- •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
Electrical injury
Fig. 3. Carpal tunnel release
don), and then simply pushing distally across the ligament, the carpal tunnel release is performed with relative ease (Fig. 3). A second look operation should be performed at 48–72 hours post op.
Serial debridement may be required before the patient is ready for closure or skin grafting. Care must be taken to prevent dessication of the open wound prior to closure. Moist dressings soaked every four hours with 5% mefanide acetate (sulfamylon) solution is one option. The wound vacuum assisted closure (VAC ) device may also be used in this setting.
The one instance when immediate amputation is contemplated is in the setting of mummified and contracted tissue. This occasionally occurs and most commonly involves the upper extremities. In this instance an aggressive approach can be undertaken which may include proximal disarticulation such as at the shoulder joint. These are infrequently performed operations however are relatively simple in that one must only differentiate viable from nonviable tissue (this is not a cancer operation). This is most easily accomplished with electrocautery working judiciously through muscle bundles in a deliberate fashion. Once the neurovascular structures are controlled the operative pace can be accelerated.
Wound care
Wound care follows the recommendations outlined in ABLS. Full thickness contact points are best treat-
ed with mefanide acetate ointment (sulfamylon ). The excellent eschar penetration of sulfamylon makes this a good treatment option in these deep wounds. Silver sulfadiazine for flash and flame burn areas provides good broad spectrum coverage at low cost with few side effects. Physical Medicine and Rehabilitation (PM&R) consultation should occur at admission and ongoing involvement is required to minimize scar complications. Physical therapy and functional splinting is begun on the day of admission and continued throughout the hospital stay. Meticulous neuromuscular examination is performed and careful documentation of neurologic status is required. This should be performed on admission and prior to discharge. Many of these cases end up in the court system and careful documentation is a must.
Operative debridement can begin on post burn day two or three either as a second look operation following fasciotomy or as the first procedure. All necrotic tissue should be excised while tissue of questionable viability retained and re-evaluated every 2–3 days until wound closure is achieved.
Diagnosis
There are several modalities that have been investigated in an effort to definitively differentiate viable from nonviable tissue. Radionuclide scanning with xenon-133 [6] and technetium pyrophosphate [27] have been shown to be accurate but not shown to decrease hospital length of stay or number of operations Hammod. Gadolinium enhanced MR imaging demonstrates potential viability in zones of tissue edema and good correlation with histopathology [11, 47, 39]. While these adjuncts can be sensitive and specific they add very little other than expense and we have refrained from their use in our institution.
Low voltage injuries
Low voltage injuries are generally localized to the contact points (Fig. 4). A careful evaluation for contact points including the scalp must be included in the physical examination. Contact point can be deep injuries with significant local tissue destruction how-
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ever they do not generally extend laterally. These may require amputation of digits but can usually be treated with local debridement and coverage. Oral commissure burns in children are more complex injuries. These oral cavity burns occur when a child chews on an electric cord. The child’s saliva completes the circuit between positive and neutral leads; the resulting resulting electrical short may cause significant local tissue destruction of the lips and or tongue [16]. These injuries are initially treated conservatively as the extent of injury is difficult to predict. Acutely these injuries should be evaluated and managed by a qualified burn surgeon. These children require admission for pain control and nutrition however outpatient management is possible once parents are comfortable with wound care and overall management [9, 36]. Parents should be warned that the eschar may separate and result in serious bleeding from the labial artery, which typically occurs at 10–14 days postburn. They should be instructed to hold pressure in this event and return immediately to the emergency department for suture ligation. Stretching and oral splinting gives good result in many and others may need reconstructive surgery. Plastic surgery consult is often required for complications and burns in the mid-portions of the mouth. These heal poorly and may require more aggressive surgical intervention [50, 57].
Fig. 4. Low voltage contact point
Lightning injuries
Lightning strikes cause 50–80 fatalities per year in the United States with Florida and Texas having the most deaths (Lightning-Associated deaths 1998) [22, 60]. Estimates of fatalities and overall injuries may be low however due to underreporting [7]. No outdoor location is safe from lightning strike. Lightning may strike as much as 10 miles in any direction from a thunderstorm even before the rain starts and while the sky is still clear. Risk factors are height of an object, isolation, and narrowness of the tip of the object. One must be indoors to be safe. Hard-wired telephones and television sets may become conduits for the charge however. Cell phones pose no inherent risk although they may be a risk factor due to the users inattentiveness to weather conditions.
