HEMATOLOGY

The science dealing with the formation,

composition, functions, and diseases of the
blood and the morphology of the blood-forming
organs.
Terminologies:
Morphology- The science that deals with the
form and structure of living thing, regarded as a
whole, and apart from their function .

 Anemia: decreased red blood cell (RBC) count.

Autologous donation: a donation of the
clients own blood before a scheduled
procedure
Band cell: slightly immature neutrophil.
Blast cell: primitive white blood cell ( WBC)
Cytokines: proteins produced by leukocytes
that are vital regulation of hemotopoiesis,
apoptosis(programmed cell death), and
immune responses.
Differentiation: development of functions and
characteristics that are different from those of
the parent stem cell.
Erythrocyte: a cellular component of blood
involved in the transport of oxygen and carbon

 Erythropoiesis: process of formation of RBCs.

Etyhropoietin: hormone produced primarily by
the kidney. Necessary for erythropoiesis.
Fibrin: filamentous protein; basis of thrombus
and blood clot.
Fibrinogen: protein converted into fibrin to form
thrombus and clot
Fibrinolysis: process of breakdown of fibrin clot.
Fresh frozen plasma: a blood product
administered to increase the level of clotting
factors in clients with such a deficiency
Granulocyte: granulated WBC (i.e,. Neutrophil,
eosinophil, basophil); sometimes used
synonymously with neutrophil.

 Hematocrit: percentage of total blood volume

consisting of RBCs.
Hematopoiesis: complex process of the
formation and maturation of blood cells.
Hemoglobin: iron-containing protein of RBCs;
delivers oxygen to tissues.
Hemostasis: intricate balance between clot
formation and clot dissolution.
Histiocytes: cells present in all loose
connective tissue, capable of phagocytosis.
Iron overload: a delayed transfusion
comlication that occurs in client who are
chronically dependent on blood transfusion,
such as clients with anemia or
thrombocytopenia

 Left shift, or shift to left: increased

release of immature forms of WBCs from
the bone marrow in response to need
Leukocyte: one of several cellular
components of blood involved in defense
of the body; subtypes include
neutrophils, eosinophils, basophils,
monocytes, lymphocytes.
Leukopenia: less-than-normal amount
of WBCs in circulation
Lymphocyte: form of WBC involved in
immune function.

 Lymphoid: pertaining to lymphocytes.

Macrophage: reticuloendothelial cells
capable of phagocytosis.
Monocyte: large WBC that becomes a
macrophage when it leaves the
circulation and moves into body tissues.
Myeloid: pertaining to nonlymphoid
blood cells differentiate into RBCs,
platelets, macrophages, mast cells, and
various WBCs.
Myelopoiesis: formation and maturation
of cells derived from myeloid stem cell.

 Natural killer cells: immune cells

accumulate in lymphoid tissue that are potent
killers if virus-infected and cancer cells.
Neutrophil: fully mature WBC capable of
phagocytosis; primary defense against
bacterial infection.
Nucleated RBC: immature form of red blood
cell (RBC); portion of nucleus remains within
the RBC.
Oxyhemoglobin: combined form of oxygen
and hemoglobin; found in arterial blood.
Phagocytosis: process of cellular ingestion
and digestion of foreign bodies.
Plasma: liquid portion of blood.

 Plasminogen: protein converted to plasmin to dissolve

thrombi and clots.
Platelet: a cellular component of blood involved in
blood coagulation. A blood product administered to
clients with low platelet counts and to
thrombocytopenic clients who are bleeding actively or
are scheduled for an invasive procedure.
Red blood cell (RBC): a cellular component involved
in the transport of oxygen and carbon dioxide.
Reticulocytes: slightly immature RBCs, usually in 1%
of total circulating RBCs.
Reticuloendothelial system: complex system f cells
throughout the body capable of phagocytosis.
RH factor: a person having the factor is Rh positive; a
person lacking the factor is Rh negative
Serum: portion of blood remaining after coagulation
occurs.

 Septicemia: the presence of infective agents or their

toxins in the bloodstream. Septicemia is a serious
infection and must be treated promptly; otherwise, the
infection leads to circulatory collapse, profound shock
and death
Stem cell: primitive cell, capable of self-replication and
differentiation into myeloid of lymphoid stem cell.
Stroma: component of the bone marrow not directly
related to hematopoiesis but serves important
supportive roles in this process.
Transfusion reaction: a hemolytic reaction caused by
blood type or Rh incompatibility. An allergic transfusion
reaction most often occurs in clients with a history of
allergic. A febrile transfusion reaction most commonly
occurs in client with antibodies directed against the
transfused white blood cells. A bacterial transfusion
reaction after transfusion of contaminated blood
products.

 Thrombin: enzyme necessary to convert

fibrinogen into fibrin clot.
Thrombocyte: a cellular component of
blood involved in blood coagulation/
White blood cell (WBC): one of several
cellular component of blood involved in
defense of the body; subtypes include
neutrophils, eosinophils, basophils,
monocytes, and lymphocytes.
Whole blood: whole blood is composed of
red blood cells, plasma and plasma proteins
and is administered primarily to treat
hypovolemic shock resulting from
hemorrhage

Learning Outcomes
At the end of this Chapter, the learner will be able to:
1. Conduct nursing history and physical assessment of a
client with an actual or potential hematologic disorder.
2. Teach a client about diagnostic studies used to detect
hematologic disorder.
3. Discuss risk factors, basic pathophysiology and clinical
manifestations of hematologic disorders
4. Design a plan of care for the prevention, collaborative
management and rehabilitation of clients with
hematologic disorders.
5. Implement nursing interventions that optimize the quality
of life of clients with hematologic disorders.
6. Evaluate planned clients outcomes, using outcome
criteria developed in the planning phase of care.

Overview of the Anatomy and

Physiology of the Blood:
The blood consist of blood cells and fluid called plasma.
The blood transports gases, nutrients, metabolic wastes,
blood cells, immune cells, and hormones throughout the
body.
The formed elements in the blood include red blood cells
(RBCs or erythrocytes) 4,000,000 to 6,000,000 per cu mm,
white blood cells (WBCs or leukocytes) 5,000 to 10,000 per
cu mm and platelets (thrombocytes) 200,000 to 500,000 per
cu mm.
RBCs transport oxygen and carbon dioxide to and from tissue
RBCs contain hemoglobin, the oxygen carrying substance
that gives blood its red color.
RBCs have an average lifespan of 90 to 120 days. The spleen
sequesters the old worn out RBCs, thereby removing them
from the circulation

 The surface of each RBC carries antigens

that determine a persons blood group, or
blood type A, B, AB, O.
Platelets play a major role in hemostasis
(blood-clotting).
Through a three stage process, the
circulatory system protects itself from
excessive blood loss. Vascular injury
activities a complex chain of events
namely, vasoconstriction, platelet
aggregation, and coagulation that leads to
clotting.

