Physical Therapy Protocols For Ankle and Foot Conditions

Red Flags for Potential Serious Conditions in Patients with Knee, Leg, Ankle or Foot Problems
Medical Screening for the Knee, Leg, Ankle or Foot Region

Red Flag Red Flag
Condition Data obtained during Data obtained during
Interview/History Physical Exam
Fractures1-4 History of recent trauma: crush Joint effusion and hemarthorsis
injury, MVA, falls from heights, Bruising, swelling, throbbing pain, and point
or sports injuries tenderness over involved tissues
Osteoporosis in the elderly Unwillingness to bear weight on involved leg
Peripheral Arterial Age > 55 years old Unilaterally cool extremity (may be bilateral if
Occlusive Disease5-9 History of type II diabetes aorta is site of occlusion)
History of ischemic heart disease Prolonged capillary refill time (>2 sec)
Smoking history Decreased pulses in arteries below the level of
Sedentary lifestyle the occlusion
Co-occurring intermittent Prolonged vascular filling time
claudication Ankle Brachial index < 0.90
Deep Vein Recent surgery, malignancy, Calf pain, edema, tenderness, warmth
Thrombosis10,11,17 pregnancy, trauma, or leg Calf pain that is intensified with standing or
immobilization walking and relieved by rest and elevation
Possible pallor and loss of dorsalis pedis pulse
Compartment History of blunt trauma, crush Severe, persistent leg pain that is intensified with
Syndrome12-14 injury - or - stretch applied to involved muscles
Recent participation in a rigorous, Swelling, exquisite tenderness and palpable
unaccustomed exercise or tension/hardness of involved compartment
training activity Paresthesia, paresis, and pulselessness
Septic Arthritis15 History of recent infection, surgery, Constant aching and/or throbbing pain, joint
or injection swelling, tenderness, warmth
Coexisting immunosuppressive May have an elevated body temperature
disorder
Cellulitis16 History of recent skin ulceration or Pain, skin swelling, warmth and an advancing,
abrasion, venous insufficiency, irregular margin of erythema/reddish streaks
CHF, or cirrhosis Fever, chills, malaise and weakness
History of diabetes mellitus
References:
1. Judd DB, Kim DH. Foot fractures misdiagnosed as ankle sprains. Am Fam Physician. 2002;68:785-794.
2. Hatch RL, Hacking S. Evaluation and management of toe fractures. Am Fam Physician. 2002;68:2413-2418.
3. Hasselman CT, et al. Foot and ankle fractures in elderly white woman. J of Bone Joint Surg. 2003;85:820-824.
4. Rammelt S, Zwipp H. Calcaneus fractures: facts, controversies, and recent developments. Injury. 2004;35:443-461.
5. Boyko EJ, et al. Diagnostic utility of the history and physical examination for peripheral vascular disease among patients
with diabetes mellitus. Journal of Clinical Epidemiology. 1997;50:659-668.
6. McGee SR, Boyko EJ. Physical examination and chronic lower-extremity ischemia: a critical review. Arch Intern Med.
1998;158:1357-1364.
7. Halperin, JL. Evaluation of patients with peripheral vascular disease. Thrombosis Research. 2002;106:V303-11.
8. Hooi JD, Stoffers HE, Kester AD, et al. Risk factors and cardiovascular diseases associated with asymptomatic peripheral
occlusive vascular disease. Scand J Prim Health Care. 1998;16:177-182.
9. Leng, GC, et al. Use of ankle brachial pressure index to predict cardiovascular events and death: a cohort study. BMJ.
1996;313:1440-79.
10. Constans J, et al. Comparison of four clinical prediction scores for the diagnosis of lower limb deep venous thrombosis in
outpatients. Amer J Med. 2003;115:436-440.
11. Bustamante S, Houlton, PG. Swelling of the leg, deep venous thrombosis and the piriformis syndrome. Pain Res Manag.
2001;6:200-203.
12. Bourne RB, Rorabeck CH. Compartment syndromes of the lower leg. Clin Orthop. 1989;240:97-104.
13. Swain R. Lower extremity compartment syndrome: when to suspect pressure buildup. Postgraduate Medicine. 1999:105.
14. Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: are clinical findings predictive of the disorder.
Orthop Trauma. 2002;16:572-577.
15. Gupta MN, et al. A prospective 2-year study of 75 patients with adult-onset septic arthritis. Rheumatology. 2001;40:24-30.
16. Stulberg D, Penrod M, Blatny R: Common bacterial skin infections. Am Fam Physician. 2002; 66:119-124.
17. Riddle DL, et al. Diagnosis of lower-extremity deep vein thrombosis in outpatients with musculoskeletal disorders: a
national survey study of physical therapists. Phys Ther. 2004; 84 (8): 717-728.
Robert Klingman PT, Joe Godges PT KP SoCal Ortho PT Residency

1
KNEE/LEG/ANKLE/FOOT SCREENING QUESTIONNAIRE
NAME: ________________________________________ DATE: _____________

Medical Record #: _________________________
Yes No
1. Have you recently experienced a trauma, such as a vehicle accident, a

fall from a height, or a sports injury?
2. Have you recently had a fever?
3. Have you recently taken antibiotics or other medicines for an

infection?
4. Have you had a recent surgery?
5. Have you had a recent injection to one or more of your joints?
6. Have you recently had a cut, scrape, or open wound?
7. Do you have diabetes?
8. Have you been diagnosed as having an immunosuppressive disorder?
9. Do you have a history of heart trouble?
10. Do you have a history of cancer?
11. Have you recently taken a long car ride, bus trip, or plane flight?
12. Have you recently been bedridden for any reason?
13. Have you recently begun a vigorous physical training program?
14. Do you have groin, hip, thigh or calf aching or pain that increases with
physical activity, such as walking or running?
15. Have you recently sustained a blow to your shin or any other trauma
to either of your legs?
Joe Godges DPT KP SoCal Ortho PT Residency

Normal Gait Mechanics
Normal Gait Patterns Have Two Major Periods:
1. Double Limb Support: a) weight loading

b) weight unloading
2. Single Limb Support: a) stance phase of ipsilateral side
b) swing phase of contralateral side
DOUBLE LIMB SUPPORT
WEIGHT UNLOADING: Trailing foot is rolling off floor
Phases: Terminal Stance: when heel rises

Pre-Swing: when 1st MTP rolls off floor
Joint Motions: Terminal Stance Æ Pre-Swing

Ankle Heel rise Æ Max. plantarflexion (20 o)
Knee Full extension Æ Flexes to approx. 40o
Hip Max. extension (20o) Æ Flexes to approx. 0o (neutral)
Pelvis Relative anterior rotation Æ Less anterior rotation
Posterior depression Æ Begin anterior elevation
Trunk Aligned between legs Æ Aligned towards wt. loading leg
WEIGHT LOADING: Weight is transferred to contralateral leg
Phases: Initial Contact: when heel contacts floor

Loading Response: when sole of foot contacts floor
Joint Motions Initial Contact Æ Loading Response

Ankle Neutral Æ Plantarflexes 10o
Knee Knee extended Æ Knee flexes 15o
Hip Flexed 25o Æ Stable 25o flexion
Relative abduction
Pelvis Level Æ Lateral drop to swing leg
Trunk Aligned between legs Æ Aligned towards wt. bearing leg
Joe Godges DPT 1

SINGLE LIMB SUPPORT Body is aligned over the stationary foot
Contralateral leg is off the floor
STANCE PHASE: (Initial Mid-Stance, Mid-Stance, Late Mid-Stance)
Joint Motions Initial Mid-Stance Æ Late Mid-Stance

Ankle Slight plantarflexion Æ Max. dorsiflexion (10 o)
Knee Slight flexion Æ Extended
Hip Flexed, Æ Extended,
Relative adduction 10o Relative adduction
Pelvis Lateral drop to swing leg, externally rotated
Trunk Toward stance leg Æ Away from stance leg
Trunk rises in an arc over the stationary foot
SWING PHASE: Leg shortens via hip and knee bend to simplify floor clearance
Sub Phases: Initial Swing: big toe leaves ground

Mid-Swing: contralateral leg is at high point – mid-stance
Terminal Swing: leg reaching forward for next floor contact
Joint Motions Initial Swing Æ Mid-Swing Æ Terminal Swing

Ankle Plantarflexed Æ Neutral Æ Neutral
Knee Max. flexion (60 o) Æ Flexion Æ Max. extension (0o)
Hip Flexion, Æ Max, flexion (25 o) Æ Flexion,
Relative abduction Max. abduction (10o) Relative abducted
Pelvis Lateral drop to swing leg, medial rotated
Trunk Aligned over stance leg
Pathway of Center of Gravity

Sagittal Plane: Rhythmical up and down motion
Highest point: Over extended single leg (MSt)
Lowest point: Double limb support (PSw/LR)
Vertical displacement of 4-5 cm. (sinusoidal wave)
Frontal Plane: Rhythmical side-to-side motion

Most lateral point: Mid-Stance
C. O. G. swings laterally in as arc over the stationary foot
Lateral displacement of 4-5 cm. (sinusoidal wave)
References:
Greenman PE. Clinical aspects of sacroiliac function in walking. Manual Medicine. 1990;5:125-
130.
Koerner I. Observation of Human Gait. Edmonton, Alberta, Canada: University of Alberta;
1986.
Observational Gait Analysis. Downey, CA: Rancho Los Amigos Research and Education
Institute; 1993.
Perry J. Gait Analysis. Normal and Pathological Function. Thorofare, NJ: Slack; 1992.
Joe Godges DPT 2

Critical Events During Gait
Joint Sagittal Plane Frontal Plane Transverse Plane
1st MTP 65o extension at PSw
Midtarsal: Control of Abduction at TSt
Calcaneocuboid PF of 1st Ray at TSt/PSw
(Peroneus Longus)
Oblique MT Jnt Axis stability
at TSt
Talonavicular Control of Eversion at MSt
(Tib Ant and Tib Post)
Longitudinal MT Jnt Axis
stability at TSt
Subtalar 4-6o eversion at IC/LR
Ankle 10o-20o DF at TSt
Control of DF (tibial
advancement) after
MSt
(Gastroc. and Soleus)
Knee Control of flexion at LR Patellar Medial Glide
(Quadriceps and VMO)
o
0 extension at TSt
60o flexion at ISw
Produce full ext. at TSw
Hip Control of flexion at LR Control of lateral pelvic tilt
(Hip extensors) at MSt
20o extension at TSt (Hip Abductors)
Common Lower Extremity Musculoskeletal Impairments Associated With Gait

Deviations
Joint ROM/Muscle Length Motor Control/Strength Joint Hypermobility/Instability

Deficits Deficits
1st MTP Dorsiflexion Tibialis Anterior Calcaneocuboid/Oblique MTJA
Talocalcaneal Eversion Tibialis Posterior Talonavicular/Longitudinal MTJA
Talocrural Dorsiflexion Peroneus Longus
Tibiofemoral Extension Gastrocnemius/Soleus
Tibiofemoral Flexion Quadriceps/VMO
Patellofemoral Medial Glide Gluteus Medius/Minimus
Hip Extension Gluteus Maximus
Joe Godges DPT 3

1
Foot Capsule Disorders
"Midtarsal Joint Capsulitis"
ICD-9-CM: 845.11 Sprain of tarsometatarsal joint
Diagnostic Criteria
History: Arch area pain - medial or lateral

Pain worse with single limb support phase of gait
Recent strain or repetitive use
Physical Exam: Pain at end range of one or more of the following accessory
movement tests (dorsal glide or plantar glide of the distal bone on
a stabilized proximal bone):
Medial Foot Lateral Foot

Talus - Navicular Calcaneus – Cuboid
Navicular - 1st Cuneiform Navicular/3rd Cuneiform – Cuboid
Talus - Navicular Accessory Movement Test
Cues: Patient sits on edge of table to allow knee flexion

Proximal forearm rests on tibia, index finger metacarpal (MCP) stabilizes dorsal
surface of talus, PIP and DIP stabilize talus using sustentaculum tali of
calcaneus
Distal index finger MCP provides the planter glide and PIP and DIP provide the
dorsal glide of the navicular
Alter forearm/upper extremity angle to align force with the "treatment plane"
(move the navicular with a glide parallel to the plane of the talonavicular
joint)
Determine symptom response, available motion, and end feel
Joe Godges PT, Robert Klingman PT Loma Linda U DPT Program KPSoCal Ortho PT Residency
2
Navicular - 1st Cuneiform Accessory Movement Test
Cues: Proximal MCP, PIP, and DIP stabilize navicular

Distal MCP, PIP, and DIP move 1st cuneiform
Calcaneus - Cuboid Accessory Movement Test
Cues: Calcaneus rests on stabilizing hand which rests on table, outside hand grabs
cuboid
Thumb on plantar surface, index and/or middle finger on dorsal surface of cuboid
"Up and out, down and in" - using a straight plane, translatory force (in line with
the "treatment plane")
3
Navicular/3rd Cuneiform - Cuboid Accessory Movement Test
Cues: Inside hand now stabilizes navicular and 3rd cuneiform (Thumb on plantar
surface, index and middle finger on dorsal surface)
Move cuboid "up and out, down and in"
"Hallux Rigidus"
ICD-9-CM: 735.1 Hallux rigidus
Diagnostic Criteria
History: Stiffness
Pain with barefoot walking - symptoms worse at pre-swing ("toe-
off")
Physical Exam: Limited motion of 1st metatarsophalangeal (MTP) extension

Pain at end range of extension ROM
Limited MTP accessory movements - especially volar glide
1st MTP Extension ROM
Cues: Depress 1st metatarsal plantarly, extend proximal phalanx of big toe dorsally
Measure angle of metatarsal shaft to proximal phalanx.
Normal ROM is 65 degrees
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1st MTP Accessory Movement Test

Dorsal Glide of Proximal Phalanx
Cues: Loose pack position is 10 degrees of dorsiflexion

"Bunch Skin"
Glide parallel to articulating surface of the proximal phalanx
Compare with opposite side for normal amount of movement (if the opposite side
has normal range of motion)
Determine symptom response at end range
5
Hallux Rigidus
ICD-9: 735.1
Description: Hallux rigidus is considered a progressive disorder of the 1st MTP joint
marked by pain, decreased dorsiflexion, and degenerative changes in the joint.
Etiology: Hallux rigidus can be caused by osteoarthritis, repetitive trauma, or anatomic

abnormalities of the foot. Patients with hallux rigidus present with complaints of pain
localized at the first MTP joint and/or joint stiffness. These symptoms can be insidious
or as the result of an injury. The pain associated with this condition is often noted with
increased activities that require a patient to extend the first MTP joint as in squatting,
jumping, kicking, and dancing. Another cause of symptoms is shoes that irritate the soft
tissues at the subcutaneous bony prominences and shoes such as high-heels that require
extended amounts of time in MTP extension and MTP jamming. According to the
Clinical Practice Guideline First Metatarsophalangeal Joint Disorders Panel, “the
hallmark of hallux rigidus is the typical dorsal bunion caused by both the proliferative
disease and the flexion at the first MTP joint. This position of hallux equinus results in
retrograde elevation of the metatarsal and the uncovering of the dorsal portion of the
articulation. Dorsiflexion is generally limited because of abutment of the articular
surfaces of the phalanx and metatarsal head, and motion is painful with/without crepitus.”
The patient will generally walk with an antalgic gait, which can lead to problems in other
joints of the foot. Radiographic findings are consistent with those of osteoarthrosis. The
division of hallux rigidus into stages is based on the progression of osteoarthrosis. A
patient with stage I may present with little or no radiographic joint changes and a patient
with stage IV will demonstrate severe end-stage arthrosis. The majority of the medical
literature acknowledges these 4 stages; however, Magee divides hallux rigidus into two
categories: acute and chronic. The following lists describe the signs and symptoms
associated with both the stage divisions and the acute/chronic divisions.
The stages are taken from J Foot Ankle Surg. 42(3):124-36. 2003.
Stage I: Stage of Functional Limitus

• Hallux equinus/flexus
• Plantar subluxation proximal phalanx
• Metatarsus primus elevatus
• Joint dorsiflexion may be normal with nonweightbearing, but ground reactive
forces elevate the first metatarsal and yield limitation
• No degenerative joint changes noted radiographically
• Hyperextension of the hallucal interphalangeal joint
• Pronatory architecture
Stage II: Stage of Joint Adaptation

• Flattening of the first metatarsal head
• Osteochondral defect/lesion
• Cartilage fibrillation and erosion
• Pain on end ROM
• Passive ROM may be limited
• Small dorsal exostosis
6
• Subchondral eburnation
• Periarticular lipping of the proximal phalanx, the first metatarsal head, and the
individual sesamoids
Stage III: Stage of Established Arthrosis

• Severe flattening of the first metatarsal head
• Osteophytosis, particularly dorsally
• Asymmetric narrowing of the joint space
• Degeneration of articular cartilage
• Erosions, excoriations
• Crepitus
• Subchondral cysts
• Pain on full ROM
• Associated inflammatory joint flares
Stage IV: Stage of Ankylosis

• Obliteration of joint space
• Exuberant osteophytosis with loose bodies within the joint space or capsule
• <10° ROM
• Deformity and/or misalignment
• Total ankylosis may occur
• Inflammatory joint flares possible
• Local pain is most likely secondary to skin irritation or bursitis caused by the
underlying osteophytosis
The following classification is taken from: Magee DJ. Orthopedic Physical Assessment:
Acute (adolescent)
• Primarily in young people with long, narrow, pronated feet
• Boys > girls
• Constant, burning, throbbing, or aching pain and stiffness come on quickly
• Palpable tenderness over MTP joint
• 1st metatarsal head may be elevated, large, and tender
• Antalgic gait
Chronic
• Primarily in adults
• Men > women
• Frequently bilateral
• Usually result of repeated minor trauma leading to osteoarthritic changes
• Stiffness gradually develops and the pain persists
7
Intervention Approaches / Strategies
If the patient chooses to first attempt conservative/non-surgical treatment it is essentially

the same for stages I-IV (along with acute and chronic). This is an inflammatory joint
disorder so the most important thing is to reduce inflammation and not aggravate the
condition.
Stage I-IV (non-surgical)

Goals: 1) decrease inflammation and pain
2) restore ROM
3) if conservative treatment does not work, but patient is unwilling to have
surgery it is important to teach patient how to manage pain and function with
decreased 1st MTP motion
• Physical Agents: phonophoresis/iontophoresis, US, NSAIDS, steroid injection,

grade I-II joint mobs for pain relief, rest, ice, whirlpool, HVGC
• External Devices: Orthoses, shoe modifications to limit extension at 1st MTP
• Therapeutic Exercises: painfree AROM or passive ROM exercises
• Re-Injury Prevention Instruction: Temporarily cease/reduce aggravating

activities.
When conservative treatment does not reduce the impairments and the patient is not
willing to live with hallux rigidus there are several surgical options. If the patient is in
stage I or II they are usually good candidates for joint-salvage procedures. These include
cheilectomy, metatarsal astronomy, phalangeal osteotomy, and chondroplasty. If the
joint has progressed to stage III or IV often a joint destructive procedure if appropriate.
These include resection arthroplasty, implant arthroplasty, and arthrodesis. The two
procedures that are utilized most often are cheilectomy and arthrodesis. While individual
surgeons have slightly different protocol for post-surgical treatment, there are general
guidelines that most surgeons request.
Post-Surgical Management – Guidelines taken from J Bone Joint Surg. 85A(11):2072-

87.2003.
Cheilectomy: Passive ROM exercises are begun within 10 days post-operatively.

Aggressive stretching is allowed as pain and swelling subside. Weight bearing as
tolerated is allowed following surgery with the patient wearing a stiff-soled postoperative
shoe. Final stages of rehab include teaching the patient a normal, functional gait pattern.
Arthrodesis of the 1st MTP Joint: The foot is placed in a stiff-soled postoperative shoe
after surgery, and weight-bearing on the heel and the lateral aspect of the involved foot is
permitted. The first ray remains unweighted until there is radiographic evidence of a
fusion.
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Selected References
Andrews JR. Harrelson GL, Wilk KE. Physical Rehabilitation of the Injured Athlete, 2nd
Edition. Philadelphia, PA: W.B. Saunders; 1998.
Brotzman SB. Clinical Orthopaedic Rehabilitation. Philadelphia, PA: Mosby; 1996.
Coughlin MJ, Shurnas PS. Hallux Rigidus Grading and Long-Term Results of Operative
Treatment. J Bone and Joint Surg. 2003;85A(11):2072-87.
Donatelli R, Wooden MJ. Orthopaedic Physical Therapy, 2nd Edition. Churchill

Livingstone; 1994.
Feltham GT, Hanks SE, Marcus RE. Age-based outcomes of cheilectomy for the
treatment of hallux rigidus. Foot Ankle Int. 2001;22(3):192-7.
Haddad SL. The use of osteotomies in the treatment of hallux limitus and hallux rigidus.
Foot Ankle Clin. 2000;5(3):627-61.
Lau JT, Daniels TR. Outcomes following cheilectomy and interpositional arthroplasty in
hallux rigidus. Foot Ankle Int. 2001;22(6):462-70.
Makwana NK. Osteotomy of the hallux proximal phalanx. Foot Ankle Clin.
2001;6(3):455-71.
Nawoczenski D. Nonoperative and Operative Intervention for Hallux Rigidus. J Orthop

