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Faulty equipment blamed for improper diagnosis: $78M verdict … and more

AT 36 WEEKS’ GESTATION, a woman went to the emergency department (ED) with abdominal pain. After ultrasonography (US), a nurse told her the fetus had died in utero, but the mother continued to feel fetal movement. The ED physician requested a second US, but it took 75 minutes for a radiology technician to arrive. This US showed a beating fetal heart with placental abruption. After cesarean delivery, the child was found to have cerebral palsy.
PATIENT’S CLAIM The first US was performed by an inexperienced technician using outdated equipment and the wrong transducer. An experienced technician with newer equipment should have been immediately available. The ED physician did not react when fetal distress was first identified.
DEFENDANTS’ DEFENSE The ED physician was told that the baby had died. Perhaps the child’s heart had started again by the time the second US was performed and a heartbeat found. The hospital denied negligence.
VERDICT A Pennsylvania jury found the ED physician not negligent; the hospital was 100% at fault. A $78.5 million verdict included $1.5 million in emotional distress to the mother, $10 million in pain and suffering for the child, $2million in lost future earnings, and the rest in future medical expenses.
Ligated ureter found after hysterectomy
A 50-YEAR-OLD WOMAN underwent laparoscopically assisted vaginal hysterectomy. She went to the ED with pain 6 days later. Imaging studies indicated a ligated ureter; a nephrostomy tube was placed. She required a nephrostomy bag for 4 months and underwent two repair operations.
PATIENT’S CLAIM The patient’s ureter was ligated and/or constricted during surgery. The gynecologist was negligent in failing to recognize and repair the injury during surgery.
PHYSICIAN’S DEFENSE The ureter was not ligated during surgery; therefore it could not have been discovered. In addition, injury to a ureter is a known risk of the procedure.
VERDICT An Arizona defense verdict was returned.
Myomectomy after cesarean; mother dies
IMMEDIATELY AFTER A WOMAN with preeclampsia had a cesarean delivery, she underwent a myomectomy. The day before discharge, her abdominal incision opened and a clear liquid drained. The day after discharge, she went to the ED with intense abdominal pain. Necrotizing fasciitis was found and debridement surgery performed. She was transferred to another hospital but died of sepsis several days later.
ESTATE’S CLAIM The infection occurred because the myomectomy was performed immediately following cesarean delivery. Prophylactic antibiotics were not prescribed before surgery. The mother was not fully informed as to the risks of concurrent operations. The ObGyns failed to recognize the infection before discharging the patient.
PHYSICIANS’ DEFENSE The patient was fully informed of the risks of surgery; it was reasonable to perform myomectomy immediately following cesarean delivery. There were no signs or symptoms of infection before discharge. Cesarean incisions open about 30% of the time—not a cause for concern. Prophylactic antibiotics for cesarean procedures are not standard of care. The patient’s infection was caused by a rapidly spreading, rare bacterium.
VERDICT A Michigan defense verdict was returned.
TOLAC to cesarean: baby has cerebral palsy
A WOMAN WANTED A TRIAL OF LABOR after a previous cesarean delivery (TOLAC). During labor, fetal distress was noted, and a cesarean delivery was performed. Uterine rupture had occurred. The baby has spastic cerebral palsy with significantly impaired neuromotor and cognitive abilities.
PARENTS’ CLAIM The hospital staff and physicians overlooked earlier fetal distress. A timelier delivery would have prevented the child’s injuries.
DEFENDANTs’ DEFENSE The hospital reached a confidential settlement. The ObGyns claimed fetal tracings were not suggestive of uterine rupture; they met the standard of care.
VERDICT A Texas defense verdict was returned.

WHEN GESTATIONAL DIABETES WAS DIAGNOSED at 33 weeks’ gestation, a family practitioner (FP) referred the mother to an ObGyn practice. Two ObGyns performed amniocentesis to check fetal lung maturity. After the procedure, fetal distress was noted, and the ObGyns instructed the FP to induce labor.
The baby suffered brain damage, had seizures, and has cerebral palsy. She was born without kidney function. By age 10, she had 2 kidney transplant operations and functions at a pre-kindergarten level.
PATIENT’S CLAIM The mother was not fully informed of the risks of and alternatives to amniocentesis. Although complications arose before amniocentesis, the test proceeded. The ObGyns were negligent in not performing cesarean delivery when fetal distress was detected.
DEFENDANTS’ DEFENSE The FP and hospital settled prior to trial. The ObGyns claimed that their care was an appropriate alternative to the actions the patient claimed should have been taken.
VERDICT Costs for the child’s care had reached $1.4 million before trial. A $9 million Virginia verdict was returned that included $7 million for the child and $2 million for the mother, but the settlement was reduced by the state cap.
Did HT cause breast cancer?
A 52-YEAR-OLD WOMAN was prescribed conjugated estrogens/medroxyprogesterone acetate (Prempro, Wyeth, Inc.) for hormone therapy by her gynecologist.
After taking the drug for 5 years, the patient developed invasive breast cancer. She underwent a lumpectomy, chemotherapy, and three reconstructive surgeries.
PATIENT’S CLAIM The manufacturer failed to warn of a woman’s risk of developing breast cancer while taking the product.
DEFENDANT’S DEFENSE Prempro alone does not cause cancer. The drug is just one of many contributing factors that may or may not increase the risk of developing breast cancer.
VERDICT A $3.75 million Connecticut verdict was returned for the patient plus $250,000 to her husband for loss of consortium.
Failure to diagnose preeclampsia—twice
AT 28 WEEKS’ GESTATION, a woman with a history of hypertension went to an ED with headache, nausea, vomiting, cramping, and ringing in her ears. After waiting 4 hours before being seen, her BP was 150/108 mm Hg and normal fetal heart tones were heard. The ED physician diagnosed otitis media and discharged her.
Later that evening, the patient returned to the ED with similar symptoms. A urine specimen showed significant proteinuria and the fetal heart rate was 158 bpm. A second ED physician diagnosed a urinary tract infection, prescribed antibiotics and pain medication, and sent her home.
A few hours later, she returned to the ED by ambulance suffering from eclamptic seizures. Her BP was 174/121 mm Hg, and no fetal heart tones were heard. She delivered a stillborn child by cesarean delivery.
PATIENT’S CLAIM The ED physicians were negligent in failing to diagnose preeclampsia at the first two visits.
PHYSICIANS’ DEFENSE The first ED physician settled for $45,000 while serving a prison sentence after conviction on two sex-abuse felonies related to his treatment of female patients at the same ED. The second ED physician denied negligence.
VERDICT A $50,000 Alabama verdict was returned for compensatory damages for the mother and $600,000 punitive damages for the stillborn child.
Inflated Foley catheter injures mother
DURING A LONG AND DIFFICULT LABOR, an ObGyn used forceps to complete delivery of a 31-year-old woman’s first child. The baby was healthy, but the mother has suffered urinary incontinence since delivery. Despite several repair operations, the condition remains.
PATIENT’S CLAIM The ObGyn was negligent in failing to remove a fully inflated Foley catheter before beginning delivery, leading to a urethral sphincter injury.
PHYSICIAN’S DEFENSE The decision regarding removal of the catheter was a matter of hospital policy. The ObGyn blamed improper catheter placement on the nurses.
VERDICT A Kentucky defense verdict was returned.
These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.
We want to hear from you! Tell us what you think.

AT 36 WEEKS’ GESTATION, a woman went to the emergency department (ED) with abdominal pain. After ultrasonography (US), a nurse told her the fetus had died in utero, but the mother continued to feel fetal movement. The ED physician requested a second US, but it took 75 minutes for a radiology technician to arrive. This US showed a beating fetal heart with placental abruption. After cesarean delivery, the child was found to have cerebral palsy.
PATIENT’S CLAIM The first US was performed by an inexperienced technician using outdated equipment and the wrong transducer. An experienced technician with newer equipment should have been immediately available. The ED physician did not react when fetal distress was first identified.
DEFENDANTS’ DEFENSE The ED physician was told that the baby had died. Perhaps the child’s heart had started again by the time the second US was performed and a heartbeat found. The hospital denied negligence.
VERDICT A Pennsylvania jury found the ED physician not negligent; the hospital was 100% at fault. A $78.5 million verdict included $1.5 million in emotional distress to the mother, $10 million in pain and suffering for the child, $2million in lost future earnings, and the rest in future medical expenses.
Ligated ureter found after hysterectomy
A 50-YEAR-OLD WOMAN underwent laparoscopically assisted vaginal hysterectomy. She went to the ED with pain 6 days later. Imaging studies indicated a ligated ureter; a nephrostomy tube was placed. She required a nephrostomy bag for 4 months and underwent two repair operations.
PATIENT’S CLAIM The patient’s ureter was ligated and/or constricted during surgery. The gynecologist was negligent in failing to recognize and repair the injury during surgery.
PHYSICIAN’S DEFENSE The ureter was not ligated during surgery; therefore it could not have been discovered. In addition, injury to a ureter is a known risk of the procedure.
VERDICT An Arizona defense verdict was returned.
Myomectomy after cesarean; mother dies
IMMEDIATELY AFTER A WOMAN with preeclampsia had a cesarean delivery, she underwent a myomectomy. The day before discharge, her abdominal incision opened and a clear liquid drained. The day after discharge, she went to the ED with intense abdominal pain. Necrotizing fasciitis was found and debridement surgery performed. She was transferred to another hospital but died of sepsis several days later.
ESTATE’S CLAIM The infection occurred because the myomectomy was performed immediately following cesarean delivery. Prophylactic antibiotics were not prescribed before surgery. The mother was not fully informed as to the risks of concurrent operations. The ObGyns failed to recognize the infection before discharging the patient.
PHYSICIANS’ DEFENSE The patient was fully informed of the risks of surgery; it was reasonable to perform myomectomy immediately following cesarean delivery. There were no signs or symptoms of infection before discharge. Cesarean incisions open about 30% of the time—not a cause for concern. Prophylactic antibiotics for cesarean procedures are not standard of care. The patient’s infection was caused by a rapidly spreading, rare bacterium.
VERDICT A Michigan defense verdict was returned.
TOLAC to cesarean: baby has cerebral palsy
A WOMAN WANTED A TRIAL OF LABOR after a previous cesarean delivery (TOLAC). During labor, fetal distress was noted, and a cesarean delivery was performed. Uterine rupture had occurred. The baby has spastic cerebral palsy with significantly impaired neuromotor and cognitive abilities.
PARENTS’ CLAIM The hospital staff and physicians overlooked earlier fetal distress. A timelier delivery would have prevented the child’s injuries.
DEFENDANTs’ DEFENSE The hospital reached a confidential settlement. The ObGyns claimed fetal tracings were not suggestive of uterine rupture; they met the standard of care.
VERDICT A Texas defense verdict was returned.

WHEN GESTATIONAL DIABETES WAS DIAGNOSED at 33 weeks’ gestation, a family practitioner (FP) referred the mother to an ObGyn practice. Two ObGyns performed amniocentesis to check fetal lung maturity. After the procedure, fetal distress was noted, and the ObGyns instructed the FP to induce labor.
The baby suffered brain damage, had seizures, and has cerebral palsy. She was born without kidney function. By age 10, she had 2 kidney transplant operations and functions at a pre-kindergarten level.
PATIENT’S CLAIM The mother was not fully informed of the risks of and alternatives to amniocentesis. Although complications arose before amniocentesis, the test proceeded. The ObGyns were negligent in not performing cesarean delivery when fetal distress was detected.
DEFENDANTS’ DEFENSE The FP and hospital settled prior to trial. The ObGyns claimed that their care was an appropriate alternative to the actions the patient claimed should have been taken.
VERDICT Costs for the child’s care had reached $1.4 million before trial. A $9 million Virginia verdict was returned that included $7 million for the child and $2 million for the mother, but the settlement was reduced by the state cap.
Did HT cause breast cancer?
A 52-YEAR-OLD WOMAN was prescribed conjugated estrogens/medroxyprogesterone acetate (Prempro, Wyeth, Inc.) for hormone therapy by her gynecologist.
After taking the drug for 5 years, the patient developed invasive breast cancer. She underwent a lumpectomy, chemotherapy, and three reconstructive surgeries.
PATIENT’S CLAIM The manufacturer failed to warn of a woman’s risk of developing breast cancer while taking the product.
DEFENDANT’S DEFENSE Prempro alone does not cause cancer. The drug is just one of many contributing factors that may or may not increase the risk of developing breast cancer.
VERDICT A $3.75 million Connecticut verdict was returned for the patient plus $250,000 to her husband for loss of consortium.
Failure to diagnose preeclampsia—twice
AT 28 WEEKS’ GESTATION, a woman with a history of hypertension went to an ED with headache, nausea, vomiting, cramping, and ringing in her ears. After waiting 4 hours before being seen, her BP was 150/108 mm Hg and normal fetal heart tones were heard. The ED physician diagnosed otitis media and discharged her.
Later that evening, the patient returned to the ED with similar symptoms. A urine specimen showed significant proteinuria and the fetal heart rate was 158 bpm. A second ED physician diagnosed a urinary tract infection, prescribed antibiotics and pain medication, and sent her home.
A few hours later, she returned to the ED by ambulance suffering from eclamptic seizures. Her BP was 174/121 mm Hg, and no fetal heart tones were heard. She delivered a stillborn child by cesarean delivery.
PATIENT’S CLAIM The ED physicians were negligent in failing to diagnose preeclampsia at the first two visits.
PHYSICIANS’ DEFENSE The first ED physician settled for $45,000 while serving a prison sentence after conviction on two sex-abuse felonies related to his treatment of female patients at the same ED. The second ED physician denied negligence.
VERDICT A $50,000 Alabama verdict was returned for compensatory damages for the mother and $600,000 punitive damages for the stillborn child.
Inflated Foley catheter injures mother
DURING A LONG AND DIFFICULT LABOR, an ObGyn used forceps to complete delivery of a 31-year-old woman’s first child. The baby was healthy, but the mother has suffered urinary incontinence since delivery. Despite several repair operations, the condition remains.
PATIENT’S CLAIM The ObGyn was negligent in failing to remove a fully inflated Foley catheter before beginning delivery, leading to a urethral sphincter injury.
PHYSICIAN’S DEFENSE The decision regarding removal of the catheter was a matter of hospital policy. The ObGyn blamed improper catheter placement on the nurses.
VERDICT A Kentucky defense verdict was returned.

AT 36 WEEKS’ GESTATION, a woman went to the emergency department (ED) with abdominal pain. After ultrasonography (US), a nurse told her the fetus had died in utero, but the mother continued to feel fetal movement. The ED physician requested a second US, but it took 75 minutes for a radiology technician to arrive. This US showed a beating fetal heart with placental abruption. After cesarean delivery, the child was found to have cerebral palsy.
PATIENT’S CLAIM The first US was performed by an inexperienced technician using outdated equipment and the wrong transducer. An experienced technician with newer equipment should have been immediately available. The ED physician did not react when fetal distress was first identified.
DEFENDANTS’ DEFENSE The ED physician was told that the baby had died. Perhaps the child’s heart had started again by the time the second US was performed and a heartbeat found. The hospital denied negligence.
VERDICT A Pennsylvania jury found the ED physician not negligent; the hospital was 100% at fault. A $78.5 million verdict included $1.5 million in emotional distress to the mother, $10 million in pain and suffering for the child, $2million in lost future earnings, and the rest in future medical expenses.
Ligated ureter found after hysterectomy
A 50-YEAR-OLD WOMAN underwent laparoscopically assisted vaginal hysterectomy. She went to the ED with pain 6 days later. Imaging studies indicated a ligated ureter; a nephrostomy tube was placed. She required a nephrostomy bag for 4 months and underwent two repair operations.
PATIENT’S CLAIM The patient’s ureter was ligated and/or constricted during surgery. The gynecologist was negligent in failing to recognize and repair the injury during surgery.
PHYSICIAN’S DEFENSE The ureter was not ligated during surgery; therefore it could not have been discovered. In addition, injury to a ureter is a known risk of the procedure.
VERDICT An Arizona defense verdict was returned.
Myomectomy after cesarean; mother dies
IMMEDIATELY AFTER A WOMAN with preeclampsia had a cesarean delivery, she underwent a myomectomy. The day before discharge, her abdominal incision opened and a clear liquid drained. The day after discharge, she went to the ED with intense abdominal pain. Necrotizing fasciitis was found and debridement surgery performed. She was transferred to another hospital but died of sepsis several days later.
ESTATE’S CLAIM The infection occurred because the myomectomy was performed immediately following cesarean delivery. Prophylactic antibiotics were not prescribed before surgery. The mother was not fully informed as to the risks of concurrent operations. The ObGyns failed to recognize the infection before discharging the patient.
PHYSICIANS’ DEFENSE The patient was fully informed of the risks of surgery; it was reasonable to perform myomectomy immediately following cesarean delivery. There were no signs or symptoms of infection before discharge. Cesarean incisions open about 30% of the time—not a cause for concern. Prophylactic antibiotics for cesarean procedures are not standard of care. The patient’s infection was caused by a rapidly spreading, rare bacterium.
VERDICT A Michigan defense verdict was returned.
TOLAC to cesarean: baby has cerebral palsy
A WOMAN WANTED A TRIAL OF LABOR after a previous cesarean delivery (TOLAC). During labor, fetal distress was noted, and a cesarean delivery was performed. Uterine rupture had occurred. The baby has spastic cerebral palsy with significantly impaired neuromotor and cognitive abilities.
PARENTS’ CLAIM The hospital staff and physicians overlooked earlier fetal distress. A timelier delivery would have prevented the child’s injuries.
DEFENDANTs’ DEFENSE The hospital reached a confidential settlement. The ObGyns claimed fetal tracings were not suggestive of uterine rupture; they met the standard of care.
VERDICT A Texas defense verdict was returned.

