Digiulio M., Keogh J. Medical-Surgical Nursing Demystified
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CHAPTER 4 Hematologic System
NURSING INTERVENTION
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No IM injections.
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No aspirin.
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To stop bleeding:
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Elevate site.
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Apply direct pressure to the site.
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Explain to the patient:
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Wear a medical alert identification.
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Contact physician for any injury.
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Avoid situations where injury might occur.
Leukemia
WHAT WENT WRONG?
Replacement of bone marrow by abnormal cells results in unregulated proliferation
of immature white blood cells entering the circulatory system. These leukemic cells
may also enter the liver, spleen, or lymph nodes, causing these areas to enlarge.
Leukemia is classified according to the type of cell it is derived from, lymphocytic
or myelocytic, and as either acute or chronic. Lymphocytic leukemias involve imma-
ture lymphocytes originating in the bone marrow and typically infiltrate the spleen,
lymph nodes, or central nervous system. Myelogenous or myelocytic leukemia
involves the myeloid stem cells in the bone marrow and interferes with the matura-
tion of all blood cell types (granulocytes, erythrocytes, thrombocytes).
The exact cause of leukemia is unknown. There is a higher incidence in people
who have been exposed to high levels of radiation, who have had exposure to ben-
zene, or who have a history of aggressive chemotherapy for a different type of can-
cer. There may be a genetic predisposition to develop acute leukemia. Patients
with Down’s syndrome, Fanconi’s anemia, or a family history of leukemia also
have a higher-than-average incidence of this disease.
PROGNOSIS
Patients with acute leukemia typically have a more aggressive disease process,
which may have a shorter course from the time of diagnosis. Patients with chronic
leukemia are more likely to have a less aggressive disease process that runs over
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a longer course. The chronic patients typically have an insidious onset and a bet-
ter prognosis.
HALLMARK SIGNS AND SYMPTOMS
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Acute patients:
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Fatigue and weakness due to anemia
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Fever due to increased susceptibility to infection
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Bleeding, petechiae, ecchymosis (bruising), epistaxis (nosebleed), gingival
(gum) bleeding—due to decreased platelet count
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Bone pain due to bone infiltration and marrow expansion
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Lymph nodes (lymphadenopathy) enlarged as leukemic cells invade nodes
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Liver (hepatomegaly) and spleen (splenomegaly) enlarged as leukemic cells
invade
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Headache, nausea, vomiting, and weight loss
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Papilledema, cranial nerve palsies, seizure if there is central nervous sys-
tem involvement
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Chronic patients:
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Fatigue due to anemia
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Weight loss due to chronic disease process and loss of appetite
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Poor appetite
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Enlarged lymph nodes (lymphadenopathy) due to infiltration of lymph nodes
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Enlarged spleen (splenomegaly) due to involvement of the spleen
INTERPRETING TEST RESULTS
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Low RBC count, low hemoglobin—anemia.
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Low platelet count—thrombocytopenia.
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Elevated WBC count—leukocytosis.
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Abnormal amount of immature WBC shown in bone marrow biopsy.
TREATMENT
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Acute myelogenous leukemia.
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Administer an anthracycline (idarubicin or daunorubicin) plus cytarabine.
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Combination: Daunorubicin, vincristine, prednisone, asparaginase.
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Administer platelet transfusions.
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Administer Filgrastim for neutropenia.
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Administer antibiotics for infections.
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Bone marrow transplant.
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Administer immunosuppressives to avoid transplant rejection.
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Chronic myelogenous leukemia.
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Administer Signal transduction inhibitor:
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Imatinib
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Interferon-α
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Busulfan
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Hydroxyurea
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Chronic lymphocytic leukemia.
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Administer alkylating agents:
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cyclophosphamide
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chlorambucil
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Administer antienoplastics:
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Vincristine
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Prednisone
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Doxorubicin
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Monoclonal antibody targeted therapy:
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alemtuzumab
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Combination of fludarabine and rituxumab.
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Transfusion if hemolytic anemia or bleeding:
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Packed RBCs.
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Whole blood.
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Platelets.
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Bone marrow transplant and immunosuppression.
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High protein diet.
