Mother dies after cesarean delivery: $4.5M verdict
A 31-year-old woman gave birth to her first child by cesarean delivery. Over the next 3 days she reported nausea, vomiting, severe abdominal pain, and had an elevated heart rate. On day 4, she was discharged from the hospital. She went to the ObGyn’s office the next day and was told, after several hours, to return to the hospital. There she was found to have sepsis and acute renal failure. A transfer to another hospital was attempted that night, but she died during transport. 

Estate's Claim: The ObGyn should have responded to her reported symptoms prior to discharge by ordering tests. The ObGyn should have called an ambulance to transport her to the hospital from his office.

Defendants’ Defense: The hospital settled for an undisclosed amount before the trial. The ObGyn claimed that there was no negligence in the patient’s treatment.

Verdict: A $4.5 million North Carolina verdict was returned.

Brain-damaged child dies at age 2
A woman was admitted to the hospital in labor. Ninety minutes later a nonreassuring fetal heart-rate tracing was noted. Two hours after that, the ObGyn decided to perform an emergency cesarean delivery.

The child was depressed at birth and required resuscitation. She was transferred to another hospital’s neonatal intensive care unit (NICU), where she was found to have had a severe and catastrophic brain injury. The child died at 2 years of age. 

Parent's Claim: An emergency cesarean delivery should have been performed as soon as the fetal heart-rate tracing was found to be nonreassuring. The ObGyn failed to respond to phone calls from the nurses to report fetal distress.

Physician's Defense: The delivery was performed in a timely manner. Brain damage was due to encephalopathy that occurred prior to labor.

Verdict: A Mississippi defense verdict was returned.

Who or what was at fault for ureter injury?
A 45-year-old woman underwent hysterectomy performed by her ObGyn. During surgery, the patient’s ureter was injured. Several additional operations were needed to repair the injury. 

Patient's Claim: The patient was not fully informed of the extent of the surgery or possible complications. The ObGyn was negligent in injuring the ureter.

Defendants' Defense: Three months after surgery, the physician entered notes into the patient’s chart that indicated that the ureter injuries were due to a defective monopolar device that had been provided by the hospital. Informed consent included surgical options and complications.

The hospital argued that its equipment was not defective; other surgeons had used the device without any problems. The ObGyn had not used the device before; any injuries were due to his inexperience and negligence.

Verdict: A $2 million South Carolina verdict was returned against the ObGyn. The hospital received a defense verdict.

Did excessive force cause child’s C7 injury?
During delivery, shoulder dystocia was encountered. The child has nerve root avulsion at C7 with damage to adjacent nerve trunks at C5–C6. As a result of the brachial plexus injury, the patient underwent cable grafting and muscle surgeries, but he has permanent weakness and dysfunction in his left arm. 

Parent's Claim: Excessive force was used to deliver the child during manipulations for shoulder dystocia.

Physician's Defense: The ObGyn denied using excessive traction. She claimed that she had never used upward traction during a shoulder dystocia presentation. Suprapubic pressure, McRoberts’ maneuver, and delivery of the posterior arm were used. The damage occurred prior to delivery of the head.

Verdict An Illinois defense verdict was returned.

 

Laparoscopic sheath and coils found at exploratory surgery
In april 2007, a woman underwent a sterilization procedure (Essure) after which she reported pelvic pain. In September 2007, she consented to right salpingo-oophorectomy plus appendectomy. The ObGyn performed the surgery using a robotic device. After surgery, the pathology report indicated that the resected organs were normal and functional.

The patient moved to another state. She continued to have pain and sought treatment with another physician. A computed tomography (CT) scan more than 3 years after robotic surgery revealed foreign objects in the patient’s body. One full Essure coil, a non-fired coil, a second partial coil, and a robotic laparoscopy sheath were surgically removed.

Patient's Claim: The ObGyn was negligent in the performance of the sterilization and robotic surgery procedures. The healthy ovary and fallopian tube should not have been removed and caused her to have surgical menopause.

Physician's defense: The right ovary appeared diseased. The Essure device dropped the coils. The robot malfunctioned during the salpingo-oophorectomy. 

Verdict: A $110,513 Oregon verdict was returned, including $10,500 in medical expenses and $100,000 for pain and mental anguish.

Discrepancy in fundal height; child has CP
During her second pregnancy, a 37-year-old woman saw Dr. A, her ObGyn, for regular prenatal care. At 37 weeks’ gestation, the fundal height was not consistent with the fetus’ gestational age: the measurement was higher by 2 cm. No additional testing was scheduled.

At 39.5 weeks’ gestation, the mother reported decreased fetal movement. Because her regular ObGyn was on vacation, she was evaluated by another ObGyn (Dr. B). The fetal heart-rate monitor showed nonreactive results with minimal variability. Dr. B told the mother to drive herself to the emergency department (ED) for additional evaluation. At the hospital, when fetal heart-rate monitoring confirmed fetal distress, an emergency cesarean delivery was performed.

At birth, the baby was not breathing and resuscitation began. The infant was taken to a transitional care unit and then to the NICU, where he was intubated. Cord blood testing confirmed metabolic acidosis. The baby was later found to have dystonic cerebral palsy (CP). He is unable to speak, walk, eat, or care for himself, and he requires 24/7 nursing care. 

Parents' Claim: Dr. A failed to order testing after the fundal height discrepancy was found. Testing could have led to an earlier delivery and avoided the injury. The pediatrician failed to ensure adequate oxygenation after delivery. The baby should have been transferred immediately to the NICU and intubated.

Physician's Defense: The fundal height discrepancy was explained by the baby’s position within the uterus. The pediatrician acted heroically to save the child’s life.

Verdict: A $3.5 million Massachusetts settlement was reached.

NT scans misread, not reported; child has Down syndrome
At 13 weeks’ gestation, a 38-year-old woman saw a maternal-fetal medicine (MFM) specialist, who interpreted a nuchal translucency (NT) scan as normal. At 20 weeks’ gestation, an ObGyn performed a second screening that indicated the fetus was at high risk for Down syndrome. However, no further testing was ordered.

At 26.5 weeks’ gestation, amniocentesis was performed after ultrasonography and an echocardiogram revealed fetal abnormalities. A diagnosis of Down syndrome was made at 29 weeks’ gestation, too late for termination of pregnancy. 

Parent's Claim: The MFM specialist misread the first NT scan. The ObGyn did not inform the mother of the results of the second screening. Proper interpretation and reporting would have initiated further testing and determination that the baby had Down syndrome before the deadline for termination of pregnancy.

Defendants' Defense: The case was settled during trial.

Verdict: A $3 million New Jersey settlement was reached, including $2 million from the medical center where the second test was performed, $940,000 from the ObGyn, and $60,000 from the MFM specialist.

Uterine rupture, baby dies: $2.15M award
At 38 weeks’ gestation, a mother was admitted to a hospital for induction of labor due to pregnancy-induced hypertension. The fetus was estimated to be large for its gestational age. A uterine rupture occurred during labor. The baby was stillborn.

Parents' Claim: The uterine rupture was not immediately recognized. The ObGyn failed to come to the mother’s bedside until after the fetus had receded up the birth canal, which indicated that a rupture was occurring. The ObGyn ordered oxytocin instead of performing an immediate cesarean delivery. Eleven minutes later, the cesarean was ordered, but the baby had died.

Physician's Defense: There was no negligence; proper protocols were followed. A uterine rupture cannot be predicted.

Verdict: A $650,000 settlement was reached with the hospital before trial. Because the ObGyn was employed by a federally qualified clinic, the matter was filed in federal court. The Illinois court issued a bench decision awarding $1.5 million.

Migrated IUD causes years of pain
In september 2006, an ObGyn inserted an intrauterine device (IUD) in a patient. In February 2007, the patient had an ectopic pregnancy. The IUD was not found during dilation and curettage. The patient continued to report pain to the ObGyn. She sought treatment from another physician in November 2010 due to continuing pain. A CT scan revealed that the IUD had migrated to her abdomen. The IUD was surgically removed.

Patient's Claim: The ObGyn was unwilling to figure out why the patient had continuing pain, and told her to “just deal with it.” He should have found and removed the IUD after the ectopic pregnancy.

Physician's Defense: It was reasonable to assume that the IUD had been expelled, as 2 ultrasonographies performed after ectopic pregnancy revealed nothing. Since the IUD had not caused an abscess, infection, or inflammation, the patient suffered no injury.

Verdict: A Virginia defense verdict was returned.

Profoundly disabled child dies at age 5
A 17-year-old woman with a history of miscarriage received prenatal care from her ObGyn. A July due date was established by ultrasonography in January.

In May, the mother went to the ED with pelvic pain. She was treated for preterm labor and discharged 2 days later.

In early July, ultrasonography showed a fetus in cephalic position with a posterior-located placenta.

