Obstetrics

Eculizumab therapy led to “acceptable” outcomes among pregnant women with paroxysmal nocturnal hemoglobinuria, investigators reported Sept. 9 in the New England Journal of Medicine.

No woman who received eculizumab died while pregnant or within 6 months of delivery; historic mortality rates for these patients are 8%-20%, said Dr. Richard Kelly at St. James’s University Hospital in Leeds, England, and his associates. Treatment with the monoclonal antibody, “has reduced mortality and morbidity associated with PNH and has allowed patients who were previously severely affected to lead a relatively normal life.”

The fetal death rate was 4%, resembling rates of 4%-9% from the era before eculizumab, the researchers said. The rate of premature births also was high (29%) as a result of preeclampsia, suspected intrauterine growth retardation, maternal thrombocytopenia, and slowed fetal movements, they said.

Paroxysmal nocturnal hemoglobinuria is a rare, chronic stem-cell disease in which complement-mediated intravascular hemolysis causes anemia, fatigue, and venous thromboembolism (Adv Exp Med Biol. 2013;735:155-72.). Increased complement activation during pregnancy intensifies the risk of severe hemolytic anemia, fetal morbidity, and fetal mortality for women with PNH. Eculizumab blocks terminal complement activation by binding complement protein C5, and has improved PNH symptoms to the extent that treated women are more likely to consider pregnancy than in the past.

Dr. Kelly and his associates surveyed members of the International PNH Interest Group to study pregnancy outcomes among these women (N Engl J. Med. 2015;373:1032-9). A total of 80% of clinicians responded, reporting data for 75 pregnancies among 61 women, the investigators said. All patients had PNH diagnosed by flow cytometry, and 61% had begun eculizumab therapy before conception. Median age at first pregnancy was 29 years, with a range of 18 to 40 years. The patients received weekly 600-mg IV infusions for 4 weeks, followed by 900 mg every 14 days. Clinicians increased the dose or treatment frequency at their own discretion if patients showed signs of breakthrough intravascular hemolysis.

Two women experienced thrombotic events during treatment, both of which happened soon after delivery. One was a lower-limb deep venous thrombosis, but the other occurred after a patient received a plasma infusion for postpartum hemorrhage. “Plasma contains high levels of complement and can overcome the effects of eculizumab and thereby render the patient susceptible to complications of PNH,” noted the investigators. “The use of plasma should thus be avoided if possible.” Ten samples of breast milk were negative for eculizumab, they added.

Dr. Kelly and 14 of 15 coauthors reported financial relationships outside this work with Alexion Pharmaceuticals, the maker of eculizumab. One coauthor also reported grant support outside this work from Alnylam Pharmaceuticals, Novartis, and Ra Pharma.

Eculizumab therapy led to “acceptable” outcomes among pregnant women with paroxysmal nocturnal hemoglobinuria, investigators reported Sept. 9 in the New England Journal of Medicine.

No woman who received eculizumab died while pregnant or within 6 months of delivery; historic mortality rates for these patients are 8%-20%, said Dr. Richard Kelly at St. James’s University Hospital in Leeds, England, and his associates. Treatment with the monoclonal antibody, “has reduced mortality and morbidity associated with PNH and has allowed patients who were previously severely affected to lead a relatively normal life.”

The fetal death rate was 4%, resembling rates of 4%-9% from the era before eculizumab, the researchers said. The rate of premature births also was high (29%) as a result of preeclampsia, suspected intrauterine growth retardation, maternal thrombocytopenia, and slowed fetal movements, they said.

Paroxysmal nocturnal hemoglobinuria is a rare, chronic stem-cell disease in which complement-mediated intravascular hemolysis causes anemia, fatigue, and venous thromboembolism (Adv Exp Med Biol. 2013;735:155-72.). Increased complement activation during pregnancy intensifies the risk of severe hemolytic anemia, fetal morbidity, and fetal mortality for women with PNH. Eculizumab blocks terminal complement activation by binding complement protein C5, and has improved PNH symptoms to the extent that treated women are more likely to consider pregnancy than in the past.

Dr. Kelly and his associates surveyed members of the International PNH Interest Group to study pregnancy outcomes among these women (N Engl J. Med. 2015;373:1032-9). A total of 80% of clinicians responded, reporting data for 75 pregnancies among 61 women, the investigators said. All patients had PNH diagnosed by flow cytometry, and 61% had begun eculizumab therapy before conception. Median age at first pregnancy was 29 years, with a range of 18 to 40 years. The patients received weekly 600-mg IV infusions for 4 weeks, followed by 900 mg every 14 days. Clinicians increased the dose or treatment frequency at their own discretion if patients showed signs of breakthrough intravascular hemolysis.

Two women experienced thrombotic events during treatment, both of which happened soon after delivery. One was a lower-limb deep venous thrombosis, but the other occurred after a patient received a plasma infusion for postpartum hemorrhage. “Plasma contains high levels of complement and can overcome the effects of eculizumab and thereby render the patient susceptible to complications of PNH,” noted the investigators. “The use of plasma should thus be avoided if possible.” Ten samples of breast milk were negative for eculizumab, they added.

Dr. Kelly and 14 of 15 coauthors reported financial relationships outside this work with Alexion Pharmaceuticals, the maker of eculizumab. One coauthor also reported grant support outside this work from Alnylam Pharmaceuticals, Novartis, and Ra Pharma.

Eculizumab therapy led to “acceptable” outcomes among pregnant women with paroxysmal nocturnal hemoglobinuria, investigators reported Sept. 9 in the New England Journal of Medicine.

No woman who received eculizumab died while pregnant or within 6 months of delivery; historic mortality rates for these patients are 8%-20%, said Dr. Richard Kelly at St. James’s University Hospital in Leeds, England, and his associates. Treatment with the monoclonal antibody, “has reduced mortality and morbidity associated with PNH and has allowed patients who were previously severely affected to lead a relatively normal life.”

The fetal death rate was 4%, resembling rates of 4%-9% from the era before eculizumab, the researchers said. The rate of premature births also was high (29%) as a result of preeclampsia, suspected intrauterine growth retardation, maternal thrombocytopenia, and slowed fetal movements, they said.

Paroxysmal nocturnal hemoglobinuria is a rare, chronic stem-cell disease in which complement-mediated intravascular hemolysis causes anemia, fatigue, and venous thromboembolism (Adv Exp Med Biol. 2013;735:155-72.). Increased complement activation during pregnancy intensifies the risk of severe hemolytic anemia, fetal morbidity, and fetal mortality for women with PNH. Eculizumab blocks terminal complement activation by binding complement protein C5, and has improved PNH symptoms to the extent that treated women are more likely to consider pregnancy than in the past.

Dr. Kelly and his associates surveyed members of the International PNH Interest Group to study pregnancy outcomes among these women (N Engl J. Med. 2015;373:1032-9). A total of 80% of clinicians responded, reporting data for 75 pregnancies among 61 women, the investigators said. All patients had PNH diagnosed by flow cytometry, and 61% had begun eculizumab therapy before conception. Median age at first pregnancy was 29 years, with a range of 18 to 40 years. The patients received weekly 600-mg IV infusions for 4 weeks, followed by 900 mg every 14 days. Clinicians increased the dose or treatment frequency at their own discretion if patients showed signs of breakthrough intravascular hemolysis.

Two women experienced thrombotic events during treatment, both of which happened soon after delivery. One was a lower-limb deep venous thrombosis, but the other occurred after a patient received a plasma infusion for postpartum hemorrhage. “Plasma contains high levels of complement and can overcome the effects of eculizumab and thereby render the patient susceptible to complications of PNH,” noted the investigators. “The use of plasma should thus be avoided if possible.” Ten samples of breast milk were negative for eculizumab, they added.

Dr. Kelly and 14 of 15 coauthors reported financial relationships outside this work with Alexion Pharmaceuticals, the maker of eculizumab. One coauthor also reported grant support outside this work from Alnylam Pharmaceuticals, Novartis, and Ra Pharma.

A mother’s untimely death in childbirth is a grave loss that sends shock waves of grief across generations of her family and community. As obstetricians practicing in the United States, we face a terrible problem. We have a continually rising rate of maternal death in a country with exceptional medical resources (FIGURE).¹ Our national decentralized approach to dealing with maternal mortality is a factor contributing to the decades-long increase in the maternal mortality ratio. Let’s get organized to better respond to this public health crisis.

 

8

Medical education—
Let’s get focused on 
maternal mortality

The 140-page Council on Resident Education in Obstetrics and Gynecology CREOG Educational Objectives: Core Curriculum in Obstetrics and Gynecology provides a detailed enumeration of the key learning objectives for residents in obstetrics and gynecology.² Surprisingly, the CREOG objectives do not mention reducing maternal mortality as an important curricular goal. Learning clinical processes and practices that decrease the risk of maternal 
mortality should be an important educational goal for all residents training in obstetrics and gynecology.

Nationwide action is needed to address 
the problem

Many countries have organized widespread efforts to reduce maternal mortality. In the United Kingdom and France there are nationwide reviews of maternal deaths with detailed analyses of clinical events and identification of areas for future improvement. These reviews result in the dissemination of countrywide clinical recommendations that change practice and hopefully reduce the risk of future maternal deaths. For example, following the identification of pulmonary embolism as a leading cause of maternal death in the United Kingdom there was a nationwide effort to increase the use of mechanical and pharmacologic prophylaxis to prevent deep venous thrombosis.

