Understanding and Management of Amniotic Fluid Embolism
Juraj Sprung, MD, PhD,* Eugene Y. Cheng, MD,? Smita Patel, MD,+ John P. Kampine, MD, PhD$ Department
of Anesthesiology,
Amniotic&id embolism CAFE) is a rare obstetric problem characterized by sudden onset of hypotension, hypoxemia, and coag~l@at&y. Thi,s case represents the difficulty in dvjferentiuting AFE from other etiologies of cardiopulmonary compromise. The definitive diagnosis of AFE Zs made at autopsy with the demonstration offetal cell elements in the pulmonavy uasculature. Diagnosis ran be highly suspected if squamous cells and other debris of presumed fetal origin are demonstrated in blood aspirated from the central venous or pulmonary urtevy circulation of .symptomatic parturients. Predisposing factors for AFL in&de advanced maternal age, multiparity, large fetal size, and short lumv~ltuouslabor, especially if uterine stimulants are used. CmrdiopvLlmorl~~ry resuscitation is the key to the treatment of @rhrient.s with AFE. A pulmonay artery ratheter CCL~ be help,fvcl in diugnosis and hemodynamic management of.parturients zoith AFE.
Keywords: Obstetrics,
complications; coagulopathy, disseminated intravascular coagulation; embolism, amniotic fluid; anesthesia, epidural.
Amniotic fluid embolism (AFE), the forced entrance of amniotic fluid into the maternal circulation through uteroplacental sinusoids or endocervical veins to the pul-
*Resident Professor
*Assistant
Professor
$Professor
and Chairman
Address reprint requests to Dr. Cheng at the Department of Anesthesiology, Froedtert Memorial Lutheran Hospital, 9200 W. Wisconsin Avenue, Milwaukee, WI 53226, USA. Received for publication July 12, 1991; revised cepted for publication November 22, 1991. 0 1992 Butterworth-Heinemann J. Clin. Anesth.
4:235-240,
1992.
manuscript
Milwaukee, WI.
monary circulation, is a rare obstetrical complication with a reported frequency in the United States of approximately 1 in 20,000 to 1 in 30,000 deliveries.’ The associated mortality with AFE is 86%,? which represents approximately 12% of all maternal deaths.’ In other areas of the world, the frequency ranges from 1 in 27,000 deliveries in Southeast Asia’ to 1 in 80,000 deliveries in England and Wales.” AFE characteristically presents with respiratory distress, hypotension, and coagulopathy, often followed within minutes by sudden cardiovascular collapse. It is often difficult to differentiate AFE from other types of thromboembolic events or other causes of cardiopulmonary collapse, although basic treatment principles are the same: oxygenating the patient, stabilizing hemodynamic parameters, and treating the underlying medical condition. This case report describes a patient with clinically suspected AFE and discusses diagnostic and management plans.
Case Report
Introduction
tAssociate
Medical College of Wisconsin,
ac-
A 27-year-old healthy female, gravida 2, para 1, was admitted to the hospital for labor induction due to postmaturity (42 weeks by date) and intrauterine growth retardation assessed by transabdominal ultrasonography. An attempt to induce labor with oxytocin was complicated by the failure to progress, and the decision was made to proceed with a cesarean delivery. A regional anesthetic was agreed on. An epidural catheter was placed atraumatically for the titration of local anesthetic, and sensory block to a T, level was achieved with 15 ml of 2% lidocaine after a 3 ml test dose of 1.5% lidocaine with epinephrine 1:200,000. A moderate decrease in blood pressure (BP) from 130180 mmHg to 100/65 mmHg occurred. Fourteen minutes after incision, a normal, vigorous baby was delivered. While the surgeon was manually delivering the placenta from the exteriorized uterus, an oxytocin bolus dose of 2 units (U) was given intravenously (IV) and an infusion of- 20 U in 1 liter, to be administered over 1 hour, was started. Shortly afterward, the patient became confused, and within 30 secJ. Clin. Anesth.,
vol. 4, May/June
1992
235
Case Reports
