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M6 13-005

Exam 10: Neuro & MS Complications of Newborn

Hydrocephalus A Condition caused by an imbalance in the production & absorption of CSF in the ventricles of the brain.
Hydrocephalus: Pathophysiology (1) Either congenital (maldevelopment or intrauterine infection) or acquired (neoplasm, trauma, or infection).
Communicating Hydrocephalus impaired absorption of CSF within the subarachnoid space.
Non-communicating Hydrocephalus Obstruction to the flow of CSF within the ventricles.
Development defects account for most cases of hydrocephalus from birth to 2 years of age.
Hydrocephalus: Assessment In infancy, head enlargement is the predominant sign. -Fontanel is full or bulging, & sutures may separate. -Head is enlarged, especially in frontal area. -Neurologic signs are present and progressive for age.
Hydrocephalus: Diagnostic Evaluation (1) Two factors influence the clinical picture: (a) Time of onset. (b) Presence of preexisting structural lesions. (2) Primary diagnostic tools: (a) CT. (b) MRI.
Hydrocephalus: Therapeutic Management Treatment is directed toward: (a) Relief of hydrocephalus. (b) Treatment of complications. (c) Management of problems related to the effect of the disorder on psychomotor development.
Hydrocephalus: Surgical Management (a) Direct removal of an obstruction (such as tumor). Or (b) Placement of a shunt that provides primary drainage of the CSF from the ventricles to an extracranial compartment, usually the peritoneum (ventriculoperitoneal VP shunt).
Hydrocephalus: Nursing Considerations (Pre-Op) Observe signs of ICP. Measure head circumference daily. Palpate fontanels & suture lines (bulging during crying or straining). Observe for altered behaviors. Maintain adequate nutrition and frequency to avoid vomiting. Support head and neck when movi
Hydrocephalus: Nursing Considerations (Post-Op) Position on UNOPERATED side to prevent pressure on shunt. Keep flat to avert complications. Monitor for ICP. Monitor for ABD distention. Infection precautions. Watch LOC (older children). Assess and relieve pain. Monitor site for healing.
Hydrocephalus: Family Support Educate on shunt malfunction and infection. Teach how and when to "pump" the shunt by pressing against the valve behind the ear. Discuss transport and the type of child restraint system needed. Educate on support groups.
Neural Tube Defects Abnormalities that are derived from the embryonic neural tube.(b) Normally the spinal cord and cauda equine are encased in a protective sheath of bone and meninges. Failure of neural tube closure produces defects of varying degrees.
Spina Bifida Midline defect involving failure of the bony spine to close
Two types of Spina Bifida Spina Bifida Occulta. Spina Bifida Cystica.
Spina Bifida Occulta Refers to a defect that is not visible externally. -Occurs mostly in the Lumbosacral area. -May not be apparent unless cutaneous manifestations or neuromuscular disturbances. -Failure of the vertebral arch to close. -Back dimple, may have hair on it
Spina Bifida Cystica refers to a visible defect with an external saclike protrusion.
Two major forms of Spina Bifida Cystica Meningocele. Myelomeningocele.
Meningocele encases meninges and spinal fluid but no neural elements. Because spinal cord is not involved, paralysis does not occur. Is not associated with neurologic deficits.
Myelomeningocele protrusion of a membrane covered sac through the spina bifida.
Neural Tube Defects: Pathophysiology The primary defect in NTDs is failure of the neural tube closure during early development (first 3 to 5 weeks) of the embryo.
Neural Tube Defects: Diagnostic Evaluation MRI, ultrasound, CT and myelography. Prenatal detection by elevated AFP and fetal ultrasound. CVS is also used for detection.
Neural Tube Defects: Therapeutic Management Initial Care: (a)Prevention of infection. (b)Neurologic assessment, including observation for associated anomalies. (c)Dealing with the impact of anomaly on the family.
