From the Editor

Amniotic fluid embolism (AFE) occurs in about 1 in 20,000 to 1 in 40,000 deliveries.^1,2 Although the condition is rare, the case fatality rate is high, and AFE is a common cause of maternal death in developed countries. AFE cannot be predicted or prevented. Moreover, the condition is difficult to precisely define and is often a diagnosis of exclusion.

AFE should be considered in the differential diagnosis of a pregnant woman with sudden onset of shortness of breath, hypotension, or cardiac arrhythmia or arrest, followed by coagulopathy and hemorrhage. Premonitory symptoms, including restlessness, confusion, disorientation, agitation, chills, nausea, numbness, and tingling, are commonly reported just before the cardiorespiratory collapse. AFE is less likely if the initial obstetric event is hemorrhage in the absence of cardiorespiratory compromise or a preceding coagulopathy.³

Typically, the onset is just before birth, during birth, or within the first few hours after delivery. In the United Kingdom, which has a robust centralized registry for reporting AFE, about 56% of cases occur before birth and 44% after birth.⁴

Related article: Is the incidence of amniotic fluid embolism rising? John T. Repke, MD (Examining the Evidence, August 2010)

The resources available to obstetric units vary greatly. Each unit needs to assess its resources and develop an AFE treatment protocol that builds on the unique strengths of the unit. Treatment of AFE requires the coordinated actions of anesthesiologists, obstetricians, nurses, the blood bank, pharmacy, and cardiovascular specialists. Coordinated activity among the members of such a large multidisciplinary team requires a written protocol that is practiced on a regular basis.

Six important components of a multidisciplinary response to AFE treatment protocol are:

1. high-quality cardiopulmonary resuscitation (CPR)
2. a protocol for massive transfusion
3. treatment of diffuse bleeding and coagulopathy
4. treatment of uterine and pelvic bleeding
5. extracorporeal lung and heart support
6. post-AFE intensive care.

1. Initiate high-quality CPR
Hypotension and hypoxemia due to cardiac and pulmonary dysfunction are prominent features of AFE. Dysrythmias such as pulseless electrical activity, bradycardia, ventricular fibrillation, and asystole are common. Rapid institution of high-quality CPR is critical to the survival of women with AFE.

Interventions often used in CPR of patients with AFE include initiation of high-quality chest compressions, early defibrillation if indicated, immediate administration of 100% oxygen by mask ventilation followed by early intubation, and rapid establishment of peripheral, arterial, and central venous access. Volume assessment, fluid replacement, and administration of vasopressors and inotropes are also important.

CPR of pregnant women requires special interventions, including maximal left lateral displacement of the uterus to reduce compression of the descending aorta and vena cava. Lateral displacement of the uterus can be accomplished by left lateral tilt or by manual uterine displacement. To optimize the effectiveness of chest compressions, many experts recommend placing the woman in a supine position and using manual uterine displacement rather than a left lateral tilt.⁵ For chest compressions, the hands should be placed just above the center of the sternum to adjust for the elevation of the diaphragm caused by the gravid uterus.

The gravid uterus can compromise the effectiveness of CPR. Fetal viability and neurologic outcome are best if delivery occurs within 5 minutes of the onset of cardiopulmonary arrest. If the gestational age of the fetus is consistent with extrauterine viability and initial CPR has not restored cardiac function, it is best to initiate fetal delivery within 4 minutes of the onset of cardiopulmonary arrest with the intent to deliver the fetus within 5 minutes.^6,7 If the fetus is beyond 20 weeks’ gestational age, delivery early in the course of CPR improves the effectiveness of maternal resuscitation and may increase the probability of maternal survival.

In one study of the response of anesthesiologists, obstetricians, and nurses to a simulated cardiac arrest caused by an AFE, the participants did not routinely use defibrillation when indicated, did not place a firm support under the back for chest compressions, and did not switch the provider of chest compressions every 2 minutes.⁸ This study indicates that additional training and routinely scheduled multidisciplinary simulation of the response to cardiopulmonary arrest could improve the quality of our CPR.

2. Use a massive transfusion protocol
Severe coagulopathy and diffuse bleeding are commonly encountered in AFE. Target goals for the replacement of blood products include:

• hemoglobin concentration ≥8 g/dL
• fibrinogen ≥150 to 200 mg/dL
• platelets ≥50,000/μL
• prothrombin time international normalized ratio (INR) ≤1.5.

Most massive transfusion protocols provide for the rapid delivery of 4 to 8 units of red blood cells and a similar number of units of fresh frozen plasma to the patient’s bedside. In the management of AFE, 20 to 30 units of red blood cells and a similar quantity of fresh frozen plasma may need to be transfused. Cryoprecipitate takes 20 to 30 minutes to thaw, so preparations to transfuse cryoprecipitate should be initiated as soon as the massive transfusion protocol is triggered. A case of AFE can completely empty the blood bank of all available blood products and necessitate the use of alternative agents.

Lyophilized fibrinogen concentrate (RiaSTAP) is approved by the US Food and Drug Administration for the treatment of congenital hypofibrinogenemia and also may be useful to replace fibrinogen in cases of AFE. In many hospitals, large quantities of fresh frozen plasma are not immediately available; lyophilized fibrinogen concentrate may be especially useful in these settings. Another advantage of fibrinogen concentrate is that large amounts of fibrinogen can be administered in a small volume of intravenous fluid. Fibrinogen concentrate typically is used at a dose of 70 mg/kg of body weight.^9,10

Intraoperative red cell salvage occasionally is used in cases of obstetric hemorrhage. In one case report of the use of red cell salvage with leukocyte depletion filtration during treatment of an AFE, acute hypotension developed in the patient after the transfusion of salvaged red cells.¹¹ This case report raises safety concerns about the use of salvaged cells in women with severe AFE.

Related article: 10 practical, evidence-based recommendations for the management of severe postpartum hemorrhage  Baha M. Sibai, MD (June 2011)

3. Treat diffuse bleeding and coagulopathy
In addition to the initiation of the massive transfusion protocol, additional treatments that may be helpful in managing the coagulopathy of AFE include tranexamic acid, recombinant factor VIIa (rFVIIa), and exchange transfusion.

AFE is often associated with hyperfibrinolysis, which can cause excessive bleeding.¹² Tranexamic acid blocks the lysine binding sites on plasminogen and thereby reduces the lysis of fibrin clots. Clinical trials in patients who have undergone trauma have demonstrated that the administration of tranexamic acid reduces blood loss.¹³ The dose of tranexamic acid is approximately 10 to 20 mg/kg of body weight, or approximately 1 g.

Controversy exists about the use of rFVIIa to treat the coagulopathy and bleeding caused by AFE. Some authorities believe that rFVIIa is associated with an increased AFE case fatality rate.¹⁴ Other authorities believe rFVIIa may be useful in the treatment of AFE coagulopathy, especially when bleeding persists despite aggressive blood and component replacement.”¹⁵ The dose of rFVIIa is approximately 90 µg/kg of body weight. rFVIIa is extremely expensive.

Exchange transfusion has been used successfully to treat AFE.¹⁶ In women with AFE, exchange transfusion removes circulating cells, cell fragments, and substances that trigger systemic anaphylaxis and coagulopathy, thereby enhancing rapid recovery.

Related article: Act fast when confronted by a coagulopathy postpartum Robert L. Barbieri, MD (Editorial; March 2012)

4. Treat uterine and pelvic bleeding
Obstetrician-gynecologists are experts in the control of uterine and pelvic bleeding. Interventions that commonly are used to control uterine and pelvic bleeding in cases of postpartum hemorrhage, uterine rupture, or placenta accreta also can be applied in cases of AFE with uncontrolled uterine and pelvic bleeding. These techniques include:

• use of uterine compression sutures
• the Bakri balloon
• a uterine tourniquet
• vascular clamps on the ovarian vessels.^17,18

In many cases of AFE, total or supracervical hysterectomy is necessary to control uterine bleeding. Uterine artery embolization, if available, has been reported to be helpful in select cases. However, many women with AFE are too unstable to survive transfer to an interventional radiology suite. Additional interventions to control bleeding include hypogastric artery ligation, infrarenal aortic compression, and pelvic packing.

Cross-clamping the aorta below the renal vessels can reduce blood flow to the pelvis and provide time for cardiopulmonary and volume resuscitation. Alternatively, placing pressure on the infrarenal aorta with a sponge or directly by hand can help reduce blood flow to the pelvis.¹⁹

In many cases of AFE, pelvic hemorrhage is difficult to control. Even if surgical pedicles are ligated securely, the coagulopathy of AFE may cause persistent oozing from areas of minor tissue trauma. Uncontrolled blood loss can be a proximate cause of death in women with AFE. All written protocols for responding to an AFE should include a plan to use pelvic packing for patients in whom standard operative procedures do not produce adequate control of bleeding. A “mushroom,” “parachute,” or “umbrella” pack has been reported to help stabilize the severely ill patient with pelvic bleeding and permit effective resuscitation and blood product replacement.²⁰

Related articles:
A stitch in time: The B-Lynch, Hayman and Pereira uterine compression sutures Robert L. Barbieri, MD (Editorial, December 2012)
Have you made the best use of the Bakri balloon in PPH? Robert L. Barbieri, MD (Editorial, July 2011)

5. Consider extracorporeal lung and heart support
In many cases of AFE, both lung and cardiac function are severely compromised. Both veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and full cardiopulmonary bypass provide support for the failing lung and heart. Based on a small number of case reports, extracorporeal lung and heart support appear to be useful in the treatment of AFE.^21–26 Using the Seldinger technique,²⁷ it is technically feasible to rapidly access a major vein and artery to provide the input and output ports for VA-ECMO. Unlike the cardiopulmonary bypass pump, the VA-ECMO pump does not have a reservoir that needs to be primed with blood and is smaller and more portable. To provide a patient with VA-ECMO or cardiopulmonary bypass, a cardiac interventionist and a perfusionist must be available. Extracorporeal lung and heart support require heparinization of the patient’s blood, which may result in increased bleeding. Both VA-ECMO and cardiopulmonary bypass, along with the diseases for which they are used, may cause renal dysfunction, neurologic injury, and infection.²⁸

Alternative approaches that provide support of the heart—but not lung—are the Impella pump, TandemHeart, and the intra-aortic balloon pump. An alternative that provides lung support—but not cardiac support—is veno-venous ECMO.