Vascular Injury
A VASOCONSTRICTION
Smooth muscle spasm
Contraction of blood vessels
B PLATELET AGGREGATION
Adherence of Circulating Platelets to collagen fibers
Adenosine diphosphate causes platelets to breakdown
and stick together
Platelets aggregate to plug the wound
C COAGULATION

Extrinsic System
Factors III and VII activate in presence of Factor IV (Calcium) and phospholipids

Factor X activates; extrinsic factor ends

Intrinsic System
Plasma Thromboplastin activates
Calcium, factor XII activate Factor XI, initiating Factor IX activity
In the presence of platelet phospholipids, factor IX converts Factor VII and
helps form Factor ends

Factor X reacts with Prothrombin (Factor V) to form prothrombinconverting complex

In the presence of Calcium and platelets, Factor X and Factor
V convert pathrombin to thrombin

Thrombin hydrolyses Fibrinogen

(factor I)
XIII)

Thrombin activates fibrin

stabilizing factor (factor

Fibrin monomers from fibrin

Threads that build polymer network
Fibrin polymer strengthen; firm clot forms

 WBCs serve as bodys defense and immune

system
The two groups of WBCs and granulocytes and
agranulocytes.
The granulocytes (polymorphonuclear leukocytes)
include neutrophils, eosinophils, and basophils.
Neutrophils are phagocytic; they engulf, ingest
and digest foreign materials.
Eosinophils participate in allergic responses
Basophils secrete histamine in response to certain
inflammatory and immune stimuli. They also
secrete heparin which prevents abnormal clotting
in the blood vessels.
Granulocytes serves as bodys first line of cellular
defense against foreign organism

 The agranulocytes (mononuclear leukocytes)

include monocytes and lymphocytes
Monocytes enlarge and mature to become
macrophages or histiocytes; they perform
phagocytosis.
Lymphocytes (T-lymphocytes and Blymphocytes) are responsible for specific
immune responses. T-cells are involved in cellmediated immunity, while B-cells are involved
in humoral immunity

ASSESSMENT OF THE CLIENT WITH

HEMATOLOGIC DISORDER
History
Complete health history
Present condition
Medical history
Use of medications
Exposure to chemicals or radiation
Family history
Psychosocial history lifestyle data
Review of system

Chief Complaint
Chills, fever, fatigue, weight loss, physical discomfort

Medical history
Previous hematologic problems (anemia, recurrent
infections, delayed wound, healing, DVT, liver disease or
excessive bleeding)

 Use of medications
ASA, ASA containing compounds, antibiotics
Allergic reactions
Blood or blood product reactions as well as complications.

Family history
Bleeding disorders (e.g. hemophilia)
Jaundice, anemia, leukemia
Congenital blood dyscracias

Psychosocial History and Lifestyle

Occupation exposure to chemicals or radiation
Habits
Nutritional habits
Use or abuse of alcohol
Use of recreational drugs (accompanied by malnutrition and vitamin
deficiency; alcohol causes liver damage)

Review of System
Fatigue, weakness, chills, fever, night sweats, lethargy,
malaise, delayed wound healing

DISORDERS AFFECTING THE RBCs

Polycythemia
increased rbc and hgb production
Compensatory response to chronic hypoxia

Hypoxia
Erythropoietin production by the kidneys
Stimulation of the bone marrow to rbc
production (this is the bodys attempt to
increase the oxygen-carrying capacity of the
blood )

 Polycythemia Vera
Hyperplasia(increase the number of new
cells) of the bone marrow
rbc (erythrocytosis); wbc (leukocytosis);
platelets (thrombocytosis)
Cause is unknown; associated with genetics
Pathophysiology of Polycythemia Vera

rbc, wbc, platelets

blood
viscosity
Thromboemboli
sm

Organ
infiltration

Hepatomegaly
Splenomegaly
Arthralgia
Celebral hypoxia

Capillary over
distention
Rupture

Hemorrhage

SIGNS AND SYMPTOMS OF POLYCYTHEMIA VERA

Ruddy complexion - ruddy is used to describe
something that is reddish, it is commonly used to
describe someones complexion. Ruddy skin has a
reddened and irritated appearance.
Headache
Dizziness
Fatigue
Blurred vision
Hepatosplenomegaly - is a disorder where both the
liver and the spleen swell beyond their normal size,
usually due to infection such as mononucleosis or
viral hepatitis.
Increased risk of CVA and MI due to
thromboembolism.

 Collaborative Management for Polycythemia Vera

Increase fluid intake to reduce blood viscosity
Monitor for signs and symptoms of bleeding
Monitor for signs and symptoms of thromboembolism.
o Angina
o Claudication- a condition in w/c cramping pain on the leg is induced by
exercise, typically caused by obstruction of the arteries or due to
inadequate blood flow to the muscles. The pain usually caused the
person to limp, typically is felt while walking and subsides with rest.
o Thrombophlebitis
o Pruritus

Administer analgesic as ordered

Administer antihistamine to decrease pruritus
Therapeutic phlebotomy to reduce circulating volume
Chemotherapy to inhibit hyperactivity of the bone marrow
Radiation therapy (Na Phosphate / IV)
Patient teaching: Avoid high altitude (mountains, airplane travel).
Low oxygen levels in high altitude tend to stimulate the kidneys
to increase secretion of erythropoietin. This cause increased rbc
production

ANEMIAS
The primary problem in anemia is decreased availability of oxygen to
the tissues.
Types of Anemia (in Adults)
Iron deficiency anemia
Folate Deficiency Anemia
Aplastic Anemia
Pernicious Anemia

Causes of Anemia
Acute or chronic blood loss.
Inadequate dietary intake of vitamins and minerals needed for rbc
production
Decreased rbc production by the bone marrow, e.g., aplastic anemia
Increased destruction of rbc, e.g., hemolytic anemia, severe
infection, cancer.
Increased demands of vitamins and minerals needed for rbc
production, e.g., infants, adolescents, pregnant clients.

 Classification of Anemia: Classified based

on the size of RBC as measured by Mean
Corpuscular volume (MCV)
a. Microcytic- MCV of less than 80m3(80fL); in the
case of iron deficiency anemia.
b. Normocytic- MCV 80-100m3(80-100fL); may be
caused by Chronic Disease, hemolysis or bone
marrow disorders.
c. Macrocytic- MCV is greater than 100m3(100fL);
Conditions involving Vit. B12 and Folate deficiency,
and Thyroid Function.

 Common Clinical Manifestation of Anemia

Pallor
Easy fatigability
Weakness
Anorexia
Weight loss
SOB (shortness of breath)
Headache / Dizziness
Tachycardia / Palpitation
Syncope- temporary loss of consciousness caused by
fall of blood flow.
Brittle hair and nails
Paresthesia is the abnormal sensation of the body;
such as numbness. Tingling, or burning caused chiefly
by pressure on or damage to peripheral nerves.
Cold sensitivity
Amenorrhea

IRON DEFICIENCY ANEMIA

(Microcytic, hypochromic anemia)
Assessment
Vinson Plummers Syndrome
Stomatitis
Dysphagia
Atrophic glossitis (smooth, sore tongue)

Cheilosis (cracks at the side of the lips)

Koilonychia (spoon shaped or concave fingernails)
Pica (craving of non edible substances like clay, laundry
starch, ice, uncooked rice, etc). This may cause food poisoning
Tinnitus humming noises that accompany certain types of
hearing disorder.
Cardiovascular symptoms (if hgb = 7.5 g / dl.or below)
PR, chest pain, SOB, CHF
Blood transfusion is necessary

 Collaborative Management
Medical Management
1. Iron Supplement

Oral
Ferrous Sulfate. Given after meals to prevent GI irritation
Ferrous Gluconate. Given before meals. These do not
cause GI irritation
Ferrous Fumarate. Given before meals for adequate
absorption
Parenteral: Iron Dextran (Imferon). Administered by Ztrack method to prevent staining of the skin. Do not
massage site of injection. To prevent leakage of
medication into the subcutaneous layer
Oral liquid iron to be administered with straw to prevent
permanent staining of the teeth.
Vitamin C increases iron absorption, e.g., orange juice.
Do not administer with tea, milk, antacid. These will
inhibit absorption of iron.

- Iron salts change color of stool to dark green or black.

