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Keys To Diagnosing And Treating Plantar Keratosis

Due to the varying presentations and causes of plantar keratosis, it is crucial to make an accurate diagnosis to facilitate effective treatment. These authors present a comprehensive guide to biomechanical and dermatological lesions as well as options for management.

Plantar keratosis is a common pathological foot condition that requires ascertaining a comprehensive history and conducting a physical examination to diagnose the lesion accurately, which is critical to precise treatment. After obtaining the appropriate information, we can classify plantar keratosis into either biomechanical or dermatological lesions. Differentiation between the two types of lesions is critical for treatment.

Biomechanical etiologies for plantar keratosis range from hallux abducto valgus and equinus to pes planus and trauma (see “A Guide To Biomechanical Etiologies Of Callus Formation In The Foot” at left).

One should base the ultimate treatment of a biomechanical lesion on the treatment of the biomechanical deformity. This applies to both conservative and surgical treatment.
For definitive treatment, treat the “why” of the lesion or the lesion will recur. Additionally, palliative care for plantar keratosis can be an acceptable method of treatment based on the needs of the individual patient.

What You Should Know About Biomechanical Causes Of Plantar Keratosis
Hallux abducto valgus.
In normal feet without hallux abducto valgus deformity, plantar aponeurosis causes plantarflexion of the first metatarsal during the first half of the stance phase. As the hallux valgus deformity develops, the first metatarsal may not be plantarflexed during stance phase. This causes extra pressure on the second metatarsal and leads to callus formation at the second metatarsal.1

Hypermobile first ray. During the stance phase, if there is hypermobility of the first metatarsophalangeal joint (MPJ), the pressure transfers to the lesser metatarsal heads. Since the lesser metatarsals have tighter articulation at the tarsometatarsal joint, they remain stable during stance phase, which causes elevated pressure at the second and third metatarsal heads. This abnormal pressure causes diffuse callus formation under the second and third metatarsal heads. The fourth and fifth rays are more mobile than rest of the rays. Therefore, a callus rarely forms under the fourth or fifth metatarsal head unless there is an osseous deformity or an abnormal global foot deformity.1

Equinus. Charles and colleagues observed functional range of motion of the ankle joint and proposed a two stage definition of equinus.2 They noted that patients with greater than 10 degrees of dorsiflexion did not experience any compensation and had normal forefoot pressures. Accordingly, those with stage 1 equinus have 5 to 10 degrees of dorsiflexion at the ankle joint with minimal gait compensation and slightly abnormal forefoot pressure. With stage 2 equinus, one would have less than 5 degrees of dorsiflexion at the ankle joint with significant gait compensation, increased forefoot pressures and a greater incidence of forefoot pathologies.

When patients have equinus, pronation of the subtalar joint is a common compensation that can unlock the midtarsal joint during midstance phase of the gait cycle. As a result, the peroneus longus muscle loses a mechanical advantage as well as the ability to plantarflex the first metatarsal during midstance. This leads to a transfer of pressure from the first metatarsal head to the second metatarsal head. Therefore, patients with compensated equinus may develop a callus under the second metatarsal head.

For uncompensated equinus, during the midstance and terminal stance phases of the gait cycle, there is an abnormally high pressure on the forefoot, which causes callus formation under the first, second and third metatarsal heads. In patients with insensate feet, this deformity can lead to ulcerations.3,4

Pes cavus. Patients with a true cavus foot deformity may have the calcaneus in a dorsiflexed position and the forefoot in an equinus position or plantarflexed relative to the rearfoot. As a result, there is an abnormally diminished weightbearing area and increased pressure under the metatarsal heads and at the heel. The foot with flexible pes cavus usually produces a callus under the second metatarsal head. This condition results from the arch’s inability to dissipate forces and a lack of shock absorption.

On the other hand, a rigid pes cavus deformity produces diffuse calluses that are usually present under the first, second and fifth metatarsal heads. Patients with pes cavus deformity also suffer from hammertoe deformity as the extensor digitorum longus tendon has a mechanical advantage over lumbricals. Hammertoes can cause retrograde buckling and can cause a plantarflexory force on the metatarsal heads. This subsequently creates extra pressure under the metatarsal heads during the terminal swing phase of gait. Such abnormal pressure under the metatarsal heads can cause callus formation under the respective metatarsals as well.5

Forefoot valgus. Forefoot valgus may be associated with a pes cavus deformity. In an uncompensated foot with forefoot valgus deformity, there may be a plantarflexed first metatarsal and subsequent development of a diffuse callus under the first metatarsal head.1

Pes planus. A foot with pes planus deformity usually does not develop a callus due to wider weight distribution across the foot. However, in a foot with hallux limitus or rigidus deformity, a callus may develop under the first metatarsal head. When these patients also have hypermobility of the first ray, a callus would develop under the second metatarsal head. In patients with hallux valgus deformity, a callus may develop along the plantar medial aspect of the hallux interphalangeal joint.1

Forefoot varus. A foot with uncompensated forefoot varus deformity and a plantarflexed fifth metatarsal can produce a callus along the plantar lateral aspect of the fifth metatarsal head.1

When Rheumatoid Arthritis Causes Plantar Keratosis
Patients with rheumatoid arthritis (RA) suffer a wide range of forefoot pathologies due to the destruction of osseous and soft tissue structure. In patients with RA, synovitis with ingrowth of pannus and cytokines causes destruction and erosion of the joint cartilage of the metatarsal heads and proximal phalanges of the toes. Synovitis causes distension and slacking of the capsules and ligaments at the joint level.

