REVIEW URRENT C OPINION
Postoperative respiratory failure: pathogenesis, prediction, and prevention Jaume Canet a and Lluı´s Gallart b
Purpose of review This review discusses our present understanding of postoperative respiratory failure (PRF) pathogenesis, risk factors, and perioperative-risk reduction strategies. Recent findings PRF, the most frequent postoperative pulmonary complication, is defined by impaired blood gas exchange appearing after surgery. PRF leads to longer hospital stays and higher mortality. The time frame for recognizing when respiratory failure is related to the surgical-anesthetic insult remains imprecise, however, and researchers have used different clinical events instead of blood gas measures to define the outcome. Still, studies in specific surgical populations or large patient samples have identified a range of predictors of PRF risk: type of surgery and comorbidity, mechanical ventilation, and multiple hits to the lung have been found to be relevant in most of these studies. Recently, risk-scoring systems for PRF have been developed and are being applied in new controlled trials of PRF-risk reduction measures. Current evidence favors carefully managing intraoperative ventilator use and fluids, reducing surgical aggression, and preventing wound infection and pain. Summary PRF is a life-threatening event that is challenging for the surgical team. Risk prediction scales based on large population studies are being developed and validated. We need high-quality trials of preventive measures, particularly those related to ventilator use in both high risk and general populations. Keywords acute respiratory distress syndrome, postoperative respiratory failure, prediction, prevention, risk factors
INTRODUCTION The full spectrum of postoperative pulmonary complications (PPCs) includes widely differing events in addition to respiratory failure: pneumonia, prolonged or unplanned mechanical ventilation, hypoxemia, atelectasis, bronchospasm, pleural effusion, pneumothorax, ventilatory depression, and aspiration pneumonitis among others. In the literature on PPC outcomes, many investigators have studied a composite of several possible respiratory events that might occur in the course of postoperative recovery [1–3]. Others have focused on specific events, mostly pneumonia [4] and postoperative respiratory failure (PRF) [5,6]. Unfortunately, the individual PPCs – PRF among them – are not always defined in the same ways. Another aspect that varies in this literature is the postoperative time frame, meaning the moment when PPCs of interest appear during the postoperative period [7]. PRF is the commonest PPC, with an incidence in general surgical populations that ranges between www.co-criticalcare.com
0.2 and 3.4% [3,5,6]. Depending on the definition used and characteristics of the patients studied, associated mortality can exceed 25% [5]. This article reviews current knowledge of the pathogenesis of this life-threatening but imprecisely defined postoperative complication. We also summarize recent findings relevant to risk identification and prevention.
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Department of Anesthesiology and Postoperative Care, Hospital Universitari Germans Trias i Pujol and bDepartment of Anesthesiology, Hospital del Mar, Institut Hospital del Mar d’Investigacions Me`diques (IMIM), Universitat Auto`noma de Barcelona, Barcelona, Spain Correspondence to Dr Jaume Canet, Department of Anesthesiology, Hospital Universitari Germans Trias i Pujol, Carretera del Canyet s/n, Badalona, 08916 Barcelona, Spain. Tel: +34 934978904; e-mail: [email protected] Curr Opin Crit Care 2014, 20:56–62 DOI:10.1097/MCC.0000000000000045 Volume 20 Number 1 February 2014
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Postoperative respiratory failure Canet and Gallart
KEY POINTS PRF, characterized by pulmonary gas exchange impairment appearing during the postoperative period, is the most devastating of all complications and a cause of high postoperative mortality. Factors associated with the patient’s health status and kind of surgery determine baseline risk. When these are combined with additive intraoperative and postoperative factors, the risk of lung damage rises sharply. There is evidence that several respiratory and nonrespiratory measures can reduce PRF risk. Beneficial strategies include strict intraoperative ventilatory and anesthetic management, avoiding fluids and transfusions whenever possible, choosing less aggressive surgical approaches, avoiding residual curarization, preventing surgical site and pulmonary infection, and providing adequate postoperative analgesia. Future studies on PRF should use arterial blood gas measurements to define the event, and consensus is needed on the most useful postoperative time frame to specify. Data should be gathered prospectively, and risk scores should be properly validated before they are considered transportable to new settings.
ventilatory support. Severity can range from transient hypoxemia in the early postoperative period to the most life-threatening form, late-stage acute respiratory disease syndrome (ARDS). According to the recent international consensus on ARDS, PRF may be classified as mild (PaO2/FIO2 300 mmHg and >200 mmHg), moderate (PaO2/ FIO2 200 mmHg and > 100 mmHg), or severe (PaO2/FIO2 100 mmHg) [8].
