bunch of management and treatments and concerns idk Flashcards
1
Q
pharmaceutical therapy for SCI
A
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
2
Q
recovery (possible forever) phase concern for SCI
A
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
3
Q
autonomic dysreflexia
A
sudden onset severe hypertension severe throbbing headache profuse diaphoresis/flushing nasal stuffiness blurred vision nausea bradycardia
4
Q
intervention for autonomic dysreflexia
A
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
5
Q
interventions for SCI
A
● 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
6
Q
difference between PEEP and CPAP
A
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
7
Q
BIPAP
A
- 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 **
8
Q
positives of CPAP and BIPAP
A
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
9
Q
what could false or low o2 readings be due to
A
vasoconstruction
cold extremities or finger
hypothermia or hypovolemia
10
Q
false high readings could be due to
A
anemia… not as many RBCs floating around so the ones floating around are fully saturated
carbon monoxide poisoning
11
Q
is coughing apart of incentive spirometry
A
good for getting secretions out BUT not apart of IS
12
Q
PULMONARY EMBOLISM
A
blocking of the blood vessels!! NOT THE AIRWAYS!
13
Q
respiratory response to pulmonary embolism
A
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
14
Q
diagnostics for pulmonary embolism
A
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 **
15
Q
GOLD STANDARD FOR PE
A
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
16
Q
risk factors for PE
A
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
17
Q
Priorities of PE
A
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
18
Q
Human response
A
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
19
Q
PE severity index
A
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.
20
Q
Pre-PE nursing interventions
A
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
21
Q
EMERGENCY nursing interventions PE
A
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
22
Q
emergency medical management PE
A
Protect airway Manage pain/anxiety Confirm diagnosis Pharmacology Surgery
23
Q
Pharm medical management PE
A
Thrombolytic (Tissue plasminogen activator or t-PA)
Anticoagulation (i.e. heparin, warfarin)
24
Q
Surgery medical management PE
A
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
25
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
```
26
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…
```
27
patient education on post-op PE
Activity
Incision care
Notify MD if/when…
28
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….
29
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
30
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, Phenobarbital
```
31
seizure 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.
32
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
33
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.
34
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
35
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.
36
bacterial meningitis CSF results
```
Increased WBC
Low Glucose
Increased Protein
Gram Stain - postivie ( 60-90% )
Culture – positive
Contagious
```
37
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
38
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
39
nursing care for meningitis
```
ABC’s
Cerebral edema
Seizure control
Antibiotics ( if bacterial )
Steriods
Fowler’s Position
```
40
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.
41
SPECIAL needs of children w disabilities
```
Growth & development
Body image/Self-esteem
Autonomy
Socialization/schooling
Communication
Family interactions – sibling needs
Financial needs
```
42
assisting chonically ill child's transition to adult life
Individualized transition plan
Adult-oriented healthcare
Alternate living arrangements
Work skills
43
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
44
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
45
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
```
46
ataxic type
Lack of balance and position sense
Muscular instability
Gait disturbances
47
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 ??.
48
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
49
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!
50
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
51
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
52
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)
53
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
54
structural defects
Hydrocephalus
Spina Bifida
Craniosynostosis
55
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.
56
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)
57
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
58
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
59
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.
60
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
61
spina bifida types
Spina Bifida Occulta,
- Meningocele,
- Myelomeningocele.
62
SB occulta
Usually does not affect the spinal cord. External signs: dimple or hair patch. Small gap/indent but no opening.
63
SB meningocele
fluid-filled sac; protrudes outside the vertebrae (cord & root…OK).
64
myelomeningocele
fluid-filled sac;
(spinal cord & nerve roots) PROTRUDE. Possible muscle weakness/paralysis, urinary bowel problems, joint/bone deformities.
65
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.
66
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.
67
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.
68
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
69
lead poisoning
One of the most common pediatric problems in the United States.
2. Highest incidence: late infancy and toddlerhood.
70
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.
71
why are children at greater risk of lead poisoning
because they absorb and retain more lead in proportion to their weight.
72
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
73
how is lead absorbed
GI
inhalation
transplacental
74
clinical manifestations of lead poisoning
Decreased IQ scores
Cognitive deficits
Loss of hearing
Growth delays
75
assessment findings of lead poisoning
a history of pica??
| inquire as to housing conditions
76
more clinical manifestations of lead poisoning
Hematologic: anemia. ( offer multi- vitamin )
- Renal: urine abnormalities.
- GI: acute crampy abdominal pain, vomiting, constipation, and anorexia.
- Musculoskeletal: short stature &lead lines in bones x‑ray .