At a prenatal examination a week later, the patient reported vaginal discharge. Her ObGyn suspected premature rupture of membranes (PROM) and admitted her to the hospital. Oxytocin was used to induce labor. Intact membranes were artificially ruptured and an internal fetal heart-rate monitor was placed. The ObGyn recorded that the pregnancy was at term.

Hours later, the mother told the nurses that she thought the fetal monitor had become disconnected; the monitor’s placement was not confirmed. The mother was given a sedative. After a few hours, she awoke with intense pain and dizziness. She used her call button, but no one immediately responded.

When full cervical dilation was reached, the fetus was at –1, 0 station. When the fetus reached +1 station, delivery was attempted. The baby was delivered using vacuum extraction.

The child’s Apgar score was 0 at 1 minute of life. Resuscitation was started with intubation and mechanical ventilation. The child’s birth weight was 6.87 lb; arterial blood gas pH measured 6.9; and gestational age was estimated at 38 to 39 weeks.

An electro-encephalogram performed in the NICU suggested intraventricular hemorrhage. The child was found to have perinatal asphyxia, hypoxic ischemic encephalopathy, left parietal skull fracture and cephalohematoma, severe metabolic acidosis, suspected sepsis, transient oliguria, and seizure episodes. The baby was hospitalized for 3.5 months and then followed regularly.

The mother and child moved from Puerto Rico to New York City to obtain better medical care. The child was regularly hospitalized until she died at age 5. 

Parent's Claim: There was a discrepancy in gestational age assessment. The nurses failed to monitor fetal heart-rate tracings at proper intervals, and they were unresponsive to the mother. Informed consent did not include vacuum extraction.

Defendants' Defense: The case was settled during trial.

Verdict: A $1.125 million Puerto Rico settlement was reached.

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.

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

Mother dies after cesarean delivery: $4.5M verdict
A 31-year-old woman gave birth to her first child by cesarean delivery. Over the next 3 days she reported nausea, vomiting, severe abdominal pain, and had an elevated heart rate. On day 4, she was discharged from the hospital. She went to the ObGyn’s office the next day and was told, after several hours, to return to the hospital. There she was found to have sepsis and acute renal failure. A transfer to another hospital was attempted that night, but she died during transport. 

Estate's Claim: The ObGyn should have responded to her reported symptoms prior to discharge by ordering tests. The ObGyn should have called an ambulance to transport her to the hospital from his office.

Defendants’ Defense: The hospital settled for an undisclosed amount before the trial. The ObGyn claimed that there was no negligence in the patient’s treatment.

Verdict: A $4.5 million North Carolina verdict was returned.

Brain-damaged child dies at age 2
A woman was admitted to the hospital in labor. Ninety minutes later a nonreassuring fetal heart-rate tracing was noted. Two hours after that, the ObGyn decided to perform an emergency cesarean delivery.

The child was depressed at birth and required resuscitation. She was transferred to another hospital’s neonatal intensive care unit (NICU), where she was found to have had a severe and catastrophic brain injury. The child died at 2 years of age. 

Parent's Claim: An emergency cesarean delivery should have been performed as soon as the fetal heart-rate tracing was found to be nonreassuring. The ObGyn failed to respond to phone calls from the nurses to report fetal distress.

Physician's Defense: The delivery was performed in a timely manner. Brain damage was due to encephalopathy that occurred prior to labor.

Verdict: A Mississippi defense verdict was returned.

Who or what was at fault for ureter injury?
A 45-year-old woman underwent hysterectomy performed by her ObGyn. During surgery, the patient’s ureter was injured. Several additional operations were needed to repair the injury. 

Patient's Claim: The patient was not fully informed of the extent of the surgery or possible complications. The ObGyn was negligent in injuring the ureter.

Defendants' Defense: Three months after surgery, the physician entered notes into the patient’s chart that indicated that the ureter injuries were due to a defective monopolar device that had been provided by the hospital. Informed consent included surgical options and complications.

The hospital argued that its equipment was not defective; other surgeons had used the device without any problems. The ObGyn had not used the device before; any injuries were due to his inexperience and negligence.

Verdict: A $2 million South Carolina verdict was returned against the ObGyn. The hospital received a defense verdict.

Did excessive force cause child’s C7 injury?
During delivery, shoulder dystocia was encountered. The child has nerve root avulsion at C7 with damage to adjacent nerve trunks at C5–C6. As a result of the brachial plexus injury, the patient underwent cable grafting and muscle surgeries, but he has permanent weakness and dysfunction in his left arm. 

Parent's Claim: Excessive force was used to deliver the child during manipulations for shoulder dystocia.

Physician's Defense: The ObGyn denied using excessive traction. She claimed that she had never used upward traction during a shoulder dystocia presentation. Suprapubic pressure, McRoberts’ maneuver, and delivery of the posterior arm were used. The damage occurred prior to delivery of the head.

Verdict An Illinois defense verdict was returned.

 

Laparoscopic sheath and coils found at exploratory surgery
In april 2007, a woman underwent a sterilization procedure (Essure) after which she reported pelvic pain. In September 2007, she consented to right salpingo-oophorectomy plus appendectomy. The ObGyn performed the surgery using a robotic device. After surgery, the pathology report indicated that the resected organs were normal and functional.

The patient moved to another state. She continued to have pain and sought treatment with another physician. A computed tomography (CT) scan more than 3 years after robotic surgery revealed foreign objects in the patient’s body. One full Essure coil, a non-fired coil, a second partial coil, and a robotic laparoscopy sheath were surgically removed.

Patient's Claim: The ObGyn was negligent in the performance of the sterilization and robotic surgery procedures. The healthy ovary and fallopian tube should not have been removed and caused her to have surgical menopause.

Physician's defense: The right ovary appeared diseased. The Essure device dropped the coils. The robot malfunctioned during the salpingo-oophorectomy. 

Verdict: A $110,513 Oregon verdict was returned, including $10,500 in medical expenses and $100,000 for pain and mental anguish.

Discrepancy in fundal height; child has CP
During her second pregnancy, a 37-year-old woman saw Dr. A, her ObGyn, for regular prenatal care. At 37 weeks’ gestation, the fundal height was not consistent with the fetus’ gestational age: the measurement was higher by 2 cm. No additional testing was scheduled.

At 39.5 weeks’ gestation, the mother reported decreased fetal movement. Because her regular ObGyn was on vacation, she was evaluated by another ObGyn (Dr. B). The fetal heart-rate monitor showed nonreactive results with minimal variability. Dr. B told the mother to drive herself to the emergency department (ED) for additional evaluation. At the hospital, when fetal heart-rate monitoring confirmed fetal distress, an emergency cesarean delivery was performed.

At birth, the baby was not breathing and resuscitation began. The infant was taken to a transitional care unit and then to the NICU, where he was intubated. Cord blood testing confirmed metabolic acidosis. The baby was later found to have dystonic cerebral palsy (CP). He is unable to speak, walk, eat, or care for himself, and he requires 24/7 nursing care. 

Parents' Claim: Dr. A failed to order testing after the fundal height discrepancy was found. Testing could have led to an earlier delivery and avoided the injury. The pediatrician failed to ensure adequate oxygenation after delivery. The baby should have been transferred immediately to the NICU and intubated.

Physician's Defense: The fundal height discrepancy was explained by the baby’s position within the uterus. The pediatrician acted heroically to save the child’s life.

Verdict: A $3.5 million Massachusetts settlement was reached.

NT scans misread, not reported; child has Down syndrome
At 13 weeks’ gestation, a 38-year-old woman saw a maternal-fetal medicine (MFM) specialist, who interpreted a nuchal translucency (NT) scan as normal. At 20 weeks’ gestation, an ObGyn performed a second screening that indicated the fetus was at high risk for Down syndrome. However, no further testing was ordered.

At 26.5 weeks’ gestation, amniocentesis was performed after ultrasonography and an echocardiogram revealed fetal abnormalities. A diagnosis of Down syndrome was made at 29 weeks’ gestation, too late for termination of pregnancy. 

Parent's Claim: The MFM specialist misread the first NT scan. The ObGyn did not inform the mother of the results of the second screening. Proper interpretation and reporting would have initiated further testing and determination that the baby had Down syndrome before the deadline for termination of pregnancy.

Defendants' Defense: The case was settled during trial.

Verdict: A $3 million New Jersey settlement was reached, including $2 million from the medical center where the second test was performed, $940,000 from the ObGyn, and $60,000 from the MFM specialist.

Uterine rupture, baby dies: $2.15M award
At 38 weeks’ gestation, a mother was admitted to a hospital for induction of labor due to pregnancy-induced hypertension. The fetus was estimated to be large for its gestational age. A uterine rupture occurred during labor. The baby was stillborn.