MECHANISMS RESPONSIBLE FOR POSTOPERATIVE RESPIRATORY FAILURE General anesthesia induces an immediate reduction of muscle tone, which in turn reduces thorax diameters, lung volumes, and airway dimensions. Airway closure and atelectasis then develop, mainly in the dependent parts of the lungs, leading to abnormal gas exchange and ventilation-perfusion mismatch and shunt. Functional imbalance worsens with manipulation of structures above or below the diaphragm during surgery [9]. The decrease in PaO2 that occurs in most patients under general anesthesia is compensated for by administering a high oxygen concentration. However, if the oxygen concentration is over 80% there is risk of adsorption atelectasis [10,11 ]. The hypoxemia that commonly develops after general anesthesia or even after only slight sedation [12] can be aggravated by factors such as hypoventilation due to the residual effects of anesthetics, lung edema, laryngospasm, and bronchospasm. As time passes atelectasis resolves, but at different rates in relation to the patient’s condition and the surgical procedure. Thus, even as gas exchange normalizes and hypoxemia is alleviated, atelectasis may remain for some time after surgery. In one study of patients after abdominal surgery, atelectasis affected the most extensive area of the lung 2 h after surgery and remained more or less the same 2 days later [13]. Atelectasis had decreased by the fourth postoperative day, when involvement extended to only about 20–25% of the area affected during anesthesia. This reduction was accompanied by increased lung volumes and improved gas exchange. If low lung volumes persist, however, atelectasis may not resolve. Eventually, the risk of other complications, such as pneumonia, increases as a result. Unplanned mechanical ventilation may become necessary or support may have to be prolonged. PRF is usually directly related to anesthesia and surgery when it appears within a few days of surgery. A recent study found that the median time until the appearance of postoperative ARDS in a general surgical population was only 2 days [14 ]. Yet, most &&
DEFINITION OF POSTOPERATIVE RESPIRATORY FAILURE By itself, respiratory failure is well defined as inadequate exchange of oxygen and carbon dioxide. It is diagnosed when exchange does not meet metabolic needs, leading to hypoxemia with or without hypercapnia. Arterial blood gas measurement provides the grounds for diagnosis: when partial pressure of oxygen (PaO2) falls below 60 mmHg and/or partial pressure of carbon dioxide exceeds 50 mmHg breathing air at sea level [inspiratory oxygen fraction (FIO2), 0.21], gas exchange is clearly inadequate. Under physiological conditions, with no displacement of the hemoglobin dissociation curve due to acidosis or hypercarbia, a PaO2 of 60 mmHg corresponds to arterial oxygen saturation of 90%. In the clinical setting, the degree of gas exchange impairment is defined by calculating the ratio of PaO2 to FIO2. Thus, when this ratio is lower than 300 mmHg respiratory failure is diagnosed. PRF, then, can be considered as pulmonary gas exchange impairment that presents after a surgical procedure and as a result of the changes induced by anesthesia and surgery. Respiratory failure secondary to cardiac dysfunction is thereby excluded from this definition. PRF is usually managed with some kind of nonroutine respiratory support: oxygen therapy, physiotherapy, or invasive or noninvasive
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authors choose a time frame of 3–7 days to record PRF as an outcome [5,14 ,15,16,17 ] while some have defined PRF as appearing up to 30 days after surgery [18,19 ]. The postoperative time frame, especially in high-risk cases, is so dynamic and is affected by so many preoperative, intraoperative, and postoperative factors acting synergistically that it is difficult to define a single postoperative moment when we can consider PRF to be a direct complication of anesthesia and surgery or a late consequence of additional events. Yet, the lack of such precision is an obstacle to comparing the findings of research, and hence a hindrance in the effort to promote evidence-based management of PRF. &
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POSTOPERATIVE RESPIRATORY MUSCLE DYSFUNCTION Respiratory muscle function in the postoperative period is a key to whether a patient develops PRF or not [20 ]. The normal physiology of the respiratory system relies on balance between respiratory pump muscles – which create a negative pressure leading to an urge to ventilate – and the upper airway dilator muscles – which counterbalance the collapsing forces of the negative pressure and ensure upper airway patency. During emergence from anesthesia and over the postoperative period, respiratory muscle function is affected to different degrees. Early after surgery, residual effects of sedatives and opiates reduce central stimulation of both the upper airway (hypoglossal nerve) and pump muscles (phrenic nerve) [21]. At the same time, residual curarization is often present, affecting the upper airway dilator muscles to a greater extent than the diaphragm [22]. Taken together, these events increase upper airway collapsibility and predispose patients to PRF, particularly in the presence of comorbid conditions such as obesity, obstructive sleep apnea, chronic obstructive pulmonary disease, or smoking addiction. Later, the effects of surgery or trauma can further favor the development of PRF, mainly due to functional disruption of the respiratory muscles, postoperative pain, or direct diaphragmatic dysfunction due to phrenic nerve injury [23]. &&
POSTOPERATIVE ACUTE RESPIRATORY DISEASE SYNDROME Under certain circumstances, some postoperative patients can develop ARDS, which is the worst presentation of PRF, occurring when hypoxemia is the result of lung damage. After the recent Berlin consensus [8], ARDS is now diagnosed if respiratory failure appears within a week of a recognized insult (such as surgery and anesthesia), specific radiological 58
