Professional Documents
Culture Documents
Pedia 2
Pedia 2
A neonate is considered to be high risk if he has an increased chance of dying during or shortly after birth
or has a congenital or perinatal problem that requires prompt intervention.
RISK NEONATES are NB who are in danger of having difficulty establishing adjustment to their new
environment as a result of some contributing factors
The very young or very old pregnant women, pregnant mothers with disease such as DM, HPN, etc, drug abuse
A. According to size
1. Low BW infant (LBW)
- BW is less than 2,500g regardless of gestational age
2. Very Low BW (VLBW)
- BW of less than 1,500g
3. Extremely LBW
- BW less than 1,000g
4. Appropriate for gestational age (AGE)
- Birth weight expected for the specific gestation
- An infant whose weight between the 10th and 90th percentiles on intrauterine growth chart
- Ex. Baby born on the 34th week who weighs 5lbs
5. Small for gestational age (SGA)
- Term infants who weigh less than 2,500g or birth weight is less than expected for the specific
gestational age
- Birth weight below 10th percentile in intrauterine growth
- May be referred small for date and intrauterine growth retardation
- SGA infant may be preterm, term or post term
Etiology:
The effect of these factors upon the fetus is dependent on the stage of fetal development.
A. Early gestation is a time of rapid cell proliferation. An insult at this time results in organs that contain
normal size cells, but they are fewer in number. Infants are symmetrical (heads and bodies grew
proportionally) but their organs are smaller.
- Usually these infants have a poor prognosis and may never catch up
B. Later in gestation, growth of the fetus results from an increase in cell size. An insult at this time
results in organs with a normal number of cells that are smaller in size heads and causes asymmetric
growth. These infants have appropriate-sized heads and body lengths, but their weight and organ sizes
are decreased.
- These infants usually have a better prognosis since they have an adequate number of cells
- They growth catches up if they are provided with good nutrition postnatally.
ASSESSMENT FINDINGS
1. Clinical manifestations
a. Soft tissue wasting and dysmaturity
b. Loose, dry and scaling skin
c. Perinatal asphyxia (due to small placenta that is less efficient in gas exchange)
d. Sunken abdomen
e. Decreased chest and abdomen circumferences
f. Decreased subcutaneous fat
g. Thin, dry umbilical cord
h. Sparse scalp hair
2. Laboratory and diagnostic study findings
a. Glucose testing reveal decreased glycogen stores, which increases the potential for hypothermia
and hypoglycaemia
b. Hematocrit level may be increase (65%), which indicates polycythemia as a result of chronic fetal
hypoxia
Treatment
1. Supportive care
2. Nutritional support
NURSING INTERVENTIONS
1. Provide adequate fluid and electrolytes and nutrition
a. Provide a high calorie formula for feeding (more than 20 calories per ounce) to promote steady
weight gain (15 to 30 grams per day; growth plotted on curves shows normal growth rate.)
b. If the infant is breast feeding, add human milk fortifier to expressed breast milk
2. Decrease metabolic demands when possible.
a. Provide small frequent feedings
b. Provide gavage feeding if the infant does not have a steady weight gain
c. Provide a neutral thermal environment
d. Decrease iatrogenic stimuli
3. Prevent hypoglycemia
a. Monitor glucose screening
b. Provide early feedings
c. Provide frequent feedings (every 2 to 3 hours)
d. Administer IV glucose if blood sugar does not normalize with oral feedings. >40mg/dl
4. Maintain a neutral thermal environment
5. Monitor serum hematocrit. (normal 45%-65%)
a. If an initial high hematocrit was obtained by heel stick capillary sample, a follow-up sample
should be done by venipuncture
b. Observe for signs, symptoms and complications of polycythemia
Ruddy appearance
Cyanosis
Lethargy, jitteriness and seizures
Jaundice
c. Provide adequate hydration to prevent hyperviscosity
d. MIO
e. Administer IV fluid therapy as ordered
6. Assess the prenatal history for possible toxoplasmosis, rubella, cytomegalovirus, and herpes simplex
infections during pregnancy. Assess maternal and infant antibody titers. Use isolation precautions
when congenital infections are suspected.
7. Support respiratory efforts; monitor respiratory status closely for changes; institute respiratory care
measures, as indicated by the neonate’s condition
8. Provide meticulous skin care
9. Provide education and emotional support
a. Explain the possible causes of intrauterine growth retardation
b. Inform parents of the infant’s goal weight for discharge
c. Provide instruction on managing the infant at home
Explain how to prepare a higher calorie formula or breastfeeding
Explain the importance of follow up with a developmental specialist who will screen for
milestone achievements.
