CHAPTER 43: NURSING CARE OF A

FAMILY WHEN A CHILD HAS AN

Infectious Disease in Children
INFECTIOUS DISORDER
The Infectious Process #1  Infectious diseases remain a leading
cause of morbidity in children.
Stages of Infectious disease:  Almost all childhood infectious
diseases include a fever or rash;
a. Incubation period
nursing care must address
b. Prodromal period
identification and relief of these
c. Convalescent period
symptoms.
The Infectious Process #2
ASSESSING VIRAL INFECTIONS #1
Viral exanthems (rashes)
o Xanthem subitum (roseola
infantum)
o Rubella (German measles)
o Measles (rubeola)
o Chickenpox (varicella)

XANTHEM SUBITUM (ROSEOLA

INFANTUM)

 Causative agent: human

herpesvirus 6 (HHV-6)
The Infectious Process #3
 Incubation period: approximately
CHAIN OF INFECTION:
10 days
 Reservoir
 Period of communicability: during
 Portal of exit
febrile period
 Means of transmission
 Portal of entry  Mode of transmission: unknown
 Susceptible host
 Occurs in children between 6
The Infectious Process #4 months to 3 years.
METHODS BY WHICH INFECTIONS (spring and fall; anytime of the year)
SPREAD
 Immunity: contracting the disease
Portal of Means of Portal of Prevention offers lasting natural immunity; no
Exit Transmissi Entry Measures artificial immunity is available.
on
Blood -Anthropod Injection -Decreasing ASSESSMENT:
exposure to
vectors into the vectors.
-Blood the -Careful
 The first symptom is a high fever
sampling bloodstrea handling of (104 to 105 degree fahrenheit) or
blood sampling
- m equipment.
40.0 to 40.6 degree celcius)
Transfusion -Prescreening of
blood for  Irritable and anorexic
organisms such
as HIV or Hepa  Pharynx may be slightly inflamed
B
Respirato -Airborne Respirtaor -Wearing a
mask  Enlarged lymphnodes (occipital,
ry droplets y tract -Droplet and cervical, and postauricular)
secretion -Fomites airborne
s precautions
-Handwashing  Decreased WBC
Feces -Water, Gastrointe -Handwashig
food stinal tract
before eating,  Rash appears (rosepink macules,
after using
-Fomites bathroom or approximately 2 to 3 mm in size)
-Vectors after handling
diapers.  The rash lasts 1 to 2 days
such as
flies  Apperance of a rash immediately
Exudate -Direct Skin, -Contact
precautions after decline in fever (Hallmark
from contact mucous -Self screening symptom)
lesions -Contact membrane for sexual
with soiled s contacts
-Gloves
ressings
  Occurs usually during winter or
early spring
INTERVENTIONS:
 Predisposing factor:
 Measures to reduce the discomfort underimmunized immigrant
of the rash populations and underimmunized
college-age populations.
 Acetaminophen (tylenol) or
ibuprofen (motrin) Signs and Symptoms:

Complication: febrile seizure, standard 1. High fever (39.5-40 degree celsius)

