TY - JOUR
AU1 - MD, John E. McCall,
AU2 - RRT, Thomas J. Cahill,
AB - A major burn is one of the most devastating physiologic and psychologic insults known. Although many organ systems are affected by a burn, the pulmonary system often sustains the most damage. Consequently, pulmonary injury is a major source of morbidity and mortality for the burn patient.1 Pulmonary injury in the burn patient may assume many forms. The injury may result directly from smoke inhalation injury to the lungs or indirectly from inflammatory mediators associated with infection, sepsis, or the burn wound itself.2 The result is a potentially life-threatening complication that may present as acute respiratory distress syndrome (ARDS): one study has estimated that the incidence of ARDS among mechanically ventilated burn patients is as high as 54%3 whereas the mortality associated with ARDS remains between 30% and 40%.4 Regardless of the pattern of injury, appropriate respiratory care of the burn patient is as important as other major components of burn care, such as fluid management, wound coverage, and infection control. As with most aspects of burn care, a team approach is essential to the provision of excellent respiratory care. The respiratory therapist, the physician, the nurse, and all other caregivers must understand the important nature of respiratory care of the burn patient. EARLY-PHASE RESPIRATORY INJURY Most patients who sustain major burns also will suffer some degree of pulmonary insult that will be manifest in the first few days as burn resuscitation is being completed. The severity of this insult may range from mild to life threatening. Although most pulmonary injuries are related to the size of the cutaneous burn, smoke inhalation injury may cause a significant pulmonary injury even without other burns. The term smoke inhalation injury complex (referred to hereafter as inhalation injury) describes a variety of insults that are attributable to the inhalation of superheated, noxious gases. Inhalation injury increases fluid requirements for resuscitation from burn shock by approximately 50%5 and is a major source of mortality in burn patients.6 A history of exposure to a closed space fire, loss of consciousness, and the presence of chemical irritants, along with a physical exam revealing carbonaceous sputum, singed nasal, or facial hair, are all suggestive of inhalation injury. The mechanism of inhalation injury consists of a combination of 1) direct thermal injury to the upper airway from inhalation of hot gases, 2) damage to cellular and oxygen transport mechanisms by inhalation of carbon monoxide and cyanide, and 3) chemical injury to the lower airways caused by inhalation of toxic products of combustion. Thermal Damage to the Upper Airway The air temperature in a room containing a fire may exceed 1000°F.7 Because of the combination of efficient heat dissipation in the upper airway, low heat capacity of air, and reflex closure of the larynx, superheated air usually will cause thermal injury only to airway structures above the carina.8 Thermal injury to these airway structures may result in massive swelling of the tongue, epiglottis, and/or aryepiglottic folds with resultant airway obstruction. Airway swelling develops over a matter of hours as fluid resuscitation is ongoing; therefore, the initial evaluation will not be a good indicator of the severity of obstruction that may occur later. A high index of suspicion must be maintained, and respiratory status must be continuously monitored to assess the need for airway control and ventilator support. If the history and initial examination leads one to suspect significant thermal injury to the upper airway, intubation for airway protection and possible ventilatory support should be considered early in the course of resuscitation. If these measures are delayed, the anatomic distortion caused by the massive swelling will make intubation very difficult. Carbon Monoxide/Cyanide Exposure Carbon monoxide is an odorless, tasteless, nonirritating gas that is a product of incomplete combustion. Carbon monoxide poisoning is a major source of early morbidity in the burn patient, with many fatalities occurring at the scene of the fire.7 Carbon monoxide levels may exceed 10% in a closed space fire; significant injury may occur in a short period of time with exposure to as little as 1% (Figure 1). With an affinity for hemoglobin 200 times greater than for oxygen, carbon monoxide effectively competes with oxygen for hemoglobin binding. This competition not only shifts the oxyhemoglobin dissociation curve to the left, but it also alters its shape. Oxygen delivery to tissues is severely compromised as the result of both the reduced oxygen-carrying capacity of blood and the less efficient dissociation of oxygen from hemoglobin at the tissue level (Figure 2). In addition, carbon monoxide competitively inhibits intracellular