HEMATOLOGIC

NURSING
RALPH R. DELOS SANTOS
BACHELOR OF SCIENCE IN NURSING
PAMANTASAN NG LUNGSOD NG MAYNILA
4TH PLACER, DECEMBER 2012, NLE
DOCTOR OF MEDICINE
PAMANTASAN NG LUNGSOD NG MAYNILA
EMERGENCY AND TRAUMA DEPARTMENT STAFF NURSE
GAT ANDRES BONIFACIO MEMORIAL MEDICAL CENTER
CITY GOVERNMENT OF MANILA
 PRINCIPLES OF HEMATOLOGY

Hematologic system is composed of the

blood, the bone marrow, and the
Reticuloendothelial System

Blood is a fluid tissue

 PRINCIPLES OF HEMATOLOGY

BLOOD COMPONENTS
RBC
WBC
Platelets
Continuously
be replenished via
HEMATOPOIESIS
 PRINCIPLES OF HEMATOLOGY

The blood is approximately 5-6 L in volume

Fluidity of the blood allows its functions
To deliver oxygen and nutrients
To transport WBC to sites of infection and
inflammation
To transport Platelets to sites of tissue trauma
 BONE MARROW

Site of hematopoiesis (contains stem cells)

May differentiate as MYELOID or LYMPHOID
Seen in flat bones of adults
Marrow may be damaged and be replaced by
fat
Marrow destruction forces extramedullary
hematopoiesis
 RBC

Disk-shaped
Oxygen and carbon dioxide transporter (made possible
by Hemoglobin)
Immature RBCs (RETICULOCYTES) may be released in
the circulation
Differentiation and maturation depends on
ERYTHROPOIETIN
Production is dependent on Vitamins B12, B9, B6
 IRON STORES AND METABOLISM

There is a tight regulation of iron in the body

Absorption is dependent on what is present
already in the body
Pre-menopausal women have higher iron
requirements
Majority of iron in the body is present as Hgb (3 g)
 IRON STORES AND METABOLISM

Ferritin: Measure of Iron Stores

Transferrin: Protein Transporter for Iron to RBC
precursors
 VITAMINS B 9 & 12

Important in the biosynthesis of nucleotides

(DNA/RNA)
Deficiency leads to failure of maturation
B9: Absorbed in the proximal small intestine
B12: Binds with INTRISIC FACTOR and absorbed in
the terminal ileum
 THE RBC RECYCLING FACTORY

Normal lifespan of RBC is 90-120 days

SenescentRBCs are trapped by the
SPLEEN (RES)
Metabolism of Hgb
 WBC

GRANULOCYTES
and the
AGRANULOCYTES
The MILITARY CELLS
of the body
 GRANULOCYTES

Neutrophil Increases in bacterial infection

Eosinophil Increases in parasitism and allergy
Basophil Least in number, secretes histamine
 CLINICAL SIGNIFICANCE OF
IMMATURE WBCs

Immature WBC is called a BAND

They are limited in number but increases during
infection
Increase in bands is called a SHIFT TO THE LEFT
SHIFT TO THE RIGHT on the other hand means an
increase in mature WBCs
 AGRANULOCYTES

Monocyte
Lymphocyte
 PLATELETS

Are fragments of Megakaryocyte

Involved in clotting mechanism
Production
is stimulated by
thrombopoietin
 PLASMA

Fluid portion of the blood

90% water
Contains plasma proteins ALBUMIN, FIBRINOGEN,
GLOBULIN
When allowed to clot, the remaining fluid is called
SERUM (no clotting factors)
 HEMOSTASIS

Physiologic process of combating blood loss

Starts with VASOCONSTRICTION Platelet
Aggregation Plug Formation
Involves platelet and the clotting factors
Deficiency in important factors and platelets
places the patient at risk for bleeding
THE CLOTTING CASCADE
SH*T ANO YAN ?!
WALA BANG MAS SIMPLE?
THE CLOTTING CASCADE
 ASSESSMENT AND DIAGNOSTICS

CBC
Bone Marrow Aspiration and Biopsy
 BONE MARROW ASPIRATION AND BIOPSY

To define the quality and quantity

of cells
Semifluid appearance
Taken from the iliac crests
Explain the procedure to the
patient
 BONE MARROW ASPIRATION AND BIOPSY