In the United States, experts have proposed that a national program of clinical review of severe maternal morbidity cases should be mandatory. (There are many more cases of “near misses” with severe 
maternal morbidity than there are maternal deaths.) The greater number of cases available for review should help institutions to quickly recognize potential areas for clinical improvement. One group of experts has recommended that all deliveries in which a pregnant woman received 4 or more units of blood or was admitted to an intensive care unit should be thoroughly reviewed to identify opportunities for 
clinical improvement.³

In the United Kingdom a contemporary clinical problem that is being addressed in an organized and systematic manner is how to respond to the rising rate of severe maternal morbidity caused by placenta accreta. Experts have concluded that women with a suspected placenta accreta should deliver in regional centers with advanced clinical resources—including an emergency surgical response team, interventional radiology, a high capacity blood bank, and an intensive 
care unit.

A similar approach has been proposed for managing placenta accreta in the United States.⁴ The American College of Obstetricians and Gynecologists (ACOG) and the Society of Maternal Fetal Medicine (SMFM) have proposed a tiered 
system of obstetric care with more complex cases being referred to regional perinatal centers.⁵ Regionalization of trauma services has been an important part of the US health care system for decades. Cases of severe trauma are brought to regional centers equipped to emergently treat complex injuries. A similar system of regulation and regionalization could be adapted for optimizing 
maternity care.

High-risk clinical events: Is your unit prepared?

In the United States the leading causes of maternal mortality, in descending order, are⁶⁻⁸:

 

• cardiovascular diseases
• infection
• hemorrhage
• cardiomyopathy
• pulmonary embolism
• hypertension
• amniotic fluid embolism
• stroke
• anesthesia complications.

Over the last decade, the Joint Commission has recommended that birthing centers develop standardized protocols and use simulation to improve the institution’s ability to respond in a timely manner to clinical events that may result in maternal morbidity or death.

The quality of published protocols dealing with hemorrhage, hypertension, and thromboembolism is continuously improving, and every birthing center should have written protocols that are updated on a regular timetable for these common high-risk events.^9,10 Does your birthing unit have written protocols to deal with cardiac diseases, infection, obstetric hemorrhage, thromboembolism, and severe hypertension? Are simulation exercises used to strengthen familiarity with the protocols?

High-risk patients

An amazing fact of today’s medical care is that sexually active women of reproductive age who have high-risk medical problems often have not been counseled to use a highly effective contraceptive, resulting in an increased risk of unintended pregnancy and maternal death. For example, adult women with a history of congenital heart disease are known to be at increased risk of death if they become pregnant. In a recent study, women with a history of congenital heart disease had 178 maternal
deaths per 100,000 deliveries—a rate approximately 10-fold higher than the US maternal mortality ratio.¹¹ Yet, many of these women are not using a highly effective contraceptive, and this results in a high rate of unplanned pregnancy.¹²

 

In order to reduce the risk of unintended pregnancy in women with high-risk medical problems, health systems could make contraception an important “vital sign” for women with high-risk medical conditions.

 

Let’s get organized

In a country with a history of embracing the “live free or die” ethic, it is often difficult for physicians to enthusiastically embrace the need for a higher level of organization and a potential reduction in individual freedom in order to improve health outcomes. And with a US maternal mortality ratio of 1 maternal death for every 5,400 births, many obstetricians will never have one of their patients die in childbirth. In fact, most obstetricians will have only 
1 maternal death during their entire career. In this reality, when clinical events occur rarely, it is not possible
for any single clinician, working alone, to impact the overall outcomes of those rare events. Therefore, teamwork and national efforts, such as the National Partnership for Maternal Safety,¹³ will be necessary to reverse our alarming trend of increasing 
maternal mortality. Let’s get organized to stop the rise of maternal deaths in the United States.

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.

A mother’s untimely death in childbirth is a grave loss that sends shock waves of grief across generations of her family and community. As obstetricians practicing in the United States, we face a terrible problem. We have a continually rising rate of maternal death in a country with exceptional medical resources (FIGURE).¹ Our national decentralized approach to dealing with maternal mortality is a factor contributing to the decades-long increase in the maternal mortality ratio. Let’s get organized to better respond to this public health crisis.

 

8

Medical education—
Let’s get focused on 
maternal mortality

The 140-page Council on Resident Education in Obstetrics and Gynecology CREOG Educational Objectives: Core Curriculum in Obstetrics and Gynecology provides a detailed enumeration of the key learning objectives for residents in obstetrics and gynecology.² Surprisingly, the CREOG objectives do not mention reducing maternal mortality as an important curricular goal. Learning clinical processes and practices that decrease the risk of maternal 
mortality should be an important educational goal for all residents training in obstetrics and gynecology.

Nationwide action is needed to address 
the problem

Many countries have organized widespread efforts to reduce maternal mortality. In the United Kingdom and France there are nationwide reviews of maternal deaths with detailed analyses of clinical events and identification of areas for future improvement. These reviews result in the dissemination of countrywide clinical recommendations that change practice and hopefully reduce the risk of future maternal deaths. For example, following the identification of pulmonary embolism as a leading cause of maternal death in the United Kingdom there was a nationwide effort to increase the use of mechanical and pharmacologic prophylaxis to prevent deep venous thrombosis.

In the United States, experts have proposed that a national program of clinical review of severe maternal morbidity cases should be mandatory. (There are many more cases of “near misses” with severe 
maternal morbidity than there are maternal deaths.) The greater number of cases available for review should help institutions to quickly recognize potential areas for clinical improvement. One group of experts has recommended that all deliveries in which a pregnant woman received 4 or more units of blood or was admitted to an intensive care unit should be thoroughly reviewed to identify opportunities for 
clinical improvement.³

In the United Kingdom a contemporary clinical problem that is being addressed in an organized and systematic manner is how to respond to the rising rate of severe maternal morbidity caused by placenta accreta. Experts have concluded that women with a suspected placenta accreta should deliver in regional centers with advanced clinical resources—including an emergency surgical response team, interventional radiology, a high capacity blood bank, and an intensive 
care unit.

A similar approach has been proposed for managing placenta accreta in the United States.⁴ The American College of Obstetricians and Gynecologists (ACOG) and the Society of Maternal Fetal Medicine (SMFM) have proposed a tiered 
system of obstetric care with more complex cases being referred to regional perinatal centers.⁵ Regionalization of trauma services has been an important part of the US health care system for decades. Cases of severe trauma are brought to regional centers equipped to emergently treat complex injuries. A similar system of regulation and regionalization could be adapted for optimizing 
maternity care.

High-risk clinical events: Is your unit prepared?

In the United States the leading causes of maternal mortality, in descending order, are⁶⁻⁸:

 

• cardiovascular diseases
• infection
• hemorrhage
• cardiomyopathy
• pulmonary embolism
• hypertension
• amniotic fluid embolism
• stroke
• anesthesia complications.

Over the last decade, the Joint Commission has recommended that birthing centers develop standardized protocols and use simulation to improve the institution’s ability to respond in a timely manner to clinical events that may result in maternal morbidity or death.

The quality of published protocols dealing with hemorrhage, hypertension, and thromboembolism is continuously improving, and every birthing center should have written protocols that are updated on a regular timetable for these common high-risk events.^9,10 Does your birthing unit have written protocols to deal with cardiac diseases, infection, obstetric hemorrhage, thromboembolism, and severe hypertension? Are simulation exercises used to strengthen familiarity with the protocols?

High-risk patients

An amazing fact of today’s medical care is that sexually active women of reproductive age who have high-risk medical problems often have not been counseled to use a highly effective contraceptive, resulting in an increased risk of unintended pregnancy and maternal death. For example, adult women with a history of congenital heart disease are known to be at increased risk of death if they become pregnant. In a recent study, women with a history of congenital heart disease had 178 maternal
deaths per 100,000 deliveries—a rate approximately 10-fold higher than the US maternal mortality ratio.¹¹ Yet, many of these women are not using a highly effective contraceptive, and this results in a high rate of unplanned pregnancy.¹²

 

In order to reduce the risk of unintended pregnancy in women with high-risk medical problems, health systems could make contraception an important “vital sign” for women with high-risk medical conditions.

 

Let’s get organized

In a country with a history of embracing the “live free or die” ethic, it is often difficult for physicians to enthusiastically embrace the need for a higher level of organization and a potential reduction in individual freedom in order to improve health outcomes. And with a US maternal mortality ratio of 1 maternal death for every 5,400 births, many obstetricians will never have one of their patients die in childbirth. In fact, most obstetricians will have only 
1 maternal death during their entire career. In this reality, when clinical events occur rarely, it is not possible
for any single clinician, working alone, to impact the overall outcomes of those rare events. Therefore, teamwork and national efforts, such as the National Partnership for Maternal Safety,¹³ will be necessary to reverse our alarming trend of increasing 
maternal mortality. Let’s get organized to stop the rise of maternal deaths in the United States.

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.

A mother’s untimely death in childbirth is a grave loss that sends shock waves of grief across generations of her family and community. As obstetricians practicing in the United States, we face a terrible problem. We have a continually rising rate of maternal death in a country with exceptional medical resources (FIGURE).¹ Our national decentralized approach to dealing with maternal mortality is a factor contributing to the decades-long increase in the maternal mortality ratio. Let’s get organized to better respond to this public health crisis.

 

8

Medical education—
Let’s get focused on 
maternal mortality

The 140-page Council on Resident Education in Obstetrics and Gynecology CREOG Educational Objectives: Core Curriculum in Obstetrics and Gynecology provides a detailed enumeration of the key learning objectives for residents in obstetrics and gynecology.² Surprisingly, the CREOG objectives do not mention reducing maternal mortality as an important curricular goal. Learning clinical processes and practices that decrease the risk of maternal 
mortality should be an important educational goal for all residents training in obstetrics and gynecology.

