In this thesis the use of real-time ultrasound in the assessment and management of preterm labour has been studied, with particular reference to the observation of fetal breathing movements, gross fetal body movements and the state of the uterine cervix. In addition, a longitudinal analysis of the trends in preterm labour in the John Radcliffe Hospital in Oxford between 1973 and 1981 has been performed. Finally, an attempt has been made to clarify the relationship between prostaglandin E2 and fetal breathing movements. The analysis of the trends in preterm labour in Oxford has shown that the incidence of preterm delivery remains unaltered. Of these patients, however, those eligible for tocolytic therapy (unexplained spontaneous preterm labour) form a small proportion. The incidence of extreme prematurity in this group is very low and the neonatal outcome is good. The presence or absence of Fetal Breathing Movements (FBM) by defined criteria is shown to be a highly sensitive index of whether the preterm labour is going to progress to delivery or not in singleton pregnancies with intact membranes. Its significance is lost when the membranes are ruptured and in multiple pregnancies. In pregnancies complicated by antepartum haemorrhage the presence or absence of Fetal Breathing Movements does not predict further haemorrhage leading to delivery. Fetal Breathing Movement status on admission bears no relationship to neonatal outcome and gives no indication of the presence of intrauterine infection. Silent chorioamnionitis has been highlighted as an important cause of "unexplained" preterm labour. Gross Fetal Body Movements (FM) are shown to give no early indication of impending preterm delivery. Evidence is presented to suggest that significant diminution in Fetal Movements is related to poor neonatal outcome. Ultrasonic measurement of the uterine cervix has been found to be technically feasible but of no benefit in the diagnosis of ongoing preterm labour. The relationship between prostaglandin E2 (PGE2) and the cessation of fetal breathing movement has been approached by elucidating the maternal absorption of PGE2 from a vaginal pessary. This then enabled me to sample fetal blood at the time of maximal maternal concentrations (the time we expect the fetal concentration to be greatest). This was performed by fetoscopy and demonstrated that a significant rise in fetal bicycleprostaglandin-E-metabolite (bicyclo-PGEM) occurs following maternal vaginal administration of PGE2. Using this information FBM has been assessed two and a half hours following the vaginal administration of PGE2. Although inconclusive, no reduction in FBM was demonstrated. as the bicyclo-PGE metabolite is used to assess PGE levels, this evidence decreases the probability that PGE mediates the reduction in FBM with the onset of labour.

Objetivo: Avaliar as lesões placentárias encontradas em gestantes com SAF e correlacionar com as intercorrências na gestação e repercussões perinatais. Casuística e Método: Foram acompanhadas 72 gestantes com diagnóstico confirmado de SAF, excluídas gestações gemelares e fetos mal-formados. Colhida placenta para análise histológica. O grupo SAF foi distribuído em três subgrupos baseando-se na história clíncia prévia e títulos de aCL e aL, e o risco de desenvolver trombose e insuficiência placentária na gestação, a saber: moderado, A(n=20), alto risco, B(n=37) e alto risco C(n=15). As pacientes foram tratadas com AAS 100mg/dia, suspensa com 36 semanas, e heparina, cuja dose era modificada de acordo com alterações na dopplervelocimetria obstétrica. Anotadas as intercorrências materno-perinatais e os achados no estudo anátomo-patológico das placentas com a aplicação de protocolo terapêutico. Um grupo de 32 gestantes normais serviu de controle. No subgrupo A, as pacientes não apresentavam colagenoses, outras trombofilias nem trombose prévia. No subgrupo B, 17 (46%) tinham LES;15(40%) fenômeno de Raynaud; 13(35%) toxemia; 12(32%) trombose prévia; nove (24,3%) outras trombofilias associadas e sete (19%) HAC. No subgrupo C, 14(93%) tinham tido trombose anterior, 4 (26,6%) LES e 2 (13,3%) outras trombofilias. As perdas fetais prévias eram 86,8%, 83% e 82,7% para subgrupos A, B e C, respectivamente. A média de início pré-natal foi de 11,8 semanas sem predominância entre os grupos. O início de AAS e heparina foi em média de 12,3 e 14,5 semanas de gestação respectivamente, igual nos subgrupos. Resultados: 1. As principais complicações maternas na média geral, foram: TPP (49,3%) e toxemia (25%). 2. Os resultados perinatais apresentaram: partos prematuros 44%; ILA diminuído 41%; SFA 40%; RCF 34%; oligoâmnio 31%.(1) e (2) semelhantes entre os subgrupos e com significância estatística com o grupo-controle. 3. A idade gestacional no parto foi em média de 35,8 semanas, e peso fetal 2493g, sem diferença estatística entre os subgrupos e grupo-controle. 