14438524 Physical Therapy Protocols for Ankle and Foot Conditions

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

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

Condition

Red Flag Data obtained during

Interview/History

Red Flag Data obtained during

Physical Exam Fractures1-4 History of recent trauma: crush

injury, MVA, falls from heights, or sports injuries

Osteoporosis in the elderly

Joint effusion and hemarthorsis Bruising, swelling, throbbing pain, and point

tenderness over involved tissues Unwillingness to bear weight on involved leg

Peripheral Arterial Occlusive Disease5-9

Age > 55 years old History of type II diabetes History of ischemic heart disease Smoking history Sedentary lifestyle Co-occurring intermittent

claudication

Unilaterally cool extremity (may be bilateral if aorta is site of occlusion)

Prolonged capillary refill time (>2 sec) Decreased pulses in arteries below the level of

the occlusion Prolonged vascular filling time Ankle Brachial index < 0.90

Deep Vein Thrombosis10,11,17

Recent surgery, malignancy, pregnancy, trauma, or leg immobilization

Calf pain, edema, tenderness, warmth Calf pain that is intensified with standing or

walking and relieved by rest and elevation Possible pallor and loss of dorsalis pedis pulse

Compartment Syndrome12-14

History of blunt trauma, crush injury - or -

Recent participation in a rigorous, unaccustomed exercise or training activity

Severe, persistent leg pain that is intensified with stretch applied to involved muscles

Swelling, exquisite tenderness and palpable tension/hardness of involved compartment

Paresthesia, paresis, and pulselessness Septic Arthritis15 History of recent infection, surgery,

or injection Coexisting immunosuppressive

disorder

Constant aching and/or throbbing pain, joint swelling, tenderness, warmth

May have an elevated body temperature

Cellulitis16 History of recent skin ulceration or abrasion, venous insufficiency, CHF, or cirrhosis

History of diabetes mellitus

Pain, skin swelling, warmth and an advancing, irregular margin of erythema/reddish streaks

Fever, chills, malaise and weakness

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.

Joe Godges DPT 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 1

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 Pre-Swing Ankle Heel rise Max. plantarflexion (20 o) Knee Full extension Flexes to approx. 40o Hip Max. extension (20o) Flexes to approx. 0o (neutral)

Pelvis Relative anterior rotation Less anterior rotation Posterior depression Begin anterior elevation

Trunk Aligned between legs 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 Loading Response Ankle Neutral Plantarflexes 10o Knee Knee extended Knee flexes 15o Hip Flexed 25o Stable 25o flexion

Relative abduction Pelvis Level Lateral drop to swing leg Trunk Aligned between legs Aligned towards wt. bearing leg

Joe Godges DPT 2

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 Late Mid-Stance Ankle Slight plantarflexion Max. dorsiflexion (10 o) Knee Slight flexion Extended Hip Flexed,

Relative adduction

10o Extended,

Relative adduction

Pelvis Lateral drop to swing leg, externally rotated Trunk Toward stance leg 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 Mid-Swing Terminal Swing Ankle Plantarflexed Neutral Neutral Knee Max. flexion (60 o) Flexion Max. extension (0o) Hip Flexion,

Relative abduction Max, flexion (25 o)

Max. abduction (10o) Flexion,

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 3

Critical Events During Gait

Joint Sagittal Plane Frontal Plane Transverse Plane 1st MTP 65o extension at PSw Midtarsal: Calcaneocuboid

Control of Abduction at TSt 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

(Quadriceps and VMO) 0o extension at TSt 60o flexion at ISw Produce full ext. at TSw

Patellar Medial Glide

Hip Control of flexion at LR

(Hip extensors) 20o extension at TSt

Control of lateral pelvic tilt at MSt

(Hip Abductors)

Common Lower Extremity Musculoskeletal Impairments Associated With Gait Deviations

Joint ROM/Muscle Length Deficits

Motor Control/Strength Deficits

Joint Hypermobility/Instability

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 PT, Robert Klingman PT Loma Linda U DPT Program KPSoCal Ortho PT Residency

1Foot 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


2

Navicular - 1st Cuneiform Accessory Movement Test Cues: Proximal MCP, PIP, and DIP stabilize navicular Distal MCP, PIP, and DIP move 1st cuneiform Determine symptom response, available motion, and end feel

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") Determine symptom response, available motion, and end feel


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


4

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


5Hallux 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


7Intervention 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.


