Leukemia
Background
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Etiology
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Group of cancer affecting the blood and blood forming tissues of
○ Bone marrow
○ Lymph system
○ Spleen
Affects all age groups
Accumulation of dysfunctional cells due to loss of regulation in cell division
Combo of genetic + environment
○ Abnormal genes
○ Chemical agents, chemo drugs, virus, radiation, immunologic
increase
Clinical Manifestations
Cause: bone marrow failure or infiltration of leukemia to tissues
● Bone marrow failure by overcrowding of abnormal cells and not enough
production of bone marrow elements
What occurs…
● Anemia
○ Sx: fatigue, SOB, pallor, tachycardia, systolic murmurs
● Thrombocytopenia
○ Sx: increased risk for bleeding, petechiae, ecchymosis, bleeding
● Decreased WBC
○ Sx: increase risk for infection, fever, lymphadenopathy (swelling of
lymph nodes)
Leukemia can travel to other organs causing…
● Splenomegaly
● Hepatomegaly (w/ or w/o jaundice)
● Lymphadenopathy
● Bone pain
● Meningeal irritation
● Oral lesions
● Seizures, disorientation, confusion
Diagnostic Studies
First do (to dx and classify)…
● Peripheral blood evaluation
● Bone marrow exam
Other options include… (cells outside of blood and bone marrow)
● Lumbar puncture
● PET/CT scan
Interprofessional Care
GOAL: ATTAIN REMISSION
-how to attain it…
1. Combo drug therapy
2. Chemotherapy
Stages of chemo:
1. Induction
a. Goal: bring about a remission
b. Destroy all leukemia cells in 3 areas to restore hematopoiesis (blood
cell production)
i.
Tissues
ii.
Peripheral blood
iii.
Bone marrow
c. Normal findings: pt will become ill from..
i.
Neutropenia
ii.
Thrombocytopenia
iii.
Anemia
2. Consolidation (postinduction or post remission)
a. Start after induction
b. Time frame: months
c. Goal: eliminate remaining cells that may not be clinically or
pathologically evident
3. Maintenance
a. Goal: Keep body free of leukemia cells
Combo drug therapy
1. Corticosteroids
2. Radiation therapy
a. Total body radiation (TBI) prepares pt for bone marrow transplant
3. Immunotherapy and target therapy
a. Use for specific types
4. Hematopoietic stem cell transplant (bone marrow transplant)
a. GOAL: eliminate all leukemia cells using combo of chemo w/ or w/o
TBI
i.
End result: eliminates pt stem’s cells are replace w/ new
ones
b. Categories
i.
Allogeneic
1. Complications (cells did not originate from
themselves)
a. Graft v. host disease
b. Relapse of leukemia
c. Infection & sepsis
ii.
Syngeneic
iii.
Autologous
c. Source of cells
i.
Bone marrow
ii.
Peripheral blood
iii.
Umbilical cord blood
Nursing Management
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Ask for health hx
○ Questions to ask include:
■ Exposure to toxins
■ Chromosome abnormalities
■ Frequent infections
Perform routine assessments
Monitor lab results
○ Look at platelet count, Hgb, Hct, WBC
Monitor for chemo S/E
○ N/V, hair loss
Monitor for bleeding
Institute neutropenic precautions
○ Watch your diet
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Education
1.
4.
5.
Med management
a. Pt should recognize acute S/E of tx are temporary
b. Review long term A/E
i.
Fertility
Infection prevention
a. HANDWASHING!
Neutropenic precautions
a. Avoid uncooked food!!!!
i.
Fresh fruit, veggies, raw meat
Bleeding precautions
Anticipated course of illness (set realistic goals)
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Increase risk for infection
Risk of sepsis
Relapse
Tx related death
2.
3.
Complications
Additional Info
○ Limit your exposure to germs. ...
○ Pay attention to your skin. ...
○ Get enough rest. ...
○ Seek medical help immediately for a fever.
