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6002 Knee & Lower Leg Cheat Sheet by

Condition of knee & lower leg

Anterior Cruciate Ligament (ACL) Injuries

YELLOW
Intro:
- Stabilises the knee joint along w/ the PCL (forms a cross "X")
- Prevent excessive forward or backward motion of the tibia relative to the femur during FX & EXT
- Nerve supply: middle geniculate artery; Innerv­ation: posterior articular n. (branch of tibial n.)
- Origin: antero­medial aspect of tibial plateau; Insertion: Medial aspect of the lateral femoral condyle
- Has 2 bundles (anter­omedial & posterolateral)
-
Aetiology (risk factors):
- Most commonly injured ligament in the knee (almost ½ of all knee injuries)
- F>M (esp. F athletes 4.5:1)
- Possible factors contri­buting to increased F risk include: weaker hamstr­ings, prefer­ential recrui­tment of quads during decele­ration, & weaker core stability
Biomec­hanics & landing factors:
- F landing mechanics mat ↑ injury risk, w/ ↑ valgus angulation & knee EXT
- ↓ hip & knee FX & ↓ fatigue resistance also contribute to ↑ stress on the ACL
Other risk factors:
- Anatom­ical: high BMI, smaller femoral notch, imping­ement on the notch, smaller ACL, hyperm­obi­lity, joint laxity, & previous ACL injury
Hormonal & genetic factors:
- Preovu­latory phase, may affect coordi­nation & predispose females to ACL injury
- Females on OCP were noted less affected
Associated injuries w/ ACL ruptures:
- Both intra & extra-­art­icular injuries can accompany acute ACL ruptures
- Meniscal tears are common, w/ lateral meniscus injury more prevalent in acute cases, & medial meniscus more involved in chronic cases
- Other ligaments (PCL, LCL, & PLC) could also be injured in conjun­ction w/ ACL
Chronic ACL deficiency effects:
- Detrim­ental effects on the knee
- Develo­pment of chondral injuries & complex, unrepa­irable meniscal tears is observed (e.g bucket handle medial meniscus tears)
Pathop­hys­iology:
- Common in non-co­ntact sports, esp. non-co­ntact pivoting injuries
- Tibia transl­ation anteriorly during slight knee FX & valgus
- Direct hits to the lateral knee can also cause ACL injuries
- Injury occurs during activi­ty/­sports partic­ipation that involves sudden changes in the direction of movement, abrupt stopping or slowing down while running, or jumping & abnormal landing
Clinical presen­tation:
- Hx of injury mechanisms
- Pt would complain of hearin­g/f­eeling a sudden "­pop­" w/ associated deep knee px
- About 70% would experience immediate swelling due to haemarthrosis
- Other Ssx: knee "­giving way", difficulty ambula­ting, reduced knee ROM
Physical examin­ation:
- Pt demons­trates quadriceps avoidance gait (no active knee EXT)
- Varus knee malali­gnment should be noted as it increases risk of ACL re-rupture
- Palpation: swollen knee, & potential joint line tenderness w/ an associated meniscal injury
- Move: knee may be locked due to associated meniscal injury (other meniscal & ligame­ntous structures to be assessed)
- Lachman test, Anterior drawer test, Pivot shift test
Diagnosis:
- MRI is the 1° modality to diagnose ACL pathology
- Knee arthro­scopy to differ­entiate complete from partial tears & chronic tears (gold standard test)
- Radiog­raphy to rule out fractures & other osseous injuries
Compli­cat­ions:
- Surgical: tunnel malpos­iti­oning, posterior wall blowout, graft failure due to various other issues
- Post op: infection & septic arthritis
- Stiffness & arthrofibrosis
- Infrap­atellar contra­cture syndrome
- Patella tendon rupture
- CRPS
- Patella fracture
- Tunnel osteolysis
- OA in the long term
- Saphenous n. irritation
- Cyclops lesion
Manage­ment:
Non-op­erative manage­ment:
- Indica­tion: when there's reduced ACL laxity on low-demand pts or athletes involved in no cutting or pivoting activities or partial ACL tears
- RICE
- Non-WB (crutches or wheelchair)
- NSAIDs
- Phase 1: acute sympto­matic treatment
- Phase 2: 12 weeks of supervised physio­therapy starting w/ regaining full ROM & progre­ssion to quad, hamstring, hip ABD & core strengthening
Operative manage­ment:
- Indica­tion: complete ACL rupture in younger or older active, high-d­emand pts, & partial ACL rupture w. functional instability
- Two options: ACL recons­tru­ction or repair
Ddx:
- ACL tear
- Epiphyseal fracture of femur/tibia
- MCL injury
- Meniscal tear
- Osteoc­hondral fracture
- Patellar dislocation
- Posterior cruciate ligament injury
- Tibial spine fracture

Lateral Collateral (LCL) & PLC Injuries

YELLOW
Intro:
- 1° resistor of varus stress
- Provides poster­ola­teral stability (preve­nting medial transl­ation of the tibia)
- LCL & PLT resist external tibial rotation in 0-30° of knee FLX
- Minor role in tibial transl­ation (stabi­lises anterior & posterior tibial transl­ation when cruciate ligaments are torn)
- Origin: lateral epicondyle of the femur, Insertion: fibular head
- Blood supply: branches of popliteal artery, Innerv­ation: common fibular n.
- Surrou­nding struct­ures: popliteus tendon (PLT) & iliotibial band (ITB)
Aetiology (risk factors):
- 40% of PLC (poste­rol­ateral corner) & LCL injuries result from contact sports
- Other causes include trauma, motor vehicle accidents, & falls
- F>M
- High-c­ontact sports
- Sports involving high-v­elocity pivoting & jumping
- Tennis & gymnastics are most specific fro isolated LCL injuries
- Prior knee, ankle, or hip injury increases the risk
Pathop­hys­iology:
- LCL injuries rarely occur in isolation
- High-e­nergy blow to the antero­-medial knee
- Involves hyperEXT & extreme varus force
- Non-co­ntact hyperEXT & varus stressors can also cause LCL injuries
Clinical presen­tation:
- Acute event consistent w/ a medial blow to the knee while fully EXT, or extreme non-co­ntact varus bending
- Complain of sudden onset lateral knee px, swelling, & ecchymosis after the injury
- May report thrust gait, inc. foot kicking in mid-stance
- May complain of parest­hesias over the lateral lower extremity, & weakness &/or a foot drop
- Gain complete Hx inc. bleedi­ng/clot disorders, previous surgeries, occupa­tion, gait, ambula­tio­n-a­ssisted devices, living situation (stairs at home)
Physical examin­ation:
- Limited ROM
- Lateral knee TTP
- Ecchym­osis, swelling, & warmth
- Gait: classical varus thrust finding
- Special tests: Varus stress test, EXT ROT recurvatum test, Poster­ola­teral drawer test, Reverse pivot shift test, Dial test
Diagnosis:
- MRI is the gold standard
- US useful for rapid diagnosis
Classi­fic­ation of injury:
- Grade 1: Mild sprain - diagnosed w/ lateral knee tender­ness, no instab­ility mechanical Ssx
- Grade 2: Partial tear - diagnosed w/ more severe localised lateral & poster­ola­teral knee px, as well as swelling
- Grade 3: Complete tear - px & swelling vary in pts, usually associated w/ PLC & other related injuries, & mechanical Ssx
Compli­cat­ions:
- Undiag­nosed LCL & PLC injuries have several long-term complications
- Continued knee instab­ility & chronic px
- 35% of PLC injuries may have an associated peroneal n. palsy (probs due to its proximity to the LCL)
- Pts may develop long-term foot drop, as well as lower extremity weakness & decreased sensation
- Post op: hardware irritation & stiffness
Manage­ment:
- Acutely, all grades treated w/ RICE & NSAIDs
- Grade 1 & 2: non-op­era­tive, non-WB for 1 week for better px control; next 3-6 weeks, the pt should be in a hinged­-knee brace while performing functional rehab
- Grade 3: surgical recons­tru­ction (best results), post op rehab and functional exercises
Ddx:
- ACL/PCL tears
- Lateral meniscus tears
- Popliteal injury
- Bone contusion
- ITB syndrome

