Professional Documents
Culture Documents
01 Physical and Developmental Challenge
01 Physical and Developmental Challenge
The nurse should teach the mother to perform baby neck stretching exercises.
Help parents to understand that their actions are important therapy. In the few instances
in which simple exercises are not effective and the condition still exists at 1 year of age,
surgical correction followed by a neck immobilizer may be necessary.
CRANIOSYNOSTOSIS
Craniosynostosis is the premature closure of the sutures of the skull. This may occur in
utero or early in infancy because of rickets or irregularities of calcium or phosphate
metabolism; it also occurs as a dominantly inherited trait and occurs more often in boys
than in girls.
Nursing Care:
Be certain to demonstrate to parents that, if a pseudodisorder is present, the foot can easily be brought
into line or is not deformed.
Stretching the foot into line every day will solve the problemin a short time.
A true talipes disorder can be one of four separate types:
Varus deviation or valgus deviation
Most children with talipes deformities have a combination of these conditions or have
an equinovarus or a calcaneovalgus disorder (a child walks on the heel with the foot
everted).
Assessment
The earlier a true disorder is recognized, the better will be the correction. Make a habit, therefore, of
straightening all newborn feet to the midline as part of the initial assessment to detect this disorder
Therapeutic Management
Correction is achieved best if it is begun in the newborn period.
For correction, a series of casts or braces are applied to gradually mold the foot into good alignment
The cast or brace extends above the knee to ensure a firm correction (every 1 or 2 weeks; 6 weeks)
Changing of diapers
Assess for good circulation
DEVELOPMENTAL DYSPLASIA OF THE HIP
Congenital hip dysplasia is improper formation and function of the hip socket and is considered a spectrum of
abnormalities affecting the hip joint.
Common musculoskeletal condition found in newborns, with the prevalence estimated to range from 1.6 to 28.5
per 1,000 infants, averaging about 5% of newborns
Leading cause of orthopedic disability in childhood and adult life because it can lead to premature arthritis
requiring hip replacement
Dislocation of the head of the femur
CAUSE:
Unknown
may be from a polygenic inheritance pattern
It may also occur from a uterine position that causes less-than-usual pressure of the femur head on the
acetabulum.
more likely to occur with breech birth, a female infant
It is usually unilateral and found 6 times more frequently in girls than in boys,
Additional risk factors include family history of DDH, oligohydramnios, large birth weight for gestational age
Generally plain radiography (X-ray) is not as effective in children less than 6 months of age due to
musculoskeletal immaturity and unreliability to accurately screen for DDH
Assessment
performing the Ortolani & Barlow maneuver up to 3 months
Therapeutic Management
Close monitoring in mild DDH cases because 60% to 80% of clinically identified abnormalities and
90% of ultrasonographic abnormalities spontaneously resolve without treatment in early infancy.
Flexion-abduction splinting devices.
Positioning the hip into a flexed, abducted (externally rotated) position to press the femur head
against the acetabulum and cause the acetabulum to deepen its contour from the pressure.
Corrective and therapeutic hip surgery, which may involve having a pin inserted to stabilize the hip.
Pavlik harness or Spica cast
PHYSICAL DEVELOPMENT DISORDERS OF
THE GASTROINTESTINAL SYSTEM
Most common congenital anomalies of the gastrointestinal system, such as
cleft lip and cleft palate, occur because of midline closure failure extremely early in
intrauterine life.
ANKYLOGLOSSIA
An abnormal restriction of the tongue occurring by an abnormally tight frenulum, the membrane
attached to the lower anterior tip of the tongue
Congenital anomaly in which a tight or shortened lingual frenulum causes restricted tongue
mobility and impaired tongue function.
ASSESSMENT
Tongue tie is often evaluated based on the mobility and how close to the tip of the tongue the
leading edge of the frenulum is attached.
Types 1 and 2 are the most common, accounting for 75% of tongue-ties and are often called
“classic” and “anterior ties.”
