Algorithm 12-1. Protocol for frostbite injury.
PHYSIOLOGY OF BURNS
Most patients with large burn or inhalation injuries will meet criteria for systemic inflammatory response syndrome (SIRS) (body temperature less than 36°C [96.8°F] or greater than 38°C [100.4°F], heart rate greater than 90 beats per minute, tachypnea greater than 20 breaths per minute, arterial partial pressure of carbon dioxide less than 4.3 kPa [32 mm Hg], blood leukocyte count less than 4,000 cells/mm3, or greater than 12,000 cells/mm3); or the presence of greater than 10% immature neutrophils (band forms). SIRS with infection is defined as sepsis and sepsis in addition to hypoperfusion is defined as “septic shock.” Burn shock does not equate to septic shock in the acute setting as true sepsis from a burn injury with subsequent infection usually does not occur until after the first 48 to 72 hours.
Burn shock is unique in the degree of vascular permeability coupled with increased hydrostatic pressure.26 This increased permeability is thought to result from the release of histamine from mast cells in burned skin following burn injury.27 Histamine interferes with the venous tight junctions and thereby allows efflux of fluid and proteins causing intravascular hypovolemia despite total volume hypervolemia.
Platelet activation products such as eicosanoids and serotonin also act to increase pulmonary vascular resistance and amplification of the vasoconstrictive effects of norepinephrine and angiotensin II.28 In addition to the increased vascular leak, platelet-activating factor and clotting factor dysregulation creates a hypercoagulable state with bleeding that resembles disseminated intravascular coagulation. This coagulation disorder is further amplified if patients become hypothermic during their resuscitation.29 Thus, patient temperature monitoring and maintenance is crucial during resuscitation.
Arachidonic acid metabolism products such as eicosanoids also play a role in burn edema. Eicosanoids increase prostaglandins such as PGE2 and prostacyclin which cause arterial dilation and increased blood flow and hydrostatic pressure in regions of injury resulting in increased edema.
Changes in cardiac output are also seen acutely in burn patients as these patients often have an increase in heart rate, and systemic vascular resistance but hypovolemia. Though not defined as “cardiogenic shock,” cardiac function is altered due to inflammatory mediators.30–33 With appropriate burn resuscitation, cardiac output should return to normal levels within 24 to 72 hours.
Metabolic Response to Burn Injury
Hypermetabolism is a physiologic response unique to burn injury. Hypermetabolism is characterized by increased body temperature, glycolysis, gluconeogenesis, proteolysis, lipolysis, and prolonged substrate cycling.34,35 The degree of the hypermetabolic response is proportional to the size of burn injury and appears to plateau at 70% TBSA. Overall the basal level of glucose is elevated despite a high insulin state which can complicate outcomes and exacerbate muscle catabolism.
Lipolysis also occurs at a rate that is higher than normal due to abnormal substrate cycling. This results in hepatic accumulation of triglycerides causing steatosis. Recent work to combat peripheral lipolysis has had some success using propranolol.36
Proteolysis is also increased in burn patients compared to nonburn patients. This is due to a combination of increased muscle breakdown and increased plasma protein production by the liver. Wound healing requires an increase in protein synthesis leading to the recommendation of enteral nutrition with elevated protein levels.
There are three ways to influence hypermetabolism: nutrition, medication, and surgery. Current protocols preferentially recommend continuous enteral nutrition with a high-carbohydrate diet consisting of 82% carbohydrate, 3% fat, and 15% protein. This diet is thought to stimulate protein synthesis, increase endogenous insulin production, and improve overall lean body mass when compared to standard formulas.35
Catecholamines are significantly elevated following a burn injury and are thought to play a role in the hypermetabolic response. This elevation is one reason why propranolol administration is thought to be helpful. Interestingly, growth hormone levels have been shown to be decreased in burn shock leading clinicians to supplement patients with the anabolic steroid oxandrolone in large burn injuries. Positive results to avoid or reduce the loss of muscle mass with oxandrolone have made its use standard in most burn units for large TBSA burn patients.37–44 With regard to thyroid hormone, total thyronine and thyroxin (T3 and T4) are reduced whereas reverse T3 is elevated. Burn injuries also cause alterations in diurnal glucocorticoid levels leading to persistent hypercortisolemia.
Surgery represents the last way to combat hypermetabolism as early debridement and grafting is the mainstay to mitigate the hypermetabolic syndrome.
Immunologic Response to Burn Injury
The immune system in burn patients demonstrates significant dysregulation that may explain increased risk of infection. Serum levels of IgA, IgG, and IgM are decreased indicating decreased B-cell function. T-cell function or cell-mediated immunity is also impaired which is why prolonged homograft and xenograft take is seen. Interleukin 2 (IL-2) production is also decreased whereas IL-10 is increased. Similar to other types of nonthermal trauma, burn patients also have elevated tumor necrosis factor alpha and IL-6. Polymorphonuclear neutrophils have impaired chemotaxis as well as decreased oxygen consumption and impaired bactericidal capabilities.
