NCMA 219 LEC | 2ND Year – 2nd Semester ~ TRANSCRIBED BY: B ~

BACHELOR OF SCIENCE IN NURSING

NCMA 219 LEC Nursing Care of a Family with High-
CARE OF THE MOTHER & CHILD AT RISK Risk Newborn
WEEK 7 Newborn Priorities of First Days of Life
Prof: Mrs. Shiella May Edquibal, Man, RN All newborns have eight (8) priority needs in the first few days
Pediatric Nursing of life:
Classification according size & gestational age
Identification of High-Risk Newborn 1. Initiation and maintenance of respirations
• Premature Infant Effective loud crying is critical for Ductus Arteriosus (will
• Postmature infant be closed by effective crying); connected to maternal
• Small-for-Gestational Age circulation
• Large-for-Gestational Age 2. Establishment of extrauterine circulation
Acute Conditions of the Newborn
• Respiratory Distress Syndrome Perfusion comes from the placenta: once baby is out, s/he
• Meconium Aspiration Syndrome should be able to establish extrauterine circulation
• Apnea of Prematurity (tumitibok ‘yung puso)
• Neonatal Sepsis > Check FHR
• Hyperbilirubinemia 3. Control of body temperature
Diseases of the Newborn
• Necrotizing Enterocolitis
Babies are Non-shivering Thermoregulation
• Retinopathy Other ways to produce heat/ thermoregulate
• Hemolytic Diseases > Breaking down its own serum glucose → hypoglycemia
• Transient Tachypnea of Newborn > Break down Fats –> Ketones –> Acid –> Acidosis
• Trisomy 21 4. Intake of adequate nourishment
> Promote breastfeeding
PEDIATRIC NURSING 5. Establishment of waste elimination
> baby should establish past first stool/ Meconium
Pediatric Nursing or Child Health Nursing 6. Prevention of Infection
Is the nursing specialty of caring for infants, children and 7. Prevention of an infant-parent relationship
adolescents. > promotion of skin-to-skin contact
A nurse who specializes in this area is usually referred to > promote early bonding; baby will be rooming-in
as a pediatric nurse. 8. Developmental care, or care that balances physiologic
needs and stimulation for best development
Roles of the Pediatric Nurse:
❖ Primary Caregiver – provide promotive, preventive, Initiating and Maintaining Respirations
curative and rehabilitative nursing care in all levels of • Resuscitation
health services. > CPR, give oxygen
❖ Coordinator and Collaborator – maintains good • Airway
interpersonal communication with the child, family, and > should be open/ patent
health team members. > use Bulb syringe for
❖ Nurse Advocate – safeguard’s the child’s right, to assist Suctioning (last resort)
and provide the best care from the health care team. • Lung Expansion
❖ Health Educator – provide information to children, • Drug Therapy
parents, and significant others, about the prevention of > if baby is not crying
illness, health promotion, or maintenance. bcos of incorrect
❖ Nurse Consultant – guides parents for maintenance and administration of sedation in the 2nd stage of labor
promotion of health. • Ventilation Maintenance
❖ Nurse Counselor – provides guidance to parents in hazards > w/out oxygen for 3 mins of life it can lead to irreversible
of children and health team for own decision making in fetal death
different situations. Epinephrine/Adrenaline

Establishing Extrauterine Circulation

➢ Although establishing respirations is the usual priority at a
high-risk infant’s birth, lack of cardiac function may be
present concurrently or may develop if respiratory function
cannot be quickly initiated and maintained.
➢ If an infant has no audible heartbeat, or if the cardiac rate
is below 80 beats per minute, closed-chest massage
should be started.
➢ Hold an infant with fingers supporting the back and depress
the sternum with two fingers.

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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
➢ Continue to monitor transcutaneous oxygen or pulse
oximetry to evaluate respiratory function and cardiac
efficiency. If the pressure and the rate of massage are
adequate, it should be possible, in addition, to palpate a
femoral pulse.
➢ If heart sounds are not resumed above 80 bpm after 30
seconds of combined positive-pressure ventilation and
cardiac compressions, 0.1 to 0.3 mL/kg epinephrine
(1:1000)
Central line/ Umbilical line to administer epinephrine
Can also administer epinephrine in the endotracheal tube
Maintaining Fluid and Electrolyte Balance
➢ After an initial resuscitation attempt, hypoglycemia
(decreased blood glucose) may result from the effort the
newborn expended to begin breathing.
demand for ↑ glucose level lead to ↓ blood glucose
Risk for: Hypoglycemia
Problem: ↑ respiration = Dehydration
➢ Dehydration may result from increased insensible water
loss from rapid respirations. Infants with hypoglycemia are
treated initially with 10% dextrose in water to restore their
blood glucose level.
➢ Fluids such as Ringer’s lactate or 5% dextrose in water are
commonly used to maintain fluid and electrolyte levels.
Ringer’s lactate – IV Fluids with electrolytes.
o Maintain of TFR – Total Fluid Rate
o Ex. Maintain TFR of 200mL/24 hours
o Strict intake and output/monitoring of I and O
▪ Make sure that the baby is urinating, weigh the
used pad (1g=1ml)
o Dextrose 5% in water
o Dextrose 10% in water
o Dextrose 50% in water
If glucose dextrose can’t be established, it can be
administer in umbilical line (pag natuyo, it can’t be used
na)
Cut down – Periphery area, Central line, via IV, cutting
down the area to expose the infant’s vein to directly
catheter the veins.
o HGT/CBG Test every 3 to 4 hours
▪ Normal Blood glucose level is >45mg mg/dl
▪ <45mg/dl → Alarming baby will be
Hypoglycemic, Notify the physician
➢ The rate of Fluid administration must be carefully
monitored because a high fluid intake can lead to patent
ductus arteriosus or heart failure. When using a radiant
warmer, there is an increase in water loss from convection
and radiation. A newborn on a warmer, therefore, will
require more fluid than if he or she were placed in a double-
walled incubator.
Nursing Considerations: Lab Findings
➢ Dehydration monitored by urine output and urine-
specific gravity measures.
o output less than 2 mL/kg/hr = oliguria
o urine specific gravity greater than 1.015 to 1.020 =
inadequate fluid intake.
Report right away, it can be kidney problem
➢ Elevated specific gravity may also be caused by
inappropriate antidiuretic hormone secretion or kidney
failure because of a primary illness.
Hypotension (↓ BP) – there’s no enough perfusion in the
brain, tissue, and organ
➢ If an infant has hypotension without hypovolemia, a
vasopressor such as dopamine may be given to increase
blood pressure and improve cell perfusion.
➢ If hypovolemia is present, the cause is usually fetal blood
loss from a condition such as placenta previa or twin-to-
twin transfusion. With Hypovolemia, typically tachypnea,
pallor, tachycardia, decreased arterial blood pressure,
decreased central venous pressure, and decreased tissue
perfusion of peripheral tissue with a progressively
developing metabolic acidosis, will be present.
o give fluids
o increased breastfeeding
o Increase OGT – Oral Gastric Feeding (Oral
Gastric Tube)
Regulating the Temperature of the baby
➢ All high-risk infants may have difficulty maintaining a
normal temperature. This is because, in addition to stress
from an illness or immaturity, the infant’s body is often
exposed during procedures such as resuscitation and blood
loss/ drawing.
Normal Temp: 36.5 – 37.2 or 37.5
Ways to Regulate Temperature:
o Radiant Heat Sources
o Incubators
o Skin-to-Skin Care
Nursing Consideration: Maintain Hydration and close
monitoring of I and O due to high temperature.
Possible Nursing Diagnosis
• Ineffective airway clearance related to presence of mucus
or amniotic fluid in airway.
• Ineffective cardiovascular tissue perfusion related to
breathing difficulty.
• Risk for deficient fluid volume related to insensible water
loss.
• Ineffective thermoregulation to newborn status and stress
from birth weight variation
• Risk for imbalanced nutrition, less than body requirements
related to lack of energy for sucking.
• Risk for infection related to lowered immune response in
newborns.
• Risk for impaired parenting related to illness in newborns
at birth.
• Deficient diversional activity (lack of stimulation) related
to illness at birth.
• Readiness for developmental care to decrease
overstimulation easily caused by necessary lifesaving
procedures.
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The newborn at Risk because of
ALTERED GESTATIONAL AGE OR BIRTH
WEIGHT
Classification According to Gestational Age
• Premature (preterm) infant – an infant born before the
completion of 37 weeks of gestation, regardless of birth
weight.
• Full-term infant – an infant born between the beginning of
38 weeks and the completion of 42 weeks of gestation,
regardless of birth weight
• Postmature (postterm) infant – an infant born after 42
weeks of gestational age, regardless of birth weight.
PRETERM VS. FULL TERM
Classification According to Size
• Low-birthweight (LBW) infant
– infant whose birth weight is less than 2,500 grams (5.5
lbs), regardless of gestational age
• Very low birthweight (VLBW) infant
– An infant whose birth weight is less than 1,500 grams
(3.3 lbs)
• Extremely low birthweight (ELBW) infant
– An infant whose birth weight is less than 1,000 grams
(2.2 lbs)
• Appropriate for Gestational Age (AGA) infant
– An infant whose weight falls between the 10th and 90th
percentiles on intrauterine growth curves.
• Small-for-date (SFD) or Small-for-gestational-age (SGA)
infant
– An infant whose rate of intrauterine growth was slowed
and whose birth weight falls below 10th percentile on
intrauterine growth curves.
• Intrauterine Growth Restriction (IUGR)
– Found in infants with those intrauterine growth is
restricted.
• Large-for-gestational age (LGA) infant
– An infant whose birth weight falls above the 90 th
percentile on intrauterine growth charts.
THE SMALL-FOR-GESTATIONAL-AGE INFANT
➢ An infant is SGA if the birth weight is below the 10th
percentile on an intrauterine growth curve for that age.
SGA infants may be born preterm (before 38 weeks of
gestation), term (between weeks 38 and 42), or post term
(past 42 weeks).
➢ SGA infants are small for their age because they have
experienced intrauterine growth restriction (IUGR) or
failed to grow at the expected rate in utero.
Etiology
➢ A woman’s nutrition during pregnancy plays a major role
in fetal growth, so lack of adequate nutrition may be a
major contributor to IUGR. Pregnant adolescents have a
high incidence of SGA infants. Because adolescents must
meet their own nutritional and growth needs, needs of a
growing fetus can be compromised.
➢ However, the most common cause of IUGR is a placental
anomaly; either the placenta did not obtain sufficient
nutrients from the uterine arteries or it was inefficient at
transporting nutrients to the fetus. Placental damage, such
as partial placental separation with bleeding, limits
placental function because the area of placenta that
separated becomes infarcted and fibrosed, reducing the
placental surface available for nutrient exchange.
o Placental Anomaly:
▪ Partial placental separation
o Mothers with systemic disease
Risk Factor
• Developmental defect in the placenta
• Women with systemic diseases that decrease blood flow to
the placenta
o Severe mellitus or pregnancy induced hypertension
(both are diseases in which blood vessel lumens are
narrowed) are at higher risk for delivering SGA babies
than others.
• Women who smoke heavily or use narcotics also tend to
have SGA infants.
Assessment
• The SGA infant may be detected in utero when fundal
height during pregnancy becomes progressively less than
expected. However, if a woman is unsure of the date of her
last menstrual period, this discrepancy can be hard to
substantiate.
• A sonogram can demonstrate the decreased size.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
• A biophysical profile including a nonstress test, placental
grading, amniotic fluid amount, and ultrasound
examination can provide additional information on
placental function. If poor placental function is apparent
from such determinations, it can be predicted the infant will
do poorly during labor because of periods of relative
hypoxia during contractions may result.
• Cesarean birth is the birth method of choice in such
circumstances.
• Appearance
o Generally, an infant who suffers nutritional
deprivation early in pregnancy, when fetal growth
consists primarily of an increase in the number of body
cells, is below average in:
▪ weight
▪ length
▪ head circumference
o An infant who suffers deprivation late in pregnancy,
who growth consists primarily of an increase in cell
size, may have only a reduction in weight.
• Regardless of when deprivation occurs, an infant tends
to:
o Have an overall wasted and old and sick appearance
o Small liver, which can cause difficulty regulating
glucose, protein, and bilirubin levels after birth.
o Poor skin turgor
o Head look bigger
o Skull sutures may be widely separated
o Hair is dull and lusterless.
o Abdomen may be sunken.
o Umbilical cord appears dry and have yellow staining.
• Laboratory findings: Blood studies at birth usually show a
high hematocrit level (less than normal amounts of
plasma in proportion to red blood cells are present because
of a lack of fluid in utero) and an increase in the total
number of red blood cells (polycythemia).
o The increase in red blood cells occurs because anoxia
during intrauterine life stimulates the development of
red blood cells. The polycythemia that results causes
increased blood viscosity, a condition that puts extra
work on the infant’s heart because it is more difficult
to effectively circulate thick blood.
• As a consequence, acrocyanosis (blueness of the hands
and feet) may be prolonged and persistently more marked
than usual. If the polycythemia is extreme, vessels may
actually become blocked and thrombus formation can
result. If the hematocrit level is more than 65% to 70%, an
exchange transfusion
o Exchange transfusion: Done in the umbilical
cord/central line/carotid, where bad blood (high
hematocrit, high RBC) infuses good blood to defuse
bad blood. To dilute high viscous blood of the baby
> Done to baby with Hyperbilirubinemia
• Because SGA infants have decreased glycogen stores, one
of the most common problems is hypoglycemia (decreased
blood glucose, or a level below 45mg/dL). Such infants
may need IV Glucose to sustain blood sugar until they are
able to suck vigorously enough to take sufficient oral
feedings.
LARGE FOR GESTATIONAL AGE
➢ An infant is LGA (also termed macrosomia) if the birth
weight is above the 90th percentile on an intrauterine
growth chart for the gestational age. Such a baby appears
deceptively healthy at birth because of the weight, but a
gestational age examination will reveal immature
development.
➢ It is important that LGA infants be identified immediately
so that they can be given care appropriate to their
gestational age rather than being treated as term newborns.
Etiology
➢ Infants who are LGA have been subjected to an
overproduction of growth hormone in utero. This happens
most often to infants of women with diabetes mellitus or
women who are obese.
➢ Extreme macrosomia occurs in fetuses of diabetic women
whose symptoms are poorly controlled, because these
fetuses are exposed to high glucose levels.
➢ Multiparous women are also prone to have large babies
because with each succeeding pregnancy, babies tend to
grow bigger.
➢ Other condition associated:
o Transposition of the great vessels,
o Beckwith syndrome (a rare condition characterized by
overgrowth), and
o Congenital anomalies such as omphalocele.
Assessment
• A fetus is suspected of being LGA when a woman’s uterus
is unusually large for the date of pregnancy.
• Abdominal size can be deceptive, however – because a
fetus lies in a flexed fetal position, he or she does not
occupy significantly more space at 10 lb than at 7 lb.
• Sonogram – to see if the fetus is growing at an abnormal
rate
• Nonstress Test – assess the placenta’s ability tosustain a
large fetus during labor may be performed
• Lung maturity assessed by amniocentesis – to see if an
LGA fetus is mature
• Fundic height measurement
• Ultrasound
Appearance
• At birth, LGA infants may show immature reflexes and
low scores on gestational age examinations in relation to
their size. They may have extensive bruising or a birth
injury such as a broken clavicle or Erb-Duchenne
paralysis from trauma to the cervical nerves if they were
born vaginally.
• Because the head is large, it may have been exposed to
more than the usual amount of pressure during birth,
causing a prominent caput succedaneum,
cephalhematoma, or molding.
Cardiovascular Dysfunction
➢ Observe LGA Infants closely for signs of
hyperbilirubinemia (increased serum bilirubin level),
which may result from absorption of blood from bruising
and polycythemia.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
➢ Polycythemia has been caused by an infant’s system
attempting to fully oxygenate all body tissues. This effort
puts extra stress on the heart, so the heart rate of LGA
infants should be carefully observed.
➢ If cyanosis is present, it may be a sign of transportation of
the great vessels, a serious heart anomaly associated with
macrosomia.
Hypoglycemia
➢ LGA infants also need to be carefully assessed for
hypoglycemia in the early hours of life because infants
require large amounts of nutritional stores to sustain their
weight.
➢ If the mother had diabetes that was poorly controlled, the
infant will have had an increased blood glucose level in
utero causing the infant to produce elevated levels of
insulin.
➢ After birth, these increased insulin levels will continue for
up to 24 hours of life, possibly causing rebound
hypoglycemia.
ACUTE CONDITIONS OF THE NEWBORN
Illness of the High-Risk Newborn
Respiratory Distress Syndrome
➢ a.k.a Hyaline Membrane Disease
➢ A condition of surfactant deficiency and physiologic
immaturity of the thorax
➢ Seen almost exclusively in PRETERM infant (multifetal
pregnancies, infants of diabetic mother, C/S delivery, etc)
Alveoli is the main gas exchange unit of the lungs, without
the alveoli, there will be no gas exchange
o (hindi siya mag i-inhale – exhale nang maayos)
Surfactants during the 24th week of AOG
If the baby is born before 24th weeks of AOG the baby will
not be able to spontaneously breathe.
Type 2 cells (work with surfactants) in the lungs, develop
during the 36th weeks AOG
Pathophysiology
Inadequate inflation
Immaturity of Surfactant
due to increased
the lungs deficiency
surface tension
• Substernal retractions
• Flaring of nares
• Fine respiratory crackles
• Central cyanosis (late and serious sign)
Diagnostic Evaluation
• Pulse Oximetry (Determine hypoxia)
o Normal: 95 – 100
• Radiography
o Heart anomaly
o Chest Xray
• L/S ratio (Lecithin/Sphingomyelin)
o Normal: 2:1
• TDx Fetal Lung Maturity assay (determines PG level in
amniotic fluid or neonatal tracheal aspirate)
o PG – ex. if ↓ Phosphatidyl glycerol/ Phosphatidyl
choline → ↓ Lung surfactant → Respiratory distress
Therapeutic Management
• Administration of exogenous surfactant
▪ Upon intubation endotracheal
▪ Baby preterm w/ respiratory distress, this surfactant
stimulate lung function
• Nitric oxide (Pulmonary Dilation)
• Oxygen therapy (Maintains correct PO2 and pH)
• IV therapy (hydration and nutrition)
Nursing Management
✓ Close monitoring
✓ Keep oxygen consumption as low as possible (handle
infants as little as possible)
Do not hyper-oxygenate! Hyperoxygenation can lead to
Retinopathy (irreversible blindness of the neonate)
✓ Suction only when necessary (Gently but quickly)
✓ Encourage parents to verbalize feelings.
Meconium Aspiration Syndrome
Nakalunok/Naka-inhale ng meconium or first poop of the
baby.
➢ Relaxation of the anal sphincter and passage of meconium
into amniotic fluid due to intrauterine urine.
Risk for: Full term/ Post term infants