infection precautions 2. Enlarged lymphnodes
3. Malaise
RUBELLA (GERMAN MEASLES) 4. Coryza (rhinitis, sore throat)
 Also known as 3-day measles 5. Conjunctivitis
6. Photophobia
 Causative agent: rubella virus
7. Cough
 Incubation period: 14-21 days
8. KOPLIK SPOT on bucal membrane
 Period of communicability: 7 days 9. Deep red maculopapular rash
before onset of rashes and 5 days 10. After 5-6 days rash fades and leaves
after fin desquamation on the skin.
 MOT: droplets – direct or indirect
contact Therapeutic Management:
 Most common during spring; school
1. Comfort measure for rash
age and adolescent
2. Antipyretic
 Immunity: natural 3. Apply lubricant or emollient to
 Active artificial immunity: MMR prevent excoriated area for constant
vaccine nasal discharge.
 Passive artificial immunity: 4. Cough suppressant
immune serum globulin (pregnant
woman)
MEASLES VS RUBELLA
Signs and Symptoms:
Measles or rubeola – is a viral infection of
 Prodromal period (1-5 days) the respiratory system. Measles is a very
1. Low grade fever contagious disease that can spread through
2. Headache contact with infected mucus an saliva.
3. Malaise
4. Anorexia Rubella – is a contagious disease that
5. Mild conjunctivitis mostly affects children. It causes symptoms
6. Sore throat like a rash, fever, and eye redness. It’s
7. Mild cough usually mild in kids, but it can be more
8. Coryza serious in pregnant woman.
9. Swollen lymph CHICKEN POX (VARICELLA)
10. Congestion
 After prodromal period  Causative agent: varicella zoster
1. Pink red maculopapular rash virus
 Incubation period: 10-21 days
Therapeutic Management:
 Period of communicability: 1 days
1. Comfort measures for the rash before onset of rash to 5-6 days
2. Antipyretic (acetaminophen after its appearance when all vesicle
(Tylenol); Ibuprofren (Motrin) have crusted.
 MOT: direct or indirect contact of
MEASLES (RUBEOLA; 7 DAY MEASLES) saliva and open vesicles.
 Causative agent: measles virus Signs and Symptoms:
 Incubation period: 10-12 days
 Period of communicability: 5th 1. Low grade fever
days of incubation through the 2. Malaise
first few days of rash. 3. Vesicular rashes
 MOT: direct or indirect contact Therapeutic Management:
with droplets
 Immunity: contracting the 1. Advise not to scratch or remove
disease scabs
 Active artificial immunity: 2. Antihistamine
immune serum globulin
Complications: secondary infections of the  Red and appears first on the face;
lesions, pneumonia, encephalitis. maculopapular and coalesce lesions
on the cheeks “slapped face”
ASSESSING VIRAL INFECTIONS #2
appearance
Viral exanthems (rashes) – cont.  Rash appears on the extensor
surfaces of the extremities, flexor
o Herpes zoster surfaces and the trunk
o Smallpox (variola)  Rashes fade from the center
o Erythema infectiosum (fifth disease) outward, giving the lesions a
o Nonpolio enteroviruses lacelike appearance.
HERPES ZOSTER  It may reappear if precipitated by
skin irritation such as trauma,
 It is caused by varicella – zoster sunlight, hot or cold.
virus  Persistent arthritis
 Signs and symptoms: pruritis,
Therapeutic Management:
vesicular lesions, pain
 Treatment: analgesia 1. Antipyretics and analgesics
 Provide measures to reduce pruritis 2. Comfort measures for the rash
 Administer acyclovir (inhibits viral 3. Avoid contact with pregnant women
DNA synthesis) as prescribed 4. Use droplet precautions in a
 Varicella-zoster immune globulin hospital.
(VZIG) (minimizes symptoms) 5. Children can return to school as
soon as the rash appears because
SMALL POX (VARIOLA) they are no longer infectious after
 Causative agent: smallpox virus this point.
 Incubation period: 7-17 days POLIOMYELITIS (INFANTILE
 Period of communicability: onset PARALYSIS)
of rash until crusts hae been shed.
 Signs and Symptoms:  Causative agent: poliovirus
1. Prodromal (3-4 days) fever,  Incubation period: 7-14 days
chills, headache, vomiting  Period of communicability:
2. Rash, high grade fever, pustular greatest shortly before and after
lesions (crusting at 13-14th day onset of symptoms (1-6 weeks)
period)  MOT: direct and indirect contact
 Therapeutic Management:
1. Vaccinia immune globulin (VIG)
to reduce disease process. Signs and Symptoms:
2. Administer antibiotic as
1. Fever
prescribed.
2. Headache
3. Oxygen
3. Nausea
ERYTHEMA INFECTIOSUM (FIFTH 4. Vomiting
DISEASE) 5. Abdominal pain
6. Mild stiffness of the neck, back and
 Causative agent: parvovirus B19 legs
 Incubation period: 6 to 14 days 7. Intense pain, tremors, paralysis
 Period of Communicability: 8. Diificulty swallowing (laryngeal
uncertain paralysis)
 Mode of Transmission: droplet 9. Respiratory paralysis
 Immunity: none
Therapeutic Management:
1. Bedrest
ASSESMENT: 2. Analgesia
3. Moist hot packs to relieve pain
 Occurs most often in children 2 to 12
4. Long term ventilation is involvement
years of age.
of respiratory muscles
 First phase
a. Fever For survivors: may develop progressive
b. Headache muscle atrophy (postpoliomyelitis
c. Malaise muscular atrophy syndrome or severe
d. Rash arthritis (late adulthood)
WEST NILE VIRUS DISEASE
  MOT: contaminated blood products; 3. Droplet precautions, standard
bite of a mosquito precautions
 Assessment:
INFECTIOUS MONONUCLEOSIS
a. Asymptomatic
b. Fluidlike symptoms (fever,  An acute infectious disease of the
fatigue, and malaise) lymphatic system
c. Encephalitis (mental confusion,  Causative agent: Epstein-Barr virus
lethargy, photophobia,  Incubation period: probably 2-8
headache, muscle weakness, weeks; unknown
and coma)  Period of communicability:
 West Nile Virus disease is unknown; probably only during acute
diagnosed when antibodies to the illness.
virus are recovered from blood  MOT: direct or indirect contact
serum. (saliva and intimate physical contact
HEALTH PROMOTION AND RISK like kissing and sharing of utensils)
MANAGEMENT #1  Immunity: one episode apparently
gives lasting immunity. NO
PATIENT EDUCATION VACCINATION IS AVAILABLE.
o Educate children and families to ASSESSMENT:
maintain in general good health.
o Educate families as to the  Sorethroat (initial)
importance of keeping up to date on  Chills
immunizations.  Fever
 Headache
PREVENTION  Anorexia
o Health care-associated infections  Malaise
and infection control.  Enlarged lymphnodes; tender to
touch (cervical most markedly
NURSING PROCESS: INFECTIOUS affected)
DISORDER  Enlarged, reddened tonsils
o Assesment  Petchiae on palate
o Nursing diagnosis Nursing diagnosis: Pain
o Outcome identification and planning
o Implementation INTERVENTIONS:
o Outcome evaluation 1. Bedrest (acute stage)
MUMPS (EPIDEMIC PAROTITIS) 2. Avoid lifting, strenuous exercise and
contact sports (until recovery; may
 Causative agent: mumps virus experience weakness and fatigue for
 Incubation period: 14-21 days up to 2-3 months)
 Period of communicability: shortly 3. Observe for LUQ abdominal pain
before and after onset of parotitis which radiates to the left scapula
 NOT: direct or indirect contact (splenic rupture). Be careful in
turning the child to avoid pressure
Signs and Symptoms: on the splenic area)
4. Maintain fluid intake (cool non-acidic
1. Fever
fluids)
2. Anorexia
5. Expression of feelings and offer
3. Headache
support.
4. Malaise
5. Pain chewing and ear ache (within ASSESSING BACTERIAL INFECTIONS #1
24 hours)
6. Swollen parotid glands Streptococcal diseases:
