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Program improves depression treatment in cancer
Credit: NIH
Results of a large study suggest major depression is common—but largely untreated—among cancer patients in Scotland.
And 2 additional studies of Scottish patients showed that a program specifically designed for individuals with cancer can treat depression and improve quality of life more effectively than current methods of care.
These studies appear in The Lancet, The Lancet Oncology, and The Lancet Psychiatry.
In The Lancet Psychiatry, researchers recounted their analysis of data from 21,151 patients treated at cancer clinics in Scotland. The team found that major depression was substantially more common in cancer patients than in the general population.
Major depression was most common in patients with lung cancer (13%) and lowest in those with genitourinary cancer (6%). Moreover, nearly three-quarters (73%) of depressed cancer patients were not receiving treatment.
To address the problem of inadequate treatment, researchers initiated the SMaRT Oncology-2 trial. They reported the results in The Lancet.
The team evaluated a new treatment program called “Depression Care for People with Cancer” (DCPC). DCPC is delivered by specially trained cancer nurses and psychiatrists, working in collaboration with the patient’s cancer team and general practitioner, and is given as part of cancer care. It is a systematic treatment program that includes both antidepressants and psychological therapy.
The trial included 500 adults with major depression and a cancer with a good prognosis (predicted survival of more than 12 months).
Patients were randomized to receive either DCPC or “usual care,” which was provided by a patient’s general practitioner and might have included prescribing antidepressants or referring the patient to mental health services for assessment or psychological treatment.
Results showed that DCPC was more effective than usual care in reducing depression. At 6 months, 62% of patients who received DCPC responded to treatment (experiencing at least a 50% reduction in the severity of their depression), compared with 17% of those who received the usual care (P<0.0001). This benefit was sustained at 12 months.
In addition, DCPC improved anxiety, pain, fatigue, functioning, and overall quality of life (all P<0.05). The researchers also noted that the cost of providing DCPC was modest (£613 per patient).
“The huge benefit that DCPC delivers for patients with cancer and depression shows what we can achieve for patients if we take as much care with the treatment of their depression as we do with the treatment of their cancer,” said study author Michael Sharpe, MD, of the University of Oxford in the UK.
To see if patients with a poor-prognosis cancer could also benefit from DCPC, researchers initiated the SMaRT Oncology-3 trial. They reported the results in The Lancet Oncology.
The team tested a version of DCPC adapted for cancer patients with a poor prognosis. The trial included 142 patients with lung cancer and major depression.
Patients who received the modified version of DCPC had a significantly greater improvement in depression than those who received the usual care during 32 weeks of follow-up (P=0.0003). DCPC also improved patients’ anxiety (P=0.046), functioning (P=0.0019), and quality of life (P=0.018).
“Patients with lung cancer often have a poor prognosis,” said study author Jane Walker, MBChB, PhD, of the University of Oxford and Sobell House Hospice in Oxford, UK.
“If they also have major depression, that can blight the time they have left to live. This trial shows that we can effectively treat depression in patients with poor-prognosis cancers, like lung cancer, and really improve patients’ lives.” 
Credit: NIH
Results of a large study suggest major depression is common—but largely untreated—among cancer patients in Scotland.
And 2 additional studies of Scottish patients showed that a program specifically designed for individuals with cancer can treat depression and improve quality of life more effectively than current methods of care.
These studies appear in The Lancet, The Lancet Oncology, and The Lancet Psychiatry.
In The Lancet Psychiatry, researchers recounted their analysis of data from 21,151 patients treated at cancer clinics in Scotland. The team found that major depression was substantially more common in cancer patients than in the general population.
Major depression was most common in patients with lung cancer (13%) and lowest in those with genitourinary cancer (6%). Moreover, nearly three-quarters (73%) of depressed cancer patients were not receiving treatment.
To address the problem of inadequate treatment, researchers initiated the SMaRT Oncology-2 trial. They reported the results in The Lancet.
The team evaluated a new treatment program called “Depression Care for People with Cancer” (DCPC). DCPC is delivered by specially trained cancer nurses and psychiatrists, working in collaboration with the patient’s cancer team and general practitioner, and is given as part of cancer care. It is a systematic treatment program that includes both antidepressants and psychological therapy.
The trial included 500 adults with major depression and a cancer with a good prognosis (predicted survival of more than 12 months).
Patients were randomized to receive either DCPC or “usual care,” which was provided by a patient’s general practitioner and might have included prescribing antidepressants or referring the patient to mental health services for assessment or psychological treatment.
Results showed that DCPC was more effective than usual care in reducing depression. At 6 months, 62% of patients who received DCPC responded to treatment (experiencing at least a 50% reduction in the severity of their depression), compared with 17% of those who received the usual care (P<0.0001). This benefit was sustained at 12 months.
In addition, DCPC improved anxiety, pain, fatigue, functioning, and overall quality of life (all P<0.05). The researchers also noted that the cost of providing DCPC was modest (£613 per patient).
“The huge benefit that DCPC delivers for patients with cancer and depression shows what we can achieve for patients if we take as much care with the treatment of their depression as we do with the treatment of their cancer,” said study author Michael Sharpe, MD, of the University of Oxford in the UK.
To see if patients with a poor-prognosis cancer could also benefit from DCPC, researchers initiated the SMaRT Oncology-3 trial. They reported the results in The Lancet Oncology.
The team tested a version of DCPC adapted for cancer patients with a poor prognosis. The trial included 142 patients with lung cancer and major depression.
Patients who received the modified version of DCPC had a significantly greater improvement in depression than those who received the usual care during 32 weeks of follow-up (P=0.0003). DCPC also improved patients’ anxiety (P=0.046), functioning (P=0.0019), and quality of life (P=0.018).
“Patients with lung cancer often have a poor prognosis,” said study author Jane Walker, MBChB, PhD, of the University of Oxford and Sobell House Hospice in Oxford, UK.
“If they also have major depression, that can blight the time they have left to live. This trial shows that we can effectively treat depression in patients with poor-prognosis cancers, like lung cancer, and really improve patients’ lives.”
Credit: NIH
Results of a large study suggest major depression is common—but largely untreated—among cancer patients in Scotland.
And 2 additional studies of Scottish patients showed that a program specifically designed for individuals with cancer can treat depression and improve quality of life more effectively than current methods of care.
These studies appear in The Lancet, The Lancet Oncology, and The Lancet Psychiatry.
In The Lancet Psychiatry, researchers recounted their analysis of data from 21,151 patients treated at cancer clinics in Scotland. The team found that major depression was substantially more common in cancer patients than in the general population.
Major depression was most common in patients with lung cancer (13%) and lowest in those with genitourinary cancer (6%). Moreover, nearly three-quarters (73%) of depressed cancer patients were not receiving treatment.
To address the problem of inadequate treatment, researchers initiated the SMaRT Oncology-2 trial. They reported the results in The Lancet.
The team evaluated a new treatment program called “Depression Care for People with Cancer” (DCPC). DCPC is delivered by specially trained cancer nurses and psychiatrists, working in collaboration with the patient’s cancer team and general practitioner, and is given as part of cancer care. It is a systematic treatment program that includes both antidepressants and psychological therapy.
The trial included 500 adults with major depression and a cancer with a good prognosis (predicted survival of more than 12 months).
Patients were randomized to receive either DCPC or “usual care,” which was provided by a patient’s general practitioner and might have included prescribing antidepressants or referring the patient to mental health services for assessment or psychological treatment.
Results showed that DCPC was more effective than usual care in reducing depression. At 6 months, 62% of patients who received DCPC responded to treatment (experiencing at least a 50% reduction in the severity of their depression), compared with 17% of those who received the usual care (P<0.0001). This benefit was sustained at 12 months.
In addition, DCPC improved anxiety, pain, fatigue, functioning, and overall quality of life (all P<0.05). The researchers also noted that the cost of providing DCPC was modest (£613 per patient).
“The huge benefit that DCPC delivers for patients with cancer and depression shows what we can achieve for patients if we take as much care with the treatment of their depression as we do with the treatment of their cancer,” said study author Michael Sharpe, MD, of the University of Oxford in the UK.
To see if patients with a poor-prognosis cancer could also benefit from DCPC, researchers initiated the SMaRT Oncology-3 trial. They reported the results in The Lancet Oncology.
The team tested a version of DCPC adapted for cancer patients with a poor prognosis. The trial included 142 patients with lung cancer and major depression.
Patients who received the modified version of DCPC had a significantly greater improvement in depression than those who received the usual care during 32 weeks of follow-up (P=0.0003). DCPC also improved patients’ anxiety (P=0.046), functioning (P=0.0019), and quality of life (P=0.018).
“Patients with lung cancer often have a poor prognosis,” said study author Jane Walker, MBChB, PhD, of the University of Oxford and Sobell House Hospice in Oxford, UK.
“If they also have major depression, that can blight the time they have left to live. This trial shows that we can effectively treat depression in patients with poor-prognosis cancers, like lung cancer, and really improve patients’ lives.”
Drug granted orphan status for PNH in EU
A novel compound has received orphan status in the Europe Union to treat paroxysmal nocturnal hemoglobinuria (PNH), a life-threatening disease that causes severe anemia and confers a high risk of thrombosis.
The compound, AMY-101, works by inhibiting C3, a central component of the complement immune system.
AMY-101 was developed by John Lambris, PhD, of the University of Pennsylvania, and subsequently licensed to Amyndas Pharmaceuticals.
AMY-101’s orphan status provides Amyndas with benefits such as tax incentives, market exclusivity for 10 years, possibilities for additional research funding, and additional guidance from the European Medicines Agency during clinical development.
How AMY-101 works
PNH is caused by the defective expression of regulatory proteins on the surface of blood cells, which leaves them vulnerable to complement attack. This can lead to hemolysis, which results in severe anemia and contributes to a high risk of thrombosis.
The monoclonal antibody eculizumab is often successful in treating PNH, but roughly a third of patients do not respond well to the drug and still require blood transfusions to manage their anemia.
Research has suggested this lack of response is due to fragments of complement C3 proteins on the surface of the patients’ red blood cells, which are eventually attacked by immune cells.
In an attempt to overcome this problem, Dr Lambris and his colleagues developed AMY-101. The drug is designed to inhibit the complement cascade, thereby preventing hemolysis and immune cell recognition.
The researchers have investigated the effects of AMY-101 on self-attack and the resulting hemolysis in human PNH cells and found the drug to be active.
These results have not been published, but the group has published results with a C3 inhibitor known as Cp40, and AMY-101 is based on Cp40.
The researchers reported in Blood that Cp40 and its long-acting form, PEG-Cp40, effectively inhibited hemolysis and efficiently prevented the deposition of C3 fragments on red blood cells from patients with PNH.
A novel compound has received orphan status in the Europe Union to treat paroxysmal nocturnal hemoglobinuria (PNH), a life-threatening disease that causes severe anemia and confers a high risk of thrombosis.
The compound, AMY-101, works by inhibiting C3, a central component of the complement immune system.
AMY-101 was developed by John Lambris, PhD, of the University of Pennsylvania, and subsequently licensed to Amyndas Pharmaceuticals.
AMY-101’s orphan status provides Amyndas with benefits such as tax incentives, market exclusivity for 10 years, possibilities for additional research funding, and additional guidance from the European Medicines Agency during clinical development.
How AMY-101 works
PNH is caused by the defective expression of regulatory proteins on the surface of blood cells, which leaves them vulnerable to complement attack. This can lead to hemolysis, which results in severe anemia and contributes to a high risk of thrombosis.
The monoclonal antibody eculizumab is often successful in treating PNH, but roughly a third of patients do not respond well to the drug and still require blood transfusions to manage their anemia.
Research has suggested this lack of response is due to fragments of complement C3 proteins on the surface of the patients’ red blood cells, which are eventually attacked by immune cells.
In an attempt to overcome this problem, Dr Lambris and his colleagues developed AMY-101. The drug is designed to inhibit the complement cascade, thereby preventing hemolysis and immune cell recognition.
The researchers have investigated the effects of AMY-101 on self-attack and the resulting hemolysis in human PNH cells and found the drug to be active.
These results have not been published, but the group has published results with a C3 inhibitor known as Cp40, and AMY-101 is based on Cp40.
The researchers reported in Blood that Cp40 and its long-acting form, PEG-Cp40, effectively inhibited hemolysis and efficiently prevented the deposition of C3 fragments on red blood cells from patients with PNH.
A novel compound has received orphan status in the Europe Union to treat paroxysmal nocturnal hemoglobinuria (PNH), a life-threatening disease that causes severe anemia and confers a high risk of thrombosis.
The compound, AMY-101, works by inhibiting C3, a central component of the complement immune system.
AMY-101 was developed by John Lambris, PhD, of the University of Pennsylvania, and subsequently licensed to Amyndas Pharmaceuticals.
AMY-101’s orphan status provides Amyndas with benefits such as tax incentives, market exclusivity for 10 years, possibilities for additional research funding, and additional guidance from the European Medicines Agency during clinical development.
How AMY-101 works
PNH is caused by the defective expression of regulatory proteins on the surface of blood cells, which leaves them vulnerable to complement attack. This can lead to hemolysis, which results in severe anemia and contributes to a high risk of thrombosis.
The monoclonal antibody eculizumab is often successful in treating PNH, but roughly a third of patients do not respond well to the drug and still require blood transfusions to manage their anemia.
Research has suggested this lack of response is due to fragments of complement C3 proteins on the surface of the patients’ red blood cells, which are eventually attacked by immune cells.
In an attempt to overcome this problem, Dr Lambris and his colleagues developed AMY-101. The drug is designed to inhibit the complement cascade, thereby preventing hemolysis and immune cell recognition.
The researchers have investigated the effects of AMY-101 on self-attack and the resulting hemolysis in human PNH cells and found the drug to be active.
These results have not been published, but the group has published results with a C3 inhibitor known as Cp40, and AMY-101 is based on Cp40.
