What Is The Most Common Cause Of Hemolytic Anemia – Hemolytic Anemia is defined as the destruction of Red Blood Cells (RBCs) before their normal lifespan of 120 days. It includes many separate and distinct entities whose common clinical features can help identify hemolysis. Hemolytic anemias range from chronic to life-threatening and require consideration in all patients with unexplained normocytic or macrocytic anemia.
When ADAMTS13 cannot be easily measured, the PLASMIC score can be used to assess the likelihood of thrombotic thrombocytopenic purpura.
What Is The Most Common Cause Of Hemolytic Anemia
Do not give antibiotics to children with E. coli diarrhea because antibiotics can increase the risk of hemolytic uremic syndrome.
Hemolytic Uremic Syndrome In Children
G6PD activity should be measured in infants who are jaundiced and whose family history or geographic background suggests possible deficiency.
Premature destruction of Red Blood cells may occur intravascularly or extravascularly in the reticuloendothelial system, although the latter is more common. The major extravascular mechanisms are sequestration and phagocytosis due to poor deformability of red blood cells (i.e., inability to change shape enough to pass through the spleen). Antibody-mediated hemolysis results in phagocytosis or complement-mediated destruction and can occur intravascularly or extravascularly. Intravascular mechanisms include direct cell destruction, fragmentation, and oxidation. Direct cell destruction is caused by toxins, trauma, or lysis. Fragmentary hemolysis occurs when external factors cause red blood cells to shear and rupture. Oxidative hemolysis occurs when the cell’s protective mechanisms are overwhelmed.
There are many causes of hemolysis (Table 1). Hemoglobin disorders can lead to destruction of the spleen, and in the case of sickle cell disease, multiple mechanisms of destruction may result. Inherited protein defects lead to increased destruction in membrane diseases. Enzymopathy leads to hemolysis due to overwhelming oxidative stress or reduced energy production. In immune-mediated hemolytic anemia, antibodies bind to red blood cells, leading to phagocytosis or complement-mediated destruction. Extrinsic nonimmune causes include microangiopathic hemolytic anemia (MAHA), infection, direct trauma, and drug-induced hemolysis.
Hemolysis should be considered when a patient develops acute jaundice or hematuria in the setting of anemia. Symptoms of chronic hemolysis include lymphadenopathy, hepatosplenomegaly, cholestasis, and common bile duct stones. Other nonspecific symptoms include fatigue, dyspnea, hypotension, and tachycardia.
Hemolytic Disease Of The Newborn: Video & Anatomy
When hemolysis is suspected, the history should include known medical diagnoses, medications, personal or family history of hemolytic anemia, and a complete examination of the systems. Physical examination should focus on identifying associated diseases, such as infection or malignancy (Table 2).
Initial workup for hemolytic anemia begins with a complete blood count showing normocytes (mean red blood cell volume 80 to 100 μm)
) anemia (Figure 1). When anemia is detected, testing should include measurement of lactate dehydrogenase, haptoglobin, reticulocyte, and unconjugated bilirubin levels and urinalysis (Table 3). Lactate dehydrogenase is located within cells and its levels increase when red blood cells rupture. Haptoglobin binds to free heme, and its concentration decreases during hemolysis. When the production of unconjugated bilirubin exceeds the ability to eliminate it, its levels rise. Hemolysis usually causes reticulocytosis, resulting in an increase in large red blood cells, unless there is significant iron deficiency or bone marrow suppression. Although there are no visible red blood cells under the microscope, a urinalysis may be positive for hemoglobinuria in hemolytic anemia. Hemolysis was confirmed by reticulocytosis, elevated lactate dehydrogenase levels, elevated unconjugated bilirubin levels, and decreased haptoglobin levels. The absence of these findings should prompt a search for other causes. After hemolysis is confirmed, supportive treatment should be initiated as needed.
Identifying the specific cause of hemolytic anemia begins with a peripheral blood smear to check for abnormal red blood cells, such as spheroids, lobulated red blood cells, bite cells, or bleb cells
Warm Autoimmune Hemolytic Anemia
(Figures 2 and 3). Spherical red blood cells are caused by membrane defects or repeated membrane removal by macrophages. Spherocytosis does not diagnose hemolytic anemia because both hereditary spherocytosis and immune causes (eg, autoimmune hemolytic anemia [AIHA], drug-induced immune hemolytic anemia) can cause spherocytosis. Schistocytes are fragmented cells caused by damage within blood vessels, which occurs in MAHA syndrome. Bites and vesicles are caused by partial phagocytosis and occur from oxidative causes such as glucose-6-phosphate dehydrogenase (G6PD) deficiency.
AIHAs are divided into two main subgroups based on binding temperature, called cold agglutinins and warm agglutinins. Many causes of AIHA are idiopathic; however, viral and bacterial infections, autoimmune diseases, connective tissue disorders, lymphoproliferative malignancies, transfusions, and transplantation have been associated with AIHA.
Hot AIHA is more common than cold AIHA and involves immunoglobulin G (IgG) antibodies, usually Rh complexes, that react with red blood cell membranes at normal body temperature. Reticuloendothelial macrophages then clear and sequester the IgG-coated red blood cells in the spleen, sometimes resulting in splenomegaly. Treatment of warm AIHA typically includes corticosteroids, treatment of the underlying disease, blood transfusions (if necessary), and supportive care.
