Definition

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

8 PRIORITY NEEDS OF HIGH-RISKS NEONATES:

1. Initiation and maintenance or respirations

2. Establishment of extrauterine circulation
3. Control of body temperature
4. Intake of adequate nourishment
5. Establishment of waste elimination
6. Prevention of infection
7. Establishment of an infant-parent relationship
8. Adequate stimulation of mental development

CLASSIFICATION OF HIGH-RISK INFANTS

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:

1. Maternal condition associated with SGA babies include:

a. Hypertension (chronic or pregnancy-induced)
b. Cardiac, pulmonary, or renal disease
c. Diabetes mellitus
d. Poor nutrition
e. Use of alcohol, tobacco, or drugs
f. Age older than 35
 g. Multiple gestation
h. Placental insufficiency
i. Placental fetal abnormalities
j. Pregnancy occurred at high altitudes
k. Drug abuse
2. Fetal conditions associated with SGA infants include:
a. Normal genetically small infant
b. Chromosomal abnormality
c. Malformations
d. Congenital infections, especially rubella and cytomegalovirus
e. Intrauterine infection

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.

6. Large for gestational age (LGA)

- BW more that expected for the specific gestational age
- BW at or above the 90th percentile on the intrauterine growth
- Also called macrosomia
- The LGA infant can be pre-term, term or post-term
- Ex. Baby born on 38 wks who weigh 4000 grams

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

 LGA may result from a genetic factor

 Male neonates tend to be larger than females
 Neonates of large parents tend to be large
 Neonates of multiparous women tend to be larger
 Neonates of diabetic mothers also tend to be LGA
 High maternal blood glucose levels provide a stimulus for continued insulin production
by the fetus
 This constant state of hyperglycemia leads to excessive growth and fat deposition

ASSESSMENT FINDINGS

 Weight generally more than 4,000g (8lb or 13oz)

 Plump and full faced
 Fractures or intracranial haemorrhage due to exposure to trauma during vaginal delivery
 Immature reflexes
 Possible asymmetry of chest secondary to diaphragmatic paralysis occurring from edema of
phrenic nerve

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

B. ACCORDING TO GESTATIONAL AGE

1. premature or preterm newborn

- Neonate born before the end of the 37th week gestation.

- Associated with numerous problems

- All body systems are immature

- 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

1. Cardiac and respiratory assessment and assistance

2. Resuscitation if necessary
3. Maintenance of fluid and electrolyte balance
4. Nutritional support
5. Prevention of infection
6. Assessment of neurologic status
7. Maintenance of body temperature
8. Monitoring of renal function
9. Emotional support to parents
10. Assessment of glucose and bilirubin levels

NURSING INTERVENTION

1. Closely assess all body systems

2. Anticipate the need for endotracheal intubation and mechanical ventilation
- Administer oxygen as ordered, avoiding concentrations that are too high. O2 should never be more
than 40% because it can lead to retrolental fibroplasia or retinopathy of prematurity (an
overgrowth of retinal blood vessels causing blindness)
- Monitor transcutaneousor pulse oxygen levels or pulse oximetry readings
- Have emergency resuscitation equipment readily available
3. Administer medications to support cardiac and respiratory function
4. Institute measures to maintain a neutral thermal environment; anticipate need for incubator or radiant
warmer
a. Skin to skin or kangaroo care- the parents wear loose-fitted, open-front top that provides modified
carrier for the child
b. Incubator care:
- Temp.- 92 deg.F of 33.3deg. C- 34.4deg. C
- Humidity 55-65%
- Frequent positioning at the right side will favour closure of the foramen ovale because of the increase
pressure on the left

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

1. Early feeding 2-3 hours after to prevent hypoglycaemia, increasing 3-4ml/feeding

- Less than 1,250 grams parenteral feeding 5-10% glucose solution e.g. IVF D10W at 65 ml/KBW day
- D10IMB at 80ml/KBW/day for succeeding days
2. Full-term infant
- Infant born after beginning of week 38 and before week 42 gestation regardless of weight
3. Post term or post mature infants
- Neonate born after 42 weeks’ gestation
- May be LGA, AGA, SGA, or dysmature, depending on placental function

ETIOLOGY

 The cause of prolonged pregnancy is unknown

 Factors associated with post maturity include
- Anencephaly
- Trisomy 16 to 18
- Primigravida mother