WHEN GESTATIONAL DIABETES WAS DIAGNOSED at 33 weeks’ gestation, a family practitioner (FP) referred the mother to an ObGyn practice. Two ObGyns performed amniocentesis to check fetal lung maturity. After the procedure, fetal distress was noted, and the ObGyns instructed the FP to induce labor.
The baby suffered brain damage, had seizures, and has cerebral palsy. She was born without kidney function. By age 10, she had 2 kidney transplant operations and functions at a pre-kindergarten level.
PATIENT’S CLAIM The mother was not fully informed of the risks of and alternatives to amniocentesis. Although complications arose before amniocentesis, the test proceeded. The ObGyns were negligent in not performing cesarean delivery when fetal distress was detected.
DEFENDANTS’ DEFENSE The FP and hospital settled prior to trial. The ObGyns claimed that their care was an appropriate alternative to the actions the patient claimed should have been taken.
VERDICT Costs for the child’s care had reached $1.4 million before trial. A $9 million Virginia verdict was returned that included $7 million for the child and $2 million for the mother, but the settlement was reduced by the state cap.
Did HT cause breast cancer?
A 52-YEAR-OLD WOMAN was prescribed conjugated estrogens/medroxyprogesterone acetate (Prempro, Wyeth, Inc.) for hormone therapy by her gynecologist.
After taking the drug for 5 years, the patient developed invasive breast cancer. She underwent a lumpectomy, chemotherapy, and three reconstructive surgeries.
PATIENT’S CLAIM The manufacturer failed to warn of a woman’s risk of developing breast cancer while taking the product.
DEFENDANT’S DEFENSE Prempro alone does not cause cancer. The drug is just one of many contributing factors that may or may not increase the risk of developing breast cancer.
VERDICT A $3.75 million Connecticut verdict was returned for the patient plus $250,000 to her husband for loss of consortium.
Failure to diagnose preeclampsia—twice
AT 28 WEEKS’ GESTATION, a woman with a history of hypertension went to an ED with headache, nausea, vomiting, cramping, and ringing in her ears. After waiting 4 hours before being seen, her BP was 150/108 mm Hg and normal fetal heart tones were heard. The ED physician diagnosed otitis media and discharged her.
Later that evening, the patient returned to the ED with similar symptoms. A urine specimen showed significant proteinuria and the fetal heart rate was 158 bpm. A second ED physician diagnosed a urinary tract infection, prescribed antibiotics and pain medication, and sent her home.
A few hours later, she returned to the ED by ambulance suffering from eclamptic seizures. Her BP was 174/121 mm Hg, and no fetal heart tones were heard. She delivered a stillborn child by cesarean delivery.
PATIENT’S CLAIM The ED physicians were negligent in failing to diagnose preeclampsia at the first two visits.
PHYSICIANS’ DEFENSE The first ED physician settled for $45,000 while serving a prison sentence after conviction on two sex-abuse felonies related to his treatment of female patients at the same ED. The second ED physician denied negligence.
VERDICT A $50,000 Alabama verdict was returned for compensatory damages for the mother and $600,000 punitive damages for the stillborn child.
Inflated Foley catheter injures mother
DURING A LONG AND DIFFICULT LABOR, an ObGyn used forceps to complete delivery of a 31-year-old woman’s first child. The baby was healthy, but the mother has suffered urinary incontinence since delivery. Despite several repair operations, the condition remains.
PATIENT’S CLAIM The ObGyn was negligent in failing to remove a fully inflated Foley catheter before beginning delivery, leading to a urethral sphincter injury.
PHYSICIAN’S DEFENSE The decision regarding removal of the catheter was a matter of hospital policy. The ObGyn blamed improper catheter placement on the nurses.
VERDICT A Kentucky defense verdict was returned.
These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.
We want to hear from you! Tell us what you think.
These cases were selected by the editors of OBG Management from Medical Malpractice Verdicts, Settlements & Experts, with permission of the editor, Lewis Laska (www.verdictslaska.com). The information available to the editors about the cases presented here is sometimes incomplete. Moreover, the cases may or may not have merit. Nevertheless, these cases represent the types of clinical situations that typically result in litigation and are meant to illustrate nationwide variation in jury verdicts and awards.
We want to hear from you! Tell us what you think.
Ins and outs of straight-stick laparoscopic myomectomy
Watch 3 videos illustrating laparoscopic myomectomy
These videos were provided by Gaby Moawad, MD, and James Robinson, MD, MS.
By age 50, almost 70% of white women and more than 80% of black women will have a uterine leiomyoma.1 These benign, hormone-sensitive neoplasms1 are asymptomatic in the majority of women, but they can cause infertility, abnormal uterine bleeding, and bulk symptoms.2
When symptomatic, fibroids are amenable to multiple management options, ranging from expectant management to medical therapy to uterine artery embolization to myomectomy to hysterectomy. Myomectomy remains the surgical option of choice for women with symptomatic fibroids who wish to retain their fertility. It is also an option for some women who may not desire fertility retention but who do wish to maintain their uterus.
Compared with traditional myomectomy by laparotomy, laparoscopic myomectomy offers the advantages of:
- less blood loss
- less postoperative pain
- less postoperative adhesions formation
- faster recovery
- better cosmesis.3,4
Current technology makes performing laparoscopic myomectomy by either “straight-stick” or robotic assistance a viable option for most women.
In this article, we describe our technique in performing straight-stick laparoscopic myomectomy.
Preoperative evaluation: The first key to success
Laparoscopic myomectomy is an advanced, delicate, and challenging surgery. Preoperative evaluation is integral to its planning and a successful outcome.
Imaging
We recommend magnetic resonance imaging (MRI) as a standard order whenever a laparoscopic approach to myomectomy is being considered, for several reasons. First, MRI of the abdomen and pelvis with contrast allows for a precise map of the location of fibroids in relation to the myometrium and the uterine cavity. Reviewing the MRI results with the patient preoperatively gives both you and the patient a clearer picture of the challenges ahead. Patients tell us they appreciate these easier-to-understand images of their anatomy and, in cases when the decision is made to proceed abdominally, it is more clear to the patient why the decision is being made.
Surgically, the MRI helps compensate for the lack of tactile feedback when faced with deep intramural fibroids laparoscopically. The MRI also helps avoid operative surprises. Experience teaches us that, when relying on transvaginal ultrasound alone, adenomyotic regions can be identified mistakenly as fibroids. Preoperative MRI can help you avoid this discovery at the time of surgery.
A flexible office hysteroscopy serves as an adjunct to MRI for precise preoperative cavitary evaluation, especially when fibroids are present in close proximity to the endometrial cavity or the patient reports menorrhagia as a component of her symptomatology. When small submucosal fibroids exist in addition to larger fibroids, we frequently perform a combined hysteroscopic and laparoscopic approach to myomectomy.
Although bowel preparation does not diminish complications from bowel surgery or improve outcome,5 we generally use laxative suppositories the night prior to surgery to improve access to the posterior cul-de-sac and reduce bulk resulting from a sigmoid full of feces.
Preoperative laboratory evaluation should always include complete blood count, beta hCG, blood type testing, and antibody screen. In patients with known anemia or large intramural fibroids, we typically match the patient for 2 units of packed red blood cells. Additionally, if significant blood loss is anticipated, cell saver technology can be modified to accommodate a laparoscopic suction tip, allowing the patient’s own blood to be collected and readministered.
Aside from the standard risks of surgery, including bleeding, transfusion, infection, and injury to adjacent organs, myomectomy has its own unique risks that need to be made clear to patients preoperatively.
Surgery timing. Initially, women with symptomatic fibroids are at significant risk for developing more fibroids in the future. In fact, 25% of women who undergo myomectomy will require a second surgery at some point in their lives to address recurrent symptoms.1 If women are young, not yet ready to conceive, and are still relatively asymptomatic, waiting to perform myomectomy may be the most prudent course.
Future uterine rupture. There are no good myomectomy data to guide us with respect to the risk of uterine rupture at future pregnancy. When we perform deep intramural myomectomy (regardless of endometrial disruption), we extrapolate from classical cesarean section data and counsel our patients to have planned cesarean sections for all future pregnancies. Patients are also counseled that uterine rupture has been well described after laparoscopic myomectomy prior to the onset of labor so any sudden onset of pain or bleeding during the late second or third trimester of pregnancy has to be regarded as a medical emergency.
Pregnancy. Again, no good data exist to guide us with respect to postoperative timing of future pregnancy. We typically suggest patients refrain from conceiving following myomectomy for at least 6 months. We are aware that other well-respected surgeons have different thresholds.
Reference
1. Andiani GB, Fedele L, Parazzini F, Villa L. Risk of recurrence after myomectomy. Br J Obstet Gynaecol. 1991;98(4):385-389.
How to minimize blood loss
Blood loss during laparoscopic myomectomy generally is less than during laparotomy due to venous compression from pneumoperitoneum. However, blood loss remains a chief concern when performing laparoscopic myomectomy. A variety of techniques have been described to minimize blood loss, including injection of dilute vasopressin6 and tourniquet placement around uterine vessels.7
Injection. To temporarily minimize bleeding in the surgical field, we routinely utilize subserosal injection of dilute vasopressin (20 IU in 100 mL of normal saline) until visible vessels blanch. This practice is more effective than deep myoma or myometrial injection.
Tourniquet. We selectively use a laparoscopically placed tourniquet to compress uterine arteries at the mid-cervix during surgery. One approach is as follows (see VIDEO 1):
- Open windows in bilateral broad ligaments lateral to the uterine pedicles and medial to the ureters.
- Pass the end of a 14-16 French red rubber catheter through one of the low lateral port sites with the port removed.
- Tag the trailing end of the tourniquet outside the abdomen and replace the port alongside the catheter.
- Pass the end of the catheter down through the ipsilateral broad ligament window and under the posterior cervix.
- Pass the end of the catheter up through the contralateral broad ligament window and over the anterior cervix.
- Pass the end of the catheter through each of the broad ligament windows a second time and then out through the contralateral port site.
- Pull the tourniquet tight from both port sites (which will occlude the uterine arteries). Place Kelly clamps on the catheter ends where they exit the port sites to maintain tension until the end of the uterine repair.
Lateral ports can still be utilized with the tourniquet in place.
Permanent occlusion. In women undergoing laparoscopic myomectomy who have completed child bearing, we advocate permanent uterine artery occlusion at the origin of the uterine arteries retroperitoneally. This can be performed in a number of ways— utilizing clips, suture, or transection. Uterine artery occlusion not only leads to less operative blood loss but preliminary studies also suggest it decreases the risk of fibroid recurrence.8
After the patient is prepped and draped in low lithotomy position with her arms tucked at her sides, drain the bladder with an indwelling catheter. Insert a uterine manipulator, such as the VCare (Conmed Corporation), into the uterus.
Obtain umbilical entry for a 30° optic scope, and place the patient in steep Trendelenburg position. We use two 5-mm lateral ports and one 12-mm suprapubic port. The level of placement of the lateral ports is tailored to the size of the fibroids; it can be anywhere from the level of the anterior iliac spine to the level of the umbilicus for fibroids contained in the pelvis or in the abdomen, respectively.
Uterine incision
After vasopressin injection, tourniquet placement, or permanent uterine artery occlusion is performed as described above, we advocate a transverse uterine incision. We do so mainly because:
- The transverse incision runs parallel to the arcuate vessels of the myometrium, leading to less bleeding.
- We suture from the lateral ports so the transverse incision facilitates a more ergonomic repair.
Perform the uterine incision (we use the Harmonic Ace [Ethicon Endo-Surgery, Inc]) through the uterine serosa deep toward the myoma. Incision size should be appropriate to the diameter of the fibroid; smaller incisions result in unnecessary struggling during enucleation of the fibroid. Incision depth should reach the fibroid capsule, and this incision should be developed over the entire fibroid. Tunneling in the myometrium is undesirable and should be avoided because it increases myometrial injury as well as the risk of hematoma.
Fibroid enucleation
Once the initial uterine incision is complete, enucleate the fibroid using a combination of traction, countertraction, sharp, and blunt dissection (see VIDEO 2). Pearls to successful enucleation include:
- Maintain traction and countertraction when cutting tissue. This helps to identify appropriate planes and allows tissue to separate quickly, minimizing thermal energy spread.
- Replace the tenaculum or myoma screw regularly at the border of the myoma and myometrium. The ultrasonic scalpel blade can be drilled into the myoma in order to create traction on the myoma.
- Bluntly peel tissue from the myoma outward. Ideally all myometrium and vessels should stay with the uterus. A properly enucleated fibroid will be pearly in appearance and avascular.
- Be particularly careful when in contact with the endometrium. Even submucous fibroids can be enucleated regularly without entering the endometrial cavity.
Uterine repair
If the endometrial cavity is inadvertently entered, close the defect (we use a 2-0 monocryl or Vicryl suture). Next, imbricate the endometrium over with successive layers, taking special care not to pass a needle into the endometrial cavity. In cases in which significant endometrial disruption cannot be avoided, use a postoperative intrauterine balloon stent. This is placed postoperatively and left in place for 2 weeks. To stimulate endometrial proliferation, we prescribe oral estradiol 1 mg twice per day for 4 weeks. Following endometrial stimulation, we prescribe a 10-day progestin withdrawal and ask the patient to return to the office for a flexible diagnostic hysteroscopy following her first menses to ensure cavitary integrity.
Once fibroid enucleation is complete, perform a multilayer closure of the defect using an absorbable, unidirectional barbed suture (V-Loc, Covidien). Eliminate all dead space in the closure. The last two throws of each barbed suture should be in the direction of the prior two throws to secure the suture. Finally, cut the suture at the tissue edge without leaving any trailing tail or knot.
Why use a barbed suture? The advantages of using absorbable barbed suture include:
- elimination of knot tying
- shorter closure time
- better tension distribution throughout the wound.
Close the seromuscularis layer in a hemostatic baseball stitch fashion to minimize suture exposure and subsequent adhesions (FIGURE). Use of the suprapubic port for the needle retrieval device facilitates placement of the alternating “inside-out” baseball stitch (see VIDEO 3).

