BLOOD DISORDERS

COURSE OUTLINE
• Course objectives
• Review of anatomy and physiology
• Hematologic studies

Conditions
 Anaemia
 Sickle cell anaemia
 Leukaemia
 Deep venous thrombosis.
 Anatomy and physiology
• Blood is a connective tissue consisting of cells, surrounded by
a liquid matrix(plasma).blood cells make up 45% and plasma
55% of total blood volume.
• Total blood volume in adults is 5L.
• Plasma- consists of 91% water, 7%proteins and 2% of other
substances. plasma proteins include: albumin, globulin
&fibrinogen
• Cellular components include erythrocytes (red blood cells),
leukocytes and lymphocytes (white blood cells), and platelets.
• These cells are derived from pluripotent stem cells in the
bone marrow, a process known as hematopoiesis.
 Blood cells
• Red blood cells (erythrocytes). These carry oxygen from
the lungs to the rest of the body and carbon dioxide as a
waste product, away from the tissues and back to the
lungs
• Normal are disk shaped (biconcave)which increases the
surface area hence increased movement of gases into
and out red blood cells. life span is 120 days.
• 98% of O2 is transported in combination with
hemoglobin in red blood cells.
• Erythropoeisis – is the process by which new red blood
cells are produced.
• Hemoglobin is the pigmented protein & main
component of RBC. It is responsible for its red
color. There four globin bound to 4 heme, each
heme contain one iron atom and associated
with each O2 molecule. Iron is necessary for
O2 transport
• The primary function of platelets, or
thrombocytes, is blood clotting. Platelets are
much smaller in size than the other blood cells.
 White blood cells
• The primary function is to fight infection. There are several
types of white blood cells and each has its own role in
fighting bacterial, viral, fungal, and parasitic infections.
Types of white blood cells that are most important for
helping protect the body from infection and foreign cells
include the following:
– Neutrophils
– Eosinophils
– Lymphocytes
– Monocytes
– Basophil
 What is the function of blood?

• 1. Transport functions: it carries O2 and

nutrients to tissues and waste products of
metabolism, e.g. CO2 and urea to lungs and
kidney.
• 2.Homeostatic functions: it distributes heat
around the body from warmer organs, e.g.
liver and gut to peripheral organs in order to
maintain the body temperature constant.
3- Buffer functions: it keeps H+ concentration of
extracellular fluid constant at pH of 7.4 by
buffers like Hb, plasma proteins and
bicarbonate
4- Protective functions: against infection by
leucocytes and antibodies in the plasma.
5- Clotting functions: stops further loss of blood
during injury
 Hematologic studies
CBC
Peripheral blood smear
Complete blood count
Identifies total number of blood
cells(leucocytes,erythrocytes and
platelets),hemoglobin) and RBC indices. as well
as the hemoglobin levels,hematocrit.
hematocrit (percentage of blood consisting of
RBCs), and RBC indices
 ct
• Hemoglobin level- decreased in anaemia, increased in
polycethemia.male- 13.5-17.5g/dl,female- 11.5- 15.5g/dl.
• Mean corpuscular volume (MCV)- ndicates size of RBCs; very
useful in differentiating types of anemia .normal 81–96 µm3
• Prothrombin time- Measure time elapsed until clot forms;
measures extrinsic and common pathways. Increased in
liver disease, disseminated intravascular coagulation (DIC).
• International normalized ratio (INR)-A standard method of
measuring PT independent of the thromboplastin reagent
used in the test. Increased with anticoagulant excess and
conditions that cause increased PT.
 Haematological disorders
ANEMIA
• It is not a specific disease state but a sign of an
underlying disorder.
• a condition in which the hemoglobin
concentration is lower than normal, reflects the
presence of fewer than normal RBCs within the
circulation. As a result, the amount of oxygen
delivered to body tissues is also diminished. There
are many different kinds of anemia etiologic
categories:
 causes
• Loss of RBCs—occurs with bleeding, potentially from any major
source, such as the gastrointestinal tract, the uterus, the nose, or
a wound
• Decreased production of RBCs —can be caused by a defi- ciency in
cofactors (including folic acid, vitamin B12, and iron) required for
erythropoiesis; RBC production may also be reduced if the bone
marrow is suppressed (eg, by tumor, medications, toxins) or is
inadequately stimulated because of a lack of erythropoietin (as
occurs in chronic renal disease).
• Increased destruction of RBCs —may occur because of an
overactive RES (including hypersplenism) or because the bone
marrow produces abnormal RBCs that are then de- stroyed by the
RES (eg, sickle cell anemia)
 Hypoproliferative Anemias
IRON DEFICIENCY ANEMIA
• results when the intake of dietary iron is
inadequate for hemoglobin synthesis. Develops
when body iron stores are depleted.
causes
• inadequate intake of iron (seen with vegetarian
diets)
• Increased need for iron in the body –I.e in
children, adolescents, and pregnant women
blood loss
 from intestinal hookworm.
 bleeding (from ulcers, gastritis, inflammatory bowel disease,
or gastrointestinal tumors, patient multiple trauma).
 premenopausal women is menorrhagia (excessive
menstrual bleeding)
• Patients with chronic alcoholism often have chronic blood
loss from the gastrointestinal tract, which causes iron loss
and eventual anemia. Other causes include iron
malabsorption, as is seen after gastrectomy or with celiac
disease
 Clinical Manifestations

