Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Anemia

  • Author: Joseph E Maakaron, MD; Chief Editor: Emmanuel C Besa, MD  more...
 
Updated: Jul 22, 2016
 

Practice Essentials

Anemia is strictly defined as a decrease in red blood cell (RBC) mass. The function of the RBC is to deliver oxygen from the lungs to the tissues and carbon dioxide from the tissues to the lungs. This is accomplished by using hemoglobin (Hb), a tetramer protein composed of heme and globin. In anemia, a decrease in the number of RBCs transporting oxygen and carbon dioxide impairs the body’s ability for gas exchange.[1] The decrease may result from blood loss, increased destruction of RBCs (hemolysis), or decreased production of RBCs.

Anemia, like a fever, is a sign that requires investigation to determine the underlying etiology. Often, practicing physicians overlook mild anemia. This is similar to failing to seek the etiology of a fever. The purpose of this article is to provide a method of determining the etiology of an anemia. (See the image below.) (See Etiology, Presentation, and Workup.)

Microcytic anemia. Microcytic anemia.

Methods for measuring RBC mass are time consuming and expensive and usually require transfusion of radiolabeled erythrocytes. Thus, in practice, anemia is usually discovered and quantified by measurement of the RBC count, Hb concentration, and hematocrit (Hct). These values should be interpreted cautiously, because they are concentrations affected by changes in plasma volume. For example, dehydration elevates these values, and increased plasma volume in pregnancy can diminish them without affecting the RBC mass. (See Workup.)

Complications

The most serious complications of severe anemia arise from tissue hypoxia. Shock, hypotension, or coronary and pulmonary insufficiency can occur. This is more common in older individuals with underlying pulmonary and cardiovascular disease. (See Pathophysiology.)

Next

Pathophysiology

Erythrocyte life cycle

Erythroid precursors develop in bone marrow at rates usually determined by the requirement for sufficient circulating Hb to oxygenate tissues adequately. Erythroid precursors differentiate sequentially from stem cells to progenitor cells to erythroblasts to normoblasts in a process requiring growth factors and cytokines.[2] This process of differentiation requires several days. Normally, erythroid precursors are released into circulation as reticulocytes.

Reticulocytes are so called because of the reticular meshwork of rRNA they harbor. They remain in the circulation for approximately 1 day before they mature into erythrocytes, after the digestion of RNA by reticuloendothelial cells. The mature erythrocyte remains in circulation for about 120 days before being engulfed and destroyed by phagocytic cells of the reticuloendothelial system.

Erythrocytes are highly deformable and increase their diameter from 7 µm to 13 µm when they traverse capillaries with a 3-µm diameter. They possess a negative charge on their surface, which may serve to discourage phagocytosis. Because erythrocytes have no nucleus, they lack a Krebs cycle and rely on glycolysis via the Embden-Meyerhof and pentose pathways for energy. Many enzymes required by the aerobic and anaerobic glycolytic pathways decrease within the cell as it ages. In addition, the aging cell has a decrease in potassium concentration and an increase in sodium concentration. These factors contribute to the demise of the erythrocyte at the end of its 120-day lifespan.

Response to anemia

The physiologic response to anemia varies according to acuity and the type of insult. Gradual onset may allow for compensatory mechanisms to take place. With anemia due to acute blood loss, a reduction in oxygen-carrying capacity occurs along with a decrease in intravascular volume, with resultant hypoxia and hypovolemia. Hypovolemia leads to hypotension, which is detected by stretch receptors in the carotid bulb, aortic arch, heart, and lungs. These receptors transmit impulses along afferent fibers of the vagus and glossopharyngeal nerves to the medulla oblongata, cerebral cortex, and pituitary gland.

