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TABLE. Immersion time to produce full-thickness burns Time Temperature (°F) 1 second 158 2 seconds 150 10 seconds 140 30 seconds 130 1 minute 127
TABLE. Immersion time to produce full-thickness burns • Time Temperature (°F) • 1 second 158 • 2 seconds 150 • 10 seconds 140 • 30 seconds 130 • 1 minute 127 • 10 minutes 120
Causes • Scalds % 72 • Fires • 85% of burn mortality • Chemical • Electrical high tension >1000V • Scalds % 72 • Firesflame • 85% of burn mortality • Chemical • Electrical high tension >1000V Low tension <1000V Low tension <1000V
Pathophysiology • Cell damage and death causes vasoactive mediator release:Histamine, thromboxane, cytokine • Increasing capillary permeability causes edema, third spacing and dehydration • Possible obstruction to circulation (compartment syndrome) and/or airway
First degree Red, erythematous Very sensitive to touch Very painful .Usually moist No blisters Surface markedly and widely blanches to light pressure Second degree Erythematous or whitish with a fibrinous exudate Wound base is sensitive to touch Painful Commonly have blisters Surface may blanch to pressureThird degreeSurface may be: White and pliable Black, charred, and leathery Pale and mistaken for normal skin Bright red from hemoglobin fixed in the subdermisGenerally anesthetic or hypoestheticSubdermal vessels do not blanchNo blisters .Hair easily pulled from its follicleFourth degreeInvolves deep tissues including fascia, muscle, bone, and tendons
Zones of BURN • ZONE 1: Coaggulation Zone 2: Ischemia Zone 3: Errythemia
Burn extent • The overall extent of the burn injury is best estimated by recording the affected areas on a burn diagram and estimating the percentage of the body surface area using the 'rules of nines' in the adult or using the Lund–Browder chart in children. Special consideration is necessary in children, in whom the head forms a much greater percentage and the lower extremities a lower percentage of the total body surface area than in adults.
Management • Airway • Any respiratory complications consider PICU • Most swelling occurs in first 24 hours to 3 days • Oxygen for all burn patients • Clinical signs to watch for: • Hoarseness, stridor, cough, and visible redness of pharynx • Overt respiratory distress or hypoxia • Consider early intubation for thermal injury to airway, face and neck, inhalation injury and central nervous system (CNS) dysfunction • For intubation use Vecuronium (no Succinylcholine due to possible high K+) • Children burnt in confined spaces may suffer carbon monoxide poisoning • Loss of consciousness, confusion or disorientation are likely signs • Give high concentration oxygen even if SaO2 is high (Carbon monoxide will bind with the hemoglobin causing a false SaO2 reading) • Consider carboxyhemoglobulin level • Consider hyperbaric oxygen
Fluid resuscitation and maintenance • Two large bore IV’s (might need to be sutured),start with forearm veins ,intraosseous catheter may be needed in children. • Bolus with normal saline (NS) or lactated ringers (LR) to restore perfusion • Blood pressure might be high due to high systemic vascular resistance (SVR) but perfusion poor • LR most often used because it has physiologic concentrations of Na+, K+, CL- & HCO3- • Albumin in the first 12 to 24 hours may leak into the interstitium and can worsen tissue edema • Goal is to normalize vital signs and maintain end organ perfusion thus improving capillary refill and urine output • First degree burns: use normal maintenance formula (tissue and fluid losses are minor) • Second and Third degree burns use Parkland Formula: • LR 4cc/Kg x % burned over 24hrs plus maintenance • Give half of the volume in 8 hours • Important: clock starts when burned occurred • Give second half in 16 hours
Other Brooke :colliod 0.5ml Xkg X% crystaliod 1.5ml Xkg X % + 5%D 2000ml/m2 Modefied Brooke crystaliod 2ml Xkg X % Evans :colliod 1ml Xkg X% crystaliod 1ml Xkg X% Monafo :250meq Na 150meq lactate 100meq Cl titer to UOP
Foley placement • Normal urine output > 1cc/kg • Teenagers > 30cc/hr • If urine output is low – increase fluids • Pain control • IV use of morphine, fentanyl or ketamine • IM route not well absorbed • Wound control • Clean with sterile normal saline or sterile water and cover with non-adherent dressing • Asses neurovascular status of circumferential burns • Chest, limbs, fingers/toes • Keep patient warm • Cover with warm blankets • No ice packs- hypothermia causes more tissue injury
Chest X-ray • I-Stat on transport • Electrolytes, BUN, Creatinine • Low K+ needs to be supplemented • In compartment syndrome or excessive tissue burn: Rhabdomyolysis (skeletal muscle decompostion) can occur causing a high K+, Phosphorus and CPK; low Ph and Ca+ are common • NaHCo3 1meq/kg will reduce the Serum K+ and damage to kidneys • CaCl 10mg/kg will stabilize cardiac cell membrane and lower phosphorus • Tetanus boostershould be given if tetanus is incomplete or if > 5 years have elapsed since last given • Transport to a Burn Center (UCSD
