopathy is attributable to an acute intrapartum event, and they provide criteria that must be fulfilled to establish a reasonable causal link between an intrapartum event and subsequent long-term neurologic disability.⁹ However, there continues to be a belief in the medical, scientific, and lay communities that birth asphyxia, secondary to adverse intrapartum events, is the leading cause of CP. A “brain-damaged infant” remains one of the most common malpractice claims, and birth injury one of the highest paid claims. Such claims generally allege that intrapartum asphyxia has caused long-term neurologic sequelae, including CP.

While it is true that prematurity, infection, hypoxia-ischemia, and pre- and perinatal stroke all have been implicated as contributing to CP risk, large population-based studies have shown that birth asphyxia accounts for less than 12% of CP cases.¹⁰ Specifically, recent data indicate that acute intrapartum hypoxia-ischemia occurs only in about 6% of CP cases. In other words, it does occur and may contribute to some cases, but this is likely a smaller percent than previously thought, and genetic factors now appear to be far more significant contributors.¹¹

Continue to: Exploring a genetic etiology...

In considering the etiologies of CP, it is important to note that 21% to 40% of individuals with CP have an associated congenital anomaly, suggesting a genetic origin in at least some individuals. Moreover, a 40% heritability has been estimated in CP, which is comparable to the heritability rate for autism spectrum disorders.¹²

In the recent study by Moreno-De-Luca and colleagues, some of the gene variants detected were previously associated with other forms of neurodevelopmental disability, such as epilepsy and autism spectrum disorder.³ Many individuals in the study cohort were found to have multiple neurologic comorbidities, for example, CP as well as epilepsy, autism spectrum disorder, and/or intellectual disability. The presence of these additional comorbidities increased the likelihood of finding a genetic cause; the authors found that the diagnostic yield ranged from 11.2% with isolated CP to 32.9% with all 3 comorbidities. The yield was highest with CP and intellectual disability and CP with all 3 comorbidities. A few genes were particularly common, and some were reported previously in association with CP and/or other neurodevelopmental disorders. In some patients, variants were found in genes or gene regions associated with disorders that do not frequently include CP, such as Rett syndrome.³

Implications for ObGyns

The data from the study by Moreno-De-Luca and colleagues are interesting and relevant to pediatricians, neurologists, and geneticists, as well as obstetricians. Understanding the cause of any disease or disorder improves care, including counseling regarding the cause, the appropriate interventions or therapy, and in some families, the recurrence risk in another pregnancy. The treatment for CP has not changed significantly in many years. Increasingly, detection of an underlying genetic cause can guide precision treatments; thus, the detection of specific gene variants allows a targeted approach to therapy.

Identification of a genetic cause also can significantly impact recurrence risk counseling and prenatal diagnosis options in another pregnancy. In general, the empiric recurrence risk of CP is quoted as 1% to 2%,¹³ and with de novo variants this does not change. However, with inherited variants the recurrence risk in future children is substantially higher. While 72% of the genetic variants associated with CP in the Moreno-De-Luca study were de novo with a low recurrence risk, in the other 28% the mode of inheritance indicated a substantial risk of recurrence (25%–50%) in another pregnancy.³ Detecting such causative variant(s) allows not only accurate counseling about recurrence risk but also preimplantation genetic testing or prenatal diagnosis when recurrence risk is high.

In the field of obstetrics, the debate about the etiology of CP is important largely due to the medicolegal implications. Patient-oriented information on the internet often states that CP is caused by damage to the child’s brain just before, during, or soon after birth, supporting potential blame of those providing care during those times. Patient-oriented websites regarding CP do not list genetic disorders among the causes but rather include primarily environmental factors, such as prematurity, low birth weight, in utero infections, anoxia or other brain injury, or perinatal stroke. Even the Centers for Disease Control and Prevention website lists brain damage as the primary etiology of CP.¹⁴ Hopefully, these new data will increase a broader understanding of this condition.

Exome sequencing is now recommended as a first-tier test for individuals with many neurodevelopmental disorders, including epilepsy, intellectual disability, and autism spectrum disorder.¹⁵ However, comprehensive genetic testing is not typically recommended or performed in cases of CP. Based on recent data, including the report by Moreno-De-Luca and colleagues, it would seem that CP should be added to the list of disorders for which exome sequencing is ordered, given the similar prevalence and diagnostic yield. ●

Cerebral palsy (CP) is the most common cause of severe neurodisability in children, and it occurs in about 2 to 3 per 1,000 births worldwide.¹ This nonprogressive disorder is characterized by symptoms that include spasticity, dystonia, choreoathetosis, and/or ataxia that are evident in the first few years of life. While many perinatal variables have been associated with CP, in most cases a specific cause is not identified.

Other neurodevelopmental disorders, such as intellectual disability, epilepsy, and autism spectrum disorder, are often associated with CP.² These other neurodevelopmental disorders are often genetic, and this has raised the question as to whether CP also might have a substantial genetic component, although this has not been investigated in any significant way until recently. This topic is of great interest to the obstetric community, given that CP often is attributed to obstetric events, including mismanagement of labor and delivery.

Emerging evidence of a genetic-CP association

In an article published recently in JAMA, Moreno-De-Luca and colleagues sought to determine the diagnostic yield of exome sequencing for CP.³ This large cross-sectional study included results of exome sequencing performed in 2 settings. The first setting was a commercial laboratory in which samples were sent for analysis due to a diagnosis of CP, primarily in children (n = 1,345) with a median age of 8.8 years. A second cohort, recruited from a neurodevelopmental disorders clinic at Geisinger, included primarily adults (n = 181) with a median age of 41.9 years.

As is standard in exome sequencing, results were considered likely causative if they were classified as pathogenic or likely pathogenic based on criteria of the American College of Genetics and Genomics. In the laboratory group, 32.7% (440 of 1,345) had a genetic cause of the CP identified, while in the clinic group, 10.5% (19 of 181) had a genetic etiology found. Although most of the identified genetic variants were de novo (that is, they arose in the affected individual and were not clearly inherited), some were inherited from carrier parents.³

A number of other recent studies also have investigated genetic causes of CP and similarly have reported that a substantial number of cases are genetic. Several studies that performed chromosomal microarray analysis in individuals with CP found deleterious copy number variants in 10% to 31% of cases.^4-6 Genomic variants detectable by exome sequencing have been reported in 15% to 20% of cases.³ In a recent study in Nature Genetics, researchers performed exome sequencing on 250 parent-child “trios” in which the child had CP, and they found that 14% of cases had an associated genetic variant that was thought to be causative.⁴ These studies all provide consistent evidence that a substantial proportion of CP cases are due to genetic causes.

Contributors to CP risk

Historically, CP was considered to occur largely as a result of perinatal anoxia. In 1862, the British orthopedic surgeon William John Little first reported an association between prematurity, asphyxia, difficult delivery, and CP in a paper presented to the Obstetrical Society of London.⁷ Subsequently, much effort has gone into the prevention of perinatal asphyxia and birth injury, although our ability to monitor fetal well-being remains limited. Nonreassuring fetal heart rate patterns are nonspecific and can occur for many reasons other than fetal asphyxia. Studies of electronic fetal monitoring have found that continuous monitoring primarily leads to an increase in cesarean delivery with no decrease in CP or infant mortality.⁸

While some have attributed this to failure to accurately interpret the fetal heart rate tracing, it also may be because a substantial number of CP cases are due to genetic and other causes, and that very few in fact result from preventable intrapartum injury.

The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics agree that knowledge gaps preclude definitive determination that a given case of neonatal encephalopathy is attributable to an acute intrapartum event, and they provide criteria that must be fulfilled to establish a reasonable causal link between an intrapartum event and subsequent long-term neurologic disability.⁹ However, there continues to be a belief in the medical, scientific, and lay communities that birth asphyxia, secondary to adverse intrapartum events, is the leading cause of CP. A “brain-damaged infant” remains one of the most common malpractice claims, and birth injury one of the highest paid claims. Such claims generally allege that intrapartum asphyxia has caused long-term neurologic sequelae, including CP.

While it is true that prematurity, infection, hypoxia-ischemia, and pre- and perinatal stroke all have been implicated as contributing to CP risk, large population-based studies have shown that birth asphyxia accounts for less than 12% of CP cases.¹⁰ Specifically, recent data indicate that acute intrapartum hypoxia-ischemia occurs only in about 6% of CP cases. In other words, it does occur and may contribute to some cases, but this is likely a smaller percent than previously thought, and genetic factors now appear to be far more significant contributors.¹¹

Continue to: Exploring a genetic etiology...

In considering the etiologies of CP, it is important to note that 21% to 40% of individuals with CP have an associated congenital anomaly, suggesting a genetic origin in at least some individuals. Moreover, a 40% heritability has been estimated in CP, which is comparable to the heritability rate for autism spectrum disorders.¹²

In the recent study by Moreno-De-Luca and colleagues, some of the gene variants detected were previously associated with other forms of neurodevelopmental disability, such as epilepsy and autism spectrum disorder.³ Many individuals in the study cohort were found to have multiple neurologic comorbidities, for example, CP as well as epilepsy, autism spectrum disorder, and/or intellectual disability. The presence of these additional comorbidities increased the likelihood of finding a genetic cause; the authors found that the diagnostic yield ranged from 11.2% with isolated CP to 32.9% with all 3 comorbidities. The yield was highest with CP and intellectual disability and CP with all 3 comorbidities. A few genes were particularly common, and some were reported previously in association with CP and/or other neurodevelopmental disorders. In some patients, variants were found in genes or gene regions associated with disorders that do not frequently include CP, such as Rett syndrome.³

Implications for ObGyns

The data from the study by Moreno-De-Luca and colleagues are interesting and relevant to pediatricians, neurologists, and geneticists, as well as obstetricians. Understanding the cause of any disease or disorder improves care, including counseling regarding the cause, the appropriate interventions or therapy, and in some families, the recurrence risk in another pregnancy. The treatment for CP has not changed significantly in many years. Increasingly, detection of an underlying genetic cause can guide precision treatments; thus, the detection of specific gene variants allows a targeted approach to therapy.

Identification of a genetic cause also can significantly impact recurrence risk counseling and prenatal diagnosis options in another pregnancy. In general, the empiric recurrence risk of CP is quoted as 1% to 2%,¹³ and with de novo variants this does not change. However, with inherited variants the recurrence risk in future children is substantially higher. While 72% of the genetic variants associated with CP in the Moreno-De-Luca study were de novo with a low recurrence risk, in the other 28% the mode of inheritance indicated a substantial risk of recurrence (25%–50%) in another pregnancy.³ Detecting such causative variant(s) allows not only accurate counseling about recurrence risk but also preimplantation genetic testing or prenatal diagnosis when recurrence risk is high.

In the field of obstetrics, the debate about the etiology of CP is important largely due to the medicolegal implications. Patient-oriented information on the internet often states that CP is caused by damage to the child’s brain just before, during, or soon after birth, supporting potential blame of those providing care during those times. Patient-oriented websites regarding CP do not list genetic disorders among the causes but rather include primarily environmental factors, such as prematurity, low birth weight, in utero infections, anoxia or other brain injury, or perinatal stroke. Even the Centers for Disease Control and Prevention website lists brain damage as the primary etiology of CP.¹⁴ Hopefully, these new data will increase a broader understanding of this condition.

Exome sequencing is now recommended as a first-tier test for individuals with many neurodevelopmental disorders, including epilepsy, intellectual disability, and autism spectrum disorder.¹⁵ However, comprehensive genetic testing is not typically recommended or performed in cases of CP. Based on recent data, including the report by Moreno-De-Luca and colleagues, it would seem that CP should be added to the list of disorders for which exome sequencing is ordered, given the similar prevalence and diagnostic yield. ●

Cerebral palsy (CP) is the most common cause of severe neurodisability in children, and it occurs in about 2 to 3 per 1,000 births worldwide.¹ This nonprogressive disorder is characterized by symptoms that include spasticity, dystonia, choreoathetosis, and/or ataxia that are evident in the first few years of life. While many perinatal variables have been associated with CP, in most cases a specific cause is not identified.

Other neurodevelopmental disorders, such as intellectual disability, epilepsy, and autism spectrum disorder, are often associated with CP.² These other neurodevelopmental disorders are often genetic, and this has raised the question as to whether CP also might have a substantial genetic component, although this has not been investigated in any significant way until recently. This topic is of great interest to the obstetric community, given that CP often is attributed to obstetric events, including mismanagement of labor and delivery.

Emerging evidence of a genetic-CP association

In an article published recently in JAMA, Moreno-De-Luca and colleagues sought to determine the diagnostic yield of exome sequencing for CP.³ This large cross-sectional study included results of exome sequencing performed in 2 settings. The first setting was a commercial laboratory in which samples were sent for analysis due to a diagnosis of CP, primarily in children (n = 1,345) with a median age of 8.8 years. A second cohort, recruited from a neurodevelopmental disorders clinic at Geisinger, included primarily adults (n = 181) with a median age of 41.9 years.

