25/10/2013

NURSING MANAGEMENT FOR PATIENTS WITH

HEMATOLOGY PROBLEMS

Kusman Ibrahim, PhD

Faculty of Nursing, Padjadjaran University

OVERVIEW OF HEMATOLOGY

Hematology is the study of blood which is composed of

plasma (~55%), and the formed elements which are:
The erythrocytes (RBCs) (~45%)
Contain hemoglobin

Function in the transport of O2 and CO2

The Leukocytes (WBCs) and platelets (thrombocytes)

(~1%)
Leukocytes are involved in the bodys defense
against the invasion of foreign antigens.
Platelets are involved in hemostasis which forms a
barrier to limit blood loss at an injured site.

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COMPOSITION OF BLOOD

BLOOD
Suspension of cells in a solute of
water, proteins, and electrolytes
Average volume is 5 liters
70mL per kg body weight
Plasma
Blood from which the cellular
components (RBCs, WBCs,
platelets) have been removed by
centrifuge
Color is yellow
Contains coagulation proteins (clotting
factors)

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HEMATOPOIESIS
Development of blood cells and other formed elements
Sites vary throughout development
Fetal: yolk sac, liver, spleen
Pediatric: axial and appendicular skeleton
Adult: axial skeleton (sternum and pelvis)
Stem cells
Primitive; self-replicate and differentiate to become
increasingly specialized progenitor cells which form mature
cells
Process regulated by growth factors (interleukins, erythropoietin,
thrombopoietin, G-CSF)
Early lineage division between progenitors for lymphoid and
myeloid cells

HEMATOPOIESIS

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HEMATOPOIESIS

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RED BLOOD CELLS

Transport oxygen via hemoglobin
from lungs to peripheral tissues
and organs
Normal lifespan = 120 days
Reticulocytes
Immature red blood cells
Calculating proportion within
circulation assists in determining cause
of anemia
Normal is 1-2%

Low suggests decreased production

(i.e. nutritional or marrow problem)

High suggests bleeding or premature

destruction of red blood cells (i.e.

hemolysis)

RED BLOOD CELLS

Peripheral blood smear
Normal

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STRUCTURE OF BONE MARROW

BONE MARROW

Hyperplastic
Normal

Hypoplastic

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SUMMARY OF BLOOD FORMING ORGANS

DERIVATION OF BLOOD CELLS

Mature blood cells have a limited life span
and with the exception of lymphocytes,
are incapable of self-renewal.
Replacement of peripheral hematopoietic cells
is a function of the pluripotential
(totipotential) stem cells found in the bone
marrow
Pluripotential stem cells can differentiate into all of
the distinct cell lines with specific functions and they
are able to regenerate themselves.
The pluripotential stem cells provide the cellular
reserve for the stem cells that are committed to a
specific cell line.

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HEMATOLOGIC DISORDERS
Disorders associated with Erythrocytes
Disorders of bleeding

Disorders associated with white blood cells

Lymphomas

Majuvy L. Sulse

ANEMIA
(DECREASED IN NUMBER OF RBCS)

Low Hgb H/H, Bone marrow

Abnormal & deficient
production, blood loss, aspiration,
destruction of RBC Peripheral smear

( Causes) ( Diagnosis)
Less 02 carrying capacity

Hypoxia

Pallor, Fatigue, Palpitation, Low BP, SOB, DOE, MI, Renal failure

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MANAGEMENT OF ANEMIA

Medical:
Identify cause
Treat cause

Relieve symptoms

Prevent
complications
Nursing:
Assess
Educate

CLASSIFICATION OF ANEMIA
Based on the size of the RBC
Normocytic
Microcytic
Macrocytic

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IRON DEFICIENCY ANEMIA

Causes:
Inadequate iron supply

Chronic blood loss without iron replacement

Decreased iron absorption in the intestines

Signs/ Symptoms:
Hypochromic (low MCH), microcytic ( low MCV)

Elevated serum binding capacity

Brittle, spoon-shaped nails with longitudinal ridges

Cheilosis (painful mouth cracks/ sores)

