- •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
Acute treatment of burned children
Table 2. Age-specific vital signs and laboratory variables (lower values for heart rate, leukocyte count, and systolic blood pressure are for the 5th and upper values for heart rate, respiration rate, or leukocyte count for the 95th percentile, [34])
|
Heart Rate, Beats/Min |
|
|
|
|
|
Age group |
Tachycardia |
Bradycardia |
Respiratory |
Leukocyte Count, |
Systolic Blood |
|
|
|
|
Rate, |
Leukocytes × 103/ |
Tachycardia |
|
|
|
|
Breaths/Min |
mm3 |
Bradycardia |
|
|
|
|
|
|
Pressure, mm Hg |
|
Newborn: 0 days to 1 wk |
> 180 |
> 100 |
> 50 |
> 34 |
> |
65 |
Neonate: 1 wk to 1 mo |
> 180 |
> 100 |
> 40 |
> 19.5 or > 5 |
> |
75 |
Infant: 1 mo to 1 yr |
> 180 |
> 90 |
> 34 |
> 17.5 or > 5 |
> 100 |
|
Toddler and preschool: 2–5 yrs |
> 140 |
N/A |
> 22 |
> 15.5 or > 6 |
> |
94 |
School age child: 6–12 yrs |
> 130 |
N/A |
> 18 |
> 13.5 or > 4.5 |
> 105 |
|
Adolescent and young adult: |
|
|
|
|
|
|
13 to > 18 yrs |
> 110 |
N/A |
> 14 |
> 11 or > 4.5 |
> 117 |
NA, not applicable
mentioned above, if early evidence of upper airway edema is present, early intubation is required because the upper airway edema normally increases over 9 to 12h. Prophylactic intubation without good indication however should not be performed.
Advances in ventilator technology and treatment of inhalation injury have resulted in some improvement in mortality. A multi-center, randomized trial in patients with acute lung injury and acute respiratory distress syndrome showed that mechanical ventilation with a lower tidal volume than traditionally utilized, resulted in decreased mortality and increased the number of days without ventilator use [39]. Pruitt’s group showed that since the advent of high-frequency ventilation, mortality has decreased to 29% from 41% reported in an earlier study [40]. Management of inhalation injury consists of ventilatory support, aggressive pulmonary toilet, bronchoscopic removal of casts, and nebulization therapy [11]. Nebulization therapy can consist of heparin,-mimetics, or polymyxin B and is applied between 2–6 times a day. Pressure-control ventilation with permissive hypercapnia is a useful strategy in the management of these patients and P CO2 levels of as much as 60 mm Hg can be well tolerated if arrived at gradually. Prophylactic antibiotics are not indicated, but imperative with documented lung infections. Clinical diagnosis of pneumonia includes two of the following [32]: Chest x-ray revealing a new and persistent infiltrate, consolidation, or cavitation; sepsis (as defined in Table 3) and/or a recent change in sputum or purulence in the sputum, as well as quan-
titative culture. Clinical diagnosis can be modified after utilizing microbiologic data three categories according to the “American Burn Association Consensus Conference to Define Sepsis and Infection in Burns” [32]. Empiric choices for the treatment of pneumonia prior to culture results, should include coverage of methicillin-resistant Staphylococcus aureus and gram-negative organisms such as Pseudomonas and Klebsiella [41].
Burn wound excision
Methods for handling burn wounds have changed in recent decades and are similar in adults and children. Early excision and closure of the burn wound has been probably the single greatest advancement in the treating patients with severe thermal injuries during the last twenty years; leading to substantially reduced resting energy requirements, subsequent improvement of mortality rates and substantially lower costs in this particular patient population [11, 42–45]. Early wound closure has been furthermore found to be associated with decreased severity of hypertrophic scarring, joint contractures and stiffness, and promotes quicker rehabilitation [11, 42].
Techniques of burn-wound excision have envolved substantially over the past decade. In general most areas are excised with a hand skin graft knife or powered dermatome. Sharp excision with a knife or electrocautery is reserved for areas of functional cosmetic importance such as hand and face. In partial
245
G. G. Gauglitz, M. G. Jeschke
Table 3. Formulas for estimating caloric requirements in pediatric burn patients
Formula |
Sex/Age (years) |
Equation (Daily Requirement in kcal) |
WHO (155) |
Males |
|
|
0–3 |
(60.9 × W) – 54 |
|
3–10 |
(22.7 × W) + 495 |
|
10–18 |
(17.5 × W) + 651 |
|
Females |
|
|
0–3 |
(61.0 × W) – 51 |
|
3–10 |
(22.5 × W) + 499 |
|
10–18 |
(12.2 × W) + 746 |
RDA (156) |
0–6 months |
108 × W |
|
6 months–1 year |
98 × W |
|
1–3 |
102 × W |
|
4–10 |
90 × W |
|
11–14 |
55 × W |
Curreri junior (157) |
> 1 |
RDA + (15 × %BSAB) |
|
1–3 |
RDA + (25 × %BSAB) |
|
4–15 |
RDA + (40 × %BSAB) |
Galveston infant (158) |
0–1 |
2 100 kcal/m2 BSA + 1 000 kcal/m2 BSAB |
Galveston revised (75) |
1–11 |
1 800 kcal/m2 BSA+ 1 300 kcal/m2 BSAB |
Galveston adolescent (159) |
12+ |
1 500 kcal/m2 BSA+ 1 500 kcal/m2 BSAB |
WHO = World Health Organization |
|
%BSAB = Percentage of Total Body Surface area Burned |
RDA = Recommended Dietary Allowance (US) |
BSAB = Body surface area Burned |
|
BSA = Body Surface area |
|
|
thickness wounds an attempt is being made to preserve viable dermis, where as in full thickness injury all necrotic and infected tissue must be removed leaving a viable wound bed of either fascia, fat or muscle [46]. The following techniques are mainly utilized:
Tangential excision. This technique first described Janzekovic in the 1970s requires repeated shaving of deep dermal partial thickness burns using a Braithwaite, Watson or Goulian or dermatome set at depth 5–10/1,000 inch until a viable dermal bed is reached, which is manifested clinically by punctuate bleeding from the dermal wound bed [46].
