MSK Flashcards
What is the definition of sign?
Observable findings detected during objective exam (e.g., swelling, skin colour changes, clubbing)
What is the definition of symptom?
Subjective reports that are perceived by a person and cannot be observed (e.g., pain, numbness, tingling, burning, nausea, dizziness)
What alerts a PT to the need for referral? What key factors create the need to screen? When may the PT know to screen or refer?
-Red flags
-Screening questions
-Screening tests
-Side effects of meds
-comorbidities
-visceral pain mechanism
-patient doesn’t get better, or initially gets better than worse, other S + S develop
How can a PT improve the screening process?
-Know what questions to ask
-Know what medical conditions can cause pain superficially and in what areas
-Become familiar with risk factors for various conditions and diseases
What are red flags?
-indicate serious pathology needing immediate attention for further screening questions and/or tests for referral
-if after screen.. PT decides physio is appropriate… continue objective, if not appropriate..referral to appropriate health care practionner
can continuously screen
What are constitutional symptoms?
-Cluster of symptoms that typically present with a systemic disease
-Diaphoresis
-Dizziness/syncope
-Fatigue
-Fever
-Nausea
-Night sweats
-Pallor
-Unexplained weight loss
-Vomiting / Diarrhea
When to refer out?
-require medical intervention
-interventions do not fall in scope of practice
-findings remain inconsistent with what is expected
-no apparent movement dysfunction, causative factors or syndromes can be identified
-client fails to improve with intervention
Immediate medical attention (emergencies) is advised when…?
Angina - not relieved (20 minds) with rest and/or NTG
- has nausea, vomiting or profuse sweating
CES-b/b incontinence, saddle anesthesia
Respiratory - inadequate ventilation, respiratory acidosis
Anaphylactic shock
Stroke - FAST
Chest - throbbing in chest, back or abdomen that increases with exertion with sensation of heart beat when lying down
-pulsating palpable abdominal mass possibly indicating an aneurysm
Explain the applied anatomy for the TMJ
Joint
-Mandibular condyle
-Glenoid fossa
-Articular disc (helps with congruency and lubrication)
Ligaments
-Lateral ligament - strongest, thickening of capsule
-Sphenomandibular and stylomandibular ligament
Movement
-Opening - lateral ptyergoid
-Closing- medial pterygoid, temporalis and masseter
-Protrusion - medial and lateral pterygoid
-Retrusion - temporalis
-Lateral deviation - contralateral - medial and lateral pterygoid and masseter, ipsilateral - temporalis
Innervation
-Trigeminal nerve (CN5), V3 branch - mandibular branch
Blood supply
-Secondary arteries of the external carotid arteries
Differential diagnosis
-trigeminal neuralgia - sensory input from the V3 trigeminal nerve
What are the cardinal signs for TMD? What are the types of TMD?
-Orofacial pain
-Restricted jaw movement
-Joint noise
-Myofascial
-Discal
-Capsular
-Ligamentous
-Joint
What are the S + S of osteoarthritis TMD?
-Signs of degeneration
-Crepitus
-Reduced ROM - especially in the morning, then increases as time goes on
-Diffuse pain - especially when biting firm foods
-Muscle weakness and atrophy
Explain disc displacement in TMD?
Disc displacement with reduction
-Click 1 : Reduction of disc
-Click 2 : Dislocation of Disc
*typically anterior disc displacement
Disc displacement without reduction
-Closed locked - anterior disc displacement, can’t open
-Open locked - posterior disc displacement, can’t close
What are the S + S of hypermobile and hypomobile TMD?
Hypermobile
-increase ROM, especially excessive anterior translation
-May be joint noise at end range
-lateral deviation contralaterally
-generalized laxity
-pain with opening
Hypomobile
-decreased ROM
-potential contracture
-history of trauma
-secondary myofascial pain
-lateral deviation ipsilaterally
-localized pain at end range
What are the S + S of myofascial pain syndrome?
-increase pain in full opening, trigger points refer pain
-NO JOINT NOISE
-Traumatic or insidious (dentist, FHP, grinding)
-May result in deceased ROM
What is the objective exam for TMD?
Observation
-Cx Ax and posture
-Asymmetry of face
-Occlusion (over/under/cross bite or normal)
-Facial profile
-Teeth
AROM
-Cx
-TMJ
-Mandibular measurement
-Tongue and swallowing
-Cranial nerve function
AROM of TMJ
-Functional opening (40mm, 25mm for rotation, 15mm for translation) can do with tongue touching, when lifts off would be around 30mm, can see where the problem is
-Max opening (50mm)
-Retrusion (1-2mm), protrusion (9mm)
-Lateral deviation (9mm)
look for quality, quantity, pain, clicking
Opening - 2 knuckles = functional, 3=max - with retrusion, not protrusion = anterior disc displacement with reduction
PROM
Isometrics
Functional Ax
Special tests
-Auscultation - crepitus = OA or disc lesion, clicking = hypermobile, late = anterior disc displacement
-Knuckle test - +ve if can’t fit knuckles
What are the interventions for TMD?
-Education
-Fascial muscle relaxation
-Tongue and jaw proprioception and control
-Strengthening
-Manual therapy - passive stretching, ST techniques, mobilization, joint manipulations
-Modalities
Joint manipulations - if anterior, can pull caudal and anterior to relocate disc (J-stroke), often hear click
Postural - education, jaw posture, TMJ mobilization/manipulations, SOM interventions, mandibular and tongue proprioception
What is the applied anatomy for the Cspine?
7 vertebrae - C1/C2 - upper, C3-C7 is lower
8 nerves - go out above, with extra C8 between C7 and T1 then they go out below
Discs - not between C1/C2, C2/C3 is starts and continues
-Thick anterior for flexion, thin to maintain mobility
What is cervical radiculopathy? What is the etiology?
Compression or irritation of the spinal nerves
- Disc herniation -
-Typically goes postero-lateral since weakest part of annulus fibrosus
-For people in flexion with weight usually as less pressure posterior and it ruputres
-*if compresses straight posterior - more likely on to SC = UMNL - Stenosis
-Osteophyte formation
-Spondylosis - degeneration plus decrease hydration = thin = compress IVF
-Ligament thickening - ligamentum flavum - get central compression because of the area of that ligament - Swelling / inflammation (from local trauma)
What are the components for neuro scan for physical exam of cervical spine? What is it testing?
-Myotome - group of muscles or muscle supplied by spinal nerve
-Dermatomes - area of skin supplied by spinal nerve
-Reflexes - involuntary and instant response to a stimuli
-Special tests
What is myotomal testing comprised of for cervical spine? Including each myotome
Test bilaterally, hold for 5-8 secs as fatigable, testing in comfortable, neutral position
C1/C2 - neck flexion
C3 - SLF
C4 -shoulder elevation
C5 - shoulder abduction
C6 - elbow flexion, wrist extension
C7 - elbow extension, wrist flexion
C8 - thumb extension, ulnar deviation
T1 - finger abduction/adduction
What is dermatomal testing comprised of for cervical spine? Including the main testable dermatomes
Area of skin supplied by one nerve
Needs to be on bare skin, relaxed, testing bilaterally, demonstrate on non-affected area, eyes closed
Start light touch, if impaired do sharp/blunt, hot/cold
see book for pictures
C5, C6,C7,C8,T1 - most important - think of the spock hand
What are the upper region LMN reflexes? What can be included with testing? What is the rating scale?
C5 - deltoid
C6 - biceps/ brachioradialis
C7 - triceps
C8 - pronator quadratus
T1 - abductor digiti minimi
*Use jendrassik - pull legs apart for upper, hands apart for lower
Put tendons on slight stretch
Rating 0-4 with increasing response - 0, no, 1, decreased, 2, normal 3, exaggerated 4, is clonus/very brisk
What are the UMNL reflexes?
Potential lesion in brainstem, brain or spinal cord
Babinski - lateral across foot - abnormal, splaying of toes or great toe extension
Clonus - more than 5 times - hold DF
What are the neuro special tests for cervical radiculopathy?
-Cervical distraction test
-Spurlings (foraminal compression) test
-Upper limb tension (neuro provocation tests)
Cx distraction test - decrease symptoms +ve
Foraminal (spurlings) compression
-Compress in neutral, no symptoms - then with extension and rotation of unaffected, then of affected then side flexion to affected
-+ve if increased symptoms on affected
ULNT
-Unaffected side first - so they know what it feels like and compare
-Order → shoulder, forearm, wrist, fingers, elbow
-Added sensitizing and desensitizing movements to see if makes a difference
+ve if symptoms
Describe how you would do the ULTT for each nerve?
Median 1 - ULNT 1
-Shoulder depression, abduction, supination, wrist and finger extension, elbow extension
Median 2 - ULNT 2
-Shoulder depression, shoulder lower abduction, forearm supination, wrist and finger extension, elbow extension
Radial - ULNT 3
-Shoulder depression and abduction (10 degrees), forearm pronation, wrist flexion and ulnar deviation, finger and thumb flexion, elbow extension
Ulnar - ULNT 4
-Shoulder depression and abduction, forearm pronation, wrist extension and radial deviation, and finger extension, elbow flexion
What is the intervention for cervical radiculopathy?
Stenosis - unload the nerve - SLF and rotation away, flexion based exercises, traction
-Can also floss / tension
Disc - graduated retraction, then add extension when ready being careful not to make things worse
-The UCS in to flexion - no discs so don’t worry, LCS in to extension
Name and describe the two brachial plexus injures
Erb- Duchenne’s Palsy
-C5/C6 injury
-Shoulder and elbow effected, not hand
-Elbow extension, shoulder internal rotation, forearm pronation
-Sensation - limited on deltoid area and along radial side
-From traumatic birth traction of head when shoulder gets stuck
Klumke’s Palsy
-C8/T1
-Present with Horner’s syndrome - drooping eyelids (ptosis) and small pupils (miosis)
-Effects the forearm, wrist and hand - elbow flexion, forearm supination, wrist and MCP extension, finger flexion
-Sensation on ulnar side of forearm and hand
-Hyperabduction injury on birth or grabbing something and hanging off of it
Explain facet syndrome
Pain with extension, SLF (ipsilateral) and rotation (ipsilateral) - all compression stress
May refer to neck or scapula
Direction of Cx is 45 degrees towards eyes - able to get more rotation
Tested using coupled or combined movements
Physiological coupled - SLF and rotation to same side
Can use manual therapy of either because they are the same arthrokinematics
Non-physiological coupled - SLF and rotation to opposite side - more provocative
Explain vertebrobasilar insufficiency (VBI) and the 5 D’s and 3N’s
Compression of vertebral artery = decrease BF to brain
Dizziness
Drop attacks
Dysarthria
Dysphagia
Diplopia
Nausea
Nystagmus
Other neurological signs
What are the vertebrobasilar insufficiency special tests?
Vertebral artery (cervical quadrant) test
Bring patient in to extension and SLF holding for 10-30 sec
The into ipsilateral rotation holding for 10-30 sec
Dizziness or nystagmus = +ve on contralateral side artery is being compressed
keep eyes open
What is SCM innervation?
Accessory nerve (CNXI)
Branches of cervical plexus C2,C3
What is torticollis?
Can be congenital or acquired
-Congenital - unknown etiology - trauma during birth or positioning in utero
-Positional plagiocephaly - flattened head cause of positioning - change positions or wear a helmet (cranial remodeling orthosis)
Primarily tightness of SCM causing ipsilateral SLF and contralateral rotation
-Cause and decrease AROM and PROM the opposite way
Postural education, stretch muscles and strengthening opposite side for treatment
What is postural dysfunction within the c-spine? Including interventions
Upper cross syndrome
Weak - lev scap and upper trapezius, DNF
Tight - pects and lower trapezius and lev scap
Chin poking leads to tight upper extensors and lower flexors which lead to weak DNF
Puts more stress on posterior structures (discs and facet)
good alignment when sitting at desk
Interventions - stretch tight muscles, strengthening of weak ones, appropriate positioning
What is cervical instability? Including contraindication for treatment
Excessive motion between two adjacent vertebrae
Due to joint damage, muscle weakness, fracture, dislocation, ligament damage
Caused by trauma, long term corticosteroid use, congenital or secondary to other conditions (RA,OA, downs syndrome)
*DO NOT MOBILIZE OR MANIPULATE
What are the S + S of cervical instability
Severe headaches especially with movement
Fear to movement head or neck especially in to flexion
Dizziness
Pupil dysfunction
Nystagmus
Lip or facial paraesthesia
Lump in thorat
Nausea/committing
Severe muscle spasm
Soft end feel
*may have SCI S + S as well
What are the special tests for cervical instability?
Anterior shear or sagittal stress test
Test: anterior ligaments and capsular tissues
How: stabilize at TP below, anterior force on adjacent vertebrae above through SP or posterior arch (lamina)
Positive: excessive motion or S + S
Lateral flexion alar ligament stress test
Test: contralateral alar ligaments
How: stabilize C2 at SP and lamina, side flexes C1 and head
Positive: excessive side flexion
Lateral (transverse) shear test
Test: lateral ligaments and capsular tissues
How: radial aspect of one hand on one vertebrae, other side radial aspect of one hand on another vertebrae and push together
Positive: excessive motion or symptoms of instability, SC or vascular pathology
Sharp purser test
Test: Determine subluxation between C1 (atlas) and C2 (axis) - potentially torn transverse ligament as stops C1 moving forward on C2 in flexion
How: Hand on forehead and thumb on C2, patient to flex forward and to push forehead back
Positive: head slide backwards during the movement, potential clunk
Cervical flexion-rotation test
Test: Determines C1/C2 dysfunction or CGH
How: full Cx flexion then rotate to right and left
Positive: increased or decreased ROM 45 UCS rotation = C1/C2 dysfunction or headaches = CGH
What is segmental instability?What are the interventions?
Inner unit muscles - attach segmental - postural control, not that strong but have good endurance
DNF, deep neck extensors and SOM
Global muscles - strong but don’t have good endurance
if IUM are weak or inhibited by pain then the global muscles take over to work but they are not meant for that task
This leads to segmental instability - aberrant movements between segments and causing pain
Strength DNF - coordination and timing, analgesic effect
What is the special test for segmental instability?
