Practice EssentialsA decline in the hemoglobin level was long considered a natural and expected consequence of aging. The frequently-used phrase “anemia of the elderly” to describe this phenomenon implied that it is unnecessary to conduct a thorough workup to identify a treatable underlying cause. However, emerging data show that anemia in this age group does reflect poor health status and results in adverse outcomes. Consequently, the phrase “anemia in the elderly” has come into use, indicating that anemia in an elderly patient mandates a workup to identify correctable causes of anemia, so that treatment can prevent the resulting morbidity and mortality. Show
The importance of this condition is set to increase significantly in the coming years. The World Health Organization (WHO) estimates that between 2015 and 2050, the percentage of the world's population over age 60 years will nearly double, from 12% to 22% (rising from 900 million in 2015 to 2 billion in 2050). [1] Go to Anemia, Iron Deficiency Anemia, and Chronic Anemia for complete information on these topics. For patient education information, see Anemia.  Anemia ThresholdsCurrently the only universally used definition of anemia in adults is the one proposed by WHO in 1968 as hemoglobin less than 13 g/dL in men and less than 12 g/dL in women. [2] This definition has since been used in population studies for anemia in elderly groups as well, though it is not an “elderly specific” definition. Some investigators have questioned this definition, based on the National Health and Nutrition Survey (NHANES) and the Scripps-Kaiser database and outcome studies. [3, 4, 5, 6] The limitation of those population studies is that they included both healthy elderly persons with few or no comorbidities as well as those with various comorbidities. However, studies on small cohorts of elderly patients without any significant chronic medical condition have shown that the hemoglobin decline during aging tends to be minimal or insignificant, even in very older individuals. [7, 8, 9] Therefore, the1968 WHO definition of anemia has remained the standard and universally used by researchers. [10] EpidemiologyIn addition to the varying thresholds for anemia, the highly heterogeneous nature of the elderly population has led to multiple estimates of anemia prevalence in the elderly. An analysis of NHANES data from 2001-2016 cycles found that in the United States population aged 65 years and older, the overall anemia prevalence was 14.1% in men (95% confidence interval [CI] 11.8–16.7%) and 10.2% in women (95% CI 8.5–12.1%). [12] An increase in the prevalence of anemia with increasing age was noted in all survey cycles for men and all but one survey cycle for women. In 2013–2016, for example, anemia prevalence by age was as follows:
Rates of anemia in the elderly may have been increasing. The NHANES data from 2001–2004 to 2013–2016 showed a statistically insignificant trend toward increased prevalence of anemia in men aged 75 to 84 years, and a significant increase (from 24.2% to 39.5%) in men aged 85 and older. The prevalence of anemia in elderly US women also increased over that period, although for the most part the trends were not significant. [12] Even if rates of anemia in the elderly were to remain stable, however, the number of elderly patients with anemia is likely to increase dramatically in the coming years because of the aging population globally. [1, 13, 14] It should be noted that NHANES estimates are representative of the general noninstitutionalized US population. They do not include institutionalized persons, a population with higher rates of anemia. [15] A study of homebound older adults found that the rate of anemia was 4 times as high as that reported from NHANES III data. [16] Studies from Europe, Japan, China, and Ecuador indicate a fairly similar prevalence of anemia in elderly adults in those parts of the world as in the United States. [17] A systematic review of 34 studies showed that, in Europeans older than 65 years, the prevalence of anemia was 12% in community-dwelling persons, 40% in hospitalized persons, and 47% in nursing home residents. [18] In this study overall, an estimated 17% of those older than 65 years (nearly 15 million elderly persons living in the European Union) were found to have anemia. Similarly, in Japan the prevalence of anemia has been reported to be 17.1% in individuals older than 65 years [19] and 22.3% in those 69–91 years. [20] In rural China the prevalence of anemia in those older than 60 years has been reported as 12.9%. [21] Racial and sexual demographicsAnemia is approximately 3 times more prevalent in elderly Blacks than in non-Hispanic Whites, with the median hemoglobin (Hb) concentration for elderly Blacks being approximately 0.8 g/dL lower than for Whites. [22] In older Mexican Americans, the prevalence of anemia is fairly similar to that of elderly whites, The reason for the higher prevalence of anemia in Blacks