Anemia

Anemia 150 150 Tony Guo

Anemia

 

  • A deficiency in
    • Number of erythrocytes (RBCs)
    • Quantity of hemoglobin
    • Volume of packed RBCs (hematocrit)
  • RBC function
    • Transport oxygen (O2) from lungs to systemic tissues 
    • Carry carbon dioxide from tissues to lungs
  • Not a specific disease 
  • Manifestation of a pathologic process
  • Diagnosed based on 
    • Complete blood count (CBC)
    • Reticulocyte count
    • Peripheral blood smear

 

Cause of anemia

  • Decreased RBC production
    • Deficient nutrients
      • Iron
      • Cobalamin
      • Folic acid
    • Decreased erythropoietin
    • Decreased iron availability
  • Blood loss
    • Chronic
      • Bleeding duodenal ulcer
      • Colorectal cancer
      • Liver disease
    • Acute
      • Acute trauma
      • Ruptured aortic aneurysm
      • GI bleeding
  • Increased RBC destruction
    • Hemolysis
      • Abnormal hemoglobin (Sickle cell disease)
      • Medication (e.g., methyldopa [Aldomet]) and chemicals (e.g., chemotherapy, lead)
      • Incompatible blood
        • Antibodies against RBCs
      • Physical destruction
        • Prosthetic heart valves
        • Extracorporeal circulation
        • Disseminated intravascular coagulopathy (DIC)
        • Thrombotic thrombocytopenic purpura (TTP)
      • Trauma (e.g., cardiopulmonary bypass)
      • Infectious agents (e.g., malaria) and toxins
      • Radiation

 

Erythrocyte production

  • Life span of an RBC is 120 days
  • Three alterations in erythropoiesis may decrease RBC production:
    • Decreased hemoglobin synthesis 
    • Defective DNA synthesis in RBCs
    • Diminished availability of erythrocyte precursors

 

Hematologic problems

  • Sickle cell disease has a high incidence among African Americans.
  • Thalassemia has a high incidence among African Americans and people of Mediterranean origin.
  • Tay-Sachs disease has the highest incidence in families of Eastern European Jewish origin, especially the Ashkenazi Jews.
  • Pernicious anemia has a high incidence among Scandinavians and African Americans.

 

Clinical manifestations

  • Caused by body’s response to tissue hypoxia
    • Manifestations vary based on rate of development, severity of anemia, presence of co-existing disease
  • Hemoglobin (Hgb) levels are used to determine severity of anemia

Integumentary manifestations

  • Pallor
    • Decreased hemoglobin 
    • Decreased blood flow to the skin
  • Jaundice
    • Increased concentration of serum bilirubin
  • Pruritus 
    • Increased serum and skin bile salt concentrations

Cardiopulmonary manifestation

  • Result from additional attempts by heart and lungs to provide adequate O2 to tissues
  • Cardiac output maintained by increasing heart rate and stroke volume

 

Nursing assessment

  • Subjective Data
    • Important health information
      • Past health history
      • Medications 
      • Surgery or other treatments
      • Dietary history
    • Functional health patterns

Nursing diagnosis and planning

  • Fatigue related to inadequate oxygenation of the blood
  • Imbalanced nutrition: less than body requirements related to inadequate nutritional intake and anorexia
  • Ineffective health management related to lack of knowledge about appropriate nutrition and medication regimen
    • Assume normal activities of daily living
    • Maintain adequate nutrition
    • Develop no complications related to anemia

Nursing interventions

  • Patients with fatigue
    • Alternate rest and activity
    • Prioritize activities 
      • Accommodate energy levels
      • Maximize O2 supply for vital functions
    • Provide assistance to minimize risk for injury
    • Evaluate nutritional needs

 

Nutritional therapy for erythropoiesis

Nutrient Role Source
Cobalamin (Vitamin B12) RBC maturation Red meats, especially liver, eggs, enriched grain products, milk and dairy foods, fish
Copper Mobilization of iron from tissues to plasma Shellfish, whole grains, beans, nuts, potatoes, organ meats
Folic Acid RBC maturation Green leafy vegetables, liver, meat, fish, legumes, whole grains, orange juice, peanuts, avocado
Iron Hemoglobin synthesis Liver and muscle meats, dried fruits, legumes, dark green leafy vegetables, whole-grain and enriched bread and cereals, beans
Niacin RBC maturation Peanut butter, beans, meats, avocado; enriched and fortified grains
Pantothenic Acid (Vitamin B5) Heme synthesis Meats, vegetables, cereal grains, legumes, eggs, milk
Pyridoxine (Vitamin B6) Heme synthesis Meats, fortified cereals, whole grains, legumes, potatoes, cornmeal, bananas, nuts
Riboflavin (Vitamin B2) Oxidative reactions Milk and dairy foods, enriched bread and other grain products, salmon, chicken, eggs, green leafy vegetables
Vitamin E Heme synthesis 