Craniocervical flexion test
Use blood pressure cuff - inflate to 20mmHg, continue to add by 2’s if patient successful. See if they can perform upper cervical flexion and hold is for 10 sec getting it up to 22mmHg
Most can get it up to 26mmHg
Positive: unable to get to 26mmHg, hold it, raise pressure in small increments, uses compensatory patterns (using superficial neck muscles - SCM, extends the head)
What is the applied anatomy for the Tx? Including thoracic rib movements
Costochondral
Costovertebral
Facet joints
Transitional vertebrae
Thoracic rib motion
Pump handle action- ribs 1-6 - up and forward
Bucket handle action - ribs 7- 10 - lateral and forward
Caliper action - ribs 8-12 - lateral
Where does the typical line of gravity travel?
From external auditory meatus
Acromion
Greater trochanter
Posterior to patella
Anterior to lateral malleolus
Name and explain the types of kyphosis deformities
Round back
-Entire spine is kyphosis - decreased pelvic inclination (20 degrees) with thoracolumbar and thoracic kyphosis
-Associated with FHP and rounded shoulders
Scheuermann’s disease
-Uneven growth = excessive wedge shape increasing kyphosis
-Typically T10-12
-Rare congenital and/or degenerative weakening of vertebral end plate
-Most common deformity in adults, 2nd decade, “growing pains”
Hump back
-Gibbus (localized, sharp, posterior angulation) in Tx caused by structural deformity (e.g., anterior wedging) due to fracture, tumour or bone disease
-May or may not have pelvic inclination
Flat back
-Decrease pelvic inclination and decrease curve in Tx - mobile though
Dowager’s hump
-Increased kyphosis, typically postmenopausal OP with older women creating anterior wedge fracture across several vertebrae (result from trunk flexion)
-Happens in upper and middle Tx, decreases height
What are the interventions for kyphosis deformities?
Posture education
Extension approach
Stabilization exercises
Stretching as needed
Mobilization as needed
* DO NOT JOINT MANIPULATE AND AGGRESSIVE MOBILIZATION IN SCHEUERMANN’S DISEASE AND DOWAGER’S HUMP*
Explain compression fracture
Secondary to OP, F>M (post-menopause), 60-70 yo
Most common in thoracolumbar region, typically anterior vertebral body (wedge shaping)
Causes - falls, trauma, trunk flexion
Increased kyphosis (multiple fractures = increase)
What are the interventions for compression fracture?
Posture education
Extension approach
Stabilization exercises
Scapular stabilization exercises
Weight bearing activity and exercises
Light mobilizations as needed with precautions
JOINT MANIPULATIONS AND AGGRESSIVE MOBILIZATION, TRUNK FLEXION EXERCISES ARE CONTRAINDICATED*
Explain scoliosis including how it is named and the different types
Named based on the direction of the convexity, and level of apex
-If two - minor and major names
-Cobb angle - >10 is significant, <10 is not
Non-structural
-Based on muscle guarding or spasm, nerve irritation, inflammation, postural, leg length discrepancy
-LLD - if R higher- pelvis, sacrum, Lx all shift to R then thoracic shifts to L in order to compensation. Adducted on R, abducted on L - more stress on hip joints
-Easy to correct once you know the difference
-Adam’s test - disappears with forward flexion
Structural
-Due to the bony structures - congenital or acquired
-Severe (>60 degrees) - cardiopulmonary system compromised
-Rotation of vertebrae is towards the convexity, creates a rib hump
-This is palpable along back, might be confused with SP
-If severe = razor back spine
-Can’t fix bones but can manage that non-structral doesn’t exacerbate structural
What are the interventions for scoliosis?
Posture education
Stretch concavity
Strengthen convexity
Stabilization exercises
Scapular stabilization exercises
Mobilization as needed
Bracing as needed - boston, milwaukee
Surgery if severe
What is herpes zoster?
AKA shingles
Viral infection of nerve causing skin rash along the typical dermatomal pattern (stripe like in Tx, just on one side)
May be with fever
Names the visceral referral pain patterns for all organs
Right
Liver and gallbladder - right neck and shoulder, right upper quadrant
Appendix - right lower quadrant
Left
Lung and diaphragm - left neck and shoulder
Heart - Left chest and arm and between scapula
Pancreas - left upper quadrant
Center
Stomach - center of chest and back
Small intestine - center of abdominal area
Colon - center of groin area
Both
Kidney - left and right lower quadrants and upper legs
Bladder - lower groin, inner legs
What is the applied anatomy for the Lx?
5 vertebrae
5 spinal nerves coming out below
5 discs
-Thicker anterior - why lumbar lordosis
-Posterolateral weaker - that is why it herniations here
-Also not posterior cause of the posterior longitudinal ligament
Motion segment - disc + above and below vertebrae
What is the neural exam for Lx radiculopathy? Including how to test for each
Dermatomes - same procedure as cervical
-L4 - patella, and to great toe
-L5 - plantar and dorsal digits, lateral ankle
-S1 - 5th digit
Myotome - same procedure as cervical
-L1/L2 - hip flexion
-L3 - knee extension
-L4 - Ankle DF
-L5 - Great toe extension
-S1 - PF, hip extension and eversion at ankle
-S2 - PF, hip extension and knee flexion
Reflexes - same procedure as cervical (and same rating)
-L3/L4 - patella
-L4/ L5 - tibialis posterior
-L5/S1 - medial hamstring
-S1/S2 - lateral hamstring
-S1/S2 - achilles
UMN - same as cervical spine as this doesn’t change
What are the special tests of Lx radiculopathy?
Slump - get patient to slump down and tuck chin then passively extend their unaffected leg, then their affected
If no symptoms - add DF
If symptoms - ask them to lift head without moving from slump
Positive - symptoms become worse with DF, or better when lifting head indicated neural tension/restriction of lumbosacral roots or dura/neural tissues
*If symptoms at any stages - don’t add movements
SLR - testing unaffected side first, add medial rotation and adduction, then flex at hip, if pain/tightness lower slightly until disappears, then DF or flex patient’s neck to see if symptoms or reproduced
ROM - 35-70 = sciatic nerve
-Before 35 - slack taken up
-35- under tension
-60-70 sciatic roots tense over disc
->70 - pain is likely MSK (hamstring stretch)
Further stress nerves
-SID - sural, inversion, DF
-TED - tibial, eversion, DF
-PIP - peroneal, inversion, PF
Crossover sign - if when doing unaffected side they feel it in affected - suggests a large disc bulge as pulling the nerves into the disc
Sign of the buttock - do after SLR - go to point of restriction then back off, add knee flexion and see if can get further hip flexion
Positive - hip flexion does not increase - pathology behind hip joint (bursitis, tumour, abscess) - refer to GP
Bow-string test - SLR produces symptoms, slightly flex the patient’s knee (20 degrees) to reproduce symptoms, pushing then in to popliteal area
Positive - reproduces radicular symptoms, pressure or tension on sciatic nerve
What is spinal stenosis? How does it present in Lx?
Narrowing of the central canal (central stenosis) or lateral canal (lateral stenosis) which may compress the nerve roots or spinal cord
Onset is insidious and usually >60
Due to osteophytes, spondylosis, ligament thickening
May result in neurogenic claudication - neural leg pain
Better with flexion, worse with extension
How do you differentiate between neurogenic claudication and intermittent claudication?
IC is similar leg pain symptoms but more to do with the use of muscles. Increase pain leads to increase activity and it is relieved by rest
*see chart to differentiate between NC and IC *
Use bicycle test as main measure to differentiate the two
What are the intervention for spinal stenosis in Lx?
Flexion based exercises initially and positioning (e.g., z-posture)
Avoid aggravating movements
Surgical management - laminectomy
What is a disc herniation? What are the types? How does it present?
Disc herniations posterolateral - due to PLL and weak annulus fibrosis, may compress nerve root
Typically acute onset, 30-50
Levels
-Protrusion
-Prolapse
-Extrusion
-Sequestration
Happens with flexion MOI, hurts in flexion, better in extension
Worse in morning - due to larger disc = more herniation, worse with cough, sneeze, Valsalva
May present with lateral shifting away from bulge (named based on the shoulders shift)
What are the interventions for disc herniation in Lx?
Postero-lateral bulge
-Extension based exercises with progressions
-Lumbar roll to promote extension when sitting
Lateral bulge
-Shift back towards the affected side
Anterior bulge
-Happens when bulge comes out anteriorly - less common, but there is no spinal nerves but the disc has nociception therefore can still feel pain
-Flexion based exercises
May be painful initially but complete entire set to evaluate the effect
CENTRALIZATION is the priority
Green (centralized or with an increase in pain), yellow (no change), red (no change and increase pain and peripheralized)
Avoidance of aggravating movements and positions
Surgical - laminectomy, discectomy
What is schmorl’s node?
The nucleus goes up or down, typically from a compression force, which goes through the cartilaginous end plate and vertebral body
Typically in higher lumbar levels
What is the postural dysfunction in Lx? What is the intervention for this?
Lower cross syndrome
Tight hip flexors, hamstrings, ES
Hamstrings tight from trying to correct pelvis and compensating for glutes
Weak glutes and core
Anteriorly rotates the pelvis = more lumbar lordosis
Intervention
Strengthening weak, stretch tight
What is spondylosis in Lx?
Degenerative changes within spinal motion segment
Increase incidence with age, typically around >50, insidious
Loss of disc height, approximation of vertebrae (initially unstable because ligaments longer = more laxity, then becomes stiff), degeneration of plates, fibrotic in discs, osteophyte formation
Presents with loss of lordosis - results in increased stiffness, muscle spasms and back pain (Ache)
Worse with prolonged flexion, specifically load. Better unloaded, position changes and gentle movement
What is facet syndrome in Lx? What are the coupled (physiological) and non-physiological movements in the Lx?
Syndrome cause by facet - worse with compression of facet joints
May refer to low back, glutes, hips, groin, thighs (not below knees)
Coupled movements
-Flexion - SLF and rotation to same side
-Extension - SLF and rotation to opposite sides
Non-physiological coupled - the opposite of this
What is the special test to determine facet syndrome in Lx?
Quadrant Test
-Patient extended Lx and side flexes and rotates to side of pain
-If increase - indicate facet involvement
What are the intervention for facet syndrome in Lx?
Flexion based exercises and positioning
Avoidance of aggravating movements and positions
What is lumbar instability? What is the intervention?
Excessive motion between two vertebrae
Can be ligament damage, fracture, dislocation,muscle weak, joint damage, poor neuromuscular control
May be caused by trauma, long term corticosteroid use, congenital or secondary to other conditions
Do not mobilize or manipulation
Control system (CNS), active system (muscles and neural control) and passive system (bones and ligaments)
Intervention = inner unit core stability training
What is clinical instability in Lx?
Inner unit muscles - stabilizers - timing and endurance is important
Transverse abdominis, PF muscles, diaphragm, lumbar multifidus
Neurophysiological connected - meaning that they all fire at once, anticipatory before movement
Often weak, trouble with timing - leads to aberrant movement and increased recruitment of global muscles to maintain stability
Active muscle systems
-Local and global - see chart in book
What are the special tests to Ax Lx instability?
H and I (*start with pain free direction first)
-If two positive - hypomobility
-If one positive - instability
-as the first movement providing stability for the second movement if this is the one that is unstable
-direction of instability is based on the first movement
Prone segmental instability test
-Upper body prone, legs on floor
-PA by therapist, if pain - lift legs - not present, then need core strengthing/stability exercises
What is inner unit core stability training for each muscle?
TA isolation
Make sure deep tension, no bulge
2 inch medial to ASIS, 1 inch inferior - then draw in abdomen and hold for 10 secs
May coactivate with multifidus and PF muscles and progress to sitting / standing
Correct
-Normal, relaxed breathing
-Slow, inward movement of lower abdomen
-Deep tension under palpated area
Incorrect - global muscle use
-No movement of lower abdomen
-Rapid contraction and/or tremor
-Visible contraction
-Swelling or bulging
-Upper abs and rib cage movement
-Breathing - unable to relax abdomen, holding breath
-Spinal movement - PPT or APT, flex or extension of spine
Multifidus
Lateral to both sides of lower lumbar SP - contract for 10 secs - swell muscle, pushing fingers away
May coactivate with TA or PF muscles
PF
Contract PF, stop urine from flowing,
NO peri-anal or glute gripping
Diaphragmatic
Breath through belly, not chest
Progression
Isolate inner unit
Train inner unit
Maintain control of inner unit while training outer unit
Integrate into function
Describe spondylolysis, spondylolithesis (and types), retrolisthesis.
Spondylolysis - fracture of one pars articularis - no slippage
Spondylolisthesis - fracture of two and get anterior slippage
-Traumatic - from trauma
-Isthmic - repetitive micro trauma - common in L5/ S1 (excess movement of L5, carry weight of body, angulation is greatest)
-Degenerative - degenerative changes - decrease joint space, increased laxity and risk of slippage
-Dysplastic (congenital) - defect in formation of vertebrae
-Pathological - secondary to another disease process or treatment
Retrolisthesis - fracture of two and get posterior slippage
What are the grades of spondylolithesis and the intervention?
1 - <25
2 - 25-50
3- 50-75
4 - >75
5 - 100
*4 and 5 - need fixation, others core stability exercises
What are the S + S of spondylolithesis?
Hyperlordotic
Pain with hyperextension
Tight hamstrings
Scotty dog with collar or decapitation
Step deformity maybe
S + S of central and lateral stenosis
What is the intervention for spondylolithesis?
Inner core stability
Education - avoid aggravating movements
Spinal fusion surgery
*don’t manipulate
What is the post-operative management of spondylolithesis?
Max protection -
Patient education
-Expectations
-No heavy lifting >10 pounds for up to 3 months
-Signs of inflammation and infection
-No getting incision wet (1 to 2 weeks)
-Surgeons guidelines
–Based on preference and surgery dependent - no rotation and avoid hyperflexion/extension
Bed mobility
Exercise - walking, gentle exercise
C/I - extension exercises for laminectomy
Moderate and minimum
Scar tissue mobilization
Progressive stretching and joint mobilization - grade I or II for pain relief
Exercise - walking, strengthening - start with inner unit then progress
C/I - joint manipulation at level of spinal fusion, extension exercises
What are the sinister pathologies for Lx and what are the S + S to look for
CES
-Below L1 - variable nerve root damage
-Flaccid paralysis
-LMN injury - areflexic B + B and sacral anesthesia
-Leaking but don’t notice as don’t know when it is full
-Emergency
Malignancy
-Spinal pain common-
-Age >50
-Previous history of cancer
-Unexplained weight loss
-Constant unrelenting pain
-Pain unrelieved by rest
-Pain worsens at night
-Failure to improve with conservative therapy (1 month)
What is the action and innervation of serratus anterior?