- Neurologic (central nervous system) manifestations: Low-dose lead exposure causes behavioral changes such as distractibility, hyperactivity, and impulsivity; learning problems; hearing impairment; and mild intellectual deficits.
High-dose lead exposure causes lead encephalopathy, which is manifested by seizures, mental retardation, paralysis, blindness, coma, and death.
77
lead poisoning tests
Laboratory and diagnostic study findings
| Lead tests will reveal a serum lead level exceeding 10 mcg/dL (considered positive for lead poisoning).
78
treatment of lead poisoning
Chelation Tx is indicated if BLL is greater that 45ug/dl
| EDTA – binds with lead, excreted in urine
79
child/fam teaching of lead poisoning
* Assure that your child does not have access to peeling paint or chewable surfaces that are coated with lead-based paint.
* Wash and dry your child=s hands frequently.
* If soil is likely to be contaminated, plant grass or other ground cover.
* If you are remodeling an old home, follow correct procedures.
* Use only cold water from the tap for consumption, especially when preparing formula.
* Have your water and soil tested by a competent laboratory.
* Do not store food in opened cans.
* Do not use inadequately fired ceramic ware or pottery for food or drink.
* Do not store food or drink in lead crystal.
* Avoid folk remedies or cosmetics that may contain lead.
* Avoid home exposure to lead from occupations or hobbies.
* Make sure that your child eats regular meals and consumes adequate amounts of iron and calcium.
80
peds resp system
nares– infants up to 4-6 wks obligate nose breathers
mouth- sm. oral cavity proportion to lg. tongue/tonsils
upper airway- short & narrow diameter
- Faster respiratory rate
- bronchioles & intercoastal muscles immature
- short, horizontal Eustachian tubes
81
peds assessment triangle
appearance
circulation
work of breathing
82
peds assessment triangle
```
Appearance : T I C L S
Tone
Interactiveness
Consolability
Look/Gaze
Speech/Cry
```
WOB : - Rate, Retraction, Position, Anxiety
** supraclavicular contractions... means individual is struggling to get air in
*** anxiety... when you can't breathe you start to get anxious and stressed
Circulation : - Color (pale, cyanosis, ashen, modeled )
83
peds resp assessment
Assess: Color, cap refill
Irregular or difficulty breathing
Feeding/swallowing problems
Nasal congestion, runny nose
Cough/stridor
Behavior changes, irritability,
lethargy
Tests: CXR, Pulse ox, Cultures.
84
nursing diagnosis for peds resp disorders
- Ineffective breathing pattern
- Ineffective airway clearance
- Activity intolerance
- Fear & Anxiety
_ Knowledge deficit re: condition,
treatment plan, self care and
discharge plan
85
peds resp management
If O2 sats are less than 94%.....
Confirm that the reading is believable
( machine reading correlates with heart rate )
Determine O2 sat probe is functioning
Raise the HOB or sit child up if able
Open airway ( ie: suction )
Administer O2 (blow by, n/c or face mask)
Signs of respiratory distress needs action and reporting to instructor, RN and MD!!
86
additional resp management of peds
- vital signs, esp. HR, RR and BP
- mentation/responsiveness
- tone
- color
Alert the appropriate person to communicate
changes in O2 and responses to treatment,
obtain order for O2 and further actions.
87
foreign body aspiration... who is at risk
Who is at risk?
- Infants, toddlers, preschoolers
exploration and imitation
- Older children & teens
activity while eating, laughing, too much, too fast,
high risk activities, especially if intoxicated
- Severity depends on location & type of object
(popcorn, peanuts, carrots, peanut butter, coins, nails, toys)
88
FBA clinical presentation
-choking, cough, gagging, hoarseness, wheezing,
stridor , drooling and/or asymmetric breath
sounds.
89
FBA diagnostic findings
CXR
| bronchoscopy
90
FBA clinical management
- Assess s/s : location & degree of obstruction
- Chest thrusts & back blows for infant,
abdominal thrusts…etc.
- Bronchoscopy: sedation/surgery to remove
the object.
- Passage thru GI tract: normal diet no laxatives
- Best approach…..PREVENTION !!
clean up small objects/toys, use Mylar balloons not latex, positive role model, supervised meals, appropriate size bites………..
91
apnea in peds
cessation of respir > 10 sec.
- May or may not be accompanied by
cyanosis, pallor, hypotonia, bradycardia
- May be first sign of distress in infant
( respir. dysfunction, illness or sepsis)
- Apnea of prematurity: occurs in preterm
infants d/t lack of maturity of
neuro/respiratory systems.
92
apparent life threatening event
Episode of apnea accompanied by color change, hypotonia, choking, gagging in infant born > 37 weeks and aged >60 days.