Causes:
- Overproduction of growth hormone in uterus. This happens most often to mothers with poorly
controlled diabetes mellitus, multiparous woman
- Ex. A baby born on the 34th week gestation who weigh 8 lbs
Etiology:
Predisposing factors:
1. Genetic predisposition
2. Excessive maternal weight gain during pregnancy
3. Poorly controlled material diabetes
LGA places the neonate at risk for certain problems
Increase incidence of caesarean deliveries; birth trauma and injury
Hypoglycemia
Polycythemia
Pathophysiology
ASSESSMENT FINDINGS
Treatment
- Close observation
- Supportive care
NURSING INTERVENTIONS
Monitor for, and manage, birth injuries and complications of birth injuries
a. Clavicle fracture
1. Confirm by x-ray
2. Assess the infant for crepitus, hematoma, or deformity over the clavicle; decrease
movement of arm on the affected side; and asymmetrical or absent Moro reflex
3. Limit arm motion by pinning the infant’s sleeve to the shirt
4. Manage pain
b. Facial nerve injury
1. Assess for symmetry of mouth while crying
2. Wrinkles are deeper on the unaffected side
3. The paralyzed side is smooth with a swollen appearance
4. The nasolabial fold is absent
5. If the eye is affected, protect it with patches and artificial tears
c. Erb-Duchenne palsy and Klumpke paralysis
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.
d. Phrenic nerve palsy
1. Assess for respiratory distress with diminished breath sound
2. X-ray usually shows elevation of the diaphragm on the affected side
3. Provide pulmonary toilet to avoid pneumonia during recovery phase (1-3 months)
e. Skull fracture
-assess for soft-tissue swelling over fracture site, visible indentation in scalp,
cephalhematoma, positive skull x-ray, and CNS signs with intracranial haemorrhage (e.g.
lethargy, seizures, apnea and hypotonia)
Klumpke paralysis
Assess for absent grasp on the affected side. The hand appears claw-shaped
Management includes:
a. X-ray studies of the shoulder and upper arm to rule out bony injury
b. Examination of the chest to rule out phrenic nerve injury
c. Delay of passive movement to maintain range of motion of the affected joints until the nerve
edema resolves (7 to 10 days)
d. Splints may be useful to prevent wrist, and digit contractures on the affected side, phrenic
nerve injury
- The extent of immaturity depends on the gestational age and level of development at delivery
- preterm neonates between 28 to 37 weeks’ gestation have the best chance of survival
Etiology
Causes of prematurity
A. Maternal Factors:
1. Malnutrition
2. Chronic diseases (heart disease, renal disease, DM)
3. Lack of prenatal care
4. Cigarette smoking
5. Maternal history of preterm delivery
6. Maternal substance abuse (cocaine)
7. Maternal age less than 18 years old
B. Factors related to pregnancy
1. Hypertension
2. Abruptio or placenta previa
3. Incompetent cervix
4. Premature rupture of membrane
5. Polyhydramnios
6. Multiple pregnancy
C. Fetal factors
1. Chromosomal abnormalities
2. Intrauterine infection
3. Anatomic abnormalities
PATHOPHYSIOLOGY
Preterm birth may occur because of maternal disease that necessitates delivery of the neonate for the health
of the mother (ex. Preeclampsia)
Preterm birth may be also a direct result of preterm labor
Preterm newborns exhibits anatomic and physiologic immaturity in all body systems; this immaturity
hinders the adaptations to extrauterine life that the newborn must make
ASSESSMENT FINDINGS
A. Inspection findings
- Low birth weight (less than 2,500 grams)
- Minimal subcutaneous fat deposits
- Proportionally large head in relation to body
- Prominent sucking pads in the cheeks
- Wrinkled features
- Thin, smooth, shiny skin that’s almost translucent (have underdeveloped subcutaneous tissue and less
fat to act as insulator)
- Veins clearly visible under the thin, transparent epidermis
- Lanugo hair over the body
- Sparse, fine, fuzzy hair on the head
- Soft, pliable ear cartilage; the ear may fold easily
- Assume frog like position
- Minimal creases in the soles and palms
- Prominent eyes, possibly closed
- Few scrotal rugae (males)
- Undescended testes (males)
- Prominent labia and clitoris (female)
B. Neurologic examination findings
- Inactivity (unusually active after birth)
- Extension of extremities
- Absence of sucking reflex
- Weak swallow, gag and cough reflex
Ability to bring the neonate’s elbow across the chest when eliciting or elbow asses the midline of the
-
body scarf sign
- Wrist at 90 degree angle- square window wrist
- Heal is easily brought to ear with no resistance heal to ear maneuver
C. Additional findings
- Inability to maintain body temperature or they easily take the temperature of the environment-
poikilothermic
- Limited ability to excrete solute in the urine
- Increased susceptibility to infection, hyperbilirubinemia, and hypoglycaemia
- Periodic breathing, hypoventilation and period of apnea
- CNS center for respiration are underdeveloped which result to irregular breathing with short periods of
apnea
TREATMENT
NURSING INTERVENTION
Kangaroo (skin-skin) care facilitates closeness and attachment between parents and their premature infant
5. Avoid vigorous stroking and rubbing use firm but gentle touch when handling neonate
6. Support the head and maintain extremities close to the body during position changes
7. Monitor fluid and electrolyte balance, assess intake and output, and administer I.V. fluid therapy as ordered
