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STUDY GUIDE

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Table of Contents
1. Acute Trauma …………………………………………………………………………………… 7

2. Basic Science ……………………………………………………………………………………. 71

3. Complications…………………………………………………………………………………… 107

4. Diagnostic Evaluation/Medical Imaging……………………………………………. 137

5. Neoplasm/ Tumors/ Masses……………………………………………………………… 175

6. Other Conditions………………………………………………………………………………. 201

7. Procedural Perioperative management…………………………………………….. 255

8. Surgical Principals……………………………………………………………………………… 270

9. Surgical Procedures and Techniques………………………………………………….. 291

10. Surgically Relevant Medical Management…………………………………………. 327

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PART 1:
ACUTE TRAUMA

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Achilles Tendon Ruptures
I. Mechanism of Acute Stage Rupture

A. Push off weight bearing of FF with knee joint extended and contracted calf muscles (e.g. sprinters start)
B. Excessive ankle joint dorsiflexion (e.g. downhill skiing)
C. Violent dorsiflexion of a plantar flexed foot (e.g. coming down from a basketball rebound)
D. Contraction of calf muscles beyond the strength of the Achilles (e.g. carrying heavy items upstairs)
E. Risk Factors
1. Recreational athlete (weekend warrior)
2. Relatively older age (30-50 year old)
3. Previous Achilles tendon injury or rupture
4. Previous tendon steroid injections or fluoroquinolone use
5. Abrupt changes in training, intensity, or activity level
6. Participation in a new activity

II. Anatomy

A. Gastro-soleus complex

1. Function: Major supinator and plantarflexor of the foot. Also acts as a shock absorber of the lower extremity during athletic
activity.
2. Nerve innervation: Tibial nerve (S1 & S2).

B. Plantaris

1. Runs between the gastrocnemius and soleus. Assists in plantarflexion of the foot and flexion of the knee.
2. Nerve innervation: Tibial nerve (L4, L5, and S1).

C. Achilles Tendon

1. The strongest and thickest tendon in the body. Tendon is narrowest approximately 4 cm proximal to its insertion.
2. The blood supply for the Achilles tendon is derived from the posterior tibial artery and its contributions to the musculotendinous
junction. The mesosternal vessels also contribute by crossing the paratenon and infiltrating the tendon and the bone-tendon
junction at the calcaneus. Most Achilles tendon ruptures occur in the "watershed zone " (The watershed zone is an area 2-6 cm
proximal to the calcaneus, in which the blood supply is less abundant and becomes even sparser with age. It is in this region that
most degeneration and therefore rupture of the Achilles tendon occurs.") The left Achilles tendon is torn more frequently due to
the handedness of a person; right-handed individuals "push off" more frequently with the left foot and there are more right
handed people.

III. Patient History:

A. Patients frequently present with complaints of a sudden snap in the lower calf associated with acute/ severe pain, weakness and/or functional
loss.
B. Attempted ambulation elicits a limp or guarded gait.
C. Patients are unable to perform single -leg toe rise on injured foot.
D. The physician should question the patient about any recent use of fluoroquinolones, corticosteroids, or of corticosteroid injections.

IV. Clinical Presentation of Ruptured Achilles

A. Edema, ecchymosis of the foot, ankle and lower posterior leg.

B. Palpable delve at site of ruptured tendon.
C. Excessive passive dorsiflexion of ankle with patient prone and knee flexed to 90 degrees as compared to the contralateral side.
D. Clinical Tests
1. Positive Thompson test (squeezing of the calf muscle does not result in plantar flexion of the foot).
2. Hyper-dorsiflexion sign – With the patient prone and knees flexed to 90º, maximal passive dorsiflexion of both feet may reveal
excessive dorsiflexion of the affected leg.
3. O’Brien needle test –A 25 gauge needle is inserted at a right angle to the leg through the skin of the calf muscle just medial to
midline. This should be performed 10 cm proximal to the calcaneal insertion of the Achilles tendon. Motion of the hub of the
needle in a direction opposite that of the tendon during passive dorsiflexion and plantarflexion of the foot confirms an intact
tendon distal to the level of needle insertion.

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V. Workup

a. Standard radiographs (X-rays) are more useful in ruling out other injuries than in ruling in Achilles tendon ruptures. You may
observe clinical findings such as soft-tissue swelling, increased ankle dorsiflexion on stress views, calcifications (spurs), accessory
ossicles, calcaneal fractures or a Haglund's deformity. You may also see disruption of Kager's triangle (Kager's triangle can be
visualized on a lateral view of the ankle. It is located in the retro malleolar region and is defined anteriorly by the flexor hallucis longus
muscle and tendon and posteriorly by the Achilles tendon, with the base being the proximal aspect of the calcaneus. The space
contained within this triangle is filled with fatty tissue, producing a well-defined area.) View image below Upon rupture of the
Achilles tendon, this space becomes poorly demarcated and the normally transparent space occupied by fatty tissue becomes
obliterated on radiograph.
A.

i.

B. MRI's are very helpful in confirming the diagnosis.

Example MRI: Radiology Report

Achilles Tendon Complete Tear Radiology Report

MRI of the Left Ankle:

A small ankle effusion is present. Complete tear of the Achilles tendon is present with a gap of approximately 1.5 - 2 cm. Fluid and blood are present in this
region. The tendon proximal to this has a shredded appearance compatible with partial tear in the proximal portion of the tendon. This extends to the
myotendinous junction. The tear is approximately 4 cm proximal to the calcaneus. The posterior tibial tendon and the peroneal tendons are intact.
IMPRESSION:
1. Complete tear of the Achilles tendon with approximately 1.5 -2 cm separation of the tendinous ends. Diffuse partial tear involves the proximal
Achilles tendon to the myotendinous junction.
2. Small ankle effusion.

Views

Axial View T1 ( Fat Image) Below Tear:

Complete Achilles Tendon Rupture (Axial View T1)

This is a T1 or fat image because it has a short TR (300-800 msec) and a short TE (15-30 msec). Tendon tissue is
dark (black) and fat tissue is light (white). This is at a level below the tear where the Achilles tendon is intact.
Note the small sagittal view of the foot in the lower right corner. This shows the level of the axial slice. These
small scout views are present on each MRI slice or view. Use them to figure out your location.

Axial View T1 ( Fat Image) At Myotendinous Junction

Complete Achilles Tendon Rupture (Axial View T1) At

Myotendinous Junction

Again, this is a T1 or fat image because it has a short TR (300-800 msec) and a short TE (15-30
msec). Tendon tissue is dark (black), fat tissue is light (white), and muscle tissue is in between (dark gray).
This is at the myotendinous junction (note the scout view, the line is up higher in the leg). There is a
shredded appearance compatible with a partial tear at this level.

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Sagittal View T1 (Fat Image)

Complete Achilles Tendon Rupture (Sagittal View T1)

Again, this is a T1 or fat image because it has a short TR (300-800 msec) and a short TE (15-30 msec).
Tendon tissue is dark (black), fat tissue is light (white), and muscle tissue is in between (dark gray).

Sagittal View T2 (Water Image)

Complete Achilles Tendon Rupture (Sagittal View T2)

This is a T2 or water image because it has a long TR (1500-3500 msec) and a long TE (60-120 msec). The
Tendon and bone tissues appear dark (black) and the blood or fluid appears light (white).

VI. Achilles Rupture Differential Diagnosis

Ankle Fracture
2. Ankle Sprain
3. Calcaneofibular Ligament Injury
4. Talofibular Ligament Injury
5. Calcaneal fracture

VII. Achilles Rupture Treatment

A. Kuwada Classification:

Kuwada in 1990 published a classification system to guide surgical treatment for Achilles tendon injuries

Type 1: A partial tear. Recommended treatment: casting.

Type 2: A complete rupture with defect up to 3 cm. Recommended treatment: End-to-end anastomosis.

Type 3: A 3- to 6-cm defect in length following surgical debridement of the tendon ends to healthy tissue. Recommended treatment:
Tendon graft flap, +/- a synthetic graft augment. Additionally, a V-Y advancement, a Bosworth turndown, tendon transfer, or a
combination of these may also be used for type 3 injuries.

Type 4: A defect >6 cm that requires a gastrocnemius recession, a turndown, tendon transfer, free tendon graft, +/- synthetic graft, or a
combination of these surgical options.

B. Conservative Treatment:

The literature is filled with studies that compare conservative verses surgical management of ruptured Achilles tendons and list the pros and
cons of each treatment modality. The discussion should be decided on a case by case basis. There are many protocols for conservative
treatment, however, most recently protocols employ a period of non-weight-bearing casting. This is performed as either an above or below
the knee cast with the foot in equinus for approximately 2-4 weeks. This is generally followed by serial casting or functional splinting at 2 to
4 week intervals with gradually decreasing degrees of plantar flexion to obtain a neutral ankle position. Recent studies are coming to the
conclusion that longer treatment protocols appear less favorable than protocols of a shorter duration. Good functional results and relatively
low rates of re-rupture were reported in the shorter protocols. Non-operative treatment is usually indicated for patients who are elderly
and/or sedentary and for those with systemic illnesses. Patients with diabetes, wound healing problems, vascular disease, neuropathies, or
serious systemic diseases are often encouraged to opt for non-operative treatment as risk of complications may outweigh the benefits of
surgery.

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 1. Conservative Achilles Protocol
i. A short-leg cast is applied to the affected leg while the ankle is placed in slight plantar flexion (gravity
equinus). Immobilization is generally continued for 6-10 weeks.
ii. The ankle may gradually be dorsiflexed (forced dorsiflexion is contraindicated) to a more neutral position after a
period of immobilization (~4-6 wk). This position is sustained with serial casting or an adjustable ankle orthotic. Walking
in the cast is allowed after the assigned period of immobilization.
iii. Following cast removal, a 2-cm heel lift is worn in the shoe for an additional 2-4 months. It is during this time that
physical therapy is generally initiated.

C. Surgically Repair

1. Percutaneous surgery: Through stab wounds, sutures are passed through the distal and proximal ends, which are approximated while the ankle
is held in maximal equinus. Postoperatively, patients are placed in short leg, non-weight-bearing casts for 4 weeks, followed by an additional 4
weeks in a weight-bearing, low-heel cast. Some studies have revealed high rates of sural nerve entrapment with this procedure.

2. Open surgical repair: In general, surgical treatment is advocated for young and athletic individuals who frequently subject their Achilles tendon
to relatively high-demand activity. It has lower re-rupture rates; Increased postoperative muscle strength, power, and endurance. It also allows
earlier return to activities when compared with non-operative treatment.

a. A medial longitudinal approach is used to better visualize the Plantaris tendon and to avoid injury to the sural nerve. Midline
incisions are rarely used because of higher rates of wound complications and adhesions.

b. The paratenon is divided longitudinally to expose the

ruptured ends, which are irrigated and debrided. The ends
are then re-approximated and sutured with a heavy non-
absorbable suture using either a modified Kessler, Krackow,
or Bunnell technique. Care should be taken to avoid
overtightening of the Achilles tendon during repair.

c. If the repair is insecure, a pull-out wire or multiple

interrupted sutures may be used to reinforce the
site. Further augmentation is possible with a turn-down
fascial graft or a woven tendon graft.

d. Following surgery, the ankle is maintained in plantar-

flexion in a cast. After a period of immobilization, the foot is gradually brought into neutral or slight plantar flexion in a rigid orthosis,
and the patient is allowed to be partial weight bearing. Immobilization is typically discontinued 4-6 weeks after repair. At this point,
active and active-assisted range of motion, swimming, stationary cycling and walking in a shoe fitted with a heel lift can be initiated.
In most cases, patients can progress to full activity within 4 months of surgery.

e. Other Techniques

i. Lynn Technique: 2 ends approximated and sutured. The most commonly used suture technique is the
Bunnell or modified Bunnell. The plantaris tendon, if present can be stretched into a membrane and fanned
around tendon as an autogenous reinforcement/ autograft.
ii. Lindholm: 2 flaps created proximally are brought down and sutured to tendon.

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Ankle Ligamentous Injuries
I. Classification of Ligamentous ankle injuries (3 categories, based on the extent of ligament damage):

A. Grade I - Micro-injury; No macroscopic tears or mechanical instability to ankle ligaments. Minimal pain and tenderness.

B. Grade II - Partial tear; Mild to moderate joint instability may be present. Moderate pain and tenderness.

C. Grade III - Complete tear; significant joint instability and inability to bear weight. Severe pain and tenderness.

II. Anatomy

A. Ankle (Talocrural Joint) a modified ginglymus or hinged synovial joint.

1. Motion: displays triplane motion. The motion occurs primarily in the sagittal plane (dorsiflexion and plantar flexion), with small
amounts of transverse and frontal plane motion (abduction/adduction and eversion/inversion respectively).

2. Articular surfaces:

i. The ankle mortise. Consists of the concave distal tibial bearing surface (aka: tibial plafond).
ii. Triangular facet of the lateral malleolus
iii. Comma-shaped facet of the medial malleolus.

3. Soft tissue structures

a. Fibrous Capsule: Completely surrounds the ankle joint and is thin anteriorly and posteriorly. Strong collateral ligament
both medially and laterally support the fibrous capsules.
b. Deltoid Ligament (aka: medial collateral ligament): Fans out in a triangular shape and contains one deep and three
superficial portions. 3 total attachments from the tibia to the talus, calcaneus and navicular bones.

a. Superficial Fibers of Deltoid Ligament:

• Tibionavicular (anterior fibers) - attaches to the tuberosity of the navicular bone.
• Tibiocalcaneal (middle fibers) - travels inferiorly from the tibia and attaches perpendicularly
to the entire length of the sustentaculum tali of the calcaneus. These fibers also blend with
the spring ligament
• Posterior Tibiotalar (posterior fibers) - travels posteriorly and laterally from the medial
aspect of the tibia and ultimately attaches to both the medial side of the talus and the
medial tubercle of the talus.

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 b. Deep Fibers:
• Anterior Tibiotalar (deepest fibers) - These fibers are well developed and attach to both the
tip of the medial malleolus superiorly and the non-articular aspect of the medial surface of
the talus inferiorly.

Note: The Tibialis Posterior and the Flexor Digitorum Longus cross over the Deltoid Ligament.

c. Lateral Ligament of the Ankle:

• Anterior Talofibular Ligament: (Intracapsular and shortest lateral ligament) from the anterior margin of the
lateral malleolus to the lateral aspect of the neck of the talus. It is a capsular thickening.
• Posterior Talofibular Ligament: (Intracapsular but extra-synovial and the strongest) from the lower part of
the lateral malleolar fossa to the lateral tubercle of the posterior process of the talus.
• Calcaneofibular Ligament: (extracapsular and deep to the peroneal tendons) a long rounded cord running
from the apex of the fibular malleolus to a tubercle on the lateral surface of the calcaneus. It stabilizes the
ankle joint and the subtalar joint.

Calcaneofibular ligament will be seen underneath retracted peroneal tendons.

Note: The best way to evaluate the integrity of the CFL is to examine the ankle in a dorsiflexed position.

b. Tibiofibular Joints: The tibiofibular joints include the proximal and distal tibiofibular joints and middle tibiofibular joint
(crural interosseous membrane).
• Motion: Allow motion in both the frontal and transverse planes, and resist ankle dorsiflexion as the wider
anterior portion of the dome of the talus engages the mortise.
• Proximal tibiofibular joint: A plane synovial joint supported by the:

i. Anterior superior tibiofibular ligament

ii. Posterior superior tibiofibular ligament.

• Middle tibiofibular joint: The crural interosseous membrane consists of obliquely oriented, dense fibrous
connective tissue running from proximal-medial to distal-lateral from the tibia to the fibula.

• Distal tibiofibular joint: A Syndesmosis: supported by the:

• Anterior inferior tibiofibular ligament

• Interosseous tibiofibular ligament
• Posterior inferior tibiofibular ligament.

Notes: The Talofibular ligaments along with the Calcaneal Fibular Ligament are components of the lateral ligament complex. This complex becomes
stressed when the ankle is inverted and plantar flexed. Supination of the foot in neutral flexion usually results in injury of the Calcaneal Fibular
Ligament. Supination and adduction injuries tear both the Anterior Talofibular Ligament and the Calcaneal Fibular Ligaments. The Posterior Talofibular
Ligament is the strongest of the lateral ligaments, and extreme inversion with plantar flexion is required to place the PTFL under stress; as a result, the PTFL
is less commonly injured. Transient subluxation or dislocation of the talus from the tibial mortise usually results in injury of all 3 lateral ligaments.
Prevention of anterior displacement of the talus is primarily a function of the ATFL. Little additional motion occurs when the CFL also is damaged.
Instability to inversion is greater when both the CFL and the ATFL are injured than when either ligament is injured alone.

I. Causes of Ankle Instability

1. Post-traumatic ligamentous disruption

2. Osteochondral dome fractures
3. Degenerative Joint Disease
4. Peroneal Subluxation
5. Muscular weakness or paralysis
6. Talofibular meniscoid
7. Generalized ligamentous laxity
8. Tibial-fibular diastasis
9. Non-union of previous ankle fracture
10. Poorly reduced yet healed fracture
11. Fixed calcaneal varus
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 12. Tibial varum
13. Rigid plantarflexed first ray
14. Torsional deformities

Note: The Anterior Draw Sign is a push - pull examination of the ankle used to identify weakness or tears of the anterior talofibular ligament (ATF).

Note: Positive abduction stress to the ankle indicates rupture of the deep Deltoid.

II. Repair

A. Attempt to repair ligament injury in active athletic people, especially in light of a talar tilt, approximately 10 degrees greater than non-injured side.
B. Can perform a delayed primary repair with chronic pain and instability after ligamentous injury months earlier.
C. Incision is J-shaped for primary or delayed primary repair, from behind lateral malleolus to extensor tendon. Attempt to stay in between sural and
IDCN.
D. Anterior talofibular ligament is inherently involved with capsule. Repair with 2-0 non-absorbable and reinforce with 2-0 or 3-0 absorbable, Cast 4-6
Weeks Non-weight bearing

III. Procedures that stabilize one ligament

A. Lee Ankle Stabilization Procedure

Detach brevis tendon as high as possible. Suture brevis muscle belly to longus.
Drill hole posterior to anterior on fibula. Route tendon through & suture on itself.

B. Evans Ankle Stabilization Procedure

Detach brevis. Make tunnel in fibula from anterior inferior to posterior superior. Tendon passed through and sutured
at both ends of tunnel.

C. Watson - Jones Ankle Stabilization Procedure

Section brevis. Drill holes through fibula from front to back one on top of another. Another hole in talus neck from
dorsal to plantar. Route tendon through upper hole in fibula, through talar upper hole, out bottom hole in talus and
in bottom fibula hole and tie to itself.

D. Nilson Ankle Stabilization Procedure

Section brevis and tie muscle to longus. Gouge sub periosteal area on lateral malleolus. Place brevis tendon in
defect and suture periosteum over.

IV. Procedures that stabilize two Ligaments:

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E. Christman - Snook Ankle Stabilization Procedure
Detach brevis. Take brevis through front to back holes on fibula. Then take into hole on lateral calcaneus.

F. Elmslie Ankle Stabilization Procedure

Use facia lata. Similar to a figure eight at right angles to each other through neck of talus - lateral malleolus - calcaneus.

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Ankle Fractures
I. Terminology

a. Chaput-Tillaux Fracture
i. Avulsion fracture of tibial from anterior inferior tibial fibular ligament
b. Wagstaffe Fracture
i. Avulsion fracture of fibula from anterior inferior tibial fibular ligament
c. Tillaux Kleiger (juvenile Tillaux)
i. Occurs because of a closure of the medial tibial physis before the lateral physis.
d. Volkmann's Fracture
i. Fracture of the posterior tibia (posterior malleolus) from the posterior inferior tibiofibular ligament.

II. Lauge Hansen Classification

(First word - position of foot, second word - direction of deforming force, movement of the foot or talus)

A. Supination-Adduction: involves pure inversion of heel and talus

1. Stage I - rupture of lateral collateral ligaments or classic transverse avulsion fracture of lateral malleolus. The
fracture is transverse (horizontal) at or below the ankle joint level.

2. Stage II - with further force of talus, there is an abutment of talus against the medial malleolus causing a short
oblique fracture (classic vertical fracture of the medial malleolus).

a. The tibial-fibular syndesmosis and syndesmotic ligaments are always intact

B. Pronation-Abduction

1. Stage I - rupture of the deltoid ligament or transverse avulsion fracture of medial malleolus.

2. Stage II - rupture of the anterior and posterior inferior tibial-fibular ligaments or avulsion of small fragments
of bone from tibial or fibula.

3. Stage III - Classic short oblique fracture of the lateral malleolus.

a. X-rays: On lateral view, the fracture appears transverse.

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C. Supination External Rotation (SER) consider the talus rotating about an axis comprised of medial malleolus and deltoid
ligament (Picture) Most common type (60 –80 % of ankle fractures are of this type).

1. Stage I - disruption of the anterior-inferior tibial-fibular ligaments or avulsion fractures of

Wagstaffe or Chaput-Tillaux

2. Stage II - Classic spiral fracture of the lateral malleolus, beginning at the joint line. The fracture line
runs laterally from anterior inferior to superior posterior. X-ray views

3. Stage III - Disruption of posterior-inferior tibial-fibular ligaments or avulsion fracture of the

posterior inferior portion of the tibia from Volkman triangle (posterior malleolus).

4. Stage IV - Rupture of deltoid ligaments or transverse fracture of medial malleolus.

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 D. Pronation External Rotation (PER) external rotation of talus about an axis consisting of lateral malleolus and
lateral collateral ligaments

1. Stage I - Disruption of deltoid ligament or transverse avulsion fracture of medial malleolus.

2. Stage II - rupture of anterior-inferior tibial-fibular ligament or fracture of Wagstaf or Tillaux-

Chaput.

3. Stage III - Interosseous membrane torn above syndesmosis and below fibular head and then a
classic high fibular fracture occurs approx. 4-5 cm above joint line.

4. Stage IV - disruption of posterior-inferior tibial-fibular ligaments or avulsion fracture of tibia

(Volman) or fibula

Classic Fractures to remember:

Use this for quick reference only. It is better to understand the process and think it through, but in a pinch, this may help.

Fibular (Lateral) Malleolus Fractures:

Transverse fibular malleolus = Supination-adduction stage I

Short oblique fibular malleolus (only on AP view) = Pronation-abduction stage III

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 Spiral fibular malleolus (on both AP & Lat) = Supination-eversion stage II

High fibular malleolus = Pronation-eversion stage III

Tibial (Medial) Malleolus Fractures:

Vertical medial malleolus (Short oblique fracture) = Supination-adduction stage II

Posterior Malleolus Fractures:

Avulsion fracture Volkman triangle (posterior malleolus)

plus spiral fracture of the lateral malleolus = Supination-eversion stage III

Avulsion fracture Volkman triangle (posterior malleolus)

plus high fibular fracture = Pronation-eversion stage IV

III. Danis Weber Classification - describes whether the fibular fracture line begins: below the inferior tibia- fibular syndesmosis
(Type A), at the level (Type B), or above the level of the syndesmosis (Type C)

A. Type A

1. Involves transverse avulsion fracture of fibular at level of ankle joint or distal.

2. Inferior tibial-fibular ligaments are intact
3. May see associated medial malleolar short oblique fracture
4. Corresponds to Lauge Hansen Supination Adduction injury

B. Type B

1. Spiral or oblique fracture beginning at inferior tibial-fibular syndesmosis

2. Tibial-fibular ligaments are usually disrupted but interosseous membrane intact
3. May have disruption of deltoid or transverse medial malleolar fracture
4. Corresponds to Lauge Hansen External Rotation or Pronation Abduction

C. Type C

1. Fibular fracture above the level of the tibial-fibular syndesmosis up to fibular head
2. Rupture of tibial-fibular syndesmosis and interosseous membrane
3. Deltoid rupture of transverse medial malleolar fracture
4. Corresponds to Lauge Hansen Pronation Eversion

IV. Key Points for Fixation

1. Fibular fracture is known as the dominant fracture and is most important

2. Restoration of length of fibular takes precedence over repair of inferior tibial-fibular syndesmosis
3. Realign ankle mortise
4. Evaluation of talar dome and tibial plafond
5. Reapproximation of soft tissue supporting structures
6. A roentgenographic pathognomonic sign identifying an avulsion fracture off the distal lateral fibula associated with
acute peroneal tendon subluxation is best seen on a Mortise (Medial Oblique) View.

V. Treatment

A. Closed Reduction

1. Plays a role in immediate reduction if neurovascular compromise has resulted

2. Used in debilitated patients or ones at operative risk
3. Fractures with minimal displacement
4. Need to sedate patient - have anesthesiologist there to administer general, or give IV sedation of Demerol and Valium
5. Basic concepts

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 • Recreate injury
• Apply distal traction
• Reverse mechanism of injury
• Use curved plaster cast with 3 point pressure (minimal padding)
• 6-8 weeks non-weightbearing

________________________________________________________________

Radiographic Criteria for Adequate Reduction of Displaced Ankle Fractures

a. No widening of medial clear space

b. No displacement of malleoli on AP views
c. Less than 2mm of posterior displacement of lateral malleolus on
d. lateral view
i. No angulation
ii. Fracture of less than 25-30% of the posterior malleolus

_________________________________________________________________

B. Open Reduction

a. Best time-immediately after injury before severe edema and hematoma form
b. After 6-12 hours, edema with hematoma may prevent wound closures
c. In this case, close reduce, put Jones on, ice, wait 4-14 days
d. Wait until fracture blisters heal

VI. Specific Fracture Reductions with ORIF

A. Supination-Adduction

a. Use two .062 inch K-wires with 22 gauge tension band wire for transverse fibular fracture
b. Use two 4.0 mm cancellous screws perpendicular to fracture line and parallel to each other to fix oblique medial malleolar fracture

B. Pronation-Abduction

1. Fix the short oblique lateral malleolar fracture with five or six hole 1/3 tubular axial compression plate with 3/5
mm cortical screws to secure the plate above the fracture line (through both fibular cortices) but not below the
fracture line, as you'll damage talus. Only purchase one cortex.
2. Repair inferior tibial-fibular ligaments with 0 non-absorbable suture. If Tillaux fracture, use 4.0 mm cancellous
screw
3. Transverse medial malleolar fracture is fixed with two 4.0 mm cancellous screws perpendicular to fracture line and
parallel to each other

C. Supination-External Rotation

1. Spiral fracture is fixed with interfragmental 4.0 mm cancellous screws or 3.5 mm cortical screws. Supplement with
one-third 5-6-hole tubular neutralization plate placed perpendicular to plane of the interfragmental screws. (Plate
anchored with 3.5 mm cortical screws/ or posterior anti-glide plate technique.
2. Repair of anterior inferior tibial fibular syndesmosis or avulsions.
3. If small posterior fracture fragment occurs, it should reduce with reduction of the fibula since the posterior inferior
tibial-fibular ligament is intact.
4. If large fragment posteriorly (greater than 25% of posterior malleolus) it must be reduced. Use 4.0 Cancellous
screw posterior to anterior
5. Two 4.0 mm cancellous screws perpendicular to transverse avulsion medial malleolar fracture and parallel to each
other.

D. Pronation-Eversion

1. For fibular fractures mid-diaphyseal level or lower, use intrafragmental compression screws, with 4.0mm cancellous or
3.5 mm cortical screws, then augment with 1/3 tubular neutralization plate. (use transfixing screw through plate for
fractures distal diaphysis)

The goal of tibiofibular transfixation is to stabilize the mortise without compression (you do not want to use a lag screw technique which would
result in compression). Two fully threaded 3.5 mm cortical screws or a single 4.5 mm are used to rigidly position the fibula in relation to the tibia.

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The screws should be directed from posterolateral to anteromedial at an angle of 25-30 degrees from the sagittal plane of the leg. The transfixation
screw must purchase both cortices of the fibula and the lateral cortex of the tibia.

Placement of the transfixation screws varies with the level of the fibular fracture. If a distal diaphysis fibular fracture is fixated with a one-third
tubular plate, the transfixation screw is incorporated through a hole in the plate located 3 to 5 cm proximal to the anterior inferior tibiofibular
ligament. If the fibula fractures at a mid-diaphyseal level and is fixated with a one-third tubular plate, the transfixion screw/screws may be placed
distal to the fracture line but 3 to 5 cm proximal to the syndesmosis. With a Maisonneuve fracture, two 3.5 mm cortical screws are placed 3 to 5 cm
proximal to the syndesmosis.

The patient bears absolutely no weight for 6 to 8 weeks. However active range-of-motion exercises are initiated as early as the first postoperative
day. Transfixation screws are generally removed before full weight bearing begins at 6 to 8 weeks.

2. In Maisonneuve fractures - *** don't open reduce due to complication with peroneal nerve ***

3. First fix distal fibula into fibular notch on tibia and temporarily transfix tibia and fibula with 5/64 Steinmann pins and x-ray to visualize mortise
and length of fibula. If good, suture interosseous membrane and then use final fixation with two 3.5 mm cortical screws. Goal is to stabilize
without compression of the mortise.

4. Remove transfixing screws at 6-8 weeks and hardware at four to six months.

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Bite Wounds
I. General Information

A. Dog bites are one of the most common causes of nonfatal injuries in the US and the lower extremity is one of the most common sites for
all animal bites.
B. Human bites, although less common in the lower extremity, are potentially even more dangerous because it is true that the human
mouth is "dirtier" than an animal's.
C. Many patient variables determine the potential for a bite to become infected.

i. The type of animal

1. Cat bites are more likely to become infected, because they are more commonly deep puncture wounds.
2. The location of the wound.
a. Extremity bites are more likely to become infected than bites in other locations.
b. If the byte is near a joint or bone, you must consider the possibility of direct inoculation. Septic arthritis
and osteomyelitis.
3. The general medical condition of the patient. The presence of diabetes, chronic alcohol usage. and other
immunocompromising conditions.
4. The type of injury:
a. Puncture wound, is the most dangerous and most common with cats.
b. Tear
c. Crush
d. Scratch
5. Treatment delay (more than 12 hours on the extremities).

II. Clinical Presentation

1. localized cellulitis may occur as soon as 12 hours following the injury.

2. A local abscess with purulence and drainage then forms.
3. Systemic involvement very rarely occurs except in cases that present very late. These include fever, chills and malaise.
4. Dog bites very often present with significant soft tissue damage and devitalized tissue. Some dogs may exert up to 2000
pounds PSI of pressure on tissue which is very destructive.
5. if the bite is near a joint, painful range of motion or other signs of septic arthritis may be seen following puncture wounds.

III. Laboratory Findings

1. Gram stain of any purulent exudate usually reveals multiple organisms, both gram-positive and gram-negative.
2. These wounds are usually localized and unless any systemic involvement is apparent, blood studies usually prove
noncontributory. However, in late untreated wounds with systemic symptoms. The usual parameters for infection will be
seen (elevated ESR, elevated WBC with a shift to the left, etc.).

IV. Bacterial Etiology

V. Treatment

A. A careful history should be taken, which includes when the bite occurred and the behavior of the animal prior to the
attack. Most dog attacks occur by animals known to the victim so observation of behavior is possible. Rabies vaccination is
administered as indicated.

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Tetanus Prophylaxis

Complete (all ages) Online Guideline

I. Unimmunized, Uncertain, or Incomplete Immunization

A. Low risk wounds -- one dose Tetanus Toxoid (T.D.)

B. Tetanus prone wounds -- one dose of T.D. plus 250 to 500u of human Tetanus Immune Globulin (TIG)
NOTE: Use separate syringe and sites for T.D. and TIG.
II. Full Primary Immunization and Booster Within 10 Years of Wound

A. Low risk wound -- nothing.

B. Tetanus prone wound -- if more than 5 years since last dose, give one dose of T.D.
C. Neglected wound greater than 24 hrs. --one dose of T.D. and 250-500u TIG.
III. Full Primary Immunization, But more Than 10 Years

A. Low risk wound -- one dose T.D.

B. Tetanus prone wound -- one dose T.D.
C. Neglected wound -- one dose T.D. plus 250-500u TIG.
Note: Primary immunization is two .5 ml. T.D. injections 4-6 weeks apart followed by a third injection 6-12 months later.

B. Tetanus prophylaxis should be administered, per the guidelines

C. I&D any abscess and debridement of necrotic wound edges, with the cultural sensitivity should be performed. The area
should then be copiously irrigated, preferably with Povidone iodine solution.

D. If the possibility of bone or joint involvement exist baseline radiographs should be taken.

E. In cases without established infection, prophylactic antibiotics is controversial. However, because of the high bacterial
inoculum and the potential for devastating infections, antibiotic therapy should be initiated.

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1. Drugs of first choice. Any of the Beta -lactamase inhibitor compounds, including amoxicillin/clavulanic acid
(oral), piperacillin/tazobactam, ticarcillin/clavulanic acid or ampicillin sulbactam (parenteral).

2. Levofloxacin or one of the other newer generation quinolones such as moxifloxacin

3. Azithromycin (strictly as an alternative)

4. Cefuroxime axetil or other later generation cephalosporins (also as an alternative)

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Calcaneal Fractures
Peak age group - 45 years

Men 5 times more prone than women

Calcaneal fractures are associated with spinal fractures 20% of time, T12 - L2 area, L1 most common vertebrae fractured. Other associated fractures
include femoral neck fractures and tibial plateau fractures.

I. Mondor's Sign

A. Ecchymosis going to sole of foot, pathognomic of calcaneal fracture

II. Bohler's Angle

A. 25 - 40 degrees
B. Used to access degree of intra-articular depression of talocalcaneal joint
C. No Take x-rays of other foot to determine this angle

III. Radiologic evaluation of calcaneal fractures

A. AP - assess calcaneal cuboid joint

B. Lateral - assess posterior facet, Bohler's angle, depression of STJ
C. Medial Oblique - assess anterior process and calcaneal cuboid
D. Axial - assess posterior facet and sustentaculum tali
E. X-rays of ankle, legs, low back, etc.

Ligaments & Muscle Attachments to Calcaneus

IV. Rowe Classification of Extra-Articular Calcaneal Fractures

A. Type I-A
1. Fracture of calcaneal tuberosity from fall with heel everted or inverted. Can have splaying and widening which may interfere with
peroneals.
2. Treatment - BK cast, 6 weeks, WB if non-displaced (manually reduce widening), ORIF if displaced

B. Type I-B

1. Fracture of sustentaculum tali from fall with twist on supinated foot

2. Clinical exam by flexing and extending hallux due to FHL
3. Axial calcaneal x-ray best view
4. Treatment - cast 6 weeks if non-displaced
5. ORIF if displaced

C. Type I-C

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 1. Fracture of anterior process (most common Type I fracture)
2. Only calcaneal fracture where females have higher incidence
3. Is an avulsion injury of bifurcate ligament
4. Force is plantar flexion on a supinated foot
5. See clearly on lateral or medial oblique views
6. May need tomograms to visualize
7. Treatment - BK walking cast for 6 weeks, excise fragment if symptoms persist

D. Type II

1. Beak and/or Avulsion fracture of calcaneus

2. May or may not involve Achilles

a. Beak fracture - does not affect Achilles insertion, treat with cast for 6 weeks in plantar flexion if non- displaced

b. Avulsion fracture - pull off of Achilles, must reduce ORIF if displaced

E. Type III

1. Fracture of body without involvement of STJ (most common extra-articular fracture)

2. Results from fall with edge of talus going into calcaneus
3. Lateral x-ray and axial views most helpful

a. Axial view determines STJ involvement

4. Treatment - cast with knee flexed, ORIF if displaced

F. Type IV

1. Fracture of body of calcaneus involving STJ

G. Type V

1. Central depression fracture with degree of comminution

(usually Essex Lopresti system used to describe intra-articular fractures)

V. Essex Lopresti System of Intra-Articular Fractures

A. Comprise 75% of all calcaneal fractures, usually results from fall from high place, talus driven down into calcaneus (Types A and B are
differentiated by secondary fracture line and shape of fragments)

B. Type A (tongue fracture)

1. Primary fracture line is from superior to inferior, extending from Gissanes critical angle to plantar aspect calcaneus.

2. Usually a direct force will cause fracture to go out through back.

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 C. Type B - (joint depression)

1. Primary fracture line exactly as in tongue fracture

2. Secondary fracture is that the posterior facet is driven down causing joint depression and possible comminution

VI. Sanders Classification:

B. Advances in cross-sectional imaging, particularly in computed tomography (CT), have given this modality an important role in identifying and
characterizing calcaneal fractures.

C. This classification is based on the number of intraarticular fracture lines and their location on semi coronal CT images. It is useful not only in
understanding typical fracture patterns of the calcaneus, but also in predicting outcome. As you move from type 1 to type 4 injuries, expected
outcomes are progressively worse.

D. The calcaneum is divided into three columns by two fracture lines A and B. A third fracture line C, separates the sustentacular fragment from the
posterior facet of the calcaneum, thereby giving rise to four potential articular fragments.

Type 1: includes all intraarticular fractures that have less than 2mm of articular displacement, regardless of the number of
fracture lines/fragments present.

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Type 2a: involves one primary fracture line that courses through the lateral aspect of the posterior facet; the primary
fracture usually assumes a "y" shaped configuration as it exits medially and laterally out of the calcaneal body; this
fracture is often accompanied by one or more accessory fracture lines that do not involve the posterior articular facet.

Type 2b: involves one primary fracture line that courses through the central aspect of the posterior facet;
the primary fracture usually assumes a "y" shaped configuration as it exits medially and laterally out of the
calcaneal body; this fracture is often accompanied by one or more accessory fracture lines that do not
involve the posterior articular facet.

Type 2c: involves one primary fracture line that courses through the medial aspect of the posterior facet and is
accompanied by a transverse fracture through the body of the calcaneus; this fracture is often accompanied by
one or more accessory fracture lines that do not involve the posterior articular facet.

Type 3ab: involves two primary fracture lines, one coursing through the lateral aspect of the posterior facet
and the second through the central aspect; this subtype usually presents with depression of the central
fragment; the two primary fracture lines may be accompanied by additional accessory fracture lines that do
not involve the posterior articular facet.

Type 3ac: involves two primary fracture lines, one coursing through the lateral aspect of the posterior facet and the
second through the medial aspect; this subtype usually presents with depression of the central fragment. The two
primary fracture lines may be accompanied by additional accessory fracture lines that do not involve the posterior
articular facet.

Type 3bc: involves two primary fracture lines, one coursing through the central aspect of the posterior facet and the
second through the medial aspect; this subtype usually presents with depression of the central fragment; the two
primary fracture lines may be accompanied by additional accessory fracture lines that do not involve the posterior
articular facet.

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 Type 4: involves three or more primary fracture lines with greater than 2mm of articular displacement, and are therefore severely
comminuted (usually with 4 or more parts).

Image of All Sanders Classification Types

VII. Initial Management

• Watch for neurovascular insult - need to perform immediate reduction

• Wait to reduce if fracture blisters
• Ice, Compression, elevation to reduce severe edema
• If seen within hours, best to operate then

VIII. Mechanics

A. The calcaneal tuberosity is lateral to center of talus

B. With vertical compressive force, you get two primary fracture fragments

1. Supero-medial fragment (sustentaculum tali)

2. Tuberosity fragment with lateral 1/3 to 1/2 of lateral posterior facet

C. If force continues, the talus and sustentaculum tali are driven down and medial

D. If force still continues

1. Postero-lateral edge of talus is driven into superolateral posterior facet driving into cancellous bone of tuberosity fragment
2. May now get blow out of lateral wall of calcaneus with possible extension into calcaneal cuboid joint
3. Usually a step deformity results

IX. Palmer's three constant components of intra-articular fracture

A. Vertical shearing fracture

B. Fracture of lateral cortex
C. Depression fracture of lateral posterior subtalar joint

X. Deformity to foot after major fracture

A. Increased calcaneal width

B. Decreased calcaneal height and length
C. Intra-articular fx of the posterior STJ
D. Outward bulging of the lateral wall of tuberosity fragments

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 1. Possible impingement of peroneal tendons, sural nerve

XI. Treatment

A. Simple immobilization, often combined with early weightbearing1.

1. Eliminates risk of pin tract infection
2. Limited weightbearing after one week, progressing to full at 6-12 weeks
B. Manipulation with skeletal traction or cast (Boehler method)
1. Not utilized much today, due to crush injury to soft tissue and pin tract infection
C. Early subtalar (Gallie) or triple arthrodesis
D. Palmer method (for joint depression)
1. With elevator, lever up the depressed fragment bearing the articular surface.
2. Inserted an autogenous iliac crest bone graft beneath the fragment for stability
3. Short leg NWB cast 12 weeks
E. Essex Lopresti method
1. Used only in tongue fractures
2. Steinmann pin in posteriorly to lift fragment
3. Lateral compression with palms to reduce heel broadening
4. For joint depression fractures, elevate depressed fragment under direct visualization then maintain it by Gissane spike
through tuberosity from behind
5. Use drains

XII. Complications

A. Post traumatic STJ arthritis

B. Ankle joint arthritis
C. Tenosynovitis of peroneals
D. Plantar heel pain due to diminished hydraulics of fat pad
E. Sural or PT nerve entrapment
F. Shuffling gait from stiffness

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 Compartment Syndrome
I. Definition

A. Compartment syndrome is a condition where the perfusion pressure drops below the tissue pressure within an enclosed anatomic space. The
elevated pressure results in muscle and nerve ischemia which can cause permanent injury.

B. Potentially Fatal Complications

1. Rhabdomyolysis
2. Renal Failure
3. Ischemic Contractures

II. Causes of Compartment Syndrome

• Tibial Fractures
• Crush Injuries
• Motor Vehicle Accidents
• Reperfusion Injuries
• Post-Op Complication
• Drug Overdose
• Tight Cast or Tight Dressing
• Severe DVT
• Minor Trauma

III. Clinical Examination

A. Visible Signs and Symptoms

1. Patients with local trauma to arms or lower extremities

2. Patients with gross deformities as a result of trauma

B. The Five P's

1. Pain Out of Proportion

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 1. Often the most reliable indicator of CS
2. Patients typically complain of a deep, dull, aching pain that will not go away
3. Pain is worsened by passive stretching of the involved muscles located within the suspected anatomical space
4. Compare pain with passive stretching to the unaffected limb
2. Pallor
3. Pulselessness
4. Paresthesias
1. Sensory nerves are typically affected earlier

C. Loss of two-point discrimination

D. Loss of vibratory sensation
1. Poikilothermia

IV. Diagnostic Testing for Compartment Syndrome

B. Compartmental Pressures
1. Performed by inserting a Wick's catheter or pressure tonometer directly into the involved anatomical space

1. Normal compartmental pressures in the foot are 8 mmHg

2. Abnormal is a resting pressure greater than or equal to 30 mmHg and would require emergency treatment
3. Because vascular occlusion will occur when a patients intracompartmental pressure equals the patients current diastolic
pressure it is also important to consider any intracompartmental pressures 30 mmHG (or less) below their current diastolic
pressure as requiring emergency treatment

C. Plain Film X-rays (to visualize potential fractures)

D. Serum Myoglobin and CK levels (indicates muscle damage)
E. Potassium Levels (Indicates potentially fatal rhabdomyolysis)
F. BUN/Creatinine (Indicates renal failure)

V. Anatomical Compartments of the Foot

A. Original Theory

1. The foot has 4 compartments Medial, Lateral, Central, and Interosseous

B. First Alternative Theory and Tonometer Insertion Methods sub 4th

1. A more recent study using dye injections into cadaver feet has revealed that the foot actually has 9 compartments (Manoli & Weber,
1990)

a. (1) Medial Compartment runs the entire length of the foot - Enter via placing the catheter 4cm inferior to the medial
malleolus

b. (1) Lateral Compartment runs the entire length of the foot - Access by inserting catheter inferior to the 5th metatarsal

c. (1) Superficial compartment - Access by inserting catheter into the flexor digitorum brevis muscle in the arch

d. (4) Interosseous compartments in the forefoot located between the metatarsals

e. (1) Adductor compartment in the forefoot - Located deep to the interosseous compartment

f. (1) Calcaneal compartment which communicates with the deep posterior compartment of the leg - Can be entered by
pushing the catheter deeper into the foot after making your entry into the medial compartment

C. Second Alternative Theory

1. A paper done by Ling in 2008 has proposed that the foot has only 3 compartments running from hindfoot to midfoot divided by thick
fascia bands and that the forefoot does not have a distinct compartment

a. Medial Compartment

b. Intermediate Compartment

c. Lateral Compartment

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 D. Compartments of the Leg

a. Anterior Compartment: Tibialis anterior, Extensor hallucis longus, extensor digitorum longus, and Peroneus
tertius

b. Lateral Compartment: Peroneus longus and Peroneus brevis

c. Superficial Posterior Compartment: Gastrocnemius, Soleus, and Plantaris

d. Deep Posterior Compartment: Tibialis posterior, Flexor hallucis longus, Flexor digitorum longus, and
Popliteus

NOTE: The Anterior Compartment of the leg is the compartment

most commonly affected regarding compartment syndrome.

VI. Emergency Treatment of Compartment Syndrome

A. Preventing Nerve Damage and Muscle/Tissue Necrosis via Emergency Fasciotomy

1. Functional nerve deficits may start to occur as soon as 30

minutes after the onset of occlusion and subsequent ischemia

2. Permanent nerve damage may result as soon as 12 hours

after onset of the ischemia

3. Muscle damage may start to occur as soon as 2 - 4 hours

after the onset of ischemia

4. Prolonged ischemia may result in scar tissue and adhesion

formation within and adjacent to the muscle tissue

5. The sooner a fasciotomy is performed after CS has been

diagnosed the better

VII. Fasciotomy to Treat Compartment Syndrome

A. Fasciotomy is performed as soon as possible under general anesthesia without a tourniquet

B. Incisions for this procedure generally involve a dorsal approach, a medial approach, or both

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 i.

C. Continue to monitor intracompartmental pressures over post-operative course

D. Wet to dry dressing changes with normal saline beginning on the second post-op day
E. Elevation is contraindicated and the limb is to be kept at heart level during the post-op recovery period
F. Alternative treatments include hyperbaric oxygen therapy

VIII. Complications Post Compartment Syndrome Fasciotomy

A. Loss of sensation
B. Claw toes or cavus foot as a result of muscle infarction
C. Death from renal failure or sepsis
D. Note: Patients may develop fibromyalgia or CRPS due to nerve damage despite performing an emergency open fasciotomy. It may be
beneficial to refer patient to a chronic pain management specialist if this happens.
See CRPS also (Full notes in medicine section)

Digital Fractures and Dislocations

I. Initial approach

A. Same as for basic approach to fractures

1. Emergent care
2. History & physical exam
3. X-rays & labs
4. Treatment

B. Mechanisms - direct or indirect trauma, most commonly caused by falling objects or stubbing injuries

C. Rarely open

D. Fifth toe most commonly injured

E. X-ray evaluation

1. Order AP, MO< Lateral

a. Order LO - view medial hallux

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 2. When unsure - order bilateral films
3. Evaluation & classification

a. same as basic approach to fractures

4. Normal Phalanges

a. Phalangeal epiphyses are at the base

b. Appearance of the bases

• proximal phalanx 1-3 years

• middle phalanx 2-6 years
• distal phalanx 3-6 years

c. Closure of epiphyses

• proximal phalanx 14-16 years

• middle phalanx 14-16 years
• distal phalanx 14 - 16 years

d. Supernumerary bones - IPJ sesamoids - hallux IPJ most common

Note: Closed reduction of a dislocated MPJ is best accomplished by dorsiflexion, longitudinal

traction, and then plantar flexion)

II. Fractures of Hallux

A. Comminuted fracture of distal phalanx tuft

1. Mechanism

a. Direct trauma

2. Treatment

a. Local anesthesia & prep

b. Avulse nail plate atraumatically

c. If Closed a shoe

1) Reduce any gross prominences

2) Replace nail plate as part of compression dressing
3) Patient told to check vascular status frequently
4) Biven shoe, ICE, NSAIDs until asymptomatic, then return to shoe gear

d. If Open

5. Appropriate tetanus prophylaxis & antibiotics

6. Re-prep in OR
7. Debride necrotic tissue and loose, exposed bone, leave no bony prominences

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 8. Irrigate copiously
9. Accurately close nail bed, if permissible
10. Replace nail plate as part of dressing
11. Post-op wound inspection and antibiotics per open fracture protocol
12. Biven shoe until asymptomatic, then return to regular shoes

B. Intra-articular dorsal avulsion fracture of distal phalanx base

1. Mechanism

a. Forced plantar flexion of the HIPJ (stubbing) resulting in avulsion of the EHL insertion

2. Treatment - displaced (common)

a. ORIF followed by Biven shoe or full-length slipper cast for 6 weeks

3. Treatment - nondisplaced (uncommon)

a. Closed treatment with full length slipper or BK walking cast for 6 weeks (with or without percutaneous pinning)

C. Hallux IPJ intra-articular fractures of the distal or proximal phalanx

1. Mechanism

a. Transverse plane torque (stubbing) resulting in a push off fracture of the medial or lateral condyle of either the distal
phalanx base or the proximal phalanx head

2. Treatment - displaced (common)

a. First attempt closed reduction

b. If closed reduction succeeds, pad first interspace with felt, cotton, or webril and tape to the second toe (buddy splitting).
Continue splinting and biven shoe for 4-6 weeks. Note when using buddy splinting - instruct patient to check vascular
status frequently

c. If closed reduction fails, ORIF larger fragments, excise smaller fragments. Biven shoe for 4-6 weeks.

3. Treatment - nondisplaced (common)

a. Splint to second toe, Biven shoe for 4-6 weeks

D. Proximal phalanx shaft fracture

1. Mechanism

a. Direct or indirect trauma resulting in a transverse or oblique fracture

2. Treatment - displaced

a. Closed reduction with or without percutaneous pinning, followed by buddy splinting and Biven shoe for 6 weeks

3. Treatment - nondisplaced

a. Buddy splint to second toe and Biven shoe for 6 weeks.

E. First MPJ intra-articular condylar fractures of the proximal phalanx

1. Mechanism

a. Transverse plane torque (stubbing) resulting in avulsion of the insertion of the medial or lateral intrinsic

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 2. Treatment - displaced

a. ORIF followed by a Biven shoe for 6 weeks

b. Smaller fragments may be excised and intrinsics reinserted as needed

3. Treatment - nondisplaced

a. If no change in hallux abductus, buddy splint and Biven shoe for 6 weeks

b. If the hallux abductus changed, consider surgical treatment

III. Fractures of Lesser Toes Stache is us

A. Distal & intermediate phalanx fractures - rare

B. Non-articular proximal phalanx fractures

1. Mechanism

a. Direct or indirect trauma (stubbing most common) resulting in a transverse, oblique or spiral fracture appearing sub-
capitally, mid-shaft, or at base or epiphysis

2. Treatment - displaced (less common)

a. Closed reduction followed by buddy splinting and Biven shoe for 4-6 weeks

b. ORIF for gross reduction failures, follow same aftercare

3. Treatment - nondisplaced (more common)

a. Buddy splinting and Biven shoe for 4-6 weeks

C. PIPJ intra-articular proximal phalanx fractures

1. Mechanism

a. Usually a stubbing injury with axial forces resulting in oblique push off or comminuted fractures

2. Treatment - displaced or nondisplaced

a. Closed reduction aimed at restoring digital alignment, followed by buddy splinting and Biven shoe for 4-6 weeks. Delayed
arthroplastic procedure prn symptoms.

b. Primary arthroplasty with or without digital implant followed by Biven shoe for 2-4 weeks, as an alternative or when digital
alignment cannot be restored.

D. MPJ intra-articular proximal phalanx fractures

1. Mechanism

a. Usually a stubbing injury

2. Treatment - displaced

a. ORIF or primary implant depending on the size of the fragment and comminution. Aftercare of Biven shoe for 6 weeks

3. Treatment - non-displaced

a. Biven shoe for 6 weeks. Delayed implantation prn symptoms

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IV. Interphalangeal Joint Dislocations

A. Rarely involves distal interphalangeal joints

B. Fifth toe PIPJ most common

C. Mechanism

1. Indirect stubbing trauma with transverse plane torque

D. Treatment

1. Closed reduction, (dorsiflexion, longitudinal traction, and plantar flexion) buddy splinting, Biven shoe for 4-6 weeks
2. Closed reduction occasionally fails due to protrusion of a bone end through the capsule (button hole). In this case, open reduction is
required.

Epiphyseal Plate Fractures

I. Anatomy
A. Diaphysis: (Primary growth center) the lengthy central aspect of the developing bone.
B. Metaphysis: A wider portion of the osseous shaft between the epiphyseal complex and the diaphysis.
C. Physis: (growth plate) A radiolucent cartilaginous plate located between the metaphysis and the epiphysis. It is the primary structure of
concern in pediatric and adolescent skeletal trauma.
D. The epiphyseal complex consists of the epiphysis, physis, and the metaphysis.
1. Epiphyses are either of the pressure or traction type. Pressure epiphyses are located at the end of a long bone and provide rapid
longitudinal growth. Traction epiphyses are non-articular, and located where muscle or tendon attaches to bone, and do not contribute to
axial growth.
2 Anatomically the physis displays three distinct zones. (see below)

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 a. The zone of growth is closest to the epiphysis and contains resting chondrocytes that progress to dividing cells that
arrange in columns.
b. The next component is the zone of cartilage maturation, which is the weakest region due to loss of intracellular
matrix.
c. Finally, the zone of cartilage transformation displays cartilage converting to bone. Periosteum is more
vascularized, thicker, and stronger in the child. The cartilage is strongly attached to the metaphysis, and more
loosely attached to the diaphysis. The periosteum also acts as a check rein to resist fracture displacement.

II. Vascular Supply of Growth Plate Complex

E. Metaphysis—supplied by the nutrient artery of the diaphysis, vessels from periosteum and perichondrium, and these sources extend to
the zone of hypertrophied cells.
F. Epiphysis—supplied by nutrient epiphyseal vessels
G. Physis—supplied by nutrient arteries from both the metaphysis and the epiphysis, as well as direct perichondrial vessels to the physis.
If the metaphyseal supply is compromised or lost, there is usually very little change in physeal perfusion. If, however, either the
epiphyseal or perichondrial supply is lost, the physis may die and premature partial or total closure may ensue. The epiphyseal
vessels supply the physeal zone of growth. Partial closure may cause angular deformity.

The osseous ring of Lacroix is an extension of metaphyseal cortical bone that stabilizes the physis at the zone of Ranvier, where the
physis interfaces with the metaphysis.

Evaluation of physeal injury requires at least three radiographic views and comparison with the uninjured extremity.

Compression is the force most likely to create growth arrest in a child with a fracture.

Epiphyseal fractures are categorized by Salter-Harris and Aiken-Mueller.

III. Salter-Harris (SH) Classification of Epiphyseal Plate Fractures

A. Type I
1. Separation of epiphysis from metaphysis between layers of hypertrophy and calcification.
2. Resting cells remain with the epiphysis.
3. Minimal displacement usually due to strong periosteum.

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 B. Type II
1. Most common acute physeal injury.
2. Separation of epiphysis from metaphysis between layers of hypertrophy and calcification.
3. Fracture line runs through physis then through metaphysis.
4. Thurston-Holland sign:
metaphyseal fragment where the periosteum is intact adjacent to the metaphyseal fragment.
5. Werenskiold sign:
small fragment of metaphyseal fragment on X-ray.
C. Type III
1. Fracture begins in joint, runs up to the physis then makes a 90o turn through the layer of hypertrophied cells to
periphery.
2. Area of concern for blood supply to free fragment as well as congruity of joint surface.
3. Most germinal cells remain intact.

D. Type IV
1. Injury runs from joint, through epiphysis, through physis and out through metaphysis.

E. Type V
1. Crushing injury that destroys all layers of physis.
2. Premature closure usually ensues
F. Type VI
1. Injury associated with removal of bone loss at the zone of Ranvier, due to trauma such as a burn or degloving injury.

G. Type VII
1. Avulsion fracture of the epiphysis, not involving the physis.

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 IV. THE AIKEN-MUELLER EPIPHYSEAL PLATE FRACTURE CLASSIFICATION SYSTEMS.
Aiken Mueller

1 = Salter II A = Salter I, II

2 = Salter III B = Salter III, IV, VI

3 = Salter IV C = Salter V

V. Triplane Fracture
A. This is special distal tibial epiphyseal fracture that usually occurs in older children, about 1 year prior to closure of the epiphysis, and results from
external rotation.
B. The 2-part triplane fracture occurs when the medial part of the distal tibial epiphysis has already closed, and the lateral radiograph displays a
Salter-Harris IV fracture, and the posterior tibial plafond fragment extends to the metaphysis, and may be comminuted.
C. The 3-part triplane fracture consists of a combination of a Salter-Harris II and a Salter-Harris III fracture, and occurs when the middle portion of
the distal tibial epiphysis has closed. The lateral radiograph displays a Salter-Harris II fracture,while the mortise view shows a Salter-Harris III fracture. The
tibia displays a large posterior fragment consisting of a large posterior fragment of posterior and medial portions of the metaphysis, while the medial 1/3-1/4
of the tibial plafond and medial malleolus remains intact. The fibula is also usually fractured.

VI. Treatment recommendations for epiphyseal plate fractures entail the following guidelines:
A. Types I and II
2. Usually respond well to closed reduction, especially if seen early.
3. If seen 7 days after injury, the attempt at closed reduction may do more harm than good due to fast healing that occurs at this site.
B. Types III, IV, V, and VI
1. Should attempt closed reduction first, but usually requires ORIF. 2. Must anatomically reduce the physis and preserve
joint congruity.
2. Try to keep threaded K-wires or screws out of physis.
3. Try and maintain fixation devices in metaphysis.

Lisfranc Fracture Dislocation

This type of injury constitutes 1% of all reported fractures
Once sustained, however, this injury is missed 20% of the time.

I. Anatomical Considerations
A. "Keystone" nature of the recessed 2nd metatarsal base provides a significant amount of stability to the midfoot complex in the transverse
plane. (Cuneiform Mortise)
B. The metatarsals are bound together by a series of transverse dorsal and plantar ligaments as well as an intermetatarsal ligament
1. Exception - lack of ligament between 1st and 2nd metatarsals
C. The ligaments that tether the metatarsals to the lesser tarsus are disrupted
D. The ligaments are stronger plantar than dorsal. Dorsal dislocation more common than plantar
E. Ligament attaching the medial cuneiform to the 1st metatarsal is the largest ligament of this level
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 F. Most significant ligament of the tarsometatarsal articulation is the 1st interosseous cuneometatarsal ligament (Lisfranc Ligament),
attaching the base of the second metatarsal medial to the lateral aspect of 1st or medial cuneiform. (Can produce an avulsion fracture
"Fleck Sign" here or dislocation)

II. Patterns of Injury

The fracture patterns are variable and described in generalized terms. The best way to categorize the injuries is based on the amount of energy the foot
absorbs during the injury. This can go from high-energy, high-impact to low-energy subtle events. These low energy type events can produce injuries that
go undiagnosed.
The current classification schemes only describe the direction of the various dislocations but do not address the energy level of the injury and do not
determine prognosis. The prognosis is associated with a level of impact energy.

III. Classification Schemes

The classification in most common use is that of Quenu and Kus for s (1909) as modified by Hardcastle (1979), and Meyerson (1986) relabeled the
classification as follows;
A. Total incongruity (Type A) - can be either medially or laterally displaced. A disruption of the entire Lisfranc joint complex in sagittal or
transverse plane (almost always lateral)

B. Partial incongruity, either medial (Type B1) or lateral (Type B2 Partial) or (Type B2 Complete) - the most common group

C. Divergent displacement, either a partial (Type C1) or total (Type C2)

IV. Mechanism
A. Wide variety of mechanisms
1. Can range from severe motor vehicle accidents to misguided steps (the injury may seem trivial to the patient).
2. Seen commonly in sports injuries
3. It is a dislocation of the metatarsals from the tarsals most commonly centered around the 2nd ray.
4. Direct
a. Crushing injury to dorsum of foot
5. Indirect
a. The forefoot is plantarflexed on the midfoot and rupture of the dorsal ligaments result in dislocations of the
metatarsals in a dorsal direction. This initiates a cascade of dislocation patterns discussed above.
B. Pathomechanics of the Dislocation

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 1. Extreme plantarflexion with an axial load usually through the heel can provide sufficient stress to cause dorsal displacement of
the second metatarsal base and results in the Lisfranc dislocation patterns.

V. Diagnosis
A. Diagnosis can range from simple "doorway" diagnosis of obvious high energy injuries to difficult (subtle low energy injuries) that may or
may not have focal tenderness. However, even low energy subtle injuries almost always demonstrate localized edema around the tarso-
metatarsal junction.
B. Patients with a history of injury involving midfoot bending and a grossly swollen foot suggest Lisfranc
C. If unclear palpation directly over the tarso-metatarsal joints will usually elicit intense pain in most patients
D. Must evaluate pulses (Doppler) and CFT and watch closely and evaluate for compartment syndrome
E. Can present with deformity of foot, with apparent shortening in the obvious "doorway Diagnosis" cases.

VI. Signs and Symptoms:

A. Midfoot pain: In subtle cases the pain may be sever at the time of the injury, however, it may then dissipate over the next few
weeks. When the patient presents to your office the pain may or may not be present. Also, their pain may migrate to different areas
due to compensatory gait.
B. However, in virtually all cases (acute or semi-acute), there will be some degree of midfoot swelling.
C. Patients may or may not be able to bear weight. However, generally the more severe the injury, the less likely they will be able to bear
weight.
D. Gentle forefoot movement against a stable hindfoot will usually elicit pain. However, do not rely on the maneuver alone to make the
diagnosis.
E. X-rays
1. Foot and ankle. AP, LAT (look at dorsal displacement of Mets on Cuneiforms, Oblique)
2. Get comparison views
3. Evaluate 1st met- cuneiform space closely
4. Evaluate base of 2nd metatarsal closely. (Medial cortical edges of metatarsal and cuneiform is generally very stable)
5. Look for compression fracture of cuboid
6. May need transverse or sagittal stress views

VII. Treatment
A. Always attempt closed reduction
1. Forefoot suspended from table by Chinese Finger traps
2. After adequate relaxation, suspend weights from ankle
3. Try to reduce 2nd metatarsal into cuneiform keystone and others may reduce due to Vassal phenomenon/principle
4. Reduce 1st metatarsal if type C
B. If closed reduction fails, it may be due to
1. Tibialis anterior interposition
2. Peroneus longus interposition
3. Avulsed fragment from Lisfranc ligament
C. Open Reduction
1. You must open reduce if vascular compromise is evident or if the injury is non-reducible after attempted closed reduction
2. Usually 3 incisions
a. 1st - medial dorsal first met-cuneiform
b. 2nd - between 2nd and 3rd met- cuneiforms
c. 3rd - between 4th and 5th met - cuboid
3. First metatarsal is fixed first
4. Use wire fixation if unstable open or closed
a. Type A - one wire, 1st met- cuneiform/ one wire 5th met-cuboid
b. Type B. - medial type - two wires at 1st met-cuneiform
c. Type C - 2 medial/ one lateral
5. Pins removed 6-8 weeks
6. BK Cast 8-12 weeks, non-weight bearing 6 weeks

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P a g e 43 | 368
 Management of Open Fractures
I. Four essentials when presented with open fractures
A. Recognize any life-threatening injuries before injuries to lower extremities
B. Evaluate the extent of associated soft tissue damage
C. Open fractures are considered contaminated (60-70% incidence of bacterial growth) at initial inspection

D. Should be treated within 8 hours, or is then considered an infected wound

II. Gustillo's Classification of Open Fractures

A. Type I - Small wounds of 1cm or less caused by low-velocity trauma with minimal damage to soft tissue. Exp.: the protrusion of a fragment
of bone out from within or a low-velocity bullet passing in from without.
B. Type II - Wounds >1 cm. but little or no avascular or devitalized soft tissue and relatively little foreign material.
C. Type III - Wounds of moderate or massive size >10 cm. with considerable devitalized soft tissue and/or foreign material, or traumatic
amputation. There are three subtypes:
Type IIIA - Wounds with extensive soft tissue laceration, flaps, or high- energy trauma but with adequate soft tissue to
cover the fractured bone.
Type IIIB - Wounds with extensive soft tissue injury or loss with periosteal stripping and bone exposure. Requires free
tissue flap or rotational flap coverage.
Type IIIC - Open fractures associated with arterial injuries requiring repair. Exposed fracture with arterial damage that
requires repair.

Gustillo Type I II IIIA IIIB IIIC

Energy Low energy Moderate High High High

Wound Size < 1 cm > 1cm >10cm >10cm

>10cm
Soft Tissue Minimal Moderate Extensive Extensive Extensive

Moderate
Contamination Clean Extensive Extensive Extensive
contamination

Simple fx pattern with Moderate Severe comminution or Severe comminution or Severe comminution or
Fracture Pattern
minimal comminution comminution segmental fractures segmental fractures segmental fractures

Periosteal Stripping No No Yes Yes Yes

Requires free tissue flap or Typically requires flap

Skin Coverage Local coverage Local coverage Local coverage including
rotational flap coverage coverage

Exposed fracture with arterial

Neurovascular Injury Normal Normal Normal Normal
damage that requires repair

• 1st generation • 1st generation cephalosporin for gram positive coverage.

cephalosporin for 24 hours after • Aminoglycoside (such as gentamicin) for gram negative coverage in type III
closure injuries
o the cephalosporin/aminoglycoside should be continued for 24-72
hours after the last debridement procedure
• Penicillin should be added if concern for anaerobic organism (farm injury)
Antibiotics
aminoglycoside (such as gentamicin) for gram negative coverage
1st cephalosporin (ancef) for gram positive coverage.

the cephalosporin/aminoglycoside should be continued for 72 hours after the last

debridement procedure

penicillin should be added if concern for anaerobic organism (farm injury

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 • Fluoroquinolones
o should be used for fresh water wounds or salt water wounds
Antibiotics (other o can be used if allergic to cephalosporins or clindamycin
considerations)
• Doxycycline and ceftazidime
o can be used for salt water wounds

III. Principles of Treatment

A. Treated as an emergency - stabilize life threatening injuries first
B. Adequate debridement and irrigation begun (warm physiologic saline)
1. All macerated, nonviable, mutilated skin should be debrided and soft tissue excised.
a. To test for viability of skin - note if skin remains pale after tourniquet release or use Fluorescein test (inject IV 10-15
mg/kg and observe skin under Wood's light. If no diffusion of dye into skin, not viable).
2. Fascia is expendable as it is poorly vascularized and prone to infection. For tendon to be viable, it must cover with skin graft,
flaps, primary closure or cover with muscle.
3. Muscle viability determined by
a. Consistency or elasticity when probed (important)
b. Contractibility (pinch or zap with stimulator) - very important
c. Color
d. Ability to bleed
4. Conservative debridement of bone unless dirty fragments that add no stability
C. Take culture and sensitivity and gram stain after debridement and irrigation
D. Place on appropriate antibiotic therapy
1. Usually begin on Cefazolin 1 or 2 grams stat IV, then 1 gram every 6-8 hours
2. If farm environment, must cover for Clostridia infection. Give Pen G 10-20 million units IV daily
3. Use antibiotics for three days. Culture should be available to determine organism and switch antibiotics if necessary
4. Continue antibiotics for three additional days in non-infected wound if
a. Delayed primary closure
b. Secondary wound closure
c. Open reduction and internal fixation
d. If changing internal or external fixation devices
5. Give tetanus

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 6. Stabilize Open Fractures
a. Realigning and stabilizing the fracture optimize local wound conditions for soft tissue healing and thereby plays a
major role in the prevention of infection
b. K-wires are a good choice for stabilization as they allow minimal amount of hardware near fracture site, are easy to
insert percutaneously without excessive dissection and trauma to site.
7. Cancellous Grafting
a. Type I can be used at time of fixation
b. Gustillo recommends cancellous bone grafting in type III open fractures with extensive soft tissue injury, large bone
exposure or loss, and when there is no callous formation after three months. Best applied at time of delayed
primary closure when non- evidence of infection. If may be necessary to have graft stabilize at time of fixation. If
infection occurs, graft may still take.
8. Wound Closure
a. Can close Type I, and many Type II fractures primarily if
1) No tension exists on wound
2) No evidence of contamination or crush injury to tissue
3) Wound is not open for more than 8 hours
b. Delayed primary closure - closing wound in 3 - 10 days
1) Can do so if bacteria count is less than 10 bacteria in gr of tissue

IV. Emergency Fracture Treatment

In general, open fractures are associated with severe trauma.
A. Evaluation Guidelines
1. Check airway to make sure no obstruction
2. Evaluate for external and internal hemorrhage
3. Evaluate for shock - check vital signs, pulse, respiratory rate, blood pressure and level of consciousness
a. Obtain blood for typing and cross matching
b. While waiting for compatible whole blood, IV infusion of glucose and water, plasma, or plasma expanders or ringers
lactate will control shock temporarily
c. Give whole blood for severe loss of blood
4. Evaluate fracture and dislocation of main concern as well as other areas of body

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Metatarsophalangeal Joint Trauma
I. Initial approach
A. Same as basic approach to fractures
1. Emergent care
2. History & physical
3. X-rays
4. Labs
5. Treatment
B. First MPJ is the most often injured and the most important to recover in terms of function

II. Turf Toe

A. Mechanism
1. Hyper dorsiflexion, hyper plantarflexion, hyper adduction, or hyperabduction stress resulting in a first metatarsophalangeal joint
sprain without alignment changes
B. X-ray evaluation
1. Order AP and lateral
a. Order MO, LO, or plantar axial depending on the area of tenderness
2. Rule out dislocation, osteochondral injury, or sesamoid fracture
C. Treatment
1. Ice, rest, Biven shoe, NSAIDs initially
2. Begin graded return to activity and shoes when symptoms resolve
3. Modify athletic shoe
4. Corticosteroid injection to be used cautiously

III. First Metatarsophalangeal Joint Dislocation

A. Mechanism
1. Hyperextension is the primary force that creates the injury
B. X-ray Evaluation
1. Order AP, Lateral and Plantar Axial
2. Rule out osteochondral fracture and sesamoid fracture

C. Types
1. Type I
a. The inter-sesamoid ligament remains intact and the sesamoids are not fractured. The joint capsule is torn
transversely under the metatarsal neck
b. Proximal phalanx, plantar capsule, and sesamoids dislocated dorsally on the first metatarsal head
c. First metatarsal protrudes through the capsule, depressed plantarly by the hallux retrograde forces.
d. Hallux IPJ is flexed
e. Usually not reducible by closed technique due to interposed soft tissue or bony fragments.

2. Type IIA
a. Same as Type I except that rather than entire plantar capsule and sesamoid apparatus dislocated dorsally, the
intersesamoidal ligament ruptures and the sesamoids sublux to each side of the metatarsal head
b. X-rays readily show sesamoids medial and lateral to the metatarsal head
c. Easier to close reduce than Type I

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 3. Type IIB
a. Same as Type IIA except a sesamoid fracture instead of the intermetatarsal ligament rupturing
b. X-rays show a sesamoid fracture
c. Easier to reduce than Type I

4. Type IIC has been proposed and represents a combination of Type IIA and Type IIB.
a. A complete disruption of the intersesamoidal ligament combined with fracture of either sesamoid

D. Treatment Type I
1. Closed reduction technique
a. General Anesthesia
b. Increase dorsiflexion and longitudinal traction
c. Push the proximal phalanx onto contact with the metatarsal head
d. Then plantar flexion into the reduced position
e. Apply a full-length slipper cast or BK walking cast with the toe in slight plantar flexion
2. Maintain casting for 3 to 4 weeks, followed by Biven shoe for 3 more weeks
3. Open reduction if closed reduction fails. Follow same aftercare.
E. Treatment - Type IIA
1. Closed reduction, full length slipper cast or BK walking cast for 3 weeks followed by Biven shoe for 3 more weeks
2. Open reduction with same aftercare if closed reduction fails
F. Treatment - Type IIB
1. Closed reduction, full length BK NWB cast for 6 weeks
a. Follow casting with Biven shoe or stiff soled shoe with sesamoid accommodation prn sesamoid symptoms
b. Delayed sesamoid excision prn symptoms
2. Open reduction with excision of fractured sesamoid, followed by full length slipper cast or BK walking cast for 3 weeks and Biven
shoe for 3 more weeks if -
a. Closed reduction of the dislocation fails
b. Sesamoid articular surface is uneven on post-reduction x-rays
IV. Lesser Metatarsophalangeal Joint Dislocation

A. Less common than first met joint dislocations

B. Mechanism
1. Hyper dorsiflexion most common
2. Rarely, adduction or abduction torque
C. X-ray evaluation
1. Order AP, MO, Lateral
2. Rule out osteochondral fracture
D. Treatment
1. Same as for Type I first MPJ dislocations
V. Osteochondral Fractures of the First MPJ

A. Phalangeal
1. Mechanism
a. Transverse plane torque (stubbing) resulting in avulsion of the insertion of the medial or lateral intrinsics at the
proximal phalanx base
2. X-ray evaluation
a. Order AP. Lateral and either LO or MO depending on side of suspected injury
3. Treatment- displaced
a. ORIF followed by Biven shoe for 6 weeks

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 b. Smaller fragments may be excised and intrinsics reinserted as needed
4. Treatment- nondisplaced
a. If no change in hallux abductus, buddy splint and Biven shoe for 6 weeks
b. If hallux abductus changed, consider surgical treatment
5. Hemi or total joint replacement implant is considered if symptoms persist after initial treatment of either displaced or
nondisplaced fractures
B. Metatarsal
1. Mechanism
a. Hyper dorsiflexion, resulting in a shearing or impaction osteochondral fracture
2. X-ray evaluation
a. Order AP, Lateral, MO
3. Treatment - displaced
a. ORIF larger fragments followed by Biven shoe for 6 weeks
b. Excise and drill smaller defects, followed by early ROM, Biven shoe for 3-6 weeks
4. Treatment - nondisplaced
a. Full length slipper cast or BK walking cast for 6 weeks or alternatively, NWB for 3 weeks then WB for 3 weeks
b. Delayed curettage and drilling of defect prn symptoms
5. Total joint replacement implant is considered if symptoms persist after initial treatment of either displaced or nondisplaced
fractures
VI. Osteochondral Fractures of the Lesser MPJ

A. Phalangeal
1. Mechanism
a. Stubbing injury
2. X-ray evaluation
a. Order AP, MO, Lateral
3. Treatment - displaced
a. ORIF or primary implant depending on the size of the fragment and comminution. Aftercare of Biven shoe for 6
weeks
4. Treatment - nondisplaced
a. Biven shoe for 6 weeks. Delayed implantation prn symptoms
5. Delayed joint replacement implant if symptoms persist after initial joint preservation treatments
B. Metatarsal
1. Mechanism
a. Same as for first MPJ
2. X-ray evaluation
a. Order AP. MO, Lateral
3. Treatment - displaced
a. ORIF, excision and drilling, or primary implantation depending on the size of the fragment and comminution,
followed by 3-6 weeks in Biven shoe depending on treatment
4. Treatment - nondisplaced
a. Full length slipper cast or Bk walking cast for 6 weeks
5. Delayed joint replacement implant if symptoms persist after initial joint preservation treatments

VII. Sesamoid Fractures

A. Mechanism
1. Fall from a height
2. Repetitive direct trauma (i.e. dancing)
3. Repetitive indirect trauma (i.e.- traction of intrinsics)
B. Presentation
1. Timing
a. Acute
b. After course of progressive symptoms similar to stress fractures
c. Chronic - misdiagnosed or mismanaged
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 2. Sesamoid involved
a. Tibial more common than fibular
b. Rarely, both are injured
c. Almost never bilateral

3. Exam
a. Pain on direct palpation
b. Pain on hallux dorsiflexion

C. Differential diagnosis of sesamoid area pain

1. Joplin's neuroma
2. Sesamoiditis
3. Osteochondritis dissecans of the sesamoid
4. Osteochondrosis of the sesamoid
5. Ruptured bipartite sesamoid
6. Turf toe
7. DJD/eroded crista
8. Hypertrophic sesamoid with painful plantar callus
9. Fractured sesamoid

D. X-ray evaluation
1. Order bilateral AP, Plantar Axial, Lateral films
a. Order LO for tibial sesamoid
b. Order MO for fibular sesamoid
2. Bilateral films may help evaluation when ruling out bipartite sesamoid
a. Look for symmetry in location, smoothness of edges, width of space
b. 75% of bipartite sesamoids are unilateral
3. When in doubt, order bone scan
4. Normal sesamoids
a. Ossification appears at 8-10 years
b. Bipartite sesamoids more common in tibial than in fibular
c. 75% of bipartite sesamoids are unilateral
d. Sesamoids may be multipartite
E. Treatment
1. Non-weightbearing full length slipper cast or BK cast for 6-8 weeks, followed by Biven shoe until asymptomatic
a. Prognosis for complete healing is guarded
2. Primary excision of the fractured sesamoid if
a. Immobilization therapy is unacceptable for the patient
b. Articular surface uneven
3. Delayed excision of the sesamoid if symptoms persist after conservative treatment
4. Tibial sesamoid excision has risk of hallux abductovalgus formation, especially in round metatarsal heads
a. Consider lateral joint and adductor release
5. Removal of both sesamoids will decrease intrinsic muscle strength
a. Decrease hallux purchase
b. Hallux hammertoe
c. Prophylactically fuse hallux IPJ

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Metatarsal Fractures
I. Initial approach
A. Same as basic approach to fractures
B. X-ray evaluation
1. Order AP, Lateral, MO
a. Plantar axial PRN
2. Order bilateral films when unsure
3. Evaluation & classification
a. As described for basic approach to fractures
4. Normal metatarsals
a. First metatarsal epiphysis at the base. Base appears at 2-3 years. Epiphysis closes at 14-16 years
b. Lesser metatarsal epiphysis at the neck. Head appears at 2-4 years. Epiphysis closes at 14-16 years.
c. Apophysis of the fifth metatarsal styloid appears at 9-14 years and fuses at 12 - 15 years. It is oriented close to
parallel to the fifth metatarsal shaft.
d. Supernumerary bones: Os Vesalianum

II. Basic Tenants of Treatment

A. It is imperative that accurate anatomic reduction is achieved
1. Length
2. Angulation
a. Transverse plane
b. Sagittal plane
B. Do not attempt to open a comminuted fracture

III. First Metatarsal Fracture

A. Osteochondral fracture of the first MPJ
1. See MPJ trauma outline
B. Neck, Shaft, or base fractures
1. Mechanism
a. Direct or indirect trauma - rare due to the bone's strength
2. Treatment - displaced
a. ORIF followed by NWB BK casting for 4-6 weeks and then WB, BK casting for 2-4 more weeks.
3. Treatment - non-displaced
a. Maintain position with percutaneous pinning. Aftercare identical to displaced fractures

IV. Metatarsal 2, 3, 4 Fractures

A. Osteochondral fractures of the lesser MPJ
1. See MPJ trauma
B. Neck fracture - isolated metatarsal
1. Mechanism
a. Direct or indirect trauma, usually resulting in a transverse or mildly oblique fracture
2. Treatment - displaced (common)
a. Closed reduction with or without percutaneous pinning followed by Biven shoe for 6 weeks
b. ORIF if accurate reduction not obtainable, follow same aftercare
3. Treatment - non-displaced (uncommon)
a. Biven shoe for 6 weeks
C. Neck fracture - multiple metatarsals

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 1. Mechanism
a. Same as for isolated

2. Treatment - displaced (common)

a. Closed reduction with or without percutaneous pinning followed by NWB BK cast for 4 weeks, then WB, BK cast for
2 more weeks
b. ORIF if accurate reduction not obtainable. Follow same aftercare
3. Treatment - nondisplaced (uncommon)
a. NWB BK cast for 4 weeks, then WB, BK cast for 2 more weeks.
D. Shaft fractures
1. Mechanism
a. Direct or indirect trauma resulting in oblique, spiral transverse, or comminuted fractures
2. Treatment - displaced (common)
a. Closed reduction with or without percutaneous pinning, followed by NWB BK cast for 4 weeks, then WB BK cast for
2 weeks
b. ORIF if accurate reduction not obtainable. Follow same aftercare
3. Treatment - nondisplaced (uncommon)
a. NWB BK cast for 4 weeks, then WB BK cast for 2 more weeks
E. Base fractures
1. Mechanism
a. Direct or indirect trauma resulting in transverse fracture
2. Treatment - displaced (uncommon)
a. Same as for displaced shaft fractures
3. Treatment - nondisplaced (common)
a. Same as for nondisplaced shaft fractures
F. Associated with Lisfranc fracture/dislocation
1. See Lisfranc fracture/dislocation

V. Fifth Metatarsal Fractures

A. Osteochondral fracture of the MPJ
1. See MPJ trauma
B. Neck and shaft fractures
1. Mechanism
a. Direct or indirect trauma
b. A common injury here occurs with indirect trauma acting on the metatarsal head lateral to medial with axial
compression. The resultant fracture is angulated distal lateral to proximal medial with a lateral butterfly
fragment
2. Treatment - displaced
a. Same as for displaced metatarsal 2, 3, 4 shaft fractures
3. Treatment - nondisplaced
a. Same as for nondisplaced metatarsal 2, 3, 4, shaft fractures
C. Jones Fracture
1. Mechanism
a. Medial or lateral cutting or pivoting movement, producing a transverse fracture distal to the 4th/5th intermetatarsal
articulation
b. Not produced by inversion injuries
2. Treatment - athletes and active individuals
a. ORIF followed by NWB BK cast for 4-6 wks, then WB BK cast for 2-4 more wks
3. Treatment - others
a. Closed reduction followed NWB BK cast 6 wks, and WB BK cast for 2 more wks
D. Metatarsal/ Cuboid joint intra-articular styloid fracture

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 1. Mechanism
a. Inversion injury with traction buy Peroneus Brevis or lateral slip of plantar fascia resulting in an avulsion-type
fracture that enters the tarso-metatarsal joint
2. Treatment - displaced
a. ORIF followed by WB BK cast for 6 weeks
3. Treatment - nondisplaced
a. WB BK cast for 6 weeks
E. Non-articular styloid fracture
1. Mechanism
a. Same as for intra-articular type
2. Treatment - displaced (uncommon)
a. ORIF followed by WB BK cast for 6 wks
3. Treatment - nondisplaced (common)
a. Ice, compression, Biven shoe for 6 weeks
b. Alternative for more pain relief is to utilize a WB BK cast for 3 weeks, then a Biven shoe for 3 more weeks

VI. Metatarsal Stress Fractures

A. Mechanism
1. Repetitive stress beyond what the bone is accustomed to:
a. New exercise program
b. Increase in exercise
c. Biomechanical abnormalities
d. Long metatarsal or plantarflexed metatarsal
e. Loss of adjacent metatarsal support
B. Presentation
1. Gradual onset, progressive course
a. Initially with rigorous activity
b. Later - any activity
2. Well localized pain and swelling dorsally
a. Localized well enough that the exact center of pain can be measured clinically from the MPJ and used for x-ray
correlation
b. Usually located in neck region
3. Usually metatarsals 2, 3, 4
4. Differential diagnosis
a. Neuroma
b. Capsulitis/arthritis
c. Extensor tenosynovitis
C. X-Ray findings
1. Initially - might see a small cortical break at site of maximum clinical tenderness
2. Periosteal reaction usually develops at the stress fracture site
a. Takes 10 days or longer from onset of pain
3. Repeat x-rays 2-3 weeks may be needed to confirm diagnosis
a. Consider bone scan if still no reaction
D. Treatment
1. Biven shoe for 4-6 weeks or until symptoms resolve
2. Initial low-dye strapping with Biven shoe and begin evaluation and casting for functional orthoses
3. Athletes may be placed on an alternative, non-impact exercise program during treatment
4. Post-recovery orthoses, patient education on risk factors, gradual return to full activity

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Nail Trauma
I. Initial Assessment

A. Emergent care
B. History, physical examination
C. Radiographs
D. Lab tests
E. Treatment
II. Intra-ungual Hematoma

A. Contusion to eponychia area, appears days after episode

B. No treatment, just reassurance
III. Sub-ungual Hematoma

A. Contusion of nail apparatus

B. Treatment
1. Prep nail, and then avulse (atraumatically) under local anesthesia. Nail will fall off eventually
2. May have underlying nail bed/ matrix disruption
a. Treat accordingly
3. If nail bed/matrix intact
a. Cleanse bed & matrix
b. Cleanse nail plate in betadine, tidy it
c. Use nail plate as part of dressing to maintain proper shape of bed while nail regrows
d. Reduce fractures of distal phalanx causing tenting of nail bed
IV. Tennis Toe

A. Recurrent retrograde trauma on nail causing pain at base of nail with swelling and erythema of the eponychium
B. Treatment
1. Rest, Ice
2. Education
a. Shoe styles
b. Nail trimming
V. Nail Avulsion

A. Total or partial avulsion without nail bed or matrix disruption

B. Treatment
1. Local anesthesia & prep
2. Inspect & detach all remaining nail
3. Cleanse nail bed
4. If nail plate available, cleanse and use as part of dressing
5. Substitute adaptic for nail plate if needed
VI. Nail Bed or Matrix Disruption

A. Manage according to principles of open wound management

B. Laceration

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 1. Appropriate tetanus prophylaxis
2. Usually, no antibiotics are required
3. Local anesthesia and prep
4. Detach remaining nail atraumatically
5. Reprep
6. Appropriate irrigation and debridement
7. Exact closure of laceration, fine suture
8. Dressing with replacement of cleansed, tidy nail plate, or adaptic placed similarly

C. Avulsion
1. Same as for laceration
a. Avulsed tissue (if available) should be meticulously cleansed and replaced accurately
b. Defects not replaced
1) Split thickness nail bed graft
2) Mobilize adjacent tissue for primary closure
3) Allow to close by secondary intention
D. Pulp or tip injury
1. Same treatment as for laceration or avulsion
a. Pulp or tip loss may be addressed with local flaps
b. Primary Lapidus
E. Associated with fracture of distal phalanx
1. Usually, fracture is comminuted
2. Treatment
a. Appropriate tetanus prophylaxis
b. Appropriate antibiotics after obtaining gram stain and culture specimens
c. Local anesthesia and prep
d. Remove nail
e. Reprep
f. Irrigation and debridement - remove exposed bone fragments, leave no sharp edges or prominences
g. Primary wound closure vs. delayed primary closure, based on age of wound, vitality of tissues, and adequacy of
irrigation & debridement
h. Nail plate incorporated into dressing, adaptic as a substitute
i. Continue antibiotics per open fracture protocol
j. Biven shoe until asymptomatic, return to shoes
VII. Crush Injuries

A. Treat according to severity

B. Delayed primary closure and appropriate antibiotic therapy
X. Complications

A. Delayed regrowth of nail - 6 months to a year

B. Cryptosis on regrowth
C. Splitting or bipartite nail
D. Roughened surface
E. Thickening
F. Abnormal longitudinal orientation
G. Abnormal curvatures
H. Infection
I. Varying amounts of attachment

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Peroneal Tendon Injuries
I. Dislocation of peroneal tendons
A. Cause
1. Eversion/ dorsiflexion injuries
2. Direct blow to lateral ankle
3. Congenital absence of groove in lateral malleolus
B. Symptoms
1. Ankle edema, pain
2. Tendonitis
3. Clicking sound
4. Ridge over lateral ankle
5. Avulsion flake from fibula
C. Treatment
1. Strapping
2. Cast immobilization in acute injuries 3-6 weeks
3. Surgical repair

II. Stenosing Tenosynovitis

A. Cause
1. Direct trauma
2. Chronic trauma
3. Enlarged peroneal tubercle
4. Calcaneal fracture
5. Arthritis
B. Symptoms
1. Pain
2. Trigger point pain
3. Thickened tendon sheath
4. Pain with ankle inversion
5. Chronic edema
C. Diagnostic Studies
1. Calcaneal axial view
2. CT scan, MRI
3. Peroneal Tenogram
D. Treatment
1. Surgical repair of osseous pathology and/or tendon sheath
2. Injection therapy
3. Physical therapy

III. Peroneal Tendon Rupture

A. Cause
1. Laceration
2. Chronic degeneration

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B. Symptoms
1. Pain, edema
2. Loss of eversion strength
3. Inability to plantar flex 1st ray
4. Increased soft tissue mass
C. Diagnostic Studies
1. Peroneal tenogram
2. CT scan, MRI
D. Treatment
1. Cast immobilization/ 6 weeks
2. Surgical repair: w/primary repair cast immobilize 6 wks; w/ graft cast immobilize 8 wks

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Puncture Wounds
I. Work-up
A. Complete history.
B. X-rays (rule out foreign body and get baseline x-rays for comparison if osteomyelitis develops.
C. I & D
D. Leave open and pack.
E. Monitor temperature and have patient back for re-evaluation.
F. Tetanus prophylaxis.
G. Antibiotics (controversial but medicolegally do it:
1. Amoxicillin/clavulanic acid 250-500 mg TID.
a. Clindamycin 300 mg TID.
b. Cephalexin 500 mg. TID.
2. Empiric parental for soft tissue:
a. Cefazolin 1q Q8h.
b. Clindamycin 600-900 mg q8h
3. Empiric for osteomyelitis:
a. Ciprofloxacin 750 mg q12h P.O.
b. Ceftazidime 2g of 12h I.V.
NOTE: For osteomyelitis antibiotics should be continued for 4-6 weeks following definitive I & D.

