The ever common presentation of focal hyperkeratosis on the plantar aspect of the foot...how do you treat it and what kind of success rate do you see?  These are painful lesions that are often sub metatarsal head, but clearly distinct from a simple shear or pressure callus.  I usually treat them with debridement and custom orthototics with offloading to the site of the lesion(s).

Here is a representative photo:

I've treated many of these focal nucreated lesions over the years, and was able to get a definative cure about 2/3rds of the time with a good application of the vessicant Cantharone Plus ( a mixture of the vessicants Cantharidin/Podophyllin and Salicylkic Acid) under occlusion.  Theoretically, any powerful vessicant should work, but I learned to like the controlled effect of Canthrone Plus.

The method I used was to debride the lesion as thoroughly as possible, even using a small currette or 69 beaver blade to scoop out as much of the keratotic plug as possible. I would then apply a drop of Cantharone Plus with the wooden end of a wood stcik cotton applicator, allow it to dry, and then repeat this 1 time, for a total of 2 applications.  I would then cover the spot and the surrounding area, usually the entire forefoot, with Elastoplast.  This materials sticks like fly paper and is occlusive.  It must maintain a good occusion to work, so I would run some tape between 2 adjacent toes and wrap the Elastoplast around the dorsum of the foot. I gave then a shower protector, and an analgesicand have the patient return to the office the next day. If you've ever had a blister on the bottom of your foot, you know what it feels like. 75% of the time, they would present with a nice sterile vessicle surrounding the lession.  Most often without anesthesia, I would take a tissue nipper and remove the roof of the vessicle, and then you find out how much of the core of the lesion you weren't able to remove with debridement ! Usually, you pull out what looks like a keratin plug that was embedded into the dermis.  There is usually no bleeding with this step.  Occasionally, this step is too painful to do without anesthersia, and I would do a field block from dorsal into the area to achieve anesthesia.  I estimated that I'd get about a third of these lesions recurring over time after this treatment, but it often took years to recoccur..and 2/3rds never reoccur.

What is a porokeratosis ?  It's still debated, but I became convinced over time that they represented clogged up sweat ducts.  The epidermis invaginates into sweat ducts, and all epidermal cells slough over time as a continuous process.  If the duct becomes blocked, the cells pile up and compacts from weight bearing.  I believe that is what causes these lesions.

Cantharone Plus was last manufactured by a Canadian company called Dormer. A google search on it revealed a number of current sources.

I treat by enucleation and off-loading the lesions with straight metatarsal padding and orthotics.  On occasion, I will surgically excise these lesions with a minimal plantar metatarsal condylectomy or straight excisional biopsy if they located on the heel or anywhere else on the plantar surface of the foot.  I have found that cryotherapy and laser cauterization rarely works. 

As far as etiology, I'm convinced these lesions, whether they are actual porokeratotic lesions or straight regions of focal hyperkeratosis, are probably traumatically induced by nature. 

This is from an earlier blog post in The Foot Blog from 2006.

The histological characteristics of a ‘corn’ or punctuate keratodermal lesion is a thickened stratum corneum, hyperplastic stratum malpighii, atrophic changes to the stratum malpighii at the base of the plug.  There is focal loss of the stratum granulosum with fibrosis of the dermis and dilation of the eccrine sweat ducts. 

Porokeratosis plantaris discretum is classified in some texts as a benign skin tumor.  Since the lesion is common and found on the bottom of the foot, and is keratotic, I have included this lesion as a plantar keratoderma. Porokeratosis plantaris discretum is characterized as a translucent keratinous plug surrounded by white rim of macerative tissue believed to be the plugged rim of an eccrine sweat duct.  Variants will show a keratin plug, and others will not have an associated plug.   They measure anywhere from 1-3 mm in diameter, so they are small.  It is theorized to be a blocked eccrine sweat gland secondarily to the stimulation of intraepidermal portion of the eccrosyringium.  There is some debate whether this is true microscopically.   In 1951, Marvin Steinberg, DPM, reported on a plantar hyperkeratotic lesion and labeled it plugged duct cyst.  In 1970, Steinberg and Taub reported a previously unrecognized dermatopathological entity and called it porkeratosis plantaris discreta.  Of 649 biopsies taken between 1963 and 1969, only 13.5% were found to be interpreted as consequence of sweat pore obstruction.  However, in 1990, Yanklowitz and Harkless reported the term as a misnomer.  They could not corroborate the microscopic (using light and electron microscopy) findings.  It has been my experience that the lesions can be very deep and painful.  They also respond well to surgical excision.  They are sometimes located under a bone prominence and sometimes not associated with pressure points. 

