Advances in burn critical careKyros Ipaktchi, MD; Saman Arbabi, MD, MPH    Background: Management of burn patients require...
icant decrease in reintubation rates, in the    accurate diagnosis of infectious compli-          Crystalloid solutions, s...
patients, with the possible exception of       there is significant increase in energy ex-        ment of surgical patients...
nases was observed. The authors recom-           experimental burn-injured sheep was as-         may attenuate systemic in...
duction in mortality in pediatric patients              effect of massive resuscitation after burn in-         gan dysfunc...
Effect of atenolol on mortality and cardiovas-   71. Hart DW, Wolf SE, Ramzy PI, et al: Anabolic      83. Dubick MA, Willi...
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Burn

  1. 1. Advances in burn critical careKyros Ipaktchi, MD; Saman Arbabi, MD, MPH Background: Management of burn patients requires a complex of burn patients includes strategies to minimize iatrogenic injury withinteraction of surgical, medical, critical care, and rehabilitation low tidal volume ventilation, to improve ventilation/perfusion mis-approaches. Severe burn patients are some of the most challeng- match, and to diagnosis pneumonia. Many aspects of burn resusci-ing critically ill patients who may have multiple-system organ tation remain controversial, and the best form of fluid resuscitationfailure with life-threatening complications. has yet to be identified. Recent research in the metabolic response to Objective: To review and highlight some of the recent ad- thermal injury has identified many potentially beneficial treatments.vances in burn critical care. We focused on some of the new Although immunomodulation therapy is promising, currently most oftreatment modalities in the management of respiratory complica- these treatments are not clinically viable, and further clinical andtions, advances in burn resuscitation, management of the meta- translational research is warranted. (Crit Care Med 2006; 34[Suppl.]:bolic response to burns, and recent ideas in burn immunotherapy. S239 –S244) Data Source: A search of the MEDLINE database and manual KEY WORDS: burn; critical care; inflammation; signal transduc-review of published articles and abstracts from national and tion; mitogen-activated protein kinase (MAPK); adrenergic recep-international meetings. tors; immunotherapy Data Syntheses and Conclusions: The respiratory managementT reating patients with burn patients face complex critical care issues. bating acute lung injury. Institution of injuries requires a complex, The present article will be a brief report low tidal volume ventilation, allowing multidimensional approach. on some of the new advances in burn permissive hypercapnia, was shown to re- Burn patients may have exten- critical care. Rather than being all inclu- duce the development of ventilator-sive damage to skin, which may require sive, we focused on four critical care issues: associated lung injury and significantlymultiple surgical interventions, burn new approaches in management of respira- improve outcomes (4). In addition, use ofwound management, physical and occu- tory complications, advances in the resus- alternate ventilation strategies such aspational therapy, and scar management. citation strategies, complex management high-frequency oscillatory ventilationIn the last decade, there have been major of the metabolic response to burns in- and high-frequency percussive ventila-advances in this aspect of burn care, cluding nutritional support, and recent tion may be beneficial in selected burnwhich includes early excision and graft- ideas and approaches in immunotherapy. patients (5). Although there are limiteding with autologous or allogeneic skin or comparative data regarding these twobiosynthetic dermal substitutes (1). Al- AIRWAY MANAGEMENT AND strategies, it seems that high-frequencythough this approach has decreased mor- VENTILATORY STRATEGIES percussive ventilation is especially usefulbidity and mortality, burn patients con- in inhalation injuries (6). Extracorporealtinue to face many serious complications. Most severely burn-injured patients are intubated early for airway manage- membrane oxygenation is described byThermal insult may induce a major distur- some authors as an ultimate salvage op-bance in the homeostatic mechanisms, ment and respiratory support. Pulmonary insufficiency and failure in severely tion in the pediatric population (7). Forwith severe disturbance in hemodynamic, adult patients, extracorporeal membranerespiratory, and metabolic pathways (2). burned patients is multifactorial. The pathogenesis can be differentiated into oxygenation is to be considered when pa-Potential postburn complications are se- tients face respiratory death from inhala-vere systemic inflammatory response direct pulmonary and upper airway inha- lation injury and indirect or secondary tion injury (8).syndrome, sepsis, acute respiratory dis- acute lung injury due to activation of the Adjunct therapies such as inhaled ni-tress syndrome, multiple-system organ systemic inflammatory response. There is tric oxide have gained momentum infailure, and death. Addition of inhalation also secondary delayed pulmonary injury treating hypoxic vasoconstriction in burninjury may double the mortality rate and due to sepsis and pneumonia. In addition, patients, improving ventilation/perfusionact as a synergistic insult on the pulmo- ventilator-associated lung injury has mismatches and thereby tissue oxygen-nary system (3). Physicians treating burn been described as an important iatro- ation (9, 10). In an animal model of in- genic factor contributing to the second- halation injury, aerosolized heparin at- ary accentuation of pulmonary injury (4). tenuated cellular infiltrates, lung edema, From the University of Michigan Burn Center, AnnArbor, MI. The reduced pulmonary compliance and congestion, and cast formation and im- Copyright © 2006 by the Society of Critical Care chest wall rigidity of burn patients can proved oxygenation (11). In a study of 90Medicine and Lippincott Williams & Wilkins lead to aggressive ventilatory manage- consecutive burn pediatric patients who DOI: 10.1097/01.CCM.0000232625.63460.D4 ment and high airway pressures, exacer- had inhalation injury, there was a signif-Crit Care Med 2006 Vol. 34, No. 9 (Suppl.) S239
