N124: Pediatric Neurological Alterations

INCREASING THE RISK OF CNS/NEURO TUBE DISORDERS: Populations w poor nutrition and hx of siblings or others in fam w sinal bifida A. HYDROCEPHALUS imbalance between production and absorption of CSF -As excess CSF accumulates in the ventricular system, the ventricles become dilated and the brain is compressed against the skull 1. CSF flow (see picture) CSF production in ventricles a. Produced by choroid plexus (80-120 mL), drained to 5 subarachnoid space (where the shit flows) 4 b. Regulated at 80 mmHg pressure 5 c. Consistency is clear, with proteins, glucose, and 1 some lymphocytes (cloudy presence of bacteria) d. Purpose is for cushioning and circulation of nutrients, 2 wastes and gas exchange 2. Excess CSF causes: 3 a. Enlargement of the skull if the sutures/fontanels are open less s/s if fontaneles are open bc that shit will flow through b. S/S of increased ICP if the sutures/fontanels are fused 3. Incidence a. 1-2 in 1000 live births b. 3-4 in 1000 hydrocephalus with Spina Bifida c. Outcome varies with complications -Normal lifespan & intelligence -Possible learning disabilities 4. Forms a. Communicating -Impaired absorption b. Noncommunicating this one is bad -Overproduction (rare) -Obstruction (99%) there is something obstructing flow c. Causes of obstruction: -Congenital (in order of incidence) -Acquired Arnold-Chiari Malformations MOST COMMON herianation in ceribreal region, common in spinal bif Neoplasm Dandy Walker Cyst common in 4th ventricle Hemorrhage Arachnoid cysts or tumors Infection (most common in meningitis) Aqueductal stenosis 5. Clinical Manifestations a. Infants to 2 yrs (CRANIAL PRESSURE) -Early signs -Late signs Irritability Bossing (irreversible forehead protrusion) Poor feeding Setting-sun sign (can see sclera at top of eyes) Bulging, non-pulsating fontanels Vomiting, lethargy Rapid head growth Shrill high pitched cry Increased muscle tone (hyperreflexia) Sluggish or unequal pupils widely separated suture VS; SBP, DBP, widened pulse pressure, HR, T, RR becomes
more irregular
(eventually progressing to Cheyne stokes respirations)

b. Children > 2yrs shit is fused -Early signs -Late signs S/S of increased ICP Seizures cushings triad (dec PR, widenins PP, irreg RR) (frontal HA, Vomiting, ataxia, irritability) VS (cushings triad) SBP, DBP, pulse pressure, Altered LOC
upper arms and wrists)

HR, T, RR become irregular

Decerebrate rigidity

(extension of upper extremities with internal rotation of

Strabismus

(squint, cross eyes, condition where eyes are not straight d/t lack of coordination of the extraocular muscles)

Blindness from herniation

6. Diagnostic evaluation
a. Serial measurements; of the head circumference done on a regular basis b. Serial transilluminations; light up head to visualize progression or resolution c. CT scan or MRI; detailed visualization d. Lumbar puncture; to measure pressure e. EEG; electroencephalography for brain activity to detect seizure risk f. Glasgow Coma Scale; standardized scale to assess LOC to provide an objective measure h. Labs; ABGs, CBC, serum & urine electrolytes, increased WBC

7. Management: Surgical removal of obstruction (not always possible) -or- Create a new pathway via Shunt (put xt fluid somewhere else)

a. Shunts: Ventriculoperitoneal (VP) shunt -or- Ventriculaoatrial (VA) shunt b. Complications: infection or occlusion (both result in increased ICP) 8. Nursing management Pre-op shunt placement Post-op shunt placement
-Measure head circumference unaffected side -VS, assess resp pattern -Seizure precautions -Support their heavy head -Skin care (turning d/t immobility)

(into the Rt atrium, not as common as VPS)

-Positioning; flat initially or as ordered (sometimes semi-fowlers) or on -Monitor for infection and increased ICP s/s

