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SKIN SIGNS OF DIABETES

Numerous skin lesions may be associated with diabetes or its treatment (Table 12.2). Many of these are not specific and are discussed elsewhere, such as cutaneous xanthomas (Ch.11), scleredema (Ch.11), arterial disease (Ch.15), lipodystrophies (Ch.22), and drug reactions (Ch.18). Vitiligo is increased in frequency but is discussed in detail in (Chapter 21). Perforating disorders are discussed in the section on renal disease in this chapter.

Infections

Neurovascular changes and the diabetic foot

Diabetes predisposes to atheroma of large vessels, and also to microangiopathy. The most frequent site at which these changes are of dermatologic importance is the foot, where three factors may combine to cause severe morbidity (Figs 12.9 – 12.11).

    Ulceration is the most important complication, which is usually associated with reduced sensation and variably with signs of vascular compromise. Impaired skin sensation increases the risk of penetrating injury, but the ulcers often arise under areas of callosity that are due to the combination of rigid keratin (because of glycosylation) and altered weight-bearing (due to foot deformity caused by neuropathy affecting the intrinsic foot muscles). Regular foot examination is important in diabetic patients, with particular attention to treatment of tinea pedis, checking sensation, and checking that there are no irregular areas within the sole of footwear. Special footwear may need to be made to avoid pressure, or lightweight casts designed to remove pressure from areas of neuropathic ulceration.

Figure 12.9   Hypothyroidism in a teenaged boy (left) who was referred due to eyelid edema but also had dramatic palmar carotenemia (shown with a normal hand for comparison).

Figure 12.10   Smooth, shiny, red skin, with a small digital ulcer, and a ‘Terry nail’ (pale, with a distal band of reddish brown color) due to chronic renal failure. This combination is highly suspicious of diabetic complications.

Figure 12.11   Neuropathic ulceration of the foot. (a) Neuropathy in a diabetic patient. This patient requires careful attention to his footwear, and regular review to exclude secondary infection (which may be asymptomatic due to the neuropathy). (b) An example in which infection has occurred; this patient has a toe web sinus due to spina bifida and has developed local cellulitis, which would normally be painful at this site even before development of redness.

Necrobiosis lipoidica

Two-thirds of individuals with necrobiosis lipoidica have diabetes, and a further 20% develop it later or have a positive family history of diabetes; conversely, 0.3% of diabetic patients will develop this complication. In such cases, it is known as necrobiosis lipoidica diabeticorum (NLD); however, most discussion of NLD is equally applicable to non-diabetic necrobiosis lipoidica. The lesions are most frequent on the shin, with a female predominance, and bilateral disease in 10–20%. Active lesions have a yellowish-colored atrophic center with visible cutaneous blood vessels, and an erythematous inflammatory border (Figs 12.12 – 12.14).

    Topical corticosteroids may have a role in reducing this inflammatory component, but they should be used with care in view of the central atrophy, which can be worsened by excessive topical steroid administration. A variety of agents with antiplatelet effects have been used therapeutically, with mixed results, based on the fact that there are changes in the vessel wall intima in diabetes and also increased platelet aggregation. Photochemotherapy (PUVA) has been used with success in several recent reports. Excision and grafting can be effective, but there is potential for poor healing and graft failure, so this procedure is usually reserved for patients with recurrent or severe ulceration of the atrophic lesions, in whom the balance of risks and benefit is most favorable. Cultured tissue grafts may be useful for ulceration but are expensive.

Figure 12.12   Ulceration is a feature in a minority of cases of necrobiosis lipoidica, usually in larger lesions at areas prone to injury (the shin is the most common site for this disorder). Secondary infection of ulcerated areas should be treated promptly, especially in diabetic patients, and adherent dressings should be avoided, as they may cause further damage when removed from the fragile atrophic skin around the ulcers.

Figure 12.13   A typical lesion of necrobiosis lipoidica in which there is cutaneous atrophy, telangiectasia (easily visible dermal vessels), and a background yellowish color. (From Lawrence CM, Cox NH. Physical Signs in Dermatology, 2nd edn. London: Mosby, 2002.)

Figure 12.14  Older lesions of necrobiosis lipoidica are often pigmented as well as obviously atrophic, but often lose the more inflamed appearance of more recent lesions.