Lightning strikes are high voltage injuries with the potential of reaching into the millions of volts. They are however brief, on the order of milliseconds. Current often flows around the victim in what is known as a flash-over-phenomenon which accounts for survival in a majority of individuals [12, 43, 48]. The most common cause of death is cardiac standstill and paralysis of the respiratory center. Cardio pulmonary resuscitation (CPR) is particularly effective when promptly initiated [45]. The pathognomonic cutaneous sign of a lightning strike is a dendritic fern-like branching erythematous pattern on the skin (Lichtenberg figure). This pattern on the skin fades rapidly much like a wheal and flare reaction. Major cutaneous injury is rare unless a nearby object is turned incandescent, causing a flash/flame injury, such as when a bag of golf clubs on a victims is struck. A rare and interesting complication is keraunoparalysis, which is a transient paralysis associated with extreme vasoconstriction and sensory disturbances of one or more extremity. This usually lasts only an hour but may be as long as twenty-four. Ruptured tympanic membrane is common and may be complicated by vertigo [31]. Neurologic complications ranging from loss of consciousness, seizures and traumatic brain injuries should prompt a high index of suspicion and consideration of head CT scan. Systemic effects of these injuries are managed in a fashion similar to high-voltage injuries.
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Electrical injury
Complications
Early complications are related to critical care issues such as cardiac, renal failure, sepsis. Neurologic complications may present at any time from admission to months after injury [33, 55, 58]. Neuromuscular defects include paresis, paralysis, GuillainBarre syndrome, transverse myelitis or amyotrophic lateral sclerosis [51]. In a key paper by Grube of 90 patients with electrical injuires 64 had high-voltage injury [13]. Two-thirds of the 64 patients had immediate central or peripheral neurologic symptoms with twenty-nine patients having loss of consciousness of whom 6 remained comatose. Three of these 6 ultimately died, and three awoke but had neurologic sequelae. One-third of the high-voltage group had one or more acute peripheral neuropathies, approximately two-thirds of these resolved or improved. The late onset peripheral neuropathies had a propensity to be more permanent. The most common clinical finding in electrically injured patients with peripheral neuropathy is weakness [15]. Reflex sympathetic dystrophy (now more commonly known as complex regional pain syndrome), is also seen in these patients and is often difficult to manage. These patients present with neuropathic pain, edema, and skin changes that may be disabling. Patients with chronic pain are also at high risk for depression [19, 20]. Depression occurs in 77% of patients with chronic pain although 89% of these patients never had been depressed before the onset of their pain [18]. Not only do survivors of electrical injury and lightning strikes have problems with depression but a whole spectrum of neuropsychological issues may be present. These range from cognitive dysfunction, memory impairment, attention disturbances, affective problems, anxiety, irritability and poor frustration tolerances, to physically aggressive outbursts [21, 29, 49, 53] Post traumatic stress disorder is also more common after electrical burns than after thermal burns [40].
Cataract formation is the most common ocular complication in electrical injury, although ocular manifestations may affect all portions of the eye [5, 30]. Ocular changes may affect 5–20% of patients with electrical injury. Saffle reported seven patients with 13 cataracts, noting a high degree of bilaterality with little association to voltage. Associated contact points
were more commonly on the head, neck, and upper trunk [56]. Seventy-seven percent of these ultimately progressed to where surgical intervention was required. This complication may present rarely within months or as late as many years after injury [46].
Heterotopic ossification (HO) occurs at the cut ends of amputation sites in this patient population. This may occur in about 80% of patients with long bone amputations but not those with disarticulations or small bone amputation [17]. In a recent report of one center’s experience over 21-years 42 patients were identified with HO and of these 7% were high-voltage electrical burns. Those patients requiring surgery can be managed by the burn team without need of orthopaedic consultation. Work-up includes plain films of the involved bodypart and PM&R consultation for postoperative care.
Electrical burn patients make up a relatively small number of overall injured patients in large burn and trauma centers. They do however consume large amounts of resources in these centers. The definitive care of these patients should be delivered in specialized centers in order to maximize good longterm outcomes and properly utilize scare resources.
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Correspondence: Brett D. Arnoldo, M.D., UT Southwestern
MedicalCenter,5323HarryHinesBlvd.,Dallas,TX75390–9158,
USA, E-mail: Brett.arnoldo@utsouthwestern.edu
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