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changes are evident, and a cardiac origin can be ruled out. A variety of mechanical, chemical, and biological insults are necessary for provoking an exudative phase, which involves diffuse alveolocapillary membrane damage occurring heterogeneously across the lung regions [24]. Three levels of respiratory impairment – mild, moderate, and severe – have been defined as described above. The condition formerly termed acute lung injury (ALI) [25], before the Berlin consensus statement [8], represented what we would today refer to as the mild and moderate levels of impaired gas exchange in ARDS. ARDS-associated mortality is very high, ranging from 17% in the mild form to more than 58% in the severe form [26]. In a recent multicenter study, a third of all patients who developed ALI (today, mild or moderate ARDS) had undergone surgery, usually a major procedure such as cardiothoracic, aortic, abdominal, or spine surgery [27]. The mean incidence of ALI after these high-risk interventions was 7.8% in that study, with the highest rate (10.2%) in cardiac surgery. However, in another recent article the incidence of ARDS was 0.2% in a general surgical population from which high-risk surgery had been excluded [14 ]. The pathogenesis of postoperative ARDS is multifactorial. According to the multiple-hit theory of this condition’s development [24,28], the first hit comes from factors related to a patient’s initial status and the scheduled procedure, including the anesthetic technique. Together they describe the epidemiologic background features that can be foreseen and which include a patient’s initial pulmonary or extrapulmonary condition. Although such factors would not by themselves lead directly to alveolar damage, the addition of second hits will further increase the likelihood of ARDS. Possible second hits in the surgical setting include aspects of intraoperative ventilatory management, aspiration, fluid therapy, transfusion, and inadequate control of infection. These second-hit events have all been shown to be direct causes of the lung damage that increases the risk of ARDS. At this point, it is worth remembering the role of persistent postoperative atelectasis, which can trigger an inflammatory reaction, and thus create a locus for postoperative lung inflammation and later pulmonary infection [29], thus also favoring ARDS. &
POSTOPERATIVE RESPIRATORY FAILURE PREDICTION In only the last 3 years, six studies have addressed the issue of the prediction of respiratory failure specifically in the postoperative period [14 ,15,16,17 , 18,19 ] (Table 1). The overall incidence of PRF in &
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Postoperative respiratory failure Canet and Gallart Table 1. Comparison of recent studies on postoperative respiratory failure &
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First author
Gupta [18]
Kor [15]
Ramachandran [16] Hua [19 ]
Blum [14 ]
Brueckmann [17 ]
Outcome
Mechanical ventilation >48 h
Surgical lung injury (ARDS)
Unplanned intubation
Unplanned intubation
ARDS
Unplanned intubation
Outcome definition
NSQIP definitiona
ALI/ARDS [25]
NSQIP definition
NSQIP definition
Mechanical ventilation P/F ratio < 300, bilateral infiltrates on X-ray
Any intubation after extubation
Time gap for 30 outcome (days)
5
3
30
7
3
Patients (n)
468 795
4336
222 094
231 548
50 367
33 769
Database
Retrospective Retrospective (ACS–NSQIP) (previous investigation)
Retrospective (ACS–NSQIP)
Retrospective Retrospective (ACS–NSQIP) (anesthetic records)
Retrospective (anesthesia and billing)
Inclusion criteria
Adult in-patient
Adult in-patient surgery > 3 h
Adult in-patient
Adult in-patient
Adult in-patient
Adult in-patient
Main exclusion criteria
None
Previous mechanical Emergency and ventilation, trauma, cardiac sepsis, shock, acute CHF, and emergency
Trauma and transplant
Cardiac, thoracic, Patients not transplant, extubated at trauma, and the end of vascular surgery
Score
Yes
Yes
Yes
Yes
No
Yes
Validation
Internal
None
Internal
Internal
None
Internal
Incidence of outcome (%)
3.1
2.6
0.8–0.9
1.9–2.2
0.2
0.4
ACS–NSQIP, American College of Surgeons–National Surgical Quality Improvement Program; ALI, acute lung injury; ARDS, acute respiratory distress syndrome; CHF, congestive heart failure. a NSQIP definition of PRF: 1/unplanned intubation during surgery or postoperatively; 2/reintubation once extubated; or 3/mechanical ventilation for > 48 h postoperatively.
those studies ranged from 0.2 to 3.1%. The results must be interpreted cautiously, taking into account how the outcome was defined (including time frames ranging from 3 to 30 days), how patients were selected, and what statistical analyses were used. All six studies were retrospective, using administrative and/or routinely recorded clinical information from multicenter or single-center databases, although one study [15] also included information from a secondary analysis of an earlier prospective study. Three of them [16,18,19 ] were based on data from the American College of Surgeons–National Surgical Quality Improvement Program. This retrospective approach can be very useful for the study of rare events such as PRF, but it has limitations [30–32,33 ] such as low positive predictive values and moderate reliability, errors in the collection data and a high percentage of missing values, lack of information on some variables of clinical interest, and little intraoperative information. These problems are compounded by a lack of external validation in the literature. The shortcomings of administrative databases for grading performance without &
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standardizing definitions, data collection, and management was demonstrated by the recent finding of only poor or moderate concordance between PRF diagnosis of patients included in an administrative database (of the Agency for Healthcare Research and Quality Patient Safety Indicators, a national clinical registry and the National Surgical Quality Improvement Program) and an institutional clinical registry (Cardiovascular Information Registry) [32]. PRF was defined in four of the six studies by prolonged mechanical ventilation or unplanned intubation [16,17 ,18,19 ]; two studies took into consideration arterial blood gases [14 ,15]. The actual incidence of PRF in these recent studies is probably underestimated, however, because currently up to 74% of patients with PRF can be managed with noninvasive ventilation [34], which several studies have shown to be very effective for treating even severe levels of hypoxemia [35–38]. Five studies proposed predictive scores based on weighted preoperative and intraoperative predictors, but information about comorbidity and demographic variables was heterogeneous and even scant
