HEMATOLOGIC DISORDERS FORMED ELEMENTS OF THE BLOOD

Erythrocytes
HEMATOLOGY • Also called Red Blood Cells or RBC’s
• The hematologic or hematopoietic system includes • Function primarily to ferry Oxygen in the blood
the blood, blood vessels, and blood forming to all cells in the body
organs ( bone marrow, spleen, liver, lymph • Also transports Carbon dioxide out of the body
nodes, and thymus gland). • Lifespan of 120 days only
• Major function of blood is to carry necessary • Hemoglobin in the RBC binds with the Oxygen
materials ( oxygen, nutrients ) to cells and to as it is transported in the blood
remove CO2 system and metabolic waste • Female : 12 – 16 g/100ml
products. • Male : 13 – 18 g/100ml
• It also plays a role in hormone transport,
inflammatory and immune responses, • Normal RBC count: about 4 – 6 million/mm³
temperature regulation, fluid-electrolyte balance, • Hematocrit (HCT) – percentage of RBC per
and acid-base balance. given volume of blood and is an important
indicator of the Oxygen-carrying capacity of
THREE BROAD FUNCTIONS OF BLOOD : the blood
1. Transportation • Female : 37 – 48%
• Respiratory – transport of gases by the RBC • Male : 45 – 52%
• Nutritive – transport of digested nutrients from Leukocytes
the GIT to the different cells of the body • Also called White Blood Cells or WBC’s
• Excretory – transport of metabolic wastes to the • Average value : 4,000 – 11,000 / mm³
kidneys and excreted as urine • Protects the body against any damage
2. Regulation • Are able to slip in and out of the blood vessels
• Hormones and other molecules that help regulate by ameboid fashion – in a process called
metabolism are also carried in the blood diapedesis
• Thermoregulation • When mobilized, the body speeds up
• Protection production which usually indicates the
• Blood clotting presence of infection in the body
• Leukocytes • Leukocytosis – total WBC count above
11,000 / mm³
COMPONENTS OF THE BLOOD : • Leukopenia – an abnormally low WBC count
1. Plasma Types:
2. Formed Elements 1. Granulocytes
• Erythrocytes or RBC
– Neutrophils -Basophils
• Leukocytes or WBC
– Eosinophils
• Thrombocytes or Platelets
2. Agranulocytes
BLOOD
• Average volume is 5 – 6 liters or approximately 6 – Lymphocytes -Monocytes
quarts
• pH is 7.35 – 7.45 Cells of the Immune System
• Arterial blood is usually bright red in color • Lymphocytes
compared to venous blood which has a darker – Lymphocytes are created in the bone marrow
color, due primarily to the large concentration of and migrate to the Thymus where they
oxyhemoglobin found in arterial blood mature
– After becoming immunocompetent, the B & T
cells transfer to the lymph nodes & spleen
a.) Plasma - fluid portion of the blood – Types
Contains :
1.B lymphocytes or B cells – produces
proteins / albumin fibrinogen
antibodies to incapacitate the antigen
clotting factors electrolytes
waste products nutrients 2.T lymphocytes or T Cells – attacks
antigens directly
b.) Cellular Components • Macrophages
1. Leukocytes (WBC) • Literally means “Big Eaters”
2. Erythrocyte (RBC) • Arise from monocytes formed in the
3. Thrombocyte (Platelets) bone marrow
• Major role : to engulf foreign particles
Hematopoiesis– occurs in the bone marrow ( pelvis,
ribs, vertebrae and sternum. Cellular (Cell-Mediated) Immune Response
• T – Cells
Extramedullary Hematopoiesis- the liver and the • Responds directly to antigens
spleen produces blood cells • Will destroy target cells thru secretions of
Lymphokines and Perforin ( “Kiss of Death”)
PLASMA which is inserted to the cell membrane, shortly
after that, the target cell ruptures
• The liquid part of the blood;approximately 90%
• They have a:
water
• License to KILL
• Also contains nutrients, ions (salts, primarily Na),
• License to HELP
respiratory gases, hormones, plasma proteins,
• License to Suppress
antibodies and various wastes and products of
• Three types :
cellular metabolism
• PLASMA PROTEINS – the most abundant solutes in • Killer T Cells – binds to the surface of