A; Draws scapula anterolaterally, Suspends scapula on thoracic wall, Rotates scapula (draws inferiorly angle laterally)
N: Long thoracic nerve (C5- C7) (SALT)
What is the action and innervation of supraspinatus?
A: Shoulder joint: abduction of arm, stabilization of the humeral head in the glenoid cavity
N:Suprascapular nerve (C5, C6)
What is the action and innervation of biceps brachii
A: Flexion and supination of the forearm at the elbow joint, weak flexor of the arm at the glenohumeral joint
N: Musculocutaneous nerve (C5- C6)
What is the action and innervation of infraspinatus?
A: Shoulder joint: Arm external rotation;
Stabilizes humeral head in glenoid cavity
N: suprascapular nerve (C5, C6)
What is the action and innervation of teres minor?
A: Shoulder joint: Arm external rotation, arm adduction;
Stabilizes humeral head in glenoid cavity
N: Axillary nerve (C5, C6)
*can be injuried with axillary nerve damage from shoulder dislocation
What is the action and innervation of subscapularis?
A; Shoulder joint: Arm internal rotation
Stabilizes humeral head in glenoid cavity
N: Upper and lower subscapular nerves (C5 - C6)
What is the action and innervation of deltoid?
A: Clavicular part: flexion and internal rotation of the arm,
Acromial part: abduction of the arm beyond the initial 15°
Spinal part: extension and external rotation of the arm.
N: Axillary nerve (C5, C6)
What is the applied anatomy for the shoulder joint?
Sternoclavicular joint - attaches shoulder to axial skeleton, ligaments very strong, more likely to fracture clavicle
Acromioclavicular joint - attached scapula to axial skeleton
Glenohumeral joint
-ER>abduction>IR - closed packed
-30 degrees flexion, 60 degrees abduction, internal rotation - loose packed
Scapulothoracic joint - false joint since no capsule and no bony articulation
What are the borders and contents of the thoracic outlet?
Borders
-Anterior - pect minor, coracoid process, clavicle
-Posterior - scapula, UFT
-Medial - 1st rib, scalenes
-Lateral - axilla
Content
-Brachial plexus
-Subclavian artery
-Subclavian vein
What is Thoracic outlet syndrome? And what are the types?
Diagnosis of exclusion - results from compression of nerve or vascular structures in outlet
Types
Neurogenic (True TOS)
-From anatomical anomaly - compression of nerve
Non specific (symptomatic) neurogenic
-Most common, diagnosis of exclusion - nothing shows up on scan, muscle atrophy or anatomical anomaly
-Maladaptive postures - tight scalenes or pect minor
Vascular - arterial
-Compression of subclavian artery from anatomical anomaly
-Worse with upper arm movements
Vascular - vein
-Does not typically result in TOS complaints - result of another cause (thrombus)
What are the S + S of all types of TOS? What is the epidemiology?
Neurogenic
-Tingling, numbness, paraesthesia
-Harder fine movements
-Weak grip strength
Vascular - artery
-Cold and pale
-Decrease pulses
-Rapid fatigue of limb
-Lower BP on affected side
Vascular - vein
-Mottled skin, blueish
-Painful swelling in arm
F>M, onset 20-50 - neuro most common
Involves C8,T1 (ulnar nerve distribution)
Athletes with abduction and external rotation
What is the etiology of TOS ?
Congenital anatomical anomaly
Inflammation or scar tissue
Hypertrophy of scalenes, pect minor, subclavius
Pressure
Posture
Overhead movements
Trauma
Thrombus (vascular TOS)
Pancoast tumor
What are the classifications of TOS?
- Scalenus anterior syndrome
Compress = interscalene triangle - between scalene anterior and medius (SUPRACLAVICULAR) - Costoclavicular syndrome
Compress = costoclavicular space - between clavicle and 1st rib (subclavicular) - Hyperabduction syndrome
Compress - axillary interval - under coracoid process and behind pect minor (infraclavicular) - Cervical rib syndrome
What are the special tests for TOS?
Adson’s
Allen’s
Costoclavicular syndrome
Halstead
Wright test
above are all vascular and have to do with different positioning and decreasing the pulse
Roos - opening and closing hands - see why they stop
Shoulder girdle passive elevation - do to patient and see if they get decrease in symptoms
What is shoulder separation? What is the etiology?
The AC joint separation - the ligaments that hold the joint together (AC and coracoclavicular)
Etiology
-Downward pressure on acromion, or fall on acromion
-Fall on outstretched hand or elbow
What are the S + S of shoulder separation? What are the special tests? How do they xray?
Step deformity
-Distal end of clavicle raises
-Grade III separation
-Torn deltoid and trapezius also possible
Pain with
-Horizontal adduction - compressing together
-Elevation - causes posterior rotation of clavicle
-HBB - causes anterior rotation of clavicle
Tenderness and swelling
Horizontal adduction or cross body test
Stress view xray - provide traction (inferior pressure) to see if there is separation
What are the grades of shoulder separation?
Grade 1 (SPRAIN) - no separation, capsule intact
Grade 2 (SUBLUXATION) - increased AC joint spacing
Grade 3 (DISLOCATION) - torn AC and coracoclavicular ligaments, joint surfaces not in contact
What is the classification of glenohumeral instability? What is the epidemiology?
Direction - anterior, posterior, inferior, multidirectional
Degree - subluxation, dislocation
Etiology - traumatic, atraumatic
Timing - acute, recurrent
Epidemiology - M, <30
What is the difference between shoulder dislocation and subluxation?
Shoulder dislocation - separate of humerus from scapula, common (and common anterior - for MSK)
Shoulder subluxation - incomplete dislocation
What is the etiology of shoulder dislocation?
Traumatic - direct, indirect
-Most common abduction, ER
-Stability provide - subscapularis, GH ligaments, long head biceps
-Anterior dislocation injuries - subscapularis, long head of biceps, GH ligaments, anterior capsule, anterior glenoid labrum
Atraumatic - general laxity lead to instability
*surgery - only if recurrent - tighten subscap - no stretching or resisted activities
What are the S +S of glenohumeral joint instability?
Feeling of slippage with pain or insecurity with certain activities
Pain or apprehension when approaching extreme ROM
Decrease ROM - acute
Increase ROM - chronic
Normal on clinical examination - more apparent after repeated activities with fatigue
Atrophy due to disuse (chronic)
Sulcus sign - multidirectional instability, loss of muscle control, groove inferior/lateral of acromion
What are the complications to glenohumeral instability?
Axillary nerve injury - deltoid or teres minor
Axillary artery
Brachial plexus - posterior cord especially
Bankart lesion - anterior dislocation = labrum damage
Hill-Sach’s lesion - damage to posterolateral humerus (indentation) as humeral head is compressed against anterior-inferior glenoid rim
What is the spectrum of instability for glenohumeral instability?
AMBRI - born loose
-Atraumatic, multidirectional, bilateral, rehab, inferior capsule shift if surgery required
TUBS - torn loose
-Traumatic, unidirectional, bankart, surgery
What are the special tests for glenohumeral instability?
Anterior instability
Crank, apprehension test with relocation
Apprehension release (surprise)
Load and shift test
Posterior instability
Posterior apprehension test
Load and shift test
Jerk test
Inferior and multidirectional instability
Sulcus sign
Feagin test - push inferior with their hand on your shoulder
What are the types of glenohumeral labral tears? Including S + S
Bankart
Anterior-inferior of labrum
From anterior dislocation, common from overhead sports
S + S
Clicking and/or popping
Diffuse shoulder pain
Worse with HBB
Weakness and instability
SLAP
Superior labrum anterior, posterior
Long head of biceps attaches to superior labrum - can tear if forceful, shoulder can become unstable
From
-Repetitive throwing and overhead activity
-Deceleration when throwing
-Direct trauma
-FOOSH
-Traction injury (to biceps) in inferior direction
S + S
Clicking and/or popping
GIRD - internal rotation deficit
Pain with overhead activity (elevation) and lying on affected side
Loss of strength and endurance in RC and scapular stabilization
“Dead arm”
What are the special tests for glenohumeral labral tears?
Clunk test
Active compression test of O’brien - SLAP
Biceps load test
What is adhesive capsulitis and was is the epidemiology?
Idiopathic - pain with more decrease ROM in capsular pattern from dense adhesions and capsular thickening
F>M, 40-60 yo, non-dominant shoulder, increased with diabetes
What is the etiology of adhesive capsulitis?
1 - primary - idiopathic
2- secondary - other conditions
*high correlation with psychosocial issues
What are the S + S of adhesive capsulitis?
Progressive ROM restriction in capsular pattern
Hard with HBB, HBH, overhead
Reverse scapulo-humeral rhythm (normal is 1:2, this is 2:1)
Trick movements
General muscle weakness and poor endurance
What are the stages of adhesive capsulitis?
1
Pain starts, increased with movement, present at night
Loss of ER
<3 months
2 - Freezing
More intense pain, restricted ROM in all directions
3-9 months
3 - Frozen
Pain only with movement
Hard capsular end feel - significant adhesions
Restricted ROM in all directions with increased scapula compensation movements
Atrophy of deltoid, RC, biceps, tricpes
9-15 months
4 - Thawing
Minimal pain
Increased ROM
15-24 months
What is subacromial impingement syndrome, including structures compressed
Increased pressure on structures under a narrowed sub-acromial space
Subacromial bursa
Supraspinatus tendon
Long head biceps tendon
Coracoacromial ligament
Joint capsule
What is the etiology of subacromial impingement syndrome?
Primary - congenital or degenerative
Secondary - abnormal force coupling action - muscle imbalance and abnormal movement patterns (scapula or GH)
-Secondary after instability (loose anterior capsule)
-From tight pect minor (anterior tip), weak LFT (less post tilt), winging of scapula (internal rotation of scapula), kyphotic posture (no posterior tilt since blocked by ribs)
Calcific tendinitis - typically supraspinatus
What are the S + S of subacromial impingement syndrome?
Pain arc (60-120)
Pain - with overhead, anterior lateral shoulder, not below elbow, no pain at rest
TOP - SSp, LHB, bursa
Revered scapula-humeral rhythm
Decreased HBB or HBH
Pain and weakness on resisted abduction and ER
Anterior-superior placed HH at rest
Decreased posterior-inferior glide
What are the special tests for subacromial impingement syndrome?
Hawkins kennedy
Neers
Scapular assist - help scapula move
Describe the terms used for muscle/tendon pathology
Tendonitis - inflammation
Tendinosis - chronic degenerative changes without inflammation
Tenosynovitis - inflammation of synovium
Tendon rupture - tendon rupture
What are the S + S for tendinopathy?
Pain with muscle contraction
TOP
What are the special tests for tendinopathy?
Biceps
-Speed
-Yergasons
Supra
-Drop arm
-Empty can
Subscap
-Belly press
-Lift off
-Internal rotation lag sign
Infra
-Infraspinatus test
-Lateral rotation lag sign
Teres minor
-Hornblower’s sign
What is scapular dyskinesia? What are the types?
Abnormal movement
-Static - structural deformity, winging at rest
-Dynamic - winging with movement
Long thoracic nerve
Serratus anterior weakness
Other causes
What are the special tests for scapula dyskinesia?
Wall or floor push up
Scapular load test
Punch out test
What is the applied anatomy for the elbow joint?
Ulnohumeral joint
Ulnar / Medial collateral ligament
Trochlea and coronoid process
Radiohumeral joint
Radial / lateral collateral ligament
Capitulum and radius
Proximal radioulnar joint
Head of radius with notch on ulna
Annular ligaments holds together
What are the normal carrying and abnormal carrying angles for the elbow?
NORMAL: female 10-15, male 5-10 (a little valgus)
Excessive cubitus valgus: 30
Cubitus varus: -5
Gun stock deformity: -15
What are the grades for ligament sprains in the elbow?
Grade I - no laxity, pain and inflammation
Grade II - moderate swelling, ecchymosis and pain. Increased ligament laxity but still firm end feel
Grade III - severe swelling, ecchymosis and pain. Gross laxity present. No end feel noted.
What is the ulnar collateral ligament?
Fan shape - anterior, posterior and transverse portions
Resists valgus
What is the etiology, S + S and special test for the ulnar collateral ligament tear?
Valgus stress (chronic or acute - FOOSH with elbow stressed or forced ER)
S + S
-Pain, TOP
-Joint effusion
-Instability with valgus stress
-Limited ROM
-May have heard audible pop
Special test
Valgus stress test
What is the interventions for an ulnar collateral ligament tear?
Activity modification
Correcting faulty technique
Decrease pain
Decrease swelling
Bracing (medial strapping of elbow)
Strengthening (focus on forearm flexors and pronators)
Restore ROM
Surgical - ligament reconstruction (take from other tendon typically hamstring)
Immobilize to 90 degrees elbow flexion, neutral pro/sup = stiff especially in to elbow extension
What are the 5 types of elbow dislocations and what are their MOIs?
Posterior
Most common, ulna and radius (distal segment) moves posterior
MOI: FOOSH
*often involves disruption of UCL and RCL
*often involves fracture of coronoid process or radial head
Major complications from impairment of vascular supply (CHECK DISTAL PULSES)
Anterior
Distal segment moves anterior
MOI: High energy trauma (MVA)
Lateral
Distal segment moves lateral
MOI: humerus moves medial
Medial
Distal segment moves medial
MOI: humerus moves lateral
Divergent
Ulna and radius move apart
MOI: driving force inferiorly
What is nursemaid’s elbow? What is the etiology, S +S, interventions?