This is harmless. These can cause adverse reactions like
nausea, vomiting, epigastric pain, pallor, drowsiness.
- Iron may cause constipation. Increase fluid intake.

2. Oxygen therapy for SOB (shortness of breath)

3. Blood transfusion as needed.

Nursing Interventions
Promote rest to reduce oxygen demands of tissues. This
is the priority nursing intervention
Provide good oral care. To prevent and relieve
stomatitis
Provide good skin care. To prevent pressure sore,
especially among bedridden clients.
Diet: Iron rich foods.
o.
o.
o.
o.

Organ meats, lean meats, egg yolk.

Beans
Green, leafy vegetables
Raisins; other dried fruits.

FOLATE DEFICIENCY ANEMIA (Megaloblastic

Anemia)
This is due to chronic deficiency of folic acid.

Causes

Poor dietary intake

Rarely eat uncooked (raw) fruits and vagetables
Alcoholism
Chronic malnutrition
Pregnancy
Anorexia nervosa
Malabsorption
Malignancy
Prolonged TPN
Chronic hemodialysis

 Clinical manifestation of folate deficiency anemia are

as follows:
1. Cracked lips, sore tongue
2. Macrocytic, hyperchromic RBCs.
3. Decreased RBC, hemoglobin, hematocrit, increased MCV and
MCHC.

Collaborative management for folate (Folic

Acid) deficiency Anemia:
1. Well balance diet that includes green vegetables
(asparagus, broccoli, spinach), yeast, liver and
other organ meats, some fresh fruits; avoid over
cooking vegetables.
2. Folic acid 1 mg./day per orem as prescribed.

NOTE: Folic acid deficiency among pregnant

clients may cause congenitally acquired neural
tube defects (spina bifida)

PERNICIOUS ANEMIA
A type of megaloblastic associated with Vitamin B 12
deficiency
It is also called gastric surgery, Chrohns disease,
autoimmune gastric mucosal atrophy.
Decreased intrinsic factor production by the parietal cells
of the stomach causes decreased Vitamin B12 absorption.
Vitamin B12 has to blind with intrinsic factor so that it can
be absorbed in the small intestine.
Decreased Vitamin B12 absorption results to the following:
1.Decreased RBC production.
2.Decreased DNA synthesis in maturing RBCs; the RBCs do not
divide normally so, they grow big resulting to megaloblastic cells.
3.Impaired integrity of cells in the GI tract (mouth, stomach, anus),
vagina, and axon of neurons.

 Pathophysiology of Pernicious Anemia

INTRINSIC FACTOR production
by the parietal cells of the stomach
VITAMIN B12 absorption
RBC production
DNA synthesis in maturing RBC
(megaloblastic cells)
Impairment of integrity of cells (mouth,
stomach, anus, vagina, axon of neurons)

 Diagnostic Tests for Pernicious Anemia

1. Tubeless Gastric Analysis

Diagnex blue / Azuressin tablet per orem

Collect urine specimen
Blue
Blue
HCI is present
(Archlorhydria)
(-) Pernicious Anemia
Pernicious Anemia

(-) HCL

(+)

NOTES:
1. HCL and intrinsic factors are both produced
by the parietal cells of the stomach.
2. CBC and blood smear show deceased
hemoglobin and hematocrit; with unusually
large RBCs.
3. Gastric analysis shows volume and acidity of
gastric juice are diminished.
4. Schillingis s Test. This is the most definitive
diagnostic test for pernicious anemia.
5. The test involves administration of small
amount of radioactive. B12 orally and 24hour urine collection to measure uptake.
Decreased excretion of vitamin B12 in the
urine supports the diagnosis of pernicious

 The clinical manifestations of pernicious anemia

are as follows:
1. Beefy red, inflamed tongue this is the most
characteristic manifestation.
2. Neurologic involvement due to destruction of axons
of neurons: paresthesia, lack of balance,
uncoordinated movements, paralysis, altered
thought processes, bladder and bowel dysfunction,
psychiatric symptoms caused by celebral
dysfunction.
3. Jaundice due to faulty erythropoiesis

 Collaborative management for pernicious anemia include

the following:
1. Monthly vitamin B12 IM for life. Oral vitamin B12 cannot be
absorbed because of inadequate intrinsic factor.
2. Folic acid (Folvite). up to 1mg/day p.o.; given IM to patients with
malabsorption.
3. Ferrous Sulfate (Feosol) or Ferrous Gluconate (Fergon) 0.3g TID
p.o., as needed, to correct nutritional deficit.
4. Hydrochloric acid (HCI), 4 to 10 ml. p.o., well diluted in water TID
(three times a day) with meals during first week of vitamin B12
therapy.
5. Blood transfusion as needed.
6. Physical examination every 6 moths for hematologic studies and
GI evaluation. The client may develop hematologic or neurologic
relapse if therapy is inadequate.

NOTE: Patients with pernicious anemia have higher

incidence of gastric cancer and thyroid dysfunction;
periodic stool examinations for occult blood, gastric
cytology, and thyroid function tests are done.

APLASTIC ANEMIA
Is a disorder characterized by bone marrow hyploplasia or aplasia
resulting in pancytopenia (decreased numbers of RBCs, WBCs and
platelets)
The causes of aplastic anemia are as follows: congenital (Fanconis
anemia); exposure to chemical toxins; idiopathic; ionizing radiation; viral
infection, especially hepatitis; certain drugs (e.g., Chloramphenicol).
Bone marrow aspiration and biopsy show bone marrow is fatty,
hypocellular or empty with greatly reduced or absent hematopoiesis.
The clinical manifestation of aplastic anemia are as follows:
1.From anemia; pallor, weakness, fatigue, exertional dyspnea, palpitations.
2.From infections associated with neutropenia(decreased in the number of
cells called neutrophils): fever, headache, malaise; abdominal pain,
diarrhea; adventitious breath sounds; erythema, pain, exudates at
wounds or sites of invasive procedures.
3.From thrombocytopenia: bleeding from gums, nose, gastrointestinal, or
genitourinary tracts; purpura, petechiae, ecchymoses.

 Collaborative for management aplastic

anemia include the following:
1. Medical Management
Bone marrow transplantation
Immunosuppressive therapy
Corticosteroids
Sandimmune (Cyclosporine)
Cytoxan (Cyclophosphamide)
ATG (antithymocyte globulin)
ALG (antilymphocyte globulin)
Imuran (Azathioprine)
Tacrolimus (Prograf)
Blood transfusion as necessary.

 Nursing Interventions
Asses for signs and symptoms of tissue hypoxia, infection,
and bleeding.
Frequent rest periods to reduce oxygen demands of
tissues.
To minimize risk of infection:
Implement Reverse / Protective Isolation. Provide private room;
practice strict hand washing..
Encourage good personal hygiene including good oral care daily,
shower or bath with mild soap, and perirectal care after using
the toilet.
Monitor vital signs including temperature frequently, notify
health care provider of fever
Avoid eating raw foods; do not permit fresh fruits or fresh flowers
in the clients unit
Limit visitors, do not allow people with signs and symptoms of
infection to visit the client.
Avoid crowds. To prevent contracting infections especially
respiratory infections.
Minimize invasive procedures or possible trauma to skin or
mucous membranes.

To minimize risk of bleeding:

Use soft toothbrush or toothettes for mouth care,
electric razor for shaving, keep nails, short by filing.
Avoid intramuscular (IM) injections and other
invasive procedures.
Prevent constipation by use of stool softener
(Colace/Docussate Na) as prescribed.
Restrict activity based on platelet count and active
bleeding.
Monitor pad count for menstruating patient; avoid
use of vaginal tampons.
Control bleeding by applying pressure to the site,
using ice packsand prescribed topical hemostatic
agents.
Advise client to use water soluble lubricants as
needed, during sexual intercourse.

