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Successful cardiopulmonary resuscitation of a parturient with amniotic fluid embolism
International Journal of Obstetric Anesthesia
(1992)1~205-207
© 1992LongmanGroup UK Ltd
international Journal of Obstetric Anesthesia
!
CASE REPORT
Successful cardiopulmonary resuscitation of a parturient with amniotic fluid embolism E. Alon, P. G. Atanassoff
Department of Anesthesiology, University Hospital, Zurich, Switzerland S U M M A R I1. A case of presumed amniotic fluid embolism is presented. Diagnosis is based on clinical findings in a 21-year-old parturient, who was admitted to hospital at 39 weeks gestation. During labor the patient became dyspneic and cyanotic, had convulsions and finally suffered a cardiac arrest. During cardiopulmonary resuscitation she was placed in a left semilateral position and an emergency cesarean section was performed immediately. Following delivery of the baby the heart rhythm returned to normal. The prolonged resuscitation produced serious neurological sequelae in both mother and infant in the first few months following delivery, though with complete long-term recovery. This case report highlights the importance of displacing the uterus laterally and performing an emergency cesarean section during resuscitation.
restarted. Briefly afterwards when turning on to her side and back again, the patient suddenly became cyanotic and complained of respiratory distress. She then convulsed and the fetal heart rate slowed to 60 beats/rain. The obstetricians immediately decided to proceed to emergency cesarean section. A few minutes later dyspnea and cyanosis worsened and the patient became unresponsive; she was rapidly intubated by the anesthesiologist using thiopental 4 mg/kg and succinylcholine 1 mg/kg. There was a sudden cardiovascular collapse, that finally resulted in cardiac arrest. Cardiopulmonary resuscitation was started. Simultanously catheters were inserted into the femoral artery and, after several attempts, into the subclavian vein. Further measures included intravenous administration of epinephrine, sodium bicarbonate, steroids and adequate fluid support. Surgery started during resuscitation and, following delivery of the baby, sinus rhythm and an adequate circulation returned. CPR lasted for approximately 30 rain during which time the patient lay on her back with a wedge under her right hip. Intraoperatively excessive and persistent bleeding due to uterine atony required a hysterectomy. Following removal of the uterus the patient's circulation stabilized. The intraoperative bleeding tendency confirmed the suspicion of a coagulopathy as part of an amniotic fluid embolism. It was verified by immediate postoperative coagulation tests in the intensive care unit (ICU) featuring fibrinogen less than 0.7 g/liter (normal 1.5-4g/liter), a prothrombin time of 78 s (normal 12.5 s), a partial
Amniotic fluid embolism is a very dangerous condition in obstetrics which can be neither predicted nor prewmted. The maternal mortality has been estimated to be 86% 1 and the perinatal and neonatal mortality 40%. 2 This report deals with a patient who suffered from amniotic fluid embolism during labor.
CASE REPORT A 21-year-old primigravid woman came to hospital at 39 weeks gestation with regular uterine contractions. She had a history of hepatitis B infection and a more than average increase in body weight during pregnancy. Additionally glucose tolerance was impaired with evidence of gestational diabetes. Shortly after admission the membranes ruptured and intense and painful but ineffective contractions followed. The cervix did not dilate. An oxytocin infusion was started to accelerate labor; a short time later a first prolonged deceleration of fetal heart rate was noted. The oxytocin infusion was stopped. As there was evidence of a prolonged first stage of labor with continuously increasing pain, the anesthesiologist inserted an epidural catheter with subsequent injection of 8 ml of plain bupivacaine 0.25%. This was repeated once 45 rain later. As there was still no cervical dilatation, the oxytocin infusion was Eli Alon MD, P. J. Atanassoff MD, Department of Anesthesiology, University Hospital, R~imistrasse 100, 8091 Zurich, Switzerland. Correspondence to: Dr Eli Alon. 205
206
International Journal of Obstetric Anesthesia
