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microscopy shows IgM, IgA, brinogen, and C3in the blood vessels causing vascular thickening [31].

Excess lipid deposition in the dermis has as a result the yellow appearance [32]. HGlut-1 (the human erythrocyte glucose transporter) is expressed by the broblasts in areas of sclerotic collagen from biopsies of patients with necrobiosis lipoidica [33]. The mainstay of treatment is currently steroids, either topical, intralesional, or rarely systemic. Steroids are cost-effective and have low side-effect proles. Other treatments include systemic cyclosporine or ticlopidine [34], CO2 laser therapy [35], and platelet-rich plasma [36]. Lesions may be excised with skin grafting, but patients with diabetes may be poor surgical candidates. Most recently, TNF-α antagonists, such as etanercept and iniximab, have been selected as possible therapies [37, 38].

Granuloma Annulare

Granuloma annulare (GA) is an idiopathic, benign, and asymptomatic granulomatous condition that is more frequently seen in women rather than men. The prevalence of granuloma annulare is estimated to be 0.1–0.4%, and the estimated incidence is 0.1–0.4%. Women are affected more commonly than men, and the disease can affect persons of any age. More than two-thirds of patients are 30years of age or younger (Figs. 12.7 and 12.8). The exact etiology and pathogenesis of GA remains unknown. Several mechanisms have been implicated in the pathogenesis of GA such as cell- mediated immunity, vasculitis, abnormalities in macrophage function, and primary collagen degeneration. Impaired neutrophil chemotaxis has been found in patients with granuloma annulare. Macrophages take over an inammatory site because of the impaired neutrophil response, which leads to the granulomatous inammation seen in granuloma annulare as opposed to a suppurative neutrophil type inammation. Some believe that granuloma annulare is caused by a delayed-type hypersensitivity reaction, more specically a Th1 reaction involving IFNgamma stimulating macrophages to release matrix metalloproteinases. This ultimately results in connective tissue degradation. Possible trigger factors include infections, sun light exposure, and the hepatitis B vaccine. Clinical subtypes include localized, subcutaneous, perforating, generalized, and papular GA.Only the generalized form shows consistent and signicant correlation with diabetes across most studies and 21–77% of patients with generalized GA have diabetes (predominantly type 2 diabetes) [39]. Generalized GA is an inammatory lesion that usu-

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Fig. 12.7 Granuloma annulare. A 40-year-old woman with T2DM (erythematous annular plaques)

Fig. 12.8 Granuloma annulare. A 38-year-old woman with T2DM (conuent erythematous plaques)

ally takes the form of multiple, small, rm, skin-colored or red dermal papules in an annular arrangement that tend to be found on the distal extremities. The skin lesions of GA are similar to necrobiosis lipoidica but GA does not exhibit epidermal atrophy and yellow discoloration. The histopathology shows lymphohistiocytic granulomatous inammation of the dermis and collagen degeneration (Figs.12.9,

12.10, and 12.11). Colloidal iron stain reveals abundant

deposition of mucin. The presence of mucin and the absence of plasma cells help to distinguish histologically GA from NL.Treatment is similar to NL.In addition to the therapy mentioned above, vitamin E, isotretinoin, tetracyclines, intralesional interferons, topical imiquimod, niacinamide,

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Fig. 12.9 Granuloma annulare. H&E shows necrobiotic granuloma surrounded by lymphocytes and histiocytes (×100)

Fig. 12.10 Granuloma annulare. H&E shows necrobiotic granuloma surrounded by lymphocytes and histiocytes (×100)

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oral calcitriol, dapsone, hydroxyurea, topical tacrolimus, clofazimine, and rifampin have been tried and reported to be effective in small studies.