Neural Tube Defects: Nursing Considerations Prevent trauma to the sac during infant transport. Observe movement below defect to determine degree of paralysis. Examine for relaxed anus & dribbling of stool & urine. Care of the sac. Positioning (prone, legs abducted, feeding is a problem). Diape
Neural Tube Defects: Postoperative Nursing Care (a) Avoid pressure on operative site. Maintain prone position. (b) Assess for signs of leakage of CSF. (c) Basic post-op care: 1) Monitor VS. 2) I &O. 3) Feeding. 4) Observation for signs of infection. 5) Managing pain.
Why provide a latex-free environment with spina bifida patients? Many spina bifida patients will develop a latex allergy.
Neural Tube Defects: Patient (Family) Teaching 1) Positioning. 2) Feeding. 3) Skin care. 4) ROM exercises. 5) Signs of complications and how to access assistance if needed. 6) Bowel and bladder care. 7) Importance of folic acid during pregnancy.
Cleft Lip and Cleft Palate Facial malformations that occur during embryonic development. The most common congenital deformities of the head and neck, and they occur together or separately, on one or both sides.
Cleft Lip (CL) Minor notching of the lip or complete separation through the lip and into floor of nose. Caused from failure of the maxillary and median nasal processes to fuse.
Cleft Palate (CP) Midline fissure of the palate that result from failure of the two sides to fuse. May include the hard and soft palate.
CL/P is more common than CP and varies by ethnicity. Approximately 60% to 80% are male. Unilateral clefts are nine times more common than bilateral clefs and occur twice as frequently on the left side.
Cleft Lip and Cleft Palate: Etiology Isolated anomaly, or may occur with recognized syndrome. May be from exposure to teratogens such as: -Alcohol. -Smoking (twice the risk). -Certain medications such as phenytoin (Dilantin) which is associated with a tenfold increase in incidence of C
Cleft Lip and Cleft Palate: Pathophisiology Represent a genetic defect in cell migration. CL and CP are distinct malformations embryologically, occurring at different times during the developmental process.
Cleft Lip and Cleft Palate: Diagnostic Evaluation Severe clefts are obvious at birth. CP is less obvious. Palpate the hard and soft palate of all neonates during initial assessment. Prenatal diagnosis with US is not reliable until the soft tissues of the fetal face can be visualized at 13 to 14 weeks.
cTherapeutic Management Advances in anesthesia and surgical technique allow many surgeons to perform palate repairs in the early neonatal period. Palate repair is done first to avoid disturbing the lip after it has been repaired.
Cleft Lip and Cleft Palate: Nursing Considerations Initial nursing problems are related to feeding and dealing with the parental reaction to the defect.
Cleft Lip and Cleft Palate: Nursing Considerations (Feeding) Breastfeeding (soft breast tissue fills in the cleft of the lip). Soft preemie nipples directed away from a cleft palate. Large, soft nipples (Binkie) with enlarged holes. Special “cleft palate” nipples. Rubber-tipped medicine dropper if infant strugg
ESSR feeding technique E - Enlarge the nipple S – Stimulate the suck reflex S – Swallow fluid appropriately R- Rest when the infant signals with facial expression.
Post-Op Care CL Protecting the operative site. Prevent infant from sucking and crying which could cause tension on the suture line. Prevent injury to the operative site by using elbow restraints. Position on back or side. Prevent infection. Prevent pain.
Post-Op Care CP Child able to lie on abdomen immediately postoperatively. Child may resume feeding by bottle, breast. Oral packing may be secured to the palate after surgery. Diet will progress from clear to full liquids. Avoid use of suction in the mouth.
Cleft Lip and Cleft Palate: Parent Education Teach feeding techniques. Prevent Infections. Importance of follow ups. Long-term follow ups. Offer psychosocial support.
Congenital Clubfoot (1) A complex deformity of the ankle and foot that includes forefoot adduction, midfoot supination, hindfoot varus and ankle equinus.
Talipes varus an inversion or bending inward
Talipes valgus an eversion or bending outward.
