bunch of management and treatments and concerns idk Flashcards
pharmaceutical therapy for SCI
glucocorticoids: to suppress immune response
vasopressors (dopamine): hypotension
plasma expanders (dextran): maintain volume/treat shock
atropine: bradycardia
muscle relaxants and antispasmodics
histamine 2 receptor antagonists: prevent GI ulcers
anticoagulants: prevent DVT
stool softeners
vasodilators: hypertension (if BP gets too high)
anti-seizure medications
recovery (possible forever) phase concern for SCI
aspiration ineffective thermoregulation spinal shock ineffective airway clearance impaired physical mobility DVT imbalanced nutrition urinary incontinence bowel incontinence and/or constipation impaired skin integrity ineffective coping anticipatory grieving sexual dysfunction
autonomic dysreflexia
sudden onset severe hypertension severe throbbing headache profuse diaphoresis/flushing nasal stuffiness blurred vision nausea bradycardia
intervention for autonomic dysreflexia
elevate HOB to sitting
check BP
check/remove/treat possible causes (kink catheter or distended bladder/bowel)
administer anti-hypertensive prn
monitor every 3-4 hours after symptoms subside
interventions for SCI
● Spinal Cord Injury Interventions
○ Suction set-up at bedside
○ Supplemental oxygen therapy
○ Encourage coughing
○ Turning and positioning
○ Chest PT
○ Core temp every 4 hours during first 72 hours after injury
○ Control environmental temperature
○ Monitor for abdominal/bladder distention
○ Bladder training
○ Check post-void residual
■ Use bladder scan
■ Catheterize only if necessary
○ Baseline weight
○ Presence/absence of bowel sounds determines nutrition route
○ Education on calorie-activity relationship
○ AE stockings
○ SCDs
○ Subcutaneous heparin or Lovenox (enoxaparin)
○ Education on signs and symptoms of DVT
■ May not have the calf pain, so frequent assessment necessary
○ Encourage independence in ADL’s
○ Use adaptive equipment in bed and for transfers
○ Prevent contractures – wrist drop, foot drop – with ROM
○ Safety - Assist with transfers and ambulation
○ Use of braces, wheelchairs
○ Good skin care
■ Wheelchair pressure reduction seating cushions
■ Teach strategies for frequent position changes
● With the commercials, after every radio song, etc.
■ Teach skin inspection with a mirror
■ Ischial ulcers are common due to lack of sensation
difference between PEEP and CPAP
PEEP = maintains airway pressure above atmospheric airway pressure at the end of expiration
PEEP can be used with either spontaneous or mechanical ventilation
CPAP = maintains a positive airway pressure throughout the whole respiratory cycle
CPAP = used with spontaneous ventilation (not mechanical ventilation) CPAP is always pushing a certain amount of air in throughout entire respiratory cycle
BIPAP
- bilevel… two levels… one for inhalation and one for exhalation
- noninvasive
- delivers two levels of pressure with the higher pressure during inhalation ** allows for airways to stay open and not get closed off ** doesn’t allow for periods of time without gas exchange
- used for COPD, sleep apnea, pneumonia
- adds slight extra pressure to keep airways open **
positives of CPAP and BIPAP
helps to prevent some atelectasis that can occur by giving + airway pressure to keep airways open - allows lower % of O2 use and better gas exchange
- adjunct method to support gas exchange - don’t need as much o2 and whatever you’re taking in used more efficiently
what could false or low o2 readings be due to
vasoconstruction
cold extremities or finger
hypothermia or hypovolemia
false high readings could be due to
anemia… not as many RBCs floating around so the ones floating around are fully saturated
carbon monoxide poisoning
is coughing apart of incentive spirometry
good for getting secretions out BUT not apart of IS
PULMONARY EMBOLISM
blocking of the blood vessels!! NOT THE AIRWAYS!