  2. 2. icant decrease in reintubation rates, in the accurate diagnosis of infectious compli- Crystalloid solutions, such as lactatedprevalence of atelectasis, and in mortality cations such as pneumonia. The National Ringers solution and normal saline, arefor patients treated with the regimen of Infection Surveillance System uses phys- still first-line fluid replacements in burnaerosolized heparin and N-acetylcysteine iologic data, laboratory evaluation, and resuscitation. Due to reduced intravascu-when compared with controls (12). radiographic data to define pneumonia. lar fluid retention, large volumes have Although most recent studies demon- Recognizing the difficult diagnosis of to be infused, which accentuate tissuestrate improved outcomes with early tra- ventilator-associated pneumonia in the edema, and the development of tissuecheostomy, controversy still exists on the injured patients (21), many investigators edema can lead to worsening outcomesgeneral “optimal” tracheostomy tech- have demonstrated the improved sensi- (30). Hypertonic saline (HTS) resuscita-nique and timing (13). A retrospective tivity and specificity by including quanti- tion (7.5% NaCl) has been promoted forstudy of pediatric burn patients demon- tative cultures obtained via bronchoal- its efficient intravascular volume resusci-strated that early tracheostomy was safe, veolar lavage (22, 23). In a retrospective tation, rapid restoration of blood pressureprovided a secure airway, and improved review of adult burn patients, the use of and cardiac output with improved cere-the ventilatory management of patients bronchoalveolar lavage eliminated the bral perfusion, and potential for expand-(14); but there was no significant change unnecessary antibiotic treatment of 21% ing circulating volume by reabsorption ofin oxygenation, minute ventilation, or pH of patients and was associated with a fluid from the interstitial space (31).after tracheostomy. In a retrospective re- lower rate of ventilator-associated pneu- More recently, HTS has been studied as aview of adult patients with severe burn monia (24). fluid with significant modulation of sys-injury, there were no differences in ven- temic inflammatory response secondarytilatory support, length of stay, preva- RESUSCITATION to reperfusion injury, which may be ben-lence of pneumonia, or survival (15); eficial in patients with shock (32, 33). Inhowever, patients with tracheostomy had Burn trauma leads to a combination animal models of trauma and burn, use ofa significantly shorter time to extubation. of hypovolemic and distributive shock HTS resuscitation has been associatedAlthough there is controversy regarding on the basis of generalized microvascu- with decreased edema and improved or-improved pneumonia rate and mortality, lar injury and interstitial third-spacing gan perfusion and outcomes (34 –36).most researchers agree that tracheos- through collagen and matrix degenera- Data on the effectiveness of HTS to pre-tomy offers some advantages in terms of tion. Burn injury is marked by dynamic vent organ damage in the clinical settingpatient comfort and security. Regarding and ongoing fluid shifts, which have led are inconsistent (37). Some of the studiesthe preferred tracheostomy technique, re- to the development of fluid resuscitation in burn patients have demonstrated thatcent studies demonstrate that percutane- formulas based on percentage of total HTS may have decreased the fluid load,ous tracheostomy may be safe in burn pa- body surface area burn and weight. Fluid tissue edema, and complications such astients (16, 17). Addition of fiberoptic resuscitation based on the Parkland burn abdominal compartment syndrome (38 –assistance may avoid rare but serious com- formula is extensively used in burn cen- 40). But others have noted no benefit inplications (18). The enthusiasm for percu- ters and has helped minimize the occur- fluid requirement and potential increasetaneous tracheostomy should be tempered rence of burn shock (25). However, a risk of renal failure (41). It seems that thein patients with severe facial and neck recent survey of 28 burn centers found benefit of HTS is seen in early resuscita-burns or upper airway edema because loss that in 58% of patients, actual fluid re- tion (42), and some researchers have rec-of airway in these patients may be associ- suscitation exceeded the 4 mL/kg recom- ommended stopping HTS infusion whenated with significant complications. mended by Baxter and Shires (26). Over- serum sodium concentration exceeds 160 resuscitation has been shown to correlate mEq/L (29, 43). Currently, HTS is not Pneumonia. Pneumonia is still one of directly with increasing intraabdominal routinely used in burn patients, and fur-the most common infectious complica- pressure and the development of abdom- ther research is required to better definetions in severe burn patients. Ventilator- inal compartment syndrome (27). Apart potential benefits, the timing, and theassociated pneumonia is very common in from the well-described extremity com- optimal volume.burn patients, and similar to other criti- partment syndrome, orbital compart- Theoretically, the use of colloids incally ill patients, it is associated with in- ment syndrome requiring canthotomy in resuscitation of hypovolemic patientscreased risk of fatal outcome (19, 20). patients receiving supranormal resuscita- may be associated with preservation ofSeveral factors prime burn victims for tion was recently described (28). The cur- plasma osmotic pressure, more efficientincreased susceptibility for pneumonia: rent high-volume fluid regimens have plasma volume expansion, and decreasedrelative immunosuppression, dysfunc- shifted postburn resuscitation complica- tissue and pulmonary edema. However,tional ciliary movement in inhalational tions from renal failure to pulmonary clinical studies have not demonstrated ainjuries leading to impaired secretory edema, with increased requirement for significant improvement in patient out-clearance, pulmonary inflammatory acti- ventilatory support, the need for fascioto- comes with colloid resuscitation (31, 44,vation with acute lung injury, and in- mies in unburned limbs, and the occur- 45). In burn patients, treatment with al-creased leakage of nutrient-rich plasma rence of the abdominal compartment bumin did not improve outcomes (44).into lung parenchyma. Due to severe un- syndrome (29). The increased use of sed- A prospective randomized study dem-derlying inflammatory pulmonary pa- ative and analgesic medication may have onstrated that a restrictive strategy ofthology, accurate clinical diagnosis of contributed to increased fluid volumes red-cell transfusion (hemoglobin concen-ventilator-associated pneumonia can be given to burn patients. In essence, the tration maintained at 7.0 –9.0 g/dL) mayvery difficult in burn patients. The recent pendulum may have swung from insuffi- be superior to a liberal transfusion strat-emergence of multi– drug-resistant bac- cient resuscitation to excessive volume egy (hemoglobin concentration main-terial pathogens has mandated a more loading. tained at 10.0 –12.0 g/dL) in critically illS240 Crit Care Med 2006 Vol. 34, No. 9 (Suppl.)
