Hyperviscosity syndrome (HVS) is clinically manifested by retinal changes, neurological symptoms, and bleeding in humans.¹ It occurs secondary to the elevation of blood or plasma viscosity, leading to tissue ischemia. Therefore, HVS can be distinguished between plasma and cellular.¹ The most common cause is hypergammaglobulinemia, either monoclonal as in malignancies, like multiple myeloma, or polyclonal.^2,3 Leishmania infantum and Ehrlichia canis infections are examples of nonneoplastic diseases that lead to dysproteinemia and possibly to HVS. ^4-7 Increased numbers of red blood cells, as in polycythemia, can also result in viscous blood.¹

Vascular disturbances play a significant role and can mainly be observed in the retinal microvascular bed. Dilated and tortuous vessels (DTV) is the earliest and most common ocular sign; nevertheless, retinal hemorrhages, retinal detachment, papilledema, retinal edema, retinal degeneration, blindness, uveitis, and secondary glaucoma have also been reported.^2,5

In this work, we review the funduscopy findings in four patients with HVS secondary to different systemic diseases. In 3/4 cases had severe hyperproteinemia (Total Protein>10g/dL) while 1/4 had cellular HVS which reflects the results of previous reports.^2,4,5,7 Retinal hemorrhages observed in case 1 and 2, are the most common forms of bleeding in patients with HVS.³ All cases had DTV in different locations. In 1/4 cases, systemic hypertension was detected and may contribute to the retinal lesions. Although the diagnosis of HVS may base on serum viscosity, a prompt approach could be made from the eye examination, which enables the institution of appropriate therapy.