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Thermal injury
SPECIAL COMMUNICATION
Thermal Injury David J. Dries, MSE, MD, FACS, FCCP, FCCM’
1, Loyola Lifestar, Loyola University Center, Maywood, IL
Medical
Address for correspondence and reprints: David J. Dries, MSE, MD, Loyola University Medical Center, Burn & Shock Trauma Institute, 2160 S. First Ave., Bldg. 100, Room 4233, Maywood, IL 60153 Copyright Associates
0 1997
1067-991
X/97/$5.00
Reprint
by the Air Medical
EDITOR’S NOTE: The author provides an
overview of bum care based on 15 years of practice in the field. Although not formally referenced, the paper includes an annotated bibliography offering access to key references pertinent to recent bum care.
Journal
Epidemiology
no. 74/l/831
Air Medical
Journal
Burns are a significant public health problem in the United States.The magnitude of this problem is reflected in data reported by each state to the National Center for Injury Prevention and Control. Burn deaths totaled more than 5000 in the United States and ranged from 4 in Hawaii and 8 in Vermont to 337 in California and 359 in Texas during 1991. Age-adjusted rate of fire and bum deaths excluding patients of unknown age ranged from 0.164 per 100,000 population in Colorado to 3.75 per 100,000 pop ulation in Mississippi. Deaths occur with greatest frequency in residential fires, particularly in multifamily dwellings and low-income census tracts. Four of five unintentional deaths and three of four deaths as a result of bums from fire result from house fires. Approximately 12 individuals die in residential fires each day; young children and the elderly are the most likely victims. Overall, an estimated 2 to 2.5 million people seek treatment for burns in the United States each year; 100,000 to 150,000 are hospitalized. Like other forms of injury, bums tend to be a disease of the young. Thirty-eight percent of victims are younger than 15 years old, a second group of similar size (31%) is in the 15- to 44-year-old range, 24%
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are between 44 and 64 years old, and 7% are 65 or older. Scalds are the most common form of childhood injury, whereas electrical and chemical injuries affect adults in the workplace. Factors that have been shown to relate to bum mortality include size of cutaneous injury, patient age, and the presence or absence of inhalation injury. The Burn Wound
Skin characteristics affect patterns of cutaneous injury. Skin is very thin in infants and increases in thickness until 30 to 40 years of age, after which it progressively thins. Men tend to have thicker skin than women. Average skin thickness is 1 to 2 mm. In general, dermis is 10 times thicker than associatedepidermis. A variety of cell types make up the epidermis. The predominant cell type is the keratinocyte, which provides the superficial layering effect seen on visualization of the skin. Melanocytes provide pigment generation against ultraviolet radiation. Iangerhans cells have a cutaneous immune function; Merkel cells serve as mechanoreceptors in the epidermis. Cell layers in the epidermis include the basal layers with the stratum germinativum, a site for superficial cell mitosis, and the stratum spinosum, where protein synthesis occurs. The stratum granulosum is the site of keratin production and the locus for formation of the stratum corneum. This latter stratum contains the layers of dead cells seen on superficial examination of the skin. The cell types and layers in the epidermis take their origin in the ectoderm. The dermis is derived from the meso81
derm. The dominant cell type is the fibroblast, which produces collagen, elastin, and ground substance of glycosaminoglycans and proteoglycans. Plasticity of the dermis associated with PATIENT ICIYOLA collagen remodeling allows the skin to reSKIN ASSESSMENT main intact under varying types of stress. The dermis consists of two layers: a superficial papillary dermis and a thicker reticular dermis. The dermoepidermal junction contains fibrinectin and mucopolysaccharides.Hemidesmosomes anchor the cells of the basal epidermal layer INDETERMINANT to the basement membrane, which divides epidermis and dermis. FULL THICKNESS When thermal injury occurs, a variety of skin functions are lost. Most important is the protective barrier against infection DONOR AREA and other environmental stimuli. The skin also provides an immunologic barrier and serves as an antigen presenting pi1 GRAFT AREA the source for immune cells. Sebum pro duced by skin glands has been noted to have antibacterial properties. Other skin functions include fluid protection, protein and electrolyte hemostasis, neurosensory stimuli processing, and vitamin D production as a metabolic activity. In thermal injury, injurious effects of heat are a function of the temperature of the heat source and the duration of skin exposure. At 40” to 44” C, enzymatic failure of the cell occurs with rising intracellular sodium concentration and swelling as a result of failed membrane sodium pumps. At exposure to 45” C, skin necro sis occurs within 1 hour with release of oxygen radicals. Three zones of cutaneous injury have been described: fluid resuscitation, and topical an- creased vascular permeability is related l The zone of coagulation is the site of timicrobial agents. to the release of several vasoactive and irreversible cell death with new esl The zone of hyperemia is characteroxidative products. char formation from local protein degradation. ized by minimal cellular injury but The size of thermal injury is assessed l The zone of stasis is the site of local prominent vasodilation and in- by the well-known rule of nines (Figure circulatory impairment with initial 1). Anatomic criteria also can be used to creased blood flow. Cell recovery cell viability. If ischemia follows in generally occurs in this zone. recognize the depth of injury and coincithis zone, cell death will occur. Vasoactive mediators, including dent likelihood of healing. Partial-thickImpaired circulation is believed to thromboxane A2 with platelet adherence ness injuries should heal within 3 weeks be a result of platelet and neutrophil and vasoconstriction, typically are seen and leave the stratum germinosum intact. aggregates, fibrin deposition, en- in the burn wound. Beyond the vasocon- Third-degree or full-thickness injuries indothelial cell swelling, and loss of stricting effects seen in the zone of stasis, volve all layers of the epidermis and dererythrocyte deformability. These the predominant effect and resuscitation mis. Some authors speak also of fourth-de tissues are susceptible to secondary issue is significant vasodilation and in- gree injuries that involve deep structures, insults, such as dehydration, pres- creased vascular permeability. The initial such as tendon, muscle, and bone. Table 1 sure, overresuscitation, and infec- increase in vascular permeability may be discussesbum depth classification. tion. Measures implemented to min- related to short-term histamine release Local care begins with serial debrideimize further tissue loss include occurring soon after injury. The second ment of nonviable tissue and blisters. nondesiccating dressings, careful longer period of vasodilation and in- Topical antimicrobials, one of the major 82
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Classification Degree
Depth of tissue penetration
of burn
First
Superficial
Deep
Third
partial
partial
Injury to the superficial epidermis, usually caused or brief heat flashes. Classically can be described
thickness
Injury has destroyed both the epidermis and the dermis. Wound appears white, will not blanch, and is anesthetic. Tough, nonelastic, and tenacious coagulated protein (eschar) tissue may be present on the surface. This wound will not heal without surgical intervention.
Antimicrobial
Agents
Advantages
Disadvantages
Silver sulfadiazine
Painless application Broad spectrum Easy application Rare sensitivities
May produce transient leukopenia Minimal penetration of eschar Some gram-negative species resistant
Mafenide acetate
Broad spectrum Easy application Penetrates eschar
Painful application Promotes acid-base Frequent sensitivities
Bacitracin, Polysporin
Painless application Nonirritating Transparent May be used on nonburn wounds
No eschar
Silver (0.5%
Painless application Broad spectrum Rare sensitivity
No eschar penetration Electrolyte imbalances Discolors wound and environment Must be kept moist
Povidoneiodine
Broad
Painful application Systemically absorbed Requires frequent reapplication Discolors wounds
Gentamicin
Painless application Broad spectrum
spectrum
advances in bum wound care, are applied twice daily after washes with antiseptic solutions. These topical antimicrobials are applied in moist dressings that also help maintain fluid balance. The burn wound affords a warm, moist, proteinladen growth medium to gram-positive and later gram-negative bacteria. Treatment for these organisms centers on good local care and topical antimicrobials (Table 2). In general systemic antibiotics are not used. Biologic dressings are used when relMedical
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to sunlight
Injury is through the epidermis and may affect isolated areas of the deep dermal strata from which cells arise. This wound may appear red and wet or white and dry, depending on extent of deep dermal damage. It heals without grafting but requires > 3 weeks with suboptimal cosmesis. Excision and splitthickness skin grafting are recommended.
Agent
nitrate solution)
by overexposure as a sunburn.
