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• GREEN
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• Intro:
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- Muscle / tendon strain is equivalent to ligament sprain in terms of injury type
- Happens when muscle fibres are overworked, resulting in fibre tearing |
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• Aetiology (risk factors):
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- ↑ incidence in athletes
- Commonly occurs when there's sudden ↑ in duration, intensity, or frequency of activity 3 types of muscles at risk: - Two-joint muscles: motion at one joint can ↑ passive tension, leading to overstretching injuries - Eccentric contractions:. common during deceleration phase, may change muscle tension & cause myofibril overload injuries - Muscles w/ ↑ % of type II fibres: fast-twitch muscles w/ high-speed contractions, making them more prone to injury (running & sprinting) → Hamstrings, gastrocnemius, quadriceps, hip flexors, hip adductors, ES, deltoids, & rotator cuff |
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• Pathophysiology:
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- Contraction induced injury caused by extensive mechanical stress
- Often occurs due to powerful eccentric contractions or over-stretching of the muscle Muscle lesions are classified as grade I, II, & III Grade I (mild): - Affect a limited number of muscle fibres - No decrease in strength - Full AROM & PROM - Px & tenderness may be delayed to the next day Grade II (moderate): - Nearly half of muscle fibres torn - Acute & significant px - Accompanied by swelling - Minor decrease in muscle strength Grade III (severe): - Complete rupture of the muscle - Tendon separated from the muscle belly or muscle belly torn in 2 parts - Severe swelling & px - Complete loss of function |
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• Sx & Ssx:
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- Swelling, bruising, or redness
- Px at rest - Inability to use the muscle at all - Weakness of muscle or tendons |
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• Management:
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- First phase: protection, rest, ice, compression, elevation (PRICE) & NSAIDs
- Second phase: mobilisation should occur ASAP but gradually & within limits of px, Mobs/Drops, low impact exercises - 3-6 weeks for the muscle fibres to recover = full ROM, pain free, & 90% strength bilaterally - Third phase: proprioceptive & endurance, SMT / STW, TrPs |
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• YELLOW
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• Intro
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- Degenerative bone condition resulting from the death of bone cells due to disruption in the subchondral blood supply
- Also known as AVN, aseptic necrosis, & ischemic bone necrosis - Typically affects the epiphysis of long bones at WB joints, w/ severe cases potentially causing subchondral bone destruction or joint collapse - Common sites include femoral head, knee, talus, & humeral head - Less common occurrences in other bones like the carpus & jaw |
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• Aetiology (risk factors):
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- 30-65 yrs
- M>F - Females more at risk w/ PMHx of lupus 6 groups of risk factors: - Direct cellular toxicity: chemo/radiotherapy, thermal injury, smoking - Extraosseous arterial fracture: hip dislocation, femoral neck fracture, iatrogenic post-surgery, congenital arterial abnormalities - Extraosseous venous: venous abnormalities, venous stasis - Intraosseous extravascular compression: haemorrhage, elevated bone marrow pressure, fatty infiltration of bone barrow due to prolonged high-dose corticosteroid use, cellular hypertrophy & marrow infiltration (Gaucher disease), bone marrow oedema, displaced fracture - Intraosseous intravascular occlusion: coagulation disorders (thrombophilias & hypofibrinolysis), sickle cell crises - Multifactorial |
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• Pathophysiology:
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1. Reduction in subchondral blood supply
2. Induces hypoxia 3. Loss of cell membrane integrity 4. Necrosis of cells (osteonecrosis) |
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• Clinical & physical exam presentation:
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Non-traumatic cases:
- Mechanical px w/ variable onset & severity - Difficult to localise - Normal physical exam in early disease (causing delay in Dx) - Focused Hx considerations: recent trauma, steroid use, autoimmune disease, Sickle cell, alcoholism, tobacco use, manual labour, change in gait, connective tissue disorders, insidious onset px, decreased ROM AVN of the hip: - Early stages often asymptomatic - Hip & groin px - Late-stage. progression indicated by px at rest - Associated Ssx: referred px in buttock & thigh, stiffness, changes in gait AVN of the knee: - Acute onset knee px while WB & at night - Typical responses in Hx: osteoporosis or osteopenia, no recent trauma - Physical exam findings: px w/ palpation over medial femoral condyle, decreased ROM AVN of the talus: - Associated w/ polyarticular disease & trauma - Complaints of px & difficulty ambulating beyond expected recovery time post-trauma |
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• Diagnosis:
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MRI findings:
- Osteosclerotic changes - Decreased bone resorption due to disrupted osteoclast function - Low on T1 (fat is white) - High on T2 (fat is dark) |