Posterior Cruciate Ligament (PCL) Injuries

YELLOW
Intro:
- 1/4 major ligaments of the knee that function to stabilise the tibia on the femur
- Origin: antero­lateral aspect of the medial femoral condyle in the area of the interc­ondylar notch, Insertion: posterior aspect of the tibial plateau
- Prevents posterior transl­ation of the tibia on the femur
- Lesser extent, the PCL functions to resist varus, valgus, & EXT ROT forces
Aetiology (risk factors):
- Caused by extreme anterior force applied to the proximal tibia of the FX knee
- Dashboard injuries during car accident or falling forward onto a FX knee
- M>F (2:1)
- Motorcycle accidents (28%) & soccer­-re­lated injuries (25%) are the leading causes
Pathop­hys­iology:
- Least common knee injury
- Antero­lateral portion is more commonly injured due to majority of injuries occurring in knee FX
- Resists posterior transl­ation w. the assistance of the poster­ola­teral joint capsule, popliteus, MCL, & posterior oblique ligament
Clinical presen­tation:
- Pts often present w/ acute onset of posterior knee px, swelling, & instability
- Hx includes mechanism of injury, ic. falling onto FX knee or recent vehicle accident
Physical examin­ation:
- Pulses
- SMR
- Mild to moderate joint effusion
- Swelling usually less than in ACL tear
- Pt may present w/ antalgic gait & potential difficulty walking up & down stairs
- Palpation: potential effusion, joint line for tenderness (sugge­stive of meniscal tears)
- Muscle strength test: should be normal, but there may be weakness w/ knee EXT & FX 2° to guarding
- Limited ROM
- Special tests: Posterior drawer test, Quadriceps active test, Dial test or EXT ROT test, Varus/­valgus stress
Diagnosis:
- MRI is the gold standard
- Initial imaging w/ plain X-rays
Classi­fic­ation of injury:
- Grade 1 (partial tear) - 1-5mm posterior transl­ation, tibia remains anterior to femoral condyles
- Grade 2 (complete isolated) - 6-10mm posterior tibial transl­ation, complete tear of PCL w/o another injury, anterior tibia flush w/ femoral condyles
- Grade 3 (complete PCL w/ combined capsular &/or ligame­ntous injury) - >10mm posterior tibial transl­ation, tibia posterior to femoral condyles which may indicate a concom­itant capsul­oli­gam­entous injury
Compli­cat­ions:
- Intra & postop­erative compli­cations of PCL surgery
- Neurom­uscular injury (e.g. popliteal artery injury)
- Fracture
- Residual instability
- Osteoa­rth­ritic progression
- Osteonecrosis
- Stiffness
- Failure of associated ligament recons­tru­ctions or meniscal repairs
- Revision of PCL recons­tru­ction
Manage­ment:
- Variables to consider: Acute or chronic; isolated or combined
Non-op­era­tive:
- Acute grade 1 & 2 injuries w/ posterior tibial transl­ation (8-12mm)
- Grade 3 injuries w/ mild Ssx or low-demand activities
- Acute treatment inv. RICE, initial knee bracing, & crutches
- Rehab focuses on knee EXT strengthening
- Est. return­-to­-play in 2-4 weeks for Grade 1 & 2 injuries
- Grade 3 may inv. knee immobi­lis­ation followed by rehab
Operative:
- Acute injuries w/ tibial transl­ation >12mm, associated meniscal tears, disloc­ation, bony avulsions, & combined injuries
- Chronic injuries w/ posterior tibial transl­ation >8mm, sympto­matic cases, instab­ility, & combined injuries
- Arthro­scopic procedures
- Reconstruction
- Graft fixations
- High tibial osteotomy
Ddx:
- ACL injury
- LCL injury
- MCL injury
- Meniscus injury
- Talofi­bular ligament injury

Baker's Cyst

GREEN
Intro:
- Also known as popliteal or parame­dical cyst
- Fluid-­filled sac, typically between semime­mbr­anosus & medial head of the gastroc
- Common in adults & associated w/ degene­rative knee conditions
- Often linked to degene­rative meniscal tears as one of the most common causes
- In children, popliteal cysts more commonly arise as a 1° condition (resulting from herniated post knee joint synovi­um/­cap­sule)
Aetiology (risk factors):
- Children aged 4-7 yo
- Adults aged 35-70
- Most commonly found in adults w/ Hx of trauma, knee joint diseases (OA, RA, etc), or as incidental findings
- They form due to accumu­lation & extrusion of synovial fluid between the semime­bra­nosus & medial head of the gastroc
- Popliteal cysts are located on the medial side of the popliteal fossa just below the crease at the posterior knee
- Prevalence increases w/ age, likely due to an increase in knee-b­urial commun­ication
Pathop­hys­iology:
Several mechan­isms:
1. Joint-cyst communication
2. Seques­tration of synovial fluid in popliteal fossa due to a valve-like effect between the joint & cyst (contr­olled by gastro­c-s­emi­mem­bra­nosus m. w/ FX & EXT at the knee)
3. Negative intraa­rti­cular knee pressure during partial FX combined w/ a positive pressure during extension (as a result directing fluid flow towards the cyst from the suprap­atellar bursa during FLX)
4. Gastro­c-s­emi­mem­bra­nosus bursa enlarg­ement resulting from micro-­traumas to the bursa w/ muscle contractions
5. Herniation of the joint capsule into the popliteal fossa
Clinical presen­tation:
- Sensation of tightness, discom­fort, or px behind the knee
- Swelling Moree noticeable when standing w/ full knee EXT
- Swelling reduces or disappears when the knee is flexed to 45° (Foucher's sign)
- Px worsens w/ increased activity & may limit full knee FX & EXT
Physical examin­ation:
- Compre­ssion of surrou­nding vessels
- Lower extremity oedema due to venous obstruction
- Enlarg­ement into the calf m. (disse­cting cyst) can cause swelling, erythema, distal oedema, & +ve Homan's sign
- Venous obstru­ction can mimic Ssx of DVT or thromb­oph­lebitis
Diagnosis:
Diagnosis methods:
- Pt stand & full knee EXT
- Mass is most prominent in this position
- Mass often softens or disappears when the knee is FX to 45° (Foucher's sign)
- Supine exam: knee passively moved from full EXT to at least 90° FX
Imaging:
- Plain radiograph & US
- MRI is recomm­ended, esp. if consid­ering surgery
Compli­cat­ions:
Compli­cations & Ssx of ruptured Baker's cyst:
- Rapid fluid accumu­lation may cause cyst rupture
- Released fluid into surrou­nding tissues can lead to inflammation
- Ssx similar to thromb­oph­leb­itis: sharp pc in the knee & calf; swelling or erythema of the calf; sensation of water running down the calf
Compli­cations of cyst rupture:
- Post tibial n. entrap­ment: posterior plantar numbness & calf px
- Popliteal artery occlusion: lower extremity oedema
- Anterior compar­tment syndrome: foot drop, oedema of antero­lateral leg
- Posterior compar­tment syndrome: plantar dysest­hesia, weakness of toes, calf swelling, px worsens w/ passive toe extension
Manage­ment:
- Asympt­omatic cases are managed through observ­ation & reassu­rance alone
- Essential to treat any underlying joint disorder in pts w/ sympto­matic Baker's cysts
- Helps reduce synovial fluid accumu­lation & cyst enlargement
Non-op­era­tive:
- Rest/a­ctivity modification
- NSAIDs
- Physical therapy & rehab regimes are effective for minimal Ssx & smaller degene­rative meniscal tears
- Aspiration & steroid injection
- Lower recurrence in younger pts
- Higher recurrence rates in older pts & those w/ degene­rative meniscal tears
Operative:
- Arthroscopy
- Open cyst excision (not recomm­ended in case of underlying degene­ration due to recurrence risk)
Ddx:
- Abscess
- Arteri­ovenous fistula
- DVT
- Ganglion cyst
- Hemangioma
- Lipoma
- Lymphadenopathy
- Malignancy (e.g. fibros­arcoma, liposarcoma)
- Popliteal (Balker's) cyst