Burn centers referral criteria • Second and third degree burns >10% body surface area (BSA) in patients <10 or >50 years old. • Second and third degree burns >20% BSA in other groups. • Second and third degree burns with serious threat of functional or cosmetic impairment that involve face, hands, feet, genitalia, perineum, and major joints. • Third-degree burns >five% BSA in any age group. • Electrical burns, including lightening injury. • Chemical burns with serious threat of functional or cosmetic impairment. • Inhalation injury with burn injury. • Circumferential burns with burn injury. • Burn injury in patients with pre-existing medical disorders that could complicate management, prolong recovery, or affect mortality. • Any burn patient with concomitant trauma (for example fractures) in which the burn injury poses the greatest risk of morbidity or morality. However , if the trauma poses the greater immediate risk, the patient may be treated in a trauma center initially until stable, before being transferred to a burn center. Physician judgement will be necessary in such situations, and should be in concert with the regional medical control plan and triage protocols. • Hospital without qualified personnel or equipment for the care of children should Thermal injury suggested fluid resuscitation (modified Parkland formula
Inhalation injury • Pulmonary problems are a major source of morbidity and mortality in the burn patient. To help clarify this process, the burn injury can be divided into the following phases. 1) The Resuscitation Phase, 2) The Early Post Resuscitation Phase and the 3) Inflammation, Infection or Hypermetabolic Phase. The pulmonary problems specific to each phase will be discussed
I) Resuscitation Phase (0-48 hrs) • Smoke Inhalation Injury ComplexPulmonary insufficiency caused by the inhalation of heat and smoke is the major cause of mortality in the fire-injured person, accounting for more than 50% of fire-related deaths. The magnitude of the problem has been much better appreciated in recent years. The use of many new synthetics in home furnishings and clothing have resulted in a much more complex form of injury, due to the extremely toxic combustion products of these advances in technology. A closed space fire can result in a severe hypoxic insult as well as lung damage from the inhalation of the toxic fumes. The exposure time, the concentration of fumes, the elements release, and the degree of concomitant body burn are critical variables. These factors cause a very complex injury with morbidity and mortality risks, especially when combined with a body burn. Improved knowledge of the pathophysiology combined with an aggressive treatment plan has made it possible to improve the outcome.
a) Carbon Monoxide Toxicityb) Upper Airway Injury from Smoke Exposurec) Chemical Burn to Upper and Lower Airwaysd) Restrictive Chest Wall Burn
II) Post-Resuscitation Period (2-6 days)This period is often the calm before the storm of the hypermetabolic catabolic state. However, during this period a number of major pulmonary problems can occur, especially the progression of a severe inhalation injury to respiratory dysfunction. The most common disorders are described below.
A. Continued Upper Airway InjuryB. Decreased Chest Wall ComplianceC. Tracheobronchitis from inhalation injuryd) Pulmonary Edema (High Pressure )
III. Pulmonary problems in the inflammation-infection phase (7 days to wound closure) • A) Nosocomial pneumoniaB) Hypermetabolism Induced Respiratory Dysfunction (Power Failure) C) Adult Respiratory Distress Syndrome (Low Pressure Pulmonary Edema)
Adult Respiratory Distress Syndrome • The lung damage is the result of a systemic process initiated by burn tissue, infection or inflammation rather than a direct lung injury. Phase One on the first, or initialphase dyspnea and tachypnea Phase Two Hypoxemia is now evident, along with continuing dyspnea.Phase Three acute respiratory failure Phase Four progressive pulmonary fibrosis and recurrent pneumonias
TreatmentMortality rate of ARDS caused by burn inflammation and infection is extremely high. The major reason for the lethal nature of the process is that resolution will not occur until the initiating process is removed: the wound especially in the large burn, cannot be readily excised and closed at this stage of the post burn process. The most important early treatment is prevention, i.e., early removal of as much of the potential source of the systemic inflammatory response as is feasible. A variety of new low pressure ventilation systems are available for management, which appear to be effective.
