What's new in critical care of the burn injured patient
What ’s New in CriticalCare of the Burn - InjuredPatient?Tina L. Palmieri, MD, FACS, FCCMa,b,* KEYWORDS Burns Sepsis Inhalation injury Critical care Glycemic controlMortality after burn injury has decreased markedly (ARDS).4 The risk for mortality from ALI and ARDSin the past 30 years. Survival after burn injury to approaches 40% to 50%.5 This mortality may bemore than 90% of the total body surface area is directly due to respiratory failure and hypoxia, orcommon in children, with some authors maintain- it may result from associated multisystem organing that virtually all children with burn injury should failure or ventilator-associated pneumonia. Newbe resuscitated.1 Unfortunately, the improvement strategies for mechanical ventilation are currentlyin survival does not apply to all age groups: being used to support burn patients who havesurvival in the elderly burn patient remains prob- respiratory insufficiency, ALI, and ARDS. Theselematic. The increases in survival after burn injury strategies include changes in traditional mechan-have been linked, in part, to a variety of wound ical ventilation paradigms (such as the use oftreatment modalities, including early excision and low-tidal-volume ventilation) and the use of alter-grafting, cultured epithelial autografting, and the native modes of ventilation.institution of broad-spectrum topical antimicrobialtherapy.2,3 Advances in critical care management, Low-tidal-volume Ventilationparticularly with respect to ventilator manage-ment, resuscitation, and sepsis management, ALI and ARDS are caused by burn injury, sepsis,have also contributed to the improved survival pancreatitis, and drug toxicity, and they are alsoafter burn injury. This article describes the present in inflammatory states. ALI and ARDSadvances in critical care management that have are characterized by diffuse alveolar damage,contributed to the decline in mortality in burn with associated increases in capillary perialvolarpatients. permeability. Protein-rich fluid is transmitted from the intravascular to the extravascular spaces andADVANCES IN VENTILATOR MANAGEMENT alveoli. This results in increases in cytokine release, the accumulation of macrophages andMechanical ventilation is frequently required after neutrophils in the alveolar-arteriolar interstitium,major burn injury, especially when the patient has and decreases in surfactant production.6,7 All ofconcomitant inhalation injury. The term ‘‘acute these factors combine to result in airway damagelung injury’’ (ALI) is used to designate the acute and alveolar collapse.onset of impaired oxygen exchange that results Endotracheal intubation and mechanical ventila-from lung injury, and the condition is characterized tion are often necessary to support the patient whoby a PaO2/FiO2 ratio of less than 300. Severe has burn or inhalation injury with ALI and ARDS.cases of ALI, in which this ratio is less than 200, Twenty years ago, the goal of ventilatory support plasticsurgery.theclinics.comare termed ‘‘acute respiratory distress syndrome’’ was normalization of arterial blood gases (ie, a Shriners Hospital for Children Northern California, 2425 Stockton Boulevard, Suite 718, Sacramento, CA 95817, USA b University of California Davis, Medial Center, 2315 Stockton Boulevard, Sacramento, CA 95817, USA * Corresponding author. University of California Davis, Medial Center, 2315 Stockton Boulevard, Sacramento, CA 95817, USA. E-mail address: email@example.com Clin Plastic Surg 36 (2009) 607–615 doi:10.1016/j.cps.2009.05.012 0094-1298/09/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.
608 Palmieri a pH as close as possible to 7.4, pCO2 at 35–45 because its use may decrease the incidence of mm Hg, and oxygen saturation greater than VILI and improve overall survival. However, given 95%). This was accomplished using high pres- that this strategy has not been assessed in sures, inspired oxygen concentration, and minute a prospective randomized trial in patients who ventilation delivered by volume-controlled ventila- have burn injury, care must be taken in the applica- tors. Tidal volumes of 10 to 15 mL/kg were the tion and monitoring this type of mechanical venti- standard, rationalized by the need for increased lation in patients who have burn injury. The use recruitment of collapsed alveoli. of this ventilator strategy should not replace the These traditional ventilator-management strate- use of escharotomy for patients who have chest gies were challenged in several prospective, wall compartment syndrome, and care needs to randomized trials. Reports of ventilator-induced be taken to guard against airway obstruction in lung injury (VILI), associated with hyperinflation of patients who have inhalation injury. normal regions of aerated lung due to high tidal volumes began to appear. Overexpansion of New Methods of Mechanical Ventilation normal alveoli leads to high transpulmonary pres- sures in aerated regions, making them susceptible Several nonconventional modes of ventilation to direct physical damage. Data from animal have been proposed for the treatment of severe studies resulted in the recommendation to reduce ARDS in patients who have burn injury, including plateau pressures to 35 mm Hg to lessen the contri- airway pressure release ventilation (APRV) and bution of VILI to the altered physiology of ALI and high-frequency oscillatory ventilation. Both of ARDS. Peak transpulmonary pressure reduction these methods use lower tidal volumes and are was accomplished by increasing positive end- designed primarily to improve oxygenation. expiratory pressure and decreasing