An Overview of Dermatological Conditions Commonly Associated with the Patient with Obesity

   According to 2004 statistics from the National Health and Nutrition Examination Survey, nearly two thirds of US adults are overweight and 30.5% are obese as determined by body mass index (BMI).¹ Body mass index is calculated by dividing the patient’s weight by his/her height squared. This figure significantly correlates with body fat content and is generally accepted as the indicator for measuring excess weight. If the BMI is >25, a person is considered overweight; >30, obese; and >40, severely or morbidly obese.¹

   Obesity increases the risk of or is associated with more than 30 medical problems, including dermatological conditions. Commonly seen dermatological conditions include acanthosis nigricans, skin tags, hyperandrogenism, striae distensae, plantar hyperkeratosis, and candidal intertrigo. Friction and excessive moisture in skin folds can lead to skin injury and incisional healing may be impaired due to increased tension on suture lines and decreased blood supply in the adipose tissue.² Clinicians need to be cognizant of the impact of obesity on health in general and on skin, specifically.

Acanthosis Nigricans

   Acanthosis nigricans is characterized by hyperpigmented, velvety, irregular plaques in body folds. The surface of the lesions may be warty, leathery, or papillomatous; the disease may be benign or malignant. The condition is considered to be a cutaneous marker of systemic disease that requires intervention; it has a well established association with obesity. As the frequency and degree of obesity increase, a concomitant increase in acanthosis nigricans also can be expected.³ Hud et al³ reported that out of 34 patients in an obesity clinic who were randomly selected and examined, 25 (74%) exhibited acanthosis nigricans; of that group, 33% of those 120% to 170% of ideal body weight (IBW), 77% of those 150% to 200% of IBW, and 100% of those >250% of IBW had acanthosis nigricans.

   Generally, acanthosis nigricans is considered to be a sign of endocrine disease (diabetes mellitus) or cancer, especially gastric cancer.⁴ When associated with obesity and diabetes, onset of the condition is gradual; when associated with cancer, the onset is more rapid and sudden. The condition may be asymptomatic or the person may experience itching.⁴ Classically, acanthosis nigricans presents in the axillae or back of the neck. Less pronounced presentations include the scalp, elbows, umbilical areas, knees, and knuckles.⁵ In the mildest form, the velvety hyperpigmented thickened lesions may resemble dirty skin or the plaques may be confused with psoriasis. When obese patients are seen with hyperkeratotic plaques, acanthosis nigricans should be considered. The plaques of acanthosis nigricans are not inflamed.⁵

   Although the precise development of acanthosis nigricans is unclear, a growing body of evidence strongly associates it with hyperinsulinemia, a condition that leads to the binding of insulin to insulin-like growth factor receptors on the keratinocytes and fibroblasts with resultant hyperplasia of the skin.⁶ An elevated fasting insulin level confirms the presence of hyperinsulinemia. Patients with high insulin levels often maintain normal glucose levels even with insulin resistance. Commonly, blood glucose levels are in the normal range, although non-insulin dependent diabetes may be present.⁷

   Insulin resistance causes acanthosis nigricans in the following sequence:
  • Severe insulin resistance leads to hyperinsulinemia
  • Increased amounts of serum insulin interact with insulin-like growth factor (IGF) receptors in the tissues
  • Large amounts of insulin bind to the IGF receptors and activate the proliferation of keratinocytes and dermal fibroblasts
  • The increased amount of insulin stimulates DNA synthesis and cell development in vitro through the IGF-I receptor present in skin keratinocytes. This series of events leads to the development of the skin lesions.^5,8

   The pathogenesis of acanthosis nigricans associated with malignancy is not clear. It is likely that a humoral factor is produced by the tumor because the skin disorder may improve or even resolve following treatment of the tumor.⁹ Elevated levels of transforming growth factor a and its receptor (epidermal growth factor receptor) have been found in patients with acanthosis nigricans and gastric cancer.¹⁰

   If the patient is obese and hyperinsulinemia is not present, a work-up for malignancy should be considered. When possible, the underlying cause of the lesions should be treated. If the lesions are asymptomatic, no treatment may be necessary. Katz⁵ reported that once patients begin to lose weight, rapid improvement in the acanthosis nigricans can be expected; hence, the most effective treatment is weight loss and exercise if the lesions are caused by hyperinsulinemia.