Types 3 and 4 account for remaining 25 % and are often referred as “posterior ties.”
frenotomy release
THYROGLOSSAL CYSTS
Arises from an embryogenic fault that leaves a cyst formed at the base of the tongue, which then
drains through a fistula (an abnormal or surgically made passage between a hollow or tubular organ
and the body surface, or between two hollow or tubular organs) to the anterior surface of the neck
Thyroglossal cysts are congenital defects located in or around the midline of the neck, extending to the
base of the tongue.
The cyst may involve the hyoid bone (the bone at the anterior surface of the neck at the root of the
tongue) and may contain aberrant thyroid gland tissue.
As the cyst fills with fluid, swelling and obstruction can lead to respiratory difficulty from pressure on
the trachea.
If infected, the cyst often appears swollen and reddened, with drainage of mucus or pus from the
anterior neck and requires antibiotic therapy.
Management:
Removal of csyt
Position infants on their sides so secretions drain freely from their mouths.
Intravenous (IV) fluid therapy is given after surgery until the edema at the incision recedes
If the mother is breastfeeding, encourage her to express her milk via a hospital-grade pump or manual
expression
Be certain parents have a chance to feed their infant before the infant is discharged from the surgical
unit.
OROFACIAL CLEFTS: CLEFT LIP AND CLEFT PALATE
The maxillary and median nasal processes normally fuse between weeks 5 and 8 of intrauterine life.
The disorder ranges from a small notch in the upper lip to total separation of the lip and facial structures up into
the floor of the nose, with even the upper teeth and gingiva absent.
The deviation may be unilateral or bilateral. The infant’s nose generally appears flattened because the
incomplete fusion of the upper lip has allowed it to expand in a horizontal dimension
It is more prevalent among boys than girls
It appears to be caused by the transmission of multiple genes aided by teratogenic factors present during weeks 5 to
8 of intrauterine life, such as a viral infection, certain seizure medicines such as phenytoin, maternal smoking or
binge drinking, hyperthermia, stress, and maternal. Folic acid deficiency may also be associated with incomplete
anterior midline closures.
A cleft palate is an opening of the palate and occurs when the palatal process does not close as usual at
approximately weeks 9 to 12 of intrauterine life.
Assessment
Ultrasound
Inspection of the mouth at birth
Therapeutic Management
Surgery can repair the condition, between 2 and 12 weeks of age. Because the deviation of the lip
Early repair also helps infants experience the pleasure of sucking and increases speech development as
soon as possible.
Parent may need caring support to bond with an infant whose face is deformed in this way
Nasal rhinoplasty to straighten a deviated nasal septum may be necessary when the child reaches 4 to 6
years of age.
Surgery may be recommended as a two-stage palate repair, with soft palate repair at 3 to 6 months of age
and hard palate repair at 6 to 18 months of age, called the Malek protocol
Unknown cause
children born with Pierre Robin syndrome have associated disorders of congenital glaucoma; cataracts;
cardiac disorders; or other genetic, chromosomal, or medical concerns.
What can you do:
Monitor infants for possible airway obstruction (as a result of their small jaw, their tongue tends to
drop backward and obstruct their airway).
Suctioning to remove secretions may be necessary.
A side-lying rather than a supine sleeping position
The airways of older children can be well maintained using nasal continuous positive airway pressure
(CPAP); obstructive sleep apnea decrease.
The jaw will grow somewhat, although the mandible will always be small. Parents need instructions
on how to feed these infants until the cleft palate can be repaired. The child may have a gastrostomy
tube or button inserted to relieve feeding difficulty
ESOPHAGEAL ATRESIAS AND TRACHEOSOPHAGEAL FISTULA
Between weeks 4 and 8 of intrauterine life, the laryngotracheal groove in the chest develops into the
larynx, trachea, and beginning lung tissue; the esophageal lumen forms parallel to this. A number of
anomalies can occur if the trachea and esophagus are affected by some teratogen that does not allow the
two organs to fully form separately and possibly become connected.
Esophageal atresia is the incomplete formation of the esophageal lumen, resulting in the proximal
(upper) esophagus forming a “blind pouch,” which then does not connect to any other structure.
Tracheoesophageal fistula occurs when an opening develops between the closed distal (lower)
esophagus and the trachea.
