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CHAPTER37 Nutritional requirements in burn patients
Increased nutritional requirements
afterburns
Hypermetabolism can last for up to 36 months following burns, covering
more than 30% of total body surface area (TBSA), raising calorie requirements up to 200% above baseline. Cachexia and lean muscle loss ensue,
resulting in adverse outcomes. For example, losses in total body mass
of 10%, 20%, 30%, and 40% can lead to immune dysfunction, decreased
wound healing, severe infections, and death respectively. Therefore, alongside resuscitation, surgery and pharmacological measures (anabolic agents),
nutritional supplementation is crucial in ameliorating hypermetabolism. It
not only treats dietary deciencies, but also supports healing and recovery.
Route and timing offeeding
Where feasible, nasogastric or nasojejunal enteral feeding is preferred for
several reasons including reduced bacterial translocation and sepsis, increased splanchnic blood ow, and preservation of alimentary structure.
For burns >20% TBSA, enteral tubes may be more appropriate than oral
feeding as patients may have altered mentation, endotracheal ventilation,
and require large volumes of feed to meet metabolic needs. Enteral nutrition should ideally commence within 12 hours post burn as this improves
outcomes. Nasojejunal feeding reduces pneumonia rates, improves nutritional intake, and may be preferable. When safe, such as when post- burn
ileus has resolved, the oral route may be used. Parenteral nutrition may be
necessary where requirements cannot be met enterally. However, parenteral feeding is associated with overfeeding and a greater incidence of complications including catheter- related sepsis.
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ENERGY REQUIREMENTS
Energy requirements
Both over- and underfeeding can lead to poor outcomes. It is therefore
crucial that supplementation closely matches requirements. Measurement
of resting energy expenditure by indirect calorimetry remains the gold
standard for assessing caloric requirements. However, since many centres
do not possess calorimetric equipment, predictive equations are often used
(Table 37.1). Only the recommended adapted Toronto equation correlates
highly with indirect calorimetry but may be too complicated for routine
clinical practice. Pragmatism may be required since controversy regarding
the most accurate equation is ongoing.
Table37.1 Daily caloric requirement estimation equations foradults
and children
Equation Patient Group Requirement (kcal/ day)
Galveston infant 0– 1 2,100 kcal/ m2 + 1,000 kcal/ m2 burn
Galveston
revised
Galveston
adolescent
Toronto Adults – 4,343 + (10.5 × %TBSA) + (0.23×kcal)
Schoeld Female 3– 10years (16.97 × weight in kg) + (1,618 × height
Schoeld Male 3– 10years (19.6 × weight) + (1033 × height) +
Schoeld Female 10– 18years (8,365 × weight) + (4.65 × height) + 200
Schoeld Male 10– 18years (16.25 × weight) + (1372 × height) +
Curreri formula 16– 59 25 kcal/ kg of weight + (40) TBSA
Curreri formula >60 20 kcal/ kg of weight + (65) TBSA
Modied Harris– Benedict equation (f or basal requirements without stress or activity allowance).
Male:BEE (kJ)=278 + (57.5 × kg Wt) + (20.9 × cm Ht)– (28.3 v age).
Female:BEE (kJ)=2741 + (40 × kg Wt) + (7.7 × cm Ht)– (19.6 × age).
Data sourced from Rousseau AF, etal. SPEN endorsed recommendations:nutritional therapy in
major burns. Clinical Nutrition 32(4):497– 502, Copyright © 2013.
Elsevier, and Rodriguez NA, et al. Nutrition in burns: Galveston contributions. Journal of
Parenteral and Enteral Nutrition 35:704e14, Copyright © 2011 SAGE Publications.
1– 11 1,800 kcal/ m2 + 1,300 kcal/ m2 burn
12– 16 1,500 kcal/ m2 + 1,500 kcal/ m2 burn
+ (0.84 × Harris– Benedict) +
(114×temperature °C)– (4.5 × days
after injury)
Where kcal=calorie intake in last 24 hours
in cm) + 371.2
414.9
515.5
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CHAPTER37 Nutritional requirements in burn patients
Food types
Proteins
Patients with large burns, and without protein supplementation, usually
have a negative protein balance due to proteolysis, which aims to provide
substrates for gluconeogenesis. This contributes to cachexia and reduces
immune function. Protein replacement is therefore a key goal of nutritional
supplementation. Protein requirements of 1.2– 2 g/ kg/ day and 2.5– 4 g/
kg/ day are widely accepted as appropriate for burned adults and children
respectively.
