Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
92 Cards in this Set
- Front
- Back
|
Cerebral Palsy (CP)
1 |
Characterized by early onset and
impaired movement and posture Incidence 1.5-3 per 1000 live births Most common permanent physical disability in childhood |
|
|
Etiology of CP
2 |
Intrauterine hypoxia/asphyxia
ntrapartum asphyxia 1 2%-23% of CP occurs in term infants with intrapartum asphyxia Postnatal Often no identifiable immediate cause |
|
|
Etiology of CP (cont)
3 |
•Preterm birth of ELBW and VLBW is single most important determinant of CP
Anoxia—most common cause of brain damage whenever it occurs |
|
|
Types of CP
4 |
Spastic
Athetoid/dyskinetic Ataxic Mixed/dystonic |
|
|
Types of CP
5 |
Spastic
Most common clinical type Presents most often as hypotonia |
|
|
Types of Spastic CP
6 |
Quadriparesis (tetraparesis)
Four extremities involved/severe disability Speech and swallowing difficulties Tongue protrusion (incomplete) Labile emotions in some patients |
|
|
Types of CP (cont'd)
7 |
Diplegia
Monoplegia Triplegia Paraplegia |
|
|
Possible Motor Signs
of CP 8 |
Poor head control after age 3 mos
Stiff or rigid limbs Arching back/pushing away Floppy tone Unable to sit without support at age 8 mos Clenched fists after age 3 mos |
|
|
Possible Behavioral Signs
9 |
Excessive irritatbility
No smiling by age 3 mos Feeding Difficuties Persistent tongue thrusting Frequent gagging or choking with feeds |
|
|
CP and IQ
10 |
Wide variation
70% of CP patients have normal IQ Difficult to assess Rigid, atonic, and quadriparetic CP have highest incidence of profound impairment |
|
|
Neural Tube Defects
11 |
Failed closure of neural tube
May involve entire length of the neural tube or small portion Incidence More girls than boys Occurs three times more often in whites than African-Americans |
|
|
Neural Tube Defects (cont'd)
12 |
Cause
50% or more = folic acid deficiency Other cases = multifactorial |
|
|
Neural Tube Defects (cont'd) 2
13 |
Treatment = prevention
Supplementation—0.4 mg/ day If history of NTD—4.0 mg/day In 1998 FDA fortifies cereal grains with folic acid Begin at preconception; can reduce risk by 50% |
|
|
Antenatal Diagnosis
14 |
Elevated alpha-fetoprotein in amniotic fluid—16-18 wks gestation
Uterine ultrasound Why do we want to know? |
|
|
Types of Neural Tube Defects
15 |
Two most common types
Anencephaly Spina bifida/myelomeningocele |
|
|
Anencephaly
16 |
Absence of cerebral hemispheres
Brainstem function may be intact Incompatible with life Few hours to few days Death due to respiratory failure |
|
|
Spina Bifida
17 |
Failure of osseous spine to close
Two types Spina bifida occulta Not visible externally Spina bifida cystica Visible defect •Sa c-like protrusion |
|
|
Spina Bifida Occulta
18 |
Usually lumbosacral, L5 S1
Skin indicators (absent, singly or combos) Sacrat dimple Sacral angioma or port wine nevus Sacral tufts of dark hair Sacral lipoma |
|
|
Spina Bifida Occulta
19 |
"Tethered cord"
Abnormal adhesion to bony or fixed structure Puts traction on the cord Altered gait Bowel/bladder problems Foot deformities May not be seen in early infancy |
|
|
Spina Bifida Occulta (cont'd)
20 |
Diagnostics -X-ray -MRI -CT - Ultrasonography
|
|
|
Spina Bifida Cystica
21 |
Definition: visible defect with external sac-like protrusion
Two types Meningocele Myelomeningocele |
|
|
Meningocele
22 |
Sac contains meninges and spinal fluid but no neural elements
No neurologic deficits |
|
|
Myelomeningocele
23 |
Neural tube fails to close
May be anywhere along the spinal column Lumbar and lumbosacral areas most common May be diagnosed prenatally or at birth |
|
|
Myelomeningocele (cont'd)
24 |
Sac contains meninges, spinal fluid, and nerves
Varying and serious degrees of neurologic deficit Clinically "myelomeningocele" term is interchangeably with phrase "spina bifida" |
|
|
Myelomeningocele: The SAC
25 |
May be fine membrane
Prone to leakage of CSF, easily ruptured May be covered with dura, meninges, or skin Rapid epithelialization |
|
|
Myelomeningocele (cont'd)2
26 |
Location and magnitude of defect
determine nature and extent of impairment If defect below 2nd lumbar vertebra Flaccid paralysis of lower extremities Sensory deficit Not necessarily uniform on both sides of defect |
|
|
Initial Management of Myelomeningocele
27 |
Prevent infection
Assessment of neuro and associated anomalies Early closure in 12-72 hrs after birth Prevent stretching of other nerve roots and further damage |
|
|