Address psych needs
○ Anxiety, fear, depression (common)
Classifications -based on WBC
● Acute lymphocytic leukemia (ALL)
○ Common in children
● Acute myelogenous leukemia (AML)
○ ⅓ of all leukemias
■ Most of which are adults
○ Onset: abrupt, dramatic
■ Manifestations: serious infections, abnormal bleeding
● Chronic myelogenous leukemia (CML)
○ Philadelphia chromosome***
■ Genetic marker
■ Seen in majority of cases
○ Onset: chronic, stable → acute, aggressive (blastic phase)
● Chronic lymphocytic leukemia (CLL)
○ Common in adults (old ppl)
Hodgkin Lymphoma
Background
Etiology
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Rapid increase of abnormal giant multinucleated cells- Reed-Sternberg cells***
Males 2x more likely to have it then females**
Most pt are cured
Cause: unknown
Factors that play a role in development:
● Infection w/ EBV virus
● Genetic predisposition
● Exposure to work toxins
● Presence of HIV infection*
Spreads by infiltrating other organs: 3 main organs
● Lung
● Spleen
● Liver
Additional Notes
Clinical
Manifestations
Stages
● Involves # of lymph nodes above or below diaphragm
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Other
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Onset: gradual
Initial sign: enlargement of cervical, auxiliary, or inguinal lymph nodes
(cause unknown)
○ Other location: mediastinal node mass
Nodes are movable and nontender
Not painful
○ Unless exert pressure on adjacent surrounding nerves
Asymptomatic pt
Flu-like sx
○ Weight loss
○ fatigue/ weak
○ fever/chills
○ Tachycardia
○ Night sweats
○ Generalized itchy w/o lesions
Sx if you have worse prognosis (B SYMPTOMS)**
● fever #> 100.4F
● Drenching night sweats
● Weight loss exceeding 10% in 6 months
Non-Hodgkin's Lymphoma
Background
Broad group of cancers consisting of…
● B cells
● T cells
● Natural killer cells
Affect all ages
Etiology
Cause: unknown
Factors that play a role:
● Chromosomal translocations
● Infections
● Environmental factors
● Weakened immune system
Clinical
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Present w/ widespread disease at time of dx
Manifestations
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Primary manifestation includes:
○ Painless lymph node enlargement (gets big or small over time)
Other sx
○ Hepatomegaly
○ Jaundice w/ liver involvement
Lymphoma
Background
Diagnostic studies
Originate in bone marrow and lymphatic structures
2 major types
● Hodgkin’s lymphoma
● Non-Hodgkin’s lymphoma (NHL)
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Management
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Complications
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Lab testing
○ Peripheral blood analysis
○ Expected findings:
■ Increased ESR
■ Hypercalcemia (bone involvement
■ Hypoalbuminemia (liver involvement)
Lymph node biopsy
○ Expected finding
■ Hodgkin lymphoma= Reed-Sternberg Cell
Bone marrow exam
Testing specific for NHL
○ MRI
■ To determine CNS involvement
○ Lumbar punctures
Tx
○ Chemo
○ Biotherapy
○ Radiation
○ Sometimes phototherapy and topical therapy
Nursing care focuses on managing
○ Problems related to disease
○ Pancytopenia
○ S/E of therapy
○ Psychosocial considerations
■ Physical & spiritual consequences
■ Fertility issues
■ Long term effects of therapy
Infection
Sepsis
Tx failure (relapse of disease)
Increased risk for secondary cancer later in life
Tx-related death
Multiple Myeloma
Background
Cancerous plasma cells proliferate in bone marrow —> destroy bone
Accounts for 18% of all hematologic cancers
● Occurs between ages of 65-74
Etiology
Cause: unknown
Factors that play a role:
● Exposure to organic chemicals (benzene)
● Herbicides
● Insecticides
● Viral infections (HIV) increase risk*
Involves excess production of plasma cells creating monoclonal antibodies
(monoclonal= one of a kind= ineffective)
● Infiltrates bone marrow
● Monoclonal proteins (M proteins)- consists of light and heavy chains
● Bence Jones- proteins that are the light chain part of monoclonal antibodies
○ Manifestation in urine
Clinical Manifestation
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Diagnostic Studies
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Treatment
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Onset: slow and subtle (gradual)
Main sx: skeletal pain
○ Location: pelvis, spine, ribs
Development of diffuse osteoporosis (M-protein begins to destroy bone)
including…
○ Osteolytic lesions occurring in skull, vertebrae, long bones, ribs
○ Vertebral compression→ vertebral collapse of vertebrae + spinal
cord compression
Calcium loss from bones causes hypercalcemia
○ Hypercalcemia sx include
■ Renal, GI, neuro problems
● Polyuria
● Anorexia
● Confusion
● Heart problems
Lab testing
○ Increased plasma cells in bone marrow
○ M-protein found in blood + urine
○ Pancytopenia (deficiency in WBC, RBC, platelets)
○ Hypercalcemia
○ Bence Jones protein in urine
○ High serum creatinine (measure of how well your kidneys are
performing their job of filtering waste from your blood)
Radiologic (show thinning of bones or fractures)
○ MRI
○ PET
○ CT scan
○ Skeletal bone survey
Corticosteroids
○ Prednisone
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Interprofessional +
Nurse Management
○ Methylprednisolone
Chemo
Immunotherapy
Target therapy
Bisphosphonates
○ For tx of osteoporosis that ends of developing
Bone marrow transplant
NO CURE!