Chondr­oca­lci­nosis (pseud­ogout)

YELLOW
Intro:
Overview:
- Calcium pyroph­osphate deposition disease (CPPD)
- Crystal deposition arthro­pathy involving synovial & periar­ticular tissues
- Asympt­omatic to acute or chronic inflam­matory arthritis
Phenotypes & termin­ology:
- Various terms used for different phenotypes
- Acute CPP deposition arthritis: "­Pse­udo­gou­t"
- Chronic CPP deposition arthritis: informally called "­pse­udo­-rh­eum­atoid arthri­tis­"
- Charac­terised by a waxing & waning clinical course, resembling RA
Radiol­ogical findings:
- Term: chondr­oca­lci­nosis
- Describes intra-­art­icular fibroc­art­ilage calcification
Commonly affected joints:
- Hips
- Knees
- Shoulders
Underlying factors:
- Often associated w/ underlying joint disease or metabolic abnormalities
- Predis­posing factors: OA, trauma, surgery, RA
Aetiology (risk factors):
- Often pts >65 yo, w/ 30-50% >85 yo
- M>F
- Rare <60 yo
- High prevalence of radiog­raphic chondr­oca­lci­nosis in the general population
Comorb­idities associated w/ CPPD:
- Hyperparathyroidism
- Gout
- OA
- RA
- Hemochromatosis
Other related comorb­idi­ties:
- Osteoporosis
- Hypomagnesium
- Chronic kidney disease
- Calcium supple­men­tation
Pathop­hys­iology:
- Caused by an imbalance between pyroph­osphate production & pyroph­osphate levels in diseased cartilage
- Pyroph­osphate deposits in the synovium & adjacent tissues combine w/ calcium to form CPP
- Deposition of calcium pyres-hate can activate the immune system, leading to inflam­mation & soft tissue injury
Clinical & physical presen­tation:
Acute cases:
- Typically, self-l­imi­ting, & inflam­mation resolves within days - weeks w/ treatment
- Similar to acute rate arthropathy
- Joint oedema, erythema, & tenderness
- Up to 50% may have a low-grade fever
- Most commonly affected joint: knee
- Other affected joints: hip, shoulders
Chronic cases:
- May show Ssx of RA inc. morning stiffness, localised oedema, & ↓ ROM
- Waxing & waning episodes of non-sy­nch­ronous, inflam­matory arthritis
- Affeects multiple non-WB joint: wrist & MCP joint
- Causes "­crowned dens syndro­me" (depos­ition of CPP around C2)
- Mostly asympt­omatic
Diagnosis:
- Confirm diagnosis through synovial fluid analysis
Imaging:
- For involved joints is recommended
- Presence of chondr­oca­lci­nosis in imaging supports CPPD Dx
- Absence of chondr­oca­lci­nosis doesn't rule out CPPD
- US may reveal early signs like cartilage abnormalities
- Radiog­raphic imaging may show joint cartilage calcification
- MRI is useful - can evaluate crystal deposition in joint cartilage
Compli­cat­ions:
- Potential of triggering inflam­matory responses
- Presence of chondr­oca­lci­nosis has associ­ations w/ degrad­ation of menisci & synovial tissue
- Pts rarely present w/ palpable nodules (resem­bling gout) that may lead to further joint degradation
- Rare spinal involv­emen, causing clinical manife­sta­tions like spine stiffness & bony ankylosis (resem­bling AS)
- Some pts present w/ manife­sta­tions similar to DISH w/ PLL calcif­ication leading to spinal cord compre­ssion Ssx
Manage­ment:
- 1st step reduce inflam­mation & addressing underlying metabolic conditions
- NSAIDs
- Acute flares inv. 1-2 joints often treated w/ joint aspiration
- Medication
- Low-al­kaline diet
Ddx:
- Tenosy­novitis w/ carpal or cubital tunnel s. can occur (multiple joints affected)
- RA
- AS
- Erosive OA
- Gout

Acute Compar­tment Syndrome

RED
Intro:
- Increased pressure in closed osteof­ascial compartmetn
- Leads to impaired local circulation
- Surgical emergency
-Untreated ACS can lead to ischemia & necrosis
Compar­tments:
- Lg has 4 compar­tments: anterior, lateral, deep posterior, & superf­icial posterior
- Anterior compar­tment is most common ACS
- Contains extensor m., tibialis anterior m., deep peroneal n., & tibial artery
*Open fractures:
- Skin laceration doesn't relieve compar­tment pressure
- ACS is still predic­table, esp. in open Gustily type 2 & 3 lesions in proximal intra-­art­icular tibia fractures
Aetiology (risk factors):
- M>F (7.3:0.7)
- Majority of cases result from trauma, w/ tibial shaft fracture being the most common
- More common in males <35 yo, possibly due to larger muscle mass & high-e­nergy trauma involvement
- Pts w/ bleeding diathesis (e.g. hemoph­ilia) are at high risk
- ACS reported w/o trauma in paediatric leukaemia cases
- Pts w/o fractures at high risk of compli­cations & delayed treatment
- Other causes:** soft tissue injuries, burns, vascular injuries, crush injuries, drug overdoses, reperc­ussion injuries, thromb­osis, bleeding disorders, infect­ions, improperly placed casts or splints, tight circum­fer­ential bandages, penetr­ating trauma, intense athletic activity, & poor positi­oning during surgery
- In children, suprac­ondylar # of the humerus & ulnar/­radial # are associated w/ compar­tment syndrome
Pathop­hys­iology:
- Caused by ↓ intrac­omp­art­mental space OR ↑ fluid volume, making the surrou­nding fascia non-compliant
- ↑ compar­tment pressure impairs hemody­namics, disrupting the equili­brium between venous outflow & arterial inflow
- Elevated compar­tment pressure leads to reduced venous outflow, ↑ venous capillary pressure
- If intrac­omp­art­mental pressure surpasses arterial pressure, arterial inflow ↓, causing tissue ischemia
- Reduced venous outflow & arterial inflow result in ↓ tissue oxygen­ation, potent­ially leading to irreve­rsible necrosis
- Normal compar­tment pressure is <10­mmHg, while reading of 30mmHg or higher indicates ACS
Clinical presen­tation:
- Can occur within few hours to up to 48h after trauma
- Px is severe & dispro­por­tionate to the injury; may be felt as a burning sensation or deep ache
- Initially, px may only occur w/ passive stretching but can be absent in advanced cases
- Parest­hesia, hypoes­thesia, or poorly localised deep muscular px may be present
- The "5 P's" (px, pulsel­ess­ness, parest­hesia, paralysis, & pallor) are classic signs, but they're typically late findings
- Parest­hesia may occur earlier
- In some cases, a pulse may still be present, even in a severely compro­mised extremity
Physical examin­ation:
- Earliest objective physical finding is the tense, or 'wood-­like' feeling int he involved compartment
Focus on neurov­ascular exam:
*
- Observe skin for lesions, swelling, or colour change
- Palpate compar­tment, noting °C, tension, & tenderness
- Check pulses in the affected area
- Evaluate two-point discri­min­ation & sensation
- Assess motor function
- Due to potential rapid progre­ssion, serial exam should be performed to monitor changes over time
Diagnosis:
- Radiog­raphs are recomm­ended if # suspected
- Measur­ement of intrac­omp­art­mental pressure (not required), can aid in Dx
- Normal pressure: 0-8mmHg
- Abnormal: exceeding 30mmHg indicates compar­tment s. & necess­itates intervention
- Pressure within 10-30mmHg of diastolic blood pressure suggests inadequate perfusion & relative ischemia, prompting clinical attention
- DUS can be used to detect occlusion or thrombus
- Elevated CPK levels may suggest muscle breakdown from ischemia, damage, or rhabdomyolysis
- Pre-op­erative studies: CBC & coagul­ation studies
Compli­cat­ions:
- Px
- Contractures
- Rhabdomyolysis
- N. damage & associated numbness &/or weakness
- Infection
- Renal failure
- Death
Manage­ment:
- Immediate surgical consult
- Keeping extremity at heart level
Ddx:
- DVT
- Cellulitis
- Peripheral vascular injury

