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  /Title (6002-knee-and-lower-leg.pdf)
  /Creator (Cheatography)
  /Author (bee.f (bee.f))
  /Subject (6002 Knee \& Lower Leg Cheat Sheet)
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    \vspace{-2pt}\large{\bf{\textcolor{DarkBackground}{\textrm{6002 Knee \& Lower Leg Cheat Sheet}}}} \\
    \normalsize{by \textcolor{DarkBackground}{bee.f (bee.f)} via \textcolor{DarkBackground}{\uline{cheatography.com/180201/cs/42420/}}}
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  \vspace{-2pt}bee.f (bee.f) \\
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  \mymulticolumn{1}{p{5.377cm}}{\bf\textcolor{white}{Cheat Sheet}}  \\
   \vspace{-2pt}Published 11th March, 2024.\\
   Updated 11th March, 2024.\\
   Page {\thepage} of \pageref{LastPage}.
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Anterior Cruciate Ligament (ACL) Injuries}}  \tn
% Row 0
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
% Row Count 1 (+ 1)
% Row 1
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• {\bf{Intro:}} & - Stabilises the knee joint along w/ the PCL (forms a cross "X")\{\{nl\}\}- Prevent excessive forward or backward motion of the tibia relative to the femur during FX \& EXT\{\{nl\}\}- {\bf{Nerve supply:}} middle geniculate artery; {\bf{Innervation:}} posterior articular n. (branch of tibial n.)\{\{nl\}\}- {\bf{Origin:}} anteromedial aspect of tibial plateau; {\bf{Insertion:}} Medial aspect of the lateral femoral condyle\{\{nl\}\}- Has 2 bundles (anteromedial \& posterolateral)\{\{nl\}\}- \tn 
% Row Count 22 (+ 21)
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• {\bf{Aetiology (risk factors):}} & - Most commonly injured ligament in the knee (almost $\frac{1}{2}$ of all knee injuries)\{\{nl\}\}- F\textgreater{}M (esp. F athletes 4.5:1)\{\{nl\}\}- Possible factors contributing to increased F risk include: weaker hamstrings, preferential recruitment of quads during deceleration, \& weaker core stability\{\{nl\}\}{\bf{Biomechanics \& landing factors:}}\{\{nl\}\}- F landing mechanics mat ↑ injury risk, w/ ↑ valgus angulation \& knee EXT\{\{nl\}\}- ↓ hip \& knee FX \& ↓ fatigue resistance also contribute to ↑ stress on the ACL\{\{nl\}\}{\bf{Other risk factors:}}\{\{nl\}\}- Anatomical: high BMI, smaller femoral notch, impingement on the notch, smaller ACL, hypermobility, joint laxity, \& previous ACL injury\{\{nl\}\}{\bf{Hormonal \& genetic factors:}}\{\{nl\}\}- Preovulatory phase, may affect coordination \& predispose females to ACL injury\{\{nl\}\}- Females on OCP were noted less affected\{\{nl\}\}{\bf{Associated injuries w/ ACL ruptures:}}\{\{nl\}\}- Both intra \& extra-articular injuries can accompany acute ACL ruptures\{\{nl\}\}- Meniscal tears are common, w/ lateral meniscus injury more prevalent in acute cases, \& medial meniscus more involved in chronic cases\{\{nl\}\}- Other ligaments (PCL, LCL, \& PLC) could also be injured in conjunction w/ ACL\{\{nl\}\}{\bf{Chronic ACL deficiency effects:}}\{\{nl\}\}- Detrimental effects on the knee\{\{nl\}\}- Development of chondral injuries \& complex, unrepairable meniscal tears is observed (e.g bucket handle medial meniscus tears) \tn 
% Row Count 86 (+ 64)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Anterior Cruciate Ligament (ACL) Injuries (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - Common in non-contact sports, esp. non-contact pivoting injuries\{\{nl\}\}- Tibia translation anteriorly during slight knee FX \& valgus\{\{nl\}\}- Direct hits to the lateral knee can also cause ACL injuries\{\{nl\}\}- 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 \tn 
% Row Count 18 (+ 18)
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• {\bf{Clinical presentation:}} & - Hx of injury mechanisms\{\{nl\}\}- Pt would complain of hearing/feeling a sudden {\bf{"pop"}} w/ associated deep knee px\{\{nl\}\}- About 70\% would experience immediate swelling due to haemarthrosis\{\{nl\}\}- Other Ssx: knee "giving way", difficulty ambulating, reduced knee ROM \tn 
% Row Count 31 (+ 13)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Anterior Cruciate Ligament (ACL) Injuries (cont)}}  \tn
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• {\bf{Physical examination:}} & - Pt demonstrates quadriceps avoidance gait (no active knee EXT)\{\{nl\}\}- Varus knee malalignment should be noted as it increases risk of ACL re-rupture\{\{nl\}\}- Palpation: swollen knee, \& potential joint line tenderness w/ an associated meniscal injury\{\{nl\}\}- Move: knee may be {\bf{locked}} due to associated meniscal injury (other meniscal \& ligamentous structures to be assessed)\{\{nl\}\}- Lachman test, Anterior drawer test, Pivot shift test \tn 
% Row Count 20 (+ 20)
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• {\bf{Diagnosis:}} & - {\bf{MRI}} is the 1° modality to diagnose ACL pathology\{\{nl\}\}- Knee arthroscopy to differentiate complete from partial tears \& chronic tears (gold standard test)\{\{nl\}\}- Radiography to rule out fractures \& other osseous injuries \tn 
% Row Count 31 (+ 11)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Anterior Cruciate Ligament (ACL) Injuries (cont)}}  \tn
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• {\bf{Complications:}} & - Surgical: tunnel malpositioning, posterior wall blowout, graft failure due to various other issues\{\{nl\}\}- Post op: infection \& septic arthritis\{\{nl\}\}- Stiffness \& arthrofibrosis\{\{nl\}\}- Infrapatellar contracture syndrome\{\{nl\}\}- Patella tendon rupture\{\{nl\}\}- CRPS\{\{nl\}\}- Patella fracture\{\{nl\}\}- Tunnel osteolysis\{\{nl\}\}- OA in the long term\{\{nl\}\}- Saphenous n. irritation\{\{nl\}\}- Cyclops lesion \tn 
% Row Count 18 (+ 18)
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• {\bf{Management:}} & {\bf{Non-operative management:}}\{\{nl\}\}- {\bf{Indication:}} when there's reduced ACL laxity on low-demand pts or athletes involved in no cutting or pivoting activities or partial ACL tears\{\{nl\}\}- RICE\{\{nl\}\}- Non-WB (crutches or wheelchair)\{\{nl\}\}- NSAIDs\{\{nl\}\}- Phase 1: acute symptomatic treatment\{\{nl\}\}- Phase 2: 12 weeks of supervised physiotherapy starting w/ regaining full ROM \& progression to quad, hamstring, hip ABD \& core strengthening\{\{nl\}\}{\bf{Operative management:}}\{\{nl\}\}- {\bf{Indication:}} complete ACL rupture in younger or older active, high-demand pts, \& partial ACL rupture w. functional instability\{\{nl\}\}- Two options: ACL reconstruction or repair \tn 
% Row Count 48 (+ 30)
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• {\bf{Ddx:}} & - ACL tear\{\{nl\}\}- Epiphyseal fracture of femur/tibia\{\{nl\}\}- MCL injury\{\{nl\}\}- Meniscal tear\{\{nl\}\}- Osteochondral fracture\{\{nl\}\}- Patellar dislocation\{\{nl\}\}- Posterior cruciate ligament injury\{\{nl\}\}- Tibial spine fracture \tn 
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Lateral Collateral (LCL) \& PLC Injuries}}  \tn
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
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• {\bf{Intro:}} & - 1° resistor of varus stress\{\{nl\}\}- Provides posterolateral stability (preventing medial translation of the tibia)\{\{nl\}\}- LCL \& PLT resist external tibial rotation in 0-30° of knee FLX\{\{nl\}\}- Minor role in tibial translation (stabilises anterior \& posterior tibial translation when cruciate ligaments are torn)\{\{nl\}\}- {\bf{Origin:}} lateral epicondyle of the femur, {\bf{Insertion:}} fibular head\{\{nl\}\}- {\bf{Blood supply:}} branches of popliteal artery, {\bf{Innervation:}} common fibular n.\{\{nl\}\} - {\bf{Surrounding structures:}} popliteus tendon (PLT) \& iliotibial band (ITB) \tn 
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• {\bf{Aetiology (risk factors):}} & - 40\% of PLC (posterolateral corner) \& LCL injuries result from contact sports\{\{nl\}\}- Other causes include trauma, motor vehicle accidents, \& falls\{\{nl\}\}- F\textgreater{}M\{\{nl\}\}- High-contact sports\{\{nl\}\}- Sports involving high-velocity pivoting \& jumping\{\{nl\}\}- Tennis \& gymnastics are most specific fro isolated LCL injuries\{\{nl\}\}- Prior knee, ankle, or hip injury increases the risk \tn 
% Row Count 44 (+ 17)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Lateral Collateral (LCL) \& PLC Injuries (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - LCL injuries rarely occur in isolation\{\{nl\}\}- High-energy blow to the antero-medial knee\{\{nl\}\}- Involves hyperEXT \& extreme varus force\{\{nl\}\}- Non-contact hyperEXT \& varus stressors can also cause LCL injuries \tn 
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• {\bf{Clinical presentation:}} & - Acute event consistent w/ a medial blow to the knee while fully EXT, or extreme non-contact varus bending\{\{nl\}\}- Complain of sudden onset lateral knee px, swelling, \& ecchymosis after the injury\{\{nl\}\}- May report thrust gait, inc. foot kicking in mid-stance\{\{nl\}\}- May complain of paresthesias over the lateral lower extremity, \& weakness \&/or a foot drop\{\{nl\}\}- Gain complete Hx inc. bleeding/clot disorders, previous surgeries, occupation, gait, ambulation-assisted devices, living situation (stairs at home) \tn 
% Row Count 34 (+ 24)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Lateral Collateral (LCL) \& PLC Injuries (cont)}}  \tn
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• {\bf{Physical examination:}} & - Limited ROM\{\{nl\}\}- Lateral knee TTP\{\{nl\}\}- Ecchymosis, swelling, \& warmth\{\{nl\}\}- Gait: classical {\emph{varus thrust}} finding\{\{nl\}\}- {\bf{Special tests:}} Varus stress test, EXT ROT recurvatum test, Posterolateral drawer test, Reverse pivot shift test, Dial test \tn 
% Row Count 12 (+ 12)
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• {\bf{Diagnosis:}} & - MRI is the gold standard\{\{nl\}\}- US useful for rapid diagnosis\{\{nl\}\}{\bf{Classification of injury:}}\{\{nl\}\}- {\bf{Grade 1:}} Mild sprain - diagnosed w/ lateral knee tenderness, no instability mechanical Ssx\{\{nl\}\}- {\bf{Grade 2:}} Partial tear - diagnosed w/ more severe localised lateral \& posterolateral knee px, as well as swelling\{\{nl\}\}- {\bf{Grade 3:}} Complete tear - px \& swelling vary in pts, usually associated w/ PLC \& other related injuries, \& mechanical Ssx \tn 
% Row Count 33 (+ 21)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Lateral Collateral (LCL) \& PLC Injuries (cont)}}  \tn
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• {\bf{Complications:}} & - Undiagnosed LCL \& PLC injuries have several long-term complications\{\{nl\}\}- Continued knee instability \& chronic px\{\{nl\}\}- 35\% of PLC injuries may have an associated peroneal n. palsy (probs due to its proximity to the LCL)\{\{nl\}\}- Pts may develop long-term foot drop, as well as lower extremity weakness \& decreased sensation\{\{nl\}\}- Post op: hardware irritation \& stiffness \tn 