NURSING DIAGNOSES
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Risk for infection
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Chronic pain
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Imbalanced nutrition, less than what body requires
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NURSING INTERVENTION
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Monitor for bleeding—platelet count may be decreased.
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Monitor for infection—patients have increased susceptibility to infection.
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Monitor pain control.
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Small, frequent meals.
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Teach patients about infection control:
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Avoid others with infection.
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Report signs of infection, sore throat, fevers, etc.
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Explain to the patient:
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Use an electric razor.
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Use soft toothbrush.
•
Watch for bleeding or bruising.
Multiple Myeloma
WHAT WENT WRONG?
A malignancy of the plasma cells causes an excessive amount of plasma cells in
the bone marrow. Masses within the bone marrow cause destructive lesions in the
bone. Normal bone marrow function is reduced as the abnormal plasma cells con-
tinue to grow. Immune function is diminished and the patient develops anemia.
The disease typically affects older adults.
PROGNOSIS
Patients are susceptible to infection and often have significant pain from bone
involvement of the disease. The survival time from diagnosis averages about 3 years.
HALLMARK SIGNS AND SYMPTOMS
•
Severe bone pain due to involvement in back or ribs
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Anemia due to invasion of the bone marrow
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Skeletal fractures due to loss of normal bone structure (osteoporosis)
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Increased risk of infection due to bone marrow failure to produce white
blood cells
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Spinal cord compression as mass enlarges
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Renal failure due to protein effect in renal tubules
INTERPRETING TEST RESULTS
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Presence of the Bence Jones protein in urine.
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Serum protein electrophoresis shows a monoclonal protein spike.
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CBC shows anemia.
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Rouleau formation on peripheral smear, a group of RBCs clump together in
a stack (like a stack of coins).
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Abnormal plasma cells in bone marrow biopsy.
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X-rays of bone show lytic lesions.
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Elevated calcium in blood (hypercalcemia).
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Protein in urine (proteinuria).
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Elevated erythrocyte sedimentation rate.
TREATMENT
Treatment regimens undergo changes based on patient response and current research
findings. Combination therapy is common in treatment of multiple myeloma.
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Pain management.
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Combination chemotherapy:
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alkylating agent (melphalan) and prednisone
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thalidomide and dexamethasone
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nonalkylating combination (vincristine, doxorubicin, and dexamethasone)
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proteosome inhibitor (borteozomib) and thalidomide derivative (lena-
lidomide)
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Diet high in protein, carbohydrates, vitamins, and minerals.
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Small frequent meals.
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Transfusion of packed RBCs if anemia is severe.
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Bone marrow transplantation.
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NURSING DIAGNOSES
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Pain
•
Impaired mobility
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Risk for injury
NURSING INTERVENTION
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Protect the patient from falling.
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Monitor input and output due to renal function changes.
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Perform muscle-strengthening exercises.
•
Explain to the patient:
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No lifting.
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Be alert for fractures.
Polycythemia Vera
WHAT WENT WRONG?
A myeloproliferative disorder that results in an overproduction of blood cells and
a thickening of blood. The hallmarks of polycythemia vera include excessive
production of red blood cells, white blood cells, and platelets. The excess of cells
present in the blood causes problems with the flow of blood through vessels,
especially the smaller ones. There will be an increase in peripheral vascular
resistance causing increased pressure, and vascular stasis in the smaller vessels,
potentially causing thrombosis or tissue hypoxia. Organ damage may result
because of these changes.
PROGNOSIS
After diagnosis of polycythemia vera, the average survival time is 10 to 15 years
with appropriate treatment, less than 2 years without treatment. Some patients may
go on to develop acute leukemia. Complications usually arise from thrombosis or
tissue hypoxia.
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CHAPTER 4 Hematologic System
HALLMARK SIGNS AND SYMPTOMS
•
Facial skin and mucous membranes dark and flushed (plethora)
•
Hypertension due to increased peripheral vascular resistance and thickening
of the blood
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Itching worse after warm shower due to histamine release from increased
basophils within dilated vessels
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Headache and difficulty concentrating
•
Vision blurred, tinnitus (ringing in ears), and hearing changes
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Thrombosis due to vascular stasis
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Spleen enlargement (splenomegaly)
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Tissue hypoxia and possible infarction of heart, spleen, kidneys, and brain
due to thrombosis
INTERPRETING TEST RESULTS
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Increased RBC count.