In developing a written protocol for responding to an AFE, obstetricians should explore the potential availability of VA-ECMO, cardiopulmonary bypass, or other cardiopulmonary support devices as options for patients who have not responded to standard treatment of AFE and are at high risk of death.

6. Post-AFE intensive care
After stabilization, most women with AFE will require intensive care for 48 to 96 hours. Some experts have proposed that all survivors of cardiopulmonary arrest who are successfully resuscitated and stabilized be transferred to hospitals that specialize in post−cardiac arrest care to improve outcomes.

Assessment of organ injury is important after an AFE. In addition, encephalopathy is a common complication of AFE, and sequential neurologic examination is a priority. Therapeutic hypothermia (TH) may help to preserve neurologic function after AFE.²⁹ However, TH may cause a mild coagulopathy by inhibiting platelet activation and enzyme activity of clotting factors. Because coagulopathy is a prominent feature of AFE, TH may be contraindicated if the patient has a clinically significant baseline coagulopathy.³⁰

DEVELOP AN AFE PROTOCOL AND PRACTICE THE COMPONENTS
Practicing the components of obstetric protocols can improve unit performance and patient outcomes.³¹ The components of an AFE protocol, as described in this article, include high-quality CPR, a protocol for massive transfusion, treatment of diffuse bleeding and coagulopathy, treatment of uterine and pelvic bleeding, extracorporeal lung and heart support, and post-AFE intensive care. Practicing these components of an AFE protocol will enhance performance across many common obstetric complications including postpartum hemorrhage, uterine rupture, placenta accreta, and pulmonary embolism.

When Chesley “Sully” Sullenberger and his copilot landed Flight 1549 in the Hudson River in New York, he had never practiced that specific response to twin engine failure, but he had practiced many emergency responses involving related scenarios. The combination of exceptional flight experience and years of practicing the response to emergency scenarios in simulation exercises permitted him and his copilot to execute a uniquely clever plan to solve a life-threatening
emergency. In a related way, practicing the components of AFE treatment will help obstetricians, obstetric anesthesiologists, and their multidisciplinary team to improve the responses to all major obstetric emergencies. 

INSTANT POLL
Does your obstetric unit have a written protocol for treating an amniotic fluid embolism (AFE)? Has your obstetric unit practiced any of the components of the AFE treatment protocol: 1) high-quality cardiopulmonary resuscitation, 2) a protocol for massive transfusion protocol, 3) treatment of diffuse bleeding and coagulopathy, 4) treatment of uterine and pelvic bleeding, 5) extracorporeal lung and heart support, and 6) post-AFE intensive care?
Tell us—at rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Amniotic fluid embolism (AFE) occurs in about 1 in 20,000 to 1 in 40,000 deliveries.^1,2 Although the condition is rare, the case fatality rate is high, and AFE is a common cause of maternal death in developed countries. AFE cannot be predicted or prevented. Moreover, the condition is difficult to precisely define and is often a diagnosis of exclusion.

AFE should be considered in the differential diagnosis of a pregnant woman with sudden onset of shortness of breath, hypotension, or cardiac arrhythmia or arrest, followed by coagulopathy and hemorrhage. Premonitory symptoms, including restlessness, confusion, disorientation, agitation, chills, nausea, numbness, and tingling, are commonly reported just before the cardiorespiratory collapse. AFE is less likely if the initial obstetric event is hemorrhage in the absence of cardiorespiratory compromise or a preceding coagulopathy.³

Typically, the onset is just before birth, during birth, or within the first few hours after delivery. In the United Kingdom, which has a robust centralized registry for reporting AFE, about 56% of cases occur before birth and 44% after birth.⁴

Related article: Is the incidence of amniotic fluid embolism rising? John T. Repke, MD (Examining the Evidence, August 2010)

The resources available to obstetric units vary greatly. Each unit needs to assess its resources and develop an AFE treatment protocol that builds on the unique strengths of the unit. Treatment of AFE requires the coordinated actions of anesthesiologists, obstetricians, nurses, the blood bank, pharmacy, and cardiovascular specialists. Coordinated activity among the members of such a large multidisciplinary team requires a written protocol that is practiced on a regular basis.

Six important components of a multidisciplinary response to AFE treatment protocol are:

1. high-quality cardiopulmonary resuscitation (CPR)
2. a protocol for massive transfusion
3. treatment of diffuse bleeding and coagulopathy
4. treatment of uterine and pelvic bleeding
5. extracorporeal lung and heart support
6. post-AFE intensive care.

1. Initiate high-quality CPR
Hypotension and hypoxemia due to cardiac and pulmonary dysfunction are prominent features of AFE. Dysrythmias such as pulseless electrical activity, bradycardia, ventricular fibrillation, and asystole are common. Rapid institution of high-quality CPR is critical to the survival of women with AFE.

Interventions often used in CPR of patients with AFE include initiation of high-quality chest compressions, early defibrillation if indicated, immediate administration of 100% oxygen by mask ventilation followed by early intubation, and rapid establishment of peripheral, arterial, and central venous access. Volume assessment, fluid replacement, and administration of vasopressors and inotropes are also important.

CPR of pregnant women requires special interventions, including maximal left lateral displacement of the uterus to reduce compression of the descending aorta and vena cava. Lateral displacement of the uterus can be accomplished by left lateral tilt or by manual uterine displacement. To optimize the effectiveness of chest compressions, many experts recommend placing the woman in a supine position and using manual uterine displacement rather than a left lateral tilt.⁵ For chest compressions, the hands should be placed just above the center of the sternum to adjust for the elevation of the diaphragm caused by the gravid uterus.

The gravid uterus can compromise the effectiveness of CPR. Fetal viability and neurologic outcome are best if delivery occurs within 5 minutes of the onset of cardiopulmonary arrest. If the gestational age of the fetus is consistent with extrauterine viability and initial CPR has not restored cardiac function, it is best to initiate fetal delivery within 4 minutes of the onset of cardiopulmonary arrest with the intent to deliver the fetus within 5 minutes.^6,7 If the fetus is beyond 20 weeks’ gestational age, delivery early in the course of CPR improves the effectiveness of maternal resuscitation and may increase the probability of maternal survival.

In one study of the response of anesthesiologists, obstetricians, and nurses to a simulated cardiac arrest caused by an AFE, the participants did not routinely use defibrillation when indicated, did not place a firm support under the back for chest compressions, and did not switch the provider of chest compressions every 2 minutes.⁸ This study indicates that additional training and routinely scheduled multidisciplinary simulation of the response to cardiopulmonary arrest could improve the quality of our CPR.

2. Use a massive transfusion protocol
Severe coagulopathy and diffuse bleeding are commonly encountered in AFE. Target goals for the replacement of blood products include:

• hemoglobin concentration ≥8 g/dL
• fibrinogen ≥150 to 200 mg/dL
• platelets ≥50,000/μL
• prothrombin time international normalized ratio (INR) ≤1.5.

Most massive transfusion protocols provide for the rapid delivery of 4 to 8 units of red blood cells and a similar number of units of fresh frozen plasma to the patient’s bedside. In the management of AFE, 20 to 30 units of red blood cells and a similar quantity of fresh frozen plasma may need to be transfused. Cryoprecipitate takes 20 to 30 minutes to thaw, so preparations to transfuse cryoprecipitate should be initiated as soon as the massive transfusion protocol is triggered. A case of AFE can completely empty the blood bank of all available blood products and necessitate the use of alternative agents.

Lyophilized fibrinogen concentrate (RiaSTAP) is approved by the US Food and Drug Administration for the treatment of congenital hypofibrinogenemia and also may be useful to replace fibrinogen in cases of AFE. In many hospitals, large quantities of fresh frozen plasma are not immediately available; lyophilized fibrinogen concentrate may be especially useful in these settings. Another advantage of fibrinogen concentrate is that large amounts of fibrinogen can be administered in a small volume of intravenous fluid. Fibrinogen concentrate typically is used at a dose of 70 mg/kg of body weight.^9,10

Intraoperative red cell salvage occasionally is used in cases of obstetric hemorrhage. In one case report of the use of red cell salvage with leukocyte depletion filtration during treatment of an AFE, acute hypotension developed in the patient after the transfusion of salvaged red cells.¹¹ This case report raises safety concerns about the use of salvaged cells in women with severe AFE.

Related article: 10 practical, evidence-based recommendations for the management of severe postpartum hemorrhage  Baha M. Sibai, MD (June 2011)

3. Treat diffuse bleeding and coagulopathy
In addition to the initiation of the massive transfusion protocol, additional treatments that may be helpful in managing the coagulopathy of AFE include tranexamic acid, recombinant factor VIIa (rFVIIa), and exchange transfusion.

AFE is often associated with hyperfibrinolysis, which can cause excessive bleeding.¹² Tranexamic acid blocks the lysine binding sites on plasminogen and thereby reduces the lysis of fibrin clots. Clinical trials in patients who have undergone trauma have demonstrated that the administration of tranexamic acid reduces blood loss.¹³ The dose of tranexamic acid is approximately 10 to 20 mg/kg of body weight, or approximately 1 g.