Hypoxemia (in the Pathophysiology

Atelectasis lungs), and Transudation
(lung
Increased pulmonary (lung injury)
collapsed)
vascular pressure

Lungs become stiffer

(hyaline membrane)

Clinical Manifestations
o Silverman Andersen Index – is the type of assessment to
check for respiratory distress
▪ 0 = no respiratory distress
▪ 10 = severe respiratory distress
• Chest indrawing and retractions
• Tachypnea
• Labored breathing
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Clinical Manifestations Therapeutic Management
➢ There will be ↑ carbon dioxide in the blood than can lead • Methylxanthines (Aminophylline, theophylline, caffeine)
to respiratory acidosis. o CNS Stimulates to breathing
➢ There will be no enough oxygenation due to lack of inhaled o Observe for Sx of toxicity (Tachycardia at rest,
oxygen vomiting, irritability, diuresis)
o Stained from meconium stool • Cafcit (Caffeine Citrate)
o Tachypneic o Urine output should be closely monitored (mild
o Expiratory grunting, nasal flaring, retractions diuretic effect)
o Initially cyanotic
o Classic Barrel chest Nursing Management
o Respiratory distress with gasping ✓ Observation combine with monitoring is the most effective
means of identifying neonatal apnea
Diagnostic Evaluation
(if apnea begun)
• Laryngoscopy – there will be a scope with video at the end
✓ Gentle tactile stimulation (rubbing the back or chest gently)
down to the larynx to visualize aspirated/meconium in the
✓ Flow-by oxygen and suctioning
area.
✓ Chin is raised gently to open airway
• Chest x-rays
✓ Infant is NEVER SHAKEN
• Pulse Oximetry – check for hypoxemia ✓ Record episodes of apnea
• Echocardiography

Therapeutic Management Sudden Infant Death Syndrome (SIDS)

• Tracheal suctioning (poor respiratory effort, low heart rate, • Sudden death of infant under 1 year of age
poor tone) • “Crib death”
• Ventilatory support Etiology: UNKNOWN (idiopathic)
• Exogenous surfactant administration Contributing Factors:
• IV Fluids
✓ Prone sleep position
• Systemic antibiotics – for prevention of infection
✓ Soft bedding
o Ampicillin – 2x a day
✓ Use of pillow
o Gentamicin – once a day
✓ Brainstem abnormality
✓ Co-sleeping with parents
Nursing management
✓ Maternal smoking
✓ Same with high-risk neonates
Manifestations and Diagnosis
Apnea of Prematurity (AOP) Manifestations:
• Common phenomenon in preterm infants May be seen:
• Characterized by apneic spells • Frothy-blood tinged fluid in the mouth
The baby is not breathing for 20 seconds • Lying face down in the secretions
Preterm baby • Hands clutching in the sheets
Premature is not sensitive to hypoxemia and hypercarbia Diagnosis:
✓ Autopsy
TYPES ✓ Investigation of the Scene
• Central Apnea
o CNS does not transmit signals to the respiratory Nursing Management
muscles. ✓ Allow the parents to say goodbye
• Obstructive Apnea ✓ Encourage to hold their infant
o Airflow ceases due to upper airway obstruction. ✓ Encourage verbalization of feelings
✓ Provide a quiet room with dim lighting
• Mixed Apnea
✓ Explain that the death is due to SIDS and it is not
o Combination of central and obstructive apnea (*most
preventable or predictable
common)
Recommendation in preventing SIDS
Pathophysiology
✓ Place infants on their back when sleeping
Immature respiratory centers (of the (Plagiocephaly: change head position periodically)
brain) ✓ Use firm mattress
✓ Avoid exposure to smoke
Weakness of muscles of the thorax ✓ Offer a pacifier to sleep
and diaphragm

Apneic Episodes

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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Neonatal Sepsis Therapeutic Management
• Handwashing
➢ Generalized bacterial infection in the blood stream. • Antibiotic Therapy
➢ Breastfeeding – has a protective effect.
• Regulation of fluids
➢ Colostrum – contains agglutinins (affective against gram-
• Oxygen therapy
negative bacteria), IgA and iron-binding proteins, as well
as macrophages and lymphocytes.
Sepsis – or septicemia, refers to a generalized bacterial Hyperbilirubinemia
infection in the bloodstream. Neonates are highly susceptible ➢ An excessive level of accumulated bilirubin in the blood
to infection because of diminished nonspecific (inflammatory) and is characterized by jaundice (ICTERUS)
and specific (humoral) immunity. (a yellowish discoloration of the skin, sclera and other
Sources of infection – From the mother itself – Sepsis in the organs)
neonatal period can acquired prenatally across the placenta ➢ Hyperbilirubinemia is a common finding on the newborn
from the maternal bloodstream or during labor from ingestion and in most instance is relatively benign. However, in
or aspiration of infected amniotic fluid. extreme cases, it can indicate a pathologic state.
Early-onset sepsis (<3 days after birth) is acquired in the NOT NORMAL!
perinatal period. Infection can occur from maternal infection. ▪ Jaundice appears in 2nd or 3rd day
Late-onset sepsis (1 to 3 weeks after birth) is primarily ▪ Peaks on 3rd – 5th day
nosocomial (healthcare associated or hospital-acquired ▪ Declines on the 5th – 7th day
infection or HAI), and the offending organisms are usually
o Staphylococci Causes:
o Klebsiella organisms • Physiologic
o Enterococci • Breastfeeding-associated
o E. coli
• Excessive production of bilirubin
o Candida species
• Liver problem
o Coagulase-negative staphylococci – older children and
• Combined overproduction and underexcretion
adults, found to be cause of septicemia in ELBW and
VLBW • Other conditions (G6PD, hypothyroidism, galactosemia,
infant of a diabetic mother)
Pathophysiology • Genetic predisposition to increased production (Native
Americans, Asians)

Pathophysiology

After to 2 – 4 days the The output is

Starts with baby will start to bilirubin
excess RBC destroy or breakdown (Stool and
the excess RBC Urine)

Jaundice Increase
Liver is premature
bilirubin in the
skin and and can’t
yellow blood that will go
metabolize yet
sclera in the tissue
properly
levels
Clinical Manifestations/ Diagnostic Evaluation
NORMAL -PATHOPHYSIOLOGY- PROBLEM
CBC – leukocytosis or leukopenia. (blood)
(↑ WBC) (↓ WBC)
CSF Analysis (Cerebrospinal Fluid)
Blood Culture and sensitivity test (blood)
CRP or C-Reactive Protein test (blood) – determine or
diagnose if there is an inflammation or bleeding in the body
Antibiotic therapy for 7 – 10 days
• Because of sepsis is easy to confuse with other neonatal
distress
• Antibiotic therapy is continued 7 to 10 days if culture are
positive, discontinued in 36 to 48 hours if cultures are
negative and the infant is asymptomatic, and most often
administered via IV infusion. Antifungal and antival
therapies are implemented
• Prognosis
o Infection was assessed early on – GOOD prognosis
o Infection spread out in the brain – POOR prognosis
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Nursing Care Management
✓ Vit. D/ Sunlight – can help dilute the bilirubin so it can be
excreted out in the urine.
✓ Phototherapy (partial sunlight)
▪ Wear eye shield
▪ Genital shield/ Diaper
▪ Clothes
✓ Periodically turn infants (*has not been shown to accelerate
clearance)
✓ Check hydration status
o manifestation of dehydration in infants:
– poor skin turgor (>2 – 3 secs) (N: <2-3 secs)
– sunken eyeball
Clinical Manifestations – sunken fontanel
• Jaundice – the yellowish discoloration primarily of the – ↓ UO
sclera, nails, or skin. – dry & cracked lips
• Appears within 24 hours – Sepsis or HDN or one of the – ↓ capillary refill (> 2 secs) (N: 1-2 secs)
maternally derived diseases such as diabetes mellitus or
infections.
• Appears on the 2nd or 3rd day, peaks at the 3rd to 5th day, and
decline at the 5th to 7th day – Physiologic jaundice
o Serum bilirubin test more than 200 mumol/L
▪ (Normal Level: Below 200 mumol/L)

Complications:
o High Bilirubin levels can lead to Bilirubin
encephalopathy.
o Kernicterus – (bilirubin-induced neurologic
dysfunction) yellow staining of brain cells and brain
necrosis.

Diagnostic Evaluation
• Serum bilirubin
o If more than 200 mumol/L
▪ Normal Level: Below 200 mumol/L
: Unconjugated bilirubin (0.2 to 1.4 mg/dL)
• Transculatenous bilirubinometry
• Hour-specific serum bilirubin levels – GOLD
STRANDARD

Therapeutic Management
• Phototherapy
o consists of exposing the infant’s skin to an
inappropriate light source.
o Light promotes bilirubin excretion by
photoisomerization.
o Alters the structure of bilirubin to a soluble form
(Lumirubin)
o Enhance excretion but not production
• Exchange Transfusion

• Phenobarbital – for infants w/ hemolytic disease

o Effective if given to mother days before the delivery
o Promotes hepatic synthesis of glucuronyl transferase
• Intravenous Immunoglobulin – ABO incompatibility
and Rh isoimmunization
• Early initiation of feeding/ breastfeeding
• Encourage frequent and effective BF
• Monitor early stooling – loose stools may indicate
accelerated excretion (check perineal irritation)

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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
DISEASES OF THE NEWBORN Diagnostic Evaluation
❖ Necrotizing Enterocolitis (NEC) • Abdominal X-ray
❖ Retinopathy of Prematurity o See “sausage-like” or sausage-shaped dilation
❖ Hemolytic Disorder
❖ Transient
o Pneumatosis intestinalis – “soapsuds” gas forming
bacteria
NECROTIZING ENTEROCOLITIS (NEC) • CBC
➢ Inflammation and death of intestinal tissue. It may involve just the lining o Anemia (↓ RBC),
of the intestine or the entire thickness of the intestine. In severe cases, the o Leukopenia (↓ WBC) – severe preterm
intestine may even perforate. o Leukocytosis (↑ WBC) – a bit older infants
➢ If this happens, the bacteria normally found only in the intestine can leak
into the abdomen and cause widespread infection.
o Metabolic acidosis
➢ Acute inflammatory disease of the bowel with increased o Electrolyte imbalance
incidence in preterm and other high-risk infants
➢ Cause is uncertain Therapeutic Management
➢ May be due to vascular compromise 1) Prevention
o Intestinal immaturity: o If baby is suspected – Dr order: NPO
▪ Gastrointestinal dysmotility > Oral Feedings withheld for at least 24 – 48 hours
▪ Impaired gastric capacity 2) Breastmilk
▪ Altered anti-inflammatory control o After 24 – 48 hours, u can do breastfeeding
▪ Impaired host defense o Have some passive immunity (IgA), macrophages,
lysozymes.
Necrotize – namamatay, infection, inflamed 3) Maternal steroid administration – promotes early gut
Enterocolitis closure and maturation of gut barriers
↓ ↓ 4) Probiotics
colon infection/ inflammatory
Necrotizing enterocolitis – nabubulok ang small or large Medical Management
intestines due to inflammation. o NPO – nothing per orem
Risk: Premature Infants o DR order:
o It usually develops within two weeks of birth. ▪ Gastric decompression (Lavage);
o 80% occurs in premature babies, 10% of infants who ▪ Drain gastric acid
weigh less than 3 pounds and 5 ounces develop NEC. – Hanggat kaya, it should be empty
o Intravenous Antibiotics
Pathophysiology o Abdominal X-ray – EVERY 4 – 6 HOURS
• Hypoxic event – (di nakakahinga agad yung baby = ▪ If upon Xray, the patient is not improving
vascular compromise sa bituka) ▪ GOAL: To prevent perforation
– Di pumutok ang bituka
• Asphyxia
– If pumutok = Peritonitis
• Vascular compromise – Intestinal ischemia
▪ Do: Bowel Resection (cut) & Anastomosis (dikit)
• Ischemia – there will be bacterial proliferation, – 16 hours OR
inflammation and infection will happen Depends on the extent of injury
(intestinal mucosa will not secrete proteolytic enzyme to
protect the intestine)
Complications:
Risk: not enough IgM & Prematurity
• Fat malabsorption – unable to gain weight, unable to
Clinical Manifestation absorb calories
1. Abdominal distention Nursing Care Management
2. Gastric residuals o Do not put diapers
o To feed: nilalagyan ng OGT (Oral Gastric Tube)
– thru OGT – if may backflow ng milk, it’s a sign RETINOPATHY OF PREMATURITY (ROP)
– Normal: when u feed a baby 30-40 mins, there is no ➢ A disorder involving immature retinal vasculature
gastric residual ➢ Formerly known as the “Retrolental Fibroplasia”
Reto – back
3. Hematochezia Lental – lense
o Blood in the stool Fibro – scar
▪ Milena – black tarry stool = Upper G.I bleed Plasia – proliferation
▪ Hematochezia – fresh blood in the stool = Lower ➢ Proliferation of scar at the back of the lens.
G.I bleed ➢ Occurs when abnormal blood vessels grow and spread
4. Nonspecific Sign throughout the retina, the tissue that lines the back of the
o Lethargy, poor feeding, hypotension, apnea, vomiting eye. These abnormal blood vessels are fragile and can leak,
(bile-stained), decreased urine output, hypothermia scarring the retina and pulling it out of position.
o Onset: between 4 and 10 days
▪ 4 – 10 days after the initiation of feedings.
▪ Especially if preterm has history of hypoxia
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Etiology Pathophysiology
• Hyperoxemia, Hypoxia, Hypercarbia, Hypocarbia, Rh antibodies
Rh (–)
Prenatal Complicatin, Exposure to light mother
Rh (+) baby enter fetal
Risk: Premature Baby circulation

Pathophysiology
Severe vascular Stimulation of Erythroblastosis RBC
constriction in Hypoxia in vascular fetalis destruction
retinal the area proliferation (Severely Anemia) and hemolysis
vasculature towards the lens

Aqueous and Clinical Manifestations

Retinal
Vitreous humor
edema &
Retinal 1. Jaundice within the 1st 24 hours.
becomes detachment 2. Fetal hydrops (generalize edema)
hemorrhage
TURBID
3. Elevated serum unconjugated bilirubin
4. Anemia – (< hemoglobin)
Irreversible – Hemoglobin
blindness Normal: Female: 12 – 14 mg/dL
: Male: 14 – 16 mg/dL
Severe vascular constriction in retinal vasculature = lead 5. Hepatosplenomegaly
to hypoxia
Hypoxic event – body will try to compensate by Diagnostic Evaluation
proliferating (pinapadami) the vasco chuchuness of Mommy Rh (–) will conduct a blood test
capillaries If she develops antibodies
Risk for: Preterm = The baby is Rh (+)
91 – 94 % 1. Maternal antibody titer (Indirect Coombs test)
Nothing to be alarm of 2. Amniocentesis – test fetal blood type
DON’T INCREASE OXYGEN! 3. Ultrasound/ Ultrasonography