II. Bacterial Etiology

A. In cases with superficial cellulitis or abscess formation occurs the most prevalent organism is Staph Aureus and Streptococci.
B. If the wound progresses to osteomyelitis Pseudomonas Aeruginosa is the organism 93% of the time.

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Talar Dome Fractures
H. Bernt Hardy Classification

A. Events that take place

1. Trauma
2. Development of avascular, aseptic necrosis of osseous not cartilage portion
3. Either union of fracture by creeping substitution (if immobilized) or
4. Sequestration and nonunion leading to osteoarthritis
B. Types

1. Stage I small area of subchondral bone compressed (small compression fracture)

2. Stage II partially detached osteochondral fragment (Incomplete avulsion of a fragment)
3. Stage III completely detached fragment, remaining in crater (Complete avulsion without displacement)
4. Stage IV displaced osteochondral fragment (Avulsed fragment displaced within the joint)

Note: A stage I lesion may occur without disruption of the lateral collateral ligaments.
STAGES II through IV require rupture.

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 C. Incidence
1. Medial Talar Dome (posterior third) = 56%
2. Lateral Talar Dome (middle or anterior half) = 44%
3. Central Talar Dome Fracture = .3% (very rare)
4. Anterior Talar Dome Fracture = .1% (Extremely rare)

D. Mechanism
1. Medial-posterior lesion - Inversion and plantarflexion with lateral rotation (i.e. external rotation force applied to a plantarflexed and
inverted foot).
2. Lateral-middle, lateral-anterior lesion - Inversion and dorsiflexion (i.e. Inversion force applied to a dorsiflexed ankle.
3. Eversion does not produce talar dome lesions due to the anatomic configuration of the medial malleolus.
E. MRI Examples

Medial Talar Dome Fracture

Medial Talar Dome Fx Radiology Report

MRI RIGHT FOOT:

Comparison plain films from an outside center dated 11/1/94. No recent plain films are available.
FINDINGS:

Extensive marrow edema in the talus surrounds an ovoid focus of signal alteration in the subchondral space of the talar dome medially. This focal
signal alteration in the talar dome measures approximately 7.5 x 4.0 mm and is of intermediate signal on T1 weighted images and hyperintense on
T2 weighted images. A very thin hypo intense rim surrounds this signal alteration; this may present fibrosis or sclerosis. Peroneus and flexor
tendons are intact with normal signal and caliber. The other navicular bones demonstrate normal marrow signal characteristics. The finding is
compatible with a transchondral fracture; the described signal characteristics may be explained by synovial invagination into an osteochondral
defect. However, no definite loose body is identified. Less likely, a non-displaced Grade III transchondral fracture may be present. Current plain
films for comparison would be useful to distinguish between Grade III and Grade IV lesions. The overlying cartilage is indistinct over this portion of
the talar come. A small joint effusion is present distending the anterior joint capsule.
IMPRESSION:

1. Transchondral fracture of the medial talar dome measures approximately 7.5 x 4.0 mm. If clinically relevant, current plain films of the
right ankle may be useful in distinguishing between Grade III and Grade IV transchondral fracture in this case, for reasons described
above.
2. Although a small anterior capsular joint effusion is present, no definitive loose bodies are identified.

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 Views
Sagittal T1 (Fat Image)

Sagittal T2 (Water Image)

Axial T1 (Fat Image) One

Axial T1 (Fat Image) Two

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 Standard X-ray

Lateral Talar Dome Fracture

Radiology Report
Radiology Report

MRI OF THE RIGHT FOOT:

Multiple axial, sagittal, and coronal images of the right foot are obtained. In the lateral corner of the talar dome, there is a detached but
nondisplaced osteochondral fragment noted. Extending into the talus from this lesion, which measures 1.2 cm in diameter, is a reticular edema
pattern, which involves a majority of the dome of the talus. There is transgression of the reticular cartilage at the site of this defect and a small
amount of fluid is present between the defect and underlying bone. This fragment is tilted slightly but remains in place in the defect in the
superolateral aspect of the talus. This appearance can be seen with osteochondritis dissecans, may also be posttraumatic in origin. No pattern
consistent with edema is noted throughout the dome of the talus and the talar neck has a normal bone marrow signal pattern. Tendons,
ligaments fascial planes, and musculature about the right ankle and forefoot demonstrate no abnormality.
IMPRESSION:

1. Chronic osteochondral fracture, superior and lateral corner talar dome. The osteochondral fragment measures 1.2 cm in diameter and
is in situ, detached but not displaced and transgression of the articular cartilage is noted.
2. Small effusion tibiotalar joint.

Views Sagittal T1 (Fat Image)

Coronal T1 (Fat Image) Axial T1 (Fat Image)

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Sagittal T2 (Water Image) Axial T2 (Water Image)

F. Treatment

1. Stage I, II and Medial III lesion cast 6-12 weeks. Some use patellar tendon brace. Surgery if not responding.

Note: To be effective the fracture should be nondisplaced and of recent origin (a few weeks). After that period
dense fibrous tissue usually has formed between the fragment and the talus impeding any further capillary
ingrowth. This is seen radiographically as sclerosis formed along the margin of the defect.

2. Stage IV, or lateral stage III - excise fragment, saucerize crater, drill holes to aid re-vascularization and produce fibrocartilage - ROM

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Talar Fractures
I. Anatomy
A. 2/3 of talus is articular cartilage, therefore most fractures are intra-articular
B. No muscles or tendons taking origin or insertion into talus
C. Extended neck is part most vulnerable to injury
D. Medial wall is vertical, lateral is extended into lateral process

II. Vascular Supply

A. General: The 3 major blood supplies to the talus are the posterior tibial artery, the dorsalis pedis artery and the peroneal artery. The
blood supply to the talar body enters through the inferior talar neck via the artery of the tarsal canal. This key vessel originates from the
posterior tibial artery. Secondary blood supply to the body is derived from the deltoid branch of the posterior tibial artery, entering the
talar body along its medial surface. Circulation to the neck, head, and lateral body is supplied via the dorsalis pedis, tarsal sinus, and
lateral tarsal sinus arteries. This last artery is an anastomosis between the peroneal and dorsalis pedis arteries.
B. Body
1. The deltoid branches of the artery of the tarsal canal supply the medial side of the talus.
2. The artery of the tarsal canal (which arises from the posterior tibial artery) then enters the canalis tarsi to supply the middle third of
the talus.
C. Head and neck –
1. A small twig off the anterior tibial artery enters the superior surface of the talar neck.
2. The artery of the sinus tarsi off the lateral tarsal artery, a branch of the dorsalis pedis, supplies the neck and dorsal head of the talus.
D. Posterior talus –
1. Calcaneal branches of peroneal artery supply the posterior region and a portion of the lateral talus
2. The calcaneal branches of the posterior tibial artery form a network over the posterior tubercle.

III. Avascular Necrosis

A. When 2/3 of vascular channels are injured, this will occur
B. Hawkins says it takes 6-8 weeks to recognize its presence after fracture-dislocation
C. May not appear from 1 - 6 months
D. Signs and symptoms
1. Intractable pain
2. Relative sclerosis or opacity of involved bone (AP and mortise views demonstrates this best)
3. Hawkins sign: appearance of decreased subchondral bone density (subchondral resorption) in the dome of talus 6 to 8 wks following
injury indicates that there is sufficient vascular supply to bone to allow normal disuse osteopenia to occur. In other words,
subchondral bone atrophy (radiolucency) in the body of the talus is a sign of viability.
E. Treatment of Avascular Necrosis
1. NWB in BK cast 6-8 months until revascularization occurs

IV Types of Talar Fractures

A. Fractures of the neck of the talus
B. Fractures of the posterior process of the talus (Shepherd's Fracture).
C. Osteochondral fractures of the talar dome
D. Fractures of the lateral process of the talus
E. Shear fracture of the talar head and neck
F. Fractures of the body of the talus

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V. Mechanisms of Fractures
1. Posterior Process - Hyperflexion (forced plantar flexion) causing the posterior process of the talus to become wedged between the
tibia and the calcaneus.
2. Osteochondral Dome Fractures - Compression with inversion and dorsiflexion of the foot (lateral lesion) or compression with
inversion and plantar flexion of the foot (medial lesion).
3. Lateral Process - Hyperextension (dorsiflexion) and inversion of the foot. Pull of the lateral Talocalcaneal ligament.
4. Shear Fracture of the Talar Head - Impact or fall on an extended foot, which compresses the talar head on the tibia.
5. Body of Talus - Fall from height on an extended foot.

VI. Hawkins Classification of Talar Neck Fracture

A. Type I
1. Vertical non-displaced fracture of talar neck
2. Occurs with 20% frequency
3. Only blood supply to neck disrupted
4. Reports of 0-7% avascular necrosis
B. Type II
1. Vertical fracture through neck with dislocation of STJ not ankle
2. Occurrence 42%
3. Two areas of blood supply disrupted
4. 46% incidence of avascular necrosis
C. Type III
1. Vertical fracture of neck with displacement of STJ and ankle joint
2. Occurrence 34%
3. Disrupts all 3 areas of blood supply
4. 88 % avascular necrosis

D. Type IV
1. Vertical fracture of neck with displacement of STJ, ankle, and T-N joint
2. 4% occurrence
3. Nearly 100% avascular necrosis

VII. Treatment of Talar Neck Fractures

A. Type I
1. BK NWB cast for 6-8 weeks, (some say AK cast with foot plantarflexed, then another cast neutral for four weeks) then therapy,
but still NWB for another 8 weeks or more
B. Type II, III, IV
1. Closed reduction attempt
2. Usually ORIF
Note: Avascular necrosis is virtually assured with type III & IV. Type IV is a medical emergency if the body compresses the posterior
tibial neurovascular bundle.

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VIII. Complications of Talar fractures
A. Avascular necrosis
B. Degenerative arthritis of ankle and STJ
C. Non-union or mal-union
D. Infection

IX. Os Trigonum (present in 10% of population)

A. Posterior process of talus (2 of them form groove for FHL, lateral largest) develops as secondary center of ossification between 8 - 11 years.
Ossification will then usually occur within one year
B. Differentiate from posterior process fracture of talus. (Fractured Steida's process or Shepard's Fracture)
1. Injury either way is plantar flexion injury
2. Os trigonum may be bilateral so take opposite x-rays
3. Fractured posterior process may be jagged and rough edges
4. Os trigonum injury may be smooth
5. Plantar flex foot and dorsiflex hallux to have FHL irritate site
C. Treatment
1. Conservative
a. BK cast for 6 weeks, local anesthetic, PT
2. Surgical - lateral incision parallel to peroneal tendons, between fibula and Achilles. The most likely complication of this procedure is
severing the Flexor Hallucis Longus Tendon. Also, be sure to isolate and protect the Sural Nerve.

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Thermal Injuries
I. Soft Tissue Burns
A. Soft tissue will burn at temperatures >115 degrees Fahrenheit. Thermal injuries are caused by both hot and cold, chemical and electrical
injury.
B. The extent of thermal injury is determined by the depth of damage and as a % of the Total Body Surface Area (TBSA). The Rule of 9's is
often used to determine the % of damage.
C. New classification system for thermal injuries includes the following categories:
1. Partial Thickness Superficial – Epidermis only
a. Characterized by erythema, flat red macules, WITHOUT blistering
b. Mild to moderate pain levels
c. Example = Sunburn
2. Partial Thickness Deep – Epidermis with partial Dermis
a. Characterized by erythema
b. Blisters/Bullae
c. Mottled Skin
d. Spotty White Skin
e. Severe pain
3. Full Thickness – All of Epidermis/Dermis and any part of sub Q tissue
a. Mottled white or black skin with eschar present
b. Painless due to total nerve destruction within tissue
c. Skin may appear leathery or have a black eschar present
d. Burn injury may be deep enough to involve tendon, capsule, or
bone

II. Progression of Burn Injuries

A. Three Zones of Tissue Injury (from superficial to deep)
1. The zone of coagulation (epidermis)
2. The zone of stasis (dermis)
3. The zone of hyperemia (Sub Q tissue)
NOTE: Energy absorbed by the soft tissue in the process of a burn injury moves
between these tissue zones causing further damage after the initial burn has
occurred. This why immediate cooling is an important step in the treatment
process.

III. Estimating the % surface area of a burn injury:

In addition to the depth of a Thermal injury, the total area is significant. Burns are measured as a percentage of total body area. The "rule of nines" is
often used, (this measurement is adjusted for infants and children). The calculation is based upon the fact that the surface area of the following parts of
an adult body each correspond to approximately 9% (or a factor of 9%) of the total body area (100%):

A. The “Rule of 9's”

1. Anterior Head/Neck = 4.5%
2. Posterior Head/Neck = 4.5%
3. Anterior Trunk = 18%
4. Posterior Trunk = 18%
5. Anterior Arm = 4.5%
6. Posterior Arm = 4.5%
7. Anterior Leg = 9%

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 8. Posterior Leg = 9%
9. Perineum/Groin = 1%

IV. Burn Treatment

A. Immediate cessation of burning agent
1. Immediate removal from contact with the skin
a. Check for possible chemical in clothing or shoe material
2. Assess Circulation, Airway, and Breathing of patient
3. Assess neurovascular status of the affected limb
a. Hemostasis
4. Cooling with towels (not direct ice)
5. Arrange for transportation to the hospital
6. Flush the Tissue (More helpful with topical chemical burns)
7. Consider providing standard blister care (It is advised to either leave blisters intact if they do not interfere with joint motion or to
drain without de-roofing the blister depending on the patient and severity of the burn)
8. Provide pain management via narcotics or OTC pain medication depending on pain levels the patient is currently experiencing
9. Provide tetanus prophylaxis if needed for burns including any of the dermis or deeper structures
10. Antibiotics - Topical Cream (Silvadene), oral antibiotics, or broad spectrum IV antibiotic depending on the patient
11. If the burn injury is severe one must consider admission to a local burn center for possible escharectomy and skin grafting as soon
as possible

B. Fluids – It is important to maintain organ perfusion and prevent hypovolemic shock

1. Fluid Replacement using Baxter’s Rule: 1st 24 Hours of treatment
a. Infusion of Lactated Ringers: 4mg Crystalloid
Formula: (4mg crystalloid) X (Kg) X (% surface area of Burn previously determined by using the rule of nines.
b. After 48 hours
Fluids are administered based on the following lab values:
Serum and Urine Osmolarity
Electrolytes Levels

V. Criteria for admission to the hospital (Consider admission for any of the following)
A. Plantar Foot Burns: (Partial Deep and Full Thickness)
1. Partial Deep (>15%)
2. Full Thickness (>2%)
B. Patients < 2 years old or patients > 60 years old
C. Electrical Burns (Due to higher risk of internal organ damage)
D. Chemical Inhalation Burns

VI. Diagnosing Hypothermia Frostbite (via core rectal temperature)

A. Mild Hypothermia = >32 degrees Celsius
B. Moderate Hypothermia = Between 28 and 32 degrees Celsius
C. Severe Hypothermia = < 28 degrees Celsius

VII. Frostbite
A. Superficial Frostbite
1. Involves the skin and subcutaneous tissue
2. Signs of superficial frostbite are clear fluid in blisters can also show other positive prognostic signs of return to normal skin color
and return of sensation
B. Deep Frostbite
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 1. damage extends down to the level of bone/joint/tendon
2. Signs of deep frostbite are hemorrhagic fluid noted within blisters, loss of color/sensation.
3. This condition generally has a poor prognosis and will likely result in some level of amputation and/or tissue loss

VIII. Treatment of Hypothermia/Frostbite

A. Immediate rewarming must be accomplished
1. Forced warm air blankets
2. Warm O2 (consider placing patient on warm air vent for severe hypothermia)
3. Warm IV fluids
B. Patient will likely develop bullae over the affected tissue
1. These bullae should be allowed to rupture while the patient is admitted and being monitored for signs of infection in the hospital
2. In severe cases where amputation and/or irreversible tissue damage occurs the affected areas should be allowed to demarcate
and an amputation at the appropriate level should then be considered
3. After amputation consider referring the patient for psychological monitoring and social services at home

IX. Older Classification for Burns (Note that the older “degree” classification system for burns is
still taught in some settings and may be included in a board level question.)
A. First Degree
1. Superficial
2. Involves outer layer of skin
3. Hyperemia with blanching usually present
4. Does NOT result in blister formation
5. Extremely painful
B. Second Degree
1. May be superficial or deep
2. May or may not involve blisters
3. Blanching erythema usually present
4. Firm yellow skin sometimes present
5. Extremely painful
C. Third Degree
1. Full thickness skin destruction
2. May involves fat, tendons, joint capsules, and Bones
3. Electrical burns, radiation, frostbite can lead to symmetrical growth arrest of physis
4. These burns involve minimal or sometimes no pain at all
5. The remaining skin may feel like leather and appear to be white or yellow

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 Tscherne Soft Tissue Injury Classification
Grade Description

0 Minimal soft tissue damage indirect injury to limb (torsion) simple fracture pattern. Little or no soft-tissue injury

1 Superficial abrasion with local contusional damage to skin or muscle with mild fracture pattern

2 Deep abrasion skin or muscle contusion severe fracture pattern direct trauma to limb associated with localized muscle damage

3 Extensive Soft tissue contusion or crushing, compartment syndrome, vascular injury and multi-fragmentary fracture pattern

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PART 2:
BASIC SCIENCE

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Basic Science Part I: PATHOMECHANICS

Bunions / Hallux Abducto Valgus

I. Anatomy of 1st Metatarsal Phalangeal Joint

Six tendons are associated with the first MPJ (three intrinsic and three extrinsic).
Intrinsic
Flexor hallucis longus
Extensor hallucis longus

Extrinsic
Abductor hallucis
Extensor hallucis brevis
Adductor hallucis
Flexor hallucis longus

II. Pathomechanics of HAV

A. Normal biomechanics of the first ray

1. Consist of the first metatarsal and first cuneiform

2. Axis runs from anterolateral/slightly plantar to posteromedial/slightly dorsal.
3. Axis is angled about 45 degrees from both the frontal and sagittal planes with little divergence from Transverse
4. Roughly equal DF(5mm) and PF(5mm) Total ROM=1cm.
5. As the first ray DF it also inverts. As it PF it also everts.
6. During midstance & propulsion the first ray must plantar flex for normal propulsion to occur. As weight is transferred
from lateral to medial, inversion of the RF & FF elevates the medial FF from the ground. The First ray must then plantar flex
to allow the first metatarsal to maintain ground contact.

B. Normal Biomechanics of the First MPJ

1. 1st MPJ has two axis; Vertical (DF/PL) & horizontal (ABD/ADD) there is no longitudinal axis & therefore any frontal plane
motion of the great toe is abnormal.
2. During static examination the ROM is only 45 degrees (Hallux DF 21-25 degrees + 20 degrees of metatarsal declination)
without movement of the first ray.
3. During gait the hallux is stable against the ground with the 1st met moving in closed Kinetic chain motion. Any DF
greater than 20 degrees at the 1st MPJ during gait requires PF of the first ray & pronation of the longitudinal midtarsal joint.
With PF of the 1st ray, the metatarsal head moves posteriorly over the sesamoids (sesamoids articulate with the distal end
of the first met.) This posterior movement occurs by the windlass mechanism.
4. The total ROM of the 1st MPJ during closed kinetic chain motion is 65-75 degrees (because of post. movement of the met
head)

C. Normal biomechanics of the midtarsal/subtalar joints

1. At heel lift no forces go to the subtalar joint. It is all transferred to the midtarsal joint. The midtarsal joint must be locked
at heel lift. In order to have a locked midtarsal joint, the subtalar joint must be supinated.

D. Normal first ray essentials

1. Supinated position of the foot in propulsion

2. Normal metatarsal length pattern (2 longer than 3)
3. Normal strength & phasic activity of muscles
4. Normal sesamoid apparatus
5. Stable base of the proximal phalanx

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 E. Pathomechanics of HAV

1. Subtalar joint pronation is necessary for hypermobility of the first ray and HAV to develop. As the calcaneus everts and
the subtalar joint pronates, the longitudinal midtarsal joint supinates to its end ROM to maintain FF contact & prevent tibial
sesamoiditis. When the degree of calcaneal eversion is greater than the amount of longitudinal midtarsal joint supination
(4-6 degrees), the 1st ray dorsi flexes & inverts as a result of the FF eversion. As the 1st met DF, the joint capsule is pulled
lateral because it is anchored to a stable second metatarsal by the deep intermetatarsal ligament. This results in a frontal
plane rotation at the MPJ. The lateral soft tissue structures are shortened & contract. The medial structures are stretched
and lengthened. This results in a lateral & valgus position of the hallux & sesamoids. The extrinsic muscles of the hallux
bowstring across the MPJ and the sesamoids rotate laterally. The ABD hallucis assumes a more plantar position and loses
the tibial sesamoid as a fulcrum for action. The Add hallucis maintains a sesamoid relationship, which results in a muscle
imbalance favoring the lateral aspect of the MPJ. As the hallux drifts laterally a retrograde force is applied to the metatarsal
resulting in an increase in the IMA.

F. Etiology of HAV

1. Hypermobility of the first ray: (most common cause)

a. Subtalar joint pronation as explained above
b. Generalized ligament laxity (effects the naviculocuneiform articulation not the metatarsocuneiform greater DF
of the first ray and greater deformity)
2. Metatarsal Deviation: (rare & usually seen in the adolescent pt.)
a. Caused by asymmetric growth of the 1st met base
b. Diagnosed by drawing a line perpendicular to the tangent of the 1st met base and comparing it to the bisection
of the 1st met. The increased IMA precedes and causes the abduction of the hallux. Therefore CBWO is indicated for
correction.
3. Metatarsus Primus Varus:
a. Causes an increased IMA due to the medial cuneiform
b. Diagnosed by comparing the longitudinal bisection of the 1st met & first cuneiform. If the angle between these
two lines is greater than 20-25 degrees, Met Primus Varus exists.
c. Correct with a CBWO, Lapidus fusion of first metatarsocuneiform joint with bone graft, or OWO of the medial
cuneiform with bone graft.
4. Relative Metatarsal Protrusion Length:
a. Protruding hallux abducts to compensate for its length
b. Correct with a shortening osteotomy (no more than 2 mm)
5. Rotational deformities:
a. Internal rotation of hip, femur, knee, tibia, or foot will result in HAV.
6. Inflammatory Joint Disease:
a. Joint destructive procedures are preferred.

III. Angular Relationships

A. Hallux Abduct o Angle

1. An angle formed by a line representing a bisection of the shaft

of proximal phalanx and a line representing a bisection of the shaft of first metatarsal.
2. Normal: 15 degrees
3. Represents: The relative position of the hallux in relation to the first metatarsal

B. Distal Articular Set Angle (DASA)

1. An angle formed by a perpendicular to the effective cartilage of the base of the proximal phalanx and a line representing
the bisection of the shaft of the proximal phalanx
2. Normal 7.5 degrees
3. Represents the position of the effective cartilage to the shaft of the proximal phalanx. An increase in the angle may show
a deformity in the shaft of the proximal phalanx

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C. Proximal Articular Set Angle (PASA)

1. An angle formed by a perpendicular to a bisection of the first metatarsal

and a line representing the effective articular cartilage.
2. Normal 7.5
3. This represents the effective cartilage in relation to the shaft of the metatarsal.
A high PASA shows that the cartilage is laterally deviated.

D. Metatarsus Primus Adductus Angle (IMA)

1. An angle formed by a line representing a bisection of the shaft of the

first metatarsal and a line representing a bisection of the shaft of the
second metatarsal.
2. Normal 8 Degrees
3. Represents the relationship of the first metatarsal to the second metatarsal.
An increase in the angle makes the head of the first metatarsal more prominent

E. Hallux Interphalangeus Angle (HIA)

1. An angle formed by a line representing the bisection of the shaft of the proximal
phalanx and a line representing the bisection of the distal phalanx
2. Normal 0-10 degrees
3. Represents a deformity at the interphalangeal joint or within the shaft of the proximal phalanx

F. Metatarsal Protrusion Angle

1. Distance between two arcs, which represent the length of the first metatarsal and second metatarsal. A line representing
the bisection of the first metatarsal is extended to intersect with a line representing the bisection of the second metatarsal.
A compass is placed at the point of intersection and an arc drawn from the distal portion of the first metatarsal and one
drawn from the distal portion of the second metatarsal. A positive millimeter distance is used to indicate the first metatarsal
being longer than the second metatarsal. A negative distance is used to indicate the second metatarsal being longer than
the first metatarsal.
2. Normal: + or - 2 mm
3. Represents the relative length between the first and second metatarsals

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 G. Metatarsus Adductus Angle (MAA)

1. An angle formed by a perpendicular to the bisection of the lesser tarsus and a line representing the lesser metatarsus.
The lesser tarsus is bisected by obtaining a median point (E) between the anterior portion of the first cuneiform (A) and the
posterior portion of the navicular (B) and a median point (F) of the anterior portion of the cuboid (C) and posterior portion
of the cuboid (D). These median points are then connected. A perpendicular is then drawn to this line. The lesser
metatarsus is represented by a bisection of the shaft of the second metatarsal.
2. Normal 10-20 degrees
3. As this angle is increased and the foot becomes more adducted, the greater is the chance for a hallux abductus
deformity. Also, the metatarsus primus adductus angle becomes more significant at a lower point than with a rectus type
foot.

H. Tibial Sesamoid Position

1. The position of the tibial sesamoid is compared to a line bisecting the shaft of the first metatarsal measured on a scale of
1-7
2. Normal 1-3
3. The position is used as an indication to remove the fibular sesamoid. Generally, the fibular sesamoid should be removed
when the tibial sesamoid is in a position of 4 or more. In this position, the sesamoid is resting on or over the crista of the
first metatarsal and thus is usually eroded.
4. With plantarflexed metatarsal, the sesamoids are distal. With dorsiflexed met, they are proximal.

IV. Shape of Metatarsal Head

A. Round
1. Represents the approximate shape of the metatarsal head. Has to do with the intrinsic stability of the first MPJ.
2. The round head is the most unstable type
B. Square
1. Relatively stable situation
C. Square with Ridge
1. This is most stable type of joint

V. Joint Position

A. Congruous
1. Comparison of a line representing the effective articular cartilage of the first metatarsal and a line representing the
effective articular cartilage of the base of the proximal phalanx
2. Normal - the lines are parallel

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 3. Represents - that the head of the first metatarsal completely articulates with the base of the proximal phalanx and that
the joint space is equal
B. Deviated
1. Comparison of a line representing the effective articular cartilage of the first metatarsal and a line representing the
effective articular cartilage of the base of the proximal phalanx
2. Deviated - the lines intersect outside the joint
3. Represents - an abductus of the hallux within the joint. The base is not displaced off of the head; however, the medial
aspect of the head is exposed. The joint space is no longer equal throughout.
C. Subluxed
1. Comparison of a line representing the effective articular cartilage of the first metatarsal and a line representing the
effective articular cartilage of the base of the proximal phalanx
2. Subluxed - the lines intersect within the joint
3. Represents - an abductus of the hallux within the joint. The base of the proximal phalanx does not completely articulate
with the metatarsal head. The medial aspect of the head is very much exposed and the joint space is no longer equal.

VI. Metatarsal Length

A. Long 1st Metatarsal - related to hallux limitus/rigidus hallux valgus

B. Second Metatarsal slightly longer than 1st by 2mm
C. In HAV
1. Abductor Hallucis insertion is more plantar & becomes a flexor

VII. Types of Bunion/HAV deformities

EXAMPLE 1 (Positional Deformity)

Hallux abductus angle = 35

DASA = 2
PASA = 6
8 <35 MPJ (deviated or subluxed)

EXAMPLE 2 (Structural Deformity)

Hallux Abductus angle = 35

DASA = 8
PASA = 27
35 = hallux abductus angle (MPJ congruous)

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 EXAMPLE 3 (Combined Deformity)

Hallux abductus angle = 35

DASA = 2
PASA = 17
19 < HAA but the PASA is abnormal (MPJ deviated.)

Basic Science Part II: Anatomy

Accessory Ossicles
These are developmental anomalies, often separations of normal processes or tubercles, and need to be differentiated from
avulsion fracture fragments if there is a history of injury.1. Os tibiale externum (accessory navicular) - located at the
posteromedial aspect tuberosity of navicular, within insertional fibers of tibialis posterior

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2. Os Vesalianum - located proximal to well-formed tip of the tuberosity of the fifth metatarsal base. To be differentiated
form fracture of the tip of the fifth metatarsal base, ununited apophysis, or ossification or fragmentation of the
apophysis. Often found to be within the fibularis brevis muscle tendon at it's attachment point to the 5th metatarsal base.
3. Os peroneum (Os Fibularis)- a sesamoid bone located within the peroneus longus tendon near the cuboid.
4. Os supranaviculare (os talonaviculare dorsale) - located at dorsal aspect talonavicular joint.
5. Os intermetatarseum - located between the medial cuneiform and the first and second metatarsal bases.
6. Os sustentaculi - located at posterior aspect of sustentaculum tali.
7. Os Calcaneus Secondarius - located dorsally at the anterior process of the calcaneus, at the junction of the calcaneus,
cuboid, head of the talus and the navicular.
8. Os trigonum - a separated posterolateral tubercle of the talus (differentiate from the trigonal process and fracture
thereof, a Shepherd's fracture).
9. Os subfibulare - located distal to the tip of the fibular malleolus. To be differentiated form avulsion fracture of lateral
malleolus.
10. Os subtibiale - located distal to the tip of the tibial malleolus. To be differentiated from avulsion fracture of the medial
malleolus.
11. Os Cuneo 1 metatarsale 1 plantare - a rare accessory ossicle located at the plantar aspect of the first metatarsal -
medial cuneiform articulation.
12. Os Cuboides Secundarium – Found on the plantar aspect of the foot, between the cuboid/navicular/talus/os calcis. This
is very rare.
13. Os Intercuneiforme - on the dorsum of the foot, between the proximal segments of the internal and middle cuneiforms
and in front of the navicular.

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Anatomy of the 1st Metatarsal

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Ankle Anatomy
Ankle (Talocrural Joint):
A modified ginglymus or hinged synovial joint.
1. Motion: displays triplanar motion. The motion occurs primarily in the sagittal plane, as dorsiflexion and plantar flexion, small amount
of abduction/adduction and eversion/inversion.
2. Articular surfaces: The ankle mortise consists of the concave distal tibial bearing surface (plafond), the triangular facet of the lateral
malleolus, and the comma-shaped facet of the medial malleolus.
3. Soft tissue structures (ligaments)

A. Fibrous Capsule: It surrounds the joint. Thin in the front and behind. It is supported on each side by strong collateral
ligaments.

B. Deltoid Ligament (or the medial collateral ligament): Fans out as a triangle and contains one deep and three superficial
portions. It attaches to the talus, calcaneus and navicular.

A. Superficial Fibers:

a. Tibionavicular anterior fibers - attach to the tuberosity of the navicular.

b. Tibiocalcaneal (blends with the spring ligament) middle fibers descend perpendicularly to the whole
length of the sustentaculum of the calcaneus.

c. Posterior Tibiotalar posterior fibers - pass backwards and laterally to the medial side of the talus and
its medial tubercle.

B. Anterior Tibiotalar (deepest fibers) are well developed and are fixed to the tip of the medial malleolus above
and the non-articular part of the medial surface of the talus below.

Note: The Tibialis Posterior and the Flexor Digitorum Longus cross over the Deltoid Ligament.
Lateral Ligament of the Ankle:

1. Anterior Talofibular Ligament: (Intracapsular and shortest lateral ligament) From the anterior margin of the lateral malleolus to the
lateral aspect of the neck of the talus. It is a capsular thickening.

2. Posterior Talofibular Ligament:(Intracapsular but extrasynovial and the strongest) From the lower part of the lateral malleolar
fossa to the lateral tubercle of the posterior process of the talus.

3. Calcaneofibular Ligament: (extracapsular and deep to the peroneal tendons) A long rounded cord running from the apex of the
fibular malleolus to a tubercle on the lateral surface of the calcaneus. It stabilizes the ankle joint and the subtalar joint.

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Note: The Peroneus Longus and Brevis tendons cross the Calcaneofibular Ligament.
Note: The best way to evaluate the integrity of the CFL is to examine the ankle in a dorsiflexed position.

Tibiofibular Joints:
The tibiofibular joints include the proximal and distal tibiofibular joints and middle tibiofibular joint (crural interosseous membrane).
1. Motion: Allow motion in both the frontal and transverse planes, and resist ankle dorsiflexion as the wider anterior portion
of the dome of the talus engages the mortise.
2. Proximal tibiofibular joint: A plane synovial joint supported by the:
a. Anterior superior tibiofibular ligament
b. Posterior superior tibiofibular ligament.
3. Middle tibiofibular joint: The crural interosseous membrane consists of obliquely oriented, dense fibrous connective tissue
running from proximal-medial to distal-lateral from the tibia to the fibula.
4. Distal tibiofibular joint: A Syndesmosis: supported by the:
a. Anterior inferior tibiofibular ligament
b. Interosseous tibiofibular ligament
c. Posterior inferior tibiofibular ligament.
d. Posterior talofibular ligament
e. Inferior transverse ligament
f. The interosseous membrane

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Arterial Supply to the Lower Extremities

I. Arterial Supply to the Lower Extremities

A. Popliteal artery
1. Direct continuation of the femoral artery as it passes through the adductor hiatus
B. Anterior Tibial Artery
1. Begins as the popliteal artery, ends at the lower border of the popliteus muscle
C. Relationship of Anterior Tibial Artery to anterior leg muscles
1. Upper 1/3 of leg the anterior tibial artery is between TA and EDL
2. Middle 1/3 of leg - it is between TA and EHL
3. Just above ankle joint - the EHL cross medial to the artery
D. Branches of anterior tibial artery
1. Posterior recurrent tibial
2. Anterior recurrent tibial
3. Muscular branches
4. Anterior medial malleolar artery
5. Anterior lateral malleolar artery
E. Key Points
1. All anterior leg muscles are supplied by muscular branches of anterior tibial
2. Anterior medial malleolar artery anastomoses with branches of posterior tibial and medial plantar arteries
3. Anterior lateral malleolar artery anastomoses with perforating of peroneal and lateral tarsal artery
F. At ankle joint, the anterior tibial artery becomes the dorsalis pedis artery, where it continues to the 1st intermetatarsal space.
Then dives deep as the deep plantar branch to joint the plantar arch

G. Branches of dorsalis pedis artery

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 1. Lateral tarsal artery
2. Medial tarsal artery
3. Arcuate artery
4. 1st dorsal metatarsal artery
5. Deep plantar perforating

H. Key Points
1. Lateral tarsal artery lies under extensor digitorum brevis and supplies it
2. Arcuate artery passes over bases of metatarsal bones and gives off 2nd, 3rd and 4th dorsal metatarsal arteries
a. Dorsal metatarsal arteries lie in corresponding intermetatarsal spaces and lie deep to extensor tendons
b. Branch off as anterior perforating branches and then continues as common digital arteries for a short way,
then divide into proper dorsal digital arteries
c. Near bases of 2nd, 3rd, 4th dorsal metatarsal arteries, they give off posterior perforating branches which
anastomose with those of the plantar arch
d. The first metatarsal artery supplies the medial 1st and 1st web space.
I. Posterior tibial artery is the other terminal branch of the popliteal artery
J. Branches of the posterior tibial artery
1. Circumflex fibular
2. Peroneal artery
3. Nutrient artery
4. Muscular branches
5. Communicating branches
6. Medial malleolar branches
7. Medial calcaneal branches
8. Medial plantar artery
9. Lateral plantar artery
K. Key points
1. Peroneal artery is a large branch running parallel and lateral to PT in posterior leg. It supplies muscular twigs to soleus,
tibialis posterior, FHL, P. longus and P. brevis and nutrient branch to fibula. About 5 cm above the lateral malleolus, it sends
a perforating branch through interosseous membrane, which anastomoses with lateral malleolar, lateral tarsal and lateral
plantar.
2. Muscular arteries supply soleus, tibialis posterior, FHL and FDL
3. Medial malleolar branches join with twigs from anterior tibial artery to form rete over medial malleolus
4. Medial calcaneal branches pierce flexor retinaculum to supply area around Achilles and medial side of heel
5. Medial plantar artery is the smaller of terminal branches (it lies medial to medial plantar nerve) and supplies medial side
of great toe, then sends other branches to join the 2nd, 3rd and 4th plantar metatarsal arteries
6. Lateral plantar artery (lies lateral to lateral plantar nerve) At base of 5th metatarsal it curves medially along met bases
and is called plantar arch. This supplies all muscles except abductor hallucis and FHB and 1st lumbrical, FDB. Plantar arch
runs across to first intermetatarsal space where it anastomoses with deep plantar perforating branch of dorsal artery. This
arch separates the 3rd and 4th layers of muscles. There are anterior and posterior perforating arteries given off here to join
with arteries from dorsal.
7. Plantar metatarsal arteries
a. 1st made of union of lateral plantar and deep branch from dorsal
b. 2nd, 3rd, 4th are given off from plantar arch
c. Medial hallux is from 1st plantar metatarsal
d. Lateral 5th is from 4th plantar metatarsal artery or from lateral plantar

II. Vascular supply to the talus

Relies on small vessels from each of the main arteries running near it. The anterior tibial/dorsalis pedis, posterior tibial, and
peroneal.
A. Body
1. The deltoid branches of the artery of the tarsal canal supply the medial side of the talus.
2. The artery of the tarsal canal (which arises from the posterior tibial artery) then enters the canalis tarsi to supply more of
the talus.
B. Head and neck
1. A small twig off the anterior tibial artery enters the superior surface of the talar neck.
2. The artery of the sinus tarsi off the lateral tarsal artery, a branch of the dorsalis pedis.
C. Posterior talus - from calcaneal branches of peroneal artery

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III. Venous Structure of the Foot

A. Superficial veins carry blood from inferior to superior

B. Common dorsal digital veins (8) collect blood from the toe and drain into the dorsal metatarsal veins.
C. Proper dorsal digital vein of the hallux becomes the medial marginal vein
D. Proper dorsal digital vein of the 5th toe becomes the lateral marginal vein
E. Medial marginal vein drains into the great saphenous vein
F. Lateral marginal vein drains into the small saphenous vein
G. Dorsal metatarsal veins (4) drain into Dorsal venous arch
H. Dorsal venous arch drains into Great saphenous vein medially and the small saphenous vein laterally

IV. Branches of the Profunda Femoris

A. Lateral femoral circumflex artery

B. Medial femoral circumflex artery
C. Perforating arteries

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Arthrology
Interphalangeal Joint (IPJ)
The digital interphalangeal joints are ginglymus (hinge) articulations consisting of a joint capsule that is hooded dorsally by the
fibrous digital extensor expansion, and thicken plantarly to form a plantar plate (plantar ligament). The joints are reinforced
with medial and lateral collateral ligaments running obliquely from the head of one phalanx to the base of the next phalanx,
in a proximal-superior to distal-plantar direction. Occasionally an interphalangeal sesamoid may be present plantarly.

Lesser Metatarsophalangeal Joint (MTPJ)

The MPJ's are spheroidal joints contained within a capsule that is contiguous with the extensor hood expansion dorsally, and the
thickened plantar plate (ligament). The capsule is reinforced medially and laterally by collateral and suspensory ligaments.
The collateral ligament runs obliquely, proximal-superior to distal-plantar, from the metatarsal head to the phalangeal base.
The suspensory ligament is actually a continuation of the extensor hood expansion that traverses vertically to the plantar
plate. The plantar plate is tethered to the adjacent plantar plate by the deep transverse intermetatarsal ligament.
Occasionally, a plantar sesamoid bone may be invested with in the flexor (plantar) plate of a lesser MTPJ.

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 First Metatarsophalangeal Joint (First MTPJ)
Anatomy of 1st Metatarsal

The first MTPJ is of particular importance because of the sesamoid apparatus and its relationship to the deformity of hallux
abductovalgus. Two sesamoids, tibial and fibular, are present. The ligamentous arrangement differs from a lesser MTPJ in
that a plantar sesamoidal ligament is present medially and laterally, running from each sesamoid to the phalangeal base.
Moreover, and intersesamoidal ligament is present. The conjoined head of m. adductor hallucis inserts into the plantarlateral
aspect of the fibular sesamoid, the first MTPJ lateral ligaments, and the base of the proximal phalanx.

Tarsometatarsal Joints (TMJ or Lisfranc's Joint)

This joint complex consists of the articulations of the metatarsal bases with the cuneiforms and the cuboid. Stability is
enhanced by the proximal inset of the base of the second metatarsal into the intercuneiform recess. The complex is
arched dorsally in both the frontal and sagittal planes.
There are three synovial joints:
1. Medial tarsometatarsal joint: between the first metatarsal base and medial cuneiform
2. Intermediate tarsometatarsal joint: between the second and third metatarsal bases and the intermediate
and lateral cuneiform
3. Lateral tarsometatarsal joint: between the fourth and fifth metatarsal bases and the cuboid.
Dorsal intercuneiform and cuneocuboid ligaments, tarsometatarsal ligaments, intermetatarsal base ligaments, and plantar
tarsometatarsal ligaments reinforce the capsular elements. The second plantar tarsometatarsal ligament originates
from the plantar surface of the first cuneiform and extends to the plantar surfaces of both the second and third
metatarsals
Of particular interest, with respect to TMJ trauma is the Medial interosseous ligament (Lisfranc's plantar ligament), which
runs obliquely from the medial cuneiform to the second metatarsal base and is the strongest.

Intertarsal Joint (Great Tarsal Joint)

Consist of the following joints
1. Cuboideonavicular Joint (Syndesmosis or planar synovial)
2. Cuneonavicular joint
3. Intercuneiform joints: forms part of the transverse pedal arch. The intermediate cuneiform is the highest point of the arch.
4. Cuneocuboid joint
5. Tarsometatarsal joints (2nd and 3rd)
6. Intermetatarsal joints (bases of the 2nd and 3rd)

Calcaneocuboid Joint (CCJ)

This is a saddle shaped synovial joint.
1. Articular surfaces: Posterior surface of the cuboid and the anterior surface of the calcaneus.
2. Capsule: Surrounds the entire joint and is reinforced with dorsal, lateral, and medial capsular ligaments.
a. The medial ligament is actually the lateral, or calcaneocuboid, portion of the bifurcate ligament.
b. Lateral Calcaneocuboid ligament
c. Dorsal Calcaneocuboid ligament

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 3. Extracapsular ligaments:
a. Long plantar calcaneocuboid ligament, which actually extends from the calcaneal tuberosity to the bases
of the second through fifth metatarsals. This is the longus ligament in the foot.

Talocalcaneonavicular Joint
It is essentially a condylar joint complex that suspends the head of the talus in the midfoot's acetabulum pedis. This is commonly,
and somewhat inaccurately, referred to as the talonavicular joint.
1. Motion: gliding and rotatory
2. Articular Surfaces: Head of the talus, which is convex in all directions and the acetabulum pedis. The acetabulum pedis
consists of:
a. The concavity of the posterior surface of the navicular
b. The anterior and middle facets of the sustentaculum tali of the calcaneus
c. The plantar calcaneonavicular ligament (spring ligament).
3. Soft tissue structures:
a. Fibrous Capsule:
b. Capsular ligaments:

i. Plantar calcaneonavicular ligament (spring ligament)

ii. Calcaneonavicular portion of the bifurcate ligament: "Y" shaped with the stem attached to
the calcaneus and one arm to the cuboid and the other to the navicular.

iii. Dorsal talonavicular ligaments

Subtalar Joint (STJ)

This is a modified ginglymus (hinge) joint

Note: The "Anatomic" STJ is defined as the synovial articulation between the posterior facets of the calcaneus and the talus.
The "Functional" STJ includes two joint cavities, the "subtalar joint proper" (the posterior facets of the calcaneus and the talus),
and the "talocalcaneal part" (The anterior and middle calcaneal facets of the sustentaculum which is an anatomical component of
the talocalcaneonavicular joint). The tarsal canal separates them from each other.

1. Motion: displays triplanar motion. The motion occurs primarily in the frontal plane, as inversion and eversion.
2. Articular Surfaces: The triangular shaped posterior facets of the talus (concave) and the calcaneus (convex).
3. The sinus tarsi is a deep depression seen laterally between the talus and the calcaneus. It extends posteriorly and
medially to become continuous with the canal formed by the sulcus tali and sulcus calcanei (tarsal canal). The tarsal canal is
often considered part of the sinus tarsi. The sinus tarsi is widest at its lateral aspect.
4. Soft tissue structures
a. Fibrous Capsule: It completely surrounds the joint and is reinforced by the capsular ligaments.
b. Ligaments:

i. Lateral talocalcaneal ligament - lateral thickening of the capsule

ii. Medial talocalcaneal ligament - medial thickening of the capsule

iii. Anterior talocalcaneal ligament - thickening of the capsule, which blends with the
interosseous talocalcaneal ligament.

iv. Posterior talocalcaneal ligament (the Y ligament) - reinforces the STJ posteriorly. It
also envelops the FHL tendon between the posterior processes of the body of the talus.

v. Interosseous talocalcaneal ligament (ligament of the tarsal canal) is situated posteriorly

within the tarsal canal (just anterior to the posterior facets). Prevents over eversion of the
foot.

vi. Second interosseous ligament (Cervical ligament) is located anterior to the interosseous
talocalcaneal ligament and arises from the floor of the sinus tarsi and attaches to the neck of
the talus. Prevents over inversion.

Note: The tibialis anterior and the tibialis posterior are the most important STJ supinators. The peroneus longus and the
peroneus brevis are the most important STJ pronators.

Talocrural (Ankle) Joint:

A modified ginglymus (hinged) synovial joint.

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 1. Motion: Displays triplanar motion. The motion occurs primarily in the sagittal plane, as dorsiflexion and plantar flexion,
small amount of abduction/adduction and eversion/inversion.
2. Articular surfaces: The ankle mortise consists of the concave distal tibial bearing surface (plafond), the triangular facet of
the lateral malleolus, and the comma-shaped facet of the medial malleolus.
3. Soft tissue structures (ligaments)
a. Fibrous Capsule: It surrounds the joint. Thin in the front and behind. It is supported on each side by strong
collateral ligaments.
b. Deltoid Ligament (or the medial collateral ligament): Fans out as a triangle and contains one deep and three
superficial portions. It attaches to the talus, calcaneus and navicula.

i. Superficial Fibers:

Tibionavicular anterior fibers - attach to the tuberosity of the navicular.

Tibiocalcaneal (blends with the spring ligament) middle fibers descend perpendicularly to
the whole length of the sustentaculum of the calcaneus.

Posterior Tibiotalar posterior fibers - pass backwards and laterally to the medial side of the
talus and its medial tubercle.

ii. Anterior Tibiotalar (deepest fibers) are well developed and are fixed to the tip of the medial
malleolus above and the non-articular part of the medial surface of the talus below.

Note: The Tibialis Posterior and the Flexor Digitorum Longus cross over the Deltoid Ligament.
c. Lateral Ligament of the Ankle:
i. AnteriorTalofibular Ligament: (Intracapsular and shortest lateral ligament) From the anterior
margin of the lateral malleolus to the lateral aspect of the neck of the talus. It is a capsular thickening.

ii. Posterior Talofibular Ligament:(Intracapsular but extrasynovial and the strongest) From
the lower part of the lateral malleolar fossa to the lateral tubercle of the posterior process of the
talus.

iii. Calcaneofibular Ligament: (extracapsular and deep to the peroneal tendons) a long
rounded cord running from the apex of the fibular malleolus to a tubercle on the lateral surface of the
calcaneus. It stabilizes the ankle joint and the subtalar joint.

Note: The Peroneus Longus and Brevis tendons cross the Calcaneofibular Ligament.
Note: The best way to evaluate the integrity of the CFL is to examine the ankle in a dorsiflexed position.

Tibiofibular Joints:
The tibiofibular joints include the proximal and distal tibiofibular joints and middle tibiofibular joint (crural interosseous
membrane).
1. Motion: Allow motion in both the frontal and transverse planes, and resist ankle dorsiflexion as the wider anterior portion
of the dome of the talus engages the mortise.
2. Proximal tibiofibular joint: a plane synovial joint supported by the:

i. Anterior superior tibiofibular ligament

ii. Posterior superior tibiofibular ligament.

iii. Middle tibiofibular joint: The crural interosseous membrane consists of obliquely
oriented, dense fibrous connective tissue running from proximal-medial to
distal-lateral from the tibia to the fibula.

iv. Distal tibiofibular joint: a syndesmosis supported by the:

Anterior inferior tibiofibular ligament

Interosseous tibiofibular ligament

Posterior inferior tibiofibular ligament

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Bone Ossification Dates
APPEARS EPIPHYSIS (BASES) FUSE
Phalanges
Prox Birth 2-3 years 15-21
Middle Birth 2-3 years 15-21
Distal Birth 2-3 years 15-21

Metatarsals
1st Birth 2-3 years (base) 15-18
2nd Birth 2-3 years (head) 15-18
3rd Birth 2-3 years (head) 15-18
4th Birth 2-3 years (head) 15-18
5th Birth 2-3 years (head) 15-18

Cuneiforms
Medial 3-4 years
Middle 3-4 years
Lateral Birth-1 yr

Cuboid Birth-1 yr

Talus Birth

Calcaneus Birth 5-12 yrs (Apophyses) 15-20

Navicular 3-4 years

Sesamoids 9-11 years

Fibula Birth (proximal 3-4) 14-21

(Distal 2 yrs) 11-14

Tibia Birth (Proximal-Birth) 19-21

(Distal-2 yrs) 17-19

Note: At birth, the following bones are not present: Medial and middle cuneiforms and the navicular.

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Extrinsic Pedal Musculature
I. Osteofascial compartments of the leg:

A. The anterior leg compartment contains:

1. Tibialis anterior (TA)
2. Extensor hallucis longus (EHL)
3. Extensor digitorum longus (EDL)
4. Peroneus tertius (PT) muscle
Note: Each of these is innervated by the deep peroneal nerve and supplied by the anterior tibial artery. The tendons of these
muscles traverse deep to the transverse and cruciate crural ligaments.

1. Tibialis anterior (TA): is the most medial of the anterior crural muscles.
Origin: From the lateral superior condyle and shaft of the tibia, interosseous membrane, deep crural fascia,
and intermuscular septum adjacent to EDL.
Insertion: Approximately 90% of the tendon inserts into the medial cuneiform, and 10% into the base of the
1st metatarsal.
Functions:

Dynamic:

• Accelerate and decelerate the foot during gait.

• It assist in dorsiflexion at toe off and dorsi flexes the first ray during swing phase.

• Resists plantar flexion of the foot at heel strike.

Static:

• Dorsiflexes the foot on the leg.

2. Extensor digitorum longus (EDL):

Origin: From superior lateral condyle of the tibia and the proximal 3/4 of the fibula, interosseous membrane,
crural fascia, and intermuscular septae common to TA and PL.
Insertion: The tendon divides into four major slips that insert into each of the four lesser toes. In the digit,
the tendon divides into a central slip that inserts into the dorsal and central aspect of the base of the
middle phalanx, and two collateral slips (one medial and the other lateral) that course along the medial
and lateral aspects of the middle phalanx before they reunite and insert as a single tendon into the
dorsal surface of the distal phalanx. The tendons also yield medial and lateral fibrous expansions at the
level of the head of the metatarsal and MTPJ, creating the extensor hood apparatus which also serves
as an insertion point for the dorsal and plantar interossei and the lumbricales. The 2nd, 3rd, and 4th
slips receive tendons from the EDB on their lateral sides.
Functions:

Dynamic:

•Stabilizes and accelerates the foot during gait.

•Helps create a "rigid beam effect" during the propulsive phase of gait.

•Assists in dorsiflexion in swing phase of gait.

Static:

•Dorsiflexes the foot on the leg, extends the 4 lateral toes, and extends the
phalanges upon each other.

3. Extensor hallucis longus (EHL):

Origin: From the anterior surface of the fibula, and the adjacent interosseous membrane.
Insertion: Into the dorsal aspect of the base of the hallux distal phalanx.
Functions

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 Dynamic
•It accelerates the foot immediately after toe off.
•During swing phase it acts as the strongest dorsiflexor of the foot
•During stance it creates a "rigid beam effect" for the hallux.
Static:
•Dorsiflexes the leg on the foot, extends the hallux and extends the distal phalanx
on the proximal phalanx. It also assists in inverting the foot.

Extensor hallucis accessorius originates from the medial aspect of EHL in the distal
leg, ankle, or foot, and inserts into the dorsal and medial aspect of the
base of the proximal hallucal phalanx.

4. Peroneus tertius (PT) muscle:

Origin: From the inferior third of the anteromedial surface of the fibula and the interosseous membrane.
Insertion: Into the base of the fifth metatarsal dorsally.
Functions:

Dynamic:

•Assists in dorsiflexion of the foot.

•During the swing phase it helps prevent excessive supination of the foot.

Static:

•Flexion and eversion of the foot on the leg.

B. The lateral leg compartment (peroneal compartment) contains:

1. Peroneus longus (PL)
2. Peroneus brevis (PB)
•The muscles are supplied by the superficial peroneal nerve, and the peroneal artery.
•They traverse deep to the peroneal retinaculum distal to the lateral malleolus.

1. Peroneus longus (PL):

Origin: From the head and proximal half of the lateral surface of the fibula, the deep crural fascia, and the
anterior and posterior peroneal septae.
Insertion: Into the plantarlateral aspect of the base of the first metatarsal (90%) and the adjacent portion of
the medial cuneiform. It also gives off a slip that gives origin to the first dorsal interosseous
muscle.
The muscle is superficial to the peroneus brevis at the myotendinous junction proximal to the lateral
malleolus, and must be retracted when harvesting the underlying brevis for lateral ankle stabilization
procedures.
Functions:

Dynamic:

•During propulsion it assists in the transfer of body weight in the forefoot from
lateral to medial.

•In stance phase (it is a stance phase muscle) it stabilizes the base of the first ray
against the tarsal bones and the head of the 1st metatarsal against the
ground.

Static:

•Plantar flexion and eversion of the foot on the ankle.

2. Peroneus brevis (PB):

Origin: Anterior to PL from the distal 2/3 of the lateral surface of the fibula, and the anterior and posterior
peroneal septae. Just distal to the lateral malleolus, the PB tendon is superior and anterior to the
tendon of PL.
Insertion: Into the lateral aspect of the tuberosity of the 5th metatarsal.
Functions:
Dynamic:

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 •(stance phase muscle): During midstance and propulsion it stabilizes the lateral column,
assists the PL in transferring the body weight of the forefoot from lateral to medial, and resists
supination of the foot and external rotation of the leg.

Static:

•Plantar flexion and eversion of the foot on the ankle.

C. The posterior compartment (divided into superficial and deep)

The superficial compartment of the posterior leg contains:
1. Gastrocnemius
2. Soleus
3. Plantaris
•These muscles make up the Triceps surae, which converge to form the tendoachilles (the thickest and
strongest tendon in the body) which inserts into the posterior aspect of the calcaneus.
•They are all innervated by branches of the tibial nerve, and supplied by the posterior tibial artery.
•Proximally the fibers of the soleus are anterior to those of the gastrocnemius. Distally the fibers of the soleus
are medial to those of the gastrocnemius because the gastroc fibers take a lateral turn.
•The triceps surae plantar flex the ankle, with some inversion, and also extend the knee by virtue of the
femoral origin of the gastrocnemius.
1. Gastrocnemius:
Origin: The lateral head from the lateral femoral condyle. The medial head (Largest) from the medial
condyle of the femur and the posterior aspect of the knee joint capsule.
Insertion: Fuses with the soleus to form the Achilles tendon, which inserts into the back end of the
calcaneus.
Functions:
Dynamic:
•Swing phase muscle
•Initiates propulsion by flexing the knee and lifting the heel.
•Prevents hyperextension of the knee.
•The tendon of the lateral head of the gastrocnemius sometimes contains a sesamoid
bone called the fabella.
•The gastrocnemius crosses the knee joint, the ankle, and the subtalar joint (3
joints).
2. Soleus:
Origin: From the head and proximal third of the fibula and the middle third of the tibia above the popliteal
line.
Insertion: Fuses with the gastrocnemius to form the Achilles tendon, which inserts into the back end of the
calcaneus.
Functions:

Dynamic:

•Stance phase muscle

•Assists in heel lift during propulsion.

•In late contact and midstance it stabilizes the lateral forefoot against the ground.

•Assists in extending the knee in midstance.

•The soleus attaches to the medial 2/3 of the deep surface of the Achilles tendon.
•The soleus crosses 2 joints (the ankle and the subtalar joints).
•The plantaris is absent 7 % of the time.
3. Plantaris:
Origin: Medial to the lateral head of the gastrocnemius at the lateral condyle of the femur. It courses from
lateral to medial.
Insertion: Into the medial aspect of the tendoachilles and, along with the Achilles, into the calcaneus.
Functions:
Dynamic:
•Assists the gastrocnemius.

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 Static:

•Flexes the leg on the thigh and plantar flexes the foot on the leg.

The (deep compartment) of the posterior leg contains:

1. Tibialis posterior (TP)
2. Flexor digitorum longus (FDL)
3. Flexor hallucis longus (FHL)
•The muscles are innervated by the tibial nerve, and supplied by the posterior tibial artery.
•The tendons of these muscles traverse deep to the flexor retinaculum (laciniate ligament).
1. Tibialis posterior (TP):
Origin: From the posteromedial aspect of the fibula, the posterior aspect of the tibia distal to the popliteal
line and lateral to the vertical line, the interosseous membrane, and adjacent intermuscular septae. FHL
and FDL both overlap the belly of TP.
Insertion: The primary insertion of TP is into the tuberosity of the navicular, with many additional slips
inserting into the plantar aspect of the intermediate three metatarsal bases and every tarsal bone
with the exception of the talus.
Functions:

Dynamic:

•A stance phase muscle.

•Decelerates STJ pronation and internal rotation of the leg during contact.

Static:

•Plantar flexes and inverts the foot on the leg.

The tendon passes through the first (medial) canal of the tarsal tunnel.
2. Flexor digitorum longus (FDL):
Origin: From the posterior aspect of the tibia distal to the soleal line, and from fascia of TP.
Insertion: The tendon splits into four slips that insert into the middle of the distal phalanx of the lesser four
toes, plantarly.
Functions:

Dynamic:

•Stance phase muscle

•During propulsion it stabilizes the lesser digits against the ground.

Static:

•Platarflexes the foot on the leg

•Flexes the lateral four toes on the metatarsals.

•Flexes the phalanges of each toe upon each other.

•The tendon traverses the second canal of the tarsal tunnel to enter the foot
•It first crosses superficial to FHL, and then over TP.
•The tendons share a vinculus where they interconnect.
3. Flexor hallucis longus (FHL):
Origin: From the distal 2/3 of the posterior surface of the fibula, the posterior aspect of the peroneal
septum, the anterior surface of the deep transverse intermuscular septum (separating the superficial
and deep posterior groups), and the fascia of TP.
Insertion: Into the plantar aspect of the base of the distal phalanx of the hallux.
Functions:
Dynamic:
•Maintains stability of hallux against the ground during propulsion.

Static:

•Flexes the hallux at the MPJ and the IPJ.

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 •Plantar flexes the foot on leg.

•The tendon courses through the fourth canal of the tarsal tunnel

II. Retinacula of the ankle: considered superficial ligaments

A. Extensor Retinacula (divided into two distinct portions)

1. Transverse crural ligament (superior portion)
•Attaches to the tibia and fibula above the malleoli (entirely on the leg).
•Separates the tendons of:

Tibialis Anterior (only one with a synovial sheath at this level)

Extensor hallucis longus

Extensor digitorum longus

Peroneus tertius

2. Cruciate crural ligament (inferior portion)

•Forms a transverse "Y"
•A lateral stem (base of "Y") and two medial arms.
•The superior arm is separated into superficial and deep layers by the EHL, which runs through it
(sometimes the Tibialis Anterior also).
•The medial arm attaches to the medial aspect of the plantar fascia. Some of the fibers bifurcate to envelope
the abductor muscle belly and form a tunnel.

B. Flexor Retinacula: (Laciniate ligament)

1. Forms part of the tarsal tunnel
2. Contents of the tarsal tunnel:
•1st (Medial) compartment: tibialis posterior
•2nd compartment: FDL
•3rd compartment: tibial vessels and nerve. Note the nerve runs deep to the artery. Remember Deep =>
superficial (NAV) nerve, artery, vein.
•4th (lateral) compartment: FHL

C. Peroneal Retinacula: (Divided into superior and inferior surfaces)

1. Superior peroneal retinaculum:
•Encloses the tendons of the peroneus longus and brevis
•quadrilateral in shape
2. Inferior peroneal retinaculum:
•Continuous with the main stem of the inferior extensor retinaculum.
•Forms a septum that separates the 2 peroneal tendons.

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Nail Anatomy
I. Basic Nail Anatomy

A. Nail plate: A hardening of the epidermis; cells have no nuclei and function is to protect the distal end of the digit/ toe
B. Maxtrix: Function of this structure is to produce nail plate
C. Eponychium/ proximal nail fold: The skin fold at the proximal edge of the nail plate which overlies the matrix seals nail
plate and protects against infection
D. Cuticle: Small ridge of transparent skin dorsal to the proximal edge of the nail plate which is continuous with the
eponychium and the function is to prevent infection by sealing the area adjacent to the nail plate
E. Nail bed: Skin directly beneath the nail plate to anchor the nail plate and allow its distal growth
F. Lunula: The small pale half-moon shaped area near eponychium composed of living nucleated cells.
G. Free edge of the nail plate: Distal edge of nail plate that overhangs the toe to protect the distal tufts of the toe from blunt
trauma
H. Hyponychium: The thickened skin adjacent to the free edge of the nail plate
I. Distal nail groove: The shallow transverse groove between the hyponychium and the skin of the distal tuft of the toe
NOTE: It takes 9 months for a toe nail to fully regrow. (See nail trauma and nail surgery)

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 Nerve Supply to the Lower Extremity

NERVE DISTRIBUTION

Saphenous Nerve -Skin on the medial aspect of the foot.

Superficial Peroneal Nerve - Skin on the dorsum of the foot.

Deep Peroneal Nerve -EDB (Extensor Digitorum Brevis)

- Skin on the contiguous sides of the great toe and
2nd toe.

Medial Plantar Nerve -AB. Hall (Abductor hallucis)

-FDB (Flexor Digitorum Brevis)
-FHB (Flexor Hallucis Brevis)
-First Lumbrical
-Skin of the plantar surface medial to a line
Splitting the fourth toe.

Lateral Plantar Nerve -Supplies all the muscles not supplied by the
medial plantar nerve and the deep peroneal nerve.
-Skin of the plantar surface lateral to a line splitting
the fourth toe.

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I. Nerve Supply to the Lower Extremities

A. In lower 1/3 of thigh, the sciatic nerve divides into the Tibial Nerve and the Common Peroneal Nerve
B. Common Peroneal Nerve
1. Deep peroneal nerve (anterior tibial) begins at the bifurcation of the common peroneal nerve between the fibula and
upper P. Longus. It passes under EDL on the interosseous membrane. At ankle it divides into
a. Lateral terminal nerve

1) Passes beneath the EDB which it innervates and gives off 3 interosseous
branches which supply 2, 3, 4th interosseous muscles

b. Medial terminal nerve

1) Follows and is lateral to DP artery. The nerve divides at first interspace into two
dorsal digital nerves supplying adjacent sides of great and second toes, supplying
adjacent sides of great and 2nd toes and first dorsal interossei.

c. Muscular branches of deep peroneal

1) Supply all anterior leg muscles and P. tertius

2. Superficial peroneal nerve - supplies both peroneals & sensory innervation to the anterolateral aspect of the leg (the
distal half) and the dorsum of the foot (the exception is the webspace between the hallux and second digit).

1) Medial dorsal cutaneous nerve - divides into two dorsal digital nerves, the medial
dorsal digital branch that communicates with the medial terminal nerve
branch from deep peroneal to supply medial side of hallux. The lateral
dorsal digital branch supplies the adjacent sides of toes 2, 3 dorsally.

2) Intermediate dorsal cutaneous nerve - is smaller than medial nerve. The medial
branch supplies the adjacent sides of the 3rd and 4th toes while the lateral
branch supplies the adjacent sides of the 4th and 5th toes.

C. Tibial Nerve - in lower third of leg runs parallel and medial to Achilles tendon
1. Sural Nerve
a. Formed by junction of the medial sural cutaneous branch of the posterior tibial nerve along with
the sural communicating branch of the lateral sural cutaneous branch of the common peroneal
nerve. This runs below lateral malleolus along lateral side of the foot.
2. Muscular branches of the tibial nerve
a. Supply the gastroc, soleus, tibialis posterior, FHL, and FDL
3. Medial Calcaneal nerve
a. Perforates the laciniate ligament and supplies the medial side of the heel and the plantar heel.
4. Medial plantar nerve
a. Larger of the two nerves. It is in the 3rd compartment of the flexor retinaculum and has the medial
plantar vessels lying medial to it.
b. Gives off the following branches:

1) Cutaneous branches - supplies medial plantar aspect of sole of foot

2) Muscular branches - supply FDB, FHB, Abductor hallucis and first lumbrical

3) Proper digital nerve of the medial plantar nerve supplies the medial plantar
aspect of the great toe

4) The 2nd, 3rd, 4th common digital nerves - give rise to two proper digital nerve
supplies of toes 1, 2

5. Lateral Plantar nerve

a. Cutaneous branch supplies lateral plantar sole of foot
b. Muscular branches supply quadratus plantae, abductor digit minim
c. Superficial branch - supplies lateral side 5th toe and communicates with 3rd common digital branch of
medial plantar nerve
d. Supplies 4th dorsal interossei, 3rd plantar interossei, flexor Digiti Quinti Brevis (Superficial branch)
e. Deep branch supplies Adductor Hallucis, all lumbricales except 1st and the rest of the interossei

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I. Dermatomes/Myotomes:

A. A dermatome is an area of skin that is mainly supplied by a single spinal nerve. There are eight cervical nerves (C1 being an
exception with no dermatome), twelve thoracic nerves, five lumbar nerves and five sacral nerves.

B. Spinal nerves have motor fibres and sensory fibres. The motor fibres innervate muscles, while the sensory fibres innervate
certain areas of skin. A skin area innervated by the sensory fibres of a single nerve root is known as a dermatome. A group of
muscles primarily innervated by the motor fibres of a single nerve root is known as a myotome. Although slight variations do
exist, dermatome and myotome patterns of distribution are relatively consistent in humans.

C. Dermatomes of the lower extremities:

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D. Dermatomes of the Foot:

E. Myotomes: Each muscle in the body is supplied by a particular level or segment of the spinal cord and by its corresponding
spinal nerve. The muscle, and its nerve make up a myotome.
F. Lower Extremity Myotomes:
L2 bends the hip.
L3 straightens the knee.
L4 pulls the foot up (Dorsiflexion of the foot)
L5 wiggles the toes (1st toe extension)
S1 pulls the foot down (Plantarflexion of the foot)
S3,4 and 5 supply the bladder. bowel and sex organs and the anal and other pelvic muscles.

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Plantar Foot Musculature
Important Points:

The fixed length of the flexor tendons passively PF the IPJ's when the extensors actively DF the MPJ.
Note: The interossei counter balance the flexors and the lumbricales neutralize the extensors.

The interossei pass above the deep transverse intermetatarsal ligament but below the transverse axis of the
MPJ. They stabilize the proximal phalanx just prior to contraction of the flexor tendons.

The lumbricales go beneath the transverse intermetatarsal.

I. The Four Muscle Layers

Layer I - Abductor hallucis, flexor digitorum brevis & abductor digit minimi
Layer II - Quadratus plantae and lumbricals
Layer III - Flexor hallucis brevis, adductor hallucis, flexor digiti minimi brevis
Layer IV - Four dorsal and three plantar interossei
Note: The muscles in layer one are the muscles removed when performing a Steinler stripping.

LAYER I

A. Abductor Hallucis originates from medial calcaneus, attaches tibial sesamoid and medial base of proximal phalanx of hallux.
B. Flexor Digitorum Brevis originates from calcaneal tuberosity and travels to base of proximal phalanx then divides, then inserts
into undersurface of the middle phalanx.
C. Abductor Digiti Quinti originates lateral calcaneus and inserts into lateral aspect of base of proximal phalanx

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 LAYER II

A. Quadratus Plantae originates from two calcaneal heads and inserts into lateral aspect of FDL tendon before it divides
B. Lumbricales The Lumbricales insert into the expansions of the tendons of the Extensor digitorum longus on the dorsal surfaces
of the proximal phalanges. All four lumbricals insert into extensor hoods of the phalanges, thus creating extension at the
inter-phalangeal (PIP and DIP) joints. However as the tendons also pass inferior to the metatarsal phalangeal (MTP) joints it
creates flexion at this joint.

1. 1st arises from medial aspect of FDL tendon to the 2nd toe and inserts medially into the middle of the proximal
phalange of the 2nd toe
2. 2nd arises from contiguous 1st and second FDL tendons and inserts medially into the middle of the proximal phalange
of the 3rd toe
3. 3rd arises from contiguous sides of 2nd & 3rd FDL tendon and inserts medially into the middle of the proximal
phalange of the 4th toe
4. 4th arises from contiguous sides of 3rd & 4th FDL tendons and inserts medially into the middle of the proximal
phalange of the 5th toe

LAYER III

A. Flexor Hallucis Brevis originates from tendons of Tibialis posterior and 2nd arm originates from cuboid and 3rd cuneiform. Then
inserts into base of proximal phalanx on medial and lateral sides.
B. Adductor Hallucis oblique head arises from 2nd, 3rd, 4th met bases and inserts into fibular sesamoid and lateral base proximal
phalanx. Transverse head arises from plantar plates of 3rd, 4th, 5th MPJ's and inserts into fibular sesamoid and lateral base
proximal phalanx.
C. Flexor digiti minimi brevis originates from plantar cuboid 5th met base and inserts into plantar base of proximal phalanx of 5th
toe

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 LAYER IV
A. Dorsal Interossei (4 of them) The dorsal interossei abducts at the metatarsophalangeal joints of the third and fourth toes.
Because there is a pair of dorsal interossei muscles attached on both sides of the second toe, contraction of these muscles
results in no movement (i.e. the midline of the hand is in the third finger, but the midline of the foot is in the second
toe). Abduction is of little importance in the foot, but, together with the plantar interossei, the dorsal interossei also produce
flexion at the metatarsophalangeal joints. Although small, the dorsal interossei are powerful muscles that, together with their
plantar counterparts, controls the direction of the toes during violent activity, and thus allow the long and short flexors to
perform their actions. Because of the relationship to the metatarsophalangeal joints, the interossei muscles also contributes
to maintaining the anterior metatarsal arch of the foot and also, to a limited extent, to the medial and lateral longitudinal
arches of the foot.
1. 1st originates from adjacent sides of 1st & 2nd met and inserts into base of proximal phalanx of 2nd toe medially.
2. 2nd arises from adjacent sides of 2nd & 3rd met and attaches to the base of the 2nd proximal phalanx laterally.
3. 3rd arises from adjacent sides of 3rd & 4th met and attaches to the base of the 3rd proximal phalanx laterally.
4. 4th arises from adjacent sides of 4th & 5th met. attach to the base of the 4th proximal phalanx laterally.

B. Plantar interossei (3 of them) Originate from medial side of 3rd, 4th, and 5th metatarsal shafts and bases. Insert into base of
proximal phalanges medially of toes 3, 4, and 5. Since the interosseous muscles cross on the metatarsophalangeal joint,
they act on that specific joint and cause adduction of toes III, IV, and V. Adduction itself isn't of extreme importance to the
toes, but the these muscles work together with the dorsal interosseous muscles in flexion of the foot. They also work
together to strengthen the metatarsal arch.

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Reflexes and Nerve Plexuses
I. Segmental Innervation of Reflexes:

A. Patellar Reflex (knee extension)= L3, L4

B. Achillis Reflex (ankle plantar flexion) = L5, S1

II. Lumbosacral Plexus:

The innervation of the lower extremity is entirely through the branches of the Lumbosacral plexus.
The lumbar plexus and the sacral plexus form the lumbosacral plexus.
A. Lumbar Plexus

1. The lumbar plexus is formed by L1, L2, L3, L4, and L5.
2. L2, L3, L4 contribute to the two major branches of the lumbar plexus;
a. The obturator nerve which supplies ventral musculature of the front of the thigh and the adductor group.
b. The femoral nerve, which supplies the dorsal muscles of the front of the thigh.

B. Sacral Plexus

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 1. The sacral plexus is formed by L3, L4, L5, S1, S2, S3, and S4.
2. L4, L5, S1, S2, S3 contribute to the sciatic nerve which subsequently separates into:
a. The common peroneal nerve (L4, L5, S1, S2), which supplies the dorsal musculature and one posterior
muscle of the thigh, the anterolateral muscles of the leg, and the dorsal muscles of foot
(Extensor Hallucis Brevis and Extensor Digitorum Brevis).
b. The tibial nerve (L4, L5, S1, S2, S3) which supplies the ventral muscles of the thigh, all the muscles of
the calf, and all the muscles of the plantar aspect of the foot (all the other muscles). It divides into
the medial plantar nerve and the lateral plantar nerve.

III. Motor innervation of the leg and foot:

Muscle Peripheral Nerve Spinal Level

Tibialis Anterior Deep Peroneal L4, 5

EDL Deep Peroneal L4, 5
EHL Deep Peroneal L4, 5
Peroneus tertius Deep Peroneal L4, 5
Gastrocnemius Tibial S1, 2
Soleus Tibial S1, 2
Plantaris Tibial S1, 2
Popliteus Tibial L4, 5 S1
FHL Tibial S2, 3
FDL Tibial S2, 3
Tibialis Posterior Tibial L4, 5
Peroneus Longus Superficial Peroneal L5 S1, 2
Peroneus Brevis Superficial Peroneal L5 S1, 2
EDB Deep Peroneal S1, 2
Abductor Hallucis Medial Plantar S2, 3
FDB Medial Plantar S2, 3
First Lumbricalis Medial Plantar S2, 3
FHB Medial Plantar S2, 3
Abductor Digiti Quinti Brevis Lateral Plantar S2, 3
Quadratus Plantae Lateral Plantar S2, 3
2nd, 3rd, 4th Lumbricalis Lateral Plantar S2, 3
Adductor Hallucis Lateral Plantar S2, 3
Flexor Digiti Quinti Brevis Lateral Plantar S2, 3
Plantar Interossei Lateral Plantar S2, 3
1st & 2nd Dorsal Interossei Deep Peroneal, Lateral Plantar S1, 2,3
3rd & 4th Dorsal Interossei Lateral Plantar S2, 3

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Tendons, Sheaths and Bursae
I. Tendon Structure, Gliding Mechanism, and Blood Supply

A. Structure:
•Tendons consist of dense regular connective tissue made up of tropocollagen units, created by fibroblasts, and organized
to form collagen fibers.
•The collagen fibers are surrounded and grouped into fasciculi by the endotenon.
•The fascicles are contained within an outer epitenon. The epitenon defines the anatomical tendon and is the visceral layer
responsible for the intrinsic repair response.
•Golgi tendon organs located within the tendon fibers register tension. Tendons are supported as they traverse through the
tissues, in such a way as to allow gliding motion.
•The organized tendon is further surrounded, outside of the epitenon, by a loose, areolar and highly vascularized paratenon,
wherever the tendon courses a straight line. Paratenon is contained deep to, and adherent to, the deep fascia (muscle
fascia); or it is adherent to a neighboring intermuscular septum (fascia) between intact skeletal muscle bellies; or it may be
adherent to deeper periosteum.
•A tendon sheath exists where a tendon's course changes direction, such as about the ankle deep to the extensor, peroneal,
and flexor retinaculum. The sheath is distinct from paratenon, and consists of a fibrous outer septum with a synovial lining,
much akin to a joint capsule. Synovial fluid bathes the tendon within the sheath as the tendon changes direction, such as at
the anterior aspect of the ankle where the long extensors enter the dorsum of the foot. On the tendon's deep (non-friction)
surface, within the sheath, a synovium lined fold of connective tissue, the mesotenon, conveys vascularity and supports the
tendon. The mesotenon attaches to the epitenon at the hilus.
B. Gliding Mechanism
•At the proximal margin of the tendon sheath a double fold of paratenon, termed a plicae duplicata, invaginates a short
distance into the sheath and adheres to epitenon. Similarly, at the distal margin of the sheath, a single fold of paratenon,
termed a plica simplex protrudes into the sheath. As muscle contracts, the plicae unfold and elongate as the tendon glides
within the sheath at the point of direction change, and within the loosely arranged paratenon where the course is straight.
C. Blood Supply
•Proximally, at the myotendinous junction, blood vessels within the perimysium supply the tendon.
•Centrally along the tendons course, blood is supplied from paratenon and, within a sheath, the mesotenon.
•Distally, at the tendon's insertion, blood vessels from periosteum supply the tendon. Synovial fluid within the sheath, and
local lymphatics within the paratenon, also nourish and drain metabolites from the tendon. Occasionally, a condensed,
highly organized fibrous connection, know as a vinculus, may also convey vascularity between closely approximated
tendons. The Master Knot of Henry, between the tendons of FHL and the more superficial (plantar) FDL, at a level
consistent with the distal margin of the sustentaculum, is just such a vinculus. Vinculi also exist between FHB and FDL near
their phalangeal insertions.

II. Subfascial and Subcutaneous Bursae

A variety of bursae occur in the foot and ankle. Bursae protect tendon and muscle from excessive friction or pressure caused by
adjacent muscle, ligament or bone.
•Subfascial bursae include the retrocalcaneal or pre-Achilles bursa, those at the insertions of TA, TP, and the IO; and those
between the bellies of adductor digiti minimi and the 5th metatarsal, and the belly of FHB and the medial cuneiform.
•Subcutaneous bursae are usually adventitious in origin, and may present at the head of the first and fifth metatarsals,
plantar to the tuberosity of the calcaneus (present in about 50% of specimens), at the medial and lateral malleoli, and
occasionally posterior to the insertion of the Achilles tendon.