Parents' Claim: The uterine rupture was not immediately recognized. The ObGyn failed to come to the mother’s bedside until after the fetus had receded up the birth canal, which indicated that a rupture was occurring. The ObGyn ordered oxytocin instead of performing an immediate cesarean delivery. Eleven minutes later, the cesarean was ordered, but the baby had died.

Physician's Defense: There was no negligence; proper protocols were followed. A uterine rupture cannot be predicted.

Verdict: A $650,000 settlement was reached with the hospital before trial. Because the ObGyn was employed by a federally qualified clinic, the matter was filed in federal court. The Illinois court issued a bench decision awarding $1.5 million.

Migrated IUD causes years of pain
In september 2006, an ObGyn inserted an intrauterine device (IUD) in a patient. In February 2007, the patient had an ectopic pregnancy. The IUD was not found during dilation and curettage. The patient continued to report pain to the ObGyn. She sought treatment from another physician in November 2010 due to continuing pain. A CT scan revealed that the IUD had migrated to her abdomen. The IUD was surgically removed.

Patient's Claim: The ObGyn was unwilling to figure out why the patient had continuing pain, and told her to “just deal with it.” He should have found and removed the IUD after the ectopic pregnancy.

Physician's Defense: It was reasonable to assume that the IUD had been expelled, as 2 ultrasonographies performed after ectopic pregnancy revealed nothing. Since the IUD had not caused an abscess, infection, or inflammation, the patient suffered no injury.

Verdict: A Virginia defense verdict was returned.

Profoundly disabled child dies at age 5
A 17-year-old woman with a history of miscarriage received prenatal care from her ObGyn. A July due date was established by ultrasonography in January.

In May, the mother went to the ED with pelvic pain. She was treated for preterm labor and discharged 2 days later.

In early July, ultrasonography showed a fetus in cephalic position with a posterior-located placenta.

At a prenatal examination a week later, the patient reported vaginal discharge. Her ObGyn suspected premature rupture of membranes (PROM) and admitted her to the hospital. Oxytocin was used to induce labor. Intact membranes were artificially ruptured and an internal fetal heart-rate monitor was placed. The ObGyn recorded that the pregnancy was at term.

Hours later, the mother told the nurses that she thought the fetal monitor had become disconnected; the monitor’s placement was not confirmed. The mother was given a sedative. After a few hours, she awoke with intense pain and dizziness. She used her call button, but no one immediately responded.

When full cervical dilation was reached, the fetus was at –1, 0 station. When the fetus reached +1 station, delivery was attempted. The baby was delivered using vacuum extraction.

The child’s Apgar score was 0 at 1 minute of life. Resuscitation was started with intubation and mechanical ventilation. The child’s birth weight was 6.87 lb; arterial blood gas pH measured 6.9; and gestational age was estimated at 38 to 39 weeks.

An electro-encephalogram performed in the NICU suggested intraventricular hemorrhage. The child was found to have perinatal asphyxia, hypoxic ischemic encephalopathy, left parietal skull fracture and cephalohematoma, severe metabolic acidosis, suspected sepsis, transient oliguria, and seizure episodes. The baby was hospitalized for 3.5 months and then followed regularly.

The mother and child moved from Puerto Rico to New York City to obtain better medical care. The child was regularly hospitalized until she died at age 5. 

Parent's Claim: There was a discrepancy in gestational age assessment. The nurses failed to monitor fetal heart-rate tracings at proper intervals, and they were unresponsive to the mother. Informed consent did not include vacuum extraction.

Defendants' Defense: The case was settled during trial.

Verdict: A $1.125 million Puerto Rico settlement was reached.

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.

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

Mother dies after cesarean delivery: $4.5M verdict
A 31-year-old woman gave birth to her first child by cesarean delivery. Over the next 3 days she reported nausea, vomiting, severe abdominal pain, and had an elevated heart rate. On day 4, she was discharged from the hospital. She went to the ObGyn’s office the next day and was told, after several hours, to return to the hospital. There she was found to have sepsis and acute renal failure. A transfer to another hospital was attempted that night, but she died during transport. 

Estate's Claim: The ObGyn should have responded to her reported symptoms prior to discharge by ordering tests. The ObGyn should have called an ambulance to transport her to the hospital from his office.

Defendants’ Defense: The hospital settled for an undisclosed amount before the trial. The ObGyn claimed that there was no negligence in the patient’s treatment.

Verdict: A $4.5 million North Carolina verdict was returned.

Brain-damaged child dies at age 2
A woman was admitted to the hospital in labor. Ninety minutes later a nonreassuring fetal heart-rate tracing was noted. Two hours after that, the ObGyn decided to perform an emergency cesarean delivery.

The child was depressed at birth and required resuscitation. She was transferred to another hospital’s neonatal intensive care unit (NICU), where she was found to have had a severe and catastrophic brain injury. The child died at 2 years of age. 

Parent's Claim: An emergency cesarean delivery should have been performed as soon as the fetal heart-rate tracing was found to be nonreassuring. The ObGyn failed to respond to phone calls from the nurses to report fetal distress.

Physician's Defense: The delivery was performed in a timely manner. Brain damage was due to encephalopathy that occurred prior to labor.

Verdict: A Mississippi defense verdict was returned.

Who or what was at fault for ureter injury?
A 45-year-old woman underwent hysterectomy performed by her ObGyn. During surgery, the patient’s ureter was injured. Several additional operations were needed to repair the injury. 

Patient's Claim: The patient was not fully informed of the extent of the surgery or possible complications. The ObGyn was negligent in injuring the ureter.

Defendants' Defense: Three months after surgery, the physician entered notes into the patient’s chart that indicated that the ureter injuries were due to a defective monopolar device that had been provided by the hospital. Informed consent included surgical options and complications.

The hospital argued that its equipment was not defective; other surgeons had used the device without any problems. The ObGyn had not used the device before; any injuries were due to his inexperience and negligence.

Verdict: A $2 million South Carolina verdict was returned against the ObGyn. The hospital received a defense verdict.

Did excessive force cause child’s C7 injury?
During delivery, shoulder dystocia was encountered. The child has nerve root avulsion at C7 with damage to adjacent nerve trunks at C5–C6. As a result of the brachial plexus injury, the patient underwent cable grafting and muscle surgeries, but he has permanent weakness and dysfunction in his left arm. 

Parent's Claim: Excessive force was used to deliver the child during manipulations for shoulder dystocia.

Physician's Defense: The ObGyn denied using excessive traction. She claimed that she had never used upward traction during a shoulder dystocia presentation. Suprapubic pressure, McRoberts’ maneuver, and delivery of the posterior arm were used. The damage occurred prior to delivery of the head.

Verdict An Illinois defense verdict was returned.

 

Laparoscopic sheath and coils found at exploratory surgery
In april 2007, a woman underwent a sterilization procedure (Essure) after which she reported pelvic pain. In September 2007, she consented to right salpingo-oophorectomy plus appendectomy. The ObGyn performed the surgery using a robotic device. After surgery, the pathology report indicated that the resected organs were normal and functional.

The patient moved to another state. She continued to have pain and sought treatment with another physician. A computed tomography (CT) scan more than 3 years after robotic surgery revealed foreign objects in the patient’s body. One full Essure coil, a non-fired coil, a second partial coil, and a robotic laparoscopy sheath were surgically removed.

Patient's Claim: The ObGyn was negligent in the performance of the sterilization and robotic surgery procedures. The healthy ovary and fallopian tube should not have been removed and caused her to have surgical menopause.

Physician's defense: The right ovary appeared diseased. The Essure device dropped the coils. The robot malfunctioned during the salpingo-oophorectomy. 

Verdict: A $110,513 Oregon verdict was returned, including $10,500 in medical expenses and $100,000 for pain and mental anguish.

Discrepancy in fundal height; child has CP
During her second pregnancy, a 37-year-old woman saw Dr. A, her ObGyn, for regular prenatal care. At 37 weeks’ gestation, the fundal height was not consistent with the fetus’ gestational age: the measurement was higher by 2 cm. No additional testing was scheduled.

At 39.5 weeks’ gestation, the mother reported decreased fetal movement. Because her regular ObGyn was on vacation, she was evaluated by another ObGyn (Dr. B). The fetal heart-rate monitor showed nonreactive results with minimal variability. Dr. B told the mother to drive herself to the emergency department (ED) for additional evaluation. At the hospital, when fetal heart-rate monitoring confirmed fetal distress, an emergency cesarean delivery was performed.

At birth, the baby was not breathing and resuscitation began. The infant was taken to a transitional care unit and then to the NICU, where he was intubated. Cord blood testing confirmed metabolic acidosis. The baby was later found to have dystonic cerebral palsy (CP). He is unable to speak, walk, eat, or care for himself, and he requires 24/7 nursing care. 

Parents' Claim: Dr. A failed to order testing after the fundal height discrepancy was found. Testing could have led to an earlier delivery and avoided the injury. The pediatrician failed to ensure adequate oxygenation after delivery. The baby should have been transferred immediately to the NICU and intubated.

