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The feet actively supporting the rest of the body, tend to be covered up all day. Thereby restricting the follow of air that helps reduce sweat and decrease bacteria activity on the feet. Which can cause the feet to smell worse than other parts of the body. Smelly feet and foot odour can become problematic and if not treated accordingly leads to not only embarrassing moment, but affect your self confidence and freedom to wiggle those feet of yours
At one point in time we all tend to sweat and perspire on the feet due to several reasons like those listed below. When these sweat itself can not evaporate then it leads to smell or stinking feet. This is usually caused by skin bacteria breakdown and secretes. Fungal infection, such as Athletes’ feet and other factors listed below can cause foot odour.
To help prevent this condition of smelly feet or foot odour at the office, during sport practice, at your loved ones home or just simply stretching your feet out at garden or when having a picnic at the park. Dr. Babajide Ogunlana has a few tips:
Condition that can lead to such foot odour and smelly foot are;
The authors of a recent study suggest that patients with some dermatologic diseases, such as superficial fungal infections and psoriasis, may be at higher risk for the COVID-19 virus, due to a possible similarity between cutaneous and mucosal immunity.
In the study, published by Dermatologic Therapy, researchers assessed dermatological comorbidities of 93 patients with the COVID-19 virus. They found that the most common skin conditions in this patient cohort in the past three years were superficial fungal infections (25.8 percent), seborrheic dermatitis (11.8 percent), actinic keratosis (10.8 percent), psoriasis (6.5 percent) and eczema (6.5 percent).
In addition, 17 of the patients in the study also presented to the dermatology clinic in the last three months. Among this subcohort, the most common dermatological conditions included superficial fungal infections (25 percent), psoriasis (20 percent) and viral skin diseases (15 percent).
Tracey Vlahovic, DPM, FFPM, RCPS (Glasg), says the study authors have made broad assumptions and do not mention other comorbidities or contributing factors. She adds that the study is also problematic since it combines groups receiving topical and systemic/biologic therapy, and suggests that both groups are at risk. Dr. Vlahovic, who is board-certified by the American Board of Foot and Ankle Surgery, recommends monitoring the National Psoriasis Foundation and the International Psoriasis Council websites for guidance.
“The National Psoriasis Foundation recommends those who are on systemic and/or biologic therapy should remain on therapy unless they develop a COVID-19 infection. Patients who have other comorbidities should speak with their physicians regarding staying on their current treatment or changing it,” maintains Dr. Vlahovic, an Associate Professor in the Department of Podiatric Medicine at the Temple University School of Podiatric Medicine.
Joel Morse, DPM agrees that the premise that those with fungal infections or inflammatory skin disease are more likely to contract COVID-19 is suspect.
He wonders if major comorbid conditions such as diabetes could be contributing to an increased risk of developing the COVID-19 virus. Can the virus move through the skin if the stratum corneum is compromised? These are important questions to consider, says Dr. Morse, a Past President of the American Society for Foot and Ankle Dermatology.
Annette Joyce, DPM concurs that this study has limitations including: a small sample size; lack of specificity as to the location and type of fungal infections involved; and failure to link immunosuppression specifically to these superficial fungal infections.
“Fungal infections of the nails and skin are harder to treat in some patients due to immune system phenotype,” says Dr. Joyce, the Medical Conference Chair for the DERMfoot conference.
Dr. Joyce also notes that organ-specific immune response in the evolving knowledge of antifungal immunity could play a role in future immune-based COVID-19 therapies, but there are still so many unknowns.
Dr. Morse advocates for investigation of other viruses in patients with skin disease, and whether this heightens the risk for infection.
“When someone is in the hospital with COVID-19 life- and limb-threatening issues, we are probably not looking for tinea pedis or scaling on the elbow … but maybe we should,” suggests Dr. Morse, who is board-certified by the American Board of Foot and Ankle Surgery.
Regardless of the degree of plantar plate injury, adding a plantar plate repair to a shortening second metatarsal osteotomy may improve outcomes, according to a recent study published in the Journal of Foot and Ankle Surgery.