Work on tx the sx → produce remission → prolong life
Goals:
1. Control pain
2. Prevent pathologic features
Major focus of nursing care= SAFETY
● Due to bone involvement and bone breakdown
● Considerations
○ Use caution when moving and ambulating pt
■ Potential to cause a fracture
Tx options
1. Immunotherapy and target therapy
2. Ambulation (helps bone reabsorb more calcium)
3. Hydration (tx of elevated calcium, prevent kidney failure)
a. Give IV fluids
i.
Goal: maintain urine output of 1.5-2L/day
4. Use of braces
a. To help with pain
5. Prompt assessment/ tx of infections
6. Psychosocial needs
If final and acute, pt is unresponsive to tx
● Initiate convo about palliative or hospice care
Complications
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Hypercalcemia
Dehydration
Fluid and electrolyte imbalance
Renal damage
Neurologic changes (peripheral neuropathy)
Patient education
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Focus on bleeding risk and infection risk
Prevention of fractures
When to call HCP
Thrombocytopenia
Background
Normal Hemostasis (stoppage of blood flow)
● Involves the vascular endothelium, platelets, and coagulation factors
● Function
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Etiology
○ Stop hemorrhage
○ Repair vascular injury
Abnormalities (disruption in components)
○ Bleeding
○ Thrombotic disorders
Reduction of platelets below 150,000/ul (150 x 10^9/L)
[NORMAL PLATELET COUNT : 150k to 450k/ul)
Low platelets result in…
● Abnormal hemostasis
○ Prolonged bleeding from minor trauma
○ spontaneous bleeding where there is no known cause
Cause: genetic or acquired
1. Inherited
2. acquired*
a. Due to ingestion of certain meds
b. Immune thrombocytopenia purpura (ITP)
i.
Most common
ii.
Abnormal platelet destruction
iii.
Manifestation
1. Acute in children
2. Chronic in adults
iv.
Onset from…
1. Viral infection
2. H. pylori
3. Autoimmune (lupus)
v.
Etiology
1. Shortened platelet survival
2. Antibodies mistake as foreign bodies causing them
to be killed off
c. Thrombotic thrombocytopenic purpura (TTP)
i.
Characteristics
1. MAHA (anemia)
2. Thrombocytopenia
3. Neurologic changes
4. Fever (absence of infection)
5. Renal problems
ii.
Uncommon
iii.
Enhanced aggregation of platelets that form into
microthrombi
iv.
Medical emergency!
1. Bleeding and clotting occur at same time
v.
Manifestations
1. Females
2. Healthy adults
vi.
Onset from…
1. Autoimmune
2. Ingestion of certain meds
3. Pregnancy
4. Preeclampsia
5. infection
d. Heparin-induced thrombocytopenia (HIT)
i.
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iv.
Clinical Manifestations
Diagnostic studies
Assoc. w/ use of heparin
Life threatening!