   Other approaches to reducing acanthosis nigricans include 5-month treatment with octreotide, which can reduce insulin secretion.^11,12 Topical treatment includes antibiotics, retinoids, and keratolytics.¹³ A 12% ammonium lactate (lactic acid) cream may be used twice a day.⁴ Blobstein,¹⁴ using case reports of five patients who served as their own controls, reported on the successful use of the combination of ammonium hydrate and tretinoin for the treatment of acanthosis nigricans; this combined therapy improved the condition 85% to 95% compared to control area.

Skin Tags

   Skin tags are pedunculated, flesh-colored lesions with smooth or irregular surfaces. They are usually found in the axillae, neck, or eyelids. Skin tags, reported in up to 44% of obese patients,¹⁵ may be associated with acanthosis nigricans. Women are affected more often than men.¹⁵

   In a randomized study involving 34 patients with obesity, skin tags, and acanthosis nigricans were observed in up to 25 (74%) of the patients studied and their prevalence correlated positively with the severity of obesity.³ A subset of patients was found to have mean fasting insulin levels twice that of the patients without skin lesions.³

   Asymptomatic skin tags require no treatment. Skin tags can be removed by clipping with scissors, electrodesiccation, or cryotherapy. They are most commonly removed for cosmetic reasons and do not seem to regress with weight loss.⁴

Hyperandrogenism

   Adipose tissue synthesizes testosterone; the hyperinsulinemia commonly seen with obesity increases the production of ovarian androgens.¹⁶ Testosterone primarily binds to albumin and sex hormone-binding globulin. Because insulin inhibits the synthesis of sex hormone-binding globulins, the free testosterone in a woman’s serum is increased. This increase of testosterone may lead to male-patterned baldness and hirsutism acne in obese women.¹⁶

   Skin biopsy specimens from persons administered high doses of testosterone and anabolic-androgenic steroids revealed increased surface lipids, hypertrophy of sebaceous glands, and populations of Propionibacterium acnes. Hence, higher levels of testosterone and anabolic steroids may increase the risk of striae atrophica, acne, hirsutism, and furunculosis.¹⁷

   A woman experiencing hyperandrogenism should have an endocrinological workup. Disorders such as tumors, Cushing’s syndrome, and non-classic congenital adrenal hyperplasia must be ruled out. Physicians recommend that an evaluation should be completed to determine glucose tolerance, insulin resistance, or dyslipidemia.¹⁸

   The goals of treatment include reducing insulin levels. Insulin-sensitizing agents such as metformin improve hyperinsulinemia and may lower androgen levels.¹⁹ Weight loss, antiandrogenic therapy, and oral contraceptives in combination with conventional treatment are other measures have been shown to reduce hyperandrogenism.¹⁹

Striae Distensae

   Striae distensae (stretch marks) are smooth, linear bands of skin. When they first appear, they are red, then progress to purple and finally to white. At that point, they also will flatten.²⁰ These lesions occur most commonly on the abdomen, thighs, buttocks, and arms. They generally are perpendicular to the direction of the greatest tension on the tissues.²¹ Their formation has been attributed to stretching and thinning of the connective tissue and subsequent formation of dermal scars as a result of collagen rupture. The gap is filled with new collagen.^21,22

   Although the exact cause is unknown, other theories on the etiology include:
  • Endogenous or exogenous hyperadrenocorticism, including patients using topical corticosteroids²⁰
  • Insufficient development of the skin
  • Rapid stretching of the skin.²

   Singh and Kumar²¹ reported that striae distensae are a form of dermal scarring in which the dermal collagen ruptures and separates; the intervening gap is filled with newly synthesized collagen, which then becomes aligned in response to local stress forces. Stretch marks correlate closely with obesity — one cross-sectional study¹⁵ of 156 patients with obesity found that 43% of had striae distensae (P = 0.3).

   Striae distensae causes significant cosmetic concern for many people. Treatment must be instituted early before the development of scar tissue (while lesions are still red or purple) and/or before the scarring process is complete.²³ Tretinoin can increase the deposition of collagen and increase the number of fibroblasts where it is applied. In a double-blind, randomized, vehicle-controlled study²⁴ of 22 patients, tretinoin was applied for 6 months. After 2 months of treatment, seven patients (32%) showed significant improvement (P = .05) in the severity (as rated by investigators, self-assessment, and punch biopsy) of striae distensae; after 6 months, 80% had a marked improvement in the severity of the striae (P = .002). After 6 additional months, little further improvement was noted.