• Headache, dizziness, fatigue, tinnitus

• Palpitations, dyspnea on exertion, pallor of skin
and mucous membranes
• Smooth, sore tongue; cheilosis (lesions at
corners of mouth)
• Koilonychia (spoon-shaped fingernails)
• Pica (craving to eat unusual substances)
• In children:irritability,poor cognitive function
and decline in psychomotor development
Assessment and diagnostic findings
 Bone marrow aspiration
There is complete absence of iron from
stores and erythroblasts.
Erythroblasts are small and have a ragged
cytoplasm
Labaratory tests
 MCV and mean corpuscular hemoglobin
reduced in relation to the severity of anemia
 Diagnostic Evaluation

• CBC and iron profile decreased hemoglobin,

hematocrit, serum iron, and ferritin;
• Determination of source of chronic blood loss
may include sigmoidoscopy, colonoscopy,
upper and lower GI studies, stool and urine for
occult blood examination.
 Medical Management

• The cause of iron deficiency should be investigated. Stool

specimens should be tested for occult blood. colonoscopy,
endoscopy, or other examination of the gastrointestinal
tract to detect ulcerations, gastritis, polyps, or cancer.
• Several oral iron preparations—ferrous sulfate, ferrous
gluconate, and ferrous.
• In cases, oral iron is poorly absorbed or poorly tolerated,
or iron supplementation is needed in large amounts.
intravenous or intramuscular administration of iron
dextran may be needed. Several doses are required to
replenish the patient’s iron stores.
 Cont:
 Health education especially in high risk groups
e.g. pregnant women
 Nutritional counseling on Iron rich foods
e.g.meat,liver,beans and leafy green vegetables
 Health education on iron therapy compliance
 Advice the patient to take iron supplement an
hour before meals since iron is best absorbed in
an empty stomach
 It can be taken with food in case of side effects. It can
also be taken in the liquid form though it stains the
teeth. To avoid staining, advice the client/patient to use
a straw or rinse the mouth with water after taking it.
 Antacids and dairy products should not be taken
together with iron because they diminish its absorption
 To prevent gastrointestinal distress where more than
one is prescribed a day, start with one tablet for few
days, then increase to two
 Cont :
Increasing Activity Tolerance
• Assess level of fatigue and normal sleep pattern; determine
activities that cause fatigue.
• Assist in developing a schedule of activity, rest periods, and sleep.
• Encourage conditioning exercises to increase strength and
endurance.
Maximizing Tissue Perfusion
• Assess patient for palpitations, chest pain, dizziness, and
shortness of breath; minimize activities that cause these
symptoms.
• Elevate head of bed and provide supplemental oxygen .
• Monitor vital signs and fluid balance.
 MEGALOBLASTIC ANEMIAS
• The anemias caused by deficiencies of vitamin
B12 or folic acid, both vitamins are essential for
normal DNA synthesis.
• A megaloblast is a large, nucleated erythrocyte
with delayed and abnormal nuclear maturation.
PERNICIOUS ANAEMIA
• a type of megaloblastic anemia associated with
vitamin B12deficiency
Cont
 PATHOPHYSIOLOGY
• Vitamin B12 is necessary for normal DNA synthesis in
maturing RBCs.
• Normal gastric mucosa secretes a substance called intrinsic
factor, necessary for absorption of vitamin B12 in ileum. If a
defect exists in gastric mucosa, or after gastrectomy or small
bowel disease, intrinsic factor may not be secreted and
orally ingested B12 not absorbed.
• Some drugs interfere with B12 absorption, notably ascorbic
acid, cholestyramine, colchicine, neomycin, cimetidine, and
hormonal contraceptives.
• Primarily a disorder of older people
 Clinical Manifestations

