- Email: [email protected]
Acute intrapartum fetoplacental transfusion in monochorionic twin pregnancy
able, so we had no adequate therapy to offset any major bleeding. As illustrated by our case, fetal intracranial hemorrhage can occur in a pregnant woman with BernardSoulier syndrome.
References 1. Bussel JB. Management of infants of mothers with immune thrombocytopenic purpura. J Pediatr 1988;113:497–9. 2. Meuller-Eckhardt C, Kiefel V, Grubert A. 348 cases of suspected neonatal alloimmune thrombocytopenia. Lancet 1989;ii:363– 6. 3. Johnson JA, Ryan G, al-Musa A, Farkas A, Blanchette VS. Prenatal diagnosis and management of neonatal alloimmune thrombocytopenia. Semin Perinatol 1997;21:45–52. 4. Shibata Y, Juji T, Nishizawa Y, Sakamoto H, Ozawa N. Detection of platelet antibodies by a newly developed mixed passive agglutination with platelets. Vox Sang 1981;41:25–31. 5. Peng TC, Kickler TS, Bell WR, Haller E. Obstetric complications in a patient with Bernard-Soulier syndrome. Am J Obstet Gynecol 1991;165:425– 6. 6. Catanzarite VA, Schrimmer DB, Maida C, Mendoza A. Prenatal sonographic diagnosis of intracranial haemorrhage: Report of a case with a sinusoidal fetal heart rate tracing, and review of the literature. Prenat Diagn 1995;15:229 –35.
Acute intrapartum fetoplacental transfusion in monochorionic twin pregnancy Jukka Uotila, MD, PhD, and Outi Tammela, MD, PhD Background: The risk of antenatal fetofetal transfusion in monochorionic twin pregnancies has been noted, but possible acute intrapartum transfusion has not been studied extensively. Acute fetoplacental transfusion after the birth of the first twin can be disastrous to the second twin, so it deserves description. Cases: We present three cases of acute intrapartum fetoplacental transfusion after successful deliveries of first twins. After the births of their cotwins, the second twins rapidly deteriorated and were born severely hypovolemic and anemic. Conclusion: The risk of acute intrapartum transfusion should be kept in mind when planning delivery of mono-
7. Freeman RK, Garite TJ, Nageotte MP. Fetal heart rate monitoring. 2nd ed. Baltimore: Williams & Wilkins, 1991. 8. Peaceman AM, Katz AR, Laville M. Bernard-Soulier syndrome complicating pregnancy: A case report. Obstet Gynecol 1989;73: 457–9.
Address reprint requests to:
Keiya Fujimori, MD Department of Obstetrics and Gynecology School of Medicine, Fukushima Medical University 1 Hikarigaoka, Fukushima City Fukushima 960-1295 Japan E-mail: [email protected]
Received October 20, 1998. Received in revised form December 28, 1998. Accepted January 28, 1999.
Copyright © 1999 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
chorionic twins. (Obstet Gynecol 1999;94:819 –21. © 1999 by The American College of Obstetricians and Gynecologists.)
Approximately one third of all twin pregnancies are monozygotic, and two thirds of those are monochorionic.1 Monochorionic twin pregnancies have threefold to fivefold higher risk of perinatal mortality and an eightfold higher morbidity rate compared with dichorionic twin pregnancies,1 which is attributed mostly to the vascular anastamoses between twin circulations.2 Chorionicity in twin gestations should be determined with ultrasound at the end of the first trimester by thickness of dividing membranes3 for antenatal diagnosis and care.1,2 Monochorionic twin pregnancies should be watched closely for fetofetal transfusion. Untreated fetofetal transfusion has a mortality rate of up to 90%.4 Monochorionic second twins can also lose blood rapidly into the placentas of first twins after first twins’ deliveries.2 Acute intrapartum fetoplacental transfusion has been reported infrequently. We report three cases of acute intrapartum fetoplacental transfusion after successful deliveries of monochorionic first twins. Cases Case 1
From the Departments of Obstetrics and Gynecology and Pediatrics, Tampere University Hospital, Tampere, Finland.
