Assessment of

Hematologic Function
and
Treatment Modalities
Prepared by: Judd Wilson T. Pasculado RN
ANATOMIC AND
PHYSIOLOGIC OVERVIEW
ANATOMIC AND PHYSIOLOGIC
OVERVIEW
The hematologic system consists of the blood and the sites where
blood is produced, including the bone marrow and the
reticuloendothelial system (RES)

Plasma is the fluid portion of blood

contains various proteins, as albumin, globulin, fibrinogen, and other

factors necessary for clotting, as well as electrolytes, waste
products, and nutrients

55% of blood volume is plasma

STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Blood
Cellular component of blood consists of three primary cell types:

1. erythrocytes (red blood cells [RBCs], red cells)

2. Leukocytes (white blood cells [WBCs])
3. thrombocytes (platelets)

40% to 45% of the blood volume

The primary site for hematopoiesis is the bone marrow

STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Bone Marrow
Site of hematopoiesis, or blood cell formation

Marrow is one of the largest organs of the body, making up 4% to 5%

of total body weight

Within it are primitive cells called Stem Cells

• These stem cells are committed to produce specific types of blood
cells
• Lymphoid stem cells produce either T or B lymphocytes
• Myeloid stem cells differentiate into three broad cell types:
erythrocytes, leukocytes, and platelets
STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Blood Cells

Erythrocytes (Red Blood Cells)

• Consist primarily of hemoglobin

• Contains iron and makes up 95% of the cell mass
• Marrow releases slightly immature forms of erythrocytes, called
reticulocytes
• Important property of heme is its ability to bind to oxygen loosely
and reversibly
• Oxygen readily binds to hemoglobin in the lungs and is carried as
oxyhemoglobin
STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Blood Cells
Leukocytes (White Blood Cells)

Leukocytes are divided into two general categories:

1. Granulocytes
2. Lymphocytes

Total leukocyte count is 4000 to 11,000 cells/mm3

STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Blood Cells
Leukocytes (White Blood Cells)

Granulocytes

• presence of granules in the cytoplasm of the cell

• eosinophils, basophils, and neutrophils

Agranulocytes

• Monocytes - remove debris as Macrophages

• Lymphocytes – Natural killer (NK) cells
STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Blood Cells
Platelets (Thrombocytes)

• Platelets play an essential role in the control of bleeding

• They adhere to the site of injury and to each other, forming a
platelet plug that temporarily stops bleeding
• Substances released from platelet granules activate coagulation
factors in the blood plasma and initiate the formation of a stable
clot composed of fibrin
STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Plasma and Plasma Proteins
• Liquid portion of the blood is called plasma

• 90% of plasma is water.

• The remainder consists primarily of plasma proteins;

-clotting factors(particularly fibrinogen); nutrients, enzymes, waste products,
and gases

• Plasma proteins consist primarily of albumin and globulins

1. Globulins carry various substances in bound form in the Circulation

2. Albumin is particularly important for the maintenance of fluid balance within the
STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Reticuloendothelial System (RES)

Composed of special tissue called macrophages

Defend the body against foreign invaders (i.e., bacteria and other
pathogens) via phagocytosis

Stimulates the inflammatory process and present antigens to the

immune system

The spleen is the site of activity for most macrophages

STRUCTURE AND FUNCTION OF
THE HEMATOLOGIC SYSTEM
Hemostasis

process of preventing blood loss from intact vessels and of stopping

bleeding from a severed vessel, which requires adequate numbers of
functional platelets

severed blood vessel constricts  Circulating platelets aggregate at

the site  adhere to the vessel and to one another  unstable
hemostatic plug is formed coagulation process  formation of fibrin
ASSESSMENT
of the
HEMATOLOGIC SYSTEM
ASSESSMENT of the HEMATOLOGIC
SYSTEM
HEALTH HISTORY

Family History Assessment Specific to Hematologic Disorders

1. Collect family history information on maternal and paternal

relatives from three generations of the family.
2. Assess family history for other family members with histories of
blood disorders or episodes of abnormal bleeding.
3. If a family history or personal risk is suspected, the person should
be carefully screened for bleeding disorders prior to surgical
procedures.
ASSESSMENT of the HEMATOLOGIC
SYSTEM
HEALTH HISTORY

Patient Assessment Specific to Hematologic Disorders

Assess for specific symptoms of hematologic diseases:

1. Extreme fatigue (the most common symptom of hematologic
disorders)
2. Delayed clotting of blood
3. Easy or deep bruising
4. Abnormal bleeding (e.g., frequent nosebleeds)
5. Abdominal pain (hemochromatosis) or joint pain (sickle cell
disease)
6. Review blood cell counts for abnormalities.
7. Assess for presence of illness despite low risk for the illness (e.g.,
ASSESSMENT of the HEMATOLOGIC
SYSTEM
HEALTH HISTORY
ASSESSMENT of the HEMATOLOGIC
SYSTEM
PHYSICAL ASSESSMENT

The physical assessment should be comprehensive and include

careful attention to the skin, oral cavity, lymph nodes, and spleen
ASSESSMENT of the HEMATOLOGIC
SYSTEM
PHYSICAL ASSESSMENT
ASSESSMENT of the HEMATOLOGIC
SYSTEM
PHYSICAL ASSESSMENT
ASSESSMENT of the HEMATOLOGIC
SYSTEM
PHYSICAL ASSESSMENT
ASSESSMENT of the HEMATOLOGIC
SYSTEM
PHYSICAL ASSESSMENT
ASSESSMENT of the HEMATOLOGIC
SYSTEM
BONE MARROW ASPIRATION AND BIOPSY

Bone marrow aspiration procedure. The

posterior superior iliac crest is the
preferred site for bone marrow
aspiration and biopsy because no vital
organs or vessels are nearby.

The patient is placed either in the

lateral position with one leg flexed or in
the prone position. The anterior iliac
crest or sternum may also be used
Therapeutic Approaches
to Hematologic Disorders
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
SPLENECTOMY

• The surgical removal of the spleen

• Enlarged spleen may be the site of excessive destruction
of blood cells
• Enlarged spleens develop severe thrombocytopenia
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
THERAPEUTIC APHERESIS

Apheresis is a Greek word meaning “separation.”

Blood is taken from the patient and passed through a centrifuge, where a specific
component is separated from the blood and removed
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
HEMATOPOIETIC STEM CELL TRANSPLANTATION
Hematopoietic stem cells may be transplanted from either allogeneic
or autologous donors

For most hematologic diseases, allogeneic transplant is more

effective
here, stem cells are obtained from a donor whose cells match those
of the patient.

