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Year : 2022  |  Volume : 6  |  Issue : 1  |  Page : 1-5

Fluid and diet management in acute skin failure

1 Department of Dermatology, Marsleeva Medicity, Kottayam, Kerala, India
2 Department of Dermatology, Sri Siddhartha Medical College, Tumkur, Karnataka, India
3 Department of Dermatology, ESIC Medical College and PGIMSR, Bengaluru, Karnataka, India

Date of Submission02-Jan-2021
Date of Decision25-Feb-2021
Date of Acceptance25-Mar-2021
Date of Web Publication25-Feb-2022

Correspondence Address:
Neethu Mary George
Onnarayil, Olamattom, Thodupuzha, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/cdr.cdr_1_21

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Acute skin failure (ASF) is due to dermatological conditions that cause total dysfunction of skin. Normal skin resists mechanical damage, protects body from external contaminants, regulates heat loss from the body, and retains body fluids and protein, all of which are lost in ASF. The treatment includes a multidisciplinary approach with aims to arrest the progression and heal the already formed lesions, wound care, fluid, electrolyte, and diet management. Along with medical management, it is extremely important to equally consider supportive therapy with correction of fluid and nutrient losses. Fluid and diet correction should neither be underdone, which can delay recovery, nor be overdone, which can lead to complications. The article covers the basis of fluid and nutritive loss and methods of correction in this dermatological emergency.

Keywords: Dermatological emergencies, fluid correction, pemphigus vulgaris, Stevens–Johnson syndrome

How to cite this article:
George NM, Potlapati A, Shivanna R. Fluid and diet management in acute skin failure. Clin Dermatol Rev 2022;6:1-5

How to cite this URL:
George NM, Potlapati A, Shivanna R. Fluid and diet management in acute skin failure. Clin Dermatol Rev [serial online] 2022 [cited 2022 Aug 19];6:1-5. Available from: https://www.cdriadvlkn.org/text.asp?2022/6/1/1/338572

  Introduction Top

Acute skin failures (ASFs) are dermatological emergencies due to total dysfunction of skin and comprise conditions such as Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), other severe drug reactions, erythroderma, and autoimmune bullous disorders and can be broadly divided into wet and dry types. Extensive epidermal detachment is also associated with loss of large amounts of electrolytes and protein from blister fluid. A good diet given through proper mode starting from day 1 helps in healing of the lesions, rectifying metabolic disturbances, and providing raw materials for the body to regenerate lost skin components. Furthermore, majority of these conditions are associated with severe mucosal involvement, and hence, the type of diet and mode of nutrition in these patients become factors of utmost importance. If we assess a spectrum of mucosal involvement in conditions such as SJS/TEN, they include erosions, ulcerations, and bleeding starting from oral cavity to anus with severe pain, bleeding, malabsorption, and rarely perforation and in later stages can form strictures, pseudodiverticular sacs, pseudomembranes, stenosis, and necrosis.[1] Hence, the care of mucosa along with skin becomes equally important. Furthermore, the lack of direct visibility prevents us from assessing the progression of disease or improvement in mucosa.

  Spectrum of Gastrointestinal and Mucosal Involvement Top

In a study by Jha et al., the symptoms, signs, and complications of gastrointestinal (GI) involvement in SJS/TEN were assessed.[1] The symptoms were GI bleeding (68%), diarrhea (52%), abdominal pain (40%), abdominal distension (12%), vomiting (8%), and complications including luminal erosions/inflammation (60%), ulcer (36%) involving large bowel, small bowel, esophageal, and gastric mucosa, perforation (12%) (small bowel/colon), strictures (8%) (ileal/ileocolonic), mesenteric ischemia, intestinal infarction, ileoileal intussusceptions, pseudodiverticular sacs, intra-abdominal abscess, pseudomembrane formation, subacute intestinal obstruction, malabsorption, hypoalbuminemia, and protein-losing enteropathy. The role of steroid in patients with SJS or TEN with GI involvement is doubtful as it may exacerbate mucosal sloughing and GI bleeding in SJS or TEN. Pancreatic involvement as elevated pancreatic enzymes and asymptomatic pancreatitis was described in a study by Dylewski et al. in pediatric SJS/TEN, and all children with elevated enzymes tolerated enteral feeding. Hence, in the absence of symptomatic pancreatitis, patients with SJS or TEN can be supported with enteral nutrition (EN).[2]

  Pathophysiology of Fluid Loss Top

Total water loss through the skin is 400 ml/day which exceeds in patients with ASF. This is due to impaired barrier function of the skin causing increased transepidermal water loss (TEWL) and enhanced percutaneous fluid loss by transpiration. Fluid and electrolyte loss will be more in wet type of ASF, whereas dry ASF will have more protein loss.