The researchers reported in Blood that Cp40 and its long-acting form, PEG-Cp40, effectively inhibited hemolysis and efficiently prevented the deposition of C3 fragments on red blood cells from patients with PNH.
Genes aid classification of polycythemia vera
Credit: AFIP
New research has revealed a molecular method for classifying patients with polycythemia vera (PV).
Investigators identified 102 genes that can be used to distinguish patients with aggressive PV from those with indolent disease.
The 2 patient groups exhibited significant differences with regard to leukemic transformation, disease duration, survival, hemoglobin level, thrombosis, splenomegaly, splenectomy, and chemotherapy exposure.
Jerry L. Spivak, MD, of the Johns Hopkins University School of Medicine in Baltimore, and his colleagues conducted this research and recounted the results in NEJM.
The researchers analyzed gene expression in CD34+ cells from 19 patients with PV and compared the results to healthy control subjects of the same sex.
Males with PV had roughly twice as many differentially regulated genes as females with PV—571 and 253, respectively.
The investigators subtracted the genes with sex-specific expression and were left with 102 genes that were differentially regulated (68 upregulated and 34 downregulated) between PV patients and controls.
And the team found they could use these genes to separate patients with indolent PV from those with aggressive disease, as the expression of the genes differed markedly between the 2 groups.
The 2 groups also differed significantly with regard to a number of clinical characteristics. The median disease duration was 14 years for patients with aggressive disease and 6 years for those with indolent disease (P=0.05).
The number of patients who transformed to acute leukemia was 4 and 1, respectively (P=0.04). And the number of patients who were still alive at the time of analysis was 1 and 11, respectively (P=0.001).
There were also significant differences with regard to hemoglobin level (P=0.007), the incidence of thromboembolic events (P=0.04), the frequency of palpable splenomegaly (P=0.03), the rate of splenectomy (P=0.007), and chemotherapy exposure (P=0.03).
However, there were no significant differences between the 2 groups with regard to age, JAK2 V617F neutrophil allele burden, white cell count, or platelet count.
Credit: AFIP
New research has revealed a molecular method for classifying patients with polycythemia vera (PV).
Investigators identified 102 genes that can be used to distinguish patients with aggressive PV from those with indolent disease.
The 2 patient groups exhibited significant differences with regard to leukemic transformation, disease duration, survival, hemoglobin level, thrombosis, splenomegaly, splenectomy, and chemotherapy exposure.
Jerry L. Spivak, MD, of the Johns Hopkins University School of Medicine in Baltimore, and his colleagues conducted this research and recounted the results in NEJM.
The researchers analyzed gene expression in CD34+ cells from 19 patients with PV and compared the results to healthy control subjects of the same sex.
Males with PV had roughly twice as many differentially regulated genes as females with PV—571 and 253, respectively.
The investigators subtracted the genes with sex-specific expression and were left with 102 genes that were differentially regulated (68 upregulated and 34 downregulated) between PV patients and controls.
And the team found they could use these genes to separate patients with indolent PV from those with aggressive disease, as the expression of the genes differed markedly between the 2 groups.
The 2 groups also differed significantly with regard to a number of clinical characteristics. The median disease duration was 14 years for patients with aggressive disease and 6 years for those with indolent disease (P=0.05).
The number of patients who transformed to acute leukemia was 4 and 1, respectively (P=0.04). And the number of patients who were still alive at the time of analysis was 1 and 11, respectively (P=0.001).
There were also significant differences with regard to hemoglobin level (P=0.007), the incidence of thromboembolic events (P=0.04), the frequency of palpable splenomegaly (P=0.03), the rate of splenectomy (P=0.007), and chemotherapy exposure (P=0.03).
However, there were no significant differences between the 2 groups with regard to age, JAK2 V617F neutrophil allele burden, white cell count, or platelet count.
Credit: AFIP
New research has revealed a molecular method for classifying patients with polycythemia vera (PV).
Investigators identified 102 genes that can be used to distinguish patients with aggressive PV from those with indolent disease.
The 2 patient groups exhibited significant differences with regard to leukemic transformation, disease duration, survival, hemoglobin level, thrombosis, splenomegaly, splenectomy, and chemotherapy exposure.
Jerry L. Spivak, MD, of the Johns Hopkins University School of Medicine in Baltimore, and his colleagues conducted this research and recounted the results in NEJM.
The researchers analyzed gene expression in CD34+ cells from 19 patients with PV and compared the results to healthy control subjects of the same sex.
Males with PV had roughly twice as many differentially regulated genes as females with PV—571 and 253, respectively.
The investigators subtracted the genes with sex-specific expression and were left with 102 genes that were differentially regulated (68 upregulated and 34 downregulated) between PV patients and controls.
And the team found they could use these genes to separate patients with indolent PV from those with aggressive disease, as the expression of the genes differed markedly between the 2 groups.
The 2 groups also differed significantly with regard to a number of clinical characteristics. The median disease duration was 14 years for patients with aggressive disease and 6 years for those with indolent disease (P=0.05).
The number of patients who transformed to acute leukemia was 4 and 1, respectively (P=0.04). And the number of patients who were still alive at the time of analysis was 1 and 11, respectively (P=0.001).
There were also significant differences with regard to hemoglobin level (P=0.007), the incidence of thromboembolic events (P=0.04), the frequency of palpable splenomegaly (P=0.03), the rate of splenectomy (P=0.007), and chemotherapy exposure (P=0.03).
However, there were no significant differences between the 2 groups with regard to age, JAK2 V617F neutrophil allele burden, white cell count, or platelet count.
Was fetus’ wrist injured during cesarean delivery?
Was fetus’ wrist injured during cesarean delivery?
At 34 weeks’ gestation, a 39-year-old woman went to the hospital in preterm labor. Her history included a prior cesarean delivery. Ultrasonography (US) showed that the fetus was in a double-footling breech position. The ObGyn decided to perform a cesarean delivery when the fetal heart-rate monitor indicated distress.
After making a midline incision through the earlier scar, the ObGyn created a low transverse uterine incision with a scalpel. The mother’s uterus was thick because labor had not progressed. When the ObGyn was unable to deliver the baby through the low transverse incision, she performed a T-extension of the incision using bandage scissors while placing her free hand inside the uterus to shield the fetus from injury. After extensive manipulation, the baby was delivered and immediately handed to a neonatologist. After surgery, the neonatologist told the mother that the baby had sustained two lacerations to the ulnar side of the right wrist. The newborn was airlifted to another hospital for treatment of sepsis. There, an orthopedic hand surgeon examined the child and determined that the lacerations were superficial and only required sutures. The orthopedist saw the infant a month later and believed there was no significant wrist injury.
When the child began preschool, she started to experience cold intolerance and difficulty writing with her right hand. The child was referred to a pediatric neurologist, who found no nerve damage and ordered occupational therapy.
The original orthopedic surgeon examined the child when she was 7 years old and determined that the flexor carpi ulnaris tendon had been completely severed with a partial injury to the ulnar nerve. He recommended a return visit at age 14 for full assessment of the wrist injury.
PARENTS’ CLAIM The ObGyn did not properly shield the fetus when performing the T-extension incision during cesarean delivery. The child’s weakness will increase with age, ruling out some occupations.
PHYSICIAN’S DEFENSE The ObGyn was not negligent; she had provided adequate protection of the fetus during both incisions.
VERDICT An Illinois defense verdict was returned.
Woman dies after tubal ligation
After a 42-year-old woman underwent tubal ligation, her surgeon was concerned about a possible bowel perforation and admitted her to the hospital. The next morning, a computed tomography (CT) scan of the abdomen did not reveal bowel injury.
That afternoon, when the patient reported shortness of breath, the surgeon called the hospitalist with concern for pulmonary embolism (PE). The hospitalist immediately ordered a CT scan of the chest, initiated PE protocol, and wrote “r/o PE” on the chart. A radiologist reminded the hospitalist of the earlier CT scan with concern for kidney damage from another dye study. The hospitalist cancelled the CT scan and PE protocol. After waiting 17 hours to run any further tests, a CT scan revealed massive bilateral PE. The patient was transferred to the ICU, but died the next day.
PATIENT’S CLAIM The 17-hour delay was negligent.
PHYSICIAN’S DEFENSE There was no negligence. The patient died of septic shock, not PE.
VERDICT A $4 million Virginia verdict was returned.
Child born without hand and forearm
During prenatal care, a mother underwent US at 20 and 36 weeks; both studies were reported as normal. The child was born missing his left hand and part of his left forearm due to a congenital amputation. The child will require prosthetics for life.
PATIENT’S CLAIM The condition should have been seen during prenatal US; an abortion was still an option at 20 weeks.
DEFENDANTS’ DEFENSE US was properly performed and evaluated. It can be difficult to differentiate the right from left extremities.
VERDICT A California defense verdict was returned.
After starting Yasmin, woman has stroke with permanent paralysis: $16.5M total award
When a 37-year-old woman reported irregular menstruation, her ObGyn prescribed drospirenone/ethinyl estradiol (Yasmin; Bayer). Thirteen days after starting the drug, the patient had a stroke. She is paralyzed on her left side, has limited ability to speak, cannot use her left arm and leg, and requires 24-hour care.
PATIENT’S CLAIM The ObGyn should have recognized that Yasmin was not appropriate for this patient because of the drug’s clotting risks. The patient’s risk factors included her age (over 35), borderline hypertension, overweight, history of smoking, and high cholesterol. The ObGyn should have offered safer alternatives, such as a progesterone-only pill. The US Food and Drug Administration (FDA) issued a safety warning that all drospirenone-containing drugs may be associated with a higher risk of venous thrombosis during the first 6 months of use.
DEFENDANTS’ DEFENSE According to Bayer, Yasmin is safe, and remains on the market. It was an appropriate drug to treat her irregular bleeding.
VERDICT Claims against the medical center that referred the patient to the ObGyn were settled for $2.5 million before trial. A $14 million Illinois verdict was returned against the ObGyn, for a total award of $16.5 million.
Who is at fault when pelvic mesh erodes?
In January 2011, an ObGyn implanted the Gynecare TVT Obturator System (TVT‑O; Ethicon) during a midurethral sling procedure to treat stress urinary incontinence (SUI) in a woman in her 60s. Shortly thereafter, the ObGyn left practice because of early-onset Alzheimer’s disease, and the patient’s care was taken over by a gynecologist.
At the 2-month postoperative visit, the gynecologist found that the mesh had eroded into the patient’s vagina. The gynecologist simply cut the mesh with a scissor, charted that a small erosion was present, and prescribed estrogen cream.
The patient continued to report pain, discomfort, pressure, difficulty voiding urine, continued incontinence, vaginal discharge, scarring, infection, odor, and bleeding.
PATIENT’S CLAIM The polypropylene mesh used during the midurethral sling procedure has been shown to be incompatible with human tissue. It promotes an immune response, which stimulates degradation of the pelvic tissue and can contribute to the development of severe adverse reactions to the mesh. Ethicon negligently designed, manufactured, marketed, labeled, and packaged the pelvic mesh products.
DEFENDANTS’ DEFENSE Proper warnings were provided about the health risks associated with polypropylene mesh products. The medical device was not properly sized.
VERDICT A Texas jury rejected the patient’s claims that Ethicon did not provide proper warnings about the sling’s health risks and declined to award punitive damages.
However, the jury decided that the mesh implant was defectively designed, and returned a $1.2 million verdict against Ethicon.
Was suspected bowel injury treated properly?
A 40-year-old woman was referred to an ObGyn after reporting abnormal uterine bleeding to her primary care physician. The patient had very light menses every few weeks. The ObGyn performed an ablation procedure, without relief. A month later, the ObGyn performed robot-assisted laparoscopic hysterectomy. The next day, the patient reported abdominal pain. Suspecting a bowel injury, the ObGyn ordered a CT scan; the bowel appeared normal, so the ObGyn referred the patient to a surgeon. During exploratory laparotomy, the surgeon found and repaired a bowel injury. The patient developed significant complications from a necrotizing infection that included respiratory distress and ongoing wound care.
PATIENT’S CLAIM Conservative treatment should have been offered before surgery. The ObGyn should have waited longer after the ablation procedure before doing the hysterectomy. The ObGyn should have checked for a possible bowel injury before closing the hysterectomy.
PHYSICIAN’S DEFENSE The bowel injury is a known complication of the procedure and was recognized and repaired in a timely manner.
VERDICT A Kentucky defense verdict was returned.
Pap smear improperly interpreted: Woman dies from cervical cancer
A 37-year-old woman underwent a pap smear in 2008 that was read by a cytotechnologist as normal. Two years later, the patient was found to have a golf-ball–sized cancerous tumor. She died from cervical cancer in 2011.
ESTATE’S CLAIM The cytotechnologist was negligent in misreading the 2008 Pap smear. If treatment had been started in 2008, the cancer could have been resolved with a simple conization biopsy.
DEFENDANTS’ DEFENSE The Pap smear interpretation was reasonable. The cancer could not have been diagnosed in 2008. The patient was at fault for failing to follow-up Pap smears during the next 2 years.
VERDICT After assigning 75% fault to the cytotechnologist and 25% fault to the patient, a Florida jury returned a $20,870,200 verdict, which was reduced to $15,816,699.
Disastrous off-label use of anticoagulation
When a pelvic abscess was found, a 50-year-old woman was admitted to the hospital for treatment. She was taking warfarin due to a history of venous thromboembolism.
Before the procedure, her physicians attempted to temporarily reverse her anticoagulation by administering Factor IX Complex (Profilnine SD, Grifols Biologicals). The dose ordered for the patient was nearly double the maximum recommended weight-based dose. Almost immediately after receiving the infusion, the patient went into cardiopulmonary arrest and died. An autopsy found the cause of death to be pulmonary emboli (PE).
ESTATE’S CLAIM An excessive dose of Profilnine caused PE. At the time of the incident, Profilnine was not FDA approved for warfarin reversal, although some off-label uses were recognized in emergent situations, such as intracranial bleeds.
DEFENDANTS’ DEFENSE The case was settled during the trial.
VERDICT A $1.25 million Virginia settlement was reached.