Latex Allergy
28 |
Identified as serious health hazard when a child with SB experienced anaphylaxis due to latex allergy
SB patients at high risk for latex allergy due to repeated exposure to latex products from multiple surgeries and repeated urinary catheterizations |
|
|
Allergic Reactions to Latex
29 |
Range from urticaria, wheezing, rash, toanaphylaxis
Reactions tend to increase in severity when latex comes in contact with mucous membranes, wet skin, bloodstream, or airway Cross-reactions with foods:b banana, avocado, kiwi, chestnuts |
|
|
Populations at Risk for Latex Allergy
30 |
Patients with urogenital anomalies
Patients with multiple surgeries Healthcare workers |
|
|
Goals
31 |
To reduce exposure to latex for SB clients who are at risk of developing allergy
To create a latex-safe environment for allergic individuals |
|
|
Muscular Dystrophies (MDs)
32 |
Largest group of muscular diseases in children
All have genetic origin with gradual degeneration of muscle fibers, progressive weakness and wasting of skeletal muscles All have increasing disability and deformity with loss of strength |
|
|
Duchenne Muscular Dystrophy (DMD)
33 |
AKA pseudohypertrophic muscular
dystrophy Most severe and most common of muscular dystrophies in childhood X-linked inheritance pattern; one third are fresh mutations Incidence: 1 in 3500 male births |
|
|
Characteristics of DMD
34 |
Onset between age 3-5 yrs
Progressive muscle weakness, wasting and contractures Calf muscles hypertrophy in most patients Progressive generalized weakness in adolescence Death from respiratory or cardiac failure |
|
|
Diagnostic Evaluation of DMD
35 |
Suspected based on clinical appearance
Confirmation by EMG, muscle biopsy, and serum enzyme measurement Serum CPK and AST levels high in first 2 yrs of life, before onset of weakness; levels diminish as muscle deterioration continues |
|
|
Clinical Manifestations of DMD
36 |
Waddling gait, frequent falls, "Gower sign"
Lordosis Enlarged muscles, especially thighs and upper arms Profound muscular atrophy in later stages Mental deficiency common |
|
|
Therapeutic Management of DMD
37 |
No effective treatment established
Primary goal: maintain function in unaffected muscles as long as possible Keep child as active as possible ROM, bracing, performance of ADLs, surgical release of contractures prn Genetic counseling for family |
|
|
Nursing Considerations of DMD
38 |
Helping child and family cope with chronic, progressive, debilitating disease
Help design a program to foster independence and activity as long as possible Teach child self-help skills Appropriate healthcare assistance as child's needs intensify (home health, skilled nursing facility, respite care for family, etc.) |
|
|
Spinal Cord Injuries
39 |
Generally the result of indirect trauma
Especially in MVC without child restraints Vertebral compression from blows to the head or buttocks (diving, surfing, falls from horses) Birth injuries from traction force on spinal cord during breech delivery |
|
|
Levels of Spinal Cord Injuries
40 |
Higher injury—more extensive damage
Paraplegia: complete or partial paralysis of lower extremities Tetraplegia: lacking functional use of all four extremities (formerly called "quadriplegia") High cervical cord injury affects phrenic nerve, paralyzes diaphragm—>vent dependent |
|
|
Spinal Cord Injury
41 |
Therapeutic management: stabilization and transport to pediatric trauma center
environment Management is complex and controversial Nursing considerations Stabilization, careful assessment, prevention of complications, maintain maximum function Rehabilitation: evaluation and support |
|
|
Increased Intracranial Pressure (ICP)
42 |
Early signs and symptoms may be subtle
As pressure increases, signs and symptoms become more pronounced and level of consciousness (LOC) deteriorates |
|
|
Clinical Manifestations of Increased ICP in Infants
43 |
Irritability, poor feeding
High pitched cry, difficult to soothe Fontanelles: tense, bulging Cranial sutures: separated Eyes: setting-sun sign Scalp veins: distended |
|
|
Clinical Manifestations of Increased ICP in Children
44 |
Headache
Vomiting: with or without nausea Seizures Diplopia, blurred vision |
|
|
Behavioral Signs of Increasing ICP
45 |
Irritability, restlessness
Drowsiness, indifference, decrease in physical activity and motor skills C/O fatigue, somnolence Inability to follow commands, memory loss Weight loss |
|
|
Late Signs of Increasing ICP
46 |
Decreased LOC