tidal volume. Although both methods have shown promise, The subsequent reduction in minute ventilation re- neither has been extensively tested in patients sulted in hypercapnia, which became popularly who have burn injury. known as permissive hypercapnia.8 A series of clin- APRV, which was first described in 1987, is ical trials and a review by the Cochrane Anesthesia a time-triggered, pressure-limited, and time- Review group demonstrated that mortality could be cycled mode of ventilation that uses two different decreased in patients who had ALI and ARDS with levels of airway pressures (high and low) over the use of tidal volumes of 6 mL/kg of ideal body two different time periods (high and low).19 In weight.9–14 These protective effects were accom- essence, APRV involves the maintenance of plished using tidal volumes of less than 7 mL/kg a high, continuous, positive airway pressure that of measured body weight and plateau pressures intermittently time-cycles to a lower airway pres- of less than 31 cm of water.12,13,15 The reductions sure. APRV is designed to optimize and maintain in mortality and the duration of mechanical ventila- airway recruitment throughout the respiratory tion correlated directly with the magnitude of differ- cycle by maintaining a higher mean airway pres- ence in tidal volume between the control and sure despite using lower tidal volumes and end treatment groups. The two studies showing the expiratory pressures than other forms of ventila- highest protective value of low-tidal-volume venti- tion.20,21 The key to the successful use of APRV lation10,11 calculated the delivered tidal volume is to set the high pressure just a bit higher than based on ideal, rather than measured, patient the alveolar closing pressure, which allows alve- weight, suggesting that ventilator management in olar recruitment without alveolar collapse. Alveolar patients who have ALI and ARDS should be guided recruitment is maintained during the inflation not by the actual weight, but by the ideal body phase. The release phase, which is relatively short, weight. This is an important consideration in allows for passive exhalation and ventilation.22 patients who have a major burn injury because Oxygenation is achieved, with increases in inspira- they often have vast increases in body weight due tory pressure and time. to massive fluid resuscitation. However, this APRV thus allows for spontaneous breathing strategy is not without risk. Adverse effects of while decreasing the work of breathing and the a low-pressure ventilation strategy include need for sedation. These salutary effects also increased intracranial pressure, decreased can potentially minimize the impact of VILI and myocardial contractility, reductions in renal blood improve hemodynamic parameters. Studies of flow, and pulmonary hypertension. However, APRV have been restricted primarily to cases of multiple studies have shown that modest permis- ARDS, and there are few reports of its use for sive hypercapnia is safe.16–18 patients who have burns. Two randomized, Low-pressure ventilation should be considered controlled trials have been performed to assess for burn patients who have severe ALI and ARDS APRV, with variable results.23,24 Although neither
What’s New in Critical Care of the Burn Patient? 609study demonstrated differences in mortality or ventilation has become the standard of care forlength of stay, one study of trauma patients re- mechanical ventilation in patients who have ARDSported lower end-inflation pressures, improved and ALI.oxygenation, decreased ventilator duration, anddecreased ICU stay in the APRV group comparedwith the pressure control ventilation group. RESUSCITATION AND FLUID MANAGEMENTCaution must be exercised before using APRV,however, because it theoretically could result in One of the greatest advances in burn treatment inlung overinflation and injury. the twentieth century was the development and adoption of guidelines for burn resuscitation. Fluid estimation formulas, such as the Parkland formula,High-frequency Oscillatory Ventilation which allow for the adjustment of intravenous fluidHigh-frequency oscillatory ventilation (HFOV), administration based on urine output, providedwhich has been used for decades in neonatal clinicians with easily identifiable endpoints ofICUs, is still under investigation for use in adults resuscitation. Patients who had major burn injurywho have ARDS. HFOV, like APRV, improves were seldom dying from underresuscitation.oxygenation by maintaining elevated mean airway However, issues related to overresuscitationpressure to recruit alveoli.25–28 It differs from volu- began to develop. ‘‘Fluid creep,’’ the term usedmetric diffusive ventilation, the current standard of to describe the use of excessive intravenous fluidcare for inhalation injury, in its use of higher during resuscitation, is being increasinglyfrequencies and time cycling. To achieve airway described in the literature.42–45 Abdominalrecruitment and improved oxygenation, HFOV compartment syndrome, considered by some touses extremely small tidal volumes (1–2 mL/kg) be a consequence of excessive resuscitation,at high frequencies (3–15 Hz), as opposed to also is being increasingly documented in the liter-frequencies of 300 to 600 Hz used in volumetric ature.46–49diffusive ventilation. The result is the generation Perhaps one of the most important issues inof sustained mean airway pressures of 30 to burn resuscitation is that the optimal measurable40 cm H2O. Oxygenation and ventilation are endpoint of resuscitation remains poorly defined.essentially uncoupled and can be controlled Studies attempting to