In the medulla, sympathetic outflow is enhanced, while parasympathetic activity is diminished. Increased sympathetic outflow leads to norepinephrine release from sympathetic nerve endings and discharge of epinephrine and norepinephrine from the adrenal medulla. Sympathetic connection to the hypothalamic nuclei increases antidiuretic hormone (ADH) secretion from the pituitary gland.[3] ADH increases free water reabsorption in the distal collecting tubules. In response to decreased renal perfusion, juxtaglomerular cells in the afferent arterioles release renin into the renal circulation, leading to increased angiotensin I, which is converted by angiotensin-converting enzyme (ACE) to angiotensin II.

Angiotensin II has a potent pressor effect on arteriolar smooth muscle. Angiotensin II also stimulates the zona glomerulosa of the adrenal cortex to produce aldosterone. Aldosterone increases sodium reabsorption from the proximal tubules of the kidney, thus increasing intravascular volume. The primary effect of the sympathetic nervous system is to maintain perfusion to the tissues by increasing systemic vascular resistance (SVR). The augmented venous tone increases the preload and, hence, the end-diastolic volume, which increases stroke volume. Therefore, stroke volume, heart rate, and SVR all are maximized by the sympathetic nervous system. Oxygen delivery is enhanced by the increased blood flow.

In states of hypovolemic hypoxia, the increased venous tone due to sympathetic discharge is thought to dominate the vasodilator effects of hypoxia. Counterregulatory hormones (eg, glucagon, epinephrine, cortisol) are thought to shift intracellular water to the intravascular space, perhaps because of the resultant hyperglycemia. This contribution to the intravascular volume has not been clearly elucidated.

Previous
Next

Etiology

Basically, only three causes of anemia exist: blood loss, increased destruction of RBCs (hemolysis), and decreased production of RBCs. Each of these causes includes a number of disorders that require specific and appropriate therapy. Genetic etiologies include the following:

  • Hemoglobinopathies
  • Thalassemias
  • Enzyme abnormalities of the glycolytic pathways
  • Defects of the RBC cytoskeleton
  • Congenital dyserythropoietic anemia
  • Rh null disease
  • Hereditary xerocytosis
  • Abetalipoproteinemia
  • Fanconi anemia

Nutritional etiologies include the following:

  • Iron deficiency
  • Vitamin B-12 deficiency
  • Folate deficiency
  • Starvation and generalized malnutrition

Physical etiologies include the following:

  • Trauma
  • Burns
  • Frostbite
  • Prosthetic valves and surfaces

Chronic disease and malignant etiologies include the following:

  • Renal disease
  • Hepatic disease
  • Chronic infections
  • Neoplasia
  • Collagen vascular diseases

Infectious etiologies include the following:

  • Viral - Hepatitis, infectious mononucleosis, cytomegalovirus
  • Bacterial - Clostridia, gram-negative sepsis
  • Protozoal - Malaria, leishmaniasis, toxoplasmosis

Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome may be a cause of anemia. Hereditary spherocytosis either may present as a severe hemolytic anemia or may be asymptomatic with compensated hemolysis. Similarly, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency may manifest as chronic hemolytic anemia or exist without anemia until the patient receives an oxidant medication. Immunologic etiologies for anemia may include antibody-mediated abnormalities. In the emergency department (ED), acute hemorrhage is by far the most common etiology for anemia.

Drugs or chemicals commonly cause the aplastic and hypoplastic group of disorders. Certain types of these causative agents are dose related and others are idiosyncratic. Any human exposed to a sufficient dose of inorganic arsenic, benzene, radiation, or the usual chemotherapeutic agents used for treatment of neoplastic diseases develops bone marrow depression with pancytopenia.

Conversely, among the idiosyncratic agents, only an occasional human exposed to these drugs has an untoward reaction resulting in suppression of one or more of the formed elements of bone marrow (1:100 to 1:millions). With certain types of these drugs, pancytopenia is more common, whereas with others, suppression of one cell line is usually observed. Thus, chloramphenicol may produce pancytopenia, whereas granulocytopenia is more frequently observed with toxicity to sulfonamides or antithyroid drugs.