Decreased motor response to command Decreased sensory response to painful stimuli Alterations in pupil size and reactivity Papilledema Decerebrate or decorticate posturing Cheyne-Stokes respirations |
|
|
Levels of Consciousness (Continued Descending Order)
47 |
Obtundation: arouses with stimulation
Stupor: responds only to vigorous and repeated stimulation Coma: no motor or verbal response to noxious stimuli Persistent vegetative state: permanently lost function of cerebral cortex |
|
|
Levels of Consciousness (in Descending Order)
48 |
Full consciousness
Confusion: impaired decision making Disorientation: to time and place Lethargy: sluggish speech |
|
|
Special Diagnostic Procedures
49 |
Lab tests: glucose, CBC, lytes, blood culture if fever, evaluate for toxic
substances, liver function Imaging: CT, MRI, echoencephalography, ultrasound, nuclear brain scan, PET Lumbar puncture EEG X-ray (r/o skull fractures, dislocations; evaluate degenerative changes, suture |
|
|
Nursing Care for Child with Increased ICP
50 |
Patient positioning
Avoid activities that may increase ICP Eliminate or minimize environmental noise Suctioning issues |
|
|
Encephalitis p1
51 |
•Herpes Simplex most
common; severe and life threatening Causes cerebral edema and ICP •LP- normal to cloudy, WBC si elevated w/ increased lymphs, Protein normal to si elevated, IgM for type 1 herpes simplex |
|
|
Encephalitis p2
52 |
• Sx: HA, malaise, fever,
dizziness, apathy, stiffness of neck, n&v, tremors, hyperactivity, speech difficulties Severe: High fever, stupor, seizures, disorientation, spasticity, coma, death Rx: acyclovir, antibiotics Mgt: Neuro checks, LOC, ICP monitor |
|
|
Meningitis
53 |
Hib, strep most common
Sx: Child/Adolescents: abrupt with fever, chills, HA, vomiting, sz, Kernig and Brudenski signs, nuchal rigidity Infants and Neonates: poor feeding, poor tone with lack of mvt, poor cry, hypothermia or fever, full, tense, bulging fontanel may not be Dx: LP with elevated WBC, decreased glucose, increased protein, increased pressure Mgt IVF, Isolation, analgesics, anitbiotics, antipyretics, monitor respirations, dexamethasone for ICP (short term) |
|
|
Hydrocephalus
54 |
A syndrome or sign, resulting
from disturbances in fluid balance of CSF caused by impaired absorption or obstruction of flow thru ventricular system • Sx: Infancy- head grows abnormal, ant fontanel tense. bulging, dilated scalp veins. bones of skull become thin. frontal protrusion, setting-sun sign, irritable, feeds poorly, cries when picked up Childhood-caused by ICP ie, HA, papilledema, strabismus, ataxia, irritable, lethargic, apathetic, confused, incoherent |
|
|
VP Shunt Complications
55 |
Infection
Malfunction |
|
|
Signs and Symptoms of Shunt Malfunction
56 |
Emergency
Increased ICP Worsening neurologic status/altered LOC |
|
|
Signs and Symptoms of Shunt Infection
57 |
Shunt malfunction
Fever and inflammation of tract Abdominal pain |
|
|
Seizures
58 |
Caused by malfunctions of brain's electrical system
Determined by site of origin Most common neurologic dysfunction in kids Occur with wide variety of CNS conditions |
|
|
Seizures (cont'd)
59 |
Sign and symptoms
Change in LOC Involuntary movements Posturing Changes in perception, behaviors, or sensations |
|
|
Types of Seizures
60 |
Epileptic
Non-epileptic Most seizures are idiopathic |
|
|
Etiology of Seizures
61 |
Idiopathic (no known cause)
Genetic factors Acquired |
|
|
Incidence and Occurrence
62 |
2.3 million Americans affected
Especially children and elderly More seizures in those under 2 yrs than any other age group |
|
|
Epilepsy
63 |
Definition: S2 "unprovoked" seizures
Idiopathic epilepsy: cause unknown Seizures are indispensable characteristic of epilepsy |
|
|
Seizures
64 |
A single seizure not generally classified as epileptic
Single seizure not generally treated with LTRx |
|
|
Major Causes of Seizures in Children
65 |
Birth injuries [anoxia] or congenital defects of CNS
Acute infections in late infancy and early childhood Usually idiopathic in children >3 yrs |
|
|
Absence Seizures
66 |
Formerly called "petit mal" or "lapses"
Brief loss of consciousness Minimal or no change in muscle tone Almost always appear in childhood (4-12) |
|
|
Absence Seizures (cont'd)p2
67 |
Sudden onset of up to 20+ events per day
No warning/no aura Duration 5-10 seconds Motor: lip smacking, twitching of eyes, face, slight hand movements May drop object, child rarely falls No incontinence |
|
|
Absence Seizures (cont'd)p3