Escharotomies and fasciotomies • Edema may develop underneath circumferential burns of extremities and compromise the arterial circulation to the more distal aspects. Early after the injury, the adequacy of the peripheral circulation can usually be assessed by palpation of the peripheral pulses, but these pulses frequently become impossible to identify as edema develops under a circumferential eschar
Increased compartment pressures can completely obstruct arterial inflow, leading to distal ischemia, necrosis, and gangrene. Signs and symptoms of peripheral ischemia can be difficult to identify in patients with large burns, who are often intubated, receiving narcotics, and have peripheral edema due to administration of resuscitation fluid. The classic signs and symptoms of peripheral ischemia (pain, paraesthesias, pallor, pulselessness, and paralysis) may therefore be masked, and Doppler ultrasonography is the only reliable method for its early detection. When vascular compromise occurs, escharotomies (incisions made through burned epidermis and dermis) are necessary to restore both arterial and venous circulation
Nutritional support • Protein should be infused at a rate of 1.5 to 2.5 g/kg per day, depending on the size of injury and the presence of sepsis. This rate will maintain a positive nitrogen balance in adults and in children, but neither the exact protein requirements nor the optimal mixture of amino acids required by seriously injured patients are known. Unfortunately, studies of nitrogen balance do not produce the exact information necessary to determine the quantity and composition of the proteins required. Until rates of synthesis of muscle protein, collagen components of host defense, and other proteins can be accurately measured in vivo, this protein-replacement rate remains only an estimate.
Calculating the caloric equivalent received by a seriously burned patient given glucose at 5 mg/kg per minute and protein at 2.5 g/kg per day shows that their caloric requirement (calculated as basal metabolic rate × 2) is not achieved. Fats are therefore given to meet the remaining caloric requirement, via either the enteral or parenteral routes
Wound care and infections • Infection of the burn wound is a major cause of complications and death in burn patients: the best approach to the problem is the prevention of wound infection. Infection is most likely to affect a large, open wound containing necrotic tissue; susceptibility is increased by the lowered host resistance that results from serious trauma, and this is more important than the virulence of most infecting bacteria in determining the seriousness of the infection. Decreased host resistance must be corrected or prevented. Necrotic tissue must be removed and wounds properly closed. Secondary derangements in physiology and metabolism leading to caloric and protein starvation must be corrected. Cross-contamination of wounds must be prevented, and antibiotic treatment to prevent invasive infections should be administered only at times of increased
The goals for therapy are to • 1. Delay colonization of the wound. • 2. Keep the wound bacterial density lower than would otherwise occur 3. Keep the wound flora more homogeneous and less diverse than without therapy
Prophylactic antibiotics may be useful against the high incidence of bacteremia that occurs during and after excision of colonized burn eschar. Treatment should begin immediately before the operation and last through the immediate postoperative period, until normal cardiovascular hemodynamics are restored (usually within 24 h) and other normal physiologic signs return. The perioperative antibiotic given should be chosen on the results of previous cultures from the burn wound and the sensitivities of the organisms. If these are unavailable, general antimicrobial coverage for both Gram-positive cocci and Gram-negative rods is recommended. Intravenous antibiotics should be directed toward the commonly encountered Staphylococcus aureus, Pseudomonas aeruginosa, E. coli, Enterobacter, Klebsiella, Acinetobacter, and Proteus spp. Serum concentrations of both vancomycin and aminoglycoside should be measured when these antibiotics are used perioperatively but continued for more than 48 to 72 h.
The risk of death for a burn patient without a significant inhalation injury is highest from systemic sepsis. There are many dose-related factors that make the burn patient highly susceptible to the development of invasive sepsis. First is the burn wound itself, representing a major compromise in the body’s defense mechanism. The burn wound, in addition to being locally susceptible to infection, is associated with dose-related immunosuppression of the specific and nonspecific immune systems. Further, because these patients are often critically ill, they are subjected to a variety of invasive devices that bypass normal defense mechanisms; these devices include endotracheal tubes, bladder catheters, and arterial or venous intravascular catheters. Depending on other associated injuries, devices such as chest tubes, intracranial pressure monitors, and pulmonary artery catheters may be present for extended periods.