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P a g e 106 | 368
PART 3:
COMPLICATIONS

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Hallux Varus
I. Definition

A. An adductus and/or varus deviation of the hallux at the 1st MPJ

II. Etiology

A. Congenital
1. Neuromuscular conditions (Thompson Classification)
a. Primary Hallux Varus: 1st ray and the hallux are deviated medially
b. Secondary Hallux Varus: All the metatarsals are deviated medially
-Metatarsus Adductus

-Talipes Equinovarus

2. Joseph's Classification
a. Primary Congenital Hallux Varus: Proximal phalanx is medially deviated at the MPJ and the abductor
hallucis tendon is the deforming force.
b. Secondary Congenital Hallux Varus: First metatarsal is deviated medially at the metatarsal cuneiform joint
and the tibialis anterior is the deforming force (i.e. Clubfoot).
c. Teratogenic Congenital Hallux Varus: Is associated with other forefoot anomalies (many).
Summary: Congenital causes of Hallux Varus Are:
1. Metatarsus Adductus
2. Talipes Equinovarus
3. Accessory Bones or toes
4. As a result of arthrosis following rheumatic fever.
B. Traumatic
1. Sesamoid Fracture
2. MPJ dislocation
3. Mal-aligned Metatarsal Fracture
C. Iatrogenic
1. Staked 1st head (excessive resection)
2. Over tightening of the medial capsule
3. Overcorrection of the IMA
4. Overcorrection of the PASA
5. Overcorrection secondary to bandaging
Note: Any of the above etiologies in conjunction with a fibular sesamoidectomy significantly increases the
chance of developing hallux varus. A combination of any two of the above causes will also greatly increase the
chance.

III. Symptoms

A. Previous bunionectomy
B. Inability to wear conventional shoes
C. Pain along medial aspect of hallux secondary to shoe pressure
D. Pain may be present along the medial aspect of the arch secondary to muscle contracture
E. Pain may be present at the MPJ with or without shoes

IV. Signs

A. Presence of adducted position and/or varus rotation of the hallux

B. Contracture of the interphalangeal joint of the hallux
C. Contracture of the extensor hallucis longus tendon
D. Contracture of the abductor hallucis muscle
E. Pain on palpation to the abductor hallucis muscle
F. Pain an crepitation may be present at 1st MPJ
G. Presence of a limitus or rigidus may be present at the first Metatarsophalangeal joint

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V. Radiographic Signs

A. Hallux will be in an adducted position at first MPJ

B. Intermetatarsal angle will usually be reduced
C. Head of the first metatarsal may be staked
D. Fibular sesamoid may be absent
E. Presence of a previous osteotomy site on the 1st met
F. Negative proximal articular set angle may be present
G. Arthritic changes may be present at the 1st MPJ

VI. Operative Considerations

A. Not every hallux varus requires surgery, but when a sufficient deformity is present, the deformity should be corrected as early
as possible, to prevent resultant degenerative arthritis
B. There is no one surgical procedure, but rather the causative factor or factors must be determined and corrected along with any
secondary deformities that may have developed.
C. A Reverse Austin is an acceptable procedure for addressing a Hallux Varus Deformity

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Infection
Diagnosis And Treatment:

I. Recognizing Infection
A. Symptoms:
1. Pain (elevated intensity out of proportion to
the procedure performed).
2. Redness
3. Heat
4. Swelling
5. Loss of function

B. Fever (4 w's)
1. Wind (pulmonary) 8-10 hours post-op
2. Water (urinary) 2-3 days post-op
3. Wound (infection) greater than 3 days
4. Walk (thrombophlebitis) post-op

CHRONOLOGICAL SEQUENCE OF POSTOPERATIVE TEMPERATURE CHANGES

Note: Pasteurella multocida is the most common organism found in dog and cat bites.

II. Hematologic Tests

A. CBC with a deferential: look for a shift to the left [increased number of immature leukocytes (granulocytes)].
Types of WBC:
1. Polymorphonuclear neutrophils
2. Polymorphonuclear eosinophils
3. Polymorphonuclear basophils
Note: All 3 are considered Granulocytes
4. Monocytes
5. Lymphocytes
6. Plasma Cells
Note: a WBC greater than 10,000 usually indicates an infection.
Note: With a localized infection (i.e. abscess) the shift to the left is less pronounced.

B. ESR (Erythrocyte Sedimentation Rate)

1. Good indicator if a base line was taken.
2. Not specific (can be elevated by systemic steroids and cigarette smoking or any inflammatory process.
3. Warfarin use may cause an elevated ESR in patients post operatively.

C. Glucose
D. SMA-6 (electrolytes)
E. Creatinine (most important) run on everyone getting parental antibiotics. 1:1 ratio (i.e. CCL = 30% then 30% renal
function).

Estimated creatinine clearance rate (eCCr) using Cockcroft-Gault formula

Est. Creatinine Clearance = [[140 - age(yr)]*weight(kg)]/[72*serum Cr(mg/dL)] (multiply by 0.85 for women).

This formula expects weight to be measured in kilograms and creatinine to be measured in mg/dL, as is standard in the
USA. The resulting value is multiplied by a constant of 0.85 if the patient is female.

One interesting feature of the Cockcroft and Gault equation is that it shows how dependent the estimation of CCr is
based on age. The age term is (140 - age). This means that a 20-year-old person (140-20 = 120) will have twice the
creatinine clearance as an 80-year-old (140-80 = 60) for the same level of serum creatinine (120 is twice as great as

P a g e 110 | 368
 60). The C-G equation assumes that a woman will have a 15% lower creatinine clearance than a man at the same level
of serum creatinine.

F. Bun

G. Liver function test: (some antibiotics are metabolized by the liver like Clindamycin and erythromycin).
1. Bilirubin
2. Serum protein
3. SGOT
4. SGP

H. C&S (culture and Sensitivity)

1. If possible get C&S before antibiotics are started. If the patient is currently taking antibiotics, they should be stopped
for at least 48 hours if possible.
2. Tissue if possible.
3. Use proper technique. If skin is being penetrated, use topical antiseptic to prevent contamination. The base of
ulceration's should be curetted before a tissue sample is taken to remove superficial contaminants.

I. Gram Stain:
Gram positive = purple
Gram negative = pink
Reagent Time Gram + Gram-
Smear and Heat Fix
Primary Stain Crystal violet 20 secs. purple purple
Distilled H2O wash
Mordant Gram's iodine 1 min purple purple
Distilled H20 wash
Decolorizing agent 95% alcohol 10-20 secs purple colorless
Distilled H20 wash
Counterstain Safranin 20 secs purple pink
Distilled H20 wash & Blot Dry Examine with microscope (x100) immediately

IDENTIFICATION OF BACTERIA:
Organism Appearance

Gram positive ( Blue )

Cocci
Staphylococcus Cocci in "grape like"
Clusters
Streptococcus Cocci in chains

Bacillus (Rods)
Clostridium Rods with a "Racquet shaped"
caused by spore
Corynebacterium Rods in "Chinese characters"

Gram Negative ( Red )

Cocci
Gonococcus Diplococcus within the
WBC

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 Rods
Pseudomonas Slightly curved rod
Klebsiella Diplococcoid bacillus may show a
heavy capsule

Gram Neg Rods (Enteric) Red Rods

Bacteroides
Citrobacter
Enterobacter
E. Coli
Klebsiella
Morganella Morganii
Proteus
Providencia
Serratia

•The cytoplasm of the WBC is light pink and the nucleus is dark pink-mauve.
•Cocci are dark blue-purple, unless gonococci are suspected.
•Streptococci occur in chains and/or pairs. Differentiated by hemolytic properties: Alpha hemolytic strep, Beta hemolytic
strep, and non-hemolytic strep.
•It is difficult to identify most other gram-negative rods on the basis of gram stain only.
•if the gram stain reveals many organisms of different morphology and the culture reveals only a few, anaerobes should
be suspected.

J. Blood cultures
•Use if patient looks septic, temp greater than 103 , or has "Fever of unknown origin".
•At least 3 sets of 2 cultures over 24 hrs.
•Cultures are drawn from rotating sites (separate sites) at least 30 mins apart.
•Twenty millimeters of blood should be drawn each time.
•If after 5 -6 cultures over two days, no organisms have been recovered, no further cultures are indicated.
•Blood cultures cannot be considered negative until after at least 2 weeks.

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III. Hospitalization: (When to Hospitalize Patient)
A. Systemic Manifestations and Constitutional Signs:
1. Fever (greater than 101F - oral)
2. Lymphangitis, ascending cellulitis, or lymphadenopathy.
3. Malaise, chills, or shakes.
4. High WBC (above 13,000)

B. Debilitated Patient:
1. Diabetes Mellitus.
2. PVD.
3. Alcoholic.
4. Nutritionally deficient.
5. Immuno-deficient.

C. Infections Requiring Parental Antibiotic:

1. Resistant organisms.
2. Gram negative or anaerobic infections.
3. Deep space infections
4. Suspected bone involvement (osteomyelitis):
a. Acute.
b. Chronic.
5. Failure of outpatient therapy.
6. Surgical debridement bone/soft tissue.

IV. Anaerobic Infection

A. Signs
1. Foul smelling discharge
2. Necrotic tissue or organism
3. Infection involves muscle
4. Gas in tissue, crepitus (on x-ray evaluation) doesn't have to be Clostridia
5. Bacteremia picture with jaundice

B. Anaerobic Organisms
1. In this type of infection, aerobic organisms use up O2 and provide a better environment for anaerobic bacteria.
Organisms responsible for this synergistic relationship include: S. aureus, S. Epidermitis, Peptococcus,
Peptostreptococcus, Corynebacterium, Bacteroides, Clostridia

V. Aerobic Organisms
A. Coagulase producing staph aureus is most common infecting organism
B. Coagulase negative staph epidermitis is also infecting organism
C. Beta hemolytic group A strep
1. Usually no pus, but intense cellulitis and can cause lymphangitis and lymphadenopathy
D. Gram (-) aerobes, E. coli, Klebsiella, pseudomonas, Enterobacter, Serratia
E. Clostridium Myonecrosis (gas gangrene)
1. Most severe anaerobic infection
2. Involves muscle tissue
3. See brown, watery, foul smelling exudate
4. See gas in soft tissue
5. Get infectious disease consult, & general surgical consult
F. Necrotizing Fasciitis

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 1. Dissecting up fascial planes
2. No muscle involvement
3. Primarily involves Pepto streptococcus, but also S. aureus, Strep pyogenes, Clostridia, Bacteroides

VI. Specific Infections

Lyme Disease: See Lyme Disease

Bite Wounds:
Dog:
Pasteurella multocida
S. Aureus
S. Epidermidis
 - Hemolytic streptococci
Cat:
Pasteurella multocida
S. Aureus
 - Hemolytic streptococci
Human:
Eikenella corrodens (gram negative anaerobic organism)
S. Aureus
Streptococcus
Bacteroides fragilis
Puncture Wounds:
Staphylococcus aureus (>50%)
 - Hemolytic streptococci
S. Epidermidis
Escherichia coli/Proteus
Osteomyelitis: Pseudomonas aeruginosa (90%)
Open Fractures:
S. Aureus
S. Epidermidis
Pseudomonas aeruginosa
Streptococcus
Enterobacteriaceae
B. Fragilis
Burns:
Early (1-2 days):
 - Hemolytic streptococci
S. Aureus
S. Epidermidis
Late (>3 days)
S. Aureus
S. Epidermidis
Pseudomonas aeruginosa
Streptococcus
Enterobacteriaceae
B. Fragilis
Post-Operative Infection:
Staphylococcus aureus

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VII. Treatment of Infection (4 D's)
A. Decompression
1. Remove some sutures, release pus
B. Drainage
1. Open tissue, pack wide pickets with iodoform gauze
2. Leave Penrose drains in for 24 - 48 hours
C. Debridement
1. A wet to dry dressing with povidone iodine-normal saline mixture absorbs fluid exudates, debrides tissue on its
removal and provides physiologic cover.
D. Drugs
1. Antibiotics
a. Always consider: Frequency of Administration, Toxicity, Duration of treatment
b. Monitoring antibiotic therapy: fever, pain CBC & Diff, ESR CRP, Insulin requirement in diabetic
E. Cellulitis
1. Koch-Mason dressing-wrap an area of cellulitis with saline soaked gauze. This is covered with plastic wrap, which
forms an occlusive dressing. A water based heating apparatus is placed around the dressing. Leave this on 5 hours and
off one hour to prevent maceration.

VIII. General Principles

A. No tourniquets with infections
1. Allows accurate debridement of devitalized tissue.
B. Sterile prep should be done
C. Release sutures
D. Explore extent of infection
1. Determine which structures are affected.
E. Remove implants
1. Internal fixation should be left intact if it is providing stability.
F. Leave all viable tissue intact
G. C&S of deep tissue
1. C&S of implant if removed
H. Following thorough debridement
1. Copiously irrigate the surgical site
2. Pack the wound open with sterile Iodoform Nugauze
3. Change post operatively once-twice a day.
I. After 3 negative cultures, delayed primary closure can be considered.
BONE IMAGING TECHNIQUES WITH INFECTIONS

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DRUGS FOR BUGS:
I. Staphylococcus Aureus and EPI

A. Penicillin sensitive -- Pen G, first generation cephalosporin, Vancomycin (IV, IM).

B. Methicillin Sensitive -- Penicillinase--resistant penicillin (nafcillin or oxacillin), clindamycin, erythromycin, Vancomycin (IV,
IM).
C. Methicillin resistant (MRSA) See MRSA (Below)
II. Streptococci
A. Group A& B -- Penicillin, first generation or cephalosporins, Clindamycin, Erythromycin, Vancomycin (IM, IV).
B. Group D (S. faecalis and S. faecium) (Enterococci) --Penicillin, ampicillin or mezlocillin with gentamicin, vancomycin &
gentamicin. Use oral Amoxicillin in mild cases.

III. Clostridium Tetanus

-- Penicillin, Tetracycline.

IV. Clostridium perfringens

-- Penicillin, Imipenem, Tetracycline, Clindamycin.

V. Neisseria Gonorrhoeae

-- Ceftriaxone, ciprofloxacin, Penicillin (if not resistant).

VI. Gram Neg. Rods

(Bacteroides, Citrobacter, Enterobacter, E. Coli, Klebsiella, proteus, Providencia, Serratia -- Imipenem, Ciprofloxacin.

VII. Pseudomonas Aeruginosa

--Ciprofloxacin (oral)
--Imipenem
-- Antipseudomonal Penicillins:
1. Piperacillin
2. Mezlocillin.
3. Ticarcillin.
--Aminoglycosides:
1. Gentamicin
2. Tobramycin.
3. Amikacin.

VIII. Pseudomonas Cepacia and Xanthomonas maltophilia

-- TMP/SMX.

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SPECIFIC DRUGS
I. Pen. G
A. Up to 20-24 million units/day (5-6 million units q 4h IM) I.V.
B. 1.2 million units IV a day.
C. Concomitant administration of probenecid 1-2 gms/day will markedly increase the duration of serum levels.
Note: Probenecid will also increase the serum levels of other penicillins and almost all cephalosporins.

D. If creatine Clearance is lower than 30 ml/min reduce dosage.

II. Erythromycin

A. 250-500 mg Q.I.D. P.O.

B. Metabolize by liver--not kidney.

III. Tetracycline

A. 250-500 mg Q.I.D. P.O.

B. Minocycline (100 mg q 12 h - 24 h P.O.)
C. Good for Lyme disease, Madura foot, Mycobacterium Marinum.
D. Good for Staph or Strep infection in patient who's allergic to penicillin.

IV. Vancomycin

A. Oral form strictly for use in colitis (pseudomembranous colitis).

B. No gram neg. aerobic/anaerobic spectrum.
C. Bactericidal against all gram-positive organisms.
D. Nephrotoxic -- evaluate renal function ototoxic--rare & reversible. Redman/Redneck Syndrome--flush of face and hot
feeling and pruritus. This is self-limiting but you can use antihistamines. Infuse slowly to avoid.
E. DOSAGE:
1. Maximum = 2q/day.
2. 500 mg q8h for less severe infections.
3. Oral dose for colitis is 125 mg Q.I.D..
4. Infuse slowly (over 45 to 60 minutes).
5. Do Peak and Trough levels:
Normal levels Peak = 15-30 mg/ml.
Trough = less than 10 mg/ml..

V. Gentamycin

A. No effect on anaerobes (the drug needs 02 to cross the cell membrane)

B. Adverse effects:
1. Nephrotoxic (usually reversible). Concurrent use of vancomycin may potentiate this nephrotoxicity.
2. Ototoxic (irreversible). Concurrent use of loop diuretics may predispose a patient to these toxicities.
3. Neuromuscular blockade (infuse slowly to avoid).
C. DOSAGE:
1. Loading dose = 2mg/kg (regardless of patient's renal function.)
2. 3-5mg/kg/day q8h to 12h.
3. First calculate creatinine clearance
CCL = (140 - age) x weight (in kg)/Serum creatine x 72
For Females: CCL x .85
1:1 relationship -- I.E. if CCL = 50 then patient has 50% renal function. Then half the dose.
4. Peak and Trough levels:
a. Draw trough sample immediately (no more than 30 minutes) prior to infusion. Draw peak sample at least 30 minutes (no
more than 90 minutes) after 90 minute infusion. Clearly label specimens with times.
b. Order after 3rd dose. If within normal range the level need not be ordered again unless there is an increase in the serum
creatinine level.
c. Run a serum creatinine 3 times a week.
d. Normal Peak = 6-10 mg/ml. and normal Trough = less than 2 mg/ml.
e. If peak is high and trough is normal decrease the amount.
f. If peak is low and trough is normal increase the amount.
g. If peak is O.K. and trough is high, increase the interval time.

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 H. If both are high, decrease the dose and increase the interval time.

VI. Clindamycin

A. DOSAGE:
1. 300 mg Bid to T.I.D. P.O. for outpatient therapy.
2. 600 - 900 mg q8h I.V. or I.M.
3. Metabolized by liver, therefore, O.K. for renal impaired patients.

NOTE: Possible drug of choice for staphylococcal osteomyelitis due to its excellent penetration
into bone and its ability to dissolve slime layer.

NOTE: Can be used for gram + organisms in patients who are allergic to Penicillin.
VII. Ciprofloxacin

A. Drug interactions:
1. Theophylline can be potentiated. Should check serum levels.
2. Patients should avoid coffee, tea, and soft drinks with caffeine. (Potentiates effects of caffeine).
3. Antacids and Irons supplements decrease absorption.
4. Do not use in children with open growth plates. May cause degeneration of cartilage.
A. DOSAGE:
500 mg bid P.O. -- mild infections
750 mg bid P.O. -- severe infections and osteomyelitis
NOTE: Decrease to once daily in patients with severe renal insufficiency.

VIII. TMP/SMX (Bactrim, Septra)

A. This is a Sulfonamide.
B. DOC for pseudomonas cepacia and Xanthomonas maltophilia.
C. DOSAGE:
One double strength tablet B.I.D. P.O.

IX. Imipenem

A. Broadest spectrum of any available drug (referred to jokingly as (gorillamycin:)

B. Adverse reactions:
1. Nausea/vomiting if infused to fast.
2. Cross reactivity in patients with penicillin allergy.
3. Seizures in patients with history of seizure disorders or renal dysfunction.
C. DOSAGE:
500 mg q6 to 8h
250 mg q6h unless severe infections
DOC in severe life or limb threatening infections in diabetics (gas gangrene or necrotizing fascitis.

X. Rifampin

A. Spectrum:
1. All mycobacteria.
2. Very active against Staph and Strep.
B. Always use in combination, never alone.
C. Dosage:
300 mg B.I.D. P.O.
D. Side effects:
1. Red discoloration of all body fluids (will permanently discolor soft contact lens).
2. Flu-like symptoms with prolonged use.

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Prophylactic Antibiotics

A. Golden Rules of prophylactic antibiotics

1. Rule 1: The antibiotic must have achieved its maximum levels at the time of initial incision or insult.
a. Timing is everything!
b. This rule helps to answer the important questions about the timing of administration and length of usage.
2. Rule 2: The antibiotic should be directed against the most common organism found if an infection were to occur in
that particular situation
a. Following this rule requires a thorough understanding of the pathophysiology, microbial etiology, and
antibacterial susceptibility of a variety of infections.
B. Indication
1. Following wounds (commonly present in the lower extremity):
a. Puncture wounds: If the "first rule" is implied in these situations, antibiotics are not indicated. By the
time the patient presents to your office gets the prescription filled and the drug is absorbed, too much
time has passed since the insult. Most studies show that prophylactic antibiotics do not alter the
incidence of infection following puncture wounds and lacerations. Only if less than a few hours have
past would there be any benefit at all.
b. Lacerations (same as puncture wounds)
c. Bite wounds are highly contaminated with numerous types of organisms. Because of this, antibiotic
therapy should be initiated along with aggressive debridement and irrigation.

2. For surgery: There is no hard and fast data to support the use of antibiotic prophylaxis in foot and ankle surgery.
However, it is generally considered to be indicated in the following surgical situations:
a. Prolonged surgery lasting longer than two hours
b. Surgery on immunocompromised patient

i. Uncontrolled diabetic patient

ii. Patients on immunosuppressive agents (chemotherapy)

iii. Patient on systemic corticosteroids (rheumatoid arthritis patient)

iv. Genetic or acquired defects

Note: HIV infection does not alter the postoperative infection rate for lower
extremity surgery. It tends to mediate infection by parasites, fungi and viruses, not
bacteria.

c. Trauma surgery
d. Implant surgery

3. Prophylaxis against bacterial endocarditis in the surgical patient with a compromise heart valve:
a. Guidelines (based on whether or not the procedure has a high potential for a bacteremia)

i. Any clean elective surgery performed through surgically prepared skin is

considered low risk and prophylaxis is not indicated.

ii. I&D of an abscess or cutting through infected tissue may cause bacteremia
and therefore is considered a high risk. Prophylaxis should be used. The antibiotic
used should be directed against any pathogens found to be causing the infection.

4. Prosthetic Joint Patient's

a. if a patient has a prosthetic joint elsewhere in the body (hip, knee), is it necessary to use prophylaxis
when performing foot or ankle surgery?
b. Formal guidelines state that prophylaxis is not required for pins, plates or screws. Only when a total joint
replacement is in place, prophylactic antibiotics are recommended in limited cases.

i. All patient's during the first 2 years following joint replacement.

ii. Immunocompromised and immunosuppressed patient's

iii. Patient's with co-morbidities

Previous prosthetic joint infection

malnourishment
HIV infection
malignancy
insulin-dependent diabetes
hemophilia

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C. Selection and administration of agents
1. Follow the second rule. In most lower extremity operations, S. aureus is the most common postoperative pathogen.
a. Variables with Staphylococcus include its susceptibility to MRSA and the tolerance to vancomycin.
b. When do you prophylax for MRSA?
i. Patients with a prior history of MRSA infection

ii. In hospitals with an unacceptably high rate of MRSA

iii. In patient's whom the risk of a MRSA post-op infection is great enough to warrant
MRSA prophylaxis

2. Implant infection are most frequently caused by S. epidermidis, often methicillin-resistant.

3. Agents should have a sufficient half-life to provide adequate levels throughout the procedure and into the early
postoperative period.

4. Recommended guidelines ("idealized" suggestions)

a. IV infusion should be administered by the anesthesiologist in the operating room a few minutes before
the elevation of a tourniquet or initial incision.
b. IM antibiotics should be given approximately 45 minutes to one hour prior to the start of surgery.
c. Oral antibiotics should be given at least one hour prior to surgery.

5. The duration of the antibiotic is very debatable. It has changed over the years back and forth. The bottom-line is that
no one is certain. Generally, most lower extremity surgery follow these guidelines;
a. For most relative short surgeries, the initial preoperative dose is sufficient.
b. For surgery lasting longer than 2 hours, a postoperative, or intraoperative (for very long
procedures) should be given.
c. For patients that are significantly compromise or extensive surgeries (e. g., internal fixation of a severely
fractured ankle) a full 24 hour dose should be used.

D. Specific Agents
1. Cefazolin (the most frequently used antibiotic for lower extremity surgical prophylaxis).
a. Dosage: 1 to 2 grams IV or IM prior to surgery. 1 gram should be given following long procedures.

2. Vancomycin
a. Primarily used in patients with documented severe penicillin or cephalosporin allergy.
b. Some hospitals are now limiting the use of this drug for routine prophylaxis because of the development
of vancomycin resistance gram-positive organisms.
c. If a high level of MRSA is suspected
d. Dosage: 1 gram, one hour prior to surgery and infused slowly over that hour. Vancomycin should not be
administered in a bolus. If postoperative administration is desired, 1 gram can be given 12 hours
following the first dose.

3. Clindamycin
a. Not frequently used for surgical prophylaxis
b. It is however effective at penetrating the bacterial glycocalyx, and therefore theoretically may prove
useful in prophylaxis for implant surgery.
c. Maybe a useful substitute for the now more carefully regulated vancomycin in beta-lactam allergic
patients.
d. Dosage: 600 to 900 mg. IV

4. Ciprofloxacin should not be used for surgical prophylaxis for lower extremity surgery. It has very poor anti-
staphylococcal activity.

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MRSA
I. Classification: All MRSA contain what is known as the “mecA gene”. This gene sets on what is known as the staphylococcal
chromosomal cassette (SCCmec). Currently there are about seven different varieties of this SCCmec I through VII. These can be divided
into two broad classifications. It is important to differentiate between these two types of MRSA because they each have unique antibiotic
sensitivity patterns along with varying levels of virulence. The CA-MRSA being the most dangerous organism.

A. Healthcare Associated MRSA (HA-MRSA)

1. Previously known as "hospital acquired" or “healthcare acquired”
2. Usually contains SCCmec I,II,III gene.
3. Traditional risk factors:
a. Previous antibiotic therapy within the past year
b. Recent hospitalization
c. Recent Nursing home stay
d. Chronic illness
e. IV drug use
B. Community Associated MRSA (CA-MRSA)
1. Previously known as "Community Acquired"
2. Contains the SCCmec IV (most common) or V Gene
3. Most common synonym is the "USA 300" strain
4. Traditional risk factors do not seem to apply to the CA-MRSA and some authors are now talking about the (Five C’s)
of CA-MRSA risk:

a. Close Contact
b. Crowding
c. lack of Cleanliness
d. Exposure to Contaminated items
e. Compromised Skin Integrity

II. Differentiating HA-MRSA and CA-MRSA:

A. The easiest and most clinically relevant way to determine one from the other is to examine the antibiotic sensitivities on the
C&S report.
B. CA-MRSA tends to be relatively susceptible to a wide range of antibiotics other than beta-lactam drugs. The SSCmec IV gene is
known as a (short segment) cassette so there is little room on it for resistant genes. This results in drugs such as
trimethoprim/sulfamethoxazole (TMP/SMX) or doxycycline being effective against this organism.
C. HA-MRSA tends to be relatively resistant to most all antibiotics other than those designated specifically to work against
resistant gram-positive organisms (Linezolid, vancomycin and Daptomycin).
D. New diagnostic test such as PCR and PGFE (pulse gel field electrophoresis) do exist to look for specific gene unique to each
Type of MRSA, unfortunately, most hospitals are not currently using these techniques.

III. Virulence:

A. Hierarchy of virulence
1. MRSA may be more virulent than MSSA
2. CA-MRSA is more virulent than HA-MRSA
3. CA-MRSA produces various toxins that cause tissue destruction, death of white blood cells and allow rapid spread of
the organism.
a. (PVL) Panton Valentine Leukocidin is the best known and most study of the virulence factors. It is almost
exclusively associated with CA-MRSA.
b. Cytolytic Peptides have the ability to recruit, activate and subsequently lyse human neutrophils which
eliminates the main cellular defense against staph aureus.

IV. Clinical Presentation:

A. A pathognomonic phrase patient's use to describe a potential MRSA lesion is “Doc, I have a spider bite”. Always assume a
spider bite or any insect bite reported to you by patient is a CA-MRSA abscess until proven otherwise. Any
infection has the potential to be a MRSA infection including surgical site infections, diabetic foot infections, osteomyelitis,
cellulitis, impetigo, etc.

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V. Treatment:

A. Empirical Therapy should be considered if;

1. A patient has had a past MRSA infection.
2. Recent hospitalization within the past year
3. A course of either oral or parental antibiotics in the past year.
4. The patient is residing in a long-term care facility
5. Chronic disease
6. A severe infection: A patient with an infection severe enough to warrant hospitalization, will usually be started on
empirical anti-MRSA therapy until cultures prove them unnecessary.
B. Antibiotic Therapy:
1. Older generic orals
a. Trimethoprim/sulfamethoxazole (TMP/SMX): BACTRIM

i. This medication has many side effects and drug interactions. It is one of the
greatest causes of Stephen Johnson syndrome. The drug can cause a number of
adverse events including renal complications and neurologic disturbances.
ii. Dosing: usually one double strength (DS) tablet BID. In severe cases and a
probably more correct dosing would be two DS tablets BID. However, doubling the
dose also increases the risk of adverse events.

b. Doxycycline, Minocycline (later generation tetracycline’s):

i. There's More published evidence supporting the use of these drugs for CA-
MRSA then TMP/SMX.

ii. Some patients have G.I. side effects and the standard precautions such as
avoidance of sun because of photosensitivity, not taking the pill with dairy
products, and not using during pregnancy should still be observed.

iii. Dosing: The Usual Dose Is 100 Mg Q12h. Some recommend a first dose load of 200
mg.

c. Clindamycin:

i. The Drug is a protein synthesis inhibitor and as such it can be very effective in
reducing the production of some of the toxins released by MRSA.

ii. A physician must be very cautious, however, when interpreting C&S results with
MRSA and clindamycin. MRSA may contain a gene that encodes for inducible
Macrolide, Lincosamide, streptogramin resistance (iMLS), and if clindamycin is
begun the organism will rapidly develop resistance to that antibiotic. The physician
must examine the sensitivity to the macrolide line, usually represented by
erythromycin. If the erythromycin line reads (R) or resistant, you cannot use
clindamycin regardless of the sensitivity results on clindamycin. Some reports
suggest 80% erythromycin resistance and therefore clindamycin has become a
rarely usable antibiotic.

iii. Many laboratories will either automatically or on specific request run a D-Test (a
specific test for inducible clindamycin resistance). Two Kirby-Bauer discs (one for
clindamycin and one for erythromycin), are placed side-by-side in a plate of MRSA.
If the organism is sensitive to both, a sideways "figure 8" zone of inhibition will be
seen. If it is resistant to both, no zone will be found. However, if it is sensitive to
clindamycin and resistant to erythromycin, where the two drugs elute together a
straight line will form. That line makes the backbone of the D with the curve zone
around the susceptible clindamycin forming the rounded side of the letter. This is
read as a "positive D-Test” and means that clindamycin should not be used.

iv. Dosage: 300 mg po q8-12h

d. Quinolones: Because of increasing resistance, even with a “S” on the C&S report, they are not an
appropriate selection in most cases.
e. Rifampin:

i. It is not the dependable for single agent use because of rapid resistance
development. For this reason it is frequently used in combination with any of the
above listed older generic agents in the treatment of MRSA.

C. Antibiotics for more severe MRSA infections

1. Vancomycin:
a. The “Gold Standard” for the treatment of resistant gram-positive infections. However, with the
epidemic of MRSA and its widening use, organisms started to become resistant. Some studies show
50% or more of clinical failures. Although frank vancomycin resistance is still extremely rare.
b. MIC Creep: in the past, the majority of MRSA strains could be inhibited by 0.5 ug of vancomycin or less.
Over the past 10 years, that number has begun to "creep" from 0.5ug to 1.0ug, all the way up to 2.0ug
or more. Even at 2.0ug, the C&S reported it as sensitive; however, studies have shown failure rates
increase dramatically at that level. For that reason, if the MIC is 2.0ug or greater than alternative
therapy may be indicated.

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 c. Despite the presence of MIC Creep, and high level evidence showing increasing failure rates,
vancomycin continues to be first-line therapy for MRSA at most hospitals. However, monitor it
carefully especially with increasing MICs and don't be afraid to switch to another drug.
d. Dosage: the usual dosage, given normal renal function, is 1gm q12h IV.
2. Zyvox (Linezolid)

a. It Is the Only antibiotic that is approved in its oral form for complicated skin, and skin structure
infections caused by MRSA.
b. Unlike vancomycin, dosing does not have to be altered in patients with renal insufficiency.
c. It is one of three antibiotics with a specific indication for the treatment of diabetic foot infections.
d. Dosage: 600 mg q12h IV or po
3. (Cubicin) Daptomycin
a. used as an alternative agent to vancomycin for IV treatment of complicated skin and skin structure
infections (cSSSI)
b. Dosage: This drug is only available in an IV formulation but does have the advantage of once daily
dosing. The usual dose is 4 mg/kg. A higher dose of 6 mg/kg is generally reserved for bloodstream
infections and right-sided endocarditis, but it has also been used for more severe cSSSI infections.
4. (Tygacil) Tigecycline:
a. This drug is a derivative of minocycline and is unique due to its broad spectrum. It is active against a
broad range of gram-positive, gram-negative and anaerobic bacteria. It is also effective against ESBL
producing gram-negative rods with the exception of Pseudomonas.
b. Effective for mixed cSSSI containing MRSA.
c. Dosage: an initial 100 mg followed by 50 mg q12h IV. Patients are sometimes either pre-medicated or
simultaneously dosed within anti-emetic agent due to the high rate of nausea and vomiting on this
antibiotic

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Non-Union / Delayed Union
I. General Information:

A. Following fracture, excessive motion and/or inadequate vascularity can lead to the formation of hypertrophic irritation
callus, malunion, delayed union, non-union or pseudo arthrosis.
B. Conditions such as Paget's disease, osteitis fibrosa cystica, rickets, hyperparathyroidism, osteomalacia and osteoporosis, and
debilitated or compromised host (immunocompromised, antimetabolite or steroid therapy, anemia, anticoagulation therapy,
elderly patient) can also impede bone healing.
C. The presence of irritation callus rules out primary bone healing, and indicates instability between fragments.
D. Delayed and non-unions are determined primarily via serial radiographic inspection, combined with clinical evidence of
persistent edema and pain.
E. A bone scan is useful in confirming vascularity at the delayed or non-union site. If the fracture cleft is large enough,
or in the presence of a large-enough synovial pseudo arthrosis, a bone scan may reveal a cold cleft. Otherwise, bone scans
are not of much use in distinguishing between delayed and non-unions. CT scans, linear tomography, MRI imaging, stress
fluoroscopy, and intramedullary venography, can also be used to evaluate a delayed or non-union of bone. A CT scan is
particularly valuable when trying to identify intervening fracture fragments.
F. Pathophysiological Risk Factors
1. Systemic status of the patient
a. Age of patient
b. Genetics
c. Malnutrition

i. Vitamin D., calcium and phosphorus

ii. Protein deficiency (Screening tests include serum albumin and total
lymphocyte count). A serum albumin level of less than 3.5 and lymphocytes are
less than 1500 cells/ml is quite significant.

iii. Anemia (low oxygen tension environment is very poor for healing)

d. Diabetes
e. Hormone deficiency (post-menopausal females not on hormone therapy are at risk)
f. Smoking (Decreases peripheral oxygen tension and decreases peripheral blood flow.)
2. Local limb status
3. Nature of injury
a. Type of injury (high impact, fragmentation type injuries with extensive soft tissue disruption are more
prone to nonunion) Not all high energy type injuries result in open fractures. The
Tscherne soft
tissue classification emphasizes the importance of a viable soft tissue envelope at the zone of
injury.

b. Location of fracture

i. Position relative to nutrient vessel

ii. Metaphyseal (better chance of healing) versus diaphyseal

c. Infection (alters micro and macro environment) Of all the things that cause a bad outcome with a
nonunion infection is the worst.
d. Nerve damage
4. Local Host Post-injury Responds
a. Growth Factors

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 b. Collagen
c. Prostaglandins
d. Bone Morphogenic Proteins
e. Mineralization
5. Orthopedic fracture care
a. iatrogenic (poor surgical choices)
b. Fracture Gap (no gaps greater than 2 mm is a general rule)
c. Motion (You want primary bone healing versus secondary or indirect bone healing which occurs with
excessive motion.)
6. Pharmacologic variables

II. Delayed Union:

A. Delayed union simply means the fracture has not healed within a reasonable period of time, and can be identified
radiographically by the presence of unchanged irritation callus and persistence of a fracture cleft.
B. Causes of delayed union, and ultimately non-union; include inadequate fracture reduction and/or immobilization, over
aggressive soft tissue (periosteal) stripping or injury, osteomyelitis, and local vascular compromise secondary to severe
injury.
C. Depending upon the clinical needs and indicators, delayed unions are treated with continued immobilization and non-weight
bearing, revisional surgery for callus channelization or bone grafting or re-fixation (internal and external), or employment of
electrical bone growth stimulation.

III. Non Union:

A. A non-union is classically defined as a fracture that is a minimum of 9 months post occurrence and is not healed and has not
shown radiographic progression for 3 months. It is not necessary to wait 9 months before intervening surgically, either
revisional or as an initial operation, when treating a delayed union, however appropriate non-surgical intervention should be
applied before deciding to go to the operating room.

B. (Weber and Cech Classification of Non-unions 1976) Non-unions are classified on their ostoegenic
potential as either hypertrophic or atrophic.
1. Hypertrophic:

a. The hypertrophic non-union displays radiographic evidence of the bone ends flaring or mushrooming.
They are classified as:

i. Elephant's foot type (maximum callous / hypertrophy and best chance for
healing).

ii. Horses’ hoof/shoe type (where there is moderate callus flaring)

b. Typically, only needs stability to consolidate

c. Vascularized
d. Callus formation present on x-ray

2. Oligotrophic type (minimal callous/ hypertrophy and least reactive).

a. A Technetium 99 (Tc MDP) bone scan shows an increase in bony activity or a "hot spot" with hypertrophic
nonunion.
b. The treatment of a hypertrophic non-union involves immobilization and non-weight bearing, electrical
bone growth stimulation, and continued monitoring. The decision may also be made to operate.

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3. Atrophic:

a. The atrophic non-union, also termed non-reactive, displays radiographic evidence of the bone ends
rounding off and the absence of bone callus. Atrophic non-unions are classified as:
i. Torsion wedge type, where a necrotic butterfly fragment impedes healing
(unilateral healing)

ii. Comminuted, with multiple fragments and gapping

iii. Defect type (no osseous integrity)

iv. Simply atrophic, where the ends are wasted or markedly rounded

4. Pseudo arthrosis:
a. When a non-union involves a fibrocartilaginous interface between the fracture fragments, it is
termed a pseudoarthrosis.
b. An articular fracture non-union may develop into a synovial pseudoarthrosis.
c. A pseudoarthrosis can also be classified

i. Actively

ii. Previously infected

iii. Non-infected

iv. metaphyseal

v. diaphyseal.

d. An atrophic non-union, an infected pseudoarthrosis or synovial pseudoarthrosis, requires operative

intervention for resection of necrotic or problematic tissue, bone grafting or reapproximation of bone,
followed by application of electrical bone growth stimulation and immobilization and non-weight bearing
5. Treatment:
a. Treatment is determined by multiple factors as discussed above.

i. Comorbidities such as vascular disease, diabetes mellitus and cognitive function of

the patient.

ii. Location and type of a nonunion, soft tissue envelope and the presence of infection.

b. Nonoperative

i. Most patient's will have already progressed through many of these nonoperative
treatments by the time they present to you.
ii. Continued immobilization

iii. Ultrasound

iv. Electric Stimulator (three modalities)

a. Direct Current -- percutaneous or implanted electrodes

b. Electromagnetic Stimulation -- uses time varying magnetic fields (noninvasive)
c. Capacitive Coupling -- uses electrodes placed on skin (noninvasive)
d. Contraindication to electric stimulation would be in a patient with an
absent biological response such as a synovial pseudo-arthrosis.

v. Bio adjuvant Modalities

c. Operative

i. Bone Graft

ii. Plate osteosynthesis

iii. Intra-medullary nailing

iv. External fixation

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 Note: Bone scans can differentiate between a hypertrophic/elephant type (positive bone scan) and an
atrophic/non-reactive type (neg bone scan) since it is relatively avascular. Generally speaking, they cannot
differentiate delayed vs. non-unions.
Note: Generally speaking, electrical bone growth stimulation is ineffective in the treatment of pseudoarthrosis,
or if the gap between fracture fragments is greater than one half the diameter of the bone.

Osteomyelitis
I. Definitions

A. Osteomyelitis - infection of bone and marrow

B. Infectious osteitis - suppuration of cortex without marrow
C. Infectious periostitis - contamination of periosteum

II. Classifications of Osteomyelitis

A. Hematogenous - result of bloodstream dissemination of bacteria emanating from an identifiable focus of infection or
developing during a transient bacteremia unrelated to infection
1. Age of onset - peaks from 1-20 then over 50
2. Blunt trauma to long bones precedes 33% of time (femur, tibia, humerus in that order)
3. Infected skin in child from measles, chicken pox can cause
a. Streptococcal Acute Hematogenous Osteomyelitis (AHO)
4. Middle ear infection in child can cause
a. Hemophilus
b. Pneumococcus
c. Staph
5. Acute hematogenous osteo. Localizes in the metaphyseal region because of paucity phagocytic cells in this area as well
as turbulent flow in sinusoidal loops
6. AHO in infant - (0-1 year)
a. In newborn, capillaries traverse epiphysis, therefore joint infection with possible permanent
damage to epiphysis
b. Get joint effusion 60-70% of time
c. Group B strep, staph aureus and E. coli are most frequent organism
7. AHO in child
a. In child, the joint is protected in most cases from infection
b. Hip, shoulder, ankle joint (distal lateral tibial metaphysis are intra- articular however, and can have joint
infections
c. See extensive cortical damage with involucrum formation
d. Rarely see damage to growth plate and joint
e. Staph aureus and epidermitis in 60-90% of cases
1) Salmonella in SS or Sc hemoglobinopathy

2) Hemophilus influenza in children less than two years old

8. AHO in adult
a. Seen in over 50-year-old age group
b. See increased incidence of pseudomonas osteo. in IV drug users
c. High incidence of spread in normal population from
1) IV devices

2) Urinary tract infection

3) Pulmonary infections

d. Infections of bone occurring over 24 months after surgery are probably AHO
e. May see accompanying joint infection
B. Contiguous - most common form of osteo in podiatry practice, seen in patients over 40, may occur following puncture,
laceration ulceration or postop.
1. Postop infections are broken down as follows:
a. Acute postop osteo - within one month of surg.
b. Delayed postop osteo - from one month to two years following surgery
c. Late postop osteo - 2 years on

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 2. Majority are delayed or late
3. Staph aureus common pathogen, but can see mixed infection
4. Diagnosis of contiguous infection osteo
a. Complete history and physical
b. Evaluate for ulcers or soft tissue lesion which may produce contiguous infection
C. Direct Inoculation - secondary to trauma or surgery
D. Vascular insufficiency

A. Cierny and Mader (1985) proposed the University of Texas Medical Branch (UTMB) classification of adult osteomyelitis. They
introduced a clinical staging of osteomyelitis that includes both an anatomic and physiologic category in a single classification.
The classification of adult osteomyelitis combines four anatomic types (the disease) with three physiologic classes (the host)
to define 12 clinical stages.

Clinical Stage
Type + Class = Clinical Stage
Example:
Stage IVBs osteomyelitis = a diffuse lesion in a systemically compromised host

III. Radiographic Diagnosis of Osteomyelitis

A. Lytic process in bone in not visible on x-ray until 30-50% of osseous mineralization has been lost
B. First bone changes occur at 10-14 days after onset of symptoms
C. First radiographic sign of osteomyelitis is due to loss of bone density know as radiolucency
D. Further radiographic changes include:
1. Sclerosis
2. Sequestration - devascularized, dead bone
3. Involucrum - new bone formation
E. Nuclear Medicine Studies

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 1. In most cases bone scintigrams become positive within 48-72 hours
2. Technetium 99M half-life is six hours
3. Tc-99m is sensitive but is not specific for osteo
4. Three phase bone scan:
a. Radio angiogram (1st phase) - demonstrates dynamic blood flow to area. Consists of several images
taken 1-2 seconds apart.
b. Blood pool image (2nd phase) - demonstrates relative vascular flow. Taken minutes after injection. These
first two phases will be hot in either soft tissue or bone infection
c. Delayed image (3rd phase) 2-4 hours after injection - demonstrates skeletal uptake
d. Recent fourth phase, taken 24 hours after injection, may help when dealing with diabetic with PVD who
has slow localization of isotope in bone, and slow excretion
5. If soft tissue infection alone is present, 3rd & 4th phases of bone should demonstrate comparatively less activity and less
diffuse activity
6. If 3rd & 4th phases seem to demonstrate similar or greater activity with discrete focal uptake, osteo is suspected
7. Osteoarthropathy can give you hot all four phases

F. Gallium 67 Scans
1. Used predominantly for the detection of acute inflammation or infection since isotope binds to white blood cells and
plasma proteins
2. Not used alone to detect osteo in foot
G. Use of Technetium and Gallium in combination
1. First perform Tc scan, then 24-72 hours later perform Ga scan
2. An increased uptake of technetium without increased uptake Ga, 85% chance no osteo is present
3. Increased uptake both 70% chance osteo is present
H. Indium 111 Scan
1. Neutrophils are taken from patient and tagged with In-111 and injected back. scan 18-24 hours later
2. Can differentiate osteoarthropathy (-) from acute osteomyelitis (+).
3. May not be beneficial in chronic osteo due to predominantly a lymphocytic pattern

IV. Diagnostic Workup

A. Aspiration of joint or bone

1. Can identify organisms
2. If wound closed needle biopsy through unaffected soft tissue (may need to perform under fluoroscope) can wash with
saline then aspirate if no frank material is noted.
B. Blood Cultures
1. Are positive in 50% of septic arthritis and osteomyelitis
C. Wound culture
1. Sinus tract culture often not responsible for underlying bone infection
2. If grow out staph aureus - approximately 50% chance that this organism is producing the associated osteo
D. Bone Cultures
1. Most definitive diagnostic tool to diagnose osteomyelitis
2. Get aerobic, anaerobic, maybe acid fast and fungal cultures

V. Chronic Osteomyelitis

A. Microorganisms residing in dead bone if not removed along with sequestra can cause acute flare-ups as late as 50 years after
initial episode
B. Squamous cell Ca has been reported to be late sequelae.

VI. Treatment

A. Indication for surgical drainage and debridement of bone in AHO

1. Pus on aspiration of the area
2. Failure of symptoms to resolve within 36 hours of antibiotic therapy
B. In frank osteomyelitis of bone

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 1. Excise necrotic bone and small portion of non-infected bone
2. Can pack open and close later
3. Can use closed suction irrigation
4. Can close over antibiotic impregnated beads
5. Antibiotics after culture
6. Monitor sed rate (or blood sugar in diabetic patient) for response to therapy as well as other signs and symptoms

VII. Workup of Patient presenting with wounds on foot with possible osteomyelitis

Diabetic presenting to office with acute, hot, swollen foot with draining wound on bottom of foot for two day duration

A. Check to see if medical status is fine - are they coherent, hypotensive, septic initially before anything
1. If not alert and coherent, may be in sepsis and ketoacidosis
2. Get stat glucose reading from Glucometer and admit to hospital
B. Get complete history and physical after determining medical status immediately
C. Inform patient, this is emergency, need to open and drain foot in hospital
D. Contact internist, patient needs I & D immediately, need to have H & P performed stat in hospital
E. Get infectious disease consult
F. Send patient to hospital and get CBC, DIFF, Sed Rate (can monitor response to treatment) Chem 24, Blood Cultures x 3, NPO
status
G. Once cleared for surgery, take to O.R.
1. Probe area to determine depth and areas that tissue are undermined
2. Make wide incision on bottom of foot across draining wound, to clear non-infectious looking tissue
3. Deepen incision to determine undermined areas
4. Open abscesses and pockets
5. Take culture of material
6. Copious high pressure irrigation
7. Probe bone gently to determine if involved. If acute infection of only a few days onset, probably not
8. Pack wound open with iodoform gauze and change BID and irrigate and debride
9. Start patient on antibiotics based on gram stain
10. If not responding to treatment either;
a. Missed all abscesses & pockets of infection
b. Inappropriate antibiotics
11. Wait for good granular bed and negative cultures then may attempt to close or may need graft.

VIII. Chronic wound on Bottom of Foot Draining for Months presents

A. Check for sepsis and control of blood sugar

B. X-ray may be suspicious for bone infection
C. Get labs as above
D. Bone scan to see if osteo, and to see how much bone involved
E. Depending on bone scan, may need Ga or Indium scan
F. Take to surgery, but don't go through chronic infection to debride bone, instead go through non-infected area off weightbearing,
i.e. dorsal metatarsal shaft for osteo of metatarsal
G. Culture bone at surgery
H. Start on antibiotics based on gram stain
I. Pack open
J. If patient with wet gangrenous or dry gangrenous skin changes and tissues changes, debride tissue with bone

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Postoperative Medical Complications
I. Defined

A. Any untoward event occurring within 30 days after surgery is considered to be a complication.

II. Non-fatal medical complications

A. Pulmonary
1. Atelectasis
2. Aspirations (rare)
3. Pulmonary embolus (uncommon, but important cause of postoperative mortality)
B. Gastrointestinal
1. Minor: gastritis or esophagitis, constipation, fecal impaction
2. Major: Post-Op jaundice (biliary tract obstruction or halothane hepatitis), paralytic ileus (rare)
C. Genitourinary
1. Urinary retention and U.T.I.
D. Cardiac
1. Congestive heart failure
2. M.I.
3. Arrhythmia, (generally rare)
E. Lower extremity
1. Superficial and deep venous thrombosis
F. Fever
G. Wound complications
1. Dehiscence
2. Hematoma

III. Pulmonary Complications

A. General
1. More common in patients with COPD from longstanding cigarette smoking (bronchitis/emphysema)
2. PFT's not CXR is best screening test for COPD
3. Associated with failure to re-expand lungs after anesthesia
4. Prolonged immobility increases risk as patients can't fully aerate lower lung fields until they are upright

B. Atelectasis: collapsed, non-ventilated lung, segments with accumulating pulmonary secretions

1. Temp to 39 degrees C (102 F.) may occur within 48 hours of surgery with tachycardia and tachypnea
2. Exam shows decreased breath sounds and crackles (collapsed lung)
3. Collapsed lung is perfused but not ventilated, which may result in hypoxemia depending on cardiopulmonary reserve.
Not improved by oxygen inhalation
4. Treatment
a. Stimulate coughing
b. Frequent change in body position (side to side) and chest percussion
c. Steam inhalation
d. Endotracheal sectioning or bronchoscopy and sectioning as last resort
C. Aspiration
1. Usually occurs with anesthesia induction
a. Saliva mild pneumonia results
2. If gastric contents, severe chemical pneumonitis results (important patient being NPO)
3. Treatment: prompt suctioning
4. Pneumonia - later complication of atelectasis or aspiration. Rare before 3rd day postoperative.
5. Increased secretions with cough, fever, infiltrate on CXR
6. Need sputum gram stain to choose appropriate antibiotic

D. Pulmonary Embolus - usually seen as late complication (7-10 days postop)

1. Rising pulse & respiratory rate out of proportion to fever

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 2. <10% go on to infarction with classic hemoptysis pleuritic chest pain and wedge shaped infiltrate on CXR
a. Diagnosis: ABG's, V/Q lung scan
3. Treatment: oxygen full doses of heparin
a. Prevention - see venous thrombosis

IV. Gastrointestinal - severe obstruction or postop paralytic ileus usually only occurs with abdominal surgery

A. Constipation- common in elderly patients who are immobilized in bed (activity has direct result on bowel function)
1. Avoid irritative cathartics (M.O.M., Dulcolax, etc if possible)
2. Bulk cathartics (bran Metamucil) preferred or stool softeners - dioctyl sodium sulfosuccinate (DDS, Colace, Doxinate)

B. Fecal Impaction - can present as postop diarrhea

1. If rectal exam reveals hard stool, patient need oil retention enema, then digital disimpaction
C. Gastritis/Reflux Esophagitis
1. Common in patients kept NPO and lying supine with legs elevated
2. Rx with elevating head and giving antacids

D. Postop Jaundice, or just Nausea

1. Check LFT's and review anesthetic record
2. With symptoms of marked right upper quadrant pain (colic), ultrasound or oral cholecystogram is indicated

V. Urinary Complications

A. Retention
1. Common in bed ridden patients, especially elderly males (high incidence of BPH) or in patients with urethral stricture
from previous catheterization, infection, or surgery
a. Atropine or other anticholergics in high doses can cause retention
b. Review intake and output
2. Excessive fluids during surgery may cause bladder
3. distention (normal bladder capacity approx 500 CCS)
4. If patient hasn't voided by 6 hrs post op, look for distended bladder on palpation and percussion
5. Treatment
a. Stand male patients to encourage voiding
b. Pass catheter if attempted voiding unsuccessful

i. If < 300 CCS, take catheter out

ii. If close to 500 CCS leave catheter in until patient more active and can void on his
own

B. Urinary Tract Infection

1. Caused by prolonged retention or unskilled catheterization
2. Treat after obtaining clean catch urine for c/s with appropriate antibiotics and adequate hydration\

VI. Cardiac Complications - generally rare during most elective surgery

A. Rarely fluid overload can precipitate CHF

B. Arrhythmias more common during anesthesia and secondary to hypoxia or cardiac toxicity of anesthetic (halothane, Ethrane)
1. Protocol - how much lidocaine to give is not the answer
C. Avoid any elective surgery within 6 months of documented M.I.

VII. Lower Extremity Venous Thrombosis

A. Results from combination of

1. Abnormality in vein wall (inflammation)
2. Decreased blood flow (stasis)
3. Hypercoagulability (Changes occur post-partum, with surgery, oral contraceptives, malignancy, trauma)
B. Increase risk in patients with chronic venous insufficiency (chronic pitting edema, hyperpigmentation especially above medial
malleolus and in obese patients with lower blood flow)
C. Clinical Presentation of Deep Vein Thrombosis
1. Aching discomfort, tightness or frank pain in the lower extremity
2. Pain on active dorsiflexion of ankle (Homan's sign) is nonspecific, but tenderness on compressing muscles
against tibia is more specific. It has fallen out of favor because a positive sign does not indicate DVT (Likelihood ratio
positive = 1) and a negative sign does not rule it out (Likelihood ratio negative = 1). It is estimated to have a sensitivity

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 of 60-88% and a specificity of 30-72%. A positive sign is present when there is pain in the calf on forceful and abrupt
dorsiflexion of the patient's foot at the ankle while the knee is extended.
3. Application of tourniquet above suspected site with resulting pain with 30-45 seconds is suggestive
4. Difference in circumference between both lower extremities very suggestive finding and often only
detectable with measuring tape

D. Laboratory diagnosis of Deep Vein Thrombophlebitis

1. Non-invasive tests (All have specificity problems and are more accurate on larger vessels)
a. Radioactive - Iodine fibrinogen scanning sensitive but not specific
b. Impedance plethysmography
c. Doppler ultrasound
d. b, c, are more accurate in picking up proximal large vessel thrombosis (femoral or iliac)
2. Invasive - venography - 90% accurate

E. Differentiate DVT from

1. Superficial thrombosis
a. Pain, tenderness, induration along course of superficial vein
b. Palpable cord
c. Absence of significant swelling in extremity
d. Treatment consists of moist heat, bed rest, elevation, and aspirin 10 grams every four hours
2. Cellulitis - warmth, adenopathy, portal of entry, fever
3. Contusion of calf muscle or tendon rupture, history of trauma, ecchymosis around foot and ankle
4. Arterial embolus - usually more pain, less swelling, temperature, loss of sensation occurs early
F. Treatment of Deep Venous Thrombosis
1. Bed rest, elevation 15-20 degrees above level of heart
2. 7-8 days for thrombi to be firmly adherent to vessel wall, and eliminate risk for P.E.
3. Use elastic bandages to increase velocity of venous flow
4. Anticoagulation
a. Heparin then Coumadin
b. 4-6 weeks for isolated calf DVT
c. 3-6 months of Coumadin for proximal vein thrombosis
d. Lovenox is indicated for:

i. the inpatient treatment of acute deep vein thrombosis with or without pulmonary
embolism, when administered in conjunction with warfarin sodium.

ii. the outpatient treatment of acute deep vein thrombosis without pulmonary
embolism when administered in conjunction with warfarin sodium.

G. DVT Prophalaxis
1. Enoxaparin (Lovenox®) is indicated for the prophylaxis of deep vein thrombosis (DVT), which may lead to
pulmonary embolism
2. The usual dosage for DVT prophylaxis is 30 mg SC every 12 hours or 40 mg SC once daily
3. Anti-Factor Xa may be used to monitor the anticoagulant effect of the drug

4. Prothrombin Time (PT) and Activated Partial Thromboplastin Time (aPTT) are relatively insensitive measures of it's
activity

VIII. Postoperative Fever

A. Definition
1. Core (Rectal) temperature 37.8 degrees C. (100 F.) should be considered abnormal
2. Temperature 38.3 degrees C (101 F) indicates major problem
B. Evaluation
1. History
a. Aspiration during anesthesia?
b. Unusual pain at operative site
c. Catheterization, possible UTI
d. Pain at IV line site
e. Respiratory, genitourinary or gastrointestinal symptoms

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 2. Physical
a. Pulmonary congestion/atelectasis
b. Red, tender, warm incision site
c. Red streak or irritation at IV
d. Abdominal findings
C. Causes
1. Atelectasis
a. Pulse, respiratory rate & temp elevated
b. Common within 24 hours of surgery
c. Pneumonitis -rare before 3rd postop day
2. Wound
a. Hemolytic strep can cause fever within 24-48 hours of surgery
b. Other bacterial infections require several days of incubation
3. Urinary - rare cause if just cystitis. Fever occurs with upper tract involvement
4. Operative site infection
5. I.V. catheters - more common with indwelling plastic
6. Drug reactions:
a. Drugs such as Lamictal, Progesterone, and sulfa drugs have been known to induce hyperthermia
D. Diagnosis - workup depends on severity & length of time from surgery
1. Lab - WBC with differential, UA, Cultures of urine, sputum, blood, drainage fluid, CXR
E. Treatment
1. Debilitating high fever (> 38.5 degrees C) give antipyretics, cooling blanket
2. If diagnosis unclear remove, IV lines and stop drugs

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Complex Regional Pain Syndrome (CRPS)
I. What is complex regional pain syndrome?

Complex regional pain syndrome is a relatively new term to encompass the older terms of reflex sympathetic dystrophy (RSDS) and
causalgia. It is a serious chronic pain condition, characterized with severe spontaneous pain and associated abnormal autonomic
features that can occur after an injury. The hallmark symptom is unrelenting, progressively worsening, intense pain out of
proportion to the severity of the injury or inciting event. It is most commonly associated with incomplete nerve trauma or soft
tissue injury, and commonly affects the distal extremities.
CRPS I, often referred to as reflex sympathetic dystrophy syndrome (RSDS) occurs with tissue injury that does not involve
direct underlying nerve trauma.
CRPS II, often referred to as causalgia, is associated with known trauma involving a known anatomical nerve trunk.

II. What are the symptoms of CRPS?

There are five major components:

1 Excessive pain: Disproportionate pain is the most prevalent characteristic for most patients. The pain is
usually continuous, spontaneous, and can be provoked by a variety of stimuli including innocuous mechanical or thermal
stimuli (Allodynia- pain elicited from a non-noxious stimulus to normal skin). Typically non-painful sensations such as:
showering, sheet irritation while in bed, weather changes, and mechanical vibrations can become painful experiences to
these patients. Therefore, light touch sensory testing is often a very effective tool in evaluating patients that might
be developing CRPS.

2 Autonomic dysfunction: Vasomotor instability that causes the affected part to be colder or warmer
than the contralateral limb, swelling, and sweating. Discoloration is usually present that includes mottled blue,
pallor, purple or red.

3 Edema: Unilateral edema

4 Movement abnormalities: Motor abnormalities are quite common and can be expressed very early in
the disease process. These include muscle weakness, spasm, intention tremor, difficulty initiating movements
(pseudo paralysis), as well as dystonia that affects the ipsilateral extremity and may extend to other
extremities. Symptoms may be heightened by emotional stress, and depression secondary to chronic pain.

5 Trophic changes: Textural changes that include thin, shiny skin; hypertrophy or atrophy of digital hair
and nail growth; fusiform digital swelling and stiffness.
Note: The clinical signs and symptoms of CRPS I and II are the same and vary in severity and length. Although there
is no definitive cut off between signs and symptoms that define distinct stages, some experts believe there are three
stages associated with CRPS, marked by progressive changes in the skin, muscles, joints, ligaments, and bones of
the affected area. The true length of each stage varies considerably from weeks to years and current staging is
neither time nor clinical expression dependent. These classical clinical staging schemes have never been validated
and their clinical usefulness has never been proven. However, for this review they are being included.
Stage one is thought to last from 1 to 3 months and is characterized by severe, burning pain,
along with muscle spasm, joint stiffness, rapid hair growth, and alterations in the blood vessels that
cause the skin to change color and temperature.
Stage two lasts from 3 to 6 months and is characterized by intensifying pain, swelling,
decreased hair growth, cracked, brittle, grooved, or spotty nails, softened bones, stiff joints, and
weak muscle tone.
Stage three extends beyond six months and entails irreversible skin and bone atrophy (Sudek's
atrophy of bone), and permanent pain and limb contracture. The syndrome progresses to the
point where changes in the skin and bone are no longer reversible. Pain becomes unyielding and
may involve the entire limb or affected area. There may be marked muscle loss (atrophy), severely
limited mobility, and involuntary contractions of the muscles and tendons that flex the joints.

III. What causes CRPS?

The pathophysiology of CRPS is not fully understood, although it is believed that the sympathetic nervous system plays an
important role in maintaining the pain, as pain receptors in the affected part of the body become sensitive to a family of
nervous system messengers known as catecholamines. It has also been theorized that post-injury CRPS (CRPS II) is caused
by a triggering of the immune response, which leads to the characteristic inflammatory symptoms of redness, warmth, and
swelling in the affected area. CRPS may therefore represent a disruption of the healing process. In all likelihood, CRPS does
not have a single cause, but is rather the result of multiple causes that produce similar symptoms. Soft tissue injuries such as
ankle sprains are a common inciting mechanism of CRPS.

IV. How is CRPS diagnosed?

The diagnosis of CRPS is based on the clinical presentation. There is no gold standard diagnostic imaging or laboratory test
to establish the diagnosis. Due to the complexity of the symptoms and similarities with other conditions, the diagnosis of
CRPS can be difficult to make, especially early in the course of the disease. It is important to rule out other conditions so that
the diagnosis can be made by exclusion. A triphasic bone scan may be useful, and often shows a splotchy uptake of
radiotracer in cases of CRPS.

In1993 the ISAP (International Association for the Study of Pain) developed specific criteria for the clinical diagnosis of
CRPS. Note: Results of validation studies suggest that the IASP CRPS diagnostic criteria are adequately sensitive; however,
both internal and external validation research suggests that utilization of these criteria causes problems of over diagnosis due
to poor specificity.

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 CRPS Type I (2-4 must be satisfied)

1. The presence of an irritating noxious event, or a cause of immobilization.

2. Continuing pain, Allodynia, or Hyperalgesia (a shifting of the stimulus-response function which
lowers the pain threshold and/or increases pain above pain threshold stimuli. Often described
in mechanical or thermal terms. Allodynia is included under hyperalgesia) with which the pain
is disproportionate to any inciting event.
3. Evidence at some time of edema, changes in skin blood flow, or abnormal pseudo-motor
activity in the region of the pain.
4. This diagnosis is excluded by the existence of conditions that would otherwise account for the
degree of pain and dysfunction.

CRPS Type II (all three criteria must be satisfied)

1. The presence of continuing pain, Allodynia, or hyperalgesia after a nerve injury, not necessarily
limited to the distribution of the injured nerve.
2. Evidence at some time of edema, changes in skin blood flow, or abnormal pseudo-motor
activity in the region of the pain.
3. The diagnosis is excluded by the existence of conditions that would otherwise account for the
degree of pain and dysfunction.

V. What is the prognosis?

The prognosis for CRPS varies from person to person. Spontaneous remission from symptoms occurs in certain people while
others can have unremitting pain and crippling, irreversible changes in spite of treatment.

VI. How is CRPS treated?

Early referral to a pain specialist and forming a multidisciplinary team will help lessen the time from diagnosis to
treatment and provide the best possible outcome for the patient. It is also important for the podiatrist on the multidisciplinary
team to be familiar with the various treatments that are available to the patient. Generally, it is agreed that the best results
have been when treatments are initiated early in the disease, and often when the treatment includes physical therapy
modalities.
The following therapies are often used:

• Physical therapy: Physical therapy is the keystone in the treatment of CRPS. A gradually increasing exercise
program to keep the painful limb or body part moving may help restore some range of motion and function.

• Psychotherapy: CRPS often has profound psychological effects on people and their families. Those with CRPS may
suffer from depression, anxiety, or post-traumatic stress disorder, all of which heighten the perception of pain and
make rehabilitation efforts more difficult.

• Sympathetic nerve block: Some patients will get significant pain relief from sympathetic nerve blocks.
Sympathetic blocks can be done in a variety of ways. One technique involves intravenous administration of
phentolamine, a drug that blocks sympathetic receptors. Another technique involves placement of an anesthetic
next to the spine to directly block the sympathetic nerves.

• Medications: Many different classes of medication are used to treat CRPS, including topical analgesic drugs that
act locally on painful nerves, skin, and muscles; antiseizure drugs; antidepressants, corticosteroids, and
opioids. However, no single drug or combination of drugs has produced consistent long-lasting improvement in
symptoms.

• Surgical sympathectomy: The use of surgical sympathectomy, a technique that destroys the nerves involved in
CRPS, is controversial. Some experts think it is unwarranted and makes CRPS worse; others report a favorable
outcome. Sympathectomy should be used only in patients whose pain is dramatically relieved (although
temporarily) by selective sympathetic blocks.

• Spinal cord stimulation: The placement of stimulating electrodes next to the spinal cord provides a pleasant
tingling sensation in the painful area. This technique appears to help many patients with their pain.

• Intrathecal drug pumps: These devices administer drugs directly to the spinal fluid, so that opioids and local
anesthetic agents can be delivered to pain-signaling targets in the spinal cord at doses far lower than those
required for oral administration. This technique decreases side effects and increases drug effectiveness.

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PART 4:
DIAGNOSITIC
EVALUATION

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Clinical Laboratory Testing
I. CBC (complete blood count) with differential cell count is a general screening for a variety of conditions. CBC includes:
A. Hgb (hemoglobin)
1. Normal ranges:
• Males = 13.5-17 gm/100 ml
• Females = 12.5-16 gm/100 ml
2. Values below 11 gm/100 ml are considered to represent anemia, and should be evaluated.
3. Elevation above 18 gm/100 ml may represent polycythemia, an increases blood viscosity and increases
risk of thrombosis.
B. Hct (Hematocrit)
1. Normal ranges:
• Males = 40-50 %
• Females = 37-47%
• Varies with the Hgb
C. RBC (Red blood cell count)
1. Normal ranges:
▪ Males = 5.4 (+/-) 0.8 X 108 /mm3
▪ Females = 4.8 (+/-) 0.6 X 108 /mm3
▪ The RBC Count increases in individuals living at high altitudes, in environmentally hot
workplaces, and in athletically fit individuals.

Red Blood Cell Indices: Red blood cell indices are blood tests that provide information about
the hemoglobin content and size of red blood cells. Abnormal values indicate the presence of
anemia and which type of anemia it is

Corpuscular indices and anemia

Microcytic/
Normocytic Macrocytic
Hypochromic

Mean corpuscular volume 82-92 95-150 50-80

Mean corpuscular Hgb 25-30 30-50 12-25

Mean corpuscular Hgb
concentration 32-36 32-36 25-30

Normocytic anemia can be observed with acute hemorrhage, hemolytic anemia, and abnormal hemopoiesis.

Macrocytic anemia occurs with pernicious anemia, sprue, pregnancy, antimetabolic therapy, and other megaloblastic
conditions.

Microcytic anemia occurs with iron deficiency or malabsorption, hemorrhage, and increase iron metabolism.

Remember the phrase "90, 30, 30," for normal MCV (mean corpuscular volume), MCH (mean corpuscular Hgb), and
MCHC (mean corpuscular Hgb concentration) values.

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I. WBC ( White blood cell count)
II. Normal Range: 5,000 - 10.000 mm3
III. Leukocytosis: Causes include: acute infection, metabolic acidosis, gout, uremia, heavy metal toxicity, tissue
necrosis or injury (burns, gangrene, tumor, myocardial infarction, pulmonary embolism), secondary to
hemorrhage or menstruation, and myeloproliferative diseases.
IV. Leukopenia: Causes include: adverse drug reactions to Thorazine, phenylbutazone, various antifungal and
antibiotics; pernicious anemia, aplastic anemia, and certain severe infections (septic shock).

II. WBC with differential The proportions of the different types of white cells in the blood.

A. White blood cells, or leukocytes, are classified into two main groups: granulocytes and nongranulocytes (also known as
agranulocytes).

• The granulocytes, which include neutrophils, eosinophils, and basophils,

have granules in their cell cytoplasm. Neutrophils, eosinophils,
and basophils also have a multilobed nucleus. As a result they are also called
polymorphonuclear leukocytes or "polys." The nuclei of neutrophils also appear to
be segmented, so they may also be called segmented neutrophils or "segs."
• The nongranuloctye white blood cells, lymphocytes and monocytes, do not
have granules and have nonlobular nuclei. They are sometimes referred to as
mononuclear leukocytes.
•
B. Normal Values: (These values fluctuate from lab to lab and are reported differently throughout the literature).

• Bands or stabs: 3 - 5 %

• Granulocytes (or polymorphonuclears)

• Neutrophils (or segs): 40 - 60%

• Eosinophils: 1 - 5%

• Basophils: 0 - 1%

• Agranulocytes (or mononuclears)

• Lymphocytes: 20 - 40%

• Monocytes: 4 - 8%
C. Neutrophilia: Causes include acute infection, necrosis, pain, exercise or post convulsion, anoxia, hemorrhage, sunburn.
D. Neutropenia: Causes include overwhelming infection, marrow depression, antimetabolite therapy, and autoimmunity.
E. Lymphocytosis: May indicate viral syndrome, hepatitis, chronic TB and measles.
F. Monocytosis: Occurs with leukemia, Hodgkin's disease, collagen vascular diseases and arthritides, sarcoidosis, subacute
bacterial endocarditis, and other infections and wounds.
G. Eosinophilia is indicative of allergy, asthma, eczema and Uticaria; parasitic infection; scarlet fever; pemphigus and
dermatitis herpetiformis; leukemia and pernicious anemia.
H. Eosinopenia is seen in Cushing's disease, excess ACTH, chronic steroid therapy, post operative state, shock, and labor.
I. Basophilia occurs in polycythemia, chronic myelogenous leukemia, chicken-pox, small-pox, hypothyroid myxedema, and
renal disease.

III. Platelet Count

A. Normal range: 140,000 - 340,000 mm3
B. Elevation is seen in collagen vascular disease, iron deficiency anemia, acute infection or injury, aquatic disease,
cardiac disease, malignancy, and polycythemia Vera.

IV. Serum chemistries

• Calcium - normal is 8.5-10.5 mg%. Elevated in primary hyperparathyroidism or secondary to chronic renal failure,
metastatic bone disease, lymphoma or multiple myeloma, sarcoidosis; or lung or renal carcinoma that produce
parathormone; or hypervitaminosis D (excessive intake of cod liver oil), diuretic use, or acidosis. Decreased in
hypoparathyroidism, chronic renal failure (perhaps postoperative, and classically seen with simultaneous elevation of
phosphorous), malabsorption or steatorrhea, alkalosis, pancreatitis, and when EDTA used to anticoagulate the blood
specimen.

• Phosphorus - normal is 2.5-4.5 mg%. Elevated in chronic renal failure, diabetic ketoacidosis, fracture healing,
acromegaly, growing children (physiological), and hypervitaminosis D. Decreased in negative nitrogen balance

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 (simultaneous decreased BUN and alkaline phosphatase), hepatic disease, Fanconi syndrome, osteomalacia, and with
longterm IV glucose infusion in a non-diabetic patient.

• Glucose - normal is 65-110 mg%. Elevated in diabetes mellitus (serum phosphorous remains normal), Cushing's
disease, corticosteroid administration, pheochromocytoma, and brain injury or tumor. Decreased in hyperinsulinism,
pancreatic islet cell tumor, Addison's disease, bacterial septicemia, and advanced hepatic necrosis.

• Blood urea nitrogen (BUN) - normal is 10-20 mg%. Elevated in renal failure (with or without obstructive uropathy),
dehydration, G.I. bleed. Decreased in hepatic failure (urea production reduced), carbon tetrachloride toxicity, and
associated with a negative nitrogen balance.

• Uric acid - normal is 2.5-8 mg%. Uric acid is the end product of purine metabolism, and may precipitate out of
serum into the tissues as monosodium urate crystals, which is responsible for acute gouty arthritis as well as chronic
tophaceous gout. Elevated in conditions where there is excessive purine intake (tyramine, cheese, dark beer, game
meats), over-production of uric acid (rapid cell proliferation as in neoplasms such as lymphoma or leukemia; extensive
tissue necrosis), or under excretion of uric acid (renal disease), eclampsia, starvation, thiazide diuretics, lead
poisoning, and metabolic acidosis. Decreased with use of uricosuric agents, Fanconi syndrome or Wilson's disease.

• Cholesterol - normal is 150-275 mg% (this is controversial). Elevated in obstructive jaundice, hypothyroidism,
nephrosis, uncontrolled diabetes, endotoxic shock or gram-negative septicemia, and pregnancy. Decreased in
malabsorption syndromes, hepatic disease (about 2/3 of the cholesterol is esterified in the liver), hyperthyroidism,
anemia, septicemia, and chronic stress.

• Albumin - normal is 3.5-5 gm%. Hyperalbuminemia is rare. Decreased in protein malnutrition, hepatic failure, renal
disease (nephrosis), GI wasting (diarrhea) or mal-absorption, burn wounds, or extensive exfoliative dermatitis.

• Total protein - normal range is 6-8 gm%. Hyperproteinemia is typically caused by an elevation of globulin, as in
collagen vascular disease, chronic infection, or malignancy such as multiple myeloma. Hypoproteinemia results from
the same causes of hypoalbuminemia. Note the following general formula for total protein: 3 gm% globulin + 4 gm%
albumin = 7 gm% total protein

• Lactate dehydrogenase - normal is 90-200 mU/ml. Lactate dehydrogenase catalyzes lactic acid t pyruvic acid in the
citric acid cycle (glycolytic cycle). Increased in cytolysis and cytonecrosis (acute myocardial, pulmonary, renal, hepatic,
skeletal muscle, and major organ infarction); pernicious anemia, malignant neoplasm, and sprue. Decreased with
radiation therapy.

• Bilirubin - normal is 0.1-1 mg%. Elevated in jaundice (hepatic, obstructive, or hemolytic), Crigler-Najjar syndrome
and Gilbert's disease. Hemolysis and hemorrhagic or hematoma due to pulmonary injury or other major trauma will
elevate serum bilirubin.

• Alkaline phosphatase - normal is 30-85 mU/ml. Elevated in the growing individual; bone diseases such as
sarcoma, fracture healing, Paget's disease, metastatic carcinoma to bone (usually normal in osteomalacia); other
metastatic disease, histiocytosis, pulmonary embolism, and congestive heart failure. Decreased hypophosphatasia, an
inherited condition similar to rickets however, the alkaline phosphatase and leukocyte counts are decreased. Also
decreased in magnesium deficiency, chronic diarrhea, malabsorption, uncontrolled diabetes mellitus with magnesium
deficient parenteral fluid administration, malnutrition, and pernicious anemia.

• Serum glutamic-oxaloacetic transaminase (SGOT) - normal is 10-50 mU/ml. SGOT is found in liver > heart >
skeletal muscle > kidney, pancreas, red blood cells, and lung. Elevated in cardiac and hepatic disease (myocardial
infarction, liver cancer or injury or hepatitis), acute tubular necrosis, acute pancreatitis, hemolytic anemia, leukemia,
myonecrosis or injury, pulmonary injury or necrosis, and dermatomyositis. Decreased in conditions with elevated
serum lactate or pyruvate such as beriberi, thiamin deficiency, diabetic ketoacidosis, and liver disease.

• Serum glutamic-pyruvic transaminase (SGPT) - normal is 5-35 mU/ml. SGPT is found primarily in the liver, and is
elevated in liver disease. Microbiological Testing

V. Coagulation Studies
• Partial thromboplastin time (PTT) - normal range is 25-35 seconds. Used as a reliable screening test, however
may not detect subtle defects. Also used to monitor heparin anticoagulation therapy. The PTT can be used to
evaluate the three stages of coagulation, with the exception of factor VII or platelet factors. The PTT remains normal in
von Willebrand's disease, platelet dysfunction, and thrombocytopenia. The PTT is prolonged by defects in clotting
factors I, II, V, VIII, IX, X, XI, and XII.

• Prothrombin time (PT) - normal range is 11-16 seconds. The PT is used to monitor longterm Coumadin
(Warfarin) anticoagulation therapy. The PT is prolonged with defects in factors I, II, V, VII, and X; as well as in
vitamin-K deficiency, fat malabsorption (steatorrhea, colitis, jaundice), salicylate or warfarin therapy, and advanced
hepatic disease.

• Bleeding time - normal range (Duke) is 1-4 minutes. The bleeding time is prolonged in thrombocytopenia, abnormal
platelet function, and von Willebrand's disease.

• Clotting time - normal range (Lee-White) is 3-6 minutes in a capillary tube, and 6-17 minutes in a test tube. This is a
routine, nonspecific screening test used to determine the presence of major clotting deficiencies.

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 VI. Urinalysis
It is preferable to evaluate the first morning specimen. Physical and chemical properties are assessed.

• Color - normal is amber to pale yellow. Black urine is noted in alkaptonuria, malignant melanoma, and malaria. Red urine
is noted in hematuria, hemoglobinuria, methemoglobinuria, and myoglobinuria. Blue urine may be noted in porphyria.
Brown to green urine may occur with bilirubinuria. Dark brown urine occurs in sickle cell anemia. Acidic urine appears
orange.

• Odor - normal urine smells like ammonia. A putrid odor may indicate bacteria. Mousy urine occurs with phenylketonuria
(PKU). Asparagus effects a peculiar urine odor.

• Clarity - generally the urine is relatively clear, with some sediments. Cloudy urine may represent infection, crystaluria,
hemorrhage, or cellular debris.

• Specific gravity - normal range is 1.003 - 1.026. pH - normal is 4.6 - 8.0

• Urine chemistries - glucose, ketones, protein, and drug by-products and metabolites can all be measured.

• Microscopic findings - blood and epithelia cells, casts, crystals, and bacteria can be identified.

VII. Important Labs in Rheumatoid Disease

A. Erythrocyte sedimentation rate (ESR) - normal anticoagulated blood shows very little settling, however, elevated globulin and
fibrinogen associated with inflammation leads to Rouleaux formation and the clumped red cells settle rapidly. An elevated ESR is indicative of a
measurably higher column of red cells settled at the bottom of the tube within a set time. The ESR can be used to distinguish inflammatory
from non-inflammatory conditions, and is used to monitor resolution of inflammation during the course of therapy. The ESR is very
sensitive, however, nonspecific. The ESR is elevated in acute infection, rheumatoid arthritis, polyarteritis, ankylosing spondylitis, septic
arthritis, acute gout, metastasis, and other connective tissue diseases.
B. C-reactive protein (CRP) - is a glycoprotein that reacts with C-mucopolysaccharide of many pneumococci. It is commonly
produced during the acute phase of inflammation. It rises before the ESR, and normalizes in the presence of NSAIDs, aspirin and
steroids. It rises in acute flare of rheumatoid arthritis, Strep. infection, in the last half of pregnancy, and in females using an IUD and/or oral
contraceptives.
C. Antinuclear antibody (ANA) - appears months after onset of connective tissue disease, and may have its greatest value in
monitoring SLE. It is more accurate than the LE cell test because it is unaffected by steroids. The significance of ANA titers less than 16 is
uncertain, as healthy persons may display titers in this range. Elevated ANA titers suggest connective tissue disease, while absent or low titers
do not rule out connective tissue disorders. High titers are common in SLE, scleroderma, and mixed connective tissue disorders, and Raynaud's
phenomenon.

Pattern Associated Antigens Clinical Conditions

Homogenous Deoxyribonucleoprotein Collagen-Vascular DS

Particulated Extractable Nuclear Antigen Mixed C.T. DS., Scleroderma, SLE, Malignancy

Peripheral Native DNA and Histones Active SLE with Nephritis

Nucleolar Nucleolar RNA Scleroderma, Raynaud's

Positive ANA is found in the following percentages in the following diseases

Systemic lupus erythematosus-----------------(100%, high titer)
Rheumatoid arthritis---------------------------- (< 60%, very low titer)
Sjogren syndrome------------------------------- (75%, low titer)
Systemic sclerosis--------------------------------(38%, low titer)
Liver cirrhosis-------------------------------------(45%, low titer)
Polymyositis--------------------------------------(20%, low titer)
Dermatomyositis---------------------------------(20%, low titer)
Malignancy ---------------------------------------(18%, low titer)
Bullous pemphigus------------------------------(rare, low titer)
Polyarteritis nodosa or ulcerative colitis------(rare, low titer)
Waldenstrom's macroglobulinemia------------(rare, low titer)
Drug reaction-------------------------------------(rare, low to high titer)
Myasthenia gravis--------------------------------(rare, very low titer)

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 D. Rheumatoid factor (RF) - IgM or IgG auto-antibodies that react with the Fc portion of denatured human IgG. There are two
methods of measurement: latex fixation (75% sensitive and 75% specific for RA at 1:80 dilution), and sheep cell agglutination (75% sensitive
and 95% specific for RA at 1:160 dilution). RF is found in the following percentages: Sjogren syndrome (75-100%), adult RA (70-80%), juvenile
RA (10%), SLE (20-40%), scleroderma (5-10%), polyarteritis nodosa and dermatomyositis (0-5%).
E. Lupus erythematosus (LE) cell - mature polymorphonuclear neutrophil that has phagocytosed a spherical, homogenous
inclusion derived from another neutrophil. Characteristic of SLE, and observed in the following percentages: SLE (70-80%), Sjogren syndrome
(10-20%), RA (5-10%), scleroderma and polyarteritis nodosa and dermatomyositis (0-5%).
F. Serum complement - series of enzymatic proteins that combine with antigen-antibody complexes and effect lysis when the
antigen is an intact cell. Complement remains normal in Sjogren syndrome, scleroderma, polyarteritis nodosa, and dermatomyositis; is normal
or decreased in SLE; and normal or slightly elevated in acute phase of RA.
G. Anti-streptolysin O (ASO) - antibody against streptolysin "O" of group A streptococci (Strept. pyogenes). It is present in 80-
85% of patients with acute rheumatic fever or other streptococcal infection.
H. HL-A B27 - histocompatability antigen found in the following percentages in the following diseases: ankylosing spondylitis
(90%), Reiter's syndrome (75%), psoriatic arthritis and juvenile RA (high concentration).
I. HL-A B15 - histocompatability antigen found in 33% of patients with SLE.
J. Uric acid (UA) - elevated in gout, malignancy, renal disease, and familial hyperuricemia. Normal is 7-9 mg% in males, and slightly
less in females. UA may be normal in the acute stage (first 10 days) of gouty arthritis, as much has precipitated out of the serum into the
affected joint. Monosodium urate (gouty) crystals are needle-shaped, and form the "martini sign" when phagocytosed by a neutrophil.
K. Calcium pyrophosphate - crystals are rhomboid, and observed in pseudogout.
L. Differential Diagnosis Based on the Joint Fluid Analysis Chart
1. Group-I: Non-inflammatory conditions such as DJD, trauma, osteochondritis dissecans, osteochondromatosis,
neuropathic hypertrophic osteo-arthropathy (Charcot), resolving or early inflammation, hypertrophic pulmonary arthropathy, and
pigmented villonodular synovitis.
2. Group-II: Inflammatory conditions such as RA, gout, pseudogout, Reiter's syndrome, ankylosing spondylitis, psoriatic
arthritis, arthritis associated with ulcerative colitis or Crohn's regional enteritis, rheumatic fever, SLE, and progressive systemic
sclerosis.
3. Group-III: Septic arthritis due to bacterial infection.
Note: Hemarthrosis results in a hemorrhagic joint fluid specimen, and can be caused by hemophilia and other bleeding
diatheses, ligamentous trauma with or without fracture, neuropathic arthropathy, pigmented villonodular synovitis, synovioma,
hemangioma, and other neoplasms.

