Acute lunginjurycuropinanaesthesiol

  • 693 views
Uploaded on

 

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
    Be the first to like this
No Downloads

Views

Total Views
693
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
11
Comments
0
Likes
0

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. Acute lung injury and outcomes after thoracic surgery Marc Lickera, Pascal Fauconneta, Yann Villigera and Jean-Marie Tschoppb a Department of Anaesthesiology, Pharmacology and Purpose of review Intensive Care, rue Micheli-du-Crest, University Hospital of Geneva, Geneva and bDepartment of The present review evaluates the evidence available in the literature tracking Internal Medicine, Chest Medical Centre, Montana, perioperative mortality and morbidity as well as the pathogenesis and management of Switzerland acute lung injury (ALI) in patients undergoing thoracotomy. Correspondence to Marc Licker, MD, Service Recent findings ´ ˆ ` d’Anesthesiologie, Hopitaux Universitaires de Geneve, Rue Micheli-du-Crest, CH-1211 Geneva, Switzerland Over the last decade, despite increasing age and comorbid conditions, the operative Tel: +41 22 3827439; fax: +41 22 3827403; mortality has remained unchanged for patients undergoing lung resection, whereas e-mail: licker-marc-joseph@diogenes.hcuge.ch procedure-related complications have declined. Better clinical outcomes are achieved Current Opinion in Anaesthesiology 2009, in high-volume hospitals and when procedures are performed by a thoracic surgeon. 22:61–67 Postthoracotomy ALI has become the leading cause of operative death, its incidence has remained stable (2–5%) and earlier diagnosis can be made by assessing the extravascular lung water volume with the single-indicator dilution technique. The pathogenesis of ALI implicates a multiple-hit sequence of various triggering factors (e.g. oxidative stress and surgical-induced inflammation) in addition to injurious ventilatory settings and genetic predisposition. Summary Knowledge of the perioperative risk factors of major complications and understanding of the mechanisms of postthoracotomy ALI enable anesthesiologists to implement ‘protective’ lung strategies including the use of low tidal volume (VT) with recruitment maneuvers, a goal-directed fluid approach and prophylactic treatment with inhaled b2-adrenergic agonists. Keywords acute lung injury, lung resection, mechanical ventilation, thoracotomy, tidal volume Curr Opin Anaesthesiol 22:61–67 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins 0952-7907 Introduction Risk factors of operative mortality Thoracotomies with lung resection are classified as inter- Outcomes following lung resection largely differ between mediate-to-major surgical procedures with in-hospital specialized and nonspecialized medical centres. mortality rates expected to be less than 2% for lobectomy Mortality rates as low as 2.2% have been reported in a and less than 6% for pneumonectomy [1,2]. Among French survey including 15 183 patients managed by 512 578 thoracic procedures performed from 1988 to specialized thoracic teams, whereas fatality rates as high 2002 in the United States, several changes have been as 12% have been observed in the US nationally repre- identified: surgical candidates are more likely to be older sentative samples of Medicare patients aged over 65 years (mean age of 63 years), women (40%) and to undergo [4,5]. Qualified cardiothoracic surgeons devoting their lobectomy instead of pneumonectomy due to earlier practice entirely or mainly to thoracic surgery achieve diagnosis of cancer stages [3]. Despite higher comorbid better results than nonspecialized surgeons [6]. Improved status, operative mortality has remained unchanged and short and long-term results are also achieved in hospitals the length of hospital stay has become shorter along with with a high volume of any complex procedure, emphasiz- a reduction of procedure-related complications. Nowa- ing the key role of multidisciplinary teams, the avail- days, the main causes of mortality have shifted from ability of intensive care resources with an acute pain cardiac and surgical complications towards infectious service as well as the implementation of scientifically complications (pneumonia, empyema and sepsis) and evidence-based practices [7,8]. the acute lung injury (ALI) syndrome with its most severe form the acute respiratory distress syndrome Apart from these organizational factors, analysis of the (ARDS). European Thoracic Surgery Database and of the French 0952-7907 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins DOI:10.1097/ACO.0b013e32831b466c Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