cytochrome oxidase enzyme systems, most notably cytochrome P-450, resulting in an inability of cellular systems to use oxygen.9 Inhaled hydrogen cyanide, which is produced during the combustion of numerous household materials, also inhibits the cytochrome oxidase system and may have a synergistic effect with carbon monoxide, producing tissue hypoxia and acidosis as well as a decrease in cerebral oxygen consumption and metabolism.10 Figure 1. View largeDownload slide Hemoglobin is converted rapidly to carboxyhemoglobin in the presence of carbon monoxide. Abstracted from Stewart RD, Stewart RS, Stamm W, et al. JAMA 1976;235:3990. Figure 1. View largeDownload slide Hemoglobin is converted rapidly to carboxyhemoglobin in the presence of carbon monoxide. Abstracted from Stewart RD, Stewart RS, Stamm W, et al. JAMA 1976;235:3990. Figure 2. View largeDownload slide Carboxyhemoglobin-induced changes in the oxygen–hemoglobin dissociation curve. Oxygen-carrying capacity is markedly diminished when carboxyhemoglobin values reach 40% to 50%. In addition, the leftward displacement of the oxygen–hemoglobin dissociation curve makes the oxygen that is bound to hemoglobin less available for delivery to tissues. Reproduced with permission from Fein, Leff, A, Hopewell PC. Crit Care Med 1980;8:94–8. Figure 2. View largeDownload slide Carboxyhemoglobin-induced changes in the oxygen–hemoglobin dissociation curve. Oxygen-carrying capacity is markedly diminished when carboxyhemoglobin values reach 40% to 50%. In addition, the leftward displacement of the oxygen–hemoglobin dissociation curve makes the oxygen that is bound to hemoglobin less available for delivery to tissues. Reproduced with permission from Fein, Leff, A, Hopewell PC. Crit Care Med 1980;8:94–8. Carbon monoxide poisoning may be difficult to detect. The absorbance spectrum of carboxyhemoglobin and oxyhemoglobin are very similar; therefore, pulse oximeters cannot distinguish between the two forms of hemoglobin. Oximeter readings will be normal even when lethal amounts of carboxyhemoglobin are present. The PaO2 measured from an arterial blood gas reflects the amount of oxygen dissolved in the plasma but does not quantitate hemoglobin saturation, which is the most important determinant of the oxygen-carrying capacity of the blood. Carboxyhemoglobin levels may be measured directly, but this test is rarely available at the scene. Because of the inevitable time delay between exposure and testing, levels measured upon arrival at a health care facility will not reflect the true extent of poisoning, especially when the patient has been breathing high concentrations of oxygen. The half life of carboxyhemoglobin is 250 minutes for the victim breathing room air; this is reduced to 40 to 60 minutes with the inhalation of 100% oxygen.11 If the patient is unconscious or cyanotic, intubation for the administration of high oxygen concentrations is indicated. Although hyperbaric oxygenation will further reduce the half life of carboxyhemoglobin, the hyperbaric chamber is a difficult environment in which to monitor the patient, perform fluid resuscitation, and provide early burn care, such as escharotomies and dressing changes. It is the opinion of most burn experts that hyperbaric oxygen treatment should be reserved for the patient with minimal-to-no cutaneous burns or other injuries.12 Chemical Injury to the Lower Airway The combustion of most substances generates materials toxic to the respiratory tract. For example, burning rubber and plastic products produce sulfur dioxide, nitrogen dioxide, ammonia, and chlorine, which form strong acids and alkali when combined with water in the airways and alveoli. Glues in laminated furniture and wall paneling may release cyanide gas. Burning cotton or wool produce toxic aldehydes.13 Smoke-related toxins damage both epithelial and capillary endothelial cells of the airway. Histologic changes resemble those observed with tracheobronchitis. Mucociliary transport is destroyed, inhibiting the clearance of bacteria. Alveolar collapse and atelectasis occur because of surfactant loss.14 Alveolar macrophages are damaged and produce chemotaxins, further enhancing the inflammatory response.15 The early inflammatory changes that occur in the airway are followed by a period of diffuse exudate formation.16 Bronchiolar edema may become quite severe. The combination of necrotizing bronchitis, bronchial swelling, and bronchospasm results in obstruction of both large and small airways. Wheezing occurs as a result of bronchial swelling and irritant receptor stimulation. A generalized increase in capillary permeability aggravates airway and pulmonary edema. Inhaled bronchodilators and mechanical methods of enhancing clearance of debris from the lower airways may be beneficial. The end result is pulmonary failure occurring 12 to 48 hours after the smoke exposure caused by a decrease in lung