Talipes equines plantar flexion in which the toes are lower than the heel.
Talipes calcaneus dorsiflexion, in which the toes are higher than the heel
talipes equinovarus (TEV) The most frequently occurring type (95% of cases). Talies (talus, "heel" and pes, "foot") equinovarus (equinus, "extension" and varus, "bent inward")
Congenital Clubfoot: Classification Positional. Syndromic. Congenital.
Congenital Clubfoot: Positional responds to simple stretching and casting
Congenital Clubfoot: Syndromic a more severe form associated with other anomalies such as myelomeningocele. Usually requires surgical intervention.
Congenital Clubfoot: Therapeutic Management Goal achieve a painless, plantigrade, and stable foot.
Congenital Clubfoot: Therapeutic Management Treatment (3 stages) 1) Correction of the deformity. 2) Maintenance of the correction until normal muscle balance is regained. 3) Follow-up observation to avert possible recurrence of the deformity.
Congenital Clubfoot: Serial Casting Manipulation and casting are repeated weekly to accommodate rapid growth within 8 to 12 weeks. Failure to achieve normal alignment by 3 months indicates the need for surgical intervention, between 6 and 12 months of age.
Congenital Clubfoot: Parent Teaching Observation of the skin and circulation. Infant may outgrow cast. how to identify potential complications with skin and circulation. Encourage normal child development.
Developmental Hip Dysplasia (DDH) Spectrum of disorders related to abnormal development of the hip that may develop at any time during fetal life, infancy, or childhood.
Developmental Hip Dysplasia (DDH): Varieties of hip Abnormalities shallow acetabulum, subluxation, or dislocation.
Developmental Hip Dysplasia (DDH): Incidences 10 per 1000 live births. 60% are girls. ↑ in caucasian children. Cause is unknown.
Developmental Hip Dysplasia (DDH): Risk factors Gender. Birth order. Family Hx. Multiple gestations (twins) 5) Oligohydramnios 6) Intrauterine position (breech) 7) Delivery type. 8) Joint laxity. 9) Postnatal positioning. (tight swaddling or use of “papoose boards”)
Developmental Hip Dysplasia (DDH): Degrees Acetabular dysplasia (or preluxation). Subluxation. Dislocation.
Developmental Hip Dysplasia (DDH): Acetabular Dysplasia (or preluxation) a)Mildest form in which there is neither subluxation nor dislocation. b)Femoral head remains in the acetabulum., but socket is shallow and the osseus roof of the acetabulum is less developed.
Developmental Hip Dysplasia (DDH): Subluxation a) Largest percentage of DDH implies incomplete dislocation of the hip. b) Femoral head remains in contact with acetabulum, but a stretched capsule and ligamentum teres cause the head to be partially displaced.
Developmental Hip Dysplasia (DDH): Diagnogstic Evaluation 1) DDH is often not detected at the initial examination after birth. 2)Ortolani or Barlow tests demonstrate the tendency for subluxation and dislocation. Other signs of DDH are shortening of the limb on the affected side.
Developmental Hip Dysplasia (DDH): Therapeutic Management Tx is begun as soon as the condition is recognized. Tx varies with age of child and extent of dysplasia.
Developmental Hip Dysplasia (DDH): Therapeutic Management Newborn to Age 6 months : hip joint is maintained by dynamic splinting in a safe position with the proximal femur centered in the acetabulum in an attitude of flexion.
Developmental Hip Dysplasia (DDH): Therapeutic Management Ages 6 to 18 months in this age-group the dislocation is not recognized until child begins to stand and walk
Developmental Hip Dysplasia (DDH): Therapeutic Management Older Children Correction is more difficult due to secondary adaptive changes (muscle contracture and bone deformities).
Developmental Hip Dysplasia (DDH): Nursing considerations Teach parents how to use Pavlik Harness. Care of the infant or small child requires care to reduce irritation & to maintain cleanliness to child and cast, particularly in diaper area. Include child in activities within own age group.
Created by: jtzuetrong