VOL. 94, NO. 5, PART 2, NOVEMBER 1999
A 39-year-old primigravida presented at 33 weeks’ gestation with mild contractions. Her twin pregnancy had progressed
0029-7844/99/$20.00 PII S0029-7844(99)00441-X
819
Figure 1. Internal heart rate tracing of second twin after the birth of first twin, showing absent beat-to-beat variability (single arrow) and acceleration-deceleration patterns (double arrow).
uneventfully. The fetuses were of equal size, there was no polyhydramnios, and fetal heart rate tracings were reactive. Two doses of 12 mg betamethasone were given 24 hours apart. Spontaneous rupture of the first twin’s membranes occurred at 34 weeks’ gestation, and after 3 hours’ labor, she delivered the first twin, an 1880-g male infant with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively, and a 70% hematocrit (normal 40 – 65%) without symptoms of polycythemia. The infant did well and was discharged at 4 weeks of age. Until delivery of the first twin, the external heart rate monitoring of the second twin was excellent. After the first twin was born, the second twin was turned externally from transverse to cephalic lie. Heart rate was normal on ultrasound. The cervix was dilated 6 –7 cm with the fetal head out of the pelvis. Membranes were ruptured, amniotic fluid was clear, and internal fetal monitoring was begun. Within 5–10 minutes, there was decreased beat-to-beat variability and large deceleration-acceleration swings (Figure 1). Thirty minutes after the first twin was born, the second twin, a 1740-g male infant, was delivered by cesarean. The second twin was pale, hypotonic, and without cardiac activity. Despite intubation, resuscitation, umbilical vein catheterization, and a 20-mL packed red blood cell transfusion, the infant died. Umbilical vein pH was 6.91. Hematocrit was not measured before treatment because the infant had severe hypovolemic shock and taking blood samples would have unnecessarily delayed therapy. Hematocrit was 37% after transfusion. The second twin’s side of the placenta was pale and bloodless, whereas the first twin’s was congested with blood. The placenta was monochorionic with vascular anastamoses confirmed by injection and histologic studies. Case 2 A 29-year-old woman with her third uneventful twin pregnancy had labor induced by amniotomy at 38 weeks’ gestation. After 90 minutes, a 2550-g female infant with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively, was born without difficulty. Her hematocrit was 71%, but no symptoms of polycythemia developed, and she was discharged at 7 days of age.
820 Uotila and Tammela
Fetoplacental Transfusion
Within 5 minutes after the birth of the first twin, the heart rate of the second twin showed absent beat-to-beat variability and large acceleration-deceleration patterns. The second twin, a 2635-g female infant, was delivered spontaneously 22 minutes after the first, and was pale and hypotonic, with Apgar scores of 1, 2, and 3 at 1, 5, and 10 minutes, respectively. Central venous pressure was 0 mmHg and umbilical vein pH was 7.46. The infant was intubated, ventilated, and transfused rapidly with 52 mL of packed red blood cells through the umbilical vein. After another 25 mL of packed red blood cells and 20 mL of fresh frozen plasma, hematocrit was 47%. Dopamine infusion and assisted ventilation were needed for 12 hours because of hypotension. At 6 days of age, another 30 mL of packed red blood cells were needed. The infant recovered and was discharged with the first twin at 7 days of age. Her development at 6 months was normal. The placenta was monochorionic, with vascular anastamoses confirmed by injection and histologic studies.
Case 3 A 28-year-old primigravida had a twin pregnancy with fetuses of equal size. Preeclampsia developed at 37 weeks’ gestation and labor was induced with amniotomy. Heart rate tracings of both twins were reassuring. After 7 hours’ labor the first twin was born, a 2430-g male infant with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively, and hematocrit of 64%. The membranes of the second twin spontaneously ruptured soon after the first twin was delivered. The second twin was in transverse lie presenting his right foot and left hand. With an internal monitor on the fetal leg, we recorded decreased beat-to-beat variability and heart rate decelerations. Twentyfive minutes after birth of the first twin, a 2600-g male infant was delivered by internal version and extraction. The infant was pale and hypotonic, with Apgar scores of 1, 1, and 5 at 1, 5, and 10 minutes, respectively, and umbilical vein pH was 7.13. We immediately intubated the infant, catheterized the umbilical vein, and infused 25 mL of 5% glucose and 20 mL of packed red blood cells. After an additional 30 mL of packed red blood cells hematocrit was 36%. Forty milliliters of red blood cells were transfused at 2 and 5 days of age. At age 2 days, phenobarbital therapy was started for convulsions. The infant was discharged at 1 month of age. Anticonvulsive medication was stopped at 3 months of age, and at 6 months neurologic development was normal. The placenta was monochorionic, with vascular anastamoses.