FIGURE Use of a hemostatic baseball stitch (with absorbable, unidirectional barbed suture) to close the seromuscularis layer of the uterus, thereby minimizing suture exposure and subsequent adhesions.
Morcellation
Mechanically morcellate the fibroids through the suprapubic port site. We use an electrical morcellator (Karl Storz Endoscopy). In cases of massive fibroids (>15 cm) we utilize cold- knife morcellation with a # 10 scalpel through an extended 3-cm suprapubic incision with a vertical fascial incision protected by a self-retaining wound retractor. It is important to be vigilant to remove all fibroid pieces as postoperative disseminated leiomyomatosis is well described.
Adhesion prevention
Myomectomy is notorious for creating dense and challenging postoperative adhesions. Given the high rate of repeat surgery for patients undergoing the procedure, anything you can do to limit the adhesion load will be appreciated by both your patient and her next surgeon. Without exception, the most important adhesion-prevention strategy is meticulous attention to tissue handling and hemostasis. In general, laparoscopy leads to fewer adhesions than laparotomy, but a bloody field and raw uterine serosa will create an environment ripe for adhesions regardless of surgical approach. If the operative field is dry, use commercial adhesion prevention aids according to manufacturers’ recommendations.
- Use preoperative MRI to tailor your surgical approach
- When menorrhagia is a presenting symptom, assess the endometrial cavity preoperatively and consider combining the laparoscopic myomectomy with hysteroscopic myomectomy
- Minimize blood loss with vasopressin or a laparoscopic tourniquet
- Utilize a transverse uterine incision and a lateral suturing technique
- Use delayed absorbable barbed suture to close the myometrial defect
- Bury the seromuscular closure suture by utilizing an “inside-out” baseball stitch
- If the risk for postoperative cavitary adhesions is high, consider postoperative balloon placement with close postoperative follow-up
- Advise patients to wait 6 months prior to attempting to conceive and have a low threshold for scheduled cesarean delivery to minimize the risk of uterine rupture
Concluding thoughts, from experience
Laparoscopic myomectomy is a challenging yet rewarding procedure. For essential points to our approach, see “Laparoscopic myomectomy: Key takeaways” on this page.
Other important things to keep in mind:
- Fibroid presentation is as varied as the women who have them—meticulous preoperative preparation is an absolute must.
- Utilize well-established approaches to preventing blood loss, removing fibroids, and repairing the uterine defects. The accomplished gynecologic laparoscopist will be successful in the majority of cases.
- Practice suturing in a box-trainer setting before taking on initial cases. Early cases should focus on straightforward subserosal fibroids and, as skills progress, more and more difficult cases will become reasonable.
- Do not place any hard and fast limit on either the number or size of fibroids you are willing to remove laparoscopically. Rather, rely on sound surgical judgment, an honest assessment of your limitations, and a healthy dose of caution as you approach every new patient. Never sacrifice the quality of your repair for a less invasive approach to surgery.
Laparoscopic myomectomy: 8 pearls
Jon I. Einarsson, MD, MPH (March 2010)
Give vasopressin to reduce bleeding in gynecologic surgery
Robert L. Barbieri, MD (Editorial, March 2010)
Barbed suture, now in the toolbox of minimally invasive gyn surgery
Jon I. Einarsson, MD, MPH; James A. Greenberg, MD (September 2009)
When necessity calls for treating uterine fibroids
William H. Parker, MD (Surgical Techniques, June 2008)
Advising your patients–Uterine fibroids: Childbearing, cancer, and hormone effects
William H. Parker, MD (May 2008)
We want to hear from you! Tell us what you think.
1. Baird DD, Dunson DB, Hill MC, Cousins D, Schectman JM. High cumulative incidence of uterine leiomyoma in black and white women: ultrasound evidence. Am J Obstet Gynecol. 2003;188(1):100-107.
2. Wallach EE, Vlahos NF. Uterine myomas: an overview of development clinical features, and management. Obstet Gynecol. 2004;104(2):393-406.
3. Stringer NH, Walker JC, Meyer PM. Comparison of 49 laparoscopic myomec- tomies and 49 open myomectomies. J Am Assoc Gynecol Laparosc. 1997;4(4):457-464.
4. Bulletti C, Polli V, Negrini V, Giacomucci E, Flamigni C. Adhesion formation after laparoscopic myomectomy. J Am Assoc Gynecol Laparosc. 1996;3(4):533-536.
5. Ram E, Sherman Y, Weil R, Vishne T, Kravarusic D, Dreznik Z. Is mechanical bowel preparation mandatory for elective colon surgery? A prospective randomized study. Arch Surg. 2005;140(3):285-288.
6. Frederick J, Fletcher H, Simeon D, Mullings A, Hardie M. Intramyometrial vasopressin as a haemostatic agent during myomectomy. Br J Obstet Gynaecol. 1994;101(5):435-437.
7. Taylor A, Sharma M, Tsirkas P, Di Spiezio Sardo A, Setchell M, Magos A. Reducing blood loss at open myomectomy using triple tourniquets: a randomised controlled trial. BJOG. 2005;112(3):340-345.
8. Burbank F, Hutchins FL, Jr. Uterine artery occlusion by embolization or surgery for the treatment of fibroids: A unifying hypothesis-transient uterine ischemia. J Am Assoc Gynecol Laparosc. 2000;7(suppl 4):S1-S49.
Watch 3 videos illustrating laparoscopic myomectomy
These videos were provided by Gaby Moawad, MD, and James Robinson, MD, MS.
By age 50, almost 70% of white women and more than 80% of black women will have a uterine leiomyoma.1 These benign, hormone-sensitive neoplasms1 are asymptomatic in the majority of women, but they can cause infertility, abnormal uterine bleeding, and bulk symptoms.2
When symptomatic, fibroids are amenable to multiple management options, ranging from expectant management to medical therapy to uterine artery embolization to myomectomy to hysterectomy. Myomectomy remains the surgical option of choice for women with symptomatic fibroids who wish to retain their fertility. It is also an option for some women who may not desire fertility retention but who do wish to maintain their uterus.
Compared with traditional myomectomy by laparotomy, laparoscopic myomectomy offers the advantages of:
- less blood loss
- less postoperative pain
- less postoperative adhesions formation
- faster recovery
- better cosmesis.3,4
Current technology makes performing laparoscopic myomectomy by either “straight-stick” or robotic assistance a viable option for most women.
In this article, we describe our technique in performing straight-stick laparoscopic myomectomy.
Preoperative evaluation: The first key to success
Laparoscopic myomectomy is an advanced, delicate, and challenging surgery. Preoperative evaluation is integral to its planning and a successful outcome.
Imaging
We recommend magnetic resonance imaging (MRI) as a standard order whenever a laparoscopic approach to myomectomy is being considered, for several reasons. First, MRI of the abdomen and pelvis with contrast allows for a precise map of the location of fibroids in relation to the myometrium and the uterine cavity. Reviewing the MRI results with the patient preoperatively gives both you and the patient a clearer picture of the challenges ahead. Patients tell us they appreciate these easier-to-understand images of their anatomy and, in cases when the decision is made to proceed abdominally, it is more clear to the patient why the decision is being made.
Surgically, the MRI helps compensate for the lack of tactile feedback when faced with deep intramural fibroids laparoscopically. The MRI also helps avoid operative surprises. Experience teaches us that, when relying on transvaginal ultrasound alone, adenomyotic regions can be identified mistakenly as fibroids. Preoperative MRI can help you avoid this discovery at the time of surgery.
A flexible office hysteroscopy serves as an adjunct to MRI for precise preoperative cavitary evaluation, especially when fibroids are present in close proximity to the endometrial cavity or the patient reports menorrhagia as a component of her symptomatology. When small submucosal fibroids exist in addition to larger fibroids, we frequently perform a combined hysteroscopic and laparoscopic approach to myomectomy.
Although bowel preparation does not diminish complications from bowel surgery or improve outcome,5 we generally use laxative suppositories the night prior to surgery to improve access to the posterior cul-de-sac and reduce bulk resulting from a sigmoid full of feces.
Preoperative laboratory evaluation should always include complete blood count, beta hCG, blood type testing, and antibody screen. In patients with known anemia or large intramural fibroids, we typically match the patient for 2 units of packed red blood cells. Additionally, if significant blood loss is anticipated, cell saver technology can be modified to accommodate a laparoscopic suction tip, allowing the patient’s own blood to be collected and readministered.
Aside from the standard risks of surgery, including bleeding, transfusion, infection, and injury to adjacent organs, myomectomy has its own unique risks that need to be made clear to patients preoperatively.
Surgery timing. Initially, women with symptomatic fibroids are at significant risk for developing more fibroids in the future. In fact, 25% of women who undergo myomectomy will require a second surgery at some point in their lives to address recurrent symptoms.1 If women are young, not yet ready to conceive, and are still relatively asymptomatic, waiting to perform myomectomy may be the most prudent course.
Future uterine rupture. There are no good myomectomy data to guide us with respect to the risk of uterine rupture at future pregnancy. When we perform deep intramural myomectomy (regardless of endometrial disruption), we extrapolate from classical cesarean section data and counsel our patients to have planned cesarean sections for all future pregnancies. Patients are also counseled that uterine rupture has been well described after laparoscopic myomectomy prior to the onset of labor so any sudden onset of pain or bleeding during the late second or third trimester of pregnancy has to be regarded as a medical emergency.
Pregnancy. Again, no good data exist to guide us with respect to postoperative timing of future pregnancy. We typically suggest patients refrain from conceiving following myomectomy for at least 6 months. We are aware that other well-respected surgeons have different thresholds.
Reference
1. Andiani GB, Fedele L, Parazzini F, Villa L. Risk of recurrence after myomectomy. Br J Obstet Gynaecol. 1991;98(4):385-389.
How to minimize blood loss
Blood loss during laparoscopic myomectomy generally is less than during laparotomy due to venous compression from pneumoperitoneum. However, blood loss remains a chief concern when performing laparoscopic myomectomy. A variety of techniques have been described to minimize blood loss, including injection of dilute vasopressin6 and tourniquet placement around uterine vessels.7
Injection. To temporarily minimize bleeding in the surgical field, we routinely utilize subserosal injection of dilute vasopressin (20 IU in 100 mL of normal saline) until visible vessels blanch. This practice is more effective than deep myoma or myometrial injection.
Tourniquet. We selectively use a laparoscopically placed tourniquet to compress uterine arteries at the mid-cervix during surgery. One approach is as follows (see VIDEO 1):
- Open windows in bilateral broad ligaments lateral to the uterine pedicles and medial to the ureters.
- Pass the end of a 14-16 French red rubber catheter through one of the low lateral port sites with the port removed.
- Tag the trailing end of the tourniquet outside the abdomen and replace the port alongside the catheter.
- Pass the end of the catheter down through the ipsilateral broad ligament window and under the posterior cervix.
- Pass the end of the catheter up through the contralateral broad ligament window and over the anterior cervix.
- Pass the end of the catheter through each of the broad ligament windows a second time and then out through the contralateral port site.
- Pull the tourniquet tight from both port sites (which will occlude the uterine arteries). Place Kelly clamps on the catheter ends where they exit the port sites to maintain tension until the end of the uterine repair.
Lateral ports can still be utilized with the tourniquet in place.
Permanent occlusion. In women undergoing laparoscopic myomectomy who have completed child bearing, we advocate permanent uterine artery occlusion at the origin of the uterine arteries retroperitoneally. This can be performed in a number of ways— utilizing clips, suture, or transection. Uterine artery occlusion not only leads to less operative blood loss but preliminary studies also suggest it decreases the risk of fibroid recurrence.8
After the patient is prepped and draped in low lithotomy position with her arms tucked at her sides, drain the bladder with an indwelling catheter. Insert a uterine manipulator, such as the VCare (Conmed Corporation), into the uterus.
Obtain umbilical entry for a 30° optic scope, and place the patient in steep Trendelenburg position. We use two 5-mm lateral ports and one 12-mm suprapubic port. The level of placement of the lateral ports is tailored to the size of the fibroids; it can be anywhere from the level of the anterior iliac spine to the level of the umbilicus for fibroids contained in the pelvis or in the abdomen, respectively.
Uterine incision
After vasopressin injection, tourniquet placement, or permanent uterine artery occlusion is performed as described above, we advocate a transverse uterine incision. We do so mainly because:
- The transverse incision runs parallel to the arcuate vessels of the myometrium, leading to less bleeding.
- We suture from the lateral ports so the transverse incision facilitates a more ergonomic repair.
Perform the uterine incision (we use the Harmonic Ace [Ethicon Endo-Surgery, Inc]) through the uterine serosa deep toward the myoma. Incision size should be appropriate to the diameter of the fibroid; smaller incisions result in unnecessary struggling during enucleation of the fibroid. Incision depth should reach the fibroid capsule, and this incision should be developed over the entire fibroid. Tunneling in the myometrium is undesirable and should be avoided because it increases myometrial injury as well as the risk of hematoma.
Fibroid enucleation
Once the initial uterine incision is complete, enucleate the fibroid using a combination of traction, countertraction, sharp, and blunt dissection (see VIDEO 2). Pearls to successful enucleation include:
- Maintain traction and countertraction when cutting tissue. This helps to identify appropriate planes and allows tissue to separate quickly, minimizing thermal energy spread.
- Replace the tenaculum or myoma screw regularly at the border of the myoma and myometrium. The ultrasonic scalpel blade can be drilled into the myoma in order to create traction on the myoma.
- Bluntly peel tissue from the myoma outward. Ideally all myometrium and vessels should stay with the uterus. A properly enucleated fibroid will be pearly in appearance and avascular.
- Be particularly careful when in contact with the endometrium. Even submucous fibroids can be enucleated regularly without entering the endometrial cavity.
Uterine repair
If the endometrial cavity is inadvertently entered, close the defect (we use a 2-0 monocryl or Vicryl suture). Next, imbricate the endometrium over with successive layers, taking special care not to pass a needle into the endometrial cavity. In cases in which significant endometrial disruption cannot be avoided, use a postoperative intrauterine balloon stent. This is placed postoperatively and left in place for 2 weeks. To stimulate endometrial proliferation, we prescribe oral estradiol 1 mg twice per day for 4 weeks. Following endometrial stimulation, we prescribe a 10-day progestin withdrawal and ask the patient to return to the office for a flexible diagnostic hysteroscopy following her first menses to ensure cavitary integrity.
Once fibroid enucleation is complete, perform a multilayer closure of the defect using an absorbable, unidirectional barbed suture (V-Loc, Covidien). Eliminate all dead space in the closure. The last two throws of each barbed suture should be in the direction of the prior two throws to secure the suture. Finally, cut the suture at the tissue edge without leaving any trailing tail or knot.
Why use a barbed suture? The advantages of using absorbable barbed suture include:
- elimination of knot tying
- shorter closure time
- better tension distribution throughout the wound.
Close the seromuscularis layer in a hemostatic baseball stitch fashion to minimize suture exposure and subsequent adhesions (FIGURE). Use of the suprapubic port for the needle retrieval device facilitates placement of the alternating “inside-out” baseball stitch (see VIDEO 3).

FIGURE Use of a hemostatic baseball stitch (with absorbable, unidirectional barbed suture) to close the seromuscularis layer of the uterus, thereby minimizing suture exposure and subsequent adhesions.
Morcellation
Mechanically morcellate the fibroids through the suprapubic port site. We use an electrical morcellator (Karl Storz Endoscopy). In cases of massive fibroids (>15 cm) we utilize cold- knife morcellation with a # 10 scalpel through an extended 3-cm suprapubic incision with a vertical fascial incision protected by a self-retaining wound retractor. It is important to be vigilant to remove all fibroid pieces as postoperative disseminated leiomyomatosis is well described.
Adhesion prevention
Myomectomy is notorious for creating dense and challenging postoperative adhesions. Given the high rate of repeat surgery for patients undergoing the procedure, anything you can do to limit the adhesion load will be appreciated by both your patient and her next surgeon. Without exception, the most important adhesion-prevention strategy is meticulous attention to tissue handling and hemostasis. In general, laparoscopy leads to fewer adhesions than laparotomy, but a bloody field and raw uterine serosa will create an environment ripe for adhesions regardless of surgical approach. If the operative field is dry, use commercial adhesion prevention aids according to manufacturers’ recommendations.
- Use preoperative MRI to tailor your surgical approach
- When menorrhagia is a presenting symptom, assess the endometrial cavity preoperatively and consider combining the laparoscopic myomectomy with hysteroscopic myomectomy
- Minimize blood loss with vasopressin or a laparoscopic tourniquet
- Utilize a transverse uterine incision and a lateral suturing technique
- Use delayed absorbable barbed suture to close the myometrial defect
- Bury the seromuscular closure suture by utilizing an “inside-out” baseball stitch
- If the risk for postoperative cavitary adhesions is high, consider postoperative balloon placement with close postoperative follow-up
- Advise patients to wait 6 months prior to attempting to conceive and have a low threshold for scheduled cesarean delivery to minimize the risk of uterine rupture
Concluding thoughts, from experience
Laparoscopic myomectomy is a challenging yet rewarding procedure. For essential points to our approach, see “Laparoscopic myomectomy: Key takeaways” on this page.
Other important things to keep in mind:
- Fibroid presentation is as varied as the women who have them—meticulous preoperative preparation is an absolute must.
- Utilize well-established approaches to preventing blood loss, removing fibroids, and repairing the uterine defects. The accomplished gynecologic laparoscopist will be successful in the majority of cases.
- Practice suturing in a box-trainer setting before taking on initial cases. Early cases should focus on straightforward subserosal fibroids and, as skills progress, more and more difficult cases will become reasonable.
- Do not place any hard and fast limit on either the number or size of fibroids you are willing to remove laparoscopically. Rather, rely on sound surgical judgment, an honest assessment of your limitations, and a healthy dose of caution as you approach every new patient. Never sacrifice the quality of your repair for a less invasive approach to surgery.
Laparoscopic myomectomy: 8 pearls
Jon I. Einarsson, MD, MPH (March 2010)
Give vasopressin to reduce bleeding in gynecologic surgery
Robert L. Barbieri, MD (Editorial, March 2010)
Barbed suture, now in the toolbox of minimally invasive gyn surgery
Jon I. Einarsson, MD, MPH; James A. Greenberg, MD (September 2009)
When necessity calls for treating uterine fibroids
William H. Parker, MD (Surgical Techniques, June 2008)
Advising your patients–Uterine fibroids: Childbearing, cancer, and hormone effects
William H. Parker, MD (May 2008)
We want to hear from you! Tell us what you think.
Watch 3 videos illustrating laparoscopic myomectomy
These videos were provided by Gaby Moawad, MD, and James Robinson, MD, MS.
By age 50, almost 70% of white women and more than 80% of black women will have a uterine leiomyoma.1 These benign, hormone-sensitive neoplasms1 are asymptomatic in the majority of women, but they can cause infertility, abnormal uterine bleeding, and bulk symptoms.2
When symptomatic, fibroids are amenable to multiple management options, ranging from expectant management to medical therapy to uterine artery embolization to myomectomy to hysterectomy. Myomectomy remains the surgical option of choice for women with symptomatic fibroids who wish to retain their fertility. It is also an option for some women who may not desire fertility retention but who do wish to maintain their uterus.
Compared with traditional myomectomy by laparotomy, laparoscopic myomectomy offers the advantages of:
- less blood loss
- less postoperative pain
- less postoperative adhesions formation
- faster recovery
- better cosmesis.3,4
Current technology makes performing laparoscopic myomectomy by either “straight-stick” or robotic assistance a viable option for most women.
In this article, we describe our technique in performing straight-stick laparoscopic myomectomy.
Preoperative evaluation: The first key to success
Laparoscopic myomectomy is an advanced, delicate, and challenging surgery. Preoperative evaluation is integral to its planning and a successful outcome.
Imaging
We recommend magnetic resonance imaging (MRI) as a standard order whenever a laparoscopic approach to myomectomy is being considered, for several reasons. First, MRI of the abdomen and pelvis with contrast allows for a precise map of the location of fibroids in relation to the myometrium and the uterine cavity. Reviewing the MRI results with the patient preoperatively gives both you and the patient a clearer picture of the challenges ahead. Patients tell us they appreciate these easier-to-understand images of their anatomy and, in cases when the decision is made to proceed abdominally, it is more clear to the patient why the decision is being made.
Surgically, the MRI helps compensate for the lack of tactile feedback when faced with deep intramural fibroids laparoscopically. The MRI also helps avoid operative surprises. Experience teaches us that, when relying on transvaginal ultrasound alone, adenomyotic regions can be identified mistakenly as fibroids. Preoperative MRI can help you avoid this discovery at the time of surgery.
A flexible office hysteroscopy serves as an adjunct to MRI for precise preoperative cavitary evaluation, especially when fibroids are present in close proximity to the endometrial cavity or the patient reports menorrhagia as a component of her symptomatology. When small submucosal fibroids exist in addition to larger fibroids, we frequently perform a combined hysteroscopic and laparoscopic approach to myomectomy.
Although bowel preparation does not diminish complications from bowel surgery or improve outcome,5 we generally use laxative suppositories the night prior to surgery to improve access to the posterior cul-de-sac and reduce bulk resulting from a sigmoid full of feces.
Preoperative laboratory evaluation should always include complete blood count, beta hCG, blood type testing, and antibody screen. In patients with known anemia or large intramural fibroids, we typically match the patient for 2 units of packed red blood cells. Additionally, if significant blood loss is anticipated, cell saver technology can be modified to accommodate a laparoscopic suction tip, allowing the patient’s own blood to be collected and readministered.
Aside from the standard risks of surgery, including bleeding, transfusion, infection, and injury to adjacent organs, myomectomy has its own unique risks that need to be made clear to patients preoperatively.
Surgery timing. Initially, women with symptomatic fibroids are at significant risk for developing more fibroids in the future. In fact, 25% of women who undergo myomectomy will require a second surgery at some point in their lives to address recurrent symptoms.1 If women are young, not yet ready to conceive, and are still relatively asymptomatic, waiting to perform myomectomy may be the most prudent course.
Future uterine rupture. There are no good myomectomy data to guide us with respect to the risk of uterine rupture at future pregnancy. When we perform deep intramural myomectomy (regardless of endometrial disruption), we extrapolate from classical cesarean section data and counsel our patients to have planned cesarean sections for all future pregnancies. Patients are also counseled that uterine rupture has been well described after laparoscopic myomectomy prior to the onset of labor so any sudden onset of pain or bleeding during the late second or third trimester of pregnancy has to be regarded as a medical emergency.
Pregnancy. Again, no good data exist to guide us with respect to postoperative timing of future pregnancy. We typically suggest patients refrain from conceiving following myomectomy for at least 6 months. We are aware that other well-respected surgeons have different thresholds.
Reference
1. Andiani GB, Fedele L, Parazzini F, Villa L. Risk of recurrence after myomectomy. Br J Obstet Gynaecol. 1991;98(4):385-389.
How to minimize blood loss
Blood loss during laparoscopic myomectomy generally is less than during laparotomy due to venous compression from pneumoperitoneum. However, blood loss remains a chief concern when performing laparoscopic myomectomy. A variety of techniques have been described to minimize blood loss, including injection of dilute vasopressin6 and tourniquet placement around uterine vessels.7
Injection. To temporarily minimize bleeding in the surgical field, we routinely utilize subserosal injection of dilute vasopressin (20 IU in 100 mL of normal saline) until visible vessels blanch. This practice is more effective than deep myoma or myometrial injection.
Tourniquet. We selectively use a laparoscopically placed tourniquet to compress uterine arteries at the mid-cervix during surgery. One approach is as follows (see VIDEO 1):
- Open windows in bilateral broad ligaments lateral to the uterine pedicles and medial to the ureters.
- Pass the end of a 14-16 French red rubber catheter through one of the low lateral port sites with the port removed.
- Tag the trailing end of the tourniquet outside the abdomen and replace the port alongside the catheter.
- Pass the end of the catheter down through the ipsilateral broad ligament window and under the posterior cervix.
- Pass the end of the catheter up through the contralateral broad ligament window and over the anterior cervix.
- Pass the end of the catheter through each of the broad ligament windows a second time and then out through the contralateral port site.
- Pull the tourniquet tight from both port sites (which will occlude the uterine arteries). Place Kelly clamps on the catheter ends where they exit the port sites to maintain tension until the end of the uterine repair.
Lateral ports can still be utilized with the tourniquet in place.
Permanent occlusion. In women undergoing laparoscopic myomectomy who have completed child bearing, we advocate permanent uterine artery occlusion at the origin of the uterine arteries retroperitoneally. This can be performed in a number of ways— utilizing clips, suture, or transection. Uterine artery occlusion not only leads to less operative blood loss but preliminary studies also suggest it decreases the risk of fibroid recurrence.8
After the patient is prepped and draped in low lithotomy position with her arms tucked at her sides, drain the bladder with an indwelling catheter. Insert a uterine manipulator, such as the VCare (Conmed Corporation), into the uterus.
Obtain umbilical entry for a 30° optic scope, and place the patient in steep Trendelenburg position. We use two 5-mm lateral ports and one 12-mm suprapubic port. The level of placement of the lateral ports is tailored to the size of the fibroids; it can be anywhere from the level of the anterior iliac spine to the level of the umbilicus for fibroids contained in the pelvis or in the abdomen, respectively.
Uterine incision
After vasopressin injection, tourniquet placement, or permanent uterine artery occlusion is performed as described above, we advocate a transverse uterine incision. We do so mainly because:
- The transverse incision runs parallel to the arcuate vessels of the myometrium, leading to less bleeding.
- We suture from the lateral ports so the transverse incision facilitates a more ergonomic repair.
Perform the uterine incision (we use the Harmonic Ace [Ethicon Endo-Surgery, Inc]) through the uterine serosa deep toward the myoma. Incision size should be appropriate to the diameter of the fibroid; smaller incisions result in unnecessary struggling during enucleation of the fibroid. Incision depth should reach the fibroid capsule, and this incision should be developed over the entire fibroid. Tunneling in the myometrium is undesirable and should be avoided because it increases myometrial injury as well as the risk of hematoma.
Fibroid enucleation
Once the initial uterine incision is complete, enucleate the fibroid using a combination of traction, countertraction, sharp, and blunt dissection (see VIDEO 2). Pearls to successful enucleation include:
- Maintain traction and countertraction when cutting tissue. This helps to identify appropriate planes and allows tissue to separate quickly, minimizing thermal energy spread.
- Replace the tenaculum or myoma screw regularly at the border of the myoma and myometrium. The ultrasonic scalpel blade can be drilled into the myoma in order to create traction on the myoma.
- Bluntly peel tissue from the myoma outward. Ideally all myometrium and vessels should stay with the uterus. A properly enucleated fibroid will be pearly in appearance and avascular.
- Be particularly careful when in contact with the endometrium. Even submucous fibroids can be enucleated regularly without entering the endometrial cavity.
Uterine repair
If the endometrial cavity is inadvertently entered, close the defect (we use a 2-0 monocryl or Vicryl suture). Next, imbricate the endometrium over with successive layers, taking special care not to pass a needle into the endometrial cavity. In cases in which significant endometrial disruption cannot be avoided, use a postoperative intrauterine balloon stent. This is placed postoperatively and left in place for 2 weeks. To stimulate endometrial proliferation, we prescribe oral estradiol 1 mg twice per day for 4 weeks. Following endometrial stimulation, we prescribe a 10-day progestin withdrawal and ask the patient to return to the office for a flexible diagnostic hysteroscopy following her first menses to ensure cavitary integrity.
Once fibroid enucleation is complete, perform a multilayer closure of the defect using an absorbable, unidirectional barbed suture (V-Loc, Covidien). Eliminate all dead space in the closure. The last two throws of each barbed suture should be in the direction of the prior two throws to secure the suture. Finally, cut the suture at the tissue edge without leaving any trailing tail or knot.
Why use a barbed suture? The advantages of using absorbable barbed suture include:
- elimination of knot tying
- shorter closure time
- better tension distribution throughout the wound.
Close the seromuscularis layer in a hemostatic baseball stitch fashion to minimize suture exposure and subsequent adhesions (FIGURE). Use of the suprapubic port for the needle retrieval device facilitates placement of the alternating “inside-out” baseball stitch (see VIDEO 3).

