Exam IV Study Guide Flashcards
DVT
40-90% of all patients
Signs and symptoms
Swelling
Erythema
Pain
Homan’s sign (but not on its own)
Point tenderness in calf
Avascular Necrosis
Hip is most common joint
-Men ages 30-60 years
-*Trauma
-Long term steroid use
-RA/Lupus
-Alcoholism
Avascular Necrosis Symptoms
Antalgic gait
Pain in the groin down to medial knee
Throbbing deep hip pain
Restricted hip internal rotation, flexion, and abduction
Hip Osteoarthritis
Osteoarthritis: focal loss of articular cartilage with variable subchondral bone reaction. Joint pain and functional impairment seen.
Hip Osteoarthritis conservative treatments
Gait and balance training
Manual therapies
Systematically progressed therapeutic strengthening, flexibility and endurance, (Keeping an eye on symptoms)
Anterior THA
Access b/t sup gluteal & femoral nerves
Possibly assoc’d w/:
-Fewer dislocations
-Less time in hospital
Relatively muscle-sparing
Femur less exposed
-Could make it difficult to place hardware
Posterior THA
most common, Good femur visibility during procedure, Deep ER muscles get cut, May increase dislocation risk, May compromise sciatic nerve, No ABD muscle cuts, Preserves frontal plane gait mechanics.
Lateral/Direct lateral THA
Glut med and min reflected away from troch
Allows for better distal access if necessary
More proximal access from the entry point could risk neurovascular compromise
Again, dislocation risk lower than that for posterior approach
Frontal plane gait problems are possible
Greater Trochanteric Bursitis
Common in active patients
Bursa irritated from excessive compression/friction
Greater Trochanteric Bursitis treatment
Relieve pain and inflammation (rest, ice, NSAIDs)
Eliminate activities that make it worse
Focus on functional exercise
If truly shortened, stretching is advocated (Glutes/TFL)
Ischial bursitis (Weaver’s bottom)
Pain over the ischial tuberosity
Caused by direct pressure from prolonged sitting
Can mimic a hamstring strain
Affects thinner people and cyclists
Ischial bursitis (Weaver’s bottom) interventions
Rest, ice, NSAIDs
Injection with corticosteroids
Muscle strain acute phase rehab
1-7 days
-Initial: cold prn pain
-Avoid motions that cause pain (crutches may be used)
-Sleeping with pillows under both knees to support the injured limb
-PRICEMEM
-Painless PROM or AAROM
Muscle strain sub acute phase rehab
1-3 weeks
-Begin AROM and initiate strengthening
-Aquatic therapy to decrease weightbearing loads
-Pain free submaximal isometrics
-Pain free concentric (AROM)
-UE strengthening
-CV training- swimming with pull buoy
Muscle strain repair phase rehab
3-8 weeks
Isometric contractions at 100% without pain
No pain on full ROM
Minimal to no pain with palpation
muscle strain repair/function phase rehab
8 weeks-6 months
-Normal gait pattern without pain
-Begin fast walking
-Once ambulating 30 min at fast speed without pain, jogging can begin
-Once jogging 30 min, sprinting can begin
-Then adapt to sport/function
2 types of hamstring strain
High-speed running (biceps femoris)
-Associated with recurrence
Extensive lengthening, e.g. kick motions (proximal semimem)
-Associated with prolonged RTS
MCL Sprain (Grade I, II, III)
Mechanism = valgus force or tibiofemoral (external) torsion
Esp. w/ planted foot
Grade I = pain, but minimal tearing
Grade II = Grade I + partial macroscopic tear, swelling, ↓ ROM
-Medial capsular ligament involvement
Grade III = Grade II + complete tear; marked instability, swelling, and loss of ROM
-Possible ACL and PCL involvement
Grade I MCL management
Crutches if needed, progressive ROM & exercise as permitted by pain
RTP by 1 month
Grade II MCL management
-Crutches during acute phase
Splint or immobilizer (< 1 week)
-Progress from isometrics to full-range resistance as pain allows
-Use brace when running
Grade III MCL management
Conservative care if isolated (plan on ~ 7 weeks for return to activity)
Surgical repair more if ACL or PCL involved
LCL Sprain
Mechanism = varus force, esp. when tibia is internally rotated
Managed similarly to MCL injury, but with prolonged timeframe (~ 6 months) for conservative care
ACL Sprain
Mechanism = Noncontact with multiplanar forces (e.g. valgus collapse); other mechanisms possible
Risk factors include female gender, fatigue, various weakness, alignment, laxity, and/or joint position sense characteristics
ACL Injury Management
Conservative and surgical (repair/reconstruction) approaches are both common
-Highly dependent on patient & nature of injury
Return to activity may range 2 – 6 months
PCL Sprain
Mechanism = fall on bent knee or direct, posteriorly-oriented blow to proximal anterior tibia
Favorable outcomes with conservative management for grade I and II
If surgically repaired, patient may be immobilized in extension for 6 weeks, followed by ROM, and finally PRE at ~4 months.
Meniscus injuries
medial more commonly injured than lateral, mechanisms of injury are femur-on-tibia internal rotation with planted foot and forced knee extension while tibia is rotated
Surgical resection more common than repair
-Partial meniscectomy preferred
Resistance exercise at full ROM ~ 6 weeks
Plica
Plica (synovial folds) are vestiges of embryological cavities, inflamed or damaged plica may cause, catching, snapping, pain going up/down stairs.