respiratory response to pulmonary embolism
air is getting into the lungs but not enough o2 can get into obstructed blood stream… leading to SOB, dyspnea
NOT EXCHANGING O2
** most clots going to lungs originate in venous system
diagnostics for pulmonary embolism
chest xray - dilated pulmonary artery
spiral CT scan - CT scan that gives 360 degree view of lungs
EKG sinus tachycardia, right heart strain, no dx for PE
d-dimer rules out blood clot by seeing if there are any breakdown products (neg less than or equal to 0.5)
VQ scan - comparison of ventilation (air) and perfusion (blood) in each of several specific lung fields ** are there any gaps where air is not meeting blood **
GOLD STANDARD FOR PE
PULMONARY ANGIOGRAM!
taking a picture of the blood vessels in lungs
dye is injected through a catheter that is treaded through the vena cava into the right side of the heart
allows for direct visualization of obstruction using fluoroscopy
allows for accurate assessment of perfusion deficit (can show us if specific areas are not being perfused)
requires specially trained team
risk factors for PE
Age 50+ Venous stasis Prolonged immobility Hypercoagulability Pregnant/postpartum women, cancer pts Previous history of thrombophlebitis Damage to vessel walls Orthopedic surgery Hip>knee for PE Certain disease states: heart disease, trauma, postoperative, diabetes mellitus, COPD Other conditions: pregnancy, post-partum, supplemental estrogen, birth control pill, obesity, constrictive clothing
Priorities of PE
Early recognition of clinical picture Depends on the: Size of the clot/amount of obstruction Location of clot The amount of lung tissue affected Early treatment
Human response
Non-specific, non-diagnostic
Anxiety, fear
Chest pain
Sudden, pleuritic; substernal
May become worse with deep breaths, coughing, eating, bending, or stooping
Worsens with exertion but won’t recede with rest
Cough
May produce bloody sputum
Crackles and/or a rub near area of the embolus
Sudden dyspnea (when clot lodges)
Syncope, tachycardia, tachypnea, diaphoresis
PE severity index
This scale can provide some indication of the outcome for a patient who suffers a PE. Although not the purpose, it can also give you an early indication of impending PE if you check your patient’s status against the predictors, and notice early changes in those dimensions – climbing heart and respiratory rate, decreasing O2 sat before any complaints of substernal chest pain, as an example.
Pre-PE nursing interventions
Identify presence of risk factors Early ambulation Reposition frequently Active/passive leg exercises AE hose/SCDs Change IV sites according to best practices Patient/family education Avoid prolonged sitting, legs and feet in dependent position, knees crossed, adequate hydration, wear AE hose/SCDs, etc. Recognize PE clinical presentation
EMERGENCY nursing interventions PE
Independent Vital Signs Assess lung sounds (airways DON’T sound different) Assess respiratory rate/effort Administer O2 Low flow systems High Fowler’s position EKG Dysrhythmia R-side failure With Order Establish IV access Labs: H&H Electrolytes d-Dimer Medications Morphine Sedation Anti-anxiety Goal: Stabilize pulmonary and cardiovascular systems
emergency medical management PE
Protect airway Manage pain/anxiety Confirm diagnosis Pharmacology Surgery
Pharm medical management PE
Thrombolytic (Tissue plasminogen activator or t-PA)
Anticoagulation (i.e. heparin, warfarin)
Surgery medical management PE
Transvenous catheter embolectomy for major/massive PE
Implantation of umbrella filter (Greenfield or IVC filter)
Goes in inferior vena cava
Holds onto and traps blood clots but doesn’t block blood flow, body will eventually break them down
Go through a femoral vein
post-PE nursing interventions
Post-embolectomy or umbrella: Routine post-op care Assessment, activity/ROM, AE/SCDs, C/T/DB, skin/incision care, hydration, O2 prn ALL Post-PE: Monitor labs PT/INR/PTT, platelets Monitor pulmonary parameters Monitor respiratory effort Evaluate all assessment data against previous data Intervene as appropriate Alert PCP Document Patient/family education
patient education on anti-coagulant medication PE
Importance of Labs as ordered Dosing as ordered Safety S/S of bleeding – joints, brain OTCs Alert of HCPs Self care Notify MD if/when…
patient education on post-op PE
Activity
Incision care
Notify MD if/when…
Post-PE
Alert all future HCP of PE history
Stay active; get out of bed as soon as possible after illness (now at risk for future blood clots)
On long car or plane trips, take breaks/walk at least every 2 hours
Change positions often
Do leg exercises if you are on bed rest
Don’t cross your legs
Get immediate medical attention for….