FIGURE Use of a hemostatic baseball stitch (with absorbable, unidirectional barbed suture) to close the seromuscularis layer of the uterus, thereby minimizing suture exposure and subsequent adhesions.
Morcellation
Mechanically morcellate the fibroids through the suprapubic port site. We use an electrical morcellator (Karl Storz Endoscopy). In cases of massive fibroids (>15 cm) we utilize cold- knife morcellation with a # 10 scalpel through an extended 3-cm suprapubic incision with a vertical fascial incision protected by a self-retaining wound retractor. It is important to be vigilant to remove all fibroid pieces as postoperative disseminated leiomyomatosis is well described.
Adhesion prevention
Myomectomy is notorious for creating dense and challenging postoperative adhesions. Given the high rate of repeat surgery for patients undergoing the procedure, anything you can do to limit the adhesion load will be appreciated by both your patient and her next surgeon. Without exception, the most important adhesion-prevention strategy is meticulous attention to tissue handling and hemostasis. In general, laparoscopy leads to fewer adhesions than laparotomy, but a bloody field and raw uterine serosa will create an environment ripe for adhesions regardless of surgical approach. If the operative field is dry, use commercial adhesion prevention aids according to manufacturers’ recommendations.
- Use preoperative MRI to tailor your surgical approach
- When menorrhagia is a presenting symptom, assess the endometrial cavity preoperatively and consider combining the laparoscopic myomectomy with hysteroscopic myomectomy
- Minimize blood loss with vasopressin or a laparoscopic tourniquet
- Utilize a transverse uterine incision and a lateral suturing technique
- Use delayed absorbable barbed suture to close the myometrial defect
- Bury the seromuscular closure suture by utilizing an “inside-out” baseball stitch
- If the risk for postoperative cavitary adhesions is high, consider postoperative balloon placement with close postoperative follow-up
- Advise patients to wait 6 months prior to attempting to conceive and have a low threshold for scheduled cesarean delivery to minimize the risk of uterine rupture
Concluding thoughts, from experience
Laparoscopic myomectomy is a challenging yet rewarding procedure. For essential points to our approach, see “Laparoscopic myomectomy: Key takeaways” on this page.
Other important things to keep in mind:
- Fibroid presentation is as varied as the women who have them—meticulous preoperative preparation is an absolute must.
- Utilize well-established approaches to preventing blood loss, removing fibroids, and repairing the uterine defects. The accomplished gynecologic laparoscopist will be successful in the majority of cases.
- Practice suturing in a box-trainer setting before taking on initial cases. Early cases should focus on straightforward subserosal fibroids and, as skills progress, more and more difficult cases will become reasonable.
- Do not place any hard and fast limit on either the number or size of fibroids you are willing to remove laparoscopically. Rather, rely on sound surgical judgment, an honest assessment of your limitations, and a healthy dose of caution as you approach every new patient. Never sacrifice the quality of your repair for a less invasive approach to surgery.
Laparoscopic myomectomy: 8 pearls
Jon I. Einarsson, MD, MPH (March 2010)
Give vasopressin to reduce bleeding in gynecologic surgery
Robert L. Barbieri, MD (Editorial, March 2010)
Barbed suture, now in the toolbox of minimally invasive gyn surgery
Jon I. Einarsson, MD, MPH; James A. Greenberg, MD (September 2009)
When necessity calls for treating uterine fibroids
William H. Parker, MD (Surgical Techniques, June 2008)
Advising your patients–Uterine fibroids: Childbearing, cancer, and hormone effects
William H. Parker, MD (May 2008)
We want to hear from you! Tell us what you think.
1. Baird DD, Dunson DB, Hill MC, Cousins D, Schectman JM. High cumulative incidence of uterine leiomyoma in black and white women: ultrasound evidence. Am J Obstet Gynecol. 2003;188(1):100-107.
2. Wallach EE, Vlahos NF. Uterine myomas: an overview of development clinical features, and management. Obstet Gynecol. 2004;104(2):393-406.
3. Stringer NH, Walker JC, Meyer PM. Comparison of 49 laparoscopic myomec- tomies and 49 open myomectomies. J Am Assoc Gynecol Laparosc. 1997;4(4):457-464.
4. Bulletti C, Polli V, Negrini V, Giacomucci E, Flamigni C. Adhesion formation after laparoscopic myomectomy. J Am Assoc Gynecol Laparosc. 1996;3(4):533-536.
5. Ram E, Sherman Y, Weil R, Vishne T, Kravarusic D, Dreznik Z. Is mechanical bowel preparation mandatory for elective colon surgery? A prospective randomized study. Arch Surg. 2005;140(3):285-288.
6. Frederick J, Fletcher H, Simeon D, Mullings A, Hardie M. Intramyometrial vasopressin as a haemostatic agent during myomectomy. Br J Obstet Gynaecol. 1994;101(5):435-437.
7. Taylor A, Sharma M, Tsirkas P, Di Spiezio Sardo A, Setchell M, Magos A. Reducing blood loss at open myomectomy using triple tourniquets: a randomised controlled trial. BJOG. 2005;112(3):340-345.
8. Burbank F, Hutchins FL, Jr. Uterine artery occlusion by embolization or surgery for the treatment of fibroids: A unifying hypothesis-transient uterine ischemia. J Am Assoc Gynecol Laparosc. 2000;7(suppl 4):S1-S49.
1. Baird DD, Dunson DB, Hill MC, Cousins D, Schectman JM. High cumulative incidence of uterine leiomyoma in black and white women: ultrasound evidence. Am J Obstet Gynecol. 2003;188(1):100-107.
2. Wallach EE, Vlahos NF. Uterine myomas: an overview of development clinical features, and management. Obstet Gynecol. 2004;104(2):393-406.
3. Stringer NH, Walker JC, Meyer PM. Comparison of 49 laparoscopic myomec- tomies and 49 open myomectomies. J Am Assoc Gynecol Laparosc. 1997;4(4):457-464.
4. Bulletti C, Polli V, Negrini V, Giacomucci E, Flamigni C. Adhesion formation after laparoscopic myomectomy. J Am Assoc Gynecol Laparosc. 1996;3(4):533-536.
5. Ram E, Sherman Y, Weil R, Vishne T, Kravarusic D, Dreznik Z. Is mechanical bowel preparation mandatory for elective colon surgery? A prospective randomized study. Arch Surg. 2005;140(3):285-288.
6. Frederick J, Fletcher H, Simeon D, Mullings A, Hardie M. Intramyometrial vasopressin as a haemostatic agent during myomectomy. Br J Obstet Gynaecol. 1994;101(5):435-437.
7. Taylor A, Sharma M, Tsirkas P, Di Spiezio Sardo A, Setchell M, Magos A. Reducing blood loss at open myomectomy using triple tourniquets: a randomised controlled trial. BJOG. 2005;112(3):340-345.
8. Burbank F, Hutchins FL, Jr. Uterine artery occlusion by embolization or surgery for the treatment of fibroids: A unifying hypothesis-transient uterine ischemia. J Am Assoc Gynecol Laparosc. 2000;7(suppl 4):S1-S49.
DEXA screening—are we doing too much?
Reconsider the intervals at which you recommend rescreening for osteoporosis; for post-menopausal women with a baseline of normal bone mineral density (BMD) or mild osteopenia, a 15-year interval is probably sufficient.1
STRENGTH OF RECOMMENDATION
B: Based on a single cohort study
Gourlay ML, Fine JP, Preisser JS, et al. Bone density testing interval and transition to osteoporosis in older women. N Engl J Med. 2012;366: 225-233
ILLUSTRATIVE CASE
A 67-year-old woman whose recent dual-energy x-ray absorptiometry (DEXA) scan showed mild osteopenia asks when she should have her next bone scan. What should you tell her?
One in 5 people who sustain a hip fracture die within a year,2 and as many as 36% die prematurely.3 Osteoporosis is the primary predictor of fracture risk and, in older white women in particular, low bone mineral density (BMD) increases the likelihood of fracture by 70% to 80%.4
Optimal screening frequency not known
The US Preventive Services Task Force (USPSTF) guideline for osteoporosis screening concludes that there is a lack of evidence about optimal rescreening intervals and states that intervals >2 years may be necessary to better predict fracture risk.5 In addition, the USPSTF cites a prospective study showing that repeat measurement of BMD after 8 years added little predictive value compared with baseline DEXA scan results.6
The prospective cohort study detailed below was undertaken to help guide decisions about how frequently to screen
STUDY SUMMARY: Longer intervals are reasonable for those at low risk
Gourlay et al followed 4957 women age ≥67 years with normal BMD or osteopenia and no history of hip or clinical vertebral fracture or osteoporosis treatment. The primary outcome was the estimated time it would take for 10% of the women to develop osteoporosis. The time until 2% of the women developed such a fracture was the secondary outcome
Participants had baseline DEXA scans, which were repeated at years 2, 6, 8, 10, and 16. The researchers followed the women until they were diagnosed with osteoporosis, started on medication for osteoporosis, or developed a hip or clinical vertebral fracture
After adjusting for multiple covariates (age, body mass index, smoking status, use of glucocorticoids, fracture after age 50, estrogen use, and rheumatoid arthritis), the intervals between baseline testing and the development of osteoporosis were:
- 16.8 years (95% confidence interval [CI], 11.5-24.6) for women with normal BMD
- 17.3 years (95% CI, 13.9-21.5) for women with mild osteopenia
- 4.7 years (95% CI, 4.2-5.2) for women with moderate osteopenia
- 1.1 year (95% CI, 1.0-1.3) for women with advanced osteopenia
Intervals until 2% of the cohort developed fractures were similar
Overall, the authors used a sensible approach to estimate reasonable intervals between DEXA screenings (TABLE)
TABLE
Suggested rescreening intervals based on DEXA scan results1
| DEXA result (T-score) | Rescreening interval* |
|---|---|
| Normal/mild osteopenia (> -1.50) | 15 years |
| Moderate osteopenia (-1.50 to -1.99) | 5 years |
| Advanced osteopenia (-2.0 to -2.49) | 1 year |
| *Consider reducing these intervals by one-third for women older than 80 years. | |
WHAT’S NEW: Many DEXA scans can be eliminated
Rescreening all postmenopausal women every 2 years is unlikely to reduce osteoporotic fractures. This cohort study provides evidence that rescreening can often be delayed for many years, depending on the patient’s baseline risk. Changing practice based on these findings can reduce resource utilization without adversely affecting women’s health
CAVEATS: Questions about applicability may remain
This analysis was limited to women ≥67 years, so different results might be obtained from analyses that included younger postmenopausal women. In addition, 99% of the participants were white. Because the prevalence of osteoporosis of the hip among white women is equal to or slightly higher than it is among nonwhite women, it is likely that the suggested intervals are reasonable estimates for women of all races
In women >80 years, the interval between baseline testing and the development of osteoporosis was shorter than that of their younger counterparts. Thus, it might be reasonable to reduce rescreening intervals by a third for women in their 80s
CHALLENGES TO IMPLEMENTATION: Education needed for patients and docs
This study is the best so far to address the frequency of rescreening. In order to implement it, patients as well as clinicians will need to be educated. Effective long-term (>10 y) reminder systems would improve implementation
The recommendations of professional associations may also be a factor. The National Osteoporosis Foundation recommends assessing BMD every 2 years, but notes that more frequent testing may sometimes be warranted.7 The American College of Preventive Medicine recommends that screening for osteoporosis not occur more often than every 2 years.8
Acknowledgement
The PURLs Surveillance System is supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of health.
1. Gourlay ML, Fine JP, Preisser JS, et al. Bone-density testing interval and transition to osteoporosis in older women. N Engl J Med. 2012;366:225-233.
2. Leibson CL, Tosteson AN, Gabriel SE, et al. Mortality, disability, and nursing home use for persons with and without hip fracture. J Am Geriatr Soc. 2002;50:1644-1650.
3. Abrahamsen B, van Staa T, Ariely R, et al. Excess mortality following hip fracture: a systematic epidemiological review. Osteoporosis Int. 2009;20:1633-1650.
4. Smith J, Shoukri K. Diagnosis of osteoporosis. Clin Cornerstone. 2000;2:22-33.
5. US Preventive Services Task Force. Screening for osteoporosis: U.S. Preventive Services Task Force recommendation statement. Available at: http://www.uspreventiveservicestaskforce.org/uspstf10/osteoporosis/osteors.htm. Accessed June 15, 2012.
6. Hillier TA, Stone KL, Bauer DC, et al. Evaluating the value of repeat bone mineral density measurement and prediction of fractures in older women. Arch Intern Med. 2007;167:155-160.
7. National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. 2010. Available at: http://www.nof.org/sites/default/files/pdfs/NOF_ClinicianGuide2009_v7.pdf. Accessed June 30, 2012.
8. Lim LS, Hoeksema LJ, Sherin K. ACPM Prevention Practice Committee. Screening for osteoporosis in the adult US population: ACPM position statement on preventive practice. Am J Prev Med. 2009;36:366-375.
Reconsider the intervals at which you recommend rescreening for osteoporosis; for post-menopausal women with a baseline of normal bone mineral density (BMD) or mild osteopenia, a 15-year interval is probably sufficient.1
STRENGTH OF RECOMMENDATION
B: Based on a single cohort study
Gourlay ML, Fine JP, Preisser JS, et al. Bone density testing interval and transition to osteoporosis in older women. N Engl J Med. 2012;366: 225-233
ILLUSTRATIVE CASE
A 67-year-old woman whose recent dual-energy x-ray absorptiometry (DEXA) scan showed mild osteopenia asks when she should have her next bone scan. What should you tell her?
One in 5 people who sustain a hip fracture die within a year,2 and as many as 36% die prematurely.3 Osteoporosis is the primary predictor of fracture risk and, in older white women in particular, low bone mineral density (BMD) increases the likelihood of fracture by 70% to 80%.4
Optimal screening frequency not known
The US Preventive Services Task Force (USPSTF) guideline for osteoporosis screening concludes that there is a lack of evidence about optimal rescreening intervals and states that intervals >2 years may be necessary to better predict fracture risk.5 In addition, the USPSTF cites a prospective study showing that repeat measurement of BMD after 8 years added little predictive value compared with baseline DEXA scan results.6
The prospective cohort study detailed below was undertaken to help guide decisions about how frequently to screen
STUDY SUMMARY: Longer intervals are reasonable for those at low risk
Gourlay et al followed 4957 women age ≥67 years with normal BMD or osteopenia and no history of hip or clinical vertebral fracture or osteoporosis treatment. The primary outcome was the estimated time it would take for 10% of the women to develop osteoporosis. The time until 2% of the women developed such a fracture was the secondary outcome
Participants had baseline DEXA scans, which were repeated at years 2, 6, 8, 10, and 16. The researchers followed the women until they were diagnosed with osteoporosis, started on medication for osteoporosis, or developed a hip or clinical vertebral fracture
After adjusting for multiple covariates (age, body mass index, smoking status, use of glucocorticoids, fracture after age 50, estrogen use, and rheumatoid arthritis), the intervals between baseline testing and the development of osteoporosis were:
- 16.8 years (95% confidence interval [CI], 11.5-24.6) for women with normal BMD
- 17.3 years (95% CI, 13.9-21.5) for women with mild osteopenia
- 4.7 years (95% CI, 4.2-5.2) for women with moderate osteopenia
- 1.1 year (95% CI, 1.0-1.3) for women with advanced osteopenia
Intervals until 2% of the cohort developed fractures were similar
Overall, the authors used a sensible approach to estimate reasonable intervals between DEXA screenings (TABLE)
TABLE
Suggested rescreening intervals based on DEXA scan results1
| DEXA result (T-score) | Rescreening interval* |
|---|---|
| Normal/mild osteopenia (> -1.50) | 15 years |
| Moderate osteopenia (-1.50 to -1.99) | 5 years |
| Advanced osteopenia (-2.0 to -2.49) | 1 year |
| *Consider reducing these intervals by one-third for women older than 80 years. | |
WHAT’S NEW: Many DEXA scans can be eliminated
Rescreening all postmenopausal women every 2 years is unlikely to reduce osteoporotic fractures. This cohort study provides evidence that rescreening can often be delayed for many years, depending on the patient’s baseline risk. Changing practice based on these findings can reduce resource utilization without adversely affecting women’s health
CAVEATS: Questions about applicability may remain
This analysis was limited to women ≥67 years, so different results might be obtained from analyses that included younger postmenopausal women. In addition, 99% of the participants were white. Because the prevalence of osteoporosis of the hip among white women is equal to or slightly higher than it is among nonwhite women, it is likely that the suggested intervals are reasonable estimates for women of all races
In women >80 years, the interval between baseline testing and the development of osteoporosis was shorter than that of their younger counterparts. Thus, it might be reasonable to reduce rescreening intervals by a third for women in their 80s
CHALLENGES TO IMPLEMENTATION: Education needed for patients and docs
This study is the best so far to address the frequency of rescreening. In order to implement it, patients as well as clinicians will need to be educated. Effective long-term (>10 y) reminder systems would improve implementation
The recommendations of professional associations may also be a factor. The National Osteoporosis Foundation recommends assessing BMD every 2 years, but notes that more frequent testing may sometimes be warranted.7 The American College of Preventive Medicine recommends that screening for osteoporosis not occur more often than every 2 years.8
Acknowledgement
The PURLs Surveillance System is supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of health.
Reconsider the intervals at which you recommend rescreening for osteoporosis; for post-menopausal women with a baseline of normal bone mineral density (BMD) or mild osteopenia, a 15-year interval is probably sufficient.1
STRENGTH OF RECOMMENDATION
B: Based on a single cohort study
Gourlay ML, Fine JP, Preisser JS, et al. Bone density testing interval and transition to osteoporosis in older women. N Engl J Med. 2012;366: 225-233
ILLUSTRATIVE CASE
A 67-year-old woman whose recent dual-energy x-ray absorptiometry (DEXA) scan showed mild osteopenia asks when she should have her next bone scan. What should you tell her?
One in 5 people who sustain a hip fracture die within a year,2 and as many as 36% die prematurely.3 Osteoporosis is the primary predictor of fracture risk and, in older white women in particular, low bone mineral density (BMD) increases the likelihood of fracture by 70% to 80%.4
Optimal screening frequency not known
The US Preventive Services Task Force (USPSTF) guideline for osteoporosis screening concludes that there is a lack of evidence about optimal rescreening intervals and states that intervals >2 years may be necessary to better predict fracture risk.5 In addition, the USPSTF cites a prospective study showing that repeat measurement of BMD after 8 years added little predictive value compared with baseline DEXA scan results.6
The prospective cohort study detailed below was undertaken to help guide decisions about how frequently to screen
STUDY SUMMARY: Longer intervals are reasonable for those at low risk
Gourlay et al followed 4957 women age ≥67 years with normal BMD or osteopenia and no history of hip or clinical vertebral fracture or osteoporosis treatment. The primary outcome was the estimated time it would take for 10% of the women to develop osteoporosis. The time until 2% of the women developed such a fracture was the secondary outcome
Participants had baseline DEXA scans, which were repeated at years 2, 6, 8, 10, and 16. The researchers followed the women until they were diagnosed with osteoporosis, started on medication for osteoporosis, or developed a hip or clinical vertebral fracture
After adjusting for multiple covariates (age, body mass index, smoking status, use of glucocorticoids, fracture after age 50, estrogen use, and rheumatoid arthritis), the intervals between baseline testing and the development of osteoporosis were:
- 16.8 years (95% confidence interval [CI], 11.5-24.6) for women with normal BMD
- 17.3 years (95% CI, 13.9-21.5) for women with mild osteopenia
- 4.7 years (95% CI, 4.2-5.2) for women with moderate osteopenia
- 1.1 year (95% CI, 1.0-1.3) for women with advanced osteopenia
Intervals until 2% of the cohort developed fractures were similar
Overall, the authors used a sensible approach to estimate reasonable intervals between DEXA screenings (TABLE)
TABLE
Suggested rescreening intervals based on DEXA scan results1
| DEXA result (T-score) | Rescreening interval* |
|---|---|
| Normal/mild osteopenia (> -1.50) | 15 years |
| Moderate osteopenia (-1.50 to -1.99) | 5 years |
| Advanced osteopenia (-2.0 to -2.49) | 1 year |
| *Consider reducing these intervals by one-third for women older than 80 years. | |
WHAT’S NEW: Many DEXA scans can be eliminated
Rescreening all postmenopausal women every 2 years is unlikely to reduce osteoporotic fractures. This cohort study provides evidence that rescreening can often be delayed for many years, depending on the patient’s baseline risk. Changing practice based on these findings can reduce resource utilization without adversely affecting women’s health
CAVEATS: Questions about applicability may remain
This analysis was limited to women ≥67 years, so different results might be obtained from analyses that included younger postmenopausal women. In addition, 99% of the participants were white. Because the prevalence of osteoporosis of the hip among white women is equal to or slightly higher than it is among nonwhite women, it is likely that the suggested intervals are reasonable estimates for women of all races
In women >80 years, the interval between baseline testing and the development of osteoporosis was shorter than that of their younger counterparts. Thus, it might be reasonable to reduce rescreening intervals by a third for women in their 80s
CHALLENGES TO IMPLEMENTATION: Education needed for patients and docs
This study is the best so far to address the frequency of rescreening. In order to implement it, patients as well as clinicians will need to be educated. Effective long-term (>10 y) reminder systems would improve implementation
The recommendations of professional associations may also be a factor. The National Osteoporosis Foundation recommends assessing BMD every 2 years, but notes that more frequent testing may sometimes be warranted.7 The American College of Preventive Medicine recommends that screening for osteoporosis not occur more often than every 2 years.8
Acknowledgement
The PURLs Surveillance System is supported in part by Grant Number UL1RR024999 from the National Center for Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of health.
1. Gourlay ML, Fine JP, Preisser JS, et al. Bone-density testing interval and transition to osteoporosis in older women. N Engl J Med. 2012;366:225-233.
2. Leibson CL, Tosteson AN, Gabriel SE, et al. Mortality, disability, and nursing home use for persons with and without hip fracture. J Am Geriatr Soc. 2002;50:1644-1650.
3. Abrahamsen B, van Staa T, Ariely R, et al. Excess mortality following hip fracture: a systematic epidemiological review. Osteoporosis Int. 2009;20:1633-1650.
4. Smith J, Shoukri K. Diagnosis of osteoporosis. Clin Cornerstone. 2000;2:22-33.
5. US Preventive Services Task Force. Screening for osteoporosis: U.S. Preventive Services Task Force recommendation statement. Available at: http://www.uspreventiveservicestaskforce.org/uspstf10/osteoporosis/osteors.htm. Accessed June 15, 2012.
6. Hillier TA, Stone KL, Bauer DC, et al. Evaluating the value of repeat bone mineral density measurement and prediction of fractures in older women. Arch Intern Med. 2007;167:155-160.
7. National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. 2010. Available at: http://www.nof.org/sites/default/files/pdfs/NOF_ClinicianGuide2009_v7.pdf. Accessed June 30, 2012.
8. Lim LS, Hoeksema LJ, Sherin K. ACPM Prevention Practice Committee. Screening for osteoporosis in the adult US population: ACPM position statement on preventive practice. Am J Prev Med. 2009;36:366-375.
1. Gourlay ML, Fine JP, Preisser JS, et al. Bone-density testing interval and transition to osteoporosis in older women. N Engl J Med. 2012;366:225-233.
2. Leibson CL, Tosteson AN, Gabriel SE, et al. Mortality, disability, and nursing home use for persons with and without hip fracture. J Am Geriatr Soc. 2002;50:1644-1650.
3. Abrahamsen B, van Staa T, Ariely R, et al. Excess mortality following hip fracture: a systematic epidemiological review. Osteoporosis Int. 2009;20:1633-1650.
4. Smith J, Shoukri K. Diagnosis of osteoporosis. Clin Cornerstone. 2000;2:22-33.
5. US Preventive Services Task Force. Screening for osteoporosis: U.S. Preventive Services Task Force recommendation statement. Available at: http://www.uspreventiveservicestaskforce.org/uspstf10/osteoporosis/osteors.htm. Accessed June 15, 2012.
6. Hillier TA, Stone KL, Bauer DC, et al. Evaluating the value of repeat bone mineral density measurement and prediction of fractures in older women. Arch Intern Med. 2007;167:155-160.
7. National Osteoporosis Foundation. Clinician’s guide to prevention and treatment of osteoporosis. 2010. Available at: http://www.nof.org/sites/default/files/pdfs/NOF_ClinicianGuide2009_v7.pdf. Accessed June 30, 2012.
8. Lim LS, Hoeksema LJ, Sherin K. ACPM Prevention Practice Committee. Screening for osteoporosis in the adult US population: ACPM position statement on preventive practice. Am J Prev Med. 2009;36:366-375.
Copyright © 2012 The Family Physicians Inquiries Network. All rights reserved.
An evidence-based approach to treating pediatric anxiety disorders
Anxiety disorders are remarkably common among pediatric patients1,2 and are associated with significant morbidity3 and increased risk of suicidality in adolescents.4,5 Effective diagnosis and treatment of pediatric anxiety disorders are critical for reducing psychosocial morbidity,3,6 suicidality, and the risk of secondary mood disorders.7
This article summarizes open-label studies and randomized controlled trials (RCTs) of selective serotonin reuptake inhibitors (SSRIs), selective serotonin-norepinephrine reuptake inhibitors, atypical anxiolytics, and benzodiazepines in children and adolescents with generalized anxiety disorder (GAD), social phobia, separation anxiety disorder, and panic disorder. Although we focus on psychopharmacologic treatments, the best outcomes generally are observed with multimodal treatments that combine psychotherapy and pharmacotherapy.
Generalized anxiety disorder
Researchers have evaluated SSRIs, benzodiazepines, and buspirone in pediatric patients with GAD. In a double-blind, placebo-controlled trial of 22 patients age 5 to 17, sertraline, 50 mg/d, was associated with improvement in Hamilton Anxiety Rating Scale (HAM-A), Clinical Global Impression-Severity (CGI-S), and Clinical Global Impression-Improvement (CGI-I) scores over 9 weeks.8 The Child-Adolescent Anxiety Multimodal Study compared cognitive-behavioral therapy (CBT) to sertraline or sertraline plus CBT in 488 patients age 7 to 17, 78% of whom had GAD.9 Sertraline monotherapy was superior to placebo and not statistically different from CBT, while combination treatment was superior to both monotherapy conditions in improving CGI score. In both trials, sertraline was well tolerated.
One study evaluated fluoxetine, 5 to 40 mg/d, or CBT in 14 youths with GAD; both treatments improved symptoms.10 In a study of 320 GAD patients age 6 to 17, venlafaxine extended-release (XR) initiated at 37.5 mg/d was associated with improved HAM-A scores.11 In general, venlafaxine was well tolerated; adverse effects included increased blood pressure, asthenia, pain, anorexia, somnolence, weight loss, and possibly treatment-emergent suicidal ideation.
Two RCTs of buspirone, 15 to 60 mg/d, that evaluated 559 children and adolescents age 6 to 17 with GAD did not observe significant differences between buspirone and placebo.12 By contrast, 2 open-label studies of youths with anxiety suggested improvement associated with buspirone.12 Treatment-emergent adverse events included nausea, stomachache, and headache.
Clinical trials of benzodiazepines in anxious children and adolescents have yielded mixed results. A 4-week, open-label trial of alprazolam, 0.5 mg to 1.5 mg/d, in 12 adolescents with overanxious disorder—the DSM-III forerunner of GAD—found improvements in anxiety, depression, psychomotor excitation, and hyperactivity, but patients experienced sedation, activation, headache, and nausea.13 However, a double-blind RCT in 30 youths age 8 to 16 found no statistically significant difference between alprazolam and placebo.14 Alprazolam generally was well tolerated; fatigue and dry mouth were reported, but no withdrawal symptoms. Additionally, benzodiazepine use may be associated with tolerance and—in young children—disinhibition.
Social phobia
Researchers have evaluated paroxetine, citalopram, fluoxetine, and venlafaxine for treating social phobia in pediatric patients. In an RCT, 78% of paroxetine-treated patients with social phobia responded compared with 38% for placebo over 16 weeks. Adverse events—including withdrawal symptoms—were twice as likely in patients who received paroxetine. Additionally, 4 paroxetine patients exhibited suicidal ideation vs 0 patients who received placebo.15
In an RCT of 293 children and adolescents age 8 to 17 with social phobia, venlafaxine XR was initiated at 37.5 mg/d and titrated to 112.5 mg/d, 150 mg/d, or 225 mg/d, depending on body weight.16 The venlafaxine group experienced significantly improved anxiety symptoms and the medication generally was well tolerated, although 3 venlafaxine-treated patients developed suicidal ideation compared with 0 in the placebo group.
An RCT compared Social Effectiveness Therapy for Children (SET-C) and fluoxetine, 10 to 40 mg/d, for 139 patients age 7 to 17 with social phobia.17 SET-C is a CBT for children and adolescents that focuses on increasing interpersonal skills and becoming more comfortable in social situations; it involves psychoeducation, social skills training, and exposure exercises. At endpoint, 53% of patients in the SET-C group no longer met diagnostic criteria for social phobia. Fluoxetine was well tolerated; no severe adverse events were reported.
In an open-label study of sertraline (mean dose = 123 mg/d) for 14 young persons with social phobia, 36% of patients responded and 29% partially responded at 8 weeks.18 Adverse events generally were mild and included nausea, diarrhea, and headache. In a 12-week study, 12 pediatric patients with social phobia received citalopram, 10 to 40 mg/d, and eight 15-minute counseling sessions. At endpoint, clinicians rated 83% of patients as much improved or very much improved. The medication generally was well tolerated.19
Separation anxiety disorder
In a 4-week, double-blind crossover pilot study, researchers randomly assigned 15 children age 7 to 13 with separation anxiety disorder to clonazepam, up to 2 mg/d, or placebo.20 There was no significant difference in CGI-I score between clonazepam and placebo. Side effects—including drowsiness, irritability and “oppositional behavior”—were more frequent in patients treated with clonazepam.
Panic disorder
Only 2 open-label studies of SSRIs have been conducted in pediatric patients with panic disorder. The first evaluated the effectiveness and tolerability of fluoxetine, sertraline, or paroxetine over 6 months in 12 patients; 67% no longer met criteria for panic disorder at endpoint.21 In this study, benzodiazepines—including clonazepam and lorazepam—were used in 67% of patients at the start of SSRI treatment. The authors suggested this strategy may be clinically useful for patients with panic disorder.
In the second study, Fairbanks et al22 examined the use of fluoxetine for 6 to 9 weeks in 16 outpatients with mixed anxiety disorders who did not respond to psychotherapy. Patients age ≤12 were given 5 to 40 mg/d and those age ≥13 received 5 to 80 mg/d. Fluoxetine was associated with clinically significant improvement in 3 of the 5 patients who had panic disorder. Although overall fluoxetine was well tolerated, drowsiness, dyssomnia, decreased appetite, nausea, and abdominal pain were the most common side effects. Fluoxetine was not associated with suicidal ideation.
Mixed anxiety disorders
Most trials of pediatric anxiety have evaluated patients with “mixed anxiety disorders” because GAD, social phobia, and separation anxiety disorder are highly comorbid and share diagnostic features (Figure 1).9 An RCT of fluvoxamine, up to 300 mg/d, in 128 pediatric patients with ≥1 anxiety disorders found significant differences in CGI-I and endpoint Pediatric Anxiety Rating Scale (PARS) scores.23 Fluvoxamine was well tolerated but associated with increased motor activity and abdominal discomfort compared with placebo.
Two open-label trials of pediatric patients with mixed anxiety disorders suggested fluoxetine may be beneficial. Fairbanks et al22 documented clinical improvement in 10 of 10 patients with separation anxiety disorder, 8 of 10 with social phobia, 4 of 6 with specific phobia, 3 of 5 with panic disorder, and 1 of 7 with GAD. Birmaher et al24 evaluated 21 pediatric patients with overanxious disorder, social phobia, or separation anxiety who had not responded to psychotherapy and were not depressed; all patients received flexibly-dosed fluoxetine for up to 10 months. Fluoxetine was well tolerated and 81% of patients improved.
Finally, in a 12-week RCT of 74 patients age 7 to 17 with GAD, separation anxiety disorder, and/or social phobia, fluoxetine, 10 to 20 mg/d, was associated with improved scores on the Screen for Anxiety Related Emotional Disorders, PARS, CGI-I, CGI-S, and Children’s Global Assessment Scale.25 A follow-up open-label trial suggested that maintenance treatment is associated with sustained improvement.26
Figure 1: The pediatric anxiety disorders triad: Comorbidity is common