Controversy exists about the use of rFVIIa to treat the coagulopathy and bleeding caused by AFE. Some authorities believe that rFVIIa is associated with an increased AFE case fatality rate.¹⁴ Other authorities believe rFVIIa may be useful in the treatment of AFE coagulopathy, especially when bleeding persists despite aggressive blood and component replacement.”¹⁵ The dose of rFVIIa is approximately 90 µg/kg of body weight. rFVIIa is extremely expensive.

Exchange transfusion has been used successfully to treat AFE.¹⁶ In women with AFE, exchange transfusion removes circulating cells, cell fragments, and substances that trigger systemic anaphylaxis and coagulopathy, thereby enhancing rapid recovery.

Related article: Act fast when confronted by a coagulopathy postpartum Robert L. Barbieri, MD (Editorial; March 2012)

4. Treat uterine and pelvic bleeding
Obstetrician-gynecologists are experts in the control of uterine and pelvic bleeding. Interventions that commonly are used to control uterine and pelvic bleeding in cases of postpartum hemorrhage, uterine rupture, or placenta accreta also can be applied in cases of AFE with uncontrolled uterine and pelvic bleeding. These techniques include:

• use of uterine compression sutures
• the Bakri balloon
• a uterine tourniquet
• vascular clamps on the ovarian vessels.^17,18

In many cases of AFE, total or supracervical hysterectomy is necessary to control uterine bleeding. Uterine artery embolization, if available, has been reported to be helpful in select cases. However, many women with AFE are too unstable to survive transfer to an interventional radiology suite. Additional interventions to control bleeding include hypogastric artery ligation, infrarenal aortic compression, and pelvic packing.

Cross-clamping the aorta below the renal vessels can reduce blood flow to the pelvis and provide time for cardiopulmonary and volume resuscitation. Alternatively, placing pressure on the infrarenal aorta with a sponge or directly by hand can help reduce blood flow to the pelvis.¹⁹

In many cases of AFE, pelvic hemorrhage is difficult to control. Even if surgical pedicles are ligated securely, the coagulopathy of AFE may cause persistent oozing from areas of minor tissue trauma. Uncontrolled blood loss can be a proximate cause of death in women with AFE. All written protocols for responding to an AFE should include a plan to use pelvic packing for patients in whom standard operative procedures do not produce adequate control of bleeding. A “mushroom,” “parachute,” or “umbrella” pack has been reported to help stabilize the severely ill patient with pelvic bleeding and permit effective resuscitation and blood product replacement.²⁰

Related articles:
A stitch in time: The B-Lynch, Hayman and Pereira uterine compression sutures Robert L. Barbieri, MD (Editorial, December 2012)
Have you made the best use of the Bakri balloon in PPH? Robert L. Barbieri, MD (Editorial, July 2011)

5. Consider extracorporeal lung and heart support
In many cases of AFE, both lung and cardiac function are severely compromised. Both veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and full cardiopulmonary bypass provide support for the failing lung and heart. Based on a small number of case reports, extracorporeal lung and heart support appear to be useful in the treatment of AFE.^21–26 Using the Seldinger technique,²⁷ it is technically feasible to rapidly access a major vein and artery to provide the input and output ports for VA-ECMO. Unlike the cardiopulmonary bypass pump, the VA-ECMO pump does not have a reservoir that needs to be primed with blood and is smaller and more portable. To provide a patient with VA-ECMO or cardiopulmonary bypass, a cardiac interventionist and a perfusionist must be available. Extracorporeal lung and heart support require heparinization of the patient’s blood, which may result in increased bleeding. Both VA-ECMO and cardiopulmonary bypass, along with the diseases for which they are used, may cause renal dysfunction, neurologic injury, and infection.²⁸

Alternative approaches that provide support of the heart—but not lung—are the Impella pump, TandemHeart, and the intra-aortic balloon pump. An alternative that provides lung support—but not cardiac support—is veno-venous ECMO.

In developing a written protocol for responding to an AFE, obstetricians should explore the potential availability of VA-ECMO, cardiopulmonary bypass, or other cardiopulmonary support devices as options for patients who have not responded to standard treatment of AFE and are at high risk of death.

6. Post-AFE intensive care
After stabilization, most women with AFE will require intensive care for 48 to 96 hours. Some experts have proposed that all survivors of cardiopulmonary arrest who are successfully resuscitated and stabilized be transferred to hospitals that specialize in post−cardiac arrest care to improve outcomes.

Assessment of organ injury is important after an AFE. In addition, encephalopathy is a common complication of AFE, and sequential neurologic examination is a priority. Therapeutic hypothermia (TH) may help to preserve neurologic function after AFE.²⁹ However, TH may cause a mild coagulopathy by inhibiting platelet activation and enzyme activity of clotting factors. Because coagulopathy is a prominent feature of AFE, TH may be contraindicated if the patient has a clinically significant baseline coagulopathy.³⁰

DEVELOP AN AFE PROTOCOL AND PRACTICE THE COMPONENTS
Practicing the components of obstetric protocols can improve unit performance and patient outcomes.³¹ The components of an AFE protocol, as described in this article, include high-quality CPR, a protocol for massive transfusion, treatment of diffuse bleeding and coagulopathy, treatment of uterine and pelvic bleeding, extracorporeal lung and heart support, and post-AFE intensive care. Practicing these components of an AFE protocol will enhance performance across many common obstetric complications including postpartum hemorrhage, uterine rupture, placenta accreta, and pulmonary embolism.

When Chesley “Sully” Sullenberger and his copilot landed Flight 1549 in the Hudson River in New York, he had never practiced that specific response to twin engine failure, but he had practiced many emergency responses involving related scenarios. The combination of exceptional flight experience and years of practicing the response to emergency scenarios in simulation exercises permitted him and his copilot to execute a uniquely clever plan to solve a life-threatening
emergency. In a related way, practicing the components of AFE treatment will help obstetricians, obstetric anesthesiologists, and their multidisciplinary team to improve the responses to all major obstetric emergencies. 

INSTANT POLL
Does your obstetric unit have a written protocol for treating an amniotic fluid embolism (AFE)? Has your obstetric unit practiced any of the components of the AFE treatment protocol: 1) high-quality cardiopulmonary resuscitation, 2) a protocol for massive transfusion protocol, 3) treatment of diffuse bleeding and coagulopathy, 4) treatment of uterine and pelvic bleeding, 5) extracorporeal lung and heart support, and 6) post-AFE intensive care?
Tell us—at rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Amniotic fluid embolism (AFE) occurs in about 1 in 20,000 to 1 in 40,000 deliveries.^1,2 Although the condition is rare, the case fatality rate is high, and AFE is a common cause of maternal death in developed countries. AFE cannot be predicted or prevented. Moreover, the condition is difficult to precisely define and is often a diagnosis of exclusion.

AFE should be considered in the differential diagnosis of a pregnant woman with sudden onset of shortness of breath, hypotension, or cardiac arrhythmia or arrest, followed by coagulopathy and hemorrhage. Premonitory symptoms, including restlessness, confusion, disorientation, agitation, chills, nausea, numbness, and tingling, are commonly reported just before the cardiorespiratory collapse. AFE is less likely if the initial obstetric event is hemorrhage in the absence of cardiorespiratory compromise or a preceding coagulopathy.³

Typically, the onset is just before birth, during birth, or within the first few hours after delivery. In the United Kingdom, which has a robust centralized registry for reporting AFE, about 56% of cases occur before birth and 44% after birth.⁴

Related article: Is the incidence of amniotic fluid embolism rising? John T. Repke, MD (Examining the Evidence, August 2010)

The resources available to obstetric units vary greatly. Each unit needs to assess its resources and develop an AFE treatment protocol that builds on the unique strengths of the unit. Treatment of AFE requires the coordinated actions of anesthesiologists, obstetricians, nurses, the blood bank, pharmacy, and cardiovascular specialists. Coordinated activity among the members of such a large multidisciplinary team requires a written protocol that is practiced on a regular basis.

Six important components of a multidisciplinary response to AFE treatment protocol are:

1. high-quality cardiopulmonary resuscitation (CPR)
2. a protocol for massive transfusion
3. treatment of diffuse bleeding and coagulopathy
4. treatment of uterine and pelvic bleeding
5. extracorporeal lung and heart support
6. post-AFE intensive care.

1. Initiate high-quality CPR
Hypotension and hypoxemia due to cardiac and pulmonary dysfunction are prominent features of AFE. Dysrythmias such as pulseless electrical activity, bradycardia, ventricular fibrillation, and asystole are common. Rapid institution of high-quality CPR is critical to the survival of women with AFE.

Interventions often used in CPR of patients with AFE include initiation of high-quality chest compressions, early defibrillation if indicated, immediate administration of 100% oxygen by mask ventilation followed by early intubation, and rapid establishment of peripheral, arterial, and central venous access. Volume assessment, fluid replacement, and administration of vasopressors and inotropes are also important.

CPR of pregnant women requires special interventions, including maximal left lateral displacement of the uterus to reduce compression of the descending aorta and vena cava. Lateral displacement of the uterus can be accomplished by left lateral tilt or by manual uterine displacement. To optimize the effectiveness of chest compressions, many experts recommend placing the woman in a supine position and using manual uterine displacement rather than a left lateral tilt.⁵ For chest compressions, the hands should be placed just above the center of the sternum to adjust for the elevation of the diaphragm caused by the gravid uterus.

The gravid uterus can compromise the effectiveness of CPR. Fetal viability and neurologic outcome are best if delivery occurs within 5 minutes of the onset of cardiopulmonary arrest. If the gestational age of the fetus is consistent with extrauterine viability and initial CPR has not restored cardiac function, it is best to initiate fetal delivery within 4 minutes of the onset of cardiopulmonary arrest with the intent to deliver the fetus within 5 minutes.^6,7 If the fetus is beyond 20 weeks’ gestational age, delivery early in the course of CPR improves the effectiveness of maternal resuscitation and may increase the probability of maternal survival.

