Burns-1.pptx prestigious company and the winter

singhtanmay120 185 views 43 slides Aug 31, 2025
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About This Presentation

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Slide Content

MODERATOR DR VIPIN KUMAR PROFESSOR DEPT OF GENERAL SURGERY BURNS BY DR NEELOTPAL SINGODIA JUNIOR RESIDENT 1 DEPT OF GENERAL SURGERY

BACKGROUND Burn injury historically carried a poor prognosis. With advances in fluid resuscitation and the advent of early excision of the burn wound, survival has become an expectation even for patients with severe burns. Continued improvements in critical care and progress in skin bioengineering herald a future in which functional and psychologic outcomes are equally important as survival alone. With this shift in priority, the American Burn Association (ABA) has emphasized referral to specialized burn centers after early stabilization. Specific criteria should guide transfer of patients with more complex injuries or other medical needs to a burn center.

The ABA has published standards of care and created a verification process to ensure that burn centre’s meet those standards. Because of increased prehospital, safety measures, burn patients are transferred longer distances for definitive care at regional burn centres. Data from one burn center with a particularly wide catchment area confirmed that even transport times averaging several hours did not affect the long term outcomes of burn patients.

Assessing depth from the history The first indication of burn depth comes from the history. The burning of human skin is temperature and time dependent. It takes 6 hours for skin maintained at 44°C to suffer irreversible changes, but a surface temperature of 70°C for 1 second is all that is needed to produce epidermal destruction. Taking an example of hot water at 65°C: exposure for 45 seconds will produce a full-thickness burn; for 15 seconds a deep partial-thickness burn; and for 7 seconds a superficial partial-thickness burn (Figure 46.3).

Superficial partial-thickness burns The damage in these burns goes no deeper than the papillary dermis. The clinical features are blistering and/or loss of the epidermis. The underlying dermis is pink and moist and will exudate fluid for up to 36 hours post burn injury. The capillary return is clearly visible when blanched. There is little or no fxed capillary staining. Pinprick sensation is normal. Superficial partial-thickness burns heal without residual scarring in 2 weeks (Figure 46.4). The treatment is supportive.

Deep partial-thickness burn These burns involve damage to the deeper parts of the reticular dermis. Clinically, the epidermis is usually lost. The exposed dermis is not as moist as that in a superficial burn. There is often abundant fixed capillary staining, especially if examined after 48 hours. The colour does not blanch with pressure under the examiner’s finger. Sensation is reduced, and the patient is unable to distinguish sharp from blunt pressure when examined with a needle. Deep dermal burns take 3 weeks or more to heal without surgery and usually lead to hypertrophic scarring.

Full-thickness burns The whole of the dermis is destroyed in these burns. Clinically, they have a hard, leathery feel. The appearance can vary from that similar to the patient’s normal skin to charred black, depending upon the intensity of the heat. There is no capillary return. Often, thrombosed vessels can be seen under the skin. These burns are completely anaesthetic – a needle can be stuck deep into the dermis without any pain or bleeding.

THE PATHOPHYSIOLOGY OF BURN INJURY TO THE SKIN Burns cause a multisystem injury, but by far the most common organ affected is the skin. An understanding of the function and the structure of the skin is essential when assessing and treating a burn injury

INJURY TO THE AIRWAY AND LUNGS Burns can also damage the airway and lungs, with life-threatening consequences. Inhalation injury of hot, smoked-filled air has three components, each of which can present alone or in any combination. They are: upper airway injury, lower airway injury (true smoke inhalation) and metabolic poisoning. Airway injuries occur when the face and neck are burned; the significance of being trapped in an enclosed space (burning room or car) cannot be underestimated.

Metabolic poisoning Incomplete combustion of carbonaceous materials may produce carbon monoxide, and burning of nitrogen-containing polymers releases hydrogen cyanide. Carbon monoxide poisoning is the most common immediate cause of death from fire. It is an odourless, colourless gas that binds with erythrocyte haemoglobin approximately 250 times more avidly than oxygen. Carboxyhaemoglobin is inactive in oxygen transport and impairs oxygen delivery at the tissue level.