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Increased hemoglobin.
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Increased hematocrit level.
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Increased WBC count.
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Increased basophils.
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Increased eosinophils.
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Increased platelet count.
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Increased uric acid level.
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Increased potassium.
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Increased vitamin B
12
level.
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Bone marrow panhyperplasia; iron stores absent.
TREATMENT
Treatment is aimed at maintaining bloodflow to the smaller vessels and diminish-
ing the amount of excess blood cells being made by the bone marrow.
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Periodic scheduled phlebotomy—the removal of 500 ml of blood—to reduce
the hematocrit level to below 45; may be done weekly.
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Adequate hydration.
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Anticoagulants such as aspirin.
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Administer myelosuppressive medication:
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hydroxyurea
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anagrelide
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radioactive phosphorus 32
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Administer medication to lower uric acid level if necessary:
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allopurinol
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Alkylating agents:
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melphalan
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busulfan
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Radiation therapy.
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Antihistamine for pruritis.
NURSING DIAGNOSES
•
Ineffective tissue perfusion
•
Disturbed sensory perception
•
Risk for injury
NURSING INTERVENTION
•
Monitor vital signs.
•
Monitor for bleeding.
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Monitor for signs of infections.
•
Keep the patient mobilized to decrease chance of clot formation.
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Increase fluid intake.
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Explain to the patient:
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Maintain activity.
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Use electric razor, use soft toothbrush, and avoid flossing to decrease
chances of bleeding.
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Avoid activities that could cause injury.
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CHAPTER 4 Hematologic System
Sickle Cell Anemia
WHAT WENT WRONG?
This is an autosomal recessive disorder in which an abnormal gene causes damage
to the RBC membrane. The abnormal hemoglobin within the red blood cell is called
hemoglobin S. Dehydration or drying of the RBC makes it more vulnerable to sick-
ling (forming a crescent-like shape), as do hypoxemia and acidosis. Hemolytic ane-
mia results as RBCs are destroyed due to the damage to the outer membrane. The
sickled cells can also clump together, causing difficulty getting through the smaller
vessels.
PROGNOSIS
Sickle cell anemia will become a chronic multisystem disease. Causes of death in
these patients are usually related to organ failure. Patients may also inherit a single
gene for sickle cell. These patients may develop sickle cell trait, in which symp-
toms would only be present in the setting of extreme circumstances (vigorous
exercise at high altitude, especially with rapid ascent).
HALLMARK SIGNS AND SYMPTOMS
•
Acute pain (especially back, chest, and long bones) from vascular occlusion
of the small vessels as the sickled cells clump
•
Fever as body responds to acute sickling episode and accompanying pro-
voking event
•
Painful, swollen joints due to vaso-occlusive process
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Fatigue due to chronic anemia
•
Stroke (cerebrovascular accident) due to vaso-occlusive process
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Enlarged liver (hepatomegaly)
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Enlarged heart and systolic murmur
INTERPRETING TEST RESULTS
•
Low RBC count due to chronic hemolytic anemia; the RBCs have a shorter
lifespan.
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Elevated WBCs.
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Increased reticulocytes.
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Presence of Howell-Jolly bodies and target cells.
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Sickle cells appear in blood smear.
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Indirect bilirubin level elevated.
•
Hemoglobin electrophoresis shows majority hemoglobin S (80 to 98 percent).
TREATMENT
During acute episodes pain control, hydration, and oxygenation are the focus of
treatment. The underlying cause that sent the patient into crisis will also need to be
treated concurrently.
•
Administer analgesics to alleviate the pain associated with the vaso-occlusive
process:
•
narcotic pain control necessary when pain is severe
•
Warm compresses on joint.
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Blood transfusion of packed RBC when anemia indicates.
•
Supplemental oxygen if hypoxic.
•
Adequate hydration, using IV fluids.
•
Treat infections.
NURSING DIAGNOSES
•
Fatigue
•
Acute pain
•
Impaired gas exchange
NURSING INTERVENTION
•
Increase fluid intake.
•
Monitor IV fluids.
•
Monitor pain control.