Muscle Strains
• GREEN |
• Intro: |
- Muscle / tendon strain is equivalent to ligament sprain in terms of injury type
- Happens when muscle fibres are overworked, resulting in fibre tearing |
• Aetiology (risk factors): |
- ↑ 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 |
• Pathophysiology: |
- 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 |
• Sx & Ssx: |
- Swelling, bruising, or redness
- Px at rest
- Inability to use the muscle at all
- Weakness of muscle or tendons |
• Management: |
- 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 |
AVN / Osteonecrosis
• YELLOW |
• Intro |
- 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 |
• Aetiology (risk factors): |
- 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 |
• Pathophysiology: |
1. Reduction in subchondral blood supply
2. Induces hypoxia
3. Loss of cell membrane integrity
4. Necrosis of cells (osteonecrosis) |
• Clinical & physical exam presentation: |
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 |
• Diagnosis: |
MRI findings:
- Osteosclerotic changes
- Decreased bone resorption due to disrupted osteoclast function
- Low on T1 (fat is white)
- High on T2 (fat is dark) |
• Complications: |
Postoperative complications:
- Surgical site infection
- Prosthesis malfunctions
- Neuromuscular compromise |
• Management: |
- 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 |
• Ddx: |
- OA
- Osteoporosis
- Osteomyelitis
- Neoplastic bone conditions
- Inflammatory synovitis
- CRPS
- Soft tissue trauma |
Bursitis
• YELLOW |
• Intro: |
- 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 |
• Aetiology (risk factors): |
- 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 |
• Pathophysiology: |
- 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 |
• Clinical presentation: |
- ↓ 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 |
• Physical examination: |
- 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 |
• Diagnosis: |
- 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 |
• Management: |
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 |
• Ddx: |
- 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 |
Calcific Tendonitis
• GREEN |
• Intro: |
- Self-limiting disorder characterised by deposition of calcium in the tendon / muscle
- Leads to px & reduced ROM |
• Aetiology (risk factors): |
- 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 |
• Pathophysiology: |
- 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 |
• Clinical presentation: |
- Px w/ or w/o loss of ROM
- Stiffness, usually after periods of inactivity (morning)
- Swelling
- TTP |
• Physical examination: |
- Limited ROM
- Crepitus
- Muscle weakness
- Warmth & redness
- Palpable calcium deposits |
• Diagnosis: |
- 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 |
• Complications: |
- Chronic px
- Tendon rupture
- Compression of adjacent structures
- Bursitis
- 2° OA
- Functional impairment
- Psychosocial impact
- Recurrence |
• Management: |
- Pts w/ chronic calcific tendonitis often don't respond to conservative care
- Anti-inflammatory NSAIDs (ibuprofen)
- Injections
- Surgery |
• Ddx: |
- Adhesive capsulitis
- Tendinopathy
- Bursitis
- Arthritis
- Ossifying tendinitis |
Osteoarthritis
• GREEN |
• Intro: |
- 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 |
• Aetiology (risk factors): |
- 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 |
• Pathophysiology: |
- 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 |
• Clinical presentation: |
- 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 |
• Physical examination: |
- 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" |
• Diagnosis: |
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 |
• Complications: |
- 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 |
• Management: |
- Exercise program
- STW
- Mobs/drops
- SMT
- NSAIDs (preferably topical) |
• Ddx: |
- RA
- Gout
- Pseudogout
- Septic arthritis
- Hemochromatosis
- Fibromyalgia
- Lyme disease
- Ankylosing spondylitis
- Psoriatic arthritis
- Neuropathic arthropathy
- Parvovirus-associated arthritis |
Inflammatory arthropathies
• YELLOW |
• Intro: |
- 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 |
• Aetiology (risk factors): |
- 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 |
• Pathophysiology: |
- 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 |
• Clinical presentation: |
- 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 |
• Physical examination: |
- 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 |
