- •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
Nursing management of the burn-injured person
Box 1. Burn severity factors
1.Extent of body surface area burned
2.Depth of tissue damage
3.Age of person
4.Part of body burned
5.Past medical history
amongst all cultures and across all age ranges. In the developed world, about two-thirds of those injured are male and about one-third are less than 16 years of age. A number of identifiable factors place someone at greater risk for sustaining a burn injury such as inattention, carelessness, lack of knowledge and resources, a sense of invincibility, and ingestion of alcohol, alone or in combination with drugs. Some incidents, however, are the result of unfortunate cir-
cumstances or medical illness, such as epilepsy or Fig. 1. Rule of Nines method for estimating extent of burn diabetes. Burn prevention programs aim to identify
these risk factors, educate and heighten awareness of individual risk, and encourage people to practice safe strategies in order to decrease their level of risk at home, work or play.
Pathophysiology
Severity factors
There are five factors that need to be considered when determining the severity of a burn injury (Box 1).
i) Extent – The larger the area of the body burned, the more serious the injury. There are several methods available to accurately calculate the percentage of body surface area involved. The simplest and most easily recalled is the Rule of Nines (Fig. 1). However, it is only for use with the adult burn population. It cannot be used for persons under the age of 15 years. The Lund and Browder method (Fig. 2) is useful for all age groups, but is more complicated to use.
The chart assigns a certain percentage to various parts of the body and includes a table indicating adjustments necessary for different ages. For the pediatric population, there is a modified version of the Lund and Browder method (Fig. 3). If the burned areas are small and irregularly-shaped, the Rule of Palm can be used. One looks at the palmer surface of
Fig. 2. Lund and Browder method for estimating extent of burn
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J. Knighton, M. Jako
Fig. 3. Pediatric estimation of burn area using modified Lund and Browder
the burned person’s hand, which represents 1% body surface area, and uses that to calculate the scattered areas of burn. If approximately 10% or more of the body surface of a child or 15% or more of that of an adult is burned, the injury is considered serious. The person requires hospitalization and fluid replacement to prevent shock.
ii) Depth – Two factors determine the depth of a burn wound – temperature of the burning agent and duration of exposure time. In other words, the hotter the source and the longer it is in contact with the skin, the deeper the injury. Previously the terminology used to describe burn depth was first, second and third degree. In recent years, these terms have been replaced by those more descriptive in nature: superficial partial-thickness, deep partial-thickness and fullthickness. A description of each is included (Table 3).
Superficial burns, such as those produced by sunburn, are not taken into consideration when assessing extent and depth. The skin is divided into 3 layers, which include the epidermis, dermis and subcutaneous tissue (Fig. 4). The epidermis is the thin, outer, nonvascular layer. Its role is one of protection, heat regulation and fluid/electrolyte conservation. Below the epidermis lies the dermis, perhaps
Fig. 4. Anatomy of burn tissue depth
the most important layer of skin, where the depth of burn has a profound impact. The dermis contains connective tissue, blood vessels, hair follicles, sweat and sebaceous glands. Skin-reproducing cells are located throughout the dermis and the sufficient presence or absence of these epidermal cells determines whether the wound will re-epithelialize or require skin grafting.
The subcutaneous tissue lies below the dermis and contains fat, lymphatics, nerves and vascular networks. Below the subcutaneous tissue is the muscle and bone, which may be affected by deep flame and major electrical injuries.
iii)Age – In patients less than 2 years of age and greater than 50, there is a higher incidence of morbidity and mortality. The severity of the burn increases with age. Infants, toddlers and the elderly have thinner skin, making the risk of a deeper burn greater in these age groups. Persons of this age also have weaker physical resources to mount a resistance against the debilitating effects brought on by a burn. Sadly, the infant, toddler and elderly are at increased risk for abuse by burning.
iv)Part of the body burned – Burn location is an important factor to consider. Patients with burns to the face, neck, hands, feet or perineum have greater challenges to overcome and require the specialized care offered by a burn centre. The challenges are both functional and esthetic in nature. Specialized care can minimize loss of permanent function, reduce infection and maximize esthetic outcomes.