Sports Phys Ther. 1999;29(12):727-735.
Notni A, Fahrmann M, Fuhrmann RA. Early results of implantation of an unconstrained

metatarsophalangeal joint prosthesis of the firs toe. Z Orthop Ihre Grenzgeb.
2001;139(4):326-31.
Schwetzer ME, Maheshwari S, Shabshin N. Hallux valgus and hallux rigidus: MRI
findings. Clin Imaging. 1999;23(6):397-402.
Solan MC, Calder JD, Bendall SP. Manipulation and injection for hallux rigidus. Is it
worthwhile? J Bone Joint Surg Br. 2001;83(5);706-8.
Vanore JV, Christensen JC, Kravitz SR, Schuberth JM, Thomas JL, Weil LS, Zlotoff HJ,
Mendicino RW, Couture SD;. Diagnosis and Treatment of First Metatarsophalangeal
Joint Disorders. Section 2: Hallux Rigidus. J Foot Ankle Surg. 2003; 42(3):124-36.
9
Posterior Medial Calf Posterior Lateral Calf
10
Impairment: Limited Ankle Dorsiflexion

Limited Inferior Tibiofibular Accessory Movements
Fibular Posterior Glide
Cues: Stabilize the tibia by 1) resting in on the treatment table, and 2) using the thenar
eminence of one hand to stabilize the medial malleolus
Slightly internally rotate the tibia (to line up the treatment plane perpendicular to
gravity)
Posteriorly glide the fibula using the thenar eminence of the other hand (“catch”
the skin on the anterior aspect of the ankle to provide a firmer grip on the
fibular)
Fibular Anterior Glide
Cues: Position the patient prone with feet of the edge off the table - but keep the distal
tibia on the table
Stabilize the tibia with one hand - internally rotate it a bit
Glide the fibula anteriorly
The following reference provides additional information regarding this procedure:

Freddy Kaltenborn PT: Manual Mobilization of the Extremity Joints, p. 158, 1989
11

Limited Talar Posterior Glide
Talar Posterior Glide
Cues: Stabilize tibia with one hand - cushion the Achilles tendon with your fingers
between the tendon and the table
Contact the talus with a “V” formed between your thumb and your index finger
metacarpal head
Posteriorly glide the talus using a weight shift from the lateral side of the table

12

Limited Talar Posterior Glide
Talar Posterior Glide MWM
Cues: Stand facing the patient

Place a towel pad between the Achilles tendon and the table
Grasp the calcaneus with the palm of one hand and the talus with the web space of
the
other hand
Elicit active dorsiflexion
Maintain the dorsiflexion with pressure from your abdomen
“Relax” the dorsiflexors
Glide the talus and calcaneus posteriorly - using a slight knee bent
Maintain the posterior glide of the calcaneus and again elicit active dorsiflexion –
take up
the slack with your abdomen
Repeat the posterior glide of the talus and calcaneus
Again, “relax” the dorsiflexors
Repeat the sequence several times

Brian Mulligan MNZSP, DipMT: Manual Therapy, p. 96-97, 1995
13
Impairment: Limited and Painful Talocrural Dorsiflexion
Ankle Dorsiflexion MWM
Cues: Position the patient standing on a secure treatment table with the patient using a
wide base of support and another person or a stationary object for balance
assist
Using a belt, glide the tibia and fibular anteriorly
Match the anterior glide with an equal and opposite posteriorly glide on the talus
using a dummy thumb and thenar eminence
If the opposing forces are balanced the patient remains stable
Attempt to keep the midtarsal joint in the supinated position
Sustain both glides and midtarsal supination while the patient actively dorsiflexes
(by shifting weight forward and bending the involved knee)

14
Impairment: Limited and Painful Talocrural Plantarflexion
Ankle Plantarflexion MWM
Cues: Position patient supine with a partially flexed knee

Glide the tibia and fibula posteriorly with one hand
Grasp the talus with the web space of your other hand
Sustaining the posterior glide, “roll” the talus anteriorly as the foot is actively
and/or passively plantar flexed

15
Impairment: Limited Ankle Plantarflexion

Limited Talar Anterior Glide
Talar Anterior Glide
Cues: Stabilize the tibia with one hand - use your fingers as a pad between the anterior
tibia and the table
Glide the calcaneus (and, thus, also the talus) anteriorly using a weight shift from
the lateral side of the involved ankle

16
Impairment: Limited Subtalar Eversion

Limited Calcaneal Lateral Glide
Calcaneal Lateral Glide
Cues: Position the patient lying on the involved side with the involved heel off the side
of the treatment table
Stabilize and pad the lateral malleolus against the table with one hand
Mobilize either 1) the posterior talocalcaneal, or 2) the anterior talocalcaneal
joint(s) with the thenar eminence of the other hand - use a weight shift
from the end of the table
The procedure is contrary to convex - concave principles but the consensus of the
“foot nerds” of Southern California (including myself) is the lateral glides
work best for restoring calcaneal eversion (probably because the
talocalcaneal joint surfaces are more planar than spheroid)
17
Impairment: Limited Navicular Plantar Glide

(at the talonavicular joint)
Navicular Plantar Glide
Cues: Flex the knee and stabilize the calcaneus and, thus, also the talus, on a wedge
Slightly internally rotating the limb and placing a finger under the medial side of
the talus provides additional stabilization
Contact the navicular with the index finger metacarpal head and mobilize the
navicular plantarly
Be sure that your mobilization is parallel to the treatment plane
Modifications of this procedure can be used for any of the tarsal plantar glide
mobilizations (i.e., stabilize the dorsal surface of the proximal bone on a
wedge and mobilize the distal bone plantarly)

18
Impairment: Limited Cuboid Dorsal Glide

(at the calcaneocuboid joint)
Cuboid Dorsal Glide
Cues: Position the patient prone with the dorsal lateral surface of the calcaneus on the
wedge
Slight internal rotation of the tibia provide additional calcaneal stabilization
Contact the cuboid with either 1) the head of the index finger metacarpal, or 2) a
“dummy” thumb under the mobilizing thenar eminence

Freddy Kaltenborn PT: Manual Mobilization of the Extremities
1
Ankle Muscle Power Deficit
"Achilles Tendinitis"
ICD-9-CM: 726.71 Achilles bursitis or tendinitis
Diagnostic Criteria
History: Gradual onset of aching in of Achilles tendon - may be able to identify a

recent increase in activity
Symptoms worse with activity
Physical Exam: Swelling 1 – 2 inches above Achilles tendon insertion

Palpable tenderness of Achilles tendon 1 – 2 inches above Achilles tendon
insertion
“Posterior Calcaneal Bursitis”
ICD-9-CM: 726.73 Calcaneal spur
Diagnostic Criteria
History: Posterior heel pain and swelling

Irritated by pressure (e.g., from shoe)
Physical Exam: Tender bump on posterior aspect of calcaneus – reproduces pain complaint
2
Achilles Tendinitis/Tendonosis
ICD-9: 726.71 achilles bursitis or tendinitis
Description: Repetitive strain injury to the Achilles tendon typically producing posterior ankle
inflammation and pain.
Etiology: Inflammation of the Achilles tendon and calcaneal insertion as well frequently the
retrocalcaneal bursa. Generally the result of over-use activities such as running or jumping,
repetitive over-stretching and/or a biomechanically deficient foot conditions such as pes cavus
and varus heels. In contrast, tendonosis involves a slow onset with chronic and recurrent
responses where the tendon may never regain its former structure, and is always sensitive to
load. Tendonosis includes intratendonous degeneration commonly due to aging, microtrauma
over a prolonged period, or vascular compromise. Collagen disorganization, focal necrosis and
calcification (may never regain normal structure, making it always sensitive to load).
Misconception Evidence Based Finding
Tendonopathies are self-limiting Tendonopathies are often recalcitrant

conditions that take only a few to treatment and may require months
weeks to resolve to resolve
Imaging techniques (MRI, Imaging does not predict prognosis; it
ultrasound, etc) can predict adds to the chance of a tendonopathy
prognosis Dx, but does not prove it
Cyst-like abnormalities found with Surgery should be based on clinical

ultrasound are indications for grounds;cyst-like ultrasound findings
surgery can be asymptomatic
Surgery provides fast recovery of After surgery, return to sport takes at
symptoms in almost all patients least 4-6 months. Not all do well.
Acute Stage / Severe Condition
• Focal palpatory pain and swelling 4 to 5 cm proximal to insertion

• Possible palpable tissue disruption
• Pain with resisted plantarflexion; especially with walking and running
• Pain at end range dorsiflexion
• Decreased plantarflexion strength
3
Sub Acute Stage / Moderate Condition
As above with the following differences:
• Possible increased ankle stiffness

• Compensatory gait pattern
• Progressive tendon nodular thickening
• Increased retrocalcaneal bursa pain
Settled Stage / Mild Condition
• Limited ankle dorsiflexion

• Residual nodule thickening
• Pain response limited to forceful loading (i.e., running or jumping) or static
overstretching such as maintained squat position (e.g., baseball catcher position)
4
Goals: Decrease swelling and pain

Limit aggravating causes
• Physical Agents
Ultrasound/ phonophoresis
Electrical stimulation
Heat or ice (contrast bath)
• Therapeutic Exercises
Gentle mobility exercises to maintain ankle range of motion (avoiding end range
dorsiflexion)
Strengthening exercises for the foot intrinsic muscles
• External Devices (Taping/Splinting/Orthotics)

Heel lifts and orthotics where indicated
• Re-injury Prevention Instruction

Instruct patient in appropriate exercises, stretches, application of ice and heat and
instruct in the use of lifts and orthotics
Sub-Acute Stage / Moderate Condition
Goals: Restore normal, pain free motion

Normalize biomechanics for standing and walking tasks
• Approaches / Strategies listed above
• Manual Therapy
May begin gentle soft tissue mobilization techniques to the Achilles tendon and
surrounding tissues (e.g., soleus myofascia, ankle retincula) where indicated
Progressive strengthening activities. In cases where tendonosis is likely, increase
tissue thickness and strength, with eccentric loading.
Proprioceptive training
Progressive stretching techniques
5
Goal: Allow patient to return to most normal activities including community ambulation,
unlevel surfaces and stairs without pain
• Functional Training
Introduce inclined walking, light jogging and gentle jumping activities
Intervention for High Performance / High Demand Functioning in Workers and Athletes
Goal: Return to unrestricted sport or work activity
Review desired activity and progress to ballistic activity specific exercises.
• Patient Education/Ergonomics Instruction

Educate patient to recognize signs and symptoms of recurrent tendinitis.
Issue final home exercise and stretching program to prevent recurrence.
Selected References
Anderson DL, Taunton JE, Davidson RG. Surgical management of chronic Achilles tendonitis.
Clin J Sport Med. 1992; 2 (1): 38-42
Khan KM, Cook JL, Taunton JE, et al. Overuse tendonosis, not tendonitis: a new paradigm for a
difficult clinical problem. The Phys and Sport Med. 2000; 28 (5)
Knight C, Rutledge C, et al. Effects of superficial heat, deep heat and active exercise warm-up on
the extensibility of the plantar flexors. Phys Ther. June 2001
Galloway M, Jokl P, Dayton O. Achilles tendon overuse injuries. Clin Sports Med. Oct 1992 pp
771-82
Mercier, L. Practical Orthopedics 3rd ed. Mosby Year Book, St. Louis, 1991
Nielson-Vertommmen SL, Taunton JE, Clement DB. The effect of eccentric versus concentric
exercise in the management of Achilles tendonitis. Clin J Sport Med. 1992; 2 (2) : 109-113.
Sammarco, J. Rehabilitation of the Athlete’s Foot and Ankle. Mosby Year Book, St. Louis, 1995
Scioli M. Achilles tendinitis. Orthop Clin North Am. Jan 1994 pp 177-82
6
Retrocalcaneal Bursitis
ICD-9: 726.73 calcaneal spur
Description: Inflammation, hypertrophy, and

adherence of the bursa and surrounding tissue
located between the insertion of the Achilles
tendon and the calcaneus producing posterior
heel pain, which is often most severe in the
morning or when just starting to walk
Etiology: Inflammation of the calcaneal bursae is commonly caused by repetitive overuse and
cumulative trauma, as seen in runners wearing tight-fitting shoes. Additional causes of
retrocalcaneal bursitis include: direct trauma, rheumatoid arthritis, and biomechanical
abnormalities such as rearfoot varus, rigid plantar flexed first ray, and Haglund’s deformity.
Physical Examinations Findings (Key Impairments)
• Antalgic gait pattern

• Swelling, redness, and warmth of the posterior heel (“pump bump”)
• Positive two-finger squeeze test (positive = pain when applying pressure both
medially and laterally with two fingers superiorly and anterior to the insertion of the
Achilles tendon)
• Pain with dorsiflexion and plantarflexion
Careful examination can help the clinician distinguish whether the inflammation is posterior
(superficial) to the Achilles tendon (within the subcutaneous bursa) or anterior (deep) to the
Achilles tendon (within the subtendinous bursa). Differentiating Achilles tendonitis from
bursitis may be impossible. At times, the two conditions coexist.
Isolated subtendinous bursitis is characterized by tenderness that is best isolated by palpating just
anterior to both the medial and lateral edges of the distal Achilles tendon.
Insertional Achilles tendonitis is notable for tenderness located slightly more distally, where the
Achilles tendon inserts on the posterior calcaneus.
A patient with plantar fasciitis has tenderness along the posterior aspect of the sole, but should
not have tenderness with palpation of the posterior heel.
7
A patient with a complete avulsion or rupture of the Achilles tendon demonstrates a palpable
defect in the tendon, weakness in plantarflexion, and positive Thompson test on physical
examination.
8
As above along with the following:
• Pain during passive end-range dorsiflexion

• Pain during terminal stance of gait
• Pain with tight-fitting shoes
Settled Stage/Mild Condition
• Pain with running or other athletic activities

• Limited ankle dorsiflexion
9
Goal: Decrease swelling and pain. Limit aggravating causes.
• Physical Agents
Ice (The patient should be instructed to ice the posterior heel and ankle to reduce
inflammation and pain. Icing can be performed 15-20 minutes at a time, several
times a day during the acute period.)
Ultrasound/ phonophoresis
Iontophoresis
Contrast baths
Gentle mobility exercises to maintain ankle range of motion (avoiding end range
dorsiflexion)

Heel lifts and orthotics where indicated

Instruct patient in appropriate exercises, stretches, and application of ice
Use of and open-backed shoe or a better-fitting shoe may relieve the pressure of
the affected region
• Immobilization (consider if above is not effective)

Walking boot
Cast for 4-6 weeks
Goal: Restore normal, pain free motion

Normalize biomechanics of gait
• Approaches/ Strategies listed above
• Manual Therapy
May begin gentle soft tissue mobilization techniques to the Achilles tendon and
surrounding tissues (e.g., soleus myofascia, ankle retincula) where indicated
Gradually progressive stretching of the Achilles tendon may help to relieve
impingement on the subtendinous bursa
Ballistic stretches should be avoided to prevent clinical exacerbation.
10

Changing footwear may be the most important treatment for calcaneal bursitis.
Inserting a heel cup within the shoe may help raise the inflamed region slightly
above the restricting heel counter of the shoe. If this approach is implemented, a
heel cup also should be placed in the other shoe to avoid introducing a leg length
discrepancy.
Goal: Return to most normal pain free activities including ambulating over uneven surfaces and
short community distances
• Approaches/ Strategies listed above
• Functional training:
Heavy-load eccentric calf muscle training

Avoid footwear that fits excessively tight or causes excessive friction at the
posterior heel
Note: If chronic pains persists and conservative treatment is unsuccessful, patient may
consider ultrasound-guided cortisone injection or surgery
Intervention for High Performance/High Demand Functioning in Workers and Athletes
Goal: Return to desired recreational or occupational level of activity
• Functional training: light jogging

• Patient education/Ergonomic instruction
Instruct patient in signs and symptoms to prevent re-injury
Review home exercise program to prevent recurrence
11
Selected References
Alfredson H, Pietila T, Jonsson P, et al. Heavy-load eccentric calf muscle training for treatment
of chronic Achilles tendinosis. Am J Sports Med. 1998; 26(3): 360-366. Retrieved January 28,
2004, from the MD Consult database.
Cunnane G, Brophy DP, Gibney RG, et al. Diagnosis and treatment of heel pain in chronic
inflammatory arthritis using ultrasound. Sem Arth Rheum. 1996; 25(6): 383-389.
Foye P., Nadler SF. Retrocalcaneal bursitis. (2003, August 12). Retrieved January 21, 2004,
from eMedicine database.
Mazzone MF. Common conditions of the Achilles tendon. Am Fam Physician. 2002;
65(9):1805-1810. Retrieved January 28, 2004, from the MD Consult database.
Myerson MS, McGarvey W. Disorders of the insertion of the Achilles tendon and Achilles
tendonitis. J Bone Joint Surg. 1998; 80A(12): 1814-1824.
Paavola M, Kannus P, Paakkala T, et al. Long-term prognosis of patients with Achilles

tendinopathy: an observational 8-year follow-up study. Am J Sports Med. 2000; 28(5): 634-642.
Schepsis AA, Jones H, Haas AL. Achilles tendon disorders in athletes. Am J Sports Med. 2002;
30(2): 287-305.
Schepsis AA, Wagner C, Leach RE. Surgical management of Achilles tendon overuse injuries: a
long-term follow-up study. Am J Sports Med. 1994; 22(5): 611-619.
Stephens M. Haglund’s deformity and retrocalcaneal bursitis. Orthop Clin North Am. 1994;
25(1): 41- 46.
1
Ankle Movement Coordination Deficit
"Lateral Ankle Sprain"
ICD-9-CM: 845.02 Sprain of calcaneofibular ligament
Diagnostic Criteria
History: Inversion sprain

Swelling
Pain
If chronic - instability
Physical Exam: Antalgic gait

Lateral ankle effusion
Tender anterior talofibular ligament and possibly also the calcaneofibular lig.
Pain reproduced with inversion stress (usually worse with plantarflexion
and inversion)
If severe sprain, or recurring sprains - laxity with anterior drawer
Anterior Talofibular Ligament
Cues: 1 = Lateral malleolus (fibula); 2 = Anterior talofibular lig.; 3 = Calcaneofibular ligament

Locate lateral malleolus - palpate anteriorly and slightly inferiorly
Palpate using graduated pressure to avoid inadvertent further injury
2
Inversion Stress Test (Talar Tilt)
Cues: Apply graduated force to avoid inadvertent injury

Slightly reproduce reported pain complaint (must not assume all lateral ankle
pain/effusion is from anterior talofibular and/or calcaneofibular ligament tears).
If not symptomatic with gentle inversion – consider tarsal or metatarsal fracture, or
inferior tibiofibular syndesmosis sprain
Anterior Drawer Anterior Drawer
Cues: Either (1) Stabilize tibia and fibula and pull calcaneus and talus anteriorly, or
(2) Bend knee to 90 degrees, place calcaneus on table and hold ankle in about 10
degrees of plantar flexion – push tibia and fibula posteriorly to create a relative
anterior glide of talus
3
Lateral Ankle Sprain

ICD-9: 845.02 sprain of calcaneofibular ligament
Description: Lateral ankle sprains are usually caused by an inversion and plantar flexion injury,
followed by ankle swelling and decreased function. After the initial recovery from a lateral
ankle sprain, some patients exhibit residual pain that limits their activities. Also, some patients
are prone to reinjure the ankle. This re-injury predisposition is thought to be caused by
neuromuscular deficits following the sprain that result in functional instability.
Etiology: With an inversion force of foot, there is injury to anterolateral capsule, anterior
talofibular ligament, and anterior tibiofibular ligament – about 40% of patients will have this
injury type. As the inversion force progresses, the calcaneofibular ligament is injured as well. In
about 58% of cases, there will be a tear of both the anterior talofibular ligament and the
calcaneofibular ligament. Finally, in a small number of cases (3%), there will be tears of the
above two ligament and the posterior talofibular ligaments.
Physical Examination Findings (Key Impairments)
• Severe swelling (more than 4 cm about the fibula)

• Severe ecchymosis
• Loss of function and motion (patient is unable to bear weight or ambulate)
• Positive anterior drawer test
• Inversion will bring on pain and apprehension
• Tenderness over Anterior Talofibular Ligament, Calcaneofibular Ligament, and
Posterior Talofibular Ligament
• Possible anterior shift/displacement of lateral malleolus
• Moderate pain and swelling

• Mild to moderate ecchymosis
• Some loss of motion and function (patient has pain with weight-bearing and
ambulation)
• Mild to moderate instability (mild positive anterior drawer)
• Pain with inversion
• Mild to moderate tenderness with swelling/effusion over the lateral malleolus
4
• Mild tenderness and swelling

• Slight or no functional loss (patient is able to bear weight and ambulate with minimal
pain)
• No mechanical instability (negative anterior drawer test)
• Slight to no apprehension when taken into inversion
5
Goals: Limit effusion

Reduce pain and protect from further injury
Prevent movement induced inflammatory reactions
• Physical Agents
Cryotherapy / Ice
Gentle, active dorsiflexion and plantarflexion in painfree ranges
Progress to ankle pumps, ankle circles, and ankle alphabet
Note: In grade III and severe grade II injuries, AROM exercises for
inversion and plantar flexion should be limited until tenderness over the
ligament decreases in order to avoid disrupting healing structures.
Towel stretch for the calf myofascia
Pain free-isometrics strengthening exercises – all directions
Towel toe curls
Note: Early Mobilization of joints following ligamentous injury actually
stimulates collagen bundle orientation and promotes healing, although full
ligamentous strength is not reestabilished for several months.
Limiting soft-tissue effusion speeds healing.