Discussion A MEDLINE search from May 1966 to December 1998, using the search terms “fetoplacental transfusion,” “acute perinatal transfusion,” and “acute intrapartum transfusion” found one German report (Niesen M, Leyendecker G. Ana¨mie des Neugeborenen durch fetoplazentare Transfusion. Arch Gynaek 1977;224:263), but it was not connected with twin pregnancies. Machin and Keith2 recently reported the possibility of second
Obstetrics & Gynecology
twins losing or gaining blood from the placenta after the first cord has been clamped. The time between twin deliveries is usually short enough to prevent development of severe hypovolemia in second twins, so a part of fetoplacental transfusions might not be clinically evident. Although acute fetoplacental transfusion occurs infrequently, we treated three cases during a 2-year period in which a total of 8900 singletons and 180 twins were born in our hospital. Chronic antenatal or acute intrapartum fetofetal transfusion could be causes of the hematocrit differences of our twins, instead of fetoplacental transfusion, especially because of high hematocrit levels in all first twins, ranging from 64 –71%. None of the first twins had symptoms of polycythemia or hypervolemia, but all second twins had severe hypovolemia with 0 mmHg central venous pressure, so significant chronic or acute transfusion from second to first twin seems unlikely. Results of heart rate monitoring of second twins were normal until delivery of first twins, and there was rapid deterioration after first twins’ cords were clamped, so there was acute blood loss between deliveries. All three second twins lost about 40 – 45% of their blood volumes. Placental abruption between deliveries might cause acute blood loss in the second twin, but there were no clinical or histologic signs of abruption. Transfusion into placenta is a possible explanation, because second twins have the sole connection to the placenta after first twins’ delivery. Substantial amounts of blood might be transfused through anastamosing vessels because of decreased resistance in the first twin’s part of the placental vasculature after clamping the umbilical cord.2 The possibility of acute fetoplacental transfusion should be kept in mind when planning the delivery of monochorionic twin pregnancies. If vaginal delivery occurs, care should be taken to monitor the second twin after delivery of the first. If there are signs of acute
VOL. 94, NO. 5, PART 2, NOVEMBER 1999
blood loss, immediate delivery should be undertaken and the infant resuscitated and transfused, as necessary. The risk of acute intrapartum transfusion raises the issue of optimal time between births of monochorionic twins. At our institution, external version and spontaneous labor have been preferred to internal version and extraction of second twins. In the light of this case report, active measures to deliver monochorionic second twins shortly after the first should be considered.
References 1. Denbow M, Fisk N. Chorionicity and twins. Curr Obstet Gynecol 1996;6:212–9. 2. Machin G, Keith L. Can twin-to-twin transfusion syndrome be explained, and how is it treated? Clin Obstet Gynecol 1998;41:105– 13. 3. Winn H, Gabrielli S, Reece E, Roberts J, Salafia C, Hobbins J. Ultrasonographic criteria for the prenatal diagnosis of placental chorionicity in twin gestations. Am J Obstet Gynecol 1989;161: 1540 –2. 4. Weiner C, Ludomirski A. Diagnosis, pathophysiology, and treatment of chronic twin-to-twin transfusion syndrome. Fetal Diagn Ther 1994;9:283–90.