May occur during sleep or wakefulness or feeding
Usually admitted to monitor, find cause
Home apnea/CPR teaching
May be GE Reflux, also consider “shaken baby syndrome”
93
SIDS
Sudden death of infant < 1yr of age that remains unexplained after a complete autopsy, death scene investigation and review of history. Death usually occurs during sleep.
Leading cause of death for infants (1 month - 1 yr )
Etiology – unknown. It is unpredictable
and unpreventable.
Risks- prematurity, drug exposure, siblings who have died of SIDS, prenatal/postnatal maternal smoking.
** Also increased incidence in infants who sleep in prone position.
94
NURSING MANAGEMENT SIDS
Evaluate family coping and grieving patterns.
2. Provide anticipatory guidance for typical feelings.
3. Allow parents to verbalize; listen & validate feelings.
4. Refer family for counseling, if needed.
5. Refer to appropriate community self-help groups.
6. Monitor infants at risk for apnea
95
teach parents how to minimize the risk of SIDS
a. Avoid smoking during and after pregnancy
b. Encourage putting infants to sleep in supine position
unless contraindicated
c. Avoid soft, moldable mattresses and overheating.
d. Avoid use of pillows
e. Avoid bed sharing
96
Obstructive sleep apnea
```
Excessive snoring then apnea:
- Asleep, then airway muscles relaxed
- Decrease tone/obstruction
- Decreased ventilation, hypoxia, incr. CO2
Causes:
- Craniofacial abnormalities
- Obesity
- Large Tonsils/Adenoids
Complications:
- FTT, cognitive impairment
Diagnostic/Treatment:
- Sleep study, Tonsillectomy, Craniofacial repair, CPAP machine
```
97
croup syndromes
Classified as upper airway syndrome
Can have swelling of epiglottis, larynx,
trachea, and/or bronchi
Viral and bacterial causes
- Acute spasmodic laryngitis
- Acute laryngotracheobronchitis (LTB)
- Epiglottitis
98
acute spasmodic laryngitis
- Viral/Allergic
- Sudden onset
- Peaks at night, resolves by morning
but often reoccurs
- Clears with humidity, cool fluids.
- Mild hoarseness & slight stridor.
99
laryngotracheo bronchitis (LTB)
- Viral
- Usually in the winter, quick onset
- Barking cough, inspiratory stridor,
and retractions, low fever.
- Potential for airway obstruction !!!
- Treatment: humidity, steroids,
racemic epinephrine via nebulizer
100
epiglottitis
- **Bacterial ( Haemophilus influenzae B )
- Incidence does decrease with higher immunization
of HIB vaccine
- **Always severe, rapid onset, high fever
- Inflammation of epiglottis causing airway obstruction
within minutes to hours.
101
treatment of epiglottitis
- Treatment: maintain airway
(intubate, tracheotomy set at bedside),
O2, along with IV fluids and antibiotics.
102
epiglottitis special considerations
- *course is rapid, progressive & life threatening
- Child insists on sitting up, leaning
forward with mouth open, drools saliva
d/t difficulty in swallowing. KEEP CHILD CALM!!
- cough is absent
- Avoid throat culture, tongue depressor
or palpation of throat area, this manipulation
could produce severe laryngospasms
…..progressing to resp. arrest !!!
103
Upper airway disorder Nasopharyngitis
A “Cold” is the most
common infection of the respiratory tract.
- Principle cause is rhinovirus, which is spread from
person to person by sneezing, coughing or direct contact
- Nasal discharge, irritability, sore throat, cough,
general discomfort.
104
Nasopharyngitis treatment
- Treatment: Clear airways (esp. before feeding),
saline drops, bulb syringe for infants,
humidifier.
Adequate fluid intake
Prevention of fever
105
pharyngitis (UAD)
: Inflammation/infection
of the throat. Viral or Bacterial ??
……That is the question ????
Must treat all strep to prevent
rheumatic fever, peritonsillar abscess
If it occurs often…… recommend
tonsillectomy & adenoidectomy ( T&A )
106
T&A post op care
Observe for bleeding. Frequent swallowing is early sign of bleeding.
Prevent bleeding by discouraging coughing and throat clearing.
**Relieve pain; encourage fluids
Position on side to facilitate drainage.
Patient teaching:
- Soft, cold diet; no milk, hot fluids or citrus liquids
- Monitor for bleeding, especially 5-10 days post-op
- Relieve pain, encourage fluids consistently at home
107
acute otitis media (AOM)
Inflammation/Infection of the middle ear.
Very common and can recur often.