peds differences
Head is large, neck muscles underdeveloped
Prone to head injury with falls
Unfused sutures <18mos
Prone to fracture or brain injury
Highly vascular brain; less CSF to cushion
Brain prone to hemorrhage and trauma
Cervical spine immature: increased mobility
Myelination incomplete at birth
Usually matured by 4-5yrs of age, continues thru to late adolescence
peds seizures
Febrile seizure- sudden, rapid rise in temp,
may be hereditary, no other cause.
Incidence decreases with age.
Epilepsy: Chronic seizure disorder
Meds: Dilantin, Phenobarbitalseizure types
Generalized: Tonic-clonic – loss of consciousness ( grand mal/convulsive – widespread activity )
Partial: Simple, affect one hemisphere of brain.
Absence: may have non or minor motor movement.
bacterial meningitis
Bacterial etiology
Infants at greatest risk: 70% < 5yr old
May occur secondary to otitis media, sinusitis, pneumonia
Or brain trauma or neurosurg procedure
BM clinical manifestations in infant
Infant:
fever, change in feeding, vomiting, anterior fontanel flat or bulging, restless, lethargic or irritable
Hard to consol, even by the parent.
Piercing cry or lethargic, listless.
BM clinical manifestations in older child
Older Child :
Fever, irritable, lethargic, confused, combative, headache, back/neck pain, photophobia, nuchal rigidity.
May have a rash, petechiae, purpura
Associated with meningococcal meningitis
opisthotonus posturing
peds BM clinical therapy/sequelae
History, PE, Labs
Lumbar Puncture to evaluate CSF
WBC’s, protein, glucose, gram stain & culture
Administer antibiotics as soon as all culture specimens are obtained _______________________________
Neurologic damage, seizures, hearing loss, developmental delays, multisystem organ failure or death.
bacterial meningitis CSF results
Increased WBC Low Glucose Increased Protein Gram Stain - postivie ( 60-90% ) Culture – positive Contagious
viral (aseptic) meningitis
Inflammatory process
Glucose & protein in CSF normal
Culture will not grow any bacteria
Patient does not appear as ill
Yet, treatment is aggressive until the 48hr cultures are negative
reye’s syndrome
Etiology unclear
Acute swelling of the brain caused by toxin, or injury, - causes inflammation.
Assoc with viral illness & use of aspirin
Now it’s rare with acetaminophen and NSAIDS
TEACH ! Educate parents: NO ASA
nursing care for meningitis
ABC’s Cerebral edema Seizure control Antibiotics ( if bacterial ) Steriods Fowler’s Position
GBS
Post infectious Polyneuritis
Autoimmune response to some infectious process: GI or Resp 2-3 wks prior
Deteriorating motor function and paralysis in ascending pattern (LE’s 1st)
Treatment: Immunoglobulin
Rarely fatal; but respiratory difficulty may require ventilation.
SPECIAL needs of children w disabilities
Growth & development Body image/Self-esteem Autonomy Socialization/schooling Communication Family interactions – sibling needs Financial needs
assisting chonically ill child’s transition to adult life
Individualized transition plan
Adult-oriented healthcare
Alternate living arrangements
Work skills
cerebral palsy overview
Non-progressive brain injury or malformation that effects movement, muscle tone or posture.
secondary to brain damage: congenital, hypoxic, or traumatic origin
Before birth, during birth or soon after birth.
Most common chronic disorder is childhood
CP spastic
Spastic CP is the most common type and may involve one or both sides of the body.