In one study of the response of anesthesiologists, obstetricians, and nurses to a simulated cardiac arrest caused by an AFE, the participants did not routinely use defibrillation when indicated, did not place a firm support under the back for chest compressions, and did not switch the provider of chest compressions every 2 minutes.⁸ This study indicates that additional training and routinely scheduled multidisciplinary simulation of the response to cardiopulmonary arrest could improve the quality of our CPR.

2. Use a massive transfusion protocol
Severe coagulopathy and diffuse bleeding are commonly encountered in AFE. Target goals for the replacement of blood products include:

• hemoglobin concentration ≥8 g/dL
• fibrinogen ≥150 to 200 mg/dL
• platelets ≥50,000/μL
• prothrombin time international normalized ratio (INR) ≤1.5.

Most massive transfusion protocols provide for the rapid delivery of 4 to 8 units of red blood cells and a similar number of units of fresh frozen plasma to the patient’s bedside. In the management of AFE, 20 to 30 units of red blood cells and a similar quantity of fresh frozen plasma may need to be transfused. Cryoprecipitate takes 20 to 30 minutes to thaw, so preparations to transfuse cryoprecipitate should be initiated as soon as the massive transfusion protocol is triggered. A case of AFE can completely empty the blood bank of all available blood products and necessitate the use of alternative agents.

Lyophilized fibrinogen concentrate (RiaSTAP) is approved by the US Food and Drug Administration for the treatment of congenital hypofibrinogenemia and also may be useful to replace fibrinogen in cases of AFE. In many hospitals, large quantities of fresh frozen plasma are not immediately available; lyophilized fibrinogen concentrate may be especially useful in these settings. Another advantage of fibrinogen concentrate is that large amounts of fibrinogen can be administered in a small volume of intravenous fluid. Fibrinogen concentrate typically is used at a dose of 70 mg/kg of body weight.^9,10

Intraoperative red cell salvage occasionally is used in cases of obstetric hemorrhage. In one case report of the use of red cell salvage with leukocyte depletion filtration during treatment of an AFE, acute hypotension developed in the patient after the transfusion of salvaged red cells.¹¹ This case report raises safety concerns about the use of salvaged cells in women with severe AFE.

Related article: 10 practical, evidence-based recommendations for the management of severe postpartum hemorrhage  Baha M. Sibai, MD (June 2011)

3. Treat diffuse bleeding and coagulopathy
In addition to the initiation of the massive transfusion protocol, additional treatments that may be helpful in managing the coagulopathy of AFE include tranexamic acid, recombinant factor VIIa (rFVIIa), and exchange transfusion.

AFE is often associated with hyperfibrinolysis, which can cause excessive bleeding.¹² Tranexamic acid blocks the lysine binding sites on plasminogen and thereby reduces the lysis of fibrin clots. Clinical trials in patients who have undergone trauma have demonstrated that the administration of tranexamic acid reduces blood loss.¹³ The dose of tranexamic acid is approximately 10 to 20 mg/kg of body weight, or approximately 1 g.

Controversy exists about the use of rFVIIa to treat the coagulopathy and bleeding caused by AFE. Some authorities believe that rFVIIa is associated with an increased AFE case fatality rate.¹⁴ Other authorities believe rFVIIa may be useful in the treatment of AFE coagulopathy, especially when bleeding persists despite aggressive blood and component replacement.”¹⁵ The dose of rFVIIa is approximately 90 µg/kg of body weight. rFVIIa is extremely expensive.

Exchange transfusion has been used successfully to treat AFE.¹⁶ In women with AFE, exchange transfusion removes circulating cells, cell fragments, and substances that trigger systemic anaphylaxis and coagulopathy, thereby enhancing rapid recovery.

Related article: Act fast when confronted by a coagulopathy postpartum Robert L. Barbieri, MD (Editorial; March 2012)

4. Treat uterine and pelvic bleeding
Obstetrician-gynecologists are experts in the control of uterine and pelvic bleeding. Interventions that commonly are used to control uterine and pelvic bleeding in cases of postpartum hemorrhage, uterine rupture, or placenta accreta also can be applied in cases of AFE with uncontrolled uterine and pelvic bleeding. These techniques include:

• use of uterine compression sutures
• the Bakri balloon
• a uterine tourniquet
• vascular clamps on the ovarian vessels.^17,18

In many cases of AFE, total or supracervical hysterectomy is necessary to control uterine bleeding. Uterine artery embolization, if available, has been reported to be helpful in select cases. However, many women with AFE are too unstable to survive transfer to an interventional radiology suite. Additional interventions to control bleeding include hypogastric artery ligation, infrarenal aortic compression, and pelvic packing.

Cross-clamping the aorta below the renal vessels can reduce blood flow to the pelvis and provide time for cardiopulmonary and volume resuscitation. Alternatively, placing pressure on the infrarenal aorta with a sponge or directly by hand can help reduce blood flow to the pelvis.¹⁹

In many cases of AFE, pelvic hemorrhage is difficult to control. Even if surgical pedicles are ligated securely, the coagulopathy of AFE may cause persistent oozing from areas of minor tissue trauma. Uncontrolled blood loss can be a proximate cause of death in women with AFE. All written protocols for responding to an AFE should include a plan to use pelvic packing for patients in whom standard operative procedures do not produce adequate control of bleeding. A “mushroom,” “parachute,” or “umbrella” pack has been reported to help stabilize the severely ill patient with pelvic bleeding and permit effective resuscitation and blood product replacement.²⁰

Related articles:
A stitch in time: The B-Lynch, Hayman and Pereira uterine compression sutures Robert L. Barbieri, MD (Editorial, December 2012)
Have you made the best use of the Bakri balloon in PPH? Robert L. Barbieri, MD (Editorial, July 2011)

5. Consider extracorporeal lung and heart support
In many cases of AFE, both lung and cardiac function are severely compromised. Both veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and full cardiopulmonary bypass provide support for the failing lung and heart. Based on a small number of case reports, extracorporeal lung and heart support appear to be useful in the treatment of AFE.^21–26 Using the Seldinger technique,²⁷ it is technically feasible to rapidly access a major vein and artery to provide the input and output ports for VA-ECMO. Unlike the cardiopulmonary bypass pump, the VA-ECMO pump does not have a reservoir that needs to be primed with blood and is smaller and more portable. To provide a patient with VA-ECMO or cardiopulmonary bypass, a cardiac interventionist and a perfusionist must be available. Extracorporeal lung and heart support require heparinization of the patient’s blood, which may result in increased bleeding. Both VA-ECMO and cardiopulmonary bypass, along with the diseases for which they are used, may cause renal dysfunction, neurologic injury, and infection.²⁸

Alternative approaches that provide support of the heart—but not lung—are the Impella pump, TandemHeart, and the intra-aortic balloon pump. An alternative that provides lung support—but not cardiac support—is veno-venous ECMO.

In developing a written protocol for responding to an AFE, obstetricians should explore the potential availability of VA-ECMO, cardiopulmonary bypass, or other cardiopulmonary support devices as options for patients who have not responded to standard treatment of AFE and are at high risk of death.

6. Post-AFE intensive care
After stabilization, most women with AFE will require intensive care for 48 to 96 hours. Some experts have proposed that all survivors of cardiopulmonary arrest who are successfully resuscitated and stabilized be transferred to hospitals that specialize in post−cardiac arrest care to improve outcomes.

Assessment of organ injury is important after an AFE. In addition, encephalopathy is a common complication of AFE, and sequential neurologic examination is a priority. Therapeutic hypothermia (TH) may help to preserve neurologic function after AFE.²⁹ However, TH may cause a mild coagulopathy by inhibiting platelet activation and enzyme activity of clotting factors. Because coagulopathy is a prominent feature of AFE, TH may be contraindicated if the patient has a clinically significant baseline coagulopathy.³⁰

DEVELOP AN AFE PROTOCOL AND PRACTICE THE COMPONENTS
Practicing the components of obstetric protocols can improve unit performance and patient outcomes.³¹ The components of an AFE protocol, as described in this article, include high-quality CPR, a protocol for massive transfusion, treatment of diffuse bleeding and coagulopathy, treatment of uterine and pelvic bleeding, extracorporeal lung and heart support, and post-AFE intensive care. Practicing these components of an AFE protocol will enhance performance across many common obstetric complications including postpartum hemorrhage, uterine rupture, placenta accreta, and pulmonary embolism.

When Chesley “Sully” Sullenberger and his copilot landed Flight 1549 in the Hudson River in New York, he had never practiced that specific response to twin engine failure, but he had practiced many emergency responses involving related scenarios. The combination of exceptional flight experience and years of practicing the response to emergency scenarios in simulation exercises permitted him and his copilot to execute a uniquely clever plan to solve a life-threatening
emergency. In a related way, practicing the components of AFE treatment will help obstetricians, obstetric anesthesiologists, and their multidisciplinary team to improve the responses to all major obstetric emergencies. 

INSTANT POLL
Does your obstetric unit have a written protocol for treating an amniotic fluid embolism (AFE)? Has your obstetric unit practiced any of the components of the AFE treatment protocol: 1) high-quality cardiopulmonary resuscitation, 2) a protocol for massive transfusion protocol, 3) treatment of diffuse bleeding and coagulopathy, 4) treatment of uterine and pelvic bleeding, 5) extracorporeal lung and heart support, and 6) post-AFE intensive care?
Tell us—at rbarbieri@frontlinemedcom.com. Please include your name and the city and state in which you practice.

Along with many others who are rapidly fading from the American surgical scene, I was born as a baby boomer. Most of us from that generation who embraced surgery as a career held fast to the values of the era. First and foremost among these was a high premium put on hard work, long hours, and an unwavering dedication to our profession and to our patients. We were particularly proud of the continuity of care that we provided to our patients.

