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close this bookStandard Treatment Guidelines for District Hospital - Ethiopia (DACA; 2004; 277 pages)
View the documentACKNOWLEDGEMENTS
View the documentABBREVIATIONS/NOTATIONS*
View the documentFOREWORD
Open this folder and view contentsChapter 1: INTRODUCTION
Open this folder and view contentsChapter 2: INFECTIOUS DISEASES
Open this folder and view contentsChapter 3: SEXUALLY TRANSMITTED DISEASES
Open this folder and view contentsChapter 4: COMMON SKIN PROBLEMS
close this folderChapter 4: NON-INFECTIOUS DISEASES
View the documentAcute Pulmonary Edema
View the documentAnemia
View the documentAnxiety Disorder
View the documentArrhythmia (Common Rhythm disorders)
View the documentAtrioventricular (AV) Block
View the documentBronchial Asthma
View the documentConstipation
View the documentDiabetic Keto Acidosis
View the documentDiabetes Mellitus
View the documentEpilepsy
View the documentGout
View the documentHeart Failure
View the documentHemorrhoids
View the documentHypertension
View the documentImmune Thrombocytopenic Purpura (ITP)
View the documentMigraine
View the documentMood Disorders
View the documentMyocardial Infarction
View the documentNausea and Vomiting
View the documentNon-Ulcer Dyspepsia
View the documentOsteoarthritis
View the documentPeptic Ulcer (PUD)
View the documentPortal Hypertension
View the documentRheumatic Fever
View the documentRheumatic Heart Disease (Chronic)
View the documentRheumatoid Arthritis
View the documentSchizophrenia
View the documentThyrotoxicosis
Open this folder and view contentsChapter 6: OBSTETRICS AND GYNECOLOGICAL CONDITIONS
Open this folder and view contentsChapter 7: PEDIATRIC DISEASES
Open this folder and view contentsChapter 8: ACUTE /EMERGENCY CONDITIONS
Open this folder and view contentsANNEXES
 

Anemia

Megaloblastic Anemia

Megaloblastic anemia (MA) is a descriptive morphologic term that refers to abnormal hematopoiesis characterized by dyssynchronous nuclear and cytoplasmic maturation. More than 95% of megaloblastic anemias are due to deficiency or deranged metabolism of either cobalamin (vitamin B12) or folate. Folate deficiency MA is more common in Ethiopians. All the causes of megaloblastic anemia produce a common set of hematologic, laboratory and histologic abnormalities in the host. Folate deficient patients are usually malnourished. Neuropsychiatric manifestations are encountered in cobalamin deficiency, but not in folate deficiency states.

Diagnosis:

1. Complete blood count and red blood cell indices
2. Peripheral blood smear examination and reticulocyte count
3. Serum cobalamin and folate levels and RBC folate content
4. Bone marrow aspiration and/or biopsy


Treatment:

General:

• Correctable or treatable causes must be identified and accordingly dealt with.
• Patients should be advised to take dairy products (cobalamin) and green vegetables (folate).


Drug Treatment:

Specific therapy is directed toward replacing the deficient factor.


Vitamin B12 (cobalamin)

A typical regimen for the correction of vitamin B12 deficiency is the administration of 1 mg vitamin B12 i.m. twice during the first week, followed by 1 mg weekly until the blood count is normal.Treatment (1 mg every 2-3 months) is continued for life if the cause cannot be corrected.

S/E: Itching, fever chills, hot flushes, nausea and dizziness.

Dosage forms: Injection, 100 mcg/ml, 1000 mcg/ml in 1 ml ampoule.


Folic Acid

Folate deficiency MA is treated with folate replacement therapy, 5 mg per os for 4 months; child up to 1 year, 500 micrograms/kg daily; over 1 year, as adult dose. Higher doses may be required in malabsorption states.

C/I: Folate-dependent malignancies

Dosage forms: Tablet, 200 mcg, 1 mg, 5 mg; injection, 5 mg/ml in 1 ml ampoule.

Caution: Folic acid should never be given without vitamin B12 in undiagnosed megaloblastic anemia or other vitamin B12 deficiency states.


Note:

The hematologic picture normalizes in about 2 months in both cobalamin and folate replacement therapy. Large doses of folate may produce hematologic response in cobalamin deficiency states. This masks the cobalamin deficiency state and allows the neurologic damage to progress. Therefore, if both folate and cobalamin are deficient, cobalamin is administered first, followed by folate.


Anemia

Iron Deficiency Anemia (IDA)

Iron deficiency denotes a deficit in total body iron resulting from iron requirements that exceed its supply. IDA is a manifestation of an underlying disease condition and is not in itself a complete diagnosis. Common causes of IDA include: increased iron requirements (growth-spurt, pregnancy and lactation), blood loss (blood donation, frequent phlebotomy, chronic bleeding), worm infestation (hookworm), and inadequate iron supply (malnutrition, malabsorption). The symptoms of IDA include fatigue, giddiness, headache, tinnitus, palpitations, sore tongue and dysphagia and are not specific to IDA.

Diagnosis:

1. Complete blood count and red blood cell indices
2. Peripheral blood smear examination and reticulocyte count
3. Serum ferritin level and bone marrow iron studies
4. Stool for ova and parasites and occult blood, digital per rectum examination, upper and lower GI radiologic and endoscopic studies, and genitourinary gynecologic and urologic examinations complete the workup of a patient with IDA.


Treatment:

General:

• The underlying cause of anemia should be identified and treated or corrected.

• Patients should be encouraged to take diet with optimal bioavailable iron such as meat.

• Patients with symptomatic anemia (such as congestive heart failure) should be transfused packed red blood cells, cautiously.


Drug Treatment

First Line

Ferrous sulfate, 325 mg tablets (65 mg elemental iron), or any other iron salt, taken tid between meals to maximize absorption is the treatment of choice. Treatment is continued for at least 3 months following correction of the anemia to replenish iron stores.

S/E: Nausea, abdominal cramps and dyspeptic symptoms, constipation or diarrhea. For patients who do not tolerate ferrous sulfate tablets, they may be advised to take it with meals, or to start a smaller dose, or to change the brand to ferrous gluconate or fumarat tablets or elixir forms.

D/I: Antacids, tetracyclines, chloramphenicol, and quinolone antibiotics interfere with the absorption and metabolism of iron.


Alternative

Iron dextran, 50 mg/ml in 2 ml ampoule; administered by deep i.m. injection. The amount of iron required for i.v. administration can be calculated from the deficit and an additional of 500 to 1000mg iron is added to replenish the iron stores. Total dose of iron to be injected in mg = Body weight (kg) x 2.3x (15 - patient's Hb) + 500-1000 mg.

S/E: pain, swelling, and staining at site of injection; nausea, vomiting and taste disturbances; hypersensitivity reactions.

C/I: history of allergic reactions (including asthma); severe hepatic or renal impairment; pregnancy.

Dosage forms: Injection, 50 mg/ml in 2 ml ampoule


Note:

Iron parenteral therapy is rarely indicated; indications include oral iron intolerance despite modifications in dosage and regimen, malabsorption, presence of an inflammatory bowl and active peptic ulcer disease, inability or unwillingness by the patient to take oral iron. A dose of 25mg (0.5ml) IV is given first to test for a hypersensitivity reactions and the patient is observed closely for possible complications.

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