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Eisenmenger's syndrome and pregnancy
Eur. J. Obstet. Gynecol. Reprod. BioL, 28 (1988) 69-74 Elsevier
I30
69
00586
Eisenmenger’s syndrome and pregnancy Mikael
Bitsch,
Christoffer
Johansen,
Alf Wennevold
Department of Gynecology and Obstetrics, and Cardiovascular Copenhagen, Denmark Accepted
for publication
27 October
and Mogens
Laboratoty,
Osler
Rigshospitalet,
1987
Summary
Two cases of successfully managed Eisenmenger’s syndrome during pregnancy are reported. A woman suffering from Eisenmenger’s syndrome who becomes pregnant should be advised to have her pregnancy terminated. On the basis of the available literature and our own experiences we suggest the following plan, if a woman, despite medical advice, chooses to continue her pregnancy: admission to hospital at approximately 25 weeks of gestation; bed rest during the remaining period of pregnancy; oxygen face-mask during episodes of dyspnoea; determination of serial blood gases to detect changes in the shunt flow. At the onset of labour, arterial and epidural catheters should be inserted, a fall in blood pressure should immediately be counteracted by the administration of norepinephrine, and loss of blood by transfusion. The patient should remain in hospital for 7-14 days after delivery. Eisenmenger’s
Syndrome;
High-risk
pregnancy
Introduction The Eisenmenger syndrome is defined by an abnormal connection between the systemic circulation and the pulmonary circulation (ventricular septal defect (VSD)), atria1 septal defect (ASD), and/or patent ductus arteriosus (PAD), and a predominant venous-arterial shunt caused by an increased vascular resistance in the pulmonary circulation [l]. Conventional surgery is not possible for this condition; recently, however, combined heart and lung transplantations have been performed.
Correspondence: M. Bitsch, M.D., Department of Gynecology Laboratory, Rigshospitalet, Copenhagen, Denmark.
0028-2243/88/$03.50
0 1988 Elsevier Science Publishers
and
Obstetrics,
B.V. (Biomedical
Division)
and
Cardiovascular
Since the maternal mortality rate is 26-66% [2-51 women are strongly dissuaded from becoming pregnant. Nevertheless, some women prefer to run the risks associated with pregnancy and delivery despite medical advice. In 1979, Gleicher and coworkers [5] published a review of 115 cases reported in the literature; in 44 cases Eisenmenger’s syndrome (ES) was adequately assessed by cardiac catheterization, cardiac surgery, or autopsy. The maternal mortality rate was 52%, highest in connection with caesarean section and during the week after delivery. VSD increases the risk seen in relation to ASD and PDA. Since 1979, 7 well-documented cases of ES during pregnancy have been reported. [6-111. Abortion is significantly safer than any form of delivery. In the light of two cases of Eisenmenger’s syndrome during pregnancy, where the pregnancies reached term without maternal mortality, a review of the literature on this subject is given, and a treatment of this patient group is proposed. Case 1
A 27-yr-old woman, para 0, with congenital heart disease was referred to the antenatal clinic for examination at the 12th weekof gestation. Her medical adviser had suggested abortion, which she refused. Heart catherization performed at ages 4,15 and 19 had shown VSD together with patent foramen ovale and slight to moderate valvular and infundibular pulmonary stenosis, but with increasing pulmonary hypertension (Table I). The condition
TABLE
I
Serial heart catheterizations pregnancy
in case 2 with the haemodynamics
of Eisenmenger’s
syndrome
at time of
Age (years) 4 Pressures (in mmHg) Pulmonary ‘wedge’ (mean) Pulmonary artery Right ventricle Right atrium (mean) Left atrium (mean) Left ventricle
Pulmonary resistance (in mmHg) a
42/3 88/2 2 4
1
Qp/Q, ratio Pulmonary vascular (dynes.s.cm-s)
15
12 50/15 100/4 2
1.4
19
29
72/12 105/5 2 8
75/12 120/5 0 4 165/D
1.4
1
resistance 231
611
factor rr 12
11
24
29
a Defined as rr = (Ppa, - Pcv,)/FR mmHg. (Ppa m = mean pressure in the pulmonary artery, Pcv, = mean pulmonary ‘wedge’ pressure, and FR = flow ratio = Qp/Qs ratio). An rr < 10 mmHg is normal, rf increased and rf 2 50 mmHg is 11-20 mmHg is slightly increased, rr 21-49 mmHg is moderately severely elevated.