• pallor, fatigue, dyspnea on exertion, palpitations. May

be angina pectoris and heart failure in the elderly or
those predisposed to heart disease.
• Of underlying GI dysfunction - sore mouth, glossitis,
anorexia, nausea, vomiting, loss of weight,
indigestion, epigastric discomfort, recurring diarrhea
or constipation.
• Of neuropathy (occurs in high percentage of untreated
patients) paresthesia that involves hands and feet, gait
disturbance, bladder and bowel dysfunction,.
 Diagnostic Evaluation

• CBC and blood smear - decreased hemoglobin

and hematocrit; marked variation in size and
shape of RBCs with a variable number of
unusually large cells
• Gastric analysis - volume and acidity of gastric
juice diminished.
• Schilling test- for absorption of vitamin B12
 Management

• Parenteral replacement with hydroxocobalamin or

cyanocobalamin (B12) is necessary by I.M. injection from health
care provider, generally every month.
Nursing Interventions
• Administering parenteral vitamin B12.
• Provide patient with quiet, supportive environment; reorient to
time, place, and person if needed; give instructions and
information in short, simple sentences and reinforce frequently..
• Refer patient for physical therapy and occupational therapy as
appropriate.
• Provide safe, uncluttered environment ;
 FOLIC ACID DEFICIENCY
• Chronic megaloblastic anemia caused by folic acid (folate)
deficiency.
causes
• Dietary deficiency, malnutrition, marginal diets, excessive
cooking of foods.
• Impaired absorption in jejunum (eg, with small bowel disease).
• Increased requirements (eg, with chronic hemolytic anemia,
pregnancy).
• Impaired utilization from folic acid antagonists (methotrexate)
and other drugs (phenytoin, broad spectrum antibiotics,
alcohol, hormonal contraceptives).
Clinical Manifestations
• fatigue, weakness, pallor, dizziness, headache,
tachycardia.
• sore tongue, cracked lips.
Diagnostic Evaluation
• Vitamin B12 and folic acid level folic acid will be
decreased.
• CBC will show decreased RBC, hemoglobin, and
hematocrit with increased mean corpuscular volume
and mean corpuscular hemoglobin concentration.
 Management

• Oral folic acid(5mg) replacement on daily

basis.
• Assess diet for inclusion of foods rich in folic
acid: beef liver, peanut butter, red beans
Complications
• Folic acid deficiency has been implicated in
the etiology of congenitally acquired neural
tube defects.
 APLASTIC ANEMIA

• Aplastic anemia is a disorder characterized by bone

marrow hypoplasia or aplasia resulting in insufficient
numbers of RBCs, WBCs, and platelets.
Pathophysiology and Etiology
• Destruction of hematopoietic stem cells is thought to
be through an immune-mediated mechanism.
• May be idiopathic or caused by exposure to chemical
toxins; ionizing radiation; viral infections, particularly
hepatitis; certain drugs (eg, chloramphenicol).
• May be congenital.
 Clinical Manifestations

• From anemia: pallor, weakness, fatigue, exertional

dyspnea, palpitations.
• From infections associated with neutropenia: fever,
headache, malaise; adventitious breath sounds;
abdominal pain, diarrhea; erythema, pain, exudate
at wounds or sites of invasive procedures.
• From thrombocytopenia: bleeding from gums,
nose, GI or GU tracts; purpura, petechiae,
ecchymoses.
 Management

• Removal of causative agent or toxin.

• Allogeneic bone marrow transplantation
• bone marrow regeneration;.
• Immunosuppressive treatment with
corticosteroids, cyclosporine,
cyclophosphamide,.
• Supportive treatment includes platelet and
RBC transfusions, antibiotics, and antifungals
 Nursing management
• Minimizing Risk of Infection-
– strict hand washing and avoidance of any contaminants.
– Encourage good personal hygiene
– Monitor vital signs, including temperature,
Minimizing Risk of Bleeding
– Use only soft toothbrush to prevent more gum bleeding
– Avoid I.M. injections and other invasive procedures..
– Monitor pad count for menstruating patient; avoid use of vaginal
tampons.
– Control bleeding by applying pressure to site, using ice packs and
topical hemostatic agents.
– Administer blood product replacement ; monitor for allergic reaction,
anaphylaxis, and volume overload.
 Hemolytic anemia
Hemolytic anemia is a disorder in which the red blood
cells are destroyed faster than they can be made.
The term for destruction of red blood cells is
hemolysis
2 types of haemolytic anaemia - intrinsic and extrinsic.
intrinsic ( the destruction of the red blood cells is due
to a defect within the red blood cells themselves.
Intrinsic hemolytic anemias are often inherited.
Examples include sickle cell anemia and
thalassemia )
 Extrinsic (Normal red blood cells are made but are later
destroyed by becoming trapped in the spleen, destroyed by
infection, or destroyed from drugs that can affect red blood
cells. In severe cases, the destruction takes place in the
circulation). Possible causes:
Infections e.g cytomegalovirus, hepatitis,typhoid fever
Medications e.g penicilin,antimalarials, sulfa medications
Leukemia or lymphomas
An overactive spleen hypersplenism
Autoimmune haemolytic disease
Autoimmune disorders e.g rheumatoid arthritis
 Sickle cell anemia
 Sickle cell anemia is a genetic disease of the
red blood cells (RBCs).It results from
inheritance of the sickle hemoglobin gene.
This gene causes the hemoglobin molecule to
be defective. The sickle hemoglobin (HbS)
acquires a crystal-like formation when
exposed to low oxygen tension.
• Normally RBCs are shaped like a disk. This
gives them the flexibility to travel through
even the smallest blood vessels. However, in
people with sickle cell, the RBCs have an
abnormal crescent shape. This makes them
sticky and rigid. They can get trapped in small
vessels and block blood from reaching
different parts of the body. This can cause pain
and tissue damage
 Clinical manifestation