Patient’s own stem cells are harvested and then used in autologous
transplant
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
THERAPEUTIC PHLEBOTOMY

Therapeutic phlebotomy is the removal of a certain amount of blood

under controlled conditions.

Patients with elevated hematocrits or excessive iron absorption can

usually be managed by periodically removing 1 unit (about 500 mL)
of whole blood.

Over time, this process can produce iron deficiency, leaving the
patient unable to produce as many erythrocytes.
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
BLOOD COMPONENT THERAPY
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
BLOOD COMPONENT THERAPY
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
BLOOD COMPONENT THERAPY
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
TRANSFUSION

Administration of blood and blood components requires

knowledge of
correct administration techniques and possible
complications.

Refer to your LECLAB on Blood Transfusions for the

procedure!!!
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
TRANSFUSION

POSTPROCEDURE
1. Obtain vital signs and auscultate breath sounds; compare with
baseline
measurements. If signs of increased fluid overload present, consider
obtaining prescription for diuretic, as warranted.
2. Dispose of used materials properly.
3. Document procedure in patient’s medical record, including patient
assessment findings and tolerance to procedure.
4. Monitor patient for response to and effectiveness of procedure. A
CBC may be ordered 1-6 hours after transfusion to facilitate this
evaluation.
5. If patient is at risk for transfusion-associated circulatory overload
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
TRANSFUSION COMPLICATIONS

1. Febrile Nonhemolytic Reaction

2. Acute Hemolytic Reaction
3. Allergic Reaction
4. Transfusion-Associated Circulatory Overload (TACO)
5. Bacterial Contamination
6. Transfusion-Related Acute Lung Injury (TRALI)
7. Delayed Hemolytic Reaction
8. Disease Acquisition
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
Common Complications Resulting from
Long-Term Packed Red Blood Cell Transfusion
Therapy
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
Nursing Management for Transfusion Reactions

Stop the transfusion. Maintain the IV line with normal saline solution through new
IV tubing, given at a slow rate.

Assess the patient carefully. Compare the vital signs with baseline, including
oxygen saturation. Assess the patient’s respiratory status carefully. Note the
presence of adventitious breath sounds; the use of
accessory muscles; extent of dyspnea; and changes in mental status, including
anxiety and confusion.
Note any chills, diaphoresis, jugular vein distention, and reports of back pain or
urticaria.

Notify the primary provider of the assessment findings, and implement any
treatments prescribed. Continue to monitor the patient’s vital signs and
respiratory, cardiovascular, and renal status.
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
Nursing Management for Transfusion Reactions

If a hemolytic transfusion reaction or bacterial infection is suspected, the nurse

does the following:

1. Obtains appropriate blood specimens from the patient

2. Collects a urine sample as soon as possible to detect hemoglobin in the urine
3. Documents the reaction according to the institution’s policy
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
DISEASES POTENTIALLY TRANSMITTED BY BLOOD
TRANSFUSION
Hepatitis (Viral Hepatitis B, C)
There is greater risk from pooled blood products and blood of paid donors than
from volunteer donors.

A screening test detects most hepatitis B and C.

Transmittal risk for Hepatitis B is estimated at 1:350,000 donated units.

THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
DISEASES POTENTIALLY TRANSMITTED BY BLOOD
TRANSFUSION
AIDS (HIV and HTLV)

Donated blood is screened for antibodies to HIV.

Transmittal risk is estimated at 1:1.5 million donated units.

People with high-risk behaviors (multiple sex partners, anal sex, IV/injection drug
use) and people with signs and symptoms that suggest AIDS should not donate
blood.
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
DISEASES POTENTIALLY TRANSMITTED BY BLOOD
TRANSFUSION
Cytomegalovirus (CMV)

Transmittal risk is greater for premature newborns with CMV antibody–negative

mothers and for immunocompromised recipients who are CMV negative (e.g.,
those with acute leukemia, organ or
tissue transplant recipients).

Blood products rendered “leukocyte reduced” help reduce transmission of virus.

THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
DISEASES POTENTIALLY TRANSMITTED BY BLOOD
TRANSFUSION
Graft-Versus-Host Disease (GVHD)

GVHD occurs only in severely immunocompromised recipients (e.g., Hodgkin

disease, bone marrow transplantation).

Transfused lymphocytes engraft in recipient and attack host lymphocytes or body

tissues; signs and symptoms are fever, diffuse reddened skin rash, nausea,
vomiting, and diarrhea.

Preventive measures include irradiating blood products to inactivate donor

lymphocytes (no known radiation risks to transfusion recipient) and processing
donor blood with leukocyte reduction filters.
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
DISEASES POTENTIALLY TRANSMITTED BY BLOOD
TRANSFUSION
Creutzfeldt-Jakob Disease (CJD)

CJD is a rare, fatal disease that causes irreversible brain damage.

There is no evidence of transmittal by transfusion.

All blood donors must be screened for positive family history of CJD.

Potential donors who spent a cumulative time of 5 years or more (January 1980 to present)
in certain areas of Europe cannot donate blood; blood products from a donor who develops
CJD are recalled.
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
PHARMACOLOGIC ALTERNATIVES TO BLOOD TRANSFUSIONS

Growth Factors
Recombinant technology has provided a means to produce
hematopoietic growth factors necessary for the production of blood
cells within the bone marrow

Erythropoietin
Effective alternative treatment for patients with chronic anemia
secondary to diminished levels of erythropoietin, as in chronic renal
disease

Granulocyte Colony-Stimulating Factor (G-CSF)

Cytokine that stimulates the proliferation and differentiation of
THERAPEUTIC APPROACHES TO
HEMATOLOGIC DISORDERS
PHARMACOLOGIC ALTERNATIVES TO BLOOD TRANSFUSIONS

Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)

Cytokine that is naturally produced by a variety of cells, including
monocytes and endothelial cells

Thrombopoietin
Cytokine that is necessary for the proliferation of megakaryocytes
and subsequent platelet formation
Management of
Patients
With
Nonmalignant
Hematologic
Disorders
ANEMIA
ANEMIA
Hemoglobin concentration is lower than normal

