What's new in critical care of the burn injured patient
1. What ’s New in Critical
Care of the Burn - Injured
Patient?
Tina L. Palmieri, MD, FACS, FCCMa,b,*
KEYWORDS
Burns Sepsis Inhalation injury Critical care
Glycemic control
Mortality after burn injury has decreased markedly (ARDS).4 The risk for mortality from ALI and ARDS
in the past 30 years. Survival after burn injury to approaches 40% to 50%.5 This mortality may be
more than 90% of the total body surface area is directly due to respiratory failure and hypoxia, or
common in children, with some authors maintain- it may result from associated multisystem organ
ing that virtually all children with burn injury should failure or ventilator-associated pneumonia. New
be resuscitated.1 Unfortunately, the improvement strategies for mechanical ventilation are currently
in survival does not apply to all age groups: being used to support burn patients who have
survival in the elderly burn patient remains prob- respiratory insufficiency, ALI, and ARDS. These
lematic. 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 of
treatment 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 antimicrobial
therapy.2,3 Advances in critical care management, Low-tidal-volume Ventilation
particularly 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 also
after burn injury. This article describes the present in inflammatory states. ALI and ARDS
advances 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 perialvolar
patients. permeability. Protein-rich fluid is transmitted from
the intravascular to the extravascular spaces and
ADVANCES IN VENTILATOR MANAGEMENT alveoli. This results in increases in cytokine
release, the accumulation of macrophages and
Mechanical 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 of
concomitant inhalation injury. The term ‘‘acute these factors combine to result in airway damage
lung 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 who
by 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.com
are 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: tina.palmieri@ucdmc.ucdavis.edu
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.
2. 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
3. What’s New in Critical Care of the Burn Patient? 609
study demonstrated differences in mortality or ventilation has become the standard of care for
length of stay, one study of trauma patients re- mechanical ventilation in patients who have ARDS
ported lower end-inflation pressures, improved and ALI.
oxygenation, decreased ventilator duration, and
decreased ICU stay in the APRV group compared
with the pressure control ventilation group. RESUSCITATION AND FLUID MANAGEMENT
Caution must be exercised before using APRV,
however, because it theoretically could result in One of the greatest advances in burn treatment in
lung 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 fluid
High-frequency oscillatory ventilation (HFOV), administration based on urine output, provided
which has been used for decades in neonatal clinicians with easily identifiable endpoints of
ICUs, is still under investigation for use in adults resuscitation. Patients who had major burn injury
who have ARDS. HFOV, like APRV, improves were seldom dying from underresuscitation.
oxygenation by maintaining elevated mean airway However, issues related to overresuscitation
pressure to recruit alveoli.25–28 It differs from volu- began to develop. ‘‘Fluid creep,’’ the term used
metric diffusive ventilation, the current standard of to describe the use of excessive intravenous fluid
care for inhalation injury, in its use of higher during resuscitation, is being increasingly
frequencies and time cycling. To achieve airway described in the literature.42–45 Abdominal
recruitment and improved oxygenation, HFOV compartment syndrome, considered by some to
uses 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.46–49
diffusive ventilation. The result is the generation Perhaps one of the most important issues in
of sustained mean airway pressures of 30 to burn resuscitation is that the optimal measurable
40 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 accurately
animal models by limiting alveolar stretch and predicts the fluid resuscitation needs for all
avoiding atelectrauma, which is caused by the patients during burn shock.50 This lack of clarity
repeated opening and collapse of alveoli.29–33 is caused by the many confounding factors
The 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 in
adults 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 on
ized, prospective trials have found no difference physiologic endpoints. To date, urine output has
in outcomes between the use of HFOV and been the most commonly used endpoint, although
conventional mechanical ventilation; however, the value of using urine output to adjust fluid rates
a current randomized, prospective trial is during burn shock has been challenged.51
underway and should define the use of HFOV in In recent years, the use of invasive monitoring
cases 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 been
lation and severe respiratory acidosis due to popularized, especially in the elderly, but recent
increases in pCO2. reports raise questions about the utility of the
Although both APRV and HFOV are promising pulmonary artery catheter in critically ill
modalities for use in burn patients who have patients.52–55 Even central venous pressure has
ARDS 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 atrial
who have burns. Likewise, the ability to decrease pressure.56
the incidence of volutrauma by reducing tidal Thus, although the pulmonary artery catheter
volumes during mechanical ventilation has not and central venous pressure provide additional
been thoroughly evaluated in patients who have information regarding heart function, studies failed
burn and inhalation injury. However, low-tidal-volume to demonstrate improved survival with their use.
4. 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
5. What’s New in Critical Care of the Burn Patient? 611
more than 20 units of blood as compared with The definition of sepsis in the patient who has
similar children receiving less than 20 units. The burns requires that an infection be documented
other two studies, one in children and one in by way of a positive culture result, a pathologic
adults, 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 that
a restrictive transfusion strategy is efficacious, 1. Temperature greater than 39 C or less than
a prospective, randomized trial is needed to define 36.5 C
the optimal burn blood transfusion strategies. In 2. Progressive tachycardia (adults, 110 beats
the interim, the use of blood transfusion after per minute; children, more than 2 SD above
burn 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 SD
SEPSIS PREVENTION AND MANAGEMENT above age-specific norms)
Sepsis continues to be one of the leading causes 4. Thrombocytopenia beginning 3 days after initial
of morbidity and mortality after burn injury. Recent resuscitation (adults 100,000/ml; children, 2
advances 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 preexisting
definition of sepsis in burns, and the prevention diabetes mellitus (untreated plasma glucose
of sepsis. This section provides an overview of 200 mg/dL, or equivalent mM/L or insulin
each of these areas. resistance)
The development of sepsis guidelines was de- 6. Inability to continue enteral feedings for more
signed to standardize the treatment of sepsis than 24 hours.
throughout all ICUs. The latest guidelines were These criteria form the foundation for all future
developed by an international panel of sepsis clinical studies and trials of sepsis in patients
experts spanning all ICU specialties.75 The guide- who have burns.
lines were created and rated based on available
evidence from the literature. The current recom-
mendations for the treatment of sepsis, which
Glycemic Control
are broad based, include those listed in Box 1.
The applicability of these recommendations in Critically ill adults and children frequently develop
certain 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 glucose
data 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 or
and the application of sepsis guidelines in patients elevated plasma insulin concentrations during
who have burns is a lack of a burn-specific defini- hyperglycemia.78 Early hyperglycemia and
tion of sepsis. Although sepsis definitions have glucose variability after admission to the ICU
been 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 associated
because 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 increased
persistently hypermetabolic, resulting in tachy- mortality in severely burned children and adults,
cardia, tachypnea, and elevated body tempera- and the administration of exogenous insulin to
ture. These physiologic alterations would result in minimize hyperglycemia after critical illness has
a sepsis definition in the vast majority of patients been shown to impact outcome in adult patients.80
who have burn injury, many of whom would not In a landmark study, van den Berghe and
have an ongoing infection. To address these colleagues81 demonstrated that, in critically ill
issues, 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/dL
and Canada was held in January 2007 to define plasma glucose level) reduced in-hospital
sepsis 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 showed
for the diagnosis of sepsis in burns clinically and improved long-term survival when they were
for all future trials related to clinical burn sepsis treated using insulin therapy that targeted a plasma
and infection. glucose level of less than 215 mg/dL.82
6. 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.
7. 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 Respir
10. 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 patients
11. 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 high
13. 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 with
14. 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
8. 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
9. 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 Burn
62. 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 after
68. 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.