has not been established. However, some of the disparity is likely related to biologic differences. Whether anemia has different adverse consequences in Blacks is unclear. In elderly persons, anemia is more common in men than in women. Some of the difference stems from employing a lower Hb threshold for women than for men (12 versus 13 g/dL, respectively). Hb levels decline slightly and anemia prevalence rises with advancing age in both men and women, but the change is more pronounced in men. [22] HematopoiesisHematopoiesis—the production of blood elements—occurs in an orderly, hierarchical fashion. Blood cell production requires stem cells, a functioning bone marrow microenvironment, nutrients, and cytokines. A pluripotent hematopoietic stem cell gives rise to committed progenitors of myeloid, erythroid, and megakaryocytic lineages. Erythropoiesis is the arm of hematopoiesis that generates erythrocytes. In adults, normal erythropoiesis occurs exclusively in the bone marrow and is generally restricted to the pelvis, vertebrae, sternum, ribs, and proximal femurs. The earliest committed erythroid lineage progenitors include the burst-forming unit-erythroid (BFU-E), which later gives rise to the colony-forming unit-erythroid (CFU-E). The reticulocyte, an early red blood cell (RBC) that has lost the nucleus but retained the polyribosomal reticular network, eventually emerges into the blood. After 1-4 days, reticulocytes lose this ribosomal network and mature into RBCs. Mature RBCS have an average lifespan in the blood of 100-120 days. Macrophages engulf senescent RBCs in the spleen, liver, and marrow. Iron extracted from RBCs in this process is recycled back to bone marrow to maintain erythropoiesis. EtiologyMultiple conditions can lead to anemia in elderly persons. Moreover, the anemia may be multifactorial. The most common causes are iron deficiency (with or without blood loss), chronic disease/inflammation, and chronic kidney disease. [11] Other etiologies of anemia in the elderly include the following:
See the table below. Table 1. Prevalence of Various Etiologies of Anemia in Elderly Persons [23] (Open Table in a new window)
Up to 35-40% of anemia in older adults is “unexplained”. [23] In some of these cases, however, additional studies, including a bone marrow biopsy and next-generation sequencing, may identify the anemia as part of one of the following potential pre-MDS conditions [11] :
Nutrient deficienciesIron deficiency anemia represents 12-32.4% of cases of anemia among the elderly. [23] The RBCs serve as the largest storage compartment of iron in the body, and RBC loss often leads to iron deficiency. Identifying iron deficiency anemia in elderly persons is essential, as the condition can be corrected. More importantly, iron deficiency, particularly in elderly persons, often points to an underlying gastrointestinal pathology, including malignancy. [24] Folic acid, vitamin B12, zinc, and copper are essential macronutrients that directly affect hematopoiesis. To the extent that such reversible micronutrient deficiencies suggest other conditions (eg, pernicious anemia or hemolysis), they remain important to identify. Low vitamin B12 levels in elderly persons is common. [25] Folate deficiency is considered uncommon, in part because of mandatory fortification of grain products in the US and many other countries, but may occur at higher rates in certain populations. [26] Copper deficiency appears to be becoming more common. [27] Copper deficiency can cause not only anemia (typically macrocytic) but also other cytopenias, such as neutropenia and thrombocytopenia. [28] Malnutrition, malabsorption, small bowel surgeries requiring total parenteral nutrition or jejunal feeding, and bariatric surgery increase the risk of copper deficiency in the elderly. Zinc deficiency can be acquired or inherited. Acquired deficiency can result from decreased intake, impaired absorption, increased metabolic demand, or excessive loss. [29] In developing countries, acquired zinc deficiency is common and is attributable to malnutrition and high dietary phytate; in developed countries it is associated with aging and many chronic illnesses. Anemia of chronic disease and inflammationAnemia of chronic disease appears to be primarily related to inflammation, thus leading to the term anemia of chronic inflammation (ACI). ACI is a hypoproliferative anemia characterized by low serum iron without evidence of low iron stores. Inflammatory markers implicated in ACI include interleukin-6 (IL-6), interleukin-1 beta (IL-1β), Stat3, C/EBP alpha, and p53. [30] Conditions associated with ACI include cancer, chronic infection, and autoimmune diseases. [31] Other chronic diseases (eg, osteoarthritis, hypertension) often contribute indirectly to anemia. Use of nonsteroidal anti-inflammatory drugs for treatment of osteoarthritis may lead to gastrointestinal bleeding and iron deficiency, whereas hypertension may contribute to anemia by