Glutamine, an immune- enhancing amino acid, is of particular interest
but remains controversial. Although glutamine signicantly reduces the incidence of Gram- negative bacteraemia and inpatient mortality, the duration
of admission, wound infections, or the number of positive blood cultures
are not aected. Further high- quality trials are required to further test the
utility of glutamine in burns.
Carbohydrates
Glucose is the preferred fuel for metabolic pathways. Increased glucose
requirements, secondary to hyperanabolism, increase the rate of carbohydrate hydrolysis potentially causing deciency. Carbohydrate deciency
may lead to cachexia and proteolysis and therefore requires correction.
Current guidelines advise delivering 55– 60% of daily caloric requirements
as carbohydrate without exceeding a 5 mg/ kg/ min limit for both adults
and children.
Patients with large burns may be insulin resistant. Therefore, to maintain
ICU- recommended blood glucose levels of 5– 8 mmol/ L, insulin may be
required although the evidence for metformin and exenatide remains weak.
Lipids
Fat supplementation should be judicious. Post- burn lipolysis increased free
fatty acids but 70% of this is re- esteried and may accumulate in the liver
since hypermetabolism reduces fat utilization capacity. Evidence on which
the recommendation to supply <35% of caloric requirements as fat
is weak.
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Vitamins and trace elements
Micronutrient deciencies result in diminished skeletal, neuromuscular,
and immune function. Micronutrient requirements are usually increased to
levels where enteral nutrition alone becomes insucient (Table 37.2).
Grade C evidence supports the recommendation to replace zinc, selenium, copper, and the vitamins B1, C, D, and E.However, early supplementation of high- dose vitamin C is not yet standard practice and the eect
of vitamin D (400 IU/ day) supplementation on osteoporosis incidence remains unclear.
Table37.2 Reference daily intakes ofmicronutrients inburned patients
Age Vitamin
0– 13 250– 500 Unclear Unclear 12.5– 25 60– 140 0.8– 2.8
Over 13s 1000 Unclear Unclear 25– 40 300– 500 4
IU, international units; mg, milligrams
Adapted with permission from Rodriguez NA, etal. Nutrition in burns:Galveston contributions.
Journal of Parenteral and Enteral Nutrition 35: 704e14, Copyright © 2011 SAGE Publications.
Source data:Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and
Fluoride (1977); Dietary Reference Intakes for Thiamin, Riboavin, Niacin, Vitamin B6, Folate,
Vitamin B12, Pantothenic Acid, Biotin, and Choline (1988); Dietary Reference Intakes for Vitamin
C, Vitamin E, Selenium, and Carotenoids (2000); and Dietary Reference Intakes for Vitamin A,
Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel,
Silicon, Vanadium, and Zinc (2001). These reports may be accessed at http:// www.nap.edu
C, IU
Vitamin
D, IU
Vitamin
Zinc, mgSelenium, mgCopper,
E, IU
Monitoring
Nutritional requirements vary throughout the post- injury period. Patients
require vigilant multidisciplinary monitoring to avoid over- or underfeeding
and identication of complications such as refeeding syndrome. Weight is
regarded among the best indicators of nutritional status, and may be used
alongside other indicators such as serum proteins and nitrogen balance.
Feeding regimes which meet requirements can usually be prepared in liaison
with pharmacy departments. Alternatively, there are several commercial
formulas with varying concentrations of ingredients (see Rodriguez etal.1).
MONITORING
mg
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CHAPTER37 Nutritional requirements in burn patients
Further reading
Herndon DN, Tompkins RG. Support of the metabolic response to burn injury. Lancet
2004;36:1895– 902.
Heyland, DK, Wischmeyer, P, Jeschke, MG, Wibbenmeyer, L, Turgeon, AF, Stelfox, HT, Day, AG,
Garrel, D. A Randomized trial of ENtERal Glutamine to minimIZE thermal injury (The REENERGIZE Trial):a clinical trial protocol. Scars, Burns & Healing 2017;3:2059513117745241.