Address reprint requests to:
Jukka Uotila, MD, PhD Department of Obstetrics and Gynecology Box 2000 Tampere University Hospital Tampere, 33521 Finland
Received January 19, 1999. Received in revised form May 12, 1999. Accepted June 10, 1999. Copyright © 1999 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
Uotila and Tammela
Fetoplacental Transfusion
821
References 1. Bussel JB. Management of infants of mothers with immune thrombocytopenic purpura. J Pediatr 1988;113:497–9. 2. Meuller-Eckhardt C, Kiefel V, Grubert A. 348 cases of suspected neonatal alloimmune thrombocytopenia. Lancet 1989;ii:363– 6. 3. Johnson JA, Ryan G, al-Musa A, Farkas A, Blanchette VS. Prenatal diagnosis and management of neonatal alloimmune thrombocytopenia. Semin Perinatol 1997;21:45–52. 4. Shibata Y, Juji T, Nishizawa Y, Sakamoto H, Ozawa N. Detection of platelet antibodies by a newly developed mixed passive agglutination with platelets. Vox Sang 1981;41:25–31. 5. Peng TC, Kickler TS, Bell WR, Haller E. Obstetric complications in a patient with Bernard-Soulier syndrome. Am J Obstet Gynecol 1991;165:425– 6. 6. Catanzarite VA, Schrimmer DB, Maida C, Mendoza A. Prenatal sonographic diagnosis of intracranial haemorrhage: Report of a case with a sinusoidal fetal heart rate tracing, and review of the literature. Prenat Diagn 1995;15:229 –35.
Acute intrapartum fetoplacental transfusion in monochorionic twin pregnancy Jukka Uotila, MD, PhD, and Outi Tammela, MD, PhD Background: The risk of antenatal fetofetal transfusion in monochorionic twin pregnancies has been noted, but possible acute intrapartum transfusion has not been studied extensively. Acute fetoplacental transfusion after the birth of the first twin can be disastrous to the second twin, so it deserves description. Cases: We present three cases of acute intrapartum fetoplacental transfusion after successful deliveries of first twins. After the births of their cotwins, the second twins rapidly deteriorated and were born severely hypovolemic and anemic. Conclusion: The risk of acute intrapartum transfusion should be kept in mind when planning delivery of mono-
7. Freeman RK, Garite TJ, Nageotte MP. Fetal heart rate monitoring. 2nd ed. Baltimore: Williams & Wilkins, 1991. 8. Peaceman AM, Katz AR, Laville M. Bernard-Soulier syndrome complicating pregnancy: A case report. Obstet Gynecol 1989;73: 457–9.
Address reprint requests to:
Keiya Fujimori, MD Department of Obstetrics and Gynecology School of Medicine, Fukushima Medical University 1 Hikarigaoka, Fukushima City Fukushima 960-1295 Japan E-mail: [email protected]
Received October 20, 1998. Received in revised form December 28, 1998. Accepted January 28, 1999.
Copyright © 1999 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
chorionic twins. (Obstet Gynecol 1999;94:819 –21. © 1999 by The American College of Obstetricians and Gynecologists.)
Approximately one third of all twin pregnancies are monozygotic, and two thirds of those are monochorionic.1 Monochorionic twin pregnancies have threefold to fivefold higher risk of perinatal mortality and an eightfold higher morbidity rate compared with dichorionic twin pregnancies,1 which is attributed mostly to the vascular anastamoses between twin circulations.2 Chorionicity in twin gestations should be determined with ultrasound at the end of the first trimester by thickness of dividing membranes3 for antenatal diagnosis and care.1,2 Monochorionic twin pregnancies should be watched closely for fetofetal transfusion. Untreated fetofetal transfusion has a mortality rate of up to 90%.4 Monochorionic second twins can also lose blood rapidly into the placentas of first twins after first twins’ deliveries.2 Acute intrapartum fetoplacental transfusion has been reported infrequently. We report three cases of acute intrapartum fetoplacental transfusion after successful deliveries of monochorionic first twins. Cases Case 1
From the Departments of Obstetrics and Gynecology and Pediatrics, Tampere University Hospital, Tampere, Finland.
