ANEMIA, MEGALOBLASTIC ANEMIA, B12 DEFICIENCY, FOLIC ACID DEFICIENCY,

ANEMIA OF CHRONIC DISEASE , APLASTIC ANEMIA, ACUTE /CHRONIC BLOOD LOSS, SICKLE CELL DISEASE

Zoya Minasyan, RN-MSN-Edu

Anemia

A deficiency in the Number of erythrocytes

(red blood cells [RBCs]) Quantity of hemoglobin Volume of packed RBCs (hematocrit)

Diverse causes such as Blood loss Impaired production of erythrocytes Increased destruction of erythrocytes

Causes of Anemia; GI

Anemia

RBC function Transport oxygen (O2) from lungs to systemic

tissues Carry carbon dioxide from the tissues to the

lungs

Anemia

Classified as Morphologic

Cellular characteristics (erythrocyte size and color )

Descriptive, objective laboratory information Etiologic

Underlying cause (clinical conditions)

Anemia: Clinical Manifestations

Caused by the body’s response to tissue hypoxia

Hemoglobin (Hb) levels are used to determine the severity of anemia.

•Mild states of anemia (Hb 10 to 14 g/dL) may exist without causing symptoms. Symptoms include palpitations, dyspnea, and mild fatigue.

• In cases of moderate anemia (Hb 6 to 10 g/dL), cardiopulmonary symptoms are increased and the patient may experience them while resting, as well as with activity.

•The patient with severe anemia (Hb less than 6 g/dL) has many clinical manifestations involving multiple body systems.

Anemia: Manifestations Pallor

↓ Hemoglobin ↓ Blood flow to the skin

Jaundice ↑ Concentration of serum bilirubin Pruritus (Itching) ↑ Serum and skin bile salt concentrations

Additional attempts by the heart and lungs to provide adequate O2 to the tissues

Cardiac output maintained by increasing the heart rate and stroke volume

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Megaloblastic Anemias

Group of disorders caused by impaired DNA synthesis

Characterized by the presence of large RBCs (megaloblasts) Easily destroyed because of fragile cell

membrane Majority result from deficiency in

Cobalamin (vitamin B12) Folic acid

Megaloblastic Anemias

Classification Cobalamin (vitamin B12) deficiency Folic acid deficiency Drug-induced suppression of DNA synthesis Inborn errors Erythroleukemia

Cobalamin Deficiency Intrinsic factor (IF)

Protein secreted by the parietal cells of the gastric mucosa

IF is required for cobalamin absorption in the small intestine.

Causes Pernicious anemia Gastrectomy Nutritional deficiencies Chronic alcoholism Hereditary enzymatic defects

Cobalamin Deficiency: Etiology

GI surgery Chronic diseases of the GI tract Long-term users of H2-histamine

receptor blockers Absence of IF

Cobalamin Deficiency Clinical Manifestations

General symptoms of anemia Sore tongue Anorexia Nausea/Vomiting Abdominal pain Neuromuscular manifestations

Weakness Paresthesias of the feet and hands ↓ Vibratory and position senses Ataxia (lack of muscle coordination) Muscle weakness Impaired thought processes

Cobalamin Deficiency: Collaborative Care

Parenteral or intra-nasal administration of cobalamin

Important to emphasize adequate dietary intake

• The dosage and frequency of cobalamin administration may vary. A typical treatment schedule consists of 1000 mg of cobalamin IM daily for 2 weeks and then weekly until the hematocrit is normal, then monthly for life.

• High-dose oral cobalamin and sublingual cobalamin are also available for those in whom GI absorption is intact.

• As long as supplemental cobalamin is used, the anemia can be reversed. However, if the person has had long-standing neuromuscular complications, they may not be reversible.

Cobalamin Deficiency: Nursing Management

Early detection and treatment.

Ensure that injuries are not sustained because of the patient’s diminished sensation to heat and pain.

Compliance with treatment. Evaluate patient for gastric

carcinoma.

