Critical Care in the Severely Burned: Organ Support and Management of Complications

Introduction

Approximately 4000 burn victims die each year from complications related to thermal injury. Burn deaths generally occur in a bimodal distribution, either immediately after the injury or weeks later due to multisystem organ failure (MOF), a pattern covered in Chapter 30 . Recent reports reveal a 50% decline in burn-related deaths and hospital admissions in the United States over the previous 20 years. In 1949, Bull and Fisher reported 50% mortality rates for children aged 0–14 years with burns of 49% of total body surface area (TBSA), 46% TBSA for patients aged 15–44, 27% TBSA for those aged between 45 and 64, and 10% TBSA for those 65 and older. These dismal statistics have improved, with the latest studies reporting a 50% mortality for greater than 95% TBSA burns in children 14 years and under, 75% TBSA burns in adults, and around 30% TBSA in the elderly. Therefore, a healthy young patient with almost any size burn should be expected to live, and the prospects for the older demographic are improving with modern wound treatment and critical care techniques.

Burned patients generally die from one of two causes: early deaths resulting from “burn shock” and immolation, or MOF leading to late deaths. With the advent of vigorous fluid resuscitation protocols in the severely burned, irreversible burn shock has been replaced by sepsis and the ensuing MOF as the leading cause of death associated with burns in those who do not die at the scene by a margin of 2 to 1. Those with a risk of mortality who do not die precipitously will be treated by what is termed critical care , a service performed in specialized units containing the equipment, supplies, and personnel to institute intensive monitoring and life-sustaining organ support to promote recovery.

Critical illness in burned patients is most commonly beset by sepsis. In a pediatric burn population with massive burns of greater than 80% TBSA, 17.5% of the children developed sepsis, defined as bacteremia with clinical signs of infection. Mortality in the whole group was 33%, most of whom succumbed to MOF. Some were bacteremic and “septic,” but the majority were not. These findings highlight the observation that the development of severe critical illness and MOF often associate with infection, but they are by no means required to develop this syndrome. What is requisite is an inflammatory focus, which is the massive skin injury in severe burns requiring inflammation to heal.

It is postulated that the progression of patients to MOF exists in a continuum with the systemic inflammatory response syndrome (SIRS). Nearly all burn patients meet the criteria for SIRS as defined by the consensus conference of the American College of Chest Physicians and the Society of Critical Care Medicine. It is therefore not surprising that severe critical illness and MOF are common in burned patients.

Patients who develop dysfunction of various organs, such as the cardiopulmonary system, renal system, and gastrointestinal system, can be supported to maintain homeostasis until the organs repair themselves or a chronic support system can be established. Critical care may be loosely defined as the process of high-frequency physiologic monitoring coupled with short response times for pharmacologic and procedural interventions. Entire textbooks and many of the preceding chapters in this book are dedicated to critical care. This chapter will focus on synthesizing a critical care system for burn injury, including the organization of specialized burn intensive care units (BICUs) and organ-specific management.

Burn Intensive Care Unit Organization

Physical Plant

Optimally, a BICU should exist within a designated burn center, ideally verified by the American Burn Association (ABA), and in conjunction with a recognized trauma center, thus providing the capability to treat both thermal and nonthermal injuries. This unit, however, need not be physically located in the same space as that designated for nonburned trauma patients. In fact, the requirement for the care of wounds in burned patients necessitates additional equipment, such as shower tables and overhead warmers, so a separate space dedicated to the severely burned should be standard. This space may be located in a separate hospital with established guidelines for transfer or a specialized unit.

The optimal number of beds in the unit should be calculated by the incidence of moderate to severe burns in the referral area, which in the United States is approximately 20 per 100,000 people per year. The Committee on Trauma of the American College of Surgeons and the ABA recommend that 100 or more patients should be admitted to this facility yearly, with an average daily census of three or more patients to maintain sufficient experience and acceptable access to specialized care.