Red shiny tongue

Insidious development of fatigue

DIAGNOSIS/TREATMENT

Treatment:
Identify cause

Diagnosis:
Laboratory values

Gastroscopy

Sigmoidoscopy

Occult blood in stools

Radiographic studies of
GI
Iron supplement

Nutritional/dietary

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MEGALOBLASTIC ANEMIA
Predominance of megaloblasts & lack of
normoblasts
Includes pernicious anemia, Vit. B12 & Folic acid
deficiencies
Related to surgery particularly of terminal ileum
where B12 is absorbed; vegetarian diet;
prolonged exposure to nitrous oxide
Related to aging & long term gastritis
Related to alcohol malnutrition & malabsorption
(Folic acid deficiency)
Macrocytic, normochromic RBC
Lack of Intrinsic factor
Autoimmune response

DIAGNOSIS & TREATMENT:

(MEGALOBLASTIC ANEMIA)

Schilling test- definitive dx of pernicious anemia

Gastric secretion analysis- pH, free HCL, low

gastric secretion

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DIAGNOSIS & TREATMENT :

(MEGALOBLASTIC ANEMIA)
Management-
Lifelong tx with Vit B12 injection

Iron & Folic acid supplement

Nutritional/ dietary changes

Foods that are rich in folic acid and vitamin B12 include the
following:
eggs
meat
poultry
milk
shellfish
fortified cereals

APLASTIC ANEMIA-MANIFESTATIONS &

DX
Manifestations-
Exertional dyspnea, fatigue, pallor, infections
Bleeding (nasal,oral, rectal,vaginal)
ecchymosis, petechiae, pupura
Low platelets (less 30, 000), RBCs, WBCs
Dry bone marrow on aspiration
Diagnosis-

Differential count
Manifestations
History of exposure to myelotoxins

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APLASTIC ANEMIA
Medical
Remove causative
Idiopathic cause- treat with steroids, hormone therapy
Autoimmune cause- bone marrow transplants (younger than
30 or those who have not received transfusions yet
Antithymocyte & cyclosporine therapy- skin testing & watch
for allergic reactions
Blood transfusions
Frequent CBCs esp for those on radiation therapy
Nursing management
Infection control

Client education

ANEMIA FROM BLOOD LOSS

Types
Acute-trauma, complications from surgery
Hypovolemia, hypotension, hypoxemia, weakness,
tachycardia, stupor
Chronic- bleeding ulcer, hemorrhoids
Gradual and vague symptoms as fatigue, pallor, dyspnea
Medical/ Nursing Interventions
Identify source of bleeding
Control through medical or surgical
interventions
Blood transfusions

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HEMOLYTIC ANEMIA
Abnormal destruction of RBCs by
Intrinsic-defective RBCs, enzyme
deficit(G6PD)
extrinsic factors- toxins, injury as in
prosthetic heart valves
Failure of bone marrow to replace destroyed
RBCs
Sites of hemolysis:
Intravascular-circulation
Extravascular- macrophages of spleen, liver &
bone marrow

FINDINGS/ TREATMENT
Findings Treatment
Normocytic anemia Identify/Treat cause
Reticulocytosis as
IV fluids to flush
compensatory kidneys
mechanism
NAHCO3 or Na
Increased RBC
fragility Lactate to alter
Short lifespan
urine pH (decrease)
precipitation in
Hyperbilirubinemi
a- blood, urine, renal tubules
stools Splenectomy

S/S as in Anemia

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SICKLE CELL ANEMIA AND SICKLE

CELL TRAIT
Inherited, autosomal, recessive disorders of HB
synthesis resulting in decrease O2 to the tissues
(hypoxia) and obstruction of blood vessels
Substitution of valine for glutamic acid in B-
globin gene
Primarily seen in the black population

Sickle cell trait is a mild form of the disease and

it is the commonest
Sickle cell trait is prevalent in Africa

Resistant to the parasite that causes malaria

Genetically inherited from each parent

Inheritance

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PATHOPHYSIOLOGY

Sickling of RBC-triggered by
Hypoxia- low O2 tension in blood
High altitude
Emotional/ physical stress
Surgery

Blood loss

Infection-bacterial & viral

Dehydration
Acidosis
Decreased plasma volume-
Increased blood viscosity
Hypothermia
Stress

PATHOPHYSIOLOGY
Sickled cell-rigid & elongated causes tissue
injury (as cells cant pass through small vessels)
results in local hypoxia anemia as more cells are
hemolyzed by spleen
Initially reversible with re-oxygenation then
becomes irreversible due to cell membrane
damage from recurrent sickling