Injury is to epidermis and upper layers of the dermis. Wounds characteristically appear red, wet, or blistered, blanchable, and extremely painful. Will heal within 3 weeks from epidermal regeneration from remaining remnants found in the tracts of hair follicles.
thickness
Full thickness
Topical
Air
Characteristics
Partial thickness
Second
of Burn Depth
imbalance
penetration
Oto/nephrotoxic Encourages development resistant organisms
of
atively clean wounds are present to reduce pain, decrease bacterial colony counts, and control fluid and protein losses.The rate of reepithelialiiation has been shown to be increased by applying biologic dressings. Epithelialiiation is increased with biologic dressings over topical antimicrobials, which tend to cause relative inhibition of wound epithelialization. Biologic dressings sometimes are placed on newly debrided partial-thickness burns in anticipation of healing without surgery. Biologic dressings also 1997
may be used to cover granulating excised wounds awaiting skin grafts. Early adherence of biologic dressings may indicate readiness of a wound bed for permanent skin grafting. Finally, biologic dressings may facilitate removal of necrotic tissue from granulating wounds. When circumferential extremity injury with second- or third-degree depth exists, the bum wound may need to be divided at lateral aspects of extremities or on the torso to facilitate extremity perfusion or chest wall movement, respectively. Division of wound eschar for this purpose is termed escharotomy. Usually the need for escharotomy is clear within 48 hours of injury. Progressive tissue edema during resuscitation creates the need for escharotomy even if initial perfusion of distal extremities or chest wall movement in circumferential torso bums appears to be adequate. Abdominal wall escharotomy or laparotomy for abdominal compartment syndrome with respiratory embarrassment sometimes is required. Excision of burned tissue that clearly will not heal (clinical assessment) generally is performed within 3 to 5 days of injury. Not more than 20% total body surface area (IBSA) is excised at a time. If possible, wounds are covered with sheet or meshed autograft, harvested .0003- to .OOl@inchthickness from unburned sites. Good sites for donor skin are the thighs, back, and scalp. Grafts can be meshed to increase surface area covered with the assumption the wound will reepithelialize within the mesh network. Generally meshing greater than 1:3 is not used be83
cause of increased incidence of contractures and graft shear. If donor skin is unavailable, cadaveric allograft can be used as a temporary cover of excised areas after burned tissuesare removed. In general, sequential tangential excision of burned tissue is used to the level of viable recipient beds as assessed by visible punctate bleeding. Although blood loss is greater with this method, cosmetic outcome is improved, and the maximum amount of viable tissue is pre served. Excision to fascia is limited to large, full-thickness injuries in which the risks of blood loss and potential graft compromise from a suboptimal recipient bed may cause increased mortality. Current research is directed at developing dermal and epidermal substitutes. Cultured epidermal autografts may be grown from uninjured skin samples ob tained after injury. This process takes several weeks and to date has produced grafts that are flawed by easy shear loss and relatively poor take. A collagen-based artificial dermis has been developed and marketed that may be used with ultrathin (.0003-inchthickness) skin grafts.
I
Resuscitation Formulas and Their Calculation PARKLAND First 24 hours: 4 ml/kg/% TBSA burn lactated Ringer’s solution; give 50% total volume during the first 8 hours after burn and the remaining 50% during the subsequent 16 hours Thereafter: 5% dextrose in water, K+, plasma to maintain normal serum sodium and potassium levels and colloid oncotic pressure BROOKE First 24 hours: 2 ml/kg/% TBSA burn lactated Ringer’s solution; during the first 8 hours after burn and the remaining 50% during Thereafter: Maintain urine output 0.5 to 1 .O ml/kg/hr SHRINE
First 24 hours: 5000 ml/m2 TBSA burn plus 2000 ml/m2 body surface area lactated Ringer’s solution; give 50% total volume during the first 8 hours after burn and the remaining 50% during the subsequent 16 hours Thereafter: 3750 ml/m2 TBSA burn plus 1500 ml/m2 body surface area; may replace intravenous fluid with enteral feedings if gastrointestinal function is normal
and vasoactive amines. PGE2 and PG12 cause arterial dilation in burned tissue with increased blood and hydrostatic pressure favoring edema formation. In addition, serotonin is released by platelet aggregation and serves to amplify the vasoconstrictive effect of norepinephrine and angiotensin II. Proteolytic cascades, including coagulation, fibrinolysis, complement, and the kinm family, have been Burn Shock Resuscitation found in activated states after burn Burn shock has both hypovolemic and trauma. The end result of these changes is disruption of normal capillary barriers cellular components. Current understanding of mediator cascadesand resus- between interstitial and intravascular comcitation strategies is based on fundamen- partments with rapid equilibration betal observations of patients and animals tween them. Plasmavolume loss, manifest after burn injury. The variety of resuscita- as hypovolemia, coincideswith edema fortion approaches available suggests the mation and increased extracellular fluid. value of careful observation and adjustBaxter described the cellular changes ment of any treatment plan based on pa- that provide the foundation of current re suscitation strategies. He noticed a detient clinical response (Table 3). Increased capillary permeability is one crease in cell membrane potential involvof the key components of the bum shock ing burned and unburned tissues. This response. In small bums, maximal edema potential change is associated with inis seen in as few as 8 to 12 hours after in- creased intracellular sodium probably a jury, whereas larger burns manifest result of a fall in sodium ATPase activity. edema at 12 to 24 hours. The initial medi- Resuscitation only partly restores normal ators of vascular effects seen after bum intracellular sodium and membrane potentials. Inadequate resuscitation leads to injury are histamine and bradykinin. Histamine release from mast cells in skin further decline in cell membrane potential is seen early after injury but appears to be and cell death. Later work on bum shock transient. The chief site of histamine ac- concluded this phenomenon is a result tion appears to be the venules. Blocker not only of intravascular hypovolemia but studies suggest that histamine explains also extracellular sodium depletion. only part of early changes in bum wound Global hemodynamic changes include a fall in extracellular fluid of as much as vascular permeability. Other mediators for vascular changes 30%to 50%in unresuscitated animal modin burns include complement, pros- els by 18 hours after being burned. taglandins, leukotrienes, stress hormones, Cardiac output falls to 25%of control at 4 84
give 50% total volume the subsequent 16 hours
hours after injury and rises to only 40%of control at 18 hours after a 30%TBSA injury. The principal site of volume loss driving some of these changes is the functional extracellular intravascular fluid space. Subsequent studies with salt solutions confirmed a variety of approaches to minimize extracellular fluid loss and maximize hemodynamic response in the first 24 hours after the burn occurs. During the first 24 hours, Baxter’s work showed that plasma volume changes were independent of the fluid type used. Thus colloids should not be used in the first 24 hours of bum resuscitation. After 24 hours, infused colloids may increase plasma volume by anticipated amounts as capillary integrity is restored. Peripheral vascular resistance actually may be very high in the initial 24 hours after a bum injury but falls as cardiac output improves to supranormal levels coincident with the end of plasma and blood volume losses. Bum wound edema is caused by dilation of precapillary arterioles and increased extravascular osmotic activity as a result of various products of thermal injury, some of which have been described above. All elements in the vascular space except red blood cells may escape from this site during this initial period of increased vascular permeability. In bum injury, intracellular and interstitial volume increase at the expense of plasma and blood volume. Edema formation is affected by fluid administration during resuscitation. Thus two principles are agreed on: first, the least amount of fluid
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should be given that is necessaryto maintain adequate organ perfusion as determined by vital signs, urine output, or other function studies; and second, lost extracellular salt is replaced in cells and burned tissue with crystalloids (and lactated Ringer’s solution in particular), the most popular solutions. A common resus citation approach uses a modified Parkland formula giving 4 ml/kg/% TBSA bum of fluid (Iactated Ringer’s); half the 24-hour volume required is given in the first 8 hours. Several other formulas have been described that represent guidelines for initiating resuscitation. Continuing this process requires perfusion as indicated by a urine output of 30 to 50 ml/hr in the adult. Hypoproteinemia and edema formation complicate the use of isotonic crystalloids for resuscitation. Hypertonic resuscitation solutions have the theoretical advantages of improved hemodynamic response and diminished overall fluid needs as intracellular water is shifted into the extracellular space by these hyperosmolar solutions. Nonetheless, a clear role for hypertonic resuscitation after bum injury has not been defined yet. Some groups add colloid to resuscitation fluids as protein formulations or dextran after the first 8 hours when much of the capillary leak has subsided. Patients most likely to benefit from supplemental colloid are the elderly, those with large bums (>50%TBSA), and/or patients suffering from inhalation injury, which may increase the overall fluid requirement of the burned patient from both volume and total salt requirement standpoints. Overall, patients in good health with bums less than 10%TBSA frequently can be resuscitated with crystalloids alone. In cases when coexistent injury, comorbid conditions, limited cardiac reserve, and inhalation injury complicate burn trauma, a combination of crystalloid and colloids may be optimally used. In general, the resuscitation target is 30 to 50 ml of urine output per hour with acceptable vital signs. In the patient with complications, a pulmonary artery catheter may be needed. Patients begun on crystalloid resuscitation protocols frequently will require supplemental colloid during the second 24 hours after bum injury. Maintenance fluids also must allow for evaporative Air Medical
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losses and may come from intravenous repletion or enteral feeding. Evaporative losses may be estimated at (25 + %TBSA burn) x TBSA (in m”) x 24 hours. Potassium, calcium, magnesium, and phosphorous losses also should be monitored carefully and these electrolytes aggressively replaced. In general, after 24 to 48 hours, a urine output of 30 to 50 ml/hr may be an inadequate guide to perfusion. This is because of relative osmotic diuresis with the metabolite loss of burns and deranged ADH metabolism. Adults require 1500 to 2000 ml/24 hours of urine output to excrete the osmolar products of large burns. Serum sodium concentration, weight change, intake and output records, and physical examination may guide ongoing fluid administration.