v)Past medical history – A person’s past medical history is an important variable to consider postburn. Someone with pre-existing cardiovascular,
390
Nursing management of the burn-injured person
Table 3. Classification of burn injury depth
Degree of Burn |
Cause of Injury |
Depth of Injury |
Appearance |
Treatment |
First degree |
Superficial sunburn |
Superficial damage to |
Erythematous, blanching |
Complete healing within |
|
Brief exposure to hot |
epithelium |
on pressure, no blisters |
3–5 days with no |
|
liquids or heat flash |
Tactile and pain |
|
scarring |
|
|
sensations intact |
|
|
Superficial partial- |
Brief exposure to |
Destruction of epider- |
Moist, weepy, blanching |
Complete healing within |
thickness |
flame, flash or hot |
mis, superficial damage |
on pressure, blisters, |
14–21 days with no |
(2nd degree) |
liquids |
to upper layer of dermis, |
pink or red colour |
scarring |
|
|
epidermal appendages |
|
|
|
|
intact |
|
|
Deep partial-thick- |
Exposure to flame, |
Destruction of epider- |
Pale and less moist; no |
Prolonged healing time |
ness |
scalding liquids or |
mis, damage to dermis, |
blanching or prolonged, |
usually > 21 days with |
(deep 2nd degree) |
hot tar |
some epidermal |
deep pressure sensation |
scarring. Skin grafting |
|
|
appendages intact |
intact, pinprick sensa- |
may be necessary for |
|
|
|
tion absent |
improved functional |
|
|
|
|
and esthetic outcome |
Full-thickness |
Prolonged contact |
Complete destruction of |
Dry, leathery, pale, |
Requires skin grafting |
(3rd degree) |
with flame, steam, |
epidermis, dermis and |
mottled brown or red in |
|
|
scalding liquids, hot |
epidermal appendages; |
colour; visible throm- |
|
|
objects, chemicals or |
injury through most of |
bosed vessels insensitive |
|
|
electrical current |
the dermis |
to pain and pressure |
|
Full-thickness |
Major electrical |
Complete destruction of |
Dry, black, mottled |
Requires skin grafting |
(4th degree) |
current, prolonged |
epidermis, dermis and |
brown, white or red; no |
and likely amputation |
|
contact with heat |
epidermal appendages; |
sensation and limited |
|
|
source (i.e. uncon- |
injury involving connec- |
movement of burned |
|
|
scious patient) |
tive tissue, muscle and |
limbs or digits |
|
|
|
bone |
|
|
pulmonary or renal disease will have a poorer predicted outcome than a previously healthy individual, since a burn injury will exacerbate pre-existing conditions. Persons with diabetes or peripheral vascular disease have a more difficult time with wound healing, a central factor in burn recovery, particularly if the burns are on the legs and/or feet. Burn patients with poor nutritional status pre-burn or with previous drug and/or alcohol abuse patterns have fewer physical reserves to draw from and, as such, require more resources for a prolonged period of time. Finally, burn patients, who have also sustained inhalation injuries, head trauma, fractures or internal damage, have a poorer prognosis overall.
Local damage
Burn wounds are produced when there is contact between a source of energy, such as heat, chemicals,
electricity or radiation, and body tissue. Local damage varies, depending upon the temperature of the agent, duration of contact time and the type of tissue involved. There are 3 zones of tissue damage in the burn wound. The deepest zone of coagulation (fullthickness) is the site of irreversible cell death, where blood vessels and re-epithelializing cells have been completely destroyed. These areas require skin grafting for permanent coverage. The middle layer, or zone of stasis, is the area of deep, partial-thick- ness injury where there are some skin-reproducing cells present in the dermis and circulation to the area is partially intact. Healing will occur generally within 14 – 21 days, as long as infection or desiccation are prevented. The outermost zone of hyperemia is the area of least damage. This superficial, partial-thickness wound has minimal cell involvement and will generally recover spontaneously within 7–10 days.
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J. Knighton, M. Jako
Coagulation necrosis occurring at the time of the injury damages or destroys tissues and vessels. During the inflammatory process post-burn, leukocytes and monocytes begin to appear at the site of the injury. Fibroblasts and collagen fibres gather within 6–12 hours after the burn to begin the task of wound repair. White blood cells begin the process of phagocytosis and necrotic burn tissue begins to slough. Fibroblasts and collagen fibres form granulation tissue. Areas of partial-thickness injury, devoid of infection and desiccation, will heal in by primary intention from the edges of the wound and from below. Full-thickness wounds require early excision and skin grafting. Over time, the collagen fibres and reepithelializing cells continue to heal and add strength to the newly formed tissue. The healed areas initially look pale and flat. However, as the blood supply increases to those areas over the next month or so, they become red and raised. In addition to these scars forming, there is a natural tendency for burned tissue to shorten and contractures to develop. Over the next year to 18 months, the burn scars will fully mature and become less red and less raised.
Fluid and electrolyte shifts
The immediate post-burn period is marked by dramatic circulation changes, producing what is known as “burn shock” (Fig. 5). Blood flow increases to the area surrounding the wound. The burned tissue then releases vasoactive substances, which results in increased capillary permeability. As early as 15 minutes post-injury, there is a shift of fluid from the intravascular compartment to the interstitial space, producing edema, decreased blood volume and hypovolemia. The hematocrit increases in response to the decrease in blood volume and the blood becomes more viscous. This increase in viscosity, coupled with a decreased blood volume, results in increased peripheral resistance. Hypovolemic or “burn” shock follows shortly thereafter. As the capillary walls continue to leak, water, sodium and plasma proteins (primarily albumin) move into the interstitial spaces in a phenomenon known as “second spacing”. Potassium levels rise initially in the extracellular spaces due to release from injured cells and hemolyzed red blood cells. When the fluid begins to
Fig. 5. Burn shock
accumulate in areas where there is normally minimal to no fluid, the term “third spacing” is used. This phenomenon is found in exudate and blister formation. As intravascular volumes are depleted, the edema increases and the body begins to respond to the hypovolemic shock ( pulse and blood pressure). There is also insensible fluid loss through evapouration from large, open body surfaces. A nonburned individual loses about 30–50 mL/hr. A severely burned patient may lose anywhere from 200 to 400 mL/hr.
Circulation is also impaired in the burn patient due to hemolysis of red blood cells. Hemolysis can be due to direct insult from the burn, circulating factors released post-injury and capillary thrombosis in burned tissue. The hematocrit is elevated secondary to hemoconcentration and returns to more normal levels once fluids shift back to the intravascular space. Following successful completion of the fluid resuscitation phase, capillary membrane permeability is restored. Fluids gradually shift back from the interstitial space to the intravascular space, bringing with them sodium to the vascular space and potassium to the cells. The patient is no longer grossly edematous and diuresis is ongoing.
392