During my early years as a surgeon, it was a 24/7 job. Saturday mornings were consumed by Surgery Grand Rounds followed by usually prolonged and detailed patient rounds. Most of us visited our hospitalized patients 7 days a week. When one of my patients developed a complication, I, rather than the surgeon on call, managed it. I missed soccer matches, baseball games, dance recitals, and even some family birthdays because etched into my conscience was the concept that duty to my patients trumped duty to my family. Although there is much to admire in this singular focus on patient care, it took its toll on the other aspects of what should be a more balanced professional life.

Two factors, one of them cultural and the other regulatory, have altered this all-consuming aspect of a surgeon’s life, with implications for the ideal of continuity of care. First was the arrival of freshly minted surgeons from generations X and Y who had a different set of priorities than their predecessors. They insisted on a more even balance between professional and family obligations. In part this resulted from the need for them to be more involved in child rearing since many of their spouses were engaged in time-intensive careers of their own. As they gravitated onto academic surgical faculties and joined private practice groups, they insisted on moving educational programs such as Surgery Grand Rounds to weekdays so they could participate in family activities. They entrusted the care of their patients to their partners, freeing them for entire weekends that could be devoted to family events.

The healthier balance they have brought to a career in surgery is to be admired. Much to the benefit of their senior colleagues, it has become their way of life as well. The trade-off has been some decay of the ideals of patient ownership and continuity of care.

The next and potentially more serious challenge to the cherished concept of continuous care of our patients was the mandate of an 80-hour work week by the Accreditation Council for Graduate Medical Education (ACGME) in 2003. As to its effects on graduate surgical education, I believe the 80-hour work week has been a double-edged sword. On the positive side, at a time when interest in general surgery was waning, institution of duty hours restrictions along with the advent of minimally invasive surgery made our specialty more attractive to medical school graduates, including women, who now constitute 50% of most medical school classes. Another plus was that teaching hospitals were forced to hire physician extenders and other personnel to perform some of the noneducational tasks previously carried out by residents.

On the negative side, since many of the lost hours were in the evenings and weekends, residents’ exposure to urgent and emergency cases was diminished. More significantly, surgery residents began to work in shifts to accommodate increasingly inflexible rules. Ownership of their patients could no longer be held as a high priority in surgical education. Several classes of surgery residents who were educated under these fairly restrictive guidelines have now graduated and have brought a "shift mentality" with them to their positions in private practice groups and on academic faculties.

Since work hour restrictions are highly unlikely to disappear from our training programs and may in fact be applied in the future to all working physicians and surgeons, what can be done to preserve the time-honored value of continuous care of our patients? The answer probably lies in seeking reasonable flexibility within the rules rather than elimination of them. A bright light in this regard is an upcoming randomized controlled trial to assess the feasibility of more flexible work hours rules for general surgery residents. This trial is sponsored by the American Board of Surgery and the American College of Surgeons, and has the support of the ACGME. It will be conducted in hospitals that have instituted the National Surgical Quality Improvement Program (NSQIP) and also sponsor general surgery residencies. Beginning in July 2014, these residencies will be randomized to one of two arms – one using the extensive and rigid present duty hour standards and the second utilizing more flexible standards limited to an 80-hour work week, one night in three on call, and one day in seven free of clinical responsibilities, all averaged over a month. Patient outcomes in each arm will be determined from NSQIP data.

The trial will be conducted over 1 year, with residents’ opinions being surveyed at its midpoint. If patient outcomes are similar in the two arms or superior in the arm with more flexible rules and resident opinion is favorable, this would lend strong support for more flexibility in all general surgery residencies. As of this date, more than 100 general surgery programs have agreed to randomization.

The sponsoring agencies are to be congratulated for designing a trial that for the first time will objectively evaluate just how restrictive work rules need to be. Their efforts may effectively preserve a value that is at the core of our profession – the continuous care of our surgical patients.

Dr. Rikkers is the Editor in Chief of ACS Surgery News.

Along with many others who are rapidly fading from the American surgical scene, I was born as a baby boomer. Most of us from that generation who embraced surgery as a career held fast to the values of the era. First and foremost among these was a high premium put on hard work, long hours, and an unwavering dedication to our profession and to our patients. We were particularly proud of the continuity of care that we provided to our patients.

During my early years as a surgeon, it was a 24/7 job. Saturday mornings were consumed by Surgery Grand Rounds followed by usually prolonged and detailed patient rounds. Most of us visited our hospitalized patients 7 days a week. When one of my patients developed a complication, I, rather than the surgeon on call, managed it. I missed soccer matches, baseball games, dance recitals, and even some family birthdays because etched into my conscience was the concept that duty to my patients trumped duty to my family. Although there is much to admire in this singular focus on patient care, it took its toll on the other aspects of what should be a more balanced professional life.

Two factors, one of them cultural and the other regulatory, have altered this all-consuming aspect of a surgeon’s life, with implications for the ideal of continuity of care. First was the arrival of freshly minted surgeons from generations X and Y who had a different set of priorities than their predecessors. They insisted on a more even balance between professional and family obligations. In part this resulted from the need for them to be more involved in child rearing since many of their spouses were engaged in time-intensive careers of their own. As they gravitated onto academic surgical faculties and joined private practice groups, they insisted on moving educational programs such as Surgery Grand Rounds to weekdays so they could participate in family activities. They entrusted the care of their patients to their partners, freeing them for entire weekends that could be devoted to family events.

The healthier balance they have brought to a career in surgery is to be admired. Much to the benefit of their senior colleagues, it has become their way of life as well. The trade-off has been some decay of the ideals of patient ownership and continuity of care.

The next and potentially more serious challenge to the cherished concept of continuous care of our patients was the mandate of an 80-hour work week by the Accreditation Council for Graduate Medical Education (ACGME) in 2003. As to its effects on graduate surgical education, I believe the 80-hour work week has been a double-edged sword. On the positive side, at a time when interest in general surgery was waning, institution of duty hours restrictions along with the advent of minimally invasive surgery made our specialty more attractive to medical school graduates, including women, who now constitute 50% of most medical school classes. Another plus was that teaching hospitals were forced to hire physician extenders and other personnel to perform some of the noneducational tasks previously carried out by residents.

On the negative side, since many of the lost hours were in the evenings and weekends, residents’ exposure to urgent and emergency cases was diminished. More significantly, surgery residents began to work in shifts to accommodate increasingly inflexible rules. Ownership of their patients could no longer be held as a high priority in surgical education. Several classes of surgery residents who were educated under these fairly restrictive guidelines have now graduated and have brought a "shift mentality" with them to their positions in private practice groups and on academic faculties.

Since work hour restrictions are highly unlikely to disappear from our training programs and may in fact be applied in the future to all working physicians and surgeons, what can be done to preserve the time-honored value of continuous care of our patients? The answer probably lies in seeking reasonable flexibility within the rules rather than elimination of them. A bright light in this regard is an upcoming randomized controlled trial to assess the feasibility of more flexible work hours rules for general surgery residents. This trial is sponsored by the American Board of Surgery and the American College of Surgeons, and has the support of the ACGME. It will be conducted in hospitals that have instituted the National Surgical Quality Improvement Program (NSQIP) and also sponsor general surgery residencies. Beginning in July 2014, these residencies will be randomized to one of two arms – one using the extensive and rigid present duty hour standards and the second utilizing more flexible standards limited to an 80-hour work week, one night in three on call, and one day in seven free of clinical responsibilities, all averaged over a month. Patient outcomes in each arm will be determined from NSQIP data.

The trial will be conducted over 1 year, with residents’ opinions being surveyed at its midpoint. If patient outcomes are similar in the two arms or superior in the arm with more flexible rules and resident opinion is favorable, this would lend strong support for more flexibility in all general surgery residencies. As of this date, more than 100 general surgery programs have agreed to randomization.

The sponsoring agencies are to be congratulated for designing a trial that for the first time will objectively evaluate just how restrictive work rules need to be. Their efforts may effectively preserve a value that is at the core of our profession – the continuous care of our surgical patients.

Dr. Rikkers is the Editor in Chief of ACS Surgery News.

Along with many others who are rapidly fading from the American surgical scene, I was born as a baby boomer. Most of us from that generation who embraced surgery as a career held fast to the values of the era. First and foremost among these was a high premium put on hard work, long hours, and an unwavering dedication to our profession and to our patients. We were particularly proud of the continuity of care that we provided to our patients.

During my early years as a surgeon, it was a 24/7 job. Saturday mornings were consumed by Surgery Grand Rounds followed by usually prolonged and detailed patient rounds. Most of us visited our hospitalized patients 7 days a week. When one of my patients developed a complication, I, rather than the surgeon on call, managed it. I missed soccer matches, baseball games, dance recitals, and even some family birthdays because etched into my conscience was the concept that duty to my patients trumped duty to my family. Although there is much to admire in this singular focus on patient care, it took its toll on the other aspects of what should be a more balanced professional life.

Two factors, one of them cultural and the other regulatory, have altered this all-consuming aspect of a surgeon’s life, with implications for the ideal of continuity of care. First was the arrival of freshly minted surgeons from generations X and Y who had a different set of priorities than their predecessors. They insisted on a more even balance between professional and family obligations. In part this resulted from the need for them to be more involved in child rearing since many of their spouses were engaged in time-intensive careers of their own. As they gravitated onto academic surgical faculties and joined private practice groups, they insisted on moving educational programs such as Surgery Grand Rounds to weekdays so they could participate in family activities. They entrusted the care of their patients to their partners, freeing them for entire weekends that could be devoted to family events.

The healthier balance they have brought to a career in surgery is to be admired. Much to the benefit of their senior colleagues, it has become their way of life as well. The trade-off has been some decay of the ideals of patient ownership and continuity of care.