Sublux radial head - commonly young children
Longitudinal traction force with wrist in pronation
S + S
Child doesn’t move arm
Arm is held at side in slight flexion
Interventions
Reduction of subluxed radial head
Hyper pronation
Supination / flexion maneuver
Compressive manipulation on radius with arm in supination
What is olecranon bursitis? Including etiology, S + S, interventions
Inflammation of bursa (fluid filled sac between bones, ligaments or tendons)
Etiology
Trauma
Pressure - chronic
Infection
more at risk if RA/gout
S + S
Swelling, TOP
Redness
Interventions
Activity modification, ice, compression, decrease swelling
Medical - NSAIDs, corticosteroid injection, aspiration (drain excess fluid), antibiotics (if infected), bursectomy (if repeated bursitis or antibiotics don’t work)
What is lateral epicondylosis? Including epidemiology, etiology, S + S and special tests
Degenerative changes to wrist extensor tendons inserting into lateral epicondyle CEO
Most common ECRB
Etiology (>35 years olds)
Repetitive use
E.g., people that do extension/pro/sup all day
Poor technique
Heavy racquet
Heavy ball
Small grip
*Load> person’s capacity to recover = degeneration of tendon
Load = capacity = no degeneration
Decrease BS also limits someone’s ability to recover
S + S
Aching pain - down to proximal forearm - insidious onset
TOP near lateral epicondyle
Pain with resisted wrist extension and/or gripping
Pain with stretching of wrist extensors
Decreased wrist extension or grip strength
Special test
Maudsleys - resisted D3
Cozen - resisted wrist extension
Mill’s - passive wrist flexion
What are the differential diagnosis for lateral epicondylosis?
Cervical radiculopathy C5, C6
Radial nerve entrapment
Musculocutaneous nerve tunnel syndrome
Supraspinatus referral
Radial head fracture
Radiohumeral synovitis
What is the treatment for lateral epicondylosis?
Activity modification
Counterforce brace
Stretching
Strengthening - eccentric
Mobilization
DTFM
Pain modalities
Medical - NSAIDs, corticosteroids
What is medial epicondylosis? Including epidemiology, etiology, S + S and special tests
Degenerative changes to wrist flexors tendons inserting into medial epicondyle CFO
Most common pronator teres and FCR
Etiology (>35 years olds)
Repetitive use
S + S
Aching pain - down to proximal forearm - insidious onset
TOP near medial epicondyle
Pain with resisted wrist flexion and/or gripping
Pain with stretching of wrist flexors
Decreased wrist flexion, pronation or grip strength
Special test
Medial epicondylitis (golfers elbow test) - reverse mills - passive wrist extension
Resisted wrist flexion
Resisted pronation
What is the treatment for medial epicondylosis?
Activity modification
Stretching
Strengthening - eccentric
Mobilization
DTFM
Pain modalities
Medical - NSAIDs, corticosteroids
What are the peripheral nerve injuries?
Median (C6-C8, T1)
-Humerus supracondylar process syndrome - ENTRAPPED - under the ligament of struthers (anomaly)
-Pronator syndrome - ENTRAPPED - between heads of pronator teres (does not lose innervation though)
-Anterior interosseous nerve syndrome - between heads of pronator teres
—Occurs with forearm fracture
—Pinch deformity - can’t go tip to tip, pulp to pulp
—Just the motor - FPL, lat ½ of FDP and pronator quadratus
—Branch of median nerve
Ulnar (C7, C8, T1)
-Cubital tunnel syndrome - ENTRAPPED - cubital tunnel between two heads of FCU
-More stress on nerve if more valgus or shallow tunnel
-Special tests - cubital tunnel compression test, tinnel’s test at the elbow, elbow flexion test
-Interventions
—Nerve mobilization
—Medial - NSAIDs, corticosteroids, ulnar nerve transposition surgery - reposition the bitch
Radial (C5-C8, T1)
-Posterior interosseous nerve (a branch) ENTRAPPED
—Two head of supinator in arcade of Frohse (anomaly)
—Entrance of radial tunnel anterior to radial head
—Near brachioradialis and ECRL
—Between ulnar half of ECRB tendon and fascia
—At distal border of supinator
may mimic tennis elbow
-Superficial branch of radial nerve
-ENTRAPPED - under tendon of brachioradialis
-*common with fractures mid-humerus - doesn’t affect triceps
-Interventions
—Mobilization
—Medial - NSAIDs, corticosteroids, radial tunnel release surgery
What is the applied anatomy for the wrist and hand complex?
Phalanges - Distal, Proximal and Middle
MC
Carpals - scaphoid, lunate, triquetrum, pisiform, trapezium, trapezoid, capitate, hamate
Radius
Ulna
Joints
DIP
PIP
MCP
CMC
Midcarpal
Intercarpal
Radiocarpaul
Distal radioulnar
*there is no ulnocarpal joint because the TFCC (triangular fibrocartilage complex) articulates with ulna and triquetrum
What is a Colles’ fracture? Including etiology, complications, S + S and interventions
Distal radial fracture where the fragment moves more dorsally
-SMITH’S fracture - the distal segments moves more anterior
Complications
-Compression neuropathy (commonly median nerve)
-CRPS
-Arthritis
From FOOSH - with wrist extended
-SMITH’s - with wrist flexed
-More common in osteoporotic women - because they have a weak radius therefore it is the first thing to give)
S +S
-“Dinner fork” deformity
-Dorsal wrist pain and TOP
-Swelling - which may cause the compression of the median nerve
-May have bruising or paraesthesia
-Difficulty lifting or grasping
Interventions
-Medical - immobilization (either stable in cast (thumb spica), or unstable/displaced in ORIF)
-PT - mobilization, strengthening
-In cast - move everything above and below - NO PRO/SUP - makes sense cause radius moves around ulna = pain and delayed healing
What is complex regional pain syndrome? Including types, etiology and S + S
Chronic pain disorder caused by SNS malfunction and is characterized by pain out of proportion to original injury
Types
I - injury to tissue - also known as regional sympathetic dystrophy (RSD)
II - injury to nerve - also known as causalgia
Unknown etiology - association with injury to affected area, F>M
S + S
Severe pain (burning)
Sensory abnormalities
-Allodynia - pain response to non-painful stimuli
-Hyperalgesia - exaggerated response to stimuli
Abnormal blood flow (vasomotor changes) and sweating (sudomotor changes)
Abnormal motor function - weakness and poor coordination and stiffness
Trophic changes
-Color changes
-Temperature changes
-Edema
-Shiny tight skin
-Abnormal hair and nail growth
Late stages may develop OP
What are the stages of CRPS?
Stage 1 - acute / reversible - days to weeks
Characteristics - pain, hyperhidrosis, warmth, erythema, rapid nail growth and edema
VASODILATION PHASE
Stage 2 - dystrophic or vasoconstriction (ischemic) stage - 3 months lasting 3-6 months
Characteristics - burning pain, sympathetic hyperactivity, hyperesthesia exacerbated by cold weather, mottling and coldness, brittle nails and OP
VASOCONSTRICTION PHASE - careful with OP
Stage 3 - Atrophic stage - 6 months to a year and lasts for months or years
Characteristics - pain decreases or becomes worse, severe OP, muscle wasting, contractures
CHRONIC PHASE - careful of OP
What are the interventions for CRPS?
Education
Mobility - early AROM, tendon gliding, nerve mobilization
Encourage ADLs
Compression loading
Distraction
Desensitization
Edema control - Elevate, compression, retrograde massage
Modalities - TENS, US, ice
Mirror therapy
Aerobic activity
What are the warning signs and precautions for immobilization ? What are the dos and don’ts?
Increased pain
Cast tightness
Cast looseness
Changes in skin colour / sensation - CRPS, nerve/blood vessel compression
Increase swelling
DO
Maintain ROM above and below
Check skin integrity above and below
Check capillary refill
Education - reduce swelling warning signs / precautions
Remove tight jewelry
DONT
Stick something inside case
Get cast wet
What is a scaphoid fracture? Including complications, etiology, S + S and interventions
Fracture of scaphoid - common, from FOOSH or MVA. Common in young males
Complications
Avascular necrosis
Radial artery branch affected - no longer supplies blood, bone cause disintegrate
Nonunion of fracture
Arthritis
S + S
Radial sided pain
Tenderness and swelling in anatomical snuffbox (EPL, EPB), scaphoid in floor
Pain with longitudinal compression of thumb - pushing in to scaphoid
Interventions
Immobilization - stable (cast - thumb spica), unstable/displaced - ORIF
Non - union - bone graft, avascular necrosis - vascular graft
PT - mobilization and strengthening
What is De Quervain’s Tenosynovitis? Including etiology, S + S, special tests and interventions
Inflammation in sheath (synovium) of ABL and EPB - compression between sheath and radial styloid process
Etiology
Chronic overuse - repetitive wrist (ulnar deviation) and thumb movements
Direct trauma - to radial styloid process
S + S
Radial side wrist pain
Tenderness and swelling
Wrist with wrist and thumb movements - contraction and stretching of APL and EPB
May have crepitus
Special tests - Finklestein’s
Interventions
PT
Activity modification
Cryotherapy
Splinting (thumb spica)
Gradually stretching and strengthening (as tolerated)
Medical
NSAIDs
Corticosteroid injections *
Surgical release
What is a TFCC tear? Including etiology, S + S, special tests, interventions
Tear to TFCC on ulnar side of wrist
TFCC - transmits and distributes load, stabilizes area (therefore causes radius to bear more load)
Etiology
Compressive loads to wrist - while in ulnar deviation - degenerative or traumatic
Distal radial - ulnar fracture
S + S
Ulnar side wrist pain
Tenderness and swelling over dorsal ulnar aspect of wrist
CLICKING with wrist movements - HALLMARK
Pain with (or resisted) wrist extension and ulnar deviation
Special tests
TFCC load test - compressive load with ulnar deviation with flexion/extension
Press test - pushing up in chair
Interventions
Activity modification
Bracing (widget - two straps)
Cryotherapy
Progressive strengthening and mobility exercises when able to tolerated
*after extension period of immobilization
Medical management -NSAIDs, Corticosteroid injection, Surgery
What muscles does each nerve innervate?
Median nerve
2 lumbricals - 1 and 2
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
Ulnar nerve
Lumbrical 3 and 4
Hypothenar muscles
-Abductor digiti minimi
-Opponens digiti minimi
-Flexor digiti minimi
-Palmaris brevis
Interossei muscles
-PAD DAB
-Palmar - adductor
-Dorsal - abductor
Adductor pollicis brevis
Radial nerve
Brachioradialis
Extensors
Supinator
Triceps and anconeus
What are the hand deformities?
Median
Ape hand - thumb in same plane, stuck in adduction - no other thumb movements
Lower level lesion
Hand of benediction - cannot flexion digits 1-3, so when make a fist those digits remain (ONLY SEE WITH FIST)
High level lesion
Ulnar
Claw hand - hyperextension of MCP, flexion of digits 4 and 5
Radial
Wrist drop - cannot extend wrist or MCP
What is carpal tunnel syndrome? Including what is the contents of the carpal tunnel and the etiology
Compression medial nerve as through carpal tunnel (made by flexor retinaculum and carpal bones)
Contents
FDP, FDS, FPL
Median nerve
Etiology
Typically insidious onset, F > M
Repetitive hand movements
Vibrations
Associated conditions
-RA and other inflammatory conditions
-Colles’ fracture
-Lunate subluxation - encroach on space
-Hypothyroidism - fluid retention
-Pregnancy - 2nd trimester - fluid
-DM - fluid
-Obesity - fluid and tissue larger
What is the S + S, special tests and interventions of CTS?
S +S
Paresthesia and pain in median nerve distribution
Worse with sustained or repetitive wrist movements
Nocturnal numbness and pain
Relieved by “flicking”
Weakness and clumsiness in hand - decrease grip strength and frequently dropping objects
Severe - atrophy and thenar eminence and lumbricals 1 and 2
Special tests
Tinel’s test
Phalen’s test - reverse prayer
Reverse Phalen’s - Prayer
Carpal compression test
Resisted APB - only one exclusively innervation by median nerve
ULTT median nerve
Nerve conduction velocity test
Electromyography (EMG)
Interventions
Activity modification
Splinting in neutral
Mobility techniques
Nerve mobilization
Tendon gliding exercises
Joint mobilization
Improve muscle performance (no symptoms)
Gentle multi-angle muscle setting
Progress to resistance and endurance
Fine-finger dexterity
Medial - NSAIDs, corticosteroids, carpal tunnel release surgery
What is the post-operative management for CTS?
Post-operative management
Immobilized 7-10 days in slight extension
Splint removed during surgery
cannot do active flexion past neutral or use finger flexors with wrist flexion for first 10 days
Pillar pain = pain in thenar and hypothenar eminences
Max protection
Patient education
Wound management
Control of edema
Control of pain
Active tendon/nerve gliding
Upper extremity exercises
Finger and thumb movements
Wrist extension
Active radial and ulnar deviation
Pronation and supination
Elbow and shoulder movements
Moderate and minimum
Suture removed post op 10-12
Return to full activity by 6 - 12 weeks
Residual impairments
-Weakness
-Sensory deficits
-Persistent edema
-Limited ROM
-Hypersensitivity
-Pain
Scar tissue mobilisation
Progressive stretching / joint mobilisation
Progressive strengthening
-Isometrics - 4 weeks
-Grip and pinch - 6 weeks
Dexterity exercises
Sensory reeducation
What is double crush syndrome?
Nerve compression in more than one place for same nerve
Proximal compression increases vulnerability at distal point
What is ulnar tunnel syndrome? Including etiology, S + S , special tests
Compression of ulnar nerve as it passes through Guyon’s canal - between pisiform and hook and hamate
Etiology
Trauma - FOOSH with or without hamate fracture
Chronic pressure
Space occupying lesion
Extended use of crutches
Higher risk of cyclist, baseball catches, karate players and use of jack hammers
S +S
Pain and paresthesia in ulnar nerve distribution
Motor weakness of muscles innervated by ulnar nerve
Decreased grip strength
Fatigue with repetitive or sustained activities
Severe - claw hand and atrophy of hypothenar eminence
Special tests
Froment’s sign - pinch paper and pull away - need to use adductor pollicus and if not then go in to thumb flexion instead
Guyon canal compression test
Tinel’s test over guyon’s canal
ULTT ulnar nerve
Nerve conduction velocity test
Interventions
Activity modification
Cock up splint - into extension
Ergonomic and padded equipment
Frequent changes of hand positions
Nerve mobilization
Medical - NSAIDs, corticosteroid injections, guyon’s canal release
What is gamekeeper’s thumb? Including etiology, S + S, special tests and interventions
Sprain of ulnar collateral ligament - occurs with valgus force of MCL joint (seen in gamekeepers, skiers, volleyball players)
S +S
Pain and tenderness at base of thumb on ulnar side of MCP
Pain with movement - worse with abduction and extension
Decreased pinch and grip
Swelling and dislocation at base of thumb
Special test
Thumb UCL laxity or instability test- valgus stress test
Interventions
Acitvity modification
Splint MCL in slight flexion
Gentle ROM as tolerated
Strengthening
Medical - surgical repair - complete or displaced avulsion fracture
What is thumb CMC OA? Including etiology, S + S, special tests, interventions
CMC OA - common
Etiology
Repetitive movement
Joint injury
F>M, advanced age
S + S
Pain at base of thumb
Worse at night, changes in weather and with overuse
Tenderness at CMC
Decreased pinch and grip strength
Muscle wasting at thenar eminence (disuse)
Possible instability (sublux or dislocation)
Lead to hyperextension deformity of MCP
Special tests
Grind test - compression with rotation
Interventions
Activity modification
Splinting
Larger grip handles
AROM within limits
Strengthening
Medical - NSAIDs, corticosteroids, 1st CMC arthroplasty (replaced trapezium with something else / arthrodesis (fuse bones)
What are the finger deformities?