Chronic (Exert­ional) Compar­tment Syndrome

RED
Intro:
- Often a Dx of exclusion charac­terised by ↑ pressures in a muscular compar­tment , leading to ischemia & px
- CECS inv/ recurrent, reversible ischemic episodes after activity cessation, leading to predic­table ↓ in fascial compar­tment pressures
- Rare condition w/ delayed diagnosis, resembling ACS
- Requires surgical emergency interv­ention through fascio­tomies to prevent irreve­rsible m. ischemia & neurov­ascular injury
- Usually occurs in the LL but can also affect forearm, thigh, or hand
Aetiology (risk factors):
- Relatively common among young adult athletes (running, endurance training, soccer, field hockey, & lacrosse)
- Anterior compar­tment most commonly affected (70% of cases), then deep posterior
- B limb in 37-82% of sympto­matic cases
- 20-25 yo, M>F, & often B
- Associated w/ sports like running or skating, & higher activity intensities
- Can result from overuse injuries, repetitive mechanisms causing tissue degene­ration, scar formation, & military training
- Pts w/ decreased fascial elasticity may be at risk for nerve entrapment & quicker rises in pathol­ogical pressures
Pathop­hys­iology:
- Has multiple etiologies
- Muscle compar­tment swelling during exercise, leading to increased pressure within muscul­ofa­scial compartments
- Rise in pressure compro­mises blood flow, causing px, motor weakness, & parest­hesia, in corres­ponding neurov­ascular distributions
- Specific Ssx depend on the affected compar­tment: e.g. anterior & lateral compar­tment involv­ement in the LL may present w/ px & tingling on the dorm of the foot
- Increased intrac­omp­art­mental pressure results in reduced myocyte oxygen­ation, leading to myonec­rosis & neurol­ogical damage
Clinical presen­tation:
- Pts often present following sport-­related activity ro exertion w/ non-sp­ecific leg px & persist after strenuous or repetitive activity
- Ssx will predic­tably abate following activity cessation
- Particular attention to pts charac­ter­isation of px during strenuous activity, well-l­oca­lised to a specific compar­tment, & the px/Ssx disappear quickly after the cessation of activity
- Pts will generally complain of discomfort described as squeezing, cramping, aching, or burning that typically begins within 15-20 minutes of activity
- Discomfort resolves completely w/ rest, although the duration may vary
Physical examin­ation:
- In 70-95% of cases B px
- Physical exam often unrema­rkable, esp. if not done during or immedi­ately after exercise
- Suspected cases should undergo pre- & post-e­xercise physical exams
- After exercise, the affected compar­tment may feel tender, bulge, or be tight, & passive stretching may cause px
- Focal neuro findings may inc. ↓ sensation, parest­hesia, or weakness
Stryker pressure monitoring system:
- Baseline measur­ements w/ pt at rest
- Pts then perform controlled exercise until severe Ssx occur
- After 5-minute rest, compar­tment pressure measured again
Diagnosis:
Pedowitz criteria:
-Rule out a Dx of CECS
- Resting pressure ≧ 15mmHg &/or a pressure of ≧ 30mmHg at 1 min post-e­xercise in any compar­tment, &/or;
- Post-e­xercise pressure greater than 20mmHg at 5 min post-e­xercise
Compli­cat­ions:
- Benign condition charac­terised by resolution of Ssx w/ rest
Manage­ment:
- Conser­vative treatment generally ineffe­ctive, inc. rest, activity modifi­cation, stretc­hing, orthotics, & physical therapy
- Non-op­erative modalities inc. NSAIDs, inject­ions, gait training (forefoot strike patterns)
- Open fasciotomy is the predom­inant surgical technique
Ddx:
- Initially gets misDx as shin splints or medial tibial stress syndrome (MTSS)
- Vascular pathol­ogies (inter­mittent claudi­cation, popliteal artery impingement)
- Tibial stress #
- Tendon pathol­ogies (tendi­nitis, tendin­osis, or tendon rupture)
- N. entrapment

Fibular Nerve (Peroneal N.) entrapment

GREEN
Intro:
- Branches off the sciatica n. in the distal posterior thigh & receives fibres from L4-S2 nerve roots
- Runs down the thigh, posterior to the biceps femoris m., & crosses laterally to the head of the lateral gastroc m.
- Provides sensory innerv­ation to the lateral leg via the lateral sural n.
- Two branches: superf­icial which innervates the lateral compar­tment of the leg, & deep which innervates the anterior compar­tment of the leg & foot dorsum
- Both have roles in foot eversion & dorsiflexion
Innerv­ation of superf­icial
Motor:
- Lateral compartment
- Peroneus longus
- Peroneus brevis
Sensory:
- Antero­lateral leg
Innerv­ation of deep
Motor:
- Anterior compartment
- Tibialis anterior
- Extensor hallucis longus
- Extensor digitorum longus
- Peroneus tertius
Sensory:
- First dorsal webspace
Aetiology (risk factors):
- Most common monone­uro­pathy in the LL & 3rd most common focal neuropathy overall (after carpal tunnel s. & ulnar neuropathies)
- Common in traumatic injuries in young athletes (e.g. football, soccer) & following high energy trauma (car accidents) in adults
- Occurs in about 16-40% of knee dislocations
Trauma or injury to the knee:
- Knee dislocation
- Direct impact, penetr­ating trauma, or lacerations
- Fibula #, esp. proximal fibula
External compre­ssion sources:
- Tight splint/cast
- Compre­ssion wrapping/bandage
- Habitual leg crossing
- Prolonged bed rest
- Positi­oning during anaest­hesia & surgery (important to pad bony prominences)
Systemic causes:
- Diabetes mellitus
- Inflam­matory conditions
- Anorexia nervosa
Others:
- Intramural ganglion
- Peripheral nerve tumour
- Iatrogenic injury following surgery to the hip, knee, & ankle
Clinical presen­tation:
- Varies based on location, severity, & anatomic variations
- Commonly presents w. weakness in ankle dorsiflexion
- Classic result is foot drop or catching toes while walking
- Develo­pment of acute or gradual, complete or partial
- Numbness or parest­hesia along lateral leg, dorsal foot, &/or first toe webspace
- Possible px in traumatic cases
Physical examin­ation:
- Gait: signif­icant for chronic peroneal nerve palsy w/ foot drop, high stoppage gait weakened dorsif­lexors to prevent toe dragging
Locali­sation of lesions:
- Proximal lesions (e.g. knee disloc­ations) may present w/ numbness in both superf­icial & deep n. distributions
- Upper lateral leg numbness indicates a lesion proximal to fibular head (possibly inv. sciatic n. or lumbos­acral n. roots)
- Lower lateral leg & dorms of the foot involv­ement suggests superf­icial peroneal n.
- Altered sensation in the dorsal aspect of the first web space implicates the deep peroneal n.
Motor involv­ement testing:
- Assess foot eversion (super­ficial n.) & foot/toe dorsif­lexion (deep n.)
- Weakness in both suggests common Peroneal n. involvement
- Proximal lesion may result in both distributions
- Detailed examin­ation of dorsif­lexion ability is crucial
Tinel sign:
- Tapping along the nerve course, esp. around the fibular neck
- +ve test = tingling or parest­hesia distally
Diagnosis:
- CT can be used to assess osseous abnormalities
- MRI/US suitable fro evaluating soft-t­issue sources or masses (es. in cases of traumatic knee dislocations)
- Electr­odi­aag­nostic studies (inc. NCV & EMG) are used to Dx peroneal nerve palsy
- They evaluate motor & sensory axons of the peroneal n. aiding in locali­sation of the nerve injury
- Useful in post-o­per­ative setting of a known traumatic injury for long-term management planning & pt care
Manage­ment:
- Full physical therapy
- Ankle-foot orthoses, even for foot-drop when surgery isn't warranted
- Surgical indica­tors: rapid deteri­oration & no signs of improv­ement within 3 months & open injuries w. suspected nerve laceration
-Open lacera­tions should undergo explor­ation & surgical repair within 72h
Ddx:
- Peroneal tendon pathology
- Other compre­ssive neurop­athies (tarsal tunnel s., anterior tarsal tunnel s., non-sp­ecific tendinitis affecting lower limb m./t.)
- Chronic ankle px

