Home Print this page Email this page Users Online: 407
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 


 
 Table of Contents  
CME ARTICLE
Year : 2013  |  Volume : 21  |  Issue : 1  |  Page : 17-23

Respiratory burn injuries: An overview


The Arizona Burn Center, Maricopa Medical Center, Department of Surgery, University of Arizona College of Medicine, Phoenix, Division of Community, Environment and Policy, Mel and Enid Zuckerman College of Public Health, University of Arizona Health ­Sciences Center, Tucson, Arizona, USA

Date of Web Publication22-Nov-2013

Correspondence Address:
Michael Peck
The Arizona Burn Center, Maricopa Medical Center, Phoenix, Arizona, USA. University of Arizona College of Medicine, Phoenix, Arizona, USA
USA
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-653X.121876

Rights and Permissions
  Abstract 

Respiratory burns are caused by the aspiration of heated gases or toxic products of incomplete combustion. The extent of damage is determined by the temperature of the inhaled gases, their composition and the duration of exposure. Along with age and size of full-thickness burn injury, the presence of respiratory burns is one of the most powerful predictors of poor outcome in patients admitted to burn centers. There are three types of respiratory burns: (a) Inhalation of systemic asphyxiants such as carbon monoxide. (b) Thermal damage to airway above vocal cords. (c) Injury to tracheobronchial tree and pulmonary parenchyma by inhaled toxicants. The goals of initial management of the airway and breathing are to protect the patency of the airway to prevent suffocation and to ensure adequate ventilation and oxygenation. High levels of inspired oxygen are necessary to treat carbon monoxide poisoning. Intubation and mechanical ventilator support with low tidal volumes is required to treat subglottic respiratory burns. Because there are no known antidotes to the poisonous effects of inhaled smoke, treatment of respiratory burns is protective and supportive.

Keywords: Pulmonary burns, respiratory burns, ventilator


How to cite this article:
Peck M. Respiratory burn injuries: An overview. Indian J Burns 2013;21:17-23

How to cite this URL:
Peck M. Respiratory burn injuries: An overview. Indian J Burns [serial online] 2013 [cited 2019 Dec 16];21:17-23. Available from: http://www.ijburns.com/text.asp?2013/21/1/17/121876


  Introduction Top


Respiratory burn injuries result from the aspiration of superheated gas, steam, or hot liquids, or the poisonous products of incomplete combustion. The toxicant gases produced in a fire can be categorized into separate classes: The asphyxiants, which induce cellular functioning impairment and the irritants, which inflame the respiratory tract. The gravity of the injury is affected by the characteristics of the offending agents, such as temperature, composition and duration of exposure.

The three categories of respiratory burn injuries are:

  • Injury caused by exposure to poisonous gases such as carbon monoxide (CO) and cyanide,
  • Injury above the vocal cords due to thermal or chemical damage, leading to loss of airway patency from edema and
  • Injury below the vocal cords resulting from inhaled toxicants, resulting in pulmonary edema, pneumonia and acute respiratory failure.


The majority of fatalities from fire and burns in the United States occur due to the inhalation of smoke. [1] In addition, respiratory burns have a telling effect on the clinical outcome from cutaneous burns, such as increasing rates of infectious complications, length of hospital stay and mortality. For example, in US burn centers the mortality rate of patients with respiratory burns is nearly 10 times the mortality rate of patients without respiratory burns. [2]

Treatment for respiratory burns is largely confined to providing appropriate support, such as endotracheal intubation and mechanical ventilation. Until date, researchers have not identified specific antidotes for the noxious effects of inhaled poisons.

The remainder of this commentary describes the author's approach to the diagnosis and treatment of respiratory burns, with the objective of minimizing unnecessary deaths and improving clinical outcomes.


  Emergency Management Top


During the first 24 h after injury, management of the airway is effected to prevent asphyxia. Effective management using modes of ventilation that do not aggravate damage to the lungs guarantees patency of the airway and ensures the satisfactory provision of oxygen (O 2 ) and the clearance of carbon dioxide (CO 2 ). Care should be taken to avoid the use of agents that may confound subsequent care, such as systemic corticosteroids and prophylactic antibiotics.