7. Complications: o Scarlet fever
meningoencephalitis, severe hearing
o Impetigo
impairment, orchitis, complete
o Cat-scratch disease
subfertility.
SCARLET FEVER
Therapeutic Management:
1. Soft, bland or liquid foods  Causative agent: Beta-hemolytic
2. Administer analgesic and antipyretic streptococci, group A
 Incubation period: 2 to 5 days
  Period of communicability:  Papulovesicular lesion
greatest during acute phase of surrounded by localized
respiratory illness; 1 to 7 days erythema (Honey-colored crust)
 Mode of transmission: direct  Local swollen lymph nodes
contact and large droplets
INTERVENTIONS:
 Immunity: one episode of disease
gives lasting immunity to scarlet  Penicillin or Erythromycin (oral)
fever toxin. No vaccinationis  Mupirocin (Bactroban) ointment for
available. 7-10 days
ASSESSMENT:  Wash the crust with soap and water
adily
 Streptococcal pharyngitis: fever,  Observe contact precautions until 24
sore throat, headache, chills, and hours after initiation of antibiotic
malaise  Complications: rheumatic fever,
 Rash appears 12 to 48 hours after AGN
the onset of the pharyngeal
symptoms. DIPTHERIA
 Increased PR.  Causative agent: Corynebacterium
(cont.) diptheriae
 Incubation period: 2-6 days
 The rash of scarlet fever is both  Period of Communicability: rarely
enanthematous and exanthematous more than 2 weeks to 4 weeks in
(on both mucuous membrane and untreated person; 1-2 days in
skin) children treated with antibiotcs
 Inflamed and enlarged tonsils with  MOT: Direct or indirect contact with
white exudate respiratory secretions
 Beefy red color uvula and pharynx  Immunity: contracting the disease
 The palate is isually covered with often lasting natural immunity
erythematous punctiform (pinpoint)
lesions (petechiae) ASSESSMENT:
 Tongue is “white strawberry a. Headache, chill, fever
appearance.” b. Purulent nasal discharge
 “Strawberry tongue” is distinctive c. Brassy cough
for scarlet fever d. Difficulty swallowing
 Hyperpigmentation in skin folds at e. Muscle weakness
the joints (Pastia’s sign) f. Pseudomembrane (grayish
membrane on the throat)
Therapeutic Management:
g. Neuritis with paralysis of the
 Soft liquid diet diaphragm and pharyngeal and
 Analgesic an antipyretic, such as laryngeal muscles.
acetaminophen (Tylenol) or h. May lead to myocarditis with heart
children’s ibuprofen (Motrin) failure and conduction disturbances
 Comfort measures for the rashes INTERVENTIONS:
 Administer penicillin as prescribed
 Droplet precautions until 24 hours a. Bedrest
after therapy is started, in addition to b. Administration of antitoxin
standard infection precautions. c. Penicillin or Erythromycin (IV)
d. Direct precautions until cultures are
IMPETIGO negative
e. Diagnostic test: throat culture
 Causative agent: B-Hemolytic
streptococcus group A; Aureus; WHOOPING COUGH (PERTUSSIS)
MRSA
 Incubation period: 2-5 days  Causative agent: Bordetella
 Period of communicability: from pertussis
outlet of lesions until lesions are  Incubation period: 5-21 days
healed  MOT: Direct and indirect contact
 MOT: direct contact with lesions  Period of Communicability:
 Immunity: none greatest catarrhal stage (respiratory
illness)
ASSESSMENT:  Immunity: contracting the disease
often lasting natural immunity
  Droplet precaution until 5 days e. Sardonic smile (sardonic grin) sign
after a child starts antibiotic therapy.
Interventions:
ASSESMENT:
a. Provide quiet stimulation-free room
1. Catarrhal stage: (1-2 weeks) b. Total parenteral nutrition
 Upper respiratory symptoms c. Provide muscle relaxant as ordered
a. Coryza d. Debridement of the wound
b. Sneezing e. Tetanus immune globulin
c. Lacrimation administration
d. Cough f. Penicillin G or erythromycin (IV)
e. Low grade fever g. Intubation and mechanical
ventilation to maintain respiratory
ASSESSMENT: function.
2. Paroxysmal stage: (4-6 weeks) Types of Tetanus: Trismus, Generalized
a. 5-10 short, rapid coughs followed tetanus, and Sardonic smile of tetanus
by rapid inspiration. (risus sardonicus)
b. “whoop” or high pitched crowing
sound of whooping cough OTHER INFECTIOUS DISEASES #1
c. May look cyanotic or red faced
Rickettsia diseases
d. Thick, tenacious mucus
e. Vomit after coughing  Rocky mountain spotted fever
3. Convalescent stage: (gradual
cessation of the coughing and ROCKY MOUNTAIN SPOTTED FEVER
vomiting)  Causative agent: rickettsia
INTERVENTIONS: rickettsia
 Incubation period: 3 to 12 days
1. Maintain bedrest  Period of communicability: not
2. Keep children secluded from communicable from one person to
environmental factors (e.g. dust, another
cigarette smoke, strenous activities)  MOT: Wood, dog, or rabbit tick
3. Small frequent feedings
 Active artificial immunity: rocky
4. Administer Azithromycin or
mountain spotted fever vaccine
Erythromycin as prescribed.
Assessment:
Complications:
 Occurs most often during the spring
1. Alkalosis
and early summer
2. Ehydration
 A reddened area evelops at the site
3. Pneumonia
of the tick bite.
4. Atelactasis or emphysema (due to
plugged bronchioles)  Rash (reddened macule change to
5. Epistaxis, subconjunctival and petechiae), persistent headache,
subarachnoid bleeding, or seizures fever (as high as 104 F or 40 C) and
(due to asphyxia) mental confusion begin.
 CNS involvement (stiff neck and
TETANUS (LOCKJAW) seizures) and cardiac and
pulmonary symptoms such as heart
 Causative agent: clostridium
failure and pneumonia.
tetani
 Nitrogen loss in the urine becomes
 Incubation period: 3 days – 3
extreme. With hyponatremia
weeks
 MOT: direct or indirect Management: Tetracycline or Erythromycin
contamintion of closed wound for 7 to 10 days
 Portal of entry: open wound,
burn site
Assessment:
a. Stiffness of the neck and jaw
b. Muscle rigidity of the trunk and
extremities
c. Opisthotonus (arching of the back)
d. Stiffness of the abdominal muscles
(board like)
 and respiratory tract, and works apparently
by preventing adherence of pathogens to
mucosal cells.
IgD – found in plasma. It may be the
receptor that binds antigens to lymphocyte
surfaces but its true function is unclear.
CHAPTER 42: NURSING CARE OF A
FAMILY WHEN A CHILD HAS AN IgE – involved in immediate hypersensivity
IMMUNE DISORDER reactions. It exists bound to mast cells on
tissue surfaces. When contacted by an
IMMUNE SYSTEM antigen cellular granules are released. It is
1. First barrier associated with allergy and parasitic
2. Phagocytosis infections.
 Macrophages ALLERGY
 Inflammatory response
 Antibody-antigen reaction  Allergic deceases results from
typical types of abnormal antigen-
Immune response antibody responses which may have
Body’s action to fight invading organisms or minor and chronic or acute and
substances by leukocyte and antibody severe symptoms.
activity.  Allergic disorders occurs when the
involved organism is an allergen
THE IMMUNE SYSTEM #1 rather than a simple immunogen.
Immune response
ALLERGY #1
 Antigen: any foreign substance
capable of stimulating an immune Hypersensitivity:
response.  Type 1: Anaphylaxis
 Immunity: did you get to destroy  Type 2: Cytotoxic response
like antigens  Type 3: Immune complex
 Immunogen: an antigen that is  Type 4: Cell-mediated
capable of inducing an immune hypersensitivity
nurse
 Allergen: substance that causes an CLASSIFICATIONS OF
allergic reaction HYPERSENSITIVITY REACTIONS:

THE IMMUNE SYSTEM #3 Type 1 allergic response: Anaphylaxis

Locations and Functions of  Involved cell: IgE which attached to

IMMUNOGLOBULINS mast cell surface and trigers release
of intracellular granules from mast
IgM – effective in agglutinating antigen as cells on contact with antigens.
well as lysing cell wall; discovered early in  Effect: allergies, asthma, atopic,
the course of an infection in the dermatitis, anaphylaxis
bloodstream as it is the first response to
pathogenic antigens. Type 2: Cytotoxic response

IgG – most frequently occuring antibody in  Involved cell: IgG or IgM where the
plasma during secondary response, it is the antigen-antibody reaction leading to
major immunoglobulin to be synthesized. It antigen destruction; complement is
freely diffuses into extravascular spaces to activated.
contact antigens. In prenatal life, it diffuses  Effect: Hemolytic anemia,
across the placenta to supply passive transfusion reaction erythroblastosis
inmune protection to the fetus until the fetalis.
infant can effectively produce
Type 3: Immune complex
immunoglobulins. It has the major
responsibility for neutralizing bacterial toxins  Immune complex disease
and in activating phagocytosis (destruction  Involved cell: IgG or IgE
of bacteria).  Antigen-antibody complexes
precipitate, complement is activated,
IgA – found in external body secretions
resulting to inflammatory response
such as saliva, sweat. Tears. Mucus, bile,
 Effects: Rheumatoid arthritis
and colostrum. It provides defense against
 SLE
pathogens on exposed mucosal surfaces,
especially those of the gastrointestinal tract Type 4: Cell-mediated hypersensitive
  Delayed hypersensitivity response  Urticaria
 Involves cell: T lymphocyte  Angioedema
 T cells combine with antigen to  Allergic contact dermatitis,
induce inflammatory reactions by pruritis, and purpura
direct cell involvement or the release  Wheezing or rhinitis
of lymphokines (ex Mantoux test or  Thrombocytopenia and
PPD) hemolytic anemia
 Effect: contact dermatitis, transplant  Anaphylactic shock and
graft reaction serum sickness
ASSESSMENT: MANAGEMENT:
a.
Reddened; watery eyes  Wear a medical identification
b.
Allergic “shiners” bracelet
c.
Sneezing, clear nasal discharge  Discontinue the drug
d.
Rapid heart rate  Antihistamine (such as
e.
Dyspnea (anaphylaxis) diphenhydramine hydrochloride
f.
Papular, vesicular lesions (atopic [Benadryl])
dermatitis)
FOOD ALLERGIES
g. Urticaria and angioedema
h. Joint pain ASSESSMENT:
i. Itching, reddened areas (contact
dermatitis) o Urticaria
j. Diagnostic tests: o Angioedema
 Radioallergosorbent (RAST) o Pruritis
 IgE serum antibodies o Stomach pain
 Eosinophil count (total count of o Colic, cramps, diarrhea
250 or more cells/mm3 o Respiratory symptoms
 Skin testing o Atopic dermatitis
THERAPEUTIC MANAGEMENT: STINGING INSECT HYPERSENSITIVITY
Goal of therapy:  Severe hypersensitivity reactions to
stings from bees, wasps, hornets, or
1. Reduce the child’s exposure to
yellow jackets.
allergen
 Serum sickness reaction (immediate
2. Hyposensitive the child to produce a
type 1 hypersensitivity reaction)
state of increased clinical tolerance
to the allergen ASSESSMENT:
3. Modify the child’s response to the
allergen with a pharmacologic agent a. Local edema at the site
4. Pharmacologic therapy: intranasal b. Generalized urticaria, pruritis,
cromolyn sodium prophylactically and edema
(reduce symptoms) c. Wheezing and dyspnea
 Ceterizine (Zyttec); Loratidine d. Shock and death
(Claritin) MANAGEMENT:
5. Antihistamines (question the use
for G6PD, can cause severe  Administer epinephrine (SC)
hemolysis)  Teach parents learn to administer;
6. Decongestants (e.g Sudafed – school nurse
pseudophedrine)  Antihistamine medication
7. Sublingual immunotherapy (SLIT)  Ice applied to the site minimizes the
amount of venom absorbed.
ALLERGY #3  Teach children who are allergic to
 Drug and Food allergies stinging insects not to use scented
o Drug allergies preparations because these attract
bees and wasps.
o Food allergies
 Avoid barefoot when going outside
o Milk hypersensitivity
o Peanut hypersensitivity COMMON IMMUNE REACTIONS:
 Stinging insect hypersensitivity
 Anaphylactic shock
 Contact dermatitis
 Urticaria and angioedema
 Serum sickness
ASSESSMENT:
ANAPHYLACTIC SHOCK
  Immediate, life-threatening type 1 Causes: drugs, infectious agents, vaccine
hypersensitivity reaction which or blood products
results from exposure to an allergen
Symptoms begin: 7-12 days after serum
in a previously sensitized child
injection

THERAPEUTIC MANAGEMENT
Signs and Symptoms:
 Symptomatic treatment
 Nausea and vomiting  NSAID (e.g ibuprofen (motrin)
 Diarrhea  Corticosteroid
 Urticaria
ATOPIC DISORDERS:
 Angioedema
 Bronchospasm (dyspnea,  Allergic rhinitis
hypoxemia, hypoxic)  Atopic dermatitis (infantile eczema)
 Hypotension and bradycardia  Atopic dermatitis in older children
 Lead to seizure, then death
ALLERGIC RHINITIS
THERAPEUTIC MANAGEMENT:
 It is caused by a type 1 or immediate
1. Determine if the child has previous hypersensitivity immune response.
reaction to a drug before  It occurs in 10% to 40% of child.
administering
2. Advise to undergo hyposensitization ASSESSMENT:
therapy (for children who have  Sneezing
hypersensitivity reactions to insect  Nasal engorgement
stings)
 Profuse watery nasal discharge
3. Drug of choice for treatment of
 Pale mucous membrane of the nose
anaphylaxis: Epinephrine
4. Apply ice to the injection or sting site  Edematous and with nasal
to slow absorption (in place or congestion
tourniquet) Have a EPINEN – a  Watery eyes
device that injects epinephrine.  Pruritic (conjunctiva), pebbly
5. Administer antihistamine as appearance
prescribed.  Allergic salute, allergic crease,
allergic shiners
URTICARIA AND ANGIOEDEMA  Full frontal headache
Urticaria: flat wheals, erythema, pruritic,  Lethargic
elevation of lesions.  Recurrent otitis media may occur
because of the swollen pharyngeal
Angioedema: edema of skin and tissue
subcutaneous tissue on the eyelids, hands,  Increased eosinophil count
feet, genitalia, and lips. It is not dependent
and asymmetrically distributed. THERAPEUTIC MANAGEMENT:

 Laryngeal edema that leads to  Avoid allergens

airway obstruction and asphyxiation,  Use of pharmacologic agents
then death. (antihistamines, leukotriene
inhibitors or corticosteroids)
Common causes: drugs, foods, insect
 Immunotherapy
stings, hypersensitivity to hot or cold.
 Parents usually ask how sick
THERAPEUTIC MANAGEMENT: children should be before they need
epinephrine injection, oral antihistamine, to.
corticosteroid (cyclosporine and
ATOPIC DERMATITIS (INFANTILE
omalizumab (Xolair)
ECZEMA)
SERUM SICKNESS
 A disease which may be related to
 An inflammatory reaction that food allergy
occurs to blood vessel walls and  SYMPTOMS:
surrounding tissues a. Pruritis (sweating, heat, tight
clothing, and contact irritants
Signs and symptoms: fever, malaise, such as soap)
lymphadenopathy, arthralgia, urticarial,
arthritis
 b. Popular and vesicular skin Nursing Diagnoses associated with
eruptions with surrounding allergic responses:
erythema.
 Situational low self-esteem
c. Linear excoriations
 Ineffective breathing patterns
d. Skin is depigmented and
 Anxiety
lichenified (shiny), and dry, flaky
 Powerlessness
scales
 Risk for delayed growth and
e. Swollen local lymph nodes
development
f. Low grade fever
 Risk for infection
g. Increased eosinophil count
h. The common sites for lesions THERAPEUTIC TECHNIQUES: ALLERGIC
includes scalp, and forehead, the RHINITIS AND PERENNIAL ALLERGIC
cheeks, neck, behind the ears, RHINITIS
and the soles of the feet.
i. Fussy and irritable  Avoidance of offending allergens
 Pharmacologic agents
THERAPEUTIC MANAGEMENT: (Antihistamines, Leukotriene
inhibitors, Corticosteroids)
o Reduce exposure to allergen
 Immunotherapy
(milk, eggs, wheat, chocolate, fish.
 Environmental control
Tomatoes, and peanuts)
o Reducing incidence of pruritis THERAPEUTIC TECHNIQUES: DRUG
a. Hydrating the skin by bathing or AND FOODS ALLERGIES
applying wet dressings (wet with
tap water or Burow’s solution)  Avoidance of allergen
for 15 to 20 minutes  Patient education
b. Apply hydrating emollient 1. Alert bracelets
(petroleum jelly, Vaseline) or 2. Diet choices and food shopping
even vegetable shortening  Peanut allergy
(Crisco) 1. Desensitization
c. Do not allow infants to become 2. Anaphylaxis treatment
chilled if a large portion of the THERAPEUTIC TECHNIQUES: STINGING
body is to be covered with wet INSECT HYPERSENSITIVITY
dressings.
d. A stockinette dressing with  Hyposensitization by immunotherapy
holes cut out for the eyes, nose,  Anaphylaxis treatment
and mouth pulled over the head  Patient education
will hold wet dressings in place
on the face and neck.
e. Antihistamine, topical steroids.

ASSESSING ALLERGY:
1. History
2. Laboratory testing
3. Skin testing

ASSESSING ATOPIC DISORDER #3

Comparison of Seborrheic Dermatitis and
Atopic Dermatitis
Seborrheic dermatitis is a benign
condition of infants requiring little treatment
other than frequent shampooing of the hair
and soaking the lesions in mineral oil and
combining them away.
Nursing Diagnoses associated with
Immune Dysfunction
 Risk for infection
 Impaired skin integrity
 Activity intolerance
  Chronic infection anemia

CHAPTER 44: NURSING CARE OF A APLASTIC ANEMIA

FAMILY WHEN A CHILD HAS
HEMATOLOGIC DISORDER  Result from depression of
hematopoletic activity in the bone
HEMATOLOGIC DISORDERS marrow.
 It also affects the formation and
development of WBCs, platelets,
 Often called blood dyscrasias and RBCs
 Occurs when components of the  Congenital aplastic anemia
blood are formed incorrectly or either (Fanconi syndrome) is inherited as
increase or decrease in amount an autosomal recessive trait. A child
beyond normal ranges. is born with several congenital
COMMON HEMATOLOGIC DISORDERS anomalies such as skeletal and
#1 renal abnormalities, hypogenitalism,
and short stature. Between 4 and
ANEMIA 12 years of age, a child begins to
manifest symptoms of
 Can be caused by multiple factors
pancytopenia, or reduction of all
 Blood loss, acute infection,
blood components.
inadequate nutrition (iron, folic acid,  Acquired aplastic anemia is a
vitamin B12) decrease in bone marrow
HEMOLYTIC ANEMIAS production.
Causes: excessive exposure to
 Sickle cell disease, thalassemia, and radiation, drugs, or chemicals
other autoimmune disorders Drugs: chloramphenicol,
sulfonamides, arsenic (contained in
THE BLOOD: STRUCTURE AND
rat poison, sometimes eaten by
FUNCTION #1
children), hydantoin, benzene, or
Blood formation and components: quinine.
o Exposure to insecticides
 BLOOD PLASMA
o Chemotherapeutic drugs
 ERYTHROCYTES
o A serious infection such as
 LEUKOCYTES
meningococcal pneumonia
 THROMBOCYTES
THE BLOOD: STRUCTURE AND ASSESSMENT:
FUNCTION #2
o Pale
ERYTHROCYTES:
o Fatigues easily
 Hemoglobin o Anorexia
 Bilirubin o Bruises easily or has petechiae
o Excessive nosebleeds or
THE BLOOD: STRUCTURE AND
gastrointestinal bleeding
FUNCTION #3
o May contract an increased number
LEUKOCYTES: of infectious and respond poorly to
antibiotic therapy
 Granulocytes o Signs of cardiac decompensation
 Agranulocytes (tachycardia, tachypnea,
THROMBOCYTES shortness of breath, or cyanosis)
o Bone marrow samples will show a
ASSESSING FOR DISORDERS OF RED reduced number of blood elements;
BLOOD CELLS #2 blood-forming spaces become
infiltrated by fatty tissue.
HYPOCHROMIC ANEMIAS:

 Iron-deficiency anemia
THERAPEUTIC MANAGEMENT:
o Causes in infants
o Causes in older children o Stem cell transplantation
 o Using procedures to suppress T-  Sclerae are generally icteric
lymphocyte-dependent autoimmune (yellowed)
responses with antihymocyte  Cell priapism or persistent, painful
globulin (ATG) or cyclosporine or erection
transfusion of new blood elements
o Packed RBCs and platelet
transfusions
o Prophylactic platelet transfusions
may be given INTERVENTIONS:
o RBC-stimulating factor  Three primary needs:
(erythropoletin) 1. Adequate hydration – priority
o Colony-stimulating factors may also 2. Pain relief
improve bone marrow function. 3. Oxygenation
o Oral corticosteroid (prednisone)  Maintain adequate and blood flow
o Be conservatively optimistic when intravenously (normal saline); oral
discussing with the parents. fluids
 Administer analgesics (RTC)-
SICKLE CELL ANEMIA Acetaminophen (Tylenol)
 Electrolyte replacement
 It is the severe chronic, haemolytic
anemia with the presence of  Do not administer potassium
abnormally shaped (elongated) intravenously until kidney function
RBCs causing occlusion of small has been determined (the child is
blood vessels characterized by voiding).
episodes of pain blood vessels  Blood and urine cultures, a chest
characterized by episodes of pain. radiograph, and a CBC (infection)
 An autosomal recessive inherited  Administer antibiotics as prescribed
disorder on the beta chain of  Refer the parents to geneticist
haemoglobin.  Report s/s of vaso-occlusion, MI or
 Erythrocytes are elongated and CVA
crescent-shaped (sickled) when OTHER INTERVENTIONS:
there is to low oxygen tension (less
than 60% to 70%), a low blood pH  Assist the child on comfortable
(acidosis), or increased blood position, keep the extremities
viscosity (e.g. dehydration or extended to promote venous return;
hypoxia) HOB not more than 30 degrees,
 Stasis and sickling occur (a sickle- avoid putting strain on painful joints
cell crisis) and do not raise the knee gatch of
 Hemosiderosis (iron deposits into the bed.
body organs) is a complication of the  High-calorie, high protein diet, folic
disease. supplementation
 Ensure that the child receives
ASSESSMENT:
vaccination (pneumococcal, h.
 Diagnostic test: Hemoglobin influenza type B, meningococcal)
electrophoresis susceptible to infection from
 Initial s/s: growth retardation functional asplenia
 Fever and anemia (approximately 6 SICKLE-CELL CRISIS:
months)
 Local pain (stasis of blood and  Denotes a sudden, severe onset of
infarction may occur in any body sickling
part)  Can occur when a child has an
 Swelling of the hands and feet (a illness causing dehydration or a
hand-foot syndrome) probably respiratory infection that results in
caused by aseptic infarction of the lowered oxygen exchange and a
bones of the hands and feet. lowered arterial oxygen level, or
 Have a slight build long arms and after extremely strenuous exercise
legs, protruding abdomen because (enough to lead to tissue hypoxia)
of an enlarged spleen and liver.  Symptoms: are sudden, severe,
 An acute chest syndrome with and painful
symptoms of pulmonary infiltrates  Laboratory results:
with chest pain, fever, tachypnea, a. Hemoglobin level of only 6 to 8
wheezing, or cough g/100 Ml.
 b. A peripheral blood smear  Avoid contact sports (such as
demonstrates sickled cells football) and long distance running
c. WBC count elevated to 12,000 to  Caution parents against taking the
20,000/mm3 child on board an unpressurized
d. Bilirubin and reticulocyte levels aircraft in which the oxygen
are increased. concentration may fall during flight.
e.
TWO TYPES OF SICKLE CELL DISEASE:
MANIFESTATIONS:
Sickle cell trait (asymptomatic)
 Hgb level ranges 6 to 9 g/dL or lower
 Blood of the patient contains a o Child is pale, tires easily, and
mixture of Hgb A and sickle (Hgb S) has little appetite
 Proportions of Hgb S are low  Sickle cell crises are painful and can
because the disease is inherited be fatal
from only one parent Symptoms: severe abdominal pain,
 Hgb and RBC counts are normal muscle spasms, leg pain, or painful
swollen joints may be seen.
Sickle cell anemia (more severe)
o Fever, vomiting, hematuria,
 Clinical symptoms do not appear convulsions, stiff neck, coma,
until the last part of the first year of or paralysis can result
life. o Risk for stroke as a
 May be an unusual swelling of the complication of a vaso-
fingers and toes occlusive sickle cell crisis.
 Symptoms caused by enlarging
bone marrow sites that impair THALASSEMIA
circulation to the bone and the
abnormal sickle cell shape that  Autosomal recessive anemias
causes clumping, obstruction in the associated with abnormalities of the
vessel, and the ischemia to the beta chain of adult hemoglobin
organ the vessel supplies. (HgbA).
 Most common in the Mediterranean
COMPLICATIONS: population may occur also in
 Aseptic necrosis of the head of the children of African and Asian
femur with increased joint pain heritage.
 A cerebrovascular accident that  RBCs are abnormal in size and
occurs from a blocked artery, shape and are rapidly destroyed;
causing loss of motor function, results in chronic anemia
coma, seizures, or even death THALASSEMIA MINOR
 If there is renal involvement, (HETEROZYGOUS BETA-THALASSEMIA)
hematuria or flank pain may be
present. o A mild form of this anemia, produce
both defective beta hemoglobin and
 Blood transfusion (usually packed normal hemoglobin
RBCs) may be necessary to o Occurs when the child inherits a
maintain the hemoglobin above 12 gene from one parent (heterozygous
g/dL (termed hypertransfusion) inheritance)
 Should not be given supplementary  RBC count will be normal
iron or iron-fortified formula or  Hemoglobin concentration will be
vitamins; too much iron may lead to decreased 2 to 3 g/100 mL below
(hemochromatosis) and normal levels
(hemosiderosis). Oral folic acid can  Pallor
be prescribed. o Require no treatment, and life
 Monitor the child’s nutrition intake expectancy is normal.
during this drug therapy. o Should not receive a routine iron
 Immunization (measles and supplement because their inability to
pertussis, meningococcal, incorporate it well into hemoglobin
pneumococcal, and influenza may cause them to accumulate too
vaccines). much iron.
 Oral penicillin as prophylaxis for the
first 5 years. THALASSEMIA MAJOR (homozygous
 Counseling and support Beta-Thalassemia)
 o Also called Cooley’s anemia or o Low sodium diet
Meditarranean anemia because o A splenectomy may be
thalassemia is a beta chain. needed to increase comfort,
o RBCs are hypochromic (pale) and increase ability to move
microcytic (small) about and to allow for more
o Hemoglobin level is less than 5 normal growth
g/100 mL. Iron saturation is 100% o Genetic counseling
o Progressive severe anemia
o Evident within the second 6 months
of life HEMOPHILIA A
o Child is pale, hypoxic, poor appetite,
o Is an inherited disorder of blood
and may have a fever
o Jaundice that progresses to a coagulation. There are numerous
hemophilia types, each involving
muddy bronze color resulting from
deficiency of a different blood
hemosiderosis
coagulation factor.
o Liver enlarges and the spleen grows
enormously Most common types:
o Abdominal distention
 Hemophilia B (Christmas disease [a
o Cardiac failure caused by profound
factor IX deficiency]
anemia is a constant threat.
 Hemophilia A (a deficiency in factor VIII)
ASSESSMENT B-THALASSEMIA  A deficiency in any one of the factors will
interfere with normal blood clotting.
o Frontal bossing
o Maxillary prominence MANIFESTATIONS OF HEMOPHILIA
o Wide eyes set with flattened nose
 Can be diagnosed at birth because
o Greenish-yellow skin tone factor VIII cannot cross the placenta
o Hepatosplenomegaly and be transferred to the fetus
o Severe anemia  Usually not apparent in the newborn
o Microcytic, hypochromic RBCs unless abnormal bleeding occurs at
the umbilical cord or after
circumcision
THALASSEMIA MAJOR
 Normal blood clots in 3 to 6 minutes
Nursing measures:  In severe hemophilia, it can take up
to 1 hour or longer
o Adhere to the principles of long term
care ASSESSMENT:
o Whenever possible, have the same
 Bleeds excessively after
nurse assigned to the child
circumcision
o Observing the patient during blood
 Bruises
transfusions for any adverse
 Soft tissue bleeding and painful
reactions
hemorrhage into the joints, which
o Monitoring vital signs
become swollen and warm
o Providing for the emotional health of
 Hemarthrosis, severe loss of joint
the child and family is essential.
mobility.
INTERVENTIONS:  Severe bleeding may also occur into
the gastrointestinal tract, peritoneal
 Transfusion of packed RBCs every 2 cavity, or central nervous system
to 4 weeks (hypertransfus therapy)  Platelet count and prothrombin time
will maintain hemoglobin between 10 are normal, depending on the level
and 12 g/100 mL. of factor VIII present.
 Because of the number of  A thromboplastin generation test is
transfusions, hemosiderosis is seen abnormal.
in the spleen, liver, heart, pancreas,  Partial thromboplastin time (PTT) is
and lymph glands. the test that best reveals the low
o Deferoxamine mesylate levels of factor VIII.
(Desferal), an iron-chelating
agent is given to counteract  Hemophilia A (Factor VIII
this side effect. Deficiency) The classic form of
o Administer medications as hemophilia is caused by deficiency of
prescribed (Digitalis, the coagulation component factor VIII,
diuretics) the antihemophilic factor. It is
 transmitted as a sex-linked recessive
trait.
o Factor VIII is an intrinsic factor of
coagulation, so the intrinsic
system for manufacturing
thromboplastin is incomplete.
 Aim of therapy is to increase level of
factor VIII to ensure clotting
 This is checked by a blood test call
partial thromboplastin time (PTT)
THERAPEUTIC MANAGEMENT:

 Control bleeding by the

administration of factor VIII, (fresh
whole blood or by fresh or frozen
plasma, concentrate of factor VIII.
 Administration of desmopressin
(DDAVP), which stimulates the
release of factor VIII.
 In a few children, antibodies (termed
inhibitors) to factor VIII develop,
rendering the factor ineffective. If
this happens, epsilon-aminocaproic
acid, a fibrinolytic enzyme that helps
to stabilize clot formation and
promote wound healing, can be self-
administered every 6 hours if
needed.
 Children with inhibitors to factor VIII
can also be given a factor IX
concentrate (Proplex or Konyne).
This concentrate enters the
coagulation cascade after VIII and
halts bleeding.
VON WILLEBRAND’S DISEASE

 An inherited autosomal dominant

disorder affecting both sexes, is
often reffered to as
angiophemophilia
 Along with a factor VIII defect, there
is also an inability of the platelets to
aggregate.
 Blood vessels cannot constrict to aid
in coagulation
ASSESSMENT:

 Prolonged bleeding time

 Hemorrhages (mucous membrane
sites)
 Epistaxis
 Heavy menstrual flow
INTERVENTIONS:

 Factor VIII replenishment or by

administration of DDAVP

 2. Infection from neutropenia
3. Bleeding from decreased platelets
4. Fractures due to bone marrow
involvement

LEUKEMIA PREDNISONE:

 Malignant disease of the bone Side effects:

marrow and lymphatic system a. Masking symptoms of infection
 Disruption of bone marrow function b. Increase fluid retention
caused y the overproduction of c. Induce personality changes
immature WBCs in the marrow d. Moon-face appearance
TYPES: METHOTREXATE AND 6-
a. Acute Lymphoid Leukemia (most MERCAPTOPURINE
common child)  Maintains remissions by acting
b. Acute Nonlymphoid Leukemia against chemical vital to the WBC
Diagnostic tests that differentiate the life
types:  Side effects: nausea, rash, fever,
anemia, peripheral neuropathy,
a. Cytochemical markers diarrhea, hair loss, anuria, and bone
b. Chromosome studies marrow depression
c. Immunological markers
AUTOLOGOUS BONE MARROW
Bone marrow aspiration: (iliac crest) TRANSPLANT:
Signs and Symptoms:  Child’s own bone marrow that has
1. Low grade fever been purged of malignant cells
2. Pallor ALLOGENEIC BONE MARROW
3. Bruising tendency TRANSPLANT:
4. Leg and joint pain
5. Listlessness  From a donor that matches the child
6. Abdominal pain  Hematopoietic stem cell
7. Enlargement of the lymph nodes transplant: used for children who
8. Liver and spleen enlargement don’t respond to chemotherapy.
9. Anorexia, vomiting, weight loss,
dyspnea INTERVENTIONS:
10. Hematuria  Observe for signs of infection
11. Ulcerations  Observe for inflammation
INTERVENTIONS:  Monitor vital signs
 Provide good nutrition and
1. Refer to specialized center and supplemental feedings (high protein
support groups and calories)
2. Chemotherapy  Observe for petechiae and
3. Hydration to prevent kidney damage ecchymosis
4. Active routine immunizations may be  Check for nose bleeding, mouth, and
delayed gum ulcerations
5. TPN
 Use lip balm, soft bristle toothbrush
6. I & O monitoring
 Provide gentle oral hygiene, soft
7. Maintain meticulous oral hygiene
bland foods, increase fluid
8. Report any incidence of exposure
 Provide for frequent rest periods.
from infections
9. Offer hat or wig If blood transfusion reaction occurs:
PRIORITIES IN CARE OF LEUKEMIC  Stop infusion
CHILDREN:  KVO with NSS
1. Complications of anemia from  Notify the charge nurse and doctor
decreased RBC infection  Take the patient’s V/S
  Observe closely THERAPEUTIC MANAGEMENT:

 Diagnosis: Bone marrow aspiration

and biopsy
 Chemotherapy: Cytarabine (Ara-C),
etoposide (VePesid), daunorubicin
(DaunoXome) commonly used drug
regimen
 Bone marrow transplantation