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• {\bf{Management:}} & - Acutely, all grades treated w/ RICE \& NSAIDs\{\{nl\}\}- 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\{\{nl\}\}- Grade 3: surgical reconstruction (best results), post op rehab and functional exercises \tn 
% Row Count 31 (+ 14)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Lateral Collateral (LCL) \& PLC Injuries (cont)}}  \tn
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• {\bf{Ddx:}} & - ACL/PCL tears\{\{nl\}\}- Lateral meniscus tears\{\{nl\}\}- Popliteal injury\{\{nl\}\}- Bone contusion\{\{nl\}\}- ITB syndrome \tn 
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\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK560847/"\}\}link text\{\{/popup\}\}}  \tn 
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Posterior Cruciate Ligament (PCL) Injuries}}  \tn
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
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• {\bf{Intro:}} & - 1/4 major ligaments of the knee that function to stabilise the tibia on the femur\{\{nl\}\}- {\bf{Origin:}} anterolateral aspect of the medial femoral condyle in the area of the intercondylar notch, {\bf{Insertion:}} posterior aspect of the tibial plateau\{\{nl\}\}- Prevents posterior translation of the tibia on the femur\{\{nl\}\}- Lesser extent, the PCL functions to resist varus, valgus, \& EXT ROT forces \tn 
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• {\bf{Aetiology (risk factors):}} & - Caused by extreme anterior force applied to the proximal tibia of the FX knee\{\{nl\}\}- Dashboard injuries during car accident or falling forward onto a FX knee\{\{nl\}\}- M\textgreater{}F (2:1)\{\{nl\}\}- Motorcycle accidents (28\%) \& soccer-related injuries (25\%) are the leading causes \tn 
% Row Count 32 (+ 13)
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• {\bf{Pathophysiology:}} & - Least common knee injury\{\{nl\}\}- Anterolateral portion is more commonly injured due to majority of injuries occurring in knee FX\{\{nl\}\}- Resists posterior translation w. the assistance of the posterolateral joint capsule, popliteus, MCL, \& posterior oblique ligament \tn 
% Row Count 13 (+ 13)
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• {\bf{Clinical presentation:}} & - Pts often present w/ acute onset of posterior knee px, swelling, \& instability\{\{nl\}\}- Hx includes mechanism of injury, ic. falling onto FX knee or recent vehicle accident \tn 
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• {\bf{Physical examination:}} & - Pulses\{\{nl\}\}- SMR\{\{nl\}\}- Mild to moderate joint effusion\{\{nl\}\}- Swelling usually less than in ACL tear\{\{nl\}\}- Pt may present w/ antalgic gait \& potential difficulty walking up \& down stairs\{\{nl\}\}- Palpation: potential effusion, joint line for tenderness (suggestive of meniscal tears)\{\{nl\}\}- Muscle strength test: should be normal, but there may be weakness w/ knee EXT \& FX 2° to guarding\{\{nl\}\}- Limited ROM\{\{nl\}\}- {\bf{Special tests:}} Posterior drawer test, Quadriceps active test, Dial test or EXT ROT test, Varus/valgus stress \tn 
% Row Count 46 (+ 25)
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Posterior Cruciate Ligament (PCL) Injuries (cont)}}  \tn
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• {\bf{Diagnosis:}} & - MRI is the gold standard\{\{nl\}\}- Initial imaging w/ plain X-rays\{\{nl\}\}{\bf{Classification of injury:}}\{\{nl\}\}- Grade 1 (partial tear) - 1-5mm posterior translation, tibia remains anterior to femoral condyles\{\{nl\}\}- Grade 2 (complete isolated) - 6-10mm posterior tibial translation, complete tear of PCL w/o another injury, anterior tibia flush w/ femoral condyles\{\{nl\}\}- Grade 3 (complete PCL w/ combined capsular \&/or ligamentous injury) - \textgreater{}10mm posterior tibial translation, tibia posterior to femoral condyles which may indicate a concomitant capsuloligamentous injury \tn 
% Row Count 26 (+ 26)
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• {\bf{Complications:}} & - Intra \& postoperative complications of PCL surgery\{\{nl\}\}- Neuromuscular injury (e.g. popliteal artery injury)\{\{nl\}\}- Fracture\{\{nl\}\}- Residual instability\{\{nl\}\}- Osteoarthritic progression\{\{nl\}\}- Osteonecrosis\{\{nl\}\}- Stiffness\{\{nl\}\}- Failure of associated ligament reconstructions or meniscal repairs\{\{nl\}\}- Revision of PCL reconstruction \tn 
% Row Count 42 (+ 16)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Posterior Cruciate Ligament (PCL) Injuries (cont)}}  \tn
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• {\bf{Management:}} & - {\bf{Variables to consider:}} Acute or chronic; isolated or combined\{\{nl\}\}{\bf{Non-operative:}}\{\{nl\}\}- Acute grade 1 \& 2 injuries w/ posterior tibial translation (8-12mm)\{\{nl\}\}- Grade 3 injuries w/ mild Ssx or low-demand activities\{\{nl\}\}- Acute treatment inv. RICE, initial knee bracing, \& crutches\{\{nl\}\}- Rehab focuses on knee EXT strengthening\{\{nl\}\}- Est. return-to-play in 2-4 weeks for Grade 1 \& 2 injuries\{\{nl\}\}- Grade 3 may inv. knee immobilisation followed by rehab\{\{nl\}\}{\bf{Operative:}}\{\{nl\}\}- Acute injuries w/ tibial translation \textgreater{}12mm, associated meniscal tears, dislocation, bony avulsions, \& combined injuries\{\{nl\}\}- Chronic injuries w/ posterior tibial translation \textgreater{}8mm, symptomatic cases, instability, \& combined injuries\{\{nl\}\}- Arthroscopic procedures\{\{nl\}\}- Reconstruction\{\{nl\}\}- Graft fixations\{\{nl\}\}- High tibial osteotomy \tn 
% Row Count 38 (+ 38)
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• {\bf{Ddx:}} & - ACL injury\{\{nl\}\}- LCL injury\{\{nl\}\}- MCL injury\{\{nl\}\}- Meniscus injury\{\{nl\}\}- Talofibular ligament injury \tn 
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
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• {\bf{Intro:}} & - Also known as popliteal or paramedical cyst\{\{nl\}\}- Fluid-filled sac, typically between semimembranosus \& medial head of the gastroc\{\{nl\}\}- Common in adults \& associated w/ degenerative knee conditions\{\{nl\}\}- Often linked to degenerative meniscal tears as one of the most common causes\{\{nl\}\}- In children, popliteal cysts more commonly arise as a 1° condition (resulting from herniated post knee joint synovium/capsule) \tn 
% Row Count 21 (+ 20)
% Row 2
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• {\bf{Aetiology (risk factors):}} & - Children aged 4-7 yo\{\{nl\}\}- Adults aged 35-70\{\{nl\}\}- Most commonly found in adults w/ Hx of trauma, knee joint diseases (OA, RA, etc), or as incidental findings\{\{nl\}\}- They form due to accumulation \& extrusion of synovial fluid between the semimebranosus \& medial head of the gastroc\{\{nl\}\}- Popliteal cysts are located on the medial side of the popliteal fossa just below the crease at the posterior knee\{\{nl\}\}- Prevalence increases w/ age, likely due to an increase in knee-burial communication \tn 
% Row Count 44 (+ 23)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Baker's Cyst (cont)}}  \tn
% Row 3
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• {\bf{Pathophysiology:}} & {\bf{Several mechanisms:}}\{\{nl\}\}{\bf{1.}} Joint-cyst communication\{\{nl\}\}{\bf{2.}} Sequestration of synovial fluid in popliteal fossa due to a valve-like effect between the joint \& cyst (controlled by \seqsplit{gastroc-semimembranosus} m. w/ FX \& EXT at the knee)\{\{nl\}\}{\bf{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)\{\{nl\}\}{\bf{4.}} \seqsplit{Gastroc-semimembranosus} bursa enlargement resulting from micro-traumas to the bursa w/ muscle contractions\{\{nl\}\}{\bf{5.}} Herniation of the joint capsule into the popliteal fossa \tn 
% Row Count 30 (+ 30)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Baker's Cyst (cont)}}  \tn
% Row 4
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• {\bf{Clinical presentation:}} & - Sensation of tightness, discomfort, or px behind the knee\{\{nl\}\}- Swelling Moree noticeable when standing w/ full knee EXT\{\{nl\}\}- Swelling reduces or disappears when the knee is flexed to 45° (Foucher's sign)\{\{nl\}\}- Px worsens w/ increased activity \& may limit full knee FX \& EXT \tn 
% Row Count 13 (+ 13)
% Row 5
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• {\bf{Physical examination:}} & - Compression of surrounding vessels\{\{nl\}\}- Lower extremity oedema due to venous obstruction\{\{nl\}\}- Enlargement into the calf m. (dissecting cyst) can cause swelling, erythema, distal oedema, \& +ve Homan's sign\{\{nl\}\}- Venous obstruction can mimic Ssx of DVT or thrombophlebitis \tn 
% Row Count 26 (+ 13)
% Row 6
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• {\bf{Diagnosis:}} & {\bf{Diagnosis methods:}}\{\{nl\}\}- Pt stand \& full knee EXT\{\{nl\}\}- Mass is most prominent in this position\{\{nl\}\}- Mass often softens or disappears when the knee is FX to 45° (Foucher's sign)\{\{nl\}\}- Supine exam: knee passively moved from full EXT to at least 90° FX\{\{nl\}\}{\bf{Imaging:}}\{\{nl\}\}- Plain radiograph \& US\{\{nl\}\}- MRI is recommended, esp. if considering surgery \tn 
% Row Count 43 (+ 17)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Baker's Cyst (cont)}}  \tn
% Row 7
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• {\bf{Complications:}} & {\bf{Complications \& Ssx of ruptured Baker's cyst:}}\{\{nl\}\}- Rapid fluid accumulation may cause cyst rupture\{\{nl\}\}- Released fluid into surrounding tissues can lead to inflammation\{\{nl\}\}- Ssx similar to thrombophlebitis: sharp pc in the knee \& calf; swelling or erythema of the calf; sensation of water running down the calf\{\{nl\}\}{\bf{Complications of cyst rupture:}}\{\{nl\}\}- Post tibial n. entrapment: posterior plantar numbness \& calf px\{\{nl\}\}- Popliteal artery occlusion: lower extremity oedema\{\{nl\}\}- Anterior compartment syndrome: foot drop, oedema of anterolateral leg\{\{nl\}\}- Posterior compartment syndrome: plantar dysesthesia, weakness of toes, calf swelling, px worsens w/ passive toe extension \tn 
% Row Count 32 (+ 32)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Baker's Cyst (cont)}}  \tn
% Row 8
\SetRowColor{LightBackground}
• {\bf{Management:}} & - Asymptomatic cases are managed through observation \& reassurance alone\{\{nl\}\}- Essential to treat any underlying joint disorder in pts w/ symptomatic Baker's cysts\{\{nl\}\}- Helps reduce synovial fluid accumulation \& cyst enlargement\{\{nl\}\}{\bf{Non-operative:}}\{\{nl\}\}- Rest/activity modification\{\{nl\}\}- NSAIDs\{\{nl\}\}- Physical therapy \& rehab regimes are effective for minimal Ssx \& smaller degenerative meniscal tears\{\{nl\}\}- Aspiration \& steroid injection\{\{nl\}\}- Lower recurrence in younger pts\{\{nl\}\}- Higher recurrence rates in older pts \& those w/ degenerative meniscal tears\{\{nl\}\}{\bf{Operative:}}\{\{nl\}\}- Arthroscopy\{\{nl\}\}- Open cyst excision (not recommended in case of underlying degeneration due to recurrence risk) \tn 