In a prospective study, the authors evaluated 86 adult patients who had second metatarsal Weil osteotomies with and without concomitant plantar plate repair for sub-second metatarsal head pain over a 3.5-year period, and followed them for one year. Patients in the group who had a plantar plate repair with their second metatarsal osteotomy showed better foot-specific quality of life and pain scores at one year despite this group having more severe baseline injuries to the plantar plate. Researchers noted no difference in pre- or postoperative radiographic parabolas, second toe alignment or complication rates between the two groups.
Adam Fleischer, DPM, MPH, FACFAS, the lead author on the study, shares that after successful plantar plate repair from a dorsal approach, he observes patients are less “aware” of their previous foot ailment, which correlates with a higher level of confidence and higher quality of life scores.
Erin Klein, DPM, MS, AACFAS, a co-author of the study, finds in her practice that repairing the plantar plate helps with stability of the MPJ as well as pain.
Dr. Fleischer notes that in his experience, magnetic resonance imaging (MRI) and ultrasound both correlate closely with intraoperative evaluation of the extent of plantar plate injury, which he finds helpful during operative repair.
Dr. Klein agrees. She elaborates that a special MRI protocol with 0.2 to 0.3 mm slices through the metatarsal head/plantar plate region will help the surgeon understand the pathology much better.
“Correcting instability by repairing the plantar plate and then addressing the deforming osseous force (metatarsal length) provides pain relief and improved function postoperatively,” explains Dr. Klein.
Lowell Weil, Jr., DPM, MBA, FACFAS, a co-author of the study, emphasizes the clear necessity to address and correct metatarsal length.
“The plantar plate is a truly important structure that one should repair appropriately when pathology is present,” notes Dr. Weil, CEO of the Weil Foot and Ankle Institute. “Doing this combined procedure yields the highest level results in our research.”
“If patients demonstrate clinical instability of the lesser metatarsophalangeal joint and require a Weil osteotomy, (I recommend) a low threshold for anatomic repair of the plantar plate,” says Dr. Fleischer, who likens it to mechanical instability of the lateral ankle, which benefits from imbrication and advancement of the native tissues.
What organisms might one expect to see upon bone biopsy in cases of osteomyelitis? A new study in the Journal of Foot and Ankle Surgery takes a closer look at patterns that may help in prescribing effective antibiotics.
Reviewing two random cohorts of 151 patients each in 2005 and 2010, the authors examined demographics, comorbidities, microorganisms found on bone biopsy and culture, location and pre-biopsy antibiotic use. Gram-positive bacteria, specifically methicillin-sensitive Staphyloccus aureus (MSSA), was most common in both groups. However, methicillin-resistant Staphyloccus aureus (MRSA) decreased from a prevalence of 28.3 percent to 10.6 percent from 2005 to 2010. The most common gram-negative bacteria was the Pseudomonas species and patients with peripheral vascular disease exhibited a higher incidence.
Mitzi Williams, DPM, FACFAS, one of the authors on the study, was not surprised by the results as they align with her clinical experience.
Regarding the reduction in MRSA between 2005 and 2010, Dr. Williams personally feels the reason is multifactorial and could include antibiotic stewardship and striving to minimize admissions and returns to the operating room.
Windy Cole, DPM agrees that the findings correlate with her clinical practice. She adds that S. aureus is readily found in the environment as well as the normal skin flora of healthy individuals.
“It is when the bacteria enter into the deep tissues or bloodstream that potentially serious infections can occur,” explains Dr. Cole, the Director of Wound Care Research at Kent State University College of Podiatric Medicine.
MRSA infection reduction could also be attributed to better hygiene, sterilization and cleaning techniques in the hospital setting and the community, adds Dr. Cole.
Dr. Williams also feels podiatrists approach amputations in a way that prevents future infection.
“We recognize that removal of a central ray will likely result in a transfer lesion and may subsequently become infected,” notes Dr. Williams. “Hence, we do not simply remove what is infected. We perform a functional amputation, which carries lower long-term risks.”
