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Nutritional Dermatoses in the Hospitalized Patient

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Nutritional Dermatoses in the Hospitalized Patient HOSPITAL CONSULT IN PARTNERSHIP WITH THE SOCIETY FOR DERMATOLOGY HOSPITALISTS Nutritional Dermatoses in the Hospitalized Patient Melissa Hoffman, MS; Robert G. Micheletti, MD; Bridget E. Shields, MD Nutritional deficiencies may arise from inadequate nutrient intake, abnormal nutrient absorption, or improper nutrient PRACTICE POINTS utilization.4 Unfortunately, no standardized algorithm for • Nutritional deficiencies are common in hospitalized screening and diagnosing patients with malnutrition exists, patients and often go unrecognized. making early physical examination findings of utmost • Awareness of the risk factors predisposing patients importance. Herein, we present a review of acquired nutri- to nutritional deficiencies and the cutaneous manifes- tional deficiency dermatoses in the inpatient setting. tations associated with undernutrition can promote copy early diagnosis. Protein-Energy Malnutrition • When investigating cutaneous findings, undernutri- tion should be considered in patients with chronic Protein-energy malnutrition (PEM) refers to a set of infections, malabsorptive states, psychiatric illness, related disorders that include marasmus, kwashiorkor and strict dietary practices, as well as in those using (KW), and marasmic KW. These conditions frequently are certain medications. seen in developing countries but also have been reported 5 • Prompt nutritional supplementation can prevent patient in developed nations. Marasmus occurs from a chronic morbidity and mortality and reverse skin disease. deficiencynot of protein and calories. Decreased insulin pro- duction 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 Cutaneous disease may be the first manifestation of an underlying nutri- 7 tional deficiency, highlighting the importance of early recognition by der- (IBW) without edema or hypoproteinemia. Kwashiorkor matologists. Undernutrition occurs when there is an imbalance between is the edematous form of PEM that develops from iso- nutrient intake and metabolic demand. Many hospitalized patients are lated protein deficiency, resulting in edema, diarrhea, and Do 6 in catabolic states due to chronic illness, infection, malabsorption, or immunosuppression. Micronutrient deficiencies, oxida- medication. These patients are at an increased risk for undernutrition tive stress, slow protein catabolism, and excess antidi- and therefore associated cutaneous disease. This review details the risk uretic hormone have been proposed as potential drivers factors for nutritional deficiency, illustrates the presentations of cutane- 8 ous disease, reviews diagnostic workups, and provides suggestions for of KW. Kwashiorkor affects children between 60% and supplementation in the undernourished patient. 80% IBW. Marasmic KW has features of both diseases, Cutis. 2020;105:296-302, 308. including children who are less than 60% IBW but with associated edema and/or hypoproteinemia.9 Although PEM is uncommon in adults, hospitalized he World Health Organization defines malnutri- patients carry many predisposing risk factors, including tion as deficiencies, excesses, or imbalances in infections, malabsorptive conditions, psychiatric disease, T an individual’s intake of energy and/or nutrients.1 and chronic illness (eTable). Patients with chronic infec- This review will focus on undernutrition, which may tions present with findings consistent with marasmic KW result fromCUTIS macronutrient or micronutrient deficiencies. due to lean body mass loss. Undernutrition in the hospitalized patient is a common The cutaneous findings in PEM are related to dysmatu- yet underrecognized phenomenon, with an estimated ration of epidermal keratinocytes and resultant epidermal prevalence of 20% to 50% worldwide.2 Malnutrition is an atrophy.10 Patients with marasmus exhibit dry, wrinkled, independent risk factor for patient morbidity and mortality loose skin due to subcutaneous fat loss. Emaciated chil- 3 and has been associated with increased health care costs. dren often lose their buccal fat pads, and reduced perianal From the Department of Dermatology, University of Pennsylvania Perelman School of Medicine, Philadelphia. The authors report no conflict of interest. The eTable is available in the Appendix online at www.mdedge.com/dermatology. Correspondence: Bridget E. Shields, MD, 3400 Civic Center Blvd, Philadelphia, PA 19104 ([email protected]). 296 I CUTIS® WWW.MDEDGE.COM/DERMATOLOGY Copyright Cutis 2020. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. HOSPITAL CONSULT HOSPITAL CONSULT adipose may lead to rectal prolapse. Increased lanugo hair small amounts and frequent intervals.5 Skin-directed therapy may be present on the face, and alopecia of the scalp may is aimed at restoring epidermal function and hydration, with occur.6 In KW, cutaneous disease progresses from conflu- regular moisturization and application of barrier creams, such ent hyperkeratosis to a dry atrophic epidermis that erodes as zinc oxide ointment or petrolatum.10 easily, leaving underlying pale erythema. The resultant pattern is one of hyperpigmented plaques with slightly Zinc Deficiency raised borders, and hypopigmented patches and erosions Zinc is an essential trace element that provides regulatory, described as flaky paint dermatitis (Figure 1).5 Lesions structural, and catalytic functions across multiple bio- appear first in areas of friction. The hair often is dry and chemical pathways6 and serves as an enzymatic cofactor brittle; curly hair may straighten and scale.11 Red-yellow and key component for numerous transcription factors.17 to gray-white hypopigmentation may develop, denoting Zinc is derived from food sources, and its concentration periods of inadequate nutrition. The flag sign describes correlates with protein content.18 Zinc is found in both alternating horizontal bands of hypopigmentation inter- animal and plant-based proteins, albeit with a lower oral spersed with bands of pigmented hair. The nails usually bioavailability in the latter. Zinc deficiency may be inher- are thin and soft and may exhibit the nail flag sign, char- ited or acquired. Primary acrodermatitis enteropathica is acterized by horizontal bands of white and red.12 Cheilitis, an autosomal-recessive disorder of the solute carrier fam- angular stomatitis, and vulvovaginitis may be present.6 ily 39 member 4 gene, SLC39A4 (encodes zinc transporter In adults, weight loss and body mass index can be ZIP4 on enterocytes); the result is abnormal zinc absorp- used to assess nutritional status, along with a focused tion from the small intestine.18 history and physical examination. Complete blood cell Acquired zinc deficiency copyoccurs from decreased dietary count, electrolyte levels, and blood urea nitrogen should be zinc intake, impaired intestinal zinc absorption, excessive assessed, as hypoglycemia and anemia often accompany zinc elimination, or systemic states of high catabolism or PEM.13 In KW, hypoalbuminemia and hypoproteinemia low albumin (eTable). Total parenteral nutrition–associated are invariably present. Although prealbumin may be a deficiency has arisen when nutritional formulations did not valid prognostic indicator of disease outcomes and mor- contain trace elements during national shortages or when tality in patients at risk for malnutrition, checking other prolonged TPN was not anticipated and trace elements were serum biomarkers remains controversial.14 Focused testing removed.19 Zinc levels may already be low in patients with may be warranted in patients with risk factors for chronic chronicnot illness or inflammation, so even a short period on infectious processes, such as human immunodeficiency TPN can precipitate deficiency.18,19 Diets high in phytate may virus or tuberculosis.6 Skin biopsy may solidify the diagno- result in zinc deficiency, as phytate impairs intestinal zinc sis of PEM. Hypertrophy of the stratum corneum, atrophy absorption.20 Approximately 15% of patients with inflamma- of the stratum spinosum and stratum granulosum, and tory bowel disease experienced zinc deficiency worldwide.21 increased basal layer melanin have been reported.15 In Crohn disease, zinc deficiency has been associated with Treatment involves initial fluid resuscitation and cor- active intestinal inflammation, increased risk for hospitaliza- Do 22,23 rection of electrolyte imbalances, followed by nutritional tion, surgeries, and disease-related complications. replacement.13 Oral or enteral tube feedings are preferred Medications such as antiepileptics, antimetabolites, over total parenteral nutrition (TPN), as they enhance recov- or penicillamine may induce zinc deficiency, highlight- ery of the gastrointestinal tract.16 Refeeding should occur in ing the importance of medication review for hospitalized patients (eTable). Catabolic states, frequently encoun- tered in hospitalized patients, increase the risk for zinc deficiency.24 Patients with necrolytic migratory erythema (associated with pancreatic glucagonomas) often experi- ence low serum zinc levels.25 The skin is the third most zinc-abundant tissue in the human body. Within keratinocytes, zinc is critical to normal proliferation and suppression of inflammation.17 CUTIS Zinc also plays an important role in cutaneous immune function.26 Zinc deficiency presents with sharply demar- cated, flaccid pustules and bullae that erode into scaly,
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