Diabetic Bullae

Diabetic bullae (DB), or bullosis diabeticorum, is a rare, noninammatory, bullous disorder characterized by tense, painless, bullae that develop abruptly on normal-appearing skin, primarily on the dorsa and the sides of the lower legs and feet, and less often affecting the hand or forearm (Fig.12.12) [40]. The blisters are non-inammatory in nature and heal in several weeks without scarring. Blisters tend to be painless and nonpruritic. The etiology of blister formation is unclear, but is postulated to involve trauma, ultraviolet (UV) light exposure, hypoglycemia or highly uctuating blood glucose levels, an autoimmune condition, vascular insufciency, neuropathy, and changes in calcium or magnesium metabolism [41, 42]. The microscopic ndings are non- specic and the level of the bullae formation is variable. The bullae contain brin and occasional inammatory cells but in case of subepidermal bullae, the cavity is lled with blood. Immunouorescence is not reliable in establishing accurate diagnosis and only helps to exclude other bullae diseases. The differential diagnoses include bullous pemphigoid, porphyria, and pseudo-porphyria, which can be ruled out by submitting a biopsy of the lesion for direct and indirect immunouorescence [20]. Treatment of DB is focused on skin protection and preventing secondary infection. These lesions usually resolve without intervention within a matter of weeks. Uncomplicated blisters should be left intact, but sterile aspiration of uid may prevent rupture in some cases. Ulcerated blisters should be treated with aggressive wound management [43].

Fig. 12.11 Granuloma annulare. H&E (×200). Necrobiotic collagen matrix with mucin surrounded by lympho-histiocytic inltrates

Fig. 12.12 Diabetic bullae. (Reproduced From Pannu AK, Suryadevara V.Image Diagnosis: Bullosis Diabeticorum. The Permanente Journal. Perm J. 2019;23:19.042, with permission from The Permanente Federation. www.thepermanentejournal.org)

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Fig. 12.13 Diabetic dermopathy. Brownish batches and rough spots on shins. (Reproduced From Brzezinski P, Chiriac AE, Pinteala T, Foia L, Chiriac A (2015). Diabetic dermopathy (“shin spots”) and diabetic bullae (“bullosis diabeticorum”) at the same patient. Pak J Med Sci, 31(5):1275–1276. DOI: 10.12669/pjms.315.7521, PMID: 26649029, PMCID: PMC4641298)

Diabetic Dermopathy

Diabetic dermopathy (DD), also known as spotted leg syndrome, is the most common cutaneous nding in diabetic and seen in about 40% of diabetic patients [29, 44]. It is characterized by atrophic, hyperpigmented and irregularly shaped papules or plaques predominantly on the pretibial skin (Fig. 12.13). The lesions are asymptomatic and may persist indenitely or disappear without treatment. Diabetic dermopathy is a clinical diagnosis. The histopathology of the lesion is relatively non-specic, while the fully developed lesions show epidermal atrophy with a mild perivascular lymphohistiocytic inltrate and hemorrhage in papillary dermis. Dermal changes include broblastic proliferation, dermal edema, and thickening of the collagen bundles with fragmentation and separation [45]. Currently, there is no recommended medical intervention for DD because the lesions are asymptomatic and may resolve spontaneously. Treatment should take into consideration the possibility of a secondary infection. Patients with this ndings may be prone to other microangiopathic complications and coronary artery disease, because of their association with diabetic dermopathy [46].

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tive perforating collagenosis, (3) Kyrle’s disease, and (4) perforating folliculitis. APD is associated with diabetes, chronic renal failure and dialysis, or a combination of these factors [48–50]. These lesions appear as pruritic, hyperkeratotic, dome-shaped papules and nodules, often with central umbilication, mainly occurring on the extensor surface of the limbs, but also on the trunk, hands, and face. Histologically, transepidermal channels traverse an acanthotic epidermis and are lled with keratin, pyknotic nuclear debris, inammatory cells, elastin, and collagen depending on the nature of the underlying disease. They all share a common microscopic nding, which is the intaepidemal elimination of these substances. In elastosis perforans serpiginosa, altered elastic bers pass through channels from dermis to epidermis. The pathogenesis is not well understood, and it mainly includes minor skin trauma from scratching, manifestation of microangiopathy, metabolic disorders causing an epidermal or dermal alteration, and a deposition of some substances not removed by dialysis, which the immune system then treats as foreign [51]. APD in the setting of diabetes is relatively unresponsive to therapy, but may resolve slowly if trauma and scratching are avoided (Fig.12.14). Therefore, the key treatment strategy is the symptomotic relief of pruri-