Dr. Cole adds that bone biopsies and deep tissue cultures are the foremost way to isolate pathogenic bacteria and form the best treatment plan.
Currently, empiric antibiotic use should cover MSSA, says Dr. Williams, a Diplomate of the American Board of Foot and Ankle Surgery. Careful analysis for a history of MRSA, chronic ulcerations or a finding of liquefactive necrosis may lead one to redirect empiric therapy. She adds that one should choose empiric antibiotics based on the most likely organism(s) involved.
After 20 years in practice, I have found that one of the more complicated issues is the treatment of lesser metatarsophalangeal joint (MPJ) instability. The MPJ is a very complicated joint, which is connected by collateral ligaments and pulled on by multiple external and internal foot tendons. All of these can cause strain on the joint and be sources of deformity and pain.
A common problem causing instability of the lesser MPJ is a plantar plate injury. Overall, there have been significant advances over the years in repairing the plantar plate but correcting hammertoes with complicated MPJ instability continues to be challenging.
It is essential to listen closely to patients in order to understand their concerns and needs. Not every patient needs surgery or has pain that requires extensive repair. Most patients are more concerned initially with the new and worsening pain under the metatarsal head. They will sometimes note their toe is starting to shift. Patients with more long-standing pain will often have a more severe shift of the toe and even a crossover toe syndrome (most commonly the second toe crossing over the great toe). Overall, it is vital to understand what the patient expects. A stiff but straight toe after an arthrodesis may not be what the patient needs.
Most commonly, the patient wants to be pain-free and perform his or her normal activities. However, in addition to concerns about pain and toe position, one needs to ask more subtle, specific questions of the patient. Does the patient have difficulty in all shoes or just a certain type? What activities does the patient prefer and does a stiff toe preclude that activity? These questions will ultimately help with treatment selection.
The physical examination also needs to be fairly detailed. When a dorsal drawer test reveals instability of the toe, this is a sign that the plantar plate is lax or partially torn. However, we need to ascertain more information to inform our treatment plan. Is there a tendon imbalance? Is there more weakness on one side of the toe versus the other, suggesting only a partial plantar plate tear? What is the level and rigidity of the digital contracture? Is the metatarsal head very prominent? Finally, is there a bunion deformity, causing overloading of the second MPJ?
Diagnostically, standard radiographs are a good start. The goal is to see the general position of the foot and bone architecture. Furthermore, metatarsus adductus and the level of toe deviation are also important factors along with the size and extent of any present bunion deformity.
If surgical intervention is a consideration, obtaining a magnetic resonance imaging (MRI) study of the foot can help the surgeon assess the level of plantar plate tear, check for a neuroma and also ensure the articular surfaces are not badly damaged. Plantar plate damage can be subtle. The surgeon should interpret the MRI as well, not just the radiologist. Get to know your radiologist and explain what you are looking for as the radiologist may not know what you suspect or be as familiar with the intricacies of the plantar plate.
Unless the patient has significant deformity, one should first attempt non-surgical care. For acute pain less than three months in duration, patients may respond to plantarflexory strapping of the toe and the use of a stiff shoe or boot to prevent strain. Physical therapy and oral steroids are also options. I do not recommend using a steroid injection as this can cause further damage and rupture to the plantar plate.
When it comes to more chronic and non-inflammatory pain that is greater than three months in duration, I prefer to add a platelet-rich plasma (PRP) or amniotic injection to the region to increase healing potential. Anecdotally, I have found this to be successful in early cases. Clinicians must convey to patients that strapping, the use of a boot or injection treatments will not correct the toe position. Again, this is why it is critical to understand the patient’s needs and expectations.
For many older or sedentary patients, fitting into shoes is impossible due to severe toe contracture. Strapping alone may improve this. For patients in this population who have a severe bunion and medially deviated third toe with a dislocated second toe, one might consider a second toe amputation.
As I noted above, there have been significant advances in surgical repair of the plantar plate. The question is what works and what does not. I have experience with many systems, plantar and dorsal approaches, all with or without osteotomy or hammertoe correction.
