REVIEW ARTICLE |
https://doi.org/10.5005/jp-journals-11010-04204 |
Year in review 2015: Recruitment manoeuvres in ards
Email: heerart2007@gmail.com
Assistant Professor, Dept. of Respiratory Therapy, School of Allied Health Sciences, MANIPAL
Abstract
Refractory hypoxaemia is a problem in patients with acute respiratory distress syndrome (ARDS). Although mechanical ventilation is the mainstay of management of ARDS, this therapy itself can cause damage to the lungs due to high tidal volume and high airway pressures. Lung protective strategies are used to reduce damage to the lungs due to mechanical ventilation. Use of small tidal volumes can cause alveolar derecruitment and arterial hypoxaemia. Lung recruitment manoeuvre (RM) opens up collapsed segments of the ARDS lung but the collapse may reappear once the RM is complete. Although RM has been shown to improve oxygenation there is still no clear data showing improvement in clinical outcome. This review summarises the different techniques used for RM, physiological effects of RM on lung mechanics along with monitoring RM at the bedside.
Keywords: ARDS, hypoxaemia, recruitment manoeuvres, lung protective ventilation.
How to cite this article: Mahto HL. Year-in review - Recruitment Manoeuvre in ARDS. Ind J Resp Care 2015; 4(2): 611-7.
Introduction
Refractory hypoxaemia is a problem in patients with acute respiratory distress syndrome (ARDS). Although mechanical ventilation is the mainstay of management of ARDS, this therapy itself can cause damage to the lungs due to high tidal volume and high airway pressures.1,2 There is strong evidence that low tidal volume ventilatory strategies improve survival.3 Lung protective strategies are used to reduce damage to the lungs due to mechanical ventilation. However, the use of small tidal volumes can cause alveolar derecruitment and arterial hypoxaemia. In the ARDSNet trial, patients randomised to the low tidal volume group had lower PO2 levels, possibly due to alveolar derecruitment.3 The lung in ARDS have regions of collapse which can possibly be recruited. It is known that damage to ARDS lungs can occur not only due to volutrauma or barotrauma but also due to atelectrauma. Recruitment and prevention of derecruitment of the collapsed areas can be expected to reduce atelectrauma, improve gas exchange as well as reduce ventilator-induced lung injury. Lung recruitment manoeuvre (RM) is one of the many lung-protective strategies that can be used to open up these collapsed areas in the lung.4
Physiological effects of recruitment manoeuvre
Historically, RM was found to safely improve arterial oxygenation in patients who develop atelectasis due to general anaesthesia,5 and in neonates undergoing high-frequency oscillation for respiratory distress syndrome.6 Literature review shows that RM inflation pressure range of 30–60 cm H2O for a duration 3 s to 3 min, have reported various improvements in gas exchange.7–14 Recruiting the lung may benefit by two mechanisms: The first is the increase in the aerated lung mass, minimising the lung heterogeneity and increasing the size of the baby lung. The second is the prevention of repeated opening and closure of the terminal respiratory units reducing shear stress. Pelosi et al showed that recruiting manoeuvres improved lung mechanics and oxygenation only in patients with extrapulmonary ARDS. RM did not improve lung mechanics in pulmonary ARDS and also did not influence the amount of improvement in arterial oxygenation after application of the recruitment manoeuvre.15 Mahto et al found that only 50 % of patients responded to initial recruitment manoeuvre suggesting the heterogeneity of disease presentation. They concluded that not all patients respond to recruitment manoeuvre and show an increase in oxygenation.16
The use of high tidal volumes produce higher peak pressures in these lungs with very low compliance leading to higher incidence of barotrauma.17 Such ventilation can also lead to release of inflammatory mediators such as interleukins 1 and 6, tumour necrosis factor alpha causing biotrauma.18 Ventilation with low tidal volumes also result in progression of lung injury.19 Thus, careful attention needs to be given to tidal volumes and at least intermittent application of distending pressures much higher than that recommended for the ventilation of patients with ARDS. Chen YM et al in animal experiments showed that RM and lung protective ventilation in rabbits with ARDS improved oxygenation and reduced extravascular lung water.20,21
Techniques of recruitment manoeuvre