generate variables predic-independently. tive of resuscitation nonresponders have been HFOV has been shown to decrease VILI in unsuccessful, and no single formula accuratelyanimal models by limiting alveolar stretch and predicts the fluid resuscitation needs for allavoiding atelectrauma, which is caused by the patients during burn shock.50 This lack of clarityrepeated opening and collapse of alveoli.29–33 is caused by the many confounding factorsThe sustained recruitment of alveoli results in surrounding burn injury, such as burn depth, inha-improved oxygenation. HFOV has been used in lation injury, associated injuries, age, delays inadults primarily as a rescue mode of ventilation resuscitation, the need for escharotomies or fas-in cases of severe ARDS in different scenarios, ciotomies, and the use of alcohol or drugs. Ideally,including burn injury.34–39 To date, two random- fluid resuscitation should be adjusted based onized, prospective trials have found no difference physiologic endpoints. To date, urine output hasin outcomes between the use of HFOV and been the most commonly used endpoint, althoughconventional mechanical ventilation; however, the value of using urine output to adjust fluid ratesa current randomized, prospective trial is during burn shock has been challenged.51underway and should define the use of HFOV in In recent years, the use of invasive monitoringcases of severe ARDS.40,41 One of the potential methods, such as central venous pressure moni-major limitations of HFOV is difficulties with venti- toring or the pulmonary artery catheter, has beenlation and severe respiratory acidosis due to popularized, especially in the elderly, but recentincreases in pCO2. reports raise questions about the utility of the Although both APRV and HFOV are promising pulmonary artery catheter in critically illmodalities for use in burn patients who have patients.52–55 Even central venous pressure hasARDS and ALI, neither has been rigorously studied been shown to be influenced more by intra-in a prospective, randomized fashion in patients abdominal pressures than actual right atrialwho have burns. Likewise, the ability to decrease pressure.56the incidence of volutrauma by reducing tidal Thus, although the pulmonary artery cathetervolumes during mechanical ventilation has not and central venous pressure provide additionalbeen thoroughly evaluated in patients who have information regarding heart function, studies failedburn and inhalation injury. However, low-tidal-volume to demonstrate improved survival with their use.
610 Palmieri New invasive monitors continue to be devel- United States.69 The mean pretransfusion hemo- oped in an attempt to improve outcomes. Clini- globin level was 8.6 Æ 1.7 g/dL, indicating that cians can now continuously measure mixed the majority of patients were still being transfused venous oxygenation, intrathoracic blood volume, at a hemoglobin level higher than what was recom- total blood volume index, and extravascular lung mended in the TRICC study. Once again, the water using specialized thermodilution tech- number of units of red blood cell transfusions the niques.54,57 Pulse contour analysis, transesopha- patients received was independently associated geal echocardiography, partial carbon dioxide with longer ICU length of stay and increased rebreathing, and impedance electrocardiography mortality. The CRIT study excluded burn patients; are all recently developed techniques that are thus, it provides no data on burn center transfusion used to estimate cardiac output.58–61 Although practices and the outcomes related to those these techniques show great promise, their utility practices. in burn resuscitation remains unclear. Finally, Limited data exists regarding the effects of tissue perfusion monitors, such as gastric tonom- a restrictive blood transfusion policy in adult burn eters or devices that measure oxygen and carbon patients. In one study by Sittig and Deitch,70 14 dioxide saturations in the subcutaneous tissues, patients admitted to a burn center during a 6- have not been shown to improve resuscitation in month interval were transfused when their hemo- burn patients. These techniques demonstrate low globin level was less than 6.0 g/dL. The outcomes perfusion capabilities despite other signs of of patients who had burns over less than 20% of providing adequate resuscitation and may actually their total body surface area or patients who lead to overresuscitation.62,63 required excision and grafting of less than 10% of their total body surface area were retrospec- tively compared with a matched group of 38 Blood Transfusion patients who had been treated the previous year Each year in the United States, more than $3 billion using a nonrestrictive policy (hemoglobin level are spent on blood transfusions, with approxi- maintained at greater than 9.5–10 g/dL). No differ- mately 25% of critically ill patients receiving at ences existed in the hospital length of stay. The least one blood transfusion to treat anemia.64–66 patients treated using the liberal strategy received Although critically ill patients may be predisposed 3.5 times as much blood as their restrictive-policy to the adverse effects of anemia, they are also counterparts. Although this study is an important subject to the adverse consequences of blood first step in the evaluation of blood transfusion in transfusion, including infection, pulmonary edema, burn patients, it is limited by its retrospective immune suppression, and microcirculatory alter- nature, review bias, and inadequate number of ations.67 Traditionally, blood transfusions have patients. been administered when the patient’s