Professional Documents
Culture Documents
City of Makati
UNIVERSITY OF MAKATI
COLLEGE OF ALLIED HEALTH STUDIES
CENTER OF NURSING
J.P Rizal Extension, West Rembo, Makati City 1215
Telephone No.: (+632) – 881 – 1571
Submitted by:
Balaoy, Ruth C.
Terrado, Debbie
4AN3B
TETRALOGY OF FALLOT
Tetralogy of Fallot is a rare condition caused by a combination of four heart defects that are present at
birth (congenital).
These defects, which affect the structure of the heart, cause oxygen-poor blood to flow out of the heart
and to the rest of the body. Infants and children with tetralogy of Fallot usually have blue-tinged skin
because their blood doesn't carry enough oxygen.
Tetralogy of Fallot is often diagnosed during infancy or soon after. However, tetralogy of Fallot might not
be detected until later in life in some adults, depending on the severity of the defects and symptoms.
With early diagnosis followed by appropriate surgical treatment, most children and adults who have
tetralogy of Fallot live relatively normal lives, though they'll need regular medical care throughout life
and might have restrictions on exercise.
Etiology
In the laboratory setting, destruction of these cells reproduced results displayed with certain cardiac
malformations.
Symptoms
Tetralogy of Fallot symptoms vary, depending on the extent of obstruction of blood flow out of the right
ventricle and into the lungs. Signs and symptoms may include:
Clubbing of fingers and toes — an abnormal, rounded shape of the nail bed
Irritability
Prolonged crying
A heart murmur
Tet spells
Sometimes, babies who have tetralogy of Fallot will suddenly develop deep blue skin, nails and lips after
crying or feeding, or when agitated.
These episodes are called tet spells and are caused by a rapid drop in the amount of oxygen in the blood.
Tet spells are most common in young infants, around 2 to 4 months old. Toddlers or older children might
instinctively squat when they're short of breath. Squatting increases blood flow to the lungs.
Causes
Tetralogy of Fallot occurs during fetal growth, when the baby's heart is developing. While factors such as
poor maternal nutrition, viral illness or genetic disorders might increase the risk of this condition, in most
cases the cause of tetralogy of Fallot is unknown.
Pulmonary valve stenosis. Pulmonary valve stenosis is a narrowing of the pulmonary valve — the
valve that separates the lower right chamber of the heart (right ventricle) from the main blood
vessel leading to the lungs (pulmonary artery).
Narrowing (constriction) of the pulmonary valve reduces blood flow to the lungs. The narrowing
might also affect the muscle beneath the pulmonary valve. In some severe cases, the pulmonary
valve doesn't form properly (pulmonary atresia) and causes reduced blood flow to the lungs.
Ventricular septal defect. A ventricular septal defect is a hole (defect) in the wall (septum) that
separates the two lower chambers of the heart — the left and right ventricles. The hole allows
deoxygenated blood in the right ventricle — blood that has circulated through the body and is
returning to the lungs to replenish its oxygen supply — to flow into the left ventricle and mix with
oxygenated blood fresh from the lungs.
Blood from the left ventricle also flows back to the right ventricle in an inefficient manner. This
ability for blood to flow through the ventricular septal defect reduces the supply of oxygenated
blood to the body and eventually can weaken the heart.
Overriding aorta. Normally the aorta — the main artery leading out to the body — branches off
the left ventricle. In tetralogy of Fallot, the aorta is shifted slightly to the right and lies directly
above the ventricular septal defect.
In this position the aorta receives blood from both the right and left ventricles, mixing the oxygen-
poor blood from the right ventricle with the oxygen-rich blood from the left ventricle.
Right ventricular hypertrophy. When the heart's pumping action is overworked, it causes the
muscular wall of the right ventricle to thicken. Over time this might cause the heart to stiffen,
become weak and eventually fail.
Some children or adults who have tetralogy of Fallot may have other heart defects, such as a hole between
the heart's upper chambers (atrial septal defect), a right aortic arch or abnormalities of the coronary
arteries.
Risk factors
While the exact cause of tetralogy of Fallot is unknown, various factors might increase the risk of a baby
being born with this condition. These risk factors include:
Nursing Diagnosis : Decreased Cardiac Output r / t ineffective circulation, secondary to the presence
of cardiac malformations
Intervention:
1. Monitor vital signs, peripheral pulses, capillary refill by comparing measurements at both
extremities while standing, sitting and lying down if possible.
2. Assess and record the apical pulse for 1 full minute.
3. Observation of cyanotic attacks.
4. Give a knee-chest position in children.
5. Observe for signs of decreased sensory: lethargy, confusion, and disorientation.
6. Monitor intake and output adequately.
7. Provide adequate rest time for children and accompany children during activity.
8. Serve foods that are easily digestible and reduce the consumption of caffeine.
9. Collaboration in the examination serial ECGs, chest radiographs, administration of anti
dysrhythmias.
