- •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
M. M. Berger et al.
Hypercalcemia remains a poorly recognized cause of acute renal failure in patients with major burns that occurs as early as 3 weeks after injury [62]. The triad of hypercalcemia, arterial hypertension and acute renal failure is well known in other critical illnesses [40, 77], while the association of hypercalcemia and renal failure in patients with major burns is much less reported in the literature. In a recent retrospective study, hypercalcemia was shown to occur in 19 % of the burned patients with hospital lengths of stay of more than 28 days, and was noted to be associated with an increased mortality [88].
In our own setting, 30% of patients developed hypercalcemia: median time to the first hypercalcemia value was 21 days [88]. Hypercalcemia may also occur in patients with smaller burns requiring a stay of more than 20 days in the ICU. Ionized calcium determination enabled earlier detection, while using total calcium determination ‘with albumin correction’ was only slightly sensitive, as shown by normal corrected values in 15 cases with ionized hypercalcemia.
Treatment of hypercalcemia includes hydration, volume expansion and early mobilization. As most causes of severe hypercalcemia depend on increased osteoclast activation, drugs that decrease bone turnover are effective [50]. The treatment of choice in cases that do not resolve with the simple measures relies on the bisphosphonates, pamidronate disodium and zoledronic acid, which are available in intravenous forms [37]. In burned children, acute intravenous pamidronate administration has been shown to help to preserve bone mass [60], achieving a sustained therapeutic effect on bone [81]. An alternative treatment of the latter in burns includes anabolic agents such as oxandrolone [61]. The bisphosphonates have been advocated in the prevention of heterotrophic ossification, a complication that occurs in 1.2% of burn patients.
Bone demineralization and osteoporosis
Due to the substantial alterations of calcium and phosphorus metabolism and bone formation is reduced both in adults and children when burns exceed 40% TBSA. Bone mineral density is significantly lower in burned children compared with the same
age normal children. Girls have improved bone mineral content and percent fat compared with boys [52]. The consequences are increased risk of fractures, decreased growth velocity and stunting [11]. The bone is affected by various means: alteration of mineral metabolism, elevated cytokine and corticosteroid levels, decreased growth hormone (GH), nutritional deficiencies, and intra-operative immobilization. Cytokines contribute to the alterations, particularly interleukin-1(and interleukin-6, both of which are greatly increased in burns and stimulate osteoblast-mediated bone resorption. The increased cortisol production in thermal injury, leads to decreased bone formation, and the low GH levels fail to promote bone formation [59], further exacerbating the situation. Various studies suggest that immobilization plays a significant role in the pathogenesis of burn-associated bone disease [58]. Alterations of magnesium and calcium homeostasis constitute another cause. Hypocalcemia and hypomagnesemia are constant findings, and ionized calcium levels remain low for weeks [97]. The alterations are partly explained by large exudative magnesium and phosphorus losses [11] A close monitoring of ionized calcium, magnesium, and inorganic phosphate levels is mandatory, since burn patients usually require substantial supplementation by intravenous or enteral routes.
Micronutrients and antioxidants
Critically ill burned patients are characterized by a strong oxidative stress, an intense inflammatory response, and a hyper-metabolic state that can last months. Trace element (TE) deficiencies have repeatedly been described. The complications observed in major burns such as infections and delayed wound healing, can be partly attributed to TE deficiencies [16]. Plasma TE concentrations are low as a result of TE losses in biological fluids, low intakes, dilution by fluid resuscitation, and redistribution from plasma to tissues mediated by the inflammatory response. The large exudative losses cause negative TE balances. Intravenous supplementation trials show that early substitution improves recovery (IV doses: Cu 3.5 mg/d, Se 400–500 mcg/d, Zn 40 mg/d), reduces infectious complications (particularly noso-
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Critical care of thermally injured patient
comial pneumonia) [14], normalize thyroid function, improve wound healing and shorten hospital length of stay [16]. The mechanisms underlying these improvements are a combination of antioxidant effects (particularly of selenium through restoration of glutathione peroxidase activity), but also immune (Cu, Se, Zn) and anabolic effects (Zn particularly).