PATHOPHYSIOLOGY

 The placenta has the growth potential of only 40 to 42 weeks

 After that time, calcium deposits collect, making the placenta unable to function, resulting in lack of
oxygen, fluids and nutrients
 If placental function decreases, the fetus may not receive adequate nutrition. The fetus will utilize its
subcutaneous fat stores for energy
 Wasting of subcutaneous fat occurs, resulting in fetal dysmaturity syndrome
 There are 3 stages of fetal dysmaturity syndrome
a. Stage 1- Chronic placental insufficiency
1. Dry, cracked, peeling, loose, and wrinkled skin
2. Malnourished appearance
3. Open-eyed and alert baby
b. Stage 2- Acute placental insufficiency
1. All features of stage 1 except point 3
2. Meconium staining
3. Perinatal depression
c. Stage 3- Sub acute placental insufficiency
 1. Findings of stage 1 and 2 except point 3
2. Green staining of skin, nails, cord, and placental membrane
3. A higher risk of fetal intrapartum or neonatal death
 The newborn is at risk for developing complications related to compromised ureteroplacental perfusion and
hypoxia
 Chronic membrane hypoxia causes increased fetal erythropoietin and red blood cell production resulting in
polycythemia
 Post term infants are susceptible to hypoglycaemia because of the rapid use of glycogen stores

ASSESSMENT FINDINGS

1. “old man face”- classic sign

2. Long thin body with wasted appearance
3. Parchment- like skin, nails and umbilical cord
4. Long fingernails
5. Absence of vernix caseosa and lanugo
6. One month alert look
7. Wide-eyed look
8. Profuse scalp hair
9. Loose, dry skin
10. Decreased or absent subcutaneous fat

TREATMENT

1. Close observation
2. Supportive care

NURSING INTERVENTIONS

1. Manage meconium aspiration syndrome

a. Suction the infant’s mouth and nares while the head is on the perineum and before the first breath is
taken to prevent aspiration of meconium that is in the airway
b. Once the infant is dry and on the warmer, intubate with direct tracheal suctioning
c. Perform chest physiotherapy with suctioning to remove excess meconium and secretions
d. Provide supplemental oxygen and respiratory support as needed
2. Obtain serial blood glucose measurements
3. Provide early feeding to prevent hypoglycaemia, if not contraindicated by respiratory status
4. Maintain skin integrity
a. Keep the skin clean and dry
b. Avoid the use of powders, creams, and lotions
c. Avoid the use of tape

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

- birth in which absence of any signs of life after birth

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

5. Post Natal death

- death that occurs at 28 days to 1 year birth

A. HYPERBILIRUBINEMIA

 Also called pathologic jaundice

 Refers to excessive accumulation of bilirubin in the blood and is characterized by jaundice, or icterus, a
yellowish discoloration of the skin and other organs
 Characterized by a bilirubin level that exceeds 6mg/dl within the first 24 hour after delivery in a preterm
neonate
 Bilirubin level that rises by more than 5mg/day
 A level that is greater than 12 mg/dl in premature or term neonates
 Conjugated (direct) bilirubin level that exceeds 1.5 to 2 mg/dl

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

 Hyperbilirubinemia can develop several ways

 Ceratin drugs (such as aspirin, tranquilizers, and sulphonamides) and conditions (such as hypothermia,
anoxia, hypoglycaemia, and hypoalbuminemia) can disrupt conjugation and unsurp albumin-binding
sites
  Decreased hepatic function can result in reduced bilirubin conjugation
 Increased erythrocytes production or breakdown can accompany a haemolytic disorder or Rh or ABO
incompatibility
 Biliary obstruction or hepatitis may block normal bile flow
 Maternal enzymes present in breastmilk can inhibit the neonate’s glucoronyl transferase-conjugating
activity
 As erythrocytes breakdown at the end of their neonatal life cycle, haemoglobin
 Separates into globin (protein) and heme (iron) fragments
 Heme fragments from unconjugated (indirect) bilirubin, which binds with albumin for transport to liver
cells to conjugate with glucuronide, forming direct bilirubin
 Unconjugated bilirubin is a fat-soluble and cannot be excreted in the urine or bile; it may escape to
extravascular tissue, especially fatty tissue and the brain, resulting in hyperbilirubinemia
 Unconjugated bilirubin can infiltrate the nuclei of the cerebral cortex and thalamus, leading to
kernicterus (bilirubin encephalopathy) – staining of brain cells with bilirubin, causing brain damage or
even death
 Kernicterus may occur with serum bilirubin levels at or above 20mg/dl (full-term) and at lower levels
(about 14mg/dl) in preterm neonates
 Signs and symptoms of kernicterus include lethargy, decreased reflexes, seizures, opisthotonos, and
high-pitched cry
 Possible causes include haemolytic disease of the neonate, sepsis, impaired hepatic functioning
polycythemia, enclosed haemorrhage, hypothermia, hypoglycaemia, and asphyxia neonatorum
 Glucose 6-phosphate deficiency (G6pD) increases the incidence of jaundice. It is more common in
populations of the Mediterranean

