The World Health Organization defines malnutrition as deficiencies, excesses, or imbalances in an individual’s intake of energy and/or nutrients.1 This review will focus on undernutrition, which may result from macronutrient or micronutrient deficiencies. Undernutrition in the hospitalized patient is a common yet underrecognized phenomenon, with an estimated prevalence of 20% to 50% worldwide.2 Malnutrition is an independent risk factor for patient morbidity and mortality and has been associated with increased health care costs.3 Nutritional deficiencies may arise from inadequate nutrient intake, abnormal nutrient absorption, or improper nutrient utilization.4 Unfortunately, no standardized algorithm for screening and diagnosing patients with malnutrition exists, making early physical examination findings of utmost importance. Herein, we present a review of acquired nutritional deficiency dermatoses in the inpatient setting.
Protein-energy malnutrition (PEM) refers to a set of related disorders that include marasmus, kwashiorkor (KW), and marasmic KW. These conditions frequently are seen in developing countries but also have been reported in developed nations.5 Marasmus occurs from a chronic deficiency of protein and calories. Decreased insulin production and unopposed catabolism result in sarcopenia and loss of bone and subcutaneous fat.6 Affected patients include children who are less than 60% ideal body weight (IBW) without edema or hypoproteinemia.7 Kwashiorkor is the edematous form of PEM that develops from isolated protein deficiency, resulting in edema, diarrhea, and immunosuppression.6 Micronutrient deficiencies, oxidative stress, slow protein catabolism, and excess antidiuretic hormone have been proposed as potential drivers of KW.8 Kwashiorkor affects children between 60% and 80% IBW. Marasmic KW has features of both diseases, including children who are less than 60% IBW but with associated edema and/or hypoproteinemia.9
Although PEM is uncommon in adults, hospitalized patients carry many predisposing risk factors, including infections, malabsorptive conditions, psychiatric disease, and chronic illness (eTable). Patients with chronic infections present with findings consistent with marasmic KW due to lean body mass loss.
The cutaneous findings in PEM are related to dysmaturation of epidermal keratinocytes and resultant epidermal atrophy.10 Patients with marasmus exhibit dry, wrinkled, loose skin due to subcutaneous fat loss. Emaciated children often lose their buccal fat pads, and reduced perianal adipose may lead to rectal prolapse. Increased lanugo hair may be present on the face, and alopecia of the scalp may occur.6 In KW, cutaneous disease progresses from confluent hyperkeratosis to a dry atrophic epidermis that erodes easily, leaving underlying pale erythema. The resultant pattern is one of hyperpigmented plaques with slightly raised borders, and hypopigmented patches and erosions described as flaky paint dermatitis (Figure 1).5 Lesions appear first in areas of friction. The hair often is dry and brittle; curly hair may straighten and scale.11 Red-yellow to gray-white hypopigmentation may develop, denoting periods of inadequate nutrition. The flag sign describes alternating horizontal bands of hypopigmentation interspersed with bands of pigmented hair. The nails usually are thin and soft and may exhibit the nail flag sign, characterized by horizontal bands of white and red.12 Cheilitis, angular stomatitis, and vulvovaginitis may be present.6
In adults, weight loss and body mass index can be used to assess nutritional status, along with a focused history and physical examination. Complete blood cell count, electrolyte levels, and blood urea nitrogen should be assessed, as hypoglycemia and anemia often accompany PEM.13 In KW, hypoalbuminemia and hypoproteinemia are invariably present. Although prealbumin may be a valid prognostic indicator of disease outcomes and mortality in patients at risk for malnutrition, checking other serum biomarkers remains controversial.14 Focused testing may be warranted in patients with risk factors for chronic infectious processes, such as human immunodeficiency virus or tuberculosis.6 Skin biopsy may solidify the diagnosis of PEM. Hypertrophy of the stratum corneum, atrophy of the stratum spinosum and stratum granulosum, and increased basal layer melanin have been reported.15
Treatment involves initial fluid resuscitation and correction of electrolyte imbalances, followed by nutritional replacement.13 Oral or enteral tube feedings are preferred over total parenteral nutrition (TPN), as they enhance recovery of the gastrointestinal tract.16 Refeeding should occur in small amounts and frequent intervals.5 Skin-directed therapy is aimed at restoring epidermal function and hydration, with regular moisturization and application of barrier creams, such as zinc oxide ointment or petrolatum.10
Zinc is an essential trace element that provides regulatory, structural, and catalytic functions across multiple biochemical pathways6 and serves as an enzymatic cofactor and key component for numerous transcription factors.17 Zinc is derived from food sources, and its concentration correlates with protein content.18 Zinc is found in both animal and plant-based proteins, albeit with a lower oral bioavailability in the latter. Zinc deficiency may be inherited or acquired. Primary acrodermatitis enteropathica is an autosomal-recessive disorder of the solute carrier family 39 member 4 gene, SLC39A4 (encodes zinc transporter ZIP4 on enterocytes); the result is abnormal zinc absorption from the small intestine.18
Acquired zinc deficiency occurs from decreased dietary zinc intake, impaired intestinal zinc absorption, excessive zinc elimination, or systemic states of high catabolism or low albumin (eTable). Total parenteral nutrition–associated deficiency has arisen when nutritional formulations did not contain trace elements during national shortages or when prolonged TPN was not anticipated and trace elements were removed.19 Zinc levels may already be low in patients with chronic illness or inflammation, so even a short period on TPN can precipitate deficiency.18,19 Diets high in phytate may result in zinc deficiency, as phytate impairs intestinal zinc absorption.20 Approximately 15% of patients with inflammatory bowel disease experienced zinc deficiency worldwide.21 In Crohn disease, zinc deficiency has been associated with active intestinal inflammation, increased risk for hospitalization, surgeries, and disease-related complications.22,23