Some children anatomically prone to AOM
due to poor Eustachian tube dysfunction
with or without an URI.
Caused by Hemophilus influenzae, Streptococcus pneumoniae
Other factors: feeding infant in supine position & passive smoking.
108
acute otitis media nursing management
- Assess child for fever and pain level
- Administer prescribed meds. ( antibiotics, antipyretics )
- Frequency may warrant surgery
109
myringotomy
sm. incision in tympanic
membrane, “tubes” placed which allows for
proper drainage of fluid.
- Purpose is to relieve symptoms, restore hearing
- Teaching: keep ear dry, will fall out by themselves
or primary care provider can take them out.
110
bronchiolitis lower airway disorders
– Inflammation & obstruction of bronchioles. Viral cause - ( RSV, Influenza type A & B).
Can be caused by bacteria or allergen
- signs & symptoms: rhinorrhea, pharyngitis,
coughing, sneezing, wheezing, intermittent fever.
* If severe: tachypnea (RR > 70 ) , listless, diminished
breath sounds, apneic spells
111
bronchiolitis
supportive humidified O2,
rest, push po fluids, IVF’s if tachypneic
to prevent aspiration.
112
respiratory syncytial virus RSV
Transmitted through close or direct contact
( Day care, shelters, high density group living, older siblings)
Airways swell, produce excess secretions
causing obstruction and bronchospasm.
URI, fever, rhinitis, progressing to wheeze & course breath sounds, less po intake, less energy, increase sleepiness.
113
RSV diagnosis
Transmitted through close or direct contact
( Day care, shelters, high density group living, older siblings)
Airways swell, produce excess secretions
causing obstruction and bronchospasm.
URI, fever, rhinitis, progressing to wheeze & course breath sounds, less po intake, less energy, increase sleepiness.
114
diagnosis rsv
viral culture done from
| nasal secretions, child put on contact precautions
115
RSV therapy/management
- Humidified O2 , CPT, isolation precautions,
handwashing, IVF’s, suction, family support.
- Meds: bronchodilators (Albuterol, xopenex)
*Synagis- recomm for premies and children
with underlying medical conditions.
Provides passive immunity, IM injection
given 1X month Oct-April
*Respigam- same passive immunity, given IV
116
pneumonia
Viral or Bacterial
Inflammation or infection of bronchioles and alveolar spaces of lungs
End result is exudate, creating areas of plugging & consolidation that interferes with gas exchange.
Increase cough, SOB with exertion
117
pneumonia nursing management
- frequent, persistent coughing can
cause muscle strain and interrupted
sleep for both child and parent.
- Tylenol or Ibuprofen for fever/pain control.
- Cough suppressants not routinely advised for children
but may use on older children at night for sleep.
- supportive therapy: fluids, nutrition, O2 prn
118
asthma
Chronic inflammatory, obstructive airway disease characterized by wheezing.
Effects the large and small airways with
increased mucous, swelling & bronchospasm
```
Triggers: exercise, infection, allergies and
environmental irritants (smoke, weather change)
```
Most common chronic disease in children
119
asthma assessment/management
- Assess for degree of resp. distress:
(RR, HR, color/O2 sat, cap refill)
- Breath sounds, air movement, peak flow
- Assess fluid status: increased RR leads to
insensible loss of water, dries out mucous
airways and risk of aspiration.
- Monitor output: strict I&O (weigh diapers)
- Promote rest to conserve energy,
decrease O2 need.
120
asthma management
Nebulizer inhilation with mask for children
- B-adrenergic agonists (short acting, rescue med)
* - Albuterol ( Proventil )
*- Levabuterol (Xopenex)
- B-adrenergic agonists (long acting)
*- Salmeterol (Serevent)
- Corticosteroid
* - Pulmicort “put your $$ where your mouth is”
Put the steroid to reduce inflammation where the lungs are,
not just po or IV with higher systemic side effects.
MDI (metered dose inhaler) with spacer
121
asthma management at home
Primary Goal is PREVENTION !!
- use peak flow meter to monitor degree
of obstruction; divided into zones
- Keep a home log of need for Tx’s
- Avoid triggers ( no ice cold drinks, encase pillow/mattresses, no dust
collectors in room, no pets, change clothes after outside, no cockroaches)
- Determine need for home nebulizer vs MDI’s
- Determine need for steroids for maintenance
and prevention
- Have a clear follow-up plan with PCP.
122
status asthmaticus
Severe, unrelenting respiratory distress
with bronchospasm
Persists despite medication and supportive
interventions
Medical emergency requiring endotracheal
intubation with assisted ventilation
Death can be a direct result of poor teaching and mismanagement of medications.