8. Administer nutritionally therapy as ordered
- Keep in mind that neonates born before 34 weeks gestation have uncoordinated sucking and
swallowing reflexes, so gavage feeding or I.V. feeding may be necessary
- Provide non-nutritive sucking via pacifier as appropriate
9. Provide education, support, and guidance to the parents and family
10. Explain all procedures and treatments to the parents, allow parents to verbalize their concerns, correct any
misconception or erroneous information
11. Assist with referrals for supportive services
Preterm feeding
ETIOLOGY
PATHOPHYSIOLOGY
ASSESSMENT FINDINGS
TREATMENT
1. Close observation
2. Supportive care
NURSING INTERVENTIONS
C.ACCORDING TO MORTALITY
1. Live births
- birth in which the neonate manifest any heartbeat, mother is dispense voluntarily movement regardless of
gestational
2. Fetal death
3. Neonatal Death
- death that oocurs in the 12th week of life, late neonatal death occurs at 7 to 27 days
4. Perinatal Mortality
- describes the total number of fetal and early neonatal death per 1,000 live birth
A. HYPERBILIRUBINEMIA
Bilirubin
Is one of the breakdown products of haemoglobin that results from red blood cell destruction
When RBC are destroyed, the breakdown products are released into the circulation, where the hemologbin
splits into two fractions: heme and globin
The globin (protein) portion is used by the body; the heme portion is converted to unconjugated bilirubin,
an insoluble substance bound to albumin
In the liver the bilirubin is detached from the plasma protein and, in the presence of the enzyme glucoronyl
transferase, is conjugated with glucoronic acid to produce a highly soluble substance, conjugated bilirubin
glucoronide, which is then excreted into the bile. In the intestine bacterial action reduces the conjugated
bilirubin to urobilinogen and stercobilin, the pigment that gives stool its characteristics color
Most of the reduced bilirubin is excreted through the feces; a small amount is eliminated as urobilinogen in
the urine.
PATHOPHYSIOLOGY
ASSESSMENT FINDINGS
Jaundice appearing anytime after the first day of life and persisting beyond 7 days
Usual pattern of progression is from head to feet. Blanch skin cover bony area or look at conjunctiva and
buccal membranes as dark-skinned infants
Elevated serum bilirubin levels- greater than 12mg/100ml in a term neonate, levels greater that
15mg/100 ml in a preterm
Hepatosplenomegaly
Pallor
Dark concentrated urine
Behavior changes (irritability, lethargy)
Polycythemia
Increased serum bilirubin (direct, indirect, and total)
TREATMENT
Exchange transfusion to replace the neonate’s blood with fresh blood (less than 48 hours), removing
some of the unconjugated bilirubin in serum
Phototherapy
Considered the treatment of choice for hyperbilirubinemia due to haemolytic disease of the neonate
Use fluorescent light to decompose bilirubin in the skin by oxidation
Exposure to light triggers the liver to
Usually discontinued after bilirubin levels falls below 10mg/100ml and continue to decrease for 24 hours
Albumin administration (1g/kg of 25% salt-poor albumin) to provide additional albumin) to provide
additional albumin for binding unconjugated bilirubin; done 1 to 2 hours before exchange or as a substitute
for a portion of the plasma in transfuse blood
Treatment of anemia caused by haemolytic disease
Pharmacological treatment:
Nursing Intervention
1. To prevent hyperbilirubinemia encourage the mother to breastfeed at least 8 to 12 times per day. Don’t skip
feeding because fasting stimulates the conversion of heme to bilirubin. Also, don’t supplement non-
dehydrated breastfed infants with water or water and dextrose
2. Assess and record the neonates jaundice in the first 24 hours after birth, and note the time it began,
immediately report the jaundice and serum or transcutaneous bilirubin levels
3. Obtained lab values as ordered, which may include blood type, Coombs’ test, complete blood count, G6pD,
urinalysis, and total and direct (conjugated) bilirubin
4. Institute phototherapy
a. Expose all areas of the body by turning the infant every 2 hours
b. Cover eyes and genitalia. To protect from ultraviolet light and burning. Bright light is harmful to NB;s
retina
c. Clean the neonate’s eyes periodically to remove drainage
d. Check for loose stool and increased body temperature
e. Maintain temperature 36 to 37 degree Celsius to prevent overheating
f. Give plenty of fluids to promote bilirubin excretion and to prevent dehydration
g. Assess skin turgor and MIO
h. Remove from phototherapy for feeding; hold infant to provide human contact
i. Ensure feeding every 3 hour
j. Explain that the neonate’s stool contains some bile and greenish color
k. Record phototherapy time
5. Assist with an exchange transfusion if indicated
6. Reassure parents that most neonates experience some degree of jaundice
7. Explain hyperbilirubinemia, its causes, diagnostic tests and treatment
8. Explain the importance of follow-up visit to assess for hyperbilirubinemia
Assessment Findings
Diagnostic Test
Treatment
Antibiotic administration
Nursing Interventions
C.ANEMIA
Risk Factors:
Prematurity
Maternal DM
Stress during delivery
Pathophysiology
RDS is characterized by poor gas exchange and ventilator failure due to lack of surfactant in the lungs
Surfactant is a phospholipids secreted by the alveolar epithelium
It coats the alveoli, keeping them open so gas exchange occur
