Anemia

1. Hg<13g/dL in M, <12 in F; incidence increases w/ age; low Hg indicates physiologic decline;

anemia is independent risk factor for increased morbidity and mortality and decreased QOL
(table 1); increasing functional deterioration associated w/ decreasing Hg; even low NORMAL Hg
may be marker for decline; despite possible benefits of Tx in older adults who are frail or at end
of life, discomfort from tests and interventions may exceed benefits when dz burden and
disability become severe; valid reasons to defer evaluation: limited overall benefits, risk of false
(+)’s, pt preference

2. Etiologies (table 2)- ~1/3rd have nutritional def., 1/3rd have chronic inflammation, CKD, or both,
1/3rd are unexplained

3. Clinical Diagnosis
a. Onset often insidious; acute drop in Hg will cause Sx of volume depletion (dizziness,
increased falls etc.); older pts can’t increase HR and CO as much as young pts w/
dyspnea, fatigue, and confusion developing as anemia worsens; preexisting cardiac dz
(CAD, CHF) become more symptomatic as Hg decreases; pale conjunctiva when Hg<9;
high index of suspicion when older pts presents w/ even subtle Sx of decline; CBC or
point-of-care Hct confirms Dx
b. Signs/Sx associated w/ blood loss (chronic indigestion, dark stools) suggest GI bleed;
dark urine suggests hematuria; ask about recent surgery; strict vegans (vitB12 def);
heavy alcohol consumption (folate def, bleeding from PUD and varices); long-standing
anemia (familial d/o’s like thalassemias and spherocytosis); meds that increase risk of
bleed (NSAIDs, warfarin); malignancy and/or chronic infection (wt loss, LAD, localized
bony pain)
4. Lab testing and evaluation- once anemia confirmed, get CBC (if not already done); if bleeding or
FeDef anemia suspected, get serum ferritin
a. Microcytic anemia (fig1)
i. Usually FeDef, ferritin <35ng/mL highly suggestive but it is an acute phase
reactant hence can increase w/ acute illness and inflammation hence it could be
elevated in pts w/ FeDef anemia + acute inflammatory process hence cutoff of
45ng/mL has higher sensitivity in older adults
ii. Often caused by GI bleed hence requires further investigation in older adults;
FeDef anemia markedly increases likelihood of GI malignancy especially in pts
>65; >1/2 of pts (even if asymptomatic) have bleeding-related lesion on
endoscopy (EGD or colonoscopy); higher rates of GI bleed associated w/:
advanced age, MCV<60, (+) FOBT; risks of perforation w/ colonoscopy increase
w/ age, comorbidities, obstruction and invasive interventions hence invasive Dx
interventions best used when they are likely to affect dz management and
improve prognosis

b. Normocytic anemia
i. Many are secondary to chronic dz including CKD however exclusion of EARLY
nutritional def and hemolysis is required b/c many pts w/ vitB12 or folate def
have a NORMAL MCV; peripheral smear, reticulocyte count, and vitB12 and
folate levels should be ordered
ii. Retic index >2%
1. Hemolysis
2. (+) direct Coombs- AIHA which is life-threatening if untreated but has
good outcomes w/ immunosuppression
 3. Recent blood loss
4. Hypersplenisms
iii. Low reticulocyte count (bone marrow failure)- most pts w/ anemia; when
reticulocyte count is low, next step is to obtain vitB12 and folate levels
iv. Many older pts have mixed anemia w/ >1 etiology
1. Soluble transferrin receptor >2.5mg/L in FeDef anemia
2. Soluble transferrin receptor/log(ferritin)<1.5- anemia of chronic dz
3. Soluble transferrin receptor/log(ferritin)>1.5- FeDef anemia + chronic dz

c. Macrocytic anemia- drug therapy, alcoholism, liver dz, hypothyroidism, vitB12 or folate
def., myelodysplastic syndrome, myeloproliferative conditions, other malignancies
(MULTIPLE MYELOMA)
i. Increased reticulocytes- hemolysis, hypersplenism, recent blood loss
ii. Low reticulocytes next step is to obtain vitB12 and folate levels if
borderline low, obtain serum homocysteine and MMA (normal homocysteine
and MMA exclude folate and B12 def)
iii. Abnormal peripheral smear- myelodysplastic syndrome, malignancy (especially
multiple myeloma), myeloproliferative conditions
 1. Bone marrow biopsy should be acquired b/c findings affect Tx

5. Treatment
a. ALL persons w/ nutritional def should be Tx except very ill pts at end of life or those who
decline intervention; effective Tx noted by reticulocytosis w/in 1wk, followed by more
gradual increase in Hg
b. FeDef Anemia- Tx for 6mo to replete iron stores
i. Usual replacement dose is ferrous sulfate 325mg/d or ferrous gluconate
325mg/d
ii. Low-dose iron therapy (<15mg of elemental Fe) corrects Hg and ferritin w/
fewer GI AE’s than higher doses
iii. Parenteral Tx w/ iron dextran or iron sucrose in pts who fail oral iron Tx
c. VitB12 def- high-dose oral cyanocobalamin (1-2mg/d)
d. Folate def- 1mg/d of folic acid
e. ACD
i. Initial and preferred Tx is to correct underlying d/o which will minimize
inflammation and lessen bone marrow suppression
ii. Most anemias in older pts are mild and do NOT require further intervention
iii. Two options to Tx severe anemia (Hg<10)
1. Blood transfusion- immediate relief of dyspnea, fatigue, dizziness; risks:
volume overload, iron overload, infections, acute rxns
2. Erythropoiesis-stimulating agents (table 4)
a. Goals for CKD are avoiding transfusions and Hg<12 b/c goal of
13 resulted in increased rate of death and CV events
iv. For most pts w/ ACD or unexplained anemia, there is little evidence that
correcting Hg decreases morbidity and mortality or improves QOL; in these pts
anemia may be marker of frailty and physiologic decline; limit use of
 erythropoietin-stimulating agents to Tx of severe anemia associated w/ CKD and
other approved indications

f. Hematology consult if Tx desired for myelodysplastic syndrome and MM