In the Child-Adolescent Multimodal Treatment Study, GAD was the most common disorder; however, GAD, SAD, and SoP were highly comorbid
GAD: generalized anxiety disorder; SAD: separation anxiety disorder; SoP: social phobia
Source: Reference 9
Anxiety disorders with ADHD
Anxiety disorders often are comorbid with attention-deficit/hyperactivity disorder (ADHD). An RCT of patients age 8 to 17 with ADHD and comorbid anxiety found that atomoxetine was associated with improved PARS scores and ADHD symptoms.27 The target dose was 1.2 mg/kg/d. Atomoxetine was well-tolerated; decreased appetite was the only significant adverse event in the treatment group vs placebo.
Multimodal treatment
Although this article reviews evidence for psychopharmacologic treatments, psychotherapeutic treatment of young patients with anxiety disorders has seen significant advances.28 Most psychotherapy studies have evaluated the efficacy of CBT,29-31 although there is evidence for psychodynamic therapy and interpersonal therapy.32 The American Academy of Child & Adolescent Psychiatry recommends a multimodal treatment approach because combination treatment appears to be more effective than monotherapy.8,28,33 Also, clinicians who treat pediatric patients who have an anxiety disorder should evaluate the family’s role on anxiety symptoms and may consider family therapy.
Treatment considerations
Evidence supports the efficacy of sertraline, citalopram, paroxetine, fluvoxamine, fluoxetine, and venlafaxine for treating children and adolescents with anxiety disorders (Figure 2).8,9,11,15,16,23,25 Some practitioners suggest using differing dosing strategies for pediatric anxiety disorders compared with those used to treat adults (Table).34 When considering SSRIs for children and adolescents, keep in mind the “black-box” warning regarding suicidality in these patients. Carefully monitor patients for treatment-emergent suicidality and routinely reassess for the presence and severity of suicidal ideation and suicide risk.
Figure 2: Number needed to treat for SSRIs and SNRIs in pediatric anxiety disorders

