Results from presence of deoxygenated hemoglobin

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Results from presence of deoxygenated hemoglobin (hemoglobin NOT bound to O 2 ) Usually apparent when arterial O 2 saturations are 80% – 85% Heart defects that cause hypoxemia and cyanosis result from desaturated venous blood (blue blood) entering systemic circulation without passing through lungs number of RBCs due to chronic hypoxia O 2 -carrying capacity of blood Anemia may result if iron is not readily available for formation of hemoglobin viscosity of blood + crowd out clotting factors = risk for clotting = risk for stroke if dehydrated Thickening and flattening of tips of fingers and toes Occurs due to chronic tissue hypoxemia and polycythemia Bacterial endocarditis (BE) infection of heart valves and inner lining of heart Most often a sequela of bacteremia in child with acquired or congenital anomalies of heart or great vessels Affects children with valvular abnormalities, prosthetic valves, shunts, recent cardiac surgery with invasive lines, and rheumatic heart disease with valve involvement Most common causative agent = Streptococcus viridians Pathophysiology organisms enter bloodstream (from any site of localized infection or from interruption of skin integrity, such as dental work, cardiac surgery, long-term indwelling catheters) to grow on heart endocardium Lesion may invade adjacent tissues, such as aortic and mitral valves, and may break off and embolize elsewhere, especially in spleen, kidney, and CNS Manifestations onset usually insidious Unexplained fever (low grade and intermittent) Anorexia, weight loss, malaise Treatment started immediately with high doses of appropriate IV antibiotics for 2 – 8 weeks Prevention = administration of prophylactic antibiotic therapy 1 hour before any procedures known to risk of entry of organisms in very high risk patients dental work Educate parents to report any unexplained fever, weight loss, or change in behavior (lethargy, malaise, anorexia) to HCP
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Sickle cell anemia (SCA) normal adult Hgb (Hgb-A) is partly or completely replaced by abnormal sickle Hgb (Hgb-S) Sickle cell disease (SCD) includes all hereditary disorders with clinical, hematologic, and pathologic features that are related to presence of Hgb-S Characterized by vasoocclusion, infarcts, hemolysis, anemia, pain, ischemia, and hypoxia RBCs are hard, inflexible, and sickle-shaped Etiology autosomal recessive disorder = 25% chance of producing offspring with SCA if both parents are carriers Primarily affects African-Americans Newborn with SCA is generally asymptomatic due to Hgb-F concentrations > Hgb-S concentrations Pathophysiology primarily result of obstruction caused by sickled RBCs and RBC destruction (7 – 10 day life span) Abnormal adhesion, entanglement, and enmeshing of rigid sickle-shaped cells with one another block microcirculation = causes vasoocclusion blood flow to adjacent tissues = local hypoxia =
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  • Spring '17
  • varies
  • Respiratory distress, respiratory tract

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