% Row Count 33 (+ 33)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Baker's Cyst (cont)}}  \tn
% Row 9
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• {\bf{Ddx:}} & - Abscess\{\{nl\}\}- Arteriovenous fistula\{\{nl\}\}- DVT\{\{nl\}\}- Ganglion cyst\{\{nl\}\}- Hemangioma\{\{nl\}\}- Lipoma\{\{nl\}\}- Lymphadenopathy\{\{nl\}\}- Malignancy (e.g. fibrosarcoma, liposarcoma)\{\{nl\}\}- Popliteal (Balker's) cyst \tn 
% Row Count 10 (+ 10)
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\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK430774/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chondrocalcinosis (pseudogout)}}  \tn
% Row 0
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
% Row Count 1 (+ 1)
% Row 1
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• {\bf{Intro:}} & {\bf{Overview:}}\{\{nl\}\}- Calcium pyrophosphate deposition disease (CPPD)\{\{nl\}\}- Crystal deposition arthropathy involving synovial \& periarticular tissues\{\{nl\}\}- Asymptomatic to acute or chronic inflammatory arthritis\{\{nl\}\}{\bf{Phenotypes \& terminology:}}\{\{nl\}\}- Various terms used for different phenotypes\{\{nl\}\}- Acute CPP deposition arthritis: {\emph{"Pseudogout"}}\{\{nl\}\}- Chronic CPP deposition arthritis: informally called {\emph{"pseudo-rheumatoid arthritis"}}\{\{nl\}\}- Characterised by a waxing \& waning clinical course, resembling RA\{\{nl\}\}{\bf{Radiological findings:}}\{\{nl\}\}- Term: {\bf{{\emph{chondrocalcinosis}}}}\{\{nl\}\}- Describes intra-articular fibrocartilage calcification\{\{nl\}\}{\bf{Commonly affected joints:}}\{\{nl\}\}- Hips\{\{nl\}\}- Knees\{\{nl\}\}- Shoulders\{\{nl\}\}{\bf{Underlying factors:}}\{\{nl\}\}- Often associated w/ underlying joint disease or metabolic abnormalities\{\{nl\}\}- Predisposing factors: OA, trauma, surgery, RA \tn 
% Row Count 46 (+ 45)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chondrocalcinosis (pseudogout) (cont)}}  \tn
% Row 2
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• {\bf{Aetiology (risk factors):}} & - Often pts \textgreater{}65 yo, w/ 30-50\% \textgreater{}85 yo\{\{nl\}\}- M\textgreater{}F\{\{nl\}\}- Rare \textless{}60 yo\{\{nl\}\}- High prevalence of radiographic {\bf{chondrocalcinosis}} in the general population\{\{nl\}\}{\bf{Comorbidities associated w/ CPPD:}}\{\{nl\}\}- Hyperparathyroidism\{\{nl\}\}- Gout\{\{nl\}\}- OA\{\{nl\}\}- RA\{\{nl\}\}- Hemochromatosis\{\{nl\}\}{\bf{Other related comorbidities:}}\{\{nl\}\}- Osteoporosis\{\{nl\}\}- Hypomagnesium\{\{nl\}\}- Chronic kidney disease\{\{nl\}\}- Calcium supplementation \tn 
% Row Count 21 (+ 21)
% Row 3
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• {\bf{Pathophysiology:}} & - Caused by an imbalance between pyrophosphate production \& pyrophosphate levels in diseased cartilage\{\{nl\}\}- Pyrophosphate deposits in the synovium \& adjacent tissues combine w/ calcium to form CPP\{\{nl\}\}- Deposition of calcium pyres-hate can activate the immune system, leading to inflammation \& soft tissue injury \tn 
% Row Count 37 (+ 16)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chondrocalcinosis (pseudogout) (cont)}}  \tn
% Row 4
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• {\bf{Clinical \& physical presentation:}} & {\bf{Acute cases:}}\{\{nl\}\}- Typically, self-limiting, \& inflammation resolves within days - weeks w/ treatment\{\{nl\}\}- Similar to acute rate arthropathy\{\{nl\}\}- Joint oedema, erythema, \& tenderness\{\{nl\}\}- Up to 50\% may have a low-grade fever\{\{nl\}\}- Most commonly affected joint: knee\{\{nl\}\}- Other affected joints: hip, shoulders\{\{nl\}\}{\bf{Chronic cases:}}\{\{nl\}\}- May show Ssx of RA inc. morning stiffness, localised oedema, \& ↓ ROM\{\{nl\}\}- Waxing \& waning episodes of non-synchronous, inflammatory arthritis\{\{nl\}\}- Affeects multiple non-WB joint: wrist \& MCP joint\{\{nl\}\}- Causes {\emph{"crowned dens syndrome"}} (deposition of CPP around C2)\{\{nl\}\}- Mostly asymptomatic \tn 
% Row Count 33 (+ 33)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chondrocalcinosis (pseudogout) (cont)}}  \tn
% Row 5
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• {\bf{Diagnosis:}} & - Confirm diagnosis through synovial fluid analysis\{\{nl\}\}{\bf{Imaging:}}\{\{nl\}\}- For involved joints is recommended\{\{nl\}\}- Presence of {\emph{chondrocalcinosis}} in imaging supports CPPD Dx\{\{nl\}\}- Absence of {\emph{chondrocalcinosis}} doesn't rule out CPPD\{\{nl\}\}- US may reveal early signs like cartilage abnormalities\{\{nl\}\}- Radiographic imaging may show joint cartilage calcification\{\{nl\}\}- MRI is useful - can evaluate crystal deposition in joint cartilage \tn 
% Row Count 23 (+ 23)
% Row 6
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• {\bf{Complications:}} & - Potential of triggering inflammatory responses\{\{nl\}\}- Presence of {\emph{chondrocalcinosis}} has associations w/ degradation of menisci \& synovial tissue\{\{nl\}\}- Pts rarely present w/ palpable nodules (resembling gout) that may lead to further joint degradation\{\{nl\}\}- Rare spinal involvemen, causing clinical manifestations like spine stiffness \& bony ankylosis (resembling AS)\{\{nl\}\}- Some pts present w/ manifestations similar to DISH w/ PLL calcification leading to spinal cord compression Ssx \tn 
% Row Count 48 (+ 25)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chondrocalcinosis (pseudogout) (cont)}}  \tn
% Row 7
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• {\bf{Management:}} & - 1st step reduce inflammation \& addressing underlying metabolic conditions\{\{nl\}\}- NSAIDs\{\{nl\}\}- Acute flares inv. 1-2 joints often treated w/ joint aspiration\{\{nl\}\}- Medication\{\{nl\}\}- Low-alkaline diet \tn 
% Row Count 11 (+ 11)
% Row 8
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• {\bf{Ddx:}} & - Tenosynovitis w/ carpal or cubital tunnel s. can occur (multiple joints affected)\{\{nl\}\}- RA\{\{nl\}\}- AS\{\{nl\}\}- Erosive OA\{\{nl\}\}- Gout \tn 
% Row Count 18 (+ 7)
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\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK540151/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Acute Compartment Syndrome}}  \tn
% Row 0
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{RED}}} \tn 
% Row Count 1 (+ 1)
% Row 1
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• {\bf{Intro:}} & - Increased pressure in closed osteofascial compartmetn\{\{nl\}\}- Leads to impaired local circulation\{\{nl\}\}- Surgical emergency\{\{nl\}\}-Untreated ACS can lead to ischemia \& necrosis\{\{nl\}\}{\bf{Compartments:}}\{\{nl\}\}- Lg has 4 compartments: anterior, lateral, deep posterior, \& superficial posterior\{\{nl\}\}- Anterior compartment is most common ACS\{\{nl\}\}- Contains extensor m., tibialis anterior m., deep peroneal n., \& tibial artery\{\{nl\}\}{\emph{*Open fractures:}}\{\{nl\}\}- Skin laceration doesn't relieve compartment pressure\{\{nl\}\}- ACS is still predictable, esp. in open Gustily type 2 \& 3 lesions in proximal intra-articular tibia fractures \tn 
% Row Count 30 (+ 29)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Acute Compartment Syndrome (cont)}}  \tn
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• {\bf{Aetiology (risk factors):}} & - M\textgreater{}F (7.3:0.7)\{\{nl\}\}- Majority of cases result from trauma, w/ tibial shaft fracture being the most common\{\{nl\}\}- More common in males \textless{}35 yo, possibly due to larger muscle mass \& high-energy trauma involvement\{\{nl\}\}- Pts w/ bleeding diathesis (e.g. hemophilia) are at high risk\{\{nl\}\}- ACS reported w/o trauma in paediatric leukaemia cases\{\{nl\}\}- Pts w/o fractures at high risk of complications \& delayed treatment\{\{nl\}\}- 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\{\{nl\}\}- In children, supracondylar \# of the humerus \& ulnar/radial \# are associated w/ compartment syndrome \tn 
% Row Count 39 (+ 39)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Acute Compartment Syndrome (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - Caused by ↓ intracompartmental space OR ↑ fluid volume, making the surrounding fascia non-compliant\{\{nl\}\}- ↑ compartment pressure impairs hemodynamics, disrupting the equilibrium between venous outflow \& arterial inflow\{\{nl\}\}- Elevated compartment pressure leads to reduced venous outflow, ↑ venous capillary pressure\{\{nl\}\}- If intracompartmental pressure surpasses arterial pressure, arterial inflow ↓, causing tissue ischemia\{\{nl\}\}- Reduced venous outflow \& arterial inflow result in ↓ tissue oxygenation, potentially leading to irreversible necrosis\{\{nl\}\}- Normal compartment pressure is \textless{}10mmHg, while reading of 30mmHg or higher indicates ACS \tn 
% Row Count 31 (+ 31)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Acute Compartment Syndrome (cont)}}  \tn
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• {\bf{Clinical presentation:}} & - Can occur within few hours to up to 48h after trauma\{\{nl\}\}- Px is severe \& disproportionate to the injury; may be felt as a burning sensation or deep ache\{\{nl\}\}- Initially, px may only occur w/ passive stretching but can be absent in advanced cases\{\{nl\}\}- Paresthesia, hypoesthesia, or poorly localised deep muscular px may be present\{\{nl\}\}- The {\bf{"5 P's"}} (px, pulselessness, paresthesia, paralysis, \& pallor) are classic signs, but they're typically late findings\{\{nl\}\}- Paresthesia may occur earlier\{\{nl\}\}- In some cases, a pulse may still be present, even in a severely compromised extremity \tn 
% Row Count 28 (+ 28)
% Row 5
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• {\bf{Physical examination:}} & - Earliest objective physical finding is the {\bf{tense{\emph{, or }}'wood-like'{\bf{ feeling int he involved compartment\{\{nl\}\}}}Focus on neurovascular exam:}}*\{\{nl\}\}- Observe skin for lesions, swelling, or colour change\{\{nl\}\}- Palpate compartment, noting °C, tension, \& tenderness\{\{nl\}\}- Check pulses in the affected area\{\{nl\}\}- Evaluate two-point discrimination \& sensation\{\{nl\}\}- Assess motor function\{\{nl\}\}- Due to potential rapid progression, serial exam should be performed to monitor changes over time \tn 
% Row Count 51 (+ 23)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Acute Compartment Syndrome (cont)}}  \tn
% Row 6
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• {\bf{Diagnosis:}} & - Radiographs are recommended if \# suspected\{\{nl\}\}- Measurement of intracompartmental pressure (not required), can aid in Dx\{\{nl\}\}- Normal pressure: 0-8mmHg\{\{nl\}\}- Abnormal: exceeding 30mmHg indicates compartment s. \& necessitates intervention\{\{nl\}\}- Pressure within 10-30mmHg of diastolic blood pressure suggests inadequate perfusion \& relative ischemia, prompting clinical attention\{\{nl\}\}- {\bf{DUS}} can be used to detect occlusion or thrombus\{\{nl\}\}- Elevated CPK levels may suggest muscle breakdown from ischemia, damage, or rhabdomyolysis\{\{nl\}\}- Pre-operative studies: CBC \& coagulation studies \tn 