Anaemia 7- 10 g/dl
Jaundice –rapid haemolysis of sickle cell
Tachycardia
Cardiac murmurs
Cardiomegaly
Pt susceptible to pneumonia and osteomyelitis
Heart failure and dysrthymias occurs in adults.
 Sickle cell crisis
• It is a painful episode that occurs in people
with sickle anemia.it happens when sickle cell
shaped red blood cells block blood vessels
such that blood cant get into tissues causing
pain
 Painful vaso-occlusive crises

 Most frequent
 results from tissue hypoxia and necrosis due to inadequate
blood flow to a specific region of tissue or organ.
 Precipitated by infection,acidosis,dehydration or deoxygenation
 Infarcts can occur in bones( hips, shoulders and vertebrae are
most affected),lungs and spleen
 The most serious crisis is of the brain or spinal cord
 Doppler ultrasonography detects abnormal blood flow
indicative of arterial stenosis and this predicts stroke in children
 Can be largely prevented by blood transfusions
 Visceral sequestration crises
 Results from trapping of large amounts of red
cells in the spleen and liver.during the crisis
the sequestreted cell cause the spleen to
become grossily enlarged.
 Most kids with this have had a splenic
infarction by 10 yrs where the spleen is no
longer funtional.in adults sequestration is in
liver & lungs.
 The patient is severly anemic
• Treatment is with analgesia,oxygen,exchange
transfusion and ventilatory support
• .Transfuse and monitor at regular intervals
• Attacks tend to be recurrent and splenectomy
is often needed
 Aplastic crises
• It results from infection with parvovirus or
from folate deficiency
• There is sudden fall in Hb and the marrow
cannot compensate as evidenced by absence
of reticulocytes
• Requires transfusion
 Hemolytic crises
• Increased rate of hemolysis
• Fall in Hb
• Rise in reticulocytes
• Accompany a painful crises
 Other clinical features
• Ulcers of the lower legs due to vascular stasis
and local ischaemia
• Spleenomegaly in infancy
and early childhoood but later is reduced in size
as a result of infarcts(autosplenectomy)
• Pulmonary hypertension detected by doppler
echochardiography and increased tricuspid
regurgitant velocity
 Lab findings

• Hb 6-9g/dl
• The patient with sickle cell trait usually has a
normal hemoglobin level, a normal hematocrit,
and a normal blood smear. In contrast, the patient
with sickle cell anemia has a low hematocrit
• Sickled cells
• Sickling test is positive.
• Hb electrophoresis:in Hb SS,no Hb A is seen
 treatment
• there are only three primary treatment
modalities for sickle cell diseases: Bone
marrow transplant, hydroxyurea, and long-
term RBC transfusion.
• Hydroxyurea (Hydrea), a chemotherapy agent,
has been shown to be effective in increasing
hemoglobin F levels in patients with sickle cell
anemia, thereby decreasing the permanent
formation of sickled cells.
 Treatment

• daily folic acid replacements to maintain the supply required for

increased erythropoiesis from hemolysis.
• Infections must be treated promptly with appropriate
antibiotics; infection remains a major cause of death in these
patients.
• Analgesics to relieve pain
• Red blood cell transfusion
• Good general nutrition and hygiene
• Pneumococcal and meningococcal vaccine should be given as
well as oral penicillin
• Hepatitis B vaccine as blood transfusion is sometimes needed
 treatment
• Acute chest syndrome is managed by prompt initiation of
antibiotic therapy
. In severe cases, bronchoscopy may be required to identify
the source of pulmonary disease.
Adminster supplemental ovygen
Fluid restriction may be more beneficial than aggressive
hydration.
Corticosteroids may also be useful.
Transfusions reverse the hypoxia
. Pulmonary function should be monitored regularly to detect
pulmonary hypertension early.
 Crisis