Though the burn wound, especially when covered with necrotic eschar, is a common site of primary infection in the septic burn patient, other sites are common, including the upper and lower respiratory tracts, the urinary tract, and, less frequently, infections from osteomyelitis or suppurative phlebitis. By far the most common sites of primary infection in burn patients are the blood stream, the burn wound,
Silver sulfadiazine Broad antibacterial actionAD Fair penetration of eschar, Painless DIS.Occasional sulfonamide sensitivity (rash) Safety in pregnancy unknown Occasional leucopenia, which is reversible
Mafenide Excellent antibacterial action AD.Good eschar penetration DIS. Very painful(10%) sulfonamide sensitivity rash Common carbonic anhydrase inhibition leading to metabolic acidosis
Silver nitrate Universal antibacterial action AD.Effective for donor sites, newly-grafted areas, and burn wounds DIS.Poor penetration of eschar(0.5%) Leaches sodium and chloride, causing hyponatremia, or hypochloremic alkalosis Stains all it touches
Wound debridements and dressing changes Classical burn wound care has been performed in a Hubbard tank or some other immersion facility. This creates for the patient, a warm, pleasant, antigravity environment, where range of motion can be performed comfortably by physical and occupational therapists. Concern regarding potential cross-contamination has led many burn centers to shower patients on a cart rather than immerse them, especially patients with large, deep burn wounds. This procedure is somewhat more uncomfortable for the patient and must be done more quickly. There is a greater tendency towards hypothermia, even with a high ambient temperature in the tub room. There are advantages, however, in terms of infection control. Even intubated patients can be debrided and cleansed very adequately in this fashion.
Critically ill patients are still debrided and dressed in their beds, though this is done less frequently with increased use of the shower cart. We still use tubbing for smaller wounds and in preparing patients to take care of their wounds after discharge. Initially, dressings must be bulky in the presence of eschar to absorb the substantial exudate created. Post-grafting, after the graft is revascularized, a properly applied dressing will protect the fragile grafts until they gain strength. However, if dressings are too bulky, they may decrease range of motion.
Recognition&management of sepsis • There are many dose-related factors that make the burn patient highly susceptible to the development of invasive sepsis. First is the burn wound itself, representing a major compromise in the body’s defense mechanism. The burn wound, in addition to being locally susceptible to infection, is associated with dose-related immunosuppression of the specific and nonspecific immune systems. Further, because these patients are often critically ill, they are subjected to a variety of invasive devices that bypass normal defense mechanisms; these devices include endotracheal tubes, bladder catheters, and arterial or venous intravascular catheters. Depending on other associated injuries, devices such as chest tubes, intracranial pressure monitors, and pulmonary artery catheters may be present for extended periods. Though the burn wound, especially when covered with necrotic eschar, is a common site of primary infection in the septic burn patient, other sites are common, including the upper and lower respiratory tracts, the urinary tract, and, less frequently, infections from osteomyelitis or suppurative phlebitis. By far the most common sites of primary infection in burn patients are the blood stream, the burn wound, the lower respiratory tract, and the urinary tract.
Because of the immunocompromised state of these patients as well as their intense and long-lasting hypermetabolism, they do not exhibit the usual clinical parameters of infection found in other immunosuppressed populations (e.g., organ allograft recipients). Thus, the burn surgeon must be constantly aware of the clinical status of the patient and be alert for any subtle changes. These are often the first indicators of incipient sepsis.
The burn wound may change in appearance with the development of sepsis. It may exhibit softening of the eschar or surrounding cellulitis, purulent material may begin to issue from the wound, or once-healthy granulation tissue may begin to deteriorate. Equally common, however, is the absence of change in wound appearance. Infection from the urinary or lower-respiratory tract is infrequently accompanied by symptoms in these ill patients. Thus, periodic culture surveillance is advisable to monitor the flora in these areas.
Careful serial clinical and laboratory monitoring of the patient is the most sensitive method of diagnosing sepsis before disastrous hemodynamic effects occur. We perform twice weekly eschar biopsies for quantitative culture, though their value is debatable. Wound colonization with >100,000 organisms/gram tissue is an indication to perform expedient eschar excision rather than to begin antibiotics. • Clinically, any change in the patient’s general status should lead to a high suspicion of sepsis. Possible changes include unexplained hypotension, tachypnea, spiking fevers above the patient’s daily baseline, tachycardia, new onset of ileus, altered mental status, thrombocytopenia, hyper- or hypoglycemia, hypoxia or hypothermia, and decreased urine output or progressive leukocytosis with “left shift,” including myelocytes and promyelocytes in the peripheral smear. The development of hypothermia and leukopenia are particularly ominous signs in the patient who is clinically becoming septic and demand aggressive intervention.
Pseudomonas aeruginosa and Staphylococcus aureus are the dominant pathogens in burn centers. This is a generalization only; it is more helpful for each burn center to know and monitor its own resident flora. Candida species are the most commonly isolated fungal organisms recovered from burn patients; other fungal infections are uncommon. Viral infections, particularly with cytomegalovirus, are reported with increasing frequency, though their clinical impact is undetermined. There is little place for prophylactic antibiotic usage in burn patients. Penicillin G used to be recommended for the first post burn week to prevent group A beta-hemolytic Streptococcal burn wound cellulitis. There is still arguably a place for this prophylaxis if topical antibiotics are not used (e.g., with Biobrane), but several studies suggest it is not necessary in addition to usual topical antibiotic treatment.