thromboplastin time of more than 150 s and extensively elevated fibrin split products. Additionally there was a drop in hemoglobin to 7.3 g/dl, and a hematocrit of 212%; platelets dropped from initially more than 200 x 109/liter to 120 x 109/liter. Blood samples obtained from the right side of the heart did not reveal any amniotic fluid material. The patient remained intubated and mechanically ventilated in the ICU for 11 days. Immediate therapeutic measures in the ICU consisted of fibrinogen, fresh fi:ozen plasma and low dose heparin infusions. The coagulation status improved and became normal within 36 h. Chest X-rays revealed bilateral pleural effusions which on draining proved to be bloodtinged. Lung perfusion scintigraphy did not show any signs of lung embolism. The neurological status of the mother detoriated postoperatively. There were signs of hypoxic brain damage with recurrent tonicclonic ,convulsions and spastic extensions of all four extremities, that could only be controlled by continuous infusion of midazolam. Several EEGs were not conclusive. Brain computer tomography (CT) showed no signs of hematoma. After weaning from mechanical ventilation and following extubation of the trachea there was slight improvement of the neurological status. Following release from the University Hospital the patient was transferred to a rehabilitation center. Five months later gait, language, and movements were still described as being slowed with an additional loss of memory. Apraxia was prominent with impaired ability to imitate body movements. A late inquiry revealed that the woman had recovered with no residual serious neurological disturbance. The patient gave birth to a male infant of 3500 g with an Apgar score of 2/3/5. Blood gas analysis revealed an umbilical vein pH of 6.71, a PCO 2 of 142 mmHg and a PO2 of 0 mmHg. The infant was rapidly' intubated by the neonatotogist with simultaneous correction of acidosis. Post partum the infant demonstrated signs of severe perinatal hypoxia with increased muscle tone, hyperexcitability, and fine tremor of the upper extremities. Brain CT demonstrated signs of edema due to hypoxia and magnetic resonance imaging (MRI) showed hypoxic lesions in the basal ganglia and the internal capsule. The latest follow-up, after 2 years, showed almost normal development in terms of neurology, language and growth. The latest MRI of the brain was also completely normal[.
DISCUSSION It is generally accepted that the true incidence of amniotic fluid embolism is between 1:20000 and 1 : 30 000 deliveries.3'4 The condition is lifethreatening and in some medical centers it is the
leading cause of maternal death during labor, delivery and the immediate post partum period. 1 The literature describes four cardinal signs of amniotic fluid embolism, namely respiratory distress, coma, cyanosis and cardiovascular collapse. The 272 cases reviewed by Morgan 1 presented respiratory difficulties with cyanosis in 51% as the initial symptom; in 27% there was a drop in blood pressure and 10% of patients had convulsions. Our patient became cyanotic, complained of respiratory distress, was bleeding, and had convulsions. A short time later she was dyspneic, unresponsive and had a cardiovascular collapse. The radiological findings of pleural effusions are probably the result of multiple subclavian vein punctures during CPR. The effect of the pregnant uterus on circulation was described by Depace et al: 5 a woman at 36 weeks of gestation had a respiratory arrest. Despite endotracheal intubation, cardiac massage, fluid and electrolyte therapy, the physicians were not able to raise the blood pressure. Immediately following delivery of the baby by cesarean section, however, arterial blood pressure rose to systolic 80 mmHg. Marx 6 described 5 cases of CPR during late pregnancy; all women were resuscitated for 10 min. In 3 of them the baby was delivered early, resulting in survival of all 3 women and most important, none of them exhibited neurological deficits. In the other 2 patients delivery was delayed, leading to irreversible neurological damage. After 32 weeks of gestation many authors v-9 recommend immediate cesarean section if CPR proves ineffective for more than 15 rain. The hemodynamic effects of the uterus must be managed by displacing it to the left thus promoting venous return and aiding in CPR. Additionally early delivery by cesarean section favours a long-term positive outcome. Serious long-term neurological complications resulting from amniotic fluid debris with subsequent occlusion of the vasculature of the central nervous system (CNS) are said to be rare. 1° The emboli usually consist of admixtures of squames and mucin, involving only the small capillaries. The resultant CNS hypoxia leads to loss of vision and hemiplegia. 11'12' The serious but short-term neurological complications in both mother and infant of the present case may be due to prolonged tissue hypoxia as evidenced by the newborn's blood gas analysis after delivery, and also, in the case of the mother, to the occlusion of small vessels in the CNS. In animal experiments, Steiner and Lushbaugh ~3 could reproduce human symptoms of amniotic fluid embolism. They found that complete occlusion of small vessels resolved after 14 days. These findings are in accordance with the clinical course of our patient and other women that survived amniotic fluid embolism. In our case both mother and infant fortunately recovered in the course of time without serious sequelae.