Fit patient with knee support if pain relief requires temporary use of an external
device
Compression ankle strapping
An ankle brace, such as air cast splint, or a walking boot

Crutch walking for 2-3 days depending on grade of sprain
Wear a brace or have ankle taped when doing activities that have high incidence
of ankle injuries.
Wear correct footwear for each sport
Be aware of uneven terrain, potholes, and high curbs
Turn a light on at night when out of bed
Watch out for slippery floors
6
Goals: Decrease and eliminate pain

Increase pain-free range of motion
Limit loss of strength and proprioception
• Manual Therapy
Manual joint mobilization if dorsiflexion or eversion range of motion is limited
Progress active dorsiflexion / plantarflexion and eversion and inversion in
painfree ranges – add resistance of tolerated (e.g., with rubber tubing or gravity
via toe raises)
Initiate proprioceptive exercises, such as single leg standing, seated BAPS board
– progressing to standing BAPS board type exercises
Goals: Regain full pain-free motion

Regain normal strength
Regain normal proprioception
Gradual return to sport activities through use of functional progression, such as
activity-specific exercise – for example:
Running in pool, swimming
Gradual progression of functional activities
Pain free hopping on both legs progressing to single leg
Stand on toes and hop on toes
Step up / over / forward / sideways on high step pain free
Begin stairmaster, treadmill, biking
Initiate running when fast pace walking is pain free
Figure 8’s, cross-over walking
Jump rope
Ball on wall
Weight bearing wobble board
Heel raises

Reinjury is common with ankle sprains; so external bracing is recommended and
can include taping, lace-up braces, and air splints
7
Intervention for High Performance / High Demand Functioning with Workers or Athletes
Goals: Return to desired occupational or leisure time activities

Prevention of recurring injury
Progress functional activies related to desired sport activity – for example:
Walk-jog, 50/50 backwards, forwards, patterns, circles
Jog-running, backwards, forwards, patterns
Jumping rope single limb
Figure 8’s, cross-over running
Improve strength and endurance through use of progressive resistive training
Consider early mobilization with the movitated athlete. However, when choosing
the specific intervention strategy, consider the patient’s activity level, age, goals
for recovery, degree of injury, previous history of injury, and general motivation.
Selected References
Wolfe MW, Uhl ML, Mccluskey LC. Management of Ankle Sprains. American Family
Physician 2001; 63: 93-104
Young CC. Ankle Sprain. EMedicine Journal 2002; (1) 3
Hammer WI. Functional Soft Tissue Examination and Treatment By Manual Methods. 2nd ed.
Aspen Publishers, Inc. Gaithersburg, Maryland. 1999
Renstrom, PA. Persistently Painful Sprained Ankle. J Am Acad Orthop Surg 1994;2(5):270-280.
Hertel, J. Functional instability following lateral ankle sprain. Sports Med. 2000;29(5):361-71.
Hertel, J; Denegar, CR; Monroe, MM; and Stokes, WL. Talocrural and subtalar joint instability
after lateral ankle sprain. Med Sci Sports Exerc 1999;31(11):1501-8.
Seto, JL; and Brewster, CE. Treatment approaches following foot and ankle injury. Clinics in
Sports Medicine. 1994;13(4):695-719.
Mascaro, TB; and Swanson, LE. Rehabilitation of the Foot and Ankle. Orthopedic Clinics of
North America. 1994;25(1):147-160.
8
Impairment: Limited and Painful Ankle Inversion
Distal Tibiofibular MWM
Cues: Glide the fibula posteriorly on a stable tibia

Sustain the posterior glide while the patient actively inverts his/her foot
As always: 1) alter the direction and amplitude of the glide to achieve painfree active
motion, 2) repeat movement several times (sets of ten) 3) add overpressure, if
indicated, at the end of available painfree active movement

Ankle Nerve Disorder
“Tarsal Tunnel Syndrome”
ICD-9-CM: 355.5 Tarsal tunnel syndrome
Diagnostic Criteria
History: Medial foot pain

Paresthesias
Numbness
Physical Exam: Symptoms reproduced with tibial nerve tension test

Symptoms reproduced with palpation/provocation of tibial nerve in tarsal
tunnel
Tibial Nerve Tension Test
Cues: SLR to first resistance

Full dorsiflex and evert the ankle and foot.
Assess symptom reproduction/elimination with alteration to hip flexion
Provocation of Tibial Nerve in Tarsal Tunnel
Cues: Determine ability to reproduce symptoms

Remember Tom, Dick, “an" Harry
T = Tibialis Posterior
D = Flexor Digitorum Longus
A = Posterior Tibial Artery
N = Posterior Tibial Nerve
H = Flexor Hallucis Longus
Tarsal Tunnel Syndrome
ICD-9: 355.5 tarsal tunnel syndrome
Description: An extrinsic or intrinsic compression neuropathy of the posterior tibial nerve or one
of its branches. Patients with TTS often report 1) burning pain in the heel and medial arch
and/or plantar aspect of the foot, 2) tightness, swelling, and “fullness” in the medial portion of
the foot, and 3) sensory disturbances including burning, tingling, and numbness. Pain located
around the ankle and extending to the toes is increased with walking and is relieved by rest.
Nerve conduction tests demonstrate a time delay across the tarsal tunnel area. EMG may
demonstrate fibrillation potential and positive sharp waves in tibial innervated muscles. MRI
showed TTS abnormality 88% of time. Positive tinel’s sign is a common finding. Mixture of
corticosteroids and local anesthetics may be injected for pain relief. Foot taping and the use to
orthotics may be used to reduce pressure on the nerve. If all other treatment fail, surgery (tarsal
tunnel release) may be necessary to alleviate pain. There is another less common type TTS,
anterior tarsal tunnel syndrome, which entraps the deep peroneal nerve.
Etiology: Any lesion that occupies space within the tarsal region may cause pressure on the
nerve and subsequent symptoms. Examples of intrinsic factors include ganglions, tenosynovitis,
lipomas, varicose veins, fibrosis, and synovial hypertrophy. Extinsic factors may also place
trauma and tension across the flexor retinaculum. Examples include bone fracture, hypertrophic
flexor hallucis tendon, or pronation and subtalar eversion, which can stretch the flexor
retinaculum and cause a narrowing of the tunnel. Half of the patients who present with tarsal
tunnel syndrome relate a history of a previous sprain or ankle fracture. Other causes may include
repetitive stress with activities, flat feet, and excess weight.
Acute Stage/ Severe Condition
• Tenderness over the nerve at the tarsal tunnel

• Positive Tinel sign (percussion over the flexor retinaculum of the tarsal tunnel)
• Diminution of two point discrimination and hypothesisas to pin prick
• With prolonged, extreme compression, nerve demyelination with Wallerian degeneration
may take place with numbness, muscular weakness, and atrophy
Sub Acute Stage/ Moderate condition
As above: Now when less acute, signs of coexisting foot disorders may be revealed, For
example:
• Tight Achilles tendon

• Increased hind foot valgus and the appearance of “too many toes sign”
• Weak or absent inversion of the heel
• Rear foot valgus/calcaneous eversion
• Depressed medial longitudinal arch
• Inability to do unilateral heel raises
• Gait lacks effective push-off
Settled Stage/ Mild condition
As above with the following differences
• Resolving symptoms
• Decreased paresthesia and pain
• Improved pain-free soft-tissue motion along the course of the tibial nerve
• Improved strength of tibialis posterior
• Improved functional activity tolerance; standing and walking
Acute Stage/ Severe Condition
Goal: Reduce pain and inflammation and tissue stress
• Physical Agents
Ice
Contranst baths
Pulsed ultra sound/ phonophoresis with 0.5 percent hydrocortisone or 2.5 percent
lidocane ointment
Iontophoresis
Interferential current therapy
• Orthotics or Taping
University of California Berkeley Laboratory (UCBL) orthosis to improve hind
foot alignment
Ankle braces, controlled ankle motion (CAM) walkers
Plantar arch taping to reduce tissue stress
Medial Heel Wedge or Heel Seat – may assist by inverting the heel and removing
traction from tibial nerve
Advise regarding footgear, such as the use of wider shoes, may be beneficial
• Therapeutic Exercise
Calf stretching exercises
Nerve mobility exercises
• Manual Therapy
Soft tissue mobilization to fascial of myofascial tissues suspected of creating the
entrapment
Neural mobilization
Sub Acute Stage/ Moderate Condition
Goal: Restore muscle strength and flexibility
As above with following differences
Posterior tibialis strengthening exercise
Settled Stage/ Mild Condition
Goal: Normalize strength, flexibility, and restore lower extremity functional mobility
As above with following differences
Posterior tibialis strengthening exercise in weight bearing.
Selected References
Daniels TR, Lau JT, Hearn TC. The Effects of Foot Position and Load on Tibial Nerve Tension.
Foot Ankle International. 1998 Feb; 19(2); 73-8
Meyer J, Kulig K, Landel R. Differential diagnosis and treatment of subcalcaneal heel pain: a
case report. Journal of Orthopaedic & Sports Physical Therapy. 2002; 32(3):114-124.
Kinoshita M MD, Okuda R MD, Morikawa J MD, Tsuyoshi J MD, Abe M MD. The dorsiflexion
test for diagnosis of tarsal tunnel syndrome. Journal of Bone & Joint Surgery. 2001;83-
A(12):1835-1839.
Romani W, Perrin DH, Whiteley T. Tarsal tunnel syndrome: Case study of a male collegiate
athlete. Journal of Sport Rehabilitation. 1997;6:364-370.
Patla CE, Abbott HJ. Tibialis posterior myofascial tightness as a source of heel pain: diagnosis
and treatment. Journal of Orthopaedic & Sports Physical Therapy. 2000;30(10):624-632.
Geideman WM MD, Johnson JE MD. Posterior tibial tendon dysfunction. Journal of

Orthopaedic & Sports Physical Therapy. 2000;30(2):68-77
Kupper, BC. Tarsal tunnel syndrome. Orthopaedic Nursing. 1998;17(6):9-16.
1
Foot Pain
"Pronatory Disorder"
ICD-9-CM: 734 Flat foot (pes planus-acquired)
Diagnostic Criteria
History: Aching in arch of foot - worse after prolonged weight bearing
Physical Exam: Excessive pronation at loading response and mid-stance (talonavicular

joint) terminal stance (calcaneocuboid) joint
Delayed or absent mid-tarsal or forefoot supination (normal = supination
begins immediately following loading response)
Inability to form rigid arch with lower external rotation when weight
bearing or with full calcaneal inversion when non weight-bearing
Tibial Internal Rotation Normal Foot Pronation
Tibial External Rotation Normal Foot Supination
Cues: Pronatory disorder - foot remains pronated with tibial external rotation
2
Longitudinal Mid Tarsal Joint Axis Mobile with Calcaneal Eversion
Longitudinal Mid Tarsal Joint Axis Rigid with Calcaneal Inversion
Cues: Grasp navicular and 1st cuneiform

Supinate and pronate wrist to provide inversion and eversion motion - compare mobility
with full calcaneal eversion and full calcaneal inversion
Normal - LMTJ axis becomes relatively rigid with full calcaneal (subtalar) inversion
3
Oblique Mid Tarsal Joint Axis Mobile with Calcaneal Eversion
Oblique Mid Tarsal Joint Axis Rigid with Calcaneal Inversion
Cues: Grasp cuboid

Move cuboid parallel to the plantar surface of the foot to provide adduction and abduction
motion - compare with full calcaneal eversion and full calcaneal inversion
Normal - OMTJ axis becomes relatively rigid with full calcaneal (subtalar) inversion
4
Pronatory Disorder
ICD-9: 734 flat foot (pes planus-acquired)
Description: Excessive pronation is defined as pronation that occurs for too long a time period
or of too great an amount. The subtalar joint is the most common location of this excessive
motion. The loss of a normal medial longitudinal arch will be evident and may result in a
talonavicular subluxation throughout the stance phase of gait.
Etiology: A pronatory disorder may be caused by congenital, neurological, and/or acquired

factors. The etiology of acquired factors will be discussed here, as the congenital and
neurological causes are listed under a different ICD9 diagnosis.
Acquired factors resulting in excessive pronation can be divided into extrinsic and intrinsic
causes. Extrinsic causes are a result of factors outside the foot/ankle complex such as the lower
leg or knee. Gastocsoleus tightness, femoral anteversion, tibial internal rotation, and postural
deformities are examples of extrinsic factors. Intrinsic causes of pronatory disorders are located
within the foot and ankle region. These causes are usually fixed deformities of the subtalar joint,
the midtarsal joints, and the first ray. It is common to see forefoot valgus (abduction), calcaneal
eversion, a flattened medial longitudinal arch, midfoot ligament laxity, talar subluxation,
posterior tibial tendon dysfunction, and plantarfascia rupture. A combination of extrinsic and
intrinsic factors often results in excessive compensatory subtalar joint pronation. This
compensatory motion may produce various soft tissue stresses resulting in pain, inflammation,
and/or tissue deformity.
• Excessive pronation (navicular drop) at mid-stance and terminal stance

• Forefoot valgus, subtalar pronation, and calcaneal eversion deformities are common
• Limited ankle dorsiflexion and excessive calcaneal eversion are common.
• Weak ankle plantar flexors, ankle/foot inverters (tibialis posterior) and ankle/foot
everters (peroneus longus - aka fibularis longus), and intrinsic pedal musculature
(abductor hallucis) are common.
• Excessive midtarsal motions (hypermobile talonavicular, calcaneocuboid
articulations, and excessive first ray dorsiflexion).
• Palpable tenderness of the peroneal tendons, tibialis posterior tendon, tarsal
ligaments, and talonavicular and calcaneocuboid articulations
• Other dysfunctions in the lower kinematic chain (i.e. knee, hip) are commonly
associated with excessive subtalar pronation.
5
• The above impairments may be present – however with less severe functional limitations.
• The above impairments may be present – however with less severe functional limitations.
6
Goal: Restore pain free performance of daily activities
• Physical Agents
Ultrasound
Phonophoresis
Electrical Stimulation
Ice
• Manual Therapy
Joint mobilization for restricted accessory movements associated with talocrural
dorsiflexion and talocalcaneal eversion
Soft tissue mobilization for restricted posterior calf myofascia
Strengthening exercises for weak calf muscles and foot intrinsics
Stretching for tight calf muscles
Instruct in exercises and functional movements to maintain the improvements in
mobility gained with joint and soft tissue manipulations

Anti-pronation type taping procedures
In-shoe orthotics to stabilize the hindfoot and medial longitudinal arch

Proper footgear and/or inserts to limit pronation
Goals: Restore pain free performance of functional activities

Improve foot proprioception/afferent activity
Normalize ankle and foot mobility and strength
• Neuromuscular Re-education
Training for neutral foot position with daily activities – including single leg standing
activities with/without unstable surfaces or visual cuing
7
Goal: Return patient to prior level of function or desired functional goals
Progress stretching and strengthening exercises – include exercises that address
impairments of the pelvis, hip, and knee which may be associated with excessive
pronation, such as weak hip abduction and external rotation
• Neuromuscular Re-education
Progress neutral foot position training

Consider foot orthotic prescription/fabrication
Intervention for High Performance / High Demand Functioning in Workers or Athletes
Goal: Return to desired work or sport specific activity levels
Progress stretching and strengthening exercises – include exercises/activities that
challenge the patient with work related or sport specific demands addressing
strength, flexibility, proprioception and endurance.
Selected References
Bennett JE, Reinking MF, Pluemer B, Pentel A, Seaton M, Killian C. Factors contributing to the
development of medial tibial stress syndrome in high school runners. J Orthop Sports Phys
Ther. 2001;31(9):504-510.
Boerum DH, Sangeorzan, BJ. Biomechanics and pathophysiology of flat foot. Foot Ankle Clin
N Am. 2003(8):419-430.
Donatelli R. Orthopaedic Physical Therapy. Second Edition. Churchill Livingstone inc. 1994.
Donatelli R. Normal biomechanics of the foot and ankle. J Orthop Sports Phys Ther.
1985;7(3):91-95.
Elftman NW. Nonsurgical treatment of adult acquired flat foot deformity. Foot Ankle Clin N
Am. 2003(8):473-489.
8
Fiolkowski P, Brunt D, Bishop M, Woo R, Horodyski M. Intrinsic pedal musculature support of
the medial longitudinal arch: an electromyography study. J Foot Ankle Surg. 2003;42(6):327-
333.
Glasoe WM, Yack HJ, Salzman CL. Anatomy and biomechanics of the first ray. Physical
Therapy. 1999;79(9):854-859.
Greisberg J, Hansen ST, Sangeorzan B. Deformity and degeneration in the hindfoot and midfoot
joints of the adult acquired flatfoot. Foot Ankle Int. 2003;24(7):530-534.
Hintermann B, Boss A, Shäfer D. Arthroscopic findings in patients with chronic ankle

instability. Am J Sports Med. 2002;30(3):402-409.
Holmes CF, Wilcox D, Fletcher JP. Effect of a modified, low-dye medial longitudinal arch
taping procedure on the subtalar joint neutral position before and after light exercise. J Orthop
Sports Phys Ther. 2002;32(5):194-201.
Imhauser CW, Abidi NA, Frankel DZ, Gaven K, Siegler S. Biomechanical evaluation of the
efficacy of external stabilizers in the conservative treatment of acquired flatfoot deformity. Foot
Ankle Int. 2002:22(8):727-737.
Munn J, Beard DJ, Refshauge KM, Lee RYW. Eccentric muscle strength in functional ankle
instability. Med Sci Sports Exerc. 2003;35(2):245-250.
Nakamura H, Kakurai, S. Relationship between the medial longitudinal arch movement and the
pattern of rearfoot motion during the stance phase of walking. J Phys Ther Sci. 2003;15(1):13-
18.
Ogon, M. Does arch height affect impact loading at the lower back level in running? Foot Ankle
Int. 1999;20(4):265-269.
Root ML, Orien WP, Weed JH. Normal and abnormal function of the foot: Clinical
Biomechanics. Vol. 2. 1997.
Shrader JA, Siegel KL. Nonoperative management of functional hallus limitus in a patient with
rheumatoid arthritis. Physical Therapy. 2003;83(9):831-843.
Snook AG. The relationship between excessive pronation as measured by Navicular drop and
isokinetic strength of the ankle musculature. Foot Ankle Int. 2001;22(3):234-40.
Staheli L, Chew D, Corbett M. The Longitudinal Arch. A survey of eight hundred and eighty-
two feet in normal children and adults. J Bone Surg. 1987;69a:426-428.
Vicenzino B, Griffiths SR. Effect of antipronation tape and temporary orthotic on vertical
navicular height before and after exercise. J Orthop Sports Phys Ther. 2000;30(6):333-9.
Wenger DR, Mauldin D, Speck G, Morgan D, Lieber RL. Corrective shoes and inserts as
treatments for flexible flatfoot in infants and children. J Bone Joint Surg Am. 1989;71(6):800-
10.
SUMMARY OF ANKLE AND FOOT DIAGNOSTIC CRITERIA AND PT MANAGEMENT STRATEGIES
DISORDER HISTORY PHYSICAL EXAM PT MANAGEMENT

Ankle & Foot Mobility Deficits Arch area pain SR w/: End range accessory motion Joint Mob (to specific hypomobility)
Recent strain or repetitive wt. Test of one or more of the Ther Ex’s
“Midtarsal Joint Capsulitis” bearing midtarsal articulations (Stretch/strengthen related muscles)
Sx’s worse w/ SLS or prolonged Taping/footgear/orthotics
wt. bearing
Ankle & Foot Mobility Deficits Stiffness ROM deficit: 1st MTP extension Joint Mob
Hallux Rigidus Pain at “toe-off” phase of gait Pain at end range of 1st MTP ext. Ther Ex’s
Limited MTP accessory movements Patient Ed: Proper footgear
Ankle Muscle Power Deficits Gradual onset of Achilles area Swelling 1-2 inches above Achilles Activity modification
aching insertion Proper footgear and/or heel lift
Achilles Tendinitis Sx’s worse with activity SR w/palpation of tendon in same area Calf stretching
Strengthening – esp. eccentric
Ankle Muscle Power Deficits Posterior heel pain Swelling near Achilles insertion Physical agents
Swelling SR w/provocation of insertion on (Ice, US, Phono, Ionto)
“Posterior Calcaneal Bursitis” Irritated by pressure, i.e., from a posterior aspect of calcaneus Activity and Shoe Modifications
shoe
Ankle Movement Coordination Inversion stress Antalgic gait P.R.I.C.E. Instructions
Deficit Swelling Lateral ankle effusion Physical agents (Ice, E. Stim,)
Pain SR w/: Palpation of lateral ligaments Friction massage
“Lateral Ankle Sprain” If chronic – instability Inversion stress Inferior Tib-Fib Mobs
May have laxity w/anterior drawer Proprioceptive Training
Calf stretching
Functional Strengthening
Ankle & Foot Radiating Pain Medial foot pain SR w/: Tibial Nerve bias LLTT Rx entrapment
Paresthesias Provocation of Tibial Nerve in (STM/JM to Med. Ankle and Foot)
Tarsal Tunnel Syndrome Numbness Tarsal Tunnel Tibial Nerve Mob
(PROM and AROM Ex’s)
Foot Pain Aching in arch of foot Excessive pronation at LR, MSt, or Joint mob/manip (to hypermobile of
Sx’s worse after prolonged weight TSt subluxed tarsal articulations)
“Pronatory Disorder” bearing Deficient Midtarsal supination or Ther Ex’s (stretch shortened and
Forefoot eversion at TSt strengthen weak myofascia of LE)
Inability to form arch w/tibial external Taping
rotation and calcaneal inversion Proper footgear or orthotics
Joe Godges DPT KPSoCal Ortho PT Residency