• Treat by rest
• rehydration by oral fluids or intravenous normal
saline 3 litres in 24 hours
• Supplemental oxygen may also be needed.
• Analgesics to relieve pain i.e asprin,NSAIDS and
opiates
Blood transfusion is given in very severe
anaemia
 Nursing management
MANAGING PAIN
• Any joint that is acutely swollen should be supported and
elevated until the swelling diminishes.
• Relaxation techniques, breathing exercises, and distraction
are helpful for some patients.
Preventing and managing infection
• monitoring the patient for signs and symptoms of infection.
• antibiotics should be initiated promptly,
• assess the patient for signs of dehydration.
.
 Nursing management
• Promoting coping skills
• Patient education- patient understanding on what situations
can precipitate a sickle cell crisis and the steps they can take to
prevent or diminish such crises,i.e keeping warm &hydration
• Monitoring and managing potential complications. i.e leg ulcers
– ensure measures to prevent it from trauma,referring to
specialist
 Priapism- The patient is taught to empty his bladder at the
onset of the attack, exercise, and take a warm bath.
 Chronic pain and prevention of substance abuse especially
opioid analgesics
 complications
Stroke
Pulmonary hypertension
Leg ulcers
Renal failure ,heart failure
Infections osteomyelitis
 THALASSEMIA
• These are a group of hereditary disorders
associated with defective hemoglobin-chain
synthesis.
• the production of one or more globulin chains
within the hemoglobin molecule is reduced.
This increases the rigidity of the RBCs and thus
the premature destruction of these cells.
• classified into two major groups according to the
globin chain diminished: alpha and beta.
• If left untreated, severe beta-thalassemia can be
fatal within the first few years of life. If it is treated
with regular transfusion of RBCs, patients may
survive into their 20s and 30s. Patient teaching
during the reproductive years should include pre-
conception counseling about the risk of congenital
thalassemia major.
Clinical features
• hypochromia(an abnormal decrease in the hemoglobin
content of RBCs)
• Paleness
• frequent infections
• poor appetite
• jaundice,
• extreme microcytosis (smaller-than-normal RBCs),
• destruction of blood elements (hemolysis)
• variable degrees of anemia
 management
• blood transfusions
• a bone marrow transplant (BMT)
• medications and supplements
• possible surgery to remove the spleen or
gallbladder
Cont: Blood disorders.

Bonus notes
 DISORDERS OF WHITE BLOOD CELLS
LEUKEMIA
 Leukemias are malignant disorders of the blood and
bone marrow that result in an accumulation of
dysfunctional, immature cells that are caused by loss of
regulation of cell division
 the proliferation of leukemic cells leaves little room for
normal cell production.
 These abnormal cells cause symptoms because of bone
marrow failure and infiltration of organs such as
liver,spleen,lymph nodes,meninges,brain,skin or testes.
 Predisposing factors

– Exposure to ionizing radiation.

– Exposure to certain chemicals and toxins (eg,
benzene, alkylating agents).
– Human T-cell leukemia lymphoma virus
– Familial susceptibility.
– Genetic disorders (e.g., Down syndrome, Fanconi's
anemia).
 pathogenesis of acute leukemia

 Malignant transformation occurs in the

haemopoietic stem cell or early progenitors
 There is an increased rate of proliferation,
reduced apoptosis and a block in cellular
differentiation
 Together these events cause accumulation of
blast cells resulting to bone marrow failure
although organ infiltration also occurs
 Classification of leukemia
 The leukemias are commonly classified according to the stem cell line
involved, either lymphoid or myeloid.
 They are also classified as either acute or chronic, based on the time it
takes for symptoms to evolve and the phase of cell development that
is halted.
 In acute leukemia, the onset of symptoms is abrupt, often occurring
within a few weeks. WBC development is halted at the blast phase, so
that most WBCs are undifferentiated or are blasts. Acute leukemia
progresses very rapidly; death occurs within weeks to months without
aggressive treatment. In chronic leukemia, symptoms evolve over a
period of months to years, and the majority of WBCs produced are
mature
.
 Acute lymphoblastic leukemia
 Caused by accumulation of lymphoblasts in the
bone marrow
 Most common malignancy of childhood
 Origin is precursor to B lymphocyte in
approximately 75% and t lymphocyte in 25% of
all cases
 Its incidence is highest at 3-7years,falling off by
10 years with a secondary rise after the age of
40 years
 Clinical features
 Clinical features are a result of the following:
1) Bone marrow failure:anaemia(pallor,lethargy,
dyspnoea),
2) neutropenia(fever,malaise,soreness of
mouth,throat,skin,respiratory,perianal or
recurrrent infections)
thrombocytopenia(spontaneous
bruises,purpura,bleeding gums and
menorrhagia)
2)Organ infiltration:
 bone and joint pain, splenomegaly,
hepatomegaly, lympoadenopathy,neurologic
dysfunction. And meiningeal
syndrome(headache,blurring vision)
 Diagnosis
 History taking
 Physical examination
• CBC and blood smear peripheral WBC count
varies widely from 1,000 to 100,000/mm3 and
may include significant numbers of abnormal
immature (blast) cells; anemia may be
profound; platelet count may be abnormal
and coagulopathies may exist.
• Bone marrow aspiration and biopsy cells also
studied for chromosomal abnormalities
(cytogenetic) and immunologic markers to
classify type of leukemia further.
• Lymph node biopsy to detect spread.
• Lumbar puncture and examination of
cerebrospinal fluid for leukemic cells
(especially in ALL).
 Management