Successful cardiopulmonary resuscitation of a parturient with amniotic fluid embolism 207 References 1. Morgan M. Amniotic fluid embolism. Anaesthesia 1979; 34'.' 20-32. 2. Clark S L. Amniofic fluid embolism. Clin Perinatol 1986; 13:: 801-811. 3. Killam A. Amniotic fluid embolism. Clin Obstet Gynecol 1985; 28: 32-36. 4. Sperry IC Amniotic fluid embolism. To understand an enigma. JAMA 1986; 255: 2183-2186. 5. Depace IN L, Betesh J S, Kotler M N. Postmortem cesarean section with recovery of both mother and offspring. J Am Med Worn Assoc 1982; 248: 971-973. 6. Marx G. Cardiopulmonary resuscitation of latepregnanlL women. Anesthesiology 1982; 56: 156. 7. Lee R V, Rodgers B D, White L M, Harvey R C. Cardiopulmonary resucitation of pregnant women. Am J Med i986; 81: 311-318.
8. Rees G A D and Willis B A. Resuscitation in late pregnancy. Anaesthesia 1988; 43: 347-349. 9. Mauer D, Dick W, Leyser K H, Gaida J B, Gervais H. Besonderheiten der kardiopulmonalen Reanimation (CPR) bei Schwangeren. Anaesthesist 1990; 39: 393-397. 10. Peterson E P, Taylor H B. Amniotic fluid embolism: an analysis of 40 cases. Obstet Gynecol 1970; 35: 787-793. 11. Fischbein F I. Ischemic retinopathy following amniotic fluid embolization. Am J Ophthalmol 1969; 67: 351. 12. Goldstein P J. Amniotic fluid embolism complicating intrauterine saline abortion. Am J Obstet Gynecol 1968; 101: 858. 13. Steiner P E, Lushbaugh C C. Maternal pulmonary embolism by anmiofic fluid as a cause of obstetric shock and unexpected death in obstetrics. J A M A 1986; 255: 2187-2203.
(1992)1~205-207
© 1992LongmanGroup UK Ltd
international Journal of Obstetric Anesthesia
!
CASE REPORT
Successful cardiopulmonary resuscitation of a parturient with amniotic fluid embolism E. Alon, P. G. Atanassoff
Department of Anesthesiology, University Hospital, Zurich, Switzerland S U M M A R I1. A case of presumed amniotic fluid embolism is presented. Diagnosis is based on clinical findings in a 21-year-old parturient, who was admitted to hospital at 39 weeks gestation. During labor the patient became dyspneic and cyanotic, had convulsions and finally suffered a cardiac arrest. During cardiopulmonary resuscitation she was placed in a left semilateral position and an emergency cesarean section was performed immediately. Following delivery of the baby the heart rhythm returned to normal. The prolonged resuscitation produced serious neurological sequelae in both mother and infant in the first few months following delivery, though with complete long-term recovery. This case report highlights the importance of displacing the uterus laterally and performing an emergency cesarean section during resuscitation.
restarted. Briefly afterwards when turning on to her side and back again, the patient suddenly became cyanotic and complained of respiratory distress. She then convulsed and the fetal heart rate slowed to 60 beats/rain. The obstetricians immediately decided to proceed to emergency cesarean section. A few minutes later dyspnea and cyanosis worsened and the patient became unresponsive; she was rapidly intubated by the anesthesiologist using thiopental 4 mg/kg and succinylcholine 1 mg/kg. There was a sudden cardiovascular collapse, that finally resulted in cardiac arrest. Cardiopulmonary resuscitation was started. Simultanously catheters were inserted into the femoral artery and, after several attempts, into the subclavian vein. Further measures included intravenous administration of epinephrine, sodium bicarbonate, steroids and adequate fluid support. Surgery started during resuscitation and, following delivery of the baby, sinus rhythm and an adequate circulation returned. CPR lasted for approximately 30 rain during which time the patient lay on her back with a wedge under her right hip. Intraoperatively excessive and persistent bleeding due to uterine atony required a hysterectomy. Following removal of the uterus the patient's circulation stabilized. The intraoperative bleeding tendency confirmed the suspicion of a coagulopathy as part of an amniotic fluid embolism. It was verified by immediate postoperative coagulation tests in the intensive care unit (ICU) featuring fibrinogen less than 0.7 g/liter (normal 1.5-4g/liter), a prothrombin time of 78 s (normal 12.5 s), a partial
Amniotic fluid embolism is a very dangerous condition in obstetrics which can be neither predicted nor prewmted. The maternal mortality has been estimated to be 86% 1 and the perinatal and neonatal mortality 40%. 2 This report deals with a patient who suffered from amniotic fluid embolism during labor.