the plasma invading cells, disrupt the cell membrane &
– Three Types destroy it by altering it’s environment
1. Albumin • Helper T cells – helps to stimulate the B
2. Globulin Cells to mature into Plasma Cells which
3. Fibrinogen synthetize & secrete immunoglobulins
4. (Antibodies)
 • Suppressor T Cells – Reduces the = transported to bone marrow via
Humoral response TRANSFERIN & reclaimed for new Hgb
production

ERYTHROPOIESIS- RBC production

Requirements :
a. Erythropoietin
b. Iron
c. Folic Acid
d. Vitamin B6, Vitamin B12
e. Vitamin C

`` Liver and Spleen- Graveyard of the RBC

Hemostasis (Blood Clotting)

• -Three Major Phases
1. Platelet Plug Formation
– Platelets adhere and stick to vessel lining that
are damaged forming a Platelet Plug or
White Thrombus
Humoral (Antibody-Mediated) Immune Response – Platelets release chemicals to attract more
platelets to the injured site
B Cells 2. Vascular Spasms
– Matures into Plasma Cells responsible for – Platelets release Serotonin causing spasms of
Antibody production the blood vessel, constricting it & decreasing
– 5 Classes of Immunoglobulins (MADGE) : blood flow
– Immunoglobulin M (IgM) 3. Coagulation or Blood Clotting
• 1st immunoglobulin produced in an immune – Thromboplastin is released by damaged cells
responsepresent in plasma, too big to cross – plasma Clotting Factors form an activator
membrane barriers that triggers the Clotting Cascade
– Immunoglobulin A (IgA) – a Blood Clot is formed
• Sound in body secretions like saliva, tears, – Serum is squeezed out within the hour pulling
mucus, bile, milk & colostrum the ruptured edges together
– Immunoglobulin D (IgD)
• Present only in the plasma & is always Plasma Clotting Factors
attached to the B Cell I Fibrinogen
– Immunoglobilin G (IgG) II Prothrombin
• 80% of circulating antibodies III Tissue Thromboplastin
• Can cross the placenta and provide passive IV Calcium
immunity V Proacelerin
• Present in all body fluids VII Proconvertin
– Immunoglobulin E (IgE) VIII Antihemophilic Factor
• Responsible for Allergic & hypersensitivity IX Christmas Factor
reactions X Stuart – Prower Factor
• Stimulates Mast cells & Basophils to release XI Plasma Thromboplastin
Histamine which mediates inflammation & the Antecedent
allergic response XII Hageman Factor
XIII Fibrin Stabilizing Factor
Thrombocytes Compatible Blood Types
• Also called Platelets
• Average value : 250,000 – 450,000 / mm³
• Lives for about 5 – 10 days ANEMIA
• Important in blood clotting • Conditions in which the number of RBC’s or
amount of hemoglobin is lower than normal leads to
Hematopoiesis (Blood Cell Formation) hypoxia and ischemia
• Occurs in the Red Bone Marrow, chiefly in flat
bones like Skull, ribs, pelvis, sternum and Classifications of Anemia According to Etiology
proximal epiphyses of the humerus and femur
• Erythropoiesis – RBC production, is a very
active process
• RBC are continuously being destroyed by the
liver & spleen
• RBC’s have a lifespan of 120 days
• As RBC’s are destroyed, iron is recycled to the
bone marrow for use in the formation of new
RBC’s
• Erythropoietin – secreted by the kidneys &
released when blood levels of Oxygen begins
to decline for any reason; which stimulates the
Red Bone Marrow to produce more RBC’s
ERYTHROCYTES Iron Deficiency Anemia
> destruction • most common type of anemia
- mature cells removed chiefly by • Iron stores are depleted, resulting in a decreased
spleen & liver supply of iron for the manufacture of hemoglobin in
* BILIRUBIN = byproduct of Hgb released RBC’s
when RBC’s destroyed Commonly results from blood loss, increased metabolic
demands, syndromes of gastrointestinal malabsorption,
* IRON = freed from Hgb during bilirubin
and dietary inadequacy
formation
 • cause : inadequate absorption or excessive • Measures absorption of radioactive vitamin B12
loss of iron both before and after parenteral administration
• Bleeding – principal cause in adults of intrinsic factor.