A substance responsible for maintaining expansion of alveolar walls after initial respiration
Acting much like a detergent, this substance reduces surface tension of fluids that line the alveoli and
respiratory passages, resulting in uniform expansion at low intra alveolar pressure
In preterm neonates, the lungs not fully developed and therefore may not have sufficient surfactant
available
Deficient surfactant production causes unequal inflation of alveoli on inspiration and collapse of alveoli on
end expiration
Without surfactant, infants are unable to keep their lungs inflated and therefore exert a great deal of effort
to re-expand the alveoli with each breath. As a result, infants use more oxygen to expend this energy than
they take in, which rapidly leads to exhaustion
The lack of expansion of affected alveoli decreases alveolar ventilation
This results in inadequate exchange of O2 and CO2 leading to hypoxia
Hypoxia increases capillary permeability, causing effusion from pulmonary capillaries into the alveoli and
terminal bronchioles
With increasing exhaustion they are able to open fewer alveoli. This instability to maintain lung expansion
produces widespread atelectasis
Inadequate pulmonary perfusion and ventilation produce hypoxemia and hypercapnea
Prolonged hypoxemia activates anaerobic glycolysis, which produces increased amounts of lactic acid
An increase in lactic acid causes metabolic acidosis
Lowered pH causes further vasoconstriction
Hyaline-like membrane form around the alveoli and bronchioles causing further hypoxia and atelectasis
With deficient pulmonary circulation and alveolar perfusion, the PaO2 continues to fall, the pH falls, and
materials needed for surfactant production are not circulated to the alveoli
With worsening atelectasis, pulmonary vascular resistance increases, with decreases blood flow to the lungs
Sequelae of RDS
1. Hyperbilirubinemia
2. Retrolental fibroplasia- retinal changes visual impairment and eventually blindness, resulting from too
high oxygen levels during treatment
3. Bronchopulmonary dysplasia
4. Necrotizing enterocolitis- an ischemic attack to the intestine resulting in thrombosis and infarction of
affected bowel, mucosal ulceration and inflammation
5. Pseudomembrane formation and inflammation
Assessment Findings
RDS can produce respiratory distress acutely after birth or within a few hours at birth
Initial assessment may reveal various finding
Increased respiratory rate- more tha 70/min, tachypnea
Retractions
Good air movement on auscultation
As respiratory distress becomes more obvious, other findings may be noted
Further increased respiratory rate
Labored breathing
Fine crackles on auscultation
Cyanosis
Nasal flaring
Expiratory grunting (major symptoms) prolonged expiratory time. The sound denotes that closure of the
glottis is occurring. Glottis closure increases pressure in alveoli on expiration
Rales (abnormal sound heard on auscultation of lungs when fluid is present)
Respiratory distress
Signs and symptoms- such as hypoxemia, hypercapnia, and acidosis- are non specific to RDS
Specific laboratory tests must be carried out to evaluate the neonate for complications
Lecithin/spingomyelin ratio (L/S ration)2:0
These may include blood, urine, and cerebrospinal fluid CSF. Cultures and blood glucose, serum calcium,
and arterial blood gas (ABG) levels
Blood values:
Low pH level (normal= 7.35-7.45)
Low pO2 level (normal 40-60mmHg)
High pCO2 level (normal 35-45)
Radiographic evaluation reveals various findings
Alveolar atelectasis shown by a diffuse granular pattern that resembles ground glass over all lung fields
Dilated bronchioles shown by dark streaks within granular pattern
Treatment
1. When premature labor cannot be arrested, Betamethasone maybe administered to enhance surfactant
2. Thermoregulation
3. Oxygen administration
4. Mechanical ventilation, if needed. Continuous positive air pressure (cpap) or positive end expiratory
pressure (peep)
5. Prevention of hypotension
6. Prevention of hypovolemia
7. Correction of respiratory acidosis by ventilatory support
8. Correction of metabolic acidosis by sodium bicarbonate administration
9. Administration of surfactant and such other drugs as an antibiotic, a sedative, and a diuretic
10. Protection from infection
11. Administration of parenteral feeding
Nursing Intervention
1. Provide continuous monitoring and close observation. (vital signs, arterial blood gases, skin color and
muscle tone)
2. Maintain temperature at 97 degree F or 36.2 degree C
3. Obtain necessary specimen for laboratory testing
4. Continuously monitor pulse oxymetry or transcutaneous oxygen levels
Administer oxygen as needed. Monitor O2 concentration every 2-4hrs; maintain less than 40%
concentration
Anticipate the need for ventilatory support, including mechanical ventilation, continuous positive airway
pressure, or positive end-expiratory pressure
5. Suction the neonate as indicated
6. Institute measures to maintain thermoregulation
7. Provide parenteral nutrition and avoid gavage and oral feedings during acute stage of the disease because
these situations increase respiratory rate and oxygen consumption
8. Cluster nursing activities to provide the neonate with rest periods; disturb the neonate with RDS as little as
possible to decrease oxygen consumption
9. Provide meticulous skin care and mouth care
10. Administer drugs as ordered
11. Educate parents about the disease, treatments and procedures as well as what to expect