High vitamin C requirements after major burns were identified already in the 40s, and have been confirmed since. Very interesting studies by Dubick et al. [34] and Tanaka et al. [99] have demonstrated that high doses of vitamin C administered during the first 24 hours after a major injury reduced the capillary leak, probably through antioxidant mechanisms, resulting in significant reductions in fluid resuscitation requirements. This has not yet become standard of clinical practice, but might do so in the coming years.
Thrombosis prophylaxis
Hematological alterations observed after burns are complex and can last for several months and can be summarized as follows:
uring the early phase after burns, fibrin split products increase.
Dilution and consumption explain the early low PT values.
The coagulation cascade is activated.
Fibrin, factors V and VIII increase as part of acute phase response.
Antithrombin deficiency is frequent [64, 72].
Thrombocytosis develops when wounds are closing.
The risk of deep venous thrombosis and of pulmonary embolism is at least as high as in any other surgical condition [38]. In our CHUV experience, 13% of patients develop some form of thrombotic complication. Specific risk factors include central venous lines, prolonged bed-rest and an intense inflammatory state. Prophylaxis should be started from admission. Interruptions for surgery should be reduced to minimum and discussed with the surgical team.
Conclusion
The critical care of the thermally injured patient, is complex and challenging for all involved. The result are however rather rewarding. The field has evolved tremendously over the last few decades and will continue to improve in-order to provide these challenging patients with the best care possible. Many questions remain in the etiology and thus treatment of these patients. Many of these can only be answered by the ongoing research in the field. This brief chapter highlights some of the important aspects of the care, and serves simply as a guide to the care of these patients.
References
[1]Agay D, Sandre C, Ducros V et al (2005) Optimization of selenium status by a single intra-peritoneal injection of Se in Se deficient rat: possible application to burned patient treatment. Free Rad Biol Med 39(6): 762–768
[2]Alderson P, Bunn F, Lefebvre C et al (2004) Human albumin solution for resuscitation and volume expansion in critically ill patients. Cochrane Database Syst Rev 2004(4):CD001 208
[3]Alvarado R, Chung KK, Cancio LC et al (2009) Burn resuscitation. Burns 35(1): 4–14
[4]Arbabi S, Ahrns KS, Wahl WL et al (2004) Beta-blocker use is associated with improved outcomes in adult burn patients. J Trauma 56(2): 265–269; discussion 269–271
[5]Arlati S, Storti E, Pradella V et al (2007) Decreased fluid volume to reduce organ damage: a new approach to burn shock resuscitation? A preliminary study. Resuscitation 72(3): 371–378
[6]Arturson G, Jakobsson OP (1985) Oedema measurements in a standard burn model. Burns 12: 1–7
[7]Arturson G, Bode G, Brizio-Molteni L et al (1990) Endocrinology of thermal trauma. Lea & Febiger, London
[8]Ballian N, Rabiee A, Andersen DK et al (2010) Glucose metabolism in burn patients: The role of insulin and other endocrine hormones. Burns;e-pub:Jan 12
[9]Barillo DJ, Goode R, Esch V (1994) Cyanide poisoning in victims of fire: analysis of 364 cases and review of the literature. J Burn Care Rehabil 15: 46–57
[10]Belmonte Torras JA, Marin de la Cruz D, Sune Garcia JM et al (2006) [Burns produced by lighters]. An Pediatr (Barc) 64(5): 468–473
[11]Berger MM, Rothen C, Cavadini C et al (1997) Exudative mineral losses after serious burns: A clue to the alterations of magnesium and phosphate metabolism. Am J Clin Nutr 65: 1473–1481