causing chronic kidney disease (CKD). Emerging evidence suggests that conditions such as CKD, diabetes mellitus, obesity, liver disease, heart failure, and pulmonary hypertension can be classified as inflammatory conditions. Inflammation inhibits erythropoiesis through a variety of mechanisms. The discovery of hepcidin has considerably clarified the pathophysiology of ACI. Hepcidin, synthesized by the liver, is a 25–amino acid peptide that serves as a primary regulator of iron homeostasis. Inflammation, particularly with IL-6, increases hepcidin expression. Hepcidin directly inhibits ferroportin, a protein that transports iron out of cells that store it. [32] This leads to reduced enteral iron resorption and trapping of iron in reticuloendothelial cells, resulting in functional iron deficiency. [33] ACI and the disordered iron homeostasis that is typically found with it is explained by increased hepcidin expression. [34, 35] Impaired erythropoietin (EPO) production and activity and EPO receptor responsiveness have also been observed. Kidney insufficiencyVarious hematopoietic growth factors support stem cell proliferation, differentiation, and survival. EPO, a glycoprotein that is a hematopoietic growth factor, serves as a primary regulator of RBC production. Synthesis and regulation of EPO occurs primarily in the kidney, with a smaller contribution by liver hepatocytes. [36, 37, 38, 39] Reduced tissue oxygenation (rather than diminished RBC production), typically from anemia or hypoxia, potently stimulates a logarithmic enhancement of EPO synthesis. [40] CKD is an important cause of anemia in elderly persons, especially considering that kidney function declines with aging. [41] In one study of older residents in a skilled nursing facility, 43% had CKD (defined as a creatinine clearance of less than 60 mL/min), and the residents with CKD were more likely to have anemia. [42] Reduced renal EPO production is the primary factor leading to anemia in CKD. The precise degree of kidney dysfunction sufficient to cause anemia remains controversial. Serum EPO levels have been shown to be low at a creatinine clearance of less than 40 mL/min. However, mild anemia in adults may be detected at a creatinine clearance of 40-60 mL/min. [43, 44, 45] The InCHIANTI study, which was performed among community-dwelling elderly persons, suggested that anemia and low EPO levels are independent of age and other factors at a creatinine clearance of less than 30 mL/min. [46] EndocrinopathiesEndocrine dysfunctions that result in anemia include the following:
Relative EPO deficiency In the prototypical model of complete kidney failure, inadequate endogenous EPO secretion rather than a primary marrow problem leads to anemia. [47] Even in kidney disorders without overt glomerular filtration abnormalities, endocrine function as measured by the endogenous EPO response to anemia may be impaired. For example, children with nephritic syndrome, before significant renal clearance impairment, have a blunted endogenous EPO response to anemia. [48] A decline in kidney function may be a feature of aging [49] that is accentuated by hypertension and diabetes. [50] Thus, a relative EPO deficiency, potentially from early and undiagnosed kidney damage, likely contributes to unexplained anemia. [46, 51] Thyroid disease Anemia has been recognized as a complication of thyroid dysfunction. [52] Hypothyroidism and hyperthyroidism may be associated with pernicious anemia and both conditions may also lead to a correctable anemia, but most patients with thyroid abnormalities are not anemic. [53] Hypothyroidism reduces RBC mass and may lead to a normocytic anemia. [54] Occasionally, hypothyroidism may lead to macrocytosis without anemia. [55] The degree of thyroid dysfunction leading to anemia remains unknown. Generally, the more severe the thyroid dysfunction, the more likely anemia will occur. Kim et al found that a low-normal level of serum free T4 was associated with a lower serum Hb level and a higher risk of anemia in euthyroid adults, especially in younger participants. [54] A therapeutic trial correcting the thyroid abnormalities may be necessary to definitively determine their role in causing lower Hb concentration. Low testosterone A large epidemiologic study showed that men with lower testosterone levels were more likely to have anemia. [56] The general Hb difference between men and women relates in large part to the erythropoietic effects of testosterone, which can be illustrated by the fact that after orchiectomy [57] or androgen deprivation therapy for prostate cancer, [58] Hb falls by 1.2 to 1.5 g/dL on average. Testosterone levels decline with aging in men. [59] The greater rate of Hb decline in men than in women with advancing age raises the suspicion that falling testosterone may cause the “unexplained" anemia in this population. Further, testosterone replacement raises Hb in older men. [60] Whether testosterone replacement improves quality