hemoglobin To evaluate actual burn center transfusion prac- level is less than 10 g/dL or the hematocrit is less tices, the Burn Multicenter Trials Group reviewed than 30%. However, a multicenter, prospective, the actual use of blood transfusion in patients randomized study of transfusion in ICU patients, who had burn injury to 20% or more of their total the TRICC study (Transfusion Requirements in body surface area for a 1-year period.71 Data Critical Care), challenged this standard.68 A total was collected from 21 different burn centers on of 838 patients were randomized to receive blood a total of 666 patients. The overall hemoglobin transfusion based on a liberal (maintain hemo- level at which the first transfusion was adminis- globin level at 10–12 g/dL) versus a restrictive tered was 9.35 Æ 0.8 g/dL for all patients, and (maintain hemoglobin level at 7–8 g/dL) strategy. the mean number of blood transfusions was 13.7 The restrictive strategy was at least as effective Æ 1.1 units, with the vast majority of transfusions as the liberal strategy in critically ill patients. Signif- given in the burn ICU (9.4 Æ 1.1). Mortality, as in icant differences favoring the restrictive strategy other studies of transfusion, was related to the included the in-hospital mortality rate, the cardiac number of units of blood transfused. In addition, complication rate, and organ dysfunction. This each transfusion increased the risk for infection study suggested that blood transfusion should by 11%. be restricted to patients who have a hemoglobin Three other retrospective studies were con- level of less than 7 g/dL. ducted to evaluate blood transfusion after burn The impact of the TRICC study on transfusion injury: two in children and one in adults. One study practices in the United States has been limited. by Jeschke and colleagues72 that evaluated the The CRIT study, a prospective, multicenter, obser- use of blood transfusion in 227 children who had vational study of ICU patients, analyzed the trans- major burn injury demonstrated increased rates fusion practices of 284 ICUs in 213 hospitals in the of sepsis and mortality in children who received
What’s New in Critical Care of the Burn Patient? 611more than 20 units of blood as compared with The definition of sepsis in the patient who hassimilar children receiving less than 20 units. The burns requires that an infection be documentedother two studies, one in children and one in by way of a positive culture result, a pathologicadults, demonstrated decreased mortality in tissue source, or a clinical response to antimicro-patients treated using a restrictive transfusion bials and three of the following:strategy.73,74 Although these studies suggest thata restrictive transfusion strategy is efficacious, 1. Temperature greater than 39 C or less thana prospective, randomized trial is needed to define 36.5 Cthe optimal burn blood transfusion strategies. In 2. Progressive tachycardia (adults, 110 beatsthe interim, the use of blood transfusion after per minute; children, more than 2 SD aboveburn injury should be scrutinized. age-specific norms) 3. Progressive tachypnea (adults 25 beats per minute not ventilated, or with minute ventilation, 12 l/min ventilated; children, more than 2 SDSEPSIS PREVENTION AND MANAGEMENT above age-specific norms)Sepsis continues to be one of the leading causes 4. Thrombocytopenia beginning 3 days after initialof morbidity and mortality after burn injury. Recent resuscitation (adults 100,000/ml; children, 2advances in sepsis treatment fall into several cate- SD under age-specific norms)gories: the development of sepsis guidelines, the 5. Hyperglycemia in the absence of preexistingdefinition of sepsis in burns, and the prevention diabetes mellitus (untreated plasma glucoseof sepsis. This section provides an overview of 200 mg/dL, or equivalent mM/L or insulineach of these areas. resistance) The development of sepsis guidelines was de- 6. Inability to continue enteral feedings for moresigned to standardize the treatment of sepsis than 24 hours.throughout all ICUs. The latest guidelines were These criteria form the foundation for all futuredeveloped by an international panel of sepsis clinical studies and trials of sepsis in patientsexperts spanning all ICU specialties.75 The guide- who have burns.lines were created and rated based on availableevidence from the literature. The current recom-mendations for the treatment of sepsis, which Glycemic Controlare broad based, include those listed in Box 1. The applicability of these recommendations in Critically ill adults and children frequently developcertain aspects of burn treatment may be prob- stress-induced hyperglycemia secondary to alter-lematic because the majority of the supporting ations in the control mechanisms for glucosedata does not include burn patients. supply and demand.77 An ‘‘insulin-resistant’’ state One of the major limitations in sepsis research develops, in which patients have either normal orand the application of sepsis guidelines in patients elevated plasma insulin concentrations duringwho have burns is a lack of a burn-specific defini- hyperglycemia.78 Early hyperglycemia andtion of sepsis. Although sepsis definitions have glucose variability after admission to the ICUbeen developed for critically ill patients, their appli- have been associated with adverse outcomes;cability in patients who have burns is limited prolonged hyperglycemia has been associatedbecause of the innate differences in the physiology with a sixfold increase in mortality.79 Hypergly-of burn patients. For example, a burn patient is cemia has also been associated with increasedpersistently