deteriorated in the course of time because of increasing pulmonary vascular resistance. The shunt was balanced, and at rest the arterial oxygen saturation was normal. She was considered to have the haemodynamics of Eisenmenger’s syndrome. On admission, the patient was not cyanotic and had no dyspnoea at rest. She was able to climb the stairs to the second floor before she showed signs of exertional dyspnoea. The electrocardiogram showed normal sinus rhythm and revealed right axis deviation and right ventricular hypertrophy. Chest X-ray showed the heart to be of normal size but with prominent pulmonary arteries. A team consisting of obstetricians, cardiologists and anaesthesiologists was set up to provide optimum guidelines for her pregnancy and delivery. At week 19 she was hospitalized for 24 h because of minor vaginal bleeding. The ultrasonography showed normal fetal growth. At 29 weeks, the patient had exertional dyspnoea on only slight physical activity. There was dyspnoea at rest, in the supine position, and she therefore had to sleep with head elevated. She was hospitalized for the rest of her pregnancy and confined to bed. No medication was given. The cardiac condition was unchanged until delivery; blood pressure was 140/90 mmHg and heart rate about 90/min; haemoglobin was 10 rnmol/l. There was no chest pain, but occasional palpitations. Physical examination revealed slight cyanosis of nails and lips. There was no neck vein engorgement. A grade 4 (of 6) holo-systolic murmur was heard at the left sternal border; no diastolic murmur was heard. The liver was not palpable and there were no oedemas of the legs. From 35 weeks, there were symptoms of imminent premature delivery, and at 37 weeks there were increasing uterine contractions. The cardiotocography showed normal fetal heart activity, but insufficient and uncoordinated uterine contractions. On the indication of labores veri inertes oxytocin infusion (Syntocinon@) was begun, a lumbar epidural catheter was inserted, and an arterial cannula was inserted into the radial artery. After 10 h, a viable boy, weighing 3720 g, and 53 cm long, was delivered after vacuum extraction and episiotomy. Apgar score 9/l, 10/5, blood pH 7.32. The blood pressure was kept constant (150/100) by intravenous administration of norepinephrine. Immediately after delivery, the mother was transferred to the cardiac intensive care unit, where the administration of norepinephrine was stopped on the second postpartum day, and the patient was gradually activated from the third day and discharged in well-being together with her child on postpartum day fourteen. Heart catheterization two years later (Table I) showed no significant deterioration compared with investigation at age 19. Case 2 A 28-yr-old woman, para 0, with congenital heart disease was referred department from her local hospital for further control of her pregnancy. Heart catheterization performed at the age of 21 had shown a patent arteriosus together with marked pulmonary hypertension and a veno-arterial
to our ductus shunt.
72
She had been advised not to become pregnant, but she had now reached 30 weeks of gestation and insisted on carrying through her pregnancy. On admission, she was slightly cyanotic. There was dyspnoea at rest. Chest X-ray showed a slightly enlarged heart, prominent pulmonary arteries and oligemic peripheral lung fields. An electrocardiogram showed right axis deviation, right ventricular hypertrophy and normal sinus rhythm. The haemoglobin was 11.7 mmol/l, blood pressure 110/70. At auscultation no murmurs were heard, but the second heart sound over the pulmonary area was accentuated. The remainder of the physical examination was within normal limits. From childhood she had had moderate, stable dyspnoea on exertion. The cardiac condition was unchanged until admission. It was decided to keep the patient in hospital for the rest of her pregnancy. Low values of serum estriol and placental lactogen together with physical evaluation aroused suspicion of fetal growth retardation. At 37 weeks, the patient went into spontaneous labour and after 3 h she delivered a premature live boy, weighing 1340 g, in foot-breech presentation. Apgar score: 7/l, 10/5. The child was immediately transferred to the neonatal intensive care unit and put into an incubator; because of dyspnoea during the following hours a respirator had to be connected. The child showed signs of cerebral haemorrhage with convulsions, and he died four and a half days after birth. An autopsy showed haemorrhage of the subarachnoidea and congenital malformation of the heart (ASD and PDA). The mother revealed no heart failure during delivery or puerperium and had no episodes of hypotension. Due to the rapid course it was not possible to set up intra-arterial pressure measurement. The patient was sterilized three months after delivery.
