Megaloblastic anemia
Causes :
•Vit B12 (cobalamine) def. including Pernicious anemia
Vit B12 def : (2-3mg/day)
Ø ↓ intake, vegetarianism
Ø ↓ absorption – IF def, gastrectomy, malabs, fish tape worm infestation
Ø ↑ requirement – pregnancy, cancer
•
•Folate (folic Acid) deficiency
Ø Folate def : (50-200mg/day)
Ø Alcohol, malabsorption, pregnancy, cancer, folate antagonists(anticonvulsants, oral contraceptives)
Unresponsive to B12 & folate therapy – methotrexate,
Pernicious anemia, the most common type of megaloblastic anemia, is caused by malabsorption of vitamin B12. AGE ALERT Onset typically occurs between the ages of 50 and 60 years, and incidence increases with age. It's rare in children. If not treated, pernicious anemia is fatal. Its manifestations subside with treatment, but some neurologic deficits may be permanent.
Pathophysiology
Pernicious anemia is characterized by decreased production of hydrochloric acid in the stomach, and a deficiency of intrinsic factor, which is normally secreted by the parietal cells of the gastric mucosa and is essential for vitamin B12 absorption in the ileum. The resulting vitamin B12 deficiency inhibits cell growth, particularly of RBCs, leading to production of few, deformed RBCs with poor oxygen-carrying capacity. It also causes neurologic damage by impairing myelin formation.
Possible causes of pernicious anemia include:
Ø genetic predisposition (suggested by familial incidence)
Ø immunologically related diseases, such as thyroiditis, myxedema, and Graves' disease (significantly higher incidence in these patients)
Ø partial gastrectomy (iatrogenic induction)
Ø older age (progressive loss of vitamin B12 absorption).The elderly often have a dietary deficiency of B12 in addition to or instead of poor absorption.
Characteristically, pernicious anemia has an insidious onset but eventually causes an unmistakable triad of symptoms:
Ø weakness due to tissue hypoxia
Ø sore tongue due to atrophy of the papillae
Ø numbness and tingling in the extremities as a result of interference with impulse transmission from demyelination.
Other common manifestations include:
Ø pale appearance of lips and gums
Ø faintly jaundiced sclera and pale to bright yellow skin due to hemolysis-induced hyperbilirubinemia
Ø high susceptibility to infection, especially of the genitourinary tract.
Ø Pernicious anemia may also have gastrointestinal, neurologic, and cardiovascular effects.
Gastrointestinal symptoms include:
Ø nausea, vomiting, anorexia, weight loss, flatulence, diarrhea, and constipation from disturbed digestion due to gastric mucosal atrophy and decreased hydrochloric acid production
Ø gingival bleeding and tongue inflammation (may hinder eating and intensify anorexia).
Neurologic symptoms include:
Ø neuritis; weakness in extremities
Ø peripheral numbness and paresthesia
Ø disturbed position sense
Ø lack of coordination; ataxia; impaired fine finger movement
Ø positive Babinski and Romberg signs
Ø light-headedness
Ø altered vision (diplopia, blurred vision), taste, and hearing (tinnitus); optic muscle atrophy
Ø loss of bowel and bladder control; and, in males, impotence, due to demyelination (initially affects peripheral nerves but gradually extends to the spinal cord) caused by vitamin B12 deficiency
Ø irritability, poor memory, headache, depression, and delirium (some symptoms are temporary, but irreversible central nervous system [CNS] changes may have occurred before treatment).
Cardiovascular symptoms include:
Ø low hemoglobin levels due to widespread destruction of RBCs caused by increasingly fragile cell membranes
Ø palpitations, wide pulse pressure, dyspnea, orthopnea, tachycardia, premature beats, and, eventually, heart failure due to compensatory increased cardiac output.
Possible complications include:
Ø hypokalemia (first week of treatment)
Ø permanent CNS symptoms (if the patient is not treated within 6 months of appearance of symptoms)
Ø gastric polyps
Ø stomach cancer.
Laboratory screening must rule out other anemias with similar symptoms but different treatments, such as:
Ø folic acid deficiency anemia
Ø vitamin B12 deficiency resulting from malabsorption due to GI disorders, gastric surgery, radiation, or drug therapy.
Ø Decreased hemoglobin levels by 1 to 2 g/dl in elderly men and slightly decreased hematocrit in both men and women reflect decreased bone marrow and hematopoiesis and, in men, decreased androgen levels; they aren't an indicator of pernicious anemia.
Diagnosis of pernicious anemia is established by:
Ø positive family history
Ø hemoglobin 4 to 5 g/dl
Ø low RBC count
Ø mean corpuscular volume greater than 120 µl due to increased amounts of hemoglobin in larger-than-normal RBCs
Ø serum vitamin B12 less than than 0.1 µg/ml
Ø bone marrow aspiration showing erythroid hyperplasia (crowded red bone marrow), with increased numbers of megaloblasts but few normally developing RBCs
Ø gastric analysis showing absence of free hydrochloric acid after histamine or pentagastrin injection
Ø Schilling test for excretion of radiolabeled vitamin B12 (definitive test for pernicious anemia)
Stage I
—Oral dose – radiolabelled, 1ug
—Parenteral dose – 4mg
—24 hr urine – N >7%, ↓ PA
Stage II : repeat with IF supplements
Stage III : if I & II abnormal, repeat after course of antibiotics / antimicrobial
o Used to detect lack of intrinsic factor
o Fast client for 6-12hrs
o A radioactive Vit B12 is given by mouth and nonradioactive B12 IM to saturate tissue binding site and permit excretion of radioactive via urine
o 24-48 hr urine collection-encourage fluid intake
o If indicated, repeat after 1 week w/ intrinsic factors
Ø serologic findings including intrinsic factor antibodies and antiparietal cell antibodies.
Treatment for pernicious anemia is:
Ø early parenteral vitamin B12 replacement (can reverse pernicious anemia, minimize complications, and possibly prevent permanent neurologic damage)
Ø concomitant iron and folic acid replacement to prevent iron deficiency anemia (rapid cell regeneration increases the patient's iron and folate requirements)
Ø after initial response, decrease vitamin B12 dosage to monthly self-administered maintenance dose (treatment must be given for life)
Ø bed rest for extreme fatigue until hemoglobin rises
Ø blood transfusions for dangerously low hemoglobin
Ø digoxin (Lanoxin), diuretic, low-sodium diet (if patient is in heart failure)
Ø antibiotics to combat infections.
Assessment for Folic Acid Deficiency:
Folic acid deficiency:
Serum folic acid ↓
Ø —FIGLU in urine
Ø ↑ (intermediate product in conversion of histidine to glutamate)
Bone Marrow assessment for megaloblastic anemia :
Ø hypercellular, may completely replace the fatty marrow
Ø Megaloblasts – larger in size, open seive-like chromatin and well hemoglobinized cytoplasm
Ø Giant metamyelocytes and band forms
Ø Megakaryocytes – large and bizarre multilobate nuclei
Treatment for megaloblastic anemia
Ø Drug therapy
Ø Vit B12 injections for monthly maintenance
Ø Folic acid supplements
Ø Transfusion therapy
Nursing Intervention For Megaloblastic Anemia
Ø Provide diet high in protein, iron and vitamins
Ø Avoid seasoned or hot foods if client has mouth sores
Ø Provide mouth care w/ soft toothbrush and non irritating rinses
Ø Safety precautions
Ø Bed rest
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