GAD: generalized anxiety disorder; RUPP: Research Unit on Pediatric Psychopharmacology; SAD: separation anxiety disorder; SNRI: serotonin-norepinephrine reuptake inhibitor; SoP: social phobia; SSRI: selective serotonin reuptake inhibitorTable
Practical dosing of SSRIs and SNRIs in pediatric patients with anxietya
| Medication | Initial child dose (age <12; mg/d) | Initial adolescent dose (age 12 to 17; mg/d) | Target dose (mg/d) |
|---|---|---|---|
| Citalopram | 5 to 10 | 10 | 20 to 40 |
| Escitalopram | 2.5 to 5 | 5 to 10 | 10 to 20 |
| Fluoxetineb | 10 | 20 | 20 to 40 (children), 40 to 60 (adolescents) |
| Paroxetineb | 5 to 10 | 10 | 20 |
| Sertralinec | 10 to 12.5 | 25 | 150 |
| Venlafaxine | 37.5 | 37.5 | 150 |
| aGeneralized anxiety disorder, social phobia, and separation anxiety disorder bMay consider cytochrome P450 genotyping for 2D6, which may suggest an alternate dosing strategy cSertraline is available in a liquid formulation (20 mg/mL) SNRI: serotonin-norepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor Source: Adapted from reference 34 | |||
Related Resources
- Connolly SD, Bernstein GA; Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2007;46(2):267-283.
- Anxiety and Depression Association of America. www.adaa.org.
- American Academy of Child & Adolescent Psychiatry. www.aacap.org.
Drug Brand Names
- Alprazolam • Xanax
- Atomoxetine • Strattera
- Buspirone • BuSpar
- Citalopram • Celexa
- Clonazepam • Klonopin
- Fluoxetine • Prozac
- Fluvoxamine • Luvox, Luvox CR
- Lorazepam • Ativan
- Paroxetine • Paxil, Paxil CR
- Sertraline • Zoloft
- Venlafaxine • Effexor, Effexor XR
Disclosures
Dr. Strawn has received research support from the American Academy of Child & Adolescent Psychiatry, Eli Lilly and Company, and Shire, and is an employee of the University of Cincinnati, Cincinnati, OH.
Dr. McReynolds was employed by Eli Lilly and Company from 1997 to 2005.
1. Beesdo K, Knappe S, Pine DS. Anxiety and anxiety disorders in children and adolescents: developmental issues and implications for DSM-V. Psychiatr Clin North Am. 2009;32(3):483-524.
2. Beesdo K, Pine DS, Lieb R, et al. Incidence and risk patterns of anxiety and depressive disorders and categorization of generalized anxiety disorder. Arch Gen Psychiatry. 2010;67(1):47-57.
3. Ialongo N, Edelsohn G, Werthamer-Larsson L, et al. The significance of self-reported anxious symptoms in first grade children: prediction to anxious symptoms and adaptive functioning in fifth grade. J Child Psychol Psychiatry. 1995;36(3):427-437.
4. Foley DL, Goldston DB, Costello EJ, et al. Proximal psychiatric risk factors for suicidality in youth: the Great Smoky Mountains Study. Arch Gen Psychiatry. 2006;63(9):1017-1024.
5. Jacobson CM, Muehlenkamp JJ, Miller AL, et al. Psychiatric impairment among adolescents engaging in different types of deliberate self-harm. J Clin Child Adolesc Psychol. 2008;37(2):363-375.
6. Ialongo N, Edelsohn G, Werthamer-Larsson L, et al. The significance of self-reported anxious symptoms in first-grade children. J Abnorm Child Psychol. 1994;22(4):441-455.
7. Pine DS, Cohen P, Gurley D, et al. The risk for early-adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders. Arch Gen Psychiatry. 1998;55(1):56-64.
8. Rynn MA, Siqueland L, Rickels K. Placebo-controlled trial of sertraline in the treatment of children with generalized anxiety disorders. Am J Psychiatry. 2001;158(12):2008-2014.
9. Walkup JT, Albano AM, Piacentini J, et al. Cognitive behavioral therapy, sertraline, or a combination in childhood anxiety. N Engl J Med. 2008;359(26):2753-2766.
10. Maslowsky J, Mogg K, Bradley BP, et al. A preliminary investigation of neural correlates of treatment in adolescents with generalized anxiety disorder. J Child Adolesc Psychopharmacol. 2010;20(2):105-111.
11. Rynn MA, Riddle MA, Yeung PP, et al. Efficacy and safety of extended-release venlafaxine in the treatment of generalized anxiety disorder in children and adolescents: two placebo-controlled trials. Am J Psychiatry. 2007;164(2):290-300.
12. BuSpar [package insert] Princeton NJ: Bristol-Myers Squibb; 2010.
13. Simeon JG, Ferguson HB. Alprazolam effects in children with anxiety disorders. Can J Psychiatry. 1987;32(7):570-574.
14. Simeon JG, Ferguson HB, Knott V, et al. Clinical, cognitive, and neurophysiological effects of alprazolam in children and adolescents with overanxious and avoidant disorders. J Am Acad Child Adolesc Psychiatry. 1992;31(1):29-33.
15. Wagner KD, Berard R, Stein MB, et al. A multicenter, randomized, double-blind, placebo-controlled trial of paroxetine in children and adolescents with social anxiety disorder. Arch Gen Psychiatry. 2004;61(11):1153-1162.
16. March JS, Entusah AR, Rynn M, et al. A randomized controlled trial of venlafaxine ER versus placebo in pediatric social anxiety disorder. Biol Psychiatry. 2007;62(10):1149-1154.
17. Beidel DC, Turner SM, Sallee FR, et al. SET-C versus fluoxetine in the treatment of childhood social phobia. J Am Acad Child Adolesc Psychiatry. 2007;46(12):1622-1632.
18. Compton SN, Grant PJ, Chrisman AK, et al. Sertraline in children and adolescents with social anxiety disorder: an open trial. J Am Acad Child Adolesc Psychiatry. 2001;40(5):564-571.
19. Chavira DA, Stein MB. Combined psychoeducation and treatment with selective serotonin reuptake inhibitors for youth with generalized social anxiety disorder. J Child Adolesc Psychopharmacol. 2002;12(1):47-54.
20. Graae F, Milner J, Rizzotto L, et al. Clonazepam in childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 1994;33(3):372-376.
21. Renaud J, Birmaher B, Wassick SC, et al. Use of selective serotonin reuptake inhibitors for the treatment of childhood panic disorder: a pilot study. J Child Adolesc Psychopharmacol. 1999;9(2):73-83.
22. Fairbanks JM, Pine DS, Tancer NK, et al. Open fluoxetine treatment of mixed anxiety disorders in children and adolescents. J Child Adolesc Psychopharmacol. 1997;7(1):17-29.
23. The Research Unit on Pediatric Psychopharmacology Anxiety Study Group. Fluvoxamine for the treatment of anxiety disorders in children and adolescents. N Engl J Med. 2001;344(17):1279-1285.
24. Birmaher B, Waterman GS, Ryan N, et al. Fluoxetine for childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 1994;33(7):993-999.
25. Birmaher B, Axelson DA, Monk K, et al. Fluoxetine for the treatment of childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2003;42(4):415-423.
26. Clark DB, Birmaher B, Axelson D, et al. Fluoxetine for the treatment of childhood anxiety disorders: open-label, long-term extension to a controlled trial. J Am Acad Child Adolesc Psychiatry. 2005;44(12):1263-1270.
27. Geller D, Donnelly C, Lopez F, et al. Atomoxetine treatment for pediatric patients with attention-deficit/hyperactivity disorder with comorbid anxiety disorder. J Am Acad Child Adolesc Psychiatry. 2007;46(9):1119-1127.
28. Connolly SD, Bernstein GA. Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2007;46(2):267-283.
29. Kendall PC. Treating anxiety disorders in children: results of a randomized clinical trial. J Consult Clin Psychol. 1994;62(1):100-110.
30. Kendall PC, Flannery-Schroeder E, Panichelli-Mindel SM, et al. Therapy for youths with anxiety disorders: a second randomized clinical trial. J Consult Clin Psychol. 1997;65(3):366-380.
31. Reynolds S, Wilson C, Austin J, et al. Effects of psychotherapy for anxiety in children and adolescents: a meta-analytic review. Clin Psychol Rev. 2012;32(4):251-262.
32. Strawn JR, Wehry AM, DelBello MP, et al. Establishing the neurobiologic basis of treatment in children and adolescents with generalized anxiety disorder. Depress Anxiety. 2012;29(4):328-339.
33. Ginsburg GS, Kendall PC, Sakolsky D, et al. Remission after acute treatment in children and adolescents with anxiety disorders: findings from the CAMS. J Consult Clin Psychol. 2011;79(6):806-813.
34. Findling RL, Kowatch RA. How (not) to dose antidepressants and antipsychotics for children. Current Psychiatry. 2007;6(6):79-83.
Anxiety disorders are remarkably common among pediatric patients1,2 and are associated with significant morbidity3 and increased risk of suicidality in adolescents.4,5 Effective diagnosis and treatment of pediatric anxiety disorders are critical for reducing psychosocial morbidity,3,6 suicidality, and the risk of secondary mood disorders.7
This article summarizes open-label studies and randomized controlled trials (RCTs) of selective serotonin reuptake inhibitors (SSRIs), selective serotonin-norepinephrine reuptake inhibitors, atypical anxiolytics, and benzodiazepines in children and adolescents with generalized anxiety disorder (GAD), social phobia, separation anxiety disorder, and panic disorder. Although we focus on psychopharmacologic treatments, the best outcomes generally are observed with multimodal treatments that combine psychotherapy and pharmacotherapy.
Generalized anxiety disorder
Researchers have evaluated SSRIs, benzodiazepines, and buspirone in pediatric patients with GAD. In a double-blind, placebo-controlled trial of 22 patients age 5 to 17, sertraline, 50 mg/d, was associated with improvement in Hamilton Anxiety Rating Scale (HAM-A), Clinical Global Impression-Severity (CGI-S), and Clinical Global Impression-Improvement (CGI-I) scores over 9 weeks.8 The Child-Adolescent Anxiety Multimodal Study compared cognitive-behavioral therapy (CBT) to sertraline or sertraline plus CBT in 488 patients age 7 to 17, 78% of whom had GAD.9 Sertraline monotherapy was superior to placebo and not statistically different from CBT, while combination treatment was superior to both monotherapy conditions in improving CGI score. In both trials, sertraline was well tolerated.
One study evaluated fluoxetine, 5 to 40 mg/d, or CBT in 14 youths with GAD; both treatments improved symptoms.10 In a study of 320 GAD patients age 6 to 17, venlafaxine extended-release (XR) initiated at 37.5 mg/d was associated with improved HAM-A scores.11 In general, venlafaxine was well tolerated; adverse effects included increased blood pressure, asthenia, pain, anorexia, somnolence, weight loss, and possibly treatment-emergent suicidal ideation.
Two RCTs of buspirone, 15 to 60 mg/d, that evaluated 559 children and adolescents age 6 to 17 with GAD did not observe significant differences between buspirone and placebo.12 By contrast, 2 open-label studies of youths with anxiety suggested improvement associated with buspirone.12 Treatment-emergent adverse events included nausea, stomachache, and headache.
Clinical trials of benzodiazepines in anxious children and adolescents have yielded mixed results. A 4-week, open-label trial of alprazolam, 0.5 mg to 1.5 mg/d, in 12 adolescents with overanxious disorder—the DSM-III forerunner of GAD—found improvements in anxiety, depression, psychomotor excitation, and hyperactivity, but patients experienced sedation, activation, headache, and nausea.13 However, a double-blind RCT in 30 youths age 8 to 16 found no statistically significant difference between alprazolam and placebo.14 Alprazolam generally was well tolerated; fatigue and dry mouth were reported, but no withdrawal symptoms. Additionally, benzodiazepine use may be associated with tolerance and—in young children—disinhibition.
Social phobia
Researchers have evaluated paroxetine, citalopram, fluoxetine, and venlafaxine for treating social phobia in pediatric patients. In an RCT, 78% of paroxetine-treated patients with social phobia responded compared with 38% for placebo over 16 weeks. Adverse events—including withdrawal symptoms—were twice as likely in patients who received paroxetine. Additionally, 4 paroxetine patients exhibited suicidal ideation vs 0 patients who received placebo.15
In an RCT of 293 children and adolescents age 8 to 17 with social phobia, venlafaxine XR was initiated at 37.5 mg/d and titrated to 112.5 mg/d, 150 mg/d, or 225 mg/d, depending on body weight.16 The venlafaxine group experienced significantly improved anxiety symptoms and the medication generally was well tolerated, although 3 venlafaxine-treated patients developed suicidal ideation compared with 0 in the placebo group.
An RCT compared Social Effectiveness Therapy for Children (SET-C) and fluoxetine, 10 to 40 mg/d, for 139 patients age 7 to 17 with social phobia.17 SET-C is a CBT for children and adolescents that focuses on increasing interpersonal skills and becoming more comfortable in social situations; it involves psychoeducation, social skills training, and exposure exercises. At endpoint, 53% of patients in the SET-C group no longer met diagnostic criteria for social phobia. Fluoxetine was well tolerated; no severe adverse events were reported.
In an open-label study of sertraline (mean dose = 123 mg/d) for 14 young persons with social phobia, 36% of patients responded and 29% partially responded at 8 weeks.18 Adverse events generally were mild and included nausea, diarrhea, and headache. In a 12-week study, 12 pediatric patients with social phobia received citalopram, 10 to 40 mg/d, and eight 15-minute counseling sessions. At endpoint, clinicians rated 83% of patients as much improved or very much improved. The medication generally was well tolerated.19
Separation anxiety disorder
In a 4-week, double-blind crossover pilot study, researchers randomly assigned 15 children age 7 to 13 with separation anxiety disorder to clonazepam, up to 2 mg/d, or placebo.20 There was no significant difference in CGI-I score between clonazepam and placebo. Side effects—including drowsiness, irritability and “oppositional behavior”—were more frequent in patients treated with clonazepam.
Panic disorder
Only 2 open-label studies of SSRIs have been conducted in pediatric patients with panic disorder. The first evaluated the effectiveness and tolerability of fluoxetine, sertraline, or paroxetine over 6 months in 12 patients; 67% no longer met criteria for panic disorder at endpoint.21 In this study, benzodiazepines—including clonazepam and lorazepam—were used in 67% of patients at the start of SSRI treatment. The authors suggested this strategy may be clinically useful for patients with panic disorder.
In the second study, Fairbanks et al22 examined the use of fluoxetine for 6 to 9 weeks in 16 outpatients with mixed anxiety disorders who did not respond to psychotherapy. Patients age ≤12 were given 5 to 40 mg/d and those age ≥13 received 5 to 80 mg/d. Fluoxetine was associated with clinically significant improvement in 3 of the 5 patients who had panic disorder. Although overall fluoxetine was well tolerated, drowsiness, dyssomnia, decreased appetite, nausea, and abdominal pain were the most common side effects. Fluoxetine was not associated with suicidal ideation.
Mixed anxiety disorders
Most trials of pediatric anxiety have evaluated patients with “mixed anxiety disorders” because GAD, social phobia, and separation anxiety disorder are highly comorbid and share diagnostic features (Figure 1).9 An RCT of fluvoxamine, up to 300 mg/d, in 128 pediatric patients with ≥1 anxiety disorders found significant differences in CGI-I and endpoint Pediatric Anxiety Rating Scale (PARS) scores.23 Fluvoxamine was well tolerated but associated with increased motor activity and abdominal discomfort compared with placebo.
Two open-label trials of pediatric patients with mixed anxiety disorders suggested fluoxetine may be beneficial. Fairbanks et al22 documented clinical improvement in 10 of 10 patients with separation anxiety disorder, 8 of 10 with social phobia, 4 of 6 with specific phobia, 3 of 5 with panic disorder, and 1 of 7 with GAD. Birmaher et al24 evaluated 21 pediatric patients with overanxious disorder, social phobia, or separation anxiety who had not responded to psychotherapy and were not depressed; all patients received flexibly-dosed fluoxetine for up to 10 months. Fluoxetine was well tolerated and 81% of patients improved.
Finally, in a 12-week RCT of 74 patients age 7 to 17 with GAD, separation anxiety disorder, and/or social phobia, fluoxetine, 10 to 20 mg/d, was associated with improved scores on the Screen for Anxiety Related Emotional Disorders, PARS, CGI-I, CGI-S, and Children’s Global Assessment Scale.25 A follow-up open-label trial suggested that maintenance treatment is associated with sustained improvement.26
Figure 1: The pediatric anxiety disorders triad: Comorbidity is common

In the Child-Adolescent Multimodal Treatment Study, GAD was the most common disorder; however, GAD, SAD, and SoP were highly comorbid
GAD: generalized anxiety disorder; SAD: separation anxiety disorder; SoP: social phobia
Source: Reference 9
Anxiety disorders with ADHD
Anxiety disorders often are comorbid with attention-deficit/hyperactivity disorder (ADHD). An RCT of patients age 8 to 17 with ADHD and comorbid anxiety found that atomoxetine was associated with improved PARS scores and ADHD symptoms.27 The target dose was 1.2 mg/kg/d. Atomoxetine was well-tolerated; decreased appetite was the only significant adverse event in the treatment group vs placebo.
Multimodal treatment
Although this article reviews evidence for psychopharmacologic treatments, psychotherapeutic treatment of young patients with anxiety disorders has seen significant advances.28 Most psychotherapy studies have evaluated the efficacy of CBT,29-31 although there is evidence for psychodynamic therapy and interpersonal therapy.32 The American Academy of Child & Adolescent Psychiatry recommends a multimodal treatment approach because combination treatment appears to be more effective than monotherapy.8,28,33 Also, clinicians who treat pediatric patients who have an anxiety disorder should evaluate the family’s role on anxiety symptoms and may consider family therapy.
Treatment considerations
Evidence supports the efficacy of sertraline, citalopram, paroxetine, fluvoxamine, fluoxetine, and venlafaxine for treating children and adolescents with anxiety disorders (Figure 2).8,9,11,15,16,23,25 Some practitioners suggest using differing dosing strategies for pediatric anxiety disorders compared with those used to treat adults (Table).34 When considering SSRIs for children and adolescents, keep in mind the “black-box” warning regarding suicidality in these patients. Carefully monitor patients for treatment-emergent suicidality and routinely reassess for the presence and severity of suicidal ideation and suicide risk.
Figure 2: Number needed to treat for SSRIs and SNRIs in pediatric anxiety disorders