Initial care in the field and emergency room is similar to that of any trauma patient. The airway should be stabilized, IV access should be obtained, concomitant life-threatening injuries should be excluded, and escharotomies should be performed if there are any circumferential areas of full-thickness injury. Escharotomies should be placed on the lateral aspects of the extremities avoiding the sites of potential nerve and large vessel injury (Fig. 12-1). Escharotomies should be extended across the chest if there is full-thickness injuries and if difficult ventilation arises. Abdominal escharotomies can also help with ventilation.
Figure 12-1. Incision lines for escharotomies. In general incisions should be kept on the lateral aspect of extremities to avoid damage to neurovascular structures. (From Holzman RS, Mancuso TJ, Polaner DM, eds. A Practical Approach to Pediatric Anesthesia, 2e. Philadelphia, PA: Wolters Kluwer; 2016.)
Table 12-1 Burn Center Referral Criteria45
Guidelines from the American College of Surgeons Advanced Trauma Life Support and the ABA Advanced Burn Life Support programs have standardized the care of trauma patients and have improved overall patient outcomes. A complete history and physical should be performed with specific focus placed on the cause and timing of the injury, risk of smoke inhalation injury, concomitant injuries, and treatments including IV fluids received prior to patient arrival. The primary goal is to stabilize the patient, ensure standard injury assessment, and transfer to a burn center as necessary. The ABA has published criteria to follow regarding when to transfer a patient to a verified burn center (Table 12-1).
Primary survey assessment should begin with evaluation of the airway. Inhalation injuries occur in approximately 10% of all burn patients, but are present in 70% of those who eventually die of their burn injury.46 Thus, it is important to specifically note such findings as soon as the patient presents. Risk for inhalation injury can be first assessed by the history. In general, patients burned outside (not in an enclosed space) very rarely suffer inhalational injuries. If, however, the patient was in a burning home or a burning building, one’s suspicions should be raised. Close physical examination should note facial burns, changes in voice, shortness of breath, singed nasal vibrissae, carbonaceous sputum, and intraoral swelling. If these findings are present and the patient appears to be in distress, oral intubation should be performed immediately by an experienced airway physician. In addition to a laryngoscope, the trauma team should have a video laryngoscope available and a surgeon present in case a surgical airway is required. If the patient is not in extremis and the level of inhalation injury is unknown, nasoendoscopy or bronchoscopy should be performed to directly visualize the airway and vocal cords. If significant swelling exists and the patient is expected to receive large volume IV fluid resuscitation, the airway should be immediately secured. If a patient is transferred with an endotracheal tube that the accepting physician feels is no longer needed, a spontaneous breathing trial should be performed followed by direct laryngoscopy to assess for cord swelling and assessment for a cuff leak should be performed before removing the endotracheal tube.
Oxygenation in a burned patient may be altered by carbon monoxide (CO) poisoning. Physical examination findings include red lips and altered mental status. Formal diagnosis should be based on history and evidence of CO levels in the blood. CO binding is assessed by measuring the level of carboxyhemoglobin in a peripheral arterial blood gas sample. Symptoms of CO poisoning typically begin with headaches at levels around 10%, while CO in the blood becomes lethal at around 50% to 70%. The half-life of CO is normally 4 hours when breathing room air, however, half-life is shortened considerably with administration of supplemental oxygen. Treatment with 100% oxygen (FiO2 100%) reduces the half-life of CO to 30 to 90 minutes. Hyperbaric oxygen treatment can reduce the half-life of CO to 15 to 23 minutes. However, if the patient has additional burn injuries or is unstable, the patient should not be placed in a hyperbaric chamber. Also, the time needed to transfer patients to hyperbaric facilities and the subsequent difficulty of resuscitating a critically ill patient in a closed chamber make hyperbaric oxygen an impractical option. Prompt and aggressive evaluation and maintenance of the airway is the most important initial step in management of a burn patient.