Reflects the presence of fewer than the normal number of

erythrocytes (i.e., red blood cells [RBCs]) within the
circulation

Amount of oxygen delivered to body tissues is also

diminished

Not a specific disease state but a sign of an underlying

disorder
ANEMIA
Classification of Anemias
ANEMIA
Classification of Anemias

HYPOPROLIFERATIVE ANEMIAS

Iron Deficiency Anemia - intake of dietary iron is inadequate

Anemias in Renal Disease - lack of erythropeitin in the kidneys
Anemia of Inflammation- chronic diseases of inflammation, infection,
and malignancy as causes for this type of anemia
Aplastic Anemia - decrease in or damage to marrow stem cells
Megaloblastic Anemias - caused by deficiencies of vitamin B12 or
folic acid
ANEMIA
Classification of Anemias

HEMOLYTIC ANEMIAS

Sickle Cell Disease - inheritance of the sickle hemoglobin (HbS) gene, which
causes the hemoglobin molecule to be defective
Thalassemias - group of hereditary anemias characterized by hypochromia (an
abnormal decrease in the hemoglobin content of erythrocytes),
extreme microcytosis (smaller-than-normal erythrocytes), hemolysis,
and variable degrees of anemia.
Glucose-6-Phosphate Dehydrogenase Deficiency - The G-6-PD gene is the source of
the abnormality in this disorder; this gene
produces an enzyme within the erythrocyte
that is essential for membrane stability
Immune Hemolytic Anemias - anemias can result from exposure of the erythrocyte
to antibodies
ANEMIA
CLINICAL MANIFESTATIONS

Symptoms may vary on the rapidity, duration(i.e., its chronicity), the metabolic
requirements of the patient, other concurrent disorders or disabilities (e.g., cardiac
or pulmonary disease), and complications or concomitant features of the condition
that produced the anemia

More rapidly an anemia develops, the more severe its symptoms

A person who has become gradually anemic, with hemoglobin levels between 9
and 11 g/dL, usually has fewer
or no symptoms other than slight tachycardia on exertion and possibly fatigue.

Patients with hypothyroidism with decreased oxygen needs may be completely

asymptomatic
ANEMIA
ASSESSMENT AND DIAGNOSTIC FINDINGS

Hematologic studies

Bone marrow aspiration

Diagnostic studies may be performed to determine the

presence of underlying chronic illness, such as malignancy,
or the source of any blood loss, such as polyps or ulcers
within the gastrointestinal (GI) tract
ANEMIA
COMPLICATIONS

• Heart failure
• Paresthesias
• Delirium
• Patients with underlying heart disease are far more likely
to have angina or symptoms of heart failure
ANEMIA
MEDICAL MANAGEMENT

Directed toward correcting or controlling the cause of the

anemia

May be replaced with a transfusion of packed red blood

cells
NURSING PROCESS (ANEMIA)
ASSESSMENT

Physical Assessment
Weakness, fatigue, and general malaise are common, as are pallor of the
skin and mucous membranes, jaundice; angular cheilosis (ulcerated corners of
the mouth); and brittle, ridged, concave nails may be present in patients with
megaloblastic anemia (characterized by the presence of abnormally large,
nucleated RBCs) or hemolytic anemia, tongue may be beefy red and sore in
megaloblastic anemia, or smooth and red in iron deficiency anemia
Patients with iron deficiency anemia may infrequently crave ice, starch, or
dirt; this craving is known as pica

Health History
Should include a medication history, history of alcohol intake, Family
history, athletic endeavors, nutritional assessment
Cardiac status should be carefully assessed.
GI system
Neurologic examination
NURSING PROCESS (ANEMIA)

NURSING DIAGNOSES

Based on the assessment data, major nursing diagnoses

may include:

• Fatigue related to decreased hemoglobin and diminished

oxygen carrying capacity of the blood
• Imbalanced nutrition, less than body requirements,
related to inadequate intake of essential nutrients
• Activity intolerance related to inadequate hemoglobin
and hematocrit
NURSING PROCESS (ANEMIA)

Collaborative Problems/Potential Complications

Potential complications may include the following:

• Heart failure
• Angina
• Paresthesias
• Confusion
• Injury related to falls
• Depressed mood
NURSING PROCESS (ANEMIA)

Planning and Goals

The major goals for the patient may include

decreased fatigue, attainment or maintenance of adequate
nutrition, maintenance of adequate tissue perfusion,
compliance with prescribed therapy, and absence of
complications.
NURSING PROCESS (ANEMIA)

NURSING INTERVENTIONS

1. Managing fatigue
2. Maintaining adequate nutrition
3. Maintaining adequate nutrition
4. Promoting adherence with prescribed therapy
5. Monitoring and managing potential complications
NURSING PROCESS (ANEMIA)
EVALUATION

1. Reports less fatigue

a. Follows a progressive plan of rest, activity, and exercise
b. Prioritizes activities
c. Paces activities according to energy level

2. Attains and maintains adequate nutrition

a. Eats a healthy diet
b. Develops a meal plan that promotes optimal nutrition
c. Maintains adequate amounts of iron, vitamins, and protein from diet or
supplements
d. Adheres to nutritional supplement therapy when prescribed
e. Verbalizes understanding of rationale for using recommended nutritional
supplements
f. Verbalizes understanding of rationale for avoiding nonrecommended nutritional
supplements
NURSING PROCESS (ANEMIA)
EVALUATION

3. Maintains adequate activity level

a. Has vital signs within baseline for patient
b. Has pulse oximetry (arterial oxygenation) value within normal limits

4. Absence of complications
a. Avoids or limits activities that trigger dyspnea, palpitations, dizziness, or
tachycardia
b. Uses rest and comfort measures to alleviate dyspnea
c. Has vital signs within baseline for patient
d. Has no signs of increasing fluid retention
e. Remains oriented to time, place, and situation
f. Remains engaged in social situations, exhibits no signs of depression
g. Ambulates safely, using assistive devices as necessary
h. Remains free of injury
i. Verbalizes understanding of importance of serial CBC measurements
j. Maintains safe home environment; obtains assistance as necessary
POLYCYTHEMIA
POLYCYTHEMIA

Refers to an increased volume of RBCs

Hematocrit is elevated (more than 55% in males, more than 50% in

females)

Dehydration (decreased volume of plasma) can cause an elevated

hematocrit but not typically to the level to be considered
polycythemia.

Polycythemia is classified as either primary or secondary.

Primary polycythemia, also called polycythemia vera, is a proliferative

POLYCYTHEMIA
SECONDARY POLYCYTHEMIA

Caused by excessive production of erythropoietin.