Vesicovaginal fistula from ureteral injury
At a women’s health clinic, a patient reported continuous, heavy vaginal bleeding; pain; and shortness of breath when walking. She had a history of endometritis and multiple abdominal surgeries. Examination disclosed a profuse vaginal discharge, a normal cervix, and an enlarged uterus. The patient consented to abdominal hysterectomy and bilateral salpingo-oophorectomy performed by an ObGyn assisted by a resident.
During surgery, the ObGyn found that the patient’s uterus was at 16 to 20 weeks’ gestation size, with multiple serosal uterine fibroids and frank pus and necrosed fibroid tumors within the uterine cavity. The procedure took longer than planned because of extensive adhesions. After surgery, the patient was anemic and was given a beta-blocker for tachycardia. She was discharged 3 days later with 48 hours’ worth of intravenous antibiotics.
A month later, the patient reported urinary incontinence. She saw a urologist, who found a vesicovaginal fistula. The patient underwent nephrostomy-tube placement. Right ureterolysis and a right ureteral reimplant was performed 4 months later.
PATIENT’S CLAIM The ObGyn injured the right ureter during surgery.
DEFENDANTS’ DEFENSE The ureter injury is a known risk of the procedure. The injury was due to an infection or delayed effects of ischemia. The patient had a good recovery with no residual injury.
VERDICT A Michigan defense verdict was returned.
Why did mother die after delivering twins?
After a 35-year-old woman gave birth to twins by cesarean delivery, she died. At autopsy, 4 liters of blood were found in her abdomen.
ESTATE’S CLAIM The ObGyn failed to recognize and treat an arterial or venous bleed during surgery.
DEFENDANTS’ DEFENSE The patient died from amniotic fluid embolism. Autopsy results showed right ventricular heart failure, respiratory failure, and disseminated intravascular coagulation.
VERDICT A Florida 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.
Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Was fetus’ wrist injured during cesarean delivery?
At 34 weeks’ gestation, a 39-year-old woman went to the hospital in preterm labor. Her history included a prior cesarean delivery. Ultrasonography (US) showed that the fetus was in a double-footling breech position. The ObGyn decided to perform a cesarean delivery when the fetal heart-rate monitor indicated distress.
After making a midline incision through the earlier scar, the ObGyn created a low transverse uterine incision with a scalpel. The mother’s uterus was thick because labor had not progressed. When the ObGyn was unable to deliver the baby through the low transverse incision, she performed a T-extension of the incision using bandage scissors while placing her free hand inside the uterus to shield the fetus from injury. After extensive manipulation, the baby was delivered and immediately handed to a neonatologist. After surgery, the neonatologist told the mother that the baby had sustained two lacerations to the ulnar side of the right wrist. The newborn was airlifted to another hospital for treatment of sepsis. There, an orthopedic hand surgeon examined the child and determined that the lacerations were superficial and only required sutures. The orthopedist saw the infant a month later and believed there was no significant wrist injury.
When the child began preschool, she started to experience cold intolerance and difficulty writing with her right hand. The child was referred to a pediatric neurologist, who found no nerve damage and ordered occupational therapy.
The original orthopedic surgeon examined the child when she was 7 years old and determined that the flexor carpi ulnaris tendon had been completely severed with a partial injury to the ulnar nerve. He recommended a return visit at age 14 for full assessment of the wrist injury.
PARENTS’ CLAIM The ObGyn did not properly shield the fetus when performing the T-extension incision during cesarean delivery. The child’s weakness will increase with age, ruling out some occupations.
PHYSICIAN’S DEFENSE The ObGyn was not negligent; she had provided adequate protection of the fetus during both incisions.
VERDICT An Illinois defense verdict was returned.
Woman dies after tubal ligation
After a 42-year-old woman underwent tubal ligation, her surgeon was concerned about a possible bowel perforation and admitted her to the hospital. The next morning, a computed tomography (CT) scan of the abdomen did not reveal bowel injury.
That afternoon, when the patient reported shortness of breath, the surgeon called the hospitalist with concern for pulmonary embolism (PE). The hospitalist immediately ordered a CT scan of the chest, initiated PE protocol, and wrote “r/o PE” on the chart. A radiologist reminded the hospitalist of the earlier CT scan with concern for kidney damage from another dye study. The hospitalist cancelled the CT scan and PE protocol. After waiting 17 hours to run any further tests, a CT scan revealed massive bilateral PE. The patient was transferred to the ICU, but died the next day.
PATIENT’S CLAIM The 17-hour delay was negligent.
PHYSICIAN’S DEFENSE There was no negligence. The patient died of septic shock, not PE.
VERDICT A $4 million Virginia verdict was returned.
Child born without hand and forearm
During prenatal care, a mother underwent US at 20 and 36 weeks; both studies were reported as normal. The child was born missing his left hand and part of his left forearm due to a congenital amputation. The child will require prosthetics for life.
PATIENT’S CLAIM The condition should have been seen during prenatal US; an abortion was still an option at 20 weeks.
DEFENDANTS’ DEFENSE US was properly performed and evaluated. It can be difficult to differentiate the right from left extremities.
VERDICT A California defense verdict was returned.
After starting Yasmin, woman has stroke with permanent paralysis: $16.5M total award
When a 37-year-old woman reported irregular menstruation, her ObGyn prescribed drospirenone/ethinyl estradiol (Yasmin; Bayer). Thirteen days after starting the drug, the patient had a stroke. She is paralyzed on her left side, has limited ability to speak, cannot use her left arm and leg, and requires 24-hour care.
PATIENT’S CLAIM The ObGyn should have recognized that Yasmin was not appropriate for this patient because of the drug’s clotting risks. The patient’s risk factors included her age (over 35), borderline hypertension, overweight, history of smoking, and high cholesterol. The ObGyn should have offered safer alternatives, such as a progesterone-only pill. The US Food and Drug Administration (FDA) issued a safety warning that all drospirenone-containing drugs may be associated with a higher risk of venous thrombosis during the first 6 months of use.
DEFENDANTS’ DEFENSE According to Bayer, Yasmin is safe, and remains on the market. It was an appropriate drug to treat her irregular bleeding.
VERDICT Claims against the medical center that referred the patient to the ObGyn were settled for $2.5 million before trial. A $14 million Illinois verdict was returned against the ObGyn, for a total award of $16.5 million.
Who is at fault when pelvic mesh erodes?
In January 2011, an ObGyn implanted the Gynecare TVT Obturator System (TVT‑O; Ethicon) during a midurethral sling procedure to treat stress urinary incontinence (SUI) in a woman in her 60s. Shortly thereafter, the ObGyn left practice because of early-onset Alzheimer’s disease, and the patient’s care was taken over by a gynecologist.
At the 2-month postoperative visit, the gynecologist found that the mesh had eroded into the patient’s vagina. The gynecologist simply cut the mesh with a scissor, charted that a small erosion was present, and prescribed estrogen cream.
The patient continued to report pain, discomfort, pressure, difficulty voiding urine, continued incontinence, vaginal discharge, scarring, infection, odor, and bleeding.
PATIENT’S CLAIM The polypropylene mesh used during the midurethral sling procedure has been shown to be incompatible with human tissue. It promotes an immune response, which stimulates degradation of the pelvic tissue and can contribute to the development of severe adverse reactions to the mesh. Ethicon negligently designed, manufactured, marketed, labeled, and packaged the pelvic mesh products.
DEFENDANTS’ DEFENSE Proper warnings were provided about the health risks associated with polypropylene mesh products. The medical device was not properly sized.
VERDICT A Texas jury rejected the patient’s claims that Ethicon did not provide proper warnings about the sling’s health risks and declined to award punitive damages.
However, the jury decided that the mesh implant was defectively designed, and returned a $1.2 million verdict against Ethicon.
Was suspected bowel injury treated properly?
A 40-year-old woman was referred to an ObGyn after reporting abnormal uterine bleeding to her primary care physician. The patient had very light menses every few weeks. The ObGyn performed an ablation procedure, without relief. A month later, the ObGyn performed robot-assisted laparoscopic hysterectomy. The next day, the patient reported abdominal pain. Suspecting a bowel injury, the ObGyn ordered a CT scan; the bowel appeared normal, so the ObGyn referred the patient to a surgeon. During exploratory laparotomy, the surgeon found and repaired a bowel injury. The patient developed significant complications from a necrotizing infection that included respiratory distress and ongoing wound care.
PATIENT’S CLAIM Conservative treatment should have been offered before surgery. The ObGyn should have waited longer after the ablation procedure before doing the hysterectomy. The ObGyn should have checked for a possible bowel injury before closing the hysterectomy.
PHYSICIAN’S DEFENSE The bowel injury is a known complication of the procedure and was recognized and repaired in a timely manner.
VERDICT A Kentucky defense verdict was returned.
Pap smear improperly interpreted: Woman dies from cervical cancer
A 37-year-old woman underwent a pap smear in 2008 that was read by a cytotechnologist as normal. Two years later, the patient was found to have a golf-ball–sized cancerous tumor. She died from cervical cancer in 2011.
ESTATE’S CLAIM The cytotechnologist was negligent in misreading the 2008 Pap smear. If treatment had been started in 2008, the cancer could have been resolved with a simple conization biopsy.
DEFENDANTS’ DEFENSE The Pap smear interpretation was reasonable. The cancer could not have been diagnosed in 2008. The patient was at fault for failing to follow-up Pap smears during the next 2 years.
VERDICT After assigning 75% fault to the cytotechnologist and 25% fault to the patient, a Florida jury returned a $20,870,200 verdict, which was reduced to $15,816,699.
Disastrous off-label use of anticoagulation
When a pelvic abscess was found, a 50-year-old woman was admitted to the hospital for treatment. She was taking warfarin due to a history of venous thromboembolism.
Before the procedure, her physicians attempted to temporarily reverse her anticoagulation by administering Factor IX Complex (Profilnine SD, Grifols Biologicals). The dose ordered for the patient was nearly double the maximum recommended weight-based dose. Almost immediately after receiving the infusion, the patient went into cardiopulmonary arrest and died. An autopsy found the cause of death to be pulmonary emboli (PE).
ESTATE’S CLAIM An excessive dose of Profilnine caused PE. At the time of the incident, Profilnine was not FDA approved for warfarin reversal, although some off-label uses were recognized in emergent situations, such as intracranial bleeds.
DEFENDANTS’ DEFENSE The case was settled during the trial.
VERDICT A $1.25 million Virginia settlement was reached.
Vesicovaginal fistula from ureteral injury
At a women’s health clinic, a patient reported continuous, heavy vaginal bleeding; pain; and shortness of breath when walking. She had a history of endometritis and multiple abdominal surgeries. Examination disclosed a profuse vaginal discharge, a normal cervix, and an enlarged uterus. The patient consented to abdominal hysterectomy and bilateral salpingo-oophorectomy performed by an ObGyn assisted by a resident.
During surgery, the ObGyn found that the patient’s uterus was at 16 to 20 weeks’ gestation size, with multiple serosal uterine fibroids and frank pus and necrosed fibroid tumors within the uterine cavity. The procedure took longer than planned because of extensive adhesions. After surgery, the patient was anemic and was given a beta-blocker for tachycardia. She was discharged 3 days later with 48 hours’ worth of intravenous antibiotics.
A month later, the patient reported urinary incontinence. She saw a urologist, who found a vesicovaginal fistula. The patient underwent nephrostomy-tube placement. Right ureterolysis and a right ureteral reimplant was performed 4 months later.
PATIENT’S CLAIM The ObGyn injured the right ureter during surgery.
DEFENDANTS’ DEFENSE The ureter injury is a known risk of the procedure. The injury was due to an infection or delayed effects of ischemia. The patient had a good recovery with no residual injury.
VERDICT A Michigan defense verdict was returned.
Why did mother die after delivering twins?
After a 35-year-old woman gave birth to twins by cesarean delivery, she died. At autopsy, 4 liters of blood were found in her abdomen.
ESTATE’S CLAIM The ObGyn failed to recognize and treat an arterial or venous bleed during surgery.
DEFENDANTS’ DEFENSE The patient died from amniotic fluid embolism. Autopsy results showed right ventricular heart failure, respiratory failure, and disseminated intravascular coagulation.
VERDICT A Florida 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.
Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Was fetus’ wrist injured during cesarean delivery?
At 34 weeks’ gestation, a 39-year-old woman went to the hospital in preterm labor. Her history included a prior cesarean delivery. Ultrasonography (US) showed that the fetus was in a double-footling breech position. The ObGyn decided to perform a cesarean delivery when the fetal heart-rate monitor indicated distress.
After making a midline incision through the earlier scar, the ObGyn created a low transverse uterine incision with a scalpel. The mother’s uterus was thick because labor had not progressed. When the ObGyn was unable to deliver the baby through the low transverse incision, she performed a T-extension of the incision using bandage scissors while placing her free hand inside the uterus to shield the fetus from injury. After extensive manipulation, the baby was delivered and immediately handed to a neonatologist. After surgery, the neonatologist told the mother that the baby had sustained two lacerations to the ulnar side of the right wrist. The newborn was airlifted to another hospital for treatment of sepsis. There, an orthopedic hand surgeon examined the child and determined that the lacerations were superficial and only required sutures. The orthopedist saw the infant a month later and believed there was no significant wrist injury.
When the child began preschool, she started to experience cold intolerance and difficulty writing with her right hand. The child was referred to a pediatric neurologist, who found no nerve damage and ordered occupational therapy.
The original orthopedic surgeon examined the child when she was 7 years old and determined that the flexor carpi ulnaris tendon had been completely severed with a partial injury to the ulnar nerve. He recommended a return visit at age 14 for full assessment of the wrist injury.
PARENTS’ CLAIM The ObGyn did not properly shield the fetus when performing the T-extension incision during cesarean delivery. The child’s weakness will increase with age, ruling out some occupations.
PHYSICIAN’S DEFENSE The ObGyn was not negligent; she had provided adequate protection of the fetus during both incisions.