   However, the use of tretinoin can lead to severe adverse effects, primarily skin irritation (35% of patients in the aforementioned study) — dermatitis was most prominent during the first 2 months of treatment. The severity of the dermatitis decreased progressively during the period when the striae showed improvement.²⁴

   The use of lasers, alone or with other therapeutic modalities, also can reduce the appearance of both red and white striae distensae.²⁵ In a prospective study of 39 stretch marks treated with four different treatment protocols, continued clinical improvement was seen in patients for 6 to 12 months after treatment. Even patients who initially responded poorly experienced up to 60% improvement 6 months after the initial treatment.

Plantar Hyperkeratosis

   Plantar hyperkeratosis is defined as “diffuse thickening of the stratum corneum in a horseshoe pattern, affecting the heel, foot arch area, and plantar-medial aspect of the great toe at the level of the interphalangeal joint.”¹⁵ The clinical significance of plantar hyperkeratosis has not been determined because it is a recently reported finding in the patient with obesity. In one cross-sectional study of 156 obese patients, the association between diabetes and was not statistically significant (P = 0.11). However, plantar hyperkeratosis was the most common dermatological manifestation in patients who weighed 76% to 100% more than their IBW.¹⁵ The excess weight of the patient with obesity disrupts the normal foot anatomy. Excessive weight causes transference of pressure to other foot areas, leading to increased pressure and friction over bony prominences. Thickening of the stratum corneum after injury may be a purely physiologic process — a protective response to mechanical trauma.

   The use of insoles fitted by an orthotist helps lessen the symptoms. However, long-term therapy must include weight loss.²

Candidal Intertrigo/Perineal Dermatitis

   Patients with obesity have excessive fat folds and sweat more profusely due to the thick layers of subcutaneous fat. Skin conditions commonly occurring in skin folds include intertrigo, yeast dermatitis, and fissures. Common locations are the abdominal skin folds, submaxillary area, axillae, and the perineal area. Friction between these surfaces leads to intertrigo and maceration of the skin from excess moisture. Infections may occur, commonly caused by yeast. The skin may become erythematous, pustules may form and then rupture, and new pustules may develop on the periphery. This, in turn, leads to areas of inflammation and rashes (see Figure 1).² Patients may complain of itching or burning. Diagnosis is confirmed via inspection of the area, potassium hydroxide (KOH) preparation, or fungal culture.²⁶ Bacterial superinfections are common.⁴
The most common clinical presentation of candidiasis on the skin, intertrigo is more common in patients with obesity and those with diabetes mellitus. Predisposing factors include hot weather, poor hygiene, tight clothing, other skin disorders such as psoriasis, and the use of topical steroids.²⁷

   Standard practice²⁸ involves keeping the skin clean and dry using a gentle soap or no-rinse skin cleanser and applying an antifungal powder, cream, or ointment locally. If these agents fail to resolve the antifungal infection, oral antifungal medications will be needed.¹⁷ Fluconazole may be effective; it is highly water-soluble, transported to the skin in perspiration, and concentrated by evaporation.²⁷ For severe cases, Burrow’s solution (water and aluminum acetate) soaks several times a day may help promote dryness.⁴ Using a 1% acetic acid solution as a compress several times a day also has been suggested.²⁵

   For patients with incontinence, standard practice includes the use of a moisture barrier with a petrolatum, dimethicone, or zinc oxide base. Tucking dry gauze or washcloths into the skin folds also may help reduce moisture.²⁸

Incision Complications

   Following incision, healing is expected to involve the formation of a watertight seal within 24 hours.²⁹ Wound healing may be slower in patients with obesity. Surgical wounds are more prone to dehiscence and evisceration in the obese patient due to increased tension on the edges of the fascia at the time of wound closure. This increases the pressure on the tissues, reducing perfusion and oxygen delivery.²⁸ Wound healing also may be slower in the patient with obesity due to poor nutrition, tension on wound edges, reduced microperfusion, and emotional stress.

   Seroma formation, wound dehiscence, and wound infections are common postoperative complications in patients with obesity. In a prospective, randomized study of 331 patients undergoing gastric bypass surgery, 49 (15%) experienced complications; 7% were superficial wound complications, seromas, or hematomas and 8% were deep surgical site infections, or fascial dehiscence.³⁰ Wound infections can be a serious complication for these patients because many also have diabetes mellitus that can contribute to slower wound healing. Fatty tissue that was not excised may have a reduced blood supply, leading to tissue necrosis and infection.²⁹ The collection of pooled serous fluid or blood is an additional problem for obese patients, increasing internal pressure and tension on suture lines and subsequently reducing oxygenation to the tissues.³¹ Poorly vascularized tissue is believed to lack sufficient oxygen to enable neutrophils to effectively phagocytize bacteria.³²

   In the patient with obesity, extensive retraction (especially during abdominal surgeries) is thought to traumatize subcutaneous tissues, leading to wound infections.³³ Increased abdominal distension in the postoperative period may increase tension on abdominal incisions.

