Brittain et al.
August 199 1
Am
creased oncotic pressure, and increased hydrostatic pressure that resulted in a net fluid shift from the intravascular to extravascular tissues. This edema was probably most pronounced in the labia because of their dependent nature that was caused by bed rest. We believe that the cause of the fluid retention was a complication of the administration of tocolytic agents.
J Obslet Gynecol
REFERENCES I. Goodlin RC, Frederick IB. Postpartum vulvar edema associated with the birthing chair. AM J OBSTET GYNECOL 1983; 146:334. 2. Hankins GD. Defenses against side effects of tocolytic therapy. Contemp Ob /Gyn 1986;3:65-79. A complete list of 1'efeunces is available from the authors on request.
Uterine activity after preterm premature rupture of the membranes B.A. Campbell, MD, R.B. Newman, MD, and S.L. Stramm, RN Charleston, South Carolina Preterm premature rupture of the membranes complicates few pregnancies but is a major contributor to overall perinatal morbidity and mortality. Although a reduced incidence of preterm premature rupture of fetal membranes has been reported in women who had antepartum uterine activity monitoring, there are few data regarding uterine activity after preterm premature rupture of fetal membranes. Therefore daily uterine activity monitoring was performed in 101 consecutive women with preterm premature rupture of fetal membranes between 26 and 34 weeks' gestation. The mean gestational ages at rupture and delivery were 31.4 ± 2.3 and 33.7 ± 4.5 weeks, respectively. A significant increase in contraction frequency was identified within 24 hours of onset of preterm labor (p < 0.005) . A contraction frequency of four or more per hour predicted the onset of labor within 24 hours with a sensitivity of 72%, a specificity of 90%, a positive predictive value of 54%, and a negative predictive value of 95%. These results indicate that most women with preterm premature rupture of fetal membranes exhibit a baseline contraction frequency that is similar to that of women with intact membranes and premature labor. An abrupt increase in contraction frequency is a warning of impending labor. (AM J OBSTET GYNECOL 1991 ;165:422-5.)
Key words: Preterm premature rupture of the membranes, uterine contraction frequency Although preterm premature rupture of the membranes is an infrequent complication of pregnancy, it contributes significantly to perinatal morbidity and mortality. I The most common sequela is respiratory distress syndrome, which occurs in 10% to 40% of preterm infants whose mothers had premature rupture of fetal membranes. Other possible complications include neonatal sepsis, skeletal malformations, pulmonary hypoplasia, abnormal presentations, and cord prolapse. The perinatal mortality associated with pre term premature rupture of fetal membranes has been reported to range as high as 20% to 50% ." The cause of preterm preFrom the Maternal-Fetal Medicine Section, Department of Obstetrics and Gynecology, Medical University of South Carolina. Received for publication August 29, 1990; revised January 1, 1991; accepted January 28,1991. R eprint requests: Berry A. Campbell, MD, Department of Obstetri cs and Gynecology, 171 Ashley Ave., Charleston, SC 29425.
611 /28331
mature rupture of fetal membranes is unknown but is likely to be multifactorial. Preterm premature rupture of fetal membranes has been associated with uterine overdistention, cervical incompetence, malpresentation, asymptomatic genital tract infection, and local defects within the membranes.3•7 Subclinical preteI'm labor also may have a role in preterm premature rupture of fetal membranes, but no direct supporting evidence exists. This study assesses daily uterine activity monitoring in a large cohort of women with expectant management after preterm premature rupture of fetal membranes. This study was performed to evaluate the possible relationship of preterm premature rupture of fetal membranes and increased uterine activity. Material and methods
A prospective evaluation of daily uterine activity was performed in 101 consecutive women with preterm
Volume 165 Number 2