turn. Chest x-ray films frequently are normal on admission, and hypoxia on blood gasses frequently is not appreciated. Chemical injury to the lung stimulates the release of substances including histamine, serotonin, and kallikreins with recruitment of leukocytes to airways and lung parenchyma. Edema of airway mucosa and sloughing can combine with the formation of plugs of fibrin and purulent material to create casts that obstruct small airways. Neutrophils and other activated intlammatory cells also may release oxygen radicals and lytic enzymes that magnify tissue change. Pulmonary edema also is seen as a result of increased capillary permeability magnitied by cutaneous bums if present. Patients with cutaneous injury alone do not experience increased extravascularlung water. Inhalation Injury Three stages of clinical inhalation inInhalation injury has emerged as a per- jury have been identitled. Acute hypoxia sisting cause of increased mortality in with asphyxia typically occurs at the bum victims. Upper airway injury is fre- scene of the fire itself, sometimes in asso quently a result of direct heat exposure, ciation with high CO exposure, and is folwhereas laryngeal reflexes protect the lowed by acute upper airway and pullung from thermal injury in all cases ex- monary edema. Pulmonary edema with cept possibly high-pressure steam expo- acute airway swelling usually resolves sure. The upper airways are an ex- within several days after injury. Later tremely efficient heat sink. Lower airway complications are infectious, with the injury (below the larynx) is predomimorbidity of pneumonia complicating nantly a result of chemical products of that of inhalation exposure to heat and combustion carried on soot particles to chemical irritants. the lung (typical particle size is 5 pm). Inhalation injury treatment is largely Aldehydes, oxides of sulfur and hy- supportive. In any situation in which indrochloric acid, may combine with water halation injury with coexposure is possiin the lung to yield corrosive acids and ble, 100% oxygen should be provided. oxygen free radicals. Polyvinyl chloride Signs of airway loss require intubation degradation, for example, yields up to 75 with mechanical ventilation. The role of toxic compounds. Carbon monoxide early tracheostomy in these patients is (CO) exposure also is associated with in- debated; some data link this procedure halation injury but does not define this with improved outcome. Resuscitation process because the true degree of expo should not be delayed or withheld in pasure to CO frequently is not detected. tients with inhalation injury. In fact, these The half-life of CO in association with he individuals may require additional fluid moglobin in room air is 4 hours; at 100% as already noted. oxygen, the half lie of CO is only 30 minHumidification of all gases helps conutes. Elevated carboxyhemoglobin lev- trol secretions and reduces desiccation els, thus, often are not found. injury. The role of early hyperbaric oxyThe diagnosis of inhalation injury gen is minimized in the bum care commost commonly is made with bronmunity for CO intoxication but remains choscopy revealing airway edema, ery- popular among pulmonologists. thema, soot accumulation, and some- Unfortunately, prospective, randomized times mucosal sloughing. This test picks clinical data are not available to establish up far more injuries than standard clini- the value of hyperbaric oxygen therapy. cal criteria, including history of closed- Heparin nebulization currently also is space bum injury, facial bums with nasal used during the initial days after inhalasinging, wheezing, and soot in the spu- tion injury because of presumed mu-
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colytic and antiinflammatory effects. Heparin nebulization may stimulate expectoration of large amounts of accumulated proteinaceous material. Electrical
Lightning
Injury/Lightning
Electrical injury is described as a syndrome rather than a discreet clinical entity because of the various ways this problem may present. In general, when the patient is exposed to an electrical source with fewer than 1000 volts, it is considered a low-voltage injury, which will result in patient response similar to that seen in other cutaneous injuries de scribed above. When exposure exceeds 1000 volts, the potential for massive deep and cutaneous injury exists. Two models for electrical injury have been proposed. One model suggests differential tissue resistance with varied energy distribution (heat) to explain patchy soft tissue loss beneath normal skin. In this model, nerves are the best conductors, followed by the vascular system, muscle, tendon, fat, and bone. The second model views injured tissue in electrocution as uniformly involved with current and differential tissue loss of heat as the explanation for patchy deep loss of muscle, which frequently is seen. Electrical injury may cause cell wall disruption with complement activation and release for arachidonic acid metabolites, particularly thromboxane. Local thromboxane AZ blockade has been associated with increased soft tissue salvage in burn models. Three types of injury to the skin can occur with electrocution. Patients will suffer characteristic entrance and exit skin wounds. Typically, these are circumscribed deep lesions, occurring at points of contact with the electrical source or ground on the hands and feet. Cutaneous burns similar to those seen with fire may be caused by arc injury to adjacent body parts. Finally, clothing ignition also may create a standard pattern of injury seen with flame exposure. Beware of pneumothorax, airway loss, cardiac arrest, and blunt injury as a result of falls and violent muscle contraction. Muscle compartment pressures may increase necessitating fasciotomy, not just escharotomy. Check the ECG for rhythm or ischemic changes and the urine for pigment deposits. If they are present in 86
Lightning versus Technical Electricity
Exposure Current Shock wave Flashover Cardiac Burns Renal failure Fasciotomy/amputation
Technical
Brief 3000-200,000 A (DC) Present Present Asystole Superficial Rare Rare
urine, alkali&e the urine and push output to 70 to 100 ml/hr until pigment is no longer seen. Patients may have ileus after electrocution. A normal ECG on presentation with no cardiac events suggests no problem of this kind will occur. The initial priority in managing electrocution is removing necrotic tissue and decompressing deep tissue compartments, particularly muscle. Resuscitation is begun at 4 ml/kg/% TBSA cutaneous injury and titrated to maintain urine output of 0.5 to 1 ml/kg unless pigments are present in the urine and higher urine output is therefore desirable. Use topical antimicrobials as in other burn types. Where large areas of soft tissue injury exist, these should be debrided and closed as rapidly as possible during the course of hospitalization to minimize infection risks. Infection is the chief risk in electrical injury as in other burn types. Other problems that may be anticipated after electrocution are myocardial and vascular injury, encephalopathy, cataract, and gut perforation. In general, fractures should be stabilized after treatment of overlying soft tissue. Lightning injury may be thought of as massive exposure to direct current. Most injury is topical because of extremely brief exposure times; a characteristic pattern of injury frequently is seen. Mortality associated with lightning relates to early cardiac and pulmonary arrest. Aggressive basic and advanced lie support may be a lifesaving measure in these patients. At least 80% of patients who are victims of lightning incidents are estimated to be long-term survivors. Artificial and natural electricity may be compared using various parameters shown in Table 4.
