2F – SICK GROWING CHILD
NCM109 (THEORY) – CARE OF MOTHER,
AND CHILD AT-RISK OR WITH
PROBLEMS (ACUTE AND CHRONIC)
MODULE 2F – SICK GROWING CHILD
Source: Wong’s-Pillitteri Book, Reporting
ALTERATIONS
FUNCTIONS
IN
RESPIRATORY
9. Bronchopulmonary Dysplasia – Xray, CBC, Echocardiogram, Pulse
Oximetry, Nasal Continuous Positive
Airway
Pressure,
Surfactant
Replacement Therapy
10. Cystic Fibrosis – Stool analysis, CBC,
Sweat Chloride Test, Sputum Culture,
Chest X-ray, Genetic Test
1. Apnea – med history, PE, sleep study,
positive airway pressure therapy,
Somnoplasty, Tonsillectomy, UPPP,
Mandibular, Nasal Surgery
11. Bronchitis – Pulmonary Functioning
Testing, High Resolution Computed
Tomography (HRCT), X-Ray, Sputum
Examination
2. Apparent Life-Threatening Event –
med., PE, CBC, Serum Bicarbonate &
Lactate (acidosis), Urinalysis, Chest
Radiography
12. Bronchiolitis
–
CBC,
Chest
Radiograph, Nasopharyngeal Swabs,
Bacterial Cultures
3. Sudden Infant Death Syndrome
4. Respiratory
Failure
–
CBC,
Spirometry, Pulmonary Functioning
Test, Peak Flow, Arterial Blood Gas
5. Croup Syndrome – Lateral Neck
Radiograph, CBC, Heliox
6. Asthma – PE, Spirometry, Peak Flow,
Methacholine Challenge, Chest X-ray,
Skin Test/Allergy Test, Nitric Oxide,
Sputum
Eosinophils,
provocative
testing for exercise and cold asthma
7. Status Asthmaticus – Spirometry,
Peak Flow Meter Tests, Exhaled Nitric
Oxide Test, Challenge Tests, CBC, Xray, Gas & Diffusion Tests
2F
8. Neonatal
Respiratory
Distress
Syndrome – Blood Gas Analysis, Xray, Blood Test, Echocardiography
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
ALTERATIONS
FUNCTIONS
IN
CARDIOVASCULAR
12. Truncus
Arteriosus
–
Echocardiogram, Cardiac Cath
Xray,
1. Patent
Ductus
Arteriosus
–
Echocardiogram, Sound waves, X-ray
13. Total Anomalous Pulmonary Venous
Return – ECG, Cardiac Cath., Xray
2. Atrial Septal Defect – X-ray,
Electrocardiogram, Echocardiogram,
Cardiac Catheterization
14. Rheumatic Fever – Throat Swab,
CBC, ECG, Echocardiogram
3. Atrioventricular Septal Defect –
Prenatal
Ultrasound,
ECG,
Echocardiogram, X-Rays, Cardiac
Catheterization
4. Ventricular Septal Defect – Cardiac
Catheterization,
ECG,
X-Ray,
Echocardiography
15. Infectious Endocarditis – Blood
Culture,
CBC,
Echocardiogram,
Electrocardiogram, Xray, CT Scan
16. Kawasaki Disease – CBC, ECG,
Echocardiogram, Urine Testing
5. Pulmonic
Stenosis
–
X-Ray,
Electrocardiogram, Echocardiogram,
Cardiac Cath.
6. Aortic Stenosis – X-ray, ECG,
Echocardiogram,
Cardiac
Catheterization, Exercise Testing,
Pulse Oximetry
7. Coarctation of the Aorta – X-ray,
ECG,
Echocardiogram,
Cardiac
Catheterization, CT Scan, MRI
8. Tetralogy of Fallot – Chest X-Ray,
Echocardiography, Cardiac Cath.,
ECG, PO
9. Transposition of the Great Arteries –
Echocardiogram, X-ray, ECG, Cardiac
Cath.
2F
10. Hypoplastic Left Heart Syndrome –
Echocardiogram, ECG, Xray, PO,
Cardiac Cath, Cardiac MRI
11. Tricuspid Atresia/Pulmonary Atresia
– Echocardiogram, ECG, PO, Xray,
Cardiac Cath
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
ALTERATIONS
FUNCTION
IN
HEMATOLOGIC
1. Iron Deficiency Anemia – CBC,
Peripheral Smear, Serum Iron, Total
Binding Capacity, Serum Ferritin,
Hemoglobin
Electrophoresis
and
Measurement of Hemoglobin A2,
Reticulocyte Hemoglobin Content,
Stool Testing, Incubated Osmotic
Fragility, Issue Lead Concentrations,
Bone Marrow Aspiration
2. Normocytic
Anemia
–
CBC,
Reticulocyte Test, Bone Marrow Biopsy
3. Sickle-Cell Anemia – Hemoglobin
Electrophoresis Test
ALTERATIONS IN CELLULAR GROWTH
1. Neuroblastoma – Blood and Urine
Tests, Biopsy, Bone Marrow Biopsy, CT
Scan,
MRI
Scan,
Methyliodobenzylguanine
(MIBG),
Ultrasound, Xray
2. Wilm’s Tumor (Nephroblastoma) –
Abdominal Ultrasound, MRI, Xray, CT
Scan, Inferior Venacavogram, Bone
Marrow
Aspiration,
Excretory
Urography, CBC
3. Bone Tumors
a. Osteosarcoma – Xray, MRI, CT
Scan, PET Scan
4. B-Thalassemia – CBC, Hemoglobin
Electrophoresis Test, Splenectomy,
Cholecystectomy
b. Ewing’s Sarcoma – CBC, Xray,
CT Scan, MRI, PET Scan, Bone
Scan, Biopsy, Bone Marrow
Aspiration and Biopsy
5. Aplastic Anemia – Bone Marrow
Biopsy, CBC
4. Leukemia – PE, Blood Test, Bone
Marrow Test
6. Hemophilia – CBC, Activated Partial
Thromboplastin Time (APTT) Test,
Prothrombin
Time
(PT)
Tests,
Fibrinogen Test
5. Soft Tissue Tumors
a. Hodgkin’s Disease – Lymph
Node Biopsy, Lab Results, CT
Scan, XRay, Bone Marrow
Analysis, Liver Function Tests,
MRI Scans, Lymphangiography,
Abdominal Biopsy
7. Von Willebrand Disease – Factor VIII
Clotting Activity, Von Willebrand Factor
Antigen
8. Disseminated
Intravascular
Coagulation – CBC, Prothrombin Time
(PT), Partial Thromboplastin Time
(PTT), Comprehensive Metabolic Panel
(CMP), D-Dimer Tests, Peripheral
Blood Smear, Serum Fibrinogen Tests
2F
9. Idiopathic
Thrombocytopenic
Purpura – CBC, PE, Bone Marrow
Aspiration
b. Non-Hodgkin’s Disease –
Physical Examination, Total
Body Imaging, Bone Marrow
Aspiration and Biopsy, Blood
and
Urine
Tests,
Blood
Chemistry
Tests,
Lumbar
Puncture
(Spinal
Tap),
Cytogenetics, Fluorescent in
Situ Hybridization (FISH)
c. Rhabdomyosarcoma
–
Imaging Studies, Biopsy, Blood
Tests, Bone Marrow Aspiration
and Biopsy
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
d. Retinoblastoma – PE, Health
History, Bone Scan, Bone
Marrow Aspiration and Biopsy,
Lumbar
Puncture,
Electroretinography, RB1 Gene
Test, Ultrasound, MRI
Renal
Ultrasonography,
Sonography
Cranial
10. Umbilical Hernias – PE, Abdominal
Ultrasound, CT Scan
11. Colic – Clinitest, Stool Exam
ALTERATIONS
FUNCTION
IN
GASTROINTESTINAL
1. Cleft lip and cleft Palate – Ultrasound,
Amniocentesis,
Cheiloplasty,
Platoplasty
2. Esophageal Atresia and Tracheoesophageal Fistula – Esophagram,
Bronchoscopy, Echocardiography
3. Pyloric Stenosis – Electrolyte Lvl, pH
Lvl, BUN Lvl, Creatinine Lvl,
Ultrasonography, Radiography
4. Gastroesophageal Reflux – 24 hr
Intraesophageal pH Monitoring Study,
Upper
GI
Series,
pH
Probe,
Esophageal Manometry, Endoscopy
5. Omphalocele
–
Prenatal
Ultrasonography, Amniocentesis, Fetal
Echocardiogram
6. Intussusception – Abdominal XRay,
Ultrasound, Air or Contrast Enema
7. Hirschsprung’s Disease – Abdominal
XRay, Rectal Biopsy, Contrast Enema,
Anal Manometry
2F
8. Anorectal
Malformations
–
Abdominal XRay, Renal Ultrasound,
Pelvic Ultrasound, Spinal Ultrasound,
MRI
9. Diaphragmatic Hernias – Chest
Radiography,
Cardiac
Ultrasonography, Echocardiography,
12. Rumination – Endocrine Hormone
Functions, Test for Anemia, Serum
Electrolytes
13. Celiac Disease – PE, Blood Test, HLA
Genetic Test, Endoscopy
ALTERATIONS
FUNCTION
IN
GENITOURINARY
1. Bladder Exstrophy – MRI, Xray
2. Hypospadias & Epispadias – Dorsal
Hood, Chordee, Mucosal Strip
3. Obstructive Uropathy – PE, Med His.,
Ultrasonography,
IV
Pyelogram,
Diethylenetriamine Pentacetic Acid
(DTPA),
Dimercaptosuccinic
Acid
(DMSA) Renal Scan, VCUG
4. Nephrotic Syndrome – Urine test,
CBC, Kidney Biopsy
5. Glomerulonephritis – Urinalysis,
CBC, Ultrasound, Kidney Biopsy
6. Phimosis – PE
7. Cryptorchidism – MRI, Laparoscopy,
Open Surgery, PE, Ultrasound
8. Inguinal Hernia & Hydrocele –
Ultrasound, Transillumination, Duplex
Ultrasonography, Plain Abdominal
Radiography
9. Testicular
Torsion
Ultrasound, Urinalysis
–
Doppler
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
ALTERATIONS
FUNCTION
IN
NEUROLOGIC
ALTERATIONS IN MUSCULOSKELETAL
FUNCTION
1. Seizure Disorders – Neuro Exam,
CBC, Spinal Tap, EEG, MRI, CT
1. Metatarsus Adductus – PE, Leopold’s
Maneuver,
Ultrasound,
Hip
Examination, Interview, MRI
2. Infectious Disease
a. Reye’s Syndrome – CT, MRI,
Urine Test, Blood Test, Skin
Biopsy, Spinal Tap, Liver Biopsy
b. Guillain-Barre Syndrome –
Spinal Tap, Electromyography,
Nerve Conduction Studies
2. Clubfoot – Ultrasound, Radiography,
MRI, CT, Xray
3. Genu Varum & Genu Valgum – PE,
Xray, Blood Test, CT Scan,
4. Dysplasia of the Hip – Ortolani Test,
Barlow Maneuver, Ultrasound, Xray
3. Hydrocephalus – Ultrasound, MRI,
CT, Spinal Tap, ICP, Fundoscopic
Examination
5. Legg-Calve-Perthes Disease – Xray,
MRI, CBC
4. Spina Bifida – Blood tests, MSAFP
Test, Amniocentesis
6. Supped Capital Femoral Epiphysis –
PE, Xray
5. Craniosynostosis – PE, CT Scan,
Ultrasound
7. Scoliosis – Plumb Line Test, Xray
“Cobb Technique”, Risser Scale
6. Cerebral Palsy – Brain Imaging Tests,
Metabolic and Genetic Testing, EEG,
Functional Independence and WeeFIM,
Pediatric Evaluation of Disability
Inventory
8. Torticollis – Xray, CT, Ultrasound,
CBC
9. Kyphosis – CT, MRI, Bone Scan
10. Lordosis – PE, Xray, CT Scan
11. Osteomyelitis – Xray, MRI, CT, Biopsy
12. Skeletal Tuberculosis – Tuberculin
Skin Test, CBC, Xray, Bone Biopsy
13. Septic Arthritis – Joint Fluid Analysis,
Blood Tests, Imaging Tests
2F
14. Osteogenesis Imperfect – Xrays, Lab
tests,
Dual
Energy
XRay
Absorptiometry Scan
15. Duchenne’s Muscular Dystrophy –
PE, Muscle Biopsy
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
16. Becker’s Muscular Dystrophy –
Creatine Kinase Level, Muscle Biopsy,
Genetic Testing
9. Klinefelter’s
Syndrome
–
Amniocentesis, Hormone Testing,
Chromosome Analysis
17. Fascioscapulohumeral Dystrophy –
Serum Creatinine Kinase, EMG,
Surgical Removal, Microscopic Exam
10. Phenylketonuria – Guthrie Bacterial
Inhibition Assay, PKU Screening Test
18. Emery-Dreyfuss
Muscular
Dystrophy – CPK Test, Transaminase,
Lactate
dehydrogenase,
aldolase
levels, PCR, ultrasonography, EMG,
ECG, PFT, Muscle biopsy
11. Galactosemia – CBC, Urine Test,
Newborn Screening, Buetler Test
12. Maple Syrup Urine Disease – Plasma
Amino Acids Testing, CBC, Urinalysis,
Chorionic
Villus
Sampling,
Amniocentesis
19. Congenital Muscular Dystrophy –
EMG, Lab Test, Biopsy, Genetic testing
ALTERATIONS IN SKIN INTEGRITY
ALTERATIONS IN ENDOCRINE FUNCTION
1. Growth Hormone Deficiency – PE,
Blood Test, Imaging Tests
2. Hyperpituitarism – CBC,
Ultrasound, Thyroid Scan
Thyroid
3. Diabetes Insipidus – Urine Collection,
Water Deprivation Test, Vasopressin
Test, MRI
1. Contact Dermatitis – Patch Test,
CBC, Challenge Test, Nasal Smear
Test
2. Diaper Dermatitis – PE, Lab Tests
3. Seborrheic Dermatitis – PE, Lab, Skin
Biopsy
4. Eczema – Allergic Skin Test, CBC, Skin
Biopsy
4. Precocious Puberty – CBC, Xray, MRI
5. Impetigo – PE, Swab Test
5. Cushing’s
Syndrome
–
Urine
Collection, Saliva Test, Steroid Test
6. Congenital Adrenal Hyperplasia –
ACTH Stimulation Test, Genetic Test,
Urine Test, Karyotypes Test, Pelvic
Ultrasound, Bone Age Studies
2F
6. Scabies – Scabies Ink Test,
Tetracycline
Solution,
Videodermatoscopy,
Dermoscopy,
Skin Scraping, Adhesive Tape Test
7. Addison’s Disease – CBC, ACTH
Stimulation Test, Xray, CT Scan,
Thyroid Functioning Test
8. Furner’s Syndrome – Karyotype
Analysis, CBC, Echocardiography,
MRI, Maternal Serum Screening
MINGUITO, SHANIA D. | BSN 2-B
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some15
APNEA
URGENT RESPIRATORY THREATS
Apnea is a pause in respirations longer than
20 seconds with accompanying bradycardia
(cyanosis also may be present).
