- •Preface
- •List of contributers
- •History, epidemiology, prevention and education
- •A history of burn care
- •“Black sheep in surgical wards”
- •Toxaemia, plasmarrhea, or infection?
- •The Guinea Pig Club
- •Burns and sulfa drugs at Pearl Harbor
- •Burn center concept
- •Shock and resuscitation
- •Wound care and infection
- •Burn surgery
- •Inhalation injury and pulmonary care
- •Nutrition and the “Universal Trauma Model”
- •Rehabilitation
- •Conclusions
- •References
- •Epidemiology and prevention of burns throughout the world
- •Introduction
- •Epidemiology
- •The inequitable distribution of burns
- •Cost by age
- •Cost by mechanism
- •Limitations of data
- •Risk factors
- •Socioeconomic factors
- •Race and ethnicity
- •Age-related factors: children
- •Age-related factors: the elderly
- •Regional factors
- •Gender-related factors
- •Intent
- •Comorbidity
- •Agents
- •Non-electric domestic appliances
- •War, mass casualties, and terrorism
- •Interventions
- •Smoke detectors
- •Residential sprinklers
- •Hot water temperature regulation
- •Lamps and stoves
- •Fireworks legislation
- •Fire-safe cigarettes
- •Children’s sleepwear
- •Acid assaults
- •Burn care systems
- •Role of the World Health Organization
- •Conclusions and recommendations
- •Surveillance
- •Smoke alarms
- •Gender inequality
- •Community surveys
- •Acknowledgements
- •References
- •Prevention of burn injuries
- •Introduction
- •Burns prevalence and relevance
- •Burn injury risk factors
- •WHERE?
- •Burn prevention types
- •Burn prevention: The basics to design a plan
- •Flame burns
- •Prevention of scald burns
- •Conclusions
- •References
- •Burns associated with wars and disasters
- •Introduction
- •Wartime burns
- •Epidemiology of burns sustained during combat operations
- •Fluid resuscitation and initial burn care in theater
- •Evacuation of thermally-injured combat casualties
- •Care of host-nation burn patients
- •Disaster-related burns
- •Epidemiology
- •Treatment of disaster-related burns
- •The American Burn Association (ABA) disaster management plan
- •Summary
- •References
- •Education in burns
- •Introduction
- •Surgical education
- •Background
- •Simulation
- •Education in the internet era
- •Rotations as courses
- •Mentorship
- •Peer mentorship
- •Hierarchical mentorship
- •What is a mentor
- •Implementation
- •Interprofessional education
- •What is interprofessional education
- •Approaches to interprofessional education
- •References
- •European practice guidelines for burn care: Minimum level of burn care provision in Europe
- •Foreword
- •Background
- •Introduction
- •Burn injury and burn care in general
- •Conclusion
- •References
- •Pre-hospital and initial management of burns
- •Introduction
- •Modern care
- •Early management
- •At the accident
- •At a local hospital – stabilization prior to transport to the Burn Center
- •Transportation
- •References
- •Medical documentation of burn injuries
- •Introduction
- •Medical documentation of burn injuries
- •Contents of an up-to-date burns registry
- •Shortcomings in existing documentation systems designs
- •Burn depth
- •Burn depth as a dynamic process
- •Non-clinical methods to classify burn depth
- •Burn extent
- •Basic principles of determining the burn extent
- •Methods to determine burn extent
- •Computer aided three-dimensional documentation systems
- •Methods used by BurnCase 3D
- •Creating a comparable international database
- •Results
- •Conclusion
- •Financing and accomplishment
- •References
- •Pathophysiology of burn injury
- •Introduction
- •Local changes
- •Burn depth
- •Burn size
- •Systemic changes
- •Hypovolemia and rapid edema formation
- •Altered cellular membranes and cellular edema
- •Mediators of burn injury
- •Hemodynamic consequences of acute burns
- •Hypermetabolic response to burn injury
- •Glucose metabolism
- •Myocardial dysfunction
- •Effects on the renal system
- •Effects on the gastrointestinal system
- •Effects on the immune system
- •Summary and conclusion
- •References