217
M. M. Berger et al.
[12]Berger MM, Pictet A, Revelly JP et al (2000) Impact of a bicarbonated saline solution on early resuscitation after major burns. Intensive Care Med 26(9): 1382–1385
[13]Berger MM, Reymond MJ, Shenkin A et al (2001) Influence of selenium supplements on the post-traumatic alterations of the thyroid axis – a prospective placebo controlled trial. Intensive Care Med 27: 91–100
[14]Berger MM (2006) Acute copper and zinc deficiency due to exudative losses – substitution versus nutritional requirements. Burns 32: 393
[15]Berger MM, Eggimann P, Heyland DK et al (2006) Reduction of nosocomial pneumonia after major burns by trace element supplementation: aggregation of two randomised trials. Crit Care 10:R153:e-pub 2 Nov
[16]Berger MM, Shenkin A (2007) Trace element requirements in critically ill burned patients. J Trace Elem Med Biol 21 [Suppl 1]: $24–48
[17]Berger MM, Baines M, Raffoul W et al (2007) Trace element supplements after major burns modulate antioxidant status and clinical course by way of increased tissue trace element concentration. Am J Clin Nutr 85: 1293–1300
[18]Berger MM, Davadant M, Marin C et al (2010) Impact of a pain protocol including hypnosis in major burns. Burns 36(5): 639–646
[19]Borron SW, Baud FJ, Megarbane B, Chantal B (2007) Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med 25: 551–8
[20]Breitenstein E, Chioléro RL, Jéquier E et al (1990) Effects of beta-blockade on energy metabolism following burns. Burns 16: 259–264
[21]Brusselaers N, Monstrey SJ, Vandijck DM, Blot SI (2007) Prediction of morbidity and mortality on admission to a burn unit. Plast Reconstr Surg 120: 360–1; author reply 361
[22]Burke JF, Wolfe RR, Mullany CJ et al (1979) Glucose requirements following burn injury. Ann Surg 190: 274–285
[23]Bushinsky DA, Monk RD (1998) Electrolyte quintet: Calcium. Lancet 352(9124): 306–311
[24]Carlson DL, Horton JW (2006) Cardiac molecular signaling after burn trauma. J Burn Care Res 27(5): 669–675
[25]Carter EA, Tompkins RG, Babich JW et al (1996) Decreased cerebral glucose utilization in rats during the ebb phase of thermal injury. J Trauma 40(6): 930–935
[26]Cheatham ML, Malbrain ML, Kirkpatrick A et al (2007) Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med 33(6): 951–962
[27]Chrysopoulos MT, Jeschke MG, Dziewulski P et al (1999) Acute renal dysfunction in severely burned adults. J Trauma 46: 141–144
[28]Chung KK, Juncos LA, Wolf SE et al (2008) Continuous Renal Replacement Therapy Improves Survival in Severely Burned Military Casualties With Acute Kidney Injury. J Trauma 64:S179 –S187
[29]Coca SG, Bauling P, Schifftner T et al (2007) Contribution of acute kidney injury toward morbidity and mortality in burns: a contemporary analysis. Am J Kidney Dis 49: 517–523
[30]Cox RA, Burke AS, Soejima K et al (2003) Airway obstruction in sheep with burn and smoke inhalation injuries. Am J Respir Cell Mol Biol 29: 295–302
[31]de Jonghe B, Lacherade JC, Sharshar T, Outin H (2009) Intensive care unit-acquired weakness: Risk factors and Prevention. Crit Care Med 37(10)[Suppl]: S309S315
[32]Ding HQ, Zhou BJ, Liu L et al (2002) Oxidative stress and metallothionein expression in the liver of rats with severe thermal injury. Burns 28: 215–221
[33]Donner B, Tryba M, Kurz-Muller K et al (1996) [Anesthesia and intensive care management of severely burned children of Jehovah’s Witnesses]. Anaesthesist 45(2): 171–517
[34]Dubick MA, Williams C, Elgjo GI et al (2005) High-dose vitamin C infusion reduces fluid requirements in the resuscitation of burn-injured sheep. Shock 24(2): 139–144
[35]Erdman AR (2007) Is hydroxocobalamin safe and effective for smoke inhalation? Searching for guidance in the haze. Ann Emerg Med 49: 814–816
[36]Etherington L, Saffle J, Cochran A (2009) Use of transesophageal echocardiography in burns:a retrospective review. J Burn Care Res 31(1): 36–39