68 |
Often misdiagnosed
Inattention/daydreaming ADD/ADHD |
|
|
Absence Seizures (cont'd)p4
69 |
School issues
Behavioral management |
|
|
Atonic Seizures
70 |
Sudden momentary loss of muscle tone
Onset usually age 2-5 May or may not have LOC Sudden fall to ground, often on face Less severe—head droops forward several times |
|
|
Myoclonic Seizures
71 |
Sudden brief contractions of muscle group
May be single or repetitive NoLOC Often occur with falling asleep May be nonspecific symptom in many CNS disorders May be mistaken as exaggerated startle reflex |
|
|
Infantile Spasms
51 |
Onset in first 6-8 months of life
Usuallv associated with some dearee of mental retardation Cause: possibly due to disturbance of central neurotransmitter regulator at specific phase of brain development |
|
|
Infantile Spasms (cont'd)p2
52 |
Specific spike seen on EEG
Two times more frequent in males Head and neck flex forward; knees drawn up (jackknife position) May or may not have LOC No postictal drowsiness Other variants |
|
|
Infantile Spasms (cont'd)p3
53 |
Often associated with cerebral
anomalies, anoxic brain injury, PKU May also have microcephaly, tonic posture, or other abnormal movements Poor prognosis (mental and developmental) Treatment |
|
|
Pediatric Diagnosis of Seizure Disorders
54 |
Ascertain type of seizure
History, observation Determine the cause of the event Diagnostics EEG ,MRI Labs: glucose, lytes, BUN, Ca" LP |
|
|
Common Pediatric Seizure Triggers
55 |
Changes in dark-light patterns (camera flashes, headlights, rotating fan blades, reflections off snow or water)
Sudden loud noises Extreme temperature changes Dehydration Fatigue |
|
|
Febrile Seizures
56 |
Transient disorder of childhood
Affect approximately 3% of children Usually occur between ages 6 mos and 3 yrs Rare after age 5 Two times more frequent in males |
|
|
Febrile Seizures p2
57 |
Cause?
Usually in temps >101.8°F Seizure occurs when temp is increased, not after Seizure usually over before arriving in ER |
|
|
Febrile Seizure Treatment
58 |
Fever reduction
Evaluate history (episodic and family) Seizure control if ongoing Diazepam (rectal) |
|
|
Febrile Seizures p3
59 |
95%-98% of children with febrile seizures will not have epilepsy or neurologic damage
Management Avoid tepid baths—usually ineffective Vigorous use of antipyretics Protect child from injury during seizure Call 911 if seizure >5 minutes duration |
|
|
Febrile Seizure Treatment
60 |
Prophylaxis with medications
If focal or prolonged seizures If neurologic anomalies If first degree relative has seizure history Child <1 yrold If multiple seizures in 24 hr period |
|
|
Phenobarbital
61 |
Febrile seizures, neonatal seizures
Also for other seizures: front line IV choice if patient does not respond to diazepam High dosage may require respiratory support |
|
|
Phenytoin (Dilantin)
62 |
PO or slow IV push (<50 mg/minute)
Precipitates when mixed with glucose Side effects: gingival hvperplasia, ataxia, rashes, acne, hirsutism, osteoporosis Onset 5-30 minutes; duration 12-24 hrs |
|
|
Fosphenytoin
63 |
May be given with saline or glucose
Rate up to 150 mg/min IVorIM |
|
|
Valproic Acid
64 |
AKA depakote, depakene
IVorPO IV for status epilepticus S.E.: hepatotoxicity |
|
|
Diazepam
65 |
AKA Valium IV, Diastat (rectal gel)
Rx of choice for status epilepticus Rectal gel for home or prehospital management Onset 3-10 min short duration (minutes) Concurrent loading with phenytoin for sustained control of seizures |
|
|
Afivan
66 |
Alternative to diazepam Mav be preferable to diazepam Longer duration of action LOSS respiratory distress in kids >2 yrs
|
|
|
Midazolam (Versed)
67 |
Intranasat route
For acute epileptic seizures Onset 3-5 minutes; duration |
|
|
Pharmacologic Management
68 |
Monitor therapeutic levels
he. i,3se dosage as child grows Mocii-or for known side effects Avoid abrupt discontinuation—gradual dose reduction |
|
|
When to Discontinue
Pharmacologic Management 69 |
When seizure free for 2 years
Normal EEG Avoid during puberty or when subject to frequent infections Recurrence possible within first year |
|
|
Nursing Interventions
70 |
Observe and document episode - Protect from injury
Stay cairn Remain with child Privacy if possible |
|
|
Home Management of Seizures
71 |
CPR training for family members
Rectal diazepam available for intractable seizures Activity restriction on individual basis Safety devices—helmets, no swimming alone, awareness of school, other caregivers |