Chemical
Electricity
Prolonged lo-10,000 A (AC) Absent Uncommon Fibrillation Deep Common Common
Injury
Many types of chemicals may be encountered; acids (cleaning products, industrial applications), alkalis (hydroxides of sodium, potassium, and sodas of ammo nia), and organic compounds (petroleum products) are most common. Injury severity relates to the agent involved, the concentration of the agent that comes in contact with the patient, and the duration of contact. Initial care involves immediate removal of the patient from the source of chemical injury. In general, removing the patient’s clothing is essential. In most cases,wounds then must be copiously irrigated with water to dilute the toxin. Two specific cases of chemical injury are noteworthy, Contact with petroleum products is associated with rapid skin penetration and late multiple organ failure involving lungs and hepatic and renal functions. Patients may be exposed to pe troleum from spilled gasoline at a motor vehicle crash scene. Rapid removal of the patient from the petroleum source and vigorous irrigation with supportive care are warranted. Hydrofluoric acid is the most tissue-reactive inorganic acid commonly available and is used in many industrial applications, including the semiconductor industry. This acid binds calcium to form salts and may be treated with topical, intravenous, or intraarterial calcium injection to neutralize toxic effects. These procedures, however, are associated with the risk of significant complications and should be performed in referral centers only. Cold Injury/Frostbite
A variety of changes are described in soft tissue injury resulting from cold exposure. Chilling with plasma leakage and
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vasospasticity occurs at 3” to 10” C with loss of sensation appreciated at 10” C. When skin cools to -4” C, freezing occurs. After freezing, tissue becomes poikilothermic; endothelium, marrow, and nerves are more sensitive than muscle. Vascular stasis with hypothermia contributes to coagulation, shunting, and plasma loss. Prolonged exposure and end-stage response to significant cold injury is ischemia with gangrene and arteriovenous shunting. Type and duration of contact are key factors. In the presence of moist skin, significant windchill, and metal contact, the adverse effects of cold exposure will be magnified. A general approach to treatment of patients with cold injury includes gentle rewarming in water heated to 40” to 42” C without massage but with spontaneous movement as possible. Blisters should be debrided. Injured extremities should be elevated and splinted. Apply topical antimicrobials to open wounds. Edema may appear within hours of rewarming and last for many days. An eschar develops within 9 to 15 days with early deep injury; later demarcation may not occur for as many as 3 to 6 weeks
when surgery may be needed to remove lost tissue. Late changes that may be anticipated include autonomic dysfunction, sensory changes, temperature sensitivity, and hyperhidrosis. The Time Line A characteristic response may be anticipated in the setting of most thermal injury. The initial phase corresponds to resuscitation during the first 36 hours after injury. Airway and pulmonary support at this time entail recognition and response to early compromise of the airway with identification of the nature and degree of injury present. Cardiovascular support bolsters losses associated with increased capillary permeability and early depression of cardiac function until the patient shifts into the later hyperdynamic response to burn injury. Wound care begins with assessment, topical antimicrobials, and debridement with escharotomy if urgently needed. During the postresuscitation phase 2 to 5 days after injury, airway care focuses on continued support of ventilation, oxygenation, and airway patency as fluid begins to shift back into the vascular com-
partment. Cardiac function improves during this time and begins the transition to the hyperdynamic response, which may persist for weeks after major bum injury. Fluids must be given in the face of increasing evaporative wound losses. At this time, local wound care gives way to surgical excision and grafting. Optimally, operative procedures begin here before later inflammatory and infectious complications arise. The third stage is one of chronic inflammation complicated by infection, which may last for weeks after major bum injury. A hyperdynamic cardiovascular state exists in which sepsisand normal patient response are difficult to distinguish. Pulmonary, burn wound, and device infections are significant risks; topical therapy with antimicrobials may be altered to compensate for changing pathogens noted in the burn wound. Enteral nutrition support, good cardiovascular reserve, and judicious management with careful wound surveillance, including biopsies to detect infection, are essential to recovery.
Bibliography Andrew CJ, Cooper MA, Daneviza M, Mackerass D, editors. Lightning injuries: electrical, medical, and legal aspects. Boca Raton (FL): CRC Press; 1992. This is the only recent book on lightning injuries of which I am aware. Much of the recent work in this area is summarized by an internationalgroup
ofauthon.
Cherrington M, Cooper MA, editors. Lightning and electrical injuries, parts I and II. Semin Neurol 1995;15(3,4):227-404. These are two recent issues born the Seminars in Neurology series devoted totally to lightning and electrical injuries. Again, Mze editors and authors represent leaders in research related to these problems. This is an excellent resource for anyone treating these patients.
p. 31527. Although slightly older than some of the other references, this is an excellent overview of the burn problem from the highly successful Current Therapy reference series. Goodwin MA. Barrie care.
36. This is another excellent discussion of burn resuscitation and provides a view complementary to Nzat offered in Total Bum Care.
is part of the Trauma Management Series akd has an excellent overview of the physiologic problems associated with burn injury and a temporal stepwise approach to their management.
Desai MH, Herndon DN. Burns. In: Lewis FR, Trunkey DD, editors. Current therapy of trauma. 3rd ed. Philadelphia: BC Decker; 1991. Air Medical
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summarized. Monafo WW. Initial management of bums. N Engl J Med 1996;335:1581-6. This is the most recent overview
on acute burn
management from The The author is
New England Journal of Medicine. a long-established
authority.
Pruitt BA, Goodwin CW, Cioff WG. Thermal injuries. In: Davis JH, Sheldon GF, editors. Surgery: a problem-solving approach. 2nd ed. St. Louis: Mosby; 1995. p. 642-720. This is an
This is a summaq of recent thinking and management approaches in the patient sustaining electrical injaw. It is part of a major recent text on surgical critical care.
overview of the thermal injuv problem from the perspective of the Army Institute of Surgical Research at Fort Sam Houston, Texas. This group has been widely regarded as the leader in burn care for both this country and the world.
today and is
Demling RH, LaLorde C. Bum trauma. New York: Thieme Medical Publishers; 1989. This volume
halation injury written in a monograph with other issues in trauma and resuscitation. Much of the recent thinking about Nzis specific problem is
Grube BJ, Heimbach DM. The pathophysiolagy and management of electrical injury. In: Barrie PS, Shires GT, editors. Surgical intensive care. Boston: Little, Brown, & Co; 1993. p. 115572.
Deitch EA. The management of burns. N Engl J Med 1990;323:1249-53. This recent overview on burn management remains pertinent concise and easily read.
CW, Finkelstein JL, Madden MR, Marano Resuscitation of the burned patient. In: PS, Shies GT, editors. Surgical intensive Boston: Little, Brown, & Co; 1993. p. 1125
the new millennium. Austin (TX): RG Landis; 1992. p. 44-63. This is a recent overview on in-
Heimback DM, Engrav LA, editors. Surgical management of the bum wound. New York: Raven Press; 1984. This is an excellent atlas describing an approach to management of the burn wound. Illustrations provide good visual evidence of the types of bum injuy and surgical approaches.
Miles RH, Dries DJ, Gamelli RL. Inhalation injury: pathophysiology and treatment. In: Dries DJ, Gamelli RL, editors. Trauma 2000: strategies for
1997
Pruitt BA, graphic, jury. In: London:
Mason AD. Epidemiological, demoand outcome characteristics of bum inTotal bum care. Herndon DN, editor. Saunders; 1996. p, 515. This is a good
overview of the epidemiological the burn problem.
Sheridan RL, Tompkins LJ, editor. Surgery:
characteristics
of
RG. Bums. In: Greenfield scientific principles and
87
practice. 2nd ed. Philadelphia: Lippincott-Raven; 1997. p. 422-38. This is another overview on burn management from the Shriner’s Hospital in Boston. Again many things will be consistent with previous references. This is one source that could be read to obtain in one sitting an overview of the burn problem.
‘Iibbles PM, Edelsberg JS. Hyperbaric oxygen therapy. N Engl J Med 1996;334:1642-8. This article summarizes recent thinking regarding the role of hyperbaric oxygen therapy in a variety of disorders. Although its use in some forms of acute ther-
88
ma1 injuy resuscitation is advocated, the data on which this recommendation is based are not the results of randomized, prospective, multicenter work and thus are not widely accepted in the burn care community.
Williams WG, Phillips IG. Pathophysiology of the burn wound. In: Herndon DN, editor. Total bum care. London: Saunders; 1996. p. 63-70. This chapter provides a recent review from a
Warden GD. Fluid resuscitation and early management. In: Herndon DN, editor. Total bum care. London: Saunders; 1996. p. 53-60. An excellent overvie; is provided of fluid resuscitation and permeability changes after burn i&y. In particular, Baxter’s work is placed in context of current resuscitation strategies.
July-September
major center regarding pathologic changes occurring in the burn wound. Total Bum Care is the most recent comprehensive textbook on bum care, currently is a leading reference in this area, and includes a discussion of common forms of thermal injuly, including electrocution.
