- •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
Adult burn management
2.The zone of ischemia–represents an ongoing microvascular injury that surrounds the zone of necrosis. Following burn injury to the skin inflammatory mediators are released via the arachidonic acid pathway and inflammatory cells. These include
histamine, prostaglandins (PGE2), prostacyclins (PGI2), leucotrienes, thromboxanes, kinins, serotonin, catecholamines, free O2 radicals and platelet activating factor. Local action of these inflammatory mediators includes increase in microvascular permeability giving rise to oedema formation, microvascular stasis and thrombosis. These actions can lead to progressive injury and cell death leading to clinical deepening of the burn wound.
This process can be influenced by desiccation, infection and hypoperfusion of the burn wound. There is ongoing interest into the manipulation of this area of injury to preserve viable tissue and prevent progression of tissue necrosis.
3.The zone of inflammation (hyperaemia) surrounds zone of ischemia and is manifested by increased vascular permeability with extravasation of fluid from the intravascular to the interstitial space leading to oedema.
Assessment of the burn wound
Key to management of the adult burn patient is the formulation of a treatment plan. The burn wound must be assessed clinically before a treatment plan can be formulated. The depth of the burn wound, the size of the burn and the anatomical site of injury are all vitally important factors that must be assessed and considered in the treatment plan.
Depth of burn
This is determined mainly by clinical wound inspection. Determining the depth of the burn wound can be difficult. In general superficial partial thickness wounds are pink, moist, blistered, blanch on pressure and are very painful. Deep partial thickness burns will either be white or red with fixed staining. They do not blanch on pressure. Full thickness burns characteristically have a leathery appearance and are insensate. It is usually easy to diagnose a very superficial burn or a full thickness burn. Deep dermal burns can be a
little more difficult to assess and are often indeterminate on first assessment. Techniques such as Laser Doppler scanning can give an estimate of dermal blood flow and depth of burn injury. Healing times and timing of surgical have been correlated to the incidence of hypertrophic scarring. Wounds that heal spontaneously within 14 days have a very low incidence of hypertrophic scarring [3]. Surgical intervention is associated with a higher incidence of hypertrophic scarring up to 3 weeks following injury [4].
Size of the burn
This is usually represented as percent of total body surface area (%TBSA) injured using
a)Wallace’s “Rule of Nines” useful for initial rapid estimation in the emergency setting
b)Lund and Browder Chart for a more precise estimation
c)Patient’s palm ~ 1% of their body surface.
Initial management of the burn wound
A general systematic approach must be undertaken to manage fluid resuscitation, smoke inhalation and other injuries in the first instance. Maintenance of the airways, breathing and establishing venous access are paramount and are discussed in other chapters.
Following assessment of the depth, size and anatomical distribution of wound the following procedures should be considered:
First aid
Cooling the burn wound soon after the injury (within 30minutes) is beneficial in removing heat from the wound and limiting tissue damage. It can also reduce early oedema and protein extravasation. Care must be taken, as prolonged or excessive cooling can be detrimental and lead to hypothermia. Irrigating the wound in a drench shower for at least 20 minutes is essential in chemical injury to dilute the chemical [6].
Burn blisters
There is ongoing debate about management with evidence of blister fluid having both beneficial and
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deleterious effects. In general blisters should be removed if large, over joints and if they produce functional impairment. Small intact blisters can be left in situ to act as a biological dressing. One of the key indications for blister removal is that the dermal wound beneath can be inspected and the depth diagnosed [7].
Escharotomy
Escharotomy is required in circumferential full thickness burns of chest, limbs or digits.
In limbs/digits such burns impair circulation, produce distal ischemia and can lead to compartment syndromes, digital and limb loss. Circumferential full-thickness chest burns can restrict chest wall excursion and impair ventilation.
Such burns require mid-axial escharotomies performed either at bedside or in the operating room. A scalpel or electrocautery device can be used to incise through the full thickness burns down to bulging fat. The incisions should extend into adjacent non burned or less deeply burned tissue. Since the wounds are full thickness, minimal analgesia or anaesthesia should be required, but extension into less damaged tissue can be very painful. Current humane practice involves anaesthesia for this procedure. The decision to perform escharotomy is a clinical one. In a full thickness burn an escharotomy incision should improve outcome with minimal risk as the area will require excision and grafting later on during treatment.