• Vegetarian diets • Definitive test for pernicious anemia.
• Vitamin C – increases iron absorption • Used to detect lack of intrinsic factor.
Assessment Findings • Fasting client is given radioactive vitamin B12
-fatigue, dyspnea, palpitatations & dizziness, pallor, brittle by mouth and nonradioactive vitamin B12 IM
hair & nails, pica, glossitis, cheilosis, koilonychia to saturate tissue binding sites and to permit
some excretion of radioactive vitamin B12 in
Mild cases – asymptomatic the urine if it is absorbed.
• 24-48 hour urine collection is obtained;
Cheilosis
client is encouraged to drink fluids.
Laboratory findings :
• If indicated, a second stage Schilling test will
RBC’s are small / microcytic and pale
be performed 1 week after first stage.
• ↓ hemoglobin & hematocrit • Fasting client is given radioactive vitamin B12
• ↓serum iron & ferritin combined with human intrinsic factor and the
test will be repeated.
Nursing Interventions
1. Identify the cause Nursing Interventions / Treatment
2. Monitor S/Sx of bleeding – stool, urine and GI 1. Drug Therapy
contents a. Vit. B12 injections monthly for life
3. Provide rest b. Iron Preparations
4. Give iron preparations ( 6 – 12 months ) c. Folic Acid
-Ferrous Sulfate, Gluconate, Fumarate 2. Transfusion therapy
a. always give after meals or snacks 3. Bed rest
b. dilute liquid preps and give thru straw 4. Mouth care
c. give with orange juice (Vitamin C enhances 5. Dietary teaching
absorption) 6. Teach about importance of lifelong Vitamin B12
d. warn clients the stool will become black and can therapy
cause constipation
5. For clients with poor absorption or continuous Hemolytic Anemias
blood loss • ↑ rate of RBC destruction
-IM or IV of Iron Dextran • short life span of RBC
a. Use 1 needle to withdraw and another for • G6PD
injection • Sickle cell anemia
b. Use z-track method • Thalassemia
c. don’t massage but encourage ambulation • DIC
d. usually, deep IM at buttocks • Transfussion incompatibilities
6. Give dietary teaching – liver, meats, nuts, egg
yolk, shellfish, legumes, etc. Sickle Cell Anemia
7. Increase intake of roughage and fluids to • Most common inherited disease among black
prevent constipation. Americans.
• Also found in Arabian, Mediterranean and
Pernicious Anemia Caribbean descent
• Vitamin B12 Deficiency Anemia
• Hgb S ( abnormal hemoglobin ), which has
• caused by inadequate Vit. B12 intake or deficiency reduced oxygen carrying capacity, replaces all
in intrinsic factor Vit. B12 combines with intrinsic or part of the hemoglobin in the RBC’s.
factor so it can be absorbed in the ileum into the • Life span is 6-20 days instead of 120, causing
bloodstream hemolytic anemia.