Other cutaneous features of diabetes

Granuloma annulare

The association between granuloma annulare (GA) and diabetes has been the subject of debate for some time. This disorder is clinically distinct from NLD but has many similar histologic features, in particular the presence of necrobiotic collagen. The typical clinical appearance is of a small plaque that gradually expands; the border is raised and thickened, often with
a cobblestoned morphology, whereas the central skin may be slightly pigmented or purplish in color. Lesions tend to occur over bony prominences of the knuckles, elbows, knees, or dorsum of the foot. Large studies of this disorder do not confirm a significant association between this ‘ordinary' pattern of GA and diabetes, and investigation is not usually performed in the typical young and otherwise well patient who develops this disorder. There is greater uncertainty about patients with some rare forms of GA, in whom it appears prudent to perform urinalysis.

    Diffuse GA is an uncommon variant that presents as myriad tiny papules, which usually show some degree of grouping and sometimes a vaguely annular patterning. This usually affects older individuals, and the suspicion of an increased frequency of diabetes may simply reflect the predominant age group.

    Perforating GA is a rare variant in which the necrobiotic collagen is expelled through the surface of the skin (Fig.12.15). The lesions are often acral, and are scabbed or discharging papules. About 30% of patients have diabetes.

    Deep and systemic variants of GA are rare but appear to be associated with higher risk of diabetes.

    Treatment of GA can be difficult. Topical corticosteroids may reduce inflammation in the border of active lesions, but many lesions are seen at a static and asymptomatic phase, in which case active treatment is often not required: about 50% resolve spontaneously within 2 years. As with NLD, photochemotherapy can be quite useful (usually for disseminated or extensive plaque forms of GA).

Figure 12.15  Perforating granuloma annulare (GA). The palm is an uncommon site for GA, and perforating disorders generally are associated with diabetes; both the atypical site and variant of GA therefore suggest this possibility.

Diabetic dermopathy

This disorder is common in diabetes but is found fairly commonly in other endocrine disorders, and occasionally in healthy individuals. It consists of small, red papules that subside to leave small, brown, atrophic patches (Fig.12.16). Within the skin in these areas, there is evidence of thick-walled blood vessels, but this is seen to some extent in the skin of the lower leg in all individuals. One theory is that the disorder is due to minor trauma, in which case the inherently abnormal vasculature in diabetic patients may lead to a more obvious residual defect compared with non-diabetic skin.

Figure 12.16  Diabetic dermopathy (skin spots). These small, brown lesions are relatively non-specific; the extent of lesions in this case is uncommon (except in diabetes). They probably represent microvascular damage and tend to occur at sites of minor trauma.

Stiff skin, cheirarthropathy, and similar disorders

An interesting phenomenon in diabetes is the development of stiff, thick skin that resembles the changes in scleroderma but without the vascular and other features of this disorder (Figs 12.17 and 12.18). This is most apparent at acral sites, and may be associated with limited joint mobility (also known as cheirarthropathy) due to the abnormal collagen. The physical sign that demonstrates this entity is known as the prayer sign. When the two palms are pressed together at 90 8 to the forearms, affected patients cannot oppose the fingers and palms fully. The condition is particularly prominent in patients with poor glycemic control over many years. The proposed mechanism is an increased cross-linking of collagen, known as non-enzymatic glycosylation (NEG), which produces stiffer collagen. In support of this concept, it has been demonstrated that NEG of skin collagen is related to duration of diabetes and to other features of poor glycemic control.

    Diabetic finger pebbles (Fig. 12.19) are another interesting skin texture change in diabetic patients.

Figure 12.17  Cheirarthropathy prayer sign. (Courtesy of Dr. S. Russell.)

Figure 12.18  Sclerederma in a patient with cheirarthropathy. (Courtesy of Dr. S. Russell.)

Figure 12.19  Diabetic finger pebbles are an exaggeration of the skin markings over the knuckles and on the dorsal aspect of the terminal phalanges. They are more cobblestoned than knuckle pads (Ch. 22), with which they may be confused.

Diabetic bullosis

This is a poorly defined entity (or entities, as various intraepidermal and subepidermal sites of blistering have been described). Blisters are usually acral, vary in size but are usually of diameter one to a few centimeters, arise on a non-inflamed background, and may be induced by trauma or by sunlight in some individuals. Diagnosis is largely by exclusion of some common blistering conditions (pompholyx eczema and friction blisters), mechanobullous disorders (inherited types of epidermolysis bullosa), porphyrias (especially if photosensitive), and immunobullous disorders (especially epidermolysis bullosa acquisita).

PRACTICE POINTS

White/Cox: Diseases of the Skin, 2ed.(c) 2006, Elsevier Inc. All rights reserved.