Thalassemia Major (Cooleys Anemia)

It is the most severe of the beta-thalassemia
syndromes. Beta thalassemia refers to an
inherited hemolytic anemia, characterized by
a reduction or absence of beta globulin
chain in hemoglobin synthesis. This RBC has
a decreased amount of hemoglobin, resulting
in a fragile RBC with a short lifespan.
The disease is most prevalent in the
Mediterranean basin, Middle East, Southeast
Asia and Africa. In the US, it is most common
in children of Italian, Greek and Southeastern
Asian Ancestry.

 The clinical manifestation of Thalassemia

major are as follows:
1. Expansion of bone marrow cavities of the
bone. This is due to increase in erythoid
activity, in an attempt to overcome the
increased rate of destruction of RBCs. there
is thinning of the bony cortex. These lead to
skeletal deformities (frontal and maxillary
bossing), growth retardation, pathologic
fractures.
2. Hemosiderosis. This is increased iron level in
the blood, which may be deposited on organ
tissues especially in the heart. This is due to
rapid destruction of defective RBCs,
decreased production of hemoglobin, and

 Collaborative management for Thalassemia include

the following:
1. Frequent and regular blood transfusion of packed RBCs.
2. Iron chelation therapy with Desperal (Deferoxamine).
This reduces the toxic side effects of excess iron;
increases excretion through urine an feces. Be alert for
visual and hearing deficits associated with use of
Desferal.
3. Splenectomy. To reduce rate of hemolysis or RBCs.
4. Decrease dietary iron
5. Monitor cardiovascular status. (CHF is a usual cause of
death).
6. Relieve bone pain (e.g., NSAIDs).
7. Avoid contract sports (skateboarding, football, soccer,
etc.) to reduce risk of fracture.
8. Encourage prompt medical attention for fever or signs
of infection.

SICKLE CELL ANEMIA

Sickle cell anemia is a genetically determined abnormality in the
structure of hemoglobin.
The inheritance pattern is classic Mendelian.
Heterozygotes have sickle cell trait while homozygotes have two
abnormal S genes, and have sickle cell disease.
The HbS crystallizes under conditions of deoxygenation, thus deforming
he entire red blood cell (RBC) into an elongated, crescent shape.
Such cells become trapped in capillaries, producing ischemia and/or
necrosis of tissues; hemolysis of trapped RBCs result in anemia.
Individuals with sickle cell trait experience few clinical problems and have
a normal life expectancy; RBCs sickle only under conditions of extremely
low Pao2 .
Those with sickle cell disease experience recurrent episodes of sickle cell
crisis, require multiple hospitalizations and transfusions, and have
significantly higher mortality rates than normal persons. The mutation
arose in Africans and imparted protection against malaria to
heterozygotes.
About 10% of African Americans carry the sickle cell trait; 0.15% have
the disease.

 The sickling response is reversible under condition of

adequate oxygenation and hydration.
After repeated sicking, the cell becomes permanently sickled.
Sickle cell crisis are acute exacerbation of the disease, which
vary considerably in severity and frequency; these includes
vasoocclusive crisis, splenic sequestration, and aplastic
crisis.
Assessment of the Sickle Cell Crisis:
vasoocclusive crisis- is the most common type of crisis. Caused
bystasis of blood with clumping of the cells in the microcirculation,
ischemia, and infarction.

Signs incude fever, pain, and tissue engorgement.

splenic sequestration- life-threatening crisis, caused by the pooling
of the blood in the spleen.

Signs include profound anemia, hypovolemia and shock.

aplastic crisis- is caused by diminished production and increased
destruction of the red blood cells, triggered by viral infection or the
depletion of folic acid.

Signs include profound anemia and pallor.

CAUSES

Point mutation in hemoglobin gene produces abnormal hemoglobin S.

Trait is passed genetically to offspring.
Insufficient oxygen causes the cells to assume a sickle shape; and the cells become
rigid and clumped together, obstructing the capillary blood flow.
Situations that precipitate sickling include fever, and emotional or physical stress; any
condition that increases the need for oxygen or alters the transport of oxygen can
result to sickle cell crisis.
SIGNS & SYMPTOMS

S/S of anemia; pallor, fatigue, shortness of breath, tachycardia.

Chronic tissue/organ damage in heart, lung, kidney, spleen, liver, gall bladder, skin,
eye, nerve
Sickle cell crisis may be precipitated by viral or bacterial infection, changes in
environmental temperatures, or any condition producing decreased Pao 2, such as
asthma
Pain is ischemic(local temporary reduction of blood supply of an area) and may be
located anywhere, but most often is in the abdomen, chest, joints, or back
Jaundice
DIAGNOSTICS

Complete blood count (CBC) shows decreased hemoglobin, hematocrit, and RBC count.
Peripheral blood smear will show characteristic RBC sickle morphology.
Sickle cell prep will be positive with neither the trait or the disease (no distinction).
Hemoglobin electrophoresis will provide a definitive diagnosis.

MEDICAL INTERVENTIONS
Care focuses on the prevention (preventing
exposure to infection and maintaining normal
hydration) and treatment (oxygen, hydration,
pain management, and bed rest) of the crisis.
Folic acid is administered to meet the increased
demands of the bone marrow
Hydration therapy is administered to clients in
sickle cell crisis to improve blood flow, reduce
pain, and prevent renal damage. Analgesics are
given for pain.
Blood transfusions may be necessary in severe
cases and for pregnant women.
Genetic counseling is important for clients and
significant others at risk for sickle cell anemia

SELECTED NURSING DIAGNOSES WITH INTERVENTIONS

Pain
Ask the client to rate the pain on a scale of 0 to 10. also assess the
clients nonverbal cues indicating pain.
Administer analgesics as prescribed, and assess the clients
response.
Teach the client alternative, non-pharmacologic measures to reduce
pain, such as meditation, guided imagery, and distraction.
Altered Tissue Perfusion
Administer oxygen as prescribed for the client in sickle cell crisis.
Ensure adequate hydration by offering non-caffeinated beverages
and administering normal saline IV, as prescribed.
Encourage the client to wear loose, non-constrictive clothing.
Tell the client to avoid flexion of the knees and hips to promote
venous return.
Maintain a room temperature of at least 72F.
Avoid taking blood pressure with an external cuff. Avoid use of
tourniquets for extended periods of time.
Perform neurovascular checks of extremities every hour, including
pulse oximetry of fingers and toes

CLIENT TEACHING
Teach the client the disease process, the genetic
component, treatment options, and how to avoid
conditions that lead to crisis.
Discuss manifestations that signal the need for
prompt medical treatment.
HOME CARE CONSIDERATIONS
Discuss the hereditary nature of the disease, and
refer the client for prenatal testing and genetic
counseling as appropriate.
Stress the need for lifelong medical supervision
of the disease and its manifestation.
A referral to a support group or other information
resource may be helpful in increasing the clients
coping skills.