compliance, an increase in ventilation perfusion mismatch, and an increase in dead space ventilation. In several days, the injury may progress to sloughing of airway mucosa and intrapulmonary hemorrhage, resulting in mechanical obstruction of the lower airways and flooding of the alveoli. Air trapping occurring distal to airway obstruction may result in barotrauma. Because of ulceration and extensive necrosis of the respiratory epithelium, patients are predisposed to secondary bacterial invasion and development of a superimposed bacterial pneumonia several days after injury.17,–19 Pulmonary function may not return to normal for several months.20 TREATMENT OF AIRWAY/PULMONARY INJURY Need for Intubation If inhalation injury is suspected, fiberoptic bronchoscopy may contribute to the diagnosis21 but should not take the place of clinical judgment. Blood gases may be normal for the first few hours after injury and thus may not be helpful, especially before fluid resuscitation is complete. Intubation and mechanical ventilation also may be indicated in a patient with carbon monoxide poisoning and depressed airway reflexes, even without thermal injury. Intubation Technique Not every patient with a face burn requires intubation; however, a delay in establishing an airway may result in a much more difficult intubation several hours later. The American Society of Anesthesiologists difficult airway algorithm22 suggests the use of fiberoptic intubation for the difficult airway; however, if intubation is delayed to the point that airway edema has developed to any significant degree, the fiberoptic technique will not be helpful because airway edema and secretions will immediately obscure the endoscopic view. Direct laryngoscopy with a rigid blade allows for the mechanical displacement of edematous tissues and affords the best-possible view of the airway. These patients should not be given muscle relaxants because this may lead to a “cannot intubate, cannot ventilate” situation. Awake intubation or the judicious administration of intravenous ketamine (1–1.5 mg/kg) allows intubation while maintaining spontaneous ventilation. If long-term intubation is anticipated, a nasal endotracheal tube may be preferable for patient comfort, stability, mouth care, and potential ability to communicate by lip reading. The American Heart Association 2000 Standards recommend the use of a commercially available device to secure the endotracheal tube; however, facial burns present a unique challenge. At our facility a 10-year review of transport records demonstrates a 100% success rate when using the staple-and-tape technique for patients with facial burns (Figure 3). The tube is secured with cloth tape, benzoin (or skin preparation), and staples. Three pieces of cloth tape are used to provide anchors above and below the tube. Figure 3. View largeDownload slide Technique of securing nasal endotracheal tube with tape and skin staples. Figure 3. View largeDownload slide Technique of securing nasal endotracheal tube with tape and skin staples. Some authors contend that intubation of an inflamed airway increases the risk of damage to the larynx.23 Because the airway obstruction is the result of supraglottic edema, the laryngeal mask airway (LMA) may in theory provide a useful temporary airway until intubation or a surgical airway is accomplished. Although we have extensive experience with the LMA in the operating room,24 the use of the LMA for airway maintenance in the patient with acute burns has not been reported. If intubation is predicted to be or proves to be impossible, a tracheostomy may be considered. In the past, authors have stated that a tracheostomy in a patient with a burned airway was associated with a mortality of close to 100%.25 More recent studies have refuted this26,27 and have proven that tracheostomy is safe and may actually improve patient comfort. In our institution, a tracheostomy is the preferred airway for the patient who we predict will require greater than 2 to 3 weeks of mechanical ventilation. Ventilation Strategies The patient with a major burn has an increased cardiac output, increased levels of oxygen consumption, and increased CO2 production. Minute ventilation will need to be at least double the normal value. Failure to adjust ventilation accordingly will lead to hypercapnia and hypoxemia. The patient with an inhalation injury or ARDS may have noncompliant lungs; an extensive burn of the trunk may produce a noncompliant chest wall. Surfactant is depleted in these patients, leading to alveolar closure. These conditions require meticulous attention to ventilation. An open lung-gentle ventilation strategy,28 which maintains airway and alveolar patency and functional residual capacity through sufficient levels of positive end-expiratory pressure (PEEP) while avoiding alveolar overdistension, will help prevent further pulmonary injury.29 Maintenance of