Five usual types of esophageal atresia that result are:
Assessment
Esophageal atresia must be ruled out in any infant born to a woman with hydramnios (excessive
amniotic fluid).
diagnosing a child who has an esophageal atresia/tracheoesophageal fistula before the infant is first
fed is important. The infant will cough, become cyanotic, and have obvious difficulty breathing as
fluid is aspirated.
Newborns who have so much mucus in their mouths that they appear to be blowing bubbles should
be suspected of having either disorder.
Esophageal atresia can be diagnosed with certainty if a catheter cannot be passed through the
infant’s esophagus
An X-ray will reveal a radiopaque catheter coiled in the blind end of the esophagus.
Ultrasound also may reveal a stomach distended with the air that has passed from the trachea into
the esophagus and stomach, demonstrating that a fistula is present.
Either a barium swallow or a bronchial endoscopy examination can also reveal the blind-end
esophagus and fistula.
Therapeutic Management
Emergency actions are required for the infant with this group of esophageal disorders in order to
prevent the development of pneumonia, one of the major complications that is apt to occur from
leakage of oral or stomach secretions into the lungs.
The best position for the infant is an upright, 60-degree angle so acid stomach fluids stay in the
stomach
Nasogastric tube can be inserted into the distal end of the esophagus and connected to low intermittent
suction, oral secretions will no longer collect in the blind pouch, decreasing aspiration risks.
IV fluids and parenteral nutrition are begun to prevent dehydration and an electrolyte imbalance from
lack of oral intake.
IV medications that restrict the stomach’s ability to produce acid may be prescribed, and an antibiotic
may be prescribed to help prevent an infection.
Surgery consists of closing the fistula and anastomosing the esophageal segments. If the defect was
only a simple fistula, surgery may be done by thoracoscopy to minimize the time required for surgery
If the repair will be more complex, it may be necessary for the surgery to be completed in different
stages and to use a portion of the intestine to complete the anastomosis if the esophageal segments are
too far apart to join readily.
After an anastomosis repair, observe infants closely at postoperative days 7 to 10 because this is the
point when their internal sutures will dissolve, possibly allowing a leak from the anastomosis site to
occur at this time. If such a leak occurs, fluid and air can leak out into the chest cavity, and
pneumothorax (collapse of a lung) can occur.
Nursing Diagnosis: Risk for imbalanced nutrition, less than body requirements, related to inability to take in
oral feedings
Outcome Evaluation: Child maintains weight within 10% of birth weight and maintains weight in same
percentile on growth curve.
Nursing Diagnosis: Risk for infection related to aspiration or seepage of stomach secretions into lungs
Outcome Evaluation: Child’s temperature remains below 98.6°F (37°C) axillary; here is absence of rales on
auscultation.
Postoperative Care. The baby will return from final surgery with multiple tubes (e.g., chest tubes, endotracheal
tube, Foley catheter, multiple IV lines, probably an arterial line, possibly a gastrostomy tube if not previously
inserted), oxygen saturation, and electrocardiography monitoring equipment. The posterior chest tube drains
collecting fluid, and the anterior tube allows air to leave the chest space so the lungs can reexpand
ABDOMINAL WALL DEFECTS
Umbilical Hernias is a protrusion of a portion of the intestine through the umbilical ring, muscle, and
fascia surrounding the umbilical cord. This creates a bulging protrusion under the skin at the umbilicus. It is
rarely noticeable at birth while the cord is still present but becomes increasingly noticeable at healthcare visits
during the first year.
low–birth-weight infants, and more often in girls than in boys
The size of the protruding mass is not as important as the size of the fascial ring through which the intestine
protrudes. If this fascial ring is less than 2cm, closure will usually occur spontaneously after the child begins to walk
to around 2 years of age, so surgical repair is often not necessary for mild (small) cases.
Omphaloceles is a protrusion (herniation) of abdominal contents through the abdominal wall at the
point of the junction of the umbilical cord and abdomen.
The herniated organs involved are usually the intestines, but they may include the stomach and liver.
The organs are usually covered and contained by a thin transparent layer of amnion and chorion with the
umbilical cord protruding from the exposed sac.