Occur in response to a reduced amount of oxygen, which acts as a hypoxic

stimulus, as in heavy cigarette smoking, obstructive sleep apnea (OSA), chronic
obstructive pulmonary disease (COPD), or cyanotic heart disease, or with
conditions such as living at a high altitude or exposure to low levels of carbon
monoxide.

It can also result from certain hemoglobinopathies (e.g., hemoglobin

Chesapeake), in which the hemoglobin has an abnormally high affinity for
oxygen or from genetic mutations.

Secondary polycythemia can also occur from neoplasms (e.g., renal cell
carcinoma) that stimulate
erythropoietin production, excess erythropoietin-stimulating agent use, or
POLYCYTHEMIA
MEDICAL MANAGEMENT

Mild, treatment may not be necessary

When treatment is necessary, it involves treating the primary

condition.

Therapeutic phlebotomy may be necessary in symptomatic

patients to reduce blood viscosity and volume as well as when the
hematocrit is significantly elevated.

Therapeutic phlebotomy should not be used when the cause for an

elevated
RBC level is an appropriate, compensatory response to tissue
POLYCYTHEMIA
MEDICAL MANAGEMENT

Mild, treatment may not be necessary

When treatment is necessary, it involves treating the primary

condition.

Therapeutic phlebotomy may be necessary in symptomatic

patients to reduce blood viscosity and volume as well as when the
hematocrit is significantly elevated.

Therapeutic phlebotomy should not be used when the cause for an

elevated
RBC level is an appropriate, compensatory response to tissue
NEUTROPENIA
NEUTROPENIA
A neutrophil count of less than 2000/mm3

results from decreased production of neutrophils or

increased destruction of these cells

Neutrophils are essential in preventing and limiting

bacterial infection.

A patient with neutropenia is at increased risk for

infection from both exogenous and endogenous sources
NEUTROPENIA
CAUSES OF NEUTROPENIA

DECREASED PRODUCTION OF NEUTROPHILS

Aplastic anemia, due to medications or toxins
Chemotherapy
Metastatic cancer, lymphoma, leukemia
Myelodysplastic syndromes
Radiation therapy
INEFFECTIVE GRANULOCYTOPOIESIS
Megaloblastic anemia
INCREASED DESTRUCTION OF NEUTROPHILS
Bacterial infections
Hypersplenism
Immunologic disorders (e.g., systemic lupus erythematosus)
Medication induceda
Viral disease (e.g., infectious hepatitis, mononucleosis)
NEUTROPENIA
CLINICAL MANIFESTATIONS

There are no definite symptoms of neutropenia until the

patient develops
an infection. A routine CBC with differential, as obtained after
chemotherapy treatment, can reveal neutropenia before the onset
of infection.
NEUTROPENIA
MEDICAL MANAGEMENT

Treatment of the neutropenia varies depending on its cause.

medication induced, the offending agent is stopped immediately, if possible.

Corticosteroids may be used if the cause is an immunologic disorder.

growth factors such as granulocyte colony-stimulating factor or granulocyte-

macrophage colonystimulating factor can be effective in increasing neutrophil
production

Withholding or reducing the dose of chemotherapy or radiation therapy may be

required
NEUTROPENIA
NURSING MANAGEMENT

Nurses in all settings have a crucial role in assessing the

severity of
neutropenia and in preventing and managing complications, which
most
often include infections.
NEUTROPENIA
The Patient at Risk for Infection

At the completion of education, the patient and/or caregiver will be

able to:

• State the impact of alterations in neutrophils, lymphocytes, immunoglobulins

on physiologic functioning, ADLs, IADLs, roles, relationships, and spirituality.
• State changes in lifestyle (e.g., diet, activity) or home environment necessary
to decrease risk for infection.
• Maintain good hand hygiene technique, oral hygiene, total body hygiene, and
skin integrity.
• Avoid cleaning birdcages and litter boxes; consider avoiding garden work
(soil) and fresh flowers in stagnant water.
• Maintain a high-calorie, high-protein diet, with fluid intake of 3000 mL daily
(unless fluids are restricted).
NEUTROPENIA
The Patient at Risk for Infection

At the completion of education, the patient and/or caregiver will be

able to:

• Avoid people with infections and crowds.

• Perform deep breathing; use incentive spirometer every 4 hours while awake
if mobility is restricted.
• Provide adequate lubrication with gentle vaginal manipulation during sexual
intercourse; avoid anal intercourse.
• Identify signs and symptoms of infection
• Demonstrate how to monitor for signs of infection.
• Describe to whom, how, and when to report signs of infection.
• Describe appropriate actions to take should infection occur
NEUTROPENIA
The Patient at Risk for Infection

At the completion of education, the patient and/or caregiver will be

able to:

• Avoid people with infections and crowds.

• Perform deep breathing; use incentive spirometer every 4 hours while awake
if mobility is restricted.
• Provide adequate lubrication with gentle vaginal manipulation during sexual
intercourse; avoid anal intercourse.
• Identify signs and symptoms of infection
• Demonstrate how to monitor for signs of infection.
• Describe to whom, how, and when to report signs of infection.
• Describe appropriate actions to take should infection occur
LYMPHOPENIA
LYMPHOPENIA
Lymphocyte count less than 1500/mm3

Result from ionizing radiation, long-term use of corticosteroids,

uremia, infections
(particularly viral infections), some neoplasms (e.g., breast and
lung cancers, advanced Hodgkin disease), and some protein-losing
enteropathies (in which the lymphocytes within the intestines are
lost)

Mild, it is often without sequelae;

Severe, it can result in bacterial infections (due to low B

lymphocytes) or in opportunistic infections (due to low T
lymphocytes).
BLEEDING
DISORDERS
BLEEDING DISORDERS
Failure of normal hemostatic mechanisms can result in bleeding,

Bleeding is commonly provoked by trauma; however, in certain

circumstances, it can occur spontaneously.

When the cause is platelet or coagulation factor abnormalities, the

site of bleeding can be
anywhere in the body.

When the source is vascular abnormalities, the site of bleeding

may be more localized.

Some patients have simultaneous defects in more than one

hemostatic mechanism.
BLEEDING DISORDERS
The bone marrow may be stimulated to increase platelet
production
(thrombopoiesis) as a reactive response to bleeding

Sometimes, the increase in platelets does not result from

increased production but from a loss in platelet pooling within the
spleen.
BLEEDING DISORDERS
CLINICAL MANIFESTATIONS

Signs and symptoms of bleeding disorders vary according to the type of

defect.