There are many techniques of providing RM in the clinical setting as well as in experimental model (Table 1). Lapinsky et al showed increase in oxygen saturation in all 14 patients while using sustained inflation manoeuvre of 45 cm of H2O for a period of 20 seconds.22 There were no adverse effects observed in his study. Lim et al used volume controlled mode, VT (tidal volume) reduced by 2 ml/kg and positive end expiratory pressure (PEEP) increased by 5 cm of H2O every 30 seconds.23 At VT 2 ml/kg and PEEP 25, continuous positive airway pressure (CPAP) 30 cm H2O was applied for 30 seconds. He found that there was increase in PaO2 and static compliance, sustained for the duration of the study. Grasso et al applied CPAP of 40 cm H2O for 40 seconds found that there was improvement in oxygenation only in early ARDS group and in patients with low lung elastance.24 Oczenski el al applied sustained inflation (CPAP 50 cm H2O for 30 s) found that significant increase in P/F ratio at 3 min post-RM, no significant differences in P/F ratio between RM and control group at baseline and after 30 min.25 Constantin et al did comparative study between CPAP of 40 cm H2O for 40 sec and sigh by PEEP of 10 cm H2O above lower inflection point on pressure-volume (P–V) curve for 15 minutes; found that both manoeuvres improved oxygenation at 5 and 60 minutes.26 Drop in systolic pressure <70 mm Hg on two occasions in the CPAP group was observed. No significant drop in systolic blood pressure (SBP) was observed in sigh group. Some level of sedation is usually required to carry out an RM but neuromuscular blockade is not absolutely necessary. Monitor the patient carefully for hypotension and desaturation during the RM. The RM should be followed up with an appropriate PEEP level to prevent derecruitment.16
Monitoring recruitment manoeuvre at the bedside
Computed tomography (CT) scan provides a wealth of information such as presence and distribution of inflated and collapsed areas of the lung, change in these areas with ventilation and whether recruiting the collapsed areas is a possibility. However, CT cannot still be used for everyday management, especially at the patient bedside, and is limited for use during clinical research.
The physiological effects of recruitment manoeuvre have been evaluated based on changes in respiratory mechanics, improvement in the ventilation–perfusion ratio and oxygenation. However, measurement of oxygenation alone is insufficient as several factors can influence oxygenation.33, 34 The multiple pressure–volume curves method has been proposed as an acceptable bedside assessment of recruitment.35 However, performing multiple pressure–volume curves is difficult in clinical practice, and alveolar recruitment can be underestimated.36
Direct measurement and monitoring of end expiratory lung volume (EELV) could be used to assess both alveolar recruitment and derecruitment at the bedside. Chiumello et al37 demonstrated that, although CT remains the gold standard for gas lung volume, EELV measurement using an automated system based on the nitrogen washout technique that is incorporated into a ventilator (Engstro¨m Carestation; GE Medical System, Helsinki, Finland) is an acceptable alternative. Several studies opine an improvement in lung aeration can be assessed and detected by lung ultrasound (LUS).38,39 Although LUS is an easily repeatable technique, it remains time-consuming, unsuitable for continuous monitoring and obviously inappropriate to detect lung hyperinflation.
| Trails | Year of Publication | Type of RM Used | Findings |
| Pelosi et al.15 | 1999 | Three consecutive sighs of plateau pressure 45 cm of H2O every minute for an hour | Increase in the end expiratory lung volume, reduction in the intrapulmonary shunt and improvement in oxygenation |
| Lapinsky et al.22 | 1999 | Sustained inflation manoeuvre of 45 cm of H2O for a period of 20 seconds | Improvement in oxygen saturation in all 14 Patients, sustained up to four hours in 10 patients. No significant adverse effects noted |
| Rothen et al.27 | 1999 | Sustained inflation of 40 cm of H2O for 26 seconds in anesthetized patients | May re-expand all previously collapsed lung tissue, as detected by lung computed tomography, and improve oxygenation |
| Lim et al.23 | 2001 | On volume controlled mode, VT reduced by 2 ml/kg and PEEP increased by 5 cm of H2O every 30 seconds. At Vt 2 ml/kg and PEEP 25, CPAP 30 cm of H2O was applied for 30 seconds. | Increase in PO2 and static compliance, sustained for the duration of the study. No major respiratory or haemodynamic complications |
| Bein et al.28 | 2002 | Progressive increase in peak airway pressure (within 30 sec) up to 60 cm H2O and sustained for the next 30 seconds | Marginal improvement in oxygenation Deterioration of cerebral haemodynamics |
| Patroniti et al.29 | 2002 | CPAP of 20% higher than peak airway pressure for 3–5 seconds every minute on pressure support ventilation | Improvement in oxygenation Improved lung compliance |
| Grasso et al.24 | 2002 | CPAP of 40 cm H2O for 40 seconds | Improved oxygenation noted only in early ARDS and in patients with low lung elastance |
| Meade et al.30 | 2002 | Sustained inflation (CPAP 35–40 cm H2O for 20–40 s) | No net effect on oxygenation or pulmonary mechanics after first or subsequent RMs |
| Oczenski et al.25 | 2004 | Sustained inflation (CPAP 50 cm H2O for 30 s) | Significant increase in PaO2/FiO2 (P/F) ratio at 3 min post-RM, no significant differences in P/F ratio between RM and control group at baseline and after 30 min |