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in some models [15,19 ]. PRF predictors that have been proposed are as follows: (1) Preoperative (a) Age (b) Male sex (c) American Society of Anesthesiologists (ASA) class at least 3 (d) Functional dependency (e) Sepsis or septic shock (f) Congestive heart failure (g) Chronic obstructive pulmonary disease (h) Diabetes mellitus (i) Gastroesophageal reflux disease (j) Alcohol abuse (k) Current smoker (l) Dyspnea (m) Hypertension (n) Liver disease (o) Cancer (p) Prolonged hospitalization (q) Weight loss (r) Renal failure (s) Number of anesthetics during the admission (t) Surgery (i) Upper abdominal (ii) Cardiac (iii) Vascular (iv) Thoracic (v) Neurosurgery (vi) Neck (vii) Urology (viii) Emergency (ix) Transplant (x) General (xi) Burn (xii) High-risk surgery (2) Intraoperative (a) Pulmonary drive pressure (b) Inspired oxygen fraction (c) Volume of crystalloid administration (d) Erythrocyte transfusion (e) Duration of surgery ASA class was included in four of the studies’ models [14 ,17 ,18,19 ], raising the problematic issue that this summary of the patient’s health status is so potent that its inclusion in a model causes specific comorbidities to drop out of the score even though some of those clinical conditions could be managed effectively and are, therefore, of interest [31,39]. The low interobserver reliability of the ASA class [40] also argues against its inclusion in models exploring clinically identifiable risk factors that can be targeted in management strategies. &
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The PRF predictors listed above – which have also been identified in the studies of PPC risk with wider scope [7,39] – can be grouped in time frames (preoperative and intraoperative), consistent with the multiple-hit theory [14 ,41] according to which new predictive models should stratify risk at two stages. The first stage would consider threats associated with the patient’s condition and the foreseen procedure (preoperative information). The second would consider intraoperative events, which would modulate first-hit risk and indicate the patient’s definitive risk. &
PREVENTION OF POSTOPERATIVE RESPIRATORY FAILURE Intraoperative and postoperative measures to prevent the development of PRF, some of which are still under investigation, are listed below: (1) Ventilatory (a) Accurate FiO2 (b) Avoid atelectotrauma (i) Positive end-expiratory pressure (PEEP) (ii) Recruitment maneuvers After intubation After disconnections During relative hypoxemia Before extubation (c) Avoid volutrauma (i) Limit airway plateau pressure to 20 cmH2O (ii) Limit tidal volume to 10 ml/kg in nonrisk patients (iii) Limit tidal volume to 6 ml/kg in highrisk patients (2) Nonventilatory (a) Anesthetic technique (i) Choose neuroaxial or regional techniques (ii) Inhaled anesthetics to decrease pulmonary inflammatory response to mechanical ventilation (iii) Accurate administration and monitoring of neuromuscular blockade (b) Emergence (i) Complete reversal of the neuromuscular blockade (ii) No atelectasis (iii) Adequate postoperative analgesia (iv) Avoid overuse of opiates and excessive sedation (c) Restrictive use of fluids (d) Avoid transfusion (i) Alleviate preoperative anemia (ii) Apply blood saving strategies Volume 20 Number 1 February 2014
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(e) Decrease risk of pulmonary infection (i) Antibiotic prophylaxis (ii) Tooth brushing and oral decontamination (iii) Orotracheal tube management Check cuff pressure Appropriate cuff shape Appropriate material (iv) Avoid nasogastric tubes (f) Surgical technique (i) Choose a thoracoscopic or laparoscopic approach (ii) Reduce surgical duration (iii) Defer surgery whenever possible Thinking in terms of the multiple-hit theory, we suggest that preventive measures that seek to reduce the impact of the second hits produced by anesthetic and surgical management might be the following: (1) Intraoperative lung-protective management of ventilation: this concept has been the subject of two recently published studies [42 ,43 ], and another ongoing study also deals with this approach [44]. Ventilatory management aims to avoid ventilator-induced lung injury, so it is used in all patients, not just those at high risk [9,45,46]. When management is approached in a way that protects the lung, the goal is avoidance of damage from atelectotrauma from the repeated opening and closing of alveoli when alveolar expansion measures, including PEEP, are applied. This approach also relies on the avoidance of volutrauma or overdistension, achieved by holding airway pressure and tidal volume within limits. (2) Accurate oxygen administration: oxygen is adjusted throughout the anesthetic procedure as the administration of a high oxygen concentration (to prevent surgical site infection [47 ]) is balanced against the risks of promoting atelectasis [11 ]. However, a recent meta-analysis concluded that applying a high intraoperative FIO2 (over 80%) for this purpose does not promote atelectasis [47 ]. During emergence from anesthesia, applying recruitment maneuvers and 40% oxygen concentration has been shown to improve oxygenation in comparison to administering 100% oxygen due to the development of readsorption atelectasis [48]. (3) Intraoperative nonventilatory measures: this large set of measures includes infection prevention [49 ,50,51], fluid therapy management [52], avoiding transfusion, and using appropriately chosen and accurately dosed anesthetics [52] and neuromuscular blocking agents [20 ]. &&
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(4) Surgical approach: measures for reducing the aggressiveness of procedures have been shown to reduce the risk of PRF [52]. (5) Postoperative strategies: a multimodal approach includes effective analgesia [52,53], physiotherapy [54 ], and early treatment of postoperative hypoxemia [38,55] as the pillars of PRF prevention. &
CONCLUSION PRF, the postoperative complication responsible for the highest number of deaths, is the result of interacting factors related to patient status, kind of surgery, and intraoperative events, which can cause lung damage. The chest wall and lung changes that anesthesia induces promote atelectasis in the dependent parts of the lung, providing the context in which some patients will develop life-threatening PRF. Although lung-protective strategies are always in place, patients at greatest risk of PRF must be identified in the interest of optimizing management if this complication develops. Further studies are therefore needed to improve PRF prediction. New controlled trials assessing intraoperative and postoperative measures to reduce the incidence of PRF are under way, but we already have some evidence for several respiratory and nonrespiratory measures that can be applied perioperatively to reduce PRF risk. Nonetheless, it is imperative to arrive at consensus on the most relevant postoperative time frame for this event and to use arterial blood gas measurements to define PRF in research so that findings can be usefully compared. Until research designs converge, it will remain difficult to apply current knowledge in the actual clinical settings. Acknowledgements Funding: Grant 041610–2003 from the Catalan public television network (TV3) Marathon fund (’Fundacio´ La Marato´ de TV3’), Barcelona, Spain. Mary Ellen Kerans gave advice on English expression in a version of this article. Conflicts of interest There are no conflicts of interest.