% Row Count 28 (+ 28)
% Row 7
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• {\bf{Complications:}} & - Px\{\{nl\}\}- Contractures\{\{nl\}\}- Rhabdomyolysis\{\{nl\}\}- N. damage \& associated numbness \&/or weakness\{\{nl\}\}- Infection\{\{nl\}\}- Renal failure\{\{nl\}\}- Death \tn 
% Row Count 35 (+ 7)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Acute Compartment Syndrome (cont)}}  \tn
% Row 8
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• {\bf{Management:}} & - Immediate surgical consult\{\{nl\}\}- Keeping extremity at heart level \tn 
% Row Count 4 (+ 4)
% Row 9
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• {\bf{Ddx:}} & - DVT\{\{nl\}\}- Cellulitis\{\{nl\}\}- Peripheral vascular injury \tn 
% Row Count 7 (+ 3)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
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\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK448124/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chronic (Exertional) Compartment Syndrome}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{RED}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Often a Dx of exclusion characterised by ↑ pressures in a muscular compartment , leading to ischemia \& px\{\{nl\}\}- CECS inv/ recurrent, reversible ischemic episodes after activity cessation, leading to predictable ↓ in fascial compartment pressures\{\{nl\}\}- Rare condition w/ delayed diagnosis, resembling ACS\{\{nl\}\}- Requires surgical emergency intervention through fasciotomies to prevent irreversible m. ischemia \& neurovascular injury\{\{nl\}\}- Usually occurs in the LL but can also affect forearm, thigh, or hand \tn 
% Row Count 25 (+ 24)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & - Relatively common among young adult athletes (running, endurance training, soccer, field hockey, \& lacrosse)\{\{nl\}\}- Anterior compartment most commonly affected (70\% of cases), then deep posterior\{\{nl\}\}- B limb in 37-82\% of symptomatic cases\{\{nl\}\}- 20-25 yo, M\textgreater{}F, \& often B\{\{nl\}\}- Associated w/ sports like running or skating, \& higher activity intensities\{\{nl\}\}- Can result from overuse injuries, repetitive mechanisms causing tissue degeneration, scar formation, \& military training\{\{nl\}\}- Pts w/ decreased fascial elasticity may be at risk for nerve entrapment \& quicker rises in pathological pressures \tn 
% Row Count 53 (+ 28)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chronic (Exertional) Compartment Syndrome (cont)}}  \tn
% Row 3
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• {\bf{Pathophysiology:}} & - Has multiple etiologies\{\{nl\}\}- Muscle compartment swelling during exercise, leading to increased pressure within musculofascial compartments\{\{nl\}\}- Rise in pressure compromises blood flow, causing px, motor weakness, \& paresthesia, in corresponding neurovascular distributions\{\{nl\}\}- 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\{\{nl\}\}- Increased intracompartmental pressure results in reduced myocyte oxygenation, leading to myonecrosis \& neurological damage \tn 
% Row Count 27 (+ 27)
% Row 4
\SetRowColor{white}
• {\bf{Clinical presentation:}} & - Pts often present following sport-related activity ro exertion w/ non-specific leg px \& persist after strenuous or repetitive activity\{\{nl\}\}- Ssx will predictably abate following activity cessation\{\{nl\}\}- 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\{\{nl\}\}- Pts will generally complain of discomfort described as squeezing, cramping, aching, or burning that typically begins within 15-20 minutes of activity\{\{nl\}\}- Discomfort resolves completely w/ rest, although the duration may vary \tn 
% Row Count 56 (+ 29)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chronic (Exertional) Compartment Syndrome (cont)}}  \tn
% Row 5
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• {\bf{Physical examination:}} & - In 70-95\% of cases B px\{\{nl\}\}- Physical exam often unremarkable, esp. if not done during or immediately after exercise\{\{nl\}\}- Suspected cases should undergo pre- \& post-exercise physical exams\{\{nl\}\}- After exercise, the affected compartment may feel tender, bulge, or be tight, \& passive stretching may cause px\{\{nl\}\}- Focal neuro findings may inc. ↓ sensation, paresthesia, or weakness\{\{nl\}\}{\bf{Stryker pressure monitoring system:}}\{\{nl\}\}- Baseline measurements w/ pt at rest\{\{nl\}\}- Pts then perform controlled exercise until severe Ssx occur\{\{nl\}\}- After 5-minute rest, compartment pressure measured again \tn 
% Row Count 28 (+ 28)
% Row 6
\SetRowColor{white}
• {\bf{Diagnosis:}} & {\bf{Pedowitz criteria:}}\{\{nl\}\}-Rule out a Dx of CECS\{\{nl\}\}- Resting pressure ≧ 15mmHg \&/or a pressure of ≧ 30mmHg at 1 min post-exercise in any compartment, \&/or;\{\{nl\}\}- Post-exercise pressure greater than 20mmHg at 5 min post-exercise \tn 
% Row Count 39 (+ 11)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Chronic (Exertional) Compartment Syndrome (cont)}}  \tn
% Row 7
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• {\bf{Complications:}} & - Benign condition characterised by resolution of Ssx w/ rest \tn 
% Row Count 3 (+ 3)
% Row 8
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• {\bf{Management:}} & - Conservative treatment generally ineffective, inc. rest, activity modification, stretching, orthotics, \& physical therapy\{\{nl\}\}- Non-operative modalities inc. NSAIDs, injections, gait training (forefoot strike patterns)\{\{nl\}\}- Open fasciotomy is the predominant surgical technique \tn 
% Row Count 16 (+ 13)
% Row 9
\SetRowColor{LightBackground}
• {\bf{Ddx:}} & - Initially gets misDx as shin splints or medial tibial stress syndrome (MTSS)\{\{nl\}\}- Vascular pathologies (intermittent claudication, popliteal artery impingement)\{\{nl\}\}- Tibial stress \#\{\{nl\}\}- Tendon pathologies (tendinitis, tendinosis, or tendon rupture)\{\{nl\}\}- N. entrapment \tn 
% Row Count 29 (+ 13)
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\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK544284/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Fibular Nerve (Peroneal N.) entrapment}}  \tn
% Row 0
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
% Row Count 1 (+ 1)
% Row 1
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• {\bf{Intro:}} & - Branches off the sciatica n. in the distal posterior thigh \& receives fibres from L4-S2 nerve roots\{\{nl\}\}- Runs down the thigh, posterior to the biceps femoris m., \& crosses laterally to the head of the lateral gastroc m.\{\{nl\}\}- Provides sensory innervation to the lateral leg via the lateral sural n.\{\{nl\}\}- {\bf{Two branches:}} {\emph{superficial}} which innervates the lateral compartment of the leg, \& {\emph{deep}} which innervates the anterior compartment of the leg \& foot dorsum\{\{nl\}\}- Both have roles in foot eversion \& dorsiflexion\{\{nl\}\}{\bf{Innervation of superficial}}\{\{nl\}\}{\bf{Motor:}}\{\{nl\}\}- Lateral compartment\{\{nl\}\}- Peroneus longus\{\{nl\}\}- Peroneus brevis\{\{nl\}\}{\bf{Sensory:}}\{\{nl\}\}- Anterolateral leg\{\{nl\}\}{\bf{Innervation of deep}}\{\{nl\}\}{\bf{Motor:}}\{\{nl\}\}- Anterior compartment\{\{nl\}\}- Tibialis anterior\{\{nl\}\}- Extensor hallucis longus\{\{nl\}\}- Extensor digitorum longus\{\{nl\}\}- Peroneus tertius\{\{nl\}\}{\bf{Sensory:}}\{\{nl\}\}- First dorsal webspace \tn 
% Row Count 44 (+ 43)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Fibular Nerve (Peroneal N.) entrapment (cont)}}  \tn
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• {\bf{Aetiology (risk factors):}} & - Most common mononeuropathy in the LL \& 3rd most common focal neuropathy overall (after carpal tunnel s. \& ulnar neuropathies)\{\{nl\}\}- Common in traumatic injuries in young athletes (e.g. football, soccer) \& following high energy trauma (car accidents) in adults\{\{nl\}\}- Occurs in about 16-40\% of knee dislocations\{\{nl\}\}{\bf{Trauma or injury to the knee:}}\{\{nl\}\}- Knee dislocation\{\{nl\}\}- Direct impact, penetrating trauma, or lacerations\{\{nl\}\}- Fibula \#, esp. proximal fibula\{\{nl\}\}{\bf{External compression sources:}}\{\{nl\}\}- Tight splint/cast\{\{nl\}\}- Compression wrapping/bandage\{\{nl\}\}- Habitual leg crossing\{\{nl\}\}- Prolonged bed rest\{\{nl\}\}- Positioning during anaesthesia \& surgery (important to pad bony prominences)\{\{nl\}\}{\bf{Systemic causes:}}\{\{nl\}\}- Diabetes mellitus\{\{nl\}\}- Inflammatory conditions\{\{nl\}\}- Anorexia nervosa\{\{nl\}\}{\bf{Others:}}\{\{nl\}\}- Intramural ganglion\{\{nl\}\}- Peripheral nerve tumour\{\{nl\}\}- Iatrogenic injury following surgery to the hip, knee, \& ankle \tn 
% Row Count 44 (+ 44)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Fibular Nerve (Peroneal N.) entrapment (cont)}}  \tn
% Row 3
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• {\bf{Clinical presentation:}} & - Varies based on location, severity, \& anatomic variations\{\{nl\}\}- Commonly presents w. weakness in ankle dorsiflexion\{\{nl\}\}- Classic result is {\emph{foot drop}} or {\emph{catching toes}} while walking\{\{nl\}\}- Development of acute or gradual, complete or partial\{\{nl\}\}- Numbness or paresthesia along lateral leg, dorsal foot, \&/or first toe webspace\{\{nl\}\}- Possible px in traumatic cases \tn 
% Row Count 17 (+ 17)
% Row 4
\SetRowColor{white}
• {\bf{Physical examination:}} & - Gait: significant for chronic peroneal nerve palsy w/ foot drop, high stoppage gait weakened dorsiflexors to prevent toe dragging\{\{nl\}\}{\bf{Localisation of lesions:}}\{\{nl\}\}- Proximal lesions (e.g. knee dislocations) may present w/ numbness in both superficial \& deep n. distributions\{\{nl\}\}- Upper lateral leg numbness indicates a lesion proximal to fibular head (possibly inv. sciatic n. or lumbosacral n. roots)\{\{nl\}\}- Lower lateral leg \& dorms of the foot involvement suggests superficial peroneal n.\{\{nl\}\}- Altered sensation in the dorsal aspect of the first web space implicates the deep peroneal n.\{\{nl\}\}{\bf{Motor involvement testing:}}\{\{nl\}\}- Assess foot eversion (superficial n.) \& foot/toe dorsiflexion (deep n.)\{\{nl\}\}- Weakness in both suggests common Peroneal n. involvement\{\{nl\}\}- Proximal lesion may result in both distributions\{\{nl\}\}- Detailed examination of dorsiflexion ability is crucial\{\{nl\}\}{\bf{Tinel sign:}}\{\{nl\}\}- Tapping along the nerve course, esp. around the fibular neck\{\{nl\}\}- +ve test = tingling or paresthesia distally \tn 
% Row Count 65 (+ 48)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Fibular Nerve (Peroneal N.) entrapment (cont)}}  \tn
% Row 5