  • 2. 62 Thoracic anaesthesia Table 1 Overview of studies on the postthoracotomy acute lung injury syndrome Incidence (%) Reference n Risk factors Overall P L <L Mortality (%) Licker et al. [11] 879 MV, high Pinsp aw, fluid overload (first 24 h), 4.2 8.4 3.1 3.4 37 pneumonectomy, alcohol abuse Ruffini et al. [12] 1221 NA 2.2 3.8 2 3.2 52 Kutlu et al. [13] 1139 Age > 60 years, male sex, lung cancer, extended 3.9 6 3.7 1 64 resection Alam et al. [14] 1428 ppoFEV1, ppoDLC0, fluid overload (intraoperative) 3.1 10.1 5.5 4.1 25 Dulu et al. [15] 2192 NA 2.5 7.9 3 0.9 40 Fernandez-Perez [16] 170a High VT (8.3 vs. 6.7 ml/kg), fluid overload NA 8.8 40 (intraoperative) van der Werff et al. [17] 197 MV, high Pinspir aw, fresh-frozen plasma 2.5 100 Turnage et al. [18] 806 NA 2.6 100 Verheijen-Breemhar et al. [19] 243 NA 4.5 27 Waller et al. [20] 205 NA 4.4 56 Algar et al. [21] 242a Operative time, ppoFEV1, prior cardiac disease, 2.5 2.5 COPD, no chest therapy (preoperative) Song et al. [22] 635 NA 3.6 48 Katzenelson et al. [23] 146a Prior chemotherapy, prior chemotherapy, FEV1 15 15 < 45% predicted, predicted postoperative lung perfusion < 55%, fluid overload (intraoperative) COPD, chronic obstructive pulmonary disease; <L, lesser resection than lobectomy; L, lobectomy; MV, mechanical ventilation; Pinspir aw, inspiratory airway pressure; P, pneumonectomy; ppoDLCO, predicted postoperative diffusion lung capacity to carbon monoxide; ppoFEV1, predicted post- operative forced expiratory volume in 1 s; VT, tidal volume; NA, not applicable. a Only pneumonectomy cases. national dataset have identified independent risk factors from almost 100% to less than 40% owing to improved of perioperative death: age, male sex, dyspnea score, ICU medical management (Table 1) [11–22]. functional performance status, American Society of Anesthesiologists (ASA) score and the extent of surgical New semiinvasive monitoring tools have appeared in the resection [4,9]. These models of risk have been validated perioperative arena providing valuable information for in second sets of population, with good predictive accu- early diagnosis of ALI and haemodynamic treatment. racies (c-index ! 0.85). The single-indicator thermal dilution method (Pulsion, Munich, Germany) has been validated against the gravi- metric method to assess the extravascular lung water Epidemiology and diagnostic criteria of acute index (EVLWI) [23]. This simple technique has proven lung injury sensitive to detect infraclinical variations in EVLWI, to The guidelines set out by the American–European estimate a pulmonary vascular permeability index while Consensus Conference on ARDS have been widely monitoring cardiac output using pulse contour analysis of adopted to describe postthoracotomy ALI, previously the arterial pressure [24]. Pulmonary artery catheters coined postpneumonectomy pulmonary oedema, low- have been replaced by ultrasound imaging for cardiocir- pressure oedema or permeability pulmonary oedema. culatory assessment. Chest ultrasound scans can also be Although the diagnosis of ALI/ARDS relies on specific used to detect excess lung water content. ‘Comet-tail criteria [acute onset of hypoxemia, arterial oxygen pres- images’ fanning out from the lung surface and originating sure (PaO2)/fraction of inspired oxygen (FIO2) less than from water-thickened interlobular septa have been 300 for ALI and less than 200 for ARDS, diffuse radio- shown to correlate closely with lung water content logical infiltrates and no evidence of elevated hydrostatic [25,26]. capillary pressure], a wide spectrum of lung injuries is encountered [10]. Importantly, two clinical patterns of postthoracotomy ALI should be distinguished corre- Clinical risk factors and pathophysiology of sponding to different pathogenic triggers: ALI develop- postthoracotomy acute lung injury ing within 48–72 h after lung resection (primary ALI) and Several risk factors of the early form of postthoracotomy a delayed form triggered by postoperative complications ALI have been identified in cohorts of thoracic surgical such as bronchoaspiration or pneumonia [11]. patients. Using multivariate regression analysis, the strongest predictors of postthoracotomy ALI are related Contrasting with other cardiopulmonary complications, to the preoperative condition of the patient (severe the incidence of postthoracotomy ALI has not shown any pulmonary dysfunction and chronic alcohol consump- noticeable decrease over the last two decades (between 2 tion) and to perioperative medical care (extended lung and 4%) although the case-fatality rate has decreased resection, ‘injurious’ ventilation and fluid overhydration) Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
  • 3. ALI and outcomes after thoracic surgery Licker et al. 63 [11]. Moreover, the occurrence of ALI is more frequently [e.g. antioxidant, heat-shock protein, p75 receptor for reported after right pneumonectomy in elderly patients tumor necrosis factor (TNF)-a] counteract the initial with colonized airways or in those requiring multiple inflammatory and oxidative responses [38,39]. The in- transfusions or receiving neoadjuvant chemoradiotherapy creased permeability of the alveolar–capillary barrier along [27–29]. with a decreased lung compliance initially results from the disruption of intercellular endothelial cell junction, cytos- Rather than a unified stereotyped response, a multiple- keleton contraction and alveolar cell death consequent hit sequence of deleterious events likely interacts to activation of endothelial/epithelial cell receptors by resulting in alveolar epithelial and capillary endothelial systemic/alveolar inflammatory mediators [e.g. thrombine, injuries, with alterations in extracellular matrix (ECM), vascular endothelial