Current evidence suggests that susceptibility to idiosyncratic reactions involves certain genetic polymorphisms involving cellular detoxifying enzymes. As a result, exogenous toxins that would normally be converted to nontoxic compounds are instead metabolized into reactive compounds that  modify cellular proteins, which can be recognized by the immune system and trigger autoimmunity.[4]

The idiosyncratic causes of bone marrow suppression include multiple drugs in each of the categories that can be prefixed with anti- (eg, antibiotics, antimicrobials, anticonvulsants, antihistamines). The other idiosyncratic causes of known etiology are viral hepatitis and paroxysmal nocturnal hemoglobinuria. In approximately one half of patients presenting with aplastic anemia, a definite etiology cannot be established, and the anemia must be regarded as idiopathic.

Rare causes of anemia due to a hypoplastic bone marrow include familial disorders and the acquired pure red cell aplasias. The latter are characterized by a virtual absence of erythroid precursors in the bone marrow, with normal numbers of granulocytic precursors and megakaryocytes. Rare causes of diminished erythrocyte production with hyperplastic bone marrow include hereditary orotic aminoaciduria and erythremic myelosis.

A study of 2688 patients undergoing cardiac surgery in the United Kingdom from 2008-2009 found that 1463 (54.4%) met the World Health Organization definition for anemia. This prevalence was much greater than previously reported, although the reason for this association is unclear.[5]

Previous
Next

Epidemiology

Occurrence in the United States

The prevalence of anemia in population studies of healthy, nonpregnant people depends on the Hb concentration chosen for the lower limit of normal values. The World Health Organization (WHO) chose 12.5 g/dL for both adult males and females. In the United States, limits of 13.5 g/dL for men and 12.5 g/dL for women are probably more realistic. Using these values, approximately 4% of men and 8% of women have values lower than those cited. A significantly greater prevalence is observed in patient populations. Less information is available regarding studies using RBC or Hct.

International occurrence

The prevalence of anemia in Canada and northern Europe is believed to be similar to that in the United States. In underprivileged countries, limited studies of purportedly healthy subjects show the prevalence of anemia to be 2-5 times greater than that in the United States. Although geographic diseases, such as sickle cell anemia, thalassemia, malaria, hookworm, and chronic infections, are responsible for a portion of the increase, nutritional factors with iron deficiency and, to a lesser extent, folic acid deficiency play major roles in the increased prevalence of anemia. Populations with little meat in the diet have a high incidence of iron deficiency anemia, because heme iron is better absorbed from food than inorganic iron.

Sickle cell disease is common in regions of Africa, India, Saudi Arabia, and the Mediterranean basin. The thalassemias are the most common genetic blood diseases and are found in Southeast Asia and in areas where sickle cell disease is common.

Race-related demographics

Certain races and ethnic groups have an increased prevalence of genetic factors associated with certain anemias. Diseases such as the hemoglobinopathies, thalassemia, and G-6-PD deficiency have different morbidity and mortality in different populations due to differences in the genetic abnormality producing the disorder. For example, G-6-PD deficiency and thalassemia have less morbidity in African Americans than in Sicilians because of differences in the genetic fault. Conversely, sickle cell anemia has greater morbidity and mortality in African Americans than in Saudi Arabians.

Race is a factor in nutritional anemias and anemia associated with untreated chronic illnesses to the extent that socioeconomic advantages are distributed along racial lines in a given area;[6] socioeconomic advantages that positively affect diet and the availability of health care lead to a decreased prevalence of these types of anemia.[7, 8, 9] For instance, iron deficiency anemia is much more prevalent in the populations of developing nations, who tend to have little meat in their diets, than it is in populations of the United States and northern Europe.

Similarly, anemia of chronic disorders is commonplace in populations with a high incidence of chronic infectious disease (eg, malaria, tuberculosis, acquired immunodeficiency syndrome [AIDS]), and this is at least in part worsened by the socioeconomic status of these populations and their limited access to adequate health care.