Persistent hypertonia, rigidity is classic hallmark (scissoring)
Exaggerated DTRs (deep tendon reflexes )
Persistent primitive reflexes(moro, rooting)
Leads to contractures and abnormal spinal curvatures
CP dyskinetic
The dyskinetic type involves abnormal involuntary movements that disappear during sleep and increase with stress. Impaired voluntary muscle control Bizarre twisting movements Tremors Exaggerated posturing Inconsistent muscle tone
ataxic type
Lack of balance and position sense
Muscular instability
Gait disturbances
assessment for CP
Assessment
Most common manifestation in all types of CP is delayed gross motor development
Failure to achieve milestones may be the FIRST SIGN.
Additional manifestations include:
Abnormal motor performance (early hand preference,
poor sucking)
Alterations of muscle tone (e.g., difficulty in diapering)
Abnormal postures (e.g., scissoring legs or persistent infantile posturing)
Reflex abnormalities (persistent primitive reflexes or
hyper-reflexia).
Mental retardation, seizures, ADHD, & sensory impairment ??.
clinical therapy for CP
Any child with devel. delays and
poor suck should be referred for eval.
Focus is on child reaching his/her maximum potential
Referrals to PT, OT, speech, special ed, ortho, hearing and vision
Cerebral palsy goals
KEY: HELPING CHILD REACH MAXIMUM POTENTIAL
Prevent physical injury: safe environment, appropriate toys, and protective gear (helmet, knee pads)
Prevent physical deformity: prescribed braces and other devices, ROM
Promote mobility: age‑ and condition‑appropriate motor activities.
Ensure adequate nutrition by providing a high‑protein, high‑calorie diet and utilizing feeding devices as needed, G-tube feedings as needed
Foster relaxation and general health by providing rest periods.
Administer medications (muscle relaxants, anti-seizure)
Encourage self‑care and independence when possible
Because many have normal intellect.
WANT THEM TO BE MOBILE!
Duchenne muscular dystrophy
MD is a group of disorders that cause progressive degeneration and weakness of skeletal muscles.
Duchenne muscular dystrophy is the most common and most severe
Duchenne is progressive and leads to death, usually in adolescence, from infection or cardiopulmonary failure.
Half of all cases are X‑linked
Pathophysiology
1. Dystrophin, a protein product in skeletal muscle, is absent in the muscles
2. There is a gradual degeneration of muscle fibers
initial symptoms of muscular dystrophy
Assessment findings: Symptoms begin between 2 and 6 years old.
Initial signs and symptoms include:
(1) Delays in further motor development
(2) Frequent falls, trouble getting up from lying/sitting position
(3) Difficulties in running, riding a bicycle, and climbing stairs
progressive symptoms of muscular dystrophy
Progressive signs and symptoms include:
(1) Abnormal gait becomes apparent.
(2) Walking ability ceases between 9-12 years old.
(3) Pseudohypertrophy of calf muscles ( fatty/fibrous tissue )
(4) Cardiac problems (weakened heart muscles)
nursing management muscular dystrophy
Assess the child for signs of disorder progression, and complications.
Maintain optimal physical mobility
Compensate for disuse syndrome: positioning, skin care, fluids, Chest PT & bowel routine.
Support the child and family in coping with this progressive disorder.
Refer family members to support agencies such as the MDA.
Teach the family and child about: Diagnosis; Treatment, Devices (braces, feeding devices); Complications; & Prognosis
structural defects
Hydrocephalus
Spina Bifida
Craniosynostosis
hydrocephalus
Description
1. Hydrocephalus condition caused by an imbalance in the production and absorption of CSF in the ventricular system. When production exceeds absorption, CSF accumulates, usually under pressure, producing dilation of the ventricles.
Congenital hydrocephalus : born with defects.
It is associated with Spina Bifida.
Acquired hydrocephalus usually results from space‑occupying lesions, hemorrhage, intracranial infections, or dormant developmental defects.
patho hydrocephalus
Pathophysiology
COMMUNICATING HYDROCEPHALUS:
CSF flows freely but has impaired absorption within the arachnoid space
NON-COMMUNICATING HYDROCEPHALUS: obstruction to the flow of CSF through the ventricular system *(most common)
clinical manifestations of hydrocephalus infants
First sign in infancy is bulging fontanels, irritability, then head enlargement, sutures become palpably separated.