Fungal infections are an uncommon but difficult problem. It is our current practice to systemically treat burn patients with fungus found in two sites (i.e., sputum, intravenous catheter tip, urine or wound). This is most often Candida species and occurs two to three weeks postburn. We have aggressively treated these patients with systemic amphotericin B. This drug has a number of side effects. It has clearly decreased morbidity and mortality from fungal infections. Delaying treatment until fungemia occurs is associated with a high mortality rate. Other adjunctive measures may be necessary in the patient with life-threatening infection. Adequate fluid must be given to maintain intravascular volume and urine output. Invasive monitoring should be added as the clinical situation demands. Often a change in topical antibiotic or an increase in the frequency of wound care is added to the management of the burn patient with invasive infection and a large eschar burden. Certainly, if one topical agent has been used for a long period, a change to another may be of benefit. In particular, mafenide has a much greater ability to penetrate the burn wound than other topical agents. It should be strongly considered in the presence of invasive burn wound infection, keeping in mind its complications.
When sepsis is suspected, support of the cardiopulmonary and GI system should be of primary concern. Consideration should be given to eschar debridement, depending on the character of the burn wound. Empiric antibiotic therapy should be started after cultures are obtained. Depending on the resident flora of a particular burn center, some combination of agents to cover Staphylococcus aureus and gramnegative rods should be initiated. Aminoglycoside dosage requirements are difficult to predict in burn patients; individualized therapy is mandatory. Drug level monitoring is also advised for Vancomycin, which is used increasingly for methicillin-resistant Staphylococcus aureus. It is important to obtain culture results as soon as possible, including in vitro sensitivities. These may not correlate with in vivo behavior. Antibiotic therapy should then be targeted for the likely infecting organism(s). The use of new antibiotics or untested combinations of antibiotics is recommended only as part of an investigational study or with the assistance of a physician fully versed in their usage and complications.
Order of excision • In the absence of significant inhalation injury, it is rare for burns to cause significant infectious complications before the fifth through the tenth post burn day. In the presence of a large burn, the highest priority is to diminish the overall necrotic tissue load. Broad areas like the trunk and lower extremities are given priority for excision. Lower priority is given burns on the face and hands. They take more time to excise and cover with autograft. Delayed excision of hands can result in very acceptable function if accompanied by meticulous therapeutic assistance. • In a major burn, the posterior trunk should be given high priority as the first area to be excised. The patient is stable and will generally tolerate the prone position better than later in his course. The posterior trunk and buttocks are frequent sites of burn wound infection and are difficult to inspect and keep well debrided; the flat, broad area lends itself well to quick excision and grafting. Complete full-thickness burns of the back are quite rare, due to the thickness of the skin. We therefore recommend tangential excision for all but the most obvious full-thickness back burns (for which excision to fascia is only rarely indicated).
Tangantial excision • Excision of full-thickness eschar may be assisted by dressing the eschar with povidone-iodine foam 12 hours prior to operation. This dehydrates the eschar and makes it more physically amenable to tangential excision. A variety of dermatomes (manual and powered) may be used. Manual knives (e.g., Weck, Goulian) are especially advantageous for small, irregular surfaces, such as the hands and face, while a powered dermatome can be used to remove quickly uniform sheets of eschar from larger surfaces. Excision is continued until punctate uniform brisk bleeding is seen. If there is dermis left when this viable tissue level is reached, it will be white and shiny. Gray, dull appearing dermis is nonviable and will not support an immediately-placed skin graft. If the dermis is completely destroyed, tangential excision should be continued into the subcutaneous fat
Tangential excision can be performed under tourniquet control. The cadaveric appearance of the tissues distal to the inflated tourniquet makes differentiation of viable and nonviable tissues difficult, but with experience this can be appreciated. With concern about blood transfusions, this technique is increasing in popularity. Tangential excisions are bloody procedures, and adequate blood should be available. We routinely type and cross-match six units of packed red cells for major excisions of the trunk, four units for each lower extremity and four units for each upper extremity, including two units for hand excision alone (if tourniquets are not used). Without a tourniquet, the best method to limit blood loss is to work on only one area at a time, completing that area before proceeding. Extremities should be excised from distal to proximal so that hemostatic compressive dressings applied after excision do not produce a tourniquet effect.