As is standard in exome sequencing, results were considered likely causative if they were classified as pathogenic or likely pathogenic based on criteria of the American College of Genetics and Genomics. In the laboratory group, 32.7% (440 of 1,345) had a genetic cause of the CP identified, while in the clinic group, 10.5% (19 of 181) had a genetic etiology found. Although most of the identified genetic variants were de novo (that is, they arose in the affected individual and were not clearly inherited), some were inherited from carrier parents.³

A number of other recent studies also have investigated genetic causes of CP and similarly have reported that a substantial number of cases are genetic. Several studies that performed chromosomal microarray analysis in individuals with CP found deleterious copy number variants in 10% to 31% of cases.^4-6 Genomic variants detectable by exome sequencing have been reported in 15% to 20% of cases.³ In a recent study in Nature Genetics, researchers performed exome sequencing on 250 parent-child “trios” in which the child had CP, and they found that 14% of cases had an associated genetic variant that was thought to be causative.⁴ These studies all provide consistent evidence that a substantial proportion of CP cases are due to genetic causes.

Contributors to CP risk

Historically, CP was considered to occur largely as a result of perinatal anoxia. In 1862, the British orthopedic surgeon William John Little first reported an association between prematurity, asphyxia, difficult delivery, and CP in a paper presented to the Obstetrical Society of London.⁷ Subsequently, much effort has gone into the prevention of perinatal asphyxia and birth injury, although our ability to monitor fetal well-being remains limited. Nonreassuring fetal heart rate patterns are nonspecific and can occur for many reasons other than fetal asphyxia. Studies of electronic fetal monitoring have found that continuous monitoring primarily leads to an increase in cesarean delivery with no decrease in CP or infant mortality.⁸

While some have attributed this to failure to accurately interpret the fetal heart rate tracing, it also may be because a substantial number of CP cases are due to genetic and other causes, and that very few in fact result from preventable intrapartum injury.

The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics agree that knowledge gaps preclude definitive determination that a given case of neonatal encephalopathy is attributable to an acute intrapartum event, and they provide criteria that must be fulfilled to establish a reasonable causal link between an intrapartum event and subsequent long-term neurologic disability.⁹ However, there continues to be a belief in the medical, scientific, and lay communities that birth asphyxia, secondary to adverse intrapartum events, is the leading cause of CP. A “brain-damaged infant” remains one of the most common malpractice claims, and birth injury one of the highest paid claims. Such claims generally allege that intrapartum asphyxia has caused long-term neurologic sequelae, including CP.

While it is true that prematurity, infection, hypoxia-ischemia, and pre- and perinatal stroke all have been implicated as contributing to CP risk, large population-based studies have shown that birth asphyxia accounts for less than 12% of CP cases.¹⁰ Specifically, recent data indicate that acute intrapartum hypoxia-ischemia occurs only in about 6% of CP cases. In other words, it does occur and may contribute to some cases, but this is likely a smaller percent than previously thought, and genetic factors now appear to be far more significant contributors.¹¹

Continue to: Exploring a genetic etiology...

In considering the etiologies of CP, it is important to note that 21% to 40% of individuals with CP have an associated congenital anomaly, suggesting a genetic origin in at least some individuals. Moreover, a 40% heritability has been estimated in CP, which is comparable to the heritability rate for autism spectrum disorders.¹²

In the recent study by Moreno-De-Luca and colleagues, some of the gene variants detected were previously associated with other forms of neurodevelopmental disability, such as epilepsy and autism spectrum disorder.³ Many individuals in the study cohort were found to have multiple neurologic comorbidities, for example, CP as well as epilepsy, autism spectrum disorder, and/or intellectual disability. The presence of these additional comorbidities increased the likelihood of finding a genetic cause; the authors found that the diagnostic yield ranged from 11.2% with isolated CP to 32.9% with all 3 comorbidities. The yield was highest with CP and intellectual disability and CP with all 3 comorbidities. A few genes were particularly common, and some were reported previously in association with CP and/or other neurodevelopmental disorders. In some patients, variants were found in genes or gene regions associated with disorders that do not frequently include CP, such as Rett syndrome.³

Implications for ObGyns

The data from the study by Moreno-De-Luca and colleagues are interesting and relevant to pediatricians, neurologists, and geneticists, as well as obstetricians. Understanding the cause of any disease or disorder improves care, including counseling regarding the cause, the appropriate interventions or therapy, and in some families, the recurrence risk in another pregnancy. The treatment for CP has not changed significantly in many years. Increasingly, detection of an underlying genetic cause can guide precision treatments; thus, the detection of specific gene variants allows a targeted approach to therapy.

Identification of a genetic cause also can significantly impact recurrence risk counseling and prenatal diagnosis options in another pregnancy. In general, the empiric recurrence risk of CP is quoted as 1% to 2%,¹³ and with de novo variants this does not change. However, with inherited variants the recurrence risk in future children is substantially higher. While 72% of the genetic variants associated with CP in the Moreno-De-Luca study were de novo with a low recurrence risk, in the other 28% the mode of inheritance indicated a substantial risk of recurrence (25%–50%) in another pregnancy.³ Detecting such causative variant(s) allows not only accurate counseling about recurrence risk but also preimplantation genetic testing or prenatal diagnosis when recurrence risk is high.

In the field of obstetrics, the debate about the etiology of CP is important largely due to the medicolegal implications. Patient-oriented information on the internet often states that CP is caused by damage to the child’s brain just before, during, or soon after birth, supporting potential blame of those providing care during those times. Patient-oriented websites regarding CP do not list genetic disorders among the causes but rather include primarily environmental factors, such as prematurity, low birth weight, in utero infections, anoxia or other brain injury, or perinatal stroke. Even the Centers for Disease Control and Prevention website lists brain damage as the primary etiology of CP.¹⁴ Hopefully, these new data will increase a broader understanding of this condition.

Exome sequencing is now recommended as a first-tier test for individuals with many neurodevelopmental disorders, including epilepsy, intellectual disability, and autism spectrum disorder.¹⁵ However, comprehensive genetic testing is not typically recommended or performed in cases of CP. Based on recent data, including the report by Moreno-De-Luca and colleagues, it would seem that CP should be added to the list of disorders for which exome sequencing is ordered, given the similar prevalence and diagnostic yield. ●

Obesity affects approximately 30% of American women, and while it is easy to diagnose, it is often difficult to address with our patients. Healthy eating and regular physical activity are the time-tested ways to achieve and maintain an appropriate weight.

For women with moderate obesity, leveraging technology is a great way to help them sensibly achieve weight loss. To evaluate the quality of a mobile app targeted to address obesity, it is particularly important to consider an app’s usefulness, functionality, and design. Clinicians can evaluate these elements with the use of the ACOG-recommended rubric, which provides criteria for judging usefulness, accuracy, authority, objectivity, timeliness, functionality, design, security, and value.

Obesity app considerations

A particularly valuable app feature that rates high on the usefulness measure is the capability for real-time motivational guidance that encourages the user to meet her daily goals. The ability to quickly and accurately scan and upload food items to an app and quantify portions using common comparative illustrations for measurement would give an app a high score on functionality. Coveted design features to enhance the user’s experience, such as syncing real time with wearable devices and catering to both visual and text learners, increase the value of an app.

In addition, an app with the combined features of a personal dietitian and a fitness trainer can employ techniques to encourage healthy eating and physical activity to self-monitor food intake and exercise. Features that calculate the user’s calorie level based on age, sex, height, and activity and offer a personalized dashboard to track carbohydrates, proteins, and fat breakdown (including nutrients and water intake) also can increase effectiveness. These features engage users to become more motivated toward an active lifestyle to balance food intake.

By incorporating apps that combine behavioral strategies with individualization, community presence, and feedback, we can successfully partner with our patients to address obesity. ●

Obesity affects approximately 30% of American women, and while it is easy to diagnose, it is often difficult to address with our patients. Healthy eating and regular physical activity are the time-tested ways to achieve and maintain an appropriate weight.

For women with moderate obesity, leveraging technology is a great way to help them sensibly achieve weight loss. To evaluate the quality of a mobile app targeted to address obesity, it is particularly important to consider an app’s usefulness, functionality, and design. Clinicians can evaluate these elements with the use of the ACOG-recommended rubric, which provides criteria for judging usefulness, accuracy, authority, objectivity, timeliness, functionality, design, security, and value.

Obesity app considerations

A particularly valuable app feature that rates high on the usefulness measure is the capability for real-time motivational guidance that encourages the user to meet her daily goals. The ability to quickly and accurately scan and upload food items to an app and quantify portions using common comparative illustrations for measurement would give an app a high score on functionality. Coveted design features to enhance the user’s experience, such as syncing real time with wearable devices and catering to both visual and text learners, increase the value of an app.

In addition, an app with the combined features of a personal dietitian and a fitness trainer can employ techniques to encourage healthy eating and physical activity to self-monitor food intake and exercise. Features that calculate the user’s calorie level based on age, sex, height, and activity and offer a personalized dashboard to track carbohydrates, proteins, and fat breakdown (including nutrients and water intake) also can increase effectiveness. These features engage users to become more motivated toward an active lifestyle to balance food intake.

By incorporating apps that combine behavioral strategies with individualization, community presence, and feedback, we can successfully partner with our patients to address obesity. ●

Obesity affects approximately 30% of American women, and while it is easy to diagnose, it is often difficult to address with our patients. Healthy eating and regular physical activity are the time-tested ways to achieve and maintain an appropriate weight.

For women with moderate obesity, leveraging technology is a great way to help them sensibly achieve weight loss. To evaluate the quality of a mobile app targeted to address obesity, it is particularly important to consider an app’s usefulness, functionality, and design. Clinicians can evaluate these elements with the use of the ACOG-recommended rubric, which provides criteria for judging usefulness, accuracy, authority, objectivity, timeliness, functionality, design, security, and value.

Obesity app considerations

A particularly valuable app feature that rates high on the usefulness measure is the capability for real-time motivational guidance that encourages the user to meet her daily goals. The ability to quickly and accurately scan and upload food items to an app and quantify portions using common comparative illustrations for measurement would give an app a high score on functionality. Coveted design features to enhance the user’s experience, such as syncing real time with wearable devices and catering to both visual and text learners, increase the value of an app.

In addition, an app with the combined features of a personal dietitian and a fitness trainer can employ techniques to encourage healthy eating and physical activity to self-monitor food intake and exercise. Features that calculate the user’s calorie level based on age, sex, height, and activity and offer a personalized dashboard to track carbohydrates, proteins, and fat breakdown (including nutrients and water intake) also can increase effectiveness. These features engage users to become more motivated toward an active lifestyle to balance food intake.

By incorporating apps that combine behavioral strategies with individualization, community presence, and feedback, we can successfully partner with our patients to address obesity. ●

Emerging data suggest that molecular classification of vascular anomalies can improve prognostication and treatment for babies born with these malformations, according to Beth Drolet, MD.

“We now know that 75%-80% of vascular malformations have gene mutations that make the cells either live longer, grow faster, or make them bigger in size,” Dr. Drolet, professor and chair of dermatology at the University of Wisconsin–Madison, said during the Society for Pediatric Dermatology pre-AAD meeting. “The basic binary premise of the current ISSVA [International Society for the Study of Vascular Anomalies] classification dividing vascular anomalies into tumors and malformations is wrong; the biology is not that straightforward. It may be helpful to differentiate between an infantile hemangioma and a capillary malformation during infancy as the hemangioma will grow in the next month, but we now know that patients with capillary malformations also have significant overgrowth of their tissue. We’ve all seen that; it just takes years, not months for us to notice it.”

The change in thinking about the root causes of vascular anomalies, she noted, stems from scientific advances in the understanding of embryonic mosaicism, DNA variation that happens after the zygote is formed, but before birth. “We know that each cell in a zygote will undergo 40 cell divisions before a baby is born,” she said. “Those cell divisions are not as neat as we thought they were. That cell and DNA duplication is actually quite messy, so there are mutations that happen purely because of embryonic cell division.”

Everyone is born with 120 somatic mutations per cell, she continued, “so we have multiple genomes in one human. Not all of those mutations are going to cause disease. Not all of those are going to be functional. About 10% of those mutations will actually be in a coding region of the gene and have the potential to change the function of the protein. If it changes the function of the protein so that the cell can’t survive, that cell dies off, but it gives the cell an advantage. It grows a little bit faster, let’s say. That cell survives, divides, producing a line of cells that can cause disease.”

In 2011, Dr. Drolet and colleagues from the Hemangioma Investigator Group and the Pediatric Dermatology Research Alliance (PeDRA) launched a multisite collaborative group to investigate the role of mosaic genetics in patients with vascular anomalies and discrepancy of growth. To date, 365 patients are enrolled, and the researchers have sequenced 97 of 165 affected tissue samples collected. “What’s nice about the registry is that we enrolled a wide spectrum of diseases: very mild diseases that might be treated by dermatologists to complex, syndromic diseases that might end up in an interdisciplinary vascular anomalies clinic,” she said.