Once the patient is suspected of having sustained respiratory injury, supplemental inhaled oxygen should be provided as humidified gas. Ideally, this step should be taken at the scene of the accident as well as during transport to the hospital, but that will only be possible in regions with developed pre-hospital response systems. The primary reason for providing oxygen is for treatment of carbon monoxide poisoning [Box 1] [Additional file 1], but oxygen will also assist patients in whom respiratory gas exchange is impaired.

The inhalation of soot and other particles as well as irritants in smoke leads to increased respiratory secretions and coughing. Inhalation of inhaled humidified oxygen provides moisture to reduce desiccation of secretions and sloughed mucosa and gives the patient some relief of symptoms.


  Intubation Top


Clearly the most important decision to make early in the assessment and treatment of patients with respiratory burns is whether or not to intubate. The key issue for consideration is that thermal and chemical injury of the upper airway will result in inflammation of the soft-tissues and edema formation in the mucosa of the oral and nasal cavities, the pharynx and the larynx. This edema causes tissue expansion into the airway space, impeding air movement. Treatment of thermal inflammation of the upper airway with inhaled corticosteroids or epinephrine has not proved to slow progression of edema formation or reduce the risk of airway compromise. The only truly effective treatment of airway burns is tracheal intubation.

Unlike the signs and symptoms of CO poisoning, which are subtle and often only detected on arterial blood gas analysis - the clinical presentation of upper airway burns is more obvious. The most reliable symptom in the awake patient is the subjective perception of difficulty in breathing. Once the patient complaints of trouble with air exchange, tracheal intubation is the next step. Earlier signs and symptoms include hoarse voice, stridor and the use of accessory muscles for breathing. Less reliable signs include the presence of burns on the face, singed nasal or facial hairs or soot in the mouth. A quick inspection using the direct laryngoscopy can identify erythema or swelling of the larynx and vocal cords consistent with thermal burns.

Diagnosis of upper airway burns in the comatose patient is challenging. Again, direct laryngoscopy may be helpful, but the single most significant factor to consider is the mechanism of injury - that is, was the patient burned by a fire in a closed space or by his or her own flaming clothing? If flames and smoke production were present at the scene, the unconscious patient should be presumed to suffer from respiratory burns and intubation should be performed expeditiously.

It is crucial to understand that in the first 24 h information provided from chest radiographs and arterial blood gas analyses will not help the diagnosis of respiratory burns. The appearance of the chest radiograph may not change for several hours; it is not unusual for patients with severe respiratory burns to present with normal chest radiographs. Similarly, hypercarbia will not be evident for some time after injury. Hypoxemia is the most common result of early alteration of blood gases, but again may not be present at the time of the initial evaluation.

Occasionally, it is necessary to perform prophylactic intubation on patients suspected of respiratory burns. Even if the patient is awake and has not complained of breathing difficulty, tracheal intubation should be performed if the patient is to be transferred from one facility to another, such as from a regional hospital to a specialty care facility with a burn center. Another circumstance in which prophylactic intubation may be useful is for the patient with large burns (for example, over 40% of the body surface area). When patients with large burns undergo aggressive resuscitation with crystalloid fluids using a technique such as the Parkland formula, capillary leakage will result in extravasation of large amounts of fluid into the soft-tissues throughout the body, including the upper airway. Even patients without respiratory burns may die of loss of airway patency caused by whole body edema and can be salvaged by early tracheal intubation.

The options for early tracheal intubation include using either the nasotracheal or orotracheal routes. The advantages of using the nasotracheal route are that it can be performed without endangering the cervical spinal cord in patients who have sustained spinal trauma and that the tubing can be secured more safely in patients with facial burns. On the other hand, a higher incidence of paranasal sinusitis results from the use of nasotracheal tubes. Orotracheal tubes can be inserted with direct vision using a laryngoscope, and skilled practitioners performing this technique can avoid endangering the cervical spine by keeping the spine in axial (in-line) traction. Adults should be intubated with endotracheal tubes of at least a 7.5 mm inner diameter (French size) to facilitate suctioning, pulmonary toilet and fiberoptic bronchoscopy.