M. Joint Fluid Analysis

Joint Fluid Normal Group -I Group -II Group -III

Volume --------------- Increased Increased Increased

Clarity Clear Clear Cloudy Opaque

Color Clear Yellow Opalescent Yellow green Yellow

Viscosity High High Low Variable

WBC/ mm3 < 200 200 - 2,000 2,000 - 100,000 >100,000

% PMNs <25% <25% >50% >75%

Culture (-) (-) (-) (+)

Mucin Clot Firm Firm Friable Friable

Glucose (mg%) = Serum = Serum < Serum < Serum

VIII. Microbiological Testing

A. Culture and sensitivity (C&S) - used to identify micro-organisms involved in an infectious process. Standard C&S involves
aerobic and anaerobic testing. Acid fast, chocolate agar, sheep's blood, fungal culture, and other specific test media may be indicated based on
individual case requirements. Sensitivity of an organism to a particular antibiotic is determined by Kirby-Bauer disk sensitivity, wherein
antibiotic impregnated disks are placed on the culture medium surface and areas of "no growth" are observed surrounding disks containing
antibiotic that kill the bacteria. Minimal inhibitory concentration (MIC) and minimal bactericidal concentration (MBC) are also used to test
sensitivity to specific antibiotics, wherein the inhibitory concentration stops cell growth and the cidal concentration kills the organism.
B. Gram's stain - used to identify the presence of bacteria, their morphology, and staining characteristics. Wound exudate suspected
of infection should be stained as follows:
1. Gentian violet - H2O rinse
2. Alcohol - H2O rinse
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 3. Gram's iodine - H2O rinse
4. Safranin - H2O rinse.
Microscopic observation should reveal granulocytes indicative of inflammation, and the presence of bacteria. The combination of granulocytes
and bacteria is indicative of infection. Antibiotic selection is made based upon bacterial morphology and staining. Gram-positive bacteria appear
violet-purple (gentian violet), while gram-negative bacteria appear red (Safranin). Interpretation of the Gram's stain is particularly important
when considering anaerobic bacteria, as it can be difficult to grow such organisms in the microbiology lab. See Also (this links to the infection
section from complications)

A. KOH prep - squamous epithelial cells are dissolved in keratinolytic potassium hydroxide, leaving microscopically evident fungal
hyphae and/or spores and yeast. Also known as a tissue exam for fungus.
B. PAS - periodic acid Schiff stain for fungal hyphae/spores and yeast.
C. Acid fast staining - for suspected tuberculin infection (Mycobacterium tuberculi).
D. Blood agar culture medium - for certain fastidious microbes, such as Neisseria.
E. Chocolate agar - predisposes to growth of Neisseria.

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Vascular Diagnostic Evaluation
I. Basic Vascular Examination:
The basic clinical vascular evaluation involves inspection of the skin color, temperature, turgor, and digital trichosis; as well
as palpation of the arterial pulse at the popliteal, posterior tibial and dorsalis pedis levels. If indicated, arterial pulse at the
perforating peroneal, femoral, and abdominal aortic levels are also assessed. Edema is noted to be either pitting, brawny or
spongy. The skin barrier is inspected for areas of open compromise or gangrene. Vasospastic instability may elicit Livedo
reticularis, while arterial insufficiency may elicit dependent rubor associated with intermittent claudication or even rest pain.
• Livedo Reticularis: a condition in which dilation of capillary blood vessels and stagnation of blood
within these vessels causes mottled discolouration of the skin. It is described as being reticular (net-
like) cyanotic (reddish blue discolouration) cutaneous discolouration surrounding pale central areas. It
occurs mostly on the legs, arms and trunk and is more pronounced in cold weather
• Dependent Rubor: Reddish-blue discoloration of the extremities; indicative of severe peripheral arterial
damage in vessels that remain dilated, as they are unable to constrict. Rubor may be observed with 20
seconds to 2 minutes after the extremity becomes dependent (lowest area, most affected by gravity).
The extremity will begin to turn pale when elevated (referred to as blanching

II. Non-Invasive Vascular Examination

A. The non-invasive vascular examination is performed with the duplex Doppler ultrasound machine, and correlated with the
clinical findings.
B. The non-invasive arterial exam measures segmental arterial pressures and waveform analysis. Ipsilateral segmental pressure
differences indicative of a 20-30 mmHg pressure drop from the proximal to the distal segment, are strongly suggestive of
occlusive disease. Moreover, arterial pulsation waveforms should be triphasic with a dicrotic notch, or at least biphasic.
Monophasic Doppler tracings and sounds are indicative of arterial occlusive disease with decreased flow.
C. Determining the ankle systolic pressure involves pneumatic cuff placement above the ankle and elevated until no arterial
pulsation can be identified with the Doppler ultrasound over the PT artery. The cuff is then deflated until the ultrasound
identifies flow in the posterior tibial artery, and the pressure recorded. The maneuver is repeated while measuring the
opening pressure in the dorsalis pedis artery, and then again for the peroneal artery. The highest of the three values is used
as the "ankle" systolic pressure.
D. Forefoot and digital systolic pressures, as well as pulse volume recordings using infrared sensors on the toe pulps can also be
determined. The ankle/arm ratio (also know as ankle/brachial index or ischemic index) is calculated by dividing the ankle
systolic opening pressure by the arm systolic opening pressure. Deceptively high opening pressures can be measured in the
presence of medial calcific sclerosis.

Ankle/Arm Ratio Guidelines in the Non-Diabetic Patient

Ankle/Arm Ratio Clinical Finding

> 0.96 Normal

0.31 - 0.95 Intermittent claudication

0.25 - 0.3 Rest Pain

0 - 0.3 Impending gangrene

III. Ischemic Index Guidelines for Reconstructive Surgery

A. Foot:
1. If ankle/arm index < 0.75, then generally do not operate.
2. If ankle/arm index > 0.75, then check toe/arm index.
3. If ankle/arm index > 0.75 and toe/arm index < 0.65, then generally do not operate.
4. If ankle/arm index > 0.75 and toe/arm index > 0.65, then may operate. If you can't get a measurement on toe
because of deformity, use forefoot/arm index. If ankle/arm index > 0.75 and forefoot/arm index > 0.65, then check
Doppler flow of digital arteries.
B. Hallux:
1. If ankle/arm index > 0.75, and toe/arm or forefoot/arm index > 0.65 and two of four digital arteries identified with
Doppler, then generally may operate.
C. Lesser Toe:
1. If ankle/arm index > 0.75 and toe/arm or forefoot/arm index > 0.65 and either both dorsal arteries and one plantar
or both plantar arteries identified with Doppler, then generally may operate.

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IV. ABI's and ischemic Index in Diabetic ulcerations and healing
A. Calcification in the arteries can result in inaccurate doppler flow readings. Calcifications falsely elevate the ABI's due to
decreased compliance of the calcified vessels.
B. Ratio of ankle to brachial pressures (< 0.6 is abnormal and concerning)
C. Index of 0.6, absolute ankle pressure of > 40 mmHg, and absolute toe pressure of 40 mmHg or more are good
indicators that a diabetic ulcer will heal.
D. Index of < 0.45 is associated with poor wound healing
E. Note: calcification of vessels will alter readings

EXAMPLE:

V. Transcutaneous oxygen tension (Tc-pO2) for assessment of pedal perfusion.

TcPO2 is a noninvasive and highly reproducible measure of skin oxygenation and reflects very well the metabolic state of lower limbs. Given
that TcPO2 measurement is not affected by arterial calcification, it is particularly useful in evaluating and managing vascular
disease in diabetic patients. It can be used to determining amputation level, the need of revascularization, and wound
healing evaluation.

A. The skin is warmed to 44°C, and a Clark electrode is placed on the foot and leg to measure Tc-pO2, using the chest as a
reference site
B. Normal transcutaneous oxygen tension levels are approximately 60 mm Hg
C. Good healing potential is likely to heal if the Tc-pO2 is at least 40 mmHg
D. Healing is questionable if the Tc-pO2 is between 26-40 mm Hg
E. Transcutaneous oxygen tension levels of 20 mm Hg or less are indicative of severely reduced blood flow to the area of
evaluation and strongly suggest that revascularization will be required to achieve healing.

VI. Invasive arterial testing

A. Angiography with radiopaque contrast media, is usually obtained only if reconstructive vascular surgery is being entertained.
Infusion of contrast medium is not a risk-free undertaking, and conveys the risk of hypersensitivity reaction, as well as renal
failure in dehydrated or predisposed individuals.
B. Digital subtraction angiography can further enhance identification of patent and occluded vessels. Although noninvasive, MRI
can also be used to evaluate blood vessels and yields considerably accurate images.
C. Venous non-invasive Doppler assessment is used when deep vein thrombophlebitis is suspected, and a venogram may further
enhance identification of a thrombosis, particularly one that is propagating or associated with embolism and consideration is
given to surgical intervention.

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X-rays Of The Foot And Ankle
I. Foot Views:

Standard pedal radiographic views are taken with the patient weight bearing, with the feet in the angle and base of gait.
This allows reproducible and reliable images, from which standard angles and relationships can be assessed. Variations can
be useful, depending upon specific needs. The primary views of the ankle include the mortise and lateral projections. Ankle
views do not necessitate positioning the foot in the angle and base of gait. Contralateral radiographs can be obtained for
comparison, particularly when evaluating the skeletally immature, or when concerned about secondary centers of
ossification.
A. Dorsoplantar foot - the patient standing on film cassette, beam angled 15 degrees from vertical and aimed at the navicular.
B. Lateral foot - the foot is positioned beside (against) the film cassette, which is vertical to the substrate, beam angled 90° from
vertical and aimed at the midfoot.
C. Lateral oblique foot - the patient standing on film cassette, beam angled 45° from vertical and aimed at the lateral aspect
of the foot. Useful in assessment of the calcaneus, cuboid, fifth metatarsal and little toe.
D. Medial oblique foot - the patient standing on film cassette, beam angled 45° from vertical and aimed at the medial aspect
of the foot. An unconventional view, useful in assessment of the medial aspect of the foot, the first metatarsal and hallux
and, in particular, the plantar medial border of the foot. It is also useful in evaluation of the tuberosity of the calcaneus, as in
the case of suspected plantar heel spur.
E. Calcaneal axial - the patient standing on film cassette, beam angled 45° to vertical and aimed at posterior aspect of the
heel. Modifications include Harris and Beath projections, wherein the beam angle ranges from 10° above and 10°
below the lateral view declination angle of the posterior facet of the STJ (as determined by a scout lateral view) or,
more simply, 30°, 45° and 60° from vertical. Useful in assessment of the posterior aspect of the calcaneus, suspected
calcaneal fracture or inspection of the posterior facet of the STJ or the sustentaculum.
F. Sesamoidal or metatarsal axial - the patient standing on orthoposer with the film vertical to the substrate, and the toes
dorsiflexed against the film. The hindfoot is supported with enough radiolucent foam to elevate the heel above the substrate,
with the beam angled from posterior-to-anterior parallel to the substrate and aimed at the metatarsal heads. Positioning
devices are available to aid in stabilizing the patient for these views.
G. Isherwood views - a rarely used set of three non-weight-bearing views that display the STJs. The lateral oblique view shows
the anterior facet, the medial oblique view shows the middle and posterior facets, and the lateral oblique axial view shows the
posterior facet. CT and linear tomography are more typically used, as positioning for Isherwood views is difficult and time
consuming. Other sets of radiographic views used to image the STJs, and generally superseded by linear and axial
tomography, include Anthansen and Broden projections.

II. Ankle Views:

A. Mortise ankle -
The heel is backed against the vertical film cassette, with the foot medially rotated 15°, the beam angled parallel to the
substrate and aimed at the ankle. This is the standard view for assessment of the tibiotalar and tibiofibular joints, and the dome
of the talus and tibial bearing surface.
B. Lateral ankle –
The medial aspect of the foot is positioned against the vertical film, the beam angled parallel to the substrate and aimed at the
ankle.
C. Anterior-posterior ankle –
The heel is backed against the vertical film cassette, with the toes pointing straight ahead, the beam angled parallel to the
substrate and aimed at the ankle. The lateral malleolus is rotated posterior to and superimposed behind the tibia in this view,
and the distal tibiofibular syndesmosis is obscured. The mortise view is much more useful for evaluation of the tibiotalar and
tibiofibular joints.
D. Medial oblique ankle –
Oriented the same as in the AP or mortise of the ankle, however the foot is medially rotated 45°, thereby further opening the
tibiofibular syndesmosis.
C. Lateral oblique ankle –
Oriented the same as the AP or mortise of the ankle, however the foot is laterally rotated 45o. May be used to assess the medial
malleolar cortex and the medial aspect of the talus.
E. Stress Radiography
Stress radiography can be performed with static radiographs, or dynamically under fluoroscopic image intensification. Stress
radiographs are used to identify occult fractures and ligamentous instability, and can be used to evaluate any bone or joint in the
leg, foot, or ankle. The examiner should wear protective gloves, thyroid shield, and body apron whenever stress films are made.
a. Anterior drawer of the ankle View You Tube Video (https://www.youtube.com/watch?v=zjauu5gXF2A) -
with the patient supine, the lateral aspect of the foot is placed against the film cassette and the heel is cupped
with one hand while the opposite hand stabilizes the anterior aspect of the tibia. The foot is rotated
medially about 15°, thereby allowing visualization of the talar dome, while the talus is pulled forward
out of the mortise. The distance between the nearest point on the posterior aspect of the dome of the talus and
the most posterior margin of the distal tibial bearing surface is measured, and a distance of > 4 mm is indicative

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 of disruption of the anterior talofibular ligament. A Telos apparatus can be useful for applying anterior drawer in a
reproducible fashion.

b. Inversion ankle stress (talar tilt) View you Tube Video

(https://www.youtube.com/watch?v=2qF_DOe2jPE&feature=related)- with the patient supine, the ankle is
oriented in a fashion similar to that used in the mortise view, while the tibia is stabilized medially and the talus
(hindfoot with the STJ stabilized) forced into the tibial malleolus in an effort to stress the lateral collateral
ligaments. The angle created between the plane of the distal tibial bearing surface and the dome of the talus is
measured. Angles < 5° are considered normal, between 5-20° may be normal or abnormal, and larger angles
are suggestive of lateral collateral ligament disruption. Loose bodies may be identified between the tibia and
talus.
c. Stress ankle dorsiflexion (charger) - a weight-bearing lateral view of the ankle is taken with the ipsilateral
knee flexed and the ankle relatively dorsiflexed, This is used to depict osseous ankle equinus.
Note: A positive push-pull with a negative inversion stress laterally generally indicates disruption of the anterior ligament alone,
while positive findings in both views implies rupture of both the anterior and calcaneofibular ligaments.

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 MRI
How it works

Protons in the body spin randomly on their long axis, which produces a magnetic field. When the patients body is placed in the
MRI machine, the protons line up parallel to the magnetic field of the machine. Then we hit the body with radio waves, which
excite the protons, and energy is released (producing an image).
Note: Spin-echo pulse sequencing is the most common form of MRI used clinically. This consists of a 90-degree
pulse followed by a 180-degree pulse, which produces a signal (echo).

Definitions

- (Repetition time) TR = time between successive 90 degree pulse.

- (Echo time) TE = time from beginning of 90 degree pulse to the peak of the echo.
- T1 image (Fat Image) has a short TR (300-800 msec) and a short TE (20-30 msec).
- T2 image (Water Image) has a long TR (1500-3500 msec) and a long TE (60-120 msec).
- Proton image has a long TR and short TE
- Imaging Time is directly proportional to TR.
- T1 is better for anatomic definition (example: TR500/TE30).
- T2 is best for soft tissue contrast (neoplasm, inflammation, pathologic process)

T1 (Fat Image)

DARK BLACK AREAS

o Tendon

o Subchondral cortex of bone

o Blood vessels with moving blood

o Ligament

o Muscles

o Tumors
LIGHT AREAS

o Fat (whitest)

o Medullary bone

o Stationary blood

T2 (Water Image)

DARK AREAS

o Ligaments

o Compact bone
INTERMEDIATE AREAS (GRAY)

o Subcutaneous fat

o Bone marrow

o Muscle
LIGHT AREAS

o Stationary blood tumor

MRI Facts

- MRI cannot predict malignancy vs non-malignancy

- MRI is better than CT for medullary canal bone tumors. CT has higher resolution for tumors of the cortex.
- MRI is the modality of choice for avascular neurosis.
- MRI gives imaging in any plane (sagittal, axial, and coronal).
- Osteomyelitis has a characteristic decreased signal on the T1 and an increased signal on T2 weighted images.

Contraindications

- Implanted metallic objects near eye orbit

- First trimester pregnancy
- Cerebral (aneurysm clips)
- Pace maker

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No Signal on T1 & T2 Images

- Air
- Rapidly flowing blood
- Cortical bone
- Ligaments
- Tendons
- Scar Tissue
- Calcifications

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MRI Examples
1. Achilles Tendon Rupture
A. Radiology Report

B. Views

Complete Achilles Tendon Rupture (Axial View T1)

This is a T1 or fat image because it has a short TR (300-800 msec) and a short TE (15-30 msec). Tendon tissue is dark
(black) and fat tissue is light (white). This is at a level below the tear where the Achilles tendon is intact. Note the small
sagittal view of the foot in the lower right corner. This shows the level of the axial slice. These small scout views are present
on each MRI slice or view. Use them to figure out your location.
Axial View T1 ( Fat Image) Below Tear:

Complete Achilles Tendon Rupture (Axial View T1) At Myotendinous Junction

Again, this is a T1 or fat image because it has a short TR (300-800 msec) and a short TE (15-30 msec). Tendon tissue is
dark (black), fat tissue is light (white), and muscle tissue is in between (dark gray). This is at the myotendinous junction
(note the scout view, the line is up higher in the leg). There is a shredded appearance compatible with a partial tear at this
level.
Axial View T1 ( Fat Image) Below Tear:

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 Complete Achilles Tendon Rupture (Sagittal View T1)
Again, this is a T1 or fat image because it has a short TR (300-800 msec) and a short TE (15-30 msec). Tendon tissue is
dark (black), fat tissue is light (white), and muscle tissue is in between (dark gray).
Sagittal View T1 (Fat Image)

Complete Achilles Tendon Rupture (Sagittal View T2)

This is a T2 or water image because it has a long TR (1500-3500 msec) and a long TE (60-120 msec). The Tendon and
bone tissues appear dark (black) and the blood or fluid appears light (white).
Sagittal View T2 (Water Image)

2. Medial Talar Dome Fracture

A. Radiology Report

Medial Talar Dome Fx Radiology Report

MRI RIGHT FOOT:

Comparison plain films from an outside center dated 11/1/94. No recent plain films are available.

FINDINGS:

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 Extensive marrow edema in the talus surrounds an ovoid focus of signal alteration in the subchondral space of the
talar dome medially. This focal signal alteration in the talar dome measures approximately 7.5 x 4.0 mm and is of
intermediate signal on T1 weighted images and hyperintense on T2 weighted images. A very thin hypo intense rim
surrounds this signal alteration; this may present fibrosis or sclerosis. Peroneus and flexor tendons are intact with
normal signal and caliber. The other navicular bones demonstrate normal marrow signal characteristics. The finding is
compatible with a transchondral fracture; the described signal characteristics may be explained by synovial
invagination into an osteochondral defect. However, no definite loose body is identified. Less likely, a non-displaced
Grade III transchondral fracture may be present. Current plain films for comparison would be useful to distinguish
between Grade III and Grade IV lesions. The overlying cartilage is indistinct over this portion of the talar come. A
small joint effusion is present distending the anterior joint capsule.

IMPRESSION:

1. Transchondral fracture of the medial talar dome measures approximately 7.5 x 4.0 mm. If clinically
relevant, current plain films of the right ankle may be useful in distinguishing between Grade III and Grade
IV transchondral fracture in this case, for reasons described above.
2. Although a small anterior capsular joint effusion is present, no definitive loose bodies are identified.

B. Views

Medial Talar Dome Fracture (Sagittal T1)

Extensive marrow edema in the talus surrounds an ovoid focus of signal alteration in the subchondral space of the talar dome
medially.
Sagittal T1 (Fat Image)

Medial Talar Dome Fracture (Sagittal T2)

The focal signal alteration in the talar dome is hypertensive in this T2 weighted image.
Sagittal T2 ( Water Image)

Medial Talar Dome Fracture (Axial T1) One

The focal signal alteration in the talar dome is of intermediate signal in this T1 weighted image.
Axial T1 ( Fat Image) One

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 Medial Talar Dome Fracture (Axial T1) Two

Axial T1 (Fat Image) Two

Medial Talar Dome Fracture Standard X-ray

This current plain film was used to confirm a grade IV lesion. Note the displaced fragment at the medial talar dome.
Standard X-ray

3. Osteomyelitis of the calcaneus

A. Radiology Report

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 Radiology Report

MRI Of the Right Foot:

The arch is destroyed by collapse of the calcaneus and destruction of the calcaneus due to infiltrative edema and
osteomyelitis. Foci of hypointensity are compatible with susceptibility effect from prior surgery but also likely gas
bubble formation. Pathologic collapse from infiltration of the calcaneus has resulted in flat foot and there is extension
of the inflammation up to the calcaneocuboid joint or transverse tarsal joint. There is also involvement of the posterior
facet with relative sparing of the talar side of the joint. Extension into the sinus tarsi and canal is noted. Inflammation
in the plantar soft tissues especially the deep compartment and quadratus planta is noted. Extensive soft tissue
change with fistulous communication or sinus tract extending out the posterolateral aspect of the subcutis and dermal
layer. Reactive talar edema is noted on the sagittal T2 fat suppressed images. This inflammatory process engulfs the
peroneus tendons.

CONCULSION:

EXTENSIVE HIND FOOT OSTEOMYELITIS IN DISTRIBUTIONS DESCRIBED.

B. Views

Osteomyelitis of the calcaneus (Sagittal T1)

Foci of hypointensity are likely gas bubble formation.
Sagittal T1 (Fat Image)

Osteomyelitis of the calcaneus (Axial T1)

The inflammatory process engulfs the peroneal tendons.
Axial T1 (Fat Image)

Osteomyelitis of the calcaneus (Axial T2)

Axial T2 (Water Image)

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4. Osteomyelitis of the Fourth Metatarsal
A. Radiology Report

Radiology Report

MRI of the Right Foot and Toes:

Comparison is made with 3 phase bone scintigraphy dated 6/14/95, at which time there was increased flow to the right foot
that persisted on the immediate and delayed static images in the region of the metatarsals, particularly metatarsals 3 and 4.
Old conventional radiographs demonstrate a remote healed fibular fracture and injury to the medial collateral complex. On
the current MR examination, extensive dorsal subcutis space swelling and edema is associated with edema in the shaft of the
4th metatarsal, compatible with osteomyelitis and cellulitis. Subtle patterns of edema are noted in the cuboid and cuneiform
metatarsal junctions, particularly in the lateral tarsometatarsal aspect of the foot, where either sterile inflammatory arthritis
producing edema or extension of the inflammatory infection is favored.

Conclusion:

Extensive signal alteration throughout the shaft of the 4th metatarsal, for which direct extension of infection with
osteomyelitis is strongly favored along with extensive dorsal cellulitis. Sterile or infectious edema in the distal intermediate
and lateral cuneiforms and cuboid.

B. Views

Osteomyelitis of the Fourth Metatarsal (Sagittal T1)

Subtle patterns of edema are noted in the cuboid and cuneiform metatarsal junctions, particularly in the lateral
tarsometatarsal aspect of the foot. Extension of inflammatory infection is favored.
Sagittal T1 (Fat Image)

Osteomyelitis of the Fourth Metatarsal (Coronal T2)

Extensive dorsal subcutis space swelling and edema is associated with edema in the shaft of the fourth metatarsal, compatible
with osteomyelitis and cellulitis.
Coronal T2 (Water Image)

Osteomyelitis of the Fourth Metatarsal (Axial T2)

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 Extensive Edema is noted in this water-weighted image.
Axial T2 (Water Image)

5. Lateral Talar Dome Fracture

A. Radiology Report

Radiology Report

MRI OF THE RIGHT FOOT:

Multiple axial, sagittal, and coronal images of the right foot are obtained. In the lateral corner of the talar dome, there is a
detached but nondisplaced osteochondral fragment noted. Extending into the talus from this lesion, which measures 1.2
cm in diameter, is a reticular edema pattern, which involves a majority of the dome of the talus. There is transgression of
the reticular cartilage at the site of this defect and a small amount of fluid is present between the defect and underlying
bone. This fragment is tilted slightly but remains in place in the defect in the superolateral aspect of the talus. This
appearance can be seen with osteochondritis dissecans, may also be posttraumatic in origin. No pattern consistent with
edema is noted throughout the dome of the talus and the talar neck has a normal bone marrow signal pattern. Tendons,
ligaments fascial planes, and musculature about the right ankle and forefoot demonstrate no abnormality.

IMPRESSION:

1. Chronic osteochondral fracture, superior and lateral corner talar dome. The osteochondral fragment measures
1.2 cm in diameter and is in situ, detached but not displaced and transgression of the articular cartilage is
noted.
2. Small effusion tibiotalar joint.

B. Views

Lateral Talar Dome Fracture (Sagittal T1)

Sagittal T1 (Fat Image)

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Lateral Talar Dome Fracture (Coronal T1)

Coronal T1 (Fat Image)

Lateral Talar Dome Fracture (Axial T1)

Axial T1 (Fat Image)

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 Lateral Talar Dome Fracture (Sagittal T2)

Sagittal T2 (Water Image)

Lateral Talar Dome Fracture (Axial T2)

Axial T2 (Water Image)

6. High-Grade Chronic Peroneus Brevis Tear

A. Radiology report

Radiology Report

MRI OF LEFT HEEL:

The tarsal tunnel is intact, with no evidence of mass or tendon injury.

There is a high-grade tear of the inframalleolar peroneus brevis tendon with a slightly hypertrophic component at
the more proximal aspect. Peritendinous fluid is also seen and is consistent with peritendinitis.
Increased T2 signal is seen along the plantar surface of the calcaneus and in the proximal aspect of the plantar
fascia, without any evidence of tendon rupture. The findings are consistent with plantar fascitis, and associated
enthesopathy of the calcaneal insertion.

IMPRESSION:

1. SIGNAL ALTERATION WITHIN THE PLANTAR FASCIA AND PLANTAR CALCANEUS CONSISTENT WITH
PLANTAR FASCIITIS. NO EVIDENCE OF HIGH-GRADE TEAR.
2. HIGH-GRADE CHRONIC PERONEUS BREVIS TEAR.
3. NORMAL TARSAL TUNNEL.

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B. Views

Peroneus Brevis Tendon Tear (Sagittal T1)

There is a high-grade tear of the inframalleolar peroneus brevis tendon with a slightly hypertrophic component at the more
proximal aspect.
Sagittal T1 (Fat Image)

Peroneus Brevis Tendon Tear (Axial T1)

Axial T1 (Fat Image)

Peroneus Brevis Tendon Tear (Axial T2)

Axial T1 (Fat Image)

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 Peroneus Brevis Tendon Tear ( Axial T2)

Axial T2 (Water Image)

7. Chronic Posterior Tibial Tendon Rupture

A. Radiology report

Radiology Report

MRI OF RIGHT ANKLE AND HINDFOOT REGION:

Flatfoot:
Inflammatory change and soft tissue mass from trauma to the deep and superficial fibers of the deltoid ligament
are noted, without complete transection.
A proteinaceous water signal mass is noted about the superficial deltoid complex and follows the anatomic
distribution of the tibialis posterior tendon.
The findings are most compatible with chronic PT rupture and associated peritendinous chronic ganglion-like
collection. The tear is high grade to complete and appears to extend proximally to a level just at the ankle joint or
mortise. Some corrugation of retraction of the PT complex is noted and the distal end of the tendon can be isolated
just behind the malleolus at the level of the proximal talus.
The presence of severe flatfoot strongly raises consideration of concomitant injury to the tibial spring and
calcaneonavicular or spring ligament complex.

CONCLUSION:

Flatfoot:
1. Low grade inflammation about the deltoid complex.
2. Pseudo-mass of either fluid or ganglion about a complete rupture of the PT tendon with proximal PT
retraction, an anatomic distribution described.

B. Views

Posterior Tibial Tendon Rupture (Sagittal T1)

Sagittal T1 (Fat Image)

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Posterior Tibial Tendon Rupture (Axial T1)

Axial T1 (Fat Image

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 CT Scan
CT numbers (Hounsfield units):

A. 1000 = air and +1000 = dense bone

B. These numbers (readings) are translated into a gray scale.
C. The range of CT numbers describes the window width.
D. The center of the gray scale designates the window level.
E. A bone window has a wide window width (2000) and a high window level (300)
F. A soft tissue window has a narrower window width and lower window level.

Image planes:

Axial image: Calcaneal-cuboid JT., talar dome, distal tibial articulation.

Coronal (frontal): middle and posterior subtalar JT., plantar compartments of the FF and MF, talar dome, distal tibial articulation.
Sagittal Image: good for calcaneal Fx's.

Indications:

Provide diagnostic information in region of suspect pathology.

Surgical planning

Uses:

Establish the presence and nature of tumors.

Evaluate trauma (Dislocations/ Fx's of calcaneus, talus, mid-tarsus, stress Fx's).
Note: In old calcaneal Fx's use both windows to evaluate bone & soft tissue.
To diagnosis coalitions and degenerative changes in the tarsus and lesser tarsus. The middle facet is well visualized in the coronal
and axial plane.
Evaluate the subtalar JT. (Coronal CT should now be considered the modality of choice to evaluate this joint.)
For non-invasive clinical investigation of aseptic necrosis, osteoporosis, osteomalacia, and other metabolic bone diseases.
Evaluate unilateral swelling.
Comparison of MRI & CT (see at beginning of MRI section)

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Bone Scan
I. General Information:

A. It is extremely sensitive, however, not highly specific.

B. The Technetium-phosphate complex is incorporated into bone that has increased osteoblastic activity.

II. Types:

A. Tc-99m (MDP) Technetium-99m Methyl diphosphate: bone-imaging radionuclide. (6 hour half-life)

B. Tc-99m (PYP) Technetium-99m Pyrophosphate: Used to determine muscle damage (MI, Electric, Thermal injuries).
C. Tc-99m (HMPAO) Technetium-99m hexamethylpropyleneamineoxime. Used to image inflammatory processes, in particular
osteomyelitis. Selectively labels leukocytes (granulocytes) and is similar to indium - 111. It has similar accuracy, more
convenient to use, requires lower radiation and is capable of imaging low-level inflammation more readily.
D. Gallium-67: Inflammatory imaging radionuclide. Used for neoplasm and Inflammatory disorders.
E. Indium111: Inflammatory radionuclide. This is best for acute infection.

III. Tc-99 (MDP) Triphasic bone scan:

Phase 1 (Blood Flow - radionuclide Angiogram): Evaluates arterial supply. Rapid sequence of pictures as blood flows into area.
Phase 2 (Blood pool image): evaluates arterial blood in capillaries & venous system immediately after phase 1.
Phase 3 (Delayed image): Evaluates regional rate of bone metabolism. 3-4 hours later.
Phase 4 (New & used in diagnosis of active osteo) Taken at 24 hours. Compare the region of interest with a normal area. This ratio
is compared with the same ratio taken from phase 3. If the ratio increases by one whole number it is positive.
Note: Bone scan (skeletal survey) is the procedure of choice in searching for osseous metastatic disease. In a
neurotrophic foot it is better to use bone biopsy and bone culture. Scan is of little value.

IV. Gallium-67:

6-24 hours after injection for chronic infection.

24-72 hours after injection for tumors.
It is very useful for differentiating malignant Vs benign and for delineating the local extent of primary bone tumors.

V. Indium 111:

Better for acute infection, however, it is not widely available, requires technical expertise in its prolonged preparation, has poor
resolution, requires high radiation and when performed alone does not differentiate from infection disorders that alter bone
marrow activity.

VI. Indications for bone scan:

1. Total skeletal scan is good for detection & staging of metastatic disease.
2. Diagnosing malignant Vs benign lesions.

Scan Malignant Benign

Tc99 Diffuse increased No

uptake in increased
adjacent uptake in
epiphysis & these
metaphysis areas

Gallium Marked increase Mild or

except in no
chondroblastoma uptake

3. Differentiating between osteomyelitis and cellulitis.

Condition Tc99 Gallium

Chronic Osteo + -

Cellulitis - +

Acute osteo/septic Arthritis + +

Normal Scan - -

4. Used to determining bone viability. Tc99 is neg. (cold) with atrophic nonunion & Pos. (hot) with hypertrophic reactive
nonunion. Infarct or aseptic necrosis shows neg.

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5. Evaluate Fx's & implants for infection or loosening. Failure to reveal focal uptake excludes Fx. For implants do Tc99 &
Gallium.
a. A pos. Tc99 & a neg. gallium usually indicates loosening, ectopic bone or normal bone.
b. If both are Pos. and congruent (similar size & shape) again this usually indicates loosening, ectopic bone
or normal bone.
c. If both are Pos. and incongruent (tc99 is greater then Gallium) this is consistent with infection.
d. If both are Pos. and incongruent (Gallium is greater then Tc99) this is consistent with bursitis, cellulitis or
other nonosseous problem.
6. Evaluate bone healing after grafting or osteotomy.
a. Pos. = viable graft
b. Neg. = nonviable graft.
7. Selecting biopsy sites
8. Evaluate unidentified pain.

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 Electromyography and Nerve Conduction
Velocity Testing
I. Electromyography
A. Evaluation of the electrical activity (action potentials) produced by muscle cells when activated. Used to detect many different
diseases and abnormalities associated with muscle contraction and function.
B. Often used to detect a state of actual muscle weakness as opposed to weakness due to a mental disorder
C. Procedure
1. A trained technician will first insert a needle (or several needles depending on the size of the muscle being observed)
directly into the patient's muscle
2. The electrical activity of the muscle is then displayed on an oscilloscope for the technician to analyze

3. The patient will often be asked to contract the muscle being observed in order to record the absence or presence of
electrical activity during normal function
4. The electrical activity represented by a waveform should have several observable characteristics

a. Presence
b. Shape
c. Size (Amplitude)
d. NOTE: Nerve conduction velocity testing is usually performed on the patient at the same time as EMG
testing

E. Normal Values
1. Normal EMG values can range from 20 - 50 microvolts and these values will vary depending on the muscle

2. Repetition rate of firing ranges from 7 - 20 Hz and also varies depending on the muscle. Values between 450 and 780
are indicative of motor nerve damage

II. Nerve Conduction Velocity

A. Measures how fast a signal (action potential) travels down a nerve. Abnormal values indicate nerve damage, nerve
demyelination, or nerve destruction.
B. Types of fibers and normal conduction velocities
1. Motor

a. Alpha Fibers: 80 - 120 m/s

b. Gamma Fibers: 4 - 24 m/s
2. Sensory

a. Alpha Fibers: 80 - 120 m/s

b. Beta Fibers: 33 - 75 m/s
c. Delta Fibers: 3 - 30 m/s
d. Group C Fibers: 0.5 - 2 m/s
NOTE: Normal values may fluctuate from patient to patient. Several factors may affect nerve conduction studies and alter the results
considerably.

C. Variable Factors Affecting Nerve Conduction Velocity

1. Temperature of the nerve being measured (Temperature of the room and any abnormalities affecting patient
temperature at that moment may alter results)
2. Patient's Age (Conduction velocities naturally decline after 30 years of age)

3. Natural anatomic variation in nerve segments

4. Technician Skill, Technique Used, and Operator Error (Kimura, 1984)

D. Procedure

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1. Several electrodes are attached to an area on the patients skin adjacent to the path of the nerve or nerves being
studied
2. A low voltage electrical pulse (similar in nature to an action potential being delivered to the nerve) is administered to
the patient
3. If a motor nerve is being studied the patients muscle will contract in response to the stimuli

4. To measure sensory nerves the stimulation electrodes will be placed at an area of distally and the recording electrodes
will be placed proximal. (Toes distal and ankle proximal for sensory nerves in the foot)
5. The time it takes for an impulse delivered to travel down the patient's nerves to the receiving electrode is then
measured and reported back to the technician
NCV procedure:

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Classification of Ulcerations
I. Wagner Ulceration Classification

The Wagner system assesses ulcer depth and the presence of osteomyelitis or gangrene by using the following grades:

grade 0 (pre-or post-ulcerative lesion)

grade 1 (partial/full thickness ulcer)

grade 2 (probing to tendon or capsule)

grade 3 (probing to bone)

grade 4 (partial foot gangrene)

grade 5 (whole foot gangrene)

II. UT Ulceration Classification System

The UT (University of Texas) system assesses ulcer depth, the presence of wound infection, and the presence of clinical signs of
lower-extremity ischemia. This system uses a matrix of grade on the horizontal axis and stage on the vertical axis. The grades of the
UT system are as follows:

grade 0 (pre-or post-ulcerative site that has healed)

grade 1 (superficial wound not involving tendon, capsule, or bone)

grade 2 (wound
0 1 2 3 penetrating to
tendon or capsule)
pre-or post- superficial wound wound penetrating wound penetrating
ulcerative site not involving to tendon or capsule bone or joint grade 3 (wound
that has healed tendon, capsule, or penetrating bone or
bone joint).

Within each wound

grade there are
four stages:
Stage
stage A (clean
wounds)
A clean wounds clean wounds clean wounds clean wounds
stage B (non-
ischemic infected
wounds)
B non-ischemic non-ischemic non-ischemic infected non-ischemic infected
stage C (ischemic
infected wounds infected wounds wounds wounds
non-infected
wounds)

stage D (ischemic
infected wounds)

C ischemic non- ischemic non- ischemic non-infected ischemic non-infected

infected wounds infected wounds wounds wounds

Grade

D ischemic infected ischemic infected ischemic infected ischemic infected

wounds wounds wounds wounds

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 III. UT Diabetic Foot Risk Classification

University of Texas Diabetic Foot Risk Classification System:

Click Here to view an in depth UT Foot Risk Classification

UT Diabetic Foot Classification System

The University of Texas Diabetic Foot Classification System

Category 0 Category 1a Category 2a Category 3a

No Neuropathy, Neuropathy History of

Pathology No Deformity with Deformity Pathology
Patient diagnosed with diabetes Protective sensation absent by Protective sensation absent Protective sensation absent
mellitus Semmes Weinstein test

Protective sensation intact by Semmes ABI > 0.8 and toe systolic pressure > ABI > 0.8 and toe systolic pressure > 45 mm ABI > 0.8 and toe systolic pressure > 45 mm Hg
Weinstein test 45 mm Hg Hg

Ankle-brachial index (ABI) > 0.08 and No history of ulceration History of neuropathic ulceration No history of neuropathic ulceration
toe brachial index > 0.45 mm Hg

Foot deformity may be present No history of Charcot's joint No history of Charcot's joint History of Charcot's joint

No history of ulceration No foot deformity Foot deformity present Foot deformity present

Possible Treatment Possible Treatment Possible Treatment Possible Treatment

Shoe accommodations Same as category 0 plus: Same as category 1 plus: Same as category 2 plus:

Patient education
Follow up 6 to 12 months
Possible shoe gear accommodation
Quarterly visits to assess shoe gear
and monitor for signs of irritation
Follow up 3 to 4 months
Pedorthist/orthotist consultation for possible Pedorthist/orthotist consultation for possible custom-
custom-molded/ extra-depth shoe molded/ extra-depth shoe accommodation
accommodation
Possible prophylactic surgery to alleviate foot deformity
Possible prophylactic surgery to alleviate foot
deformity
More frequent visits may be indicated for monitoring

Follow up 2 to 3 months
Follow up 1 to 2 months

Category 4A Category 4B Category 5 Category 6

Neuropathic Acute The Infected The Ischemic

Wound Charcot's Foot Diabetic Foot Limb
Protective sensation absent Protective sensation absent Protective sensation may be present Protective sensation may not be present

ABI > 0.8 and toe systolic pressure > Hg ABI > 0.8 and toe systolic Infected wound ABI < 0.8 or toe systolic pressure < 45 mm Hg or pedal
45 mm Hg pressure > 45 mm Hg transcutaneous oxygen present tension < 40 mm Hgtension
< 40 mm Hg

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Foot deformity normally present Non-infected neuropathic ulcer may Charcot's joint may be present Ulceration may be present
be present

No Charcot's joint present Charcot's joint present Possible Treatment Possible Treatment

Possible Treatment
Same as category 3 plus:
Pressure reduction program instituted
Wound care program instituted
Possible Treatment
Same as category 3 plus:
Pressure reduction program
instituted
Thermometric and radiographic
monitoring
Debridement of infected, necrotic tissue and/or Vascular consult, possible revascularization
bone as indicated
If infection present, treat as in Category 5. Vascular
Possible hospitalization, institute antibiotic consultation with control of sepsis
regimen
Medical management

If ulcer present, same treatment as

category 4A

a Categories 1-3 contain risk factors for ulceration; categories 4-6 contain risk factors for amputation

Prioritize Infection Vs. Ischemia

In general, if there is no rapidly ascending infection (no aggressive ascending cellulitis, no deep-space abscess), leave the wound alone and
get a stat vascular consult. If infection is acute and ascending then infection takes priority. Debride the wound first and then get the area re-
vascularized.

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SVS WIFI Classification System
(new on ABFAS)
I. Lower Extremity Threatened Limb Classification System (WIFI):

A. The SVS (Society for Vascular Surgery) has developed a new lower extremity threatened limb classification system based on Wound, Ischemia, and foot Infection
(WIfI).

B. After grading each category, a physician can then clinically stage the affected limb to estimate the risk of amputation at 1 year. It can also standardize outcome
comparisons for accurate analysis of the increasing numbers of therapies.

C. The system is intended for any patient with a diabetic foot ulceration, non-healing foot ulcer present for 2 or more weeks, foot/lower extremity gangrene, or ischemic
rest pain. It is not meant for patients with acute ischemic emboli, trauma, non-atherosclerotic disease such as vasospastic disorders or pure venous ulcers.

D. This classification basically merges portions of 3 other classification systems into a single concise system.

1. The Fontaine and Rutherford Systems is used to classify risk of amputation and likelihood of benefit from revascularization. It has two subcategory
groups: ischemic rest pain and tissue loss.

2. The Infectious Disease Society of America (IDSA) clinical classification works well for infection and strongly correlates with amputation risk but does
not address wound type or perfusion status.

3. The existing major wound classification systems (Wagner, UT (University of Texas) system) are primarily ulcer classifications, and generally do not
distinguish ulcers from gangrene and lack adequate assessment of perfusion.

E. Wound category accounts for the degree of tissue loss

F. Ischemia category assesses perfusion status to the foot using objective hemodynamic indices. Toe pressure measurement is preferred due to calcified vessels or non-
compressible ABI's often found in diabetics and end stage renal disease.

G. Foot Infection category describes the foot infection if present.

H. After calculating the WIFI score a physician then uses the classification system to asses the clinical stage 1-5 (with stage 5 being an unsalvageable foot). The physician
can then estimate the risk of major amputation at 1 year and the benefit or requirement for revascularization.

1. The stages are derived from a grid of 64 theoretically possible outcomes assigned by a 12 member expert group using a Delphi consensus method.

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 a. Estimated risk of amputation at 1 year for each combination

fI = foot infection; I, ischemia; W, wound

b. Estimated benefit of/requirement for revascularization (assuming infection is controlled)

fI, foot infection; I, ischemia; W, wound

c.

Stage 1: Amputation risk: very low

Stage 2: Amputation risk: low

Stage 3: Amputation risk: moderate

Stage 4: Amputation risk: high

Stage 5: Amputation risk: Unsalvageable foot

To view a discussion of the WIFI system Click Here

The SVS has an interactive practice guidelines app which contains the 2016 diabetic foot guidelines.

Click here for more information about the App.

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Angiosomes
I. General Information:

A. Angiosomes divide the body into three-dimensional anatomic vascular regions supplied by specific arteries and drained by specific veins.

B. There are at least 40 angiosomes in the body

C. Angiosomes are interconnected by anastomotic arteries or reduced caliber choke vessels which can supply blood to an adjacent Angiosome

D. Angiosomes generate multiple pathways to augment blood supply to ulcerations/wounds

E. Angiosomal distribution should be considered in any surgery on a diabetic foot.

F. Understanding angiosomes and their vascular connections provides;

1. A basis for designing incisions and tissue exposure that preserve blood flow for the surgical wound to heal.

2. Allows prediction of whether a given amputation will heal.

3. Helps guide the vascular surgeon in choosing the bypass or endovascular procedure that has the best chance of healing existent ischemic ulcers.

G. Doppler evaluation of these connections can map the existing vascular tree and the direction of flow.

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II. Lower Extremity Vascular Anatomy:

III. Angiosomes of the foot and ankle:

A. There are six angiosomes in the foot originating from three major arteries in the lower leg (posterior tibial, anterior tibial/dorsalis pedis,
and the peroneal arteries)

1. The three branches of the posterior tibial artery each supply distinct portions of the plantar foot.

2. The two branches of the peroneal artery supply the anterolateral portion of the ankle and rear foot.

3. The anterior tibial artery supplies the anterior ankle, and its continuation (the dorsalis pedis artery) supplies the dorsum of the foot.

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P a g e 174 | 368
PART 5:
NEOPLASMS
TUMORS &
MASSES

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Bone Tumors
I. Three Types of Lytic Destruction Patterns

A. Geographic

1. Least aggressive pattern

2. Indicative of slow growing lesion
3. Uniquely well-defined sclerotic margin that is separated from surrounding bone
4. Usually benign lesions such as giant cell tumors, bone cysts, and enchondromas
5. Short zone of transition from tumor changes to regular bone

B. Moth-Eaten

1. Lacks a definitive shape

2. Faster growth than geographic pattern which indicates malignancy
3. Seen more commonly in cancellous bone
4. Multiple small lesions lacking definitive shape
5. These lesions have less well-defined sclerotic margins
6. Long zone of transition from abnormal to normal bone

C. Permeative

1. Usually seen in cortical bone

2. Aggressive lesions with very rapid growth potential suggesting malignancy
3. Less well-defined margins not easily separated from surrounding normal bone
4. May be imperceptibly merged with uninvolved segment
5. Long zone of transition from abnormal to normal bone

II. Trabecular Patterns of Some Bone Tumors

A. Giant Cell Tumor - delicate, thin

B. Chondromyxoid Fibroma - coarse, thick
C. Aneurysmal Bone Cyst - delicate, horizontal
D. Non-ossifying Fibroma/Fibrous Cortical Defect - lobulated "soap bubble" appearance
E. Hemangioma - striated, radiating

III. Periosteal Reactions of Bone Tumors

A. One layer of periosteum laid down against and separated from cortex solitary bone cyst
B. Multiple layers of periosteum - osteosarcoma (osteogenic sarcoma), Ewing's
C. Radiating spicules (starburst) - osteosarcoma
D. Hair on end radiating spicules - Ewing's sarcoma
E. Triangular elevation of periosteum - Codman's triangle as seen below:

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IV. Position of Lesion in Transverse Plane (Refer to Pocket Pod)

A. Central: Within the medullary canal

1. Enchondroma, solitary bone cyst, and fibrous dysplasia

B. Eccentric: Arising from one side of the central axis of the bone

1. Giant cell tumor, osteosarcoma, chondrosarcoma, fibrosarcoma, chondromyxoid fibroma

C. Cortical: Arising in or near the cortex

1. Non-ossifying fibroma, osteoid osteoma

D. Periosteal: Arising within the periosteum

1. Periosteal sarcoma, osteochondroma

V. Common Tumor Locations Within Bone

A. Tumors of Diaphyseal Bone

1. Ewing's Sarcoma
2. Multiple Myeloma
3. Osteoid Osteoma
4. Osteoblastoma
5. Fibrous Dysplasia
6. Fibrosarcoma
7. Eosinophilic granuloma

B. Tumors of Metaphyseal Bone

1. Osteosarcoma
2. Enchondroma
3. Solitary (Unicameral) Bone Cyst
4. Aneurysmal Bone Cyst
5. Osteochondroma
6. Chondrosarcoma
7. Non-Ossifying fibroma
8. Chondromyxoid Fibroma
9. Giant Cell Tumor (Children before
plate closure)

C. Tumors of Epiphyseal Bone

1. Chondroblastoma
2. Intraosseous Ganglion
3. Hemangioma
4. Giant Cell Tumor (Adults after
plate closure)

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VI. Characteristics of Malignant Lesions

A. Cortical destruction
B. Poorly defined margins suggesting an aggressive lesion
C. Codman Angle or lamellated "onion skin" periosteal reactions
D. Divergent "sunburst" or spiculated "hair on end" periosteal reactions
E. Moth-eaten or permeative appearance
F. Soft tissue invasion with swelling and occasionally ossification
G. Metastases (most commonly to the lungs)

VII. Lab Tests for Possible Malignant Bone Tumors

A. CBC
B. Calcium - Increased when bone is being destroyed or remodeled (8.5-10.5)
C. Alkaline Phosphatase (ALP) - Increased with osteoblastic activity (30 - 120)
D. Acid Phosphatase - High levels seen with prostate cancer (.1 - .6)
E. Total Protein - Increase seen in multiple myeloma (6 - 8)
F. Bone biopsy is still the gold standard of diagnostic tools and the most definitive test
G. See Enneking classification system also
H. Other tests to consider include the following:

1. Arteriography - Not used to determine malignancy. Used when a concomitant limb salvage procedure is required.
2. CT scan - Best for visualizing cortical integrity of the bone and lesion definition
3. MRI - Best for visualizing the non-mineralized matrix and marrow involvement
4. Bone Scintigraphy (Bone Scan) - Best imaging modality in identifying an infectious process

VIII. Cartilaginous Tumors of Bone

A. Enchondroma (Benign tumor of hyaline cartilage)

1. Seen in patients ages 10 - 35 years old

2. Well defined margins
3. Usually asymptomatic (If painful consider progression of the lesion to malignant chondrosarcoma)
4. Most common benign tumor of the phalanges (50% found in the hands/fingers)
5. Lesions are usually centrally located within the medullary cavity of metaphyseal bone
6. Consider Ollier's disease for patients with multiple enchondromas and severe deformities
7. Consider Maffucci's Syndrome for patients with multiple enchondromas and soft tissue hemangiomas

B. Periosteal (Juxtacortical) Chondroma

1. Presents as a "crater-like" cortical erosion usually in metaphyseal bone

2. Seen in males more commonly 2:1
3. Often present with dactylitis of the toes
4. More commonly seen in the first three decades of life
5. Most frequently seen in the femur and the humerus
6. May present as a "buttress" periosteal reaction

C. Chondroblastoma

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 1. Seen in 15 - 30-year-old age group
2. Most common location in the body is the knee
3. Most common location in the foot is the calcaneus
4. Typically appears as a juxta-articular well defined lytic lesion of epiphysis

D. Chondromyxoid Fibroma

1. Seen most commonly in the first two decades of life (Growth plates)
2. Lesions are usually oval shaped and located in metaphyseal bone
3. See course trabeculation
4. Seen more commonly in males (2:1)
5. Most frequently seen in the proximal tibia (or the talus amongst pedal bones)
6. Lesions are eccentrically located and frequently seen with a "buttress" periosteal
reaction

E. Osteochondroma

1. The most common benign bone tumor of the human skeleton

2. Most frequently seen in the 1st and 2nd decades of life
3. Seen most frequently in the knee or distal femur (also the small tubular bones of the foot)
4. The lesions most commonly appear to be pedunculated "mushroom-shaped" exostosis where the cortex of the lesion is commonly seen to expand into the
cortex of the underlying bone
5. The lesion typically points toward the diaphysis of the involved bone and away from the nearest joint
6. Lesions can also appear to be sessile or "plateau-like" (highest risk of malignant transformation)
7. Seen more commonly in males (2:1)
8. Most frequent site involved is metaphyseal bone

F. Chondrosarcoma

1. Can arise from enchondroma, periosteal chondroma, and osteochondroma

2. Slow growing malignant tumor of cartilage
3. Usually seen in patients from age 30 - 60 years old (Rare in children)
4. 3rd most common primary malignant bone tumor in the body
5. Most common malignant bone tumor of foot (Most commonly seen in the calcaneus)
6. Typically seen as a radiolucent lesion centrally located in the medullary cavity of metaphyseal bone
7. Poorly defined margins with endosteal "scalloping"
8. Matrix may appear to be "stippled", "fluffy", or appear to have "rings and arcs" due to ongoing calcification within the lesion
9. Most commonly seen to have metastases to the lungs (CXR)
10. Excise with a wide margin of surrounding normal bone (May still require amputation)

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IX. Bone Forming Tumors

A. Osteoid Osteoma

1. 75% occur between ages 5 and 25

2. More commonly seen in males (2:1) than females
3. Most common location in the body is the proximal femur then diaphysis of tibia
4. In the foot the talus is the most commonly involved pedal bone
5. Patient typically complains of an aching pain that is worse at night.
6. Many patient experience complete relief of this pain by taking aspirin
7. Round lesion with a radiolucent centralized nidus no larger than 1 cm commonly found in the cortex
8. Suggested treatment is to have patients continue with pain relief via NSAID use and monitor the lesion for
signs of ossification (healing) in 3 - 6 months

B. Osteoblastoma

1. Seen in young adults - usually 2nd - 3rd decades

2. Round lesion with a lucent centralized nidus larger than 1 cm commonly found in the cortex

C. Osteosarcoma (Osteogenic Sarcoma)

1. Second most common primary bone lesion in the body next to multiple myeloma
2. Seen most commonly in the 2nd - 3rd decades
3. The knee is the most common location (65%) followed by the femur then tibia
4. Only 1% occur in pedal bones (most commonly the tarsal bones)
5. Can develop from Paget's disease
6. May involve periosteal reactions that are commonly associated with malignant lesions such as "sunburst" or "hair on end" reactions
7. Cortical break through with destruction is commonly seen
8. Frequently originates from the metaphysis of long bones
9. Lifted periosteum can result in appearance of a Codman's triangle on radiographs
10. Seen in males twice as often as females
11. Moth-eaten or permeative internal bone destruction patterns are commonly seen

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X. Tumors of Connective Tissue

A. Non-Ossifying Fibroma

1. Seen in 1st - 2nd decades of life

2. Most frequently seen in the metaphyseal region
3. These lesions appear to be multiloculated (bubbled appearance) and are eccentrically located
4. Lesions tend to have a sharply demarcated with a thick sclerotic border
5. Internal cortical "scalloping" is a hallmark feature for diagnosis
6. Very large Non-Ossifying fibromas have been associated with pathologic fractures
7. May convolute into a bone island over time

B. Fibrosarcoma

1. Malignant mesenchymal tumor of fibrous connective tissue

2. 67% appear in medullary bone of the knee, femur, and hip
3. Appears more commonly in males ages 35 - 55 years old
4. Treatment involves wide surgical resection and chemotherapy

XI. Locally Aggressive Tumors

A. Giant Cell Tumor (Osteoclastoma)

1. 75% occur in male patients ages 15-40 years old

2. Seen most commonly in the 3rd - 4th decades (skeletally mature patients)
3. Most common location is diaphyseal bone, but they have also been seen crossing over into the metaphysis and
epiphysis eventually ballooning under the subchondral bone plate
4. These rapidly expanding radiolucent lesions typically have a "soap bubble" appearance on radiographs and do not
have a visible matrix
5. Presence of a "fallen fragment sign" within the lesion indicates possible pathological fracture
6. In the foot they are most commonly seen in the small tubular bones (phalanges and metatarsals)

XII. Tumors of Vascular Origin

A. Hemangioma

1. Most commonly seen in the 4th - 5th decade of life

2. Has a characteristic "spoke wheel" periosteal reaction on radiographs

B. Glomus Tumor

1. Most commonly seen in the 4th - 5th decade of life

2. May present as a lytic lesion of the distal phalanx
3. May appear clinically as a purple/blue soft tissue mass

XIII. Tumor and Tumor-Like Lesions of Bone - Unknown Origin

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A. Solitary Bone Cyst (also known as simple or unicameral bone cyst)

1. The most common fluid filled bone cyst

2. Seen in 1st - 2nd decades
3. Seen more commonly in males (2:1)
4. Most commonly involved pedal bone is the calcaneus (neutral
triangle)
5. Typically seen in metaphyseal bone centrally located
6. May display "fallen fragment sign" indicating pathologic fracture with
very large lesions

B. Aneurysmal Bone Cyst

1. Most commonly seen in patients age 5 - 20 years old

2. Patients may present clinically with a rapid onset of pain and limited range of motion
3. Rapidly expanding lesion that may appear to be "balloon-like"
4. Horizontal trabeculation can usually be seen within the lesion
5. Lesions are typically the result of trauma and therefore usually filled with blood
6. Difficult to differentiate from malignant lesion due to it's aggressive appearance

C. Ewing's Sarcoma

1. Typically seen in patients age 5 - 30 years old

2. Seen in males more commonly (3:2)
3. Lesions are typically located in diaphyseal bone and involve cortical destruction
4. Lesions may present as having an "Onion skin" (lamellated) or "hair on end" periosteal reaction
5. Most commonly affected pedal bone is the calcaneus
6. Has a very high rate of metastasis and a generally poor prognosis
7. Commonly seen with an adjacent soft tissue mass

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D. Fibrous Dysplasia

1. Replaces normal bone with fibrous bone tissue

2. Typically found in diaphyseal bone
3. Occurs most commonly in children ages 3 - 15 years old
4. Has a characteristic "ground glass" appearance on radiographs
5. Significant boney deformities can be seen and pathological fractures may occur

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Malignant Melanoma
I. Background
A. Definition: Malignant Melanoma arises from melanocytes and are the most malignant of skin cancers. Melanocytes have dendritic processes, are of epidermal germ cell
origins and reside in the basal layer of the epidermis. They function to produce "sun-protective" melanin pigment that guards the underlying living cells on the basal layer of
the epidermis from the mutagenic effects of UV radiation.
B. Incidence among men and women appear equal, but lower extremity melanomas are more common in females
C. Majority present between 30 - 60 years of age
D. Anatomic sites
1. Sun exposed areas
2. "BANS" area, (back, arms, neck, scalp) B A N S
E. Diagnostic signs
1. Focus on size, shape and contour, color, location and duration of a lesion. The ABCD Criteria (Asymmetry, Border, Color, Dimension) are commonly
used.
2. Presence of ulceration, irregularity in the margin, bleeding.
3. Palpation of regional lymph nodes and major internal organs should be routine
4. In foot, plantar and periungual lesions should be suspected for malignant melanoma until proven otherwise
5. Any lesion on the foot that is greater than 5 mm in diameter, heterogeneous in color, or displaying an irregular or notch border should be biopsied if it
has not been present since birth.
6. Melanoma grows in a radial (horizontal, or latent) phase, and an invasive (vertical) phase. In the horizontal or radial growth phase the lesion appears
macular, while the vertical growth phase appears with surface elevation (papular or nodular) and is associated with a more aggressive tumor. Poor prognostic
indicators include lesions displaying a whitish or amelanotic color, tumor regression (notched border), progressive nodularity (consistent with deeper invasion of
the dermis), change in size or shape, ulceration, hemorrhage, pain, or pruritus, should be considered malignant and treated after accurate identification.
7. Poor prognostic indicators include lesions displaying a whitish or amelanotic color, tumor regression (notched border), progressive nodularity
(consistent with deeper invasion of the dermis), change in size or shape, ulceration, hemorrhage, pain, pruritus. should be considered malignant.
II. Clinical Histologic Types of Melanoma
A. Superficial Spreading Melanoma (SSM)
1. May develop on any portion of the body with peak incidence around 5th decade
2. This type comprised 70% of cutaneous melanomas and is the most commonly encountered form of melanoma
3. Variegated (several colors) color pattern and lesion is elevated. Classic SSM displays the "red, white, and blue" of advanced
malignancy showing tumor regression. These are very common on the trunks of males.

B. Lentigo Malignant Melanoma (LMM)

1. Predominance on BANS regions of the body

2. It is the most benign of the four major types of melanoma and slowest growing legion

3. Median age is 70 years

4. It is more tan in color and not as nodular as Superficial Spreading Melanoma

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 C. Nodular Melanoma (NM)

1. Most malignant of the melanomas

2. Comprises 12% of cutaneous melanomas

3. Seen more commonly in males, approx age 50

4. Uniformly blue, black, or dark brown

5. Nodular

6. Ulceration is not uncommon

7. Develop quickly so there is no radial growth phase

D. Acral Lentiginous Melanoma (ALM): Predilection for soles, palms, nail beds

1. Most commonly found in the soles, palms, oral mucosa, and nail beds

2. Hutchinson's sign

• Periungual extension of brown-black pigmentation from longitudinal melanonychia onto the proximal and
lateral nailfolds, is an important indicator of subungual melanoma. However, experience has demonstrated
that Hutchinson's sign, although valuable, is not an infallible predictor of melanoma. Periungual
pigmentation is present in a variety of benign disorders and, therefore, may lead to overdiagnosis of
subungual melanoma. Periungual hyperpigmentation occurs in at least one nonmelanoma skin cancer,
Bowen's disease of the nail unit. Hyperigmentation of the nail bed and matrix may reflect through the
"transparent" nailfolds simulating Hutchinson's sign. "Pseudo-Hutchinson's sign" is a phrase coined to
encompass these three simulants of Hutchinson's sign. Each represents a misleading clue to the diagnosis of
subungual melanoma. Total reliance on the (apparent) presence or absence of periungual pigmentation may
lead to overdiagnosis or underdiagnosis of subungual melanoma. All relevant clinical and historical
information, including the presence or absence of periungual pigmentation, must be carefully evaluated in a
patient suspected of having subungual melanoma. Ultimately, the diagnosis of subungual melanoma is
made histologically.

3. Melanonychia striata (Longitudinal black, tan, or brown band in the nail plate)

4. Any new/sudden areas of pigmentation on the hands or feet can be a warning sign

5. More common in patients ages 60 – 70 years old

6. Account for 3.5% of cutaneous melanomas

7. Most common of melanoma in African American and Asian patients
8. Unlike other forms of melanoma it is NOT linked to sun exposure
9. Melanotic Whitlow

• A melanoma beginning in the skin at the border of or beneath the nail

III. Clinical Staging:

Note: The most important determinant of survival rate for malignant melanoma is clinical staging. Survival of a clinical stage I lesion is far more likely than survival of a clinical
stage II lesion, whereas clinical stage III lesions are usually fatal.

A. Stage I: malignant melanoma involves a primary lesion, or one with a local satellite within 5 cm.

B. Stage II: malignant melanoma entails in transit metastasis and regional lymph node involvement (identified by palpable adenopathy or node biopsy).

C. Stage III: malignant melanoma entails distant metastasis. Melanoma can go anywhere in the body, including the choroid of the eye and internal parenchyma.

IV. Pathologic Staging:

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 Note: The microstage of malignant melanoma is determined by the vertical thickness in millimeters (Breslow's classification) and/or the anatomic level of local invasion
(Clark's classification) on histologic examination. The Breslow stage more accurately predicts subsequent behavior of malignant melanoma and has been shown to correlate
better with survival rate.

A. Clark's classification (anatomic level of local invasion)

Level I: Lesion extends into epidermis but does not penetrate basement membrane

Level II: Lesion extends through basement membrane into part of papillary dermis

Level III: Lesion involves all of the papillary dermis and line up against but do not penetrate into the reticular dermis (papillary-reticular interface).

Level IV: Lesion extends into reticular dermis

Level V: Lesion extends into subcutaneous fat

B. IV. Breslow's Classification (Depth of the lesion)

Thickness (mm) 5-year survival rate (%)

0.75 mm or less 83-100
0.76 mm to 1.50 mm 37-90
1.51 mm to 3.5 mm 44-72
> then 3.5 mm 9-55

To view a complete staging and grouping for malignant melanoma Click Here.

Malignant Melanoma Staging and grouping

TNM Staging (NOT ON CURRENT BBN?)

Primary tumor (pT)

• pTX - Primary tumor cannot be assessed

• pT0 - No evidence of primary tumor
• pTis - Melanoma in situ; involves only epidermis (CL I)
• pT1 - Tumor 1 mm or less in thickness; invades papillary dermis (CL II) (or to papillary-reticular dermal interface (CL III) (pT1b can mean that
either the melanoma is £ 1 mm with ulceration or is <1 mm but is Clark level IV or V with or without ulceration.)
• pT2 - Tumor 1.01-2 mm in thickness

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 • pT3 - Tumor 2.01-4 mm in thickness
• pT4 - Tumor greater than 4 mm in thickness and/or invades subcutaneous tissue (CL V) and/or satellite(s) within 2 cm of the primary tumor
• pT4a - Tumor greater than 4 mm in thickness with or without ulceration
• Any Ta - Not ulcerated
• Any Tb - Ulcerated

Regional lymph nodes (N)

o NX - Regional lymph nodes cannot be assessed

o N0 - No regional lymph node metastasis
o N1 - Metastasis in 1 lymph node
o N2 - Metastasis in 2-3 lymph nodes or spread of melanoma in the skin toward a nearby lymph node area
o N3 - Metastasis in 4 or more lymph nodes or spread of melanoma in the skin toward a lymph node area and into the lymph node(s)
o Any Na - Melanoma only seen under the microscope
o Any Nb - Melanoma in the lymph node visible to naked eye

Distant metastasis (M)

▪ MX - Distant metastasis cannot be assessed

▪ M0 - No distant metastasis
▪ M1 - Distant metastasis
▪ M1a - Metastases to skin or subcutaneous (below the skin) tissue or distant lymph nodes
▪ M1b - Metastases to lung
▪ M1c - Metastases to other organs

AJCC (American Joint Committee on Cancer) Groupings

▪ Stage 0 (pTis, N0, M0): The melanoma is in situ, meaning that it involves the epidermis but has not spread to the dermis (lower layer).
▪ Stage IA (pT1a, N0, M0): The melanoma is less than 1 mm in thickness and Clark level II or III. It is not ulcerated, appears to be localized in the
skin, and has not been found in lymph nodes or distant organs.
▪ Stage IB (pT1b or pT2a, N0, M0): The melanoma is less than 1 mm in thickness and is ulcerated or Clark level IV or V, or it is 1.01-2 mm and is
not ulcerated. It appears to be localized in the skin and has not been found in lymph nodes or distant organs.
▪ Stage IIA (pT2b or pT3a, N0, M0): The melanoma is 1.01-2 mm in thickness and is ulcerated, or it is 2.01-4 mm and is not ulcerated. It appears
to be localized in the skin and has not been found in lymph nodes or distant organs.
▪ Stage IIB (pT3b or pT4a, N0, M0): The melanoma is 2.01-4 mm in thickness and is ulcerated, or it is thicker than 4 mm and is not ulcerated. It
appears to be localized in the skin and has not been found in lymph nodes or distant organs.
▪ Stage IIC (pT4b, N0, M0): The melanoma is thicker than 4 mm and is ulcerated. It appears to be localized in the skin and has not been found in
lymph nodes or distant organs.
▪ Stage III (any pT, N1-3, M0): The melanoma has spread to lymph nodes near the affected skin area. No distant spread is present. The thickness of
the melanoma is not a factor, although it is usually thick in people with stage III melanoma.
▪ Stage IV (any pT, any N, any M1): The melanoma has spread beyond the original area of skin and nearby lymph nodes to other organs, such as
the lungs, liver, or brain, or to distant areas of the skin or lymph nodes. Neither the lymph node status nor thickness is considered, but in general,
the melanoma is thick and has spread to lymph nodes.

V. Biopsy Consideration

Note: As podiatrists it is our duty to provide patients with a timely/accurate diagnosis via the appropriate biopsy procedure and the appropriate consultations
such as a referral to an oncological surgeon.

Note: Clinical stage I lesions can be definitively excised by the podiatric surgeon. Clinical stage II lesions have regional lymph node involvement and therefore
will require lymph node dissection by a general or vascular surgeon who is familiar with malignant melanoma.

A. Ideally, an excisional biopsy should include 1 to 3 mm of normal appearing skin around the lesion and must include subcutaneous fat (full-thickness skin). The biopsy
should also be made through the most malignant appearing portion of lesion and oriented in a fashion that will allow the biopsy wound to be excised in toto when subsequent
definitive surgery is performed.

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 1. Lesions under 2 cm can be done under local by the following method:

a. Make two semi-elliptical incisions.

b. Dissection from proximal to distal to decrease potential spread of tumor.

c. Dimensions should be (3:1 length:width)

d. Depth should be full-thickness (includes the subcutaneous fat)

e. The proximal normal margin of skin should be marked with a suture for pathological orientation.

2. Complete excision of lesions over 2 cm in diameter will not be possible without creating a large defect. In these cases a punch biopsy or incisional biopsy
should be performed.

VI. Treatment

Note: The most definitive treatment of malignant melanoma is surgical excision.

A. Definitive treatment is based on clinical and pathological assessment and involves the following:

1. Chest x-rays and a constitutional evaluation are required since malignant melanoma may exist as a systemic disease.

2. Oncological consultation for use of chemotherapy prior to surgical excision of the lesion. This is done to decrease the size of the tumor and therefore
minimize the risk of metastasis. Preoperative chemotherapy has been shown to increase the overall survival rates of patients undergoing the procedure.

Guidelines for definitive excision are as follows:

Recommended margin of normal

Melanoma Depth (mm)
appearing skin (cm) around lesion
<0.76 2
0.76 - 4.0 3
> 4.0 5(with excision of underlying deep fascia)

B. Subungual Melanoma

1. The definitive treatment of a subungual melanoma is digital amputation at the level of the metatarsophalangeal joint.

2. Therapeutic lymph node dissection remains somewhat controversial for clinical stage II melanoma, particularly with lesions of Clark's level II and

3. Therapeutic lymph node dissection is recommended for lesions with a Clark's level II - V, (This decision must be made by the oncological surgeon.
Some patients may also receive adjunct chemotherapy depending on prognosis after node dissection.

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Soft Tissue Masses & Tumors
I. General Considerations for Clinical Workup and Treatment of a Soft Tissue Mass

A. Assess nearby skin for pigmentation and texture

B. Assess nearby skin and tissue for uniformity of coloration and changes in color over time

C. Assess lesion for active bleeding or a history of bleeding

D. Assess the mobility of the mass (Generally tumors above the deep fascia are movable and tumors below the deep fascia are fixed in place)

E. Assess patient for any sensory or motor disturbance around the mass

F. Perform a thorough vascular exam (Pulses, temperature, edema, located near large vessel?)

1. May need a vascular consult for angiogram

G. Palpate the popliteal and inguinal lymph nodes

1. If the nodes are hard, fixed, and/or painful consider metastasis

H. Attempt to transilluminate the mass with a penlight (Generally the benign fluid filled cysts will allow light to pass through)

I. Consider using an ultrasound to visualize the soft tissue mass (Document the size)

J. Ancillary Imaging

1. CT scan best to visualize surrounding bone involvement

2. MRI most sensitive tool for detection of soft tissue masses (Consider ordering T1, T2, and STIR images in all planes to best visualize the mass and its
involvement with surrounding structures)

K. Radiography

1. Consider ordering a chest x-rays (15% of soft tissue sarcomas will have metastases to the lungs)

2. X-ray the adjacent osseous structures to check for bone involvement

L. Biopsy is still the gold standard of soft tissue mass identification

Biopsies should be performed by the surgeon who accepts responsibility for the complete surgical management of the patient. Biopsies performed by one surgeon who
then refers the patient to a tumor surgeon may compromise the ideal surgical approach for complete treatment by the subsequent tumor surgeon. Scope of practice varies
throughout the country and throughout the podiatry community. In general, if you are suspicious of a mass, referral to a tumor specialist is recommended. The
following information is presented for educational and exam purposes. If a question has "referral to the appropriate medical specialist" as a choice, that would be
your best response particularly for malignant lesions. However, some questions will not have that choice and then you need to proceed as if you are a podiatrist who
specializes in tumor resection, even if you do not in your practice.

a. Skin Biopsies: The epidermis, dermis and/or subcutaneous tissue should be included in the biopsy.

i. Core needle biopsy can be done in office using a cannulated needle with inner trocar and specimen notch. The specimen is then sent to
pathology for analysis. A fine-needle aspiration sample may also occasionally be sent.

ii. Incisional biopsy is widely considered to be the procedure of choice when dealing with potentially malignant lesions. It is a
segment of the lesion removed for diagnosis only. Incision is made over the mid-portion of the mass in the OR removing a small portion
of the mass for pathological study. This is done to minimize risk of metastasis.

iii. Excisional biopsy with wide margins may be a better option for smaller benign appearing soft tissue masses. It is a completely cut-out
of the lesion for diagnosis and treatment.

iv. A punch biopsy is 2-6 mm of tissue removed for diagnostic purpose

v. A curette consists of fragments of tissue removed using a spoon-shaped bone curette primarily for treatment (warts)

vi. A shave biopsy is a horizontal section of the skin, removed either for diagnosis or treatment.

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 b. Musculoskeletal Tumor biopsy:

i. The main issue is that sarcomas are highly implantable and

the biopsy track needs to be removed with the tumour.

ii. Don’t contaminate new compartments or critical anatomical structures unnecessarily

iii. Needle biopsies are the “industry standard”

iv. If you do an open biopsy, use a vertical incision (easier to re-excise), make sure you
have good hemostasis and if you need to drain, take it out close to or through the wound

v. Talk to the pathologist – some specimens go fresh

vi. Make sure you get enough tissue

vii. Excision biopsies are only performed for small (<5cm) superficial tumors which do

not involve the deep fascia.

M. Musculoskeletal Staging Systems: Staging systems are useful for assigning treatment priorities, and determining the role of adjuvant therapies. No universally
accepted staging system for soft-tissue sarcomas exists. However, in adults, the most commonly used staging system is the Enneking classification system.

II. Types of Soft Tissue Masses

A. Epidermal Inclusion Cyst

1. Precipitated by trauma (Epidermal tissue displaced after a puncture wound produces a subcutaneous mass of keratin)

2. Lesion presents clinically as a firm round subcutaneous

3. Is typically very slow growing

4. These masses are generally not excised unless they become painful

B. Eccrine Poroma

1. A benign neoplasm that is typically composed of tubular (ductal) epithelial cells

2. Presents clinically as an asymptomatic solitary flesh colored nodule 1 - 2 cm in diameter

3. Commonly presents on the plantar aspect of the foot

4. Treatment consists of an excisional biopsy if the lesion becomes painful

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C. Squamous Cell Carcinoma

1. A malignant epithelial neoplasm with predilection for skin and mucous membranes

2. The second most common form of skin cancer on the body

3. Primary cause is cumulative skin damage due to sun exposure

4. Patients at highest risk are older patients with previous diagnosis of actinic keratosis

5. Affects males more commonly than females (3:1)

6. Appears clinically as a superficial flesh colored lesion with telangiectasias

7. Lesions are typically freely movable and may be tender to palpation

8. Most common site for these lesions to appear is the sun exposed areas such as the head and neck

9. Lesions can metastasize depending on depth

10. Treatment is excision with wide margins (95% cure rate) or excision via Moh's surgery (99% cure rate)

D. Basal Cell Carcinoma

1. Most common form of skin cancer on the body

2. Lesions arise from epithelial tissue due to cumulative damage from ultraviolet radiation

3. Seen most frequently on sun exposed skin (Uncommon on the foot)

4. Lesions are slow growing, painless, and generally asymptomatic for patients

5. Clinically the lesion will typically appear as a fixed shiny nodule with a central depression

6. The borders of this lesion commonly appear to be translucent and rolled inward

7. Lesions may also appear to bleed easily and have telangiectasias and crusting present

8. Some subtypes include the following:

a. Nodular: The most common subtype

b. Pigmented Basal Cell Carcinoma: More common in black patients

c. Sclerosing Basal Cell Carcinoma: Waxy appearance resembling a scar. Most prominent telangiectasias. Most difficult to treat

d. Superficial Basal Cell Carcinoma: Scaly appearance similar to psoriasis

9. Metastasis of these lesions is possible but rare and usually due to incomplete excisions

10. Treatment is excision with wide margins (95% cure rate) or excision via Moh's surgery (99% cure rate)

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E. Bowen's Disease (Squamous Cell Carcinoma In Situ)
1. An in situ squamous cell carcinoma involving skin and mucocutaneous junctions
2. Clinically may appear as a nodule with crusting (removal of crust reveals a moist red patch)
3. Histologically the epithelial cells will have a characteristic "windblown" appearance with
haphazardly arranged hyperchromatic cells with irregular nuclei
4. May also appear clinically as keratotic lesion on bottom of foot resembling a heloma dura
5. Treatment is simple excision for small lesions and Moh's surgery for larger lesions

F. Periungual Fibroma (Kernan's Tumor)

1. Benign flesh colored nodules
2. Tends to bleed easily if disturbed but otherwise typically asymptomatic for the patient
3. Usually the nodule can be seen near the nail bed protruding from the nail folds
4. 50% of cases are associated with tuberous sclerosis
5. Other causes include trauma, previous nail surgery, and shoe gear irritation
6. Kernan's tumor or periungual fibroma with tuberous sclerosis
7. Treatment not required unless symptomatic in which case a local excision is performed
8. These lesions have a high recurrence rate after excision

G. Plantar Fibromatosis
1. Firm nodular lesion(s) found on the plantar aspect of the foot
2. These benign lesions are typically composed of fibrous tissue
3. Frequently seen alongside a thickening of the plantar fascia (>4mm) and plantar
fasciitis
4. Most commonly seen in patients 20 - 40 years old
5. Conservative treatment involves the use of orthotics and steroid injections
6. If mass has become invested in the tendon a wide excision is recommended
taking .5 cm of healthy tissue in all directions around the lesion to avoid recurrence
(65% will reappear)

H. Fibrosarcoma
1. Can be encountered in lower extremities but relatively rare in the foot and ankle
2. Lesions typically present as painless small nodular or large irregular masses in the deep fascia
3. These lesions tend to be very aggressive and can easily metastasize (usually to the lungs)
4. Immediate wide excisional biopsy is recommended
5. A Symes amputation or vascular consult for a BKA may be required for cases in which the lesion cannot be reliably extracted
I. Lipoma
1. Most common benign soft tissue mass found in the body
2. Masses are typically soft, movable, and pain free (Patients may experience pain if the mass is compressing a nearby nerve)
3. Lipomas are composed of adipose tissue (mature fat cells)
4. Lipomas have been seen to occur more frequently in obese patients
5. Treatment for these lesions is a local excision with subsequent pathological analysis

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J. Liposarcoma
1. Asymptomatic malignant tumor arising from adipose tissue. In the early stages, a
sarcoma is small and does not produce symptoms. As the tumor grows, it may push
aside normal body structures, causing symptoms. The most common symptom of a
sarcoma is a lump or swelling that may or may not be painful.
2. The 2nd most common soft tissue sarcoma in the body
3. Most commonly seen in patients ages 40 - 60 years
4. Most lesions are located in the deep fascia
5. Treatment for these lesions can vary from a wide excisional biopsy followed by
chemotherapy to amputation of the extremity in advanced cases

K. Ganglion Cyst
1. Most common soft tissue mass found in the foot and ankle
2. Filled with a thick viscous fluid that is normally clear or straw colored
3. These cysts are frequently found to be the result of previous trauma
4. Most frequently found on the dorsum of the foot
5. The freely movable mass is typically soft and non-tender with palpation
6. Cyst forms as a herniation of joint or synovial tissue
7. Complications involve compression of nearby nerves or tendons
8. Baker's cyst is a ganglion cyst found in the popliteal fossa just behind the knee
9. Treatment involves aspiration of the viscous fluid in these soft tissue masses using an 18 gauge
needle (Multiple aspirations may be required due to a very high recurrence rate)

L. Mucoid Cysts (Mucous Cyst)

1. Presents as a small flesh colored ganglion that is soft and painless to palpation
2. Usually located dorsal to the distal interphalangeal joint or near the nail bed
3. They are seen more commonly in the hands than the feet
4. The lesions are fluid filled and therefore will transilluminate with a penlight
5. Typically seen in older patients after age 30 and can commonly exist alongside Hebereden nodes
typically seen in patients with osteoarthritis
6. Treatment is similar to ganglion cyst and involves aspiration of the fluid or excisional biopsy
7. Advanced cases or lesions that have become painful may require an arthroplasty

M. Leiomyoma (Angioleiomyoma)
1. Benign encapsulated tumor arising from smooth muscle
2. Patients will typically complain of an painful area that gets much worse in cold
3. Pain is the result of impingement of the surrounding neurovascular structures
4. These lesions are more common in adults than children and more common in females (2:1)
5. Can present clinically as a single firm flesh colored nodule

N. Rhabdomyoma

1. Rare benign tumor of striated muscle cells

2. Most commonly seen in men ages 25 - 40 years old
3. Most commonly seen in the head and neck (90% of all cases)
4. Excision is treatment

O. Rhabdomyosarcoma
1. Rare malignant tumor arising from skeletal muscle
2. Typically seen in the head and neck regions of children
3. Treatment consists of referral to pediatric oncologist for excision and chemotherapy

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P. Giant Cell Tumor of Tendon Sheath
1. True benign neoplasm of synovial structures
2. Arises from the synovial lining of tendon sheaths
3. These lesions are generally asymptomatic for patients
4. They occur most commonly along the dorsal surface o the foot near the ankle
5. More commonly seen in patients ages 30 - 50 years old
6. 2nd most common tumor of the tendon (after ganglion)
7. Treatment is a wide excision (25% recurrence rate after excision)

Q. Synovial Sarcoma
1. Lesions are typically slow growing but can be very aggressive
2. These lesions are very metastatic and should be treated aggressively
3. They are typically seen in younger patients age 20 - 30 years old
4. The most common site for these lesions is the knee followed by the ankle
5. Treatment typically consists of a radical resection or amputation of the extremity in some cases

R. Schwannoma
1. A lesion arising from the peripheral nerve sheath in the lower extremities
2. These fluctuant lesions are typically slow growing and usually appear on the flexor surfaces
3. These patients tend to have a history of trauma in the area of the lesion
4. Lesions can present with or without pain and can be removed via local excision

S. Neurofibroma
1. Benign, well circumscribed, often non-tender lesions that can often occur in multiples
2. The lesion originates from the spindle cells of peripheral nerves
3. Occurs more frequently in men than women
4. Patients are typically asymptomatic (If pain does occur excision is recommended)
5. Patients with multiple neurofibromas must be examined for presence of neurofibromatosis type I (formerly known as Von Recklinghausen
Disease) These patients have multiple involved organ systems, may exhibit "cafe au lait" spots on the skin, and are at high risk of developing malignant
neurosarcoma
6. Von Recklinghausen Disease ( neurofibromatosis type 1)

T. Hemangioma
1. Most common benign tumor of blood vessels in the foot and ankle
2. Can exist as two types:

a. Capillary (Strawberry) Hemangioma

i. Superficial, painless, and most commonly sound form

ii. Typically are noticed on children in the first 6 months of life

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 b. Cavernous Hemangioma

i. Typically, deeper involving both capillaries and veins

ii. Blue/Purple color lesion may be visible on the skin

iii. Clinically may feel like a "bag of worms" upon palpation

iv. Can become very large or painful and may require excision

v. If excision is warranted then a vascular consult should be ordered

for an arteriogram of the area around the lesion. This is required prior to
excision due to high degree of involvement with the normal foot vasculature

U. Kaposi's Sarcoma
1. Nodules, patches, macules, or plaques ranging in color from red to blue to purple
2. Can appear virtually anywhere on the skin and in the mouth
3. Very high incidence in AIDS patients
4. High incidence in Jewish, Mediterranean, and African males over age 40
5. Lesions are caused by human herpesvirus-8
6. The result of a proliferation of capillaries and connective tissue
7. Treatment consists of checking HIV status and performing a punch biopsy or wide excision

V. Glomus Tumor (Glomangioma/Angiomyoneuroma)

1. Typically they are benign solitary lesions more common in females
2. They typically appear as blueish subungual tumors but can also be red/purple
3. These lesions are usually very painful for the patient and require surgical excision

W. Benign Vascular Tumors

1. Gorham's Disease (Vanishing Bone Disease) Rare skeletal condition characterized by uncontrolled proliferation of thin walled vascular structures
leading to replacement of bone with angiomas or fibromas
2. Hemangioendothelioma

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 a. Vascular tumors associated with an enlarging soft tissue mass

b. Malignant proliferation of the capillaries

c. Most commonly seen in lungs, liver, and skeletal muscle

X. Pigmented Villonodular Synovitis (PVNS)

1. General Information:
A. PVNS is a joint disease characterized by inflammation and overgrowth of the joint lining as well as hemosiderin (iron) build-up inside
the joint. In PVNS the lining of the joint (the synovium), becomes swollen and grows. This growth may harm the bone next to the joint.
The lining also makes extra fluid that can cause swelling and make movement painful. PVNS is idiopathic, it doesn't seem to run in
families or be caused by certain jobs or activities. Surgery can help but, even with treatment, PVNS has a high rate of reoccurrence
(50% or higher). It occurs most commonly in the third and fourth decades of life.
B. Pigmented villonodular synovitis occurs in two forms: localized or nodular and diffuse

I. Localized (Nodular) pigmented villonodular synovitis: When the pain and swelling occurs in just one area of the joint, it is
called localized pigmented villonodular synovitis. This type usually responds well to treatment. It does not show the same
destructive changes as the diffuse form of PVNS. It may cause recurrent hemarthrosis and aspirate may be of normal
color (may not show classic brown color).