For gene sequencing, the researchers drew from solid tumor biology and used next-generation sequencing with semi-target hybrid capture, “so we’re only looking at a subset of genes,” she said. “Right now, the chip we’re using has 180 cancer-related genes. It sequences the entire exome of the gene with a high depth of coverage, usually over 1,000 X. We use a specific pipeline that can detect very low allele frequency mutation: down to 1%, and robust criteria to determine variant pathogenicity.”

In 75% of tissue samples so far, the researchers have found a gene mutation in one of 13 genes: AKT1, AKT3, BRAF, GNA11, GNAQ, KRAS, MAP2K1, NRAS, PIK3CA, PIK3R1, PTPN11, RASA1, and TEK. According to Dr. Drolet, the common thread in these 13 genes is that they are implicated in cancer and have direct control over the cell cycle. “They’re intracellular proteins that control the cell cycle,” she explained. “These are proteins that are in the cell but interact with transmembrane proteins that receive extracellular messengers of cell growth”.

Understanding and recognizing genetic conditions is complicated, she said, because it involves determining which gene is altered, where in the DNA the gene is altered, how the gene variation will influence the function of the protein, and what tissue expresses that gene. “Then you get your phenotype,” Dr. Drolet said. “If you add mosaicism onto that, you have several additional variables. You need to know: When in embryogenesis did the mutation occur? What region of the body is affected? What cell lineage is affected? That predicts what phenotype you’re going to have.”

While molecular classification efforts continue to be refined, Dr. Drolet incorporates genotyping at every opportunity, like when she counsels parents of a baby born with a vascular stain on its face. “What can we tell them about what else might be wrong? What can we tell them about how this will change over time? What can we tell them about how we can treat it? I think genotyping absolutely helps to clarify that for me,” she said. “I can’t use that alone, but it gives me another piece of evidence to help do a better job in predicting when I need to screen, what I need to screen for, and what might happen in the future. If you combine your genotype with your clinical exam, I really do believe we can start to offer some prognostication for our families, to say, ‘this is the degree of overgrowth we may see over time; these are the complications I predict that you might have.’ ”

Even the vascular stain can give you a clue. “If it’s light and lacey, you probably don’t have a lot of cell cycle activation,” Dr. Drolet said. “If it’s dark and there’s blebs and you’ve got some bleeding at a young age, you’ve got a highly activated mutation, and there’s everything in between.”

Dr. Drolet disclosed that she is a consultant for Venthera and Novartis and is a board member for the Isthmus Project. She also holds intellectual property rights in and is a patent holder for Peds Derm Development Group. Dr. Drolet has also received funding from the Spirit Foundation, Kayleigh’s Crew Endowment, the SPD, PeDRA, and the National Institutes of Health.

[email protected]

Emerging data suggest that molecular classification of vascular anomalies can improve prognostication and treatment for babies born with these malformations, according to Beth Drolet, MD.

“We now know that 75%-80% of vascular malformations have gene mutations that make the cells either live longer, grow faster, or make them bigger in size,” Dr. Drolet, professor and chair of dermatology at the University of Wisconsin–Madison, said during the Society for Pediatric Dermatology pre-AAD meeting. “The basic binary premise of the current ISSVA [International Society for the Study of Vascular Anomalies] classification dividing vascular anomalies into tumors and malformations is wrong; the biology is not that straightforward. It may be helpful to differentiate between an infantile hemangioma and a capillary malformation during infancy as the hemangioma will grow in the next month, but we now know that patients with capillary malformations also have significant overgrowth of their tissue. We’ve all seen that; it just takes years, not months for us to notice it.”

The change in thinking about the root causes of vascular anomalies, she noted, stems from scientific advances in the understanding of embryonic mosaicism, DNA variation that happens after the zygote is formed, but before birth. “We know that each cell in a zygote will undergo 40 cell divisions before a baby is born,” she said. “Those cell divisions are not as neat as we thought they were. That cell and DNA duplication is actually quite messy, so there are mutations that happen purely because of embryonic cell division.”

Everyone is born with 120 somatic mutations per cell, she continued, “so we have multiple genomes in one human. Not all of those mutations are going to cause disease. Not all of those are going to be functional. About 10% of those mutations will actually be in a coding region of the gene and have the potential to change the function of the protein. If it changes the function of the protein so that the cell can’t survive, that cell dies off, but it gives the cell an advantage. It grows a little bit faster, let’s say. That cell survives, divides, producing a line of cells that can cause disease.”

In 2011, Dr. Drolet and colleagues from the Hemangioma Investigator Group and the Pediatric Dermatology Research Alliance (PeDRA) launched a multisite collaborative group to investigate the role of mosaic genetics in patients with vascular anomalies and discrepancy of growth. To date, 365 patients are enrolled, and the researchers have sequenced 97 of 165 affected tissue samples collected. “What’s nice about the registry is that we enrolled a wide spectrum of diseases: very mild diseases that might be treated by dermatologists to complex, syndromic diseases that might end up in an interdisciplinary vascular anomalies clinic,” she said.

For gene sequencing, the researchers drew from solid tumor biology and used next-generation sequencing with semi-target hybrid capture, “so we’re only looking at a subset of genes,” she said. “Right now, the chip we’re using has 180 cancer-related genes. It sequences the entire exome of the gene with a high depth of coverage, usually over 1,000 X. We use a specific pipeline that can detect very low allele frequency mutation: down to 1%, and robust criteria to determine variant pathogenicity.”

In 75% of tissue samples so far, the researchers have found a gene mutation in one of 13 genes: AKT1, AKT3, BRAF, GNA11, GNAQ, KRAS, MAP2K1, NRAS, PIK3CA, PIK3R1, PTPN11, RASA1, and TEK. According to Dr. Drolet, the common thread in these 13 genes is that they are implicated in cancer and have direct control over the cell cycle. “They’re intracellular proteins that control the cell cycle,” she explained. “These are proteins that are in the cell but interact with transmembrane proteins that receive extracellular messengers of cell growth”.

Understanding and recognizing genetic conditions is complicated, she said, because it involves determining which gene is altered, where in the DNA the gene is altered, how the gene variation will influence the function of the protein, and what tissue expresses that gene. “Then you get your phenotype,” Dr. Drolet said. “If you add mosaicism onto that, you have several additional variables. You need to know: When in embryogenesis did the mutation occur? What region of the body is affected? What cell lineage is affected? That predicts what phenotype you’re going to have.”

While molecular classification efforts continue to be refined, Dr. Drolet incorporates genotyping at every opportunity, like when she counsels parents of a baby born with a vascular stain on its face. “What can we tell them about what else might be wrong? What can we tell them about how this will change over time? What can we tell them about how we can treat it? I think genotyping absolutely helps to clarify that for me,” she said. “I can’t use that alone, but it gives me another piece of evidence to help do a better job in predicting when I need to screen, what I need to screen for, and what might happen in the future. If you combine your genotype with your clinical exam, I really do believe we can start to offer some prognostication for our families, to say, ‘this is the degree of overgrowth we may see over time; these are the complications I predict that you might have.’ ”

Even the vascular stain can give you a clue. “If it’s light and lacey, you probably don’t have a lot of cell cycle activation,” Dr. Drolet said. “If it’s dark and there’s blebs and you’ve got some bleeding at a young age, you’ve got a highly activated mutation, and there’s everything in between.”

Dr. Drolet disclosed that she is a consultant for Venthera and Novartis and is a board member for the Isthmus Project. She also holds intellectual property rights in and is a patent holder for Peds Derm Development Group. Dr. Drolet has also received funding from the Spirit Foundation, Kayleigh’s Crew Endowment, the SPD, PeDRA, and the National Institutes of Health.

[email protected]

Emerging data suggest that molecular classification of vascular anomalies can improve prognostication and treatment for babies born with these malformations, according to Beth Drolet, MD.

“We now know that 75%-80% of vascular malformations have gene mutations that make the cells either live longer, grow faster, or make them bigger in size,” Dr. Drolet, professor and chair of dermatology at the University of Wisconsin–Madison, said during the Society for Pediatric Dermatology pre-AAD meeting. “The basic binary premise of the current ISSVA [International Society for the Study of Vascular Anomalies] classification dividing vascular anomalies into tumors and malformations is wrong; the biology is not that straightforward. It may be helpful to differentiate between an infantile hemangioma and a capillary malformation during infancy as the hemangioma will grow in the next month, but we now know that patients with capillary malformations also have significant overgrowth of their tissue. We’ve all seen that; it just takes years, not months for us to notice it.”

The change in thinking about the root causes of vascular anomalies, she noted, stems from scientific advances in the understanding of embryonic mosaicism, DNA variation that happens after the zygote is formed, but before birth. “We know that each cell in a zygote will undergo 40 cell divisions before a baby is born,” she said. “Those cell divisions are not as neat as we thought they were. That cell and DNA duplication is actually quite messy, so there are mutations that happen purely because of embryonic cell division.”

Everyone is born with 120 somatic mutations per cell, she continued, “so we have multiple genomes in one human. Not all of those mutations are going to cause disease. Not all of those are going to be functional. About 10% of those mutations will actually be in a coding region of the gene and have the potential to change the function of the protein. If it changes the function of the protein so that the cell can’t survive, that cell dies off, but it gives the cell an advantage. It grows a little bit faster, let’s say. That cell survives, divides, producing a line of cells that can cause disease.”

In 2011, Dr. Drolet and colleagues from the Hemangioma Investigator Group and the Pediatric Dermatology Research Alliance (PeDRA) launched a multisite collaborative group to investigate the role of mosaic genetics in patients with vascular anomalies and discrepancy of growth. To date, 365 patients are enrolled, and the researchers have sequenced 97 of 165 affected tissue samples collected. “What’s nice about the registry is that we enrolled a wide spectrum of diseases: very mild diseases that might be treated by dermatologists to complex, syndromic diseases that might end up in an interdisciplinary vascular anomalies clinic,” she said.

For gene sequencing, the researchers drew from solid tumor biology and used next-generation sequencing with semi-target hybrid capture, “so we’re only looking at a subset of genes,” she said. “Right now, the chip we’re using has 180 cancer-related genes. It sequences the entire exome of the gene with a high depth of coverage, usually over 1,000 X. We use a specific pipeline that can detect very low allele frequency mutation: down to 1%, and robust criteria to determine variant pathogenicity.”

In 75% of tissue samples so far, the researchers have found a gene mutation in one of 13 genes: AKT1, AKT3, BRAF, GNA11, GNAQ, KRAS, MAP2K1, NRAS, PIK3CA, PIK3R1, PTPN11, RASA1, and TEK. According to Dr. Drolet, the common thread in these 13 genes is that they are implicated in cancer and have direct control over the cell cycle. “They’re intracellular proteins that control the cell cycle,” she explained. “These are proteins that are in the cell but interact with transmembrane proteins that receive extracellular messengers of cell growth”.

Understanding and recognizing genetic conditions is complicated, she said, because it involves determining which gene is altered, where in the DNA the gene is altered, how the gene variation will influence the function of the protein, and what tissue expresses that gene. “Then you get your phenotype,” Dr. Drolet said. “If you add mosaicism onto that, you have several additional variables. You need to know: When in embryogenesis did the mutation occur? What region of the body is affected? What cell lineage is affected? That predicts what phenotype you’re going to have.”

While molecular classification efforts continue to be refined, Dr. Drolet incorporates genotyping at every opportunity, like when she counsels parents of a baby born with a vascular stain on its face. “What can we tell them about what else might be wrong? What can we tell them about how this will change over time? What can we tell them about how we can treat it? I think genotyping absolutely helps to clarify that for me,” she said. “I can’t use that alone, but it gives me another piece of evidence to help do a better job in predicting when I need to screen, what I need to screen for, and what might happen in the future. If you combine your genotype with your clinical exam, I really do believe we can start to offer some prognostication for our families, to say, ‘this is the degree of overgrowth we may see over time; these are the complications I predict that you might have.’ ”

Even the vascular stain can give you a clue. “If it’s light and lacey, you probably don’t have a lot of cell cycle activation,” Dr. Drolet said. “If it’s dark and there’s blebs and you’ve got some bleeding at a young age, you’ve got a highly activated mutation, and there’s everything in between.”

Dr. Drolet disclosed that she is a consultant for Venthera and Novartis and is a board member for the Isthmus Project. She also holds intellectual property rights in and is a patent holder for Peds Derm Development Group. Dr. Drolet has also received funding from the Spirit Foundation, Kayleigh’s Crew Endowment, the SPD, PeDRA, and the National Institutes of Health.

[email protected]

A 31-year-old Hispanic man presented for evaluation of numerous disfiguring growths on his scalp. They first appeared when he was 19 years old. A review of his family history revealed that his father had 2 “cysts” on his body.