Most moderate to severe burns with hospital admission will require intensive monitoring for at least the day of admission during the resuscitative phase. Thereafter approximately 20% will undergo prolonged cardiopulmonary monitoring for inhalation injury, burn shock, cardiopulmonary compromise, renal dysfunction, and the development of SIRS and MOF. In these severely burned patients, the average length of stay in the BICU is approximately 1 day per % TBSA burned. Using an average of 25 days admission for a severely burned patient (20% of the burns, 4/100,000 per capita) and 2 days for those not so severely injured (80%, 16/100,000 per capita), this suggests 132 BICU inpatient days per 100,000 persons in the catchment area. Thus a 10-bed BICU should serve a population of 3,000,000 sufficiently when considered independently. Space provided should be at least 3,000 sq ft, including patient beds and support space for nursing/charting areas, office space, wound care areas, and storage.

Multiply-resistant bacteria and fungi are commonly encountered in the BICU owing to the presence of open wounds. To prevent transmission of these organisms to other patients, isolation of burned patients from all other patients is recommended and should be considered when designing units for this purpose. Single rooms with negative-pressure ventilation are advisable. In addition, strict guidelines for contact precautions in wound care and interventions, and hand-washing are standard.

Personnel

A BICU functions best by using a team approach among surgeons/intensivists, nurses, laboratory support staff, respiratory therapists, occupational and physical therapists, mental health professionals, prosthetists, dietitians, and pharmacists ( Box 32.1 ). The unit should have a designated medical director, ideally a burn surgeon, to coordinate and supervise personnel, quality management, and resource utilization. The medical director will usually work with other qualified surgical staff to provide sufficient care for the patients. It is recommended that medical directors and each of their associates be well versed in critical care techniques and that each physician care for at least 50 patients per year to maintain skills. In teaching hospitals, three to four residents or other qualified medical providers should be assigned to the 10-bed unit described. A coverage schedule should be devised to provide 24-hour prompt responses to problems.

Box 32.1

Assigned Burn Unit Personnel

▪
Experienced burn surgeons (burn unit director and qualified surgeons)
▪
Dedicated nursing personnel
▪
Physical and occupational therapists
▪
Social workers
▪
Dietitians
▪
Pharmacists
▪
Respiratory therapists
▪
Phychiatrists and clinical psychologists
▪
Prosthetists

Nursing personnel should consist of a nurse manager with at least 2 years of intensive care and acute burn care experience and 6 months of management responsibilities. The rest of the nursing staff in the BICU should have documented competencies specific to the care of burned patients, including critical care and wound care. Owing to the high intensity of burn intensive care, at least five full-time equivalent nursing providers are required per BICU bed to provide sufficient 24-hour care. Additional personnel are required for respiratory care, occupational and physical therapy, and other support. A dedicated respiratory therapist for the burn unit at all times is optimal.

Owing to the nature of critical illness in burned patients, complications may arise that are best treated by specialists not generally in the field of burn care ( Box 32.2 ). As such, these specialists should be available for consultation when the need arises. Given the regularity with which burn surgeons encounter subspecialty problems, such as corneal injuries, routine injuries are often managed directly by the burn surgeon without additional consultation.

Box 32.2

Consultants for the Burn ICU

▪ General surgery	▪ Pediatrics
▪ Plastic surgery	▪ Psychiatry
▪ Anesthesiology	▪ Cardiology
▪ Cardiothoracic surgery	▪ Gastroenterology
▪ Neurosurgery	▪ Hematology
▪ Obstetrics/gynecology	▪ Pulmonology
▪ Ophthalmology	▪ Nephrology
▪ Orthopedic surgery	▪ Neurology
▪ Otolaryngology	▪ Pathology
▪ Urology	▪ Infectious disease
▪ Radiology

Equipment

The equipment needs of the BICU include those items common to all ICUs, but some of which are specialized ( Box 32.3 ). Each BICU bed must be equipped with monitors to measure heart rate, continuous electrocardiography, noninvasive blood pressure, invasive arterial and venous blood pressures, end tidal carbon dioxide monitoring, and right heart cardiac output using dilution techniques or data derived from arterial pressure tracings. Arterial blood oxygen saturation measurement is also required, but continuous mixed venous saturation monitoring or the technical equivalent is optional. Equipment to measure weight and body temperature should be standard. Oxygen availability with at least two vacuum pumps must be present for each bed.