Discussion Eisenmenger’s syndrome is associated with risk of sudden death [9-121. This is explained by an increase in the veno-arterial shunt with decreasing arterial oxygen saturation and ensuing reflex bradycardia. In connection with pregnancy and delivery hypotension with ensuing increase of the veno-arterial shunt may occur either because of bleeding or because of decreasing peripheral vascular resistance. The maternal mortality in the cases reported was highest during delivery and puerperium [2,5,6,10,11]. In a study of the ratio of pulmonary systemic blood flow (QJQ,) during labour, delivery and puerperium, Midwall et al. [S] found that uterine contractions and delivery decrease the Qr/Q, ratio. Epidural anaesthesia, oxytocin and the supine position did not affect pulmonary haemodynamics or shunt flow adversely. Since oxygen has a beneficial effect on pulmonary vascular resistance and, simultaneously, causes a reduction of the veno-arterial shunt, oxygen in high concentrations is recommended. To counteract hypotension, infusion with vasopressors, e.g. norepinephrine, in doses of 5-15 pg/min can be used. Caesarean section is accompanied by a high risk of maternal mortality [2,4,5]; consequently, vaginal delivery assisted by vacuum extractor is recommended. When obstetric complica-
13
tions make section necessary, the choice of a general or regional anaesthetic technique may arise. We prefer epidural anaesthesia as described by Spinnato [7], but other authors recommend general anaesthesia [12]. Some authors recommend anticoagulation treatment with heparin until labour begins, and again during the puerperium, since autopsies have frequently shown microthrombi in the pulmonary circulation. Pitts and coworkers have found heparin treatment of no value [3]. In most cases, anticoagulation treatment was not used. In some reports, antibiotic treatment is suggested to prevent endocarditis, e.g. cephalosporin, either alone or in combination with gentamycin [5,6,8]. There is no reason to believe that a woman with Eisenmenger’s syndrome who has carried a pregnancy to a successful termination is less exposed to risk than she was before, if she wants to become pregnant again. This is illustrated by a case in which the patient died during the puerperium of her 3rd pregnancy [14]. Cardiac catheterization of patient 1 and physical examination of patient 2 did not show any aggravation of the cardiac condition after the two successfully managed pregnancies. Clinical management The pregnant woman should be hospitalized approximately at 25 weeks of gestation, dependent on the cardiac condition. During episodes of dyspnoea, bed rest is recommended, and high concentrations of oxygen should be administered through a face mask. The oxygen tension should be assessed through determination of serial arterial blood gases to detect changes in shunt flow. Usually, anticoagulation treatment is not indicated. From a cardiac point of view, premature delivery has no beneficial effect. If necessary, oxytocin can be administered. At the onset of labour, the patient should be carefully monitored by electrocardiograms and arterial and epidural catheters. Intravenous infusion with norepinephrine and blood should be held in readiness to counteract blood loss, and a drop in blood pressure should be counteracted by the infusion of vasopressors; oxygen is recommended to counteract pulmonary hypertension. Vaginal delivery, assisted by vacuum extractor in the 2nd state of delivery is recommended. The patient should be kept in bed for the first day after delivery and should be monitored continuously and then gradually activated. We suggest that the patient stays in hospital for a period of 7-14 days after delivery under careful observation due to the continued risk of sudden death. References 1 2 3 4 5
Wood P. The Eisenmenger syndrome. Br Med J. 1958;2:701-755. Jones AM, Howitt G. Eisenmenger syndrome in pregnancy. Br Med J 1965;1:1627-1631. Pitts JA, Crosby WM, Basta LL. Eisenmenger’s syndrome in pregnancy. Am Heart J 1977;93:321-325. Neilson G, Galea EG, Blunt A. Eisenmenger’s syndrome and pregnancy. Med J Austr 1971;1:431-434. Gleicher N, Midwall J, Hochberger D, Jaffin H. Eisenmenger’s syndrome and pregnancy. Obstet Gynecol Surv 1979;34:721-741.