10. Collaboration of oxygen.
11. Collaboration IV fluid administration.
INCIDENCE
RDS is at the top 3 of Infant mortality leading causes as of 2009 with a number of 2,438 per 1000
live births. (© DOH)
RISK FACTORS
Preterm infants
Infants of diabetic mothers
Infants born by cesarean birth
Baby boy
The baby has a sibling born with RDS
DIAGNOSIS
Antenatal Period
o Examination of Amniotic fluid - Lecithin sphingomyelin ratio; < 1.5
Laboratory tests
o pCo2 elevated
o pO2 low
o Calcium low
o Serum glucose low
Chest Xray
o “ground – glass appearance” or “ white wash lung”
NURSING INTERVENTIONS
1. Clearing of airway, ensuring adequate breathing and circulation are the first line of management.
A baby in obvious respiratory distress needs to be on continuous pulse oximeter monitoring to
decide when intubation and ventilation is required.
2. Warm, humidified oxygen is given. Oxygen should be given in the correct dose, as it is toxic to
preterm neonates.
3. Maintenance of correct temperature is essential. RDS is aggravated by hypothermia.
4. Surfactant is the drug of choice in a baby with RDS. This may be given either prophylactically if
the baby is less than 28 weeks of gestation or within the first two hours of onset of symptoms in
older babies. Prophylactic surfactant is given in the labour room after the baby has been
stabilized.
5. Fluid and electrolyte management: Electrolyte balance, fluids, calcium and glucose homeostasis
are all equally important.
6. All preterm babies with respiratory distress should be started on broad spectrum antibiotics. In
term babies, decision to start antibiotics would depend on the clinical situation.
7. Maintenance of respiration with ventilation support, if necessary.
COMPLICATIONS
Pulmonary Hemorrhage
Pneumothorax
Bronchopulmonary
Neurological abnormalities
PATHOPHYSIOLOGY
SUDDEN INFANT DEATH SYNDROME
DEFINITION
SIDS is the sudden death of an infant under one year of age which remains unexplained after a
thorough case investigation, including performance of a complete autopsy, examination of the death
scene, and review of the clinical history.
INCIDENCE
The annual mortality rate per 100,000 people from sudden infant death syndrome in Philippines
has decreased by 15.8% since 1990, an average of 0.7% a year.
RISK FACTORS
Smoke
Sleeping.
Maternal age
Anemia
Genetics
DIAGNOSIS
Postmortem laboratory tests are done to rule out other causes of death (for example, electrolytes
are checked to rule out dehydration and electrolyte imbalance; bacterial and viral cultures are
obtained to evaluate whether an infection was present).
An autopsy provides clues as to the cause of death. In 15%-25% of sudden, unexpected infant
deaths specific abnormalities of the brain or central nervous system, the heart or lungs, or
infection may be identified as the cause of death.
A thorough investigation of the death scene consists of interviewing the parents, other caregivers,
and family members, collecting items from the death scene, and evaluating that information.
NURSING INTERVENTIONS
Health teaching
o Sleeping practices
• Back to sleep for every sleep, no side sleeping
• Use a crib/bassinet that conforms to the safety standards
• Firm sleeping surface
• No loose soft objects in bed
• Room sharing without bed sharing
• Avoid overheating
• Offer a pacifier during sleep
• No sleeping in sitting devices (car seats, swings)
• No devices promoted to make bed sharing protected (wedges, positioners)
o Feeding practices
• Promote breastfeeding
o Health care maintenance
• Regular prenatal care
• Avoid smoke exposure, alcohol, illicit drug use during pregnancy and after birth
• Immunizations in accordance with the AAP recommendation.
INTUSSUSCEPTION
It is the invagination of one portion of the intestine into another, usually occurs in the second half of the
first year of life. The point of invagination is generally at the juncture of the distal ileum and proximal
colon.
In infants younger than 1 year, intussusception generally occurs for idiopathic reasons. In infants older
than 1 year, a “lead point” (polyp or tumor) on the intestine likely cues the invagination. It can be caused
by lymphoid hyperplasia, enlargement of lymph tissue. There are tons of tiny lymph nodes sprinkled to
the intestines called “Peyer’s patches” and they are particularly common in the ileum. When a child
caught off some sort of viral infection in the gastrointestinal tract usually caused by rota virus, the lymph
nodes enlarge to light off infection and sometimes becomes a lead point that drags the ileum into the
cecum which causes intussusception. Can also be caused by MECKEL’S DIVERTICULUM-
outpouching of GI tissue, or bowel tumors.
ASSESSMENT
- Intermittent abdominal pain- children with this disorder suddenly draw up their legs and cry as if
they are in severe pain; they may vomit. After the peristaltic wave that caused the discomfort
passes, they are symptom-free and play happily. In approximately 15 minutes, the same
phenomenon of intense abdominal pain strikes again.
- Vomitus will begin to contain bile because the obstruction is invariably below the ampulla of
Vater, the point in the intestine where bile empties into the duodenum.
- Approximately after 12 hours, blood occurs in the stool and possibly in vomitus, “Currant jelly”
appearance
- The abdomen becomes distended as the bowel above the intussusception distends.