growth factor (VEGF), transforming ultimately leading to the characteristic histopathological growth factor-beta (TGF-b) and thromboxane A2 (TxA2)] features of ALI [30]. [40–42]. The ‘neutrophil hypothesis’ suggests that circulating Clinical studies neutrophils are activated by proinflammatory mediators In the ICU setting, the benefits of a protective lung such as granulocyte and macrophage–colony stimulating ventilation (PLV) strategy have been clearly documented factors in concert with various chemokines. These neu- in large observational studies and meta-analysis of random- trophils experience delayed apoptosis and sustained ized controlled trials (RCTs) [43]. In clinical practice, PLV release of proteolytic enzymes, reactive oxygen inter- entails the delivery of low VT (less than 7 ml/kg) with mediates/reactive nitrogen intermediates (ROIs/RNIs) pressure-limited ventilation (less than 30 cm of H2O) and as well as proinflammatory mediators [31]. the application of positive end-expiratory pressure (PEEP) with periodic recruitment maneuvers [44]. The ‘epithelial hypothesis’ emphasizes the role of both lung parenchymal cell apoptosis and chemotactic/inflam- During short periods of mechanical ventilation (4–6 h), matory responses, which are associated with increased atelectatic areas are common and so-called ‘low-volume’ expression of Fas on epithelial cells, along with enhanced injuries may result from repetitive opening and closing of extravasation of Fas ligand-expressing cells [32]. unstable lung units owing to inactivation of surfactant and excessive mechanical stress between neighboring lung Ventilatory strategy areas [45,46]. Recent experimental and clinical studies have empha- sized the ‘injurious’ aspects of physical stress and hyper- Several RCTs including surgical patients with healthy oxia associated with mechanical ventilation that may lungs have questioned whether different ventilatory set- trigger inflammatory changes at the alveolar–capillary tings could modulate pulmonary/systemic inflammation barrier in ‘vulnerable’ surgical patients as characterized while influencing oxygenation index and respiratory by genetic factors, disrupted lympathic vessels and pro- mechanical properties [47]. As summarized in Table 2 inflammatory circulating mediators associated with pre- [48–59], no benefit could be demonstrated by varying the existing lung disease or surgical trauma. VT for surgical procedures lasting less than 5 h [48,49]. In contrast, in all studies, except one including more severe Basic science surgical stresses (e.g. major operations exceeding 5 h and Even ‘physiological’ low VT (4–8 ml/kg) delivered over cardiac surgery), intraoperative ventilation with lower VT several hours in healthy lungs may produce subtle lung (5–6 ml/kg) and PEEP was associated with stable or injuries: neutrophil infiltration, rupture of alveolar–bron- improved oxygenation, reduced expression of alveolar chial attachment and chondroitin–sulfate proteoglycan and systemic inflammation and reduced procoagulant fragmentation in the ECM [33]. With larger VT, there is activity in the bronchoalveolar lavage fluid (BALF) [50– further macromolecular fragmentation, activation of 55]. In agreement with these data, Lee et al. [57] reported a matrix metalloprotease and upregulation of collagen syn- trend for lower incidence in pulmonary complications and thesis in the ECM that represent an autoregulatory for shorter intubation periods in patients ventilated with response to maintain low pulmonary compliance while small VT (6 vs. 12 ml/kg) after major noncardiac surgery. protecting the ECM against fluid overload [34–36]. Inter- estingly, induction of unilateral ventilator-induced injury In patients undergoing thoracotomy and requiring one- (VILI) in one lung with high VT does not trigger a lung ventilation (OLV), three RCTs have evaluated concomitant inflammatory response in the contralateral the impact of different ventilatory settings. Schilling normally ventilated lung [37]. et al. [58] found reduced alveolar concentrations of TNF-a and soluble intercellular adhesion molecules Ventilation with large VT is not sufficient per se to induce (ICAMs) in patients ventilated with small vs. large VT ALI in healthy lungs, as defense and repair mechanisms (5 vs. 10 ml/kg). Confirming these positive results, Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
  • 4. 64 Thoracic anaesthesia Table 2 Randomized controlled trials assessing the effects of different modes of ventilation Reference n Type of surgery Ventilation strategy Effects of low vs. high VT Two-lung ventilation Wrigge et al. [48] 39 Visceral, orthopedic 5 ml/kg ZEEP vs. 5 ml/kg Similar plasma cytokine levels and vascular 10 cmH2O PEEP vs. 15 ml/kg 10 PEEP Wrigge et al. [49] 32 Visceral 6 ml/kg 10 cmH2O PEEP Similar time course of cytokines in tracheal vs. 12–15 ml/kg ZEEP aspirate and plasma Choi et al. [50] 40 Visceral 6 ml/kg cmH2O PEEP Thrombin–antithrombin complex, activated vs. 12 ml/kg ZEEP protein C in BALF, thrombomodulin in BALF Wolthuis et al. [51] 40 Visceral 6 ml/kg 10 cmH2O PEEP Similar levels of TNF-a, IL-1, MIP-1 in BALF, vs. 12 ml/kg ZEEP IL-8 in BALF, myeloperoxidase and elastase in BALF, similar