Protection against oxidative damage to RBCs

Vegetable oils, meat, eggs, wheat germ, whole-grain products, seeds, nuts, peanut butter
Amino Acids Heme and plasma membrane synthesis Eggs, meat, milk and milk products (cheese, ice cream), poultry, fish, legumes, nuts, tofu
Ascorbic Acid (Vitamin C) Conversion of folic acid to its active forms, aids in iron absorption Citrus fruits, green leafy vegetables, strawberries, potatoes, kiwi fruit

 

Iron-deficiency anemia

  • Inadequate dietary intake
    • 5% to 10% of ingested iron is absorbed
  • Malabsorption 
    • Iron absorption occurs in the duodenum
    • Diseases or surgery that alter, destroy, or remove absorption surface of this area of intestine cause anemia
  • Blood loss
    • 2 mL whole blood contain 1 mg iron
    • Major cause of iron deficiency in adults
    • Chronic blood loss most commonly through GI and GU systems
  • Hemolysis
  • Pregnancy contributes to this condition
  • At-risk groups
    • Premenopausal women
    • Pregnant women
    • Persons from low socioeconomic backgrounds
    • Older adults
    • Individuals experiencing blood loss

Clinical manifestations

  • General manifestations of anemia 
    • Pallor is most common
    • Glossitis is second
      • Inflammation of tongue
    • Cheilitis is also found
      • Inflammation of lips

Diagnostic studies

  • Laboratory findings
    • Hgb, Hct, MCV, MCH, MCHC, reticulocytes, serum iron, TIBC, bilirubin, platelets
  • Stool occult blood test
  • Endoscopy 
  • Colonoscopy

Interprofessional care

  • Goal 
    • Treat underlying disease causing reduced intake or absorption of iron
  • Replace iron
    • Nutritional therapy
    • Oral iron supplements
    • Transfusion of packed RBCs

Drug therapy

  • Parenteral iron
    • Indicated for malabsorption, oral iron intolerance, need for iron beyond normal limits, poor patient compliance
    • Can be given IM or IV
    • IM may stain skin
      • Z-track

 

Anemia caused by blood loss (Acute and Chronic)

  • Anemia resulting from blood loss may be caused by either acute or chronic problems
    • Acute blood loss occurs as a result of sudden hemorrhage
    • Sources of chronic blood loss are similar to those of iron-deficiency anemia
  • Acute blood loss
    • Causes of sudden hemorrhage 
      • Trauma
      • Complications of surgery
      • Conditions or diseases that disrupt vascular integrity
        • Hypovolemic shock 
        • Compensatory increased plasma volume with diminished O2 -carrying RBCs
    • Clinical manifestations
      • Pain
        • Internal hemorrhage
  • Tissue distention, organ displacement, nerve compression
  • Retroperitoneal bleeding
  • Numbness 
  • Pain in lower extremities
  • Shock is major complication
  • Diagnostic studies
    • With sudden blood volume loss, values may seem normal or high for 2 to 3 days
    • Once plasma volume is replaced, low RBC concentrations become evident
      • Low RBC, Hgb, and Hct levels show up and reflect actual blood loss
  • Interprofessional care
    • Replacing blood volume to prevent shock
    • Identifying source of hemorrhage and stopping blood loss
    • Correcting RBC loss 
    • Providing supplemental iron
    • May be impossible to prevent if caused by trauma
    • Postoperative patients
      • Monitor blood loss
      • Administer blood products for anemia
    • No need for long-term treatment

 

Hemolytic Anemia

  • General manifestations of anemia
  • Specific manifestations including
    • Jaundice
    • Enlargement of the spleen and liver
  • Maintenance of renal function is a major focus of treatment

 

Sickle Cell Disease

  • Group of inherited, autosomal recessive disorders
    • Characterized by presence of an abnormal form of Hgb in RBC 
    • Genetic disorder usually identified during routine neonatal screening
    • Incurable and often fatal by middle age