Asepsis is maintained
Under local anesthesia, patient
may feel pressure
After aspiration, pressure is applied
Monitor for bleeding, avoid aspirin
for pain
 ANEMIA

Not a disease but a manifestation of an underlying

disease
Most common hematologic condition
Reduction in Hgb Decreased oxygen carrying
capacity
 POSSIBLE MECHANISMS OF ANEMIA

RBC Loss: Bleeding

Decreased RBC Production: B 9/12-
deficiency, Fe deficiency,
Decreased EPO
Increased RBC Destruction
 MANAGEMENT

Correction of underlying cause

Transfusion with PRBC
 NURSING CONSIDERATIONS
Hx and PE:
History of blood diseases, transfusion history, Hx of
excessive bleeding
Symptoms experienced (weakness, fatigue, malaise)
PE: Pallor, jaundice, tongue morphology, cracking of
mouth corners
NrDx:
Activity intolerance r/t weakness and fatigue
Imbalanced nutrition less than body requirements
 NURSING INTERVENTIONS

Manage the most common symptom: FATIGUE

Provide adequate rest
Dietary therapy
No to alcoholic drinks
VS monitoring for possible complications
 IRON DEFICIENCY ANEMIA

Inadequate iron intake for Hgb synthesis

Most common type of anemia
Can be due to Hookworm Infection in endemic
areas
In adults, rule out bleeding as cause (ulcers,
gastritis, tumors)
 CLINICAL MANIFESTATIONS

Anemic presentation
Glossitis, brittle ridged nails, cheilosis
Pica
LOW SERUM FERRITIN and increased Total
Iron Binding Capacity
 MANAGEMENT

Investigate the cause

Examine patient for tumors and possible occult
GI bleeding
Treat with Iron Preparations (oral, IM, IV)
Iron Dextran should be administered only ANST,
prepare Epi.
 NURSING MANAGEMENT

Dietary therapy using food sources (organ

meats/liver, beans, green leafy veggies)
Take with Vit C to improve absorption
Take medication on empty stomach, 1H before
or 2H after meals, no dairy foods
If more than 1 tab is prescribed, start with one
then increase until the prescribed number of
pills can be tolerated
 NURSING MANAGEMENT

Eat foods high in fiber to combat constipation

If patient develops GI distress upon taking meds
on empty stomach, patient may take
medication with meals but prolongs the therapy
If parenteral iron, use Z-track method at the
gluteus maximus
 APLASTIC ANEMIA

A rare disease characterized by damage to the

bone marrow
Reduced hematopoiesis
Pancytopenia
Associated with the antibiotic Chloramphenicol
Confirmed by biopsy
 MANAGEMENT

MEDICAL
Bone marrow transplantation
Immunosuppresive medication
Supportive therapy

NURSING
Deficiency-specific nursing management
 MEGALOBLASTIC ANEMIA

Failure of maturation due to deficiency in

important factors
Hyperplastic bone marrow
Pancytopenia
 FOLIC ACID DEFICIENCY ANEMIA

Folic acid is important in DNA synthesis

Reduced due to dietary (within 4 months)
and lifestyle factors
Can be caused by malabsorption
 B12 DEFICIENCY

Inadequate intake among vegetarians

Faulty absorption because of GI diseases
PERNICIOUS ANEMIA
 MANIFESTATIONS

Almost the same

B12 deficiency is more associated with
neurologic s/sx
B12 Deficiency: Beefy Red Tongue
 DIAGNOSTICS

SCHILLING TEST (under 24H urine collection)

Patient will take a small amount radiolabeled B12
After few hours, patient will take large amount of parenteral non-
labeled B12
If oral B12 is absorbed, >8% will be excreted in the urine within 24H
If no radioactivity is detected, the cause is malabsorption
If radioactivity is detected, the cause of the deficiency is not ileal
IF is added, if absorbed, the it is really ileal/pernicious

DETERMINE ANTIBODIES
 MANAGEMENT

MEDICAL
Increase FA in the diet or give 1mg FA daily
Once Hgb is normal, FA is stopped but for alcoholics, it is continued.
B12 deficiency is treated with replacement
Tongue manifestation will improve in several days
Neurologic manifestations require more time for recover.
To prevent recurrence, may be continued for life.