Acquired Perforating Dermatosis

Acquired perforating dermatosis (APD) denes a group of chronic skin disorders characterized by transepidermal perforation and elimination of a dermal component of the skin [47]. This disorder is historically classied by the predominant dermal material identied microscopically such as keratin, collagen, or elastic tissue. Hence, APD can be divided into four types: (1) elastosis perforans serpiginosa, (2) reac-

Fig. 12.14 Perforating collagenosis. Skin surgical biopsy. H&E (×100) shows skin biopsy from the foot. Altered collagen is eliminated through epidermis into the thick keratin layer

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tus. Further treatments with benecial effects are reported, among these are topical keratolytics, topical and systemic retinoids, allopurinol, PUVA, UVB phototherapy, topical and intralesional injection of steroids, antibiotics (doxycycline), oral antihistamine, cryotherapy, and renal transplantation [47, 52, 53].

Diabetic Thick Skin

Diabetic patients often exhibit thickening of the skin caused by excessive accumulation of abnormal collagen. Clinically, thickened skin is divided in three distinct categories: (1) asymptomatic benign skin thickening; (2) scleroderma-like skin changes in the ngers with limited joint mobility, also known as diabetic hand syndrome or limited joint mobility syndrome; and (3) diabetic scleredema. Thickened skin is thought to be a manifestation of the abnormal glycosylation of collagen occurring in a hyperglycemic state, leading to increased cross-linking of collagen bers that become resistant to degradation by collagenase [54]. Others have suggested that excess insulin acting as a growth factor promotes collagen proliferation [55].

A scleroderma-like syndrome develops in 8–50% of diabetic patients. Skin on the dorsal part of the hand can thicken, resulting rst in stiffness of the metacarpophalangeal and proximal interphalangeal joints of the ngers [54]. Thickened skin on the ngers, known as Huntley’s papules or nger pebbles, appears as grouped indurate papules on the extensor surface of the ngers, knuckles, or periungual area. Decreased joint mobility is manifested as a limited ability for active extension, but later in the course of this syndrome, limited exion may occur. The literature suggests that diabetic hand syndrome is a cutaneous marker for the development of diabetes- related microvascular complications [54, 56].

Diabetic scleredema is a rare chronic connective tissue disorder primarily associated with type 2 diabetes. It consists of a dramatic increase in the thickness of the reticular dermis, initially on the face, and extends to the posterior neck and upper back. Diabetic scleredema is usually asymptomatic, but neck discomfort and back pain may occur, especially in more severe cases [57]. The affected skin is hard, thick, and indurated, sometimes erythematous, and may have a peau d’ orange appearance. Unequivocal diagnosis of scleredema by histologic examination requires a full thickness excisional biopsy to examine the dermis. Histologically, diabetic scleredema reveals a markedly thickened reticular dermis, increased mast cells, thick collagen bundles, and accumulated hyaluronic acid between the collagen bundles, and there is no sign of edema nor sclerosis [58]. The diagnosis is usually based on history and physical examination. Histologically special stains such as Alcian blue and Colloidal iron reveal interstitial mucin deposits in between

the collagen bundles. There is no highly effective treatment for diabetic scleredema. Therapies include potent intralesional glucocorticoids, low-dose methotrexate, and UV light phototherapy. Although strict glycemic control does not show consistent therapeutic benet in scleredema diabeticorum, it is proposed to be an effective preventive measure [59–61].