123
bronchopulmonary dysplasia (BPD)
A fibrous or thickening of the lung caused by persistent oxygen need (O2 toxicity) and ventilation given to newborns for a prolonged period of time.
Respiratory distress syndrome(RDS) in
the newborn is major reason O2 & vents are used
Main cause of RDS for the newborn is…. prematurity.
124
BPD clinical symptoms
-resp distress, tachypnea, wheezing,
retractions, cyanosis on exertion, grunting,
irritability.
- long term dyspnea = barrel chest, clubbing
Normal activities such as feeding, playing or mild URI, incr. O2 demand = resp. distress
125
medical management BPD
- resp. support= humidified O2, mechanical
ventilation, suction, CPT 3-4x/day
- med support= bronchodilators, diuretics,
anti-inflammatories, and antibiotics if needed
*think prevention:
Respigam and or Synagis
- nutritional support= NG tube feedings to conserve energy
126
nursing management BPD
- support safe weaning from oxygen
- promote normal growth & development
- prepare family for home care needs
- teach close monitoring of RR,HR,color & behavioral changes, and how the family unit is coping with caring for this child with special needs.
- Discuss clear parameters for follow up in an acute illness: re-admission to the hospital is common and they become ill very quickly.
127
cystic fibrosis
Major cause of serious chronic lung disease
in children, inherited from both parents carrying
a gene for the disease (autosomal recessive)
Involves the exocrine glands which excrete a thick fluid that affects functioning of the respiratory, GI, endocrine, skin and reproductive systems.
Mostly seen in the white population
Equal distribution among gender
Median life span is 30 yrs.
128
CF multi-systems impacted
* Resp. system – lungs plugged with thick mucous that cannot be easily expectorated, causing atelectasis, air trapping, fibrosis and frequent infections.
Assess s/s – wheezing, dyspnea, cough and cyanosis. Also, gerneralized obstructive emphysema produces such characteristic features as barrel chest & finger clubbing
129
CF digestive system
secretions prevent
digestive from flowing to GI tract, results
in poor absorption of food
- great appetite, weight loss, FTT, bulky
& foul smelling stools are frothy d/t
undigested food.
- Rectal prolapse
- pancreatic ducts blocked thus Insulin
dependent diabetes is not uncommon.
130
CF reproductive system and CV system
Reproductive system-
- Females will have delayed puberty &
decreased fertility ( thick cervical mucus ).
- Males also with decr fertility
(decr. sperm motility, blockage of vas deferens )
Cardiovascular system-
- Right sided heart enlargement & CHF, from
obstruction of pulmonary blood flow.
131
integumentary system CF
Increased concentrations of sodium
and chloride in sweat;
have salty skin surface, tears, saliva
132
CF primary presentation and diagnosis
- Meconium ileus in the new born
- small bowel obstruction as young infant
- fecal impaction and/or intussesception
- steatorrhea ( bulky,fatty stools )
- productive cough, frequent URI’s
and weight loss
- elevated chloride on a Sweat Test (>50-60)
133
nursing management of CF
- Therapy: Oxygen prn, antibiotic, aerosol & MDI’s,
postural drainage, breathing exercises,
prevention of infection.
- Dietary: supplemental pancreatic enzymes
- Other: general hygiene( skin/diaper area), teeth may
be poor condition d/t dietary deficiencies.
- Promote growth & development
- Assist family to adjust to chronic disease,
and long term implications.
134
Rheumatic and rheumatism
These are diseases characterized by inflammation (signs include redness or heat, swelling, and symptoms such as pain) and loss of function of one or more connecting or supporting structures of the body. They especially affect joints, tendons, ligaments, bones, and muscles.
135
systemic rheumatic diseases
Generally have a primary systemic and autoimmune pathology
Rheumatoid arthritis
Systemic lupus erythematosus
Systemic sclerosis (Scleroderma)
136
rheumatoid arthritis
An inflammatory disease of exacerbations and remissions that attacks joints predominantly, but can also affect other tissues because of its systemic effects.
Joint disease is characterized by synovitis that leads to destruction of the joint cartilage and underlying bone.
Most often seen in women between 40 and 60, though can be seen in all ages, including children (when is termed Juvenile Idiopathic Arthritis or JIA)
137
rheumatoid arthritis cause
No clear cause found for the condition, but clearly has a genetic component as well as immune-mediated inflammation in joints and body tissues.
Can be thought of as an “over-activation” of the immune system, where the body produces antibodies against itself (autoantibodies)
Seems to involve activation of CD4 helper T cells, and then production of cytokines such as TNF, interleukins, etc.)