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• Complications:
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Postoperative complications:
- Surgical site infection - Prosthesis malfunctions - Neuromuscular compromise |
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• Management:
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- Pharmacological therapy in early stages
- Surgery - Exercises to maintain joint mobility & strengthen muscles around - Later in therapy implement endurance & coordination training - Post-surgery & recovery full conservative care |
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• Ddx:
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- OA
- Osteoporosis - Osteomyelitis - Neoplastic bone conditions - Inflammatory synovitis - CRPS - Soft tissue trauma |
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• YELLOW
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• Intro:
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- Swelling or inflammation of a bursa
- Bursae are found near bony provinces & between bones, muscles, tendons, & ligaments (approx. 150 facilitate MSK movement) - Bursitis causes the bursa to enlarge w/ fluid, resulting in px w/ movement & pressure - Not all forms of bursitis are due to 1° inflammation, some result from swelling due to a noxious stimulus |
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• Aetiology (risk factors):
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- Overuse of the joint
- Repetitive strain: picking up & lifting heavy loads - Trauma: falling / bumping against things - Pressure: "student's elbow" & "housemaid's knee" - Bacterial infection: unattended wound (causing septic bursitis) - Other inflammatory disease: e.g. Gout (crystals can form in the bursa & cause inflammation) - Immunocompromised individuals: diabetes, rheumatological disorders, alcoholism, or HIV, are at risk of septic bursitis |
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• Pathophysiology:
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- Bursa is a synovial lining sac
- Collapses upon itself until triggered, leading to irritation & filling with synovial fluid - Px occurs when the inflamed bursa is compressed against bone, muscle, tendon, ligaments, or skin - Not all bursitis is linked to an overt inflammatory process - Subacromial bursa examination shows ↑ inflammatory mediators |
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• Clinical presentation:
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- ↓ ROM due to px in involved joint
- Px with AROM, but not w/ PROM in some cases - Two forms of bursitis: acute & chronic Acute: - Caused by trauma, infection, or crystalline joint disease - Pts experience px on palpation of bursa - Px w/ FX, but no px w/ EXT in certain types (e.g. prepatellar & olecranon bursitis) Chronic: - Often results from inflammatory arthropathies & repetitive pressure/overuse - Often painless - Bursa has had time to expand to accommodate increased fluid, resulting in significant swelling & thickening of the bursa |
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• Physical examination:
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- Evaluate skin for trauma, erythema, & warmth
- Temperature increase of 2.2°C over affected bursa compared to unaffected indicative of septic bursitis - Deep bursitis may not show tenderness or obvious skin changes - Normal ROM in septic bursitis |
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• Diagnosis:
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- Plain radiography: recommended w/ Hx of trauma, concern for foreign body, or fracture causing swelling or px
- MRI: for evaluating deeper bursa - US: helpful in differentiating cellulitis from infectious bursitis - Bursa fluid punction: can rule out infections |
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• Management:
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Bursitis w/o infection:- Most often self-limiting
- RICE - NSAIDs - Injections - Mobs - Gradual ↑ in exercise - Immobilising is a risk towards adhesive capsulitis Septic bursitis: - Antibiotics - Aspiration (needle) - NEVER inject w/ steroids - Surgical removal of bursa (in case of tuberculous bursitis) - Surgical incision & drainage |
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• Ddx:
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- OA
- RA - Can mimic other conditions in specific locations (e.g. shoulder - rotator cuff / labral tear) - Pathologies can coexist w/ or precipitate bursitis (e.g. gout) - Ischial bursitis can mimic sciatica (sitting-induced px distinguishes it from sciatica) - Trochanteric bursitis differs from ITB syndrome, w/ tenderness in IT band more distal compared to proximal location of trochanteric bursa - Iliopsoas bursitis can resemble arthritis, overuse injuries, synovitis, labral tears, or AVN - Knee bursitis typically doesn't cause effusion, aiding in differentiation from other knee pathologies - Retrocalcaneal bursitis may initially resemble achilles tendinitis, enthesopathy, px from bone spurs, or plantar fasciitis |
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• GREEN
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• Intro:
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- Self-limiting disorder characterised by deposition of calcium in the tendon / muscle
- Leads to px & reduced ROM |
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• Aetiology (risk factors):
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- 30-50yrs
- F>M - Occupational risk (construction, agriculture, certain sports) - Metabolic conditions (e.g. diabetes) - Mechanical stress: repetitive microtrauma or overuse of tendons - Vascular factors: poor blood supply (reduced clearance of metabolic waste) - Genetic predisposition |