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APLASTIC ANEMIA
Low Hb & pancytopenia
Unknown etiology / autoimmune disturbance
Direct injury by Myelotoxins- agents causing bone marrow
damage when received in large doses
Medication induced:

Chemo, chloramphenicol, sulfonamides, mephenytoin, quinine

Exposure to environmental hazards:
Benzene, insecticides, radiation & radioactive materials
Infections
Hepatitis, miliary TB, EPBV
Congenital/hereditary causes

SICKLE CELL CRISIS

Exacerbation of RBC sickling
Vaso- occlusion (Vaso-occlusive crises) -
vasospasm
Changes in membrane permeability plasma
loss & hemoconcentration development of
thrombi, tissue ischemia, infarction, necrosis
Shock is a life threatening consequence
Frequency, extent, & severity of episode is
dependent on percentage of HbS present

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CAUSES OF SICKLE CELL CRISIS

Vaso - Occlusion
Aplastic crisis

Hemolytic crisis

Sequestration crisis

Mixed crisis

TYPES OF SICKLE CELL DISEASE

Sickle cell anemia
Sickle cell Thalassemia
Sickle cell HbC-

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CLINICAL MANIFESTATIONS
Cardiovascular changes
Skin changes

Abdominal changes

Musculoskeletal changes

Central nervous system changes

CLINICAL MANIFESTATION
Noticed after 6 months when fetal Hb is
no longer present
Improper growth related to anemia

Retarded growth and delay in sexual

maturity
Hand- foot syndrome- edema of hands and
feet
Pain from tissue ischemia-hands, feet ,
joints

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CLINICAL MANIFESTATION
Weakness and fatigue-exercise intolerance
Jaundice- development of gallstones
Pallor-of mucous membrane-grayish cast on skin
Priapism-occlusion of penile veins
Infarct on the spleen - small and scarred
Leg ulcers in about 75% of cases

COMPLICATIONS
CHF from ischemia &
heart enlargement
Acute Chest syndrome-
fever, chest pains, cough,
dyspnea
Autosplenectomy-
shrinking of spleen
from repetitious
scarring
CVA- thrombus

Pulmonary infarct-
formation
pulmonary HTN, MI, Cor Osteoporosis/

Pulmonale
Blindness from retinal
obstruction-hemmorhage-
detachment
Renal failure-
hemoconcentration
Osteosclerosis
Leg ulcers esp. at
ankles-tissue hypoxia
Infection- absence of
phagocytic activity by
spleen

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DIAGNOSTIC FINDINGS
Peripheral Smear
Sickling Test

DNA

Elevated serum bilirubin levels

Skeletal xrays-reveal bone/joint deformities &

flattening
MRI-check for clots (CVA)

MEDICAL/ NURSING MANAGEMENT

No cure
Supportive interventions: pain relief,
Hydration, O2, rest, blood transfusions
Patient Teaching to avoid factors that cause
crisis
Assessment of family understanding of the
disease & coping mechanism
Links for support
Genetic counseling

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GET INVOLVED CLASS!

What nursing diagnosis should receive the
highest priority in a client with sickle cell crisis?
A nurse is preparing a teaching plan for a sickle
cell client, what should the nurse emphasize on
to prevent sickle cell crisis?

POLYCYTHEMIA VERA
Excessive production of erythrocytes,
leukocytes, platelets due to excessive
activation of pluripotent stem cells
Manifestations
HTN- headache, vertigo, tinnitus, dizziness, visual
disturbances
CHF- angina- hypervolemia & viscosity
Intermittent claudication- thrombophlebitis

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POLYCYTHEMIA VERA
Stroke- thrombi formation
Pruritus- histamine release from basophils
Hemmorrhage- vessel rupture from tissue distention
Hepatomegaly & Slenomegaly from organ
engorgement
Plethora- Ruddy complexion
Gouthyper uric acid production from RBC
destruction

DIAGNOSIS
RBC=8-12 million
Hgb=18-25 gm
Increased platelet count
HCT= >54% in men; 49% in women
Elevated WBCs with basophilia
Increased serum uric acid, B12
Splenomegaly
Hyperplastic bone marrow