Nationwide action is needed to address 
the problem

Many countries have organized widespread efforts to reduce maternal mortality. In the United Kingdom and France there are nationwide reviews of maternal deaths with detailed analyses of clinical events and identification of areas for future improvement. These reviews result in the dissemination of countrywide clinical recommendations that change practice and hopefully reduce the risk of future maternal deaths. For example, following the identification of pulmonary embolism as a leading cause of maternal death in the United Kingdom there was a nationwide effort to increase the use of mechanical and pharmacologic prophylaxis to prevent deep venous thrombosis.

In the United States, experts have proposed that a national program of clinical review of severe maternal morbidity cases should be mandatory. (There are many more cases of “near misses” with severe 
maternal morbidity than there are maternal deaths.) The greater number of cases available for review should help institutions to quickly recognize potential areas for clinical improvement. One group of experts has recommended that all deliveries in which a pregnant woman received 4 or more units of blood or was admitted to an intensive care unit should be thoroughly reviewed to identify opportunities for 
clinical improvement.³

In the United Kingdom a contemporary clinical problem that is being addressed in an organized and systematic manner is how to respond to the rising rate of severe maternal morbidity caused by placenta accreta. Experts have concluded that women with a suspected placenta accreta should deliver in regional centers with advanced clinical resources—including an emergency surgical response team, interventional radiology, a high capacity blood bank, and an intensive 
care unit.

A similar approach has been proposed for managing placenta accreta in the United States.⁴ The American College of Obstetricians and Gynecologists (ACOG) and the Society of Maternal Fetal Medicine (SMFM) have proposed a tiered 
system of obstetric care with more complex cases being referred to regional perinatal centers.⁵ Regionalization of trauma services has been an important part of the US health care system for decades. Cases of severe trauma are brought to regional centers equipped to emergently treat complex injuries. A similar system of regulation and regionalization could be adapted for optimizing 
maternity care.

High-risk clinical events: Is your unit prepared?

In the United States the leading causes of maternal mortality, in descending order, are⁶⁻⁸:

 

• cardiovascular diseases
• infection
• hemorrhage
• cardiomyopathy
• pulmonary embolism
• hypertension
• amniotic fluid embolism
• stroke
• anesthesia complications.

Over the last decade, the Joint Commission has recommended that birthing centers develop standardized protocols and use simulation to improve the institution’s ability to respond in a timely manner to clinical events that may result in maternal morbidity or death.

The quality of published protocols dealing with hemorrhage, hypertension, and thromboembolism is continuously improving, and every birthing center should have written protocols that are updated on a regular timetable for these common high-risk events.^9,10 Does your birthing unit have written protocols to deal with cardiac diseases, infection, obstetric hemorrhage, thromboembolism, and severe hypertension? Are simulation exercises used to strengthen familiarity with the protocols?

High-risk patients

An amazing fact of today’s medical care is that sexually active women of reproductive age who have high-risk medical problems often have not been counseled to use a highly effective contraceptive, resulting in an increased risk of unintended pregnancy and maternal death. For example, adult women with a history of congenital heart disease are known to be at increased risk of death if they become pregnant. In a recent study, women with a history of congenital heart disease had 178 maternal
deaths per 100,000 deliveries—a rate approximately 10-fold higher than the US maternal mortality ratio.¹¹ Yet, many of these women are not using a highly effective contraceptive, and this results in a high rate of unplanned pregnancy.¹²

 

In order to reduce the risk of unintended pregnancy in women with high-risk medical problems, health systems could make contraception an important “vital sign” for women with high-risk medical conditions.

 

Let’s get organized

In a country with a history of embracing the “live free or die” ethic, it is often difficult for physicians to enthusiastically embrace the need for a higher level of organization and a potential reduction in individual freedom in order to improve health outcomes. And with a US maternal mortality ratio of 1 maternal death for every 5,400 births, many obstetricians will never have one of their patients die in childbirth. In fact, most obstetricians will have only 
1 maternal death during their entire career. In this reality, when clinical events occur rarely, it is not possible
for any single clinician, working alone, to impact the overall outcomes of those rare events. Therefore, teamwork and national efforts, such as the National Partnership for Maternal Safety,¹³ will be necessary to reverse our alarming trend of increasing 
maternal mortality. Let’s get organized to stop the rise of maternal deaths in the United States.

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.

NEW YORK – The “perfect storm” of pregnancy and lactation can throw breastfeeding moms into a painful deep freeze.

Almost 25% of women with lactation pain may actually be experiencing symptoms of Raynaud’s, Dr. Honor Fullerton Stone said at the American Academy of Dermatology summer meeting.

 

©lokisurina/thinkstockphotos.com

“Breastfeeding mothers are in a perfect storm,” of physical developments that predispose them to this vasoconstrictive phenomenon, said Dr. Fullerton Stone, who practices dermatology in Menlo Park, Ca. “Estrogen increases the alpha-adrenergic receptors on smooth muscle. Nerve irritation from constant breastfeeding upregulates those receptors. And emotional stress – crying baby, anyone? – increases epinephrine, which contributes further to vasoconstriction.”

She conducted a review of 88 of her own patients with nursing-related breast pain. Of these, about a quarter ended up with a diagnosis of nipple vasoconstriction. None of the women had a history of Raynaud’s disease.

Pain during a nursing session is the presenting complaint, but breastfeeding pain is incredibly nonspecific as a symptom. It’s the quality of the pain, Dr Stone said, that should ring a bell.

“There’s let-down pain, which occurs at latch and then comes on again later, with refill. There’s pain from candidiasis, which is dramatic at latch, like a radiating heat, but goes away rapidly after a few days of antifungals,” she noted. But with Raynaud’s, “the pain is persistent. It’s throbbing, which makes sense since it’s vascular. And it’s constant,” lasting through every nursing session, which she said is the kind of experience that makes mothers stop breastfeeding.

Since pain is such a pervasive symptom in breastfeeding complaints, women with vasoconstriction of the nipple are often misdiagnosed. They can go for months trying to improve latch technique or receiving antifungal therapy with no improvement, she said.

Dr. Stone considers a diagnosis of Raynaud’s if two of the following criteria are met:

• Color change of nipple, cold sensitivity, or color change of acral surfaces with cold exposure.

• Chronic deep breast pain for 4 or more weeks.

• Failure of oral antifungals and or antibiotics.

Treatment is both supportive and systemic and avoiding cold is key. She recalled a young mother who arrived in her office bundled up in a down parka on a warm California spring day. “I don’t know why, but this really seems to help,” she said.

 

“I suggest taking two hot showers a day and all the better if they can be right before nursing. Hot pads and compresses are not going to help. You need to warm up the entire body to calm this vascular reactivity.”

Women should also avoid consuming anything that can cause vasoconstriction, including caffeine and tobacco, she advised.

Nifedipine is a very effective medication, and is safe for nursing infants, Dr. Stone said. The sustained-released 30 mg/day dose is typically recommended, but she has changed her thinking on this a bit.

Her internal study showed that, although 83% responded very well to the drug, about a third of them also had a vasodilation-related side effect.

“For this reason, I usually now start with the 10 mg nonsustained form, and warn about things like headache, dizziness, postural hypotension, and fainting,” she said. Typically, patients adjust well to the drug’s effects and then the dose can be individually titrated.

Dr. Fullerton Stone had no relevant financial disclosures.

[email protected]

On Twitter @Alz_Gal

NEW YORK – The “perfect storm” of pregnancy and lactation can throw breastfeeding moms into a painful deep freeze.

Almost 25% of women with lactation pain may actually be experiencing symptoms of Raynaud’s, Dr. Honor Fullerton Stone said at the American Academy of Dermatology summer meeting.

 

©lokisurina/thinkstockphotos.com

“Breastfeeding mothers are in a perfect storm,” of physical developments that predispose them to this vasoconstrictive phenomenon, said Dr. Fullerton Stone, who practices dermatology in Menlo Park, Ca. “Estrogen increases the alpha-adrenergic receptors on smooth muscle. Nerve irritation from constant breastfeeding upregulates those receptors. And emotional stress – crying baby, anyone? – increases epinephrine, which contributes further to vasoconstriction.”

She conducted a review of 88 of her own patients with nursing-related breast pain. Of these, about a quarter ended up with a diagnosis of nipple vasoconstriction. None of the women had a history of Raynaud’s disease.

Pain during a nursing session is the presenting complaint, but breastfeeding pain is incredibly nonspecific as a symptom. It’s the quality of the pain, Dr Stone said, that should ring a bell.

“There’s let-down pain, which occurs at latch and then comes on again later, with refill. There’s pain from candidiasis, which is dramatic at latch, like a radiating heat, but goes away rapidly after a few days of antifungals,” she noted. But with Raynaud’s, “the pain is persistent. It’s throbbing, which makes sense since it’s vascular. And it’s constant,” lasting through every nursing session, which she said is the kind of experience that makes mothers stop breastfeeding.

Since pain is such a pervasive symptom in breastfeeding complaints, women with vasoconstriction of the nipple are often misdiagnosed. They can go for months trying to improve latch technique or receiving antifungal therapy with no improvement, she said.

Dr. Stone considers a diagnosis of Raynaud’s if two of the following criteria are met:

• Color change of nipple, cold sensitivity, or color change of acral surfaces with cold exposure.

• Chronic deep breast pain for 4 or more weeks.

• Failure of oral antifungals and or antibiotics.

Treatment is both supportive and systemic and avoiding cold is key. She recalled a young mother who arrived in her office bundled up in a down parka on a warm California spring day. “I don’t know why, but this really seems to help,” she said.