9. Seizures: abnormal discharge of neurons a. Generalized akaTonic Clonic Gran Mal; involves entire brain (both hemispheres), alters consciousness b. Partial (focal); occurs in focal area -Simple partial; may or may not alter consciousness -Complex partial; more likely to alter consciousness c. Nursing management of seizures -Protect from injury (area around) -Keep airway open; O2 if necessary by holding mask in front of face -Observe and record: the three stage of seizure Preictal pattern of behavior before seizure begins Ictal actual seizure (record time & observations) Postictal should be coherent, often dont remember, will be tired, fatigued sometimes for up to 2 hrs
(*very telling as far as pts who fakeseizures, they usually arent tired after)

-Provide client and family teaching; Care during seizure, drug therapy, medic alert ID 10. Parent teaching for Hydrocephalus
a. Life-long management b. Assess current knowledge c. Shunt revision; may need to take place periodically d. Expected development e. Infection (risk with VPS or VAS); S/S of infection, wound care, aseptic, pump site (where shunt is) f. Obstruction S/S g. Diet; fruit, vegetables, cereals, fluids for fiber to straining h. Position; HOB elevated i. Safety; protect shunt site, helmet use with bikes, some epileptics may need to wear daily j. Support groups

B. SPINA BIFIDA a congenital neural tube defect characterized by incomplete closure of the vertebrae & neural tube during fetal develpmt 1. Etiology & Incidence: a. 1-5 in 1,000 (variables), Actual etiology is unknown b. Increased incidence in: -Maternal folic acid deficiency -Sibling with neural tube defect -Environmental factors (theory); Chemicals, Medications 2. Pathophysiology (*add pic of Bones of the backbone spine, see h/o p. 9) a. CNS defect @ 4th week of GA b. Degree of impairment depends on location of defect -T12: Flaccid LE Sensation (risk for skin breakdown, burns and injury) Incontinence (risk for bladder infections & bowel obstructions) -L2: 90% of cases; Varying ortho problems Hip flexion, flail feet, hip adduction, hip extension, knees flexion May need to wear braces -S3: No motor impairment 3. Spina Bifida Occulta: L5-S1 with failure to fully close sometimes ppl dont even know they have it a. May have NO sensory or motor defects b. Clinical Manifestations: Dimple/Hair Tuft/Hemangioma/Lipoma in the lower lumbar or sacral area 4. Spina Bifida Cystica: incomplete closure of vertebrae and neural tube, evidenced by saclike protrusion in lumbar/sacral areas a. Varying degrees of nervous tissue involvement greatest risk is infection bc it is poorly covered b. Further described as: Meningocele or Myelomeningocele Saclike protrusion Herniation most severe Meninges (Dura, Pia & Arachnoid) & CSF Meninges (Dura, Pia & Arachnoid), CSF & Nerves Translucent or membranous Poorly covered, usually translucent
*high risk for infection, goes to surgery ASAP to close

Least Common More Common 5. Anencephaly: upper end of neural tube fails to close, absence of cerebral hemispheres, will not survive Tx is comfort measures

6. Diagnostic evaluation a. Prenatal: AFP dones at 16-18 wks GA, if elevated then Amniocentesis & Fetal US are warranted b. Postnatal: CT scan, Myelography, Neurological evaluation 7. Therapeutic Management: a. Surgical repair -Perinatal; 19-25 wks GA -Risks: premature birth, fetal death, maternal risks are directly r/t hysterotomy (abruption
placenta, uterine rupture)