It is important to have large bore IV access with 16- or 18G peripheral IVs. IV access catheters should preferentially be placed in nonburned areas of skin although this is not always possible. If the patient will require invasive hemodynamic monitoring, a central line should be placed under sterile conditions. Peripherally inserted central catheter (PICC) lines can be used in burn patients, however, their infection rate remains high. If a central line is used, this does not need to be changed out at a certain timepoint but rather should be monitored daily for signs of infection. Ideally, burn and critical care surgeons would have access to a minimally invasive monitor of cardiac output. Though several technologies exist including esophageal Dopplers, arterial waveform monitors, and thermodilution modalities, the trend of these values is more useful than the absolute values. If a PiCCO device (Pulsion Medical Systems AG, Munich, Germany) is used to monitor the patient, it is best to have the central venous line located in the internal jugular vein and the arterial line in the femoral artery. This technology uses thermodilution to determine cardiac performance. Studies have demonstrated efficacy of this technology when compared to use of a pulmonary artery catheter.47 Burn injury and soft tissue edema make noninvasive blood pressure measurement difficult and inaccurate, hence arterial line placement is frequently necessary.
The Parkland or Consensus formula is most commonly used to estimate fluid requirements for the first 24 hours and should be used to guide initial fluid infusion rates. This is a start point and should not be construed as a dogmatic prescription of the total fluid volume to be given during the first day after injury.48 It is extremely important to note that the original time of the injury is used in the calculation, not the time of initial presentation to care providers. Partial- and full-thickness burns are totaled to calculate burned TBSA.
Consensus formula: First 24-hour requirement= 2–4 cc × %TBSA × weight (kg)
Half of this fluid volume is planned to be administered in the first 8 hours after burn injury and the second half is administered over the next 16 hours. For example, if a 70-kg patient with 20% TBSA burn sustained at 10 AM presents 2 hours later, the crystalloid fluid to be administered in the first 8 hours is calculated using the following formula: ([4 cc × 20% × 70 kg]/2)/6 hours. Lactated Ringers crystalloid solution is recommended as the first choice fluid to avoid complications associated with metabolic acidosis.48 Currently data do not support hypertonic saline, dextran, or albumin during the first 24 hours of resuscitation in standard clinical situations.49,50 Studies have suggested that limited albumin usage may play a role in reducing the rate of abdominal compartment syndrome when the patient requires substantially more fluid administration than estimated by the Parkland formula (>1.5 times).51 Additionally, D5/LR is commonly used for maintenance of fluid in children under 1 year of age to avoid hypoglycemia. Once the Parkland formula is begun, the patient’s vital signs and urine output should be closely monitored and laboratory studies should be drawn frequently. Although such formulas exist, it is important to note that proper fluid resuscitation should be guided by overall clinical response and the trend of vital signs and laboratory values. IV fluid infusion rate should be increased or decreased based on the response of the patient on an hourly basis with fluid administration titrated to maintain urine output goals of 0.5 to 1 mL/kg/hr in adults and 1 to 1.5 mL/kg/hr in children. Blood pressure and heart rate should be monitored; burn patients are often tachycardic regardless of the degree of resuscitation. Though urine output is considered a “gold standard,” it often lags the fluid status and thus clinicians must be cautious not to reflexively increase fluids with low urine output but rather consider the entire clinical picture. In addition, close monitoring of the patient’s laboratories is necessary to determine the trend in organ perfusion. Laboratory values that help assess organ perfusion include lactate, base deficit, central venous O2, and/or pH. Although any one of these values alone does not provide a sensitive marker of the patient status, trending these values during resuscitation can help direct resuscitation adjustments if the current fluid rate is causing a positive trend. If the end organs are adequately perfused, decrease in lactate and base deficit as well as increase in central venous O2 and normalization of pH should be observed.
In the second 24 hours, all patients should receive crystalloid sufficient to maintain urine output and to maintain parameters of perfusion including lactate, pulse volume variation, and cardiac output. Infusion rate will often be at a maintenance rate plus adjustment for losses of fluid into the burn wound. Nutritional support should be started enterally within 24 hours. After 24 to 36 hours, providers can cut fluids by 1/3 if the patient continues to make adequate urine. One may decrease fluids again by 1/3 for hours 36 to 48 (assuming urine output does not drop off). Colloid can be given after initial crystalloid resuscitation (5% albumin at 0.3 to 0.5 mL/kg per %TBSA over 24 hours).
After 48 hours, fluid infusion rate should maintain urine output at 0.5 to 1 mL/kg body weight per hour. Insensible losses and hyperthermia are associated with hyperdynamic states and increase fluid requirements. Daily patient weights can be helpful to determine insensible fluid loss or retention.
Pediatric fluid resuscitation does have some differences with regard to fluid management. Due to the limited reserve in children under 20 kg, a glucose-based maintenance fluid is recommended. Additionally, fluid requirements may be as high as 6 mL/kg per TBSA and their urine output should be 1.0 to 1.5 mL/kg/hr.52 Since burn resuscitation should be considered in the setting of a 10% TBSA in children, transfer to a burn center is recommended.
Pulmonary status is also an indicator of fluid status but in a delayed fashion. Complications such as pulmonary edema result from fluid overload and necessitate daily evaluation of oxygen requirements and ventilator settings.