The hammertoe contracture is an important deforming force. Correction of the hammertoe increases the plantar strength of the flexor tendons and helps with relocation of the toe. If there is a severe dorsal contracture, an extensor lengthening can help relax the dorsal strain. It is important to remember that if the toe is medially deviated as well, one must not neglect this during hammertoe correction. During my procedures, I prefer to preserve the length of the proximal interphalangeal joint (PIPJ) length and not use a saw. I primarily employ a cup and cone technique with a rongeur, and do subsequent rounding with a burr. I also try to keep the joint fairly tight but still maintain reducibility at the PIPJ so there is less gapping at final reduction.
My preferred implant is the Hammertoe Fixation System (Ossio), which is made out of a natural fiber material that incorporates easily into bone. There is no absorption and the material has a sticky quality, which keeps the bones from separating. It is also trimmable, allowing one to reduce length if the intermediate phalanx is smaller. Surgeons can also cut through this implant in case of revision or conversion to an arthroplasty. The implant can also go through an MRI without signal. I no longer use metal in my hammertoes as it is mainly intramedullary and is very difficult to remove without severe damage to the toe.
When correcting the MPJ, one must consider the stability of the joint, the amount of medial deviation, partial versus complete plantar plate tears and the amount of time that has passed since complete dislocation. The MRI and exam should help with decision making.
I divide my cases into mild, moderate and severe dislocations. A mild dislocation is a somewhat unstable joint with a very mild medial shift of the toe and very little dorsal contraction. A moderate case is one with a fairly lax joint on a dorsal drawer test and enough medial deviation that the great toe and second toe are touching or mildly overlapping. A severe case has significant medial deviation with crossover of the second toe or a complete plantar plate tear and dislocation at the MPJ. Each of these categories has some overlap so be prepared to treat and classify in a fluid fashion.
A metatarsal osteotomy and a possible extensor lengthening are often applicable in mild cases. I try to avoid a tenotomy because transfer of strain to the other digits may cause them to contract over time. I find extensor lengthening to be far better. The biggest pearl for my metatarsal osteotomies is to shift the metatarsal medially and shift the toe laterally, much like a bunion correction. I will, at times, imbricate the lateral capsule and collateral ligament for mild cases. In these instances, there is very minimal plantar plate tear and therefore, I find no need to repair it. It will heal during the post-surgical period and there is less stiffness of the joint without repair.
Moderate cases require plantar plate repair. Performing a metatarsal osteotomy shifts the metatarsal medially to help with repositioning the toe. One should examine and repair the plantar plate prior to repair of the metatarsal. A majority of plantar plate tears are lateral or central-lateral. I do not free up the entire plantar plate as I find this causes a great deal of scar tissue. I prefer to release the lateral plantar plate in the region of the tear, remove a triangular wedge and then utilize one of the plantar plate repair systems.
My system of choice currently is the Hat-Trick Lesser Toe Repair System (Smith & Nephew). I utilize the full repair system and pass two sutures, one on the medial side of the repair site and one on the lateral edge. I pass these two sutures through one or two holes, and hold them in place with PEEK interference fixation. More often than not, I use a single hole from lateral to medial and pass the sutures through that hole with one interference pin to stabilize the joint. The Hat-Trick system provides me with better correction of the medial deviation and less scarring. It is very rare for me to perform a flexor tendon transfer for a moderate case but I suggest being comfortable with it in case of poor plantar plate quality or if damage is apparent during repair.
A severe case either has a great deal of medial deviation or dislocation. In such cases, I find the plantar plate is either very poor quality or non-existent. For these patients, I now perform a flexor tendon transfer as I find it far more reproducible and successful in stabilizing a severe joint shift. I harvest the flexor tendon at the PIPJ prior to performing my hammertoe fusion. One then splits the tendon and pulls it medially and laterally along the proximal phalanx to the base of the toe on either side. The surgeon should place the tendon directly against the bone in order to avoid neurovascular damage before tensioning it and placing a single temporary stitch to hold it.