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Respir Care 2012; 57:743–752. 35. Squadrone V, Coha M, Cerutti E, et al. Continuous positive airway pressure for treatment of postoperative hypoxemia: a randomized controlled trial. JAMA 2005; 293:589–595. 36. Michelet P, D’Journo XB, Seinaye F, et al. Noninvasive ventilation for treatment of postoperative respiratory failure after oesophagectomy. Br J Surg 2009; 96:54–60. 37. Jaber S, Michelet P, Chanques G. Role of noninvasive ventilation (NIV) in the perioperative period. Best Pract Res Clin Anaesthesiol 2010; 24:253–265. 38. Glossop AJ, Shephard N, Bryden DC, et al. Noninvasive ventilation for weaning, avoiding reintubation after extubation and in the postoperative period: a meta-analysis. Br J Anaesth 2012; 109:305–314. 39. Canet J, Gallart L. Predicting postoperative pulmonary complications in the general population. Curr Opin Anaesthesiol 2013; 26:107–115. 40. Castillo J, Canet J, Gomar C, et al. Imprecise status allocation by users of the American Society of Anesthesiologists classification system: survey of Catalan anesthesiologists [in Spanish]. Rev Esp Anestesiol Reanim 2007; 54:394– 398. 41. Wanderer JP, Anderson-Dam J, Levine W, et al. Development and validation of an intraoperative predictive model for unplanned postoperative intensive care. Anesthesiology 2013; 119:516–524. 42. Severgnini P, Selmo G, Lanza C, et al. Protective mechanical ventilation && during general anesthesia for open abdominal surgery improves postoperative pulmonary function. Anesthesiology 2013; 118:1307–1321. A comprehensive ventilation strategy (low tidal volumes, PEEP, and recruitment maneuvers) can improve postoperative pulmonary function. 43. Futier E, Constantin JM, Paugam-Burtz C, et al. A trial of intraoperative low-tidal&& volume ventilation in abdominal surgery. N Engl J Med 2013; 369:428–437. A comprehensive ventilation management strategy (low tidal volumes, PEEP, and recruitment maneuvers) can decrease PPCs in patients at intermediate to high risk. The control group received none of these strategies and high tidal volumes, a rare combination nowadays. 44. Hemmes SN, Severgnini P, Jaber S, et al. Rationale and study design of PROVHILO: a worldwide multicenter randomized controlled trial on protective ventilation during general anesthesia for open abdominal surgery. Trials 2011; 12:111. 45. Hemmes SN, Serpa Neto A, Schultz MJ. Intraoperative ventilatory strategies to prevent postoperative pulmonary complications: a meta-analysis. Curr Opin Anaesthesiol 2013; 26:126–133. 46. Melo MF, Eikermann M. Protect the lungs during abdominal surgery: it may change the postoperative outcome. Anesthesiology 2013; 118:1254–1257. 47. Hovaguimian F, Lysakowski C, Elia N, et al. Effect of intraoperative high & inspired oxygen fraction on surgical site infection, postoperative nausea and vomiting, and pulmonary function: systematic review and meta-analysis of randomized controlled trials. Anesthesiology 2013; 119:303–316. A meta-analysis on the beneficial effects of high inspired oxygen fraction. 48. Benoit Z, Wicky S, Fischer JF, et al. The effect of increased FIO(2) before tracheal extubation on postoperative atelectasis. Anesth Analg 2002; 95:1777–1781. 49. Diez-Sebastian J, Herruzo R, Garcia-Caballero J. Prevention of early-onset & pneumonia in surgical patients by chemoprophylaxis. Am J Surg 2012; 204:441–446. Surgical site infection prevention could also decrease postoperative pneumonia – an interesting hypothesis to follow. 50. Zolfaghari PS, Wyncoll DL. The tracheal tube: gateway to ventilatorassociated pneumonia. Crit Care 2011; 15:310. 51. El-Orbany M, Salem MR. Endotracheal tube cuff leaks: causes, consequences, and management. Anesth Analg 2013; 117:428–434. 52. Guldner A, Pelosi P, de Abreu MG. Nonventilatory strategies to prevent postoperative pulmonary complications. Curr Opin Anaesthesiol 2013; 26:141–151. 53. van Lier F, van der Geest PJ, Hoeks SE, et al. Epidural analgesia is associated with improved health outcomes of surgical patients with chronic obstructive pulmonary disease. Anesthesiology 2011; 115:315–321. 54. Cassidy MR, Rosenkranz P, McCabe K, et al. I COUGH: reducing post& operative pulmonary complications with a multidisciplinary patient care program. JAMA Surg 2013; 148:740–745. Guided physiotherapy can decrease pulmonary complications in surgical patients. 55. Chiumello D, Chevallard G, Gregoretti C. Noninvasive ventilation in postoperative patients: a systematic review. Intensive Care Med 2011; 37:918–929.
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Postoperative respiratory failure: pathogenesis, prediction, and prevention Jaume Canet a and Lluı´s Gallart b
Purpose of review This review discusses our present understanding of postoperative respiratory failure (PRF) pathogenesis, risk factors, and perioperative-risk reduction strategies. Recent findings PRF, the most frequent postoperative pulmonary complication, is defined by impaired blood gas exchange appearing after surgery. PRF leads to longer hospital stays and higher mortality. The time frame for recognizing when respiratory failure is related to the surgical-anesthetic insult remains imprecise, however, and researchers have used different clinical events instead of blood gas measures to define the outcome. Still, studies in specific surgical populations or large patient samples have identified a range of predictors of PRF risk: type of surgery and comorbidity, mechanical ventilation, and multiple hits to the lung have been found to be relevant in most of these studies. Recently, risk-scoring systems for PRF have been developed and are being applied in new controlled trials of PRF-risk reduction measures. Current evidence favors carefully managing intraoperative ventilator use and fluids, reducing surgical aggression, and preventing wound infection and pain. Summary PRF is a life-threatening event that is challenging for the surgical team. Risk prediction scales based on large population studies are being developed and validated. We need high-quality trials of preventive measures, particularly those related to ventilator use in both high risk and general populations. Keywords acute respiratory distress syndrome, postoperative respiratory failure, prediction, prevention, risk factors
INTRODUCTION The full spectrum of postoperative pulmonary complications (PPCs) includes widely differing events in addition to respiratory failure: pneumonia, prolonged or unplanned mechanical ventilation, hypoxemia, atelectasis, bronchospasm, pleural effusion, pneumothorax, ventilatory depression, and aspiration pneumonitis among others. In the literature on PPC outcomes, many investigators have studied a composite of several possible respiratory events that might occur in the course of postoperative recovery [1–3]. Others have focused on specific events, mostly pneumonia [4] and postoperative respiratory failure (PRF) [5,6]. Unfortunately, the individual PPCs – PRF among them – are not always defined in the same ways. Another aspect that varies in this literature is the postoperative time frame, meaning the moment when PPCs of interest appear during the postoperative period [7]. PRF is the commonest PPC, with an incidence in general surgical populations that ranges between www.co-criticalcare.com
0.2 and 3.4% [3,5,6]. Depending on the definition used and characteristics of the patients studied, associated mortality can exceed 25% [5]. This article reviews current knowledge of the pathogenesis of this life-threatening but imprecisely defined postoperative complication. We also summarize recent findings relevant to risk identification and prevention.