II. Diffuse pigmented villonodular synovitis: When the condition involves the entire joint, it tends to be more destructive. This
form is more difficult to treat and is significantly more common than localized pigmented villonodular synovitis. Look for
peri-articular erosions on radiographs. Diffuse mass may be present on exam.

III. Most have hemorrhagic, dark brown synovial fluid.

IV. Biopsy is diagnostic.

2. Pathology:
A. Grossly, pigmented villonodular synovitis appears as a proliferative synovial process with brownish villonodular fronds in the affected
joints.
3. Histology:
A. Histologic characteristics are similar to GCT of tendon sheath.
B. Classic cytoarchitecture consists of subsynovial nodular proliferation of large round, polyhedral, or spindle cells with prominent cytoplasm and pale
nuclei.
C. Phagocytic histiocyte-like cells are also present.
D. Lipid-laden foam cells and multinucleated giant cells are interspersed with hemosiderin-
laden cells that resemble lining cells.
E. Giant cells appear to have phagocytic role.
F. Findings include deposition of iron, foam cells, or giant cells.
G. Histologically, diffuse disease is characterized by a mononuclear stromal cell infiltrate
in the synovial membrane. Hemosiderin-laden macrophages give the characteristic
brown color. Additional cell populations include foam cells and multinucleated giant
cells.

H. Mononuclear stromal cell infiltrate (white arrow) and hemosiderin-laden

macrophages (black arrow).
1. Radiographic findings

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 A. Soft-tissue swelling around joint from effusion and synovial proliferation
B. Dense soft-tissues from hemosiderin deposits
C. Subchondral pressure erosions at margins of joint may occur from hypertrophied synovium
D. May display multiple sites of deossification appearing as cysts
E. No calcifications
F. No osteoporosis
G. No joint space narrowing (until late)
2. MRI Findings:
A. Most characteristic feature of PVNS on MRI is the presence of intraarticular nodular masses of low signal intensity on T1, T2-weighted, and
proton-density-weighted images (due to presence of iron) characteristic of this lesion.
B. Diseased synovium and focal masses may be best demonstrated on T2 images, showing up as a void of signal intensity due to hemosiderin deposition.
C. Hypo-intense signal is also seen on T1 images
D. MRI differential diagnosis:
i. Hemophilic arthropathy
ii. Soft-tissue sarcoma
iii. Fibromatosis
iv. Synovial chondromatosis
v. Septic arthritis
vi. Degenerative arthritis (Displays joint space narrowing and subchondral sclerosis)
vii. Inflammatory arthropathies
viii. Hemorrhagic synovitis
ix. Synovial sarcoma (Mass around, but outside of, joint and frequently calcify).

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Enneking Classification System
A. The Enneking system for the surgical staging of bone and soft-tissue tumors is based on grade (G), site (T), and metastasis (M) and uses histologic, radiologic,
and clinical criteria. The system should be reserved for staging mesenchymal lesions rather than nonmesenchymal (marrow or reticuloendothelial system),
such as lymphomas, multiple myeloma, plasmacytoma, Ewing’s sarcoma, other round cell neoplasms, and metastatic carcinomas. There are separate staging
systems for benign and malignant mesenchymal tumors.
B. Surgical Grade looks at the histologic features of a lesion. A G1 (low-grade lesion) corresponds to Broder’s Grades 1 or 2, with a low risk for distant spread (<
25%). These tumors are characterized by low mitotic rates, low nuclear to cytoplasmic ratio, and limited pleomorphism. G2 (high-grade lesions)- Broder’s
Grades 3 and 4, have a higher incidence of metastasis. They are characterized by mitotic figures, prominent nucleoli, and pleomorphism. Some tumors are
high grade by definition, such as a dedifferentiated chondrosarcoma. The stage of the tumor dictates the extent of surgical resection and margin.
C. Local Extent evaluates clinical and radiographic features. Axial imaging may be used to determine the anatomic confines of the primary tumor and the presence
of metastasis. Local extent refers to the lesions containment in anatomic boundaries of a compartment and determines the approach for surgical procedure and
desired surgical margins. A high-grade lesion is more likely to invade surrounding tissue and indicates a greater risk of local recurrence and metastasis. The
use of adjuvant therapies is then indicated to eradicate tumor cells that would remain after surgical resection.
T0 - A benign tumor that is confined within a true capsule and the lesion's anatomic compartment of origin (such as a benign intra-
capsular, intra-compartmental lesion)
T1- An aggressive benign or malignant tumor that is still confined within its anatomic compartment (an intra compartmental lesion)
T2 - A lesion that has spread beyond its anatomic compartment of origin ( an extra-compartmental lesion)

D. The Enneking staging system for benign musculoskeletal tumors consists of three categories, 1 (latent), 2 (active), and 3 (aggressive). The classification is based
on radiographic characteristics of the tumor host margin. Well-demarcated borders are indicative of latent lesions whereas indistinct borders result from
permeation into host bone and a more aggressive lesion. For benign tumors, local aggressiveness and incidence of recurrence increase with increase in surgical
grade. Metastases are rare for locally aggressive benign lesions but do rarely occur in giant cell tumor and chondroblastoma.

E. The Enneking surgical staging system for malignant mesenchymal tumors looks at the surgical grade (G0, G1, G2), local extent (T0, T1, T2), and presence or
absence of metastasis (M0, M1). It consists of three stages. Stages I and II are based on surgical grade of the tumor and Stage III represents any tumor with
distant metastasis. Each stage is further divided into two subcategories (A, B) based on the local extent of tumor. The stage of the tumor dictates the extent of
surgical resection and margin.

F. Procedures

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PART 6:
OTHER
CONDITIONS
&
DEFORMITIES

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Brachymetatarsia
I. Definition

A. Hereditary anomaly characterized by premature closure of the epiphyseal plate of one or more metatarsals
B. Most commonly affects 4th metatarsal but can affect any or multiple metatarsals.
C. Can be associated with congenital anomalies, Downs syndrome, pseudohypoparathyroidism, poliomyelitis and may be
idiopathic
D. Usually not seen at birth
E. Becomes evident between 4 - 15 years of age

II. Surgical Procedure

Obtain autogenous bone graft from medial upper tibia, fibula, etc.
V-Y skin plasty to reduce tension of skin and to gain length
Z-plasty lengthening of EDL
Provide distal traction to toe by retrograding K-wire
Insert bone graft
Retrograde K-Wire
Avoid stretching tissue and neurovascular structure to toe
Take intraoperative x-rays
Close
Non-weightbearing 2 1/2 months or longer pending radiographic evidence of host-graft consolidation.

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Calcaneal Valgus Foot
I. At birth, the foot lies in an acutely extended position with the dorsal surface of the foot in contact with the anterolateral
surface of the leg.

II. The foot and heel are in a complete valgus position to the point that when the foot is pulled into plantar flexion, the
following are noted:

A. Flexion is limited to the neutral position, maybe slightly beyond.

B. Skin & subcutaneous tissues are stretched tightly due to their contracture - to the point where a tight band is prominent. This
band often appears blanched in comparison to normal surrounding skin.
C. The underlying tendons are not contracted.
D. The heel is in valgus.
E. No deviation of the rearfoot in relation to the forefoot.
F. The foot is fairly flexible & the heel and midfoot can be brought into a corrected varus position.

III. In the normal neonate foot, the foot can only be passively extended to 45 degrees (not to front of leg as in calcaneal
valgus foot). Additionally, passive flexion will result in approximately 50 degrees (not only to neutral or slightly past it).

IV. RADIOLOGIC COMPARISON OF NORMAL FOOT VS. CALCANEAL VALGUS FOOT

NORMAL: The talus sits on top of calcaneus with no overlap of anterior edges of bone. On lateral view, a line bisecting talus will
pass through the superior half of the cuboid.
CALCANEAL VALGUS: The talus is plantarflexed and the talar head overlaps the forward edge of calcaneus. The bisection line
falls plantar to cuboid on the lateral. If deformity very severe, talus may line in a vertical position.
Parents do not usually bring child into office until six to eight months old, (time when the child first stands). A
complete absence of arch and severe valgus foot type is noted. Increased plantar flexion of talus will be visible
on lateral view. Also Kite's angle will be over 35 degrees on dorsal plantar view.

V. Conservative treatment

A. Casting technique
1. Use two layers thickness of webril on tincture of Benzoin.
2. Assistant hold foot from tips of toes in an equinus position with no varus or valgus deviation of forefoot.
3. Apply cast to tips of toes to just above ankle.
4. Mold very well in arch and around heel.
5. Forefoot in plantar flexion and adducted position to correct the talonavicular joint.
6. Take lateral x-rays to confirm reduction.
7. Extend cast above knee.
8. Hold position two weeks in neonate, changing every 3 - 4 days.

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Charcot Joints (Osteoarthropathy)
Charcot arthropathy is a relatively painless, progressive, and destructive disorder, which can occur in single or multiple joints
secondary to underlying neuropathy and concomitant trauma. In Charcot foot, there is a hypervascularity caused by the loss
of normal sympathetic tone on the blood vessels. This leads to hyperemia and increased osteoclastic resorption of bone.
The foot is usually warm & dry, markedly swollen (increased blood flow results in abnormal venous pooling ->
edema) and often deformed. Radiographically it resembles an acute fracture or a severely destructive form of degenerative
arthritis.

I. Causes

A. Central (Upper motor)

• Syphilis (get FTA if suspect this with Charcot foot)
• Syringomyelia
• Meningomyelocele
• Trauma
• Multiple Sclerosis
• Charcot Marie Tooth disease
• Cord compressor or degeneration
B. Peripheral (lower motor neuron)
• Diabetes (can see superimposed osteomyelitis or septic joint)
• Alcoholism
• Infection (T. B., leprosy)
• Amyloidosis
• Pernicious anemia
• Steroids
C. Other
• Disorder called Congenital Indifference to pain
Note: In most cases all three forms of peripheral neuropathy (autonomic, motor and sensory) will be
implicated in the development of a Charcot joint.

II. Pathogenesis of Charcot Joint

Neuropathy
Loss of deep sensation (protective pain sensation)
Loss of proprioception

Ambulation on insensitive joint

Recurrent microtrauma
Possible major

Joint Instability
Malalignment

Joint degeneration and subluxation

Erosion of cartilage, subchondral sclerosis, fracture and
fragmentation

(Charcot Joint)
Joint derangement

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 III. Stages of Charcot Foot Eichenholtz outlined three distinct stages

A. Development:

• Characterized by capsular distention, fragmentation of the subchondral bone and attached articular
cartilage, and debris formation at the articular margins.
• Hypertrophic changes consisting of intra-articular debris and joint mice, and osteochondral fragmentation. Cartilage
debris becomes imbedded in the synovial cavity.
• Bony eburnation, subluxation, fracture, joint effusion, and soft tissue swelling.

B. Coalescence:

• Characterized by absorption of fine debris and fusion of large fragments, which eventually adhere to the adjacent
bones. Sclerosis of the end of bones may be present, occurring as a result of a loss of vascularization that
developed during the first stage
• Subchondral sclerosis (avascular necrosis)
• Periosteal new bone formation, and marginal osteophytes.

C. Reconstruction:

• Reformation of joint architecture takes place. The bone ends and major fragments become rounded and there is a
decrease in sclerosis as a result of re-vascularization.
• Diminished swelling.

The original Eichenholtz staging system lacked correlation between radiographic findings and associated clinical findings. Staging of the
Charcot deformity based solely on radiographic findings is difficult. A more accurate staging can be accomplished when the associated clinical
findings are correlated with radiographic findings.

• In the initial stage of the deformity, the Charcot patient exhibits increased temperature, edema, and redness. Edema and
warmth are profound at this time, and pedal pulses are often bounding. An increase in joint mobility may also be noted on
examination.
• A progressive decrease in skin temperature, edema, and redness occurs as the patient progresses through stages 2 and 3.
The pedal pulses return to normal when the inflammatory cycle ceases. A progressive decrease in joint mobility and increased
stabilization occur as the reconstruction process progresses. The patient who has progressed through all three stages usually has
significant residual deformity or joint instability.

An updated version of the Eichenholtz classification system identifies a pre-fragmentation (or acute inflammatory) stage 0 (zero).
Radiographic evaluation of the stage 0 patient may show simple or comminuted fracture, widening of joint spaces, dislocation, or, in some
cases, normal anatomy. Clinical evaluation of the patient will demonstrate swelling, warmth, and possible joint instability as a result of
weakening of the periarticular structures. Differentiating stage 0 from stage 1 on the basis of radiographic evaluation can be difficult following
an acute injury in the neuropathic patient. Radiographic findings of osteopenia and fracture fragmentation indicate that the condition has
progressed from stage 0 to stage 1.

Classification of Charcot arthropathy into one of four stages by a modified Eichenholtz system

The stages are:

Stage 0: Early or inflammatory – There is localized swelling, erythema, and warmth with little or no radiological abnormalities.

Stage 1: Development – Swelling, redness, and warmth persist, and bony changes such as fracture, subluxation/dislocation, and
bony debris start to appear radiologically.

Stage 2: Coalescence – The clinical inflammatory signs decrease, and radiological signs of fracture healing, bony debris resorption,
and new bone formation occur.

Stage 3: Remodelling – The redness, warmth, and swelling has settled, and bony deformity which may be stable or unstable is
present. Radiographic appearances may show mature fracture callus and decreased sclerosis.

Note: Ankle equinus is one of the biggest deforming forces on the neuropathic foot.

Note: The most common joint to break down by Charcot disease in the foot is the LisFranc's (tarsal-metatarsal)
joint.

Note: Shards of cartilage and bone in synovium is diagnostic of Charcot joint.

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 The most reliable specialized test during the earliest stage of Charcot’s Neuroarthropathy is Triphasic bone
scan (technetium-99m MDP) which reveals significant and impressive uptake in all three phases within the
affected bone 3 to 6 hours following the initial injection.

In cases of suspected osteomyelitis, a labeled white blood cell scan (indium-111 or technetium-99m
hexamethylpropyleneamine oxime [HMPAO]) will demonstrate positive uptake 3 to 6 hours after injection, but
it should not be considered positive until a 24-hour follow-up reading is obtained. A positive indium- 111 or
technetium-99m HMPAO scan should be considered a false positive for osteomyelitis unless positive uptake is
demonstrated at 24 hours. A negative indium-111 or technetium-99m HMPAO scan at 3 to 6 hours essentially
rules out an active, underlying infectious process of bone.

IV. Differential Diagnoses

•Includes various arthritides (gout, osteoarthritis, psoriatic arthritis, rheumatoid arthritis, septic arthritis).
Note: These systemic arthritides do not demonstrate the characteristic stages and non-weight bearing does
not halt the progression. Appropriate serologic tests should be ordered to rule out these arthritides as well as
joint cultures to rule out a pyogenic process.
•Neoplasms

V. Treatment

•Treatment is directed at prevention of further trauma to the joint.

•Avoid weight bearing on the foot and allow healing to occur.
•Once the acute stage has subsided start limited protected weight bearing to prevent the onset of disuse osteoporosis and
potential reactivation of the destructive process.
•Long-term treatment requires protective shoe gear and supportive devices (custom molded shoes).

VI. Surgical considerations

A. Wait until acute inflammatory process subsides

B. Use arthrodesis procedures (use rigid internal fixation)
C. If equinus involved, need to deal with it.

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Charcot-Marie-Tooth Disease
I. General information:

A. An inherited familial neuromuscular disease that effects peripheral nerves and causes slowing of sensory and motor
conduction velocities (NCVs). It is classified as a HMSN (Hereditary Motor and Sensory Neuropathy).
B. CMT is caused by mutations in genes that produce proteins involved in the structure and function of either the
peripheral nerve axon or the myelin sheath.
C. The gene mutations in CMT disease are usually inherited. Each of us normally possesses two copies of every gene, one
inherited from each parent. Most forms of CMT are inherited in an autosomal dominant fashion , which
means that only one copy of the abnormal gene is needed to cause the disease. Other forms of CMT are inherited in
an autosomal recessive fashion, which means that both copies of the abnormal gene must be present to cause the disease.
Still other forms of CMT are inherited in an X-linked fashion, which means that the abnormal gene is located on the X
chromosome.
D. The genes responsible for CMT have been linked to chromosome 1 and 17. It is caused by an abnormality in three myelin
genes
1. Peripheral myelin protein22 (PMP22)
2. Myelin Protein 0 (MPZ)
3. Connexin 32 (Cx32)

II. Classification:

The original Dyck and Lambert classification of CMT1 or demyelinating (HMSN type I, hypertrophic neuropathy) and CMT2 or axonal
(HMSN type II, neuronal type) is still valid. However, the newer classifications are based on the clinical presentation, pathologic
conditions, electrodiagnostic criteria, mode of inheritance, and genetic analysis.

A. CMT1 (hypertrophic CMT)

1. Characterized by a microscopic abnormality called the onion bulb (enlargement of the nerve).
2. Subdivided based on specific gene mutation:

a. CMT1A most frequent (60 to 90%)

b. CMT1B (4-5%)

c. CMT1C (very rare)

B. CMT2 (neuronal or axonal type)

1. Onset of symptoms occurs later without hypertrophy and slightly reduced or normal NCVs.
2. More pronounced distal lower extremity weakness (characteristic "Stork leg" appearance).

C. CMTX (Sex linked)

1. Manifests in the second decade of life with marked deformity developing in the third decade
2. Males are more common and more severe

D. CMT4 (The most severe disability is found in patients with autosomal recessive inheritance of the disease or CMT4)
1. Appear around 8 years of age
2. Profound weakness by the second decade
The earlier the onset the poorer the prognosis
3. HMSN type III (Dejerine-Sottas disease) is sometimes considered a subgroup of CMT4. It is still used to define severe
cases of hypodemyelinating neuropathy of early onset. Many authors consider CMT1 and Dejerine-Sottas disease as
simply variants of different severity of the same disease. It is a severe demyelinating neuropathy that begins in infancy.
Infants have severe muscle atrophy, weakness, and sensory problems. This rare disorder can be caused by a specific
point mutation in the P0 gene or a point mutation in the PMP-22 gene.

III. Evaluation and Diagnosis

A. Look for evidence of muscle weakness in the individual's arms, legs, hands, and feet, decreased muscle bulk, reduced tendon
reflexes, and sensory.
B. Look for evidence of deformities, bilateral pes cavovarus and claw toe deformities.
C. Evaluate each muscle (not as a group) using the polio Foundation rating (0-5).

0 = No muscle activity

1 = Muscle contracts, but no motion

2 = Motion with gravity eliminated

3 = Muscle motion against gravity

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 4 = Movement against mild resistance

5 = Movement against resistance (normal muscle)

D. If CMT is suspected, you may to order electrodiagnostic tests. This testing consists of two parts: nerve conduction studies
and electromyography (EMG).
E. Genetic testing is available for some types of CMT and results are usually enough to confirm a diagnosis. In addition, genetic
counseling is available to assist individuals in understanding their condition and plan for the future.
F. If the diagnostic work-up in inconclusive or genetic testing comes back negative, a nerve biopsy may be performed to confirm
the diagnosis.

IV. Treatment

A. Conservative Treatment

There is no cure for CMT, but physical therapy, occupational therapy, braces and other orthopedic devices, and surgery can
help individuals cope with the disabling symptoms of the disease. Patients with mechanically controllable deformity, slowly
progressing deformity or poor surgical candidates may benefit from conservative treatment.
1. Extra-depth shoes, High-top shoes or boots
2. Accommodative orthotics
3. Light weight plastic AFO's (Ankle Foot Orthoses)
4. Physical and occupational therapy, involves muscle strength training, muscle and ligament stretching, stamina
training, and moderate aerobic exercise.
B. Surgical Treatment
1. General discussion
A. Surgical treatment is individualized by patient. There is no single surgical solution.
B. Distinguishing between fixed and flexible deformity is extremely important.
C. Selection of the surgical procedure is based on multiple factors. The patients age, prognosis,
primary deforming forces, and muscle inventory (Most important).
D. Three principles for a reconstructive surgical approach to CMT or any other progressive
neuromuscular disease have been proposed;

i. All fixed deformities must be corrected.

ii. Muscle balance and function must be restored or at least limited.

iii. Prevent recurrence of the deformity.

2. Types of Deformity
A. Digital Deformity:
i. Claw Toe Stabilization of the lesser digits by arthrodesis of the PIPJ is preferred.
B. Metatarsal Deformity:
i. The first metatarsal is usually in some degree of equinus secondary to the unopposed pull of the
peroneus longus tendon, the effect of which is generally localized to the 1st metatarsal.
ii. It is best treated with a dorsiflexory wedge osteotomy at the base of the first metatarsal.
C. Mid-foot Deformity:
i. When the apex of the deformity is at the mid-foot a dorsiflexory mid-foot osteotomy can be used
(i.e. Japas and Cole procedures)
ii. Japas Procedure:

V osteotomy in the coronal plane made from dorsal to plantar through the mid-foot at the apex of
the deformity in conjunction with plantar fasciotomy.

Contraindicated in children <7 years old and in patients with fixed deformity.

Not used frequently due to failure to preserve joint motion and other drawbacks
iii. Cole Procedure:

Older procedure but used more frequently

Dorsal based wedge osteotomy through the mid-foot (navicular-cuneiform joints and the cuboid).

Shortens the foot, interference with tarsal motion and a high rate of pseudoarthrosis (30%) are
some drawbacks.

Indicated for patients with slow progressing neuromuscular diseases and sagittal plane pes cavus.

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 D. Rearfoot Deformity:

i. The goal is to reduce the rearfoot varus and the cavus deformities.

ii. In mild cases that do not correct with the Coleman Lateral Block Test, a Dwyer calcaneal
osteotomy is adequate. Click here to view a video of the Coleman block test.

If STJ is flexible the hindfoot will go from

varus to rectus. This is secondary to
forefoot pronation

E. The Coleman block test evaluates hindfoot flexibility and pronation of the forefoot. The test is
performed by placing the patient's foot on a wood block, 2.5 to 4 cm thick, with the heel and
lateral border of foot on the block and bearing full weight while the first, second, & 3rd
metatarsals are allowed to hang freely into plantar flexion and pronation. It is based on premise
that there is fixed flexion of 1st metatarsal. It negates the effect that the forefoot (first
metatarsal in plantar flexion) may have on the hindfoot in stance. If heel varus corrects while the
patient is standing on the block, the hindfoot is considered flexible. If the subtalar joint is supple
& corrects with the block test, then surgical procedures may be directed to correcting forefoot
pronation, which is usually due to plantar flexion of 1st metatarsal. If the hindfoot is rigid, then
surgical correction of both forefoot & hindfoot are required

i. Triple Arthrodesis remains the main procedure for pes cavus caused by CMT. Indicated in
patients with severe rigid cavus deformity, limited subtalar joint mobility and
degenerative changes. In younger patients with mild deformity try other combinations of
procedures before a triple.

F. Drop-foot Deformity:

i. If an AFO does not work or the patient does not want an AFO, a muscle tendon transfer
may be indicated. If the disease has progressed to include all lower limb musculature or
balance and stability are severely compromised, ankle fusion may be indicated.

G. Ankle Equinus Deformity:

i. The overpowering of the posterior muscles results in limited dorsiflexion or posterior

ankle equinus. A triple arthrodesis can take care of this by virtue of reduction of the
calcaneal inclination angle and subtalar joint resection. However, it the ankle equinus is
still present, a TAL or gastrocnemius recession may be indicated.

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Club Foot
I. General Information

A. A.k.a Talipes equinovarus

B. Incidence: 1:1,000 births
C. Sex Predilection: males 2:1
D. 50% are unilateral
E. If first child has clubfoot, the second has a 20-30 times greater chance.

II. Classification

A. Congenital
1. Extrinsic (Type I/Flexible Clubfoot)

a. Tarsal subluxation is usually not present

b. No abnormality in the head and neck of the talus

c. little lower leg atrophy

d. Normal heel size

e. This deformity responds well to conservative treatment consisting of manipulation and serial
casting

f. If left untreated this condition will progress to the rigid form

2. Intrinsic (Type II/Rigid Clubfoot)

a. More common than extrinsic form
b. Tarsal subluxation is present
c. Extensive lower leg atrophy present
d. Fibula and sinus tarsi become obliterated

e. Significant decrease in heel size

f. Deep creases are usually found medially along the foot and ankle

g. Osseous prominences along the medial aspect of the foot are changed

h. Medial malleolus, talar head, navicular become poorly defined

NOTE: This form usually requires surgical intervention

B. Acquired (Potential Causes)
1. Neuromuscular Diseases/Conditions

a. polio

b. spina bifida

c. Meningitis

d. Postcerebral vascular accident

e. Cerebral palsey (Little's syndrome)

f. Diastematomyelia

2. Trauma

a. Distal tibial epiphyseal injuries

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 b. Spinal trauma

c. Peripheral nerve trauma

d. Neglected lower extremity tendon ruptures and lacerations

e. Contractures of soft tissue after burns

f. Neglected fractures

g. Volkman's contracture/paralysis

III. Etiology of Congenital Clubfoot

A. Idiopathic
B. Hereditary germ plasm defect
C. Abnormal intrauterine pressure
D. Intrauterine trauma
E. Nerve lesions
F. Arrested fetal development
G. Bone abnormalities
H. Circulatory abnormalities of the tarsal bones
I. Muscle Contractures
J. Open defects: myelomeningocele/meningocele
K. Closed defects: spina bifida, myelodysplasia, and errors in skeletal segmentation
L. Myogenic: abnormal muscle/tendon insertions
M. Osteogenic: absence of the tibia or medial malleolus
N. Collagenous: amniotic bands and arthrogryposis
O. Cartilaginous: diastrophic dwarfism

IV. Basic Deformities of Clubfoot

A. Three Main Components

1. Ankle Equinus
2. Rearfoot Varus
3. Forefoot Adduction

B. Other Components
1. Talar Navicular Subluxation
NOTE: Talonavicular subluxation is usually present when rearfoot
varus is present.

V. Pathological Anatomy

A. Transverse Plane: The talar head and neck are adducted 80° on the talar
body
B. Sagittal Plane: The talar head and neck are plantarflexed 45 to 65°
C. Dislocated talonavicular joint
D. Subluxed subtalar joint and calcaneocuboid joint
E. The posterior talocalcaneal facet is usually normal
1. Normal:

a. The head and neck of the talus are aligned 15-20 degrees on the body

b. Talar head and neck normally plantarflexed 25-30 degrees

2. Clubfoot

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 a. Head and neck of the talus relationship oriented at 60-90 degrees to one another

b. Talar head and neck are plantarflexed 45-65 degrees

F. Equinus of clubfoot due to

1. Primarily; posterior capsule
2. Secondarily; tight Achilles
NOTE: You see that the wide anterior portion of the articulating cartilage on the dorsum of the talus which
does not reside in ankle due to equinus deformity.

G. Influence Changes
1. Calcaneal

a. Medial rotation of anterior calcaneus due to contracture of posterior tibial and anterior
deltoid.

b. External rotation of posterior calcaneus due to calcaneal fibular ligament

2. Navicular

a. Tethering of posterior tibial tendon can pull navicular medially enough to force it to articulate
with the medial malleolus

3. Cuboid

a. Follows the navicular due to it's ligamentous attachments

H. Osseous Changes
1. Talus: Depending on the form we may see a 25% decrease in size. The head and neck are typically adducted and
plantarflexed. It is usually positioned anteriorly in the ankle mortise
2. Calcaneus: Slight varus and equinus positioning. Hypoplastic. It is usually displaced in a supinated position beneath
the talus
3. Navicular: We may see a decrease in size to 66% of normal. It is typically positioned far more medial than in a normal
patient. It may also articulate with the tibia
4. Forefoot: The metatarsals and phalanges are typically adducted and rotated into a varus position. In the intrinsic form
the 1st ray is typically plantarflexed
I. Soft Tissue Changes
1. Tendons

a. Contracted Achilles tendon, posterior tibialis, flexor hallucis longus, flexor digitorum longus,
and abductor hallucis

b. The Achilles tendon and the long extensor tendons are typically medially displaced

c. The peroneal tendons are typically elongated and posteriorly displaced

d. The intrinsic plantar tendons are typically contracted

2. Ligaments

a. Contracted posterior talofibular, tibionavicular, calcaneonavicular, tarsometatarsal, and

deltoid ligaments

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 3. Shortened blood vessels medially
4. Decreased calf size

VI. Radiographic Analysis

A. AP View Angles:

1. Kites Angle: The anteroposterior

talocalcaneal angle (Bi-section of the
talus and calcaneus). The angle is
formed by the intersection of two lines
coincident with the longitudinal axes of
both the talus and the calcaneus on the
horizontal plane, and it indicates the
normal divergence of the two bones in
the standing position. 20-40 degrees in
normal a foot.

NOTE: In clubfoot deformity Kite's angle is usually less than 15 degrees. It is not uncommon for this angle to
be close to zero.

2. Talar - 1st metatarsal angle

a. The lines drawn through the long axis of the

talus and the 1st metatarsal. The normal
range is 0-15 degrees. Patients with
clubfoot typically have a negative Talar 1st
metatarsal angle (angle less than zero).

B. Lateral View
1. The Kite’s angle will also be decreased. These angular relationships represent Simon’s rule of fifteen (i.e., Kite’s angle
less than 15° and the talo-first metatarsal angle greater than 15°). In the neglected clubfoot angular relationships are
more difficult at times because of a rigid contracted foot not amenable to standard positioning.
2. In clubfoot the lateral talocalcaneal angle is less than 35 which indicates hind foot equinus. It is not uncommon for
this angle to approach zero.
NOTE: In order to best determine the extent of the patient's equinus in clubfoot deformity it may be wise to
compare lateral stress dorsiflexion with relaxed views.
3. Calcaneal Inclination Angle: Normally 20-25 degrees. Typically we see a CI angle of less than 17 degrees with
clubfoot.

VII. Conservative Treatment

A. Early intervention is the key to successful conservative treatment

1. Treatment is most successful in the first 12 months of life with earlier starts being most advantageous
B. The gold standard of conservative care is manipulation followed by immobilization
1. The following devices are commonly used to achieve this goal:

a. Dennis Brown Bar

b. Ganley Splint

c. Strapping/Taping

d. Molded plaster casting

NOTE: The key to achieving a successful conservative treatment plan when dealing with clubfoot is to address
the deformities in the proper order. The forefoot adduction is addressed first, rearfoot varus second, and ankle
equinus last.

C. Corrective Manipulations

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NOTE: Your manipulations correct the deformity. The cast retains any corrections you have made and does not
apply a corrective force.

1. Pre-Manipulation

a. The foot should be manipulated at 30 to 60 intervals for five minutes

b. Distal traction at the ankle joint and distal traction of the forefoot

2. Manipulation

a. The forefoot is abduct it against the cuboid

b. The Talar head is pushed immediately

c. The heel is everted

d. Multiple repetitions of 10 second intervals for 10 minutes

3. Application of cast

a. Apply a slipper cast below the malleoli first. Bi-plane manipulation, sealing forefoot and heal
correction in plaster.

b. After the slipper cast hardens, the foot and ankle are everted, and the cast is carried
proximally to the knee.

c. No excessive dorsiflexion at the ankle, which might cause a mid-tarsal breach.

d. The knee should be locked at 90 to 120° with plaster. To prevent cast slippage.

e. An additional optional layer of fiberglass may be applied for additional reinforcement.

4. Frequency of cast changes

a. Ideally 2X/week for the first three months

b. Once a week after three months

c. Every other week after maintaining your alignment up to one year after correction has been
verified by x-ray

NOTE: Serial X-rays should be taken at every cast change. If corrections are not seen or treatment stagnates
then consider surgical intervention.

5. Additional treatment after correction has been achieved includes the following:

a. Apply a bi-valved retention cast

b. Night splints

c. Orthopedic shoes

d. Orthotics

e. Shoe wedging

6. Complications of casting

a. Pressure sores

b. Rocker bottom deformity (Radiographs will reveal a midfoot breach)

c. Muscle atrophy

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 D. The Ponseti Technique
1. Indicated for infants 3-4 months old
2. Based on the principle that the forefoot is pronated in relation to the rearfoot
3. Manipulation involves supinating the forefoot and dorsiflexing the first metatarsal
4. Counter pressure on the lateral aspect of the head of the talus which should abduct the calcaneus
5. A percutaneous tendo-Achilles lengthening is then usually needed to correct the equinus

VIII. Surgical Treatment

A. Indications for Surgical Intervention

1. Recalcitrant to conservative treatment. Recommended that at least 6 weeks of conservative treatment be attempted
2. Appearance of complications of conservative treatment

a. rocker-bottom deformity (reversible)

b. flat-topped talus (non-reversible)

3. Foot length should be at least 8 cm. -Less than this can result in tearing of tendons and other vital tissue in an
attempt to straighten foot.

Note: Surgery should be planned in a progressive manner. The foot and ankle should be evaluated at the
completion of each step to determine if further surgery is indicated.

B. Surgical Age/Procedure Guidelines

1. Birth to 4 years: Soft tissue procedures
2. 4 - 8 years: Either soft tissue or bone procedures
3. 8-12 years: Bone procedures
4. > 12 years: Joint procedures

NOTE: Guidelines are based on ossification ages of bones in the midfoot and rearfoot.

C. Surgical Procedures
1. Turco: (Modified "hockey stick" incision)

a. This approach provides a good exposure to the medial, plantar and posterior structures

b. It does not interrupt the vascular supply to the skin

c. Disadvantage is that it has limited exposure to the lateral structures which may require a
separate incision

2. Cincinnati Incision (Most commonly used approach for clubfoot surgery)

a. It provides excellent exposure

b. May risk disrupting the vascular supply to the skin

c. Has limited exposure of the superior portion of the Achilles tendon

3. Talipes Equinovarus Surgery

a. Posterior Release
i. Tendo-Achilles lengthening
ii. Posterior capsulotomy of the ankle joint and the sub talar joint
iii. Release of the posterior inferior tibiofibular ligament, posterior tibiofibular
ligament, and most importantly, the calcaneofibular ligament

iv. Assess your correction before proceeding to the next phase

b. Medial Release

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 i. lengthening of the posterior tibial tendon, the flexor digitorum longus, and
the flexor hallucis longus

ii. Incise the subtalar joint and interosseous ligament

iii. Perform a medial capsulotomy of the subtalar joint, talonavicular joint and
the 1st metatarsocuneiform joint

iv. Insert a K-wire through the talus into the navicular in order to maintain a
corrected alignment of the talonavicular joint

v. Assess your correction before proceeding to the next phase

c. Adjunctive procedures

i. Lateral release of the Bifurcate ligament and subtalar joint release

ii. Plantar releases

iii. McCauley procedure (A lengthening of the abductor hallucis)

iv. Cuboid osteotomy or calcaneocuboid fusion.

v. Talectomy (Adults)

vi. Triple Arthrodesis (Adults)

D. Post-Op Care
1. Maintain corrections with casting
2. Typically 12 weeks in an above knee cast which is changed every four weeks
3. Window the cast and remove the sutures in two weeks
4. Remove pins in a week
5. Maintain with night splints for another 4-6 weeks after the 12th week
E. Osseous Procedures
1. Calcaneal Osteotomy

a. Dwyer procedure

b. Corrects heel varus

c. Closing wedge osteotomy with an 8-14mm bone wedge being excised

2. Cuboid Osteotomy

a. Shortens the lateral column of foot

b. Evans procedure

c. Closing wedge of cuboid

d. Calcaneal cuboid fusion

e. Corrects talonavicular dislocation

3. Tarsal Osteotomy
4. Cervical Osteotomy of Talus

a. High incidence of avascular necrosis with this procedure

5. Talectomy
6. Naviculectomy
7. Metatarsal Osteotomy

a. Berman and Gartland pan metatarsal base osteotomies

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 b. Corrects any associated metatarsus adductus

c. Most appropriate for patients ages 8-12 years

F. Joint Procedures
1. Tarsal Fusion (wedge arthrodesis)

a. Used on older uncorrected clubfoot conditions

b. Usually performed on patients ages 10 year or older

c. Corrects associated adducted forefoot

2. Triple Arthrodesis
3. Pantalar Arthrodesis
G. Complications of Clubfoot Surgery
1. Infection
2. Wound Dehiscence
3. Under correction
4. Overcorrection
5. Growth disturbances
6. Neurovascular Insult

Congenital Dysplasia & Dislocated Hip

I. Terminology:

A. Dislocation: The head of the femur lies outside of the socket (no contact between the femoral head and the acetabulum).
B. Subluxation: This is a partial dislocation. The articular surfaces of the femur head and the acetabulum are in contact, however
the head of the femur is moved out, over and back) not concentrically reduced).
C. Hip Dysplasia (Dislocatable or unstable Hip): Describes some degree of instability or abnormality of the anatomical structures
of the hip joint (femur, innominate bone, capsule, ligamentum teres, and the musculo-tendinous structures). It may be
present in the newborn child, later infancy, childhood, adolescence, or adult life. Characterized by an inadequate acetabulum
and/or a significant deformity of the upper femur.

II. Etiology:

A. Acetabular Dysplasia
1. Hip acetabulum is dysplastic (not formed properly). It may be shallow or anteriorly displaced
2. Teratologic (Germ plasm defect): Hip is abnormal due to a primary genetic disorder with polygenetic inheritance. Exp.
arthrogryposis multiplex congenital (high percentage of CDH)
B. Ligamentous Laxity
1. The strong Ligament Teres is weakened by some external factor. Relaxin hormone secreted by the mother to relax her
ligaments during the birth process is able to cross the placenta and affects the ligaments of the infant.
C. Intrauterine Malposition
1. Breech birth is an important factor in causing CDH. During a breech birth the infants hip is extended and traction is
placed on the infants lower limbs. This position can cause CDH. 30% of breech births result in CDH.
2. During gestation, the fetus is in a hip flexed position with the left leg crossed over the right. The force on the left limb
can vary, however, 80-90% of unilateral cases of CDH are found on the left side.
D. Post-Natal Environmental Factors
1. Higher incidence of CDH in northern Italy and Germany because infants are wrapped up in blankets for warmth. This
AD-Ducts the infant’s legs, which causes CDH.
2. Low incidence in Africa, China, India where babies are carried on mom's hip. This AB-Ducts the infant’s thighs and
helps to put the femur head back into the acetabulum.
Note: Females are more affected than males

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III. Clinical Picture (Signs):

A. Limitation of AB-Duction (most important clinical finding) with the child supine and the hips
and knees flexed, gently abduct the hip. There will be restriction on the dislocated side.
With bilateral dislocations abduction will be symmetrical but limited (normal is 90 degrees).
Most reliable after 2 months of age.
B. Shortening of the limb due to the position of the femur head (up and out).
C. Telescoping Sign: The child is placed on his/her back with hips either flexed to 90 degrees or
extended to 180 degrees. You push the femur in a posterior direction. If you can push the
femur beyond the usual hip joint articulation and you feel pistoning mobility, you have CDH.
D. Anchor Sign Asymmetry of thigh and gluteal folds and gluteal and popliteal creases). This is
seen in 50 % of all newborns or infants. The sign is more reliable from 4 months to 18
months. It is less reliable after 18 months.

E. Limping or waddling during gait analysis.

IV. Clinical Test: (memorize these test)

These test are done on newborns that are 6 months old or less.

A. Ortolani Test

Steps:
1. Place baby in the supine position with hips and knees flexed to 90 degrees.
2. Examine hips one at a time by lifting and abducting the thigh to be examined while stabilizing the opposite thigh and
pelvis.
3. If the hip is dislocated you will feel a "palpable click or clunk" as the femoral head goes back into the acetabulum.

Important Points:
-Most reliable in early months of post-natal life.
-Although a very good sign, it is not pathognomonic for CDH.
B. Barlow Test

Steps:
1. Place baby in the supine position with hips and knees flexed to 90 degrees.
2. Place your middle fingers over the greater trochanter and your thumbs to the inner side of the thigh opposite the
position of the lesser trochanter.
3. Place thighs into mid abduction.
4. Apply pressure backwards and outwards with the thumbs.
5. If the femoral head slips out over the posterior lip of the acetabulum and back again immediately when the pressure is
released, the hip is "unstable" (the hip is not dislocated but is dislocatable).
Important Points:
-Most reliable at birth to four weeks (although can be tried up to seventh month).

C. Galeazzi Test (also called Allis sign)

Steps:
1. Place baby in the supine position with hips and knees flexed.
2. Look at the level of the knees. The height of the knee on the affected side will
appear lower.
Important Points:
-Most reliable after the age of 18 months.
-The test only works with a child that has unilateral CDH.
- To rule out limb length difference, do a full body x-ray and measure the bones.
D. Trendelenburg Test

Steps:
1. Have the child stand on both feet.
2. Then have the child stand on alternate feet.
3. When the child stands on the affected side, the opposite (normal) hip will drop down due to weakness of the
abductors on the affected side.
Important Points:
-Test is performed on older children.
Order x-rays if any of the above test are positive.

V. Radiographic Findings:

A. General Information:

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 1. Order Anterior-posterior hip position and a frog lateral.
2. Look for lateral and upward displacement of the femur and abnormalities of the acetabulum (shallow or elongation of
the acetabular roof).
B. Quadrant System: By drawing Hilgenreiner's and Ombredanne's lines, a four-quadrant system can be superimposed over
each hip. Normally the developing femoral head should be in the lower medial quadrant. A dislocated hip will show at least
part of the femoral head in the upper outer quadrant.
C. Hilgenreiner's Line (Y Line) A horizontal line that connects the two most medial and inferior points of the acetabular cavity
(just below the visible ossified aspect of the acetabular roof on both sides). Normally the head of the femur is below this line.
If it is above the line, the hip is dislocated.
D. Ombredanne's Line (Perkins Vertical Line) A vertical line from the most lateral ossified margin of the roof of the
acetabulum perpendicular to the Y line to form quadrants.
E. Acetabular Index: The angle formed between Hilgenreiner's line and a line drawn from the most inferior ossified margin of
the acetabular roof, across the acetabulum to the most lateral ossified margin of the acetabular roof.

Normal is 27 to 30 degrees at birth, which decreases to 20 degrees at two years of age.

If > 30, the hip is dislocated.
F. Shenton's Curved Line (Menard's Line): Draw an arc along the medial border of the femoral neck and the superior portion
of the obturator foramen. Normally a continuous arc is formed. In a dislocated hip, you will have a broken arc.

VI. Treatment of CDH:

A. AB-Duct the leg Anything that AB-Ducts the leg will force the femoral head back into the acetabular cavity.
B. Casting (This is the hallmark treatment).
1. Use on infants that are between 2 and 18 months old.
2. Types of cast:
a. Bachelor Cast:
i. Runs from groin to ankle.
ii. Knee is flexed at 15 - 20 degrees
iii. A bar joins the two casted legs to keep the patients foot in position.
b. Frog or Lorenze Cast (a.k.a spica cast):
i. Runs from below nipple line down to ankle.
ii. AB-Ducts the hip at 45 degrees

c. Pavlik Harness

i. Maintains the hip and knee in flexion and the thigh in abduction

NOTE: The key to treatment is catch the deformity as early as possible and then maintain the patient in
hip/knee flexion with the thigh abducted.

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Congenital Vertical Talus
(CONGENITAL CONVEX PES VALGUS)

I. Definition

A. Congenital Vertical Talus (also known as congenital convex pes valgus) is a fairly rare malformation of the foot that may be
seen and diagnosed in newborns.
B. Characteristics
1. Contracture of the peroneal and achilles tendons resulting in a fixed rearfoot equinovalgus

2. A dislocated navicular resulting in rigid midfoot dorsiflexion

3. Contractures of the extensor hallucis longus, extensor digitorum longus, and anterior tibialis muscles
resulting in a forefoot which is abducted and dorsiflexed
NOTE: A hallmark visual feature of the deformity is a foot with a convex rockerbottom plantar, prominent talar
head, and is dorsiflexed to the point of making contact with the anterior aspect of the leg at birth.

NOTE: Early diagnosis of the deformity is critical to successful treatment.

II. Etiology

A. 50% of cases are associated with either a genetic disorder or neuromuscular disorder
1. Transmission believed to be via autosomal dominant inheritence (Stern, 1989)

2. Myelodysplasia is the most commonly seen disorder to co-exist with vertical talus at birth

B. More commonly seen in males than females

C. Most deformities are bilateral

III. Clinical Features

A. Palpable talar head on the dorsomedial aspect of the foot

B. Rigid rockerbottom plantar aspect of the foot
C. Foot often dorsiflexed to the point of contacting the anterior aspect
of the leg
D. Very prominent skinfold can be noted dorsolateral to the ankle joint
E. Rearfoot in fixed equinovalgus
F. Rigid forefoot valgus
G. Rigid pronation of the foot
H. Patient may exhibit a clumsy peg-like gait due to the protrusion of
the talar head plantarly

IV. Ligamentous Changes

A. Shortening of the dorsal talonavicular ligament, tibionavicular ligament, calcaneofibular ligament, calcaneocuboid ligament, and
interosseous talocalcaneal ligament
B. Posterior ankle joint and subtalar joint capsules contracted
C. Elongation of the spring ligament

V. Radiographic Features

A. Suggested views are AP, Lateral, and Lateral with forced plantarflexion
B. Findings
1. AP

a. Increased talocalcaneal angle

b. NOTE: A talocalcaneal angle greater than 50 degrees in infants and 40 degrees in children
older than 5 is consistent with vertical talus deformity.

2. Lateral

a. Most notably a line bisecting the talus will be seen to be parallel or nearly parallel to a line
bisecting the tibia indicating that the talus is indeed in a vertical orientation

b. Increased talocalcaneal angle

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 NOTE: When examining this view a talocalcaneal angle greater than 50 is considered to be abnormal.

c. Calcaneus in equinus and forefoot is dorsiflexed

d. Negative calcaneal inclination angle

3. Lateral with forced plantarflexion

a. Normally the 1st metatarsal and talar axises are parallel to one another. In this view the talar
axis with extends through the sole of the foot and the 1st metatarsal

NOTE: Some deformities may involve a flexible vertical talar orientation that may be reduced by forced
plantarflexion (talipes calcaneovalgus, pes planovalgus with gastroc equinus, and paralytic forms of pes
planovalgus such as cerebral palsy and polio most notably). In convex pes valgus (vertical talus) the deformity
will NOT be reduced when this view is analyzed.

NOTE: To differentiate between a paralytic pes planovalgus deformity with supple reducibility and other causes
of a vertical talar orientation it may be useful to order a lumbosacral x-ray on neonates with CVT.

b. Dorsal dislocation of the navicular may be evident in patients after age 3 when the bone
normally ossifies

VI. Treatment

A. The primary goal of treatment is to restore a normal relationship between the talus, calcaneus, and navicular in the patient as
early as possible
B. Conservative treatment may be attempted but is rarely successful
1. Conservative Treatment
a. Initiate during the first 3 weeks of life for best results
b. A closed reduction of the talus, calcaneus, and navicular can be performed using percutaneous pinning
c. 3 to 4 months of serial casting, skin stretching, and soft tissue manipulation is often required to restore a
normal orientation via the following procedure:
i. The triceps surae and calcaneal fibular ligament should be stretched gently via distal and
medial traction.
ii. In order to stretch the dorsiflexors and everters the forefoot must be pulled into plantar
flexion and adduction.
iii. Apply distal traction on forefoot (navicular). Then move the forefoot into adductus and varus
which stretches the tibionavicular and talonavicular ligaments. Hold the forefoot in this position for 15 seconds.
iv. Apply a long leg cast, which is changed twice a week for at least six weeks.
v. At this time it is now advisable to attempt a closed reduction of the navicular onto the talus
by applying distal traction on forefoot (navicular) and then dorsiflexion and eversion in order to increase the
deformity. The forefoot is then brought into plantar flexion as the talar head is pushed into dorsiflexion. The
calcaneus should then be pulled under talus thus reducing the deformity.
NOTE: The closed reduction should be held in place via percutaneous pinning.
c. NOTE: Conservative treatment is usually not successful even if performed early. Therefore surgical
correction of the deformity is recommended after the 4th month of conservative treatment in order to prevent
the soft tissues from adapting to the deformity.

2. Surgical Treatment
a. The preferred surgical treatment for vertical talus deformity is an open reduction.

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 i. Begin the skin incision at the medial cuneiform and extend to the inferior aspect of
the medial malleolus. Then extend the incision in a curvilinear fashion just superior to Achilles
tendon.
ii. Retract the neurovascular bundle.
iii. Release any contracted ligaments at this time and lengthen any tendons visible.
iv. Lengthen the talonavicular, bifurcate, calcaneofibular, interosseous talocalcaneal
and tibionavicular ligaments. Lengthen the dorsal calcaneocuboid joint capsule.
v. Perform a Z-plasty lengthening on the triceps surae, tibialis anterior, extensor
hallucis longus, and peroneal muscle tendons.
vi. Manipulate talar head while plantar flexing and inverting the navicular in order to
reestablish a normal anatomic alignment.

vii. A 0.062 inch K-wire is then driven from the posterior talus anteriorly passing
through the talonavicular articulation, naviculocuneiform joint and finally into the first
intermetatarsal space.

viii. The spring ligament is then tightened at this time.

ix. Postoperatively the patient is placed in a above the knee cast for 4 months with K-
wires to be removed at 6 weeks.

VII. Complications

A. Avascular Necrosis
B. Skin Sloughing
C. Rigid Athrogryphosis may develop between ages 3 and 6
NOTE: The treatment for this complication is to excise the navicular.

D. Recurrence due to failure of OR adaptation to the releases performed. Typically seen after age 6.
NOTE: A triple arthrodesis is recommended for these patients.

VIII. Differential Diagnosis

A. Talipes calcaneal valgus and pes planus with gastroc-soleus equinus

B. Paralytic pes plano valgus, myelomengocele or polio has suppleness in reducibility Note: Take a lumbosacral x-ray on a
neonate with CVT.
C. Spastic flatfoot secondary to tarsal coalition can be differentiated by radiographic signs

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Equinus/Ankle
I. Definition: limitation of passive ankle joint dorsiflexion to less than degrees. Equinus is generally considered to be a
plantarflexed sagittal plane attitude of the foot to the leg with maximum ankle joint dorsiflexion

A. Anatomy
1. Triceps Surae

a. Gastrocnemius: medial head is thicker, more broad, and extends more distally. Attaches to
lateral side of tendo-Achilles

b. Soleus: Attaches to medial 2/3 of deep surface of tendo-Achilles. Origin from:

i. broad aponeurotic bands from back of the head of the fibula

ii. Upper 3rd of the posterior surface of the fibula

iii. The soleal line and middle 3rd of the tibia

c. Plantaris: Arises from lateral femoral condyle, absent 7% of time. Attaches medially

2. Innervation

a. Tibial nerve (sacral level 1, 2)

3. Vascularization

a. Posterior Tibial Artery

4. Action

a. Gastrocnemius: Plantarflexes foot and flexes the knee

b. Soleus: Plantarflexes the foot

c. Gait

i. The gastrocnemius and soleus fire toward end of the contact period and
continue to work during midstance into the first portion of the propulsive
period of normal gait

B. The Achilles Tendon

1. 15 cm in length, begins near middle of leg and inserts at the posterior middle third of the calcaneus
2. It is the thickest and strongest tendon in the body
3. Gastrocnemius crosses 3 joints (The knee, the ankle, and the subtalar joint)
4. Soleus crosses 2 joints (The ankle and the subtalar joint)
5. The watershed zone: An area located 2-6 cm superior to the insertion of the Achilles tendon on the calcaneus.

NOTE: This area has the weakest blood supply along the length of the tendon and is also the most frequent
area for the Achilles tendon to rupture

II. Etiology

A. The 5 etiologic types of equinus

1. Talipes Equinus
2. Osseous equinus
3. Gastrocnemius-soleus equinus

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 4. Metatarsal equinus: Forefoot plantarflexion to the rear foot at the Lisfranc’s joint
5. Forefoot equinus: Plantarflexion of the forefoot on the rear foot at the Chopart's joint
B. The 3 Forms of Equinus
1. Muscular

a. Spastic Equinus (The oldest known form) seen in patients with neuromuscular diseases such
as cerebral palsy

i. Patients with spastic equinus may exhibit hypertonicity, clonus,

hyperreflexia, and toe-walking

ii. Posterior crural muscles overpower the weaker anterior muscles of the leg

b. Non-spastic (Congenital) Equinus:

i. Short posterior leg muscle group

ii. May have accessory soleus

iii. May have a low soleus insertion point

NOTE: This condition is usually diagnosed by exclusion and toe walking is considered to be normal up till the
age of 3-6 months

c. Acquired: As the result of trauma, iatrogenic causes, prolonged casting, or the wearing high-
heeled shoes causing a progressive shortening of the Achilles tendon

2. Osseous

NOTE: This condition is characterized by a hard end feel when testing the ankle joint ROM.

a. Talotibial Exostosis: Osseous projections from the margins of the trochlear surface of the talus
and the distal articular surface of the tibia

b. Osseous bridging: Usually between the tibia and fibula at the distal syndesmotic area

c. Pseudoequinus: False ankle equinus in an anterior cavus foot type due to the angular
relationship of the forefoot to the leg in the sagittal plane. Most often confused with equinus

d. Types

i. Metatarsal Equinus: Usually at the Lisfanc joint

ii. Forefoot equinus: Usually at the Chopart joint

iii. Lesser tarsal equinus

iv. Combination equinus

3. Combined

III. Clinical Exam

A. Replicating maximum ankle joint dorsiflexion

1. Clinical measurement performed with patient laying in the supine with the knee fully extended and the STJ in neutral
2. Ankle equinus is a sagittal plane measurement of the rearfoot to a bisection of the leg
B. The Silverskiold Test is used to determine if a patient's equinus is due to the gastrocnemius muscle only or if it is a combined
gastroc-soleus problem.
• A test used to determine what type of equinus is present. If ankle dorsiflexion is less than 10 degrees
with the knee extended, but increases or returns to 10 degrees or more with the knee flexed, this
indicates a positive test result and the presence of a gastrocnemius equinus. If the test reveals less
than 10 degrees of dorsiflexion when the knee is extended and when it is flexed the test is negative
and the condition is due to a gastroc-soleus equinus.

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 NOTE: In cases of gastrocnemius only equinus a gastrocnemius recession is indicated. In cases of a gastroc-
soleus equinus a tendoachilles lengthening procedure would be indicated.

C. Proximal compensations for equinus

1. Changes the body may undergo in order to return the bodies center of gravity to a normal alignment

a. Lumbar lordosis

b. Hip flexion

c. Knee flexion

d. Genu recurvatum

D. Distal compensation for equinus

1. STJ pronation
2. MTJ pronation
3. Forefoot dorsiflexes on the rearfoot
E. Types of distal compensation
1. No distal compensation: True toe walkers where the heel is totally unable to make contact with the ground. The
forefoot bears all the weight and the patient appears to walk on their toes during gait
2. Full distal compensation: Involves STJ and MTJ pronation with hypermobile flatfoot deformity. Any of the following
may also co-exist with this compensation method:

a. Forefoot dorsiflexed at the MTJ

b. Rearfoot maximally everted in relation to the floor

c. Forefoot everted on the rearfoot

d. Excessive internal leg rotation

e. Lower back pain

f. Genu valgum

g. Flexor substitution contractures at the digits

h. A hypermobile 1st ray with associated HAV or metatarsus primus adductus deformity

i. Callusing under metatarsal heads

3. Partial distal compensation: Involves some STJ pronation and little to no MTJ pronation. Visible pathology here seems
to be entirely dependent on the degree of MTJ motion available during compensation. You may see the following in
partially compensated patients:

a. Early heel off

b. Heel contact during early stance phase

IV. Conservative Treatment

A. Custom molded foot orthoses

B. Custom shoegear
C. Physical Therapy
1. Strengthening the anterior crural muscle groups
2. Stretching the posterior crural muscle groups
3. Reserved for mild cases or moderate equinus in older patients who may not be good candidates for surgical
intervention
D. Shoe padding
E. Exercising and stretching routines
F. Serial casting or bracing (This is typically reserved for very young patients)

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 NOTE: The primary goal of conservative treatment is to prevent the development or progression of potentially
pathologic accommodations to the existing equinus.

V. Surgical Treatment

A. Gastrocnemius Equinus Procedures

1. Volpius & Stoffel

a. Distal resection of the gastrocnemius aponeurosis using an inverted V incision without

suturing to the underlying muscle

2. Strayer

a. Transverse incision of the gastrocnemius aponeurosis followed by suturing of the proximal

portion of aponeurosis to the underlying soleus muscle

3. Baker

a. Distal tongue-in-grove recession of the gastrocnemius with a dissected central soleus

aponeurosis

4. Fulp & McGlammary Modification of the Baker

a. A distal tongue and grove recession of the gastrocnemius as originally described by Baker
only using inverted cuts (Medial and lateral cuts are made proximally and central cut made distally)
b. Now believed to have a high risk of causing atrophy of the medial gastrocnemius head
c. Make a 6 cm incision extending from the myotendinous junction distally
d. Incision should be slightly medial to the midline in order to avoid the small saphenous vein
and the sural nerve
e. The deep fascia and paratenon are reflected together in one layer
f. The plantaris is then transected
g. The foot is then plantarflexed as the medial and lateral 1/3 of the gastrocnemius is then
transected

h. The foot is then dorsiflexed and the distal middle 1/3 of the gastrocnemius is transected

i. Let slide

j. Dorsiflex to 10 degrees and hold in a neutral position

k. Use 2-0, 3-0 Dexon to suture the ends

l. Close the paratenon and deep fascia with 3-0 Dexon

B. Alternative procedures for Gastrocnemius Equinus

1. Stoffel: A neurectomy of the tibial nerve motor branches usually reserved for spastic forms of equinus
2. Silfverskiold: Involves the reinsertion of the muscular heads of the gastrocnemius from the femur to the proximal tibia
3. Silver & Simon: Involves the reinsertion of the gastrocnemius to the proximal tibia and is usually followed with a
neurectomy of the tibial nerve motor branches
C. Gastroc-Soleus Equinus Procedures
1. Neurectomy: A neurectomy of the soleus muscle is typically reserved for cases involving the presence of clonus in the
patient and is combined with a lengthening of the gastroc-soleus complex
2. Achilles Tendon Advancement

a. Original Murphy procedure

i. Advance the Achilles tendon to the dorsum of calcaneus just posterior to

the posterior facet

ii. Doing so will shorten the lever arm of the ankle joint fulcrum by 50% yet
only shortens the lever arm of the MPJ fulcrum by 15%

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 b. Murphy modification of tendo-Achilles advancement

i. Involves rerouting the Achilles deep (anterior) to the flexor hallucis

longus tendon

ii. A Bunnell suture is used

iii. Resect a wedge of bone 1 cm thick

iv. Place an above knee cast on the patient in neutral position

v. Most useful in treating moderate, sever, and spastic forms of equinus

c. The McGlamry Modification: Involves passing suture to medial and lateral calcaneus

3. Tenotomy

a. Frontal plane Z-lengthening

b. Open sagittal plane Z-lengthening will allow for the most exact corrections to be made

NOTE: An Achilles tendon lengthening is the procedure of choice when treating a patient with a non-spastic
gastroc-soleus equinus that has not responded to conservative treatment.

D. Osseous Equinus Procedures

1. The primary goal of a surgical intervention is to resect the osseous block
2. May use an open ankle arthrotomy or an ankle arthroscopy

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Flexible Flatfoot Deformity
I. Definition

A. A.k.a. pes planus, Pes planus, Pes valgoplanus, Pes planovalgus, Idiopathic hypermobile flatfoot
B. Visible loss of the medial arch when patient becomes weight bearing
C. Flexible flatfoot is defined by the restoration of the medial arch when performing the Hubscher maneuver.
NOTE: The Hubscher Maneuver involves passive dorsiflexion of the hallux while the patient stands in a normal
relaxed position. If the deformity is flexible, the medial longitudinal arch will increase in height and the
rearfoot will supinate. If the deformity is rigid (typical in tarsal coalitions) no change in the arch will be seen.

NOTE: Flexible flatfoot is more common than rigid.

II. Etiology

A. Hereditary
B. Tibialis posterior muscle weakness (can follow local trauma)
C. Ligament weakness and laxity (Ehlers Danlos)
D. Forefoot varus - subtalar pronation allows lowering of medial column to floor
E. Flexible forefoot valgus - The midtarsal joint supinates making it unstable
F. Ankle joint equinus - compensation occurs at the subtalar joint and midtarsal joint if the patient is observed to have an early
heel off during gait analysis
G. Calcaneovalgus - limited ankle plantar flexion with everted foot position.
H. Tibial torsion, femoral anteversion, metatarsus adductus, and metatarsus abductus
1. Internal tibial torsion results in open kinetic chain pronation and an abducted foot position
2. External tibial torsion results in a medial shift of body weight causing excessive STJ pronation
I. Neurotrophic feet (Charcot foot)
J. Abnormal insertion of the posterior tibialis tendon

III. Clinical Appearance

A. Rearfoot valgus
B. STJ subluxation
C. Prominent talar head (usually a plantar medial bump)
D. Laterally angled midtarsal joint
E. Forefoot supinatus

IV. Planes of Flatfoot Deformity

A. Normal: An equal amount of STJ motion in the transverse and frontal planes with very little motion in the sagittal plane
NOTE: Plane dominance is generally determined radiographically.

NOTE: Determining which plane is dominant is vital to determining the appropriate surgical treatment for the
patient.

NOTE: The more that a joint axis deviates from a cardinal body plane, the more motion will occur in that plane

B. Frontal Plane Deformity

1. A more horizontal STJ axis means more motion in frontal plane
2. Rearfoot valgus
3. Superimposition of metatarsals
4. Decreased 1st metatarsal declination angle
5. Decreased height of the sustentaculum tali, midtarsal joint, and the STJ
C. Transverse Plane Deformity
1. Determined via AP view
2. A more vertical STJ axis means more motion in transverse plane
3. Increased Kite angle
4. Increased cuboid abduction
5. Decrease in the % of T-N congruency
D. Sagittal Plane Deformity
1. An STJ axis closer to the frontal plane means more motion in sagittal plane
2. Decrease in the calcaneal inclination angle
3. Increased talar declination angle
4. Navicular cuneiform breach
5. Increased talocalcaneal angle on lateral view

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V. Radiographic Presentation

A. DP View
1. The talocalcaneal angle (Kite's) Normally 35-50 degrees reduced to 17-21 degrees by age 5.

2. NOTE: By age five you should see 75% articulation of the talonavicular joint. A decrease in this value
denotes excessive pronation typical of flatfoot deformity.

B. Lateral View
1. Calcaneal Inclination Angle 18-21 degrees, Talar declination
angle 21 degrees. Lateral Talocalcaneal angle 35-50 degrees.

VI. Conservative Treatment

A. Gastroc/soleus stretching
B. Oral NSAIDs
C. Educate patient on acquiring the appropriate shoegear if existing shoes appear to be worn out or not supportive enough (A stiff
sole with a firm heel counter is best)
D. Custom shoe orthotics
E. Ankle foot orthoses (Usually reserved for severe cases)
F. CAM Walker Boot
G. Casting/Immobilization (usually reserved for incalcitrant patients or those with posterior tibialis tendinitis)
NOTE: Most flexible flatfoot cases can be successfully treated via conservative measures.

VII. Surgical Treatment

A. When is flatfoot surgery appropriate?

1. Failure of conservative therapy
2. Instability during gait
3. Postural complaints with proximal compensation
4. Pain in the arch, sinus tarsi, rearfoot, and gastroc/soleus muscle
5. Difficulty walking or inability to maintain normal activity level
6. A pediatric patient showing decreased activity level
B. When is a flexible flatfoot procedure contraindicated?
1. Rigid plantarflexed talus
2. Osseous equinus
3. Tarsal coalitions
4. Extreme obesity
5. Rigid flatfoot deformity (Negative Hubscher Maneuver)

VIII. Surgical procedures correct flexible flatfoot deformity?

A. Procedures to address sagittal plane dominance

1. Tendoachilles Lengthening/Gastrocnemius Recession
2. Kidner procedure - excise the tibiale externum and transpose the tibialis posterior to the underside of the navicular
3. Young - Used to correct flexible deformities with forefoot supinatus. Procedure involves rerouting the tibialis anterior
through the navicular
4. Lowman - A talonavicular arthrodesis. Procedure involves rerouting the tibialis anterior under navicular and suturing it
to the spring ligament
5. Miller - A naviculocuneiform arthrodesis of the medial cuneiform and 1st metatarsal
6. Hoke - Arthrodesis of the navicular with medial and intermediate cuneiforms
7. Cotton - An opening wedge osteotomy of medial cuneiform. This procedure is performed in order to plantarflex the
medial column
B. Procedures that restrict STJ motion (Extra-articular)
1. Chambers

a. Typically reserved for patients younger than 8 years of age

b. Procedure involves a bone graft being place under the sinus tarsi in order to block talar
motion on calcaneus

2. Baker and Hill

a. Procedure involves an osteotomy with lifting of a bone graft under the posterior facet

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 3. Selakovich

a. Procedure involves an opening osteotomy and bone graft of the sustentaculum tali

C. Procedures to address transverse plane dominance

1. Evans

a. Procedure involves an opening osteotomy 1.5 cm proximal to the calcaneocuboid joint on the
lateral aspect of the calcaneus using an autogenous bone graft

b. Medial base wedge osteotomy shortening the medial column

D. Procedures to address frontal plane dominance

1. Gleich

a. Involves an oblique calcaneal osteotomy

2. Dwyer

a. Contraindicated on patients under 3 years of age

b. Involves an opening wedge from lateral side or closing wedge form medial side of the
calcaneus

3. Silver

a. Involves an opening wedge bone graft on the lateral side of the calcaneus

4. Koutsogiannis

a. Involves a posterior displacement osteotomy performed in the frontal plane

5. Subtalar Arthroereisis

NOTE: An x-ray of the patient should be taken in neutral position in order to view any potential metatarsus
adductus component of the flatfoot deformity.

a. Involves an implant being placed within the sinus tarsi in order to block excessive subtalar
joint pronation

i. Implant Types

ii. Lelievre: A silastic plug in the sinus tarsi

iii. Sta-Peg polyethylene: Elevates the floor of the sinus tarsi which restricts
talar motion

iv. Viladot: An hour glass shaped silastic implant

v. Valente: Screws in using guides. Ideally you want to allow the foot to
pronate 4-5 degrees after this procedure is finished

b. Most successful on patients 4-8 years of age

c. Excellent for addressing deformities where the patient has a talocalcaneal angle over 30
degrees on the AP view

d. 50% articulation of T-N joint

e. Rearfoot valgus of 8-10 degrees

f. Forefoot varus of 10 degrees

g. Suited for calcaneal valgus foot with severe forefoot supinatus (Patient demonstrates an
overlap of the lesser metatarsals on the lateral x-ray)

For a complete in depth review of Adult flatfoot, please view the Journal of Foot and Ankle Clinical Practice Guideline

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Metatarsus Adductus
I. Definition

A. A transverse plane deformity in which the forefoot is adducted in relation to the midfoot/rearfoot. The apex of the deformity is
located at the Lisfranc joint.
B. 55% of cases are bilateral
C. The disorder appears to be a familial trait
D. The disorder occurs 1:1,000 live births

II. Classification

NOTE: Classification is done clinically and is based clinical

assessment, foot flexibility, and the location of the heel
bisector. (Bleck)

NOTE: The heel bisector is found on a weight bearing

patient where the heel forms an ellipse. The line
extending from the major axis of this ellipse (the
reference line) can then be used to determine the severity
of the deformity.

A. Mild: Reference line intersects 3rd digit

B. Moderate: Reference line passes between 3rd and 4th digits
C. Severe: Reference line passes between 4th and 5th digits

III. Etiology

NOTE: A wide variety of theories exist with regard to the cause of metatarsus adductus

A. Familial Trait
B. Intrauterine position and Tight Intrauterine Packing
C. tight/hyperactive abductor hallucis muscle
D. Osseous Deformities
1. Elongated lateral column
E. Soft Tissue Contractures
F. Abnormal Muscle Insertions
1. Tibialis Anterior
2. Abductor Hallucis
G. Abnormal Fetal Limb Rotation

IV. Clinical Presentation of Metatarsus Adductus

A. The lateral border of the foot is convex while the medial border is concave (“C-shaped” Foot)
B. The metatarsals appear to be adducted with the 1st metatarsal being greater than the 2nd and the 2nd greater than the 3rd
etc.
C. Patient may trip often during their gait due to in-toeing
D. Excessive lateral shoe wearing
E. If there is no STJ compensation the patient may have a high medial arch or a flatfoot with STJ compensation
NOTE: The primary compensation for metatarsus adductus is STJ pronation.

F. Prominent styloid process

G. Tight abductor hallucis due to hyperactivity
H. Maybe slight hyperactivity of tibialis anterior in walking or when foot stroked medially

V. Differential Diagnoses

A. Metatarsus Primus Varus

B. Hyperactive Abductor Hallucis
C. Internal Tibial Torsion
D. Femoral Anteversion
E. Clubfoot
F. Skewfoot

VI. Radiographic Evaluation of Metatarsus Adductus

A. AP View

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 1. Increased metatarsus adductus (MA) angle

a. How the MA angle is determined

i. Longitudinal axis is the lesser tarsal bones to the 2nd metatarsal bone

ii. Transect the TMTJ by dotting the “Rhomboid” shaped midfoot at the 5th
met-cuboid joint, calcaneocuboid joint, anterior medial corner of the
medial cuneiform, and the inflection point (where concave turns to
convex) of the proximal medial navicular – any lines perpendicular to this
bisection will be your long axis lines

b. Evaluating the metatarsus adductus angle on AP view

i. Normal = 0-15 degrees

ii. Mild deformity = 15-17 degrees

iii. Moderate deformity = 18-22 degrees

iv. Severe deformity = >23 degrees

NOTE: Pediatric normals are higher than adult normals for metatarsus adductus all the way up to 6 years old
where angles should start to resemble adult normal values.

2. An alternative method for determining metatarsus adductus angle is the Engle's Angle. It measures the angle
between the long axis of the second metatarsal relative to the second cuneiform and the normal value is about 18
degrees.
3. Long term compensation for MA may reveal the following:

a. moderate to severe HAV deformity

b. cuboid abduction

c. digital abductus as toes align with the rearfoot

d. increased angle of Kite

B. Lateral View
1. Compensated

a. Anterior break in cyma line

b. Plantarflexed talus in relation to 1st metatarsal

c. Decreased calcaneal inclination angle

2. Uncompensated

a. Will resemble cavus foot

VII. Conservative Treatment of Metatarsus Adductus

A. sequential reduction followed by serial casting is usually successful on patients 0-3 years of age consisting of the following
steps:
1. Apply lateral force on the metatarsals while holding the calcaneus in rectus in order to avoid creating a valgus rearfoot
2. Parents can be taught how to perform these manipulations
3. Apply below knee cast after manipulations have been performed making sure to also manipulate and hold the foot in
the desire positioning until the plaster has dried
4. Reinforce the ankle at 90 degrees with additional plaster
5. Modify the patients sitting and sleeping positions by turning the child's feet outward using a Dennis Brown bar
6. Appropriate shoe gear for the child should have a straight last with no arch

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 7. Serial casting should be continued 4 - 6 weeks after a rectus position has been attained and verified radiographically
8. After serial casting manipulations have completed a Wheaton brace may then be best to maintain corrections for up to
1 year.
NOTE: The Wheaton brace, Ganley splint, and Bebax shoe are all devices that can be used to treat metatarsus
adductus.
B. Stretching and Manipulation
1. Best if used in very early weeks of life for children with mild metatarsus adductus deformities
2. Hold the STJ in neutral or varus
3. Abduct the forefoot for 10-20 seconds and perform 10 repetitions of this stretching exercise. Educate parents to
perform this stretch 2-3 times daily
C. Serial Plaster Casting
1. Still considered to be the “gold standard” of conservative metatarsus adductus treatment
2. Involves 3 point bending of the patient's foot in the transverse plane to attain correction

a. Maintain the foot in equinus

b. Compress the tarsal bones from medial to lateral

c. Abduct at the metatarsals

3. Cast the patient weekly until a rectus position has been attained and verified radiographically
NOTE: Use of too much cast padding is a primary cause of failure when treating metatarsus adductus via serial
casting.

VIII. Surgical Treatment of Metatarsus Adductus

NOTE: Surgical intervention is rarely required as conservative treatment is usually successful.

NOTE: If patient is >3 years of age or if patient has not responded to conservative treatment at all after 6
months surgical intervention is advised.
A. Soft Tissue Repair
1. Generally reserved for patients 2 to 8 years of age that have not responded to conservative treatment
2. Procedurea. Heyman Herndon and Strong

i. Originally described as transverse incision

ii. Better to use three longitudinal incision

iii. Cut ligaments and capsule except lateral 1/3 of plantar ligament

iv. Complications include malposition of the metatarsals in the sagittal plane,

growth plate disturbance, and development of arthritis

b. Chondrotomy (usually done on patients between the ages of 6 and 8 years old) as originally
described by Johnson

i. Resect lateral based wedge of cartilaginous enlarge of base of metatarsal

2, 3, 4, and 5 with apex medially

ii. Remove 2.5 mm wedge from these lesser metatarsals

iii. Use lateral base wedge osteotomy distal to epiphysis on 1st

iv. Lengthen abductor hallucis

c. Thompson

i. Resect abductor hallucis muscle

ii. Primary indication is hallux varus with adductus

iii. Primary complication is HAV

d. Lange

i. Capsulotomy 1st metatarsal cuneiform articulation with division of

abductor hallucis

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 ii. Serial casting following surgery

e. Lichtblau

i. Sectioning of hyperactive abductor hallucis especially in equinovarus foot

with met adductus

f. Brown

i. Transfer tibialis posterior into navicular from anomalous insertion, medial

capsulotomy of naviculocuneiform joint

g. Ghali

i. Anterior medial release of 1st met cuneiform and naviculo-cuneiform joint

with division of tibialis anterior at medial aspect of medial cuneiform.

B. Osseous Repair
1. Usually reserved for patients >8 years of age
2. Cormick and Blount

a. Arthrodesis of 1st metatarsal cuneiform articulation with osteotomy of 2, 3, 4 metatarsals

3. Fowler

a. Opening wedge osteotomy of the medial cuneiform

b. Ganley does the same if articular cartilage is extremely deviated medially

4. Peabody- Muro
a. Excise bases of 2, 3, 4, osteotomy of 5, mobilize 1st met, cuneiform

b. No longer performed as it is more of a procedure of historical

significance

5. Gartland Berman

a. Most popular osseous procedure for metatarsus adductus correction

b. Involves osteotomies of metatarsals 1 – 5

6. Lepird
a. Uses a 3 incision approach (Over the shaft of the 1st metatarsal, between the 2nd and 3rd
metatarsal bases, and between the 4th and 5th metatarsal bases)
b. Perform an oblique abductory wedge osteotomy on the 5th metatarsal
c. Perform osteotomies of metatarsals 2, 3, and 4 from dorsal distal to plantar proximal (parallel
to the weight bearing plane)
i. Leave dorsal-distal-medial cortex intact
ii. Insert 2.7 mm cortical screw, but don't tighten
iii. Cut remaining cortex left intact

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 iv. X-ray foot

v. Adjust metatarsals (distal portion on proximal potion) and tighten screws.

7. Oblique osteotomy on 1st.

8. Bankhart

a. Excise cuboid

9. Tachdjian-Grice

a. Juxta-articular arthrodesis for rearfoot and soft tissue release for

forefoot

10. Steytler & VanDerWalt

a. V osteotomy of all metatarsals

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Cavus Foot
I. Definition:

Pes cavus is primarily a sagittal plane deformity of plantarflexion of the forefoot on the rearfoot, with secondary multi-planar forefoot and
rearfoot rigid and flexible possibilities, coupled with neuromuscular concerns.

II. Etiology:

A. Neuromuscular (Neurological is the #1 cause 75% of cases)

1. Muscular level (Muscular dystrophy)
2. Peripheral or spinal nerve root level

a. Dejerine Sottas

b. Charcot Marie Tooth Disease

c. Polyneuritis and trauma to spinal nerve

3. Spinal Cord level (anterior Horn cells)

a. Poliomyelitis

b. Myelomeningocele

c. Diastematomyelia and tumors in spinal cord

4. Heterofamilial affection of spino-cerebellar tracts

a. Roussy Levy

b. Friedreich's Ataxia

5. Pyramidal or Extrapyramidal system of the brain

a. Cerebral palsy (spastic hemiplegia and athetoid)

6. Cerebral level

a. Hysteria

B. Congenital
1. Talipes Equinovarus
2. Club Foot
3. Spina Bifida
C. Idiopathic
D. Iatrogenic
1. Trauma
2. Peroneal Nerve Injury
3. Post surgery
4. Weak Anterior Muscles
5. Over Powering Posterior Muscles

III. Pathogenesis (Muscle Imbalances and Spasms)

A. Weakness of anterior tibial muscle

1. Get increased plantarflexed first ray due to unopposed P. longus
2. EDL & EHL substitute and give hammer and claw toes
B. Weakness of Peroneus brevis
1. Get increased activity of longus giving plantarflexed first ray
2. Posterior tibial muscle supinates rearfoot unopposed
C. Paralysis of Intrinsics (described by Duchenne)
1. Extrinsics work unopposed and lead to hammertoes with buckling of metatarsals
D. Triceps Surae Weakness (paralysis)
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 1. Long flexors substitute and result in claw toes
2. Peroneus longus substitutes and causes plantarflexed 1st ray
3. Posterior tibial muscles compensates and supinates foot
E. Spastic Posterior tibial muscle
F. Spastic peroneus longus

IV. Classification

Classification is based primarily on the position of the foot in the sagittal plane. There are a variety of classifications and many of
these overlap which can lead to confusion.

Based on the apex of the deformity

A. Anterior Cavus Foot

• Primarily a sagittal plane deformity - excessive plantar declination attitude of the forefoot or
part of the forefoot in relation of the rearfoot
• Divided into four basic types according to the apex of the deformity
• The four types may be further classified as structural (rigid) or positional (flexible)

1. Metatarsus Cavus (apex at Lisfranc’s joint)

a. Local - involves only plantar flexion of 1st ray

b. Global - involves entire Lisfranc Articulation

Note: Differentiating these two is important in determining proper surgical procedure

2. Lesser Tarsal Cavus (apex at the lesser tarsal area)

a. Prominence noted at lesser tarsus

3. Forefoot Cavus (apex at Chopart’s joint)

a. Occurs at MTJ

b. Pathognomonic dorsolateral prominence of the Talar head

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 4. Combined Anterior Cavus - 2 or more of above (apex generalized to the lesser tarsus)
5. Compensations with anterior cavus

a. Flexible anterior cavus compensation

i. Retraction of toes - because EDL has longer distance to course, it will pull
toes

ii. Reverse buckling at MPJ

iii. Anterior cavus is seen non-weight bearing and reduces with weight
bearing, due to lesser tarsus adapting (lesser tarsal sagittal plane
flexibility)

b. Rigid anterior cavus compensation

i. Dorsiflexion of foot on ankle

ii. Functional limitation of ankle joint dorsiflexion caused by premature use of

the ankle joint motion to compensate for pure sagittal plane anterior pes
cavus deformity

iii. No STJ compensation

iv. CIA increases from dorsiflexion of foot at ankle. Called pseudoequinus

B. Posterior Cavus
1. A perspective of excessive dorsiflexion attitude of the rearfoot in relation to the forefoot
2. May not be a truly separate cavus entity
3. Less common than anterior pes cavus
4. Primarily STJ deformity
5. Deformity in rearfoot resulting in a high C.I.A.
6. Meary’s angle < 10°
7. Meary’s angle intersects proximal to Chopart’s joint
8. Frontal plane- varus (fixed) rearfoot - non-reducible
9. Posterior Cavus Compensation (Sagittal plane)

a. Flexible: Plantarflexion compensation (no change in CIA)

b. Rigid: Forefoot Plantarflexion compensation (decreased CIA)

C. Combined Cavus - combination of the above two types

1. Increased C.I.A.
2. Increased talar declination angle
3. Increased metatarsal declination angle

a. Primary Anterior

i. C.I.A. ~ 30°

ii. Meary’s angle intersects at N-C joint

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 b. Primary Posterior

i. C.I.A. > 30°

ii. Talar varus

iii. Meary’s angle intersects at Chopart’s joint

c. Pes Cavus Rearfoot Varus

i. Functional forefoot deformity with a rigid rearfoot varus

ii. Coleman Block test used to determine if RF varus is 1° or 2° deformity

Based on flexibility of the deformity

A. Flexible pes cavus (primarily reducible with weight bearing)
B. Rigid pes cavus (little reduction of cavus with weight bearing)
C. Semi-rigid pes cavus (significant reduction of cavus with weight bearing but maintaining a moderately
increased calcaneal inclination angle)

V. Preoperative assessment

A. Thorough family history & exam siblings & parents

B. Examine muscles to rule out paralytic disease (Muscle strength assessment)
C. Neurologic consult (Neurologic picture - is deformity progressive)
D. Nerve conduction and EMG studies
E. X-ray of spine
F. Orthopedic exam
1. Gait analysis

a. High stepping indicative of weak anterior muscles

b. Wide based gait with short steps suggests neurological etiology

2. Position of hindfoot
3. Rigidity of hindfoot and forefoot
4. Coleman Lateral block test is used to determine if the hindfoot is mobile.
Place a 2.5 to 4 cm thick block on the floor and have the patient stand with the heal and lateral edge of
the foot bearing full weight on the block while the medial forefoot (1st, 2nd and 3rd metatarsals) hang
off the block. Examine the heel from the rear. The test is based on the premise that the first metatarsal
is in fixed flexion. It negates the effect that the forefoot (fixed flexion of the 1st metatarsal) may have
on the hindfoot in stance. If the heel varus corrects to neutral position, the hindfoot is mobile
(flexible). Thus, the deformity seen clinically is due to plantar flexion of 1st metatarsal and surgical
procedures may be directed at correcting forefoot pronation due to the 1st metatarsal flexion. If the
hindfoot remains in varus there is fixed hindfoot inversion deformity (or possibly spasticity of the
tibialis posterior). Isolated correction of the excessive plantar flexion of 1st metatarsal alone will not
be successful. Surgical correction of both the forefoot and hindfoot are required. Click here to view a
video of the Coleman block test.
https://www.youtube.com/watch?v=TCp25F0l7hc

5. Can forefoot be reduced with rearfoot

6. Evaluate for ankle equinus
7. Kelikian push-up test to determine the flexible or rigid digital deformities
G. Locate apex of deformity
H. What type of cavus (Classification)

VI. Radiographic Evaluation

A. X-rays should be taken both non-weight bearing and weight-bearing

B. Increased calcaneal inclination angle - greater than 30 degrees

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C. Normal cyma line to posterior break in the cyma line
D. Accentuated sinus tarsi
E. Decreased Hibbs angle

F. Meary's angle: Is used to determine the apex of the deformity

1. Meary's Angle or lateral talo-first metatarsal angle has been used to identify the apex of deformity in patients with pes
cavus and pes planus on lateral weight bearing radiograph. It is the angle between lines drawn from the centers of the
longitudinal axes of the talus and the first metatarsal. In the normal weight-bearing foot, the midline axis of the talus is in
line with the midline axis of the first metatarsal.