Additionally, it competes with, and inhibits, oxygen binding to cytochrome oxidase. This disrupts aerobic metabolism and decreases the capacity for cellular respiration. The treatment for carbon monoxide poisoning is early recognition and therapy with high flow, high concentration oxygen. Cyanide combines with trivalent iron in the mitochondrial cytochrome A3 complex, inhibiting electron transport and cellular respiration.

INFLAMMATION AND CIRCULATORY CHANGES The circulatory changes initiated by a burn injury are complex and multifactorial, originating from both the actual injury of burned skin (eschar) and the inflammatory cascade. It is governed by a complex series of events. The release of neuropeptides and the activation of complement are initiated by the stimulation of pain fibres and the alteration of proteins by heat. The activation of Hageman factor initiates a number of protease-driven cascades, altering the arachidonic acid, thrombin and kallikrein pathways. Fluid is lost from capillaries and oedema formation occurs.

OTHER LIFE-THREATENING EVENTS WITH MAJOR BURNS The inflammatory changes caused by the burn have an effect on the patient’s immune system. Cell-mediated immunity is significantly reduced in large burns, leaving them more susceptible to bacterial and fungal infections. There are many potential sources of infection, primarily from the burn wound and from the lung if this is injured, but also from any central venous lines, tracheostomies or urinary catheters present. The immune system and infection

Changes to the intestine The inflammatory stimulus and shock can cause microvascular damage and ischaemia to the gut mucosa. This reduces gut motility and can prevent the absorption of food. Failure of enteral feeding in a patient with a large burn is a life-threatening complication. This process also increases the translocation of gut bacteria, which can become an important source of infection in large burns. Gut mucosal swelling, gastric stasis and peritoneal oedema can also cause abdominal compartment syndrome, which splints the diaphragm and increases the airway pressures needed for respiration.

Danger to peripheral circulation In full-thickness burns, the collagen fibres are coagulated. The normal elasticity of the skin is lost. A circumferential full thickness burn to a limb acts as a tourniquet as the limb swells. If untreated, this will progress to limb-threatening ischaemia.

IMMEDIATE CARE OF THE BURN PATIENT Good prehospital care is essential in ensuring rapid assessment and transfer. The key principles are: Ensure rescuer safety. This is particularly important in the case of electrical and chemical injuries and building fires. Stop the burning process. Stop, drop and roll is a good method of extinguishing fre burning on a person. Check for other injuries . A standard ABC (airway– breathing–circulation) check followed by a rapid secondary survey will ensure that no other significant injuries are missed. Patients burned in explosions or even escaping from fire can have coexisting fractures or blast pattern injuries. Prehospital care

Cool the burn wound . This provides analgesia and slows the delayed microvascular damage that can occur after a burn injury. Cooling should occur for a minimum of 20 minutes and is effective up to 1 hour after the burn injury. It is a particularly important frst aid step in partial-thickness burns, especially scalds. In temperate climates, cooling should be at about 15°C – tepid water – and hypothermia must be avoided, particularly in the extremes of age. Give oxygen . Anyone involved in a fire in an enclosed space should receive oxygen, especially if there is an altered consciousness level. Elevate . Sitting a patient up with a burned airway may prove life-saving in the event of a delay in transfer to hospital care. Elevation of burned limbs will reduce swelling and discomfort. Analgesia . Administration of analgesia prior to or during transfer will subside pain.

Hospital care The principles of managing an acute burn injury follow the advanced trauma life support (ATLS) principles as per any major trauma: A, airway control; B, Breathing and ventilation C, Circulation D, disability – neurological status E, exposure with environmental control F, fluid resuscitation

The possibility of injury additional to the burn must be sought both clinically and from the history, and treated appropriately . The major determinants of severity of any burn injury are the percentage of total body surface area (TBSA) that is burned, the presence of an inhalation injury, the depth of the burn and the age/co-morbidities of the patient. Not all burned patients will need to be admitted to a burns unit, but the main criteria are given in the following table.

ASSESSMENT OF THE BURN WOUND The defining feature of any burn referral and usually the first question to seek clarification is ‘What is the size of the burn?’ From this simple question the burn team can establish the correct method of transfer and the resources needed to appropriately manage the patient with burn on arrival. Assessing size

The standard method of estimating burn size is to use percentage body surface area. As per the Emergency Management of Severe Burns (EMSB) the distal wrist crease to fingertips of an adult patient’s hand is approximately 1% TBSA (1.25%), due to the inherent error in measurement this is useful for small burns of up to 10% TBSA. An estimation of burn size (greater than 15% in an adult; 10% in extremes of age) will also determine whether fluid resuscitation is required.

