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6002 General LL Cheat Sheet by

General LL conditions

Muscle Strains

- 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
- 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
- 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

- 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
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
MRI findings:
- Osteos­cle­rotic changes
- Decreased bone resorption due to disrupted osteoclast function
- Low on T1 (fat is white)
- High on T2 (fat is dark)
Postop­erative compli­cat­ions:
- Surgical site infection
- Prosthesis malfunctions
- Neurom­uscular compromise
- 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
- OA
- Osteoporosis
- Osteomyelitis
- Neoplastic bone conditions
- Inflam­matory synovitis
- Soft tissue trauma


- 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
- 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
- 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)
- 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
- 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
Bursitis w/o infection:- Most often self-limiting
- 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
- 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

- 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
- 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
Physical examin­ation:
- Limited ROM
- Crepitus
- Muscle weakness
- Warmth & redness
- Palpable calcium deposits
- 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
- Chronic px
- Tendon rupture
- Compre­ssion of adjacent structures
- Bursitis
- 2° OA
- Functional impairment
- Psycho­social impact
- Recurrence
- Pts w/ chronic calcific tendonitis often don't respond to conser­vative care
- Anti-i­nfl­amm­atory NSAIDs (ibuprofen)
- Injections
- Surgery
- Adhesive capsulitis
- Tendinopathy
- Bursitis
- Arthritis
- Ossifying tendinitis


- 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
- 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"
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
- 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
- Exercise program
- Mobs/drops
- NSAIDs (prefe­rably topical)
- RA
- Gout
- Pseudogout
- Septic arthritis
- Hemochromatosis
- Fibromyalgia
- Lyme disease
- Ankylosing spondylitis
- Psoriatic arthritis
- Neurop­athic arthropathy
- Parvov­iru­s-a­sso­ciated arthritis

Inflam­matory arthro­pathies

- 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
- 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
- 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
- Benefi­cial, especially when radiog­raphs are nondiagnostic
- More sensitive than plain film in evaluating synovitis, erosions, sacroiliitis
- Higher sensit­ivity than X-rays
- 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
- Inflam­mation is revers­ible, while joint destru­ction is not
- Antibiotic therapy
- Education
- Manual therapy
- Diet
- Lifestyle modifi­cation
- RA
- AS
- Psoriatic arthritis
- Lupus arthritis
- Gout
- Juvenile idiopathic arthritis
- Reactive arthritis
- Spondy­loa­rth­ritis

Septic arthritis

- Same day referral
- 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
- 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)
- 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
- Synovial WBC count
Plain radiog­raphs:
- May reveal widened joint spaces
- Soft tissue bulging
- Subcho­ndral bony changes (late finding)
- Normal plain radiograph doesn't rule out septic arthritis
- Useful for identi­fying & quanti­fying joint effusion
- Aids needle aspiration
- Sensitive for early detection of joint fluid
- Reveals abnorm­alities in surrou­nding soft tissue & bone
- Cartil­aginous involv­ement
- Osteomyelitis
- Chronic px
- Osteon­ecrosis / AVN
- Leg length discrepancies
- Sepsis
- Death
- Same day referral to GP
- Antibiotics
- Aspiration of joints
- Infections
- OA
- Fractures
- AVN/osteonecrosis
- Other inflam­matory arthropathies
- Systemic infections
- Tumour


- 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
- 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
- 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
- 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
- Healing as long as 3-6 months
- Mobs/drops
- 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

- 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
- 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
- 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
- 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
- Rest & activity modification
- NSAIDS & neurop­athic px medication
- Injections
- Occupation & ergonomic modifications
- Weight management
- Surgery
- Pt education
- Streng­thening & mobilising
- Peripheral neuropathy
- Lx radiculopathy
- 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

- 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)
- 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 #
- 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
- First is plain radiography
- CT
- 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
- Splinting
- Resting / non-WB
- Supple­men­tation of vitamin D, magnesium
- Potential surgery
- Post-s­urgery / healing rehab
- Streng­thening /mobs
- Cellulitis
- Osteomyelitis
- Tendonitis
- Tendinopathy
- Exertional compar­tment syndrome
- Tumours (benign & malignant)
- Nerve entrapment
- Arterial entrapment
- Coagul­ation disorders
- Compar­tment s.
- Neurop­athic px


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