 

“I suggest taking two hot showers a day and all the better if they can be right before nursing. Hot pads and compresses are not going to help. You need to warm up the entire body to calm this vascular reactivity.”

Women should also avoid consuming anything that can cause vasoconstriction, including caffeine and tobacco, she advised.

Nifedipine is a very effective medication, and is safe for nursing infants, Dr. Stone said. The sustained-released 30 mg/day dose is typically recommended, but she has changed her thinking on this a bit.

Her internal study showed that, although 83% responded very well to the drug, about a third of them also had a vasodilation-related side effect.

“For this reason, I usually now start with the 10 mg nonsustained form, and warn about things like headache, dizziness, postural hypotension, and fainting,” she said. Typically, patients adjust well to the drug’s effects and then the dose can be individually titrated.

Dr. Fullerton Stone had no relevant financial disclosures.

[email protected]

On Twitter @Alz_Gal

NEW YORK – The “perfect storm” of pregnancy and lactation can throw breastfeeding moms into a painful deep freeze.

Almost 25% of women with lactation pain may actually be experiencing symptoms of Raynaud’s, Dr. Honor Fullerton Stone said at the American Academy of Dermatology summer meeting.

 

©lokisurina/thinkstockphotos.com

“Breastfeeding mothers are in a perfect storm,” of physical developments that predispose them to this vasoconstrictive phenomenon, said Dr. Fullerton Stone, who practices dermatology in Menlo Park, Ca. “Estrogen increases the alpha-adrenergic receptors on smooth muscle. Nerve irritation from constant breastfeeding upregulates those receptors. And emotional stress – crying baby, anyone? – increases epinephrine, which contributes further to vasoconstriction.”

She conducted a review of 88 of her own patients with nursing-related breast pain. Of these, about a quarter ended up with a diagnosis of nipple vasoconstriction. None of the women had a history of Raynaud’s disease.

Pain during a nursing session is the presenting complaint, but breastfeeding pain is incredibly nonspecific as a symptom. It’s the quality of the pain, Dr Stone said, that should ring a bell.

“There’s let-down pain, which occurs at latch and then comes on again later, with refill. There’s pain from candidiasis, which is dramatic at latch, like a radiating heat, but goes away rapidly after a few days of antifungals,” she noted. But with Raynaud’s, “the pain is persistent. It’s throbbing, which makes sense since it’s vascular. And it’s constant,” lasting through every nursing session, which she said is the kind of experience that makes mothers stop breastfeeding.

Since pain is such a pervasive symptom in breastfeeding complaints, women with vasoconstriction of the nipple are often misdiagnosed. They can go for months trying to improve latch technique or receiving antifungal therapy with no improvement, she said.

Dr. Stone considers a diagnosis of Raynaud’s if two of the following criteria are met:

• Color change of nipple, cold sensitivity, or color change of acral surfaces with cold exposure.

• Chronic deep breast pain for 4 or more weeks.

• Failure of oral antifungals and or antibiotics.

Treatment is both supportive and systemic and avoiding cold is key. She recalled a young mother who arrived in her office bundled up in a down parka on a warm California spring day. “I don’t know why, but this really seems to help,” she said.

 

“I suggest taking two hot showers a day and all the better if they can be right before nursing. Hot pads and compresses are not going to help. You need to warm up the entire body to calm this vascular reactivity.”

Women should also avoid consuming anything that can cause vasoconstriction, including caffeine and tobacco, she advised.

Nifedipine is a very effective medication, and is safe for nursing infants, Dr. Stone said. The sustained-released 30 mg/day dose is typically recommended, but she has changed her thinking on this a bit.

Her internal study showed that, although 83% responded very well to the drug, about a third of them also had a vasodilation-related side effect.

“For this reason, I usually now start with the 10 mg nonsustained form, and warn about things like headache, dizziness, postural hypotension, and fainting,” she said. Typically, patients adjust well to the drug’s effects and then the dose can be individually titrated.

Dr. Fullerton Stone had no relevant financial disclosures.

[email protected]

On Twitter @Alz_Gal

Infectious disease morbidity and mortality continue to disproportionately impact pregnant women and young infants.

In California, the incidence of pertussis approximates 100 cases per 100,000 in infants less than 5 months of age; a rate threefold greater than any other age group. Seven of nine (77%) deaths in 2013/2014 occurred in infants less than 3 months of age (California Department of Public Health Pertussis Report, Aug. 3, 2015).

Influenza severity and mortality is increased in pregnant women, and there is a greater risk of fetal morbidity and wastage. In the 2009 H₁N₁ pandemic, there was a 20% case fatality rate in women sick enough to be admitted to the ICU. The incidence of low birth weight also was increased among pregnant women delivering while hospitalized for influenza-related illness. These examples highlight the burden of vaccine-preventable disease in two vulnerable populations, pregnant women and infants too young to be protected by vaccines mandated by the U.S.immunization program.

The American College of Obstetricians and Gynecologists, the American Academy of Pediatrics, the Centers for Disease Control and Prevention, and many other national and state organizations endorse immunization of pregnant women to improve women’s and infants’ outcomes. Recent studies demonstrate that infants born to women vaccinated with influenza are 45%-48% less likely to be hospitalized for culture-proven influenza.

Benowitz et al. reported a 91.5% effectiveness for maternal influenza vaccination for prevention of hospitalization of infants caused by influenza in the first 6 months of life. The presumed mechanisms of protection are both the transplacental transfer of protective antibody as well as indirect protection from disease prevention in the mother (Clin Infect Dis. 2010 Dec 15;51(12):1355-61). The recommendation is that inactivated influenza vaccine can be given at any time during pregnancy; however, live attenuated influenza vaccine (LAIV; FluMist) is contraindicated, as are all live-virus vaccines. In contrast, Tdap is recommended for use either during pregnancy or post partum.

However, Healy et al. (Pediatr Infect Dis J. 2015;34(1):22-60) failed to demonstrate a benefit to postpartum immunization and cocooning for reducing pertussis illness in infants 6 months of age or younger. The likely explanation for this failure is revealed in a recent study in infant baboons where immunization with Tdap failed to decrease colonization or transmission of Bordetella pertussis, compared with natural disease or whole-cell pertussis. Thus, even though protective against disease, Tdap failure to prevent transmission within the community still occurs. The current Advisory Committee on Immunization Practices recommendation, immunization between 27 and 36 weeks, is designed to ensure high antibody concentrations in both mother and newborn at the time of birth and bridge the time period until infant immunization can elicit protective antibody.

The benefits achieved with maternal immunization must be weighed against potential for adverse events. There is no evidence of risk to either mother or infant from inactivated vaccines administered during pregnancy. Still, the recommendations for influenza and Tdap vaccine incorporate the high likelihood of exposure, the risk of morbidity or mortality from the infectious agent, and the likelihood of harm. During the H₁N₁ epidemic, a cohort study by Chambers et al. of H₁N₁ vaccine in exposed and unexposed pregnant women concluded that there was no increase in risk for major congenital defects, spontaneous abortion, or small for gestational age (Vaccine. 2013 Oct 17;31(44):5026-32). There was a signal for increase in prematurity, but the difference between H₁N₁-vaccinated and unvaccinated pregnancies was 3 days. In addition, a review of 11 studies, including one of 10,428 pregnant women, concluded there were no harmful maternal or fetal effects.

Additionally, no adverse risks have been identified in women who were inadvertently vaccinated during pregnancy with live-attenuated rubella, influenza, and yellow fever vaccines. Tetanus vaccination has been administered safely to several millions of pregnant women without documented serious adverse outcomes. Ongoing postmarketing surveillance continues as an important tool for identification of potential adverse effects.

One potential limitation is the blunting of infant immune responses to vaccination due to high serum antibody concentrations at the time of primary immunizations. Some studies have found lower antibody concentrations prior to booster vaccinations at 1 year of age. However, as morbidity and mortality is greater in the first months of life for many infectious diseases, this may be an acceptable trade off if high morbidity and mortality can be reduced in the first months of life.

Immunization during pregnancy represents only one aspect of prevention of vaccine preventable diseases. Preconception, prenatal, and postpartum visits with health care professionals represents an opportune time to discuss the benefits of immunization and their contribution to a healthy pregnancy outcome. Inactivated vaccines are safe for administration during pregnancy, live virus vaccines, despite being attenuated, are a theoretical risk if spread to the fetus occurs and therefore are contraindicated and should be administered during preconception counseling if indicated. The table below outlines vaccines that can be administered before, during, and after pregnancy.

 

Although once considered potentially contraindicated in pregnant women, evidence now supports specific vaccines as both safe for a pregnant woman and her fetus and effective for preventing serious disease in both. Universal immunization with influenza vaccine and Tdap, as recommended by multiple national professional medical organizations, will improve the outcome of pregnancy by prevention of morbidity and mortality from common community pathogens.

Dr. Pelton is chief of pediatric infectious disease and coordinator of the maternal-child HIV program at Boston Medical Center. E-mail him at [email protected].

Infectious disease morbidity and mortality continue to disproportionately impact pregnant women and young infants.

In California, the incidence of pertussis approximates 100 cases per 100,000 in infants less than 5 months of age; a rate threefold greater than any other age group. Seven of nine (77%) deaths in 2013/2014 occurred in infants less than 3 months of age (California Department of Public Health Pertussis Report, Aug. 3, 2015).

Influenza severity and mortality is increased in pregnant women, and there is a greater risk of fetal morbidity and wastage. In the 2009 H₁N₁ pandemic, there was a 20% case fatality rate in women sick enough to be admitted to the ICU. The incidence of low birth weight also was increased among pregnant women delivering while hospitalized for influenza-related illness. These examples highlight the burden of vaccine-preventable disease in two vulnerable populations, pregnant women and infants too young to be protected by vaccines mandated by the U.S.immunization program.