A useful aide-memoire in the prehospital and emergency setting is the Wallace rule of nines. In this schematic each body part is assigned a burn percentage: each upper limb is 9%, head is 9%, lower limbs are 18% each, posterior torso and buttocks is 18% and the anterior torso 18% (chest 9% and abdomen 9%). The remaining 1% is assigned to the genitalia. The rule of nines has been in established clinical practice for 70 years but it is not without drawbacks.

In terms of accuracy there is a tendency to overestimate burn size, and in the obese patient the proportion of surface area of the arms and head decreases as the surface area of the torso and legs increase. A modification of 5% for the arms, 20% for the legs and 50% for the torso has been suggested but is not widely used. However, the rule of nines is an excellent means to quickly and reliably assess the size of a burn in an emergency setting, providing the clinician is aware of the limitations; it is not suitable for children under 10 years of age.

On arrival at a burns unit, the standard formatting for assessment and documentation is the Lund and Browder chart (Figure 46.2). Developed in 1942 following a mass casualty burn event at a nightclub in Boston, MA, USA, the chart is a schematic representation of the anterior and posterior body. It further subdivides body areas and allows for differentiation of burn depth by shading. The Lund and Browder chart can be completed at multiple points during a burn admission to document changes in burn size/depth and can also be used as an adjunct to surgical notes, when skin graft donor sites and grafted areas can be shaded.

In an increasingly digital era, it is worth noting the easy availability of burn management apps that are readily compatible with smart phones. These invariably involve shading a pictorial representation of the body, which then calculates a burn size. Additional features include adding age and weight to allow automatic estimation of fluid resuscitation requirements.

Burn size calculation: children The body proportions of children necessitate adjustment of the above-mentioned scales. An infant’s head is proportionally larger than an adult’s and this adjustment is represented on the modified Lund and Browder chart for children, where at birth the head represents 18% and the lower limbs 13.5% each. For each year 1% is subtracted from the head, with 0.5% being added to each lower limb until the age of 10, when the body proportions are roughly equivalent to those of an adult.

FLUID RESUSCITATION As the understanding of ‘fluid shifts’ developed, the introduction of fluid resuscitation guidelines greatly improved the survival rates for patients with large burns. Standard guidelines and formulae are taught to emergency department and first- responder personnel. Resuscitation fluid should commence from time of burn injury and any delay in commencement must be caught up.

Intravenous resuscitation is appropriate for any adult with a burn greater than 15% TBSA and any child with a burn greater than 10% TBSA. Extremes of age require extra care: for children, additional maintenance fluid is required; in the elderly, judicious monitoring is necessary owing to concurrent comorbidities and the inherent physiology of ageing. Depending on resources available, the commencement of intravenous fluid resuscitation approaches 30% TBSA in some countries. If oral resuscitation is necessary then additional salt solutions (such as Dioralyte) are required as hyponatraemia and water intoxication can be fatal.

There are three variables in the calculation of fluid requirements: the percentage of TBSA burned, the weight of the patient and the rate/type of fluid. Fluid loss is maximum in the first 8 hours and slows by 24–36 hours, by which stage normal fluid replacement is required. There are three main fuids used in the resuscitation stage: crystalloid (by far the most common), colloid and, in some centres, hypertonic saline. Each resuscitation fuid has advantages and disadvantages.

Crystalloid resuscitation Hartmann’s solution or Ringer’s lactate is the most commonly used crystalloid as it most closely replicates the osmolality of plasma. It is considerably less expensive than colloid and can maintain intravascular volume. The modified Parkland formula is the most commonly used: TBSA% burn × weight (kg) × 4 = volume in mL The first half is given in 8 hours and the second over 16 hours to complete the 24-hour resuscitation time frame.

In children maintenance fluid must also be given. This is normally dextrose–saline given as follows: 100 mL/kg for 24 hours for the frst 10 kg 50 mL/kg for the next 10 kg; 20 mL/kg for 24 hours for each kilogram over 20 kg bodyweight. Crystalloid resuscitation requires eight-fold greater vol- umes than colloid which can result in increased tissue oedema.