[37]Evans RA, Lawrence PJ, Thanakrishnan G et al (1986) Immobilization hypercalcaemia due to low bone formation and responding to intravenous sodium sulphate. Postgrad Med J 62(727): 395–398
[38]Fecher AM, O’Mara MS, Goldfarb IW et al (2004) Analysis of deep vein thrombosis in burn patients. Burns 30(6): 591–593
[39]Forni JG, Hilton PJ (1997) Continuous hemofiltration in the treatment of acute renal failure. N Engl J Med 336: 1303–1309
[40]Forster J, Querusio L, Burchard KW et al (1985) Hypercalcemia in critically ill surgical patients. Ann Surg 202: 512–518
[41]Gore DC, Chinkes D, Heggers J et al (2001) Association of hyperglycemia with increased mortality after severe burn injury. J Trauma 51(3): 540–544
[42]Herndon DN, Hart DW, Wolf SE, Chinkes DL, Wolfe RR (2001) Reversal of catabolism by beta-blockade after severe burns. N Engl J Med 345: 1223–1229
[43]Herndon DN, Wolf SE, Chinkes DL et al (2001) Reversal of catabolism by beta-blockade after severe burns. N Engl J Med 345: 1223–1229
[44]Holm C, Horbrand F, von Donnersmarck GH et al (1999) Acute renal failure in severely burned patients. Burns 25: 171–178
[45]Holm C, Melcer B, Hörbrand F et al (2000) Intrathoracic blood volume as an endpoint in resuscitation of the severely burned: an observational study of 24 patients. J Trauma 48: 728–734
218
Critical care of thermally injured patient
[46]Holm C, Mayr M, Tegeler J et al (2004) A clinical randomized study on the effects of invasive monitoring on burn shock resuscitation. Burns 30(8): 798–807
[47]Horton JW, Garcia NM, White DJ et al (1995) Postburn cardiac contractile function and biochemical markers of postburn cardiac surgery. J Am Coll Surg 181: 289–298
[48]Horton JW, White DJ, Maass DL et al (2001) Antioxidant vitamin therapy alters burn trauma-mediated cardiac NF-kappaB activation and cardiomyocyte cytokine secretion. J Trauma 50(3): 397–406
[49]Huang PP, Stucky FS, Dimick AR et al (1995) Hypertonic sodium resuscitation is associated with renal failure and death. Ann Surg 221: 543–557
[50]Inzucchi SE (2004) Management of hypercalcemia: diagnostic workup, therapeutic options for hyperpararthyroidism and their common causes. Postgrad Med J 115(5): 27–36
[51]Ivy ME, Atweh NA, Palmer J et al (2000) Intra-abdom- inal hypertension and abdominal compartment syndrome in burn patients. J Trauma 49: 387–391
[52]Jeschke MG, Barrow RE, Mlcak RP et al (2005) Endogenous anabolic hormones and hypermetabolism: effect of trauma and gender differences. Ann Surg 241(5): 759–767
[53]Jeschke MG, Micak RP, Finnerty CC, Herndon DN (2007) Changes in liver function and size after a severe thermal injury. Shock 28: 172–177
[54]Jeschke MG, Finnerty CC, Suman OE et al (2007) The effect of oxandrolone on the endocrinologic, inflammatory, and hypermetabolic responses during the acute phase postburn. Ann Surg 246(3): 351–360; discussion 360–352
[55]Jeschke MG, Finnerty CC, Kulp GA et al (2008) Combination of recombinant human growth hormone and propranolol decreases hypermetabolism and inflammation in severely burned children. Pediatr Crit Care Med 9(2): 209–216
[56]Jeschke MG, Gauglitz GG, Song J, MD et al (2009) Calcium and ER Stress Mediate Hepatic Apoptosis after Burn Injury. J Cell Mol Med 13(8B):1857–1865
[57]Kealey GP (2009) Effects/Treatment of Toxic Gases. J Burn Care Res 30(1): 146–155
[58]Klein GL, Kikuchi Y, Sherrard DJ et al (1996) Burn-asso- ciated bone disease in sheep: roles of immobilization and endogenous corticosteroids. J Burn Care Rehabil 17: 518–521
[59]Klein GL, Wolf SE, Langman CB et al (1998) Effect of therapy with recombinant human growth hormone on insulin-like growth factor system components and serum levels of biochemical markers of bone formation in children after severe burn injury. J Clin Endocrinol Metab 83: 21–24