VERDICT An Illinois defense verdict was returned.
Woman dies after tubal ligation
After a 42-year-old woman underwent tubal ligation, her surgeon was concerned about a possible bowel perforation and admitted her to the hospital. The next morning, a computed tomography (CT) scan of the abdomen did not reveal bowel injury.
That afternoon, when the patient reported shortness of breath, the surgeon called the hospitalist with concern for pulmonary embolism (PE). The hospitalist immediately ordered a CT scan of the chest, initiated PE protocol, and wrote “r/o PE” on the chart. A radiologist reminded the hospitalist of the earlier CT scan with concern for kidney damage from another dye study. The hospitalist cancelled the CT scan and PE protocol. After waiting 17 hours to run any further tests, a CT scan revealed massive bilateral PE. The patient was transferred to the ICU, but died the next day.
PATIENT’S CLAIM The 17-hour delay was negligent.
PHYSICIAN’S DEFENSE There was no negligence. The patient died of septic shock, not PE.
VERDICT A $4 million Virginia verdict was returned.
Child born without hand and forearm
During prenatal care, a mother underwent US at 20 and 36 weeks; both studies were reported as normal. The child was born missing his left hand and part of his left forearm due to a congenital amputation. The child will require prosthetics for life.
PATIENT’S CLAIM The condition should have been seen during prenatal US; an abortion was still an option at 20 weeks.
DEFENDANTS’ DEFENSE US was properly performed and evaluated. It can be difficult to differentiate the right from left extremities.
VERDICT A California defense verdict was returned.
After starting Yasmin, woman has stroke with permanent paralysis: $16.5M total award
When a 37-year-old woman reported irregular menstruation, her ObGyn prescribed drospirenone/ethinyl estradiol (Yasmin; Bayer). Thirteen days after starting the drug, the patient had a stroke. She is paralyzed on her left side, has limited ability to speak, cannot use her left arm and leg, and requires 24-hour care.
PATIENT’S CLAIM The ObGyn should have recognized that Yasmin was not appropriate for this patient because of the drug’s clotting risks. The patient’s risk factors included her age (over 35), borderline hypertension, overweight, history of smoking, and high cholesterol. The ObGyn should have offered safer alternatives, such as a progesterone-only pill. The US Food and Drug Administration (FDA) issued a safety warning that all drospirenone-containing drugs may be associated with a higher risk of venous thrombosis during the first 6 months of use.
DEFENDANTS’ DEFENSE According to Bayer, Yasmin is safe, and remains on the market. It was an appropriate drug to treat her irregular bleeding.
VERDICT Claims against the medical center that referred the patient to the ObGyn were settled for $2.5 million before trial. A $14 million Illinois verdict was returned against the ObGyn, for a total award of $16.5 million.
Who is at fault when pelvic mesh erodes?
In January 2011, an ObGyn implanted the Gynecare TVT Obturator System (TVT‑O; Ethicon) during a midurethral sling procedure to treat stress urinary incontinence (SUI) in a woman in her 60s. Shortly thereafter, the ObGyn left practice because of early-onset Alzheimer’s disease, and the patient’s care was taken over by a gynecologist.
At the 2-month postoperative visit, the gynecologist found that the mesh had eroded into the patient’s vagina. The gynecologist simply cut the mesh with a scissor, charted that a small erosion was present, and prescribed estrogen cream.
The patient continued to report pain, discomfort, pressure, difficulty voiding urine, continued incontinence, vaginal discharge, scarring, infection, odor, and bleeding.
PATIENT’S CLAIM The polypropylene mesh used during the midurethral sling procedure has been shown to be incompatible with human tissue. It promotes an immune response, which stimulates degradation of the pelvic tissue and can contribute to the development of severe adverse reactions to the mesh. Ethicon negligently designed, manufactured, marketed, labeled, and packaged the pelvic mesh products.
DEFENDANTS’ DEFENSE Proper warnings were provided about the health risks associated with polypropylene mesh products. The medical device was not properly sized.
VERDICT A Texas jury rejected the patient’s claims that Ethicon did not provide proper warnings about the sling’s health risks and declined to award punitive damages.
However, the jury decided that the mesh implant was defectively designed, and returned a $1.2 million verdict against Ethicon.
Was suspected bowel injury treated properly?
A 40-year-old woman was referred to an ObGyn after reporting abnormal uterine bleeding to her primary care physician. The patient had very light menses every few weeks. The ObGyn performed an ablation procedure, without relief. A month later, the ObGyn performed robot-assisted laparoscopic hysterectomy. The next day, the patient reported abdominal pain. Suspecting a bowel injury, the ObGyn ordered a CT scan; the bowel appeared normal, so the ObGyn referred the patient to a surgeon. During exploratory laparotomy, the surgeon found and repaired a bowel injury. The patient developed significant complications from a necrotizing infection that included respiratory distress and ongoing wound care.
PATIENT’S CLAIM Conservative treatment should have been offered before surgery. The ObGyn should have waited longer after the ablation procedure before doing the hysterectomy. The ObGyn should have checked for a possible bowel injury before closing the hysterectomy.
PHYSICIAN’S DEFENSE The bowel injury is a known complication of the procedure and was recognized and repaired in a timely manner.
VERDICT A Kentucky defense verdict was returned.
Pap smear improperly interpreted: Woman dies from cervical cancer
A 37-year-old woman underwent a pap smear in 2008 that was read by a cytotechnologist as normal. Two years later, the patient was found to have a golf-ball–sized cancerous tumor. She died from cervical cancer in 2011.
ESTATE’S CLAIM The cytotechnologist was negligent in misreading the 2008 Pap smear. If treatment had been started in 2008, the cancer could have been resolved with a simple conization biopsy.
DEFENDANTS’ DEFENSE The Pap smear interpretation was reasonable. The cancer could not have been diagnosed in 2008. The patient was at fault for failing to follow-up Pap smears during the next 2 years.
VERDICT After assigning 75% fault to the cytotechnologist and 25% fault to the patient, a Florida jury returned a $20,870,200 verdict, which was reduced to $15,816,699.
Disastrous off-label use of anticoagulation
When a pelvic abscess was found, a 50-year-old woman was admitted to the hospital for treatment. She was taking warfarin due to a history of venous thromboembolism.
Before the procedure, her physicians attempted to temporarily reverse her anticoagulation by administering Factor IX Complex (Profilnine SD, Grifols Biologicals). The dose ordered for the patient was nearly double the maximum recommended weight-based dose. Almost immediately after receiving the infusion, the patient went into cardiopulmonary arrest and died. An autopsy found the cause of death to be pulmonary emboli (PE).
ESTATE’S CLAIM An excessive dose of Profilnine caused PE. At the time of the incident, Profilnine was not FDA approved for warfarin reversal, although some off-label uses were recognized in emergent situations, such as intracranial bleeds.
DEFENDANTS’ DEFENSE The case was settled during the trial.
VERDICT A $1.25 million Virginia settlement was reached.
Vesicovaginal fistula from ureteral injury
At a women’s health clinic, a patient reported continuous, heavy vaginal bleeding; pain; and shortness of breath when walking. She had a history of endometritis and multiple abdominal surgeries. Examination disclosed a profuse vaginal discharge, a normal cervix, and an enlarged uterus. The patient consented to abdominal hysterectomy and bilateral salpingo-oophorectomy performed by an ObGyn assisted by a resident.
During surgery, the ObGyn found that the patient’s uterus was at 16 to 20 weeks’ gestation size, with multiple serosal uterine fibroids and frank pus and necrosed fibroid tumors within the uterine cavity. The procedure took longer than planned because of extensive adhesions. After surgery, the patient was anemic and was given a beta-blocker for tachycardia. She was discharged 3 days later with 48 hours’ worth of intravenous antibiotics.
A month later, the patient reported urinary incontinence. She saw a urologist, who found a vesicovaginal fistula. The patient underwent nephrostomy-tube placement. Right ureterolysis and a right ureteral reimplant was performed 4 months later.
PATIENT’S CLAIM The ObGyn injured the right ureter during surgery.
DEFENDANTS’ DEFENSE The ureter injury is a known risk of the procedure. The injury was due to an infection or delayed effects of ischemia. The patient had a good recovery with no residual injury.
VERDICT A Michigan defense verdict was returned.
Why did mother die after delivering twins?
After a 35-year-old woman gave birth to twins by cesarean delivery, she died. At autopsy, 4 liters of blood were found in her abdomen.
ESTATE’S CLAIM The ObGyn failed to recognize and treat an arterial or venous bleed during surgery.
DEFENDANTS’ DEFENSE The patient died from amniotic fluid embolism. Autopsy results showed right ventricular heart failure, respiratory failure, and disseminated intravascular coagulation.
VERDICT A Florida 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.
Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Overcorrection of Hyponatremia
Q) A clinic patient of mine was recently admitted to the hospital with hyponatremia (serum sodium, 115 mEq/L). She was treated with 2 L of normal saline and discharged home 48 hours later, at her baseline mental status with a serum sodium level of 132 mEq/L. Two days later, she was readmitted for mental status changes, and MRI showed brain swelling. The neurologist stated this was a result of the initial treatment for her hyponatremia. How is this possible?
The cause-and-effect relationship between rapid correction of chronic hyponatremia and subsequent development of neurologic problems was discovered in the late 1970s. Central pontine and extrapontine myelinolysis (known as osmotic demyelination syndrome or ODS) is a neurologic condition that can occur from rapid sodium correction. It is diagnosed by MRI, which shows hyperintense lesions on T2-weighted images. Clinical signs include upper motor neuron signs, pseudobulbar palsy, spastic quadriparesis, and mental status changes ranging from mild confusion to coma.2
Treatment for hyponatremia should be guided by symptom management.2,3 If a patient is asymptomatic, a simple and effective strategy is to keep NPO for 24 hours, except for medications. Simple food and fluid restriction will likely increase the serum sodium level because of obligate solute losses and urinary electrolyte free water loss.2,4 While the first instinct is to feed these patients, as they often appear malnourished, this can cause a solute load leading to a too-rapid sodium correction. After 24 hours, if intake restriction is not effective, use 0.5% normal saline but with limited dosing orders, as usual saline dosing can cause too rapid a correction.2
For symptomatic patients (confusion, seizures, coma), the goal is to initially elevate sodium by 1 to 2 mEq/L per hour for the first two to three hours. Do not exceed 10 mEq/L in 24 hours or 18 mEq/L in 48 hours. Exceeding these limits puts patients at high risk for ODS. In fact, even when staying within these parameters, there is some risk for overcorrection. It is always better to go slowly.2,3
In the patient with hyponatremia due to low solute intake (eg, beer potomania), diuresis can start spontaneously after a period of food and fluid restriction. It can also be initiated with just a small amount of solute. For example, administering an IV antibiotic with a base solution of 100 mL of normal saline or a “banana bag” (an IV solution containing 0.5 to 1 L of normal saline with multivitamins/minerals that cause the fluid to be yellow) can produce several liters of diuresis.2 Once you open the floodgate, you can unintentionally cause too-rapid correction that could lead to ODS.
In chronic hyponatremic patients, low antidiuretic hormone (ADH) levels are often found; thus when a solute is introduced, there is little ADH in the system to protect against excessive water loss and electrolyte imbalance. At the same time, excessive water loss can translate to higher sodium levels and increase the risk for cerebral edema. If rapid diuresis occurs, an infusion of D5W (5% dextrose in water) to match the rate of urine output may prevent a rapid serum sodium level rise. Frequent monitoring of serum sodium levels is often necessary. In instances where ODS is already present, there are case studies of improved neurologic outcomes with reduction of serum sodium levels.2,3
While the treatment of hyponatremia at first glance seems straightforward—replace that which is lost—it can actually transform a seemingly simple problem into a complicated clinical course requiring intensive care, due to the need for frequent monitoring and intervention.
Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John
Medical Center
Longview, WA
REFERENCES
1. Hilden T, Swensen TL. Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.
2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.
3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.
4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.
5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.
| Clinician Reviews in partnership with |
|
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, who is a physician assistant with Metropolitan Nephrology in Alexandria, Virginia, and Clinton, Maryland; she is also past chair of the NKF-CAP. This month’s responses were authored by Kristina Unterseher, MSN, FNP, CNN-NP, who practices at Peacehealth St. John Medical Center in Longview, Washington.
| Clinician Reviews in partnership with |
|
|
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, who is a physician assistant with Metropolitan Nephrology in Alexandria, Virginia, and Clinton, Maryland; she is also past chair of the NKF-CAP. This month’s responses were authored by Kristina Unterseher, MSN, FNP, CNN-NP, who practices at Peacehealth St. John Medical Center in Longview, Washington.
| Clinician Reviews in partnership with |
|
|
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, who is a physician assistant with Metropolitan Nephrology in Alexandria, Virginia, and Clinton, Maryland; she is also past chair of the NKF-CAP. This month’s responses were authored by Kristina Unterseher, MSN, FNP, CNN-NP, who practices at Peacehealth St. John Medical Center in Longview, Washington.
Q) A clinic patient of mine was recently admitted to the hospital with hyponatremia (serum sodium, 115 mEq/L). She was treated with 2 L of normal saline and discharged home 48 hours later, at her baseline mental status with a serum sodium level of 132 mEq/L. Two days later, she was readmitted for mental status changes, and MRI showed brain swelling. The neurologist stated this was a result of the initial treatment for her hyponatremia. How is this possible?