THE PYRAMID OF SUCCESS

Pyramid points focus on the safe administration of
blood components, managing and providing care
related to the procedure for administering blood
components, and monitoring for complications.
Focus is on the safe procedure for administering
blood and on the signs and symptoms of transfusion
reaction. Pyramid points also focus on the immediate
interventions if a transfusion reactions occurs, and
evaluation and documentation of expected and
unexpected effects of the therapy. Integrated
Processes addressed in this chapter are Nursing
Process, Caring, Communication and Documentation
and Teaching/Learning

CLIENT NEEDS
Safe, Effective Care Environment
Clients rights
Continuity of care and close supervision during
transfusion
Establishment of priorities
Ethical practice and legal responsibilities
Handling of hazardous and infectious materials
Informed consent for the administration of blood
products
Medical and surgical asepsis
Standard, transmission-based, and other precautions.

Health Promotion and Maintenance

Client education about the signs of a transfusion
reaction
Lifestyle choices related to receiving blood transfusion

 Psychosocial Integrity
Religious, spiritual and cultural considerations related
to blood administration
Therapeutic interactions with the client regarding the
procedure for blood administration

Physiological Integrity
Documentation of the clients response to receiving
the blood product
Management of medical emergencies if a transfusion
reaction or other complication occurs
Monitoring for complications related to blood
administration
Monitoring of laboratory values
Monitoring for expected effects
Safe administration of blood and blood products
Venous access devices for blood administration

TYPES OF BLOOD COMPONENTS

A. Red blood cells
1. Red blood cells are a blood product used to replace
erythrocytes
2. Packed red blood cells usually are supplied in 250-mL unit
bags; however, they can be supplied in other amounts
such as 250- to 350- or 350- to 400-mL bags. Always
check the unit for the volume of the blood component
3. Each unit increases the hemoglobin by 1g/dL and
hematocrit by 2% to 3%; the change in laboratory values
takes 4 to 6 hours after completion of the blood
transfusion
4. Evaluation of an effective response is based on the
resolution of the symptoms of anemia and an increase in
the erythrocyte count

B. Whole Blood
1. Whole blood rarely is used; treatment with a specific blood component usually
is prescribed
2. Whole blood is used to resolve hypovolemic shock resulting from hemorrhage.
3. Whole blood contains red blood cells, plasma, and plasma proteins, and each
unit normally contains 500 mL. always check the bag for the volume of the
blood component
4. Evaluation of an effective response is based on the resolution of the
symptoms of hypovolemia

C. Platelets
1. Platelets are used to treat thrombocytopenia(deficiency of platelets in the
blood, causing bleeding into the tissues, bruising, and slow blood clotting
after an injury.), and platelets dysfunctions
2. Crossmatching is not required but usually is done (platelet concentrates
contain few red blood cells).
3. The volume in a unit of platelets may vary from 50 to 70 mL per unit to 200
to 400 mL per unit. Always check the bag for the volume of the blood
component.
4. Platelets are administered immediately on receipt from the blood bank and
are given rapidly, usually over 15 to 30 minutes.
5. Evaluation of an effective response is based on improvement in the platelet
count, and platelet counts normally are evaluated 1 hour and 18 to 24 hours
after the transfusion

D. Fresh Frozen Plasma

1. Fresh frozen plasma may be used to provide
clotting factors or volume expansion; it
contains no platelelets
2. Fresh frozen plasma is infused within 6 hours
of thawing, while clotting factors are still
viable, is infused as rapidly as possible.
3. Rh compatibility and ABO compatibility are
required for the transfusion of plasma
products
4. A unit usually contains 200 to 250 mL.
Always check the bag for the volume of the
blood component
5. Evaluation of an effective response is
assessed by monitoring coagulation studies,

E. Albumin
1. Albumin is prepared from plasma and can be
stored for 5 years
2. Albumin is used to treat hypovolemic shock
or hypoalbuminemia.
3. Albumin 25g/100 mL is equal to 500 mL of
plasma.

F. Cryoprecipitates
1. Cryoprecipitates are prepared from fresh
frozen plasma and can be stored for 1 year;
once thawed the product must be used
2. Cryoprecipitates are used to replace clotting
factors, especially factor VIII and fibrinogen

PRECAUTION AND NURSING

RESPONSIBILITIES
GENERAL PRECAUTIONS
A large volume of refrigerated blood infused rapidly through a
central catheter into the ventricle of the heart can cause cardiac
dysrhytmias
No solution other than normal saline should be added to blood
components
Medications are never added to blood components or piggybacked
into a blood transfusion
To avoid the risk of septicemia, infusion (1 unit) should not exceed
4 hours
The blood administration set should be changed every 4 to 6 hours
or according to institution policy to reduce the risk of septicemia
Always check the blood bag for the date of expiration; components
expire at midnight on the day marked on the bag unless otherwise
specified.

 Inspect the blood bag for leaks, abnormal color, clots, and
bubbles.
Blood must be administered as soon as possible (within 20
to 30 minutes) from its being received at the blood bank, as
this is the maximal allowable time out of monitored storage
Never refrigerate blood in refrigerators other than those
used in blood banks; if the blood is not administered within
20 to 30 minutes, return it to blood bank
The recommended rate of infusion varies with the blood
component being transfused and depends on the clients
condition allows
Components containing few red blood cells and platelets
may be infused rapidly, but caution should be taken to
avoid circulatory overload
The nurse should measure vital signs and assess lung
sounds before the transfusion and again after the first 15
minutes and every 1 hour after the transfusion is completed

BLOOD BANK PRECAUTIONS

Blood will be released from the blood
bank only to personnel as specified by
agency policy
The name and identification number of
the intended recipient must be provided
to the blood bank, and a documented
permanent record of this information
must be maintained
Blood should be transported from the
blood bank to only one client at a time to
prevent blood delivery to the wrong client

CLIENT IDENTITY AND COMPATIBILITY

The most critical phase of the transfusion is confirming
product compatibility and verifying client identity
Two registered nurses need to check the physicians
order, the clients identity, and the clients
identification band or bracelet and number, verifying
that the name and number are identical to those on
the blood component bag
At the bedside, the nurse asks the client to state his or
her name, and the nurse compares the name with the
name on the identification band or bracelet
The nurse checks the blood bag tag, label, and blood
requisition form to ensure that ABO and Rh types are
compatible
If the nurse notes any inconsistencies when verifying
client identity and compatibility, the nurse notifies the
blood bank immediately

CLIENT ASSESSMENT
Assess for any cultural or religious beliefs regarding
blood transfusions
A Jehovah Witness cannot receive blood or blood
products; this group believes that blood transfusions
have eternal consequences
Ensure that an informed consent has been obtained.
Determined whether the client has ever experienced
any previous reactions to blood transfusions
Check the clients vital signs; assess renal, circulatory,
and respiratory status and the clients ability to
tolerate intravenously administered fluids
If the clients temperature is elevated, notify the
physician before beginning the transfusion; a fever
may be a cause for delaying the transfusion in addition
to masking a possible symptom of an acute
transfusion reaction

ADMINISTRATION OF THE TRANSFUSION

Maintain standard , transmission-based, and other
precautions as necessary
Insert an intravenous (IV) line and infuse normal saline;
maintain the infusion at a keep vein open rate
An 18- or 19-gauge IV needle will be needed to achieve a
maximum flow rate of blood products and prevent damage
to red blood cells; if a smaller-gauge needle must be used,
red blood cells may be diluted with normal saline
A central catheter is an acceptable venous access option
for blood transfusions
Always check the bag for the volume of the blood
component
Blood products should be infused through administration
sets designed specifically for blood; use a Y tubing or
straight tubing blood administration set that contains a
filter designed to trap fibrin clots and other debris that
accumulate during blood storage