levels of IL-6 and IL-8 in plasma Reis-Miranda et al. [52] 62 Cardiac 4–6 ml/kg 10 cmH2O IL-8 and IL-10 in plasma PEEP þ RM vs. 6–8 ml/kg 3 cmH2O PEEP Chaney et al. [53] 25 Cardiac 6 ml/kg 10 cmH2O PEEP PaO2/FIO2, static lung compliance vs. 12 ml/kg ZEEP Zupancich et al. [54] 40 Postcardiac 6 ml/kg 10 cmH2O PEEP IL-6 and IL-8 in BALF and plasma vs. 10–12 ml/kg 3 cmH2O PEEP Koner et al. [56] 44 Cardiac 6 ml/kg 5 cmH2O PEEP Similar plasma TNF-a and IL-1, similar vs 0.10 ml/kg ZEEP vs. PaO2/FIO2 10 ml/kg 10 cmH2O PEEP Lee et al. [57] 103 General 6 vs. 12 ml/kg Pulmonary infection, duration of MV Wrigge et al. [55] 44 Cardiac 6 ml/kg 10 PEEP TNF-a in BALF, similar plasma cytokine levels vs. 12 ml/kg ZEEP One-lung ventilation Wrigge et al. [49] 32 Lung resection 6 ml/kg 10 cmH2O PEEP Similar time course of cytokines in tracheal vs. 12–15 ml/kg ZEEP aspirate and plasma Schilling et al. [58] 32 Lung resection 5 ml/kg ZEEP vs. 10 ml/kg ZEEP TNF-a and sICAM in BALF, similar levels of albumine, elastase, IL-8 and IL-10 Michelet et al. [59] 52 Esophagectomy 5 ml/kg 5 cmH2O PEEP vs. IL-1, IL-6, IL-8 in plasma, PaO2/FiO2 and 9 ml/kg ZEEP lung water content, duration of MV BALF, bronchoalveolar lavage fluid; MV, mechanical ventilation; PaO2/FIO2, ratio of arterial oxygen pressure to fractional inspiratory oxygen pressure; PEEP, positive end-expiratory pressure; RM, recruitment maneuver; sICAM, soluble intercellular adhesion molecules; TNF, tumor necrosis factor; ZEEP, zero-end expiratory pressure. Michelet et al. [59] reported an attenuated systemic proin- trigger formation of ROIs/RNIs and induce complex flammatory response [lower plasma levels of interleukin patterns of cell death. These findings have been con- (IL)-6], reduced EVLWI and improved oxygenation index firmed in animal and human studies. allowing earlier extubation in patients undergoing esopha- gectomy who received low VT (5 ml/kg) with a PEEP level In rabbits ventilated with large VT and moderate hyperoxia of 5 cmH2O (compared with VT of 10 ml/kg with zero (FIO2 ¼ 0.5), Sinclair et al. [60] reported a loss of alveolar– PEEP). In contrast, Wrigge et al. [49] failed to document capillary barrier integrity and larger increase in local any difference in systemic inflammatory markers, blood inflammatory mediators (IL-8 and TNF-a) than animals oxygenation index and respiratory mechanics between exposed either to room air or to hyperoxia without large VT. thoracic surgical patients assigned to receive either mech- Consistent with these results, Funakoshi et al. [61] anical ventilation with VT of 6 ml/kg and PEEP of reported an upregulation of proinflammatory cytokines 10 cmH2O or a VT of 12–15 ml/kg without PEEP. and myeloperoxidase upon reventilation, though indices of pulmonary capillary permeability remained unchanged. Although a growing body of scientific knowledge indicates Likewise, in anesthetized pigs subjected to thoracotomy that the ‘traditional’ ventilatory settings may be injurious and OLV (VT of 10 ml/kg, PEEP of 5 cmH2O and FIO2 of in the healthy lungs, a clear demonstration of clinical 0.4), Kozian et al. [62] showed hyperperfusion, ventilation– outcome benefits induced by LPV is still lacking. There- perfusion mismatch and diffuse tissue damage that pre- fore, we are awaiting the results of well designed RCTs dominated in the dependent nonoperated lung. with sufficient power and pertinent clinical endpoints, comparing conventional ventilation to LPV protocols. In three patients with reexpansion pulmonary oedema, Her and Mandy [63] observed leukocyte-mediated ALI Hyperperfusion and oxidative injuries in the contralateral lung along with decreased leuko- In-vitro studies have shown that cyclic stretch and hyper- cytes and platelet counts upon reoxygenation of the col- oxic exposure of lung epithelial and endothelial cells lapsed lung. In another clinical study involving patients Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
  • 5. ALI and outcomes after thoracic surgery Licker et al. 65 undergoing lobectomy, Cheng et al. [64] reported for- have been incriminated as initiating or aggravating factors mation of ROIs during lung reinflation after OLV (VT of [71]. Likewise, the interactions with ROIs/RNIs and 10 ml/kg and FIO2 of 1.0) although antioxidant markers nuclear factor-kB-dependent activation of the inducible and EVLWI remained unchanged. nitric oxide synthase may result in downregulation of b2- adrenergic receptor in response to surgical trauma and Taken together, these data suggest that hyperoxic/ OLV/reoxygenation. Hence, early and severe interstitial/ mechanical injuries predominate in the nonoperated alveolar lung edema may develop in patients with lung, whereas the operated lung is prone to atelectasis deficient b-adrenergic-mediated fluid clearance mechan- formation due to impaired surfactant and direct surgical isms. manipulation. An imbalance between antioxidants and excess production of RNIs/ROIs has been incriminated in perpetuating the inflammatory process and causing Novel perioperative approaches cellular damage by oxidizing nucleic acids, proteins and Preliminary data suggest some advantages for volatile membrane lipids [65]. anesthetics during