1
Achilles Tendon Repair and Rehabilitation
Surgical Indications and Considerations
Anatomical Considerations: The poorest blood supply to the Achilles tendon is in the central
part of the tendon – approximately 2 to 6 cm proximal to the calcaneal insertion – which may
account for the fact that most of the ruptures occur in this area.
Pathogenesis: Tendons rupture when the mechanical loads exceed the physiologic capacity of
the tendon. The physiologic capacity of the Achilles tendon may be compromised by intrinsic
factors such as hypovascularity, repetitive microtrauma and the associated inflammation and
degeneration, endocrine function and nutrition. Extrinsic, mechanical forces may also exceed
the physiologic capacity of the Achilles tendon, such as when 1) an individual forcefully pushes
off the forefoot while extending the knee (e.g., when cutting, sprinting or jumping), 2) an
individual experiences a sudden dorsiflexion with full weightbearing (e.g., a slip, fall, or sudden
deceleration), or 3) an individual experiences violent dorsiflexion when jumping from a height
and landing on a plantar-flexed foot.
Epidemiology: Achilles tendon ruptures are one of the most frequently ruptured tendons – about
40% or all tendon ruptures are of the Achilles. Most Achilles tendon ruptures occur in male,
recreational athletes between the ages of 30 and 40 years. Athletic activities that require sudden
acceleration or deceleration are most likely to cause a rupture. Ruptures not attributed to athletic
activity are usually caused by falls or stumbles that also produce sudden acceleration and
deceleration movements.
Diagnosis
• Most patients describe a “pop” as though someone has shot them in the back of the ankle
• Palpable defect in the tendon between 2 to 6 cm proximal to the calcaneus
• Positive Thompson’s test
• Radiograph’s rule out bony injury
• MRI can be helpful in demonstrating the presence, location, and severity of the tear(s)
Nonoperative Versus Operative Management: Surgical repair is typically recommended for

patients who expect to return to relatively high functional activities required of recreational
athletics. Surgical repairs allow quicker mobilization and return to activity – thus lessening the
deleterious effects on prolonged cast immobilization with the ankle in a plantarflexed position.
The main surgical risk is wound infection and breakdown, which can be a distrastrous
complication because soft tissue coverage can only be resolved with vascularized flaps and a
reconstructive tendon procedure will likely be required. Indications for nonoperative
management include patients with poor wound healing potential (e.g., those with moderately
severe diabetes), concomitant illnesses, a sedentary lifestyle or lower functional/athletic goals.
The prolonged cast immobilization required of nonoperative management promotes the
2
following common problems associated with immobilization: muscle atrophy, joint stiffness,
cartilage atrophy, degenerative arthritis, adhesion formation, and deep venous thrombosis. The
average re-rupture rate is about 18% in nonoperative patients compared with approximately 2%
in operatively treated patients.
Surgical Procedure: Surgery is usually performed about one week after rupture. This delay
allows consolidation of the tendon ends, making the repair technically easier. Various suture
techniques have been described to approximate the ruptured ends of the tendon. Augmentations
using either the plantaris tendon or gastrocnemius fascia flaps have also been described.
Mandelbaum et al promotes the use of a Krackow modified suture technique to provide a
stronger fixation – thus, allowing an accelerated rehabilitation emphasizing early motion, weight
bearing and conditioning in motivated, higher-level athletes. Neglected acute ruptures or re-
ruptures may require reconstruction using endogenous materials (e.g., fascia lata, peroneus
brevis transfer) or exogenous materials (e.g., carbon fiber, Marlex mesh, Dacron vascular graphs,
polypropylene braid).
Preoperative Rehabilitation
• Further injury protection using a splint or cast – with the ankle in about 20o or
plantarflexion
• Instruction in use of crutches to maintain the desired non-weight bearing or partial weight
bearing status
• Instructions/review post-operative rehabilitation plan
POSTOPERATIVE REHABILITATION
Note: The following rehabilitation progression is a summary of the guidelines provided by

Mandelbaum, Gruber, and Zachazewski. Refer to their publication to obtain further
information regarding criteria to progress from one phase to the next, anticipated
impairments and functional limitations, interventions, goals, and rationales.
Phase I for Traditional Immobilization and Rehabilitation: Weeks 1-4
Goals: Control edema and pain

Protect repair
Minimize deconditioning
Intervention:
• Cast with ankle in plantarflexion

• Elevation and ice
• Instruct and monitor non-weight-bearing crutch ambulation
• General cardiovascular and muscular conditioning program
3
Phase II for Traditional Immobilization and Rehabilitation: Weeks 5-8
Goals: Control any residual symptoms of edema and pain

Continue to protect repair
Progressive weightbearing status
Intervention:
• Re-casted with ankle in neutral dorsiflexion

• Instruct in progressive weight-bearing, as allowed, using the appropriate assistive devices
and encouraging normal gait mechanics
• Modify/progress cardiovascular and muscular conditioning program
Phase III for Traditional Immobilization and Rehabilitation: Weeks 9-16
Goals: Normal gait mechanics

Limit scar tissue adhesions
Full range of motion (ROM)
Improve strength of all ankle and foot musculature
Modify/progress cardiovascular and muscular conditioning program
Intervention:
• Gait training – use a the appropriate height heel lift, if necessary, to attain normal loading
response and stance phase mechanics
• Soft tissue mobilization to hypomobile tissue in superficial fascia near surgery site and to
shortened posterior calf myofascial
• Joint mobilization to hypomobile accessory motions of the talocrural, talocalcaneal, and
mid-tarsal articulations
• Progressive passive stretching to painfree tolerance
• Active range of motion (AROM) exercises, isometric exercises, progressing to resisted
exercises using tubing or manual resistance – to all weakened ankle and foot musculature
• Modify/progress cardiovascular and muscular conditioning
4
Phase IV for Traditional Immobilization and Rehabilitation: Weeks 17-20
Goals: Normal gait mechanics for walking and running on level surfaces
Symmetric ankle mobility and single-leg proprioception
Improved ability to perform repeated single leg heel raises
Initiate sport-specific or job-specific skill development
Intervention:
• Continue intervention strategies listed in Phase III as indicated by remaining impairments

• Progress stretching exercises to initiate body weight stretching over incline or wedge
• Progress resistive exercises to body weight exercises such as repeated heel raises (if no
increase in symptoms occurs with previous exercises)
• Progress proprioceptive and balance training to include pertabative surfaces (such as a
wobble board) or advanced single-leg balance activities
• Near the end of phase IV, begin running progression and/or sport-specific or job-specific
skill development
Phase I for Early Motion and Rehabilitation: Day 1-7
Goals: Prevent wound complications

Control edema and pain
Active dorsiflexion to –5o
50% of active plantar flexion (compared to opposite side)
Intervention:
• Instruct in surgical site protection

• Toe curls, ankle pumping (full active dorsiflexion and plantar flexion – out of splint - by
day 3)
• Instruct and monitor non-weight-bearing crutch ambulation
5
Phase II for Early Motion and Rehabilitation: Weeks 2-8
Goals: Active dorsiflexion to 0o by week 4

Active dorsiflexion to +5o by week 8
Full weight bearing beginning on day 14
Normal gait mechanics on level surfaces without brace by end of week 8
Initiate progressive resistive training program for the gastrocnemius-soleus complex
Intervention:
• Pool therapy – walk or run under full buoyancy conditions (non-weight bearing only),
heel raises in chest deep water after Week 5
• Ankle AROM (out of splint) exercises
• Initiate gentle passive dorsiflexion stretching with towel or strap after Week 3
• Initiate gentle, painfree, weight-bearing dorsiflexion starting at Week 5
• Gait training wearing protective splint – with weight bearing to tolerance until Week 5
• Gait training out of walking splint to painfree tolerance starting at Week 5
• Painfree resistive ankle exercises using elastic tubing or band
• Initiate double-leg heel raises at Week 5
• Initiate single-leg heel raises in chest-deep water after Week 5
• Initiate submaximal isokinetic dorsiflexion and plantarflexion – emphasizing endurance
• Cardiovascular conditioning on stationary bicycle to painfree tolerance using walking
splint until Week 5 – without splint to painfree tolerance starting at Week 5
• Resistive exercises for unaffective muscle groups
Phase III for Early Motion and Rehabilitation: Weeks 9-20
Goals: Normal gait mechanics for all activities of daily living

Normal ankle and foot ROM
Ability to perform repeated single-leg heel raises
Fast walking, progressing to slow jogging, progressing to sport-specific or job specific
skill development – all to painfree tolerance
Intervention:
• Continue intervention strategies listed in Phase II as indicated by remaining impairments

• Pool therapy – walking, gentle hopping and jumping in waist deep water
• Gait training – progress to treadmill walking on level surfaces and later on a slight
incline, gradual progressing to jogging if symptom free – and – progress to skiping,
hopping, and easy jumping after Week 17. Careful not to progress gait or sport specific
training too soon and accentuate the risk of re-rupture.
• Progress submaximal isokinetic dorsiflexion and plantarflexion – emphasizing endurance
• After Week 17, develop and individualized strength and flexibility program to address
6
remaining impairments on the involved and uninvolved lower extremities. Then,

gradually initiate a functional training program – leading toward the ability to perform
the desired sport-specific or job-specific skills.
Selected References:
Mandelbaum B, Gruber J, Zachazewski J. Achilles Tendon Repair and Rehabilitation. In Maxey

L, Magnusson J, eds., Rehabilitation for the Postsurgical Orthopedic Patient. St. Louis, Mosby,
2001.
Certi R, Steen-Erik C, Ejsted R, Jensen NM, Jorgensen U. Operative versus nonoperative

treatment of Achilles tendon rupture. A prospective randomized study and review of the
literature. Am J Sports Med. 1993;21:791-799.
Curwin S. Tendon injuries. Pathology and Treatment. In Zachazewski JE, Magee DJ, Quillen
WS, eds., Athletic Injuries and Rehabilitation. Philadelphia, WB Saunders, 1996.
Kannus P, Jozsa L. Histopathological changes preceding spontaneusos rupture of a Achilles

tendon. J Bone Joint Surg. 1991;73A:1507-1525.
Lagerrgren C, Lindholm A. Vascular distributon in the Achilles tendon. an arteriographic and

microangiographic study. Acta Chir Scand. 1958;116:491-495.
Mandelbaum BR, Myerson MS, Forster R. Achilles tendon ruptures. a new method of repair,
early range of motion, and functional rehabilitation. Am J Sports Med. 1995;23:392-95.
1
Ankle – Open Reduction Internal Fixation
Anatomical Considerations: Damage to neurovascular and tendonous structures must be

considered with ankle fractures. Medially, the posterior tibial artery, tibial nerve, posterior tibial
and flexor tendons, and deltoid ligament are subject to trauma. Laterally, the peroneous
longus/brevis tendons, lateral collateral ligaments, superficial peroneal nerve and sural nerve are
potentially at risk.
Pathogenesis: Ankle fractures result from similar mechanisms as ankle sprains. For example,
an inversion injury may result in a medial malleolus fracture as well as a sprain of the lateral
collateral ligaments. In contrast, an eversion injury may fracture the lateral malleolus and sprain
the medial deltoid ligament. Ankle fractures are based on the classification system developed by
Lauge-Hansen in 1948. The classification system has five groups of ankle fractures and is
dependent on the foot position and direction of force when the injury occurred. It also indicates
the injured structures. Since the mechanism of injury for ankle sprains and fractures is virtually
the same, ankle sprains that do not respond to conservative treatment after 4 to 5 weeks should
be reevaluated for a fracture.
Lauge-Hansen Classification (Lesic & Bumbasirevic)

Type of Fracture Stage Injured Structures
Supination-adduction 1 Avulsion fracture of the lateral malleolus
Supination-adduction 2 Vertical fracture of the medial malleolus
Supination-eversion 1 Lesion of the anterior tibiofibular ligament
Supination-eversion 2 Oblique fracture of the lateral malleolus
Supination-eversion 3 Posterior malleolus fracture or rupture of the
posterior tibiofibular ligament
Supination-eversion 4 Fracture of the medial malleolus or rupture of
the deltoid ligament
Pronation-abduction 1 Transverse avulsion fracture of the medial
malleolus
Pronation-abduction 2 Rupture of tibiofibular ligaments
Pronation-abduction 3 High transverse bending fracture of the lateral
malleolus
Pronation-eversion 1 Rupture of deltoid ligament or avulsion fracture
of the medial malleolus
Pronation-eversion 2 Failure of the anterior tibiofibular ligament
Pronation-eversion 3 Oblique or spiral fibular fracture
Pronation-eversion 4 Disruption of the posterior tibiofibular ligament
or fracture of the third metatarsal
Pronation- 5 Pilon fractures stages 1/3
dorsiflexion
2
Epidemiology: Ankle fractures are one of the most common injuries in the lower extremity
occurring at a rate of 107 fractures per 100,000 persons per year. Young athletic males and
middle age women are most commonly affected. Talus fractures represent 3% of foot fractures
and tend to be associated with high-energy traumas such as a fall from a height or a motor
vehicle accident. Eversion fractures are the most common whereas pronation-dorsiflexion
(pilon) fractures are the rarest but more severe.
Diagnosis:
Physical Examination:
• Acute trauma
• Pain with weight bearing
• Local tenderness
• Instability
• Obvious swelling- Ankle effusion of 13 mm or more has been shown to be indicative of a
fracture with an 82% predictive value.
Radiological Examination: Plain film radiographs using a minimum of three views

(anterior-posterior, lateral and mortise view with the foot internally rotated 15o) are used.
Magnetic Resonance Imaging may be utilized if ligamentous, tendon or chondral lesions are
suspected. Computed tomography is also used in complex fractures to better identify
fracture comminution and displacement as well as soft tissue injury.
The following radiological criteria are used to assess ankle integrity:
• The medial joint space measures less than 4 mm.
• There is less than 5 mm of interosseous clear space.
• The anterior tibial tubercle and fibula overlap at least 10mm.
• Normal talcrural angle is 83o + 4o
• 0o of talar tilt allowing for 5o of difference between the two joints.
• The tibiotalar line must pass through both the center of the tibia and the talus on anterior-
posterior and lateral views.
Nonoperative Versus Operative Management: Nonoperative versus operative treatment depends

on the type of fracture (displaced versus nondisplaced), skin integrity, circulation status as well
as the patient's age and current health. Stable, nondisplaced fractures are typically treated
conservatively with immobilization. Some displaced fractures may undergo closed reduction
under general or spinal anesthesia if possible. Some indications for conservative treatment
include: peripheral vascular disease, peripheral neuropathy, diabetes mellitus, poor health, age,
sedentary lifestyle, open wounds, infections, paraplegia, and debilitated mental status (i.e. ability
to maintain weight-bearing status post-operatively). The patient is typically nonweight-bearing
in a cast for 3-4 weeks and may then be weight-bearing as tolerated or partial weight-bearing in a
walking cast for another 8-12 weeks depending on the stability of the fracture.
Open reduction internal fixation is indicated in unstable, displaced fractures especially if
the talus is subluxed. Pronation type fractures are typically treated with open reduction and
internal fixation whereas supination/eversion type fractures can be treated either conservatively
or surgically with about equal results.
3
Fractures and dislocations should be reduced as quickly as possible to prevent circulatory

impairments and neuropraxia. Swelling and inflammation severely limit reduction. Depending
on the extent of the fracture, pins, screws, plates and intramedullary nails and rods are used to
secure the fracture site(s). The surgical approach depends on the location of the fracture.
Phase I: Weeks 1-4
Goals: Decrease pain and edema

Protect surgical repair
Maintain/improve general cardiovascular and muscular fitness
Intervention:
• Ice and elevation

• Gait train nonweight-bearing with crutches/front wheeled walker. Step/stair training as
needed
• Immobilize with below-the-knee plaster cast with ankle in neutral
• General cardiovascular and total body strengthening program
Phase II: Weeks 5-10
Goals: Control pain and edema

Protect surgical repair
Gradually progress weight-bearing status
Increase ankle plantarflexion/dorsiflexion range of motion
Intervention:
• Continue gait training as weight-bearing status changes (walking cast to short leg
walking brace) with assistive device as needed
• Compression garments as needed to control edema
• Begin active and passive ankle dorsiflexion and plantarflexion
• General cardiovascular and total body strengthening program
4
Phase III: Weeks 10-14
Goals: Control edema

Full ankle range of motion
Normalize gait
Increase strength
Intervention:

• Continue range of motion exercises adding ankle inversion/eversion
• Lower extremity stretching focusing on the gastrocnemius/soleus complex (may begin
with passive seated towel stretch and progress to standing)
• Begin ankle/foot strengthening (begin with isometric progressing to isotonic with
theraband to standing ankle dorsiflexion/plantarflexion)
• Scar mobilization and desensitization
• Joint mobilization to decrease capsular tightness
• General cardiovascular and strengthening program
Phase IV: Week 14-24
Goals: Increase ankle muscle strength/endurance

Increase balance/proprioception/neuromuscular control
Begin sport/job specific activities
Normalize gait/running on varied surfaces
Intervention:
• Continue to progress lower extremity stretching and strengthening

• Balance/proprioception exercises on varied surfaces/conditions (single leg stance/tandem,
compliant/noncompliant surface, eyes open/closed)
• Gait training/running on varied surfaces and inclines
• General cardiovascular and strengthening program
• Sport/job specific skill training
5
Bernier J, Sieracki K, Levy L. Functional rehabilitation of the ankle. Athletic Therapy Today.
2000;23:38-44.
Hannu L, Teppo J, Seppo H, Markku N, Kimmo V, Markku J. Use of a cast compared with a
functional ankle brace after operative treatment of an ankle fracture. JBJS. 2003;85:205-215.
Lesic A, Bumbasirevic M. Ankle fractures. Trauma. 2004;2(1).
Nilsson G, Nyberg P, Ekdahl C, Eneroth M. Performance after surgical treatment of patients

with ankle fractures – 14-month follow-up. Physiotherapy Research International. 2003;8:69-
82.
Prentice W. Ankle fractures and dislocations. In Malinee V, Reed S, eds., Rehabilitation

Techniques. Boston, McGraw-Hill, 1999.
1
Talar Fracture Repair and Rehabilitation
Anatomical Considerations: The talus is made up of a body (consisting of a dome, central

portion, a lateral process, and a posterior process. Along with that is the talar neck and head.
There are no tendons attached to the talus, it is held by ligamentous as well as bony structures. It
articulates with the tibia, medial and lateral malleoli, calcaneus, and the navicular bone. The
talus has a rich vascular network made up of three main arteries, the posterior tibial artery,
anterior tibial artery, and peroneal artery.
Pathogenesis: Decreased osteoblast activity in the bone makes it become weak to stresses
placed on it. Strong axial and shear forces accompanied with activity or trauma can cause bones
in the body to break. Therefore talar fractures usually occur with a severe impact like trauma to
an either dorsiflexed foot or with an increased load on a hyper-plantar flexed foot. Examples
range from involvement in a motor vehicle accident to forces produced by ballerinas while
dancing.
Epidemiology: Talar fractures are quite rare, they account for about 0.14% - 0.32% for all
fractures throughout the body. Of all foot fractures talar fractures make up about 3-5%, but they
can be underreported. Roughly about 50% of the fractures of the talus involve the talar neck.
Fractures of the main portion of the talar body and of the talar head are uncommon. Fractures of
the talar dome, lateral process, and posterior process occur primarily in young athletes. But
other talar fractures can occur at any age, primarily from a motor vehicle accident or a fall from a
height.
Diagnosis:
• Chronic ankle pain and non-union can be present after an undetected fracture that is
misdiagnosed as a “chronic ankle sprain”.
• Patient may complain of chronic hindfoot pain.
• Possible tear of lateral collateral ligament or injury to flexor hallucis longus.
• Plain radiographs of the foot and ankle are use to diagnose a talar fracture.
• A CT Scan is used to evaluate displacement of the bone and plan for surgery.
• MRI and CT are used to diagnose clinically occult fractures.
2
Hawkins Classification of Talar Neck Fractures
Radiographic findings Risk of AVN*
Type I Nondisplaced fracture line 0-13%
Type II Displaced fracture, plus subluxation or 20-50%

dislocation of subtalar joint
Type III Displaced fracture, dislocation subtalar 69-100%

AND tibiotalar joints
Type IV Displaced fracture and disruption of talonavicular joint high

*AVN=Avascular necrosis
Nonoperative vs. Operative Management: There is a general consensus that dislocated talar
fractures should be operated on. The collapse rate of the talus has been shown to be lowered due
to surgical intervention. Surgical repair allows better healing and decreases the chance of any
further complications such as avascular necrosis or severe arthrosis of the ankle. Immediate
reduction of fracture dislocations is essential to preserve blood supply to the talus and to also
avoid secondary soft tissue edema. Unlike non-operative treatment it also permits early
mobilization of the joint. Indications for non-operative treatment are used solely for undisplaced
talar fractures. If stable fixation with surgical treatment is not used than prolonged
immobilization of the ankle is used. A non-weight bearing status is usually preferred. Due to
the long term immobilization of the ankle significant problems can arise such as secondary
arthrosis, muscle atrophy, and cartilage atrophy (with 2/3 of the bone surface being covered by
cartilage).
Surgical Procedure: According to both Kundel and Frawley et al careful closed fracture
reduction should be attempted as early as possible during assessment in the emergency room.
Most of the blood supply runs along the neck of the talus, with the neck being the most common
fracture site. Immediate reduction of fracture dislocations is vital to maintain blood supply to the
talus and therefore the antero-medial approach is usually preferred. The approach goes from the
navicular to the medial malleolus between the tibialis anterior and the tibialis posterior tendons.
K-wire transfixation of a mobile fragment can be used to maintain the reduction during the
insertion of usually 2 titanium screws. Open reduction along with stable internal fixation of a
talar fracture can speed along recovery. Earlier motion is then achieved leading to increased
weight bearing status as well as preservation of the blood supply to help with healing and post-
operative rehabilitation.
3
Preoperative Rehabilitation:
• Immobilization of ankle with temporary splint or cast before surgery is performed in the
emergency room.
• Instruction in assistive device for ambulation while maintaining a non-weight bearing
status.
• Instruction and review of post-operative rehabilitation.
Phase I for Early Motion and Rehabilitation: Week 1-6
Goals: Initiate early active motion

Control edema and pain
Maintain motion of affected/unaffected joints in the foot
Intervention:
• Surgical scar protection

• Mobilization to ankle/foot to increase joint mobility
• Elevation with intermittent ice compression
• Active ROM exercises (i.e. ankle pumps) to increase circulation to the foot and promote
cartilage healing
• PROM to joints of the ankle/foot (increase ROM, control pain, once edema is lowered)
• Instruction in non-weight bearing crutch ambulation
Phase II for Early Motion and Rehabilitation: Weeks 6-8
Goals: Partial weight bearing

Prevention of necrosis of the talus
Continue with joint mobilization in Phase I as needed
Increase AROM to 50-75% of normal
Intervention:
• Initiate instruction in partial weight bearing restriction with crutch ambulation.