Box 32.3

Equipment for a Fully Equipped Burn ICU

Standard

▪
Monitors (heart rate, electrocardiography, blood pressure, cardiac output, oxygen saturation, temperature)
▪
Scales
▪
Ventilators
▪
Advanced cardiac life support (ACLS) cardiac cart
▪
Laboratory support (blood gas analysis, hematology, chemistry, microbiology)

Specialty

▪
Fiberoptic bronchoscopes
▪
Fiberoptic gastroscopes/colonoscopes
▪
Dialysis equipment (peritoneal dialysis and hemodialysis)
▪
Portable plain radiography
▪
Computed tomography/fluoroscopy/angiography
▪
Indirect calorimeters

Ventilator equipment must also be available for all beds. The availability of a number of types of ventilator is optimal, including conventional ventilators with the capability to deliver both volume-targeted and pressure-targeted modes, as well as high-frequency ventilators that are oscillatory and/or percussive in design. An emergency cardiac cart containing advanced cardiac life support (ACLS) medications and a battery-powered electrocardiograph/defibrillator must be present in the unit. Infusion pumps to deliver continuous medications and intravenous/intraarterial fluids must also be readily available. A laboratory providing blood gas analysis, hematology, and blood chemistry should be located on site. Point-of-care blood analysis for glucose, arterial blood gas, and basic chemistries is strongly advised. Microbiologic support to complete frequent, routine bacterial and fungal cultures and sensitivities must also be present, as well as virology.

Available specialty equipment should include various sizes of fiberoptic bronchoscopes for the diagnosis and treatment of pulmonary disorders, as well as personnel competent with these techniques. Fiberoptic gastroscopes and colonoscopes for gastrointestinal complications are also necessary for diagnosis, bleeding control, decompression, and difficult feeding access. For renal support, equipment to provide intermittent and/or continuous renal replacement should be present. Portable radiographic equipment for standard chest/abdominal/extremity radiographs must be immediately available. Equipment for computed tomography (CT), fluoroscopy, and angiography should be available. Indirect calorimeters to measure metabolic rate are strongly advised. Overhead warmers and central heating with individualized ambient temperature controls must be available for each room as a specialized requirement.

Hemodynamic Monitoring in the Burn Intensive Care Unit

Most burned patients follow an anticipated course of recovery, which is monitored in the BICU by measuring physiologic parameters. Experienced clinicians assess these physiologic measures in a repeated and sequential fashion to discern when potential interventions may be initiated to improve outcomes. Often no intervention will be necessary from the unit's standard care protocol as the patient is following the anticipated course. At other times this is not the case, and procedural or pharmacologic intervention is beneficial. Physiologic monitoring is then used further to determine the adequacy of the interventions. The following is a survey of monitoring techniques used in the BICU.

Cardiovascular Monitoring

Arterial Lines

Hemodynamic monitoring is directed at assessing the results of resuscitation and maintaining organ and tissue perfusion. Currently used measures are only estimates of tissue perfusion because the measurement of oxygen and nutrient transfer to cells cannot be made directly at the bedside. Instead global physiologic measures of central pressures still serve as the principal guides.

