• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Acs0716 Miscellaneous Burns And Cold Injuries
 

Acs0716 Miscellaneous Burns And Cold Injuries

on

  • 1,728 views

 

Statistics

Views

Total Views
1,728
Views on SlideShare
1,728
Embed Views
0

Actions

Likes
1
Downloads
0
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Adobe PDF

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Acs0716 Miscellaneous Burns And Cold Injuries Acs0716 Miscellaneous Burns And Cold Injuries Document Transcript

    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 1 16 MISCELLANEOUS BURNS AND COLD INJURIES David M. Heimbach, M.D., F.A.C.S., and Nicole S. Gibran, M.D., F.A.C.S. Electrical Injury negligible. When the high current is terminated, the heart usually Three main forms of electrical injury exist: low-voltage burns (i.e., reverts back to sinus rhythm, just as happens in cardiac defibrilla- burns resulting from contact with circuits of less than 440 volts tion, when such high currents are deliberately applied to the chest [V]), high-voltage burns (i.e., burns resulting from circuits of to depolarize the entire heart. greater than 1,000 V), and super–high-voltage burns (caused In the event that the victim of electric shock is unconscious, the by lightning). There is also a poorly defined “intermediate-volt- initial responder should remove the source of the current (taking age” category, which includes burns caused by contact with indus- care not to become a victim of shock himself or herself) and then trial circuits of 440 to 800 V; these burns have characteristics provide cardiopulmonary resuscitation (CPR); paramedics may of both high-voltage and low-voltage burns, depending on the then begin defibrillation. If a sinus rhythm has not been established circumstances. on arrival at the emergency department (ED), the physician A common “electrical,” though noncontact, injury is an intense should treat the patient as he or she would any other dysrhythmia flash burn resulting from the short-circuiting of an industrial cir- patient. If sinus rhythm has been established, the patient should be cuit by an electrician with a metal tool. Such a short-circuiting treated as a sudden death victim, with evaluation for anoxic dam- causes the metal part of the tool to vaporize, as if it were an uncon- age and cardiac monitoring. trolled arc welder; this vaporization results in a very high tempera- Many patients come to the ED after receiving an electric shock ture flash that causes deep burns to the hand holding the tool and from household current. If the electrocardiogram and rhythm strip less deep burns to the upper body and face. Clothing can catch are normal, the patient should be reassured and discharged with- fire, compounding the problem. These burns are not, however, out hospital admission. Muscle soreness will resolve spontaneous- associated with the problems of contact electrical burns, and they ly in 24 to 48 hours and may be treated with analgesics, such as should be treated in much the same way as other thermal burns. nonsteroidal anti-inflammatory drugs (NSAIDs). An electrical burn is managed in essentially the same way as any Cutaneous burns with significant tissue necrosis rarely result other burn except that a higher urinary output is necessary in the from contact with low-voltage current. Usually, the area of contact presence of myoglobinuria. In addition to the potentially devastat- is large enough to dissipate the heat of the current, and underlying ing tissue destruction seen with high-voltage injury, electrical tissue destruction is minimal. injuries can lead to chronic and debilitating nonsurgical conditions that must be addressed. Mouth Burns in Children The exception to this rule is a child who may chew on the end LOW-VOLTAGE INJURIES of a live electric extension cord. The child’s saliva completes the The human body is three to four times as sensitive to alternat- circuit between the positive and neutral leads; the resulting electri- ing current as it is to direct current. Alternating current has gener- cal short may cause significant tissue destruction of the lips, ally replaced direct current for all commercial power applications tongue, or both [see Figure 1].These burns should be evaluated and because it is cheaper to transmit and can be more easily trans- treated by a plastic surgeon or a burn surgeon.The patient is often formed to any required voltage. The amount of 60-cycle alternat- admitted to ensure he or she receives proper nourishment and that ing current that can just be perceived in the hand is about 1.1 mil- the parent is comfortable with pain management and wound liamperes (mA), which produces a tingling sensation. Skin resis- cleansing. The parent should be forewarned that the eschar might tance, however, varies according to the thickness of the epidermal separate in a few days, resulting in bleeding from the labial branch keratin layer, as well as the cleanliness and dryness of the skin.The of the facial artery. In an emergency setting, this bleeding can be calloused hand may provide resistance of as much as 1,000,000 easily treated by pinching the lip between thumb and forefinger ohms/in2 while dry; normal skin provides resistance of 5,000 while the child is brought to the ED for suture ligation. ohms/in2; and wet skin provides resistance of only 1,000 ohms/in2. There are two plans for definitive care.1-3 Long-term results With currents higher than 2 to 4 mA, the tingling gives way to appear to be about equal for nonoperative and operative acute muscle contractions, which get stronger as the current increases. management. If nonoperative management is chosen, splinting is The “let go” current is reached at approximately 15 mA, above usually recommended to keep the mouth stretched to prevent con- which the victim cannot release his or her grasp of the conductor. tracture, but patients and parents do not always comply fully with Above 20 mA, there is sustained spasm of the respiratory muscles. splint use. Immediate coverage with flaps hastens the healing but If the passage of current lasts less than 4 minutes, respiration will leaves a permanent scar and may result in the sacrifice of some resume; however, if it lasts longer than 4 minutes, asphyxiation normal tissue. may occur, and mouth-to-mouth resuscitation may be required. At HIGH-VOLTAGE INJURIES levels above 30 to 40 mA, ventricular fibrillation (VF) may be induced. As the current is increased, the heart’s susceptibility to Current in wires containing 1,000 V or more may cause massive fibrillation first increases and then decreases. At 1 to 5 A, the heart tissue destruction. The tissue destruction results from electrical goes into sustained contraction, and the likelihood of VF becomes energy being converted to heat as it meets resistance in the tissues.
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 2 in adults, especially in the presence of myoglobinuria.With signif- icant myonecrosis, rhabdomyolysis results in increased levels of circulating myoglobin and hemoglobin, as well as cell fragments, which can plug the renal tubules and cause acute tubular necrosis. Myoglobin precipitation is accentuated by acidic urine and decreased by alkaline urine.There has never been a report of a cor- relation between exact myoglobin levels in the urine or the blood and development of renal failure.4,5 Because urinary myoglobin levels can be significantly elevated even when the urine is clear, the clinical relevance of quantifying such levels is unclear. However, gross myoglobin in the urine should be treated with aggressive fluid hydration. If the urine is red or reddish black, urinary flow of at least 1 ml/kg/hr is indicated until the pigment clears, and acido- sis should be corrected. An osmotic diuretic such as mannitol (25 g bolus, followed by 12.5 g every 2 to 4 hours) may be necessary to maintain adequate urinary output. Use of sodium bicarbonate to maintain urinary pH above 7 without raising blood pH above 7.5 theoretically may minimize protein precipitation in the urine. SURGICAL CONSIDERATIONS Figure 1 Shown is an electrical burn caused by a 110-volt house- hold current. The injury resulted from the patient’s sucking on an There are two indications for early operation in a patient with a extension plug. The burn was treated conservatively with a mouth high-voltage electrical burn. If the burn is making the patient sick splint, which resulted in a nearly normal-appearing mouth with (e.g., myoglobin will not clear or acidosis will not resolve), the good function. wound should be explored and all grossly necrotic tissue removed. If the burn is making an extremity sick (e.g., there are signs of a compartment syndrome), early escharotomy, fasciotomy, or both The smaller the size of the body part through which the electrici- should be performed. Otherwise, delaying surgical exploration by ty passes, the more intense the heat and the less the heat is dissi- a few days can often allow definitive debridement and wound clo- pated. Fingers, hands, forearms, feet, and lower legs frequently are sure through a single operation.6,7 totally destroyed; areas of larger volume (e.g., the trunk) usually dissipate enough current to prevent extensive damage to viscera Escharotomy and Fasciotomy unless the contact wound is on the abdomen or the chest. As cur- In general, an escharotomy is indicated for a circumferential rent passes through the body, arc burns, as well as the usual con- deep burn when there is evidence of impaired distal perfusion. tact wounds, are common. These deep wounds, which may be as Fasciotomy is indicated for concomitant electrical injury to under- destructive as contact wounds, occur when current takes a direct lying muscle when there is evidence of increased compartment path, often between joints in close apposition to one another at the pressure, myoglobinuria, tense muscle compartments, or nerve or time of injury. Burns of the volar aspect of the wrist, the antecu- vessel compression. Careful monitoring, including measurement bital fossa when the elbow is flexed at the time of injury, and the of compartment pressures, is mandatory, and escharotomies and axilla are most common. Such injuries should