hypermetabolic, resulting in tachy- mortality in severely burned children and adults,cardia, tachypnea, and elevated body tempera- and the administration of exogenous insulin toture. These physiologic alterations would result in minimize hyperglycemia after critical illness hasa sepsis definition in the vast majority of patients been shown to impact outcome in adult patients.80who have burn injury, many of whom would not In a landmark study, van den Berghe andhave an ongoing infection. To address these colleagues81 demonstrated that, in critically illissues, a consensus conference consisting of patients, intensive intravenous insulin therapy, de-burn experts from throughout the United States signed to maintain normoglycemia (80–110 mg/dLand Canada was held in January 2007 to define plasma glucose level) reduced in-hospitalsepsis and infection for patients after burn injury.76 mortality by 34%. Similarly, patients who had dia-The findings of this group formed the foundation betes and acute myocardial infarction showedfor the diagnosis of sepsis in burns clinically and improved long-term survival when they werefor all future trials related to clinical burn sepsis treated using insulin therapy that targeted a plasmaand infection. glucose level of less than 215 mg/dL.82
612 Palmieri Box 1 22. Institute glycemic control that targets Current recommendations for the treatment patients who have a blood glucose level of of sepsis less than 150 mg/dL. 23. Maintain an equivalency of continuous 1. Provide early, goal-directed resuscitation veno-veno hemofiltration and intermittent within 6 hours of sepsis diagnosis. hemodialysis. 2. Check blood cultures before starting antibi- 24. Use prophylaxis for patients who have otic therapy. deep-vein thrombosis. 3. Use imaging studies to confirm the infection 25. Use stress ulcer prophylaxis with H2 blockers source. or proton pump inhibitors. 4. Start the administration of broad-spectrum 26. Consider the limitation of support, when antibiotics within 1 hour of diagnosis of appropriate. septic shock or severe sepsis. 5. The narrowing of antibiotic coverage should be based on culture sensitivity Several studies have been completed evaluating results. 6. Use a 7- to 10-day antibiotic duration, the impact of tight glycemic control after major burn guided by clinical response. injury. Two studies, one in adults and one in chil- 7. Use source control. dren, have been performed in patients who had 8. Provide resuscitation using colloid or crystal- burn injury.83,84 Both studies demonstrated that loid agents. a strict glycemic control protocol that maintained 9. Use a fluid challenge to restore mean circu- blood glucose levels at less than 120 mg/dL could lating filling pressures. be developed and safely applied for patients who 10. Use a reduction in fluid administration in had burns, with an incidence of hypoglycemia of cases with rising filling pressures and no 5%. These studies also demonstrated a decrease improvement in tissue perfusion. in infectious complications and mortality. Although 11. The vasopressor preference should be for norepinephrine or dopamine to maintain these studies are suggestive of a salutary effect of the target arterial pressure at greater than continuous exogenous insulin administration, 65 mm Hg when fluid resuscitation fails to further prospective, randomized trials are needed improve hemodynamics. to confirm these findings because other studies 12. Use dobutamine when the cardiac output of glycemic control in critical illness have reported remains low despite the use of fluid resusci- differing results.85–87 Perhaps some of the tation and combined inotropic and vaso- disparity in findings can be explained by the vaga- pressor therapy. ries of glucose measurement for strict glycemic 13. Use stress-dose steroid therapy only in cases control protocols. Blood glucose levels can of septic shock when the blood pressure is differ by as much as 20%, based on whether poorly responsive to fluid and vasopressor therapy. the blood is drawn from a central venous cath- 14. Provide recombinant-activated protein C eter or an arterial line.88 In addition, anemia to patients who have severe sepsis and may introduce an error rate of 15% to 20% in a high risk for death based on clinical point of care glucose testing readings.89 Hence, assessment. care needs to be taken in the development of 15. Maintain hemoglobin levels at 7 to 9 g/dL, a protocol, including planning how and when except in patients who have coronary artery blood glucose levels will be measured. Addi- disease or acute hemorrhage. tional care needs to be taken to avoid the devel- 16. Use low-tidal-volume ventilation and a limi- opment of hypoglycemia during dressing tation of inspiratory plateau pressure in changes, during operative interventions, and patients who have ALI and ARDS. 17. Minimize the positive end-expiratory pres- after the administration of certain medications. sure in patients who have ALI. 18. Use a conservative fluid management strategy for patients who have ALI and REFERENCES ARDS who are not in shock. 1. Wolf SE, Rose JK, Desai MH, et al. Mortality determi- 19. Follow the protocols for weaning and seda- nants in massive pediatric burns. An analysis of 103 tion and analgesia. 20. Use intermittent bolus sedation or contin- children with or 5 80% TBSA burns ( or 5 70% uous infusion sedation with daily full-thickness). Ann Surg 1997;225:554–65. interruption. 2. Xiao-Wu W, Herndon DN, Spies M, et al. Effects of 21. Avoidance the use of a neuromuscular delayed wound excision and grafting in severely blockade. burned children. Arch Surg 2002;137:1049–54.