Therapeutic Management Therapeutic Management

✓ Strict oxygen management
o Maintain oxygen
o Do not increase oxygen level right away!
o Refer to Doctor
✓ Cryotherapy ablation
o Using cold to kill blood vessels that may cause ROP
✓ Laser Therapy
o Using heat as a destroying medium.
Cryotherapy and laser – pinapahinto yung proliferation,
slowing or reversing the abnormal growth of blood vessels
Nursing Care Management
• ↓ constant bright environmental light
• Inform the parents that infants eyelid will be closed and
edematous post operatively.
• If mother is nanganak na – give Rh Isoimmunization (Rh
Ig) (Rhoga) is administered at 28 weeks of pregnancy and
72 hrs after birth
o This will deactivate antibodies in mother.
o Blood type can see if ↓ RBC & h = fetal anemia
• Intrauterine Transfusion
o Ultrasound guided sa umbilical cord
o Gaano kadaming blood? Depends sa Doctor or sa
gaano karami ang need
• Exchange Transfusion
o If nakalabas na si baby from mother
o Infant’’s blood is removed in small amounts and
replaced with compatible blood
• Phototherapy
Risk for: Miscarriage or Preterm labor

HEMOLYTIC DISEASES OF THE NEWBORN Nursing care Management

➢ Term “hemolytic” is derived from the Latin word for • Assessment: see early jaundice, history of Rh
“destruction” (lysis) of red blood cells. incompatibility
➢ Abnormally rapid rate of RBC destruction. • Baby – NPO
➢ Anemia caused by this destruction stimulates the o Monitor for clinical manifestation of blood transfusion
production of RBC. reaction (fever, difficulty of breathing, rashes)
• Phototherapy
Causes:
o Eye shield and Genital shield
• Rh Incompatibility (Fetal anemia) • Urine, Intake and Output
• ABO Incompatibility (can cause jaundice but not really • VS
hemolytic disease)

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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
TRANSIENT TACHYPNEA OF NEWBORN Therapeutic Management
➢ Short period of time NO CURE.
➢ Can happen to ALL infants. 1. Therapy
➢ Preterm, term, post term 2. Referral to the Doctor of all at risk complications
Can happen if baby aspirate meconium. • Surgeries to correct congenital anomalies
• Hearing and vision testing/ evaluation
Clinical Manifestations • Thyroid function tests
• Increased RR (Tachypnea)
o Normal RR of newborn: 40 – 60 or 30 – 50 bpm Nursing Care Management
• Retraction • Supporting the family at the time of Diagnosis
• Nasal flaring o Culture has significant effect
• Cyanosis • Assist the Family in Preventing Physical problems

Diagnostic Evaluation If hindi na-diagnose agad…

• T/C Trisomy 21 (Do karyotype)
Determine the cause by:
• At risk of injury, environment should be safe.
• Chest X-ray
• Promote the Child Developmental Progress
• CBC and Blood culture
• Assist in Prenatal Diagnosis and Genetic Counseling.
Therapeutic Management and Outcome
• Oxygenate because after 2 – 3 days, mawawala na

TRISOMY 21
➢ “DOWN SYNDROME”
➢ Physical and cognitive abnormalities
➢ Typical life expectancy 60 YEARS OLD
With proper treatment and therapy
Therapy – as early as 18 months
➢ know thru Karyotyping: The 21st Chromosome instead of
2, it became 3. Attributable to extra chromosome 21.

Etiology: UNKNOWN

➢ Can happen to anyone

➢ Higher incidences with mother who delivers over 35 years
of age.

Clinical Manifestations
PHYSICAL
o Slanted eyes
o Low set ears
o Transverse palmar creases
o Additional fats or skin in neck part
o Flat face, nose, forehead
Other symptoms:
• Intelligence
o Severe – Low average intelligence
o Mild – Moderate range of Cognitive Impairment
• Social Development
• At risk of Congenital abnormalities
o Heart, kidney diseases, muscoskeletal defects
o Cervical spine mobility
• Sensory problems
o Poor muscle strength
• Growth
o Small stature than general
o Weight gain rapid more than normal
• Sexual development
o May be delayed, incomplete, or both
o Female – can have menstruation, ovulation
o Male – genitalia & facial hair – undeveloped
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
NCMA 219 LEC PHENYLKETONURIA (PKU)
CARE OF THE MOTHER & CHILD AT RISK
Phenylalanine – a substance that we get from food we eat
WEEK 8 (meat, milk, eggs)
Prof: Mrs. Shiella May Edquibal, Man, RN Phenylalanine is needed to convert –> tyrosine
Newborn Screening To convert, it needs Phenylalanine hydroxylase
• Congenital Hypothyroidism ➢ Phenylketonuria – NO Phenylalanine hydroxylase
• Phenylketonuria
➢ If there’s no tyrosine, it will lead to neurotransmitter.
• Galactosemia
• G6PD (Glucose-6-Phosphate Dehydrogenase Deficiency)
• Congenital Adrenal Hyperplasia • Increased phenylalanine will lead to:
Infant and Young Problems o Brain injury
• Failure to thrive. o
• Colic
o Seizure
Phenylpyruvic acid in the urine
NEWBORN SCREENING (NBS) – Iniihi mo yung excess Phenylalanin
➢ Has 3 parts
➢ Very important to be done to all babies. Pathophysiology
➢ Should be done to 24 – 48 hours after birth.
↓ tyrosine
➢ Mandatory
➢ Hospital
➢ Health Center
Screening is until 2 days after birth. ↓ Tryptophan ↓ Dopamine ↓ Melanin

Three parts:
Decreases Decreased plasma Fair skin,
1. Blood Spot Screening levels of
level of Blue eyes,
2. Pulse Oximetry Screening (heart condition) serotonin catecholamines Blond hair
3. Hearing Screening (responsible for
o (OAE) stress response)

Where do you get the blood needed for NBS? Therapeutic Management
✓ Heel of the foot • Diet (no to meat!)
o ↓ Phenylalanine : ↑ tyrosine
Diseases that can be diagnoses with NBS o No meat, nuts is an ecemption.
Metabolic Diseases • No medication
CONGENITAL HYPOTHYROIDISM Nursing Management
➢ Thyroid – regulates metabolism, stress response, ability • If the child grow until he can understand anything – s/he
thermoregulate need to know his/ her disease, s/he needs to be aware of it.
➢ Hypothyroidism – ↓ thyroxine • Parent – basic understanding
➢ With congenital hypothyroidism – thyroid is not
functioning at all or not secreting enough thyroxine.
GALACTOSEMIA
Signs and Symptoms ➢ Baby doesn’t have 3 hepatic enzyme. Which is needed
• 1st few days/ months – looks normal convert the galactose to glucose.
• Without proper treatment can lead to: o Galt
o Intellectual disability – developmental delay, o Galk
detoriation o Gale
o Physical deformity ➢ Baby with galactosemia can’t convert galactose to glucose.
➢ What the baby drink (breastfeed), doesn’t have an effect,
Treatment no nutrients
• Levothyroxine (oral medicine) – maintenance drug
Clinical Manifestations
How to feed the baby? • ↑ unmotabolize milk = ↑ sugar, damage the eyes, liver &
o Crash the tablet and mixed it in the breastmilk or brain
formula, bottle feed; • If left untreated = Fetal death
o Given ONCE daily.
If not be able to be given medication right away during Therapeutic Management
infancy, it can lead to Irreversible intellectual disability. • Stop feeding with breastmilk or formula feeding.
• Soymilk products
• Lactose/ Galactose-free formula feedings
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Nursing Care Management • Ultrasound – to see if the baby has ovaries and uterus
• Diet modification
• Don’t eat food with galactose and lactose INFANT AND YOUNG INFANT PROBLEMS
• Don’t eat – dairy products, cheese FAILURE TO THRIVE
• Mother and children should be aware. Bata – di nag d-develop ng normal, not gaining weight/
doesn’t have the weight appropriate to his/her age.
G6PD (GLUCOSE – 6 – PHOSPHATE Normal: after 6 months = 2x gain weight
DEHYDROGENASE) : 1 year = 3x bigat

➢ RBC – lifespan is up to 120 days Pathophysiology

➢ G6PD – enzyme that can help RBC to sustain life up to 120
1. Inadequate Caloric intake
days until mapalitan
2. Inadequate absorption
➢ G6PD DEFICIENCY
o Chron’s disease, cystic, fibrosis
o No G6PD
3. Increases Metabolism
o Nagh-hemolyze or namamatay agad yung RBC even
o Hyperthyroidism, sickly
before mapalitan ng bago in 120 days
4. Defective Utilization
Complication: Hemolytic Anemia
o Genetic anomaly
Clinical Manifestations
Clinical Manifestations
• Pale skin
• Developmental delay
• Yellow skin, eyes, mouth (jaundice)
• No fear of stranger
• Fever
• Apathy
• Weakness
• Under nutrition
• Dizziness
• Confusion Diagnostic Evaluation
• Dark-colored urine
• Weigh the baby
• Heart murmur
• ↑ RR
Therapeutic Management
• Know the reason
Therapeutic Management
• Iron supplement
COLIC
• Blood/ Iron Transfusion
➢ Paroxysmal Abdominal Pain
➢ “KABAG” in Filipino
CONGENITAL ADRENAL HYPERPLASIA
➢ Most fatal Clinical Manifestation
➢ RARE • Baby is crying for 3 hours a day
➢ Adrenal glands (in the tip of both kidney), produce: • 3x a week for almost a month
o Androgens (steroid hormone) After 3 week, mawawala na.
o Aldosterone (maintain urine ↑ Androgen
production & water reabsorption) ↑ Aldosterone
Etiology
o Cortisol (stress response) ↓ Cortisol
Theories
Hyperplasia – lumalaki • Too rapid breathing
Adrenal hyperplasia – lumalaking adrenal glands
• Overeating
• Swallowing excessive air
Clinical Manifestation
• Ambiguous Genitalia (lumalaki and clitoris) Therapeutic Management
• Precocious Genitalia • Order different kind of milk
• Medication:
Therapeutic Management o Antispasmodics
• Glucocorticoids – suppress the abnormally high secretion o Antihistamines
of ACTH and adrenal androgens o Anti flatulent
o ACTH – Adrenocorticotrophic Hormone
• Ambiguous and Precocious – infertile Nursing Management
o Ambiguous – will not show secondary sex, not • Know what the baby eats, how much, for how long.
develop • Time of day
o Precocious – not develop spermatogenesis • Smoking and nicotine – can cause colic (theory)
• Know the characteristics of …
Nursing Care Management
• Ambiguous – explain to the patient
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
NCMA 219 LEC
CARE OF THE MOTHER & CHILD AT RISK
WEEK 9
Prof: Mrs. Shiella May Edquibal, Man, RN
Problems in toddlers and preschool
• Accidental Poisoning (Lead/Salicylate)
• Falls
• Drowning
• Aspiration and suffocation
• Conjunctivitis
Problems in school age
• Enuresis
• Encopresis
• ADHD
• Bullying
Problems in adolescents
• Amenorrhea
• Dysmenorrhea PATHOPHYSIOLOGY AND CLINICAL MANIFESTATION
• Vaginitis (female)
• Gynecomastia (male)

PROBLEMS IN TODDLERS &PRESCHOOL

LEAD POISONING
Metallic substance, an ingredient that we use to create
paint, metals, that could also be found in soil, environment.
There are toys and things that have lead and toddlers and
preschooler could reach out, and they can ingest those.
➢ The use of lead in paint and leaded gasoline has been
banned in the United States.
In the Philippines, it’s also banned.
➢ After this change in policy, the average blood lead level
(BLL) in the United States for people ages 1 to 74 years
dropped from 12.8 mcg/dl in 1980 to 1.3 mcg/dl in 2010.