Onset
1. 5-14 days after heparin therapy
Characteristics
1. Platelet count < 250k
2. Platelet destruction
3. Vascular endothelial injury
4. VTE*** (DVT)
Symptomatic
● Common sx: bleeding (mucosal or cutaneous)
○ Results in…
■ Petechiae
● Flat, small, red brown microhemorrhages that
develop in the skin
■ Purpura
● Many petechiae
● Pain and tenderness present
■ Bruising (ecchymosis)
● Due to hemorrhage
Major complication: hemorrhage
● Onset
○ Acute (drastic)
○ Subtle (less noticeable)
■ First detection the anemia from blood loss
○ Internal
■ Manifestations
● Weakness
● Dizzy
● Tachycardia
● Hypotension
● Abdominal pain
■ Prolonged bleeding after routine procedures
○ External
● Areas affected
○ Joints
○ Retina
○ Brain
● Monitor for
○ Epistaxis (nose bleeds)
○ Gingival bleeding
○ Joint bleeding
○ Brain bleeding
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Decreased platelet count on CBC <150,000/ul
○ Prolonged bleeding count <50,000/ul
○ Spontaneous hemorrhage count <20,000/ul
Hx and assessment*
Lab testing (PT, APTT)
○ Findings: normal
Interprofessional care
Nursing Management
Tx based on cause
1. ITP
a. Corticosteroids
b. Immunoglobulins
c. Monoclonal antibodies
d. Removal of spleen (splenectomy)
2. TTP
a. Corticosteroids
b. Immunosupressive therapy
c. Plasmapheresis
3. HIT
a. STOP HEPARIN (including fushing)
b. Maintain anticoagulation w/ other meds (ex: warfarin)
i.
Only start warfarin if platelet count 150,000/ul
c. Plasmapheresis- if severe clotting
d. Considerations
i.
Never give heparin again (lovenox)
Avoid aspirin or other drugs that affect platelet fx or production
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Discourage use of OTC meds
○ Especially those caused acquired thrombo and reduced platelet fx
(ASPIRIN)
○ Have pt check with HCP
● Have pt know when to seek care if they notice S/S assoc. w/ bleeding
○ If they see prolonged nosebleeds, petechiae
● Observe early sx if pt receives chemo
○ Thrombo. Known S/E of chemo
In acute care settings..
1. Assess for bleeding***
a. Any bleeding needs eval and tx
GOAL: PREVENT OR CONTROL HEMORRHAGE
2. Admin platelets per orders
3. Monitor labs
a. Platelet count
b. Coagulation studies
c. Hbg, Hct
4. Use small gauge needles if need to do SUBQ injections
a. Apply direct pressure for at least 5-10 min after injection
b. Can use ice pack
5. AVOID IM!
6. Teach importance of following self-care measures to reduce risk of bleeding
Anaphylaxis
Background
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Hypersensitivity reactions
○ Immune response is overreactive against foreign antigens or reacts
against its own tissue→ tissue damage
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Classifications based on
■ Source
■ Time sequence (immediate or delayed response)
■ Immunological mechanisms causing injury
○ Types
■ IgE-mediated-TYPE 1
■ Cytotoxic- TYPE 2
■ Immune complex- TYPE 3
■ Delayed hypersensitivity-TYPE 4
○ TYPES 1-3
■ Immediate
■ Examples of humoral immunity
○ TYPE 4
■ Delayed
■ Related to cell-mediated immunity
Type 1 hypersensitivity reaction
● acute , potentially life threatening
● Occur only in ppl who are highly sensitized to specific allergens
○ Sx include
■ Smooth muscle contraction
■ Increased vascular permeability
■ Vasodilation
■ Hypotension
■ Increased secretion of mucus
■ Itching
Genetic predisposition o the development of allergic diseases
Etiology
Common allergic rxns are:
● Food
○ Milk
○ Peanuts
○ Tree nuts
○ Fish
○ Chocolate
○ Strawberries
● Insect stings
● Latex
● Meds (common penicillin)****
Clinical Manifestations
When localized…
● Cutaneous wheal and flare rxn
● Occurs in min or hrs
● Usually not dangerous
When systemic…
● Occurs within min
● Life threatening
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Diagnostic studies
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Interprofessional Care
○ Due to bronchial constriction
○ Airway obstruction
○ Vascular collapse
Dyspnea
Bronchial edema and angioedema
○ Swelling in the deeper layers of skin
■ Often around face and lips
Progression to shock
○ Rapid or weak pulse
○ Hypotension
○ Dilated pupils
○ Cyanosis
○ LOC or death ← if not tx
Lab testing
○ CBC w/ differential
■ Elevated eosinophils
○ IgE level
■ High antibodies
Skin allergy testing
○ Allergen applied to skin prick or scratch or injected into skin (ID)
○ Causes wheal and flare responses if positive allergy
Blood allergy testing
○ RAST testing
■ Use for pt that present with allergies to medications,
foods, etc
Emergency tx ALWAYS starts w/ ABC
● Ensure and establish a patent airway **
● Assess respirations
● Establish IV access for emergency fluids/med
○ to tx hypotension
Expected meds
● Drug of choice: epinephrine**
○ Given parenterally
■ IM
● Pt over 60 kgs: give 0.3-0.5 mg
○ Give in mid-outer thigh
○ Repeat every 5-15 min
■ IV
Make sure to know what meds pt is on (beta blockers= metoprolol)
■ Resistance to tx w/ epi
Give high flow oxygen
○ Usually 8-10L/min via face mask
■ Give up to 100%, if needed
Nebulized albuterol tx
○ For bronchospasms resistant to epi
IV benadryl or diphenhydramine
○ For itching or urticaria (hives)
Corticosteroids
○ Given IV
○ Common med: methylprednisolone
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Nurse management
Teaching
1.