Meniscal Tears

YELLOW
Intro:
- Lateral & medial menisci function in load transm­ission & shock absorption in the tibiof­emoral joint
- Inner 2/3 (white zone) of the menisci is avascular, likely receiving nutrition through synovial fluid diffusion
- Peripheral 1/3 (red zone) is well-v­asc­ula­rised, supplied by branches of the medial & lateral vehicular arteries
- Medial meniscus is less mobile than the lateral one, firmly attached to the joint capsule & deep fibres of the MCL
- Lateral miscues doesn't connect w/ the LCL & has looser attach­ments w. the joint capsule
- Anterior margins of the menisci are connected by the transverse inter meniscal ligament
- Peripheral 2/3 of the menisci contain nocice­ptive free endings (pain percep­tion), while mechan­ore­ceptors are in the anterior & posterior horns, suggesting a propri­oce­ptive function
- Posterior horn of the lateral meniscus connects to the femur via menisc­ofe­moral ligaments & the adjacent popliteus tendon
Aetiology (risk factors):
- 61/100,000 in general population (USA), 9/1000 in military population
- 15% of sports injuries
- M>F
- Age >40 yo
- ACL deficient knees, esp. if ACL recons­tru­ction is delayed beyond 1 year from initial injury
- Medial­>la­teral meniscal tears
- Increased risk factors: infant­ry-­related duties, frequent squatt­ing­/kn­eeling, & partic­ipation in sports like soccer, rugby, football, basket­ball, baseball, skiing, & wrestling
- Traumatic impacts to the knee can lead to isolated meniscal tears or tears concom­itant w/ bony lesions or damage to primary stabil­ising ligaments (ACL & MCL)
- Less force is required for tears in indivi­duals w/ degene­rative changes of the menisci, typically seen in adults >40 w. concom­itant OA
- Isolated meniscal tears result from rotational or shearing forces across the tibiof­emoral joint, esp. during activities w/ increased closed kinematic chain FX, heavy lifting, rapid accele­rat­ion­/de­cel­era­tion, change of direction, & jumping
Pathop­hys­iology:
- Charac­terised by shape & location on MRI
- Horizontal (cleavage) run parallel to the tibial plateau, associated w/ degene­rative changes in people >40 w/o specific causes
- Longit­udinal run perpen­dicular to the tibial plateau & parallel to the meniscus axis
- Radial run perpen­dicular to both the tibial plateau & the meniscus axis, origin­ating from the inner free edge
- Complex involve combin­ations of horizo­ntal, longit­udinal, or vertical tears
- Displaced involve complete detachment or flipping of a piece still attached to the meniscal body
- Bucket­-handle are complete longit­udinal tear fragments that migrate centrally
- Parrot­-break are radial tears w/ partially detached fragments
- Flap are partially detached fragments of horizontal tears
- Tears in the outer 1/3 vascular zone are "­red­-re­d"; those extending into the inner 2/3 avascular zone are "­red­-wh­ite­", & tears within the inner 2/3 avascular zone are "white-white"
- Tears in the red zone have the highest potential for sponta­neous healing w/ conser­vative management or successful outcomes after meniscal repair
Clinical presen­tation:
- "­POP­" sensation w/ immediate knee effusion suggests ACL tear w/ possible medial meniscal involvement
- Gradual effusion over 24h indicates an isolated meniscal tear
- Ssx can be insidious, featuring low-grade effusi­on& stiffness w/o a specific triggering event
- Px commonly reported along the antero­medial or antero­lateral joint line
- Additional Ssx: locking, clicking, catching, interm­ittent inability to fully EXT the knee, & a sense of the knee giving way
Physical examin­ation:
- Inspection of edema, palpation of joint line, standing & supine ROM, muscle strength testing, special testing
- Antero­medial & antero­lateral joint line tenderness at 90° FX
- Px & deficits in FX or EXT ROM may vary based on tear type & effusion extent
- Deficits in open kinetic chain knee FX/EXT strength testing are unlikely
- Antalgic gait or increased px w/ squatting may indicate meniscal issues due to compre­ssive forces
- Special tests: Thessaly test, McMurray's test, Apley's compre­ssion test
Diagnosis:
- Begin w/ radiog­raphs - AP, lateral, oblique, sunrise, & WB views to assess concom­itant bony pathol­ogies, loose bodies, & OA
- Arthro­scopy is the gold standard
- MRI is the best mode of imaging to Dx & charac­terise tears
Manage­ment:
- RICE
- NSAIDs
- Early px-free knee & ankle ROM exercise (help limit motion loss & aid edema)
- Bracin­g/s­leeves (prote­ction & compression)
Simple tears (outer 1/3 of the meniscus) & degene­rative tears:
- 4-6 weeks relative rest & physical therapy
- Despite conser­vative manage­ment, pts w/ persistent px, swelling, & mechanical Ssx should be evaluated for surgical intervention
Surgical tears:
- Meniscal repair is preferred over menisc­ectomy (risk of accele­rated OA)
- Factors ↑ success: tears that occur in red zone of the meniscus, shorter than 2cm, vertical longit­udinal tears, & acute tears
Rehab:
- First 6 weeks inc. restri­ctions in knee FX ROM & WB status (depending on tear & repair type)
- Strengthening
- Mobs
Ddx:
- ACL injury
- Contusions
- ITB syndrome
- Knee osteochondritis
- LCL injury
- Lumbos­acral radiculopathy
- MCL injuy
- Medial synovial plica irritation
- Patell­ofe­moral joint syndrome
- PCL injury

Osgood­-Sc­hlatter Disorder (OSD)