of life is yet to be systematically studied. [61] Primary hematologic disordersA variety of primary hematologic disorders have anemia as a manifestation. Thrombotic thrombocytopenic purpura (TTP), although rare, should be considered in every patient with anemia, as this a medical emergency requiring prompt intervention. Often (but not always), patients with TTP will have other cardinal features of the disorder, including thrombocytopenia, altered mental status, and kidney insufficiency. Patients with myeloproliferative diseases often have an elevated white blood cell (WBC) count. However, elderly patients with acute leukemia can have a more smoldering disease course than younger patients. These patients may present with a low, high, or even normal WBC count, although in most individuals the WBC differential is abnormal. This fact emphasizes the importance of performing a manual differential in all patients with an abnormal complete blood cell count (CBC). [62] Chronic lymphocytic leukemia (CLL) is common in elderly persons. Although most patients will have either an elevated WBC count or lymphadenopathy at presentation, some patients will present with autoimmune hemolytic anemia. [63] Plasma cell disorders should always be considered, particularly in patients with elevated globulin levels. Patients with aplastic anemia may or may not have a low WBC and/or platelet count. However, some patients with myelofibrosis will have anemia as the prominent abnormality. Myelodysplastic syndromes represent a heterogeneous group of disorders characterized by clonal hematopoiesis and peripheral blood cytopenias. They are more common in older adults and initially may present as an isolated anemia. In the elderly, anemia in conjunction with macrocytosis, thrombocytopenia, or neutropenia in the absence of another cause raises the suspicion of myelodysplastic syndrome. [64] When evaluating mean corpuscular volume (MCV), the clinician must be cognizant that recent RBC transfusions will alter the values. Thus, determining hematology values before a transfusion is critical. Finally, anemia can be a sign of bone marrow infiltration from lymphoma and leukemia or metastatic solid tumors. Not uncommonly, the patient will not have palpable lymphadenopathy, but computed tomography (CT) scans could reveal extensive internal lymphadenopathy. In these patients, measurement of a lactate dehydrogenase (LDH) level is essential. PrognosisAlthough anemia in elderly population is a prevalent condition, it is underrecognized and undertreated. [65] Multiple epidemiologic studies show an association between anemia, or even mildly low hemoglobin (Hb) above the WHO threshold for anemia (ie, < 14 g/dL), and adverse health and economic outcomes. [66, 67] Anemia impairs quality of life and increases frailty; an increase of 1 g/dL in Hb is associated with a 14% reduction in risk of being frail (odds ratio [OR] 0.86, 95% CI 0.79–0.94). [68, 69] A Dutch study of 562 elderly persons aged 85 years, with a 5-year annual follow-up, found that the 26.7% of study participants who had anemia at baseline had more disability in instrumental activities of daily living than did the other participants. [70] Fall and fracture risk rises as Hb level decreases, but importantly, even individuals with the mildest anemia (Hb 12–12.9 g/ dl) are at significantly greater risk of the following:
Anemia also adversely affects the outcome of various procedures in elderly, from spinal procedures to carotid endarterectomy and knee arthroscopy. [82, 83, 84, 85] Overall, anemia in the elderly is associated with increased mortality and hospitalization. [79, 86, 87, 88] Older patients with anemia have longer hospital stays—from 4 to 10 days longer, depending on severity of anemia. [89, 90, 91] Therefore, medical costs are more than twice as high as patients without anemia matched for age, sex, comorbidities, and insurance status. [92] Anemia also increases the medical cost associated with various comorbidities. [93, 94, 95] Additionally, the increased risk of injurious falls and fractures contributes to increased cost of care for this patient population. [96, 97, 98] History and Physical ExaminationMedical historyObtaining a detailed medical history can be extremely valuable in the diagnosis of anemia and its cause. Inquiries should include the following:
Diseases that frequently cause anemia should be noted, including the following:
Conditions that are associated with specific types of anemia should be clearly identified. Lymphoproliferative and autoimmune disease may cause autoimmune hemolytic anemia. Previous chemotherapy or radiotherapy raises the possibility of therapy-related myelodysplastic syndrome. Alcohol overuse may go unrecognized in the elderly and can lead to deficiencies of vitamin B12 and folate, as well as marrow hypoproliferation and gastrointestinal bleeding. Family history and racial backgroundFamily history can be useful for suggesting a coexistent thalassemia trait, hemoglobinopathies, and other inherited anemias. Racial ancestry should be considered, with recognition that Hb concentrations may be approximately 0.8 g/dL lower in Blacks than in Whites. Signs and symptomsMost symptoms of anemia are nonspecific (eg, fatigue, shortness of breath, tinnitus). Nevertheless, a detailed history often identifies the presence of anemia-related symptoms. Obvious blood loss should be directly inquired about (eg, melena, hematuria, hemoptysis, hematemesis, abnormal vaginal bleeding). A temporal relation between falling Hb and symptom exacerbation is very useful. Symptoms relate to the rapidity of the development of anemia, the depth of the Hb fall, and concomitant medical conditions. Inquiries about specific tasks, such as walking upstairs, can provide useful objective information. Fatigability was found to be a predictor of subclinical and clinical anemia in a longitudinal analysis of 905 well-functioning men and women aged 60-89 years who were followed for 1-5 years from the Baltimore Longitudinal Study of Aging conducted at the National Institute of Aging. [99] Special attention should be paid to elements that indicate a cause for the anemia (eg, presence or symptoms of cancer, gastrointestinal blood loss, infection, arthritis) and symptoms related to anemia. Patients may mistakenly attribute decreased energy to aging or medications. General signs and symptoms include the following:
Signs and symptoms of iron deficiency may include the following:
Signs and symptoms of vitamin B12 deficiency may include the following:
Signs and symptoms of hemolysis may include the following:
Physical examinationThe physical examination may uncover an anemia etiology, signs related to the anemia, or both. Thus, the examination must be comprehensive. Special attention should be paid to the following:
An abdominal ultrasonogram can be helpful if the patient's body habitus makes examination for hepatosplenomegaly difficult. Differential DiagnosisThe differential diagnosis of anemia in the elderly should include the following:
WorkupInitiate an evaluation under the following conditions:
Numerous algorithms have been proposed for the evaluation of anemia and anemia in elderly persons. They are often based on kinetic measures made by first assessing the reticulocyte count, RBC size (using mean corpuscular volume [MCV]), or peripheral smear (see the image below). Such an investigation must account for the unique epidemiology in this population. The following commonalities guide the evaluation:
Potential causes for microcytic anemia include the following:
Potential causes for normocytic anemia include the following:
Potential causes for macrocytic anemia include the following:
Should the anemia's etiology not be apparent from the initial history and physical examination, a comprehensive evaluation is useful. Recommended studies include the following:
In about two thirds of elderly persons with anemia, this evaluation will lead to a presumed etiology for the anemia. A reiterative process is essential: Once a deficiency is identified, blood counts should be reevaluated after identifying the problem, correcting the deficiency, or both. Additional tests often performed include the following:
Possible hemolysis may be evaluated with the following:
Androgen insufficiency may be evaluated with testosterone and sex hormone–binding globulin (SHBG) levels. A peripheral blood smear is invaluable, especially when determining if a primary bone marrow process accounts for macrocytic anemia. This generally requires a hematology or pathology review of the peripheral smear, rather than a technician-reported analysis. If no cause is identified, a hematology referral and/or bone marrow examination should be considered. The more severe the anemia and the more severe the macrocytosis, the more likely a specific cause will be identified. Diagnostic pitfallsEtiologies of anemia in the elderly that can pose diagnostic challenges include the following:
Iron deficiency Serum iron is not an adequate test to exclude iron deficiency. Nor does a normocytic anemia exclude iron deficiency, as iron deficiency can coincide with deficiencies of other nutritients, such as vitamin B12, folate, zinc, or copper, which may mask the microcytosis. Because iron deficiency is correctable and often reflects gastrointestinal pathology, including malignancy, every elderly anemic adult requires a thorough evaluation to determine the underlying cause of iron deficiency, including a gastroenterology consult to perform endoscopy, colonoscopy, or a capsule study. Although in some conditions (eg, thalassemia [100] ) serum ferritin may underestimate body iron stores, serum ferritin remains the most useful test for diagnosing iron deficiency anemia. Low serum ferritin (eg, < 30 ng/mL) is highly specific for iron deficiency anemia. [24, 26] On the other hand, as an acute--phase reactant, ferritin can be elevated in inflammation, complicating