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• {\bf{Diagnosis:}} & - CT can be used to assess osseous abnormalities\{\{nl\}\}- MRI/US suitable fro evaluating soft-tissue sources or masses (es. in cases of traumatic knee dislocations)\{\{nl\}\}- Electrodiaagnostic studies (inc. NCV \& EMG) are used to Dx peroneal nerve palsy\{\{nl\}\}- They evaluate motor \& sensory axons of the peroneal n. aiding in localisation of the nerve injury\{\{nl\}\}- Useful in post-operative setting of a known traumatic injury for long-term management planning \& pt care \tn 
% Row Count 22 (+ 22)
% Row 6
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• {\bf{Management:}} & - Full physical therapy\{\{nl\}\}- Ankle-foot orthoses, even for foot-drop when surgery isn't warranted\{\{nl\}\}- Surgical indicators: rapid deterioration \& no signs of improvement within {\bf{3 months}} \& open injuries w. suspected nerve laceration\{\{nl\}\}-Open lacerations should undergo exploration \& surgical repair within 72h \tn 
% Row Count 37 (+ 15)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Fibular Nerve (Peroneal N.) entrapment (cont)}}  \tn
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• {\bf{Ddx:}} & - Peroneal tendon pathology\{\{nl\}\}- Other compressive neuropathies (tarsal tunnel s., anterior tarsal tunnel s., non-specific tendinitis affecting lower limb m./t.)\{\{nl\}\}- Chronic ankle px \tn 
% Row Count 9 (+ 9)
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\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK549859/\#article-27038.s8"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Meniscal Tears}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
% Row Count 1 (+ 1)
% Row 1
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• {\bf{Intro:}} & - Lateral \& medial menisci function in load transmission \& shock absorption in the tibiofemoral joint\{\{nl\}\}- Inner 2/3 (white zone) of the menisci is avascular, likely receiving nutrition through synovial fluid diffusion\{\{nl\}\}- Peripheral 1/3 (red zone) is well-vascularised, supplied by branches of the medial \& lateral vehicular arteries\{\{nl\}\}- Medial meniscus is less mobile than the lateral one, firmly attached to the joint capsule \& deep fibres of the MCL\{\{nl\}\}- Lateral miscues doesn't connect w/ the LCL \& has looser attachments w. the joint capsule\{\{nl\}\}- Anterior margins of the menisci are connected by the transverse inter meniscal ligament\{\{nl\}\}- Peripheral 2/3 of the menisci contain nociceptive free endings (pain perception), while mechanoreceptors are in the anterior \& posterior horns, suggesting a proprioceptive function\{\{nl\}\}- Posterior horn of the lateral meniscus connects to the femur via meniscofemoral ligaments \& the adjacent popliteus tendon \tn 
% Row Count 46 (+ 45)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Meniscal Tears (cont)}}  \tn
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• {\bf{Aetiology (risk factors):}} & - 61/100,000 in general population (USA), 9/1000 in military population\{\{nl\}\}- 15\% of sports injuries\{\{nl\}\}- M\textgreater{}F\{\{nl\}\}- Age \textgreater{}40 yo\{\{nl\}\}- ACL deficient knees, esp. if ACL reconstruction is delayed beyond 1 year from initial injury\{\{nl\}\}- Medial\textgreater{}lateral meniscal tears\{\{nl\}\}- {\bf{Increased risk factors:}} infantry-related duties, frequent squatting/kneeling, \& participation in sports like soccer, rugby, football, basketball, baseball, skiing, \& wrestling\{\{nl\}\}- 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)\{\{nl\}\}- Less force is required for tears in individuals w/ degenerative changes of the menisci, typically seen in adults \textgreater{}40 w. concomitant OA\{\{nl\}\}- {\bf{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 \seqsplit{acceleration/deceleration}, change of direction, \& jumping \tn 
% Row Count 46 (+ 46)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Meniscal Tears (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - Characterised by shape \& location on MRI\{\{nl\}\}- {\bf{Horizontal}} (cleavage) run parallel to the tibial plateau, associated w/ degenerative changes in people \textgreater{}40 w/o specific causes\{\{nl\}\}- {\bf{Longitudinal}} run perpendicular to the tibial plateau \& parallel to the meniscus axis\{\{nl\}\}- {\bf{Radial}} run perpendicular to both the tibial plateau \& the meniscus axis, originating from the inner free edge\{\{nl\}\}- {\bf{Complex}} involve combinations of horizontal, longitudinal, or vertical tears\{\{nl\}\}- {\bf{Displaced}} involve complete detachment or flipping of a piece still attached to the meniscal body\{\{nl\}\}- {\bf{Bucket-handle}} are complete longitudinal tear fragments that migrate centrally\{\{nl\}\}- {\bf{Parrot-break}} are radial tears w/ partially detached fragments\{\{nl\}\}- {\bf{Flap}} are partially detached fragments of horizontal tears\{\{nl\}\}- 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"\{\{nl\}\}- Tears in the red zone have the highest potential for spontaneous healing w/ conservative management or successful outcomes after meniscal repair \tn 
% Row Count 53 (+ 53)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Meniscal Tears (cont)}}  \tn
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• {\bf{Clinical presentation:}} & - {\bf{"POP"}} sensation w/ immediate knee effusion suggests ACL tear w/ possible medial meniscal involvement\{\{nl\}\}- Gradual effusion over 24h indicates an isolated meniscal tear\{\{nl\}\}- Ssx can be insidious, featuring low-grade effusion\& stiffness w/o a specific triggering event\{\{nl\}\}- Px commonly reported along the anteromedial or anterolateral joint line\{\{nl\}\}- {\bf{Additional Ssx:}} locking, clicking, catching, intermittent inability to fully EXT the knee, \& a sense of the knee giving way \tn 
% Row Count 23 (+ 23)
% Row 5
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• {\bf{Physical examination:}} & - Inspection of edema, palpation of joint line, standing \& supine ROM, muscle strength testing, special testing\{\{nl\}\}- Anteromedial \& anterolateral joint line tenderness at 90° FX\{\{nl\}\}- Px \& deficits in FX or EXT ROM may vary based on tear type \& effusion extent\{\{nl\}\}- Deficits in open kinetic chain knee FX/EXT strength testing are unlikely\{\{nl\}\}- Antalgic gait or increased px w/ squatting may indicate meniscal issues due to compressive forces\{\{nl\}\}- {\bf{Special tests:}} Thessaly test, McMurray's test, Apley's compression test \tn 
% Row Count 48 (+ 25)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Meniscal Tears (cont)}}  \tn
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• {\bf{Diagnosis:}} & - Begin w/ radiographs - AP, lateral, oblique, sunrise, \& WB views to assess concomitant bony pathologies, loose bodies, \& OA\{\{nl\}\}- Arthroscopy is the gold standard\{\{nl\}\}- MRI is the best mode of imaging to Dx \& characterise tears \tn 
% Row Count 11 (+ 11)
% Row 7
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• {\bf{Management:}} & - RICE\{\{nl\}\}- NSAIDs\{\{nl\}\}- Early px-free knee \& ankle ROM exercise (help limit motion loss \& aid edema)\{\{nl\}\}- Bracing/sleeves (protection \& compression)\{\{nl\}\}{\bf{Simple tears (outer 1/3 of the meniscus) \& degenerative tears:}}\{\{nl\}\}- 4-6 weeks relative rest \& physical therapy\{\{nl\}\}- Despite conservative management, pts w/ persistent px, swelling, \& mechanical Ssx should be evaluated for surgical intervention\{\{nl\}\}{\bf{Surgical tears:}}\{\{nl\}\}- Meniscal repair is preferred over meniscectomy (risk of accelerated OA)\{\{nl\}\}- Factors ↑ success: tears that occur in red zone of the meniscus, shorter than 2cm, vertical longitudinal tears, \& acute tears\{\{nl\}\}{\bf{Rehab:}}\{\{nl\}\}- First 6 weeks inc. restrictions in knee FX ROM \& WB status (depending on tear \& repair type)\{\{nl\}\}- Strengthening\{\{nl\}\}- Mobs \tn 
% Row Count 48 (+ 37)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Meniscal Tears (cont)}}  \tn
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• {\bf{Ddx:}} & - ACL injury\{\{nl\}\}- Contusions\{\{nl\}\}- ITB syndrome\{\{nl\}\}- Knee osteochondritis\{\{nl\}\}- LCL injury\{\{nl\}\}- Lumbosacral radiculopathy\{\{nl\}\}- MCL injuy\{\{nl\}\}- Medial synovial plica irritation\{\{nl\}\}- Patellofemoral joint syndrome\{\{nl\}\}- PCL injury \tn 
% Row Count 11 (+ 11)
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\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK431067/\#article-23936.s9"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osgood-Schlatter Disorder (OSD)}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
% Row Count 1 (+ 1)
% Row 1
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• {\bf{Intro:}} & - Common cause of anterior knee px in skeletally immature athletes\{\{nl\}\}- Also known as {\emph{osteochondrosis}} or {\emph{traction apophysitis of the tibial tubercle}}\{\{nl\}\}- Common in sports like basketball, volleyball, sprinting, gymnastics, \& football\{\{nl\}\}- Self-limiting \& results from repetitive stress on the extensor mechanism (jumping/sprinting)\{\{nl\}\}- While benign, OSD can lead to prolonged recovery \& absence from sports \tn 
% Row Count 21 (+ 20)
% Row 2
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• {\bf{Aetiology (risk factors):}} & - Leading cause of knee px in adolescent athletes\{\{nl\}\}- Onset typically aligns w/ growth spurts: 10-15 M \& 8-13 F\{\{nl\}\}- M\textgreater{}F\{\{nl\}\}- 9.8\% of adolescents 12-15 yo (11.4\% M; 8.3\% F)\{\{nl\}\}- B Ssx observed in 20-30\% of pts\{\{nl\}\}- Overuse injury due to repetitive strain from patellar tendon\{\{nl\}\}- Force increases w/ higher activity levels, after rapid growth\{\{nl\}\}- {\bf{Predisposing factors:}} poor flexibility of quadriceps \& hamstrings, extensor mechanism misalignment \tn 
% Row Count 43 (+ 22)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osgood-Schlatter Disorder (OSD) (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - Tibial tubercle develops as a 2° ossification centre for patellar tendon attachment\{\{nl\}\}- Bone growth surpasses \seqsplit{muscle-tendon-bone-attachment}, susceptible to injury from repetitive stress\{\{nl\}\}- Repeated quadriceps muscle contraction, esp. in sports involving running \& jumping, can cause apophyseal ossification centre softening \& partial avulsion, resulting in osteochondritis\{\{nl\}\}{\bf{Tibial tubercle development sequence:}}\{\{nl\}\}- Entirely cartilaginous before age 11\{\{nl\}\}- Apophysis forms between 11-14\{\{nl\}\}- Apophysis fuses w/ proximal tibial epiphysis between 14-18\{\{nl\}\}- Proximal tibial epiphysis \& tibial tubercle apophysis fuse w/ the rest of the proximal tibia after age 18\{\{nl\}\}- {\bf{Prevailing theory:}} repeated traction over tubercle causes microvascular tears, fractures, inflammation \tn 
% Row Count 37 (+ 37)
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osgood-Schlatter Disorder (OSD) (cont)}}  \tn