Although cricothyroidotomy and emergency tracheostomy are always options, their use is less desirable in the early management of respiratory burns than that of tracheal intubation. Tissue edema distorts cervical anatomy, often creating severe technical challenges for the surgeon. Obviously, when excessive edema in the upper airway disallows tracheal intubation, a surgical procedure is the only option. However, it is preferable to avoid such situations by intubating the patient early in the 1 st h after injury.

Patient with respiratory burns should also be treated from the earliest opportunity for CO poisoning. The diagnosis of CO poisoning depends on the assay of the percentage of hemoglobin (Hgb) sites bound with CO; this percentage can be obtained with an arterial blood gas analyzer. In the absence of such specific information, however, treatment should not be delayed. Supplemental oxygen should be delivered with a tightly fitted, non-rebreathing mask. If the patient is intubated, ventilator settings should be adjusted to deliver a fraction of inspired oxygen (FIO 2 ) of 100%. Treatment with high levels of FIO 2 should be continued for 6 h (the half-life of CO bound to Hgb is 4 h when the patient is breathing room air (FIO 2 21%); it decreases to 1 h when the patient is breathing air heavily enriched with O 2 (FIO 2 90-100%). Thus using FIO 2 100%, over 98% of CO can be cleared from the blood within 6 h).


  Causation of Injury Top


Respiratory burns below the vocal cords result from exposure of the respiratory tract tissues to noxious chemicals present in the inhaled gases and smoke particles produced from incomplete combustion. The pharynx is so efficient at removing heat from inhaled smoke that the only thermal damage from smoke occurs above the vocal cords (the exception results from inhalation of superheated steam, the droplets of which are capable of carrying heat down into the small airways; this is frequently a fatal injury because of thermal damage to the lung parenchyma). Changes associated with subglottic respiratory burns include sloughing of airway epithelium, increased mucous secretion, impairment of ciliated cells lining the trachea, diffuse inflammation, inactivation of surfactant secretion, increased blood flow and spasm of the smooth muscle lining of the bronchi and bronchioles [Box 2] [Additional file 2].

Toxicants present in inhaled smoke diffuse from the alveoli to the capillaries and arterioles that surround the air sacs, leading to damage of these vessels as well. Not only do the perialveolar capillaries become inflamed, but the release of cytokines attracts leucocytes to the site of injury. Inflammation results in exudation of plasma into the perialveolar space, leading to widening of the alveolar-capillary space, pulmonary edema and hypoxemia, characteristics of acute lung injury (ALI). Leucocytes infiltrate the inflamed tissue by diapedesis, releasing contents of their lysosomes and exacerbating tissue damage. As fluid accumulates in the alveolar-capillary space throughout the lungs, compliance is diminished and CO 2 exchange is compromised. Innate immune function becomes impaired and the combination of reduced ciliary clearance, fluid accumulation and epithelial necrosis create conditions in which bacterial pneumonia is likely.

Thus two clinical syndromes may result from respiratory burns : p0 neumonia and acute respiratory distress syndrome (ARDS). Both are associated with acute respiratory failure, and if untreated, can progress to death. Treatment of bacterial pneumonia of course requires appropriate antibacterial therapy, but both conditions may increase the likelihood of prolonging intubation and mechanical ventilator support.


  Ventilator Support Top


The goal of ventilator support is to provide adequate ventilation for oxygenation and elimination of CO 2 without further damaging the lungs. Ventilator-induced lung injury (VLI) is associated with hyperinflation of normal regions of aerated lung because of high tidal volumes. Alveolar rupture and accumulation of extra-alveolar air (barotrauma) result from higher inflating pressures. Because compliance in poorly aerated regions of diseased lung is low, the rapid cyclic inflation-deflation of normal, inflated alveoli consecutive to the collapsed alveoli creates high shear forces. In addition, the overexpansion of normal alveoli leads to high transpulmonary pressures in the aerated regions, making them susceptible to direct physical damage, including disruption of alveolar epithelia and capillary endothelia. The flood of cytokines both locally and systemically may also increase as the inflammatory response is aggravated.

In the past, the goal of employing ventilator support was to normalize arterial blood gases, bringing pH as close as possible to 7.4 and keeping oxyhemoglobin saturation above 95%. This was accomplished using high concentrations of inspired oxygen and high minute ventilations delivered by volume-controlled ventilators. Tidal volumes of 10-15 mL/kg were not unusual, rationalized by the need for increased recruitment of collapsed alveoli. Unfortunately, this approach frequently resulted in VLI.

