5010 - Exam 3

Biophysical agents

modalities, physical agents, energy applied to pt to assist rehab, heat/cold/water/sound/electricity

3 categories of biophysical agents

thermal, mechanical, electromagnetic

Hot packs are what mode of heat transfer

conduction

Ice massage is what mode of heat transfer

convection

Physiological effects of heating tissue for MMT

MMT prior to or more than 2 hours after heat application

Temp of tissue for theraputic effects

104-113

5 potential contraindications for biophysical agents

pregnancy, malignancy, pacemaker/electronic deivce, impaired sensation, impaired mentation

When should strength testing be done for cooling tissue

only prior to cold application

Adverse signs of response to cryotherapy

wheeling, syncope

3 categories of biophysical agents

thermal (US, hot pack), mechanical (traction, whirlpool), electromagnetic (laser, TENS)

APTA statement on physical agents

utilized only as component of patient/client management (use with other interventions and NOT alone)

How long after applying hot pack should you check on the patient

10 minutes

How long should a hotpack be on for

20-25 minutes

How long should a coldpack be on for

15-20 min (don’t want frostbite)

Vasodiliation

HR decrease and BP decrease

Vasoconstriction

HR increase and BP increase

Adverse response to cold

wheels, redness, swelling, face flush, decrease BP, increase pulse, fainting

Hot pack amount (ex: prone)

6-8

Hot pack amount (ex: supine)

10-12

Scapular Dyskinesis Type I

inferior angle dysfunction — angle more prominent due to anterior tilting —> correlated with subacromial impingement or RC dysfunction

Scapular Dyskinesis Type II

medial border dysfunction — border prominance —> due to IR of scap secondary to weak rhomboids and serratus

Scapular Dyskinesis Type III

excessive elevation of superior border vs upward rotation of scap —> RC pathology or adhesive capsulitis

Lower trap exercises

low row, lawn mower, standing W, wall slide with lift off

lower trap exercise advanced

Progression

1. prone row

2. prone horiz ABD/prone T

3. prone 90/90 ER

4. superman/prone Y

** other: seated pike/press up

mid trap/rhomboid exercises

Progression

1. prone 90/90 ER

2. prone row

3. prone H ABD/prone T,

4. superman/prone Y

serratus anterior

prone 90/90 ER, ceiling pounch, scap plane elevation, dynamic hug 90 and 120, push up plus, wheelbarrow

infraspinatus/teres minor

standing (base) ER, sidelying ER, standing 90/90 ER, prone 90/90 ER, standing 90/90 ER windshield wiper

supraspinatus

standing (base) ER, sidelying ER, scap plane elevation 80 and 120, prone 90/90 ER, prone Y

subscapularis

belly press, standing base IR, standing 90/90 IR

GIRD

glenohumeral internal rotation deficit —> lack of GH IR

GIRD degree loss

>20 degree of dominate side IR OR >5 degree loss total arc of motion on dominate side

GIRD causes

1. humeral retroversion

2. post GH jt capsule tightness

3. post RC muscle tightness/stiffness (IS and TM)

4. acute post RC muscle stiffness (IS and TM)

glenohumeral retroversion (HRV)

bony torsion (twist) in shaft of humerus — HH turned posterior on glenoid

throwing exposure does what to de-rotation

slows

if there is an increase in HRV, what happens to ER and IR

ER has more ROM and IR has less ROM

A loss in IR for HRV means what for ER

gain in ER — bony issue only

Total arc of motion is what

IR ROM + ER ROM (both supine)

if total arc is = dom vs non dom

anatomic GIRD (DO NOT TREAT)

if dominate shld total arc is < 5 degree

pathological GIRD (can treat)

Is posterior RC tightness/stiff is a greater factor than posterior capsule tightness in pathologic gird?

YES

What is frozen shoulder

inflammation of shoulder from subacromial pain syndrome, small tear, or other trauma

Why do people not move their shoulder with frozen shoulder?