- •Anesthesia for patients with acute burn injuries
- •Introduction
- •Preoperative evaluation
- •Monitors
- •Pharmacology
- •Postoperative care
- •References
- •Diagnosis and management of inhalation injury
- •Introduction
- •Effects of inhaled gases
- •Carbon monoxide
- •Cyanide toxicity
- •Upper airway injury
- •Lower airway injury
- •Diagnosis
- •Resuscitation after inhalation injury
- •Other treatment issues
- •Prognosis
- •Conclusions
- •References
- •Respiratory management
- •Airway management
- •(a) Endotracheal intubation
- •(b) Elective tracheostomy
- •Chest escharotomy
- •Conventional mechanical ventilation
- •Introduction
- •Pathophysiological principles
- •Low tidal volume and limited plateau pressure approaches
- •Permissive hypercapnia
- •The open-lung approach
- •PEEP
- •Lung recruitment maneuvers
- •Unconventional mechanical ventilation strategies
- •High-frequency percussive ventilation (HFPV)
- •High-frequency oscillatory ventilation
- •Airway pressure release ventilation (APRV)
- •Ventilator associated pneumonia (VAP)
- •(a) Prevention
- •(b) Treatment
- •References
- •Organ responses and organ support
- •Introduction
- •Burn shock and resuscitation
- •Post-burn hypermetabolism
- •Individual organ systems
- •Central nervous system
- •Peripheral nervous system
- •Pulmonary
- •Cardiovascular
- •Renal
- •Gastrointestinal tract
- •Conclusion
- •References
- •Critical care of thermally injured patient
- •Introduction
- •Oxidative stress control strategies
- •Fluid and cardiovascular management beyond 24 hours
- •Other organ function/dysfunction and support
- •The nervous system
- •Respiratory system and inhalation injury
- •Renal failure and renal replacement therapy
- •Gastro-intestinal system
- •Glucose control
- •Endocrine changes
- •Stress response (Fig. 2)
- •Low T3 syndrome
- •Gonadal depression
- •Thermal regulation
- •Metabolic modulation
- •Propranolol
- •Oxandrolone
- •Recombinant human growth hormone
- •Insulin
- •Electrolyte disorders
- •Sodium
- •Chloride
- •Calcium, phosphate and magnesium
- •Calcium
- •Bone demineralization and osteoporosis
- •Micronutrients and antioxidants
- •Thrombosis prophylaxis
- •Conclusion
- •References
- •Treatment of infection in burns
- •Introduction
- •Clinical management strategies
- •Pathophysiology of the burn wound
- •Burn wound infection
- •Cellulitis
- •Impetigo
- •Catheter related infections
- •Urinary tract infection
- •Tracheobronchitis
- •Pneumonia
- •Sepsis in the burn patient
- •The microbiology of burn wound infection
- •Sources of organisms
- •Gram-positive organisms
- •Gram-negative organisms
- •Infection control
- •Pharmacological considerations in the treatment of burn infections
- •Topical antimicrobial treatment
- •Systemic antimicrobial treatment (Table 3)
- •Gram-positive bacterial infections
- •Enterococcal bacterial infections
- •Gram-negative bacterial infections
- •Treatment of yeast and fungal infections
- •The Polyenes (Amphotericin B)
- •Azole antifungals
- •Echinocandin antifungals
- •Nucleoside analog antifungal (Flucytosine)
- •Conclusion
- •References
- •Acute treatment of severely burned pediatric patients
- •Introduction
- •Initial management of the burned child
- •Fluid resuscitation
- •Sepsis
- •Inhalation injury
- •Burn wound excision
- •Burn wound coverage
- •Metabolic response and nutritional support
- •Modulation of the hormonal and endocrine response
- •Recombinant human growth hormone
- •Insulin-like growth factor
- •Oxandrolone
- •Propranolol
- •Glucose control
- •Insulin
- •Metformin
- •Novel therapeutic options
- •Long-term responses
- •Conclusion
- •References
- •Adult burn management
- •Introduction
- •Epidemiology and aetiology
- •Pathophysiology
- •Assessment of the burn wound
- •Depth of burn
- •Size of the burn
- •Initial management of the burn wound
- •First aid
- •Burn blisters
- •Escharotomy
- •General care of the adult burn patient
- •Biological/Semi biological dressings
- •Topical antimicrobials
- •Biological dressings
- •Other dressings
- •Exposure
- •Deep partial thickness wound