Measurement of arterial blood pressure is the mainstay for the assessment of tissue perfusion. In critical illness, this measurement can be made using cuff sphygmomanometers; however in practice this technique is not useful because the measurement is episodic and placement of these cuffs on burned extremities is problematic. Diastolic pressures can also be artificially elevated in the elderly and obese. Instead continuous monitoring for hemodynamic instability through the use of intraarterial catheters is generally preferable when the patient is in the BICU for a prolonged period. Lines are typically placed in either the radial or the femoral artery. The radial artery is the preferred site for critically ill patients because of safety, with the dual arterial supply to the hand as backup should a complication arise. However it has been shown that radial artery catheters are inaccurate in the measurement of central blood pressure when vasopressors are used and are notoriously inaccurate in children because of greater vascular reactivity. Furthermore femoral cannulation sites are often unburned due to the insulation provided by undergarments, and they do not preclude mobilization with physical therapy or rehabilitation goals. For these reasons, we recommend femoral arterial blood pressure measurement in most burned patients.

For arterial catheters, systolic, diastolic, and mean arterial pressures (MAPs) should be displayed continuously on the monitor screen. Either systolic or MAP can be used to determine adequacy of pressure, although a MAP of greater than 70 mm Hg is considered a more accurate descriptor of normal tissue perfusion on the whole. Reasons for this include the finding that, as the arterial pressure wave traverses proximally to distal, the systolic pressure gradually increases and the diastolic pressure decreases; the MAP determined by integrating areas under the curve, however, remains constant. The adequacy of the waveform must also be determined, with a diminished waveform indicative of catheter damping, requiring catheter replacement. Care must be taken to ensure that the diminished waveform is not true hypotension, which can be determined using a manual or cycling sphygmomanometer. Exaggerated waveforms with elevated systolic pressure and additional peaks in the waveform (generally only two are found) may be a phenomenon known as “catheter whip,” which is the result of excessive movement of the catheter within the artery. Typically this problem is self-limited, but care must be taken not to interpret normal systolic blood pressure values with evidence of catheter whipping as unexceptional because the effect generally overestimates pressures. Again, use of MAP as the principal guideline for the assessment of blood pressure is optimal, as effects of catheter whip or other problems with intraarterial monitoring are then diminished.

Complications associated with arterial catheters include distal ischemia associated with vasospasm and thromboembolism, catheter infection, and arterial damage/pseudo-aneurysm during insertion and removal. Although these complications are uncommon, the results can be devastating. Physical evidence of ischemia in the distal hand or foot should prompt immediate removal of the catheter and elevation of the extremity. If improvement in ischemic symptoms is not seen promptly (within an hour), angiography and intervention must be considered. Should thromboembolism be found, the clot can be removed with operative embolectomy or clot lysis at the discretion of the treating physician. If, during angiography, extensive arterial damage is found with ischemia, operative repair may be indicated. Consideration for anticoagulation must be made while balancing the risk of hemorrhage from open wounds versus the benefit of tissue salvage.

Evidence of catheter infection hallmarked by purulence and surrounding erythema should instigate removal of the catheter, which often will suffice. With continued evidence of infection, antibiotics and incision and drainage of the site should be entertained. Great caution must be exercised to avoid arterial bleeding if an incision is made over the catheter site. If a pseudo-aneurysm is encountered after arterial catheterization and removal without signs of distal ischemia, injection of thrombin or compression with a vascular ultrasound device until no further flow is seen in the pseudo-aneurysm will often alleviate the problem without operative intervention.

Cardiac Output Measurement

Pulmonary artery catheters placed percutaneously through a central vein (internal jugular, subclavian, or femoral) and “floated” into the pulmonary artery through the right heart have been used extensively in hemodynamic monitoring in BICUs. By measuring the back pressure through the distal catheter tip “wedged” into an end-pulmonary branch, an estimate of left atrial pressure can be measured. In addition, dyes or isotonic solutions injected into a proximal port can be used to determine cardiac output from the right heart. These data are used to estimate preload delivery to the heart, cardiac contractility, and afterload against which the heart must pump, which then directs therapy at restoration of hemodynamics. These catheters are used in BICUs under conditions of unexplained shock, hypoxemia, renal failure, and monitoring of high-risk patients.