VOL. 94, NO. 5, PART 2, NOVEMBER 1999
A 39-year-old primigravida presented at 33 weeks’ gestation with mild contractions. Her twin pregnancy had progressed
0029-7844/99/$20.00 PII S0029-7844(99)00441-X
819
Figure 1. Internal heart rate tracing of second twin after the birth of first twin, showing absent beat-to-beat variability (single arrow) and acceleration-deceleration patterns (double arrow).
uneventfully. The fetuses were of equal size, there was no polyhydramnios, and fetal heart rate tracings were reactive. Two doses of 12 mg betamethasone were given 24 hours apart. Spontaneous rupture of the first twin’s membranes occurred at 34 weeks’ gestation, and after 3 hours’ labor, she delivered the first twin, an 1880-g male infant with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively, and a 70% hematocrit (normal 40 – 65%) without symptoms of polycythemia. The infant did well and was discharged at 4 weeks of age. Until delivery of the first twin, the external heart rate monitoring of the second twin was excellent. After the first twin was born, the second twin was turned externally from transverse to cephalic lie. Heart rate was normal on ultrasound. The cervix was dilated 6 –7 cm with the fetal head out of the pelvis. Membranes were ruptured, amniotic fluid was clear, and internal fetal monitoring was begun. Within 5–10 minutes, there was decreased beat-to-beat variability and large deceleration-acceleration swings (Figure 1). Thirty minutes after the first twin was born, the second twin, a 1740-g male infant, was delivered by cesarean. The second twin was pale, hypotonic, and without cardiac activity. Despite intubation, resuscitation, umbilical vein catheterization, and a 20-mL packed red blood cell transfusion, the infant died. Umbilical vein pH was 6.91. Hematocrit was not measured before treatment because the infant had severe hypovolemic shock and taking blood samples would have unnecessarily delayed therapy. Hematocrit was 37% after transfusion. The second twin’s side of the placenta was pale and bloodless, whereas the first twin’s was congested with blood. The placenta was monochorionic with vascular anastamoses confirmed by injection and histologic studies. Case 2 A 29-year-old woman with her third uneventful twin pregnancy had labor induced by amniotomy at 38 weeks’ gestation. After 90 minutes, a 2550-g female infant with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively, was born without difficulty. Her hematocrit was 71%, but no symptoms of polycythemia developed, and she was discharged at 7 days of age.
820 Uotila and Tammela
Fetoplacental Transfusion
Within 5 minutes after the birth of the first twin, the heart rate of the second twin showed absent beat-to-beat variability and large acceleration-deceleration patterns. The second twin, a 2635-g female infant, was delivered spontaneously 22 minutes after the first, and was pale and hypotonic, with Apgar scores of 1, 2, and 3 at 1, 5, and 10 minutes, respectively. Central venous pressure was 0 mmHg and umbilical vein pH was 7.46. The infant was intubated, ventilated, and transfused rapidly with 52 mL of packed red blood cells through the umbilical vein. After another 25 mL of packed red blood cells and 20 mL of fresh frozen plasma, hematocrit was 47%. Dopamine infusion and assisted ventilation were needed for 12 hours because of hypotension. At 6 days of age, another 30 mL of packed red blood cells were needed. The infant recovered and was discharged with the first twin at 7 days of age. Her development at 6 months was normal. The placenta was monochorionic, with vascular anastamoses confirmed by injection and histologic studies.
Case 3 A 28-year-old primigravida had a twin pregnancy with fetuses of equal size. Preeclampsia developed at 37 weeks’ gestation and labor was induced with amniotomy. Heart rate tracings of both twins were reassuring. After 7 hours’ labor the first twin was born, a 2430-g male infant with Apgar scores of 9 and 9 at 1 and 5 minutes, respectively, and hematocrit of 64%. The membranes of the second twin spontaneously ruptured soon after the first twin was delivered. The second twin was in transverse lie presenting his right foot and left hand. With an internal monitor on the fetal leg, we recorded decreased beat-to-beat variability and heart rate decelerations. Twentyfive minutes after birth of the first twin, a 2600-g male infant was delivered by internal version and extraction. The infant was pale and hypotonic, with Apgar scores of 1, 1, and 5 at 1, 5, and 10 minutes, respectively, and umbilical vein pH was 7.13. We immediately intubated the infant, catheterized the umbilical vein, and infused 25 mL of 5% glucose and 20 mL of packed red blood cells. After an additional 30 mL of packed red blood cells hematocrit was 36%. Forty milliliters of red blood cells were transfused at 2 and 5 days of age. At age 2 days, phenobarbital therapy was started for convulsions. The infant was discharged at 1 month of age. Anticonvulsive medication was stopped at 3 months of age, and at 6 months neurologic development was normal. The placenta was monochorionic, with vascular anastamoses.