12. Orient the parents to the intensive care unit
13. Provide emotional support especially during the acute stage
14. Assist with referrals to social services, chaplain, and other supportive resources as necessary
E. BRONCHOPULMONARY DYSPLASIA
Is a chronic pulmonary disease of infancy marked by the need for oxygen therapy beyond 28 days after
birth
Most commonly affects very low-birth weight (under 2,500g) and extremely low-birth weight (under
1,000g) infants with lung disorders
A premature neonate who is mechanically ventilated and receives high concentration of oxygen
Etiology
The exact cause is unknown, but is thought that it is the response of a premature lung to early injury
Mechanical ventilation and a high inhaled oxygen concentration are the two major causes of BpD
May occur after mechanical ventilation therapy for such conditions as RDS, meconium aspiration,
persistent pulmonary hypertension, and cyanotic heart disease
Pathophysiology
Positive inspiratory pressures and high concentration of oxygen can injure the alveoli saccules and small
airway epithelium and leaf to fibrosis of these structures
Areas of cystic foci and atelectasis appear in the lung parenchyma. In addition, airway smooth-muscle
hypertrophy results in bronchospasm and endothelial damage, causing interstitial edema
These changes further aggravate airway obstruction and necessitate long term oxygen
Assessment Findings
1. Clinical Manifestations
a. Cyanosis when breathing room air, tachypnea, retractions, grunting, nasal flaring, increased
anteroposterior diameter of the chest, wheezing, crackles, and copious secretions
b. Manifestations of right sided heart failure may be present including periorbital edema, hepatomegaly,
and jugular vein distention; pulmonary edema, clubbing of the fingers is seen with severe disease
c. Thin with height and weight measurement in the bottom of 50th percentile
2. Laboratory and diagnostic study findings
a. Pulmonary function test will reveal increased airway resistance, decreased compliance and increased
functional residual capacity
b. Chest x-rays show characteristic streakiness with areas of hyperinflation and atelectasis
c. Electrocardiography and echocardiogram may show evidence of right-sided cardiac hypertrophy
Nursing Management:
Risk Factors:
Maternal diabetes
Maternal hypertension
Difficult labor
Fetal distress
Intrauterine hypoxia
Advanced gestational age (greater than 40 weeks)
Poor intrauterine growth
Pathophysiology
Asphyxia in utero leads to increased fetal peristalsis, relaxation of the anal sphincter, passage of meconium
into amniotic fluid, and reflex gasping of amniotic fluid into the lungs
- Neonates with MAS increase respiratory effort to create greater negative intrathoracic pressures and
improve airflow to the lungs
- Hyperinflation, hypoxemia, and acidemia cause increase peripheral vascular resistance
- Right-to-left shunting commonly follows
Meconium creates a baoo-valve effect, trapping air in the alveolus and preventing adequate gas exchanging
Chemical pneumonitis result, causing the alveolar walls and interstitial tissue to thicken, again preventing
adequate gas exchange
Cardiac efficiency can compromised from pulmonary hypertension
Assessment Findings
Treatment
Definition
1. ESOPHAGEAL ATRESIA- failure of the esophagus to form continuous passage from the pharynx to the
stomach
2. TRACHEOESOPHAGEAL FISTULA (TEF)- abnormal sinus connection between the esophagus and
the trachea
TYPES OF ESOPHAGEAL ATRESIA AND FISTULA
1. TYPE 1/A- both upper and lower segment of the esophagus end in blind pouches; no connection to the
trachea
2. TYPE III/C- the most frequent type of esophageal atresia. The esophagus ends in blind pouch. The trachea
communicates by a fistula with the lower esophagus and stomach
3. TYPE IV/D- the upper and lower segments communicate with the trachea
4. TYPE II/B- upper end of the esophagus opens into the trachea, blind lower segment
5. TYPE V/E- “H TYPE”, no esophageal atresia but with fistula, rare type
6. TYPE VI/F- stenosis occurs 2/3 of the way down the esophagus. Obstruction maybe partial or complete
30-50% of cases are associated with other congenital anomalies, usually in the cardiac, GI or CNS.
Premature and LBW infants have increased incidence of TEF
Clinical Manifestations:
1. Excessive amount of secretions- outstanding symptom which occurs soon after birth
a. Constant drooling of saliva
b. Large amount of secretions from the nose
2. Intermittent cyanosis- due to aspiration from the blind upper pouch
3. Abdominal distention- air from the trachea passes through the fistula into the stomach
4. When fed, infant responds violently after first and second swallow
a. Cough and chokes
b. Fluid returns through the nose and mouth
c. Infant struggles; becomes cyanotic, dyspneic
5. Inability to pass catheter through the nose or mouth into the stomach
Diagnostic Evaluation:
1. Maternal history of polyhydramnios (helpful clue) excessive amount of amniotic fluid due to inability of
the fetus to swallow. A normal fetus swallow amniotic fluid during intrauterine life
2. Flat plate x-ray of the abdomen and chest reveals presence of gas in the stomach and chest
3. X-ray with radiopaque catheter, radiopaque contrast medium never used because of aspiration
Management: Surgery
1. Position NB with the head and chest elevated 20-30 deg to prevent reflux of gastric juices into the
tracheobronchial tree.