138
RA pathology
Neutrophils, macrophages, and lymphocytes are attracted to the area (joint, connective tissue, etc.) where the autoantibodies are present.
The autoantibodies are phagocytized, and release destructive enzymes.
These enzymes (lysozymes) attack joint cartilage.
An inflammatory response follows, and attracts additional inflammatory cells.
The cycle is begun…
Inflammatory process leads to reactive hyperplasia in the synovium – causes vasodilation and increased blood flow (increased vascular permeability)
Warmth
Redness
Pain
Swelling
139
RA patho continued
New blood vessels are formed in the synovium in response to the inflammation.
This profusion of inflammatory granulation tissue is called PANNUS – and becomes destructive to the cartilage and underlying bone.
Pannus eventually spreads throughout the joint, and causes deformity, reduced joint motion, and stiffness.
These destructive changes are irreversible.
140
RA course
Can vary from mild and involving a few joints, to a serious and disabling condition.
Many new drugs have been produced recently to halt or slow the disease progression – these drugs work to block various components of the immune response.
141
joint manifestations in RA
Usually symmetric and polyarticular
Can involve any diarthrodial joint – fingers, hands, wrists, knees, and feet
Pain and stiffness lasts longer than 30 minutes in the AM, and after rest.
Exacerbations and remissions
If affects spine – usually involves the cervical spine.
In hands, PIP and MCP joints are affected (proximal interphalangeal and metacarpophalangeal) causing swelling and deformity
142
classic deformities in RA
Swan neck deformity – hyperextension of PIP (proximal interphalangeal) joint with flexion of the DIP (distal interphalangeal) joint
Boutonniere deformity – flexion of the PIP joint and hyperextension of the DIP joint
143
Other joints involved in RA
```
Frequent knee damage including
Contractures
Instability
Genu valgum (knock-knee)
Ankle involvement
Can interfere with walking
Toes
Rheumatoid nodules
Neck discomfort
Can cause neurologic complications
```
144
Systematic manifestations in RA
During active disease:
fatigue, weakness, weight loss, low-grade fever, and anorexia
Elevation of ESR (erythrocyte sedimentation rate)
Anemia
Rheumatoid nodules found over pressure points
Vasculitis – causes ischemic areas, neuropathy, and ulcerations and visceral organs (heart, lungs, GI tract)
145
more systemic manifestations in RA
Hematologic abnormalities
Pulmonary disease
Cardiac disease (SIGNIFICANT increase in heart disease and MI in people with RA)
Eye lesions – e.g. slceritis
Infection
Felty syndrome = splenomegaly with leukopenia
146
Diagnostics in RA
History
Physical exam
Examination of synovial fluid
Laboratory tests
Rheumatoid Factor (RF) may be present (~80%), but is not always.
Anti-CCP (anti-cyclic citrullinated peptide antibodies) or ACPA (anti-citrullinated protein antibodies). These may be more specific.
147
Treatment overview in RA
```
Medications
DMARDs – disease-modifying anti-rheumatic drugs
NSAIDs
Corticosteroids
Biologics – many now
Etanercept
Inflximab
Leflunomide, etc.
Exercise
Physical and emotional rest
Assistive devices
Splints
Surgery – synovectomy, fusion, and joint replacements
```
148
osteoarthritis
Osteoarthritis (OA) is also known as degenerative joint disease (DJD)
Is NOT a systemic condition like RA; is localized in joints
Is the most common form of arthritis
Is frequently a cause of joint pain and disability – especially in the elderly
149
primary vs secondary osteoarthritis
Primary - localized or generalized involvement of joints with no obvious cause
Secondary – caused by congenital or acquired joint defects, trauma, metabolic disorders, or inflammatory diseases
150
demographics of OA
Men affected earlier than women, but both genders affected.
Some clear genetic clues – (i.e. more hand OA in white women, more knee OA in black women, less hip OA in some Asians)
151
risk factors for OA
Obesity – esp. knee involvement in women
Trauma (sports injuries, occupation…)
Repetitive use syndromes
Age
152
patho OA
Involves changes in the underlying cartilage of a joint in both composition and mechanics
Weakening and breaking of collagen – thought due to release of cytokines. These cytokines cause release of enzymes that are destructive to joint structures.
Body is unable to repair the damage because of an imbalance in normal cartilage turnover.
Articular cartilage is eroded and destroyed, exposing the underlying bone.
Eventual rubbing of “bone on bone.”