| ARDSNet31 | 2003 | CPAP of 35–45 cm H2O for 30 seconds | Effects of RM were inconsistent and transient |
| Stewart et al.32 | 2007 | Sustained inflation (CPAP 40 cm H2O for 40 s) | None reported |
| Constantin et al.26 | 2008 | Comparative study between CPAP of 40 cm H2O for 40 sec and sigh by PEEP of 10 cm H2O above lower inflexion point on P -V curve for 15 minutes | Both manoeuvres improved oxygenation at 5 and 60 minutes Drop in systolic pressure <70 mm Hg on two occasions in the CPAP group No significant drop in BP during sigh |
| Mahto et al.16 | 2013 | During the RM, PEEP was increased from baseline to 15, 20 and 25 cm H2O sequentially (every 30 s from the baseline PEEP until 25 cm H2O). The VT was decreased by 25%, 50% and 75% respectively from the baseline VT during the incremental PEEP trial phase. | Significant increase in P/F ratio post recruitment manoeuvre after 30 minutes |
Electrical impedance tomography (EIT), allows real-time rather than intermittent monitoring, measures relative impedance changes in lung tissue during tidal breathing and provides images of the lungs divided into regions of interest.40
Recruitment manoeuvre and prone position
Prone position has become an established method for pulmonary recruitment and increase in oxygenation in many ARDS patients. Kacmarek suggested that the recruitment manoeuvre in prone position is more effective for PaO2 increase, and that the PEEP level required to sustained PaO2 increase is lower in prone than in the supine position.41
-Lim et al performed an experimental trial with seven acute lung injury dog models. 42 They showed that lower PEEP levels are needed for preserving the recruitment manoeuvre in prone position. Another study by Cakar et al showed that the alveolar recruitment more effectively improves oxygenation with lower PEEP levels in prone position as compared to supine position.43
Complications
Studies done by Lim et al and Kloot TE et alhave shown increased intrathoracic pressure resulting from recruitment manoeuvre transiently compromises haemodynamic function by impeding venous return with an increase in right atrial pressure, decreasing cardiac output and arterial pressure. RM should be used with caution in patients with haemodynamic instability.44–47 Substantial reductions (20–30%) in cardiac output and mean arterial blood pressure have been reported during sustained inflations of 40 cm H2O.24 Bein T et al found 17% decrease in cerebral perfusion pressure, along with a marked, sustained decrease in jugular venous oxygen saturation, from 69 to 59%, due to recruitment manoeuvre in head- injured patients with ARDS.48 Eddy et al after a systematic review of 31 studies involving 985 patients concluded that the majority of adverse events occurred during RM, with hypotension (12%) and desaturation (8%) being the most common complications.49 Serious adverse events, such as barotrauma (1%) and arrhythmias (1%), were uncommon. Only 10 (1%) patients were reported to have had RM terminated prematurely due to adverse events. Seventeen studies (287 patients) reported no adverse events from RM. Translocation of bacteria from the lung due to increased stretch during RMs is more a theoretical concern.50–52 Study done by Cakar et al in a rat model, showed that a sustained inflation RM of 45 cm of H2O for 30 seconds at fifteen minute intervals did not result in bacterial translocation as evident on blood cultures.53
Summary
Recruitment manoeuvre may improve oxygenation and further prevent derecruitment of alveoli if antiderecruitment strategy of RM is used. It also prevents repetitive opening and closing of alveoli thus reducing the chances of VILI. Extrapulmonary ARDS is more likely to respond to RMs compared to pulmonary ARDS; consolidated lungs may not be recruitable. RM is more likely to be beneficial during the early stages of ARDS, compared to later stages when fibroproliferative changes set in. Patients who are already on optimal PEEP are unlikely to benefit from RM. Overdistention due to recruitment manoeuvre can lead to decrease in venous return and cardiac output causing significant haemodynamic compromise. Thus haemodynamic effects of RM should be considered among patients who are on inotropes and blood pressures should be continuously monitored during RM. Monitoring the effects of recruitment manoeuvre at the bedside have become an integral part of the strategy. The optimal technique of recruitment is unclear and may vary depending on individual clinical circumstances. Prone position has become an established method for pulmonary recruitment and increase in oxygenation in many ARDS patients. RM have been clearly shown to improve gas exchange, there is no evidence that suggests improved morbidity or mortality. Routine use of RM should be avoided as it may not be associated with benefit. RM may be used as rescue therapy in refractory hypoxaemia and in patients with severe ARDS.