• the result is abnormally large erythrocytes and • Death often occurs in early adulthood due to
hypochlorhydria ( a deficiency of hydrochloric acid occlusion or infection.
in gastric secretions). • During decreased O2 tension, lowered pH,
• Lack of intrinsic factor is caused by gastric mucosal dehydration and severe infections, RBC’s
atrophy (possibly due to heredity, prolonged iron change from round to sickle or crescent shape
deficiency, or an autoimmune disorder), can also • Sickled cells don’t slide thru vessels as normal
result in client who have had a total gastrectomy RBC’s do, causing clumping, thrombosis,
• Usually occurs in men and women over age 50, arterial obstruction, increased blood viscosity,
with an increase in blue eyed persons. hemolysis and eventual tissue ischemia and
necrosis
Assessment :
Anemia- symptoms are: Sickle Cell Crisis :
• Fatigue, weakness • dyspnea Cause : infection, dehydration, fever, cold
• Palpitations & dizziness • paresthesias exposure, hypoxia, strenuous exercise, extreme
• Pallor • wt. loss fatigue or extreme changes in altitude
•Confusion VASO-OCCLUSIVE CRISIS:
• ↓ intellectual function -most common and most painful type of crisis
•Sore tongue • caused by stasis of blood with clumping of the
cells in the microcirculation leading to ischemia &
Lab Results infarction.
-Decrease RBC -signs include fever, pain, and tissue engorgement
-Decreased free Hydrochloric acid -trreatment
-Large RBC / Megaloblast • hydration, electrolyte replacement, bed rest,
-Positive Schilling Test– definitive test for Pernicious broad spectrum antibiotics, transfusions &
anemia oxygen therapy.
- used to detect lack of intrinsic factor
SPLENIC SEQUESTRATION:
Positive schilling test -Life - threatening crisis caused by the pooling of
blood in the spleen. (from congestion of sickled
 cells)
-signs include profound anemia, hypovolemia, and
shock
-treatment : blood transfusions and splenectomy
APLASTIC CRISIS:
-Occurs infrequently and is caused by:
• diminished production of RBC
• increased destruction of RBC’s
• triggered by a viral infection or the
depletion of folic acid.
-signs include profound anemia, pallor, and
PANCYTOPENIA.
-treatment – Transfusion of packed RBC’s
• Frequent infection esp. with H. influenzae
• Infants may have Dactylitis (hand – foot
syndrome) symmetrical painful soft tissue
swelling in the hands and feet in the absence
of trauma
Assessment
• Signs and symptoms of anemia – pallor,
weakness
• Hepatospleenomegaly
• Dactylitis (Symmetric swelling of the hands
and feet) – called hand-foot syndrome
• Other problems :
– CVA
– MI
– Growth retardation – initial
manifestation
– Decreased fertility
– Priapism
– Recurrent severe infections
MEDICAL MANAGEMENT
A. Drug therapy
> analgesic/narcotics to control pain
• Avoid meperidine (Demerol) due increased risk
of seizures in children
> antibiotics to control infection.
B. Blood transfusions
C. Hydration:oral and IV
D. Bed rest
E. Surgery: splenectomy
INTERVENTIONS
• Administer O2 & Blood Transfusion as Rx
• Maintain adequate hydration
• Avoid tight clothing that could impair
circulation.
• Keep wounds clean and dry.
• Provide bed rest to decrease energy
expenditure and oxygen use.
• Encourage patient to eat foods high in calories,
CHON, with folic acid supplementation.
• Analgesics:
– Acetaminophen
– Morphine
– avoid aspirin as it enhances
acidosis,which promotes sickling
• Avoid anticoagulants( sludging is not due to
clotting ).
• Antibiotics.
• Avoid activities that require so much energy.
• Keep arms and legs from extreme cold.
• Decrease emotional stress.