premature rupture of fetal membranes who were between 26 and 34 weeks' gestation. Patients were excluded if there was evidence of active labor, chorioamnionitis, fetal distress, or fetal lung maturity during an initial 24-hour observation period. During the initial observation, membrane rupture was confirmed by Nitrazine paper testing, ferning of vaginal fluid, and ultrasonographic evaluation of amniotic fluid volume. A visual assessment of cervical dilatation and effacement was performed, and a cervicovaginal culture for group B streptococcus was obtained. Each patient was given antibiotics pending the culture results. Tocolysis was used only during the initial 24 hours. Betamethasone (12 mg intramuscularly, 24 hours apart) was optional in gestations of 70% of the patients studied. Martin et at. 10 previously reported very similar findings in a small group of patients with premature rupture of fetal membranes that was managed conservatively. Among women with preterm premature rupture of fetal membranes, the positive predictive value and sensitivity of a baseline contraction frequency of four or more contractions per hour were 54% and 72%, respectively. A contraction frequency of fewer than four contractions per hour was reassuring that labor would not ensue within the next 24 hours (negative pl"edictive value, 95%, specificity, 90%). This predictive information regarding impending preterm labor could be helpful in the management of women with abnormal presentations who are at risk for cord prolapse or birth trauma. Some investigators have suggested the use of antibiotics and tocolysis to prolong pregnancy complicated by preterm premature rupture of fetal membranes. 11 The early identification of impending preterm labor may be of value in determining the role of ascending genital tract infection in premature rupture of fetal membranes and in maximizing the therapeutic potential of tocolytic agents. This information would be of great use if other management plans were used that placed a premium on the early diagnosis of preterm labor in women with preterm premature rupture of fetal membranes. After preterm premature rupture of fetal membranes, the crescendo of uterine activity leading to the diagnosis of spontaneous labor is very similar to the pattern demonstrated by women with intact membranes. It appears that the status of the membranes does not affect the evolution of uterine activity necessary to initiate preterm labor. Although rupture of the membranes does not appear to be associated with excessive uterine contractility in most cases, the short latent period indicates that preterm premature rupture of fetal membranes is a powerful facilitator of preterm labor. We believe that the ultimate onset of labor in this patient population is often associated with an ascending decidual or chorioamniotic infection. REFERENCES 1. Cox SM, Williams ML, Leveno KJ. The natural history of preterm ruptured membranes: what to expect of expectant management. Obstet Gynecol 1988;71 :558. 2. Bourne G. The human amnion and chorion. London: Lloyd-Luke Medical Books, 1960.
Volume 165 Number 2
3. Ibrahim M, Bou-Resli M, AI-Zaid N, Bishay L. Intact fetal membranes. Morphological pre disposal to rupture. Acta Obstet Gynecol Scand 1983;62:48l. 4. Lavery J, Miller C. Deformation and creep in the human choriomaniotic sac. AM J OBST£T GYNECOL 1979; 134:366. 5. Evaldson G, Malmborg AS, Nord C. Premature rupture of the membranes in ascending infection. Br J Obstet Gynaecol 1982;89:793. 6. Regan J, Chao S, James LS. Premature rupture of the membranes, preterm delivery and group B streptococcal colonization of mothers. AM J OBSTET GYNECOL 1981; 141: 184. 7. Katz M, Newman RB, Gill PJ. Assessment of uterine activity in ambulatory patients at high risk of preterm labor and delivery. AM J OBST£T GYNECOL 1986; 154:44.
Uterine activity after preterm premature membrane rupture
8. Katz M, Gill PJ, Newman RB. Detection of pre term labor by ambulatory monitoring of uterine activity: a preliminary report. Obstet Gynecol 1986;68:773. 9. Morrison JC, Martin IN, Martin RW, Godkin KS, Wiser WL. Prevention of premature birth by ambulatory assessment of uterine activity: a randomized study. AM J OBSTET GYNECOL 1987;156:536. 10. MartinJN, McColgin SW, Martin RW, Roach H, Morrison JC. Uterine activity among a diverse group of patients at risk for preterm delivery. Obstet Gynecol 1990; 76(suppl):4 7S. Il. Morales WJ, AngelJL, O'Brien WF, Knuppel RA. Use of ampicillin and corticosteroids in premature rupture of membranes: a randomized study. Obstet Gynecol 1989;73:72l.
Obstetric complications in a patient with Bernard-Soulier syndrome Thomas C. Peng, MD, Thomas S. KickIer, MD, William R. Bell, MD, and Emily Haller, MD Baltimore, Maryland We describe the obstetric complications and management of a patient with Bernard-Soulier syndrome. Severe bleeding at the time of delivery and delayed postpartum hemorrhage were prominent features of her pregnancies. Further complicating this woman's pregnancies was the development of antibodies to platelet glycoprotein IB/IX, leading to neonatal alloimmune thrombocytopenia. (AM J OBSTET GVNECOL 1991 ;165:425-6.)