Difficult to Resuscitate Patients
If the fluid resuscitation required during the first 24 hours is 1.5 times greater than initially estimated, the physician should reassess the clinical picture. Giving excessive crystalloid fluids and failure to use appropriate early resuscitation adjuncts are associated with significantly worse outcomes. Physicians often will give additional fluid due to low urine output not realizing that the kidney, like other organs during burn shock, often lags behind the clinical picture. Specific complications associated with excessive resuscitation include compartment syndrome of both the extremities and the abdomen. Signs of abdominal compartment syndrome include abdominal distention, decreased urine output, elevated ventilator pressures, and desaturation. Surgeons should have a low threshold to assess for this devastating complication in any patient requiring resuscitation above the Parkland formula. Diagnosis can be made both by observing clinical signs as well as by assessment of bladder pressure transduced through a Foley catheter. Pressures over 20 mm Hg are considered abnormal and pressures greater than 25 mm Hg with evidence of organ failure indicate the urgent need for intervention. Strategies to intervene should begin with decreasing the rate of fluid administration. If the patient has full-thickness burns on the abdomen or torso, escharotomies should be performed. The bed should be reclined and a chemical paralytic can be given to relax the musculature. If elevated bladder pressures remain despite these maneuvers, a decompressive laparotomy is often required. Some surgeons will attempt decompression with a suprapubic peritoneal drainage catheter; however, the morbidity of these procedures is significant in burn patients. Therefore, attempts should be made to minimize fluid overload with early vigilant monitoring of fluid administration.
When patients are difficult to resuscitate, additional monitoring devices can be used including monitors of cardiac output and cardiac index. Examples include esophageal Doppler, bedside echo as well as transthoracic echo. Serial echo examinations after providing a fluid bolus allow monitoring of cardiac filling, IVC variation, and wall motion changes.53,54
Burns are considered tetanus-prone wounds and therefore tetanus status should be obtained upon presentation. Previous immunization within 5 years requires no treatment whereas immunization within 10 years requires a tetanus toxoid booster and unknown immunization requires both.
Thoracic escharotomy is rarely required, however, if a patient has early respiratory distress, this may be due to compromised ventilation caused by chest wall inelasticity. If chest wall compliance is limited due to eschar, thoracic escharotomies should be performed bilaterally in the anterior axillary lines with additional release under the costal margin. Extremity eschartomy can be limb or digit saving. Edema of the underlying tissue under the thick, stiff eschar can produce vascular compromise. Though Doppler and pulse oximeters can be used to follow perfusion, once perfusion is lost, it is often too late to intervene. Thus, patients with circumferential full thickness extremity burns should have an escharotomy as soon as their airway is stable and vascular access has been obtained. Extremity eschartomy should be carried out medially and laterally and should extend the entire area of the full thickness burns. Additional compartments to assess include the orbital compartment. Opthomology should be consulted in large volume fluid resuscitation to assess intra-ocular pressure. If abnormally elevated, a lateral canthotomy should be performed.
For full-thickness burns and partial-thickness burns, identifying the extent of the burn injury is crucial. TBSA is useful to guide fluid resuscitation administration and defines the overall prognosis of patients. Only partial- and full-thickness burns are totaled to calculate TBSA.
Figure 12-2. Rule of 9s used to estimate percent burns in adults (A), children (B), and infants (C). (From Stedman’s Medical Dictionary for the Health Professions and Nursing, Illustrated, 6e. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.)
If small areas in various distributions are affected, it may be easier to use the patient as a ruler with one palm size (patient’s) representing 1% TBSA. Another useful guide is the rule of 9s, where the adult body is partitioned into several areas that each constitutes 9% of the TBSA (Fig. 12-2). Regions on the adult that constitutes 9% of the TBSA include the head and arms, while the legs, anterior trunk, and posterior trunk account for 18% of TBSA each. In children and infants, the body surface area of the lower extremities constitutes a lower percentage while the head is higher. Careful estimation of TBSA is essential for proper early management of burn patients, as patients who have burns of more than 20% TBSA commonly require IV fluid resuscitation.
Acute burn injuries require prompt intervention and serial examinations. On initial evaluation, it is important to recognize and treat constrictive circumferential burns that can lead to tissue ischemia and subsequent necrosis by limiting perfusion to the distal tissues.46 The overarching concept, however, in acute burn care is early debridement and grafting. All blisters and nonviable tissue must be debrided upon presentation. After the initial debridement, dressing changes are initiated while the patient is stabilized from a systemic standpoint. If patients suffer from full-thickness or deep partial-thickness injuries, debridement and grafting within 72 hours should be the standard of care.
