DOI: 10.1111/j.1471-0528.2006.01152.x
Maternal medicine
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Maternal pseudo primary hyperaldosteronism in twin-to-twin transfusion syndrome IL Gussi, J Nizard, M Yamamoto, R Robyr, Y Ville Department of Obstetrics and Gynecology, CHI Poissy Saint Germain, Universite´ de Versailles Saint-Quentin-en-Yvelines, Poissy, France Correspondence: Prof Y Ville, Department of Obstetrics and Gynecology, CHI Poissy Saint Germain, Universite´ de Versailles Saint-Quentin-en-Yvelines, 10, rue du Champ Gaillard, 78300 Poissy, France. Email
[email protected] Accepted 2 October 2006.
Objective To monitor changes in the maternal renin–angiotensin–
aldosterone system following laser therapy and amnioreduction in severe twin-to-twin transfusion syndrome (TTTS). Design Observational prospective study. Setting Single university hospital in Poissy, France. Population Sixty cases of TTTS at 16–26 weeks of gestation. Method Maternal blood sampling before, 6 and 24 hours
following the procedure. Main outcome measures Plasma levels of aldosterone, renin,
angiotensin II (AII), atrial natriuretic peptide (ANP), vasopressin, sodium, potassium and plasma proteins together with full blood count were measured before, 6 and 24 hours following the procedure.
Results TTTS is associated with maternal hyperaldosteronism dissociated from renin–angiotensin changes. Correcting TTTS by placental surgery and amnioreduction triggers incomplete correction of hyperaldosteronism, as early as 6 hours following the procedure, without changes in AII but an increase in the levels of ANP in plasma. Electrolyte concentrations remained stable despite haemodilution, while vasoactive hormone levels such as that of vasopressin remained unchanged. Conclusion Mechanisms involved in marked fluid retention in
TTTS are rapidly corrected by laser therapy followed by amnioreduction while maintaining electrolyte homeostasis. Keywords Aldosterone, amnioreduction, haemodilution, laser
therapy, plasma volume expansion, twin-to-twin transfusion syndrome.
Please cite this paper as: Gussi I, Nizard J, Yamamoto M, Robyr R, Ville Y. Maternal pseudo primary hyperaldosteronism in twin-to-twin transfusion syndrome. BJOG 2007;114:65–69.
Introduction Pregnant women show both intravascular and extravascular volume expansion with progressive sodium retention.1 Sodium balance is the most important determinant of maternal circulating volume and one of the most challenging adaptative mechanisms. Increased sodium requirements develop simultaneously with natriuretic mechanisms such as increased glomerular filtration rate and the antimineralocorticoid effect of increased circulating progesterone. These changes in maternal physiology are balanced by early supra-physiological renin– angiotensin–aldosterone system (RAS) activation, which increases throughout gestation.2 Both aldosterone and renin receptors are reset to activate at a lower threshold of sodium levels during gestation.3 However, increase in the levels of aldosterone in plasma appears earlier in pregnancy than that of renin, and the interaction with renin is weakened,4 thus mimicking primary hyperaldosteronism.1
These adaptive changes are even more pronounced in twin pregnancies,5 especially when there is polyhydramnios in twin-to-twin transfusion syndrome (TTTS). In these cases, plasma volume and sodium concentrations are reported to be normal but with a more pronounced hyperaldosteronism than that in matched, uncomplicated, monochorionic pregnancies.6 TTTS can be corrected following photocoagulation of placental anastomoses and amnioreduction.7 The aim of this study was to monitor changes in maternal RAS and water–electrolyte balance following placental surgery and amnioreduction in severe mid-trimester TTTS.
Material and methods Sixty cases of TTTS at 16–26 weeks of gestation were investigated prospectively between April 2004 and January 2005. All twin pregnancies were diagnosed as monochorionic diamniotic by ultrasound examination at 6–14 weeks of gestation.
ª 2007 The Authors Journal compilation ª RCOG 2007 BJOG An International Journal of Obstetrics and Gynaecology
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TTTS was diagnosed when there was evidence of polyuria in the recipient twin (severe polyhydramnios with a deepest pool of liquor of at least 100 mm and a distended bladder) and oliguria in the donor twin (oligohydramnios and a small or absent bladder on ultrasound). None of them had undergone any therapeutic intervention prior to referral to our centre. Women were treated by placental surgery followed by rapid amnioreduction, as described elsewhere.7 Briefly, local anaesthetic with lidocaine 2% was injected down to the myometrium. Percutaneous insertion of the trocar and the endoscope into the polyhydramniotic cavity was performed under ultrasound guidance. Endoscopic inspection of the chorionic plate was followed by selective coagulation of vessels identified as being intertwin anastomoses, as well as those failing to clearly show that they belonged to only one twin. Amnioreduction was then performed until the deepest pool of amniotic fluid returned to a maximum of 50–60 mm. Tocolysis consisted of a single dose of 100 mg of indomethacin given intrarectal 3 hours before surgery. Perioperative intravenous fluids were limited to a maximum of 500 ml intravenous crystalloid, administered at a maximum rate of 125–150 ml per hour. Over the next 24 hours, women had preserved venous access only if painkillers were needed and no or very little fluid was infused. Women were allowed normal unrestricted food and fluid intake from 2 hours after the procedure. In a recumbent position, 35 ml of maternal cubital venous blood was collected before, 6 hours and 12–24 hours after surgery. Samples were centrifuged, and plasma was immediately separated and stored at –20C. Aldosterone levels in plasma were measured by radioimmunoassay using Immunotech kits (Marseille, France) (interassay coefficient of variation (CV) 11.06% for 214.2 pg/ml). Angiotensin II (AII) and arginine vasopressin (AVP) were also measured by radioimmunoassay using Nichols Institute Diagnosis kits (Paris, France) (interassay CV 16.62% for 68.98 pg/ml for AII and CV 16.35% for 13.7 pg/ml for AVP). Renin was measured by radioimmunoassay using Biorad Laboratory (Hercules, CA, USA) kits (interassay CV 8.45% for 32.93 ng/l). Atrial natriuretic peptide (ANP) was measured by radioimmunoassay using Cisbio International (Bagnets-sur-Ceze,
France) kits (interassay CV 10.19% for 12.98 pg/ml). Results were compared with normal nonpregnant ranges as provided by the laboratory according to each kit used (Table 1); these were 68–300, 3–33, 19.9–39.7,
