Week 9 Flashcards
Variations in Pediatric Anatomy and Physiology first 3-4 weeks’ gestation
Infection, trauma, teratogens, and malnutrition can cause physical defects and may affect normal CNS development
Variations in Pediatric Anatomy and Physiology: birth
Cranial bones not well developed or fused: increased risk for fracture
Brain is highly vascular: increased risk for hemorrhage
Variations in Pediatric Anatomy and Physiology: child
Spine is mobile: high risk for cervical spine injury
clinical manifestations for Infant with ^ICP
Irritability, poor feeding
Macewen sign
High-pitched cry,
bulging fontanels
Separated cranial sutures
Sunsetting sign
Distended scalp veins
Increased frontooccipital circumference
clinical manifestations for child with ^ICP
Headache
Forceful vomiting
Seizures
blurred vision
drowsiness
increased sleep
Lethargy
Inability to follow simple commands
late signs of ^ ICP
Bradycardia
Decreased motor response to command; decreased sensory response to painful stimuli
Alterations in pupil size and reactivity
Cheyne -Stokes respirations
Decreased consciousness
Coma
Respiratory Care
Airway management is the primary concern.
Cerebral hypoxia lasting more than 4 minutes may cause irreversible brain damage.
The child may have minimal gag and cough reflexes.
Hydrocephalus Infancy (early)
Abnormally rapid head growth
Bulging fontanels (especially anterior)
Nonpulsatile
Dilated scalp veins
Separated sutures
Macewen sign
Thinning of skull bones
Hydrocephalus Infancy (General)
Irritability
Lethargy
Early infantile reflex acts may persist
Normally expected responses failing to appear
Change in level of consciousness
Opisthotonos (often extreme)
Lower extremity spasticity
Vomiting
Advanced cases: Difficulty in sucking and feeding Shrill, brief, high-pitched cry
Cardiopulmonary compromise
Hydrocephalus Infancy (Later)
Frontal enlargement, or bossing
Depressed eyes
Setting-sun sign (sclera visible above the iris)
Pupils sluggish, with unequal response to light
Hydrocephalus Childhood
Headache on awakening
Papilledema
Strabismus
Irritability
Lethargy
Apathy
Confusion
Incoherence
Vomiting
Shunt Treatment for Hydrocephalus
Period of greatest risk is 1 to 2 months after placement
Infections:
Septicemia
Bacterial endocarditis
Wound infection
Shunt nephritis
Meningitis
Ventriculitis
Antibiotics or shunt removal
Seizure Disorders
Caused by excessive and disorderly neuronal discharges in the brain
Determined by site of origin
Most common treatable neurological disorder in children
Occur with wide variety of CNS conditions
Epilepsy
Two or more unprovoked seizures
Caused by a variety of pathological processes in the brain
Optimal treatment and prognosis require an accurate diagnosis and determination of cause.
Etiology of Seizures
Acute symptomatic
Associated with head trauma or meningitis
Remote symptomatic
Prior brain injury such as encephalitis, meningitis, or stroke
Cryptogenic
No clear cause
Idiopathic
Genetic in origin
Partial Seizures
Local onset and involves a relatively small location of the brain
Generalized Seizures
Involves both hemispheres without local onset
tonic phase of tonic-clonic
Lasts about 10 to 20 seconds
Eyes roll upward
Immediate loss of consciousness
Entire body musculature stiffens in symmetrical tonic contraction
Legs, head, and neck extended and person may utter a peculiar cry
Increased salivation and loss of swallowing reflex
clonic phase of tonic-clonic
Lasts about 30 seconds but can last up to 30 minutes
Violent jerking movements
May foam at mouth
May be incontinent of urine and feces
Absence Seizures
Brief loss of consciousness
Minimum or no alteration in muscle tone
Almost always appear in childhood (4 to 12 years old)
More common in girls than in boys
Usually cease at puberty
Atonic and Akinetic Seizures
Sudden momentary loss of muscle tone and postural control
Onset usually at ages 2 to 5
May or may not have loss of consciousness
Sudden fall to ground, often on face; may incur facial, head, or shoulder injury
Myoclonic Seizures
Sudden brief contractions of a muscle or group of muscles
May be single or repetitive
May or may not include loss of consciousness
No postictal state
May or may not be symmetrical
Infantile Spasms
Onset in first 6 to 8 months of life
Twice as common in boys than in girls
Poor outlook for normal intelligence
Possibly caused by disturbance of central neurotransmitter regulator at specific phase of brain development
Febrile Seizures
Transient disorder of childhood
Affect approximately 2 to 5% of children
Usually occur between ages 6 and 60 months
Cause is uncertain
Tepid sponge baths are not recommended.