ottds, she responded only by withdrawing to pain. Respiration became labored, and progressive bradycardia developed down to a rate of approximately 35 beats per minute (bpm). Noninvasive BP was t 1970 mmHg. The patient developed perioraf cyanosis and tonic-clonic seizures. Pulse oximetry readings failed. The airway was secured by endotracheaf intubation after administration of thiopental sodium 50 mg, which stopped the seizures, attd succinytchotine 120 mg, to enable direct tat-yngoscopy. After intubation, the patient continued to be cyanotic despite hand ventilation and receiving art inspired oxygen tension (FIO,) of 1 .O. Heart rate (HK) was stiff bratfycardic (30 bpttt) after intubatiott, but BP could not be detected and no pulse could be palpated. Af’ter atropine 0.5 mg IV was given, a supraventricufar tachycardia was seen on the cardiac monitor, but no pulse or BP was detectable. (~ardiopuftnottary resuscitation (CPK) was stat-ted, and after several minutes of’ chest cotttpression and the adtninistra~iott of a 250 ml fluid challenge. ephedrinr 1.5 tng, and phenylephrine 100 pg, the patient was able to sustain ;I BP of 801.50 mmHg ant1 an HR of’ 1 10 bpm. A radial arterial catheter was placed. .I‘he first arterial blood gas, obtained approximately 5 minutes after intubation, showed pH 7.30, arterial carbon dioxide tension (PaCO,) 4 1 mntHg, arterial oxygen tension (Pa0.6) and lhe patient is still inadequately oxygenated, PEEP is used f’or alveolar recruitment and improvement of’ ox\genation. (:ommonly, PEEP is started at .i cmH,O and increased in 2 to :3 cmH,O increments, with carefill asscssment of’lung compliance, peak airway pressures, BP. antl (:O. until satisfactory levels of’ PaO, are reached OIunacceptable htY~~0dynamic~ compromise occurs. Ftilid challenges should be the first response to hvpotension or shock. Larger than expected quantities ;,fisotonic fluid IWIY be necessary, as in this case, due ro a c-ombination of‘ an epidural anesthetic block of‘ the syrnpat hetic svstem, hemorrhage secondary to coagulopath). antiio~- acute lef’r ventricular f‘ailure from AFE. To mon-
Amniotic fluid
itor intravascular volume, a central venous catheter, instead of a pulmonary artery catheter, was used in our case because BP and HR stabilized rapidly. In addition, the placement of a pulmonary artery catheter was not thought necessary because the PEEP requirement was 10 cmH,O or less and therefore had minimal, if any, impact on myocardial function.*7 However, a pulmonary artery catheter is often inserted after AFE because of the known difficulties optimizing preload. This catheter helps practitioners monitor the effects of vasoactive drugs and follow the effect of PEEP on myocardial function. Dopamine, epinephrine, and norepinephrine are often used separately or in combination to increase BP and
Juraj Sprung, MD, PhD,* Eugene Y. Cheng, MD,? Smita Patel, MD,+ John P. Kampine, MD, PhD$ Department
of Anesthesiology,
Amniotic&id embolism CAFE) is a rare obstetric problem characterized by sudden onset of hypotension, hypoxemia, and coag~l@at&y. Thi,s case represents the difficulty in dvjferentiuting AFE from other etiologies of cardiopulmonary compromise. The definitive diagnosis of AFE Zs made at autopsy with the demonstration offetal cell elements in the pulmonavy uasculature. Diagnosis ran be highly suspected if squamous cells and other debris of presumed fetal origin are demonstrated in blood aspirated from the central venous or pulmonary urtevy circulation of .symptomatic parturients. Predisposing factors for AFL in&de advanced maternal age, multiparity, large fetal size, and short lumv~ltuouslabor, especially if uterine stimulants are used. CmrdiopvLlmorl~~ry resuscitation is the key to the treatment of @rhrient.s with AFE. A pulmonay artery ratheter CCL~ be help,fvcl in diugnosis and hemodynamic management of.parturients zoith AFE.
Keywords: Obstetrics,
complications; coagulopathy, disseminated intravascular coagulation; embolism, amniotic fluid; anesthesia, epidural.
Amniotic fluid embolism (AFE), the forced entrance of amniotic fluid into the maternal circulation through uteroplacental sinusoids or endocervical veins to the pul-
*Resident Professor
*Assistant
Professor
$Professor
and Chairman
Address reprint requests to Dr. Cheng at the Department of Anesthesiology, Froedtert Memorial Lutheran Hospital, 9200 W. Wisconsin Avenue, Milwaukee, WI 53226, USA. Received for publication July 12, 1991; revised cepted for publication November 22, 1991. 0 1992 Butterworth-Heinemann J. Clin. Anesth.