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MEDICAL/NURSING MANAGEMENT
Goal of treatment is
Reduce blood volume & viscosity
Phlebotomy to Hct levels of 45-48% (about 300-
500ml/day)
Reduce bone marrow activity- myelosuppressive
agents & radioactive phosphorous
Hydration therapy with I & O

DISORDERS OF BLEEDING-
THROMBOCYTOPENIA
Decreased production of platelets below
150,000/uL
Manifests as bleeding- skin bruises easily

Maybe
acquired food, drugs, infections, aplastic anemia
inherited- pancytopenia, hereditary
thrombocytopenia

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DIAGNOSIS/ MANAGEMENT
CBC shows low platelet & Hb count
Assess for hx of NSAIDS

Avoid injury

Good oral hygiene & skin care

Rectal enemas & suppository-avoid

constipation
Avoid IM, SC injections, rectal temperatures

Apply pressure on any bleeding source

Monitor signs of bleeding

IMMUNE THROMBOCYTOPENIA PURPURA-

( ITP)
Autoimmune bleeding disorder
Platelets coated with antibodies

Destroyed by macrophages in liver & spleen

Survival is 1-3 days instead of 8-10

Gradual onset & transient remissions occur

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CLINICAL MANIFESTATIONS
Petecchiae-small, flat, pinpoint red
Purpura-numerous petecchiae

Ecchymosis-large purplish lesions

Epistaxis-

Bleeding gums

Heavy menses

Complication=hemorrhage

DIAGNOSIS
Platelet Ct<100, 000
Prolonged bleeding time with normal
coagulation time
Increased capillary fragility

Positive platelet antibody test

Bone marrow aspirate contains normal or

increased megakaryocytes

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MANAGEMENT
Cortecosteroids (prednisone)-suppreses the
phagocytic response of Spleenic macrophages,
depress antibody formation, reduce capillary
permeability & bleeding time
IV immunoglobulin (IVIG)

Immunosuppressive therapy

Splenectomy-

Platelet transfusions

HEMOPHILIA
Characterized by prolonged bleeding after
surgical/ dental or small trauma or cuts
Types

Hemophilia A- factor Vlll-most common-80%

cases
Hemophilia B- factor lX deficiency-inherited
gene
Von Willebrands disease- deficient Vlll &
platelet dysfunction

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ETIOLOGY
Sex linked genetic disorder
Transmitted by females but males express the
disorder
Carriers transmit the gene to half their
daughters and the disorder to half their sons
Males transmit the gene to all their daughters
but none to their sons

CLINICAL MANIFESTATIONS
Slow persistent bleeding from
cuts/scratches
Delayed hemorrhage-hours/days after
injury
Severe bleeding after dental surgery

GI bleed

Nosebleed

Hematoma

Prolonged APTT

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TREATMENT
Goal is to stop bleeding
Increase anti-hemophilic factor-give factor Vlll,
lX
Prevent complications

Support therapy

LEUKEMIA
DESCRIPTION
Malignant exacerbation in the number of
leukocytes, usually at an immature stage, in
the bone marrow
May be acute, with a sudden onset and short
duration, or chronic, with a slow onset and
persistent symptoms over a period of years
Affects the bone marrow, causing anemia,
leukopenia, the production of immature cells,
thrombocytopenia, and a decline in immunity

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LEUKEMIA
DESCRIPTION
The cause is unknown and appears to involve gene
damage of cells leading to the transformation of cells
from a normal state to a malignant state
Risk factors include genetic, viral, immunological,
and environmental factors and exposure to radiation,
chemicals, and medications

CLASSIFICATION OF LEUKEMIA
ACUTE LYMPHOCYTIC LEUKEMIA (ALL)
Mostly lymphoblasts present in bone marrow
Age of onset is less than 15 years
CNS manifestation common-leukemic meningitis
Normally, the lymphocytes fight infection by
making antibodies that attack harmful elements.
But, in ALL, the cells are immature and
overabundant. They crowd out other blood cells,
and may collect in the blood, bone marrow, and
lymph tissue.