8Selected 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 Impairment: Limited Ankle Dorsiflexion

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 Impairment: Limited Ankle Dorsiflexion

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

The following reference provides additional information regarding this procedure: 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 The following reference provides additional information regarding this procedure: Brian Mulligan MNZSP, DipMT: Manual Therapy, p. 95-96, 1995


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 The following reference provides additional information regarding this procedure: Freddy Kaltenborn PT: Manual Mobilization of the Extremity Joints, p. 155, 1989


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 The following reference provides additional information regarding this procedure: 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 conditions that take only a few

weeks to resolve

Tendonopathies are often recalcitrant to treatment and may require months

to resolve Imaging techniques (MRI, ultrasound, etc) can predict

prognosis

Imaging does not predict prognosis; it adds to the chance of a tendonopathy

Dx, but does not prove it

Cyst-like abnormalities found with ultrasound are indications for

surgery

Surgery should be based on clinical grounds;cyst-like ultrasound findings

can be asymptomatic Surgery provides fast recovery of symptoms in almost all patients

After surgery, return to sport takes at 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

Intervention Approaches / Strategies

Acute Stage / Severe Condition 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

Settled Stage / Mild Condition 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

• Therapeutic Exercises 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) Acute Stage / Severe Condition

• 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

Sub-Acute Stage / Moderate Condition 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

Intervention Approaches / Strategies Acute Stage / Severe Condition 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 Electrical stimulation Contrast baths


Gentle mobility exercises to maintain ankle range of motion (avoiding end range dorsiflexion)


Heel lifts and orthotics where indicated

• Re-injury Prevention Instruction 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

Sub-Acute Stage / Moderate Condition 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

• Re-injury Prevention Instruction

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.

Settled Stage / Mild Condition 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) Acute Stage / Severe Condition

• 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

Sub Acute Stage / Moderate Condition

• 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


Acute Stage / Severe Condition Goals: Limit effusion

Reduce pain and protect from further injury Prevent movement induced inflammatory reactions

• Physical Agents

Cryotherapy / Ice Electrical stimulation


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

Sub Acute Stage / Moderate Condition 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

• Therapeutic Exercises 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

Settled Stage / Mild Condition 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


• Therapeutic Exercises 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.

Physical Examination Findings (Key Impairments)

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


Intervention Approaches / Strategies 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

• Therapeutic Exercise Posterior tibialis strengthening exercise


Settled Stage/ Mild Condition Goal: Normalize strength, flexibility, and restore lower extremity functional mobility As above with following differences

• Therapeutic Exercise 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


4Pronatory 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.

Physical Examination Findings (Key Impairments) Acute Stage / Severe Condition

• 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 Sub Acute Stage / Moderate Condition

• The above impairments may be present – however with less severe functional limitations. Settled Stage / Mild Condition

• The above impairments may be present – however with less severe functional limitations.


6Intervention Approaches / Strategies

Acute Stage / Severe Condition 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

• Re-injury Prevention Instruction Proper footgear and/or inserts to limit pronation

Sub Acute Stage / Moderate Condition 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


7Settled Stage / Mild Condition Goal: Return patient to prior level of function or desired functional goals


• Therapeutic Exercises 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

• External Devices (Taping/Splinting/Orthotics) 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


• Therapeutic Exercises 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.


8Fiolkowski 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.

Joe Godges DPT KPSoCal Ortho PT Residency

SUMMARY OF ANKLE AND FOOT DIAGNOSTIC CRITERIA AND PT MANAGEMENT STRATEGIES DISORDER HISTORY PHYSICAL EXAM PT MANAGEMENT Ankle & Foot Mobility Deficits “Midtarsal Joint Capsulitis”

Arch area pain Recent strain or repetitive wt. bearing Sx’s worse w/ SLS or prolonged

wt. bearing

SR w/: End range accessory motion Test of one or more of the

midtarsal articulations

Joint Mob (to specific hypomobility) Ther Ex’s (Stretch/strengthen related muscles) Taping/footgear/orthotics

Ankle & Foot Mobility Deficits Hallux Rigidus

Stiffness Pain at “toe-off” phase of gait

ROM deficit: 1st MTP extension Pain at end range of 1st MTP ext. Limited MTP accessory movements

Joint Mob Ther Ex’s Patient Ed: Proper footgear

Ankle Muscle Power Deficits Achilles Tendinitis

Gradual onset of Achilles area aching Sx’s worse with activity

Swelling 1-2 inches above Achilles insertion

SR w/palpation of tendon in same area

Activity modification Proper footgear and/or heel lift Calf stretching Strengthening – esp. eccentric

Ankle Muscle Power Deficits “Posterior Calcaneal Bursitis”