• Provide good skin care
THALASSEMIA MAJOR
(Cooley’s anemia)
• B - thalassemia refers to an inherited
hemolytic anemia, characterized by reduction
or absence of the B-globulin chain in Hgb
synthesis
• Fragile RBC & short life span
• Autosomal recessive pattern of inheritance
• Insufficient B-globulin chain synthesis allows
large amounts of unstable chains to
accumulate
• Precipitates of alpha chains that form cause
RBC’s to be rigid & easily destroyed, leading to
severe hemolytic anemia = chronic hypoxia
• Skeletal deformities: pathologic fractures
• Hemosiderosis – excess iron supply, which
leads to iron deposits in the organ tissues
leading to decreased function
CLINICAL MANIFESTATIONS
• onset is usually insidious
• Sx are primarily related to progressive
anemia, expansion of marrow cavities of the
bone & developmemnt of hemosiderosis
• Early Sx often include progressive pallor, poor
feeding & lethargy
• Further signs: hemorrhage, bone pain,
exercise intolerance, jaundice, & protuberant
abdomen
hemosiderosis of the eye and lungs
DIAGNOSTIC EVALUATION
• Decrease hemoglobin
• RBC= increase in number
• Hgb elctrophoresis
– elevated levels of HgF ( doesn’t hold
O2 well )
– limited amount of HgA
–
Management
• Frequent and regular transfusion of packed
RBC’s to maintain Hgb levels above 10 g/dL
• Iron chelation therapy with deferoxamine
(Desferal) – reduces toxic effects of excess
iron & increases iron excretion thru urine &
feces
• Splenectomy
• Supportive management of symptoms
• Bone marrow transplant
• Prognosis and Survival rate is poor because of
no known cure
• Often fatal in late adolescence or early
adulthood
Complications
• Splenomegaly
• Growth retardation in the second decade
• Endocrine abnormalities :
– delayed development of secondary sex
characteristics – most boys fail to
undergo puberty, girls – menstruation
problems
– DM – due to iron deposits in the
pancreas
– Hypermetabolic rates
• Skeletal complications
– Frontal & parietal bossing
(Enlargement)
– Maxillary hypertrophy – leading to
occlusion
– Premature closure of epiphyses of long
bones
– Osteoporosis & pathologic fractures
• Cardiac problems: pericarditis & CHF – usual
cause of death
Complications
• Gallbladder disease
– Gallstones that often require surgery
• Skin – bronze pigmentation caused by iron
deposits in the dermis
• Leg ulcers
ERYTHROBLASTOSIS FETALIS
Rh Incompatibility
 • Destruction of RBCs that result from Ag-Ab rxn • Implement phototherapy or exchange
• Characterized by hemolytic anemia or transfusion.
hyperbilirubinemia
• Possibly caused by Rh incompatibility NURSING INTERVENTIONS
between the mother & the fetus (Ag & • Administer Rh0 (D) immune globulin to the
Ab reaction) mother during the first 72 hrs. after
delivery if the Rh(-) mother delivers an Rh (+)
ERYTHROBLASTOSIS FETALIS fetus but remains unsensitized
• Sensitization of Rh (-) woman by transfusion of • Assist with exchange transfusion as
Rh (+) blood prescribed.
• Sensitization of Rh (-) woman by presence of • The baby undergoes transfusion of blood to
Rh (+) RBCs from her fetus conceived with stop the destruction of the baby’s RBC
Rh (+) man - the transfused blood is replaced with the baby’s
• Approximately 65% of infants conceived by own blood gradually
this combination of parents will be Rh (+) • Reassure the mother that the newborn will
• Mother is sensitized by passage of Rh (+) suffer no untoward effects from the
RBCs thru placenta, either during condition
pregnancy (break/leak in membrane) or
at the time of separation of the placenta MYELOPROLIFERATIVE DISORDER
after delivery. POLYCYTHEMIA VERA
• Underlying cause is unknown
RH INCOMPATIBILTY • Hyperplasia of all bone marrow elements
• FIRST PREGNANCY > increase RBC mass
- mother may become sensitized, baby rarely > increase blood volume viscosity
affected > decrease marrow iron reserve
INDIRECT COOMB’S TEST > Splenomegaly