What’s New in Critical Care of the Burn Patient? 613 3. Sheridan RL, Tompkins RG. What’s new in burns and permissive hypercapnia: a prospective study. Crit metabolism. J Am Coll Surg 2004;198:243–63. Care Med 1994;22:1568–78. 4. Bernard GR, Artigas A, Brigham KL, et al. Report of 17. Laffey JG, O’Croinin D, McLoughlin P, et al. Permis- the American-European Consensus Conference on sive hypercapnia: role in protective lung ventilatory acute respiratory distress syndrome: definitions, strategies. Intensive Care Med 2004;30:347–56. mechanisms, relevant outcome, and clinical trial 18. Bidani A, Tzouanakis AE, Cardenas VJ, et al. coordination. J Crit Care 1994;9:72–81. Permissive hypercapnia in acute respiratory failure. 5. Lewandowski K. Epidemiological data challenge JAMA 1994;272:957–62. ARDS/ALI definition. Intensive Care Med 1999;25: 19. Stock MC, Downs JB, Frolicher DA. Airway pressure 884–6. release ventilation. Crit Care Med 1987;15:462–6. 6. Slutsky AS, Tremblay LN. Multiple system organ 20. Habashi NM. Other approaches to open lung venti- failure: is mechanical ventilation a contributing lation: airway pressure release ventilation. Crit care factor? Am J Respir Crit Care Med 1998;157: Med 2005;33:S228–40. 1721–5. 21. Myers TR, MacIntyre NR. Does airway pressure 7. Dreyfuss D, Saumon G. From ventilator-induced lung support ventilation offer important new advantages injury to multiple organ dysfunction? Intensive Care in mechanical ventilation support? Respir Care Med 1998;24:102–4. 2007;52:452–8. 8. Slutsky AS. Mechanical ventilation: American 22. Haitsma JJ, Lachmann B. Lung protective ventilation College of Chest Physicians’ Consensus Confer- in ARDS: the open lung maneuver. Minerva Aneste- ence. Chest 1993;104:1833–59. siol 2006;72:117–32. 9. Petrucci N, Iacovelli W. Lung protective ventilation 23. Putensen C, Zech S, Wrigge H, et al. Long-term strategy for the acute respiratory distress syndrome. effects of spontaneous breathing during ventilatory Cochrane Database Syst Rev 2007;(3):CD003844. support in patients with acute lung injury. Am J Respir10. Amato MB, Barbas CS, Medeiros DM, et al. Effect of Crit Care Med 2001;164:43–9. a protective-ventilation strategy on mortality in the 24. Varpula T, Jousela I, Niemi R, et al. Combined acute respiratory distress syndrome. N Engl J Med effects of prone positioning and airway pressure 1998;338:347–54. release ventilation on gas exchange in patients11. Ventilation with lower tidal volumes as compared with acute lung injury. Acta Anaesthesiol Scand with traditional tidal volumes for acute lung injury 2003;47:516–24. and the acute respiratory distress syndrome. The 25. Derdak S. High-frequency oscillatory ventilation for Acute Respiratory Distress Syndrome Network. acute respiratory distress syndrome in adult N Engl J Med 2000;342:1301–8. patients. Crit Care Med 2003;31:S317–23.12. Brochard L, Roudot-Thoraval F, Roupie E, et al. Tidal 26. Ferguson ND, Stewart TE. New therapies for adults volume reduction for prevention of ventilator- with acute lung injury: high frequency oscillatory induced lung injury in the acute respiratory distress ventilation. Crit Care Clin 2002;18:1–13. syndrome. Am J Respir Crit Care Med 1998;158: 27. Suzuki H, Papazoglou K, Bryan AC. Relationship 1831–8. between PaO2 and lung volume during high13. Stewart TE, Meade MO, Cook DJ, et al. Evaluation of frequency oscillatory ventilation. Acta Paediatr Jpn a ventilation strategy to prevent barotrauma in 1992;34:494–500. patients at high risk for acute respiratory distress 28. Kolton M, Cattran CB, Kent G, et al. Oxygenation syndrome. N Engl J Med 1998;338:355–61. during high-frequency ventilation compared with14. Villar J, Kacmarek RM, Perez-Mendez L, et al. A conventional mechanical ventilation in two models high positive end-expiratory pressure, low tidal of lung injury. Anesth Analg 1982;61:323–32. volume ventilatory strategy improves outcome in 29. Hamilton PP, Onayemi A, Smyth JA, et al. Compar- persistent acute respiratory distress syndrome: ison of conventional and high-frequency oscillatory a randomized, controlled trial. Crit Care Med ventilation: oxygenation and lung pathology. J Appl 2006;34:1311–8. Physiol 1983;55:131–8.15. Brower RG, Shanholtz CB, Fessler HE, et al. 30. McCulloch PR, Forkert PG, Froese AB. Lung Prospective randomized, controlled clinical trial volume maintenance prevents lung injury during comparing traditional vs. reduced tidal volume venti- high frequency oscillatory ventilation in surfactant- lation in ARDS patients. Crit Care Med 1999;27: deficient rabbits. Am Rev Respir Dis 1988;137: 1492–8. 1185–92.16. Hickling KG, Walsh J, Henderson S, et al. Low 31. Bond DM, Froese AB. Volume recruitment maneu- mortality rate in acute respiratory distress syndrome vers are less deleterious than persistent low lung using low-volume, pressure-limited ventilation with volumes in the atelectasis-prone rabbit lung during