Normally Meary's angle is 0 degree.

angle> 4 degrees (convex upward) - pes cavus
angle> 4 degrees (convex downward) - pes planus

It can also be used to assess severity of the pes cavus deformity

angle < 15 degrees - mild deformity
angle 15-30 degrees - moderate deformity
angle > 30 degrees - severe deformity

G. Line through proximal and distal articulations of medial cuneiform may be seen to converge instead of being parallel
H. Coalition views should be used to assess the subtalar joint

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 I. An axial view of the calcaneus should be performed to rule out a structural varus

VII. Treatment

A. Underlying etiology MUST be determined

B. Determine the plane of the deformity
C. The cavus foot may require multilevel correction ie. Digits, Lisfranc’s joint, Midfoot, Rearfoot
D. Non surgical treatment
1. Indicated in mild pes cavus or when surgery is contraindicated
2. Orthotics, AFO's, Shoe modification, physical therapy
E. Surgical classification
1. Type I - Mild Pes Cavus Flexible

a. May appear normal when weight bearing

b. Tylomas, metatarsalgia, contracted digits (extensor substitution)

c. Surgery

i. MPJ release

ii. PIPJ fusions

iii. Hibbs procedure

iv. Other soft tissue releases

2. Type II – Moderate Pes Cavus

a. More rigid and more evident clinically

b. Primarily sagittal plane deformity

c. Hammertoes, tylomas, metatarsalgia

d. Surgery

i. DFWO of 1st metatarsal

ii. Dwyer calcaneal osteotomy

iii. Digital procedures

3. Type III – Severe Pes Cavus

a. Marked rigid deformity

b. Gait abnormalities

c. Multiplanar

d. Surgery

i. Major tarsal fusions or osteotomies

ii. Digital procedures

iii. Triple arthrodesis

VIII. Procedures

A. Soft Tissue Procedures

1. Plantar Fascia Release
2. Steindler Stripping

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 a. Release plantar fascia, abductor hallucis, FDB, abductor digiti quinti, and often the quadratus
plantae muscle attachment to the heel

3. Tendon Transfers
a. Jones
i. Transfer EHL from the hallux to the 1st metatarsal
ii. Indications: A flexible Platarflexed 1st ray, weak Tibialis Anterior
b. Hibbs
i. Transfer EDL from each toe out to the midfoot (lateral cuneiform or
cuboid)
ii. Indications: flexible anterior cavus, flexible claw toes, patients with
extensor substitution or weak tibialis Anterior, EDL, EHL
c. STATT (Split Tibialis Anterior Tendon Transfer)
i. Split Tibialis Anterior tendon in half. The lateral half is transferred to
insert with the peroneus tertius, lateral cuneiform, or cuboid
ii. Indications: weak anterior muscle, swing phase supination
d. Posterior Tibial Tendon Transfer/ Lengthening procedures
i. Transfer Tib. Post. to dorsum of foot through EDL, peroneus tertius or Tib.
Ant. tendon sheath.
ii. Indications: A weak anterior muscle group
iii. Very difficult to perform and it is an out of phase transfer
e. Peroneus Longus Tendon Transfer

i. Transfer the peroneus longus to the dorsum of lesser tarsus through EDL
tendon sheath or split through Tibalis Anterior & peroneus tertius sheaths.

ii. STOP procedure : Suture Peroneus Longus to Peroneus Brevis

• indications: flexible 1st ray, heel varus

iii. Peroneus Longus Lengthening

• Decreases plantaflexion of 1st ray

• Indications: Flexible 1st ray or weak tibialis anterior muscle

B. Osseous Procedures
1. Digital Reduction to restore MPJ alignment

a. PIPJ arthrodesis

b. Extensor hood resection

c. Extensor tendon lengthening

d. Flexor plate release

e. Fixate (K-wire)

2. DFWO metatarsals
3. Cole Wedge Osteotomy Procedure

a. Described a closing wedge osteotomy with removal of a dorsally based wedge. The wedge is
removed from a distal cut through the cuboid and cuneiforms coupled with a proximal cut through the cuboid
and navicular. This elevates the forefoot out of equinus.
b. Primarily indicated for patients with a static or non-progressive pes cavus deformity
c. The Cole osteotomy corrects mainly in the sagittal plane, and is primarily indicated for rigid
anterior pes cavus. In the strictest terms, it is indicated for a global anterior cavus or lesser tarsus cavus
when the apex of the deformity occurs near the naviculo-cuneiform joints, or over the lesser tarsus. It is
contraindicated when the apex of the deformity is any place other than the midfoot.
d. The procedure is not indicated for the skeletally immature foot, as this can lead to shortening.

e. It is important that the talonavicular and calcaneal-cuboid joints are spared during this
procedure.

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 f. It may be combined with other procedures to achieve multiplanar correction

4. Japas V Osteotomy Procedure

a. Described a through-and-through V-shaped osteotomy. The transverse plane V-shaped

osteotomy is performed with the apex proximal in the navicular and the
arms extending distally through the cuboid and the first cuneiform.

b. Indicated for anterior pes cavus

c. The procedure is not indicated for the skeletally immature foot

5. Dwyer

a. A lateral closing wedge osteotomy (wider laterally than medially) to correct fixed varus of the
calcaneus

b. Indications:

i. Calcaneal varus

ii. Posterior cavus

iii. Non-reducible deformity

c. Contraindications:

i. Reducible calcaneal varus 2° to plantarflexion of the 1st ray.

ii. Note: It is important to do Coleman Block test to determine reducibility or

not

6. Triple Arthrodesis See Triple Arthrodesis (in surgical procedures/techniques section)

a. Can correct all planal deformities

b. Commonly performed for severe cases of pes cavus

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Polydactyly
I. Preaxial Polydactyly

A. If it involves the tibial side of foot

B. Would involve duplication of hallux
C. Occurs in 15%

II. Postaxial polydactyly

A. Involves the fibular side of foot

B. Duplication of 5th toe
C. Most common type - occurs in 80% of cases
D. Two types
1. Type A - a well developed articulated digit
2. Type B- a vestigial rudimentary digit devoid of osseous tissue

III. Central Ray Polydactyly

A. Occurs in 5% of cases

IV. Mixed Polydactyly

A. Pre and post axial occurs in same patient

B. This condition occurs over nine times more frequently in blacks
than white.
C. 50% of cases are bilaterally

V. Radiographic Evaluation

A. Six patterns associated with duplicated digits.

1. Short block metatarsal
2. Y-shaped metatarsal
3. T-shaped metatarsal
4. Normal metatarsal shaft with wide head
5. Partial or complete ray duplication
6. Normal metatarsal with distal phalangeal duplication

VI. Treatment

A. As digital supplication often involves osseous, tendinous and neurovascular structures, surgeon must determine the digit which
has the most potential for normal growth, and which is most functional
B. Excise the toe that would allow the foot to assume the most normal contour & facilitate shoe wear
1. Usually amputating the most medial toe when the great toe is involved
2. Amputating the most lateral toe when the fifth toe is duplicated
C. Preaxial Polydactyly
1. Standard route is usually disarticulation of the medial involved digit
2. Increased incidence of Hallux varus following this, so one may need to K-wire across the MPJ or lengthen the abductor
hallucis

D. Post Axial Polydactyly

1. Allow the plantar skin that was under 6th metatarsal or skin located on the plantar lateral side of the foot to be the
new thick skin located on the lateral 5th metatarsal.
2. Scar should be dorsal to 5th met shaft
3. In case of abnormal metatarsal configuration (Y or T), the prominent bone portion should be trimmed flush with the
metatarsal shaft.

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 4. If wide metatarsal head is present, it should be narrowed. Make
cuts perpendicular to physis and no growth disturbance will occur.
E. Central Ray Duplications
1. Usually require a dorsal racquet shaped incision at the base of
the toe.
Step-By-Step Procedure

Tarsal Coalitions
I. Etiology

A. Definition: The formation of an osseous bridge between two bones that normally articulate with one another and have a well-
defined joint space between them. This union typically results in absent or decreased motion between the bones which can
become quite painful for the patient. The union may also result in peroneal spastic flatfoot in the patient.
NOTE: Tarsal Coalition is the most common cause of peroneal spastic flatfoot in patients though not all tarsal
coalitions will result in its development. In fact some coalitions may develop without symptoms at all.
B. Development
1. Congenital: There are two theories that attempt to explain the congenital malformations resulting in a tarsal coalition.

a. A study done by Leonard supports the theory in which the mutation of an autosomal gene
resulting in a failure of differentiation and segmentation of primitive mesenchyme. This
results in the lack of normal joint formation between two tarsal bones. Furthermore the
evidence suggests that this form of tarsal coalition displays autosomal dominant inheritance
among the patient’s offspring.

b. An alternate theory proposed earlier by Pfitzner suggests that congenital coalitions may
develop due to the incorporation of nearby ossicles into the joint space resulting an osseous
bridge between the two bones in the fetus.

2. Acquired: Coalitions may develop as a result of arthritis, infections, trauma, and neoplasms.

II. Incidence

A. Tarsal coalitions occur equally among male and female patients

B. The talocalcaneal and calcaneonavicular coalitions are the most common type of coalition (90% of all cases) though it is
currently debated as to which of the two is more common it is believed that talocalcaneal coalitions are slightly more common
C. 50% of all coalitions are seen to be bilateral

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 D. Tarsal coalitions show no racial preference

III. Classification

A. Extra-articular Coalitions: These occur outside of the joint and are commonly referred to as “bars”
1. Calcaneonavicular
2. Cubonavicular
B. Intraarticular: These occur at a joint and are commonly referred to as “bridges”
1. Talocalcaneal (Anterior Facet, Middle Facet, Posterior Facet, and Combination)
NOTE: Coalitions involving the middle facet are the most common.
2. Talonavicular (More typically seen in very young patients)
3. Calcaneocuboid
4. Naviculocuneiform
C. Types of Coalitions
1. Syndesmosis - Fibrous
2. Synostosis - Osseous
3. Synchondrosis - Cartilaginous
View Coalition Classification

IV. Clinical Signs & Symptoms

A. Age when ossification begins & possible onset of symptoms

1. Talonavicular: 3-5 years of age (The least symptomatic coalition)
2. Calcaneonavicular: 8-12 years of age
3. Talocalcaneal: 12-16 years of age
NOTE: The onset of pain is usually insidious, aggravated by activity, and relieved by rest.

B. Symptoms of Tarsal Coalition

1. Painful Range of Motion
2. Typically a deep aching pain in the area of the coalition itself

a. In patients with the most common type of coalition (talocalcaneal middle facet) the patient
may point to the dorsal midfoot area as being the source of the most pain

3. Limited Range of Motion

a. Decreased midtarsal joint and/or subtalar joint range of motion is one of the most common
finding in patients

4. Tonic Peroneal Spasms

5. Negative Hubscher Maneuver
• involves passive dorsiflexion of the hallux while the patient stands in a normal relaxed position. If the
deformity is flexible, the medial longitudinal arch will increase in height and the rearfoot will supinate.
If the deformity is rigid (typical in tarsal coalitions) no change in the arch will be seen.

V. Diagnosis

A. Primarily done via radiographs. Note: Osseous coalitions with clear bony bridging are more easily diagnosed than fibrous or
cartilaginous coalitions in which cases MRI and CT are a better modality for evaluation).
1. Lateral Foot View: The middle and posterior facet joint lines can be well visualized on a lateral view

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 a. Primary Signs

i. C-Sign

ii. Anteater Sign

b. Secondary Signs
i. Talar Beaking
ii. Narrowing of the posterior talocalcaneal facet
iii. Flattening/Widening of the lateral talar process
iv. Rounded cortical margins
v. Altered calcaneal trabecular pattern
vi. Decreased Boehler angle

vii. Degenerative ankle joint changes

viii. Radiographic finding typical of flatfoot deformity

NOTE: One of the most reliable indicators of a tarsal coalition is the absence of the middle facet of the subtalar
joint.

2. Medial Oblique Foot View (45 degrees)

a. Typically used to better visualize a calcaneonavicular bar coalition

3. Ischerwood Views

a. Typically used to visualize the anterior facet

b. No longer in regular use due to the difficulty in holding the patient in the proper position while
the views are acquired

4. Harris Beath Views

a. Best used when attempting to visualize a talocalcaneal

coalition
b. Normally the middle and posterior facets lie on the same
plane. A talocalcaneal coalition is indicated by obliquity (difference
of greater than 20 degrees between the two facets) of the middle
facet in this particular view

c. Irregular sustentaculum tali and rounded lateral talar

process on these views are also indicative of a tarsal
coalition

5. Broden's Views

a. Best used to visualize the posterior facet in tarsal coalitions

6. Computed Tomography

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 a. Often considered to be the most definitive technique for visualizing tarsal coalitions when
plain film x-rays are inconclusive or when a more thorough view of the coalition is desired by
the surgeon

b. For TC coalitions frontal or coronal plane images 2-4 mm thick are most helpful in visualizing
the coalition

c. Other coalitions are best visualized using transverse plane CT images

7. MRI

a. MRI may detect concomitant pathology, some of which may be secondary to the underlying
coalition, such as stress fracture or stress reaction due to altered biomechanics, or ankle
sprains

NOTE: Although CT and MRI both provide detailed information for diagnosing and determining the extent of
tarsal coalitions, MRI can be more accurate in subtle cases of fibrous coalition, where osseous changes may
not be as conspicuous.

VI. Treatment

A. Conservative
1. Splinting
2. Below Knee Casting (Non-weightbearing)
3. Shoe modification (Thomas Heel, Medial heel wedge, longer medial heel counter, or medial longitudinal padding)
4. Custom Shoe Orthotics (Limit STJ range of motion)
5. Steroid Injections (into the sinus tarsi)
6. Physical Therapy
B. Surgical
NOTE: Surgical intervention typically consists of either resection of the bar or fusion of the involved joint
depending on many patient dependent factors like the type of coalition, age of the patient, mobility of the
patient, and any degenerative joint changes. (Resection is the preferred method for younger patients in order
to maintain as much mobility as possible)

1. Extra-articular coalitions respond best to resection via the following Badgley procedure:

a. Ollier (curvilinear) incision beginning over the lateral sinus tarsi and ending medially to the
lateral aspect of the talonavicular joint

b. Identify and avoid severing the intermediate dorsal cutaneous nerve which travels medially in
this area as well as the sural nerve which travels laterally

c. Resect the bar. Be certain to resect enough of the coalition (at least 1 cm).

d. Identify the extensor digitorum brevis muscle and sever at its origin

e. Interpose the EDB muscle belly into the space created between the navicular and calcaneus

NOTE: Interposition of the muscle belly into the defect created by the resection serves as a spacer that will
prevent complications such as recurrence of the bar as well as hematoma and seroma.

f. Keith needles may be used to then pass suture through the bottom of the patient's foot tying
the suture to a button with gauze placed at the base

g. Place a large drain in the area before closure

h. Place the patient in a below knee non-weightbearing cast for 4-6 weeks

i. Complications include dehiscence due to hematoma, seroma, and infection. As

well as recurrence of the bar

NOTE: Calcaneonavicular bars are best resected by age 14 in order to prevent secondary changes.
NOTE: Triple arthrodesis is typically used to resolve issues of recurrence or continued pain in patients that do
not respond well to resection.

2. Intraarticular coalitions typically respond better to arthrodesis. If the patient is young and does not also have
degenerative joint changes in the area then one must consider first attempting a resection
a. Resection of a middle facet talocalcaneal coalition (medial approach)

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 i. Linear incision made posterior and inferior to the medial malleolus to
plantar medial aspect of the first cuneiform
ii. Identify and retract the tibialis posterior and flexor digitorum longus
muscle tendons dorsal then the neurovascular bundle and flexor hallucis longus tendon
plantar
iii. Identify and resect the middle facet coalition which should immediately
result in an observable increase in the patient's subtalar joint motion

iv. Adipose tissue may then be

transplanted from the Kagar's triangle into the newly created deficit after the resection has
been performed (The adipose tissue is to act as a spacer) Alternatives options to consider
would be to split the flexor hallucis longus and interpose it into the space instead

v. Close then apply a below knee cast

to the patient and keep them non-weightbearing for 4-6 weeks

NOTE: A resection may fail even with juvenile patients having no associated degenerative changes. In that
case the patient may go on to require a triple arthrodesis.

Intraarticular Surgical Guidelines

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Tarsal Tunnel Syndrome
I. Definition

A. An entrapment or compression neuropathy of the posterior tibial nerve or one of its three main branches, the medial and
lateral plantar and medial calcaneal nerves as the nerve passes under the flexor retinaculum at the level of the ankle or
distally.

II. Anatomy

A. The Tarsal Tunnel

1. Formed by the flexor retinaculum (laciniate ligament) as it passes from medial malleolus to the posterior inferior
aspect of the calcaneal tuberosity.
2. Borders of the tarsal tunnel are flexor retinaculum (medially), the posterior aspect of the calcaneus and talus (laterally),
and the medial malleolus (anteriorly)
3. The contents of the tarsal tunnel listed from medial to lateral are the tibialis posterior muscle tendon, the flexor digitorum
longus muscle tendon, the posterior tibial artery, the posterior tibial vein, the posterior tibial nerve, and the flexor hallucis
longus muscle tendon.
4. Porta pedis (Abductor Canal): A canal created by abductor hallucis muscle belly through which the medial and lateral
plantar nerves pass.
B. The Divisions of the Posterior Tibial Nerve
1. The division into its three main branches most commonly occurs proximal to the flexor retinaculum.
2. The divisions may also occur within the flexor retinaculum or distal (uncommon) to it.

a. Branches

i. Medial Calcaneal Nerve: sensory nerve that may pierce the flexor
retinaculum

ii. Medial Plantar Nerve: Provides sensory innervation to the plantar aspect of
the hallux, second, and third toes as well as the medial aspect of the
fourth toe and medial aspect of the plantar foot; Motor innervation to the
abductor hallucis and flexor digitorum brevis muscles

iii. Lateral Plantar Nerve: Provides sensory innervation to the plantar lateral
aspect of the fourth toe, plantar aspect of the fifth toe, and plantar lateral
aspect of the foot; Motor innervation to the abductor digiti quinti and
quadratus plantae muscles.

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III. Etiology

A. Most common cause is idiopathic. 36% of patients suffering from tarsal

tunnel syndrome had no identifiable cause at the time of surgical
decompression. (McGlammary)
B. Local trauma (fractures, dislocations, and ankle sprains) were found to
be the most common (34.5%) identifiable cause of tarsal tunnel
syndrome (Grumbine)
C. Space occupying lesions (varicosities, lipomas, neurofibromas,
neurilemmomas, ganglions, synovial cysts) lying within or adjacent to
the tarsal tunnel.
1. The most common space occupying lesion causing tarsal tunnel
has been identified as varicosities (dilated posterior tibial veins)
(Lau & Daniels, 1999)
D. Systemic disease with synovial thickening and urate or arthritic deposits
in the surrounding joints and soft tissues.
1. Rheumatoid arthritis, Reiter's syndrome
2. Diabetes mellitus (neuropathy)
E. Mechanical - neuritis associated with specific trauma of compensatory eversion at the subtalar joint associated with midtarsal
and subtalar joint pronation
1. Rearfoot Varus
2. Rearfoot Valgus
F. Thickening of the Flexor Retinaculum

IV. Clinical Signs and Symptoms

A. History may or may not involve an injury.

1. Ankle sprains are frequently associated with the later development of tarsal tunnel syndrome
B. The patient may relate a history of intermittent burning, tingling, or numbness over a diffuse area of the foot
1. These sensations typically progress from intermittent to constant over time
2. Sensations are typically aggravated by long periods of exercise, walking, or standing and relieved by rest
C. Positive Hoffman-Tinel sign with paresthesia radiating proximally into the calf and/or distally into the foot.
• The Hoffman-Tinel sign, although originally described by Paul Hoffman, is commonly referred to as just
"Tinel sign". It is a tingling sensation triggered by a mechanical stimulus to an injured nerve. This
sensation radiates peripherally, from the point where it is triggered to the cutaneous distribution of the
nerve. The tingling response can be compared with that produced by a weak electric current, The
unpleasant sensation is not a severe pain and does not persist.

D. Valleix point Note: There is a lot of controversy about the tinel's sign and the Valleix sign in the literature. Most of us were
taught that a Tinel's sign was a tingling sensation distal from the point of palpation and a Valleix sign was tingling distal and
proximal to the point of palpation. Some of the new terminology can be confusing.

• Valleix point, Any of various points in the course of a nerve upon which pressure is painful in cases of
neuralgia.

V. Diagnosis (not always sharply definitive)

A. History of previous trauma or radiographic evidence of previous injury

B. History associated systemic disease or conditions (appropriate lab studies for arthritides, diabetes, etc.)
C. Hoffman-Tinel sign Note: If you percuss too hard, you'll get tingling even if there is no entrapment. Only significant if
unilateral.

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D. Forced eversion of the foot on the affected side may produce symptoms
E. MRI may be used to identify any space occupying lesions present in the area

F. Needle Electromyography and Motor/Sensory Nerve Conduction Velocity Testing

1. Not definitive for the diagnosis of tarsal tunnel syndrome, however, very helpful in
patients with very vague or poorly localized complaints of pain where conservative
treatments have failed and another cause cannot be identified
2. Normal NCV versus abnormal NCV seen in patients suffering from tarsal tunnel

See also: EMG/NCV

Normal NCV

Abnormal Tarsal Tunnel NCVs

Note: The normal images contain action potentials which are of a higher amplitude and the AP waveform itself
is better defined. In the abnormal image the action potentials are all in the 20's which is considered to be a
relatively "low" amplitude for the nerves that are being tested. The deformed AP waveform and it being
relatively lower amplitude than normal.

3. The compound nerve action potential (CNAP) has been noted to be absent or abnormally prolonged in many patients
experiencing tarsal tunnel syndrome. In some patients this action potential has been noted to return after performing a
tarsal tunnel release (Oh, 1991)
Tarsal Tunnel Release Action Potential

G. When electrodiagnostic studies are negative, the use of pressure- specified sensory device (PSSD) has been recommended.
1. PPSD is a quantitative sensory testing device that measures cutaneous pressure thresholds, similar to the Semmes-
Weinstein monofilament test.
2. PPSD records one-point static and moving touch and static and moving two-point discrimination

H. The Cuff Test involves inflating a pneumatic pressure cuff at the proximal ankle above the patient's diastolic blood pressure
(generally it is inflated to 60- 80 mm Hg). This results in venous engorgement and reproduces symptoms. A positive cuff
test is highly suggestive of a nerve entrapment secondary to venous pressure.
I. Local anesthetic injection of the posterior tibial nerve can also be used. Immediate resolution of the symptoms indicates poster
tibial nerve involvement. If there is no improvement then consider a further workup to elicit the etiology of the patient's pain.

J. Differential Diagnoses

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 1. Amyloid neuropathy
2. Charcot disease
3. Ganglion cyst
4. Hereditary motor and sensory neuropathies
5. Lumbar disc disease (If pain radiates to lower back consider radiculopathy)
6. Peripheral neuropathies
7. Plantar fasciitis
8. Posterior tibialis dysfunction
9. Reactive arthritis (Rieter's syndrome)
10. Rheumatoid arthritis
11. Stress fractures

VI. Treatment

A. Conservative Measures

a. NSAIDS

b. Steroid Injections (Local posterior tibial nerve blocks with the local infiltration of
corticosteroids deep into the flexor retinaculum over the area of tenderness with
immobilization in the neutral position)

c. Physical Therapy

d. Functional orthotics for those with excessive pronation

e. (AFO) Ankle/Foot Orthotic

f. Compressive Stockings for patients presenting with varicosities and/or evidence of venous
insufficiency

B. Surgical treatment
Note: (done without a tourniquet to visualize the posterior tibial artery and the tortuous veins that need
ligation)

1. Decompression of the tarsal tunnel

a. 4-6 cm curvilinear incision behind the medial malleolus

b. Release flexor retinaculum

c. Dissect distally toward the abductor hallucis removing any hypertrophic tissue from the
abductor hallucis as needed

d. Release abductor fascia of porta pedis then expose the medial and lateral plantar nerves
incising the septum between them

e. Remove any soft tissue masses present and ligate or excise any varicosities as needed near
the nerves of the tarsal tunnel

f. Free posterior tibial nerve and any branches in the area from surrounding entrapments

g. Flush and drain the involved

h. Close without reapproximating the retinaculum

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 i. A dry sterile Jones compression dressing is applied and the patient is kept non-weight
bearing for 3 weeks and then partial weight bearing till 8 weeks

VII. Complications

A. Recurrence secondary to fibrosis

B. Permanent or temporary loss of sensation due to severing or damaging one of the nerves during the procedure
C. Tenosynovitis
D. Severed posterior tibial artery (requires microvascular repair)
E. Hematoma/Seroma/Infection
F. Wound Dehiscence

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PART 7:
PERI-
OPERATIVE
MANAGEMENT

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Perioperative Management of Patients
I. Diabetic Patient

A. Local anesthetic: no change in diet, or medication regimens. Closely monitor post-op blood sugars to avoid stress-associated
hyperglycemia.
B. General anesthetic:
1. Well controlled on diet: - nothing
2. Well controlled on oral agents (minor surgery):
a. Discontinue the medication one day before surgery
b. No insulin - no glucose protocol during surgery
c. Reinstate oral medication when patient starts eating.
3. Well controlled on oral agents (major surgery):
a. Better to use continuous I.V. insulin during surgery.
4. IDDM well controlled (minor short procedure) --no insulin no glucose.
5. IDDM well controlled (long procedures):
a. 1/3 to 1/2 of patient’s usual dose of intermediate acting insulin sub-Q on the morning of
surgery
b. Followed by dextrose infusion with insulin added. (i.e.-- 500 ml. of 5% dextrose over the first hour
then 125 ml/hr. of 5% dextrose plus 2u/hr. of regular insulin).(1u/hr. in patients taking less than
20u/day pre-operatively).
c. During long cases adjustments should be made for blood glucose levels taken intraoperatively.
e. Post-op:
1. Closely monitor blood glucose

2. Check hydration of the patient

3. Check plasma potassium (insulin tends to lower K.)

II. Patient on Steroid Therapy

A. Asthmatic, COPD, cancer therapy, transplant patient, autoimmune diseases (rheumatoid, SLE, Crohn's disease)
B. Steroids effects:
1. Suppresses hypothalamic-pituitary-adrenal (HPA) axis (can cause hypotension/cardio-vascular collapse).
2. Poor wound healing
3. Predisposition to infection
NOTE: If a patient takes 7.5 mg/day or more of prednisone for longer than a week during the year preceding
surgery you should suspect their adrenal reserve to be decreased.
C. Prophylactic antibiotic is not indicated
D. Oral vitamin A 1 week pre-operatively will improve wound healing.
E. An ACTH stimulation test can assess a patient's ability to undergo stressful surgery.
F. If a patient has been on steroid therapy during the previous year or during emergencies (no time for ACTH test) do coverage.
G. For minor cases:
1. Hydrocortisone IV or IM
2. 100 mg the evening before surgery
3. 100 mg at the beginning of surgery
4. 100 mg q8h for 24 hours.
H. For major cases: same as above except continue the q8h dose until all stress from postoperative period has passed.
NOTE: tapering is necessary only if coverage is needed for more than 24 hours.

III. Hypertensive Patient

A. Let patient take their meds as usual pre-operatively.

B. Postpone surgery for severely hypertensive patients until they are controlled.
C. Immediate post-op acute elevation of B.P. can occur (pain volume overload, tube).
D. Treatment
1. Remove noxious stimuli (tube)
2. If no response:
a. Diuretics (furosemide 40-80 mg I.V. over 5 mins.)
b. Or beta blocker (propranolol 1-3 mg I.V.).

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IV. Patients with Clotting Abnormalities

A. When history and examination suggest bleeding problems order

1. Platelet count
2. PT
3. PTT
4. Bleeding time
B. Drugs that alter platelet function
1. Aspirin
2. NSAID
3. Steroids
4. Antihistamines
5. High doses of I.V. penicillin (especially carbenicillin)
C. Abnormalities that cause bleeding problems
1. Hemophilia
a. Three types:

1. Factor VIII All three affect the intrinsic

2. Factor IX pathways, therefore PTT is affected.

3. Factor XI

2. Vit K deficiency:
a. Vit. K is used by liver to produce factors II,VII, IX, X.
b. Effects both intrinsic and extrinsic pathways (therefore, effects PT & PTT)
3. Von Willebrand's Disease
a. Impairment in the synthesis or function of von Willebrand factor (VWF).
b. For the treatment of minor bleeding or minor surgery, the use of intravenous or intranasal DDAVP
(Desmopressin) in patients who have shown a prior response to this agent. If bleeding is not
adequately controlled, a von Willebrand factor (VWF) concentrate should be used.
c. For the treatment of major bleeding or major surgery, or for patients whose bleeding does not respond to
DDAVP (Desmopressin) or need therapy for longer than three days, use a VWF concentrate.
d. Can causes abnormal PTT, bleeding time & platelet adhesion.

D. Management
1. Hemophilia:
a. Use cryoprecipitate or antihemophilic factor.
b. Dosage: amount necessary to raise factor VII to 80% of normal is infused 2 hrs before surgery. Then 1/2
of that dose q12h for 10-14 days.
2. Vit K deficiency:
a. 10 mg Vit K sub Q will normalize patient in 8 hrs.
b. Immediate control of homeostasis requires fresh frozen plasma.
c. If the liver is bad Vit K will not work.
3. Von Willebrand's Disease:
a. Fresh frozen plasma or cryoprecipitate.

V. Anticoagulant Therapy Patients

A. Heparin
1. Inhibits intrinsic pathway
2. Monitor with PTT
3. Use protamine to reverse
4. Used as prophylaxis against DVT and initiation of long-term therapy.
5. Prophylaxis:
5,000 u Subq 2 hrs before surgery
5,000 u Subq q12h until patient ambulates.
B. Coumadin (warfarin)
1. Inhibits extrinsic pathway
2. Monitored by P.T.
3. Reverse effects with Vit K or rapidly by fresh plasma or frozen plasma.

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 C. Perioperative Management
1. Minor procedures (under local): keep them on their meds if P.T. is stable.
2. Major procedures: stop oral meds 3 days prior to surgery and start back post-operatively.

Mnemonic (Think of alphabetic order)

A Coumadin PT Extrinsic K (vitamin) 2 times the control
Z Heparin PTT Intrinsic Protamin 2-3 times the control

VI. Patients with Cardiac Disease

A. Management
1. Good history: identify risk factors pre-operatively (i.e.--previous MI, CHF, hypertension, smoking, unstable angina). All
risk factors should be stabilized preoperatively.
2. Elective surgery should not be performed within 6 months of a myocardial infarct and in patients with
uncompensated congenital heart disease.
3. EKG is usually recommended for patients older than 50 years of age or patients with a positive history of heart
disease.
4. Pre-operative test: CBC, SMA6, baseline EKG & CXR. See EKG Interpretation.
1. Nitrates and beta-blockers should be continued during the perioperative period.
2. Endocarditis prophylaxis should be considered for patients with acquired and congentital valvular heart disease with a rheumatic
murmur and prosthetic valves.
a. Amoxicillin: 3 Gms pre-op and 1.5 gm post-op (taken 1 hour pre-op and 6 hours post-op.
b. If patient has a penicillin allergy, use Clindamycin 300 Mg pre-op and 150 Mg post-op.
1. Post-op monitoring is imperative.
a. ICU for 3 days watch for silent MI's

VII. The Anemic Patient

A. Lowest pre-operative hemoglobin level is 9-10g/dl

B. 4 g/dl is acceptable with sickle cell anemia and anemia associated with chronic renal failure.
C. If transfusion is necessary do it at least 24 hrs pre-operatively.
D. Note: In patients demonstrating anemia after a surgical procedure due to blood loss it is recommended that the physician
type and cross the patient and transfuse as soon as possible.
E. Note: After receiving a blood transfusion the patient may display signs of hyperthermia, leukocytosis, nausea, puritis, and
urticaria.

VIII. The Malnourished Patient

A. Diagnosis
1. History:
a. Diet
b. Weight loss
c. Anorexia
d. Vomiting and/or diarrhea
2. Physical:
a. Koilonychia (soft thin, brittle nails)
b. Anemia
c. Bruising
e. Dehydration
3. Tests:
a. CBC
b. SMA-6
c. Serum albumin (less than 3mg/dl)
d. Serum transferrin (less than 200mg/dl)
4. Treatment:
a. Perioperative oral or parenteral
b. Nutrition

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Interpretation of EKG's
The EKG is reliable for diagnosing ischemic heart disease, myocardial infarction, frequent premature ventricular contractions and
other pathologic arrhythmias. It is usually recommended for patients older than 50 years of age or patients with a positive history of
heart disease.
See Perioperative Management of Patients with Cardiac Disease also.

I. Basic principles:

• Heart cells are charged or polarized in the resting state, but when electrically stimulated, they "depolarize" and contract.
• The wave of depolarization (cells become positive inside) and repolarization (cells return to negative) are recorded on the EKG.

• Fig 1 The SA node begins the electrical impulse, which spreads in a wave
fashion, stimulating both atria. This electrical impulse yields a P wave on the
EKG. Thus, the P wave represents the electrical activity of the
contraction of both atria.

• Fig 2 The impulse reaches the AV node, where there is a 1/10 of the second pause,
allowing blood to enter the ventricles. The flat line between the P wave and the QRS
complex represents this.

• Fig 3 The QRS complex represents the electrical activity of ventricular contraction.
The neuro-muscular conduction system of the ventricles is composed of the AV node,
the AV bundle, and the right and left bundle branches, which terminate in the fine
Purkinje fibers. This system allows for rapid conduction of the electrical impulses to all
the heart cells in the ventricles.

• Fig 4 The Q-wave is the first downward stroke of the QRS complex NOT preceded by an R wave and is
often not present. The R-wave is the first upward deflection of the QRS complex. Any downward stroke
preceded by an upward stroke is an S-wave.

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 • Fig 5 There is a pause again after the QRS complex. This is the ST segment and is represented
as a flat line again between the QRS complex and the T-wave. The T-wave represents
the repolarization of the ventricles. The ventricles have no physical response to
repolarization. It is strictly and electrical phenomenon recorded on EKG.

• Fig 6 So, one cardiac cycle is represented by the P-wave, QRS complex,
and T-wave.

• Fig 6a Several intervals are regularly measured. They provide a significant amount of
information concerning the progression of action potentials throughout the myocardium.

• PR Interval
This is the time from the initiation of SA nodal depolarization to the initiation of ventricular depolarization. It
encompasses the time it takes for the action potential to pass through the AV node. The normal PRI is 120-200
msec. This demonstrates that the electrical impulses are originating from the atria and following the proper
conduction pathways. It is normal for the PRI to shorten slightly during tachycardia, and lengthen during
bradycardia within the limits stated above.
• QRS Duration
The normal QRS duration is 60-100 msec. It is measured from the initiation of ventricular depolarization at the Q
or R wave, to the last wave of the complex. This point where the R or S wave returns to baseline is called the J
point. Prolonged QRS indicated conduction problems. Bundle branch blocks often cause this.
• QT Interval
This interval spans the onset of depolarization of the ventricles to the completion of repolarization of the
ventricles. Electrolyte balance, drugs, and ischemia influence the QT interval. Lengthened QT intervals indicated
slowed ventricular repolarization. This may be due to hypokalemia, or other electrolyte imbalances. Shortened
QTs are seen with hypercalcemia and digitalis toxicity.

II. Systematic examination of an ECG

A. Rate:
1. The rate is read as cycles per minute.
2. The rate is normally set by the SA node (the normal cardiac pacemaker), which is located in the posterior wall of the
right atrium.
3. Other areas of the heart have the ability to set a pace if normal pacemaking mechanisms fail. We referred to these
potential pacemakers as "ectopic" pacemakers, which generally function only in disease or emergency conditions.
4. Ectopic foci in the atria, AV node, and ventricles can discharge at their own inherent rate when normal peacemaking
fails.
a. Atria = 75/min.
b. AV node = 60/min.
c. Ventricles = 30-40/min.

Note: In emergency or pathological conditions the ectopic foci may discharge at a rapid rate
(150-250/min.). This rapid rate is the same for all three areas.

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 5. Quick method of determining rate: Fig 8

• Find an R wave (of a QRS complex) that falls on a heavy black line on the EKG tracing. Count off "300,
150, 100, 75, 60, 50" for each heavy black line that follows.
Memorize these triplicates: "300,150,100" and "75,60,50"
• Where the next R wave falls determines the rate.
• For rates below 50, count the number of complete cycles (R to R wave) that occur in 6 sec (two 3 sec
markers across the top of an EKG) and multiply this number by 10.
6. Sinus Tachycardia Fig 9 is a rate of greater than 100/minute with a normal rhythm (a regular rhythm which
proceeds normally from the SA node, and each repeated cycle takes the same amount of time which results in a
steady continuous rate).

7. Sinus Bradycardia Fig 10 is a rate of less than 60 per minute (with a normal rhythm).

B. Rhythm: Note: There are many abnormal arrhythmias that go beyond the scope of this review. For a more in depth
discussion of ECG's please review Rapid Interpretation of EKGs by Dale Dubin, MD (sold on Amazon.com). For our purpose we
will review some of the more common and serious arrhythmias.
1. Sinus arrhythmia: Fig 11
• Often caused by coronary artery disease (sick SA node disease).
• Normal waves similar in size and shape but irregular timing between cycles.

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2. Atrial Flutter: Fig 12
• Originates in atrial ectopic foci.
• Characterized by rapid succession of the waves, which are identical to each other.
• Occasionally an atrial stimulus will stimulate the AV node, which results in the typical appearance of a
few flutter waves in a series before a QRS complex is seen.

3. Atrial fibrillation: Fig 13

• Is caused by the firing of multiple foci in the atria. Since no single impulse depolarizes the
atria completely you will not see any real P waves. Only an occasional impulse gets through
to the AV node.

• Always presents with totally irregular rhythm sense only random impulses get to the AV node
to initiate a QRS complex.

4. P.V.C.’s (Premature Ventricular Contractions): Fig 14

• Caused by an ectopic foci somewhere in one of the ventricles.

• Like all other premature beats it occurs very early in the cycle (before a P-wave is expected).

• The impulse of the PVC does not follow the usual bundle branch conduction system; herefore
conduction is slow (a very wide QRS complex).

• There is a long (compensatory) pause after the PVC during which the heart is electrically
silent.

• Numerous PVCs may originate from the same foci. More than six PVCs per minute is
considered pathological.

• PVCs may indicate that the hearts blood supply is poor, so their appearance alerts us that
something may be wrong.

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 5. Ventricular Flutter: Fig 15

• Is produced by a single ventricular ectopic focus firing at a rate of 200-300/min.

• Characterized by the smooth sine wave appearance.

• Ventricular flutter deteriorates into deadly arrhythmias.

• True ventricular flutter almost always becomes ventricular fibrillation.

6. Ventricular Fibrillation: Fig 16

• Is caused by stimuli from many ventricular ectopic foci (each firing at a certain rate), which
results in a chaotic twisting of the ventricles.

• Often referred to as a "bag of worms"

• When ventricular fibrillation occurs, there is no effective cardiac pumping.

7. Myocardial Infarction: The classical triad of an acute myocardial infarction is "ischemia", "injury"
and "infarction". All three are not required to establish the diagnosis of myocardial infarction. However,
they do provide a good set of criteria to routinely check for. The "three I" Triad is the basis for
recognizing and diagnosing the signs of myocardial infarction.

1. Ischemia: Fig 17

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 • Ischemia (decreased blood supply) is characterized by inverted T-waves. This may
vary from a slightly flat or depressed wave to the inversion. The inversion is
symmetrical.
• Inverted T-waves may indicate ischemia in the absence of myocardial infarction.
• Sense the chest leads are nearest the ventricles always check the V1-V6 leads.

2. Injury: Fig 18

• Injury indicates acute infarct.

• ST segment (the section of baseline between the QRS complex and the T-wave)
elevation denotes injury (acute or fresh infarct). It may be slightly elevated, or as
much as 10 or more millimeters above the baseline.
• The ST segment rises above the baseline with an acute infarction but later returns
to the level of the baseline. If the diagnosis of infarction has been made it is
important to know whether the infarction just occurred and needs immediate
treatment or if the infarction is old (normal ST segment).
• Pericarditis may elevate the ST segment also. However, the T-wave is also
elevated.
• A ventricular aneurysm may also cause ST elevation. However, the ST segment
does not return to the baseline with time.
• Therefore, ST elevation by itself could represent any of the above conditions.

3. Infarction: Fig 19

• The Q-wave makes the diagnosis of infarction.

• Note: the Q-wave is the first downward part of the
QRS complex and is never preceded by anything in the
complex.
• Q waves are absent in most of the leads in tracings
from a normal person. However, leads I, II, V5 and V6
commonly containing insignificant Q waves which are
considered normal and do not signify the presence of an
infarction.
• A significant Q wave is one small square wide (one
millimeter = .04 sec.) or one third the size of the QRS
complex. Fig 20
• Check all leads except the AVR lead (it can exhibit a
phony Q-wave which is really an upside down R-wave)
for significant Q waves.

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8. Asystole: Fig 21

• Is a state of no cardiac electrical activity, hence no contractions of the myocardium

and no cardiac output or blood flow.

9. Heart Blocks: occur in any one of three areas: The SA Node, AV Node or the Bundle branches

• SA (Node) block Fig 22 causes the pacemaker to temporarily stop for at least one
cycle, but then the pacemaker resumes the pacing activity.

• AV (Node) block creates a delay of the atrial impulse at the AV node, making a
longer than normal pause before stimulating the ventricle. The delay of AV block
prolongs the P-R interval more than one large square (.2 seconds) on EKG.
• 1° (first degree) AV block Fig 23 is present when the P--QRS--T sequence is
normal, but the P-R interval is prolonged.

• 2° (second degree) AV block is present when it takes two or more atrial

impulses to stimulate the ventricular (QRS) response (2:1 Fig 24 or 3:1 block Fig
25).

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24

25

● Note: The Wenckebach Phenomenon occurs when the

P-R interval becomes progressively longer until the AV
node is not stimulated (no QRS). (pronounced Winky-
bok) Fig 26

is often seen in a type of second-degree AV block

called Mobitz I. Fig 27

It is characterized by progressive prolongation of the PR

interval on the electrocardiogram (ECG) on consecutive
beats followed by a blocked P wave (i.e., a 'dropped'
QRS complex). After the dropped QRS complex, the PR
interval resets and the cycle repeats.

● Mobitz II block Fig 28

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 is noted, when occasional ventricular depolarization is
missed after a normal P wave and generally uniform PR
interval in the preceding cycle. Mobitz II often heralds
serious AV node problems with progressively more
involved blocking of nodal conduction. The medical
significance of this type of AV block is that it may
progress rapidly to complete heart block, in which no
escape rhythm may emerge. In this case, the person
may experience a Stokes-Adams attack, cardiac arrest,
or Sudden Cardiac Death. The definitive treatment for
this form of AV Block is an implanted pacemaker.

● 3° (complete block): Fig 29

occurs when none of the atrial impulses stimulate the AV node

(no ventricular response). The ventricles must be paced
independently,and as a result, the unstimulated ventricles or AV
node call into action an ectopic pacemaker. In this case, there
is an atrial rate, and an independent ventricular rate. If the
QRS's appear normal, the rhythm is often said to be "ideonodal"
(AV node pacer) and if the QRS's are wide and bizarre. The
rhythm is often called "ideoventricular" (ventricle
pacemaker). The location of the ectopic pacemaker is
sometimes assumed by the ventricular rate, i.e. ventricular rate
of 60 -- nodal pacemaker, ventricular rate of 30 to 40 is a
ventricular ectopic pacemaker. Note: In 3° block the pulse
(ventricular rate) may be so slow that the blood flow to the
brain is diminished. As a result, a person with third-degree
block may lose consciousness. This is strokes-Adam's
syndrome.

● Bundle Branch Block: Fig 30

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is caused by a block of the impulse in the right or left bundle branch,
which causes one ventricle to fire slightly later than the other resulting in
two "joined QRS's" The depolarization of both the right and left sides are
of normal duration. Because of this they do not fire simultaneously,
which makes the "widened QRS" appearance that we see on EKG.
Because the "widened QRS" represents the non-simultaneous
depolarization of both ventricles, we usually see two R waves named in
order R and R'.

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Steroid Replacement Therapy
I. Patient on cortisone therapy

Asthmatic, COPD, cancer therapy, transplant patient, autoimmune diseases (rheumatoid, SLE, Crohn's disease)
NOTE: If a patient takes 7.5 mg/day or more of prednisone for longer than a week during the year preceding
surgery you should suspect their adrenal reserve to be decreased.

II. Coverage:

For minor cases:

1. Hydrocortisone IV or IM
2. 100 mg the evening before surgery
3. 100 mg at the beginning of surgery
4. 100 mg q8h for 24 hours.
For major cases: same as above except continue the q8h dose until all stress from postoperative period has passed.

III. Complications of long term steroid therapy

A. Suppression of the hypothalamic - pituitary - adrenal (HPA) axis

Symptoms of adrenal insufficiency:
1. Hypotension
2. Nausea, Vomiting
3. Dizziness
B. Predisposition to infection: decreased white count, so infections can be masked.
C. Decreased epithelization and wound contraction for first three days.
D. Poor wound healing
1. Inhibit production of fibroblast
2. Prolong healing time
3. Decrease the inflammatory process
4. Increase risk of infection due to decreased WBC

IV. Physical Characteristics of long term therapy with steroids:

A. Moon face
B. Truncal obesity
C. Buffalo hump
D. Abdominal striae

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PART 8:
SURGICAL
PRINCIPALS

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Biopsy Techniques
I. Types of Biopsy

A. Excisional Biopsy - entire lesion is removed

B. Incisional Biopsy - portion of lesion is removed

II. Method of Biopsy

A. Punch Biopsy

1. Best to select the most mature and well-developed lesion. Biopsies on leg & feet heal
more slowly.
2. Cleanse area, taking care to leave scabs, crusts, and vesicles intact
3. Anesthetize with local anesthetic of 1:100,000 or 1:200,000 epinephrine. Ring area
to be biopsied or field block with local anesthetic. Intradermal injection directly
into or below a lesion appears to cause little or no perceptible microscopic
alteration.
4. Biopsy punches are available in sizes ranging from 2-8mm in diameter. 4 mm
punch is most commonly used. Removal of specimen less than 4mm in
diameter may allow the histologic confirmation of a tumor, but is inadequate for
diagnosis of inflammatory process.
5. Skin surrounding the lesions should be stretched taut perpendicular to the wrinkle
lines before the circular punch is inserted. The punch biopsy is firmly pressed
downward into the lesion with a rotary back and forth cutting motion until it is well
into the subcutaneous tissue.
6. Gently grasp biopsy plug with forceps and cut base with scissors and place sample into 10% formalin
7. 4 mm punch or greater needs to be sutured, less than 4 mm punch apply sterile dressing or steri-strips and sterile dressing.
8. Simple pressure is adequate for hemostasis. Linear defect heals more readily than round defect.

B. Shave Biopsy

This removes that portion of the skin elevated above the plane of surrounding tissue and is useful for
biopsy or removing many benign epidermal growths. This is also a convenient procedure for diagnosis of
malignant lesions such as BCE.
1. Cleanse area
2. Inject anesthetic, use a #15 blade to remove elevated growth, put tissue in 10% formalin.
3. Pressure for hemostasis.

C. Surgical Excision Biopsy

This should be considered under the following circumstances

1. There are lesions with active and spreading borders
2. The junction of the lesion and normal skin is important to survey
3. The lesions are atrophic and sclerotic
4. It is important to acquire adequate full-thickness skin (e.g. in
panniculitis and erythema nodosum)

D. Curettage

This is a useful technique for removal of benign cutaneous lesions such as warts. Also, effective in treating basal
and squamous cell carcinoma. 4 mm curette is most common size.

EXCISION TECHNIQUES

There are several common skin lesions, which are necessary to excise as the treatment of choice at certain times.
1. Verruca
2. Inclusion cyst
3. Hypertrophic scar
4. Nucleated fibrotic keratotic plug.

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 These are handled in a manner similar to that of the surgical excision biopsy technique.
1. Mark area to be excised
2. Avoid depositing the anesthetic solution in the area to be excised
3. The length of the ellipse should be three to four times the width.
4. Place long axis of the wound in the direction of the crease lines.
5. Undermine the wound edges if necessary to keep tension off wound edges.
6. Avoid weight bearing on plantar wounds for approximately two - three weeks.

Bone Grafting Techniques

I. Terminology

A. Transplantation: Transfer of viable tissue that will thrive in host bone.

B. Implantation: Transfer of nonliving tissue (i.e. Freeze-dried bone) to host.

II. Biology and Physiology of Bone Grafting

A. Osteogenesis is defined as the synthesis of new bone by cells residing within the graft itself or cells of the host.
B. Osteoinduction refers to the ability of substances in the graft to induce nonosseous tissue to become osteogenic in the presence of a
favorable environment.
C. Osteoconduction is where the graft provides a lattice-work, scaffold, or trellis that allows surviving host tissue to invade and
propagate enabling new bone formation or graft replacement. It is the primary method by which freeze-dried allogenic bone
heals. This process may last several months in cancellous autografts, but it can persist for years in allografts. Osteoconduction is the
means by which creeping substitution can take place.
D. Creeping Substitution is the process by which the "cutting cone" of new osteoclasts, followed by osteoblasts, will invade the graft
from host bone.

III. Types of Bone Grafts

A. From one's own bone- autograft or isograft.

B. From identical twin - isograft
C. Living bone from same species - allograft or homograft.
D. Dead bone from same species - alloimplant or homoimplant
E. Bone from different species (not recommended for general use) - xenograft or heterograft.

IV. Functions of Grafting

A. Osteogenesis
B. Immobilization
C. Replacement

V. Specific Functions

A. Treatment of delayed union, nonunion and pseudarthrosis.

B. Augment defects - pack defects from trauma or removal of cysts.
C. Facilitate of arthrodesis of joints
D. Bone blocks to limit motion
E. Reconstructive procedures - i.e. Evans, repair of brachymetatarsia.

VI. Forms of Grafts:

A. Cortical grafts - densely compact, contain few transferrable viable cells, and provide stable graft that can be fixed to
surrounding bone with fixation devices.
B. Cancellous grafts - less dense bone and contains viable transferable cells (osteogenesis). Is incorporated much more rapidly.
C. Corticocancellous grafts - (i.e. iliac crest) provides stability and osteogenesis (best of both worlds). This may explain why
the iliac crest tricortical auto-grafts have become the favored material in many settings.
Cortical Verses Cancellous Bone Grafts

Characteristic Cortical Cancellous

Incorporation Slow More Rapidly

Maturation Slow Faster

Initial Mechanical Strength Very strong Little to none

Predominant Initial Activity Osteoclastic Osteoblastic

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Strength Weakens during the first 6 weeks Becomes stronger initially

VII. Advantage of Autogenous bone

A. Viable cells - the amount depending on if cancellous or cortical.

B. Immunologically compatible with host tissue.

VIII. Complications of Autogenous grafts

A. Creates stress point of donor site with possible fracture and need for immobilization in many cases.
B. Adds another surgical procedure, which increases anesthesia and chance of hematoma, infection, etc.
C. May be insufficient quantity of donor bone.
D. Donor site can be painful and reveal scar.

IX. Allografts and Alloimplants

A. Considerations
1. Immunologic compatibility
2. Sterile
B. Functions best as a spacer for osteoconduction (ingrowth of vessels for new bone) Scaffolding effect.

X. Composite Grafting (a mixture of autogenous and allograft)

A. Uses autogenous bone for osteogenic effect and allogenic graft for structural effect.

XI. Management of Autogenous Bone Grafts:

A. Irrigation and cooling during cutting of bone

B. Use sharp drill, saws or osteotomes (some studies show osteotomes best)
C. Avoid excessive high RPM's of power
D. Put graft in container and cover container with moistened saline sponge. ** Do not store in saline solution**
E. Use Cefazolin 30 minutes preop and no more than 24 postop.
F. Take from same extremity to prevent damage to two extremities.

XII. Sites for Autogenous graft

A. Iliac crest
B. Greater trochanter
C. Proximal and distal tibia
D. Calcaneus

E. Fibula (midshaft is almost all cortical)

F. Rib

XIII. Graft healing

A. Prerequisites
1. Mechanical stability
2. Vascularization of graft bed
3. Close contact of graft and host environment
B. Radiographic appearance
1. Slow amorphous sclerosis followed by radiolucency

XIV. Complications of Grafting

A. Failure of 15 - 20%

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 1. Used wrong type graft (i.e. cancellous graft when cortical graft needed)
2. Inadequate mechanical stabilization (fixation)
When grafting a nonunion, autogenous graft preferable.

External Fixation
I. History
a. Today, most external fixators are based on the Hoffmann and Ilizarov constructions.
b. Dr. Gavriel A. Ilizarov, a Russian physician is credited with making most of the advances for current external
fixation.
II. General principles of external fixation
a. External fixation can be used to compress, distract, angulate or rotate bone segments with respect to each
other.
b. Decreased soft tissue dissection, which provides minimal trauma.
c. Can obtain immobilization of multiple regions while applying compression or distraction at various sites.
d. Avoids areas of vascular supply.
e. Allows for post-operative adjustment.
f. With stable external fixation, early range-of-motion exercises are possible and with the Ilizarov and some
hybrid fixators, full weight bearing immediately post-operatively can be achieved.
g. Behrens 3 basic principles:
i. The frame should avoid and respect all vital anatomic structures.
ii. It should allow access to the injured area for later fixation, bone grafting,
debridement and soft tissue reconstruction.
iii. It should meet the mechanical demands of the patient and the injury.
III. Placement of pins and limb anatomy
a. The lower leg and foot have four corridors (anatomic compartments) each. These corridors allow for save pin
insertion.
b. The tibia and foot have an eccentric position, which allows easy osseous access and placement of pins closer to
the anatomic axis of the osseous segment. This increases overall stability.
c. The entire medial and anterior surface of the tibia are relatively safe for pin insertion.
d. At the ankle and foot, the corridors become narrow. Avoid the fibular neck where the common peroneals nerve
is found.
e. In the foot avoid the area of the tarsal tunnel and the dorsum of the foot.
f. If a question of neurovascular injury exists, remove the pin and reposition it.
IV. Types of Fixators
a. General information
i. When all pins used in a fixator are placed in the same plane (i.e., coplanar) the frame is
considered uniplanar.
ii. There are two types of uniplanar frames.
a. Unilateral pins encompass less then a 90 degree arc (half pins).
b. Bilateral pins have a 180 degree arc (transfixation pins).
iii. Most external fixators used in the foot and ankle do not allow for early weight bearing.
However, circular tensioned wire configurations do allow for axial loading of the
extremity.
iv. Frame stability is determined by:
a. Pin diameter.
b. The number of pins.
c. The pin spread.

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 d. The distance of the connecting bar from the mechanical axis of the bone being fixed.
v. The stiffness of the frame and, therefore, the amount of motion at the healing bone
interface is determined by the:
a. Frame configuration.
b. Size of pins
c. Number of pins.
vi. The bending moments of the tibia are greater in the anterior posterior plane than in the
coronal plane.
vii. In the foot the primary displacing forces occur in the dorsoplantar direction.
b. Unilateral Fixators:
i. Produce monoplane distraction or compression. (Note: articulated unilateral fan produce
triplane motion).
ii. Indications for use:
a. Fixation of fractures.
b. Fusion joints.
c. Lengthening of bone.
d. Special techniques:
i.Treatment of monoplanar deformities.
ii.Osteomyelitis.
iii.Bone transport in the foot, leg, hand and arm are possible.
iii. Biomechanics:
a. Primary weakness is lack of stability in the sagittal plane. Therefore, immediate weight
bearing is not indicated. Weight bearing may begin 6-8 weeks into osseous healing phase.
c. Circular Frames:
i. Can be used in monoplane and biplane deformities.
ii. Has the ability to create distraction and rotation in two planes at the same time.
iii. Used most often in the leg, arm and rearfoot, but can be used in the small bones of the
foot and hand.
iv. Indications for use:
a. Limb lengthening.
b. Bone transport.
c. Non-unions.
d. Fixation of fractures.
e. Correction of biplane deformities.
f. Primary joint fusion.
g. Soft tissue lengthening.
v. Biomechanics:
a. Provide sagittal plane stability, white allowing axial rotation.
b. Allows for immediate full weight bearing through the use of transosseous wires and
distal circular fixators.
d. Hybrid fixators:
i. Combination of unilateral or bar fixator and one or more circular or ring fixator.
ii. Indications for use:
a. Treatment of Pilon and tibial plateau fractures.
b. Primary fusion of the ankle.
iii. Biomechanics:
a. Provides sagittal plane compression or distraction and through the use of olive wires
provide additional transverse plane compression.
b. Limitation in full weight bearing in the foot and ankle without the addition of a
footplate and multiple rings. Therefore, when used in the rearfoot, immediate weight
bearing cannot be permitted.
e. Taylor spatial frame fixators:
i. Allows for the reduction of triplane complex deformities.
ii. Indications for use:
a. Reduction of deformity and stabilization of fractures.
V. Application of External Fixation in the Foot and Leg
a. Mechanical distraction (limb lengthening):
i. Limb lengthening involves the clinical application of the Law of Tensionstress. Tension
stress effect is the governing principle that allows for the gradual distraction of osseous
and soft tissues to achieve lengthening of the skeletal system. The Law of Tensionstress
is directly affected by:
a. The stability of the fixator.

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 b. The rate of distraction.
c. The frequency of distraction.
d. The position and type of osteotomy.
ii. Methods of lengthening through mechanical distraction:
a. Epiphyseal distraction or chondrodiatasis.
i. Had complication and not used now.
b. Metaphyseal corticotomy distraction.
i. Allows better preservation of osseous vascular supply.
ii. Initial distraction occurs between 7 and 14 days (a delay in distraction allows for
an increased volume of callus).
iii. Distraction then begins at a rate of .25 mm every 6 hours for a total of 1 mm
per day.
b. Angular deformity:
i. Uniplane deformities can be corrected using a special T-type fixator.
ii. Biplane and triplane deformities require circular or Taylor spatial fixators.
iii. A hinge system is set to allow distraction of the opposite side of the deformity. Circular
fixation uses one or two parallel hinges most of the time, while unilateral fixation uses
one hinge most of the time.
iv. When correcting biplane and triplane deformities, angular correction is preceded by
distraction. The bone callous allows correction without jamming the opposite cortical
bone.
c. Fractures:
i. The use of unilateral fixators in the treatment of metatarsal fractures allows for
weight bearing within 4-6 weeks.
ii. Distraction causes ligamentotaxis (pulling of fracture fragments into alignment). This
phenomenon works well with calcaneal fractures.
d. Arthrodesis:
i. Triple Arthrodesis.
ii. Tibiocalcaneal arthrodesis.
iii. Ankle or ankle and subtalar arthrodesis.
iv. First metatarsophalangeal joint arthrodesis.
VI. Fixator Management
a. Generally, pin-skin junction sites are cleansed with peroxide or sterilizing scrub solution on a daily, weekly or
biweekly basis. Povidone-iodine (Betadine) is not used due to potential corrosion.
b. Topical antibiotic cream or ointment is the applied and initially dressings (gauze).
c. Inspect the fixator and its components regularly for worn or damaged parts.
VII. Postoperative Management
a. The last phase in the use of external fixation is the dynamizing process. This consists of the release of
tension from the transosseous wires and loosening of all half-pin connections to the fixator. This
allows the bone to strengthen and decreases the risk of fracture when the fixator is removed.
b. The appearance of cortical bone on three sides of the healing bone is sufficient for removal of the fixator. This is
for distraction.
VIII. Complications
a. Minor: pin tract infections, fractured transosseous wires or half-pins, and pain from the wires.
b. Major: non-union, osteomyelitis, neurovascular injury, joint subluxation and bone fracture.

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Internal Fixation Techniques
I. Stability of fractures is determined by two entities:

A. Intrinsic Factors
1. Fracture Configuration

a. Stable fractures-transverse fracture configuration

b. Potentially stable fractures - those with intact cortical walls (greenstick and torus)

c. Unstable fracture - oblique or spiral fractures tend to be displaced with axial loads resulting in
shortening

2. Bone Composition

a. Cancellous fractures usually have greater degree of friction between fragments owing to bone-
to-bone contact.

b. Cortical fracture sites will have less stabilizing effect

3. Bone Quality

a. Purchase of fixation devices are compromised in bone with poor quality

B. Extrinsic Factors (Soft tissue attachments play a major role in the stability of a fracture)
1. Tendons, ligaments and periosteum - can either aid manipulation of a fracture or prevent successful reduction
2. When multiple fractures exist, soft tissue attachments between larger fragments can be instrumental in providing
satisfactory realignment and stabilization
3. Vassal phenomenon - fixation of the dominant fracture will afford stabilization to the subordinate fracture
4. Mechanical forces that affect fractures stability include: bending, torsion, shearing. Compression tends to cause fractures
but once fracture occurs, it will usually be a stabilizing force.

II. Goals of Internal Fixation

A. Anatomic Reduction
B. Stable Internal Fixation
C. Atraumatic technique - will preserve the vascular supply
D. Active mobilization

III. Splintage Techniques

A. K-Wires come in smooth or threaded with sizes .035, .045 and .062. Steinman pins are larger, most frequent size is .078
inches.
1. Advantage of single pin fixation

a. Has advantage with small fragments that have minor tendency to disruption.

b. Also good in displaced transverse metatarsal fracture and is the method of choice when
crossing physeal plate.

2. Disadvantage of single pin fixation

a. Poor resistance to distraction and rotatory forces (can be diminished by using additional pins
in divergent directions.

b. Hazards of smooth pins are that they have a tendency to migrate into the wound (bend wire to
prevent). Proper bandaging prevents dislodgement.

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 3. Threaded K-wires resist distraction or pullout, but care must be taken to prevent separation of the fracture fragments as
the far fragment is penetrated (this is accomplished by compressing fragments as wire is inserted). Fatigue and failure can
occur since the core diameter is decreased.
B. Stainless Steel Wire
1. Intraosseous wire loop

a. Used to stabilize small fracture fragments

b. Bones with thick cortical walls are best suited for this type of fixation to prevent the
complication of pull through.

c. Wire loops should be placed perpendicular to the fracture at 90 degrees to each other for
maximum stability

2. Cerclage wire
a. Used to prevent telescoping of an oblique fracture
b. Also used as a gathering influence to control small fragments and used with other forms of fixation

c. Sizes are measured in gauges from 18 to 30 (larger numbers = smaller gauges)

d. Fatigue and failure of the wire has been a common complication of its use in internal fixation,
due to back & forth bending

3. Staple Fixation

a. Designed or use almost exclusively in cancellous bone

b. Since force of impact is great, staples in thick cortical bone carries significant risk of fracture
(may pre drill to prevent this)

c. Staples resist distraction forces across site, but do not withstand shear or bending

d. Two more points of fixation provide better resistance to rotation forces and a 90 degree angle
between staples affords the most secure fixation

e. Insert staple with as few strikes as possible to prevent loss of contact between bone and
staple

f. Excellent choice for an opening Wedge osteotomy.

IV. Rigid Internal Fixation

A. Motion between bone ends is primary cause for unpredictable healing and lack of differentiation of callus to bone tissue
B. Fractures healing without callus formation do so when they are rigidly fixed
1. Known as primary vascular bone healing
2. Rigid internal fixation: no minimal gap and no motion
C. Types of Internal Fixation
1. Interfragmental Compression
a. Static interfragmental compression - result of tension exerted on the pre stressed implant at the fracture
interface. (Example is lag effect by screw fixation)

b. Dynamic interfragmental compression - utilizes a combination of static forces in conjunction

with physiologic loads that naturally occur about extremity. (Example - tension-band
technique)

2. Lag Screw Technique

a. Most significant and versatile method of achieving static interfragmental compression

b. Lagged screw is one that engages only the far fragment with its threads. Compression occurs
as head of screw contacts the near cortex and the threads purchasing the far fragment pull
the fragments together.

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 3. Types of Screws
a. Cortical screws
1. Fully threaded, since degree of purchase is directly related to the number of threads in
contact with bone
2. Full thread pattern allows the maximum amount of threads to purchase a thin cortical wall
3. Screw size = diameter of threads
4. Comes in 1.5 mm, 2.0 mm, 2.7 mm, 3.5 mm and 4.5 mm sizes
b. Cancellous screws
1. Only partially threaded so over drilling of near cortex is not necessary to produce
interfragmental compression
2. No threads should cross fracture line (distraction occurs)
3. Cancellous screws have wider thread pattern and thinner core
4. Sizes are 4.0 mm, 4.5 malleolar, and 6.5 long and short thread

5. Normally used in metaphyseal bone.

6. Is considered the Classical "Lag Screw"

V. Techniques of Screw Fixation Screw Quide

A. Ideally, screws perpendicular to fracture line, perpendicular to near cortex. Unfortunately, situation does not exist many times)
B. When screw is placed perpendicular to oblique fracture line, the axial loading can cause poor stability and telescoping of the
fragment
C. When single screw is used, must be oriented 1/2 between perpendicular to center and fracture line
D. In long oblique or spiral fracture, this is amenable to multiple screws. Therefore, 1st screw is oriented perpendicular to cortex
and others are oriented perpendicular to fracture line.
E. Screw Insertion Techniques

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 1. Guide hole is drilled through both fragments with K-wire or drill bit
2. Glide hole (overdrill) the initial guide hole of the near fragment is increased in diameter by over drilling. This allows
threads to pass through this near cortex without purchase
3. Thread hole - the guide hole is enlarged in the far fragment by use of hand driven drill bit (can use drill guide)
4. Countersink - it reduces prominence of screw head, and shapes bone to fit undersurface of screw head, giving even force
distribution (preventing stress fractures)
5. Depth Gauge - add 1 to 2mm to size measured to insure purchase of far cortex.
6. Tap - cuts thread pattern through the thread hole. (Use tap sleeve to prevent soft tissue wrapping around)

VI. Plate Fixation

A. Another method of obtaining rigid internal fixation, and in some cases, can create interfragmental compression.
B. In most cases, plates are used as splintage to provide protection of the interfragmental compression provided by lag screws
C. Function of plates
1. Axial Interfragmental Compression

a. Can only be obtained with a pre- stressed plate

b. Relatively transverse fracture configuration is required to obtain axial interfragmental

compression, since oblique fractures under this type of fixation become displaced.

c. One needs to eccentrically drill either a tubular or dynamic compression plate to accomplish
axial interfragmental compression

1. Dynamic compression plate is thick

2. Can pre-bend a tubular plate to compensate for loss of thickness

3. When possible, one should apply the plate to the side of bone under tension

2. Neutralization
a. Some fractures (long, spiral, oblique, comminuted) are not amenable to axial compression.
Interfragmental compression can be obtained by lag screws. Once fixation with lag screws, protection of shear,
bending and torsional forces about the fracture site can be reduced by using plate as neutralization plate

b. Any plate can be used as a neutralization plate as long as it is well molded, although tubular
plates work the best.

3. Buttressing

a. Are used in the fixation of unstable fractures to maintain alignment of the fracture fragments

b. No interfragmental compression is achieved

c. Plate bridges between larger fragments with intervening small fragments. Cancellous bone
grafts under protection of a buttress plate can replace devitalized bone fragments removed.

4. Anti-Glide used as a neutralization plate but placed on the back of the fibula.

VII. Techniques of Plate Fixation

A. Rules
1. Four Cortices are to be purchased in metatarsal fractures
2. In proximal skeleton, five cortices recommended
3. Axial intrafragmental compression need 6 cortices
B. Axial Compression with Tubular Plate
1. Plate is contoured and pre-bent
2. Eccentric drilling of hole adjacent to fracture without needing to overdrill
3. Other holes are drilled centrally
C. Neutralization Plates
1. Can use separate interfragmental screw and can use lag screw through neutralization plate.
2. All screws are centrally drilled

VIII. Tension Band Principles

A. When a bone is eccentrically loaded and subjected to bending forces:

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 1. Tension side is on the convex side
2. Compression side is on the concave side
B. To achieve tension banding, the bone must be able to withstand compression and plate or wire must absorb the tensile forces.
C. Tension band device can be either stainless steel wire or a plate
D. Avulsion fractures (malleolar and 5th met bases) very amenable
E. K-wires are often aids to tension band wiring to enhance rotational stability. K-wire is crossed over the area of the fracture to
center compression force

IX. External Fixation

A. Primary application is for fractures associated with soft tissue defects, comminuted or osteoporotic bone and infection.
B. Device can be used to provide rigid fixation (if fracture transverse), can be used as a splint or to maintain distraction of an open
comminuted fracture
C. Main Difficulty is placement of percutaneous pins

Neutralization plates are not a specific type of plate. Neutralization refers to how a plate functions in fracture
fixation. A neutralization plate removes the loading forces on a fracture by spanning the fracture and
transmitting the loading forces through the plate rather than through the fracture site. This allows the primary
fracture fixation to be accomplished with other devices such as lag screws.

Buttress plates are used to rigidly hold in place fractures at the end of long bones, especially at the knee and
ankle, where the fracture site experiences large compressive and other distorting forces. To provide adequate
fixation, these plates are broadened and carefully contoured at the joint end of the plate. For this reason, they
are often referred to as periarticular plates. The periarticular surfaces of long bone are complex having several
surfaces and unique topographic feature at each surface. Buttress plates are contoured to a particular surface
(medial, lateral, anterior, etc.), and thus several different plate designs may be necessary for an individual
periarticular region. There are a large number of buttress plates. Some of the more common configurations are
T-shaped, L-shaped and bulbous end shaped plates. The contoured, periarticular portion of the plate give these
plates a three dimensional configuration.

In general, Buttress plates are used frequently in more distal (Metaphyseal) and comminuted fractures where
as Neutralization plates are used in more proximal (diaphyseal) fracture and counter Axial load forces.

Tumor Resection
Interlesional:

Curettage, debulking, resection within capsule of tumor.

Marginal:

Resection of tumor capsule, leave reactive zone (therefore a chance of reoccurrence).

Wide a.k.a. En Bloc:

Resection of tumor capsule, and reactive zone

Radical:

Resection of tumor capsule, and reactive zone plus normal tissue

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Plastic Surgery
I. Criteria for designing an incision

A. Parallel to relaxed skin tension lines (RSTL)

B. Adequate length and direction of exposure (length to width ratio = 3.5:1)

C. Avoidance of neurovascular structures

II. Incisions

A. Incisions made parallel to RSTL will remain approximated.

B. While those made perpendicular to RSTL will gap apart.
C. Pinching skin of foot parallel to RSTL will give regularly shaped furrow.
D. Pinching it obliquely will give "S" shaped.
E. Pinching it perpendicular will give limited skin mobility.

III. Problem

A. Difficulty arises when RSTL are in a transverse direction, but exposure needs to be longitudinal (example - plantar fibromatosis)
B. Answer - use zigzag incision. This will give longitudinal exposure and will keep most of incision in RSTL

IV. Skin Grafting

A. Success Rates
1. If bacteria less than 10Λ5 per gram of tissue, success of graft is 94%
2. If bacteria greater than 10Λ5 per gram of tissue, success is 19%
B. Free skin graft
1. Completely detached from body
2. Nourishment must be derived from new vascular connections at recipient site.
C. Autograft - transfer of graft within same individual
1. Allograft - graft is from same species but different
E. Isograft - from identical twins
F. Xenograft - different species - does not take, functions as biologic dressing
G. Bare bone, tendon, cartilage, nerve will not support graft

V. Split Thickness

A. Thin split thickness skin graft (.008 - .012 inches) heals readily
1. Wound contracts a lot
B. Intermediate split thickness skin graft (.012 - .016)
1. More small blood vessels contact recipient site
2. More durable, but doesn't heal as readily as thin
3. Usually best choice
C. Thick split thickness skin graft - 0.16 - .020 inches
1. Much greater chance of failure
2. Contain all of epidermis and dermis
3. Has no superficial fascia or fat
4. Wound contracts very little
D. Ways to obtain graft
1. Blair and Humby Knives - most common hand knives
2. Electric Dermatome - most commonly utilized

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VI. Steps Utilized in Skin Grafting

A. Lubricate skin with sterile mineral oil

B. Apply pressure to donor site
C. Use electric dermatome with slow even pressure
D. Assistant grasps corners of skin at each end as it comes through dermatome
E. Once graft obtained, you can perform the following
1. Graft meshing - gives uniform fishnet appearance to expand the graft, allowing it to cover more area, and allow drainage
to prevent hematoma
2. Pie crusting - allows surgeon to get smaller amount of expansion and drainage, make sharp cuts in graft
F. Prepare recipient site
1. Sharply debride wound edges and curette base to remove excessive fibrous tissue
2. If excessive bleeding, use gauze soaked in local anesthetic with epinephrine or topical thrombin
3. Cut graft to fit wound and suture in place
4. Can store excessive graft for 21 days at 0-5 degrees C
5. Apply pressure to wound
6. Immobilize limb
7. Leave dressing in place 3-4- days
8. If fluid buildup evident, puncture with #11 blade to drain
9. After 3 days, graft should pink up
10. If necrotic areas, excise it and use stored graft

VII. Donor sites

A. Thigh/buttock (irregular surface, but hidden from view)

1. Use "Op Site" polyurethane film - allows epidermal regeneration in this moist environment. Less pain on removal

VIII. Graft healing

A. Must be complete contact between graft and recipient bed

B. Three stages
1. Plasmatic 24-48 hours fibrin layer found in between
2. Inosculation - blood vessels traverse across fibrin layer
3. Reorganization and reinnervation - may take months to heal
C. Failure of Graft
1. Fluid accumulation
2. Movement across graft host interface
3. Excessive tension

IX. Skin Flaps (retain their vascular attachments) can be used to cover up to 2.5 cm defect. If defect larger, use split
thickness

A. Specific Indications
1. Areas with poor vascularity (bare bone or tendon)
2. Reconstruction for full thickness
3. Pad bony prominences
4. Coverage of areas requiring surgery at later date

B. Local flaps
1. Flaps that rotate about a pivot point (rotation, transposition)

a. Rotation flap: semi-circular flap (ideally 1/2 circle) that is rotated to adjacent defect. Donor
site is closed or grafted

2. Advancement flaps (V-Y, Y-V, single, bipedal)

a. Move directly forward to cover defect without rotation

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 C. Myocutaneous Flaps
1. Can produce bulky padding, skin coverage and vascularity to area
2. Muscles can support a segment 50% larger than the size of muscle (i.e. - heel defect can be covered with FDB and skin
graft)
D. Z-Plasty
1. Transposition of 2 triangular flaps
2. Make transverse central incision parallel to the contracted skin.
3. Arms of Z are equal with flap to tip angle 60 Degrees (can give about 75% increase in length)
E. V-Y Plasty for skin lengthening
1. Apex of V is proximal in foot - distal skin is advanced
2. Entire V may be undermined beneath superficial fascia for exposure

Tourniquets
I. Application of Pneumatic Cuff

A. Wrap extremity with several thicknesses of cotton cast padding (even and snug).
B. Apply pneumatic cuff smoothly and evenly - wrinkles cause skin to be pinched resulting in blisters. Apply it to an area of
maximum circumference.
C. Elevate the extremity for three minutes or express the blood from the extremity with an Esmarch bandage before inflating the
cuff.
Note: Exsanguination is contraindicated in surgery dealing with open traumatic wounds, in the presence of
infection, or when resecting a tumor.

II. Determining Inflation Pressure

A. Three variable in determining correct pressure

1. Placement of tourniquet
2. Systolic blood pressure
3. Size of extremity
B. Thigh Cuff
1. Requires inflation to a minimum of 100mmhg over the systolic blood pressure adjusted to the size of the extremity.
2. Maximum pressures are 500 mmHg in adults and 200 mmHg in a child.
C. Ankle Cuff
1. Inflate cuff 70 - 100 mm Hg above preoperative systolic blood pressure
2. Maximum pressures are 250 mmHg in adults and 150 mmHg in a child.
3. Calibration of the pressure indicator gauge of pneumatic cuff needs to be checked with mercury manometer regularly

III. Contraindications

A. Absolute Contraindications
1. Sickle cell disease
2. Peripheral vascular disease (prior bypass or angioplasty)
3. Deep vein thrombophlebitis
B. Relative Contraindications
1. Sickle cell trait
2. Diabetes mellitus
3. Rheumatoid vasculitis

IV. Complications

A. Paralysis

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 1. Compression paralysis from direct pressure to the nerve can cause loss motor function prior to loss of sensation with pain
perception spared.
2. Insufficient pressure resulting in passive congestion of the part with hemorrhagic infiltration of the nerve
3. Ischemia causing numbness and weakness
4. Keeping tourniquet on too long
5. Application without considering the local anatomy
B. Ischemia
1. Ischemia for more than 3 hours will cause sublethal damage to muscle cellular components
2. General rule - inflation time limit - 2 hours on healthy adult under 50. If operation requires more time, deflate for 15-20
minutes, then reinflate
3. Intervals of time necessary for the readjustment of tissue and blood PH, PCO2, PO2

a. The time period should not exceed 1 ½ to 2 hours at the ankle and 2 to 2 ½ hours at the upper
thigh. If longer times are required, an appropriate breather time is necessary. Once a
tourniquet is reinflated there are no reported "safe" time periods for the tourniquets.

Every 30 minutes of inflation time requires 3-5 minutes of breathing time.

b. Shorter modifications are necessary for children

C. Alterations of Clotting Mechanism

1. Increased bleeding tendency with use of pneumatic tourniquet, resulting in profuse bleeding from wound following
surgery (Reactive Hyperemia)
2. Liberation of plasminogen activators occurs with hypoxia, which results in lysis (fibrinolytic activity). Fibrinolytic activity
increases with deflation of the tourniquet, reaches a maximum 15 minutes after release, and returns to normal 30 minutes
after release.
3. Increased bleeding from wound for the first 30 minutes following release of tourniquet
4. Venous occlusion or direct pressure of the wall of the vein releases activators of fibrinolysis (especially plasminogen) into
free-flowing blood
D. Thrombophlebitis
1. Rare complication with use of pneumatic cuff in patients with no previous history of thrombophlebitis or venous stasis.
E. Chemical Burn - any solution running under tourniquet can cause a chemical burn (Betadine)

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Wound Healing
I. Dermal healing:

A. Inflammatory Phase (Substrate phase or lag phase)

1. 10% of the healing process
2. First reaction is Vasoconstriction which lasts 5-10 minutes
3. Second reaction is Vasodilation which lasts 3-4 days
4. The Fibroblast forms collagen which adds tensile strength
5. Epithelialization occurs at the end of the first phase
6. Contact Inhibition occurs when lead cells touch each other
B. Fibroblastic Phase or Proliferative Phase
1. 20% of the healing process
2. This phase lasts 2-3 weeks
3. The tensile strength of the wound equals 35% of the original strength of the skin at 14 days at this point the tensile
strength of the wound equals the tensile strength of the suture.
Note: Collagen synthesis is directly responsible for a wound obtaining tensile strength.
C. Maturation Phase
1. 70% of the healing process
2. This phase lasts up to one year

II. Bone Healing:

Bone heals via either callus bone healing or primary bone healing. Healing always demands an intact vascular supply.
A. Secondary Bone Healing (Callus bone healing) occurs in six phases:
1) Hematoma formation phase: lasts 1-3 days, and entails hematoma formation between fracture fragments.
2) Hematoma organization phase: lasts from 3-10 days, and entails inflammation with recruitment of osteoclasts and
osteoblasts.
3) Fibrocartilaginous callus phase: lasts from 10 days to 6 weeks, depending upon the degree of immobilization and
fragment stability; and entails osteoclastic phagocytosis of necrotic bone, chondroblastic and osteoblastic differentiation into
cartilage (low oxygen tension) or bone (high oxygen tension), and neovascularization derived primarily from endosteal, and
to a lesser degree periosteal, blood supplies. Fracture instability leads to progressive irritation (fibrocartilaginous callus)
formation, and delays the development of bone.
4) Primary bone callus phase: lasts from 6-10 weeks, and entails condensation of the fibrocartilaginous callus into bone that
bridges the fracture interface.
5) Primary bone callus absorption phase: lasts from 2.5-4 months, and entails new bone remodeling into secondary bone
callus.
6) Remodeling (maturation) phase: entails alteration of bone in response to applied forces in accordance with Wolff's law,
and continues from about 4 months post-injury.
B. Primary Bone Healing
Primary bone healing requires fracture reduction and rigid stabilization, and preservation of fragment vascularity. When
bone fragments are reduced and rigidly stabilized, the fibrocartilaginous callus phase can be bypassed and new bone
formation and remodeling occur simultaneously via Haversian remodeling. Primary bone healing can occur via either contact
or gap healing. As the names imply, contact healing involves stabilization of bone-to-bone contact, while gap healing
involves stabilization of the fragments with maintenance of a small (up to 2 mm) gap between the bone ends. Stabilization
is enhanced by compression, which increases friction between bone fragments and promotes rigidity. Fracture stability can
be achieved in a variety of ways, and will be discussed elsewhere in this manual (see Internal and External Fixation of
Bone).
Haversian remodeling is the underlying process of normal bone remodeling. When fracture fragments are reduced and
stabilized, capillary budding from Haversian canals occurs at points of contact, and bridge the fracture interface by means
of the cutting cone. The cutting cone consists of a leading tip of osteoclasts, which phagocytose osteoid, a central capillary
emanating from the Haversian canal, and osteoblasts, which are organized about the margins of the capillary and lay down
lamellar new bone.
C. Avascular Necrosis (AVN) of Bone:
1. Bone necrosis has many causes:
•trauma (accidental and surgical)

•steroid therapy

•occlusive vascular disease

•venous thrombosis

•collagen vascular disease (rheumatoid, arteritis)

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 •status-post renal transplant

•sickle cell anemia

•pancreatitis and chronic alcohol abuse

•radiation therapy

•hyperuricemia and gout

•hyperlipidemia

•barotrauma (caisson's disease)

•osteoporosis and osteomalacia.