Key words: Neonatal alloimmune thrombocytopenia, Bernard-Soulier syndrome Individuals may lack the membrane glycoprotein IB/IX, leading to Bernard-Soulier syndrome, which is characterized by platelet dysfunction. Life-threatening bleeding may occur spontaneously or after invasive procedures. Women lacking these glycoproteins are also at risk of being immunized by fetal platelets during pregnancy. We report on a mother with BernardSoulier syndrome who was immunized to platelet glycoprotein IB I IX, leading to neonatal thrombocytopenia.
Case report A 35-year-old woman had Bernard-Soulier syndrome. Her first pregnancy, which occurred in 1972, From the Departments of Obstetrics and Gynecology, Medicine, and Pathology, The Johns Hopkins University School of Medicine. Receivedforpublication October 3,1990; revised February 1,1991; accepted February 27, 1991. Reprint requests: Thomas S. Kickier, MD, The Johns Hopkins Hospital, 600 N. Wolfe St., Baltimore, MD 21205.
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was uneventful. Postpartum hemorrhage necessitated 11 units of blood. In 1986 her second pregnancy ended with in utero fetal death at 38 weeks' gestation, concomitant with severe third-trimester gastrointestinal bleeding. Vaginal bleeding necessitating 8 units of blood occurred 2 weeks after delivery. Treatment with aminocaproic acid significantly reduced the vaginal bleeding. In 1987 a third pregnancy resulted in an infant with a platelet count of 51,0001 mm'. In 1988 she was seen for her fourth pregnancy. At the onset of labor she received 50 gm 'V-globulin intravenously. Vaginal delivery of a non thrombocytopenic infant occurred 28 hours later. E-Aminocaproic acid was initiated post partum, 5 gm intravenously, then 2 gm every 6 hours for 24 hours. Post partum she experienced moderate vaginal bleeding that necessitated four units of blood. After the addition of methergine, the bleeding decreased. The E-aminocaproic acid was continued for 4 weeks. Platelet antibody studies. After the third pregnancy the patient'S serum was tested with an antiglobulin test that had a radioactive label against platelets from 20
425
August 199 1
Am
creased oncotic pressure, and increased hydrostatic pressure that resulted in a net fluid shift from the intravascular to extravascular tissues. This edema was probably most pronounced in the labia because of their dependent nature that was caused by bed rest. We believe that the cause of the fluid retention was a complication of the administration of tocolytic agents.
J Obslet Gynecol
REFERENCES I. Goodlin RC, Frederick IB. Postpartum vulvar edema associated with the birthing chair. AM J OBSTET GYNECOL 1983; 146:334. 2. Hankins GD. Defenses against side effects of tocolytic therapy. Contemp Ob /Gyn 1986;3:65-79. A complete list of 1'efeunces is available from the authors on request.
Uterine activity after preterm premature rupture of the membranes B.A. Campbell, MD, R.B. Newman, MD, and S.L. Stramm, RN Charleston, South Carolina Preterm premature rupture of the membranes complicates few pregnancies but is a major contributor to overall perinatal morbidity and mortality. Although a reduced incidence of preterm premature rupture of fetal membranes has been reported in women who had antepartum uterine activity monitoring, there are few data regarding uterine activity after preterm premature rupture of fetal membranes. Therefore daily uterine activity monitoring was performed in 101 consecutive women with preterm premature rupture of fetal membranes between 26 and 34 weeks' gestation. The mean gestational ages at rupture and delivery were 31.4 ± 2.3 and 33.7 ± 4.5 weeks, respectively. A significant increase in contraction frequency was identified within 24 hours of onset of preterm labor (p < 0.005) . A contraction frequency of four or more per hour predicted the onset of labor within 24 hours with a sensitivity of 72%, a specificity of 90%, a positive predictive value of 54%, and a negative predictive value of 95%. These results indicate that most women with preterm premature rupture of fetal membranes exhibit a baseline contraction frequency that is similar to that of women with intact membranes and premature labor. An abrupt increase in contraction frequency is a warning of impending labor. (AM J OBSTET GYNECOL 1991 ;165:422-5.)