Dupuytren’s contracture - of palmar fascia
Fixed in flexion of MCP and PIP, usually D4 and D5
Skin is adherent to the fascia
Splint in extension after release
Trigger finger
Thickening of flexor tendon sheath (Notta’s nodule)
Tendon sticking, catching or locking when flexing
More common D3-D4
Associated with RA
Mallet finger
Flexion of DIP at rest
Rupture or avulsion of extensor tendon at insertion in distal phalanx
Splint DIP for 6-8 weeks
Bouchard nodes
OA enlargement of PIP on dorsal
Heberden nodes
OA enlargement of DIP on dorsal
Swan neck deformity (RA)
Boutonniere deformity (RA)
Ulnar drift (RA)
What is the cutaneous innervations of upper extremity?
See image
What is the applied anatomy for the hip joint?
Acetabulum
-Ischium
-Ilium
-Pubis
Femur
Labrum - suction, and capsule also help support
Hard to dislocate unless deformity, extreme force or poor stability from passive and active structures
Ligaments (*strong)
-Ischiofemoral
-Iliofemoral
-Pubofemoral
-Ligamentum teres
Describe the angle of inclination in the frontal and transverse plane and the resulting impacts
Frontal plane
-Normal: 120-135
-Coxa valgus - >135
—Creates varus at the knees
-Coxa vara- <120
—Creates valgus at the knees
Transverse plane
-Anteverted - femoral moved anteriorly, creates internal rotation force at foot
—Associated with W sitting - already in the position, greater BoS
-Retroverted - femoral head moves posteriorly, creates external force at foot
-*doesn’t mean someone has pain, just different body mechanics acting on joint - might need to have variations in how they do things
What is OA of the hip? Including etiolgy and risk factors (modifiable and non-modifiable)
Degeneration of articular cartilage and subchondral bone = narrow joint space, bone on bone (no articular cartilage) and osteophyte formation
Etiology
Unknown
Risk factors
Non- Modifiable
-Age
-Genetics
-Gender (F>M)
-Congenital malformation
Modifiable
-Obesity
-Abnormal repetitive stress
-Trauma
-Joint mechanics (may or may not be able to modify)
What are the S + S of hip OA? What are the special tests?
S + S
Pain around hip, groin, glutes, thigh, back or knee
Pain with weight bearing
Decrease pain in loose packed position (30 flexion, 30 abduction, slight ER)
Stiffness
Firm capsular end feel, limited ROM
Capsular pattern - flexion, abduction, IR
Initially lose IR, then hip is fixed in adduction (no abduction), no IR or extension past neural and limitation in hip flexion to 90
Decrease muscle stretch
Limited functional abilities (PROGRESS to this)
STS
Walking on uneven surfaces
Difficulty with ADLs
Decrease walking distance
Decrease time in standing
Special tests
1. Scour - in to flexion and adduction
May also be iliopsoas, pectineus, TFL, sartorius pain as well if +ve
2. FABER or Patrick’s
Decrease ROM, knee isn’t parallel or lower = hip pathology, SIJ, iliopsoas spasm
3. Hip quadrant - flexion adduction without scouring
+ve if pain
What are the interventions for hip OA?
Education
-Safe ambulation
-Minimize aggravating activities
Decrease pain
-Grade I or II mobilizations
-Assistive device for ambulation
-LLD - shoe lifts
-Modify chairs and commodes
-Modalities
Increase ROM
-ROM exercises
-Grade III or IV mobilizations
-Stretching if chronic
Strengthening
-OKC first then progress to CKC
-Hip strengthening as tolerated
What is a total hip arthroplasty and what are the indications? What is the rehab pre-operatively?
Replacement of the femoral head and acetabulum
Indications
Severe hip pain, loss of function, decrease QoL associated with OA, RA, AS, avascular necrosis with failure of conservative treatment
Nonunion fracture, instability or deformity of hip
Bone tumours
Failure of previous joint reconstruction surgery
Preoperatively
Examine patient’s status
Education - operative procedures, post-operative precautions and rationale
Functional training for early post-op days and exercises
Criteria for discharge
What are the types of THA surgical approaches? What are the muscles incised or not and the benefits/disadvantages of each?
Posterior / posterolateral
Keep - Glute med and TFL
Cut - Glute max and tendon, posterior capsule, small ER and piriformis, interval between glute max and medius
Good for gait, bad for dislocation and subluxation in post-op
Lateral
Keep - NOTHING
Cut - glute med, min, TFL, vastus lateralis, capsulotomy
Bad recovery in gait and weakness of hip abductors, possible pelvic obliquity
Anterior
Keep - ALL
Cut - (move sartorius and rectus femoris out of way), anterior capsulotomy
WBAT immediately, good recovery, good gait
What are the complications for a THA?
Intra-operatively
Malpositioning
Femoral fracture
Nerve injury
Peroneal division of sciatic - most common = drop foot
Also superior gluteal or obturator or femoral nerve
LLD - either prosthesis not in place or dislocated
Early post- op
DVT
Infection
Wound healing problems
Pneumonia - HAP, immunity decreased
Dislocation of prosthetic joint
Late post - op
Prosthesis doesn’t fit - mechanical loosening, atraumatic wearing out
What are the post-op precautions for THA?
Posterior / posterolateral
No flexion past 90 degrees
-Pay attention for STS
No internal rotation past neutral
-Pay attention for pivoting when walking - turn towards the sounds leg
No adduction past neutral
-Pay attention for transfer
Anterior/anterolateral and direct lateral
No flexion past 90 degrees
No adduction past neutral
No external rotation
No hip extension
No hip abduction (resisted or antigravity) if muscles cut 6 - 8 weeks
No combined movements of FABER
less precautions that are more natural so that is why better for patient’s with dementia
What are the interventions after THA?
Max
Prevent complications
Ankle pumps, deep breathing and secretion clearance
Reduce risk of complications education (precautions, safe bed mobility, transfers, S + S of infection)
Prevent muscle atrophy
Isometric quads, hip extensors and hip abductors (if not cut)
Regain active mobility and control
AAROM / AROM in ranges
CKC weight shift, balance, heel raises, mini squats
Achieve independent functional mobility
Bed mobility
STS
Transfer training
Ambulation with assistive device
Stairs training
Moderate
Continue
Minimal
Continue - resume return to spots - avoid high intensity/ impact sports with slippery surfaces
What are hip fractures? Including etiology
Fracture of the hip - majority in elderly women (>75 years old)
Extracapsular
Intracapsular
-Risk of avascular necrosis
-Not congruent - wears out acetabulum
-Delayed healing
-Non-union
Etiology
Falls
Decreased walking speed and balance- more likely to fall sideways on the hip
Decreased muscle strength and flexibility
Poor vision
Cognitive decline
Medications
Osteoporosis
Sudden twisting motion of LE
What are the S + S for hip fractures and the interventions
S + S
Pain in groin or hip
AROM or PROM of hip
Pain with LE weight bearing
LLD
LE assumed ER and abduction position
Intervention
Surgery
ORIF - younger people
Hemiarthroplasty - just femur and if acetabulum in good shape
THA
What is the post-operative rehab for hip fracture
Minimize adverse effects of bed rest
-Bed mobility, transfers, ambulative with assistive device (walker), deep breathing and coughing, LE edema control
Exercise program - ROM, strengthening, balance
What are the S + S of failure of internal fixation for hip fracture?
Severe pain increasing with weight bearing or hip movement
Shortening that was not immediately present
Positive trendelenburg on involved side that doesn’t resolve
Damage to superior gluteal nerve
Lurching gait - getting CoG over stance leg
Persistent external rotation
What are common neuropathies in LE?
Sciatic
Entrapped from piriformis
Obturator
Uterine pressure and damage during labour
Femoral
Fracture of upper femur or pelvis, reduction of congenital dislocation or pressure during a forceps labor and delivery
What are hip muscle imbalance test?
Modified thomas test
Iliopsoas or rectus femoris - hip stays flexed, bent knee and if continues then rectus femoris
TFL and sartorius - if abducted - if in external rotation - sartorius, if internal - TFL
Ely’s test
Prone, flex knee - if hip flexes = rectus femoris tightness
Ober’s test
Tight ITB
Piriformis test
Sidelying, forward flex (60-90) and adduct the hip
90/90 SLR
More accurate than just SLR (isolating hamstrings)
In reverse table top and straight the leg
What is developmental hip dysplasia? Including etiology, S + S
General instability resulting in increased risk of hip fractures, common in infants (F>M)
Etiology
Genetics
F>M - gender
First born
Breech birth
Narrow uterus
Tight swaddling
Signs and symptoms
Asymmetry (if unilateral)
-LLD or gluteal folds
Hip abduction limitations
Hip clicks
*diagnosis through US, not XRAY
What is the screening for hip dysplasia?
Barlow’s maneouver
Hip adduction with a posterior force - +ve if sublux or dislocation
Ortolani maneouver
Hip flexed to 90 then abduction with anterior force - +ve if click when hip reduces
What are the intervention for developmental hip dysplasia?
Pavlik’s harness - in flexion and abduction (*avoid extension and adduction)
Hip spica - if severe instability or above doesn’t work - more fixed
Closed reduction - if didn’t catch it soon enough
Open reduction - if tissue is stopping it
What is Legg-Calve Perthes Disease? Including etiology, S + S and interventions
Avascular necrosis of femoral head due to interruption of blood supply (etiology unknown but risks factors - trauma, infection, family Hx, low birth weight)
Children 2-15 (common 4-8)
S + S
Limp of insidious onset
+ve trendelenberg
Pain aggravated by activity and relieved by rest
Pain in hip which may refer to anteromedial thigh or knee
Decreased hip ROM (especially abduction, internal rotation)
*XRAY - flattened femoral head, if not - MRI or bone scan
Interventions
Petrie’s cast - in abduction
Low impact, strengthening, ROM, reduction of weight bearing if pain is severe, hemiarthroplasty
heals fairly well since young
What is the slipped capital femoral epiphysis? Including etiology, S +S, interventions
Fracture through growth plate (physis) causing slippage of end of femur (metaphysis)
Shaft moves anterior (and external rotated), head moves posterior
Seen in adolescent M>F
Etiology
Obesity
Family history
Endocrine disorders
S + S
Pain in hip or anterior thigh
Pain with activity
ROM limitations - flexion, abduction, IR
Limp present
Interventions - surgery - same rehab as ORIF
Get screw through but don’t change the femoral head cause more risk for avascular necrosis
Describe the meniscus including blood supply, shape, ligaments, movement during movement (i.e., flexion), what is attached to them? What is their role?
Medial (C-shaped - thicker anterior / posterior) and lateral (O-shaped) meniscus
-Thicker on peripheries
-Vascular on lateral ⅓ - easier to heal, avascular on inner 2/3s - harder to heal, get surgery
-Attach to tibia by coronary ligament and to each other by transverse ligament
During flexion, the meniscus both move posterior but the lateral meniscus moves more (10mm) the medial moves less (2mm) making the lateral one less prone to injury
-Lateral meniscus is less prone to injury because ot this and because it is attached to less structures
Lateral meniscus - attaches to PCL and tendon of popliteus through capsular connections
Medial meniscus - attached to ACL, MCL (terrible triad), PCL, semimembranosus
-Because of semimem - if eccentric contraction can disrupt the meniscus
Roles
-Increase congruency
-Shock absorber
-Lubrication and nutrition of joint
-Improve weight distribution
-Reduce friction
-Aid ligaments and capsule preventing hyperextension
What is a meniscal tear? Including etiology, S + S and types
Typically occurs in vascular region
Etiology
Occurs with shearing / twisting forces
Compression with hyperflexion (>90 degrees) common MOI
Early flexion = anterior, deep flexion = posterior
Internal rotation = lateral, external rotation = medial
Also think of femur - if internal rotation when cutting = external rotation of tibia so medial meniscus tear
S + S
Swelling, joint line tenderness
“Locking” if bucket handle tear, need an external force to unlock it
This and osteocondritis dyskinesis - bones get caught
Clicking noise with movement
Knee “gives way” - because of swelling - quads because inhibited
Loss of ROM
“Springy block” - bucket handle tear instead of soft tissue approximation
Types of meniscal tears
Posterior tear
-Most common - hyperflexion and compression
Transverse tear
-Common in lateral meniscus, and associated with ACL injuries
Longitudinal tear
Bucket handle tear
-Longitudinal tear but a inner edge flips up getting caught in intercondylar notch
-Medial meniscus tear - associated with ACL injuries
-refer to surgery
What are the special tests and interventions for menisical tears?
Special tests
Mcmurrys - deep flexion with external (medial) or internal (lateral) rotation into extension - can also add a varus/valgus force
Apley’s - compression/ distraction in prone
Thessalys - twist in SLS
Bounce home test - extension and test end feel
Interventions
Physio - decrease swelling, increase ROM, strengthening
Medical
Meniscal repair
-WBAT in extension
->90 flexion in 4-6 weeks
-WB in flexion >90 3-4 months
-No pivoting or cutting 3-4 months
Partial or total meniscectomy
-Recovering easier - RTW in 5-7-days, sport in 3-6 weeks
-Focus on decrease swelling, improve ROM and gait
-More prone to OA - redistribute load
What are the grades of ligament sprains for knee complex?