- •Total wound excision
- •Serial wound excision and conservative management
- •Full thickness burns
- •Excision and autografting
- •Topical antimicrobials
- •Large full thickness burns
- •Serial excision
- •Mixed depth burn
- •Donor sites
- •Techniques of wound excision
- •Blood loss
- •Antibiotics
- •Anatomical considerations
- •Skin replacement
- •Autograft
- •Allograft
- •Other skin replacements
- •Cultured skin substitutes
- •Skin graft take
- •Rehabilitation and outcome
- •Future care
- •References
- •Burns in older adults
- •Introduction
- •Burn injury epidemiology
- •Pathophysiologic changes and implications for burn therapy
- •Aging
- •Comorbidities
- •Acute management challenges
- •Fluid resuscitation
- •Burn excision
- •Pain and sedation
- •End of life decisions
- •Summary of key points and recommendations
- •References
- •Acute management of facial burns
- •Introduction
- •Anatomy and pathophysiology
- •Management
- •General approach
- •Airway management
- •Facial burn wound management
- •Initial wound care
- •Topical agents
- •Biological dressings
- •Surgical burn wound excision of the face
- •Wound closure
- •Special areas and adjacent of the face
- •Eyelids
- •Nose and ears
- •Lips
- •Scalp
- •The neck
- •Catastrophic injury
- •Post healing rehabilitation and scar management
- •Outcome and reconstruction
- •Summary
- •References
- •Hand burns
- •Introduction
- •Initial evaluation and history
- •Initial wound management
- •Escharotomy and fasciotomy
- •Surgical management: Early excision and grafting
- •Skin substitutes
- •Amputation
- •Hand therapy
- •Secondary reconstruction
- •References
- •Treatment of burns – established and novel technology
- •Introduction
- •Partial thickness burns
- •Biological membranes – amnion and others
- •Xenograft
- •Full thickness burns
- •Dermal analogs
- •Keratinocyte coverage
- •Facial transplantation
- •Tissue engineering and stem cells
- •Gene therapy and growth factors
- •Conclusion
- •References
- •Wound healing
- •History of wound care
- •Types of wounds
- •Mechanisms of wound healing
- •Hemostasis
- •Proliferation
- •Epithelialization
- •Remodeling
- •Fetal wound healing
- •Stem cells
- •Abnormal wound healing
- •Impaired wound healing
- •Hypertrophic scars and keloids
- •Chronic non-healing wounds
- •Conclusions
- •References
- •Pain management after burn trauma
- •Introduction
- •Pathophysiology of pain after burn injuries
- •Nociceptive pain
- •Neuropathic pain
- •Sympathetically Maintained Pain (SMP)
- •Pain rating and documentation
- •Pain management and analgesics
- •Pharmacokinetics in severe burns
- •Form of administration [21]
- •Non-opioids (Table 1)
- •Paracetamol
- •Metamizole
- •Non-steroidal antirheumatics (NSAID)
- •Selective cyclooxygenasis-2-inhibitors
- •Opioids (Table 2)
- •Weak opioids
- •Strong opioids
- •Other analgesics
- •Ketamine (see also intensive care unit and analgosedation)
- •Anticonvulsants (Gabapentin and Pregabalin)
- •Antidepressants with analgesic effects
- •Regional anesthesia
- •Pain management without analgesics
- •Adequate communication
- •Psychological techniques [65]
- •Transcutaneous electrical nerve stimulation (TENS)
- •Particularities of burn pain
- •Wound pain
- •Breakthrough pain
- •Intervention-induced pain
- •Necrosectomy and skin grafting
- •Dressing change of large burn wounds and removal of clamps in skin grafts
- •Dressing change in smaller burn wounds, baths and physical therapy
- •Postoperative pain
- •Mental aspects
- •Intensive care unit
- •Opioid-induced hyperalgesia and opioid tolerance
- •Hypermetabolism
- •Psychic stress factors
- •Risk of infection
- •Monitoring [92]
- •Sedation monitoring
- •Analgesia monitoring (see Fig. 2)
- •Analgosedation (Table 3)
- •Sedation
- •Analgesia
- •References
- •Nutrition support for the burn patient
- •Background
- •Case presentation
- •Patient selection: Timing and route of nutritional support
- •Determining nutritional demands
- •What is an appropriate initial nutrition plan for this patient?