- Tests for anti-Rh(+) Ab in mother’s circulation
- performed during pregnancy at first visit & again ASSESSMENT
about 28 week’s gestation. • Reddish purple hue of skin & mucosa, pruritus
RESULTS: • Splenomegaly, hepatomegaly
- If (-) at 28 weeks, a small dose of (MicroRhogam) • Epigastric discomfort, abdominal discomfort
is given prophylactically to prevent sensitization • Painful fingers & toes from paresthesias
in the 3rd trimester. • Altered mentation
- Rhogam may also be given after 2nd trimester • Weakness, fatigue, night sweats, bleeding
amniocentesis tendency
- If (+), levels are titrated to determine potential • Hyperuricemia – from increased RBD formation
effects on the fetus and destruction
DX TESTS
DIRECT COOMBS’ TEST • CBC
- Tests done on the cord blood at delivery to • BONE MARROW ASPIRATION & Biopsy
determine presence of (+) Ab on fetal RBCs
RESULTS MANAGEMENT
- If both indirect & direct Coombs’ test is NEGATIVE • HYPERVISCOSITY
& infant is Rh(+): = phlebotomy @ intervals determined by CBC
- NEGATIVE: No formation of Anti-Rh (+) Ab results to decrease RBC mass
- Rhogam (Rho[D] human immune globulin is =generally 250-500ml removal @ a time
given to the Rh(-) mother to prevent development of • HYPERPLASIA
anti-Rh(+) Ab as the result of sensitization from = myelosuppressive therapy,
present or just terminated pregnancy. = generally using hydroxyurea or IV
• In each pregnancy, an Rh(-) mother who radioactive phosphorus (32P), biologic response
carries an Rh (+) fetus receives Rhogam modifier, ie alpha interferon
if both the mother and infant is (-) to both • HYPERURICEMIA= allupurinol (Zyloprim)
direct & indirect Coombs’ test.
• PRURITUS = antihistamines (cimitidine), low
• If mother is has been sensitized:
dose acetyl salicylic acid; certain anti-
- anti-Rh(+) Ab are present
depressants (paroxetin), phototherapy,
- Rhogam is not indicated
cholestyramine
• Rhogam must be injected into unsensitized
mother’s system within 72 hours of delivery of
INTERVENTION
Rh(+) infant
• Encourage/assist ambulation
• Assess for early S/Sx of thromboembolic
ERYTHROBLASTOSIS FETALIS
complications : swelling of limbs, increased
CLINICAL FINDINGS
warmth, pain
• Anemia
• Monitor CBC & assist with phlebotomy as
• Jaundice that develops rapidly after birth and
ordered
before 24 hours or that occurs within 24 -
Patient Education
36 hours
• Educate about risk of thrombosis; encourage
• Enlarged placenta
patient to maintain normal activity pattern &
• Edema
avoid long periods of rest
• Ascites
• Avoid hot showers
• Report @ regular intervals for follow up blood
NURSING INTERVENTIONS
• Determine blood type and Rh early in
DISORDERS OF PLATELETS and CLOTTING
pregnancy.
MECHANISM
• Determine results of direct Coomb’s test early
in pregnancy & again at 28 week’s.
HEMOPHILIA
• Determine results of direct Coomb’s test on
• Hereditary coagulation defect, usually
cord blood.
transmitted to affected male by female carrier
- type & Rh, Hgb, Hct
 through sex – linked recessive gene, resulting
in prolonged clotting time.
• Most common type is Hemophilia A or Classic
Hemophilia - factor VIII deficiency (called
Antihemophilic Factor / AHF)
• Hemophilia B or Christmas Disease – factor IX
deficiency (called the Christmas Factor)
• Male inherits hemophilia from their mothers,
and females inherit the carrier status from
their fathers.
– Found predominantly, but not
exclusive, in male offsprings
• Bleeding occurs due to impaired ability to form
fibrin clot
ASSESSMENT
• Abnormal bleeding in response to trauma or
surgery. (muscles/joints)
• Joint bleeding causing pain, tenderness,
swelling, and limited range of motion.
• Tendency to bruise easily.
• Epistaxis
• Hemarthrosis (bleeding in joints causing pain,
swelling and limited movement)
IMPLEMENTATION
• Administer factor VIII concentrate.
• Monitor for bleeding and maintain bleeding
precautions.
