Plantar Verruca (Warts)

Verrucase Vulgaris, also known as the common wart, are skin infections caused by the human papilloavirus (HPV). There are over 100 different strains of the virus that occur all over the body. They are spread by physical contact. 

ANATOMY 

Plantar warts infect the epidermis, most superficial layer of skin, specifically keratinocyctes. 

EXAM AND DIAGNOSIS

Warts are diagnosed clinically by the following observations: 

• Absence of skin lines in the lesion. 
• Thickening of overlying skin, often mistaken for a callus. 
• Presence of multiple dots or a single black dot caused by small capillaries that have developed to nourish the infected tissue. 
• Tenderness with lateral pressure (pinching it). 

They can present as either single lesions (solitary) or in clusters of lesions (mosaic). 

TREATMENT

There are many different treatment options available ranging from oral medications, topical medications, laser therapy, cryotherapy (freezing), and surgical removal. While approx 65% of warts resolve without intervention after 2 years many patients want faster relief. This is an area that is in need of more research to figure out which of the long list of treatments is most effective. Treatments that are currently used include the following: 

Topical Medications

• Salicylic Acid - can be purchased over the counter and an effective first line treatment. 
• Imiquimod 
• Cantharone
• 5-flourouracil 5% Cream

Intralesional Tharpy (injections)

• bleomycin

Oral Medications

• cimetidine

Other Treatments

• Duct Tape Occlusion - shown not to work
• Cryotherapy
• Laser Therapy

PREVENTION

Because HPV is spread by contact prevention consists of protecting your feet. These suggestions include: 

• Avoid walking barefoot through public places. 
• Clean feet daily with soap and water. 

Foot and Toenail Fungus

Tinea is a fancy name for fungus. There have been shown to be more than 80 different strains of fungus on the average person's foot with the highest concentrations being on the heel. These fungi live in a balance that isn't a problem until that balance is disturbed. People at risk for fungal infections include those with:

• Compromised immune systems (HIV, Diabetes, Oral Steroid use)
• Advanced age
• History of trauma to the toenail.  
• Poor blood flow in their toes. 
• Frequent use public/locker room showers (thus the term athlete's foot). 
• Poor pedal hygiene (improved hygiene has even shown to cure 35% of existing fungal skin infections).
• Genetically prone.  

ANATOMY INVOLVED

While tinea can get into the blood and cause systemic infections it most commonly affects the most superficial layer of skin, the epidermis, and the nail plates. The areas that are most resistant to treatment are the plantar foot and the nail plates due to the high amount of keratin which makes it difficult for topical medications to penetrate the structure.

THE EXAM AND DIAGNOSIS

Signs of a fungal infection of the skin, also known as athlete's foot or tinea pedia can include:

• redness (erythema)
• itchiness (pruritus)
• foul odor 
• macerated (white over-hydrated skin) or hyperkaratotic (dry callused skin) scaling
• fissures (cracking)

They present in three main patterns; interdigital, moccasin, and vestibulobullous(fluid filled blisters). Interdigital infections are usually more macerated while the moccasin pattern in more hyperkaratotic.

Research has shown that the most common fungal strains resulting in tinea pedis are Trichophyton rubrum and Trichophyton mentagrophytes (more aggressive strain). T. mentagrophytes has been shown to be more common in the younger healthier individual.

Signs of a fungal infection of the toenails, also known as onychomycosis, include:

• nail discoloration; yellow, orange or brown patches or streaks. 
• nail detachment from nail bed (onycholysis).
• subungual (under the nail plate) debris. 
• nail thickening
• nail crumbling

The "gold standard" method for diagnosis of pedal fungal infections is microscopic examination of skin subungual (skin under the nail plate) scrapings prepared in potassium hydroxide (KOH). The examiner can see hyphae. Today's podiatrists send these scrapings to a lab where they are read in a lab.

TREATMENT

Treatments for fungal infections include topical powders and creams for less severe infections and oral medications for more sever or resistant infections. Due to the resistive nature of onychomycosis (toenail fungus) the most effective treatments are oral medications. The downside of oral antimicrobial medications are that many have been shown to cause liver damage to a very small percentage of individuals. The internet is full of many home remedies and other remedies for treatment of toenail fungus (Vick's Vapor Rub, Colloidal Silver, Tea Tree Oil....). Due to the high number of these types of treatments and the low level of effectiveness I am not going to discuss all of them. The below list of medications that have been proven with varying degrees of effectiveness which I have put in order of effectiveness.