alveolar patency is important because reopening alveoli requires much higher airway pressure.30 FiO2 should be reduced to less than 0.6 as soon as possible to minimize oxygen-related pulmonary damage. A mild-to-moderate degree of respiratory acidosis is acceptable to prevent the exacerbation of the pulmonary injury. Ventilation Techniques Mechanical ventilation of the burn patient can be accomplished by several methods. The two that will be discussed in this article are conventional mechanical ventilation and the Volume Diffusive Respirator™ (VDR™; Percussionaire, Sandpoint, ID). Conventional Ventilation. The two most common methods of conventional ventilation include volume control ventilation and pressure control ventilation. Volume control ventilation delivers a consistent tidal volume (TV) and minute ventilation to the patient regardless of the compliance of the lungs. This consistent TV and minute ventilation stabilizes the PaCO2, but results in variable peak airway pressures. Pressure control ventilation uses a set inspiratory pressure to deliver tidal volume to the patient. TV is determined by lung compliance and the inspiratory time. This mode will limit inflation pressure and thereby decrease the risk of alveolar over distention. It also may improve the patient–ventilator synchrony.31 Because of the variability in TV, the precise control of PaCO2 is not possible. The most common settings or targets for both modes of ventilation are TV of 5 to 7 ml/kg, rate 4 to 20 breaths per minute, PEEP optimized for maximum recruitment, and an FiO2 of 0.21 to 1.0. Rates should be adjusted to maximize ventilation initially, then weaned as tolerated to promote spontaneous ventilation and reduce the occurrence of muscle atrophy. FiO2 is adjusted to maintain PaO2 between 80 mm Hg and 100 mm Hg. The waveform graphics package available on all fourth-generation microprocessor ventilators provides a visual means of determining effective ventilation and the adequacy of lung protective strategies. The pressure–volume loop is one of the easier waveforms to understand and can be used to determine optimal PEEP, lung overdistention, and lung compliance. The lower inflection point is where the slope of the lower curve begins to increase. This demonstrates the airway pressure below which alveolar collapse occurs. By observing the lower inflection point during a mechanical breath, one can estimate the opening pressure of the alveoli and set the optimal PEEP just above this level to prevent collapse (Figure 4). A flattening of the upper portion of the pressure–volume loop indicates the lung is over pressurized; airway pressure should be reduced to protect the lung (Figure 5). The slope of the curve (Figure 6) demonstrates the compliance of the lung by displaying the volume achieved with the pressure used. Decreased compliance results in a decrease in lung volumes at a given airway pressure and a decrease in slope. Figure 4. View largeDownload slide Using the pressure–volume loop to determine optimal levels of positive end-expiratory pressure (PEEP). Figure 4. View largeDownload slide Using the pressure–volume loop to determine optimal levels of positive end-expiratory pressure (PEEP). Figure 5. View largeDownload slide Lung overdistension is demonstrated by the flattening of the upper portion of the pressure-volume loop. Figure 5. View largeDownload slide Lung overdistension is demonstrated by the flattening of the upper portion of the pressure-volume loop. Figure 6. View largeDownload slide A decrease in the lung compliance is demonstrated as a decrease in slope of the pressure–volume loop. Figure 6. View largeDownload slide A decrease in the lung compliance is demonstrated as a decrease in slope of the pressure–volume loop. Airway pressure-release ventilation (APRV) is specialized mode of conventional ventilation that may facilitate maintenance of a lung protective strategy. APRV uses inverse ratio ventilation (inspiratory time longer than expiratory) at two levels of PEEP. The patient should be allowed to spontaneously breathe at the high PEEP level with a quick drop to the low PEEP level to facilitate CO2 elimination. APRV reduces the need for paralytics and sedation, improves patient–ventilator synchrony, improves the mean airway pressure, increases oxygenation by alveolar recruitment, lowers peak inspiratory pressure, and decreases physiologic deadspace. An additional benefit of this mode of ventilation is that the patient is breathing spontaneously, which improves venous return by lowering intrathoracic pressure during a spontaneous breath. APVR potentially is indicated in patients requiring full or partial ventilatory support and patients diagnosed with acute lung injury or ARDS, refractory hypoxemia caused by alveolar collapse, and/or massive atelectasis.31 Volume Diffusive Respirator™. VDR™ is a high-frequency time-cycled pressure ventilator that provides