• Monitor for joint pain; IMMOBILIZE the
affected extremity if joint pains occur.
• Monitor urine for hematuria.
• Instruct the parents regarding activities for the
child, emphasizing the avoidance of contact
sports.
• Instruct the parents on how to control bleeding
(direct/indirect pressure)
• DDVAP (Desmopressin) – promotes the release
of Factor VIII in hemophilia A
• Use soft toothbrush and point out need for
regular dental checkups
• Refer to National Hemophilia Association
• Emphasize avoidance of Aspirin
• Provide diet information as excess weight
places further stress on joints
IMPLEMENTATION
R - Rest
I - Immobilize
C - Cold Compress
E - Elevate
Dissimenated Intravascular Coagulation
• DIC is a disorder of diffuse activation of the
clotting cascade that results in depletion of
clotting factors in the blood.
• occurs when the blood clotting mechanisms
are activated all over the body instead of being
localized to an area of injury.
• grave coagulopathy resulting from
overstimulation of clotting & anticlotting
processess in response to disease & injury
• Small blood clots form throughout the body,
and eventually the blood clotting factors are
used up and not available to form clots at sites
of tissue injury.
• Clot - dissolving mechanisms are also
increased stimulated by many factors including
infection in the blood & severe tissue injury –
burns and head injury, reactions to blood
transfusions, carcinomas and obstetrical
complications such as retained placenta after
delivery.
ASSESSMENT
• purpura on lower extremities & abdomen
• hemorrhagic bullae, acral cyanosis, focal
gangrene in skin
Dx Tests:
• marked decrease of blood platelets
• low levels of fibrinogen & other clotting factors
• prolonged prothrombin & partial
thromboplastin times & abnormal erythrocyte
morphologic characteristics
Nursing Interventions / Treatment
1. The objective of treatment is to determine the
underlying cause of DIC and provide treatment for it.
2. Replacement therapy of the coagulation factors is
achieved by transfusion of fresh frozen plasma.
Cryoprecipitates may also be used if fibrinogen is
significantly decreased. Platelet transfusions if platelets
are diminished
3. Heparin, a medication used to prevent thrombosis,
is sometimes used in combination with replacement
therapy. ( still controversial )
4. Prevent further injury
a. avoid IM injections
b. apply pressure to bleeding sites
c. turn patient frequently and gently
d. provide mouth care – soft bristled
toothbrush
5. Teach patient the importance of avoiding aspirin.
IDIOPATHIC THROMBOCYTOPENIA PURPURA
• Increased destruction of platelets with
resultant platelet count of less that
100,000/mm3 characterized by petechiae and
ecchymoses of the skin.
• Exact cause unknown; may be autoimmune.
• Spleen is the site for destruction of platelets
• often triggered by URTI or Childhood
communicable disease – Measles & chickenpox
ASSESSMENT:
• Petechiae
• Ecchymosis
• Blood in any body secretions, bleeding form
mucous membranes, nosebleeds.
• Decreased platelet count
• Anemia
• easy bruising
• blood in stool or urine
• CBC reveals platelet count below 20,000/mm3
• Bone marrow aspiration done to rule out
leukemia
MEDICAL MANAGEMENT:
 Drug therapy:
– Prednisone – decreases anti-platelet antibodies
(monitor for infection)
– IVIG (Intravenous Immune Globulin) – helps to
effectively increase platelet count
– Anti-D Antibody – one dose treatment
• Given to pt’s 1 year but less than 19 years
old
• Normal WBC and hemoglobin
• no active bleeding present
• no concurrent infection
• Diphenhydramine and hydrocortisine are
made ready for possible allergic reactions to
the medication
 Platelet transfusion
Splenectomy
Intervention
• Prevent, control and minimize bleeding.
• Prevent bruising
• Provide support to client and be sensitive to
change in body image.
• Protect from infection.
• Administer analgesics (acetaminophen) as
ordered; avoid aspirin.
• administer meds orally, rectally, or I.V. rather
than I.M.