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• {\bf{Clinical presentation:}} & - Common Ssx: anterior knee px\{\{nl\}\}- Presentation: w/ or w/o swelling, unilateral or bilateral\{\{nl\}\}- Onset: typically insidious, w/o preceding trauma\{\{nl\}\}- Nature of px: dull ache localised over tibial tubercle\{\{nl\}\}- Px progression: gradually increases w/ activity\{\{nl\}\}- Px relief: typically improves w/ rest\{\{nl\}\}- Duration of relief: subsides minutes to hours after stopping activity or sport\{\{nl\}\}- Exacerbating factors: running, jumping, direct knee trauma, kneeling, \& squatting \tn 
% Row Count 23 (+ 23)
% Row 5
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• {\bf{Physical examination:}} & - Enlarged prominence at the tibial tubercle\{\{nl\}\}- Tenderness over the patellar tendon insertion site\{\{nl\}\}- Reproduction of px: resisted knee EXT \& active/passive knee FX can reproduce px \tn 
% Row Count 32 (+ 9)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osgood-Schlatter Disorder (OSD) (cont)}}  \tn
% Row 6
\SetRowColor{LightBackground}
• {\bf{Diagnosis:}} & - 1° Dx clinically, radiographic evaluation typically not necessary\{\{nl\}\}- Consider comparing B images to help delineate normal vs abnormal in the pt\{\{nl\}\}{\bf{Radiographic use:}}\{\{nl\}\}- Plain radiographs may be employed in severe or atypical presentations\{\{nl\}\}- Used to rule out additional conditions like fractures, infections, or bone tumours\{\{nl\}\}- Assessment fro avulsion injury or other traumas may necessitate radiographic evaluation\{\{nl\}\}{\bf{Classic findings:}}\{\{nl\}\}- Elevated tibial tubercle w/ soft tissue swelling\{\{nl\}\}- Fragmentation of the apophysis\{\{nl\}\}- Calcification in the distal patellar tendon \tn 
% Row Count 28 (+ 28)
% Row 7
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• {\bf{Complications:}} & - Prominence of tibial tubercle\{\{nl\}\}- Ongoing px\{\{nl\}\}- Ssx continue to adulthood if treatment isn't provided or poor compliance w/ recommended treatment \tn 
% Row Count 35 (+ 7)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osgood-Schlatter Disorder (OSD) (cont)}}  \tn
% Row 8
\SetRowColor{LightBackground}
• {\bf{Management:}} & - Excellent prognosis\{\{nl\}\}- Self-limiting but time to resolution can take up to 2 yrs until apophysis fuses\{\{nl\}\}- Surgery rarely indicated, low benefit \& high complication risk\{\{nl\}\}- Relative rest \& activity modification based on px levels\{\{nl\}\}- Participation in sports allowed if px resolves w/ rest \& doesn't limit activities\{\{nl\}\}{\bf{Px management:}}\{\{nl\}\}- Ice \& NSAIDs\{\{nl\}\}- Protective knee pad recommended over tibial tubercle to prevent direct trauma\{\{nl\}\}- Hamstring \& quadriceps stretching, \& strengthening\{\{nl\}\}- In severe cases, short knee immobilisation might be considered\{\{nl\}\}{\bf{Refractory cases:}}\{\{nl\}\}- In up to 10\%, Ssx may persist \textgreater{}1-2 yrs beyond skeletal maturity\{\{nl\}\}- Ossicle excision may be performed in skeletally mature pts w/ persistent Ssx \tn 
% Row Count 35 (+ 35)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osgood-Schlatter Disorder (OSD) (cont)}}  \tn
% Row 9
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• {\bf{Ddx:}} & - Patella tendonitis\{\{nl\}\}- Osteomyelitis of the tibia\{\{nl\}\}- Perthes disease\{\{nl\}\}- Synovial place injury\{\{nl\}\}- Infectious apophysitis \tn 
% Row Count 7 (+ 7)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK441995/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteochondritis Dissecans (OCD)}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
% Row Count 1 (+ 1)
% Row 1
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• {\bf{Intro:}} & - Rare condition affecting the knee, categorised as a form of osteonecrosis in the subchondral bone\{\{nl\}\}- 1° occurs in school-aged children \& adolescents, w/ manifestations of the dysfunction \& px\{\{nl\}\}- Juvenile OCD occurs in pts w/ open growth plates, while adult OCD applies to skeletally mature pts\{\{nl\}\}- If left untreated, OCD can lead to degenerative changes, chronic px, \& mechanical Ssx such as 'locking' \& 'clicking' \tn 
% Row Count 21 (+ 20)
% Row 2
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• {\bf{Aetiology (risk factors):}} & - Highest incidence 12-19 yo\{\{nl\}\}- 9.5-29 / 100,00\{\{nl\}\}- M\textgreater{}F\{\{nl\}\}- 75\% of affected pts have knee lesion, w/ 64\% localised in the medial femoral condyle\{\{nl\}\}- 32\% of knee lesions are found in the lateral condyle, while other cases localise to the trochlea, patella, \& tibial plateau\{\{nl\}\}- Usually unilateral, but 7-25\% of pts have B disease\{\{nl\}\}- Theories inc. micro-trauma, ischemia, \& genetic predisposition\{\{nl\}\}- Pts w. extreme obesity \& elevated BMI face an increased risk of developing OCD\{\{nl\}\}- Repetitive trauma is widely considered the 1° cause of OCD of the knee\{\{nl\}\}- Adult form of OCD is believed to result from vascular insult \tn 
% Row Count 51 (+ 30)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteochondritis Dissecans (OCD) (cont)}}  \tn
% Row 3
\SetRowColor{LightBackground}
• {\bf{Pathophysiology:}} & - Disruption of epiphyseal vessels, leading to ischemia \& necrosis at trauma site\{\{nl\}\}- Softening, tearing, fissuring, \& erosion of hyaline cartilage follow as a consequence of the disrupted blood supply\{\{nl\}\}- Advancement of the affected area result in focal demineralisation \& repeated shear forces, causing detachment of bone \& overlying cartilage\{\{nl\}\}- Repetitive axial loading, esp. w/ increased valgus \& varus stress, is suggested by experts as a contributing factor tot he condition\{\{nl\}\}- OCD lesions can introduce irregularities in the articular surface, potentially leading to degenerative arthritis \tn 
% Row Count 28 (+ 28)
% Row 4
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• {\bf{Clinical presentation:}} & - Vague, poorly localised knee px that worsens w/ activity\{\{nl\}\}- Stiffness \& occasional swelling may occur during or after activity as the disease progresses\{\{nl\}\}- Advanced stages may be indicated by {\bf{locking or catching}}, suggesting the presence of a sizeable loose body in the knee\{\{nl\}\}- Hx of trauma, recent increase in activity level, previous knee injuries, \& the presence of mechanical Ssx\{\{nl\}\}- Approx. 80\% of pts report px when WB\{\{nl\}\}- Juvenile: intermittent, activity-associated px poorly localised around the anterior aspect of the joint\{\{nl\}\}- Adult: more likely effusion, limited ROM, or mechanical Ssx such as 'catching or locking'\{\{nl\}\}- Depending on chronicity of the lesion, pts may report quadriceps dysfunction \& intermittent knee instability \tn 
% Row Count 63 (+ 35)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteochondritis Dissecans (OCD) (cont)}}  \tn
% Row 5
\SetRowColor{LightBackground}
• {\bf{Physical examination:}} & - Genu varus, associated w/ lesions at medial femoral condyle\{\{nl\}\}- Genu valgus, associated w/ lesions at lateral femoral condyle\{\{nl\}\}- Quadriceps atrophy or weakness may be evident\{\{nl\}\}- Foreign body may be palpable\{\{nl\}\}- FX of knee during joint palpation can reveal effusion or bony tenderness along the femoral condyles\{\{nl\}\}- ROM may be restricted due to px, swelling, or the presence of a loose body\{\{nl\}\}- Antalgic gait or lateral rotation of the foot on the affected side may indicate efforts to alleviate WB px\{\{nl\}\}{\bf{Wilson sign:}}\{\{nl\}\}- Identifies lesions of the lateral aspect of the medial femoral condyle\{\{nl\}\}- +ve test: px w/ INT ROT, relieved by EXT ROT, indicating impingement of the OCD lesion\{\{nl\}\}- Absence of the Wilson sign does not rule out OCD \tn 
% Row Count 36 (+ 36)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteochondritis Dissecans (OCD) (cont)}}  \tn
% Row 6
\SetRowColor{LightBackground}
• {\bf{Diagnosis:}} & - Arthroscopy is the gold standard for assessing lesion stability\{\{nl\}\}- Plain radiographs used to locate the lesion, assess growth plates, \& rule out other conditions\{\{nl\}\}- Initial radiographs may appear normal in OCD\{\{nl\}\}{\bf{Lesion characteristics:}}\{\{nl\}\}- Distinct Lucent areas w/ varying density levels\{\{nl\}\}- Calcifications \& Lucent lines may or may not be present, depending on lesion severity\{\{nl\}\}- B comparison\{\{nl\}\}{\bf{Classification:}}\{\{nl\}\}- Lesion location can provide important prognostic info\{\{nl\}\}- Atypical locations like trochlea or patella may not respond effectively to conservative management\{\{nl\}\}{\bf{MRI evaluation:}}\{\{nl\}\}- Useful for assessing unstable lesions presenting w/ mechanical Ssx or knee effusion\{\{nl\}\}- Unstable lesions on mRI may exhibit increased T2 signal, destruction of overlying articular cartilage, or multiple cyst-like foci\{\{nl\}\}- Gadolinium contrast may be necessary for assessing blood supply \& stability uncertainties\{\{nl\}\}- Line of high signal intensity between fragment \& underlying bone is a sensitive prognosticator \tn 
% Row Count 49 (+ 49)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteochondritis Dissecans (OCD) (cont)}}  \tn
% Row 7
\SetRowColor{LightBackground}
• {\bf{Complications:}} & - If left untreated, adults often progress to arthritis\{\{nl\}\}- Degenerative articular changes over time\{\{nl\}\}- A non-union \& dissociation of the bony fragment\{\{nl\}\}- Chronic px \& mechanical Ssx\{\{nl\}\}- Surgical complications inc. postop infection, pneumonia, haemorrhage, \& reactions to anesthesia\{\{nl\}\}- Venous thrombosis due to immobility \tn 
% Row Count 16 (+ 16)
% Row 8
\SetRowColor{white}
• {\bf{Management:}} & - Prognosis influenced by age, location \& appearance of lesion\{\{nl\}\}{\bf{Non-operative:}}\{\{nl\}\}- Recommended for juvenile pts w/o a displaced fragment OR stage 1-3 disease\{\{nl\}\}- Immobilisation \& protected WB for 4-6 weeks\{\{nl\}\}- Physical therapy initiated after immobilisation \& continued until pain-free, achieving full ROM, strength, power, \& mobility\{\{nl\}\}- NSAIDs for px \& edema\{\{nl\}\}{\bf{Operative:}}\{\{nl\}\}- Surgery recommended if conservative treatment ineffective after 3-6 months or if not suitable\{\{nl\}\}- 1° treatment for Ssx related to OCD in adults, stage 2 disease, or expanding lesions on radiographs\{\{nl\}\}- Surgical intervention warranted in juveniles w/ stage 4 disease, loose bodies, unstable lesions, or impending physeal closure \tn 
% Row Count 50 (+ 34)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Osteochondritis Dissecans (OCD) (cont)}}  \tn
% Row 9
\SetRowColor{LightBackground}
• {\bf{Ddx:}} & {\bf{Juvenile:}}\{\{nl\}\}- Patellofemoral syndrome\{\{nl\}\}- Patellar tendonitis\{\{nl\}\}- Osgood-Schlatter disease\{\{nl\}\}- \seqsplit{Sinding-Larsen-Johansson} syndrome\{\{nl\}\}- Fat pad impingement\{\{nl\}\}- Symptomati discoid meniscus\{\{nl\}\}- Symptomatic synovial plica\{\{nl\}\}{\bf{Adult:}}\{\{nl\}\}- Patellofemoral px\{\{nl\}\}- Knee OA\{\{nl\}\}- Chondromalacia\{\{nl\}\}- Patellar tendonitis\{\{nl\}\}- Meniscal tear\{\{nl\}\}- Fat pad impingement\{\{nl\}\}- Symptomatic synovial plica\{\{nl\}\}{\bf{Adult w/ more severe Ssx:}}\{\{nl\}\}E.g. atraumatic edema \& mechanical Ssx\{\{nl\}\}- Meniscal tear\{\{nl\}\}- Osteochondral loose body\{\{nl\}\}- Neoplasm \tn 
