Pathophysiology of unilateral pleural effusions in the ovarian hyperstimulation syndrome

Nick Wood

19 Ivygreen Road, Chorlton cum Hardy, Manchester M21 9FF, UK

Dear Sir,

The more detailed explanation of the pathophysiology of acute unilateral pleural effusion in ovarian hyperstimulation syndrome (OHSS) provided by Loret de Mola (1999) is one of the possibilities that we alluded to in our case report. I agree that in OHSS, the most plausible explanation is provided by the presence of anatomical defects in the tendinous portion of the diaphragm, which are more common on the right side. Furthermore, the presence of a unilateral effusion without gross ascites could be explained by the preferential passage of fluid into the pleural cavity secondary to the negative intrathoracic pressure. Thus prior to the rupture of the diaphragmatic bleb there would have been more ascites which would only reaccumulate once the intrathoracic pressure equilibrated with the pressure in the peritoneal cavity. I imagine that this would be associated with significant respiratory and possibly cardiac compromise, as in a tension pneumothorax.

The presence of small to moderate bilateral effusions with gross ascites in OHSS is probably more likely be due to the drainage of the diaphragmatic lymphatics as Dr Loret de Mola suggested as a mechanism for the formation of effusions in more chronic ascites such as cirrhosis. This situation also leads to respiratory compromise, but due to a combination of the space occupying pleural effusion and diaphragmatic splinting by the tense ascites.

The number and size of the defects in the tendinous portion of the diaphragm I am sure varies, as does the pressure at which the membranous blebs rupture. This a certain portion of the population will be predisposed to suffering an `acute' unilateral (or bilateral) pleural effusion. In some, this predisposition may be compounded by previous abdominal surgery as in the case illustrated in our article.

Where the fluid ends up is more about `plumbing' than `production', in that I agree that it is unlikely that a systemic factor will target its vascular permeability effects on a pleural space unilaterally, without affecting any other serosal membrane. The cause of the production of the fluid, i.e. the aetiology of OHSS remains unexplained.

References

Loret de Mola, J.R. (1999) Pathophysiology of unilateral pleural effusions in ovarian hyperstimulation syndrome. Hum. Reprod., 14, 272–273.[Free Full Text]