Fragments of bone and cartilage can become dislodged and “float” throughout the joint
New bone forms at the edges of the joints – called osteophytes or “spurs”
153
Findings in OA
Aching pain that worsens with use, and usually decreases with rest
In later disease, the pain can be experienced during rest as well
Joint enlargement
Frequent sites for OA (weight-bearing joints, mainly)
Hips
Knees
Lumbar and cervical vertebrae
Hands and feet
154
Diagnostics in OA
```
History
Physical exam
X-rays
Joint space narrowing
Osteophytes
Laboratory studies that EXCLUDE other diseases ( no lab test for OA); may be slight elevation of ESR
Synovial fluid analysis (usually normal)
```
155
Treatment overview in OA
Balance of rest and exercise
Use of heat and cold to control discomfort
Weight loss, if indicated
Medications
NSAIDs
Corticosteroids (oral and by injection)
Viscosupplementation (injection of sodium hyaluronate into joint to increase lubrication)
e.g. Hyalgan, Synvisc
Surgery
Joint replacement, osteotomy, and spinal decompression
156
Gout
Refers to a condition characterized by joint and surrounding inflammation, accumulation of crystalline deposits in joints and other tissues, nerve damage, renal damage, and uric acid stones
Most commonly, gout is considered to be uric acid or monosodium urate crystals deposited in joint cavities
157
gout arthritis
The disorder is termed “primary gout” when the cause is unknown, and mainly shows hyperuricemia and joint effects.
Usually seen in men in their 30’s – 50’s
But, MANY individuals have hyperuricemia, - most do not develop gout
158
patho of gout
Is a disorder of purine metabolism that results in elevated serum uric acid levels.
Primary = 90% of gout; is likely a result of enzyme defects that result in overproduction, inadequate elimination, or both
Secondary = increased breakdown of nucleic acids, as when rapid tumor cells are broken down from treatment of lymphoma or leukemia
Also seen with some diuretics and chronic kidney disease
159
patho pt 2 gout
Monosodium urate crystals precipitate within joints and initiate the inflammatory response
Usually occurs in peripheral areas of the body, very often the great toe
Over time, small, hard nodules called microtophi accumulate in the synovial lining and joint cartilage
The inflammatory process continues, and eventually causes destruction of the cartilage and bone
160
tophi
Repeated attacks lead to the formation of large, hard, nodules with irregular surfaces in synovium, helix of the ear, olecranon bursa, and the Achilles’ tendon
161
manifestations of gout
Acute “attacks” are usually monoarticular – and the person reports sudden, severe pain
Most often in great toe, but also instep, wrist, tarsal joints, knees, elbows, and ankles
The affected area will appear red, swollen, warm, and will be EXTREMELY tender to touch
Attack may begin at night, or after excessive exercise, foods, medications, alcohol, and dieting
162
diagnosis of gout
Health history, risk factors, pain assessment, joint assessment
Serum uric acid level greater than 7.5 mg/dL
Increased WBC and ESR during attacks
24-hour urine collection to assess uric acid excretion
*Definitive = Joint fluid analysis – will show urate crystals
163
management of gout
For acute attacks = analgesics, NSAIDs, corticosteroids, and colchicine
Prevention between attacks – aim to normalize uric acid levels with drugs like allopurinol
Non-pharmacologic approaches include weight loss, dietary modification (decrease alcohol and purine-rich foods)
Maintain high fluid intake if risk for kidney stones
164
rheumatoid disease management
Group of chronic, systemic disorders
Characterized by diffuse inflammation and degeneration in the connective tissue
Clinical course of exacerbations and remissions
An autoimmune reaction in the synovial fluid
Most frequently diagnosed 35 – 50 years of age
Affects 1% of general population
Affects females disproportionally
Cause ? immunologic abnormalities? environmental triggers?