Topical Treatments:

• 2% Miconazole Nitrate Powder - Available Over the Counter
• 1% Clotrimazole Cream- Available Over the Counter
• 1% Clotrimazole Solution (better penetration into nail plate). 
• 1% Terbinafine Cream (Lamisil)
• 1% Terbinafine Gel
• 0.77% Ciclopirox Cream/Gel
• 8% Ciclopirox Solution (Penlac Nail Lacquer)
• 20% Urea Cream*
• 40% Urea Cream*
• Salycilic Acid*

*can be used with topical medications to soften the nail plate and callused skin improving penetration of medication.

Oral Medications:

• 250mg Terbinafine (Lamisil); liver enzymes from a blood test are also monitored while this medication is given to ensure that there is not irreparable damage occurring. 

Other Treatment Options

• Cleaning feet daily has shown to cure about 35% of cases. 
• Laser Treatment (for onychomycosis) is available and is very expensive. Its efficacy is still being investigated. 
• Toenail Avulsion (removal of toenail). In sever cases the complete removal either permanently or temporarily, is always an option. This options will prevent spread to other toes and is a sure cure. Toenails serve no real purpose beyond their aesthetic appeal. 

PREVENTION

The best option is to take proper precautions to prevent fungal infections from getting out of control in the first place. Most toenail infections begin as athlete's foot that has been neglected and the fungus gets into the nail. Once in the nail it is extremely difficult to cure and the fungus can damage the cells that cause the nail to grow making the nail thick and disfigured. Once a nail has become thick and disfigured the chances of being able to return to nail to its appearance prior to the infection if very low. Here are some suggestions as for prevention:

• Wash your feet daily with soap. Fungal spores are EVERYWHERE and washing them will decrease the amount on your feet and will remove the dirt and grim that harbors colonies. 
• Alternate shoes to allow them to dry out. The environment in your shoes (moist, dark, warm) is prefect for fungus to thrive so allowing your shoes to dry out will inhibit growth. 
• Wear well ventilated shoes, synthetic socks and use shoe powders occasionally to keep feet dry. 
• Treat fungal skin infections early on to prevent them from getting out of control and into the tissue that is more difficult to get to with medication like callused skin and toenails. 
• Avoid going barefoot in public area such as showers and pools. Fungal spores and live on for months to years. 

Hsu AR, Hsu J. Topical Review: Skin Infections in the Foot and Ankle Patient. Foot & Ankle International. 33(7):612-619, 2012 

Primary vs Secondary Bone Healing

Primary bone healing occurs when cortical bone is touching each other and is fixed rigidly by other cortical bone or hardware. The bone fuses together by bone cones which consists of leading osteoclasts and trailed by osteoblasts forming a cone.

Secondary bone healing goes through the process similar to wound healing such as hemostasis, inflammation, callus bone formation and reconstruction to produce the same, if not better bone.

Stages of Wound Healing

There are 4 phases of wound healing:

1. Hemostasis: Clotting sequence is activated, vasoconstriction, thrombin --> fibrinogen --> fibrin. 
2. Inflammation: During this phase debris and bacteria are phagocytosed. Neutrophils then Monocyctes and Macrophages(approx 4 days after injury)  then
3. Proliferation: Angiogensis, Collogen deposition, granulation tissue formation, epithelialization and wound contraction. 
4. Remodeling: Occurs for about a year. Scar tissue regains about 2/3 or original strength but is never as strong. 

Over-drill Sizes for Lag Technique

Screw Size-->Initial Drill Size --> Glide Hole Bit Size

Non-canulated
2.7mm-->2.0mm-->2.7mm
3.5mm-->2.5mm-->3.5mm
4.0mm-->2.5mm(cancelous), 2.9(cortical)-->4.0mm
4.5mm-->3.2mm-->4.5mm
6.5mm-->3.2mm-->6.5mm

Cannulated
3.5mm-->2.7mm-->3.5mm
4.5mm-->3.2mm-->4.5mm
7.0mm-->5.3mm-->7.0mm
7.3mm-->5.0mm-->7.3mm


Synthes Reference Sheet found here: http://www.rcsed.ac.uk/fellows/lvanrensburg/classification/commonfiles/Synthes%20screws.pdf

Ankle Blocks

Ankle Blocks

Nerves blocked: Tibia N (5mL), Saphenous N, Medial Dorsal Cutaneous, Deep Peroneal N (needle advanced to bone btw EHL and EDL, 5mL), Intermediate Dorsal Cutaneous, Sural.

Mayo Block

Nerves blocked: Medial Plantar N, Saphenous N, Medial Dorsal Cutaneous N, Deep Peroneal.