Hypertonic saline Hypertonic saline is used in some centres; it produces hyper- osmolality and hypernatraemia, resulting in a reduction in the shift of intracellular water to the extracellular space. Proponents of this resuscitation fluid cite advantages that include less tissue oedema and a resultant decrease in escharotomies and intubations. However, prolonged hypernatraemia without careful monitoring can be problematic and lead to renal dysfunction.

Colloid resuscitation The most commonly used colloid is human albumin solution. Plasma proteins are responsible for inward oncotic pressure that counteracts the outward capillary hydrostatic pressure. Albumin should be preferably administered after the first; 12 hours post burn as the massive fluid shifts drive proteins out of the cells. The most common colloid-based formula is the Muir and Barclay formula, which estimates the amount of fluid that needs to be infused during the first 36 hours post burn:

TREATMENT OF THE BURN WOUND Multitudes of topical therapies exist for the treatment of burn wounds, many of which contain antimicrobial properties. A recent Cochrane Database Review nicely summarizes the data surrounding antisepsis for burns; however, much of the data is inconclusive. Silver sulfadiazine is one of the most widely used in clinical practice. Silver sulfadiazine has a wide range of antimicrobial activity, primarily as prophylaxis against burn wound infections rather than treatment of existing infections. It has the added benefits of being inexpensive, being easily applied, and having soothing qualities. It is not significantly absorbed systemically and thus has minimal metabolic derangements. Silver sulfadiazine has a reputation for causing neutropenia, but this association is more likely due to neutrophil margination from the inflammatory response following burn injury.

True allergic reactions to the sulfa component of silver sulfadiazine are rare, and at-risk patients can have a small 257 test patch applied to identify a burning sensation or rash. Silver sulfadiazine destroys skin grafts and is contraindicated on burns or donor sites in proximity to newly grafted areas. Also, silver sulfadiazine may retard epithelial migration in healing partial- thickness wounds.

Mafenide acetate, either in cream or solution form, is an effective topical antimicrobial. It is effective even in the presence of eschar and can be used in both treating and preventing wound infections; the solution formulation is an excellent antimicrobial for fresh skin grafts. Use of mafenide acetate may be limited by pain with application to partial-thickness burns. As mafenide is a carbonic anhydrase inhibitor, a historically described side effect is metabolic acidosis. However, multiple studies have been performed using mafenide to treat burn wounds without any significant incidence of metabolic acidosis.

Silver nitrate has broad-spectrum antimicrobial activity as a topical solution. The solution used must be dilute (0.5%), and prolonged topical application leads to electrolyte extravasation with resulting hyponatremia. A rare complication is methemoglobinemia. Although inexpensive, silver nitrate solution causes black stains, and laundry costs may offset any fiscal benefit to the hospital. Although there is no definitive evidence regarding use in the burn population, Dakin’s solution (0.5% sodium hypochlorite solution) is an acceptable alternative as an inexpensive topical antimicrobial.

For smaller burns or larger burns that are nearly healed, topical ointments such as bacitracin, neomycin, and polymyxin B can be used. These are also useful for superficial partial- thickness facial burns as they can be applied and left open to air without dressing coverage. Meshed skin grafts in which the interstices are nearly closed are another indication for use of these agents, preferably with greasy gauze to help retain the ointment in the affected area. All three have been reported to cause nephrotoxicity and should be used sparingly in large burns. Recent media coverage of methicillin-resistant Staphylococcus aureus (MRSA) has led to widespread use by community practitioners of mupirocin for new burns. Unless the patient has known risk factors for MRSA, mupirocin should only be used in culture-positive burn wound infections to prevent emergence of further resistance.

Silver-impregnated dressings are increasingly being used for donor sites, skin grafts, and partial-thickness burns because of their potential to avoid daily dressing changes. These may be more comfortable for the patient, reduce the number of dressing changes, and shorten hospital length of stay, but they limit serial wound examinations. Biologic membranes such as Biobrane (Smith & Nephew Global Products) provide a prolonged barrier under which wounds may heal. Because of the occlusive nature of these dressings, these are typically used only on fresh, superficial, partial-thickness burns that are clearly not contaminated.