References
1. Dreyfuss D, Basset F, Soler P, Saumon G. Intermittent positive pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats. Am Rev Respir Dis 1985; 132:880-4.
2. Kolobow T, Moretti MP, Fumagalli R, et al. Severe impairment in lung function induced by high peak airway pressure during mechanical ventilation. Am Rev Respir Dis 1987; 135:312-5.
3. The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes in acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000;342:1301-8.
4. Gattinoni L, Caironi P, Cressoni M, et al. Lung recruitment in patients with the acute respiratory distress syndrome. N Engl J Med 2006; 354:1775-86.
5. Rothen HU, Sporre B, Engberg G, Wegenius G, Hedenstierna G. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993;71(6): 788-95.
6. Froese AB. Role of lung volume in lung injury: HFO in the atelectasis- prone lung. Acta Anaesthesiol Scand Suppl 1989;33:126-30.
7. Borges JB, Okamoto VN, Matos GF, Caramez MP, Arantes PR, Barros F, et al. Reversibility of lung collapse and hypoxemia in early acute respiratory distress syndrome. Am J Respir Crit Care Med 2006;174(3):268-78.
8. Po'voa P, Almeida E, Fernandez A, Mealha R, Moreira P, Sabino H. Evaluation of a recruitment manoeuvre with positive inspiratory pressure and high PEEP in patients with severe ARDS. Acta Anaesthesiol Scand 2004;48(3):287-93.
9. Lapinsky SE, Aubin M, Mehta S, Boiteau PE, Slutsky AS. Safety and efficacy of a sustained inflation for alveolar recruitment in adults with respiratory failure. Intens Care Med 1999;25(11):1297- 301.
10. Pelosi P, Bottino N, Chiumello D, Caironi P, Panigada M, Gamberoni C, et al. Sigh in supine and prone position during acute respiratory distress syndrome. Am J Respir Crit Care Med 2003; 167(4):521-7.
11. Grasso S, Mascia L, Del Turco M, Malacarne P, Giunta F, Brochard L, et al. Effects of recruiting manoeuvres in patients with acute respiratory distress syndrome ventilated with protective ventilatory strategy. Anesthesiology 2002;96(4):795-802.
12. Foti G, Cereda M, Sparacino ME, De marchi L, Villa F, Pesenti A. Effects of periodic lung recruitment manoeuvres on gas exchange and respiratory mechanics in mechanically ventilated acute respiratory distress syndrome (ARDS) patients. Intensive Care Med 2000;26(5): 501-7.
13. Barbas CSV, Silva E, Garrido A, Assuncao M, Hoelz EC, Knobel E. Recruitment manoeuvres with different pressure control levels in ARDS patients. Am J Respir Crit Care Med 2001;163:A767.
15. Dreyfuss D, Saumon G: Ventilator-induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med 1998, 157:294-323.
16. Pelosi P, Cadringher P, Bottino N, Panigada M, Carrieri F, Riva E, Lissoni A, Gattinoni. Sigh in acute respiratory distress syndrome. Am J Respir Crit Care Med 1999; 159: 872–80.
17. Mahto HL, Shanbhag V, Shenoy A. Efficacy of recruitment manoeuvre with or without antiderecruitment strategy in ARDS patients: A prospective study. Ind J Resp Care 2013; 2: 284-91.
18. Gammon RB, Shin MS, Buchalter SE. Pulmonary barotrauma in mechanical ventilation. Patterns and risk factors. Chest 1992;102:568- 72.