Folic Acid Deficiency

Also a cause of megaloblastic anemia Folic acid is required for DNA

synthesis. RBC formation and maturation Common causes

Dietary deficiency Malabsorption syndromes Drugs Increased requirement Alcohol abuse and anorexia Loss during hemodialysis

Folic Acid Deficiency

Clinical manifestations are similar to those of cobalamine deficiency.

Absence of neurologic problems Treated by replacement therapy

Encourage patient to eat foods with large amounts of folic acid.

•GI disturbances include dyspepsia (upset stomach or indigestion) and a smooth, beefy red tongue.

•During diagnostic studies, the serum folate level is low (normal is 3 to 25 mg/mL)

•Replacement therapy: The usual dose is 1 mg per day by mouth. In malabsorption states, up to 5 mg per day may be required.

Anemia of Chronic Disease

Underproduction of RBCs Mild shortening of RBC survival Causes

End-stage renal disease Primary factor: ↓ Erythropoietin

Chronic liver disease Chronic inflammation Malignant tumors Chronic endocrine diseases

Anemia of Chronic Disease

Treating underlying cause. Rarely blood transfusions. Erythropoietin therapy

Erythropoietin therapy (Epogen, Darbepoetin) is used for anemia related to renal disease and may be used for anemia related to cancer and its therapies. However, it is used conservatively because the risk of thromboembolism and mortality is increased in some patients.

Aplastic Anemia

Pancytopenia Decrease in all blood cell types

RBCs White blood cells (WBCs) Platelets

Hypocellular bone marrow Types

Congenital Chromosomal alterations

Acquired Results from exposure to ionizing radiation,

chemical agents, viral and bacterial infections

Aplastic Anemia: Clinical Manifestations

Abrupt or gradual development Symptoms caused by suppression of any or all

bone marrow elements General manifestations of anemia

Fatigue, dyspnea Cardiovascular and cerebral responses Neutropenia-low neutrophil count (WBC, fighting

disease) The patient with neutropenia is susceptible to infection

and is at risk for septic shock and death. Even a low-grade temperature (>100.4o F) should be considered a medical emergency.

Treatment options Hematopoietic stem cell transplantation Immunosuppressive therapy

Acute Blood Loss

Result of sudden hemorrhage Trauma Complications of surgery Disrupted vascular integrity

Concerns Hypovolemic shock Reduced plasma volume

Diminished O2 because fewer RBCs are available

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Acute Blood LossClinical Manifestations

Cause Body’s attempt to maintain adequate blood

volume and O2

Pain Internal hemorrhage Tissue distention, organ displacement, nerve

compression Retroperitoneal bleeding

Numbness Pain in the lower extremities

Shock is the major complication22

Acute Blood LossCollaborative Care

Replacing blood volume to prevent shock Identifying the source of the hemorrhage Stopping blood loss Correcting RBC loss Providing supplemental iron

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Acute Blood LossNursing Management

May be impossible to prevent if caused by trauma

Postoperative patients Monitor blood loss.

No need for long-term treatment

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Chronic Blood Loss

Reduced iron stores Bleeding ulcer Hemorrhoids Menstrual and postmenopausal blood loss

Management Identify source. Stop bleeding. Use supplemental iron if needed.

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Hemolytic Anemia

Destruction or hemolysis of RBCs at a rate that exceeds production

Intrinsic hemolytic anemia Abnormal hemoglobin Enzyme deficiencies RBC membrane abnormalities

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Hemolytic Anemia

Extrinsic hemolytic anemia More common than intrinsic Acquired

Sites of hemolysis Intravascular Extravascular

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Sequences of Events in Hemolysis

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Hemolytic Anemia

Jaundice Destroyed RBCs cause increased bilirubin.

Enlarged spleen and liver Hyperactive with macrophage phagocytosis of

defective RBCs Accumulation of hemoglobin molecules

can obstruct renal tubules. Tubular necrosis

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Sickle Cell Disease (SCD)

Group of inherited, autosomal recessive disorders

Presence of an abnormal form of hemoglobin in the erythrocyte

Hemoglobin S (HbS), abnormal HbS causes the RBC to stiffen and

elongate. Sickle shape in response to ↓ O2 levels Substitution of valine for glutamic acid on the β-

globin chain of hemoglobin Genetic disorder Incurable disease, often fatal

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Sickle Cell Hemoglobin Aggregates and Alters Shape of RBC

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Sickle Cell DiseaseClinical Manifestations

Typical patient is asymptomatic, except during sickling episodes.