1997
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Thermal Injury David J. Dries, MSE, MD, FACS, FCCP, FCCM’
1, Loyola Lifestar, Loyola University Center, Maywood, IL
Medical
Address for correspondence and reprints: David J. Dries, MSE, MD, Loyola University Medical Center, Burn & Shock Trauma Institute, 2160 S. First Ave., Bldg. 100, Room 4233, Maywood, IL 60153 Copyright Associates
0 1997
1067-991
X/97/$5.00
Reprint
by the Air Medical
EDITOR’S NOTE: The author provides an
overview of bum care based on 15 years of practice in the field. Although not formally referenced, the paper includes an annotated bibliography offering access to key references pertinent to recent bum care.
Journal
Epidemiology
no. 74/l/831
Air Medical
Journal
Burns are a significant public health problem in the United States.The magnitude of this problem is reflected in data reported by each state to the National Center for Injury Prevention and Control. Burn deaths totaled more than 5000 in the United States and ranged from 4 in Hawaii and 8 in Vermont to 337 in California and 359 in Texas during 1991. Age-adjusted rate of fire and bum deaths excluding patients of unknown age ranged from 0.164 per 100,000 population in Colorado to 3.75 per 100,000 pop ulation in Mississippi. Deaths occur with greatest frequency in residential fires, particularly in multifamily dwellings and low-income census tracts. Four of five unintentional deaths and three of four deaths as a result of bums from fire result from house fires. Approximately 12 individuals die in residential fires each day; young children and the elderly are the most likely victims. Overall, an estimated 2 to 2.5 million people seek treatment for burns in the United States each year; 100,000 to 150,000 are hospitalized. Like other forms of injury, bums tend to be a disease of the young. Thirty-eight percent of victims are younger than 15 years old, a second group of similar size (31%) is in the 15- to 44-year-old range, 24%
+ 0 66
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1997
are between 44 and 64 years old, and 7% are 65 or older. Scalds are the most common form of childhood injury, whereas electrical and chemical injuries affect adults in the workplace. Factors that have been shown to relate to bum mortality include size of cutaneous injury, patient age, and the presence or absence of inhalation injury. The Burn Wound
Skin characteristics affect patterns of cutaneous injury. Skin is very thin in infants and increases in thickness until 30 to 40 years of age, after which it progressively thins. Men tend to have thicker skin than women. Average skin thickness is 1 to 2 mm. In general, dermis is 10 times thicker than associatedepidermis. A variety of cell types make up the epidermis. The predominant cell type is the keratinocyte, which provides the superficial layering effect seen on visualization of the skin. Melanocytes provide pigment generation against ultraviolet radiation. Iangerhans cells have a cutaneous immune function; Merkel cells serve as mechanoreceptors in the epidermis. Cell layers in the epidermis include the basal layers with the stratum germinativum, a site for superficial cell mitosis, and the stratum spinosum, where protein synthesis occurs. The stratum granulosum is the site of keratin production and the locus for formation of the stratum corneum. This latter stratum contains the layers of dead cells seen on superficial examination of the skin. The cell types and layers in the epidermis take their origin in the ectoderm. The dermis is derived from the meso81
derm. The dominant cell type is the fibroblast, which produces collagen, elastin, and ground substance of glycosaminoglycans and proteoglycans. Plasticity of the dermis associated with PATIENT ICIYOLA collagen remodeling allows the skin to reSKIN ASSESSMENT main intact under varying types of stress. The dermis consists of two layers: a superficial papillary dermis and a thicker reticular dermis. The dermoepidermal junction contains fibrinectin and mucopolysaccharides.Hemidesmosomes anchor the cells of the basal epidermal layer INDETERMINANT to the basement membrane, which divides epidermis and dermis. FULL THICKNESS When thermal injury occurs, a variety of skin functions are lost. Most important is the protective barrier against infection DONOR AREA and other environmental stimuli. The skin also provides an immunologic barrier and serves as an antigen presenting pi1 GRAFT AREA the source for immune cells. Sebum pro duced by skin glands has been noted to have antibacterial properties. Other skin functions include fluid protection, protein and electrolyte hemostasis, neurosensory stimuli processing, and vitamin D production as a metabolic activity. In thermal injury, injurious effects of heat are a function of the temperature of the heat source and the duration of skin exposure. At 40” to 44” C, enzymatic failure of the cell occurs with rising intracellular sodium concentration and swelling as a result of failed membrane sodium pumps. At exposure to 45” C, skin necro sis occurs within 1 hour with release of oxygen radicals. Three zones of cutaneous injury have been described: fluid resuscitation, and topical an- creased vascular permeability is related l The zone of coagulation is the site of timicrobial agents. to the release of several vasoactive and irreversible cell death with new esl The zone of hyperemia is characteroxidative products. char formation from local protein degradation. ized by minimal cellular injury but The size of thermal injury is assessed l The zone of stasis is the site of local prominent vasodilation and in- by the well-known rule of nines (Figure circulatory impairment with initial 1). Anatomic criteria also can be used to creased blood flow. Cell recovery cell viability. If ischemia follows in generally occurs in this zone. recognize the depth of injury and coincithis zone, cell death will occur. Vasoactive mediators, including dent likelihood of healing. Partial-thickImpaired circulation is believed to thromboxane A2 with platelet adherence ness injuries should heal within 3 weeks be a result of platelet and neutrophil and vasoconstriction, typically are seen and leave the stratum germinosum intact. aggregates, fibrin deposition, en- in the burn wound. Beyond the vasocon- Third-degree or full-thickness injuries indothelial cell swelling, and loss of stricting effects seen in the zone of stasis, volve all layers of the epidermis and dererythrocyte deformability. These the predominant effect and resuscitation mis. Some authors speak also of fourth-de tissues are susceptible to secondary issue is significant vasodilation and in- gree injuries that involve deep structures, insults, such as dehydration, pres- creased vascular permeability. The initial such as tendon, muscle, and bone. Table 1 sure, overresuscitation, and infec- increase in vascular permeability may be discussesbum depth classification. tion. Measures implemented to min- related to short-term histamine release Local care begins with serial debrideimize further tissue loss include occurring soon after injury. The second ment of nonviable tissue and blisters. nondesiccating dressings, careful longer period of vasodilation and in- Topical antimicrobials, one of the major 82
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Classification Degree
Depth of tissue penetration
of burn
First
Superficial
Deep
Third
partial
partial
Injury to the superficial epidermis, usually caused or brief heat flashes. Classically can be described
thickness
Injury has destroyed both the epidermis and the dermis. Wound appears white, will not blanch, and is anesthetic. Tough, nonelastic, and tenacious coagulated protein (eschar) tissue may be present on the surface. This wound will not heal without surgical intervention.
Antimicrobial
Agents
Advantages
Disadvantages
Silver sulfadiazine
Painless application Broad spectrum Easy application Rare sensitivities
May produce transient leukopenia Minimal penetration of eschar Some gram-negative species resistant
Mafenide acetate
Broad spectrum Easy application Penetrates eschar
Painful application Promotes acid-base Frequent sensitivities
Bacitracin, Polysporin
Painless application Nonirritating Transparent May be used on nonburn wounds
No eschar
Silver (0.5%
Painless application Broad spectrum Rare sensitivity
No eschar penetration Electrolyte imbalances Discolors wound and environment Must be kept moist
Povidoneiodine
Broad
Painful application Systemically absorbed Requires frequent reapplication Discolors wounds
Gentamicin
Painless application Broad spectrum
spectrum
advances in bum wound care, are applied twice daily after washes with antiseptic solutions. These topical antimicrobials are applied in moist dressings that also help maintain fluid balance. The burn wound affords a warm, moist, proteinladen growth medium to gram-positive and later gram-negative bacteria. Treatment for these organisms centers on good local care and topical antimicrobials (Table 2). In general systemic antibiotics are not used. Biologic dressings are used when relMedical
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to sunlight
Injury is through the epidermis and may affect isolated areas of the deep dermal strata from which cells arise. This wound may appear red and wet or white and dry, depending on extent of deep dermal damage. It heals without grafting but requires > 3 weeks with suboptimal cosmesis. Excision and splitthickness skin grafting are recommended.
Agent
nitrate solution)
by overexposure as a sunburn.