GAD: generalized anxiety disorder; RUPP: Research Unit on Pediatric Psychopharmacology; SAD: separation anxiety disorder; SNRI: serotonin-norepinephrine reuptake inhibitor; SoP: social phobia; SSRI: selective serotonin reuptake inhibitorTable
Practical dosing of SSRIs and SNRIs in pediatric patients with anxietya
| Medication | Initial child dose (age <12; mg/d) | Initial adolescent dose (age 12 to 17; mg/d) | Target dose (mg/d) |
|---|---|---|---|
| Citalopram | 5 to 10 | 10 | 20 to 40 |
| Escitalopram | 2.5 to 5 | 5 to 10 | 10 to 20 |
| Fluoxetineb | 10 | 20 | 20 to 40 (children), 40 to 60 (adolescents) |
| Paroxetineb | 5 to 10 | 10 | 20 |
| Sertralinec | 10 to 12.5 | 25 | 150 |
| Venlafaxine | 37.5 | 37.5 | 150 |
| aGeneralized anxiety disorder, social phobia, and separation anxiety disorder bMay consider cytochrome P450 genotyping for 2D6, which may suggest an alternate dosing strategy cSertraline is available in a liquid formulation (20 mg/mL) SNRI: serotonin-norepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor Source: Adapted from reference 34 | |||
Related Resources
- Connolly SD, Bernstein GA; Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2007;46(2):267-283.
- Anxiety and Depression Association of America. www.adaa.org.
- American Academy of Child & Adolescent Psychiatry. www.aacap.org.
Drug Brand Names
- Alprazolam • Xanax
- Atomoxetine • Strattera
- Buspirone • BuSpar
- Citalopram • Celexa
- Clonazepam • Klonopin
- Fluoxetine • Prozac
- Fluvoxamine • Luvox, Luvox CR
- Lorazepam • Ativan
- Paroxetine • Paxil, Paxil CR
- Sertraline • Zoloft
- Venlafaxine • Effexor, Effexor XR
Disclosures
Dr. Strawn has received research support from the American Academy of Child & Adolescent Psychiatry, Eli Lilly and Company, and Shire, and is an employee of the University of Cincinnati, Cincinnati, OH.
Dr. McReynolds was employed by Eli Lilly and Company from 1997 to 2005.
Anxiety disorders are remarkably common among pediatric patients1,2 and are associated with significant morbidity3 and increased risk of suicidality in adolescents.4,5 Effective diagnosis and treatment of pediatric anxiety disorders are critical for reducing psychosocial morbidity,3,6 suicidality, and the risk of secondary mood disorders.7
This article summarizes open-label studies and randomized controlled trials (RCTs) of selective serotonin reuptake inhibitors (SSRIs), selective serotonin-norepinephrine reuptake inhibitors, atypical anxiolytics, and benzodiazepines in children and adolescents with generalized anxiety disorder (GAD), social phobia, separation anxiety disorder, and panic disorder. Although we focus on psychopharmacologic treatments, the best outcomes generally are observed with multimodal treatments that combine psychotherapy and pharmacotherapy.
Generalized anxiety disorder
Researchers have evaluated SSRIs, benzodiazepines, and buspirone in pediatric patients with GAD. In a double-blind, placebo-controlled trial of 22 patients age 5 to 17, sertraline, 50 mg/d, was associated with improvement in Hamilton Anxiety Rating Scale (HAM-A), Clinical Global Impression-Severity (CGI-S), and Clinical Global Impression-Improvement (CGI-I) scores over 9 weeks.8 The Child-Adolescent Anxiety Multimodal Study compared cognitive-behavioral therapy (CBT) to sertraline or sertraline plus CBT in 488 patients age 7 to 17, 78% of whom had GAD.9 Sertraline monotherapy was superior to placebo and not statistically different from CBT, while combination treatment was superior to both monotherapy conditions in improving CGI score. In both trials, sertraline was well tolerated.
One study evaluated fluoxetine, 5 to 40 mg/d, or CBT in 14 youths with GAD; both treatments improved symptoms.10 In a study of 320 GAD patients age 6 to 17, venlafaxine extended-release (XR) initiated at 37.5 mg/d was associated with improved HAM-A scores.11 In general, venlafaxine was well tolerated; adverse effects included increased blood pressure, asthenia, pain, anorexia, somnolence, weight loss, and possibly treatment-emergent suicidal ideation.
Two RCTs of buspirone, 15 to 60 mg/d, that evaluated 559 children and adolescents age 6 to 17 with GAD did not observe significant differences between buspirone and placebo.12 By contrast, 2 open-label studies of youths with anxiety suggested improvement associated with buspirone.12 Treatment-emergent adverse events included nausea, stomachache, and headache.
Clinical trials of benzodiazepines in anxious children and adolescents have yielded mixed results. A 4-week, open-label trial of alprazolam, 0.5 mg to 1.5 mg/d, in 12 adolescents with overanxious disorder—the DSM-III forerunner of GAD—found improvements in anxiety, depression, psychomotor excitation, and hyperactivity, but patients experienced sedation, activation, headache, and nausea.13 However, a double-blind RCT in 30 youths age 8 to 16 found no statistically significant difference between alprazolam and placebo.14 Alprazolam generally was well tolerated; fatigue and dry mouth were reported, but no withdrawal symptoms. Additionally, benzodiazepine use may be associated with tolerance and—in young children—disinhibition.
Social phobia
Researchers have evaluated paroxetine, citalopram, fluoxetine, and venlafaxine for treating social phobia in pediatric patients. In an RCT, 78% of paroxetine-treated patients with social phobia responded compared with 38% for placebo over 16 weeks. Adverse events—including withdrawal symptoms—were twice as likely in patients who received paroxetine. Additionally, 4 paroxetine patients exhibited suicidal ideation vs 0 patients who received placebo.15
In an RCT of 293 children and adolescents age 8 to 17 with social phobia, venlafaxine XR was initiated at 37.5 mg/d and titrated to 112.5 mg/d, 150 mg/d, or 225 mg/d, depending on body weight.16 The venlafaxine group experienced significantly improved anxiety symptoms and the medication generally was well tolerated, although 3 venlafaxine-treated patients developed suicidal ideation compared with 0 in the placebo group.
An RCT compared Social Effectiveness Therapy for Children (SET-C) and fluoxetine, 10 to 40 mg/d, for 139 patients age 7 to 17 with social phobia.17 SET-C is a CBT for children and adolescents that focuses on increasing interpersonal skills and becoming more comfortable in social situations; it involves psychoeducation, social skills training, and exposure exercises. At endpoint, 53% of patients in the SET-C group no longer met diagnostic criteria for social phobia. Fluoxetine was well tolerated; no severe adverse events were reported.
In an open-label study of sertraline (mean dose = 123 mg/d) for 14 young persons with social phobia, 36% of patients responded and 29% partially responded at 8 weeks.18 Adverse events generally were mild and included nausea, diarrhea, and headache. In a 12-week study, 12 pediatric patients with social phobia received citalopram, 10 to 40 mg/d, and eight 15-minute counseling sessions. At endpoint, clinicians rated 83% of patients as much improved or very much improved. The medication generally was well tolerated.19
Separation anxiety disorder
In a 4-week, double-blind crossover pilot study, researchers randomly assigned 15 children age 7 to 13 with separation anxiety disorder to clonazepam, up to 2 mg/d, or placebo.20 There was no significant difference in CGI-I score between clonazepam and placebo. Side effects—including drowsiness, irritability and “oppositional behavior”—were more frequent in patients treated with clonazepam.
Panic disorder
Only 2 open-label studies of SSRIs have been conducted in pediatric patients with panic disorder. The first evaluated the effectiveness and tolerability of fluoxetine, sertraline, or paroxetine over 6 months in 12 patients; 67% no longer met criteria for panic disorder at endpoint.21 In this study, benzodiazepines—including clonazepam and lorazepam—were used in 67% of patients at the start of SSRI treatment. The authors suggested this strategy may be clinically useful for patients with panic disorder.
In the second study, Fairbanks et al22 examined the use of fluoxetine for 6 to 9 weeks in 16 outpatients with mixed anxiety disorders who did not respond to psychotherapy. Patients age ≤12 were given 5 to 40 mg/d and those age ≥13 received 5 to 80 mg/d. Fluoxetine was associated with clinically significant improvement in 3 of the 5 patients who had panic disorder. Although overall fluoxetine was well tolerated, drowsiness, dyssomnia, decreased appetite, nausea, and abdominal pain were the most common side effects. Fluoxetine was not associated with suicidal ideation.
Mixed anxiety disorders
Most trials of pediatric anxiety have evaluated patients with “mixed anxiety disorders” because GAD, social phobia, and separation anxiety disorder are highly comorbid and share diagnostic features (Figure 1).9 An RCT of fluvoxamine, up to 300 mg/d, in 128 pediatric patients with ≥1 anxiety disorders found significant differences in CGI-I and endpoint Pediatric Anxiety Rating Scale (PARS) scores.23 Fluvoxamine was well tolerated but associated with increased motor activity and abdominal discomfort compared with placebo.
Two open-label trials of pediatric patients with mixed anxiety disorders suggested fluoxetine may be beneficial. Fairbanks et al22 documented clinical improvement in 10 of 10 patients with separation anxiety disorder, 8 of 10 with social phobia, 4 of 6 with specific phobia, 3 of 5 with panic disorder, and 1 of 7 with GAD. Birmaher et al24 evaluated 21 pediatric patients with overanxious disorder, social phobia, or separation anxiety who had not responded to psychotherapy and were not depressed; all patients received flexibly-dosed fluoxetine for up to 10 months. Fluoxetine was well tolerated and 81% of patients improved.
Finally, in a 12-week RCT of 74 patients age 7 to 17 with GAD, separation anxiety disorder, and/or social phobia, fluoxetine, 10 to 20 mg/d, was associated with improved scores on the Screen for Anxiety Related Emotional Disorders, PARS, CGI-I, CGI-S, and Children’s Global Assessment Scale.25 A follow-up open-label trial suggested that maintenance treatment is associated with sustained improvement.26
Figure 1: The pediatric anxiety disorders triad: Comorbidity is common

In the Child-Adolescent Multimodal Treatment Study, GAD was the most common disorder; however, GAD, SAD, and SoP were highly comorbid
GAD: generalized anxiety disorder; SAD: separation anxiety disorder; SoP: social phobia
Source: Reference 9
Anxiety disorders with ADHD
Anxiety disorders often are comorbid with attention-deficit/hyperactivity disorder (ADHD). An RCT of patients age 8 to 17 with ADHD and comorbid anxiety found that atomoxetine was associated with improved PARS scores and ADHD symptoms.27 The target dose was 1.2 mg/kg/d. Atomoxetine was well-tolerated; decreased appetite was the only significant adverse event in the treatment group vs placebo.
Multimodal treatment
Although this article reviews evidence for psychopharmacologic treatments, psychotherapeutic treatment of young patients with anxiety disorders has seen significant advances.28 Most psychotherapy studies have evaluated the efficacy of CBT,29-31 although there is evidence for psychodynamic therapy and interpersonal therapy.32 The American Academy of Child & Adolescent Psychiatry recommends a multimodal treatment approach because combination treatment appears to be more effective than monotherapy.8,28,33 Also, clinicians who treat pediatric patients who have an anxiety disorder should evaluate the family’s role on anxiety symptoms and may consider family therapy.
Treatment considerations
Evidence supports the efficacy of sertraline, citalopram, paroxetine, fluvoxamine, fluoxetine, and venlafaxine for treating children and adolescents with anxiety disorders (Figure 2).8,9,11,15,16,23,25 Some practitioners suggest using differing dosing strategies for pediatric anxiety disorders compared with those used to treat adults (Table).34 When considering SSRIs for children and adolescents, keep in mind the “black-box” warning regarding suicidality in these patients. Carefully monitor patients for treatment-emergent suicidality and routinely reassess for the presence and severity of suicidal ideation and suicide risk.
Figure 2: Number needed to treat for SSRIs and SNRIs in pediatric anxiety disorders

