852: peds and non MSK knee conditions

Osgood schlatter disease medical diagnosis

• juvenile osteochondrosis of LE excluding foot

• Tibial apophysitis

• Tibial tubercle apophysitis

Osgood schlatter disease PT diagnosis

May include knee flexion, dynamic knee valgus

Osgood schlatter disease Pathobiological mechanisms

It’s a traction apophysitis of the tibial tuberosity

• inflammation at the growth region of the bone due to repetitive pulling and strain

Occurs during periods of rapid growth

• quads activation causes increased stress into the patellar tendon insertion onto the partially developed part of the tib tube

• May cause softening and partial avulsion of the growth plate at the tib tube

Osgood schlatter disease Potential pertinent history

• reports recent spike in growth

• Involved in multiple sports

• Especially with running, jumping, gymnastics, football, basketball

Osgood schlatter disease Potential predisposing factors

Age: during growth spurt

• females: 8-13

• Males: 10-15

Symptoms of Osgood schlatter disease

Pain over tibial tuberosity, distal patellar tendon

Thickening, swelling over tibial tuberosity

Osgood schlatter disease Symptom descriptors

Dull to sharp aching

Osgood schlatter disease Aggravating factors

Running, jumping, squatting, stairs, kneeling, cutting activity

Osgood schlatter disease Easing factors

Rest, ice, knees positioned in passive extension

Osgood schlatter disease 24 hr pattern

Increased symptoms with increased activity

Osgood schlatter disease Objective exam: observation

Swelling, thickening over distal patellar tendon at tibial tuberosity

Ankle/foot malalignment, or motor control deficits could be present

Osgood schlatter disease Objective exam: palpation

Pain with palpation over tibial tuberosity

Osgood schlatter disease Objective exam: flexibility/muscle length

Likely length deficits in rec fem, HS, and gastroc

Osgood schlatter disease Objective exam: joint mobility

May have hypomobility in all directions with PF joint

Osgood schlatter disease PT management

Requires activity modification

• load reduction, reduce pain and stay active

Stretching to quads or other LE musculature with flexibility deficits

Manual therapy

• soft tissue mobs, joint mobs to PF joint, ankle, foot, or hip

Strengthening once symptom irritability and intensity improves

Appropriate progression towards return to sport

Osgood schlatter disease Medical management

• pharm: NSAIDs or acetaminophen as needed

• Surgery: not needed

• Conservative: activity modification, ice, brace

• Imaging: radiographs

Sinding Larsen Johansson disease

Palpation tender over inferior patellar pole - thickening/swelling noted here

Salter Harris fracture

Physeal growth plate fracture

• more common in sports

• Concerning due to risk of impeding growth progress

Type II salter-Harris fracture

Fracture line runs along physis through metaphysis, but the epiphysis is not involved

• bony fragment of metaphysis is formed

Type I and II usually heal well

Usually only require casting/immobilization

May occasionally need closed reduction

Type III and IV involve growth plate AND the joint surface which leads to a higher complications rate

• can result in permanent damage to growth plate if not identified and treated promptly

• Typically need surgery to fixate in correct anatomical alignment

Salter-Harris fracture symptoms

• inability to WB on involved side

• Localized joint pain

• Swelling, tenderness at the physis

PT management of salter Harris fracture

• occurs after casting/surgery

• ROM not often limited, and typically is regained quickly

• Focus on improving strength and mobility

• Gait, balance, proprioceptive training

2+

Score indicates DVT likely

Score of 1 or less

Should still refer for d-dimer testing

Wells Criteria for DVT

• active cancer

• Paralysis of lower extremities

• Recently bedridden for 3 days or surgery within 12 weeks requiring anesthesia

• Localized tenderness along distribution of the deep venous system

• Entire leg swollen

• Calf swelling at least 3 cm larger than other side

• Pitting edema

• Collateral superficial veins

• Previously documented DVT

Vascular claudication

• due to atherosclerotic build up in the arteries or veins causing partial or complete occlusion

• Atherosclerosis is a complex inflammatory response between vascular cells, thrombotic factors, cholesterol, and inflammatory mediators

Neurogenic claudication

• due to neural tissue irritation, usually occurring at the nerve root

• Inflammation from repeated mechanical irritation

• Ischemia due to degenerative changes: disc bulge, osteophyte formation, ligamentous thickening

• Usually BL

Vascular claudication predisposing factors

• > or = 40-60

• Males > females

• Lumbar stenosis

• Advanced DM

• Smoking

• HTN

• Hypercholesterolemia

• Obesity

Neurogenic claudication predisposing factors

• > 60

• Diagnosis of lumbar spinal stenosis

• Spina bifida

• RA

• Paget disease

• Ankylosing spondylitis

Vascular claudication symptoms

• cramping sensation

• Fatigue

• Weakness

• Paresthesias

• Activity dependent: all exercise induced

• Usually BL

• Many patients deny pain

Neurogenic claudication symptoms

• burning pain

• Paresthesia

• Weakness

• Symptoms in legs, back, and or buttocks

• Position dependent > activity dependent

Vascular claudication aggravating factors

Exercise, walking uphill, stairs, elevating legs during rest

Easing factors for vascular claudication

Rest and dangling legs off edge of bed/couch

Aggravating factors for neurogenic claudication

Walking, extending spine, less painful when walking uphill

Easing factors for neurogenic claudication

Trunk flexion in standing or sitting, laying down

Vascular claudication objective exam

• may see decreased pedal pulses

• Color, changes

• Decreased temp, dry, scaly, or shiny skin

• Ankle brachial index < 0.9

• Differentiating tests: bicycle test of van gelderen and two stage treadmill test

Neurogenic claudication objective exam

• normal pulses

• +SLR

• Familiar leg symptoms with lumbar extension, extension quadrant AROM

• Lumbar flexion decreases symptoms

• May have + neuro exam for multiple segments

Vascular claudication medical management

• imaging: Doppler ultrasonography, MRA

• Pharm management to address comorbidities

• Patient education

• Supervised exercise therapy programs

Supervised exercise therapy program for vascular claudication

• treadmill walking program

• 3x week for 12 weeks

• Walking to onset of moderate claudication symptoms, rest, repeat for 30-60 mins

• Stretching, strengthening in addition to walking program beneficial

Neurogenic claudication medical management

• imaging: MRI, CT, NCV or EMG testing

• Conservative and non surgical methods preferred initially

• PT: stretching, strengthening, aerobic fitness, manual therapy

• Anti inflammatory meds, gabapentin, epidural steroid injections

Mechanisms of Baker’s cyst

• synovial fluid filled mass in popliteal fossa

• Enlargement of bursa that is located beneath medial gastroc or semimembranosus

• Chronic effusion that herniates between the heads of the gastrocs

Baker’s cyst predisposing factors

• adults 35-70

• History of trauma or injury to the knee

• Often present with concurrent degenerative joint disease in the knee

• May be asymptomatic and incidental finding

• RA

Bakers cyst symptoms

• tightness

• Pain

• Swelling more visible in knee extension

• Symptoms tend to be in posterior aspect of the knee

• Pain increases with activity

• May limit knee ROM

Bakers cyst objective exam

Palpable and visible mass in posterior aspect of knee near popliteal fossa

Bakers cyst management

• imaging: radiography, ultrasonography, MRI

• Conservative: rest, activity modification, and NSAIDs

• PT: focus on stretching, ROM, manual therapy, strengthening as appropriate

• Corticosteroid injections

• Ultrasound guided aspiration

• Surgery: arthroscopic debridement, open excision