74 6 Gummerus M, Laasonen H. Eisenmenger complex and pregnancy. Ann Chir Gynaecol 1981;70:339-341. 7 Spinnato JA, Kraynack BJ, Cooper MW. Eisenmenger’s syndrome in pregnancy: epidural anaesthesia for elective cesarean section. N Engl J Med 1981;20:1215-1217. 8 Midwah J, Jaffin H, von Herman M, Kupersmith J. Shunt flow and pulmonary hemodynamics during labour and delivery in the Eisenmenger syndrome. Am J Cardiol 1978;42:299-303. 9 Huyghe de Mahence A, Andre-Fouet X, Bernet D, Sehgman G, Wilner LC, Gayet C, Robert D, Pont M. Syndrome d’Eisenmenger et grossesse. Arm Cardiol Angeiol (Paris) 1985;34:547-549. 10 Heytens L, Alexancer JP. Maternal and neonatal death associated with Eisenmenger’s syndrome. Acta Anaesthesiol Belg 1986;37:45-51. 11 Lieber S, et al. Eisenmenger’s syndrome and pregnancy. Acta Cardiol 1985;40:421-424. 12 Young D, Mark H. Fate of the patient with Eisenmenger syndrome. Am J Cardiol 1971;28:658-659. 13 Foster JMG, Jones RM. The anaesthetic management of the Eisenmenger syndrome. Ann R Co11 Surg Engl 1984;66:353-355. 14 Bueman B, Kragelund E. Clinical assessment of heart disease during pregnancy. Acta Obstet Gynaecol Stand 1962;41:57-79.
I30
69
00586
Eisenmenger’s syndrome and pregnancy Mikael
Bitsch,
Christoffer
Johansen,
Alf Wennevold
Department of Gynecology and Obstetrics, and Cardiovascular Copenhagen, Denmark Accepted
for publication
27 October
and Mogens
Laboratoty,
Osler
Rigshospitalet,
1987
Summary
Two cases of successfully managed Eisenmenger’s syndrome during pregnancy are reported. A woman suffering from Eisenmenger’s syndrome who becomes pregnant should be advised to have her pregnancy terminated. On the basis of the available literature and our own experiences we suggest the following plan, if a woman, despite medical advice, chooses to continue her pregnancy: admission to hospital at approximately 25 weeks of gestation; bed rest during the remaining period of pregnancy; oxygen face-mask during episodes of dyspnoea; determination of serial blood gases to detect changes in the shunt flow. At the onset of labour, arterial and epidural catheters should be inserted, a fall in blood pressure should immediately be counteracted by the administration of norepinephrine, and loss of blood by transfusion. The patient should remain in hospital for 7-14 days after delivery. Eisenmenger’s
Syndrome;
High-risk
pregnancy
Introduction The Eisenmenger syndrome is defined by an abnormal connection between the systemic circulation and the pulmonary circulation (ventricular septal defect (VSD)), atria1 septal defect (ASD), and/or patent ductus arteriosus (PAD), and a predominant venous-arterial shunt caused by an increased vascular resistance in the pulmonary circulation [l]. Conventional surgery is not possible for this condition; recently, however, combined heart and lung transplantations have been performed.
Correspondence: M. Bitsch, M.D., Department of Gynecology Laboratory, Rigshospitalet, Copenhagen, Denmark.