Abnormalities of the vascular system give rise to local bleeding, usually into the
skin.

Patients with platelet defects develop petechiae, often in clusters;

Bleeding from platelet disorders can be severe.

In contrast, coagulation factor defects do not tend to cause superficial bleeding,

because the primary hemostatic mechanisms are still intact.

Instead, bleeding occurs deeper within the body (e.g., subcutaneous or

intramuscular hematomas, hemorrhage into joint spaces).
BLEEDING DISORDERS
CLINICAL MANIFESTATIONS
BLEEDING DISORDERS
MEDICAL MANAGEMENT

Management varies based on the underlying cause of the bleeding

disorder.

transfusions of blood products may be indicated.

Hemostatic agents such as aminocaproic acid (Amicar) can be

used to
inhibit this process.

A patient scheduled for an invasive procedure, including a dental

extraction, may
need a transfusion prior to the procedure to minimize the risk of
BLEEDING DISORDERS
NURSING MANAGEMENT

Patients must be educated to observe themselves carefully and

frequently for signs
of bleeding

They need to understand the importance of avoiding activities that

increase the risk of bleeding, such as contact sports.

Examine the skin for petechiae and ecchymoses (bruises)

and the nose and gums for bleeding.

If severe, patients who are hospitalized are monitored for bleeding

by testing all drainage and excreta (feces, urine, emesis, and
BLEEDING DISORDERS
NURSING MANAGEMENT

Patients must be educated to observe themselves carefully and

frequently for signs
of bleeding

They need to understand the importance of avoiding activities that

increase the risk of bleeding, such as contact sports.

Examine the skin for petechiae and ecchymoses (bruises)

and the nose and gums for bleeding.

If severe, patients who are hospitalized are monitored for bleeding

by testing all drainage and excreta (feces, urine, emesis, and
SECONDARY THROMBOCYTOSIS
Increased platelet production is the primary mechanism of
secondary, or reactive, thrombocytosis.

The platelet count is above normal, an increase of more than 1

million/mm3 Platelet function is normal; survival time is normal or
decreased.

disorders or conditions can cause a reactive increase in platelets,

including infection, iron deficiency, chronic inflammatory
disorders, malignant disease, acute hemorrhage, and splenectomy.

Treatment is aimed at the underlying disorder. With successful

management, the platelet count usually returns to normal.
THROMBOCYTOPENIA

Thrombocytopenia (low platelet level) can result from

various factors:

1. Decreased production of platelets within the bone

marrow
2. Increased destruction of platelets
3. Increased consumption of platelets (e.g., the use of
platelets in clot formation).
THROMBOCYTOPENIA

CLINICAL MANIFESTATIONS

Bleeding and petechiae usually do not occur with platelet counts greater than
50,000/mm3

When the platelet count drops to less than 20,000/mm3, petechiae can appear,
along with nasal and gingival bleeding, excessive menstrual bleeding, and
excessive bleeding after surgery or dental extractions.

When the platelet count is less than 5000/mm3, spontaneous, potentially fatal
central nervous system or GI hemorrhage can occur.

If the platelets are dysfunctional as a result of disease (e.g., MDS) or

medications (e.g.,
aspirin), the risk of bleeding may be much greater even when the actual
platelet count is not significantly reduced, because the function of the platelets
is altered.
THROMBOCYTOPENIA

MEDICAL MANAGEMENT

The management of secondary thrombocytopenia is usually

treatment of the underlying disease.

If platelet production is impaired, platelet transfusions may

increase the platelet count and stop bleeding or prevent
spontaneous hemorrhage.

In some instances, splenectomy can be a useful therapeutic

intervention, but often it is not an option.
THROMBOCYTOPENIA

NURSING MANAGEMENT

the nurse considers the cause of the thrombocytopenia, the likely duration, and
the overall condition of the patient.

Education is important, as are interventions to promote patient,safety,

particularly fall prevention in the older adult or patient who is frail.

The interventions for a patient with thrombocytopenia are the same as those for
a patient with cancer who is at risk for bleeding
THROMBOCYTOPENIA

NURSING MANAGEMENT

the nurse considers the cause of the thrombocytopenia, the likely duration, and
the overall condition of the patient.

Education is important, as are interventions to promote patient,safety,

particularly fall prevention in the older adult or patient who is frail.

The interventions for a patient with thrombocytopenia are the same as those for
a patient with cancer who is at risk for bleeding
IMMUNE THROMBOCYTOPENIC
PURPURA
More common among children and young women.

Also called idiopathic thrombocytopenic purpura and immune

thrombocytopenia.

Primary ITP occurs in isolation

Secondary ITP often results from autoimmune diseases (e.g.,

antiphospholipid antibody syndrome), viral infections (e.g.,
hepatitis C, HIV), and various drugs (e.g., sulfa drugs).

Primary ITP is defined as a platelet count less than 100 × 109/L

with an inexplicable absence of a cause for thrombocytopenia
IMMUNE THROMBOCYTOPENIC
PURPURA
PATHOPHYSIOLOGY

Antiplatelet antibodies develop in the blood and bind to the

patient’s platelets  ingested and destroyed by the
reticuloendothelial system (RES) or tissue macrophages  body
attempts to compensate for this destruction by increasing platelet
production within the marrow  platelet production also be
impaired as the antibodies may also induce cell death (via
apoptosis) of the megakaryocytes  inhibit platelet production
within the bone marrow
IMMUNE THROMBOCYTOPENIC
PURPURA
CLINICAL MANIFESTATIONS

Many patients have no symptoms, and the low platelet count is an incidental
finding (often less than 30,000/mm3; less than 5000/mm3 is not uncommon).

Common physical manifestations are easy bruising, heavy menses, and

petechiae on the extremities or trunk

Simple bruising or petechiae (“dry purpura”) tend to have fewer complications

from bleeding than those with bleeding from mucosal surfaces, such as the GI
tract (including the mouth) and pulmonary system (e.g., hemoptysis), which is
termed wet purpura.

Severe thrombocytopenia (platelet count less than 20,000/mm3)

IMMUNE THROMBOCYTOPENIC
PURPURA
ASSESSMENT AND DIAGNOSTIC FINDINGS

A careful history and physical assessment must be obtained to exclude causes of

the thrombocytopenia and identify evidence of bleeding.

Patients should be tested for hepatitis C and HIV, if not previously done to rule out
these potential causes.