ventilation and oxygenation while promoting pulmonary hygiene through secretion removal. The VDR™ facilitates a lung-protective strategy by providing ventilation at lower airway pressures then those required in the pressure control mode.32 Manipulation of the amplitude (peak pressure), frequency, inspiratory and expiratory time, PEEP, and FiO2 provide for optimal ventilation. The chart below illustrates the effects of manipulation of these individual parameters.3 Setting changes in relationship with the PaCO2 and PaO2: ↑ inspiratory time may ↑ PaO2 but possibly ↑ PaCO2 ↓ inspiratory time may ↓ PaO2 but possibly ↓ PaCO2 ↑ expiratory time may ↑ PaCO2 ↓ expiratory time may ↓ PaCO2 ↑ frequency may ↑ PaO2 and ↑ PaCO2 ↓ frequency may ↓ PaO2 and ↓ PaCO2 ↑ amplitude may ↑ PaO2 and ↓ PaCO2 ↓ amplitude may ↓ PaO2 and ↑ PaCO2 No one factor determines whether a patient will respond best to conventional ventilation or to the VDR™. Oftentimes a trial of each mode will be required to determine which is the best mode for each individual patient. The respiratory therapists and physicians in the burn unit must be familiar with a number of modes of ventilation and be willing to alter strategies as dictated by patient response. Other Respiratory Issues Airway resistance is increased in the patient with chemical injury of the airway as the result of both injury-induced bronchial edema and bronchospasm. Bronchodilators are best delivered directly to the airway via the ventilator circuit;34 the use of a spacer will maximize delivery of properly sized particles to the distal airways. Fluid resuscitation must be adequate because both under- and over-resuscitation are detrimental to pulmonary function.35 Pulmonary infection may complicate the course of the patient with a chemical injury of the airway because host defenses are compromised by a major burn. The presence of an artificial airway makes bacterial colonization of the airway inevitable. Meticulous attention to detail and technique during suctioning and other airway related care will help to minimize the incidence of ventilator-associated pneumonia (VAP). The American Association for Respiratory Care also has recommended disposable ventilator circuits be changed only when visibly soiled or no longer functional. Not only does this reduce costs, but it also leads to a reduction in VAP.36 Aggressive pulmonary hygiene is indicated for the patients with suspected pulmonary injury because mechanical obstruction of small airways by soot and secretions may occur. Techniques include bronchial lavage with some type of mucolytic that includes aerosolized heparin37 or our local practice of using small quantities (3–5 ml) of diluted sodium bicarbonate instilled directly into the artificial airway. Suctioning is performed using an inline device, which eliminates the need to enter the ventilator circuit and may decrease VAP. The American Association for Respiratory Care has developed evidence-based clinical practice guidelines that address the issues of passive and active humidification of the artificial airway. It has been our practice to use active humidification in the burn patient.38 SEDATION AND CARE OF THE VENTILATED PATIENT Sedation often is required by the ventilated burn patient. Although morphine and midazolam are sufficient for most, occasional patients will require deeper sedation and/or paralysis. We have found dexmedetomidine (Precedex®; Abbott Laboratories, Abbott Park, IL), an alpha-2 adrenergic agonist recently approved by the Food and Drug Administration, provides effective sedation with minimal respiratory depression or other side effects. If paralysis is necessary, it is important to minimize the amount of neuromuscular blocking agent used and to frequently reassess the need for continued paralysis in order to minimize complications. Oral endotracheal tubes are uncomfortable for the patient and make oral care difficult. In addition, oral tubes are difficult to secure, especially in a patient with a facial burn, and may be “tongued out” by a determined patient. We have found in our pediatric population that nasal endotracheal tubes are more comfortable for the patient and easier to secure. If tape does not adhere well to the skin because of a facial burn, we do not hesitate to use staples to secure the endotracheal tube (Figure 3). As mentioned earlier, tracheostomy is indicated if ventilation will be required for more than two to three weeks. Noninvasive Ventilation Little has been written describing the use of noninvasive positive pressure ventilation (NPPV) in the burn patient. We have found NPPV to be useful in the setting of mild-to-moderate respiratory distress either attributable to primary injury or after extubation. NPPV should not be attempted in a patient who is uncooperative, unconscious, or does not have intact airway reflexes. NPPV may be provided via a continuous positive airway pressure