First degree or epidermal burns. These burns only involve the epidermis and therefore do not blister. They do, however, have erythema and can cause pain. These burns will often desquamate by days 4 to 5.
Superficial partial thickness (second degree). Superficial partial thickness burns include the upper layers of the dermis and usually form blisters at the interface of the epidermis and dermis. When the blisters are removed, the wound is pink and wet and often is the site if significant pain. The wound should blanch with pressure and the hair follicles should be visible. Assuming no infection sets in, these burns should heal on their own in 3 to 4 weeks. They can be treated with xenograft to decrease pain.
Deep partial thickness (second degree). Deep partial thickness burns extend into the deep or reticular dermis. These will also blister, but appear a “lobster” red. The patient often has some pain and there is slow to absent capillary refill with applied pressure. The wound is often dry and if hair is present, it is usually easily depilated. These burns usually require debridement and grafting.
Full thickness (third degree). Full thickness burns involve all layers of the dermis. These burns appear white, insensate, and without capillary refill. The skin may appear depressed and leathery compared to surrounding tissues. These burns require debridement and grafting as nondebrided eschar forms a nidus for infection and inflammation.
Fourth degree. Fourth degree is used to describe burn into the deeper subcutaneous structures such as muscle, fat, fascia, and bone. These are common in electrical burns and patients who were either unconscious or insensate.
CRITICAL CARE OF THE BURN PATIENT
Ideally, a critical care physician would be able to assess real time responses to fluid administration through accurate cardiac output readings. Unfortunately, no such noninvasive devices to directly assess cardiac output exist and those invasive devices that estimate cardiac output lack definitive studies supporting their use. Some centers use a PiCCO device which provides cardiac output based on temperature changes and use of the Fick equation, however, this requires a femoral arterial line and a large bore IJ or SVC catheter which introduce potential for complications. Some surgeons use pulse volume variation (>25% being abnormal), however, this too lacks accuracy. Though goal-directed therapies with a pulmonary artery catheter, esophageal Doppler, transesophageal echo, or CVP monitor have demonstrated promising results in some critical care populations, their use in burn patients has been mixed.55,56 Frequently, the output of monitors such as pulmonary artery catheters or CVP monitors fails to reflect the actual resuscitation of the patient.57,58
Treatment for Inhalational Injury
Manifestations of inhalation injury include wheezing and air hunger. Within a few hours, the tracheobronchial epilthelium slughs and hemorrhagic tracheobronchitis develops. In cases with thermal injury interstitial edema can cause acute respiratory distress syndrome (ARDS) and oxygenation difficulty. If inhalation injury is suspected, the patient should undergo urgent airway assessment and be placed on supplemental oxygen. Inhalation injury has three components that must be considered: (1) upper airway thermal injury which can cause swelling and obstruction, (2) CO poisoning, and (3) lower airway chemical injury from toxic agents found in smoke. Upper airway thermal injury is treated by intubation of the airway and CO poisoning is treated by 100% oxygen administration. Lower airway injury is diagnosed by evidence of soot or mucosal irritation on bronchoscopy. Airway mucosal injury from chemical pneumonitis leads to increased secretions while compromising the patient’s ability to clear those secretions. This leads to increased risk of mucous plugging. Airway mucosal sloughing can also result in bleeding and clot formation that further obstruct airways. The use of aerosolized heparin, albuterol, and Mucomyst (HAM) following smoke inhalation to promote airway clearance is advocated in some centers, however, larger studies are needed to validate these treatments.53,54,59–61
Early endotracheal intubation and mechanical ventilator support are important in patients with inhalation injury or in large TBSA burns expected to receive large volume resuscitation. Ventilator management should follow ARDSnet protocol recommendations.62,63 Low volume protective lung ventilation is used to avoid barotrauma: 4 to 6 mL/kg tidal volume, peak airway pressures should not exceed 30 cm H2O. Assess best positive end expiratory pressure (PEEP) to determine an optimal setting, but a PEEP of at least 5 should be used to avoid lung derecruitment. Consider esophageal monitor to aid in settings if the patient is obese. Recruitment maneuvers may be needed to improve oxygenation and/or ventilation. Permissive hypercapnia is preferred over large tidal volumes to avoid lung barotrauma. Limited studies have shown a potential role for high-frequency percussive ventilation in burn patients.64 Elevating the head of bed to 45 degrees helps decrease airway swelling, prevents aspiration and ventilator-associated pneumonia (VAP) for ventilated patients. Daily mouth care with chlorhexidine should be used for ventilated patients.
