- •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
J. Knighton, M. Jako
Fig. 10. Inhalation injury
2.Inhalation injury below the glottis – Most injuries below the glottis are chemically-produced through the inhalation of noxious products of combustion, resulting in tracheobronchitis. Major airway involvement (tracheobronchial tree) occurs about 30% of the time, with bronchopneumonia being the chief concern. Patients may not show symptoms until 12–24 hours post-burn. Since gases are usually cooled before they reach the lung parenchyma, there is only a 10% injury occurrence at the level of the terminal bronchioli and alveoli. Primary concerns here are pulmonary edema and adult respiratory distress syndrome (ARDS).
3.Carbon monoxide poisoning. Most fatalities at a fire scene are caused by carbon monoxide poisoning or asphyxiation. Carbon monoxide is produced by the incomplete combustion of burning materials. It then displaces the oxygen being carried by the hemoglobin molecules, resulting in less oxygen being delivered throughout the body. Carboxyhemoglobin levels should be measured following admission of the person to an emergency department or
Table 5. Signs and symptoms of carbon monoxide poisoning
Carboxyhemoglobin |
Signs and Symptoms |
Saturation (%) |
|
5–10 |
Visual acuity impairment |
11–20 |
Flushing, headache |
21–30 |
Nausea, impaired dexterity |
31–40 |
Vomiting, dizziness, syncope |
41–50 |
Tachypnea, tachycardia |
>50 |
Coma, death |
burn centre (Table 5). Treatment consists of the administration of 100% humidified oxygen until the carboxyhemoglobin falls to acceptable levels.
Radiation
These burns involve overexposure to the sun or radiant heat sources, such as tanning lamps or tanning beds. Nuclear radiation burns require government intervention and specialized treatment.
Clinical manifestations
Recovery from a burn injury involves successful passage through 3 phases of care: emergent, acute and rehabilitative. Principles of care for the emergent period involve resolution of the immediate problems resulting from the burn injury. The time required for this to occur is usually one to two days. The emergent phase ends with the onset of spontaneous diuresis. Principles of care for the acute period include the avoidance, detection and treatment of complications, and wound care. This second phase of care ends when the majority of burn wounds have healed. During the third, and final, phase of rehabilitative care, the goals are for the burn patient to return to an acceptable place in society and to accomplish functional and cosmetic reconstruction. This phase ends when there is complete resolution of any outstanding clinical problems resulting from the burn injury.
Subjective symptoms
It is essential throughout all phases of a burn patient’s recovery to seek out his/her perspective, when
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possible, and attempt to incorporate individual wishes into the plan of care. During the emergent period, patients and their families are in a state of physical and psychological shock. As a result of hypoxia, patients may also be disoriented or not able to recall what happened. Others remain very lucid throughout the ordeal and recall events with remarkable clarity. Some may not realize how serious their injuries are and be unrealistic about the care they require. Some may be intubated and sedated and not be aware for weeks to come. Pain may be a concern, while others experience little discomfort. Thirst may be a symptom, depending upon the degree of fluid loss. Some may complain of feeling cold or be seen to shiver as a result of heat loss, anxiety and pain. The combination of hypovolemic shock, facial edema, intubation and analgesics/sedative agents may alter a patient’s sensory perception significantly over the first few days post-injury. If he/she is able to talk, common themes include “Will I die? What happened? Why me? I can’t believe this is happening”. In the acute phase, patients experience varying levels of pain during dressing changes and physical/occupational therapy, and may describe significant muscular discomfort, resulting from functional positioning and use of splinting materials. Unable to do any number of self-care activities, patients may become very frustrated about how dependent they have become on others. Concerns may be expressed regarding finances, family and work obligations. Adaptation to the hospital environment and necessary treatments may absorb a considerable amount of the patient’s physical and emotional energy. Adjustment to a variety of losses (personal and property), feelings of grief, guilt and blame, a need for information about what to expect over the coming weeks, and a search for meaning behind the event, are also experienced. Patients may feel angry or depressed postinjury. Relationships with family may become strained as everyone seeks to readjust and cope with this unexpected and traumatic event. During the rehabilitative phase of care, patients come to realize they have completed the most difficult part of their recovery. However, they may experience impatience with the time required for complete healing and physical rehabilitation. There is usually a desire to resume as much independence as possible, sometimes coupled with slight fear and hesitation about
leaving the protective environment of the burn centre. Questions, such as “What will it be like when I leave the hospital? How will I manage when the nurses and therapists are no longer around to help?” reflect the primary concerns for patients and family members at this time. There may be concerns about resumed sexual intimacy with a partner and self-ac- ceptance of an altered body image. A request may be made to speak with a recovered burn survivor, who can offer words of support and advice based on personal experience. Over time, burn patients express feelings of pride at having overcome such tremendous physical and emotional challenges, and begin to reflect on the path their lives will take post-burn as they move from burn “victim” to burn “survivor” and, perhaps, burn “thriver”.