4:235-240,
1992.
manuscript
Milwaukee, WI.
monary circulation, is a rare obstetrical complication with a reported frequency in the United States of approximately 1 in 20,000 to 1 in 30,000 deliveries.’ The associated mortality with AFE is 86%,? which represents approximately 12% of all maternal deaths.’ In other areas of the world, the frequency ranges from 1 in 27,000 deliveries in Southeast Asia’ to 1 in 80,000 deliveries in England and Wales.” AFE characteristically presents with respiratory distress, hypotension, and coagulopathy, often followed within minutes by sudden cardiovascular collapse. It is often difficult to differentiate AFE from other types of thromboembolic events or other causes of cardiopulmonary collapse, although basic treatment principles are the same: oxygenating the patient, stabilizing hemodynamic parameters, and treating the underlying medical condition. This case report describes a patient with clinically suspected AFE and discusses diagnostic and management plans.
Case Report
Introduction
tAssociate
Medical College of Wisconsin,
ac-
A 27-year-old healthy female, gravida 2, para 1, was admitted to the hospital for labor induction due to postmaturity (42 weeks by date) and intrauterine growth retardation assessed by transabdominal ultrasonography. An attempt to induce labor with oxytocin was complicated by the failure to progress, and the decision was made to proceed with a cesarean delivery. A regional anesthetic was agreed on. An epidural catheter was placed atraumatically for the titration of local anesthetic, and sensory block to a T, level was achieved with 15 ml of 2% lidocaine after a 3 ml test dose of 1.5% lidocaine with epinephrine 1:200,000. A moderate decrease in blood pressure (BP) from 130180 mmHg to 100/65 mmHg occurred. Fourteen minutes after incision, a normal, vigorous baby was delivered. While the surgeon was manually delivering the placenta from the exteriorized uterus, an oxytocin bolus dose of 2 units (U) was given intravenously (IV) and an infusion of- 20 U in 1 liter, to be administered over 1 hour, was started. Shortly afterward, the patient became confused, and within 30 secJ. Clin. Anesth.,
vol. 4, May/June
1992
235
Case Reports
ottds, she responded only by withdrawing to pain. Respiration became labored, and progressive bradycardia developed down to a rate of approximately 35 beats per minute (bpm). Noninvasive BP was t 1970 mmHg. The patient developed perioraf cyanosis and tonic-clonic seizures. Pulse oximetry readings failed. The airway was secured by endotracheaf intubation after administration of thiopental sodium 50 mg, which stopped the seizures, attd succinytchotine 120 mg, to enable direct tat-yngoscopy. After intubation, the patient continued to be cyanotic despite hand ventilation and receiving art inspired oxygen tension (FIO,) of 1 .O. Heart rate (HK) was stiff bratfycardic (30 bpttt) after intubatiott, but BP could not be detected and no pulse could be palpated. Af’ter atropine 0.5 mg IV was given, a supraventricufar tachycardia was seen on the cardiac monitor, but no pulse or BP was detectable. (~ardiopuftnottary resuscitation (CPK) was stat-ted, and after several minutes of’ chest cotttpression and the adtninistra~iott of a 250 ml fluid challenge. ephedrinr 1.5 tng, and phenylephrine 100 pg, the patient was able to sustain ;I BP of 801.50 mmHg ant1 an HR of’ 1 10 bpm. A radial arterial catheter was placed. .I‘he first arterial blood gas, obtained approximately 5 minutes after intubation, showed pH 7.30, arterial carbon dioxide tension (PaCO,) 4 1 mntHg, arterial oxygen tension (Pa0.6) and lhe patient is still inadequately oxygenated, PEEP is used f’or alveolar recruitment and improvement of’ ox\genation. (:ommonly, PEEP is started at .i cmH,O and increased in 2 to :3 cmH,O increments, with carefill asscssment of’lung compliance, peak airway pressures, BP. antl (:O. until satisfactory levels of’ PaO, are reached OIunacceptable htY~~0dynamic~ compromise occurs. Ftilid challenges should be the first response to hvpotension or shock. Larger than expected quantities ;,fisotonic fluid IWIY be necessary, as in this case, due ro a c-ombination of‘ an epidural anesthetic block of‘ the syrnpat hetic svstem, hemorrhage secondary to coagulopath). antiio~- acute lef’r ventricular f‘ailure from AFE. To mon-
Amniotic fluid
itor intravascular volume, a central venous catheter, instead of a pulmonary artery catheter, was used in our case because BP and HR stabilized rapidly. In addition, the placement of a pulmonary artery catheter was not thought necessary because the PEEP requirement was 10 cmH,O or less and therefore had minimal, if any, impact on myocardial function.*7 However, a pulmonary artery catheter is often inserted after AFE because of the known difficulties optimizing preload. This catheter helps practitioners monitor the effects of vasoactive drugs and follow the effect of PEEP on myocardial function. Dopamine, epinephrine, and norepinephrine are often used separately or in combination to increase BP and