The American College of Obstetricians and Gynecologists, the American Academy of Pediatrics, the Centers for Disease Control and Prevention, and many other national and state organizations endorse immunization of pregnant women to improve women’s and infants’ outcomes. Recent studies demonstrate that infants born to women vaccinated with influenza are 45%-48% less likely to be hospitalized for culture-proven influenza.

Benowitz et al. reported a 91.5% effectiveness for maternal influenza vaccination for prevention of hospitalization of infants caused by influenza in the first 6 months of life. The presumed mechanisms of protection are both the transplacental transfer of protective antibody as well as indirect protection from disease prevention in the mother (Clin Infect Dis. 2010 Dec 15;51(12):1355-61). The recommendation is that inactivated influenza vaccine can be given at any time during pregnancy; however, live attenuated influenza vaccine (LAIV; FluMist) is contraindicated, as are all live-virus vaccines. In contrast, Tdap is recommended for use either during pregnancy or post partum.

However, Healy et al. (Pediatr Infect Dis J. 2015;34(1):22-60) failed to demonstrate a benefit to postpartum immunization and cocooning for reducing pertussis illness in infants 6 months of age or younger. The likely explanation for this failure is revealed in a recent study in infant baboons where immunization with Tdap failed to decrease colonization or transmission of Bordetella pertussis, compared with natural disease or whole-cell pertussis. Thus, even though protective against disease, Tdap failure to prevent transmission within the community still occurs. The current Advisory Committee on Immunization Practices recommendation, immunization between 27 and 36 weeks, is designed to ensure high antibody concentrations in both mother and newborn at the time of birth and bridge the time period until infant immunization can elicit protective antibody.

The benefits achieved with maternal immunization must be weighed against potential for adverse events. There is no evidence of risk to either mother or infant from inactivated vaccines administered during pregnancy. Still, the recommendations for influenza and Tdap vaccine incorporate the high likelihood of exposure, the risk of morbidity or mortality from the infectious agent, and the likelihood of harm. During the H₁N₁ epidemic, a cohort study by Chambers et al. of H₁N₁ vaccine in exposed and unexposed pregnant women concluded that there was no increase in risk for major congenital defects, spontaneous abortion, or small for gestational age (Vaccine. 2013 Oct 17;31(44):5026-32). There was a signal for increase in prematurity, but the difference between H₁N₁-vaccinated and unvaccinated pregnancies was 3 days. In addition, a review of 11 studies, including one of 10,428 pregnant women, concluded there were no harmful maternal or fetal effects.

Additionally, no adverse risks have been identified in women who were inadvertently vaccinated during pregnancy with live-attenuated rubella, influenza, and yellow fever vaccines. Tetanus vaccination has been administered safely to several millions of pregnant women without documented serious adverse outcomes. Ongoing postmarketing surveillance continues as an important tool for identification of potential adverse effects.

One potential limitation is the blunting of infant immune responses to vaccination due to high serum antibody concentrations at the time of primary immunizations. Some studies have found lower antibody concentrations prior to booster vaccinations at 1 year of age. However, as morbidity and mortality is greater in the first months of life for many infectious diseases, this may be an acceptable trade off if high morbidity and mortality can be reduced in the first months of life.

Immunization during pregnancy represents only one aspect of prevention of vaccine preventable diseases. Preconception, prenatal, and postpartum visits with health care professionals represents an opportune time to discuss the benefits of immunization and their contribution to a healthy pregnancy outcome. Inactivated vaccines are safe for administration during pregnancy, live virus vaccines, despite being attenuated, are a theoretical risk if spread to the fetus occurs and therefore are contraindicated and should be administered during preconception counseling if indicated. The table below outlines vaccines that can be administered before, during, and after pregnancy.

 

Although once considered potentially contraindicated in pregnant women, evidence now supports specific vaccines as both safe for a pregnant woman and her fetus and effective for preventing serious disease in both. Universal immunization with influenza vaccine and Tdap, as recommended by multiple national professional medical organizations, will improve the outcome of pregnancy by prevention of morbidity and mortality from common community pathogens.

Dr. Pelton is chief of pediatric infectious disease and coordinator of the maternal-child HIV program at Boston Medical Center. E-mail him at [email protected].

Infectious disease morbidity and mortality continue to disproportionately impact pregnant women and young infants.

In California, the incidence of pertussis approximates 100 cases per 100,000 in infants less than 5 months of age; a rate threefold greater than any other age group. Seven of nine (77%) deaths in 2013/2014 occurred in infants less than 3 months of age (California Department of Public Health Pertussis Report, Aug. 3, 2015).

Influenza severity and mortality is increased in pregnant women, and there is a greater risk of fetal morbidity and wastage. In the 2009 H₁N₁ pandemic, there was a 20% case fatality rate in women sick enough to be admitted to the ICU. The incidence of low birth weight also was increased among pregnant women delivering while hospitalized for influenza-related illness. These examples highlight the burden of vaccine-preventable disease in two vulnerable populations, pregnant women and infants too young to be protected by vaccines mandated by the U.S.immunization program.

The American College of Obstetricians and Gynecologists, the American Academy of Pediatrics, the Centers for Disease Control and Prevention, and many other national and state organizations endorse immunization of pregnant women to improve women’s and infants’ outcomes. Recent studies demonstrate that infants born to women vaccinated with influenza are 45%-48% less likely to be hospitalized for culture-proven influenza.

Benowitz et al. reported a 91.5% effectiveness for maternal influenza vaccination for prevention of hospitalization of infants caused by influenza in the first 6 months of life. The presumed mechanisms of protection are both the transplacental transfer of protective antibody as well as indirect protection from disease prevention in the mother (Clin Infect Dis. 2010 Dec 15;51(12):1355-61). The recommendation is that inactivated influenza vaccine can be given at any time during pregnancy; however, live attenuated influenza vaccine (LAIV; FluMist) is contraindicated, as are all live-virus vaccines. In contrast, Tdap is recommended for use either during pregnancy or post partum.

However, Healy et al. (Pediatr Infect Dis J. 2015;34(1):22-60) failed to demonstrate a benefit to postpartum immunization and cocooning for reducing pertussis illness in infants 6 months of age or younger. The likely explanation for this failure is revealed in a recent study in infant baboons where immunization with Tdap failed to decrease colonization or transmission of Bordetella pertussis, compared with natural disease or whole-cell pertussis. Thus, even though protective against disease, Tdap failure to prevent transmission within the community still occurs. The current Advisory Committee on Immunization Practices recommendation, immunization between 27 and 36 weeks, is designed to ensure high antibody concentrations in both mother and newborn at the time of birth and bridge the time period until infant immunization can elicit protective antibody.

The benefits achieved with maternal immunization must be weighed against potential for adverse events. There is no evidence of risk to either mother or infant from inactivated vaccines administered during pregnancy. Still, the recommendations for influenza and Tdap vaccine incorporate the high likelihood of exposure, the risk of morbidity or mortality from the infectious agent, and the likelihood of harm. During the H₁N₁ epidemic, a cohort study by Chambers et al. of H₁N₁ vaccine in exposed and unexposed pregnant women concluded that there was no increase in risk for major congenital defects, spontaneous abortion, or small for gestational age (Vaccine. 2013 Oct 17;31(44):5026-32). There was a signal for increase in prematurity, but the difference between H₁N₁-vaccinated and unvaccinated pregnancies was 3 days. In addition, a review of 11 studies, including one of 10,428 pregnant women, concluded there were no harmful maternal or fetal effects.

Additionally, no adverse risks have been identified in women who were inadvertently vaccinated during pregnancy with live-attenuated rubella, influenza, and yellow fever vaccines. Tetanus vaccination has been administered safely to several millions of pregnant women without documented serious adverse outcomes. Ongoing postmarketing surveillance continues as an important tool for identification of potential adverse effects.

One potential limitation is the blunting of infant immune responses to vaccination due to high serum antibody concentrations at the time of primary immunizations. Some studies have found lower antibody concentrations prior to booster vaccinations at 1 year of age. However, as morbidity and mortality is greater in the first months of life for many infectious diseases, this may be an acceptable trade off if high morbidity and mortality can be reduced in the first months of life.

Immunization during pregnancy represents only one aspect of prevention of vaccine preventable diseases. Preconception, prenatal, and postpartum visits with health care professionals represents an opportune time to discuss the benefits of immunization and their contribution to a healthy pregnancy outcome. Inactivated vaccines are safe for administration during pregnancy, live virus vaccines, despite being attenuated, are a theoretical risk if spread to the fetus occurs and therefore are contraindicated and should be administered during preconception counseling if indicated. The table below outlines vaccines that can be administered before, during, and after pregnancy.

 

Although once considered potentially contraindicated in pregnant women, evidence now supports specific vaccines as both safe for a pregnant woman and her fetus and effective for preventing serious disease in both. Universal immunization with influenza vaccine and Tdap, as recommended by multiple national professional medical organizations, will improve the outcome of pregnancy by prevention of morbidity and mortality from common community pathogens.

Dr. Pelton is chief of pediatric infectious disease and coordinator of the maternal-child HIV program at Boston Medical Center. E-mail him at [email protected].

Missed Preeclampsia

A 24-year-old woman, gravida 1, para 1, aborta 0, presented to the ED complaining of a 1-day history of shortness of breath. Four days earlier, she had delivered a healthy baby boy via normal vaginal delivery and without complication. She denied chest pain, fever, or abdominal pain. She was otherwise in good health, stating that she was not taking any medications. She also denied smoking cigarettes.

