Chapter 8 Flashcards
How is immobility treatment gauged?
By improvement in function
Definition of immobility
A limitation in independent, purposeful physical movement; it is a measure of function (or lack of), not a dz
Importance of small improvements
Can decrease incidence and severity of complications, and improve function, sense of well being, caregiver burden
Musculoskeletal causes of immobility
Arthritides Osteoporosis Fxs (esp hip and femur) Podiatric problems Other (e.g., Paget's dz)
Neurological causes of immobility
Stroke Nl pressure hydrocephalus Parkinson's dz Dementia Other (cerebellar dysfunction, neuropathies)
Cardiovascular causes of immobility
CHF (severe- low output/perfusion)
Coronary artery dz (frequent angina)
Peripheral vascular dz (frequent claudication)
Pulmonary causes of immobility
COPD (severe)
Sensory factors in immobility
Impairment of vision, proprioception, touch
Fear (from instability and fear of falling)
Environmental causes of immobility
Forced immobility (in hospitals and nursing homes) Inadequate aids for mobility
Other causes of immobility
Acute and chronic pain
Malnutrition
Severe systemic illness (e.g., widespread malignancy)
Depression
Deconditioning (after prolonged bed rest from acute illness)
Drug side effects (e.g., antipsychotic-induced rigidity
Apathy, fear of falling, lack of motivation
Skins complications of immobility
Pressure ulcers
MS complications of immobility
Muscular deconditioning and atrophy
contractures
Bone loss (osteoporosis)
Cardiovascular complications of immobility
Deconditioning
Orthostatic hypotension
Venous thrombosis, embolism
Pulmonary complications of immobility
Decreased ventilation
Atelectasis
Aspiration pneumonia
GI complications of immobility
Anorexia
Constipation
Fecal impaction, incontinence
GU complications of immobility
Urinary infection
Urinary retention
Bladder calculi
Incontinence
Metabolic complications of immobility
Altered body composition (e.g., decreased plasma volume)
Negative nitrogen balance
Impaired glucose tolerance
Altered drug pharmacokinetics
Psychological complications of immobility
Sensory deprivation
Isolation
Delirium
Depression
Hx components in assessment of immobile geriatric pts
Medical conditions contributing to immobility
Nature and duration of disabilities causing immobility
Pain
Drugs that can affect mobility
Motivation and other psychological factors
Environment
Two things to check in the start for PE
Skin
Cardiopulmonary status
MS examination
Muscle tone and strength; symmetry
Joint-ROM; heat; swelling; deformity; erythema; crepitus; mono-poly; large vs small; symmetry
Foot deformities and lesions
Neuro exam
Focal weakness
Sensory and perceptual eval
Affect, cognition
Levels of mobility
Bed mobility Ability to transfer (bed to chair) Wheelchair mobility Standing balance Gait Pain with movement
General assessment of immobile pts
Ascertain pts perceived cause; there is frequently some volitional component, need pt education!
Assess mood and fear (subjective) and affect (objective); fear may be denied, ask caregivers
Assess nutrition, protein, and vit D levels
Pt function with reevaluations
Lab assessment
ESR- helpful in following pts with PMR; nonspecific (infection, malignancy)
Rheumatoid factor- false positives (rate increases with age); false negatives (esp early in process)
Uric acid- blood levels may support suspicion, but: crystals in synovial required for diagnosis of gout, CPPD
ANA: sensitive for autoimmune dz; positive only 20-30% for RA
Anti-CCP: specific and sensitive for RA
Maxims of immobility managment
Goal driven (prevention of complication, optimize function and mobility)
Target diseases and disabilities (by diagnosis)
Multispecialty involvement (PT, OT)
Frequent reassessment
Environmental manipulation
Algorithm for joint pain
Is it joint or periarticular (tendonitis, bursitis) or polymyalgia?
Is it monoarticular (OA) or polyarticular?
Is it inflamed or not?