Cold AIHA involves IgM antibodies (cold agglutinin titers) that react at low temperatures with polysaccharide antigens on the surface of red blood cells and then cause lysis on rewarming via complement fixation and intravascular hemolysis. The production of these antibodies is associated with infection or malignant processes. Mycoplasma pneumonia and mononucleosis are two of the most common diseases. Treatment of patients with cold AIHA typically includes supportive measures, avoidance of triggers, and management of the underlying disease.
Introduction To Hemolytic Anemia| Molecular Basis
Acute transfusion reactions are caused by reactions of alloantibodies with incompatible red blood cells. Hemolysis can be acute or delayed and can be life-threatening. Transfusion reactions have been previously discussed in American Family Physician (https:///afp/2011/0315/p719.html).
Drug-induced immune hemolytic anemia is a rare condition caused by drug-induced antibodies. Patients with this disease have positive DAT results. Historically, methyldopa and penicillins were the classic causes, but cefotetan (Cefotan), ceftriaxone, piperacillin (piperacillin/tazobactam combination [Zosyn]), and nonsteroidal antibiotics Inflammatory drugs now dominate
(Table 4). The progression of the disease is usually gradual, and treatment involves removal of the causative agent.
3. 4-Methylenedioxymethamphetamine (ecstasy), bupropion (Wellbutrin), chemotherapy, clopidogrel (Plavix), cocaine, cyclosporine (Sandimmune), bupropion Profen, interferon, mefloquine, metronidazole (Flagyl), nitrofurantoin, quetiapine (Seroquel), quinine, simvastatin (Zocor), tacrolimus (Prograf), trimethoprim /sulfamethoxazole,
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MAHA is a descriptive term for hemolytic anemia, which occurs when red blood cells are shattered, resulting in sharded red blood cells visible on peripheral blood smears. This may be caused by trauma from an intravascular device or microthrombosis. Thrombotic microangiopathy (TMA) is a diverse group of clinical disorders with MAHA as a core feature (Table 1).
Thrombotic thrombocytopenic purpura (TTP) is characterized by a significant decrease in ADAMTS13 enzyme activity. The ADAMTS13 enzyme cleaves von Willebrand factor aggregates, and when it is absent or not functioning, large von Willebrand factor multimers form. These polymers capture platelets and cause microthrombi and red blood cell destruction through shearing, producing fragmented red blood cells. Approximately 95% of TTP cases are associated with acquired autoantibodies, usually without a precipitating event or disease.
TTP is life-threatening and requires prompt diagnosis and treatment. Thrombocytopenia, fever, renal impairment, MAHA, and neurological dysfunction are hallmarks of TTP. Other laboratory test results included a negative DAT result and a normal coagulation test. Assessment of ADAMTS13 enzyme activity is diagnostic of TTP, but results are often delayed, necessitating a presumptive diagnosis. The PLASMIC score can be used to predict severe reduction in ADAMTS13 enzyme activity and initiate early treatment (Table 5).
Once a presumptive diagnosis is made, plasmapheresis and glucocorticoid therapy should be initiated immediately. Plasma exchange removes affected platelets and autoantibodies while replenishing ADAMTS13 enzyme levels. Although plasmapheresis is more effective, fresh frozen plasma transfusion is beneficial and should be initiated if transfer to a center with plasmapheresis capability is delayed.
Haemolytic Uraemic Syndrome
Hemolytic uremic syndrome (HUS) is characterized by MAHA and acute kidney injury, often accompanied by thrombocytopenia and neurological deficits. Based on ADAMTS13 enzymatic activity, HUS is a TTP-independent entity. Shiga toxin-producing Escherichia coli HUS (STEC-HUS, also known as classic HUS) accounts for 90% of HUS cases and is caused by STEC organisms such as O157:H7 and Shigella dysenteriae.
It mainly affects children. STEC-HUS has the classic positive symptoms of abdominal pain with diarrhea, usually preceded by MAHA, acute kidney injury, and thrombocytopenia by 5 to 10 days. STEC urinary tract infection can lead to diarrhea-negative STEC-HUS.
In rare cases, Streptococcus pneumoniae, human immunodeficiency virus, and influenza have also been associated with HUS without the classic prodromal symptoms. There is an atypical form of HUS that also has no prodromal symptoms, is caused by complement dysregulation rather than infection, and can be inherited. Upper respiratory tract infections may cause exacerbations.
Undercooked ground beef is a major source of STEC infections, but fruits, vegetables, poultry and contaminated drinking water are also affected. In STEC-HUS, Shiga toxin is absorbed and attaches to specific receptors that are primarily expressed in children’s glomeruli and brain, causing endothelial cell damage that initiates a cascade that produces large amounts of von Weiler Brand factor multimers, thereby inducing MAHA. Treatment of STEC-HUS is supportive care and ongoing assessment of renal function. Antibiotics are not recommended for gastrointestinal STEC because they may increase the risk of HUS.
Autoimmune Hemolytic Anemia: Video & Anatomy
Other clinical conditions leading to MAHA include HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count) and disseminated intravascular coagulation. HELLP syndrome is associated with pregnancy and shares many features with TTP and HUS, both of which may also occur during pregnancy. TTP and HUS generally do not cause elevations in liver-related enzymes as does HELLP syndrome.
A lower lactate dehydrogenase to aspartate aminotransferase ratio helps differentiate HELLP syndrome from higher rates of hemolysis in other TMAs and higher hepatic involvement in HELLP syndrome.
Disseminated intravascular coagulation can also cause MAHA due to fibrin-rich microthrombi. Disseminated intravascular coagulation resulting in prolonged coagulation studies, positive d-dimer test results, and decreased fibrinogen
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