-Postnatal; 24-48 hrs after birth*most common b. Lifelong management: -Neurologic; shunt revisions -Orthopedic; braces, surgery, PT -Urinary; bladder emptying program 8. Major problems of Myelomeningocele a. Hyrdrocephalus b. Infection of sac (initially) c. Bowel and Bladder dysfunction d. Risk for Latex allergy 18-40% d/t several catherizations per day e. Paralysis/Sensory loss 9. Nursing management a. Protect the sac (pre & post op); positioning, clean & sterile dressings b. Provide adequate nutrition c. Prevent complications; observe for S/S (Infection, ICP, obstruction if shunt is used) d. Promote mobility e. Teaching & d/c planning; wound care/S/S of complications/Med Regimen (seizures)/PT/Elimination/Sensory Stimulation f. Weight control is big issue; d/t phys impairments, wt control can improve independence & quality of life g. Emotional support; support groups 10. Nursing Diagnoses a. Risk for infection r/t rupture or bacterial invasion of the neural tube sac b. Constipation r/t sensory deficit c. Risk for imbalanced nutrition, less than body requirements r/t difficulty assuming feeding position C. MENINGITIS inflammation of the meninges dura, pia, subarachnoid 1. Causes a. Primary disease; Bacterial (more lethal) or Viral b. Secondary complication; Trauma to brain or Systemic infection (ie. sinus infxn or OM untreated) 2. Pathophysiology a. Pathogen enters the CNS and causes an inflammatory response that results in: -Increased ICP -Subdural empyema (ous will make CFS cloudy think and obstruct flow, no pus = viral; CSF contains glucose and protein and leuko [ineffective] bacteria loves glucose, a good indication is low BG bc the bacteria is eating it; intracranial focal collection of pus located btwn the dura and arachnoid mater) -Potential spread to ventricles b. Remember CSF contains glucose & protein -Leukocytes ineffective, d/t low presence -Bacteria can multiply quickly; loves glucose, lumbar puncture may show glucose levels 3. Incidence a. 1 month 5 yrs b. Immunosuppressed c. VP shunt d. Crowded living conditions; day care, college dormitories e. Boy > Girls f. Decrease incidence since HIB vaccine 4. Etiology a. Bacterial -Ages 2-12 yrs; Haemophilus influenzae type B, Streptococcus pneumoniae, *Neisseria meningitides
(meningococcal) *nasty, bad one

-Newborns; E.coli, *Group B strep (*from vaginal canal, mom will be given Abx) b. Viral (aseptic) -Enterovirus (80%), Mumps, Herpes virus, Paramyxoviruses c. Secondary to other infections -Otitis Media / Pharyngitis / Pneumonia / Tuberculosis / Septic arthritis d. Secondary to brain trauma (penetrating) e. Secondary to a neurosurgical procedure (VP shunts, Cochlear Implants) 5. Clinical Manifestations: Depend on Age, Pathogen, and Length of illness a. Neonate -Poor feeding -Fever -Vomiting/Diarrhea -Irritability -Lethargy -Seizures