General care of the adult burn patient
Adult patients with major burn injuries must be managed in a dedicated facility used to looking after such complex problems. Patients requiring Intensive Care support should be managed in a Burn ICU. Recent analysis of the effects of burn centre volume and mortality revealed a complex relationship not only dependent on patient characteristics but also where the patient was treated [8].
Fluid resuscitation using Parkland formula is currently standard care and although fluid resuscitation is the cornerstone of acute burn management it is apparent that in most centres patients today are receiving more fluid per percent total body surface
area (TBSA) giving rise to the concept of ‘fluid creep’. It has been show that patients receiving larger volumes of resuscitation fluid are prone to increased complications and mortality [9].
Burn patients with respiratory failure may require ventilation using lung protective ventilation strategies designed to minimise shear and stress forces in the alveoli. Pressure limited low tidal volume ventilation is the currently favoured strategy although high frequency percussive ventilation based strategies are becoming increasingly popular especially for rescue ventilation. A recent trial comparing the two strategies showed similar clinical outcomes in burn patients with respiratory failure however a higher percentage of low tidal volume strategy patients required rescue ventilation [10].
Vascular access in adult burn patients can be a significant challenge. Obviously central venous catheters represent a risk in terms of catheter related blood stream infections. Central venous catheters in burn patients are usually change after about 7 days following insertion either to a new site or over a guide wire. A recent study showed no difference in the incidence of catheter-related bloodstream infections between lines placed by new site or by guide wire exchange. Subset analysis of adults in this study revealed rewires having less catheter related blood stream infections compared to new sites [11].
Other studies have shown the incidence of sepsis increasing with increasing number of central line days and increasing number of central line changes. No statistically significant difference in the incidence of sepsis between upper-and lower-body central line sites was demonstrated [12].
Other intensive care bundles routinely undertaken in general intensive care practise may also have benefits in care of critically ill burn patients. These included protocols for deep venous thrombosis prophylaxis, stress ulcer prophylaxis, daily weaning parameters, sedation holidays, elevation of the head-of-bed up at 30 degrees and tight glucose control. Implementing these care bundles into the burn critical care setting was associated with reduction in ventilator associated pneumonias, and blood stream infection rates and lower mortality [13].
The hypermetabolic response in critically ill burn patients is characterized by hyperdynamic circulatory, catabolic and immune system responses. En-
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ergy and protein requirements are massive during critical illness and inadequate replacement can lead to multiorgan failure, increased susceptibility to infection, and death. Attenuation of the hypermetabolic response using pharmacologic modalities is an essential part of care of the severely injured adult burn patients.
Current modalities include beta-adrenergic blockade with propranolol, growth hormone, insu- lin-like growth factor, oxandralone and intensive insulin therapy [14].
Early nutritional support is an essential component of burn care to prevent ileus, stress ulceration, the effects of hypermetabolism and should be initiated as soon as possible following admission. Multicentre analysis has demonstrated that patients fed within 24hrs of injury had no increase in complications and a lower rate of wound infections and shorter ICU length of stay [15]. There are a variety of techniques in assessing nutritional requirements ranging from formulae based on the age and weight and the percentage burn to the use of indirect calorimetry and the respiratory quotient. Nutrition is usefully provided using high energy, high protein enteral feeds via the nasogastric or nasojejunal route.
Pain control in the burn population is an essential part of care yet control of pain remains a difficult task that is often inadequately performed. The adverse sequelae of inadequate pain control in the burn population have long been recognised. Burn pain is dynamic and has a peripheral and central component. A therapeutic plan for pain control must be dynamic and flexible to address background, breakthrough, procedural and post-operative pain. Regular, ongoing and documented pain assessment is key in directing this process. The simple analgesic paracetamol (acetaminophen) has both anti-pyretic and opioid-sparing properties and justly deserves its place in the pharmacological treatment of every burn patient Opioid analgesics provide the backbone of analgesia to burn patients but must be used judiciously (Fig. 1). Other centrally acting drugs such as ketamine and gabapentin are increasingly being used as opioid sparing adjuncts. Non-pharmacolog- ical methods such as distraction therapy can also play a role. Pain specialists must be integral part of the modern burn multi-disciplinary team and pain control must be given a high clinical priority [16].