On physical examination, the patient’s vital signs were remarkable for the following: heart rate (HR), 86 beats/minute; blood pressure (BP), 164/94 mm Hg; respiratory rate, 18 breaths/minute; temperature, 98.6^oF. Oxygen saturation was 96% on room air. The head, eye, ear, nose and throat examination was unremarkable. The lungs were clear to auscultation bilaterally, and HR and heart rhythm were normal. The abdomen was soft and nontender without guarding or rebound. The lower extremities were remarkable for 1+ pedal and pretibial edema bilaterally.

Since this patient was 4 days postpartum, the emergency physician (EP) was concerned for pulmonary embolism (PE). A complete blood count, basic metabolic profile, and a serum troponin T level were ordered. The electrocardiogram revealed normal sinus rhythm without evidence of strain or injury. The chest X-ray was interpreted by radiology services as normal. Given the concern for PE, computed tomography angiography (CTA) of the chest was ordered. All laboratory studies, including the troponin T level, were reported as normal. The CTA scan of the chest was interpreted by radiology services as normal and without evidence of PE. The patient was discharged home with a diagnosis of “shortness of breath of unknown etiology.”

The patient presented to the same ED 2 days later, again with the chief complaint of shortness of breath. On examination, her BP was noted to be elevated and she had 1+ dependent edema bilaterally. Again, the EP was concerned for a PE and ordered a repeat CTA scan of the chest. This study, similar to the first, was read as normal, and showed no evidence of PE. The patient was diagnosed again with “shortness of breath of unknown etiology” and discharged home. The patient’s obstetrician-gynecologist (Ob/Gyn) was not consulted; however, the patient was encouraged to follow up with him.

The next day, the patient presented to the same ED via emergency medical services, this time with seizures; she had no prior history of a seizure disorder. On presentation to the ED, she was noted to be postictal, with an elevated BP and tachycardic with an HR of 104 beats/minute. On examination, the lungs were clear to auscultation and the lower extremities exhibited 1+ pedal and pretibial edema. A urinalysis revealed proteinuria. The patient was given 4 g of magnesium sulfate intravenously (IV) and her Ob/Gyn was consulted.

The patient was admitted to the hospital with a diagnosis of eclampsia. She was given an IV drip of magnesium and labetalol for the high BP. Unfortunately, the patient apparently had suffered an anoxic brain injury from the previous seizures and died on hospital day 3.

The family sued the treating EPs and the hospital for failure to diagnose preeclampsia on two separate ED presentations. They noted the patient’s Ob/Gyn was never consulted; no action was taken to treat the hypertension; and no urinalysis was ordered on either visit. The EPs and hospital settled the case prior to trial for several million dollars.

Discussion

This is an incredibly sad case, and the EPs and hospital were right to settle and not go to trial. While PE was a reasonable diagnosis to consider in this patient on her first ED visit, it should not have been the only one in the differential diagnosis. The EP became anchored to this single diagnosis and refused to consider other alternative diagnoses—even after the CTA scan of the chest ruled out PE. Moreover, it appears the EP either never considered the significance of the elevated BP and dependent edema or just ignored these findings. To repeat essentially the same exact workup on the second visit does not make sense—one should “cast a wider net, not the same net.”

The diagnosis of “shortness of breath of unknown etiology” is similarly unacceptable. While this is a common and accepted diagnosis when it pertains to abdominal pain, the same is not true for dyspnea.

Preeclampsia is characterized by hypertension (BP >140/90 mm Hg) and proteinuria; associated symptoms include edema and hyperreflexia. Postpartum preeclampsia occurs infrequently and can develop up to 4 weeks after delivery.¹ In one 10-year retrospective case series, the incidence of preeclampsia in the postpartum period was 5.7%, and nearly 16% went on to develop eclampsia.² In a retrospective study of 22 postpartum preeclamptic patients, the median time to presentation was 5 days postpartum.¹ In a similar retrospective study of 152 patients, 90% of such patients presented within 7 days.³ The patient in this case initially presented on postpartum day 4.

 

Interestingly, in a study by Al-Safi et al,³ 63% of postpartum preeclamptic patients had no antecedent diagnosis of hypertensive disease during pregnancy. These findings are consistent with the findings of others that 33% to 69% of such patients show no evidence of preeclampsia in the ante- or peripartum period.

The clinical presentation of postpartum preeclampsia is similar to preeclampsia complicating pregnancy after gestation week 20. In the study by Al-Safi et al,³ headache was the most common presenting symptom (69%), followed by shortness of breath (30%), blurry vision (21%), nausea (12.5%), and epigastric abdominal pain (5%). Similarly, Yancey et al¹ found headache (82%) to be the most common presenting symptom in their series. Unfortunately, it is not known whether the patient in this case complained of headache or blurred vision as the published records note neither their presence nor absence.

The management of patients with preeclampsia includes IV magnesium to prevent seizures (ie, eclampsia) and BP control.¹ A bolus of 4 to 6 g IV magnesium sulfate over 15 to 30 minutes is recommended, followed by an infusion of 2 g/h IV. Historically, IV hydralazine has been used to manage preeclamptic patients with a BP greater than 160/110 mm Hg. More recently, however, IV labetalol has become popular.⁵ All such patients require admission to the hospital with Ob/Gyn involvement.

Missed Subdural Hematoma

A 59-year-old man presented to the ED with a chief complaint of headache, the onset of which he stated started gradually 2 days prior. He noted the headache was worse than normal but without associated nausea, vomiting, fever, chills, or change in vision. His past medical history was significant for a lower extremity deep vein thrombosis 3 months prior, for which he was taking warfarin.

The patient’s vital signs were all normal. The physical examination, including a thorough neurological examination, was also normal. The EP ordered a prothrombin time (PT), an international normalized ratio (INR), and a noncontrast CT scan of the head. The PT/INR results were therapeutic at 22 seconds and 2.3. The CT scan was interpreted by radiology services as normal. The patient’s headache was treated with IV prochlorperazine and diphenhydramine. After treatment, the patient reported feeling better and was discharged home with instructions to follow up with his primary care physician.

Over the next several months, the patient presented to the same ED on seven different occasions, each time with the chief complaint of headache. At each of these presentations, the history and physical examination were documented as unremarkable, with no history of trauma. The thoroughness, however, of the documentation varied considerably for each ED encounter. No head CT scan was ordered on the subsequent seven visits, and at each presentation, the patient was treated symptomatically and discharged home.

Two days after his eighth visit to the same hospital ED, the patient presented to a different ED, again with a chief complaint of headache. The EP at this ED ordered a noncontrast CT of the head, which demonstrated a left subdural hematoma. The patient was admitted to the hospital, given IV vitamin K and fresh frozen plasma, and underwent evacuation of the hematoma by neurosurgery. The patient’s hospital course was unremarkable, and he was discharged home without any focal weakness.

The patient, however, claimed that he suffered cognitive impairment as a result of the missed diagnosis. He sued treating EPs at the first ED as well as the hospital for failure to timely diagnose the subdural hematoma, stating that a CT scan should have been performed at each of his ED visits since he was on warfarin. The defense claimed that a CT scan was not warranted for each visit, and that the timing of when and how the brain bleed started was uncertain. At trial, a defense verdict was returned.

Discussion

It is well known that patients receiving warfarin are at an increased risk for intracranial hemorrhage (ICH) following blunt head trauma.¹ The recommendation is that all such patients have a noncontrast CT scan of the head to rule out intracranial bleeding. This is due to the fact that 60% of patients presenting with an immediate traumatic intracranial hemorrhage will have a normal mental status on examination; and 11% will have no history of loss of consciousness, a normal mental status examination, and no physical evidence of trauma above the clavicles.¹ In a study by Hart et al,² subdural hematoma accounted for 44% of all ICH in these types of patients.

More controversial is how to manage patients on warfarin who experience blunt head trauma and have a normal CT scan of the head. Because of the fear for delayed traumatic ICH, many clinicians recommend admitting such patients for neurological observation and repeat head CT scan the next morning.³ Additionally, some clinicians even recommend reversing the warfarin anticoagulation in such patients. ⁴ These recommendations, though, are based on expert consensus rather than on rigorous, prospective multicenter studies.¹  These strategies are also problematic, since such multiple repeat CT scans would not only be incredibly expensive but also would expose the patient to high doses of radiation to the brain. Moreover, the Centers for Medicare and Medicaid Services has now made CT brain scan imaging of patients presenting to the ED with complaint of nontraumatic headache a quality measure they follow. Their goal is to decrease the number of “unnecessary” head CT scans.

 

The patient in this case denied any history of trauma on the subsequent seven ED visits. Unfortunately, as pointed out, even minor trauma can result in ICH, and patients may not recall the occurrence of the event.

For patients on warfarin who present with headache, a very careful history must be taken—including inquiring about minor traumatic events. Even then, as has been shown, patients may have not experienced a loss of consciousness, have a normal mental status examination, and exhibit no external evidence of head trauma. The clinician is forced to use her or his own best judgment when evaluating such patients in the ED.

Interestingly, the risk of ICH secondary to blunt head trauma in patients on warfarin is increased if they are on concomitant aspirin therapy.² Similarly, the risk of ICH following head trauma in patients on clopidogrel is greater than for those patients taking warfarin,¹ and the risk of ICH in patients taking dabigatran is less than if taking warfarin.²

Missed Preeclampsia

A 24-year-old woman, gravida 1, para 1, aborta 0, presented to the ED complaining of a 1-day history of shortness of breath. Four days earlier, she had delivered a healthy baby boy via normal vaginal delivery and without complication. She denied chest pain, fever, or abdominal pain. She was otherwise in good health, stating that she was not taking any medications. She also denied smoking cigarettes.