165
human response to rheumatoid disease
```
Fever
Fatigue
Anemia
Scleritis
Neuropathy
Pericarditis
Splenomegaly
Weight change
Lymph node enlargement
Sensory changes of extremity
Raynaud’s phenomenon: Cold- and stress-induced vasospasm
Sjögren’s syndrome
Dry eyes and mucous membranes
Rheumatoid nodules
Non-tender, movable; found over bony prominences
Joint pain/limited function
Usually begins with small joints: Hands, wrists, feet
Progressively involves:
Knees, shoulders, hips, elbows, ankles, cervical spine, temporomandibular joints
Symptoms are usually acute, bilateral, symmetric
```
166
Rheumatoid arthritis diagnostics
Labs:
Positive rheumatoid factor (~80%)
Anti-citrullinated protein antibodies (ACPA)
Anti-cyclic citrullinated peptide antibodies (Anti-CCP)
Anemia
Elevated erythrocyte sedimentation rate
(aka sed rate or ESR)
C-reactive protein and antinuclear antibody (ANA)
tests may be positive
X-rays may also show classic deformities
Rheumatoid nodules
167
osteoarthritis
```
Most common form of arthritis
Often seen beginning in the late 20’s
and early 30’s
Common by the 40’s and 50’s
May account for more total disability
among elderly than many other diseases
Primary (idiopathic)
No precipitating cause
Secondary
From previous injury or inflammatory disease(s)
```
168
OA human response
Most common form of arthritis
Slow progressive disorder of articulating joints
Breakdown of cartilage causes decrease joint function
Limited systemic manifestations
Primarily in the joints
Hips, knees, cervical and lumbar spine
Due to weight-bearing wear-and-tear
Pain, stiffness
Most pronounced in the morning
Usually relieved with activity in 30 minutes
Functional impairment
169
OA diagnostics
```
Physical assessment
Tender, enlarged joints
X-rays
Narrowing of involved joint space
MRI
Evaluation of entire joint structure
Does not have systemic inflammation
No specific lab markers as with RA
```
170
arthritis nursing goals
```
Education
Optimize functional ability
Manage symptoms (primarily pain)
```
171
arthritis nursing interventions
```
Knowledge
Education for informed decisions/ prevention awareness
Self care
Assist as necessary; encourage independence
Pain
Assess in context; non-pharm measures; analgesia
Mobility
Encourage activity – really!; PT/OT
Fatigue
Allow rest periods
Nutrition
Dietary consult
```
172
arthritis education
```
Allows informed decision making
Recognition of activities that strain joints
Importance of early diagnosis
Disease process/symptom patterns
Correct use of assistive devices
Need for adequate rest periods
Strategies for self care/safety
Good body mechanics
Treatment options
```
173
arthritis nursing diagnosis
At risk for self care deficit
At risk for alterations in comfort: Pain
At risk for alterations in mobility: Impaired
At risk for increased fatigue
At risk for nutritional imbalance
Knowledge deficit: Education on disease process and personal management
174
human response
At risk for self care deficit
Goal: Maximize self care
*interventions -->
Assist patient to identify/recognize self care deficits
Explore alternative, work-around strategies for self care activities
Develop plan based on patient perceptions, priorities and goals
Provide assistive devices as needed
Allow adequate time for self care activities
175
human response
At risk for alterations in comfort: Pain
Goal: Control of pain and discomfort
```
Assess level of pain
Intensity, location, quality, precipitating and relieving factors
Administer medications as prescribed
Anti-inflammatory
Analgesics
Anti-rheumatic
Comfort measures
Application of heat/cold, massage, position changes, rest, supportive pillows, splints, relaxation techniques
Encourage rest of painful joints
Emphasize good body mechanics
Limit strain on non-affected joints
Encourage proper weight
Emotional support
Education on pathophysiology of disease
Enhance understanding to promote making educated choices for treatment
Encourage use of non-pharmacological pain-relief
Meditation, visualization, distraction
```
176
human response
At risk for alterations in mobility: Impaired
Goal: Maximize mobility
```
Assess ROM of all affected joints
Perform functional mobility test
Gait, ability to sit and rise from seated position, step into/out of tub, negotiate stairs
Assess need for OT, PT
Teach AROM and PROM exercises
Low impact aerobics
Plan for rest periods
```
177
human response
At risk for increased fatigue
Goal: Control level of fatigue
Education on fatigue
Relationship of disease activity to fatigue
Identify helpful comfort measures
Education on energy conserving techniques
Assist patient in ID’ing fatigue triggers
Facilitate activity-rest schedule
Encourage adherence to the treatment program
Encourage adequate nutrition
178
human response
At risk for nutritional imbalance
Goal: Maintain nutrition and appropriate weight
Obtain dietary history
Education on nutrition
Emphasis: vitamins, protein, iron for tissue building and repair
Monitor increased appetite as a side effect of medication
Consider small, frequent feedings, especially if anorexic
Consider exogenous vitamins
Vitamin D and calcium
179
human response
Knowledge deficit: Education on disease process and personal management
Goal: Education to allow development of personal self care strategies
Distinguish between “routine” side-effects and “emergent” side-effects of medication
Symptom management for “routine” side-effects of medication
Recognition of and action for emergent side-effects of medications
GI bleeding, rashes, respiratory distress, jaundice, tarry stool, localize/systemic infection
180
Human Response
At risk for alteration in body image
Goal: Reduce internal conflict over body image; reduce risk of social hibernation
Help patient identify issues of control over disease, symptoms, treatment
Emotional support
Identify area of life affected by disease
Develop plan for managing symptoms
Enlist support of family, friends to promote daily life