Types:
1. Central – Both airflow and chest wall
movement are absent.
2. Obstructive – Airflow is absent but
chest wall motion is present.
3. Mixed – Both central and obstructive
components are present.
- Medical conditions such as type 2 DM,
- congestive heart failure, high blood
pressure, Parkinson’s disease, PCOS,
hormonal disorders, prior stroke, or
chronic lung disease like asthma.
TAKE NOTE!
Gently shaking an infant or flicking the sole of
the foot often stimulates the baby to breathe
again, almost as if the child needed to be
reminded to maintain this function. If an infant
does not respond to these simple measures,
resuscitation is necessary.
As a result of:
✓ Fatigue
✓ Immaturity
of
their
respiratory
mechanisms.
✓ Secondary
stress
–
infection,
hyperbilirubinemia, hypoglycemia, or
hypothermia.
Apnea during infancy can be a symptom of any
one of many disorders – including:
Sepsis
Seizures or other Neurologic Disorder
Upper/Lower Airway Infection
Gastroesophageal Reflux
Hypoglycemia or other Metabolic
Problems
✓ Impaired regulation of breathing during
sleep or feeding
✓
✓
✓
✓
✓
Risk Assessment:
- Being overweight
- A large neck circumference that could
make
- your airways more narrow
- A narrowed airway that you inherited or
- developed from large tonsils or
adenoids
- Being male
- Older age
- A family history of sleep apnea
- Smoking
- Use of alcohol, sedatives, or
tranquilizers
- Nasal congestion
2F
APNEA: Therapeutic and Nursing Care
Management
1. Closely
observe
all
newborns,
especially preterm ones, to detect these
apneic episodes.
2. Apnea monitors that record respiratory
movements are invaluable tools to
detect failing respiration and sound a
warning an infant needs attention.
3. Infants with frequent or difficult-tocorrect episodes may be placed on
ventilators to provide respiratory
coordination until they are more mature.
4. To help prevent episodes of apnea,
maintain a neutral thermal environment
and use gentle handling to avoid
excessive fatigue.
5. Always suction gently to minimize
nasopharyngeal irritation, which can
cause bradycardia because of vagal
stimulation.
6. Using indwelling nasogastric tubes
rather than intermittent ones can also
reduce the amount of vagal stimulation.
7. After feeding, observe an infant
carefully because a full stomach can
put pressure on the diaphragm and can
potentially compromise respirations.
Careful burping also helps to reduce
this effect.
8. Never take rectal temperatures in
infants prone to apnea because the
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
resulting vagal stimulation can reduce
the heart rate (bradycardia).
9. Theophylline or caffeine sodium
benzoate may be prescribed to
stimulate respirations. → Increase the
infant’s sensitivity to carbon dioxide,
which stimulates respiratory function.
Infants who have had an apneic episode
severe enough to require resuscitation are at
a high risk for SIDS. Such infants may be
discharged home with a monitoring device to
be used for 2 to 6 months.
APPARENT LIFE-THREATENING EVENT
URGENT RESPIRATORY THREATS
Formerly referred to as aborted SIDS death or
near-miss SIDS, generally refers to
➔ An event that is sudden and frightening
to the observer in which the infant
exhibits a combination of:
▪ Apnea
▪ Change in color (pallor,
cyanosis, redness)
▪ Change in muscle tone
(usually hypotonia)
▪ Choking
▪ Gagging
▪ Coughing
➔ ALTE – May include apnea, but ALTE
may occur without apnea. (Apnea is not
an immediate precursor to SIDS)
➔ Common Risk Factor for SIS and ALTE
is maternal smoking.
Diagnostic Evaluation:
2F
✓ Who witnessed the event?
✓ Where the infant was during the event?
✓ What, if any, activities were involved?
(Such as during or after a feeding and
etc.)
✓ Prenatal and postnatal history must be
obtained.
✓ Observe the infant’s respiratory pattern
and response to feeding.
Commonly used monitoring is continuous
recording of cardiorespiratory patterns are the
following:
a) Pneumocardiogram
b) Four-channel pneumocardiograms →
monitor heart rate
c) Respirations (chest impedance)
d) Nasal Airflow
e) Oxygen Saturation
Risk Factors:
- Infants <2 months of age
- History of prematurity especially if <32
weeks at birth
- More than 1 event
Risk Assessment:
-
Male predominance
Gestational age
Low birth weight
Very low birth weight
Incident of small for gestational age
Age at the event
Multiparity
Maternal age
Smoking
Polysomnography (sleep study) → Records
brain waves, eye and body movements,
esophageal manometry, and end-tidal carbon
dioxide measurements.a
ALTE: Therapeutic Management:
✓ 24 hour observation
✓ Monitors with respiratory impedance
plethysmography (RIP) are capable of
detecting obstruction as well as central
apnea.
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
ALTE: Nursing Care Management:
1. Nurse can be a major source of support
to the family in terms of education about
the equipment.
2. Education regarding observation of the
infant’s status.
3. Instructions
regarding
immediate
intervention during apneic episodes
including CPR.
4. To help the family cope with the
numerous procedures they must learn.
5. Adequate preparation before discharge
and written instructions are essential.
6. Encourage parents to look first at the
infant if an alarm goes off and ensure
the infant is breathing, and then
determine the cause of the alarm.
7. Nurses, especially those involved in the
care at home, must become familiar
with the equipment, including its
advantages and disadvantages.
Safety is a major concern because monitor
can cause electrical burns and electrocution.
The following precautions are recommended:
Electrode placement for apnea monitoring. In
small infants, one fingerbreadth may be used.
✓ Remove leads from infant when not
attached to the monitor.
✓ Unplug the power cord from the
electrical outlet when the cord is not
plugged into the monitor.
✓ Use safety covers on electrical outlets
to discourage children from inserting
objects into sockets.
Home apnea monitor uses a soft belt with a
Velcro attachment to hold two leads in the
appropriate position on the chest.
2F
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
ALTE: TAKE NOTE!
If the infant is apneic, gently stimulate the trunk
by patting or rubbing it. Call loudly for help
even if alone. If the infant is prone, turn to the
back and flick the heels of the feet. If there is
still no response, immediately begin CPR,
starting with chest compressions. After
approximately 2 minutes of CPR, activate the
emergency medical service – “CALL 911!”and
then resume CPR until emergency responders
arrive or the infant starts breathing. Never
vigorously shake the child. No more than 10
seconds are spent on stimulation before
implementing CPR.
stimulation < IOS
SUDDEN INFANT DEATH SYNDROME
URGENT RESPIRATORY THREATS
Sudden death of an infant younger than 1 year
of age that remains unexplained after a
complete postmortem examination, including
an investigation of the death scene, and a
review of the case history.
Sudden Unexpected Early Neonatal Death
(SUEND) and Sudden Unexpected Infant
Death (SUID) share similar features but differ
in regards to the timing of death.
abnormalities
disorders.
in
CNS
and
respiratory
Health Status – History of Illness
Sleep Habits – Prone
Siblings – Siblings of SIDS victims
Maternal – Young age; cigarette smoking,
poor postnatal care and etc.
SIDS: Etiology
One hypothesis → Related to a brainstem
abnormality in the neurologic regulation of
cardiorespiratory control. → Affects arousal
and physiologic responses to a life-threatening
challenge during sleep.
Abnormalities include:
✓ Prolonged sleep apnea
✓ Increased frequency of brief inspiratory
pauses
✓ Excessive periodic breathing
✓ Impaired arousal responsiveness to
increased carbon dioxide or decreased
oxygen.
SLEEP APNEA IS NOT THE CAUSE OF
SIDS.
SUEND – Occurs in the first week of life.
SUID – Death in the postneonatal period.
SIDS: Epidemiology
Peak Age – 2 to 3 months, 95% occur by 6
months
2F
Sex – Higher % are Boys
Time of Death – During sleep
Time of Year – Increased incidence in winter.
Socioeconomic – Lower socioeconomic class.
Birth – Higher % in preterm infants → ELBW
and VLBW; multiple births; low APGAR;
Genetic Predisposition – To SIDS has been
postulated as a cause, chromosome 6q was
positively linked to a syndrome of SIDS and
dysgenesis of the testis.
Risk Factors for SIDS:
a) Underlying infant vulnerability factor
o Brain abnormality – A critical
incident
in
the
fetal
developmental period or in early
neonatal
life
and
an
environmental stressor such as
prone sleep positioning.
b) Maternal Smoking – Major factor in
SIDS.
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2F – SICK GROWING CHILD
c) Maternal Alcohol Use
d) Cosleeping – Infant sharing a bed with
an adult or older child on a noninfant
bed.
e) Prone
Sleeping
–
Causes
oropharyngeal obstruction or affect
thermal balance or arousal state.
f) Side-Lying Position – No longer
recommended for infants sleeping at
home, day care, or hospitals (unless
medically indicated).
g) Soft Bedding – Such as waterbeds,
sheepskins, beanbags, pillows, and
quilts should be avoided for infant
sleeping surfaces.
h) Viral respiratory or botulism infection.
i) Pulmonary Edema
j) Brainstem Abnormalities
k) Neurotransmitter Deficiencies
l) Heart Rate Abnormalities
m) Distorted familial breathing patterns.
n) Decreased arousal responses.
o) Possible lack of surfactant in alveoli.
Protective Factors for SIDS:
a) Breastfeeding – First 16 weeks of life.
b) Pacifier Use
c) Supine Position
d) Updated Immunization Status
Infant Risk Factors for SIDS:
a) Low birth weight or preterm birth (<37
weeks’ gestation)
b) Low APGAR Scores
c) Recent Viral Illness
d) Siblings of two or more SIDS victims
e) Male Gender
f) Infants of Native American or AfricanAmerican Ethnicity
2F
HOME
MONITORING
IS
NOT
RECOMMENDED FOR THIS GROUP OF
CHILDREN.
SIDS: Nursing Care Management
1. Educating families about the risk of
prone sleeping position in infants from
birth to 6 months of age, use of
appropriate
bedding
surfaces,
association with maternal smoking, and
the dangers of cosleeping on noninfant
surfaces.
2. Nurses have an important role in
modeling behaviors for parents to foster
practices that decrease the risk of
SIDS, including placing infants in a
supine sleeping position in the hospital.
3. Promote supine sleep positions at
home. (Can also be side-lying
positions)
4. Nurses must be proactive in further
decreasing the incidence of SIDS;
postpartum
discharge
planning,
newborn discharges, follow-up home
visits, well-baby clinic visits, and
immunization visits provide excellent
opportunities to educate parents about
safe sleep environment for infants and
other protective factors for SIDS.
5. Nurses must continue to take every
opportunity to advocate for infants by
providing information for parents and
caretakers about the modifiable risk
factors for SIDS that can be
implemented to prevent its occurrence
across all sectors of the population.
6. Parents should be counseled by a
nurse or someone else trained in
counseling at the time of the infant’s
death. It helps if they can talk to this
same person periodically for however
long it takes to resolve their grief.
7. Autopsy reports should be given to
parents asap.
8. Reading that their child’s death was
unexplained can help to reassure
parents the death was not their fault.
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2F – SICK GROWING CHILD
TAKE NOTE!
Practices that may reduce the risk of SIDS:
✓ Avoid smoking during pregnancy and near
the infant.
✓ Using supine sleeping position.
✓ Avoiding soft, moldable mattresses,
blankets, and pillows.
✓ Avoid bed sharing.
✓ Breastfeeding
✓ Avoid overheating during sleep
hypoxemia
hypoxia
hypercapnia
RESPIRATORY FAILURE
URGENT RESPIRATORY THREATS
An inadequate supply of oxygen results in
blood hypoxemia and tissue hypoxia;
inadequate carbon dioxide removal causes
hypercapnia. Often both gases may be
insufficiently exchanged.
Respiratory Insufficiency – applied to two
conditions:
a) When there is increased work of
breathing but gas exchange function
remains near normal.
b) When normal blood gas tensions
cannot be maintained and hypoxemia
and acidosis develop secondary to
carbon dioxide retention.
Respiratory Failure – Inability of the
respiratory apparatus to maintain adequate
gas exchange.
o This process involves pulmonary
dysfunction that generally results in
impaired
alveolar-capillary
gas
exchange, which can lead to
hypoxemia or hypercapnia.
2F
Respiratory Arrest – Cessation of respiration.
12
Apnea – Cessation of breathing for more than
20 seconds, or for a short period when
associated with hypoxemia or bradycardia.