NURSING
Monitor for fatigue
Frequent neurologic assessment
 MYELODYSPLASTIC SYNDROME

Abnormal development in one of the cell lines

Cells are produced but usually non-functional
Macrocytic RBCs
May evolve to Acute Myeloid Leukemia (very aggressive leukemia)
Manifestations are related to cells affected
No known cure, BMT can be of help, chemotherapy has been used.
Chelation for iron overload (given SQ over 8-10H)
 HEMOLYTIC ANEMIA

Shortened RBC lifespan

Results to hypoxia, triggers increased EPO
Increase in bilirubin
Decreased haptoglobin
Diseases:
SCA
G6PD Deficiency
Thalassemia
Hereditary Spherocytosis
 SICKLE CELL ANEMIA

Inheritance of the sickle cell

gene
HbS
Hypoxemia-sensitive RBC
Can cause obstruction
because of abnormal
morphology
Intermittent crisis
 CLINICAL MANIFESTATIONS

Ischemic effects
Anemia (7-10 g/dL)
Jaundice
Skull enlargement
 SICKLE CELL CRISIS

Sicklecrisis MOST COMMON

(painful)
Aplastic crisis
Sequestration crisis (can cause
autosplenectomy)
 ACUTE CHEST SYNDROME

Falling Hgb
Tachycardia
Fever
Bilateral infiltrates in CXR
 MANAGEMENT

MEDICAL
BMT
Hydroxyurea (chemotherapeutic)
Transfusion
Hydration
Supplemental oxygen
NSAIDs
For severe pain: Morphine is DOC
 NURSING MANAGEMENT

Manage pain through medications and

prevent vasoocclusion
Prevent leg ulcers
Ensure
hydration and adequate
oxygenation
Monitorfor any manifestation of ischemia
(include intraabdominal sources)
 THALASSEMIA

Inheritable hemoglobin-chain synthesis disorder

Microcytic hypochromic
Alpha-thalassemia (Asia, Middle East)
Beta-Thalassemia (Mediterranean
Severe Beta Thalassemia: Cooleys Anemia
Severe hemolysis
Iron overload
Regular BT and chelation
 G6PD DEFICIENCY

Defect in the gene synthesizing the enzyme G6PD, X-

linked
Decreased membrane stability prone to hemolysis
Normal Hgb levels, hemolysis is triggered by offending
agents
AVOID! Antimalarials, sulfonamides, Fava beans
Managed when hemolysis occurs (usual hemolytic
pattern)
 IMMUNE HEMOLYTIC ANEMIA

Alloantibody mediated hemolysis

Example is Rh Reaction
Warm-body antibody (most common)
Cold-body antibody
Hemolytic presentation Jaundice, splenomegaly
Coombs Test (Direct Antibody Test) detects
antibodies against RBC
 MEDICAL MANAGEMENT

Corticosteroids
Immunosuppresants
Cold-body antibody reaction can be prevented by keep patient
warm.
Manage hemolysis

NURSING MANAGEMENT
Protect patient from infection, educate on tapering steroids
Manage hemolysis
THE POLYCYTHEMIA

TEACHING MOMENT
WHAT ARE THE IMPORTANT POINTS WHEN IT COMES TO
HEMATOLOGIC MALIGNANCIES?
 ACUTE MYELOID LEUKEMIA

Malignancy of the myeloid precursors

Most common non lymphocytic leukemia
Arises from MDS
Prognosis is less than 1 year.
Proliferation of malignant myeloid cells
Gum hyperplasia
Bone marrow expansion
 DIAGNOSTICS

Apparent abnormality in CBC

BMAB reveal myeloblasts BIOPSY IS CONFIRMATORY
 COMPLICATIONS

Bleeding <10,000 major hemorrhage

Infection
 MANAGEMENT

MEDICAL
ChemoTx: Cytarabine, Daunorubicin, Etoposide
Combat anemia BT
Neutopenia G-CSF
Thrombocytopenia PC Transfusion
BMT
Tumor Lysis Syndrome: Increased Calcium and
Uric Acid
NURSING
Address fatigue
Educate about risk for infection and bleeding
Increase fluid intake
 CHRONIC MYELOID LEUKEMIA