4. Na análise microscópica predominou infartos com 60% das placentas afetadas, correlacionadas com alta incidência de resultados adversos nas gestações, assim como hiperplasia da camada média de ATV, 44,6%, com predomínio de RCF (60%) e prematuros (80%) no subgrupo C, necrose fibrinóide do trofoblasto com predomínio de ILA diminuído (60%) no subgrupo B, deposição maciça de fibrina perivilosa com predomínio de SFA (100%) no subgrupo A, vasculopatia trombótica fetal com predomínio de SFA (100%) e prematuros (75%) no subgrupo A e RCF (77%) no subgrupo B. Todas as lesões com significativa estatística em relação ao grupo-controle. Entre os subgrupos, a deposição maciça de fibrina perivilosa apresentou estatística significativa no subgrupo C em relação aos demais. 5. Conclusões: O protocolo terapêutico foi eficaz, porém ainda é elevado o índice de morbidades na gestação.A alta incidência de infartos e outras complicações trombóticas na placenta confirmam a agressão placentária e a necessidade de adequação nos protocolos de anticoagulação / Objective: Evaluate the placental injuries found in pregnant women with SAF and correlate with the morbidity in pregnancy and fetal repercussions. Methods: 72 pregnant women with SAF diagnosis were followed, except the twin pregnancies and inadequate formed fetus. Gathered placenta to histological examination. The SAF group was distributed in three subgroups based on the previous clinic history, aCL and aL titles, risk of thrombosis development and the placentary insuffiency in pregnancy to know: moderated, A (n=20); high risk, B (n=37) and even higher risk, C (n=15). The patients were treated with AAS 100mg/day, suspended within 36 weeks and enoxaparin which portion was modified according to the fetal placental circulation alteration on obstetric dopplervelocimetria. The outcome of pregnancy and placental pathological findings studies with the application of the therapeutic protocol were noted down.32 normal pregnant women were the control group. In subgroup A the patients did not presented any disease colagen or heritable thrombophilia.In subgroup B,17(46%) pacients presented LES; 15(40%) Raynaud phenomena; 13(35%) preeclampsia; 12(32%) had previous thrombosis; nine(24.3%) had other thrombophilia and seven(19%) HAC. In subgroup C, 14 (93%) pacients presented previous thrombosis; 4(26%) LES; 4(26%) HAC; 3(20%) preeclampsia; 3(20%) Raynaud phenomena and 2(13.3%) others thrombophilia. The previous fetus losses were 85%, 80% and 79% to subgroups A, B and C respectively. Prenatal started around 12 weeks with no advantage among the groups. Introduction of AAS and enoxaparin was 12 and 14 weeks respectively the same in subgroups. Results: 1. The main maternal complications in general were: TPP (49%) and toxemia (25%). 2. The fetal results presented: 44% early childbirth; 41% reduced ILA; 40% SFA; 34% RCF; 31% oligohydramnios. (1) e (2) similar between the subgroups and expressive statistic with the control group. 3. The pregnant age was in avarage 35,8 weeks with fetus weigh 2493g with no statistic differences between the subgroups and the control group. 4. In the microscopy analysis predominated infarcts with 60% of the placentas affected, correlated with the high incidence of adverse results in pregnancies, so as 44,6% reduction or obliteration of fetal stem vessels by mural hyperplasia; 60% RCF predominance and 80% early childbirth in subgroup C, fibrinoid necrosis trophoblast with reduced ILA predominance (60%) in subgroup B, massive perivillous fibrin deposition with SFA predominance (100%) in subgroup A, fetal thrombotic vasculopathy with SFA predominance (100%) and early birth (75%) in subgroup A and RCF (77%) in subgroup B. All the placental injuries with statistics significance related to the group control. Among the subgroups the massive perivillous fibrin deposition presented statistic significance in the subgroup C related to the others. Conclusions: The therapeutic protocol was effective, but is still high the morbidity indices among the pregnancies. The high incidences of infarcts and other thrombotic complications in the placenta confirm the placental aggression and the necessity of the adequation in the anticoagulation protocols

Objetivo: Avaliar as lesões placentárias encontradas em gestantes com SAF e correlacionar com as intercorrências na gestação e repercussões perinatais. Casuística e Método: Foram acompanhadas 72 gestantes com diagnóstico confirmado de SAF, excluídas gestações gemelares e fetos mal-formados. Colhida placenta para análise histológica. O grupo SAF foi distribuído em três subgrupos baseando-se na história clíncia prévia e títulos de aCL e aL, e o risco de desenvolver trombose e insuficiência placentária na gestação, a saber: moderado, A(n=20), alto risco, B(n=37) e alto risco C(n=15). As pacientes foram tratadas com AAS 100mg/dia, suspensa com 36 semanas, e heparina, cuja dose era modificada de acordo com alterações na dopplervelocimetria obstétrica. Anotadas as intercorrências materno-perinatais e os achados no estudo anátomo-patológico das placentas com a aplicação de protocolo terapêutico. Um grupo de 32 gestantes normais serviu de controle. No subgrupo A, as pacientes não apresentavam colagenoses, outras trombofilias nem trombose prévia. No subgrupo B, 17 (46%) tinham LES;15(40%) fenômeno de Raynaud; 13(35%) toxemia; 12(32%) trombose prévia; nove (24,3%) outras trombofilias associadas e sete (19%) HAC. No subgrupo C, 14(93%) tinham tido trombose anterior, 4 (26,6%) LES e 2 (13,3%) outras trombofilias. As perdas fetais prévias eram 86,8%, 83% e 82,7% para subgrupos A, B e C, respectivamente. A média de início pré-natal foi de 11,8 semanas sem predominância entre os grupos. O início de AAS e heparina foi em média de 12,3 e 14,5 semanas de gestação respectivamente, igual nos subgrupos. Resultados: 1. As principais complicações maternas na média geral, foram: TPP (49,3%) e toxemia (25%). 