Effective pulmonary gas exchange requires:
✓ Clear airways
✓ Normal lungs and chest wall
✓ Adequate pulmonary circulation
Diagnosis of Respiratory Failure
Is determined by the combined application of
three sources of information:
1. Presence or history of a condition that
might predispose to respiratory failure.
2. Observation of respiratory failure.
3. Measurement of ABGs.
Predisposing Factors:
Obstructive Lung Disease – There is
increased resistance to airflow in either the
upper or the lower respiratory tract.
✓ Obstruction
▪ Tracheomalacia Strached collapse)
▪ Choanal Atresia
▪ Vocal Paralysis
✓ Aspiration
▪ Meconium
▪ Mucus
▪ Vomitus
▪ FB
✓ Infection
▪ Epiglottis
▪ Pneumonia
▪ Pertusis
▪ Severe Tonsillitis
✓ Laryngospasm from local irritation
▪ Intubation
▪ Drowning
▪ Aspiration
S
&
MINGUITO, SHANIA D. | BSN 2-B
2F – SICK GROWING CHILD
Restrictive Lung Disease – Impaired lung
expansion results from loss of lung volume,
decreased distensibility, or chest wall
disturbance.
Causes:
RDS
Pulmonary Edema
Pleural Effusion
Near Drowning
Congenital Diaphragmatic Hernia
Abdominal Distention
Muscular Dystrophy
Paralytic Conditions (e.g., poliomyelitis,
botulism)
✓ Severe Structural Obstructions (e.g.,
sever scoliosis)
✓
✓
✓
✓
✓
✓
✓
✓
Primary Inefficient Gas Transfer –
Insufficient alveolar ventilation for carbon
dioxide removal or impaired oxygenation of
pulmonary capillary blood as a result of
dysfunction of the respiratory control
mechanism.
Causes of respiration center depression
include:
✓ Cerebral trauma (e.g., birth injuries,
shaken baby syndrome)
✓ Intracranial tumors
✓ CNS Infection (e.g., meningitis,
encephalitis, sepsis)
✓ Overdose with barbiturates, opioids, or
benzodiazepines
✓ Sever Asphyxia (e.g., hypercapnia,
hypoxemia)
✓ Tetanus
2F
Recognition of Respiratory Failure:
1. Insufficient alveolar ventilation leads to
hypoxemia and hypercapnia.
2. Evaluation of respiratory adequacy is
based on both clinical assessment and
laboratory studies.
3. In clinical situations in which impaired
ventilation can be anticipated or clinical
manifestations indicate impending
hypoxemia, serial measurements of
blood gases should be obtained and
monitored
to
detect
impending
respiratory failure, and therapy should
be implemented before respiratory
acidosis becomes extreme.
Respiratory
Management
Failure:
Nursing
Care
1. Recognize
the
situation
and
immediately
initiate
resuscitative
measures, such as opening the airway
and
positioning,
administering
supplemental oxygen and positive
pressure
ventilation,
suctioning,
performing CPR, or intubating if the
child’s status continues to deteriorate.
2. When the situation is not an arrest, the
suspicion of respiratory failure is
confirmed by assessment, and the
severity is defined by capillary or
arterial blood gas analysis.
3. When severity is established, an
attempt is made to determine the
underlying
cause
by
thorough
evaluation.
Specific Therapies – Directed
reversal of the causative factors.
toward
Nonspecific Therapies – Necessary to
maintain oxygenation and enhance carbon
dioxide removal until specific methods take
effect.
MINGUITO, SHANIA D. | BSN 2-B
13
2F – SICK GROWING CHILD
The major reasons for implementing
nonspecific treatments are:
1. Unknown etiology
2. Lack of specific treatment for a known
cause.
3. Lack of time for a specific treatment to
take effect, and
4. Need for specialized personnel or
equipment for specific treatment.
The principles of management are to:
1. Maintain ventilation and maximize
oxygen delivery.
2. Correct hypoxemia and hypercapnia.
3. Treat the underlying cause.
4. Minimize
extra-pulmonary
organ
failure.
5. Apply specific and nonspecific therapy
to control oxygen demands, and
6. Anticipate complications. Monitoring
the patient’s condition is critical.
Observation and Monitoring:
✓ Nurse monitors the child to anticipate
respiratory failure, determine a course
of action, and assess the patient’s
response to treatment.
✓ If close, continuous monitoring is
required, the child is transferred to a
pediatric
intensive
care
unit.
Observation is geared toward general
appearance, responsiveness, pulse
oximetry, and vital signs.
✓ Prone
positioning
improves
oxygenation and lung mechanics.
✓ Nurse monitors the child’s cardiac and
respiratory status by observation and
electronic means.
✓ Goal of therapy is to control the body’s
oxygen demands, assessments of
fever and pain should be frequent.
✓ Measure oxygenation by the use of
pulse oximetry or blood gas monitoring.
2F
Clinical
Failure
Manifestations
of
14
Respiratory
Cardinal Signs:
o Restlessness
o Tachypnea
o Diaphoresis
Early but Less Obvious Signs:
o Mood changes
o Headache
o Altered
depth
and
pattern
of
respirations
o Hypertension
o Exertional dyspnea
o Anorexia
o Increased cardiac output and urinary
output
o CNS Symptoms
o Nasal Flaring
o Expiratory Grunting
o Wheezing
Signs of More Severe Hypoxia:
o
o
o
o
o
o
o
o
o
o
Hypotension
Depressed respirations
Dimness of Vision
Bradycardia
Arrythmias
Somnolence (drowsy , sleepy)
Cyanosis
Stupor
(near
Coma
Dyspnea
unconsciousness)
Nursing Observation for the Child with
Respiratory Failure:
Observation of respiratory effort or distress –
Nasal flaring, grunting, gasping, retractions,
agonal respirations.
Observation of diaphragmatic movement, lung
expansion, and use of accessory muscles –
Depth, symmetry, inspiration/expiration ratio.
MINGUITO, SHANIA D. | BSN 2-B
2F – SICK GROWING CHILD
Auscultation of chest to assess:
✓ Breath sounds – presence, intensity,
quality, symmetry
✓ Abnormal sounds – stridor, wheezes,
crackles, rhonchi, increase or decrease
in sounds
✓ Endotracheal tube placement and need
for suction
Visual inspection of skin color, capillary refill.
Observation of activity level and level of
consciousness.
CROUP SYNDROME
REACTIVE AIRWAY DISORDERS
Croup – General term applied to a group of
symptoms characterized by hoarseness, a
resonant cough described as “barking” or
“brassy” (croupy), varying degrees of
inspiratory stridor, and varying degrees of
respiratory distress resulting from swelling or
obstruction in the region of the larynx.
1. Acute Epiglottitis
2. Acute LTB
3. Acute Spasmodic Laryngitis
4. Acute Tracheitis
➔ H. influenza type B
o Parainfluenza virus
o Influenza types A and B
o Human coronavirus
o Rhinoviruses
o Enteroviruses
o Metapneumoviruses
o Adenoviruses
o RSV
o Measles
➔ Mycoplasma pneumonia – can also
cause coup.
2F
CROUP: Acute Epiglottitis (2 to 5 years old)
➔ Noninfectious
➔ Obstructive inflammatory process.
o Causative Agent: H. influenza
o Caustic Agents: Hot foods,
smoke
inhalation,
foreign
bodies, and exposure to crack
cocaine.
➔ Three clinical observations that are
predictive of epiglottis are absence of
spontaneous cough, presence of
drooling, and agitation.
➔ Manifestations: Child is irritable,
restless, voice is thick and muffled,
froglike croaking sound on inspiration.
Not
hoarse,
suprasternal
and
substernal retractions may be visible.
➔ Struggles to breathe, slow, quiet
breathing provides better air exchange.
➔ Throat is red and inflamed, and a
distinctive,
large,
cherry
red,
edematous epiglottis is visible on
careful throat inspection.
o Throat inspection should only be
performed when immediate
endotracheal
intubation
or
emergency tracheotomy can be
performed if needed.
CROUP: Acute Epiglottitis Therapeutic
Management, Prevention, and Nursing
Care Management
➔ Progressive obstruction leads to:
o hypoxia
o hypercapnia
o acidosis
o decreased muscular tone
o reduced level of consciousness
o sudden death
➔ Lateral neck radiograph of the soft
tissues is indicated for diagnosis.
➔ Nasotracheal intubation → for RDS
➔ Swelling decreases after 24 hours of
antibiotic therapy.
➔ Corticosteroids for reducing edema.
MINGUITO, SHANIA D. | BSN 2-B
15
2F – SICK GROWING CHILD
➔ Recommended
to
receive
H.
influenzae type B conjugate vaccine
beginning at 2 months of age.
✓ Act quickly but calmly and provide
support without unduly increasing
anxiety.
✓ Child is allowed to remain in the
position that provides the most comfort
and security.
✓ Droplet isolation precautions are
indicated for 24 hours after initiation of
effective antibiotic therapy to control
spread of respiratory organisms.
✓ Nurses who suspect epiglottitis should
not attempt to visualize the epiglottitis
directly with a tongue depressor or take
a throat culture but should have the
child seen by the primary care provider
immediately.
✓ Resuscitation equipment and suction
should be immediately available and
ready at the child’ bedside.
CROUP: Acute Laryngitis
Causative Agents: Viruses
Therapeutic and Nursing Care Management
The disease is almost always self-limiting
without long-term sequelae. Treatment is
supportive with fluids and humidified air.
CROUP: Acute Laryngotracheobronchitis
AKA LTB → Affects children less than 5 years
of age.
2F
Organisms responsible:
1. parainfluenza virus types 1 and 2
2. parainfluenza virus type 3
3. RSV
4. influenza types A and B
5. measles
6. M. pneumoniae
➔ Onset of low-grade fever. Child wakes
up with barky, brassy cough at times
inspiratory stridor.
➔ Symptoms got worse at night, and
agitation and crying tend to exacerbate
the symptoms.
➔ Manifested by nasal flaring, intercostal
retractions, tachypnea, and continuous
stridor.
➔ Develops the classic barking or seallike cough and acute stridor after
several days of rhinitis.
➔ Can lead to respiratory acidosis or
respiratory failure.
LTB Therapeutic Management and Nursing
Care Management
➔ Major Objective: Maintain an airway
and providing for adequate respiratory
exchange.
➔ Cool mist, cool air vaporizer, cool
temperature therapy.
➔ Nebulized epinephrine is used in
children with croup that is not alleviated
with cool mist.
➔ Corticosteroids – decrease subglottic
edema.
➔ Severe Cases → helium + oxygen
(heliox) may reduce the work of
breathing and relieve the airway
obstruction.
➔ Continue to drink beverages they like.
➔ Children with severe respiratory
distress (traditionally, a respiratory rate
>60 breaths/min for infants) should not
be given anything by mouth to prevent
aspiration and increased work of
breathing.
✓ Monitor,
observe,
and
proper
assessment. – Cardiac, respiratory,
and pulse oximetry.
✓ Early signs of impending airway
obstruction include increased pulse and
respiratory
rate;
substernal,
suprasternal,
and
intercostal
MINGUITO, SHANIA D. | BSN 2-B
16
2F – SICK GROWING CHILD
retractions; nasal flaring; and increased
restlessness.
✓ Rest, sit upright, or children wanted to
be held.
CROUP: Acute Spasmodic Laryngitis
AKA MIDNIGHT CROUP or TWILIGHT
CROUP – Characterized by paroxysmal
attacks of laryngeal obstruction that occur at
night. Child awakes suddenly with the
characteristic barking,
metallic cough;
hoarseness;
noisy
inspirations;
and
restlessness.
Therapeutic
Management
and
Nursing
Care
✓ Managed at home. Cool mist is
recommended.
✓ Warm mist provided by steam from hot
running water may be helpful.
✓ Hospitalized for moderate to severe
symptoms.
✓ Corticosteroid therapy.
CROUP: Bacterial Tracheitis (5 to 7 years
old)
Infection of the mucosa and soft tissues of the
upper trachea.
o Complication of LTB.
o Thick, purulent tracheal secretions.
o May develop a life-threatening upper
airway obstruction, respiratory failure,
ARDS, and multiple organ dysfunction.
Organism responsible:
-
Staphylococcus aureus
M. catarrhalis
S. pneumoniae
S. pyogenes
H. influenzae
2F
Therapeutic
Management
and
Nursing
Care
✓ Antipyretics, fluid status, and antibiotics
(10-day course)
✓ Endotracheal
intubation
and
mechanical ventilation
ASTHMA
REACTIVE AIRWAY DISORDERS
Chronic inflammatory disorder of the airways
characterized by recurring symptoms, airway
obstruction,
and
bronchial
hyperresponsiveness.
Atopy – Genetic predisposition for the
development of an IgE-meditated response to
common aeroallergens, is the strongest
identifiable predisposing factor for developing
asthma.
Exaggerated response of bronchi to a trigger
such as URI, dander, cold air, exercise.
- bronchospasm, exudation, and edema
of bronchi
- infancy to adolescence or adulthood
- wheezing, chest tightens, cough,
labored respirations
- Treatment: inhaled corticosteroids,
bronchodilators, leukotriene modifiers,
allergen, and control of triggers.
Organisms responsible:
- viruses – RSV in infants, variety of URI
pathogens
AIM
MINGUITO, SHANIA D. | BSN 2-B
17
2F – SICK GROWING CHILD
STATUS ASTHMATICUS
REACTIVE AIRWAY DISORDERS
Medical emergency that can result in
respiratory failure and death if unrecognized
and untreated.
➔ therapy for status asthmaticus is aimed
at improving ventilation, decreasing
airway
resistance
and
reliving
bronchospasm, correcting dehydration
and acidosis, allaying child and parent
anxiety related to the severity of the
event, and treating any concurrent
infection
18
NEONATAL RESPIRATORY DISTRESS
SYNDROME
LOWER AIRWAY DISORDERS
Surfactant
deficiency
immaturity of the thorax.
and
physiologic
➔ chronic intrauterine stress (e.g.,
maternal
preeclampsia
or
hypertension)
➔ nonpulmonary cause – sepsis, cardiac
defects
More details on Module 1F.