OLV. Indeed, desflurane has been associated with lesser recruitment of neutrophils and Genetic factors reduced concentrations of inflammatory biomarkers in Only a fraction of patients exposed to ALI-inciting events the BALF [elastase, soluble intercellular adhesion mol- progress to the full clinical syndrome. Hence, major ecules (sICAM), TNF-a, IL-8 and IL-10] than propofol interest has been focused on the identification of genetic anesthesia [73]. factors characteristic of ALI susceptibility. Relevant gene variants or single-nucleotide polymorphisms (SNPs) in Regarding ventilatory settings, the emerging concept of these ALI candidate genes have been tested for differ- PLV based on the ‘open-lung approach’ aims to limit ences in allelic frequency in cohort studies [66]. This alveolar distension with low (but physiological) VT while approach has yielded a number of candidate genes con- attenuating the loss of functional residual volume and tributing towards an ALI phenotype, namely genes cod- preventing the formation of atelectasis with PEEP and ing for angiotensin-converting enzyme (ACE), surfactant lung recruitment maneuvers [74,75]. Using ‘low VT’ protein B, heat-shock protein 70, pre-B-cell colony combined with PEEP does not favor the development enhancing factor, myosin light-chain kinase and macro- of atelectasis, whereas the pressure-controlled mode of phage migration inhibitory factor. ventilation (vs. volume-controlled mode) may lower peak airway pressure with similar blood oxygenation indices, at Using microarray technology, the transcription factor least in patients without severe lung disease [76,77]. Nrf2 (NF-E2 related factor 2) has been shown to up- regulate the protective detoxifying enzymes in response Controversies still surround the question of the optimal to oxidative stress [67]. Genetic disruption of the Nrf2 FIO2; high levels (60–80%) may reduce the risk of surgi- has been associated with an overexpression of proinflam- cal-site infections but promote atelectasis and ROI for- matory cytokines and increased risk of ALI due to hyper- mation [78]. Conversely, low–moderate FIO2 (30–50%) oxia and high VT. In line with these results, Marzec et al. might be an appropriate compromise to ensure satisfactory [68] identified six novel SNPs for Nrf2 in a nested case– blood oxygenation and limit secondary lung injuries. control study. Patients with the À617 SNP (A/or C/A allele) were at greater risk of posttrauma ALI relative to Considering the importance of the hydrostatic pulmonary patients bearing the wild type (À617 C) [odds ratio (OR) pressure, a restrictive or goal-directed fluid approach 6.4; 95% confidence interval (CI) 1.3–30.8]. coupled with the assessment of intrapulmonary fluid volume is strongly recommended for the intraoperative In patients undergoing esophagectomy (n ¼ 152), pul- period and the first 24–48 h after major lung resection. monary morbidity has been associated with an ACE insertion/deletion polymorphism; the D/D genotype Postoperatively, high-risk thoracic patients may benefit was found to be highly predictive of major pulmonary from noninvasive ventilation and inhaled b2-adrenergic complications (adjusted OR 3.12; 95% CI 1.01–9.65) [69]. therapy. In a small RCT including 32 patients with a moderate degree of chronic obstructive pulmonary dis- Edema clearance mechanisms ease, better postoperative recovery of pulmonary func- Removal of the excess intraalveolar fluid is mainly influ- tion was reported when noninvasive pressure support enced by epithelial b-adrenergic receptors and lectin-like ventilation was applied prophylactically before and domain of TNF-a that regulate the active sodium trans- shortly after lung resection [79]. In 21 patients at high port through alveolar type I and II cells [70–72]. In heart risk of pulmonary edema from either a cardiogenic or failure, high-altitude lung edema and various models of noncardiogenic cause, the impact of aerosolized broncho- ALI, alterations in these b-adrenergic signaling pathways dilators has been investigated using the single-dilution Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
  • 6. 66 Thoracic anaesthesia 9 Berrisford R, Brunelli A, Rocco G, et al. The European Thoracic Surgery indicator method [80]. Using a crossover design, salbu- Database project: modelling the risk of in-hospital death following lung tamol (vs. ipratropium) was shown to accelerate the resection. Eur J Cardiothorac Surg 2005; 28:306–311. resolution of postoperative lung edema and improve 10 Villar J, Perez-Mendez L, Lopez J, et al. An early PEEP/FIO2 trial identifies different degrees of lung injury in patients with acute respiratory distress blood oxygenation without causing adverse cardiac syndrome. Am J Respir Crit Care Med 2007; 176:795–804. events. In addition, b2-adrenergic agonists may also pre- 11 Licker M, de Perrot M, Spiliopoulos A, et al. Risk factors for acute lung injury vent or attenuate ALI by blunting the release of proin- after thoracic surgery for lung cancer. Anesth Analg 2003; 97:1558–1565. flammatory cytokines, reducing chemotaxis and neutro- 12 Ruffini E, Parola A, Papalia E, et al. Frequency and mortality of acute lung injury and acute respiratory distress syndrome after pulmonary resection for phil degranulation as well as protecting the integrity of bronchogenic carcinoma. Eur J Cardiothorac Surg 2001; 20:30–36. the alveolar–capillary barrier [81]. 