614 Palmieri high-frequency oscillation. Crit Care Med 1993;21: 47. Latenser BA, Kowel-Vern A, Kimball D, et al. A pilot 402–12. study comparing percutaneous decompression with 32. Rotta AT, Gunnarsson B, Fuhrman BP, et al. Compar- decompressive laparotomy for acute abdominal ison of lung protective ventilation strategies in compartment syndrome in thermal injury. J Burn a rabbit model of acute lung injury. Crit Care Med Care Rehabil 2002;23:190–5. 2001;29:2176–84. 48. Hobson KG, Young KM, Ciraulo A, et al. Release of 33. Imai Y, Nakagawa S, Ito Y, et al. Comparison of lung abdominal compartment syndrome improves protection strategies using conventional and high- survival in patients with burn injury. J Trauma 2002; frequency oscillatory ventilation. J Appl Physiol 53:1129–34. 2001;91:1836–44. 49. Oda J, Yamashita K, Inoue T, et al. Resuscitation 34. Mehta S, Lapinsky SE, Hallett DC, et al. A prospec- volume and abdominal compartment syndrome in tive trial of high frequency oscillatory ventilation in patients with major burns. Burns 2006;32:151–4. adults with acute respiratory distress syndrome. 50. Cancio LC, Reifenberg L, Barillo DJ, et al. Standard Crit Care Med 2001;29:1360–9. variables fail to identify patients who will not respond 35. Andersen FA, Guttormsen AB, Flaatten HK. High to fluid resuscitation following thermal injury: brief frequency oscillatory ventilation in adult patients with report. Burns 2005;31:358–65. acute respiratory distress syndrome—a retrospective 51. Dries DJ, Waxman K. Adequate resuscitation of burn study. Acta Anaesthesiol Scand 2002;46:1082–8. patients may not be measured by urine output and 36. Mehta S, Granton J, MacDonald RJ, et al. High- vital signs. Crit Care Med 1991;19:327–9. frequency oscillatory ventilation in adults: the Toronto 52. Shah MR, Hasselblad V, Stevenson LW, et al. Impact experience. Chest 2004;126:518–27. of the pulmonary artery catheter in critically ill 37. Claridge JA, Hostetter RG, Lowson SM, et al. High- patients: meta-analysis of randomized clinical trials. frequency oscillatory ventilation can be effective as JAMA 2005;294:1664–70. rescue therapy for refractory acute lung dysfunction. 53. Martin RS, Norris PR, Kilgo PD, et al. Validation of Am Surg 1999;65:1092–6. stroke work and ventricular arterial coupling as 38. David M, Weiler N, Heinrichs W, et al. High- markers of cardiovascular performance during frequency oscillatory ventilation in adult acute respi- resuscitation. J Trauma 2006;60:930–5. ratory distress syndrome. Intensive Care Med 2003; 54. Rocca GD, Costa MG, Pompei L, et al. Continuous 29:1656–65. and intermittent cardiac output measurement: 39. Cartotto R, Ellis S, Gomez M, et al. High frequency pulmonary artery catheter versus aortic transpulmo- oscillatory ventilation in burn patients with the acute nary technique. Br J Anaesth 2002;88:350–6. respiratory distress syndrome. Burns 2004;30:453–63. 55. Holm C, Mayr M, Tegeler J, et al. A clinical random- 40. Derdak S, Mehta S, Stewart TE, et al. High ized study on the effects of invasive monitoring on frequency oscillatory ventilation for acute respiratory burn shock resuscitation. Burns 2004;30:798–807. distress syndrome: a randomized controlled trial. 56. Kuntscher MV, Germann G, Hartmann B. Correla- Am J Respir Crit Care Med 2002;166:801–8. tions between cardiac output, stroke volume, central 41. Bollen CW, van Well GT, Sherry T, et al. High venous pressure, intra-abdominal pressure and total frequency oscillatory ventilation compared with circulating blood volume in resuscitation of major conventional mechanical ventilation in adult respira- burns. Resuscitation 2006;70:37–43. tory distress syndrome: a randomized controlled 57. Holm C, Mayr M, Horbrand F, et al. Reproducibility of trial. Crit Care 2005;9:R430–9. transpulmonary thermodilution measurements in 42. Engrav LH, Colescott PL, Kemalyan N, et al. A patients with burn shock and hypothermia. J Burn biopsy of the use of the Baxter formula to resuscitate Care Rehabil 2005;26:260–5. burns or do we do it like Charlie did it? J Burn Care 58. Rocca G, Costa MG, Coccia C, et al. Cardiac output Rehabil 2000;21:91–5. monitoring: aortic transpulmonary thermodilution 43. Pruitt BA Jr. Protection from excessive resuscitation: and pulse contour analysis agree with standard ther- pushing the pendulum back. J Trauma 2000;49: modilution methods in patients undergoing lung 387–91. transplantation. Can J Anaesth 2003;50:707–11. 44. Shah A, Kramer GC, Grady JJ, et al. Meta-analysis 59. McGee WT, Horswell JL, Calderon J. Validation of of fluid requirements for burn injury 1980–2002. a continuous cardiac output measurement using arte- J Burn Care Rehabil 2003;24:S118. rial pressure waveforms. Crit Care 2005;9:24–5. 45. Friedrich JB, Sullivan SR, Engrav LH, et al. Is supra- 60. De Wilde RB, Breukers RB, van den Berg PC, et al. Baxter resuscitation in burns patients a new Monitoring cardiac output using the femoral and phenomenon? Burns 2004;30:464–6. radial arterial pressure waveform. Anaesthesia 46. Greenhalgh DG, Warden GD. The importance of 2006;61:743–6. intra-abdominal pressure measurements in burned 61. Bajorat J, Hofmockel R, Vagts DA, et al. Comparison children. J Trauma 1994;36:685–90. of invasive and less-invasive techniques of cardiac