2. Regular positioning
3. Put in incubator with high humidity to aid in liquefying secretions and thick mucus
4. Administer 02 prn
5. Assist in bougienage treatment (the process whereby a blunt metal instrument is used to dilate a fistula or
lengthen membranous tissue or elongation of proximal pouch using mercury-weighted dilator or firm
catheter inserted briefly each day)
6. Give antibiotics as ordered to prevent or treat associated pneumonitis
7. Monitor IV or hyperalimentation. Infant cannot be given oral fluid until the esophagus is repaired
8. Observe closely for:
a. V/S, respiratory behaviour
b. Amount of secretions
c. Abdominal distention
d. Skin color
Postoperative Care:
1. Observe for signs of stricture at the anastomosis site; refusal to feed, pronounced coughing, dysphagia,
atelectasis and pneumonia
2. Maintain patent airway
a. Suction prn. Mark catheter to determine how far it can be inserted without disturbing anastomosis
site. Suctioning must be done shallowly so that suction catheter will not touch the suture line in
the esophagus
b. Change position frequently and stimulate baby to cry but avoid hyperextension of the neck to
prevent tension on the suture line
c. Continued use of incubator
3. Maintain adequate nutrition \, infants must be kept NPO post-op until the suture line is healed. They
must be given oral fluids as soon as he begins to tolerate it and the suture line is healed.
- Also known as Chalasia, Achlasia, gastro-esophageal reflux disease (GORD), gastric reflux disease, or
acid reflux disease is chronic symptoms or mucosal damage a neuromuscular disturbance in which the
cardiac sphincter and the lower portion of the esophagus are lax, therefore allow easy regurgitation of
gastric contents into the esophagus which may lead to aspiration pneumonia.
- Can be described as the transfer of gastric contents into the esophagus
- GER occurs in everyone; it is the frequency and persistence that make it abnormal
Incidence:
- More common in premature infants due to hypotonia. Infants during 6 months of life are more prone to
GER because of underdeveloped abdominal lower esophageal sphincter
- A problem that results from immaturity of cardiac sphincter causing a reflux of stomach contents
which may lead to aspiration
Cause: unknown, self-limiting disappears spontaneously within 2-3 months when the esophageal sphincter
matures and the child begins to eat solid foods
1. Prolonged repeated non-projectile vomiting which is more pronounced when lying flat on his back
2. Often hungry after each vomiting episode
3. Aspiration may occur
4. Pressure on abdomen causes reflux of stomach contents into the esophagus
5. Regurgitation occurs almost immediately after feeding when the infant is laid down after feeding
Repeated vomiting
Effortless spitting up
Coughing, and other respiratory problems
Inconsolable crying
Failure to gain adequate weight
Refusing food
Bad breath
Belching or burping
Heartburn and abdominal pain
Pathophysiology:
- The cardiac sphincter muscles fail to function causing to be relaxed and constantly patent
- The lower esophageal sphincter is a structure of smooth muscle surrounding the distal end of the
esophagus. It is innervated by vagal nerves and multiple organs stimulate its function
- As food travels down the esophagus, the sphincter opens to allow the food to enter the stomach at
which time closes to prevent the food bolus form being forced back up the esophagus when the
stomach cotracts
- A defect in the neutral control resulting from immature development of cardiac sphincter can result to
periods of spontaneous relaxation of the sphincter allowing the stomach contents to regurgitate into the
esophagus
- Because gastric acid are mixing with the food bolus to create chime regurgitation causes the sphincter
and esophagus to come in contact with stomach acid
- Inflammation and stricture of the esophagus. Potential aspiration of regurgitated stomach contents.
Recurrent pulmonary infection
Therapeutic Management:
- Feed such infants a formula thickened with rice cereal while holding them in an upright position 30-60
deg
- Keep them in an elevated prone position for 1 hour after feeding. Hydrogen receptor antagonist to
decrease acid secretions
- Antacids or Cimetidine 3 to 4x daily to reduce stomach acid contents
- Betametachol or metochlopromide (Reglan) a prokinetic agent to hurry gastric emptying.