The patient had 10 nodules on his scalp and upper back (Figures 1A and 1B). The ones on his scalp lacked puncta and appeared in a “turban tumor” configuration. The lesions were pink, smooth, and semisoft, and ranged in size from 1 to 6 cm.

Six years earlier, the patient had been seen for evaluation of 20 protuberant nodules. At the time, he had been referred to plastic surgery, where 15 lesions were excised. No other treatment was reported by the patient during the 6-year gap between exams.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Pilar cysts (PC), also known as trichilemma cysts, wen, or isthmus-catagen cysts, are benign cysts that manifest as smooth, firm, well-­circumscribed, pink nodules. PCs originate from the follicular isthmus of the hair’s external root sheath¹ and are found in 5% to 10% of the US population.² Possible sites of appearance include the face, neck, trunk, and extremities, although 90% of PCs develop on the scalp.¹ They tend to have an autosomal dominant pattern of inheritance with linkages to the short arm of chromosome 3.³ PCs can occasionally become inflamed following infection or trauma.

Characteristic histology of PCs demonstrates semisolid, keratin-filled, subepidermal cysts lined by stratified epithelium without a granular layer (trichilemmal keratinization). Lesions excised from this patient’s scalp showed 2 subtypes of PCs: nonproliferating (FIGURE 2A) and proliferating (FIGURE 2B). Subtypes appear similar on exam but can be differentiated on histology.

With gradual growth, proliferating PCs can reach up to 25 cm in diameter.¹ Rapid growth, size > 5 cm, infiltration, or a non-scalp location may indicate malignancy.⁴

Differential diagnosis includes lipomas

The differential diagnosis for a lesion such as this includes epidermal inclusion cysts, dermoid cysts, and lipomas. Epidermal inclusion cysts have a punctum, whereas PCs do not. Dermoid cysts are single congenital lesions that manifest much earlier than PCs. Lipomas are easily movable rubbery bulges that appear more frequently in lipid-dense areas of the body.

For this patient, the striking turban ­tumor–like presentation, with numerous large cysts on the scalp, initially inspired a differential diagnosis including several genetic tumor syndromes. However, unlike the association between Gardner syndrome and numerous epidermoid cysts or Brooke-Spiegler syndrome and spiradenomas, no syndromes have been linked to numerous trichilemmal cysts.

Continue to: Excision is effective

Excision is the treatment of choice for both proliferating and nonproliferating PCs.⁵ The local recurrence rate of proliferating PCs is 3.7% with a rare likelihood of transformation to trichilemmal carcinoma.⁶

Our patient continues to be followed in clinic for monitoring and periodic excision of bothersome cysts.

A 31-year-old Hispanic man presented for evaluation of numerous disfiguring growths on his scalp. They first appeared when he was 19 years old. A review of his family history revealed that his father had 2 “cysts” on his body.

The patient had 10 nodules on his scalp and upper back (Figures 1A and 1B). The ones on his scalp lacked puncta and appeared in a “turban tumor” configuration. The lesions were pink, smooth, and semisoft, and ranged in size from 1 to 6 cm.

Six years earlier, the patient had been seen for evaluation of 20 protuberant nodules. At the time, he had been referred to plastic surgery, where 15 lesions were excised. No other treatment was reported by the patient during the 6-year gap between exams.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Pilar cysts (PC), also known as trichilemma cysts, wen, or isthmus-catagen cysts, are benign cysts that manifest as smooth, firm, well-­circumscribed, pink nodules. PCs originate from the follicular isthmus of the hair’s external root sheath¹ and are found in 5% to 10% of the US population.² Possible sites of appearance include the face, neck, trunk, and extremities, although 90% of PCs develop on the scalp.¹ They tend to have an autosomal dominant pattern of inheritance with linkages to the short arm of chromosome 3.³ PCs can occasionally become inflamed following infection or trauma.

Characteristic histology of PCs demonstrates semisolid, keratin-filled, subepidermal cysts lined by stratified epithelium without a granular layer (trichilemmal keratinization). Lesions excised from this patient’s scalp showed 2 subtypes of PCs: nonproliferating (FIGURE 2A) and proliferating (FIGURE 2B). Subtypes appear similar on exam but can be differentiated on histology.

With gradual growth, proliferating PCs can reach up to 25 cm in diameter.¹ Rapid growth, size > 5 cm, infiltration, or a non-scalp location may indicate malignancy.⁴

Differential diagnosis includes lipomas

The differential diagnosis for a lesion such as this includes epidermal inclusion cysts, dermoid cysts, and lipomas. Epidermal inclusion cysts have a punctum, whereas PCs do not. Dermoid cysts are single congenital lesions that manifest much earlier than PCs. Lipomas are easily movable rubbery bulges that appear more frequently in lipid-dense areas of the body.

For this patient, the striking turban ­tumor–like presentation, with numerous large cysts on the scalp, initially inspired a differential diagnosis including several genetic tumor syndromes. However, unlike the association between Gardner syndrome and numerous epidermoid cysts or Brooke-Spiegler syndrome and spiradenomas, no syndromes have been linked to numerous trichilemmal cysts.

Continue to: Excision is effective

Excision is the treatment of choice for both proliferating and nonproliferating PCs.⁵ The local recurrence rate of proliferating PCs is 3.7% with a rare likelihood of transformation to trichilemmal carcinoma.⁶

Our patient continues to be followed in clinic for monitoring and periodic excision of bothersome cysts.

A 31-year-old Hispanic man presented for evaluation of numerous disfiguring growths on his scalp. They first appeared when he was 19 years old. A review of his family history revealed that his father had 2 “cysts” on his body.

The patient had 10 nodules on his scalp and upper back (Figures 1A and 1B). The ones on his scalp lacked puncta and appeared in a “turban tumor” configuration. The lesions were pink, smooth, and semisoft, and ranged in size from 1 to 6 cm.

Six years earlier, the patient had been seen for evaluation of 20 protuberant nodules. At the time, he had been referred to plastic surgery, where 15 lesions were excised. No other treatment was reported by the patient during the 6-year gap between exams.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

Pilar cysts (PC), also known as trichilemma cysts, wen, or isthmus-catagen cysts, are benign cysts that manifest as smooth, firm, well-­circumscribed, pink nodules. PCs originate from the follicular isthmus of the hair’s external root sheath¹ and are found in 5% to 10% of the US population.² Possible sites of appearance include the face, neck, trunk, and extremities, although 90% of PCs develop on the scalp.¹ They tend to have an autosomal dominant pattern of inheritance with linkages to the short arm of chromosome 3.³ PCs can occasionally become inflamed following infection or trauma.

Characteristic histology of PCs demonstrates semisolid, keratin-filled, subepidermal cysts lined by stratified epithelium without a granular layer (trichilemmal keratinization). Lesions excised from this patient’s scalp showed 2 subtypes of PCs: nonproliferating (FIGURE 2A) and proliferating (FIGURE 2B). Subtypes appear similar on exam but can be differentiated on histology.

With gradual growth, proliferating PCs can reach up to 25 cm in diameter.¹ Rapid growth, size > 5 cm, infiltration, or a non-scalp location may indicate malignancy.⁴

Differential diagnosis includes lipomas

The differential diagnosis for a lesion such as this includes epidermal inclusion cysts, dermoid cysts, and lipomas. Epidermal inclusion cysts have a punctum, whereas PCs do not. Dermoid cysts are single congenital lesions that manifest much earlier than PCs. Lipomas are easily movable rubbery bulges that appear more frequently in lipid-dense areas of the body.

For this patient, the striking turban ­tumor–like presentation, with numerous large cysts on the scalp, initially inspired a differential diagnosis including several genetic tumor syndromes. However, unlike the association between Gardner syndrome and numerous epidermoid cysts or Brooke-Spiegler syndrome and spiradenomas, no syndromes have been linked to numerous trichilemmal cysts.

Continue to: Excision is effective

Excision is the treatment of choice for both proliferating and nonproliferating PCs.⁵ The local recurrence rate of proliferating PCs is 3.7% with a rare likelihood of transformation to trichilemmal carcinoma.⁶

Our patient continues to be followed in clinic for monitoring and periodic excision of bothersome cysts.

Wearing stable, supportive footwear reduces knee pain to a significantly greater extent than what’s felt with flat, flexible shoes in patients with severe knee osteoarthritis, according to results of a randomized, controlled trial presented at the OARSI 2021 World Congress.

Stockbyte/Thinkstock

Clinical guidelines for knee OA emphasize the importance of patients self-managing their condition with exercise, weight control, and appropriate footwear. However, there is limited evidence on which footwear is best, and some guidelines advocate stable supportive shoes based solely on expert opinion, Kade Paterson, PhD, of the University of Melbourne told the conference, sponsored by Osteoarthritis Research Society International.

“Recent research suggests that another type of shoe style – termed flat, flexible shoes – may be more beneficial,” Dr. Paterson said, citing a randomized, controlled trial that found greater improvement in pain and function with flat flexible shoes, compared with neutral tennis shoes. “Flat, flexible shoes are generally lighter, and have thinner, more flexible soles.”

In this study, which was published earlier this year in Annals of Internal Medicine, 164 individuals with knee OA who had experienced knee pain on most days of the past month were randomized to wear either stable, supportive shoes or flat, flexible shoes for at least 6 hours a day for 6 months. Six of each shoe type – three male styles and three female styles – were offered, having been chosen based on a survey in which participants were asked about a selection of commercially available shoes they were most likely to wear.

Researchers found participants who wore the stable, supportive shoes had significantly greater reductions in knee pain on walking during the previous week, representing a mean difference of 1.1 units on an 11-point numerical rating scale. More patients in the stable, supportive shoe arm of the study achieved minimal clinically important difference in pain than did those in the flat, flexible shoe group.

Stable, supportive shoes were also associated with greater improvements in knee-related quality of life scores and greater improvements in overall pain. However, there was no significant difference between the two groups in function. Patients wearing flat, flexible shoes reported significantly more adverse events – mainly onset of or increases in knee pain.

Dr. Paterson said the results were surprising, given previous research suggesting a benefit from lighter flat, flexible shoes. “Some previous research showed that those shoes reduced knee joint forces that were associated with pain and reduced it more than stable, supportive shoes, and based on the biomechanical research, we thought would be flat, flexible shoes,” he said in an interview.

Another observation to come from the study was the poor quality of most patients’ everyday shoes. Dr. Paterson said that most of the participants’ usual shoes were very old, and many were also wearing inappropriate footwear for knee OA, including shoes with heels or slippers.

“We would strongly recommend that clinicians ask patients to even bring in their most commonly worn shoes and then recommend new shoes, and based on our data, certainly stable supportive shoes,” he said.

Commenting on the findings, Jos Runhaar, PhD, of Erasmus University Medical Center in Rotterdam, the Netherlands, said this study provided high-quality evidence for this specific intervention in this specific group of patients, namely those with more severe, end-stage OA who had long-lasting changes in their foot posture and gait.

“Based on this, I would say that restoring the original posture of the foot – because that’s how the stable, supportive shoes are probably designed – is more beneficial than actually supporting the natural gait that people are already adapted to at that stage,” Dr. Runhaar said in an interview.

Dr. Paterson noted that the findings of the study were not generalizable to people with mild knee OA, and also that the study did not compare either shoe type with participants’ usual shoes.

The study and three authors were supported by the Australian National Health and Medical Research Council. No conflicts of interest were declared.

Wearing stable, supportive footwear reduces knee pain to a significantly greater extent than what’s felt with flat, flexible shoes in patients with severe knee osteoarthritis, according to results of a randomized, controlled trial presented at the OARSI 2021 World Congress.

Stockbyte/Thinkstock

Clinical guidelines for knee OA emphasize the importance of patients self-managing their condition with exercise, weight control, and appropriate footwear. However, there is limited evidence on which footwear is best, and some guidelines advocate stable supportive shoes based solely on expert opinion, Kade Paterson, PhD, of the University of Melbourne told the conference, sponsored by Osteoarthritis Research Society International.

“Recent research suggests that another type of shoe style – termed flat, flexible shoes – may be more beneficial,” Dr. Paterson said, citing a randomized, controlled trial that found greater improvement in pain and function with flat flexible shoes, compared with neutral tennis shoes. “Flat, flexible shoes are generally lighter, and have thinner, more flexible soles.”

In this study, which was published earlier this year in Annals of Internal Medicine, 164 individuals with knee OA who had experienced knee pain on most days of the past month were randomized to wear either stable, supportive shoes or flat, flexible shoes for at least 6 hours a day for 6 months. Six of each shoe type – three male styles and three female styles – were offered, having been chosen based on a survey in which participants were asked about a selection of commercially available shoes they were most likely to wear.

Researchers found participants who wore the stable, supportive shoes had significantly greater reductions in knee pain on walking during the previous week, representing a mean difference of 1.1 units on an 11-point numerical rating scale. More patients in the stable, supportive shoe arm of the study achieved minimal clinically important difference in pain than did those in the flat, flexible shoe group.