Posterior heel pain Swelling Irritated by pressure, i.e., from a shoe

Swelling near Achilles insertion SR w/provocation of insertion on

posterior aspect of calcaneus

Physical agents (Ice, US, Phono, Ionto) Activity and Shoe Modifications

Ankle Movement Coordination Deficit “Lateral Ankle Sprain”

Inversion stress Swelling Pain If chronic – instability

Antalgic gait Lateral ankle effusion SR w/: Palpation of lateral ligaments Inversion stress May have laxity w/anterior drawer

P.R.I.C.E. Instructions Physical agents (Ice, E. Stim,) Friction massage Inferior Tib-Fib Mobs Proprioceptive Training Calf stretching Functional Strengthening

Ankle & Foot Radiating Pain Tarsal Tunnel Syndrome

Medial foot pain Paresthesias Numbness

SR w/: Tibial Nerve bias LLTT Provocation of Tibial Nerve in

Tarsal Tunnel

Rx entrapment (STM/JM to Med. Ankle and Foot) Tibial Nerve Mob (PROM and AROM Ex’s)

Foot Pain “Pronatory Disorder”

Aching in arch of foot Sx’s worse after prolonged weight

bearing

Excessive pronation at LR, MSt, or TSt Deficient Midtarsal supination or

Forefoot eversion at TSt Inability to form arch w/tibial external

rotation and calcaneal inversion

Joint mob/manip (to hypermobile of subluxed tarsal articulations)

Ther Ex’s (stretch shortened and strengthen weak myofascia of LE)

Taping Proper footgear or orthotics


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 Minimize deconditioning

Intervention:

• Re-casted with ankle in neutral dorsiflexion • Elevation and ice • 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 • Elevation and ice • 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 Surgical Indications and Considerations 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-dorsiflexion

5 Pilon fractures stages 1/3


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.

POSTOPERATIVE REHABILITATION 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 Maintain/improve general cardiovascular and muscular fitness

Intervention:

• Ice and elevation • 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 Maintain/improve general cardiovascular and muscular fitness

Intervention:

• Ice and elevation • 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 Maintain/improve general cardiovascular and muscular fitness 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

Selected References: 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

Surgical Indications and Considerations 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 dislocation of subtalar joint

20-50%

Type III Displaced fracture, dislocation subtalar AND tibiotalar joints

69-100%

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.

POSTOPERATIVE 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

Selected References: 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.

Physical Examination Findings (Key Impairments)


• 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


• 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 • Pain with dorsiflexion and/or external rotation of the foot • Mild to moderate tenderness with swelling/effusion over the above mentioned

ligaments Settled Stage / Mild Condition

• 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 • Therapeutic Exercises

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

• External Devices (Taping/Splinting/Orthotics) 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


• Therapeutic Exercises 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 Surgical Indications and Considerations 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. Preoperative Rehabilitation:

• 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 Goals: Control edema and pain

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

Selected References: 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 Surgical Indications and Considerations 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

Preoperative Rehabilitation:

• 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 Goals: Control edema and pain

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

Goals: Control edema and pain

Prevent extension of fracture and loss of surgical stabilization Prevent contracture and loss of motion at ankle/foot joints Minimize loss of function and cardiovascular endurance

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 Minimize loss of function and cardiovascular endurance

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 Selected References: 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 Surgical Indications and Considerations 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.

POSTOPERATIVE REHABILITATION 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

Selected References:

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

Surgical Indications and Considerations 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 mild weakness and pain

Elongation of tendon, moderate pain, weakness of tendon, mobile valgus rearfoot

Fixed valgus position of rearfoot with subtalar joint 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.

Preoperative Rehabilitation: • 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 Goals: Control edema and pain

Minimize deconditioning 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 Selected References: 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

Sub Acute Stage / Moderate Condition As above with the following differences

• Moderate pain and swelling • The symptoms and functional range of motion will improve as the stability of the joint

and closure of the diastasis is resolved.


2

Settled Stage / Mild Condition As above with the following differences

• 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


Acute Stage / Severe Condition 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

Sub Acute Stage / Moderate Condition 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

• Therapeutic Exercises 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.

Settled Stage / Mild Condition 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 Gradual progression of functional activities Standing on toes Pushing off on toes Pain free hopping on both legs progressing to single leg Step up on box or stairs Begin Stairmaster, treadmill, biking Initiate running when fast pace walking is pain free 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

Surgical Indications and Considerations 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

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

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

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.

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. Preoperative Rehabilitation

• 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

Selected References: 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 Surgical Indications and Considerations 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

Preoperative Rehabilitation

• 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 Goals: Control edema and pain

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. Selected References: 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.

Documents

14438524 Physical Therapy Protocols for Ankle and Foot Conditions