Causes of Lead Poisoning

➢ In most instances of acute childhood lead poisoning, the
source is nonintact lead-based paint in an older home or
lead contaminated bare soil in the yard.
Nonintact lead based – daily accumulation/ exposure of the
child to lead. They might touch the materials and put their
hands in their mouth.
➢ Microparticles of lead gain entrance into a child’s body
through ingestion or inhalation and, in the case of an
exposed pregnant woman, by placental transfer.
Lead can transfer from the woman → placenta → baby.
➢ When measured, a mother’s lead level is nearly the same
as that of her unborn child. However, although the level of
lead may not be harmful to an adult woman, it can be
harmful to the fetus.
➢ Inhalation exposure usually occurs during renovation and
remodeling activities in the home,, ingestion happened
during normal day-to-day play and mouthing activities.
➢ Sometimes, a child will actually swallow loose chips of
lead-based paint because it has a sweet taste.
➢ Water and food may also be contaminated with lead.
➢ A child does not need to eat loose paint chips to be exposed
to the toxin; normal hand-to-mouth behavior, coupled with
the presence of lead dust in the environment that has settled
over the decades, is the usual method of poisoning.
If you are living in an environment with a high lead area/
houses, those dust settled in your floor and the toddlers and
preschoolers can inhale and touch those.
Lead can affect any part of the body including Renal
(kidneys), Hematologic (blood), Neurologic (brain)
Most common concern for young children – the developing
___ & nervous system, which are more vulnerable than
those of older children and adults.
Lead in the body moves via equilibration process between
the blood, soft tissue, organs, and the bones and teeth.
Lead ultimately settles in the bone and teeth wherein it
remains inert and in storage. This makes up the largest
portion of the body.
At the cellular level, it completes with molecules of
Calcium, interfering with the regulating action of calcium.
In the brain – lead disrupts the biochemical causes and may
have a direct effect on the release of neurotransmitters and
may cause alteration in the blood brain barrier and may
interfere with regulation of synaptic activity.
There’s also a relationship between anemia and loid lead
poisoning. Children who are iron deficient absorbed lead
more readily than those with sufficient iron storage.
Lead can interfere with binding of iron on to the heme
molecule. This sometimes create a picture of anemia.
Even though the child isn’t iron deficient, lead toxicity to
the erythrocytes needs to the release of erythrocyte
protoporphyrin, which leads to anemia.
With high levels of lead in the body:
Hematologic System:
– (Synthesis of heme – red blood cell production)
– Can interfere with the synthesis of RBC production.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
– The body will try to increase the erythrocyte
protoporphyrin (it’s a precursor to RBC production)
(u need this enzyme to help w/ production of RBC)
– Your body will work double time to produce RBC and
this can lead to anemia.
In the Renal System:
– Proximal tubules in the kidneys helps with
reabsorption of substances. With lead poisoning, there
will be increased permeability in the proximal tubules.
– Which will urinate glucose, protein, ketones.
Decreased Vit. D production.
– Urinate coproporphyrin. This can also damage the
teeth and the bone.
In the Neurologic System:
– Most problematic, mostly irreversible.
– Because if the lead poisoning is treated, the problem in
the hematologic and renal system are reversible.
– Has blood brain barrier – filters materials and things
that can go to the brain. A protective barrier for the
brain not to receive toxins, chemicals, etc.
– If there’s lead poisoning – it increases the permeability
(there will be more substances that cam enter the brain,
even the toxins)
DIAGNOSTIC EVALUATION
• Blood examination – Lead testing of a venous blood
specimen from a venipuncture.
2 types:
o Blood test of elevation of erythrocyte protoporphyrin
o Blood Lead Level (BLL)
• Collection process is important.
• Blood must be collected carefully to avoid contamination
by lead on the skin.
• Prior to 2012, the level of concern for an elevated BLL had
dropped from 80 mcg/dl in 1950 to 10 mcg/dl.
Anticipatory Guidance
• Most effective prevention of lead exposure is ensuring that
environmental exposures are reduced before children are
exposed to the hazards (e.g., paint, soil, dust, water that
contains lead).
• There has been recent concern regarding toys and other
imported items children play with that were found to
contain lead.
• Parents should carefully evaluate the source of the toy
(manufacturer) or item the child may play with and not
assume it is safe.
Check if the area that u will go was built in 1980s. if u’re buying toys,
evaluate the toys if it has lead in it.
Screening for Lead Poisoning
• Targeted screening is acceptable when an area has been
determined by existing data to have less risk.
• Children should be screened when they live in a high-risk
geographic area or are members of a group determined to
be at risk (e.g., Medicaid recipients), or if their family
cannot answer “no” to the following personal risk
questions:
o Does your child live in or regularly visit a house that
was built before 1950?
o Does your child live in or regularly visit a house built
before 1978 with recent or ongoing renovations or
remodeling within the past 6 months?
o Does your child have a sibling or playmate who has or
had lead poisoning?
• Screening should be done at ages 1 and 2 years.
• Any child between the ages 3 and 6 years who has not been
previously screened should also be tested.
• All children with risk factors should be screened more
often.
Therapeutic Management
• The degree of concern, urgency, and need for medical
intervention changes as the lead level increases.
• Education is one of the most important elements of the
treatment process.
Tell them what is lead, how does it affect, the materials with
lead, etc.
• Several areas that the nurse needs to discuss with the family
of every child who has an elevated BLL (≥ 5 mcg/dl)
include the following:
o The child’s BLL and what it means.
o Potential adverse health effects of an elevated BLL
o Sources of lead exposure and suggestions on how to
reduce exposure, such as importance of wet cleaning
to remove lead dust on floors, windowsills, and other
surfaces.
o Importance of good nutrition in reducing the
absorption and effects of lead; for persons with poor
nutritional.
(increased the iron supply for the baby, toddler or
preschool & increased calcium and vitamin D
intake)
• Chelation Therapy – Chelation is the term used for
removing lead from circulating blood and theoretically,
some lead from organs and tissues.
This attracts magnets or metals like lead to the drug and the
patient will urinate it.
Can be done outpatient.
• Equilibration process between blood, soft tissues, and
other sites in the body, there is often a rebound of the BLL
after chelation. After the body burden of lead is reduced
enough to stabilize the BLL, rebound will cease.
• Multiple chelation treatments may be necessary.
The treatment can’t be done once, bcos there’s a risk of
rebound or it will not be effective if it’s once. There will be
several chelation treatments to make sure that the lead will
flush out from the body.
• Adequate hydration is essential during therapy because
the chelates are excreted via the kidneys.
• Severe lead toxicity (lead level ≥70 mcg/dl) requires
immediate inpatient treatment, whether symptoms are
present or not.
• A less used oral chelating agent, d-penicillamine, is
sometimes used to treat lead poisoning, but low doses
should be used in children. Monitoring of renal function
and blood counts during administration is essential.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Prognosis
• Although most of the pathophysiologic effects of lead are
reversible, the most serious consequences of both high and
low lead exposure are the effects on the central nervous
system.
• In children with lead encephalopathy, permanent brain
damage can result in
o cognitive impairment
o behavior changes
o possible paralysis
o seizures
• However, low-dose exposure may also cause permanent
neurologic deficits.
• Increased distractibility, short attention span, impulsivity,
reading disabilities, and school failure have been
associated with lead exposure.
Nursing Care Management
• Primary goal in lead poisoning – Prevent the child’s initial
or further exposure to lead.
• For children with low level exposure, this requires
identifying the sources of lead in the environment.
• For children who undergo chelation therapy, the nurse
prepares them for the injections and makes all efforts to
reduce injection pain.
• Chelation Therapy – Chelating agents may be
administered deeply into a large muscle mass.
o IM – toddlers and preschooler
o IV – adults
• Calcium EDTA – medication to help with the calcium
deficit and Vit. D problem
o Local anesthetic procaine injected with the drug – to
lessen the pain from calcium EDTA.
• Rotation of sites is essential to prevent the formation of
painful areas of fibrotic tissues.
• Because calcium EDTA and lead are toxic to the kidneys
o Keep records of intake and output
o Assess the results of urinalysis to monitor renal
functioning.
Increase oral fluid intake and monitor intake and output
thru your urine monitoring. To determine if the kidneys are
still functioning.
FALLS
➢ Are still a hazard to children in this age-group, although by
the later part of early childhood, gross and fine motor skills
are well developed, decreasing the incidence of falls
downstairs or from chairs.
➢ However, playground injuries are common.
➢ Children need to learn safety at play areas, such as:
o no horseplay on high slides or jungle gyms,
o sitting on swings
o staying away from moving swings.
In developmental milestones of toddler – they want to be
independent. (Erik Erikson – autonomy vs. shame and
doubt)
They would want to roam around, unassisted.
You need to balance their safety while they’re having their
independence.
➢ The climbing and running activity of the typical toddler is
complicated by total neglect for and lack of appreciation of
danger, immature coordination, and a high center of
gravity.
➢ Falling from furniture is a major cause of injury, with
more children in this age-group sustaining head injuries
than older children.
➢ Gates must be placed at both ends of stairs.
➢ Accessible windows that are left often during warm
weather must be guarded with a rail.
➢ When children reach a height of 89 cm (35 inches), they
should sleep in a bed rather than a crib. (bcos they can
already climb the crib)
➢ If a bunk bed is selected, parents should be aware of
possible dangers, including falls from the top bed and the
ladder and head entrapment between the mattress and
guardrail or between the supporting mattress slats.
As a caregiver/ parent, remember to keep your eyes always
in the children.
DROWNING
One of the leading causes of mortality in children <5 y/o.
➢ Highest rate of drowning in the years 2000 to 2006 was in
children ages 0 to 4 years; children ages 12 to 36 months
are at higher risk for drowning during the same time period.
➢ Drowning deaths in infants occur most commonly in the
bathtub and large buckets.
➢ With well-developed skills of locomotion, toddlers are able
to reach potentially dangerous areas such as:
o Bathtubs
o Toilets
o Buckets,
o Swimming pools,
o Hot tubs, and
o Ponds or lakes.
➢ Toddlers’ intense drive for exploration and
investigation, combined with an unawareness of the
danger of water and their helplessness in water, makes
drowning always a viable threat.
➢ It is also one category of injury that results in death within
minutes, diminishing the chance for rescue and survival.
If the brain remains unoxygenated for 3 mins, it can cause
irreversible damage. >3 mins = death.
➢ Close adults supervision of children when near any source
of water is essential; many drowning in this age-group
occur when a supervising adult becomes distracted.
➢ Recommends “touch” supervision for small children; the
adult can reach out and touch or grab the child having
difficulty.
➢ Teaching swimming and water safety can be helpful but
cannot be regarded as sufficient protection.
➢ Pool fencing although critical, does not always deter fast-
moving children.
ASPIRATION AND SUFFOCATION
➢ Small children characteristically explore objects with their
hands and mouth and are prone to place FBs (foreign
bodies) into the air passages (nose and mouth).
➢ They also place objects such as beads, paper clips, plastic
toys, small magnets, or food items in the nose, which can
easily be aspirated into the trachea.
➢ Small items may also be placed into the external ear
canal; small rocks and pebbles appear to be a favorite item
for boys, whereas girls prefer colorful beads.
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➢ When such objects are placed into the nose or mouth, they
can be aspirated into the airway, causing subsequent
obstruction.
➢ Ingestion or aspiration of an FB can occur at any age but is
most common in older infants and children ages 1 to 3
years.
➢ Severity depends on the location, type of object aspirated,
and extent of obstruction.
➢ For example, dry vegetable matter, such as seed, nut,
piece of carrot, or popcorn, that does not dissolve and that
may swell when moistened creates a particularly difficult
problem.
Avoid giving dry vegetable matters to the toddlers.
➢ The high fat content of potato chips and peanuts may cause
the added risk of lipoid pneumonia.
➢ “Fun foods” such as hard candy and hot dogs are among
the worst offenders.
These cannot dissolve easily in the mouth.
➢ Offending foods, in order of frequency of aspiration, are
hot dogs, round candy, peanuts and other types of nuts,
grapes, cookies or biscuits, pieces of meat, caramels,
carrots, apples, peas, celery, popcorn, fruit and vegetable
seeds, cherry pits, gum, and peanut butter.
➢ Round foods are the most frequent offenders.
➢ The first four items together make up more than 40% of all
aspirated food items.
➢ Other items include plastic or glass beads, button or disk
batteries, burst latex balloons, pen or marker caps, and
coins.
➢ Objects such as small lithium or cadmium batteries may
cause esophageal or tracheal corrosion.
➢ Magnets can trap tissue/ mucosa in between them, which
can result in necrosis of that area.
➢ A sharp or irritating objects produces irritation and edema.
A round, pliable object that does not readily break apart is
more likely to occlude an airway than an object with a
different shape.
➢ A small object may cause little if any pathologic change,
whereas an object of sufficient size to obstruct a passage
can produce various changes, including atelectasis,
emphysema, inflammation, and abscess
Mechanism of Airway Obstruction
1st degree
o Children are a bit symptomatic at first.
o Obstruction allows passage of air in both direction.
o Patient can still breath in air and exhale air, bcos the
obstruction is just small.
o Problem – obstruction become bigger, can lead to
irritation.
o If left untreated – can lead to complete obstruction
2nd degree or Partial obstruction
o Air able to move past the obstruction in one direction
only. Air passages enlarge during inspiration and
diminish during expiration.
o Patient can inhale air but the patient can’t exhale the
Carbon dioxide which can lead to inflammation,
emphysema, respiratory problem.
Complete obstruction
o Air unable to move in either direction. FB and
edematous mucosa obliterate passage.
o Can lead to death.
Clinical Manifestations
• Initially, an FB in the air passages produces choking,
gagging, or coughing, but symptoms depend on the site of
obstruction and on the interval between aspiration and
presentation.
• Up to half of all children with FB ingestion may be
asymptomatic.
• Laryngotracheal obstruction most commonly causes
dyspnea, cough, stridor, and hoarseness because of a
decreased air entry.
• Cyanosis may also occur if the obstruction becomes worse.
• Bronchial obstruction usually produces cough (frequently
paroxysmal), wheezing, asymmetric breath sounds,
decreased airway entry, and dyspnea.
• In some cases a FB obstruction may be mistaken for croup.
• If the obstruction progresses, the child’s face may become
livid, and sometimes the child becomes unconscious and
dies of asphyxiation if the object is not removed.
• If obstruction is partial, hours, days, or even weeks may
pass without symptoms after the initial period.
• Secondary symptoms are related to the anatomic area in
which the FB is lodged and are usually caused by a
persistent respiratory tract infection located distal to the
obstruction.
• A history of recurrent intractable pneumonia is reason to
consider an FB in an airway. Often, by the time secondary
symptoms appear, the parents have forgotten the initial
episode of coughing and gagging.
• The most common symptoms observed in children brought
to medical attention ar:
o Stridor,
o Wheezing,
o Sternal Retraction,
o Cough
• When an object is lodged in the larynx, the child is unable
to speak or breath.
Diagnostic Evaluation
• The diagnosis of FB obstruction is usually suspected on the
basis of the history and physical signs.
• Radiographic examination reveals opaque FBs but is of
limited value in localizing vegetable matter and some
plastic items.
• Bronchoscopy is required for a definitive diagnosis and
removal of objects in the larynx and trachea. (video guided)
• Fluoroscopic examination is valuable in detecting FBs in
the bronchi.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
o On fluoroscopy, a check-valve – obstructed lung
remains expanded, the diaphragm remains low and
fixed on the obstructed side, and the heart and
mediastinum shift to the unobstructed side during
expiration.
o In a stop-valve obstruction, the heart and
mediastinum are drawn to the obstructed side and
remain there during both inspiration and expiration.
• The diaphragm on the obstructed side remains high,
whereas that on the unobstructed side moves normally.
• Other diagnostic evaluation:
o Endoscopy
o Bronchoscopy
o X-ray
Therapeutic Management
• FB aspiration may result in life-threatening airway
obstruction, especially in infants because of the small
diameters of their airways.
• Current recommendations for the emergency treatments of
the choking child include the use of:
o Abdominal thrusts (Heimlich maneuver) for
children over 1 year of age
o Back blows and chest thrusts for children less than 1
year of age.
• An FB is rarely coughed up spontaneously; therefore, it
must be removed by endoscopy or bronchoscopy.
• Removal of the FB must be done as soon as possible, since
the progressive local inflammatory process triggered by the
foreign material hampers removal.
• In addition, a chemical pneumonia soon develops, and
vegetable matter begins to macerate within a few days,
further complicating its removal.
Nursing Care Management
• Recognize the signs of Foreign Bodies aspiration and
implement immediate measures to relieve the obstruction.
• All persons working with children should be prepared to
deal effectively with aspiration of an FB.
• Choking on food or other material should not be fatal.
• Two simple procedures – can be used by both health
professionals and lay persons – can save lives.
o Back blows
o Abdominal thrusts
• It is the nurse’s obligation to learn these techniques and
teach them to parents and other groups.
• To aid a child who is choking, nurses need to recognize the
signs of distress.
• Not every child who gags or coughs while eating is truly
choking.
Prevention
• Small children should not be allowed access to small
objects that they might please in their nose or mouth.
• Anticipatory guidance for parents of small children is
essential. Nurses are in a position to teach prevention in a
variety of settings.
• They can educate parents singly or in groups about hazards
of aspiration in relation to the developmental level of their
children and encourage them to teach their children safety.
• Caution parents about behaviors that their children might
imitate (e.g., holding foreign objects, such as pins, nails,
and toothpick, in their lips or mouth).
CONJUNCTIVITIS
➢ “Sore eyes”
➢ Acute conjunctivitis (inflammation of the conjunctiva)
occurs from a variety of causes that are typically age
related.
• In newborns conjunctivitis can occur from infection during
birth, most often from Chlamydia trachomatis (inclusion
conjunctivitis) or Neisseria gonorrhoeae. These
organisms, as well as herpes simplex virus (HSV), cause
serious ocular damage.
• In infants, recurrent conjunctivitis may be a sign of
nasolacrimal (tear) duct obstruction.
➢ A chemical conjunctivitis may occur within 24 hours of
instillation of neonatal ophthalmic prophylaxis; the clinical
features include:
o mild lid edema
o sterile, non-purulent eye discharge.
• In children, the usual causes of conjunctivitis are viral,
bacterial, allergic, or related to a foreign body.
➢ Bacterial infection accounts for most instances of acute
conjunctivitis in children.
➢ Diagnosis is made primarily from the clinical
manifestations.
Clinical Manifestations of Conjunctivitis
Bacterial Conjunctivitis (“Pink Eye”)
o Purulent drainage
o Crusting of eyelids, especially on awakening
o Inflamed conjunctivitis
o Swollen lids
Viral Conjunctivitis
o Usually occurs w/ upper respiratory tract infection
o Serous (watery) drainage
o Inflamed conjunctivitis
o Swollen lids
Allergic Conjunctivitis
o Itching
o Watery to thick, stringy discharge
o Inflamed conjunctivitis
o Swollen lids
Conjunctivitis Caused by Foreign Body
o Tearing
o Pain
o Inflamed conjunctivitis
o Usually only one eye affected
Therapeutic Management
• Treatment depends on the cause.
• Viral conjunctivitis is self-limiting, and treatment is
limited to removal of the accumulated secretions.
• Bacterial conjunctivitis has traditionally been treated with
topical antibacterial agents such as:
o Polymyxin and bacitracin (Polysporin)
o Sodium sulfacetamide (Sulamyd)
o Trimethoprim and polymyxin (Polytrim)
• However, in one study of children with acute infective
conjunctivitis treated by placebo versus topical
chloramphenicol, there was little difference in cure rates;
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
the authors concluded that most children will get better
without antibiotic treatment.
• Fluroquinolones, approved for children ages 1 year and
older, are viewed by ophthalmologists as the best
ophthalmic antimicrobial agents available
fluoroquinolones
o Moxifloxacin
o Gatifloxacin
o Besifloxacin
Which provide broad-spectrum coverage, are bactericidal,
and are generally well tolerated.
• Drops – used during the day.
• Ointment – at bedtime.
✓ Ointment preparation remains in the eye longer but blurs
the vision.
• Corticosteroids – avoided because they reduce ocular
resistance to bacteria.
Nursing Care Management
• Keeping the eye clean and properly administering
ophthalmic medication.
• Remove accumulated secretions by wiping from the inner
canthus downward and outward, away from the opposite
eye.
• Warm, moist compresses, such as a clean washcloth
wrung out with hot top water, are helpful in removing the
crusts.
• Compresses are not kept on the eye because an occlusive
covering promotes bacterial growth.
• Instill medication immediately after the eyes have been
cleaned and according to correct procedure.
• Prevention of infection in other family members is
important consideration w/ bacterial or viral conjunctivitis.
• Keep the child’s washcloth and towel separate from those
used by others.
• Discard tissues used to clean the eye.
• Instruct the child to refrain from rubbing the eye and to
use good hand-washing technique.
PROBLEMS w/ SCHOOL AGE CHILDREN
ENURESIS
➢ “Bed-wetting”
➢ A common disorder that is defined as intentional or
involuntary passage of urine in children who are beyond
the age when voluntary bladder control should normally
have been acquired.
By the age of toddler period: 16 or 18 months – 3 y/o
A child should be able to have a bit of bladder control. They
should be able to wake up in the middle of the night/day to
tell u that they need to pee.
Enuresis happens when a child has already been past the
age of toddler hood and preschoolers (5 y/o & above), and
they still wet their bed.
➢ Medical evaluation is recommended when inappropriate
voiding of urine occurs at least twice a wee for a minimum
of 3 consecutive months and the chronologic or
developmental age of the child is at least 5 years.
➢ More common to boys than girls; nocturnal bed-wetting
usually ceases between 6 and 8 years of age.
o Primary – bed-wetting in children who have never been dry
for extended periods.
o Secondary – the onset of wetting after a period of
established urinary continence.
➢ The passage of urine may occur:
o Monosymptomatic – only during nighttime sleep,
with the child remaining dry during the day
o Polysymptomatic – where the child has daytime
urinary urgency and an occasional daytime accident in
conjunction w/ other conditions such as sleep apnea,
urinary tract infection, neurologic impairment,
constipation, or emotional stressors.
ETIOLOGY AND PATHOPHYSIOLOGY
• No clear etiology has been determined.
It is idiopathic. (unknown)
• Predictive factors have been noted:
o Longer duration of sleep in infancy,
o A positive family history
o A slower rate of physical development in children up
to 3 years of age.
• There is a high concordance rate of enuresis in
monozygotic (identical) twins and an even higher one in
dizygotic (nonidentical) twins, which suggests more than a
pure generic link in the disorder.
• Approximately 75% of all children w/ enuresis have a first-
degree relative who has, or has had, the disorder.
• Enuresis is primarily an alteration of neuromuscular
bladder functioning and as such is benign and self-limiting.
Self-limiting – as the child grows older, there’s a possibility
s/he will outgrow it.
• Emotional factors may influence the symptom. Some
children exhibit temporary regressive behavior resulting in
enuresis after the birth of a sibling or other trauma.
• Other children, such as those w/ attention deficit
hyperactivity disorder (ADHD), may have occasional
“accidents” when they become so involved in play that they
are unaware of a full bladder or “forget” to empty the
bladder.
• In other children, enuresis may be related to attempts to
toilet train before they are developmentally mature enough
to:
o Maintain bladder control,
o The emotional atmosphere surrounding the training
situation
o An excessive amount of emotional dependence on the
caregiver.
• Occasionally, enuresis can be a behavioral manifestation of
a personality disorder.
Several theories have been proposed to explain enuresis.
o The Sleep theory stems from parental reports that
these children sleep more soundly and are difficult to
arouse from sleep.
o Another theory related to functional bladder
capacity theory; the volume of urine voided after
maximum delay of micturition.
o Nocturnal polyuria theory suggests that the kidneys
of these children fail to concentrate urine during sleep
because of insufficient secretion of antidiuretic
hormone (ADH).
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The brain cannot secrete enough anti-diuretic hormone.
The baby at night will always need to urinate that can lead
to enuresis.
▪ The ADH circadian rhythm may thus be a
significant biologic marker in enuresis, but
additional research must be conducted to clarify
its role.
o Dysfunctional detrusor activity theory suggests that
an unstable bladder detrusor muscle spontaneously
contracts to produce bed-wetting, either because of
abdominal innervation or as a result of other, unknown
reasons.
• Studies to explore theses theories have yielded
contradictory and inconclusive results; ore research is
needed to clarify etiology and address contradictions.
Clinical Manifestations
• Predominant symptom – immediate urgency that is
accompanied by:
o Acute discomfort
o Restlessness
o Sometimes Urinary frequency.
• With nocturnal enuresis the child may or may not feel
urgency. If awareness of the urgency is present, the child
often reports difficulty awakening to urinate.
• Spontaneous voiding during sleep occurs, which usually
results in multiple nightly incidents.
• Spontaneous remission of nocturnal enuresis occurs in
approximately 15% of cases.
• However, is some cause nocturnal enuresis continues into
adolescence and adulthood.
Diagnostic Evaluation
During the initial phases of evaluation
• Routine physical examination – performed to rule out
physical causes, such as:
o Urinary tract infection
o Structural disorders
o Major neurologic deficits
o Nocturnal epilepsy
o Disorders that increase the nocturnal output of urine
(e.g., diabetes mellitus and diabetes insipidus)
o Disorders that impair the concentrating ability of the
kidneys (e.g., chronic renal failure or sickle cell
disease)
• Routine psychiatric evaluation – is warranted if
psychologic difficulties are evident or a personality
disorder is suspected.
• History of bed-wetting behavior is obtained, including
information about the toilet training process.
Ask the parents to check and record the number of times
and the time at night/morning when it occur if the child wet
their bed.
• Assessment – important feature
o Parental attitudes – by listening and asking parents
how they have attempted to cope w/ the bed-wetting.
o Baseline count of enuretic incidents
o Time of the day when each occurs.
• This is necessary not only to establish diagnostic reliability
but also to confirm outcome success after treatment.
• The baseline information is gathered for 1 to 2 weeks by
the child and family.
• It usually consists of:
o Chart or calendar given to the family on which they
indicate the date of the incident
o Time of the incident
o Approximate volume of the urinary output
• Physical examination may be followed by diagnostic
evaluation of functional bladder capacity.
• Functional bladder capacity is determined by having the
child hold off voiding until the strongest urgency is felt, at
which time the child voids into a measurement container.
• Normal bladder capacity (in ounces) is the child’s age + 2
Normal bladder capacity for:
o 6 years old = 8 ounces (237 ml)
• A bladder volume of 10 to 12 ounces (300 to 350 ml) is
sufficient for retention of a night’s urine.
Ex: urine is <237ml for 6 years old = the child cannot retain
the urine and they will urinate even at night
Therapeutic Management
• Conditioning therapy – involves training the child to
awaken to urinate after a stimulus is given, especially with
a urine alarm.
o The device consists of a moisture-sensitive wire pad
that is placed inside the underpants and is attached to
a bell or buzzer.
o When the system detects moisture, the bells or buzzer
sounds, which fully awakens the child.
o The child is thus conditioned to awaken at the
initiation of micturition or to the stimulus of the bell or
buzzer and eventually learns to continue voiding in the
toilet.
• The urine alarm can be very effective, but children may
relapse once they stop using it.
Relapse is addressed by reinstituting the alarm during
sleep.
• This method is inexpensive compared with drug therapy
and has no side effects.
• Retention control therapy – developed after the
observation of reduced functional bladder capacity in
children who were bed-wetters.
o The child drinks fluids while awake and alert, then
delays urination as long as can be tolerated to stretch
the bladder to accommodate increasingly larger
volumes of urine.
• Kegel, or Pelvic muscle, exercises may be helpful in
children with daytime enuresis.
• In the waking schedule treatment, the child is awakened
during the night at intervals to void. This method has been
successful in reducing, but not eliminating, bed-wetting
incidents.
• Drug therapy is increasingly being prescribed to treat
enuresis.
Three types of drugs are used:
o Tricyclic antidepressants – (if emotional stress)
o Antidiuretics – (so pt will not urinate at night)
o Antispasmodics – (to prevent spasms of the muscle)
• The selection depends on the interpretation of the cause.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
• Tricyclic antidepressant imipramine (Tofranil) – the
drug used most frequently, which exerts an anticholinergic
action in the bladder to inhibit urination.
• The dosage and time of administration are individualized,
and the drug is given in amounts sufficient to lighten sleep
but not to cause wakefulness.
U have to assess first when does enuresis usually happen;
at night or daytime or both.
• Some practitioners prescribe low doses, which reduces