  3. 3. patients, with the possible exception of there is significant increase in energy ex- ment of surgical patients. In elective non-patients with acute myocardial infarction penditure after burns, high-calorie nutri- cardiac operations, perioperativeand unstable angina (46). A recent mul- tional support was thought to decrease treatment with beta-blockers has been as-tiple-center cohort analysis found an in- muscle catabolism. However, aggressive sociated with reduced mortality and prev-creased mortality in burn patients asso- high-calorie feeding with a combination alence of cardiovascular complicationsciated with blood transfusions (47). of enteral and parenteral nutrition was (61, 62). In burn patients, beta-blockersTherefore, there is a push to decrease associated with increased mortality (56). can blunt the catecholamine effect by at-blood transfusion in burn patients. Re- Increasing enteral feeding beyond the tenuating hypermetabolism, decreasingcombinant human erythropoietin has body energy expenditure, 20 – 40% above oxygen demand and resting energy ex-been shown to be useful in treatment of the resting energy expenditure, does not penditure, and decreasing heart rate andchronic anemia and, theoretically, may improve lean body mass and is associated cardiac oxygen demand (54). Beta-decrease the need for blood transfusion in with complications such as fatty liver blockers may also attenuate catechol-the ICU. However, in a prospective, dou- (51). Most authors recommend adequate amine-induced muscle catabolism and li-ble-blind, randomized study of 40 se- calorie intake via enteral feeding and polysis (63, 64). Moreover, there are dataverely burned patients, recombinant hu- avoidance of overfeeding (54). to suggest that beta-blockers can modifyman erythropoietin did not prevent the High carbohydrate diets compared catecholamine-mediated defect in lym-development of postburn anemia or de- with high fat diets may improve the net phocyte activation and improve immunecrease transfusion requirements (48). In- balance of skeletal muscle protein (57). response with decreased infectious com-terestingly, a recent animal study dem- Increased endogenous insulin may con- plications (65). Various studies have dem-onstrated that recombinant human tribute to improved muscle metabolism. onstrated the potential beneficial effect oferythropoietin improved healing of burn In a study of six adult patients with beta-blockers in burn patients. Adminis-wound through increased epithelial pro- 40% total body surface area burn, treat- tration of propranolol (nonselective beta-liferation, maturation of the extracellular ment with insulin and metformin were antagonist) to burned children reducesmatrix, and angiogenesis (49). Currently, associated with improved muscle kinetic the release of free fatty acids from adiposemost centers do not use erythropoietin in (58). However, high carbohydrate diet tissue and decreases hepatic triacylglyc-treatment of burn patients, and further may be associated with elevated glucose, erol storage and fat accumulation (66,clinical study is required before routine which may be detrimental in critically ill 67). In a randomized study of 25 childrenclinical use. patients. In a study of 58 pediatric burn with severe burns, treatment with pro- patients, there was a significant associa- pranolol attenuated hypermetabolismMETABOLIC RESPONSE tion between poor glucose control and and reversed muscle protein catabolism complications such as increased bactere- (68). In a retrospective study of adult During the flow phase postburn, there mia, reduced skin graft take, and in- burn patients, use of beta-blockers wasis an impressive hyperdynamic response. creased mortality (59). In another study, associated with decreased mortality,For pediatric patient with 40% total tight glucose control in severe burn pa- wound infection rate, and wound healingbody surface area burn, the resting met- tients seemed to be safe and associated time (69). Although these data stronglyabolic rate is increased in the ranges be- with decreased risk of infection and im- support the use of beta-blockers in burntween 160% and 200% (50). This global proved survival (60). Therefore, aggres- patients, there are no large randomizedhypermetabolism is associated with sive monitoring and treatment of hyper- studies looking at mortality and woundtachycardia, fever, muscle protein catab- glycemia is recommended. healing in burn patients. Nevertheless,olism, and derangement in hepatic pro- Similar to all critically ill patients, ad- many burn units use beta-blockers suchtein synthesis (51, 52). This response may equate protein intake is required. Be- as propranolol or metoprolol as the mostbe