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CLASSIFICATION OF LEUKEMIA
ACUTE MYELOGENOUS LEUKEMIA (AML)
affects the young blood cells (called blasts)
that develop into a type of white blood cell
(called granulocytes). The main function of
granulocytes is to destroy bacteria. The
blasts, which do not mature and become
too numerous, remain in the bone marrow
and blood.
Age of onset is between 15 and 39 years

CLASSIFICATION
CHRONIC MYELOGENOUS LEUKEMIA (CML)
Mostly granulocytes present in bone marrow
Age of onset is after 50 years of age
CML occurs mainly in adults and is rare in children
CHRONIC LYMPHOCYTIC LEUKEMIA (CLL)
Mostly lymphocytes (B cells) present in bone marrow
Age of onset is after 50 years of age,

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DIAGNOSIS
CBC-WBC may be normal, decreased or elevated
Decreased platelet

Decreased Hb

Bone marrow aspiration- increase in marrow

cells

LEUKEMIA
ASSESSMENT
Anorexia, fatigue, weakness, weight loss
Anemia
Bleeding (nosebleeds, gum bleeding, rectal bleeding,
hematuria, increased menstrual flow)
Petechiae
Prolonged bleeding after minor abrasions or
lacerations

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ASSESSMENT
Elevated temperature
Lymphadenopathy and splenomegaly
Palpitations, tachycardia, orthostatic
hypotension
Pallor and dyspnea on exertion
Headache
Bone pain and joint swelling

LEUKEMIA
ASSESSMENT
Normal, elevated, or reduced white blood cell (WBC)
count
Decreased hemoglobin and hematocrit levels
Decreased platelet count
Positive bone marrow biopsy identifying leukemic
blast phase cells

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LEUKEMIA
INFECTION
A major cause of death in the immunosuppressed
client
Can occur through autocontamination or cross-
contamination
Common sites of infection are the skin, respiratory
tract, and gastrointestinal (GI) tract

LEUKEMIA
IMPLEMENTATION: INFECTION
Initiate protective isolation procedure-also
called Neutropenic Precautions or Reverse
isolation
Ensure frequent and thorough hand washing
Reduce exposure to environmental organisms
by eliminating raw fruits and vegetables (low-
bacteria) from the diet, fresh flowers from the
clients room, and by not leaving standing
water in the clients room
Avoid invasive procedures such as injections,
rectal temperatures, and urinary
catheterization

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LEUKEMIA
CLIENT EDUCATION: INFECTION
Avoid crowds and those with infections
Consume a low-bacteria diet and to avoid
drinking water that has been standing for
longer than 15 minutes
Avoid activities that expose the client to
infection such as changing a pets litterbox or
working with houseplants or in the garden
Neither the client nor their household contacts
should receive immunization with a live virus

LEUKEMIA
BLEEDING
During the period of greatest bone marrow
suppression (the nadir), the platelet count may be
extremely low, less than 10,000/mm3 (bleeding
risk)
Examine the client for signs and symptoms of
bleeding; examine all body fluids and excrement
for the presence of blood
Handle the client gently; use caution when taking
blood pressures to prevent skin injury
Measure abdominal girth, which can provide an
indication of internal hemorrhage
Provide safety-pad side rails and sharp corners of
the bed and furniture

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LEUKEMIA
IMPLEMENTATION: BLEEDING
Provide soft foods that are cool to warm in
temperature
Avoid injections if possible to prevent trauma
to the skin and bleeding; apply firm, gentle
pressure to a needle stick site for at least 10
minutes
Avoid rectal suppositories, enemas, and
thermometers
If the female client is menstruating, count the
number of pads or tampons used
Administer blood products as prescribed

LEUKEMIA
FATIGUE AND NUTRITION
Assist the client in selecting a well-balanced
diet
Provide small, frequent meals (high calorie,
high-protein, high-carbohydrate) that require
little chewing
Assist the client in self-care and mobility
activities
Allow adequate rest periods during care; do
not perform activities unless they are essential
Administer blood products for anemia as
prescribed

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LEUKEMIA
CHEMOTHERAPY
Induction therapy: Aimed at achieving a rapid,
complete remission of all manifestations of the
disease
Consolidation therapy: Administered early in
remission with the aim of cure
Maintenance therapy: May be prescribed for months
or years following successful induction and
consolidation therapy; the aim is to maintain
remission

LEUKEMIA
IMPLEMENTATION
Administer antibiotic, antibacterial, antiviral, and
antifungal medications
Blood replacements as needed
Prepare the client for transplantation
Administer colony-stimulating factors as prescribed
Maintain infection and bleeding precautions