Key words: Preterm premature rupture of the membranes, uterine contraction frequency Although preterm premature rupture of the membranes is an infrequent complication of pregnancy, it contributes significantly to perinatal morbidity and mortality. I The most common sequela is respiratory distress syndrome, which occurs in 10% to 40% of preterm infants whose mothers had premature rupture of fetal membranes. Other possible complications include neonatal sepsis, skeletal malformations, pulmonary hypoplasia, abnormal presentations, and cord prolapse. The perinatal mortality associated with pre term premature rupture of fetal membranes has been reported to range as high as 20% to 50% ." The cause of preterm preFrom the Maternal-Fetal Medicine Section, Department of Obstetrics and Gynecology, Medical University of South Carolina. Received for publication August 29, 1990; revised January 1, 1991; accepted January 28,1991. R eprint requests: Berry A. Campbell, MD, Department of Obstetri cs and Gynecology, 171 Ashley Ave., Charleston, SC 29425.
611 /28331
mature rupture of fetal membranes is unknown but is likely to be multifactorial. Preterm premature rupture of fetal membranes has been associated with uterine overdistention, cervical incompetence, malpresentation, asymptomatic genital tract infection, and local defects within the membranes.3•7 Subclinical preteI'm labor also may have a role in preterm premature rupture of fetal membranes, but no direct supporting evidence exists. This study assesses daily uterine activity monitoring in a large cohort of women with expectant management after preterm premature rupture of fetal membranes. This study was performed to evaluate the possible relationship of preterm premature rupture of fetal membranes and increased uterine activity. Material and methods
A prospective evaluation of daily uterine activity was performed in 101 consecutive women with preterm
Volume 165 Number 2
premature rupture of fetal membranes who were between 26 and 34 weeks' gestation. Patients were excluded if there was evidence of active labor, chorioamnionitis, fetal distress, or fetal lung maturity during an initial 24-hour observation period. During the initial observation, membrane rupture was confirmed by Nitrazine paper testing, ferning of vaginal fluid, and ultrasonographic evaluation of amniotic fluid volume. A visual assessment of cervical dilatation and effacement was performed, and a cervicovaginal culture for group B streptococcus was obtained. Each patient was given antibiotics pending the culture results. Tocolysis was used only during the initial 24 hours. Betamethasone (12 mg intramuscularly, 24 hours apart) was optional in gestations of 70% of the patients studied. Martin et at. 10 previously reported very similar findings in a small group of patients with premature rupture of fetal membranes that was managed conservatively. Among women with preterm premature rupture of fetal membranes, the positive predictive value and sensitivity of a baseline contraction frequency of four or more contractions per hour were 54% and 72%, respectively. A contraction frequency of fewer than four contractions per hour was reassuring that labor would not ensue within the next 24 hours (negative pl"edictive value, 95%, specificity, 90%). This predictive information regarding impending preterm labor could be helpful in the management of women with abnormal presentations who are at risk for cord prolapse or birth trauma. Some investigators have suggested the use of antibiotics and tocolysis to prolong pregnancy complicated by preterm premature rupture of fetal membranes. 11 The early identification of impending preterm labor may be of value in determining the role of ascending genital tract infection in premature rupture of fetal membranes and in maximizing the therapeutic potential of tocolytic agents. This information would be of great use if other management plans were used that placed a premium on the early diagnosis of preterm labor in women with preterm premature rupture of fetal membranes. After preterm premature rupture of fetal membranes, the crescendo of uterine activity leading to the diagnosis of spontaneous labor is very similar to the pattern demonstrated by women with intact membranes. It appears that the status of the membranes does not affect the evolution of uterine activity necessary to initiate preterm labor. Although rupture of the membranes does not appear to be associated with excessive uterine contractility in most cases, the short latent period indicates that preterm premature rupture of fetal membranes is a powerful facilitator of preterm labor. We believe that the ultimate onset of labor in this patient population is often associated with an ascending decidual or chorioamniotic infection. REFERENCES 1. Cox SM, Williams ML, Leveno KJ. The natural history of preterm ruptured membranes: what to expect of expectant management. Obstet Gynecol 1988;71 :558. 2. Bourne G. The human amnion and chorion. London: Lloyd-Luke Medical Books, 1960.