CASE REPORT A 21-year-old primigravid woman came to hospital at 39 weeks gestation with regular uterine contractions. She had a history of hepatitis B infection and a more than average increase in body weight during pregnancy. Additionally glucose tolerance was impaired with evidence of gestational diabetes. Shortly after admission the membranes ruptured and intense and painful but ineffective contractions followed. The cervix did not dilate. An oxytocin infusion was started to accelerate labor; a short time later a first prolonged deceleration of fetal heart rate was noted. The oxytocin infusion was stopped. As there was evidence of a prolonged first stage of labor with continuously increasing pain, the anesthesiologist inserted an epidural catheter with subsequent injection of 8 ml of plain bupivacaine 0.25%. This was repeated once 45 rain later. As there was still no cervical dilatation, the oxytocin infusion was Eli Alon MD, P. J. Atanassoff MD, Department of Anesthesiology, University Hospital, R~imistrasse 100, 8091 Zurich, Switzerland. Correspondence to: Dr Eli Alon. 205
206
International Journal of Obstetric Anesthesia
thromboplastin time of more than 150 s and extensively elevated fibrin split products. Additionally there was a drop in hemoglobin to 7.3 g/dl, and a hematocrit of 212%; platelets dropped from initially more than 200 x 109/liter to 120 x 109/liter. Blood samples obtained from the right side of the heart did not reveal any amniotic fluid material. The patient remained intubated and mechanically ventilated in the ICU for 11 days. Immediate therapeutic measures in the ICU consisted of fibrinogen, fresh fi:ozen plasma and low dose heparin infusions. The coagulation status improved and became normal within 36 h. Chest X-rays revealed bilateral pleural effusions which on draining proved to be bloodtinged. Lung perfusion scintigraphy did not show any signs of lung embolism. The neurological status of the mother detoriated postoperatively. There were signs of hypoxic brain damage with recurrent tonicclonic ,convulsions and spastic extensions of all four extremities, that could only be controlled by continuous infusion of midazolam. Several EEGs were not conclusive. Brain computer tomography (CT) showed no signs of hematoma. After weaning from mechanical ventilation and following extubation of the trachea there was slight improvement of the neurological status. Following release from the University Hospital the patient was transferred to a rehabilitation center. Five months later gait, language, and movements were still described as being slowed with an additional loss of memory. Apraxia was prominent with impaired ability to imitate body movements. A late inquiry revealed that the woman had recovered with no residual serious neurological disturbance. The patient gave birth to a male infant of 3500 g with an Apgar score of 2/3/5. Blood gas analysis revealed an umbilical vein pH of 6.71, a PCO 2 of 142 mmHg and a PO2 of 0 mmHg. The infant was rapidly' intubated by the neonatotogist with simultaneous correction of acidosis. Post partum the infant demonstrated signs of severe perinatal hypoxia with increased muscle tone, hyperexcitability, and fine tremor of the upper extremities. Brain CT demonstrated signs of edema due to hypoxia and magnetic resonance imaging (MRI) showed hypoxic lesions in the basal ganglia and the internal capsule. The latest follow-up, after 2 years, showed almost normal development in terms of neurology, language and growth. The latest MRI of the brain was also completely normal[.