The use of pulmonary artery catheters, however, has come under scrutiny from reports indicating no benefit from their use. A study of 5735 critically ill adults in medical and surgical ICUs showed an increase in mortality and use of resources when pulmonary artery catheters were used. Most of these patients had medical conditions. The authors of this report suggested that their results should prompt a critical evaluation of the use of pulmonary artery catheters under all conditions. This was followed by a clinical trial in the United Kingdom demonstrating no benefit from the use of pulmonary artery catheters in a general ICU setting. A more recent evaluation of the usefulness of these devices has demonstrated that, with proper training and in the appropriate setting, they can provide data not available through other modalities. Over the past years, the use of pulmonary artery catheters has significantly diminished except in special circumstances, such as unexpected response to treatment, as in volume replacement for oliguria. Even in this condition, new technology based on arterial waveform analysis gives an estimate of cardiac output and end-diastolic volume, which generally gives enough information to guide appropriate therapy. However, in the appropriate patients, pulmonary artery catheters may still play a valuable role.

Arterial Waveform Analysis

Multiple devices have been developed over the past decade using arterial waveform analysis to continuously measure cardiac output as well as to estimate preload. Stroke volume variation provides a good estimate of the fluid responsiveness of shock with only arterial access. The transpulmonary thermodilution technique provides an even more complete hemodynamic dataset without the use of a pulmonary artery catheter. Using only a central line and central arterial line, thermodilution allows monitoring of preload with global end-diastolic volume index, intrathoracic blood volume, continuous cardiac output, and extravascular lung water index. Numerous studies have shown that these volumetric indices represent preload more precisely than urine output or cardiac filling pressures. In a study involving 54 burned children, Herndon et al. determined pulse index continuous cardiac output (PiCCO) to be the superior measurement for cardiac parameters to transthoracic echocardiography and an objective cardiovascular monitor to guide goal-directed fluid resuscitation.

Echocardiography

Transesophageal echocardiography has been used for a number of years as an intraoperative monitor in high-risk cardiovascular patients. It has not been used extensively in other critically ill patients because of the lack of available expertise and paucity of equipment. Since this device can be used as a diagnostic tool for the evaluation of hemodynamic function, it stands to reason that it could be used to monitor critically ill, severely burned patients. A report documented the use of transesophageal Doppler measurements of cardiac output in a series of severely burned patients and showed that intravascular volume and cardiac contractility are significantly diminished the first day after burn in spite of high-volume resuscitation.

Echocardiography has also been studied as a means to supplement urine output monitoring. Investigators in China examined whether esophageal Doppler monitoring of heart function might be an improvement by studying 21 patients with massive burns (79 ± 8% TBSA burned) who were resuscitated with a goal of 1.0 mL/kg per hour. They found that cardiac output was predictably low after injury and increased linearly with time by increases in preload and contractility and decreased afterload. However changes in cardiac output were most closely associated with increased cardiac contractility and decreased afterload rather than increases in preload. Additionally urine output was not closely associated with cardiac output. Held et al. evaluated 11 adult burn patients with a mean TBSA of 37% and found that changes in volume status on echocardiography preceded changes in urine output and vital signs, and they were able to titrate inotropes and vasopressors in elderly patients.

These results call into question the validity of urine output as the primary measure of the adequacy of resuscitation. A similar study by investigators in Sweden probing the role of cardiac function, as measured by echocardiography, and myocyte damage, as measured by troponin abundance in the serum, showed that half of their patients had myocardial damage during resuscitation universally associated with some temporary cardiac wall motion abnormality. However systolic function was not adversely affected. Bedside echocardiographic equipment and skills are increasingly common in BICUs and are an increasingly common means of hemodynamic monitoring in critical care. However the intermittent nature of this procedural assessment allows it to only serve as a useful adjunct to add clarity to a difficult clinical scenario and prevents echocardiography from supplanting continuous monitoring modalities, such as thermodilution or waveform analysis. We look forward to further work regarding the optimal method of assessment of resuscitation; for the present, however, urine output remains the standard, and other measures are useful adjuncts.