Peak transpulmonary pressures can be safely reduced by increasing positive end-expiratory pressure (PEEP) and decreasing tidal volume. In addition, the philosophy of permissive hypercapnia has been adopted, allowing the pH to decline to as low as 7.2 before intervening. Furthermore, in patients without vascular disease, oxyhemoglobin saturation of 90% is adequate.

Either volume-cycled or pressure-cycled modes can be used for mechanical ventilation as long as high tidal volumes and plateau pressures (plateau pressures are measured at 0.5 s after peak inspiration) are avoided (see below for discussion of the rationale for the use of low tidal volumes for lung protective strategy). When using a volume-cycled mode such as synchronous intermittent mandatory ventilation, plateau pressures should be kept below 30 cm H 2 O. Initial tidal volumes should be set at 6 mL/kg of patient weight. When using a pressure-cycled mode, peak inspiratory pressure should be set at 20 cm H 2 O and increased as needed to keep pH >7.2.

In the first few hours after injury, patients suffering from respiratory burns may have relatively normal oxygenation (P/F ratio [P/F ratio is an expression of the capacity of inspired air to oxygenate the blood in the pulmonary capillaries: PaO 2 /FIO 2 ] >300). However, the P/F ratio quickly declines as the effects of respiratory burns become manifest and as resuscitation fluid accumulates in the lungs. The initial PEEP setting should be 5 cm H 2 O to prevent airway collapse. For the first 6 h after intubation and initiation of mechanical ventilator support, FIO 2 should be maintained at 100% to treat CO poisoning, but after this period of time, FIO 2 should be reduced to 40-50%, provided that oxyhemoglobin saturation remains above 90%.

Throughout the duration of mechanical ventilation, care should be given to pulmonary toilet. This includes frequent, but gentle suctioning with sterile catheters through the endotracheal tube, and the use of humidified nebulizers such as albuterol or salbuterol to relieve bronchoconstriction and clear secretions. Elective tracheostomy is often helpful, particularly for patients who are intubated for more than 2 weeks, because tracheostomy is more comfortable for the patient than endotracheal intubation, less sedation is required and there a lower incidence of subglottic stenosis.

Care should also be taken to reduce the risk of ventilator-associated pneumonia (VAP). Elevating the head of the bed 30-45° reduces aspiration of gastric contents into the respiratory tract. Peptic ulcer disease prophylaxis also minimizes the damage done by aspiration and reduces the risk of stress ulceration. Most importantly, the patient should be evaluated every day for the potential for extubation and weaning from ventilator support. This daily evaluation is best accomplished by temporarily reducing sedation ("sedation holiday") to allow the patient to breathe spontaneously if possible.

Once the decision has been made to wean the patient from ventilator support, protocols can be used to shorten the time required for this process. Ventilator settings from which a patient can be safely extubated include FiO 2 <30%, PEEP 5 cm H 2 O, pressure support <10 cm H 2 O and a mandatory ventilator rate of <4 breaths/min. While the patient is still intubated, short trials of spontaneous breathing may be conducted using a T-piece circuit or continuous positive airway pressure of 5 cm H 2 O without mandatory ventilator breaths.

Fortunately, the vast majority of survivors of respiratory burns have normal pulmonary function and thus do not subsequently experience chronic respiratory problems.


  Rationale for the Use of Low-Volume Ventilation as Lung Protective Strategy Top


The employment of low-volume ventilation as a pulmonary protective strategy has been described in detail elsewhere. [15] ALI denotes the acute onset of impaired oxygen exchange, which can result from smoke inhalation and is defined by an alveolar-arteriolar gradient of less than 300. Serious cases of ALI are described as ARDS, defined by an alveolar-arteriolar gradient of less than 200. [16] Chest radiographs show the presence of bilateral alveolar or interstitial infiltrates. However, there are no clinical signs of left heart failure to explain the occurrence of pulmonary edema.

