Venous thromboembolism

Venous thromboembolism occurs in 2 to 5 per 1000 deliveries. As well as pregnancy itself, additional specific and non-obstetric risk factors include advanced maternal age, multiparity, obesity, Cesarean section, instrument-assisted delivery and other surgical procedures, prolonged bed rest, hemorrhage, trauma to the lower limbs, and inherited deficiencies in natural inhibitors of coagulation ( Rutherford.,.a,D.d P.h®.iaD...,199.1.; I0.g.!i.a...,a.n.d...,We.g The role of gestational age remains controversial. Traditionally, the risk of thrombosis was considered to be higher during the third trimester and immediately postpartum. Whereas more than 50 per cent of pulmonary emboli occur postpartum, 75 per cent of deep-vein thromboses present antepartum (Togli.§..,„and.,..We.g 1996).

The risk of venous thromboembolism is five times higher in a pregnant woman than in a non-pregnant woman of similar age. This increased frequency is due to both the physiological hypercoagulable state associated with pregnancy and the venous stasis mediated by estrogens and local pressure effects of the gravid uterus on the inferior vena cava (Table 1). The levels of all clotting factors, except factors XI and XIII, increase during pregnancy. Plasma fibrinolytic activity also decreases as a result of placental inhibitors and, when the placenta separates, tissue thromboplastin is released into the circulation, further promoting thrombosis. These changes are prominent at term and in the immediate postpartum period, accounting for the maximum risk of venous thromboembolism around delivery. This hypercoagulable state is the result of stimulation of synthesis by the low-grade disseminated intravascular coagulation that takes place within the uteroplacental vasculature and that replaces the internal elastic lamina and smooth muscle in the spiral arteries with fibrin to enhance blood flow to the fetoplacental unit ( Rutherford, P.h.ela.D 1991).

Eventually, these alterations in the coagulation mechanisms that promote thrombosis help the mother to cope with the increased demand that arises on these components at the time of placental separation. By the third to fourth week following delivery these components of the coagulation and fibrinolytic systems have returned to their non-pregnant levels.

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Table 1 Pathophysiology of venous thromboembolism during pregnancy

If left untreated, deep venous thrombosis will progress to pulmonary embolism in 25 per cent of patients, with a mortality of approximately 15 per cent. Amniotic fluid embolism

Amniotic fluid embolism, although uncommon, is perhaps the most devastating critical illness specifically related to the pregnant state. The incidence is quoted as between 1 in 8000 and 1 in 80 000 live births with a fatality rate as high as 86 per cent ( Pet§rs.0.D...,§n.d...,Iayl0I..; Cjark. . ., 1991). Together with pulmonary thromboembolism, this obstetric complication is the leading cause of maternal mortality in Western countries.

Most episodes of amniotic fluid embolism occur during labor and delivery. However, this condition has been reported as early as during first- and second-trimester abortion, as late as 48 h postpartum, and following abdominal trauma or any uterine manipulation such as Cesarean section or even amniocentesis. Increased maternal age, multiparity, premature placental separation, meconium in the amniotic fluid, and intrauterine fetal death are predisposing factors, but there is no firm association with vigorous labor and hypertonic uterine contractions ( PetersoD...,a.D.d..,Ta.yj.0.Ll.97.0; .Clark...1.9").

Typical presenting features usually include sudden onset of respiratory failure and circulatory collapse, accompanied by seizures in 15 per cent of cases. Occasionally, fetal distress or hemorrhage due to disseminated intravascular coagulation herald this condition (15 per cent). Up to half the patients die within the first hour. Those who survive this initial cardiorespiratory insult face hypoxic brain damage, acute respiratory distress syndrome (up to 70 per cent), and uterine hemorrhage ascribed to consumptive coagulopathy and uterine atony (40 per cent) ( Table J).

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Table 2 Symptoms of amniotic fluid embolism

The pathogenesis of this syndrome remains controversial. Entrance of abnormal amniotic fluid into the vascular circulation through uterine tears or endocervical veins seems to be the primary event. Transient trapping of amniotic debris in the uterine veins by uterine tone may explain the occasional delay between delivery and onset of the syndrome. Before week 12 of gestation the volume of amniotic fluid is probably insufficient to trigger this syndrome, although experimentally there is no close correlation between its severity and the volume of injected fetal debris. It is the introduction of abnormal amniotic fluid into the maternal circulation rather than the infusion of amniotic fluid per se that accounts for the syndrome (Claik...1..9.9.1.).

Uterine atony and consumptive coagulopathy result from a myometrial depressant effect of amniotic fluid and from procoagulant substances in amniotic fluid respectively. Early hemodynamic data are scarce in this catastrophic condition. Transient and intense pulmonary hypertension, secondary right ventricular insufficiency, and profound hypoxemia probably account for the initial phase of cardiorespiratory failure and for the bulk of maternal death. This pulmonary hypertension may be mediated by mechanical obstruction by amniotic debris or by pulmonary arterial spasm triggered by hypoxemia and vasoactive substances such as prostaglandin F2 or mucin. Acute left ventricular dysfunction of obscure pathogenesis rapidly ensues in most surviving cases and accounts for the pulmonary edema that characterizes the second stage of amniotic fluid embolism (Clark. .etal 1985). It has not been established whether it is the particulate contents, such as mucin from meconium, or humoral factors in the amniotic fluid, such as arachidonic acid metabolites, that are responsible for these hemodynamic effects.

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