 Premedicate the client with acetaminophen (Tylenol)

or diphenhydramine (Benadryl) as prescribed if the
client has a history of adverse reactions; if
prescribed, oral medications should be administered
30 minutes before the transfusion is started
Instruct the client to report anything unusual
immediately
Determine the rate of infusion by physician order or,
if not specified, by agency policy
Begin the transfusion slowly under close supervision;
if no reaction is noted within the first 15 minutes, the
flow can be increased to the prescribed rate
During the transfusion, monitor the client for signs
and symptoms of a transfusion reaction; the first 15
minutes of the transfusion are the most critical, and
the nurse must stay with client

 If a major ABO incompatibility exists or a

sever allergic reaction occurs, the
reaction is usually evident within the first
50mL of the transfusion
Document the clients tolerance to the
administration of the blood product
Monitor appropriate laboratory values
and document effectiveness of treatment
related to the specific type of the blood
product

REACTION TO THE TRANSFUSION

If a transfusion reaction occurs, stop the transfusion, change the
IV tubing tubing down to the IV site, keep the IV line open with
normal saline, notify the physician and blood bank, and return
the blood bag and tubing to the blood bank
Do not leave the client alone, and monitor the client for any lifethreatening symptoms
Obtain appropriate laboratory samples according to agency
policies, such as blood and urine samples (free hemoglobin
indicates that red blood cells were hemolyzed)
COMPLICATION OF THE BLOOD TRANSFUSION
Transfusion reactions
Circulatory overload
Septicemia
Iron overload
Disease transmission
Hypocalcemia and citrate intoxication
hyperkalemia

A. Transfusion Reaction
1. Signs of and immediate transfusion reaction
a.
b.
c.
d.
e.
f.
g.
h.
i.
j.

Chills and diaphoresis

Muscles aches, back pain, or chest pain
Rashes, hives, itching, and swelling
Rapid, thready pulse
Dyspnea, cough, wheezing, or rales
Pallor and cyanosis
Apprehension
Tingling and numbness
Headache
Nausea, vomiting, abdominal cramping and diarrhea

2. Signs of transfusion reaction in unconscious client

a.
b.
c.
d.
e.
f.

Weak pulse
Fever
Tachycardia or bradycardia
Hypotension
Visible hemoglobinuria
Oliguria or anuria

II. NEOPLASTIC BLOOD DISORDERS

Leukemias
Are acute or chronic malignant disorders of the
blood and bone marrow. These result in the
accumulation of dysfunctional, immature cells
that are caused by loss of regulation of cell
division.
Leukemias are classified as acute or chronic as
follows:
Acute Lymphocytic Leukemia (ALL)
Acute Myelogenous Leukemia (AML)
Chronic Lymphocytic Leukemia (CLL)
Chronic Myelogenous Leukemia (CML)

 Causes of leukemias are as follows:

1.
2.
3.
4.
5.
6.

Idiopathic or unknown.
Viral infections
Familial susceptibility
Genetic disorders (Down Syndrome, Fanconis anemia)
Exposure to ionizing radiation.
Exposure to certain chemicals and toxins (e.g.,
benzene, alkylating, agents).

ALL (acute lymphocytic leukemia) is most

common in children, with peak incidence between
ages 2 and 9. childhood ALL is often cured with
chemotherapy alone, if detected early.
The primary problem in leukemia is proliferation
of immature WBCs. The client becomes immune
compromised (low resistance to infection)

 There is decreased production of RBCs and platelets.

Decreased production of RBCs causes sign and
symptoms of decreased oxygenation like pallor, fatigue,
weakness, palpitation, faintness, weight loss, shortness
of breath.
Decreased production of platelets causes abnormal
bleeding like nose bleeding, rectal bleeding, bruising,
ecchymosis, visual changes (due to retinal bleeding).
Hypertrophy of the bone marrow causes bone pain.
Organ infiltration by immature WBCs causes
hepatomegaly, splenomegaly, renal insufficiency,
hyperuricemia, arthralgia (joint pain), and increased
intracranial pressure (due to meningeal infiltration)
Hepatosplenomegaly causes abdominal pain.
Leukostasis (high numbers of circulating leukemic cells)
causes infiltration and weakening of blood vessel walls,
with high risk for rupture and bleeding, including
intracranial hemorrhage.

 Tumor lysis syndrome (rapid destruction of large

numbers of malignant cells) leads to alterations
in electrolytes (hyperuricemia, hyperkalemia,
hyperphosphatemia, and hypocalemia).
Collaborative management for leukemia:
1. Medical management include the following:

Chemotherapy
Bone marrow transplantation
Blood transfusion
Allopurinol to prevent tumor lysis syndrome.

2. Nursing interventions include the following:

Preventing infection.

Place the client in a private room with handwashing

precautions strictly enforced.

 Avoid exposure to all sources of stagnant water

(e.g., flower vases, denture cups, water pitchers,
humidifiers and plants). These are good media fir
bacterial growth.
Encourage or assist with personal hygiene mouth
care, perirectal care, daily shower of bath with mild
soap.
Monitor vital signs every 4 hours, especially body
temperature. Report fever of 101F or 38C and above.
Fever indicates infection.
Assess respiratory function every 4 hours. Neutropenic clients
are prone to bacterial or fungal pneumonia.
Assess for changes in mental status like restlessness, irritability,
confusion, headache or changes in level of consciousness. These
changes are often the first subtle signs of sepsis.
Avoid invasive procedures if possible, e.g., urinary
catheterization. Use strict aseptic technique if procedure is
unavoidable. Risk of infection from invasive procedure.

 Prevent rectal trauma by avoiding rectal

temperature, enema or suppositories. Use Sitz
bath and barrier cream for patient with diarrhea
and hemorrhoids. Use stool softeners as needed to
prevent constipation. Perianal area is high risk
site for infection, including rectal abscesses.
Obtain cultures of suspected infected sites or body
fluids. To reveal bacterial, fungal or viral
pathogens.
Avoid crowds. Immunocompromised clients can
easily be contaminated with infection, especially
in crowded places.
Avoid raw of undercooked foods. Raw or
undercooked foods increase bacterial colonization
r the GI tract.

 Preventing and managing bleeding.

Asses for signs of bleeding at least every 8 hours. Overt and
covert spontaneous bleeding is possible at platelet counts
less than 50,OOO/cu.mm.
Provide soft toothbrush for mouth care. To minimize damage
to mucous membrane.
Use only an electric razor for shaving.
Keep fingernails and toenails short and smooth.
Lubricate skin with mild soap. To minimize skin excoriation.
Avoid IM injections, and other invasive procedures.
Use stool softeners to prevent constipation. Straining at stool
causes rectal bleeding.
Teach avoidance of constipation with increased fluid and fiber.
Monitor pad count during menstruation. Avoid use of vaginal
tampon.
Control bleeding by applying pressure, ice packs, and topical
hemostatic agents (Avitene, fibrindex, Thrombinar) to site.
Promote bedrest during bleeding episode.

 Avoid use of ASA and NSAIDs.

Platelet transfusion as necessary, when platelet
count is less than 20,000/cu.mm. or with active
bleeding.
Teach clients to avoid contract sports and other
activities likely to cause injury.
Teach avoidance of forceful nose-blowing. To
prevent severe nose bleeding.

Conserving energy and increasing oxygen

supply.
Adequate rest to reduce oxygen demand of tissues.
Oxygen therapy as needed.