0028-2243/88/$03.50
0 1988 Elsevier Science Publishers
and
Obstetrics,
B.V. (Biomedical
Division)
and
Cardiovascular
Since the maternal mortality rate is 26-66% [2-51 women are strongly dissuaded from becoming pregnant. Nevertheless, some women prefer to run the risks associated with pregnancy and delivery despite medical advice. In 1979, Gleicher and coworkers [5] published a review of 115 cases reported in the literature; in 44 cases Eisenmenger’s syndrome (ES) was adequately assessed by cardiac catheterization, cardiac surgery, or autopsy. The maternal mortality rate was 52%, highest in connection with caesarean section and during the week after delivery. VSD increases the risk seen in relation to ASD and PDA. Since 1979, 7 well-documented cases of ES during pregnancy have been reported. [6-111. Abortion is significantly safer than any form of delivery. In the light of two cases of Eisenmenger’s syndrome during pregnancy, where the pregnancies reached term without maternal mortality, a review of the literature on this subject is given, and a treatment of this patient group is proposed. Case 1
A 27-yr-old woman, para 0, with congenital heart disease was referred to the antenatal clinic for examination at the 12th weekof gestation. Her medical adviser had suggested abortion, which she refused. Heart catherization performed at ages 4,15 and 19 had shown VSD together with patent foramen ovale and slight to moderate valvular and infundibular pulmonary stenosis, but with increasing pulmonary hypertension (Table I). The condition
TABLE
I
Serial heart catheterizations pregnancy
in case 2 with the haemodynamics
of Eisenmenger’s
syndrome
at time of
Age (years) 4 Pressures (in mmHg) Pulmonary ‘wedge’ (mean) Pulmonary artery Right ventricle Right atrium (mean) Left atrium (mean) Left ventricle
Pulmonary resistance (in mmHg) a
42/3 88/2 2 4
1
Qp/Q, ratio Pulmonary vascular (dynes.s.cm-s)
15
12 50/15 100/4 2
1.4
19
29
72/12 105/5 2 8
75/12 120/5 0 4 165/D
1.4
1
resistance 231
611
factor rr 12
11
24
29
a Defined as rr = (Ppa, - Pcv,)/FR mmHg. (Ppa m = mean pressure in the pulmonary artery, Pcv, = mean pulmonary ‘wedge’ pressure, and FR = flow ratio = Qp/Qs ratio). An rr < 10 mmHg is normal, rf increased and rf 2 50 mmHg is 11-20 mmHg is slightly increased, rr 21-49 mmHg is moderately severely elevated.
deteriorated in the course of time because of increasing pulmonary vascular resistance. The shunt was balanced, and at rest the arterial oxygen saturation was normal. She was considered to have the haemodynamics of Eisenmenger’s syndrome. On admission, the patient was not cyanotic and had no dyspnoea at rest. She was able to climb the stairs to the second floor before she showed signs of exertional dyspnoea. The electrocardiogram showed normal sinus rhythm and revealed right axis deviation and right ventricular hypertrophy. Chest X-ray showed the heart to be of normal size but with prominent pulmonary arteries. A team consisting of obstetricians, cardiologists and anaesthesiologists was set up to provide optimum guidelines for her pregnancy and delivery. At week 19 she was hospitalized for 24 h because of minor vaginal bleeding. The ultrasonography showed normal fetal growth. At 29 weeks, the patient had exertional dyspnoea on only slight physical activity. There was dyspnoea at rest, in the supine position, and she therefore had to sleep with head elevated. She was hospitalized for the rest of her pregnancy and confined to bed. No medication was given. The cardiac condition was unchanged until delivery; blood pressure was 140/90 mmHg and heart rate about 90/min; haemoglobin was 10 rnmol/l. There was no chest pain, but occasional palpitations. Physical examination revealed slight cyanosis of nails and lips. There was no neck vein engorgement. A grade 4 (of 6) holo-systolic murmur was heard at the left sternal border; no diastolic murmur was heard. The liver was not palpable and there were no oedemas of the legs. From 35 weeks, there were symptoms of imminent premature delivery, and at 37 weeks there were increasing uterine contractions. The cardiotocography showed normal fetal heart activity, but insufficient and uncoordinated uterine contractions. On the indication of labores veri inertes oxytocin infusion (Syntocinon@) was begun, a lumbar epidural catheter was inserted, and an arterial cannula was inserted into the radial artery. After 10 h, a viable boy, weighing 3720 g, and 53 cm long, was delivered after vacuum extraction and episiotomy. Apgar score 9/l, 10/5, blood pH 7.32. The blood pressure was kept constant (150/100) by intravenous administration of norepinephrine. Immediately after delivery, the mother was transferred to the cardiac intensive care unit, where the administration of norepinephrine was stopped on the second postpartum day, and the patient was gradually activated from the third day and discharged in well-being together with her child on postpartum day fourteen. Heart catheterization two years later (Table I) showed no significant deterioration compared with investigation at age 19. Case 2 A 28-yr-old woman, para 0, with congenital heart disease was referred department from her local hospital for further control of her pregnancy. Heart catheterization performed at the age of 21 had shown a patent arteriosus together with marked pulmonary hypertension and a veno-arterial
to our ductus shunt.