BRONCHOPULMONARY DYSPLASIA
Asthma & S. Asthmaticus: NCM:
✓ acute asthma care
✓ pulse oximetry is monitored along with
rate and depth of breathing
✓ auscultation
of
air
movement,
adventitious sounds, and any signs of
respiratory distress
✓ child w/ s. asthmaticus should be
placed on continuous cardio-respiratory
(including BP) and pulse oximetry
monitoring
✓ avoid allergens
✓ relieve bronchospasm
✓ promote self-care and normalization
✓ child and family support
2F
LOWER AIRWAY DISORDERS
Chronic lung disease, is a pathologic process
that develops primarily in ELBW and VLBW
interstitial edema
infants with RDS.
epithelial swelling
thickening& Fibrotic
walls
More details on Module 1F.
C
T
prolif of alveolar
.
CYSTIC FIBROSIS
LOWER AIRWAY DISORDERS
Exocrine
(mucus-producing)
gland
dysfunction that produces multisystem
involvement.
- autosomal recessive trait
- inherits defective gene from both
parents
- Cystic
Fibrosis
Transmembrane
Regulator (CFTR) → codes a protein of
1480 amino acids
- mechanical obstruction caused by
increased viscosity of mucous gland
secretions
- produces thick, heavy mucoprotein that
accumulates and dilates
- small organs like pancreas and
bronchioles become obstructed
- retained mucus serves as an excellent
medium for bacterial growth
- viscous and tenacious secretions are
difficult to expectorate and gradually
obstruct the bronchi and bronchioles,
causing
scattered
areas
of
MINGUITO, SHANIA D. | BSN 2-B
2F – SICK GROWING CHILD
bronchiectasis,
hyperinflation
ateltectasis,
and
TAKE NOTE: REINFORCEMENT
Is a disease of exocrine gland function that
involves multiple organ systems but results in
chronic respiratory infection.
Common symptoms are:
- progressive chronic obstructive lung
disease associated with infection
- maldigestion from exocrine pancreatic
insufficiency
- growth failure from malabsorption and
anorexia
- diabetes symptoms of hyperglycemia,
polyuria, glycosuria and weight loss
from pancreatic insufficiency
-salty sweat
Signs of a pneumothorax are usually
nonspecific and include tachypnea,
tachycardia,
dyspnea,
pallor,
and
cyanosis. A subtle drop in oxygen
saturation (measured by pulse oximetry)
may be an early sign of pneumothorax.
2F
Therapeutic
Management
and
Nursing
Care
✓ prevent or
minimize pulmonary
complications
✓ ensure adequate nutrition for growth
✓ encourage appropriate physical activity
✓ promote reasonable quality of life
✓ Pulmonary Assessment – special
attention to lung sounds, observation of
cough, and evidence of decreased
activity or fatigue
✓ Gastrointestinal
Assessment
–
Observing the frequency and nature of
the stools and abdominal distention
✓ must be alert to evidence of growth
failure or failure to thrive
✓ determine the child’s eating and
eliminating habits and confirm a history
of frequent respiratory tract infections or
bowel obstruction in infancy
✓ assess newborn for feeding and
stooling patterns
✓ nurse anticipates diagnostic testing
such as initial newborn screening,
immunoreactive trypsinogen, DNA
analysis, or sweat chloride test
Flutter mucus clearance device – Small,
handheld plastic pipe with a stainless-steel ball
on the inside. Acapella provides highfrequency oscillation as well as PEP.
MINGUITO, SHANIA D. | BSN 2-B
19
2F – SICK GROWING CHILD
Patent Ductus Arteriosus
BRONCHITIS
PDA
LOWER AIRWAY DISORDERS
CHD - ACYANOTIC DEFECTS NON-OBSTRUCTIVE
LESIONS
Inflammation of the large airways (trachea and
bronchi) that is frequently associated with a
URI.
dry, hacking, nonproductive cough
worsens at night
first 4 years of life
productive in 2 or 3 days
requires only symptomatic treatment
including analgesics, antipyretics, and
humidity
- Treatment: Cough suppressants
-
Organisms responsible:
✓ viral
✓ M. pneumoniae
✓ bacteria, fungi,
airborne irritants
Failure of the fetal ductus arteriosus (artery
connecting the aorta and pulmonary artery) to
close within the first weeks of life. The
continued patency of this vessel allows blood
to flow from the higher-pressure aorta to the
lower-pressure pulmonary artery, which
causes a left-to-right shunt.
➔ machinery-like murmur
➔ widened pulse pressure and bounding
pulses result from runoff of blood from
the aorta to the pulmonary artery
Treatment:
allergic
disorders,
BRONCHIOLITIS
LOWER AIRWAY DISORDERS
Most common infectious disease of lower
airways. Acute viral infection with maximum
effect at bronchiolar level.
- occurs in winter and spring
- 2-12 mos. of age; rare after 2 years
- labored respirations, poor feeding,
cough, tachypnea, retractions, flaring
nares, emphysema, increased nasal
mucus, wheezing, may have fever
- Treatment:
Provide
supplemental
oxygen
if
saturations
≤90%;
bronchodilators (optional), suction
nasopharynx, ensure adequate fluid
intake, maintain adequate oxygenation.
2F
Organisms responsible:
✓ caused by RSV, adenoviruses, and
parainfluenza viruses, human metapneumovirus,
Mycoplasma
pneumoniae
Medical – Administer indomethacin.
Surgical – Surgical division/ligation, videoassisted thoracoscopic surgery.
Nonsurgical – Coils to occlude the PDA.
Atrial Septal Defect
ASD
CHD - ACYANOTIC DEFECTS NON-OBSTRUCTIVE
LESIONS
Abnormal opening between the atria, allowing
blood from the higher-pressure left atrium to
flow into the lower-pressure right atrium. There
are three types of atrial septal defect (ASD).
➔ Ostium primum (ASD 1) – Opening at
lower end of septum; may be
associated
with
mitral
valve
abnormalities.
➔ Ostium secundum (ASD 2) – Opening
near center of septum.
➔ Sinus Venosus Defect – Opening near
junction of superior vena cava and right
atrium; may be associated with partial
anomalous
pulmonary
venous
connection.
➔ Left atrial pressure slightly exceeds
right atrial pressure, blood flows from
the left to the right atrium, causing an
increased flow of oxygenated blood into
the right side of the heart.
MINGUITO, SHANIA D. | BSN 2-B
20
2F – SICK GROWING CHILD
➔ Asymptomatic, may develop heart
failure, characteristic murmur
➔ RISK FOR ATRIAL DYSRHYTHMIAS
ATRIOVENTRICULAR SEPTAL
CHD - ACYANOTIC DEFECTS NON-OBSTRUCTIVE
LESIONS
Incomplete fusion of the endocardial cushions.
Consists of a low ASD that is continuous with
a high VSD and clefts of the mitral and
tricuspid valves, which creates a large central
atrioventricular (AV) valve that allows blood to
flow between all four chambers of the heart.
➔ the directions and pathways of flow are
determined by pulmonary and systemic
resistance, left and right ventricular
pressures, and the compliance of each
chamber
➔ flow is generally from LEFT TO RIGHT
➔ most common cardiac defect in children
DOWN SYNDROME
➔ MINIMUM SHUNTING OF BLOOD –
left-to-right shunting occurs and
pulmonary blood flow increases
VENTRICULAR SEPTAL
CHD - ACYANOTIC DEFECTS NON-OBSTRUCTIVE
LESIONS
Abnormal opening between the right and left
ventricles. May be classified according to
location: membranous (accounting for 80%) or
muscular. May vary in size from a small
pinhole to absence of the septum, which
results in a common ventricle.
➔ VSDs – most likely occur during the first
year of life in children having small or
moderate defects.
➔ because of the higher pressure within
the LEFT VENTRICLE and because
the systemic arterial circulation offers
more resistance than the pulmonary
circulation
➔ blood flows through the DEFECT INTO
THE PULMONARY ARTERY
2F
PULMONIC STENOSIS
CHD - ACYANOTIC DEFECTS OBSTRUCTIVE LESIONS
Narrowing at the entrance to the pulmonary
artery. Resistance to blood flow causes right
ventricular hypertrophy and decreased
pulmonary blood flow. Pulmonary atresia is the
extreme form of pulmonic stenosis (PS) is that
there is total fusion of the commissures and no
blood flows to the lungs. The right ventricle
may be hypoplastic.
➔ PS is present = resistance to blood flow
causes right ventricular hypertrophy
➔ result in reopening of the foramen
ovale, shunting of unoxygenated blood
into the left atrium, and systemic
cyanosis
➔ newborns w/ severe narrowing are
cyanotic
AORTIC STENOSIS
CHD - ACYANOTIC DEFECTS OBSTRUCTIVE LESIONS
Narrowing or stricture of the aortic valve,
causing resistance to blood flow in the left
ventricle, decreased cardiac output, left
ventricular hypertrophy, and pulmonary
vascular congestion.
➔ the prominent anatomic consequence
of aortic stenosis (AS) – is hypertrophy
of the LEFT VENTRICULAR WALL
➔ left ventricular hypertrophy also
interferes
with
coronary
artery
perfusion and may result in myocardial
infarction
➔ VALVULAR STENOSIS – most
common type usually caused by
malformed cusps
VALVULAR STENOSIS is a serious defect
because:
1. Obstruction tends to be progressive.
2. Sudden episodes of myocardial
ischemia/low cardiac output, can result
in sudden death.
3. Surgical repair rarely results in a normal
valve.
MINGUITO, SHANIA D. | BSN 2-B
21
2F – SICK GROWING CHILD
narrow part of aorta
COARCTATION OF THE AORTA
CHD - ACYANOTIC DEFECTS OBSTRUCTIVE LESIONS
Localized narrowing near the insertion of the
ductus arteriosus, which results in increased
pressure proximal to the defect (head and
upper extremities) and decreased pressure
distal to the obstruction (body and lower
extremities).
➔ narrowing within the aorta is increased
pressure proximal to the defect (upper
extremities) and decreased pressure
distal to it (lower extremities)
➔ high blood pressure and bounding
pulses in arms, weak or absent femoral
pulses, cool lower extremities with
lower blood pressure
TRANSPOSITION OF THE GREAT
ARTERIES
CYANOTIC DEFECTS
Pulmonary artery leaves the left ventricle, and
the aorta exists from the right ventricle, with no
communication between the systemic and
pulmonary circulations.
➔ SEPTAL DEFECTS/PDA must be
present to permit blood to enter the
systemic circulation or the pulmonary
circulation for mixing of saturated and
desaturated blood
➔ MOST COMMON DEFECT = Patent
Foramen Ovale
➔ severely cyanotic
Atresia
-
not normal
opening
HYPOPLASTIC LEFT HEART SYNDROME
(4) TETRALOGY OF FALLOT
CYANOTIC DEFECTS
The classic form includes four defects:
USD 1. ventricular septal defect (VSD)
stenosis
BSA 2.3. pulmonic
overriding aorta
RVH 4. right ventricular hypertrophy
➔ an example of acyanotic heart defect
➔ if pulmonary vascular resistance is
higher than systemic resistance, the
shunt is from RIGHT TO LEFT
➔ if systemic resistance is higher than
pulmonary resistance the shunt is LEFT
TO RIGHT
➔ cyanosis,
characteristic
murmur,
hypoxia – blue spells, emboli, seizures,
loss of consciousness/SID
2F
LESS COMMON CONGENITAL HEART DEFECT
Underdevelopment of the left side of the heart,
resulting in a hypoplastic left ventricle and
aortic atresia. Most blood form the left atrium
flows across the patent foramen ovale to the
right atrium, to the right ventricle, and out the
pulmonary artery.
➔ descending aorta receives blood from
the patent ductus arteriosus supplying
systemic blood flow
➔ the amount of blood flow to the
pulmonary and systemic circulations
depends on the relationship between
the pulmonary and systemic vascular
resistances
➔ the coronary and cerebral vessels
receive blood by RETROGRADE
FLOW through the HYPOPLASTIC
ASCENDING AORTA.
➔ mild cyanosis, dec. cardiac output, CVC
➔ FATAL IN FIRST MONTHS OF LIFE
WITHOUT INTERVENTION
MINGUITO, SHANIA D. | BSN 2-B
22
2F – SICK GROWING CHILD
TAP VR
TRICUSPID ATRESIA/PULMONARY
ATRESIA
TOTAL ANOMALOUS PULMONARY
VENOUS RETURN
LESS COMMON CONGENITAL HEART DEFECT
LESS COMMON CONGENITAL HEART DEFECT
The tricuspid valve fails to develop.
➔ no communication from the RIGHT
ATRIUM to the RIGHT VENTRICLE
➔ blood flows through an ATRIAL
SEPTAL DEFECT (ASD) / patent
foramen ovale to the left side of the
heart
➔ COMPLETE
MIXING
OF
UNOXYGENATED
AND
OXYGENATED BLOOD IN THE LEFT
SIDE OF THE HEART
➔ VSD – right ventricle and out to the
lungs
➔ cyanosis, tachycardia, dyspnea
Rare defect characterized by failure of the
pulmonary veins to join the left atrium. Instead,
the pulmonary veins are abnormally
connected to the systemic venous circuit via
the right atrium or various veins draining
toward the right atrium, such as the superior
vena cava.
➔ MIXED BLOOD BEING RETURNED to
the RIGHT ATRIUM and shunted from
the right to the left through an ASD –
Atrial Septal Defect.