a
Department of Anesthesiology and Postoperative Care, Hospital Universitari Germans Trias i Pujol and bDepartment of Anesthesiology, Hospital del Mar, Institut Hospital del Mar d’Investigacions Me`diques (IMIM), Universitat Auto`noma de Barcelona, Barcelona, Spain Correspondence to Dr Jaume Canet, Department of Anesthesiology, Hospital Universitari Germans Trias i Pujol, Carretera del Canyet s/n, Badalona, 08916 Barcelona, Spain. Tel: +34 934978904; e-mail: [email protected] Curr Opin Crit Care 2014, 20:56–62 DOI:10.1097/MCC.0000000000000045 Volume 20 Number 1 February 2014
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Postoperative respiratory failure Canet and Gallart
KEY POINTS PRF, characterized by pulmonary gas exchange impairment appearing during the postoperative period, is the most devastating of all complications and a cause of high postoperative mortality. Factors associated with the patient’s health status and kind of surgery determine baseline risk. When these are combined with additive intraoperative and postoperative factors, the risk of lung damage rises sharply. There is evidence that several respiratory and nonrespiratory measures can reduce PRF risk. Beneficial strategies include strict intraoperative ventilatory and anesthetic management, avoiding fluids and transfusions whenever possible, choosing less aggressive surgical approaches, avoiding residual curarization, preventing surgical site and pulmonary infection, and providing adequate postoperative analgesia. Future studies on PRF should use arterial blood gas measurements to define the event, and consensus is needed on the most useful postoperative time frame to specify. Data should be gathered prospectively, and risk scores should be properly validated before they are considered transportable to new settings.
ventilatory support. Severity can range from transient hypoxemia in the early postoperative period to the most life-threatening form, late-stage acute respiratory disease syndrome (ARDS). According to the recent international consensus on ARDS, PRF may be classified as mild (PaO2/FIO2 300 mmHg and >200 mmHg), moderate (PaO2/ FIO2 200 mmHg and > 100 mmHg), or severe (PaO2/FIO2 100 mmHg) [8].
MECHANISMS RESPONSIBLE FOR POSTOPERATIVE RESPIRATORY FAILURE General anesthesia induces an immediate reduction of muscle tone, which in turn reduces thorax diameters, lung volumes, and airway dimensions. Airway closure and atelectasis then develop, mainly in the dependent parts of the lungs, leading to abnormal gas exchange and ventilation-perfusion mismatch and shunt. Functional imbalance worsens with manipulation of structures above or below the diaphragm during surgery [9]. The decrease in PaO2 that occurs in most patients under general anesthesia is compensated for by administering a high oxygen concentration. However, if the oxygen concentration is over 80% there is risk of adsorption atelectasis [10,11 ]. The hypoxemia that commonly develops after general anesthesia or even after only slight sedation [12] can be aggravated by factors such as hypoventilation due to the residual effects of anesthetics, lung edema, laryngospasm, and bronchospasm. As time passes atelectasis resolves, but at different rates in relation to the patient’s condition and the surgical procedure. Thus, even as gas exchange normalizes and hypoxemia is alleviated, atelectasis may remain for some time after surgery. In one study of patients after abdominal surgery, atelectasis affected the most extensive area of the lung 2 h after surgery and remained more or less the same 2 days later [13]. Atelectasis had decreased by the fourth postoperative day, when involvement extended to only about 20–25% of the area affected during anesthesia. This reduction was accompanied by increased lung volumes and improved gas exchange. If low lung volumes persist, however, atelectasis may not resolve. Eventually, the risk of other complications, such as pneumonia, increases as a result. Unplanned mechanical ventilation may become necessary or support may have to be prolonged. PRF is usually directly related to anesthesia and surgery when it appears within a few days of surgery. A recent study found that the median time until the appearance of postoperative ARDS in a general surgical population was only 2 days [14 ]. Yet, most &&
DEFINITION OF POSTOPERATIVE RESPIRATORY FAILURE By itself, respiratory failure is well defined as inadequate exchange of oxygen and carbon dioxide. It is diagnosed when exchange does not meet metabolic needs, leading to hypoxemia with or without hypercapnia. Arterial blood gas measurement provides the grounds for diagnosis: when partial pressure of oxygen (PaO2) falls below 60 mmHg and/or partial pressure of carbon dioxide exceeds 50 mmHg breathing air at sea level [inspiratory oxygen fraction (FIO2), 0.21], gas exchange is clearly inadequate. Under physiological conditions, with no displacement of the hemoglobin dissociation curve due to acidosis or hypercarbia, a PaO2 of 60 mmHg corresponds to arterial oxygen saturation of 90%. In the clinical setting, the degree of gas exchange impairment is defined by calculating the ratio of PaO2 to FIO2. Thus, when this ratio is lower than 300 mmHg respiratory failure is diagnosed. PRF, then, can be considered as pulmonary gas exchange impairment that presents after a surgical procedure and as a result of the changes induced by anesthesia and surgery. Respiratory failure secondary to cardiac dysfunction is thereby excluded from this definition. PRF is usually managed with some kind of nonroutine respiratory support: oxygen therapy, physiotherapy, or invasive or noninvasive
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authors choose a time frame of 3–7 days to record PRF as an outcome [5,14 ,15,16,17 ] while some have defined PRF as appearing up to 30 days after surgery [18,19 ]. The postoperative time frame, especially in high-risk cases, is so dynamic and is affected by so many preoperative, intraoperative, and postoperative factors acting synergistically that it is difficult to define a single postoperative moment when we can consider PRF to be a direct complication of anesthesia and surgery or a late consequence of additional events. Yet, the lack of such precision is an obstacle to comparing the findings of research, and hence a hindrance in the effort to promote evidence-based management of PRF. &