machine, a bilevel device, or with a conventional ventilator using the flow-triggered pressure support mode. Either a nasal or full face mask may be used depending on patient acceptance, facial contour, and burn pattern. The benefits of NPPV usually are evident soon after institution; if the patient does not show rapid improvement, another mode of therapy should be pursued. In patients who respond well to NPPV, we will continue support as long as necessary. The patient must be assessed frequently for gastric insufflation and mask-induced pressure areas. It is essential that the team works with the patient to ensure proper fit and acceptance of the mask. Weaning and Extubation Ventilator weaning in general should follow the evidence-based guidelines developed through literature review.39 Ventilator days often are increased in the burn patient because of the staged excisions and grafting procedures that delay weaning attempts. A spontaneous breathing trial should be undertaken before extubation. Whether the spontaneous breathing trial is performed with low level CPAP, low level pressure support ventilation, or via a T-piece has little effect on outcome or predictive ability.40 Patients with mild stridor after extubation may respond to inhaled racemic epinephrine, which through vasoconstriction reduces airway swelling. Patients with more severe stridor may respond to NPPV, as mentioned previously, or to the inhalation of a mixture of helium and oxygen (heliox). Helium, because of its low density, reduces resistance to flow through a narrowed airway, thus reducing the work of breathing. To be effective, heliox must contain at least 65% helium. Heliox does not treat the cause of stridor but reduces patient fatigue, whereas other therapies or “tincture of time” reduce airway swelling. Optimal care of the burn patient requires a team approach. Respiratory care of these challenging patients demands close collaboration between the respiratory therapist, physician, nurse, physical therapist, and all other caregivers. Best outcomes are achieved when all are providing up-to-date, evidence-based care. REFERENCES 1. Weiss SM, Lakshminarayan D Acute inhalation injury.. Clin Chest Med  1994; 15: 103– 16. Google Scholar PubMed  2. Wolf SE, Prough DS, Herndon DN Critical care in the severely burned: organ support and management of complications. Herndon DN Total burn care.  2nd ed. New York Saunders Co; 2002 399– 420. Google Scholar CrossRef Search ADS   3. Dancey DR, Hayes J, Gomez Met al.   ARDS in patients with thermal injury.. Intensive Care Med  1999; 25: 1231– 6. Google Scholar CrossRef Search ADS PubMed  4. Hudson LD, Steinberg KP Epidemiology of acute lung injury and ARDS.. Chest  1999; 116: 745– 825. Google Scholar CrossRef Search ADS   5. 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Oakes D Ventilator management: a bedside reference guide.  Orono Health Educator Publications, Inc; 2002. 32. Carman B, Cahill T, Warden G, McCall J A prospective randomized comparison of the Volume Diffusive Respirator® vs. conventional ventilation for ventilation of burned children.. J Burn Care Rehabil  2002; 23: 444– 8. Google Scholar CrossRef Search ADS PubMed  33. Bird F Volume diffusive respiratory manual 1987.  34. Sheridan R Airway management and respiratory care of the burn patient.. Int Anesthesiol Clin  2000; 38: 129– 45. Google Scholar CrossRef Search ADS PubMed  35. Hughes KR, Armstrong R, Brough Met al.   Fluid requirements of patients with burns and inhalation injuries in an intensive care unit.. Intensive Care Med  1981; 15: 519. 36. AARC Evidence-Based Clinical Practice Guidelines. Care of the ventilator circuit and its relation to ventilator-associated pneumonia.. Respir Care  2003; 48: 540. PubMed  37. Desai MH, Mlcak R, Richardson Jet al.   Reduction in mortality in pediatric patients with inhalation injury with aerosolized heparin/N-acetylcystine therapy [erratum in: J Burn Care Rehabil 1999;20:49].. J Burn Care Rehabil  1998; 19: 210– 2. Google Scholar CrossRef Search ADS PubMed  38. American Association for Respiratory Care Clinical Practice Guideline. Humidification during mechanical ventilation.. Respir Care  1992; 37: 887. PubMed  39. Cook DJ, Meade MO, Guyatt GH, et al.  , for the McMaster Evidence Based Practice Center Weaning from mechanical ventilation. Agency for Healthcare Research and Quality  (Contract No. 290–97–0017, Task order number 2). 40. Jones DP, Byrne P, Morgan Cet al.   Positive endexpiratory pressure vs T-piece: extubation after mechanical ventilation.. N Engl J Med  1991; 100: 1655– 9. Copyright © 2005 by the American Burn Association
TI - Respiratory Care of the Burn Patient
JF - Journal of Burn Care & Research
DO - 10.1097/01.BCR.0000162150.32733.23
DA - 2005-05-01
UR - https://www.deepdyve.com/lp/oxford-university-press/respiratory-care-of-the-burn-patient-LY0nGvfjLp
SP - 200
EP - 206
VL - 26
IS - 3
DP - DeepDyve
ER -