➔ TAPVC – Total Anomalous Pulmonary
Venous Connection
➔ cyanosis, asymptomatic
➔ w/o intervention = CF / death
"common truncus"
TRUNCUS ARTERIOSUS
LESS COMMON CONGENITAL HEART DEFECT
Failure of normal septation and division of t he
embryonic bulbar trunk into the pulmonary
artery and the aorta.
TAPVC classified as follows:
1. Supracardiac – Attachment above the
diaphragm, such as to the superior
vena cava.
2. Cardiac – Direct attachment to the
heart, such as to the right atrium or
coronary sinus.
3. Infradiaphragmatic – Attachment
below to the diaphragm, such as to the
inferior vena cava (most severe form).
➔ PREFERENTIAL BLOOD FLOW TO
THE LUNGS
➔ results in development of SINGLE
VESSEL that OVERRIDES both
ventricles
➔ blood from both ventricles MIXES in
the COMMON GREAT ARTERY –
leads to desaturation and hypoxemia
➔ Symptomatic, Mod. – Severe HF,
cyanosis,
poor
growth,
activity
intolerance
2
common vessel instead of
-
single
Type 1 – A single pulmonary trunk arises near
the base of the truncus and divides into the left
and right pulmonary arteries.
2F
Type 2 – The left and right pulmonary arteries
arise separately but in close proximity and at
the same level from the back of the truncus.
Type 3 – The pulmonary arteries arise
independently from the sides of the truncus.
MINGUITO, SHANIA D. | BSN 2-B
23
2F – SICK GROWING CHILD
SBE
RHEUMATIC FEVER
ACQUIRED HEART DISEASE
Occurs after pharyngitis caused by group A Bhemolytic streptococci (GABHS). Self-limiting
illness that involves the joints, skin, brain,
serous surfaces, and heart.
Rheumatic Heart Disease – Cardiac valve
damage, most significant complication of RF.
- Ages 5 to 14 years old
- principal manifestations are observed
in the heart, joints, skin, and central
nervous system
- major cardiac manifestation involves
valvular endocardium, pericardium, and
myocardium
- most commonly associated in mitral
valve
Aschoff Bodies – Inflammatory hemorrhagic
bullous lesions are formed which cause
swelling, fragmentation, and alterations in the
connective tissue.
- these lesions occur at the heart, blood
vessels, brain, and serous surfaces of
the joints and pleura
↳
-
Subacute Endocarditis
✓ 10-day course for initial therapy of
Penicillin or an alternative antibiotic.
✓ SBE
prophylaxis
is
NOT
RECOMMENDED.
✓ Salicylates are used to reduce fever
and discomfort and to control the
inflammatory process, especially in the
joints.
✓ Prednisone administration may be
indicated in some patients with heart
failure.
INFECTIOUS ENDOCARDITIS
ACQUIRED HEART DISEASE
➔ infection of the valves and inner lining
of the heart
➔ potentially damage or destroy the heart
valves with high morbidity and mortality
for affected pts.
➔ children
with
CONGENITAL
ANOMALIES OF HEART/GREAT
VESSELS
➔ children with indwelling catheters are
also at risk – affecting the mitral/aortic
valve
➔ fever, malaise, murmur
Organisms responsible:
Rheumatic Fever: Therapeutic and Nursing
Care Management
✓ eradication of GABHS (primary
prevention)
✓ prevention of permanent cardiac
damage
✓ palliation of the other symptoms
✓ encourage compliance with drug
regimens
✓ facilitate recovery from the illness
✓ provide emotional support
✓ prevention of recurrences (secondary
prevention)
✓ Penicillin (PO or IM) remains drug of
choice,
with
macrolides
or
cephalosporins as a substitute in
penicillin-sensitive children.
2F
✓
✓
✓
✓
24
Prophylaxis
Streptococcus viridans
Staphylococcus aureus
Gram-negative bacteria, enterococcus
Fungi – Candida albicans
Therapeutic & NCM:
✓ administration of high-dose antibiotics
IV 2-8 weeks
✓ blood culture
✓ counsel parents of high-risk children
concerning the need for prophylactic
antibiotic therapy
✓ must maintain highest level of oral
health to reduce the chance of
bacteremia from oral infections
MINGUITO, SHANIA D. | BSN 2-B
2F – SICK GROWING CHILD
✓ educate pts. and families to bring
unexplained fever, weight loss, change
in behavior
Nursing Goals:
1. Preparation of child for IV infusion,
usually with an intermittent-infusion
device, and performance of several
venipunctures to draw blood for culture
and laboratory values.
2. Use of sterile technique when
administering IV antibiotics.
3. Observation for side effects of
antibiotics, especially inflammation
along venipuncture sites, along with
assessments of renal function.
4. Observation
for
complications,
including embolism and HF.
5. Education regarding the importance of
follow-up visits for cardiac evaluation,
echocardiographic monitoring, and
blood culturing.
KAWASAKI DISEASE
ACQUIRED HEART DISEASE
Acute systemic vasculitis of unknown cause.
resolves in 6 to 8 weeks
damage to the coronary arteries
dilation of the coronary arteries
winter and early spring outbreak
KD involves inflammation of the small
and medium-sized blood vessels →
coronary arteries being the most
susceptible to damage
- Inflammatory markers: C-reactive
protein
level
and
erythrocyte
sedimentation rate
-
2F
Acute Phase of KD – Begins with an abrupt
onset of high fever that is unresponsive to
antibiotics and antipyretics.
Subacute Phase of KD – Begins with
resolution of the fever and lasts until all
outward clinical signs of KD have disappeared.
If changes in the coronary arteries occur,
some enlargement or dilation is generally
evident by echocardiography during the
second week of illness.
Convalescent Phase of KD – Clinical signs of
KD have mostly resolved, but the laboratory
values are still abnormal. This phase is
complete when all blood values return to
normal (6 to 8 weeks after onset). At the end
of this stage, parents report that the child
appears to have returned to normal in terms of
temperament, energy, and appetite.
Kawasaki Disease: Therapeutic
Nursing Care Management
and
✓ Salicylate therapy
✓ Steroids, infliximab, cyclosporine
✓ Aspirin is given initially to control fever
and symptoms of inflammation.
✓ Additional anticoagulation therapy,
such as clopidogrel or warfarin
administration, may be indicated in
children with moderate or giant
coronary enlargement, respectively.
✓ Nurse must focus on symptomatic
relief, emotional support, diagnostic
assistance, medication administration,
and education of the child and family.
TAKE NOTE: REINFORCEMENT
It causes swelling and inflammation in the
walls of small to medium-sized blood vessels
that carry blood throughout the body.
MINGUITO, SHANIA D. | BSN 2-B
25
2F – SICK GROWING CHILD
ANEMIA
1. Replacement of bone marrow by
fibrous tissue or by neoplastic cells, as
in leukemia.
2. Depression of marrow activity by
irradiation, chemicals, or drugs; and
3. Interference with bone marrow activity
caused by systemic disorders such as
severe infection, chronic renal disease,
widespread
malignancy,
collagen
disease, or hypothyroidism.
IRON DEFICIENCY ANEMIA
ANEMIA - ALTERATIONS IN HEMATOLOGIC FUNCTION
Caused by an inadequate supply or loss of
iron.
inadequate supply of iron
impaired iron absorption
blood loss
excessive demands for iron required for
growth
- At birth the full-term infant has
approx. 0.5 supply or iron.
- Average of 0.8mg of iron must be
absorbed each day during the first
15 years of life.
- During the last trimester of pregnancy,
iron is transferred from the mother to
the fetus at the rate of 4mg/day.
-
IDA enhances the leakage of plasma proteins,
which causes edema; retarded growth; and
decreased serum concentration of the proteins
album, gamma globulin, and transferrin.
- Iron supplements are administered in
two divided doses between meals,
when the presence of free hydrochloric
acid is greatest, and are accompanied
by a citrus fruit or juice, which helps
reduce iron to its most soluble state.
2F
IDA: Therapeutic
Management
and
Nursing
Care
✓ Prevention is the primary goal. – Proper
nutrition and more iron supplements.
✓ Use only breast milk for the first 12
months.
✓ Iron suppl. of 1mg/kg/day should be
provided by 4 to 6 months of age in a
full-term infant. While, 2 mg/kg/day by 2
months of age in preterm infants.
✓ Administer iron drops.
✓ Limit the amount of formula to no more
than 1 L/day.
✓ Iron medication must continue for 2 to 3
months after blood values normalize to
replenish the body’s iron stores.
✓ Iron ingested in excessive quantities is
toxic, even fatal, parents should keep
no more than a 1-month supply in the
home and store it safely away from the
reach of children.
NORMOCYTIC ANEMIA
ANEMIA - ALTERATIONS IN HEMATOLOGIC FUNCTION
Normochromic (normal color) or normocytic
(normal cell size) anemia occur because of
impaired production of erythrocytes by the
bone
marrow
or
by
abnormal
or
uncompensated loss of circulating red blood
cells, as with acute hemorrhage. The red blood
cells appear normal in both color and size;
however, there are simply too few of them for
effective oxygen transport.
Etiology:
➔ breaking up of red blood cells
➔ decreased RBC production
➔ increased RBC destruction
➔ blood loss, or other etiologies
➔ acute blood loss
➔ bone marrow failure
➔ chronic disease
o Kidney disease, Rheumatoid
arthritis and thyroiditis
o Destruction (hemolysis)
MINGUITO, SHANIA D. | BSN 2-B
26
2F – SICK GROWING CHILD
Acute Blood-Loss Anemia – which can occur
from trauma such as an automobile accident
with internal bleeding from acute nephritis in
which blood is lost in the urine o in the newborn
from disorders such as placenta previa,
premature separation of the placenta,
maternal-fetal or twin-to-twin transfusion, or
trauma to the cord or placenta.
Risk Assessment:
- fatigue
- getting tired so much easily
- dizziness
- SOB
(shortness of
- lack of energy
- weakness
breath)
S/S:
- pale,
dizziness,
SOB,
fatigue,
weakness, lack of energy, irritability
Diagnostic Evaluation: CBC, reticulocyte
test, bone marrow biopsy
Therapeutic & NCM:
✓ Discontinue any drug or chemical
suspected of causing the bone marrow
dysfunction and remove the substance
from the child’s environment to avoid
exposure.
✓ Monitor the vital signs.
✓ History of alcohol intake.
✓ Provide an adequate nutritional diet.
✓ Blood transfusion
✓ Erythropoietin
✓ ATG IV Anti Thymocyte Globulin)
✓ Bone marrow biopsy
2F
SICKLE-CELL ANEMIA
ANEMIA - ALTERATIONS IN HEMATOLOGIC FUNCTION
Group of hereditary disorders, all of which are
related to the presence of HgbS.
Administration of pneumococcal, H. influenzae
type B, and meningococcal vaccines is
recommended.
TAKE NOTE: REINFORCEMENT
Is an inherited disorder characterized by
defective hemoglobin and affects the shape of
the cells.
Correct term: SCA are HgBSS Disease and
Homozygous Sickle Cell Disease
- SCA – The homozygous form of the
disease (HgbSS), in which valine, an
amino acid, is substituted for glutamic
acid at the sixth position of the B chain.
- Sickle Cell C Disease – A
heterozygous variant of SCD (HgbSC),
characterized by the presence of both
HgbS and hemoglobin C (HgbC), in
which lysine is substituted for glutamic
acid at the sixth position of the B chain.
- Sickle Thalassemia Disease –
Combination of sickle cell trait and Bthalassemia trait.
- Mode of Transmission: Genes
One of a group of diseases collectively termed
hemoglobinopathies.
Basic defect responsible for the sickling of
erythrocytes is contained in the globin fraction
of hemoglobin, which is composed of 574
amino acids.
Hemoglobinopathies –
Normal adult
hemoglobin (HgbA) is partly or completely
replaced by abnormal sickle hemoglobin
(HgbS).
MINGUITO, SHANIA D. | BSN 2-B
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2F – SICK GROWING CHILD
Manifestations of SCA:
B-THALASSEMIA
1. Obstruction caused by the sickled
RBCs.
2. Vascular inflammation
3. Increased RBC destruction.
Diagnostic Evaluation:
&
Nursing
Care
✓ Prevent sickling phenomenon.
✓ Prevent stroke.
✓ Hypoxia prevented when surgery is
necessary.
✓ Assessment of the child in sickle cell
crisis includes all areas and systems.
✓ Minimize tissue deoxygenation.
✓ Encourage screening and genetic
counseling.
✓ Promote hydration.
✓ Bed
rest
to
minimize
energy
expenditure and to improve oxygen
utilization.
✓ Hydration through oral and IV therapy.
✓ Electrolyte replacement, since hypoxia
results in metabolic acidosis, which also
promotes sickling.
✓ Analgesia for severe pain from
vasoocclusion.
✓ Blood replacement to treat anemia and
to reduce the viscosity of the sickled
blood.
✓ Antibiotic therapy to treat any existing
infection. – Penicillin
2F
Thalassemia, Greek of “Thalassa” → Sea
Inherited blood disorders characterized by
deficiencies in the rate of production of specific
globin chains in hemoglobin.
Refers to people
Mediterranean sea.
1. Stained blood smear
2. Sickle Turbidity Test (Sickledex)
3. Hemoglobin Electrophoresis
SCA: Therapeutic
Management:
ANEMIA - ALTERATIONS IN HEMATOLOGIC FUNCTION
living
near
the
Thalassemia → Excess of hemosiderin, the
iron-containing pigment from the breakdown of
hemoglobin,
results
from
decreased
hemoglobin
synthesis
and
increased
hemolysis of transfused erythrocytes.
- autosomal recessive disorder
TAKE NOTE: REINFORCEMENT
Is an autosomal recessive anemia associated
with abnormalities with the b chain of adult
hemoglobin.
Manifestations:
- anemia (before diagnosis)
- progressive anemia
o chronic hypoxia
o headache
o bone pain
o decreased exercise tolerance
o listlessness
o anorexia
- small stature
- delayed sexual maturation
- bone changes
Hemosiderosis – Excess iron storage in
various tissues of the body.