-S/S of ICP (high pitched cry, bulging fontanels) b. Child/Adolescent -Decreased appetite -Fever -Vomiting/Diarrhea -Altered LOC (HA) -Severe HA -Joint pain -Seizures (rare in viral) -Other symptoms r/t Meningeal irritation c. Other s/s of Meningeal irritation -(bacterial) Nuchal rigidity; when head is flexed forwardit hurts -Opisthotonic position; backed flexed seen only in 2 situations (Meningial irritation & when air starved) -Hemorrhage rash; petechiae develops into hemorrhage rash (meningococcal has entered bloodstream) -Kernigs sign; unable to straighten knee (pain with extension of leg and knee) -Brudzinski sign; hyperreflexia (flexion of head causing flexion of hips and knees) 6. Diagnostic Evaluation a. History & Clinical presentation b. Lumbar puncture to evaluate for -Pressure -Cloudy appearance -Culture (Protein, Glucose, inc WBC = bacteria) c. Labs (Culture blood, pharynx, urine); to see how systemic the infection is 7. Bacterial Meningitis Therapeutic Management (Medical Emergency) a. Isolation until 24 hr of Abx (Droplet precautions) b. IV antibiotics (broad spectrum) -Initiate before pathogen identified; empirical Tx started ASAP just in case, to not waste time while C & S is done -IM injection if unable to gain IV access -Antibiotics may change after pathogen ID c. Corticosteroids -To inflammation & reduce risk of neurologic sequelae (the pluralized sequel of shit following) d. If ICP is present -Mannitol (diuretic) -High-dose barbiturates 8. Viral Meningitis (Symtomatic & Supportive) a. Observation & hydration (PO or IV) b. Acetaminophen c. Keep room dark (d/t photosensitivity), and quiet d. Keep parents informed and educated; teaching for home care 9. Nursing interventions a. Prevention: Immunization (HIB) & Risk evaluation b. Early Recognition: Assessment of physiologic status, VS, neurological assessment, head circumference c. Treatment: During treatment, be alert to changes 10. Nursing Diagnosis a. Risk for aspiration r/t altered LOC b. Risk for fluid volume deficit r/t poor feeding, vomiting, diarrhea, fever c. Knowledge deficit r/t seriousness of meningitis, possible residual neurological deficits, home management, and prophylaxis d. Caregiver role strain r/t hospitalized child and other family responsibilities D. CEREBRAL PALSY Non progressive, chronic disorder of the upper motor neurons of the developing brain occurring pre, peri, or postnatal 1. Etiology & Incidence a. Unknown etiology b. Associated with low birth weight & preterm infants c. Theory: caused by congenital anoxia or intrauterine infection d. Most common chronic pediatric disorder (2-3/1000 births, high incidence) 2. Types of Cerebral Palsy -related to location of brain injury a. Dyskinetic or Athetoid; injury in frontal area - constant, uncontrolled motion of limbs, head and eyes -Early hypotonicity -Later involuntary movement Choreoid (jerking) Dyskinetic (slow, writhing, purposeless weaving motions) b. Spastic; tense, contracted muscles **Most common type of CP -Hypertonicity, abnormal clonus & reflexes c. Ataxic; poor sense of balance, often causing falls & stumbles injury to cerebellum -Mimics cerebellar disorders -Early hypertonicity -Coordination problems d. Mixed; Spastic & Athetoid symptoms (this is the most common mix) 3. Parts of the body affected a. Hemiplegia; arm & leg on one side affected b. Paraplegia or diplegia; both legs only with slight involvement elsewhere are affected

c. Quadriplegia; both arms & both legs are affected 4. Assessment great variance in problems a. Assess motor behaviors; doesnt meet developmental milestones b. Babies are often limp or floppy (child hang in upside down U with little or no movement) c. Stiffness or uncontrolled movements develop d. Seizures e. Intellectual function; greatly varied, RNs do not assess (ask mom to determine if pt can understand you with care) f. Sensory deficits g. Swallowing h. Nutrition i. Joint injuries (Spastic CP have incidence) 5. Diagnostic evaluation a. History b. S/S; developmental milestones, abnormal positions c. EEG (seizures do), CT (assess for damage), MRI to r/o or assess for seizures d. Labs; electrolytes (to assess for malnutrition) e. Neurological exam 6. Treatment prevention of secondary problems (injuries) a. Maximize abilities (repetition of motor activities facilitates development of new brain pathways and enhances proper motor fxn) b. Medication; only if necessary -Anticonvulsants -Control spasms; skeletal muscle relaxants (Baclofen PO or Intrathecal Pump for severe spasticity in children) or
(Benzodiazepines)

-Antiulcer; to minimize GI side effects (Rantidine or Cimetidine) -Botox treatment for spastic CP; paralyzes or weakens muscles 7. Surgical interventions a. G-tube placement; for aspiration risk b. Orthopedic surgery for hip & joint problems c. Dental work d. Foot surgery; to relax extreme contraction 8. Collaborative team a. Speech tx b. Special education c. Occupational tx d. Physical tx e. Recreational tx f. Nutritional mgmt g. Gastroenterologist h. Pulmonologist i. Ophthalmologist j. Pediatrician k. Neurologist l. Orthopedic surgeon m. NURSES n. Social work