ACUTE LYMPHOCYTIC LEUKEMIA

 Proliferation of immature WBCs SIDE EFFECTS OF CHEMOTHERAPY:
 ASSESSMENT:
 Steroids can mask signs of
 Signs and Symptoms of anemia (easy infections, cause fluid retention,
fatigability and fainting), pallor, low induce personality changes, and
grade fever cause the child’s face to appear
 Repeated infection moon-shaped.
 Bleeding  Certain chemotherapy agents can
 Weight loss cause nausea, diarrhea, rash, hair
 Night sweats loss, fever, anuria, anemia, and
 Splenomegaly bone marrow depression
 Pain on the bone, joint  Peripheral neuropathy may be
 Painless, generalized swelling of lymph signated by severe constipation
nodes caused by decreased nerve
sensations to the bowel
NURSING DIAGNOSIS: Risk for infection
HODGKIN’S DISEASE
Laboratory Data: Increased WBC count
(150,000/mm3)  Malignancy of the lymph system
involving the lymph nodes
Definitive diagnostic test: Bone marrow
 Reed-stemberg cells (giant
aspiration
multinucleated)
THERAPEUTIC MANAGEMENT:  Diagnosis: X-ray, blood tests, body
scan, biopsy
1. Watch for signs of infection and
bleeding STAGING HODGKIN’S DISEASE
2. Avoid crowded places CRITERIA
3. Avoid venipunctures
4. Prepare the client for chemotherapy I. Restricted to single site or
5. Administer Allupurinol as localized in a group of lymph
prescribed (decrease uric acid nodes, asymptomatic
production) II. Involves 2 or more lymph nodes
6. Observe neutropenic precautions in area or on same side of
a. Strict handwashing diaphragm
b. Provide private room III. Involves lymph node regions on
c. Provide a low bacteria diet, avoid both sides of diaphragm,
fresh fruits and vegetables adjacent organs or spleen
d. ANTIEMETICS to be given 1 IV. Diffuse diseases; least favorable
hour before beginning prognosis
chemotherapy, but administer SIGNS AND SYMPTOMS:
every 2-6 hours for the next 24
hours. 1. Painless, enlarged, rubbery feeling
cervical or sentinel lymph nodes
ACUTE MYELOID LEUKEMIA 2. Swelling
3. Unexplained low grade fever
 Overproliferation of granulocytes
4. Anorexia
(neutrophils, basophils, and
5. Unexplained weight loss
eosinophils)
6. Night sweats
 20% of all child leukemias
7. General malaise
 ASSESSMENT: same signs and
8. Rash
symptoms with ALL; susceptible to
9. Itchiness
infection because they do not have
mature granulocytes. NURSING DIAGNOSIS: Potential for
infection
TREATMENT: o Distal femur (40-50%), proximal tibia
(20%) and the proximal humerus
 Radiation therapy
(10%-15%)
 Chemotherapy o Metastasis to the lungs is very
 Cyclophosphamide (Cytoxan): S/E: common by the time of diagnosis. It
nausea, vomiting, cystitis, alopecia may also involve the brain and other
 Vincristine: S/E: constipation, bones.
alopecia, neurotoxicity
 Procarbazine HCL ASSESSMENT:
 Prednisone 1. Taller than average
INTERVENTIONS: 2. Has a history of recent trauma on
the affected area
1. Health teaching on s/e of radiation 3. Pain and swelling on the site
and chemotherapy (inflammation and warmth to touch)
- Lymphangiogram: buish skin and
urine TREATMENT:
- Irradiation: malaise 1. Chemotherapy (methotrexate,
- Avoid sunlight exposure and cisplatin, doxorubicin, ifosfamide-
irritation of skin common
- Delayed menstruation and 2. Surgery, bone transplant or metal
secondary sex characteristics prosthesis
appearance, sterility 3. Avoid bearing weight on the affected
2. Monitor for infection area because it may cause fracture
3. Emotional support due to weakening of the bone by the
NON-HODGKIN LYMPHOMA growth of growing tumor.

o Malignant disorders of the DIAGNOSIS:

lymphocytes (either B or T cells) 1. Blood serum for alkaline
o Cause: undocumented but many phosphatase
times like EBV is linked to its 2. Biopsy
occurrence 3. CBC, urinalysis, chest x-ray, CT
o Common age occurrence at 5-15 scan and bone scan to determine
years metastasis
o Assessment: involve lymph
glands of the neck and chest, NEUROBLASTOMA
cough or chest tightness, face o Tumors arise from the cells of the
edema, abdominal mass, pain, SNS; occurs frequently in the
diarrhea, or constipation abdomen near the adrenal glands
THERAPEUTIC MANAGEMENT: and spinal ganglia
o Occurs primarily in infants and
o Induction phase (child is put into preschool children, most common in
remission or no tumor can be boys
detected by clinical examination) o Metastasis include the bone marrow,
o Maintenance phase (up to 2 years) liver, and subcutaneous tissue
o Administer cyclosphophamide, o Can be detected through ultrasound
hydroxydaunorubicin, vincristine or at birth
(Oncovin), prednisone
o Intrathecal chemotherapy because DIAGNOSIS: IV pyelogram, MRI,
of tendency to metastasize to the arteriogram, CT scan, biopsy.
CNS. ASSESSMENT:
OSTEOGENIC SARCOMA o Abdominal mass
o A malignant tumor of long bone o Weight loss, anorexia
which involves a rapid growing bone o Excessive sweating, flushed face
tissue and hypertension
o Most common in boys and for those o Loss of motor function in lower
who had radiation for other extremities
malignancies as a later effect in life. o Dyspnea, difficulty in swallowing,
o May be hereditary neck, and facial edema
o Jaundice
o Blue or purplish nodules on arms
and legs
THERAPEUTIC MANAGEMENT:
o Tumor stage I or II: surgical
removal of primary tumor
o Tumor stage III or IV: surgery will
be followed by chemotherapy
(doxorubicin, cyclophosphamide,
etoposide, and carboplatin)
o Stem cell transplantation
o Immunotherapy

NEPHROBLASTOMA

 Also known as Wilm’s tumor

 Malignant tumor that rises from the
metanephric mesoderm cells of the
upper pole of the kidney
 NEPHROBLASTOMA: common
malignancy of early life; embryonal
adenosarcoma
DIAGNOSIS:

 Mass on the abdomen

 Kidney radiographic exams: (IV
Pyelograms)
ASSESSMENT:

 Firm, non tender abdominal mass

 Hematuria
 Low grade fever
 Anemia
 Increased blood pressure
INTERVENTIONS:

 Surgery
 Radiation therapy
 Chemotherapy
 Avoid unnecessary handling of the
abdomen
 Avoid contact sports (post)
RETINOBLASTOMA

 A malignant tumor of the retina of

the eye (congenital)
ASSESSMENT: cat’s eye reflex or grayish
appearance of the pupil
INTERVENTIONS:

 Prepare for enucleation

 Refer the parents to a geneticist.