13 Kutlu CA, Williams EA, Evans TW, et al. Acute lung injury and acute respiratory distress syndrome after pulmonary resection. Ann Thorac Surg 2000; 69:376–380. 14 Alam N, Park BJ, Wilton A, et al. Incidence and risk factors for lung injury after Conclusion lung cancer resection. Ann Thorac Surg 2007; 84:1085–1091. This review has attempted to summarize and update key 15 Dulu A, Pastores SM, Park B, et al. Prevalence and mortality of acute lung features regarding major mortality and ALI following injury and ARDS after lung resection. Chest 2006; 130:73–78. thoracic surgery. Animal studies and transitional biology 16 Fernandez-Perez ER, Keegan MT, Brown DR, et al. Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy. Anesthesiology have provided new insights into the fundamental mech- 2006; 105:14–18. anisms of ALI that might evolve towards new targeted 17 van der Werff YD, van der Houwen HK, Heijmans PJ, et al. Postpneumo- therapeutic tools. nectomy pulmonary edema. A retrospective analysis of incidence and pos- sible risk factors. Chest 1997; 111:1278–1284. 18 Turnage WS, Lunn JJ. Postpneumonectomy pulmonary edema. A retrospec- Several changes in perioperative management have tive analysis of associated variables. Chest 1993; 103:1646–1650. already been implemented, particularly in high-risk 19 Verheijen-Breemhaar L, Bogaard JM, van den Berg B, Hilvering C. Post- patients: an ‘open-lung’ approach (low VT, PEEP and pneumonectomy pulmonary oedema. Thorax 1988; 43:323–326. recruitment), titrated fluid regimen, assessment of pul- 20 Waller DA, Gebitekin C, Saunders NR, Walker DR. Noncardiogenic pulmon- ary edema complicating lung resection. Ann Thorac Surg 1993; 55:140– monary fluid compartment and early treatment of lung 143. edema with noninvasive ventilation, aerosolized b2- 21 Algar FJ, Alvarez A, Salvatierra A, et al. Predicting pulmonary complications adrenergic agonists or both. after pneumonectomy for lung cancer. Eur J Cardiothorac Surg 2003; 23:201–208. 22 Song SW, Lee HS, Kim MS, et al. Preoperative serum fibrinogen level predicts postoperative pulmonary complications after lung cancer resection. Ann Acknowledgements Thorac Surg 2006; 81:1974–1981. The present study was supported by a grant from the Lancardis 23 Katzenelson R, Perel A, Berkenstadt H, et al. Accuracy of transpulmonary Foundation in Sion (Switzerland). thermodilution versus gravimetric measurement of extravascular lung water. Crit Care Med 2004; 32:1550–1554. 24 Monnet X, Anguel N, Osman D, et al. Assessing pulmonary permeability by transpulmonary thermodilution allows differentiation of hydrostatic pulmonary References and recommended reading edema from ALI/ARDS. Intensive Care Med 2007; 33:448–453. Papers of particular interest, published within the annual period of review, have been highlighted as: 25 Agricola E, Bove T, Oppizzi M, et al. Ultrasound comet-tail images: a marker of  of special interest pulmonary edema: a comparative study with wedge pressure and extravas-  of outstanding interest cular lung water. Chest 2005; 127:1690–1695. Additional references related to this topic can also be found in the Current 26 Jambrik Z, Monti S, Coppola V, et al. Usefulness of ultrasound lung comets as World Literature section in this issue (pp. 132–133). a nonradiologic sign of extravascular lung water. Am J Cardiol 2004; 93:1265–1270. 1 Licker MJ, Widikker I, Robert J, et al. Operative mortality and respiratory 27 Brouchet L, Bauvin E, Marcheix B, et al. Impact of induction treatment on complications after lung resection for cancer: impact of chronic obstructive postoperative complications in the treatment of nonsmall cell lung cancer. pulmonary disease and time trends. Ann Thorac Surg 2006; 81:1830–1837. J Thorac Oncol 2007; 2:626–631. 2 Boffa DJ, Allen MS, Grab JD, et al. Data from The Society of Thoracic  Surgeons General Thoracic Surgery database: the surgical management 28 D’Journo XB, Michelet P, Papazian L, et al. Airway colonisation and post- operative pulmonary complications after neoadjuvant therapy for oesophageal of primary lung tumors. J Thorac Cardiovasc Surg 2008; 135:247–254. A comprehensive survey of 9033 pulmonary resections recorded in the general cancer. Eur J Cardiothorac Surg 2008; 33:444–450. thoracic surgery prospective database from 1999 to 2006. 29 Swanson K, Dwyre DM, Krochmal J, Raife TJ. Transfusion-related acute lung 3 Memtsoudis SG, Besculides MC, Zellos L, et al. Trends in lung surgery: injury (TRALI): current clinical and pathophysiologic considerations. Lung United States 1988 to 2002. Chest 2006; 130:1462–1470. 2006; 184:177–185. 4 Falcoz PE, Conti M, Brouchet L, et al. The Thoracic Surgery Scoring System 30 Ware LB. Pathophysiology of acute lung injury and the acute respiratory (Thoracoscore): risk model for in-hospital death in 15 183 patients requiring distress syndrome. Semin Respir Crit Care Med 2006; 27:337–349. thoracic surgery. J Thorac Cardiovasc Surg 2007; 133:325–332. 