always be seen fasciotomies should be performed at the slightest suggestion of immediately by a surgeon with a special interest in burns. The progression. Routine compartment pressure measurements may immediate evaluation of the patient with a major electrical burn is be helpful, but any of the signs of impending compartment syn- similar to that of any severely injured patient and includes evalua- drome (i.e., increased pain, pallor, absence of pulse, decreased tion of the ABCs (Airway, Breathing, and Circulation). sensation, and tense swelling) mandate prompt compartment In addition to burns, which may be obvious, the patient may release in the operating theater. have other associated injuries resulting from falls or may have bro- One unique injury that must be considered in patients with ken bones resulting from the tetanic spasms of major muscle electrical injuries to the hand is a carpal tunnel injury.7 With the groups. Common potential fractures include those of the lumbar associated swelling, relatively small electrical injuries can lead to spine and hip. swelling in the carpal tunnel that manifests as increasing paresthe- sias and numbness in the distribution of the median nerve. If the RESUSCITATION injury is sufficiently devastating to create a mummified hand, Flash and flame burns without electrical contact injuries are carpal tunnel release probably has no role in the treatment plan. treated in the same manner as all thermal burns are. For patients CONTACT SITES with electrical contact injuries, fluid requirements are considerably greater than are predicted by the various formulae used for ther- Because most electrical injuries result from alternating current, mal burn victims; the reason is that the cutaneous injury is usual- entrance and exit sites are better referred to as contact points. ly only the “tip of the iceberg,” and underlying deep tissue dam- These are thermal burns resulting from heat generation, but age may be extensive. A good general starting point is to adminis- unlike flame burns, they are often associated with significant ter lactated Ringer solution at two to three times the quantity spec- injury to the deep tissues.The amount of heat generated depends ified by the Baxter (Parkland) burn formula. This would initially on the resistance to current flow. A dry hand or foot in contact require providing 8 to 10 ml/kg/% of total body surface area with high voltage may generate heat in excess of 1,000° C, leading (TBSA) that is burned. Fluid administration should be adjusted, to mummification at the contact site [see Figure 2]. with the aims of correcting metabolic acidosis, normalizing vital With the passage of a large current, multiple contact sites may signs, and attaining a urinary output of approximately 100 ml/hr be seen along the route of the current, resulting in injuries that
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 3 suggest the effects of an explosion. Sites of current arcing (see above) should be treated in the same manner as primary contact sites because the underlying damage can be just as severe. WOUND MANAGEMENT Necrotic Fat, In general, if there are large amounts of necrotic muscle as a Fascia, Muscle result of high-voltage electrical contact, aggressive surgical debridement to decrease myoglobinemia is indicated. This inter- vention may minimize subsequent organ dysfunction. If gross myoglobinuria does not resolve after several hours of aggressive hydration, diuresis, and compartment release, the presence of a large amount of dead muscle is a virtual certainty. Muscle of inde- terminate viability should be spared, but if a limb is obviously unsalvageable, guillotine amputation may be appropriate and life- Bone saving. The goal of subsequent surgical procedures is to conserve viable tissue while removing neighboring dead tissue. The uneven nature of the injuries makes this approach difficult and time-con- suming. If they are not exposed, small, scattered areas of injured muscle will be replaced by fibrous tissue. A high fever and tachy- cardia, however, may be physiologic evidence that remaining non- Figure 3 Shown is the same injury seen in Figure 2 just before a viable muscle has become infected. Because bone resists current second debridement on day 7. Because this patient’s right leg was amputated, every attempt was made to salvage as much of the and becomes very hot, there may be a substantial amount of non- left foot as possible. At initial debridement, it is difficult to tell viable necrotic muscle tissue along the bone that must be debrid- precisely how much of the foot is possibly viable; note that there ed. It is not uncommon for superficial forearm muscles to appear is still considerable nonviable soft tissue under the metatarsals viable while necrotic muscle surrounds the radius and ulna. Use of and that the metatarsals are considerably exposed. After the sec- vascular grafts to replace clotted arteries is sometimes an option. ond debridement, the foot was treated in a Wound Vac to stimu- However, such grafts may actually increase morbidity and prolong late vascularization. recovery; amputation followed by use of one of the newer prosthe- ses may result in better function than would be available in a hand or foot that has poor sensation and motor function. In accordance with the principles used for thermal burns, devi- talized tissue below the skin at the contact sites should be debrid- ed within 7 days after injury [see Figure 3]. Sequential debridement of residual necrotic tissue may be necessary over the ensuing 3 to Figure 4 Shown is the same foot as in Figures 2 and 3 at the time of discharge (day 21 after injury). Two toes and the fifth metatarsal were removed, leaving a stable, sensate foot with sat- isfactory cover. 5 days. Early aggressive debridement, followed immediately by reconstructive surgery with tissue transfer by rotation or free flaps to cover remaining viable tissue, nerves, vessels, and bone, may facilitate early recovery [see Figure 4]. To help determine the optimal timing and results of operation, Figure 2 Shown is a contact-point injury caused by a 15,000-volt one group reviewed the charts of 62 patients who underwent treat- current, seen on day 1. Although the injury looks relatively sim- ment for high-voltage electrical burns of the upper extremities.6 A ple, a similar injury to this patient’s right foot led to a below-the- total of 100 upper extremities were treated. Of these, 22% under- knee amputation. Careful monitoring for compartment syn- went decompression within 24 hours because of progressive nerve drome in the leg is mandatory in such injuries. dysfunction, clinical compartment syndrome, or failure of resusci-
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 4 tation.This subset required a mean of 4.2 operations; the amputa- Peripheral neuropathies are relatively common in burned tion rate was 45%, which was similar to that reported in other extremities, resulting either from direct nerve injury or from fibro- series. For another 35% of the burned extremities, the first opera- sis occurring around the nerves. Reflex sympathetic dystrophy is tive procedure was delayed until resuscitation was complete. This not uncommon. Many patients suffer aches, headaches, chronic subset required a mean of 2.1 operations and no amputations. For pain, and various nonanatomic neurologic complaints for some the remaining 43% of the extremities, no operations were required months after injury.18-20 to achieve healing. Overall results showed a 10% amputation rate and a mean hospital stay of 27 days; these results were better than Cataracts the results reported by others. The incidence of premature cataract development may be as high as 5% to 10% after electrical injury.21-23 Surprisingly, cataracts NONSURGICAL PROBLEMS RELATED TO ELECTRICAL INJURY occur equally in patients who have obvious contact points on the face or head and in those who do not.The latent period may range Cardiac Injuries from weeks to years, with the average being 6 months.23 Therefore, Immediate cardiac arrest is the most common cause of death complete ophthalmologic examination for cataracts at the time of from electrical injury. Low-voltage exposure is likely to induce ven- hospitalization and, subsequently, with any subjective decrease in tricular fibrillation, whereas high-voltage exposure is more likely to visual acuity is warranted. For workers’ compensation claims, an produce cardiac standstill. Cardiac standstill and respiratory arrest eye examination shortly after the injury is indicated to document may revert spontaneously if CPR prevents anoxia;VF is more like- normal lens transparency in case cataracts occur as an injury-relat- ly to necessitate defibrillation. Conventional wisdom states that ed disease and not from preexisting problems. patients who have sustained high-voltage injuries should be admit- ted for 24-hour telemetry monitoring and that cardiac isoenzyme Psychological Effects levels should be followed. Studies have shown that if the ECG is Posttraumatic stress syndrome is more common after electrical normal on admission, subsequent cardiac dysrhythmias are rare burns than after thermal burns.24 However, general rehabilitation and intensive monitoring is probably not necessary.8,9 The tran- and self-assessed quality of life are comparable after thermal burns sient interest in isoenzyme and troponin levels has now waned, and and after electrical burns.25 assessment of these variables has not proved useful in predicting LIGHTNING INJURY cardiac damage.8,10-13 Myocardial infarction is uncommon, but it has been reported in A lightning strike is an extraordinarily high-voltage discharge of a small percentage of cases in each series. In one patient at the brief duration. The current generated may reach 300,000 A and University of Washington (UW) Burn Center, a papillary muscle 100 million V. Fortunately, the current often flows around the sur- ruptured within 24 hours; this led to immediate, fatal congestive face of, rather than through, the body; this “flashover” permits an heart failure. overall survival rate of 65% or higher.26-28 The most common immediate potentially fatal complications are paralysis of the