The next and potentially more serious challenge to the cherished concept of continuous care of our patients was the mandate of an 80-hour work week by the Accreditation Council for Graduate Medical Education (ACGME) in 2003. As to its effects on graduate surgical education, I believe the 80-hour work week has been a double-edged sword. On the positive side, at a time when interest in general surgery was waning, institution of duty hours restrictions along with the advent of minimally invasive surgery made our specialty more attractive to medical school graduates, including women, who now constitute 50% of most medical school classes. Another plus was that teaching hospitals were forced to hire physician extenders and other personnel to perform some of the noneducational tasks previously carried out by residents.

On the negative side, since many of the lost hours were in the evenings and weekends, residents’ exposure to urgent and emergency cases was diminished. More significantly, surgery residents began to work in shifts to accommodate increasingly inflexible rules. Ownership of their patients could no longer be held as a high priority in surgical education. Several classes of surgery residents who were educated under these fairly restrictive guidelines have now graduated and have brought a "shift mentality" with them to their positions in private practice groups and on academic faculties.

Since work hour restrictions are highly unlikely to disappear from our training programs and may in fact be applied in the future to all working physicians and surgeons, what can be done to preserve the time-honored value of continuous care of our patients? The answer probably lies in seeking reasonable flexibility within the rules rather than elimination of them. A bright light in this regard is an upcoming randomized controlled trial to assess the feasibility of more flexible work hours rules for general surgery residents. This trial is sponsored by the American Board of Surgery and the American College of Surgeons, and has the support of the ACGME. It will be conducted in hospitals that have instituted the National Surgical Quality Improvement Program (NSQIP) and also sponsor general surgery residencies. Beginning in July 2014, these residencies will be randomized to one of two arms – one using the extensive and rigid present duty hour standards and the second utilizing more flexible standards limited to an 80-hour work week, one night in three on call, and one day in seven free of clinical responsibilities, all averaged over a month. Patient outcomes in each arm will be determined from NSQIP data.

The trial will be conducted over 1 year, with residents’ opinions being surveyed at its midpoint. If patient outcomes are similar in the two arms or superior in the arm with more flexible rules and resident opinion is favorable, this would lend strong support for more flexibility in all general surgery residencies. As of this date, more than 100 general surgery programs have agreed to randomization.

The sponsoring agencies are to be congratulated for designing a trial that for the first time will objectively evaluate just how restrictive work rules need to be. Their efforts may effectively preserve a value that is at the core of our profession – the continuous care of our surgical patients.

Dr. Rikkers is the Editor in Chief of ACS Surgery News.

CASE: DISCONTINUED OXYTOCIN LEADS TO POSTPARTUM HEMORRHAGE
You have just completed a repeat cesarean delivery for a 41-year-old woman, now G2P2. You order an infusion of oxytocin, 20 U in 1 L lactated Ringer’s solution, to run at a rate of 125 mL/hr for 8 hours. Without informing you, the recovery room nurse discontinues the bag with the oxytocin solution and starts an infusion of lactated Ringer’s solution without oxytocin.

One hour later, you are called to the recovery room because your patient is having a postpartum hemorrhage (PPH). Physical examination shows that the uterus is boggy and above the level of the umbilicus. On ­bedside ­ultrasonography, the uterine cavity is demonstrated to contain minimal blood, and Doppler sonography does not demonstrate any vascular tissue within the uterine cavity. You diagnose uterine atony and initiate treatment. You massage the uterus, rapidly infuse 1 L crystalloid solution, place misoprostol 800 µg in the rectum, and reinitiate the oxytocin infusion. The uterine bleeding slows and then stops.

The following morning, the patient’s hematocrit has decreased from a preoperative value of 37% to 21%.  

Could this case of PPH have been prevented?

Cesarean delivery is one of the most commonly performed major operations in developed countries. More than 1,250,000 cesarean deliveries are performed annually in the United States. In 2012, there were 3,952,937 births and a cesarean delivery rate of 32.8%.¹ It is an important goal of obstetric care providers to continuously improve our approach to cesarean delivery in order to minimize the surgical risks of this procedure. Evidence-based, standardized protocols for cesarean delivery are critical to ensuring high- reliability surgical outcomes.

A key gap in cesarean delivery protocols is the lack of a nationwide, standardized approach to reducing the risk of postoperative bleeding by maintaining a continuous infusion of oxytocin in the hours immediately following cesarean delivery. 

OXYTOCIN: A CRITICAL INTERVENTION TO PREVENT PPH
More than half of all maternal deaths occur in the 24 hours following delivery, with the most common cause being PPH.² In addition to death, serious complications of PPH include coagulopathy, shock, emergency hysterectomy, transfusion complications, respiratory distress, and pituitary necrosis. Most cases of PPH that occur within 24 hours of delivery are caused by uterine atony.³ Other causes include retained products of conception, placenta accreta, infection, coagulation defects, and amniotic fluid embolism.

Administering a uterotonic such as oxytocin at the time of delivery reduces the risk of PPH by approximately 66% and the risk of maternal blood transfusion by about 65%.⁴ In order to prevent uterine atony and PPH, oxytocin should be routinely administered following birth of the baby or after delivery of the placenta. Appropriate doses following vaginal delivery are oxytocin 10 U administered intramuscularly or 10 U administered as a slow intravenous (IV) infusion.⁵ The onset of action of oxytocin is approximately 2 to 5 minutes after an intramuscular dose and 1 minute after an IV dose.⁶ 

Related article: Routine use of oxytocin at birth: just the right amount to prevent postpartum hemorrhage  Robert L. Barbieri, MD (Editorial, July 2012)

OXYTOCIN AND CESAREAN DELIVERY
Many clinical trials have reported that during a cesarean delivery, the routine administration of a uterotonic agent following birth of the baby reduces the risk of uterine atony and excessive bleeding. Three uterotonics: oxytocin, misoprostol, and carbetocin (a long-acting oxytocin analogue, see SIDEBAR), have been reported to reduce the risk of excessive bleeding during cesarean delivery.⁷ Oxytocin is the uterotonic most commonly used during cesarean delivery in developed countries. 

Related article: A new (to the US) first-line agent for heavy menstrual bleeding Robert L. Barbieri, MD (Editorial, October 2010)

In the United States, there is no standardized oxytocin regimen for prevention of uterine atony and hemorrhage at cesarean delivery. The most common regimen is to add 10–40 U of oxytocin in 1 L crystalloid solution and initiate the oxytocin infusion following delivery of the baby. Initially, the infusion is run at a rapid rate. Once the obstetrician reports that there is adequate uterine tone, the infusion rate is slowed to one that maintains uterine tone.

Some clinicians administer a single bolus of oxytocin following birth of the baby. However, a bolus of oxytocin commonly causes hypotension and, less commonly, ST segment changes on the electrocardiogram (EKG) suggestive of cardiac ischemia.^8–10Many experts recommend against administering one large bolus of oxytocin over a short period of time and favor a continuous infusion.

At cesarean delivery, the minimum infusion rate of oxytocin that has been reported to avoid most cases of uterine atony, as reported by the obstetrician immediately following delivery, is approximately oxytocin 0.3 U/min.¹¹ Oxytocin infusion rates of 0.2 U/min and 0.1 U/min were associated with uterine atony rates of 21% and 40%, respectively. An infusion rate of oxytocin 0.3 U/min can be achieved by the administration of 20 U of oxytocin in 1 L crystalloid solution at a rate of 15 mL/min until uterine tone is achieved. The oxytocin dose then can be titrated to maintain adequate uterine tone. Following completion of surgery, uterine tone can be maintained with a low-dose continuous infusion of oxytocin.  

4- TO 8-HOUR OXYTOCIN RULE
A key gap in our cesarean delivery protocols is a standardized recommendation concerning the duration of the oxytocin infusion following cesarean delivery. To my knowledge, no national organization has made a firm recommendation concerning the duration of oxytocin infusion following cesarean delivery.

One recent clinical trial studied PPH following cesarean delivery utilizing two oxytocin regimens: a bolus of oxytocin following delivery of the baby versus a bolus of oxytocin followed by a 4-hour IV infusion of oxytocin.¹² In this trial, 2,058 women undergoing a scheduled cesarean delivery with a singleton pregnancy were randomly assigned to an oxytocin bolus alone, oxytocin 5 U administered intravenously over 1 minute, or an oxytocin bolus plus a 4-hour oxytocin infusion at a rate of 10 U/hr. The 4-hour postoperative oxytocin infusion was formulated by adding 40 U of oxytocin to 500 mL saline and infusing the solution at 125 mL/hr, equivalent to 0.167 U of oxytocin per minute. In this trial, 65% of the women were undergoing a repeat cesarean delivery and 35% were undergoing a primary cesarean delivery.

The authors reported that women who received the oxytocin bolus alone were significantly more likely to be diagnosed with uterine atony requiring additional uterotonic treatment than women who received both the bolus and the 4-hour postoperative infusion (18.4% versus 12.2%, respectively; P <.001). There was no difference in the rate of PPH between the two groups.

The rate of PPH was 16% in women receiving an oxytocin bolus alone and 15.7% in women receiving both an oxytocin bolus and the continuous oxytocin infusion. However, among less experienced surgeons, the rate of PPH was significantly greater in the group that received the oxytocin bolus alone compared with the women receiving the bolus and continuous infusion (22.2% versus 17.3%, respectively). The authors concluded that obstetricians should consider using a 4-hour infusion of oxytocin following cesarean delivery to reduce the risk of uterine atony.

In a recent evidence-based review of optimal interventions in cesarean delivery, the authors recommended an IV infusion of 10 to 40 U of oxytocin administered over 4 to 8 hours after cesarean delivery.7 Following cesarean, an IV infusion of crystalloid solution is typically maintained for at least 4 to 8 hours. Consequently, adding oxytocin (which costs approximately $1 for 10 units) to the crystalloid infusion does not add substantially to the cost of the patient’s postoperative care and may reduce the risk of uterine atony and PPH.

