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FACP. Colegio de médicos de Tarragona Nº 4305520 / fgcapriles@gmail.com




Wednesday, July 1, 2015

Síndrome de hiperviscosidad


emDocs - By Kessler  J and Kang C - Edited by Koyfman A and Alerhand S - June 30, 2015
"Clinical presentation
The syndrome typically presents as a triad of oro-nasal bleeding, visual changes, and neurological symptoms. Additionally,cardiovascular and pulmonary symptoms may occur. These symptoms have been noted to occur when a patient’s blood viscosity, measured in centipoise, increases from a normal range of 1.4-1.8 pg to 4-5 pg. The increase in viscosity has been correlated to several corresponding serum levels including immunoglobulin M (IgM) level >3 g/dL, IgG level >4 g/dL, and IgA level >6 g/dL.
Diagnostic work-up
As an Emergency Medicine provider, you may consider several diagnostic tests if suspecting HVS. A CBC with a peripheral smear may demonstrate a rouleax formation. A CMP may demonstrate hypercalcemia, hypophosphatemia, and hyperkalemia. A total protein and albumin study may be abnormal. A coagulopathy study may reveal abnormalities. Imaging studies should include a CT and/or MRI of the brain if the patient presents with significant neurological abnormalities and/or a chest x-ray if the patient presents with additional symptoms of congestive heart failure (CHF).
Immediate therapy of symptomatic hyperviscosity is directed at reduction of blood viscosity. Plasmapheresis is the initial treatment of choice for the management and stabilization of HVS, as it is usually safe for and well tolerated by the patient. By removing the circulating excess paraproteins located in the intravascular space, serum viscosity decreases and the patient’s symptoms improve. Leukapheresis, plateletpheresis, and phlebotomy are indicated for HVS from leukostasis, thrombocytosis, and polycythemia, respectively. However, plasmapheresis and the aforementioned blood therapies are not the definitive treatment, as they do not address the underlying dysproteinemia and/or blood cell dyscrasia. Long-term management is directed at control of the underlying disease to prevent production of the monoclonal protein. A consult to ahematologist/oncologist is required."