• Patient performing PROM exercises actively to ankle.
• Aquatic therapy – ambulation in waist to chest high water (partial wt. bearing).
• Instruction in donning and doffing walking boot.
• Pain free open chain exercises with band.
• Stationary bike to pain free tolerance without walking boot.
4
Phase III for Early Motion and Rehabilitation: Weeks 12-24
Goals: Full weight bearing at 12 weeks

Normal ankle/foot ROM
Normal gait mechanics without walking boot
Intervention:
• Initiation of gait training in parallel bars

• Progressive resistive strengthening of ankle musculature with band
• Proprioceptive weight bearing activities for balance
• Gait training on treadmill with progression to incline surface
• Single leg support activities
• Fast walking with progression to jogging for patient specific activities
Crim J. Talus Fractures.July 13, 2004.http://www.emedicine.com/radio/topic672.htm#target24.
Low CK, Chong CK , Wong HP, Low YP. Operative treatment of displaced talar neck fractures.
Ann Acad Med Singapore. 1998;27:763-766.
Cronier P, Talha A, Massin P. Central talar fractures – therapeutic considerations. Int J Care
Injured. 2004; 35:S-B10 – S-B22.
Schulze W, Richter J, Russe O, Ingelfinger P, Muhr G. Surgical treatment of talus fractures. a

retrospective study of 80 cases followed for 1-15 years. Acta Orthop Scand. 2002;73:344-351.
1
Syndesmosis Ankle Sprains
ICD 9 code: 719.47 Pain in joint involving ankle and foot
Description: The mechanism of injury for syndesmotic ankle sprains can be difficult to
isolate as there are different anatomic structures involved, depending upon the
mechanism of injury. The manner in which these structures can be injured may involve
3 planes of motion. There are 3 proposed mechanisms on injury for the syndesmotic
ankle sprain. These include external rotation of the foot, eversion of the talus within the
ankle mortise, and excessive dorsiflexion. These mechanisms of injury vary significantly
from the typical lateral ankle sprain, in which the ankle and foot are plantarflexed and
inverted. Forceful external rotation of the foot results in widening of the ankle mortise.
Additionally, elevated forces with eversion of the talus can widen the mortise. Finally,
forceful dorsiflexion may widen the ankle mortise with the wider anterior aspect of the
talar dome entering the joint space. With all the above scenarios, the distal fibula is
forced laterally away from its articulation with the distal tibia.
Etiology: The mechanism of injury dictates which structures are involved with the
sydesmotic ankle sprain. The three major ligaments involved are the anterior inferior
tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), and
the interosseous ligament. Syndesmotic ankle sprains may coexist with traditional ankle
sprains, as well as deltoid ligament injuries, or occur independently. Research has shown
that between 1% and 18% of all ankle sprains involve injury to the syndesmosis. Patients
with incomplete syndesmotic ankle sprains, on average, require 55 days to recover. This
period of time is almost twice the recovery period for patients with third degree lateral
ankle sprains.
• Severe swelling
• Severe ecchymosis
• Loss of function and motion (patient may have heel raise gait pattern in order
to avoid dorsiflexion at terminal stance)
• Positive External Rotation Test, Squeeze Test, or Point Test
• Dorsiflexion may bring on pain and apprehension
• Tenderness over Anterior Inferior Tibiofibular Ligament, Posterior
InferiorTibiofibular Ligament, or Interosseous Ligament
• Possible lateral and/or anterior shift/displacement of lateral malleolus
2

• Mild to moderate ecchymosis
• Some loss of motion and function (patient has pain with weight-bearing and
ambulation)
• Mild to moderate instability
• Pain with dorsiflexion and/or external rotation of the foot
• Mild to moderate tenderness with swelling/effusion over the above mentioned
ligaments
• Mild tenderness and swelling

• Slight or no functional loss (patient is able to bear weight and ambulate with
minimal pain)
• No mechanical instability (ER test and squeeze tests are negative
• Slight to no apprehension when taken into external rotation or dorsiflexion
• Pain & Edema Control

Physical Agents: pain and swelling control; rest, ice compression, and
elevation (RICE), electrical stimulation, toe curls, ankle pumps
Note: Early Mobilization of joints following ligamentous injury actually
stimulates collagen bundle orientation and promotes healing, although
full ligamentous strength is not reestabilished for several months.
Limiting soft-tissue effusion speeds healing.
• Temporary stabilization (ie, short leg cast, splint, brace)

• Non-weight bearing with crutches
• Partial weight-bearing without pain

• Low-level balance training:bilateral standing activity or standing on balance
pad
• Lower-level strengthening with Theraband
• Manual Therapy to restore accessory and physiological mobility deficits
3
• Unilateral balance training

• Progress from double heel raises to single heel raises
• Treadmill walking with progression to fast walking
Gradual return to sport activities through use of functional progression,
such as activity-specific exercise – for example:
Running in pool, swimming
Stand on toes and hop on toes
Step up / over / forward / sideways on high step pain free
Begin stairmaster, treadmill, biking
Figure 8’s, cross-over walking
Jump rope
Ball on wall
Weight bearing wobble board
Heel raises
Reinjury is common with ankle sprains; so external bracing is
recommended and can include taping, lace-up braces, and air splints
Intervention for High Performance / High Demand Functioning with Workers or Athletes
Goals: Return to desired occupational or leisure time activities

Prevention of recurring injury
Progress functional activies related to desired sport activity – for example:
Walk-jog, 50/50 backwards, forwards, patterns, circles
Jog-running, backwards, forwards, patterns
Jumping rope single limb
Figure 8’s, cross-over running
Improve strength and endurance through use of progressive resistive
training
Consider early mobilization with the motivated athlete. However, when

choosing the specific intervention strategy, consider the patient’s activity
level, age, goals for recovery, degree of injury, previous history of injury,
and general motivation.
4
Selected References
Lin CFL, Gross MT, Weinhold P. Ankle syndesmosis injuries: anatomy, biomechanics,
mechanism of injury and clinical guidelines for diagnosis and intervention. J Orthop
Sports Phys Ther 2006: 36(6):372-384
Alonso A, Khoury L, Adams R. Clinical Tests for ankle syndesmoisis injury: reliability
and prediction of return to function. J Orthop Sports Phys Ther. 1998: 27:276-284
Fallat L, Grimm DJ, Saraco JA. Sprained ankle syndrome: prevalence and analysis of 639
injuries. J Foot Ankle Surg. 1998;37:280-285
Gerber JP, Williams GN, Scoville CR, Arciero RA. Persistent disability associated with
ankle sprains: a prospective examination of an athletic population. Foot Ankle Int.
1998;19:653-660
Hopkinson WJ, St Pierre P, Ryan JB, Wheeler JH. Syndesmosis sprains of the ankle.
Foot Ankle. 1990;10:325-330
1
Ankle – Lateral Ligament Reconstruction and Rehabilitation
Anatomical Considerations: The main lateral soft tissue stabilizers of the ankle are the
ligaments of the lateral ligamentous complex: the anterior talofibular ligament, the
calcaneofibular ligament, and the posterior talofibular ligament. As the foot goes into plantar
flexion the bony talar contribution to overall talocrural stability dissociates thereby causing the
ligamentous structures to assume a greater role in providing stability and become more
susceptible to injury.
Pathogenesis: The anterior talofibular ligament is a small thickening of the tibiotalar capsule.
When the foot is in plantar flexion, the ligament’s course becomes parallel to the axis of the leg
allowing for greater force to be placed upon it. Most sprains occur when the foot is in plantar
flexion and inversion thereby injuring the anterior talofibular ligament.
Epidemiology: Ankle sprains are the most common sport-related injury accounting for 10-15%
of all sport injuries. Approximately 85% of all ankle sprains involve the lateral structures of the
ankle: a tear of the anterior talofibular ligament and sometimes the calcaneofibular ligament and
anterior inferior tibiofibular ligament. Previous sprain is a predictive factor for lateral ankle
sprains although studies have found a decreased risk of re-injury when a brace is worn. Gender,
joint laxity, and anatomical foot type does not appear to be a risk factor as was previously
thought but the literature remains divided with regard to whether or not height, weight, limb
dominance, ankle-joint laxity, anatomical alignment, muscle strength, muscle-reaction time, and
postural sway are risk factors for ankle sprains.
Diagnosis:
Lateral ankle ligament sprains or general talocrural instability is assessed through a history of
the mechanism of injury, a physical examination with special tests, and radiographic
evaluation.
• Previous lateral ankle ligament sprain

• Foot is usually plantar flexed and inverted during injury
• Many patients state hearing a “snap”
• Immediate pain and swelling usually are localized over the anterior talofibular ligament
• Positive anterior drawer test (anterior talofibular ligament) or talar tilt test
(calcaneofibular ligament)
• Radiographic analysis to detect fractures
Nonoperative versus Operative Management: Nonoperative management of a lateral ankle

sprain includes physical therapy, bracing, activity modification, and steroid injections.
Operative management is an option when the above have failed to return the patient to a pain-
free active lifestyle. A failure occurs when the patient has recurrent giving way of the ankle with
activities of daily living or the patient’s particular activities or sports, abnormal inversion, and
2
positive anterior drawer stress x-rays. Lateral ligament repair surgery is indicated in patients all
ages. However, those older than 40 seldom have surgery secondary to decreased activity levels.
Surgical Procedure: Surgery begins with arthroscopy to identify further intraarticular ankle
pathology. If intraarticular pathology is identified, it is then addressed and the arthroscopic
surgery is completed. Arthroscopic techniques are performed, but an open stabilization gives a
reproducible result. There are numerous procedures that use the peroneus brevis tendon to
reconstruct the anterior talofibular ligament during open stabilization. More recently other
surgical procedures for direct anatomic repair have gained popularity such as direct suturing of
the ligament, imbrication, reinsertion to the bone, and in some cases augmentation with
surrounding tissues. After the repair is completed the ankle is put through total range of motion
to make sure that it has been maintained throughout surgery.
• Injury protection with ankle splint or cast
• Instruction in the use of assistive device to maintain weight-bearing status
• Instructions/review of postoperative rehabilitation plan
NOTE: The following protocol is taken from Ferkel, Donatelli, and Hall. Refer to their
publication for a full explanation of the protocol and for information regarding criteria for
advancement to next stage, anticipated impairments and functional limitations, and treatment
rationale.
Phase I for Lateral Ligament Repair: Postoperative Weeks 4-6
Goals: Decrease pain

Control edema
Increase range of motion and muscle contraction tolerance
Intervention:
• Isometric exercises
• Passive and active range of motion: plantar and dorsi flexion
• Progressive resistance exercises of the hip
• Soft tissue mobilization and modalities as needed
• Joint mobilization as indicated
• Instruct and monitor gait training progressing to full weight bearing ambulation using
appropriate device
• Patient education
3
Phase II for Lateral Ligament Repair: Postoperative Weeks 6-8

Increase strength and tolerance to single-limb stance and advanced activities
Improve proprioception and stability of ankle
Minimize gait deviations on level surfaces
Intervention:
• Isometric exercises
• Active range of motion of ankle for all ranges against gravity
• Standing bilateral heel raises and squats and lunges
• Treadmill and stationary bike and pool therapy
• Elastic tubing and balance board exercises
• Proprioceptive neuromuscular facilitation
Phase III for Lateral Ligament Repair: Postoperative Weeks 8-10
Goals: Full active and passive range of motion

Return ankle strength to 80% of uninvolved side
Self-management of edema and pain
Intervention:
• Increase elastic tubing resistance

• Isotonics and Isokinetics
Phase IV for Lateral Ligament Repair: Postoperative Weeks 11-18
Goals: Prevent reinjury with return to sport

Return to sport
Discharge to home or gym program
Intervention:
• Ankle brace
• Advanced exercises: plyometrics, trampoline, box drills, slide board, lateral shuffle,
figure eight exercises
• Increase demand of pivoting and cutting exercises
4
Baltopoulos P, Tzagarakis GP, Kaseta MA. Midterm results of a modified Evans repair for
chronic lateral ankle instability. Clin Orthop Rel Res. 2004;422:180-185.
Baumhauer JF, O’Brien T. Surgical considerations in the treatment of ankle instability. Journal
of Athletic Training. 2002;37:458-462.
Burks RT, Morgan J. Anatomy of the lateral ankle ligaments. Am J Sports Med. 1994;22:72-77.
DeMaio M, Paine R, Drez D. Chronic lateral ankle instability-inversion sprains: Part I & II.
Orthopedics. 1992;15:87-92.
Komenda G, Ferkel RD. Arthroscopic findings associated with the unstable ankle. Foot Ankle
Intern. 1999; 20: 708-14.
MacAuley D. Ankle injuries: same joint, different sports. Med Sci Sports Exerc. 1999;31(7
suppl):409-11.
1
Calcaneal Fracture and Rehabilitation
Anatomic Considerations: The calcaneus articulates with the talus superiorly at the subtalar
joint. The three articulating surfaces of the subtalar joint are the: anterior, middle, and posterior
facets, with the posterior facet representing the major weight-bearing surface. The subtalar joint
is responsible for the majority of foot inversion/eversion (or pronation/supination). The
interosseous ligament and medial, lateral, and posterior talocalcaneal ligaments provide
additional support for the joint. The tibial artery, nerve, posterior tibial tendon, and flexor
hallucis longus tendon are located medially to the calcaneus and are at risk for impingement with
a calcaneal fracture, as are the peroneal tendons located on the lateral aspect of the calcaneus.
The calcaneus serves three major functions: 1) acts as a foundation and support for the body’s
weight, 2) supports the lateral column of the foot and acts as the main articulation for
inversion/eversion, and 3) acts as a lever arm for the gastrocnemius muscle complex.
Pathogenesis: Fractures of the calcaneal body, anterior process, sustentaculum tali, and superior
tuberosity are known as extra-articular fractures and usually occur as a result of blunt force or
sudden twisting.
Fractures involving any of the three subtalar articulating surfaces are known as intra-articular
fractures and are common results of: a fall from a height usually 6 feet or more, a motor vehicle
accident (MVA), or an impact on a hard surface while running or jumping. Intra-articular
fractures are commonly produced by axial loading; a combination of shearing and compression
forces produce both the primary and secondary fracture lines.
Shearing forces are created by opposing, parallel forces, which in this case are often the upward-
moving body of the calcaneus against the downward-driving subtalar articulation. Shearing
forces often split the calcaneus into medial and lateral halves. The exact position of the hindfoot
upon impact is partially responsible for the position of the fracture line—a hindfoot in the valgus
position tends to move fractures more laterally, whereas a hindfoot in the varus position moves
fractures medially.
Axial loading also produces a compression fracture line in a characteristic “Y” pattern, as seen
from lateral and oblique radiographic views. The resulting fracture line often splits the middle
subtalar facet and creates a superomedial fragment. As described by Essex-Lopresti, the “Y”
pattern can extend more horizontally, as in a tongue-type fracture, or can extend more vertically,
as in a joint-depression fracture.
Besides the descriptions of Essex-Lopresti, two other classification systems are most widely
recognized and utilized in the evaluation of calcaneal fractures. Sanders, utilizing computerized
tomography (CT) scanning, divides calcaneal fractures into four categories:
• Type I - Undisplaced
• Type II - Two parts (split)
• Type III - Three parts (or split/depression)
2
• Type IV - Comminuted
Crosby-Fitzgibbons also using CT scans divide calcaneal fractures into three categories:
• Type I - Small fracture segments which are slightly displaced or undisplaced
• Type II - Fracture segments which are displaced by 2mm or more
• Type III - Comminuted fracture
Epidemiology: Calcaneal fractures account for 2-3% of all fractures of the body, and 60% of all
tarsal fractures. 75% of all calcaneal fractures are intra-articular and involve one or more of the
three subtalar articulating facets. Intra-articular fractures have a poorer prognosis than extra-
articular fractures. Calcaneal fractures are most often seen in young adult men. Compression
fractures of the lumbar vertebrae occur in 10-15% of cases presenting with a calcaneal fracture.
Diagnosis: Patients with a fracture of the calcaneus may present with the following symptoms:
• Pain - Most importantly pressure pain, or pain elicited when providing pressure to the
calcaneus by holding the heel of the patient’s foot and gently squeezing
• Edema
• Ecchymosis - A hematoma or pattern of ecchymosis extending distally to the sole of
the foot is specific for calcaneal fractures and is known as the Mondor sign
• Deformity of the heel or plantar arch - Widening or broadening of the heel is seen
secondary to the displacement of the lateral calcaneal border outward and
accompanying edema
• Inability to or difficulty weight-bearing on affected side
• Limited or absent inversion/eversion of the foot
• Decreased Bohler or “tuber-joint” angle - In normal anatomical alignment an angle of
25-40 degrees exists between the upper border of the calcaneal tuberosity and a line
connecting the anterior and posterior articulating surfaces. With calcaneal fractures,
this angle becomes smaller, straighter, and can even reverse.
• CT scan (both axial and coronal views) to classify the degree of injury to the posterior
facet and lateral calcaneal wall
• X-rays or Radiographs:
o Axial - Determines primary fracture line and displays the body, tuberosity,
middle and posterior facets
o Lateral - Determines Bohler angle
o Oblique/Broden’s view - Displays the degree of displacement of the primary
fracture line
Nonoperative Versus Operative Management: Great debate remains as to what is the best course
of treatment following a calcaneal fracture, especially following operative management of
displaced or intraarticular fractures. Nonoperative management is preferable when there is no
impingement of the peroneal tendons and the fracture segments are not displaced (or are
displaced less than 2 mm). Nonoperative care is also recommended when, despite the presence
of a fracture, proper weight-bearing alignment has been adequately maintained and articulating
surfaces are not disturbed. Extra-articular fractures are generally treated conservatively.
3
Patients who are over the age of 50 years old or who have pre-existing health conditions, such as
diabetes or peripheral vascular disease, are also commonly treated using nonoperative
techniques. Patients receiving nonoperative management are 5.5 times more likely to require
primary subtalar arthrodesis at some point in the future.
Surgical repair is recommended in calcaneal fractures which present with displaced fracture
segments, impinged peroneal tendons, or entrapped medial compartments. Patients who are
younger, female, have a light or moderate work load involving the foot, or who have a larger
remaining Bohler angle have better results with operative care. A 16 percent incidence of wound
complication is associated with operative management.
Using the classifications of Sanders and Crosby-Fitzgibbons, nonoperative and operative

treatment courses are preferred for the following grades of calcaneal fracture:
• Type I (Sanders), Type I (Crosby-Fitzgibbons) - Nonoperative management of
immobilization or early mobilization
• Type II (Crosby-Fitzgibbons) - Nonoperative management of immobilization or early
mobilization, or operative management including closed reduction and fixation
• Type II/III (Sanders), Type III (Crosby-Fitzgibbons) - Operative management
commonly including ORIF
• Type IV (Sanders) - Nonoperative management for non-salvageable comminuted
fractures or operative management consisting of ORIF with primary arthrodesis
Surgical Procedure: The goals of operative management of a calcaneal fracture include: 1)

restoration of normal heel height and length, 2.) realignment of the posterior facet of the subtalar
joint, 3) restoration of the mechanical axis of the hindfoot. Surgical repair is often delayed 3-14
days after the fracture, especially in the presence of significant edema or fracture blister
formation, to allow for some reduction of swelling.
There are various surgical techniques for the repair of a calcaneal fracture, including the least
invasive, closed reduction with percutaneous fixation. Open reductions include the medial,
lateral, or combined ORIF approach. The extensive lateral approach is the most popular and
allows the surgeon to visualize the entire fracture area. However, this approach requires a full-
thickness skin flap for closure. The lateral approach is indicated when: 1) the fracture occurred
two to three weeks previous to the surgical repair, 2) the fracture is severely-comminuted, 3) the
fracture fragment moves out laterally and positions itself near the talus, 4) a displaced fracture of
the calcaneocuboid joint is present, and 5) the fracture is unable to be reduced using the medial
approach. A variety of pins, plates and other fixation devices, such as the Gissane spike and
Kirschner wires are used for stabilization during surgical repair.
Primary fusion, or arthrodesis, can be used for the surgical repair of Type IV (Sanders) or Type
III (Crosby-Fitzgibbons) severely comminuted fractures, and is used in combination with an
ORIF. Subtalar joint motion is limited after primary fusion and increases the patient’s risk for
development of arthritis secondary to increased rotational forces on the ankle during walking.
4
• Immediate elevation of involved extremity to decrease swelling

• Compression including: foot pump, intermittent compression devices, or compression
wraps
• Ice
• Instruction in use of wheelchair, bedside transfers, or crutches to maintain strict non-
weight bearing status
• Instruction in appropriate nonoperative or postoperative rehabilitation plan
NONOPERATIVE AND POSTOPERATIVE REHABILITATION
Note: Both the progression of nonoperative and postoperative management of calcaneal

fractures include traditional immobilization and early motion rehabilitation protocols. In fact,
the traditional immobilization protocols of nonoperative and postoperative management are
similar, and are thereby combined in the progression below. Phases II and III of traditional and
early motion rehabilitation protocols after nonoperative or postoperative care are comparable as
well and are described together below. Much debate remains on the preferable management of
calcaneal fractures after operative management. Bohler, Burdeaux, Palmer, and Parmer
recommend traditional immobilization after surgical repair, while Buckley, Essex-Lopresti,
Lance, Paley, and Wei advocate early mobilization beginning within 24-72 hours of surgical
repair. Debate also exists on the preferable management of calcaneal fractures with
nonoperative management. Barnard proposes the use of traditional immobilization in the form
of a short leg cast, while Lance, Paley, and Parmer recommend early mobilization with
nonoperative management.
Phase I for Traditional Immobilization and Rehabilitation following Nonoperative and