The associated risk of mortality from ALI/ARDS rises when the severity of oxygen exchange becomes more impaired. Mortality in these cases has been observed to reach as high as 40% to 50%. [17] Mortality from ALI/ARDS may be due directly to inability to oxygenate sufficiently due to respiratory failure, or it may result from associated VAP or multisystem organ failure. Moreover, patients become ventilator dependent, resulting in increased length of stay in intensive care units. [18] Increased disability, reduced health-care quality of life and cognitive impairment have been observed in long-term survivors. [19]

ALI and ARDS are characterized by diffuse alveolar damage caused by increased permeability of the perialveolar capillary endothelia. Protein-rich fluid escapes from the intravascular space into the extravascular space, from which it spreads into the alveoli. Much like the buildup in the alveoli of plasma-like fluid that results with left heart failure from an elevation in hydrostatic pressure within the pulmonary veins, this non-cardiogenic pulmonary edema is associated with either inflammatory states secondary to trauma or aspiration, or with systemic diseases, such as drug toxicity, pancreatitis and sepsis. In respiratory burns, widening of cell-to-cell contact in the vascular endothelium is caused by the toxins adsorbed onto alveolar surfaces from inhaled smoke diffuse across the alveolar-arteriolar space.

Another feature of ALI/ARDS is cytokine release. Leucocytes (neutrophils and macrophages) accumulate in the alveolar-arteriolar interstitium and inflammatory cytokines are released, exacerbating the local damage done by toxins in the smoke. The cytokines that pour into the systemic circulation after respiratory burns can contribute to multisystem organ failure, seen commonly with ARDS. [20],[21] In addition, surface tension is altered because of reduction in surfactant production and hyaline membranes form in the alveoli, leading to alveolar collapse.

Endotracheal intubation and mechanical ventilation are necessary for survival because of the severe impairment in gas exchange and because of loss of pulmonary compliance due to accumulation of intra- and perialveolar fluid, both of which lead to impaired oxygenation and diminished removal of CO 2 . Two decades ago the goal of ventilatory support was to normalize arterial blood gases, keeping oxyhemoglobin saturation above 95% and bringing pH as close as possible to 7.4. This was achieved using high minute ventilations delivered by volume-controlled ventilators and elevated concentrations of inspired oxygen. Tidal volumes of 10-15 mL/kg were common, rationalized by the perceived need for increased recruitment of collapsed alveoli.

Experimental studies subsequently proposed reducing plateau pressures to35 cm of water to diminish the contribution of VLI to the pathophysiology of ALI and ARDS. This decrease in peak transpulmonary pressures was accomplished by decreasing tidal volume and increasing PEEP. The consequent reduction in minute ventilation required toleration of some degree of hypercapnia, popularly described as permissive hypercapnia. [22] This proposal led to a succession of clinical trials in the quest for evidence to buttress the assertion of benefit of a lung-protective ventilation strategy. However, respiratory acidosis and severe hypercapnia (pH < 7.2) are not without risk. Adverse effects include an increase in pulmonary hypertension and intracranial pressure as well as diminished renal blood flow and myocardial contractility. Thus, permissive hypercapnia may be relatively contraindicated for certain critically ill-patients. Despite this, multiple studies have shown that judicious use of permissive hypercapnia is benign. [23],[24],[25]

Meta-analysis of these trials was conducted to study the effect of ventilation with lower tidal volumes on morbidity and mortality of critically ill-adults with either ALI or ARDS. [26] Only randomized, controlled trials without selection bias were selected. Six out of 10 studies of probable applicability were included for the final analysis. [27],[28],[29],[30],[31],[32] In 1030 patients in three studies, [27],[28],[29] 28 day mortality showed a distinct protective benefit of a ventilation strategy using plateau pressure less than 31 cm water and tidal volume less than 7 mL/kg of measured body weight. In 288 patients in three studies, [29],[30],[31],[32] mechanical ventilation was required on fewer days.

The degree of difference in tidal volume between the control and the treatment groups correlated directly with the increase in survival. Studies employing the tactic of low tidal volumes in which the differences between tidal volumes ranged from 4.9 to 5.6 mL/kg [27],[31] showed more benefit to survival than trials in which differences in mean tidal volume between the two groups were in the range of 2.9-3.7 mL/kg. [29],[30],[32]


  Acknowledgements Top


The author would like to express gratitude for the editorial contributions of Ms. Andrea Sattinger.