Inadequate fluid replacement can lead to reduced intravascular volume and formation of hyperosmolar urine leading to dehydration and decreased urinary output. This, along with loss of electrolytes in blister fluid, can lead to electrolyte imbalance. Patients with acute generalized pustular psoriasis may develop acute hypocalcemia secondary to severe hypoalbuminemia. Correction of hypocalcemia can help in disease remission as hypocalcemia is known to precipitate pustular psoriasis.

  Pathophysiology of Nutrient Loss Top

The principal nutrients lost in ASF are protein and iron. Continuously shedding scales, increased basal metabolic rate, decreased hepatic synthesis, and dermatogenic enteropathy can lead to hypoproteinemia. Reduced iron and Vitamin B12 levels are through shed skin, impaired absorption, and increased utilization. Increased cell turnover rate can lead to folate deficiency, all of which will contribute in the development of anemia. A complex system of special enzymes, their cofactors (selenium, zinc, and iron), and vitamins (E and C) helps to counter the oxidant stress seen in the acute phase of injury or illness. Patients may have variable micronutrient deficiencies in the early phase of illness. During enteral feeding competition for absorption is also to be considered; ascorbic acid inhibits Cu absorption, whereas Cu and Zn compete for absorption. Micronutrient deficiencies have been described in critically ill adults, with low serum levels of thiamine, folate, Vitamin B12, zinc, b-carotene, Vitamin A, Vitamin C, Vitamin E, selenium, and copper.

Diffuse scaling leads to protein loss of approximately 20–30 g/m2 body surface area (BSA) per day. This amount varies with the underlying disease. In the presence of exudative skin lesions, the combined protein loss through oozing from the skin surface and urine (urinary nitrogen derived from hypercatabolism) may amount to 150–200 g/day.[3] There is increased catabolism of tissue protein in ASF. This along with altered glucose metabolism leads to loss of tissue protein which causes hypoalbuminemia and negative nitrogen balance and in long term is manifested as muscle wasting.

  Route of Diet Top

Oral intake is often difficult because of upper gastrointestinal tract (GIT) injury. Therefore, diet and fluid modifications are important. Early in the disease when dysphagia and odynophagia are severe, a fluid diet is preferable and more tolerable for the patient. If nutritional requirements exceed the ability to eat, then there is a role for parenteral or nasogastric (NG) feeding. Unless it is extensive, EN through NG tube is started, and in majority, it is changed over to oral liquid feeds in few days. In addition to feeding, a NG tube helps in assessing gastric emptying. Parenteral nutrition (PEN) appears to be recommended due to concern that the extensive epithelial loss in SJS/TEN affects the entire GIT and results in poor absorption and intolerance as well as difficulty placing enteral feeding tubes. It is also noted that majority of the patients who are put on continuous PEN have high mortality because of the risk of sepsis. The role of nil per oral is not described and could be considered in severe GI bleed, perforation, or symptomatic acute pancreatitis. Early and continuous oral nutrition reduces the risk of stress ulcers, reduces bacterial translocation infection, allows early discontinuation of venous lines, and prevents adhesions in the upper GIT. The best route has to be individualized for each patient and their needs, including assessment of total body surface area (TBSA) affected.

For micronutrient supplementation, factors such as bowel edema, bowel ischemia, hemodynamic instability, and fluid resuscitation affect absorption by the enteral route in critically ill patients. However, a meta-analysis by Visser et al. did not find clear evidence that parenteral is superior to enteral administration in terms of clinical outcomes.[4] Timing, duration, and dosing are key factors for optimal clinical benefit. The repletion of micronutrients, and specifically antioxidants, would probably achieve a greater efficacy if given before massive oxidative injury.