[60]Klein GL, Wimalawansa SJ, Kulkarni G et al (2005) The efficacy of acute administration of pamidronate on the conservation of bone mass following severe burn injury in children: a double-blind, randomized, controlled study. Osteoporos Int 16(6): 631–635
[61]Klein GL (2006) Burn-induced bone loss: importance, mechanisms, and management. J Burns Wounds 5:e5
[62]Kohut B, Rossat J, Raffoul W et al (2009) Hypercalcaemia and acute renal failure after major burns: An under-diagnosed condition. Burns 34(3): 360–366
[63]Lam NN, Tien NG, Khoa CM (2008) Early enteral feeding for burned patients: an effective method which should be encouraged in developing countries. Burns 34(2): 192–196
[64]Lavrentieva A, Kontakiotis T, Bitzani M et al (2008) Early coagulation disorders after severe burn injury:
impact on mortality. Intensive Care Med 34(4): 700–706
[65]Lund T, Onarheim H, Reed RK (1992) Pathogenesis of edema formation in burn injuries. World J Surg
16:2–9
[66]Marano MA, Fong Y, Moldawer LL et al (1990) Serum cachectin: tumor necrosis factor in critically ill patients with burns correlates with infection and mortality. Surg Gynecol Obstet 170: 32–38
[67]Mégarbane B, Delahaye A, Goldgran-Toledano D, Baud FJ (2003) Antidotal treatment of cyanide poisoning. J Chin Med Assoc 66: 193–203
[68]Morio B, Irtun O, Herndon DN et al (2002) Propranolol decreases splanchnic triacylglycerol storage in burn patients receiving a high-carbohydrate diet. Ann Surg 236(2): 218–225
[69]Mosier MJ, Pham TN (2009) American Burn Association Practice guidelines for prevention, diagnosis, and treatment of ventilator-associated pneumonia (VAP) in burn patients. J Burn Care Res 30(6): 910–928.
[70]Mustonen KM, Vuola J (2008) Acute Renal Failure in Intensive Care Burn Patients (ARF in Burn Patients). J Burn Care Res 29: 227–237.
[71]Namias N (2007) Advances in burn care. Curr Opin Crit Care 13(4): 405–410
[72]Niedermayr M, Schramm W, Kamolz L et al (2007) Antithrombin deficiency and its relationship to severe burns. Burns 33(2): 173–178
[73]Palmieri T, Enkhbaatar P, Bayliss R et al (2006) Continuous nebulized albuterol attenuates acute lung injury in an ovine model of combined burn and smoke inhalation. Crit Care Med 34: 1719–1724
[74]Pereira C, Murphy K, Herndon D (2004) Outcome measures in burn care: is mortality dead? Burns
30:761–771
[75]Pham TN, Warren AJ, Phan HH et al (2005) Impact of tight glycemic control in severely burned children. J Trauma 59(5): 1148–1154
[76]Pierre EJ, Barrow RE, Hawkins HK et al (1998) Effects of insulin on wound healing. J Trauma 44: 342–345
[77]Popp M, Friedberg D, McMillan B (1980) Clinical characteristics of hypertension in burned children. Ann Surg 191: 473–478
[78]Price LA, Thombs B, Chen CL, Milner SM (2007) Liver disease in burn injury: evidence from a national sample of 31,338 adult patients. J Burns Wounds 7: e1
219
M. M. Berger et al.
[79]Pruitt BA Jr, Foley F D, Moncrief J A (1970) Curling’s ulcer: a clinical-pathology study of 323 cases. Ann Surg 172: 523–539
[80]Pruitt BA Jr (2000) Protection from excessive resuscitation: “pushing the pendulum back”. J Trauma 49: 567–568
[81]Przkora R, Herndon DN, Sherrard DJ et al (2007) Pamidronate preserves bone mass for at least 2 years following acute administration for pediatric burn injury. Bone 41(2): 297–302
[82]Rainville P, Bao QV, Chretien P (2005) Pain-related emotions modulate experimental pain perception and autonomic responses. Pain 118(3): 306–318
[83]Rainville P (2008) Hypnosis and the analgesic effect of suggestions. Pain 134(1–2): 1–2
[84]Raff T, Hartmann B, Germann G (1997) Early intragastric feeding of seriously burned and long-term ventilated patients: a review of 55 patients. Burns 23: 19–25
[85]Richardson P, Mustard L (2009) The management of pain in the burns unit. Burns 35(7): 921–936