NUTRITION Nutritional support may be more important in patients with large burns than in any other patient population. Not only does adequate nutrition play a role in acute issues such as immune responsiveness, but the hypermetabolic response in burn injury may raise baseline metabolic rates by as much as 200%. This can lead to catabolism of muscle proteins and decreased lean body mass that may delay functional recovery. Early enteral feeding for patients with burns >20% TBSA is safe and may reduce loss of lean body mass, slow the hypermetabolic response and result in more efficient protein metabolism.

Early enteral feeds have also been associated with shorter duration of ICU stay and decreased rates of wound infection. If the enteral feeds are started within the first few hours after admission, gastric ileus may be avoided. Adjuncts such as metoclopramide promote gastrointestinal motility; if other measures for gastric feeding are unsuccessful, advancing the tube into the small bowel with nasojejunal feeding can be attempted. In endotracheally intubated patients, trips to the operating room do not necessitate holding enteral feedings. Immune-modulating supplements such as glutamine may decrease infectious com- plications in burn patients, although the effect on mortality and wound closure remains unknown. One proposed mechanism for glutamine’s immune modulating properties is via prevention of T-cell suppression in mesenteric lymph nodes.

There is currently a multicenter randomized control trial recruiting to determine the effect of glutamine on mortality, blood stream infections, and health-related quality of life. Micronutrient supplementation with antioxidant vitamins (vitamin E and ascorbic acid) and trace minerals (selenium, zinc, and copper) optimizes wound healing, enhances immune function, and fights oxidative stress.

Calculating the appropriate caloric needs of the burn patient can be challenging. A commonly used formula in non-burned patients is the Harris-Benedict equation, which calculates caloric needs using factors such as gender, age, height, and weight. This formula uses an activity factor for specific injuries, and for burns, the basal energy expenditure is multiplied by two. The Harris-Benedict equation may be inaccurate in burns of <40% TBSA, and in these patients, the Curreri formula may be more appropriate. This formula estimates caloric needs to be 25 kcal/kg per d plus 40 kcal/%TBSA. Indirect calorimetry can also be used to calculate resting energy expenditure, but in burn patients, a “metabolic cart” has not been documented to be more beneficial than the predictive equations. Titrating caloric needs closely is important because overfeeding patients will lead to storage of fat instead of muscle anabolism.

Modifying the hypermetabolic response is an area of intense study. β-Blocker use in pediatric patients decreases heart rate and resting energy expenditure and abrogates protein catabolism, even in long-term use. There may be benefits to β-blockade in adult patients, and many centers use β-blockers routinely in the adult population with limited safety and efficacy data. Some data suggests that β-blocker use in the adult burn population has a greater incidence of iatrogenic hypotension and bradycardia. As such, it is important to monitor hemodynamic status when starting β-blockers in these populations.

The anabolic steroid oxandrolone has been extensively studied in burn patients as well and has demonstrated improvements in lean body mass and bone density in severely burned children. The weight gain and functional improvements seen with oxandrolone may persist even after stopping administration of the drug. A double-blind, randomized study of oxandrolone showed decreased length of stay, improved hepatic protein synthesis, and no adverse effects on endocrine function, although the authors noted a rise in transaminases with unclear clinical significance. Oxandrolone therapy has also been associated with overall decreased mortality in patients with large burns.

Hyperglycemia has been associated with increased mortal- ity after burn injury,165 and intensive insulin therapy in critically ill patients has shown benefit, presumably from avoidance of hyperglycemia. However, in burn patients, the insulin itself may have a metabolic benefit, with improvements in lean body mass and amelioration of the inflammatory response to burn injury. Oral hypoglycemic agents such as metformin also help to avoid hyperglycemia and may contribute to prevention of muscle catabolism.

COMPLICATIONS IN BURN CARE There are several complications commonly associated with treatment of burn patients. Though not always avoidable, maintaining vigilance for typical complications and using appropriate techniques for prevention may limit the frequency and severity of complications. Ventilator-associated pneumonia, as in all critically ill patients, is a significant problem in burned patients. However, it is so common in patients with inhalation injury that a better nomenclature may be post injury pneumonia. Unfortunately, commonly used scores in critical illness such as the Clinical Pulmonary Infection Score (CPIS) have not been shown to be reliable in burn patients. Quantitative bronchoscopic cultures in the setting of clinical suspicion of pneumonia should guide treatment of pneumonia.