Pulmonary infection occurs in 30% to 50% of patients. Patients with three of the following five clinical criteria should be assessed for pneumonia with culture samples and placed on empiric antibiotic therapy; purulent sputum production, fever, elevated white blood cell count, infiltrate on chest radiograph, and increasing supplemental oxygen requirements. If the patient has pneumonia and been in the hospital for over 48 hours, he should be treated for hospital-acquired pneumonia. Sputum or a bronchoalveolar lavage samples should be sent for aerobic, anaerobic, and quantitative cultures. Empiric antibiotics including coverage of Pseudomonas sp. should be started until culture results become available. Empiric treatment should also cover methicillin resistant staphylococcus aureus and thus vancomycin or linezolid is preferred. If vancomycin is used, drug levels should be followed to adjust dosage and avoid renal toxicity.
Staphylococcus aureus and Streptococcus are common causes of early VAP. Pseudomonas aeruginosa is the most common cause of late VAP. The usual signs of pneumonia (fever, purulent sputum, or leukocytosis) are not helpful in burn patients since almost all patients are febrile, tachypneic, and have elevated white blood cell counts. The best diagnostic test is bronchoscopy-obtained bronchial alveolar lavage sample with quantification of bacteria. Bacterial counts of >103 colony forming units (CFU) are considered positive. ABA recommendations for length of VAP treatment are 8 days of antibiotic therapy for antibiotic-sensitive organisms and 15 days of therapy for multidrug-resistant organisms.65 Consideration should be given to antifungal therapy (Diflucan) if the patient does not respond to prolonged broad-spectrum antibiotics.
Electrolyte Abnormalities and Acute Renal Failure
The immediate effects of burn injury on kidney function are secondary to hypovolemia and circulating inflammatory mediators. The diuresis phase occurs at 48 to 72 hours after “third space” fluid is reabsorbed. Hyponatremia is often seen due to large volume resuscitation with hypotonic IV fluids and will usually self-correct. Open burn wounds or the use of topical silver nitrate can also cause hyponatremia. Renal hypoperfusion exacerbates hyponatremia by decreasing glomerular filtration. Hypernatremia may also occur due to insensible and evaporative water losses. Hypophosphatemia can result from dilution or refeeding syndrome. Hypocalcemia can result from use of silver nitrate.
Acute Kidney Injury
Risk factors include sepsis, large TBSA burns, organ failure, and antibiotic administration. Renal function is compromised by hypoperfusion, pharmacologic nephrotoxic insult, and sepsis which are all common following major burn injury. Physiologically there is a decrease in renal perfusion, glomerular filtration rate, and renal blood flow. The renal medulla is the most sensitive to hypoxia with damage to renal tubular cells. Patients present with oliguria and decreased creatinine clearance. Early renal failure often results from hypovolemia-induced ischemic injury. However, overresuscitation can also compromise renal perfusion by causing abdominal compartment syndrome. Late renal failure occurs after the fifth postburn day and is frequently caused by sepsis or nephrotoxic antibiotics. Continuous renal replacement therapy and pharmacologic treatments such as dopamine have not definitively been shown to improve outcomes.
The initial care of acute renal failure patients should focus on reversing underlying causes and correcting any fluid and electrolyte imbalances. The physician should ensure adequate volume status, avoid nephrotoxins, and dose medications appropriately.
Metabolic Response and Nutrition
Early nutrition is now the cornerstone of burn care. Tube feeding should begin soon after admission. Attempts to feed postpyloric should be done, however, gastric feeding is also acceptable. Tube feeds are often needed even in patients who are able to feed themselves due to the need to enable wound healing and keep up with the hypermetabolic response to burn injuries. Feedings can be continued during surgery as long as prone positioning is not planned.
The metabolic rate is significantly greater in burn patients than in other critically ill patients and leads to accelerated lean body mass wasting. Positive nitrogen balance is key to prevent skeletal muscle breakdown and highlights the importance of early nutritional support. The general composition of enteral feeding should include at least 60% calories from carbohydrates not exceeding 1,600 kcal/day, 12% to 15% from lipids and essential fatty acids, and 20% to 25% from protein. Failure to meet large energy and protein requirements can impair wound healing and alter end-organ function. Even though adequate nutrition is crucial, overfeeding must be avoided. A randomized, double-blind, prospective study demonstrated that aggressive high-calorie feeding with enteral and parenteral nutrition was associated with increased mortality.66 The daily caloric requirements can be calculated using the Curreri formula: ([25 kcal] [body wt kg]) + ( [% TBSA area burn]) 1 to 2 g/kg/day of protein for synthetic needs of the patient. Burn patients should receive a small proportion of calorie requirements from fat than other ICU patients. The liver in a burn patient produces less very low density lipoprotein causing hepatic triglyceride elevation. Increased fat leads to increased complications including fatty liver, infection, hyperlipidemia, hypoxia, and mortality. Decreased gastrointestinal absorption and increased urinary losses can also lead to deficiencies in vitamin C, E, zinc, iron and selenium. Burn patients, like a subset of trauma and gastrointestinal surgery patients have been shown to benefit from glutamine supplementation.