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• Pathophysiology:
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- Repetitive trauma → tendon degeneration → calcification
- Tendon necrosis → intracellular calcium accumulation - Active process mediated by chondrocytes arising from metaplasia → calcium deposition - Phagocytosis of metaplastic areas reforms normal tendon |
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• Clinical presentation:
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- Px w/ or w/o loss of ROM
- Stiffness, usually after periods of inactivity (morning) - Swelling - TTP |
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• Physical examination:
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- Limited ROM
- Crepitus - Muscle weakness - Warmth & redness - Palpable calcium deposits |
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• Diagnosis:
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- X-ray: identify calcifications in the tendon or adjacent soft tissue
- US: visualise extent & characteristics of calcifications & assess tendon thickness - MRI: may be used to evaluate soft tissue involvement & inflammation |
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• Complications:
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- Chronic px
- Tendon rupture - Compression of adjacent structures - Bursitis - 2° OA - Functional impairment - Psychosocial impact - Recurrence |
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• Management:
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- Pts w/ chronic calcific tendonitis often don't respond to conservative care
- Anti-inflammatory NSAIDs (ibuprofen) - Injections - Surgery |
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• Ddx:
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- Adhesive capsulitis
- Tendinopathy - Bursitis - Arthritis - Ossifying tendinitis |
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• GREEN
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• Intro:
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- Non-inflammatory, degenerative joint disease
- Characterised by loss of articular cartilage & marginal hypertrophy of bone - Accompanied by px & stiffness that is aggravated by prolonged activity - Most prevalent type of arthritis |
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• Aetiology (risk factors):
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- Higher age
- F>M - Hx of joint trauma - Obesity - 1° OA: most common subset of OA; absence of predisposing trauma or disease - 2° OA: occurrence w/ pre-existing joint abnormality; Ssx - Modifiable environmental factors: repetitive movements, obesity, metabolic syndrome, smoking, vitamin D deficiency, muscle weakness, low bone density - Commonly affects hands, knees (most common), feet, facet joints, & hips |
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• Pathophysiology:
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- Multifactorial & involves 3 major processes: mechanical degeneration (wear & tear), structural degeneration, & joint inflammation
- Overuse & aging of the joint are believed to be the main contributors, but inflammatory processes indicated by ↑ cytokines are also present - Firstly, OA involves cartilage damage, including surface fibrillation, irregularity, & focal erosions - Then, cartilage damage prompts chondrocyte proliferation, & outgrowths can ossify, forming osteophytes - Later, subchondral bone sclerosis & bone cyst formation occur, potentially increasing joint stiffness & px - Advanced OA may lead to episodic synovitis, & in rare cases, bony erosions can occur in erosive OA |
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• Clinical presentation:
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- Joint px worse w/ use & improves w/ rest
- Px peaks in late afternoon or early evening, also present in the early morning Two types of px: - Dull, aching, throbbing px (predictable & constant over time) - Intense, unpredictable px for short periods Classified into three stages based on px types: - Early OA: sharp, predictable px limiting high-impact activities - Mid OA: constant px, unpredictable joint px or locking, affecting ADLs - Advanced OA: constant dull-aching px w/ intermittent intense episodes, limiting recreational activities Additional joint Ssx: - Tenderness, stiffness, crepitus - Limited ROM - Joint swelling, deformity, or instability |
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• Physical examination:
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- Bony enlargement (commonly in DIP & PIP joint of fingers & toes)
- Crepitus - Effusions (non-inflammatory) - Joint line tenderness - Limited ROM due to px, swelling, or joint deformity Specific bony enlargements: - Heberden's nodes: posterolateral bony swelling of DIP joints - Bouchard nodes: posterolateral bony swelling of PIP joints - OA involving the base of the thumb is described as a "shoulder appearance" or "squaring" |
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• Diagnosis:
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Plain radiographs to grade OA:
- 0: no OA - 1: Doubtful narrowing of joint spaces &/or possible osteophytes - 2: Definite osteophytes & possible narrowing of joint spaces - 3: Multiple osteophytes, definite narrowing of joint space & some sclerosis & deformity of bone ends - 4: Large osteophytes, marked narrowing of joint space, severe sclerosis & definite deformity of bone ends |