the diagnosis of iron deficiency anemia or iron overload in the presence of inflammation. An elevated ferritin therefore requires confirmation of iron overload by liver magnetic resonance imaging (MRI) or liver biopsy. Intermediate ferritin values of 18 to 44 ng/mL are highly suggestive of iron deficiency in the elderly. Thus, using a higher threshold for serum ferritin in the elderly to account for aging-related inflammation and/or comorbid conditions enables reasonable sensitivity and specificity for iron deficiency anemia. [24, 30] The use of CBC indices such as red cell distribution width (RDW), MCV, or mean corpuscular hemoglobin (MCH) and reticulocyte count and peripheral smear may be additional helpful tools. A major pitfall is misinterpreting the MCV. Although microcytosis occurs in iron deficiency anemia, it is a late finding and typically occurs only after chronic iron deficiency leads to an Hb value of less than 10 g/dL. The impact of other factors may abrogate the standard changes in cell size. For example, alcohol use or liver disease leads to increased RBC size. That said, microcytic anemia in an older adult in the absence of an obvious chronic inflammatory disease is highly suspicious for iron deficiency (eg, if an initial MCV of 85 fL and an Hb of 12 g/dL changes to an MCV of 75 fL and an Hb of 9.5 g/dL). Vitamin B12 deficiency Currently there is no universally accepted definition of vitamin B12 deficiency. The WHO has suggested using a value of < 200 pg/mL. However, some consider that too low and instead suggest 400 pg/mL as a cutoff value. Homocysteine levels cannot be used to distinguish vitamin B12 deficiency from folate deficiency, as levels are elevated in both conditions. For equivocal levels of vitamin B12 (eg, a level between 200 and 400 pg/mL), checking for methylmalonic acid (MMA) will be helpful, as the combination of increased homocysteine and MMA levels with a slightly decreased vitamin B12 level is consistent with early or mild vitamin B12 deficiency, rather than folate deficiency. However some experts believe elevated MMA may also be observed at the later stage of vitamin B12 deficiency. MMA is also elevated in the setting of kidney dysfunction. [25] In dialysis patients, a level higher than 500-700 mcmol/L might be more indicative of vitamin B12 deficiency, and empiric supplementation with cobalamin that results in improvement in anemia can be confirmatory. Anemias due to vitamin B12, folate, zinc, or copper deficiency are typically macrocytic but may not be, as these cases may also be associated with iron deficiency. However, the presence of an MCV greater than 115 fL is highly suspicious for the megaloblastoid anemia that is characteristic of those deficiencies. Re-evaluating the anemia after replacing the micronutrients is essential, as persistent anemia indicates that the low nutrient level was only partially causative and other etiologies need to be investigated. However, performing bone marrow biopsy before correcting these micronutrient deficiencies can result in misdiagnosis, as the findings may be mistaken for myelodysplastic syndrome. [101, 102] Once vitamin B12 deficiency has been identified, an etiology for it (eg, pernicious anemia, malabsorption) should be investigated and vitamin B12 replenished. Chronic inflammation No established diagnostic criteria for anemia of chronic inflammation exist. Hepcidin testing has not been validated as a diagnostic test for anemia of chronic inflammation, and in any case is not clinically available. In NHANES III, anemia of inflammation was defined as a low serum iron level (eg, < 60 μg/dL) without evidence of low iron stores. [103] Other features of anemia of inflammation include inappropriately low levels of EPO and elevated inflammatory markers such as CRP or erythrocyte sedimentation rate (ESR). [104] An alternative method is to consider anemia of chronic inflammation to exist when the patient has an inflammatory comorbid condition. Evaluation of “unexplained” anemiaEven after an extensive evaluation, approximately one third of older adults with anemia do not have an obviously discernible cause of anemia. The anemia in these patients is generally mild (Hb from 9-12 g/dL), normocytic, and hypoproliferative (low reticulocyte count). Potential explanations for the anemia have included low testosterone, occult inflammation or infection, reduced hematopoietic reserve with advancing age, inappropriately low serum EPO level, and myelodysplastic syndromes (MDS). The diagnosis of unexplained anemia assumes the clinician has excluded more common known causes. Macrocytosis, thrombocytopenia, neutropenia, splenomegaly, or unexplained constitutional symptoms of fever, chills, early satiety, bone pain, or weight loss should prompt consideration of a bone marrow examination. The threshold to pursue a bone marrow examination to exclude MDS remains unknown. However, the authors advocate considering referral for further