The cause-and-effect relationship between rapid correction of chronic hyponatremia and subsequent development of neurologic problems was discovered in the late 1970s. Central pontine and extrapontine myelinolysis (known as osmotic demyelination syndrome or ODS) is a neurologic condition that can occur from rapid sodium correction. It is diagnosed by MRI, which shows hyperintense lesions on T2-weighted images. Clinical signs include upper motor neuron signs, pseudobulbar palsy, spastic quadriparesis, and mental status changes ranging from mild confusion to coma.2
Treatment for hyponatremia should be guided by symptom management.2,3 If a patient is asymptomatic, a simple and effective strategy is to keep NPO for 24 hours, except for medications. Simple food and fluid restriction will likely increase the serum sodium level because of obligate solute losses and urinary electrolyte free water loss.2,4 While the first instinct is to feed these patients, as they often appear malnourished, this can cause a solute load leading to a too-rapid sodium correction. After 24 hours, if intake restriction is not effective, use 0.5% normal saline but with limited dosing orders, as usual saline dosing can cause too rapid a correction.2
For symptomatic patients (confusion, seizures, coma), the goal is to initially elevate sodium by 1 to 2 mEq/L per hour for the first two to three hours. Do not exceed 10 mEq/L in 24 hours or 18 mEq/L in 48 hours. Exceeding these limits puts patients at high risk for ODS. In fact, even when staying within these parameters, there is some risk for overcorrection. It is always better to go slowly.2,3
In the patient with hyponatremia due to low solute intake (eg, beer potomania), diuresis can start spontaneously after a period of food and fluid restriction. It can also be initiated with just a small amount of solute. For example, administering an IV antibiotic with a base solution of 100 mL of normal saline or a “banana bag” (an IV solution containing 0.5 to 1 L of normal saline with multivitamins/minerals that cause the fluid to be yellow) can produce several liters of diuresis.2 Once you open the floodgate, you can unintentionally cause too-rapid correction that could lead to ODS.
In chronic hyponatremic patients, low antidiuretic hormone (ADH) levels are often found; thus when a solute is introduced, there is little ADH in the system to protect against excessive water loss and electrolyte imbalance. At the same time, excessive water loss can translate to higher sodium levels and increase the risk for cerebral edema. If rapid diuresis occurs, an infusion of D5W (5% dextrose in water) to match the rate of urine output may prevent a rapid serum sodium level rise. Frequent monitoring of serum sodium levels is often necessary. In instances where ODS is already present, there are case studies of improved neurologic outcomes with reduction of serum sodium levels.2,3
While the treatment of hyponatremia at first glance seems straightforward—replace that which is lost—it can actually transform a seemingly simple problem into a complicated clinical course requiring intensive care, due to the need for frequent monitoring and intervention.
Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John
Medical Center
Longview, WA
REFERENCES
1. Hilden T, Swensen TL. Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.
2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.
3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.
4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.
5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.
Q) A clinic patient of mine was recently admitted to the hospital with hyponatremia (serum sodium, 115 mEq/L). She was treated with 2 L of normal saline and discharged home 48 hours later, at her baseline mental status with a serum sodium level of 132 mEq/L. Two days later, she was readmitted for mental status changes, and MRI showed brain swelling. The neurologist stated this was a result of the initial treatment for her hyponatremia. How is this possible?
The cause-and-effect relationship between rapid correction of chronic hyponatremia and subsequent development of neurologic problems was discovered in the late 1970s. Central pontine and extrapontine myelinolysis (known as osmotic demyelination syndrome or ODS) is a neurologic condition that can occur from rapid sodium correction. It is diagnosed by MRI, which shows hyperintense lesions on T2-weighted images. Clinical signs include upper motor neuron signs, pseudobulbar palsy, spastic quadriparesis, and mental status changes ranging from mild confusion to coma.2
Treatment for hyponatremia should be guided by symptom management.2,3 If a patient is asymptomatic, a simple and effective strategy is to keep NPO for 24 hours, except for medications. Simple food and fluid restriction will likely increase the serum sodium level because of obligate solute losses and urinary electrolyte free water loss.2,4 While the first instinct is to feed these patients, as they often appear malnourished, this can cause a solute load leading to a too-rapid sodium correction. After 24 hours, if intake restriction is not effective, use 0.5% normal saline but with limited dosing orders, as usual saline dosing can cause too rapid a correction.2
For symptomatic patients (confusion, seizures, coma), the goal is to initially elevate sodium by 1 to 2 mEq/L per hour for the first two to three hours. Do not exceed 10 mEq/L in 24 hours or 18 mEq/L in 48 hours. Exceeding these limits puts patients at high risk for ODS. In fact, even when staying within these parameters, there is some risk for overcorrection. It is always better to go slowly.2,3
In the patient with hyponatremia due to low solute intake (eg, beer potomania), diuresis can start spontaneously after a period of food and fluid restriction. It can also be initiated with just a small amount of solute. For example, administering an IV antibiotic with a base solution of 100 mL of normal saline or a “banana bag” (an IV solution containing 0.5 to 1 L of normal saline with multivitamins/minerals that cause the fluid to be yellow) can produce several liters of diuresis.2 Once you open the floodgate, you can unintentionally cause too-rapid correction that could lead to ODS.
In chronic hyponatremic patients, low antidiuretic hormone (ADH) levels are often found; thus when a solute is introduced, there is little ADH in the system to protect against excessive water loss and electrolyte imbalance. At the same time, excessive water loss can translate to higher sodium levels and increase the risk for cerebral edema. If rapid diuresis occurs, an infusion of D5W (5% dextrose in water) to match the rate of urine output may prevent a rapid serum sodium level rise. Frequent monitoring of serum sodium levels is often necessary. In instances where ODS is already present, there are case studies of improved neurologic outcomes with reduction of serum sodium levels.2,3
While the treatment of hyponatremia at first glance seems straightforward—replace that which is lost—it can actually transform a seemingly simple problem into a complicated clinical course requiring intensive care, due to the need for frequent monitoring and intervention.
Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John
Medical Center
Longview, WA
REFERENCES
1. Hilden T, Swensen TL. Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.
2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.
3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.
4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.
5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.
Hyponatremia: Beer Potomania
Q) Recently, we had a patient admitted for hyponatremia with
a serum sodium level of 117 mEq/L. One of the hospitalists mentioned “beer potomania” in the differential. Not wanting to look dumb, I just agreed. What is beer potomania, and how is it related to low serum sodium?
Potomania is the excessive consumption of alcoholic beverages; beer potomania is used to refer to a dilutional hyponatremia caused by excessive consumption of beer.1 First recognized in 1971, this cause of hyponatremia is not the most common but should be in the differential if the patient is a heavy alcohol imbiber who presents with encephalopathy and low serum sodium.
When considering this diagnosis, keep in mind that hyponatremia is common among chronic alcoholics and can be due to conditions such as cirrhosis, congestive heart failure, syndrome of inappropriate antidiuretic hormone (SIADH) secretion, and hypovolemia. Less common but still belonging in the differential are pseudohyponatremia secondary to alcohol-induced severe hypertriglyceridemia and cerebral salt wasting syndrome.2,3
Beer potomania usually manifests as altered mental status, weakness, and gait disturbance with an average serum sodium concentration of 108 mEq/L.3 Other abnormal lab results consistent with this diagnosis include hypokalemia (mean potassium, 3 mEq/L) and low blood urea nitrogen and urine sodium levels.2,3 Another fairly consistent finding is a recent personal history of binge drinking (more than about 5 L, or 14 cans of beer, in 24 hours) and/or history of illness (vomiting, diarrhea) that predisposed the patient to a rapid drop in serum sodium levels.2
Based on the information presented thus far, you may ask, “Why haven’t I seen this diagnosed more often? There are a lot of beer bingers out there!” Good question. Let’s review the pathophysiology of beer potomania. When patients have poor protein and solute (food, electrolytes) intake, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia.3
Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load in-cludes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution.2
However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake ... as long as you are not drinking excessive amounts of water.5
Alcoholics get a moderate amount of their calories via beer consumption and do not experience this endogenous protein breakdown or its resultant low urea/solute level. With low solute intake, dramatically lower fluid intake (about 14 cans of beer) will overwhelm the kidneys’ ability to clear excess free water in the body.2 Fortunately, most heavy beer drinkers continue to eat at least modestly, which is sufficient to avoid this rare type of hyponatremia. Chronic alcoholics who go on a drinking binge beyond their normal baseline alcohol consumption, or who develop a flulike illness that causes electrolyte depletion (via diarrhea or vomiting), are at higher risk for beer potomania.
Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John
Medical Center
Longview, WA
REFERENCES
1. Hilden T, Swensen TL. Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.
2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.
3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.
4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.
5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.
| Clinician Reviews in partnership with |
|
|
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, who is a physician assistant with Metropolitan Nephrology in Alexandria, Virginia, and Clinton, Maryland; she is also past chair of the NKF-CAP. This month’s responses were authored by Kristina Unterseher, MSN, FNP, CNN-NP, who practices at Peacehealth St. John Medical Center in Longview, Washington.
| Clinician Reviews in partnership with |
|
|
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, who is a physician assistant with Metropolitan Nephrology in Alexandria, Virginia, and Clinton, Maryland; she is also past chair of the NKF-CAP. This month’s responses were authored by Kristina Unterseher, MSN, FNP, CNN-NP, who practices at Peacehealth St. John Medical Center in Longview, Washington.
| Clinician Reviews in partnership with |
|
|
Renal Consult is edited by Jane S. Davis, CRNP, DNP, a member of the Clinician Reviews editorial board, who is a nurse practitioner in the Division of Nephrology at the University of Alabama at Birmingham and is the communications chairperson for the National Kidney Foundation’s Council of Advanced Practitioners (NKF-CAP); and Kim Zuber, PA-C, MSPS, DFAAPA, who is a physician assistant with Metropolitan Nephrology in Alexandria, Virginia, and Clinton, Maryland; she is also past chair of the NKF-CAP. This month’s responses were authored by Kristina Unterseher, MSN, FNP, CNN-NP, who practices at Peacehealth St. John Medical Center in Longview, Washington.
Q) Recently, we had a patient admitted for hyponatremia with
a serum sodium level of 117 mEq/L. One of the hospitalists mentioned “beer potomania” in the differential. Not wanting to look dumb, I just agreed. What is beer potomania, and how is it related to low serum sodium?
Potomania is the excessive consumption of alcoholic beverages; beer potomania is used to refer to a dilutional hyponatremia caused by excessive consumption of beer.1 First recognized in 1971, this cause of hyponatremia is not the most common but should be in the differential if the patient is a heavy alcohol imbiber who presents with encephalopathy and low serum sodium.
When considering this diagnosis, keep in mind that hyponatremia is common among chronic alcoholics and can be due to conditions such as cirrhosis, congestive heart failure, syndrome of inappropriate antidiuretic hormone (SIADH) secretion, and hypovolemia. Less common but still belonging in the differential are pseudohyponatremia secondary to alcohol-induced severe hypertriglyceridemia and cerebral salt wasting syndrome.2,3
Beer potomania usually manifests as altered mental status, weakness, and gait disturbance with an average serum sodium concentration of 108 mEq/L.3 Other abnormal lab results consistent with this diagnosis include hypokalemia (mean potassium, 3 mEq/L) and low blood urea nitrogen and urine sodium levels.2,3 Another fairly consistent finding is a recent personal history of binge drinking (more than about 5 L, or 14 cans of beer, in 24 hours) and/or history of illness (vomiting, diarrhea) that predisposed the patient to a rapid drop in serum sodium levels.2
Based on the information presented thus far, you may ask, “Why haven’t I seen this diagnosed more often? There are a lot of beer bingers out there!” Good question. Let’s review the pathophysiology of beer potomania. When patients have poor protein and solute (food, electrolytes) intake, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia.3
Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load in-cludes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution.2
However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake ... as long as you are not drinking excessive amounts of water.5
Alcoholics get a moderate amount of their calories via beer consumption and do not experience this endogenous protein breakdown or its resultant low urea/solute level. With low solute intake, dramatically lower fluid intake (about 14 cans of beer) will overwhelm the kidneys’ ability to clear excess free water in the body.2 Fortunately, most heavy beer drinkers continue to eat at least modestly, which is sufficient to avoid this rare type of hyponatremia. Chronic alcoholics who go on a drinking binge beyond their normal baseline alcohol consumption, or who develop a flulike illness that causes electrolyte depletion (via diarrhea or vomiting), are at higher risk for beer potomania.
Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John
Medical Center
Longview, WA
REFERENCES
1. Hilden T, Swensen TL. Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.
2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.
3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.
4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.
5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.
Q) Recently, we had a patient admitted for hyponatremia with
a serum sodium level of 117 mEq/L. One of the hospitalists mentioned “beer potomania” in the differential. Not wanting to look dumb, I just agreed. What is beer potomania, and how is it related to low serum sodium?
Potomania is the excessive consumption of alcoholic beverages; beer potomania is used to refer to a dilutional hyponatremia caused by excessive consumption of beer.1 First recognized in 1971, this cause of hyponatremia is not the most common but should be in the differential if the patient is a heavy alcohol imbiber who presents with encephalopathy and low serum sodium.
When considering this diagnosis, keep in mind that hyponatremia is common among chronic alcoholics and can be due to conditions such as cirrhosis, congestive heart failure, syndrome of inappropriate antidiuretic hormone (SIADH) secretion, and hypovolemia. Less common but still belonging in the differential are pseudohyponatremia secondary to alcohol-induced severe hypertriglyceridemia and cerebral salt wasting syndrome.2,3
Beer potomania usually manifests as altered mental status, weakness, and gait disturbance with an average serum sodium concentration of 108 mEq/L.3 Other abnormal lab results consistent with this diagnosis include hypokalemia (mean potassium, 3 mEq/L) and low blood urea nitrogen and urine sodium levels.2,3 Another fairly consistent finding is a recent personal history of binge drinking (more than about 5 L, or 14 cans of beer, in 24 hours) and/or history of illness (vomiting, diarrhea) that predisposed the patient to a rapid drop in serum sodium levels.2
Based on the information presented thus far, you may ask, “Why haven’t I seen this diagnosed more often? There are a lot of beer bingers out there!” Good question. Let’s review the pathophysiology of beer potomania. When patients have poor protein and solute (food, electrolytes) intake, they can experience water intoxication with smaller-than-usual volumes of fluid. The kidneys need a certain amount of solute to facilitate free water clearance (the ability to clear excess fluid from the body). A lack of adequate solute results in a buildup of free water in the vascular system, leading to a dilutional hyponatremia.3
Free water clearance is dependent on both solute excretion and the ability to dilute urine. Someone consuming an average diet will excrete 600 to 900 mOsm/d of solute. This osmolar load in-cludes urea generated from protein (10 g of protein produces about 50 mOsm of urea), along with dietary sodium and potassium. The maximum capacity for urinary dilution is 50 mOsm/L. In a nutritionally sound person, a lot of fluid—about 20 L—would be required to overwhelm the body’s capacity for urinary dilution.2
However, when you don’t eat, the body starts to break down tissue to create energy to survive. This catabolism creates 100 to 150 mOsm/d of urea, allowing you to continue to appropriately excrete a moderate amount of fluid in spite of poor solute intake ... as long as you are not drinking excessive amounts of water.5
Alcoholics get a moderate amount of their calories via beer consumption and do not experience this endogenous protein breakdown or its resultant low urea/solute level. With low solute intake, dramatically lower fluid intake (about 14 cans of beer) will overwhelm the kidneys’ ability to clear excess free water in the body.2 Fortunately, most heavy beer drinkers continue to eat at least modestly, which is sufficient to avoid this rare type of hyponatremia. Chronic alcoholics who go on a drinking binge beyond their normal baseline alcohol consumption, or who develop a flulike illness that causes electrolyte depletion (via diarrhea or vomiting), are at higher risk for beer potomania.