  Type of Diet Top

Nutrition is an integral part of management as SJS/TEN is a hypermetabolic state. Glycemic control can be a problem as a result of stress and previous treatment with systemic steroids. Food given also plays an important role, and it should be able to meet the nutrition loss that has happened over the disease process. The calorie and protein requirement increases with mucosal and skin damage and is estimated to be around 30–35 kcal/kg/day and 1.5 g/kg/day. There is a significant negative correlation of energy needs with BMI and age.[5] Factors to consider with regard to oral feeds are temperature, acidity, texture, and moisture of food. Hot, cold, acidic food and beverages worsen pain. texture, and moisture of food. Soft, bland meal is initially preferred. There is hardly any literature on the types of foods that can be advised in such patients. Feed often and prepare nutritious mixes using locally available foods of good quality. Mashed banana/potato/rice, soft boiled vegetables, dal, and porridge are some of the local foods given. Adding ghee, jaggery, etc., enhances the taste and nutritive value of the feeds given. Oils/ghee also coats the alimentary tract and helps in the absorption of fat-soluble vitamins (A, D, E, and K). Calorie and protein calculation can be approximated with the help of a nutritionist. Certain mobile apps can be used by caregivers which help in the calculation of nutritive value of individual ingredients. It is important to replenish the lost nutrients including vitamins and minerals. Essential fatty acid deficiency can lead to altered barrier function and disruption in epidermal homeostasis leading to an increase in TEWL. The recommended daily allowance for ω 6 and ω 3 FA in an adult is approximately 5%–10% and 0.6%–1.2% of total daily calories, respectively. Supplementation much above the recommended dietary allowance may even lead to adverse effects such as increased bleeding tendency, decreased blood pressure, fishy aftertaste, and bloating.[6] Blenderized food is the most common type of NG feed in developing countries primarily because it is cheaper than commercially prepared feeds. It is viscous and chunks of food may block the feeding tube and there is a risk for complications like feed contamination. Commercially prepared enteral feeds such as polymeric feeds and elemental feeds are not commonly used. Disease-specific feed can be used if the situation demands.

NG tubes are fairly easy to insert but should only be done by trained staff because of the risk of misplacement and esophageal or pulmonary perforation. Misplacement can lead to pulmonary aspiration of feeds with potentially fatal results. Methods for checking the position of the tube include air insufflation and auscultation of the epigastrium, aspiration of gastric contents, and testing with litmus paper and X-ray confirmation. In general, the distance that tubes are inserted should be recorded, or even the tube itself marked with tape to identify migration.

Long-term NG tubes should usually be changed every 4–6 weeks, switching to the other nostril. To minimize aspiration, patients should be fed propped up by 30°. They must also be kept propped up for 30 min after feeding. Continuous feed should not be given overnight in patients who are at risk. Any drugs administered through an enteral tube feeding (ETF) should be liquid and should be given separately from the feed with flushing of the tube before and after. Tube clogging can be minimized by regular flushing with water. Simultaneous use of other drugs, particularly antibiotics, is usually the cause of apparent ETF-related diarrhea. Fiber-containing feeds and breaks in the feeding of 4–8 h sometimes help with ETF-related diarrhea. Avoiding gastric acid suppression and allowing breaks in feeding to let gastric pH fall will help prevent bacterial overgrowth during ETF.[7]

  Oral Care Top

Oral hygiene should be maintained with normal saline swishes or antiseptic or anesthetic mouthwashes. Saline compresses followed by the application of lubricants can be advised for the lips. This also helps soften hemorrhagic lip crusts.

Some centers do use mouthwash prepared by adding 125 ml (100 mg) of diphenhydramine, 1 ampule of 2% (100 mg) lidocaine, and 2 ampules of 8.4% sodium bicarbonate to 1000 ml of sterile saline, commonly known as diphenhydramine-lidocaine-antacid mouthwash for pain and for resolution of mucositis, but its long-term efficacy is yet to be evaluated.[8]

  Fluid Management Top

Unlike burns, TEN lacks the distinctive combination of altered capillary permeability, decreased colloid osmotic pressure, and sodium sequestration, which cause the massive interstitial shift and plasma deficits of a major burn injury. Hence, fluid requirements in TEN are generally less than the estimated volume in a burn injury of comparable size, and the fluid resuscitation followed in burns is usually unnecessary for most TEN patients.[9]

The Parkland formula estimates the fluid requirements for critical burn patients in the first 24 h after injury using the patient's body weight and the percentage of TBSA that is affected by thermal burns. The formula recommends 4 ml/kg of body weight in adults (3 ml/kg in children) per percentage burn of %TBSA of crystalloid solution over the first 24 h of care. Delivery of half the volume is in the first 8 h postburn and the remaining volume given over the next 16 h. The “Wallace rule of nines” is the most common method of determining BSA.