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4.
Recognize S/S of anaphylactic rxn
Maintain a pt airway
Admin meds (ex: epi)
a. When recommended or ordered
Recognize and tx shock w/ oxygen, fluids, necessary meds
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Have pt try to identify what the allergen is and cause for the response
Referral to specialist
Teach to min exposure to allergen
Teach epi self-injection then call 911
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Pathogen or microorganism which causes disease, invades the body,
multiplies and causes disease, usually causing harm to the host
○ S/S results from the activity of the pathogen which triggers
inflammation and other immune responses
Pathogen
○ Agents that cause disease
■ Includes bacteria, fungi, virus, protozoa, prions
Normal flora protect the body by preventing overgrowth of other
microorganisms
○ Under certain conditions and circumstances, imbalance occurs and
results in disease
Categories
○ Localized
○ Disseminated
○ Systemic
Infection
Background
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Types
1.
2.
Emerging and reemerging
a. Bacterial: H. pylori
b. Viral: COVID, flu
c. Parasitic: cryptosporidium parvum
Antimicrobial-resistant infection
a. All pathogenic organisms are highly adaptable
3.
Antimicrobial resistant
infection
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HAI
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b. Change and become resistant to tx
c. Think MRSA and VRE
Health care-associated infections (HAIs)
a. CAUTI
b. CLABSI
c. C. Diff
d. MRSA
e. Pneumonia
Rates have increased
○ HCPs have contributed:
■ Treat viral infections with antibiotics
■ Succumb to patient pressure for medications
■ Use inadequate drug regimens to treat infections
■ Use broad-spectrum or combination agents when first-line
agents could be effective
Patients have contributed:
○ Skip doses of antibiotics
○ Stop antibiotics before the full course has been taken
○ Save and use antibiotics for “later”
Also consider: Limited resources and access to care can result in inadequate
treatment of infections
Prevention
○ Standard precautions
○ Transmission-based
■ Airborne
■ Droplet
■ Contact
Sepsis
Etiology
Clinical Manifestation
Diagnostic studies
Localized infections which lead to bacteria entering the bloodstream
Systemic inflammatory response to documented or suspected infection
Progresses to organ dysfunction
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Presence of infection AND:
Altered mental status (AMS)
Fever and chills
Tachycardia
Hypotension (especially SBP <100)
Core body temp less than 97 (Hypothermia)
Extreme/unexplained pain
Tachypnea
Hyperglycemia in absence of diabetes
Potential significant edema, positive fluid balance (20mL/kg) in 24 hours
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Lab testing
○ Serum and blood sepsis findings
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■ WBC may be decreased (<4k) or increased (>12k)
■ Lactic acid increased
■ Procalcitonin increased
■ C-reactive protein increased
■ Cultures positive (blood and other samples)
○ Progression to septic shock may have indications of:
■ Decreased platelets
■ Increased PT/INR
■ Increased PTT
MEWS score (modified early warning Signs/sepsis recognition)
○ The higher the #, the worse the pt outcome is
Interdisciplinary care
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Treatment of source of infection
If bacterial, antibiotic management
Oxygen management – Sepsis (and septic shock) may indicate the presence
of inadequate tissue perfusion resulting in hypoxia
Nursing management
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Ongoing assessment of VS
Assessment of early recognition of shock manifestations
Fluid management
Skincare
Monitoring I/O, especially urine output
May be transferred to ICU for invasive cardiac monitoring