Stable, supportive shoes were also associated with greater improvements in knee-related quality of life scores and greater improvements in overall pain. However, there was no significant difference between the two groups in function. Patients wearing flat, flexible shoes reported significantly more adverse events – mainly onset of or increases in knee pain.

Dr. Paterson said the results were surprising, given previous research suggesting a benefit from lighter flat, flexible shoes. “Some previous research showed that those shoes reduced knee joint forces that were associated with pain and reduced it more than stable, supportive shoes, and based on the biomechanical research, we thought would be flat, flexible shoes,” he said in an interview.

Another observation to come from the study was the poor quality of most patients’ everyday shoes. Dr. Paterson said that most of the participants’ usual shoes were very old, and many were also wearing inappropriate footwear for knee OA, including shoes with heels or slippers.

“We would strongly recommend that clinicians ask patients to even bring in their most commonly worn shoes and then recommend new shoes, and based on our data, certainly stable supportive shoes,” he said.

Commenting on the findings, Jos Runhaar, PhD, of Erasmus University Medical Center in Rotterdam, the Netherlands, said this study provided high-quality evidence for this specific intervention in this specific group of patients, namely those with more severe, end-stage OA who had long-lasting changes in their foot posture and gait.

“Based on this, I would say that restoring the original posture of the foot – because that’s how the stable, supportive shoes are probably designed – is more beneficial than actually supporting the natural gait that people are already adapted to at that stage,” Dr. Runhaar said in an interview.

Dr. Paterson noted that the findings of the study were not generalizable to people with mild knee OA, and also that the study did not compare either shoe type with participants’ usual shoes.

The study and three authors were supported by the Australian National Health and Medical Research Council. No conflicts of interest were declared.

Wearing stable, supportive footwear reduces knee pain to a significantly greater extent than what’s felt with flat, flexible shoes in patients with severe knee osteoarthritis, according to results of a randomized, controlled trial presented at the OARSI 2021 World Congress.

Stockbyte/Thinkstock

Clinical guidelines for knee OA emphasize the importance of patients self-managing their condition with exercise, weight control, and appropriate footwear. However, there is limited evidence on which footwear is best, and some guidelines advocate stable supportive shoes based solely on expert opinion, Kade Paterson, PhD, of the University of Melbourne told the conference, sponsored by Osteoarthritis Research Society International.

“Recent research suggests that another type of shoe style – termed flat, flexible shoes – may be more beneficial,” Dr. Paterson said, citing a randomized, controlled trial that found greater improvement in pain and function with flat flexible shoes, compared with neutral tennis shoes. “Flat, flexible shoes are generally lighter, and have thinner, more flexible soles.”

In this study, which was published earlier this year in Annals of Internal Medicine, 164 individuals with knee OA who had experienced knee pain on most days of the past month were randomized to wear either stable, supportive shoes or flat, flexible shoes for at least 6 hours a day for 6 months. Six of each shoe type – three male styles and three female styles – were offered, having been chosen based on a survey in which participants were asked about a selection of commercially available shoes they were most likely to wear.

Researchers found participants who wore the stable, supportive shoes had significantly greater reductions in knee pain on walking during the previous week, representing a mean difference of 1.1 units on an 11-point numerical rating scale. More patients in the stable, supportive shoe arm of the study achieved minimal clinically important difference in pain than did those in the flat, flexible shoe group.

Stable, supportive shoes were also associated with greater improvements in knee-related quality of life scores and greater improvements in overall pain. However, there was no significant difference between the two groups in function. Patients wearing flat, flexible shoes reported significantly more adverse events – mainly onset of or increases in knee pain.

Dr. Paterson said the results were surprising, given previous research suggesting a benefit from lighter flat, flexible shoes. “Some previous research showed that those shoes reduced knee joint forces that were associated with pain and reduced it more than stable, supportive shoes, and based on the biomechanical research, we thought would be flat, flexible shoes,” he said in an interview.

Another observation to come from the study was the poor quality of most patients’ everyday shoes. Dr. Paterson said that most of the participants’ usual shoes were very old, and many were also wearing inappropriate footwear for knee OA, including shoes with heels or slippers.

“We would strongly recommend that clinicians ask patients to even bring in their most commonly worn shoes and then recommend new shoes, and based on our data, certainly stable supportive shoes,” he said.

Commenting on the findings, Jos Runhaar, PhD, of Erasmus University Medical Center in Rotterdam, the Netherlands, said this study provided high-quality evidence for this specific intervention in this specific group of patients, namely those with more severe, end-stage OA who had long-lasting changes in their foot posture and gait.

“Based on this, I would say that restoring the original posture of the foot – because that’s how the stable, supportive shoes are probably designed – is more beneficial than actually supporting the natural gait that people are already adapted to at that stage,” Dr. Runhaar said in an interview.

Dr. Paterson noted that the findings of the study were not generalizable to people with mild knee OA, and also that the study did not compare either shoe type with participants’ usual shoes.

The study and three authors were supported by the Australian National Health and Medical Research Council. No conflicts of interest were declared.

The ivory white appearance and slight atrophy of the lesions raised the possibility of extragenital lichen sclerosus (LS). A 4-mm punch biopsy confirmed the diagnosis.

LS occurs in all races and is an uncommon, chronic inflammatory disease that most often affects the vulva and perianal mucosa in postmenopausal women.¹ That said, it can also affect men and children, and manifest in places such as the trunk and neck. Extragenital lesions may appear ivory white, as in this case, or may resemble ecchymoses and raise alarm for possible abuse.

When LS is present on the extremities, a complete skin surface exam, including external genitalia, is warranted. LS is thought to be an autoimmune disease and is associated with vitiligo, autoimmune thyroid disease, and morphea.

In cases of suspected LS, it’s important to biopsy the full thickness of the skin and subcutaneous tissue. It is helpful to include an area of normal skin in the sample, as the findings are subtle and best contrasted with the architecture of unaffected skin. For this patient, a 4-mm punch biopsy was sufficient, but an incisional biopsy would be more appropriate for a larger patch or plaque.

Treatment options are based on a small case series and a few small randomized controlled trials. Medications include topical steroids, topical calcineurin inhibitors, systemic retinoids, and topical estrogens.

In this case, the patient was advised to apply topical clobetasol 0.05% cream bid to the affected area for 2 weeks, then twice weekly for 4 weeks. She had partial clearance with this approach, but small macules later appeared on her dorsal foot; the treatment was repeated.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

The ivory white appearance and slight atrophy of the lesions raised the possibility of extragenital lichen sclerosus (LS). A 4-mm punch biopsy confirmed the diagnosis.

LS occurs in all races and is an uncommon, chronic inflammatory disease that most often affects the vulva and perianal mucosa in postmenopausal women.¹ That said, it can also affect men and children, and manifest in places such as the trunk and neck. Extragenital lesions may appear ivory white, as in this case, or may resemble ecchymoses and raise alarm for possible abuse.

When LS is present on the extremities, a complete skin surface exam, including external genitalia, is warranted. LS is thought to be an autoimmune disease and is associated with vitiligo, autoimmune thyroid disease, and morphea.

In cases of suspected LS, it’s important to biopsy the full thickness of the skin and subcutaneous tissue. It is helpful to include an area of normal skin in the sample, as the findings are subtle and best contrasted with the architecture of unaffected skin. For this patient, a 4-mm punch biopsy was sufficient, but an incisional biopsy would be more appropriate for a larger patch or plaque.

Treatment options are based on a small case series and a few small randomized controlled trials. Medications include topical steroids, topical calcineurin inhibitors, systemic retinoids, and topical estrogens.

In this case, the patient was advised to apply topical clobetasol 0.05% cream bid to the affected area for 2 weeks, then twice weekly for 4 weeks. She had partial clearance with this approach, but small macules later appeared on her dorsal foot; the treatment was repeated.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

The ivory white appearance and slight atrophy of the lesions raised the possibility of extragenital lichen sclerosus (LS). A 4-mm punch biopsy confirmed the diagnosis.

LS occurs in all races and is an uncommon, chronic inflammatory disease that most often affects the vulva and perianal mucosa in postmenopausal women.¹ That said, it can also affect men and children, and manifest in places such as the trunk and neck. Extragenital lesions may appear ivory white, as in this case, or may resemble ecchymoses and raise alarm for possible abuse.

When LS is present on the extremities, a complete skin surface exam, including external genitalia, is warranted. LS is thought to be an autoimmune disease and is associated with vitiligo, autoimmune thyroid disease, and morphea.

In cases of suspected LS, it’s important to biopsy the full thickness of the skin and subcutaneous tissue. It is helpful to include an area of normal skin in the sample, as the findings are subtle and best contrasted with the architecture of unaffected skin. For this patient, a 4-mm punch biopsy was sufficient, but an incisional biopsy would be more appropriate for a larger patch or plaque.

Treatment options are based on a small case series and a few small randomized controlled trials. Medications include topical steroids, topical calcineurin inhibitors, systemic retinoids, and topical estrogens.

In this case, the patient was advised to apply topical clobetasol 0.05% cream bid to the affected area for 2 weeks, then twice weekly for 4 weeks. She had partial clearance with this approach, but small macules later appeared on her dorsal foot; the treatment was repeated.

‌

Text and photos courtesy of Jonathan Karnes, MD, medical director, MDFMR Dermatology Services, Augusta, ME. (Photo copyright retained.)

No matter where an initial fracture occurs in a postmenopausal woman, there is a subsequent increased risk of another fracture, with the risk surprisingly highest in the youngest postmenopausal group and among certain minorities, new data indicate.

“To our knowledge, no previous prospective study has reported detailed patterns of subsequent fracture locations after initial fracture according to age strata among women in the U.S.,” the authors noted in their article, published online May 5, 2021, in EClinicalMedicine.

The results show that a first fracture of the lower arm or wrist; upper arm; or shoulder, upper leg, knee, lower leg, or ankle – as well as those of the hip or pelvis – were associated with an approximately three- to sixfold increased risk for subsequent fractures. The findings have important implications for clinicians, said lead author Carolyn J. Crandall, MD, professor of medicine at the University of California, Los Angeles.

“By not paying attention to which types of fractures increase the risk of future fractures, we are missing the opportunity to identify people at increased risk of future fracture and counsel them regarding risk reduction,” she said in a press statement.

Commenting on the research, Michael R. McClung, MD, stressed this message to clinicians needs to be underscored.

“This paper is one of a series of papers highlighting the fact that having a previous fracture is a risk factor for subsequent fractures,” he said in an interview.

“This has been known for a very long time, but it is a point still not appreciated by patients and primary care doctors, so having another study pointing this out is important,” emphasized Dr. McClung, of the Oregon Osteoporosis Center in Portland.
 

30% of women’s health initiative participants had a fracture

For the study, Dr. Crandall and colleagues evaluated data on 157,282 women between the ages of 50 and 79 who were enrolled in the Women’s Health Initiative between 1993 and 2018.

The women were a mean age of 63.1 years and 47,126 (30%) experienced an incident fracture during the study period.

With a mean follow-up of 15.4 years, each type of fracture was associated with an increased risk of a subsequent fracture after adjusting for age, race/ethnicity, body mass index, hormone therapy use, and other factors.

A wide range of initial risk fractures – including an initial lower arm or wrist fracture (adjusted hazard ratio, 4.80), upper arm or shoulder fracture (aHR, 5.06), upper leg fracture (aHR, 5.11), knee fracture (aHR, 5.03), lower leg/ankle fracture (aHR, 4.10), and spinal fracture (aHR, 6.69) – increased the risk of sustaining a subsequent hip fracture. 

For initial fractures of the lower arm or wrist, there was an increased risk of a subsequent fracture of the upper arm/shoulder, upper leg, knee, lower leg/ankle, hip/pelvis, and spine (aHRs ranged from 2.63 to 5.68). 

“The finding that knee fracture has the same prognostic value for subsequent fracture as hip or wrist fracture is a novel key finding, as knee fracture is generally not considered ‘osteoporotic’,” the authors noted.

The risk of fracture after sustaining an initial hip or pelvis fracture was exceptionally high – with as much as a 27-fold higher risk of a subsequent upper leg (nonhip) fracture (aHR, 27.18).

“Thirty-four percent of women who experienced initial hip or pelvis fracture experienced a subsequent nonhip fracture,” the authors noted.

However, the risks associated with an initial hip fracture are already well established, and the study’s more notable findings are the risks of other bone breaks, Dr. Crandall told this news organization.

“The (increased risk with hip fracture) is a rather substantial result,” she said. “However, the more major point of this study is that no matter where the initial fracture happened, the risk of the future fracture was elevated.”
 