associated with significant complica- cause there is an increased oxidation rate effective catabolic treatment in burn pa-tions such as immunodeficiency, im- of amino acids in burn patients, the pro- tients.paired wound healing, sepsis, loss of lean tein requirement is increased to 1.5–2.0 Oxandrolone. Oxandrolone is an ana-body and muscle mass, cardiac ischemia, g/kg per day in treatment of severely log of testosterone, which is an anabolicand potential death. Primary treatment burned patients (54). hormone. It has been used to treat mus-modalities include avoidance of infec- cle wasting in various disease processestious complications such as sepsis and Modulation of Hormonal and such as acquired immune deficiency syn-early excision of full-thickness burns, Endocrine Response drome (70). In a study of 14 severelywhich is associated with attenuation of burned children, oxandrolone improvedhypermetabolism (52–54). Several other Burn injury is associated with in- muscle protein metabolism through en-approaches have been used to attenuate creased levels of catecholamines and cat- hanced protein synthesis efficiency (71).the burn-induced hypermetabolism (54). abolic hormones. Therefore, it is logical In adult burn patients, oxandrolone sig-This article will focus on early nutritional to assume blockade of catecholamine re- nificantly decreased weight loss and netsupport and modulation of hormonal/ sponse or use of anabolic steroids may nitrogen loss and increased donor siteendocrine response. attenuate hypermetabolism or blunt cat- wound healing compared with placebo abolic response after burn injury. In this controls (72). In a prospective random-Nutritional Support review, we will focus on beta-adrenergic ized study of 81 patients, 10 mg of oxan- receptor blockade and oxandrolone. drolone every 12 hrs was associated with The use of early enteral feeding in Beta-Adrenergic Receptor Blockade. decreased hospital stay (73). Althoughburn patients may attenuate catabolic re- There has been a recent increased enthu- there was no hepatic insufficiency, a sig-sponse after thermal injury (55). Because siasm for use of beta-blockers in treat- nificant increase in hepatic transami-Crit Care Med 2006 Vol. 34, No. 9 (Suppl.) S241
  4. 4. nases was observed. The authors recom- experimental burn-injured sheep was as- may attenuate systemic inflammatory re-mended monitoring liver function tests sociated with decreased edema and fluid sponse and acute lung injury (93, 94). Inin patients treated with oxandrolone. requirement (83). In a randomized trial these studies, topical application of p38-Enthusiasm to use oxandrolone should of critically ill surgical patients, a combi- mitogen–activated protein kinase inhibi-also be tempered by the findings of po- nation of ascorbic acid and -tocopherol tor to the burn wound decreased dermaltential increase in ventilatory days; in a reduced the prevalence of organ failure inflammation, postburn skin apoptosis,study of trauma patients, oxandrolone and ICU length of stay (84). Early use of systemic inflammatory response, and sec-was associated with increased ventila- high-dose antioxidant therapy in the in- ondary pulmonary complications. Topicaltory days (74). The authors suggested jured patients seems to be beneficial; inflammatory modulation in severe burnsthat oxandrolone may enhance collagen however, further clinical trials are re- is attractive because it can be readily useddeposition in acute respiratory distress. quired to confirm this potential effect and in patients who are already receiving top-Overall, it seems that oxandrolone may better define the timing and the required ical antimicrobial agents, and it maybe beneficial in patients with large body dose (85, 86). avoid some of the systemic complica-surface area burns. Recombinant Human Activated Pro- tions. However, currently there are no tein C. Recombinant activated protein C clinically approved topical immuno-IMMUNOTHERAPY (activated drotrecogin alfa) is the first modulators for burn patients. agent approved by the Food and Drug Severe dermal burns are known to in- Administration for treatment of severe REFERENCESduce systemic inflammatory response sepsis. The Protein C Worldwide Evalua-syndrome, which is correlated with a tion in Severe Sepsis (PROWESS) trial 1. Heimbach DM, Warden GD, Luterman A, ethigh risk of end-organ failure (5, 75). Also demonstrated a statistically significant al: Multicenter postapproval clinical trial ofsevere burn injury is associated with in- relative risk reduction of 28-day mortality Integra dermal regeneration template forcreased risk of infection, sepsis, and im- (87). Post hoc analyses of 532 possible burn treatment. J Burn Care Rehabil 