Minni-Mayo Block

Nerves blocked: Lateral Dorsal Cutaneous, 4th Common Dorsal Digital, Superficial branch of lateral plantar, 4th common plantar digital N.

Ankle Sprain

Lateral Ankle Sprain Grades (Leach's Classification)

• Type1: ATFL affected
• Type 2: Complete tear of anterior talofibular lig and some damage of the CFL lig. 
• Type 3: Rupture of all 3 ligament, associated with rupture. 

O'Donoghue's Classification

1. Partial tear of LCL with mild swelling/tenderness, no mechanical instability, pt can walk, play.
2. Incomplete tear of LCL with moderate swelling/tenderness, mild/moderate instability, pt limps after injury. 
3. Complete tear of LCL with severe swelling/tenderness, echymosis, instability, pt cannot walk after injury. 

Dias Classification (1979)

Grade I: Partial rupture of CFL.
Grade II: Rupture of ATF
Grade III: Complete rupture of CFL, ATF and /or PTF.
Grade IV: Rupture of all lateral collateral ligaments and partial failure of the deltoid ligament. 

Anterior Drawer Test: Checks ATFL by pulling cal/talus forward while stabilzing tib/fib. 5-8mm drawer --> rupture of ATF, 10-15mm drawer-->rupture of ATF + CF, >15mm drawer --> rupture of ATF, CF+PTF. 

Talar Tilt: >10mm of inverstion is indicative of CFL rupture. 

Kleiger's Test: Rotate foot and dorsiflex to check for medial pain (deltoid) or anterolateral pain (syndesmosis). 

Tinel's Sign: Tapping PT nerve causes radiation in one direction. 

Ankle Fractures

Description and ID:

X-ray read points to make: Position of talus to mortis (dislocation....), syndesmotic rupture, malleoli involved (tri, bi - mal fx), displaced or not, medial or lateral clear space (>4mm =deltoid injury), medial fibulas/anterior tibia overlap (>10mm), fibular shortening, avulsions, "Shenton Line" (tibial subchondral bone lines up with small spike on fib adjacent to syndesmotic space). 

Lauge-Hanson - Ankle fractures

Classification system described by the direction of movement on the talus on tibia (Key identifies in green). 

Supination-Adduction

Stage I: Transverse fracture of the fibula below the level of the ankle joint or rupture of the lateral collateral ligaments.

Stage II: Near vertical fracture of the medial malleolus

Supination-External Rotation

Stage I: Rupture of the anterior inferior tib-fib ligament or avulsion of the ligament (Wagstaff or Tilluax-Chaput)

Stage II: Spiral fracture of the fibula with a posterior spike on the lat X ray beginning at the level of the ankle joint

Stage III: Rupture of the posterior inferior tib-fib ligament or avulsion of the ligament off the posterior malleolus (Volkmann’s)

Stage IV: Avulsion fracture of the medial malleolus or rupture of the deltoid ligament

Pronation-Abduction

Stage I: Transverse fracture of the medial malleolus or rupture of the deltoid ligament

Stage II: Rupture of the anterior and inferior tib-fib ligaments (Wagstaff or Tillaux-Chaput Fx)

Stage III: Fibular fracture at the level of the ankle joint with the appearance of a spiral fracture on the AP X ray and a transverse fracture on the lat X ray (butterfly fragment)

Pronation-External Rotation

Stage I: Avulsion fracture of the medial malleolus or rupture of the deltoid ligament

Stage II: Rupture or avulsion fracture of the anterior inferior tib-fib ligament (Wagstaff or Tilluax-Chaput) and rupture of the interosseous membrane

Stage III: Short oblique fibular fracture starting above the ankle joint and extends up the fibula depending on the extent of the interosseous rupture. Fracture runs distal posterior to proximal anterior

Stage IV: Rupture or avulsion fracture of the posterior inferior tib-fib ligament (Volkmann’s)

Danis Weber- Lateral Malleolar Fracture

Type A: Transverse avulsion fracture of the fibula beginning below the syndesmosis (SAD)

Type B: Spiral, oblique fracture of the fibula beginning at the level of the syndesmosis (SER/PAB)

Type C: Fracture of the fibula beginning above the level of the syndesmosis (PER)

Treatment:

Initial closed reduction and stabilization (posterior splint). 

DW-A --> Tension band wiring, screw/plate depending on fragment size. 

DW-B --> Neutralization plate.

ATFL should always be repaired. 

Posterior avulsion (SER 3, PER 4) repaired of >25% of joint involved. 

DW-C --> syndesosis needs to be repaired if deltoid is ruptures. 