Injury is to epidermis and upper layers of the dermis. Wounds characteristically appear red, wet, or blistered, blanchable, and extremely painful. Will heal within 3 weeks from epidermal regeneration from remaining remnants found in the tracts of hair follicles.
thickness
Full thickness
Topical
Air
Characteristics
Partial thickness
Second
of Burn Depth
imbalance
penetration
Oto/nephrotoxic Encourages development resistant organisms
of
atively clean wounds are present to reduce pain, decrease bacterial colony counts, and control fluid and protein losses.The rate of reepithelialiiation has been shown to be increased by applying biologic dressings. Epithelialiiation is increased with biologic dressings over topical antimicrobials, which tend to cause relative inhibition of wound epithelialization. Biologic dressings sometimes are placed on newly debrided partial-thickness burns in anticipation of healing without surgery. Biologic dressings also 1997
may be used to cover granulating excised wounds awaiting skin grafts. Early adherence of biologic dressings may indicate readiness of a wound bed for permanent skin grafting. Finally, biologic dressings may facilitate removal of necrotic tissue from granulating wounds. When circumferential extremity injury with second- or third-degree depth exists, the bum wound may need to be divided at lateral aspects of extremities or on the torso to facilitate extremity perfusion or chest wall movement, respectively. Division of wound eschar for this purpose is termed escharotomy. Usually the need for escharotomy is clear within 48 hours of injury. Progressive tissue edema during resuscitation creates the need for escharotomy even if initial perfusion of distal extremities or chest wall movement in circumferential torso bums appears to be adequate. Abdominal wall escharotomy or laparotomy for abdominal compartment syndrome with respiratory embarrassment sometimes is required. Excision of burned tissue that clearly will not heal (clinical assessment) generally is performed within 3 to 5 days of injury. Not more than 20% total body surface area (IBSA) is excised at a time. If possible, wounds are covered with sheet or meshed autograft, harvested .0003- to .OOl@inchthickness from unburned sites. Good sites for donor skin are the thighs, back, and scalp. Grafts can be meshed to increase surface area covered with the assumption the wound will reepithelialize within the mesh network. Generally meshing greater than 1:3 is not used be83
cause of increased incidence of contractures and graft shear. If donor skin is unavailable, cadaveric allograft can be used as a temporary cover of excised areas after burned tissuesare removed. In general, sequential tangential excision of burned tissue is used to the level of viable recipient beds as assessed by visible punctate bleeding. Although blood loss is greater with this method, cosmetic outcome is improved, and the maximum amount of viable tissue is pre served. Excision to fascia is limited to large, full-thickness injuries in which the risks of blood loss and potential graft compromise from a suboptimal recipient bed may cause increased mortality. Current research is directed at developing dermal and epidermal substitutes. Cultured epidermal autografts may be grown from uninjured skin samples ob tained after injury. This process takes several weeks and to date has produced grafts that are flawed by easy shear loss and relatively poor take. A collagen-based artificial dermis has been developed and marketed that may be used with ultrathin (.0003-inchthickness) skin grafts.
I
Resuscitation Formulas and Their Calculation PARKLAND First 24 hours: 4 ml/kg/% TBSA burn lactated Ringer’s solution; give 50% total volume during the first 8 hours after burn and the remaining 50% during the subsequent 16 hours Thereafter: 5% dextrose in water, K+, plasma to maintain normal serum sodium and potassium levels and colloid oncotic pressure BROOKE First 24 hours: 2 ml/kg/% TBSA burn lactated Ringer’s solution; during the first 8 hours after burn and the remaining 50% during Thereafter: Maintain urine output 0.5 to 1 .O ml/kg/hr SHRINE
First 24 hours: 5000 ml/m2 TBSA burn plus 2000 ml/m2 body surface area lactated Ringer’s solution; give 50% total volume during the first 8 hours after burn and the remaining 50% during the subsequent 16 hours Thereafter: 3750 ml/m2 TBSA burn plus 1500 ml/m2 body surface area; may replace intravenous fluid with enteral feedings if gastrointestinal function is normal
and vasoactive amines. PGE2 and PG12 cause arterial dilation in burned tissue with increased blood and hydrostatic pressure favoring edema formation. In addition, serotonin is released by platelet aggregation and serves to amplify the vasoconstrictive effect of norepinephrine and angiotensin II. Proteolytic cascades, including coagulation, fibrinolysis, complement, and the kinm family, have been Burn Shock Resuscitation found in activated states after burn Burn shock has both hypovolemic and trauma. The end result of these changes is disruption of normal capillary barriers cellular components. Current understanding of mediator cascadesand resus- between interstitial and intravascular comcitation strategies is based on fundamen- partments with rapid equilibration betal observations of patients and animals tween them. Plasmavolume loss, manifest after burn injury. The variety of resuscita- as hypovolemia, coincideswith edema fortion approaches available suggests the mation and increased extracellular fluid. value of careful observation and adjustBaxter described the cellular changes ment of any treatment plan based on pa- that provide the foundation of current re suscitation strategies. He noticed a detient clinical response (Table 3). Increased capillary permeability is one crease in cell membrane potential involvof the key components of the bum shock ing burned and unburned tissues. This response. In small bums, maximal edema potential change is associated with inis seen in as few as 8 to 12 hours after in- creased intracellular sodium probably a jury, whereas larger burns manifest result of a fall in sodium ATPase activity. edema at 12 to 24 hours. The initial medi- Resuscitation only partly restores normal ators of vascular effects seen after bum intracellular sodium and membrane potentials. Inadequate resuscitation leads to injury are histamine and bradykinin. Histamine release from mast cells in skin further decline in cell membrane potential is seen early after injury but appears to be and cell death. Later work on bum shock transient. The chief site of histamine ac- concluded this phenomenon is a result tion appears to be the venules. Blocker not only of intravascular hypovolemia but studies suggest that histamine explains also extracellular sodium depletion. only part of early changes in bum wound Global hemodynamic changes include a fall in extracellular fluid of as much as vascular permeability. Other mediators for vascular changes 30%to 50%in unresuscitated animal modin burns include complement, pros- els by 18 hours after being burned. taglandins, leukotrienes, stress hormones, Cardiac output falls to 25%of control at 4 84
give 50% total volume the subsequent 16 hours
hours after injury and rises to only 40%of control at 18 hours after a 30%TBSA injury. The principal site of volume loss driving some of these changes is the functional extracellular intravascular fluid space. Subsequent studies with salt solutions confirmed a variety of approaches to minimize extracellular fluid loss and maximize hemodynamic response in the first 24 hours after the burn occurs. During the first 24 hours, Baxter’s work showed that plasma volume changes were independent of the fluid type used. Thus colloids should not be used in the first 24 hours of bum resuscitation. After 24 hours, infused colloids may increase plasma volume by anticipated amounts as capillary integrity is restored. Peripheral vascular resistance actually may be very high in the initial 24 hours after a bum injury but falls as cardiac output improves to supranormal levels coincident with the end of plasma and blood volume losses. Bum wound edema is caused by dilation of precapillary arterioles and increased extravascular osmotic activity as a result of various products of thermal injury, some of which have been described above. All elements in the vascular space except red blood cells may escape from this site during this initial period of increased vascular permeability. In bum injury, intracellular and interstitial volume increase at the expense of plasma and blood volume. Edema formation is affected by fluid administration during resuscitation. Thus two principles are agreed on: first, the least amount of fluid
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should be given that is necessaryto maintain adequate organ perfusion as determined by vital signs, urine output, or other function studies; and second, lost extracellular salt is replaced in cells and burned tissue with crystalloids (and lactated Ringer’s solution in particular), the most popular solutions. A common resus citation approach uses a modified Parkland formula giving 4 ml/kg/% TBSA bum of fluid (Iactated Ringer’s); half the 24-hour volume required is given in the first 8 hours. Several other formulas have been described that represent guidelines for initiating resuscitation. Continuing this process requires perfusion as indicated by a urine output of 30 to 50 ml/hr in the adult. Hypoproteinemia and edema formation complicate the use of isotonic crystalloids for resuscitation. Hypertonic resuscitation solutions have the theoretical advantages of improved hemodynamic response and diminished overall fluid needs as intracellular water is shifted into the extracellular space by these hyperosmolar solutions. Nonetheless, a clear role for hypertonic resuscitation after bum injury has not been defined yet. Some groups add colloid to resuscitation fluids as protein formulations or dextran after the first 8 hours when much of the capillary leak has subsided. Patients most likely to benefit from supplemental colloid are the elderly, those with large bums (>50%TBSA), and/or patients suffering from inhalation injury, which may increase the overall fluid requirement of the burned patient from both volume and total salt requirement standpoints. Overall, patients in good health with bums less than 10%TBSA frequently can be resuscitated with crystalloids alone. In cases when coexistent injury, comorbid conditions, limited cardiac reserve, and inhalation injury complicate burn trauma, a combination of crystalloid and colloids may be optimally used. In general, the resuscitation target is 30 to 50 ml of urine output per hour with acceptable vital signs. In the patient with complications, a pulmonary artery catheter may be needed. Patients begun on crystalloid resuscitation protocols frequently will require supplemental colloid during the second 24 hours after bum injury. Maintenance fluids also must allow for evaporative Air Medical
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losses and may come from intravenous repletion or enteral feeding. Evaporative losses may be estimated at (25 + %TBSA burn) x TBSA (in m”) x 24 hours. Potassium, calcium, magnesium, and phosphorous losses also should be monitored carefully and these electrolytes aggressively replaced. In general, after 24 to 48 hours, a urine output of 30 to 50 ml/hr may be an inadequate guide to perfusion. This is because of relative osmotic diuresis with the metabolite loss of burns and deranged ADH metabolism. Adults require 1500 to 2000 ml/24 hours of urine output to excrete the osmolar products of large burns. Serum sodium concentration, weight change, intake and output records, and physical examination may guide ongoing fluid administration.
