Lecture 10 Part 2 PDF

Stasis Dermatitis/Id Reactions Stasis dermatitis is common in the elderly. It is more common in obese patients and patients who have had trauma or surgery to the legs. Stasis dermatitis affects the lower extremities, below the knees. It occurs almost exclusively in patients who get leg edema, but...

Stasis Dermatitis/Id Reactions Stasis dermatitis is common in the elderly. It is more common in obese patients and patients who have had trauma or surgery to the legs. Stasis dermatitis affects the lower extremities, below the knees. It occurs almost exclusively in patients who get leg edema, but most patients with leg edema do not get stasis dermatitis. It starts with erythema, warmth, and possibly tenderness. It then progresses to scaling and possibly weeping (Figure 10.21) (Figure 10.22). The difference between stasis dermatitis and edema is that legs with stasis dermatitis become red, tender, and itchy. If the stasis dermatitis is persistent, scaling will develop in addition to the redness and itch. Over time, the leg will develop permanent brown discoloration. If the stasis is severe, ulcers are likely to develop. These ulcers most commonly develop proximal to the medial malleolus and are usually ill-defined, very moist, and exude large amounts of serous fluid (Figure 10.23). Patients with severely inflammatory stasis dermatitis may develop a generalized, pruritic eruption consisting of small, pink papules and vesicles, which, if severe enough, can become confluent and generalized (Figure 10.24). This is called an Id reaction. Venous hypertension is the primary problem in stasis dermatitis. Any cause of impaired blood flow out of the legs can cause venous hypertension (thrombosed/obliterated veins, incompetent valves, increased intra-abdominal pressure (from obesity), surgical removal of veins for use during cardiac surgery, etc.). Venous hypertension leads to distension of the venules and capillaries, followed by extravasation of fluid, protein, white blood cells, and red-blood cells. Over time, a cuff of protein may form around capillaries, and this cuff may impede oxygen exchange between the blood and the tissue. An inflammatory reaction develops in response to protein and iron in the tissue. In addition, extravasated WBC may release proteases and lysosomes, which further add to the inflammation and tissue damage. Id reactions are thought to be caused by circulating cytokines released as a result of the severely inflammatory stasis reaction. The first step in treating stasis dermatitis is making the diagnosis. Unilateral stasis dermatitis is possible, but it is more frequently bilateral. Of note, bilateral lower extremity cellulitis is rare. A patient presenting with bilateral, red, swollen, painful calves, in the absence of fever, elevated WBC, and malaise, should be treated for stasis dermatitis, not cellulitis. Diagnosing stasis dermatitis as cellulitis is a very common mistake and should be avoided, as it leads to incorrect treatment and the patient not improving. Vascular studies are usually not necessary. However, if stasis dermatitis develops suddenly, then Doppler studies should be ordered to rule out DVT. Stasis dermatitis is treated with topical steroids, leg elevation, and compression. Graduated compression stockings are the usual method of compression. They are graduated in the sense that the greatest compression occurs distally with decreasing compression proximally, so as to promote fluid movement proximally. If concerned about arterial insufficiency, compression should not be used until confirming that the arterial circulation is not compromised, because compression can significantly worsen arterial disease. Patients often find compression stockings difficult to put on and painful to wear when they have active stasis dermatitis. In this setting, the keys to treatment are: 1) keep the extremities elevated to promote fluid drainage; 2) use ace wraps to provide compression. Ace wraps are not as effective as graduated compression stockings, but are more effective than no compression at all. Topical steroids should be applied twice daily to decrease inflammation. Triamcinolone 0.1% ointment is the topical steroid of choice. This is because patients with stasis dermatitis are at incredibly high risk of developing contact dermatitis to any topicals that are applied to the affected limb(s) (antibiotic creams/ointments, moisturizers, soaps, etc.). Triamcinolone 0.1% ointment has very few ingredients and allergies to it are very rare. Allergic contact dermatitis should be suspected in all patients with chronic stasis dermatitis, and patients should be instructed to apply nothing to the stasis-affected leg(s) except plain petroleum jelly, triamcinolone 0.1% ointment, and mupirocin ointment for infection prophylaxis, if necessary. It is uncommon for a patient to be allergic to any of these three products. Patients with obvious varicose veins, difficult-to-treat stasis dermatitis, or difficult-to-heal ulcers should be referred to a vascular surgeon for vascular studies and consideration of vessel ligation. In this