Laboratory Estimates of Perfusion

Mixed venous saturation is the gold standard for the measurement of total tissue perfusion but has fallen out of favor because it requires a pulmonary artery catheter. As such, peripheral surrogates, such as base deficit and serum lactate, have become the standard values followed to monitor shock. These can be measured in minutes using point-of-care techniques and rapid guide interventions.

The base deficit is a value calculated using the Henderson-Hasselbalch equation based on the relationship between pH, pCO ₂ , and serum bicarbonate:

pH = 6.1 + \log ({HCO}_{3}^{-}) / ({pCO}_{2}) (0.03)

$pH = 6.1 + \log ({HCO}_{3}^{-}) / ({pCO}_{2}) (0.03)$

It is the stoichiometric equivalent of base required to return the pH to 7.40. Base deficit is routinely calculated on blood gas analysis and provides a reasonable estimate of the degree of tissue anoxia and shock at the whole-body level, particularly in hemorrhagic shock. A rising base deficit indicates increasing metabolic acidosis and may stratify risk of mortality in patients after major trauma. The same can be said for the use of base deficit in resuscitation of burned patients. These studies showed a correlation between higher base deficit and increased mortality, and some have suggested that this value is a better monitor of resuscitation than the time-honored monitors of urine output and arterial blood pressure. Recent studies of burned patients showed the base deficit was higher in nonsurvivors during resuscitation, although the authors could not identify a specific boundary for the effect. Despite its utility as an indicator of shock, base deficit remains a nonspecific indicator of metabolic acidosis and may be elevated with many confounding conditions other than shock, including hyperchloremia, uremia, and alcohol, cocaine, and methamphetamine use. Interpretation can be difficult under these circumstances.

Lactate is another common measure used to determine the adequacy of tissue perfusion. Under acute low-flow conditions, cells transition from primarily aerobic metabolism to anaerobic metabolism for energy production (i.e., adenosine triphosphate [ATP]). A by-product of anaerobic metabolism is lactic acid. Under ischemic conditions, plasma lactate concentration will increase, leading to a decrease in pH. Measurement of lactate is commonly performed to determine the adequacy of generalized perfusion; increases suggest ischemia. Investigators showed that lactate does increase, along with base deficit, in burned patients during resuscitation, and higher levels are associated with poorer outcomes. Later in the course, however, lactate concentrations must be used with some caution because elevated levels do not necessarily indicate ischemia. Under hypermetabolic conditions common in the severely burned, pyruvate dehydrogenase activity is sufficiently inefficient that lactate levels might be elevated without ischemia. Isolated elevations of lactate should then be interpreted with caution and confirmation of ischemia or shock by physical or other laboratory findings sought.

Multisystem Organ Failure

MOF is largely a creation of our success in critical care enabling previously moribund patients to survive long enough for organ failure to develop. Often particular organ systems are allowed to fail to maintain overall patient survival (e.g., performing an excision and grafting procedure that leads to renal failure to remove a septic burn which would otherwise be lethal). The topic of MOF is more thoroughly covered in Chapter 30 , but we will briefly summarize it here.

Humoral Mediators

Humoral inflammatory factors elaborated from the burn wound and the resultant immune, adrenal, and sympathetic activation mediate the development of SIRS.

A number of theories have been developed to explain the progression to MOF ( Box 32.4 ). In the infection theory, as organisms proliferate out of control, endotoxins and exotoxins are released that cause the initiation of a cascade of inflammatory mediators through activation of pathogen-activated molecular pathway (PAMP) receptors, such as Toll-like receptors 2, 4, and 9, as well as the recruitment of inflammatory cells. These pathways can result in organ damage and progression toward MOF if unchecked.