Sex-related demographics

Overall, anemia is twice as prevalent in females as in males. This difference is significantly greater during the childbearing years due to pregnancies and menses.

Approximately 65% of body iron is incorporated into circulating Hb. One gram of Hb contains 3.46 mg of iron (1 mL of blood with an Hb concentration of 15 g/dL = 0.5 mg of iron). Each healthy pregnancy depletes the mother of approximately 500 mg of iron. While a man must absorb about 1 mg of iron to maintain equilibrium, a premenopausal woman must absorb an average of 2 mg daily. Further, because women eat less food than men, they must be more than twice as efficient as men in the absorption of iron to avoid iron deficiency.

Women have a markedly lower incidence of X-linked anemias, such as G-6-PD deficiency and sex-linked sideroblastic anemias, than men do. In addition, in the younger age groups, males have a higher incidence of acute anemia from traumatic causes.

Age-related demographics

Previously, severe, genetically acquired anemias (eg, sickle cell disease, thalassemia, Fanconi syndrome) were more commonly found in children because they did not survive to adulthood. However, with improvement in medical care and breakthroughs in transfusion and iron chelation therapy, in addition to fetal hemoglobin modifiers, the life expectancy of persons with these diseases has been significantly prolonged.[10]

Acute anemia has a bimodal frequency distribution, affecting mostly young adults and persons in their late fifties. Causes among young adults include trauma, menstrual and ectopic bleeding, and problems of acute hemolysis. During their childbearing years, women are more likely to become iron deficient.

In people aged 50-65 years, acute anemia is usually the result of acute blood loss in addition to a chronic anemic state. This is the case in uterine and GI bleeding.

Neoplasia increases in prevalence with each decade of life and can produce anemia from bleeding, from the invasion of bone marrow with tumor, or from the development of anemia associated with chronic disorders. The use of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and warfarin also increases with age and can produce GI bleeding.

Previous
Next

Prognosis

Usually, the prognosis depends on the underlying cause of the anemia. However, the severity of the anemia, its etiology, and the rapidity with which it develops can each play a significant role in the prognosis. Similarly, the age of the patient and the existence of other comorbid conditions influence outcome.

Sickle cell anemia

Patients who are homozygous (Hgb SS) have the worst prognosis, because they tend to have more frequent crises. Patients who are heterozygous (Hgb AS) have sickle cell traits, and they have crises only under extreme conditions.

Thalassemias

Patients who are homozygous for beta thalassemia (Cooley anemia or thalassemia major) have a worse prognosis than do patients with any of the other thalassemias (thalassemia intermedia and thalassemia minor). These few years have witnessed groundbreaking advancements in the treatment of thalassemias, especially with iron chelation therapies, allowing thalassemia patients to live well into adulthood.[10] Patients who are heterozygous for beta thalassemia have mild microcytic anemia that is not clinically significant.

Aplastic anemia

Chances of survival are poorer for patients with idiosyncratic aplasia caused by chloramphenicol and viral hepatitis and better when paroxysmal nocturnal hemoglobinuria or insecticide toxicity are the probable etiology. The prognosis for idiopathic aplasia lies between these 2 extremes, with an untreated mortality rate of approximately 60-70% within 2 years after diagnosis.

The 2-year fatality rate for severe aplastic anemia is 70% without bone marrow transplantation or a response to immunosuppressive therapy.

Hyperplasia

Among patients with a hyperplastic bone marrow and decreased production of RBCs, one group has an excellent prognosis, and the other is unresponsive, refractory to therapy, and has a relatively poor prognosis. The former includes patients with disorders of relative bone marrow failure due to nutritional deficiency, in whom identification of the etiology and treatment with vitamin B-12, folic acid, or iron leads to a correction of anemia once the appropriate etiology is established. Drugs acting as an antifolic antagonist or inhibitor of DNA synthesis can produce similar effects.