Related article: Act fast when confronted by a coagulopathy postpartum Robert L. Barbieri, MD (Editorial, March 2012)

My bottom-line recommendation. In the United States, we should adopt a policy of maintaining a continuous infusion of oxytocin for 4 to 8 hours following a cesarean delivery. Following a 4- to 8-hour rule will decrease the rate of uterine atony and excessive bleeding, thereby improving the safety of our cesarean delivery surgery. 

INSTANT POLL
How many hours following cesarean delivery do you think that an oxytocin infusion should be maintained to reduce the risk of uterine atony and postpartum hemorrhage?
If the patient is a Jehovah’s Witness and refuses the transfusion of all blood products, how many hours following cesarean delivery do you think that an oxytocin infusion should be maintained to reduce the risk of uterine atony and postpartum hemorrhage?
Tell us—at rbarbieri@frontlinemedcom.com Please include your name and city and state.

CASE: DISCONTINUED OXYTOCIN LEADS TO POSTPARTUM HEMORRHAGE
You have just completed a repeat cesarean delivery for a 41-year-old woman, now G2P2. You order an infusion of oxytocin, 20 U in 1 L lactated Ringer’s solution, to run at a rate of 125 mL/hr for 8 hours. Without informing you, the recovery room nurse discontinues the bag with the oxytocin solution and starts an infusion of lactated Ringer’s solution without oxytocin.

One hour later, you are called to the recovery room because your patient is having a postpartum hemorrhage (PPH). Physical examination shows that the uterus is boggy and above the level of the umbilicus. On ­bedside ­ultrasonography, the uterine cavity is demonstrated to contain minimal blood, and Doppler sonography does not demonstrate any vascular tissue within the uterine cavity. You diagnose uterine atony and initiate treatment. You massage the uterus, rapidly infuse 1 L crystalloid solution, place misoprostol 800 µg in the rectum, and reinitiate the oxytocin infusion. The uterine bleeding slows and then stops.

The following morning, the patient’s hematocrit has decreased from a preoperative value of 37% to 21%.  

Could this case of PPH have been prevented?

Cesarean delivery is one of the most commonly performed major operations in developed countries. More than 1,250,000 cesarean deliveries are performed annually in the United States. In 2012, there were 3,952,937 births and a cesarean delivery rate of 32.8%.¹ It is an important goal of obstetric care providers to continuously improve our approach to cesarean delivery in order to minimize the surgical risks of this procedure. Evidence-based, standardized protocols for cesarean delivery are critical to ensuring high- reliability surgical outcomes.

A key gap in cesarean delivery protocols is the lack of a nationwide, standardized approach to reducing the risk of postoperative bleeding by maintaining a continuous infusion of oxytocin in the hours immediately following cesarean delivery. 

OXYTOCIN: A CRITICAL INTERVENTION TO PREVENT PPH
More than half of all maternal deaths occur in the 24 hours following delivery, with the most common cause being PPH.² In addition to death, serious complications of PPH include coagulopathy, shock, emergency hysterectomy, transfusion complications, respiratory distress, and pituitary necrosis. Most cases of PPH that occur within 24 hours of delivery are caused by uterine atony.³ Other causes include retained products of conception, placenta accreta, infection, coagulation defects, and amniotic fluid embolism.

Administering a uterotonic such as oxytocin at the time of delivery reduces the risk of PPH by approximately 66% and the risk of maternal blood transfusion by about 65%.⁴ In order to prevent uterine atony and PPH, oxytocin should be routinely administered following birth of the baby or after delivery of the placenta. Appropriate doses following vaginal delivery are oxytocin 10 U administered intramuscularly or 10 U administered as a slow intravenous (IV) infusion.⁵ The onset of action of oxytocin is approximately 2 to 5 minutes after an intramuscular dose and 1 minute after an IV dose.⁶ 

Related article: Routine use of oxytocin at birth: just the right amount to prevent postpartum hemorrhage  Robert L. Barbieri, MD (Editorial, July 2012)

OXYTOCIN AND CESAREAN DELIVERY
Many clinical trials have reported that during a cesarean delivery, the routine administration of a uterotonic agent following birth of the baby reduces the risk of uterine atony and excessive bleeding. Three uterotonics: oxytocin, misoprostol, and carbetocin (a long-acting oxytocin analogue, see SIDEBAR), have been reported to reduce the risk of excessive bleeding during cesarean delivery.⁷ Oxytocin is the uterotonic most commonly used during cesarean delivery in developed countries. 

Related article: A new (to the US) first-line agent for heavy menstrual bleeding Robert L. Barbieri, MD (Editorial, October 2010)

In the United States, there is no standardized oxytocin regimen for prevention of uterine atony and hemorrhage at cesarean delivery. The most common regimen is to add 10–40 U of oxytocin in 1 L crystalloid solution and initiate the oxytocin infusion following delivery of the baby. Initially, the infusion is run at a rapid rate. Once the obstetrician reports that there is adequate uterine tone, the infusion rate is slowed to one that maintains uterine tone.

Some clinicians administer a single bolus of oxytocin following birth of the baby. However, a bolus of oxytocin commonly causes hypotension and, less commonly, ST segment changes on the electrocardiogram (EKG) suggestive of cardiac ischemia.^8–10Many experts recommend against administering one large bolus of oxytocin over a short period of time and favor a continuous infusion.

At cesarean delivery, the minimum infusion rate of oxytocin that has been reported to avoid most cases of uterine atony, as reported by the obstetrician immediately following delivery, is approximately oxytocin 0.3 U/min.¹¹ Oxytocin infusion rates of 0.2 U/min and 0.1 U/min were associated with uterine atony rates of 21% and 40%, respectively. An infusion rate of oxytocin 0.3 U/min can be achieved by the administration of 20 U of oxytocin in 1 L crystalloid solution at a rate of 15 mL/min until uterine tone is achieved. The oxytocin dose then can be titrated to maintain adequate uterine tone. Following completion of surgery, uterine tone can be maintained with a low-dose continuous infusion of oxytocin.  

4- TO 8-HOUR OXYTOCIN RULE
A key gap in our cesarean delivery protocols is a standardized recommendation concerning the duration of the oxytocin infusion following cesarean delivery. To my knowledge, no national organization has made a firm recommendation concerning the duration of oxytocin infusion following cesarean delivery.

One recent clinical trial studied PPH following cesarean delivery utilizing two oxytocin regimens: a bolus of oxytocin following delivery of the baby versus a bolus of oxytocin followed by a 4-hour IV infusion of oxytocin.¹² In this trial, 2,058 women undergoing a scheduled cesarean delivery with a singleton pregnancy were randomly assigned to an oxytocin bolus alone, oxytocin 5 U administered intravenously over 1 minute, or an oxytocin bolus plus a 4-hour oxytocin infusion at a rate of 10 U/hr. The 4-hour postoperative oxytocin infusion was formulated by adding 40 U of oxytocin to 500 mL saline and infusing the solution at 125 mL/hr, equivalent to 0.167 U of oxytocin per minute. In this trial, 65% of the women were undergoing a repeat cesarean delivery and 35% were undergoing a primary cesarean delivery.

The authors reported that women who received the oxytocin bolus alone were significantly more likely to be diagnosed with uterine atony requiring additional uterotonic treatment than women who received both the bolus and the 4-hour postoperative infusion (18.4% versus 12.2%, respectively; P <.001). There was no difference in the rate of PPH between the two groups.

The rate of PPH was 16% in women receiving an oxytocin bolus alone and 15.7% in women receiving both an oxytocin bolus and the continuous oxytocin infusion. However, among less experienced surgeons, the rate of PPH was significantly greater in the group that received the oxytocin bolus alone compared with the women receiving the bolus and continuous infusion (22.2% versus 17.3%, respectively). The authors concluded that obstetricians should consider using a 4-hour infusion of oxytocin following cesarean delivery to reduce the risk of uterine atony.

In a recent evidence-based review of optimal interventions in cesarean delivery, the authors recommended an IV infusion of 10 to 40 U of oxytocin administered over 4 to 8 hours after cesarean delivery.7 Following cesarean, an IV infusion of crystalloid solution is typically maintained for at least 4 to 8 hours. Consequently, adding oxytocin (which costs approximately $1 for 10 units) to the crystalloid infusion does not add substantially to the cost of the patient’s postoperative care and may reduce the risk of uterine atony and PPH.

Related article: Act fast when confronted by a coagulopathy postpartum Robert L. Barbieri, MD (Editorial, March 2012)

My bottom-line recommendation. In the United States, we should adopt a policy of maintaining a continuous infusion of oxytocin for 4 to 8 hours following a cesarean delivery. Following a 4- to 8-hour rule will decrease the rate of uterine atony and excessive bleeding, thereby improving the safety of our cesarean delivery surgery. 

INSTANT POLL
How many hours following cesarean delivery do you think that an oxytocin infusion should be maintained to reduce the risk of uterine atony and postpartum hemorrhage?
If the patient is a Jehovah’s Witness and refuses the transfusion of all blood products, how many hours following cesarean delivery do you think that an oxytocin infusion should be maintained to reduce the risk of uterine atony and postpartum hemorrhage?
Tell us—at rbarbieri@frontlinemedcom.com Please include your name and city and state.

CASE: DISCONTINUED OXYTOCIN LEADS TO POSTPARTUM HEMORRHAGE
You have just completed a repeat cesarean delivery for a 41-year-old woman, now G2P2. You order an infusion of oxytocin, 20 U in 1 L lactated Ringer’s solution, to run at a rate of 125 mL/hr for 8 hours. Without informing you, the recovery room nurse discontinues the bag with the oxytocin solution and starts an infusion of lactated Ringer’s solution without oxytocin.

