Table 12.2 . Depending on the differential diagnosis, a number of other blood tests also may be performed to evaluate anemia, including (1) serum iron indices (iron levels, iron-binding capacity, transferrin saturation, and ferritin concentrations), which help distinguish among microcytic anemia caused by iron deficiency, chronic inflammation, and thalassemia; (2) plasma unconjugated bilirubin, haptoglobin, and lactate dehydrogenase levels, which are abnormal in hemolytic anemia; (3) serum and red cell folate and vitamin B12 concentrations, which are low in megaloblastic anemia; (4) hemoglobin electrophoresis, which is used to detect abnormal hemoglobin; and (5) the Coombs test, which is used to detect antibodies or complement bound to red cells in suspected cases of antibody-mediated hemolytic anemia. In isolated anemia, tests performed on the peripheral blood usually suffice to establish the cause. By contrast, when anemia occurs along with thrombocytopenia and/or granulocytopenia, it is much more likely to be associated with marrow aplasia or infiltration; in such instances a marrow examination usually is warranted.
As discussed later, the clinical consequences of anemia are determined by its severity, rapidity of onset, and underlying http://ebooksmedicine.net
Table 12.2 Adult Reference Ranges for Red Blood Cells
Hemoglobin(Hb)g/dL13.2–16.711.9–15.0 11.5–14.8 aReferencerangesvaryamonglaboratories.Thereferencerangesforthelaboratoryprovidingtheresultshouldalwaysbeusedininterpretingalaboratorytest.
pathogenic mechanism. If the onset is slow, the deficit in O2carrying capacity is compensated for by increases in cardiac output, respiratory rate, and red cell 2,3-diphosphoglycerate (DPG), a glycolytic pathway intermediate that enhances the release of O2 from hemoglobin. These adaptive changes mitigate the effects of mild to moderate anemia in otherwise healthy persons but are less effective in those with compromised pulmonary or cardiac function. Pallor, fatigue, and lassitude are common to all forms of anemia. Anemia caused by the premature destruction of red cells (hemolytic anemia) is associated with hyperbilirubinemia, jaundice, and pigment gallstones (if hemolysis is chronic), all related to increases in the turnover of hemoglobin. Anemia that stems from ineffective hematopoiesis (the premature death of marrow erythroid progenitors) is associated with inappropriate increases in iron absorption from the gut, which can lead to iron overload (secondary hemochromatosis) with consequent damage to endocrine organs and the heart. If left untreated, a severe congenital anemia such as β-thalassemia major inevitably results in growth retardation, skeletal abnormalities, and cachexia.
Microcytic(irondeficiency,thalassemia)
Normocyticbutwithabnormalshapes(hereditaryspherocytosis,sicklecelldisease)
Acute: shortnessofbreath,organfailure,shock
Pallor,fatigue,lassitude
Withhemolysis:jaundiceandgallstones
Withineffectiveerythropoiesis:ironoverload,heartandendocrinefailure
Ifsevereandcongenital:growthretardation,bonedeformitiesduetoreactivemarrowhyperplasia
ANEMIAOFBLOODLOSS:HEMORRHAGE