2. The process involves acute ischemia of bone, necrosis, then revascularization and new bone formation. Bone scans, if
used early enough and with fine localization, may show a cold spot due to ischemia. Generally, however, bone scans are
hot, consistent with new bone accretion associated with healing. An MR image can be useful in establishing the diagnosis of
AVN.
3. The radiographic classification of AVN of the first metatarsal head (or head of the femur) is as follows:

•Stage I: Pre-collapse

Early - normal density, localized "cold" bone scan

Intermediate - relative sclerosis of dead bone, due to surrounding hyperemia and disuse
osteoporosis.

Late - true sclerosis due to new bone accretion, "hot" bone scan.

• Stage II: Collapse

Early - mild step defect, loss of articular sphericity

Late - fragmentation of articular surface and metaphysis

• Stage III: Arthritis

Early - joint space narrowing, subchondral cysts and sclerosis, osteophytosis

Late - sclerosis, ankylosis, articular erosion

4. The clinical signs and symptoms include:

Stage I: usually asymptomatic, or perhaps minimal pain and stiffness

Stage II: usually significant pain and stiffness, occasionally asymptomatic

Stage III: pain and stiffness are most typical

5. The differential diagnosis should include arthrosis, RSDS, and infection. The ESR is usually not elevated in AVN and
RSDS.
6. The medical treatment of AVN entails protective or non-weight bearing, electrical bone growth stimulation, vasodilators,
NSAIDs to inhibit platelet aggregation, and the avoidance of steroids.
7. The surgical treatment of AVN includes debridement of necrotic bone or core decompression and replacement with
autogenous bone graft, revascularization with a pedicle muscle graft, and resection with endoprosthesis or arthrodesis.
8. Rates of AVN of the first metatarsal head following distal first metatarsal osteotomy have been reported to range from
less than 1% to greater than 40%. Steps for the prevention of AVN include preservation of periosteal and capsular
attachments, accurate hemostasis, avoidance of immediately subchondral osteotomies, rigid stabilization of metaphyseal
osteotomies, protective or non-weight bearing, use of sharp blades and osteotomes, and routine serial radiographs
following osteotomy or fracture.

III. Cartilage Healing

A. Normal cartilage

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 1. Consists of Chondrocytes, Matrix - a-Type II collagen and

2. Ground substance (glycosaminoglycans and water)

3. Nutrition is through synovial fluid. There is no blood supply to cartilage.

B. Healing Phase
1. Necrosis
2. Inflammation
3. Repair via metaplasia and replication
C. Types of Injury
1. Partial thickness -usually these injuries do not heal, using shaving and drilling of "articular surface" may lead to the
development of fibrocartilages ingrowth
2. Osteochondral heals via:

a. Type II collagen - similar to hyaline cartilage

b. Type I collagen - fibrocartilages

IV. Non-traumatic Dermal Wounds: Skin Ulcers

Dermal wounds that develop secondary to pressure, typically chronic, non-traumatic weight bearing or decubitus pressure,
can result in cutaneous compromise where the skin barrier is broken. Technically, skin ulceration is defined as an open wound
where the full thickness of skin is violated. The International Association for Enterostomal Therapy classifies pressure induced
cutaneous compromise as follows:
•Stage 1: Epidermis intact, however erythema remains longer than 30 minutes after pressure relieved. Reversible with
intervention.
•Stage II: Partial thickness skin loss, including epidermis and perhaps superficial dermis. There is surrounding induration,
and local bulla or vesicle with erythema, tenderness (if not insensitive), and base of wound is moist and necrosis free.
•Stage III: Full thickness skin loss, through dermis into subcutaneous fat and superficial fascia, affecting a crater. Necrotic
eschar filling the crater and covering the base must be debrided in order to accurately stage the depth and properly
categorize the wound. The central wound base is generally non-tender. There is often undermining of the margin, sinus
tract formation, local exudate, and a surrounding halo of erythema. Ascending cellulitis and infection may also be present.
Underlying osteomyelitis or, in the presence of an ischemic limb, subcutaneous gas or necrotizing infection should also be
ruled out.
•Stage IV: Deep crater with penetration through deep (muscle) fascia, with associated involvement of muscle, joint, and/or
bone. Once again, wound base is usually nontender. Must rule-out associated dissecting abscess, necrotizing infection, and
osteomyelitis.
See also Classifications of Ulcerations (in Diagnostic Eval section)

V. Keloids and Hypertrophic Scars

Keloids are reactive fibrous proliferations that develop at sites of cutaneous injury, and occur most commonly in black
individuals as well as certain families. The fibrous proliferation extends beyond the area of the original skin injury or
incision, and can be debilitating. The lesion is thought to develop due to irregular wound granulation, associated with
abnormal capillary endothelium and the presence of excessive myofibroblasts. Excessive collagenation and decreased
collagenase activity may also contribute to fibroproliferation. Hypertrophic scars are similar to keloids, however they remain
within the area of the original injury and tend to reduce in size over time. Intralesional injection of glucocorticosteroid and
surface compression, preferably with elasticized silicone polymer, may reduce keloid and hypertrophic scar formation. Peptic
ulcer disease, fibromatoses, and enostoses can be associated findings. Elective surgery should be considered only with
caution in patients with a history of hypertrophic scar or keloid formation.

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VAC® (VAC®uum Assisted Closure) Therapy
I. Nomenclature:

A. VAC® (VAC®uum assisted closure)

B. NPWT (negative pressure wound therapy) most common in the United States
C. Sub-atmospheric pressure (older nomenclature)
D. Topical negative pressure (European)

II. Definition (NPWT)

It is the controlled application (intermittently or continuously) of sub-atmospheric pressure to a specialized wound dressing (a
resilient, open-cell foam surface), using an electrical pomp, sealed with an occlusive dressing to maintain the sub-atmospheric
pressure.

III. Devices

A. Original VAC® classic

B. InfoVAC: has a build in seal check (Seal

Audio), is smaller, lighter and has easy touch screen
controls.

C. ActiVac: designed to enhance mobility and ease-of-use for home care

patients.

D. VAC® ATS: improved

E. VAC® freedom: (mini model for outpatient)
F. VAC Instill:

IV. Mechanisms of action

A. Removes interstitial fluids including infectious materials allowing tissue decompression

B. Helps promote perfusion
C. Promotes a moist wound healing environment
D. Helps draw wound edges together
E. Protects the wound environment
F. Promotes granulation
G. Helps promote flap and graft survival

V. Indicated wound types

Acute, chronic, traumatic, partial thickness burns, dehisced wounds, diabetic ulcers, pressure ulcers, flaps and grafts.

VI. Precautions

A. Active bleeding
B. Difficult wound hemostasis
C. Patient on active anticoagulants
D. Dressing in close proximity to blood vessels or organs require protective barrier
E. Avoid weakened, irritated, sutures, bone fragments or sharp edges

VII. Contraindications

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 A. Untreated osteomyelitis
B. Malignancy in wound
C. Exposed blood vessels or organs
D. Non-enteric and unexplored fistula
E. Necrotic tissue with eschar present

VIII. Components of a VAC® system

A. Therapy delivery unit

B. T.R.A.C.™ tubing
C. VAC® canisters
D. Application-specific dressings
E. Semi-occlusive drapes

IX. Specific dressings

A. VAC polyurethane foam known by the trade name GranuFoam – Do not create as much granulation tissue. They are available
as small, medium, large, and extra large foams which can be cut into specific shapes. There are also precut heel dressings
with devices that allow bridging of the track pad away from the site of the heel to reduce potential pressure necrosis. There
are also thin and round foam shapes.
B. VersaFoam (polyvinyl alcohol) –do not promote as much of a robust granulation tissue response which may be useful in certain
wound types. They come in small and large white foam dressing.

X. Application of dressing (5 step approach): after appropriate debridement and devising an off loading strategy.

A. Placement of foam
B. Application of semi-permeable dressing
C. Secure seal
D. Connecting with central unit
E. Setting device

XI. Potential Complications

A. Maceration: (most common) Use of newer VAC® freedom and VAC® ATS has allowed a much easier and consistent seal. Use
of stoma adhesive barrier and other barrier dressings also decrease maceration.
B. Cellulitis
C. Deep space infection
D. Tube Necrosis (be aware of placement)

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PART 9:
SURGICAL
PROCEDURES
&
TECHNIQUES

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Ankle & Pantalar Fusion
I. Pantalar fusion involves the bony union of:

A. Ankle joint:
1. The tibial plafond and trochlear surface of the talus
2. The medial articular surface of the fibular malleolus and the lateral articular surface of the calcaneous
3. The lateral articular surface of the tibia and the medial articular surface of the talus
4. Between the distal tibial and fibular articular surfaces
B. Subtalar joint
C. Talonavicular Joint
D. Calcaneocuboid Joint
Note: Failure to fuse any of these joints will increase the chances of nonunion and painful arthrosis
postoperatively.

II. Indications

A. Most common indication is post traumatic arthrosis (DJD) of the ankle following ankle fracture
1. Wherein a small lateral shift or shortening of the fibula produces incongruity resulting in deterioration.
2. A 1 mm shift can result in a 42% decrease in tibiotalar contact
B. Avascular necrosis of talus
C. Bone tumors destroying a portion of the ankle
D. Abnormal angulational deformity
E. Neuromuscular disease with poor stability
F. Failed ankle joint prosthesis
G. Infection (chronic osteomyelitis, septic arthritis)
H. Congenital deformities (talipes equino varus deformity)
I. Neurological deformities
J. Paralytic deformities are the primary indication for pantalar arthrodesis (poliomyelitis and Charcot-Marie-Tooth disease)

III. Evaluation of patient

A. In evaluating patient for ankle fusion, evaluate STJ and MTJ

1. Increased stress will accelerate any degeneration present
2. May need to consider pantalar arthrodesis
B. Need motion at MTJ and Lisfranc articulation to plantar flex foot when ankle is fused at 90 degrees
C. Do not put in varus rather slight valgus
D. If tibial varum is present, increase the amount of valgus or they'll be walking on side of foot.

IV. Surgical Approaches to Ankle Fusion

A. Charnley anterior approach - not used much due to injury of anterior Neurovascular structures
B. Lateral hockey stick incision
1. Begins over lateral fibular (junction of middle and distal 1/3 aspect, extends over lateral neck of talus to 4th metatarsal
base.
i. Gives anterior, lateral, posterior exposure with fibular Osteotomy
C. Medial - gives good anteromedial, medial and posteromedial exposure when combined with tibial Osteotomy
D. Combined incisional approach is the most common approach (lateral hockey stick with secondary medial incision).
E. When performing ankle fusion, we are looking to position the large cancellous mass of the tibial metaphysis in rigid apposition
to the trabecular bone of the body of the talus for osteogenesis (absolute stability) - no micro movement

V. Types of Ankle Fusion Techniques

A. Remove cartilage from each surface with bone grafts in defects

B. Sliding inlay graft from anterior tibial surface to talus
1. Modified Gallie fusion
a. Joint resection with anteromedial and anterolateral inlay allogenic graft with staple fixation
C. Lateral or medial malleolar osteotomy to gain exposure then use them as only grafts.
D. Subtotal fusion - when patients condition does not require extensive fusion, rather use trephine technique or dowel fusion.
E. Compression arthrodesis -
1. Use external fixation devices

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 F. Tibiocalcaneal fusion - Blair
G. Glissane's requirements for successful fusion
1. Removal of cartilage fibrous tissue and other material hindering raw bone contact
2. Accurate and close fitting of surfaces
3. Optimal position of ankle joint.

Note: The ideal position for a tibiocalcaneal or pantalararthrodesis fusion is 90 degrees of the foot relative to
the leg, with slight ankle and/or hindfoot valgus, and approximately 10-12 degrees of pes abductus.

4. Maintenance of apposition in undisturbed fashion until fusion is complete.

VI. Doctors Hospital/Northlake Regional Medical Center Technique

A. Lateral hockey stick approach

B. Osteotomy fibula
C. Resect cartilage
D. Ancillary approach through medial ankle to remove medial malleolar and ankle cartilage.
E. Temporarily fix with Steinmann pins - take x-ray
F. Fuse at 90 degrees (if in equinus, they'll have genu recurvatum, and 15 degrees external rotation).
G. Two criss-crossing 6.5mm cancellous screws (make sure not in STJ)
H. Fibular onlay graft with 4.5 mm screw
I. Don't fix fibular osteotomy site (can get nonunion)
J. Apply closed suction drain
K. Leave bone screws in 6 months until healed, then optional removal

VII. External fixators (Mueller, Charnley, etc) are common means of fixation - good use when skin loss

VIII. Complications

A. 20% infection rate in literature

B. Non-union, malunion, pseudarthrosis
C. Fusing joint in wrong position creates other problems
D. Stress transfer to MTJ and STJ (may need later triple)
E. Shortening of segment

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Bunionectomy Procedures
I. Silver Bunionectomy

A. Criteria / Indications
1. Bump pain,
2. No sesamoidal or deep pain in the joint
3. Medial skin & soft tissue irritation over 1st MPJ
4. Good range of motion in 1st MPJ,
5. No pain or crepitation should occur on motion of the 1st MPJ

B. Advantages:
1. Rapid Post-op recovery
2. Minimal Post-op Edema
3. Can be performed in office setting

D. Complications / Disadvantages:
1. Weakens medial aspect of 1st MPJ
2. Has poor long term results
3. Does not correct etiology of bunion deformity.

II. McBride Bunionectomy

A. Criteria / Indications:
1. No pain on motion of 1st MPJ
2. Pain associated with a fibular sesamoid
3. Adequate range of motion of first MPJ
4. Mild axial rotation of the hallux is acceptable
5. No crepitation with motion of 1st MPJ
6. Preop Radiographic Signs
a. Hypertrophy of the medial eminence is present.
b. Deviated to subluxed 1st MPJ is present
c. Tibial sesamoid position of 4 or greater

B. Complications / disadvantages:
1. Can't correct structural deformity

OSTEOTOMIES OF HALLUX

I. Akin Bunionectomy

A. Classic Akin
1. Closing adductory osteotomy in metaphyseal bone to correct increased DASA.
2. Rarely performed as isolated procedure.
3. If true hallux interphalangeus or increased DASA use Akin and don't try to tighten capsule because you'll get Varus.
a. Procedure: proximal cut parallel to joint surface at base proximal phalanx. Distal cut perpendicular to long
axis of shaft 5 - 10 mm distal to MPJ

B. Proximal Phalanx
1. Valgus rotation should be minimal to hallux
2. Need congruous MPJ unless corrected by another procedure.
3. Proximal phalanx can't be too short.
4. DASA 7-8 degrees
5. Closed epiphysis at proximal phalanx
6. Proximal Akin Corrects DASA

C Distal Akin

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 1. Congruous 1st MPJ unless corrected by another procedure
2. May be open epiphysis
3. HAI angle > 10-12 degrees
4. Phalanx should not be too short
5. Distal Akin corrects HAI

D. Cylindrical Akin
1. Designed to correct an abnormally long proximal phalanx
2. DASA or HAI can be corrected
3. Closed epiphysis
4. Can have delayed healing in diaphysis
5. Cylindrical Akin is excessive valgus rotation.
E. Regnauld: Autogenous Bone Graft of Base of Proximal Phalanx

FIRST METATARSAL OSTEOTOMIES

I. Distal Metatarsal Osteotomies

A. Reverdin Bunionectomy
1. Criteria / Indications:
a. Abnormal Proximal Articular Set Angle

2. Advantages:
a. Technically easy to perform
b. Metaphyseal osteotomy results in good healing
c. Can be performed in children due to distal placement of
osteotomy
d. Requires minimal fixation

3. Complications / Disadvantages:
a. Possible aseptic necrosis
b. Possible traumatic arthritis secondary to sesamoid damage
d. No sagittal plane correction
e. No correction of IMA

4. Post-op Management:
a. Wooden post-op shoe for 3 to 4 weeks
b. Weight bearing ambulation one day after surgery

B. Green-Reverdin
Same as Reverdin except the osteotomy is made in a fashion that avoids damage to the
sesamoids.

C. Reverdin-Laird
Same as the Green-Reverdin except the osteotomy is through and through which allows correction of the PASA & IMA

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D. Peabody
Same as the original Reverdin except the osteotomy is performed at the level of the anatomical
neck (more proximal). This avoids the sesamoids but may increase healing time due to location
of the osteotomy (not metaphyseal).

E. Mitchell
1. Criteria / Indications:
a. Mild increased IMA
b. Dorsiflexion of the first metatarsal
c. Normal PASA & DASA

2. Advantages:
a. Corrects sagittal plane deformity
b. Can be performed in children

3. Complications / Disadvantages:
a. Prolonged disability and immobilization
b. Possible avascular necrosis of the first metatarsal head
c. Possible metatarsalgia and hallux limitus due to dorsal displacement of the distal fragment

4. Post Op Management:
a. Below Knee walking cast for 4 - 6 Weeks

F. Austin Bunionectomy

Note: The original Austin is a unicorrectional procedure (Corrects abnormal IMA). The Modified bicorrectional
procedure can correct an abnormal IMA and PASA (transpositional and angulational osteotomy).

Note: You can use the "apical axis guide" to control the position of the distal fragment. For example, to
produce both shortening and plantar flexion of the capital fragment, the osteotomy must be angulated distal
medial to proximal lateral and dorso-medial to plantar lateral.

Note: The Austin procedure is an excellent choice for a structural deformity in hallux abductovalgus in a young
child because it has the least effect on growth centers.

1. Criteria / Indications:
a. Good, pain free range of motion without crepitus of the first MPJ in the corrected position unless a hemi-
implant is used.
b. Use bicorrectional procedure if the joint is trackbound (decreased sagittal plane motion when the joint is
placed in the corrected position).
c. Preop Radiographic Signs:
- Hallux abductus angle greater than 15 degrees
- Normal Hallux interphalangeal angle
- Normal DASA
- Normal PASA for unicorrectional Austin. Abnormal (7 degrees or more) for
bicorrectional Austin
- Mild to moderate increased IMA. The width of the metatarsal head determines
how much reduction you can obtain (up to 15 degrees).
- Absence of cystic changes and degenerative joint disease

- Congruous to deviated first MPJ

2. Advantages:
a. Eliminates the possibility of dorsiflexion of the metatarsal
b. Can compensate for short or long metatarsal and/or dorsiflexed or plantarflexed metatarsal by angulating
the transverse osteotomy using the apical axis guide.
3. Complications / Disadvantages:
a. Technically difficult to perform (bicorrectional)
b. It achieves a relative reduction of the IMA, not a true IMA reduction.
c. Can result in shortening of the first Metatarsal

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 4. Post Op Management: Wooden post-op shoe for 4 -6 weeks
G. Drato Procedure

Note: This procedure has very specific criteria and is therefore performed infrequently.
However when indicated it has good results. It is the only procedure that corrects a valgus
rotation of the first metatarsal head.
1. Criteria / Indications:
a. Valgus rotation of the 1st metatarsal
b. Abnormal PASA but normal DASA
c. Plantarward adaptation of articular surface of the 1st metatarsal and a mild increase in IMA.

2. Advantages: Simultaneously corrects four deformities with one osteotomy (derotational,

angulational, transpositional).

3. Complications / Disadvantages:
a. Possible Hallux Elevatus secondary to excessive dorsiflexion of the head
b. Possible metatarsalgia and/or hallux limitus
c. Possible aseptic necrosis of the first metatarsal head
d. Technically difficult to perform
e. Prolonged disability and immobilization

4. Post Op Management:
a. Same as Mitchell procedure (Below Knee walking cast for 4 - 6 Weeks).

II. Proximal Base Osteotomies

A. Crescentic Osteotomy

1. Criteria / Indications:
a. IMA (greater than 13 degrees rectus), (greater than 11 degrees in adductus)
b. Normal to negative Metatarsal protrusion
c. A plantarflexed first ray or a metatarsus primus elevatus may be present
Note: Use cross K-wires and at least 2/3 of bone needs to make contact at osteotomy

2. Advantages:
a. Allows transverse and sagittal plane correction
b. Maintains Metatarsal length

3. Complications / Disadvantages:
a. Less stable because all cortices are transected
b. Special instrumentation is required
c. Internal fixation required
d. Delayed or nonunion due to poor fixation which results in motion at the osteotomy
4. Post Op Management: 6 -8 weeks below knee walking cast

B. Opening Wedge Osteotomy

Note: This procedure should generally be performed in

conjunction with an arthroplasty procedure of the first MPJ unless
it is a redo of a previous osteotomy (length gain will not cause
jamming of the MPJ).

1. Criteria / Indications:
a. Very high IMA (greater than 15 degrees rectus),
(greater than 13 degrees in adductus)
b. Normal to negative Metatarsal protrusion
c. Normal PASA is desired
d. The epiphyseal plate should be closed
2. Advantages:
a. Can reduce a very high IMA
b. Can be performed on a short first metatarsal

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 c. If another osteotomy has to be performed to correct additional deformity the OBWO will maintain the
metatarsal length without jamming the 1st MPJ.
3. Complications / Disadvantages:
a. Osteoporosis secondary to long cast immobilization
b. Complete bone healing is prolonged
c. Technically difficult to perform
d. The osteotomy may not be structurally sound resulting in motion at osteotomy (Delayed union/nonunion,
elevatus).
4. Post Op Management: Below knee non weight bearing cast for 6 -8 weeks
C. Closing Base Wedge Osteotomy

1. Criteria / Indications: (Same as opening wedge osteotomy)

a. Very high IMA (greater than 15 degrees rectus), (greater than 13
degrees in adductus)
b. Normal to negative Metatarsal protrusion
c. Normal PASA is desired
d. The epiphyseal plate should be closed
2. Advantages:
a. Can reduce a very high IMA
b. Can be performed on a long first metatarsal
c. Can dorsiflex a plantarflexed first metatarsal

3. Complications / Disadvantages:
a. Osteoporosis secondary to long cast immobilization
b. Technically difficult to perform
c. The osteotomy may not be structurally sound resulting in motion at osteotomy (Delayed union/nonunion,
elevatus).
d. Metatarsalgia
e. Submet 2 Lesion

4. Post Op Management: Below knee non weight bearing cast for 6 -8 weeks

D. Lapidus Procedure (Fusion of 1st Met-Cuneiform)

1. Pain and hypermobility at the 1st metatarsal cuneiform

2. Corrects high IMA
3. Corrects deformities in the transverse and/or sagittal planes
4. Round 1st metatarsal cuneiform joint
5. Shortens 1st ray
6. Requires 6-8 weeks non weight bearing casting
7. When underscoring the medial capsule-ligamentous and periosteal complex at the first
metatarsocuneiform articulation, care should be taken to avoid trauma to the Anterior Tibial
Tendon.
E. Scarf-Meyer Z Plasty

1. Very stable
2. Can get troughing
3. Fixation may be with smooth or threaded K-wire Near cortex, over-drill for
fully threaded screw

F. Ludloff Procedure

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 1. Indicated for cases of metatarsus primus elevatus or a short first metatarsal
2. Not very stable
3. Requires 6 - 8 weeks non weight bearing Cast

G. Mau Procedure

1. Oblique base/shaft osteotomy from plantar-proximal to dorsal distal.

2. No wedge-no hinge.

H. Modified Juvara

1. Type A
a. Oblique base/shaft osteotomy from medial-proximal to lateral distal.
b. Intact medial hinge, wedge of bone removed, screw fixation.
2. Type B
a. Same osteotomy as in "A", but with no intact hinge. This allows dorsiflexion, plantar flexion, lengthening
and shortening.
b. Screw fixation.
3. Type C
a. Same osteotomy as in "A", but with no intact hinge and no wedge is removed.
b. Screw fixation is used.
Note: When performing a closing abductory wedge osteotomy at the base of the first metatarsal (Juvara) using
the hinge-axis concept to achieve pure abduction of the metatarsal, the axis guide should be drilled
perpendicular to the ground or weight-bearing surface.

III. Double Osteotomy of the first Metatarsal

A. Logroscino Procedure

1. A double osteotomy of the first metatarsal.

2. It combines the techniques of Reverdin with Trethowan (Opening Wedge Base
Osteotomy) or Loison-Balacescu (Closing Base Wedge Osteotomy).
3. Used in a situation where a bicorrectional Austin procedure cannot correct a very
high intermetatarsal angle and/or an abnormally long or short first metatarsal.
4. Post-op management consists of non-weight-bearing cast for 6-8 weeks.

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Digital Deformities
Types of Deformity: Flexible, Semi-rigid, Rigid
Check flexibility with Kelikian push-up test. This test for reducibility of the deformity at the MPJ.

I. Anatomic Factors and Mechanics

Dorsal Digital Anatomy

Lesser MPJ Sagittal Plane

Lesser MPJ Dorsal View

Lesser MPJ Cross Section

See also Plantar Foot Musculature (detailed in basic science)

A. Extensor Digitorum longus

1. Divides into three slips
2. Middle slip to base of middle phalanx
3. Lateral two slips to base of distal phalanx
4. Very loose connection of EDL to dorsal capsule & proximal phalanx
5. Centering EDL on toe proximally is extensor sling which extends laterally down around capsule of MPJ and inserts at
junction of flexor plate, deep transverse intermetatarsal ligament and flexor tendon sheath
6. EDL is more firmly attached to plantar MPJ then dorsal
7. Distal portion of dorsal aponeurosis is extensor wing - which extends to head of proximal phalanx
8. The entire sling and wing mechanism dorsiflexes the proximal phalanx on the metatarsal head with little force exerted
at PIPJ or DIPJ

B. Extensor Digitorum Brevis

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 1. Originates from dorsolateral aspect of calcaneus and attaches into the lateral sides of tendons of extensor digitorum
longus (the lateral aspect of the extensor expansion) of the 2nd, 3rd and 4th toes.
2. Distally attaches to base of distal phalanx
3. This along with FDB, exerts plantarflexory force at IPJ's
4. However, during weight bearing the strong plantarflexory force on the IPJ's is resisted by ground reactive forces.
Resulting in a retrograde force which may dorsiflex MPJ (this is usually resisted by interossei)

C. Flexor Digitorum Brevis

1. Arises from calcaneus in first layer of foot
2. The FDB and FDL pass plantar to the MPJ in a groove under plantar capsule
3. The FDB splits at proximal phalanx and allows FDL to pass through
4. It attaches at base of middle phalanx

D. Dorsal Interossei
1. Are dorsal to deep transverse intermetatarsal ligament
2. 1st one to medial plantar proximal phalanx second toe
3. 2nd, 3rd, 4th to lateral plantar proximal phalanx of 2nd, 3rd, 4th digits
4. Stabilize in transverse plane and plantar flex at MPJ
5. Resists dorsal buckling of proximal phalanx by FDL and FDB.

E. Plantar Interossei
1. Are dorsal to deep transverse intermetatarsal ligament
2. 2nd, 3rd and 4th tendon to plantar medial proximal phalanx of 3, 4, & 5
3. Stabilize digits in transverse plane and resist buckling by FDL and FDB

F. Flexor digiti quinti Brevis

1. Functions like interossei to lateral plantar middle phalanx of 5th toe.

G. Lumbricales
1. Plantar to deep transverse intermetatarsal ligament
2. Arise from medial aspect of each FDL tendon
3. Inserts into medial base of proximal phalanx of 2, 3, 4, & 5
4. Create plantar flexion of proximal phalanx
5. Functions to resist EDL effect on dorsiflexion of proximal phalanx

H. Quadratus Plantae
1. Originates from calcaneus and attaches to lateral FDL before tendons arise to stabilize the medial pull of this tendon
on toes.

II. Vascular and Nerve Supply to Digits

A. Arterial
1. Major Arterial supply to the digits is through the medial plantar proper digital artery
2. Lateral plantar digital artery of hallux is the main supply to this digit

B. Nerve Supply
1. Dorsal
a. Saphenous/medial dorsal cutaneous to medial first
b. Deep peroneal to interdigital 1st and 2nd
c. Lateral branch of medial dorsal cutaneous to adjacent 2nd and 3rd
d. Intermediate dorsal cutaneous nerve to adjacent 3-4, 4-5
e. Sural nerve to lateral side of fifth

2. Plantar
a. Medial plantar nerve to hallux, 2nd, 3rd and medial aspect of 4th
b. Lateral plantar nerve to lateral 4th and all of 5th digit.

III. Concepts

A. Flexor Stabilization (Most common cause of hammertoes)

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 1. FDL & FDB fire earlier in a hypermobile flatfoot deformity to stabilize the osseous structures of the foot.
2. When they fire, during stance, the force creates dorsiflexion at MPJ
3. The FDL and FDB will overpower the plantar force exerted here by the interossei
4. Can get adduct o varus 4th and 5th toes due to abductory deviation of forefoot on rearfoot

B. Flexor Substitution
1. Generally see sagittal Contractures of toes with no adductovarus deformity
2. See this condition in weak triceps surae in which posterior and lateral leg muscles substitute for the weak triceps
3. Calcaneus gait may develop
4. Muscles fire earlier and longer than usual, causing contracted digits and supinated foot
5. P. Longus can plantar flex 1st ray
6. FDL and FDB will overpower interossei
7. Least common cause of hammertoes of lesser digits

C. Extensor Substitution
1. EDL gains advantage over lumbricales
2. EDL will overpull with: anterior pes cavus, weak lumbricales, spastic condition of EDL, very tight triceps surae and
weakness of tibialis anterior
3. This deformity will contract MPJs over the normal 20 - 40 degrees on active dorsiflexion of foot by patient on exam
table
4. Get retrograde buckling of metatarsal heads

IV. Types of Deformities

A. Mallet toe

1. Sagittal plane deformity in which distal phalanx flexed on middle

2. Can be associated with long digit

B. Curly (Congenital Varus) toe

1. Usually involves 3, 4,and 5
2. Flexion and varus at DIPJ with adduction component also
3. In severe cases the PIPJ is involved

C. Hammertoes

1. Dorsiflexion of proximal phalanx, plantar flexion of middle

2. The primary deforming force is the FDL

D.Clawtoe

1. Dorsiflexion of proximal phalanx

2. Plantar flexion, middle and distal

V. Reducible Lesser Digital Deformities

A. Flexor Tendon Transfer (indicated in a young patient with a reducible hammertoe or claw toe deformity with no frontal plane
deformity.)
1. Longitudinal incision over PIPJ
2. Extensor tendon is mobilized to approximately mid shaft
3. Long flexor is isolated and severed at its insertion through a stab incision plantarly
4. FDL is split and the medial and lateral slips are brought dorsally, crossed over the neck of the proximal phalanx and
sutured together
5. The extensor tendon is repositioned and sutured
6. Reapproximate and close skin

B. Flexor Tenotomy
1. When flexion deformity at PIPJ or DIPJ that is completely reducible
2. Long flexor tendon may be only entity needing to be corrected
3. Usually plantar skin and joint is contracted as well
4. If skin is contracted, use plantar approach

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 5. If not, use medial or lateral

C. Extensor Tenotomy/capsulotomy
1. When dorsal extensor tendon and joint capsule involved

VI. Complex Hammertoe Repair Step By Step Approach

A. Prox. phal. head resection

B. Extensor hood release
C. Extensor tendon lengthening
D. Capsulotomy of MPJ (Dorsal Medial Lateral)
E. Plantar hood release
F. Arthrodesis with internal fixation
G. Hibbs suspension (special cases only)

VII. Severe Claw Toe Repair With MPJ Deformity

A. Incision as Above
B. Z-plasty EDL and retract
C. Prepare bone for peg in hole or end to end arthrodesis (end to end if toe is short), now perform pushup test
D. Extensor hood release - push up test
E. Capsulotomy at MPJ. If still can't relocate, it's probably due to
1. Capsulodesis of flexor plate to metatarsal neck or head
2. Medial or lateral dislocation of flexor plate (will cause a medial and dorsal migration of toe. This will cause an adductus
deformity of the toe on the metatarsal head. Usually caused by chronic synovitis of the supporting structures of the joint.
F. Arthrodesis toe with wire across MPJ
G. Repair extensor tendon
H. If medial or lateral dislocation of flexor plate present: you will need capsulorrhaphy on one side of MPJ. Overcorrect with wire
for 6 weeks

VIII. Various Hammertoe Procedures

A. Resection of head of proximal phalanx - Post

B. Fusion of IPJ, end to end - Soule
C. Spiked peg and hole arthrodesis - Higgs
D. Rounded peg in hole arthrodesis - Young
E. End to end fusion with K-wires - Taylor and Selig
F. Resection of base of proximal phalanx - Gotch & Kreuz
1. Poor results - flail toe
2. May need to syndactylies for stability and cosmesis
G. Flexor tendon transfer - Girdlestone, Forrester/Brown

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Hallux Interphalangeal Arthrodesis
I. Hallux Interphalangeal Arthrodesis

Five Fixation techniques used to arthrodesis the hallux interphalangeal joint:

1. Stainless steel monofilament wire, 28 gauge
2. Two .045 inch Kirschner Wires
3. 4.0 cancellous screw
4. 3.5 Cortical Screw - lag technique
5. 2.7 cortical screw - lag technique

A. Indications
1. Semi-reducible or non-reducible interphalangeal joint contracture present
2. Hyperkeratotic lesion overlying the interphalangeal joint
3. Transverse plane or frontal plane deformity of hallux
4. Clawtoe deformity
5. Abnormally short or long toe
B. Symptoms
1. Painful interphalangeal joint motion
2. Painful hyperkeratotic lesion
3. Inability to wear regular shoe gear
4. Contracted painful toe w/ painful hyperkeratotic lesion plantar aspect of 1st met head may be present
C. Radiographic
1. Contracted interphalangeal joint
2. Degenerative joint disease at interphalangeal joint
3. Abnormal hallux interphalangeal abductus angle
4. Hallux may be abnormally long or short
5. Adequate bone stock of the distal proximal phalanges must be present

D. Biomechanical Signs
1. Instability of 1st ray and/or metatarsophalangeal joint could create abnormal weight bearing position of hallux -should be
taken into consideration.
2. Severe pronotary imbalance within foot and/or lack of intrinsic or extrinsic stability of the involved toe would not
contraindicate an interphalangeal joint fusion of hallux

II. Various Fixation Methods

A. Stainless Steel Wire

1. Advantages
a. Minimal instrumentation
b. Easy to use
c. No intraoperative x-rays
d. Can be used with artificial joint at 1st MPJ
e. Can be used where a sagittal plane deformity of the hallux is maintained.
f. Does not have to be removed.
2. Disadvantages
a. Can't be used effectively in osteoporotic bone
b. Can't be used where loss or disruption of cortical surfaces adjacent to fusion site is present
c. Difficult to achieve uniform inter fragmental compression
d. Becomes a permanent fixation device
e. Stability of fusion site not as good as with screw
B. Kirschner Wire

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 1. Advantages
a. Minimal instrumentation
b. Easy
c. Can be used in osteoporotic bone
d. Non-permanent fixation
e. Can be used in presence of non-corrected sagittal plane deformity of hallux
2. Disadvantages
a. Requires intra op x-rays
b. External irritation can lead to early removal of fixation device prior to bone healing
c. External position of fixation device can be potential source of pin tract infection
d. Difficult to use in presence of artificial joint of 1st MPJ
e. Compression achieved at fusion site, not as good as with screw, but better than single K-wire
C. Screw Fixation
1. Advantages
a. Excellent inter-fragmental compression
b. More rapid fusion than other methods
c. Earlier mobilization of proximal MPJ
2. Disadvantages
a. Can't be used with artificial joint at 1st MPJ unless 2.7 cortical screw modification used
b. Can't be used if bone stock of proximal phalanx osteoporotic or too small
c. Special instrumentation
d. Special training
e. Requires removal in most cases
f. Requires intraoperative x-rays
g. Can't be used if sagittal plane deformity is maintained unless cortical screw modification used

III. Postoperative Management

A. Every effort should be made to eliminate propulsive phase of gait for six - eight weeks through
1. Wooden sole surgical shoe or
2. Below knee walking cast or
3. Keep patient non-weight bearing
B. X-rays to evaluate osseous healing - six - eight weeks
C. Any K-wires usually removed 6-weeks postop depending upon skin irritation around wires, or degree of bone healing.
D. Screw inserted from distal to proximal - remove at approx 8 weeks postop unless patient has no irritation.

IV. Lesser Digital Arthrodesis

A. Indications
1. Semi-reducible or non-reducible contracture of involved interphalangeal joint
2. Hyperkeratotic lesion overlying the interphalangeal joint
3. Transverse plane or frontal plane deformity of distal aspect of toe
4. Clawtoe deformity
5. Abnormally short or long toe
B. Symptoms
1. Painful proximal interphalangeal joint motion
2. Painful hyperkeratotic lesion
3. Inability to wear regular shoe gear
4. Contracted painful toe which is short
5. Flail distal aspect of toe secondary to previous arthrectomy
C. Radiographic
1. Contracted proximal interphalangeal joint
2. Degenerative joint disease at proximal interphalangeal joint
3. Absence of proximal phalangeal head may be present
4. Involved toe may be abnormally long or short
5. Adequate bone stock at intermediate phalanx & proximal phalanges must be present
D. Biomechanical Signs

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 1. Instability of 1st ray and/or metatarsophalangeal joint could create abnormal weight bearing position of entire involved
toe -should be taken into consideration.
2. Severe pronotary imbalance within foot and/or lack of intrinsic or extrinsic stability of the involved toe would not
contraindicate a proximal interphalangeal joint arthrodesis

II. Various Fixation Methods

A. Stainless Steel Wire

1. Advantages
a. Minimal instrumentation
b. Easy to use
c. No intraoperative x-rays
d. Can be used in small bones
e. Can be used where a sagittal plane deformity of the lesser toe is maintained.
2. Disadvantages
a. Can't be used effectively in osteoporotic bone
b. Can't be used where loss or disruption of cortical surfaces adjacent to fusion site is present
c. Difficult to achieve uniform inter fragmental compression
d. Becomes a permanent fixation device
B. Kirschner Wire
1. Advantages
a. Minimal instrumentation
b. Easy
c. Can be used in osteoporotic bone
d. Non-permanent fixation
2. Disadvantages
a. Requires intraop x-rays
b. External irritation can lead to early removal of fixation device prior to bone healing
c. External position of fixation device can be potential source of pin tract infection
d. Difficult to use in presence of artificial joint of involved MPJ
e. Difficult to achieve good compression at fusion site
f. Difficult to prevent frontal plane rotation of osseous segments
g. Difficult to use where a sagittal plane deformity exists along the involved toe

VI. Postoperative Management

A. Every effort should be made to eliminate motion between bones involved in fusion six - eight weeks through
1. Wooden sole surgical shoe or
2. Below knee walking cast or
3. Keep patient non-weight bearing
B. X-rays to evaluate osseous healing - six - eight weeks
C. Any K-wires usually removed 6-weeks postop depending upon skin irritation around wires, or degree of bone healing.

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Hallux Limitus / Rigidus
I. Types

•Structural Hallux Limitus: restriction of motion is present with first MPJ loaded (weight bearing mode) and unloaded.
•Functional Hallux Limitus: restriction of motion only in the weight-bearing mode. There is adequate ROM in the non-loaded
examination.
Note: The Range of motion of the first MPJ should be determined in a way that reproduces the position of the
foot when the maximum amount of motion is required (propulsion). Therefore the ankle should be
plantarflexed.

II. Etiology

A. Long first Metatarsal: creates overloading of the first MPJ in the propulsive phase of gait.
B. Hypermobility of the first ray: Results from abnormal subtalar joint pronation in the late midstance and propulsive phases of
gait.
C. Immobility of the first ray:
D. DJD at Lisfranc’s joint (ankylosis of the first metatarsal - cuneiform joint)
E. Congenital coalition of the first metatarsal - cuneiform joint or the calcaneus and navicula.
F. Met primus elevatus: congenital or acquired through abnormal excessive subtalar joint pronation or iatrogenic (previous
surgery).
G. DJD (Degenerative joint disease):
•Previous deformity (HAV)
•Trauma
•Systemic arthritides: rheumatoid, psoriatic, gouty, and septic.
•Primary Osteoarthritis
•Iatrogenic (previous surgery)

III. Signs

A. Dorsal bump.
B. Limited or absent 1st MPJ motion.
C. Pain and/or crepitation with 1st MPJ ROM.
D. Hallux extension distal to the interphalangeal joint.
E. Weak peroneus longus and/or hyperactive interior tibial muscle.
F. Irritation of skin over the dorsal aspect of the 1st MPJ with/without bursa formation.

IV. X-Ray Evaluation

A. Narrowing of 1st MPJ.

B. Flattening of first metatarsal head.
C. Arthritic changes of 1st MPJ.
D. Changes consistent with pronation in the foot.
E. Subchondral sclerosis of base of the proximal phalanx and/or the head of the 1st metatarsal.
F. Central subchondral cysts

V. Biomechanical Evaluation

A. Two components:
1. Structural
2. Functional
B. Determine functional component:
1. Evaluate ROM of 1st MPJ (patient weight-bearing) in both the calcaneal stance position and the calcaneal neutral
position.
2. If significant increase of ROM in the calcaneal neutral position-control with orthotics.
C. Structural component must be corrected by surgical means.
1. if patient is a poor surgical candidate, try metatarsal bar or rocker bottom shoe.

VI. Treatment

A. Conservative

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 •Orthotics (hypermobile first ray)
•Metatarsal bar (at the sulcus level)
•Morton's extension (at the sulcus level)
•Anti-inflammatory medications

B. Surgical Procedures:
Note: Two key principles must be accomplished:
1. Complete relief of excessive joint tension.
2. Ensure that there is adequate mobility of the plantar joint structures (including the flexor plate mobility).
Note: Evaluation of the Sesamoid \ flexor plate mobility should be done before surgery, and during surgery.
Procedure:
1. Pull fat pad forward and place tip of thumb in notch anterior to the sesamoids.
2. Passively dorsiflex the hallux. Distal displacement of the thumb will indicate that the Flexor Plate is mobile.

1. Joint preservation techniques (contraindicated where there is joint pain with any motion of the 1st MPJ.)

A. Soft tissue release: release what is causing the restriction of motion:

•fibrosis dorsally
•capsulodesis
•plantar adhesions (sesamoids)
•post-op care (immediate ROM exercises. Send patient to physical therapist. Patient should be seen every
three days to make sure they comply.

B. Cheilectomy: Removal of the osteophytic proliferation about the metatarsal head and or the proximal phalangeal base.

Note: If the removal of the hypertrophic bone fails to increase motion the sesamoid apparatus must be
evaluated and if needed freed up. If there is severe limitation and arthritic changes of the sesamoid an entirely
different surgical is indicated. This procedure is a very effective adjunctive procedure when combined with
metatarsal osteotomies.

C. Waterman osteotomy: consist of a removal of a trapezoidal wedge of bone from the first metatarsal head with its base
dorsally. Problems: unstable capital fragment because of complete osteotomy and damage to sesamoids due to placement
of osteotomy.
D. Modified Waterman procedure (no disruption of the plantar articular cartilage).
Note: The modified Waterman is indicated in a mild to moderate case of hallux limitus without marked arthritic
changes to the sesamoids.

E. Modified Green - Waterman Osteotomy: involves the removal of a small section of bone length, which provides relaxation
of the flexor apparatus.
F. Austin osteotomy: many modifications exist that provide shortening of the first metatarsal. However, there is no
advantage over the modified Green - Waterman procedure.
G. Lambrinudi Osteotomy: plantarflexory osteotomy of the first metatarsal used for a structural first metatarsal elevatus.
Make sure it is not functional elevatus, which can be controlled with orthotics.
H. Kessel - Bonney Osteotomy: resection of a dorsally based wedge of bone from the base of the proximal phalanx of the
hallux.
•It is most useful in adolescent patients with no arthritic changes and no met primus elevatus. Most of these
patients respond to conservative treatment.

2. Joint Destruction Techniques:

A. Keller Arthroplasty: Resection of the base of the proximal phalanx.
•The procedure of choice in Neuropathic patients with hallux limitus.
•It is a salvage procedure for iatrogenically or arthritically destroyed joints.
•Complications:

•Loss of purchase

•Diminished propulsion at toe off

•Stress fracture of the 2nd Metatarsal

•Shortening of hallux

•Metatarsalgia

B. Implant Arthroplasty:
C. Arthrodesis: fusion of the first MPJ.
•Best for older patients with apropulsive gait patterns.

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 •Check the distal interphalangeal joint first. If there are degenerative changes before the fusion the patient
will have pain following the surgery.

NOTE: If it's functional treat conservatively (orthotics). If possible, do a joint preservation procedure. If you
have to do an implant, where it is possible use a total implant. Compare the patient's physical,
psychological make-up, and post-op disability, to the expected outcome, and then decide what to do.

VII. Postop care:

•weight bearing is allowed for all procedures except proximal plantarflexory osteotomies. (6 weeks of non-weight bearing).
•Remember to institute early range of motion exercises of the first MPJ.

Heel Pathology
I. Anatomy of The Heel

A. Circulation to heel area:

1. Medially: Calcaneal branches of posterior tibial artery and lateral plantar
2. Laterally: Communicating branches of peroneal and lateral malleolar arteries
3. Posteriorly: Communicating branches
B. Structures:
1. Deep Plantar Fascia (aponeurosis) attaches to the medial process of the tuberosity.
2. Abductor Hallucis, Flexor Digitorum Brevis, Abductor Digiti Quinti originate from the calcaneal tuberosity.
3. Quadratus Plantae and the Long Plantar Calcaneocuboid Ligament originate and attach to the plantar surface of the os
calcis near the tuberosity.
4. Neutral or Vascular Triangle - Pressure trabeculae from subtalar joint combined with traction trabeculae from normal pull
of plantar fascia and Achilles tendon. This results in a radiolucent area seen under sustentaculum tali.

II. Heel Spur Syndrome

A. Etiology
1. Repetitive traction of a pathological nature at the sites of attachment of the above structures. Seen in both pronated and
supinated foot types.
2. Inflammation secondary to metabolic disease at the sites of attachment.
3. Loss of the plantar heel fat pad
4. Forrester's disease (DISH)- diffuse idiopathic skeletal hyperostosis: large irregular posterior and plantar spurring.
B. Differential Diagnosis

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 1. Plantar Fasciitis (especially with concomitant ankle equinus or subtalar hyperpronation.
2. Subcalcaneal Adventitious Bursitis
3. Contusion or stone bruise (Policeman’s Heel)
4. Tendonitis of the first layer of plantar musculature
5. Nerve entrapment
6. Heel Neuroma
7. Radiculopathy
8. Infection
9. Systemic Disease: gout, rheumatoid arthritis, and seronegative arthritides.
C.Treatment
1. Conservative therapy
a. Plantar rest strapping
b. Local physical therapy: ultrasound, ice, stretching exercises, Steroid injections, and phonophoresis.
c. Orthotic control for long term management
2. Heel Spur Surgery
a. Diagnosis

-Rule out gout, RA, seronegative arthritides (Reiter's Syndrome)

-If normal x-rays, bone scan may be hot, indicating reactive process. This is not
very informative since non-specific study.

b. Always present conservative treatment

c. Procedure Open or semi closed (Dugger Approach)

1. Incision: medial and between medial band of plantar fascia below, and abductor
hallucis above.

2. Fasciotomy or take out 1.0 - 1.5 cm of fascia (sub total plantar fasciectomy)

3. Resect exostosis and rasp

4. TLS drain

5. Jones dressing

d. Complications

1. Long term pain and edema

2. Slough secondary to excessive retraction, poor placement of incision, poor

suturing and hematoma formation

3. Too aggressive an exostectomy can cause stress fracture

4. Medial calcaneal nerve entrapment

III. Haglund’s Exostosis

A. Diagnosis
1. Fowler and Philip Angle (usually between 44 - 69 degrees) with over 75 degrees usually will present with posterior
swelling and prominence just superior to Achilles insertion.
2. According to Ruch: for more relevant criteria for patient's with Haglund’s and retrocalcaneal bursitis- add sum of Fowler
& Phillip along with calcaneal inclination angle. If over 90, patient probably has Haglund’s

3. Mechanical foot types that present with Haglund’s

a. Compensated rearfoot varus
b. Compensated Forefoot valgus
c. Rigid plantarflexed 1st ray
B. Anatomy

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 1. Superior posterior 1/3 of calcaneus is smooth and bordered superiorly by bursal projection
2. Retrocalcaneal synovial bursa separates Achilles from the upper 1/3 posterior calcaneus.
3. Pre-Achilles fat pad
a. Normally 9 mm wide, 2 cm above bursal projection
b. Outlines anterior surface of the Achilles on x-ray
c. Thickening of Achilles will widen the normal 9mm dimension as well as lose sharp interface with pre-
Achilles fat pad
4. Kager’s Triangle
a. Posteriorly: Achilles
b. Anteriorly: long flexor tendons
c. Inferiorly: superior surface of calcaneus
5. Adventitious superficial Achilles bursa - between Achilles and subcutaneous tissue
C. Incidence of Haglund’s
1. Females in 20 - 30 year old age group
D. Haglund’s Syndrome
1. + PPL (Parallel Pitch Lines)
2. Cortically intact bursal projection
3. Loss of calcaneal recess
4. Thickening of Achilles over normal 9mm
5. Loss of Achilles and pre-Achilles fat pad interface
6. Superficial Achilles bursitis
E. Treatment
1. Wait for apophysis to close, 14 - 16 years of age
2. Procedure
a. Performed best prone
b. If exostoses is mainly lateral, use lazy L or linear lateral incision
c. If exostoses is mainly medial, use second linear medial incision
3. In structural cavus foot with high CIA, but normal postero-superior prominence causes symptoms, use Keck and Kelly
osteotomy
a. This brings postero-superior aspect of calcaneus anteriorly
b. Fix with Steinmann pins or screws.

IV. Retrocalcaneal Exostosis with Calcification in Achilles

A. Diagnosis
1. See obvious retrocalcaneal exostosis and not Haglund’s
2. May see intra-tendinous calcification
B. Procedure
1. Patient prone
2. Midline incision
3. Dickinson Approach
a. From superior medial to inferior lateral
b. Don't detach distal Achilles, separate it.
4. Tendon should be split longitudinally with distal portions of Achilles remaining intact
5. Resect intra-tendinous calcification and exostoses.
6. Long leg cast after, Jones dressing, for 4-5 weeks.

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Implants
I. Patient selection

A. Adequate neurovascular status

B. Adequate skin coverage
C. Functional musculo-tendinous system
D. Adequate bone structure
E. Patient acceptance

II. Contraindications

A. Patients with profound peripheral neuropathy - may lead to breakdown (should consider 1st MPJ fusion)
B. Advanced osteoporosis (bone erosion and collapse)
C. Young and very active patients
D. Previous Joint Infection
E. Allergy to implant material
F. Abnormally short proximal phalanx

III. Goals

A. Relief of pain
B. Restore motion
C. Reduce deformity
D. Implant functions as spacer, and should not be expected to correct deformity and restore motion

IV. Complications

A. Failure to reattach FHB

B. Failure to lengthen a taut EHL
C. Cutting FHL
D. Improper angle of MPJ bony resection

V. Hemi Implant

A. Indications
1. Narrowed joint space
2. Osteoarthritis lipping base at proximal phalanx or head of metatarsal
3. Severe luxation of proximal phalanx on metatarsal head with subchondral bone changes
4. Use hemi implant if good articular surface on Metatarsal head. If subchondral bone plate has good contour and direction
and if resection of metatarsal head exostoses will not destroy functional articulating surface
B. Technique
1. Inverted "L" capsule made at base of proximal phalanx (good capsular flap).
2. Can perform Reverdin or Austin if high PASA on Metatarsal head (lateral deviated cartilage)
3. Cut base perpendicular with long axis of proximal phalanx (5 - 10 degrees of abductus is physiologic)
4. Implant should be wider then cortical width of phalanx wide implant may limit ROM
5. Two drill holes, medial dorsal, medial plantar for medial capsular flap
6. One hole plantar for medial head FHB (Avoids poor purchase)

VI. Total Implant

A. Indications- Severe adaptive and degenerative changes at both surfaces of MPJ

B. Contraindications
1. A high IM angle and excessive HAA can't be corrected and maintained by insertion of total implant
2. Implant failure or fracture and erosion through cortical surfaces can occur
C. Technique
1. Don't remove excessive bone from metatarsal head so as to maintain length (possible transference of weight to lesser
metatarsals)
2. 8 mm resection from phalanx, 3 mm resection from metatarsal head
3. Perform IM angle closing procedure in IM high or if elderly patient. Perform Mayo with total implant (i.e. more bone
removal from 1st metatarsal)
D. Complications
1. If too much bone cut from dorsal metatarsal head - hallux won't purchase ground
2. If too much bone cut from plantar metatarsal head - hallux will have limited dorsiflexion

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VII. Implant Alternatives

A. Keller Bunionectomy
1. Indications
a. MPJ pain must be present
b. Severe HAV
c. Limitus/Rigidus
d. 1st metatarsal should not be excessively short
e. Osteoporosis may be present

2. Technique
a. Lengthen EHL to prevent cock-up
b. Can use K-wire to control
3. Complications
a. Flail toe
b. Weight transfer to lesser metatarsals (stress fractures)
c. Short hallux
d. Postoperative osseous proliferation
B. 1st MPJ Arthrodesis
1. Indications
a. Flail toe
b. Failed implant
c. Failed Keller
d. Neuromuscular imbalance (Cerebral Palsy, Polio etc.)
e. Intra-articular fractures
f. Arthritic 1st MPJ
2. Contraindication
a. Limited motion of IPJ
b. Wearing heads greater than 2 inches
c. Poor bone stock
3. Optimum Fusion
a. 10 - 20 percent abduction
b. 20 - 30 percent dorsiflexion
c. Remove minimum bone from metatarsal head and base to maintain length
d. Use single retrograded 3/32 or 3/64 Steinmann pin

VII. Implant Complications

A. Under Stress
1. Plastic Deformation
2. Stress Fractures
3. Detritic synovitis
4. Thickened Synovial Tissue Capsule
B. Can get stress riser and fatigue fracture if you try to whittle or alter implant
C. Reasons for removal of Hemi implant
1. Performing procedure to correct HAV
2. Attempting to correct a structural deformity
D. Implant Arthropathy
1. Aseptic Necrosis
2. Ectopic Bone formation - will see 3-4 months after implant
3. Bone Cysts - in metaphyseal and subchondral bone
E. Reaction of Host (soft tissue)
1. Fibrous encapsulation of implant
2. Inflammatory foreign body reaction
a. Foreign body granuloma

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 b. Fibrous hyperplasia - can have resorption around stem

VIII. Digital implants

A. Preoperative Criteria
1. Pain
2. Absence of significant MPJ contracture unless reduced at time of surgery
3. Absence of significant abnormal length of the involved toe
4. Adequate bone density and size
5. Absence of a cavus foot
6.Normal skin and vascular status
B. Types
1. The Silastic Hammertoe Implant (Weil design)
a. A nonhinged, cylinder-shaped implant
b. Affords the least post-op motion
c. It produces the most internal rigidity of all three
d. A good choice for a short toe
2. The Silflex Hammertoe Implant (Sgarlato design)
a. A hinged implant designed to allow for joint motion
b. Requires more precise fabrication of the stem holes
c. Any rotation of the implant on its long axis will produce a nonfunctional result.
3. The Silastic Finger Joint Implant H.P. (Swanson design)
a. Same as Sgarlato design
C. Contraindications
1. Nonreducible contracture of the involved MPJ
2. Inadequate bone density or size to receive the implant
3. Infection in the area involved
4. Inadequate skin covering and/or vascular status
5. History of allergy to the implant material
6. Significant frontal plane deformity of the toe
7. Intraoperative fracture of the phalangeal bone while fabricating the stem holes.

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 Laser Surgery
I. General Facts:

A variety of surgical lasers are used today, however the CO2 laser remains the mainstay in podiatric surgery. Fundamental
physical properties of laser surgery are based on Planck's quantum mechanics and Einstein's stimulated emission theories. LASER
stands for Light Amplified Stimulated Emission Radiation. Laser light is monochromatic and coherent, wherein all of the light waves
line up so that the peaks and troughs are equidistant in space and time.
The laser beam (electromagnetic radiation) is characterized by its;

• frequency (Hz, or cycles per second)

• wavelength (nanometers)
• time of application (milliseconds to picoseconds)
• power density (watts per cm2)
• amount of energy delivered to the tissues (joules, or watts per second).

The coherent light is collimated by the fiberoptic or articulated arm delivery system, and can therefore be aimed by the operator.
The time of exposure to the laser beam is controlled by gating the delivery system to allow passage of light as a continuous
beam, a single pulse, or repetitive pulses varying from millisecond to picosecond intervals. The interval between pulses allows the
tissue to dissipate energy as heat, with the minimal thermal relaxation ration being 1:10 on:off.
Tissue absorption varies primarily with the wavelength and tissue type, wherein shorter wavelength light has higher energy, and
therefore penetrates deeper or creates more heat in the same tissue.
The specific wavelength is determined by the specific element or elements used in the "lasing (active) media" of the laser. The lasing,
or active media may be CO2 (with helium and nitrogen), or Nd-YAG (neodymium with yttrium, aluminum and garnet), or
other elemental gases.
Tissue interaction with laser light varies from one tissue type to another. For instance, skin and soft tissue may readily vaporize, while
bone or cartilage heats up and denatures with resultant necrosis, in response to the same laser beam. It is therefore important to
select the proper laser and settings for the tissue being manipulated. In foot and ankle surgery, the following lasers are used:
Types of Lasers Used in Foot and Ankle Surgery

Laser Characteristics and applications

Far infrared wavelength, readily absorbed by water and therefore only used for superficial (0.1 mm) penetration
CO2 such as cutting, ablation, and coagulation of skin and nail lesions.

Ho-YAG
Middle infrared wavelength, absorbed by bone and cartilage, penetrates 0.4-0.6 mm, and used for lesion ablation
non-contact tip in more dense tissue.
(holmium)

Nd-YAG
Near infrared wavelength, poorly absorbed, penetrates 6-8 mm, deep lesion ablation and coagulation.
non-contact tip

Nd-YAG contact tip Near infrared wavelength, penetrates 5-200 microns, superficial cutting or incision

KTP (potassium, titanium,

phosphate) 532 micron wavelength, absorbed by dermal vessels and superficial lesions such as verrucae, penetrates 0.5 mm
non-contact tip in pigmented skin and up to 4 mm in nonpigmented skin, used for ablation.

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 KTP contact tip Penetrates 1-2 mm, used for incising skin.

488-514 micron wavelength, penetrates 0.5-1 mm, absorbed by dermal vessels and superficial skin lesions such
Argon non-contact tip as verrucae, used for ablation of dermal lesions.

Cu (copper) vapor, 478 micron wavelength, penetrates 0.5-1 mm, absorbed by dermal vessels and superficial skin lesions, used for
ablation of dermal lesions.
non-contact tip

II. Safety

Laser safety entails special attention to instrumentation, eye protection and personal shielding, vapor evacuation and filtration, and
aiming technique. ANSI publication 136.3 serves as a standard reference for laser safety. Eye safety precautions vary with the
wavelength of the laser beam as follows:

• Class I - direct visualization of the beam effects no ocular damage

• Class II - prolonged direct visualization will effect ocular damage

• Class III - direct visualization effects immediate ocular damage

• Class IV - direct visualization effects immediate, severe ocular damage ranging from corneal burn to retinal ablation and
blindness.
All medical lasers are categorized as Class IV. They pose a fire hazard and are harmful to unprotected skin. Damaging effects
can be caused by direct or reflective laser exposure. Smoke plume evacuation systems should entail vacuum suction at the point of
creation, and 0.2 micron dual filtration with carbon. Personnel in the OR should wear proper body and eye protection and filtration
mask. The door to the OR must indicate the presence of medical laser hazard.

III. Specific Laser Procedures

Surgical laser techniques include lesion ablation and dissection primarily. As with any other form of dissection or tissue
ablation (scalpel, radiosurgery, cryotherapy), violation of the dermis results in tissue repair with scar formation.

• Incisions are made with a focused beam directed in a repetitive, linear fashion.

• Lesion ablation is achieved with a defocused beam directed in a cross-hatched linear or back-and-forth fashion, or
in an ever-increasing radius circular fashion beginning centrally in the lesion. Periodic curettage may assist lesion
ablation, as non-vaporized eschar may accrue. It should be noted that, with the exception of skin lesions, lasers
are generally used to assist with dissection and lesion ablation, while standard techniques of dissection and
arthroscopy are employed to expose lesions and underlying target structures. Patients should understand this
concept of "laser assisted" surgery. Appropriate lesion biopsy should be obtained prior to laser ablation.
Appropriate sterile bandage, with topical application of silver sulfadiazine (Silvadene) cream, and follow-up are
part of the aftercare.

Common Lesions and Procedures and Applicable Laser

Lesion Lasers

Verrucae CO2, Argon, Nd-YAG, KTP

Cavernous hemangioma Nd-YAG bare fiber

Hypertrophic scar or keloid CO2

tattoo removal CO2

cutaneous granulomatous lesions CO2

Nail Matrix Ablation CO2, Argon, Nd-YAG

Synovitis, Scar, Chondromalacia, Osteophyte Holmium-YAG

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Morton's Neuroma
I. Signs

A. Most commonly encountered in 4th - 6th decades of life

B. Tendency to see in obese patient, or ones that require excessive ambulation, or those that wear tight shoes
C. Make sure to check neurologic status (IE reflexes) to rule out proximal disk or nerve problem
D. Conservative measures first
1. Orthotics
2. Strapping
3. Injections
4. Molds

II. Surgical Approaches

A. Plantar longitudinal in interspace gives best exposure

1. Avoid weight bearing metatarsal heads to avoid painful scar
2. Keep non weight bearing for 3 weeks
B. Plantar transverse incision
1. Can evaluate adjacent interspaces
2. Avoid weightbearing area, by going distal to metatarsal heads.
C. Dorsal Linear incision
1. Allows early ambulation
2. Greater potential for dead space

III. Complications

A. Hematoma in dead space

1. To avoid - use closed suction small drain
2. Treatment - remove one or two sutures and express blood after anesthetizing foot.
B. Vascular ischemia
1. From trauma to vessels, ligating veins, transecting arteries
2. Treatment - remove ice, check capillary return, wait 6 hours, then sympathetic nerve blocks, avoid caffeine and nicotine
possible IV Vasodilan 5 mg- 10 mg.
C. Amputation neuroma
1. Can inject stump before closure, cut nerve proximal enough and away from bony areas.
D. Permanent numbness of involved digits and plantar interspace

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Nail Surgery
I. Ingrown Nail (Onychocryptosis)

A. Definition
1. Nail pathologies in which the nail plate has grown into the ungualabia and may or may not be infected
B. Classification
1. Iatrogenic Onychocryptosis
a. Most commonly seen ingrown nail
b. Characterized by a history of patient cutting own nails incorrectly
2. Congenital Abnormality of Nail Plate
a. Matrix shape is abnormal & the nail plate curves downward on one or both sides
b. Also known as incurvated nail plate
3. Primary Soft Tissue Abnormality (Hypertrophy of Ungualabia)
a. Primary pathology is in the soft tissue structures surrounding the nail plate.
b. Usually enlarged and overlapping the normal nail plate causing in growth.
4. Combinations of 1 - 3
a. Including combined problems where there may be an incurvated nail with hypertrophy of the ungualabia
or incorrect cutting of nails with an incurvated nail.
C. Surgical Treatment
1. Avulsion
a. Useful in infected nails
b. Non-permanent removal, good for 1st episode of ingrown nails
2. Phenol Technique
a. Advantages

1) Good first choice procedure for chronic ingrown nails

2) Simple & easy to perform

3) Minimal discomfort

b. Disadvantages

1) Produces chemical burns

2) Open draining wound for three - four weeks.

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Pan Met Head Resection & Implantation
I. When performing surgery on rheumatoid patient consider

A. Physiologic age of patient

B. Condition of bone stock and soft tissue
C. Medical condition of patient
D. Activity level

II. MPJ Replacement

A. Purpose
1. Primarily to alleviate pain
2. Secondarily to restore function
B. In rheumatoid patient, use total joints as opposed to hemi joints because articular cartilage on non-implanted side
will eventually deteriorate and breakdown implant
C. Give Cefazolin 2 gram IV 15-30 minutes prior to procedure

III. IPJ Replacement

A. Criteria
1. Painful IPJ
2. Adequate bone stock to receive stems of implant
3. Absence of severe MPJ subluxation unless released
4. Non need to replace MPJ of involved digit if you're replacing IPJ
5. Adequate skin coverage
B. Technique
1. If dealing with normal metaphyseal width to proximal phalanx, don't remove base of middle, rather, ream hole in
cartilage.
2. If narrow metaphyseal region remove base so that implant will not have tendency to fracture bone of proximal phalanx

III. Lesser MPJ Implants

A. Bone stock of metatarsal and phalanx should be large enough to accept stems
B. Reduce dorsal contracture because if left alone, it will overpower implant
C. Don't take excessive bone or implant may have tendency to dislocate
D. Take limited bone from phalangeal bases.

IV. 1st MPJ implants

A. 1st MPJ pain

B. Limited or absent ROM
C. Osseous proliferation
D. No excessive cystic changes in bone structure
E. Adequate bone stock
F. Normal IM angle, unless corrected by another procedure.

V. Pan Metatarsal Head Resection

A. Objectives
1. Alleviate pain
2. Restore improved weightbearing function
B. Procedures
1. Hoffman - removed metatarsal heads
2. Clayton - removed base of proximal phalanx if enlarged, because they will assume increased weightbearing function
without metatarsal heads.
C. Incisions
1. Plantar transverse
a. Make 1.5 cm proximal to web space
b. Good with severe dorsal contractures to assist pulling down the contracted digits
c. Keep fat with plantar skin (don't separate)
d. Don't dissect in between metatarsal interspaces
e. Does not allow good exposure of bases
f. Separate dorsal incisions address arthrodesis of PIPJs 2-4, & arthroplasty 5

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 2. Dorsal incisions
a. Three incision approach - one over 1st MPJ, second between 2 and 3, third between 4 and 5
b. Five dorsal incisions - 1st and 5th can be extended but middle three incisions are kept mostly on toes to
proximal metatarsal head area to avoid making long peninsulas of tissue that may compromise blood
supply.
D. Preferred length pattern after metatarsal head resection: 2, 1, 3, 4, 5
E. Bone cutting techniques
1. Make cut angled more plantar then dorsal
2. Without implant 1st met is angle medially
3. 2nd is cut perpendicular 3, 4, & 5 more laterally cut
4. If hypertrophied bases, take 1, 2, 3, & 4 but not 5
F. Most commonly fuse PIPJ 2-4 arthroplasty 5th for more stabilization
G. K-wire from tip, across metatarsals. Keep forefoot Non weightbearing by padding shoe
H. Postoperative expectations
1. Shorter and wider foot
2. Apropulsive gait.

Tailor's Bunion Surgery

I. Causes

A. Uncompensated or partially compensated rearfoot or forefoot varus creates hypermobile 5th ray from ground
reactive forces
B. Plantarflexed 5th metatarsal will abduct, evert and dorsiflex from ground reactive forces.
C. Congenitally dorsiflexed 5th ray

II. Pathomechanical X-ray Analysis

A. Rotation of lateral plantar tubercle to lateral position (seen in pronatory

eversion of 5th metatarsal).
B. Increased I.M. angle of 4th and fifth (over 9 degrees), normal is 4-5 degrees.

C. Increased lateral deviation angle or lateral bowing of 5th

metatarsal (over 7.0 degrees) normal is 0 - 3 degrees.

D. Dumbbell shaped enlarged 5th metatarsal head

E. Arthritic changes with exostosis of 5th metatarsal head
F. Combinations of above

III. Splay Foot

A. I.M. angle increased over 12 degrees for first and second metatarsals with 4th and 5th metatarsal I.M. angle over 8 degrees

IV. Surgical Goals

A. Correct enlarged lateral exostoses

B. Correct structural deviations and bowing of 5th metatarsal
C. Correct splaying of 5th and 4th with increased I.M. angle
D. Correct varus or adductovarus rotation of 5th toe

V. Procedures

A. Lateral exostectomy

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 1. Performed on mild cases with minimal structural deformity.
2. If performed aggressively to correct a severely splayed or bowed 5th metatarsal it will result in laxity of lateral joint
structure, tightness of medial structures, adductovarus 5th toe and retrograde forces on 5th metatarsal causing a
recurrence and worsening of deformity
B. Hohmann Osteotomy
1. Transverse through and through osteotomy at neck

C. Reverse Wilson
1. Displacement osteotomy or oblique osteotomy from distal lateral to proximal medial

D. Mitchell Osteotomy
1. May not be able to get good IM closure with thin metatarsal neck

E. Austin "V" Osteotomy

1. Again requires wide metatarsal neck for displacement if severe tailor's bunion

F. Closing adductory osteotomy at neck (Mercado)

G. Closing adductory osteotomy at proximal diaphysis with stainless steel wire fixation and casting (Gerbert)

H. Oblique wedge osteotomy at apex of deformity with K-wire fixation or small screw 2.0 mm screw fixation.

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Tendon Transfer Procedures
I. Fundamental points of concern are:

A. Balance of power - all of the joints of the foot and ankle are influenced by the muscle-tendon units that cross each specific joint.
Primarily the forces created by the muscle-tendon units acting upon the joint determine the ultimate position of a functional
joint, both at rest and during function. Every time a muscle-tendon unit is manipulated (transferred), there is a change in the
overall balance of the joint. In order to effectively restore function, deforming influences must be removed and it may be
necessary to stabilize (arthrodesis) deformed or dysfunctional joints upon which the transferred tendons can work (e.g. it is
not uncommon to combine triple arthrodesis with major tendon transfers crossing the ankle). Furthermore, there
is only a fixed amount of power available to influence a joint, and the total amount of power cannot be increased via
transfer. One can expect at least 1/2 grade decrease in strength following tendon transfer. Rarely would a
muscle weaker than grade 4 be considered for transfer unless another tendon transfer augments it. Only a muscle-
tendon unit of satisfactory strength and range of contraction is suitable for transfer.
B. Anatomical and physiological factors - these have been noted elsewhere in this manual, in the anatomy and physiology section.
C. Atraumatic technique - there are specific methods for handling tendon, all of which enhance healing and ultimate function.
These include:
1. Maintain tendon moisture (avoid desiccation)
2. Prepare the recipient site for transfer prior to harvesting the tendon
3. Establish physiological tension in the transferred tendon.
4. Use available naturally occurring tendon sheaths and retinacula to direct and maintain the course of the transferred
tendon.
5. Preserve the vascular supply to the transferred tendon by avoiding excessive traction on the muscle belly, or
overcrowding tendons within a sheath or fibro-osseous tunnel or hiatus in the interosseous membrane of the leg.
6. Enhanced rehabilitation based upon understanding of tendon healing.

II. Clinical assessment of muscle strength:

It is necessary to put the joint acted upon by the muscle-tendon complex in the end range of motion position, thereby providing
the tendon maximum mechanical advantage and yielding the most accurate clinical test of muscle strength. Other techniques
useful in the assessment of muscle strength include biometric testing using machines such as Cybex or Biodex, and yield
information detailing power, endurance and strength. Neurological consultation, and EMG and NCV testing are usually
indicated when gross weakness is clinically identified.

III. Grading system for gross (clinical) manual muscle testing:

Grade 5, "normal" strength, full resistance at end range of motion.

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 Grade 4, "good" strength, some resistance at end range of motion
Grade 4+, moderate resistance at end range of motion
Grade 4-, mild resistance at end range of motion
Grade 3, "fair" strength, able to move against gravity only
Grade 2, "poor" strength, able to move only after gravity eliminated
Grade 1, "trace" strength, can visualize or palpate contraction without joint motion
Grade 0, "zero" strength, no clinical evidence of muscle contraction

IV. The relationship of muscle length and strength of contraction:

Physiologically, a muscle's ideal resting length allows for optimum strength of contraction. A muscle subjected to excessive resting
tension will undergo fiber degeneration, while inadequate tension predisposes to muscle weakness. Muscle tensile strength is
approximately 75 PSI, while tendon tensile strength is 8,600-18,00 PSI. Comparing tension versus length, as the length
increases beyond resting length, tension increases up to a point after which tension decreases as the muscle belly fails to
sustain force. Thereafter, tension actually rises as the strength of the tendon, not the muscle, sustains the load. In some
cases, it may be desirable to use the transferred tendon as a sling or suspensory ligament, and not a gliding functional
tendon. The direction of pull determines the transferred tendons influence on affected joints.

V. Tendon healing (3 phases in 4 weeks):

A. Lag (substrate) phase

Week one, the ends are joined by a fibroblastic splint, strength due to sutures, immobilization required. The repair site
consists of serous material and granulation tissue (zone of degeneration) and is in its weakest state.
Week two, increasing fibroplasia and vascular, strength due to sutures, immobilization required.
B. Fibroproliferation (collagenation) phase
Week three, marked increased fibroplasia, moderate collagenation strength; can sustain gentle passive motion or isometric
(in cast or brace) exercises.
C. Remodeling phase
Week four, collagen realignment and remodeling, moderate strength (not full), gradual progressive strengthening
with passive and active exercises.

VI. Tendon anchors and reattachment:

Hole and button

Hole and bone plug
3-hole intraosseous
2-hole intraosseous
Side-to-side
Bunnell
Lateral trap
Various commercially available anchors (Staytak, Mytek, PBA, etc.)

VII. Complications of tendon transfer include:

Muscle spasm (diazepam is useful in the early postoperative phase)

Stenosing tenosynovitis and adhesion
Over correction
Under correction or weakness
Loss of correction
Bowstringing
Nerve entrapment.

VIII. Tendon lengthening procedures

A. Baker Procedure: tongue-in-groove

B. Hoke's Tenotomy: a triple tenotomy of the Achilles tendon
C. White Tenotomy: Tenotomy of the anterior 2/3 of the distal end of the Achilles tendon and the medial 2/3 of the tendon
D. Strayer: Distal recession requiring the complete severance of the aponeurosis. The proximal aponeurosis is sutured to the
underlying soleus.
E. Silverskiold: Proximal recession in which the muscular heads of the gastrocnemius are released from the femoral condyles and
reinserted to the proximal tibial area. Note: a 3 joint muscle is converted to a 2 joint muscle.
F. Sliding Z-lengthening: Used on extensor tendons or the Achilles (White procedure).
Note: These procedures are used to correct non-spastic ankle equinus secondary to gastroc shortening. For
spastic gastroc equinus you must also excise the central soleus aponeurosis.

IX. Common tendon transfers about the foot and ankle

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A. Jones suspension
1. Goals: eliminate cock-up hallux, enhance ankle dorsiflexion.
2. Indications: cock-up hallux, weak tibialis anterior, and loss of sesamoid function.
3. Adjunct procedures: hallux IP arthrodesis, Heyman-Jones panmetatarsal suspension.
4. Complications: recurrence of deformity due to tendon regeneration.
5. Aftercare: BK WB cast 2-3 weeks.

B. Hibbs suspension
1. Goals: decrease MTPJ buckling and increase ankle dorsiflexion.
2. Indications: anterior weakness (mild), flexible anterior cavus with extensor substitution, claw toes often with associated
IPK.
3. Contraindications: posterior weakness, weak interossei, gross EDL weakness, structural rigidity, and osseous instability.
4. Aftercare: BK WB cast 4-6 weeks.

C. Tibialis anterior tendon transfer (TATT)

1. Goals: decrease forefoot supinatory twist, increase true ankle dorsiflexion
2. Indications: recurrent clubfoot, flexible anterior cavus, dropfoot (CMT)
3. Contraindications: excessively weak TA (<4), pes valgus, weak PL, severe anterior cavus with claw toes.
4. Aftercare: BK WB cast 3-4 weeks.

D. Split tibialis anterior tendon transfer (STATT)

1. Goals: increase true ankle dorsiflexion, decrease long extensor swing phase overload, and decrease adductocavovarus
forefoot deformity.
2. Indications: flexible anterior cavus, extensor substitution, claw toes; spastic posterior ankle equinus, equinovarus (CP),
anterior weakness dropfoot, flexible cavovarus, overpowering invertors.
3. Contraindications: same as TATT.
4. Aftercare: same as TATT.

E. Tibialis posterior tendon transfer (TPTT)

1. Goals: eliminate dropfoot; eliminate flexor substitution (triceps surae weakness).
2. Indications: anterior muscle weakness, dropfoot, nonspastic equinovarus, recurrent clubfoot, peroneal nerve palsy
(CMT), and triceps surae weakness.
3. Contraindications: spastic TP, pes valgus, rigid clubfoot.
4. Technical considerations: approaches, interosseous window, phase conversion, often combined with arthrodesis.
5. Aftercare: BK cast 3 weeks NWB, then additional 3 weeks WB, begin ROM at 4 weeks.

F. Peroneus longus tendon transfer (PLTT)

1. Goals: increase ankle dorsiflexion, eliminate PL cavus influence.
2. Indications: anterior muscle weakness, dropfoot, and flexible cavus.
3. Technical considerations: easy phase conversion, caution sural and intermediate dorsal cutaneous nerves.
4. Contraindications: posterior weakness, pes valgus.
5. Aftercare: same as TPTT.

G. Peroneus brevis into talus tendon transfer (PBTT)

1. Goals: suspend talar neck, eliminate flexible vertical talus.
2. Indications: Type I vertical talus, severe pes valgo planus.
3. Contraindications: rigid pes valgoplanus, immature talus or compromised talar neck circulation.
4. Technical considerations: may be combined with closing adductory wedge osteotomy of talar neck, medial arch
tendosuspension (McGlamry-Young), Evans lateral column lengthening.
5. Aftercare: up to 8 weeks BK cast NWB

H. Murphy anterior advancement of the tendoachilles

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 1. Goals: eliminate spastic posterior ankle equinus.
2. Indications: CP induced dropfoot with triceps surae contracture ankle equinus.
3. Contraindications: osseous ankle equinus.
4. Technical considerations: heel prominence, routing around FHL, recurrent deformity, and weak propulsion.
5. Aftercare: up to 5-6 weeks BK NWB cast.

Triple Arthrodesis
I. Indications

A. Collapsing pes valgo planus foot

B. Tarsal coalition
C. Tarsal arthritis
D. Cavus foot
E. Recalcitrant clubfoot
F. Neuromuscular disorders (CMT frequently presents a different foot type from the others.

II. Incisions

A. Ollier incision
1. From tip of fibular malleolus, across sinus tarsi to the dorsal region of the talonavicular joint
2. This approach is good if cavus foot, but difficulty addressing TN joint in pes valgus foot.
B. Lateral incision
1. From tip of lateral malleolus to dorsum of 4th and 5th metatarsal base
2. Gives good access to STJ and C-C joint
C. Medial incision
1. From medial malleolus to navicular cuneiform joint
2. Gives good exposure to talonavicular joint and for T-C fixation
D. Laterally

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 1. Go thru superficial fascia to deep fascia, which is incised between EDB and P. brevis tendon
2. Lift EDB off of C-C joint
3. Expose CC and STJ
4. Remove fibroligamentous tissue from sinus tarsi
5. Expose lateral head and neck of talus
6. Reflect peroneal tendons for exposure to posterior facet
E. Medially
1. Avoid medial marginal vein
2. Deep fascial incision medial to Tibialis Anterior
3. Incision into capsule exposed both ankle and talonavicular joints.
Note: The relationship and viability of the dorsal soft tissues are preserved as subperiosteal dissection extends
between the two incisions.

III. Osseous Resections

A. Position of Foot
1. If knee is rotated internally 15 degrees, abduct foot about 30 degrees
2. If knee is abducted 30 degrees, do not further abduct foot.
B. Midtarsal Resection
1. Perform this first as it allows FF to be mobilized for access to STJ
2. Hold foot in reduced position and resect parallel to CC and TN articulations
C. STJ Wedging (This is the resected last and fixated first)
1. If pes valgus, slide calcaneus medially
2. If pes cavus, slide calcaneus laterally
D. Dorsiflexion or plantar flexion of FF on Rearfoot
1. Slide calcaneus posteriorly to talus which results in plantar flexion of talus and increased arch height
2. Slide calcaneus anterior to the talus which dorsi flexes talus and decreases height of arch
E. Avoid varus rearfoot, instead, place in mild valgus
F. After pleased with alignment, temporarily fix STJ, CCJ TNJ with large K-wires or small Steinmann pins
1. From dorsal neck of talus across STJ then into body of calcaneus
2. X-ray lateral and axial calcaneal views
3. Use 6.5 mm cancellous screw for all joints
G. Alternate method of fixating MTJ is by
1. Use Blount staple (2) at 90 degrees to each other at CC and TN
I. Place drains under capsule and periosteum and close

IV. Postoperative Care for Complete Rigid Fixation of All Joints

A. After 3-5 days, take out TLS drain and change to bivalved AK cast for 4 weeks
B. From 4-8 weeks, active and passive ROM exercises
C. At 10 weeks gradual weightbearing with crutches
D. At 12 weeks full weightbearing if x-rays reveal solid fusion

V. Postoperative Care for Non-Rigid Compression Fixation

A. Maintain 6 weeks non-weightbearing

B. If X-rays reveal consolidation of fusion sites
1. From 4-8 weeks, active and passive ROM exercises
2. At 10 weeks, gradual weightbearing with crutches
3. At 12 weeks, full weightbearing if x-rays reveal solid fusion

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PART 10:
GENERAL
MEDICINE

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AIDS
High Risk groups:

Homosexuals, IV drug users, hemophiliacs and anyone who had a transfusion.

Mechanism of infection:

The envelope Protein gp120 found on the surface of the viral cell has an affinity for a CD4 molecule on human target cells.
When the CD4 molecule binds with the gp120 protein the viral and target cell fuse and infection occurs. The cell is infected
for life because the retroviral RNA becomes part of the host cell genome.

A.
o T4 helper-inducer cells are the most common target cells. Normal levels are 800-1000 cells/mm3. A
count of less than 500 usually accompanies the first symptoms of aids.

o Lymphocytes, monocytes, mast cells, macrophages and Stem cells are also target cells. Macrophages and
monocytes survive HIV infection and persist as viral reservoirs.

o Aids affects the dermatologic, vascular, and neurologic systems of the lower extremity.

o
Test to Order if you suspect aids:

1. Main screening test- ELISA

(Enzyme Linked Immunosorbent Assay): is sensitive for antibodies to HIV. (Usually develops in three months) Sometime
there are false positives in patients with chronic hepatitis, Alcohol liver disease and collagen vascular disease.
2. Follow Elisa with a Western Blot Assay for confirmation of diagnosis. (It tests for antibodies to glycoprotein and antigens).
3. Also T4/T8 Ratio: Normal: 2:1 Aids: .4:1 or 1.1
4. CD 4 level: Normal: 800/900/mm3 Aids: Steady decline to less than 200/mm3
5. Baseline lab screening for HIV positive patients include CBC with Diff., Platelet, ESR Chemistry panel with liver function tests
and lymphocyte markers with % and ratio, U/A, Syphilis serology, TB skin test, and Hepatitis B panel.