31 Perl M, Chung CS, Perl U, et al. Beneficial versus detrimental effects of 5 Hammill BG, Curtis LH, Bennett-Guerrero E, et al. Impact of heart failure on neutrophils are determined by the nature of the insult. J Am Coll Surg 2007; patients undergoing major noncardiac surgery. Anesthesiology 2008; 204:840–852. 108:559–567. 32 Perl M, Chung CS, Perl U, et al. Fas-induced pulmonary apoptosis and 6 Goodney PP, Lucas FL, Stukel TA, Birkmeyer JD. Surgeon specialty and inflammation during indirect acute lung injury. Am J Respir Crit Care Med operative mortality with lung resection. Ann Surg 2005; 241:179–184. 2007; 176:591–601. 7 Urbach DR, Baxter NN. Does it matter what a hospital is ‘high volume’ for? 33 D’Angelo E, Koutsoukou A, Della Valle P, et al. Cytokine release, small airway Specificity of hospital volume-outcome associations for surgical procedures: injury, and parenchymal damage during mechanical ventilation in normal open- analysis of administrative data. BMJ 2004; 328:737–740. chest rats. J Appl Physiol 2008; 104:41–49. 8 Lien YC, Huang MT, Lin HC. Association between surgeon and hospital 34 Demoule A, Decailliot F, Jonson B, et al. Relationship between pressure- volume and in-hospital fatalities after lung cancer resections: the experience volume curve and markers for collagen turn-over in early acute respiratory of an Asian country. Ann Thorac Surg 2007; 83:1837–1843. distress syndrome. Intensive Care Med 2006; 32:413–420. Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
  • 7. ALI and outcomes after thoracic surgery Licker et al. 67 35 Pavone LA, Albert S, Carney D, et al. Injurious mechanical ventilation in the 57 Lee PC, Helsmoortel CM, Cohn SM, Fink MP. Are low tidal volumes safe? normal lung causes a progressive pathologic change in dynamic alveolar Chest 1990; 97:430–434. mechanics. Crit Care 2007; 11:R64. 58 Schilling T, Kozian A, Huth C, et al. The pulmonary immune effects of 36 Musch G, Venegas JG, Bellani G, et al. Regional gas exchange and cellular mechanical ventilation in patients undergoing thoracic surgery. Anesth Analg metabolic activity in ventilator-induced lung injury. Anesthesiology 2007; 2005; 101:957–965. 106:723–735. 59 Michelet P, D’Journo XB, Roch A, et al. Protective ventilation influences 37 Almendros I, Gutierrez PT, Closa D, et al. One-lung overventilation does not systemic inflammation after esophagectomy: a randomized controlled study. induce inflammation in the normally ventilated contralateral lung. Respir Anesthesiology 2006; 105:911–919. Physiol Neurobiol 2008; 162:100–102. 60 Sinclair SE, Altemeier WA, Matute-Bello G, Chi EY. Augmented lung injury 38 Wilson MR, Goddard ME, O’Dea KP, et al. Differential roles of p55 and p75 due to interaction between hyperoxia and mechanical ventilation. Crit Care tumor necrosis factor receptors on stretch-induced pulmonary edema in mice. Med 2004; 32:2496–2501. Am J Physiol Lung Cell Mol Physiol 2007; 293:L60–L68. 61 Funakoshi T, Ishibe Y, Okazaki N, et al. Effect of re-expansion after short- 39 Ogawa EN, Ishizaka A, Tasaka S, et al. Contribution of high-mobility group period lung collapse on pulmonary capillary permeability and pro-inflammatory box-1 to the development of ventilator-induced lung injury. Am J Respir Crit cytokine gene expression in isolated rabbit lungs. Br J Anaesth 2004; Care Med 2006; 174:400–407. 92:558–563. 40 Frank JA, Wray CM, McAuley DF, et al. Alveolar macrophages contribute to 62 Kozian A, Schilling T, Freden F, et al. One-lung ventilation induces hyperperfu- alveolar barrier dysfunction in ventilator-induced lung injury. Am J Physiol Lung sion and alveolar damage in the ventilated lung: an experimental study. Br J Cell Mol Physiol 2006; 291:L1191–L1198. Anaesth 2008; 100:549–559. 41 Ware LB, Matthay MA, Parsons PE, et al. Pathogenetic and prognostic 63 Her C, Mandy S. Acute respiratory distress syndrome of the contralateral lung significance of altered coagulation and fibrinolysis in acute lung injury/acute after reexpansion pulmonary edema of a collapsed lung. J Clin Anesth 2004; respiratory distress syndrome. Crit Care Med 2007; 35:1821–1828. 16:244–250. 42 Lowe K, Alvarez D, King J, Stevens T. Phenotypic heterogeneity in lung 64 Cheng YJ, Chan KC, Chien CT, et al. Oxidative stress during 1-lung ventila- capillary and extra-alveolar endothelial cells. Increased extra-alveolar endothe- tion. J Thorac Cardiovasc Surg 2006; 132:513–518. lial permeability is sufficient to decrease compliance. J Surg Res 2007; 65 Tasaka S, Amaya F, Hashimoto S, Ishizaka A. Roles of oxidants and redox 143:70–77. signaling in the pathogenesis of acute respiratory distress syndrome. Antioxid 43 Petrucci N, Iacovelli W. Lung protective ventilation strategy for the acute Redox Signal 2008; 10:739–753. respiratory distress syndrome. Cochrane Database Syst Rev 2007: 66 Meyer NJ, Garcia JG. Wading into the genomic pool to unravel acute lung CD003844. injury genetics. Proc Am Thorac Soc 2007; 4:69–76. 44 Verbrugge SJ, Lachmann B, Kesecioglu J. Lung protective ventilatory strate- 67 Papaiahgari S, Yerrapureddy A, Reddy SR, et al. Genetic and pharmacologic  gies in acute lung injury and acute respiratory distress syndrome: from evidence links oxidative stress to ventilator-induced lung injury in mice. Am J experimental findings to clinical application. Clin Physiol Funct Imaging Respir Crit Care Med 2007; 176:1222–1235. 