Kristina Unterseher, MSN, FNP, CNN-NP
Peacehealth St. John
Medical Center
Longview, WA
REFERENCES
1. Hilden T, Swensen TL. Electrolyte disturbances in beer drinkers: a specific “hypo-osmolaity syndrome.” Lancet. 1975;2(7928):245-246.
2. Sanghvi SR, Kellerman PS, Nanovic L. Beer potomania: an unusual cause of hyponatremia at high risk of complications from rapid correction. Am J Kidney Dis. 2007;50(4):673-680.
3. Bhattarai N, Poonam K, Panda M. Beer potomania: a case report. BMJ Case Rep. 2010; 2010: bcr10.2009.2414.
4. Campbell M. Hyponatremia and central pontine myelinolysis as a result of beer potomania: a case report. Prim Care Companion J Clin Psychiatry. 2010;12(4):PCC.09100936.
5. Thaler SM, Teitelbaum I, Beri T. “Beer potomania” in non-beer drinkers: effect of low dietary solute intake. Am J Kidney Dis. 1998;31(6):1028-1031.
“Something Abnormal” on a Chest X-ray
ANSWER
The radiograph demonstrates a fairly large (4 x 6 cm) right paratracheal mass of unclear etiology. This type of finding warrants further evaluation with contrasted CT.
Fortunately for this patient, a subsequent study demonstrated a slightly enlarged thyroid gland. This correlated with the radiographic
finding.
ANSWER
The radiograph demonstrates a fairly large (4 x 6 cm) right paratracheal mass of unclear etiology. This type of finding warrants further evaluation with contrasted CT.
Fortunately for this patient, a subsequent study demonstrated a slightly enlarged thyroid gland. This correlated with the radiographic
finding.
ANSWER
The radiograph demonstrates a fairly large (4 x 6 cm) right paratracheal mass of unclear etiology. This type of finding warrants further evaluation with contrasted CT.
Fortunately for this patient, a subsequent study demonstrated a slightly enlarged thyroid gland. This correlated with the radiographic
finding.
You are doing preoperative orders on a patient scheduled for surgery tomorrow morning. The patient is a 75-year-old woman who was admitted with an acute left subdural hematoma after sustaining a ground-level fall. Her medical history is significant for hypertension and diabetes. Social history is unremarkable. She is neurologically intact except for occasional confusion and aphasia. She moves all her extremities well. As you review her lab results, one of the nurses mentions that the radiology department called about “something abnormal” on the patient’s chest radiograph. You pull up the patient’s portable chest radiograph on the computer to review. What is your impression?
Itchy Lesion Heralds Pervasive Problem
ANSWER
The correct answer is pityriasis rosea (choice “b”), a common and very distinctive eruption related to human herpesvirus 6 and 7.
Allergic reaction to methotrexate (choice “a”), while far from unknown, does not resemble pityriasis rosea. It also would not be limited to such a relatively small area.
Pityriasis rosea is often designated as “fungal infection” (choice “c”) by the uninitiated. However, the lesions of dermatophytosis would be round, with a leading scaly edge, and unlikely to be found in this distribution.
Secondary syphilis (choice “d”) is a major item in the pityriasis rosea differential, but it almost always involves the palms and soles and the lesions would be round (not oval) scaly brown papules. Furthermore, assuming we have an honest patient, we’re also missing a source for sexually transmitted infection.
DISCUSSION
One could hardly ask for a more classic case of pityriasis rosea (PR), which primarily affects patients ages 14 to 40. Alas, that being said, one cannot depend on seeing all these clues in every PR patient.
For example, the herald patch (also known as the mother patch) is missing in at least half of cases. In others, the lesions are smaller, sparser, and more papular (especially in young black patients). The condition may even be confined to intertriginous areas (eg, the groin and/or axillae); this is known as inverse PR.
While salmon-colored scaly lesions are considered a classic presentation, PR can present with darker ovoid macules that have minimal scale and, rarely, become bullous. Involvement above the neck is rare.
What is consistent and dependable among signs of PR is the centripetal scale, seen even in the smallest lesions. This scale is so fine that the old dermatology texts called it “cigarette paper” scale or “scurf.”
After decades of speculation, researchers finally provided strong evidence of the probable cause of PR: replication of human herpesvirus 6 and 7, present in mono-
nuclear cells of lesional skin. Though universally acquired in childhood, these viruses are thought to remain latent until reactivated, leading to viremia.
Itching can be moderately severe in a minority of cases. Most patients, such as this one, are not bothered much by the condition once they understand its self-limited nature. They usually are not happy, however, to learn that it could persist for nine weeks or more, whether treated or not.
UV light exposure can be helpful in hastening PR’s departure, and topical corticosteroids (class III or IV; eg, triamcinolone 0.1% cream) can help control the itching. Neither oral nor topical antihistamines will help, since PR is not a histamine-mediated problem.
If the diagnosis is in doubt, a punch biopsy could at least rule out the more serious items in the differential, which include syphilis, drug rash, and psoriasis. In cases in which fungal origin is a possibility, a quick KOH prep will settle the issue. However, it must be remembered that one doesn’t just “get” a fungal infection. There has to be a source (animal, child), and that source is usually identified with minimal history taking.
ANSWER
The correct answer is pityriasis rosea (choice “b”), a common and very distinctive eruption related to human herpesvirus 6 and 7.
Allergic reaction to methotrexate (choice “a”), while far from unknown, does not resemble pityriasis rosea. It also would not be limited to such a relatively small area.
Pityriasis rosea is often designated as “fungal infection” (choice “c”) by the uninitiated. However, the lesions of dermatophytosis would be round, with a leading scaly edge, and unlikely to be found in this distribution.
Secondary syphilis (choice “d”) is a major item in the pityriasis rosea differential, but it almost always involves the palms and soles and the lesions would be round (not oval) scaly brown papules. Furthermore, assuming we have an honest patient, we’re also missing a source for sexually transmitted infection.
DISCUSSION
One could hardly ask for a more classic case of pityriasis rosea (PR), which primarily affects patients ages 14 to 40. Alas, that being said, one cannot depend on seeing all these clues in every PR patient.
For example, the herald patch (also known as the mother patch) is missing in at least half of cases. In others, the lesions are smaller, sparser, and more papular (especially in young black patients). The condition may even be confined to intertriginous areas (eg, the groin and/or axillae); this is known as inverse PR.
While salmon-colored scaly lesions are considered a classic presentation, PR can present with darker ovoid macules that have minimal scale and, rarely, become bullous. Involvement above the neck is rare.
What is consistent and dependable among signs of PR is the centripetal scale, seen even in the smallest lesions. This scale is so fine that the old dermatology texts called it “cigarette paper” scale or “scurf.”
After decades of speculation, researchers finally provided strong evidence of the probable cause of PR: replication of human herpesvirus 6 and 7, present in mono-
nuclear cells of lesional skin. Though universally acquired in childhood, these viruses are thought to remain latent until reactivated, leading to viremia.
Itching can be moderately severe in a minority of cases. Most patients, such as this one, are not bothered much by the condition once they understand its self-limited nature. They usually are not happy, however, to learn that it could persist for nine weeks or more, whether treated or not.
UV light exposure can be helpful in hastening PR’s departure, and topical corticosteroids (class III or IV; eg, triamcinolone 0.1% cream) can help control the itching. Neither oral nor topical antihistamines will help, since PR is not a histamine-mediated problem.
If the diagnosis is in doubt, a punch biopsy could at least rule out the more serious items in the differential, which include syphilis, drug rash, and psoriasis. In cases in which fungal origin is a possibility, a quick KOH prep will settle the issue. However, it must be remembered that one doesn’t just “get” a fungal infection. There has to be a source (animal, child), and that source is usually identified with minimal history taking.
ANSWER
The correct answer is pityriasis rosea (choice “b”), a common and very distinctive eruption related to human herpesvirus 6 and 7.
Allergic reaction to methotrexate (choice “a”), while far from unknown, does not resemble pityriasis rosea. It also would not be limited to such a relatively small area.
Pityriasis rosea is often designated as “fungal infection” (choice “c”) by the uninitiated. However, the lesions of dermatophytosis would be round, with a leading scaly edge, and unlikely to be found in this distribution.
Secondary syphilis (choice “d”) is a major item in the pityriasis rosea differential, but it almost always involves the palms and soles and the lesions would be round (not oval) scaly brown papules. Furthermore, assuming we have an honest patient, we’re also missing a source for sexually transmitted infection.
DISCUSSION
One could hardly ask for a more classic case of pityriasis rosea (PR), which primarily affects patients ages 14 to 40. Alas, that being said, one cannot depend on seeing all these clues in every PR patient.
For example, the herald patch (also known as the mother patch) is missing in at least half of cases. In others, the lesions are smaller, sparser, and more papular (especially in young black patients). The condition may even be confined to intertriginous areas (eg, the groin and/or axillae); this is known as inverse PR.
While salmon-colored scaly lesions are considered a classic presentation, PR can present with darker ovoid macules that have minimal scale and, rarely, become bullous. Involvement above the neck is rare.
What is consistent and dependable among signs of PR is the centripetal scale, seen even in the smallest lesions. This scale is so fine that the old dermatology texts called it “cigarette paper” scale or “scurf.”
After decades of speculation, researchers finally provided strong evidence of the probable cause of PR: replication of human herpesvirus 6 and 7, present in mono-
nuclear cells of lesional skin. Though universally acquired in childhood, these viruses are thought to remain latent until reactivated, leading to viremia.
Itching can be moderately severe in a minority of cases. Most patients, such as this one, are not bothered much by the condition once they understand its self-limited nature. They usually are not happy, however, to learn that it could persist for nine weeks or more, whether treated or not.
UV light exposure can be helpful in hastening PR’s departure, and topical corticosteroids (class III or IV; eg, triamcinolone 0.1% cream) can help control the itching. Neither oral nor topical antihistamines will help, since PR is not a histamine-mediated problem.
If the diagnosis is in doubt, a punch biopsy could at least rule out the more serious items in the differential, which include syphilis, drug rash, and psoriasis. In cases in which fungal origin is a possibility, a quick KOH prep will settle the issue. However, it must be remembered that one doesn’t just “get” a fungal infection. There has to be a source (animal, child), and that source is usually identified with minimal history taking.
Two weeks ago, an itchy rash appeared on a man’s back before spreading to his chest and neck. He has never experienced anything like it before, and no one else in his household is similarly affected. He denies night sweats, fever, and malaise but reports that he was recently diagnosed with rheumatoid arthritis. His rheumatologist started him on methotrexate (12.5 mg/wk) after extensive labwork (complete blood count, complete metabolic panel, and hepatitis profile) was performed. He denies any history of high-risk sexual behavior or exposure, exposure to animals or children, or history of foreign travel. The patient, who appears well, is afebrile and in no distress. The original lesion, on his upper left back, is distinctly pinkish brown and round, with an odd fine scale around its inner rim, and measures about 3 cm in diameter. Elsewhere, examination reveals about 15 more lesions. All are oval but similarly pinkish brown, averaging about 2 cm in their long axis. These smaller lesions form a necklace-like configuration, paralleling the natural skin lines of the neck. Each lesion has central scaling identical to that of the original back lesion. Examination of the patient’s palms and soles fails to reveal any cutaneous abnormalities. Likewise, examination of the oral cavity is normal. No palpable nodes are felt around the neck, in the axillae, or in the groin.
Eikenella corrodens Septic Hip Arthritis in a Healthy Adult Treated With Arthroscopic Irrigation and Debridement
A summary of the new ACOG report on neonatal brachial plexus palsy. Part 1: Can it be predicted?
Neonatal brachial plexus palsy (NBPP) after a delivery involving shoulder dystocia is not only a clinical disaster—it constitutes the second largest category of litigation in obstetrics.1
Lawsuits that center on NBPP often feature plaintiff expert witnesses who claim that the only way a permanent brachial plexus injury can occur is by a clinician applying “excessive” traction on the fetal head during delivery. The same experts often claim that the mother had multiple risk factors for shoulder dystocia and should never have been allowed a trial of labor in the first place.
The jury is left suspecting that the NBPP was a disaster waiting to happen, with warning signs that were ignored by the clinician. Jurors also may be convinced that, when the dystocia occurred, the defendant handled it badly, causing a severe, lifelong injury to the beautiful child whose images they are shown in the courtroom.
But this scenario is far from accurate.
ACOG publishes new guidance on NBPPThe American College of Obstetricians and Gynecologists (ACOG) periodically issues practice bulletins on the subject of shoulder dystocia, the most recent one written in 2002 and reaffirmed in 2013.2 These bulletins are, of necessity, relatively brief summaries of current thinking about the causes, pathophysiology, treatment, and preventability of shoulder dystocia and associated brachial plexus injuries.
