Research Paper Sample on Hemolytic Anemia

Hemolytic anemia is termed as a condition where red blood cells undergo hemolysis. The condition occurs when there is an abnormal breakdown of red blood cells in any part of the body mostly the spleen that is extravascular hemolysis or in the blood vessel, which is called intravascular hemolysis. In this condition, the bone marrow is unable to make or produce red blood cells at faster rate as the body demands them. The condition leads to other health problems like arrhythmias, enlarged heart and thus becoming life threatening at some point. However, different types of hemolytic anemia are acquired or inherited (Bass, Tuscano, & Tuscano, 2014). These types determine the kind of treatment that one will be given if suffering from hemolytic anemia.

Definition

Hemolytic anemia is a condition that comes up when red blood cells are destroyed before their normal lifespan is over and are removed from the bloodstream. The state is also referred as a type of anemia in which the number of red-blood cells in the components of blood is lower compared to how it should be normally. The condition may also occur when the erythrocytes do not have enough hemoglobin. The seriousness of this condition is dependent on the type and the beginning of hemolysis whether it is abrupt or gradual and the degree to which the destruction of erythrocytes is occurring (Bass, Tuscano, & Tuscano, 2014). For this case, therefore, the hemolytic anemia has different causes, a clinical presentation that may be different depending on the etiology. The treatment and management are also of various types.

Etiology

There are a wide range hemolytic causes that are documented. The causes determine the type of hemolytic anemia that one will have that is either acquired or inherited hemolytic anemia. The causes too may be termed as intrinsic that is from internal factors or extrinsic from internal factors that may include immune attack through the damage of red blood cells.

Intrinsic causes inherited hemolytic anemia can be caused by:

Defects in the production of enough hemoglobin. That occurs in sickle cell disease, congenital dyserythropoietic anemia, and thalassemia. If red blood cells are not replaced in the body as fast as they should and according to how the body needs them.

Inherited red blood cells membrane defects that is called hereditary elliptocytosis, spherocytosis, and pyropoikilocytosis. That is defects in production of red blood cells membrane (Bass, Tuscano, & Tuscano, 2014).

A defect in the metabolism of red cell that is a deficiency of enzymes these are; pyruvate kinase (PK) deficiency and deficiency of G6PD glucose-6-phosphate dehydrogenase (Bass, Tuscano, & Tuscano, 2014).

Marchiafava-Micheli syndrome which is also known as paroxysmal nocturnal hemoglobinuria (PNH) although it is rarely life threatening to some extents and it is composed of complement-induced intravascular hemolytic anemia.

Presence of abnormal cells that are fragile and may break anytime while in the bloodstream.Extrinsic causes the causes of acquired hemolytic anemia are immune or non-immune etiologies. They include:

Immune hemolytic anemia they are divided according to the temperatures which the antibodies bind well to the red blood cells. They can either be cold or warm reacting antibodies.

Autoantibodies is another cause which leads to immune-mediated hemolytic anemia and is mostly part of other autoimmune conditions like scleroderma, SLE, and rheumatoid arthritis or may be related to lymph proliferative disorder like chronic lymphocytic leukemia and non-Hodgkin lymphoma (Bass, Tuscano, & Tuscano, 2014).

Alloimmune hemolytic anemia which includes the transfusion reaction or the hemolytic disease of the infants.

Hypersplenism that is the increase in the spleen's size and activity like portal hypertension.Infections like malaria and as a result of physical damage like burns.

Toxic chemicals like lead poisoning that may be from a polluted environment and it cause non-immune hemolytic anemia or poisoning by stibine or arsine (Lindbergh, 2012).

Uptake of some drugs that are associated with hemolysis some through mechanisms that are immune-mediated and some that are non-immune mediated or even blood transfusion.

Paroxysmal nocturnal hemoglobinuria which results in the subsequent hemolysis and erythrocyte membrane defect although it is a rare disorder (Bass, Tuscano, & Tuscano, 2014).

Another cause of non-immune mediated hemolysis is the trauma of different forms of eclampsia, hemolytic uremic syndrome, DIC and malignant hypertension

Pathophysiology

Hemolysis of the red blood cells could be as a result of acquired or hereditary disorders. The etiology of the destruction of the premature erythrocyte is very diverse and can be a defect of an intrinsic membrane, hypersplenism or other causes. However, it may be an intravascular or extravascular phenomenon. Moreover, this type of anemia may be intramedullary that is when the precursors of fragile red blood cells are destroyed before release into the circulatory system from the bone marrow (Lindbergh, 2012). Also, hemolysis is associated with the discharge of red blood cells lactate dehydrogenase (LDH). An increase of indirect urobilinogen and bilirubin levels is also caused by the release of hemoglobin from the RBCs that are already damaged. However one may have a normal hemoglobin level if he or she has mild hemolysis. If one is in that condition, he or she may be invaded by marked anemia that is if his bone marrow manufacture of the erythrocyte is switched-off by infections or other viral causes like parvovirus (Lindbergh, 2012).