Fig. 1. Acute pain guidelines (courtesy of Dr P Richardson MB FRCA)
Treatment planning
As with all areas in medicine treatment planning is key to successful outcome. Initially the size, site, and depth of the burn wound must be assessed whilst simultaneously undertaking initial urgent measures. A burn wound treatment plan must be formulated. This management plan will include conservative and surgical options depending on the individual patient and the type and site of the wound.
Treatment planning depends on the assessment of the factors described in Fig. 2.
In general, for superficial partial thickness wounds a more conservative approach is undertaken. A more aggressive surgical approach is best
Fig. 2. Patient factors to assess for treatment planning
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for deeper wounds, to improve outcome and reduce morbidity in smaller injury and to improve survival in bigger injuries. This based on the surgical principle that excision of dead tissues saves lives.
Superficial partial thickness wound
The aim of management of this type of wounds is to promote rapid spontaneous re-epithelialisation with the minimum number of painful dressing changes and to prevent infection which can lead to deepening of the wound and subsequent increased risk of hypertrophic scarring.
The wounds can be treated either with biological or semi biological dressings, with topical antimicrobials, with standard dressings either impregnated or free from a topical agent or by exposure
Biological/Semi biological dressings
Biological dressings can be defined as the use of human or animal tissue for temporary wound covering. A semi biological dressing refers to where a component of the dressing is derived from such tissue (i. e. collagen).
Biobrane is a semibiological dressing made up of a fenestrated silicone layer bonded to a nylon mesh that has bee impregnated with Type I porcine collagen. It has been used in burn care for the past twenty years since its development. In randomised controlled studies its use has been shown to reduce pain, in patient stay and time to healing [17,18].
In patients presenting within 24h of their injury, following admission and stabilisation the patient’s burns blisters are cleaned, debrided and all burned epithelium is removed under sedation or anaesthesia. Biobrane is then applied to the wound in a circumferential fashion around the limb or trunk so that it is closely adherent to the wound. The Biobrane is secured by either by stapling it to itself or the use of sterile Hypafix tape. Care is taken not to staple the Biobrane to the patient as this can cause granulomas and the staples are painful to remove. The Biobrane is then wrapped with a standard dressing of rolled gauze covered by elastic bandages. The dressings are removed at 24–48 hrs to inspect the wound. Oral antibiotics with staphylococcal coverage are given for five
days. If the Biobrane is adherent after the first day, no further dressings are required. As re-epithelialisation occurs in 10–14 days the Biobrane spontaneously separates from the healed wound. If wound infection supervenes, the Biobrane rapidly becomes non adherent and can trap any exudate produced by the wound. For this reason Biobrane is not used in patients presenting more than 24–36h following their injury and in larger wounds (>40% TBSA). Biobrane is also relatively expensive compared to common topical antimicrobials.
Topical antimicrobials
Silver has been used as an antimicrobial agent for some time. Numerous silver containing dressings are currently used for the management of burn wounds.
Traditionally topical Silvadene/Flammazine (1% Silver Sulfadiazine) is the usual alternative for these wounds. After cleaning the wound and debridement of the blisters, Silvadene is applied topically to the wound which is then covered with rolled gauze and elasticated bandage. The Silvadene dressings are changed once or twice daily until re-epithe- lialisation occurs and the wound is healed. This method requires frequent dressing changes, which can be a painful.
Acticoat is a nanocrystalline silver dressing that can provide sustained release of silver for up to 7 days [19]. A randomised controlled trial compared Acticoat to Silver Sulfadiazine demonstrated Acticoat to have better antimicrobial activity compared to silver sulfadiazine [20]. Other studies have suggested Acticoat has fewer adverse effects and reduces healing times. It is easy to apply and requires low frequency of dressing changes makes it an ideal dressing in burn wounds [21]. It is the method of choice for patients presenting late after injury with a colonized wound.
Biological dressings
Biological dressings such as allograft skin, xenograft skin (porcine), human amnion can all be used in a similar fashion to Biobrane to physiologically close the wound while re-epithelialisation occurs. The problems associated with the use of these products
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