bed-wetting in two thirds of children.
• However, almost all children relapse when the medication
is stopped.
o Length of treatment = 6 – 8 weeks
o Gradual withdrawal – over 4 weeks
Risk of drug:
o Overdosage to continue treatment or add more
medication if enuresis is unresolved.
• Caution parents about safe use and the need to keep
supplies of the drug from the reach of younger siblings.
• Anticholinergic drugs: oxybutynin
– Reduce uninhibited bladder contractions and may be
helpful for children w/ daytime urinary frequency.
• Desmopressin acetate nasal spray – an analog of
vasopressin
– Success is achieved with this.
– Reduces nighttime urinary output to a volume less than
functional bladder capacity.
Nursing Care Management
• Support both children and parents who are coping w/ the
problem of enuresis, the treatment plan, and the difficulties
they may encounter in the process.
• Both need encouragement and patience.
• Problem is discussed w/ both the parent and the child –
since any treatment involves and require the child’s active
participation.
• Child:
o is in charge of the intervention – in some treatments
intervention.
• Parents:
o Must learn to support the child rather than intervene
themselves.
o Should also be taught to observe for side effects of any
medications used.
o Believe that enuresis – is caused by an emotional
disturbance and fear that they have somehow produced
the situation by improper childrearing practices.
o Need reassurance that the bed-wetting is NOT a
manifestation of emotional disturbance and does not
represent willful misbehavior.
o Need to understand that punishment such as scolding,
shaming, and threatening is contraindicated
because of their negative emotional impact and limited
success in reducing the behavior.
o Encouraged to be patient and understanding and to
communicate love and support to the child.
• Communication w/ children is directed toward eliminating
the emotional impact of the problem;
o Relieving feelings of shame, guilt, and the burden of
parental disapproval
o Building self-confidence
o Motivating them toward independent control
• Nurse can provide consistent support through the
inconsistent and unpredictable treatment process.
• Children need to believe that they are helping themselves
and to maintain feelings of confidence and hope.
ENCOPRESIS
➢ Repeated voluntary or involuntary passage of feces of
normal or near-normal consistency in places not
appropriate for that purpose according to the individual’s
own sociocultural setting.
Fetal accidents
They cannot control until they go to the bathroom.
o Occur at least = once a month for a minimum of 3 months
o Child’s chronologic/ developmental age = at least 4 years.
➢ Fecal incontinence must NOT be caused by physiologic
effects of a substance (e.g., laxatives) or a general medical
condition EXCEPT through a mechanism involving
constipation.
➢ Consistency of stool may vary from:
Normal or near-normal to Liquid
➢ With a more liquid stool seen especially in individuals who
have overflow incontinence secondary to fecal retention.
o Primary encopresis – child 4 years of age or older who has
never achieved fecal continence.
– This is more frequently observed as a result of neglect,
lax training methods, mental subnormalities, and
familial causes.
o Secondary encopresis – fecal incontinence occurring in a
child over 4 years of age after a period of established fecal
continence.
➢ The disorder is more common in males than in females.
Etiology
• Constipation – may be precipitated by environmental
change, such as:
o Having a new sibling
o Moving to a new house
o Changing schools
o Having to use new or unfamiliar toilet facilities
• Chronic, severe constipation – tends to impair the usual
movement and contractions of the colon, which can lead to
fecal obstruction.
Associated w/ Constipation, which can lead to encopresis:
o Abnormalities in the digestive tract:
▪ Hirschsprung disease
▪ Anorecta lesions
▪ Malformations
▪ Rectal prolapse
o Medical conditions:
▪ Hypothyroidism
▪ Hypokalemia
▪ Hypercalcemia
▪ Lead intoxication
▪ Myelomeningocele
▪ Cerebral palsy
▪ Muscular dystrophy
▪ Irritable bowel syndrome
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
• Voluntary retention of stool – may also follow an incident
of painful defecation (e.g., in a child with anal fissures)
• Involuntary retention – may be produced by emotional
problems caused by the encopresis, which sets up a tear -
pain cycle and results in learned abnormal defecation
patterns.
• Psychogenic encopresis
o the soiling is caused by emotional problems
o often related to a disturbed mother-child relationship
Normal: children and adolescents have one or two soft formed
stools per day.
• Children with soiling problems tend to form large-bore
stools, which are painful to excrete.
o And so, they tend to avoid defecation and withhold
stooling.
• Stool help in the rectum and sigmoid colon loses water and
progressively hardens, which causes successively more
painful bowel movements and a stretched rectal vault.
• Over time the child will lose the urge to defecate on his or
her own.
• A pain-retention-pain cycle is established.
• Leakage around an impaction – suggested when many
children have diarrhea or loose leakage in their clothing
and pass small amounts of hard stool.
Children may experience:
o Exacerbations w/ transitions in the school setting
o For developing retentive tendencies:
▪ Fear of using school bathrooms
▪ A busy schedule
▪ Interruption of an established time schedule for
bowel evacuation
o May react to stress w/ bowel dysfunction.
Clinical Manifestations
• Feel ashamed and may wish to avoid social situations
(camp or school) that might lead to embarrassment.
• School performance and attendance are affected – the
child’s offensive odor becomes a target for scorn and
derision by classmates.
• Child is not well liked by peers and may be severely
rejected by the parents as a result of the symptom.
• Rejection by peers and parents causes further withdrawal
and other behavioral manifestations.
Therapeutic Management
• Goal: alleviating the cause of the soiling.
Is there a problem with physical or anatomy problem or
disease or bcos of emotional trauma.
• Detailed medical history and physical examination – to
determine the CAUSE.
o Rectal examination
o Abdominal x-ray film – to determine the SEVERITY
of impaction.
• Diet, lubricants, and a toilet ritual – encourages the child
to establish normal defecation.
• Fecal impaction is relieved by:
o Lubricants
▪ Mineral oil
o Osmotic laxatives:
▪ Lactulose
▪ Sorbitol
▪ Polyethylene glycol (PEG or MiraLax)
▪ Magnesium hydroxide
• Customary dosages are usually insufficient to produce a
therapeutic response.
• Mineral oil should be avoided in children who have
dysphagia or vomiting to prevent risk of aspiration.
• Dietary changes are helpful:
o Elimination of milk and dairy products
o Consumption of increased amounts of high-fiber foods
▪ Fruits
▪ Vegetables
▪ Cereals
o Increased hydration with water
• Behavior therapy – eliminate any dear that has developed
as a result of painful defecation.
• Psychotherapeutic intervention – with the child and
family.
Nursing Care Management
• Assess the time, date, when it occur.
• Thorough history of the soiling is essential.
o When soiling began
o How often it occurs.
o Under what circumstance
o Whether the child uses the toilet successfully at all
• Direct questioning about the soiling – bcos the parents and
child are reluctant to volunteer information.
• Education of these is prerequisite to a successful outcome.
o Physiology of normal defecation
o Toilet training as a developmental process
o The treatment outlined for the particular family
• Regimen prescribed for stimulating elimination – is
explained to the parents.
• Essential in treating encopresis or chronic constipation:
o Bowel retraining with mineral oil
o High fiber diet
o A regular toileting routine
• Child encouraged to:
o sit on the toilet 10 – 15 minutes after meals.
o intervals of 10 minutes
• Placing a footstool below the feet – relax the abdomen
and make the child more comfortable.
• Enemas – for impactions, but long-term use prevents the
child from assuming responsibility for defecation.
• Lubricants – given liberally,
– Stimulant cathartics often cause abdominal cramps
that can frighten the child.
• Positive reinforcement may encourage child to participate
in the bowel regimen.
o Giving stickers
o Praising the child
o Awarding special activities
• Family counseling – directed toward reassurance that most
problems resolve successfully, although the child may have
relapses during periods of stress, such as vacations or
illness.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
• Reevaluated condition – if encopresis persists beyond
occasional relapses.
• Behavior modification techniques are explained.
• Family is assisted with a plan suited to particular situation.
ATTENTION DEFICIT HYPERACTIVE DISORDER
(ADHD)
➢ Refers to developmentally inappropriate degrees of
inattention, impulsiveness, and hyperactivity.
➢ Most common neurobehavioral disorder of childhood and
often persists into adulthood.
➢ Prevalence rates for ADHD vary depending on whether
they are based on school samples or community samples.
➢ The National Survey of Children’s Health found the
estimated prevalence of parent-reported ADHD among
children aged 4 – 17 years was 9.5%, representing 5.4
million children.
➢ The rates of diagnosis have been increasing an estimated
2% to 3% per year.
➢ ADHD is seen more in boys than girls.
➢ Early 1900s – first recognize symptoms.
Several different names have been applied to the disorder.
➢ Difficulties associated w/ ADHD are most often:
o School related or academic.
➢ Family and social relationship – if aggressive behavior and
mood liability w/ peer relationship, cause difficulties in
social interactions, or make discipline difficult.
Risk for:
• Conduct disorders
• Oppositional defiant disorders
• Depression
• Anxiety disorders
• Developmental disorders: speech and language delays and
learning disabilities
➢ Early identification of affected children is important –
characteristics of ADHD significantly interfere w/ the
normal course of emotional and psychologic development.
➢ Many children develop maladaptive behavior patterns that
hinder psychosocial adjustment.
ADHD can cause problems with social development. Since
they want to go and roam around, they cannot stay still,
they have problems with communication and mingling
with other people.
➢ Their behavior evokes negative responses from others, and
repeated exposure to negative feedback adversely affects
the child’s self-concept.
Etiology
• Exact cause is UNKNOWN.
• A combination of organic, genetic, and environmental
factors is probably involved.
• Factors that put a child at risk for symptoms of ADHD:
o Family history of ADHD
o Especially the father, brother, or uncle.
• Implicated in ADHD
o Chromosomal or genetic abnormalities
▪ Fragile X syndrome
▪ Klinefelter syndrome
• Sex linked factor – may be operating bcos the disorder is
much more common in boys than in girls.
Clinical Manifestation
• Behaviors exhibited are not unusual aspects of child
behavior.
• Difference lies in the:
o Quality of motor activity
o Developmentally inappropriate inattention
o Impulsivity
o Hyperactivity that the child displays
o Degree of severity
• May be numerous or few, mild, or sever, and vary with the
child’s developmental level.
• Mild manifestations – apparent in at least two settings
o Educational
o Family environments
Every child with ADHD is different from all other children
with ADHD.
• Most behavioral manifestations – apparent at an early age,
• Learning disabilities – may not become evident until the
child enters school.
• Distractibility – major c.m
• Stimuli may come from – External or Internal Sources
• Children frequently demonstrate immaturity relative to
chronologic age.
There is a developmental/ mental delay (ex. child is 5 or 6
y/o but acting like 2 or 3 y/o), they cannot understand and
follow instructions to stay still and listen to what others are
saying.
• Selective attention – is often seen; the child has difficulty
attending to “nonpreferred” tasks, such as:
– Completing chores
– Finishing homework
• Child may not consider the consequences of behavior
o Take excessive physical risks (often beginning early in
life)
o May demonstrate inappropriate social skills.
• In families of children w/ ADHD, there is an increased:
o Incidence of substance abuse
o Conduct disorders
o Learning disabilities
o Depression
o Antisocial personality disorder
Diagnostic Evaluation
• Complete and thorough multidisciplinary evaluation of
the child
o incorporating the efforts of the primary pediatric
health care provider and the family
o possible support from a Psychologist, Developmental
Pediatrician, Neurologist, Pediatric Nurses, Classroom
Teachers, and Administrators.
• Clinicians and professionals – must first determine whether
the child’s behavior is age appropriate or truly problematic.
• Complete medical and developmental history – obtained
prior to diagnosis.
• Detailed descriptions of the child’s behavior:
o In the home
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
o In school
o In social situations
From many observes of the child as possible, particularly
with those involved in the child’s care:
o Parents
o Teachers
o Caregiver
o Administrator
• Physical examination
o Vision and hearing screening
o Detailed neurologic evaluation
• Psychologic testing – Projective tests
o identify visual-perceptual difficulties,
o problem with spatial organization, and other
phenomena that suggest cortical or diencephalic
involvement,
o helps to identify the child’s intelligence and
achievement levels.
• Behavioral checklist and adaptive scales – be completed
by the child’s caregivers and educators and scored by the
primary care provider.
• These assessment tools are also helpful in measuring social
adaptive functioning and behavioral concerns in children
with ADHD, as well as providing benchmarks for
evaluation of improved or worsening behavioral changes
once therapy has begun.
• Psychiatric disorders, medical problems, and traumatic
experiences are ruled out, including:
– Lead poisoning
– Seizures
– Partial hearing loss
– Psychosis
– Witnessing of sexual activity
– Violence
Therapeutic Management
• Behavior therapy and Psychotherapy
o Behavior Therapy – focuses on the prevention of
undesired behavior. Families help to identify new
appropriate contingency and reward system to meet
the child’s developing needs. They may also receive
instruction in effective parenting skills such as:
delivering positive reinforcement, rewarding small
___ of desired behavior and providing age-appropriate
consequences like time-out, etc.
o Through collaborative teamwork (parents, doctors,
nurses, teachers); A parent learn techniques to help the
child become more successful at home and in school.
• Pharmacologic Therapy (Medication)
o Most effective and frequently used medication are
stimulants:
▪ Methylphenidate hydrochloride
▪ Dextroamphetamine
o Non stimulant medication including norepinephrine
reactive inhibitors and adrenergic agonist –
effective with fewer side effects with school age and
adolescents’ children.
o Children are given a small dosage initially, and dosage
is gradually increased until the desire respond is
achieved.
o Children who receive stimulants should be monitored
carefully for side-effects of medication.
▪ Decreased appetite/ appetite loss
▪ Abdominal pain
▪ Headaches
▪ Sleep disturbances
▪ Growth velocity
o Stimulants are avoided in children who have a history
of Tics-like behavior or Tourette syndrome.
o Tricyclic antidepressant an extended-release
Clonidine can be used as another therapy for ADHD.
▪ Primarily for children with co-existing condition
such as sleep disturbances.
Nursing Care Management
• School nurses are active participants in all aspects of
managements of the child w/ ADHD.
• Nurses in the community setting work with families in the
home on a long-term basis to help plan and implement
therapeutic regimens and to evaluate the effectiveness of
therapy.
• Medication
o Stimulants, Nonstimulants, Antidepressants
• Environmental Manipulation
o Encourage families to learn how to modify the
environment to allow the child to be more successful.
o Consistency – important for children w/ ADHD.
Consistency between families and teachers in terms of
reinforcing the goals is essential.
o Fostering improve organizational skills required a
more highly structured environment than most
children need.
o The child should be encouraged to make more
appropriate choices and to take responsibilities for
his/her actions.
▪ (u let them choose & decide to help them boost
their self-esteem)
o Other helpful intervention include: Teaching parents to
make organizational charts, listing all activities that
must be performed before leaving for school.
▪ (so they can have a structured environment and
they know what are the things that need to be
done, and to follow before going out)
o Suggesting how to decrease distraction in the
environment:
▪ Child completing homework: turn off tv; have a
consistent study area w/ the supplies needed so the
child will not go around; have schedule
o Helping parents to understand ways to model positive
behaviors and problem solving; the focus is on
strategies to help the child succeed and cope with
deficits while emphasizing strengths.
• Appropriate Classroom Placement
o Children with ADHD need an orderly predictable and
consistent classroom environment with clear and
consistent rules.
o Homework and classroom assignments may need to be
reduced and more time may need to be allotted to
allow the child to complete test/task.
o Verbal instruction should be accompanied by visual
references such as little instruction in the chalk board.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
o Schedules may need to be arrange, so academic
subjects are taught in the morning when the child is
experiencing the effect of morning dose of the
medication.
o Low interest and high interest classroom activity
should be integrated to maintain the child’s attention.
o Regular and frequent breaks in activities are helpful,
because sitting in one place for an extended period of
time may be difficult for patient with ADHD.
– Ice breakers
– Short snack break
o Computers are helpful for children who have difficulty
in written assignments and fine motor skills.
o If learning disabilities exist, special learning activities
may be accompanied in self-contain classes, limited to
6 – 8 children only.
• Psychiatric, Psychologic, and Social Therapies
o Refer the parents to counseling therapy.
o Counseling can be very helpful with children who
demonstrate signs of anxiety or depression.
o Therapy can help the child develop a healthier self-
esteem and practice problem solving.
o Adolescents may benefit from group work focusing on
social skills development.
o Parents of children with ADHD can cause a lot of
stress and therapy may be indicated for parent and
family members.
BULLYING
➢ The infliction of repetitive physical, verbal, or emotional
abuse by one or more individuals to harm or bother another
individual in order to establish power over someone who is
perceived as being less physically or psychologically
dominant than the aggressor(s).
➢ Can occur in varying degrees of severity in a physical,
social, or emotional context.
➢ Can occur in any setting, it usually takes place in school
hallways or on the playground where supervision is
minimal, but peers are present to witness attack.
Cyberbullying
➢ Involves an electronic medium to harm or bother another
individual.
➢ Can be more harmful than traditional bullying because the
attach can instantly reach a wider audience, while allowing
the bully to remain anonymous.
Bullies and victims of bullying are at risk for long-term
psychologic disturbances and psychiatric symptoms.
Future problems of bullies include a higher risk for:
o Conduct problems
o Hyperactivity
o School dropout
o Unemployed
o Participation in criminal behavior
Victims of bullying are at increased risk for:
o Low self-esteem
o Anxiety
o Depression
o Feelings of insecurity
o Loneliness
o Poor academic performance
o Psychosomatic complaints: feeling tense, tired or
dizzy
➢ Bullying can be reduced or prevented through:
o Supportive relationships with family
o Intervention of school personnel
o Involvement with positive peer groups
➢ Many school districts have developed bullying prevention
programs; however, results are mixed. Some programs
reporting positive results and others showing little to no
impact.
➢ All states have antibullying laws and/ or policies that
include definitions of bullying and procedures for
reporting, investigating, and responding to bullying.
Bullying can happen to all ages.
PROBLEMS WITH ADOLESCENTS
AMENORRHEA
The adolescent is not menstruating.
➢ The absence of menstrual flow, a clinical sign of a variety
of disorders.
➢ Generally, the following circumstances should be
evaluated:
(1) the absence of both menarche and secondary sexual
characteristics by age 13 years
(2) the absence of menses by age 16.5 years, regardless of
normal growth and development (primary amenorrhea)
(3) a 6-month or more cessation of menses after a period of
menstruation (secondary amenorrhea)
➢ A moderately obese girl (20% to 30% above ideal weight)
may have early-onset menstruation
➢ Delay of onset is known to be related to malnutrition
(starvation such as that with anorexia)
➢ Girls who exercise strenuously before menarche can have
delayed onset of menstruation until about age 18.
➢ Although amenorrhea is not a disease; it is often SIGN of
disease.
➢ May occur from any defect or interruption in the
hypothalamic-pituitary-ovarian-uterine axis.
➢ May result from anatomic abnormalities such as:
o Endocrine disorders such as:
▪ Hypothyroidism
▪ Hyperthyroidism
o Chronic diseases
▪ Type 1 diabetes
o Medications
▪ Phenytoin (Dilantin)
o Illicit drug abuse (e.g., opiates, marijuana, cocaine)
o Eating disorders
o Strenuous exercise
o Emotional stress
o Oral contraceptive use
➢ Secondary amenorrhea is commonly result of pregnancy.
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
➢ Exercise-associated amenorrhea – can occur in women
undergoing vigorous physical and athletic training and is
thought to be associated w/ many factors, including:
o Body composition (height, weight, and percentage of
body fat)
o Type, intensity, and frequency of exercise
o Nutritional status
o Presence of emotional or physical stressors
Greater risk: Women who participate in sports emphasizing
low body weight:
• Sports in which performance is subjectively scored (dance,
gymnastics)
• Endurance sports favoring participants with low body
weight (distance running, cycling)
• Sports in which body contour-revealing clothing is worn
(swimming, diving, volleyball)
• Sports with weight categories for participation (rowing,
martial arts)
• Sports in which prepubertal body shape favors success
(gymnastics, figure skating)
Assessment
• Begins w/ thorough history and physical examination.
• Specific components of the assessment process depend on
a patient’s:
o age
o adolescents, young adult, or perimenopausal
o whether she has menstruated previously
Nursing Care Management
You have to first know whether it’s primary or secondary
amenorrhea.
• Amenorrhea caused by hypothalamic disturbances:
o Nurse – ideal health professional to assist women
because many of the cause are potentially reversible
(stress, weight loss for nonorganic reasons)
• Counseling and Education – primary interventions and
appropriate nursing roles.
• Addressing the stressors – initial management when a
stressor is known to predispose a woman to hypothalamic
amenorrhea is identifies.
• The adolescent and nurse plan:
o How the woman can decrease or discontinue
medications known to affect menstruation
o Correct weight loss
o Deal more effectively w/ psychologic stress
o Address emotional distress
o Alter an exercise routine
• Nurse and adolescent:
o Work together to help her identify, cope with, and
eliminate sources of stress in her life.
o May have several sessions before the woman elects to
try exercise reduction.
o Should investigate other factors that may be
contributing to the amenorrhea and develop plans for
altering lifestyle and decreasing stress.
• Deep breathing exercise and relaxation techniques –
simple yet effective stress-reduction measures.
• Referral for biofeedback or Massage therapy.
• Referrals for psychotherapy (in some instances)
• If an adolescent’s exercise program is thought to contribute
to her amenorrhea, several options exist for management.
o May decide to decrease the intensity
o Decrease the duration of her training
o Modify her diet to include the appropriate nutrition for
her age
*accepting these alternative may be difficult for one who is
committed to a strenuous exercise regimen.
• Nurse – point out the connection between low bone density
and stress fractures.
– Because many young female athletes may not
understand the consequences of low bone density or
osteoporosis
DYSMENORRHEA
➢ Pain during or shortly before menstruation.
➢ One of the most common gynecologic problems in women
of all ages.
➢ Many adolescents have dysmenorrhea in the first 3 years
after menarche.
➢ Pain is usually located in the suprapubic area or lower
abdomen.
➢ Women describes pain:
o Sharp
o Cramping
o Gripping
o Steady, dull ache
➢ For some women, Pain radiates to the lower back or
upper thighs.
Primary Dysmenorrhea
➢ A condition associated with ovulatory cycles.
➢ Research – show that primary dysmenorrhea has a
biochemical basis and arises from the releases of
prostaglandins with menses.
➢ During the luteal phase and subsequent menstrual flow
= prostaglandin F2-alpha (PGF2α) is secreted.
Which lead to uterine contraction, vasospasm and ischemia
which can lead to abdominal cramps or dysmenorrhea.
➢ Excessive release of PGF2α
– increases the amplitude and frequency of uterine
contractions and causes vasospasm of the uterine
arterioles
– resulting in ischemia and cyclic lower abdominal
cramps.
➢ Systemic responses to PGF2α include:
o Backache
o Weakness
o Sweats
o Gastrointestinal symptoms
▪ Anorexia
▪ Nausea
▪ Vomiting
▪ Diarrhea
o Central nervous system symptoms
▪ Dizziness
▪ Syncope
▪ Headache
▪ Poor concentration
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Pain usually: • Exercise
• Begins at the onset of menstruation. o Helps relieve menstrual discomfort through increased
• Lasts 8 to 48 hours vasodilation and subsequent decreases ischemia.
o Releases endogenous opiates (beta-endorphins)
Primary dysmenorrhea o Suppresses prostaglandins.
• Appears 6 to 12 months after menarche when ovulation is o Shunts blood flow away from the viscera = reduced
established. pelvic congestion.
If you are not ovulating, prostaglandins cannot be secreted. o Pelvic rocking
Hence, dysmenorrhea will not occur. • Decreased salt and refined sugar intake 7 – 10 days
before expected menses – may reduce fluid retention.
Anovulatory bleeding • Natural diuretics – helps reduce edema and related
discomforts
o Common in the few months or years after menarche
o Asparagus
o Painless
o Cranberry juice
➢ Because both estrogen and progesterone are necessary for
o Peaches
primary dysmenorrhea to occur, it is experienced only w/
o Parsley
ovulatory cycles.
o Watermelon
➢ More common among women in their late teens and
early twenties than in women in older age-groups; the • Low-fat vegetarian diet – help minimize dysmenorrheal
incidence declines with age. symptoms.
➢ Psychogenic factors – may influence symptoms • NSAIDs
– But symptoms are definitely related to ovulation and o Most effective if started several days before menses or
do not occur when ovulation is suppressed. at least by the onset of bleeding.
o All NSAIDs have potential gastrointestinal side
Nursing Care Management effects:
• Medications ▪ Nausea
o Buscopan ▪ Vomiting
o Hyoscine-N-butylbromide ▪ Indigestion
* Warn all women taking them to report dark-colored stool
(this may be an indication of gastrointestinal bleeding)
• Mgt of Primary dysmenorrhea – depends on the severity
of the problem and the individual woman’s responses to
various treatments. Secondary Dysmenorrhea
• Information and support ➢ Menstrual pain that develops later in life than primary
dysmenorrhea – typically after age 25. (adult women)
Because menstruation is so closely linked to reproduction and ➢ Associated with pelvic pathology such as:
sexuality, menstrual problems such as dysmenorrhea can have o Adenomyosis (myoma)
a negative influence on sexuality and self-worth. o Endometriosis
• Nurse can provide facts about what is normal – to correct o Pelvic inflammatory disease
myths and misinformation about menstruation and o Endometrial polyps
dysmenorrhea. o Submucous or intestinal myomas (fibroids)
• Adolescent and young women need support to foster their
feelings of positive sexuality and self-worth. ➢ Pain is often characterized by:
• Heat (heating pad or hot bath) or warm compress to the o Dull
lower abdominal area, minimizes cramping by: o lower abdominal aching that radiates to the back or
o increasing vasodilation and muscle relaxation thighs.
o minimizing uterine ischemia ➢ Often women experience feelings of bloating or pelvic
fullness.
• Massaging the lower back – can reduce pain by:
o Relaxing paravertebral muscles
Therapeutic Management
o Increasing the pelvic blood supply
• Physical examination – careful pelvic examination
• Soft, rhythmic rubbing of the abdomen (effleurage) –
useful bcos it provides distraction and an alternative focal • Diagnosis may be assisted by ultrasound examination
point. • Dilation and curettage (D&C) – Raspa
• Endometrial biopsy
• Used to decrease menstrual discomfort (evidence is sufficient • Laparoscopy
to determine the effectiveness)
o Biofeedback • Treatment is directed toward – removal of the underlying
o Transcutaneous electrical nerve stimulation pathology.
(TENS) – help relax the muscle of uterus • Many of the measures described for pain relief of primary
o Progressive relaxation dysmenorrhea are also helpful for women w/ secondary
o Hatha yoga dysmenorrhea.
o Acupuncture
o Medication
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 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
VAGINITIS
Inflammation on vaginal tract.
➢ “Abnormal vaginal discharge”
➢ An infection caused by a microorganism.
➢ Most common vaginal infections:
o Bacterial vaginosis (BV)
o Candidiasis
o Trichomoniasis
➢ Group B Streptococcus is considered normal vaginal
flora, it may also cause infection.
➢ Vulvovaginitis (inflammation of the vulva and vagina) –
may be caused by vaginal infection:
o Copious leukorrhea
▪ Can causes maceration of tissues
o Chemical irritants, allergens, and foreign bodies
▪ May produce inflammatory reactions
Signs and Symptoms
• An itchy or sore vagina.
• Vaginal discharge that’s a different colour, smell or
thickness to usual.
• Vaginal dryness.
• Pain when peeing or having sex.
• Light vaginal bleeding or spotting.
• Sore, swollen or cracked skin around your vagina.
Diagnostic Evaluation
• Perform a pelvic exam.
– Pap smear – to check the cervix/ vaginal tract or canal
– u can also check the discharge – to know what type of
bacterial infection invaded the vaginal tract
• Collect a sample for lab testing.
• Perform pH testing.
– Acidic discharge – manifestation of vaginitis.
Genitourinary syndrome of menopause (vaginal
atrophy)
• Estrogen – in the form of vaginal creams, tablets or rings
– can treat this condition.
Noninfectious vaginitis
• Need to pinpoint the source of the irritation and avoid it.
It can be bcos of external environment, poor hygienic processes,
underwear, etc.
• Possible sources include new soap, laundry detergent,
sanitary napkins or tampons.
GYNECOMASTIA
➢ Some degree of bilateral or unilateral breast enlargement
occurs frequently in young boys during puberty.
➢ Approx. half of adolescent boys have transient
gynecomastia, which usually lasts less than 1 year.
➢ If gynecomastia persists or is extensive enough to cause
embarrassment – plastic surgery is indicated for cosmetic
and psychologic reasons.
➢ Administration of testosterone – has NO effect on breast
development or regression and may even aggravate the
condition.
Nursing Care Management
Consists of assuring the adolescent and his parents that this
situation is benign and temporary.
But all adolescents w/ gynecomastia should receive a
careful medical evaluation to rule out pathologic causes.
Maybe there is cyst or tumor.
Do ultrasound.
X-ray
Adolescent may benefit from the knowledge that it occurs
in more than 50% of his peers.
Common in male esp. during the onset of puberty.

