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Neurohormonal and Hemodynamic Changes in Severe Cases of the Ovarian Hyperstimulation Syndrome

Juan Balasch, MD; Vicente Arroyo, MD; Francisco Fabregues, MD; Juan Salo, MD; Wladimiro Jimenez, PhD; Juan C. Pare, MD; and Juan A. Vanrell, MD
[+] Article and Author Information

From Hospital Clinic i Provincial, Faculty of Medicine, University of Barcelona, Barcelona, Spain. Requests for Reprints: Juan Balasch, MD, Department of Obstetrics and Gynecology, Hospital Clinic i Provincial, Casanova 143, 08036 Barcelona, Spain. Grant Support: In part by a grant from the Direccion General de Investigacion Cientifica y Tecnica (DGICYT PM91-0216). Dr. Fabregues received a grant from the Hospital Clnic i Provincial. Dr. Salo is supported by Fondo de Investigaciones Sanitarias de la Seguridad Social (FISS 93/0610).


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1994;121(1):27-33. doi:10.7326/0003-4819-121-1-199407010-00005
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Objective: To evaluate systemic hemodynamics, endogenous vasoactive neurohormonal factors (renin-angiotensin and sympathetic nervous systems, antidiuretic hormone, atrial natriuretic factor, and renal prostaglandins), and renal function in the severe ovarian hyperstimulation syndrome.

Design: Prospective longitudinal study.

Setting: Assisted-reproduction unit of a tertiary care hospital in Barcelona, Spain.

Patients: 31 consecutive patients having in vitro fertilization with development of ascites because of severe ovarian hyperstimulation syndrome.

Measurements: Mean arterial pressure; cardiac output; peripheral vascular resistance; hematocrit concentration; renal function; plasma renin activity; plasma aldosterone, norepinephrine, antidiuretic hormone, and atrial natriuretic peptide determinations; and urinary excretion of prostaglandin E2 and 6-keto-prostaglandin-F1 were measured during the syndrome and 4 to 5 weeks after recovery (baseline).

Results: During the syndrome, patients showed increased hematocrits (mean of the paired difference, 0.047; 95% CI, 0.029 to 0.064), decreased mean arterial pressure (−16.6 mm Hg; CI, −19.8 to −13.6), increased cardiac output (2.6 L/min; CI, 2.13 to 3.17), and reduced peripheral vascular resistance (−709 dyne/s · cm−5; CI, −792 to −627).This was accompanied by marked increases of plasma renin (14.4 ng/L · s; CI, 9.87 to 18.90), norepinephrine (1.857 nmol/L; CI, 0.533 to 3.161), antidiuretic hormone (3.3 pg/mL; CI, 1.89 to 4.71), and atrial natriuretic peptide levels (9.7 fmol/mL; CI, 6.1 to 13.2). Hemoconcentration developed in 16 patients (mean of the paired difference in hematocrit concentration, 0.082; CI, 0.063 to 0.101) but not in 15 others (0.009; CI, 0.003 to 0.021). Both groups showed similar values for arterial pressure, cardiac output, and peripheral vascular resistance, but patients with hemoconcentration had higher (P < 0.05) levels of renin (mean, 20.97 ng/L · s [CI, 13.3 to 28.63] compared with 7.83 ng/L · s [CI, 4.08 to 11.58]), norepinephrine (3.907 nmol/L [CI, 3.057 to 4.757] compared with 2.417 [CI, 2.035 to 2.799]), and antidiuretic hormone (6.0 pg/mL [CI, 4.1 to 7.9] compared with 2.4 [CI, 1.7 to 3.03]).

Conclusions: In addition to increased capillary permeability, severe ovarian hyperstimulation syndrome is consistently associated with arteriolar vasodilation. The simultaneous occurrence of these disorders leads to hyperdynamic circulatory dysfunction with marked stimulation of the sympathetic nervous system, renin-angiotensin system, and antidiuretic hormone.

Figures

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Figure 1.
Cardiac output and peripheral vascular resistance during the ovarian hyperstimulation syndrome (OHSS) and after recovery measured in 24 patients.
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Figure 2.
The relation between plasma norepinephrine concentration and the plasma renin activity and antidiuretic hormone concentration.
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Grahic Jump Location
Figure 3.
Plasma concentration of atrial natriuretic peptide during the ovarian hyperstimulation syndrome and after recovery measured in 31 patients.
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