 
  References Top

1.Peck MD. Structure fires, smoke production, and smoke alarms. J Burn Care Res 2011;32:511-8.  Back to cited text no. 1
[PUBMED]    
2.American Burn Association, 2013. National Burn Repository, Chicago, IL, 2013. Available from: http://www.ameriburn.org/2013NBRAnnualReport.pdf. [Last accessed on 2013 Sep 24].  Back to cited text no. 2
    
3.Abdi S, Herndon D, McGuire J, Traber L, Traber DL. Time course of alterations in lung lymph and bronchial blood flows after inhalation injury. J Burn Care Rehabil 1990;11:510-5.  Back to cited text no. 3
[PUBMED]    
4.Hales CA, Barkin P, Jung W, Quinn D, Lamborghini D, Burke J. Bronchial artery ligation modifies pulmonary edema after exposure to smoke with acrolein. J Appl Physiol (1985) 1989;67:1001-6.  Back to cited text no. 4
    
5.Hinder F, Matsumoto N, Booke M, Bradford DW, Traber LD, Herndon DN, et al. Inhalation injury increases the anastomotic bronchial blood flow in the pouch model of the left ovine lung. Shock 1997;8:131-5.  Back to cited text no. 5
[PUBMED]    
6.Linares HA, Herndon DN, Traber DL. Sequence of morphologic events in experimental smoke inhalation. J Burn Care Rehabil 1989;10:27-37.  Back to cited text no. 6
[PUBMED]    
7.Abdi S, Evans MJ, Cox RA, Lubbesmeyer H, Herndon DN, Traber DL. Inhalation injury to tracheal epithelium in an ovine model of cotton smoke exposure. Early phase (30 minutes). Am Rev Respir Dis 1990;142:1436-9.  Back to cited text no. 7
[PUBMED]    
8.Barrow RE, Morris SE, Basadre JO, Herndon DN. Selective permeability changes in the lungs and airways of sheep after toxic smoke inhalation. J Appl Physiol (1985) 1990;68:2165-70.  Back to cited text no. 8
    