Syndesmotic Screws --> 1x, 2x, 3.5mm or 4.5mm screws, 3 corticies or 4 corticies inserted approx 2cm above ankle joint after tapping. Removes screws usually 8-12weeks. 

21 Points of Ankle Arthroscopy

The 21-point examination was developed by Richard D. Ferkel (22) to establish a reproducible and thorough intra-articular examination of the ankle. It consists of an 8-point anterior examination, a 6-point central examination, and a 7-point posterior examination. 

8-point anterior exam:

6-point central exam:

7-point posterior exam: 

Ferkel RD, Cheng JC. Ankle and Subtalar Arthroscopy. In: Kelikian A, ed. Operative Treatment of the Foot and Ankle. New York: Appleton-Croft, 1999:321

Erythrasma

I have often heard "erythrasma" considered as a DDx when evaluating a patient with cellulitis. Here is the low down on it:

- Commonly presents in intertriginous areas of the body (skin folds, between toes, etc).
- High incidence in humid areas and in diabetic patients.
- Often is a secondary infection to tinea

- Caused by corynebacterium minutissimum
- Can dx using a woods lamp, causing it to turn corral red.
- Clinical presentation is scaling, fissuring and slightly macerated, resembling tinea.
- Common between 3rd and 4th digits (2nd interspace)

- Treated with oral Erythromyocin(binds 50S) or Tetracycline(not currently available in US).
- Relapse is common.

Big Bugs: Pseudomonus and MRSA

MRSA (methcillin resistant staph aureus) is a gram (+), catalase (+) cocci in clusters. MRSA is often sensitive to the following drugs:

• Vancomycin 500mg IV qid
• Bactrim 80/400 or 160/800 PO BID
• Linezolid 400-600mg BID

Pseudomonas is a gram (-) rod w/pili and flagella and is often sensitive to:

• Ciprofloxacin 500mg PO BID
• 3rd Gen cephalosporins 
• Aztreonam 0.5-2mg IM/IV q6-12h
• Zosyn(piperacillin/tazobactam) 3.375g IV q4-6h
• Timentin(ticarcillin/clavulanate) 3.1g IV q4-6h

Rearfoot Varus

Rearfoot Varus is when the rearfoot has a decreased amount of STJ pronation causing the calcaneus to be positioned into an inverted position.
Effects:

This leads to the foot striking the ground in a more supinated position than normal. This more supinated position requires the foot to travel a further distance to achieve necessary pronation at midfoot. This causes the medial column to slam into the ground harder than normal. This in turn fails to give the foot enough time to adequately supinate, creating a rigid lever. Inadequate supination during toe off causes a soft midfoot and can put strain on soft tissue.

If the position of the calcaneus is more inverted then this changes the pull of the

Deformities that can result secondary to a rearfoot varum include:

1. Genu Varum
2. Forefoot Valgus (caused by lateral pressure on foot). 
3. Plantar Fasciitis (caused by rapid pronation leading to high medial GRF). 
4. Hammertoes (secondary to flexor stabilization which is activated in an attempt to stablize the foot during propulsion). 

"Supinatus"

Supinatus is a term used mainly on the west coast, or so I hear. It is also known as flexible forefoot varus. This deformity can progress to become a rigid deformity from a soft tissue adaptation. Soft tissue adaptations occur secondary to bony deformities. Two deformities that can lead to supinatus are 1) Forefoot Varus and 2) Rearfoot Varus.

Forefoot Varus is a rigid deformity that requires the STJ to compensate into a pronated position. During this process of compensation over compensation usually occurs which leads to ground reactive forces causing dorsiflexion of the midfoot. This frequent dorsiflexion eventually causes the midfoot to remain in a supinated position secondary to soft tissue accomidation, particularly shortening of the posterior tibialis. The PT shortening causes the TN joint to remain supinated, decreasing the overall ROM of the midfoot.

Rearfoot Varus is when the STJ has decreased pronatory ROM. During push off the lateral column comes off the ground first due to the limited time available to bring the foot into a rigid supinated position causing a dorsiflexory force to the medial midfoot leading the supinatus. During gait the heel strike occurs with the foot in a more inverted position causing the foot to have to pronate very quickly to get the forefoot to the ground causing a high GRF to the medial column as it slams into the ground.