In 2011, James Breeden, MD, then president-elect of ACOG, called for formation of a task force on NBPP. The task force’s report, Neonatal Brachial Plexus Palsy,3 was published earlier this year and represents ACOG’s official position on the important—but still controversial—subjects of shoulder dystocia and NBPP. This report should serve not only to help clinicians better understand and manage these entities but also as a foundational document in the prolific and complex medicolegal suits involving them.
Given the length of this report, however, a concise summary of the key takeaways is in order.
NBPP and shoulder dystocia are not always linked
Early in the report, ACOG presents three very important statements, all of which challenge claims that are frequently made by plaintiffs in brachial plexus injury cases:
- NBPP can occur without concomitant, clinically recognizable shoulder dystocia, although it often is associated with shoulder dystocia.
- In the presence of shoulder dystocia, all ancillary maneuvers necessarily increase strain on the brachial plexus, no matter how expertly the maneuvers are performed.
- Recent multidisciplinary research now indicates that the existence of NBPP after birth does not prove that exogenous forces are the sole cause of this injury.
These findings raise a number of questions, including:
- Can NBPP be predicted and prevented?
- What is the pathophysiologic mechanism for NBPP with and without shoulder dystocia?
- Are there specific interventions that may reduce the frequency of NBPP?
In Part 1 of this article, I summarize ACOG data on whether and how NBPP might be predicted. Part 2, to follow in October 2014, will discuss the pathophysiologic mechanism for NBPP and discuss potential interventions.
The data on NBPP without shoulder dystocia
The results of 12 reports published between 1990 and 2011 describe NBPP (temporary and persistent) that occurred without concomitant shoulder dystocia. These reports indicate that 46% of NBPP cases occurred without documented shoulder dystocia (0.9 cases/1,000 births).
Persistent NBPP. Two of these reports provide data on persistent NBPP without shoulder dystocia. Even when injury to the brachial plexus was documented as lasting more than 1 year, 26% of cases occurred in the absence of documented shoulder dystocia.
NBPP sometimes can occur during cesarean delivery. Four studies evaluated more than 240,000 births and found a rate of NBPP with cesarean delivery ranging from 0.3 to 1.5 cases per 1,000 live births.
All of these studies are described in the ACOG report.
When NBPP is related to shoulder dystocia
Shoulder dystocia may occur when there is a lack of fit of the transverse diameter of the fetal shoulders through the different pelvic diameters the shoulders encounter as they descend through the pelvis during the course of labor and delivery. This lack of fit can be related to excessive size of the fetal shoulders, inadequacy of pelvic dimensions to allow passage of a given fetus, or both. Abnormalities of fetal anatomy, fetal presentation, and soft tissue obstruction are rarely the cause of shoulder dystocia.
The difference between anterior shoulder obstruction behind the symphysis pubis and posterior shoulder obstruction from arrest at the level of the sacral promontory also is discussed in the ACOG report. In both cases, it is this obstruction of the affected shoulder while the long axis of the body continues to be pushed downward that widens the angle between the neck and impacted shoulder and stretches the brachial plexus.
The ACOG report acknowledges that may cases of NBPP do occur in conjunction with shoulder dystocia and that the same biomechanical factors that predispose a fetus to develop NBPP are associated with shoulder dystocia as well. However, the report takes pains to point out that the frequent conjunction of these two entities—NBPP and shoulder dystocia—may lead to an “erroneous retrospective inference of causation.”
Risk and predictive factors
The ACOG report states: “Various risk factors have been described in association with NBPP. Overall, however, these risk factors have not been shown to be statistically reliable or clinically useful predictors for...NBPP.”
For example, fetal macrosomia, defined as a birth weight of 4,000 g or more, has been reported as a risk factor for NBPP either alone or in conjunction with maternal diabetes. Although NBPP does occur more frequently as birth weight increases, seven studies over the past 20 years have shown that most cases of NBPP occur in infants of mothers without diabetes and in infants who weigh less than 4,000 g.
Other studies have shown that, if cesarean delivery were performed in cases of suspected macrosomia, it would have only a limited effect on reducing the incidence of NBPP. Specifically, in women with diabetes who have an estimated fetal weight of more than 4,500 g, the positive predictive value for NBPP is only 5%. Without maternal diabetes, that figure is less than 2%.
Estimating fetal weight by ultrasound does not significantly enhance our ability to predict NBPP. Ultrasound estimates of birth weight usually fall within 15% to 20% of actual birth weight, and the sensitivity of ultrasound in detecting birth weights more than 4,500 g is only 40%.
Therefore, ultrasound estimates of birth weight are of limited utility for contemporaneous clinical management. Furthermore, no data exist to support the claim that estimated fetal weight can be used prophylactically to reduce the incidence of NBPP.
Recurrent shoulder dystocia may be predictive of future NBPP
Whether studied alone or with NBPP, risk factors for shoulder dystocia are not reliable predictors of its occurrence. This is not the case, however, for recurrent shoulder dystocia, where the risk of neonatal brachial plexus palsy can be as high as 4.5%, compared with 1% to 2% for a first episode of shoulder dystocia.
NBPP is a rare phenomenon
The frequency of NBPP is “rare,” according to the ACOG report, which cites a rate of 1.5 cases for every 1,000 births. Favorable outcomes with complete recovery are estimated to range from 50% to 80%.3
Brachial plexus injuries are classically defined as Erb’s palsy—involving C5 and C6 nerve roots—or Klumpke’s palsy, in which there is damage to the C8 and T1 nerve roots.
Erb’s palsy is recognizable by the characteristic “waiter’s tip” position of the hand, which is caused by muscle imbalance in the shoulder and upper arm. Most NBPP injuries are Erb’s palsy, which affect 1.2 infants in every 1,000 births.
Klumpke’s palsy results in weakness of the hand and medial forearm muscles. It affects 0.05 infants in every 1,000 births. The remaining cases involve a combination of the two types of palsy.
These injuries can be temporary, resolving by 12 months after birth, or permanent. The rate of persistence of NBPP at 12 months ranges from 3% to 33%.
Can clinician maneuvers increase the likelihood of NBPP?
The ACOG report addresses the direction and angle of clinician traction at delivery. The report confirms what clinicians generally have been taught: The application of fundal pressure during a delivery in which shoulder dystocia is recognized can exacerbate shoulder impaction and can lead to an increased risk of NBPP.
Traction applied by the clinician and lateral bending of the fetal neck often are implicated as causative factors of NBPP. However, ACOG presents evidence that NBPP can occur entirely unrelated to clinician traction. The report cites studies involving both transient and persistent NBPP in fetuses delivered vaginally without evident shoulder dystocia. The same types of injury are sometimes seen in fetuses delivered by cesarean, as has been mentioned.
The report goes on to state:
Recommendations for practice
At the close of its second chapter (“Risk and predictive factors”), the ACOG report offers the same official recommendations that appear in its current practice bulletin on shoulder dystocia. It notes that there are three clinical situations in which it may be prudent to alter usual obstetric management, with an aim of reducing the risk of shoulder dystocia and NBPP:
- when fetal macrosomia is suspected, with fetal weight estimated to exceed 5,000 g in a woman without diabetes or 4,500 g in a woman with diabetes
- when the mother has a history of recognized shoulder dystocia, especially when neonatal injury was severe
- when midpelvic operative vaginal delivery is contemplated with a fetus estimated to weigh more than 4,000 g.
It is interesting to note that these recommendations are made, according to the report, “notwithstanding the unreliability of specific risk factors to predict NBPP or clinically apparent shoulder dystocia in a specific case.” The report further adds:
More to come
For ACOG’s conclusions on the pathophysiology and causation of NBPP, with a view toward formulating specific protective interventions, see Part 2 of this article, which will appear in the October 2014 issue of OBG Management.
Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
1. Physician Insurers Association of America. http://www.piaa.us. Accessed August 21, 2014.
2. American College of Obstetricians and Gynecologists. Practice Bulletin #40: shoulder dystocia. Obstet Gynecol. 2002;100(5 pt 1):1045–1050.
3. American College of Obstetricians and Gynecologists. Executive summary: neonatal brachial plexus palsy. Report of the American College of Obstetricians and Gynecologists’ Task Force on neonatal brachial plexus palsy. Obstet Gynecol. 2014;123(4):902–904.
Henry M. Lerner, MD
Dr. Lerner is Assistant Clinical Professor of Obstetrics and Gynecology at Harvard Medical School in Boston, Massachusetts.
Dr. Lerner reports that he has been a consultant to the Sullivan Group, which provides patient safety services to labor and delivery units and obstetric practices.
Henry M. Lerner, MD
Dr. Lerner is Assistant Clinical Professor of Obstetrics and Gynecology at Harvard Medical School in Boston, Massachusetts.
Dr. Lerner reports that he has been a consultant to the Sullivan Group, which provides patient safety services to labor and delivery units and obstetric practices.
Henry M. Lerner, MD
Dr. Lerner is Assistant Clinical Professor of Obstetrics and Gynecology at Harvard Medical School in Boston, Massachusetts.
Dr. Lerner reports that he has been a consultant to the Sullivan Group, which provides patient safety services to labor and delivery units and obstetric practices.
Neonatal brachial plexus palsy (NBPP) after a delivery involving shoulder dystocia is not only a clinical disaster—it constitutes the second largest category of litigation in obstetrics.1
Lawsuits that center on NBPP often feature plaintiff expert witnesses who claim that the only way a permanent brachial plexus injury can occur is by a clinician applying “excessive” traction on the fetal head during delivery. The same experts often claim that the mother had multiple risk factors for shoulder dystocia and should never have been allowed a trial of labor in the first place.
The jury is left suspecting that the NBPP was a disaster waiting to happen, with warning signs that were ignored by the clinician. Jurors also may be convinced that, when the dystocia occurred, the defendant handled it badly, causing a severe, lifelong injury to the beautiful child whose images they are shown in the courtroom.
But this scenario is far from accurate.
ACOG publishes new guidance on NBPPThe American College of Obstetricians and Gynecologists (ACOG) periodically issues practice bulletins on the subject of shoulder dystocia, the most recent one written in 2002 and reaffirmed in 2013.2 These bulletins are, of necessity, relatively brief summaries of current thinking about the causes, pathophysiology, treatment, and preventability of shoulder dystocia and associated brachial plexus injuries.
In 2011, James Breeden, MD, then president-elect of ACOG, called for formation of a task force on NBPP. The task force’s report, Neonatal Brachial Plexus Palsy,3 was published earlier this year and represents ACOG’s official position on the important—but still controversial—subjects of shoulder dystocia and NBPP. This report should serve not only to help clinicians better understand and manage these entities but also as a foundational document in the prolific and complex medicolegal suits involving them.
Given the length of this report, however, a concise summary of the key takeaways is in order.
NBPP and shoulder dystocia are not always linked
Early in the report, ACOG presents three very important statements, all of which challenge claims that are frequently made by plaintiffs in brachial plexus injury cases:
- NBPP can occur without concomitant, clinically recognizable shoulder dystocia, although it often is associated with shoulder dystocia.
- In the presence of shoulder dystocia, all ancillary maneuvers necessarily increase strain on the brachial plexus, no matter how expertly the maneuvers are performed.
- Recent multidisciplinary research now indicates that the existence of NBPP after birth does not prove that exogenous forces are the sole cause of this injury.
These findings raise a number of questions, including:
- Can NBPP be predicted and prevented?
- What is the pathophysiologic mechanism for NBPP with and without shoulder dystocia?
- Are there specific interventions that may reduce the frequency of NBPP?
In Part 1 of this article, I summarize ACOG data on whether and how NBPP might be predicted. Part 2, to follow in October 2014, will discuss the pathophysiologic mechanism for NBPP and discuss potential interventions.
The data on NBPP without shoulder dystocia
The results of 12 reports published between 1990 and 2011 describe NBPP (temporary and persistent) that occurred without concomitant shoulder dystocia. These reports indicate that 46% of NBPP cases occurred without documented shoulder dystocia (0.9 cases/1,000 births).
Persistent NBPP. Two of these reports provide data on persistent NBPP without shoulder dystocia. Even when injury to the brachial plexus was documented as lasting more than 1 year, 26% of cases occurred in the absence of documented shoulder dystocia.
NBPP sometimes can occur during cesarean delivery. Four studies evaluated more than 240,000 births and found a rate of NBPP with cesarean delivery ranging from 0.3 to 1.5 cases per 1,000 live births.
All of these studies are described in the ACOG report.
When NBPP is related to shoulder dystocia
Shoulder dystocia may occur when there is a lack of fit of the transverse diameter of the fetal shoulders through the different pelvic diameters the shoulders encounter as they descend through the pelvis during the course of labor and delivery. This lack of fit can be related to excessive size of the fetal shoulders, inadequacy of pelvic dimensions to allow passage of a given fetus, or both. Abnormalities of fetal anatomy, fetal presentation, and soft tissue obstruction are rarely the cause of shoulder dystocia.
The difference between anterior shoulder obstruction behind the symphysis pubis and posterior shoulder obstruction from arrest at the level of the sacral promontory also is discussed in the ACOG report. In both cases, it is this obstruction of the affected shoulder while the long axis of the body continues to be pushed downward that widens the angle between the neck and impacted shoulder and stretches the brachial plexus.
The ACOG report acknowledges that may cases of NBPP do occur in conjunction with shoulder dystocia and that the same biomechanical factors that predispose a fetus to develop NBPP are associated with shoulder dystocia as well. However, the report takes pains to point out that the frequent conjunction of these two entities—NBPP and shoulder dystocia—may lead to an “erroneous retrospective inference of causation.”
Risk and predictive factors
The ACOG report states: “Various risk factors have been described in association with NBPP. Overall, however, these risk factors have not been shown to be statistically reliable or clinically useful predictors for...NBPP.”