67 demonstrated that propranolol in acute burns in the pediatric population improved net muscle synthesis and increased lean body mass. Additionally, current standard of care includes providing pharmacologic agents such as oxandrolone (testosterone analog given 0.1 mg/kg q12h). Oxandrolone improves muscle synthetic activity, increases expression of muscle anabolic genes, and increases net muscle protein synthesis improving lean body mass composition and has been shown to reduce weight loss, improve donor site wound healing, and decrease hospital stay. Patients with burn injuries greater than 30% should receive oxandrolone for 6 months as the hypermetabolic state has been shown to persist following major burn injury. Despite being well tolerated, patients on oxandrolone should have liver function tests monitored weekly. Human growth hormone and insulin-like growth factor have also been investigated but results have been indeterminate.Acute response to thermal injury is biphasic with the hypodynamic shock state at 24 to 72 hours and hyperdynamic catabolic state beginning on the fifth postburn day. Patients have supraphysiologic cardiac output, elevated body temperature, supranormal oxygen consumption, supranormal glucose consumption and altered glucose metabolism, increased CO2 production, and accelerated tissue catabolism. This response is thought to be caused by excessive release of catabolic hormones including catecholamines, glucagon, and cortisol. There is a shift from anabolic–catabolic homeostasis to hypercatabolic state requiring increased substrates for energy. The resting metabolic rate is directly related to the severity of burn injury and a persistent hypermetabolic state is unsustainable. This hypermetabolism can be reduced by promptly treating sepsis as well as performing early excision and grafting of burn wounds. Recent studies have shown efficacy of a nonselective beta-blocker such as propranolol which inhibits the effect of catecholamines and slows muscle catabolism. Herndon et al
Burn injury results in an increase in hepatic gluconeogenesis and impaired insulin-mediated glucose transport into skeletal and cardiac muscles and adipose tissue. Hypermetabolism seen in burn injury also leads to hyperglycemia and insulin resistance and thus glucose should be monitored in large burn injury patients. Currently, data do not support strict glucose control (<110 mg/dL) but moderate blood glucose control is recommended (<180 mg/dL) and may decrease infectious complications.68
There are a variety of burn wound dressing materials. Patient factors such as burn wound depth, condition, location of the burn, and comfort during dressing changes dictate the choice utilized.47 Although the indications for systemic antibiotic therapy have not been clearly defined, use of antimicrobial dressings is recommended. Silvadene (silver sulfadiazine) is a silver-containing cream that has broad-spectrum coverage against both gram-negative and positive bacteria. Silvadene is commonly used on the skin of both partial- and full-thickness burn injuries. Its use is contraindicated in patients with sulfa allergies and over wounds near the eyes.69 A self-limited leukopenia is commonly seen during the initial days of Silvadene treatment, but its use can be continued as leukocyte counts recover quickly without intervention. Sulfamylon (mafenide acetate) is an analogous agent that is used over cartilaginous areas such as the nose or ear due to increased tissue penetration compared to other dressing materials. Since topical Sulfamylon cream can be used without secondary dressing, it can be used for open burn wound therapy and regular examination of the burn wound surface. Both the cream and a 5% solution of Sulfamylon are equally effective.70 Sulfamylon cream is useful for ear burns when there is risk of cartilage exposure. Sulfamylon may cause increased pain in the burn wound. In addition to the cream, Sulfamylon soaks can also be used for burn and postoperative dressings. Patients receiving large surface area Sulfamylon dressings should be monitored for complications such as hyperchloremic metabolic acidosis that can occur due to its mechanism of action as a carbonic anhydrase inhibitor.
Silver nitrate can also be used by soaking dressings in a 0.5% to 1.0% concentration solution and applied 3 to 4 times a day. These dressings offer several advantages over Sulfamylon soaks as they cover fungus in addition to bacteria and are more cost effective. If not careful, however, silver nitrate does cause significant staining of anything it contacts. If grafts are placed in an area with surrounding cellulitis, silver soaks can be used during the first few days when the compressive dressing is still needed.
Bacitracin and Xeroform are additional examples of antimicrobial-type dressing regimens and can be used after the first dressing takedown. While both can be used anywhere on the body, bacitracin is commonly used for facial burns.
For patients who are at lower risk of infection based on the appearance of burn wounds, dressings may be changed with less frequency to achieve a balance between pain control and the need for wound coverage. Acticoat is one such option that is mainly used in partial-thickness burn injuries. This dressing consists of silver-impregnated sheets that have antimicrobial properties and can be changed less frequently, reducing pain and cost.71 The nanocrystalline particles in Acticoat are able to reduce wound infection and promote wound healing compared to older silver products, including silver nitrate.72 When using Acticoat, it is important to remember to moisten it with water and not normal saline as sodium can inactivate the silver. There are other commercial products in addition to Acticoat that utilize the principle of nanocrystalline dressings. These dressings can be attached with mild adhesive (Mepilex), wrapped or placed on like a glove (Silveron).
