BLOOD IS THICKER THAN WATER: THE MANAGEMENT OF HYPERVISCOSITY IN ADULTS WITH CYANOTIC HEART DISEASE. A. DeFilippis 1 , S. Aaberg 1 ; 1 Emory University, Decatur, GA (Tracking ID #76037) LEARNING OBJECTIVES: 1. Recognize the clinical presentation of hyperviscosity syndrome in patient with chronic hypoxia. 2. To recognise the complications of phlebotomy in the treatment of erythrocytosis of cyanotic heart disease. 3. To recognise the appropriate use of hydroxyurea in the treatment of erythrocytosis of cyanotic heart disease. CASE INFORMATION: A 19-year-old male with uncorrected tetralogy of Fallot presented to the emergency room after a ground level fall after climbing two steps. The fall was preceded by two episodes of lightheadedness. He denied vertigo, bowel or bladder incontinence, chest pain, dyspnea, or palpitations. At presentation, he was afebrile with a pulse of 90 beats per minute, blood pressure of 117/63, 30 respirations per minute and an oxygen saturation of 79%. Physical examination was remarkable for a well developed, alert and oriented male in no distress, clubbing in all digits, normal S1 and S2 heart tones with a II/VI early systolic ejection murmur heard throughout the chest; a cardiac heave over the left side of the chest, no jugular venous distention, no peripheral edema or crackles. Chest radiograph revealed a large bootshaped heart and right-sided aortic arch. EKG was notable for a normal sinus rhythm with left axis deviation and right atrial enlargement. Remarkable laboratory values were hemoglobin of 24g/dL and a hematocrit of 76 %. The patient was phlebotomized 500ml of blood and discharged from the hospital after remaining in normal sinus rhythm and asymptomatic for 24 hours. IMPLICATIONS/DISCUSSION: Complications of chronic hypoxia including erythrocytosis, hyperviscosity, abnormalities of hemostasis, cerebral abscesses or stroke and endocarditis are among the most common consequences of cyanotic heart disease in adults. The compensatory erythrocytosis of cyanotic heart disease can become pathologic by causing an increase in blood viscosity, which decreases perfusion, resulting in a decrease in total oxygen delivery and an increased risk of veno-occlusive/hyperviscosity syndrome. Treatment of hyperviscosity secondary to erythrocytosis in cyanotic heart disease is controversial. Data suggest that phlebotomy has the potential to increase exercise capacity, reduce the symptoms of hyperviscosity syndrome and reduce the potential increased risk of vasoocclusive disease in selected patients with polycythemia secondary to cyanotic heart disease. Unfortunately, repeated phlebotomy can quickly lead to iron deficiency. Microcytic erythrocytes produce higher viscosity than normocytic erythrocytes at comparable hematocrits putting patients at high risk for vasoocclusive events. There is limited data on the use of hydroxyurea to suppress erythrocytosis in this patient population. Thus we concluded that until newer approaches to decreasing the hematocrit, without causing iron deficiency anemia, are shown to be safe and efficacious, phlebotomy should only be used for the acute resolution of hyperviscosity symptoms; and the use of hydroxyurea should be limited to recurrently symptomatic patients.