2003;munosuppression (76, 77). Therefore, surgical patients in the PROWESS trial 24:42– 48many investigators have studied the ben- demonstrated a favorable benefit/risk 2. Sheridan RL: A great constitutional distur- bance. N Engl J Med 2001; 345:1271–1272efit of immune modulation in severely profile in surgical patients (88, 89). In- 3. Greenhalgh DG: Hypoxic pulmonary vaso-burned patients. creased risk of bleeding was similar to the constriction after combined burn and inha- Immunonutrition. The immune-en- medical patients, and there was no fatal lation injury. Crit Care Med 2006; 34:hancing diets/agents include arginine, bleeding in the surgical cohort. Twenty- 1562–1563glutamine, omega-3 fatty acids, and anti- four patients in this group were defined 4. Ventilation with lower tidal volumes as com-oxidants such as ascorbic acid (vitamin C) as having a skin surgical procedure pared with traditional tidal volumes for acuteand -tocopherol (vitamin E). Multiple within 30 days before the study. There lung injury and the acute respiratory distressstudies looking at a combination diet of was a 12-hr waiting period after an oper- syndrome: The Acute Respiratory Distressthese agents have failed to demonstrate a ation before starting the treatment. Syndrome Network. N Engl J Med 2000; 342:benefit in critically ill patients (78, 79). Other exclusion criteria for PROWESS 1301–1308 5. Cartotto R, Ellis S, Smith T: Use of high-The controversy regarding the use of im- were pregnancy, recent cerebrovascular frequency oscillatory ventilation in burn pa-mune-enhancing diets is ongoing, with accident, intracranial pathology, active tients. Crit Care Med 2005; 33:S175–S181many studies showing benefit and others bleeding, or anticipated need for surgery 6. Cioffi WG Jr, Rue LW III, Graves TA, et al:showing no improvement in outcomes. within the ensuing 96-hr period. It Prophylactic use of high-frequency percus-For instance, whereas many previous should also be noted that because 90% of sive ventilation in patients with inhalationstudies support the use of glutamine sup- the drug is eliminated within 2 hrs after injury. Ann Surg 1991; 213:575–580; discus-plementation, a recent study demon- discontinuation of infusion, stopping the sion, 580 –572strated that addition of glutamine to the treatment should rapidly stop drotreco- 7. Goretsky MJ, Greenhalgh DG, Warden GD, etenteral feed did not improve outcomes gin alfa–induced bleeding (88). Although al: The use of extracorporeal life support in(80). Also, although many studies in there are no published trials specifically pediatric burn patients with respiratory fail- ure. J Pediatr Surg 1995; 30:620 – 623burned animal models show improve- in burn patients, based on available infor- 8. Thompson JT, Molnar JA, Hines MH, et al:ment with a specific immune supplemen- mation, burn patients with severe sepsis Successful management of adult smoke in-tation, there are no human studies to who lack the exclusion criteria should be halation with extracorporeal membraneinvestigate the response in a clinical set- considered for recombinant activated oxygenation. J Burn Care Rehabil 2005; 26:ting. As an example, in burned rats, sup- protein C. 62– 66plementation with omega-3 fatty acids Topical Immunomodulation. Thermal 9. Sheridan RL, Hurford WE, Kacmarek RM,improved protein metabolism and atten- injury induces dermal inflammatory and et al: Inhaled nitric oxide in burn patientsuated muscle breakdown (81), but no pro-apoptotic signaling. In the absence of with respiratory failure. J Trauma 1997; 42:large human trial has confirmed these inhalation injury, the burn wound is the 629 – 634finding in burned patients. Most re- inflammatory source triggering systemic in- 10. Westphal M, Cox RA, Traber LD, et al: Com- bined burn and smoke inhalation injury im-searchers agree that an indiscriminate flammatory response via liberation of a pairs ovine hypoxic pulmonary vasoconstric-use of a combination formula immu- plethora of potentially deleterious proin- tion. Crit Care Med 2006; 34:1428 –1436nonutrition diet in critically ill patients is flammatory mediators and attraction/ 11. Murakami K, McGuire R, Cox RA, et al: Hep-not beneficial (78, 82). Therefore, a more activation of neutrophils (90 –92). Stud- arin nebulization attenuates acute lung in-selective approach is proposed, and there ies using rodent models of thermal injury jury in sepsis following smoke inhalation inis a need for more clinical studies. have demonstrated that controlling the sheep. Shock 2002; 18:236 –241 Use of high doses of ascorbic acid in source of inflammation at the dermis 12. Desai MH, Mlcak R, Richardson J, et al: Re-S242 Crit Care Med 2006 Vol. 34, No. 9 (Suppl.)