turn. Chest x-ray films frequently are normal on admission, and hypoxia on blood gasses frequently is not appreciated. Chemical injury to the lung stimulates the release of substances including histamine, serotonin, and kallikreins with recruitment of leukocytes to airways and lung parenchyma. Edema of airway mucosa and sloughing can combine with the formation of plugs of fibrin and purulent material to create casts that obstruct small airways. Neutrophils and other activated intlammatory cells also may release oxygen radicals and lytic enzymes that magnify tissue change. Pulmonary edema also is seen as a result of increased capillary permeability magnitied by cutaneous bums if present. Patients with cutaneous injury alone do not experience increased extravascularlung water. Inhalation Injury Three stages of clinical inhalation inInhalation injury has emerged as a per- jury have been identitled. Acute hypoxia sisting cause of increased mortality in with asphyxia typically occurs at the bum victims. Upper airway injury is fre- scene of the fire itself, sometimes in asso quently a result of direct heat exposure, ciation with high CO exposure, and is folwhereas laryngeal reflexes protect the lowed by acute upper airway and pullung from thermal injury in all cases ex- monary edema. Pulmonary edema with cept possibly high-pressure steam expo- acute airway swelling usually resolves sure. The upper airways are an ex- within several days after injury. Later tremely efficient heat sink. Lower airway complications are infectious, with the injury (below the larynx) is predomimorbidity of pneumonia complicating nantly a result of chemical products of that of inhalation exposure to heat and combustion carried on soot particles to chemical irritants. the lung (typical particle size is 5 pm). Inhalation injury treatment is largely Aldehydes, oxides of sulfur and hy- supportive. In any situation in which indrochloric acid, may combine with water halation injury with coexposure is possiin the lung to yield corrosive acids and ble, 100% oxygen should be provided. oxygen free radicals. Polyvinyl chloride Signs of airway loss require intubation degradation, for example, yields up to 75 with mechanical ventilation. The role of toxic compounds. Carbon monoxide early tracheostomy in these patients is (CO) exposure also is associated with in- debated; some data link this procedure halation injury but does not define this with improved outcome. Resuscitation process because the true degree of expo should not be delayed or withheld in pasure to CO frequently is not detected. tients with inhalation injury. In fact, these The half-life of CO in association with he individuals may require additional fluid moglobin in room air is 4 hours; at 100% as already noted. oxygen, the half lie of CO is only 30 minHumidification of all gases helps conutes. Elevated carboxyhemoglobin lev- trol secretions and reduces desiccation els, thus, often are not found. injury. The role of early hyperbaric oxyThe diagnosis of inhalation injury gen is minimized in the bum care commost commonly is made with bronmunity for CO intoxication but remains choscopy revealing airway edema, ery- popular among pulmonologists. thema, soot accumulation, and some- Unfortunately, prospective, randomized times mucosal sloughing. This test picks clinical data are not available to establish up far more injuries than standard clini- the value of hyperbaric oxygen therapy. cal criteria, including history of closed- Heparin nebulization currently also is space bum injury, facial bums with nasal used during the initial days after inhalasinging, wheezing, and soot in the spu- tion injury because of presumed mu-
1997
85
colytic and antiinflammatory effects. Heparin nebulization may stimulate expectoration of large amounts of accumulated proteinaceous material. Electrical
Lightning
Injury/Lightning
Electrical injury is described as a syndrome rather than a discreet clinical entity because of the various ways this problem may present. In general, when the patient is exposed to an electrical source with fewer than 1000 volts, it is considered a low-voltage injury, which will result in patient response similar to that seen in other cutaneous injuries de scribed above. When exposure exceeds 1000 volts, the potential for massive deep and cutaneous injury exists. Two models for electrical injury have been proposed. One model suggests differential tissue resistance with varied energy distribution (heat) to explain patchy soft tissue loss beneath normal skin. In this model, nerves are the best conductors, followed by the vascular system, muscle, tendon, fat, and bone. The second model views injured tissue in electrocution as uniformly involved with current and differential tissue loss of heat as the explanation for patchy deep loss of muscle, which frequently is seen. Electrical injury may cause cell wall disruption with complement activation and release for arachidonic acid metabolites, particularly thromboxane. Local thromboxane AZ blockade has been associated with increased soft tissue salvage in burn models. Three types of injury to the skin can occur with electrocution. Patients will suffer characteristic entrance and exit skin wounds. Typically, these are circumscribed deep lesions, occurring at points of contact with the electrical source or ground on the hands and feet. Cutaneous burns similar to those seen with fire may be caused by arc injury to adjacent body parts. Finally, clothing ignition also may create a standard pattern of injury seen with flame exposure. Beware of pneumothorax, airway loss, cardiac arrest, and blunt injury as a result of falls and violent muscle contraction. Muscle compartment pressures may increase necessitating fasciotomy, not just escharotomy. Check the ECG for rhythm or ischemic changes and the urine for pigment deposits. If they are present in 86
Lightning versus Technical Electricity
Exposure Current Shock wave Flashover Cardiac Burns Renal failure Fasciotomy/amputation
Technical
Brief 3000-200,000 A (DC) Present Present Asystole Superficial Rare Rare
urine, alkali&e the urine and push output to 70 to 100 ml/hr until pigment is no longer seen. Patients may have ileus after electrocution. A normal ECG on presentation with no cardiac events suggests no problem of this kind will occur. The initial priority in managing electrocution is removing necrotic tissue and decompressing deep tissue compartments, particularly muscle. Resuscitation is begun at 4 ml/kg/% TBSA cutaneous injury and titrated to maintain urine output of 0.5 to 1 ml/kg unless pigments are present in the urine and higher urine output is therefore desirable. Use topical antimicrobials as in other burn types. Where large areas of soft tissue injury exist, these should be debrided and closed as rapidly as possible during the course of hospitalization to minimize infection risks. Infection is the chief risk in electrical injury as in other burn types. Other problems that may be anticipated after electrocution are myocardial and vascular injury, encephalopathy, cataract, and gut perforation. In general, fractures should be stabilized after treatment of overlying soft tissue. Lightning injury may be thought of as massive exposure to direct current. Most injury is topical because of extremely brief exposure times; a characteristic pattern of injury frequently is seen. Mortality associated with lightning relates to early cardiac and pulmonary arrest. Aggressive basic and advanced lie support may be a lifesaving measure in these patients. At least 80% of patients who are victims of lightning incidents are estimated to be long-term survivors. Artificial and natural electricity may be compared using various parameters shown in Table 4.