MALIGNANT LYMPHOMAS
A neoplastic disorder affecting the lymph nodes. It is characterized
by painless lymphadenopathy and splenomegaly. The cause is
unknown.
The main problem is infection. This is due to the inability of the
lymph nodes to produce normal lymphocytes.
There are two types of lymphomas, namely Hodgkins and nonHodgkins diseases.
Non-Hodgkins lymphomas are lymphosarcoma or Burkitts (stem
cell) lymphoma.
Hodgkins disease is more common among male adolescents, young
adults, and after age 60 years. It is characterized by presence of
Reed-Stemberg cells as detected by lymph node biopsy.
the other manifestations of Hodgkins disease are as follows: fever,
chills, general malaise, night sweats, weight loss, pruritus, pain due
to pressure on nerves, edema due to decreased venous and lymph
drainage, abdominal pain due to splenomegaly and hepatomegaly,
cough, dypnea and dysphagia due to enlarged mediastinal nodes.

 Collaborative management for Hodgkins

disease:
1. Medical Management.
Radiation therapy
Chemotherapy
MOPP regimen
M ustargen (Nitrogen mustard)
O ncovin (Vincristine)
P rocarbazine (Matulane)
P rednisone
ABVD regime
A driamycin (Doxurubicin)
B leomycin (Blenoxane)
V inblastine (Velban)
D acarbazine (DTIC)

Bone marrow transplantation

1. Nursing Interventions
Priority is prevention of infection.
Care of the client receiving radiation therapy:
o
o
o
o

Avoid rubbing powders, deodorants, lotions or

ointments or application of heat/cold to treated areas.
Keep treated areas clean and dry, bathing the areas
with tepid water and mild soap.
Encourage wearing loose fitting clothes, to prevent
skin irritation.
Protect skin from exposure to sun, chlorine, and
temperature extremes.

Frequent small meals, using bland and soft diet

at mild temperatures.
Avoid irritants such as alcohol, tobacco, spices,
extreme food temperatures (very hot or very
cold) to prevent ulcers in the oral mucosa.

Note: Chemotherapy for non Hodgkins

disease are as follows:
CAOP
C ytoxan (Cyclophosphamide)
A driamycin (Doxorubicin)
O ncovin (Vincristine)
P rednisone
BACOP
B lenoxane (Bleomycin)
A driamycin (Doxorubin)
C ytoxan (Cyclophosphamide)

P rednisone

MULTIPLE MYELONA
Is a malignant disorder characterized by proliferation
of abnormal plasma cells in the bone marrow.
The primary problems of the client with multiple
myeloma are infection due to affectation of plasma
cells, and fracture due to the affectation of the bones
(plasma cells produce osteoclast-activating factor
leading to extensive bone loss.)
Etiology is unknown; genetic and environmental factor
such as chronic exposure to low levels of ionizing
radiation, may play a part.
Generally, the disorder affects older people and is
more common among African-American men and
women.

 The clinical manifestations of multiple myeloma

include:
1. Severe bone pain due to bone destruction and pathologic
fracture. Sites most commonly affected are thoracic and
lumbar vertebrae, ribs, skull, pelvis and proximal long
bones.
2. Fatigue and weakness related to anemia cause by crowding
of marrow by plasma cells.
3. Hyperviscosity of blood due to proliferation of abnormal
plasma cells.
4. Bleeding due to abnormal platelet function.
5. Proteinuria and renal insufficiency.
6. Electrolyte disturbance:
Hypercalemia due to bone destruction.
Hyperuricemia due to cell death, renal insufficiency.

7. Decreased resistance to infection due to decreased

immunoglobulin production.
8. Bence Jones Protein in the blood and urine. This is due to
abnormal antibody in the blood and urine.

 Collaborative management for multiple

myeloma are as follows:
1. Chemotherapy
Cytoxan (Cyclophosphamide)
Alkeran (Melphalan)
Corticosteroids

2. Alpha interferon as maintenance therapy.

3. Plasmapheresis to treat hyperviscosity or
bleeding.
4. Radiation therapy for bone lesions.
5. Pamidronate to treat hypercalcemia and
alleviate bone pain. This drug should be
administered IV during 4 or more hours.
Rapid IV administration may cause renal

INFECTIOUS MONONUCLEOSIS
An infectious disorder affecting the lymphatic system, caused by Epstein Barr Virus
(EBV)
The mode of transmission is by close personal contact, like kissing (via saliva).
It is also called kissing disease.
The clinical manifestations of infectious mononucleosis include the following:
Fever, headache, fatigue
Sore throat due to pharyngitis
Anorexia, body malaise
Splenomegaly (abdominal tenderness)
Lymphadenopathy
Leukocytosis
(+) Paul Bunnel Test ; (+) Monospot Test

Infectious mononucleosis is self limiting; the course of the disease may take 2 to 4
weeks.
A dangerous complication is splenic rupture.
Collaborative management for infectious mononucleosis include:
1. Warm saline gargle to relieve sore throat.
2. Adequate rest.
3. If with splenomegaly, avoid activities that may increase the risk of injury to the spleen
(splenic rupture). Such as contact sports, bicycling, and heavy lifting. Splenic rupture
causes severe massive bleeding

III. Bleeding Disorders

Thrombocytopenia
Idiopathic Thrombocytopenia Purpura (ITP)
Disseminated Intravascular Coagulation (DIC)
Von Willebrands Disease
Thrombocytopenia
Is a decrease in circulating platelet count (less than
100,00/cu.mm.).
The cause of thrombocytopenia are as follows:
1. Decreased platelet production disease of bone marrow, leukemia,
aplastic anemia, radiation therapy.
2. Increased platelet destruction infection, drug induced, ITP, DIC.
3. Abnormal distribution of sequestration of platelets in the spleen.
4. Dilutional thrombocytopenia after hemorrhage, RBC transfusions.

The clinical manifestations of thrombocytopenia are as follows:

1. Petechiae, ecchymoses
2. Bleeding in the nose, GI and GU tracts, respiratory system and within
CNS.

 Collaborative management for

thrombocytopenia include:
1.
2.
3.
4.
5.

Treat underlying cause.

Platelet transfusion
Steroids or IV immunoglobulins.
Bleeding precautions
Evaluate urine, stool and emesis for gross
and occult blood.
6. Avoid use of ASA and NSAIDs. These
medications may cause bleeding.

Autoimmune Idiopathic Thrombocytopenic

Purpura (ITP)
Is an acute or chronic bleeding disorder that results from
immune destruction of platelets by antiplatelet
antibodies.
It usually follows viral infection in children
Clinical manifestation of ITP: bruising, petechiae, bleeding
from nares and gums, menorrhagia (excessive menstrual
bleeding).
Collaborative management for ITP include:
1. Platelet tansfusion
2. High dose corticosteroids, IV immunoglobulins (IVIG), Danazol
(Danocrine), Imuran (Azathioprine), Oncovin (Vinscristine),
Velban (Vinblastine).
3. Splenectomy removes potential site for sequestration and
destruction of platelets.
4. Bleeding precautions

Disseminated Intravascular Coagulation (DIC)

Is an acquired thrombotic and hemorrhagic syndrome.
It is characterized by abnormal activation of the clotting
cascade and accelerated fibrinolysis
This result in widespread clotting in small vessels of the
body with consumption of clotting factors and platelets,
so that bleeding and thrombosis occur simultaneously.
Causes of DIC are as follows:
1. Overwhelming infections, e.g., bacterial sepsis.
2. Obstetric complications: abruption placenta, eclampsia,
amniotic fluid embolism, retention of dead fetus.
3. Massive tissue injury: burns, trauma, fractures, major
surgery, fat embolism.
4. Vascular and circulatory collapse, shock.
5. Hemolytic transfusion reaction.
6. Malignancy: particularly of lung, colon, stomach, pancreas.