If a bone marrow aspirate is performed, an increase in megakaryocytes may be

seen. The severity of the thrombocytopenia is highly variable, but a platelet count
that is less than 20,000/mm3 is a
common finding.
IMMUNE THROMBOCYTOPENIC
PURPURA
MEDICAL MANAGEMENT

The primary goal of treatment is a “safe” platelet

Count exceeds 30,000/mm3 to 50,000/mm3 may be carefully observed without

additional intervention.

less than 30,000/mm3 or if bleeding occurs, the goal is to improve the patient’s
platelet count rather than to cure the disease.

basis is not of the patient’s platelet count but on the severity of bleeding

Aminocaproic acid—a fibrinolytic enzyme inhibitor that slows the dissolution of

clots—may be useful for patients with significant mucosal bleeding refractory to
other treatments

The mainstay of short-term therapy is the use of immunosuppressive agents.

IMMUNE THROMBOCYTOPENIC
PURPURA
NURSING MANAGEMENT

Nursing care includes an assessment of the patient’s lifestyle to determine the risk of
bleeding from activity.

A careful medication history is also obtained, including use of over-the-counter (OTC)

medications, herbs, and
nutritional supplements.

The nurse must be alert for sulfa-containing medications and others that alter platelet
function (e.g., aspirin-based or other NSAIDs).

The nurse assesses for any history of recent viral illness and reports of headache or visual
disturbances, which could be initial symptoms of intracranial bleeding.

Patients who are admitted to the hospital with wet purpura and low platelet counts should
have a neurologic
assessment incorporated into their routine vital sign measurements.

All injections or rectal medications should be avoided, and rectal temperature

PLATELET DEFECTS

Qualitative defects, the number of platelets may be normal but the platelets do not
function normally.

The morphology of platelets is often hypogranular and pale, and may be larger
than normal.

Aspirin may induce a platelet disorder.

NSAIDs can also inhibit platelet function, but the effect is not as prolonged as with
aspirin (

Other causes of platelet dysfunction include end-stage renal disease, possibly from
metabolic products affecting platelet function;

MDS; multiple myeloma (due to abnormal protein interfering with platelet function);
cardiopulmonary bypass; herbal therapy; and other medications
PLATELET DEFECTS

CLINICAL MANIFESTATIONS

Bleeding may be mild or severe.

elevated PT in the setting of a normal aPTT and platelet count may suggest factor
VII deficiency,

whereas an elevated partial thromboplastin time (PTT) in the setting of a normal PT

and platelet count may suggest
hemophilia or von Willebrand disease (vWD).

Ecchymoses are common, particularly on the extremities. Patients with platelet

dysfunction may be at
risk for significant bleeding after trauma or invasive procedures
PLATELET DEFECTS

MEDICAL MANAGEMENT
If the platelet dysfunction is caused by medication, its use should be stopped, if
possible

If platelet dysfunction is marked, bleeding can often be prevented by transfusion of

normal platelets before invasive procedures.

Antifibrinolytic agents (e.g., aminocaproic acid) may be required to prevent

significant bleeding after such procedures;

Desmopressin (DDAVP) can decrease the duration of bleeding in some situations

and improve hemostasis (Levi et al., 2016).
PLATELET DEFECTS

MEDICAL MANAGEMENT
If the platelet dysfunction is caused by medication, its use should be stopped, if
possible

If platelet dysfunction is marked, bleeding can often be prevented by transfusion of

normal platelets before invasive procedures.

Antifibrinolytic agents (e.g., aminocaproic acid) may be required to prevent

significant bleeding after such procedures;

Desmopressin (DDAVP) can decrease the duration of bleeding in some situations

and improve hemostasis
PLATELET DEFECTS

NURSING MANAGEMENT

Instruct to avoid substances that can diminish platelet function, such

as certain OTC medications, some herbal therapies, nutritional
supplements, and alcohol.

inform their health care providers (including dentists) of the

underlying condition before any invasive procedure is performed so
that appropriate steps can be initiated to diminish the risk of
bleeding.

Maintaining good oral hygiene is very important so that gingival

bleeding can be minimized.
HEMOPHILIA

Hemophilia A is caused by a genetic defect that results in deficient or defective

factor VIII.

Hemophilia B (also called Christmas disease) stems from a genetic defect that
causes deficient or defective factor IX

Both types of hemophilia are inherited as X-linked traits, so most affected people
are males; females can be carriers but are almost always asymptomatic

Hemophilia is recognized in early childhood, usually in the toddler age group.

However, patients with mild hemophilia may not be diagnosed until they
experience severe trauma (e.g., a high school football injury) or surgery.
HEMOPHILIA

CLINICAL MANIFESTATIONS

Hemorrhages into various parts of the body

Severe and can occur even after minimal trauma.

The frequency and severity of the bleeding depend on the degree of factor
deficiency as well as the intensity of the precipitating trauma.

About 75% of all bleeding in patients with hemophilia occurs into joints. The most
commonly affected joints are the knees, elbows, ankles, shoulders, wrists, and
hips.
HEMOPHILIA

CLINICAL MANIFESTATIONS
HEMOPHILIA

CLINICAL MANIFESTATIONS

Bleeding is commonly associated with dental extraction

Spontaneous hematuria and GI bleeding can also occur

Surgical procedures typically result in excessive bleeding at the surgical site

Falls carry significant risk for morbidity in adults

HEMOPHILIA

MEDICAL MANAGEMENT

Recombinant forms of factor VIII and X concentrates are available and decrease the
need for using factor concentrates, or, more infrequently, fresh-frozen plasma.

Other therapeutic options include administering recombinant factor VIIa

(Novoseven, Novo Nordixk) or activated prothrombin complex concentrates (IaPCC,
FEIBA)

Aminocaproic acid inhibits fibrinolysis and therefore stabilizes the clot

HEMOPHILIA
NURSING MANAGEMENT

Diagnosed as children, hey often require assistance in coping with the condition
because it is chronic, places restrictions on their lives, and is an inherited disorder
that can be passed to future generations

Patients need extensive education about activity restrictions and self-care

measures to diminish the chance of hemorrhage and complications of bleeding

Patients and family members are instructed how to administer the factor
concentrate at home at the first sign of bleeding so that bleeding is minimized and
complications avoided

During hemorrhagic episodes, the extent of bleeding must be assessed Carefully.