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• Complications:
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- Chronic px
- Long-term analgesics use - Reduced joint mobility - Decreased stability & increased fall risk - Joint malalignment - Deformity - Stress fractures - Hemarthrosis - Osteonecrosis - Joint infection - Gout & pseudogout - Depression |
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• Management:
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- Exercise program
- STW - Mobs/drops - SMT - NSAIDs (preferably topical) |
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• Ddx:
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- RA
- Gout - Pseudogout - Septic arthritis - Hemochromatosis - Fibromyalgia - Lyme disease - Ankylosing spondylitis - Psoriatic arthritis - Neuropathic arthropathy - Parvovirus-associated arthritis |
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• YELLOW
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• Intro:
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- Painful inflammation & stiffness of the joints
- Inflammatory arthritis is typically associated w/ classic Ssx of inflammation - Can have various factors - inc. infectious / non-infectious factors - Inflammatory arthritis may or may not be associated w/ systemic features related to the underlying condition causing the inflammation |
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• Aetiology (risk factors):
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- Increasing age
- F > M (autoimmune inflammatory arthritis) - M>F (gout & seronegative spondyloarthritis) - Smoking (strongest environmental factor) - Caucasian, FHx - W/ juvenile idiopathic arthritis presenting before 10 yrs of age |
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• Pathophysiology:
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- Varies depending on the underlying etiology
- External or self-antigens trigger an immune-mediated inflammatory response - Inflammatory cells migrate from the bloodstream into synovial membrane - Hyperplasia of synovial fibroblasts is associated with inflammatory response - Cartilage & bone damage can occur, leading to joint destruction in some cases - Infectious arthritis results from the direct invasion of the joint by infectious organisms - Infectious agents may trigger an immune response, leading to inflammatory arthritis - Autoimmune inflammatory arthropathies involve an interplay of environmental & genetic factors activating the immune system - Crystalline arthropathies involve crystals in the synovial acting as antigens, triggering a neutrophil-mediated inflammatory cascade |
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• Clinical presentation:
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- Disease progression can be chronic & progressive, leading to joint damage, deformity, & disability if left untreated
- Joint px - Joint stiffness - Joint swelling - Warmth & redness - Fatigue - Malaise - Low-grade fever - Inflammatory arthritis often follows a pattern of flares & remissions |
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• Physical examination:
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- Inflammatory eye conditions: uveitis or iritis, common in various types of IA
- Skin rashes: commonly in connective tissue diseases (systemic lupus or psoriatic arthritis) - Enthesitis: inflammation in the sites where tendons & ligaments insert into bones (common in seronegative spondyloarthropathies) - Dactylitis: swelling of an entire digit (common of certain spondyloarthropathies) - Symmetry: common in RA |
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• Diagnosis:
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Labs:
- Elevated inflammatory markers: erythrocyte sedimentation rate (ESR) & C-reactive protein (CRP) - Positive autoantibodies: such as rheumatoid factor (RF) & anti-cyclic citrullinated peptide (anti-CCP) antibodies in RA Plain radiographs: - Initially normal in early inflammatory arthritis - May show periarticular osteopenia at the disease progresses - Periarticular erosions are seen in inflammatory arthritis like RA - Gout erosions are typically juxta-articular/rat-bite erosions w/ overhanging edges - Chondrocalcinosis or CPPD deposition can be easily visualised - Axial spondyloarthropathies can later show 'bamboo' spine & SIJ function & erosions MRI: - Beneficial, especially when radiographs are nondiagnostic - More sensitive than plain film in evaluating synovitis, erosions, sacroiliitis - Higher sensitivity than X-rays |
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• Complications:
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- Arise from delay in treatment or mass Dx
- May lead to aggressive & permanent joint damage - Associated conditions w/ joint damage: chronic gout, RA, seronegative spondyloarthritis - Erosive changes in joints - Interference w/ ADLs |
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• Management:
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- Inflammation is reversible, while joint destruction is not
- Antibiotic therapy - NSAIDs - Education - Manual therapy - Diet - Lifestyle modification |
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• Ddx:
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- RA
- AS - Psoriatic arthritis - Lupus arthritis - Gout - Juvenile idiopathic arthritis - Reactive arthritis - Spondyloarthritis |
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• YELLOW
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- Same day referral
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• Intro:
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- Inflammation of joints 2° to an infectious etiology