• To eradicate leukemic cells and allow restoration of normal

hematopoiesis.
– Leukapheresis (or exchange transfusion in infants) may be used
when abnormally high numbers of white cells are present to reduce
the risk of leukostasis and tumor burden before chemotherapy.
– Radiation, particularly of central nervous system (CNS) in ALL.
– Autologous or allogeneic bone marrow or stem cell transplantation.
– Lymphoid blast cells are typically very sensitive to corticosteroids
and to vinca alkaloids; therefore, these medications are an integral
part of the initial induction therapy
• Supportive care and symptom management.
Central nervous system directed therapy: high
dose methotraxate is given intravenously.
Stem cell transplantation
Treatment protocols are complex using a wide
range of chemotherapeutic agents. This is
given up to three years
 Acute myeloid leukemia
 Occurs in all age groups
 AML results from a defect in the hematopoietic stem cell that
differentiates into all myeloid cells
 Most common in adults and increasingly common with old age
Clinical manifestations
 Anemia and thrombocytopenia
 Fever and infection
 DIC
 Gum hypertrophy and infiltration
 Bone pain due to expansion of marrow
 hepatosplenomegally
 Diagnostic findings
 General hematological and biochemical findings similar to
those seen in ALL.
 Test for DIC is positive
Treatment
 Supportive therapy: Multiple platelet transfusions and
replacement of clotting factors with fresh frozen plasma
 Specific therapy: Intensive chemotherapy usually given in
four blocks each of approximately one week
 Bone marrow & Stem cell transplantation: used in patients
under 65 years old.
 Results of therapy in patients over 70 years is poor
 supportive care may be the only option if the patient has
significant comorbidity, such as extremely poor cardiac,
pulmonary, renal, or hepatic function. In such cases, aggressive
antileukemia therapy is not used;
 occasionally, hydroxyurea (eg, Hydrea) may be used briefly to
control the increase of blast cells. Patients are more commonly
supported with antimicrobial therapy and transfusions as
needed

Complications
 Bleeding
 Infection
 Chronic myeloid leukemia
 Occur at any age
 Chronic myeloid leukemia (CML) arises from a mutation
in the myeloid stem cell. Normal myeloid cells continue
to be produced, but there is a preference for immature
(blast) forms
 involving more mature cells than acute leukemia
clinical features
Many patients are asymptomatic
 Symptoms include dyspnea,weight loss, anorexia or
night sweats,hepatomegally.
 Splenomegally
 Features of anemia such as pallor
 Bruising,epistaxis,menorrhagia or hemorrhage
 Gout or renal impairment caused by
hyperuricaemia
 Visual disturbances
 priapism
 Lab findings
Leucocytosis:A complete spectrum of myeloid
cells is seen in the peripheral blood
Bone marrow aspiration and biopsy:
hypercellular, usually demonstrates
Philadelphia (Ph1) chromosome
 Treatment
 imatinib. A protein-tyrosine kinase inhibitor, it works
by inhibiting proliferation of abnormal cells and
inducing cell death (apoptosis) in abnormal cells.
 alpha interferon frequently eliminates the Ph1
chromosome and blasts
 chemotherapy with such agents as busulfan or
hydroxyurea
 irradiation;
 splenectomy.
 Chronic lymphocytic leukemia
 Peak incidence is between 60 and 80 years
 is characterized by proliferation of
morphologically normal but functionally inert
lymphocytes. Classified according to cell
origin, it includes B cell (accounts for 95% of
cases), T cell
Assessment and diagnostic finding
• CBC and blood smear: large numbers of
lymphocytes; may also be anemia,
thrombocytopenia, hypogammaglobulinemia.
• Bone marrow aspirate and biopsy:
lymphocytic infiltration of bone marrow.
• Lymph node biopsy to detect spread.
 Clinical features
Symmetrical enlargement of cervical,axillary or
inguinal lymph nodes. The nodes are discrete and
non-tender .Tonsillar enlargement may be a feature
Features of anemia
Bruising due to thrombocytopenia
Purpura
Hepatosplenomegally
Immunosuppression: bacterial infections but later
Viral and fungal infections such as herpes zoster.
 Treatment