Close observation and
systematic assessment for emergent complications

Warm baths promote relaxation, improve mobility, and lessen pain

VON WILLEBRAND DISEASE (VWD)

Inherited as a dominant trait, vWD is a common bleeding disorder that affects

males and females equally

Deficiency of vWF, which is necessary for factor VIII activity

Type 1, the most common, is characterized by decreases in structurally normal

vWF.

Type 2 shows variable qualitative defects based on the specific vWF subtype
involved.

Type 3 is very rare (less than 5% of cases) and is characterized by a severe vWF
deficiency as well as significant deficiency of factor VIII
VON WILLEBRAND DISEASE (VWD)

CLINICAL MANIFESTATIONS

Bleeding tends to be mucosal.

Recurrent nosebleeds, easy bruising, heavy menses, prolonged bleeding from cuts,
and postoperative bleeding.

Massive soft tissue or joint hemorrhages are not often seen, unless the patient has
severe type 3 vWD.

As the laboratory values fluctuates, so does the bleeding.

VON WILLEBRAND DISEASE (VWD)

Assessment and Diagnostic Findings

The diagnosis is established by the patient meeting all of these criteria:
1. A history of bleeding since childhood
2. Reduced vWF activity in plasma
3. History of bleeding within the family

Laboratory test results show a normal platelet count but a prolonged bleeding time
and a slightly prolonged aPTT.

Ristocetin cofactor, or vWF collagen binding assay, which measures vWF activity

vWF antigen, factor VIII, and, for patients with suspected type 2 defects, vWF
multimers, which measure specific subtypes of vWF.
VON WILLEBRAND DISEASE (VWD)
MEDICAL MANAGEMENT

The goal of treatment is to replace the deficient protein (e.g., vWF or factor VIII) at
the time of spontaneous bleeding or prior to an invasive procedure to prevent
subsequent bleeding.

Desmopressin, a synthetic vasopressin analogue, can be used to prevent bleeding

associated with
dental or surgical procedures

Replacement products include Humate-P and Alphanate, which are commercial

concentrates of vWF and factor VIII

Aminocaproic acid is useful in managing mild forms of mucosal bleeding

Estrogen–progesterone compounds may diminish the extent of menses.

Platelet transfusions are useful when there is significant bleeding. While rich in vWF
ACQUIRED
COAGULATION
DISORDERS
LIVER DISEASE

Hepatic dysfunction (due to cirrhosis, tumor, or hepatitis) can result in diminished

amounts of
the factors needed to maintain coagulation and hemostasis.

Prolongation of the PT, unless it is caused by vitamin K deficiency, may indicate

severe hepatic dysfunction. Although bleeding is usually minor (e.g., ecchymoses),
these patients are also at risk for significant bleeding, related especially to trauma
or surgery.

Transfusion of fresh-frozen plasma may be required to replace clotting factors and

to prevent or stop bleeding.

Patients may also have life-threatening hemorrhage from peptic ulcers or

esophageal varices. In these cases, replacement with fresh-frozen plasma, PRBCs,
and platelets is usually required.
VITAMIN K DEFICIENCY

The synthesis of many coagulation factors depends on vitamin K.

Vitamin K deficiency is common in malnourished patients.

Prolonged use of some antibiotics decreases the intestinal flora that produces
vitamin K

Administration of vitamin K (phytonadione [Mephyton]), either orally or as a

subcutaneous injection, can correct the deficiency quickly; adequate synthesis of
coagulation factors is reflected by normalization of the PT.
DISSEMINATED INTRAVASCULAR
COAGULATION
Disseminated intravascular coagulation (DIC) is not an actual disease but a sign of
an underlying condition.

DIC may be triggered by sepsis, trauma, cancer, shock, abruptio placentae, toxins,
allergic reactions, and other conditions

the vast majority (two thirds) of cases of DIC are initiated by an infection or a
malignancy

The severity of DIC is variable, but it is potentially life-threatening.

DISSEMINATED INTRAVASCULAR
COAGULATION
PATHOPHYSIOLOGY
DISSEMINATED INTRAVASCULAR
COAGULATION
CLINICAL MANIFESTATIONS
DISSEMINATED INTRAVASCULAR
COAGULATION
ASSESSMENT AND DIAGNOSTIC FINDINGS
DISSEMINATED INTRAVASCULAR
COAGULATION
Medical Management

The most important factor in managing DIC is aggressively treating the underlying
cause

Correcting the secondary effects of tissue ischemia by improving oxygenation,

replacing fluids, correcting electrolyte imbalances, and administering vasopressor
medications is also important.

If serious hemorrhage occurs, the depleted coagulation factors and platelets may
be replaced to reestablish the potential for normal hemostasis and thereby
diminish bleeding.

Cryoprecipitate is given to replace fibrinogen and factors V and VII. Administering

fresh frozen plasma replaces coagulation factors. Platelets are transfused to correct
severely low platelet levels, control bleeding
DISSEMINATED INTRAVASCULAR
COAGULATION
NURSING MANAGEMENT

Nurses need to be aware of which patients are at risk for DIC

Patients need to be assessed thoroughly and frequently for signs and symptoms of
thrombi and bleeding and monitored for any progression of these signs

Lab values must be monitored frequently, not only for the actual result but to note
trends over time as well as the rate of change in values.

Assessment and interventions should target potential sites of end-organ damage

DISSEMINATED INTRAVASCULAR
COAGULATION
NURSING MANAGEMENT

Nurses need to be aware of which patients are at risk for DIC

Patients need to be assessed thoroughly and frequently for signs and symptoms of
thrombi and bleeding and monitored for any progression of these signs

Lab values must be monitored frequently, not only for the actual result but to note
trends over time as well as the rate of change in values.

Assessment and interventions should target potential sites of end-organ damage

THROMBOTIC DISORDERS

Altered balance within the normal hemostasis process, causing excessive

thrombosis that may be arterial (due to platelet aggregation) or venous (composed
of platelets, red cells, and thrombin).

Decreased clotting inhibitors within the circulation, altered hepatic, lack of

fibrinolytic enzymes, and tortuous or atherosclerotic vessels

Thrombosis may occur as an initial manifestation of an occult malignancy or as a

complication from a pre- existing cancer.