Treatment
Bacterial vaginosis
• Health care provider might prescribe
o Metronidazole tablets (Flagyl) – taken by mouth
o Metronidazole gel (MetroGel) – apply to the affected
area
• Clindamycin (Cleocin) cream – apply to the vagina
• Clindamycin tablets – taken by mouth or capsules put in
the vagina.
• Tinidazole (Tindamax) or Secnidazole (Solosec) – taken
by mouth
Yeast Infections
• Usually are treated with an over-the-counter antifungal
cream or suppository, such as:
o Miconazole (Monistat 1)
o Clotrimazole (Lotrimin AF, Mycelex, Trivagizole 3)
o Butoconazole (Gynazole-1)
o Tioconazole (Vagistat –1)
• Prescription of oral antifungal medication = Fluconazole
(Diflucan)
Trichomoniasis
• Health care provider may prescribe tablets like:
o Metronidazole (Flagyl)
o Tinidazole (Tindamax)
MIDTERMS // honeybunchsugarplum | 28
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
NCMA 219 LEC Classification of Congenital Heart Defect (CHD)
CARE OF THE MOTHER & CHILD AT RISK
WEEK 10
Prof: Mrs. Shiella May Edquibal, Man, RN
Alterations in Oxygenation
• Responses to Altered Cardiac and Tissue Perfusion
Congenital Heart Defects (CHD)
Congestive Heart Failure
Rheumatic Fever
Kawasaki Disease
LEGENDS:
➢ From ppt in canvas
✓ From ppt in canvas
Notes taken from what ma’am said in f2f class
• Notes taken from “ f2f
How does the NORMAL heart of the baby work?
Atrium – receive
Ventricle – release/ away from the heart
Normal heart:
UNOXYGENATED blood from Superior vena cava (from
upper body) & Inferior vena cava (from lower body) → unoxy
will all empty → RA (unoxy) → Tricuspid valve → RV →
Pulmonic valve → Pulmonary artery → Lungs
OXYGENATED blood from Lungs → Pulmonary vein → LA
→ Mitral valve → LV → Aortic valve → Aorta → Body
TPMA
T – Tricuspid valve
P – Pulmonic valve
M – Mitral (Bicuspid) valve
A – Aortic valve
Muscles that separates the diff. chambers
o Ventricular Septum – separates the R and L Ventricle
o Atrial Septum – separates the R and L Atrium
Baby inside mother’s womb – lungs are not functional; the
fetal heart does not have to pump blood to the lungs to pick
up oxygen.
The fetal heart does not need a separate pulmonary artery
and aorta, they are connected.
The umbilical cord – connected to the baby’s heart with two
holes:
o Ductus Arteriosus – another valve (butas)
▪ which connects the pulmonary artery and the
aorta.
o Foramen ovale – muscle separation (butas)
▪ located in the atrial septum
These 2 should be OPEN when the baby is inside mother’s
womb; these 2 holes bypass the lungs.
CONGENITAL HEART DEFECTS (CHD)
❖ Incidence: 1% of or about 40,000 births per year
❖ Most common anomaly is VSD.
❖ 25% of babies with CHD are critical and generally needs
surgery or other procedures in their 1st year of life (CDC)
❖ 15% of CHD are associated with genetic conditions.
❖ 28% of kids with CHD have another recognized anomaly
(trisomy 21)
Cyanotic – show manifestations of cyanotic episode
Acyanotic – newborn not showing symptom of cyanosis
ACYANOTIC
Defects w/ INCREASED PUMONARY BLOOD FLOW
ATRIAL SEPTAL DEFECT
➢ Idiopathic
➢ Abnormal opening between atria →
blood from higher pressure (LA) to
flow into lower pressure (RA).
➢ Increase O2 blood into R side of
heart
➢ RA & RV enlargement
➢ Cardiac failure is unusual in
uncomplicated ASD
May butas/ hole sa Atrial septum (muscle that separate the
R and L atrium)
Left side = need ↑ pressure – to pump blood away from
the heart to go to the body
Right side = ↓ pressure – only receives unoxy blood;
pumping is adjacent to the lungs
“Shunting” – movement or flow
– There will be shunting from the left side → right side
Clinical Manifestation
Acyanotic – may lumalabas pa ring oxygenated blood
Asymptomatic if small defect
If small – baby can still live normally.
30 – 40 y/o – possible lalabas na mga symptoms
– bcos over the decades of working, the R side of heart
will get tired;
Right side will have:
o Hypertrophy
o Increase pressure in R atrium.
o Pulmonary artery will have Pulmonary Hypertension
o Can develop Right Side Heart failure.
Problem – additional workload
Complication: lumalaki yung CHAMBER not the
opening, because of workload/ ↑ pressure
MIDTERMS // honeybunchsugarplum | 29
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Signs and Symptoms Hole is in the ventricular septum
Hear “murmur” sound. Complication:
Hollow systolic murmur o mas mabilis lumala ‘yung sakit bcos Ventricle has ↑
Subtle signs: pressure
✓ Dyspnea o mas madami and blood flow na mapupunta dito
✓ Fatigue and poor growth o Acyanotic blues – meron pa ring lalabas na oxygenated
✓ Soft systolic murmur in pulmonic area (splitting S2) blood
✓ May develop CHF
Clinical Manifestations
Laboratory/ Diagnostic Examination
• Murmur sound
DR order: 2D Echo – heart ultrasound • Hollow systolic murmur
– reveals enlarged right side of the heart and ↑
• Mas mabilis mag manifest – school age/ preschool pa lang
pulmonary circulation
– can have heart failure if left untreated.
✓ Cardiac catheterization – demonstrates separation of RA
and the↑ O2 saturation in the RA
Symptoms
✓ Tachypnea, dyspnea
Surgical Treatment
✓ Poor growth, reduced fluid intake
If detected early – can have surgery. ✓ Palpable thrills
• Surgical Dacron patch closure (pericardial patch) ✓ Systolic murmur at left lower sternal border
– Open repair with C-P bypass during school age ✓ May develop CHF
• Direct closure w/ double suture
Surgical Treatment
Non-surgical Treatment • Pulmonary artery bandaging (if not too large) or Patch
• May be closed using devices during cardiac – Support to pulmonary artery
catheterization.
• Same to VSD Non-surgical Treatment
• Same to ASD
Prognosis of ASD (and CHD) • Catheterization
• if treated, detected, have surgery early on – GOOD. o In femoral artery (singit)– ipapasok catheter papunta
• if hindi agad nadetect/ surgery – BAD can have failure. sa heart (may device sa dulo) → irrelease like an
umbrella – para takpan ‘yung butas/defect.
Nursing Management
✓ Explain to parents the purpose of tests and procedures Prognosis
✓ Teach parents ways to support nutrition, reduce stress on • If detected early on – GOOD.
heart, promote rest, and support growth and development • If left undetected/ untreated – DEATH.
during preoperative period
✓ Teach parents signs of congestive heart failure and Treatments:
infection ✓ Medications:
✓ Prepare parents and child for surgery by visiting intensive o Furosemide: a diuretic which removes excess fluid out
care unit, explaining equipment and sounds of the body
✓ Prepare older child for post-operative experience, o Digoxin: helps the heart pump more forcefully
including coughing and deep breathing and need for o Angiotensin-converting enzyme (ACE) inhibitor:
movement relaxes blood vessels and help heart to pump more
✓ Teach need for antibiotic prophylaxis to prevent subacute easily
bacterial endocarditis ✓ Surgical repair with bypass (procedure of choice)

