The causes of transient blurred vision* lasting from seconds to minutes (sometimes up to 1 to 2 hours) include:
1. Carotid Artery Disease 2. Vertebrobasilar Insufficency 3. Hyperviscosity Syndrome a. from Multiple Myeloma b. from Polycythemia Vera c. from Chronic Myelogenous Leukemia d. from acute leukemias e. from Waldenstrom’s Macoglobulinemia 4. Optic Nerve Disease a. Ischemic Optic Neuritis b. Demyelinating Optic Neuropathy c. Compressive Optic Neuropathy d. Toxic/Metabolic Optic Neuropathy 5. Macular disease 6. Refractive error 7. Papilledema (increased intracranial pressure) 8. Temporal Arteritis (Giant Cell Arteritis) 9. Impending central retinal vein occlusion 10. Migraine with aura 11. Acephalic Migraine 12. Basilar Artery Migraine
Transient visual loss can be due to a transient ischemic attack (TIA) which is an emergency.The reason to go to the emergency department right away is that patients who has a TIA are at markedly increased risk of having a stroke. It is estimated that a person with a TIA has a 10% chance of having a stroke over the next 90 days. And as much as one one quarter to one half of that increased risk occurs in the two days immediately after the TIA symptoms.
Please see my post on diagnosis and treatment of TIA titled Transient Ischemic Attack—Know What It Is and Take Immediate Action posted 12-2-2011. There are detailed instructions on the imaging evaluation of transient visual loss (and other symptoms of TIA) from the 2009 AHA TIA guidelines.
The emedicine article on transient visual loss also recommends consideration of an echocardiogram and what they call electrophysiologic studies (by which they mean EKG, Holter Monitor, and/or Event Recorder in this context).**
Laboratory evaluation of transient visual loss should include CBC, CMP, U/A, ESR and/or CRP.
Hyperviscosity syndrome is also a potential cause of transient visual loss and in 85% of cases is due to Waldenstrom’s magroglobulinemia.**
Hyperviscosity syndrome (HVS) refers to the clinical sequelae of increased blood viscosity. Increased serum viscosity usually results from increased circulating serum immunoglobulins and can be seen in such diseases as Waldenström macroglobulinemia and multiple myeloma. It can also result from increased cellular blood components (typically white or red blood cells) in hyperproliferative states such as the leukemias, polycythemia, and the myeloproliferative disorders.
The complications most commonly associated with this syndrome include mucous membrane bleeding, neurologic and pulmonary symptoms, and the associated retinopathy.
The normal relative serum viscosity ranges from 1.4-1.8 units (reported as Centipoises). Symptoms usually are not seen at viscosities of less than 4 units, and the hyperviscosity syndrome typically requires a viscosity greater than 5 units.***
WBC count is typically 100,000 or greater in leukostasis causing HVS, but it may be lower in the blast crises of the leukemias. Consider adding total protein (TP) and albumin as in the paraproteinemias; a globulin gap (TP – albumin = 4 or greater) may exist.***
When hyperviscosity is present you need to check for hypercalcemia, hyperphosphatemia, and hyperkalemia. And remember that radiocontrast is contraindicated in myeloma because it can cause renal failure. Consider a serum and urine electrophoresis.***
*The Will’s Eye Manual, 5th ed., 2008. pp. 264 – 5.