For example, fetal macrosomia, defined as a birth weight of 4,000 g or more, has been reported as a risk factor for NBPP either alone or in conjunction with maternal diabetes. Although NBPP does occur more frequently as birth weight increases, seven studies over the past 20 years have shown that most cases of NBPP occur in infants of mothers without diabetes and in infants who weigh less than 4,000 g.
Other studies have shown that, if cesarean delivery were performed in cases of suspected macrosomia, it would have only a limited effect on reducing the incidence of NBPP. Specifically, in women with diabetes who have an estimated fetal weight of more than 4,500 g, the positive predictive value for NBPP is only 5%. Without maternal diabetes, that figure is less than 2%.
Estimating fetal weight by ultrasound does not significantly enhance our ability to predict NBPP. Ultrasound estimates of birth weight usually fall within 15% to 20% of actual birth weight, and the sensitivity of ultrasound in detecting birth weights more than 4,500 g is only 40%.
Therefore, ultrasound estimates of birth weight are of limited utility for contemporaneous clinical management. Furthermore, no data exist to support the claim that estimated fetal weight can be used prophylactically to reduce the incidence of NBPP.
Recurrent shoulder dystocia may be predictive of future NBPP
Whether studied alone or with NBPP, risk factors for shoulder dystocia are not reliable predictors of its occurrence. This is not the case, however, for recurrent shoulder dystocia, where the risk of neonatal brachial plexus palsy can be as high as 4.5%, compared with 1% to 2% for a first episode of shoulder dystocia.
NBPP is a rare phenomenon
The frequency of NBPP is “rare,” according to the ACOG report, which cites a rate of 1.5 cases for every 1,000 births. Favorable outcomes with complete recovery are estimated to range from 50% to 80%.3
Brachial plexus injuries are classically defined as Erb’s palsy—involving C5 and C6 nerve roots—or Klumpke’s palsy, in which there is damage to the C8 and T1 nerve roots.
Erb’s palsy is recognizable by the characteristic “waiter’s tip” position of the hand, which is caused by muscle imbalance in the shoulder and upper arm. Most NBPP injuries are Erb’s palsy, which affect 1.2 infants in every 1,000 births.
Klumpke’s palsy results in weakness of the hand and medial forearm muscles. It affects 0.05 infants in every 1,000 births. The remaining cases involve a combination of the two types of palsy.
These injuries can be temporary, resolving by 12 months after birth, or permanent. The rate of persistence of NBPP at 12 months ranges from 3% to 33%.
Can clinician maneuvers increase the likelihood of NBPP?
The ACOG report addresses the direction and angle of clinician traction at delivery. The report confirms what clinicians generally have been taught: The application of fundal pressure during a delivery in which shoulder dystocia is recognized can exacerbate shoulder impaction and can lead to an increased risk of NBPP.
Traction applied by the clinician and lateral bending of the fetal neck often are implicated as causative factors of NBPP. However, ACOG presents evidence that NBPP can occur entirely unrelated to clinician traction. The report cites studies involving both transient and persistent NBPP in fetuses delivered vaginally without evident shoulder dystocia. The same types of injury are sometimes seen in fetuses delivered by cesarean, as has been mentioned.
The report goes on to state:
Recommendations for practice
At the close of its second chapter (“Risk and predictive factors”), the ACOG report offers the same official recommendations that appear in its current practice bulletin on shoulder dystocia. It notes that there are three clinical situations in which it may be prudent to alter usual obstetric management, with an aim of reducing the risk of shoulder dystocia and NBPP:
- when fetal macrosomia is suspected, with fetal weight estimated to exceed 5,000 g in a woman without diabetes or 4,500 g in a woman with diabetes
- when the mother has a history of recognized shoulder dystocia, especially when neonatal injury was severe
- when midpelvic operative vaginal delivery is contemplated with a fetus estimated to weigh more than 4,000 g.
It is interesting to note that these recommendations are made, according to the report, “notwithstanding the unreliability of specific risk factors to predict NBPP or clinically apparent shoulder dystocia in a specific case.” The report further adds:
More to come
For ACOG’s conclusions on the pathophysiology and causation of NBPP, with a view toward formulating specific protective interventions, see Part 2 of this article, which will appear in the October 2014 issue of OBG Management.
Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
Neonatal brachial plexus palsy (NBPP) after a delivery involving shoulder dystocia is not only a clinical disaster—it constitutes the second largest category of litigation in obstetrics.1
Lawsuits that center on NBPP often feature plaintiff expert witnesses who claim that the only way a permanent brachial plexus injury can occur is by a clinician applying “excessive” traction on the fetal head during delivery. The same experts often claim that the mother had multiple risk factors for shoulder dystocia and should never have been allowed a trial of labor in the first place.
The jury is left suspecting that the NBPP was a disaster waiting to happen, with warning signs that were ignored by the clinician. Jurors also may be convinced that, when the dystocia occurred, the defendant handled it badly, causing a severe, lifelong injury to the beautiful child whose images they are shown in the courtroom.
But this scenario is far from accurate.
ACOG publishes new guidance on NBPPThe American College of Obstetricians and Gynecologists (ACOG) periodically issues practice bulletins on the subject of shoulder dystocia, the most recent one written in 2002 and reaffirmed in 2013.2 These bulletins are, of necessity, relatively brief summaries of current thinking about the causes, pathophysiology, treatment, and preventability of shoulder dystocia and associated brachial plexus injuries.
In 2011, James Breeden, MD, then president-elect of ACOG, called for formation of a task force on NBPP. The task force’s report, Neonatal Brachial Plexus Palsy,3 was published earlier this year and represents ACOG’s official position on the important—but still controversial—subjects of shoulder dystocia and NBPP. This report should serve not only to help clinicians better understand and manage these entities but also as a foundational document in the prolific and complex medicolegal suits involving them.
Given the length of this report, however, a concise summary of the key takeaways is in order.
NBPP and shoulder dystocia are not always linked
Early in the report, ACOG presents three very important statements, all of which challenge claims that are frequently made by plaintiffs in brachial plexus injury cases:
- NBPP can occur without concomitant, clinically recognizable shoulder dystocia, although it often is associated with shoulder dystocia.
- In the presence of shoulder dystocia, all ancillary maneuvers necessarily increase strain on the brachial plexus, no matter how expertly the maneuvers are performed.
- Recent multidisciplinary research now indicates that the existence of NBPP after birth does not prove that exogenous forces are the sole cause of this injury.
These findings raise a number of questions, including:
- Can NBPP be predicted and prevented?
- What is the pathophysiologic mechanism for NBPP with and without shoulder dystocia?
- Are there specific interventions that may reduce the frequency of NBPP?
In Part 1 of this article, I summarize ACOG data on whether and how NBPP might be predicted. Part 2, to follow in October 2014, will discuss the pathophysiologic mechanism for NBPP and discuss potential interventions.
The data on NBPP without shoulder dystocia
The results of 12 reports published between 1990 and 2011 describe NBPP (temporary and persistent) that occurred without concomitant shoulder dystocia. These reports indicate that 46% of NBPP cases occurred without documented shoulder dystocia (0.9 cases/1,000 births).
Persistent NBPP. Two of these reports provide data on persistent NBPP without shoulder dystocia. Even when injury to the brachial plexus was documented as lasting more than 1 year, 26% of cases occurred in the absence of documented shoulder dystocia.
NBPP sometimes can occur during cesarean delivery. Four studies evaluated more than 240,000 births and found a rate of NBPP with cesarean delivery ranging from 0.3 to 1.5 cases per 1,000 live births.
All of these studies are described in the ACOG report.
When NBPP is related to shoulder dystocia
Shoulder dystocia may occur when there is a lack of fit of the transverse diameter of the fetal shoulders through the different pelvic diameters the shoulders encounter as they descend through the pelvis during the course of labor and delivery. This lack of fit can be related to excessive size of the fetal shoulders, inadequacy of pelvic dimensions to allow passage of a given fetus, or both. Abnormalities of fetal anatomy, fetal presentation, and soft tissue obstruction are rarely the cause of shoulder dystocia.
The difference between anterior shoulder obstruction behind the symphysis pubis and posterior shoulder obstruction from arrest at the level of the sacral promontory also is discussed in the ACOG report. In both cases, it is this obstruction of the affected shoulder while the long axis of the body continues to be pushed downward that widens the angle between the neck and impacted shoulder and stretches the brachial plexus.
The ACOG report acknowledges that may cases of NBPP do occur in conjunction with shoulder dystocia and that the same biomechanical factors that predispose a fetus to develop NBPP are associated with shoulder dystocia as well. However, the report takes pains to point out that the frequent conjunction of these two entities—NBPP and shoulder dystocia—may lead to an “erroneous retrospective inference of causation.”
Risk and predictive factors
The ACOG report states: “Various risk factors have been described in association with NBPP. Overall, however, these risk factors have not been shown to be statistically reliable or clinically useful predictors for...NBPP.”
For example, fetal macrosomia, defined as a birth weight of 4,000 g or more, has been reported as a risk factor for NBPP either alone or in conjunction with maternal diabetes. Although NBPP does occur more frequently as birth weight increases, seven studies over the past 20 years have shown that most cases of NBPP occur in infants of mothers without diabetes and in infants who weigh less than 4,000 g.
Other studies have shown that, if cesarean delivery were performed in cases of suspected macrosomia, it would have only a limited effect on reducing the incidence of NBPP. Specifically, in women with diabetes who have an estimated fetal weight of more than 4,500 g, the positive predictive value for NBPP is only 5%. Without maternal diabetes, that figure is less than 2%.
Estimating fetal weight by ultrasound does not significantly enhance our ability to predict NBPP. Ultrasound estimates of birth weight usually fall within 15% to 20% of actual birth weight, and the sensitivity of ultrasound in detecting birth weights more than 4,500 g is only 40%.
Therefore, ultrasound estimates of birth weight are of limited utility for contemporaneous clinical management. Furthermore, no data exist to support the claim that estimated fetal weight can be used prophylactically to reduce the incidence of NBPP.
Recurrent shoulder dystocia may be predictive of future NBPP
Whether studied alone or with NBPP, risk factors for shoulder dystocia are not reliable predictors of its occurrence. This is not the case, however, for recurrent shoulder dystocia, where the risk of neonatal brachial plexus palsy can be as high as 4.5%, compared with 1% to 2% for a first episode of shoulder dystocia.
NBPP is a rare phenomenon
The frequency of NBPP is “rare,” according to the ACOG report, which cites a rate of 1.5 cases for every 1,000 births. Favorable outcomes with complete recovery are estimated to range from 50% to 80%.3
Brachial plexus injuries are classically defined as Erb’s palsy—involving C5 and C6 nerve roots—or Klumpke’s palsy, in which there is damage to the C8 and T1 nerve roots.
Erb’s palsy is recognizable by the characteristic “waiter’s tip” position of the hand, which is caused by muscle imbalance in the shoulder and upper arm. Most NBPP injuries are Erb’s palsy, which affect 1.2 infants in every 1,000 births.
Klumpke’s palsy results in weakness of the hand and medial forearm muscles. It affects 0.05 infants in every 1,000 births. The remaining cases involve a combination of the two types of palsy.
These injuries can be temporary, resolving by 12 months after birth, or permanent. The rate of persistence of NBPP at 12 months ranges from 3% to 33%.
Can clinician maneuvers increase the likelihood of NBPP?
The ACOG report addresses the direction and angle of clinician traction at delivery. The report confirms what clinicians generally have been taught: The application of fundal pressure during a delivery in which shoulder dystocia is recognized can exacerbate shoulder impaction and can lead to an increased risk of NBPP.
Traction applied by the clinician and lateral bending of the fetal neck often are implicated as causative factors of NBPP. However, ACOG presents evidence that NBPP can occur entirely unrelated to clinician traction. The report cites studies involving both transient and persistent NBPP in fetuses delivered vaginally without evident shoulder dystocia. The same types of injury are sometimes seen in fetuses delivered by cesarean, as has been mentioned.
The report goes on to state:
Recommendations for practice
At the close of its second chapter (“Risk and predictive factors”), the ACOG report offers the same official recommendations that appear in its current practice bulletin on shoulder dystocia. It notes that there are three clinical situations in which it may be prudent to alter usual obstetric management, with an aim of reducing the risk of shoulder dystocia and NBPP:
- when fetal macrosomia is suspected, with fetal weight estimated to exceed 5,000 g in a woman without diabetes or 4,500 g in a woman with diabetes
- when the mother has a history of recognized shoulder dystocia, especially when neonatal injury was severe
- when midpelvic operative vaginal delivery is contemplated with a fetus estimated to weigh more than 4,000 g.
It is interesting to note that these recommendations are made, according to the report, “notwithstanding the unreliability of specific risk factors to predict NBPP or clinically apparent shoulder dystocia in a specific case.” The report further adds:
More to come
For ACOG’s conclusions on the pathophysiology and causation of NBPP, with a view toward formulating specific protective interventions, see Part 2 of this article, which will appear in the October 2014 issue of OBG Management.
Share your thoughts on this article! Send your Letter to the Editor to [email protected]. Please include your name and the city and state in which you practice.
1. Physician Insurers Association of America. http://www.piaa.us. Accessed August 21, 2014.
2. American College of Obstetricians and Gynecologists. Practice Bulletin #40: shoulder dystocia. Obstet Gynecol. 2002;100(5 pt 1):1045–1050.
3. American College of Obstetricians and Gynecologists. Executive summary: neonatal brachial plexus palsy. Report of the American College of Obstetricians and Gynecologists’ Task Force on neonatal brachial plexus palsy. Obstet Gynecol. 2014;123(4):902–904.
1. Physician Insurers Association of America. http://www.piaa.us. Accessed August 21, 2014.
2. American College of Obstetricians and Gynecologists. Practice Bulletin #40: shoulder dystocia. Obstet Gynecol. 2002;100(5 pt 1):1045–1050.
3. American College of Obstetricians and Gynecologists. Executive summary: neonatal brachial plexus palsy. Report of the American College of Obstetricians and Gynecologists’ Task Force on neonatal brachial plexus palsy. Obstet Gynecol. 2014;123(4):902–904.