res- Neurologic Complications piratory center and cardiac standstill. Cardiac activity will usually Neurologic complications are common sequelae of high-voltage resume spontaneously, but apnea may be present for 15 minutes electrical injuries and can affect the brain, spinal cord, and periph- or longer—long enough to cause anoxic brain injury in the absence eral nerves. Immediate but frequently transient symptoms include of pulmonary resuscitation. A rare but fascinating complication is varying levels of unconsciousness, respiratory paralysis, and motor keraunoparalysis, which is a transient paralysis associated with paralysis. Permanent changes include cortical encephalopathy, extreme vasoconstriction and sensory disturbances of one or more caused by the electrical injury itself or resulting from hypoxia at the extremities. It usually lasts only an hour (in rare instances, as long time of the accident. Spinal cord injuries are rare but may present as 24 hours); a lifeless appearance should not result in the patient’s as progressive muscular atrophy, amyotrophic lateral sclerosis, or being treated as a victim of sudden death.29 Cardiac and neuro- transverse myelitis. These conditions may occur days to months logic complications are frequent and are generally similar to those after the injury and progress slowly.14-16 resulting from man-made high-voltage injuries.30 Dendritic super- A study of 90 patients (82 male and 8 female) with electrical ficial skin burns, known as Lichtenberg’s flowers or fractals,31 are burns was conducted at the UW Burn Center to identify and eval- sometimes seen. These superficial burns heal rapidly without uate neurologic consequences.17 There were four deaths. Of the 86 sequelae. Ruptured tympanic membranes and vertigo are com- remaining patients, 22 sustained low-voltage injury. Of these 22, 11 mon accompaniments.32,33 Treatment of systemic effects is gener- had immediate neurologic symptoms; these symptoms resolved in ally supportive; tissue injuries are treated in the same manner as nine of the 11 patients. A total of 64 patients sustained high-volt- other high-voltage injuries. age injury; of these, two thirds had immediate central or peripher- al neurologic symptoms (or both). Loss of consciousness account- ed for the largest percentage of central nervous system sequelae in Chemical Burns the high-voltage group (45%). Of the 29 patients who lost con- GENERAL EMERGENCY CARE sciousness, 23 (79%) regained consciousness before arrival at the hospital. Six patients remained comatose, three died, and three Immediate treatment of chemical burns involves the immediate awoke but had neurologic sequelae. One third of the patients in the removal of affected clothing; the burns should then be thoroughly high-voltage group had one or more acute peripheral neu- flushed with copious amounts of water at the scene of the accident. ropathies; of these neuropathies, 64% resolved or improved. Five The only exception to this is for chemical burns involving dry pow- patients had transient initial paralysis, but there were no delayed der; for such burns, the powder should be brushed from clothing spinal cord symptoms. Eleven patients experienced one or more and skin. Chemicals will continue to burn until removed; washing delayed peripheral neuropathies; half of these delayed neuropathies for at least 15 minutes under a stream of running water may limit resolved or improved. the overall severity of the burn. No thought should be given to
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 5 searching for a specific neutralizing agent. Delay results in deepen- size the severity and long-term sequelae of the respiratory and ocu- ing of the burn, and neutralizing agents may cause burns them- lar problems.40-44 selves; they frequently generate heat while neutralizing the offend- ACIDS ing agent, adding a thermal burn to the already potentially serious chemical burn. As noted (see above), acid burns tend to denature (tan) the skin. Chemical burns, usually caused by strong acids or alkalis, are Although they may be full-thickness burns, destruction of deeper most often the result of industrial accidents, assaults, or the tissues is often limited as a result of the formation of an impervi- improper use of harsh solvents and drain cleaners. In contrast to a ous carapace of the dermis. thermal burn, chemical burns cause progressive damage until the chemicals are inactivated by reaction with the tissue or are diluted Hydrochloric and Nitric Acids by being flushed with water. Individual circumstances vary, but Hydrochloric and nitric acids are strong acids that denature pro- acid burns may be more self-limiting than alkali burns. Acid tends teins but usually do not result in systemic poisoning unless inhaled to tan the skin, creating an impermeable barrier that limits further or ingested. penetration of the acid. Alkalis combine with cutaneous lipids to create soap and thereby continue dissolving the skin until they are Chromic Acid neutralized. A full-thickness chemical burn may appear deceptive- Some acids, such as chromic acid and dichromate, cause both ly superficial, seeming to cause only a mild brownish discoloration systemic and cutaneous problems. Chromium poisoning is char- of the skin. The skin may appear to remain intact during the first acterized by complete anuria, hepatic damage, and progressive few days after the burn and only then begin to slough sponta- anemia. It can occur from the cutaneous absorption of chromi- neously. Chemical burns should be considered deep dermal or um from chromic acid burns that are as small as 1% of TBSA. full-thickness burns until proved otherwise. In general, definitive Aggressive surgical excision and prompt hemodialysis may be treatment of these burns is the same as for thermal injuries—shal- lifesaving.45-48 low burns heal with infection prevention; deep burns are excised and grafted as soon as their depth is determined. Formic Acid Some chemicals, such as phenol, cause severe systemic effects; Similarly, formic acid causes metabolic acidosis, intravascular others, such as hydrofluoric acid, may cause death from hypocal- hemolysis, and hemoglobinuria when ingested or when concen- cemia even after moderate exposure. Unless the characteristics of trated solutions contact the skin.49,50 the chemical are well known, the treating physician is advised to call the local poison control bureau for specifics on treatment. Carbolic Acid Phenol (carbolic acid) is used as a hospital, industrial, and home ALKALIS disinfectant. Exposure may lead to rapid CNS depression, vomit- Lime (calcium oxide/hydroxide) and sodium or potassium ing, coughing, stridor, and, in rare instances, seizures.51 The cuta- hydroxide are examples of common alkalis used in industry and neous burns are usually first degree. around the home. Sodium or potassium hydroxide (drain cleaner) is ingested by Hydrofluoric Acid children accidentally and by adults attempting suicide. Mouth Hydrofluoric acid burns are unique in terms of their presenta- burns are the tip of the iceberg. Emergency treatment should be tion and current treatment. Hydrofluoric acid is used in industrial directed to the oropharynx and the upper GI tract; description of cleaners and rust removers. It is used in concentrated form in the such treatment is beyond the scope of this chapter. Sodium or etching of circuit boards and in dilute form as a cleaner for glass potassium hydroxide is also used in assaults, especially in areas and milk cans. Hydrofluoric acid is a very strong acid that coagu- where people cannot afford handguns.34 Teen hoodlums some- lates skin and allows entry of fluoride ions, which then chelate cal- times fill water pistols with sodium hydroxide and squirt sleeping cium and magnesium in tissue and plasma. Local cell death homeless people. Contact of concentrated sodium hydroxide with results; with severe exposure, severe systemic hypocalcemia and the cornea results in prompt and permanent corneal destruction hypomagnesemia can result in fatal cardiac dysrhythmias.52-54 and blindness. Drain and oven cleaners are also favorite substances Fluoride, as the most electronegative element, tightly binds many of patients who deliberately and repeatedly inflict injury on them- cations essential to hemostasis, inhibiting normal blood coagula- selves (Munchausen syndrome).35-37 tion. As a metabolic poison, it stimulates some enzymes (e.g., The unwitting homeowner or novice construction worker who adenylate cyclase) and severely inhibits others (e.g., Na+,K+- does not protect the skin when working with concrete cement (cal- ATPase and the enzymes of carbohydrate metabolism).55 cium hydroxide) is often surprised at day’s end with painful red Treatment of severe poisoning requires careful monitoring in an contact areas on the hands, feet, knees, and forearms. By bedtime, ICU, replacement of magnesium and calcium, and consideration these injuries have become excruciating and require emergency of dialysis. treatment and, frequently, excision and grafting.38,39 More commonly, industrial exposure is limited to the hand.56 Strong alkali burns are invariably deep, though they may seem Exposure to concentrated solution will cause immediate symp- deceptively shallow at their onset. toms, but the more common dilute solutions may not cause symp- toms for hours. Often, the worker will go home and experience ANHYDROUS AMMONIA increasingly severe pain, which will prevent sleep and lead to a Anhydrous ammonia is a colorless, pungent gas that is stored nighttime visit to the ED.The worker will likely be unaware of the and transported under pressure in liquid form. Ammonia injury is cause of the pain; the emergency physician should question the uncommon, but it is associated with high morbidity and mortality. patient about solvents used that day. Particularly devastating is severe acute respiratory distress syn- Conventional treatment of burns to the hand and digits has drome (ARDS) and long-term restrictive disease with bronchiec- consisted of local application of calcium liquids and gels. Direct tasis. Most of the literature consists of case reports, but all empha- injection of calcium gluconate into the injury site is somewhat