- •Formulations for nutritional support
- •Monitoring nutrition support
- •Optimal monitoring of nutritional status
- •Problems and complications of nutritional support
- •Conclusion
- •References
- •HBO and burns
- •Historical development
- •Contraindications for the use of HBO
- •Conclusion
- •References
- •Nursing management of the burn-injured person
- •Introduction
- •Incidence
- •Prevention
- •Pathophysiology
- •Severity factors
- •Local damage
- •Fluid and electrolyte shifts
- •Cardiovascular, gastrointestinal and renal system manifestations
- •Types of burn injuries
- •Thermal
- •Chemical
- •Electrical
- •Smoke and inhalation injury
- •Clinical manifestations
- •Subjective symptoms
- •Possible complications
- •Clinical management
- •Non-surgical care
- •Surgical care
- •Coordination of care: Burn nursing’s unique role
- •Nursing interventions: Emergent phase
- •Nursing interventions: Acute phase
- •Nursing interventions: Rehabilitative phase
- •Ongoing care
- •Infection prevention and control
- •Rehabilitation medicine
- •Nutrition
- •Pharmacology
- •Conclusion
- •References
- •Outpatient burn care
- •Introduction
- •Epidemiology
- •Accident causes
- •Care structures
- •Indications for inpatient treatment
- •Patient age
- •Total burned body surface area (TBSA)
- •Depth of the burn
- •Pre-existing conditions
- •Accompanying injuries
- •Special injuries
- •Treatment
- •Initial treatment
- •Pain therapy
- •Local treatment
- •Course of treatment
- •Complications
- •Infections
- •Follow-up care
- •References
- •Non-thermal burns
- •Electrical injury
- •Introduction
- •Pathophysiology
- •Initial assessment and acute care
- •Wound care
- •Diagnosis
- •Low voltage injuries
- •Lightning injuries
- •Complications
- •References
- •Symptoms, diagnosis and treatment of chemical burns
- •Chemical burns
- •Decontamination
- •Affection of different organ systems
- •Respiratory tract
- •Gastrointestinal tract
- •Hematological signs
- •Nephrologic symptoms
- •Skin
- •Nitric acid
- •Sulfuric acid
- •Caustic soda
- •Phenol
- •Summary
- •References
- •Necrotizing and exfoliative diseases of the skin
- •Introduction
- •Necrotizing diseases of the skin
- •Cellulitis
- •Staphylococcal scalded skin syndrome
- •Autoimmune blistering diseases
- •Epidermolysis bullosa acquisita
- •Necrotizing fasciitis
- •Purpura fulminans
- •Exfoliative diseases of the skin
- •Stevens-Johnson syndrome
- •Toxic epidermal necrolysis
- •Conclusion
- •References
- •Frostbite
- •Mechanism
- •Risk factors
- •Causes
- •Diagnosis
- •Treatment
- •Rewarming
- •Surgery
- •Sympathectomy
- •Vasodilators
- •Escharotomy and fasciotomy
- •Prognosis
- •Research
- •References
- •Subject index
Nutrition support for the burn patient
er to institute and experienced more frequent interruptions [20, 21]. Either route can be used successfully provided that this issue is incorporated into an overall plan for nutritional management.
