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Hemolytic Anemia: Evaluation and Differential Diagnosis

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Hemolytic Anemia: Evaluation and Differential Diagnosis Hemolytic Anemia: Evaluation and Differential Diagnosis James Phillips, MD, and Adam C. Henderson, MD, Womack Army Medical Center, Fort Bragg, North Carolina Hemolytic anemia is defined by the premature destruction of red blood cells, and can be chronic or life-threatening. It should be part of the differential diagnosis for any normocytic or macrocytic anemia. Hemolysis may occur intravascularly, extravascularly in the reticuloendothelial system, or both. Mechanisms include poor deformability leading to trapping and phagocytosis, antibody-mediated destruction through phagocytosis or direct complement activation, fragmentation due to microthrombi or direct mechanical trauma, oxidation, or direct cellular destruction. Patients with hemolysis may present with acute anemia, jaundice, hematuria, dyspnea, fatigue, tachycardia, and possibly hypotension. Laboratory test results that confirm hemolysis include reticulocytosis, as well as increased lactate dehydrogenase, increased unconju- gated bilirubin, and decreased haptoglobin levels. The direct antiglobulin test further differentiates immune causes from nonimmune causes. A peripheral blood smear should be performed when hemolysis is present to identify abnormal red blood cell morphologies. Hemolytic diseases are classified into hemoglobinopathies, membranopathies, enzymopathies, immune-mediated anemias, and extrinsic nonimmune causes. Extrinsic nonimmune causes include the thrombotic micro- angiopathies, direct trauma, infections, systemic diseases, and oxidative insults. Medications can cause hemolytic anemia through several mechanisms. A rapid onset of anemia or significant hyperbilirubinemia in the neonatal period should prompt consideration of a hemolytic anemia. (Am Fam Physician. 2018;98(6):354-361. Copyright © 2018 American Acad- emy of Family Physicians.) Hemolytic anemia is defined as the destruction of red and oxidation. Direct cellular destruction is caused by blood cells (RBCs) before their normal 120-day life span. It toxins, trauma, or lysis. Fragmentation hemolysis occurs includes many separate and diverse entities whose common when extrinsic factors produce shearing and rupture of clinical features can aid in the identification of hemolysis. RBCs. Oxidative hemolysis occurs when the protective Hemolytic anemia exists on a spectrum from chronic to mechanisms of the cells are overwhelmed.1 life-threatening, and warrants consideration in all patients The etiologies of hemolysis are numerous (Table 1). The with unexplained normocytic or macrocytic anemia. hemoglobinopathies lead to splenic destruction and, in the case of sickle cell disease, likely multiple mechanisms Pathophysiology of destruction. Inherited protein deficits lead to increased Premature destruction of RBCs can occur intravascu- destruction in membranopathies. Enzymopathies result larly or extravascularly in the reticuloendothelial sys- in hemolysis due to overwhelming oxidative stress or tem, although the latter is more common. The primary decreased energy production. In immune-mediated hemo- extravascular mechanism is sequestration and phago- lytic anemia, antibodies bind with the RBCs, resulting in cytosis due to poor RBC deformability (i.e., the inabil- phagocytosis or complement-mediated destruction. The ity to change shape enough to pass through the spleen). extrinsic nonimmune causes include microangiopathic Antibody-mediated hemolysis results in phagocytosis or hemolytic anemia (MAHA), infections, direct trauma, and complement-mediated destruction, and can occur intra- drug-induced hemolysis, among others. vascularly or extravascularly. The intravascular mecha- nisms include direct cellular destruction, fragmentation, Clinical Presentation Hemolysis should be considered when a patient experiences acute jaundice or hematuria in the presence of anemia. CME This clinical content conforms to AAFP criteria for continuing medical education (CME). See CME Quiz on Symptoms of chronic hemolysis include lymphadenopathy, page 345. hepatosplenomegaly, cholestasis, and choledocholithia- Author disclosure: No relevant financial affiliations. sis. Other nonspecific symptoms include fatigue, dyspnea, hypotension, and tachycardia. Downloaded from the American Family Physician website at www.aafp.org/afp. Copyright © 2018 American Academy of Family Physicians. For the private, noncom- 354 American Family Physician www.aafp.org/afp Volume 98, Number 6 ◆ September 15, 2018 mercial use of one individual user of the website. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. HEMOLYTIC ANEMIA TABLE 1 Differential Diagnosis of Hemolysis Class/type Diseases Mechanism Site Laboratory tests Treatment Alloimmune Transfusion reactions, hemo- Trapping, Intravascular Neonatal DAT Halt transfusion, lytic disease of the fetus and phagocytosis, supportive newborn complement Autoimmune Warm or cold autoimmune Trapping, Extravascular DAT Steroids, avoid- hemolytic anemia hemolytic anemia phagocytosis, or intravascular ance, treatment of complement other disease Drug induced Drug-induced thrombotic Direct, toxin, Extravascular Schistocytes, DAT, Drug withdrawal microangiopathy, drug-in- phagocytosis, or intravascular Heinz bodies duced immune hemolytic fragmentation anemia, oxidative hemolysis Envenomation Insects, cobra, brown recluse Direct Extravascular — — spider or intravascular Enzymopathy G6PD or pyruvate kinase Oxidative lysis Intravascular Enzyme activity Avoidance, deficiencies measurement splenectomy Hemoglobinopathy Sickle cell disease, thalas- Trapping Extravascular Hemoglobin Disease-specific semias, hemoglobin defects electrophoresis treatment Infection Malaria, Babesia, Bartonella, Direct, toxin, Extravascular Pathogen-specific Infection-specific Clostridia, Rickettsia, Hae- phagocytosis, or intravascular testing treatment mophilus influenzae, human fragmentation immunodeficiency virus Membranopathy Hereditary sphero- Trapping Extravascular Osmotic fragility test, Splenectomy, cytosis, hereditary eosin-5-maleimide eculizumab elliptocytosis, paroxysmal binding (Soliris; parox- nocturnal hemoglobinuria ysmal nocturnal hemoglobinuria) Microangiopathic Thrombotic thrombocyto- Fragmentation Intravascular Peripheral blood Plasma exchange, hemolytic ane- penic purpura, hemolytic smear (showing steroids, delivery, mia/thrombotic uremic syndrome, dis- schistocytes), assess- drug withdrawal microangiopathy seminated intravascular ment of ADAMTS13 coagulation, HELLP syn- activity, liver enzyme drome, drug-induced tests, coagulation thrombotic microangiopathy study, culture Osmotic Freshwater drowning Osmotic lysis Intravascular — — Systemic disease Malignant hypertension, sys- Trapping, Extravascular Disease-specific Disease-specific temic lupus erythematosus, fragmentation or intravascular testing treatment scleroderma, liver disease, vasculitides, hypersplenism Trauma Endovascular devices, aortic Fragmenta- Intravascular — Stop trauma stenosis, extracorporeal tion, direct membrane oxygenation, arteriovenous malformation, march hemoglobinuria, burns DAT = direct antiglobulin test; G6PD = glucose-6-phosphate dehydrogenase; HELLP = hemolysis, elevated liver enzymes, and low platelet count. Evaluation The initial workup of hemolytic anemia begins with a When hemolysis is suspected, the history should include complete blood count illustrating normocytic (mean cor- known medical diagnoses, medications, personal or family puscular volume of 80 to 100 µm3 [80 to 100 fL]) or mac- history of hemolytic anemia, and a complete review of sys- rocytic (mean corpuscular volume greater than 100 µm3) tems. The physical examination should focus on identifying anemia (Figure 1). When anemia is identified, testing should associated conditions, such as infections or malignancies include measurement of lactate dehydrogenase, haptoglo- (Table 2). bin, reticulocyte, and unconjugated bilirubin levels, as well Downloaded from the American Family Physician website at www.aafp.org/afp. Copyright © 2018 American Academy of Family Physicians. For the private, noncom- September 15, 2018 ◆ Volume 98, Number 6 www.aafp.org/afp American Family Physician 355 mercial use of one individual user of the website. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. SORT: KEY RECOMMENDATIONS FOR PRACTICE Evidence Clinical recommendation rating References After hemolytic anemia is confirmed, a peripheral blood C 1 as urinalysis (Table 3). Lactate dehy- smear should be ordered to determine the etiology. drogenase is intracellular, and levels Glucocorticoids are the first-line treatment of warm C 4 increase when RBCs rupture. Hapto- autoimmune hemolytic anemia. globin binds to free hemoglobin, and levels decrease in hemolysis. Unconju- The PLASMIC score can be used to assess the likeli- C 10 hood of thrombotic thrombocytopenic purpura when gated bilirubin levels rise as its produc- ADAMTS13 cannot be easily measured. tion exceeds elimination capability. Hemolysis usually induces a reticulo- Do not give antibiotics to children with Escherichia coli B 15 diarrhea because antibiotics increase the risk of hemo- cytosis causing macrocytosis, unless lytic uremic syndrome. significant iron deficiency or mar- row suppression is present. Urinalysis G6PD activity should be measured in infants with C 28 jaundice and a family history or geographic background may be positive for hemoglobinuria in suggestive of possible deficiency. hemolytic anemia despite no visible
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