Objective signs The initial assessment of the burn patient is like that of any trauma patient and can best be remembered by the simple acronym “ABCDEF” (Box 2). During the emergent period, burn patients quickly begin to exhibit signs and symptoms of hypovolemic shock (Box 3). Lack of circulating fluid volumes will also result in minimal urinary output and absence of bowel sounds. The patient may also be shivering due to heat loss, pain and anxiety. If inhalation injury is a factor, the patient may demonstrate a number of physical findings upon visual assessment, laryngoscopy and fiberoptic bronchoscopy (Box 4). The patient may also experience pain, as exhibited by facial grimacing, withdrawing and moaning when touched, particularly if the injuries are partial-thickness in nature. Some areas of full-thick- ness burn may be anaesthetic to pain and touch if the nerve endings have been destroyed. The loss of sensation may be temporary if the nerves have been compressed by resulting edema in the hypovolemic shock phase. It is important to examine areas of cir-
Box 2. Primary survey assessment
A Airway
BBreathing
CCirculation
–C-spine immobilization
–Cardiac status
DDisability
–Neurological Deficit E Expose and evaluate
F Fluid resuscitation
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J. Knighton, M. Jako
Box 3. Signs and symptoms of hypovolemic shock
Restlessness, anxiety
Skin – pale, cold, clammy
Temperature below 37 ºC
Pulse is weak, rapid, systolic BP
Urinary output 20 mL/hr
Urine specific gravity 1.025
Thirst
Hematocrit 35; BUN
cumferential full-thickness burn for signs and symptoms of vascular compromise, particularly the extremities (Box 5).
Areas of partial-thickness burn appear reddened, blistered and edematous. Full-thickness burns may be dark red, brown, charred black or white in colour. The texture is tough and leathery and no blisters are present.
If the patient is confused, one has to determine if it is the result of hypovolemic shock, inhalation injury, substance abuse, pre-existing history or, more rarely, head injury sustained at the time of the trauma. It is essential to immobilize the c-spines until a full assessment can be performed and the c-spines cleared. At this time, a secondary survey assessment is performed (Box 6). Additional objective data can then be collected, analyzed and a plan of care developed, which includes a set of Admission Orders. In the acute phase, the focus is on wound care and potential development of complications. At this point, the burn wounds should have declared themselves as being partial-thickness or full-thickness in nature. Eschar on partial-thickness wounds is thinner and, with dressing changes, it should be possible to see evidence of eschar separating from the viable wound bed. Healthy, granulation tissue is apparent on the clean wound bed and re-epithelializing cells are seen to migrate from the wound edges and the der-
Box 5. Signs and symptoms of vascular compromise
Cyanosis
Deep tissue pain
Progressive paresthesias
Diminished or absent pulses
Sensation of cold extremities
mal bed to slowly close the wound within 10–14 days. Full-thickness wounds have a thicker, more leathery eschar, which does not separate easily from the viable wound bed. Those wounds require surgical excision and grafting.
Continuous assessment of the patient’s systemic response to the burn injury is an essential part of an individualized plan of care. Subtle changes quickly identified by the burn team can prevent complications from occurring or worsening over time. Physical examination, laboratory tests and diagnostic procedures will assist in the rapid identification and treatment of complications.
During the final, rehabilitative phase, attention turns to scar maturation, contracture development and functional independence issues. The areas of burn, which heal either by primary intention or skin grafting, initially appear red or pink and are flat. Layers of re-epithelializing cells continue to form and collagen fibres in the lower scar tissue add strength to a fragile wound. Over the next month, the scars may become more red from increased blood supply and more raised from disorganized whorls of collagen and fibroblasts/myofibroblasts. The scars are referred to as hypertrophic in nature. If oppositional forces are not applied through splinting devices, exercises or stretching routines, this new tissue continues to heal by shortening and forming contractures. A certain amount of contracture development is unavoidable, but the impact can be lessened through prompt and aggressive interventions.
