Transcript Slide 1

How Can PTNow Help You in
Orthopedic Patient Care?
Airelle Hunter-Giordano, PT, OCS, SCS
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Benign Paroxysmal
Positional Vertigo (BPPV)
• Most common cause of vertigo due to peripheral
vestibular disorder
• Illusion of movement, spinning sensation
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Episodic
Less than 1 minute
Occurs when head (labyrinth) is in certain positions
Characteristic nystagmus
Repeated provocation reduces signs and symptoms
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BPPV
• Mechanical problem resulting from displacement of
otoconia from the utricle to one of the semicircular
canals (SCCs)
• Triggers
– Lying down
– Rolling over in bed
– Bending over and looking up
• Diagnosis
– Confirmed by observation of nystagmus when the patient
is placed in a provoking position using:
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Dix Hallpike Test
Sidelying Test
Roll Test
Bow and Lean Test
– Rule out cervical and cervical-medullary disorders
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BPPV Classification
• Primarily based on the SCC involved
[*posterior (76-85%), anterior (1.2-13.0%),
horizontal (5.0-13.6%)]
• Maneuver takes a few minutes to perform
• High rate of resolution
• Which canal is involved?
– Based on the observation that nystagmus occurs
when patient is in provoking position
• Canalithiasis
• Cupulolithiasis
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Canalithiasis
• Delay in onset of vertigo of 1-40 sec after the
patient has been placed in the provoking position
• Nystagmus that appears with the same latency as
reports of vertigo
• Fluctuation in intensity of the vertigo and
nystagmus, which increases and then decreases
while the person is in a provoking position,
disappearing in 60 sec
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Cupulolithiasis
• Immediate onset of vertigo when patient is
moved into provoking position
• Presence of nystagmus appearing with the
same latency as reports of vertigo
• Persistence of vertigo and nystagmus as long
as head is maintained in provoking position
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Determining the SCC: Observed
Patterns of Nystagmus*
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Focus Areas for Examination*
Image from: http://www.youtube.com/watch?v=Ew14aZqiUrw
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Differential Diagnosis: Central
Positional Nystagmus and Vertigo
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Central positional nystagmus and vertigo
Perilymphatic fistula
Superior canal dehiscence
Vestibular hypofunction
Vertebrosbasilar artery insufficiency
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Differential Diagnosis: Central
Positional Nystagmus and Vertigo
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Summary of Treatment Options
Type of BPPV
Treatment
Posterior SCC Canalithiasis
Canalith repositioning procedure or
treatment (CRT) (Epley maneuver)
Anterior SCC Cupulolithiasis
Reverse Liberatory maneuver
Anterior SCC Canalithiasis
Canalith repositioning procedure on the
affected side
Horizontal SCC Canalithiasis
Roll treatment, Forced prolonged position,
Gufoni or Appiani maneuver
Horizontal SCC Cupulolithiasis
No treatment recommended
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Prognosis
• Posterior SCC canalithiasis
– Supported by systematic and Cochrane reviews with use of
canalith repositioning (Epley maneuver)
– Remission of symptoms usually occurs in 1-2 treatments
• If not remission in 4 treatments, reevaluate
• Horizontal and anterior SCCs
– Equally effective treatment as posterior SCC; however, level of
evidence is lacking
• Spontaneous recovery
– In ~30% of patients with posterior SCC canalithiasis, remission is
spontaneous
• Recurrence
– More common if associated with head trauma (1/3)
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Achilles Tendinopathy
• Tendinopathies are characterized by excessive loading
and overuse resulting in tendon breakdown
• Often seen in middle-aged athletes (aged 30-50) but
can also present in sedentary individuals
• Incidence:
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Running: </ 9% in a given year
Competitive athletes lifetime incidence: 24%
Runners lifetime incidence: 40-50%
Acute or progressive rupture: 8% runners
• Pain:
– Mid portion of the tendon
– Tendon’s bony insertion
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Achilles Tendon
• Largest and strongest tendon in the body
connecting the gastroc and soleus to the
calcaneous
• Tendon is 6 inches long
– 2-6 cm proximal to the tendon’s distal
insertion is a zone of hypovascularity
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Risk Factors
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Intrinsic
Abnormal DF motion
Abnormal subtalar motion
PF strength
Abnormal pronation
Abnormal foot/tendon structure
Lateral ankle instability
Age
Male sex