Box 32.4

Theories for the Development of Multiple Organ Failure

▪
Infectious causes
▪
Macrophage theory
▪
Microcirculatory hypothesis
▪
Endothelial–leukocyte interactions
▪
Gut hypothesis
▪
Two-hit theory

MOF can also be initiated by inflammation from the presence of necrotic tissue, and open wounds can incite a similar inflammatory mediator response to that seen with endotoxins. Evidence suggests that this response is due to activation of the cytokine cascade through damage-associated molecular pathways (DAMPs), which might be antigens associated with liberated mitochondria from our own cells. Four of these cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-8, are most strongly associated with sepsis and MOF in burns. The primary support of this theory is that many patients, including those burned, can develop MOF without identified infection. Regardless, it is known that a cascade of systemic events is set in motion, either by invasive organisms or from open wounds, that initiates SIRS and may progress to MOF, thus supporting early burn excision and grafting.

Another theory implicates prolonged tissue hypoxia and the subsequent generation of toxic free radicals during reperfusion as the primary mediator of end-organ damage. As discussed in Chapter 8 on burn edema, this free radical damage can be ameliorated with high-dose intravenous vitamin C during resuscitation. From in vitro models and in vivo animal models, we know tissues that were in shock initially and subsequently reperfused produce oxygen free radicals known to damage a number of cellular metabolism processes. It was found that free radical scavengers, such as superoxide dismutase, improve survival in animal models, but these results have not yet been established in humans. Endogenous natural antioxidants, such as vitamins C and E, are low in burned patients, suggesting that therapeutic interventions may be beneficial.

The final two theories revolve around the role of the gut in the generation of organ failure and the “two-hit” theory of MOF. For years, investigators have implicated the gut as the “engine” of organ failure, which is associated with loss of gut barrier function and translocation of enteric bacteria and/or their toxic metabolites. Bacterial translocation has been shown to occur after burn in patients. No studies have clearly shown whether bacterial translocation is the cause of SIRS/MOF, probably because investigators have as yet been unable to control bacterial translocation effectively during shock in humans; thus, a cause-and-effect relationship cannot be established. The “two-hit” theory ascribes a summation of insults to the development of MOF. Each of the insults alone is inadequate to cause the response, but one or more can “prime” the inflammatory response system just described, such that another normally insignificant injury causes the release of toxic mediators ending in MOF.

It is likely that some part of all of these theories is a cause for MOF in burned patients; probably the relative contribution is unique in each patient. Therefore a single solution is unlikely, and this should be kept in mind when devising strategies to improve care and outcomes.

Course of Organ Failure

Generally, MOF will begin in the renal and/or pulmonary systems and progress in a systematic fashion through the liver, gut, hematologic system, and central nervous system. The development of MOF does not inevitably lead to mortality, however. Efforts to support failed organs until they recover are justified.

Critical Care Interventions

Critical care of a burn patient in the modern era is predicated upon seven key factors:

▪
Sufficient goal-directed fluid resuscitation
▪
Early burn excision and grafting
▪
Aggressive antimicrobial and source control of sepsis
▪
Aggressive and sufficient nutritional support
▪
Active warming
▪
Aggressive physical, occupational, and respiratory therapy
▪
Aggressive and continuous support of organ failures

Sufficient fluid resuscitation of an acute burn wound is thoroughly covered in Chapter 9 on fluid resuscitation. Various formulas to predict fluid requirement, balances between crystalloid versus colloid, and resuscitation endpoints have been advocated. Early in resuscitation it is critical to provide sufficient volume to maintain preload and perfusion in the setting of fluid losses into burn edema and distributive shock while avoiding over-resuscitation, with the resultant costs such as heart failure, liver failure, and compartment syndromes.