DISCUSSION It is generally accepted that the true incidence of amniotic fluid embolism is between 1:20000 and 1 : 30 000 deliveries.3'4 The condition is lifethreatening and in some medical centers it is the
leading cause of maternal death during labor, delivery and the immediate post partum period. 1 The literature describes four cardinal signs of amniotic fluid embolism, namely respiratory distress, coma, cyanosis and cardiovascular collapse. The 272 cases reviewed by Morgan 1 presented respiratory difficulties with cyanosis in 51% as the initial symptom; in 27% there was a drop in blood pressure and 10% of patients had convulsions. Our patient became cyanotic, complained of respiratory distress, was bleeding, and had convulsions. A short time later she was dyspneic, unresponsive and had a cardiovascular collapse. The radiological findings of pleural effusions are probably the result of multiple subclavian vein punctures during CPR. The effect of the pregnant uterus on circulation was described by Depace et al: 5 a woman at 36 weeks of gestation had a respiratory arrest. Despite endotracheal intubation, cardiac massage, fluid and electrolyte therapy, the physicians were not able to raise the blood pressure. Immediately following delivery of the baby by cesarean section, however, arterial blood pressure rose to systolic 80 mmHg. Marx 6 described 5 cases of CPR during late pregnancy; all women were resuscitated for 10 min. In 3 of them the baby was delivered early, resulting in survival of all 3 women and most important, none of them exhibited neurological deficits. In the other 2 patients delivery was delayed, leading to irreversible neurological damage. After 32 weeks of gestation many authors v-9 recommend immediate cesarean section if CPR proves ineffective for more than 15 rain. The hemodynamic effects of the uterus must be managed by displacing it to the left thus promoting venous return and aiding in CPR. Additionally early delivery by cesarean section favours a long-term positive outcome. Serious long-term neurological complications resulting from amniotic fluid debris with subsequent occlusion of the vasculature of the central nervous system (CNS) are said to be rare. 1° The emboli usually consist of admixtures of squames and mucin, involving only the small capillaries. The resultant CNS hypoxia leads to loss of vision and hemiplegia. 11'12' The serious but short-term neurological complications in both mother and infant of the present case may be due to prolonged tissue hypoxia as evidenced by the newborn's blood gas analysis after delivery, and also, in the case of the mother, to the occlusion of small vessels in the CNS. In animal experiments, Steiner and Lushbaugh ~3 could reproduce human symptoms of amniotic fluid embolism. They found that complete occlusion of small vessels resolved after 14 days. These findings are in accordance with the clinical course of our patient and other women that survived amniotic fluid embolism. In our case both mother and infant fortunately recovered in the course of time without serious sequelae.
Successful cardiopulmonary resuscitation of a parturient with amniotic fluid embolism 207 References 1. Morgan M. Amniotic fluid embolism. Anaesthesia 1979; 34'.' 20-32. 2. Clark S L. Amniofic fluid embolism. Clin Perinatol 1986; 13:: 801-811. 3. Killam A. Amniotic fluid embolism. Clin Obstet Gynecol 1985; 28: 32-36. 4. Sperry IC Amniotic fluid embolism. To understand an enigma. JAMA 1986; 255: 2183-2186. 5. Depace IN L, Betesh J S, Kotler M N. Postmortem cesarean section with recovery of both mother and offspring. J Am Med Worn Assoc 1982; 248: 971-973. 6. Marx G. Cardiopulmonary resuscitation of latepregnanlL women. Anesthesiology 1982; 56: 156. 7. Lee R V, Rodgers B D, White L M, Harvey R C. Cardiopulmonary resucitation of pregnant women. Am J Med i986; 81: 311-318.
8. Rees G A D and Willis B A. Resuscitation in late pregnancy. Anaesthesia 1988; 43: 347-349. 9. Mauer D, Dick W, Leyser K H, Gaida J B, Gervais H. Besonderheiten der kardiopulmonalen Reanimation (CPR) bei Schwangeren. Anaesthesist 1990; 39: 393-397. 10. Peterson E P, Taylor H B. Amniotic fluid embolism: an analysis of 40 cases. Obstet Gynecol 1970; 35: 787-793. 11. Fischbein F I. Ischemic retinopathy following amniotic fluid embolization. Am J Ophthalmol 1969; 67: 351. 12. Goldstein P J. Amniotic fluid embolism complicating intrauterine saline abortion. Am J Obstet Gynecol 1968; 101: 858. 13. Steiner P E, Lushbaugh C C. Maternal pulmonary embolism by anmiofic fluid as a cause of obstetric shock and unexpected death in obstetrics. J A M A 1986; 255: 2187-2203.