Simple febrile seizures are benign.
Cranial Asymmetry
Increased frequency since recommendation that infants be put in supine position to sleep
Unilateral flattening of the occiput
Teach parents to position infant’s head to the side when lying in the supine position
Prone position when awake; tummy time at least 10 to 15 minutes TID
variation in pediatric Anatomy and physiology spine
Spinal cord more mobile than in adult
Myelination incomplete at birth; reaches maturity by age 2 years
Present and mature at birth:
Full range of motion
Deep tendon reflexes
Muscle tone
Cerebral Palsy
A group of permanent disorders of the development of movement and postures, causing activity limitations attributed to nonprogressive disturbances that occurred in the developing fetal or infant brain
Early Warning Signs of CP
Poor head control and clenched fists after age 3 months
Stiff or rigid limbs
Floppy tone
Unable to sit without support at 8 months
Failure to smile by 3 months
Primitive reflexes
Feeding Difficulties
Neural Tube Defects
Failure of the neural tube to close during the embryo’s early development (3 to 5 weeks)
Multifactorial etiology
Exencephaly and anencephaly
The fetus is usually aborted
If the fetus survives, degeneration of the brain to a spongiform mass occurs
Incompatible with life beyond a few days
Spina Bifida
Failure of osseous spine to close
Two types
Spina bifida occulta
Not visible externally
Spina bifida cystica
Visible defect
Myelomeningocele
Neural tube fails to close
May be anywhere along the spinal column
May be diagnosed prenatally or at birth
Sac contains meninges, spinal fluid, and nerves
Varying and serious
high incidence of latex allergy **
Duchenne Muscular Dystrophy
pseudohypertrophic muscular dystrophy
Most severe and most common
Progressive muscle weakness, wasting, and contractures
Death from respiratory or cardiac failure
Early onset, usually between 3 and 5 years of age
Symptoms of Duchenne Muscular Dystrophy
Waddling gait, frequent falls, Gower sign
Lordosis
Enlarged muscles, especially of thighs and upper arms
Profound muscular atrophy
Spinal Muscular Atrophy
Group of inherited genetic muscle-wasting disorders affecting motor neurons
Four types
Type I (severe) – also known as infantile-onset or Werdnig-Hoffman disease
Type II (intermediate) Type III (mild) – also known as Kugelberg-Welander disease
Type IV – also known as adult SMA
SMA type 1
Manifests within first few months of life
Infant lies in frog position, has weak cry, cough, generalized weakness
Active movement usually limited to fingers and toes
Normal sensation and intellect
Palliative care
Death usually by age 2 years
SMA type 2
Onset between 2 and 12 months of age
First have weakness of arms and legs, later generalized weakness
Prominent pectus excavatum
Movements absent during relaxation and sleep
Lifespan is 7 months to 7 years
SMA type 3
Onset late childhood or adolescence
Normal head control, can sit by age 6 to 8 months
Thigh and hip muscles weak
Some will learn to walk
Scoliosis common
Slowly progressive course
Normal life expectancy
Spinal Cord Injury
Generally the result of indirect trauma
Especially in motor vehicle collision without child restraints
Vertebral compression from blows to the head or buttocks
Levels of spinal cord injuries
Higher injury: more extensive damage
Paraplegia
Tetraplegia
Down Syndrome
Also known as nonfamilial trisomy 21
Extra chromosome 21 in 95% of cases
Translocation of chromosomes 15 and 21 or 22 in 3 to 4% of cases
Mosaicism, a mixture of abnormal and normal cells in 1 to 2% of cases
Maternal age
Age 35—risk is 1 in 400 births Age 40—risk is 1 in 110 births
Fragile X Syndrome
Most common inherited cause of CI and second most common genetic cause of CI after Down syndrome
Abnormal gene on the lower end of long arm of the X chromosome
Autism Spectrum Disorders
Complex neurodevelopmental disorder accompanied by intellectual and social defects
Change in DSM-5 classification, all under ASD (e.g., Asperger disorder is under ASD)
Risk: 1 in 166 children Four times more common in males