Don’t disregard risks in younger women, racial/ethnic groups

The findings regarding age are also important. The highest risk was observed in the youngest postmenopausal age group of 50-59 years (aHR, 6.45), which decreased slightly in the 60- to 69-year age group (aHR, 6.04) and further decreased in the 70- to 79-year age group (aHR, 4.99).

“This was a surprise, and it highlights that clinicians should not disregard initial fractures among young postmenopausal women,” Dr. Crandall told this news organization.

Even greater increased risks for a subsequent fracture following an initial lower extremity fracture were observed in non-Hispanic Black women, Hispanic or Latina women, and women of Asian Pacific Islander ethnicity, ranging from ninefold to 14-fold, versus a sevenfold risk among non-Hispanic White women.

“This has public health implications because it means that we may have been missing the opportunity to prevent fractures among younger postmenopausal women and underrepresented racial/ethnic groups,” Dr. Crandall noted.

Is risk greatest 1-2 years after the initial fracture?

The findings suggest that current treatment guidelines may need to be revisited in light of inconsistencies regarding when, and for which fracture types, to initiate treatment.

“It will be important to determine whether existing risk calculators can be adapted (or new calculators developed) to help refine decision-making to determine which of the women with fractures other than hip or vertebral fractures should be treated,” the authors wrote.

Dr. McClung said a randomized, controlled trial of osteoporosis treatment in people who present with all types of fractures would help determine whether having a knee or a wrist fracture does indeed warrant such therapy.

He further commented that future studies should evaluate the shorter- versus longer-term risks.

“The most recent research suggests that the risk of having a second fracture is much higher in the first year or 2 after the first or incident fracture,” he observed. “So, the next stage in research with this dataset would be to ask not what happens over a 10-year time frame but what happens over the first year or 2 after the fracture.”

The study was funded by the National Heart, Lung, and Blood Institute. Dr. Crandall reported no relevant financial relationships. Dr. McClung reported being a consultant and on the speakers bureau for Amgen and being a speaker for Alexion.

A version of this article first appeared on Medscape.com.

No matter where an initial fracture occurs in a postmenopausal woman, there is a subsequent increased risk of another fracture, with the risk surprisingly highest in the youngest postmenopausal group and among certain minorities, new data indicate.

“To our knowledge, no previous prospective study has reported detailed patterns of subsequent fracture locations after initial fracture according to age strata among women in the U.S.,” the authors noted in their article, published online May 5, 2021, in EClinicalMedicine.

The results show that a first fracture of the lower arm or wrist; upper arm; or shoulder, upper leg, knee, lower leg, or ankle – as well as those of the hip or pelvis – were associated with an approximately three- to sixfold increased risk for subsequent fractures. The findings have important implications for clinicians, said lead author Carolyn J. Crandall, MD, professor of medicine at the University of California, Los Angeles.

“By not paying attention to which types of fractures increase the risk of future fractures, we are missing the opportunity to identify people at increased risk of future fracture and counsel them regarding risk reduction,” she said in a press statement.

Commenting on the research, Michael R. McClung, MD, stressed this message to clinicians needs to be underscored.

“This paper is one of a series of papers highlighting the fact that having a previous fracture is a risk factor for subsequent fractures,” he said in an interview.

“This has been known for a very long time, but it is a point still not appreciated by patients and primary care doctors, so having another study pointing this out is important,” emphasized Dr. McClung, of the Oregon Osteoporosis Center in Portland.
 

30% of women’s health initiative participants had a fracture

For the study, Dr. Crandall and colleagues evaluated data on 157,282 women between the ages of 50 and 79 who were enrolled in the Women’s Health Initiative between 1993 and 2018.

The women were a mean age of 63.1 years and 47,126 (30%) experienced an incident fracture during the study period.

With a mean follow-up of 15.4 years, each type of fracture was associated with an increased risk of a subsequent fracture after adjusting for age, race/ethnicity, body mass index, hormone therapy use, and other factors.

A wide range of initial risk fractures – including an initial lower arm or wrist fracture (adjusted hazard ratio, 4.80), upper arm or shoulder fracture (aHR, 5.06), upper leg fracture (aHR, 5.11), knee fracture (aHR, 5.03), lower leg/ankle fracture (aHR, 4.10), and spinal fracture (aHR, 6.69) – increased the risk of sustaining a subsequent hip fracture. 

For initial fractures of the lower arm or wrist, there was an increased risk of a subsequent fracture of the upper arm/shoulder, upper leg, knee, lower leg/ankle, hip/pelvis, and spine (aHRs ranged from 2.63 to 5.68). 

“The finding that knee fracture has the same prognostic value for subsequent fracture as hip or wrist fracture is a novel key finding, as knee fracture is generally not considered ‘osteoporotic’,” the authors noted.

The risk of fracture after sustaining an initial hip or pelvis fracture was exceptionally high – with as much as a 27-fold higher risk of a subsequent upper leg (nonhip) fracture (aHR, 27.18).

“Thirty-four percent of women who experienced initial hip or pelvis fracture experienced a subsequent nonhip fracture,” the authors noted.

However, the risks associated with an initial hip fracture are already well established, and the study’s more notable findings are the risks of other bone breaks, Dr. Crandall told this news organization.

“The (increased risk with hip fracture) is a rather substantial result,” she said. “However, the more major point of this study is that no matter where the initial fracture happened, the risk of the future fracture was elevated.”
 

Don’t disregard risks in younger women, racial/ethnic groups

The findings regarding age are also important. The highest risk was observed in the youngest postmenopausal age group of 50-59 years (aHR, 6.45), which decreased slightly in the 60- to 69-year age group (aHR, 6.04) and further decreased in the 70- to 79-year age group (aHR, 4.99).

“This was a surprise, and it highlights that clinicians should not disregard initial fractures among young postmenopausal women,” Dr. Crandall told this news organization.

Even greater increased risks for a subsequent fracture following an initial lower extremity fracture were observed in non-Hispanic Black women, Hispanic or Latina women, and women of Asian Pacific Islander ethnicity, ranging from ninefold to 14-fold, versus a sevenfold risk among non-Hispanic White women.

“This has public health implications because it means that we may have been missing the opportunity to prevent fractures among younger postmenopausal women and underrepresented racial/ethnic groups,” Dr. Crandall noted.

Is risk greatest 1-2 years after the initial fracture?

The findings suggest that current treatment guidelines may need to be revisited in light of inconsistencies regarding when, and for which fracture types, to initiate treatment.

“It will be important to determine whether existing risk calculators can be adapted (or new calculators developed) to help refine decision-making to determine which of the women with fractures other than hip or vertebral fractures should be treated,” the authors wrote.

Dr. McClung said a randomized, controlled trial of osteoporosis treatment in people who present with all types of fractures would help determine whether having a knee or a wrist fracture does indeed warrant such therapy.

He further commented that future studies should evaluate the shorter- versus longer-term risks.

“The most recent research suggests that the risk of having a second fracture is much higher in the first year or 2 after the first or incident fracture,” he observed. “So, the next stage in research with this dataset would be to ask not what happens over a 10-year time frame but what happens over the first year or 2 after the fracture.”

The study was funded by the National Heart, Lung, and Blood Institute. Dr. Crandall reported no relevant financial relationships. Dr. McClung reported being a consultant and on the speakers bureau for Amgen and being a speaker for Alexion.

A version of this article first appeared on Medscape.com.

No matter where an initial fracture occurs in a postmenopausal woman, there is a subsequent increased risk of another fracture, with the risk surprisingly highest in the youngest postmenopausal group and among certain minorities, new data indicate.

“To our knowledge, no previous prospective study has reported detailed patterns of subsequent fracture locations after initial fracture according to age strata among women in the U.S.,” the authors noted in their article, published online May 5, 2021, in EClinicalMedicine.

The results show that a first fracture of the lower arm or wrist; upper arm; or shoulder, upper leg, knee, lower leg, or ankle – as well as those of the hip or pelvis – were associated with an approximately three- to sixfold increased risk for subsequent fractures. The findings have important implications for clinicians, said lead author Carolyn J. Crandall, MD, professor of medicine at the University of California, Los Angeles.

“By not paying attention to which types of fractures increase the risk of future fractures, we are missing the opportunity to identify people at increased risk of future fracture and counsel them regarding risk reduction,” she said in a press statement.

Commenting on the research, Michael R. McClung, MD, stressed this message to clinicians needs to be underscored.

“This paper is one of a series of papers highlighting the fact that having a previous fracture is a risk factor for subsequent fractures,” he said in an interview.

“This has been known for a very long time, but it is a point still not appreciated by patients and primary care doctors, so having another study pointing this out is important,” emphasized Dr. McClung, of the Oregon Osteoporosis Center in Portland.
 

30% of women’s health initiative participants had a fracture

For the study, Dr. Crandall and colleagues evaluated data on 157,282 women between the ages of 50 and 79 who were enrolled in the Women’s Health Initiative between 1993 and 2018.

The women were a mean age of 63.1 years and 47,126 (30%) experienced an incident fracture during the study period.

With a mean follow-up of 15.4 years, each type of fracture was associated with an increased risk of a subsequent fracture after adjusting for age, race/ethnicity, body mass index, hormone therapy use, and other factors.

A wide range of initial risk fractures – including an initial lower arm or wrist fracture (adjusted hazard ratio, 4.80), upper arm or shoulder fracture (aHR, 5.06), upper leg fracture (aHR, 5.11), knee fracture (aHR, 5.03), lower leg/ankle fracture (aHR, 4.10), and spinal fracture (aHR, 6.69) – increased the risk of sustaining a subsequent hip fracture. 

For initial fractures of the lower arm or wrist, there was an increased risk of a subsequent fracture of the upper arm/shoulder, upper leg, knee, lower leg/ankle, hip/pelvis, and spine (aHRs ranged from 2.63 to 5.68). 

“The finding that knee fracture has the same prognostic value for subsequent fracture as hip or wrist fracture is a novel key finding, as knee fracture is generally not considered ‘osteoporotic’,” the authors noted.

The risk of fracture after sustaining an initial hip or pelvis fracture was exceptionally high – with as much as a 27-fold higher risk of a subsequent upper leg (nonhip) fracture (aHR, 27.18).

“Thirty-four percent of women who experienced initial hip or pelvis fracture experienced a subsequent nonhip fracture,” the authors noted.

However, the risks associated with an initial hip fracture are already well established, and the study’s more notable findings are the risks of other bone breaks, Dr. Crandall told this news organization.

“The (increased risk with hip fracture) is a rather substantial result,” she said. “However, the more major point of this study is that no matter where the initial fracture happened, the risk of the future fracture was elevated.”
 

Don’t disregard risks in younger women, racial/ethnic groups

The findings regarding age are also important. The highest risk was observed in the youngest postmenopausal age group of 50-59 years (aHR, 6.45), which decreased slightly in the 60- to 69-year age group (aHR, 6.04) and further decreased in the 70- to 79-year age group (aHR, 4.99).

“This was a surprise, and it highlights that clinicians should not disregard initial fractures among young postmenopausal women,” Dr. Crandall told this news organization.

Even greater increased risks for a subsequent fracture following an initial lower extremity fracture were observed in non-Hispanic Black women, Hispanic or Latina women, and women of Asian Pacific Islander ethnicity, ranging from ninefold to 14-fold, versus a sevenfold risk among non-Hispanic White women.

“This has public health implications because it means that we may have been missing the opportunity to prevent fractures among younger postmenopausal women and underrepresented racial/ethnic groups,” Dr. Crandall noted.

Is risk greatest 1-2 years after the initial fracture?

The findings suggest that current treatment guidelines may need to be revisited in light of inconsistencies regarding when, and for which fracture types, to initiate treatment.

“It will be important to determine whether existing risk calculators can be adapted (or new calculators developed) to help refine decision-making to determine which of the women with fractures other than hip or vertebral fractures should be treated,” the authors wrote.

Dr. McClung said a randomized, controlled trial of osteoporosis treatment in people who present with all types of fractures would help determine whether having a knee or a wrist fracture does indeed warrant such therapy.

He further commented that future studies should evaluate the shorter- versus longer-term risks.

“The most recent research suggests that the risk of having a second fracture is much higher in the first year or 2 after the first or incident fracture,” he observed. “So, the next stage in research with this dataset would be to ask not what happens over a 10-year time frame but what happens over the first year or 2 after the fracture.”

The study was funded by the National Heart, Lung, and Blood Institute. Dr. Crandall reported no relevant financial relationships. Dr. McClung reported being a consultant and on the speakers bureau for Amgen and being a speaker for Alexion.

A version of this article first appeared on Medscape.com.

“Antibiotic stewardship is never easy, and sometimes it is very difficult to differentiate what is going on with a patient in the clinical setting,” said Valerie M. Vaughn, MD, of the University of Utah, Salt Lake City, at SHM Converge, the annual conference of the Society of Hospital Medicine.

“We know from studies that 20% of hospitalized patients who receive an antibiotic have an adverse drug event from that antibiotic within 30 days,” said Dr. Vaughn.