As a result of a striking upsurge in subsequent bone marrow development and hematopoiesis, in some illnesses like thalassemia, skeletal and skull deformities may occur during childhood. Hemolytic anemia can affect anyone at any age and of any race or gender. However, some hemolytic anemia types occur in certain people from specific populations than others (Lindbergh, 2012). Like in the United States of America, the condition has affected the males African Americans more than the Caucasians.

Clinical manifestation

Hemolytic anemia has diverse sign and symptoms that are due to anemia, underlying disorder, previous treatment and compensation extent. Patient suffering from long-standing or minimal hemolytic anemia may be asymptomatic, but it is still found incidentally during a laboratory test. The clinical manifestations of this condition are:

Dyspnea, weakness, angina, and tachycardia are observed in patients suffering from severe anemia, and the cardiac function has a high sensitivity to anoxia (Lindbergh, 2012).

Dark urine which may be due to hemoglobinuria.

Persistent hemolysis which occurs due to the formation of bilirubin gallstones. The patient may also suffer from severe abdominal pain (Bass, Tuscano, & Tuscano, 2014).

Iron deficiency in intravascular hemolysis because of chronic hemoglobinuria. That can exacerbate weakness and anemia.

Diabetes occurs in hemosiderosis and skin color changes to bronze. To patients who have undergone several transfusions, an iron overload occurs and in those administered with iron therapy erroneously (Lindbergh, 2012).

Leg ulcers - this may develop in those suffering from the hemolytic disorder and sickle cell anemia due to a reduced number of the red blood cells and changes in endothelial.

Fever, renal failure, thrombocytopenia and neurologic signs may occur in patients suffering from thrombotic thrombocytopenic purpura (TTP) (Bass, Tuscano, & Tuscano, 2014).

Heart failure of the right ventricle due to pulmonary hypertension. That is a symptom of ascites fluid in the abdominal cavity and peripheral edema that is fluid accumulation in the legs.Treatments

The treatment of hemolytic anemia depends mostly on the cause and the aim of treatment. Some of the aims of treatment include:

Treating and getting rid of the underlying cause of that condition.

Stopping or reducing red blood cells destruction.

Increasing the erythrocytes count to a good advisable level.

The main treatments are:

Blood transfusions the kind of hemolytic anemia that is treated using this method is one that is life-threatening. Mostly symptomatic treatment is given through transfusion in case of marked anemia. Since before treatment there have to be laboratory tests when the patient is found out to have serious disorder the transfusion is the most appropriate. In case of a positive Coombs test then there is a relative contraindication to transfuse a patient. There is an advantage of transfusing warmed blood to cold hemolytic anemia (Berentsen, S., & Tjonnfjord, 2012). The transfusion is a procedure where blood is given to a patient via an intravenous line in a specific blood vessel in our bodies. Before transfusion, the blood groups and rhesus of the donor and recipient must be well matched for better results.

Steroid therapy is also necessary for treatment of immune related hemolytic anemia which is at a severe level. Medicine can be used to improve some hemolytic anemia especially (AIHA) where corticosteroid drugs like prednisone limit the immune system from making antibodies against erythrocytes (Lindbergh, 2012).

Immunosuppressant like cyclophosphamide and azathioprine can be added, or rituximab is used in case steroids are resistant. If one does not respond to the corticosteroid medicine, then other drugs are used to suppress the immune system like cyclosporine (Berentsen, S., & Tjonnfjord, 2012). If the sickle cell anemia is too severe, then there is need to be recommended for a drug called hydroxyurea that stimulates the body to make fetal hemoglobin. That hemoglobin is also found in newborn infants.

Intravenous and methylprednisolone immunoglobulin association which are used in control of hemolysis even in acute or severe cases.

Splenectomy- this is helpful in case of predominant hereditary spherocytosis or extravascular hemolysis. That is only done via surgery for those whose level is too severe and just have to remove their spleens. If the spleen is healthy, it should be able to filter out older blood cells and those that are damaged. In case the spleen is enlarged or damaged, it has the probability of eliminating more red blood cells than it is supposed thus leading to anemia and by its removal, it helps reduce destruction of red blood cells at a high rate (Lindbergh, 2012).

Plasmapheresis this is the removal of antibodies from the blood in the body of a human. Blood is taken out of the body of a patient using a syringe and a needle from the veins. The plasma containing antibodies is separated from the other blood components. Then a donors plasma and the other blood is put back into a patients body (Berentsen, S., & Tjonnfjord, 2012). The treatment is effective if other treatments are not working.

Marrow stem cell and blood transplant this is a transplant that that is carried out to replace the stems that are damaged by function alone. The practice is like blood transfusion, and the donated stem cells are put into a vein using a tube. Once they are placed in the recipients body, they move to the bone marrow and can now manufacture other red blood cells.

Conclusion

There is a great need for patients to identify signs and symptoms of recurrence of hemolysis. If the symptoms reoccur then medical attention has to be seen. Patients should also know themselves especially those with G6PD must know the kind of medications. Patients suffering from chronic hemolytic should avoid folate consumption as it causes folate deficiency (Lindbergh, 2012). Hemolytic anemia is as found to have some risk factors. The people who are most affected by deficiency of glue-6- phosphate dehydrogenase (G6PD) are men of the African Americans. Therefore people from that population especially...