Early burn excision and grafting has been discussed thoroughly in Chapter 12 on operative management. The overriding principle is to remove inflammatory and diseased burned tissue to break the hyperinflammatory state underlying burn shock. Early grafting reduces the inflammatory load on the patient, fluid loss, heat loss, the area susceptible to infection, and the total length of critical care. Collectively it reduces the exposure time available for MOF to occur.

Furthermore, the blood loss associated with large-scale early excision often results in a functional plasma exchange. Plasma exchange has been shown to be effective in reducing burn resuscitation, ostensibly by removing the inflammatory and oxidative humoral mediators underlying burn shock. Klein et al. reviewed 44 plasma exchanges in patients reaching twice Parkland with albumin or fresh frozen plasma and found a 40% reduction in fluid resuscitation. In a plasma exchange protocol triggered at 1.2 times Parkland, Neff et al. found a 24% increase in MAP, 400% increase in urine output, and 25% reduction in resuscitation rate, with a reduction in lactic acid as well. In 37 patients undergoing plasma exchange with a mean TBSA of 48.6%, hourly fluid, base deficit, lactate, and hematocrit all improved and were associated with decreased resuscitation volume and increased urine output. Collectively these data support the notion that plasma exchange improves burn shock; however there are thus far no studies directly linking plasma exchange resulting from intraoperative blood loss with improvements in burn outcome demonstrated in early burn excision.

Chapter 11 on infection control well defines the critical nature of early surgical source control and appropriate antimicrobials, but generally emphasizes that meticulous aseptic technique, excision of infected or devitalized tissue, coverage with viable grafts, topical antimicrobials, culture surveillance, and systemic antimicrobials when appropriate are critical components. Similarly, Chapters 28 and 29 on nutrition support and hypermetabolism, respectively, effectively discuss the critical need for enteral feeding and nutritional support, physical therapy, and the requirement to keep patients warm. The remainder of this chapter is directed toward organ-specific critical care support.

Toxicological Burn Critical Care

Many toxins can affect the burn-injured patient, particularly with occupational injuries. Specific therapies for all toxins are beyond the scope of this chapter and require appropriate decontamination, antidotes, and consultation with material data safety sheets and poison control centers for known exposures if beyond the burn physician's comfort. However the most common toxins are cyanide and carbon monoxide. Cyanide can be elaborated from the combustion of various plastics, and significant exposure can result from smoke inhalation. Mounting evidence indicates that cyanide toxicity is clinically significant in inhalation injuries, being found at clinically significant levels in up to 76% of inhalation injury patients. Few clinical labs return blood cyanide labs in a clinically useful time scale, so surrogate markers of less than 15% TBSA with smoke inhalation, Glasgow Coma Scale (GCS) under 14, abnormal hemodynamics, and/or a lactate level of greater than 10 are known sensitive indicators of cyanide toxicity of greater than 1.0 mg/L. In these cases, empiric therapy is recommended with hydroxycobalamin. It is the first-line antidote for cyanide toxicity and has a very mild side effect profile of transient hypertension, bradycardia, and urine discoloration. Hydroxycobalamin is also a nitric oxide scavenger and effectively reduces the hypotension often seen in burn shock.

As a common product of combustion, carbon monoxide (CO) should be considered in any inhalation injury, enclosed fire, or patient with altered mental status. Patients with carboxyhemoglobin (COHb) levels above 25% should be mechanically ventilated on 100% F io ₂ , which reduces the half-life from 4 hours to 1 hour. There are rare indications for hyperbaric oxygen (HBO) because it can reduce the CO half-life to 15 minutes, particularly in the setting of pregnancy or seizures. HBO is only indicated in the burn setting if it can be immediately employed in conjunction with definitive burn care in specialized centers. For cases where instituting HBO unnecessarily delays burn care, mechanical ventilation can bring COHb to safe levels prior to HBO's institution, and appropriate burn care should take precedence.

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