Requested 1986 Forefoot Supinatus article from JAPMA


Random exerts from "The Foot Book":

Forefoot Supinatus:
o Fixed supinated position of the forefoot due to SOFT TISSUE ADAPTATION
o One would see MTJ total ROM DECREASED (different from Forefoot Varus)
o Example: Calcaneal Eversion  Forefoot supination via GRF  soft tissue adaptation 
supinatus  Decreased MTJ ROM
Supinatus?
 YES!
 If FF varus is 4 degrees and STJ pronatory ROM is 9 degrees.
o STJ will pronate to END ROM
o FF 4 degree varus will become SUPER-COMPENSATED
o STJ extra 5 degrees of pronation will JAM THE MEDIAL Forefoot into
the ground  Inversion  Soft Tissue adapation  SUPINATUS

Soft tissue defects are often an affect not a cause of MSK deformity.  Examples are equinus, 

supinatus 

Supinatus: soft tissue adaptation about the MTJ causing the supinatus; due to 1) rearfoot varus (the

STJ compensatory pronation jams the 1st ray into the ground, causing the soft tissue adaptation) and 2) forefoot varus (STJ compensatory pronation will pronate to end ROM which will probably jam the 1st ray into the ground causing soft tissue adaptation and, thus, the supinatus)

 Supinatus with a RF Varus: the STJ doesn’t pronate enough to jam the 1st

 met into the ground to cause the soft tissue adaptation leading to supinatus – this actually still happens because the lateral column raises FASTER than the STJ pronates, so the 1

st still slams into the ground leading to the soft tissue adaptation 

Plantarflexory force on 1st ray to cast out supinatus

Cotton indicated. 

Supinatus

 General Cause of Supinatus (see below for details on exactly how): PRONATION OF THE STJ! #1 cause is a compensated RF varus or it could also be due to over-compensated forefoot varus –when you pronate past where you need to to be able to fully compensate for the FF Varus deformity 

 Supinatus occurs at the TN joint (talo-navicular joint)

 It occurs when the TN joint SUPINATES to allow the 1st

 ray to dorsiflex during hyperpronatory gait so that the 1st ray doesn’t get slammed into the ground

 It is a “FLEXIBLE forefoot varus” type of a deformity, so soft tissue is causing the problem 

o Since it’s flexible, it can in theory be manually reduced by rotating the navicular about the

talus such that the forefoot inversion problem corrects itself 

 The only soft tissue that can cause the navicular to have a problem is the PT tendon because it’s theonly one that attaches to the navicular 

 Supinatus occurs when the PT tendon becomes functionally shorter that it’s supposed to be –

here’s how that happens: when you have a forefoot varus (rigid deformity), you pronate at the STJ

to compensate for it.  In theory, you compensate (pronate the STJ) so that you stop pronating when the 1st ray hits the ground (so that it doesn’t go through the ground).  Catch-22 is that when you pronate to compensate, you basically always pronate past full compensation to have an “overly

compensated” forefoot varus.  Well, since the ground doesn’t permit the 1st ray to go through the ground, you get SUPINATION at the TN joint to allow the 1st ray to elevate so that you can keep

pronating without crushing your sesamoids and 1st metatarsal.  THIS SUPINATION OF THE TN JOINT when the STJ pronates past full forefoot varus compensation causes the PT tendon to become functionally shorter, so the PT tendon then “holds” the navicular in the inverted position leading to the supinatus deformity 

DO NOT plantarflex the first ray (yes you Californians are probably throwing up a little…), why create an artificially high medial arch that often cannot be tolerated by pts?  When plantarflexing the first ray you are not effectively removing supinatus, only flexing the met-cuneiform joint.   Supinatus is due to contracture of soft tissues at the level of the mid foot not the first ray.  To cast out supinatus you must rotate out the supinatus at the T-N joint by pressing down on the navicular.  By plantar flexing the 1st ray you can actually create a more supinated foot that will eventually lead to a weakened peroneus longus and possible HAV. 

Amniotic Membrane for Wound Care

PubMed Search

1. 2011 French article entitled "Human amniotic membrane in the management of chronic venous leg ulcers" stated that in a review of multiple studies amniotic membrane showed benefit in promoting granulation, reducing fibrosis and enhancing re-epithelialisation. 
2. Used a lot in the eye. 

Companies producing such products and claims/indications. 

1. Amniox Medical: They claim that because it is from "fetal" tissue it doesn't activate inflammation and prevents scar formation. They have cryopreserved products for wound care and surgical covering. 
2. EpiFix: Claims it provides growth factors and prevents scar formation while enhancing repair. They have a product that can store at room temp for 5yrs. Site was broken. 

Claims

1. Decreased scar formation. 
2. Growth factor delivery
3. Collagen
4. Lack of immunological markers preventing immune reaction 
5. Antibacterial properties
6. Pain reduction on application

Sites for info:

1. http://www.medscape.com/viewarticle/773578 - Reviews technology and discussed dehydrated amniotic membrane benefits.