Physician's Defense: The fundal height discrepancy was explained by the baby’s position within the uterus. The pediatrician acted heroically to save the child’s life.

Verdict: A $3.5 million Massachusetts settlement was reached.

NT scans misread, not reported; child has Down syndrome
At 13 weeks’ gestation, a 38-year-old woman saw a maternal-fetal medicine (MFM) specialist, who interpreted a nuchal translucency (NT) scan as normal. At 20 weeks’ gestation, an ObGyn performed a second screening that indicated the fetus was at high risk for Down syndrome. However, no further testing was ordered.

At 26.5 weeks’ gestation, amniocentesis was performed after ultrasonography and an echocardiogram revealed fetal abnormalities. A diagnosis of Down syndrome was made at 29 weeks’ gestation, too late for termination of pregnancy. 

Parent's Claim: The MFM specialist misread the first NT scan. The ObGyn did not inform the mother of the results of the second screening. Proper interpretation and reporting would have initiated further testing and determination that the baby had Down syndrome before the deadline for termination of pregnancy.

Defendants' Defense: The case was settled during trial.

Verdict: A $3 million New Jersey settlement was reached, including $2 million from the medical center where the second test was performed, $940,000 from the ObGyn, and $60,000 from the MFM specialist.

Uterine rupture, baby dies: $2.15M award
At 38 weeks’ gestation, a mother was admitted to a hospital for induction of labor due to pregnancy-induced hypertension. The fetus was estimated to be large for its gestational age. A uterine rupture occurred during labor. The baby was stillborn.

Parents' Claim: The uterine rupture was not immediately recognized. The ObGyn failed to come to the mother’s bedside until after the fetus had receded up the birth canal, which indicated that a rupture was occurring. The ObGyn ordered oxytocin instead of performing an immediate cesarean delivery. Eleven minutes later, the cesarean was ordered, but the baby had died.

Physician's Defense: There was no negligence; proper protocols were followed. A uterine rupture cannot be predicted.

Verdict: A $650,000 settlement was reached with the hospital before trial. Because the ObGyn was employed by a federally qualified clinic, the matter was filed in federal court. The Illinois court issued a bench decision awarding $1.5 million.

Migrated IUD causes years of pain
In september 2006, an ObGyn inserted an intrauterine device (IUD) in a patient. In February 2007, the patient had an ectopic pregnancy. The IUD was not found during dilation and curettage. The patient continued to report pain to the ObGyn. She sought treatment from another physician in November 2010 due to continuing pain. A CT scan revealed that the IUD had migrated to her abdomen. The IUD was surgically removed.

Patient's Claim: The ObGyn was unwilling to figure out why the patient had continuing pain, and told her to “just deal with it.” He should have found and removed the IUD after the ectopic pregnancy.

Physician's Defense: It was reasonable to assume that the IUD had been expelled, as 2 ultrasonographies performed after ectopic pregnancy revealed nothing. Since the IUD had not caused an abscess, infection, or inflammation, the patient suffered no injury.

Verdict: A Virginia defense verdict was returned.

Profoundly disabled child dies at age 5
A 17-year-old woman with a history of miscarriage received prenatal care from her ObGyn. A July due date was established by ultrasonography in January.

In May, the mother went to the ED with pelvic pain. She was treated for preterm labor and discharged 2 days later.

In early July, ultrasonography showed a fetus in cephalic position with a posterior-located placenta.

At a prenatal examination a week later, the patient reported vaginal discharge. Her ObGyn suspected premature rupture of membranes (PROM) and admitted her to the hospital. Oxytocin was used to induce labor. Intact membranes were artificially ruptured and an internal fetal heart-rate monitor was placed. The ObGyn recorded that the pregnancy was at term.

Hours later, the mother told the nurses that she thought the fetal monitor had become disconnected; the monitor’s placement was not confirmed. The mother was given a sedative. After a few hours, she awoke with intense pain and dizziness. She used her call button, but no one immediately responded.

When full cervical dilation was reached, the fetus was at –1, 0 station. When the fetus reached +1 station, delivery was attempted. The baby was delivered using vacuum extraction.

The child’s Apgar score was 0 at 1 minute of life. Resuscitation was started with intubation and mechanical ventilation. The child’s birth weight was 6.87 lb; arterial blood gas pH measured 6.9; and gestational age was estimated at 38 to 39 weeks.

An electro-encephalogram performed in the NICU suggested intraventricular hemorrhage. The child was found to have perinatal asphyxia, hypoxic ischemic encephalopathy, left parietal skull fracture and cephalohematoma, severe metabolic acidosis, suspected sepsis, transient oliguria, and seizure episodes. The baby was hospitalized for 3.5 months and then followed regularly.

The mother and child moved from Puerto Rico to New York City to obtain better medical care. The child was regularly hospitalized until she died at age 5. 

Parent's Claim: There was a discrepancy in gestational age assessment. The nurses failed to monitor fetal heart-rate tracings at proper intervals, and they were unresponsive to the mother. Informed consent did not include vacuum extraction.

Defendants' Defense: The case was settled during trial.

Verdict: A $1.125 million Puerto Rico settlement was reached.

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.

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

In his March podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses two original research articles that focus on women who have survived cancer, one that looks at the effects of ArginMax on sexual functioning and quality of life in female cancer survivors, and another that examines the need for decision and communication aids among breast cancer survivors. Also included in this month’s line-up of original research is a report on the cost of palliative external beam radiotherapy for bone metastases in patients with prostate cancer and a study of the impact of an electronic medical record intervention on the use of growth factor in patients with cancer. The regular Community Translations column features the recently approved combination therapy, palbociclib plus letrozole, for first-line treatment of postmenopausal women with estrogen receptor-positive, human epidermal growth factor receptor 2-negative advanced breast cancer. Dr Henry rounds off the podcast with a discussion the Journal Club’s entry, which this month focuses on new approvals, genetic testing, and maintenance therapy in women with ovarian cancer.

In his March podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses two original research articles that focus on women who have survived cancer, one that looks at the effects of ArginMax on sexual functioning and quality of life in female cancer survivors, and another that examines the need for decision and communication aids among breast cancer survivors. Also included in this month’s line-up of original research is a report on the cost of palliative external beam radiotherapy for bone metastases in patients with prostate cancer and a study of the impact of an electronic medical record intervention on the use of growth factor in patients with cancer. The regular Community Translations column features the recently approved combination therapy, palbociclib plus letrozole, for first-line treatment of postmenopausal women with estrogen receptor-positive, human epidermal growth factor receptor 2-negative advanced breast cancer. Dr Henry rounds off the podcast with a discussion the Journal Club’s entry, which this month focuses on new approvals, genetic testing, and maintenance therapy in women with ovarian cancer.

In his March podcast for The Journal of Community and Supportive Oncology, Dr David Henry discusses two original research articles that focus on women who have survived cancer, one that looks at the effects of ArginMax on sexual functioning and quality of life in female cancer survivors, and another that examines the need for decision and communication aids among breast cancer survivors. Also included in this month’s line-up of original research is a report on the cost of palliative external beam radiotherapy for bone metastases in patients with prostate cancer and a study of the impact of an electronic medical record intervention on the use of growth factor in patients with cancer. The regular Community Translations column features the recently approved combination therapy, palbociclib plus letrozole, for first-line treatment of postmenopausal women with estrogen receptor-positive, human epidermal growth factor receptor 2-negative advanced breast cancer. Dr Henry rounds off the podcast with a discussion the Journal Club’s entry, which this month focuses on new approvals, genetic testing, and maintenance therapy in women with ovarian cancer.

Tomasz Cierpicki, PhD,

and Jolanta Grembecka, PhD

Photo courtesy of the

University of Michigan

Two small-molecule inhibitors can fight aggressive, acute leukemias by targeting a protein-protein interaction, according to preclinical research published in Cancer Cell.

The compounds, MI-463 and MI-503, work by inhibiting the interaction between menin and mixed-lineage leukemia (MLL) fusion proteins.

Menin binds to the N-terminal fragment of MLL retained in all MLL fusion proteins, and the fusion proteins require menin for leukemogenic activity.

That’s why Jolanta Grembecka, PhD, and Tomasz Cierpicki, PhD, both of the University of Michigan in Ann Arbor, have been working for several years to identify small-molecule inhibitors that would block the MLL-menin interaction.

“The MLL-menin interaction is a good drug target because it’s the primary driver in [MLL] leukemia,” Dr Grembecka said. “By blocking this interaction, it’s very likely to stop the cancer.”

With that in mind, Dr Grembecka and her colleagues tested 2 compounds they developed, MI-463 and MI-503, in cell lines and mice with MLL leukemia. The compounds blocked the MLL-menin interaction without affecting normal hematopoiesis.