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LEUKEMIA
IMPLEMENTATION
Provide an adequate diet
Provide an activity schedule that will conserve
energy
Instruct the client in appropriate home care
measures
Provide psychosocial support and support services for
home care

LEUKEMIAS

Acute Chronic
Combination Chemo Treatment based on
Induction symptoms
Rest- 3 weeks Radiation to spleen, nodes
Consolidation Interferon
Maintenace follows Autologous stem cell
remission- lasts 2-3 years transplant
Bone marrow transplant Blood transfusions: RBCs,
platelets, WBCs

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HODGKINS DISEASE
DESCRIPTION
A malignancy of the lymph nodes that originates
in a single lymph node or a single chain of nodes;
metastasis occurs to other adjacent lymph
structures and eventually invades nonlymphoid
tissue
Usually involves lymph nodes, tonsils, spleen, and
bone marrow and is characterized by the presence
of the Reed-Sternberg cell in the nodes
Possible causes include viral infections and
previous exposure to alkalyting chemical agents
Prognosis is dependent on the stage of the disease

ETIOLOGY & PATHOPHYSIOLOGY

Unknown cause
Linked to Epstein-Barr Virus

Genetics- high among Jews

Mechanism of growth & spread- unknown

Cancerous cells transforms in lymph and

progresses to other nodes or direct
infiltration of blood vessels

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CLINICAL MANIFESTATIONS
Enlargement of cervical, axillary, inguinal
lymph nodes may be painless
B symptoms-Weight loss, Fever, night
sweats
Cough, stridor, dyspnea

Hepatomegaly

Splenomegaly

SVC syndrome from intra thoracic

involvement

DIAGNOSIS & STAGING

Peripheral blood analysis-microcytic,
hypochromic anemia, leukocytosis
Lymph node biopsy-definitive dx

Bone marrow examination-staging( l-lV)

CXR, CT Scan, radioisotope studies-define sites

Lymphangiography-assess nodes & vessels

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HODGKINS DISEASE
IMPLEMENTATION
For stage 1 and 2 without mediastinal node
involvement, the treatment of choice is extensive
external radiation of the involved lymph node regions
With more extensive disease, radiation along with
multi agent chemotherapy is utilized

HODGKINS DISEASE
Implementation
Monitor for side effects related to chemo or
radiation
Monitor for signs of infection & bleeding
Maintain infection and bleeding precautions
Discuss possibility of sterility with male client
receiving radiation & inform of options related
to sperm banks
Pain management
Client & family support
If terminal- ensure client has dignified death

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NHL
NON- HODGKINS LYPHOMA
Group of malignancies with origins in
lymphoid cells affecting all ages
Most common occurring cancer & 5th
leading cancer causing death
Men are more affected than women;
survival better for women than in men
Incidence higher in whites than other
races
Painless lymph node enlargement is
primary manifestation
Symptoms will present on where disease
has spread

DIAGNOSIS & TREATMENT

Diagnostic tests are same as for Hodgkins

disease-Lymph node biopsy done
Treatment-radiation & chemotherapy

Nursing assessment for nodes

characteristics, B symptoms appearance
Support for client & family

Manage risk for infection, bleeding, sexual

& reproductive dysfunction
Nutritional management

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MULTIPLE MYELOMA
Cancer of the plasma cell, an important part
of the immune system that produces
immunoglobulins (antibodies) to help fight
infection and disease.
Hypercalcemia, anemia, renal damage,
increased susceptibility to bacterial infection,
and impaired production of normal
immunoglobulin are common clinical
manifestations of multiple myeloma. It is
often also characterized by diffuse
osteoporosis, usually in the pelvis, spine,
ribs, and skull.

DIAGNOSTICS/ MANAGEMENT
Diagnostics
Radiologic studies- lesions in bones,
demineralization, osteoporosis
Bone marrow biopsy- immature plasma
cells
Abnormal immunoglobulin
Monoclonal immunoglobulin chains in
blood & urine exam

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MULTIPLE MYELOMA
Management
Chemotherapy, radiation tx
Autologous bone marrow transplant

Plasmapheresis

Hydration, diuretics, phosphate for

treatment of Hypercalcemia
Pain management

Supportive for anemia, leukopenia,

thrombocytopenia

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