Grade I - stretching ligament with minimal disruption of fibers
Grade II - tearing 50% of ligament fibers; small hematoma; hemarthrosis may be present
Grade III - complete tear and separation of ends, hematoma and hemarthrosis
-Hemarthrosis - more likely in those with hemophilia and on anticoagulants (get greater ROM limitation, increased warmth/bruising
What is an ACL? What is an ACL tear? Including etiology and S+S
Runs back, up and lateral (BUL) - from medial tibial condyle to lateral femoral condyle
Two bands
Anterior medial - taut in flexion - more tested with anterior drawer
Posterolateral - taut in extension - more tested with lachman’s
Resists anterior drawer, medial rotation of tibia and valgus/varus on tibia
Epidemiology - F>M - hormones and q-angle
Etiology
Excessive anterior translation of tibia
Contact
-A valgus force from lateral side of knee
-Terrible triad - ACL,MCL,medial meniscus
Non-contact
-Pivoting or cutting - ER of tibia, or internal rotation of tibia or femur with planter foot
-Rapid deceleration - because quads working eccentric - pull tibia forward
-Forceful hyperextension - cause of contraction of quads
S + S
Hear audible pop or snap, tearing sensation
Pain
Contrast, throbbing, aching
Increased with movement or weight bearing
Hemarthrosis
Joint effusion
Knee “giving out” or feelings of instability - because of swelling inhibiting quads or because of actual instability
Limited ROM
What are the ACL special tests and interventions?
Special tests
Anterior drawer
-More in flexion
-Check for muscle guarding from hamstrings that won’t let you pull it forward
-Check for PCL tear as might feel like excessive motion but is because just sitting more posterior
-Posterior sag sign or Godfrey’s (that is at 90-90)
Lachman’s
-More in flexion
Pivot - shift
-In flexion when supine, anterior force on the calf then in to extension - about 20-30 degrees of flexion the ITB will kick in and pull the tibia and you can see the reduction
Interventions
Strengthening (CKC because OKC)
Decrease pain/ swelling
Bracing
Crutches if necessary
Proprioception
Restore ROM
Surgical - ACL graft
Autograft - you are donor
-Gracilis / semitendinosus
—Don’t use semimembranosus because of the attachment to the medial meniscus
—Issues with strengthening of hamstrings - is a dynamic stabilizes so prevents the tibia from going anteriorly - prone to more tears
-Patellar tendon graft
—-Harder to strengthening quads - more at risks for PFPS
Allograft - other donor
What is the applied anatomy for the knee joint?
Tibiofemoral joint
-Meniscus
-Cruciate ligaments - support anterior/posterior direction
-Collateral ligaments - supports medial/ lateral direction
Patellofemoral joint
Superior tibiofibular joint
What is a PCL? What is a PCL tear? Including etiology and S + S?
Goes from tibial lateral plateau to the medial femoral condyle
Resists posterior translation, medial rotation of tibia and valgus/varus force on tibia
Stronger and thicker than ACL - less likely to tear
Etiology
Posterior translation of tibia on femur (typically knee flexion)
Dashboard injury
Fall on knees in hyperflexion
Sudden forceful hyperflexion or hyperextension
S + S
Pain
Contrast, throbbing, aching
Increased with movement, especially kneeling or stairs
Hemarthrosis
Joint effusion
Limited ROM in acute stage
Increased passive extension ROM
Genu recurvatum (knees hyperextended on observation)
Have functional instability - so less likely to come to clinic cause don’t notice it as much
What are PCL special tests and interventions?
Special tests
Posterior drawer
Posterior sag sign
Godfrey test
Interventions
Strengthening
Decrease pain/ swelling
Bracing
Proprioception
Restore ROM
Surgical - ACL graft
Autograft - you are donor
Gracilis / semitendinosus
Patellar tendon graft
Allograft - Achilles tendon
What is a MCL? What is an MCL tear including etiology and S + S?
Two layers - superficial (just attaches to capsule) and deep (attaches to capsule and medial meniscus)
Restrains valgus, lateral rotation of tibia and anterior/posterior tibial translation
All fibers taut in extension
-Anterior - more taut in flexion
-Posterior - more taut mid range
Etiology
Valgus force (with or without compression)
S + S
Pain
Contrast, throbbing, aching
Increased with movement, especially kneeling or stairs
Joint effusion
Pay report knee “giving out” or feelings of instability
Limited ROM
What is a MCL special test and intervention?
Special tests
Valgus stress test - if full extension = capsule, so want 20-30 degrees of flexion
Interventions
Strengthening
Decrease pain/ swelling
Bracing - not in full extension due to MCL taut
Proprioception
Restore ROM
Surgical - not usually done, because of attachment to capsule - has good blood supply and therefore can heal conservatively
What is a LCL? What is a LCL tear including etiology and S + S
Round, cord like - lateral epicondyle of femur to fibular head
Restrains valgus, lateral rotation of tibia and anterior/posterior tibial translation
All fibers taut in extension, lose in 30 degrees flexion (so when testing don’t go past this)
Can feel in figure 4 position
Etiology
Varus force (with or without rotation)
S + S
Pain
Contrast, throbbing, aching
Increased with movement, especially kneeling or stairs
Joint effusion
Pay report knee “giving out” or feelings of instability
Limited ROM
What are the special tests and interventions for a LCL?
Special tests
Varus stress test
When doing this compress medial side - so pain there might be a meniscus injury
Interventions
Strengthening
Decrease pain/ swelling
Bracing - not in full extension due to MCL taut
Proprioception
Restore ROM
Surgical - not usually done
What is knee OA including etiology (modifiable and non-modifiable), S +S and imaging findings
Degeneration of articular cartilage and subchondral bone leading to joint space narrowing, rubbing of bone on bone leading to osteophyte formation
Etiology
Non-modifiable
-Age
-Gender (F>M) - hormonal, weight distribution, body shape (q-angle)
-Genetics
-Congenital malformation
Modifiable
-Obesity
-High impact activities
-Inactivity
-Muscle weakness - rely on passive structures
-Trauma
-Decreased proprioception - not optimal loading
-Joint mechanics (may or may not be able to modify)
S + S
Insidious onset
Morning stiffness (<30 mins) - if >1 hour it is more likely inflammatory (RA)
Pain with activity - worse with weight bearing, squatting, stairs, static postures, rissing after sitting, excessive activity (e.g., walking), fall in barometric pressure
Joint line tenderness
Decreased ROM / strength / function
Bony enlargement
Crepitus
Muscle atrophy, swelling, warm knee, feelings instability (decrease joint space = ligaments lax or quad inhibition), genu varum or valgum
Imaging
Decreased joint space
Osteophyte formation
What are the interventions for knee OA, including surgical
Interventions
Muscle strengthening
Low impact exercises
Decrease pain and swelling
Increase ROM (continuous passive motion machine - post -op)
Improve function
Assistive device for ambulation if needed
Bracing if needed (unloader)
Weight loss
Surgical
Aspiration
Injections - hyaluronic acid (component of synovial fluid), corticosteroids
Arthroscopic debridement
Proximal tibial osteotomy (closing wedge varus - take out piece, opening wedge valgus - put in piece)
Partial (hemi) knee replacement - unicompartmental OA
TKR - 90 degrees required by 6 weeks or manipulation under anesthetic required
What is PFPS? Including epidemiology?
Diffuse pain around knee cap from abnormal patellar tracking causing increased contact pressure on posterior surface of patella against the femur
Diagnosis made on history and physical exam
Chondromalacia patella - progression - degeneration of patella articular cartilage
Epidemiology - F>M
What is the etiology of PFPS?
Extrinsic - sudden or drastic changes in training regime
Intrinsic - abnormal patellar tracking (normally 60-90 degrees most contact, at 20- contact at apex, 90- contact at base, odd facet - side of patella - likely irritated and painful)
Increased Q angle
Measured from ASIS to mid patella, and mid patella to tibial tubercle
Angle of quad muscles and patellar tendon - represents angle of force of the quads
If increase in q-angle = larger bias to lateral quads = patella tracks more lateral
Q- angle in females 15-18, males 12-15
Q-angle <12: patella alta (high sitting patella)
Q-angle >18: patella baja (low sitting patella), genu valgum, subluxing patella - since pull patella laterally out of trochlea, PFPS
Muscle and fascial tightness
ITB tightness - lateral tracking
Patella retinaculum tightness (especially laterally)
Ankle PF tight (tight calves) → decrease ankle DF, subtalar pronation (not proper push offs), increased tibial IR (tibial torsion) - changes q-angle since tibial tubercle has changes, changes pull of quads
Hip muscle weakness
Weakness in hip abductors and ERs may results in adduction of the femur and valgus at the knee and possibly IR of femur
Glute med weakness = TFL compensation and overuse = increase femoral internal rotation
Glute med - abduction, external rotation and extension
TFL - abduction, internal rotation and flexion
*changes q-angle, TFL pulls it in to internal rotation or makes ITB more taut - patella track in different way
VMO insufficiency
Disuse or inhibition (because of joint swelling and pain)
Weakness or poor timing of VMO = lateral drifting of patella
Lax medial retinaculum
What are the S + S, special tests and interventions for PFPS?
S + S
Insidious onset (can be traumatic too)
Anterior knee pain
Pain with activities - prolonged knee flexion (theater/movie sign), loaded knee flexion/extension
“Buckle” or “give way” - inhibited quads
Crepitus
PF joint pain, swelling and tenderness - common in retropatellar area
Special tests
Clarke’s sign (patellar grind test) - proximal patella with webspace - contract quads
McConnels tests - resisted isometrics in 30,60,90 - if pain, add medial glide - if goes away = PFPS
Step - up test
Eccentric step test (step-down test)
See if goes in to dynamic valgus
Special tests for swelling
Brush tests
Patellar tap test
Interventions
Reduce activity involving high or prolonged loads
Bracing or taping to prevent/limit lateral tracking
Lateral retinaculum stretch
VMO training
Glute medius strengthening
Arch support and foot intrinsic training
Treat underlying cause(S)
Surgical - lateral retinacular release (poor outcomes), Fulkerson’s procedure (distal realignment - changing tibial tubercle to decrease q-angle-change pull of quads)
What is infrapatellar fat pad syndrome? Including etiology, S + S, special tests, interventions
Impingement of infrapatellar fat pad (Hoffa’s pad) from patella - occurs at 20 degrees knee flexion
Etiology
Patella alta
-High sitting patella - apex touching fat pad at joint line
Genu recurvatum
-Hyperextended, go into inferior patellar tilt, apex tilts backwards into joint to cause irritation
Inferior patellar tilt
-See above
Anterior pelvic tilt
-More likely to go into hyperextension - see above
Knee hyperextension injury (sudden onset)
-Irritation
S + S
Anterior inferior knee pain
Pain with extension activities (difficult from PFPS - since hurts with flexion), prolonged standing, stairs
Tenderness on Hoffa’s fat pad - joint line near outside of patella
Puffy appearance below patella
“Camel sign” - two humps (patella and inflamed bursa)
Special tests
Hoffa’s Test - palpate then go from flexion to extension - fat pad goes anterior - compressed into fingers (20 degrees knee flexion)
Interventions
Decrease inflammation
Decrease aggravating activities
Taping (tape base to tilt inferior apex of the patella off fat pad)
Address muscle imbalances
Surgical - partial or full removal of fat pad
What is plica syndrome? Including S + S, special tests and interventions
Irritation to the plica (commonly medial plica) that causes inflammation of synovial sack where the area of the plica becomes thicker - this may catch between patella and femur causing further irritation and inflammation
Plica - fold of synovial membrane - embryological remnant
S + S
Intermittent anteromedial knee pain
Pain with prolonged standing, squatting, sitting, stairs
Tenderness on plica - medial side
Audible clicking or snapping
Knee may give way, present with pseudo-locking (not real, just catching), catching
Special tests
Hughston’s plica test
Mediopatellar plica test
Patellar bowstring test
Interventions
Decrease inflammation
Decrease aggravating activities
Taping to offload plica
Address muscle imbalance and possible patellar tracking
Surgical - partial or full removal of plica
What is patellar subluxation / dislocation? Including etiology, S + S, special tests, interventions
Sublux - partially out, dislocation - completely out (lateral more common)
Etiology
Decelerated lateral cut- eccentric quads with planted foot = hip internally rotated, foot externally rotated - quads pull patella laterally and over the lateral femoral condyle
Increased likelihood of dislocation with decelerated lateral cut and external valgus force
Increased likelihood
-Shallow groove
-Patella alta
-Increased q - angle
-Foot pronation
Post TKR
Previous subluxation
S + S
Audible popping noise
Severe pain and immediate swelling
Apprehension
Knee extension relocates typically and reduces pain
Knee not feeling secure and slips out of place
Hypermobile patella
Tenderness on medial border
Special tests
Fairbank’s apprehension test - lateral glide, patient shows apprehension
Interventions
Early:
Immobilization (zimmer splints) - 3-6 weeks
Decrease inflammation
Crutches until full extension can be obtained
Normalize gait
Isometrics and ROM exercises - OKC not CKC
Later:
Progress to CKC - emphasis on VMO and gluteus medius
Patellar bracing
Surgical - medial retinaculum tightening, lateral retinaculum release, Fulkerson’s procedure
What is patellar tendinosis? What is the etiology, S + S, interventions
Degenerative injury to patellar tendon causing pain in infrapatellar region of knee - NOT inflammatory
Etiology
Jumping sports and activities
Repetitive overloading - typically eccentric quads
Increased risk in those with patella alta
S + S
Pain with quadriceps contraction
Worse with jumping, squatting, resisted knee extension
Decrease pain with compression over patellar tendon
TOP
Localized swelling, quadricep weakness
Interventions
Manage pain and swelling
Patellar tendon strap - force going through wider surface
Avoid overloading quadriceps
Progressive loading → return to activity
Eccentric quadricep contraction - realign collagen
What is osgood schlatters disease? Including etiology, S + S, interventions
Traction apophysitis of tibial tuberosity
Apophysis - bony tubercle arising as a result of secondary ossification
Apophysitis - inflammation /irritation of apophysis
*also sinding - larsen johansson - same but the inferior pole of patella
Overuse injury in growing adolescents - M>F
Etiology
Repeated tension on growth plate of tibia
Growth spurt - bones grow fast then muscles, so muscles traction
Increase incidence in sports with running and jumping (quad contraction)
S + S
Pain with quad contraction over tibial tuberosity
Worse with quad activation
Decrease with compression over patellar tendon
Pai with pressure of tibial tubercle (kneeling)
Increased prominence of tibial tubercle (remains in adulthood)
Interventions
Manage pain and swelling
Decrease parameters of aggravating activity
Patellar tendon strap
What is iliotibial band friction syndrome? Including etiology, S + S, special tests, interventions
Lateral knee pain - from irritation of structures from repeated knee flexion / extension - ITB frictions over lateral epicondyle
ITB goes over lateral femoral epicondyle around 30 degrees
Brought on by inflammation of ITB and underlying bursa
Etiology
Repetitive knee flexion / extension - e.g., sports like running/cycling
Rapid increase in training volume
Precipitating factors
TFL/ITB tightness
-Weak gluteus medius → TFL overactivity
Genu varum
-Increase distance of ITB
Tibial IR (increase tension for ITB)
-Further from gurdy’s tubercle (insertion)
S + S
Lateral knee pain
Increase pain with repetitive knee flexion / extension
Pain decreases with rest
Special tests
Noble compression test - compress lateral with extension, Pain at 30 degrees = +ve
Obers test
Thomas Test - test for ITB
Interventions
Decrease pain
Avoid aggravating activity
TFL/ITB stretches / ST
What is knee bursitis? Including etiology, S + S, common areas, interventions
Fluid filled sac providing cushion, has synovial fluid reduces friction
Etiology
Trauma
Sustained pressure
Overuse and chronic friction
Inflammatory conditions
Infections
S + S
Joint stiffness
Decreased ROM
Warmth
Pain with movement and pressure
May present as visible bump
*infection S + S - fever, red, warm, swollen
Common
Pes anserine - between sartorius, gracilis, semitendinosis
Prepatellar
Superficial infrapatellar
Deep infrapatellar
Interventions
Manage pain and inflammation
Avoid aggravating activities
Stretching / ST mobilization putting pressure on bursa
Surgical - aspiration corticosteroid injection, bursectomy
What is Baker’s cyst? Including etiology
Excess fluid behind knee (between semimem and medial gastroc) which can rupture and produce pain and swelling in calf
Etiology
Intra-articular knee pathology, increases synovial fluid in knee which spills in to bursa
May occur in children idiopathically
S + S
Swelling in popliteal fossa
Visible lump
Joint stiffness
Decreased ROM
Warmth
Pain - worse with movement, knee extension and standing
Interventions
Manage pain and inflammation
Avoid aggravating activities
Compression sleeve
Self limiting - will resolve on own
Surgical - aspiration, corticosteroid injection, excision of cyst, arthroscopy and debridement of articular pathology
What is osteochondritis dissecans?