Eruptive Xanthomas

Eruptive xanthomatoses are rare and occur more often in patients with poorly controlled type 2 diabetes, characterized by a collection of lipids in the skin. They arise suddenly in groups of multiple yellow papules with surrounding erythema, commonly located on the extensor surfaces of the extremities and on the buttocks [62]. The histopathology shows an accumulation of lipid-laden histiocytic foam cells with a mixed inltrate of lymphocytes and neutrophils in the dermis (Fig.12.15). These lesions can be the rst sign of diabetes. The reason for the increased frequency of eruptive xanthomatosis among individuals with diabetes has been well characterized. Insulin is a stimulating factor critical to the normal activity of lipoprotein lipase; the insulin-decient state of insulin-dependent diabetes results in the decrease in lipoprotein lipase activity and then leads to an accumulation of serum triglycerides [63]. Occasionally, when the serum triglyceride level reaches 2000mg/dL, lipids will deposit in the skin [64]. Eruptive xanthomas are a cutaneous manifestation of the hyperlipidemic state, especially hypertriglyceridemia. Early identication of xanthomatosis can facilitate timely treatment and possible avoidance of more serious manifestations of hyperlipidemia such as atherosclerotic complications and pancreatitis. Systemic drugs that

Fig. 12.15 Eruptive xanthoma. H&E (×100) shows inltrates with foam histiocytes in dermis

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lower lipid levels aid in both resolving the lesions and preventing other complications of hyperlipidemia, such as coronary artery disease and pancreatitis [41, 57, 65].

Cutaneous Infections

Infections are one of the major skin disorders affecting patients with diabetes. The prevalence of cutaneous infections in diabetes mellitus (DM) reported in the literature, regardless of DM type, ranged from 20 to 61% [66, 67] (Fig.12.16). These include bacterial infections, candidiasis, dermatophytosis, and rare infections. Multiple factors in patients with diabetes increase the risk for skin infections: skin barrier disruption, sensory neuropathy, autonomic neuropathy, trauma, venous or arterial insufciency, immune system dysfunction, and uncontrolled hyperglycemia [68]. The infection rate is higher in type 1 versus type 2 diabetes, strongly related to blood glucose levels. Oxidative stress, as a result of mitochondrial destruction, blocks insulin, signaling pathways and releases inammatory cells and molecules,

such as proinammatory cytokines [68]. Prolonged effect of oxidative stress causes irreversible organ damage.

Bacterial Infections

Acute bacterial skin infections can cause high morbidity and mortality in patients with DM [69]. Bacterial overgrowth and invasion are facilitated by decreased skin barrier and poor vascularization (Fig. 12.17). Streptococcal and Fournier’s gangrene, rhino-cerebral mucormycosis, and synergistic necrotizing cellulitis with severe muscular involvement are most typical and severe infections occurring in patients [70]. Staphylococcus aureus (MRSA) is more prevalent in hospitalized patients [71]. Gram-negative bacilli (GNB), such as Escherichia coli and Pseudomonas aeruginosa, have also been detected in hospitalized patients, increasing the risk of mortality [72]. Moreover, GNB affect patients with necrotizing fasciitis, causing a life-threatening condition. Patients with diabetic foot are involved in highly resistant bacteria such as Acinetobacter, Bacillus, and Citrobacter. Other common skin lesions caused by bacteria are folliculitis, abscesses, and external ear canal infection, presented with otalgia, otorrhea, hearing loss, edema, and erythema.