- Proton pump inhibitor- effective acid suppressant medications, given 30 minutes before breakfast
- E.g. omeprazole, lanzoprazole (prevalid), pantoprazole and rabeprazole
Surgical Management:
- NISSEN FUNDOPLICATION- fundus of the stomach is wrapped around the distal end of the
esophagus
- Correct the cardiac sphincter
Diagnostic Tests:
a. Upper GI series
b. Endosurgery
c. Esophageal monometry- muscle tone of cardiac sphincter reduce
d. Fluoroscopy- presence of reflux contrast material
e. Esophageal pH- contents are acidic
f. Barium swallow- is performed to observe for reflux after swallowing
Nursing Responsibilities:
IMPERFORATE ANUS
During embryonic development the cloaca becomes the common channel for the developing
urinary, genital, and rectal system
The cloaca is divided at the sixth week of gestation into an anterior urogenital sinus and posterior
intestinal channel by urorectal septum
After the lateral folds joins the urorectal septum, separation of the urinary and rectal segments
takes place. Further differentiation results in the anterior gastro urinary system and the posterior
In week 7 of intrauterine life, the upper bowel elongates to pouch and combine with a pouch
invaginating from the perineum
These two sections of bowel meet, the membrane between them are absorbed and the bowel is
then patent to the outside
If thus motion toward each other does not occur or if the membrane between the two surfaces does
not dissolve imperforate anus occur
With no negotiable opening from the large intestines to the outside fecal matter cannot be
expelled, thus leading to severe intestinal obstruction
1. No anal opening
2. No meconium or stool
3. Green-tinged urine due to fistula
4. Inability to insert rectal thermometer or small finger into the rectum
5. Abdominal distention
6. “wink reflex” is absent if sensory nerve endings in the rectum are not intact (touching the skin near the
rectum should make it contract)
Diagnostic Test
Management
1. NpO, IV fluid
2. Temporary colostomy- opening of the bowel on the surface of the abdomen to relieve bowel obstruction
3. Surgery:
a. Anoplasty- repair of the rectum
b. Abdomino- perinel pull through
- They undergo surgey before 1 year of age (6-12 months)
4. General post op care:
a. Put on prone/side lying position
b. Check bowel sounds frequently
c. NGT for gastric decompression
d. Change position from side to side to decrease tension on suture line
e. Oral feeding resume 1-2 days post op when peristalsis has resumed (fluids are retained, stools/flatus
passed)
f. 3 days after the operation dilate the anus once or twice a day to ensure patency of the rectal sphincter
g. OSTOMY- is a opening of the bowel on the surface of the abdomen to relieve bowel obstruction
h. COLOSTOMY- if the ostomy is made in the sigmoid portion of the bowel, the stoma on the LL
abdomen passes normally formed stool. In NB, this is soft and unformed
- A group of related defects of the CNS involving the cranium or spinal cord and varying from mildly to
severely disabling
Etiology
Pathophysiology
At 20 days of gestation, the neural grooves appears in the dorsal ectoderm of the embryo
During the 4th week of gestation the groove deepens rapidly & its elevated margins develop
laterally & five dorsally to form neural tube.
Neural tube formation begins in the cervical region near the center of the embryo & advances in
both directions caudally and cephalically until the end of the fourth week of gestation, the end of
the neural tube, the anterior and posterior neuropores close.
The neural tube eventually forms the spinal cord & brain. The vertebral column develops along
with the spinal cord.
The primary defect in neural tube malformation is a failure of neural tube closure. However, some
evidence indicates that the defects are a result of an abnormal increases in CSF pressure during the
first trimester.
1. Anencephaly
- This is a severe defect involving absence of the entire brain or cerebral hemispheres. The infants have
an intact brainstem & are able to maintain vital functions such as temperature regulation, cardiac &
respiratory function for few hours to several weeks but usually die of respiratory failure.
- Total anencephaly is incompatible with life, many anencephaly are aborted or still born, living infants
usually survive a few hours.
2. Encephalocele
- Meningeal & tissue protrudes in a through a defect in the skull, with the occiput being the most
common site.
- When possible, the brain is placed back in the skull.
3. Myelodysplasia
- Refers broadly to any malformation of the spinal canal & cord.
a. Spina Bifida – defective closure of the vertebral column, the most common defect of CNS
Incidence:
Clinical Manifestation
Vary widely to the degree of the spinal defect. Depends on the location, all body parts below the lesions are
affected.
1. Motor function
Feet may be deformed.
Joints of ankles, knees or hips may be immobile.
Variable degree of weakness in the lower extremities.
Spontaneous and induced movements are decrease or absent.
2. Sensory function
Sensations are usually absent below the level of the defect.
Ulcerations and induced movements are decreased or absent.
3. Impaired functioning of the automatic nervous system
Skin is dry and cool.
Sweating ability is impaired.
4. Urinary and bowel problems
Inefficient bladder causes constant urinary dribbling.
Stasis of urine causes UTI.
Possible renal destruction.
Fecal incontinence or retention due to poor innervations of the anal sphincter and bowel
musculature.
Complications
1. Hydrocephalus – occurs in 80-85% of children with myelomeningocele. Developed within the first 6
weeks of life. Can occur because the NTD itself disrupts the flow of CSF.
2. Chiari Malformation – is brain defect involving posterior fossa – type II. Seen almost exclusively with
myelomeningocele.
3. Characterized by herniation of a small cerebellum, medulla, pons and fourth ventricle into the cervical
canal through an enlarged foramen magnum.
4. Meningitis
5. Severe neurologic deficit
Diagnostic Test
A. Prenatal
1. Ultrasound image of the pregnant uterus shows fetal spinal defect and sac
2. Amniocentesis – increased alpha-fetoprotein (AFP) level prior to 18th week of gestation Y-1 globulin
indicate anencephaly or myelomeningocele.
B. Postpartal
1. X-ray of spine shows cerebral defect; ST scan of skull may show hydrocephalus
2. Magnetic resonance imaging, Myelogram shows extent or neural defect.
3. Urinalysis, culture and sensitivity (C&S) may identify organism and indicate appropriate antibacterial
therapy.