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:

 Phenobarbital given to mother several days before delivery. It promotes:

1. Hepatic glucoronyl transferase synthesis and increase bilirubin conjugation and hepatic clearance of
the pigment bile
2. Protein synthesis which increase bilirubin

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

B.INFECTION (SEPSIS OR SEPTICEMIA)

 Refers to generalized bacterial infection in the blood stream

 Occurs when pathogenic microorganism or their toxins occur in the blood or tissues
 Can occur before, during or after delivery
 Most common causative organism are the gram-negative Escherichia coli, Aerobacter, and Klebshiella and
the gram-positive beta haemolytic streptococci
Contributing factors:

 Prolonged rupture of membranes (more than 24 hours)

 Prolonged or difficult labor
 Maternal infection
 Infection in hospital personnel
 Aspiration at birth or later
 Premature are more susceptible because of the general immaturity of the immune system, IgG globulins
occurs during the last 2 weeks of delivery, he is not able to receive the necessary protection normally
obtained by full-term babies

Assessment Findings

 Behavioral changes: lethargy, irritability, poor feeding and hypotonia

 Temperature instability, low grade fever
 Apnea
 Jaundice
 Abdominal distention
 Skin color changes, including mottling, pallor and cyanosis
 Vomiting, diarrhea
 Positive blood culture

Diagnostic Test

 Lumbar puncture to rule out meningitis

 Urine, skin, blood, and nasopharyngeal cultures
 Gastric aspiration

Treatment

 Antibiotic administration

Nursing Interventions

 Collect specimens to identify the causative organisms

 Assess the neonate’s vital signs at least once per hour or more frequently as indicated
 Provide supportive care, including maintenance of a neutral thermal environment
 Administer nutritional support
 Assist with respiratory support measure, including oxygen therapy as ordered
 Monitor fluid and electrolytes balance; administer I.V. fluid therapy as ordered
 Institute measures to provide cardiovascular support
 Administer antibiotic as ordered

C.ANEMIA

 Exageration of the physiologic anemia of full term babies

 All NB’s manifest gradual drop of hgb levels for the first 6-12 weeks of life because bone marrow stops
producing RBC in response to elevated oxygenation in extrauterine respiration
  Normochromic, normocytic anemia, blood cells maybe fragmented or irregularly shaped. The fault appears
to the immaturity of the hematopoietic system combined with destruction of RBC due tolow level of
Vitamin E
 Preemies have less iron stores because transfer of iron from the mother to the baby occur during the last 2
weeks of pregnancy and smaller RBC mass, since cord was cut immediately after birth

D.RESPIRATORY DISTRESS SYNDROME

 A disease related to immaturity of lung tissue

 Also called, HYALINE MEMBRANE DISEASE
 Specific disease of premature infant
 It is a name applied to respiratory dysfunction in neonates and is primarily a disease related to
developmental delay in lung maturation

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:

1. Assess all at risk neonates for signs of BPD

2. Administer prescribed medications, such as bronchodilator, an anti-inflammatory and antibiotic. A diuretic
may be prescribed to treat heart failure
3. Administer respiratory syncytial virus (RSV) immune globulin (RespiGram) or palivizumab (Synargis) to
diminish the effects of RSV
4. Provide respiratory support through continuous mechanical ventilation and administration of oxygen via
oxygen hood, nasal catheter, or cannula
5. Support safe weaning from oxygen, which will be indicated by clinical manifestations of readiness:
a. Maintenance of normal ABG, pO2, and pCO2
b. No increase in the work of breathing
c. Normal growth and development
6. Promote adequate oxygenation and normal breathing pattern
7. Provide desired fluid and nutritional intake
8. Provide family teaching, which includes instruction on cardiopulmonary resuscitation because of the high
mortality associated with BPD during the first year of life