Fig. 12.16 Erythema and pustules should raise the suspicion of skin infection. (This gure was published in Infect Dis Clin North Am, Vol number 35, Polk C, Sampson MM, Roshdy D, Davidson LE, Skin and Soft Tissue Infections in Patients with Diabetes Mellitus, 183–97, Copyright Elsevier (2021)) Fig. 12.17 Cellulitis l, swollen, erythematous skin

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Candida Infections

Candida albicans is the most common factor causing mucocutaneous candidiasis, presenting as white plaques with exudates and pustules. Other common presentations are candida vulvovaginitis, perianal candidiasis, angular cheilitis, intertrigo (infections of the skinfolds and erosio interdigitalis blastomycetica), nger web space infection, paronychia, and onychomycosis [57]. Patients with diabetic ketoacidosis may develop mucormycosis, an acute, severe soft-tissue infection, which is progressive and does not respond to systemic antifungals [57]. Rhinocerebral mucormycosis affects mainly patients with poorly controlled diabetes. Blood vessels are diffusely invaded by fungi (Phycomycetes) causing widespread necrosis, bony erosions, and cerebral abscesses.

Dermatophyte Infections

Tinea corporis, tinea pedis, and onychomycosis are frequent dermatophyte infections in DM [73]. Trichophyton rubrum, Trichophyton mentagrophytes, and Trichophyton tonsurans are the most common dermatophytes.

Clinical Evaluation ofSkin Infections

Skin symptoms and signs raising the suspicion of infections include erythema, tenderness, pain, warmth, or induration. Moreover, patients frequently present with purulent drainage, rash, boils, furuncles, or carbuncles [74]. When active cellulitis is present, all patients should be examined for edema, erythema, or purulent discharge. Depth of ulcerations, ulcer merging, and diabetic foot ulcers should be carefully evaluated to detect the possible underlying bone infection [75]. Patients with infections should be closely monitored for cardiovascular diseases as well, due to high incidence of bacteremia, endocarditis, and systemic manifestations from heart and lung [76]. Systemic inammatory response syndrome and septic shock can be seen in patients with supercial and deep infections. When fever and leukocytosis are present, disseminated infection should be considered in differential diagnosis. Serious complications include acute kidney injury, peripheral arterial disease, puncture, wounds, trauma, and progressive infection, despite antibiotic therapy [76]. The above mentioned infections can progress rapidly and require proper treatment, a multidisciplinary care team with surgeons and infectious disease physicians. Choice of antibiotic therapy depends on cultures and patient risks, factors for methicillin-resistant staphylococcus aureus, pseudomonas, and multidrug resistant organisms as well as severity and depth of infections.

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Biomechanics oftheDiabetic Foot:

https://t.me/med1917

TheRoad toFoot Ulceration

PanagiotisV.Tsaklis andNikolaosTentolouris

Abstract

Biomechanics is a branch of the life sciences for the study of the structure and function of biological systems including humans by means of the methods of mechanics. Biomechanics is clearly relevant to diabetic foot, since the majority of the feet injuries are related to the mechanical stress applied to the structures of the feet. Thus, callus is formed in the feet when increased pressure is applied for a prolonged period of time, an ulcer will not heal if there is no sufcient ofoading, and callus or ulcers will recur if there is no proper ofoading of the vulnerable areas of the feet. Knowing, therefore, the basic biomechanics of the foot is important for understanding the mechanism of development of ulcers, for organizing prevention methods, for the treatment of ulcers, and for prevention of relapses. For the biomechanical and functional evaluation of the diabetic foot and the general mobility of the person, there must be a holistic approach which include the morphological investigation of the foot; the mobility measurements (Range of Motion) of the foot joints; the recording and evaluation of the pressures around the plantar area and the weight distribution between legs (weight shift %); the Gait assessment and evaluation through kinematic and kinetic analysis of the movement of the foot and other body segments, like pelvis and trunk; and the assessment of the static and dynamic balance.

P. V. Tsaklis (*) Laboratory of Biomechanics and Ergonomics—@ErgoMechLab, Department of Physical Education and Sport Science, University of Thessaly, Trikala, Greece

Department of Molecular Medicine and Surgery, Growth and Metabolism, Karolinska Institute, Solna, Sweden e-mail: tsaklis@uth.gr

N. Tentolouris Department of Internal Medicine, Medical School, National and Kapodistrian University of Athens, Laiko General Hospital, Athens, Greece

Foot Anatomy andFunction Related toBiomechanics

The human foot is a complex and strong mechanical structure containing 26 bones, 33 joints, and more than a hundred muscles, tendons, and ligaments. The feet support the weight of the body, and provide support during standing and fulcrum during walking. One of the principal functions of the foot is its shock-absorbing capability during walking or running. Furthermore, the foot has the particularity of forming arches which help to t even on uneven surfaces [1].