The team also noted that both compounds demonstrated metabolic stability and favorable pharmacokinetic profiles.

“Against all odds, we decided to explore finding a way to block the MLL-menin interaction with small molecules,” Dr Cierpicki said. “From nothing, we have been able to identify and greatly improve a compound and show that it’s got valuable potential in blocking MLL fusion leukemia in animal models.”

In a separate study published in Nature Medicine, the researchers discovered that menin and MLL play a role in androgen receptor signaling, a key driver of prostate cancer.

The team found that MI-503 and MI-136, another inhibitor of the menin-MLL interaction, were both active against castration-resistant prostate cancer in vitro and in vivo.

The researchers said they will continue to investigate the role of MLL in castration-resistant prostate cancer. And they plan to further refine their inhibitors and put the compounds through more advanced preclinical testing in MLL leukemia.

Tomasz Cierpicki, PhD,

and Jolanta Grembecka, PhD

Photo courtesy of the

University of Michigan

Two small-molecule inhibitors can fight aggressive, acute leukemias by targeting a protein-protein interaction, according to preclinical research published in Cancer Cell.

The compounds, MI-463 and MI-503, work by inhibiting the interaction between menin and mixed-lineage leukemia (MLL) fusion proteins.

Menin binds to the N-terminal fragment of MLL retained in all MLL fusion proteins, and the fusion proteins require menin for leukemogenic activity.

That’s why Jolanta Grembecka, PhD, and Tomasz Cierpicki, PhD, both of the University of Michigan in Ann Arbor, have been working for several years to identify small-molecule inhibitors that would block the MLL-menin interaction.

“The MLL-menin interaction is a good drug target because it’s the primary driver in [MLL] leukemia,” Dr Grembecka said. “By blocking this interaction, it’s very likely to stop the cancer.”

With that in mind, Dr Grembecka and her colleagues tested 2 compounds they developed, MI-463 and MI-503, in cell lines and mice with MLL leukemia. The compounds blocked the MLL-menin interaction without affecting normal hematopoiesis.

The team also noted that both compounds demonstrated metabolic stability and favorable pharmacokinetic profiles.

“Against all odds, we decided to explore finding a way to block the MLL-menin interaction with small molecules,” Dr Cierpicki said. “From nothing, we have been able to identify and greatly improve a compound and show that it’s got valuable potential in blocking MLL fusion leukemia in animal models.”

In a separate study published in Nature Medicine, the researchers discovered that menin and MLL play a role in androgen receptor signaling, a key driver of prostate cancer.

The team found that MI-503 and MI-136, another inhibitor of the menin-MLL interaction, were both active against castration-resistant prostate cancer in vitro and in vivo.

The researchers said they will continue to investigate the role of MLL in castration-resistant prostate cancer. And they plan to further refine their inhibitors and put the compounds through more advanced preclinical testing in MLL leukemia.

Tomasz Cierpicki, PhD,

and Jolanta Grembecka, PhD

Photo courtesy of the

University of Michigan

Two small-molecule inhibitors can fight aggressive, acute leukemias by targeting a protein-protein interaction, according to preclinical research published in Cancer Cell.

The compounds, MI-463 and MI-503, work by inhibiting the interaction between menin and mixed-lineage leukemia (MLL) fusion proteins.

Menin binds to the N-terminal fragment of MLL retained in all MLL fusion proteins, and the fusion proteins require menin for leukemogenic activity.

That’s why Jolanta Grembecka, PhD, and Tomasz Cierpicki, PhD, both of the University of Michigan in Ann Arbor, have been working for several years to identify small-molecule inhibitors that would block the MLL-menin interaction.

“The MLL-menin interaction is a good drug target because it’s the primary driver in [MLL] leukemia,” Dr Grembecka said. “By blocking this interaction, it’s very likely to stop the cancer.”

With that in mind, Dr Grembecka and her colleagues tested 2 compounds they developed, MI-463 and MI-503, in cell lines and mice with MLL leukemia. The compounds blocked the MLL-menin interaction without affecting normal hematopoiesis.

The team also noted that both compounds demonstrated metabolic stability and favorable pharmacokinetic profiles.

“Against all odds, we decided to explore finding a way to block the MLL-menin interaction with small molecules,” Dr Cierpicki said. “From nothing, we have been able to identify and greatly improve a compound and show that it’s got valuable potential in blocking MLL fusion leukemia in animal models.”

In a separate study published in Nature Medicine, the researchers discovered that menin and MLL play a role in androgen receptor signaling, a key driver of prostate cancer.

The team found that MI-503 and MI-136, another inhibitor of the menin-MLL interaction, were both active against castration-resistant prostate cancer in vitro and in vivo.

The researchers said they will continue to investigate the role of MLL in castration-resistant prostate cancer. And they plan to further refine their inhibitors and put the compounds through more advanced preclinical testing in MLL leukemia.

MRS2500 (magenta) and

BPTU (yellow) bind to P2Y1R

Image courtesy of

Yekaterina Kadyshevskaya

Researchers say they have identified 2 disparate ligand-binding sites in the human P2Y1 receptor (P2Y1R), which plays a critical role in thrombosis.

Their research has provided a detailed molecular map of P2Y1R, a G protein-coupled receptor (GPCR), in complex with a nucleotide antagonist MRS2500 and a non-nucleotide antagonist BPTU.

The researchers believe their findings, published in Nature, could aid the development of new antithrombotic drugs.

Beili Wu, PhD, of the Shanghai Institute of Materia Medica in China, and her colleagues noted that the human purinergic receptors P2Y1R and P2Y12R play a major physiological role in adenosine 5′-diphosphate (ADP)-mediated platelet aggregation, an important component of thrombosis.

Although most of the available antithrombotic drugs act on P2Y12R, research has suggested that P2Y1R may be a promising antithrombotic drug target. In addition, P2Y1R inhibitors may offer a safety advantage over P2Y12R inhibitors by reducing the risk of bleeding. However, efforts to develop new drugs have been impeded by poor understanding of receptor-ligand interaction.

“The P2Y1R structures [we mapped] help us understand how this receptor and different types of experimental drugs interact at the molecular level and could enable further exploration to design new and safer antithrombotic drugs with reduced adverse effects,” Dr Wu said.

She and her colleagues found that the nucleotide ligand MRS2500 recognizes a binding site within the transmembrane bundle of P2Y1R. And it is different in shape and location from the nucleotide-binding site in P2Y12R.

“It is amazing to observe that 2 GPCRs recognize the same ligand in such different ways,” Dr Wu said. “The finding highlights the diversity of signal recognition mechanisms in GPCRs, and this is of great value to drug design for each receptor with high selectivity.”

The researchers also found that, instead of interacting within the transmembrane bundle, the non-nucleotide ligand BPTU binds to a pocket on the outer interface of P2Y1R embedded in the cell membrane.

This is the first structurally characterized, selective, and high-affinity GPCR ligand located entirely outside of the helical bundle, and it represents a new paradigm in ligand binding to alter signaling in GPCRs, according to the researchers.

The team believes this new understanding of the P2Y1R structure provides opportunities to broaden the scope of future GPCR drug discovery to target novel sites outside of the conventional GPCR ligand-binding pocket, which may improve drug selectivity and reduce side effects.

MRS2500 (magenta) and

BPTU (yellow) bind to P2Y1R

Image courtesy of

Yekaterina Kadyshevskaya

Researchers say they have identified 2 disparate ligand-binding sites in the human P2Y1 receptor (P2Y1R), which plays a critical role in thrombosis.

Their research has provided a detailed molecular map of P2Y1R, a G protein-coupled receptor (GPCR), in complex with a nucleotide antagonist MRS2500 and a non-nucleotide antagonist BPTU.

The researchers believe their findings, published in Nature, could aid the development of new antithrombotic drugs.

Beili Wu, PhD, of the Shanghai Institute of Materia Medica in China, and her colleagues noted that the human purinergic receptors P2Y1R and P2Y12R play a major physiological role in adenosine 5′-diphosphate (ADP)-mediated platelet aggregation, an important component of thrombosis.

Although most of the available antithrombotic drugs act on P2Y12R, research has suggested that P2Y1R may be a promising antithrombotic drug target. In addition, P2Y1R inhibitors may offer a safety advantage over P2Y12R inhibitors by reducing the risk of bleeding. However, efforts to develop new drugs have been impeded by poor understanding of receptor-ligand interaction.

“The P2Y1R structures [we mapped] help us understand how this receptor and different types of experimental drugs interact at the molecular level and could enable further exploration to design new and safer antithrombotic drugs with reduced adverse effects,” Dr Wu said.

She and her colleagues found that the nucleotide ligand MRS2500 recognizes a binding site within the transmembrane bundle of P2Y1R. And it is different in shape and location from the nucleotide-binding site in P2Y12R.