What’s New in Critical Care of the Burn Patient? 615 output measurement under different haemodynamic 76. Greenhalgh DG, Saffle JR, Holmes JH 4th, et al. conditions in a pig model. Eur J Anaesthesiol 2006; American Burn Association consensus conference 23:23–30. to define sepsis and infection in burns. J Burn62. Wynne JL, Ovadje LO, Akridge CM, et al. Imped- Care Res 2007;28:776–90. ance cardiography: a potential monitor for hemodial- 77. Mizock BA. Alterations in fuel metabolism in critical ysis. J Surg Res 2006;133:55–60. illness: hyperglycaemia. Best Pract Res Clin Endo-63. Holm C, Horbrand F, Mayr M, et al. Assessment of crinol Metab 2001;15:533–51. splanchnic perfusion by gastric tonometry in 78. Siegel JH, Cerra FB, Coleman B, et al. Physiological patients with acute hypovolemic burn shock. Burns and metabolic correlations in human sepsis. Invited 2006;32:689–94. commentary. Surgery 1979;86:163–93.64. Wallace EL, Churchill WH, Surgenor DM, et al. 79. Srinivasan V, Spinella PC, Drott HR, et al. Associa- Collection and transfusion of blood and blood tion of timing, duration, and intensity of hypergly- components in the United States, 1994. Transfusion cemia with intensive care unit mortality in critically 1998;38:625–36. ill children. Pediatr Crit Care Med 2004;5:329–36.65. Hebert PC, Wells G, Martin C, et al. A Canadian 80. Gore DC, Chinkes D, Heggers J, et al. Association of survey of transfusion practices in critically ill hyperglycemia with increased mortality after severe patients. Crit Care Med 1998;26:482–7. burn injury. J Trauma 2001;51:540–4.66. Marini JJ. Transfusion triggers and Occam’s rusty 81. van den Berghe G, Wouters P, Weekers F, et al. razor. Crit Care Med 1998;26:1775–6. Intensive insulin therapy in the critically ill patients.67. Alvarez G, Hebert PC, Szick S. Debate: transfusing N Engl J Med 2001;345:1359–67. to normal haemoglobin levels will not improve 82. Malmberg K. Prospective randomised study of outcome. Crit Care 2001;5(2):56–63. intensive insulin treatment on long term survival after68. Hebert PC, Wells G, Blajchman MA, et al. A multi- acute myocardial infarction in patients with diabetes center, randomized controlled clinical trial of transfu- mellitus. DIGAMI (Diabetes Mellitus, Insulin Glucose sion requirements in critical care. N Engl J Med Infusion in Acute Myocardial Infarction) Study 1999;340:409–17. Group. BMJ 1997;314:1512–5.69. Corwin HL, Gettinger A, Pearl RG, et al. The CRIT 83. Phan TN, Warren AJ, Pham HH, et al. Impact of tight study: anemia and blood transfusion in the critically glycemic control in severely burned children. ill—current clinical practice in the United States. Crit J Trauma 2005;59:1148–59. Care Med 2004;32:39–52. 84. Cochran A, Davis L, Morris SE, et al. Safety and effi-70. Sittig KM, Deitch EA. Blood transfusions: for the ther- cacy of an intensive insulin protocol in a burn-trauma mally injured or for the doctor? J Trauma 1994;36(3): intensive care unit. J Burn Care Res 2008;29: 369–72. 187–91.71. Palmieri TL, Caruso DM, Foster KN, et al. Impact of 85. Wiener RS, Wiener DC, Larson RJ. Benefits and blood transfusion on outcome after major burn injury: risks of tight glucose control in critically ill adults: a multicenter study. Crit Care Med 2006;34:1602–7. a meta-analysis. JAMA 2008;300:933–44.72. Jeschke MG, Chinkes DL, Finnerty CC, et al. Blood 86. Devos P, Preiser J, Melot C. Impact of tight glucose transfusions are associated with increased risk for control by intensive insulin therapy on ICU mortality development of sepsis in severely burned pediatric and the rate of hypoglycaemia: final results of the patients. Crit Care Med 2007;35:579–83. glucontrol study. Intensive Care Med 2007;33:S189.73. Palmieri TL, Lee T, O’Mara MS, et al. Effects of a restric- 87. Treggiari MM, Karir V, Yanez ND, et al. Intensive tive blood transfusion policy on outcomes in children insulin therapy and mortality in critically ill patients. with burn injury. J Burn Care Res 2007;28:65–70. Crit Care 2008;12:R29.74. Kwan P, Gomez M, Cartotto R. Safe and successful 88. Kanji S, Buffie J, Hutton B, et al. Reliability of point- restriction of transfusion in burn patients. J Burn of-care testing for glucose measurement in critically Care Res 2006;27:826–34. ill adults. Crit Care Med 2005;33:2778–85.75. Dellinger RP, Levy MM, Cartet JM, et al. Surviving 89. Mann EA, Pidcoke HF, Salinas J, et al. Compar- Sepsis Campaign: International guidelines for ison of point-of-care and laboratory glucose anal- management of severe sepsis and septic shock: ysis in critically ill patients. Am J Crit Care 2007; 2008. Crit Care Med 2008;36:296–327. 16:531–2.