F. MECONIUM ASPIRATION SYNDROME

 Involves aspiration of meconium into the lungs

 Results when the neonate inhales the meconium mixed with amniotic fluid; typically occurs with the first
breath or while the neonate is in utero

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

 Fetal hypoxia as indicated by altered fetal activity and heart rate

 Dark greenish staining or streaking of the amniotic fluid noted on ruptures of membrane
 Obvious presence of meconium in the amniotic fluid
 Greenish staining of neonate’s skin
 Signs of distress at delivery, NB appear limp, ApGAR score below 6, pallor, cyanosis and respiratory
distress
 Coarse crackles when auscultating neonate’s lungs
 Chest x-ray show patches or streaks of meconium in the lungs, air trapping or hyperinflation

Treatment

 Respiratory assistance via mechanical ventilator

 Maintenance of neutral thermal environment
 Administration of surfactant and an antibiotic
 Extracorporeal membrane oxygenation in severe cases

Tracheoesophageal Atresia and Fistula

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

Etiology: failure of embryonic development

Cause: unknown in most cases

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. Primary repair- esophageal anastomosis and division of fistula

2. Emergency surgery for the infant with tracheoesophageal fistula is essential to prevent pneumonia from
leakage to stomach secretions into the lungs, dehydration or electrolyte imbalance from lack of oral intake
3. Gastrostomy (cervical esophagostomy)- temporary until infant gain weight. Under local anesthesia, the
tube allowed to drain by gravity to keep the stomach empty secretions and prevent reflux into the lungs.
Upper right lobe pneumonia is one of the major complications
- Staging (repeated operations separated by periods of time, waiting for growth) is the accepted
philosophy of treatment (G-tube)
4. Cervical esophagostomy- the distal end of the blind esophagus is brought to the surface just over the
sternum so that the mucus can drain. G-tube is placed and aspirated every 15-10 minutes and IV access is
established as the infant awaits transfer to NICU and surgey.
 Preoperative Care:

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.

Oral feeding started 6-10 days post-op

a. Low residue diet to keep stools soft

b. Feed slowly in upright position to allow time for swallowing
4. Oral hygiene to prevent bacterial growth
5. Allow infant to suck in a pacifier to meet psychological and physiologic needs
6. Encourage parental participation to promote strong parental-infant bonding

GASTROESOPHAGEAL REFLUX (GER)

- 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

- Boys are affected as often as girls

Signs and Symptoms:

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

GERD in children may cause:

 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:

1. Small frequent feedings

2. Thickened feedings (mix with cereal)
3. Feed in upright position 30-60 deg never in prone, supine
4. Burp the baby between midway of the feeding
5. Place in elevated prone position after feeding for 1 hour
6. Post op; NGT is irritated with normal saline every 2 hours to ensure its patency
7. Assess NGT drainage for coffee colored drainage (normal for the first 24 hours) would reveal bleeding
from incision

IMPERFORATE ANUS

- Also called as ANAL AGENESIS or ANAL ATRESIA

- A congenital absence of the normal anal opening
- Stricture of the anus/anal opening
- Failure of the membrane separating the rectum from the anus to absorb during the 8th week intrauterine
life (all vital organs are developed/ formed)
- A congenital malformation caused by abnormal fetal development

Cause: unknown, due to arrest embryonic development of 8 weeks intrauterine life

TYPES OF IMPERFORATE ANUS

1. Stenosis- tight stricted external sphincter

2. Membranous- obstruction in the internal sphincter
3. Agenesis- no anal opening only anal dimple
4. Atretic- there is no connection between rectal anal and rectus- sigmoid (colon) canal
 Pathophysiology

 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

Signs and Symptoms

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)

Complication: intestinal obstruction/distention

Diagnostic Test

1. Early examination of the NB to determine the patency of rectum

2. Ultrasound and CT scan to determine the type or level of lesions
3. Wangesteen-Rice Method- infant is held upside-down while abdomen is filmed to determine the distance
from the retum to anal dimple; this is an x-ray which is helpful in determining the distance the intestine is
separated from the perineum
4. Flat plate x-ray radiograph of abdomen to determine level of lesion

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

NEURAL TUBE DEFECTS

- A group of related defects of the CNS involving the cranium or spinal cord and varying from mildly to
severely disabling

Etiology

1. Heredity and environmental factors

2. Folic acid deficiency
3. Drugs like antiepileptic drug
4. Radiation
5. Maternal nutrition
6. Chemicals

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.

