Abstract
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Learning Objectives The purpose of this exhibit is: 1. Review the pathophysiology of hepatopulmonary syndrome. 2. Describe the utility of nuclear medicine evaluation of hepatopulmonary syndrome. 3. Explain imaging findings of lung perfusion and abnormal brain activity utilizing Tc-99 MAA reduced particles. 4. Perform quantitative lung and brain analysis to determine presence of a direct pulmonary anatomic shunt and brain uptake in patients with hepatopulmonary syndrome.
Scientific data will be presented in the way of a case series of nuclear medicine evaluation of hepatopulmonary syndrome utilizing Tc-99 MAA reduced particles to demonstrate abnormal activity in the brain, suggestive of direct arteriovenous communication (anatomic shunt) in the lungs with resultant arterial hypoxemia and shortness of breath. Pathophysiology of hepatopulmonary syndrome Nuclear medicine evaluation of hepatopulmonary syndrome Review of imaging findings utilizing Tc-99 MAA reduced particles -lung perfusion -static brain imaging -regions of interest Quantitative Analysis -split pulmonary perfusion -geometric mean counts -percentage brain uptake Sample cases Summary 1. Hepatopulmonary syndrome: arterial hypoxemia caused by pulmonary vasodilation which is the consequence of portal hypertension 2. Percentage brain uptake greater than or equal to 6% is considered abnormal and suggestive of presence of an anatomic shunt in the lungs 3. Diagnosis of hepatopulmonary syndrome is facilitated by nuclear medicine lung perfusion and brain uptake quantification.