“It is amazing to observe that 2 GPCRs recognize the same ligand in such different ways,” Dr Wu said. “The finding highlights the diversity of signal recognition mechanisms in GPCRs, and this is of great value to drug design for each receptor with high selectivity.”

The researchers also found that, instead of interacting within the transmembrane bundle, the non-nucleotide ligand BPTU binds to a pocket on the outer interface of P2Y1R embedded in the cell membrane.

This is the first structurally characterized, selective, and high-affinity GPCR ligand located entirely outside of the helical bundle, and it represents a new paradigm in ligand binding to alter signaling in GPCRs, according to the researchers.

The team believes this new understanding of the P2Y1R structure provides opportunities to broaden the scope of future GPCR drug discovery to target novel sites outside of the conventional GPCR ligand-binding pocket, which may improve drug selectivity and reduce side effects.

MRS2500 (magenta) and

BPTU (yellow) bind to P2Y1R

Image courtesy of

Yekaterina Kadyshevskaya

Researchers say they have identified 2 disparate ligand-binding sites in the human P2Y1 receptor (P2Y1R), which plays a critical role in thrombosis.

Their research has provided a detailed molecular map of P2Y1R, a G protein-coupled receptor (GPCR), in complex with a nucleotide antagonist MRS2500 and a non-nucleotide antagonist BPTU.

The researchers believe their findings, published in Nature, could aid the development of new antithrombotic drugs.

Beili Wu, PhD, of the Shanghai Institute of Materia Medica in China, and her colleagues noted that the human purinergic receptors P2Y1R and P2Y12R play a major physiological role in adenosine 5′-diphosphate (ADP)-mediated platelet aggregation, an important component of thrombosis.

Although most of the available antithrombotic drugs act on P2Y12R, research has suggested that P2Y1R may be a promising antithrombotic drug target. In addition, P2Y1R inhibitors may offer a safety advantage over P2Y12R inhibitors by reducing the risk of bleeding. However, efforts to develop new drugs have been impeded by poor understanding of receptor-ligand interaction.

“The P2Y1R structures [we mapped] help us understand how this receptor and different types of experimental drugs interact at the molecular level and could enable further exploration to design new and safer antithrombotic drugs with reduced adverse effects,” Dr Wu said.

She and her colleagues found that the nucleotide ligand MRS2500 recognizes a binding site within the transmembrane bundle of P2Y1R. And it is different in shape and location from the nucleotide-binding site in P2Y12R.

“It is amazing to observe that 2 GPCRs recognize the same ligand in such different ways,” Dr Wu said. “The finding highlights the diversity of signal recognition mechanisms in GPCRs, and this is of great value to drug design for each receptor with high selectivity.”

The researchers also found that, instead of interacting within the transmembrane bundle, the non-nucleotide ligand BPTU binds to a pocket on the outer interface of P2Y1R embedded in the cell membrane.

This is the first structurally characterized, selective, and high-affinity GPCR ligand located entirely outside of the helical bundle, and it represents a new paradigm in ligand binding to alter signaling in GPCRs, according to the researchers.

The team believes this new understanding of the P2Y1R structure provides opportunities to broaden the scope of future GPCR drug discovery to target novel sites outside of the conventional GPCR ligand-binding pocket, which may improve drug selectivity and reduce side effects.

Vials of drug

Photo by Bill Branson

The US Food and Drug Administration (FDA) has strengthened an existing warning that serious, potentially fatal, allergic reactions can occur with the anemia drug Feraheme (ferumoxytol).

The FDA changed the drug’s prescribing information and approved a boxed warning detailing this risk.

The agency also added a new contraindication, which advises against the use of Feraheme in patients who have had an allergic reaction to any intravenous (IV) iron replacement product.

The FDA said it is continuing to monitor and evaluate the risk of serious allergic reactions with all IV iron products, and the agency will update the public as new information becomes available.

About Feraheme

Feraheme is an IV iron replacement product used to treat iron-deficiency anemia in patients with chronic kidney disease. Like other IV iron products, Feraheme may only be given where emergency personnel and equipment are immediately available to treat the potentially life-threatening allergic reactions that can occur with treatment.

All IV iron products carry a risk of potentially life-threatening allergic reactions. At the time of Feraheme’s approval in 2009, this risk was described in the “Warnings and Precautions” section of the drug label.

Since then, serious reactions, including deaths, have occurred, despite the proper use of therapies to treat these reactions and emergency resuscitation measures.

Serious reactions reported

In the initial clinical trials of Feraheme, conducted predominantly in patients with chronic kidney disease, serious hypersensitivity reactions were reported in 0.2% (3/1726) of patients receiving Feraheme.

Other adverse reactions potentially associated with hypersensitivity (eg, pruritus, rash, urticaria, or wheezing) were reported in 3.7% (63/1726) of these patients.

In other trials that did not include patients with chronic kidney disease, moderate to severe hypersensitivity reactions, including anaphylaxis, were reported in 2.6% (26/1014) of patients treated with Feraheme.

Since the approval of Feraheme on June 30, 2009, cases of serious hypersensitivity reactions, including death, have occurred.

A search of the FDA Adverse Event Reporting System database revealed 79 cases of anaphylactic reactions associated with Feraheme administration, reported from the time of approval to June 30, 2014. Of the 79 cases, 18 were fatal, despite immediate medical intervention and emergency resuscitation attempts.

The 79 patients ranged in age from 19 to 96 years. In nearly half of all cases, the anaphylactic reactions occurred with the first dose of Feraheme. For approximately 75% (60/79) of the cases, the reaction began during the infusion or within 5 minutes after administration was complete.

Frequently reported symptoms included cardiac arrest, hypotension, dyspnea, nausea, vomiting, and flushing. Of the 79 patients, 43% (34/79) had a medical history of drug allergy, and 24% had a history of multiple drug allergies.

Recommendations for administering Feraheme

Initial symptoms of fatal and serious hypersensitivity reactions associated with Feraheme may include hypotension, syncope, unresponsiveness, and cardiac/cardiorespiratory arrest, with or without signs of rash.

All IV iron products carry a risk of anaphylaxis, so these products should be administered only in patients who require IV iron therapy.

Feraheme is only approved for use in adults with iron-deficiency anemia in the setting of chronic kidney disease. The drug is contraindicated in patients with a history of hypersensitivity to Feraheme or any other IV iron product.

Only administer Feraheme and other IV iron products when personnel and therapies are immediately available for the treatment of anaphylaxis and other hypersensitivity reactions.

Patients with a history of multiple drug allergies may have a greater risk of anaphylaxis with parenteral iron products. Carefully consider the potential risks and benefits before administering Feraheme to these patients.

Feraheme should only be administered as an IV infusion in 50-200 mL of 0.9% sodium chloride or 5% dextrose over a minimum period of 15 minutes following dilution. Do not administer Feraheme by undiluted IV injection.

Closely monitor patients for signs and symptoms of hypersensitivity reactions, including monitoring blood pressure and pulse during administration and for at least 30 minutes following each infusion of Feraheme.

Elderly patients 65 years of age and older with multiple or serious comorbidities who experience hypersensitivity reactions, hypotension, or both following administration of Feraheme may have more severe outcomes.

Advise patients to immediately report any signs and symptoms of hypersensitivity that may develop during and following Feraheme administration, such as respiratory distress, hypotension, dizziness or lightheadedness, edema, rash, or itching. Advise patients to seek immediate medical attention if these signs and symptoms occur.

Allow at least 30 minutes between administration of Feraheme and administration of other medications that could potentially cause serious hypersensitivity reactions, hypotension, or both, such as chemotherapeutic agents or monoclonal antibodies.

Report adverse events involving Feraheme to the FDA’s MedWatch Program.

Vials of drug

Photo by Bill Branson

The US Food and Drug Administration (FDA) has strengthened an existing warning that serious, potentially fatal, allergic reactions can occur with the anemia drug Feraheme (ferumoxytol).

The FDA changed the drug’s prescribing information and approved a boxed warning detailing this risk.

The agency also added a new contraindication, which advises against the use of Feraheme in patients who have had an allergic reaction to any intravenous (IV) iron replacement product.

The FDA said it is continuing to monitor and evaluate the risk of serious allergic reactions with all IV iron products, and the agency will update the public as new information becomes available.

About Feraheme

Feraheme is an IV iron replacement product used to treat iron-deficiency anemia in patients with chronic kidney disease. Like other IV iron products, Feraheme may only be given where emergency personnel and equipment are immediately available to treat the potentially life-threatening allergic reactions that can occur with treatment.

All IV iron products carry a risk of potentially life-threatening allergic reactions. At the time of Feraheme’s approval in 2009, this risk was described in the “Warnings and Precautions” section of the drug label.

Since then, serious reactions, including deaths, have occurred, despite the proper use of therapies to treat these reactions and emergency resuscitation measures.