Intractible plantar keratosis or IPK is sometimes confused with porokeratosis.  The IPK also has diffuse maceration surrounding the keratosis, but these lesions are more associated with deeper keratinisation of tissue underlying a bony prominence.  They are in general , larger than the porokeratosis sometimes measuring 20-30mm in diameter.  It is most commonly seen under the metatarsal head regions of the forefoot.  I have also observed that smokers can develop these lesions, so there may be a neural or stimulatory component to the development of these lesions.  A variability of metatarsal decompression type osteotomies have been performed to eliminate these lesions with variable success.  The IPK can be so deep, that it appears to encompass into the dermis and can bleed on deep debridement. 

I.  Non-mechanical punctuate keratosis includes various diseases and conditions such as arsenic intoxication, secondary syphilis, malignancies, autosomal dominant and recessive diseases.  There are also a few premalignant keratosis that fall into the nonmechanical keratosis such as arsenical keratosis and actinic keratosis or solar keratosis.  Although not necessarily premalignant, seborrheic keratosis can be a cutaneous sign of internal malignancy such as adenocarcinoma.  This is usually preceded by a rare sign called the sign of Leser-Trelat.  An associated erythema with a rapid increase in the number of lesions accompanied by pruritis may indicate adenocarcinoma. 

Keratosis punctata of Hallopeau is a plantar keratosis named after a French dermatologist, Francious Henri Hallopeau.  It is an autosomal dominant trait.  There are several dermatologic syndromes used to describe different type of lesions and presentations that can range from nodular to bullous in nature.  The keratosis punctata variety is an autosomal dominant disorder.  The lesions are epidermal and can present in three different forms; truncated, macular or verrucoid.  The lesions usually begin to develop between the ages of 15 and 30 years and continue to last throughout life.  Since this is also a palmoplantar keratoderma (PPK), the lesions involve the palm and feet symmetrically, bilaterally with groups of small, black-like punctuate lesions. 

Karretosis Follicularis or Dariers-White disease  is a non-mechanical, autosomal dominant disease of late childhood.  The lesions can appear a multiple papules on the heels that are cobblestone-like in appearance.  Sometimes the lesions can manifest itself on the skin behind the ears.  Pinpoint papules occur in relation to and in between corresponding hair follicles. 

Osteopoikilosis is a rare autosomal dominant disorder that affects bone.  Also called ‘spotty bones’ , it is commonly characterized by ovoid regions of periarticular sclerosing, usually affecting the hip, shoulder and knee joints.  Cutaneous, punctuate keratosis to the soles of the feet affect about 25% of this population.  It is associated with dermatofibrosis lenticularis disseminate, scleroderma, dwarfism and cleft palate. 

Richner-Hanhart’s Syndrome is an inborn disease of Tyrosinemia .  It is an autosomal recessive trait caused by hepatic tyrosine aminotransferase deficiency seen in infants in the first few months of life.  It will cause hepatomegaly and liver cirrhosis if left untreated.  The syndrome is characterized by palmoplantar keratosis, lacrimation, corneal sensitivity, mental retardation and self mutilation. 

Basal Cell Nevus Syndrome or Gorlin’s Syndrome is an autosomal dominant trait that can cause punctuate palmoplantar keratomas (PPK).  The disease was first described by Gorlin in 1960 characterized by multiple nevoid basal cell carcinomas.  It is a very rare disease with the diagnosis confirmed by calcification of the falx cerebri, odontogenic cysts of the jaw and nevoid basal cell cutaneous nevi. 

Arsenical keratosis is associated with arsenic intoxication and is rarely seen in the United States.  Arsenic is used in industrial and agricultural compounds.  It is still seen in regions of the world such as Mexico and Taiwan, where arsenic levels can be detected in drinking water.  Arsenic is naturally found in rock, which can leach into drinking aquifers.  In 1888, Hutchinson reported an increase in cases of squamous cell carcinoma insitu or Bowen’s disease  in patients ingesting arsenical medications. The lesions usually presents as small, yellow-brown like round and even wart-like along the soles of the feet.  The lesions may also coalesce to form plaques. 