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POSTOPERATIVE RESPIRATORY MUSCLE DYSFUNCTION Respiratory muscle function in the postoperative period is a key to whether a patient develops PRF or not [20 ]. The normal physiology of the respiratory system relies on balance between respiratory pump muscles – which create a negative pressure leading to an urge to ventilate – and the upper airway dilator muscles – which counterbalance the collapsing forces of the negative pressure and ensure upper airway patency. During emergence from anesthesia and over the postoperative period, respiratory muscle function is affected to different degrees. Early after surgery, residual effects of sedatives and opiates reduce central stimulation of both the upper airway (hypoglossal nerve) and pump muscles (phrenic nerve) [21]. At the same time, residual curarization is often present, affecting the upper airway dilator muscles to a greater extent than the diaphragm [22]. Taken together, these events increase upper airway collapsibility and predispose patients to PRF, particularly in the presence of comorbid conditions such as obesity, obstructive sleep apnea, chronic obstructive pulmonary disease, or smoking addiction. Later, the effects of surgery or trauma can further favor the development of PRF, mainly due to functional disruption of the respiratory muscles, postoperative pain, or direct diaphragmatic dysfunction due to phrenic nerve injury [23]. &&
POSTOPERATIVE ACUTE RESPIRATORY DISEASE SYNDROME Under certain circumstances, some postoperative patients can develop ARDS, which is the worst presentation of PRF, occurring when hypoxemia is the result of lung damage. After the recent Berlin consensus [8], ARDS is now diagnosed if respiratory failure appears within a week of a recognized insult (such as surgery and anesthesia), specific radiological 58
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changes are evident, and a cardiac origin can be ruled out. A variety of mechanical, chemical, and biological insults are necessary for provoking an exudative phase, which involves diffuse alveolocapillary membrane damage occurring heterogeneously across the lung regions [24]. Three levels of respiratory impairment – mild, moderate, and severe – have been defined as described above. The condition formerly termed acute lung injury (ALI) [25], before the Berlin consensus statement [8], represented what we would today refer to as the mild and moderate levels of impaired gas exchange in ARDS. ARDS-associated mortality is very high, ranging from 17% in the mild form to more than 58% in the severe form [26]. In a recent multicenter study, a third of all patients who developed ALI (today, mild or moderate ARDS) had undergone surgery, usually a major procedure such as cardiothoracic, aortic, abdominal, or spine surgery [27]. The mean incidence of ALI after these high-risk interventions was 7.8% in that study, with the highest rate (10.2%) in cardiac surgery. However, in another recent article the incidence of ARDS was 0.2% in a general surgical population from which high-risk surgery had been excluded [14 ]. The pathogenesis of postoperative ARDS is multifactorial. According to the multiple-hit theory of this condition’s development [24,28], the first hit comes from factors related to a patient’s initial status and the scheduled procedure, including the anesthetic technique. Together they describe the epidemiologic background features that can be foreseen and which include a patient’s initial pulmonary or extrapulmonary condition. Although such factors would not by themselves lead directly to alveolar damage, the addition of second hits will further increase the likelihood of ARDS. Possible second hits in the surgical setting include aspects of intraoperative ventilatory management, aspiration, fluid therapy, transfusion, and inadequate control of infection. These second-hit events have all been shown to be direct causes of the lung damage that increases the risk of ARDS. At this point, it is worth remembering the role of persistent postoperative atelectasis, which can trigger an inflammatory reaction, and thus create a locus for postoperative lung inflammation and later pulmonary infection [29], thus also favoring ARDS. &
POSTOPERATIVE RESPIRATORY FAILURE PREDICTION In only the last 3 years, six studies have addressed the issue of the prediction of respiratory failure specifically in the postoperative period [14 ,15,16,17 , 18,19 ] (Table 1). The overall incidence of PRF in &
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Postoperative respiratory failure Canet and Gallart Table 1. Comparison of recent studies on postoperative respiratory failure &
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&
First author
Gupta [18]
Kor [15]
Ramachandran [16] Hua [19 ]
Blum [14 ]
Brueckmann [17 ]
Outcome
Mechanical ventilation >48 h
Surgical lung injury (ARDS)
Unplanned intubation
Unplanned intubation
ARDS
Unplanned intubation
Outcome definition
NSQIP definitiona
ALI/ARDS [25]
NSQIP definition
NSQIP definition
Mechanical ventilation P/F ratio < 300, bilateral infiltrates on X-ray
Any intubation after extubation
Time gap for 30 outcome (days)
5
3
30
7
3
Patients (n)
468 795
4336
222 094
231 548
50 367
33 769
Database
Retrospective Retrospective (ACS–NSQIP) (previous investigation)
Retrospective (ACS–NSQIP)
Retrospective Retrospective (ACS–NSQIP) (anesthetic records)
Retrospective (anesthesia and billing)
Inclusion criteria
Adult in-patient
Adult in-patient surgery > 3 h
Adult in-patient
Adult in-patient
Adult in-patient
Adult in-patient
Main exclusion criteria
None
Previous mechanical Emergency and ventilation, trauma, cardiac sepsis, shock, acute CHF, and emergency
Trauma and transplant
Cardiac, thoracic, Patients not transplant, extubated at trauma, and the end of vascular surgery
Score
Yes
Yes
Yes
Yes
No
Yes
Validation
Internal
None
Internal
Internal
None
Internal
Incidence of outcome (%)
3.1
2.6
0.8–0.9
1.9–2.2
0.2
0.4
ACS–NSQIP, American College of Surgeons–National Surgical Quality Improvement Program; ALI, acute lung injury; ARDS, acute respiratory distress syndrome; CHF, congestive heart failure. a NSQIP definition of PRF: 1/unplanned intubation during surgery or postoperatively; 2/reintubation once extubated; or 3/mechanical ventilation for > 48 h postoperatively.