Serious reactions reported

In the initial clinical trials of Feraheme, conducted predominantly in patients with chronic kidney disease, serious hypersensitivity reactions were reported in 0.2% (3/1726) of patients receiving Feraheme.

Other adverse reactions potentially associated with hypersensitivity (eg, pruritus, rash, urticaria, or wheezing) were reported in 3.7% (63/1726) of these patients.

In other trials that did not include patients with chronic kidney disease, moderate to severe hypersensitivity reactions, including anaphylaxis, were reported in 2.6% (26/1014) of patients treated with Feraheme.

Since the approval of Feraheme on June 30, 2009, cases of serious hypersensitivity reactions, including death, have occurred.

A search of the FDA Adverse Event Reporting System database revealed 79 cases of anaphylactic reactions associated with Feraheme administration, reported from the time of approval to June 30, 2014. Of the 79 cases, 18 were fatal, despite immediate medical intervention and emergency resuscitation attempts.

The 79 patients ranged in age from 19 to 96 years. In nearly half of all cases, the anaphylactic reactions occurred with the first dose of Feraheme. For approximately 75% (60/79) of the cases, the reaction began during the infusion or within 5 minutes after administration was complete.

Frequently reported symptoms included cardiac arrest, hypotension, dyspnea, nausea, vomiting, and flushing. Of the 79 patients, 43% (34/79) had a medical history of drug allergy, and 24% had a history of multiple drug allergies.

Recommendations for administering Feraheme

Initial symptoms of fatal and serious hypersensitivity reactions associated with Feraheme may include hypotension, syncope, unresponsiveness, and cardiac/cardiorespiratory arrest, with or without signs of rash.

All IV iron products carry a risk of anaphylaxis, so these products should be administered only in patients who require IV iron therapy.

Feraheme is only approved for use in adults with iron-deficiency anemia in the setting of chronic kidney disease. The drug is contraindicated in patients with a history of hypersensitivity to Feraheme or any other IV iron product.

Only administer Feraheme and other IV iron products when personnel and therapies are immediately available for the treatment of anaphylaxis and other hypersensitivity reactions.

Patients with a history of multiple drug allergies may have a greater risk of anaphylaxis with parenteral iron products. Carefully consider the potential risks and benefits before administering Feraheme to these patients.

Feraheme should only be administered as an IV infusion in 50-200 mL of 0.9% sodium chloride or 5% dextrose over a minimum period of 15 minutes following dilution. Do not administer Feraheme by undiluted IV injection.

Closely monitor patients for signs and symptoms of hypersensitivity reactions, including monitoring blood pressure and pulse during administration and for at least 30 minutes following each infusion of Feraheme.

Elderly patients 65 years of age and older with multiple or serious comorbidities who experience hypersensitivity reactions, hypotension, or both following administration of Feraheme may have more severe outcomes.

Advise patients to immediately report any signs and symptoms of hypersensitivity that may develop during and following Feraheme administration, such as respiratory distress, hypotension, dizziness or lightheadedness, edema, rash, or itching. Advise patients to seek immediate medical attention if these signs and symptoms occur.

Allow at least 30 minutes between administration of Feraheme and administration of other medications that could potentially cause serious hypersensitivity reactions, hypotension, or both, such as chemotherapeutic agents or monoclonal antibodies.

Report adverse events involving Feraheme to the FDA’s MedWatch Program.

Vials of drug

Photo by Bill Branson

The US Food and Drug Administration (FDA) has strengthened an existing warning that serious, potentially fatal, allergic reactions can occur with the anemia drug Feraheme (ferumoxytol).

The FDA changed the drug’s prescribing information and approved a boxed warning detailing this risk.

The agency also added a new contraindication, which advises against the use of Feraheme in patients who have had an allergic reaction to any intravenous (IV) iron replacement product.

The FDA said it is continuing to monitor and evaluate the risk of serious allergic reactions with all IV iron products, and the agency will update the public as new information becomes available.

About Feraheme

Feraheme is an IV iron replacement product used to treat iron-deficiency anemia in patients with chronic kidney disease. Like other IV iron products, Feraheme may only be given where emergency personnel and equipment are immediately available to treat the potentially life-threatening allergic reactions that can occur with treatment.

All IV iron products carry a risk of potentially life-threatening allergic reactions. At the time of Feraheme’s approval in 2009, this risk was described in the “Warnings and Precautions” section of the drug label.

Since then, serious reactions, including deaths, have occurred, despite the proper use of therapies to treat these reactions and emergency resuscitation measures.

Serious reactions reported

In the initial clinical trials of Feraheme, conducted predominantly in patients with chronic kidney disease, serious hypersensitivity reactions were reported in 0.2% (3/1726) of patients receiving Feraheme.

Other adverse reactions potentially associated with hypersensitivity (eg, pruritus, rash, urticaria, or wheezing) were reported in 3.7% (63/1726) of these patients.

In other trials that did not include patients with chronic kidney disease, moderate to severe hypersensitivity reactions, including anaphylaxis, were reported in 2.6% (26/1014) of patients treated with Feraheme.

Since the approval of Feraheme on June 30, 2009, cases of serious hypersensitivity reactions, including death, have occurred.

A search of the FDA Adverse Event Reporting System database revealed 79 cases of anaphylactic reactions associated with Feraheme administration, reported from the time of approval to June 30, 2014. Of the 79 cases, 18 were fatal, despite immediate medical intervention and emergency resuscitation attempts.

The 79 patients ranged in age from 19 to 96 years. In nearly half of all cases, the anaphylactic reactions occurred with the first dose of Feraheme. For approximately 75% (60/79) of the cases, the reaction began during the infusion or within 5 minutes after administration was complete.

Frequently reported symptoms included cardiac arrest, hypotension, dyspnea, nausea, vomiting, and flushing. Of the 79 patients, 43% (34/79) had a medical history of drug allergy, and 24% had a history of multiple drug allergies.

Recommendations for administering Feraheme

Initial symptoms of fatal and serious hypersensitivity reactions associated with Feraheme may include hypotension, syncope, unresponsiveness, and cardiac/cardiorespiratory arrest, with or without signs of rash.

All IV iron products carry a risk of anaphylaxis, so these products should be administered only in patients who require IV iron therapy.

Feraheme is only approved for use in adults with iron-deficiency anemia in the setting of chronic kidney disease. The drug is contraindicated in patients with a history of hypersensitivity to Feraheme or any other IV iron product.

Only administer Feraheme and other IV iron products when personnel and therapies are immediately available for the treatment of anaphylaxis and other hypersensitivity reactions.

Patients with a history of multiple drug allergies may have a greater risk of anaphylaxis with parenteral iron products. Carefully consider the potential risks and benefits before administering Feraheme to these patients.

Feraheme should only be administered as an IV infusion in 50-200 mL of 0.9% sodium chloride or 5% dextrose over a minimum period of 15 minutes following dilution. Do not administer Feraheme by undiluted IV injection.

Closely monitor patients for signs and symptoms of hypersensitivity reactions, including monitoring blood pressure and pulse during administration and for at least 30 minutes following each infusion of Feraheme.

Elderly patients 65 years of age and older with multiple or serious comorbidities who experience hypersensitivity reactions, hypotension, or both following administration of Feraheme may have more severe outcomes.

Advise patients to immediately report any signs and symptoms of hypersensitivity that may develop during and following Feraheme administration, such as respiratory distress, hypotension, dizziness or lightheadedness, edema, rash, or itching. Advise patients to seek immediate medical attention if these signs and symptoms occur.

Allow at least 30 minutes between administration of Feraheme and administration of other medications that could potentially cause serious hypersensitivity reactions, hypotension, or both, such as chemotherapeutic agents or monoclonal antibodies.

Report adverse events involving Feraheme to the FDA’s MedWatch Program.

Fatih Uckun, MD, PhD

Photo courtesy of Dr Uckun

An engineered protein can enhance the effects of radiation and even overcome radiation resistance to treat B-precursor acute lymphoblastic leukemia (ALL), according to research published in EBioMedicine.

The protein, CD19L-sTRAIL, is a fusion of the CD19 ligand protein, which seeks out and binds to leukemia cells, with soluble TRAIL, a protein that can amplify the potency of radiation if it can be anchored on the membrane of leukemia cells.

Researchers found that CD19L-sTRAIL augmented the potency of radiation therapy even against the most aggressive and radiation-resistant forms of leukemia.

“Even very low doses of radiation were highly effective in mice challenged with aggressive human leukemia cells, when it was combined with [CD19L-sTRAIL],” said Fatih M. Uckun, MD, PhD, of The Saban Research Institute of Children’s Hospital Los Angeles in California.

“Due to its ability to selectively anchor to the surface of leukemia cells via its CD19L portion, CD19L-sTRAIL was 100,000-fold more potent than sTRAIL and consistently killed aggressive leukemia cells taken directly from children with ALL—not only in the test tube but also in mice.”