Symptoms may include Pain and swelling Pallor of mucous membranes Jaundice

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Clinical Manifestations of Sickle Cell Disease

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Sickle Cell Disease: Complications

Gradual involvement of all body systems Usually fatal by middle age from renal

and pulmonary failure Prone to infection

Pneumonia, most common infection Acute chest syndrome

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Sickle Cell Disease: Diagnostic Studies

Peripheral blood smear Sickling test Electrophoresis of hemoglobin(the

movement of charged particles when an electric field is applied to them)

Skeletal x-rays Magnetic resonance imaging (MRI)

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Sickle Cell Disease: Nursing Management

Alleviate symptoms of disease complications. Minimize end target-organ damage. Avoid high altitudes, maintain fluid

intake, treat infections, help with pain control.

O2 for hypoxia and to control sickling Pain management Acute chest syndrome

Antibiotics O2 therapy Fluid therapy Transfusions, if needed

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Sickle Cell Disease: Nursing Management

Blood transfusions in crisis Hydroxyurea: Antisickling agent

Erythropoietin in patients unresponsive to hydroxyurea

Hematopoietic stem cell transplant Can cure some patients with SCD

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Acquired Hemolytic Anemia

Three extrinsic categories1. Physical factors

Physical destruction of RBCs results from extreme force on the cells.Hemodialysis, prosthetic heart valves

2. Immune reactions Antigen-antibody reactions destroy RBCs. Isoimmune reactions

Antibodies develop against antigens; blood transfusions

Autoimmune reactionsDevelop antibodies against their own RBCs

3. Infectious agents and toxins Foster hemolysis in four ways

Invading RBCs and destroying contents Releasing hemolysis substances Generating an antigen-antibody reaction Contributing to splenomegaly 38

Blood cell Disorders: Hemochromatosis

Iron overload disorder Increased intestinal iron absorption and increased tissue

iron deposition Autosomal recessive, C282Y and H63D Early symptoms-fatigue, abdominal pain, weight

loss. Later symptoms-liver enlargement, cirrhosis, skin

pigment change (bronzing), cardio-myopathy, arthritis, testicular atrophy.

Treatment- to remove excess iron from the body(remove 500ml blood each week for 2-3 years until iron stores are normal in body)

Avoid vitamin C and iron supplements, uncooked seafood.

Problem with Hemostasis

Involves the vascular endothelium, platelets, and coagulation factors, which helps to stop hemorrhage and repair vascular injury.

Three major disorders Thrombocytopenia (low platelet count) Hemophilia (disorder of clotting factors) Disseminated intravascular coagulation (DIC)

Thrombocytopenia

Reduction of platelets Prolonged bleeding from minor trauma Nursing

Monitor for s/s of bleeding Monitor for PT, PTT, fibrinogen, platelets count Avoid injections (IV, IM, SubQ) to prevent bleeding Protect from trauma, Administer blood products Stop anticoagulants Avoid high impact activity (aerobics, contact

sports)

Hemophilia

X-linked recessive genetic disorder Deficient coagulation factor Hemophilia A caused by Factor VIII

deficiency Hemophilia B factor IX deficiency Complications related to prolonged

bleeding, uncontrolled hemorrhage after dental extractions, GI bleeding from gastritis or ulcers, ecchymosis or hematomas; pain, paralysis from compression of nerves

Replacement of clotting factors

Disseminated intravascular coagulation (DIC)

Decrease in clotting factor and platelets, which may lead to hemorrhage.

Is always caused by and underlining disease or condition. The underlining cause must be treated for the DIC to resolve.

Assess for petechiae, oozing at IV site, internal bleeding, heart rate, increasing in abd girth, change in mental status, pain, decrease in urine output.

Administer blood product.