- Usually monoarticular, however polyarticular also occurs - Although rare, septic arthritis is considered an orthopaedic emergency |
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• Aetiology (risk factors):
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In children:
- Diverse casues - Staphylococcus is the 1° pathogen - Kingella king affects children under 2-3 yrs - Neonates face streptococcus, staphylococcus, gonorrhea - Adolescents: gonorrhoea concern - Salmonella links w/ sickle cell disease - Prolonged antibiotic use raises fungal infection risk - Pseudomonas from puncture wounds/drug use - Hip joint commonly affected in children In adults: - Staphylococcus major in adults - Streptococcus pneumonia significant - Gonorrhoea causes non-traumatic mono-arthritis - Fungal/mycobacterial organisms challenging to Dx - SCJ/SIJ infections involve pseudomonas, common in IV drug abusers - Damaged joints, especially in RA, prone to infection w/ cartilage damage, effusions, & px Epidemiology: - Incidence peaks at 2-3 yrs & elderly - M>F (2:1) Risk factors: - Age >80 - Diabetes mellitus - RA - Recent joint surgery - Joint prosthesis - Previous intra-articular injection - Skin infections & cutaneous ulcers - HIV infection - OA - Sexual activity (gonorrhoea) |
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• Pathophysiology:
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- Bacterial invasion of synovial, followed by inflammatory processes
- Common pathogens change throughout lifetime (viz. aetiology) - Damaged joints through RA are highly susceptible to infection - Synovium lacks limiting basement membrane → systemic infection can spread to bones - Contagious spread from osteomyelitis (hip & shoulder are prone) |
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• Clinical presentation:
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In children
Local Ssx: - Px, joint swelling, warmth - Limited ROM - Limp, refusal to use or move the affected joint (pseudoparalysis) Systemic Ssx: - Ill appearance - Fever - Tachycardia - Fussiness/irritability - Decreased appetite In adults: - Acute onset monoarticular (large joints) joint px - Fever (40-60% of pts), swelling, reluctance or refusal to move the affected joint - LL (hip, knees, ankles) commonly affected - Knee most affected joint |
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• Physical examination:
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- Palpation may elicit px
- Limited ROM - Effusions are common |
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• Diagnosis:
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- Synovial WBC count
- ESR & CRP Imaging Plain radiographs: - May reveal widened joint spaces - Soft tissue bulging - Subchondral bony changes (late finding) - Normal plain radiograph doesn't rule out septic arthritis US: - Useful for identifying & quantifying joint effusion - Aids needle aspiration MRI: - Sensitive for early detection of joint fluid - Reveals abnormalities in surrounding soft tissue & bone - Cartilaginous involvement |
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• Complications:
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- Osteomyelitis
- Chronic px - Osteonecrosis / AVN - Leg length discrepancies - Sepsis - Death |
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• Management:
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- Same day referral to GP
- Antibiotics - Aspiration of joints |
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• Ddx:
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- Infections
- CPPD - OA - Fractures - AVN/osteonecrosis - Other inflammatory arthropathies - Systemic infections - Tumour |
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• GREEN
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• Intro:
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- Tendinopathy is an umbrella term to describe tendon px, w/ unknown cause
- Tendinosis describes the degenerative state of tendons (more applicable) |
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• Aetiology (risk factors):
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- Not fully understood
- Mechanical stressors, repetitive overloading, or toxic chemical exposure ca initiate tendinosis - Age, genetic predisposition, &/or comorbidities can increase susceptibility to healing failure leading to tendinosis |
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• Pathophysiology:
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- Decreased simplistically in 3 stages, but actually occurs on a continuum
Stage 1: - Begins w/ tendon experiencing the initial insult, stress, or injury - Causes: acute overload, repetitive stress, or chemical irritation - Linked to the death of tenocytes (tendon cells) Stage 2: - Characterised by failed healing of the tendon - Unclear cause, but believed to result from an altered tendon environment (steroids/NSAIDs may alter natural healing cascade) - Improper cell recruitment & a cascade of healing issues may occur Stage 3: - Characterised by apoptosis (death) of cells, disorganisation of the matrix, & neovascularisation - Pts often present at this stage, experiencing mechanical weakness or increased px - Neovascularisation theorised to supply neonerves, contributing to px (neurogenic inflammation) |
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• Clinical presentation:
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- Identify potential stressors
- Impact on ADLs - Recent changes in medication, inc. antibiotics (may influence treatment) |
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• Physical examination:
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- Tenderness
- Swelling - Other abnormalities - Special tests based on the specific tendon |
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• Diagnosis:
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- Labs: CRP & ESR (aid in identifying inflammatory processes)
- X-ray: if bone injury is suspected - US: increased spacing of fibrillar lines, reduced echogenecity, tendon thickening, neovascularisation (via colour Doppler) - MRI: valuable for evaluating tendinosis |
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• Complications:
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- Tendon rupture (if untreated)
- Contractures of the tendon, w/ reduced tendon liability - Tendon adhesions - Atrophy of muscles - Loss of functionality, even up to & including disability |
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• Management:
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- Healing as long as 3-6 months
- STW - SMT - Mobs/drops - RICE - NSAIDs |
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• Ddx:
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- Acute compartment syndrome (ACS)
- Ankle injury - Bursitis - Carpal tunnel syndrome - Gout & pseudogout - Hand infections - Reactive arthritis - Rotator cuff injuries - Soft tissue knee injury |
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• GREEN
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• Intro:
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- Umbrella term for conditions characterised by compression or entrapment of nerves, blood vessels, or tendons within anatomical tunnels in the LL
- Can lead to various Ssx inc. px, numbness, tingling, & weakness, affecting the function & sensation of the LL Common LL tunnel syndromes inc.: - Sciatica - Tarsal tunnel s. - Common peroneal n. entrapment - Anterior compartment s. (ACS) - Popliteal artery entrapment s. (PAES) |
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• Aetiology (risk factors):
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- Age-related degeneration
- Obesity - Sedentary lifestyle - Trauma - Arthritis - Tumours - Diabetes - Pregnancy - Tight clothing - Occupation-related factors |
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• Pathophysiology:
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- Increased pressure within confined spaces leads to nerve or vascular compression
- Inflammation, fibrosis, or space-occupying lesions contribute to compression - Repetitive use or trauma can exacerbate Ssx - Individual anatomical variations may predispose individuals to specific tunnel syndromes |
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• Clinical presentation:
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- Px or discomfort in the affected LL
- Numbness or tingling - Weakness in the muscles of the affected area - Altered sensation or hypersensitivity - Px may worsen w/ specific activities or movements - Swelling in the affected area - Impaired coordination or balance |
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• Physical examination:
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- Tenderness or px upon palpation of the affected nerve pathway
- Muscle atrophy in severe or chronic cases - Limited ROM in affected joint - Positive Tinel's sign: tingling or px elicited by tapping on the nerve - Positive Nerve tension tests: straight leg raise / slump test to assess nerve mobility & irritation - Changes in reflexes, such as diminished or exaggerated reflexes |
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• Diagnosis:
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- MRI: provides detailed soft tissue visualisation, helping identify nerve compression & surrounding structures
- US: useful fro dynamic imaging, assessing nerve movement during various joint positions - CT: may be used in specific cases, especially fro bony abnormalities contributing to nerve compression |
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• Complications:
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- Nerve compression & damage
- Ischemia (reduced blood supply) - Muscle atrophy & weakness - Chronic px - Motor dysfunction - Sensory abnormalities - Functional limitations - Trophic changes (skin, hair, nail condition) - Risk for 2° injuries (risk of falls) - Psychosocial impact - Surgical complications |
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• Management:
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- Rest & activity modification
- NSAIDS & neuropathic px medication - Injections - Occupation & ergonomic modifications - Weight management - Surgery - Pt education - SMT & STW - Strengthening & mobilising |
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• Ddx:
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- Peripheral neuropathy
- Lx radiculopathy - MFPD - Complex regional px s. (CRPS) - Tarsal tunnel syndrome - Morton's neuroma - Stress fractures - Compartment s. - MSK injuries (ligament sprains, tendonitis etc.) - Inflammatory arthropathies (RA etc.) - Infectious causes (cellulitis, osteomyelitis etc.) - Neoplastic conditions (tumours) - Systemic conditions (diabetes, hypothyroidism etc.) - Iliotibial band s. - Popliteal entrapment s. |
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• RED
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|
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• Intro:
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- Fractures that occur due to an imbalance between the bone strength & the chronic mechanical stress placed upon the bone (→ overuse s.)