Postoperative Management: Weeks 1-4

Prevent extension of fracture or loss of surgical stabilization
Minimize loss of function and cardiovascular endurance
Intervention:
• Cast with ankle in neutral and sometimes slight eversion,

• Elevation
• Ice
• After 2-4 days, instruct in non-weight bearing ambulation utilizing crutches or walker
• Instruct in wheelchair use with appropriate sitting schedule to limit time involved
extremity spends in dependent-gravity position
• Instruct in comprehensive exercise and cardiovascular program utilizing upper
extremities and uninvolved lower extremity
5
Phase I for Early Motion and Rehabilitation following Nonoperative and Postoperative
Managment: Weeks 1-4

Prevent extension of fracture and loss of surgical stabilization
Prevent contracture and loss of motion at ankle/foot joints
Intervention:
• Elevation of involved extremity with ankle maintained at 90 degree angle in relation to

the lower leg (or tibia)
• Ice combined with compression wrap
• After 24-72 hours, active range-of-motion exercises in small amounts of movement begin
at all joints of the foot and ankle, including: tibiotalar, subtalar, midtarsal, and toe joints,
and are completed every hour
• After 2-4 days, instruct in non-weight bearing ambulation utilizing crutches or walker
• After 14 days, instruct in proper fitting and usage of prescribed surgical shoe or orthosis
to prevent contracture
• Instruct in wheelchair use with appropriate sitting schedule to limit time involved
extremity spends in dependent-gravity position
• Instruct in comprehensive exercise and cardiovascular program utilizing upper
extremities and uninvolved lower extremity
Phase II for Traditional Immobilization/Early Mobilization and Rehabilitation following

Nonoperative and Postoperative Management:
Weeks 5-8
Goals: Control remaining or residual edema and pain

Prevent re-injury or complication of fracture by progressing weight-bearing safely
Prevent contracture and regain motion at ankle/foot joints
Intervention:
• Continued elevation, icing, and compression as needed for involved lower extremity
• After 6-8 weeks, instruct in partial-weight bearing ambulation utilizing crutches or walker
• Initiate vigorous exercise and range of motion to regain and maintain motion at all joints:
tibiotalar, subtalar, midtarsal, and toe joints, including active range of motion in large
amounts of movement and progressive isometric or resisted exercises
• Progress and monitor comprehensive upper extremity and cardiovascular program
6
Phase III for Traditional Immobilization/Early Mobilization and Rehabilitation following

Nonoperative and Postoperative Management: Weeks 9-12
Goals: Progress weight-bearing status

Normal gait on all surfaces
Restore full range of motion
Restore full strength
Allow return to previous work status
Intervention:
• After 9-12 weeks, instruct in normal full-weight bearing ambulation with appropriate
assistive device as needed
• Progress and monitor the subtalar joint’s ability to adapt for ambulation on all surfaces,
including graded and uneven surfaces
• Joint mobilization to all hypomobile joints including: tibiotalar, subtalar, midtarsal, and
to toe joints
• Soft tissue mobilization to hypomobile tissues of the gastrocnemius complex, plantar
fascia, or other appropriate tissues
• Progressive resisted strengthening of gastrocnemius complex through use of pulleys,
weighted exercise, toe-walking ambulation, ascending/descending stairs, skipping or
other plyometric exercise, pool exercises, and other climbing activites
• Work hardening program or activities to allow return to work between 13- 52 weeks
Barnard L and Odegard J. Conservative approach in the treatment of fractures of the calcaneus.
J Bone Joint Surg. 1955;37A:1231-1236.
Bohler L. Diagnosis, pathology, and treatment of fractures of the os calcis. J Bone Joint Surg.
1931;13:75-89.
Buckley R, Tough S, McCormack R, Pate G, Leighton R, Petrie D, and Galpin R. Operative

compared with nonoperative treatment of displaced intra-articular calcaneal fractures. J Bone
Joint Surg. 2002;84A:1733-1744.
Burdeaux B. The medial approach for calcaneal fractures. Clin Orths. 1993;290:96-107.
Carr J. Mechanism and pathoanatomy of the intraarticular calcaneal fracture. Clin Orthos.
1993;290:36-40.
Crosby L and Fitzgibbons T. Computerized tomography scanning of acute intra-articular

fractures of the calcaneus. J Bone Joint Surg. 1990;72A:852-859.
Essex-Lopresti P. The mechanism, reduction technique, and results in fractures of the os calcis.
7
Br. J Surg. 1951;39:395-419.
Hildebrand K, Buckley R, Mohtadi N, and Faris P. Functional outcome measures after displaced
intra-articular calcaneal fractures. J Bone Joint Surg. 1996;78-B:119-123.
Lance E, Carey E, and Wade P. Fractures of the os calcis: Treatment by early mobilization.
Clin Ortho. 1963;30:76-89.
Paley D and Hall H. Calcaneal fracture controversies—can we put Humpty Dumpty together
again? Clin Ortho. 1989;20:665-677.
Palmer I. The mechanism and treatment of fractures of the calcaneus. J Bone Joint Surg.
1948;30A:2-8.
Parmar H and Triffitt P. Intra-articular fractures of the calcaneum treated operatively or

conservatively. J Bone Joint Surg. 1993;75-B:932-937.
Randle J, Kreder H, Stephen D, Williams J, Jaglal S, and Hu R. Should calcaneal fractures be

treated surgically? Clin Ortho. 2000;377:217-227.
Wei S, Okereke E, Esmail A, Born C, and Delong W. Operatively treated calcaneus fractures:
To mobilize or not to mobilize. Univ of Penn Ortho J. 2001;14:71-73.
Wilson D. Functional capacity following fractures of the os calcis. Canada Med Ass J.
1966;95:908-911.
1
Tarsal Tunnel Release
Anatomical Considerations: The tarsal tunnel is a fibro-osseous tunnel created by the tibia
anteriorly, posteriorly by the talus, and laterally by the calcaneus. The flexor retinaculum
(laciniate ligament) overlays the contents of the tarsal tunnel, which includes the posterior
tibialis, flexor digitorum, flexor hallucis longus, posterior artery/vein, and the posterior tibial
nerve. The posterior tibial nerve has three main entrapment sites: proximal at the flexor
retinaculm, and distally at the medial and lateral plantar nerve (branches from the posterior tibial
nerve located at the distal ends of the tarsal tunnel).
Pathogenesis: Tarsal tunnel syndrome is an entrapment neuropathy, which occurs as a result of

compression of the posterior tibial nerve. In some cases, it is referred to as an ishemic
compartment syndrome and exceeding the threshold of tissue pressure at the tunnel can be
associated with a reproduction of symptoms and changed in nerve function.
Epidemiology: Specific causes of the syndrome can be identified in 60-80% of patients. The
most common causes including trauma, varicosities, heel varus, fibrosis, and heel valgus.
Tendonitis within the tunnel can cause entrapment of the posterior tibial nerve due to the
decreased space, and tethering at the abductor hallicus can cause a stretch injury at the branches
tibial nerve within the tunnel. Generally the causes of this syndrome can be placed into three
categories: 1) Trauma, 2) Space occupying lesion, and 3) Deformities of the foot. It tends to
have a slight female predominance of 56%. Other factors that predispose the patient to a tarsal
tunnel syndrome can include rapid weight gain and inflammatory arthopathies such as anklosing
spondylitis and rheumatoid arthritis. The inflammatory autoimmune diseases cause an increase
in synovium causing synovitis within the tunnel. Along with this syndrome, development of a
“Double Crush Syndrome” can occur. This is when there are multiple sites of nerve entrapment.
When pain radiates up the proximal leg, this is called “Valleix Phenomenon,” and is commonly
seen with the “Double Crush Syndrome.”
Diagnosis:
• History of pain/paresthesia along the posterior tibial nerve and its branches
• Physical examination includes: inspection of foot deformities, sensory testing, muscle
strength testing of the foot intrinsics (especially the flexion of the toes),
palpation/percussion (Tinel’s test) of the posterior tibial nerve, and tibial nerve tension
testing
• Radiograph’s to determine deformities or bony injury
• EMG study to determine motor and sensory nerve damage
• MRI to determine soft tissue damage or deformity, nerve damage, thickening of the
flexor retinaculum, and space occupying lesions.
• Differential Diagnosis: lumbosacral radiculopathy, matatarsalgia, rheumatoid arthritis,
plantar fasciitis, peripheral neuritis, diabetic neuropathy, peripheral vascular disease, and
morton neuroma.
2
Nonoperative Versus Operative Management: Nonoperative treatment is most effective when

the nerve entrapment/compression is caused by tenosynovitis and flexible foot deformities.
Space occupying lesions tend not to respond to conservative treatments. The space occupying
lesions can include ganglia’s, lipomas, chronic thrombophlebitis, and varicosities. Better
surgical results are seen in the following: young, short history of symptoms, no history of ankle
pathology, early diagnosis prior to motor involvement, and a localized lesion is identified.
Failure of the decompression or decreased satisfaction with the surgical release tends to occur
with the following factors: older, chronic symptoms with motor involvement, double crush
syndrome, valliex phenomenon, systemic disease process, idiopathic causes, inadequate release
of the tissue, and pes plantus feet.
Surgical Procedure: An incision is made 10 cm to the tip of the medial malleolus and 2 cm
posterior to the posterior margin of the tibia. During the proximal release, the flexor retinaculm
is released from its proximal extent near the medial malleolus to the sustentaculum tali. The
tunnel is followed distally, and release of the fascial arcade around the medial and lateral plantar
nerve branches should be followed through to the abductor hallucis.
Discussions of surgical complications have been infrequently reported in literature. One case
study published an incident of the posterior tibial tendon subluxing following decompression.
Follow-up studies on patients who have had decompression have also been infrequent.
Currently, the longest follow up study has been an average of 31 months post surgery, with the
result of only 44% of the patients receiving significant benefit out of a total of 32 surgical
decompressions.
Preoperative Rehabilitation: Conservative treatments include as immobilization, orthotics,

strengthening and balance exercises, pharmological medications, steroid injections, and
inflammatory reducing modalities. In some studies, conservative treatments also included
whirlpool therapy and having the patient wear wider shoes. These conservative tools are most
effective with tenosynovitis cases and flexible foot deformities. When the co-existence of
lumbar nerve root compromise or sciatic nerve entrapments occurs with tibial nerve entrapments,
the treatment of both entrapment sites is considered to be essential for a favorable outcome to
occur. Once the source of the mechanical nerve entrapments have be addressed, neural gliding
techniques may be employed in order to minimize fibrosis at peripheral nerve interfaces. It is
very important to understand patient irritability and peripheral nerve healing rates, so as to not
increase neurogenic complaints with neural gliding techniques.The ones who are most likely not
to respond to these treatments are patients with space occupying lesions, long-term nerve
irritation that has produced motor deficits, and a long, chronic history of tarsal tunnel syndrome
symptoms.
Note: The research articles only released information for phase one for post-operative
procedures. For phase two and three, common rehabilitation protocols for ankle rehabilitation
3
were taken from: Stephenson K, Saltzman C, Brotzman S. Foot and Ankle Injuries. In Brotzman
A, Wilk K., Clinical Orthopaedic Rehabilitation. Philadelphia, 2003, Mosby.
4
Phase I for Immobilization and Rehabilitation: Weeks 1-3
Goals: Protect joint/nerve Integrity

Control inflammation
Control pain/edema
Intervention:
• Immobilization with non-weight bearing precautions to protect the nerve and

overstretching of the surgical site
• Passive mobilization to prevent edema and maintain joint integrity post 1-2 weeks per
MD request. This may include selective hallux, phalange, and ankle PROM in order to
prevent fibrosis of the FHL, FDL, and Posterior Tibialis tendons as they traverse through
the tarsal tunnel.
• Instruct in surgical site protection and infection prevention strategies
• Elevation and ice to control swelling
• Educate and monitor non-weight-bearing crutch ambulation
Phase II for Immobilization and Rehabilitation: Weeks 3-6
Goals: Prevent contractions and formation of scar tissue adhesions

Maintain soft tissue and joint mobility
Intervention:
• Progress weight bearing as tolerated - starting from non-weight bearing to weight bearing
• Gentle passive, active-assist, and active ankle stretches out of splint
• Initiate gentle passive dorsiflexion stretching with towel or strap
• Initiate tibial nerve gliding techniques, starting with anti-tension techniques of the tibial
nerve (foot plantarflexed and inverted), and moving from the hip or knee. As irritability
decreases and no evidence of post-treatment latency is eveident, progressing to
mobilization of the foot into dorsiflexion and eversion.
• Initiate gentle, pain free, weight-bearing dorsiflexion stretches
• Gait training wearing protective splint, to tolerance
• Pool therapy under buoyancy conditions – walk or run
Phase III for Immobilization and Rehabilitation: Weeks 6-12 to 24
Goals: Normal gait mechanics for walking and running on level surfaces
Symmetric ankle mobility and single-leg proprioception
Ability to perform repeated single leg heel raises pain free
Initiate sport-specific or job-specific skill development exercises
5
Intervention:
• Gait training out of walking splint to pain free tolerance

• Pain free resistive ankle exercises using elastic tubing or band
• Continue intervention strategies listed in Phase II as indicated by remaining impairments
• Progress stretching exercises to initiate body weight stretching over incline or wedge
• Progress resistive exercises to body weight exercises
o Partial to full weight bearing Progression
o Evaluate compensations and muscular weakness determine specific therapeutic
exercises
• Progress proprioceptive and balance training from single to multi-planar unstable
conditions (such as a BAPS board, BOSU ball, ½ roller, foam surfaces) or advanced
single-leg balance activities
• With no pain with over pressure or during walking, patient may begin pain walk/run
progression and/or sport-specific or job-specific skill development
• Cardiovascular conditioning on stationary bicycle to pain free tolerance
• Resistive exercises for weakened muscle groups
• Initiation of low level plyometric activities for sport specific activities
Cimino W. Tarsal tunnel syndrome: review of the literature. Foot Ankle. 1990;11:47-52.
Gondring W, Shields B, Wenger S. An outcome analysis of surgical treatment of tarsal tunnel
syndrome. Foot Ankle Internat. 2003; 24:545-550.
Langan P, Weiss C. Subluxation of the tibialis posterior, a complication of the tarsal tunnel
decompression: a case report. Clin.Orthop.1980;146: 226-227.
Lau J, Daniels T. Tarsal tunnel syndrome: a review of the literature. Foot Ankle. 1999;20:201-209.
Pfeiffer W, Cracchiolo A. Clinical results after tarsal tunnel decompression. J Bone Joint Surg.
1994;76A:1222-1230.
Saal JA, et al. The psuedoradicular syndrome: lower extremity peripheral nerve entrapment
masquerading as lumbar radiculopathy. Spine. 1988;13 (8):926-930.
Sammarco G, Chang L. Outcome of surgical treatment of tarsal tunnel syndrome. Foot Ankle
Internat. 2003; 24:125-131.
Shacklock MO. Clinical application of neurodynamics, from: Moving in on Pain, Butterworth-
Heinemann. 1995; 123-131.
Stephenson K, Saltzman C, Brotzman S. Foot and Ankle Injuries. In Brotzman A, Wilk K.,
Clinical Orthopaedic Rehabilitation. Philadelphia, 2003, Mosby.
Trepman, E, Kadel N, Chisholm K, Razzano N. Effect of foot and ankle position on tarsal tunnel
compartment pressure. Foot Ankle. 1999; 20:721-726.
1
Posterior Tibialis Tendon Dysfunction & Repair
Anatomical Considerations: The posterior tibialis muscle arises from the interosseous
membrane and the adjacent tibia and fibula in the proximal 1/3 of the leg. The tendon runs
within its sheath, posterior to the medial malleolus, beneath the flexor retinaculum. The tendon
also runs posterior to the axis of the ankle joint and medial to the subtalar joint. It inserts in a
fan-like manner into the navicular, the three cuneiforms, and the plantar surfaces of the base of
the second, third, and fourth metatarsals. The posterior tibialis muscle is a plantar flexor and
invertor of the foot. At the midtarsal joint, it is an adductor of the forefoot opposing the action
of the fibularis brevis.
This muscle functions mainly in the stance phase of gait. After heel contact, the muscle acts as a
shock absorber for the subtalar joint limiting hindfoot eversion through eccentric contraction. In
midstance, contraction of the posterior tibialis muscle causes subtalar inversion thereby causing
the calcaneocuboid and talonavicular joints to lock. This locking creates a right lever for
forward propulsion of the foot over the metatarsal heads. During the swing phase, the tibialis
posterior functions to accelerate subtalar joint supination and assists in heel lift.
If there is an existing dysfunction in the posterior tibialis muscle, there is a decrease in tibial
deceleration and greater hindfoot eversion. This then leads to increased tension and stretching in
the ligaments during contact phase. This also results in a lack of a rigid lever for push-off and
decreased tarsometatarsal joint stability and hindfoot inversion. The gastrocnemius and soleus
muscles begin to act at the midfoot rather than at the metatarsal heads, which starts creating
excessive midfoot stress allowing increased midfoot abduction. All these add to a dysfunction in
gait resulting in progressive midfoot collapse, forefoot abduction, and excessive hindfoot valgus.
From an anatomical and biomechanical view, the posterior tibialis tendon hugs the undersurface
of the medial malleolus and takes on a shaper curve compared with all the other tendons passing
along the medial aspect of the ankle. The tendon is also under an increased amount of tension in
the area posterior and distal to the medial malleolus, especially during dorsiflexion and eversion
of the foot.
There is a zone of hypovascularity present in the mid-portion of the posterior tibial tendon. This
zone starts approximately forty millimeters from the medial tubercle of the navicular and runs
proximally for about fourteen millimeters.
Pathogenesis: Studies have shown that a healthy tendon will not tear with acute stress. Instead
the muscle, insertion, origin, or musculotendinous junction will fail first. On the other hand, a
diseased tendon will rupture secondary to the application of a sudden force. Rupture of the
posterior tibial tendon may be related to both local and systemic vascular impairments. Age,
hypertension, diabetes, obesity, previous foot or ankle trauma/surgery, traumatic disruption of
local blood supply, and the administration of corticosteroids may lead to vascular compromise
and subsequent tendon rupture.
2
Epidemiology: Posterior tibialis tendon ruptures occur predominantly in the late middle-aged
population (average age 57 years). For posterior tibialis dysfunction, the patient is typically a
female over the age of 40 who exhibits ligamentous laxity in multiple joints and has an
occupation that requires extended periods of standing. They usually do not recall any acute
traumatic event. There is another subset of the populations in which posterior tibial tendon
insufficiency occurs and that consists of the 20- to 40-year old athletes. They usually recall a
traumatic event, usually a direct blow to the medial malleolus. Or, they present with years of
involvement in athletics with a pronated foot.
Diagnosis
• Swelling along the medial aspect of the foot and ankle

• Progressive loss of longitudinal arch → pes planus and heel valgus
• “Too many toes” sign secondary to an increase in forefoot abduction and heel eversion
• Positive first metatarsal rise sign
• Palpable pain between medial malleolus and navicular
• Positive single heel rise (painful but normal rise; rise without inversion of the hindfoot;
no elevation of the heel possible)
• Radiographic studies taken with patient weight bearing along with the contralateral foot
to evaluate for pathologic changes secondary to the dysfunction
Classification of Posterior Tibial Tendon Dysfunction

Author Stage I Stage II Stage III
Johnson and Strom Peritendinitis with Elongation of tendon, Fixed valgus position
mild weakness and moderate pain, of rearfoot with
pain weakness of tendon, subtalar joint
mobile valgus rearfoot arthrosis, medial and
lateral rearfoot pain
**Myerson also describes an additional stage, Stage IV: rigid hindfoot, valgus angulation of the
talus with ankle joint degeneration.
Nonoperative Versus Operative Management: The patient’s age, weight, and activity level, and
the severity of the deformity influence treatment. As with many other pathologies, conservative
treatment should be attempted before any surgical interventions are considered. As the severity
of the pes planus increases, the treatment options become more and more limited. Once the
deformity reaches stage IV, arthrodesis is the only option.
Conservative treatment can be broken down into two sections, those with an acute onset and
those with a chronic condition. For the patient with an acute onset, rest and oral anti-
inflammatory medication is given initially. In 2 to 3 months, if the symptoms do not resolve, the
treatment progresses to include a lower extremity casting. This cast is left on for 4 to 6 weeks,
which provides a longitudinal arch support and guarantees rest to the posterior tibialis muscle.
With this cast, the patient is allowed to bear weight as tolerated and uses pain level as a guide. If
after the cast is removed and the patient remains to have symptoms but still does not opt for
surgical intervention, the patient is fitted for orthotics and their shoe is modified permanently.
3
During rehab, using ice after exercise and an air stirrup brace or lace-up ankle support can be
beneficial. Strengthening and lightweight stretching should also be started after the tenderness
has resolved. Orthotic control of excessive pronation and strengthening/movement re-education
of the tibialis posterior, peroneous longus, and gastrocnemius-soleus has proven to be effective.
The combination of these interventions has been shown to significantly reduce the magnitude of
rearfoot pronation more than orthotics alone. This is important to realize for both conservative
and post-operative management.
For the patients with a chronic condition, the goal of treatment is to relieve their symptoms and
to slow the pes planus progression. A molded ankle foot orthosis, or patellar tendon bearing foot
ankle orthosis, which redistribute forces proximally, thereby reducing stress in the foot and ankle
region can be helpful.
Surgical Procedure: If constant attempts at conservative intervention fail, the next progression
is operative treatment. There are several options when surgery is the treatment of choice. The
decision on which type of procedure should be completed takes into account the severity of the
rupture and the mobility of the hindfoot. Surgery types may include the following: primary
repair, synovectomy, tendon transfer, calcaneal osteotomy, and arthrodesis.
Primary repair – Completed for an acute rupture or laceration. If no sign of degeneration is

present and the tear or laceration is complete, repair consists of primary end-to-end suturing.
Synovectomy – Indicated by tenosynovitis or tendinitis of the intact tendon that continues

despite efforts of conservative management. Debridement of the tendon and opening of the
tendon sheath often results in resolution of symptoms. Failing to complete this operation may
allow the tendon to degenerate and rupture eventually.
Tendon Transfer – May be completed if foot is mobile and supple without evidence of a fixed
hindfoot or forefoot deformity. Contraindications of this procedure include obesity, large build,
sedentary lifestyle, older than 70 years, and a hypermobile foot. The tendon that is transferred is
the flexor digitorum longus.
Calcaneal Osteotomy – Those who have a flexible valgus deformity of the hindfoot may have
this procedure completed. The calcaneus is shifted medially to place the hindfoot in a varus
position. This redirects the gastrocnemius-soleus pull medial to the subtalar joint.
Arthrodesis – Indications include fixed deformities of the forefoot or hindfoot. Arthrodesis
should be completed on as few joints as possible required to stabilize the foot, reduce pain, and
establish a plantigrade position. This is due to the fact that the more joints subjected to
arthrodesis, the more stable the foot becomes, yet it comes at the cost of lesser flexibility of the
foot.
• Orthotics to prevent further hindfoot valgus
• Patient education on post-operative care
• Patient education on use of crutches secondary to non weight bearing post-operation
4
For tendon transfer procedure
Phase I for Immobilization and Rehabilitation: Weeks 1-4