% Row Count 27 (+ 27)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK538194/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Patellofemoral Pain Syndrome (PFPS)}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Also known as {\emph{Chondromalacia patella (CMP)}} \& {\emph{Runner's knee}}\{\{nl\}\}- Softening of hyaline cartilage on articular surfaces of bones\{\{nl\}\}- CMP specifically refers to the softening, tearing, fissuring, \& erosion of the patellar cartilage\{\{nl\}\}- Can occur in any joint, but common in joints w/ trauma \& deformities \tn 
% Row Count 16 (+ 15)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & - F\textgreater{}M\{\{nl\}\}- Increased Q angles in F (lateral positioning of the patella)\{\{nl\}\}- No hormonal cause has been identified\{\{nl\}\}- Active young adults (esp. running sports), \& workers who stress their patellofemoral joint (stairs, kneeling)\{\{nl\}\}- Often multifactorial\{\{nl\}\}- LL malalignment \& patellar maltracking play a significant role\{\{nl\}\}- Foot \& ankle variances: pes planus can lead to increased lateral wear of the patellofemoral joint\{\{nl\}\}- Miserable malalignment syndrome, w/ femoral ante version, gene valium, \& pronated feet\{\{nl\}\}- Muscular weakness: vests medals \& core m.\{\{nl\}\}- Patellar lesions from injuries, immobilisation, or surgical procedures causing quadriceps atrophy\{\{nl\}\}- Abnormal wear \& tear of the patellofemoral joint's hyaline cartilage\{\{nl\}\}- Iatrogenic factors: injecting chondrotoxic medications into joints \tn 
% Row Count 54 (+ 38)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Patellofemoral Pain Syndrome (PFPS) (cont)}}  \tn
% Row 3
\SetRowColor{LightBackground}
• {\bf{Pathophysiology:}} & {\bf{Pathological process:}}\{\{nl\}\}- Hyaline cartilage composed of chondrocytes, type 2 collagen, proteoglycans, \& water\{\{nl\}\}- Avascular w/ nutrients diffusing from synovial fluid\{\{nl\}\}- Poor repair due to lack of blood supply, devoid of lymphatic \& neural tissue\{\{nl\}\}{\bf{Factors leading to hyaline cartilage degeneration:}}\{\{nl\}\}- Destruction by chondrotoxic substances, cytokinins, \& proteolytic enzymes\{\{nl\}\}- Microtrauma from wear \& tear\{\{nl\}\}- Repeated compressive stress or increased loads on patellofemoral joint\{\{nl\}\}- Aging-related decrease in chondrocytes, proteoglycan production, \& water content\{\{nl\}\}- Cross-linking of collagen fibrils leads to loss of elastic properties\{\{nl\}\}- Superficial zone of hyaline cartilage is the 1st to degenerate in aging process\{\{nl\}\}{\bf{Px generation:}}\{\{nl\}\}- Anterior fat pad \& joint capsule commonly involved in generating px signals\{\{nl\}\}- SUbchondral bone less likely to cause px signals\{\{nl\}\}-{\bf{Initiation of CMP pathology:}} begins w/ softening, swelling, \& edema of articular cartilage \tn 
% Row Count 47 (+ 47)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Patellofemoral Pain Syndrome (PFPS) (cont)}}  \tn
% Row 4
\SetRowColor{LightBackground}
• {\bf{Clinical presentation:}} & - CC: anterior knee px\{\{nl\}\}- Pts may report insidious onset of diffuse retropatellar or pre patellar px, exacerbated by activities stressing the patellofemoral joint\{\{nl\}\}- Aggravating factors: stair ascending or descending, squatting, kneeling, running, \& prolonged sitting (theatre px)\{\{nl\}\}- Additional Ssx: effusion, quadriceps wasting, \& retropatellar crepitus (not specific to CMP)\{\{nl\}\}- Hx evaluation: previous trauma, comorbid conditions, joint stability, foot \& ankle issues, \& activity levels \tn 
% Row Count 23 (+ 23)
% Row 5
\SetRowColor{white}
• {\bf{Physical examination:}} & - Px is usually sharp \& achy\{\{nl\}\}- Examine quadriceps appearance, foot \& ankle orientation, \& specific evaluation of the patellofemoral joint\{\{nl\}\}- Patella malt racking signs: increased femoral anteversion, EXT tibial torsion, lateral patella subluxation, loss of medial patellar mobility\{\{nl\}\}- +ve patellar apprehension test\{\{nl\}\}- +ve Clark's test \tn 
% Row Count 39 (+ 16)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Patellofemoral Pain Syndrome (PFPS) (cont)}}  \tn
% Row 6
\SetRowColor{LightBackground}
• {\bf{Diagnosis:}} & - Reliable Dx requires excluding other conditions causing anterior knee px\{\{nl\}\}- Arthroscopy is the most efficient (invasive, so non-invasive methods essential for initial Dx)\{\{nl\}\}- Plain radiographs: lower sensitivity in earlier stages\{\{nl\}\}- CT: measures TT-TG distance \& detects torsional deformities of the LL\{\{nl\}\}- MRI: modality of choice fro articular cartilage, esp. T2 sequence \tn 
% Row Count 18 (+ 18)
% Row 7
\SetRowColor{white}
• {\bf{Complications:}} & - 2° to NSAID usage (e.g. GI Ssx)\{\{nl\}\}- Bracing may cause dermatological reactions \tn 
% Row Count 22 (+ 4)
% Row 8
\SetRowColor{LightBackground}
• {\bf{Management:}} & - {\bf{Min. 12 months}} of conservative management before considering surgery\{\{nl\}\}- May be reversible\{\{nl\}\}- Could progress to patellofemoral OA\{\{nl\}\}- Pts often fully recover (can take months to yrs)\{\{nl\}\}{\bf{Conservative 1st phase:}}\{\{nl\}\}- Activity modification\{\{nl\}\}- RICE\{\{nl\}\}- NSAIDs\{\{nl\}\}{\bf{Conservative 2nd phase:}}\{\{nl\}\}- Knee + hip exercise to increase strength, mobility \& function\{\{nl\}\}- Patella taping \tn 
% Row Count 41 (+ 19)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Patellofemoral Pain Syndrome (PFPS) (cont)}}  \tn
% Row 9
\SetRowColor{LightBackground}
• {\bf{Ddx:}} & - Patellofemoral OA\{\{nl\}\}- Osgood-Schlatter\{\{nl\}\}- Plica syndrome\{\{nl\}\}- Bursitis\{\{nl\}\}- Saphenous neuritis\{\{nl\}\}- Quadriceps tendinopathy\{\{nl\}\}- Patellar tendinopathy\{\{nl\}\}- Referred px from hip/back \tn 
% Row Count 10 (+ 10)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK459195/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Medial Tibial Stress Syndrome (MTSS)}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{GREEN}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Early stress injury leading to tibial stress fractures\{\{nl\}\}- Known also as {\emph{shin splints}}\{\{nl\}\}- Common overuse injury in athletes \& military personnel\{\{nl\}\}- Involves exercise-induced px along the anterior tibia \tn 
% Row Count 11 (+ 10)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & - 13-20\% incidence in runners\{\{nl\}\}- Up to 35\% in military\{\{nl\}\}- {\bf{Factors contributing:}} significant increasing loads, volume, \& high-impact exercises\{\{nl\}\}- {\bf{Intrinsic risk factors:}} F gender, previous MTSS Hx, high BMI, navicular drop, ankle plantar FX range, hip EXT ROT range\{\{nl\}\}- Overuse condition, specifically a tibial bony overload injury w/ associated periostitis\{\{nl\}\}- {\bf{Common for:}} recurrent impact exercise, such as running, jumping, \& military personnel\{\{nl\}\}- Suggested link between vitamin D \& increased risk of stress injury \tn 
% Row Count 36 (+ 25)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Medial Tibial Stress Syndrome (MTSS) (cont)}}  \tn
% Row 3
\SetRowColor{LightBackground}
• {\bf{Pathophysiology:}} & - Involves accumulation of unprepared micrdamage in the cortical bone of the distal tibia\{\{nl\}\}- Overlying periostitis is typically present at the site of bony injury\{\{nl\}\}- Periostitis correlates w/ tendinous attachments of soleus, flexor digitorum longus, \& posterior tibialis\{\{nl\}\}- Sharpey's fibers, perforating connective tissue linking periosteum to bone, play a role in the mechanical connection\{\{nl\}\}- Repetitive muscle traction is believed to be the underlying cause of periostitis \& cortical microtrauma \tn 
% Row Count 24 (+ 24)
% Row 4
\SetRowColor{white}
• {\bf{Clinical presentation:}} & - Presence of exercise-induced px along the distal 2/3 of the medial tibial border\{\{nl\}\}- Presence of px provoked during or after physical activity, which reduces w/ relative rest\{\{nl\}\}- The absence of cramping, burning px over the posterior compartment \&/or numbness/tingling in the foot \tn 
% Row Count 38 (+ 14)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Medial Tibial Stress Syndrome (MTSS) (cont)}}  \tn
% Row 5
\SetRowColor{LightBackground}
• {\bf{Physical examination:}} & - Presence of recognisable px reproduced w/ palpation of the posteromedial tibial border \textgreater{}5cm\{\{nl\}\}- The absence of other findings not typical of MTSS (e.g. severe swelling, erythema, loss of distal pulses, etc) \tn 
% Row Count 10 (+ 10)
% Row 6
\SetRowColor{white}
• {\bf{Diagnosis:}} & - Dx through clinical \& physical findings\{\{nl\}\}- Imaging done when uncertain about cause or to rule out other exercise-induced LL injuries\{\{nl\}\}- Plain radiographs are normal in MTSS \& early stress fractures\{\{nl\}\}- {\emph{"dreaded black line"}} indicates a {\emph{stress fracture}}\{\{nl\}\}- MRI is preferred for identifying MTSS \& higher-grade bone stress injuries like tibial stress fractures \tn 
% Row Count 28 (+ 18)
% Row 7
\SetRowColor{LightBackground}
• {\bf{Complications:}} & - Px leading to decreased performance \&/or time away from training/participation\{\{nl\}\}- May progress to tibial stress fracture\{\{nl\}\}- Severe tibial stress fractures may require surgical intervention \tn 
% Row Count 37 (+ 9)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Medial Tibial Stress Syndrome (MTSS) (cont)}}  \tn
% Row 8
\SetRowColor{LightBackground}
• {\bf{Management:}} & - Full recovery is expected\{\{nl\}\}- Rest \& activity modification w/ less repetitive, load-bearing exercise\{\{nl\}\}- {\bf{Additional therapies:}} iontophoresis, phonophoresis, ice massage, US therapy, periosteal pecking, \& extracorporeal shockwave therapy\{\{nl\}\}- {\bf{No benefit:}} low-energy laser therapy, stretching, strengthening, LL braces, \& compression stockings\{\{nl\}\}- {\bf{Slow response cases:}} optimising calcium \& vitamin D status \& gait retraining may improve recovery \& prevent further progression \tn 
% Row Count 23 (+ 23)
% Row 9
\SetRowColor{white}
• {\bf{Ddx:}} & - Tibial stress fracture\{\{nl\}\}- Compartment syndrome\{\{nl\}\}- Functional popliteal artery entrapment syndrome \tn 
% Row Count 28 (+ 5)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK538479/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Varicose Veins}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{YELLOW}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Characterised by subcutaneous dilated, tortuous veins of ≧3mm\{\{nl\}\}- Age \& FHx are important risk factors\{\{nl\}\}- Common clinical manifestations of chronic venous disease\{\{nl\}\}- Evaluating associated superficial axial venous reflux is crucial\{\{nl\}\}- Manifestations can range from limited leg discomfort to swelling \& non-healing ulcers \tn 