VENTRICULAR SEPTAL DEFECT (VSD) PATENT DUCTUS ARTERIOSUS (PDA)

➢ Idiopathic
➢ An abnormal opening between the R
and L ventricle
➢ Defect in ventricular septum – error
in early fetal development
➢ 20-25% of all CHDs are VSD
➢ Pressure LV → RV and systemic
arterial circulation resistance →
pulmonary circulation, blood flows
through the defect and into the pulmonary artery
➢ RV becomes enlarged (Hypertrophied), over time the RA
may also become distended
➢ Ductus SHOULD close by about age
15 hours after birth
➢ Some shunting of blood may occur
up to 24 hours of life
➢ DUCTUS closes because increase in
arterial oxygen concentration that
follows initiation of pulmonary
function
➢ Prostaglandin E leads to closure of
PDA
➢ Allows blood to flow from left to right and pulmonary
blood flow

MIDTERMS // honeybunchsugarplum | 30
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Ductus Arteriosus – opening/ connection in between the COARCTATION OF AORTA
Aorta (oxygenated) and Pulmonary Artery (unoxygenated) ↑ pressure sa taas
Ductus Arteriosus is maintained by Prostaglandin E. ↓ pressure pababa
If baby is inside mother’s womb – it’s okay if it’s open. ➢ The aorta is narrowed near the
In PDA – If baby is OUT from mother’s womb – open na yung insertion of the ductus arteriosus
ductus arteriosus. which result in increased
Crying of the baby will expand the lungs → Pressure will pressure proximal to the defect
close/ seal the patency → If ‘di nag close – ‘yung blood na and decreased pressure distal to
nasa Aorta ay bumabalik sa Pulmonary artery the obstruction (body).

Clinical Manifestations Signs and Symptoms

• Acyanotic – meron pa ring oxygenated blood na lalabas. • Hypertension – high BP in UPPER body and extremities
• Asymptomatic: small PDA • Bounding pulses in arms
✓ Bounding peripheral pulses • Weak or absent femoral pulses
✓ Widened pulse pressure (>25) • Cool lower extremities with low BP
✓ Complication for Large PDA: CHF with tachypnea, ✓ Patient at risk for ruptures aorta, aortic aneurysm, or stroke
dyspnea, and hoarse cry
Clinical Manifestations
Signs and Symptoms • Decreased/ diminish/ absent femoral pulses
• Machinery- like murmur • ↓ pressure
o Loud machine-like murmur at upper left sternal border • Cool extremity
(Left intraclavicular area)
Surgical Treatment
Nursing Care Management
Treatment of choice – For infants younger than 6 months
• Refer to the DR A. Resection and end – end anastamosis
o DR order – 2D Echo B. Grafting (luter positioning graft)
• Medication C. Patch Angioplasty
o To close the opening D. Subclavian Flap
o Prostaglandin E. Inhibitor
▪ INDOMETHACIN to close PDA’s – (IV) ✓ Surgical: does not require bypass since defect is outside
pericardium
Surgical Treatment ✓ Post-op complication is hypertension.
• Thoracotomy ✓ Usually done before age 2 yrs.
✓ Surgical ligation if meds fail. ✓ Risk of recurrence
✓ Surgery >> between age 1 – 2 years
Non-surgical Treatment
OBSTRUCTIVE BLOOD FLOW • Balloon Angioplasty
➢ Blood flow in heart meets an area of anatomic narrowing – Usually, effective.
(stenosis) → obstruction to blood flow – Pinapadaan sa femoral artery paakyat sa heart
➢ Pressure in ventricle & great arteries before – Ginagawa PANANDALIAN – i-inflate ‘yung balloon
obstruction is increased; pressure in area beyond hanggang masanay na dilated then id-deflate and
obstruction is decreased remove. Hoping it will remain dilated.
➢ Location of narrowing near the valve of the obstructive – May tendency na bumalik sa coarctation.
defect:
o Valvular: site of valve itself
AORTIC STENOSIS
o Sub valvular: narrowing in vent below valve
(ventricular outflow tract) ➢ Narrowing of aortic valve
o Supravalvular: narrowing in great art above valve usually malformed in BI-
➢ (+) pressure load on ventricle – decrease CO rather than Tricuspid valve
➢ s/s – CHF ➢ Causes ↑ resistance of blood
➢ Mild obstruction: asymptomatic flow in left ventricle, ↓
➢ Severe stenosis: hypoxemia (rare) Cardiac Output, Left
ventricular hypertrophy and
Stenosis – narrowing hindi harang pulmonary vascular
Stricture – narrowing congestion
Obstruction palabas ng puso ➢ Left ventricular wall is
hypertrophied>> increased pulmonary vascular resistance
& pulmonary hypertension
➢ LVH >> decrease coronary artery perfusion & increase risk
of MI.

MIDTERMS // honeybunchsugarplum | 31
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Stenosis in the aortic valve or aorta. Clinical Manifestations
Hypertrophy – lalaki ‘yung left ventricle • Asymptomatic/ Acyanotic – may lumalabas pa ring
↑ Left Atrial pressure oxygenated blood
Connected to pulmonary vein that lead to pulmonary • Progressive narrowing causes increased symptoms.
vascular congestion → Lungs → Pulmonary edema
• Cyanotic – if sobrang narrow
(magtutubig and puso)
• Characteristic Murmur
>> can lead to: Left side heart failure
or worse: Death • Cardiomegaly
• Xray
Clinical Manifestations
Treatment of Choice:
• Acyanotic – may lumalabas pa ring oxygenated blood • Balloon Angioplasty – to dilate the pulmonary artery.
• Newborns are critical. • Valvotomy (resect stenosis)
• ↓ Cardiac output:
▪ Faint pulse Balloon angioplasty has better outcome to pulmonic
▪ Hypotension stenosis compared to doing it in the coarctation of aorta.
▪ Tachycardia
▪ Poor feeding
✓ Murmur; exercise intolerance CYANOTIC
✓ Chest pain, dizziness with standing Defects w/ DECREASED PULMONARY BLOOD
FLOW
Non-surgical Treatment Obstructed pulmonary blood flow + anatomic defect (ASD
• Balloon Angioplasty or VSD) between the Right and Left side of the heart are
present.
Surgical Treatment Difficulty of blood exiting R heart via pulmonary artery
→ Pressure on the right side of the heart increases →
• Artificial Heart Valve – after balloon angioplasty; can do
exceeding pressure on the left side → allows
if school age na
desaturated blood to shunt right to left → desaturation
• Implantable heart devices – Heart Valve in the left side of the heart and in the systemic
circulation
✓ Surgery: Konne procedure (valve replacement)
✓ May require repeat procedures
TETRALOGY OF FALLOT
PULMONIC STENOSIS Involves 4 heart defects:
o Ventricular Septal Defect
➢ Pulmonary artery is stenosed. (VSD)
➢ Narrowing at entrance to pulmonary artery → o Pulmonic stenosis
resistance to blood flow >> R ventricular hypertrophy o Overriding aorta
and decreased pulmonary blood flow. o Right ventricular hypertrophy
➢ Extreme form of PS: Pulmonary atresia (total fusion of the
commissures and no blood flow to lungs) Cyanotic
➢ PS >> RVH, R ventricular failure >> R atrial pressure 1. May pulmonic stenosis.
increases and may reopen foramen ovale 2. Kulang na ‘yung dugo na pumupunta sa baga from
➢ Shunts unoxygenated blood to L atrium >> systemic oxygenation → pagbalik na oxygenated, naghahalo ‘yung
cyanosis. oxygenated and unoxygenated blood → lumalabas
➢ May lead to CHF. desaturated blood
➢ Often have PDA as well
➢ Cardiomegaly on CXR ➢ Hemodynamics vary widely.
– Depends on extent of pulmonic valve stenosis & size
Problems in pulmonary artery of VSD.
Narrowing at the entrance to the pulmonary artery. – If VSD is large, pressures are equal in R and L
ventricles. Blood is shunted in the direction of the least
Complication: resistance (pulmonary or systemic vascular resistance)
Hypertrophy ➢ PVR is > than systemic vascular resistance, shunt will be R
↑ pressure of Left Atrium to L
Systemic circulation >> overload – may tumatakas na
additional fluid pabalik sa katawan Clinical Manifestations
– Edematous
• Cyanotic
– Mamamaga ‘yung liver
• Over the years w/o surgery – lumalala ‘yung VSD
• When they cry & eating/ feeding – exhibit bluish skin.
= TET SPELLS or BLUE SPELLS
= specific C.M: “Blue Baby”