[86]Rossaint R, Falke KJ, Lopez F, Slama K, Pison U, Zapol WM (1993) Inhaled nitric oxide for the adult respiratory distress syndrome. N Engl J Med 328: 399–405
[87]Saffle JR (2007) The phenomenon of “fluid creep” in acute burn resuscitation. J Burn Care Res 28 (May/ june):382–395
[88]Sam R, Vaseemuddin M, Siddique A et al (2007) Hypercalcemia in patients in the burn intensive care unit. J Burn Care Res 28: 742–746
[89]Shankar R, Melstrom KA Jr, Gamelli RL (2007) Inflammation and sepsis: past, present, and the future. J Burn Care Res 28(4): 566–571
[90]Shepherd G, Velez LI (2008) Role of hydroxocobalamin in acute cyanide poisoning. Ann Pharmacother 42: 661–669
[91]Sheridan RL (2009) Inhaled nitric oxide in inhalation injury. J Burn Care Res 30(1): 162–163
“Opioid creep” is real and may be the cause of “fluid creep”. Burns 30(6): 583–90
[97]Szyfelbein SK, Drop LJ, Martyn JAJ (1981) Persistent ionized hypocalcemia in patients during resuscitation and recovery phases of body burns. Crit Care Med 9: 454–458
[98]Takala J, Ruokonen E, Webster NR et al (1999) Increased mortality associated with growth hormone treatment in critically ill adults. N Engl J Med 341: 785–792
[99]Tanaka H, Matsuda T, Miyagantani Y et al (2000) Reduction of resuscitation fluid volumes in severely burned patients using ascorbic acid administration. Arch Surg 135: 326–331
[100]Tappy L, Schwarz JM, Schneiter P et al (1998) Effects of isoenergetic glucose-based or lipid-based parenteral nutrition on glucose metabolism, de novo lipogenesis, and respiratory gas exchanges in critically ill patients. Crit Care Med 26: 860–867
[101]Tasaki O, Mozingo DW, Dubick MA, Goodwin CW, Yantis LD, Pruitt BA Jr (2002) Effects of heparin and lisofylline on pulmonary function after smoke inhalation injury in an ovine model. Crit Care Med 30: 637–43
[102]Thomas S, Wolf SE, Chinkes DL, Herndon DN (2004) Recovery from the hepatic acute phase response in the severely burned and the effects of long-term growth hormone treatment. Burns 30: 675–9
[103]Warden GD (1996) Fluid resuscitation and early management. In: Herndon D (ed) Total burns care. Saunders, London, pp 53–60
[104]Weaver LK (2009) Clinical practice. Carbon monoxide poisoning. N Engl J Med 360: 1217–1225
[105]Wibbenmeyer L, Sevier A, Liao J, Williams I, Light T, Latenser B, Lewis R 2nd, Kealey P, Rosenquist R (2010) The impact of opioid administration on resuscitation volumes in thermally injured patients. J Burn Care Res 31(1): 48–56
[92]Shiozaki T, Kishikawa M, Hiraide A et al (1993) Recov- [106] Wolf SE, Debroy M, Herndon DN (1997) The corner-
ery from postoperative hypothermia predicts survival in extensively burned patients. Am J Surg 165: 326–330
[93]Song J, Finnerty CC, Herndon DN, Boehning D, Jeschke MG (2009) Severe burn–induced endoplasmic reticulum stress and hepatic damage in mice. Mol Med 15(9–10): 316–320
[94]Sparkes BG (1997) Immunological responses to thermal injury. Burns 23: 106–113
[95]Stucki P, Perez MH, Cotting J, Shenkin A, Berger MM (2010) Substitution of exudative trace elements losses in burned children. Critical Care 14: 439
stones and directions of pediatric burn care. Pediatric Surgery International 12: 312–320
[107]Wolf SE, Edelman LS, Kemalyan N et al (2006) Effects of oxandrolone on outcome measures in the severely burned: a multicenter prospective randomized doubleblind trial. J Burn Care Rehab 27(2): 131–139; discussion 140–141
[108]Zhang Q, Carter EA, Ma B et al (2008) Burn-related metabolic and signaling changes in rat brain. J Burn Care Res 29(2): 346–352
[96]Sullivan SR, Friedrich JB, Engrav LH, Round KA, HeimCorrespondence: Mette M. Berger, Adult ICU and Burn
bach DM, Heckbert SR, Carrougher GJ, Lezotte DC, |
Unit, CHUV, BH D8.612, 1011 Lausanne, Switzerland, E-mail: |
Wiechman SA, Honari S, Klein MB, Gibran NS (2004) |
Mette.Berger@chuv.ch |
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