evaluation and bone marrow examination in all patients who otherwise have unexplained anemia. A bone marrow aspirate and biopsy are used when a primary marrow disease (eg, MDS, aplastic anemia) is suspected. Occasionally, the marrow is used to investigate possible marrow involvement of non-marrow diseases (eg, infection, lymphoma), or nonmalignant marrow processes (eg, hemophagocytic syndrome, Gaucher disease). MDS should be diagnosed based on a bone marrow examination and not only on the peripheral smear. Bone marrow examination generally has fewer complications and is less invasive than is generally appreciated. The glomerular filtration rate, calculated with serum cystatin C, may be a marker to uncover undiagnosed kidney dysfunction. However, this needs to be interpreted in collaboration with a nephrologist. [105] TreatmentManagement of anemia in the elderly usually requires a multidisciplinary approach. The critical element is to identify and treat reversible etiologies for the anemia (eg, nutritional deficiency, infection) and address comorbid conditions. Intervention to correct the anemia itself remains experimental. While folate deficiency has become vanishingly rare due to folate fortification of flour and other grain products, particular attention needs to be paid in certain settings, such as poor diet combined with alcoholism, or compliance failure with folate and vitamin B12 supplementation in a dialysis patient. Similarly, vitamin B12 deficiency may be infrequently diagnosed, but a diagnostic trial of vitamin B12 therapy may be necessary if the constellation of symptoms and signs are consistent with this etiology. Unless a deficiency has been identified as a cause of anemia in an elderly person, no specific dietary intervention will be fruitful, except in special circumstances such as hemolytic anemias, blood donors, or in dialysis patients receiving EPO. In those cases, ample amounts of vitamin B12, folate, and iron are required to empower effective hematopoiesis. For unexplained anemia, no treatment has been well studied. Medications include erythropoiesis-stimulating agents (ESAs), oral mineral supplements (used in mineral deficiencies), and colony-stimulating factors (used to enhance erythropoiesis when endogenous EPO levels are low). In elderly patients who may have active cardiac symptoms, activity restrictions may be considered until an appropriate cardiac evaluation has been performed. RBC transfusionFor severe symptomatic anemia, RBC transfusion is warranted. Transfusions entail numerous, and often underappreciated, risks of infection, volume overload, transfusion reactions, and costs. Two units of RBCs may represent a considerable volume for elderly patients who have preexisting cardiac dysfunction. As a general rule, geriatric patients should be transfused more slowly than younger adults, and diuretic treatment may be considered to avoid transfusion-associated circulatory overload (TACO). If one unit adequately improves symptoms and clinical status, no further units should be given, regardless of initial Hb values. Repeated transfusions can result in iron overload and clinical manifestations of hemochromatosis as well as RBCl alloimmunization in some conditions. Recommendations for Hb thresholds vary, depending on severity of anemia, patient comorbidities, and cause. The need for transfusion is also related to the rapidity of the Hb drop, as patients will be more symptomatic from a more acute drop in Hb. Prospective randomized controlled trials are required to definitively clarify the role of transfusions in older individuals with anemia and different types of cardiovascular disease. Erythropoiesis-stimulating agentsESAs approved in the United States include epoetin-alfa (Procrit, Epogen), and biosimilar epoietin alfa-epbx (Retacrit), darbepoetin-alfa (Aranesp), and methoxy polyethylene glycol/epoetin beta (Mircera). The primary indication for use of these agents is anemia due to chronic kidney disease (CKD). Although ESA therapy has found widespread use in the treatment of anemia due to CKD (based on a 2006 Kidney Disease Outcomes Quality Initiative [KDOQI] consensus statement), [106] the risks and benefits in patients with CKD, particularly older adults not on dialysis and not receiving RBC transfusions, remain underexplored. Iron supplementation is frequently needed to prevent iron-restricted erythropoiesis in elderly patients on ESA treatment. One study showed that ESAs can treat anemia of unknown etiology, and responses may be similar to those in CKD. No statistically significant increase in cardiovascular events in those receiving ESAs was detected. [107] Considering the possible adverse effects of ESA, which include thrombosis and hypertension and the potential for progression of certain cancers, caution must be exercised in populations at increased danger for such events. ESAs should be prescribed only be physicians experienced in the use and monitoring of such treatment.