Is it acute onset, 1st M-T? Think gout
If more muscle than joint, think PMR
Monoarticular joint pain
Inflammatory- consider: -Gout -CPDD (pseudogout) -Septic arthritis Noninflammatory- consider: -Osteoarthritis
Polyarticular joint pain
Inflammatory- consider:
-Rheumatoid arthritis
Noninflammatory- consider hx:
-Osteoarthritis
What is the most common joint disease?
`Osteoarthritis
The major cause of knee and hip pain in the elderly
Characteristics of OA
Cartilage destruction
Osteophyte formation
Loss of joint space (in wt-bearing joints)
Insidious, brief morning stiffness, crepitus
Usually 1 or few joints, not polyarthritis
Dx of OA
X-ray
Wt-bearing film shows narrowed joint space;
U/s, MRI more accurate, comprehensive, but more expensive
Tx of OA
Nonpharm- wt loss, PT, exercise, ice, heat
Pharm- APAP, NSAIDs, intra-articular steroids, glucosamine +/- chondroitin controversial, visco-supplementation (intra-articular injections of hyaluronan or hyaluronic acid polymers)
Surgical: joint replacement, arthroscopy
Vit D, glucosamine, chondroitin of doubtful benefit
What is helpful in diagnosing other arthritides?
Synovial fluid analysis Joint X-ray ESR H/h (anemia in RA and PR) Anti-CCP RF
Onset of RA
Usually age 20-40, but may have new onset of RA in elderly (20% of all cases)
What RA affects
PIP (ulnar deviation) MCP Wrist Elbow Shoulder TMJ C-spine Hip Knee Ankle MTP
Characteristics of OA
Inflammatory Polyarticular With symmetry Joint synovitis Prolonged morning stiffness
Lab findings in OA
RF usually, but not always, elevated, esp early
Diagnostic criteria for RA
Must have 5 of 7, 1st 4 continuous for >6 wks Morning stiffness (1 hr or more) Arthritis of 3 or more joints with swelling or fluid Swelling of 1 or more wrist, PIP, MCP joints Symmetrical joint swelling Positive serum RF Rheumatoid nodules (sub-Q, hands, fingers, knuckles, elbows) X-ray: erosions, decalcification in affected joints
Labs in RA
H/h frequently normochromic, normocytic anemia, thrombocytosis ESR, CRP elevated: not specific RF sensitivity only 70-80% Anti-CCP sensitive; specificity >90% ANA not sensitive; shows autoimmune SLE
Radiography of RA
Plain films of hands, wrists, feet initially
Lack of bony remodeling, symmetric joint space narrowing
Cortical bone erosions: indistinct margins, dot-dash pattern of cortical loss
Periarticular osteopenia
RA tx goals
Control pain
Maximize functional status
Modify disease
Advanced age doesn’t necessarily preclude use of DMARDS
RA management
Think both symptomatic management and dz-modifying
Don’t wait to start DMARDs (N-B first) 1st 2-3 mos
DMARDs from different classes additive
Refer to rheumatologist if ongoing active disease > 3 mos maximal therapy
Use steroids only for brief flare sx; but low dose c-s effective, and better than NSAIDs
Think med-induced gastritis; PPIs, surveillance, caution in Hep C, or liver dz
Screen for latent TB if using TNF inhibitors
When is PMR most common?
Older women
What is PMR associated with?
Temporal arteritis, esp when ESR >75 mm/h
Untreated, can lead to blindness
Biopsy the temporal artery; treat aggressively
Prognosis of PMR
Tends to be self-limited 1-2 yrs
Lab findings of PMR
Increased ESR
Anti-CCP usually neg
Dx of PMR
Clinical; immediate response to corticosteroids confirms
Findings of PMR
Prolonged morning stiffness Wt loss Fever Muscle pain Symmetry Hip Shoulders
Tx of PMR
Prednisone 10-20 mg/day
Most will need Rx for >2 yrs then taper off; may relapse
Inflammatory vs Noninflammatory
All newly inflamed joints with significant effusion should be tapped, cultured (with Gram stain) to r/o infection, a cause of osteomyelitis, joint destruction
OA usually not associated with inflammatory response, RA and PMR always are
First line treatments for OA, RA, PMR
OA: NSAIDs or other anti-inflammatories
RA: DMARDs
PMR: steroids