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 6 effective but may cause pressure necrosis of fingers that are already gloves, and boots. The victim’s clothing is removed, and extensive swollen. A much better treatment that can yield almost magical water lavage is provided, along with copious isotonic eye irrigation. results is direct intra-arterial infusion of a dilute calcium gluconate Once decontamination has been completed, there is no danger to solution through the radial or brachial artery.The sooner the infu- attendants; blister fluid does not contain chemicals.71 Burns are sion is started after the onset of pain, the better the result. Pain is usually of partial thickness and can be treated in the same manner immediately mitigated if not cured, and tissue destruction is often as other partial-thickness burns. minimal.57,58 This measure has become the treatment of choice in the UW Burn Center and has yielded good results with no com- plications to date. However, therapy must be started within the Cold Injury first 24 hours; after this point, tissue damage is permanent. An Cold injuries limited to digits, extremities, or exposed surfaces alternative is intravenous infusion of calcium gluconate with the are the result of either direct tissue freezing (frostbite) or more Bier block technique (i.e., a venous tourniquet applied proximal to chronic exposure to an environment just above freezing (chilblain the infusion site),59-61 but this measure can increase swelling in the or pernio; trench foot). Cold injury has been a major cause of mor- extremity. bidity during war, and it is described as being the single major injury sustained by British soldiers in the Falklands expedition. Cold injury resulted in over 7 million soldier fighting days lost by War and Chemicals of Mass Destruction Allied forces in World War II.72 NAPALM CHILBLAIN, PERNIO, AND TRENCH FOOT Napalm is jellied gasoline that is generally ignited and sprayed Chilblain and pernio are descriptive terms for a form of local on material and combatants in wartime. It causes devastating cold injury characterized by red-purple, pruritic skin lesions burns because the gasoline sticks to clothing and skin while it is (papules, macules, plaques, or nodules) that are often associated burning. Injuries are usually fourth-degree thermal burns, which with edema or blistering.These lesions are caused by a chronic vas- are treated in the same manner as other very deep thermal burns. culitis of the dermis, and their development appears to be pro- WHITE PHOSPHORUS voked by repeated exposure to cold, though not freezing, temper- atures. The injury typically occurs on the face, the anterior tibial White phosphorus is used in many types of military munitions, surface, or the dorsum of the hands and feet—areas that are poor- as well as in fireworks and in industrial and agricultural products. ly protected or are subject to long-term exposure to the environ- In the presence of oxygen, it ignites spontaneously; when in con- ment.With continued exposure, ulcerative or hemorrhagic lesions tact with skin, it causes deep thermal injuries. It may also give rise may appear and progress to scarring, fibrosis, and atrophy. to multiple organ dysfunction syndrome (MODS) because of its Treatment consists of sheltering the patient, elevating the affected toxic effects on erythrocytes, the liver, the kidneys, and the heart. part on sheepskin, and allowing gradual rewarming at room tem- Treatment of the injured patient is difficult.The particles must be perature. Rubbing or massage is contraindicated, because further debrided to prevent continued burning and systemic poisoning. damage and secondary infection may result.73-75 Conventional wisdom was to use a solution of copper sulfate to Trench foot or cold immersion foot (or hand) describes a non- convert the elemental phosphorus into copper phosphate. freezing injury of the hands or feet, typically sustained by sailors, However, this approach has fallen into disfavor because copper fishermen, or soldiers as a consequence of long-term exposure to poisoning may result, the effects of which are often as bad as those wet conditions (e.g., water or mud) and temperatures just above of phosphorus poisoning.62,63 During debridement in the operat- freezing.76-80 Alternating arterial vasospasm and vasodilatation ing theater, exposure of the particles to air can reignite the phos- appear to occur, with the affected tissue first cold and anesthetic phorus and thereby endanger the patient and the operating team. and then becoming hyperemic after 24 to 48 hours of exposure. MUSTARD GAS, LEWISITE, AND PHOSGENE With the hyperemia comes an intense, painful burning and dyses- thesia, as well as tissue damage characterized by edema, blistering, Sulfur mustard is a vesicant that alkylates DNA. In liquid or gas redness, ecchymosis, and ulceration. Complications consisting of form, its main targets are the skin, the eyes, and the lungs.64-68 Its local infection and cellulitis, lymphangitis, and gangrene may occur. clinical effects are similar to those of burns, with loss of immunity, After 2 to 6 weeks, a posthyperemic phase ensues, resulting in tis- respiratory failure, and ophthalmic, gastrointestinal, and hemato- sue cyanosis with increased sensitivity to cold. Treatment is best logic signs. In the Iraq-Iran war (1981–1989), extensive use of started during or before the reactive hyperemia state; it consists of chemical weapons such as mustard gas caused injuries with high immediate removal of the extremity from the cold, wet environment mortality and morbidity, as well as chronic side effects in vital and exposure of the extremity to warm, dry air.The limb is elevat- organs, especially the respiratory tract. In a study that examined ed to minimize edema, pressure spots are protected, and local and long-term effects of mustard gas exposure in 220 survivors, nearly systemic measures to combat infection are undertaken. Massage, all the victims complained of cough, dyspnea, and suffocation. soaking of the feet, and rapid rewarming are not indicated. Hemoptysis was found in six victims. Respiratory distress with use of accessory muscles was observed in four. Two thirds of the sub- FROSTBITE jects had wheezing and coarse rales. Most had obstructive patterns Frostbite is a common, severe form of cold injury that involves on pulmonary function testing.69 Cutaneous exposure is manifest- local freezing of tissues. Frostbite is classified into four grades of ed by a delayed erythema of skin occurring after about 4 hours, fol- severity81,82: lowed by blistering in 12 to 48 hours.The blisters rupture, leaving shallow, painful ulcers. Other vesicants are more corrosive: lewisite 1. First-degree injury involves the freezing of tissue with hyperemia (arsine) and phosgene are both more potent than mustard gas, and and edema but without blistering. symptoms appear sooner with these agents.70 2. Second-degree frostbite involves the freezing of tissue with hy- Rescuers should be protected with suitable clothing, respirators, peremia, edema, and characteristic large, clear blisters.
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 7 TREATMENT 3. Third-degree frostbite involves the freezing of tissue with the death of subcutaneous tissues and skin, resulting in hemorrhag- Prehospital or field care of a victim of cold injury should focus ic vesicles that are generally smaller than those seen in second- on removing the patient from the hostile environment and pro- degree frostbite. tecting the injured body part from further damage. Rubbing or 4. Fourth-degree frostbite is notable for tissue necrosis, gangrene, exercising the affected tissue does not augment blood flow and and, eventually, full-thickness tissue loss. risks further cold injury or mechanical trauma. Because repeated bouts of freezing and thawing worsen the injury, it is preferable for The degree of severity of frostbite is often not apparent for sev- the patient with frostbite of the hands or feet to seek definitive shel- eral days. For all forms of frostbite, the initial presentation is pain ter and care immediately rather than to rewarm the tissue in the or discomfort, as well as pruritus if the injury is mild. With more field and risk refreezing. Once rewarming has begun, weight bear- severe injury, there is a progressive decrease in range of motion, ing should be avoided. and edema becomes prominent. The injury progresses to numb- The ED treatment of a frostbite victim should first focus on the ness and eventual loss of all sensation in the affected tissue. The basic ABCs of trauma resuscitation [see 7:1 Initial Management of involved area appears white or blue-white and is firm or even hard Life-Threatening Trauma] and on identifying and correcting sys- (frozen) to the touch. The tissue is cold and insensate. Although temic hypothermia. Frostbitten tissue should be immersed in a the initial symptoms may be mild and may be overlooked by the large water bath of 40° to 42° C (104° to 108° F).The bath should patient, severe pain, burning, edema, and even necrosis and gan- be large enough to prevent rapid loss of heat, and the water tem- grene may appear with rewarming. perature should be maintained. This method of rapid rewarming Weather conditions, altitude, degree of protective clothing, may significantly decrease tissue necrosis caused by full-thickness duration of exposure, and degree of tissue wetness are all con- frostbite.88,90,91 Dry heat is not advocated, because it is difficult to tributing external factors to the development of frostbite. regulate and places the patient at risk for a burn injury. The Acclimation to cold may be protective, whereas a previous history rewarming process should take about 30 to 45 minutes for digits. of frostbite probably does predispose an individual to another cold The affected area appears flushed when rewarming is complete tissue injury. Smoking and a history of arterial disease also are con- and good circulation has been reestablished. Narcotics are tributing factors. In urban environments, more than 50% of frost- required, because the rewarming process may be quite painful. bite injuries are alcohol related, and a significant