One subsequently positions and stabilizes the metatarsal in the osteotomy region. Holding the toe in position, the surgeon crosses the tendon ends over each other and adjusts tension on each side until the toe is stable and well-positioned at the MPJ. I use a 3-0 taper needle to place three double-pass stitches through the tendon to stabilize it. Then I tie the end sitting on the lateral side of the toe to the MPJ lateral capsule for additional stability and fine-tuning of the crossover toe correction. I do not use a K-wire across the MPJ and prefer to strap the toe with dressings for stability. You may have the patient begin MPJ range of motion at week two or three to prevent scar formation and joint stiffness.
A metatarsal osteotomy is usually, if not always, necessary as are hammertoe correction and extensor tendon lengthening. One may employ strapping and dressings to facilitate stabilization until suture removal. After removing the sutures, a toe strap should suffice. I like the Darco TAS Toe Alignment Splint (Darco) as it is very solid, can also incorporate a bunion splint and has an elastic band around the midfoot that decreases edema. However, any splint that prevents toe dorsiflexion is okay.
About 20 percent of patients will still have a floating toe at three to six months postoperatively and will require an in-office tenotomy and capsulotomy of the MPJ to reduce dorsal scarring and contracture. These procedures have proven to be very good adjuncts in my patients.
I find flexor tendon transfers rarely result in a floating toe but there is a bit more stiffness. As I noted above, one can have patients initiate gentle and stabilized range of motion of the MPJ with practicing of grip strength of the MPJ. Range of motion can be more aggressive in weekly increments with physical therapy highly recommended. Wrapping the toe with a Coban wrap for two to three months is essential to avoid swelling. A Coban wrap for the midfoot is helpful but far less important than it is for the toe.
Proper planning and a solid understanding of different surgical options will make plantar plate and hammertoe repairs gratifying and fairly reproducible treatments for patients. Although plantar plate repair can be difficult, it is important for the surgeon to have a comprehensive mastery of options as one procedure does not fit every patient case.
Dr. Baravarian is an Assistant Clinical Professor at the UCLA School of Medicine. He is the Director and Fellowship Director at the University Foot and Ankle Institute in Los Angeles (https://www.footankleinstitute.com/podiatrist/dr-bob-baravarian).
Dr. Baravarian has disclosed that he is a consultant for CrossRoads Extremity Systems and OSSIO.
Given the common nature of xerotic skin disorders as well as the varied array of etiologies and treatments, these authors offer a thorough review of the literature on conditions ranging from ichthyosis and atopic dermatitis to venous stasis dermatitis and asteatotic dermatitis.
Xerosis is a very common skin disorder characterized by excessively dry skin. Other terms for this disorder include xerosis cutis and xeroderma. Xerosis can be a primary pathology associated with loss of the normal water content of the epidermis. Xerotic skin can also occur secondary to associated skin disorders and systemic disease. Underlying all xerotic skin disorders is excess water loss from the epidermis.
Skin requires a water content of 10 to 15 percent to remain intact and maintain normal function.1 Three main deficiencies in the skin lead to the development of xerosis including deficiency in natural moisturizing factors; deficiency in the skin lipids or ceramides; and deficiency in moisture in the epidermis that is mediated by aquaporin water channels.2-7 Natural moisturizing factors are isolated to the stratum corneum in high concentration in the corneocytes. These factors consist of amino acids and their derivatives including lactate, urea and inorganic salts.2 Lipids in the stratum corneum modulate water loss. Deficiencies of these cutaneous lipids can increase epidermal water loss up to 75 times that of normal skin.8
Ceramides are the main lipids in the stratum corneum. Numerous risk factors contribute to loss of cutaneous lipids and predispose individuals to develop xerotic skin disorders. This may include decreased sebaceous and sweat gland activity associated with aging; anti-androgen therapy, which decreases sebum production; exposure to degreasing agents including soaps and solvents; and exposure to dry environments.