Actinic keratosis or Solar keratosis is a premaglinant, scaling, ill-marginated, red to pink hyperkeratotic papule of the epidermis.  It is more common in light-complected individuals.  Actinic keratosis is more pronounced on sun exposed areas such as the top of the foot rather than on the sole of the foot.  The lesions are well defined, raised and usually appear as a red to pink plaque.  Sometimes, as the lesions dry, yellow to brown crusting may form over the lesions.  The lesions are also pruritic, so associated excoriations may be seen. 

Seborrheic keratosis is autosomal dominant in inheritance.  It is characterized by a classic dark, well marginated hyperkeratosis of the epidermis containing horn cysts.  It is usually a skin condition seen in the elderly population and most often appears as a ‘paste-like’ papule or plaque.  The condition can also be associated with malignant adenocarcinoma.  A rapid increase in the number or these lesions with associated pruritis is diagnostic for the sign of Leser-Trelat.  A variant of seborrheic keratosis is Stucco keratosis.  These lesions are lighter in color, often a light yellow to white lesion commonly seen in the elderly around the ankles or on top of the foot.  The lesion is loosely adherent to the outer epidermis and is crust-like.  The classic diagnosis of this lesion is the ability to ‘pick’ off the lesion directly from the skin with your finger nail. 

II.  Mechanical punctuate keratosis 

These lesions are typically hyperplastic to the epidermis.  The epidermal rete ridges arrange themselves in a haphazard pattern called pseudoepitheliomatous.  There is significant increase in the stratum corneum and is caused by reactive stresses to the skin.  The two most common types of mechanical punctuate keratosis is associated with epidermal inclusion cyst and/or foreign body implantation. 

The epidermal inclusion cyst is certainly the most common cyst of the foot.  It is basically caused by traumatic inoculation of epidermal cells into the dermis.  The characteristic appearance of this cyst is a dome shaped, firm nodule.  If a central core is found, sometimes caseated, cheesy keratinatious material can be expressed from the lesion. 

Foreign body implantation is a variant of the epidermal inclusion cyst.  Here on debridement, we see a macerated region just under the keratoma that appears very similar to a porokeratosis plantaris discreta.  However, on closer inspection, a small foreign body is seen.  When the cyst is inspected, many times a central foreign body can be found in the cyst.  Here we see a small foreign body implantation of a metal shaving removed from an inclusion keratoma.  On initial clinical inspection, the lesion looks like a typical punctuate keratoma to the bottom of the foot.  However, on sharp debridement, the small metal shaving is identified as foreign body material inducing punctuate hyperkeratosis.

During residency, John, Jolly tried a rotational advancement to excise one and move the potential area of recurrence to another site. We thought that that might take care of the problem. But instead the lesion reoccured along the incision line, giving credence to the idea that they occur in areas of trauma to the skin. Mind you that we relocated the incision to areas of low stress (no tension on the skin, no metatarsal head directly above the skin, etc.)

FYI, Dr. Gary Dockery, who has written several dermatology chapters and textbooks, uses the injection of diluted dehydrated alcohol, directly underneath the skin lesion... the same kind of alcohol solution that is commonly used in the chemical neurectomy and neuroma treatment.

When I was in training in Cleveland, I have seen cantharone used as a vessicant, for many skin lesions, anything from IPKs to plantar warts... and I think they worked pretty good, while some of the patients complained of severe pain once in a while, especially if you are treating large or multiple areas. Another vote for cantharone from me.

I largely use cantharone, as was the practice in my training program, although I have seen people use sclerosing alcohol injections for the management of these types of skin lesions, as Kazu mentions, and it seems effective.

I used to wonder what all the excitment was about until I developed a porokeratosis on my own foot.  It felt like a needle in my foot.   I have frozen them with liquid nitrogen, and also used Cantharon.,  I now use debridement with urea 40% ointment in the void after  and Plastizote inserts,  I claim only fair sucess with this method, 

I have excellent results with debridement of the core and immediate freezing with liquid nitrogen. I have them follow up in one month for one more treatment and many of them are gone at that point.

