15. Anaemia

DEFINITION
Decreased ability of the red blood cells to provide adequate oxygen supplies to body tissues. May be due to decreased number of red blood cells, decreased amount of substance in red blood cells which transports oxygen (hemoglobin), or decreased volume of red blood cells.
It can be:
- anemia ofBl2 deficiency
- anemia of chronic disease
- anemia of folate deficiency
- grug-induced immune hemolytic anemia
- hemolytic anemia
- hemolytic anemia due to g6pd deficiency
- idiopathic aplastic anemia
- idiopathic autoimmune hemolytic anemia
- immune hemolytic anemia
- iron deficiency anemia
- megaloblastic anemia
- pemicions anemia
- secondary aplastic anemia
- sickle cell anemia
Hemolytic anemia
OTHER NAMES
hemoglobin SC disease; sickle thalassemia; aplastic anemia; anemia - hemolytic
DEFINITION
A condition of inadequate number of circulating red blood cells (anemia), caused by premature destruction of red blood cells. There are a number of specific types of hemolytic anemia which are described individually.
CAUSES, INCIDENCE, AND RISK FACTORS
Hemolytic anemia occurs when the bone marrow is unable to compensate for premature destruction of red blood cells by increasing their production. When the marrow is able to compensate, anemia does not occur.
There are many types of hemolytic anemia, which are classified by the location of the defect. The defect may be in the red blood cell itself (intrinsic factor) or outside the red blood cell (extrinsic factor).
Causes of hemolytic anemia include infection, certain medications, autoimmune disorders, and
inherited disorders. Types of hemolytic anemia include:
- aplastic anemia
- secondary aplastic anemia
- hemoglobin SC disease
- hemolytic anemia due to G6PD deficiency
- hereditary elliptocytosis
- hereditary spherocytosis
- hereditary ovalocytosis
- idiopathic autoimmune hemolytic anemia
- non-immune hemolytic anemia caused by chemical or physical agents
- secondary immune hemolytic anemia
- sickle thalassemia
The over all incidence of “hemolytic anemia” is 4 out of 100,000 people.
PREVENTION
There is no known prevention for hemolytic anemia.
SYMPTOMS
- nosebleeds
- gums, bleeding
- chills
- fatigue
- pale color
- shortness of breath
- rapid heart rate
- yellow skin color (jaundice)
- dark urine ..enlarged spleen
SIGNS AND TESTS
These are test for hemolysis (red blood cell destruction). There are specific tests which identify
the specific types of hemolytic anemia; they are performed after hemolysis has been established.
- elevated indirect bilirubin levels
- low serum haptoglobin
- hemoglobin in the urine
- hemosiderin in the urine
- increased urine and fecal urobilinogen
- elevated absolute reticulocyte count
- low red blood cell count and hemoglobin
Direct measurement of the red cell life span by isotopic tagging techniques shows a decreased life span.
This disease may also alter the following test results:
- uric acid
- TIBC
- RBC indices
- protein electrophoresis - serum
- potassium test
- platelet count
- peripheral smear
- leukocyte alkaline phosphatase
- LDH isoenzymes
-LDH
- serum iron
- hematocrit
- ferritin
- febrile or cold agglutinins
- Donath-Landsteiner test
- Coombs’ test, indirect
- Coombs’ test, direct
-CBC
- blood differential
-AST
- 24-hr. urine protein

Treatment Options

Treatment Strategy

 Therapy for anemia depends on the cause and the severity of the anemia. In some anemias, the therapy is well established; in others the therapy is largely expectant, depending on the successful treatment of the underlying disease (e.g., anemia of chronic disease). Avoid oxidant medications in patients with G6PD deficiency. Other treatment options include the following. _... Supportive care (e.g., transfusions), folic acid, and fluids-for patients with sickle cell anemia _... Supportive care (e.g., transfusions), symptomatic therapy, bone marrow transplantation, and splenectomy-for the alpha and beta thalassemias _... Splenectomy-for hereditary spherocytosis

Drug Therapies

 _... Erythropoietin plus iron-for anemia of chronic renal failure _... Steroids (e.g., prednisone), splenectomy, cytotoxic agents (e.g., azathioprine), or transfusions-for autoimmune hemolytic anemia _... Analgesics (for painful crises)-for sickle-cell anemia _... Cessation of offending drugs-for acquired forms of sideroblastic anemia _... Iron replacement _... Transfusions _... Treatment of underlying disorders

Complementary and Alternative Therapies

 Most cases of macrocytic and microcytic anemias may respond well to nutritional therapy. Patients need to be counseled that excess iron is toxic and should not be taken unless indicated by abnormal lab values. Herbal and dietary treatments may be helpful as adjunctive.

Nutrition

 _... Ferrous fumerate, glycerate or glycinate (100 mg/day for three to six months) are the most absorbable forms of iron. Ferrous sulfate (325 mg/day) is poorly absorbed and more frequently causes problems with GI upset and/or constipation. Dietary sources of iron include meat, beans, green leafy vegetables, beet greens, blackstrap molasses, almonds, and brewer's yeast. _... Vitamin C-for pernicious anemia, up to 1,000 mg tid will aid in absorption of iron. _... Vitamin B12-cyanocobalamine, 1,000 IU intramuscular injection bid for one week, then weekly for one month, then every two to three months. (Note that dosing varies depending on individual case.) Dietary sources include organ meats, meats, eggs, fish, and cheese. _... Folic acid (1 to 2 mg/day)-for folic acid deficiency and hereditary spherocytosis. Good food sources include green leafy vegetables and grains. _... Omega-3 and omega-6 essential fatty acids (1,000 to 1,500 IU) have been shown to decrease the frequency of sickle-cell crisis. EFAs can increase clotting times so may need to be checked in people on anticoagulants.

EXPECTATIONS (PROGNOSIS)
The outcome depends upon the type of hemolytic anemia.
COMPLICATIONS

The complications vary with the specific type of hemolytic anemia. Severe anemia can cause cardiovascular collapse. Severe anemias can aggravate pre-existing heart disease, lung disease, or cerebrovascular disease.

Courtesy:

Compiled and Shared By: Habib Anwar 

habib.anwar@hotmail.com