Hemochromatosis – Excess iron storage that
results in cellular damage.
MINGUITO, SHANIA D. | BSN 2-B
28
2F – SICK GROWING CHILD
B-Thalassemia: Therapeutic and Nursing
Care Management
✓ promote compliance with transfusion
and chelation therapy
✓ assist the child in coping with the
anxiety-provoking treatments and the
effects of the illness
✓ foster the child’s and family’s
adjustment to a chronic illness
✓ observe for complications of multiple
blood transfusions
✓ all families with a child with thalassemia
should be tested for the trait and
referred for genetic counseling
✓ improved physical and psychologic
well-being because of the ability to
participate in normal activities
✓ decreased
cardiomegaly
and
hepatosplenomegaly
✓ fewer bone changes
✓ normal or near-normal growth and
development until puberty, and
✓ fever infections
✓ Vit C – only to pt. who are ascorbate
depleted
✓ Deferoxamine
2F
APLASTIC ANEMIA
ANEMIA - ALTERATIONS IN HEMATOLOGIC FUNCTION
Production of the formed elements of the blood
is simultaneously depressed.
- can be congenital, or present at birth, or
acquired
- human parvovirus infection, hepatitis,
or overwhelming infection
- decreased platelet count
- bone marrow → red bone marrow to
yellow, fatty bone
Diamond-Blackfan Syndrome – Congenital
condition, marked by complete or almost
complete absence of all cells of the erythroid
series.
Fanconi
Syndrome
–
Pancytopenia,
hypoplasia of the bone marrow, and patchy
brown discoloration of the skin due to the
deposition of melanin.
Aplastic Anemia: Therapeutic and Nursing
Care Management:
✓ must restore the function of the narrow
o immunosuppressive therapy –
counter presumed immunologic
responses that prolong aplasia
o bone marrow transplantation
✓ prepare the child and family for
diagnostic and therapeutic procedures,
preventing complications from severe
pancytopenia,
and
emotionally
supporting the family in the face of
potentially fatal outcome
MINGUITO, SHANIA D. | BSN 2-B
29
2F – SICK GROWING CHILD
HEMOPHILIA
CLOTTING DISORDERS - ALTERATIONS IN
HEMATOLOGIC FUNCTION
Refers to a group of bleeding disorders
resulting
from
congenital
deficiency,
dysfunction,
or
absence
of
specific
coagulation proteins or factors.
- transmitted as an x-linked recessive
disorder
- prolonged bleeding anywhere from or in
the body
- Hemarthrosis – Refers to the bleeding
into the joint cavities.
RICE →
Elevation
Rest,
Ice,
Compression,
and
VON WILLEBRAND DISEASE
CLOTTING DISORDERS - ALTERATIONS IN
HEMATOLOGIC FUNCTION
Severe: <1% - Spontaneous bleeding without
trauma
Moderate: 1% to 5% - Bleeding with trauma
Mild: >5% to 40% - Bleeding with severe
trauma or surgery
Hemophilia: Therapeutic and Nursing Care
Management:
✓ recognize the signs that indicate
bleeding
✓ prevent bleeding
✓ bleeding episodes treated early with
factor replacement
✓ exercise and physical therapy
✓ nurse must maintain a high level of
suspicion when a child with hemophilia
shows signs such as headache; slurred
speech; loss of consciousness;
bleeding, and black tarry stools
✓ primary therapy is to replace the
missing clot factor
✓ AVOID aspirin and NSAIDs because
they inhibit platelet function
✓ However, Ibuprofen are effective in
relieving pain caused by synovitis and
must be used with caution.
2F
Hereditary bleeding disorder characterized by
a deficiency of or defect in a protein called Von
Willebrand factor (vWF).
vWF Protein → Contributes to the adherence
of platelets to damaged endothelium and
serves as a carrier protein for factor VIII.
➔ results in prolonged bleeding time
because platelets fail to adhere to the
walls of the ruptured vessel to form a
platelet plug
➔ s/s: frequent nosebleeds, gingival
bleeding, easy bruising, excessive
menstrual bleeding (menorrhagia)
VWD: Nursing Care Management:
✓ be calm, to alleviate anxiety and
promote child’s cooperation
✓ nosebleed – child must breathe from
the mouth
Epistaxis Management:
1. Sit up and lean forward (do not lie
down).
2. Apply pressure to nose with thumb and
forefinger for at least 10 minutes.
MINGUITO, SHANIA D. | BSN 2-B
30
2F – SICK GROWING CHILD
3. Insert cotton into each nostril and apply
ice to bridge of nose if bleeding
persists.
4. Keep child calm and quiet.
DISSEMINATED INTRAVASCULAR
COAGULATION
CLOTTING DISORDERS - ALTERATIONS IN
HEMATOLOGIC FUNCTION
Diffuse
fibrin
deposition
in
the
microvasculature, consumption of coagulation
factors, and endogenous generation of
thrombin and plamin.
➔ secondary disorder
➔ complication of a number of pathologic
processes
➔ hallmark signs: bleeding and clotting –
occurs simultaneously
➔ petechiae, purpura, bleeding from
openings in the skin, bleeding from
umbilicus, trachea, GI bleeding,
hypotension, organ dysfunction
DIC: Therapeutic
Management:
and
Nursing
Care
✓ platelets and fresh frozen plasma may
be needed to replace lost plasma
components
✓ recognize the signs that might indicate
its presence
✓ monitor IV infusion and blood
transfusions
2F
IDIOPATHIC THROMBOCYTOPENIC
PURPURA
CLOTTING DISORDERS - ALTERATIONS IN
HEMATOLOGIC FUNCTION
Purpura – Infrequent sign at presentation.
➔ hemorrhagic
disorder
by
thrombocytopenia, absence to severe
signs of bleeding (e.g., easy bruising,
mucosal
bleeding,
petechiae,
menorrhagia), and normal bone
marrow with a normal or increased
number of immature megakaryocytes
and esinophils
Types:
- Acute – URT (MMR, or chickenpox;
after infection with human parvovirus)
- Self-Limiting Course (Chronic) - >12
months’ duration.
ITP: Therapeutic
Management:
✓
✓
✓
✓
and
Nursing
Care
activity is restricted
prevent serious bleeding episodes
treatment administered w/o SEs
anti-D antibody → after administration
of anti-D antibody, observe the child for
a min. of 1 hr. and maintain a patent IV
line. Obtain baseline VS measurements
before the infusion and again 5, 20, and
60 minutes after beginning the infusion.
If fever, chills, or headache occurs
during or shortly after the infusion, the
nurse
should
administer
acetaminophen,
diphenhydramine,
and/or hydrocortisone. Observe the
patient for an additional hr. after the
anti-D antibody infusion is complete.
MINGUITO, SHANIA D. | BSN 2-B
31
2F – SICK GROWING CHILD
NEUROBLASTOMA
ALTERATIONS IN CELLULAR GROWTH
Most common extracranial solid tumor of
childhood and the most common cancer
diagnosed in infancy.
➔ originate from embryonic neural crest
cells that normally give rise to the
adrenal medulla and the sympathetic
nervous system
➔ adrenal gland or retroperitoneal
sympathetic chain
➔ Primary Site: Within abdomen; include
head and neck region, chest, and
pelvis.
Manifestations:
- firm, nontender, irregular mass in the
abdomen that crosses the midline
- compression of kidney, ureter, or
bladder may cause urinary frequency or
retention
Stages of Neuroblastoma:
Stage 1 – Localized tumor that is confined to
the area of origin capable of complete gross
excision; representative ipsilateral lymph
nodes negative for tumor microscopically
(nodes that are attached to and removed with
the primary tumor may be positive).
Stage 2-A – Unilateral tumor with incomplete
gross resection; representative ipsilateral
nonadherent lymph nodes and contralateral
lymph
nodes
negative
for
tumor
microscopically.
Stage 2-B – Unilateral tumor with or without
complete gross excision, with ipsilateral
nonadherent lymph nodes positive for tumor;
enlarged contralateral lymph nodes must be
negative microscopically.
2F
Stage 3 – Tumor infiltrating across the midline,
with or without regional lymph node
involvement; or localized unilateral tumor with
contralateral
regional
lymph
node
involvement; or midline tumor with bilateral
lymph node involvement.
Stage 4 – Dissemination of tumor to distant
lymph nodes, bone, bone marrow, liver, skin,
and/or other organs.
Stage 4-S – Localized primary tumor (as
defined for stage 1, 2-A, or 2-B) with
dissemination limited to liver, skin, or bone
marrow but not to bone.
Neuroblastoma: Therapeutic and Nursing
Care Management:
✓ remove as much of the tumor as
possible and to obtain biopsies
✓ chemotherapy – mainstay of therapy
✓ prevent postop. complications for
abdominal, thoracic, or cranial surgery
✓ parents need much support in dealing
with these feelings and expressing
them to the appropriate people
WILM’S TUMOR (NEPHROBLASTOMA)
ALTERATIONS IN CELLULAR GROWTH
Common kidney tumor of childhood.
-
painless swelling/mass within abdomen
hematuria, anemia, hypertension
weight loss and fever
dyspnea, cough, SOB, pain in the chest
Staging of Wilms Tumor:
Stage 1 – Tumor is limited to one kidney and
completely resected.
Stage 2 – Tumor extends beyond kidney but
is completely resected; lymph nodes do not
contain tumor.
Stage 3 – Residual tumor confined to
abdomen that may have disease in nearby
lymph nodes or abdominal space.
Stage 4 – Hematogenous metastases with
disease spread to the lung, liver, bone, brain,
or distant lymph nodes.
MINGUITO, SHANIA D. | BSN 2-B
32
2F – SICK GROWING CHILD
Stage 5 – Bilateral renal involvement is
present at diagnosis.
WILMS: Therapeutic and Nursing Care
Management:
✓ surgery + chemotherapy
✓ same nursing care to other cancers
treated with surgery, irradiation, and
chemotherapy
EWING’S SARCOMA (BONE TUMOR)
ALTERATIONS IN CELLULAR GROWTH
Primitive neuroectodermal tumor of the bone,
are the second most common malignant bone
tumor.
➔ arises in the marrow spaces of the bone
rather from the osseous tissue
➔ tumor originates from the shaft of long
and trunk bones, most often affecting
the pelvis, femur, tibia, fibula, humerus,
ulna, vertebra, scapula, ribs, and skull
OSTEOSARCOMA (BONE TUMOR)
ALTERATIONS IN CELLULAR GROWTH
Most common bone cancer in children and
most commonly affects patients in the second
decade of life during their growth spurt.
Therapeutic & Nursing Care Management:
✓ surgical biopsy
✓ limb salvage procedure
✓ all gross and microscopic tumors must
be resected
✓ chemotherapy plays a vital role in
treatment of osteosarcoma
✓ straightforward honesty is essential in
gaining the child’s cooperation and trust
✓ nurse should be present at the
discussion
✓ nurse must be careful not to overwhelm
children with information
✓ nurse must be considerate and mindful
of the child’s feelings
2F
Ewing’s: Therapeutic and Nursing Care
Management:
✓ limb salvage might be feasible
✓ radiotherapy and chemotherapy
✓ prepare the client and the family on the
different tests
✓ child should wear loose-fitting clothes
over the irradiated area t o minimize
additional skin irritation
✓ protect the area from sunlight and
sudden changes in temperature
(heating pads/ice packs) – due to
increased sensitivity
✓ encourage child to use the extremity as
tolerated
MINGUITO, SHANIA D. | BSN 2-B
33
2F – SICK GROWING CHILD
LEUKEMIA
ALTERATIONS IN CELLULAR GROWTH
Cancer that starts in blood-forming tissue,
such as the bone marrow, and causes large
numbers of abnormal blood cells to be
produced and enter the bloodstream.
Types:
1. Acute Lymphocytic Leukemia (ALL)
– This is the most common type of
leukemia in young children. All can also
occur in adults. This type of leukemia
begins in the B or T lymphocytes, which
are immature white blood cells.
Lymphocytes are the building blocks of
the lymphoid tissues that make up the
immune system.
antchen
2. Acute Myelogenous Leukemia (AML)
– AML is the most common type of
acute leukemia in adults. Myeloid stem
cells usually mature in to abnormal
myeloblasts, or white blood cells. But,
they sometimes become abnormal red
blood cells or platelets. As they multiply,
they overwhelm the normal cells in the
bone marrow and blood. The cancer
cells can also spread to other parts of
the body.
adults
Signs & Symptoms:
-
fever/chills
persistent fatigue, weakness
frequent or severe infections
losing weight w/o trying
swollen lymph nodes
enlarged liver/spleen
easy bleeding/bruising
recurrent nosebleeds
tiny red spots in your skin (petechiae)
excessive sweating, esp. at night
bone pain/tenderness
Diagnostic Tests: PE, CBC, bone marrow
test
Therapeutic & NCM:
✓ Obtain health history which may reveal
some symptoms reported by the patient
before problem is detected on PE.
✓ Conduct a physical assessment.
✓ Monitor lab results.
✓ Provide emotional support, education,
listen, help in decision making.
✓ Chemotherapy – Tr for Leukemia
HODGKIN’S DISEASE
SOFT TISSUE TUMORS - ALTERATIONS IN CELLULAR
GROWTH
3. Chronic Lymphocytic Leukemia
(CLL) – Begins in the B lymphocytes.
As the abnormal cells proliferate, they
crowd out the normal cells.
Originates in the lymphoid system and
primarily involves the lymph nodes.
4. Chronic Myelogenous Leukemia
(CML) – Occurs when a genetic change
turns the myeloid cells into immature
cancer cells. These cells then grow
slowly and overwhelm the healthy cells
in the bone marrow and blood.