Dr. Vaughn identified several practical ways in which hospitalists can reduce antibiotic overuse, including in the management of patients hospitalized with COVID-19.
 

Identify asymptomatic bacteriuria

One key area in which hospitalists can improve antibiotic stewardship is in recognizing asymptomatic bacteriuria and the harms associated with treatment, Dr. Vaughn said. For example, a common scenario for hospitalists might involve and 80-year-old woman with dementia, who can provide little in the way of history, and whose chest x-ray can’t rule out an underlying infection. This patient might have a positive urine culture, but no other signs of a urinary tract infection. “We know that asymptomatic bacteriuria is very common in hospitalized patients,” especially elderly women living in nursing home settings, she noted.

In cases of asymptomatic bacteriuria, data show that antibiotic treatment does not improve outcomes, and in fact may increase the risk of subsequent UTI, said Dr. Vaughn. Elderly patients also are at increased risk for developing antibiotic-related adverse events, especially Clostridioides difficile. Asymptomatic bacteriuria is any bacteria in the urine in the absence of signs or symptoms of a UTI, even if lab tests show pyuria, nitrates, and resistant bacteria. These lab results are often associated with inappropriate antibiotic use. “The laboratory tests can’t distinguish between asymptomatic bacteriuria and a UTI, only the symptoms can,” she emphasized.
 

Contain treatment of community-acquired pneumonia

Another practical point for reducing antibiotics in the hospital setting is to limit treatment of community-acquired pneumonia (CAP) to 5 days when possible. Duration matters because for many diseases, shorter durations of antibiotic treatments are just as effective as longer durations based on the latest evidence. “This is a change in dogma,” from previous thinking that patients must complete a full course, and that anything less might promote antibiotic resistance, she said.

“In fact, longer antibiotic durations kill off more healthy, normal flora, select for resistant pathogens, increase the risk of C. difficile, and increase the risk of side effects,” she said.

Ultimately, the right treatment duration for pneumonia depends on several factors including patient factors, disease, clinical stability, and rate of improvement. However, a good rule of thumb is that approximately 89% of CAP patients need only 5 days of antibiotics as long as they are afebrile for 48 hours and have 1 or fewer vital sign abnormalities by day 5 of treatment. “We do need to prescribe longer durations for patients with complications,” she emphasized.
 

Revisit need for antibiotics at discharge

Hospitalists also can practice antibiotic stewardship by considering four points at patient discharge, said Dr. Vaughn.

First, consider whether antibiotics can be stopped. For example, antibiotics are not needed on discharge if infection is no longer the most likely diagnosis, or if the course of antibiotics has been completed, as is often the case for patients hospitalized with CAP, she noted.

Second, if the antibiotics can’t be stopped at the time of discharge, consider whether the preferred agent is being used. Third, be sure the patient is receiving the minimum duration of antibiotics, and fourth, be sure that the dose, indication, and total planned duration with start and stop dates is written in the discharge summary, said Dr. Vaughn. “This helps with communication to our outpatient providers as well as with education to the patients themselves.”
 

Bacterial coinfections rare in COVID-19

Dr. Vaughn concluded the session with data from a study she conducted with colleagues on the use of empiric antibacterial therapy and community-onset bacterial coinfection in hospitalized COVID-19 patients. The study included 1,667 patients at 32 hospitals in Michigan. The number of patients treated with antibiotics varied widely among hospitals, from 30% to as much as 90%, Dr. Vaughn said.

“What we found was that more than half of hospitalized patients with COVID (57%) received empiric antibiotic therapy in the first few days of hospitalization,” she said.

However, “despite all the antibiotic use, community-onset bacterial coinfections were rare,” and occurred in only 3.5% of the patients, meaning that the number needed to treat with antibiotics to prevent a single case was about 20.

Predictors of community-onset co-infections in the patients included older age, more severe disease, patients coming from nursing homes, and those with lower BMI or kidney disease, said Dr. Vaughn. She and her team also found that procalcitonin’s positive predictive value was 9.3%, but the negative predictive value was 98.3%, so these patients were extremely likely to have no coinfection.

Dr. Vaughn said that in her practice she might order procalcitonin when considering stopping antibiotics in a patient with COVID-19 and make a decision based on the negative predictive value, but she emphasized that she does not use it in the converse situation to rely on a positive value when deciding whether to start antibiotics in these patients.

Dr. Vaughn had no financial conflicts to disclose.

“Antibiotic stewardship is never easy, and sometimes it is very difficult to differentiate what is going on with a patient in the clinical setting,” said Valerie M. Vaughn, MD, of the University of Utah, Salt Lake City, at SHM Converge, the annual conference of the Society of Hospital Medicine.

“We know from studies that 20% of hospitalized patients who receive an antibiotic have an adverse drug event from that antibiotic within 30 days,” said Dr. Vaughn.

Dr. Vaughn identified several practical ways in which hospitalists can reduce antibiotic overuse, including in the management of patients hospitalized with COVID-19.
 

Identify asymptomatic bacteriuria

One key area in which hospitalists can improve antibiotic stewardship is in recognizing asymptomatic bacteriuria and the harms associated with treatment, Dr. Vaughn said. For example, a common scenario for hospitalists might involve and 80-year-old woman with dementia, who can provide little in the way of history, and whose chest x-ray can’t rule out an underlying infection. This patient might have a positive urine culture, but no other signs of a urinary tract infection. “We know that asymptomatic bacteriuria is very common in hospitalized patients,” especially elderly women living in nursing home settings, she noted.

In cases of asymptomatic bacteriuria, data show that antibiotic treatment does not improve outcomes, and in fact may increase the risk of subsequent UTI, said Dr. Vaughn. Elderly patients also are at increased risk for developing antibiotic-related adverse events, especially Clostridioides difficile. Asymptomatic bacteriuria is any bacteria in the urine in the absence of signs or symptoms of a UTI, even if lab tests show pyuria, nitrates, and resistant bacteria. These lab results are often associated with inappropriate antibiotic use. “The laboratory tests can’t distinguish between asymptomatic bacteriuria and a UTI, only the symptoms can,” she emphasized.
 

Contain treatment of community-acquired pneumonia

Another practical point for reducing antibiotics in the hospital setting is to limit treatment of community-acquired pneumonia (CAP) to 5 days when possible. Duration matters because for many diseases, shorter durations of antibiotic treatments are just as effective as longer durations based on the latest evidence. “This is a change in dogma,” from previous thinking that patients must complete a full course, and that anything less might promote antibiotic resistance, she said.

“In fact, longer antibiotic durations kill off more healthy, normal flora, select for resistant pathogens, increase the risk of C. difficile, and increase the risk of side effects,” she said.

Ultimately, the right treatment duration for pneumonia depends on several factors including patient factors, disease, clinical stability, and rate of improvement. However, a good rule of thumb is that approximately 89% of CAP patients need only 5 days of antibiotics as long as they are afebrile for 48 hours and have 1 or fewer vital sign abnormalities by day 5 of treatment. “We do need to prescribe longer durations for patients with complications,” she emphasized.
 

Revisit need for antibiotics at discharge

Hospitalists also can practice antibiotic stewardship by considering four points at patient discharge, said Dr. Vaughn.

First, consider whether antibiotics can be stopped. For example, antibiotics are not needed on discharge if infection is no longer the most likely diagnosis, or if the course of antibiotics has been completed, as is often the case for patients hospitalized with CAP, she noted.

Second, if the antibiotics can’t be stopped at the time of discharge, consider whether the preferred agent is being used. Third, be sure the patient is receiving the minimum duration of antibiotics, and fourth, be sure that the dose, indication, and total planned duration with start and stop dates is written in the discharge summary, said Dr. Vaughn. “This helps with communication to our outpatient providers as well as with education to the patients themselves.”
 

Bacterial coinfections rare in COVID-19

Dr. Vaughn concluded the session with data from a study she conducted with colleagues on the use of empiric antibacterial therapy and community-onset bacterial coinfection in hospitalized COVID-19 patients. The study included 1,667 patients at 32 hospitals in Michigan. The number of patients treated with antibiotics varied widely among hospitals, from 30% to as much as 90%, Dr. Vaughn said.

“What we found was that more than half of hospitalized patients with COVID (57%) received empiric antibiotic therapy in the first few days of hospitalization,” she said.

However, “despite all the antibiotic use, community-onset bacterial coinfections were rare,” and occurred in only 3.5% of the patients, meaning that the number needed to treat with antibiotics to prevent a single case was about 20.

Predictors of community-onset co-infections in the patients included older age, more severe disease, patients coming from nursing homes, and those with lower BMI or kidney disease, said Dr. Vaughn. She and her team also found that procalcitonin’s positive predictive value was 9.3%, but the negative predictive value was 98.3%, so these patients were extremely likely to have no coinfection.

Dr. Vaughn said that in her practice she might order procalcitonin when considering stopping antibiotics in a patient with COVID-19 and make a decision based on the negative predictive value, but she emphasized that she does not use it in the converse situation to rely on a positive value when deciding whether to start antibiotics in these patients.

Dr. Vaughn had no financial conflicts to disclose.

“Antibiotic stewardship is never easy, and sometimes it is very difficult to differentiate what is going on with a patient in the clinical setting,” said Valerie M. Vaughn, MD, of the University of Utah, Salt Lake City, at SHM Converge, the annual conference of the Society of Hospital Medicine.

“We know from studies that 20% of hospitalized patients who receive an antibiotic have an adverse drug event from that antibiotic within 30 days,” said Dr. Vaughn.

Dr. Vaughn identified several practical ways in which hospitalists can reduce antibiotic overuse, including in the management of patients hospitalized with COVID-19.
 

Identify asymptomatic bacteriuria

One key area in which hospitalists can improve antibiotic stewardship is in recognizing asymptomatic bacteriuria and the harms associated with treatment, Dr. Vaughn said. For example, a common scenario for hospitalists might involve and 80-year-old woman with dementia, who can provide little in the way of history, and whose chest x-ray can’t rule out an underlying infection. This patient might have a positive urine culture, but no other signs of a urinary tract infection. “We know that asymptomatic bacteriuria is very common in hospitalized patients,” especially elderly women living in nursing home settings, she noted.

In cases of asymptomatic bacteriuria, data show that antibiotic treatment does not improve outcomes, and in fact may increase the risk of subsequent UTI, said Dr. Vaughn. Elderly patients also are at increased risk for developing antibiotic-related adverse events, especially Clostridioides difficile. Asymptomatic bacteriuria is any bacteria in the urine in the absence of signs or symptoms of a UTI, even if lab tests show pyuria, nitrates, and resistant bacteria. These lab results are often associated with inappropriate antibiotic use. “The laboratory tests can’t distinguish between asymptomatic bacteriuria and a UTI, only the symptoms can,” she emphasized.
 

Contain treatment of community-acquired pneumonia

Another practical point for reducing antibiotics in the hospital setting is to limit treatment of community-acquired pneumonia (CAP) to 5 days when possible. Duration matters because for many diseases, shorter durations of antibiotic treatments are just as effective as longer durations based on the latest evidence. “This is a change in dogma,” from previous thinking that patients must complete a full course, and that anything less might promote antibiotic resistance, she said.

“In fact, longer antibiotic durations kill off more healthy, normal flora, select for resistant pathogens, increase the risk of C. difficile, and increase the risk of side effects,” she said.

Ultimately, the right treatment duration for pneumonia depends on several factors including patient factors, disease, clinical stability, and rate of improvement. However, a good rule of thumb is that approximately 89% of CAP patients need only 5 days of antibiotics as long as they are afebrile for 48 hours and have 1 or fewer vital sign abnormalities by day 5 of treatment. “We do need to prescribe longer durations for patients with complications,” she emphasized.
 

Revisit need for antibiotics at discharge

Hospitalists also can practice antibiotic stewardship by considering four points at patient discharge, said Dr. Vaughn.

First, consider whether antibiotics can be stopped. For example, antibiotics are not needed on discharge if infection is no longer the most likely diagnosis, or if the course of antibiotics has been completed, as is often the case for patients hospitalized with CAP, she noted.

Second, if the antibiotics can’t be stopped at the time of discharge, consider whether the preferred agent is being used. Third, be sure the patient is receiving the minimum duration of antibiotics, and fourth, be sure that the dose, indication, and total planned duration with start and stop dates is written in the discharge summary, said Dr. Vaughn. “This helps with communication to our outpatient providers as well as with education to the patients themselves.”
 

Bacterial coinfections rare in COVID-19

Dr. Vaughn concluded the session with data from a study she conducted with colleagues on the use of empiric antibacterial therapy and community-onset bacterial coinfection in hospitalized COVID-19 patients. The study included 1,667 patients at 32 hospitals in Michigan. The number of patients treated with antibiotics varied widely among hospitals, from 30% to as much as 90%, Dr. Vaughn said.

“What we found was that more than half of hospitalized patients with COVID (57%) received empiric antibiotic therapy in the first few days of hospitalization,” she said.