Fluid replacement requirements are about 30% lower than the volume, as required for burns affecting similar BSA.[10] A combination of intravenous and enteral supplementation has to be given. Fluid replacement with electrolyte solution (0.7 ml/kg/% affected area) and albumin solution (5% human albumin, 1 ml/kg/% affected area) is recommended, titrating to maintain a urine output of 0.5–1 ml/kg/h.[9],[11] After initial 24 h, it should be guided by previous day's output. Regular input–output chart has to be maintained. Gradually IV fluids should be decreased and NG feed should be encouraged. It must be noted that overcorrection of hypovolemia may also lead to pulmonary edema.[12] Blood transfusion may be useful in some cases and perhaps work by the dilution of drug metabolites, cytokines, cytotoxic T-cells and autoantibodies. It also provides immunoglobulin, corrects anemia and hypovolemia.[12]

Patients of TEN lose a significant amount of fluid as blister fluid and insensible fluid loss. Adult patients having involvement of 50% of BSA lose around 3–4 L of fluid every day. This is usually accompanied by the loss of electrolytes such as sodium, potassium, and chloride in blister fluid. Hypophosphatemia is a common complication in these patients, aggravating insulin resistance, which can alter the neurological status and diaphragmatic functions. If replacement is not given promptly, the patient may develop dehydration, urine becomes hyperosmolar, urine output decreases, and prerenal failure may develop. A reduction in urine volume may be an early indicator of hypovolemia or septicemia. A pulse rate of 120 or more per minute indicates a negative fluid balance, even in the presence of precipitating factors such as septicemia and fever.

It is advisable to insert peripheral and central venous lines through nonlesional skin whenever possible, and peripheral venous cannulas should be changed after 48 h if possible.[6] Monitor fluid balance carefully and catheterize if necessary. The environmental temperature should be maintained at 30°C–32°C; alternatively, an infrared lamp can be used to reduce shivering and the associated energy loss. The use of air-fluidized beds and a burn cage ensures patient comfort and helps in caregiving. However, air-fluidized beds may increase the evaporative fluid loss from the body surface and are better avoided till major fluid and electrolyte imbalance is corrected.[3]

  Monitoring Top

An hourly record of the pulse, respiratory rate, blood pressure, and urine volume is essential. Body weight and signs of edema have to be checked frequently. The body temperature and gastric emptying (measuring volume of gastric aspiration) should be recorded every 3–4 h. Serum levels of albumin and prealbumin have historically been recommended for evaluating nutrition status, although recent guidelines note that these reflect the severity of illness rather than nutrition status in acutely ill patients.[9] Serial serum lactate measurements may also help to detect tissue hypoperfusion. Laboratory signs of dehydration may include rising hematocrit and hemoglobin, urinary specific gravity >1.020, elevated serum osmolality, hypernatremia, and blood urea nitrogen-to-creatinine ratio >20:1.

[Table 1] denotes the general measures to be followed for a patient with ASF [Table 1].
Table 1: General measures and supportive care in acute skin failure

Click here to view

  Pregnant Females Top

TEN in pregnancy puts two lives at risk, and hence, it requires the immediate attention of both dermatologists and gynecologists. It is necessary to keep a close watch on fetal parameters during management. All kinds of diet can be included in the diet, but a close watch on glycemic control has to be kept. Hypoalbuminemia can aggravate the already existing edema due to fluid overload.

  Children Top

In children with severe burns, the hypermetabolic stress response and poor intake result in energy deficits, and the negative effects on nutritional status have been shown to persist for months after injury.[13] It is necessary to constantly monitor the weight of a child who is in an intensive care unit for a prolonged time to not miss undernourishment. A weight-for-age Z score lower than −2.0, which is two standard deviations below the mean for age and sex, is termed as undernourished.[14] Serum levels of Vitamin D are decreased in children with severe burns.[15]

The following formula is useful in calculating the daily energy requirements of a child with SJS or TEN. Energy requirements (in calories) for pediatric SJS/TEN patients are estimated by the following equation.[16]

Daily requirement in calories = (preinjury weight [kg] × (24.6)) + (wound size [% of BSA] × 4.1) + 940 calories.

The protein requirement is 3–4 g/kg body weight per day in children.[17]

Maintaining room temperature at 30°C–32°C is recommended in addition to strict aseptic precautions, maintenance of fluid, acid–base and electrolyte balance. SJS/TEN in children does not differ significantly in its etiology, clinical features, and management strategies from adult SJS/TEN. It has been seen that the energy needs of children with SJS/TEN are 22% less than burn patients of similar age and wound size. Currently, there are not any specific recommendations for micronutrient supplementation in the acute phase of critical illness[18] and pharmacological use of micronutrients during the acute phase remains controversial due to reports of toxicity. However, subclinical or clinical micronutrient deficiencies may affect nutritional recovery, particularly when anabolism has been restored and nutritional rehabilitation should be ensured postdischarge.