GREEN
Intro:
- Common cause of anterior knee px in skeletally immature athletes
- Also known as osteoc­hon­drosis or traction apophy­sitis of the tibial tubercle
- Common in sports like basket­ball, volley­ball, sprinting, gymnas­tics, & football
- Self-l­imiting & results from repetitive stress on the extensor mechanism (jumping/sprinting)
- While benign, OSD can lead to prolonged recovery & absence from sports
Aetiology (risk factors):
- Leading cause of knee px in adolescent athletes
- Onset typically aligns w/ growth spurts: 10-15 M & 8-13 F
- M>F
- 9.8% of adoles­cents 12-15 yo (11.4% M; 8.3% F)
- B Ssx observed in 20-30% of pts
- Overuse injury due to repetitive strain from patellar tendon
- Force increases w/ higher activity levels, after rapid growth
- Predis­posing factors: poor flexib­ility of quadriceps & hamstr­ings, extensor mechanism misali­gnment
Pathop­hys­iology:
- Tibial tubercle develops as a 2° ossifi­cation centre for patellar tendon attachment
- Bone growth surpasses muscle­-te­ndo­n-b­one­-at­tac­hment, suscep­tible to injury from repetitive stress
- Repeated quadriceps muscle contra­ction, esp. in sports involving running & jumping, can cause apophyseal ossifi­cation centre softening & partial avulsion, resulting in osteochondritis
Tibial tubercle develo­pment sequence:
- Entirely cartil­aginous before age 11
- Apophysis forms between 11-14
- Apophysis fuses w/ proximal tibial epiphysis between 14-18
- Proximal tibial epiphysis & tibial tubercle apophysis fuse w/ the rest of the proximal tibia after age 18
- Prevailing theory: repeated traction over tubercle causes microv­ascular tears, fractures, inflam­mation
Clinical presen­tation:
- Common Ssx: anterior knee px
- Presen­tation: w/ or w/o swelling, unilateral or bilateral
- Onset: typically insidious, w/o preceding trauma
- Nature of px: dull ache localised over tibial tubercle
- Px progre­ssion: gradually increases w/ activity
- Px relief: typically improves w/ rest
- Duration of relief: subsides minutes to hours after stopping activity or sport
- Exacer­bating factors: running, jumping, direct knee trauma, kneeling, & squatting
Physical examin­ation:
- Enlarged prominence at the tibial tubercle
- Tenderness over the patellar tendon insertion site
- Reprod­uction of px: resisted knee EXT & active­/pa­ssive knee FX can reproduce px
Diagnosis:
- 1° Dx clinic­ally, radiog­raphic evaluation typically not necessary
- Consider comparing B images to help delineate normal vs abnormal in the pt
Radiog­raphic use:
- Plain radiog­raphs may be employed in severe or atypical presentations
- Used to rule out additional conditions like fractures, infect­ions, or bone tumours
- Assessment fro avulsion injury or other traumas may necess­itate radiog­raphic evaluation
Classic findings:
- Elevated tibial tubercle w/ soft tissue swelling
- Fragme­ntation of the apophysis
- Calcif­ication in the distal patellar tendon
Compli­cat­ions:
- Prominence of tibial tubercle
- Ongoing px
- Ssx continue to adulthood if treatment isn't provided or poor compliance w/ recomm­ended treatment
Manage­ment:
- Excellent prognosis
- Self-l­imiting but time to resolution can take up to 2 yrs until apophysis fuses
- Surgery rarely indicated, low benefit & high compli­cation risk
- Relative rest & activity modifi­cation based on px levels
- Partic­ipation in sports allowed if px resolves w/ rest & doesn't limit activities
Px manage­ment:
- Ice & NSAIDs
- Protective knee pad recomm­ended over tibial tubercle to prevent direct trauma
- Hamstring & quadriceps stretc­hing, & strengthening
- In severe cases, short knee immobi­lis­ation might be considered
Refractory cases:
- In up to 10%, Ssx may persist >1-2 yrs beyond skeletal maturity
- Ossicle excision may be performed in skeletally mature pts w/ persistent Ssx
Ddx:
- Patella tendonitis
- Osteom­yelitis of the tibia
- Perthes disease
- Synovial place injury
- Infectious apophy­sitis

Osteoc­hon­dritis Dissecans (OCD)

YELLOW
Intro:
- Rare condition affecting the knee, catego­rised as a form of osteon­ecrosis in the subcho­ndral bone
- 1° occurs in school­-aged children & adoles­cents, w/ manife­sta­tions of the dysfun­ction & px
- Juvenile OCD occurs in pts w/ open growth plates, while adult OCD applies to skeletally mature pts
- If left untreated, OCD can lead to degene­rative changes, chronic px, & mechanical Ssx such as 'locking' & 'clicking'
Aetiology (risk factors):
- Highest incidence 12-19 yo
- 9.5-29 / 100,00
- M>F
- 75% of affected pts have knee lesion, w/ 64% localised in the medial femoral condyle
- 32% of knee lesions are found in the lateral condyle, while other cases localise to the trochlea, patella, & tibial plateau
- Usually unilat­eral, but 7-25% of pts have B disease
- Theories inc. micro-­trauma, ischemia, & genetic predisposition
- Pts w. extreme obesity & elevated BMI face an increased risk of developing OCD
- Repetitive trauma is widely considered the 1° cause of OCD of the knee
- Adult form of OCD is believed to result from vascular insult
Pathop­hys­iology:
- Disruption of epiphyseal vessels, leading to ischemia & necrosis at trauma site
- Softening, tearing, fissuring, & erosion of hyaline cartilage follow as a conseq­uence of the disrupted blood supply
- Advanc­ement of the affected area result in focal demine­ral­isation & repeated shear forces, causing detachment of bone & overlying cartilage
- Repetitive axial loading, esp. w/ increased valgus & varus stress, is suggested by experts as a contri­buting factor tot he condition
- OCD lesions can introduce irregu­lar­ities in the articular surface, potent­ially leading to degene­rative arthritis
Clinical presen­tation:
- Vague, poorly localised knee px that worsens w/ activity
- Stiffness & occasional swelling may occur during or after activity as the disease progresses
- Advanced stages may be indicated by locking or catching, suggesting the presence of a sizeable loose body in the knee
- Hx of trauma, recent increase in activity level, previous knee injuries, & the presence of mechanical Ssx
- Approx. 80% of pts report px when WB
- Juvenile: interm­ittent, activi­ty-­ass­ociated px poorly localised around the anterior aspect of the joint
- Adult: more likely effusion, limited ROM, or mechanical Ssx such as 'catching or locking'
- Depending on chronicity of the lesion, pts may report quadriceps dysfun­ction & interm­ittent knee instab­ility
Physical examin­ation:
- Genu varus, associated w/ lesions at medial femoral condyle
- Genu valgus, associated w/ lesions at lateral femoral condyle
- Quadriceps atrophy or weakness may be evident
- Foreign body may be palpable
- FX of knee during joint palpation can reveal effusion or bony tenderness along the femoral condyles
- ROM may be restricted due to px, swelling, or the presence of a loose body
- Antalgic gait or lateral rotation of the foot on the affected side may indicate efforts to alleviate WB px
Wilson sign:
- Identifies lesions of the lateral aspect of the medial femoral condyle
- +ve test: px w/ INT ROT, relieved by EXT ROT, indicating imping­ement of the OCD lesion
- Absence of the Wilson sign does not rule out OCD
Diagnosis:
- Arthro­scopy is the gold standard for assessing lesion stability
- Plain radiog­raphs used to locate the lesion, assess growth plates, & rule out other conditions
- Initial radiog­raphs may appear normal in OCD
Lesion charac­ter­istics:
- Distinct Lucent areas w/ varying density levels
- Calcif­ica­tions & Lucent lines may or may not be present, depending on lesion severity
- B comparison
Classi­fic­ation:
- Lesion location can provide important prognostic info
- Atypical locations like trochlea or patella may not respond effect­ively to conser­vative management
MRI evalua­tion:
- Useful for assessing unstable lesions presenting w/ mechanical Ssx or knee effusion
- Unstable lesions on mRI may exhibit increased T2 signal, destru­ction of overlying articular cartilage, or multiple cyst-like foci
- Gadolinium contrast may be necessary for assessing blood supply & stability uncertainties
- Line of high signal intensity between fragment & underlying bone is a sensitive progno­sti­cator
Compli­cat­ions:
- If left untreated, adults often progress to arthritis
- Degene­rative articular changes over time
- A non-union & dissoc­iation of the bony fragment
- Chronic px & mechanical Ssx
- Surgical compli­cations inc. postop infection, pneumonia, haemor­rhage, & reactions to anesthesia
- Venous thrombosis due to immobility
Manage­ment:
- Prognosis influenced by age, location & appearance of lesion
Non-op­era­tive:
- Recomm­ended for juvenile pts w/o a displaced fragment OR stage 1-3 disease
- Immobi­lis­ation & protected WB for 4-6 weeks
- Physical therapy initiated after immobi­lis­ation & continued until pain-free, achieving full ROM, strength, power, & mobility
- NSAIDs for px & edema
Operative:
- Surgery recomm­ended if conser­vative treatment ineffe­ctive after 3-6 months or if not suitable
- 1° tre­atment for Ssx related to OCD in adults, stage 2 disease, or expanding lesions on radiographs
- Surgical interv­ention warranted in juveniles w/ stage 4 disease, loose bodies, unstable lesions, or impending physeal closure
Ddx:
Juvenile:
- Patell­ofe­moral syndrome
- Patellar tendonitis
- Osgood­-Sc­hlatter disease
- Sindin­g-L­ars­en-­Joh­ansson syndrome
- Fat pad impingement
- Symptomati discoid meniscus
- Sympto­matic synovial plica
Adult:
- Patell­ofe­moral px
- Knee OA
- Chondromalacia
- Patellar tendonitis
- Meniscal tear
- Fat pad impingement
- Sympto­matic synovial plica
Adult w/ more severe Ssx:
E.g. atraumatic edema & mechanical Ssx
- Meniscal tear
- Osteoc­hondral loose body
- Neoplasm