19. Ranieri VM, Suter PM, Tortorella C, De Tullio R, Dayer JM, Brienza A, et al. Effect of mechanical ventilation on inflammatory mediators in patients with acute respiratory distress syndrome: A randomized controlled trial. JAMA 1999;282:54-61.
20. Muscedere JG, Mullen JB, Gan K, Slutsky AS. Tidal ventilaton at low airway pressures can augment lung injury. Am J Respir Crit Care Med 1994;149:1327-34.
21. Halter JM, Steinberg JM, Schiller HJ, DaSilva M, Gatto LA, Landas S, et al. Positiveend expiratory pressure after a recruitment manoeuvre prevents both alveolar collapse and recruitment/derecuitment. Am J Respir Crit Care Med 2003; 167: 1620-6.
22. Chen YM, Yang Y, Qiu HB, Li JQ, Huang YZ, Xu XT. Effect of protective ventilation and open lung strategy on extravascular lung water in rabbits with acute respiratory distress syndrome. Zhonghua Jie He He Hu Xi Za Zhi 2005; 28: 615-8.
23. Lapinsky SE, Aubin M, Mehta S, Boiteau P, Slutsky AS. Safety and efficacy of a sustained inflation for alveolar recruitment in adults with respiratory failure. Intensive Care Med 1999;25:1297-301.
24. Lim CM, Koh Y, Park W, Chin JY, Shim TS, Lee SD, et al. Mechanistic scheme and effect of “extended sigh” as a recruitment manoeuvre in patients with acute respiratory distress syndrome: A preliminary study. Crit Care Med 2001;29:1255-60.
25. Grasso S, Mascia L, Del Turco M, Malacarne P, Giunta F, Brochard L, Slutsky AS, et al. Effects of recruiting manoeuvres in patients with acute respiratory distress syndrome ventilated with protective ventilatory strategy. Anesthesiology 2002;96: 795-802.
26. Oczenski W, Hormann C, Keller C, Lorenzi N, Kepka A, Schwarz S, Fitzgerald RD. Recruitment manoeuvres after a positive end-expiratory pressure trial do not induce sustained effects in early adult respiratory distress syndrome. Anesthesiology 2004;101:620–5.
27. Constantin JM, Jaber S, Futier E, Cayot- Constantin S, Verny- Pic M, Jung B, et al. Respiratory effects of different recruitment manoeuvres in acute respiratory distress syndrome. Crit Care 2008;12:R50.
28. Rothen HU, Neumann P, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Dynamics of re-expansion of atelectasis during general anesthesia. Br J Anaesth 1999;82:551-6.
29. Bein T, Kuhr LP, Bele S, Ploner F, Keyl C, Taeger K. Lung recruitment manoeuvre in patients with cerebral injury: Effects on intracranial pressure and cerebral metabolism. Intensive Care Med 2002;28:554-8.
30. Patroniti N, Foti G, Cortinovis B, Maggioni E, Bigatello LM, Cereda M, et al. Sigh improves gas exchange and lung volume in patients with acute respiratory distress syndrome undergoing pressure support ventilation. Anesthesiology 2002;96:788-94.
31. Meade MO, Guyatt GH, Cook DJ, Lapinsky SE, Hand L, Griffith L, Stewart TE. Physiologic randomized pilot study of a lung recruitment manoeuvre in acute lung injury. Am J Respir Crit Care Med 2002; 165: A683.
32. Brower RG, Lanken PN, MacIntyre N, Matthay MA, Morris A, Ancukiewicz M, et al. National heart, lung, and blood institute ARDS Clinical Trials Network: Higher versus lower positive end- expiratory pressures in patients with the acute respiratory distress syndrome. N Engl J Med 2004;351:327-36.
33. Oczenski W, Hormann C, Keller C, Lorenzi N, Kepka A, Schwarz S, Fitzgerald RD. Recruitment manoeuvres after a positive end-expiratory
34. pressure trial do not induce sustained effects in early adult respiratory distress syndrome. Anesthesiology 2004;101:620–5.
35. Mancini M, Zavala E, Mancebo J, et al. Mechanisms of pulmonary gas exchange improvement during a protective ventilatory strategy in acute respiratory distress syndrome. Am J Respir Crit Care Med 2001;164:1448–53.
36. Cressoni M, Caironi P, Polli F, et al. Anatomical and functional intrapulmonary shunt in acute respiratory distress syndrome. Crit Care Med 2008;36:669–75.