The second group includes patients with an idiopathic hyperplasia that may respond partially to pyridoxine therapy in pharmacologic doses but more frequently does not. These patients have ringed sideroblasts in the bone marrow, indicating an inappropriate use of iron in the mitochondria for heme synthesis.

Certain patients with marrow hyperplasia (see the image below) may have refractory anemia for years, but some of the group eventually develop acute myelogenous leukemia.

Bone marrow aspirate showing erythroid hyperplasia Bone marrow aspirate showing erythroid hyperplasia and many binucleated erythroid precursors.

Hemolytic-uremic syndrome

Hemolytic-uremic syndrome carries a significant morbidity and mortality if untreated. As many as 40% of those affected die, and as many as 80% develop renal insufficiency.

Previous
Next

Patient Education

Inform patients of the etiology of their anemia, the significance of their medical condition, and the therapeutic options available for treatment.

If no effective specific treatment of the underlying disease exists, educate patients who require periodic transfusions about the symptoms that herald the need for transfusion. Likewise, they should be aware of the potential complications of transfusion.

For patient education information, see Anemia.

Previous
 
 
Contributor Information and Disclosures
Author

Joseph E Maakaron, MD Research Fellow, Department of Internal Medicine, Division of Hematology/Oncology, American University of Beirut Medical Center, Lebanon

Disclosure: Nothing to disclose.

Coauthor(s)

Ali T Taher, MD, PhD, FRCP Professor of Medicine, Associate Chair of Research, Department of Internal Medicine, Division of Hematology/Oncology, Director of Research, NK Basile Cancer Center, American University of Beirut Medical Center, Lebanon

Disclosure: Nothing to disclose.

Marcel E Conrad, MD Distinguished Professor of Medicine (Retired), University of South Alabama College of Medicine

Marcel E Conrad, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Association of Blood Banks, American Chemical Society, American College of Physicians, American Physiological Society, American Society for Clinical Investigation, American Society of Hematology, Association of American Physicians, Association of Military Surgeons of the US, International Society of Hematology, Society for Experimental Biology and Medicine, SWOG

Disclosure: Partner received none from No financial interests for none.

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.

Acknowledgements

Jose A Perez Jr, MD, MBA, MSEd Consulting Staff, Department of Medicine, Methodist Hospital; Associate Professor of Clinical Medicine, Weill Cornell Medical College

Jose A Perez Jr, MD, MBA, MSEd is a member of the following medical societies: American College of Physician Executives, American College of Physicians, Society of General Internal Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Ronald A Sacher, MB, BCh, MD, FRCPC Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, MD, FRCPC 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, and Royal College of Physicians and Surgeons of Canada

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Veng-Pedersen P, Chapel S, Schmidt RL, Al-Huniti NH, Cook RT, Widness JA. An integrated pharmacodynamic analysis of erythropoietin, reticulocyte, and hemoglobin responses in acute anemia. Pharm Res. 2002 Nov. 19(11):1630-5. [Medline].

  2. Liang R, Ghaffari S. Advances in understanding the mechanisms of erythropoiesis in homeostasis and disease. Br J Haematol. 2016 Jul 21. [Medline].

  3. Adamson JW, Longo DL. Anemia and polycythemia. Harrison's Principles of Internal Medicine. 15th ed. New York, New York: McGraw-Hill; 2001. Vol 1.: 348-354.

  4. Babushok DV, Li Y, Roth JJ, Perdigones N, Cockroft JD, Biegel JA, et al. Common polymorphic deletion of glutathione S-transferase theta predisposes to acquired aplastic anemia: Independent cohort and meta-analysis of 609 patients. Am J Hematol. 2013 Oct. 88 (10):862-7. [Medline]. [Full Text].

  5. Hung M, Besser M, Sharples LD, Nair SK, Klein AA. The prevalence and association with transfusion, intensive care unit stay and mortality of pre-operative anaemia in a cohort of cardiac surgery patients. Anaesthesia. 2011 Sep. 66(9):812-8. [Medline].