percentage (16%) The skin should be gently but meticulously cleansed and air- of patients have an underlying psychiatric illness.83,84 dried, and the affected area should be elevated to minimize edema. Current evidence suggests that frostbite injury may in fact have A tetanus toxoid booster should be administered as indicated by the two components: (1) the initial freeze injury and (2) a reperfusion immunization history. Sterile cotton should be placed between toes injury that occurs during rewarming.85-87 The initial response to or fingers to prevent skin maceration, and extreme care should be tissue cooling is vasoconstriction and arteriovenous shunting, taken to prevent infection and to avoid even the slightest abrasion. relieved intermittently (every 5 to 7 minutes) by vasodilatation. Prophylactic antibiotics and dermal blister debridement are both With prolonged exposure, this response fails, and the temperature controversial; most clinicians debride blisters and reserve antibiotics of the freezing tissue will approximate ambient temperature until a for identified infections. A 2005 study reported a lower than expect- temperature of –2° C is reached. At this point, extracellular ice ed digit amputation rate when rapid rewarming was followed by crystals form; as these crystals enlarge, the osmotic pressure of the treatment with hepatin and tissue plasminogen activator (tPA), but interstitium increases, resulting in the movement of intracellular to date, this finding has not been confirmed by other studies.94 water into the interstitium. Cells begin to shrink and become After rewarming, the treatment goals are to prevent further hyperosmolar, disrupting cellular enzyme function. If freezing is injury while awaiting the demarcation of irreversible tissue destruc- rapid (i.e., if the temperature falls by more than 10° C/min), intra- tion. All patients with second- and third-degree frostbite should be cellular ice crystal formation will occur, resulting in immediate cell hospitalized. The affected tissue should be gently cleansed in a death. Intravascularly, endothelial cell disruption and red cell warm (38° C) whirlpool bath once or twice a day; some clinicians sludging result in cessation of circulation.88-91 add an antiseptic such as chlorhexidine or an iodophor to the bath. During rewarming, red cell, platelet, and leukocyte aggregation On the basis of findings of arachidonic acid metabolites in the blis- is known to occur; this results in patchy thrombosis of the micro- ters of frostbite victims, some authors advocate the use of topical circulation.92 These accumulated blood elements are thought to aloe vera (a thromboxane inhibitor) and systemic ibuprofen or release, among other products, the toxic oxygen free radicals and aspirin. After resolution of edema, digits should be exercised dur- the arachidonic acid metabolites prostaglandin F2 and thrombox- ing the whirlpool bath, and physical therapy should begin.Tobacco, ane A2, which further aggravate vasoconstriction and platelet and nicotine, and other vasoconstrictive agents must be withheld. leukocyte aggregation. However, the exact mechanism of tissue Numerous adjuvants have been suggested and tried in an effort destruction and death after freeze injury remains poorly defined. to restore blood supply to frostbitten areas. Because of the intense Animal studies suggest that vascular injury, in the form of endothe- vasoconstrictive effect of cold injury, attention has been focused for lial cell damage and subsequent interstitial edema (but not vessel many years on increased sympathetic tone. Sympathetic blockade thrombosis) is the primary initial event in rewarming injury. It has and even surgical sympathectomy have been advocated as early been demonstrated that a marked amelioration of the frostbite therapy, the theoretical rationale being that sympathetic blockade injury can be achieved in a rabbit ear model by treating the animals should release the vasospasm that may precipitate thrombosis in (after cold injury and before rewarming) with a monoclonal anti- the affected tissue. Unfortunately, this method of treatment has body to the neutrophil CD18 glycoprotein complex.93 The impli- produced inconsistent results in experimental studies and is diffi- cation of this observation is that neutrophil adherence to the cult to evaluate clinically.89,95 Experience with intra-arterial vasodi- endothelium of frostbitten tissue during rewarming (reperfusion) lating drugs such as reserpine and tolazoline has also failed to ver- is at least partially responsible for the subsequent tissue injury. ify this hypothesis. In a controlled clinical study, immediate (mean, Clinical application of these experimental observations remains 3 hours) ipsilateral intra-arterial reserpine infusion coupled with untested. early (mean, 3 days) ipsilateral operative sympathectomy failed to
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 8 alter the natural history of acute frostbite injury.89 Sympathectomy one theory, certain offending drugs that should be metabolized are may, however, mollify the chronic pain, hyperhidrosis, and instead deposited in the epidermis, leading to an immune vasospasm of cold injuries; some clinicians also suggest that it response, which causes the body to reject the skin. In 1998, Viard reduces the risk of subsequent cold injury. Heparin, low-molecu- pointed out that keratinocytes normally express the death receptor lar-weight dextran, thrombolytic agents, and hyperbaric oxygen Fas (CD95); keratinocytes from TEN patients were found to have failed to demonstrate any substantial treatment benefit express lytically active Fas ligand (FasL). Antibodies present in (despite the suggestive results of the 2005 study by Twomey and pooled human intravenous immunoglobulins (IVIg) blocked Fas- associates94). mediated keratinocyte death in vitro. In a pilot study, 10 consecu- The difficulty in determining the depth of tissue destruction in tive individuals with clinically and histologically confirmed TEN cold injury has led to a conservative approach to the care of frost- were treated with IVIg; disease progression was rapidly reversed, bite injuries. As a general rule, amputation and surgical debride- and the outcome was favorable in all cases. The implication was ment are delayed for at least 1 month unless severe infection with that Fas-FasL interactions were directly involved in the epidermal sepsis occurs.The natural history of a full-thickness frostbite injury necrolysis of TEN and that IVIg might be an effective treatment.99 leads to the gradual demarcation of the injured area; dry gangrene This report sparked numerous small clinical series, the results of or mummification clearly delineate nonviable tissue. Often, the which have been, at best, inconclusive.100-104 A 2005 study of the permanent tissue loss is much less than originally suspected. In effect of IVIg on ocular complications was unable to demonstrate one review, only 39% of urban frostbite victims required debride- any benefit.105 There may be a role for γ-globulin, but current data ment and skin grating or amputation.84 Emergency surgery is indicate that it is no miracle cure. Because of the high cost of unusual, but during the rewarming phase, vigilance should be γ-globulin and its potential for inducing renal damage, we no maintained to detect the development of a compartment syn- longer use it to treat TEN at the UW Burn Center. drome necessitating fasciotomy. Open amputations are indicated TEN should be distinguished from a somewhat similar disease, in patients with persistent infection and sepsis that is refractory to staphylococcal scalded skin syndrome (SSSS).This entity is caused debridement and antibiotics. by a bacterial exotoxin, which splits the epidermis above the der- Frostbitten tissues seldom recover completely. Some degree of mal-epidermal junction. Although patients with SSSS experience cold insensitivity invariably remains. Hyperhidrosis (occurring in severe erythema, the skin exfoliates rather than blisters. SSSS does as many as 72% of patients), neuropathy, decreased nail and hair not involve mucosa, and the patients are in a septic state from growth, and persistent Raynaud phenomenon in the affected part the underlying staphylococcal infection. SSSS usually affects are frequent sequelae of cold injury.96 The affected tissue remains newborns, becoming much less common as people get older. at risk for reinjury and should be carefully protected during any This unusual disease is treated with antibiotics directed against cold exposure. Treatment with antiadrenergics (e.g., prazosin staphylococci.106 hydrochloride, 1 to 2 mg/day) or calcium channel blockers (e.g., The TEN-induced areas of denudation are comparable to those nifedipine, 30 to 60 mg/day) and careful protection from further affected by a very shallow second-degree burn. Oropharyngeal, exposure are often helpful. However, there is little that appears to esophageal, anal, urethral, and vaginal107,108 mucosal sloughing are afford significant relief to the chronic symptoms that follow tissue also characteristic of TEN.The disease attacks squamous epitheli- freeze injury; sympathectomy, beta- and alpha-adrenergic blocking um, so the remainder of the GI tract is usually spared.There is only agents, calcium channel blockers, topical and systemic steroids, one case report of intestinal epithelial sloughing.109 Complications and a host of home remedies have all been tried, with only occa- such as infection, malnutrition, negative nitrogen balance, severe sional individual success.78 wound pain, and MODS are identical to those seen in patients with major burns. The most common causes of death in TEN patients are systemic infection and pneumonia.The potential mor- Toxic Epidermal Necrolysis tality from TEN is high, but it is reduced by treatments and proto- Toxic epidermal necrolysis (TEN) is a devastating, though (for- cols common in burn centers (e.g., wound coverage with biologic tunately) rare, exfoliative disease of the skin and mucous mem- dressings).There is good evidence that patients affected with TEN branes that results in full-thickness epidermal necrosis. The first should be referred early for