One hour later, you are called to the recovery room because your patient is having a postpartum hemorrhage (PPH). Physical examination shows that the uterus is boggy and above the level of the umbilicus. On ­bedside ­ultrasonography, the uterine cavity is demonstrated to contain minimal blood, and Doppler sonography does not demonstrate any vascular tissue within the uterine cavity. You diagnose uterine atony and initiate treatment. You massage the uterus, rapidly infuse 1 L crystalloid solution, place misoprostol 800 µg in the rectum, and reinitiate the oxytocin infusion. The uterine bleeding slows and then stops.

The following morning, the patient’s hematocrit has decreased from a preoperative value of 37% to 21%.  

Could this case of PPH have been prevented?

Cesarean delivery is one of the most commonly performed major operations in developed countries. More than 1,250,000 cesarean deliveries are performed annually in the United States. In 2012, there were 3,952,937 births and a cesarean delivery rate of 32.8%.¹ It is an important goal of obstetric care providers to continuously improve our approach to cesarean delivery in order to minimize the surgical risks of this procedure. Evidence-based, standardized protocols for cesarean delivery are critical to ensuring high- reliability surgical outcomes.

A key gap in cesarean delivery protocols is the lack of a nationwide, standardized approach to reducing the risk of postoperative bleeding by maintaining a continuous infusion of oxytocin in the hours immediately following cesarean delivery. 

OXYTOCIN: A CRITICAL INTERVENTION TO PREVENT PPH
More than half of all maternal deaths occur in the 24 hours following delivery, with the most common cause being PPH.² In addition to death, serious complications of PPH include coagulopathy, shock, emergency hysterectomy, transfusion complications, respiratory distress, and pituitary necrosis. Most cases of PPH that occur within 24 hours of delivery are caused by uterine atony.³ Other causes include retained products of conception, placenta accreta, infection, coagulation defects, and amniotic fluid embolism.

Administering a uterotonic such as oxytocin at the time of delivery reduces the risk of PPH by approximately 66% and the risk of maternal blood transfusion by about 65%.⁴ In order to prevent uterine atony and PPH, oxytocin should be routinely administered following birth of the baby or after delivery of the placenta. Appropriate doses following vaginal delivery are oxytocin 10 U administered intramuscularly or 10 U administered as a slow intravenous (IV) infusion.⁵ The onset of action of oxytocin is approximately 2 to 5 minutes after an intramuscular dose and 1 minute after an IV dose.⁶ 

Related article: Routine use of oxytocin at birth: just the right amount to prevent postpartum hemorrhage  Robert L. Barbieri, MD (Editorial, July 2012)

OXYTOCIN AND CESAREAN DELIVERY
Many clinical trials have reported that during a cesarean delivery, the routine administration of a uterotonic agent following birth of the baby reduces the risk of uterine atony and excessive bleeding. Three uterotonics: oxytocin, misoprostol, and carbetocin (a long-acting oxytocin analogue, see SIDEBAR), have been reported to reduce the risk of excessive bleeding during cesarean delivery.⁷ Oxytocin is the uterotonic most commonly used during cesarean delivery in developed countries. 

Related article: A new (to the US) first-line agent for heavy menstrual bleeding Robert L. Barbieri, MD (Editorial, October 2010)

In the United States, there is no standardized oxytocin regimen for prevention of uterine atony and hemorrhage at cesarean delivery. The most common regimen is to add 10–40 U of oxytocin in 1 L crystalloid solution and initiate the oxytocin infusion following delivery of the baby. Initially, the infusion is run at a rapid rate. Once the obstetrician reports that there is adequate uterine tone, the infusion rate is slowed to one that maintains uterine tone.

Some clinicians administer a single bolus of oxytocin following birth of the baby. However, a bolus of oxytocin commonly causes hypotension and, less commonly, ST segment changes on the electrocardiogram (EKG) suggestive of cardiac ischemia.^8–10Many experts recommend against administering one large bolus of oxytocin over a short period of time and favor a continuous infusion.

At cesarean delivery, the minimum infusion rate of oxytocin that has been reported to avoid most cases of uterine atony, as reported by the obstetrician immediately following delivery, is approximately oxytocin 0.3 U/min.¹¹ Oxytocin infusion rates of 0.2 U/min and 0.1 U/min were associated with uterine atony rates of 21% and 40%, respectively. An infusion rate of oxytocin 0.3 U/min can be achieved by the administration of 20 U of oxytocin in 1 L crystalloid solution at a rate of 15 mL/min until uterine tone is achieved. The oxytocin dose then can be titrated to maintain adequate uterine tone. Following completion of surgery, uterine tone can be maintained with a low-dose continuous infusion of oxytocin.  

4- TO 8-HOUR OXYTOCIN RULE
A key gap in our cesarean delivery protocols is a standardized recommendation concerning the duration of the oxytocin infusion following cesarean delivery. To my knowledge, no national organization has made a firm recommendation concerning the duration of oxytocin infusion following cesarean delivery.

One recent clinical trial studied PPH following cesarean delivery utilizing two oxytocin regimens: a bolus of oxytocin following delivery of the baby versus a bolus of oxytocin followed by a 4-hour IV infusion of oxytocin.¹² In this trial, 2,058 women undergoing a scheduled cesarean delivery with a singleton pregnancy were randomly assigned to an oxytocin bolus alone, oxytocin 5 U administered intravenously over 1 minute, or an oxytocin bolus plus a 4-hour oxytocin infusion at a rate of 10 U/hr. The 4-hour postoperative oxytocin infusion was formulated by adding 40 U of oxytocin to 500 mL saline and infusing the solution at 125 mL/hr, equivalent to 0.167 U of oxytocin per minute. In this trial, 65% of the women were undergoing a repeat cesarean delivery and 35% were undergoing a primary cesarean delivery.

The authors reported that women who received the oxytocin bolus alone were significantly more likely to be diagnosed with uterine atony requiring additional uterotonic treatment than women who received both the bolus and the 4-hour postoperative infusion (18.4% versus 12.2%, respectively; P <.001). There was no difference in the rate of PPH between the two groups.

The rate of PPH was 16% in women receiving an oxytocin bolus alone and 15.7% in women receiving both an oxytocin bolus and the continuous oxytocin infusion. However, among less experienced surgeons, the rate of PPH was significantly greater in the group that received the oxytocin bolus alone compared with the women receiving the bolus and continuous infusion (22.2% versus 17.3%, respectively). The authors concluded that obstetricians should consider using a 4-hour infusion of oxytocin following cesarean delivery to reduce the risk of uterine atony.

In a recent evidence-based review of optimal interventions in cesarean delivery, the authors recommended an IV infusion of 10 to 40 U of oxytocin administered over 4 to 8 hours after cesarean delivery.7 Following cesarean, an IV infusion of crystalloid solution is typically maintained for at least 4 to 8 hours. Consequently, adding oxytocin (which costs approximately $1 for 10 units) to the crystalloid infusion does not add substantially to the cost of the patient’s postoperative care and may reduce the risk of uterine atony and PPH.

Related article: Act fast when confronted by a coagulopathy postpartum Robert L. Barbieri, MD (Editorial, March 2012)

My bottom-line recommendation. In the United States, we should adopt a policy of maintaining a continuous infusion of oxytocin for 4 to 8 hours following a cesarean delivery. Following a 4- to 8-hour rule will decrease the rate of uterine atony and excessive bleeding, thereby improving the safety of our cesarean delivery surgery. 

INSTANT POLL
How many hours following cesarean delivery do you think that an oxytocin infusion should be maintained to reduce the risk of uterine atony and postpartum hemorrhage?
If the patient is a Jehovah’s Witness and refuses the transfusion of all blood products, how many hours following cesarean delivery do you think that an oxytocin infusion should be maintained to reduce the risk of uterine atony and postpartum hemorrhage?
Tell us—at rbarbieri@frontlinemedcom.com Please include your name and city and state.

We have some interesting and insightful articles lined up for you this month, beginning with a Commentary by Samuel and Stone on treating HER2-positive breast cancer and asking whether the era of trastuzumab therapy is over. The Commentary and accompanying Community Translations report explore the use of pertuzumab and trastuzumab together, especially in the neoadjuvant setting. The Cleopatra trial has already shown that combining pertuzumab with trastuzumab plus docetaxel as a first-line treatment for HER2-positive metastatic breast cancer significantly prolonged progression-free survival with no increase in cardiac toxic effects, compared with placebo plus trastuzumab plus docetaxel, so perhaps using pertuzumab and trastuzumab upfront might be equally successful.

Click on the PDF icon at the top of this introduction to read the full article.

We have some interesting and insightful articles lined up for you this month, beginning with a Commentary by Samuel and Stone on treating HER2-positive breast cancer and asking whether the era of trastuzumab therapy is over. The Commentary and accompanying Community Translations report explore the use of pertuzumab and trastuzumab together, especially in the neoadjuvant setting. The Cleopatra trial has already shown that combining pertuzumab with trastuzumab plus docetaxel as a first-line treatment for HER2-positive metastatic breast cancer significantly prolonged progression-free survival with no increase in cardiac toxic effects, compared with placebo plus trastuzumab plus docetaxel, so perhaps using pertuzumab and trastuzumab upfront might be equally successful.

Click on the PDF icon at the top of this introduction to read the full article.

We have some interesting and insightful articles lined up for you this month, beginning with a Commentary by Samuel and Stone on treating HER2-positive breast cancer and asking whether the era of trastuzumab therapy is over. The Commentary and accompanying Community Translations report explore the use of pertuzumab and trastuzumab together, especially in the neoadjuvant setting. The Cleopatra trial has already shown that combining pertuzumab with trastuzumab plus docetaxel as a first-line treatment for HER2-positive metastatic breast cancer significantly prolonged progression-free survival with no increase in cardiac toxic effects, compared with placebo plus trastuzumab plus docetaxel, so perhaps using pertuzumab and trastuzumab upfront might be equally successful.

Click on the PDF icon at the top of this introduction to read the full article.