Classified into Four Histologic Types:
2F
- spleen, liver, bone marrow, lungs, and
mediastinum
1. lymphocytic predominance
2. nodular sclerosis
3. mixed cellularity
4. lymphocytic depletion
MINGUITO, SHANIA D. | BSN 2-B
34
2F – SICK GROWING CHILD
Staging of Hodgkin Disease:
Stage 1 – Lesions are limited to one lymph
node area or only one additional
extralymphatic site (I-E), such as the liver,
lungs, kidney, or intestines.
Stage 2 – Two or more lymph node regions on
the same side of the diaphragm or one
additional extralymphatic site or organ (II-E) on
the same side of the diaphragm is involved.
Stage 3 – Lymph node regions on both sides
of the diaphragm and has spread to one
extralymphatic site (III-3), spleen (III-S), or
both (III-SE).
Stage 4 – Cancer has metastasized diffusely
throughout the body to one or more
extralymphatic sites with
or
without
involvement of associated lymph nodes.
-
complete blood count
uric acid levels
liver function tests
C-reactive protein
radiographic tests
Hodgkin’s: Therapeutic and Nursing Care
Management:
✓ follow-up care of children no longer
receiving therapy is essential to identify
relapse and second malignancies
✓ immunizations against pneumococci
and meningococci are recommended
before the splenectomy
✓ explain the treatment side effects –
child and family support
✓ nurse should discuss a feasible school
schedule with the parents and child
2F
NON-HODGKIN’S DISEASE
SOFT TISSUE TUMORS - ALTERATIONS IN CELLULAR
GROWTH
- Disease is usually diffuse rather than
nodular.
- Cell type is evenly split between B-cell
and T-cell lineages.
- Dissemination occurs earlier, more
often, and more rapidly.
Staging of Non-Hodgkin Lymphoma:
Stage 1 – Disease is limited to one lymph
node area or only one additional
extralymphatic site (I-E).
Stage 2 – Two or more lymph node regions on
the same side of the diaphragm or one
additional extralymphatic site or organ (II-E) on
the same side of the diaphragm.
Stage 3 – Tumor on both sides of abdomen
and may have spread to an area or organ next
to the lymph nodes (IIIE), spleen (IIIS), or both
(IIISE).
Stage 4 – Tumor has spread into any organ
that is not right next to an involved node,
and/or the tumor has spread to the central
nervous system or bone marrow.
Non-Hodgkin’s: Therapeutic and Nursing
Care Management:
✓ irradiation and chemotherapy
✓ lymphoblastic
lymphoma
→
chemotherapeutic
drugs
–
cyclophosphamide
✓ nonlymphoblastic lymphoma – cyclic
drug
combinations
→
cyclophosphamide and high-dose
methotrexate
✓ administered 6 to 24 months
✓ nursing care is similar to cancer
MINGUITO, SHANIA D. | BSN 2-B
35
2F – SICK GROWING CHILD
RHABDOMYOSARCOMA
SOFT TISSUE TUMORS - ALTERATIONS IN CELLULAR
GROWTH
Most common soft tissue sarcoma in children.
Arises from embryonic mesenchyme with
three recognized subtypes.
- occurs in the head and neck
- more common in males – 6 years or
younger
- originate from:
o muscles
o tendons
o bursae
o fascia
o fibrous
o connective
o lymphatic
o vascular tissue
TAKE NOTE: REINFORCEMENT
Is a rare type of cancer that forms in soft tissue
specifically skeletal muscle tissue or hollow
organs such as bladder or uterus.
Staging of Rhabdomyosarcoma:
Group 1 – Localized disease; tumor
completely resected and regional nodes not
involved.
Rhabdomyosarcoma: Therapeutic
Nursing Care Management:
and
✓ complete removal of tumor
✓ radical procedures with high morbidity
should be avoided
✓ careful assessment for signs of the
tumor
✓ supportive care during each stage of
therapy
✓ emotional support of the family
RETINOBLASTOMA
SOFT TISSUE TUMORS - ALTERATIONS IN CELLULAR
GROWTH
Arises from the retina, most common
intraocular malignancy of childhood.
Whitish “glow” in the pupil → cat’s eye reflex
or leukocoria
- caused by genetic alterations Rb gene
- germ-line mutation
- chromosomal deletion (chromosome
13)
- increased incidence of cognitive
impairment
and
congenital
malformations
Group 2 – Localized disease with microscopic
residual that may have spread into nearby
lymph nodes.
Group 3 – Incomplete resection with gross
residual disease; disease may have spread
into nearby lymph nodes but not into distant
organs.
Group 4 – Metastatic disease present at
diagnosis.
2F
- indirect ophthalmoscopy, ultrasound,
CT, and MRI scans
MINGUITO, SHANIA D. | BSN 2-B
36
2F – SICK GROWING CHILD
International Classification for Intraocular
Retinoblastoma:
Group A – Small (3 mm or less) intraretinal
tumors away from the optic disc and foveola.
Group B – All remaining tumors that are larger
than 3 mm and/or close to the optic disc or
foveola but remain confined to the retina.
Group C – Discrete local disease with minimal
amounts of disease under the retina
(subretinal seeding) or into the gelatinous
material of the eye (vitreous seeding).
Group D – Large or poorly defined tumors with
significant vitreous or subretinal seeding;
retina may have become detached from the
back of the eye.
Group E – Tumor is very large, extending near
the front of the eye, is bleeding or causing
glaucoma, or has other features that indicate
there is no means to save the eye.
Retinoblastoma: Therapeutic and Nursing
Care Management:
✓ enucleation – no salvage of vision
✓ irradiation – for vitreous seeding
✓ chemotherapy – decrease the tumor
size (plaque brachytherapy)
✓ photocoagulation – destroy retinal
blood vessels that supply nutrition to
the tumor
✓ cryotherapy – freezing the tumor, which
destroys microcirculation to the tumor
and the cells themselves through
microcrystal formation
✓ prepare the family for diagnostic and
therapeutic procedures and home care
✓ child may not see clearly after
procedure → SENSITIVE TO LIGHT
✓ encourage the parents to participate in
dressing changes – eye patches and
etc.
✓ safety measures should be practiced at
all times
2F
CLEFT LIP AND CLEFT PALATE
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Most common birth defect.
➔ exposure to environmental factors or
teratogens may be responsible for
clefts at a critical point in embryonic
development
➔ alcohol use, cigarette smoking, and
prescription
drugs,
including
anticonvulsants, steroids, and retinoids
➔ FOLIC ACID supplements may protect
against clefting
CLEFT LIP
- multifactorial
inheritance,
environmental
factors,
familial
occurrence
- male predominance
- unilateral/bilateral
- external nose, nasal cartilages, nasal
septum, maxillary alveolar ridges,
dental anomalies
- 2-3 mos. surgical repair, early use of
orthodontics
- nasal alveolar molding
- feeding and weight gain
CLEFT PALATE
- associated
w/
syndromes
(chromosomal), familiar occurrence,
environmental factors such as maternal
alcohol
ingestion,
smoking,
or
teratogens
- female predominance
- soft palate/hard palate
- midline/posterior palate
- may involve nostril and absence of
nasal
septal
development
(communication with oral and nasal
cavity)
- surgical repair for isolated Cp between
6-12 months; infants with CL/CP
between 9-15 months
- feeding efficiency; growth failure
MINGUITO, SHANIA D. | BSN 2-B
37
2F – SICK GROWING CHILD
- feeding cup, syringe feeding, special
needs feeder, pigeon bottle, cleft palate
nurser; avoid spoon, fork
Therapeutic & NCM:
✓ cleft/craniofacial multidisciplinary team
✓ plastic
surgery,
otolaryngology,
orthodontics,
speech-language,
pediatrics, nursing, audiology, social
work, psychology
✓ surgical closure of the cleft
✓ nurse must address not only the infant’s
physical needs but also the parents’
emotional needs
✓ nurse should encourage expression of
parental grief and fears
ESOPHAGEAL ATRESIA & TRACHEOESOPHAGEAL FISTULA
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Rare malformations that represent a failure of
the esophagus to develop as a continuous
passage and a failure of the trachea and
esophagus to separate into distinct structures.
➔ EA – frothy saliva in the mouth & nose,
drooling, choking, and coughing,
mild/significant respiratory distress
➔ EA – if fed, the infant may swallow
normally but suddenly cough and gag,
with return of fluid through the nose and
mouth, the infant may become cyanotic
and apneic because of aspiration of
formula or saliva
➔ EA w/ TEF (Type C) – stomach
becomes distended with air, and
thoracic and abdominal compressions
(especially during crying) cause the
gastric contents to be regurgitated
through the fistula and into the trachea,
producing chemical PNEUMONITIS
➔ NG-orogastric (OG) catheter into the
esophagus
➔ When EA w/ TEF is suspected, the
infant is IMMEDIATELY DEPRIVED
OF ORAL INTAKE.
2F
38
Polyhdramnios – Accumulation of 2000 mL of
amniotic fluid.
Tracheomalacia – May occur as a result of
weakness in the tracheal wall that exists when
a dilated proximal pouch compresses the
trachea early in fetal life.
EA & TEF: Therapeutic & NCM:
✓
✓
✓
✓
✓
✓
✓
✓
✓
✓
maintenance of a patent airway
prevention of pneumonia
gastric/blind pouch decompression
supportive therapy
surgical repair of the anomaly
IV fluids are initiated and the infant is
positioned to facilitate drainage of
secretions and decrease the likelihood
of aspiration
accumulated secretions are suctioned
frequently from the mouth and pharynx
infants head is kept UPRIGHT to
facilitate removal of fluid collected
nursing responsibility for detection of
this serious malformation begins
immediately after birth
assist in pre-op care, post-op care,
special problems, family support,
discharge planning, and home care.
Esophagus-failure todevelop passage
Esophagus &trachea-failure toseparate
MINGUITO, SHANIA D. | BSN 2-B
2F – SICK GROWING CHILD
PYLORIC STENOSIS
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Occurs when the ferential muscle of the pyloric
sphincter becomes thickened, resulting in
elongation and narrowing of the pyloric canal.
This produces an outlet obstruction and
compensatory dilation, hypertrophy, and
hyperperistalsis of the stomach.
➔ develops in the first few weeks of life,
causing nonbilious vomiting (occurs
after feeding)
Cregurgitation)
➔ projectile vomiting may develop if the
infant is fussy and hungry after vomiting
➔ if not diagnosed asap → dehydration,
metabolic alkalosis, and failure to thrive
may occur
➔ common in FIRSTBORN MALES
➔ inheritance is polygenic, with an
increased risk in the siblings and
offspring of affected persons
Pyloromyotomy
(Fredet-Ramstedt
Operative Procedure) – Performed by
laparoscope and consists of a longitudinal
incision through the circular muscle fibers of
the pylorus down to, but not including, the
submucosa.
incision to wall of
. .
PYLOMS
Therapeutic & NCM:
✓ surgical relief of the pyloric obstruction
by pyloromyotomy is the standard
therapy
✓ pre-op → infant must be rehydrated and
metabolic alkalosis corrected with
parenteral
fluid
and
electrolyte
administration
✓ replacement fluid therapy usually
delays surgery for 24 to 48 hours
✓ stomach is decompressed with an NG
tube if the infant continues with vomiting
✓ infant = no evidence of fluid &
electrolyte imbalance → surgery is
performed without delay
✓ nurse must observe for clinical features
that help establish the diagnosis
2F
✓ careful regulation of fluid therapy
✓ reestablishment of normal feeding
patterns
✓ nurses must be alert to signs of HPS in
infants and refer them for medical
evaluation
✓ HPS should be considered a possibility
in the very young infant who appears
alert but fails to gain weight and has a
history of vomiting after feedings
✓ assessment should be based on
observation of eating behaviors,
evidence of characteristic clinical
manifestations,
hydration,
and
nutritional status
✓ careful monitoring of the IV fluids and
strict monitoring of intake and output
are important
✓ observe
VS
–
fluid/electrolyte
imbalances
GASTROESOPAGEAL REFLUX
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Transfer of gastric contents into the
esophagus. This phenomenon is physiologic,
occurring throughout the day, most frequently
after meals and at night.
➔ peak: 4 months of age
➔ PASSIVE REGURGITATION (18 mos.)
➔ failure to thrive, respiratory problems,
dysphagia develops
➔ prone to develop GER
o premature infants
o bronchopulmonary dysplasia
o tracheoesophageal/esophageal
atresia repairs
o neurologic disorders
o scoliosis
o asthma
o cystic fibrosis
o cerebral palsy
➔ avoid caffeine, citrus, tomatoes,
alcohol, peppermint, spicy/fried foods
➔ thickened
feedings
&
upright
positioning
MINGUITO, SHANIA D. | BSN 2-B
39
2F – SICK GROWING CHILD
Nissen Fundoplication – Most common
surgical procedure. This surgery involves
passage of the gastric fundus behind the
esophagus to encircle the distal esophagus.
GER: Therapeutic & NCM:
✓
✓
✓
✓
✓
✓
✓
✓
✓
adequate weight gain
limited spitting up or vomiting
good sleep habits
no recurrent pneumonias
educate parents regarding home care –
including feeding, positioning, and
medications when indicated
care for child undergoing surgical
intervention
parents should not place infants on their
sides as an alternative to fully supine
sleeping
avoid of soft bedding and soft objects in
the bed is important
if severe – NG tube feedings may
decrease the amount of emesis and
provide constant buffering of gastric
acid
OMPHALOCELE
ALTERATIONS IN GASTROINTESTINAL FUNCTION
True failure of embryonic development.
Occurs when there is failure of the caudal or
lateral infolding of the abdominal wall.