management in a burn center.110-112 published report of adult TEN appeared in 1956, when Lyell, in The role of the dermatologist is to define the diagnosis and deter- Lyon, France, compared four cases to scald burns.97 Some authors mine the potential cause. describe a similar skin sloughing but with lesser involvement, CLINICAL MANIFESTATIONS termed the Stevens-Johnson syndrome. In reality, the two diseases are exactly the same: Stevens and Johnson anticipated Lyell by 34 A prodrome of TEN usually consists of fever, sore throat, and years when they described the same pathology in two children in malaise; 1 to 2 days after these symptoms appear, the skin of the South Africa.98 Dermatologists have long known the disease as ery- face and extremities usually becomes tender and erythematous. thema multiforme majus exudativum.Thus, even though only one Lesions appear either as large areas of red skin or as target lesions disease process is involved, various names continue to be used: that are about 2 cm in diameter and consist of concentric rings of Europeans refer to this condition as Lyell disease, pediatricians call erythema. At the same time, ulcerations in the lips and mouth it the Stevens-Johnson syndrome, dermatologists refer to it as ery- appear, making oral intake painful. thema multiforme majus, and American surgeons and internists In 24 to 96 hours, the involved skin begins to form both small call it TEN. blisters and bullae. Moderate traction of the erythematous skin TEN can be precipitated by the administration of medications, results in separation of the epidermis from the dermis—a positive most commonly sulfonamides, antibiotics, and anticonvulsants. It Nikolsky sign.113 When the bullae rupture, large denuded areas of can also be caused by events such as immunizations, systemic dis- skin become apparent. Fingernails, toenails, and the skin of the eases, and viral illnesses. Some cases have no known precipitating palms and soles may also slough. cause. One hallmark of this disease is severe inflammation of the The molecular etiology of TEN remains unclear. According to mouth. Blisters develop on the oral mucosa, leaving a very raw, red
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 9 surface. The lips quickly become swollen and crusted with clotted Cardiovascular function is initially impaired as a result of hypo- blood. The oral lesions may be confined to the oral cavity or may volemia caused by plasma leaking from the blisters, increased skin extend to the larynx or even to the trachea and the esophagus.The evaporative losses, and decreased oral intake. Controlling the patient is usually unable to eat. The eyelids swell as conjunctival febrile response will also help decrease fluid losses, vasodilatation, inflammation develops. Conjunctival infection, usually caused by and the resulting hyperadrenergic response. Careful use of Staphylococcus aureus, may lead to scarring and permanent blind- NSAIDs is often necessary to keep the patient’s temperature below ness.114 The nasal and urethral mucosa may also become inflamed, 102° F (38.9° C). Adequate pain control is essential. Methadone and erosions can develop on the genital and perianal skin. is effective for long-acting pain control, and morphine is a good Renal failure can occur as a result of hypovolemia, the septic choice for procedural pain. response, or membranous glomerulonephritis. In as many as 50% Aggressive oral care is critical because of the high risk of local of cases, there are abnormalities in liver enzymes, including mod- mouth infection and consequent wound and lung infection. Early est increases in aspartate aminotransferase (AST) and alanine and continued assessment and aggressive management of corneal aminotransferase (ALT). Bilirubin levels often show modest to involvement are required. Administration of ophthalmic antibiotic severe increases.115 The mechanism of these increases, which ointments and gentle breaking of adhesions between conjunctiva appear to be a part of the toxic component of TEN, is unknown. and eyelids with a small glass rod are the standard treatment.125 TREATMENT OPTIMIZING NUTRITION The initial focus of treatment is on restoration and maintenance Nutrition is a major component of care, and it often cannot be of cardiopulmonary stability. Because TEN does not induce the delivered orally because of oral lesions. A small gastric feeding intense cytokine reaction that is associated with similar-sized tube is preferred, as the GI tract between stomach and anus is usu- burns, massive anasarca is unusual; resuscitation need not proc- ally intact and is normally functional.126 In general, standard tube- ceed in the manner recommended for burns. Maintenance of nor- feeding formulas for an individual under moderate stress are suf- mal vital signs and adequate urinary output (0.5 ml/kg) is satisfac- ficient because the full ravages of postburn hypermetabolism are tory. Because of the high incidence of catheter infection in the probably not present. When sepsis is avoided, it is very unusual absence of epidermis, use of Swan-Ganz catheters is usually avoid- for the gut to fail and for intravenous parenteral nutrition to be ed when possible.116 needed. Treatment involves aggressive wound management, similar to The role of corticosteroids in the treatment of TEN remains that of a massive second-degree burn, in which the emphasis is on unclear. Although some patients who were receiving steroids optimizing healing and controlling infection. A crucial feature of before the development of TEN still get severe disease,127 a num- TEN is an intact and uninjured dermis, which, if protected, rapid- ber of dermatologists feel that the administration of steroids when ly reepithelializes from sweat glands and hair follicles, which appear the disease process is just beginning, before skin sloughing occurs, to remain intact. Treatment must, therefore, protect the dermis can attenuate the process and thereby reduce subsequent slough- from desiccation and infection. Routine use of ointments and ing. However, once vesicles have formed and the separation has salves not only creates intense pain but also increases the risk of the occurred, corticosteroids no longer effectively attenuate skin formation of a “pseudo eschar” of crusts and devitalized dermis sloughing; in fact, the use of corticosteroids retards the rate of heal- that impairs wound healing. ing. In one study, the complication rate was found to be higher in Biologic or manufactured covers have formed an important role patients who received steroids.128 This study, however, did not take in wound treatment.111,117,118 Emergency operative wound cleans- into account the patients whose disease might have been suffi- ing and application of commercially available pigskin (porcine ciently limited by steroid use to make burn center treatment xenograft) has been the standard of care at the University of unnecessary. Washington Burn Center in more than 130 cases. The pigskin is FOLLOW-UP CARE stapled in place, the patient is treated for several days in a fluidized bed, and the pigskin is removed as the denuded areas heal. The Fortunately, when treatment is successful, the disease usually pigskin is relatively inexpensive, adheres well, is nontoxic, and resolves without hypertrophic scarring, though some mismatching probably provides some growth factors to hasten healing.With this of epidermal pigmentation may be evident. Nails may remain management plan and meticulous systemic care, mortality at the deformed, and eyes are usually dry, requiring periodic lubrication. UW Burn Center has been below 20% for the past 15 years.119 Obviously, patients must not again contact the medication that Alternative covers include Acticoat120 (Smith & Nephew, London, caused the disease; for common medications, a Medic Alert United Kingdom) and Biobrane121-124 (Mylan Laboratories, bracelet is useful. Canonsburg, Pennsylvania), which follow the same principle of dermal protection to permit uninfected healing. In addition, associated physiologic and psychological care must Ionizing Radiation Burns be meticulous. Lung function is often impaired as a result of the The burn surgeon may encounter ionizing radiation injuries in aspiration of secretions from involved oral mucosa and a reduction three settings. Of these, by far the most common involves deliber- in the clearance of secretions as a result of oral pain and overall ate exposure to radiation (i.e., radiation used in treatment) or acci- weakness. Pain control and aggressive pulmonary toilet to assist dental radiation in a hospital, a laboratory, or an industrial com- the patient’s cough are the first line of defense. Suctioning can lead plex. In such settings, a single individual is likely to be injured.The to significant bleeding and should be used either sparingly or only second scenario involves failure of a nuclear energy plant, such as after an endotracheal tube is in place. The patient should be intu- occurred at Chernobyl; in this scenario, dozens to hundreds of bated if lung function is progressively impaired. If the patient is exposures may occur. The third setting is that resulting from a intubated, partial ventilatory assistance is often required because nuclear explosion through military or terrorist action. In such a chest wall pain, systemic toxicity, and weakness can severely impair scenario, thousands of casualties will immediately overwhelm all spontaneous ventilatory efforts. resources.