Mosier MJ, Pham TN, Klein MB, etal. Early enteral nutrition in burns:compliance with guidelines and
associated outcomes in a multicenter study. Journal of Burn Care & Research 2011;32:104– 9.
Rousseau AF, Losser MR, Ichai C, Berger MM. ESPEN endorsed recommendations: nutritional
therapy in major burns. Clinical Nutrition 2013;32:497– 502.
Reference
1. Rodriguez NA, Jeschke MG, Williams FN, et al. Nutrition in bur ns: Galveston contributions.
Journal of Parenteral and Enteral Nutrition 35:704e14.
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Chapter38
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Tetanus
Introduction to tetanus 328
Classifying tetanus-prone injuries 328
Management 329
References 330
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CHAPTER38 Tetanus
Introduction totetanus
Tetanus is the clinical manifestation of Clostridium tetani infection, a Grampositive obligate anaerobic bacterium that exhibits spore- based transmission and is predominantly found in soil.
1,2
Clostridium tetani produces the
exotoxin tetanospasmin, which blocks the inhibitory GABA pathway in the
central nervous system; this results in unopposed reex activity and ultimately the classical spasm pattern of trismus or ‘lock jaw’ that is associated
with the infection.
1,2
The childhood immunization programme introduced in the UK in 1961
has eectively eradicated tetanus in the UK; however, elderly people and
those patients who have not completed a ve- vaccine program of immunization remain at risk.
1,2
Classifying tetanus- prone injuries
Tetanus- prone Injuries
• Injuries associated with sepsis and/ or open fractures
• Puncture wounds or those containing foreign bodies
• Agreater than 6- hour delay to theatre following trauma
Injuries witha high- risk oftetanus contamination
• Those occurring in immunocompromised patients
• Injuries associated with large volumes of devitalized tissue
• Heavy contamination with tetanus prone debris
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Management
Prophylaxis
Tetanus toxoid IM injection (often a combination vaccine)
• Stimulates immunity by inducing antitoxin production
• Five injections are thought to confer lifelong immunity
Tetanus immunoglobulin IM injection
• Human immunoglobulin which neutralizes the exotoxin
• 500 international units (IU) is the standard dose in burns
• Bioavailability is achieved 2– 3days after injection and it has a 3– 4 week
half- life
Clinically apparent C.tetani infection
Tetanus is a clinical diagnosis. The cornerstones of treatment are antibiotics,
surgical debridement and intensive care management. IM and intravenous
immunoglobulin (IVIg) may be of use in neutralizing circulating exotoxin
but they do not treat the existing spasm caused by tetanospasmin already
bound to neurons2 (Table 38.1).
Table38.1 Tetanus prophylaxis regimen required inall wound
types dependent uponprevious immunization and associated risk
ofClostridium tetani infection
Tetanus prophylaxis
Immunization
history
5- year vaccination
program
complete
Incomplete
course or unsure
of status
*High- risk injuries require immunoglobulin treatment to neutralize the exotoxin regardless of the
prior vaccination history.
**A full 5- vaccination course should be completed.
Data sourced from Department of Health. Tetanus. Chapter30. In Immunisation against infectious
disease:The Green Book, Public Health England, London, UK © Crown Copyright 2014, available from https:// www.gov.uk/ government/ publications/ tetanus- the- green- book- chapter- 30.
Reproduced under the Open Government Licence v3.0.
Low risk or
clean injury
Tetanus- prone injury High- risk injury
Nil required Nil required Immunoglobulin onl y*
Toxoid
booster**
Toxoid booster and
immunoglobulin**
Toxoid booster and
immunoglobulin**
MANAGEMENT
329
Tetanus is a preventable disease with a high associated mortality; with
appropriate immunization, it could be eradicated entirely.
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CHAPTER38 Tetanus
References
1. Cook TM, Protheroe RT, Handel JM. Tetanus: a review of the literature. British Journal
Anaesthesia 2001;87:477– 87.
2. Department of Health. Immunisation against infectious disease: the Green Book.
Tetanus:Chapter30. 2013. London:Public Health England.
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Chapter39
331
Desquamating skin
disorders
Introduction to desquamating skin disorders 332
Classication 332
Aetiology 332
Clinical presentation 333
Pathology 334
Management outline 336
Prognosis 338
Further reading 338
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