  5. 5. duction in mortality in pediatric patients effect of massive resuscitation after burn in- gan dysfunction score. Transfusion 2006; 46: with inhalation injury with aerosolized hep- jury. J Trauma 2006; 60:72–76 80 – 89 arin/N-acetylcystine [correction of acetyl- 29. Pruitt BA Jr: Does hypertonic burn resusci- 45. Finfer S, Bellomo R, Boyce N, et al: A com- cystine] therapy. J Burn Care Rehabil 1998; tation make a difference? Crit Care Med parison of albumin and saline for fluid resus- 19:210 –212 2000; 28:277–278 citation in the intensive care unit. N Engl13. Pelosi P, Severgnini P: Tracheostomy must 30. Ahrns KS: Trends in burn resuscitation: J Med 2004; 350:2247–2256 be individualized! Crit Care 2004; 8:322–324 Shifting the focus from fluids to adequate 46. Hebert PC, Wells G, Blajchman MA, et al: A14. Palmieri TL, Jackson W, Greenhalgh DG: endpoint monitoring, edema control, and ad- multicenter, randomized, controlled clinical Benefits of early tracheostomy in severely juvant therapies. Crit Care Nurs Clin North trial of transfusion requirements in critical care: burned children. Crit Care Med 2002; 30: Am 2004; 16:75–98 Transfusion Requirements in Critical Care In- 922–924 31. Arbabi S: Hypovolemic Shock. In: Complica- vestigators, Canadian Critical Care Trials15. Saffle JR, Morris SE, Edelman L: Early tra- tions in Surgery. Mulholland MW, Doherty Group. N Engl J Med 1999; 340:409 – 417 cheostomy does not improve outcome in GM (Eds). Philadelphia, Lippincott Williams 47. Palmieri TL, Caruso DM, Foster KN, et al: burn patients. J Burn Care Rehabil 2002; and Wilkins, 2005, pp 136 –143 Effect of blood transfusion on outcome after 23:431– 438 32. Staudenmayer KL, Maier RV, Jelacic S, et al: major burn injury: A multicenter study. Crit16. Caruso DM, al-Kasspooles MF, Matthews MR, Hypertonic saline modulates innate immu- Care Med 2006; 34:1602–1607 et al: Rationale for ‘early’ percutaneous dila- nity in a model of systemic inflammation. 48. Still JM Jr, Belcher K, Law EJ, et al: A dou- tational tracheostomy in patients with burn Shock 2005; 23:459 – 463 ble-blinded prospective evaluation of recom- injuries. J Burn Care Rehabil 1997; 18: 33. Arbabi S, Rosengart MR, Garcia I, et al: Hy- binant human erythropoietin in acutely 424 – 428 pertonic saline solution induces prostacyclin burned patients. J Trauma 1995; 38:233–23617. Gravvanis AI, Tsoutsos DA, Iconomou TG, et production by increasing cyclooxygenase-2 49. Galeano M, Altavilla D, Bitto A, et al: Recom- al: Percutaneous versus conventional trache- expression. Surgery 2000; 128:198 –205 binant human erythropoietin improves an- ostomy in burned patients with inhalation 34. Murao Y, Loomis W, Wolf P, et al: Effect of giogenesis and wound healing in experimen- injury. World J Surg 2005; 29:1571–1575 dose of hypertonic saline on its potential to tal burn wounds. Crit Care Med 2006; 34:18. Herve S, Patuano E, Ainaud P, et al: [Reflec- prevent lung tissue damage in a mouse 1139 –1146 tions on percutaneous tracheotomy: Regard- model of hemorrhagic shock. Shock 2003; 50. Hart DW, Wolf SE, Mlcak R, et al: Persistence ing a retrospective study of 106 cases with 20:29 –34 of muscle catabolism after severe burn. Sur- major burns]. Ann Otolaryngol Chir Cervi- 35. Angle N, Hoyt DB, Cabello-Passini R, et al: gery 2000; 128:312–319 cofac 1999; 116:258 –262 Hypertonic saline resuscitation reduces neu- 51. Hart DW, Wolf SE, Herndon DN, et al: En-19. Cook DJ, Brun-Buisson C, Guyatt GH, et al: trophil margination by suppressing neutro- ergy expenditure and caloric balance after Evaluation of new diagnostic technologies: phil L selectin expression. J Trauma 1998; burn: Increased feeding leads to fat rather Bronchoalveolar lavage and the diagnosis of 45:7–12; discussion, 12–13 than lean mass accretion. Ann Surg 2002; ventilator-associated pneumonia. Crit Care 36. Kien ND, Antognini JF, Reilly DA, et al: 235:152–161 Med 1994; 22:1314 –1322 Small-volume resuscitation using hypertonic 52. Hart DW, Wolf SE, Chinkes DL, et al: Deter-20. Jackson WL, Shorr AF: Update in ventilator- saline improves organ perfusion in burned minants of skeletal muscle catabolism after associated pneumonia. Curr Opin Anaesthe- rats. Anesth Analg 1996; 83:782–788 severe burn. Ann Surg 2000; 232:455– 465 siol 2006; 19:117–121 37. Murao Y, Hoyt DB, Loomis W, et al: Does the 53. Hart DW, Wolf SE, Chinkes DL, et al: Effects21. Croce MA, Swanson JM, Magnotti LJ, et al: timing of hypertonic saline resuscitation af- of early excision and aggressive enteral feed- The futility of the clinical pulmonary infec- fect its potential to prevent lung damage? ing on hypermetabolism, catabolism, and tion score in trauma patients. J Trauma