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 10 LOCALIZED INJURY WHOLE-BODY IRRADIATION AND RADIATION SICKNESS A gray (Gy) is the current unit of radiation, defined as 1 joule (J) A detailed description of whole-body radiation exposure and of energy deposited in 1 kg of tissue; 1 Gy is the equivalent of 100 its treatment is beyond the scope of this chapter. Radiation sick- rads. ness, also known as the acute radiation syndrome, may begin Localized injury is produced by local irradiation of a small area; within hours of exposure. It is initially characterized by nausea, no systemic effects are produced. As with thermal burns, the vomiting, diarrhea, and lethargy; this is followed by the degree of injury is dependent on the type of radiation encountered, hematopoietic syndrome (neutropenia and thrombocytopenia) the radiation dose delivered, and the susceptibility of the tissue. An and the gastrointestinal syndrome (severe diarrhea, bowel initial erythema appears within minutes or hours of exposure and ischemia, bacterial translocation, and sepsis).130 Treatment is subsides over 2 to 3 days. Secondary erythema occurs 1 to 3 weeks mainly supportive. after exposure and is associated with hair loss and desquamation of A nuclear explosion is characterized by a supersonic blast, a the epidermis. At about 3 weeks, blisters (after doses of about 20 fireball extending miles from the epicenter, and immense Gy) or ulcerations (after doses in excess of 25 Gy) may occur. amounts of ionizing radiation. These three components interact, Ulceration may recur months to years after injury. Blood vessels causing severe mechanical injury, flash and flame burns from the become telangiectatic, and deeper vessels become occluded, lead- ignition of clothing, and, of course, severe radiation exposure.131 ing to fibrosis, atrophy, and necrosis.129 The flash has been described as being so intense that the side of Wounds are generally treated in a manner similar to the treat- a victim facing the flash will be charred to bone while the oppo- ment of thermal burns, with the additional caveat that radiation site side is unburned. Doctors in Hiroshima after the atomic sickness is accompanied by immunosuppression, and that endar- bombing there observed that for a time, thermal burns appeared teritis obliterans will markedly diminish the blood supply. Infection to be healing, but in the second and third weeks, the wounds is common, and the optimal timing of excision and grafting of deep broke down and infection set in as the acute radiation syndrome ulcers is not known. became manifest. References 1. Milano M: Oral electrical and thermal burns in 14. Ratnayake B, Emmanuel ER, Walker CC: Neuro- injuries. Emerg Med Clin North Am 22:369, 2004 children: review and report of case. ASDC J Dent logical sequelae following a high voltage electrical 29. ten Duis HJ, Klasen HJ, Reenalda PE: Kerauno Child 66:116, 1999 burn. Burns 22:578, 1996 paralysis, a ‘specific’ lightning injury. Burns Incl 2. Canady JW, Thompson SA, Bardach J: Oral com- 15. Kanitkar S, Roberts AH: Paraplegia in an electrical Therm Inj 12:54, 1985 missure burns in children. Plast Reconstr Surg burn: a case report. Burns Incl Therm Inj 14:49, 30. Muehlberger T, Vogt PM, Munster AM: The long- 97:738, 1996 1988 term consequences of lightning injuries. Burns 3. Thomas SS: Electrical burns of the mouth: still 16. Ko SH, Chun W, Kim HC: Delayed spinal cord 27:829, 2001 searching for an answer. Burns 22:137, 1996 injury following electrical burns: a 7-year experi- 31. ten Duis HJ, Klasen HJ, Nijsten MW, et al: Super- ence. Burns 30:691, 2004 4. Gupta KL, Kumar R, Sekhar MS, et al: Myoglob- ficial lightning injuries: their ‘fractal’ shape and ori- inuric acute renal failure following electrical injury. 17. Grube B, Heimbach D, Engrav L, et al: Neurologic gin. Burns Incl Therm Inj 13:141, 1987 Ren Fail 13:23, 1991 consequences of electrical burns. J Trauma 30:254, 32. Ogren FP, Edmunds AL: Neuro-otologic findings 1990 5. Rosen CL, Adler JN, Rabban JT, et al: Early pre- in the lightning-injured patient. Semin Neurol dictors of myoglobinuria and acute renal failure fol- 18. Selvaggi G, Monstrey S, Van Landuyt K, et al: Re- 15:256, 1995 lowing electrical injury. J Emerg Med 17:783, 1999 habilitation of burn injured patients following light- ning and electrical trauma. NeuroRehabilitation 33. Jones D, Ogren F, Roh L, et al: Lightning and its 6. Mann R, Gibran N, Engrav L, et al: Is immediate 20:35, 2005 effects on the auditory system. Laryngoscope 101: decompression of high voltage electrical injuries to 830, 1991 the upper extremity always necessary? J Trauma 19. Tan SR, McDermott MR, Castillo CJ, et al: Pemphigus vulgaris induced by electrical injury. 34. Branday J, Arscott GD, Smoot EC, et al: Chemical 40:584, 1996 burns as assault injuries in Jamaica. Burns 22:154, Cutis 77:161, 2006 7. Engrav L, Gottlieb J, Walkinshaw M, et al: Out- 1996 come and treatment of electrical injury with imme- 20. Isao T, Masaki F, Riko N, et al: Delayed brain atro- phy after electrical injury. J Burn Care Rehabil 35. Barocas D, Difede J, Viederman M, et al: A case of diate median and ulnar nerve palsy at the wrist: a chronic factitious disorder presenting as repeated, retrospective review and a survey of members of the 26:456, 2005 self-inflicted burns [letter]. Psychosomatics 3:79, American Burn Association. Ann Plast Surg 21. Boozalis GT, Purdue GF, Hunt JL, et al: Ocular 1998 25:166, 1990 changes from electrical burn injuries: a literature review and report of cases. J Burn Care Rehabil 36. Lutzow-Holm C: [Psycho-cutaneous disorders in 8. Purdue GF, Hunt JL: Electrocardiographic moni- practice: self-inflicted skin diseases of psychological toring after electrical injury: necessity or luxury. J 12:458, 1991 origin.] Tidsskr Nor Laegeforen 117:3241, 1997 Trauma 26:166, 1986 22. Reddy SC: Electric cataract: a case report and review of the literature. Eur J Ophthalmol 9:134, 37. Wiechman SA, Ehde DM, Wilson BL, et al: The 9. Bailey B, Gaudreault P, Thivierge RL: Experience management of self-inflicted burn injuries and dis- 1999 with guidelines for cardiac monitoring after electri- ruptive behavior for patients with borderline per- cal injury in children. Am J Emerg Med 18:671, 23. Saffle JR, Crandall A, Warden GD: Cataracts: a sonality disorder. J Burn Care Rehabil 21:310, 2000 2000 long-term complication of electrical injury. J Trauma 25:17, 1985 38. Buckley D: Skin burns due to wet cement. Contact 10. Hammond J, Ward CG: Myocardial damage and Derm 8:407, 1982 electrical injuries: significance of early elevation of 24. Mancusi-Ungaro HR Jr, Tarbox AR, Wainwright CPK-MB isoenzymes. South Med J 79:414, 1986 DJ: Posttraumatic stress disorder in electric burn 39. Early S, Simpson R: Caustic burns from contact patients. J Burn Care Rehabil 7:521, 1986 with wet cement. JAMA 254:528, 1985 11. Murphy JT, Horton JW, Purdue GF, Hunt JL: Evaluation of troponin-I as an indicator of cardiac 25. Cochran A, Edelman LS, Saffle JR, et al: Self- 40. George A, Bang RL, Lari AR, et al: Liquid ammo- dysfunction after thermal injury. J Trauma 45:700, reported quality of life after electrical and thermal nia injury. Burns 26:409, 2000 1998 injury. J Burn Care Rehabil 25:61, 2004 41. Close L, Catlin F, Cohn A: Acute and chronic 12. Pereira C, Fram R, Herndon D: Serum creatinine 26. Milzman DP, Moskowitz L, Hardel M: Lightning effects of ammonia burns of the respiratory tract. kinase levels for diagnosing muscle damage in elec- strikes at a mass gathering. South Med J 92:708, Arch Otolaryngol 106:151, 1980 trical burns. Burns 31:670, 2005 1999 42. Leduc D, Gris P, Lheureux P, et al: Acute and long 13. Kopp J, Loos B, Spilker G, et al: Correlation be- 27. Graber J, Ummenhofer W, Herion H: Lightning term respiratory damage following inhalation of tween serum creatinine kinase levels and extent of accident with eight victims: case report and brief ammonia. Thorax 47:755, 1992 muscle damage in electrical burns. Burns 30:680, review of the literature. J Trauma 40:288, 1996 43. Kerstein MD, Schaffzin DM, Hughes WB, et al: 2004 28. O’Keefe Gatewood M, Zane RD: Lightning Acute management of exposure to liquid ammonia.
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 11 Mil Med 166:913, 2001 Clin Exp Dermatol 31:1, 2006 phologic characterization of acute injury to vascular 44. Flury K, Dines D, Rodarte J, et al: Airway obstruc- 67. Ghanei M, Moqadam FA, Mohammad MM, et al: endothelium of skin after frostbite. Plast Reconstr tion due to inhalation of ammonia. Mayo Clin Proc Tracheobronchomalacia and air trapping after mus- Surg 83:67, 1989 58:389, 1983 tard gas exposure. Am J Respir Crit Care Med 173: 93. Mileski WJ, Raymond JF,Winn RK, et al: Inhibition 45. Laitung J, Earley M:The role of surgery in chromic 304, 2006 of leukocyte adherence and aggregation for treat- acid burns: our experience with two patients. Burns 68. Hefazi M, Attaran D, Mahmoudi M, et al: Late res- ment of severe cold injury in rabbits. J Appl Physiol Incl Therm Inj 10:378, 1984 piratory complications of mustard gas poisoning in 74:1432, 1993 46. Matey P, Allison KP, Sheehan TM, et al: Chromic Iranian veterans. Inhal Toxicol 17:587, 2005 94. Twomey JA, Peltier GL, Zera RT: An open-label acid burns: early aggressive excision is the best 69. Bijani K, Moghadamnia AA: Long-term effects of study to evaluate the safety and efficacy of tissue method to prevent systemic toxicity. J Burn Care chemical weapons on respiratory tract in Iraq-Iran plasminogen activator in treatment of severe frost- Rehabil 21:241, 2000 war victims living in Babol (north of Iran). bite. J Trauma 59:1350, 2005 47. Schiffl H, Weidmann P, Weiss M, et al: Dialysis Ecotoxicol Environ Saf 53:422, 2002 95. Porter JM, Wesche DH, Rosch J, et al: Intra-arteri- treatment of acute chromium intoxication and com- al sympathetic blockade in the treatment of clinical 70. Devereaux A, Amundson DE, Parrish JS, et al: parative efficacy of peritoneal versus hemodialysis in frostbite. Am J Surg 132:625, 1976 Vesicants and nerve agents in chemical warfare: chromium removal. Miner Electrolyte Metab 7:28, decontamination and treatment strategies for a 96. Purdue GF, Hunt JL: Cold injury: a collective 1982 changed world. Postgrad Med 112:90, 2002 review. J Burn Care Rehabil 7:331, 1986 48. Terrill P, Gowar J: Chromic acid burns: beware, be 71. Mellor SG, Rice P, Cooper GJ:Vesicant burns. Br J 97. Lyell A: Toxic epidermal necrolysis: an eruption aggressive, be watchful. Br J Plast Surg 43:699, Plast Surg 44:434, 1991 resembling scalding of the skin. Br J Dermatol 1990 68:355, 1956 72. DeGroot DW, Castellani JW, Williams JO, et al: 49. Chan TC,Williams SR, Clark RF: Formic acid skin Epidemiology of U.S. Army cold weather injuries, 98. Stevens A, Johnson F: A new eruptive fever associ- burns resulting in systemic toxicity. Ann Emerg 1980–1999. Aviat Space Environ Med 74:564, ated with stomatitis and opthalmia. Am J Dis Child