While dressing changes are sometimes used to optimize a wound before and after operative interventions, dressings also have the potential to completely heal a wound without the need for surgical intervention depending on the overall appearance of the burn and patient as a whole. Thus, a proper wound care team must not only include a critical care physician and surgeon, but it must also include a specialized wound care nurse to appropriately address this central modality of care for any burn patient.
Donor sites can be the most painful area for the patient and thus consistent donor site care should be provided. Like other wounds, these wounds heal in a moist environment and though dry Xeroform can be used, this can be extremely painful for the patient. We prefer a non-adherent dressing like mepilex that maintains wound moisture in addition to having an antimicrobial silver.
Excision and Grafting
After initial stabilization of the patient, which generally takes 24 to 48 hours, surgical intervention should occur as soon as possible since there are no benefits to delaying surgery when it is clear that a burn wound is of sufficient depth that it will not heal on its own.73,74 Early excision of devitalized tissue appears to reduce the local and system effects of mediators released from burned tissue, thus reducing the progressive pathophysiologic derangements. Excision also removes dead skin which can serve as a nidus for wound infection. Tangential excision with a sharp blade on a guarded device removes necrotic tissue while preserving as much of the underlying viable tissue as possible. For large burn wounds, debridement should occur within 2 to 4 days of the initial injury. If there are insufficient donor sites to autograft all of the burn wounds, the debrided wound should be covered temporarily with allograft.75 Alternatively, the burn can be completely excised within the first several days after injury, and a temporary skin substitute can be used to close the wound remaining after available autologous skin has been harvested and grafted (Fig. 12-3). Sequential debridement and grafting is the backbone of burn care in those suffering from large TBSA burns. The use of allograft also allows the surgeon to assess the depth of the injury and the adequacy of excision. If the homograft has good take, then it is likely an autograft will also take.
Figure 12-3. Full-thickness friction burn staged with integra to allow for full declaration of the wound prior to grafting. Top row shows initial injury. Middle row shows integra placement and bottom row shows after final debridement and graft.
During tangential excision, tissue is debrided until healthy, bleeding tissue is reached. Hemodynamic stability and correction of hematologic and metabolic derangements are helpful for such operative cases given the large amount of blood that may be lost during debridement. A discussion in the preoperative time out should take place between the surgeon and anesthetist about the amount of blood loss expected, the blood products available, and the transfusion triggers for the case. Arterial lines as well as large bore IVs and often a central line should be in place prior to beginning the operation. In general, hemoglobin fluids are not an accurate during acute blood loss anemia caused by intraoperative bleeding after a large debridement. In any burn over 20%, a preoperative blood type and crossmatch should be performed and packed red blood cells should be placed in the operating room to avoid intraoperative acute blood loss anemia. Several measures can be used to decrease intraoperative blood loss, but the need to debride to bleeding tissue makes bloodless surgery impossible. Techniques to decrease blood loss include the use of tourniquets on the extremities as well as the use of topical spray thrombin and epinephrine-soaked Telfa pads placed immediately after excision followed by wrapping this area with epinephrine-soaked Kerlix gauze. We use 1:1,000,000 epinephrine in a saline solution as a hemostatic dressing after excision. In regions where circumferential wrapping cannot be performed, epinephrine solution can be used as an injectable solution to perform dermatoclysis. An 18G spinal needle on the end of a 60-cc syringe or tumescent device can be used to deliver this solution under the skin in areas of bleeding. Similarly, we use epinephrine injection solution as a preharvest tumescent solution for donor sites. This helps create a flat surface on which to run the dermatome and decreases postharvest blood loss. If working on an extremity, a good strategy is to start proximally and perform the excision followed by inflation of the tourniquet. Subsequently, the distal excision can be performed under tourniquet control.
In addition to achieving a healthy and well-vascularized wound bed after debridement, it is also essential to classify and examine the wounds further during this process. At this time, the distinction between superficial and deep partial-thickness burns must be made. While superficial partial-thickness injuries can heal on their own with dressing changes and without grafting, deeper burns must be treated with skin grafting. Given the association between early debridement and grafting with improved functional- and scar-related outcomes, the earlier this distinction is made the faster a treatment plan can be formulated.
Figure 12-4. Grafting back of donor site with 4:1 split-thickness skin graft. (Top) Intraop placement of graft back. (Bottom) 4 weeks postop from graft back.