Xerosis has variable presentation depending on its severity. Mild xerosis can exhibit accentuation of skin lines and resemble the appearance of cracked porcelain due to epidermal water loss. Xerosis affects the normal desquamation process of the epidermis, leading to the development of thin flakes on the skin surface. With more severe xerosis, one will see pruritic, dry, cracked and fissured skin. Severe xerosis can produce an inflammatory dermatitis with localized erythema and edema. Clinicians may note xerotic skin on numerous areas of the body including the lower extremity, upper extremity, abdomen and face.
Patients of increased age are at significantly higher risk of developing xerotic skin disorders.9 Sebaceous gland activity decreases significantly after 70 years of age in women and 80 years of age in men.10 Sweat gland function also declines with age.11 Skin thickness decreases with age, leading to increased water loss from the skin to the environment.12 Environmental factors are also significant risk factors for the development of xerosis. In winter months when humidity decreases, xerosis occurs much more frequently. Xerotic skin disorders are more common in dry climates with low humidity.
Basic treatment for all xerotic skin disorders aims to minimize cutaneous water loss. Lazar and Lazar identified the following methods to prevent water loss and lubricate the skin:
• reduce the frequency of bathing, showering and skin cleansing;
• increase room humidity;
• limit exposure to soaps, detergents, solvents and water;
• avoid friction from washcloths, clothing and other abrasives; and
• use emollients frequently.13
Moisturizers are a mainstay in the treatment of xerotic skin. The skin contains natural moisturizers including ceramides, glycerol, urea and lactic acid. Many moisturizers contain these elements aiming to supplement these natural moisturizing agents. Skin care products that both improve skin hydration and improve barrier function are wise choices. Specific products should contain both rehydrating and lipid-restoring components. Urea has the largest body of evidence for the treatment of xerosis.14 Combining urea with moisturizing agents and ceramides can improve its effectiveness.
Aiming to address multiple key deficiencies in skin hydration, Weber and colleagues formulated a topical formulation containing glyceryl glucoside, natural moisturizing factors and ceramide, and found it to be an effective treatment modality for xerosis.15
Asteatotic dermatitis is an inflammatory dermatitis secondary to severely xerotic skin. Other terms for this disorder include xerotic dermatitis, xerotic eczema and eczema craquelé. Asteatotic dermatitis most commonly occurs in elderly people with underlying xerosis.
Asteatotic dermatitis can be generalized or localized. Generalized disease is often associated with underlying systemic disease. Localized forms most commonly occur on the pretibial areas. Patients with asteatotic dermatitis exhibit dry, cracked and polygonal fissured skin with scaling and pruritis. Secondary erythema, edema and excoriations can develop from scratching. Fissures with superficial bleeding can occur when the skin develops cracks deep enough to damage dermal capillaries.
Known as “winter itch,” asteatotic dermatitis most commonly occurs in the winter months when environmental humidity is the lowest. Asteatotic dermatitis is prevalent in the elderly due to decreased sebaceous and sweat gland activity associated with aging. Aside from climate and age, certain medications, including diuretics, retinoids and protein kinase inhibitors, can also contribute to the development of asteatotic dermatitis.16
In addition to the preventative skin care recommended by Lazar and Lazar, topical steroid ointments under occlusion and Unna boots are treatment options for asteatotic eczema.13,17 Topical calcineurin inhibitors, including pimecrolimus and tacrolimus cream, show efficacy in the treatment of asteatotic dermatitis.18 Recently, endogenous phospholipids, N-palmitoylethanolamine and N-acetylethanolamine, that are part of the endocannabinoid system have proven to be effective treatments for asteatotic dermatitis with efficacy superior to traditional emollients.19
Ichthyosis is a group of skin disorders characterized by excessive dry, scaling skin. The name for this disorder comes from the Greek word, ichthys, meaning fish, since this disorder is known for its xerotic scales. Both inherited and acquired forms of ichthyosis exist with the most common form being ichthyosis vulgaris, an inherited autosomal-dominant disorder that commonly begins in childhood.20 Patients with ichthyosis vulgaris have xerotic skin with fine white scales. Scaling is most common on the extensor surfaces of the extremities. Acquired ichthyosis typically occurs in adults and is associated with medications that inhibit sterol synthesis in epidermal cells (nicotinic acid) or underlying systemic diseases including Hodgkin’s lymphoma, leukemia, sarcoidosis, human immunodeficiency virus (HIV), hypothyroidism, hepatitis, malabsorption and bone marrow transplantation.21 Acquired ichthyosis appears as small white scales on the extremities.