The balance between intrinsic and extrinsic muscle disappears and as a result, joint subluxation and dislocation occur at the MPJs. At the first MPJ level, this results in hallux valgus deformity. In lesser MPJs, this results in dorsolateral subluxation of the toes. The fifth phalanx usually subluxes in a varus position. The progression of the disease causes rigid claw toe deformities of the lesser MPJs and hallux abducto valgus deformity of the first MPJ. Due to retrograde buckling of the claw toes, there is a plantarflexory force on the metatarsal heads. The fat pad and soft tissue displace distally on the metatarsal heads. As a result, bursitis and callus formation may occur on the lesser metatarsal heads.

Researchers have found that patients with rheumatoid arthritis may suffer from heel valgus in 30 percent of cases in comparison to varus heel in only 2 percent of cases.1 True valgus deformity of the rearfoot pronation at the subtalar joint may occur, which in turn may cause hypermobility of the metatarsocuneiform joint. Such changes can lead to excessive pressure under the second metatarsal head and cause thick callus formation.

One may note the following callus formation patterns in patients with RA:6

• medial eminence of the first metatarsal head due to bunion;
• between the hallux and second toe due to valgus and abduction of the hallux;
• on the plantar aspect of the lesser metatarsal heads, mainly the second metatarsal;
• on the dorsal aspect of the proximal interphalangeal joint and distal interphalangeal joint; and/or
• on the lateral aspect of the fifth metatarsal head due to broadening of the forefoot.

Key Insights On Plantar Keratoses Arising From Trauma And Surgery
If the metatarsal head or neck fracture were to heal in a malunion position, it could cause abnormal pressure under the metatarsal heads. If the malunion causes a plantarflexed metatarsal head, then the callus would form under that particular metatarsal. However, if the malunion causes dorsiflexion of the metatarsal head, the callus would develop under adjacent metatarsal heads due to increased weightbearing pressure.

Any surgery that alters the weight distribution of the weightbearing surface of the foot can cause callus formation. Consider the following examples.

• A dorsiflexion metatarsal osteotomy can cause callus formation under adjacent metatarsal heads.
• A plantarflexory metatarsal osteotomy can cause callus formation under the same metatarsal head.
• A shortening first metatarsal osteotomy can create excessive pressure under the second and third metatarsal heads during midstance and terminal stance, creating calluses under the second and third metatarsal heads.

When Plantar Keratosis Is A Dermatological Condition
Plantar keratoses can also have a variety of dermatological etiologies (see the table “An Overview Of Generalized Dermatological Lesion Etiologies” at right).7-10 Some of the more common dermatological etiologies for plantar keratoses include plantar verrucae, palmoplantar psoriasis, pitted keratolysis, keratoderma climactericum (Haxthausen’s disease) and keratosis punctata palmaris et plantaris.

Plantar verrucae. Plantar verrucae are among the most common dermatological plantar keratoses. These lesions may present as solitary or grouped. Clinicians often misdiagnose these lesions as hyperkeratotic lesions. Mechanical debridement is important to allow for physical examination and diagnosis. Key physical exam findings for plantar verrucae include overlying hyperkeratosis, pain with lateral compression, encapsulated rete pegs, pinpoint bleeding with debridement and the absence of skin lines. While there are numerous treatment options for verrucae ranging from blunt dissection, cryotherapy and Candida antigen to oral cimetidine, topical retinoids like adapalene, and occlusion, there have been mixed results.9,10

Palmoplantar psoriasis. This type often arises with chronic plaque psoriasis but can be unassociated with disease elsewhere. Varieties of palmoplantar psoriasis include guttate psoriasis and pustular psoriasis.

Guttate psoriasis appears as small, salmon-colored plaques on the trunk and extremities. The condition most often occurs in individuals younger than 30. Typically, the onset is sudden and, due to the extensive involvement, one should consider systemic drug eruption in the differential diagnosis. Spontaneous resolution is not uncommon several weeks after onset. Clinical expression varies, ranging from hyperkeratotic plaques to erythematous patches containing pustules. The condition may be most painful due to the location, which frequently impacts quality of life.