Patell­ofe­moral Pain Syndrome (PFPS)

GREEN
Intro:
- Also known as Chondr­oma­lacia patella (CMP) & Runner's knee
- Softening of hyaline cartilage on articular surfaces of bones
- CMP specif­ically refers to the softening, tearing, fissuring, & erosion of the patellar cartilage
- Can occur in any joint, but common in joints w/ trauma & deform­ities
Aetiology (risk factors):
- F>M
- Increased Q angles in F (lateral positi­oning of the patella)
- No hormonal cause has been identified
- Active young adults (esp. running sports), & workers who stress their patell­ofe­moral joint (stairs, kneeling)
- Often multifactorial
- LL malali­gnment & patellar maltra­cking play a signif­icant role
- Foot & ankle variances: pes planus can lead to increased lateral wear of the patell­ofe­moral joint
- Miserable malali­gnment syndrome, w/ femoral ante version, gene valium, & pronated feet
- Muscular weakness: vests medals & core m.
- Patellar lesions from injuries, immobi­lis­ation, or surgical procedures causing quadriceps atrophy
- Abnormal wear & tear of the patell­ofe­moral joint's hyaline cartilage
- Iatrogenic factors: injecting chondr­otoxic medica­tions into joints
Pathop­hys­iology:
Pathol­ogical process:
- Hyaline cartilage composed of chondr­ocytes, type 2 collagen, proteo­gly­cans, & water
- Avascular w/ nutrients diffusing from synovial fluid
- Poor repair due to lack of blood supply, devoid of lymphatic & neural tissue
Factors leading to hyaline cartilage degene­ration:
- Destru­ction by chondr­otoxic substa­nces, cytoki­nins, & proteo­lytic enzymes
- Microt­rauma from wear & tear
- Repeated compre­ssive stress or increased loads on patell­ofe­moral joint
- Aging-­related decrease in chondr­ocytes, proteo­glycan produc­tion, & water content
- Cross-­linking of collagen fibrils leads to loss of elastic properties
- Superf­icial zone of hyaline cartilage is the 1st to degenerate in aging process
Px genera­tion:
- Anterior fat pad & joint capsule commonly involved in generating px signals
- SUbcho­ndral bone less likely to cause px signals
-Initiation of CMP pathology: begins w/ softening, swelling, & edema of articular cartilage
Clinical presen­tation:
- CC: anterior knee px
- Pts may report insidious onset of diffuse retrop­atellar or pre patellar px, exacer­bated by activities stressing the patell­ofe­moral joint
- Aggrav­ating factors: stair ascending or descen­ding, squatting, kneeling, running, & prolonged sitting (theatre px)
- Additional Ssx: effusion, quadriceps wasting, & retrop­atellar crepitus (not specific to CMP)
- Hx evalua­tion: previous trauma, comorbid condit­ions, joint stability, foot & ankle issues, & activity levels
Physical examin­ation:
- Px is usually sharp & achy
- Examine quadriceps appear­ance, foot & ankle orient­ation, & specific evaluation of the patell­ofe­moral joint
- Patella malt racking signs: increased femoral anteve­rsion, EXT tibial torsion, lateral patella sublux­ation, loss of medial patellar mobility
- +ve patellar appreh­ension test
- +ve Clark's test
Diagnosis:
- Reliable Dx requires excluding other conditions causing anterior knee px
- Arthro­scopy is the most efficient (invasive, so non-in­vasive methods essential for initial Dx)
- Plain radiog­raphs: lower sensit­ivity in earlier stages
- CT: measures TT-TG distance & detects torsional deform­ities of the LL
- MRI: modality of choice fro articular cartilage, esp. T2 sequence
Compli­cat­ions:
- 2° to NSAID usage (e.g. GI Ssx)
- Bracing may cause dermat­olo­gical reactions
Manage­ment:
- Min. 12 months of conser­vative management before consid­ering surgery
- May be reversible
- Could progress to patell­ofe­moral OA
- Pts often fully recover (can take months to yrs)
Conser­vative 1st phase:
- Activity modification
- RICE
- NSAIDs
Conser­vative 2nd phase:
- Knee + hip exercise to increase strength, mobility & function
- Patella taping
Ddx:
- Patell­ofe­moral OA
- Osgood-Schlatter
- Plica syndrome
- Bursitis
- Saphenous neuritis
- Quadriceps tendinopathy
- Patellar tendinopathy
- Referred px from hip/back

Medial Tibial Stress Syndrome (MTSS)

GREEN
Intro:
- Early stress injury leading to tibial stress fractures
- Known also as shin splints
- Common overuse injury in athletes & military personnel
- Involves exerci­se-­induced px along the anterior tibia
Aetiology (risk factors):
- 13-20% incidence in runners
- Up to 35% in military
- Factors contri­buting: signif­icant increasing loads, volume, & high-i­mpact exercises
- Intrinsic risk factors: F gender, previous MTSS Hx, high BMI, navicular drop, ankle plantar FX range, hip EXT ROT range
- Overuse condition, specif­ically a tibial bony overload injury w/ associated periostitis
- Common for: recurrent impact exercise, such as running, jumping, & military personnel
- Suggested link between vitamin D & increased risk of stress injury
Pathop­hys­iology:
- Involves accumu­lation of unprepared micrdamage in the cortical bone of the distal tibia
- Overlying perios­titis is typically present at the site of bony injury
- Perios­titis correlates w/ tendinous attach­ments of soleus, flexor digitorum longus, & posterior tibialis
- Sharpey's fibers, perfor­ating connective tissue linking periosteum to bone, play a role in the mechanical connection
- Repetitive muscle traction is believed to be the underlying cause of perios­titis & cortical microt­rauma
Clinical presen­tation:
- Presence of exerci­se-­induced px along the distal 2/3 of the medial tibial border
- Presence of px provoked during or after physical activity, which reduces w/ relative rest
- The absence of cramping, burning px over the posterior compar­tment &/or numbne­ss/­tin­gling in the foot
Physical examin­ation:
- Presence of recogn­isable px reproduced w/ palpation of the poster­omedial tibial border >5cm
- The absence of other findings not typical of MTSS (e.g. severe swelling, erythema, loss of distal pulses, etc)
Diagnosis:
- Dx through clinical & physical findings
- Imaging done when uncertain about cause or to rule out other exerci­se-­induced LL injuries
- Plain radiog­raphs are normal in MTSS & early stress fractures
- "­dreaded black line" indicates a stress fracture
- MRI is preferred for identi­fying MTSS & higher­-grade bone stress injuries like tibial stress fractures
Compli­cat­ions:
- Px leading to decreased perfor­mance &/or time away from training/participation
- May progress to tibial stress fracture
- Severe tibial stress fractures may require surgical interv­ention
Manage­ment:
- Full recovery is expected
- Rest & activity modifi­cation w/ less repeti­tive, load-b­earing exercise
- Additional therapies: iontop­hor­esis, phonop­hor­esis, ice massage, US therapy, periosteal pecking, & extrac­orp­oreal shockwave therapy
- No benefit: low-energy laser therapy, stretc­hing, streng­the­ning, LL braces, & compre­ssion stockings
- Slow response cases: optimising calcium & vitamin D status & gait retraining may improve recovery & prevent further progre­ssion
Ddx:
- Tibial stress fracture
- Compar­tment syndrome
- Functional popliteal artery entrapment syndrome