The ankle joint is the major point for controlling sagittal plane movements of the leg relative to the foot, which is essential for bipedal ambulation [1]. Τhe subtalar joint allows move- ment three planes described as pronation (combination inversion abduction and dorsiexion) and supination (a combination of inversion, adduction, and plantar exion) [2, 3]. The midtarsal joint represents the functional articulation between the rearfoot and midfoot. The inter-relationship of the subtalar and midtarsal joint provides full pronation and supination motions throughout the foot. The rst metatarsophalangeal joint (MTPJ) incorporates the rst metatarsal head (MTH), the base of the proximal phalanx, and the superior surfaces of the medial and lateral sesamoid bones within a single joint capsule. The main motion of the rst MTPJ and the lesser MTPJs is in the sagittal plane (dorsiexion and plantar exion) (Fig.13.1).

During propulsion the body weight is moving forward over the hallux creating dorsiexion of the rst MTPJ. This occurs with the hallux planted rmly on the ground and with the heel lifting for propulsion. The force acting across the rst MTPJ approximates body weight, whereas the force across other MTPJs is considerably less [4]. Maximum loading of the rst MTH and hallux is practically at the same time during stance in normal gait, highlighting the importance of the load bearing function of both the hallux and rst MTH.

The gait or walking cycle is a repetitive pattern involving steps and strides. A step is one single step, a stride is a whole gait cycle. The step time is the time from one foot hitting the oor to the other foot hitting the oor. Step width can be

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P. V. Tsaklis and N. Tentolouris

Foot Joints

Ankle joint

Talonavicular joint

Metarsocunieform joint

Subtalar joint

Calcaneocuboid joint

First MP joint

Arches of the Foot

A-B Anterior Transverse Arch

B-C Lateral Longitudinal Arch A-C Medial Longitudinal Arch

Fig. 13.1 Foot anatomy—joints and arches

described as the mediolateral space between the two feet (Fig13.2a). The gait refer to a series of events which the leg experiences during ambulation. For analyzing gait cycle, one foot is taken as reference and the movements of the reference foot are studied. Each leg experiences its own gait pattern which consists of two main phases: the stance phase (68% of the cycle) and the swing phase (38% of the cycle) (Fig13.2b).

During gait, the foot is required to be unstable for shock absorption and to adapt to the terrain, whereas during the propulsive phase, the foot has to be stable to function as a lever. Foot exibility and rigidity are mainly controlled with pronation and supination of the subtalar and midtarsal joints. As subtalar joint pronation after heel strike is a major shock- absorbing mechanism, limited joint mobility (LJM) or structural abnormality could compromise exibility and shock absorption, thereby placing increased stress on the plantar skin surface [5,

6]. For example, LJM of the rst MTPJ is the commonest cause

of recurrent ulcers under the big toe. In addition, limited ankle dorsiexion could result in increased pressure on the forefoot, in particular during the late stance phase of gait, caused by an early heel rise or compensatory pronation [5, 7, 8].

Beyond the pressure applied to the foot, another important mechanical quantity that contributes to the development of foot ulcers is the plantar shear stress, which results from the forces exerted parallel to the skin and tends to cause a tear [9, 10]. Ground reaction forces act in all three dimensions under the foot during locomotion. Among the threedimensional stresses that act on the plantar surface, vertical stress (pressure) can easily be quantied via commercial pressure measurement systems [11]. Due to technical challenges, objective determination of the horizontal shear stress was not possible in the past, but during the last few decades, a variety of methods have been developed for its measurement [12]. Data suggest that peak plantar pressure and shear

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