- •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
R. Girtler, B. Gustorff
nificantly increased during a permanent oxycodone treatment. However, the plasma concentration can be increased in patients suffering from renal and liver insufficiency.
It can be administered in non-retarded (onset of action takes place after 15 to 25 minutes, action time 4 to 6 hours) and retarded (onset of action takes place after 60 minutes, action time 8 to 12 hours) form and is also available as parenterally injectable solution (rapid onset of action within 2 to 5 minutes, action time 4 hours). 2 mg orally administered oxycodone equals 1 mg parenterally administered oxycodone. However, due to individually different responses, a careful dosage titration is essential.
L-Methadone
L-Methadone is a μ-receptor agonist with low addiction potential and a 2 to 3-fold higher potency than morphine. It is not suitable for acute pain management as its action time is relatively long and not clearly predictable. Apart from that there is a high risk of accumulation, particularly in the presence of liver insufficiency.
In addition to its action at the opioid receptors, methadone has also antagonistic properties at the NMDA receptors. During a permanent opioid treatment with tolerance development, a rotation to methadone can improve analgesia.
In a patient (TBSA 55%) with chronic neuropathic pain after wound healing, the rotation to methadone could reduce the pain by 70% and improve the quality of life significantly [47].
Remifentanil
Remifentanil is an ultra short-acting, very well controllable opioid. Its potency is 200-fold higher than morphine. It is used intraoperatively during sedoanalgesia and in the intensive care unit (see IX. intensive care patients/6.2. analgesia). In single cases remifentanil is used with adequate monitoring for the treatment of burn pain in patients not receiving artificial respiration.
Other analgesics
Ketamine (see also intensive care unit and analgosedation)
Ketamine is used during sedoanalgesia in the intensive care unit and in the treatment of opioid-induced hyperalgesia and opioid tolerance as well as in chronic pain.
Literature provides numerous studies concerning the supplementation of an opioid therapy with ketamine in low, subanesthetic doses [48]. Psychomimetic side effects have only been reported in single cases.
Repeated surgical interventions as well as opioid therapy cause the activation of NMDA receptors. The effect of opioids is reduced due to a sensitization of the NMDA receptors through opioid induced hyperalgesia and opioid tolerance [49]. The application of NMDA receptor antagonists can lessen or inhibit these antinociceptive effects [50].
Weinbroum et al. showed that administering 250 μg/kg Ketamine in postoperative ineffectiveness of strong opioids could sufficiently relieve the pain [51].
Furthermore, an intraoperative intravenous administration of ketamine can reduce the postoperative demand for opioids and the opioid-induced side effects [52]. This effect should be taken advantage of after painful interventions with high demand for opioids (e. g. debridements in burn patients). Single studies show that a perioperative intravenous administration of ketamine can reduce the incidence of postoperative chronic pain [53, 54].
When administered for sedation during painful procedures stationary, ketamine is also effective and secure in children with burn trauma. An analysis of 347 sedations with administering ketamine according to a strict protocol and adequate monitoring showed a very low number (10i. e. 2.9%) of complications that required interventions like oxygenation or volume substitution [55].
Compared to the racemate ketamine the analgesic potency of S(+)-ketamine is twice as high and has fewer psychomimetic side effects. Thus, when administering S(+)-ketamine half of the dosage of the racemate is sufficient.
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Pain management after burn trauma
Anticonvulsants (Gabapentin and Pregabalin)
Gabapentin is important in numerous clinical settings: initially is was developed as an anticonvulsant for the treatment of epileptic partial seizures. However, nowadays gabapentin is a commonly used drug in the treatment of neuropathic pain of various causes. Additionally, several clinical studies have shown its effectiveness in the treatment of anxiety disorder [56–58]. Gabapentin also reduces the postoperative need for opioids and the opioid-induced side effects [59]. It is assumed that gabapentin has an antihyperalgetic component [60].
The exact mechanism of action remains unknown. The 2- -subunits of the voltage-dependent calcium channel were identified as binding spots. By inhibiting the calcium influx, the release of substance P, glutamate and calcitonin gene related peptide (CGRP) is suppressed.
In clinically relevant concentrations gabapentin does not bind to other receptors in the brain. In several in vitro test systems gabapentin decreased partially the effect on the glutamate agonist N-methyl- D-aspartic acid, however only in concentrations over 100 μg, which cannot be achieved in vivo.
Gabapentin does not bind to plasma proteins. There is no evidence of metabolism and it is only renally excreted. The dosage of gabapentin should thus be determined depending on the renal function of the patient (e. g. dependent on creatinine clearance).
To avoid side effects it is recommended to find the correct dosage by titrating: initially 300 mg once daily and after that depending on reaction and tolerance increase of the daily dosage in steps of 300 mg every second to third day until a maximum dosage of 3 600 mg daily is reached. In children of 6 years and older the initial daily total dosage is 10 mg/kg/day to 15 mg/kg/day dependent on the dosage of the onset therapy. The maximum daily dosage should be administered in three single doses as in adults. Dosages up to 40 mg/kg have proven well tolerated in clinical studies.
The usage of gabapentin in the management of burn injuries is still not sufficiently evaluated. A small study with burn patients (mean total burned surface area 25%) showed that gabapentin could reduce significantly the opioid consumption and pain
intensity. From day 3 to day 24 after the burn accident patients were administered 2 400 mg gabapentin in 3 single doses [61].
The neuropathic component of burn pain is often misinterpreted and has not been evaluated very extensively so far. Gabapentin could be administered successfully in a case series of 6 patients, who developed burning (neuropathic) pain in the area of the burned skin or the donor sites for skin grafting within 1 to 7 days after the burn accident [5].
Furthermore, a study in 35 children (6 months to 15 years of age) with severe itching of the healing burns showed that gabapentin could improve the symptoms significantly within 24 hours [62].
Pregabalin is a structure-related anticonvulsant and has the same mechanism of action as gabapentin. However, its pharmacological properties are better (oral bioavailability independent of the dosage, linear dose-effect relation). The initial dose is 150 mg in 2 single doses, the daily maximum dosage is 600 mg.
Antidepressants with analgesic effects
Depression and pain are very often closely related and show several similarities in their psychopathology and pharmacology. A dysfunction of ascending and descending serotonergic and noradrenergic tracts not only can cause depressive syndromes but also maintain the pain syndromes.
Thus, antidepressants are a very important part of the multimodal general treatment of burn patients [63]. A study group from Texas showed that an early administration of antidepressants in children with burn trauma could treat acute stress reactions successfully [64]. An intensifying effect of descending and ascending serotonergic and noradrenergic tracts by antidepressants can inhibit the pain signals from the body’s periphery and the intestines. The analgesic effect occurs mostly with a time lag of several days up to 3 weeks. Currently, the literature does not provide any studies concerning the analgesic effects of antidepressants in burn patients.
Tricyclic antidepressant (TCA) as for example amitryptiline: For a long time the use of TCA was the golden standard in the coanalgesia with antidepressants. A downside of TCA is the high potential for anticholinergic side effects. Apart from
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