Clinicians may treat ichthyosis with topical creams and emollients to hydrate the skin and keratolytics to remove scales.
Creams containing a high percentage of urea or lactic acid can be very effective treatment options for ichthyosis.22 Oral retinoids such as acitretin (Soriatane) and isotretinoin have a general anti-keratinizing effect, and the literature suggests effectiveness in the treatment of more severe cases of ichthyosis.20
Atopic dermatitis is an inflammatory skin disorder, which is often associated with xerotic skin. This disorder presents as dry, itchy, red, swollen and cracked skin. There is often serous drainage and the presentation can vary with age. A total body distribution is more typical in infancy. For children, it is more common to see atopic dermatitis in the back of the knees and the front of the elbows. The feet and hands are the most common sites in adults.
Frequently, atopic dermatitis is associated with allergies and asthma. Several factors are thought to contribute to the development of atopic dermatitis including genetics, immune system dysfunction, environmental triggers and disruption of skin permeability. Dry skin secondary to dry climate, frequent washing and harsh chemicals increases the risk of developing atopic dermatitis.23
Treatment of atopic dermatitis varies based on the severity of the disease. Basic treatment involves avoiding aggravating environments and keeping the skin moist with moisturizers and emollients.24 Mild to moderate disease may respond to topical corticosteroids.25 Oral corticosteroids and calcineurin inhibitors are applicable for the treatment of more severe and resistant cases.23,26-28
Venous stasis dermatitis is a common inflammatory disorder affecting the skin of the lower extremities. It is frequently one of the first manifestations of chronic venous insufficiency, when retrograde blood flow through incompetent valves leads to venous hypertension and the eventual extravasation of red blood cells and ferric iron into dermal tissues. Dermal tissue changes results both directly from venous hypertension and from an inflammatory process mediated by metalloproteinases that are upregulated by ferric iron in extravasated red blood cells.29
Stasis dermatitis appears as erythematous, scaling, eczematous patches on the lower extremity. The medial ankle is the most common site, owing to its relatively poor blood supply. Skin lesions can vary in distribution from small patches to areas encompassing the entire lower leg below the knee and involving the dorsal foot. Long-standing skin lesions can present with lichenification and hyperpigmentation. Additionally, chronic venous insufficiency and hypertension can lead to skin induration and progression to lipodermatosclerosis.30
The treatment of stasis dermatitis involves management of the underlying venous insufficiency and edema. One typically treats this condition through compression therapy.29 Xerotic skin in areas of quiescent dermatitis often responds to emollients and moisturizers. Mid-potency topical steroids are applicable for short durations in the management of acute inflammation and pruritus. Long-term and high-potency topical corticosteroids are not desirable as they can lead to steroid-induced cutaneous atrophy, which can increase the risk of developing venous skin ulcerations.31,32
While topical calcineurin inhibitors are only approved for the treatment of atopic dermatitis, they are reportedly effective treatment modalities for many inflammatory skin disorders including stasis dermatitis.33,34 Tacrolimus has specifically proven effective in the treatment of stasis dermatitis.35 Maroo and colleagues found a combination of topical tacrolimus and oral doxycycline to be effective for stasis dermatitis.36
What Is The Relationship Between Systemic Disease And Xerotic Skin?
Several systemic diseases can cause xerosis and the workup of xerotic skin changes should include consideration of underlying systemic disease. Disorders including diabetes mellitus, thyroid disease and severe renal disease are frequently associated with xerotic skin. Treatment of xerosis secondary to systemic disease typically involves management of the underlying disease state as well as symptomatic management.