72
She had been advised not to become pregnant, but she had now reached 30 weeks of gestation and insisted on carrying through her pregnancy. On admission, she was slightly cyanotic. There was dyspnoea at rest. Chest X-ray showed a slightly enlarged heart, prominent pulmonary arteries and oligemic peripheral lung fields. An electrocardiogram showed right axis deviation, right ventricular hypertrophy and normal sinus rhythm. The haemoglobin was 11.7 mmol/l, blood pressure 110/70. At auscultation no murmurs were heard, but the second heart sound over the pulmonary area was accentuated. The remainder of the physical examination was within normal limits. From childhood she had had moderate, stable dyspnoea on exertion. The cardiac condition was unchanged until admission. It was decided to keep the patient in hospital for the rest of her pregnancy. Low values of serum estriol and placental lactogen together with physical evaluation aroused suspicion of fetal growth retardation. At 37 weeks, the patient went into spontaneous labour and after 3 h she delivered a premature live boy, weighing 1340 g, in foot-breech presentation. Apgar score: 7/l, 10/5. The child was immediately transferred to the neonatal intensive care unit and put into an incubator; because of dyspnoea during the following hours a respirator had to be connected. The child showed signs of cerebral haemorrhage with convulsions, and he died four and a half days after birth. An autopsy showed haemorrhage of the subarachnoidea and congenital malformation of the heart (ASD and PDA). The mother revealed no heart failure during delivery or puerperium and had no episodes of hypotension. Due to the rapid course it was not possible to set up intra-arterial pressure measurement. The patient was sterilized three months after delivery.
Discussion Eisenmenger’s syndrome is associated with risk of sudden death [9-121. This is explained by an increase in the veno-arterial shunt with decreasing arterial oxygen saturation and ensuing reflex bradycardia. In connection with pregnancy and delivery hypotension with ensuing increase of the veno-arterial shunt may occur either because of bleeding or because of decreasing peripheral vascular resistance. The maternal mortality in the cases reported was highest during delivery and puerperium [2,5,6,10,11]. In a study of the ratio of pulmonary systemic blood flow (QJQ,) during labour, delivery and puerperium, Midwall et al. [S] found that uterine contractions and delivery decrease the Qr/Q, ratio. Epidural anaesthesia, oxytocin and the supine position did not affect pulmonary haemodynamics or shunt flow adversely. Since oxygen has a beneficial effect on pulmonary vascular resistance and, simultaneously, causes a reduction of the veno-arterial shunt, oxygen in high concentrations is recommended. To counteract hypotension, infusion with vasopressors, e.g. norepinephrine, in doses of 5-15 pg/min can be used. Caesarean section is accompanied by a high risk of maternal mortality [2,4,5]; consequently, vaginal delivery assisted by vacuum extractor is recommended. When obstetric complica-
13