9.Cox RA, Burke AS, Soejima K, Murakami K, Katahira J, Traber LD, et al. Airway obstruction in sheep with burn and smoke inhalation injuries. Am J Respir Cell Mol Biol 2003;29:295-302.  Back to cited text no. 9
[PUBMED]    
10.Herndon DN, Traber LD, Linares H, Flynn JD, Niehaus G, Kramer G, et al. Etiology of the pulmonary pathophysiology associated with inhalation injury. Resuscitation 1986;14:43-59.  Back to cited text no. 10
[PUBMED]    
11.Kraneveld AD, Nijkamp FP. Tachykinins and neuro-immune interactions in asthma. Int Immunopharmacol 2001;1:1629-50.  Back to cited text no. 11
[PUBMED]    
12.Traber DL, Schlag G, Redl H, Traber LD. Pulmonary edema and compliance changes following smoke inhalation. J Burn Care Rehabil 1985;6:490-4.  Back to cited text no. 12
[PUBMED]    
13.Isago T, Fujioka K, Traber LD, Herndon DN, Traber DL. Derived pulmonary capillary pressure changes after smoke inhalation in sheep. Crit Care Med 1991;19:1407-13.  Back to cited text no. 13
[PUBMED]    
14.Basadre JO, Sugi K, Traber DL, Traber LD, Niehaus GD, Herndon DN. The effect of leukocyte depletion on smoke inhalation injury in sheep. Surgery 1988;104:208-15.  Back to cited text no. 14
[PUBMED]    
15.Peck MD, Koppelman T. Low-tidal-volume ventilation as a strategy to reduce ventilator-associated injury in ALI and ARDS. J Burn Care Res 2009;30:172-5.  Back to cited text no. 15
[PUBMED]    
16.Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, et al. Report of the American-European Consensus conference on acute respiratory distress syndrome: Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Consensus Committee. J Crit Care 1994;9:72-81.  Back to cited text no. 16
[PUBMED]    
17.Lewandowski K. Epidemiological data challenge ARDS/ALI definition. Intensive Care Med 1999;25:884-6.  Back to cited text no. 17
[PUBMED]    
18.Davidson TA, Caldwell ES, Curtis JR, Hudson LD, Steinberg KP. Reduced quality of life in survivors of acute respiratory distress syndrome compared with critically ill control patients. JAMA 1999;281:354-60.  Back to cited text no. 18
[PUBMED]    
19.Dowdy DW, Eid MP, Dennison CR, Mendez-Tellez PA, Herridge MS, Guallar E, et al. Quality of life after acute respiratory distress syndrome: A meta-analysis. Intensive Care Med 2006;32:1115-24.  Back to cited text no. 19
[PUBMED]    
20.Slutsky AS, Tremblay LN. Multiple system organ failure. Is mechanical ventilation a contributing factor? Am J Respir Crit Care Med 1998;157:1721-5.  Back to cited text no. 20
[PUBMED]    
21.Dreyfuss D, Saumon G. From ventilator-induced lung injury to multiple organ dysfunction? Intensive Care Med 1998;24:102-4.  Back to cited text no. 21
[PUBMED]    
22.Slutsky AS. Mechanical ventilation. American College of Chest Physicians' Consensus Conference. Chest 1993;104:1833-59.  Back to cited text no. 22
[PUBMED]    
23.Hickling KG, Walsh J, Henderson S, Jackson R. Low mortality rate in adult respiratory distress syndrome using low-volume, pressure-limited ventilation with permissive hypercapnia: A prospective study. Crit Care Med 1994;22:1568-78.  Back to cited text no. 23
[PUBMED]    
24.Laffey JG, O'Croinin D, McLoughlin P, Kavanagh BP. Permissive hypercapnia - Role in protective lung ventilatory strategies. Intensive Care Med 2004;30:347-56.  Back to cited text no. 24
[PUBMED]    
25.Bidani A, Tzouanakis AE, Cardenas VJ Jr, Zwischenberger JB. Permissive hypercapnia in acute respiratory failure. JAMA 1994;272:957-62.  Back to cited text no. 25
[PUBMED]    
26.Petrucci N, Iacovelli W. Lung protective ventilation strategy for the acute respiratory distress syndrome. Cochrane Database Syst Rev 2007;???:CD003844.  Back to cited text no. 26
    
27.Amato MB, Barbas CS, Medeiros DM, Magaldi RB, Schettino GP, Lorenzi-Filho G, et al. Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 1998;338:347-54.  Back to cited text no. 27
[PUBMED]    
28.Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000;342:1301-8.  Back to cited text no. 28
[PUBMED]    
29.Brochard L, Roudot-Thoraval F, Roupie E, Delclaux C, Chastre J, Fernandez-Mondéjar E, et al. Tidal volume reduction for prevention of ventilator-induced lung injury in acute respiratory distress syndrome. The Multicenter Trail Group on Tidal Volume reduction in ARDS. Am J Respir Crit Care Med 1998;158:1831-8.  Back to cited text no. 29
    
30.Stewart TE, Meade MO, Cook DJ, Granton JT, Hodder RV, Lapinsky SE, et al. Evaluation of a ventilation strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome. Pressure-and Volume-Limited Ventilation Strategy Group. N Engl J Med 1998;338:355-61.  Back to cited text no. 30
[PUBMED]    
31.Villar J, Kacmarek RM, Pérez-Méndez L, Aguirre-Jaime A. A high positive end-expiratory pressure, low tidal volume ventilatory strategy improves outcome in persistent acute respiratory distress syndrome: A randomized, controlled trial. Crit Care Med 2006;34:1311-8.  Back to cited text no. 31
    
32.Brower RG, Shanholtz CB, Fessler HE, Shade DM, White P Jr, Wiener CM, vet al. Prospective, randomized, controlled clinical trial comparing traditional versus reduced tidal volume ventilation in acute respiratory distress syndrome patients. Crit Care Med 1999;27:1492-8.  Back to cited text no. 32
[PUBMED]    




 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Emergency Management
Intubation
Causation of Injury
Ventilator Support
Rationale for th...
Acknowledgements
References

 Article Access Statistics
    Viewed7110    
    Printed185    
    Emailed1    
    PDF Downloaded312    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]