Box 4. Physical findings of inhalation injury
Carbonaceous sputum
Facial burns, singed nasal hairs
Agitation, tachypnea, general signs of hypoxemia
Signs of respiratory difficulty
Hoarseness, brassy cough
Rales, ronchi
Erythema of oropharynx or nasopharynx
Box 6. Secondary survey assessment
Head-to-toe examination
Rule out associated injuries
Pertinent history – circumstances of injury
– medical history
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Nursing management of the burn-injured person
The scar maturation process takes anywhere from 6–18 months. During this time, the scars will progress from a dark pink/red to a pale pink/whitened appearance. The final colour is usually lighter than the surrounding unburned skin. For people with darkly pigmented skin, the process of colour return may be prolonged as the melanocytes work to produce pigment in the areas where it has been lost. Pressure may be necessary to gently and continually flatten the scars which, in turn, pushes the extra blood from the area, making them lighter in colour. Pressure is usually applied in increasing amounts as the fragile skin develops tolerance. Custom-fitted pressure garments and/or acrylic face masks apply constant pressure over a wearing period of 23 ½ hours a day. Extra pressure over concave and difficult-to-fit areas can be provided through elastomer inserts or silicone sheeting under the garments or face mask. The length of time a person might have to wear the garments varies, but is in the range of 1 to 1½ years, depending upon the intensity of the scarring and the body’s response to pressure therapies. Patients will often experience itchiness and dry skin. One of the best ways to decrease the itchiness is to get at the source of the problem: the dry skin. However, burned skin is different from healthy skin. Once the skin has been damaged by a burn injury, there are less natural oils available since the oil-reproducing glands have been destroyed, in whole or in part. In other words, the skin is “internally” dry as opposed to “externally” dry, such as when hands get chapped in the cold weather. What burned skin needs is a product that will be absorbed through the outer layer of the epidermis into the dry, dermal tissues. Water-based products are needed in order to do this. The more predominant products available are oil-based and contain mineral oil, petrolatum or paraffin. These ingredients coat the surface of the skin and, in essence, block the pores. This prevents loss of natural oils from the dermis, oils which burned skin is lacking. These ingredients are not absorbed into the dry dermis and do not bring moisture back into the skin. Mineral oil also breaks down elastic fibres in pressure garments and should be avoided. Suggested water-based products include Vaseline( Intensive Rescue or Smith and Nephew’s Professional Care . Medications, such as diphenhydramine (Atarax , Benadryl ), can also be ordered to help with moder-
ate to severe itchiness on a short-term basis, as can massage therapy.
Diagnostic findings
There are a number of baseline diagnostic studies that describe the patient’s clinical condition at the time of the injury and monitor responses to care throughout the recovery period. They include laboratory tests, such as complete blood cell count (CBC), hemoglobin and hematocrit, group and screen, serum electrolyte levels, blood glucose, blood urea nitrogen (BUN), serum creatinine, calcium profile, serum lactate, liver function tests and coagulation studies (PT, PTT, INR). Drug and alcohol screens may be indicated, upon admission, if the circumstances of the accident and/or patient’s clinical presentation warrant it. If inhalation injury is suspected, a serum carboxyhemoglobin, serum cyanide and arterial blood gas should be obtained, along with a chest x-ray. Laryngoscopy and/or fiberoptic bronchoscopy may also be indicated for inhalation-in- jured patients. Routine urinalysis, along with urine for hemoglobin and myoglobin in cases in electrical injury, also need to be collected. For patients with pre-existing cardiac disease or those sustaining electrical injuries, a 12-lead electrocardiogram (ECG) should be performed. For patients with suspected, head or spinal injury, fractures or internal trauma, x- rays or scans are indicated. Antibiotic resistant organism (MRSA and VRE) screening and wound swabs for culture and sensitivity (C + S) monitor the microbiological organisms present on admission. Blood cultures, along with urine and sputum for C + S, are also helpful when investigating patients who become febrile or who may be developing sepsis. As the patient’s condition changes, medical specialists from various services may be consulted and they may order various diagnostic tests, such as ultrasound, magnetic resonance imaging (MRI) or computerized axial tomography (CAT) scans to rule out or confirm diagnoses. Placement and monitoring of transduced, invasive central and arterial lines provide the team with information on a patient’s cardiac and pulmonary functioning. Access to this wide variety of diagnostic information allows for timely clinical interventions by members of the burn team.
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