- If necrosis (cell death) occurs, children generally have an elevated temperature, peritoneal
irritation (their abdomen feels tender; they may guard it by tightening their abdominal muscles)
- Increased WBC count, often rapid pulse.
Intussusception
ISCHEMIA and INFARCTION causes SLOUGHING OFF (shedding off) OF INTESTINAL MUCOSA,
BLOOD AND MUCUS RED CURRANT JELLY
INTUSSUSCEPTION can also prevent food and fluid from passing through the body causing an
obstruction. This can lead to a large mass in the intestines which can potentially cause the intestines to be
twisted “VOLVULUS”
DIAGNOSIS:
- In children, it may be felt during rectal examination, but a definite diagnosis often requires
imaging techniques: Ultrasound, xray, CT scan which will reveal a “BULL’S EYE” or a
telescoped intestine on end which is a sign of intestinal obstruction
TREATMENT:
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 week 38 of gestation), term (between 38 weeks and 42), or
post term (after 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.
Normal birth weight- 7.5lbs (3.5kg); 5.5lbs (2.5kg) and 10lbs (4.5kg) are still normal.
ETIOLOGY
- A woman’s nutrition during pregnancy plays a major role in fetal growth, so lack of 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.
- Most common cause of IUGR is placental anomaly: either the placenta did not obtain sufficient
nutrients from the uterine arteries or it was inefficient at transporting nutrient 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.
- Women with systemic disease that decrease blood flow to the placenta, such as diabetes mellitus
or pregnancy induced hypertension (both are diseases are 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/ DIAGNOSTICS
- SGA infant can 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 then demonstrate the decreased size.
- A biophysical profile including non-stress 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. CS
is the birth method of choice in such circumstances.
APPEARANCE
- 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
and head circumference. Regardless of when deprivation occurs, an infant tends to have an
overall wasted appearance.
- Small liver- which can cause difficulty regulating glucose, protein and bilirubin levels after birth,
- Poor skin turgor
- Generally, appear to have large head because the rest of the body is so small,
- Skull sutures may be widely separated from lack of normal bone growth
- Hair is dull and lusterless
- Abdomen may be sunken
- Umbilical cord appears dry and may be stained yellow
The SGA infant needs careful assessment for possible congenital anomalies occurring as a result of poor
nutritional intrauterine environment.
Polycythemia (increased rbc) which happens because anoxia (absence of oxygen) stimulates the
development of RBC.
Polycythemia causes increase blood viscosity, a condition that puts extra work of on the infant’s
heart because it is more difficult to effectively circulate thick blood. As a result, Acrocyanosis
(blueness of hands and feet) are prolonged.
Because SGA infants have decreased glycogen stores, one of the most common problems is
hypoglycemia (Decreased blood glucose, less than 45 mg/dL). Such infants may need IV glucose
to sustain blood sugar until they are able to suck vigorously enough to take sufficient oral
feedings.
NURSING DIAGNOSIS
The average baby weighs about 7 pounds at birth. About 9 percent of all babies weigh more than 4,000
grams (8 pounds, 13 ounces). Rarely do babies weigh over 10 pounds.
Although most LGA babies are born at term (37 to 41 weeks of pregnancy), a few premature babies may
be LGA.
LGA infants are large, obese, and plethoric. The 5-min Apgar score may be low. These infants may be
listless(lacking energy) and limp(weak movement) and feed poorly
A mother's weight gain can also influence a baby's size. Excessive maternal weight gain in pregnancy
may correspond with a big baby.
Babies are weighed within the first few hours after birth. The weight is compared with the baby's
gestational age and recorded in the medical record.
After delivery, a LGA baby will be carefully examined for any birth injuries. Blood glucose testing is also
performed to check for hypoglycemia.
Prevention of LGA
Prenatal care is important in all pregnancies, especially to monitor fetal growth when a baby seems to be
too small or too large. Examinations during pregnancy that show a large baby can help identify a mother
who may have undetected diabetes, or other problems. Careful management of diabetes and proper weight
gain, according to your doctor's recommendations, can help lower some of the risks to the baby.
Nursing Management
a. Clavicle fracture
Confirm by x-ray.
Assess the infant for crepitus, hematoma, or deformity over the clavicle; decreased movement of
arm on the affected side; and asymmetrical or absent. Moro reflex.
Limit arm motion by pinning the infant’s sleeve to the shirt.
Manage the pain
c. Erb-Duchenne palsy and Klumpke paralysis (Weakness or lack of ability to use specific muscles of the
shoulder or arm)
Erb-Duchenne palsy. Assess for adduction of the affected arm with internal rotation and elbow
extension. The Moro reflex is absent on the affected side. The grasp reflex is intact.
Klumpke paralysis. Assess for absent grasp on the affected side. The hand appears claw-shaped.
Management includes:
X-ray studies of the shoulder and upper arm to rule out bony injury
Examination of the chest to rule out phrenic nerve injury
Delay of passive movement to maintain range of motion of the affected joints until the nerve
edema resolves (7 to 10 days)
Splints may be useful to prevent wrist and digit contractures on the affected side
d. Phrenic nerve palsy