Varicose Veins

YELLOW
Intro:
- Charac­terised by subcut­aneous dilated, tortuous veins of ≧3mm
- Age & FHx are important risk factors
- Common clinical manife­sta­tions of chronic venous disease
- Evaluating associated superf­icial axial venous reflux is crucial
- Manife­sta­tions can range from limited leg discomfort to swelling & non-he­aling ulcers
Aetiology (risk factors):
- Up to 30% of general population
- F>M
- Risk factors: F gender, multip­arty, high BMI, consti­pation, Hx of venous thromb­osis, smoking, & circul­ating iron levels
- Both genetic & enviro­nmental factors
Pathop­hys­iology:
- Valve dysfun­ction leads to increased pressure in veins
- Elevated pressure causes vein walls to weaken & dilate
- Ironic pressure causes the vein walls to stretch & lose elasticity
- Weakened walls contribute to the develo­pment of varico­sities
Clinical presen­tation:
- Leg heaviness
- Itching
- Cramps
- Mild tenderness
- Skin discoloration
- Exercise intolerance
- Leg fatigue
Physical examin­ation:
- Visible distended veins from thigh to ankle
- Discol­our­ation most prominent around ankle & calf
- Special test: Trende­lenburg test - assesses deep venous valve competency
Diagnosis:
CEAP classi­fic­ation:
- C0: no visible, palpable signs
- C1: spider veins
- C2: varicose veins
- C3: edema
- C4a: pigmen­tation, eczema
- C4b: lipodermatoslerosis
- C5: healed ulcer
- C6: active ulcer
- Colour duplex venous US exam is recomm­ended for suspected venous reflux
Compli­cat­ions:
- Venous ulcers
- Pain
- Poor cosmesis
- DVT
- PE (rare)
- Superf­icial thromb­oph­lebitis might be compli­cated w/ prolonged bleeding & px
- Superf­icial vein thrombosis
Manage­ment:
- No cure
- Long-term graduated compre­ssion stockings, leg elevation, & oral px medication
- Surgery (recur­rence is likely )
Ddx:
- Lymphedema
- DVT
- Cellulitis
- Dermat­olo­gical disorders (e.g. stasis dermat­itis)

Vasculitis

RED
Intro:
- Hetero­genous group of over 30 different kinds of vascul­itis. presenting either as a 1° process or 2° to another pathology
- Clinical & pathol­ogical manife­station vary based on the affected blood vessels' type & location
Aetiology (risk factors):
- Incidence of 20-40 million / year
- Gender dominance depending on type of vasculitis
- Giant cell arteritis is the most common form
- Risk factors: Behcet disease (ancient Silk route), Takayasu disease (South Asian), Kawasaki disease (children <5), hepatitis B/C
Pathop­hys­iology:
- Unknown specific cause
- Immune system activa­tion: becomes overactive
- Inflam­mation of blood vessels: immune system mistakenly identifies blood vessels as foreign invaders
- Attack on endoth­elium: attacks the endoth­elium (inner lining of blood vessels)
- Adhesion molecules & leukocyte activa­tion: cytokines. signalling molecules in the immune system, cause changes in adhesion molecules on the endoth­elium → inappr­opriate activation of leukocytes & their adherence to the blood vessel walls
- Vessel damage: combined effect of immune cells sticking to the blood vessel walls & the inflam­matory response damages the vessels
- Formation of immune complexes or antibo­dies: different forms of vasculitis may involve the formation of immune complexes or the production of antibodies targeting specific components in the blood vessels
- Granuloma formation (in some cases): in certain vasculitis types. granulomas may form. contri­buting to tissue damage
Clinical presen­tation:
- Ssx dependent on location of vasculitis
- Potential organ damage from vasculitis
- Fevers, unexpl­ained weight loss
- Nose bleeding, hemopt­ysis, hematuria
Physical examin­ation:
- Upper airway disease
- Ocular inflammation
- Limb claudication
- +ve sensor­y/motor neurop­athy, purpura, change of pulses
Diagnosis:
- Chest x-ray or high-r­eso­lution CT for respir­atory Ssx
- Vascular imaging (MRI, MRA, CTA, vascular US, PET) to detect large artery lesions in vasculitis cases
-Labs: CBC, kidney & liver function, ESR, serolo­gies, & urinalysis w/ urinary sediment
Compli­cat­ions:
- Depend on the type of vessel involved
- Large vessel involv­ement: acute MI, stroke, mesenteric ischemia, aortic s., critical extremity ischemia
- Life threat­ening compli­cations of small vessels: alveolar haemor­rhage, renal failure, intestinal ischemia
Manage­ment:
- Long-term survival highly depends on the Dx, response to treatment, & adverse effects of drugs
- Managed w/ medication
- 3 main compon­ents: remission induction, remission mainte­nance, & monitoring
Ddx:
- Infect­ions, neoplasms & certain drug toxicities can mimic vasculitis
- Coagul­opa­thies can present w/ similar Ssx to vasculitis

Venous Thromb­o-e­mbolism (VTE)

RED
Intro:
- Signif­icant compli­cation of hospitalisation
- 3rd leading CV Dx, following heart attacks & strokes
- VTE encomp­asses DVT & PE
- Growing public health concern
- Need for increased awareness among the public & healthcare providers
Aetiology (risk factors):
- Global annual burden of VTE is in millions
- Signif­icant morbidity & mortality associated w/ VTE cases worldwide
- Majority of VTE cases are hospit­al-­related or acquired (60%)
- Leading preven­table cause of death in hospit­alised pts
- Risk factor: >40 yrs, obesity, varicose veins, immobi­lity, oral contra­cep­tive, smoking, hyperc­oag­ula­bility, pregnancy, & pelvic­/hi­p/l­ong­-bone fractures
- Disease states ↑ risk: malign­ancies, spinal cord injury, nephrotic s., congestive heart failure, IBD, & recent MI
Pathop­hys­iology:
- Venous thrombosis involves the formation of a clot made of platelets & fibrin within blood vessels
- Clinically signif­icant thrombi typically form in large-­lumen vessels, such as deep veins in the legs, pelvis, & arms
- Clots can propagate & extend proxim­ally, leading to clinical Ssx when vascular flow is obstructed
- Dislodged clots may embolise to distant sites, w/ the pulmonary vascul­ature being a common location
- Obstru­ction in pulmonary vascular flow can result in impaired gas exchange, alveolar edema, & pulmonary alveolar necrosis
- Chronic repetitive pulmonary emboli­sation can increase pulmonary vascular resist­ance, ultimately causing pulmonary hypertension
- In the presence of cardiac abnorm­alities like a patent foramen ovale or atrial septal defect, parado­xical embolism may occur, leading to systemic arterial vascular involv­ement
Clinical & physical findings of DVT:
- Unilateral limb px is a common complaint
- Physical signs may include swelling, warmth, & tenderness to touch
- Physical exam signs for DVT have low Dx yield
Clinical & physical findings:
- Sudden onset of dyspnea (most common presenting complaint)
- Pleuritic chest px, cough, & hemoptysis
- Massive PE can lead to syncope, hypote­nsion, & shock
- Physical examin­ation findings for PE are variable & often nonDx
- Tachypnea (resp. rate >18­/min) is common
- In older pts, new-onset atrial fibril­lation may be a presenting Ssx
Establ­ished PE physical findings:
- Tachypnea (resp. rate >18­/min) is common
- Rales may be present in up to 50% of cases
- Tachyc­ardia (HR >10­0/min) & fever occur in about 45%
- Diapho­resis & S3 or S4 gallop may be audible in about 30%
- Pleural friction rub may indicate peripheral PE w/ pulmonary necrosis
Diagnosis:
- Chest radiography
- D-dimer assay
- US & serial US for DVT
- CTPA & VQ for PE
Compli­cat­ions:
- Bleeding
- Hepari­n-i­nduced thrombocytopenia
- Warfar­in-­induced skin necrosis
Manage­ment:
- Treatment is based on associated conditions
- 1° tre­atment is antico­agu­lation
Ddx:
- Localised Ssx of DVT can be similar to cellul­itis, arterial insuff­ici­ency, lymphe­dema, & hematoma
- PE: congestive heart failure, acute respir­atory distress s., pneumonia, & MI
       
 

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