procedure, ligation of an incompetent vessel causes blood flow to be shunted into vessels with competent valves. For patients with Id reactions, systemic steroids are usually necessary to relieve the severe pruritus. Treating the stasis dermatitis as described above (compression, elevation, and topical steroids) will prevent recurrence of the Id reaction when the systemic steroids are stopped. Ulcers are best treated with aggressive compression therapy. An inexpensive, effective option for compression is use of Unna boots. These are semi-rigid boots, similar to a cast, which are applied, kept on for a week, and replaced weekly. The material directly against the skin contains a zinc oxide ointment. They are very effective for healing stasis ulcers, but should not be used if the ulcers are grossly infected. Chronic Lymphedema Chronic lymphedema occurs most commonly following chronic stasis dermatitis and edema. It can also occur in a limb in which the draining lymphatic basin has been removed surgically or damaged through radiation therapy. Chronic lymphedema presents as thick, hardened skin of the affected extremities. There is often a pebbly or nodular surface to the skin (Figure 10.25). Patients are at risk for recurrent infections, ulcerations, pain, and loss of function in limbs with chronic lymphedema. Lymphedema is initially due to accumulated lymphatic tissue in the extremity. With chronicity, the inflammation associated with fluid and protein extravasation leads to fibrosis of the skin and subcutaneous tissue. Once the lymphedematous limb has become fibrotic, the changes are essentially permanent. At this stage, treatment revolves around trying to prevent progression, infection, and ulceration. This typically means using compression garments that apply significantly more compression than those used for stasis dermatitis. These are usually custom-made garments. Sequential compression devices (SCDs) can also be useful. These pumps are connected to garments worn on the limb. Balloons in the garment are sequentially inflated by the pump, starting at the distal aspect of the limb and progressing proximally, with the intent to squeeze the fluid from the tissue. SCDs can sometimes reverse some of the changes of lymphedema. In addition, any causative factors, such as obesity, must be addressed. If obese patients do not lose weight, there is very little chance of halting or reversing their lymphedema. Broad-spectrum antibiotic creams, such as silver sulfadiazine cream, should be used for infection prophylaxis if there is skin breakdown. Cellulitis Cellulitis is a relatively common infection. Cellulitis presents with erythema, edema, warmth, and tenderness (Figure 10.26). Patients are typically symptomatic with fevers, chills, and malaise, and often have an elevated WBC count. Cellulitis is most often caused by Staph aureus or Strep pyogenes. Cellulitis should be treated with beta-lactamase resistant antibiotics. Blood cultures should be checked prior to starting therapy. Intertrigo Intertrigo commonly occurs in elderly patients, especially in overweight individuals. Intertrigo presents in skin folds as moist, brightly erythematous, skin (Figure 10.27), and is specifically limited to areas where skin contacts skin (inframammary, sub-pannus, axillae, etc.). Intertrigo is primarily related to two factors: excessive skin moisture and overgrowth of Candida albicans. The excessive moisture is the primary factor, as Candida overgrowth cannot occur in skin that is not moist. The most important aspect of treatment is drying the affected skin. This can be accomplished by allowing air to reach the skin, rinsing it with water frequently, allowing it dry completely, and placing a dry towel between the two skin surfaces. Once the area has been dried in this manner for several days, it can be maintained by applying antiperspirant once or twice daily. In addition to drying the area effectively, anti-yeast therapy with nystatin or topical azoles can also be beneficial. However, no amount of anti-yeast therapy is likely to be effective if the area is not effectively dried. Scabies Scabies is common in children, nursing home residents, and recently-hospitalized individuals. Scabies presents with intense pruritus. Although the entire body can be affected, the finger- webs, abdomen, breasts, and groin are most common. The rash is usually mildly erythematous and somewhat scaly. The classic scabies lesions are burrows, which are thin white lines, usually most apparent in the finger-webs (Figure 10.28). In most cases, burrows cannot be appreciated, and the patient presents with a non-specific, itchy, scaly rash. There are two situations in which a clinical diagnosis of scabies can be made with certainty: 1) burrows seen on examination or 2) erythematous papules seen on the glans penis (Figure 10.29). If there is no involvement of the finger-webs of the hands, scabies is quite unlikely. Crusted scabies is a specific variant seen in patients with neurologic disease or immune compromise. In this variant, there is thick crusting, especially on the hands, feet, and scalp (Figure 10.30) (Figure 10.31). In this setting, thousands or millions of mites exist on the patient. Scabies is cause by the itch mite Sarcoptes scabiei. The typical patient with scabies has only 10- 20 mites on their body. The itch and rash are caused by an allergic reaction to the mites and their feces (Figure 10.32). Scabies should be suspected in any patient presenting with a new, intensely itchy rash, especially those recently in a nursing home or hospital. Standard treatment is topical permethrin, which is applied from the neck down before bed, left on overnight, and washed off in the shower in the morning. The sheets should be washed in hot water in the morning, along with all clothes worn in the last five days. This whole process should be repeated in one week. For severe cases or cases where compliance with the topical treatment is a concern, the oral medication, ivermectin, can be used. It consists of two doses, each one week apart, at 200 mcg/kg for each dose. Even with successful treatment, the itch and rash persists at least 2 weeks, and sometimes up to 6-8 weeks. Antihistamines can be useful for symptomatic treatment of the itch until it resolves. Herpes Zoster Zoster is common in the elderly. It becomes more common with age and with any form of immunosuppression. Zoster presents initially as erythematous plaques. Vesicles soon develop within the plaque and eventually rupture and turn into scabs. Clinically, the most useful diagnostic finding is a sharp, mid-line cutoff and dermatomal distribution (Figure 10.33) (Figure 10.34). Frequently, tingling, burning, or itch precedes the eruption. The eruption itself is often painful, and the pain may persist after the eruption has completely healed. Zoster involving the V1 dermatome is particularly concerning. If the V1 dermatome is affected, there can be ophthalmic involvement, which can lead to permanent visual impairment without treatment (Figure 10.35). Thus, any patient with V1 involvement should be immediately referred to ophthalmology to rule out ophthalmic zoster. The other common complication of zoster is post-herpetic neuralgia. In this disease, there is persistent pain at the site of a zoster eruption for months after the eruption has resolved. Zoster is caused by the varicella zoster virus. The virus remains latent in the dorsal root ganglia and trigeminal ganglion after infection during childhood. Reactivation of the virus leads to proliferation and retrograde axonal transport to the skin. Zoster is treated with antiviral medications – acyclovir and valacyclovir are the treatments of choice. Treatment is important because it decreases the probability of post-herpetic neuralgia. The likelihood of post-herpetic neuralgia is directly correlated with age of the patient, with older patients more likely to be affected. Post-herpetic neuralgia is treated with gabapentin, tricyclic antidepressants (which are often effective for chronic pain), and nerve blocks. A zoster vaccine is available now for patients over age 60, which may prevent or lessen the severity of zoster. Mycosis Fungoides/Cutaneous T-Cell Lymphoma (CTCL) CTCL is a rare malignancy. It becomes more common with age, but is very rare prior to age 50. CTCL presents with moderately pruritic, red-brown, slightly scaly patches that most commonly start on sun-protected areas, such as the back, buttocks and thighs (Figure 10.36). As the disease progresses, the patches turn into plaques, and the patients may develop cutaneous tumors as well (Figure 10.37). In advanced stages, malignant T-cells are found in the blood and lymph nodes. CTCL is a malignancy of CD4+ T-cells localized to the skin. As the disease progresses, skin localization is lost, and malignant T-cells can then be found in the lymph nodes and peripheral blood. Patch-stage CTCL is usually treated with topical treatments – topical steroids, topical chemotherapy, or phototherapy. As the disease becomes more advanced (plaque, tumor, or systemic disease), systemic therapy is employed. Bullous Pemphigoid Bullous pemphigoid is a disease of the elderly. It occurs almost exclusively in individuals over age 60 and is much more common in patients in their 70s, 80s, and 90s. BP presents with intensely pruritic, edematous, red plaques. Tense blisters then develop in these plaques (Figure 10.38) (Figure 10.39). BP is an autoimmune disease. Antibodies are directed against a protein located at the dermal- epidermal junction. The immune reaction incited by these antibodies leads to separation of the epidermis from the dermis. The epidermis, therefore, forms the roof of the blisters, and because the epidermis is relatively “tough”, the blisters are also “tough”, tense blisters. This is contrasted with the blisters in pemphigus, in which the roof of the blister is composed of partial epidermis, which does not have nearly the strength of the intact epidermis in pemphigoid. Mild cases of pemphigoid are treated with topical steroids. More severe cases are treated with systemic steroids combined with immunosuppressive medications like azathioprine, methotrexate, and cyclophosphamide.