GAD: generalized anxiety disorder; RUPP: Research Unit on Pediatric Psychopharmacology; SAD: separation anxiety disorder; SNRI: serotonin-norepinephrine reuptake inhibitor; SoP: social phobia; SSRI: selective serotonin reuptake inhibitorTable
Practical dosing of SSRIs and SNRIs in pediatric patients with anxietya
| Medication | Initial child dose (age <12; mg/d) | Initial adolescent dose (age 12 to 17; mg/d) | Target dose (mg/d) |
|---|---|---|---|
| Citalopram | 5 to 10 | 10 | 20 to 40 |
| Escitalopram | 2.5 to 5 | 5 to 10 | 10 to 20 |
| Fluoxetineb | 10 | 20 | 20 to 40 (children), 40 to 60 (adolescents) |
| Paroxetineb | 5 to 10 | 10 | 20 |
| Sertralinec | 10 to 12.5 | 25 | 150 |
| Venlafaxine | 37.5 | 37.5 | 150 |
| aGeneralized anxiety disorder, social phobia, and separation anxiety disorder bMay consider cytochrome P450 genotyping for 2D6, which may suggest an alternate dosing strategy cSertraline is available in a liquid formulation (20 mg/mL) SNRI: serotonin-norepinephrine reuptake inhibitor; SSRI: selective serotonin reuptake inhibitor Source: Adapted from reference 34 | |||
Related Resources
- Connolly SD, Bernstein GA; Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2007;46(2):267-283.
- Anxiety and Depression Association of America. www.adaa.org.
- American Academy of Child & Adolescent Psychiatry. www.aacap.org.
Drug Brand Names
- Alprazolam • Xanax
- Atomoxetine • Strattera
- Buspirone • BuSpar
- Citalopram • Celexa
- Clonazepam • Klonopin
- Fluoxetine • Prozac
- Fluvoxamine • Luvox, Luvox CR
- Lorazepam • Ativan
- Paroxetine • Paxil, Paxil CR
- Sertraline • Zoloft
- Venlafaxine • Effexor, Effexor XR
Disclosures
Dr. Strawn has received research support from the American Academy of Child & Adolescent Psychiatry, Eli Lilly and Company, and Shire, and is an employee of the University of Cincinnati, Cincinnati, OH.
Dr. McReynolds was employed by Eli Lilly and Company from 1997 to 2005.
1. Beesdo K, Knappe S, Pine DS. Anxiety and anxiety disorders in children and adolescents: developmental issues and implications for DSM-V. Psychiatr Clin North Am. 2009;32(3):483-524.
2. Beesdo K, Pine DS, Lieb R, et al. Incidence and risk patterns of anxiety and depressive disorders and categorization of generalized anxiety disorder. Arch Gen Psychiatry. 2010;67(1):47-57.
3. Ialongo N, Edelsohn G, Werthamer-Larsson L, et al. The significance of self-reported anxious symptoms in first grade children: prediction to anxious symptoms and adaptive functioning in fifth grade. J Child Psychol Psychiatry. 1995;36(3):427-437.
4. Foley DL, Goldston DB, Costello EJ, et al. Proximal psychiatric risk factors for suicidality in youth: the Great Smoky Mountains Study. Arch Gen Psychiatry. 2006;63(9):1017-1024.
5. Jacobson CM, Muehlenkamp JJ, Miller AL, et al. Psychiatric impairment among adolescents engaging in different types of deliberate self-harm. J Clin Child Adolesc Psychol. 2008;37(2):363-375.
6. Ialongo N, Edelsohn G, Werthamer-Larsson L, et al. The significance of self-reported anxious symptoms in first-grade children. J Abnorm Child Psychol. 1994;22(4):441-455.
7. Pine DS, Cohen P, Gurley D, et al. The risk for early-adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders. Arch Gen Psychiatry. 1998;55(1):56-64.
8. Rynn MA, Siqueland L, Rickels K. Placebo-controlled trial of sertraline in the treatment of children with generalized anxiety disorders. Am J Psychiatry. 2001;158(12):2008-2014.
9. Walkup JT, Albano AM, Piacentini J, et al. Cognitive behavioral therapy, sertraline, or a combination in childhood anxiety. N Engl J Med. 2008;359(26):2753-2766.
10. Maslowsky J, Mogg K, Bradley BP, et al. A preliminary investigation of neural correlates of treatment in adolescents with generalized anxiety disorder. J Child Adolesc Psychopharmacol. 2010;20(2):105-111.
11. Rynn MA, Riddle MA, Yeung PP, et al. Efficacy and safety of extended-release venlafaxine in the treatment of generalized anxiety disorder in children and adolescents: two placebo-controlled trials. Am J Psychiatry. 2007;164(2):290-300.
12. BuSpar [package insert] Princeton NJ: Bristol-Myers Squibb; 2010.
13. Simeon JG, Ferguson HB. Alprazolam effects in children with anxiety disorders. Can J Psychiatry. 1987;32(7):570-574.
14. Simeon JG, Ferguson HB, Knott V, et al. Clinical, cognitive, and neurophysiological effects of alprazolam in children and adolescents with overanxious and avoidant disorders. J Am Acad Child Adolesc Psychiatry. 1992;31(1):29-33.
15. Wagner KD, Berard R, Stein MB, et al. A multicenter, randomized, double-blind, placebo-controlled trial of paroxetine in children and adolescents with social anxiety disorder. Arch Gen Psychiatry. 2004;61(11):1153-1162.
16. March JS, Entusah AR, Rynn M, et al. A randomized controlled trial of venlafaxine ER versus placebo in pediatric social anxiety disorder. Biol Psychiatry. 2007;62(10):1149-1154.
17. Beidel DC, Turner SM, Sallee FR, et al. SET-C versus fluoxetine in the treatment of childhood social phobia. J Am Acad Child Adolesc Psychiatry. 2007;46(12):1622-1632.
18. Compton SN, Grant PJ, Chrisman AK, et al. Sertraline in children and adolescents with social anxiety disorder: an open trial. J Am Acad Child Adolesc Psychiatry. 2001;40(5):564-571.
19. Chavira DA, Stein MB. Combined psychoeducation and treatment with selective serotonin reuptake inhibitors for youth with generalized social anxiety disorder. J Child Adolesc Psychopharmacol. 2002;12(1):47-54.
20. Graae F, Milner J, Rizzotto L, et al. Clonazepam in childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 1994;33(3):372-376.
21. Renaud J, Birmaher B, Wassick SC, et al. Use of selective serotonin reuptake inhibitors for the treatment of childhood panic disorder: a pilot study. J Child Adolesc Psychopharmacol. 1999;9(2):73-83.
22. Fairbanks JM, Pine DS, Tancer NK, et al. Open fluoxetine treatment of mixed anxiety disorders in children and adolescents. J Child Adolesc Psychopharmacol. 1997;7(1):17-29.
23. The Research Unit on Pediatric Psychopharmacology Anxiety Study Group. Fluvoxamine for the treatment of anxiety disorders in children and adolescents. N Engl J Med. 2001;344(17):1279-1285.
24. Birmaher B, Waterman GS, Ryan N, et al. Fluoxetine for childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 1994;33(7):993-999.
25. Birmaher B, Axelson DA, Monk K, et al. Fluoxetine for the treatment of childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2003;42(4):415-423.
26. Clark DB, Birmaher B, Axelson D, et al. Fluoxetine for the treatment of childhood anxiety disorders: open-label, long-term extension to a controlled trial. J Am Acad Child Adolesc Psychiatry. 2005;44(12):1263-1270.
27. Geller D, Donnelly C, Lopez F, et al. Atomoxetine treatment for pediatric patients with attention-deficit/hyperactivity disorder with comorbid anxiety disorder. J Am Acad Child Adolesc Psychiatry. 2007;46(9):1119-1127.
28. Connolly SD, Bernstein GA. Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2007;46(2):267-283.
29. Kendall PC. Treating anxiety disorders in children: results of a randomized clinical trial. J Consult Clin Psychol. 1994;62(1):100-110.
30. Kendall PC, Flannery-Schroeder E, Panichelli-Mindel SM, et al. Therapy for youths with anxiety disorders: a second randomized clinical trial. J Consult Clin Psychol. 1997;65(3):366-380.
31. Reynolds S, Wilson C, Austin J, et al. Effects of psychotherapy for anxiety in children and adolescents: a meta-analytic review. Clin Psychol Rev. 2012;32(4):251-262.
32. Strawn JR, Wehry AM, DelBello MP, et al. Establishing the neurobiologic basis of treatment in children and adolescents with generalized anxiety disorder. Depress Anxiety. 2012;29(4):328-339.
33. Ginsburg GS, Kendall PC, Sakolsky D, et al. Remission after acute treatment in children and adolescents with anxiety disorders: findings from the CAMS. J Consult Clin Psychol. 2011;79(6):806-813.
34. Findling RL, Kowatch RA. How (not) to dose antidepressants and antipsychotics for children. Current Psychiatry. 2007;6(6):79-83.
1. Beesdo K, Knappe S, Pine DS. Anxiety and anxiety disorders in children and adolescents: developmental issues and implications for DSM-V. Psychiatr Clin North Am. 2009;32(3):483-524.
2. Beesdo K, Pine DS, Lieb R, et al. Incidence and risk patterns of anxiety and depressive disorders and categorization of generalized anxiety disorder. Arch Gen Psychiatry. 2010;67(1):47-57.
3. Ialongo N, Edelsohn G, Werthamer-Larsson L, et al. The significance of self-reported anxious symptoms in first grade children: prediction to anxious symptoms and adaptive functioning in fifth grade. J Child Psychol Psychiatry. 1995;36(3):427-437.
4. Foley DL, Goldston DB, Costello EJ, et al. Proximal psychiatric risk factors for suicidality in youth: the Great Smoky Mountains Study. Arch Gen Psychiatry. 2006;63(9):1017-1024.
5. Jacobson CM, Muehlenkamp JJ, Miller AL, et al. Psychiatric impairment among adolescents engaging in different types of deliberate self-harm. J Clin Child Adolesc Psychol. 2008;37(2):363-375.
6. Ialongo N, Edelsohn G, Werthamer-Larsson L, et al. The significance of self-reported anxious symptoms in first-grade children. J Abnorm Child Psychol. 1994;22(4):441-455.
7. Pine DS, Cohen P, Gurley D, et al. The risk for early-adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders. Arch Gen Psychiatry. 1998;55(1):56-64.
8. Rynn MA, Siqueland L, Rickels K. Placebo-controlled trial of sertraline in the treatment of children with generalized anxiety disorders. Am J Psychiatry. 2001;158(12):2008-2014.
9. Walkup JT, Albano AM, Piacentini J, et al. Cognitive behavioral therapy, sertraline, or a combination in childhood anxiety. N Engl J Med. 2008;359(26):2753-2766.
10. Maslowsky J, Mogg K, Bradley BP, et al. A preliminary investigation of neural correlates of treatment in adolescents with generalized anxiety disorder. J Child Adolesc Psychopharmacol. 2010;20(2):105-111.
11. Rynn MA, Riddle MA, Yeung PP, et al. Efficacy and safety of extended-release venlafaxine in the treatment of generalized anxiety disorder in children and adolescents: two placebo-controlled trials. Am J Psychiatry. 2007;164(2):290-300.
12. BuSpar [package insert] Princeton NJ: Bristol-Myers Squibb; 2010.
13. Simeon JG, Ferguson HB. Alprazolam effects in children with anxiety disorders. Can J Psychiatry. 1987;32(7):570-574.
14. Simeon JG, Ferguson HB, Knott V, et al. Clinical, cognitive, and neurophysiological effects of alprazolam in children and adolescents with overanxious and avoidant disorders. J Am Acad Child Adolesc Psychiatry. 1992;31(1):29-33.
15. Wagner KD, Berard R, Stein MB, et al. A multicenter, randomized, double-blind, placebo-controlled trial of paroxetine in children and adolescents with social anxiety disorder. Arch Gen Psychiatry. 2004;61(11):1153-1162.
16. March JS, Entusah AR, Rynn M, et al. A randomized controlled trial of venlafaxine ER versus placebo in pediatric social anxiety disorder. Biol Psychiatry. 2007;62(10):1149-1154.
17. Beidel DC, Turner SM, Sallee FR, et al. SET-C versus fluoxetine in the treatment of childhood social phobia. J Am Acad Child Adolesc Psychiatry. 2007;46(12):1622-1632.
18. Compton SN, Grant PJ, Chrisman AK, et al. Sertraline in children and adolescents with social anxiety disorder: an open trial. J Am Acad Child Adolesc Psychiatry. 2001;40(5):564-571.
19. Chavira DA, Stein MB. Combined psychoeducation and treatment with selective serotonin reuptake inhibitors for youth with generalized social anxiety disorder. J Child Adolesc Psychopharmacol. 2002;12(1):47-54.
20. Graae F, Milner J, Rizzotto L, et al. Clonazepam in childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 1994;33(3):372-376.
21. Renaud J, Birmaher B, Wassick SC, et al. Use of selective serotonin reuptake inhibitors for the treatment of childhood panic disorder: a pilot study. J Child Adolesc Psychopharmacol. 1999;9(2):73-83.
22. Fairbanks JM, Pine DS, Tancer NK, et al. Open fluoxetine treatment of mixed anxiety disorders in children and adolescents. J Child Adolesc Psychopharmacol. 1997;7(1):17-29.
23. The Research Unit on Pediatric Psychopharmacology Anxiety Study Group. Fluvoxamine for the treatment of anxiety disorders in children and adolescents. N Engl J Med. 2001;344(17):1279-1285.
24. Birmaher B, Waterman GS, Ryan N, et al. Fluoxetine for childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 1994;33(7):993-999.
25. Birmaher B, Axelson DA, Monk K, et al. Fluoxetine for the treatment of childhood anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2003;42(4):415-423.
26. Clark DB, Birmaher B, Axelson D, et al. Fluoxetine for the treatment of childhood anxiety disorders: open-label, long-term extension to a controlled trial. J Am Acad Child Adolesc Psychiatry. 2005;44(12):1263-1270.
27. Geller D, Donnelly C, Lopez F, et al. Atomoxetine treatment for pediatric patients with attention-deficit/hyperactivity disorder with comorbid anxiety disorder. J Am Acad Child Adolesc Psychiatry. 2007;46(9):1119-1127.
28. Connolly SD, Bernstein GA. Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with anxiety disorders. J Am Acad Child Adolesc Psychiatry. 2007;46(2):267-283.
29. Kendall PC. Treating anxiety disorders in children: results of a randomized clinical trial. J Consult Clin Psychol. 1994;62(1):100-110.
30. Kendall PC, Flannery-Schroeder E, Panichelli-Mindel SM, et al. Therapy for youths with anxiety disorders: a second randomized clinical trial. J Consult Clin Psychol. 1997;65(3):366-380.
31. Reynolds S, Wilson C, Austin J, et al. Effects of psychotherapy for anxiety in children and adolescents: a meta-analytic review. Clin Psychol Rev. 2012;32(4):251-262.
32. Strawn JR, Wehry AM, DelBello MP, et al. Establishing the neurobiologic basis of treatment in children and adolescents with generalized anxiety disorder. Depress Anxiety. 2012;29(4):328-339.
33. Ginsburg GS, Kendall PC, Sakolsky D, et al. Remission after acute treatment in children and adolescents with anxiety disorders: findings from the CAMS. J Consult Clin Psychol. 2011;79(6):806-813.
34. Findling RL, Kowatch RA. How (not) to dose antidepressants and antipsychotics for children. Current Psychiatry. 2007;6(6):79-83.
Sleep terrors in adults: How to help control this potentially dangerous condition
Sleep terrors (STs)—also known as night terrors—are characterized by sudden arousal accompanied by a piercing scream or cry in the first few hours after falling asleep. These parasomnias arise out of slow-wave sleep (stages 3 and 4 of nonrapid eye movement [non-REM] sleep) and affect approximately 5% of adults.1 The condition is twice as common in men than women, and usually affects children but may not develop until adulthood.1
During STs, a patient may act scared, afraid, agitated, anxious, or panicky without being fully aware of his or her surroundings. The episode may last 30 seconds to 5 minutes; most patients don’t remember the event the next morning. STs may leave individuals feeling exhausted and perplexed the next day. Verbalization during the episode is incoherent and a patient’s perception of the environment seems altered. Tachycardia, tachypnea, sweating, flushed skin, or mydriasis are prominent. When ST patients walk, they may do so violently and can cause harm to themselves or others.
The differential diagnosis of STs includes posttraumatic stress disorder; nocturnal seizures characterized by excessive motor activity and organic CNS lesions; REM sleep behavior disorder; sleep choking syndrome; and nocturnal panic attacks. Patients with STs report high rates of stressful events—eg, divorce or bereavement—in the previous year. They are more likely to have a history of mood and anxiety disorders and high levels of depression, anxiety, and obsessive-compulsive and phobic traits. One study found patients with STs were 4.3 times more likely to have had a car accident in the past year.2
Evaluating and treating STs
Rule out comorbid conditions such as obstructive sleep apnea and periodic limb movement disorder. Encourage your patient to improve his or her sleep hygiene by maintaining a regular sleep/wake cycle, exercising, and limiting caffeine and alcohol and exposure to bright light before bedtime.
Self-help techniques. To avoid injury, encourage your patient to remove dangerous objects from their sleeping area. Suggest locking the doors to the room or home, and putting medications in a secure place. Patients also may consider keeping their mattress close to the floor to limit the risk of injury.
Pharmacotherapy and psychotherapy. Along with counseling and support, your patient may benefit from cognitive-behavioral therapy, relaxation therapy, or hypnosis.3 Anticipatory arousal therapy may help by interrupting the altered underlying electrophysiology of partial arousal.
If your patient is concerned about physical injury during STs, consider prescribing clonazepam, temazepam, or diazepam.4 Trazodone and selective serotonin reuptake inhibitors such as paroxetine5 also have been used to treat STs.
Disclosure
Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Crisp AH. The sleepwalking/night terrors syndrome in adults. Postgrad Med J. 1996;72(852):599-604.
2. Oudiette D, Leu S, Pottier M, et al. Dreamlike mentations during sleepwalking and sleep terrors in adults. Sleep. 2009;32(12):1621-1627.
3. Lowe P, Humphreys C, Williams SJ. Night terrors: women’s experiences of (not) sleeping where there is domestic violence. Violence Against Women. 2007;13(6):549-561.
4. Schenck CH, Mahowald MW. Long-term nightly benzodiazepine treatment of injurious parasomnias and other disorders of disrupted nocturnal sleep in 170 adults. Am J Med. 1996;100(3):333-337.
5. Lillywhite AR, Wilson SJ, Nutt DJ. Successful treatment of night terrors and somnambulism with paroxetine. Br J Psychiatry. 1994;164(4):551-554.
Sleep terrors (STs)—also known as night terrors—are characterized by sudden arousal accompanied by a piercing scream or cry in the first few hours after falling asleep. These parasomnias arise out of slow-wave sleep (stages 3 and 4 of nonrapid eye movement [non-REM] sleep) and affect approximately 5% of adults.1 The condition is twice as common in men than women, and usually affects children but may not develop until adulthood.1
During STs, a patient may act scared, afraid, agitated, anxious, or panicky without being fully aware of his or her surroundings. The episode may last 30 seconds to 5 minutes; most patients don’t remember the event the next morning. STs may leave individuals feeling exhausted and perplexed the next day. Verbalization during the episode is incoherent and a patient’s perception of the environment seems altered. Tachycardia, tachypnea, sweating, flushed skin, or mydriasis are prominent. When ST patients walk, they may do so violently and can cause harm to themselves or others.
The differential diagnosis of STs includes posttraumatic stress disorder; nocturnal seizures characterized by excessive motor activity and organic CNS lesions; REM sleep behavior disorder; sleep choking syndrome; and nocturnal panic attacks. Patients with STs report high rates of stressful events—eg, divorce or bereavement—in the previous year. They are more likely to have a history of mood and anxiety disorders and high levels of depression, anxiety, and obsessive-compulsive and phobic traits. One study found patients with STs were 4.3 times more likely to have had a car accident in the past year.2
Evaluating and treating STs
Rule out comorbid conditions such as obstructive sleep apnea and periodic limb movement disorder. Encourage your patient to improve his or her sleep hygiene by maintaining a regular sleep/wake cycle, exercising, and limiting caffeine and alcohol and exposure to bright light before bedtime.
Self-help techniques. To avoid injury, encourage your patient to remove dangerous objects from their sleeping area. Suggest locking the doors to the room or home, and putting medications in a secure place. Patients also may consider keeping their mattress close to the floor to limit the risk of injury.
Pharmacotherapy and psychotherapy. Along with counseling and support, your patient may benefit from cognitive-behavioral therapy, relaxation therapy, or hypnosis.3 Anticipatory arousal therapy may help by interrupting the altered underlying electrophysiology of partial arousal.
If your patient is concerned about physical injury during STs, consider prescribing clonazepam, temazepam, or diazepam.4 Trazodone and selective serotonin reuptake inhibitors such as paroxetine5 also have been used to treat STs.
Disclosure
Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
Sleep terrors (STs)—also known as night terrors—are characterized by sudden arousal accompanied by a piercing scream or cry in the first few hours after falling asleep. These parasomnias arise out of slow-wave sleep (stages 3 and 4 of nonrapid eye movement [non-REM] sleep) and affect approximately 5% of adults.1 The condition is twice as common in men than women, and usually affects children but may not develop until adulthood.1
During STs, a patient may act scared, afraid, agitated, anxious, or panicky without being fully aware of his or her surroundings. The episode may last 30 seconds to 5 minutes; most patients don’t remember the event the next morning. STs may leave individuals feeling exhausted and perplexed the next day. Verbalization during the episode is incoherent and a patient’s perception of the environment seems altered. Tachycardia, tachypnea, sweating, flushed skin, or mydriasis are prominent. When ST patients walk, they may do so violently and can cause harm to themselves or others.
The differential diagnosis of STs includes posttraumatic stress disorder; nocturnal seizures characterized by excessive motor activity and organic CNS lesions; REM sleep behavior disorder; sleep choking syndrome; and nocturnal panic attacks. Patients with STs report high rates of stressful events—eg, divorce or bereavement—in the previous year. They are more likely to have a history of mood and anxiety disorders and high levels of depression, anxiety, and obsessive-compulsive and phobic traits. One study found patients with STs were 4.3 times more likely to have had a car accident in the past year.2
Evaluating and treating STs
Rule out comorbid conditions such as obstructive sleep apnea and periodic limb movement disorder. Encourage your patient to improve his or her sleep hygiene by maintaining a regular sleep/wake cycle, exercising, and limiting caffeine and alcohol and exposure to bright light before bedtime.
Self-help techniques. To avoid injury, encourage your patient to remove dangerous objects from their sleeping area. Suggest locking the doors to the room or home, and putting medications in a secure place. Patients also may consider keeping their mattress close to the floor to limit the risk of injury.
Pharmacotherapy and psychotherapy. Along with counseling and support, your patient may benefit from cognitive-behavioral therapy, relaxation therapy, or hypnosis.3 Anticipatory arousal therapy may help by interrupting the altered underlying electrophysiology of partial arousal.
If your patient is concerned about physical injury during STs, consider prescribing clonazepam, temazepam, or diazepam.4 Trazodone and selective serotonin reuptake inhibitors such as paroxetine5 also have been used to treat STs.
Disclosure
Dr. Jain reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Crisp AH. The sleepwalking/night terrors syndrome in adults. Postgrad Med J. 1996;72(852):599-604.
2. Oudiette D, Leu S, Pottier M, et al. Dreamlike mentations during sleepwalking and sleep terrors in adults. Sleep. 2009;32(12):1621-1627.
3. Lowe P, Humphreys C, Williams SJ. Night terrors: women’s experiences of (not) sleeping where there is domestic violence. Violence Against Women. 2007;13(6):549-561.
4. Schenck CH, Mahowald MW. Long-term nightly benzodiazepine treatment of injurious parasomnias and other disorders of disrupted nocturnal sleep in 170 adults. Am J Med. 1996;100(3):333-337.
5. Lillywhite AR, Wilson SJ, Nutt DJ. Successful treatment of night terrors and somnambulism with paroxetine. Br J Psychiatry. 1994;164(4):551-554.
1. Crisp AH. The sleepwalking/night terrors syndrome in adults. Postgrad Med J. 1996;72(852):599-604.
2. Oudiette D, Leu S, Pottier M, et al. Dreamlike mentations during sleepwalking and sleep terrors in adults. Sleep. 2009;32(12):1621-1627.
3. Lowe P, Humphreys C, Williams SJ. Night terrors: women’s experiences of (not) sleeping where there is domestic violence. Violence Against Women. 2007;13(6):549-561.
4. Schenck CH, Mahowald MW. Long-term nightly benzodiazepine treatment of injurious parasomnias and other disorders of disrupted nocturnal sleep in 170 adults. Am J Med. 1996;100(3):333-337.
5. Lillywhite AR, Wilson SJ, Nutt DJ. Successful treatment of night terrors and somnambulism with paroxetine. Br J Psychiatry. 1994;164(4):551-554.