Med 26:383, 1995 2003 24:526, 1922 50. Sigurdsson J, Bjornsson A, Gudmundsson ST: 73. White AD: Chilblains. Med J Aust 154:406, 1991 99. Viard I,Wehrli P, Bullani R, et al: Inhibition of toxic Formic acid burn: local and systemic effects: report epidermal necrolysis by blockade of CD95 with of a case. Burns Incl Therm Inj 9:358, 1983 74. Goette DK: Chilblains (perniosis). J Am Acad human intravenous immunoglobulin. Science Dermatol 23(2 pt 1):257, 1990 51. Spiller HA, Quadrani KDA, Cleveland P: A five 282:490, 1998 year evaluation of acute exposures to phenol disin- 75. Cribier B, Djeridi N, Peltre B, et al: A histologic 100. Abe R, Shimizu T, Shibaki A, et al: Toxic epidermal fectant (26%). J Toxicol Clin Toxicol 31:307, 1993 and immunohistochemical study of chilblains. J Am necrolysis and Stevens-Johnson syndrome are Acad Dermatol 45:924, 2001 52. Sanz-Gallen P, Nogue S, Munne P, et al: Hypocal- induced by soluble fas ligand. Am J Pathol 162: caemia and hypomagnesaemia due to hydrofluoric 76. Irwin MS, Sanders R, Green CJ, et al: Neuropathy 1515, 2003 acid. Occup Med (Lond) 51:294, 2001 in non-freezing cold injury (trench foot). J R Soc 101. French LE, Tschopp J: Protein-based therapeutic Med 90:433, 1997 approaches targeting death receptors. Cell Death 53. Mayer T, Gross P: Fatal systemic fluorosis due to hydrofluoric acid burns. Ann Emerg Med 14:149, 77. Irwin MS: Nature and mechanism of peripheral Differ 10:117, 2003 1985 nerve damage in an experimental model of non- 102. Bachot N, Revuz J, Roujeau JC: Intravenous freezing cold injury. Ann R Coll Surg Engl 78:372, immunoglobulin treatment for Stevens-Johnson 54. Ohtani M, Nishida N, Chiba T, et al: Pathological 1996 demonstration of rapid involvement into the subcu- syndrome and toxic epidermal necrolysis: a taneous tissue in a case of fatal hydrofluoric acid 78. Mills WJ Jr, Mills WJ 3rd: Peripheral non-freezing prospective noncomparative study showing no ben- burns. Forensic Sci Int, Jan 17, 2006 [Epub ahead cold injury: immersion injury. Alaska Med 35:117, efit on mortality or progression. Arch Dermatol of print] 1993 139:33, 2003 55. McIvor M: Acute fluoride toxicity: pathophysiology 79. Wrenn K: Immersion foot: a problem of the home- 103. Stella M, Cassano P, Bollero D, et al: Toxic epider- and management. Drug Saf 5:79, 1990 less in the 1990s. Arch Intern Med 151:785, 1991 mal necrolysis treated with intravenous high-dose 80. Kyosola K: Clinical experiences in the management immunoglobulins: our experience. Dermatology 56. Piraccini BM, Rech G, Pazzaglia M, et al: Peri- and of cold injuries: a study of 110 cases. J Trauma 203:45, 2001 [PMID 11549799] subungual burns caused by hydrofluoric acid. Con- tact Dermatitis 52:230, 2005 14:32, 1974 104. Paquet P, Jacob E, Damas P, et al: Treatment of 81. Cauchy E, Chetaille E, Marchand V, et al: drug-induced toxic epidermal necrolysis (Lyell’s 57. Siegel DC, Heard JM: Intra-arterial calcium infu- Retrospective study of 70 cases of severe frostbite syndrome) with intravenous human immunoglobu- sion for hydrofluoric acid burns. Aviat Space lesions: a proposed new classification scheme. lins. Burns 27:652, 2001 Environ Med 63:206, 1992 Wilderness Environ Med 12:248, 2001 105. Yip LW,Thong BY,Tan AW, et al: High-dose intra- 58. Lin TM, Tsai CC, Lin SD, et al: Continuous intra- 82. Schedule for rating disabilities: cold injuries—VA. venous immunoglobulin in the treatment of toxic arterial infusion therapy in hydrofluoric acid burns. epidermal necrolysis: a study of ocular benefits. Eye J Occup Environ Med 42:892, 2000 Final rule. Fed Regist 63:37778, 1998 19:846, 2005 59. Gupta R: Intravenous calcium gluconate in the 83. Urschel JD, Urschel JW, Mackenzie WC: The role 106. Patel GK, Finlay AY: Staphylococcal scalded skin treatment of hydrofluoric acid burns. Ann Emerg of alcohol in frostbite injury. Scand J Soc Med syndrome: diagnosis and management. Am J Clin Med 37:734, 2001 18:273, 1990 Dermatol 4:165, 2003 60. Ryan JM, McCarthy GM, Plunkett PK: Regional 84. Urschel JD: Frostbite: predisposing factors and 107. Meneux E, Paniel BJ, Pouget F, et al: Vulvovaginal intravenous calcium: an effective method of treating predictors of poor outcome. J Trauma 30:340, 1990 sequelae in toxic epidermal necrolysis. J Reprod hydrofluoric acid burns to limb peripheries. J Accid 85. Murphy JV, Banwell PE, Roberts AH, et al: Med 42:153, 1997 Emerg Med 14:401, 1997 Frostbite: pathogenesis and treatment. J Trauma 108. Meneux E, Wolkenstein P, Haddad B, et al: 61. Graudins A, Burns MJ, Aaron CK: Regional intra- 48:171, 2000 Vulvovaginal involvement in toxic epidermal venous infusion of calcium gluconate for hydroflu- 86. Zook N, Hussmann J, Brown R, et al: Microcirc- necrolysis: a retrospective study of 40 cases. Obstet oric acid burns of the upper extremity. Ann Emerg ulatory studies of frostbite injury. Ann Plast Surg Gynecol 91:283, 1998 Med 30:604, 1997 40:246, 1998 109. Sugimoto Y, Mizutani H, Sato T, et al: Toxic epi- 62. Eldad A, Wisoki M, Cohen H, et al: Phosphorous 87. Manson PN, Jesudass R, Marzella L, et al: Evidence dermal necrolysis with severe gastrointestinal burns: evaluation of various modalities for primary for an early free radical-mediated reperfusion injury mucosal cell death: a patient who excreted long treatment. J Burn Care Rehabil 16:49, 1995 in frostbite. Free Radic Biol Med 10:7, 1991 tubes of dead intestinal epithelium. J Dermatol 63. Eldad A, Simon GA:The phosphorous burn: a pre- 25:533, 1998 88. Greenwald D, Cooper B, Gottlieb L: An algorithm liminary comparative experimental study of various for early aggressive treatment of frostbite with limb 110. Kelemen JJ 3rd, Cioffi WG, McManus WF, et al: forms of treatment. Burns 17:198, 1991 salvage directed by triple-phase scanning. Plast Burn center care for patients with toxic epidermal 64. Etezad-Razavi M, Mahmoudi M, Hefazi M, et al: Reconstr Surg 102:1069, 1998 necrolysis. J Am Coll Surg 180:273, 1995 Delayed ocular complications of mustard gas poi- 89. Bouwman DL, Morrison S, Lucas CE, et al: Early 111. Heimbach DM, Engrav LH, Marvin JA, et al:Toxic soning and the relationship with respiratory and sympathetic blockade for frostbite: is it of value? J epidermal necrolysis: a step forward in treatment. cutaneous complications. Clin Experiment Oph- Trauma 20:744, 1980 JAMA 257:2171, 1987 thalmol 34:342, 2006 65. Balali-Mood M, Hefazi M, Mahmoudi M, et al: 90. Valnicek SM, Chasmar LR, Clapson JB: Frostbite 112. Honari S, Gibran NS, Heimbach DM, et al: Toxic Long-term complications of sulphur mustard poi- in the prairies: a 12-year review. Plast Reconstr Surg epidermal necrolysis (TEN) in elderly patients. J soning in severely intoxicated Iranian veterans. 92:633, 1993 Burn Care Rehabil 22:132, 2001 Fundam Clin Pharmacol 19:713, 2005 91. Reamy BV: Frostbite: review and current concepts. 113. Salopek TG: Nikolsky’s sign: is it ‘dry’ or is it ‘wet’? 66. Saladi RN, Smith E, Persaud AN: Mustard: a J Am Board Fam Pract 11:34, 1998 Br J Dermatol 136:762, 1997 potential agent of chemical warfare and terrorism. 92. Marzella L, Jesudass RR, Manson PN, et al: Mor- 114. de Felice GP, Caroli R, Autelitano A: Long-term
    • © 2006 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 7 TRAUMA AND THERMAL INJURY 16 Miscellaneous Burns and Cold Injuries — 12 complications of toxic epidermal necrolysis (Lyell’s 120. Clennett S, Hosking G: Management of toxic epi- 126. Palmieri TL, Greenhalgh DG, Saffle JR, et al: A disease): clinical and histopathologic study. dermal necrolysis in a 15-year-old girl. J Wound multicenter review of toxic epidermal necrolysis Ophthalmologica 195:1, 1987 Care 12:151, 2003 treated in U.S. burn centers at the end of the twen- 115. Masia M, Gutierrez F, Jimeno A, et al: Fulminant 121. Arevalo JM, Lorente JA: Skin coverage with Bio- tieth century. J Burn Care Rehabil 23:87, 2002 hepatitis and fatal toxic epidermal necrolysis (Lyell brane biomaterial for the treatment of patients 127. Rzany B, Schmitt H, Schopf E: Toxic epidermal disease) coincident with clarithromycin adminis- with toxic epidermal necrolysis. J Burn Care necrolysis in patients receiving glucocorticos- tration in an alcoholic patient receiving disulfiram Rehabil 20:406, 1999 teroids. Acta Derm Venereol 71:171, 1991 therapy. Arch Intern Med 162:474, 2002 122. Al-Qattan MM:Toxic epidermal necrolysis: a review 128. Halebian PH, Corder VJ, Madden MR, et al: 116. Heimbach DM, Engrav LH, Marvin JA, et al: and report of the successful use of Biobrane for early Improved burn center survival of patients with Toxic epidermal necrolysis: a step forward in treat- wound coverage. Ann Plast Surg 36:224, 1996 toxic epidermal necrolysis managed without corti- ment [published erratum appears in JAMA 123. Bradley T, Brown RE, Kucan JO, et al: Toxic epi- costeroids. Ann Surg 204:503, 1986 258:1894, 1987]. JAMA 257:2171, 1987 dermal necrolysis: a review and report of the suc- 129. Nenot JC: Medical and surgical management for 117. Sheridan RL,Weber JM, Schulz JT, et al: Manage- cessful use of Biobrane for early wound coverage. localized radiation injuries. Int J Radiat Biol 57: ment of severe toxic epidermal necrolysis in chil- Ann Plast Surg 35:124, 1995 783, 1990 dren. J Burn Care Rehabil 20:497, 1999 124. Kucan JO: Use of Biobrane in the treatment of 130. Gus’kova AK, Baranov AE, Barabanova AV, et al: 118. Yarbrough DR 3rd: Treatment of toxic epidermal toxic epidermal necrolysis. J Burn Care Rehabil [The diagnosis, clinical picture and treatment of necrolysis in a burn center. J S C Med Assoc 93: 16(3 pt 1):324, 1995 acute radiation sickness in the victims of the 347, 1997 125. Power WJ, Ghoraishi M, Merayo-Lloves J, et al: Chernobyl Atomic Electric Power Station. II. 119. Imahara SD, Holmes JHt, Heimbach DM, et al: Analysis of the acute ophthalmic manifestations of Non-bone marrow syndromes of radiation lesions SCORTEN overestimates mortality in the setting the erythema multiforme/Stevens-Johnson syn- and their treatment]. Ter Arkh 61:99, 1989 of a standardized treatment protocol. J Burn Care drome/toxic epidermal necrolysis disease spec- 131. Iijima S: Pathology of atomic bomb casualties. Res 27:270, 2006 trum. Ophthalmology 102:1669, 1995 Acta Pathol Jpn 32(suppl 2):237, 1982