Cure is rare and so the approach to therapy is

conservative aiming for symptom control rather
than normal blood count
Chemotherapy:Chlorambucil 4-6mg/day
Corticosteroids:Treat them with prednisolone alone
Radiotherapy
Combination
Immunoglobulin replacement
Stem cell transplantation
• Supportive Care
• Transfusion therapy to replace platelets and
RBCs.
• Antibiotics, antivirals, and antifungals as
needed to control infections.
• I.V. immunoglobulins or gamma globulin to
treat hypogammaglobulinemia
 NURSING MANAGEMENT
Preventing Infection
• Especially monitor for pneumonia, pharyngitis, esophagitis,
perianal cellulitis, urinary tract infection, and cellulitis,
• Monitor for fever,.
• Check results of granulocyte counts. Concentrations less than
500/mm3 put the patient at serious risk for infection.
• Avoid invasive procedures and trauma to skin or mucous
membrane to prevent entry of microorganisms.
• Care for patient in private room with strict hand-washing
practice.
• Encourage and assist patient with personal hygiene, bathing,
and oral care.
• administer antimicrobials promptly as directed
 Preventing and Managing Bleeding

• Watch for signs of minor bleeding, such as petechiae,

ecchymosis, conjunctival hemorrhage, epistaxis, bleeding
gums, bleeding at puncture sites, vaginal spotting, heavy
menses.
• Be alert for signs of serious bleeding, such as headache with
change in responsiveness, blurred vision, hemoptysis,
hematemesis, melena, hypotension, tachycardia, dizziness.
• Test all urine, stool, emesis for gross and occult blood.
• Monitor platelet counts daily.
• Administer blood components as directed.
• Keep patient on bed rest during bleeding episodes
• easing pain and discomfort – by giving analgesics,positon
changes.shoulder and back massage
• managing mucositis- by encouraging oral hygiene, use soft brush,
normal saline rinse
• improving nutritional intake- by ensuring oral hygiene, analgesisc
before & after meals,small frequent meals, high caloric diet,
antiemetics
• decreasing fatigue and deconditioning-. Nursing interven- tions
should focus on assisting the patient to establish a balance between
activity and rest.
• maintaining fluid and electrolyte balance
. In- take and output need to be measured accurately,
and daily weights should also be monitored. The
patient should be assessed for signs of dehydration
as well as fluid overload, with particular attention to
pulmonary status. Laboratory test results UECS, and
hematocrit, should be monitored.
managing anxiety and grief – by providing information
about the disease
 Venous thrombo embolism
• deep vein thrombosis is the formation of blood clot
in one of the deep veins of the body usually the
leg.
• DVT usually originates in the lower extremity
venous level, starting at the calf vein level and
progressing proximally to involve popliteal,
femoral or iliac system
• Superficial thrombosis blood clot develops in veins
close to the surface of the skin.they do not usually
travel to the lungs.
 Risk factors of dvt
• Virchow’s triad, are believed to play a significant role in its
development:
stasis of blood (venous stasis), vessel wall injury, and
altered blood coagulation
• At least two of the factors seem to be necessary for
thrombosis to occur.
1. Venous stasis- occurs when blood flow is reduced i.e in
heart failure or shock; when veins are dilated, paralysis of
the extremities, or anaesthesia, acast on the leg.
• Prolonged bed rest,obesity, spinal cord injury
 Damage to the intimal lining of blood
vessels
• Direct trauma to the vessels i.e fractures or
dislocation, diseases of the veins, and chemical
irritation of the vein from intravenous
medications or solutions
• Surgery ,
• Pacing wires ,Central venous catheters Dialysis
access catheters
• Local vein damage ,Repetitive motion injury,
chemotherapy ports, or parenteral nutrition lines
• Increased blood coagulability
• occurs most commonly in patients who have
been abruptly with drawn from anticoagulant
medications.
• Oral contraceptive use, pregnancy, obesity
pregnancy
• An inherited blood-clotting disorder.
• cancers
 Clinical Manifestations