37. Ranieri VM, Eissa NT, Corbeil C, et al. Effects of positive end-expiratory pressure on alveolar recruitment and gas exchange in patients with the adult respiratory distress syndrome. Am Rev Respir Dis 1991;144:544–51.
38. Patroniti N, Bellani G, Cortinovis B, et al. Role of absolute lung volume to assess alveolar recruitment in acute respiratory distress syndrome patients. Crit Care Med 2010; 38:1300–7.
39. Chiumello D, Cressoni M, Chierichetti M, et al. Nitrogen washout/washin, helium dilution and computed tomography in the assessment of end expiratory lung volume. Crit Care 2008; 12:R150.
40. Gargani L, Lionetti V, Di Cristofano C, et al. Early detection of acute lung injury uncoupled to hypoxemia in pigs using ultrasound lung comets. Crit Care Med 2007; 35:2769–74.
41. Bouhemad B, Liu ZH, Arbelot C, et al. Ultrasound assessment of antibioticinduced pulmonary reaeration in ventilator-associated pneumonia. Crit Care Med 2010; 38:84–92.
42. Wrigge H, Zinserling J, Muders T, et al. Electrical impedance tomography compared with thoracic computed tomography during a slow inflation manoeuvre in experimental models of lung injury. Crit Care Med 2008; 36:903–9.
43. Kacmarek RM. Strategies to optimize alveolar recruitment. Curr Opin Crit Care. 2001;7(1): 15-20.
44. Lim CM, Koh Y, Chin JY, Lee JS, Lee SD, Kim WS, Kim DS, Kim WD. Respiratory and haemodynamic effects of the prone position at two different levels of PEEP in a canine acute lung injury model. Eur Respir J. 1999;13(1): 163-8.
45. Cakar N, der Kloot TV, Youngblood M, Adams A, Nahum A. Oxygenation response to a recruitment manoeuvre during supine and prone positions in an oleic acid induced lung injury model. Am J Respir Crit Care Med. 2000;161(6):1949-56.
46. Lim SC, Adams AB, Simonson DA, et al. Transient haemodynamic effects of recruitment manoeuvres in three experimental models of acute lung injury. Crit Care Med 2004; 32: 2378–84.
47. Kloot TE, Blanch L, Melynne Youngblood A, et al. Recruitment manoeuvres in three experimental models of acute lung injury. Effect on lung volume and gas exchange. Am J Respir Crit Care Med 2000; 161:1485–94.
48. Frank JA, McAuley DF, Gutierrez JA, Daniel BM, Dobbs L, Matthay MA. Differential effects of sustained inflation recruitment manoeuvres on alveolar epithelial and lung endothelial injury. Crit Care Med 2005;33(1):181–188; discussion 254–5.
49. Odenstedt H, Lindgren S, Olegard C, Erlandsson K, Lethvall S, Aneman A, et al. Slow moderate pressure recruitment manoeuvre minimizes negative circulatory and lung mechanic side effects: evaluation of recruitment manoeuvres using electric impedance tomography. Intensive Care Med 2005;31(12):1706–14.
51. Bein T, Kuhr LP, Bele S, Ploner F, Keyl C, Taeger K. Lung recruitment manoeuvre in patients with cerebral injury: effects on intracranial pressure and cerebral metabolism. Intensive Care Med 2002; 28(5):554–58.
52. Fan E, Wilcox ME, Brower RG et al. Recruitment Manoeuvres for Acute Lung Injury A Systematic Review. Am J Respir Crit Care Med 2008; 178:1156–63.
53. Nahum A, Hoyt J, Schmitz L, Moody J, Shapiro R, Marini JJ. Effect of mechanical ventilation strategy on dissemination of intratracheally instilled Escherichia coli in dogs. Crit Care Med 1997;25:1733-43.
54. Piacentini E, Villagra A, Lopez-Aguilar J, Blanch L. Clinical review: The implications of experimental and clinical studies of recruitment manoeuvres in acute lung injury. Crit Care 2004;8:115-21.
55. Lin CY, Zhang H, Cheng KC, Slutsky AS. Mechanical ventilation may increase susceptibility to the development of bacteremia. Crit Care Med 2003;31:1429-34.
56. Cakar N, Akinci O, Tugrul S, Ozcan PE, Esen F, Eraksoy H, et al. Recruitment manoeuvre: Does it promote bacterial translocation? Crit Care Med 2002;30:2103-6.