  6. Servilla KS, Singh AK, Hunt WC, et al. Anemia management and association of race with mortality and hospitalization in a large not-for-profit dialysis organization. Am J Kidney Dis. 2009 Sep. 54(3):498-510. [Medline].

  7. Adebisi OY, Strayhorn G. Anemia in pregnancy and race in the United States: blacks at risk. Fam Med. 2005 Oct. 37(9):655-62. [Medline].

  8. Silva DG, Priore SE, Franceschini Sdo C. Risk factors for anemia in infants assisted by public health services: the importance of feeding practices and iron supplementation. J Pediatr (Rio J). 2007 Mar-Apr. 83(2):149-56. [Medline].

  9. Oliveira MA, Osorio MM, Raposo MC. Socioeconomic and dietary risk factors for anemia in children aged 6 to 59 months. J Pediatr (Rio J). 2007 Jan-Feb Epub 2007 Jan 12. 83(1):39-46. [Medline].

  10. Borgna-Pignatti C, Rugolotto S, De Stefano P, et al. Survival and complications in patients with thalassemia major treated with transfusion and deferoxamine. Haematologica. 2004 Oct. 89(10):1187-93. [Medline].

  11. Kuku I, Kaya E, Yologlu S, Gokdeniz R, Baydin A. Platelet counts in adults with iron deficiency anemia. Platelets. 2009 Aug 3. 1-5. [Medline].

  12. Stamatoyannopoulos G, Majerus PW, Perimutter RM. The Molecular Basis of Blood Diseases. Philadelphia, Pa: WB Saunders Co; 2000.

  13. Dhar R, Zazulia AR, Videen TO, et al. Red blood cell transfusion increases cerebral oxygen delivery in anemic patients with subarachnoid hemorrhage. Stroke. 2009 Sep. 40(9):3039-44. [Medline]. [Full Text].

  14. DeLoughery TG. Microcytic anemia. N Engl J Med. 2014 Oct 2. 371(14):1324-31. [Medline].

  15. Mozaffari-Khosravi H, Noori-Shadkam M, Fatehi F, Naghiaee Y. Once weekly low-dose iron supplementation effectively improved iron status in adolescent girls. Biol Trace Elem Res. 2009 Aug 4. epub ahead of print. [Medline].

  16. [Guideline] Killick SB, Bown N, Cavenagh J, Dokal I, Foukaneli T, Hill A, et al. Guidelines for the diagnosis and management of adult aplastic anaemia. Br J Haematol. 2016 Jan. 172 (2):187-207. [Medline]. [Full Text].

  17. [Guideline] Barone A, Lucarelli A, Onofrillo D, Verzegnassi F, Bonanomi S, et al. Diagnosis and management of acquired aplastic anemia in childhood. Guidelines from the Marrow Failure Study Group of the Pediatric Haemato-Oncology Italian Association (AIEOP). Blood Cells Mol Dis. 2015 Jun. 55 (1):40-7. [Medline].