Shock 2000; 14:18 –23 sepsis after severe burn. J Trauma 2003; 54: 2006; 60:523–527; discussion, 527–528 38. Bortolani A, Governa M, Barisoni D: Fluid 755–761; discussion, 761–75422. Miller PR, Johnson JC III, Karchmer T, et al: replacement in burned patients. Acta Chir 54. Herndon DN, Tompkins RG: Support of the National nosocomial infection surveillance Plast 1996; 38:132–136 metabolic response to burn injury. Lancet system: From benchmark to bedside in 39. Griswold JA, Anglin BL, Love RT Jr, et al: 2004; 363:1895–1902 trauma patients. J Trauma 2006; 60:98 –103 Hypertonic saline resuscitation: efficacy in a 55. Mochizuki H, Trocki O, Dominioni L, et al:23. Croce MA, Fabian TC, Mueller EW, et al: The community-based burn unit. South Med J Mechanism of prevention of postburn hyper- appropriate diagnostic threshold for ventila- 1991; 84:692– 696 metabolism and catabolism by early enteral tor-associated pneumonia using quantitative 40. Shimazaki S, Yukioka T, Matuda H: Fluid feeding. Ann Surg 1984; 200:297–310 cultures. J Trauma 2004; 56:931–934; dis- distribution and pulmonary dysfunction fol- 56. Herndon DN, Barrow RE, Stein M, et al: cussion, 934 –936 lowing burn shock. J Trauma 1991; 31: Increased mortality with intravenous supple-24. Wahl WL, Ahrns KS, Brandt MM, et al: Bron- 623– 626; discussion, 626 – 628 mental feeding in severely burned patients. choalveolar lavage in diagnosis of ventilator- 41. Huang PP, Stucky FS, Dimick AR, et al: Hy- J Burn Care Rehabil 1989; 10:309 –313 associated pneumonia in patients with pertonic sodium resuscitation is associated 57. Hart DW, Wolf SE, Zhang XJ, et al: Efficacy burns. J Burn Care Rehabil 2005; 26:57– 61 with renal failure and death. Ann Surg 1995; of a high-carbohydrate diet in catabolic ill-25. Baxter CR, Shires T: Physiological response 221:543–554; discussion, 554 –547 ness. Crit Care Med 2001; 29:1318 –1324 to crystalloid resuscitation of severe burns. 42. Elgjo GI, Poli de Figueiredo LF, Schenarts 58. Gore DC, Herndon DN, Wolfe RR: Compari- Ann N Y Acad Sci 1968; 150:874 – 894 PJ, et al: Hypertonic saline dextran produces son of peripheral metabolic effects of insulin26. Engrav LH, Colescott PL, Kemalyan N, et al: early (8 –12 hrs) fluid sparing in burn resus- and metformin following severe burn injury. A biopsy of the use of the Baxter formula to citation: A 24-hr prospective, double-blind J Trauma 2005; 59:316 –322; discussion, resuscitate burns or do we do it like Charlie study in sheep. Crit Care Med 2000; 28: 322–313 did it? J Burn Care Rehabil 2000; 21:91–95 163–171 59. Gore DC, Chinkes D, Heggers J, et al: Asso-27. O’Mara MS, Slater H, Goldfarb IW, et al: A 43. Shimazaki S, Yoshioka T, Tanaka N, et al: ciation of hyperglycemia with increased mor- prospective, randomized evaluation of intra- Body fluid changes during hypertonic lac- tality after severe burn injury. J Trauma abdominal pressures with crystalloid and col- tated saline solution therapy for burn shock. 2001; 51:540 –544 loid resuscitation in burn patients. J Trauma J Trauma 1977; 17:38 – 43 60. Pham TN, Warren AJ, Phan HH, et al: Impact 2005; 58:1011–1018 44. Cooper AB, Cohn SM, Zhang HS, et al: Five of tight glycemic control in severely burned28. Sullivan SR, Ahmadi AJ, Singh CN, et al: percent albumin for adult burn shock resus- children. J Trauma 2005; 59:1148 –1154 Elevated orbital pressure: Another untoward citation: Lack of effect on daily multiple or- 61. Mangano DT, Layug EL, Wallace A, et al:Crit Care Med 2006 Vol. 34, No. 9 (Suppl.) S243
  6. 6. Effect of atenolol on mortality and cardiovas- 71. Hart DW, Wolf SE, Ramzy PI, et al: Anabolic 83. Dubick MA, Williams C, Elgjo GI, et al: High- cular morbidity after noncardiac surgery: effects of oxandrolone after severe burn. Ann dose vitamin C infusion reduces fluid re- Multicenter Study of Perioperative Ischemia Surg 2001; 233:556 –564 quirements in the resuscitation of burn- Research Group. N Engl J Med 1996; 335: 72. Demling RH, Orgill DP: The anticatabolic injured sheep. Shock 2005; 24:139 –144 1713–1720 and wound healing effects of the testosterone 84. Nathens AB, Neff MJ, Jurkovich GJ, et al:62. Wallace A, Layug B, Tateo I, et al: Prophylac- analog oxandrolone after severe burn injury. Randomized, prospective trial of antioxidant tic atenolol reduces postoperative myocardial J Crit Care 2000; 15:12–17 supplementation in critically ill surgical pa- ischemia: McSPI Research Group. Anesthesi- 73. Wolf SE, Edelman LS, Kemalyan N, et al: Ef- tients. Ann Surg 2002; 236:814 – 822 ology 1998; 88:7–17 fects of oxandrolone on outcome measures in 85. Bulger EM, Maier RV: Antioxidants in critical63. Herndon DN, Nguyen TT, Wolfe RR, et al: the severely