Because of pain

Frozen shoulder capsule becomes…

thickened and fibrotic — fixed to humeral head = capsular stiffness

frozen shoulder capsular pattern

ER > ABD > IR (most common)

ER > FLEX > IR

EER > Elevation > IR

primary frozen shoulder (idiopathic)

no known cause

insidious onset

40-65 y.o

F>M

diabetes or thyroid history

obesity

resolves in 15-24 months

Risk factors for idiopathic frozen shoulder

prolonged immobilization

prolonged disuse

myocardial infarction

autoimmune disease

secondary frozen shoulder

AC that “sees you”

secondary to trauma

faster prognosis

smaller capsular pattern

50% loss

capsular pattern is based on what?

% loss of ER > Flex/ABD > IR

frozen shoulder exam pearls

spend time with ROM —> can be false positives

how many stages are there in frozen shoulder

4 stages

Stage 1 frozen shoulder

inflammation in shld

painful loss of ROM - no PROM

“pre-adhesive” stage

Stage 2 of frozen shoulder

“freezing” or pain stage

pain with AROM and PROM (more than AROM) with empty feel (7/8-10)

synovium red and angry

3-9 months

Stage 3 frozen shoulder

“frozen” stage

very little synovitis

loss of motion/impaired function

PROM = AROM

pain @ end range with firm end feel (4-6)

4-12 months

Stage 4 frozen shoulder

“thawing” stage

very little pain (0-3)

AROM = PROM

significant stiffness, firm end feel

no synovial reaction

gradual return to motion

muscle weakness

12-24+ months

CPG (A level evidence)

corticosteroid injection (CSI)

pain and muscle guarding as primary limit to motion

immediate improvements in pain and ROM after injection

use in FREEZING phase

CPG (B level evidence)

patient education on natural courses of disease

modify activities

match intensity of stretching protocol to irritability

do stretching exercises (diff in diff stages)

Freezing stage intervention

*caution — irritable tissue will stiffen further

low grade joint mobs

maintain, don’t gain

scap mobs, soft tissue norm

modify activities: open pack position

pendulum exercises

pain relieving modalities

frozen stage intervention

LLLD

— 5” for 24x up to 30” for 4x

aggressive capsular stretching

PT 1x week for 2-3 weeks

daily exercises

thawing stage intervention

aggressive stretching

LLD stretching

strength more important for AROM-PROM differences

daily stretching

strength 3x week

CPG (c level evidence)

modalities (estem, diathermy) to augment stretching

joint mobs

manipuation under anesthesia

discharge criteria for frozen shoulder

pt is out of frozen stage

independent HEP

no improvements with manual interventions

elbow traumatic injuries

MVA

collision/impact

FOOSH (fall out on stretched hand)

post elbow injury consideration

overly aggressive stretch/mobs/manipulation to elbow

anterior capsule of elbow is very thin

brachialis passes over capsule = bleeding from trauma cause capsular scarring

bleeding can lead to fibroplasia, calcification, myositis ossificans

outcomes of elbow injury

pain

ROM (elbow, forearm)

strength (elbow, grip)

functional ADL’s

elbow injury intervention

modalities as indicated

PROM, AROM, stretching (don’t be too aggressive)

joint mobs/manipulation (when safe)

dynamic splinting

strengthening (once ROM improved and trauma healed more)

instability is?

state of being unstable, lack of stability or firmness

behave in unpredictable, changeable, or erratic matter

laxity is?

state or quality of being loose

laxity in shoulder

one’s genetic predisposition of tissue elasticity

no pain

common: high beighton index

rare: marfan’s syndrome

instability in shoulder

painful hypermobility

causees for instability in shoulder

born loose: poor dynamic stability in genetic laxity

worn loose: repetitive overuse, wear out

torn loose: traumatic incident (MVA)

instability spectrum

born loose = AMBRI - congenital

worn loose = SLAP tear - repetetive stress

torn loose = TUBS - traumatic

anterior dislocation clock position

3-6

posterior dislocation clock position

6-9

SLAP tear clock position

10-2

classification of shoulder instability

direction: anterior, posterior, inferior, MDI

etiology: traumatic vs atraumatic

degree: dislocation, subluxation, apprehension

frequency: acute, recurrent, chronic

volition: voluntary vs involuntary

anterior shoulder instability (direction)