2. Os resultados perinatais apresentaram: partos prematuros 44%; ILA diminuído 41%; SFA 40%; RCF 34%; oligoâmnio 31%.(1) e (2) semelhantes entre os subgrupos e com significância estatística com o grupo-controle. 3. A idade gestacional no parto foi em média de 35,8 semanas, e peso fetal 2493g, sem diferença estatística entre os subgrupos e grupo-controle. 4. Na análise microscópica predominou infartos com 60% das placentas afetadas, correlacionadas com alta incidência de resultados adversos nas gestações, assim como hiperplasia da camada média de ATV, 44,6%, com predomínio de RCF (60%) e prematuros (80%) no subgrupo C, necrose fibrinóide do trofoblasto com predomínio de ILA diminuído (60%) no subgrupo B, deposição maciça de fibrina perivilosa com predomínio de SFA (100%) no subgrupo A, vasculopatia trombótica fetal com predomínio de SFA (100%) e prematuros (75%) no subgrupo A e RCF (77%) no subgrupo B. Todas as lesões com significativa estatística em relação ao grupo-controle. Entre os subgrupos, a deposição maciça de fibrina perivilosa apresentou estatística significativa no subgrupo C em relação aos demais. 5. Conclusões: O protocolo terapêutico foi eficaz, porém ainda é elevado o índice de morbidades na gestação.A alta incidência de infartos e outras complicações trombóticas na placenta confirmam a agressão placentária e a necessidade de adequação nos protocolos de anticoagulação / Objective: Evaluate the placental injuries found in pregnant women with SAF and correlate with the morbidity in pregnancy and fetal repercussions. Methods: 72 pregnant women with SAF diagnosis were followed, except the twin pregnancies and inadequate formed fetus. Gathered placenta to histological examination. The SAF group was distributed in three subgroups based on the previous clinic history, aCL and aL titles, risk of thrombosis development and the placentary insuffiency in pregnancy to know: moderated, A (n=20); high risk, B (n=37) and even higher risk, C (n=15). The patients were treated with AAS 100mg/day, suspended within 36 weeks and enoxaparin which portion was modified according to the fetal placental circulation alteration on obstetric dopplervelocimetria. The outcome of pregnancy and placental pathological findings studies with the application of the therapeutic protocol were noted down.32 normal pregnant women were the control group. In subgroup A the patients did not presented any disease colagen or heritable thrombophilia.In subgroup B,17(46%) pacients presented LES; 15(40%) Raynaud phenomena; 13(35%) preeclampsia; 12(32%) had previous thrombosis; nine(24.3%) had other thrombophilia and seven(19%) HAC. In subgroup C, 14 (93%) pacients presented previous thrombosis; 4(26%) LES; 4(26%) HAC; 3(20%) preeclampsia; 3(20%) Raynaud phenomena and 2(13.3%) others thrombophilia. The previous fetus losses were 85%, 80% and 79% to subgroups A, B and C respectively. Prenatal started around 12 weeks with no advantage among the groups. Introduction of AAS and enoxaparin was 12 and 14 weeks respectively the same in subgroups. Results: 1. The main maternal complications in general were: TPP (49%) and toxemia (25%). 2. The fetal results presented: 44% early childbirth; 41% reduced ILA; 40% SFA; 34% RCF; 31% oligohydramnios. (1) e (2) similar between the subgroups and expressive statistic with the control group. 3. The pregnant age was in avarage 35,8 weeks with fetus weigh 2493g with no statistic differences between the subgroups and the control group. 4. In the microscopy analysis predominated infarcts with 60% of the placentas affected, correlated with the high incidence of adverse results in pregnancies, so as 44,6% reduction or obliteration of fetal stem vessels by mural hyperplasia; 60% RCF predominance and 80% early childbirth in subgroup C, fibrinoid necrosis trophoblast with reduced ILA predominance (60%) in subgroup B, massive perivillous fibrin deposition with SFA predominance (100%) in subgroup A, fetal thrombotic vasculopathy with SFA predominance (100%) and early birth (75%) in subgroup A and RCF (77%) in subgroup B. All the placental injuries with statistics significance related to the group control. Among the subgroups the massive perivillous fibrin deposition presented statistic significance in the subgroup C related to the others. Conclusions: The therapeutic protocol was effective, but is still high the morbidity indices among the pregnancies. The high incidences of infarcts and other thrombotic complications in the placenta confirm the placental aggression and the necessity of the adequation in the anticoagulation protocols