Intervention:
• Patient has short leg cast with foot in plantar flexion and inversion
• Instruction on crutch ambulation with non-weight-bearing status on all surfaces
• Initiate cardiovascular program
• Ice (if possible) and elevate extremity
Phase II for Mobilization and Rehabilitation: Weeks 5-9

Goals: Continue to control edema and pain
Prevent cardiovascular deconditioning
Encourage full weight bearing during gait cycle
Out of cast approximately week 9
Intervention:
• Patient has short leg walking cast with foot in neutral
• Weight bearing as tolerated with appropriate assistive devices
• Gross strengthening and cardiovascular activities
Phase III for Mobilization and Rehabilitation: Weeks 9-23

Goals: Normalization of gait cycle
Obtain full ankle range of motion
Improve strength
Return to prior level of function
Intervention:
• Soft tissue mobilization to prevent scar adhesions

• Strengthening all foot musculature with focus on posterior tibialis muscle and intrinsic
muscles of the foot
• Increasing ankle proprioception
• Gait training
• Balance activities
• Functional task specific training
5
Phase IV for Mobilization and Rehabilitation: Week 24
Goals: Return to sports activities
Intervention:
• Sport specific tasks
**Progression is dependent on status of repaired tendon and per physician’s orders
Churchill R, Sferra J. Posterior tibial tendon insufficiency. Its diagnosis, management, and
treatment. Am J Orthop. 1998;27:339-347.
Fleischli J, Fleischli J, Laughlin T. Treatment of posterior tibial tendon dysfunction with tendon
procedures from the posterior muscle group. Clin Podiatr Med Surg. 1999;16:453-470.
Frey C, Shereff M, Greenidge N. Vascularity of the posterior tibial tendon. J Bone Joint Surg
Am. 1990;72:884-888.
Holmes G, Mann R. Possible epidemiological factors associated with rupture of the posterior
tibial tendon. Foot Ankle. 1992;13:70-79.
Janis L, Wagner J, Kravitz R, Greenberg J. Posterior tibial tendon rupture: classification,

modified surgical repair, and retrospective study. J Foot Ankle Surg. 1993;32:2-13.
Johnson K, Strom D. Tibialis posterior tendon dysfunction. Clin Orthop. 1989;239:196-206.
Mosier S, Pomeroy G, Manoli A. Pathoanatomy and etiology of posterior tibial tendon

dysfunction. Clin Orthop. 1999;365:12-22.
Weimer KM, Reischl SF, Requejo SM, Burnfield JM, Kulig K. Nonoperative treatment of
posterior tibialis tendon dysfunction: a randomized clinical trial. Published abstract from APTA
Combined Section Meeting, 2005.
Feltner ME, et al. Strength training effects on rearfoot motion in running. Med & Science in
Sport & Exerc. 1994:1021-1027.
1
Tarsometatarsal Joint Sprain

ICD-9: 845.11 sprain of tarsometatarsal joint
Description: The tarsometatarsal (TMT) joint, or the Lisfranc joint complex, involves the
articulations of the forefoot and the midfoot. The first through third metatarsals articulate with
corresponding cuneiforms. The fourth and fifth metatarsals articulate with the cuboid.
Transverse ligaments join each metatarsal head, however, there is no transverse ligament
between base of the 1st and 2nd metatarsal.
Etiology: A Lisfranc injury indicates an injury to the normal alignment of the cuneiforms and
metatarsal joints with loss of their normal spatial relationships. The most common injury to the
Lisfranc joint occurs at the joint involving the 1st and 2nd metatarsals and the medial cuneiform.
In athletes, injury typically is due to an axial load sustained with foot plantarflexed and slightly
rotated. If the ligaments between the medial and mid cuneiforms are disrupted, or between the
1st, 2nd metatarsals and the medial cuneiform, then the bones separate and the normal alignment
of the joints is lost. When recognized, this injury may be treated surgically and has a much
better prognosis then when it is not diagnosed. True Lisfranc sprains (with disruption of
Lisfranc’s ligament), are most often due to high-energy trauma ( e.g.,motor vehicle accidents)
rather than from sporting events. Lisfranc joint injury should be suspected when the mechanism
of injury is consistent is as described above and soft tissue edema or pain in the foot persists five
or more days after the initial injury
Physical Examinations Findings (Key Impairments)
• Pain with functional movements and activities

• Inability to bear weight while standing on tiptoe
• Inability to squat due to joint instability
• Decreased range of motion
• Pain and swelling in the midfoot (typically in the dorsum) with tenderness along
Lisfranc’s joint
• Tenderness with passive abduction and pronation of forefoot with fixed hindfoot
• Dorsalis pedis pulse may be diminished or absent
• Gross subluxation or lateral deviation of the forefoot is rare but muscle guarding and
weakness is common
• Always consider and assess, if appropriate, for compartment syndrome of the foot

• The symptoms and functional range of motion will improve as the stability of the joint
and closure of the diastasis is resolved.
2
• Even greater range of motion and ability to squat

• Improved segmental stability is commonly associated with improving symptomatology
• Important to resolve normal joint movement in the surrounding joints
3
Sprains of this joint complex must be adequately protected & immobilized until soft tissue
healing is complete. Usually 6 weeks in a non-weight bearing straight leg cast to ensure
complete healing is recommended.
If a weight bearing anterior-posterior x-ray shows any diastasis at the 2nd metatarsal/medial
cuneiform articulation, a closed reduction and percutaneous screw fixation is usually indicated.
Nonoperative Treatment
Mild or moderate sprain – weightbearing radiograph and bone scintigrams show no diastasis
Immobilization: short leg walking cast, a removable short-leg orthotic or a non weight
bearing cast is continued for four to six weeks or until symptoms have resolved. The
potential for disability following a Lisfranc joint injury justifies the use of a non-weight
bearing cast.
After immobilization: ambulation and rehabilitation exercises can be progresses if the

symptoms persist up to 2 weeks after rehabilitation has begun, a repeat weight bearing
radiograph must be obtained to evaluate the joint articulation for instability and evidence
of delayed separation (i.e., disarticulation worsened after weight bearing)
Nonoperative vs. Operative Treatment
The treatment of Lisfranc joint complex fracture/dislocations remains controversial. Some

investigators believe that nonoperative management of fractures and fracture-dislocations is
ineffective, because the reduction and alignment that occur with casting are lost when soft
tissue swelling decreases. Some investigators suggest a displacement of more than 2mm
requires open reduction and internal fixation to avoid a poor outcome, especially in athletes.
Others report no correlation between the degree of diastasis and the eventual outcome. All
studies indicate that timely diagnosis facilitates treatment and decreases long-term disability.
Goal: Restore joint stability and soft tissue healing

Limit effusion
Reduce pain and protect from further injury
• Physical Agents
Electrical stimulation, Ultrasound, Cryotherapy / Ice to provide pain relief, decrease
swelling, promote circulation, promote wound healing, and reduce muscle guarding
• Manual Therapy
Soft tissue mobilization. Joint mobilization.
Note: Early mobilization of jointson their midranges following ligamentous injury
4
can stimulates collagen bundle orientation and promote healing, although full
ligamentous strength is not reestablished for several months. Limiting soft tissue
effusion speeds healing.

Immobilization using a short leg walking cast a removable short-leg orthotic or a non
weight bearing cast is continued for four to six weeks or until symptoms have
resolved. The potential for disability following a Lisfranc joint injury justifies the use
of a non-weight bearing cast.

Instruct patient of proper application of non-weight bearing orthotic
Crutch training if necessary to facilitate non-weight bearing ambulation
Goals: Decrease and eliminate pain

Increase pain free range of motion
Limit loss of strength and proprioception
• Approaches / Strategies listed above plus
• Manual Therapy
Joint mobilization of adjacent hypomobile carpal articulation – being careful to not
strain the involved, potentially unstable and healing tarsometatarsal articulations

Midfoot taping and orthotics can be used for support with weight bearing activities
Stretching foot, ankle, and lower extremities – primarily calf musculature
Progress from passive range of motion to active range of motion exercises in
dorsiflexion, plantarflexion, inversion, eversion in pain free ranges-add resistance as
tolerated
Initiate proprioceptive exercises, such as weight bearing on effected foot, seated
BAPS board.
Goals: Regain full pain-free motion

Regain normal strength
Regain normal proprioception
• Approaches and strategies listed above plus
5
Gradual return to sport or occupational activities through use of functional
progression, such as activity-specific exercise. For example:
Running in pool or de-loaded on a treadmill
Swimming
Standing on toes
Pushing off on toes
Step up on box or stairs
Begin Stairmaster, treadmill, biking
Jump rope
Squats
Selected References
Arntz CT, Hansen ST Jr. Dislocations and fracture dislocations of the tarsometatarsal joints.
Orthop Clin North Am. 1987;18:105-14.
Boden BP, Osbahr DC, Jimenez C. Low-risk stress fractures. Am J. Sports Med. 2001;29:100-
111.
Brown DD, Gumbs RV. Lisfrancs fracture-dislocations: report of two cases. J Natl Med Assoc.
1991;83:366-9.
Brunet JA, Wiley JJ. The late results of tarsometatarsal joint injuries. J Bone Joint Surg [Br].
1987;69:437-40.
Curtis MJ, Myerson M, Szura B. Tarsometatarsal joint injuries in the athlete. Am J Sports Med.
1993;21:497-502.
Englanoff G, Anglin D, Hutson HR. Lisfranc fracture-dislocation: a frequently missed diagnosis

in the emergency department. Ann Emerg Med. 1995;26:229-33.
Faciszewski T, Burks RT, Manaster BJ. Subtle injuries of the Lisfranc joint. J Bone Surg [Am].
1990;72:1519-22.
Hardcastle PH, Reschauer R, Kutscha-Lissberg E, et al: Injuries to the tarsometatarsal joint.

Incidence, classification and treatment. J Bone Joint Surg. 1982;64B:349-356.
Heckman JD. Fractures and dislocations of the foot. In: Rockwood CA, Green DP, Bucholz
6
RD, eds. Rockwood and Green’s Fractures in adults. Vol 2. 3d ed. Philadelphia: Lippincott,
1991:2140-51.
Kraeger DR. Foot injuries. In: Lillegard WA, Rucker KS, eds. Handbook of sports medicine: a
symptom-oriented approach. Boston: Andover Medical, 1993:159-71.
Kuo RS, Tejwani NC, Digiovanni CW, Holt SK, Benirschke SK, Hansen ST Jr, Sangeorzan BJ.
Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg
Am. 2000;82-A(11):1609-18.
Lawson JP, Ogden JA, Sella E, Barwick KW. The painful accessory navicular. Skeletal
Radiology. 1984;12(4):250-62.
Mantas JP, Burks RT. Lisfranc injuries in the athlete. Clin Sports Med. 1994;13:719-30.
Markowitz HD, Chase M, Whitelaw GP. Isolated injury of the second tarsometatarsal joint. A
case report. Clin Orthop. 1989;(248):210-12.
Myerson M. The diagnosis and treatment of injuries to the Lisfranc joint complex. Orthop Clin
North Am. 1989;20:655-64.
Nunley JA, Vertullo CJ. Classification, investigation and management of midfoot

sprains:Lisfranc injuries in athletes. Am J Sports Med. 2002;30:871-878.
Requejo SM, Kulig K, Thordarson DB. Management of foot pain associated with accessory
bones of the foot: two clinical case reports. J Orthop Sports Physical Ther. 200;30(10):580-9.
Trevino SG, Kodros S, Controversies in tarsometatarsal injuries. Orthop Clin North Am.
1995;26:229-38.
Vuori JP, Aro HT. Lisfranc joint injuries: trauma mechanisms and associated injuries. J
Trauma. 1993;35:40-5.
Wiley JJ. The mechanism of tarso-metatarsal joint injuries. J Bone Joint Surg [Br].
1971;53:474-82.
1
Osteomyelitis in the Diabetic Foot

First and Second Ray Amputation
Anatomical Considerations: Osteomyelitis is an infection which involves the bone marrow,

surrounding cortical bone, and the periosteum. It results in delayed healing of wounds, more
extensive tissue damage, an increased length of stay in the hospital, and higher mortality rates.
In the diabetic/neuropathic foot, the most frequent location of a plantar ulcer is the head of
metatarsal I, with the interphalangeal joint of the first toe and the head of metatarsal II occurring
almost as frequently. Bacteria can also invade through interdigital cracks, fissures, paronychias,
and ingrown toenails. The size of the ulcer does not indicate the extent of necrosis.
Osteomyelitis is likely if the ulcer is greater than two centimeters in diameter, greater than three
millimeters deep, or probes to bone. Ray resections are more durable and functional that
transmetatarsal amputations, and are especially indicated in the patient with diabetes, whose
other foot is at risk. No more than two ray resections are recommended to preserve the
maximum foot stability. The bases of the metatarsals should be preserved if possible, to avoid
instability of the Lisfranc (tarsometatarsal) joint.
Pathogenesis: Ulcers in the neuropathic foot usually occur because of trauma, including
pressure from weight bearing, poorly fitting shoes, burns, and puncture wounds, due to loss of
protective sensation. Injuries incurred with trimming of toenails and calluses can precipitate
infection. Combined with an impaired immune response, and poor perfusion, nutrition, and
glycemic control, patients with diabetes are at high risk for pathogens to enter a wound and
extend to the bone. Autonomic neuropathy contributes to decrease in skin hydration and
formation of skin fissures, providing a portal for bacteria. The infection may cause the formation
of avascular tissue, which forms an area for persistent infection. The local infection can lead to
gangrene, necrotizing fasciitis, and sepsis. It is usually polymicrobial, with gram-positive cocci
being the most common, reportedly 50-70%. Gram-negative bacilli are increasing, up to 50%.
Epidemiology: Approximately 25% (16 million) of Americans with diabetes will have foot
problems. 90% will have no infection with early intervention. 15% will have amputations, 5%
of which will be major amputations. 85% of lower extremity amputations are preceded by foot
ulcers. 68% of diabetic ulcers lead to osteomyelitis, many of which are asymptomatic. Of the
hospital admissions for diabetes, 20% are for osteomyelitis in the foot. Drug resistant organisms
(MRSA, VRSA) have increased the incidence, with long-term sequelae and morbidity. Ray
amputations are the second most common amputation of the foot, next to toe amputations.
Diagnosis
¾ Clinical suspicion
• Chronic wound must have careful history and thorough physical exam – the wound
may not have the normal signs and symptoms of infection
• Patient can have: pain (rarely), edema, erythema, induration, tenderness, draining
2
sinus tract, venous insufficiency, impaired range of motion, loss of sensory

perception
• Any exposed joint capsule or bone should be assessed for osteomyelitis
• “Sausage toe” with pain and swelling only is a clinical sign with sensitivity and
specificity
• “Fetid foot” – foul smelling wound drainage probably anaerobic
• Any ulcer that probes to bone is 100% predictive as osteomyelitis
• Ulcer diameter greater than two centimeters: 94% predictive
• Ulcer inflammation: 77% predictive
¾ Lab tests
• Gold standard is aerobic, anaerobic, fungal, and Acid Fast Bacillus bone culture of
biopsy under direct vision during surgery
• Percutaneous needle biopsy under ultrasound or radiologic guidance – culture
multiple specimens
• Swab culture of the sinus tract usually is not accurate
• Blood cultures positive only 50-80% of cases, only in acute stages, rarely in adults
• WBC elevated only in early stages
• Erythrocyte sedimentation greater 70 mm/hour with noninflammed ulcer: 100%
predictive
• Check for hyperglycemia – people with diabetes may have normal temperature and
blood studies
¾ Imaging studies
• Plain films will show soft tissue swelling and bone erosion in about two weeks, with
periosteal reaction about four weeks later
• Three phase bone scan, radionuclide skeletal imaging, is gold standard; wide
availability, documented sensitivity; detects early stage of disease and identifies
multiple areas; specificity is low
• MR is equally sensitive, more specific; T1 has decreased signal intensity of bone
marrow, T2 is increased, as is STIR(short tau inversion recovery); MR has good
differentiation from bone tumor and infarction; useful in planning surgery
• CT can be helpful
• Often pathologic fractures with people with diabetes with osteomyelitis, especially
the distal first or proximal second toe phalanges, with no history of trauma.
¾ Differential diagnosis
• Charcot – requires clinical observations and lab tests
• Must have wound to allow bacteria to penetrate to infect the bone
• Recalcification is not present on radiograph
• RSD
• Simple fractures
• Diabetic osteopathy – no wound, pointed distal metatarsal “peppermint stick sign” on
radiograph - no surgery needed; if only clinical findings, then need biopsy
3
Nonoperative Versus Operative Management: In the acute or initial stages of osteomyelitis in

the diabetic foot, IV antibiotics are mandatory and it is precluded that coverage is in effect
before any advanced wound management is initiated by the physical therapist. This plan often
can be effective, at least in postponing surgical intervention. Irrigation and debridement with
pulsatile lavage with suction (PLWS), sharp debridement, topical antimicrobials for short term
(about two weeks) for surface bacteriostasis, advanced wound dressings (including living skin
equivalents) to provide a moist wound healing environment, negative pressure wound therapy
(NPWT), and off-loading are strategies for wound management. Infection control measures are
of paramount importance, employing standard precautions, including hand washing and proper
Personal Protective Equipment (PPE), especially with the spread of drug resistant organisms.
Systemic hyperbaric oxygen therapy (HBO) has a lethal effect on strict anaerobic and some
aerobic organisms, and has been shown to stimulate granulation, as has electrical stimulation
(ES). They are somewhat controversial, as it is important not to close off any tracts. Whirlpool
is contraindicated for neuropathic feet, as is any type of heat, to avoid burns, maceration, and
further infection. Cytotoxic agents should not be used. Physical therapy also includes exercises
for range of motion (ROM), strength, and circulation.
Glycemic control and optimization of nutritional status must be gained. If ischemia is present
operative intervention is necessary for revascularization of the lower extremity to improve large
vessel perfusion.
Systemic antibiotics, IV and oral, are necessary for six weeks to six months, until the wound
cultures are negative. In acute osteomyelitis sequential, high dose IV antibiotics can decrease
the role of surgery. Response can be evaluated by monitoring the C-reactive protein level, often
decreasing the duration to three to four weeks. The choice of antibiotics is determined by
specimen cultures or stains, obtained by aspiration, needle biopsy, or swab. Also taken into
consideration is the age and health status of the patient, the site of the infection, local sensitivity
patterns, systemic toxicity, drug allergies, and any previous antimicrobial therapy. Initial
coverage is broad spectrum, with specific antibiotics when the organism(s) is identified. With
fluoroquinolones, photosensitivity is produced, and the risk is present of tendinopathy, especially
of the Achilles, with possible rupture.
Surgical Procedure: If osteomyelitis spreads to a joint, it is considered an orthopedic

emergency. Articular cartilage can be damaged in just hours. Surgical debridement includes
removing all overlying callous, sinus tracts, infected granulation tissue, dead tendon, exposed
cartilage, bursal tissue, and all soft bone to bleeding cancellous and firm cortical bone. All
purulent exudate should be drained, and the wound left open for delayed primary closure, to
allow for inspection and further debridement if needed.
If osteomyelitis involves the entire toe, the ray should be resected: the digit plus the head and
shaft of the corresponding metatarsal (MT). Removal of the first ray is devastating to both
stance and gait, as an intact medial column is essential to proper forward progression. It is
valuable to try to save most of the MT shaft, especially the proximal portion to minimize
pronation abnormalities. If the entire MT has to be amputated and the tibialis anterior tendon is
not damaged, it should be reattached to the medial cuneiform. Loss of the anterior tibialis will
4
result not only in pronation of the foot, but will transfer excessive pressure to the MT II head,
which will lead to breakdown.
If the second toe is involved, it is wise to remove MT II at its proximal metaphysic along with
the toe, to preserve cosmesis and function (avoid valgus). The distal toes should be filleted to
create additional soft tissue for closure. The wound should be closed on the dorsum of the foot,
preserving the plantar skin. Sutures should remain intact for three-four weeks due to delayed
healing in patients with diabetes, due to impaired nutrition and oxygen delivery at the surgical
site, plus tissue ischemia. The inflammatory phase of healing is limited due to abnormal
phagocytosis, contributing to edema. Protein metabolism is also abnormal, impairing
fibroblastic proliferation, collagen synthesis, and new capillary formation. Future split thickness
skin grafts are often necessary for complete wound closure.
• Physical therapy wound management: PLWS, sharp debridement, possible NPWT,

advanced wound dressings
• Pressure ulcer prevention
• Off-loading, non-weight bearing (NWB) on affected lower extremity; wheel chair or
walker, monitoring for carpal tunnel syndrome, 11% more likely with patients with
diabetes. Crutches not advised due to neuropathy.
• Monitor and protect integumentary integrity of opposite lower extremity
• Education re: post surgery: gait, diabetic foot inspection, footwear/orthotics, opposite
lower extremity inspection and protection, nutrition, glucose control, no smoking
• If no sepsis, ROM and strengthening exercises; watch for antibiotic reactions, including
hypersensitivity; nausea, vomiting, diarrhea (may need to alter time of PT treatment)
• Ultraviolet (UV) sensitivity, with need to establish an accurate minimal erythemal dose if
utilizing UV radiation
• Social/family support
• Psychology consult
Note: There is a lack of evidence-based studies to support the rehabilitation interventions of

patients with ray amputations, especially those with diabetes following surgery due to
osteomyelitis. Research should and must be done with the explosion of new diagnoses of
diabetes in the population.
Phase I: Weeks 1-4
Goals: Control edema