Volume 165 Number 2
3. Ibrahim M, Bou-Resli M, AI-Zaid N, Bishay L. Intact fetal membranes. Morphological pre disposal to rupture. Acta Obstet Gynecol Scand 1983;62:48l. 4. Lavery J, Miller C. Deformation and creep in the human choriomaniotic sac. AM J OBST£T GYNECOL 1979; 134:366. 5. Evaldson G, Malmborg AS, Nord C. Premature rupture of the membranes in ascending infection. Br J Obstet Gynaecol 1982;89:793. 6. Regan J, Chao S, James LS. Premature rupture of the membranes, preterm delivery and group B streptococcal colonization of mothers. AM J OBSTET GYNECOL 1981; 141: 184. 7. Katz M, Newman RB, Gill PJ. Assessment of uterine activity in ambulatory patients at high risk of preterm labor and delivery. AM J OBST£T GYNECOL 1986; 154:44.
Uterine activity after preterm premature membrane rupture
8. Katz M, Gill PJ, Newman RB. Detection of pre term labor by ambulatory monitoring of uterine activity: a preliminary report. Obstet Gynecol 1986;68:773. 9. Morrison JC, Martin IN, Martin RW, Godkin KS, Wiser WL. Prevention of premature birth by ambulatory assessment of uterine activity: a randomized study. AM J OBSTET GYNECOL 1987;156:536. 10. MartinJN, McColgin SW, Martin RW, Roach H, Morrison JC. Uterine activity among a diverse group of patients at risk for preterm delivery. Obstet Gynecol 1990; 76(suppl):4 7S. Il. Morales WJ, AngelJL, O'Brien WF, Knuppel RA. Use of ampicillin and corticosteroids in premature rupture of membranes: a randomized study. Obstet Gynecol 1989;73:72l.
Obstetric complications in a patient with Bernard-Soulier syndrome Thomas C. Peng, MD, Thomas S. KickIer, MD, William R. Bell, MD, and Emily Haller, MD Baltimore, Maryland We describe the obstetric complications and management of a patient with Bernard-Soulier syndrome. Severe bleeding at the time of delivery and delayed postpartum hemorrhage were prominent features of her pregnancies. Further complicating this woman's pregnancies was the development of antibodies to platelet glycoprotein IB/IX, leading to neonatal alloimmune thrombocytopenia. (AM J OBSTET GVNECOL 1991 ;165:425-6.)
Key words: Neonatal alloimmune thrombocytopenia, Bernard-Soulier syndrome Individuals may lack the membrane glycoprotein IB/IX, leading to Bernard-Soulier syndrome, which is characterized by platelet dysfunction. Life-threatening bleeding may occur spontaneously or after invasive procedures. Women lacking these glycoproteins are also at risk of being immunized by fetal platelets during pregnancy. We report on a mother with BernardSoulier syndrome who was immunized to platelet glycoprotein IB I IX, leading to neonatal thrombocytopenia.
Case report A 35-year-old woman had Bernard-Soulier syndrome. Her first pregnancy, which occurred in 1972, From the Departments of Obstetrics and Gynecology, Medicine, and Pathology, The Johns Hopkins University School of Medicine. Receivedforpublication October 3,1990; revised February 1,1991; accepted February 27, 1991. Reprint requests: Thomas S. Kickier, MD, The Johns Hopkins Hospital, 600 N. Wolfe St., Baltimore, MD 21205.
6/1129135
was uneventful. Postpartum hemorrhage necessitated 11 units of blood. In 1986 her second pregnancy ended with in utero fetal death at 38 weeks' gestation, concomitant with severe third-trimester gastrointestinal bleeding. Vaginal bleeding necessitating 8 units of blood occurred 2 weeks after delivery. Treatment with aminocaproic acid significantly reduced the vaginal bleeding. In 1987 a third pregnancy resulted in an infant with a platelet count of 51,0001 mm'. In 1988 she was seen for her fourth pregnancy. At the onset of labor she received 50 gm 'V-globulin intravenously. Vaginal delivery of a non thrombocytopenic infant occurred 28 hours later. E-Aminocaproic acid was initiated post partum, 5 gm intravenously, then 2 gm every 6 hours for 24 hours. Post partum she experienced moderate vaginal bleeding that necessitated four units of blood. After the addition of methergine, the bleeding decreased. The E-aminocaproic acid was continued for 4 weeks. Platelet antibody studies. After the third pregnancy the patient'S serum was tested with an antiglobulin test that had a radioactive label against platelets from 20
425