This condition occurs because, at approximately weeks 6 to 8 of intrauterine life, the fetal abdominal contents,
which grow faster than the fetal abdomen, are pushed out from the abdomen into the base of the umbilical cord.
At 7 to 10 weeks, when the fetal abdomen has enlarged sufficiently, the intestine normally returns to the
abdomen.
An omphalocele occurs when abdominal contents fail to return in the usual way.
Gastroschisis a term derived from the Greek word for “stomach cleft” or “fissure,”
is a condition similar to an omphalocele, except the abdominal wall disorder is a
distance from the umbilicus, usually to the right, and abdominal organs are not
contained by a membrane but rather spill freely from the abdominal wall
The condition occurs because of failure of the abdominal wall to close, usually
during the fourth week of development,
Therapeutic Management
With both omphalocele and gastroschisis, until surgery and the bowel is effectively returned to the abdomen, the
infant will be fed by TPN to supply nutrients and keep the bowel from filling with air or stool.
Most infants with gastroschisis will have surgery within 24 hours to replace the bowel before the blood supply
becomes hampered, the intestinal membranes dry, bowel volvulus occurs, or the bowel becomes infected.
prosthetic patch repair that bridges the unformed gap on the abdomen with a synthetic material; the skin is then
drawn tight and closed over the patch.
A second approach is to replace only a portion of the bowel at one time. The remainder is contained by a Silastic
pouch termed a “silo” that is suspended over the infant’s bed.
ICE BREAKER
Maia tells the nurse her baby was born on an unlucky day because the baby
born before hers had his bowel outside his body. What is the most important
nursing consideration at birth in the care of a baby with gastroschisis?
a. Position the infant on his or her stomach so the intestine is well contained.
b. Wrap the intestines with chilled gauze to prevent intestinal swelling.
c. Keep the infant seated upright under a radiant warmer for warmth.
d. Contain the intestine in a warmed, sterile saline–lined bowel bag.
INTESTINAL OBSTRUCTIONS
If canalization of the intestine does not occur in utero at any point, an atresia (complete closure) or stenosis
(narrowing) of the fetal bowel can develop, although the most common site is the duodenum.
This twisting pattern is termed a volvulus and continues to be a potential problem for the first 6 months of life until
the infant develops firmer intestinal supports.
Yet another reason obstruction can occur is because of thicker-than-usual meconium formation, blocking the lumen
(meconium plug or meconium ileus).
Mesentery
Assessment
If more than 30 ml of stomach contents can be aspirated from the newborn stomach by catheter and
syringe at birth (fluid is not passing freely through the tract).
The infant passes no meconium or may pass one stool
The abdomen becomes distended and tender.
the infant will vomit.
True vomiting from intestinal obstruction is usually sour smelling (stomach acid has acted on it),
Vomitus may also be black from the color of meconium.
The infant may reveal that abdominal pain is developing by crying
The child’s respiratory rate will increase as the intestine fills, the diaphragm is pushed up against the
lungs, and lung capacity decreases.
Management
As soon as a bowel obstruction is confirmed, an orogastric or nasogastric tube is inserted and then
attached to low suction or left open to the air to prevent further gastrointestinal distention.
IV therapy is begun to restore fluid and electrolyte balance; immediate surgery is scheduled to relieve the
obstruction
The area of stenosis or atresia is removed, and the bowel is anastomosed.
MECONIUM PLUG SYNDROME
A meconium plug is an extremely hard portion of meconium that has completely blocked the
intestinal lumen. Meconium plugs usually form in the lower end of the bowel .
Assessment
Typically, the infant will be identified first as an infant who has had no meconium passage in the first
24 hours postbirth. A gentle rectal examination may reveal the presence of hardened stool, although
the plug may be too high up in the bowel to be palpated.
An X-ray or sonogram may reveal distended air-filled loops of bowel up to the point of obstruction.
A barium enema not only reveals the level of obstruction but also may be therapeutic in loosening the
plug.
MECONIUM ILEUS
Obstruction of the intestinal lumen by hardened meconium
The usual symptoms of bowel obstruction occur: no meconium passage, abdominal distention, and
vomiting of bile-stained fluid.