The Philadelphia Chromosome t(9,22)

BRC-ABL gene (acts via Tyrosine Kinase)
Pathophysiology resembles AML
STAGES
Chronic
Transformation
Blast Crisis
 MANAGEMENT

Imatinib (Gleevec)
ChemoTx
EPO
C-CSF
Oprelvekin
BMT
 ACUTE LYMPHOCYTIC LEUKEMIA

Proliferation of Lymphoblasts
Usually B cell
Most common in young children (peaks at 4 y/o)
Competes with normal myeloid precursors
Tx: Corticosteroids, Vinca, Methotrexate, BMT

Nursing Considerations
Supportive, symptomatic approach
 CHRONIC LYMPHOCYTIC LEUKEMIA

Common malignancy of older adult.

B lymphocytes, CD52
Competes with normal cells
The B Symptoms: Fevers, Sweating at night, unintentional weight loss
Prone to infection
ChemoTx: Cyclophosphamide, Vincristine, Doxorubicin
Anti-CD52: Alemtuzumab
 THE LYMPHOMAS

Malignancy of lymphoid origin

Usually starts in the lymph nodes but may disseminate
Hodgkins vs Non-Hodgkins
 HOGDKINS LYMPHOMA

Rare but with impressive curability

Starts in a single node
Viral theory of pathogenesis
Presence of the Reed-Sternberg Cells
(Pathognomonic)
Nodular Sclerosis Most common type
 MANIFESTATION

Painless enlargement of lymph node

Lymph obstruction manifestations
Splenomegaly
B symptoms
 MANAGEMENT

Very good prognosis

Doxorubicin, Bleomycin, Vinblastin, Dacarbazine
Surgery and Radiotherapy
 NON-HODGKINS LYMPHOMA

Diffuse infiltration with malignant cells

(-) Reed-Sternberb Cells
Associated with EBV
B symptoms
Affects multiple nodal sites
MULTIPLE MYELOMA

TEACHING MOMENT.
 PRIMARY THROMBOCYTHEMIA

Stem cell disorder of increased platelet production

Myeloproliferative
Usually >600,000 cells/mL
Asymtomatic
Triggers thrombosis
 DIAGNOSTICS

CBC with APC

BMAB
 MANAGEMENT

Focused on preventing thrombosis

Hydroxyurea, Aspirin
Increase fluid intake
Promote activity
Monitor for thrombotic complications
Avoid smoking
 IDIOPATHIC THROMBOCYTOPENIC
PURPURA

Acute: Among children, 1-6 weeks after viral illness, spontaneously resolves
after 6 months
Chronic: considered after r/o other causes of thrombocytopenia
Autoimmune mechanism (anti-platelet antibodies), drug-induced
Hypersplenism
PC: <20,000, sometimes even <5,000
Common PE: Petechia, bruises, GI bleed, Hemoptysis
 MANAGEMENT

Goal: SAFE PLATELET COUNT

Spontaneous bleeding: <10, 000, levels 30,000-50,000
should be observed
Tx: Cyclophosphamide, Azathioprine, Dexamethasone
Tx: IVIg
Sx: Splenectomy
 MANAGEMENT

NURSING CONSIDERATIONS
Be aware of drug-triggers
Monitor for signs of bleeding
Avoid Valsalva
Use electric razors
Soft bristle brush
Refrain from vigorous sexual intercourse
 HEMOPHILIA

A or B X-linked
A: F VIII
B: F IX
Hemorrhage even with minimal trauma (joints are affected)
Most dangerous: Head trauma
Tx: Before, FFP. Now, F VIII and IX transfusion
Aminocaproic Acid, DDVAP F VIII Increase
 VON WILLEBRANDS DISEASE

Most common bleeding disorder

Autosomal dominant trait
Lacks activation of F VIII
Tx: Cryoprecipitate (I, VIII, XIII) or FFP
DDVAP
FIN.