• pain, swelling and tenderness in one of your

legs (usually your calf muscle)
• With obstruction of the deep veins comes
edema and swelling of the extremity because
the outflow of venous blood is inhibited
• Homans’ sign (pain in the calf after the foot is
sharply dorsiflexed) positive
• limb pain, a feeling of heaviness, functional
impairment, ankle engorgement, and edema;
• differences in leg circumference bilaterally from
thigh to ankle;
• increase in the surface temperature of the leg,
particularly the calf or ankle; and areas of
tenderness or superficial thrombosis
• red skin, particularly at the back of your leg
below the knee
 Diagnostic Evaluation

• Venous duplex/color duplex(doppler ultrasound)

ultrasound is commonly done. This noninvasive test
allows for visualization of the thrombus, including any
emboli.
• Venography: I.V. injection of a radiocontrast agent. The
vascular tree is visualized and obstruction is identified.
• Coagulation profiles: PTT, PT/INR,
• D-dimer test- detects pieces of blood clot that have been
broken down and are loose in your bloodstream. The
larger the number of fragments found, the more likely it
is that you have a blood clot in your vein
 Medical Management

• The objectives of treatment for deep vein

thrombosis are to pre- vent the thrombus
from growing and fragmenting (risking
pulmonary embolism) and to prevent
recurrent thromboemboli.
Preventing embolization
• ANTICOAGULATION THERAPY Measures for
preventing or reducing blood clotting within
the vascular system
 Unfractionated Heparin
• Unfractionated heparin may be given I.V. Or
subcutaneously initially, followed by 3 to 6
months of oral anticoagulant therapy.
• Medication dosage is regulated by monitoring
the partial thromboplastin time, the
international normalized ratio (INR), and the
platelet count.
 Subcutaneous low-molecular- weight
heparin
It has a longer half-life than unfractionated heparin,
so doses can be given in one or two
subcutaneous injections each day. LMWH
prevents the extension of a thrombus and
development of new thrombi and is associated
with fewer bleeding complications than
unfractionated heparin. LMWH may be used
safely in pregnant women, and the patients may
be more mobile and have an improved quality of
life.
 Thrombolytic Therapy
• (eg, tissue plasminogen activator, streptokinase) May
be used in life- or limb-threatening situations.
• Most effective in dissolving existing clots within the first
24 hours of thrombolic event.is given within the first 3
days after acute thrombosis. Therapy initiated beyond 5
days after the onset of symptoms is significantly less
effective
• However, thrombolytic therapy results in approximately
a threefold greater incidence of bleeding than heparin. If
bleeding occurs and cannot be stopped, the
thrombolytic agent is discontinued.
 Nonpharmacologic Therapies

• Bed rest is used only with unfractionated heparin. When

treating a superficial thrombosis or using low-molecular-
weight heparin, the patient is encouraged to walk.
• Elevation of affected extremity: at least 10 to 20 degrees
above the level of the heart to enhance venous return and
decrease swelling.
• Compression: promotes venous return and reduces swelling.
– Electrically or pneumatically controlled stockings, boots, or sleeve
– Elastic stockings or garments (20 to 30 mm Hg with arterial
disease secondarily, 30 to 40 mm Hg for isolated venous disease)
• Dry heat:
– Warm water bottles
• Moist heat:
– Hydrotherapy
– Whirlpool bath
– Warm compresses
 relieving pain

• Elevate legs as directed to promote venous

drainage and reduce swelling.
• Apply warm compresses or heating pad as
directed to promote circulation and reduce pain.
• Administer acetaminophen (Tylenol), codeine,
or other analgesic and as needed. Avoid the
use of aspirin (or aspirin-containing drugs) and
NSAIDs during anticoagulant therapy to prevent
further risk of bleeding.
 Preventing Bleeding

• Follow precautions to prevent bleeding.

– Handle patient carefully while turning and positioning.
– Maintain pressure on I.V. and venipuncture sites for at
least 5 minutes. Apply ice if patient is prone to bleeding.
– Assist with ambulation and keep walkways/hallways free
from clutter to prevent falls.
• Observe carefully for any possible signs of bleeding
and report immediately so that anticoagulant
dosage may be reviewed and altered if necessary:
 Surgery

• Placement of a filter into the inferior vena

cava to prevent pulmonary embolism in a
patient who cannot tolerate prolonged
anticoagulant therapy or who has recurrent
emboli in the presence of adequate
anticoagulation.
• Thrombectomy may be necessary for severely
compromised venous drainage of the
extremity.
 complications
• Acute pulmonary embolism
• Post thrombotic syndrome
• Renal vein thrombosis
• Heart attack
• stroke