On physical examination, the patient’s vital signs were remarkable for the following: heart rate (HR), 86 beats/minute; blood pressure (BP), 164/94 mm Hg; respiratory rate, 18 breaths/minute; temperature, 98.6^oF. Oxygen saturation was 96% on room air. The head, eye, ear, nose and throat examination was unremarkable. The lungs were clear to auscultation bilaterally, and HR and heart rhythm were normal. The abdomen was soft and nontender without guarding or rebound. The lower extremities were remarkable for 1+ pedal and pretibial edema bilaterally.

Since this patient was 4 days postpartum, the emergency physician (EP) was concerned for pulmonary embolism (PE). A complete blood count, basic metabolic profile, and a serum troponin T level were ordered. The electrocardiogram revealed normal sinus rhythm without evidence of strain or injury. The chest X-ray was interpreted by radiology services as normal. Given the concern for PE, computed tomography angiography (CTA) of the chest was ordered. All laboratory studies, including the troponin T level, were reported as normal. The CTA scan of the chest was interpreted by radiology services as normal and without evidence of PE. The patient was discharged home with a diagnosis of “shortness of breath of unknown etiology.”

The patient presented to the same ED 2 days later, again with the chief complaint of shortness of breath. On examination, her BP was noted to be elevated and she had 1+ dependent edema bilaterally. Again, the EP was concerned for a PE and ordered a repeat CTA scan of the chest. This study, similar to the first, was read as normal, and showed no evidence of PE. The patient was diagnosed again with “shortness of breath of unknown etiology” and discharged home. The patient’s obstetrician-gynecologist (Ob/Gyn) was not consulted; however, the patient was encouraged to follow up with him.

The next day, the patient presented to the same ED via emergency medical services, this time with seizures; she had no prior history of a seizure disorder. On presentation to the ED, she was noted to be postictal, with an elevated BP and tachycardic with an HR of 104 beats/minute. On examination, the lungs were clear to auscultation and the lower extremities exhibited 1+ pedal and pretibial edema. A urinalysis revealed proteinuria. The patient was given 4 g of magnesium sulfate intravenously (IV) and her Ob/Gyn was consulted.

The patient was admitted to the hospital with a diagnosis of eclampsia. She was given an IV drip of magnesium and labetalol for the high BP. Unfortunately, the patient apparently had suffered an anoxic brain injury from the previous seizures and died on hospital day 3.

The family sued the treating EPs and the hospital for failure to diagnose preeclampsia on two separate ED presentations. They noted the patient’s Ob/Gyn was never consulted; no action was taken to treat the hypertension; and no urinalysis was ordered on either visit. The EPs and hospital settled the case prior to trial for several million dollars.

Discussion

This is an incredibly sad case, and the EPs and hospital were right to settle and not go to trial. While PE was a reasonable diagnosis to consider in this patient on her first ED visit, it should not have been the only one in the differential diagnosis. The EP became anchored to this single diagnosis and refused to consider other alternative diagnoses—even after the CTA scan of the chest ruled out PE. Moreover, it appears the EP either never considered the significance of the elevated BP and dependent edema or just ignored these findings. To repeat essentially the same exact workup on the second visit does not make sense—one should “cast a wider net, not the same net.”

The diagnosis of “shortness of breath of unknown etiology” is similarly unacceptable. While this is a common and accepted diagnosis when it pertains to abdominal pain, the same is not true for dyspnea.

Preeclampsia is characterized by hypertension (BP >140/90 mm Hg) and proteinuria; associated symptoms include edema and hyperreflexia. Postpartum preeclampsia occurs infrequently and can develop up to 4 weeks after delivery.¹ In one 10-year retrospective case series, the incidence of preeclampsia in the postpartum period was 5.7%, and nearly 16% went on to develop eclampsia.² In a retrospective study of 22 postpartum preeclamptic patients, the median time to presentation was 5 days postpartum.¹ In a similar retrospective study of 152 patients, 90% of such patients presented within 7 days.³ The patient in this case initially presented on postpartum day 4.

 

Interestingly, in a study by Al-Safi et al,³ 63% of postpartum preeclamptic patients had no antecedent diagnosis of hypertensive disease during pregnancy. These findings are consistent with the findings of others that 33% to 69% of such patients show no evidence of preeclampsia in the ante- or peripartum period.

The clinical presentation of postpartum preeclampsia is similar to preeclampsia complicating pregnancy after gestation week 20. In the study by Al-Safi et al,³ headache was the most common presenting symptom (69%), followed by shortness of breath (30%), blurry vision (21%), nausea (12.5%), and epigastric abdominal pain (5%). Similarly, Yancey et al¹ found headache (82%) to be the most common presenting symptom in their series. Unfortunately, it is not known whether the patient in this case complained of headache or blurred vision as the published records note neither their presence nor absence.

The management of patients with preeclampsia includes IV magnesium to prevent seizures (ie, eclampsia) and BP control.¹ A bolus of 4 to 6 g IV magnesium sulfate over 15 to 30 minutes is recommended, followed by an infusion of 2 g/h IV. Historically, IV hydralazine has been used to manage preeclamptic patients with a BP greater than 160/110 mm Hg. More recently, however, IV labetalol has become popular.⁵ All such patients require admission to the hospital with Ob/Gyn involvement.

Missed Subdural Hematoma

A 59-year-old man presented to the ED with a chief complaint of headache, the onset of which he stated started gradually 2 days prior. He noted the headache was worse than normal but without associated nausea, vomiting, fever, chills, or change in vision. His past medical history was significant for a lower extremity deep vein thrombosis 3 months prior, for which he was taking warfarin.

The patient’s vital signs were all normal. The physical examination, including a thorough neurological examination, was also normal. The EP ordered a prothrombin time (PT), an international normalized ratio (INR), and a noncontrast CT scan of the head. The PT/INR results were therapeutic at 22 seconds and 2.3. The CT scan was interpreted by radiology services as normal. The patient’s headache was treated with IV prochlorperazine and diphenhydramine. After treatment, the patient reported feeling better and was discharged home with instructions to follow up with his primary care physician.

Over the next several months, the patient presented to the same ED on seven different occasions, each time with the chief complaint of headache. At each of these presentations, the history and physical examination were documented as unremarkable, with no history of trauma. The thoroughness, however, of the documentation varied considerably for each ED encounter. No head CT scan was ordered on the subsequent seven visits, and at each presentation, the patient was treated symptomatically and discharged home.

Two days after his eighth visit to the same hospital ED, the patient presented to a different ED, again with a chief complaint of headache. The EP at this ED ordered a noncontrast CT of the head, which demonstrated a left subdural hematoma. The patient was admitted to the hospital, given IV vitamin K and fresh frozen plasma, and underwent evacuation of the hematoma by neurosurgery. The patient’s hospital course was unremarkable, and he was discharged home without any focal weakness.

The patient, however, claimed that he suffered cognitive impairment as a result of the missed diagnosis. He sued treating EPs at the first ED as well as the hospital for failure to timely diagnose the subdural hematoma, stating that a CT scan should have been performed at each of his ED visits since he was on warfarin. The defense claimed that a CT scan was not warranted for each visit, and that the timing of when and how the brain bleed started was uncertain. At trial, a defense verdict was returned.

Discussion

It is well known that patients receiving warfarin are at an increased risk for intracranial hemorrhage (ICH) following blunt head trauma.¹ The recommendation is that all such patients have a noncontrast CT scan of the head to rule out intracranial bleeding. This is due to the fact that 60% of patients presenting with an immediate traumatic intracranial hemorrhage will have a normal mental status on examination; and 11% will have no history of loss of consciousness, a normal mental status examination, and no physical evidence of trauma above the clavicles.¹ In a study by Hart et al,² subdural hematoma accounted for 44% of all ICH in these types of patients.

More controversial is how to manage patients on warfarin who experience blunt head trauma and have a normal CT scan of the head. Because of the fear for delayed traumatic ICH, many clinicians recommend admitting such patients for neurological observation and repeat head CT scan the next morning.³ Additionally, some clinicians even recommend reversing the warfarin anticoagulation in such patients. ⁴ These recommendations, though, are based on expert consensus rather than on rigorous, prospective multicenter studies.¹  These strategies are also problematic, since such multiple repeat CT scans would not only be incredibly expensive but also would expose the patient to high doses of radiation to the brain. Moreover, the Centers for Medicare and Medicaid Services has now made CT brain scan imaging of patients presenting to the ED with complaint of nontraumatic headache a quality measure they follow. Their goal is to decrease the number of “unnecessary” head CT scans.

 

The patient in this case denied any history of trauma on the subsequent seven ED visits. Unfortunately, as pointed out, even minor trauma can result in ICH, and patients may not recall the occurrence of the event.

For patients on warfarin who present with headache, a very careful history must be taken—including inquiring about minor traumatic events. Even then, as has been shown, patients may have not experienced a loss of consciousness, have a normal mental status examination, and exhibit no external evidence of head trauma. The clinician is forced to use her or his own best judgment when evaluating such patients in the ED.

Interestingly, the risk of ICH secondary to blunt head trauma in patients on warfarin is increased if they are on concomitant aspirin therapy.² Similarly, the risk of ICH following head trauma in patients on clopidogrel is greater than for those patients taking warfarin,¹ and the risk of ICH in patients taking dabigatran is less than if taking warfarin.²

Missed Preeclampsia

A 24-year-old woman, gravida 1, para 1, aborta 0, presented to the ED complaining of a 1-day history of shortness of breath. Four days earlier, she had delivered a healthy baby boy via normal vaginal delivery and without complication. She denied chest pain, fever, or abdominal pain. She was otherwise in good health, stating that she was not taking any medications. She also denied smoking cigarettes.