Cracks from articular cartilage and subchondral bone due to avascular necrosis
Patella or femoral trochlea
Pain, swelling, crepitus
May cause catching and locking if caught
Worse with squatting, walking, descending stairs
What is myositis ossificans?
Formation of bone instead muscle-tendon unit, capsule, ligamentous structure
Calcification may occur following injury (i.e.,. Bruising forms to bone)
Commonly quads (also brachialis)
MASSAGE, PASSIVE STRETCHING AND RESISTED EXERCISE IS C/I*
What is the applied anatomy for the lower leg and ankle complex?
Inferior tib fib
-AITFL, PITFL, interosseous, inferior transverse
Talocrural
-Lateral - ATFL, PTFL, CFL
-Medial - deltoid
Subtalar
-Medial / lateral talocalcaneal ligament
What is a lateral ankle sprain? Including etiology, S + S, special tests and interventions
Inversion sprain - tearing ligaments on the lateral aspect of ankle (ATFL, CFL, PTFL)
Etiology
Traumatic - PF and inversion
Landing on uneven surface, running on uneven ground
Increased incidence with weak peroneal or ankle instability
PF and inversion (ATFL), neutral inversion (CFL), DF and inversion (PTFL)
S + S
Acute onset
swelling/inflammation - warmth, bruising
Lateral ankle pain - worse with inversion and weightbearing
Antalgic gait
TOP
Instability
Decreased proprioception
Special tests
Anterior drawer test
Talar tilt
Other - ankle lunge test (KTW), proprioception, strength
Interventions
Manage pain and swelling
Bracing / taping
Crutches
Strengthening
Proprioception
Restore ROM - mobilizations, AROM, PROM
Cross friction massage
Describe the west point ankle sprain grading
See chart in book
What is a medial ankle sprain? Including etiology, S + S, special tests and interventions
Eversion sprain - tearing ligaments on the medial aspect of ankle (anterior tibiotalar, posterior tibiotalar, tibiocalcaneal, tibionavicular
Due to strength of deltoid - associated with avulsion fracture
Les common due to fibular blocking movement, strength of medial ligaments
Etiology
Traumatic
Eversion
Jumping and landing on uneven surface
Running and cutting
S + S
Acute onset
swelling/inflammation - warmth, bruising
Medial ankle pain - worse with eversion and weight bearing
Antalgic gait
TOP
Decreased proprioception
Special tests
Anterior drawer test
Talar tilt
External rotation stress test (Kleiger) - for high ankle sprains but if feel pain on medial side - splaying of the mortise
Other - ankle lunge test (KTW), proprioception, strength
Interventions
Manage pain and swelling
Bracing / taping
Crutches
Strengthening
Proprioception
Restore ROM - mobilizations, AROM, PROM
Cross friction massage
What is a high ankle sprain? Including etiology, S + S, special tests and interventions
Tearing of syndesmotic ligaments connecting tib-fib (inferior transverse, AITFL, PITFL, interosseous membrane / ligament)
Associated with deltoid ligament injuries or fracture of the fibula/ medial malleolus
Etiology
Traumatic
External rotation
Hyper-DF
S + S
Acute onset
swelling/inflammation - warmth, bruising
Anterior ankle pain - worse with external rotation and weight bearing
Antalgic gait
TOP over syndesmosis and interosseous membrane
Decreased proprioception
May present with widening of mortis on imaging
Special tests
External rotation stress test (Kleiger) - for high ankle sprains - splaying of the mortise since wider anterior
Squeeze test - pain, in weightbearing and do this adds stability and may get increased DF
Other - ankle lunge test (KTW), proprioception, strength
Interventions
Manage pain and swelling
Bracing / taping
Crutches
Strengthening
Proprioception
Restore ROM - mobilizations, AROM, PROM
Cross friction massage
What are the ottawa ankle rules?
Ottawa ankle rules - referred for radiographic imaging
Bony tenderness along 6cm of posterior edge of lateral malleolus
Bony tenderness along 6 cm posterior edge of medial malleolus
Bony tenderness at base of 5th MT (from peroneal brevis maybe)
Bony tenderness of navicular
Inability to weight bear immediately after injury and for 4 steps during initial evaluation
What is an achilles tendinosis? Including etiology, S + S, special tests and interventions
Degenerative changes to achilles tendon - may lead to thickening if chronic
Classification
Insertional - <2cm from calcaneal insertion
Midsubstance - 2-6cm from calcaneal insertion
Etiology
Extrinsic
Sudden and drastic changes in training regime - FOOT WEAR
Intrinsic
Age - reduced ability to recover, natural degeneration
Decreased DF - excess stress on DF
Foot pronation (static or dynamic)
Weight gain
S + S
Insidious onset
Morning stiffness
Decreased ankle DF
Decrease strength in PF
Pain
Increased with active/resisted PF, passive DF or weight bearing
Decrease pain with walking about or applying heat
TOP
Antalgic gait
Thickening of achilles tendon
Retrocalcaneal exostosis
-Excess bone - called pump bump, haglund deformity or achilles heel bone spur
-Can lead to retocalcaneal bursitis
May present with crepitus
Interventions
Avoid aggravating activities
Eccentric exercises for PF (heel drops)
Increasing shoe heel height and progressively decreasing heel height
Stretching of PF
Manage pain
Taping
Night splint
Manage inflammation if paratenonitis or retrocalcaneal bursitis is present
What is an achilles rupture? Including Etiology, S + S, special tests and interventions
Full grade III tear (~2-6cm proximal to calcaneal insertion)
Epidemiology: M>F, athletes in 30s-40s
Etiology
Direct trauma (direct blow / cut)
Rapid and forceful concentric contraction
Eccentric overload
Corticosteroid use - weakens connective tissue - more likely to rupture
S + S
Audible snap / tear
Swelling
Warmth, bruising
Obvious limp - because no PF
Palpable gap
Gross decrease in strength in PF
Present with pain
Special tests
Thompson’s test - squeeze calf, ankle in PF
Interventions
PT (conservative)
-Cast immobilization in max PF (4 weeks) then gradually progress for 4 weeks reduced DF
-Crutches NWB
-Progressive ROM and strengthening exercise following
-Proprioception exercises
-higher risk of re-rupturing
Surgical management
-Rupture repair (suturing)
-Immbolization post-op same as conservative approach - strength and ROM may be difficult to regain
-higher risk of complications but less likely to re-rupture
What is Sever’s disease? Including etiology, S + S, interventions
Traction apophysitis in calcaneal insertion of achilles tendon
Epidemiology - overuse injury in children, ages 7-10
Etiology
Repeated tension on growth plate of calcaneus
Growth spurt - bone growing faster than muscle
Over-pronation - increase stretch of tendon
Increase incidence in sports that involve running / jumping (especially hard surfaces)
S + S
Heel pain (posterior plantar side)
Worse with calf use - walking, running, jumping
May present with antalgic gait
Pain with pressure over medial and lateral calcaneus in area of growth plate
May present with decreased passive DF
ALREADY on stretch and inhibited by pain
Interventions
Manage pain
Decrease parameters of aggravating activity
Foot orthotics
Stretching
Heel lifts - decrease stress of tendon
What are the branches of shin splints?
Umbrella term = pain along medial border of the tibia synonymous with medial tibial stress syndrome (MTSS)
Classification
-Periostitis
-Stress fracture
-Compartment syndrome
please ses chart for comparison
Stress - remains same pain wise
Compartment - as use it, more pain - stops rapidly
Periostitis - initially worse, then better, then worse once stopped
What is periostitis? Including etiology, S +S
Inflammation of the periosteum- surrounds bone - chronic pulling (traction) by the muscles connected with repeated activity
Anterior shin splints
-Overuse of tib ant, EHL, EHL
-Pain over proximal ⅔ of anterolateral aspect of tibia
-Pain with resisted DF and passive PF
Posterior shin splints
-Overuse of tib post
-Pain over the distal ⅓ of posteromedial aspect of tibia
-Pain with acitve supination and with passive DF and eversion
Etiology
Sudden and drastic change in training regime
Over -pronation - tib post on stretch
Muscle dysfunction
Fatigue
Decreased flexibility
S + S
Gradual onset
Diffuse pain - increases with activity, decreases or disappears with warming up and rest
Diffuse TOP
Interventions
Avoid aggravating activities
Manage inflammation and pain
Taping - approximate muscles towards bone
Orthotics
Stretching and ST mobilization
Strengthening (graduated with an eccentric focus)
Walk-run program
Address alignment and biomechanical issues
What is a stress fracture? Including etiology, S +S, special tests and interventions
Overuse injury from repetitive loading leading to microdamage
Etiology
Sudden and drastic change in training regime
Cavus foot - increased arch, not as much shock absorption
Over pronation
Overall limb and foot alignment - overload it
LLD - overloading one side
S + S
Gradual onset
Focal pain - present with activity and rest, remains constant or slightly increases with activity, worse at night, worse with impact activities
TOP
Special tests
Stress fracture test (turning fork vibration) - irritate fracture
Interventions
Initial period of rest
Avoidance of aggravating activities
Crutches if needed
Gradual progressive loading - Wolfe’s law -bone adapts to demand
Walk-run program
get bone scan not an XRAY
What is compartment syndrome? Including etiology, compartments, S + S, interventions
Increase pressure within fascial compartments of LL - decreased BF, decreased tissue perfusion, increase ischemia, pain and permanent damance
Chronic exertional compartment syndrome - increased pressure within fascial compartment due to increased activity (increased muscle pump, increased BF = increased pressure)
Compartments
Anterior
-Muscles - EHL, EDL, tib ant, peroneous tertius
-Nerves - deep peroneal nerve (foot drop = no DF)
-Cutaneous - webbing between 1st and 2nd digit
Lateral
-Muscles - peroneous brevis and longus
-Nerve - superficial peroneal nerve (stuck in inversion since no eversion)
-Cutaneous - dorsum of foot, except webbing of 1st and 2nd digit
Posterior superficial
-Muscles - gastroc, soleus, plantaris
-Nerve - Sural - purely sensory
-Cutaneous -posterior lateral aspect of leg and lateral foot and 5th digit
Posterior deep
-Muscles - tib post, FHL, FDL, popliteus
-Nerve - tibial (does motor of above too)
-Cutaneous - plantar aspect of the foot
Etiology - unknown
S + S
Gradual onset
Diffuse pain - severe cramping, increased with activity, decreased or disappears with rest (significant in minutes)
Severe cramping
Tightness sensation
May present with motor weakness, altered or absent sensation, vascular S + S
Special tests
Compartment pressure (gauge) test - before, after exercise
Pulse palpation
MMT - strength
Sensory testing - peripheral nerve testing - see if alterations
Interventions
PT - rest, ST mobilization
Surgical - interosseous membrane release (fasciotomy)
What is tarsal tunnel syndrome?
Compression of posterior tibial nerve through tarsal tunnel (post to medial malleolus) - created by bone and flexor retinaculum
Contains
-Tib post
-FDL
-Posterior tibial artery and vein
-Tibial nerve
-FHL
-TOM DICK and A VERY NERVOUS HARRY
S + S
Pain and paresthesia
-burning , electric shock nerve pain
-Plantar surface of foot
-Increased with weight bearing, activity
-Decreased with rest
May present with swelling in the feet
Special tests
Tinel’s sign at ankle
What is the cutaneous intervention for the lower extremity?
see picture in book
What is the applied anatomy for the foot complex?