Chemical
Electricity
Prolonged lo-10,000 A (AC) Absent Uncommon Fibrillation Deep Common Common
Injury
Many types of chemicals may be encountered; acids (cleaning products, industrial applications), alkalis (hydroxides of sodium, potassium, and sodas of ammo nia), and organic compounds (petroleum products) are most common. Injury severity relates to the agent involved, the concentration of the agent that comes in contact with the patient, and the duration of contact. Initial care involves immediate removal of the patient from the source of chemical injury. In general, removing the patient’s clothing is essential. In most cases,wounds then must be copiously irrigated with water to dilute the toxin. Two specific cases of chemical injury are noteworthy, Contact with petroleum products is associated with rapid skin penetration and late multiple organ failure involving lungs and hepatic and renal functions. Patients may be exposed to pe troleum from spilled gasoline at a motor vehicle crash scene. Rapid removal of the patient from the petroleum source and vigorous irrigation with supportive care are warranted. Hydrofluoric acid is the most tissue-reactive inorganic acid commonly available and is used in many industrial applications, including the semiconductor industry. This acid binds calcium to form salts and may be treated with topical, intravenous, or intraarterial calcium injection to neutralize toxic effects. These procedures, however, are associated with the risk of significant complications and should be performed in referral centers only. Cold Injury/Frostbite
A variety of changes are described in soft tissue injury resulting from cold exposure. Chilling with plasma leakage and
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vasospasticity occurs at 3” to 10” C with loss of sensation appreciated at 10” C. When skin cools to -4” C, freezing occurs. After freezing, tissue becomes poikilothermic; endothelium, marrow, and nerves are more sensitive than muscle. Vascular stasis with hypothermia contributes to coagulation, shunting, and plasma loss. Prolonged exposure and end-stage response to significant cold injury is ischemia with gangrene and arteriovenous shunting. Type and duration of contact are key factors. In the presence of moist skin, significant windchill, and metal contact, the adverse effects of cold exposure will be magnified. A general approach to treatment of patients with cold injury includes gentle rewarming in water heated to 40” to 42” C without massage but with spontaneous movement as possible. Blisters should be debrided. Injured extremities should be elevated and splinted. Apply topical antimicrobials to open wounds. Edema may appear within hours of rewarming and last for many days. An eschar develops within 9 to 15 days with early deep injury; later demarcation may not occur for as many as 3 to 6 weeks
when surgery may be needed to remove lost tissue. Late changes that may be anticipated include autonomic dysfunction, sensory changes, temperature sensitivity, and hyperhidrosis. The Time Line A characteristic response may be anticipated in the setting of most thermal injury. The initial phase corresponds to resuscitation during the first 36 hours after injury. Airway and pulmonary support at this time entail recognition and response to early compromise of the airway with identification of the nature and degree of injury present. Cardiovascular support bolsters losses associated with increased capillary permeability and early depression of cardiac function until the patient shifts into the later hyperdynamic response to burn injury. Wound care begins with assessment, topical antimicrobials, and debridement with escharotomy if urgently needed. During the postresuscitation phase 2 to 5 days after injury, airway care focuses on continued support of ventilation, oxygenation, and airway patency as fluid begins to shift back into the vascular com-
partment. Cardiac function improves during this time and begins the transition to the hyperdynamic response, which may persist for weeks after major bum injury. Fluids must be given in the face of increasing evaporative wound losses. At this time, local wound care gives way to surgical excision and grafting. Optimally, operative procedures begin here before later inflammatory and infectious complications arise. The third stage is one of chronic inflammation complicated by infection, which may last for weeks after major bum injury. A hyperdynamic cardiovascular state exists in which sepsisand normal patient response are difficult to distinguish. Pulmonary, burn wound, and device infections are significant risks; topical therapy with antimicrobials may be altered to compensate for changing pathogens noted in the burn wound. Enteral nutrition support, good cardiovascular reserve, and judicious management with careful wound surveillance, including biopsies to detect infection, are essential to recovery.
Bibliography Andrew CJ, Cooper MA, Daneviza M, Mackerass D, editors. Lightning injuries: electrical, medical, and legal aspects. Boca Raton (FL): CRC Press; 1992. This is the only recent book on lightning injuries of which I am aware. Much of the recent work in this area is summarized by an internationalgroup
ofauthon.
Cherrington M, Cooper MA, editors. Lightning and electrical injuries, parts I and II. Semin Neurol 1995;15(3,4):227-404. These are two recent issues born the Seminars in Neurology series devoted totally to lightning and electrical injuries. Again, Mze editors and authors represent leaders in research related to these problems. This is an excellent resource for anyone treating these patients.
p. 31527. Although slightly older than some of the other references, this is an excellent overview of the burn problem from the highly successful Current Therapy reference series. Goodwin MA. Barrie care.
36. This is another excellent discussion of burn resuscitation and provides a view complementary to Nzat offered in Total Bum Care.
is part of the Trauma Management Series akd has an excellent overview of the physiologic problems associated with burn injury and a temporal stepwise approach to their management.
Desai MH, Herndon DN. Burns. In: Lewis FR, Trunkey DD, editors. Current therapy of trauma. 3rd ed. Philadelphia: BC Decker; 1991. Air Medical
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summarized. Monafo WW. Initial management of bums. N Engl J Med 1996;335:1581-6. This is the most recent overview
on acute burn
management from The The author is
New England Journal of Medicine. a long-established
authority.
Pruitt BA, Goodwin CW, Cioff WG. Thermal injuries. In: Davis JH, Sheldon GF, editors. Surgery: a problem-solving approach. 2nd ed. St. Louis: Mosby; 1995. p. 642-720. This is an
This is a summaq of recent thinking and management approaches in the patient sustaining electrical injaw. It is part of a major recent text on surgical critical care.
overview of the thermal injuv problem from the perspective of the Army Institute of Surgical Research at Fort Sam Houston, Texas. This group has been widely regarded as the leader in burn care for both this country and the world.
today and is
Demling RH, LaLorde C. Bum trauma. New York: Thieme Medical Publishers; 1989. This volume
halation injury written in a monograph with other issues in trauma and resuscitation. Much of the recent thinking about Nzis specific problem is
Grube BJ, Heimbach DM. The pathophysiolagy and management of electrical injury. In: Barrie PS, Shires GT, editors. Surgical intensive care. Boston: Little, Brown, & Co; 1993. p. 115572.
Deitch EA. The management of burns. N Engl J Med 1990;323:1249-53. This recent overview on burn management remains pertinent concise and easily read.
CW, Finkelstein JL, Madden MR, Marano Resuscitation of the burned patient. In: PS, Shies GT, editors. Surgical intensive Boston: Little, Brown, & Co; 1993. p. 1125
the new millennium. Austin (TX): RG Landis; 1992. p. 44-63. This is a recent overview on in-
Heimback DM, Engrav LA, editors. Surgical management of the bum wound. New York: Raven Press; 1984. This is an excellent atlas describing an approach to management of the burn wound. Illustrations provide good visual evidence of the types of bum injuy and surgical approaches.
Miles RH, Dries DJ, Gamelli RL. Inhalation injury: pathophysiology and treatment. In: Dries DJ, Gamelli RL, editors. Trauma 2000: strategies for
1997
Pruitt BA, graphic, jury. In: London:
Mason AD. Epidemiological, demoand outcome characteristics of bum inTotal bum care. Herndon DN, editor. Saunders; 1996. p, 515. This is a good
overview of the epidemiological the burn problem.
Sheridan RL, Tompkins LJ, editor. Surgery:
characteristics
of
RG. Bums. In: Greenfield scientific principles and
87
practice. 2nd ed. Philadelphia: Lippincott-Raven; 1997. p. 422-38. This is another overview on burn management from the Shriner’s Hospital in Boston. Again many things will be consistent with previous references. This is one source that could be read to obtain in one sitting an overview of the burn problem.
‘Iibbles PM, Edelsberg JS. Hyperbaric oxygen therapy. N Engl J Med 1996;334:1642-8. This article summarizes recent thinking regarding the role of hyperbaric oxygen therapy in a variety of disorders. Although its use in some forms of acute ther-
88
ma1 injuy resuscitation is advocated, the data on which this recommendation is based are not the results of randomized, prospective, multicenter work and thus are not widely accepted in the burn care community.
Williams WG, Phillips IG. Pathophysiology of the burn wound. In: Herndon DN, editor. Total bum care. London: Saunders; 1996. p. 63-70. This chapter provides a recent review from a
Warden GD. Fluid resuscitation and early management. In: Herndon DN, editor. Total bum care. London: Saunders; 1996. p. 53-60. An excellent overvie; is provided of fluid resuscitation and permeability changes after burn i&y. In particular, Baxter’s work is placed in context of current resuscitation strategies.
July-September
major center regarding pathologic changes occurring in the burn wound. Total Bum Care is the most recent comprehensive textbook on bum care, currently is a leading reference in this area, and includes a discussion of common forms of thermal injuly, including electrocution.
1997
16:3
Air Medical
Journal