Simple measures such as elevating the head of the bed and maintaining excel- lent oral hygiene and pulmonary toilet are recommended to help decrease the risk of post injury pneumonia. There is some question as to whether early tracheostomy decreases infectious morbidity in burn patients and whether it improves long-term outcomes. There do not seem to be any major differences in the rates of pneumonia with early tracheostomy, though there may be reduced development of subglottic stenosis compared with prolonged endotracheal intubation. Practical considerations such as protection of facial skin grafts may influence the decision for tracheostomy placement. One major consideration in deciding whether to perform a tracheostomy has been the presence of eschar at the insertion site, which complicates tracheostomy site care and increases the risk of airway infection. Bedside percutaneous dilatational tracheostomy is a facile method for performing tracheostomy and is reported to be as safe as open tracheostomy in the burn population.

Massive resuscitation of burned patients may lead to an abdominal compartment syndrome characterized by increased airway pressures with hypoventilation and decreased urine output and hemodynamic compromise. Decompressive laparotomy is the standard of care for refractory abdominal compartment syndrome but carries an especially poor prognosis in burn patients. Adjunctive measures such as minimizing fluid, performing torso escharotomies, decreasing tidal volumes, and chemical paralysis should be initiated before resorting to decompressive laparotomy. Patients undergoing massive resuscitation also develop elevated intraocular pressures and may require lateral canthotomy.

Deep vein thrombosis (DVT) and prophylaxis in the burn population has received increasing attention in the literature recently. Up to 25% of burn patients develop DVT, and fatal pulmonary emboli have been reported in burn patients. A recent prospective trial demonstrated an 8% incidence of DVT in patients with 30% to 60% TBSA burns not receiving low molecular weight heparin prophylaxis with no evidence of DVT in patients receiving prophylaxis. There were no complications from low molecular weight heparin prophylaxis. Thus, it appears that heparin prophylaxis is safe in burn patients and may help prevent thrombotic complications.

Unfortunately, the use of both prophylactic and therapeutic heparin may be associated with heparin-associated thrombocytopenia (HIT). One study of HIT in burn patients showed an incidence of 1.6% in heparinized burn patients. Thrombotic complications included DVT, pulmonary embolus, and even arterial thrombosis requiring limb amputation. Nonheparin anticoagulation for HIT commonly caused bleeding complications requiring transfusion. Although rare, a high index of suspicion for HIT should be maintained in thrombocytopenic burn patients, particularly if the platelet counts drop at hospital days 7 to 10.

SURGERIES Full-thickness burns with a rigid eschar can form a tourniquet effect as the edema progresses, leading to compromised venous outflow and eventually arterial inflow. The resulting compartment syndrome is most common in circumferential extremity burns, but abdominal and thoracic compartment syndromes also occur. Warning signs of impending compartment syndrome may include paresthesias, pain, decreased capillary refill, and progression to loss of distal pulses; in an intubated patient, the surgeon should anticipate the compartment syndrome and perform frequent neurovascular evaluations. Abdominal compartment syndrome should be suspected with decreased urine output, increased ventilator airway pressures, and hypotension. Hypoventilation, increased airway pressures, and hypotension may also characterize thoracic compartment syndrome.

Escharotomies are rarely needed within the first 8 hours following injury and should not be performed unless indicated because of the terrible aesthetic sequelae. When indicated, they are usually performed at the bedside, preferably with electrocautery to minimize blood loss. Extremity incisions are made on the lateral and medial aspects of the limbs in an anatomic position and may extend onto thenar and hypothenar eminences of the hand. Digital escharotomies do not usually result in any meaningful salvage of functional tissue and are not recommended. Inadequate perfusion despite proper escharotomies may indicate the need for fasciotomy, but this procedure should not be routinely performed as part of the eschar release. Thoracic escharotomies should be placed along the anterior axillary lines with bilateral subcostal and subclavicular extensions. Extension of the anterior axillary incisions down the lateral abdomen typically will allow adequate release of abdominal eschar.