Author Coauthor(s) Zahra Pakbaz, MD Health Science Associate Clinical Professor, Division of Hematology/Oncology, Department of Medicine, UCI Health, University of California, Irvine, School of Medicine Zahra Pakbaz, MD is a member of the following medical societies: American Society of Hematology, Medical Oncology Association of Southern California, Inc Disclosure: Nothing to disclose. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape. Ronald A Sacher, MD, FRCPC, DTM&H Professor Emeritus of Internal Medicine and Hematology/Oncology, Emeritus Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center Ronald A Sacher, MD, FRCPC, DTM&H is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Clinical and Climatological Association, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society of Blood Transfusion, International Society on Thrombosis and Haemostasis, Royal College of Physicians and Surgeons of Canada Disclosure: Nothing to disclose. Chief Editor Emmanuel C Besa, MD Professor Emeritus, Department of Medicine, Division of Hematologic Malignancies and Hematopoietic Stem Cell Transplantation, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American Society of Clinical Oncology, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Hematology, New York Academy of Sciences Disclosure: Nothing to disclose. Additional Contributors Andrew S Artz, MD, MS Clinical Professor, Division of Leukemia, Department of Hematology and Hematopoietic Cell Transplantation, Director, Program for Aging and Blood Cancers, Deputy Director, Center for Cancer and Aging, City of Hope Andrew S Artz, MD, MS is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Blood and Marrow Transplantation, American Society of Clinical Oncology, American Society of Hematology Disclosure: Nothing to disclose. Acknowledgements William B Ershler, MD Deputy Clinical Director and Senior Investigator, Clinical Research Branch National Institute on Aging, National Institute of Health; Director, Institute for Advanced Studies in Aging and Geriatric Medicine; Clinical Professor of Medicine, George Washington University College of Medicine William B Ershler, MD is a member of the following medical societies: American Association for Cancer Research, American Association for the Advancement of Science, American Federation for Aging Research, American Federation for Clinical Research, American Geriatrics Society, and Gerontological Society of America Disclosure: Nothing to disclose. How does aging affect the hematologic system?Age-related hematologic changes are marked by a decline in marrow cellularity, increased risk of myeloproliferative disorders and anemia, and a decline in adaptive immunity. The exact mechanisms that produce these changes remain undefined.
Which of the following is the most common hematologic condition affecting elderly patients?Iron deficiency anemia and the anemia of chronic disease are the most common types of anemia in the elderly.
Which age related changes occur in the hematologic system quizlet?Changes in the hematologic system that occur with aging include a decrease in the functioning of lymphocytes, including cellular immunity. Changes with aging include an increase in platelet adhesiveness, and a slight decrease in the number of stem cells in the bone marrow.
What causes low blood count in elderly?Anemia should not be accepted as an inevitable consequence of aging. A cause is found in approximately 80 percent of elderly patients. The most common causes of anemia in the elderly are chronic disease and iron deficiency.
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Which effect of aging would likely impact the hematologic function of older patients
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