Thus, it is equally important to consider fluid and nutrition in a patient with ASF as that of medical management.

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  References Top

Jha AK, Suchismita A, Jha RK, Raj VK. Spectrum of gastrointestinal involvement in Stevens-Johnson syndrome. World J Gastrointest Endosc 2019;11:115-23.  Back to cited text no. 1
Dylewski ML, Prelack K, Keaney T, Sheridan RL. Asymptomatic hyperamylasemia and hyperlipasemia in pediatric patients with toxic epidermal necrolysis. J Burn Care Res 2010;31:292-6.  Back to cited text no. 2
Inamadar AC, Palit A. Acute skin failure: Concept, causes, consequences and care. Indian J Dermatol Venereol Leprol 2005;71:379-85.  Back to cited text no. 3
[PUBMED]  [Full text]  
Visser J, Labadarios D, Blaauw R. Micronutrient supplementation for critically ill adults: A systematic review and meta-analysis. Nutrition 2011;27:745-58.  Back to cited text no. 4
Graves C, Faraklas I, Maniatis K, Panter E, La Force J, Aleem R, et al. Nutrition in toxic epidermal necrolysis: A multicentre review. Nutr Clin Pract 2016;31:708-847.  Back to cited text no. 5
Creamer D, Walsh SA, Dziewulski P, Exton LS, Lee HY, Dart JK, et al. U.K. guidelines for the management of Stevens-Johnson syndrome/toxic epidermal necrolysis in adults 2016. Br J Dermatol 2016;174:1194-227.  Back to cited text no. 6
Stroud M, Duncan H, Nightingale J; British Society of Gastroenterology. Guidelines for enteral feeding in adult hospital patients. Gut 2003;52 Suppl 7:vii1-2.  Back to cited text no. 7
Turhal NS, Erdal S, Karacay S. Efficacy of treatment to relieve mucositis-induced discomfort. Support Care Cancer 2000;8:55-8.  Back to cited text no. 8
Shiga S, Cartotto R. What are the fluid requirements in toxic epidermal necrolysis? J Burn Care Res 2010;31:100-4.  Back to cited text no. 9
Schneider JA, Cohen PR. Stevens-Johnson syndrome and toxic epidermal necrolysis: A concise review with a comprehensive summary of therapeutic interventions emphasizing supportive measures. Adv Ther 2017;34:1235-44.  Back to cited text no. 10
Mockenhaupt M. Stevens-Johnson syndrome and toxic epidermal necrolysis: Clinical patterns, diagnostic considerations, etiology, and therapeutic management. Semin Cutan Med Surg 2014;33:10-6.  Back to cited text no. 11
Gupta LK, Martin AM, Agarwal N, D'Souza P, Das S, Kumar R, et al. Guidelines for the management of Stevens-Johnson syndrome/toxic epidermal necrolysis: An Indian perspective. Indian J Dermatol Venereol Leprol 2016;82:603-25.  Back to cited text no. 12
[PUBMED]  [Full text]  
Hart DW, Wolf SE, Mlcak R, Chinkes DL, Ramzy PI, Obeng MK, et al. Persistence of muscle catabolism after severe burn. Surgery 2000;128:312-9.  Back to cited text no. 13
Mehta NM, Duggan CP. Nutritional deficiencies during critical illness. Pediatr Clin North Am 2009;56:1143-60.  Back to cited text no. 14
Gottschlich MM, Mayes T, Khoury J, Warden GD. Hypovitaminosis D in acutely injured pediatric burn patients. J Am Diet Assoc 2004;104:931-41, quiz 1031.  Back to cited text no. 15
McClave SA, Taylor BE, Martindale RG, Warren MM, Johnson DR, Braunschweig C, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). J Parenter Enteral Nutr 2016;40:159-211.  Back to cited text no. 16
Das S, Ramamoorthy R. Stevens-Johnson syndrome and toxic epidermal necrolysis in children. Indian J Paediatr Dermatol 2018;19:9-14.  Back to cited text no. 17
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Nilesh M. Micronutrients in critical illness: Essential and enigmatic. Pediatric Crit Care Med 2018;19:907-8.  Back to cited text no. 18


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Spectrum of Gast...
Pathophysiology ...
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Route of Diet
Type of Diet
Oral Care
Fluid Management
Pregnant Females
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