It is common to observe xerotic skin in patients with diabetes mellitus. Dry skin has the potential to fissure, increasing the risk of foot ulceration and infection in patients with diabetes mellitus.37,38
The nervous system plays an important role in maintaining adequate skin hydration. Diabetic polyneuropathy affects small sympathetic nerves, resulting in atrophy of sweat glands and decreased sudomotor response.39-42
Additionally, microcirculatory disease in patients with diabetes can lead to dry, rough, atrophic skin. Namgoong and team specifically examined the effect of peripheral neuropathy and microangiopathy on skin hydration in the feet of patients with diabetes mellitus.43 These researchers found a significant correlation between skin hydration and microvascularity, but no significant correlation between skin hydration and peripheral nerve function.
Hypothyroidism is a disorder of the endocrine system in which the thyroid gland fails to produce adequate amounts of thyroid hormone. Thyroid dysfunction is more common in women and people over the age of 60. This underproduction of thyroid hormones decreases the activity of the sweat glands, resulting in dry, xerotic skin.44 Skin changes in hypothyroidism include coarse, thin, scaly skin.45 The prevailing theory is that reduction of thyroid hormone alters sterol synthesis in epidermal keratinocytes, leading to xerotic skin changes.46 Treatment of hypothyroid-associated skin changes involves treatment of the underlying endocrine disorder with thyroid hormone supplementation.
Skin disorders are also extremely common in patients with chronic renal failure (CRF) and end-stage renal disease (ESRD).47 Xerosis is the most common skin disorder associated with renal disease, reportedly occurring in over 80 percent of patients with chronic renal failure.48 When it comes to the development of xerosis in chronic renal failure and ESRD, researchers have proposed several etiologies including decreased sweat production, decreased sebum production, reduced lipids in the skin surface, altered vitamin A metabolism, loss of or reduction in epidermal water content, and disruption of the integrity of the stratum corneum.49,50
In chronic renal failure and ESRD, reduced glomerular filtration rate leads to accumulation of waste products, including urea, creatinine, sodium, calcium, and phosphate, that are some of the main agents associated with the pathogenesis of skin disease in severe renal disease.51 Patients with severe xerosis secondary to renal disease can develop ichthyosis. Moisturizers with 5-10% urea cream or 2-3% salicylic acid are options for the treatment of uremic xerosis.49,52
Xerotic skin disorders are very common and have numerous etiologies including local and systemic disease. Both age and environmental factors play significant roles in the development of these disorders. Management of xerotic skin varies based on severity and pathology, and frequently involves management of environmental risk factors, emollients and moisturizers, and treatment of underlying disease states.
Dr. Hoffman is an Attending Physician in the Department of Orthopedics at Denver Health Medical Center. She is an Assistant Professor in the Department of Orthopedics at the University of Colorado School of Medicine. She is an Attending Physician for the Highland/Presbyterian St. Luke’s Medical Center Residency Program.
Dr. Jerabek is an Attending Physician in the Department of Orthopedics at Denver Health Medical Center. She is an Assistant Professor in the Department of Orthopedics at the University of Colorado School of Medicine.
1. Pons-Guiraud A. Dry skin in dermatology: a complex physiopathology. J Eur Acad Dermatol Venereol. 2007;21 Suppl 2:1-4.
2. Rawlings AV, Scott IR, Harding CR, Bowser PA. Stratum corneum moisturization at the molecular level. J Invest Dermatol. 1994;103(5):731- 741.
3. Rawlings AV, Harding CR. Moisturization and skin barrier function. Dermatol Ther. 2004;17 Suppl 1:43-48.
4. Jungersted JM, Hellgren LI, Jemec GB, Agner T. Lipids and skin barrier function–a clinical perspective. Contact Dermatitis. 2008;58(5):255- 262.
5. Elias PM, Feingold KR. Lipids and the epidermal water barrier: metabolism, regulation, and pathophysiology. Semin Dermatol. 1992;11(2):176-182.
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