ACUTE MYELOID LEUKEMIA

Kathleen Joyce Dimacali

BSN-IV
Acute myeloid leukemia(AML)

is a neoplastic disease characterized by:

 infiltration of the blood,
 bone marrow, and
 proliferative, clonal undifferentiated cells of the
hematopoietic system.
AML usually begin in cells that turn into white blood
cells, but it can start in other blood-forming cells.
• as well as with acute types of leukemia such as AML,
bone marrow cells don't grow the way they're supposed
to. These immature cells, called blasts, build up in the
body.
Other names for acute myeloid leukemia,
including:
• Acute myelocytic leukemia
• Acute myelogenous leukemia
• Acute granulocytic leukemia
• Acute non-lymphocytic leukemia
Incidence
•3.5 per 100,000 people per year
•it is higher in men than in women (4.5 vs 3.1)
•increases with age
 1.7 in individuals age <65 years
 15.9 in those age >65 years
•The median age at diagnosis is 67 years.
ETIOLOGY AND RISK FACTORS
Heredity
• Aneuploidy(trisomy21 noted in Down syndrome),
• Inherited diseases with defective DNA repair (Fanconi
anemia, Bloom syndrome, and ataxia telangiectasia)
• Congenital neutropenia(Kostmannsyndrome)
• Germline mutations of CCAAT/enhancer-binding protein α
(CEBPA), runt-related transcription factor 1 (RUNX1), and
tumor protein p53 (TP53)
Radiation
 High-dose radiation
•atomic bombs ; nuclear reactor accidents,
•increases the risk of myeloid leukemias that peaks
5–7 years after exposure.
Therapeutic radiation alone seems to add little risk
Chemical and Other Exposures
Exposure to benzene
•plastic, rubber, and pharmaceutical industries, is
associated with an increased incidence of AML.
Smoking and exposure to petroleum products
•paint, embalming fluids, ethylene oxide, herbicides,
and pesticides
Drugs
Anticancer drugs are the leading cause of therapy-
associated AML.
Alkylatingagent-associated leukemias occur on
average 4–6 years after exposure
TopoisomeraseII inhibitor associated leukemias
occur 1–3 years after exposure
• Newer agents for treatment of other hematopoietic
malignancies and solid tumors are also under scrutiny for
increased risk of AML.
CLINICAL PRESENTATION
SYMPTOMS
•Patients with AML often have several non-
specific(general) symptoms.
• These can include:
Fatigue usually the first symptom
Fever with or without an identifiable infection is the
initial symptom in approximately 10% of patients
Night sweats
Loss of appetite
 Weight loss
 Signs of abnormal hemostasis(bleeding, easy bruising)
are noted first in 5% of patients.
 On occasion, bone pain, lymph adenopathy, nonspecific
cough, headache, or diaphoresis are the presenting
symptoms
Physical Findings
 splenomegaly,
 hepatomegaly,
 lymphadenopathy,
 sternal tenderness,
 evidence of infection and hemorrhageare oftn found at
diagnosis.
•Significant gastrointestinal bleeding, intrapulmonary
hemorrhage, or intracranial hemorrhageoccurs most
often in APL.
•Bleeding associated with coagulopathymay also
occur in monocytic AML and with extreme degrees of
leukocytosisor thrombocytopenia in other
morphologic subtypes.
•Retinal hemorrhagesare detected in 15% of
patients. •Infiltration of the gingivae, skin, soft
tissues, or meninges with leukemic blasts at
diagnosis is characteristic of the monocyticsubtypes
and those with 11q23 chromosomal abnormalities.
Hematologic Findings
Anemiais usually present at diagnosis and can be
severe.
Decreased erythropoies is often results in a
reduced reticulocyte count, and red blood cell
(RBC) survival is decreased by accelerated
destruction.
Active blood loss also contributes to the anemia.
leukocyte count is about 15,000/μL.
•Between 25 and 40% of patients have counts
<5000/μL,
• 20% have counts >100,000/μL.
• Fewer than 5% have no detectable leukemic cells in the
blood.
Platelet counts <100,000/μLare found at diagnosis
• in ~75% of patients, and about 25% have counts
<25,000/μL.
Diagnosis
• 20% or more leukemic
blasts in the bone
marrow
• Immunohistochemicalst
aining for myelo
peroxidaseis the best Immunohisto chemical diagnosis of acute
myeloid leukemia(AML). (A) Bone marrow
method for determining aspirate shows increased blasts from a patient
with AML with inv(16) (Wright-Giemsastain,
which cells are 350). (B) Bone marrow biopsy from the same
committed to the patient shows 100% cellularitywith sheets of
blasts (hematoxylin-eosin stain, 340)
myeloid line age
 Diagnosis the diagnostic work-up for AML:
• Complete blood count (CBC) with manual
differential and routine chemistry profile (including
liver function tests, serum creatinine, lactate
dehydrogenase[LDH], and uric acid)
• Coagulation profile –Prothrombintime (PT), partial
thromboplastintime (PTT), fibrinogen)•Bone marrow
aspiration and biopsy, including classical
cytogenetics, immunophenotyping, and molecular
testing for c-KIT, FLT3-ITD, NPM1, and CEBPA•HLA
typing of patient and family
• Imaging studies, including dental survey and
computed tomography (CT) scan of the chest and
abdomen, or chest x-ray and abdominal ultrasound
• Sperm preservation in men (if desired by patient)
• Pregnancy test in women
Treatment
newly diagnosed patient with AML is usually divided into two
phases,
• induction –postremission management
• The initial goal is to induce Complete remission
based on the patient’s age
 <60 years -Intensifying therapy with traditional
chemotherapy agents such as cytarabine and
anthracyclinesin younger patients appears to increase the
cure rate of AML.
 >60 years -the benefit of intensive therapy is controversial;
INDUCTION CHEMOTHERAPY •
The most commonly used CR induction regimens
(for patients other than those with APL) consist of
combination chemotherapy with cytarabineand an
anthracycline(e.g., daunorubicin, idarubicin,
mitoxantrone).
<60 years

cytarabine is used either at standard dose (100–

200 mg/m2) administered as a continuous
intravenous infusion for 7 days or higher dose (2
g/m2) administered intravenously every 12 h for 6
days.
anthracycline therapy generally consists of
daunorubicin(60–90 mg/m2) or idarubicin(12
mg/m2) intravenously on days 1, 2, and 3 (the 7
and 3 regimen).
≥60 years

• outcome is poor likely due to a higher induction

treatment–related mortality rate and frequency of
resistant disease, especially in patients with prior
hematologic disorders (MDS) or who have received
chemotherapy treatment for another malignancy
*has not shown benefit due to the increased toxicity
and is not recommended.
NURSING INTERVENTION

• Education. The nurse should explain the disease

course, treatment, and adverse effects.
• Infection. The nurse should teach the patient and his
family how to recognize symptoms of infection such
as fever, chills, cough, and sore throat.
• Bleeding. The nurse should educate the patient
and the family how to recognize abnormal bleeding
through bruising and petechiae and how to stop it
with direct pressure and ice application.
• Promote good nutrition. The nurse should explain
that chemotherapy causes weight loss and
anorexia, so the patient must be encouraged to eat
and drink high-calorie and high-protein foods and
beverages.