This chapter focuses on common disorders of the hands, feet,
and extremities and is organized into the following subgroups: ulcers,
inflammatory conditions, cutaneous infections, and vascular cutaneous
Dermatitis and Venous Leg Ulcers
The vast majority of leg ulcers are venous stasis ulcers resulting from
chronic venous insufficiency. Risk factors for development of both
venous stasis dermatitis and venous leg ulcers include heredity,
older age, female sex, obesity, pregnancy, prolonged standing, and
Chronic venous insufficiency is usually caused by
episodes of phlebitis or varicose veins, both of which damage venous
valves. This situation results in poor venous return from the lower extremities,
leading to increased hydrostatic pressure and lower extremity edema
and stasis dermatitis.
Dependent edema, erythema, and orange-brown hyperpigmentation
characterize early stasis dermatitis. The medial distal legs and
the pretibial leg are the areas most frequently affected. More chronic
and severe cases may have bright weepy erythema and even ulceration
(Figure 247-1). Pruritus is common. Bacterial
infection may complicate stasis dermatitis. The presence of honey-colored
crust and pustules suggest secondary bacterial infection. Cellulitis
and lymphangitis may develop.
Venous insufficiency. Pruritic stasis dermatitis with
venous stasis ulcer. (Reproduced with permission from Wolff KL,
Johnson R, Suurmond R: Fitzpatrick’s Color Atlas
& Synopsis of Clinical Dermatology, 5th ed. © 2005,
McGraw-Hill, New York.)
Stasis ulcers often begin within areas of stasis dermatitis.
The medial and lateral malleolus and the medial aspect of the calf
are the most common sites of involvement. The ulcer often has an aching
quality with dependency. The ulcer has a punched out appearance
with orange-brown hyperpigmentation at the borders and a moist pink
base. Peripheral pulses are usually present.
Diagnosis of stasis dermatitis and stasis ulcers is clinical.
Usually, other signs of venous stasis are present (edema, hyperpigmentation,
varicose veins, and scarring), making the diagnosis straightforward.
With acute exacerbation, secondary infection is common. Coexistent
allergic contact dermatitis should also be considered.
If the ulcer does not have the clinical findings mentioned above, other
diagnoses should be considered (Table 247-1). Certain
disorders, such as arterial ulcerations, pyoderma gangrenosum, and
polyarteritis nodosa require immediate attention. For instance,
if peripheral pulses are absent and the patient has a history of
claudication, vascular blood flow studies should be performed to
exclude arterial ulcers. If the patient reports a rapidly developing
ulcer that began as a pustule or erythematous nodule and has violaceous
overhanging borders, pyoderma gangrenosum should be suspected. If
the diagnosis is in question, consultation with a dermatologist
Table 247-1 Differential
Diagnosis of Extremity Ulcers*
| Save Table
Table 247-1 Differential
Diagnosis of Extremity Ulcers*
|Injuries, burns, injections, decubitus,
chilblains (pernio), neuropathic ulcers|
|Viral: herpes simplex virus, cytomegalovirus|
|Bacterial: gangrene, ecthyma gangrenosum, ecthyma
secondary to Staphylococcus aureus and/or
group A streptococcus; osteomyelitis, methicillin-resistant S.
|Mycobacterial: Buruli ulcer (West Africa, Mycobacterium
ulcerans), Bairnsdale ulcer (Australia, M. ulcerans),
|Fungal: blastomycosis, coccidioidomycosis, paracoccidioidomycosis, chromomycosis,
|Spirochetal: syphilis, yaws|
|Parasitic: leishmaniasis, amebiasis,
|Spiders, scorpions, snakes|
|Diabetes, gout, calciphylaxis (cutaneous
necrosis from small- and medium-sized vessel calcification in diabetes,
end-stage renal disease, or hyperparathyroidism)|
|Venous: varicose veins, venous insufficiency|
|Arterial: hypertension, arterial insufficiency,
|Polyarteritis nodosa, vasculitis,
collagen vascular disease, Behçet syndrome|
|Cutaneous: squamous cell carcinoma, basal cell
|Lymphoma: T-cell or B-cell lymphoma|
|Polycythemia, sickle cell anemia|
|Bullous pemphigoid, necrobiosis lipoidica|
Venous hypertension should be reduced by leg elevation and the use
of support stockings. Weeping eruptions should be treated with an
astringent compress. A low- to mid-potency topical steroid, such
as fluocinolone acetonide 0.025% or hydrocortisone 2.5% ointment,
should be applied twice a day until erythema, scale, and pruritus
resolve. Oral antihistamines, such as diphenhydramine or hydroxyzine,
should be used for pruritus and for nighttime sedation. Secondary
bacterial infection should be treated with cephalexin, dicloxacillin,
or ciprofloxacin for 7 to 10 days. Topical neomycin, antihistamine
creams, and anesthetic creams should be avoided as they may complicate
the condition with allergic contact dermatitis.
Because venous leg ulcers are chronic and slow
to heal, ED treatment should focus on treating underlying causes
of edema, stasis dermatitis, secondarily infected ulcers, cellulitis,
or lymphangitis. Evidence of cellulitis or lymphangitis may require hospitalization
for IV antibiotics. Otherwise, follow-up should be arranged with
a dermatologist, vascular surgeon, or leg ulcer clinic for further
Pyoderma gangrenosum is a recurrent cutaneous, necrotizing, and
noninfective ulceration of the skin that most commonly occurs in
women between 30 and 50 years of age.2 Fifty percent of cases are associated with
an underlying disease, the most common of which are inflammatory
bowel disease, arthritis, and myeloproliferative disorders.3
The classic lesion of pyoderma gangrenosum begins as a superficial
pustule or erythematous nodule that expands into a large painful
ulcer on the lower extremity with a purulent base and irregular,
undermined, gunmetal-colored border (Figure 247-2).
There is no associated lymphadenopathy. Up to 50% of patients
develop lesions at the sites of trauma, such as surgery sites, injection
sites, or after blood-drawing.2 History of multiple
surgical debridements with sterile cultures should suggest a potential
diagnosis of pyoderma gangrenosum.
Pyoderma gangrenosum. (Reproduced with permission from Wolff
KL, Johnson R, Suurmond R: Fitzpatrick’s Color
Atlas & Synopsis of Clinical Dermatology, 5th ed. © 2005, ...
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