• Diagnosis: |
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 |
• Complications: |
- 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 |
• Management: |
- Inflammation is reversible, while joint destruction is not
- Antibiotic therapy
- NSAIDs
- Education
- Manual therapy
- Diet
- Lifestyle modification |
• Ddx: |
- RA
- AS
- Psoriatic arthritis
- Lupus arthritis
- Gout
- Juvenile idiopathic arthritis
- Reactive arthritis
- Spondyloarthritis |
Septic arthritis
• YELLOW |
- Same day referral |
• Intro: |
- Inflammation of joints 2° to an infectious etiology
- Usually monoarticular, however polyarticular also occurs
- Although rare, septic arthritis is considered an orthopaedic emergency |
• Aetiology (risk factors): |
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) |
• Pathophysiology: |
- 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) |
• Clinical presentation: |
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 |
• Physical examination: |
- Palpation may elicit px
- Limited ROM
- Effusions are common |
• Diagnosis: |
- 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 |
• Complications: |
- Osteomyelitis
- Chronic px
- Osteonecrosis / AVN
- Leg length discrepancies
- Sepsis
- Death |
• Management: |
- Same day referral to GP
- Antibiotics
- Aspiration of joints |
• Ddx: |
- Infections
- CPPD
- OA
- Fractures
- AVN/osteonecrosis
- Other inflammatory arthropathies
- Systemic infections
- Tumour |
Tendinopathies
• GREEN |
• Intro: |
- Tendinopathy is an umbrella term to describe tendon px, w/ unknown cause
- Tendinosis describes the degenerative state of tendons (more applicable) |
• Aetiology (risk factors): |
- 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 |
• Pathophysiology: |
- 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) |
• Clinical presentation: |
- Identify potential stressors
- Impact on ADLs
- Recent changes in medication, inc. antibiotics (may influence treatment) |
• Physical examination: |
- Tenderness
- Swelling
- Other abnormalities
- Special tests based on the specific tendon |
• Diagnosis: |
- 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 |
• Complications: |
- 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 |
• Management: |
- Healing as long as 3-6 months
- STW
- SMT
- Mobs/drops
- RICE
- NSAIDs |
• Ddx: |
- Acute compartment syndrome (ACS)
- Ankle injury
- Bursitis
- Carpal tunnel syndrome
- Gout & pseudogout
- Hand infections
- Reactive arthritis
- Rotator cuff injuries
- Soft tissue knee injury |
LL nerve entrapments / Tunnel syndromes
• GREEN |
• Intro: |
- 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) |
• Aetiology (risk factors): |
- Age-related degeneration
- Obesity
- Sedentary lifestyle
- Trauma
- Arthritis
- Tumours
- Diabetes
- Pregnancy
- Tight clothing
- Occupation-related factors |
• Pathophysiology: |
- 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 |
• Clinical presentation: |
- 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 |
• Physical examination: |
- 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 |
• Diagnosis: |
- 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 |
• Complications: |
- 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 |
• Management: |
- Rest & activity modification
- NSAIDS & neuropathic px medication
- Injections
- Occupation & ergonomic modifications
- Weight management
- Surgery
- Pt education
- SMT & STW
- Strengthening & mobilising |
• Ddx: |
- 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. |
Stress fractures
• RED |
• Intro: |
- 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 |
• Aetiology (risk factors): |
- 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) |
• Epidemiology: |
- 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 # |
• Pathophysiology: |
- 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 |
• Clinical presentation: |
- 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 |
• Physical examination: |
- 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 |
• Spondylolysis & spondylolisthesis: |
- 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 |
• Diagnosis: |
- First is plain radiography
- CT
- MRI |
• Complications: |
- 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 |
• Management: |
- NSAIDs
- Splinting
- Resting / non-WB
- Supplementation of vitamin D, magnesium
- Potential surgery
- Post-surgery / healing rehab
- Strengthening /mobs |
• Ddx: |
- 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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