Application: In the patient presented above, a naso-enteric feeding tube was placed on the morning following admission (24 hours after injury) under fluoroscopic guidance and carefully secured. Enteral nutrition (see below for a discussion of formulas) was started at a low rate, and increased gradually over the next 48 hours, so that the patient achieved goal-rate nutrition by 72 hours post-burn. We also elected to give a single enteral dose of erythromycin as a “pro motility” agent to help reduce gastric ileus and promote passage of the enteral tube into the small intestine [22].
Determining nutritional demands
Initiation of nutritional support requires estimation of a caloric goal in ICU patients[3]. This estimation can prove particularly challenging in burns because of the profound hypermetabolic response that the body mounts in response to significant burn injury. Malnutrition is associated with the development of pneumonia in critically ill patients and is known to impair wound healing. Without appropriate management, the protein-calorie malnutrition that results from burn hypermetabolism may be life threatening.
Further, although adequate nutrition is desired, care must be taken not to provide calories in excess of the patient’s needs. Overfeeding has been shown to result in fat accretion in burn patients and may contribute to difficulties with glycemic control and ventilator weaning. Estimated energy demands provide an appropriate starting point for nutritional support in major burns, with revision occurring based upon metabolic characteristics and patient tolerance of enteral feeds.
What is an appropriate initial nutrition plan for this patient?
Energy expenditure in burn patients is a heterogeneous metabolic process and the protean manifestations of burn hypermetabolism make determination of energy and protein requirements particularly dif-
ficult. However, several algebraic formulas are widely used for determination of initial assessment of energy needs. Estimation of basal energy expenditure (BEE) using the Harris-Benedict equation or kcal/ Kg formulas are used at most American Burn Association verified burn centers [23]. The baseline estimate acquired using the Harris-Benedict equation is usually multiplied by a factor of 1.2 to 1.4 to allow for the hypermetabolism associated with the burn injury. Although more varied methods are used in children, two methods are used most commonly to estimate caloric needs. The first of these is the recommended dietary allowances (RDA), recently revised and known as the Dietary Reference Index (DRI) [24]. This is a widely-used standard formula for estimating nutritional requirements. A burn-specific formula, the Galveston formula, is also widely used in pediatric burn care. Together, the RDA/DRI and/ or Galveston formulas are the routine methods of estimating energy requirements used in over 70% of US burn centers [23]. Of note, the previously used Curreri formula appears to have fallen out of favor for both adult and pediatric burns, likely because of the marked overestimation of energy demands demonstrated by this formula[25, 26]. Table 1 shows each of the more commonly used formulas and includes additional comments on many of these formulas, including information on the accuracy of each formula versus measured energy demands using indirect calorimetry (IDC) when that data is available.
The primary pitfall of these commonly used formulas for caloric demands in burned adults and children is that they frequently overestimate patients’ resting energy expenditure (REE) [3, 25, 26]. Feeding more than 1.2 times REE has been shown to increase fat accretion and does not improve maintenance of lean body mass in acute burn patients [27]. Therefore, although these formulas typically provide an appropriate method for initial estimates, measurement of energy expenditure by IDC provides a more precise representation of the burn patient’s energy expenditure over time.
Estimation of caloric needs in the obese burn patient should use ideal body weight in any algebraic formula calculations; otherwise, these equations result in substantial overfeeding. Although the concept of “permissive underfeeding” in the obese currently predominates the ICU nutrition literature, the bene-
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A. Cochran et al.