- spondylolisthesis is also classified as stress fracture |
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• Aetiology (risk factors):
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- Abrupt increase in activity or training patterns
Intrinsic factors: - Poor physical conditioning - F>M - Hormonal disorders - Menstrual disorders - Poor bone density - Reduced muscle mass - Genu valgum kness - Short leg Extrinsic factors: - High-impact sports - Abrupt increase in physical activity - Irregular or angled running surface - Poor footwear - Running shoe wear older than 6 months - Vitamin D & calcium deficiency - Smoking Common risk factors: - Abrupt increase in activity - Females - PMHx of stress fractures Common sites: - Metatarsals, tibia, tarsals, femur, fibula, & pelvis (in decreasing order) - Pelvic & metatarsal stress # common in females - UL stress # rare but reported in gymnasts, weightlifters, & throwing sports Sports-specific risks: - Runners: tibia & metatarsal stress # (F may also experience pelvic stress #) - Long-distance runners: association w/ femoral neck & pelvic injuries - Hurdlers: patella # - Gymnasts, female soccer players, certain American football positions & weightlifters: increased risk of spondylolysis (unique stress # related to repeated hyperEXT of the spine) |
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• Epidemiology:
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- Stress # are 20% of all sports injuries
- Common along military - Runners (16% of injuries): tibia (23.6%), tarsal navicular (17.6%), metatarsals (16.2%), femur (6.6%), pelvis (1.6%) - F>M - Neuromuscular factors play a role (muscle loss / fatigue decreases ability to absorb forces) - Rapid weight loss, particularly muscle loss, is associated w/ stress # - Overtraining / relative energy deficiency s. contribute (esp. in females w/ disordered menstruation & hormonal imbalances) - Male endurance athletes w/ high training volumes & restricted calorie intake (low testosterone), leading to osteoporosis & stress # |
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• Pathophysiology:
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- Wolff's law: applied force on a normal bone leads to remodelling for increased strength
- Osteocytes: most common bone cells, orchestrate osteoclastic & osteoblastic functions - Osteocyte's dendritic network: responds to biomechanical stress, secretes mediators regulating bone activites - Cycling loading impact: compromises osteocyte singling, hinders physiological repair mechanisms - Repetitive loading effect: stimulates osteoclasts for faster resorption, outpacing osteoblasts in new bone formation - Normal remodelling cycle: takes 3-4 months |
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• Clinical presentation:
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- Insidious onset of px after activity
- Progressive increase in px duration post-exercise - Px present upon waking up following training activity - Important factors in Hx: recent changes in training, nutrition, intrinsic & extrinsic risk factors, PMHx, & medications |
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• Physical examination:
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- Focal TTP
- Occasional edema at the suspected stress fracture site - Limited clinical diagnostic tests - Px percussion & vibration - Commonly used tests: "hop test" & fulcrum test - Bony tenderness on palp, often at distal to middle third junctions I the tibia or over 3rd & 4th metatarsal shafts |
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• Spondylolysis & spondylolisthesis:
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- Require high index of suspicion
- Spondylolysis may be asymptomatic & found incidentally on Lx films - Lx extension increases px in spondylolysis, Stork test or single leg hyperextension test is common - Spondylolisthesis occurs when pars defect does not heal, leading to anterior migration of the vertebral body |
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• Diagnosis:
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- First is plain radiography
- CT - MRI |
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• Complications:
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- Small for low-risk stress fractures
- Occasional residual px - Higher for high-risk stress fractures - More likely to progress to non-union & thus require surgery |
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• Management:
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- NSAIDs
- Splinting - Resting / non-WB - Supplementation of vitamin D, magnesium - Potential surgery - Post-surgery / healing rehab - Strengthening /mobs |
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• Ddx:
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- Cellulitis
- Osteomyelitis - Tendonitis - Tendinopathy - Exertional compartment syndrome - Tumours (benign & malignant) - Nerve entrapment - Arterial entrapment - Coagulation disorders - Compartment s. - Neuropathic px - CRPS |
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