- •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
Pain management after burn trauma
patients; significant correlation with applied dosages of analgesics and sedatives [95].
COMFORT-scale: Application in pediatric intensive care units; consists of 8 easily determinable parameters to evaluate the level of sedation during the daily nursing measures [96].
Analgesia monitoring (see Fig. 2)
After evaluation of the level of sedation and analgesia, an individual aim for sedation and analgesia should be determined according to these scoring systems. The achievement of this aim should be verified on a regular basis (at least every 8 hours). A reevaluation and re-defining of the level of sedation and analgesia should also be carried out regularly.
Analgosedation (Table 3)
As there is a vast number of available preparations for an analgosedation, it is necessary to develop standard operating procedures [97]. It must not necessarily be decisive which concept is applied but that the concept is consequently and correctly applied.
Apart from an adequate sedation and analgesia, an adequate anxiolysis and vegetative protection are desirable. Modern concepts for analgosedation are based on a controlled sedation of the patient’s state of awareness and an effective elimination of pain perception. They are not meant as a prolongation of a general anesthesia.
In severely burned patients a deeper sedation is often necessary. This holds true for patients with pronounced edema in the face and the upper respiratory tract. In such patients an accidental self-extubation can be a vital danger. A deeper analgosedation can also be necessary for a particular positioning of the patient due to the localization of the burn wound and to protect fresh skin grafts that are prone to shearing forces. However, this increases the risk for ventilator-induced pneumonia. In such cases the situation must be evaluated by the health care personnel depending on the patient’s general condition and the surgical and pulmonary situation [98].
Item |
Description |
Score |
|
|
|
Facial expression |
Relaxed |
1 |
|
Partially tightened (e. g., brow |
2 |
|
lowering) |
|
|
|
|
|
Fully tightened (e. g., eyelid |
3 |
|
closing) |
|
|
|
|
|
Grimacing |
4 |
Upper limbs |
No movement |
1 |
|
|
|
|
Partially bent |
2 |
|
|
|
|
Fully bent with finger flexion |
3 |
|
|
|
|
Permanently retracted |
4 |
|
|
|
Compliance with |
Tolerating movement |
1 |
ventilation |
|
|
|
|
|
|
Coughing but tolerating |
2 |
|
ventilation for most of the time |
|
|
|
|
Fig. 2. Behavioral pain scale |
|
Sedation
Today there are various methods for the sedation of intensive care patients. The medication should not be ended abruptly after long-time sedation but slowly. Sedation and weaning protocols make this process easier and respiration time is reduced [99]. Sedatives must not be administered as a replacement for analgesics.
Propofol
Propofol is approved for sedation in intensive care for a maximum of 7 days. It has sedative-hypnotic, but no analgesic effects. Due to its short and con- text-sensitive half-life and the production of inac-
Table 3. Sedoanalgesia in the intensive care unit
Midazolam |
0,03–0,15 mg/kgBW/h |
Propofol |
1–3 mg/kgBW/h |
Clonidine |
0,03–0,15 mg/kgBW/h |
S(+)-Ketamine |
0,3–1,5 mg/kgKBW/h |
Sevoflurane* |
endtidal Conc. 0,5–1,1 Vol % |
Sufentanil |
0,5–1,5 mg/kgBW/min |
Remifentanil |
0,05–2 mg/kgBW/min |
*Calculation of the pumpfrequency (ml/h)
depending on breath volume per minute by nomogram
355
R. Girtler, B. Gustorff
tive metabolites, the preparation is well controllable. Problems during application might occur through falling blood pressure and additional fat supply (1 ml = 0.1 g fat). A dosage limitation ( > 4 mg/ kg/h) is required to minimize the risk of a propofol- infusion-syndrome. This is characterized by cardiac arrythmia, heart failure, rhabdomyolysis, severe metabolic acidosis and acute renal failure. Regular checks in the laboratory (in particular ph-value and lactate) facilitate an early detection of this syndrome. Propofol is approved for the sedation of children older than 16 years.
Fröhlich et al. evaluated in a randomized pla- cebo-controlled study the effect of propofol to pain sensation with temperature stimulus (45°C, 47 °C and 49°C). Propofol was administered as targetcontrolled infusion in 2 different concentrations (0.5 μ/ml and 1.0 μ/ml) to 18 test subjects. Pain intensity was measured by the visual analogous scale. Surprisingly, the authors could prove that propofol in mild and moderate doses increased the pain intensity and the patients’ discontentment. Thus a sedation should always be combined with sufficient analgesia [100].
Benzodiazepine
Benzodiazepine centrally enforces the inhibiting effect of -aminobutyric acid and has anxioloytic, sed- ative-hypnotic, centrally relaxing and anticonvulsant effects. It is administered during long-term sedation ( > 3 days). Compared to other benzodiazepines, midazolam has a shorter context-sensitive half-life and thus is very well suited. Another benefit is an anterograde amnesia caused by benzodiazepine. Liver and renal dysfunctions cause an extensively longer action time.
Clonidine
Clonidin is a presynaptic 2-adrenoceptorantagonist with antihypertensive, analgesic, sedative and anxiolytic activity. It is administered as basic sedation (particularly in hypertensive patients), as prohylactic and in the therapy of withdrawal symptoms after long-time analgosedation and in preexisting alcoholism. Furthermore, clonidine causes a dosage reduction of sedatives and opioids and thus reduces
the side effects induced by these preparations. However, complications as for example bradycardic arrhythmia, dropping blood pressure and inhibition of the gastro-intestinal motility have to be considered. After long-time application, the administration of clonidine must be stopped slowly and gradually to avoid a rapid increase of the blood pressure.
Ketamine
Ketamine is a non-competitive NMDA-receptor-an- tagonist with dosage dependent activity. A higher dosage causes somnolence up to dissociate anesthesia (dissociation from the environment without sleeping). Due to the psychomimetic side-effects, ketamine should be administered in combination with propofol and benzodiazepine. Ketamine has proven beneficial in patients with bronchospasm or hypotensive circulation without cardiogenic reasons. However, ketamine stimulates the cardiovascular system by sensitizing the heart to catecholamines. A potential increase of the arterial blood pressure, tachycardia and increase of the myocardiac oxygen consumption have to be considered.
In subanesthetic dosages, ketamine acts exclusively as analgesic. Numerous studies have shown that ketamine can suppress effectively an opioid tolerance and an opioid-induced hyperalgesia [35, 38, 101]. The opioid-reducing property of ketamine could also be proven in intensive care patients [102].
Volatile anesthetics
A long-term sedation by intravenous preparations is associated with respiratory depression, enteroparesis, renal and liver disorders and accumulation with retarded recovery. Volatile anesthetics can be an effective alternative. For this purpose special recirculation systems for inhalational anesthetics have been developed for the use in the intensive care unit (e. g. Anesthetic Conserving Device, suitable for isoflurane and sevoflurane). At present, however, there are no sufficient studies on the importance of volatile anesthetics in analgosedation in the intensive care unit. There are single case reports of a successful application in burn patients [103].
356