burned: A multicenter prospective illness. Arch Surg 2001; 136:1201–1207 Lipolysis in burned patients is stimulated by randomized double-blind trial. J Burn Care Res 86. Demling RH: The burn edema process: Cur- the beta 2-receptor for catecholamines. Arch 2006; 27:131–139; discussion, 140 –131 rent concepts. J Burn Care Rehabil 2005; Surg 1994; 129:1301–1304; discussion, 74. Bulger EM, Jurkovich GJ, Farver CL, et al: 26:207–227 1304 –1305 Oxandrolone does not improve outcome of 87. Bernard GR, Vincent JL, Laterre PF, et al:64. Louis SN, Jackman GP, Nero TL, et al: Role ventilator dependent surgical patients. Ann of beta-adrenergic receptor subtypes in lipol- Surg 2004; 240:472– 478; discussion, 478 – 480 Efficacy and safety of recombinant human ysis. Cardiovasc Drugs Ther 2000; 14: 75. Dancey DR, Hayes J, Gomez M, et al: ARDS in activated protein C for severe sepsis. N Engl 565–577 patients with thermal injury. Intensive Care J Med 2001; 344:699 –70965. Prass K, Meisel C, Hoflich C, et al: Stroke- Med 1999; 25:1231–1236 88. Barie PS, Williams MD, McCollam JS, et al: induced immunodeficiency promotes spon- 76. Davis KA, Santaniello JM, He LK, et al: Burn Benefit/risk profile of drotrecogin alfa (acti- taneous bacterial infections and is mediated injury and pulmonary sepsis: Development of vated) in surgical patients with severe sepsis. by sympathetic activation reversal by post- a clinically relevant model. J Trauma 2004; Am J Surg 2004; 188:212–220 stroke T helper cell type 1-like immunos- 56:272–278 89. Fry DE, Beilman G, Johnson S, et al: Safety timulation. J Exp Med 2003; 198:725–736 77. Sasaki J, Fujishima S, Iwamura H, et al: Prior of drotrecogin alfa (activated) in surgical pa-66. Aarsland A, Chinkes D, Wolfe RR, et al: burn insult induces lethal acute lung injury tients with severe sepsis. Surg Infect Beta-blockade lowers peripheral lipolysis in endotoxemic mice: Effects of cytokine in- (Larchmt) 2004; 5:253–259 in burn patients receiving growth hor- hibition. Am J Physiol Lung Cell Mol Physiol 90. Hansbrough JF, Wikstrom T, Braide M, et al: mone: Rate of hepatic very low density 2003; 284:L270 –L278 Neutrophil activation and tissue neutrophil lipoprotein triglyceride secretion remains 78. Heyland D, Dhaliwal R: Immunonutrition in sequestration in a rat model of thermal in- unchanged. Ann Surg 1996; 223:777–787; the critically ill: From old approaches to new jury. J Surg Res 1996; 61:17–22 discussion, 787–779 paradigms. Intensive Care Med 2005; 31: 91. Piccolo MT, Wang Y, Verbrugge S, et al: Role67. Morio B, Irtun O, Herndon DN, et al: Pro- 501–503 of chemotactic factors in neutrophil activa- pranolol decreases splanchnic triacylglycerol 79. Kieft H, Roos AN, van Drunen JD, et al: tion after thermal injury in rats. Inflamma- storage in burn patients receiving a high- Clinical outcome of immunonutrition in a tion 1999; 23:371–385 carbohydrate diet. Ann Surg 2002; 236: heterogeneous intensive care population. 92. Till GO, Johnson KJ, Kunkel R, et al: Intra- 218 –225 Intensive Care Med 2005; 31:524 –532 vascular activation of complement and acute68. Herndon DN, Hart DW, Wolf SE, et al: Re- 80. Schulman AS, Willcutts KF, Claridge JA, et lung injury: Dependency on neutrophils and versal of catabolism by beta-blockade after al: Does the addition of glutamine to enteral toxic oxygen metabolites. J Clin Invest 1982; severe burns. N Engl J Med 2001; 345: feeds affect patient mortality? Crit Care Med 1223–1229 2005; 33:2501–2506 69:1126 –113569. Arbabi S, Ahrns KS, Wahl WL, et al: Beta- 81. Hayashi N, Tashiro T, Yamamori H, et al: 93. Ipaktchi K, Mattar A, Niederbichler A, et al: blocker use is associated with improved out- Effect of intravenous omega-6 and omega-3 Topical p38MAPK inhibition reduces dermal comes in adult burn patients. J Trauma fat emulsions on nitrogen retention and pro- inflammation and epithelial apoptosis in 2004; 56:265–269; discussion, 269 –271 tein kinetics in burned rats. Nutrition 1999; burn wounds. Shock In Press70. Strawford A, Barbieri T, Van Loan M, et al: 15:135–139 94. Arbabi S, Ipaktchi K, Mattar A, et al: Modu- Resistance exercise and supraphysiologic an- 82. Ochoa JB, Makarenkova V, Bansal V: A ratio- lating local dermal inflammatory response drogen therapy in eugonadal men with HIV- nal use of immune enhancing diets: When improves survival in post-burn pneumonia related weight loss: A randomized controlled should we use dietary arginine supplementa- model. In: First Annual Academic Surgical trial. JAMA 1999; 281:1282–1290 tion? Nutr Clin Pract 2004; 19:216 –225 Congress. San Diego, California, 2006S244 Crit Care Med 2006 Vol. 34, No. 9 (Suppl.)

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