% Row Count 17 (+ 16)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & - Up to 30\% of general population\{\{nl\}\}- F\textgreater{}M\{\{nl\}\}- {\bf{Risk factors:}} F gender, multiparty, high BMI, constipation, Hx of venous thrombosis, smoking, \& circulating iron levels\{\{nl\}\}- Both genetic \& environmental factors \tn 
% Row Count 27 (+ 10)
% Row 3
\SetRowColor{white}
• {\bf{Pathophysiology:}} & - Valve dysfunction leads to increased pressure in veins\{\{nl\}\}- Elevated pressure causes vein walls to weaken \& dilate\{\{nl\}\}- Ironic pressure causes the vein walls to stretch \& lose elasticity\{\{nl\}\}- Weakened walls contribute to the development of varicosities \tn 
% Row Count 39 (+ 12)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Varicose Veins (cont)}}  \tn
% Row 4
\SetRowColor{LightBackground}
• {\bf{Clinical presentation:}} & - Leg heaviness\{\{nl\}\}- Itching\{\{nl\}\}- Cramps\{\{nl\}\}- Mild tenderness\{\{nl\}\}- Skin discoloration\{\{nl\}\}- Exercise intolerance\{\{nl\}\}- Leg fatigue \tn 
% Row Count 7 (+ 7)
% Row 5
\SetRowColor{white}
• {\bf{Physical examination:}} & - Visible distended veins from thigh to ankle\{\{nl\}\}- Discolouration most prominent around ankle \& calf\{\{nl\}\}- {\bf{Special test:}} Trendelenburg test - assesses deep venous valve competency \tn 
% Row Count 16 (+ 9)
% Row 6
\SetRowColor{LightBackground}
• {\bf{Diagnosis:}} & {\bf{CEAP classification:}}\{\{nl\}\}- C0: no visible, palpable signs\{\{nl\}\}- C1: spider veins\{\{nl\}\}- C2: varicose veins\{\{nl\}\}- C3: edema\{\{nl\}\}- C4a: pigmentation, eczema\{\{nl\}\}- C4b: lipodermatoslerosis\{\{nl\}\}- C5: healed ulcer\{\{nl\}\}- C6: active ulcer\{\{nl\}\}- Colour duplex venous US exam is recommended for suspected venous reflux \tn 
% Row Count 31 (+ 15)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Varicose Veins (cont)}}  \tn
% Row 7
\SetRowColor{LightBackground}
• {\bf{Complications:}} & - Venous ulcers\{\{nl\}\}- Pain\{\{nl\}\}- Poor cosmesis\{\{nl\}\}- DVT\{\{nl\}\}- PE (rare)\{\{nl\}\}- Superficial thrombophlebitis might be complicated w/ prolonged bleeding \& px\{\{nl\}\}- Superficial vein thrombosis \tn 
% Row Count 9 (+ 9)
% Row 8
\SetRowColor{white}
• {\bf{Management:}} & - No cure\{\{nl\}\}- Long-term graduated compression stockings, leg elevation, \& oral px medication\{\{nl\}\}- Surgery (recurrence is likely ) \tn 
% Row Count 16 (+ 7)
% Row 9
\SetRowColor{LightBackground}
• {\bf{Ddx:}} & - Lymphedema\{\{nl\}\}- DVT\{\{nl\}\}- Cellulitis\{\{nl\}\}- Dermatological disorders (e.g. stasis dermatitis) \tn 
% Row Count 21 (+ 5)
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{\{\{popup="https://www.ncbi.nlm.nih.gov/books/NBK470194/"\}\}link text\{\{/popup\}\}}  \tn 
\hhline{>{\arrayrulecolor{DarkBackground}}--}
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Vasculitis}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{2}{x{17.67cm}}{• {\bf{RED}}} \tn 
% Row Count 1 (+ 1)
% Row 1
\SetRowColor{white}
• {\bf{Intro:}} & - Heterogenous group of over 30 different kinds of vasculitis. presenting either as a 1° process or 2° to another pathology\{\{nl\}\}- Clinical \& pathological manifestation vary based on the affected blood vessels' type \& location \tn 
% Row Count 12 (+ 11)
% Row 2
\SetRowColor{LightBackground}
• {\bf{Aetiology (risk factors):}} & - Incidence of 20-40 million / year\{\{nl\}\}- Gender dominance depending on type of vasculitis\{\{nl\}\}- Giant cell arteritis is the most common form\{\{nl\}\}- {\bf{Risk factors:}} Behcet disease (ancient Silk route), Takayasu disease (South Asian), Kawasaki disease (children \textless{}5), hepatitis B/C \tn 
% Row Count 25 (+ 13)
% Row 3
\SetRowColor{white}
• {\bf{Pathophysiology:}} & - Unknown specific cause\{\{nl\}\}- Immune system activation: becomes overactive\{\{nl\}\}- Inflammation of blood vessels: immune system mistakenly identifies blood vessels as foreign invaders\{\{nl\}\}- Attack on endothelium: attacks the endothelium (inner lining of blood vessels)\{\{nl\}\}- 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\{\{nl\}\}- Vessel damage: combined effect of immune cells sticking to the blood vessel walls \& the inflammatory response damages the vessels\{\{nl\}\}- 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\{\{nl\}\}- Granuloma formation (in some cases): in certain vasculitis types. granulomas may form. contributing to tissue damage \tn 
% Row Count 70 (+ 45)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Vasculitis (cont)}}  \tn
% Row 4
\SetRowColor{LightBackground}
• {\bf{Clinical presentation:}} & - Ssx dependent on location of vasculitis\{\{nl\}\}- Potential organ damage from vasculitis\{\{nl\}\}- Fevers, unexplained weight loss\{\{nl\}\}- Nose bleeding, hemoptysis, hematuria \tn 
% Row Count 8 (+ 8)
% Row 5
\SetRowColor{white}
• {\bf{Physical examination:}} & - Upper airway disease\{\{nl\}\}- Ocular inflammation\{\{nl\}\}- Limb claudication\{\{nl\}\}- +ve sensory/motor neuropathy, purpura, change of pulses \tn 
% Row Count 15 (+ 7)
% Row 6
\SetRowColor{LightBackground}
• {\bf{Diagnosis:}} & - Chest x-ray or high-resolution CT for respiratory Ssx\{\{nl\}\}- Vascular imaging (MRI, MRA, CTA, vascular US, PET) to detect large artery lesions in vasculitis cases\{\{nl\}\}-{\bf{Labs:}} CBC, kidney \& liver function, ESR, serologies, \& urinalysis w/ urinary sediment \tn 
% Row Count 27 (+ 12)
% Row 7
\SetRowColor{white}
• {\bf{Complications:}} & - Depend on the type of vessel involved\{\{nl\}\}- {\bf{Large vessel involvement:}} acute MI, stroke, mesenteric ischemia, aortic s., critical extremity ischemia\{\{nl\}\}- {\bf{Life threatening complications of small vessels:}} alveolar haemorrhage, renal failure, intestinal ischemia \tn 
% Row Count 40 (+ 13)
\end{tabularx}
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\begin{tabularx}{17.67cm}{x{7.7715 cm} x{9.4985 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Vasculitis (cont)}}  \tn
% Row 8
\SetRowColor{LightBackground}
• {\bf{Management:}} & - Long-term survival highly depends on the Dx, response to treatment, \& adverse effects of drugs\{\{nl\}\}- Managed w/ medication\{\{nl\}\}- 3 main components: remission induction, remission maintenance, \& monitoring \tn 
% Row Count 10 (+ 10)
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• {\bf{Ddx:}} & - Infections, neoplasms \& certain drug toxicities can mimic vasculitis\{\{nl\}\}- Coagulopathies can present w/ similar Ssx to vasculitis \tn 
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\begin{tabularx}{17.67cm}{x{8.635 cm} x{8.635 cm} }
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Venous Thrombo-embolism (VTE)}}  \tn
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\mymulticolumn{2}{x{17.67cm}}{• {\bf{RED}}} \tn 
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• {\bf{Intro:}} & - Significant complication of hospitalisation\{\{nl\}\}- 3rd leading CV Dx, following heart attacks \& strokes\{\{nl\}\}- VTE encompasses DVT \& PE\{\{nl\}\}- Growing public health concern\{\{nl\}\}- Need for increased awareness among the public \& healthcare providers \tn 
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• {\bf{Aetiology (risk factors):}} & - Global annual burden of VTE is in millions\{\{nl\}\}- Significant morbidity \& mortality associated w/ VTE cases worldwide\{\{nl\}\}- Majority of VTE cases are hospital-related or acquired (60\%)\{\{nl\}\}- Leading preventable cause of death in hospitalised pts\{\{nl\}\}- {\bf{Risk factor:}} \textgreater{}40 yrs, obesity, varicose veins, immobility, oral contraceptive, smoking, hypercoagulability, pregnancy, \& \seqsplit{pelvic/hip/long-bone} fractures\{\{nl\}\}- {\bf{Disease states ↑ risk:}} malignancies, spinal cord injury, nephrotic s., congestive heart failure, IBD, \& recent MI \tn 
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\mymulticolumn{2}{x{17.67cm}}{\bf\textcolor{white}{Venous Thrombo-embolism (VTE) (cont)}}  \tn
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• {\bf{Pathophysiology:}} & - Venous thrombosis involves the formation of a clot made of platelets \& fibrin within blood vessels\{\{nl\}\}- Clinically significant thrombi typically form in large-lumen vessels, such as deep veins in the legs, pelvis, \& arms\{\{nl\}\}- Clots can propagate \& extend proximally, leading to clinical Ssx when vascular flow is obstructed\{\{nl\}\}- Dislodged clots may embolise to distant sites, w/ the pulmonary vasculature being a common location\{\{nl\}\}- Obstruction in pulmonary vascular flow can result in impaired gas exchange, alveolar edema, \& pulmonary alveolar necrosis\{\{nl\}\}- Chronic repetitive pulmonary embolisation can increase pulmonary vascular resistance, ultimately causing pulmonary hypertension\{\{nl\}\}- 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 \tn 
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• {\bf{Clinical \& physical findings of DVT:}} & - Unilateral limb px is a common complaint\{\{nl\}\}- Physical signs may include swelling, warmth, \& tenderness to touch\{\{nl\}\}- Physical exam signs for DVT have low Dx yield \tn 
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• {\bf{Clinical \& physical findings:}} & - Sudden onset of dyspnea (most common presenting complaint)\{\{nl\}\}- Pleuritic chest px, cough, \& hemoptysis\{\{nl\}\}- Massive PE can lead to syncope, hypotension, \& shock\{\{nl\}\}- Physical examination findings for PE are variable \& often nonDx\{\{nl\}\}- Tachypnea (resp. rate \textgreater{}18/min) is common\{\{nl\}\}- In older pts, new-onset atrial fibrillation may be a presenting Ssx\{\{nl\}\}{\bf{ Established PE physical findings:}}\{\{nl\}\}- Tachypnea (resp. rate \textgreater{}18/min) is common\{\{nl\}\}- Rales may be present in up to 50\% of cases\{\{nl\}\}- Tachycardia (HR \textgreater{}100/min) \& fever occur in about 45\%\{\{nl\}\}- Diaphoresis \& S3 or S4 gallop may be audible in about 30\%\{\{nl\}\}- Pleural friction rub may indicate peripheral PE w/ pulmonary necrosis \tn 
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• {\bf{Diagnosis:}} & - Chest radiography\{\{nl\}\}- D-dimer assay\{\{nl\}\}- US \& serial US for DVT\{\{nl\}\}- CTPA \& VQ for PE \tn 
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• {\bf{Complications:}} & - Bleeding\{\{nl\}\}- Heparin-induced thrombocytopenia\{\{nl\}\}- Warfarin-induced skin necrosis \tn 
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• {\bf{Management:}} & - Treatment is based on associated conditions\{\{nl\}\}- 1° treatment is anticoagulation \tn 
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• {\bf{Ddx:}} & - Localised Ssx of DVT can be similar to cellulitis, arterial insufficiency, lymphedema, \& hematoma\{\{nl\}\}- PE: congestive heart failure, acute respiratory distress s., pneumonia, \& MI \tn 
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\end{document}