tions make section necessary, the choice of a general or regional anaesthetic technique may arise. We prefer epidural anaesthesia as described by Spinnato [7], but other authors recommend general anaesthesia [12]. Some authors recommend anticoagulation treatment with heparin until labour begins, and again during the puerperium, since autopsies have frequently shown microthrombi in the pulmonary circulation. Pitts and coworkers have found heparin treatment of no value [3]. In most cases, anticoagulation treatment was not used. In some reports, antibiotic treatment is suggested to prevent endocarditis, e.g. cephalosporin, either alone or in combination with gentamycin [5,6,8]. There is no reason to believe that a woman with Eisenmenger’s syndrome who has carried a pregnancy to a successful termination is less exposed to risk than she was before, if she wants to become pregnant again. This is illustrated by a case in which the patient died during the puerperium of her 3rd pregnancy [14]. Cardiac catheterization of patient 1 and physical examination of patient 2 did not show any aggravation of the cardiac condition after the two successfully managed pregnancies. Clinical management The pregnant woman should be hospitalized approximately at 25 weeks of gestation, dependent on the cardiac condition. During episodes of dyspnoea, bed rest is recommended, and high concentrations of oxygen should be administered through a face mask. The oxygen tension should be assessed through determination of serial arterial blood gases to detect changes in shunt flow. Usually, anticoagulation treatment is not indicated. From a cardiac point of view, premature delivery has no beneficial effect. If necessary, oxytocin can be administered. At the onset of labour, the patient should be carefully monitored by electrocardiograms and arterial and epidural catheters. Intravenous infusion with norepinephrine and blood should be held in readiness to counteract blood loss, and a drop in blood pressure should be counteracted by the infusion of vasopressors; oxygen is recommended to counteract pulmonary hypertension. Vaginal delivery, assisted by vacuum extractor in the 2nd state of delivery is recommended. The patient should be kept in bed for the first day after delivery and should be monitored continuously and then gradually activated. We suggest that the patient stays in hospital for a period of 7-14 days after delivery under careful observation due to the continued risk of sudden death. References 1 2 3 4 5
Wood P. The Eisenmenger syndrome. Br Med J. 1958;2:701-755. Jones AM, Howitt G. Eisenmenger syndrome in pregnancy. Br Med J 1965;1:1627-1631. Pitts JA, Crosby WM, Basta LL. Eisenmenger’s syndrome in pregnancy. Am Heart J 1977;93:321-325. Neilson G, Galea EG, Blunt A. Eisenmenger’s syndrome and pregnancy. Med J Austr 1971;1:431-434. Gleicher N, Midwall J, Hochberger D, Jaffin H. Eisenmenger’s syndrome and pregnancy. Obstet Gynecol Surv 1979;34:721-741.
74 6 Gummerus M, Laasonen H. Eisenmenger complex and pregnancy. Ann Chir Gynaecol 1981;70:339-341. 7 Spinnato JA, Kraynack BJ, Cooper MW. Eisenmenger’s syndrome in pregnancy: epidural anaesthesia for elective cesarean section. N Engl J Med 1981;20:1215-1217. 8 Midwah J, Jaffin H, von Herman M, Kupersmith J. Shunt flow and pulmonary hemodynamics during labour and delivery in the Eisenmenger syndrome. Am J Cardiol 1978;42:299-303. 9 Huyghe de Mahence A, Andre-Fouet X, Bernet D, Sehgman G, Wilner LC, Gayet C, Robert D, Pont M. Syndrome d’Eisenmenger et grossesse. Arm Cardiol Angeiol (Paris) 1985;34:547-549. 10 Heytens L, Alexancer JP. Maternal and neonatal death associated with Eisenmenger’s syndrome. Acta Anaesthesiol Belg 1986;37:45-51. 11 Lieber S, et al. Eisenmenger’s syndrome and pregnancy. Acta Cardiol 1985;40:421-424. 12 Young D, Mark H. Fate of the patient with Eisenmenger syndrome. Am J Cardiol 1971;28:658-659. 13 Foster JMG, Jones RM. The anaesthetic management of the Eisenmenger syndrome. Ann R Co11 Surg Engl 1984;66:353-355. 14 Bueman B, Kragelund E. Clinical assessment of heart disease during pregnancy. Acta Obstet Gynaecol Stand 1962;41:57-79.