The strategy of early excision and grafting in burned patients revolutionized survival outcomes in burn care. Not only did it improve mortality, but early excision also decreased reconstruction surgery, hospital length of stay, and costs of care. Once the initial resuscitation is complete and the patient is hemodynamically stable, attention should be turned to excising the burn wound. Burn excision and wound coverage should ideally start within the first several days, and in larger burns, serial excisions can be performed as patient condition allows. Excision is performed with repeated tangential slices using a Watson or Goulian blade until viable, diffusely bleeding tissue remains. It is appropriate to leave healthy dermis, which will appear white with punctate areas of bleeding. Excision to fat or fascia may be necessary in deeper burns.

The downside of tangential excision is a high blood loss, though this may be ameliorated using techniques such as instillation of an epinephrine tumescence solution underneath the burn. Pneumatic tourniquets are helpful in extremity burns, and compresses soaked in a dilute epinephrine solution are necessary adjuncts after excision. A fibrinogen and thrombin spray sealant also has beneficial effects on both hemostasis and graft adherence to the wound bed. The use of these techniques has markedly decreased the number of blood trans- fusions given during burn surgery.

For patients with clearly deep burns and concern for excessive blood loss, fascial excision may be employed. In this technique, electrocautery is used to excise the burned tissue and the underlying subcutaneous tissue down to muscle fascia. This technique markedly decreases blood loss but results in a cosmetically inferior appearance due to the loss of subcutaneous tissue. For excision of burns in difficult anatomic areas, such as the face, eyelids, or hands, a pressurized water dissector may offer more precision but is time consuming, has a steep learning curve, and is expensive.

LATE COMPLICATIONS Once patients have recovered from their acute burns, many face management of the hypertrophic burn scars. In patients with healed burns or donor sites, hypertrophic scar-related morbidity includes pruritus, erythema, pain, thickened tight skin, and even contractures. Within these scars, there is believed to be an increased inflammatory response, irregular neovascularization, aberrant cytokine and Toll-like receptor expression, abundant collagen production, and abnormal extracellular matrix structure. Treatment for these scars has included nonsurgical therapies such as compression garments, silicone gel sheeting, massage, physical therapy, and corticosteroid. Surgical excision and scar revision represent more invasive scar management approaches that are often necessary for functional and aesthetic recovery. HYPERTROPHIC SCAR, CONTRACTURES AND HETEROTOPIC OSSIFICATION

Laser-based therapies provide additional treatment options for symptomatic hypertrophic scars. Two of the most common ones are the pulsed dye laser (PDL) and the ablative carbon dioxide (CO2) laser. The PDL causes photothermolysis of hemoglobin, resulting in coagulative necrosis. It obliterates small capillaries close to the skin and has had success treating congenital, cutaneous vascular malformations. The CO2 laser has been used for treatment of acne and recently has been gain- ing acceptance for its use to treat hypertrophic burn scars. It works by ablating microscopic columns of tissue to flatten scars and is also believed to stimulate matrix metalloproteinases and other signaling pathways to induce collagen reorganization. Lasers are ultimately believed to help with scar remodeling and collagen reorganization.

CO2 laser therapy has been shown to decrease symptoms associated with hypertrophic scarring, including scar appearance, pliability, contracture, neuropathic pain, and pruritus. A recent prospective study utilizing PDL and CO2 laser therapy demonstrated improved signs and symptoms of hypertrophic scars based on the Vancouver Scar Scale and the University of North Carolina 4P Scar Scale. Outpatient and office-based treatment sessions are tolerated well by most patients. There is wide practice variation on when to start therapy and the number of treatments, but the literature has general support for starting treatment at 6 to 12 months and offering three treatments. More research is needed to determine the full potential of laser therapy to provide burn survivors a less invasive treatment of hypertrophic scars with improved symptoms and quality of life.

Contractures are another long-term complication of burn injury that can result in significant morbidity. Contractures result from both wound contracture and scar contracture and prevents range of motion of a particular joint. Factors influencing contracture development include burn depth and activation of dermal fibroblasts, myofibroblasts, fibrocytes, and helper T cells. Treatment of contractures includes both nonsurgical and surgical options, ranging from pressure garments and splints to laser therapy and contracture excision.

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