Knabben H, Wolf S, Remky A, Schulte K, Arend O, Reim M
Augenklinik, RWTH Aachen.
Klin Monbl Augenheilkd. 1995 Mar;206(3):152-6. doi: 10.1055/s-2008-1035420.
The hyperviscosity syndrome (e.g. plasmacytoma, cryoglobulinaemia and Waldenström's macroglobulinaemia) leads through the polymerisation of macro-molecules to an increased blood viscosity. This may result in microcirculatory disturbances in various organs. In the retina the hyperviscosity produces a pattern of retinal changes including dot and blot hemorrhages, retinal and optic nerve head edema and increased diameters of the veins. In the present study we quantified the retinal hemodynamic in patients with hyperviscosity syndrome.
Fifteen patients aged between 35 and 72 years were included in the study. Ten presented with Waldenström's macroglobulinaemia, two with cryoglobulinaemia and three with plasmacytoma. All patients underwent video fluorescein angiographic studies. The arteriovenous passage time (AVP) representing the retinal microcirculation and the arm retina time (ART) were quantified from the angiograms. In addition, hematocrit (Hct) and the plasma viscosity (ETA) were measured.
The AVP was significantly prolonged in patients with hyperviscosity syndrome in comparison to healthy volunteers (AVP: 2.6 +/- 1.5 s vs. 1.6 +/- 0.4 s; p < 0.05). The ART showed no significant differences. Plasma viscosity was doubled in the patients as compared with reference values (ETA: 2.54 +/- 2.23 mPas vs. 1.24 +/- 0.08 mPas; p < 0.01).
The simultaneous rising of plasmaviscosity and arteriovenous passage time suggests that the increase of plasmaviscosity causes retinal circulatory disturbance. All this may result in the typical fundus changes in patients with hyperviscosity syndrome.