4. BUN may be increase.
5. Creating clearance rate may be decreased.
Management
1. Surgery
a. Closure of the sac with 48 hours to prevent infection & preserve neural tissue
b. Shunt procedure if accompanying hydrocephalus
c. Orthopedic procedures to correct defects of hips, knees, or feet
d. Physical therapy
e. Skin grafting
2. Drug Therapy
a. Antibiotic for prevention of infections
b. Anticholinergic drug to increase bladder capacity of lower intravascular pressure.
c. Anticonvulsant if seizures develop
3. Immobilization (cast, braces, traction) for defects of the hips, knees or feet.
Nursing Management
Many infants have associated hydrocephalus, so prevent trauma from increased ICP
Promote optimal bowel functioning because more than 90% of children with myelomeningocele have
neurologic colon.
a. Instruct the parents on colon training, which consists of timing, diet, exercise, posture, and rectal
stimulation.
b. Encourage a diet high in fiber and low in carbohydrates
c. Exercise the lower part of the body
d. Use then knee-chest position to put pressure on the abdomen and aid in bowel evacuation.
e. Use rectal stimulation with digit finger of suppository.
MENINGITIS
- The word “meningitis” usually describes inflammation of the meninges owing to the ineffective
agents.
Description
- Is an infection of the meninges that is usually caused by bacterial invasion and less commonly by
viruses.
- The inflammation of the meninges, the membranes that surround the brain and spinal column, causing
an infectious process in the central nervous system. As a result of bacterial and viral infection.
- Such inflammation may involve the three meningeal membranes, the dura matter, the arachnoid,
and the pia matter.
- Meninges can occur as a primary condition or secondary as a complication of neurosurgery, trauma,
systemic infection, or upper respiratory infection.
Etiology
1. Escherichia coli and group B streptococci are the most common organism that cause meningitis in the
neonate.
2. Nesseria meningitis, streptococcus pnemoniae, and group B streptococci are the most common
organisms that cause meningitis in infants and children. Other causative organism include beta-
hemolytic streptococci, and staphylococcus aureus.
3. Viral meningitis (due to coxsackievirus, echovirus, or mumps) is a self-limiting disease lasting 7 to 10
days.
Pathophysiology
1. In bacterial meningitis, the bacteria enter the meninges’ through the bloodstream and spread through
the cerebrospinal (CSF); the infection may also infect the meninges directly through trauma or
neurosurgery.
2. The pathogens act as a toxin, creating a meningeal inflammatory response and a resultant release of
purulent exudate. The infection spreads quickly through the exudate. As the inflammation continues,
increased intracranial pressure (ICP) develops along with subdural empyema. If infection progresses to
the ventricles, edema and tissue scarring occur around the ventricle can lead to obstruction of cerebro
spinal fluid (CSF). Exudate can cover the choroid plexus and obstruct the subrachnoid villi, causing
hydrocephalus.
- Because CSF contains substances such as protein and glucose on which bacterial growth. In addition,
leukocytes or WBC, is one of the body’s major defense mechanisms, are unable to function in the fluid
environment of the CSF. Meningitis develop very quickly because becteria multiply rapidly without
WBCs to stop their growth.
- As the infection progresses, as second mechanism causes the ICP to increase further. This mechanism
involves changes in the permeability of capillaries and blood vessels in the dura matter, which leads to
increased passage of albumin and water into the subdural space. In turn, leads to accumulation of
protein and fluid in the brain.
3. Vascular congestion and inflammation lead to cerebral edema, which may produce increase
intracranial pressure (ICP). Necrosis of brain cells can cause permanent damage and death.
4. Complications can include obstructive hydrocephalus, thrombi in meningeal veins or venous sinses,
brain abscesses, deafness, blindness, and paralysis.
5. Meningococcal meningitis can result in meningococcal sepsis. If severe, sudden, and fulminate, it is
called Waterhouse – Friderichsen syndrome characterized by disseminated intravascular coagulation,
massive bilateral adrenal hemorrhage, and purura. Mortality is as high as 90%.
Incubation
Mode of transmission:
Classifications:
1. Acute meningococcemia
- Meningococci invade the bloodstream without with involving the meninges.
- Usually starts with nasopharyngitis followed by sudden onset of high-grade fever with chills, nausea,
vomiting, malaise, and headache.
- Petechial, purpuric, or ecchymotic hemorrhages scattered over the entire body and mucous membrane.
- The adrenal lesions start to bleed into the medulla which extends into the medulla which extends to the
cortex
- The combination of meningococcemia & adrenal medullary hemorrhage, is known as Waterhouse-
friderichsen syndrome.
- Waterhouse-friderichsen syndrome is the rapid development of petechiae to purpuric, and ecchymotic
spots in association with shock.
- The condition ruins short course and is usually fatal.
2. Aseptic meningitis
- A benign syndrome characterized by headache, fever, vomiting, and benign meningeal symptoms
- Begins suddenly with a fever up to 40 degrees, alterations in consciousness (drowsiness, confusion,
stupor), neck and spine stiffness, which is slight at first
- Characteristics sign of meningeal irrigation:
Stiff neck/nuchal rigidity
Opisthotonos
(+) Brudzinski’s sign
(+) Kernig sign
Exaggerated and symmetrical deep tendon reflexes
- Sinus arrythmia, irritability, photophobia, diplopia and other visual problems
- Delirium, deep stupor, and coma
- Signs of intra-cranial pressure
Bulging fontanel in infants
Nausea and vomiting (projectile)
Severe frontal headache
Blurring of vision
Alteration in sensorium