Therapy is difficult. Many cases of palmoplantar psoriasis fail to adequately respond to topical steroids, vitamin D analogues and retinoids. Alternative therapies include methotrexate, cyclosporine, acitretin (Soriatane, Stiefel Laboratories) and biologics such as etanercept (Enbrel, Amgen/ Pfizer) and adalimumab (Humira, AbbVie/Abbott Laboratories).11

Pustular psoriasis may appear as sterile pustules on the plantar foot and palm of the hand. The pustules are in essence microabscesses in varying stages of the lesion and are generally visible on localized areas of the skin. Once the pustules form, they evolve into an amber color and subsequently desquamate. Tinea pedis and pompholyx are part of the differential diagnosis.11

Pitted keratolysis. Also known as keratoma plantare sulcatum, pitted keratolysis, a superficial infection of the stratum corneum, is generally characterized by circular, pitted, punched-out indentations that primarily affect weightbearing regions. Three typical findings include hyperhidrosis, maceration and foul odor. Various strains of keratinase secreting bacteria, including Corynebacterium, colonize the skin and are responsible for pitted keratolysis. This condition most commonly affects physically active individuals who wear boots and athletic shoes. This is due to the bacteria, which thrive in a warm, sweaty environment.

Keratoderma climactericum (Haxthausen’s disease). This condition often presents as painful cracking and fissuring of the plantar heel as well as the palms. Clinicians often see this condition spread from the plantar heel to the sides of the foot. This condition mainly affects postmenopausal females and can be painful. It is associated with other general conditions of obesity, arthritis and hypertension (most common after menopause and/or hysterectomy). When severe, this fissuring often interferes with ambulation. Treatment consists of keratolytic and emollient topical agents to decrease the thickness of the skin and improve the epidermal skin barrier. Oral retinoids have induced remission.9  

Keratosis punctata palmaris et plantaris. This condition is most commonly inherited in an autosomal dominant manner with variable penetrance. The majority of cases usually manifest after the age of 20. Patients may complain of pruritus, discomfort or cosmetic disfigurement. There is no cure and we have yet to identify the specific genes. One can manage these patients. Mechanical debridement is a mainstay of treatment.

Final Words
Utilizing the basics of history and physical examination, clinicians can subsequently categorize the plantar keratosis as either a biomechanical or dermatological lesion in order to ensure appropriate treatment. Determining whether the etiology is biomechanical or dermatological in nature is critical to long-term successful patient outcomes.

Dr. DeHeer is a Fellow of the American College of Foot and Ankle Surgeons, and a Diplomate of the American Board of Podiatric Surgery. He is also a team podiatrist for the Indiana Pacers and the Indiana Fever. Dr. DeHeer is in private practice with various offices in Indianapolis and is the founder of Step by Step Haiti.

Dr. Leshikar is a second-year resident at St. Vincent Hospital in Indianapolis.

Dr. Patel is a first-year resident at St. Vincent’s Hospital in Indianapolis.

References

  1.     Coughlin MJ, Saltzman CL, Anderson RB, Mann RA. Mann’s Surgery of the Foot and Ankle, Volume 1, Ninth Edition, Saunders/Elsevier, Philadelphia, 2014.
  2.     Charles J, Scutter SD, Buckley J. Static ankle joint equinus: toward a standard definition and diagnosis. J Am Podiatr Med Assoc. 2012; 100(3):195-203
  3.     Aronow MS, Diaz-Doran V, Sullivan RJ, et al. The effect of triceps surae contracture force on plantar foot pressure distribution. Foot Ankle Int. 2006;27(1):43-52.
  4.     Johnson CH, Christensen JC. Biomechanics of the first ray part V: The effect of equinus deformity. A 3-dimensional kinematic study on a cadaver model. J Foot Ankle Surg. 2005; 44(2):114-20.
  5.     Franco AH. Pes cavus and pes planus. Analyses and treatment. Phys Ther. May; 67(5):688-94.
  6.     Louwerens JW, Schrier JC. Rheumatoid forefoot deformity: Pathophysiology, evaluation and operative treatment options. Int Orthoped. 2013;37(9):1719-1729.
  7.     Dockery GL. Cutaneous Disorders of the Lower Extremity. Saunders, Philadelphia, 1997, pp. 133-159;185-200.
  8.     Schleicher SM, Vlahovic TC. Skin Disease of the Lower Extremities: A Photographic Guide. HMP Communications, Malvern, PA, 2012, pp. 44-45.
  9.     Weber C, Hoffman K. How to treat recalcitrant plantar warts. Podiatry Today. 2013; 26(7):68-73.
  10.     Vlahovic T. Using a topical acne medication off-label for plantar warts. Podiatry Today. http://www.podiatrytoday.com/blogged/using-topical-acne-medication-label-plantar-warts . Published April 1, 2015.
  11.     Menter A, Gottlieb A, Feldman SR, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol. 2008;58(5):826-50.
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Patrick A. DeHeer, DPM, FACFAS, Aaron J. Leshikar, DPM, and Shrunjay Patel, DPM
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