Post-op:
✓ mechanical ventilation
✓ parenteral nutrition
✓ intraabdominal compression – prevents
effective respiration and restrict blood
flow to the lower extremities &
abdominal organs
✓ feedings may resume once adequate
bowel function is established
✓ observe for infection, evisceration,
intestinal volvulus, obstruction, and
ventral hernia
Long-term complications include:
✓
✓
✓
✓
GER
failure to thrive
ventral hernia
feeding issues
➔ 3rd week of gestation
➔ usually covered only by a translucent
peritoneal sac
➔ the sac may contain only a small portion
of the bowel or most of the bowel and
other abdominal viscera such as the
liver
2F
TAKE NOTE: REINFORCEMENT
Is a congenital abnormality in which some of
the abnormal organs protrude through an
opening in the abdominal muscles of the
umbilical cord.
MINGUITO, SHANIA D. | BSN 2-B
40
2F – SICK GROWING CHILD
INTUSSUSCEPTION
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Most common cause of intestinal obstruction
in children. Occurs when a proximal segment
of the bowel telescopes into a more distant
segment, pulling the mesentery with it.
Mesentery is compressed and angled,
resulting in lymphatic and venous obstruction.
TAKE NOTE: REINFORCEMENT
Is a condition in which part of the intestine
slides into an adjacent part of the intestine.
➔ 3 mos. – 6 years
➔ more common in males
➔ ILEOCECAL VALVE (common site)
➔ sudden acute abdominal pain
➔ child screaming and drawing the knees
onto the chest
➔ child appearing normal and comfortable
between episodes of pain
➔ vomiting, lethargy
➔ passage of red, current jelly-like stools
➔ tender, distended abdomen
➔ palpable SAUSAGE-SHAPED mass in
upper right quadrant
➔ empty lower right quadrant → DANCE
SIGN
➔ eventual fever, prostration, and other
signs of peritonitis
Therapeutic & NCM:
✓ air enema, saline enema
✓ IV fluids, NG decompression, and
antibiotic therapy
✓ nurse can help establish a diagnosis by
listening to the parent’s description of
the child’s physical and behavioral
symptoms
✓ nurse prepares the parents for the
immediate need for hospitalization
✓ maintenance of NPO status, routine lab
testing (CBC and urinalysis), signed
parental consent, and pre-anesthetic
sedation are performed
✓ children with perforation → IV fluids,
systemic
antibiotics,
bowel
decompression before undergoing
surgery
✓ observe VS, BP, intact sutures and
dressing, and the return of bowel
sounds
Passage of a normal brown stool usually
indicates that the intussusception has reduced
itself. This is immediately reported to the
practitioner, who may choose to alter the
diagnostic and therapeutic care plan.
The classic signs and symptoms of
intussusception may not be present; a more
chronic picture may occur, characterized by
diarrhea, anorexia, weight loss, occasional
vomiting, and periodic pain. The older child
may have pain without other signs or
symptoms. Because this condition is
potentially life threatening, be aware of such
signs, and closely observe and refer these
children for further medical investigation.
2F
MINGUITO, SHANIA D. | BSN 2-B
41
2F – SICK GROWING CHILD
HIRSCHSPRUNG’S DISEASE
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Congenital anomaly that results in mechanical
obstruction from inadequate motility of part of
the intestine.
TAKE NOTE: REINFORCEMENT
A birth defect characterized by the absence of
a particular nerve cells in a segment of a
bowel.
➔ more common in males
➔ SHORT-SEGMENT DISEASE
➔ relates due to the absence of
GANGLION cells in the affected areas
of the intestine, resulting in a loss of the
rectosphincteric
reflex
and
an
abdominal microenvironment of the
cells
➔ CONGENITAL
AGANGLIONIC
MEGACOLON – primary defect, which
is the absence of ganglion cells in the
myenteric plexus of Auerbach and the
submucosal plexus of Meissner
➔ LONG-SEGMENT HD – entire colon or
part of the small intestine may be
involved
➔ TOTAL CLONIC AGANGLIONOSIS –
there is no innervation of the large and
small intestine from the anus to the
ileocecal valve
2F
Therapeutic & NCM:
✓ soave
pull-through,
Swenson
procedure, Duhamel procedure
✓ main objectives are to help the parents
adjust to a congenital defect in their
child, foster infant-parent bonding
✓ prep the parents for med-surg
intervention
ANORECTAL MALFORMATIONS
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Rectal Atresia – Complete obstruction
(inability to pass stool) and requires immediate
surgical intervention.
Rectal Stenosis – May not become apparent
until later in infancy when the infant has a
history of difficult stooling, abdominal
distention, and ribbonlike stools.
Persistent Cloaca – Complex anorectal
malformation in which the rectum, vagina, and
urethra drain into a common channel opening
into the perineum.
PSARP – common surgical procedure for the
repair of anorectal malformations
POSTERIOR SAGGITAL
ANORECTOPLASTY
MINGUITO, SHANIA D. | BSN 2-B
42
2F – SICK GROWING CHILD
Therapeutic & NCM:
✓ primary management – surgical
✓ first nursing responsibility is assisting in
identification
of
anorectal
malformations
✓ a newborn who does not pass stool
within 24 hours after birth or has
meconium that appears at a location
other than the anal opening requires
further assessment
✓ pre-op care: diagnostic evaluation, GI
decompression, bowel preparation, IV
fluids
✓ (for perineal fistula) Anoplasty is
performed – involves moving the fistula
opening to the center of the sphincter
and enlarging the rectal opening
✓ feedings are started soon after the
surgical repair
✓ breastfeeding is encouraged because it
causes less constipation
✓ Cloaca
(female),
recto-urethral
prostatic fistula (male), and vestibular
fistula (female) → DESCENDING
COLOSTOMY is performed, to allow
fecal elimination and avoid fecal
contamination
✓ PSARP – common surgical procedure
for
the
repair
of
anorectal
malformations
2F
CONGENITAL DIAPHRAGMATIC HERNIA
ALTERATIONS IN GASTROINTESTINAL FUNCTION
CDH results when the diaphragm does not
form completely, resulting in an opening
between the thorax and the abdominal cavity.
➔ diaphragm forms at 4-8 weeks
gestation
➔ BOCHDALEK HERNIA or AKA LEFT
POSTEOLATERAL DEFECT (most
common type of CDH)
➔ Bochdalek – intestines and other
abdominal structures, such as the liver,
can enter the thoracic cavity,
compressing the lung
➔ lung
hypoplasia,
ventilation
is
compromised
➔ pulmonary hypertension
➔ acute RDS is present, dyspneic,
cyanotic, scaphoid abdomen, impaired
cardiac output, shock
Therapeutic & NCM:
✓ fetal surgery
✓ proper assessment, prompt recognition
of neonatal respiratory distress,
cyanosis,
scaphoid
abdomen,
mediastinal shift would alert the nurse
to investigate further
✓ any infant with a scaphoid abdomen,
moderate
to
severe
respiratory
distress, decreased breath sounds
unilaterally,
and
a
history
of
polyhydramnios should be suspected of
having a CDH
✓ ventilation should not be given with bag
and mask to prevent further intestinal
air
and
subsequent
respiratory
compromise
✓ pre-op
care
involves
prompt
recognition,
resuscitation,
and
stabilization of the infant, including
ventilatory
support,
blood
gas
monitoring, fluid volume maintenance,
and administration of IV fluids and
electrolytes
MINGUITO, SHANIA D. | BSN 2-B
43
2F – SICK GROWING CHILD
✓ post-op → routine obs, detect signs of
RDS/fluid/electrolyte imbalances
✓ monitor mediastinal
shift signs,
pulmonary air leak, and infection
UMBILICAL HERNIA
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Hernia – Protrusion of a portion of an organ or
organs through an abnormal opening.
Umbilical Hernia – Common hernia observed
in infants. Occurs when fusion of the umbilical
ring is incomplete at the point where the
umbilical vessels exit the abdominal wall.
Incarceration – Hernia is constricted and
cannot be reduced manually, is rare. (3 to 5
years)
Nursing Care Management:
✓ Need reassurance that the defect
usually is not harmful.
✓ Taping or strapping the abdomen to
flatten the protrusion does not aid in
resolution and can produce skin
irritation.
✓ Observe the child for complications
related to a hematoma or infection.
Therapeutic & NCM:
✓ investigation of possible organic
causes such as CMA, intussusception,
or other GI problem
✓ PO – Lactobacillus reuteri
✓ antispasmodics
✓ antihistamines
✓ antiflatulents
Areas that should be stressed include:
1. infant’s diet
2. diet of the breastfeeding mother
3. time of day when crying occurs
4. relationship of crying to feeding time
5. presence of specific family members
during crying and habits of family
members, such as smoking
6. activity of the mother or usual caregiver
before, during, and after crying
7. characteristics of the cry (e.g., duration,
intensity)
8. measures used to relieve crying and
their effectiveness
9. infant’s stooling, voiding, and sleeping
patterns
RUMINATION
COLIC (PAROXYSMAL ABDOMINAL
PAIN)
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Abdominal pain or cramping that is manifested
by loud crying and drawing t he legs up to the
abdomen.
Star anise tea is a remedy used by some to
treat colic. Numerous cases of star anise tea
toxicity have been recorded in the literature.
Inform parents that this remedy should not be
used in infants to treat colic.
2F
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Is a behavioral problem which causes a
regurgitation of readily eaten food.
Etiology: Unknown
Risk Factors:
- gastric distention w/ food
- abdominal pressure
- relaxation
of
lower
esophageal
sphincter
- gastric contents regurgitated
- food expelled/re-swallowed depending
on social circumstances
MINGUITO, SHANIA D. | BSN 2-B
44
2F – SICK GROWING CHILD
Risk Assessment:
- abdominal pain
- indigestion
- repeatedly bringing up (regurgitating
food)
- attempt to force back food into the
oropharynx
- spitting up/vomiting
S/S: re-chewing of the food, repeated
regurgitation, bad breath, raw & chapped lips,
malnutrition, delayed growth development
DT: endocrine hormone functions, test for
anemia, serum electrolytes
Therapeutic & NCM:
✓ Restore a nurturing environment.
✓ Provide a primary care of nursing staff
to feed the child.
✓ Talking away distractions during
feeding.
✓ Making feeding a more relaxing and
pleasurable experience.
✓ Maintain a calm and even temperament
when feeding the infant or child
throughout the meal.
CELIAC DISEASE
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Permanent intestinal intolerance to dietary
gluten. A protein present in wheat, barley, rye,
and oats, that causes damage to the villi in the
small intestine.
Risk Assessment:
-
1st degree relative with celiac disease
Northern European background
T1 DM
Down Syndrome/Turner Syndrome
Autoimmune Thyroid Disease
microscopic colitis
addison’s disease
IgA deficiency
S/S: abdominal bloating & pain, chronic
diarrhea, vomiting, constipation, pale, foulsmelling, fatty stool, IDA, weight loss, fatigue,
irritability & behavioral issues, dental enamel
defects of the permanent teeth, delayed
growth & puberty
DT: PE, CBC, HLA Genetic Test, Endoscopy
Therapeutic & NCM:
✓ gluten-free diet
✓ help the child adhere to the dietary
regimen
✓ nurse must give advise to parents of the
necessity of reading all label
ingredients carefully to avoid hidden
sources of gluten
✓ nurse can be instrumental in allowing
the child to express concerns and
frustration while focusing on ways in
which the child can still feel normal
Also known as:
2F
✓ gluten-induced enteropathy
✓ gluten-sensitive enteropathy
✓ celiac sprue
MINGUITO, SHANIA D. | BSN 2-B
45
2F – SICK GROWING CHILD
SHORT BOWEL SYNDROME
ALTERATIONS IN GASTROINTESTINAL FUNCTION
Malabsorptive disorder that occurs as a result
of decreased mucosal surface area, usually
because of extensive resection of the small
intestine.
➔ decreased intestinal surface area for
absorption of fluid, electrolytes, and
nutrients
➔ need for parenteral nutrition (PN)
Therapeutic & NCM:
✓ preserve as much length of bowel as
possible during surgery
✓ maintain optimum nutritional status,
growth, and development while
intestinal adaptation occurs
✓ stimulate intestinal adaptation with
enteral feeding
✓ minimize complications related to the
disease process and therapy
✓ most important components of nursing
care are administration and monitoring
of nutritional therapy
Therapeutic & NCM:
✓ Maintain hygiene of the bladder area to
prevent infection and excoriation of the
surrounding tissue.
✓ Adding a sterile, nonadherent, moist
dressing is placed over the exposed
bladder area to prevent infection and to
avoid the diaper form adhering to
mucosa.
✓ Inspect periodically for evidence of
pressure necrosis.
✓ Apply fluid management, IV access
should be applied early on.
✓ Preserve pelvic immobility.
✓ Maintain ureteric catheter patency.
✓ Avoid having the baby cry to decrease
chances of abdominal distention.
✓ Maintain skin hygiene.
HYPOSPADIAS
ALTERATIONS IN GENITOURINARY FUNCTION
Hypospadias – Urethral opening is located
below the glans penis or anywhere along the
ventral surface (underside) of the PENILE
SHAFT.
BLADDER EXSTROPHY
ALTERATIONS IN GENITOURINARY FUNCTION
Is a more severe defect characterized by
externalization of the bladder, splaying of the
urethra with failure of tubular formation.
Etiology: Exstrophy results from failure of the
abdominal wall and underlying structures,
including the ventral wall of the bladder, to fuse
in utero. As a result, the lower urinary tract is
exposed and the everted bladder appears
bright red through the abdominal opening.
2F
S/S: bladder is visible, smaller-capacity
bladder, lower-than-usual belly button, anus is
lower than usual, separated pelvic bones,
undescended testicles
Chordee – Ventral curvature of the penis,
results from the replacement of normal skin
with a fibrous band of tissue and usually
accompanies
more
sever
forms
of
hypospadias.
TAKE NOTE: REINFORCEMENT
Is a birth defect in which the opening of the
urethra is not located at the tip of the penis.
MINGUITO, SHANIA D. | BSN 2-B
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