   The stress response of surgery further compromises perfusion and places the patient with obesity at increased risk for impaired wound healing.³⁴ The release of epinephrine, norepinephrine, and catecholamines in response to stress may trigger further vasoconstriction that potentially can reduce perfusion of the wound site.³⁵ Excess weight also can reduce chest expansion during respirations, further reducing oxygen supply to the tissues.

   Dehiscence and evisceration commonly occur during the proliferation phase of wound healing and are a result of reduced tensile strength following impaired collagen synthesis.³² In sutured incisions, collagen synthesis usually peaks at about day 5, at which point it is possible to palpate a healing ridge under the intact suture line. Absence of the healing ridge indicates impaired wound healing and increased risk for wound dehiscence.³⁶ Serous drainage from an incision between postoperative days 5 and 12 is a classic sign of wound dehiscence.³⁴

   Obesity is a major risk factor for sternal wound infections after coronary artery bypass surgery.^37,38 In a retrospective study, Zacharias and Habib reported that 51% of the 2,317 patients with sternal wound infections were obese (P = .001).³⁷ Another study of 3,560 patients undergoing coronary artery bypass surgery found that sternal wound infections were higher in patients with higher BMI.³⁸

   Obese renal transplant patients also were more likely to experience superficial breakdown and complete wound dehiscence and tended to have more wound infections, as shown in a retrospective study³⁹ in which 59 (12%) out of 493 subjects were obese. Patients with obesity were more likely than nonobese patients to experience superficial wound breakdown (14% versus 4%, respectively; P <0.01) and complete wound dehiscence (3% versus 0%, respectively; P <0.01). Wound infections also tended to be more frequent in patients with obesity (15% versus 8%, P = 0.11).

   Nursing interventions to maintain tissue perfusion include reducing pain, anxiety, hypovolemia, and hypothermia. Systemically, adequate circulating blood volume and adequate blood pressure are necessary for adequate wound perfusion. Subcutaneous blood vessels constrict very quickly following small decreases in blood volume.⁴⁰ The use of incentive spirometry deep breathing and coughing help promote oxygenation to a surgical wound.

   Abdominal binders help reduce the tension on abdominal incisions.²⁹ However, binders must not fit too snugly to avoid reduced circulation. Binder size is determined by measuring abdomen girth; each company provides a sizing chart. For proper fit, the clinician should be able to easily slide two fingers under the binder. For female patients, surgical bras also may be helpful to reduce the tension on sternal wounds.

Cellulitis

   Cellulitis, an acute, quickly spreading, pyogenic inflammation of the dermis and subcutaneous tissue, is a comorbid condition associated with obesity.⁴¹ Predisposing factors include disruption of the cutaneous barrier, venous or lymphatic compromise, and a previous history of cellulitis. The incidence of cellulitis has not been carefully studied; however, the Agency of Health Care Policy and Research ranked cellulitis 28 among the most common diagnoses for hospitalized patients in 1996.⁴² In one study, 73% of the cases were in the lower extremities.⁴³

   In the majority of cases, cellulitis, is caused by beta hemolytic streptococci, Staphylococcus aureus, or Hemophilus influenza. Incidence of community-acquired infection has increased due to methicillin-resistant S. aureus (CA-MRSA), which primarily causes skin/soft tissue infections. In a prospective study of 1,100 MRSA infections in 2000, 75% were related to CA-MRSA.⁴⁴

   Cellulitis presents with erythema, pain, warmth, edema, and often fever. Lymphangitic streaking may be present (see Figure 2). Recurrent cellulitis is common due to damage to lymphatic drainage.⁴¹

   Standard treatment includes leg elevation, bedrest, treatment of any open wounds, and antibiotics.⁴² Wound debridement may be needed if the infection is extensive and deep. Support stockings and good skin hygiene may help decrease recurrences.⁴¹

Lymphedema

   Lymphedema of the legs may be seen in patients with obesity, especially after surgery or radiation therapy. One person in 30 throughout the world is affected by lymphedema; 90% of cases occur secondary to surgery or radiation.⁴⁵ Lymphedema reduces local blood flow, tissue oxygenation, and wound healing. Impaired lymphatic vessels are unable to pump the protein-rich, pooled lymphatic fluid into circulation, causing edema of the legs (non-pitting to minimally pitting). The proteins that have been deposited in the tissues cause a thickening of the skin and fibrosis of the soft tissues, which increases the risk of skin injury.⁴⁶ If the condition is not treated, the stagnant fluid causes dilation of the tissue channels and decreased tissue oxygenation and provides a culture medium conducive to bacterial growth and recurrent infection.⁴⁶ Minor breaks in the skin can lead to acute cellulitis, heavily exudating wounds, and infections.