2007; 27:67–90. This review addresses the physiological background of ventilator-induced lung 68 Marzec JM, Christie JD, Reddy SP, et al. Functional polymorphisms in the injury and the clinical implications of lung-protective strategies in critically ill transcription factor NRF2 in humans increase the risk of acute lung injury. patients. FASEB J 2007; 21:2237–2246. 45 Tsuchida S, Engelberts D, Peltekova V, et al. Atelectasis causes alveolar injury 69 Lee JM, Lo AC, Yang SY, et al. Association of angiotensin-converting enzyme in nonatelectatic lung regions. Am J Respir Crit Care Med 2006; 174:279– insertion/deletion polymorphism with serum level and development of pul- 289. monary complications following esophagectomy. Ann Surg 2005; 241:659– 665. 46 Pavone L, Albert S, DiRocco J, et al. Alveolar instability caused by mechanical ventilation initially damages the nondependent normal lung. Crit Care 2007; 70 Vadasz I, Schermuly RT, Ghofrani HA, et al. The lectin-like domain of tumor 11:R104. necrosis factor-alpha improves alveolar fluid balance in injured isolated rabbit lungs. Crit Care Med 2008; 36:1543–1550. 47 Schultz MJ. Lung-protective mechanical ventilation with lower tidal volumes in patients not suffering from acute lung injury: a review of clinical studies. Med 71 Guidot DM, Folkesson HG, Jain L, et al. Integrating acute lung injury and Sci Monit 2008; 14:RA22–RA26. regulation of alveolar fluid clearance. Am J Physiol Lung Cell Mol Physiol 2006; 291:L301–L306. 48 Wrigge H, Zinserling J, Stuber F, et al. Effects of mechanical ventilation on release of cytokines into systemic circulation in patients with normal pulmon- 72 Vadasz I, Raviv S, Sznajder JI. Alveolar epithelium and Na,K-ATPase in acute ary function. Anesthesiology 2000; 93:1413–1417. lung injury. Intensive Care Med 2007; 33:1243–1251. 49 Wrigge H, Uhlig U, Zinserling J, et al. The effects of different ventilatory 73 Schilling T, Kozian A, Kretzschmar M, et al. Effects of propofol and desflurane settings on pulmonary and systemic inflammatory responses during major anaesthesia on the alveolar inflammatory response to one-lung ventilation. Br J surgery. Anesth Analg 2004; 98:775–781. Anaesth 2007; 99:368–375. 50 Choi G, Wolthuis EK, Bresser P, et al. Mechanical ventilation with lower tidal 74 Puls A, Pollok-Kopp B, Wrigge H, et al. Effects of a single-lung recruitment volumes and positive end-expiratory pressure prevents alveolar coagulation in maneuver on the systemic release of inflammatory mediators. Intensive Care patients without lung injury. Anesthesiology 2006; 105:689–695. Med 2006; 32:1080–1085. 51 Wolthuis EK, Choi G, Dessing MC, et al. Mechanical ventilation with lower 75 Yilmaz M, Gajic O. Optimal ventilator settings in acute lung injury and acute tidal volumes and positive end-expiratory pressure prevents pulmonary in- respiratory distress syndrome. Eur J Anaesthesiol 2008; 25:89–96. flammation in patients without preexisting lung injury. Anesthesiology 2008; 108:46–54. 76 Cai H, Gong H, Zhang L, et al. Effect of low tidal volume ventilation on atelectasis in patients during general anesthesia: a computed tomographic 52 Reis Miranda D, Gommers D, Struijs A, et al. Ventilation according to the open scan. J Clin Anesth 2007; 19:125–129. lung concept attenuates pulmonary inflammatory response in cardiac surgery. Eur J Cardiothorac Surg 2005; 28:889–895. 77 Unzueta MC, Casas JI, Moral MV. Pressure-controlled versus volume- controlled ventilation during one-lung ventilation for thoracic surgery. Anesth 53 Chaney MA, Nikolov MP, Blakeman BP, Bakhos M. Protective ventilation Analg 2007; 104:1029–1033. attenuates postoperative pulmonary dysfunction in patients undergoing car- diopulmonary bypass. J Cardiothorac Vasc Anesth 2000; 14:514–518. 78 Aboab J, Jonson B, Kouatchet A, et al. Effect of inspired oxygen fraction on alveolar derecruitment in acute respiratory distress syndrome. Intensive Care 54 Zupancich E, Paparella D, Turani F, et al. Mechanical ventilation affects Med 2006; 32:1979–1986. inflammatory mediators in patients undergoing cardiopulmonary bypass for cardiac surgery: a randomized clinical trial. J Thorac Cardiovasc Surg 2005; 79 Perrin C, Jullien V, Venissac N, et al. Prophylactic use of noninvasive ventila- 130:378–383. tion in patients undergoing lung resectional surgery. Respir Med 2007; 101:1572–1578. 55 Wrigge H, Uhlig U, Baumgarten G, et al. Mechanical ventilation strategies and inflammatory responses to cardiac surgery: a prospective randomized clinical 80 Licker M, Tschopp JM, Robert J, et al. Aerosolized salbutamol accelerates the trial. Intensive Care Med 2005; 31:1379–1387. resolution of pulmonary edema after lung resection. Chest 2008; 133:845– 852. 56 Koner O, Celebi S, Balci H, et al. Effects of protective and conventional mechanical ventilation on pulmonary function and systemic cytokine release 81 Perkins GD, Gao F, Thickett DR. In vivo and in vitro effects of salbutamol on after cardiopulmonary bypass. Intensive Care Med 2004; 30:620–626. alveolar epithelial repair in acute lung injury. Thorax 2008; 63:215–220. Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.