The researchers found that a combination of low-dose total body irradiation (TBI) and CD19L-sTRAIL greatly improved event-free survival (EFS) in mice that had received a typically fatal dose of cells from a patient with relapsed B-precursor ALL.

The median EFS for mice treated with CD19L-sTRAIL plus low-dose TBI was 72 days, which was significantly longer than the EFS for untreated control mice (17 days, P<0.0001), mice that received TBI alone (64 days, P=0.0014), mice that received CD19L-sTRAIL alone (20 days, P=0.0022), and mice that received a combination of vincristine, dexamethasone, and PEG-asparaginase (17 days, P=0.0033).

Dr Uckun and his colleagues noted that none of the mice that received CD19L-sTRAIL and TBI experienced a toxic death or signs of treatment-related toxicity.

The team also found that TBI plus CD19L-sTRAIL improved progression-free survival (PFS) in CD22ΔE12xBCR-ABL double transgenic mice with radiation-resistant, advanced stage, CD19+ murine B-precursor ALL with lymphomatous features.

The mean PFS was 24.0 ± 4.0 days for mice that received CD19L-sTRAIL plus TBI, which was significantly longer than the PFS for control mice (0 ± 0 days, P<0.0001), mice that received CD19L-sTRAIL alone (3.4 ± 0.9 days, P=0.0003), and mice that received TBI alone (9.0 ± 4.6 days, P=0.020).

Based on these results, Dr Uckun and his colleagues believe that incorporating CD19L-sTRAIL into the pre-transplant TBI regimens of patients with very high-risk B-precursor ALL could improve survival after hematopoietic stem cell transplant.

“We are hopeful that the knowledge gained from this study will open a new range of effective treatment opportunities for children with recurrent leukemia,” Dr Uckun said.

Fatih Uckun, MD, PhD

Photo courtesy of Dr Uckun

An engineered protein can enhance the effects of radiation and even overcome radiation resistance to treat B-precursor acute lymphoblastic leukemia (ALL), according to research published in EBioMedicine.

The protein, CD19L-sTRAIL, is a fusion of the CD19 ligand protein, which seeks out and binds to leukemia cells, with soluble TRAIL, a protein that can amplify the potency of radiation if it can be anchored on the membrane of leukemia cells.

Researchers found that CD19L-sTRAIL augmented the potency of radiation therapy even against the most aggressive and radiation-resistant forms of leukemia.

“Even very low doses of radiation were highly effective in mice challenged with aggressive human leukemia cells, when it was combined with [CD19L-sTRAIL],” said Fatih M. Uckun, MD, PhD, of The Saban Research Institute of Children’s Hospital Los Angeles in California.

“Due to its ability to selectively anchor to the surface of leukemia cells via its CD19L portion, CD19L-sTRAIL was 100,000-fold more potent than sTRAIL and consistently killed aggressive leukemia cells taken directly from children with ALL—not only in the test tube but also in mice.”

The researchers found that a combination of low-dose total body irradiation (TBI) and CD19L-sTRAIL greatly improved event-free survival (EFS) in mice that had received a typically fatal dose of cells from a patient with relapsed B-precursor ALL.

The median EFS for mice treated with CD19L-sTRAIL plus low-dose TBI was 72 days, which was significantly longer than the EFS for untreated control mice (17 days, P<0.0001), mice that received TBI alone (64 days, P=0.0014), mice that received CD19L-sTRAIL alone (20 days, P=0.0022), and mice that received a combination of vincristine, dexamethasone, and PEG-asparaginase (17 days, P=0.0033).

Dr Uckun and his colleagues noted that none of the mice that received CD19L-sTRAIL and TBI experienced a toxic death or signs of treatment-related toxicity.

The team also found that TBI plus CD19L-sTRAIL improved progression-free survival (PFS) in CD22ΔE12xBCR-ABL double transgenic mice with radiation-resistant, advanced stage, CD19+ murine B-precursor ALL with lymphomatous features.

The mean PFS was 24.0 ± 4.0 days for mice that received CD19L-sTRAIL plus TBI, which was significantly longer than the PFS for control mice (0 ± 0 days, P<0.0001), mice that received CD19L-sTRAIL alone (3.4 ± 0.9 days, P=0.0003), and mice that received TBI alone (9.0 ± 4.6 days, P=0.020).

Based on these results, Dr Uckun and his colleagues believe that incorporating CD19L-sTRAIL into the pre-transplant TBI regimens of patients with very high-risk B-precursor ALL could improve survival after hematopoietic stem cell transplant.

“We are hopeful that the knowledge gained from this study will open a new range of effective treatment opportunities for children with recurrent leukemia,” Dr Uckun said.

Fatih Uckun, MD, PhD

Photo courtesy of Dr Uckun

An engineered protein can enhance the effects of radiation and even overcome radiation resistance to treat B-precursor acute lymphoblastic leukemia (ALL), according to research published in EBioMedicine.

The protein, CD19L-sTRAIL, is a fusion of the CD19 ligand protein, which seeks out and binds to leukemia cells, with soluble TRAIL, a protein that can amplify the potency of radiation if it can be anchored on the membrane of leukemia cells.

Researchers found that CD19L-sTRAIL augmented the potency of radiation therapy even against the most aggressive and radiation-resistant forms of leukemia.

“Even very low doses of radiation were highly effective in mice challenged with aggressive human leukemia cells, when it was combined with [CD19L-sTRAIL],” said Fatih M. Uckun, MD, PhD, of The Saban Research Institute of Children’s Hospital Los Angeles in California.

“Due to its ability to selectively anchor to the surface of leukemia cells via its CD19L portion, CD19L-sTRAIL was 100,000-fold more potent than sTRAIL and consistently killed aggressive leukemia cells taken directly from children with ALL—not only in the test tube but also in mice.”

The researchers found that a combination of low-dose total body irradiation (TBI) and CD19L-sTRAIL greatly improved event-free survival (EFS) in mice that had received a typically fatal dose of cells from a patient with relapsed B-precursor ALL.

The median EFS for mice treated with CD19L-sTRAIL plus low-dose TBI was 72 days, which was significantly longer than the EFS for untreated control mice (17 days, P<0.0001), mice that received TBI alone (64 days, P=0.0014), mice that received CD19L-sTRAIL alone (20 days, P=0.0022), and mice that received a combination of vincristine, dexamethasone, and PEG-asparaginase (17 days, P=0.0033).

Dr Uckun and his colleagues noted that none of the mice that received CD19L-sTRAIL and TBI experienced a toxic death or signs of treatment-related toxicity.

The team also found that TBI plus CD19L-sTRAIL improved progression-free survival (PFS) in CD22ΔE12xBCR-ABL double transgenic mice with radiation-resistant, advanced stage, CD19+ murine B-precursor ALL with lymphomatous features.

The mean PFS was 24.0 ± 4.0 days for mice that received CD19L-sTRAIL plus TBI, which was significantly longer than the PFS for control mice (0 ± 0 days, P<0.0001), mice that received CD19L-sTRAIL alone (3.4 ± 0.9 days, P=0.0003), and mice that received TBI alone (9.0 ± 4.6 days, P=0.020).

Based on these results, Dr Uckun and his colleagues believe that incorporating CD19L-sTRAIL into the pre-transplant TBI regimens of patients with very high-risk B-precursor ALL could improve survival after hematopoietic stem cell transplant.

“We are hopeful that the knowledge gained from this study will open a new range of effective treatment opportunities for children with recurrent leukemia,” Dr Uckun said.

In this video, diffuse complex endometrial hyperplasia is identified using a vaginoscopic approach with a 1.9-mm diagnostic rigid hysteroscope. The posterior fornix of the vagina is filled with saline until the cervix is elevated with the fluid and the cervical os is identified. The cervical canal is entered and gentle rotational movement and hydrodistension allows the canal to be traversed into the uterine cavity. 

Video provided by Amy L. Garcia, MD

Vidyard Video

In this video, diffuse complex endometrial hyperplasia is identified using a vaginoscopic approach with a 1.9-mm diagnostic rigid hysteroscope. The posterior fornix of the vagina is filled with saline until the cervix is elevated with the fluid and the cervical os is identified. The cervical canal is entered and gentle rotational movement and hydrodistension allows the canal to be traversed into the uterine cavity. 

Video provided by Amy L. Garcia, MD

Vidyard Video

In this video, diffuse complex endometrial hyperplasia is identified using a vaginoscopic approach with a 1.9-mm diagnostic rigid hysteroscope. The posterior fornix of the vagina is filled with saline until the cervix is elevated with the fluid and the cervical os is identified. The cervical canal is entered and gentle rotational movement and hydrodistension allows the canal to be traversed into the uterine cavity. 

Video provided by Amy L. Garcia, MD

Vidyard Video