Etiology and pathophysiology

  • Abnormal hemoglobin, HgbS, causes the RBC to stiffen and elongate
    • Erythrocytes take on a sickle shape in response to decrease O2 levels
    • Substitution of valine for glutamic acid on the β-globin chain of hemoglobin
  • Types of SCD
    • Sickle cell anemia
      • Most severe
      • Homozygous for hemoglobin S (HgbSS)
    • Sickle cell thalassemia
    • Sickle cell HgbC disease
    • Sickle cell trait (HgbAS)
  • Sickle cell hemoglobin aggregates and alters shape of RBC
Normal red blood cells Sickled red blood cells
Normal hemoglobin Sickle cell hemoglobin forms long and inflexible chains
Normal RBCs are compact and flexible, enabling them to squeeze through small capillaries Sickled RBCs are stiff and angular, causing them to become stuck in small capillaries
  • Sickling episodes
    • The major pathophysiologic event of this disease
      • Triggered by low O2 tension in blood
      • Infection is most common precipitating factor
      • Initially, sickling is reversible with re-oxygenation
    • Sickling episodes are most commonly triggered by low oxygen tension in the blood. 
    • Hypoxia or deoxygenation of the RBCs can be caused by viral or bacterial infection, high altitude, emotional or physical stress, surgery, and blood loss. 
    • Infection is the most common precipitating factor. Other events that can trigger or sustain a sickling episode include dehydration, increased hydrogen ion concentration (acidosis), increased plasma osmolality, decreased plasma volume, and low body temperature. A sickling episode can also occur without an obvious cause.
    • Initially the sickling of cells is reversible with reoxygenation, but it eventually becomes irreversible because of cell membrane damage from recurrent sickling. 
    • Thus vaso-occlusive phenomena and hemolysis are the clinical hallmarks of sickle cell disease.
  • Sickle cell crisis
    • Severe, painful, acute exacerbation of sickling causes a vaso-occlusive crisis
    • Severe capillary hypoxia eventually leads to tissue necrosis
    • Life-threatening shock is a result of severe O2 depletion of the tissues and a reduction of the circulating fluid volume

Clinical manifestations

  • Typical patient is asymptomatic except during sickling episodes
  • Symptoms may include 
    • Pain from tissue hypoxia and damage
    • Pallor of mucous membranes
    • Jaundice from hemolysis 
      • Prone to gallstones (cholelithiasis)

Complications

Body organ Complications
Brain Thrombosis or hemorrhage causing paralysis, sensory deficits, death
Eye Hemorrhage

Retinal detachment

Blindness

Retinopathy

Lung Acute chest syndrome

Pulmonary hypertension

Pneumonia

Heart  Heart failure
Liver and gallbladder Hepatomegaly

Gallstones

Spleen Splenic atrophy (autosplenectomy)
Kidney Hematuria

Renal failure

Bones and joints Hand-foot syndrome

Osteonecrosis

Penis Priapism
Skin Stasis ulcers of hands, ankles, and feet
  • Infection is a major cause of morbidity and mortality
    • Function of spleen becomes compromised from sickled RBCs
      • Autosplenectomy is a result of scarring
    • Pneumococcal pneumonia most common
    • Severe infections can cause aplastic crisis
      • Can lead to shutdown of RBC production
  • Acute chest syndrome
    • Pulmonary complications that include pneumonia, tissue infarction, and fat embolism
    • Characterized by fever, chest pain, cough, pulmonary infiltrates, and dyspnea
    • Leads to multiple serious complications

Nursing and Interprofessional management

  • Care is directed toward
    • Prevention of sequelae from disease
    • Alleviating manifestations from complications
    • Minimizing end-organ damage
    • Promptly treating serious sequelae
  • Hospitalized patients in sickle cell crisis 
    • O2 for hypoxia and to control sickling
    • Vigilance for respiratory failure
    • Rest with DVT prophylaxis
    • Administration of fluids and electrolytes
    • Transfusion therapy
      • Chelation therapy with repeat exacerbations
  • Under-treatment is a major problem
  • Pain management
    • Often pain medication tolerant
    • Require continuous and breakthrough analgesia with morphine and hydromorphone
    • Multimodal and interdisciplinary approach involving emotional and adjunctive measures
  • Treat infections
  • Administer folic acid
  • Hydrea is only antisickling agent shown to be clinically beneficial
  • Hematopoietic stem cell transplantation (HSCT) is only available cure
  • Patient and caregiver teaching and support are important
    • How to avoid crises
    • Importance of prompt medical attention
    • Pain control

 

Patient education

  • Avoidance of high altitudes
  • Maintenance of adequate fluid intake
  • Proper treatment of infections
  • Immunizations for pneumonia, Haemophilus influenzae, influenza, and hepatitis should be given.
  • Direct patient to seek medical attention quickly when symptoms return.

 

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