 The clinical manifestation of DIC are as follows:

1. Signs of Abnormal Clotting:
a. Coolness and mottling of extremities.
b. Acrocyanosis (cold, mottled extremities with clear
demarcation from normal tissue).
c. Dypsnea, adventitious breath sounds, chest pain.
d. Altered mental status.
e. Acute renal failure (hematuria).
f. Pain (related to bowel infarction).

2. Signs of abnormal bleeding:

a. Oozing, bleeding from sites of procedures, IV
catheter insertion sites, suture lines, mucous
membranes, orifices.
b. Internal bleeding leading to changes in vital organ
functions, altered vital signs.
c. Diagnostic result: low platelet count; PT, PTT
prolonged; fibrinogen level decreased.

 Collaborative management for DIC

include:
1. Treat underlying cause. Institute bleeding
precautions.
2. Replacement Therapy:
a. Fresh frozen plasma replaces clotting factors.
b. Platelet transfusions
c. Cryoprecipitate replaces clotting factors and
fibrinogen.

3. Supportive measures: fluid replacement,

oxygenation, maintenance of BP and renal
perfusion.
4. Heparin therapy inhibits clotting component
of DIC

VONWILLEBRANDs DISEASE
It is an inherited (autosomal dominant) or acquired bleeding
disorder characterized by decreased level of vonWillebrand
factor and prolonged bleeding time.
VonWilleBrand factor enhances platelet adhesion as first step in
clot formation, also acts as carrier of factor VIII in blood. Von
Willbrands disease another type of hemophilia, is a common
hereditary bleeding disorder that results from a deficiency of vW
factor and is often accompanied by a deficiency of factor VIII and
platelet dysfunction.
The clinical manifestations of vonWillebrands disease are as
follows:
1. Bruising, gingival bleeding, epistaxis, menorrhagia.
2. Prolonged bleeding from cuts or after dental and surgical procedures.
3. Bleeding time prolonged; vonWillebrands factor decreased; factor
VIII decreased.

 Collaborative management for vonWillebrands

disease are as follows:
1. Factor VIII replacement via infusions of cryocipitate.
2. Amicar (antifibrinolytic agent) to stabilize clot
formation before dental procedures and before minor
surgery
3. Desmopressin (DDAVP), to manage mild to moderate
bleeding.
4. Institute bleeding precautions.
Avoid use of plain razor, hard toothbrush or floss, IM
injections, tourniquets, rectal procedures or suppositories.
Administer stool softeners to prevent constipation.
Restrict activity and exercise when platelet cound is less
than 20,000/cu.mm. or when active bleeding occurs.
Monitor pad count and amount of saturation during menses.
Avoid use of ASA, NSAIDs.
Use of direct and steady pressure at bleeding site if
bleeding occurs.

HEMOPHILIA
Hemophilia is an X-linked hereditary bleeding
disorder, caused by a deficiency of one of several
order caused by a deficiency of one of several
plasma clotting factors.
Hemophilia A (classic hemophilia), a lack of factor
VIII, accounts for most (80%) of all hemophilias;
about 1 in 10,000 males is born with this defect.
Hemophilia B (Christmas disease), a deficiency of
factor IX, accounts for about 20% of all hemophilias;
incidence is 1 in 100,000 males.
Both forms result in abnormal bleeding into muscles,
joints, and/or body cavities following an injury.
Chronic disability usually results.

CAUSES
An X-linked recessive hereditary disease
that almost always affects males.
Females are carriers and have a 50%
chance of passing the gene to each child.
A son receiving this gene from the
mother would have hemophilia; a
daughter would be a carrier
A daughter can acquire both defective
genes only if her father has the disease
and her mother is a carrier

SIGN AND SYMPTOMS

Abnormal bleeding, which may be mild to
severe in any given individual
Spontaneous bleeding may occur
Hematoma formation, following even
slight injury
Pain tenderness
Swelling
Deformity, may follow repeated bleeding
bouts
Shock, possibly leading to death

HIV (Human Immunodeficiency Virus)

INFECTION AND AIDS
HIV
Retrovirus; nucleic acid: RNA
Body fluid:
Blood, Semen, Urine, Stool, Saliva , CSF
enter

a.
b.
c.

Blood stream
Intimate contact with body secretions
(sexual intercourse)
Contact with infected blood
(Blood Transfusion, sharing of needles)
Maternal infant transfer
attack

T4 Helper Cells
(necessary for immunity; protection from cancer, virus, parasites)
Reverse
Genetic Code: RNA
DNA (cell / virus)

Transciptase
Immunosupression

DIAGNOSIS
Factor assays; reveal decreased factor VIII in hemophilia
and von Willbrands disease, and decreased IX in hemophilia
B
Activated partial thromboplastin time (APTT) is prolonged.
Thrombocyte count, function, bleeding time, and
prrothrombin time are all normal
MEDICAL INTERVENTIONS
People with hemophilia A and B require replacement of the
deficient clotting; factors for maintenance, as a prophylactic
measure, and to control bleeding.
Von Willbrands disease may be treated with regular IV
administration of cryoprecipitate, which contains the vW
factor.

SELECTED NURSING DIAGNOSES WITH

INTERVENTIONS
Risk for Impaired Skin Integrity
Use safety measures in personal care. For example, use
an electric razor rather than a razor blade to shave a
client.
Avoid activities that place the client at risk, and minimize
safety hazards. Avoid intramuscular injections, rectal
temperatures, and enemas.
Monitor for signs of bleeding, including hematomas
ecchymoses, and purpura, as well as surface oozing or
bleeding.
If surface bleeding occurs, control blood loss: Apply
gentle pressure until bleeding stops; apply ice; apply a
topical hemostatic agent.
Notify the physician at the first sign of bleeding.

 High Risk
Homosexual Anal Intercourse
Bisexual Males Anal Intercourse
IV Drug Users
Infants : HIV infected parents
Blood / Blood Products before 1985

Signs and Symptoms

Fever
Diarrhea
Muscles aches
G.I. cramps
Rashes
Weight loss
Night sweats
Persistent generalized lymphadenopathy (PGL)

When HIV antibodies are present:

Night sweats
Fever
Weight loss
Edema
Fatigue
Abnormal T4 T8 cells ratio

No infections / No malignancy
ARC (Aids Related Complex)

Opportunistic Infections are present

AIDS

 Diagnostic Test
Elisa Test
(+) result indicates HIV infection (HIV seropositive)
False (+) multiple Blood Transfusion / pregnancy
False (-) window period (few weeks 3 months)

Western Blot
(+) result indicates AIDS

Implementation Among Health Caregivers

Practice strict hand washing.
Wear gloves when coming contract with body secretions
Avoid recapping of needles
Use heavy plastic bags to be used for articles contaminated
with body fluids (biohazard bag/red bag).
Use of 1:10 Bleach / Water Solution.
Boiling equipment (20 minutes).
Dishwashing (hot water, air drying)
Laundry (use bleach).
Do not share razors, toothbrush. These are contaminated
with body secretions.

Risk for Ineffective Management of

Therapeutic Regimen: Individual
Assess the clients knowledge of the
disorder and the related treatments
Provide information about the bleeding
disorder and the home medications and
treatments
Provide emotional support to the client,
and express confidence in the clients
self-care abilities.
Provide opportunities for the client to
learn an practice administering clotting
factors and topical hemostatic agents

 Implementation Among Clients

Client Education and Counseling
Disease transmission: blood and body fluids.
Advise client to practice safe sex as follows:
o Abstinence
o Mutual, monogamous sexual relationship.
o Avoid multiple partners
o Use of soluble lubricants and condoms

Prevention of infections
Promote
Self care
safety

THANK YOU!