Accelerate wound healing process
5
Eliminate pressure
Prevent contractures and loss of strength
Eliminate infection
Control pain
Intervention:
• Elevation of foot on one pillow if low ABI

• PLWS, sharp debridement, advanced wound dressings
• NWB with walker or wheelchair
• Suspend heel in bed or sitting; therapeutic positioning in bed
• Active, active assistive, and passive ROM exercises for adjacent joints
• Achilles tendon stretching; may require surgical lengthening in the future
• Rest, antibiotics, infection control measures with wound management
• Pain medications
Phase II: Weeks 4-8 (up to 27: wound closure)
Goals: Wound closure

Continue to eliminate pressure
Increase strength
Eliminate infection
Intervention:
• PLWS, sharp debridement, NPWT/advanced wound dressings, ES, growth factors, skin
substitutes
• NWB with walker, wheelchair, or total contact cast (TCC) if infection clears
• Avoid high intensity exercise to avoid increase in blood pressure, which could cause
further damage to retinas and kidneys. Avoid putting head below the waist to prevent
further retinal damage
• Antibiotics
• Infection control measures with wound management
Phase III: Weeks 8 (or at wound closure) - lifetime
Goals: Protect and accommodate remaining portion of foot

Equalize weight bearing to protect remaining MT heads from increased pressure (as
medial arch can collapse)
Minimize drifting of remaining toes
Improve gait
Restore functional capacity
6
Intervention:
• Consult orthotist, pedorthist, shoemaker – patient should never take an unprotected step.
Use adaptive and supportive footwear.
• Soft, moldable upper to protect and accommodate remaining foot
• Sandals for shower, night trips to bathroom
• Custom molded shoe or total contact insert with strong medial counter to support the
medial arch
• Roller or rocker bottom shoe with flare and external extended steel shank or internal rigid
carbon footplate to protect remaining MT heads and for improved gait by enhancing the
loss of toe-off and adding stability to anteroposterior plane. High top shoes may be
necessary to prevent the heel from slipping out of the heel counter
• Heel raise added to shoe to prevent dorsiflexion of the forefoot, with the same raise used
on the contralateral shoe
• Provide shoe filler for amputated portion of foot, including toe fillers
• No high heels to avoid increased forefoot pressures
• Expanded toe boxes to accommodate claw toe deformities caused by intrinsic imbalance
in remaining toes
• Exercises to strengthen remaining plantar flexors to increase power in push-off –
insertions of plantar fascia and flexor hallucis are lost
• Gait training for ascending/descending stairs
Attinger C, Venturi M, Kim K, Ribiero C. Maximizing length and optimizing biomechanics in

foot amputations by avoiding cookbook recipes for amputation. Seminars in Vascular Surgery.
2003; 16:44-66.
Eneroth M, Larsson J, Apelqvist J. Deep foot infections in patients with diabetes and foot ulcer:
an entity with different characteristics, treatments, and prognosis. Journal of Diabetes and Its
Complications. 1999; 13:254-263.
Karchmer AW, Gibbons GW. Foot infection in diabetes: evaluation and management. Current
Clinical Topics in Infectious Diseases. 1994; 14:1-22.
Lipsky BA. Osteomyelitis of the foot in diabetic patients. Clinical Infectious Diseases. 1997;
25:1318-26.
7
Nehler MR, Whitehill TA, Bowers SO, Jones DN, et al. Intermediate-term outcome of primary
digit amputations in patients with diabetes mellitus who have forefoot sepsis requiring
hospitalization and presumed adequate circulatory status. J Vasc Surg. 1999; 30:509-17.
Paluska SA. Osteomyelitis. Clinics in Family Practice. 2004; 6:127-149.
Philbin TM, Leyes M, Sferra JJ, Donley BG. Orthotic and prosthetic devices in partial foot
amputations. Foot and Ankle Clinics. 2001; 6:215-228.
Snyder RJ, Cohen MM, Sun C, Livingston J. Osteomyelitis in the diabetic patient: diagnosis and
treatment. part 2: medical, surgical, and alternative treatments. OstomyWound Management.
2001; 47(3):24-43.
1
Bunionectomy
Anatomical Considerations: Normal biplanar flexion and extension of the metatarsophalangeal

joint is maintained by counterbalance between muscles acting on the first metatarsophalangeal
joint. The action of the long and short toe extensors is normally counteracted by the long and
short toe flexors, and the abductor hallucis is counterbalanced by the adductor hallucis. Also, no
muscle inserts into the metatarsal head. Therefore, once the hallux becomes destabilized and
begins to sublux laterally, the muscles, which previously acted to stabilize the joint, become a
deforming force since their pull is lateral to the long axis of the metatarsophalangeal joint.
Pathogenesis: Bunion is associated with imbalance of the soft tissues and abnormal bony
configuration of the first cuneiform/metatarsophalangeal joint complex. As the proximal
phalanx moves laterally on the metatarsal head, it exerts pressure against the metatarsal head,
pushing it medially. As this occurs, there is progressive attenuation of the medial joint capsule,
as well as a progressive contracture of the lateral joint capsule. While this deformity is
occurring, the sesamoid sling, which is anchored laterally by the insertion of the adductor
hallucis muscle and transverse metatarsal ligament, remains in place, creating pressure on the
medial joint capsule. As a result, the abductor hallucis muscle gradually slides beneath the
medially deviating metatarsal head. Once the abductor hallucis slides underneath the metatarsal
head, two events occur. First, the intrinsic muscles no longer act to stabilize the
metatarsophalangeal joint but actually help to enhance the deformity. Second, as the abductor
hallucis rotates beneath the metatarsal head, because it is connected to the proximal phalanx, it
will spin the proximal phalanx around on its long axis, giving rise to varying degrees of
pronation.
Hallux valgus occurs due to hereditary and environmental factors. Tends to occur in families
with a genetic predisposition for laxity of the ligaments and excessive pronation of the foot (flat
feet). What generally causes the problems of pain and deformity result due to improper fitting
footwear. Wearing shoes with a narrow toe box (the part of the shoe that surrounds the front part
of the foot) squeezes the toes and cause the crowding of the big toe into the other toes. The
problem is also caused by wearing high heels that force the body weight forward onto to the toes.
Epidemiology: Adult acquired hallux valgus is found most often in women and is commonly
associated with long-term wearing of fashionable, narrow box, pointed-toe shoes. According to
the study of Lam Sim-Fook and Hodgson, 33% of shod individuals had some degree of hallux
valgus, compared with 1.9% of unshod persons. Other associated findings, which may be
implicated in the biomechanical cause of hallux valgus, include contracture of the Achilles
tendon complex, hypermobility of the first metatarsal-medial cuneiform joint, and pes planus.
The static foot posture of pes palnus, however, has not been found to contribute directly to hallux
valgus formation. In contrast, the observation of dynamic forefoot pronation has been found to
be present in as many as 84% of cases with hallux valgus. Pronation contributes to midtarsal
joint (calcaneal-cuboid joint – oblique axis) instability, and as a result, midfoot horizontal
abduction at terminal stance. This occurance creates insufficient first ray plantarflexion and an
inefficient length-tension relationship for proper peroneous longus function in stabilizing the
first metatarsal.
2
Bunions are relatively unknown in non shoe wearing populations. It is suggested that between 30
to 50% of the people in show wearing populations have some degree of hallux valgus.
According to the American Orthopedic Foot and Ankle Society, bunions are nine times more
likely to be seen in women than men. This is probably due to ill fitting shoes with a narrow toe
box and high heels. Feet naturally widen as we age so bunions do not generally become a
problem until middle age.
Diagnosis: A diagnosis of hallux valgus can usually be made based upon appearance of the big
toe.
The symptoms can include;
• Red, calloused skin at the base of the big toe

• A bursa or bony bump at the base of the first metatarsal
• Pain at the MTP joint aggravated by pressure from shoes
• Big toe turned toward the other toes.
Associated findings can include;

• Second digit hammertoe
• Callous on the bottom of the foot
• Pronated foot
• Ingrown toenail
Radiographic findings include;

• Medial prominence of the first metatarsal head
• + or – joint space abnormality
• increased HVA
• increased IMA
• lateral displacement of the sesamoids
Differential diagnosis includes;
• Hallux rigidus which presents a distinguishing distal osteophyte on radiograph

• Hallux arthrosis which presents with loss of the entire joint space on radiograph
• Gout presents as an acute condition with laboratory tests indicating elevated uric
acid and sodium urate crystals.
Diagnosis is further determined by severity. Severity is based upon the HVA and IMA and joint
deviation.
Stage 1 or mild hallux valgus indicates a HVA < 25 degrees, IMA of < 12 degrees
Stage 2 or moderate hallux valgus indicates a HVA of > 25 degrees, IMA of < 16 degrees
Stage 3 or severe hallux valgus indicates a HVA of > 35 degrees, IMA of > 16 degrees
3
Nonoperative Versus Operative Management: Most bunions do not require surgery. Those that
do end with surgical interventions produce debilitating pain or deformity that is not relieved with
conservative measures. Because most pain is produced during gait, patients limit their activity
which can lead to secondary problems of general deconditioning. Conservative measures
usually begin with patient education regarding appropriate footwear. Wide, low heeled shoes
such as athletic shoe, soft leather shoes or sandals are recommended. Protect the bunion with
moleskin or gel filled pads. Over the counter or prescribed nonsteroidal anti-inflammatory
medications may relieve the inflammation and subsequent pain. Semi soft orthotics can be
inserted into the shoe to help position the foot properly. Night splints can hold the toe straight.
Physical therapy can also be recommended with exercise instruction, stretching, taping,
application of modalities as well as education as to prevention. If these conservative measures
are not successful the patient should seek medical consultation for surgical bunionectomy.
Surgical Procedure: There are over 100 surgical procedures for bunionectomy or osteotomy and
the procedure is determined based upon the severity of the hallux valgus as well as the patient’s
age, health, and activity level. The goals of surgery are to remove the bump. realign the joint,
relieve the pain and restore normal function particularly during gait. The goal is not to fit the
patient into stylish shoes with a narrow toe box. In fact the surgery is not for cosmetic reasons.
Usually bunionectomy is performed as an outpatient procedure. However as the procedure
becomes more complicated, hospital stay may involve 1 to 3 days. Simple surgical removal of
the medial eminence can be performed if the primary complaint is a prominent medial eminence,
the deformity is mild, and rapid recovery is desirable. Distal metatarsal osteotomy such as a
chevron osteotomy is performed for mild-to-moderate deformity in a young person with no
degenerative joint disease. This procedure affords limited realignment by lateral displacement of
the head of the first metatarsal, removal of the medial prominence, and plication of the medial
capsule. For a more extensive deformity, the distal soft tissue procedure, which is a modification
of the procedure originally described by McBride, is performed. Its major components are: 1)
release of lateral metatarsophalangeal joint capsule, adductor hallucis tendon, and contractures
about the lateral sesamoid. 2) removal of medial eminence of the metatarsal head and
realignment of the sesamoid sling. 3) Osteotomy at the base of the first metatarsal. Arthrodesis
or resection arthroplasty is a choice of procedure if there is severe degenerative joint disease.
The Cochrane Library review of evidence from clinical trials showed that about one third of all
patients were dissatisfied with the result of surgery even if pain and toe alignment were
improved. This may be due to unrealistic expectations of surgery, poor post surgical rehab or a
lack of a suitable way to measure patient satisfaction. Also the survey found little evidence to
support whether conservative or surgical intervention worked best. Results from a 2001
randomized controlled trial of 209 patients performed by Torkki et al found that pain intensity,
number of painful days, cosmetic disturbance and foot wear problems were the least following
surgery as compared with the use of orthoses or watchful waiting. Functional status and
satisfaction with treatment were also the best in the surgical group. As of 2003, it is estimated
that 209,000 people in the United States undergo some type of bunion surgery each year making
it one of the most common orthopedic surgeries in western industrialized countries.
4
• Evaluation and recommendation of proper footwear specifically width of toe box.

• Foot exercises including toe spread, eat the towel, marble pick up, toe raises and toe
curls.
• Stretching of Achilles tendon if indicated
• Shoe inserts or orthotics
• Night splints
• Bunion pads or moleskin
• Pain relieving modalities such as ice packs, whirlpool, ultrasound and massage.
• Post op rehab plan instruction in the use of assistive devices if limited or non weight
bearing.
• Post op rehab plan instruction in donning and doffing brace if indicated.
POSTOPERATIVE REAHBILITATION
The rehabilitation following surgical intervention is based upon the procedure itself and the
physician’s determination. Below are some of the procedures and the post op rehab for that
procedure.
Chevron Osteotomy
• a gauze and compression dressing is applied in the operating room (OR), changed
weekly for a duration of six weeks
• Kirschner wire is removed three to four weeks post op
• PROM exercises begun when wires are removed
• Gait training allowed with weight on the heel and lateral aspect of the foot
• At 4 weeks plantigrade walking wearing a wooden-soled postoperative shoe.
McBride Procedure
• a gauze and tape compression dressing is applied in the OR and changed weekly for
eight weeks
• Gait training WBAT wearing a postoperative wooden-soled shoe
• P and AROM exercises allowed six weeks after the surgery
Triple Distal Osteotomies

• Gauze and tape compression dressing
• Gait training with walker or crutches for NWB below the knee cast.
• At four weeks, cast changed to allow weight bearing
• Cast removed in six to eight weeks dependent upon radiographic confirmation of healing
• ROM exercise initiated when cast is removed
Mitchell or Wilson Osteotomy

• Gauze and tape compression dressing applied in OR
5
• Gait training NWB with assistive device, cast applied one week after the operation.
NWB maintained for 4 weeks.
• Weight bearing cast applied at 4 weeks
• Rom begun when cast is removed usually 6 to 8 weeks post op
Keller Excisional arthroplasty

• Gauze and tape compression dressing, changed weekly for 6 weeks
• Gait training WBAT with the patient wearing a wooden soled shoe.
• Kirschner wires removed at 4 weeks then ROM and plantarflexion exercises are begun.
Phase I: Weeks 1-6/8

Protect incision site
Intervention:
• Dressing
• (Ambulation in a postoperative shoe as tolerated if patient had arthrodesis)
Phase II: Week 6/8-12
Goals: Increase range of motion

Continue edema control
Progressive weight-bearing status
Intervention:
• Passive and active range of motion

• Contrast bath and manual lymph drainage techniques
• Grade I joint mobilization
• Metatarsophalangeal stretch
• Gastrocsoleus stretch
• Ambulation as tolerated in postoperative shoe or soft, wide shoe
Phase III: Weeks 12-16
Goals: Full range of motion

Normal gait
Intervention:
6
• Strengthening exercises for foot and lower quarter muscular power/control deficits
• Grade II-IV joint mobilizations performed at end range, as symptoms allow
• Gait training
• Orthotics, as needed, to address overproantion and/or intrinsic foot deformities, which
may contribute to impaired healing and/or reocurance of hallux valgus.
Ayub A, Yale S, Bibbo C. Common Foot disorders. Clinical Medicine and Research.
2005;Vol.3No2:116-119.
Brotzman S, Wilk K Clinical Orthopedic Rehabilitation, Philadelphia, Mosby Second edition,

2003, p. 424.
Clinical Practice Guideline First Metatarsophalangela Joint Disorders Panel. Diagnosis and
treatmnet of first metatarsophalangels joint disorders. J Foot Ankle Surg. 2003 may-
June;42(3):112-54.
Coughlin MJ, Mann RA. Surgery of the Foot and Ankle. 7th ed. St. Louis, Mosby, 1999.
Coughlin MJ: Roger A Mann Award. Juvenile hallux valgus: etiology and treatment. Foot Ankle
Int. 1995;16:682.
Donatelli RA. The Biomechanics of the Foot and Ankle. 2nd ed. Philadelphia, F.A.Davis
Company, 1996.
Donnery J, Dibacco RD. Postsurgical rehabilitation exercises for hallux abducto valgus repair. J
Am Podiatr Med Assoc. 1990;80:410-413.
Eustace S, Byrne JO, Beausang O, et al: Hallux valgus, first metatarsal pronation and collapse of
the medial longitudinal arch – a radiological correlation. Skeletal Radiol. 1994;23:191.
Fink B, Mizel M. What’s New in Foot and Ankle Surgery. The Journal of Bone and Joint
Surgery. 2002;84(3):504-509.
Radl R, Kastner N, Aigner C, Portugaller H, Schreyer H, Windhager R. Venous Thrombosis

After Hallux Valgus Surgery. The Journal of Bone and Joint Surgery. 2003;85:1204-1208.
Sargas NP, Becker PJ: Comparitive radiographic analysis of parameters in feet with and without
hallux valgus. Foot Ankle Int. 1995; 16:139.
Smith A. Easy Exercises for Preventing Bunions. Medical Update 2001;Vol27 Issue 5.
Torkki M, Malmivaara A, Seitsalo S, Hoikka V, Laippala P, Paavolainen P. JAMA.

2001;285:2474-2480.

Physical Therapy Protocols For Ankle and Foot Conditions

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Red Flags for Potential Serious Conditions in Patients with Knee, Leg, Ankle or Foot Problems

Medical Screening for the Knee, Leg, Ankle or Foot Region

Robert Klingman PT, Joe Godges PT KP SoCal Ortho PT Residency

KNEE/LEG/ANKLE/FOOT SCREENING QUESTIONNAIRE

NAME: ________________________________________ DATE: _____________

1. Have you recently experienced a trauma, such as a vehicle accident, a

2. Have you recently had a fever?

3. Have you recently taken antibiotics or other medicines for an

4. Have you had a recent surgery?

5. Have you had a recent injection to one or more of your joints?

6. Have you recently had a cut, scrape, or open wound?

7. Do you have diabetes?

8. Have you been diagnosed as having an immunosuppressive disorder?

9. Do you have a history of heart trouble?

10. Do you have a history of cancer?

12. Have you recently been bedridden for any reason?

13. Have you recently begun a vigorous physical training program?

Joe Godges DPT KP SoCal Ortho PT Residency

Normal Gait Patterns Have Two Major Periods:

1. Double Limb Support: a) weight loading

DOUBLE LIMB SUPPORT

WEIGHT UNLOADING: Trailing foot is rolling off floor

Phases: Terminal Stance: when heel rises

Joint Motions: Terminal Stance Æ Pre-Swing

WEIGHT LOADING: Weight is transferred to contralateral leg

Phases: Initial Contact: when heel contacts floor

Joint Motions Initial Contact Æ Loading Response

Joe Godges DPT 1

STANCE PHASE: (Initial Mid-Stance, Mid-Stance, Late Mid-Stance)

Joint Motions Initial Mid-Stance Æ Late Mid-Stance

Sub Phases: Initial Swing: big toe leaves ground

Joint Motions Initial Swing Æ Mid-Swing Æ Terminal Swing

Pathway of Center of Gravity

Frontal Plane: Rhythmical side-to-side motion

Joe Godges DPT 2

Common Lower Extremity Musculoskeletal Impairments Associated With Gait

Joint ROM/Muscle Length Motor Control/Strength Joint Hypermobility/Instability

Joe Godges DPT 3

"Midtarsal Joint Capsulitis"

ICD-9-CM: 845.11 Sprain of tarsometatarsal joint

History: Arch area pain - medial or lateral

Medial Foot Lateral Foot

Talus - Navicular Accessory Movement Test

Cues: Patient sits on edge of table to allow knee flexion

Navicular - 1st Cuneiform Accessory Movement Test

Cues: Proximal MCP, PIP, and DIP stabilize navicular

Calcaneus - Cuboid Accessory Movement Test

Navicular/3rd Cuneiform - Cuboid Accessory Movement Test

ICD-9-CM: 735.1 Hallux rigidus

Physical Exam: Limited motion of 1st metatarsophalangeal (MTP) extension

1st MTP Extension ROM

1st MTP Accessory Movement Test

Cues: Loose pack position is 10 degrees of dorsiflexion

Etiology: Hallux rigidus can be caused by osteoarthritis, repetitive trauma, or anatomic

Stage I: Stage of Functional Limitus

Stage II: Stage of Joint Adaptation

Stage III: Stage of Established Arthrosis

Stage IV: Stage of Ankylosis

If the patient chooses to first attempt conservative/non-surgical treatment it is essentially

Stage I-IV (non-surgical)

• Physical Agents: phonophoresis/iontophoresis, US, NSAIDS, steroid injection,

• External Devices: Orthoses, shoe modifications to limit extension at 1st MTP

NAME: ____________________________ DATE: _