If serious, can be resected; otherwise, rest
Osteochondritis Dissecancs
Usually refers to floating piece of articular cartilage
-May involve other soft tissue like meniscus or synovium
In children, conservative care may be sufficient
In adults, surgery more likely
Patellofemoral Pain Syndrome
General label describing many kinds of anterior knee/patellar pain, often associated with lateral patellar tracking, activity modification should be first approach
Chondromalacia Patella
Deterioration of posterior patellar cartilage
-Progresses from swelling/softening to cartilaginous fragmentation
will lead to arthritis if not addressed
Earlier on, conservative care may work
-Activity modification, anti-inflammatories
Sometimes, surgical realignment, resurfacing, or even patellar removal will be necessary
Patellar Subluxation/Dislocation
May occur as a result of forceful plant-and-twist maneuver (e.g. cutting), or direct trauma
Repeated subluxations may compromise capsule and restrict ROM
Dislocation (lateral)
-Painful
-Requires reduction followed by extension immobilization for a month
Osgood-Schlatter
Tibial tubercle avulsion fracture caused by repetitive tensile stress
Usually occurs in youth and is resolved by growth of a callus
End result is a larger-than-normal tubercle
Conservative management
Larsen-Johansson
Like osgood schlatter but its at the apex of the patella, conservative management
Jumper’s Knee
Overuse-mediated degeneration anywhere along the patellar tendon
Early on, pain after activity
As it progresses, pain becomes more intense and/or more constant
Management involves decreasing training volume, reducing pain, and graded exercise w/ eccentric contraction modes
Knee Osteoarthritis risk factors
Age
Sex
-Females @ greater risk (65+)
-Males @ greater risk before age 50
Previous knee injury
Obesity
Malalignment(s)
-Varus/valgus
-Recurvatum
-Patellar tracking
Occupation
Knee OA idiopathic
There is probably a mechanism, but TBD
Possible involvement of genetics
Knee OA post-traumatic
Fracture or soft tissue injury
Can include consequences of surgery (e.g. meniscectomy)
Knee OA inflammatory
Pigmented villonodular synovitis
Psoriatic arthritis
Knee OA hemophilic
Caused by hemarthrosis-mediated degeneration
Primary prevention is best (only) strategy, but $$$ and requires extreme vigilance
Onset may be early (20s, 30s), and often TKA will be required
Stemmer’s Sign
A thickened skin fold at the base of the second toe or second finger that is a diagnostic sign for lymphedema
A positive result occurs when this tissue cannot be lifted but can only be grasped as a lump of tissue
In a negative result, it is possible to lift the tissue normally
Complete Decongestive Therapy (CDT)
Manual lymphatic drainage (MLD)
Short-stretch multi-layer bandaging
Limb Clearing Exercises/HEP
5 consecutive treatment days a week for 2-6 weeks.
Comprehensive Lymphedema Management
Education on basic anatomy, skin care, self-massage, self-bandaging, garment care, and infection management
Psychological and emotional support
Custom compression garments (20 mm hg-60 mm hg)
Complete Decongestive Therapy (CDT) phase one
Phase One – decongestive phase (2-6 weeks)
-Mobilize edema
-Decrease volume/circumference as much as possible
-Limit fibrosclerotic tissue
Complete Decongestive Therapy (CDT) phase two
self care (ongoing)
Maintain gains made in Phase One
Limit exacerbation of sx
Manual Lymph drainage
a gentle, manual treatment technique consisting of several basic strokes, designed to improve the activity of intact lymph vessels by providing mild mechanical stretches on the wall, does not kneading elements and is generally applied suprafascially, whereas massage is usually applied to subfascial tissues.
Manual lymph drainage indications
Edema
Swelling
Sports injuries High output failure
Arthritis
Wounds
Lymphedema
CRPS
Combined Insufficiency
Combination of a high output failure and a low output failure
-High output failure due to infection, trauma or surgery
-Low output failure due to previous injury to lymph vessels or nodes, i.e. radiation therapy
Stagnation or a blockage of lymph
immunoglobulins prevented from reaching the sites where they can perform their immune functions
Kinmonth syndrome
inguinal lymph node fibrosis
Primary lymphedema: Milroy disease
observed at birth due to gene mutation- RARE
Primary lymphedema: Lymphedema Praecox
developed before 35 y/o
Primary lymphedema: Lymphedema Tarda
developed after age 35
Symptoms of Lymphedema
Tightness/heaviness/discomfort in the area
Not usually painful
Swelling and decrease in skin mobility
Loss of strength or flexibility in a limb
Variations in skin temperature and/or color
Lipedema
Painful “Fluid in the fat” disorder
Feet are not involved
Stewart-Treves syndrome
Rare angiosarcoma that develops in people with long-standing lymphedema.
Usually people have a hx of breast CA that was treated with radical mastectomy.
Stage 0 or Latent lymphedema
lymph transport is impaired, but there is no clinical evidence of swelling. May last months or years.
Stage I lymphedema
chronic inflammatory response to the excessive protein in the interstitium
pitting on pressure
reverses with elevation
Subcutaneous tissues begin to fibrose due to protein buildup, progressing the lymphedema from Stage I to II.
Stage II lymphedema
Non-pitting
Does not reduce on elevation of the limb
Clinical fibrosis is present- skin is thick and rigid
Clear, sticky lymph fluid may ooze from pores
Chronic inflammation can lead to recurrent bacterial and fungal infections
Stage III lymphedema/ lymphostatic elephantiasis
severe non-pitting
Large lobular folds
fibrotic edema with atrophic skin changes such as thickened, leathery, keratotic skin, skin folds with tissue flaps, papillomas (warty like overgrowth)
Functional Severity: Minimal
less than 3cm difference between limbs
Less than 20% increase in limb volume
Functional Severity: Moderate
3-5 cm difference
20-40% increase in volume
Functional Severity: Severe
> 5 cm difference AND a positive Stemmers sign
40% increase in volume