However, “despite all the antibiotic use, community-onset bacterial coinfections were rare,” and occurred in only 3.5% of the patients, meaning that the number needed to treat with antibiotics to prevent a single case was about 20.

Predictors of community-onset co-infections in the patients included older age, more severe disease, patients coming from nursing homes, and those with lower BMI or kidney disease, said Dr. Vaughn. She and her team also found that procalcitonin’s positive predictive value was 9.3%, but the negative predictive value was 98.3%, so these patients were extremely likely to have no coinfection.

Dr. Vaughn said that in her practice she might order procalcitonin when considering stopping antibiotics in a patient with COVID-19 and make a decision based on the negative predictive value, but she emphasized that she does not use it in the converse situation to rely on a positive value when deciding whether to start antibiotics in these patients.

Dr. Vaughn had no financial conflicts to disclose.

Your mentor has been looking for someone to help lead a new project in your division, and tells you she’s been having a hard time finding someone – but that you would be great. The project isn’t something you are very interested in doing and you’re already swamped with other projects, but the mentor seems to need the help. What do you do?

Mentor-mentee relationships can be deeply beneficial, but the dynamics – in this situation and many others – can be complex. At SHM Converge, the annual conference of the Society of Hospital Medicine, panelists offered guidance on how best to navigate this terrain.

Vineet Arora, MD, MAPP, MHM, associate chief medical officer for clinical learning environment at the University of Chicago, suggested that, in the situation involving the mentor’s request to an uncertain mentee, the mentee should not give an immediate answer, but consider the pros and cons.

“It’s tough when it’s somebody who’s directly overseeing you,” she said. “If you’re really truly the best person, they’re going to want you in the job, and maybe they’ll make it work for you.” She said it would be important to find out why the mentor is having trouble finding someone, and suggested the mentee could find someone with whom to discuss it.

Calling mentoring a “team sport,” Dr. Arora described several types: the traditional mentor who helps many aspects of a mentee’s career, a “coach” who helps on a specific project or topic, a “sponsor” that can help elevate a mentee to a bigger opportunity, and a “connector” who can help a mentee begin new career relationships.

“Don’t invest in just one person,” she said. “Try to get that personal board of directors.”

She mentioned six things all mentors should do: Choose mentees carefully, establish a mentorship team, run a tight ship, head off rifts or resolve them, prepare for transitions when they take a new position and might have a new relationship with a mentee, and don’t commit “mentorship malpractice.”

Mentoring is a two-way street, with both people benefiting and learning, but mentoring can have its troubles, either through active, dysfunctional behavior that’s easy to spot, or passive behavior, such as the “bottleneck” problem when a mentor is too preoccupied with his or her own priorities to mentor well, the “country clubber” who mentors only for popularity and social capital but doesn’t do the work required, and the “world traveler” who is sought after but has little time for day-to-day mentoring.

Valerie Vaughan, MD, MSc, assistant professor of medicine at the University of Utah, described four “golden rules” of being a mentee. First, find a CAPE mentor (for capable, availability, projects of interest, and easy to get along with). Then, be respectful of a mentor’s time, communicate effectively, and be engaged and energizing.

“Mentors typically don’t get paid to mentor and so a lot of them are doing it because they find joy for doing it,” Dr. Vaughan said. “So as much as you can as a mentee, try to be the person who brings energy to the mentor-mentee relationship. It’s up to you to drive projects forward.”

Valerie Press, MD, MPH, SFHM, associate professor of medicine at the University of Chicago, offered tips for men who are mentoring women. She said that, while cross-gender mentorship is common and important, gender-based stereotypes and “unconscious assumptions” are alive and well. Women, she noted, have less access to mentorship and sponsorship, are paid less for the same work, and have high rates of attrition.

Male mentors have to meet the challenge of thinking outside of their own lived experience, combating stereotypes, and addressing these gender-based career disparities, she said.

She suggested that male mentors, for one thing, “rewrite gender scripts,” with comments such as, “This is a difficult situation, but I have confidence in you! What do you think your next move should be?” They should also “learn from each other on how to change the power dynamic,” and start and participate in conversations involving emotions, since they can be clues to what a mentee is experiencing.

When it comes to pushing for better policies, “be an upstander, not a bystander,” Dr. Press said.

“Use your organizational power and your social capital,” she said. “Use your voice to help make more equitable policies. Don’t just leave it to the women’s committee to come up with solutions to lack of lactation rooms, or paternity and maternity leave, or better daycare. These are family issues and everybody issues.”

Maylyn S. Martinez, MD, clinical associate professor of medicine at the University of Chicago, suggested that mentors for physicians from minority groups should resist the tendency to view their interests narrowly.

“Don’t assume that their interests are going to center on their gender or minority status – invite them to be on projects that have nothing to do with that,” she said. They should also not be encouraged to do projects that won’t help with career advancement any more than others would be encouraged to take on such projects.

“Be the solution,” she said. “Not the problem.”
 

Your mentor has been looking for someone to help lead a new project in your division, and tells you she’s been having a hard time finding someone – but that you would be great. The project isn’t something you are very interested in doing and you’re already swamped with other projects, but the mentor seems to need the help. What do you do?

Mentor-mentee relationships can be deeply beneficial, but the dynamics – in this situation and many others – can be complex. At SHM Converge, the annual conference of the Society of Hospital Medicine, panelists offered guidance on how best to navigate this terrain.

Vineet Arora, MD, MAPP, MHM, associate chief medical officer for clinical learning environment at the University of Chicago, suggested that, in the situation involving the mentor’s request to an uncertain mentee, the mentee should not give an immediate answer, but consider the pros and cons.

“It’s tough when it’s somebody who’s directly overseeing you,” she said. “If you’re really truly the best person, they’re going to want you in the job, and maybe they’ll make it work for you.” She said it would be important to find out why the mentor is having trouble finding someone, and suggested the mentee could find someone with whom to discuss it.

Calling mentoring a “team sport,” Dr. Arora described several types: the traditional mentor who helps many aspects of a mentee’s career, a “coach” who helps on a specific project or topic, a “sponsor” that can help elevate a mentee to a bigger opportunity, and a “connector” who can help a mentee begin new career relationships.

“Don’t invest in just one person,” she said. “Try to get that personal board of directors.”

She mentioned six things all mentors should do: Choose mentees carefully, establish a mentorship team, run a tight ship, head off rifts or resolve them, prepare for transitions when they take a new position and might have a new relationship with a mentee, and don’t commit “mentorship malpractice.”

Mentoring is a two-way street, with both people benefiting and learning, but mentoring can have its troubles, either through active, dysfunctional behavior that’s easy to spot, or passive behavior, such as the “bottleneck” problem when a mentor is too preoccupied with his or her own priorities to mentor well, the “country clubber” who mentors only for popularity and social capital but doesn’t do the work required, and the “world traveler” who is sought after but has little time for day-to-day mentoring.

Valerie Vaughan, MD, MSc, assistant professor of medicine at the University of Utah, described four “golden rules” of being a mentee. First, find a CAPE mentor (for capable, availability, projects of interest, and easy to get along with). Then, be respectful of a mentor’s time, communicate effectively, and be engaged and energizing.

“Mentors typically don’t get paid to mentor and so a lot of them are doing it because they find joy for doing it,” Dr. Vaughan said. “So as much as you can as a mentee, try to be the person who brings energy to the mentor-mentee relationship. It’s up to you to drive projects forward.”

Valerie Press, MD, MPH, SFHM, associate professor of medicine at the University of Chicago, offered tips for men who are mentoring women. She said that, while cross-gender mentorship is common and important, gender-based stereotypes and “unconscious assumptions” are alive and well. Women, she noted, have less access to mentorship and sponsorship, are paid less for the same work, and have high rates of attrition.

Male mentors have to meet the challenge of thinking outside of their own lived experience, combating stereotypes, and addressing these gender-based career disparities, she said.

She suggested that male mentors, for one thing, “rewrite gender scripts,” with comments such as, “This is a difficult situation, but I have confidence in you! What do you think your next move should be?” They should also “learn from each other on how to change the power dynamic,” and start and participate in conversations involving emotions, since they can be clues to what a mentee is experiencing.

When it comes to pushing for better policies, “be an upstander, not a bystander,” Dr. Press said.

“Use your organizational power and your social capital,” she said. “Use your voice to help make more equitable policies. Don’t just leave it to the women’s committee to come up with solutions to lack of lactation rooms, or paternity and maternity leave, or better daycare. These are family issues and everybody issues.”

Maylyn S. Martinez, MD, clinical associate professor of medicine at the University of Chicago, suggested that mentors for physicians from minority groups should resist the tendency to view their interests narrowly.

“Don’t assume that their interests are going to center on their gender or minority status – invite them to be on projects that have nothing to do with that,” she said. They should also not be encouraged to do projects that won’t help with career advancement any more than others would be encouraged to take on such projects.

“Be the solution,” she said. “Not the problem.”
 

Your mentor has been looking for someone to help lead a new project in your division, and tells you she’s been having a hard time finding someone – but that you would be great. The project isn’t something you are very interested in doing and you’re already swamped with other projects, but the mentor seems to need the help. What do you do?

Mentor-mentee relationships can be deeply beneficial, but the dynamics – in this situation and many others – can be complex. At SHM Converge, the annual conference of the Society of Hospital Medicine, panelists offered guidance on how best to navigate this terrain.

Vineet Arora, MD, MAPP, MHM, associate chief medical officer for clinical learning environment at the University of Chicago, suggested that, in the situation involving the mentor’s request to an uncertain mentee, the mentee should not give an immediate answer, but consider the pros and cons.

“It’s tough when it’s somebody who’s directly overseeing you,” she said. “If you’re really truly the best person, they’re going to want you in the job, and maybe they’ll make it work for you.” She said it would be important to find out why the mentor is having trouble finding someone, and suggested the mentee could find someone with whom to discuss it.

Calling mentoring a “team sport,” Dr. Arora described several types: the traditional mentor who helps many aspects of a mentee’s career, a “coach” who helps on a specific project or topic, a “sponsor” that can help elevate a mentee to a bigger opportunity, and a “connector” who can help a mentee begin new career relationships.

“Don’t invest in just one person,” she said. “Try to get that personal board of directors.”

She mentioned six things all mentors should do: Choose mentees carefully, establish a mentorship team, run a tight ship, head off rifts or resolve them, prepare for transitions when they take a new position and might have a new relationship with a mentee, and don’t commit “mentorship malpractice.”

Mentoring is a two-way street, with both people benefiting and learning, but mentoring can have its troubles, either through active, dysfunctional behavior that’s easy to spot, or passive behavior, such as the “bottleneck” problem when a mentor is too preoccupied with his or her own priorities to mentor well, the “country clubber” who mentors only for popularity and social capital but doesn’t do the work required, and the “world traveler” who is sought after but has little time for day-to-day mentoring.

Valerie Vaughan, MD, MSc, assistant professor of medicine at the University of Utah, described four “golden rules” of being a mentee. First, find a CAPE mentor (for capable, availability, projects of interest, and easy to get along with). Then, be respectful of a mentor’s time, communicate effectively, and be engaged and energizing.

“Mentors typically don’t get paid to mentor and so a lot of them are doing it because they find joy for doing it,” Dr. Vaughan said. “So as much as you can as a mentee, try to be the person who brings energy to the mentor-mentee relationship. It’s up to you to drive projects forward.”

Valerie Press, MD, MPH, SFHM, associate professor of medicine at the University of Chicago, offered tips for men who are mentoring women. She said that, while cross-gender mentorship is common and important, gender-based stereotypes and “unconscious assumptions” are alive and well. Women, she noted, have less access to mentorship and sponsorship, are paid less for the same work, and have high rates of attrition.

Male mentors have to meet the challenge of thinking outside of their own lived experience, combating stereotypes, and addressing these gender-based career disparities, she said.

She suggested that male mentors, for one thing, “rewrite gender scripts,” with comments such as, “This is a difficult situation, but I have confidence in you! What do you think your next move should be?” They should also “learn from each other on how to change the power dynamic,” and start and participate in conversations involving emotions, since they can be clues to what a mentee is experiencing.

When it comes to pushing for better policies, “be an upstander, not a bystander,” Dr. Press said.

“Use your organizational power and your social capital,” she said. “Use your voice to help make more equitable policies. Don’t just leave it to the women’s committee to come up with solutions to lack of lactation rooms, or paternity and maternity leave, or better daycare. These are family issues and everybody issues.”

Maylyn S. Martinez, MD, clinical associate professor of medicine at the University of Chicago, suggested that mentors for physicians from minority groups should resist the tendency to view their interests narrowly.

“Don’t assume that their interests are going to center on their gender or minority status – invite them to be on projects that have nothing to do with that,” she said. They should also not be encouraged to do projects that won’t help with career advancement any more than others would be encouraged to take on such projects.

“Be the solution,” she said. “Not the problem.”