Rearfoot
Talus
Calcaneus
Midfoot
Cuneiform
Cuboid
Navicular
Forefoot
Phalanges
Metatarsals
List common foot deformities
-Club foot
-Pes Cavus
-Pes Planus
-Hallux rigidus
-Hallux valgus
-Claw toe
-Hammer toe
-Mallet toe
Explain the common foot deformities
Club foot
Congenital deformity, etiology unknown - genetics or environment or intrauterine malpositioning
Most common is congenital talipes equinovarus (CTEV)
Congenital - from birth, talipes - foot and ankle, equinovarus - horse like and in varus
Ankle - PF, rearfoot - varus, midfoot - adduction and supination
foot in in PF and turned inwards
Can be rigid (can’t move, complicated surgery) and flexible (can move a lot - serial casting gradually)
During gait walking on edge laterally of foot and the heels are off the ground
Pes cavus
Longitudinal arches are accentuated with abnormally short muscles on the sole of the foot
Leads to rigid foot with poor ability to adapt to stress and absorb shock (similar to stress #/ shin splints, causes plantar fasciitis, heel stress #)
Pes planus
Medial longitudinal arch is reduced
Can cause no other problems
Can lift arch and see if it changes the pain
Hallux rigidus
Extension of great toe is limited due to OA of MTP
Hallux valgus
Great toe deviations medially (along with MT head)
Causes - tight pointed shoes, hereditary factors
Bunion = medial side callus, thickened bursa and exostosis (bone)
Can use toe wedge, change footwear, intrinsic foot exercises, mobilization or get fusion, osteotomy
Claw toe
Hyperextension of MTP and flexion of PIP and DIP
PIP and MTP get callus formation
Hammer toe
Extension of MTP and flexion of PIP (DIP may be flexed, neutral or extended)
Callus at PIP
Mallet toe
Flexion of DIP
Callus at DIP or tip of toe
all three hereditary, poor shoes, muscle imbalance - common in RA
What is plantar fasciitis? Including etiology, S +S, special tests
Overuse injury of plantar fascia leading to pain at medial tubercle of the calcaneus (attachment), and it also attaches at metatarsal heads
During great toe extension (heel/toe off) - plantar fascia tightens to bring bones together to lift the medial longitudinal arch - creates rigid foot ready for push off
Etiology
Pes planus
-Increased strain trying to maintain arch- already stretched, stretching further
Pes cavus
-Short and thick - trying to pull against tightness
Excessive walking or running
-load> capacity to recover = degeneration
Prolonged weight bearing
-Load for long time
Obesity
-Load > capacity to recover
Decreased ankle DF
-Compensate during push off for pronation or hyperextension of 1st toe to push off = further stretching
Tight calf muscles
-Same as above
Non-supportive footwear
-Excess stress
Special tests
Windlass Test - standing on step and PT extends great toe - pain at insertion of calcaneus
S + S
Insidious onset
Worse in morning and may decrease with activity
Increased pain when activity is recommenced after period of inactivity
tender on medial calcaneal tubercle which may extended into medial longitudinal arch
Antalgic gait - less / no toe off, no heel contact
What are the interventions and differential diagnosis for plantar fasciitis?
Interventions
Activity modification
ST mobilization or stretching- plantar fascia / calf
Strengthening - intrinsic foot muscles
Taping
Orthotics, insoles, heel pad
Night splints / Strassberg sock (DF over night - on stretch)
Cryotherapy - decrease inflammation and analgesic
Iontophoresis - medication given through electrodes
Extracorpeal shock wave therapy
Medical - NSAIDs, corticosteroids (inflammation and to wear down connective tissue so it eventually just breaks), plantar fasciotomy
Ddx
Fat pad contusion
-High impact on heel - increase heel strike - common with fat pad atrophy (posterior-lateral of heel)
Calcaneal stress fractures
-Common with pes cavus - heel strike hurts
Lateral plantar nerve entrapment - most common
-Extension of posterior tibial nerve
-Presents with pain - do S + S, SLR with tibial nerve stress, with head movements
-Similar Rx
What is morton’s neuroma? Including etiology, S+S, special tests, interventions
Thickening of fibrous tissue leading to entrpaemtn of digit nerve of foot (usually 3rd and 4th between MT)
Etiology
Narrow shoes
High heels (MTP in extension, balls drop)
Metatarsal injury - # = ossification encraoching
Dropped transverse arch - all bones closer together
*more common in RA *
Special tests
Morton’s test - press together MT heads
S +S
Pain between MT heads
May have associated paraesthesia
Worse with walking (especially push off), running and with high heeled or narrow shoes (compression of MT heads)
Interventions
Activity modification
Changes in footwear
Orthotics
Cryotherapy
Plantar metatarsal padding
Strengthening - intrinsic foot muscles
Medical - corticosteroid injections
Surgical excision of nerve
What is turf toe? Including etiology, S +S, interventions
Sprain of 1st MTP due to hyperextension injury combined with compression loading
Etiology
Flexible footwear
Artificial turf
Decreased ankle DF - compensate with hyperextension of toe
Decreased MTP ROM - taut ligaments - more strain
S + S
Pain, swelling, plantar tenderness at 1st MTP
Decrease ROM
Worse with extension
Interventions
Activity modification
Cryotherapy
Taping
Stiff soled shoes
Medical - NSAIDs
What are the indication and contraindication to stretching?
Indications
ROM limitations
-Adaptive muscle shortening
-Adhesions
-Contractures
-Scar tissue formation
Preventable structural deformity due to restricted movements
Component of sport to increase performance or reduce risk of injury
Potentially reduce post-exercise soreness
Contraindications
Bony block limiting ROM
Recent fracture or incomplete bone union
Evidence of acute inflammation or infection
Sharp acute pain with muscle elongation
Hematoma
Hypermobility
Functional muscle shortening
What are the different types of stretching?
Passive, assisted (something helps), active
PNF - need normal innervation and voluntary control
-Hold relax - isometric contraction
-Contract relax - concentric contraction
Incorporating into regular basis is most effective way to gain ROM
What are the anatomical planes of movement (x3)?
Sagittal (runs anterior to posterior) - separates R and L - like flexion/extension (abduction/adduction for thumb)
Coronal (separates anterior / posterior) - separates front and back - like abduction / adduction (flexion/extension for thumb)
Transverse - separates in upper and lower - rotational movements, supination/pronation
Describe physiological and accessory movements
Physiological Movements
Done actively by the patient
Accessory Movement
Cannot be actively performed by the individual
Component movements - motions that accompany physiological movements (but not voluntary)
-Scapular movements, clavicular movements
Joint play - motions that occur between joint surfaces - describe distensibility of capsule (hypo/hypermobility, normal, doing traction, compression, distraction, glide spine)
Describe osteokinematics and end-feel
Physiological movements that occur between segments (bones)
End feel
Normal
-Bone to bone
-Soft tissue approximation
-Tissue stretch
Abnormal
-Abnormal capsular - frozen shoulder
-Springy block - meniscus tear
-Muscle spasm
-Empty - can’t get to the end range
-Abnormal bone to bone
Describe arthokinematics
Accessory movements that occur between joint surfaces
Types of movement
-Slide - one point of one meets new point on other - e.g., tires sliding to a stop
-Roll - new point on one meet new point on another - tires moving normally
-Spin - doesn’t move, same surfaces but spins
-Traction
-Distraction - pulling at a right angle
-Compression
*in periphery - name based on the distal segment, in spine - named based on the vertebrae above compared to the one below
Direction of movement
What is the mobilization concept?
Concave (distal) on convex - moves in SAME direction
-E.g., MCP flexion = anterior, extension = posterior
Convex (distal) on concave - moves in OPPOSITE direction
-E.g, GH abduction - inferior, adduction - superior, flexion = posterior, extension = anterior, external rotation = anterior, internal rotation = posterior
Rule of same different same as you name joints going down
What are the indications and contraindications/precautions for mobilization?
Indications
Pain, muscle guarding, spasm
Reversible joint hypomobility
Positional faults, subluxations
Progressive limitation -frozen shoulder - need to maintain ROM
Functional immobility - isn’t moving (cast) - regain ROM
Contraindications
Hypermobility
Joint effusion
Inflammation
Precautions
Malignancy
Bone disease
Unhealed fracture
Excessive pain
Hypermobility in associated joints
Total joint replacements
Weakened connective tissue
Systemic connective tissue diseases
Elderly individuals with weakened connective tissues
What are the three types of mobilization? And the parameters
Freddy Kaltenborn - sustained glides
grades I (loosen - small distraction, pain), II (tighten - small amplitude - distraction/glide - tighten tissue around joint, joint sensitivity, helps with pain, maintain joint play), III (large amplitude - distraction or glide to stretch joint capsule and periarticular structures - helps increase joint play)
Geoffrey Maitland - oscillatory glides - grades I (small - pain and spasm), II (large - pain and spasm), III (large - regain ROM), IV (small - regain ROM), V (small - high velocity thrust)
Brain mulligan - MWM (sustained glides with movements)
Sustained accessory glide during active or passive physical movement by patient
Comparable sign - determine effectiveness
Accessory - pain free
OP - pain free
Improve comparable sign
Failure to improve - something fucked up
Parameters
Type
Direction
Grade
Speed (Hz) - how many pushes per sec (2Hz = 2 pushes per sec)
Time (reps / sets)
What do you choose an assistive gait device based on? What do they help do?
Consider - needs (stairs, environment), abilities (physical - strength, balance, energy expenditure or psychological - cognitive), preference
Help - increase support, stability, confidence (decrease fear of falling)
What are the indications for an assistive gait device?
Pain, weakness, limited PROM
Decreased strength / endurance
Impaired motor control, balance
Unstable structures
Fear of falling
Open wounds on WB surface (increase chance of infection)
What are the different weightbearing restrictions?
NWB - affected limb bearing no weight in any circumstance
-ONLY CRUTCHES AND STANDARD WALKER
TTWB - toe touch weight bearing - foot may touch for balance only (<20%)
PWB - prescribed based on percentage of weight that can be applied (25%, 50%) -
-Use two bathroom scale method (or limb load monitor, heel sensors)
WBAT - as much weight as comfortable
FWB - no restrictions, no gait aid necessary
*increase in weight bearing - progression, bone adapts to stress - Wolfe’s law
Describe parallel bars assistive gait device
Advantages - max support/stability, initiate gait training, assistive gait device measurement
Disadvantages - no portable, expensive
Describe standard walkers assistive gait devices
Advantage - high stability , wide BoS, functional mobility, unloads limb
NMB, TTWB, PWB, WBAT, FWB
Disadvantage - high energy expenditure, no stairs, difficult to transport
Describe the attachments you can put on assistive gait devices
add a storage attachment, glides or platform - e.g., weightbearing through forearm
Describe a folding walker assistive gait device
Advantage - high stability , wide BoS, functional mobility, unloads limb, can collapse easily
TTWB, PWB, WBAT, FWB (NOT NWB LIKE STANDARD)
Disadvantage - low mobility, high energy expenditure, no stairs
Describe a wheeled roller assistive gait device
Advantages - increased mobility, good stability, unload a limb
PWB, WBAT, FWB
Disadvantages - not for NWB, no stairs
Describe a posterior (reverse) walker
Advantages - promotes upright posture , less energy expenditure than standard
Disadvantages - no stairs
Describe a rollator assistive gait device
Advantages - high mobility, WBAT or FWB, sit to rest (main reason - CRT or endurance issues)
Disadvantages - low stability, no stairs, no turning if issues
Describe axillary crutches
Advantages - high mobility, used to unload limb, stairs, wide selection of gait patterns
NWB, TTWB, PWB, WBAT
Disadvantages - low stability, good balance and upper body/trunk strength, high energy expenditure, risks of brachial plexus or radial nerve compression injury (crutch palsy), temporary use only
Describe how you would fit axillary crutches
Estimate height of crutches
-Height markers
-ATNR method (sitting)
-From folding arm to the extended arm
-Axillary fold to a spot 6-8 inch lateral to heel of shoe
Estimate height of handles
-Measure axillary fold to greater trochanter
-Measure bottom of shoe to greater trochanter
Confirm fit in functional standing
-Tip 2 inch lateral, 6 inch anterior to 5th digit
-2 fingers between axilla and axillary pad
-Hand grips at wrist crease, ulnar styloid, greater trochanter (elbows 20-30 degrees flexion)
Describe forearm crutches
Advantages - high mobility, used to unload limb, stairs, wide selection of gait patterns, no risks of brachial plexus injuries or radial nerve compression, allows for release of handgrips for functional activities
NWB, TTWB, PWB, WBAT
Disadvantages - low stability, good balance and upper body/trunk strength, high energy expenditure, good coordination
mostly for those long term use of crutches that need just a little stability (SB, CP - grade II GMFCS)
Describe the fitting of forearm crutches
Handgrips
-2 inch lateral, 6 inch anterior
-Hand grips at wrist crease, ulnar styloid, greater trochanter (elbows 20-30 degrees)
Cuff
-Proximal 1/3rd forearm, 1-⅕ below olecranon or elbow cuff
-Squeeze together or pull apart for proper fit (partial contact but not binding
Describe hemi walkers
Advantages - good stability, use when stability is needed but only one UE can be used, unload limb
PWB, WBAT or FWB
Disadvantages - low mobility, high energy expenditure, cannot be used on most stairs
Describe quadruped canes
Advantages - high mobility, good stability, unload limb, stairs
WBAT or FWB
Disadvantages - minimal balance deficits, slower gait pattern
Describe single point canes
Advantages - high mobility, unload limb, stairs, lower energy expenditure
WBAT or FWB
Disadvantages - minimal balance deficits, low stability
How do you fit an assistive gait device?
Weight bearing capacity of device (standard - <300 pounds, bariatric >300 pounds)
Handgrip placement -
*wearing shoes
Elbows in 20-30 degrees of flexion
Estimate using
-Greater trochanter to heel
-Wrist crease in standing
-Ulnar styloid process
-Height markings on device
Confirm in functional standing
-Tips of cane or crutches slight forward (4-6 inches) and to the side (2 inches)
-Feet within box of walker
Describe guarding
Gait belt
-Secure when seated, usually at midsection or high if physical condition or patient’s size (breasts, incision)
-Hold with supinated grip
Stand posterior and to the side (which they are most likely to fall - weaker or side they lean to)
Maintain broad BoS in staggered stance
Describe gait pattern
-see image in book
Describe different functional skills and how you would teach them
STS
Scoot to edge, flat feet, extend restricted leg out
Lean over CoM over BoS
-*for posterior or posterolateral - do not - just lean back because don’t want hips to go over 90 degrees of flexion
Push up stable surface
-Do not push up or pull up on stable surface
Once standing - grab device
Stand to sit
Back legs up against chair, reach back and extended weight bearing restrictions, slow descent
Turning
Turn towards unaffected then can progress
With posterolateral turn towards unaffected
Use multiple slow steps progress to pivot
Stairs
Good up, bad down - device moves with affected LE - guard most likely to fall
Initially step to then progress to step through
Use handrails (no bilateral if device) - use on affected side
Describe the safety with assistive gait devices
Inspect device regularly
Replace rubber tips when signs of excessive wear
Avoid slippery surfaces
Beware of ice and snow - may need ice picks on tip in winter