Frontal protrusion or bossing
Eyes depressed downward: setting sun sign ( sclera visible above pupil)
Pupils may be sluggish with unequal response to light
clinical manifestations of hydrocephalus older kids
Presentation is different than infants after closure of the cranial sutures
No head enlargement, (no bossing)
Headache, morning vomiting, confusion, apathy, ataxia, visual defects
Overall, signs of increased ICP
treatment of of hydrocephalus
Ventriculoperitoneal (VP) Shunt:
A pathway to divert excess fluid from ventricles to….. peritoneum
Replace as child grows
Can become blocked, kinked or infected
Malfunction causes recurrent signs of increased ICP
Infection most serious complication.
neural tube defects patho
Neural tube is structure that develops into the baby’s brain and spinal cord, as well as the tissues that surround it.
If it fails to develop or close properly in 3rd-4th week of gestation then have defects in spinal cord or nerves
spina bifida types
Spina Bifida Occulta,
- Meningocele,
- Myelomeningocele.
SB occulta
Usually does not affect the spinal cord. External signs: dimple or hair patch. Small gap/indent but no opening.
SB meningocele
fluid-filled sac; protrudes outside the vertebrae (cord & root…OK).
myelomeningocele
fluid-filled sac;
(spinal cord & nerve roots) PROTRUDE. Possible muscle weakness/paralysis, urinary bowel problems, joint/bone deformities.
neural tube defects nursing management
No treatment for spina bifida occulta unless neurologic damage.
If a sinus is present, it may need to be closed.
Meningocele requires closure as soon after birth as possible. The child should be monitored for hydrocephalus, meningitis, and spinal cord dysfunction. *Location…..
Myelomeningocele requires a multidisciplinary approach (i.e., neurology, neurosurgery, pediatrics, urology, orthopedics, rehabilitation, and nursing).
Closure is performed within 2-3 days to minimize infection and prevent further damage to the spinal cord and roots.
Shunting is performed for hydrocephalus and antibiotics are initiated to prevent infection. The child will need correction of musculoskeletal deformities and management of urologic and bowel control problems.
NTD prevent infection and injury
- Surgical closure (24-48 hrs)
a. Preoperatively, apply a sterile dressing, constantly
moistened with saline, to the lesion.
b. Pre and postoperatively perform the following:
Maintain a sterile, damp dressing. Examine for leakage.
Avoid placing a diaper or other covering directly over the lesion (this could cause fecal contamination).
Monitor the child for signs of local infection and meningitis
(e.g., fever, irritability, and poor feeding).
c. Position the infant in a prone or side-lying position
to prevent contamination by stool or urine.
NTD prevention
Prevent the development of neural tube defects. Encourage women of childbearing age to consume 0.4 mg of folic acid everyday during the preconceptual period (recommended by the U.S. Department of Public Health).
They should consult their primary care provider or pharmacist to ensure that their multivitamin contain this amount.
craniosynostosis
Premature closure of the cranial sutures
Can cause deformity of the skull
Can palpate over riding of the sutures
Reconstructive surgery before the age of 1yr has better outcome
lead poisoning
One of the most common pediatric problems in the United States.
2. Highest incidence: late infancy and toddlerhood.
lead poisoning etiology
The child is exposed –eating contaminated food or nonfood substances, breathing contaminated air, or drinking contaminated water.
2. Lead dust —paint chips, powder from paint, gasoline, unglazed ceramic containers, lead crystal, water from lead pipes, batteries, folk remedies, fishing weights, furniture refinishing supplies, art supplies, cosmetics, pool cue chalk, and even certain industrial pollutants.
why are children at greater risk of lead poisoning
because they absorb and retain more lead in proportion to their weight.
lead poisoning problems with normal cell functioning
Nervous syst – irreversible damage to developing brain
Blood cells- displaces iron, which decreases Heme production
Kidneys- excreted through kidneys
Has adverse affect on vitamin D and calcium metabolism