MIDTERMS // honeybunchsugarplum | 32
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
• Characteristic murmur Therapeutic Management
• Episode of cyanosis • Give Prostaglandin E
• Hypoxia • To keep the Ductus Arteriosus open
Hindi tumatagal ‘gang pre-school unless masurgery agad. • Atrial Septostomy – if maliit ang septum opening;
✓ Anoxic after feeding or with crying. bubutasan
✓ RISK of: emboli, LOC, sudden death, seizures Note: If lumabas si baby as cyanotic – give Prostaglandin E
AGAD; then do 2D Echo
Surgical Treatment ✓ Continuous infusin of PGE 1 until Sx
A. Palliative Shunt
o Blalock Taussig Shunt (BTS) Surgical Treatment
– Maglalagay ng artificial graft deretso sa • Pulmonary – to – Systemic Artery Anastomosis
pulmonary artery – gumagawa ng artificial way para – If the ASD is small – Atrial Septostomy – palalakihin
makapunta ‘yung dugo sa pulmonary artery. ‘yung butas ng ASD or ‘yung pulmonary artery
 (Gore-Tex graft) ✓ Pulmonary artery bandaging
– Connecting subclavian artery to pulmonary artery ✓ Modified Fontan procedure
branch
– Pansamantala; can have multiple surgery. MIXED DEFECTS
B. Complete Repair Fully saturated systemic blood flow mixes with the
o Closure of VSD desaturated blood flow, causing a desaturation of the
o Repair of the pulmonic stenosis systemic blood flow.
✓ Usually in 1st year of life ➢ Survival on postnatal period depends on mixing of blood
✓ Resect stenosed area from pulmonary systemic circulation within cardiac
✓ Patch R ventricular outflow chambers.
➢ Cardiac output decreases because of volume load on
TRICUSPID ATRESIA ventricle
Atresia – wala/ didn’t develop ➢ Signs of desaturation, cyanosis, and
Walang valve only ligament/ harang CHF, but variable depending on
ASD, VSD, PDA anatomy
– Need these defects to be present for baby to survive. ➢ Degree of cyanosis not always
– Lagyan ng butas visible & signs of CHF
ASD – need to open AS or manatiling open ang foramen – TGA: severe cyanosis in 1st day
ovale. of life → CHF (later)
VSD – need para lumipat ‘yung dugo sa RA paakyat sa – Truncus arteriosus: severe CHF
pulmonary artery 1st few weeks of life and mild desaturation
Deoxygenated and oxygenated blood → (mixing) → L
Atrium → LV → RV → lalabas sa PDA or aorta TRANSPOSITION OF THE GREAT ARTERIES or
= Complete mixing (may desaturation) TRANSPOSITION OF THE GREAT BLOOD VESSELS
GOAL: Oxy Saturation = until 75% RV – connected to aorta
< 80% LV – connected to Pulmonary
Note: without ASD, VSD & PDA – DEATH Artery
The pulmonary artery leaves
➢ Failure of tricuspid valve to develop the L ventricle and the Aorta
➢ No communication from R atrium to R ventricle exits from the R ventricle with
➢ Blood flows thru an ASD or a patent FO to L side of the no communication between
heart thru a VSD to R ventricle to lungs the systemic and pulmonary
➢ Complete mixing unO2 and O2 blood in L side of the heart circulation.
→ systemic desaturation, pulmonary obstruction →
decrease pulmonary blood flow 2 Circuits
➢ At birth: presence of patent FO (or ASD) is required to 1. Oxygen poor blood (Aorta)
permit blood flow across septum into L atrium o circulates through the body by passing the lungs.
– PDA allows blood flow to pulmonary artery for Deoxygenated blood
oxygenation – unoxygenated blood → Aorta unoxygenated ulit
2. Oxygen rich blood (Pulmonary Artery)
Clinical Manifestations o Circulated from the heart to the lungs and back.
✓ Cyanosis – Pulmonary artery is oxygenated → pulmonary
✓ Tachycardia vein oxygenated pabalik
✓ Dyspnea
✓ Hypoxemia
✓ Clubbing
✓ AT RISK FOR: Bacterial endocarditis, Brain abscess,
Stroke
MIDTERMS // honeybunchsugarplum | 33
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Pathophysiology CONGESTIVE HEART FAILURE
• Associated defects such as septal defects or PDA must be ➢ Inability of the heart to pump an adequate amount of blood
present to permit blood to enter the systemic circulation or to the systemic circulation at normal filling pressures to
the pulmonary circulation for mixing of saturated and meet the metabolic demands of the body.
desaturated blood. ➢ Due to structural deformity in children (septal defects) →
o Most common defects associated: increased blood volume & pressure in the heart →
– Patent foramen ovale or ASD MYOCARDIAL FAILURE
• TGA/ TGV = PDA & Foramen ovale are not open. ➢ Can occur with cardiomyopathy, dysrhythmia, severe
• For baby to survive: there should be an opening to electrolyte imbalances
Patent Ductus Arteriosus & Foramen Ovale. ➢ Could also be due to excess demands on a normal cardiac
– For the unoxygenated blood in the R atrium → L muscle (sepsis / severe anemia)
atrium → L ventricle → Pulmonary artery → left Cause: PEDIA = structural abnormalities
lung → Pulmonary vein (helpful ang PDA) → What happens?
Mixing of blood in Aorta → palabas o Ventricular emptying
• If foramen ovale is not open → ASD o Stroke volume
Therapeutic Management o Residual volume
• Medication: 2 Types:
o Prostaglandin E • Left Side Heart Failure
– IV
• Right Side Heart Failure
– Panandalian; to maintain the opening
Surgery Management Signs and symptoms of CHF
• Balloon Atrial Septostomy ✓ Each side of the heart depends on the adequate function of
– Bubuksan Septal Defect the other
• Artificial Graft in Aorta ✓ Failure of one chamber affects the opposite chamber
✓ If not corrected, it may lead to cardiac damage →
Lifetime mixing of deoxy and oxy blood inadequate CO → decreased supply to the kidneys → Na
Desaturated patient and H2O resorption → hypervolemia, increased workload
GOAL: at least 75 % oxy saturation on the heart, pulmonary and systemic congestion
HYPOPLASTIC LEFT HEART SYNDROME (HLHS)
Hypoplastic = maliit LEFT SIDE HEART FAILURE
Underdevelopment of the Problem = Pulmonary Congestion
left side of the heart ➢ LV unable to pump blood to the systemic circulation →
resulting in Hypoplastic increased LA pressure and pulmonary artery → congestion
left ventricle & Aortic in lungs → increased pulmonary pressure → pulmonary
atresia. edema → pulmonary HPN
Most blood from the L OR
atrium flows across the LV → (-) SYSTEMIC CIRCULATION → ↑LA → ↑PA → lung
patent foramen ovale → R congestion/ pulmonary edema
atrium → L ventricle → out
to pulmonary artery. Signs and Symptoms of LSCHF
The descending aorta receives blood from the PDA to • Respiratory malfunctions
supply the systemic blood flow. • Dyspnea (Paroxysmal Nocturnal Dyspnea)
Walang lumalabas na dugo from LV and aorta. • Orthopnea
unoxy blood → RA → RV → Pulmonary Artery → Lung • Rales/ Crackles
→ pabalik → need ASD or Foramen ovale → need PDA – • Blood-Tinged Frothy Sputum
para lumabas ‘yung blood through the body • Wheezing
Therapeutic Management • Dizziness
• Prostaglandin E • Syncope
– Infusion to keep the ductus open • Weakness
• Heart Transplant – best and last option.
Surgical Treatment RIGHT SIDED HEART FAILURE
Problem = Systemic Circulation Overload
✓ Norwood procedure to create a new aorta using the main ➢ RV unable to pump blood to Pulmonary Artery →
pulmonary artery and creation of large ASD. increased pressure in RA and in the systemic venous
✓ Bidirectional Glenn Shunt at 6-9 months age to reduce circulation → Systemic venous HPN →
volume load on the R ventricle. hepatosplenomegaly.
✓ Modified Fontan procedure, similar to Tricuspid atresia OR
repair.
RV → (-)PA → ↑RA → ↑systemic circulation →
✓ Transplant may be an option for some parts. Mortality rate
is very high (30%- 50%) hepatosplenomegaly → edema
MIDTERMS // honeybunchsugarplum | 34
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
Signs and Symptoms of RSCHF Therapeutic Management
• Edema GOALS:
• Fatigue 1. Improve Cardiac Function
• Neck vein engorgement o Digitalis therapy
• Ascites ▪ Increased CO, decreased size and venous
• Enlarged liver & spleen pressure, relieve edema
• Peripheral edema ▪ Lanoxin (Digoxin) – (Pedia) – more rapid in onset
• Leg varicosities  Oral / IV doses x 24 hours followed by
• Weight gain (bcos of additional fluids) maintenance dose (BID) to maintain blood
levels (Digitalizing Dose)
If not corrected…  Help heart contractility.
 Inotropic effects
↓Blood flow → KIDNEY → ↑ABSORPTION → hypervolemia  Chronotropic effects
→ ↑workload → DAMAGE TO HEART MUSCLES
o ACE Inhibitors (Capoten/ Enalapril)
This will lead to the three groups of manifestation for CHF ▪ (-) normal function of R-A system in kidney
1. Impaired myocardial function (L & R) ▪ Blocks conversion of AI to AII (Vasodilator)
– ‘di na titibok nang maayos ‘yung puso ▪ Captopril – can be given smaller doses
2. Pulmonary congestion (L) Asess:
3. Systemic venous congestion (R) • Heart Rate before administration if below 60 or above 120
= DO NOT GIVE Lanoxin or Digoxin; refer to doctor
s/s of Impaired Myocardial Function • If given it can lead to Bradycardia or rebound Tachycardia
• Contractility of heart
• Tachycardia Digitalis Toxicity
• ↓ urine output • Bradycardia
• Fatigue • GI manifestations:
• Weakness o Anorexia
• Restlessness o Nausea and Vomiting
• Anorexia o Diarrhea
• Pale, Cool extremities • Dysrhythmias (most dangerous)
• ↓ BP • Altered visual perceptions (Halos)
• Weak peripheral pulse 2. Remove accumulated fluid/ sodium
• Cardiomegaly • To decrease cardiac workload by reducing circulating
volueme thereby reducing preload
s/s of Pulmonary Congestion o DIURETICS – pampaihi
• Respiratory problems 1. Furosemide (Lasix)
• Tachypnea 2. Thiazides (Diuril)
• Dyspnea 3. Potassium sparing (Aldactone)
• Retractions Assess:
• Flaring of nares Pt is at risk for electrolyte imbalance.
• Exercise intolerance • Hypokalemia (↓ potassium) = < 3.5 mmol/L
• Cough – DO NOT GIVE furosemide and thiazide
• Cyanosis Normal: 3.5 – 5 mmol/L
• Wheezing
Management:
s/s of Systemic Venous Congestion • If hypokalemia:
o Hook the patient to Cardiac Monitor; refer to DR
• Weight gain and hold the medication.
• Hepatomegaly (Large liver)
• DR order:
• Peripheral and periorbital edema o Potassium sparring – muscle electrolyte; will
• Ascites reabsorb potassium to go back to circulation
• Neck vein distention o Give Diuretics – best in EARLY MORNING/
EARLY AFTERNOON
Diagnostic Evaluation
3. Decrease Cardiac Demand
• Chest X-ray – to determine kung lumalaki ‘yung puso
1. Reduce metabolic needs (Diet)
• Electrocardiogram (ECG) – to determine if u have
2. Limited physical activity
arrythmia, dysrhythmia or short abnormal heart rhythm
3. Preserving body temperature
4. Positioning
5. Sedation
MIDTERMS // honeybunchsugarplum | 35
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
4. Improve tissue oxygenation and Decrease O2 Nursing Management
consumption 1. Encourage compliance to treatment
• Supplemental humidifies oxygen is given. o Encourage adherence to tx’c plan
• DR order: Oxygen therapy o (+) poor compliance: monthly injections
2. Facilitates recovery from the illness
For L and R side heart failure: 3. Provide emotional support
4. Prevent the disease
• Vasodilators – to dilate the vessels to maintain normal
blood pressure
o Captopril (Capoten) KAWASAKI DISEASE
o Hydralazine (Apresoline) ➢ MUCOCUTANEOUS LYMPH NODE SYNDROME
o Nifedipine (calcium channel blocker w/ vasodilator ➢ Acute systemic vasculitis
effects) ➢ <5 y/o (Peak: toddlers)
➢ This in itself is SELF-LIMITING.
RHEUMATIC FEVER (RF) ➢ w/o treatment the child can develop Cardiac Problems
➢ Acute inflammatory disease
➢ Has significant effect in the: ETIOLOGY
o Heart ➢ UNKNOWN
o CNS • Infectious
o Joints • Geographical
o Subcutaneous tissues • Seasonal outbreaks
Rheumatic Heart Diseases
PATHOPHYSIOLOGY
➢ Damages the mitral valves
• Extensive inflammation of the arterioles, venules, and
ETIOLOGY capillaries
➢ Group A streptococci • Formation of coronary artery aneurisms
➢ Development of RF within 2 – 6 weeks • Coronary thrombosis
– Upon exposure to Group A streptococci bacteria • Stenosis
Diagnostic Criteria for RF • Severe scar formation of the main coronary artery
Can happen if left untreated.
• Modifications of the Jones criteria
o 2 Major Manifestations and 2 Minor Manifestations
Signs and Symptoms
• If with evidence of STREP INFECTION
• Pink eye
o 1 major and 2 minor manifestation
• Oral mucosal change
5 MAJOR CRITERIA of Jones • Enlarged lymph nodes
1. Polyarthritis • Patchy rash
2. Carditis • Peeling skin
3. Subcutaneous nodules
4. Erythema marginatum • Small and medium vessel vasculitis
5. Sydenham’s chorea • Mnemonic: “Warm CREAM”
MINOR
• Fever Needs:
• Polyarthralgia • Warm – fever >5d (5 days)
• History of RF
• Increase ESR PLUS 4 of 5:
• Antecedent strep infection 1. Conjunctivitis – bilateral, non-purulent
2. Rash – erythematous, maculopapular, morbilliform
Therapeutic Management 3. Erythema palms and soles – with swelling
1. Eradication of Hemolytic Streptococci 4. Adenopathy, cervical – 1 unilateral node
o Penicillin G – IM x 1 5. Mucous Membrane – dry, red, strawberry tongue
o Penicillin V – oral x 10 days
o Sulfa – oral x 10 days Diagnostic Criteria for KD
o Erythromycin (if allergic to above) - oral x 10 days
1. Fever for 5 or more days
2. Prevention of Permanent Cardiac Damage 2. Bilateral conjunctival inflammation without exudation
3. Palliation of other symptoms 3. Changes in the oral mucous membrane “strawberry tongue”
o Salicylates (ASA) – control inflammatory process esp. 4. Changes in the extremities (EDEMA and PEELING)
joints, dec fever and discomfort 5. Polymorphous rash
o Bed rest – during febrile phase but need not be strict 6. Cervical lymphadenopathy (one lymph node >1.5cm)
o Should be followed medically x 5 years
4. Prevention or recurrence of RF

MIDTERMS // honeybunchsugarplum | 36
 NCMA 219 – BSN 2ND YEAR – 2nd SEMESTER // Transcribed by B
3 Phases Clinical Manifestations
1. Acute phase
o ABRUPT ONSET FEVER
o Very irritable
2. Subacute phase
o Begins with resolution n of the fever
o Lasts until all clinical signs of KD disappear
o GREATEST RISK FOR THE DEVT OF
CORONARY ARTERY ANEURISMS
o Still irritable
3. Convalescent phase
o All clinical signs of KD have disappeared but LAB
values not normal

Therapeutic Management
1. High doses of IV Gamma Globulin
o 2 g/kg of BW over 10 – 12 hours
2. ASPIRIN
o Anti-inflammatory dose 80 – 100 mg/ kg/ day
o Antiplatelet dose 3 – 5 mg/ kg/ day
3. COUMADIN
o 1 of GIANT Aneurisms

• Prognosis
o Curable and full recover after treatment
• Death
o Sec to THROMBOSIS

Nursing Care Management

• Help the family adjust to the disorder
• Educated the family about the disorder
• Help the family manage the illness at home
• Prepare the child and family for invasive procedures
• Provide Postoperative care
• Provide Emotional support
• Plan for discharge and home care

Surgical Intervention
• Open-Heart
• Closed heart procedures
• Staged procedures
• Prepare child and family for procedures

MIDTERMS // honeybunchsugarplum | 37