Hyperhomocysteinemia, antithrombin (AT) deficiency, protein C deficiency, protein

S deficiency, activated protein C (APC) resistance, and factor V Leiden deficiency -
hypercoagulable states
THROMBOTIC DISORDERS
THROMBOTIC DISORDERS

A recent study found that taking aspirin after completing standard

anticoagulation therapy for treating VTE reduced the risk of recurrent thrombosis

With some conditions, or with repeated thrombosis, lifelong anticoagulant

therapy is necessary.
HYPERHOMOCYSTEINEMIA
Homocysteine can promote platelet aggregation.

Increased plasma levels of homocysteine are a significant risk factor for VTE
(e.g., deep vein
thrombosis [DVT], pulmonary embolism [PE]), recurrent VTE, and arterial
thrombosis (e.g., ischemic stroke, ACS)

Hyperhomocysteinemia can be hereditary, or it can result from a nutritional

deficiency of folate and, to a lesser extent, of vitamins B12 and B6, because
these vitamins are cofactors in homocysteine metabolism.

In hyperhomocysteinemia, the endothelial lining of the vessel walls is denuded,

which can precipitate thrombus formation.

Smoking causes low levels of vitamin B6 and B12 and folate

ANTITHROMBIN DEFICIENCY
AT is a protein that inhibits thrombin and certain coagulation factors, and it may
also play a role in diminishing inflammation within the endothelium of blood
vessels.

Most commonly a hereditary condition that can cause venous thrombosis

common sites for thrombosis are the deep veins of the leg and the mesentery.

Patients tend to exhibit heparin resistance; require greater amounts of heparin

AT deficiency can also be acquired by four mechanisms:

1. Accelerated consumption of AT (as in DIC)

2. Reduced synthesis of AT (as in hepaticdysfunction)
3. Increased excretion of AT (as in nephrotic syndrome)
4. Medication induced (e.g., estrogens, L-asparaginase)
PROTEIN C DEFICIENCY
Protein C is a vitamin K–dependent enzyme synthesized in the liver; when
activated, it inhibits coagulation.

Deficient, the risk of thrombosis increases, and thrombosis can often occur
spontaneously.

Individuals with Protein C deficiency are at higher risk for recurrent PE

Complication of anticoagulation management is warfarin-induced skin necrosis.

Treatment with purified protein C concentrate is sometimes indicated.

PROTEIN S DEFICIENCY
Protein S is another natural anticoagulant normally produced by the liver.

Like patients with protein C deficiency, those with protein S deficiency have a
greater risk of recurrent venous thrombosis early in life, and also with recurrent
PE

Thromboses most commonly occur in the axillary, mesenteric, and cerebral

veins.

Warfarin-induced skin necrosis is possible.

Acquired protein S deficiency can also occur.

Pregnancy, DIC, liver disease, nephritic syndrome, HIV infection, and the use of
L-asparaginase have all been associated with reduced protein S levels.
ACTIVATED PROTEIN C RESISTANCE AND FACTOR V
LEIDEN MUTATION
APC resistance is a common condition that can occur with other hypercoagulable
states.

APC is an anticoagulant, and resistance to APC increases the risk of venous

thrombosis.

Factor V Leiden mutation is the most common cause of inherited

hypercoagulability in Caucasians,

Factor V Leiden mutation synergistically increases the risk of thrombosis in

patients with other risk factors (e.g., the use of oral contraceptives,
hyperhomocysteinemia, increased age).

The duration of anticoagulation is based upon the coexistence of other risk

factors for thrombi formation
ACTIVATED PROTEIN C RESISTANCE AND FACTOR V
LEIDEN MUTATION
MEDICAL MANAGEMENT

The primary method of treating thrombotic disorders is anticoagulation.

However, in thrombophilic conditions, when to treat (prophylaxis or not) and how

long to treat (lifelong or not) can be controversial.

Anticoagulation therapy is not without risks; the most significant risk is bleeding.
ACTIVATED PROTEIN C RESISTANCE AND FACTOR V
LEIDEN MUTATION
PHARMACOLOGIC THERAPY

1. Heparin
2. Warfarin (Coumadin)
3. Thrombin and Factor Xa Inhibitors
4. Aspirin
ACTIVATED PROTEIN C RESISTANCE AND FACTOR V
LEIDEN MUTATION
NURSING MANAGEMENT

Patients with thrombotic disorders should avoid activities that lead to circulatory
stasis (e.g., immobility, crossing the legs).

Exercise, especially ambulation, should be performed frequently throughout the

day, particularly during long trips by car or plane.

Anti-embolism stockings are often prescribed

Surgery further increases the risk of thrombosis.

Medications that alter platelet aggregation, such as low-dose aspirin or

clopidogrel (Plavix), may be prescribed.

Anticoagulants such as warfarin

ACTIVATED PROTEIN C RESISTANCE AND FACTOR V
LEIDEN MUTATION
NURSING MANAGEMENT

Assessed for concurrent risk factors for thrombosis and should avoid them if
possible.

Tobacco and nicotine products should be avoided

In many instances, younger patients with thrombophilia may not require

prophylactic anticoagulation; however, with concomitant risk factors (e.g.,
pregnancy), increasing age, or subsequent thrombotic events,prophylactic or
long-term anticoagulation therapy may be required.

Accurate health history can be extremely useful and can help guide the selection
of appropriate
therapeutic interventions.

Patients need to understand risk factors for thrombosis and what they can do to
diminish or reduce them, such asavoiding smoking, using alternative forms of
ACTIVATED PROTEIN C RESISTANCE AND FACTOR V
LEIDEN MUTATION
NURSING MANAGEMENT

Assessed for concurrent risk factors for thrombosis and should avoid them if
possible.

Tobacco and nicotine products should be avoided

In many instances, younger patients with thrombophilia may not require

prophylactic anticoagulation; however, with concomitant risk factors (e.g.,
pregnancy), increasing age, or subsequent thrombotic events,prophylactic or
long-term anticoagulation therapy may be required.

Accurate health history can be extremely useful and can help guide the selection
of appropriate
therapeutic interventions.

Patients need to understand risk factors for thrombosis and what they can do to
diminish or reduce them, such asavoiding smoking, using alternative forms of
ACTIVATED PROTEIN C RESISTANCE AND FACTOR V
LEIDEN MUTATION
NURSING MANAGEMENT

When a patient with a thrombotic disorder is hospitalized, frequent assessments

should be performed for signs and symptoms of beginning thrombus formation,
particularly in the legs (DVT) and lungs (PE).

Ambulation or range-of-motion exercises as well as the use of antiembolism

stockings

Properly fitted graduated compression stockings may reduce pain and edema
associated with the acute stage of DVT
Thank You for
Listening!