 
Previous
Next
 
Anemia. Decreased production of red blood cells is suggested in certain patients with anemia. Bone marrow biopsy specimen allows categorization of patients with anemia without evidence of blood loss or hemolysis into 3 groups: aplastic or hypoplastic disorder, hyperplastic disorder, or infiltration disorder. Each category and its associated causes are listed in this image.
Microcytic anemia.
Peripheral smear showing classic spherocytes with loss of central pallor in the erythrocytes.
Bone marrow aspirate containing increased numbers of plasma cells.
Bone marrow aspirate showing erythroid hyperplasia and many binucleated erythroid precursors.
Table 1. Microcytic Hypochromic Anemia (MCV < 83; MCHC < 31)
Condition Serum Iron Total Iron-Binding Capacity (TIBC) Bone Marrow Iron Comment
Iron deficiency 0 Responsive to iron therapy
Chronic inflammation ++ Unresponsive to iron therapy
Thalassemia major N ++++ Reticulocytosis and indirect bilirubinemia
Thalassemia minor N N - ↓ ++ Elevation of fetal hemoglobin and Hb A2, target cells, and poikilocytosis
Lead poisoning N N ++ Basophilic stippling of RBCs
Sideroblastic N ++++ Ring sideroblasts in marrow
Hemoglobin N N ++ Hemoglobin electrophoresis
↓ = decreased; ↑ = increased; 0 = absent; +'s indicate the amount of stainable iron in bone marrow specimens, on a scale of 0-4; N = normal.
Table 2. Macrocytic Anemia (MCV >95)
Megaloblastic bone marrow Deficiency of vitamin B-12
Deficiency of folic acid
Drugs affecting deoxyribonucleic acid (DNA) synthesis
Inherited disorders of DNA synthesis
Nonmegaloblastic bone marrow Liver disease
Hypothyroidism and hypopituitarism
Accelerated erythropoiesis (reticulocytes)
Hypoplastic and aplastic anemia
Infiltrated bone marrow
Table 3. Various Forms of RBCs
Macrocyte Larger than normal (>8.5 µm diameter). See Table 2.
Microcyte Smaller than normal (< 7 µm diameter). See Table 1.
Hypochromic Less hemoglobin in cell. Enlarged area of central pallor. See Table 1.
Spherocyte Loss of central pallor, stains more densely, often microcytic. Hereditary spherocytosis and certain acquired hemolytic anemias
Target cell Hypochromic with central "target" of hemoglobin. Liver disease, thalassemia, hemoglobin D, and postsplenectomy
Leptocyte Hypochromic cell with a normal diameter and decreased MCV. Thalassemia
Elliptocyte Oval to cigar shaped. Hereditary elliptocytosis, certain anemias (particularly vitamin B-12 and folate deficiency)
Schistocyte Fragmented helmet- or triangular-shaped RBCs. Microangiopathic anemia, artificial heart valves, uremia, and malignant hypertension
Stomatocyte Slitlike area of central pallor in erythrocyte. Liver disease, acute alcoholism, malignancies, hereditary stomatocytosis, and artifact
Tear-shaped RBCs Drop-shaped erythrocyte, often microcytic. Myelofibrosis and infiltration of marrow with tumor. Thalassemia
Acanthocyte Five to 10 spicules of various lengths and at irregular intervals on surface of RBCs
Echinocyte Evenly distributed spicules on surface of RBCs, usually 10-30. Uremia, peptic ulcer, gastric carcinoma, pyruvic kinase deficiency, and preparative artifact
Sickle cell Elongated cell with pointed ends. Hemoglobin S and certain types of hemoglobin C and l
Table 4. Classification of the Hemolytic Disorders
  Hereditary Acquired
Intracorpuscular defect Hereditary spherocytosis



Hereditary elliptocytosis



Hemoglobinopathies



Thalassemias



Congenital dyserythropoietic anemias



Hereditary RBC enzymatic deficiencies



Rarer hereditary abnormalities



Vitamin B-12 and folic acid deficiency



Paroxysmal nocturnal hemoglobinuria



Severe iron deficiency



Extracorpuscular defect   Physical agents: Burns, cold exposure



Traumatic: Prosthetic heart valves, march hemoglobinuria, disseminated intravascular coagulation (DIC), graft rejection



Chemicals: Drugs and venoms



Infectious agents: Malaria, toxoplasmosis, mononucleosis, hepatitis, primary atypical pneumonia, clostridial infections, bartonellosis, leishmaniasis



Hepatic and renal disease



Collagen vascular disease



Malignancies: Particularly hematologic neoplasia



Transfusion of incompatible blood



Hemolytic disease of the newborn



Cold hemagglutinin



disease



Autoimmune hemolytic anemia Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome (HUS)



Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.