Obesity
Hypertension
Diabetes
Cholesterol
Adverse drug events
Extrinsic
• Training errors (change in
intensity, duration, level)
• Environmental factors
(surfaces, temperature)
• Faulty equipment (shoe
wear)
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• Tendinitis
Classification
– Acute trauma or muscle fatigue and characterized by edema
and hyperemia of the involved tendon
– Pain and tenderness
– Crepitus
• Tendinosis
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Chronic condition, gradual onset and lacking inflammatory cells
Tender nodules around tendon
Diffuse thickening of surrounding soft tissue
More prone to injury
• Tendinopathy
– Term suggested to avoid confusion
• 2 locations
– Mid portion (2-6 cm proximal to tendon insertion)
– Insertion to calcaneus (insertional tendinopathy)
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Screening
• Differential Diagnosis
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Achilles tendon rupture
Partial tear of Achilles tendon
Calf strain
Retrocalcaneal bursitis
Posterior ankle impingement
Sural nerve irritation and/or neuroma
Tarsal tunnel syndrome
Peroneal tenosynovitis and/or dislocation
Os trigonum syndrome
Accessory soleus muscle
Ossification of Achilles tendon
Systemic inflammatory disease
Lumbar radiculopathy
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Examination & Diagnosis
• Moderate evidence supports use of a group of signs
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Achilles tendon palpation test
Decreased PF strength and endurance
Arc sign
Royal London Hospital test
• Strong evidence to incorporate validated functional
outcome measures before and after intervention
– Victorian Institute of Sport Assessment (VISA-A)
– The Foot and Ankle Ability Measure (FAAM)
• Moderate evidence to analyze walking ability, stair
decent, unilateral heel raise, single limb hop, and
participation in recreational activities
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Diagnostic Imaging
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May be needed when examination findings are ambiguous
Ultrasound and magnetic resonance imaging (MRI) were found to be most
helpful
Ultrasound slightly less sensitive than MRI
MRI is preferred due to 3-dimensional abilities and soft tissue visulaization
MRI sensitivity=94 or 95%; specificity=50% to 81%. Increased risk of false
negatives because symptomatic tendons may appear normal upon imaging.
Acute tendinitis diagnosis: presence of fluid surrounding the tendon
Tendinosis: hypoechoic areas with poorly defined structural borders
Tendon degradation and disease progression graded: (1=normal tendon,
2=enlarged tendon, 3=tendon containing a hypoechoic area)
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Intervention
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Intervention
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Prognosis
• Conservative care 6 to12 weeks’ duration: significant
decreases in pain with the maintenance of long-term
function without reinjury.
• Prognosis in the more sedentary population is not as
encouraging.
• Conservative management may be unsuccessful in as
much as 24% to 49% of patients.
• Surgery (eg, excision of fibrotic adhesions, removal of
degenerated nodules, longitudinal incisions to restore
vascularity) is a favorable option after 4 to 6 months of
failed conservative measures.
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Medical Management
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Extracorporeal Shockwave Therapy (ESWT): A series of 2 or 3 high-energy pulses
per second to promote healing through neovascularization. Research on
effectiveness limited and conflicting. ESWT is not FDA-approved for this purpose.
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Local Corticosteroid Injection: Used to decrease acute inflammation, pain, and
promote function and activity. May decrease tensile strength.
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Sclerosing Injection (Polidocanol): Used to manage the more chronic, midsubstance form of Achilles tendinopathy, especially when less invasive strategies
have failed; decreases pain via the analgesic effects of the medication and reducing
high-flow areas within the tendon.
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Oral Nonsteroidal Anti-inflammatory Drugs (NSAIDs): Used as an adjunct to other
treatments to control pain and inflammation. Side effects are common. Should be
used with consideration of comorbidities, especially in the older population.
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Surgical Intervention: Percutaneous tenotomy and open removal of the tendon
pathology. Used when conservative management fails and functional decline
continues. Prognosis based on the extent of remaining tendon structure. If condition
progresses to the point of tendon rupture, primary Achilles tendon repair is
performed.
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