Discussion A MEDLINE search from May 1966 to December 1998, using the search terms “fetoplacental transfusion,” “acute perinatal transfusion,” and “acute intrapartum transfusion” found one German report (Niesen M, Leyendecker G. Ana¨mie des Neugeborenen durch fetoplazentare Transfusion. Arch Gynaek 1977;224:263), but it was not connected with twin pregnancies. Machin and Keith2 recently reported the possibility of second
Obstetrics & Gynecology
twins losing or gaining blood from the placenta after the first cord has been clamped. The time between twin deliveries is usually short enough to prevent development of severe hypovolemia in second twins, so a part of fetoplacental transfusions might not be clinically evident. Although acute fetoplacental transfusion occurs infrequently, we treated three cases during a 2-year period in which a total of 8900 singletons and 180 twins were born in our hospital. Chronic antenatal or acute intrapartum fetofetal transfusion could be causes of the hematocrit differences of our twins, instead of fetoplacental transfusion, especially because of high hematocrit levels in all first twins, ranging from 64 –71%. None of the first twins had symptoms of polycythemia or hypervolemia, but all second twins had severe hypovolemia with 0 mmHg central venous pressure, so significant chronic or acute transfusion from second to first twin seems unlikely. Results of heart rate monitoring of second twins were normal until delivery of first twins, and there was rapid deterioration after first twins’ cords were clamped, so there was acute blood loss between deliveries. All three second twins lost about 40 – 45% of their blood volumes. Placental abruption between deliveries might cause acute blood loss in the second twin, but there were no clinical or histologic signs of abruption. Transfusion into placenta is a possible explanation, because second twins have the sole connection to the placenta after first twins’ delivery. Substantial amounts of blood might be transfused through anastamosing vessels because of decreased resistance in the first twin’s part of the placental vasculature after clamping the umbilical cord.2 The possibility of acute fetoplacental transfusion should be kept in mind when planning the delivery of monochorionic twin pregnancies. If vaginal delivery occurs, care should be taken to monitor the second twin after delivery of the first. If there are signs of acute
VOL. 94, NO. 5, PART 2, NOVEMBER 1999
blood loss, immediate delivery should be undertaken and the infant resuscitated and transfused, as necessary. The risk of acute intrapartum transfusion raises the issue of optimal time between births of monochorionic twins. At our institution, external version and spontaneous labor have been preferred to internal version and extraction of second twins. In the light of this case report, active measures to deliver monochorionic second twins shortly after the first should be considered.
References 1. Denbow M, Fisk N. Chorionicity and twins. Curr Obstet Gynecol 1996;6:212–9. 2. Machin G, Keith L. Can twin-to-twin transfusion syndrome be explained, and how is it treated? Clin Obstet Gynecol 1998;41:105– 13. 3. Winn H, Gabrielli S, Reece E, Roberts J, Salafia C, Hobbins J. Ultrasonographic criteria for the prenatal diagnosis of placental chorionicity in twin gestations. Am J Obstet Gynecol 1989;161: 1540 –2. 4. Weiner C, Ludomirski A. Diagnosis, pathophysiology, and treatment of chronic twin-to-twin transfusion syndrome. Fetal Diagn Ther 1994;9:283–90.
Address reprint requests to:
Jukka Uotila, MD, PhD Department of Obstetrics and Gynecology Box 2000 Tampere University Hospital Tampere, 33521 Finland
Received January 19, 1999. Received in revised form May 12, 1999. Accepted June 10, 1999. Copyright © 1999 by The American College of Obstetricians and Gynecologists. Published by Elsevier Science Inc.
Uotila and Tammela
Fetoplacental Transfusion
821