Table 1. Commonly used algebraic formulas for caloric needs in nutritional support
ADULT FORMULAS |
Formula |
Daily caloric estimates for |
Comments |
|
|
25 year-old male, 85 kg, |
|
|
|
180 cm, 48% TBSA |
|
Harris-Benedict [111] |
Men: 66.5 + 13.8 (Weight in Kg) |
Baseline = 1,946 kcal |
Estimates basal energy expend- |
|
+ 5 (Height in cm) – 6.76 (Age in |
If factor 1.5 = 2,918 kcal |
iture (BEE). Best stress adjust- |
|
years) |
|
ment is a factor of 1.5; results in |
|
Women: 655 + 9.6 (Weight in |
|
a % calorie variance of 19 24% |
|
|
from measured REE (MREE) |
|
|
Kg) + 1.85 (Height in cm) – 4.68 |
|
|
|
|
(p = NS). [26] |
|
|
(Age in years) |
|
|
|
|
|
|
Kcal/Kg |
35 kcal/kg |
2,975 kcal |
Variance of 23 ± 36% from |
(Common use) [26] |
|
|
MREE (p = NS) [26] |
Curreri [112] |
Age 16–59: 25 kcal/ kg/ day |
4,045 kcal |
Variance of 35 ± 35% from |
|
+ 40 kcal/ %TBSA burn/ day |
|
MREE (p = 0 001)[26] Now |
|
Age 60: 20 kcal/kg/day |
|
rarely used because of marked |
|
|
tendency to over-estimate |
|
|
+ 65 kcal/ %TBSA burn/ day |
|
|
|
|
calories. |
|
|
|
|
|
PEDIATRIC FORMULAS |
Formula |
Daily caloric estimates for |
Comments |
|
|
a 15-month old male, |
|
|
|
11 kg, 0.9 m2 BSA |
|
DRI [113] |
On-line calculator |
899 kcal/day |
Varies according to age, weight, |
|
|
If factor 1.2 = 1,078 kcal/ |
and activity level. Includes |
|
|
day |
allowances for growth and |
|
|
If factor 1.4 = 1,258 kcal/ |
activity. |
|
|
day |
|
Galveston [114–116] |
0–1 Years: 2 100 kcal/m2/day |
|
Like the Curreri formula, the |
|
+ 1 000 kcal/m2 TBSA burn/day |
|
Galveston formula was created |
|
1–11 Years: 1 800 kcal/m2/day |
2,182 kcal/day |
with the goal of maintaining |
|
+ 1 300 kcal/m2 TBSA burn/day |
|
body weight. |
|
12–18 Years: 1 500 kcal/m2/day |
|
|
|
+ 1 500 kcal/ m2 TBSA burn/day |
|
|
Curreri Junior [117] |
1 Year: RDA + 15 kcal/ %TBSA |
|
Now rarely used because of |
|
burn |
|
marked tendency to over-esti- |
|
1–3 Years: RDA + 25 kcal/ % |
2,099 kcal |
mate calories. |
|
|
||
|
TBSA burn |
|
|
|
4–15 Years: RDA + 40 kcal/ % |
|
|
|
TBSA burn |
|
|
fits and dangers of this practice have not yet been clearly established in patients with burn injury [28–30]. The physiologic principles of permissive underfeeding rely upon fat oxidation to mobilize peripheral energy stores in these patients, a pairing of metabolic processes that are known to be deranged in patients with significant burns.
Ratios for carbohydrate, protein, and fat intake must also be considered once a caloric goal has been
established. Carbohydrates may limit loss of lean body mass by stimulation of protein synthesis, meaning that carbohydrates should be the primary energy source in the hypermetabolic burn patient [31]. In addition, glucose serves as the primary metabolic fuel for wound healing. However, glucose administration rates in excess of 7 mg/kg/min cause hyperglycemia with the attendant complications of impaired wound healing, conversion of excess calories
364
Nutrition support for the burn patient
to fat, and elevated rates of carbon dioxide production [32]. Optimal nutrition support in burns consists of at least 50% carbohydrate calories, with glucose administration occurring at rate of 5–7 mg/kg/ min [33].