   If lymphatic obstruction occurs, extracellular fluid gradually assumes a higher protein content. This increases oncotic pressure and further attracts more fluid into the tissues.⁴⁷ Because the lymphatic tissue is prominent in the dermis, the edema becomes prominent in the visible skin. The skin becomes pitted, thickened, and fibrotic.⁴⁸

   Treatment consists of reducing the edema in the affected leg to allow the lymphatic fluid to flow back into the circulation and decrease the chance of infection. Edema can be reduced in the early stages of the disease by elevating the legs, wearing elastic stockings, and applying external compression pumps.⁴⁹ Severe or nonresponsive lymphedema may require complex decongestive physiotherapy (CDP), which consists of manual lymphatic drainage (MLD), compression bandaging, select exercises, and patient education. Manual lymphatic drainage, a light massage technique, is usually initiated by a specially trained therapist and involves massaging the chest or abdomen to empty the central lymphatic vessels, followed by massage from the distal to proximal aspect along the affected limb. Between sessions (two per day), the extremity is wrapped and select exercises are performed to help reduce limb size. Usually, therapy lasts 2 weeks and is repeated as needed.⁴⁹

   Another component of therapy is weight reduction. Excess weight may hinder venous return, limit exercise, and interfere with leg elevation or pneumatic pumping, thwarting the benefits of other prescribed therapies.
Treatment must be ongoing to maintain the return of lymphatic fluid to the circulation. Prevention of skin injury is also important. The skin should be cleansed with a mild soap and water. The soap should be rinsed off and the extremity dried well. The extremity should be moisturized daily, avoiding the areas between the toes.²

   Both cellulitis and lymphedema can be challenging situations for the patient and healthcare provider. The responsibility for management falls on the patient, making education about etiology and principles of management essential. Often, if patients understand the etiology of the disease process, they will develop methods to work a treatment plan into their daily routine.⁵⁰

Pressure Ulcers

   Patients who are immobile are at risk for pressure ulcers. Patients with obesity are often immobile and acutely ill when they present to the hospital. This, in addition to poor blood supply to the fatty tissue, increases their risk for pressure ulcers.⁵¹ Pressure ulcers typically develop over bony prominences; in persons with obesity, pressure created when skin folds touch may lead to pressure ulcers in unusual places. Clinical observations have revealed that pressure ulcers also may develop when beds or wheelchairs are too small for body size and the frame of the device causes pressure injury to the skin.⁵¹

   Skin inspection must be meticulous for these patients. This includes lifting, cleaning, and drying all skin folds. The caregiver must carefully assess for any pressure injury caused by catheters or other drainage tubes. During surgery, the occipital area and heels are prone to pressure injury.⁵² Care providers may need to manually reposition the head and heels to decrease pressure and implement appropriate use of support surfaces.
The intubated patient or the patient with a tracheostomy may develop skin injury in the neck skin folds due to seepage of secretions from the mouth or around the tracheostomy. Injury also may occur from the tracheostomy ties pressing into skin folds.²⁹ Clinician experience dictates that care must be taken in assessing, cleansing, and drying the neck skin folds.

   Pressure ulcer risk assessment should be initiated for patients with obesity on admission to any healthcare setting and be repeated at regular intervals to detect any change in condition that would increase the risk of pressure ulcer development.²⁸

Conclusion

   The number of obese patients continues to increase. Obesity is a chronic health problem, with numerous complications that affect the skin. These complications may simply be annoying or may be indicators of systemic disorders. Poorly healing surgical wounds and pressure ulcer development in this population may be costly healthcare issues, one of several important topics for future research related to obesity. Research relative to these special problems, interventions, and care needs of the obese patient is scant; this is a relatively new focus for the nursing profession. Studies relative to the prevalence and incidence of skin and wound conditions, best interventions, and appropriate use of products and technology are needed.

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