Types of Neural Tube Defects

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:

- Higher in girls than boys

- 3 per 1,000 live birth

Types of Spina Bifida:

1. Spina bifida occulta

- Spinal cord and meninges remain in the normal anatomic position
- Defect may not be visible or may be identified by dimple or a tuft of hair on the spine.
- Frequently, no observable manifestations, child is asymptomatic & may have a slight neuromuscular
deficit.
- Superficial cutaneous indications include a skin depression or dimple, port-wine angiomatous new
dark tuft hair, soft subcutaneous lipomas. These signs maybe absent, appear singly or be present in
combination.
- Spinal dysgraphia – the spinal cord or roots cane be distorted by fibrous bands & adhesions, an
intraspinal lipoma (fatty tumor) or subcutaneous lipoma (lipomyelomeningocele tumor). The usual
cause is abnormal adhesion or fixed structure, resulting in reaction on the spinal cord & cauda equina.
2. Spina bifida cystica – refers to visible defect with an external like sac protrusion.
a. Meningocele – sac (meninges) filled with spinal fluid provides through opening in spinal canal
uses in the lumbo sacral area, sac covered with thin skin. The spinal cord is not involved. There is
little to no neurologic involvement. No motor or sensory loss.
b. Myelomeningocele (Meningomyelocele) – congenital failure of the arches of one or more
vertebrae to unite at the back, so that the bony wall normally surrounding the spinal canal at that
place is missing there is external protrusion through transparent sac containing spinal fluid,
meninges, spinal cord and or nerve roots.
It is the most severe of spinal deformities. Develop during the first 28 days or pregnancy
when the tube fails to close and fuse at some point along its length.

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

1. Teach family about management required for the disorder.

2. Assess and monitor vital signs, measure had circumference, and assess neurologic status.
 3. Monitor the child throughout childhood to detect the true extent of the disorder. Assess neurologic status,
neuromuscular functioning, sensory perception, bowel and bladder control, sexual functioning, and
psychosocial functioning.
4. Administer prescribed medications.
5. Prevent infection and injury.
a. Preoperatively, apply sterile dressing to the lesion and constantly moisten it with saline. Handle infant
with care.
b. Preoperatively and postoperatively perform the following:
- Maintain a sterile dressing
- Examine the dressing for leakage
- Avoid placing a diaper of other covering directly over lesion (this could cause fecal
contamination)
- Monitor the infant in a prone or side-lying position to prevent contamination by stool or urine.
c. Position the infant in prone or side-lying position to prevent contamination by tool or urine.
d. Prevent hip subluxation by maintain the legs in abduction, with a pad between the knees and the feet in
a neural position, with a roll under the ankles.
e. Prevent skin breakdown by padding the bony prominences.

Many infants have associated hydrocephalus, so prevent trauma from increased ICP

a. Measure head circumference daily for any significant increase

b. Anterior fontanel for tenseness & fullness
c. Shrill, high pitch cry
d. Monitoring, irritability
e. Increasing BP and RR, widening pulse pressure
f. Minimize stress, which increases ICP

Prevent urinary complications

a. Assess urologic status

b. Instruct on catheterization
c. Prevent urinary tract infection
d. Prevent injury due to neuromuscular impairment.
e. Carefully monitor the skin condition because the child may have decreased sensation in areas distal to the
lesion, increasing the risk of pressure sores.
f. Promote mobility and turn the child frequently.
g. Use caution when positioning the child, keeping in mind that a lack of sensation makes the child unable to
detect potential skin irritants.

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.

Promote family coping.

 a. Explain the essentials of the infant care, such as nutrition and elimination
b. Promote parent-infant relationship by encouraging parental participation with feeding, cuddling, and
stimulation.
c. Emphasized infection prevention and recognition of early signs and symptoms of infection and increased
ICP
d. Explain and demonstrate bladder and bowel management and skin care.
e. Discuss the effects of immobilization and strategies for dealing with them.
f. Discuss the need for lifelong care.
g. Encourage as mush normalcy. Most children suffer some degree of physical and cognitive impairment.
h. Carefully assess the family’s ability to care for the child and refer them for further assistance if needed.
i. Encourage parents to verbalize their fears.

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

- Is variable, the extreme limits being set from 1 – 10 days.

Mode of transmission:

1. Respiratory droplets through nasopharyngeal mucosa

2. By direct invasion through otitis media
3. May also follow skull fracture, a penetrating head wound, lumbar puncture or ventricular shunting
procedures.

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