Full thickness excision. A hand knife such as the Watsonorpowereddermatomeissetatat15–30/1,000 inch and serial passes are made excising the full thickness wound. Excision is aided by traction on the excised eschar as it passes through the knife or dermatome. Adequate excision is signaled by a viable bleeding wound bed, which is usually fat [46].
Fascial excisison. This technique is reserved for burn extending down to through the fat into muscle, where the patient presents late with large infected wounds and inpatients with life-threatening invasive
fungal infections. It involves surgical excision of the full thickness of the integument including the subcutaneous fat down to the fascia using Goulian knives and number 11 blades. Unfortunately, fascial excision is mutilating and leaves a permanent contour defect, which is near impossible to reconstruct. Lymphatic channels are excised in this technique and peripheral lymphyedema may develop [46].
Most patients can be managed with layered excisions that optimize later appearance and function. Published estimates of the amount of bleeding associated with these operations range within 3.5 to 5 % of the blood volume for every 1 % of the body surface excised [47, 48]. The control of blood loss is one of the main determinants for outcome [49]. Therefore several techniques should be applied to control blood loss. Local application of fibrin or thrombin spray, topical application of epinephrine 1:10 000–1:20 000, epinephrine soaked lab-pads (1: 40 000), and immediate electrocautery of the blood vessel can control blood loss [50]. The use of a sterilized tourniquet can also limit blood loss [51]. Lastly, pre-excisional tumescence with epinephrine
246
Acute treatment of burned children
saline can be used on trunk, back, extremities, but not fingers.
Burn wound coverage
Various biological and synthetic substrates have been employed to replace the injured skin post-burn. Autografts from uninjured skin remains the mainstay of treatment for many patients. Since early wound closure using autograft may be difficult when full-thickness burns exceed 40% total body surface area (TBSA), allografts (cadaver skin) frequently serve as skin substitute in severely burned patients. While this approach is still commonly used in burn centers throughout the world, it bears considerable risks, including antigenicity, cross-infection as well as limited availability [52]. Xenografts have been used for hundreds of years as temporary replacement for skin loss. Even though these grafts provide a biologically active dermal matrix, the immunologic disparities prevent engraftment and predetermine rejection over time [53]. However, both xenografts and allografts are only a mean of temporary burn wound cover. True closure can only be achieved with living autografts or isografts. But the widespread use of cultured autografts is frequently hampered by poor long term clinical results, exorbitant costs and fragility and difficult handling of these grafts [53–55]. Alternatively, dermal analogs have been made available for clinical use in recent years. Integra was approved by the United States Food and Drug administration for use in life-threatening burns and has been successfully utilized in immediate and delayed closure of full-thickness burns, leading to reduction in length of hospital stay, favorable cosmetics, and improved functional outcome in a prospective and controlled clinical study [56–59]. Our group recently conducted a randomized clinical trial utilizing IntegraTM in the management of severe full-thickness burns of ≥ 50% TBSA in a pediatric patient population comparing it to standard autograft-allograft technique, and found Integra to be associated with attenuated hepatic dysfunction, improved resting energy expenditure and improved aesthetic outcome post-burn [60]. AllodermTM, an acellular human dermal allograft, has been advocated for the management of acute burns. Small clinical series and case
reports suggest that AllodermTM may be useful in the treatment of acute burns [61–64]. Tissue engineering technology is advancing rapidly. Fetal constructs have recently been successfully trialed by Hohlfeld et al. [65] and the bilaminar skin substitute of Boyce [66] is now routine in clinical use and promise spectacular results [50]. Advances in stem cell culture technology are expected to deliver full cosmetic restoration for burn patients [67].
Metabolic response and nutritional support
The response to burn injury, known as hypermetabolism, occurs most dramatically following severe burn its modulation constitute an ongoing challenge for successful burn treatment [68]. Increases in oxygen consumption, metabolic rate, urinary nitrogen excretion, lipolysis and weight loss are directly proportional to the size of the burn [69]. Metabolic rates of burned children can dramatically exceed those of other critical care or trauma patients and cause marked wasting of lean body mass within days after injury [10]. Failure to circumvent the subsequent large energy and protein requirements may result in impaired wound healing, organ dysfunction, susceptibility to infection and death [70]. Thus, adequate nutrition is imperative for the treatment of severely burned patients. Due to the significant increase in energy expenditure post-burn, high-calorie nutritional support was thought to decrease muscle metabolism [71]. However, a randomized, double blinded, prospective study performed by our group found that aggressive high-calorie feeding with a combination of enteral and parenteral nutrition was associated with increased mortality [72]. Most authors therefore recommend adequate calorie intake via early enteral feeding and avoidance of overfeeding to attenuate the catabolic response after injury [10, 11]. Different formulations have been developed to address the specific energy requirements of burned adult and pediatric patients [73–75]. In children, formulas based on body surface area are more appropriate because of the greater body surface area per kilogram. The formulas change with age based on the body surface area alterations that occur with growth (Table 3).
247