Unlike simple meconium plugging, the obstruction point may be too high in the intestine for enemas to
reduce it; instead, the bowel must be incised and the hardened meconium removed by laparotomy.
DIAPHRAGMATIC HERNIAS
A diaphragmatic hernia is a weakness in the musculature that permits a portion of the abdominal organs, such as
the stomach or intestine, to protrude through the chest wall.
This can cause a collapse of the left lung due to cardiac displacement on the right side of the chest
Increased frequency in boys and a decreased frequency in Blacks
CAUSE: early in intrauterine life, the chest and abdominal cavity are one; at approximately week 8 of
intrauterine growth, the diaphragm forms and divides them. If the diaphragm does not form completely, the
intestines can herniate through the diaphragm opening into the chest cavity
Assessment
At birth, breath sounds are usually absent on the affected side of the chest cavity
The infant may be cyanotic with intercostal or subcostal retractions.
The abdomen generally appears sunken because it is not as filled with intestine as usual.
Therapeutic Management
Surgery includes repair of the diaphragm and replacement of the herniated intestine and organs back
into the abdomen, possibly requiring both thoracic and abdominal incisions.
The repair can be complicated if there is not enough room in the abdomen for the intestine to be
returned. In these infants, the abdominal incision may not be closed.
If the lung that was compressed in utero and cannot function, it will be removed at the time of
surgery. If it is developed but just deflated, over the next week after surgery, the lung will gradually
expand and begin to function.
IMPERFORATED ANUS
The spinal cord is protected by three layers of meninges or membranes: the pia mater, the arachnoid, and the dura
mater.
If these membranes herniate through an unformed vertebrae, they protrude as a circular mass, about the size of an
orange, at the center of the back
The protrusion generallyoccurs in the lower lumbar and lumbosacral region, although it might be present
anywhere along the spinal canal. The protrusion is either covered by a layer of skin or, more frequently, only the
clear dura mater.
No sensory or motor deficits accompany the disorder unless the membrane sac should rupture, but damage to the
cord could occur or infection could enter the now unprotected CSF.
Meningomyelocele
The most common birth defect affecting the central nervous system and is frequently viewed as the
most complicated birth defect compatible with survival
not just the meninges protrude through the vertebrae, but the spinal cord usually ends at the point of
protrusion.
Motor and sensory function will be decreased or absent beyond this point.
Generally, the higher the defect is along the spine, the greater the degree of paralysis.
The child will have partial or complete paralysis, partial or complete lack of sensation of the lower
extremities, as well as loss of bowel and bladder control.
The infant’s legs may appear lax because the infant cannot move them; urine and stools continually
dribble because of a lack of sphincter control.
Encephalocele
An encephalocele is a cranial meningocele. These occur most often in the occipital area of the skull but may
occur as a nasal or nasopharyngeal disorder.
Encephaloceles generally are covered fully by skin, although they may be open or covered only by the dura. It is
difficult to tell from the size of the encephalocele if only CSF is trapped in the protruding meninges or whether
brain tissue could also be involved.
Transillumination of the sac will reveal whether brain tissue is in the sac. A CT, MRI, or ultrasound will reveal
the size of the skull disorder and help predict the extent of surgery, which will be needed.
ARNOLD–CHIARI (CHIARI II) MALFORMATION
Categorized as Chiari I, Chiari II, or Chiari III. Chiari
Type I malformation involves the downward herniation of the caudal end of the cerebellar vermis
through the foramen magnum.
Children with Chiari I typically show symptoms in the second or third decade of life, so it is referred to
as an “adult type,” although current sonogram scan capabilities have allowed for earlier incidental
diagnosis.
Chiari II and the very rare Chiari III types are present at birth and so are considered primary neural tube
abnormalities.
ASSESSMENT
A diagnosis is made by MRI and is sometimes accidently identified via an initial MRI because the older child is
being evaluated for chronic headaches.
The prognosis for the child with an Arnold–Chiari malformation depends on the extent of the disorder and the
surgical repair procedure possible.
Because of the upper motor neuron involvement, gagging and swallowing reflexes may be absent, increasing the risk
for tracheal aspiration.
Serious levels of sleep apnea may also occur.