To the Editor: I read with interest the valuable comments of Dr. Hassan. Traditionally, diffuse alveolar infiltrate complicating ovarian hyperstimulation syndrome (OHSS) has been attributed to an increased vascular permeability. However, OHSS is consistently associated with a circulatory dysfunction characterized by arterial hypotension, low peripheral vascular resistance, increased activity of the renin-aldosterone system, marked stimulation of the antidiuretic hormone, and sodium retention.1 Despite different theories, the exact pathogenesis of circulatory dysfunction during OHSS remains unknown. Massive hydration in patients with circulatory dysfunction may lead to further deterioration of pulmonary edema and respiratory symptoms. This theory is supported by the fact that reported cases of alveolar infiltrate complicating severe OHSS demonstrated marked improvement in patients’ conditions after fluid restriction and loop diuretics.3,4 Furthermore, an autopsy case of OHSS reported massive pulmonary edema without diffuse alveolar damage, hyaline membrane formation, or interstitial inflammatory infiltrate supporting the possibility of high pressure edema.4 The pathogenesis of pulmonary edema complicating severe OHSS appears to be multifactorial. Transient cardiac dysfunction could be one of the pathogenic causes of pulmonary edema. Future research should address different factors that may affect cardiac function in patients with severe OHSS, including the associated physiological and inflammatory changes, with a special focus on the subgroup of patients who develop severe pulmonary edema.
References
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