90% cases is anterior instability

cause anteroinferior translation

MOI traumatic, FOOSH in ER+ABD, forced position

may cause boney bankart (anteroinferior glenoid rim) or hill sachs (posterior humeral head impaction fracture)

posterior shoulder instability (direction)

1-5%

MOI repetetive or traumatic

forceful axial loading

multidirectional shoulder instability (direction)

2 directions of instability

pain w/2+ directions

inferior instability

atraumatic, overuse

superior shoulder instability (direction)

SLAP tear, superior labrum insufficient

worn loose

MOI quick traction overload

peel back

arthrokinematics for shoulder instability (caution with)

anterior: ER, EXT, HOR ABD, combo of movements

posterior: IR, hyperflex, flex w/axial load, UE weight bearing

AMBRI

atraumatic, multidirectional, bilateral, rehabilitation, inferior capsular shift

“born loose”

high beighton index

genetic collagen disorder

TUBS

traumatic, unilateral, bankart, surgery (indicated)

“torn loose”

traumatic injury

repetetive overuse

“worn loose”

shoulder dislocation degree

humeral head displaced completely from glenoid rim

may cause bony injury to HH or glenoid

shoulder subluxation degree

HH partially displaced from glenoid

shifting or clunking at injury

shoulder apprehension degree

reservations about putting arm into certain positions

frequency of shoulder instability

acute: recent traumatic incident

recurrent:" has history, or another event, <20 yo = 90% and >40 yo 10%

chronic: history with no recent events, pain or secondary dysfunction

shoulder instability volition

voluntary: hypermobile, no trauma history, born loose

involuntary: dislocate/sublux at night, serial recurrent, bone loss

shoulder instability examination

initial injury: MOI, DOI, direction, degree

pain: location, intensity

medical management: ATC/MD reduce, past history

current symptoms (SINSS): severity, irritability, nature, stage, stability

goal setting: preference, experience

examination: observation

clinical assessment: med screen

functional test: beighton, 5 item hypermob history (yes to 2 or more = extra point for beighton)

observation: scar, skin extensibility

examination: tests

AROM: guarding, side to side, scap dyskinesia

strength: RIMS, MMT, dynamometry

PROM: track and measure over time, tolerance

examination: special tests

anterior instability: apprehension, relocation, load and shift

MDI: sulcus sign

examination: diagnostic imaging

x-ray, CT, MRI

evaluation: shoulder instability

diagnosis: ex - connective tissue issue, poor strength/stability

prognosis: ex: low likelyhood, bony, pain, inflammation, recurrent, neuro

shoulder instability: surgery or no

15-25: acute repair best to decrease chance of recurrence

25-40: conservative care

40+ conservative care (10-15% recurrence)

shoulder instability: conservative treatment

phase 1: tissue protection and ROM

phase 2: muscular endurance, rhythmic stabilization, beginner strength

phase 3: progressive strengthening, stability, motor conrol

phase 4: plyometric and advanced programming

phase 5: return to sport

the big 4 exercise programming

RC strength

periscapular strength

advanced proprioceptive training

core strengthening

SAPS is…

subacromial pain syndrome

• non-traumatic, unilateral, pain around acromion w/lifting

• bursitis, tendinosis, supraspinatus tendinopathy, partial tear of RC, biceps tendinitis, etc.

stages of SAPS

stage 1: tendinitis - acute inflammatory condition

stage 2: tendinosis - repetitive impingement

stage 3: partial or full thickness RC tear

slop of acromion process

type 1: flat

type 2: curved

type 3: hooked

**leads to acromial plasty to make acromion more flat