Clinical Signs & Symptoms:

- Thrombocytopenia purpura
- Nausea
- Night sweats
- Vomiting
- Maculopapular Rash on trunk and extremities
- Diarrhea
- Myalgia
- Oral candidosis
- Malaise
- Weight loss
- Fever
- Sensory Neuropathy: Glove & Stocking along with tingling sensations

Lab Indicators:

CD4 lymphocyte count

Detection of p24 core antigens
Serum B2 microglobulin
Serum Neopterin
IgA levels

Specific Foot Disorders Found in AIDS

1. Reiter Syndrome (6-10%) Classic Triad

2. Warts
3. Vascular Lesions
4. Dermatologic diseases (Many)
5. Onychomycosis
6. Kaposi’s Sarcoma

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Preventing HIV Transmission in Podiatric Practice

-Universal precautions policy: Consider all patients as potentially infected HIV.

- Keep an Employee classification record showing that they all have been trained in preventative protocols.
- Equipment:
1.Gloves
2.Masks
3.Eye Protection (Shields, goggles, etc.)
4.Sharps Receptacles-- Leak free containers for Bio hazardous waste--these should be labeled as such (in Red) and
disposed of by a professional service such as BFI.

Protocol after possible exposure to HIV:

1. If cut immediately wash with betadine soln. and dress.

2. If mucosal membrane exposure:
a. Intact membrane- nothing
b. Non-intact membrane- wash immediately
Note: In both cases the source patient must be informed and with their consent they should be tested for HIV.
If they do not consent or if they are positive for HIV, the employee is tested immediately then at six weeks and
periodically thereafter.

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Arthritides
I. Rheumatoid Arthritis

Atrophic arthritis - a constitutional disease with inflammatory changes throughout connective tissue of the body.
A. Pathology: Chronic proliferative inflammation of synovial membrane, which can cause irreversible damage to joint
capsule and articular cartilage, which are replaced by granulation tissue.
B. Radiology:
1. Narrowing of joint spaces
2. Bone atrophy and rarefaction of cancellous bone over joint
3. Bone erosion or punched out area near joint
4. Subluxation, deformities, bone resorption (osteoporosis)
C. Location:
1. PIP and MP joints most common
2. Mid-tarsal & subtalar joint - pes planus
3. Calcaneus - posterior-superior surface near Achilles tendon insertion - heel spurs
D. Manifestations Clinically:
1. Pain - symptoms worse first thing in morning
2. Stiffness - morning, or after rest, reduced upon activity
3. Constitutional symptoms- weight loss, fever, coldness, numbness, tingling, easily fatigued
4. Cardinal objective findings: swelling, tenderness to pressure, pain with motion
5. Swelling, joint effusion & synovial membrane thickening.
6. Limitation of motion, pain, muscle spasm, fibrosis of joint capsule, shortening of muscles, or fibrosis
ankylosis/bony ankylosis
7. Symmetrical small joints of feet - pip, mpj classically affected
8. Rheumatoid nodules (subcutaneous nodules)
E. Diagnosis (Made on basis of consideration of characteristic findings and the behavior of the disease over a period of
time.)
1. Criteria: Classical RA most have 7 of following symptoms - first 5 must be present for at least six weeks

Morning stiffness

Pain on motion or tenderness in at least one joint

Swelling in at least one joint,

Swelling of at least one other joint

Symmetrical joint swelling with simultaneous involvement of the same joint on both sides of
the body, except PIP joints

Subcutaneous nodules

X-ray changes typical of rheum arthritis

Positive agglutination test - RA factor

Poor mucin PPT from synovial fluid

Characteristic histologic changes in synovial membrane

Characteristic histologic changes in nodules showing granulomatous foci.

Note: 5 of the above - definite rheumatoid arthritis
3 of the above - probable rheumatoid arthritis
2. Possible RA - any 2 of the following for three weeks.

Tenderness or pain on motion

Morning stiffness
History of joint swelling

Subcutaneous nodules

Elevated sed. rate or C-reactive protein

Iritis
3. Exclusions:

Typical rash or disseminated Le

High concentration of Le cells

Histologic evidence of periarteritis nodosa

Weakness of neck, trunk & pharyngeal muscles or swelling or dermatomyositis

Definite scleroderma

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 Clinical picture characteristic of rheumatic fever

Clinical picture characteristic of gouty arthritis

Tophi

Clinical picture characteristic of acute infectious arthritis

Clinical picture characteristic of Reiter's syndrome

Tubercle bacilli in joints

Clinical picture characteristic of shoulder-hand syndrome

Clinical picture characteristic of hypertrophic pulmonary osteoarthropathy.

Clinical picture characteristic of neuropathy

Homogentisic acid in urine

Histological evidence of sarcoid or positive Kveim test

Multiple myeloma

Characteristic skin lesions of erythema nodosum

Leukemia or lymphoma

Agammaglobulinemia

4. Lab tests

CBC - slight to moderate normocytic hypochromic anemia, white count -acute cases - is
elevated (PNMs may be increased with shift to left) - chronic - normal to slight
decrease

Sed. Rate - moderate to marked increase

RA Test - agglutination test positive 75% after several months to year

Uric acid - normal

Blood Protein - plasma fibrinogen & globin increased; Albumin - decreased total protein -
normal

Ca. & PO4 - normal

LE test - negative

Synovial Fluid Analysis reveals increased WBC's cloudy fluid, decreased viscosity.

II. Osteoarthritis

Primary - no apparent cause

Secondary - excessive stress - obesity- postural or orthopedic abnormalities
A. Pathology: degeneration of articular cartilage
B. Radiology: hypertrophy of bone at articular margins
C. Pedal locations: nearly all pedal joints can be involved
D. Clinical Manifestations:
1. Aching pain relieved by rest,
2. Pain - clinical findings may not be correlated with symptoms
3. Stiffness - symptoms more pronounced with activity as day progresses
4. Joints may appear normal or deformed
5. Crepitus noted with motion
6. Localized tenderness
7. Swelling (feels hard)
8. Range of motion, full or limited
9. Deformities - hammertoe, etc
E. Diagnosis of Osteoarthritis
Age of patient
Gradual onset of symptoms
Stiffness of joints
X-rays of hypertrophic arthritis
Normal laboratory studies
F. Differential diagnosis
RA
Gout
Charcot's joint

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III. Gout

A. Types - Etiologic
Primary metabolic
Primary renal
Secondary metabolic- myeloproliferative diseases
Secondary renal diseases with renal involvement
B. Types - Clinical
Acute gouty arthritis
Intercritical gout (period between acute attacks)
Chronic gouty arthritis (tophaceous gout)
C. Radiology
Acute gout - soft tissue or periarticular swelling
Punched out areas of erosion in joints
Chronic gout - marked deformities with erosion of entire joint surfaces and ankylosis
D. Locations
1. Classic - 1st MPJ
2. Posterior heel - insertion of Achilles tendon with calcaneus
3. Plantar inferior calcaneus
4. Other pedal articulations (MP & Midtarsal), ankle
5. Hand, wrist, elbow, knee
E. Clinical Manifestations:
1. Acute gouty arthritis
Symptoms - excruciating pain
Physical signs
1. Monarticular acute inflammation

2. Swelling, redness, heat, loss of function

3. Desquamatization of skin over site of previous inflammation

2. Chronic gouty arthritis

Symptoms: slow, insidious and painless process, may have occasional periodic moderate acute attacks.
Physical signs:
1. Tophaceous deposits (hallux, digits, Achilles tendon) subcutaneous tophi, bursa tendon

2. Marked deformities in feet: (bunion, hammer-toes, pes planus)

3. Ulcerations with white discharge (sodium urate crystals)

4. Diagnosis: history and exam, demonstration of uric acid crystals in joints; hyperuricemia
(8.0 mg% or higher is usual)
5. Differential diagnosis: pseudo gout; suppurative arthritis; acute bursitis; rheumatoid
arthritis

F. DIAGNOSIS
1. Uric acid level of 7mg/dl for males and 6 mg/dl for females indicate a supersaturated state and can precipitate crystals.
2. The only definitive diagnosis is demonstration of intracellular monosodium urate crystals in leukocytes that are strongly
birefringent.
3. Diuretic therapy is important cause of hyperuricemia.

G. TREATMENT (ACUTE GOUT)

1. Orally
a. Colchicine .5 mg q hour or 1 mq. q 2 hours until symptoms improve, GI distress or 6 mg given without
relief.
b. Indocin 50 mg q 6 hours x 24 hours then q 8 hours x 24 hours then Indocin 25 mg q 8 hours x 24 hours.
2. Parentally
a. IV colchicine 2 mg followed by 1 mg q 6 hours for two doses.
3. Prophylaxis
a. Orally .5mg q 8 hours for 2 to 3 days before surgery and continue 3 - 5 days postoperatively.
H. Long term therapy of Uric Acid
1. When uric acid excretion less than 700 mg/24 hours use Probenecid Sulfinpyrazone
2. If uric acid excretion is over 700 mg/24 hours use Allopurinol.
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IV. Ankylosing Spondylitis

A. New York Criteria, 1968

1. Limited motion of lumbar spine in anterior and lateral flexion and extension
2. History of pain or presence of pain in dorsolumbar junction or in lumbar spine
3. Limitation of chest expansion to 1" or less
4. Definite ankylosing spondylitis present if bilateral sacroiliitis associated with at least one clinical criterion. Probable
ankylosing spondylitis of bilateral sacroiliitis associated with none of the clinical criteria.
B. Prominent symptoms
1. Low back pain
2. Prolonged back stiffness
3. Ascending back pain
4. Heel pain
5. Peripheral joint pain
6. Fatigue
7. Diminished vision or eye pain
C. Roentgenographic features
1. Early
a. Sacroiliac joint blurring
b. Irregularity
c. Sclerosis
d. Erosion
e. Widening
f. Diffuse osteoporosis of spine
g. Apophyseal joint sclerosis
h. Straightening of spine
2. Advanced
a. Apophyseal joint erosion
b. Squaring of vertebrae
c. Narrowed disc space
d. Vertebral collapse
e. Pelvic whiskering
f. Involvement of symphysis pubis
3. Terminal
a. Intervertebral disc calcification
b. Paravertebral ligament calcification
c. Vertical syndesmophytes
d. Sacro-iliac joint fusion
e. Bamboo spine

V. Reiter's syndrome:

Seronegative, asymmetric, arthropathy plus one or more of the following: urethritis/cervicitis, dysentery, inflammatory eye
disease, mucocutaneous disease, balanitis, oral ulceration or keratoderma.
A. Characteristics
1. Involvement of synovial joints, symphysis and enthesis
2. Asymmetric arthritis of lower extremities
3. Predilection of small bones of the feet and ankle, the calcaneus, the SI joint and the knee.
4. Bony erosion with adjacent proliferation
5. Paravertebral ossification
6. Capsulitis and digital edema
B. Studies suggesting diagnosis of Reiter's disease include:
1. Negative test for rheumatoid factor
2. Demonstration of HLA-27
3. Pekin cells in synovial fluid. Numerous white cells in prostatic fluid
4. Fluffy periostitis particularly at insertion of Achilles tendon.

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 5. Unilateral sacroiliitis

VI. Psoriatic arthritis:

Sex distribution 3:2 female to male

Age: any age
A. Patterns of psoriatic arthritis
1. Polyarthritis with DIPJ involvement
2. Symmetric seronegative polyarthritis simulating RA
3. Monarthritis or asymmetric oligoarthritis
4. Sacroiliitis and spondylitis
5. Arthritis mutilans
B. Diagnostic features
1. Psoriasis with nail lesions
2. DIPJ arthritis
3. Sausage swelling of digits
4. Unilateral sacroiliitis
5. Simultaneous flaring of psoriasis and arthritis. Absence of subcutaneous nodules, negative rheumatoid factor, last
resorptive radiologic changes and periostitis.
C. Radiologic features in psoriatic arthritis
1. DIPJ involvement with erosion and expansion of base of distal phalanx
2. Distal phalangeal osteolysis
3. Pencil and cup appearance
4. Oligoarthritis
5. Sacroiliitis
6. Spinal involvement

VII. SEPTIC ARTHRITIS

A. Diagnosis
Should be considered when examining any monarticular erythematous, hot, swollen joint. It has a propensity for lower
extremity joints, knee most common site.
B. Pathogenesis
1. Etiology: contiguous spread, direct implantation, hematogenous sources or surgical contamination.
a. Contiguous spread occurs when osteomyelitis is present in the metaphyseal or epiphyseal bone.
Bacteria can spread into subchondral bone leading to eventual infection of joint.
b. Can result from bacteria invading the synovium through the blood stream. It is more common in children,
usually result of otitis media or upper respiratory tract infections.
c. Direct implantation of bacteria into joint may occur during puncture wound. Contamination during surgery,
resulting in joint infections is more common when joint implants used.
C. Bacteriology
1. Staphylococcus aureus - most common, all ages
a. Neonate - Streptococcus and gram negative organisms more common.
b. Children (6 months - 5 yrs) H. influenza common
c. Teenagers - Neisseria gonorrhoea - higher incidence
d. Adults - less 5% caused by E. coli, Pseudomonas mirabilis, P. aeruginosa. (P. Aeruginosa common after
puncture injuries)
e. Adults suffering from sickle cell anemia - often have salmonella.
f. Compromised patients (burn victims, drug abusers) -Serratia marcescens pyarthrosis.

D. Diagnosis
1. Patients present: extremely painful, hot, swollen joint. Also exhibits varying signs of sepsis: elevated temperature,
malaise, tachycardia, and confusion. Onset of symptoms is frequently rapid.
2. Differential Diagnosis
a. Children: Acute rheumatic fever, acute juvenile arthritis
b. Adults: trauma, gout, pseudo-gout, and foreign body synovitis.
3. Laboratory data may be helpful:
a. Blood work: elevated white blood count with shift to the left. Elevation of the sedimentation rate
and positive C-reactive protein may be found. Diagnosis of septic arthritis should not be dismissed
simply on normal results. Blood cultures are positive in 50% of cases.

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 b. Radiographs: commonly negative in early stages. Severe joint effusion and juxta-articular osteopenia
appreciated as disease continues. Nuclide 2 bone scanning techniques helpful in early diagnosis.
Technetium-99 and Gallium-67 used for this purpose. (Although studies sensitive for infection, they
lack specificity) Indium-111 labeled leukocytes reported to be both specific and sensitive for infection.
c. Joint aspiration should be performed if septic arthritis is considered. Contraindication to
arthrocentesis is present if soft tissue infection is apparent. When joint aspiration is necessary,
the joint should be penetrated through non-cellulitic areas. In order of importance, aspirate should
undergo following studies: culture & sensitivity, gram stain, examination for crystals, white blood cell
concentration & differential. In septic arthritis, aspirate will vary in color from cloudy yellow - creamy
white or gray. Most joints, white blood count will be higher than 100,000. One exception is gonococcal
arthritis - white blood count usually below 50,000 cells. Differential count consists of 90-95%
polymorphonuclear leukocytes.

E. Treatment
1. Septic joint could be thought of an abscess, requiring drainage for removal of infection. Proponents of surgical
drainage insist it is impossible to completely debride joint through a needle, & bacteria left in joint will accelerate joint
damage. Another criticism of multiple joint aspirations is associated pain & possible joint damage by the needle.
2. Open debridement: allows for direct visualization of joint and permits lysing of adhesions and debridement or necrotic
bone or soft tissue present. Proponents of non-surgical needle aspiration argue that arthrotomy can result in loss of
function of joint from fibrosis.
3. Surgery reserved for patients who don't respond to aspiration. Arthrotomy should almost always be performed in
patients with advancing osteomyelitis, infected joint implants, longstanding infections, or in the toxic patient.
Patients requiring surgical drainage may be packed open until infection cleared.
a. Following drainage, joint should initially be immobilized. After acute episode subsides, gentle
passive range of motion should be initiated. Early motion critical in preventing significant
decreases in range of motion. Immobilization can lead to extra articular fibrosis as well as intra-
articular adhesions.
b. Presumptive therapy should cover S. aureus adequately, since it is the most common organism causing
septic arthritis. Intravenous coverage consists of nafcillin or cefazolin if patient has no allergies.
Patients with documented allergy to penicillin can be placed on clindamycin presumptively.
c. Once culture & sensitivity tests return - the therapy can be modified appropriately. IV antibiotics should
be continued for a minimum of 2 weeks. If the patient is responding well - oral antibiotics can be
administered from 2 - 4 weeks.

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Heparin /Coumadin
Heparin

A. Inhibits intrinsic pathway

B. Monitor with PTT
C. Use protamine to reverse
D. Used as prophylaxis against DVT and initiation of long-term therapy.
E. Prophylaxis:
1. 5,000 u Subq 2 hrs before surgery
2. 5,000 u Subq q12h until patient ambulates.

Coumadin (warfarin)

A. Inhibits extrinsic pathway

B. Monitored by P.T.
C. Reverse effects with Vit K or rapidly by fresh plasma or frozen plasma.

Perioperative Management

A. Minor procedures (under local): keep them on their meds if P.T. is stable.
B. Major procedures: stop oral meds 3 days prior to surgery and start back post-operatively.

Mnemonic (Think of Alphabetic Order)

A Coumadin PT Extrinsic K (vitamin) 2 times the control
|||||
Z Heparin PTT Intrinsic Protamin 2-3 times the control

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Hepatitis
I. Types

There are five main types of hepatitis that are caused by a virus, A, B, C, D, and E - plus types X and G.

A. Hepatitis A
1. Is caused by eating infected food or water
2. Anal-oral contact during sex can also be a cause
3. Most patients with Hepatitis A makes a full recovery. It usually does not lead to chronic disease.

B. Hepatitis B
1. Hepatitis B is caused by the virus HBV (hepatitis B virus) and is an STD (sexually transmitted disease).
2. It is spread by contact with infected blood, semen, and some other body fluids.
3. The disease can be contracted by:

a. Unprotected sexual intercourse with an infected person.

b. Using a syringe that was previously used by an infected person (drug addicts, steroid users).

c. Unsterilized needles (getting a tattoo), or being accidentally pricked with a contaminated

needle (health care workers).

d. Sharing personal items (toothbrush, razor) with an infected person.

4. Patients with Hepatitis B can suffer serious liver damage due to infection, resulting in cancer. Some patients become
chronic (very long-term or lifelong
5. Donated blood is always tested for hepatitis B.

C. Hepatitis C
1. It is caused by the virus HCV (hepatitis C Virus).
2. Spreads through direct contact with the blood of a person who has the disease.
3. Feces is never a route of transmission in hepatitis C.
4. Donated blood is also tested for hepatitis C.
5. The liver can swell and become damaged.

D. Hepatitis D
1. It is caused by the virus HDV (Hepatitis D Virus).
2. Infection is through contact with infected blood, unprotected sex, and perforation of the skin with infected needles.
3. Only a person who is already infected with hepatitis B can become infected with hepatitis D.
4. The liver swells with hepatitis D

E. Hepatitis E
1. Is caused by HEV (hepatitis E virus).
2. Individuals can become infected by drinking water that contains HEV and through anal-oral sex.
3. The liver swells but there is no long-term consequence.

F. Hepatitis X
1. If a case of hepatitis cannot be attributed to the viruses of hepatitis A, B, C, D, or E, it is called hepatitis X or hepatitis
of an unknown virus.

G. Hepatitis G
1. Caused by the hepatitis G virus (HGV).
2. Usually there are no symptoms or very mild symptoms.

II. Symptoms

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A. Symptoms usually occur about 15 to 180 days after the person has become infected.
B. Many people with hepatitis experience either mild symptoms or none at all.
C. The initial phase of hepatitis is called the acute phase. The symptoms are like a mild flu, and may include:
1. Diarrhea
2. Fatigue
3. Loss of appetite
4. Mild fever
5. Muscle or joint aches
6. Nausea
7. Slight abdominal pain
8. Vomiting
9. Weight loss

D. The acute phase is not usually dangerous, unless it develops into the fulminant or rapidly progressing form, which can lead to
death.
E. As the patient gets worse, these symptoms may follow:
1. Circulation problems (only toxic/drug-induced hepatitis)
2. Dark urine
3. Dizziness (only toxic/drug-induced hepatitis
4. Drowsiness (only toxic/drug-induced hepatitis
5. Enlarged spleen (only alcoholic hepatitis
6. Headache (only toxic/drug-induced hepatitis
7. Hive
8. Itchy skin
9. Light colored feces, the feces may contain pus
10. Yellow skin, whites of eyes, tongue (jaundice)

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Infection
Diagnosis and Treatment:

I. Recognizing Infection

A. Symptoms:
1. Pain (elevated intensity out of proportion to the procedure performed).
2. Redness
3. Heat
4. Swelling
5. Loss of function
B. Fever (4 w's)
1. Wind (pulmonary) 8-10 hours post-op
2. Water (urinary) 2-3 days post-op
3. Wound (infection) greater than 3 days
4. Walk (thrombophlebitis) post-op
CHRONOLOGICAL SEQUENCE OF POSTOPERATIVE TEMPERATURE CHANGES

Note: Pasteurella multocida is the most common organism found in dog and cat bites.

II. Hematologic Tests

A. CBC with a deferential: look for a shift to the left [increased number of immature leukocytes (granulocytes)].
Types of WBC:
1. Polymorphonuclear neutrophils
2. Polymorphonuclear eosinophils
3. Polymorphonuclear basophils
Note: All 3 are considered Granulocytes
4. Monocytes
5. Lymphocytes
6. Plasma Cells
Note: a WBC greater than 10,000 usually indicates an infection.
Note: With a localized infection (i.e. abscess) the shift to the left is less pronounced.
B. ESR (Erythrocyte Sedimentation Rate)
1. Good indicator if a base line was taken.
2. Not specific (can be elevated by systemic steroids and cigarette smoking or any inflammatory process.
3. Warfarin use may cause an elevated ESR in patients post operatively.
C. Glucose
D. SMA-6 (electrolytes)
E. Creatinine (most important) run on everyone getting parental antibiotics. 1:1 ratio (i.e. CCL = 30% then 30% renal
function).

Estimated creatinine clearance rate (eCCr) using Cockcroft-Gault formula

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 Est. Creatinine Clearance = [[140 - age(yr)]*weight(kg)]/[72*serum Cr(mg/dL)] (multiply by 0.85 for women).

This formula expects weight to be measured in kilograms and creatinine to be measured in mg/dL, as is standard in the
USA. The resulting value is multiplied by a constant of 0.85 if the patient is female.

One interesting feature of the Cockcroft and Gault equation is that it shows how dependent the estimation of CCr is
based on age. The age term is (140 - age). This means that a 20-year-old person (140-20 = 120) will have twice the
creatinine clearance as an 80-year-old (140-80 = 60) for the same level of serum creatinine (120 is twice as great as
60). The C-G equation assumes that a woman will have a 15% lower creatinine clearance than a man at the same level
of serum creatinine.

F. Bun
G. Liver function test: (some antibiotics are metabolized by the liver like Clindamycin and erythromycin).
1. Bilirubin
2. Serum protein
3. SGOT
4. SGP
H. C&S (culture and Sensitivity)
1. If possible get C&S before antibiotics are started. If the patient is currently taking antibiotics, they should be stopped
for at least 48 hours if possible.
2. Tissue if possible.
3. Use proper technique. If skin is being penetrated, use topical antiseptic to prevent contamination. The base of
ulceration's should be curetted before a tissue sample is taken to remove superficial contaminants.
I. Gram Stain:
Gram positive = purple
Gram negative = pink
Reagent Time Gram + Gram-
Smear and Heat Fix
Primary Stain Crystal violet 20 secs. purple purple
Distilled H2O wash
Mordant Gram's iodine 1 min purple purple
Distilled H20 wash
Decolorizing agent 95% alcohol 10-20 secs purple colorless
Distilled H20 wash
Counterstain Safranin 20 secs purple pink
Distilled H20 wash & Blot Dry Examine with microscope (x100) immediately

IDENTIFICATION OF BACTERIA:
Organism Appearance
Gram positive (Blue)
Cocci
Staphylococcus: Cocci in "grape like" Clusters

Streptococcus: Cocci in chains

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Bacillus (Rods)
Clostridium Rods with a "Racquet shaped" caused by spore
Corynebacterium Rods in "Chinese characters"
Gram Negative (Red)
Cocci
Gonococcus Diplococcus: within the WBC

Rods
Pseudomonas: Slightly curved rod

Klebsiella Diplococcoid: bacillus may show a heavy capsule

Gram Neg Rods(Enteric): Red Rods

Bacteroides

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 Citrobacter
Enterobacter
E. Coli
Klebsiella
Morganella Morganii
Proteus
Providencia
Serratia

•The cytoplasm of the WBC is light pink and the nucleus is dark pink-mauve.
•Cocci are dark blue-purple, unless gonococci are suspected.
•Streptococci occur in chains and/or pairs. Differentiated by hemolytic properties: Alpha hemolytic strep, Beta hemolytic
strep, and non-hemolytic strep.
•It is difficult to identify most other gram-negative rods on the basis of gram stain only.
•f the gram stain reveals many organisms of different morphology and the culture reveals only a few, anaerobes should
be suspected.

J. Blood cultures
•Use if patient looks septic, temp greater than 103 , or has "Fever of unknown origin".
•At least 3 sets of 2 cultures over 24 hrs.
•Cultures are drawn from rotating sites (separate sites) at least 30 mins apart.
•Twenty millimeters of blood should be drawn each time.
•If after 5 -6 cultures over two days, no organisms have been recovered, no further cultures are indicated.
•Blood cultures cannot be considered negative until after at least 2 weeks.

III. Hospitalization: (When to Hospitalize Patient)

A. Systemic Manifestations and Constitutional Signs:

1. Fever (greater than 101F - oral)
2. Lymphangitis, ascending cellulitis, or lymphadenopathy.
3. Malaise, chills, or shakes.
4. High WBC (above 13,000)
B. Debilitated Patient:
1. Diabetes Mellitus.
2. PVD.
3. Alcoholic.
4. Nutritionally deficient.
5. Immuno-deficient.
C. Infections Requiring Parental Antibiotic:
1. Resistant organisms.
2. Gram negative or anaerobic infections.
3. Deep space infections
4. Suspected bone involvement (osteomyelitis):

a. Acute.

b. Chronic.

5. Failure of outpatient therapy.

6. Surgical debridement bone/soft tissue.

IV. Anaerobic Infection

A. Signs
1. Foul smelling discharge
2. Necrotic tissue or organism
3. Infection involves muscle
4. Gas in tissue, crepitus (on x-ray evaluation) doesn't have to be Clostridia
5. Bacteremia picture with jaundice
B. Anaerobic Organisms

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 1. In this type of infection, aerobic organisms use up O2 and provide a better environment for anaerobic bacteria.
Organisms responsible for this synergistic relationship include: S. aureus, S. Epidermitis, Peptococcus,
Peptostreptococcus, Corynebacterium, Bacteroides, Clostridia

V. Aerobic Organisms

A. Coagulase producing staph aureus is most common infecting organism

B. Coagulase negative staph epidermitis is also infecting organism
C. Beta hemolytic group A strep
1. Usually no pus, but intense cellulitis and can cause lymphangitis and lymphadenopathy
D. Gram - aerobes, E. coli, Klebsiella, pseudomonas, Enterobacter, Serratia
E. Clostridium Myonecrosis (gas gangrene)
1. Most severe anaerobic infection
2. Involves muscle tissue
3. See brown, watery, foul smelling exudate
4. See gas in soft tissue
5. Get infectious disease consult, & general surgical consult
F. Necrotizing Fascitis
1. Dissecting up fascial planes
2. No muscle involvement
3. Primarily involves Peptostreptococcus, but also S. aureus, Strep pyogenes, Clostridia, Bacteroides

VI. Specific Infections

Lyme Disease (Details in next section)

Bite Wounds:
Dog:

Pasteurella multocida

S. Aureus

S. Epidermidis

 - Hemolytic streptococci

Cat:
Pasteurella multocida

S. Aureus

 - Hemolytic streptococci

Human:

Eikenella corrodens (gram negative anaerobic organism)

S. Aureus

Streptococcus

Bacteroides fragilis

Puncture Wounds:

Staphylococcus aureus (>50%)

 - Hemolytic streptococci

S. Epidermidis

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 Escherichia coli/Proteus

Osteomyelitis: Pseudomonas aeruginosa (90%)

Open Fractures:

S. Aureus

S. Epidermidis

Pseudomonas aeruginosa

Streptococcus

Enterobacteriaceae

B. Fragilis

Burns:
Early (1-2 days):

 - Hemolytic streptococci

S. Aureus

S. Epidermidis

Late (>3 days):

S. Aureus

S. Epidermidis

Pseudomonas aeruginosa

Streptococcus

Enterobacteriaceae

B. Fragilis

Post-Operative Infection:

Staphylococcus aureus

VII. Treatment of Infection (4 D's)

A. Decompression
1. Remove some sutures, release pus
B. Drainage
1. Open tissue, pack wide pickets with iodoform gauze
2. Leave Penrose drains in for 24 - 48 hours
C. Debridement
1. A wet to dry dressing with povidone iodine-normal saline mixture absorbs fluid exudates, debrides tissue on its
removal and provides physiologic cover.
D. Drugs
1. Antibiotics

a. Always consider: Frequency of Administration, Toxicity, Duration of treatment

b. Monitoring antibiotic therapy: fever, pain CBC & Diff, ESR CRP, Insulin requirement in diabetic

E. Cellulitis

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 1. Koch-Mason dressing-wrap an area of cellulitis with saline soaked gauze. This is covered with plastic wrap, which
forms an occlusive dressing. A water based heating apparatus is placed around the dressing. Leave this on 5 hours and
off one hour to prevent maceration.

VIII. General Principles

A. No tourniquets with infections

1. Allows accurate debridement of devitalized tissue.
B. Sterile prep should be done
C. Release sutures
D. Explore extent of infection
1. Determine which structures are affected.
E. Remove implants

1. Internal fixation should be left intact if it is providing stability.

F. Leave all viable tissue intact

G. C&S of deep tissue
1. C&S of implant if removed
H. Following thorough debridement
1. Copiously irrigate the surgical site
2. Pack the wound open with sterile Iodoform Nugauze
3. Change post operatively once-twice a day.
I. After 3 negative cultures, delayed primary closure can be considered.

BONE IMAGING TECHNIQUES WITH INFECTIONS

DRUGS FOR BUGS:

I. Staphylococcus Aureus and EPI

A. Penicillin sensitive -- Pen G, first generation cephalosporin, Vancomycin (IV, IM).

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 B. Methicillin Sensitive -- Penicillinase--resistant penicillin (nafcillin or oxacillin), clindamycin, erythromycin, Vancomycin (IV,
IM).
C. Methicillin resistant (MRSA) (See MRSA in complications)

II. Streptococcus
A. Group A& B -- Penicillin, first generation or cephalosporins, Clindamycin, Erythromycin, Vancomycin (IM, IV).
B. Group D (S. faecalis and S. faecium) (Enterococci) --Penicillin, ampicillin or mezlocillin with gentamicin, vancomycin &
gentamicin. Use oral Amoxicillin in mild cases.

III. Clostridium Tetanus

A. Penicillin, Tetracycline.

IV. Clostridium perfringens

A. Penicillin, Imipenem, Tetracycline, Clindamycin.

V. Neisseria Gonorrhoeae

A. Ceftriaxone, ciprofloxacin, Penicillin (if not resistant).

VI. Gram Neg. Rods

A. (Bacteroides, Citrobacter, Enterobacter, E. Coli, Klebsiella, proteus, Providencia, Serratia -- Imipenem, Ciprofloxacin.

VII. Pseudomonas |Aeruginosa (FAT CIAZ)

A. Ciprofloxacin (oral)
B. Imipenem
C. Antipseudomonal Penicillins:
1. Piperacillin
2. Mezlocillin.
3. Ticarcillin.
D. Aminoglycosides:
1. Gentamicin
2. Tobramycin.
3. Amikacin.

VIII. Pseudomonas Cepacia and Xanthomonas maltophilia

A. TMP/SMX.

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SPECIFIC DRUGS
I. Pen. G
A. Up to 20-24 million units/day (5-6 million units q 4h IM) I.V.
B. 1.2 million units IV a day.
C. Concomitant administration of probenecid 1-2 gms/day will markedly increase the duration of serum levels.
Note: Probenecid will also increase the serum levels of other penicillins and almost all cephalosporins.
D. If creatinine Clearance is lower than 30 ml/min reduce dosage.

II. Erythromycin

A. 250-500 mg Q.I.D. P.O.

B. Metabolize by liver--not kidney.

III. Tetracycline

A. 250-500 mg Q.I.D. P.O.

B. Minocycline (100 mg q 12 h - 24 h P.O.)
C. Good for Lyme disease, Madura foot, Mycobacterium Marinum.
D. Good for Staph or Strep infection in patient who's allergic to penicillin.

IV. Vancomycin

A. Oral form strictly for use in colitis (pseudomembranous colitis).

B. No gram neg. aerobic/anaerobic spectrum.
C. Bactericidal against all gram-positive organisms.
D. Nephrotoxic -- evaluate renal function ototoxic--rare & reversible. Redman/Redneck Syndrome--flush of face and hot
feeling and pruritus. This is self-limiting but you can use antihistamines. Infuse slowly to avoid.
E. DOSAGE:
1. Maximum = 2q/day.
2. 500 mg q8h for less severe infections.
3. Oral dose for colitis is 125 mg Q.I.D..
4. Infuse slowly (over 45 to 60 minutes).
5. Do Peak and Trough levels:

Normal levels Peak = 15-30 mg/ml.

Trough = less than 10 mg/ml.

V. Gentamycin

A. No effect on anaerobes (the drug needs 02 to cross the cell membrane)

B. Adverse effects:
1. Nephrotoxic (usually reversible). Concurrent use of vancomycin may potentiate this nephrotoxicity.
2. Ototoxic (irreversible). Concurrent use of loop diuretics may predispose a patient to these toxicities.
3. Neuromuscular blockade (infuse slowly to avoid).
C. DOSAGE:
1. Loading dose = 2mg/kg (regardless of patient's renal function.)
2. 3-5mg/kg/day q8h to 12h.
3. First calculate creatinine clearance

CCL = (140 - age) x weight (in kg)/Serum creatine x 72

For Females: CCL x .85

1:1 relationship -- I.E. if CCL = 50 then patient has 50% renal function. Then half the dose.

4. Peak and Trough levels:

a. Draw trough sample immediately (no more than 30 minutes) prior to infusion. Draw peak sample
at least 30 minutes (no more than 90 minutes) after 90 minute infusion. Clearly label specimens with times.

b. Order after 3rd dose. If within normal range the level need not be ordered again unless there is an
increase in the serum creatinine level.

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 c. Run a serum creatinine 3 times a week.

d. Normal Peak = 6-10 mg/ml. and normal Trough = less than 2 mg/ml.

e. If peak is high and trough is normal decrease the amount.

f. If peak is low and trough is normal increase the amount.

g. If peak is O.K. and trough is high, increase the interval time.

h. If both are high, decrease the dose and increase the interval time.

VI. Clindamycin

A. DOSAGE:
1. 300 mg Bid to T.I.D. P.O. for outpatient therapy.
2. 600 - 900 mg q8h I.V. or I.M.
3. Metabolized by liver, therefore, O.K. for renal impaired patients.
NOTE: Possible drug of choice for staphylococcal osteomyelitis due to its excellent penetration into bone and
its ability to dissolve slime layer.
NOTE: Can be used for gram + organisms in patients who are allergic to Penicillin.

VII. Ciprofloxacin

A. Drug interactions:
1. Theophylline can be potentiated. Should check serum levels.
2. Patients should avoid coffee, tea, and soft drinks with caffeine. (Potentiates effects of caffeine).
3. Antacids and Irons supplements decrease absorption.
4. Do not use in children with open growth plates. May cause degeneration of cartilage.
B. DOSAGE:
500 mg bid P.O. -- mild infections
750 mg bid P.O. -- severe infections and osteomyelitis
NOTE: Decrease to once daily in patients with severe renal insufficiency.

VIII. TMP/SMX (Bactrim, Septra)

A. This is a Sulfonamide.
B. DOC for pseudomonas cepacia and Xanthomonas maltophilia.
C. DOSAGE:
One double strength tablet B.I.D. P.O.

IX. Imipenem

A. Broadest spectrum of any available drug (referred to jokingly as (gorillamycin:)

B. Adverse reactions:
1. Nausea/vomiting if infused to fast.
2. Cross reactivity in patients with penicillin allergy.
3. Seizures in patients with history of seizure disorders or renal dysfunction.
C. DOSAGE:
500 mg q6 to 8h
250 mg q6h unless severe infections
DOC in severe life or limb threatening infections in diabetics (gas gangrene or necrotizing fasciitis.

X. Rifampin

A. Spectrum:
1. All mycobacteria.
2. Very active against Staph and Strep.
B. Always use in combination, never alone.
C. Dosage:
300 mg B.I.D. P.O.
D. Side effects:

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 1. Red discoloration of all body fluids (will permanently discolor soft contact lens).
2. Flu-like symptoms with prolonged use

Prophylactic Antibiotics

A. Golden Rules of prophylactic antibiotics

1. Rule 1: The antibiotic must have achieved its maximum levels at the time of initial incision or insult.

a. Timing is everything!

b. This rule helps to answer the important questions about the timing of administration and
length of usage.

2. Rule 2: The antibiotic should be directed against the most common organism found if an infection were to occur in
that particular situation

a. Following this rule requires a thorough understanding of the pathophysiology, microbial

etiology, and antibacterial susceptibility of a variety of infections.

B. Indication
1. Following wounds (commonly present in the lower extremity):

a. Puncture wounds: If the "first rule" is implied in these situations, antibiotics are not indicated.
By the time the patient presents to your office gets the prescription filled and the drug is
absorbed, too much time has passed since the insult. Most studies show that prophylactic
antibiotics do not alter the incidence of infection following puncture wounds and lacerations.
Only if less than a few hours have past would there be any benefit at all.

b. Lacerations (same as puncture wounds)

c. Bite wounds are highly contaminated with numerous types of organisms. Because of this,
antibiotic therapy should be initiated along with aggressive debridement and irrigation.

2. For surgery: There is no hard and fast data to support the use of antibiotic prophylaxis in foot and ankle surgery.
However, it is generally considered to be indicated in the following surgical situations:

a. Prolonged surgery lasting longer than two hours

b. Surgery on immunocompromised patient

i. Uncontrolled diabetic patient

ii. Patients on immunosuppressive agents (chemotherapy)

iii. Patient on systemic corticosteroids (rheumatoid arthritic patient)

iv. Genetic or acquired defects

Note: HIV infection does not alter the postoperative infection rate for
lower extremity surgery. It tends to mediate infection by parasites, fungi
and viruses, not bacteria.

c. Trauma surgery

d. Implant surgery

3. Prophylaxis against bacterial endocarditis in the surgical patient with a compromise heart valve:

a. Guidelines (based on whether or not the procedure has a high potential for a bacteremia)

i. Any clean elective surgery performed through surgically prepared skin is

considered low risk and prophylaxis is not indicated.

ii. I&D of an abscess or cutting through infected tissue may cause bacteremia
and therefore is considered a high risk. Prophylaxis should be used. The
antibiotic used should be directed against any pathogens found to be
causing the infection.

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 4. Prosthetic Joint Patient's
a. if a patient has a prosthetic joint elsewhere in the body (hip, knee), is it necessary to use
prophylaxis when performing foot or ankle surgery?
b. Formal guidelines state that prophylaxis is not required for pins, plates or screws. Only when
a total joint replacement is in place, prophylactic antibiotics are recommended in limited cases.
i. All patient's during the first 2 years following joint replacement.

ii. Immunocompromised and immunosuppressed patient's

iii. Patient's with co-morbidities

Previous prosthetic joint infection

malnourishment
HIV infection
malignancy
insulin-dependent diabetes
hemophilia

C. Selection and administration of agents

1. Follow the second rule. In most lower extremity operations, S. aureus is the most common postoperative pathogen.

a. Variables with Staphylococcus include its susceptibility to MRSA and the tolerance to
vancomycin.

b. When do you prophylax for MRSA?

i. Patients with a prior history of MRSA infection

ii. In hospitals with an unacceptably high rate of MRSA

iii. In patient's whom the risk of a MRSA post-op infection is great enough to
warrant MRSA prophylaxis

2. Implant infection are most frequently caused by S. epidermidis, often methicillin-resistant.

3. Agents should have a sufficient half-life to provide adequate levels throughout the procedure and into the early
postoperative period.
4. Recommended guidelines ("idealized" suggestions)

a. IV infusion should be administered by the anesthesiologist in the operating room a few

minutes before the elevation of a tourniquet or initial incision.

b. IM antibiotics should be given approximately 45 minutes to one hour prior to the start of
surgery.

c. Oral antibiotics should be given at least one hour prior to surgery.

5. The duration of the antibiotic is very debatable. It has changed over the years back and forth. The bottom-line is that
no one is certain. Generally, most lower extremity surgery follows these guidelines;

a. For most relative short surgeries, the initial preoperative dose is sufficient.

b. For surgery lasting longer than 2 hours, a postoperative, or intraoperative (for very long
procedures) should be given.

c. For patients that are significantly compromise or extensive surgeries ( e. g., internal fixation
of a severely fractured ankle) a full 24 hour dose should be used.

D. Specific Agents
1. Cefazolin (the most frequently used antibiotic for lower extremity surgical prophylaxis).

a. Dosage: 1 to 2 grams IV or IM prior to surgery. 1 gram should be given following long

procedures.

2. Vancomycin

a. Primarily used in patients with documented severe penicillin or cephalosporin allergy.

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 b. Some hospitals are now limiting the use of this drug for routine prophylaxis because of the
development of vancomycin resistance gram-positive organisms.

c. If a high level of MRSA is suspected

d. Dosage: 1 gram, one hour prior to surgery and infused slowly over that hour. Vancomycin
should not be administered in a bolus. If postoperative administration is desired, 1 gram can
be given 12 hours following the first dose.

3. Clindamycin

a. Not frequently used for surgical prophylaxis

b. It is however effective at penetrating the bacterial glycocalyx, and therefore theoretically may
prove useful in prophylaxis for implant surgery.

c. Maybe a useful substitute for the now more carefully regulated vancomycin in beta-lactam
allergic patients.

d. Dosage: 600 to 900 mg. IV

4. Ciprofloxacin should not be used for surgical prophylaxis for lower extremity surgery. It has very poor anti-
staphylococcal activity.

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Lyme Disease (Lyme borreliosis)
I. General information:

A. It is now the most common vector borne disease in the United States but is also found in other parts of the world.
B. It is transmitted by its principle vector; the deer tick (Ixodes scapularis) although other ixodid ticks have been implicated as
well.
C. The tick does not act as the reservoir for the organism. The most common reservoir is the white footed mouse or deer
mouse. White tailed deer are a host for adult ticks, but are not considered an important reservoir for the bacteria.
D. There is a direct correlation between the amount of time the tick is attached to the human and the potential for developing the
disease. A minimum of 36 to 48 hours of attachment may be required to transmit the disease.

II. Bacterial Etiology:

A. The etiologic agent is Borrelia burgdorferi (a spirochete). When Borrelia burgdorferi is Gram-stained, the cells stain a weak
Gram-negative by default. Borrelia, like most spirochetes, does have an outer membrane that contains an LPS-like
substance, an inner membrane, and a periplasmic space which contains a layer of peptidoglycan. Therefore, it has a Gram-
negative bacterial type cell wall. Despite its staining characteristics, however, they are not classified as either Gram-positive
or Gram-negative.

III. Clinical Presentation:

A. The disease is usually broken down into 3 stages (some use only two stages “Early” and “Late” – classifying the first two
stages as variations of early disease i.e. “early localized” and “early disseminated”).
1. Stage 1 (localized infection):
a. Early stage marked by EM (erythema migrans) EM presents as an expanding annular ring of
erythema centered on the initial bite site. EM is present in about 90% of patients who develop the
disease, however, actual tick bites are very rarely reported because the tick is so small and their
bite is painless. The lesion starts as a small papule that slowly expands over time. Central clearing
is common and leads to the classic "Target" or "bulls eye" appearance.

2. Stage 2 (disseminated stage):

a. Secondary rings of EM may begin to appear at distant sites from the original bite usually days
or even weeks after the initial presentation.

b. Lethargy and fatigue are the most reliable and persistent symptoms of this stage.

c. Transient neurologic symptoms (such as Bell’s palsy), rheumatologic and cardiac involvement
are other symptoms that may occur.

3. Stage 3 (persistent infection):

a. Occurs months to years later and is marked by migratory arthritis (most commonly affecting
the large joints of the lower extremity, although the hands and shoulders can be
involved)and chronic neurologic symptoms.

IV. Laboratory Findings:

A. Diagnosis is mainly clinical, labs present several difficulties.

B. Serologic testing with ELISA (enzyme–linked immunosorbent assay) or Western blot techniques is fraught with false
positives (in patients previously exposed to the organism who do not develop the disease or are treated successfully) and
negatives (in early disease). The so called C6 peptide ELISA maybe the best study although still far from ideal.
C. Observation of the spirochete using special stains is diagnostic but very difficult. Biopsy from the outer margin of the EM has
the highest concentration of organisms along with fluid from joints, CSF, or blood.

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 D. Recently PCR (polymerase chain reaction)- detection of the spirochete DNA has assisted in identification of the organism from
synovial fluids.
E. Ideally the organism should be grown on culture for definitive diagnosis. However the organism is difficult to grow and the
medium is very expensive.

V. Treatment:

A. Erythema Migrans:
1. The drug of choice is oral doxycycline 100 mg bid for 10-21 days but should be avoided in children. Amoxicillin 500
mg tid for 14-21 days is an alternative as is cefuroxime axetil.
2. Macrolides should only be used in patients unable to tolerate any of the above.
3. IV Ceftriaxone is not recommended in early Lyme disease unless the patient has early neurologic symptoms.

B. Late Lyme Disease:

1. The same antibiotics listed above may be used in adults without neurologic manifestations but for 28 days.
2. Patients with arthritis and evidence of neurologic disease should receive IV Ceftriaxone 2gm/day for 2 to 4 weeks.

VI. Prophylaxis:

A. Avoid high risk areas, long pants, tucked in socks, light colored clothing and insecticides (DEET) all help.
B. IDSA recommendations call for NOT using prophylactic antibiotics (a single dose of doxycycline 200 mg) following a tick bite
with the following exceptions:
1. The attached tick can be identified as an adult or nymphal I. scapularis that is estimated to be attached for 36 or
more hours based on the amount of engorgement of the tick or on certainty of time of exposure to the tick.
2. Prophylaxis can be started within 72 hours from the time the tick was removed.
3. Etiologic information indicates that the local rate of infection of the ticks is equal to or greater than 20%
4. Doxycycline is not contraindicated

Neurologic Disorders
I. Nerve injuries

A. Neuropraxia
1. Loss of conduction without structural change in the axon
2. Fibers usually regain function promptly
B. Axonotmesis
1. Axonal continuity is lost and there is subsequent Wallerian degeneration of the distal segment.
2. Recovery depends on regeneration of nerve fibers 1 - 3 mm per day. Therefore, may take months to years to regenerate
C. Neurotmesis
1. Separation of the entire nerve, including supporting connective tissues
2. Regeneration seldom possible
Note: The order of return of function during recovery from a nerve sectioning injury is: Tinel's Sign,
Sudomotor, skeletal motor.
Note: Nerve Conduction studies will show decreased velocity when nerves are damaged as in compression
syndromes or CMT, etc.

II. Grading Deep tendon reflexes

0 = absent
+ = present but diminished
++ = normal
+++ = increased but not necessarily pathologic
++++ = marked hyperactive with clonus

III. Muscle function during gait cycle

A. TA, EHL, EDL, and Peroneus Tertius

1. Contract two times

a. From heel strike to first 10% of contact to decelerate

b. Fire at propulsive and swing

B. Peroneal Group 15 - 20% of stance throughout propulsion

C. FDL, TP, FHL, 15 - 20% of stance up throughout propulsion

IV. Upper motor neuron disease -

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 A. Lies above the level of the anterior horn cells of the spinal cord
B. Signs - muscle rigidity, spastic paralysis, hyperreflexia, positive Babinski and ankle clonus.

V. Lower Motor neuron lesion

A. Will lie at or below anterior horn cell

B. Signs - muscle weakness and wasting, areflexia, flaccid paralysis

VI. Muscle Testing:

Grade 0 = no contraction
Grade 1 = trace contraction
Grade 2 = motion with gravity eliminated
Grade 3 = motion against gravity
Grade 4 = motion against mild resistance
Grade 5 = normal strength

Osteomyelitis
I. Definitions

A. Osteomyelitis - infection of bone and marrow

B. Infectious osteitis - suppuration of cortex without marrow
C. Infectious periostitis - contamination of periosteum

II. Classifications of Osteomyelitis

A. Hematogenous - result of bloodstream dissemination of bacteria emanating from an identifiable focus of infection or developing
during a transient bacteremia unrelated to infection
1. Age of onset - peaks from 1-20 then over 50
2. Blunt trauma to long bones precedes 33% of time (femur, tibia, humerus in that order)
3. Infected skin in child from measles, chicken pox can cause

a. Streptococcal Acute Hematogenous Osteomyelitis (AHO)

4. Middle ear infection in child can cause

a. Hemophilus

b. Pneumococcus

c. Staph

5. Acute hematogenous osteo. Localizes in the metaphyseal region because of paucity phagocytic cells in this area as well
as turbulent flow in sinusoidal loops
6. AHO in infant - (0-1 year)

a. In newborn, capillaries traverse epiphysis, therefore joint infection with possible permanent
damage to epiphysis

b. Get joint effusion 60-70% of time

c. Group B strep, staph aureus and E. coli are most frequent organism

7. AHO in child

a. In child, the joint is protected in most cases from infection

b. Hip, shoulder, ankle joint (distal lateral tibial metaphysis are intra- articular however, and can
have joint infections

c. See extensive cortical damage with involucrum formation

d. Rarely see damage to growth plate and joint

e. Staph aureus and epidermitis in 60-90% of cases

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 1) Salmonella in SS or Sc hemoglobinopathy

2) Hemophilus influenza in children less than two years old

8. AHO in adult

a. Seen in over 50 year old age group

b. See increased incidence of pseudomonas osteo. in IV drug users

c. High incidence of spread in normal population from

1) IV devices

2) Urinary tract infection

3) Pulmonary infections

d. Infections of bone occurring over 24 months after surgery are probably AHO

e. May see accompanying joint infection

B. Contiguous - most common form of osteo in podiatry practice, seen in patients over 40, may occur following puncture,
laceration ulceration or postop.
1. Postop infections are broken down as follows:

a. Acute postop osteo - within one month of surg.

b. Delayed postop osteo - from one month to two years following surgery

c. Late postop osteo - 2 years on

2. Majority are delayed or late

3. Staph aureus common pathogen, but can see mixed infection
4. Diagnosis of contiguous infection osteo

a. Complete history and physical

b. Evaluate for ulcers or soft tissue lesion which may produce contiguous infection

C. Direct Inoculation - secondary to trauma or surgery

D. Vascular insufficiency
A. Cierny and Mader (1985) proposed the University of Texas Medical Branch (UTMB) classification of adult osteomyelitis. They
introduced a clinical staging of osteomyelitis that includes both an anatomic and physiologic category in a single classification.
The classification of adult osteomyelitis combines four anatomic types (the disease) with three physiologic classes (the host)
to define 12 clinical stages.

Anatomic Stage

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 Clinical Stage
Type + Class = Clinical Stage
Example:
Stage IVBs osteomyelitis = a diffuse lesion in a systemically compromised host

III. Radiographic Diagnosis of Osteomyelitis

A. Lytic process in bone in not visible on x-ray until 30-50% of osseous mineralization has been lost
B. First bone changes occur at 10-14 days after onset of symptoms
C. First radiographic sign of osteomyelitis is due to loss of bone density know as radiolucency
D. Further radiographic changes include:
1. Sclerosis
2. Sequestration - devascularized, dead bone
3. Involucrum - new bone formation
E. Nuclear Medicine Studies
1. In most cases bone scintigrams become positive within 48-72 hours
2. Technetium 99M half-life is six hours
3. Tc-99m is sensitive but is not specific for osteo
4. Three phase bone scan:

a. Radio angiogram (1st phase) - demonstrates dynamic blood flow to area. Consists of several
images taken 1-2 seconds apart.

b. Blood pool image (2nd phase) - demonstrates relative vascular flow. Taken minutes after
injection. These first two phases will be hot in either soft tissue or bone infection

c. Delayed image (3rd phase) 2-4 hours after injection - demonstrates skeletal uptake

d. Recent fourth phase, taken 24 hours after injection, may help when dealing with diabetic with
PVD who has slow localization of isotope in bone, and slow excretion

5. If soft tissue infection alone is present, 3rd & 4th phases of bone should demonstrate comparatively less activity and less
diffuse activity
6. If 3rd & 4th phases seem to demonstrate similar or greater activity with discrete focal uptake, osteo is suspected
7. Osteoarthropathy can give you hot all four phases
F. Gallium 67 Scans
1. Used predominantly for the detection of acute inflammation or infection since isotope binds to white blood cells and
plasma proteins
2. Not used alone to detect osteo in foot
G. Use of Technetium and Gallium in combination
1. First perform Tc scan, then 24-72 hours later perform Ga scan
2. An increased uptake of technetium without increased uptake Ga, 85% chance no osteo is present
3. Increased uptake both 70% chance osteo is present
H. Indium 111 Scan

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 1. Neutrophils are taken from patient and tagged with In-111 and injected back. Scan 18-24 hours later
2. Can differentiate osteoarthropathy (-) from acute osteomyelitis (+).
3. May not be beneficial in chronic osteo due to predominantly a lymphocytic pattern

IV. Diagnostic Workup

A. Aspiration of joint or bone

1. Can identify organisms
2. If wound closed needle biopsy through unaffected soft tissue (may need to perform under fluoroscope) can wash with
saline then aspirate if no frank material is noted.
B. Blood Cultures
1. Are positive in 50% of septic arthritis and osteomyelitis
C. Wound culture
1. Sinus tract culture often not responsible for underlying bone infection
2. If grow out staph aureus - approximately 50% chance that this organism is producing the associated osteo
D. Bone Cultures
1. Most definitive diagnostic tool to diagnose osteomyelitis
2. Get aerobic, anaerobic, maybe acid fast and fungal cultures

V. Chronic Osteomyelitis

A. Microorganisms residing in dead bone if not removed along with sequestra can cause acute flare-ups as late as 50 years after
initial episode
B. Squamous cell Ca has been reported to be late sequelae.

VI. Treatment

A. Indication for surgical drainage and debridement of bone in AHO

1. Pus on aspiration of the area
2. Failure of symptoms to resolve within 36 hours of antibiotic therapy
B. In frank osteomyelitis of bone
1. Excise necrotic bone and small portion of non-infected bone
2. Can pack open and close later
3. Can use closed suction irrigation
4. Can close over antibiotic impregnated beads
5. Antibiotics after culture
6. Monitor sed rate (or blood sugar in diabetic patient) for response to therapy as well as other signs and symptoms

VII. Workup of Patient presenting with wounds on foot with possible osteomyelitis

Diabetic presenting to office with acute, hot, swollen foot with draining wound on bottom of foot for two day duration
A. Check to see if medical status is fine - are they coherent, hypotensive, septic initially before anything
1. If not alert and coherent, may be in sepsis and ketoacidosis
2. Get stat glucose reading from Glucometer and admit to hospital
B. Get complete history and physical after determining medical status immediately
C. Inform patient, this is emergency, need to open and drain foot in hospital
D. Contact internist, patient needs I & D immediately, need to have H & P performed stat in hospital
E. Get infectious disease consult
F. Send patient to hospital and get CBC, DIFF, Sed Rate (can monitor response to treatment) Chem 24, Blood Cultures x 3, NPO
status
G. Once cleared for surgery, take to O.R.
1. Probe area to determine depth and areas that tissue are undermined
2. Make wide incision on bottom of foot across draining wound, to clear non-infectious looking tissue
3. Deepen incision to determine undermined areas
4. Open abscesses and pockets
5. Take culture of material
6. Copious high pressure irrigation
7. Probe bone gently to determine if involved. If acute infection of only a few days onset, probably not
8. Pack wound open with iodoform gauze and change BID and irrigate and debride
9. Start patient on antibiotics based on gram stain
10. If not responding to treatment either;

a. Missed all abscesses & pockets of infection

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 b. Inappropriate antibiotics

11. Wait for good granular bed and negative cultures then may attempt to close or may need graft.

VIII. Chronic wound on Bottom of Foot Draining for Months presents

A. Check for sepsis and control of blood sugar

B. X-ray may be suspicious for bone infection
C. Get labs as above
D. Bone scan to see if osteo, and to see how much bone involved
E. Depending on bone scan, may need Ga or Indium scan
F. Take to surgery, but don't go through chronic infection to debride bone, instead go through non-infected area off weightbearing,
i.e. dorsal metatarsal shaft for osteo of metatarsal
G. Culture bone at surgery
H. Start on antibiotics based on gram stain
I. Pack open
J. If patient with wet gangrenous or dry gangrenous skin changes and tissues changes, debride tissue with bone

Tetanus Prophylaxis
Complete (all ages) Online Guideline

(http://www.michigan.gov/documents/mdch/Tetanus_Prophy_All_Ages_Final_060412_388045_7.pdf)

I. Unimmunized, Uncertain, or Incomplete Immunization

A. Low risk wounds -- one dose Tetanus Toxoid (T.D.)

B. Tetanus prone wounds -- one dose of T.D. plus 250 to 500u of human Tetanus Immune Globulin (TIG)
NOTE: Use separate syringe and sites for T.D. and TIG.

II. Full Primary Immunization and Booster Within 10 Years of Wound

A. Low risk wound -- nothing.

B. Tetanus prone wound -- if more than 5 years since last dose, give one dose of T.D.
C. Neglected wound greater than 24 hrs. --one dose of T.D. and 250-500u TIG.

III. Full Primary Immunization, But more Than 10 Years

A. Low risk wound -- one dose T.D.

B. Tetanus prone wound -- one dose T.D.
C. Neglected wound -- one dose T.D. plus 250-500u TIG.
Note: Primary immunization is two .5 ml. T.D. injections 4-6 weeks apart followed by a third injection 6-12
months later.

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Von Willebrand Disease (VWD)
I. General Information

A. Von Willebrand Disease is the most common of the inherited bleeding disorders.
B. It is caused by mutations that lead to an impairment in the synthesis or action of von Willebrand factor (VWF).
C. VWF contributes to primary hemostasis by binding to both platelets and endothelial components. It forms an adhesive bridge
between platelets and vascular subendothelial structures and between adjacent platelets at sites of endothelial injury.
D. VWF also contributes to fibrin clot formation. It acts as a carrier protein for factor VIII. If factor VIII is not bound to VWF its
half-life is greatly reduced.

II. CLASSIFICATION OF VWD

A. Type 1, an autosomal dominant disease, is the most common, accounting for approximately 75 percent of patients. It
represents a partial quantitative deficiency of VWF. Clinical presentation varies from mild to moderately severe, as
determined by bleeding symptoms.
B. Type 2, which is usually an autosomal dominant disease, is characterized by several qualitative abnormalities of VWF. Four
subtypes have been identified: 2A, 2B, 2M, and 2N.
C. Type 3, a total deficiency of VWF, is an autosomal recessive disorder that leads to severe disease with extremely reduced or
undetectable levels of VWF.
D. Acquired VWD can develop in association with a number of disease states, including lymphoid malignancies, lymphoproliferative
and myeloproliferative disorders, autoimmune disorders, conditions of high vascular flow, and some medications.

III. Surgical Considerations

A. In preparation for any surgery, the surgeon should speak directly with the hematologist to fully understand the procedure and
evaluate the potential for bleeding.
B. If the patient has responded to a particular agent for a similar hemostatic challenge in the past, then this agent can be used
again. DDAVP (Desmopressin) should only be used for treatment or prophylaxis against bleeding in those who have
demonstrated a response to this agent. Note: When several doses of DDAVP are used, fluid intake and electrolytes should be
monitored closely to avoid hyponatremia.
1. Minor surgery — Surgery which involves a non-vital organ, little to no tissue dissection, and where the site can be
visualized directly (eg, skin surgery). However, each case must be managed individually.

a. Use intravenous or intranasal DDAVP as initial treatment of minor bleeding or at the time of
minor surgery in patients who have shown an adequate prior response to this agent. VWF
ristocetin cofactor activity levels should reach at least 30 international units/dL; 50
international units/dL is optimal. DDAVP may be used at approximately 12-hour intervals for
two to four doses. As stated above, water intake should be decreased and electrolytes
should be monitored to avoid hyponatremia.

b. Bleeding should be followed clinically and with laboratory monitoring as needed if the
expected clinical response is not seen. If the patient continues to have bleeding, the use of
VWF concentrate may be indicated.

c. You can also use antifibrinolytic and/or topical therapies as appropriate for specific
indications to supplement the above treatments.

2. Major surgery — Surgery which involves a vital organ or tissue dissection, and that in which. Again, each case must
be managed individually.

a. For episodes of major bleeding or major surgical procedures, patients should be hospitalized
at a location where expertise in management of VWD and laboratory monitoring of VWF
levels are available.

b. VWF concentrate is recommended over DDAVP in order to reach a target level of

approximately 100 international units/dL of VWF ristocetin cofactor activity. This usually
requires an initial dose of 40 to 60 international units/kg; repeated doses of 20 to 40
international units/kg should be given approximately every 12 hours to maintain a level
between 50 to 100 international units/dL of VWF ristocetin cofactor activity. (See 'VWF
replacement therapy' above.)

c. Maintain the above levels of VWF ristocetin cofactor activity for 7 to 14 days or more if
needed. When potential sites of bleeding are visible or easily detected, treatment duration
may be reduced if bleeding is controlled.

d. If the patient is taking an antiplatelet drug and bleeding is serious and not controlled by
therapy for VWD, consideration must be given to correction of the platelet defect, usually by
platelet transfusion.

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General Anesthesia
ASA classification for General Anesthesia

Class 1: Normal & Healthy

Class 2: Mild Systemic Disease
Class 3: Severe Systemic Disease (not incapacitating)
Class 4: Incapacitating Systemic Disease (is a threat to life)
Class 5: Moribund Patient (not expected to live with/without the surgery)

General Anesthesia Staging:

Stage 1:
- Plane 1: pre analgesia
- Plane 2: partial analgesia
- Plane 3: total analgesia
Stage 2: unconsciousness, irregular breathing pupils dilated
Stage 3:
- Plane 1: faint lid reflex, eyeball centrally fixed
- Plane 3: decreased B.P. diaphragmatic respiration's
Stage 4: Medullary paralysis respiratory and cardiac
Note: The medication of choice for post-op nausea is prochlorperazine (Compazine) 10 mg. I.M.
Note: Post-spinal headache is characterized by comfort when lying in bed but disabling headaches when
standing up,

General Anesthesia:

A. Perioperative Evaluation:
1. The severity of preexisting disease increases perioperative morbidity and mortality.

a. Previous myocardial infarction, of less than 6 months duration, has a perioperative rate of
reinfarction that is ten times greater then if older than 6 months.

2. There is a high incidence of postanesthetic pulmonary complications in patients with COPD (chronic obstructive
pulmonary disease) and asthmatic patients. We can reduce these complications with preoperative pulmonary function tests
and preparation.
3. It is important to know what medication the patient is taking and why. Certain medications need to be stopped and
others need to be continued.

a. Discontinuance of beta-adrenergic blockers (e.g., Inderal) may produce complications related

to the patients underlying disease (e.g., hypertension, angina, dysrhythmias).

• Stopping clonidine (Catapres) may precipitate a sudden hypertensive crisis.

• Some medications may potentiate drugs used in general anesthesia (e.g., Tolbutamide and
Coumadin bind to plasma albumin which normally binds 70% of the Pentothal injected. This
results in more available drug and a depressant effect.

Important points:

A. The currently popular inhaled anesthetics include Nitrous oxide and the halogenated hydrocarbons (Halothane, Isoflurane, and
Enflurane).
B. In Vitro all inhalation anesthetics produce a dose related cardiac depression. However, In Vivo the effect is less clear.
C. Halothane causes bradycardia while Isoflurane and Enflurane increase heart rate.
D. All three halogenated hydrocarbons decrease mean arterial blood pressure.
E. Isoflurane depresses autoregulation the most and may cause a "coronary steal" which may cause myocardial ischemia in
patients with coronary disease.
F. When supplementing with local anesthetics containing epinephrine with Halothane, the maximum allowable is 0.15 ml/kg of a
1:100,000/10 min. (not to exceed 0.45ml/kg of a 1:100,000/hr.). Epinephrine sensitizes the myocardium when used
concomitantly with halothane and can cause cardiac arrhythmias. Therefore, avoid epinephrine when halothane is being used.
G. Also, Halothane should be avoided in the presence of aminophylline because of the arrhythmogenic potential.
H. All mu receptor opioids except Demerol decrease the heart rate via a central effect on the vagal nucleus in the medulla. The
hypotension from morphine is primarily due to histamine release and can be blocked by using both histamine H1- and H2-
antagonist.
I. Succinylcholine can cause tachycardia, bradycardia, or cardiac dysrhythmia.

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 J. Halothane is used by many in the asthmatic patient because of its bronchodilatory qualities.
K. All inhalational anesthetics reduce resistance to flow to the skin and brain.

Local Anesthesia
I. Types

_____________________________________________________________
Esters: Hydrolyzed by Pseudocholinesterase of Plasma
A. Esters of para-aminobenzoic acid
1. Novocain - most toxic
2. Nesacaine - least toxic (shortest duration 20 min.)
B. Esters of benzoic acid
1. Cyclaine
2. Pontocaine (longest duration 2.5 hrs.)
______________________________________________________
Amides: Hydrolyzed by the Liver
C. Amides
1. Lidocaine - shortest duration, fastest onset
2. Carbocaine
3. Marcaine - longest duration
_____________________________________________________________
Note: Amides are detoxified in the liver and consequently their effects last longer. Esters are destroyed in the
blood stream by cholinesterases and are more quickly detoxified.
Note: Esters are most commonly associated with anaphylactic reactions and amides are most commonly
associated with toxic reactions.
Note: Bupivacaine should NOT be given to children under 12 years of age.

II. Maximal Allowable Single Dose in Adults

III. Conversion of % solutions to mg/cc

A. Whatever percentage of solution you are using, when you need to calculate the amount in milligrams, move the decimal point
one place to the right.
1. a 1% solution has 10mg/cc (1% = 1.0% = 10 mg)
2. a 2.3% solution has 23 mg/cc (2.3% = 23 mg/cc)

B. When you are using milligrams, and need to know what percentage you have, take the number of milligrams in one cc of
solution and move the decimal point to the left.
1. 65mg in 1 cc of solution is a 6.5% solution (65.0mg = 6.5%)
2. 10mg in 1 cc of solution is a 1% solution (10.0mg = 1.0% = 1%)

IV. Maximum dose in cc's

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 2% xyo = converted mg/cc = Max in cc's
max mg
20 mg/cc = 15 cc's
300 mg

V. Special maximum doses

• Debilitated geriatric patient: 1/2 or less of usual maximum adult dose and use lowest concentration.

• Pediatric patient:
Clark's Rule Children: Clark's Rule is used to evaluate the proper dosage of medicine for children aged 2-17. Take the weight of the child in
pounds and divide the weight by 150 lb., and then multiply the result by the adult dose to find the equivalent child dosage.
Formula: Pediatric Child dose = (Weight of child / 150 lbs) x adult dose

Example:
A 10 year old girl / 60 Lbs with 400mg Adult dose. Calculate the child's dose.

Solution:
Pediatric Child dose = (Weight of child / 150 lbs) x adult dose
Pediatric Child dose = (60 / 150 lbs) x 400 mg
Pediatric Child dose = 160mg

Fried's Rule Infants: Fried rule is a method, to estimate the medicine dosage for a child, by dividing the age of the child (in months) by 150
lbs. Then multiply the result by the adult's dosage
Formula: Child dose = (Age of child in month / 150 lbs) x Average adult dose

Example:
Calculate the child dose for 1 year old baby, where the adult dose of the medicine is 400mg

Solution:
Child dose = (Age of child in month / 150 lbs) x Average adult dose= (12 / 150 lbs) x 400mg
Child dose = 32mg

VI. Systemic Effects of Local General Anesthesia

1. Syncope -Tx: lie patient down, 02 (if it continues, use .4 mg atropine I.V.)
2. Overdose (CNS stimulation followed by depression) - TX: 02, Valium 5mg I.V. for convulsions. Ephedrine 20 mg. I.M. for
hypotension. CPR if necessary.
3. Anaphylactic reaction (bronchial constriction, hypotension and shock). Respiratory obstruction is the cause of death.
TX: - .5cc epinephrine (1:1000) I.V. or I.M.

(Sublingually is good)

Tourniquet and .25cc epinephrine at injection site.

O2 & keep airway open

Hydrocortisone (Solu-Cortef) 200 mg. I.V.

VII. General principles to remember when local anesthetics are used

A. Know patients past history

1. Allergies to other drugs
2. Allergies to local anesthetics

B. Know maximum dose of the local anesthetic for the particular patient.

C. Use smallest concentration of the anesthetic that will do the job

1. Higher % of local anesthetic does not last longer
2. When nerve is poisoned with lidocaine - takes 1 hr for it to recover whether you use 1 or 2%.
3. Higher doses are justified when doing thick nerve blocks to better affect penetration
D. Allow enough time for anesthetic to take effect.
1. Each anesthetic has an intrinsic time lag before anesthesia sets in
E. Food intake for office or "come & go surgery" should be restricted

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 F. When large volumes or large doses of a local anesthetic are needed, best to use epinephrine with the local to prevent too rapid
absorption of the anesthetic drug (physical condition permitting)
G. Withdraw on barrel of the syringe before making an injection. Do this each time you change the position of the needle before
you inject.
H. Do not inject local anesthetic into an infected area.
1. Infection will spread
2. Bacteria cause a drop in PH & local anesthetics are ineffective in an acid medium
I. When long bilateral procedures are scheduled, inject one foot at a time.
J. Local Anesthetics DO cross the placental barrier and fetal effect are unknown.
K. A total ankle block would block all of the following nerves: Sural, intermediate dorsal cutaneous, medial dorsal cutaneous,
saphenous, posterior tibial, deep peroneal.
L. The mechanism of action of a local anesthetic is to block the conduction of a nerve impulse by decreasing the permeability of Na
ions.

Malignant Hyperthermia
- This is a rare catastrophic reaction to general anesthesia.
- Sometimes inherited trait
- Exposure to potent volatile anesthetics (exp: Halothane) or succinylcholine causes the inability of the body to control calcium
concentrations within the muscle fiber, which leads to an increase in oxygen consumption and lactate production. This results
in heat production, muscle rigidity, and sympathetic stimulation.
- Occurs more frequently in children and adolescents.
- Treatment:
Discontinue all inhalation anesthesias and hyperventilate with 100% oxygen.
I.V. Dantrolene Sodium (The average successful dose is 2.5 mg/kg. However, much higher doses may be needed.
Administer more of the drug until therapeutic effect is obtained.).
Cool patient by all routes: surface, nasogastric, lavage, IV cold solutions, and rectally.
NOTE: If suspicious of malignant hyperthermia, do a pre-op CPK. This is elevated in 79 % of patient with M.H.

Anaphylactic Shock
I. Rapid respiratory and cardiovascular collapse.

-Laryngospasm, bronchospasm, unconsciousness, pruritus, urticaria and angioedema.

II. Treatment

A. Withdraw allergen,
B. Maintain airway,
C. Trendelenburg position
D. Inject epinephrine 1:1,000 .3 - .5 cc (If IV not attainable, inject into posterior ventral portion of the tongue where it is very
vascular) repeat q 10-20 minutes
E. Apply BP proximal to site injection (release every 5 minutes)
F. Inject .25 ccs of epi.into site of injection
G. If hypotension does not respond to epi., give metaraminol (Aramine) .5- 5 mg IV
H. If convulsions occur, give short acting barb pentobarbital 100 mg IV and be prepared to maintain respiration
I. If persistent bronchospasm, give aminophylline 250 mg over 10 minutes, and repeat every 6 hours.

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Angina Pectoris
I. Cause:

Coronary artery disease, family history of heart disease/precipitate stress & anxiety.

II. Symptoms:

Substernal chest pain, persists for 3 - 5 minutes, vitals stable

III. Treatment:

02 100%, 6 liters/minute, nitroglycerine 1/150 tables SL q 10 minutes. If persists more than 3 - 5 minutes, and patient has no
history, consider Myocardial Infarction.

Acute Asthmatic Attack

I. Causes:

Intermittent airway obstruction, if not treated can lead to respiratory arrest.

II. Signs and symptoms:

A. Recurrent attacks of wheezing

B. Dyspnea
C. Cough

III. Treatment:

A. Reassurance
B. Oxygen
C. Drug Therapy (Bronchodilator) & sedation

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CPR
View American Heart Association Video
https://www.youtube.com/watch?v=O9T25SMyz3A

The AHA 2015 updated basic life support (BLS) algorithm

Old method was (ABC):

Airway
Breathing
Compressions

New Method is (CAB)

Compressions
Airway
Breathing

I. Adult Cardiopulmonary Resuscitation (CPR)

1. Attempt to wake victim. If the victim is not breathing (or is just gasping for breath), call 911 immediately and go
to step 2. If someone else is there to help, one of you call 911 while the other moves on to step 2. If the victim is
breathing, see the Tips section at the bottom of this page for what to do.
2. Begin chest compressions. If the victim is not breathing, place the heel of your hand in the middle of his chest.
Put your other hand on top of the first with your fingers interlaced. Compress the chest at least 2 inches (4-5
cm). Allow the chest to completely recoil before the next compression. Compress the chest at a rate of at least
100 pushes per minute. Perform 30 compressions at this rate (should take you about 18 seconds). If you are
not trained in CPR, continue to do chest compressions until help arrives or the victim wakes up. It's normal to feel
pops and snaps when you first begin chest compressions - DON'T STOP! You're not going to make the victim worse.
3. Begin rescue breathing. If you have been trained in CPR, after 30 compressions, open the victim's airway using
the head-tilt, chin-lift method. Pinch the victim's nose and make a seal over the victim's mouth with yours. Use a
CPR mask if available. Give the victim a breath big enough to make the chest rise. Let the chest fall, then repeat
the rescue breath once more. If the chest doesn't rise on the first breath, reposition the head and try again.
Whether it works on the second try or not, go to step 4. If you don't feel comfortable with this step, just continue
to do chest compressions at a rate of at least 100/minute.
4. Repeat chest compressions. Do 30 more chest compressions just like you did the first time.
5. Repeat rescue breaths. Give 2 more breaths just like you did in step 3 (unless you're skipping the rescue
breaths).
6. Keep going. Repeat steps 4 and 5 for about two minutes (about 5 cycles of 30 compressions and 2 rescue
breaths). If you have access to an automated external defibrillator (AED), continue to do CPR until you can attach
it to the victim and turn it on. If you saw the victim collapse, put the AED on right away. If not, attach it after
approximately one minute of CPR (chest compressions and rescue breaths).

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 7. After 2 minutes of chest compressions and rescue breaths, stop compressions and recheck victim for breathing. If
the victim is still not breathing, continue CPR starting with chest compressions.
8. Repeat the process, checking for breathing every 2 minutes (5 cycles or so), until help arrives. If the victim wakes
up, you can stop CPR.
Tips:
1. Chest compressions are extremely important. If you are not comfortable giving rescue breaths,
still perform chest compressions! It's called Hands Only CPR.
2. If the victim is breathing, briskly rub your knuckles against the victim's sternum. If the victim
does not wake, call 911.
3. If the victim wakes up, but is confused or not able to speak, call 911.

II. Child CPR for kids 1-8 years old

1. Stay Safe
Children may be infected with contagious diseases. If you are concerned about possible exposure to contagious
disease, practice universal precautions and wear personal protective equipment, if available.
2. Try to Wake the Child
Gently tap or shake the child's shoulders and call out his or her name in a loud voice. Don't hurt the child, but be
aggressive -- you're trying to wake her up.

If the child does not wake up, have someone call 911 immediately. If no one else is available to call 911 and the
child is not breathing, continue to step 3 and do CPR for about 2 minutes before calling 911.
3. Begin chest compressions
If the child is not breathing, put one hand on the breastbone directly between the child's nipples. Push straight
down about 2 inches -- or about a third of the thickness of the child's chest -- and then let the chest all the way
back up. Do that 30 times, about twice per second.

If you've been trained in CPR and you remember how to give rescue breaths, go to step 4. If not, just keep doing
chest compressions and go to step 5.
4. Give the child two breaths
After pushing on the chest 30 times, cover the child's mouth with your mouth and pinch his nose closed with your
fingers. Gently blow until you see his chest rise. Let the air escape -- the chest will go back down -- and give one
more breath.

If no air goes in when you try to blow, adjust the child's head and try again. If that doesn't work, then skip it and
go back to chest compressions (step 3), you can try rescue breaths again after 30 more compressions.
5. Keep doing CPR and call 911 after 2 minutes
If you are by yourself, keep doing CPR for 2 minutes (about 5 groups of compressions) before calling 911. If
someone else is there or comes along as you are doing CPR, have that person call 911. Even if the child wakes up,
you need to call 911 any time you had to do CPR.

Once 911 has been called or you have someone else calling, keep doing CPR. Don't stop until help arrives or the
child wakes up.
Tips:
1. When checking for breathing, if you're not sure then assume the child isn't breathing. It's much worse to
assume a kid is breathing and not do anything than to assume he or she isn't and start rescue breaths.
2. When giving rescue breaths, using a CPR mask helps with making a proper seal and keeps vomit out of the
rescuer's mouth.
3. Put a book under the child's shoulders -- if you have time -- to help keep his or her head tilted back.
4. When asking someone else to call 911, make sure you tell them why they are calling. If not, they may not
tell the 911 dispatcher exactly what's going on. If the dispatcher knows a child isn't breathing or
responding, the dispatcher may be able to give you instructions to help. If you call 911, be calm and listen
carefully.

III. For babies under 1 year old, do infant CPR

1. Stay Safe
Again, children may be infected with contagious diseases. If you are concerned about possible exposure to
contagious disease, practice universal precautions and wear personal protective equipment, if available.
2. Try to wake the infant
Really little babies respond well having the soles of their feet rubbed or tapped. For infants more than 2 months
old, tap their shoulder or chest. In either case, call out his name in a loud voice. Don't hurt the baby but be
aggressive; you're trying to wake him up.

If the infant does not wake up, have someone call 911 immediately. If no one else is available to call 911 and the
baby is not breathing, continue to step 3 and do CPR for about 2 minutes before calling 911.
3. Begin chest compressions
If the baby is not breathing, put two fingers on the breastbone directly between the baby's nipples. Push straight
down about an inch and a half -- or about a third of the thickness of the baby's chest -- and then let the chest all
the way back up. Do that 30 times, about twice per second.

If you've been trained in CPR and you remember how to give rescue breaths, go to step 4. If not, just keep doing
chest compressions and go to step 5.
4. Give the baby two breaths
After pushing on the chest 30 times, cover the baby's entire mouth and nose with your mouth and gently blow until
you see his or her chest rise. Let the air escape -- the chest will go back down -- and give one more breath.

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 If no air goes in when you try to blow, adjust the baby's head and try again. If that doesn't work, then skip it and
go back to chest compressions (step 3), you can try rescue breaths again after 30 more compressions.
5. Keep doing CPR and call 911 after 2 minutes
If you are by yourself, keep doing CPR for 2 minutes (about 5 groups of compressions) before calling 911. If
someone else is there or comes along as you are doing CPR, have that person call 911. Even if the baby wakes up,
you need to call 911 any time you had to do CPR.

Once 911 has been called or you have someone else calling, keep doing CPR. Don't stop until help arrives or the
baby wakes up.
Tips:
1. When checking for breathing, if you're not sure then assume the baby isn't breathing. It's
much worse to assume a baby is breathing and not do anything than to assume he or she
isn't and start CPR.
2. Put a book under the baby's shoulders -- if you have time -- to help keep his head tilted
back.
3. When asking someone else to call 911, make sure you tell them why they are calling. If not,
they may not tell the 911 dispatcher exactly what's going on. If the dispatcher knows the
baby isn't breathing or responding, the dispatcher may be able to give you instructions to
help.
Source:
Travers AH, Rea TD, et al. "Part 4: CPR overview: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care." Circulation. 2010;122(suppl 3):S676 –S684.

Hypersensitivity Reactions
I. Cause

A. Allergic response in which you get histamine release, vasodilatation and bronchospasm.

II. Types

A. Urticarial Rash
1. Wheals, hives with pruritus
2. Treatment: Benadryl 50 mg po q 6 hrs prn or 50 - 75 Benadryl IM Consider 4 - 8 mg of Decadron IM
B. Angioneurotic edema
1. Swelling of eyelids, cheeks, lips, pharynx, larynx, hoarseness, wheezing, cyanosis (laryngeo & bronchospasm)
2. Treatment: withdraw allergen, aqueous epi. .2 -.5 cc 1:1,000 SC q 15 minutes Benadryl 50 - 75 mg IM with 8 mg
Decadron IM
C. Asthmatic Attack
1. Wheezing from bronchospasm, dyspnea, flush-cyanosis
2. Treatment: epi 1:1,000 .3-.5 cc SC q 15 minutes x3 then Aerosol bronchodilator (Ventolin, Proventil) 2 puffs q 4-6
hours.
D. See anaphylaxis

Hypertensive Crisis
I. Diazoxide (Hyperstat) 300 mg IV rapidly over 10 seconds

Hypoglycemic Crisis
I. Signs and symptoms

Weakness, hunger, sweating, irritability, faintness, tremors, convulsions, fast pulse, moist skin, low blood sugar, possible sugar in
urine, normal respirations

II. Treatment:

A. Conscious- able to swallow: give oral sugar and/or orange juice

B. Unconscious: Start IV 20-50 ml of D50 slowly
C. Take blood sugars
NOTE: If a diabetic is found unconscious and you don't know if it's diabetic coma or insulin reaction (When in
doubt give 50% glucose IV.)

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Myocardial Infarction
I. Cause:

Coronary artery disease

II. Symptoms:

Substernal chest pain, radiation to chin, left shoulder, wrists, irregular rate and rhythm of heart, diaphoresis, nausea, and
dyspnea.

III. Treatment

02 at 100% via mask at 6 Liters/minute. Morphine sulfate 5 - 10 mg IV push (10-15 mg I.M.),. Monitor B. P., Start IV with DSW
at 8-hour rate (KVO rate).

Syncopal Reaction
I. Cause

A. Temporary cerebral anoxia secondary to emotional stress or pain

II. Symptoms:

A. Pallor
B. Hypotension
C. Tachycardia
D. Cool, clammy diaphoresis

III. Treatments:

A. Give 02 at 4 - 6 liters/minute
B. Aromatic spirits of ammonia
C. Cool compresses

Classification of Toxic reactions to local

Anesthetics
I. CNS Stimulation

A. Elevated BP with rapid pulse and twitch may progress to convulsion

B. Treatment: 02 (combats hypoxia and stops convulsions) maintain airway, in office, give Valium 10 mg slow (best is ultrashort
barbs)

II. CNS depression

A. May progress after CNS stimulation. Low Blood pressure with weak rapid pulse, shallow, slow respiration, loss of speech
B. Treatment: maintain airway and give O2, 1st choice - ephedrine 1/2 cc IV, 1/2 cc IM, If decreased Blood pressure, with rapid
pulse, give Vasoxyl 10 mg IM

III. Peripheral Cardiovascular Collapse

A. Usually due to toxic dose where you get slow pulse and low Blood pressure.
B. Treatment: Maintain airway, give 02, Ephedrine as above, Atropine .4 mg IV.

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