Protein requirements are also heterogeneous in burn patients and must be carefully considered in the development of a nutrition care plan. Protein demands in burn injury are increased due to the catabolic response to injury as well as the need for protein for wound healing and immune function. While healthy, uninjured individuals synthesize protein at a rate of 4 grams/ kg/ day, burn patients may induce protein synthesis rates of nearly twice that [34]. Administration of nutritional support with 1.5–2 grams/ kg/ day of protein balances protein synthesis and breakdown in the course of burn hypermetabolism [35]. The calories provided by protein are usually calculated as part of the total energy support of the patient. However, this protein should always be provided in addition to significant energy in the form of carbohydrate and fat calories; otherwise, the protein will be used entirely as an energy source rather than as a specific nutrient to provide substrate for wound healing and support of muscle mass. For that reason, the amount of protein contained in various nutrients is often expressed as the ratio of nonprotein calories to nitrogen (NPCal:N2). The optimal NPCal:N2 for burn patients has long been recognized to be a function of burn size [36], but is almost always a lower ratio than in unstressed patients.
Administration of nutrition support with lipid content in excess of 15% impairs immune function [37]. Lipids are necessary as a source of free fatty acids and for carriage of lipid-soluble vitamins, and some lipid calories are helpful in avoiding requirements for excessive quantities of glucose. Enhanced lipolysis occurs in burn hypermetabolism with the rate of free fatty acid oxidation being nearly double that measured in healthy volunteers [34]. This enhanced lipolysis may result in increased recycling of free fatty acids or increased total body fat stores. Optimal lipid content for burn nutrition support is therefore less than 15%, at least during the initial highly catabolic phase [33, 38, 39]. However, as will be shown below, few commercially-available enteral products fulfill this requirement. Patients given PN may be better off if fat is withheld entirely for short
periods and given as little as once weekly [40], and this practice is recommended when instituting PN [3] even though this may contribute to aggravated glucose intolerance.
Demands for vitamins and trace minerals are increased in all critically ill patients, and this demand is marked in burn patients because of exudative losses that occur in the absence of the skin barrier. Use of micronutrient supplementation has increased remarkably over the last 20 years and now represents a widespread practice in burn nutrition. All centers that responded to a recent survey on nutrition care practices indicated daily use of a multivitamin supplement [23]. However, no evidence-based guidelines currently exist for additional micronutrient supplementation in burns [5].
Vitamins A and C are routinely supplemented in many burn centers and therefore merit consideration. Both of these vitamins show decreased levels following burn injury and demonstrate responsiveness to supplementation [41]. Vitamin A has multiple functions relevant to burn care, including prevention of free radical damage, maintenance of immune function, and assistance in wound epithelialization. Vitamin C also has antioxidant function and plays a critical role in collagen cross-linking and, therefore, wound healing. One group has recommended supplementation in burn patients with 1000 IU of Vitamin A and 500 mg of Vitamin C daily [42]. Clinicians should be mindful of the potential for toxicity with high doses of Vitamin A. High doses of Vitamin C, in contrast, seem to have no toxic effects with excess simply being excreted in urine.
Burned patients, especially children, are known to suffer bone demineralization, predisposing them to spontaneous fractures [43], and contributing to growth retardation. Reasons for this are multifactorial, including increased glucocorticoid production, reduced production of parathyroid hormone, and impaired synthesis of Vitamin D [44, 45].
Klein et al. have provided a detailed description of the events responsible for demineralization of bone following burn injury, the reduction in parathyroid hormone production, and the subsequent deficiency of 1,25 dihydroxyvitamin D. In addition, skin from burned patients cannot synthesize Vitamin D correctly and burn patients are encouraged to avoid sun exposure on the skin [46]. As a consequence,
365