Thanks, Dr.Winters.  I think all vessicants, if sufficiently powerful, work well in this situation...liquid nitrogen certainly being one of them. The application needs to be titrated based on the location of the lesion.  My experience has been that porokeratoses tend to appear under the weight bearing areas of the forefoot, and to a lesser extent, the heel. Pressure seems to be part of the etiology...facilitating the clogging up of the sweat duct.  The skin in these locations is among the thickest on the body, so a fairly potent vessicant application is required.

Since everyone has exhausted most treatment options, I'll just put in my 2 cents....

Canthone w/ occlusive dressing...if recalcitrant, I am now using the CryoProbe after enucleation and then applying Canthrone.

 For the most severe recalcitrant cases, I treat them like a verruca plantaris, CO2 laser excision and curretage, Effudex ointment with occlusion x 2 weeks.  Seems to work.

Eric 

Where does everyone order Cantharone from?  I am trying to have my hospital pharmacy order it so I can have it in my clinic for use, but they claim it is not FDA approved and is only available from Canada....

Cantharone Plus was last manufactured by a Canadian company called Dormer. A google search on it revealed a number of current sources.

Alan

Did anyone else notice that this thread has over 2600 views?

Unless it's just Alan Sherman clicking on it over and over?  :) 

I actually enjoyed this thread very much. It is interesting how we treat the same skin lesion in so many different ways.

I did my residency in Cleveland OH, Salt Lake City UT, and now practice in Los Angeles CA. I can tell you from my personal experience that how we practice (ie. osteotomy fixation method) differ completely from region to region.

For example, in Cleveland, I've seen percutaneous k-wire fixation for almost every hammer toe correction. In Salt Lake City, hammertoes were almost never fixated. In Los Angeles, many people fixate Austin with percutaneous k-wire, which I have never seen in Cleveland.

I think it's pretty cool to have this forum where we can exchange ideas so easily. 

I usually debride this down to core and apply phenol.  I repeat this every 2 to 3 months.  For the true mascerated porokeratotic lesion, it seems to work well.  There are many ways to skin the cat so to speak.  The objective is to either remodel or ablate the dermal subcutaneous region where the histologic defect occurs and have new dermis replace the defective tissue.  Dr. Kline, nice review of the differential lesions.  That should have been an ezine.  Does anyone have issues with recurrence when these are excised?

The fact that there are 2600+ viewings of this string makes an important point: there is no one completely effective treatment for all patients yet.

I have read many good ideas here. But I am not competely convinced that we are all talking about the same lesion though (as Dr. Kline indicates in his excellent educational contribution).

George, I would bet you dollars to doughnts that yes, if we are being perfectly honest and not just bragging that "in my hands.....", these do recur. If we think we have cured our patients for good because the patients don't return, they may be seeing the podiatrist across town for the same condition/different treatment! 

This is a difficult condition that we truly don't understand the etiology of yet.  Once we do, they we can develop a true treatment and possible cure.

Well, first off, the etiology of the Intractable plantar keratosis is different from the Porokeratosis plantaris discretum lesion and the treatment should follow that difference. For the true Porokeratosis plantaris discretum lesion, I have done the treatment shown to us by Harvey Lemont at the Temple School (so many years ago): numb up the area under the lesion so that you can work without a chance of the patient jerking the foot and causing a calamity. Excholeate around the rim of the lesion to raise a section and then grab it with a hemostat. Continue to excholeate the obvious, whitish colored core of the lesion to the base. The depth of this may be shocking in some cases, but success is completely dependant upon working to the base. Once at the base of the lesion, it will pluck out and leave a small diameter, somewhat deep non-bleeding evacuated site. It will be non-bleeding if you use epinephrine in your block, by the way. I use two cotton tipped sticks of phenol for 30 seconds each, constantly rotating the stick in the site. After two sticks to cauterize the site, with attendant color changes, I flush with EtOH on a cotton tipped stick, place a little topical antibiotic on it with a Band-Aid. I place no restrictions upon the patient as far as weightbearing or activity and the site is usually minimally tender once the block has worn off. I’ve averaged around an 85% success rate with one treatment, following this protocol. Thanks, Dr. Lemont!