On physical examination, the patient’s vital signs were remarkable for the following: heart rate (HR), 86 beats/minute; blood pressure (BP), 164/94 mm Hg; respiratory rate, 18 breaths/minute; temperature, 98.6^oF. Oxygen saturation was 96% on room air. The head, eye, ear, nose and throat examination was unremarkable. The lungs were clear to auscultation bilaterally, and HR and heart rhythm were normal. The abdomen was soft and nontender without guarding or rebound. The lower extremities were remarkable for 1+ pedal and pretibial edema bilaterally.

Since this patient was 4 days postpartum, the emergency physician (EP) was concerned for pulmonary embolism (PE). A complete blood count, basic metabolic profile, and a serum troponin T level were ordered. The electrocardiogram revealed normal sinus rhythm without evidence of strain or injury. The chest X-ray was interpreted by radiology services as normal. Given the concern for PE, computed tomography angiography (CTA) of the chest was ordered. All laboratory studies, including the troponin T level, were reported as normal. The CTA scan of the chest was interpreted by radiology services as normal and without evidence of PE. The patient was discharged home with a diagnosis of “shortness of breath of unknown etiology.”

The patient presented to the same ED 2 days later, again with the chief complaint of shortness of breath. On examination, her BP was noted to be elevated and she had 1+ dependent edema bilaterally. Again, the EP was concerned for a PE and ordered a repeat CTA scan of the chest. This study, similar to the first, was read as normal, and showed no evidence of PE. The patient was diagnosed again with “shortness of breath of unknown etiology” and discharged home. The patient’s obstetrician-gynecologist (Ob/Gyn) was not consulted; however, the patient was encouraged to follow up with him.

The next day, the patient presented to the same ED via emergency medical services, this time with seizures; she had no prior history of a seizure disorder. On presentation to the ED, she was noted to be postictal, with an elevated BP and tachycardic with an HR of 104 beats/minute. On examination, the lungs were clear to auscultation and the lower extremities exhibited 1+ pedal and pretibial edema. A urinalysis revealed proteinuria. The patient was given 4 g of magnesium sulfate intravenously (IV) and her Ob/Gyn was consulted.

The patient was admitted to the hospital with a diagnosis of eclampsia. She was given an IV drip of magnesium and labetalol for the high BP. Unfortunately, the patient apparently had suffered an anoxic brain injury from the previous seizures and died on hospital day 3.

The family sued the treating EPs and the hospital for failure to diagnose preeclampsia on two separate ED presentations. They noted the patient’s Ob/Gyn was never consulted; no action was taken to treat the hypertension; and no urinalysis was ordered on either visit. The EPs and hospital settled the case prior to trial for several million dollars.

Discussion

This is an incredibly sad case, and the EPs and hospital were right to settle and not go to trial. While PE was a reasonable diagnosis to consider in this patient on her first ED visit, it should not have been the only one in the differential diagnosis. The EP became anchored to this single diagnosis and refused to consider other alternative diagnoses—even after the CTA scan of the chest ruled out PE. Moreover, it appears the EP either never considered the significance of the elevated BP and dependent edema or just ignored these findings. To repeat essentially the same exact workup on the second visit does not make sense—one should “cast a wider net, not the same net.”

The diagnosis of “shortness of breath of unknown etiology” is similarly unacceptable. While this is a common and accepted diagnosis when it pertains to abdominal pain, the same is not true for dyspnea.

Preeclampsia is characterized by hypertension (BP >140/90 mm Hg) and proteinuria; associated symptoms include edema and hyperreflexia. Postpartum preeclampsia occurs infrequently and can develop up to 4 weeks after delivery.¹ In one 10-year retrospective case series, the incidence of preeclampsia in the postpartum period was 5.7%, and nearly 16% went on to develop eclampsia.² In a retrospective study of 22 postpartum preeclamptic patients, the median time to presentation was 5 days postpartum.¹ In a similar retrospective study of 152 patients, 90% of such patients presented within 7 days.³ The patient in this case initially presented on postpartum day 4.

 

Interestingly, in a study by Al-Safi et al,³ 63% of postpartum preeclamptic patients had no antecedent diagnosis of hypertensive disease during pregnancy. These findings are consistent with the findings of others that 33% to 69% of such patients show no evidence of preeclampsia in the ante- or peripartum period.

The clinical presentation of postpartum preeclampsia is similar to preeclampsia complicating pregnancy after gestation week 20. In the study by Al-Safi et al,³ headache was the most common presenting symptom (69%), followed by shortness of breath (30%), blurry vision (21%), nausea (12.5%), and epigastric abdominal pain (5%). Similarly, Yancey et al¹ found headache (82%) to be the most common presenting symptom in their series. Unfortunately, it is not known whether the patient in this case complained of headache or blurred vision as the published records note neither their presence nor absence.

The management of patients with preeclampsia includes IV magnesium to prevent seizures (ie, eclampsia) and BP control.¹ A bolus of 4 to 6 g IV magnesium sulfate over 15 to 30 minutes is recommended, followed by an infusion of 2 g/h IV. Historically, IV hydralazine has been used to manage preeclamptic patients with a BP greater than 160/110 mm Hg. More recently, however, IV labetalol has become popular.⁵ All such patients require admission to the hospital with Ob/Gyn involvement.

Missed Subdural Hematoma

A 59-year-old man presented to the ED with a chief complaint of headache, the onset of which he stated started gradually 2 days prior. He noted the headache was worse than normal but without associated nausea, vomiting, fever, chills, or change in vision. His past medical history was significant for a lower extremity deep vein thrombosis 3 months prior, for which he was taking warfarin.

The patient’s vital signs were all normal. The physical examination, including a thorough neurological examination, was also normal. The EP ordered a prothrombin time (PT), an international normalized ratio (INR), and a noncontrast CT scan of the head. The PT/INR results were therapeutic at 22 seconds and 2.3. The CT scan was interpreted by radiology services as normal. The patient’s headache was treated with IV prochlorperazine and diphenhydramine. After treatment, the patient reported feeling better and was discharged home with instructions to follow up with his primary care physician.

Over the next several months, the patient presented to the same ED on seven different occasions, each time with the chief complaint of headache. At each of these presentations, the history and physical examination were documented as unremarkable, with no history of trauma. The thoroughness, however, of the documentation varied considerably for each ED encounter. No head CT scan was ordered on the subsequent seven visits, and at each presentation, the patient was treated symptomatically and discharged home.

Two days after his eighth visit to the same hospital ED, the patient presented to a different ED, again with a chief complaint of headache. The EP at this ED ordered a noncontrast CT of the head, which demonstrated a left subdural hematoma. The patient was admitted to the hospital, given IV vitamin K and fresh frozen plasma, and underwent evacuation of the hematoma by neurosurgery. The patient’s hospital course was unremarkable, and he was discharged home without any focal weakness.

The patient, however, claimed that he suffered cognitive impairment as a result of the missed diagnosis. He sued treating EPs at the first ED as well as the hospital for failure to timely diagnose the subdural hematoma, stating that a CT scan should have been performed at each of his ED visits since he was on warfarin. The defense claimed that a CT scan was not warranted for each visit, and that the timing of when and how the brain bleed started was uncertain. At trial, a defense verdict was returned.

Discussion

It is well known that patients receiving warfarin are at an increased risk for intracranial hemorrhage (ICH) following blunt head trauma.¹ The recommendation is that all such patients have a noncontrast CT scan of the head to rule out intracranial bleeding. This is due to the fact that 60% of patients presenting with an immediate traumatic intracranial hemorrhage will have a normal mental status on examination; and 11% will have no history of loss of consciousness, a normal mental status examination, and no physical evidence of trauma above the clavicles.¹ In a study by Hart et al,² subdural hematoma accounted for 44% of all ICH in these types of patients.

More controversial is how to manage patients on warfarin who experience blunt head trauma and have a normal CT scan of the head. Because of the fear for delayed traumatic ICH, many clinicians recommend admitting such patients for neurological observation and repeat head CT scan the next morning.³ Additionally, some clinicians even recommend reversing the warfarin anticoagulation in such patients. ⁴ These recommendations, though, are based on expert consensus rather than on rigorous, prospective multicenter studies.¹  These strategies are also problematic, since such multiple repeat CT scans would not only be incredibly expensive but also would expose the patient to high doses of radiation to the brain. Moreover, the Centers for Medicare and Medicaid Services has now made CT brain scan imaging of patients presenting to the ED with complaint of nontraumatic headache a quality measure they follow. Their goal is to decrease the number of “unnecessary” head CT scans.

 

The patient in this case denied any history of trauma on the subsequent seven ED visits. Unfortunately, as pointed out, even minor trauma can result in ICH, and patients may not recall the occurrence of the event.

For patients on warfarin who present with headache, a very careful history must be taken—including inquiring about minor traumatic events. Even then, as has been shown, patients may have not experienced a loss of consciousness, have a normal mental status examination, and exhibit no external evidence of head trauma. The clinician is forced to use her or his own best judgment when evaluating such patients in the ED.

Interestingly, the risk of ICH secondary to blunt head trauma in patients on warfarin is increased if they are on concomitant aspirin therapy.² Similarly, the risk of ICH following head trauma in patients on clopidogrel is greater than for those patients taking warfarin,¹ and the risk of ICH in patients taking dabigatran is less than if taking warfarin.²