those studies ranged from 0.2 to 3.1%. The results must be interpreted cautiously, taking into account how the outcome was defined (including time frames ranging from 3 to 30 days), how patients were selected, and what statistical analyses were used. All six studies were retrospective, using administrative and/or routinely recorded clinical information from multicenter or single-center databases, although one study [15] also included information from a secondary analysis of an earlier prospective study. Three of them [16,18,19 ] were based on data from the American College of Surgeons–National Surgical Quality Improvement Program. This retrospective approach can be very useful for the study of rare events such as PRF, but it has limitations [30–32,33 ] such as low positive predictive values and moderate reliability, errors in the collection data and a high percentage of missing values, lack of information on some variables of clinical interest, and little intraoperative information. These problems are compounded by a lack of external validation in the literature. The shortcomings of administrative databases for grading performance without &
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standardizing definitions, data collection, and management was demonstrated by the recent finding of only poor or moderate concordance between PRF diagnosis of patients included in an administrative database (of the Agency for Healthcare Research and Quality Patient Safety Indicators, a national clinical registry and the National Surgical Quality Improvement Program) and an institutional clinical registry (Cardiovascular Information Registry) [32]. PRF was defined in four of the six studies by prolonged mechanical ventilation or unplanned intubation [16,17 ,18,19 ]; two studies took into consideration arterial blood gases [14 ,15]. The actual incidence of PRF in these recent studies is probably underestimated, however, because currently up to 74% of patients with PRF can be managed with noninvasive ventilation [34], which several studies have shown to be very effective for treating even severe levels of hypoxemia [35–38]. Five studies proposed predictive scores based on weighted preoperative and intraoperative predictors, but information about comorbidity and demographic variables was heterogeneous and even scant
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in some models [15,19 ]. PRF predictors that have been proposed are as follows: (1) Preoperative (a) Age (b) Male sex (c) American Society of Anesthesiologists (ASA) class at least 3 (d) Functional dependency (e) Sepsis or septic shock (f) Congestive heart failure (g) Chronic obstructive pulmonary disease (h) Diabetes mellitus (i) Gastroesophageal reflux disease (j) Alcohol abuse (k) Current smoker (l) Dyspnea (m) Hypertension (n) Liver disease (o) Cancer (p) Prolonged hospitalization (q) Weight loss (r) Renal failure (s) Number of anesthetics during the admission (t) Surgery (i) Upper abdominal (ii) Cardiac (iii) Vascular (iv) Thoracic (v) Neurosurgery (vi) Neck (vii) Urology (viii) Emergency (ix) Transplant (x) General (xi) Burn (xii) High-risk surgery (2) Intraoperative (a) Pulmonary drive pressure (b) Inspired oxygen fraction (c) Volume of crystalloid administration (d) Erythrocyte transfusion (e) Duration of surgery ASA class was included in four of the studies’ models [14 ,17 ,18,19 ], raising the problematic issue that this summary of the patient’s health status is so potent that its inclusion in a model causes specific comorbidities to drop out of the score even though some of those clinical conditions could be managed effectively and are, therefore, of interest [31,39]. The low interobserver reliability of the ASA class [40] also argues against its inclusion in models exploring clinically identifiable risk factors that can be targeted in management strategies. &
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The PRF predictors listed above – which have also been identified in the studies of PPC risk with wider scope [7,39] – can be grouped in time frames (preoperative and intraoperative), consistent with the multiple-hit theory [14 ,41] according to which new predictive models should stratify risk at two stages. The first stage would consider threats associated with the patient’s condition and the foreseen procedure (preoperative information). The second would consider intraoperative events, which would modulate first-hit risk and indicate the patient’s definitive risk. &
PREVENTION OF POSTOPERATIVE RESPIRATORY FAILURE Intraoperative and postoperative measures to prevent the development of PRF, some of which are still under investigation, are listed below: (1) Ventilatory (a) Accurate FiO2 (b) Avoid atelectotrauma (i) Positive end-expiratory pressure (PEEP) (ii) Recruitment maneuvers After intubation After disconnections During relative hypoxemia Before extubation (c) Avoid volutrauma (i) Limit airway plateau pressure to 20 cmH2O (ii) Limit tidal volume to 10 ml/kg in nonrisk patients (iii) Limit tidal volume to 6 ml/kg in highrisk patients (2) Nonventilatory (a) Anesthetic technique (i) Choose neuroaxial or regional techniques (ii) Inhaled anesthetics to decrease pulmonary inflammatory response to mechanical ventilation (iii) Accurate administration and monitoring of neuromuscular blockade (b) Emergence (i) Complete reversal of the neuromuscular blockade (ii) No atelectasis (iii) Adequate postoperative analgesia (iv) Avoid overuse of opiates and excessive sedation (c) Restrictive use of fluids (d) Avoid transfusion (i) Alleviate preoperative anemia (ii) Apply blood saving strategies Volume 20 Number 1 February 2014
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Postoperative respiratory failure Canet and Gallart
(e) Decrease risk of pulmonary infection (i) Antibiotic prophylaxis (ii) Tooth brushing and oral decontamination (iii) Orotracheal tube management Check cuff pressure Appropriate cuff shape Appropriate material (iv) Avoid nasogastric tubes (f) Surgical technique (i) Choose a thoracoscopic or laparoscopic approach (ii) Reduce surgical duration (iii) Defer surgery whenever possible Thinking in terms of the multiple-hit theory, we suggest that preventive measures that seek to reduce the impact of the second hits produced by anesthetic and surgical management might be the following: (1) Intraoperative lung-protective management of ventilation: this concept has been the subject of two recently published studies [42 ,43 ], and another ongoing study also deals with this approach [44]. Ventilatory management aims to avoid ventilator-induced lung injury, so it is used in all patients, not just those at high risk [9,45,46]. When management is approached in a way that protects the lung, the goal is avoidance of damage from atelectotrauma from the repeated opening and closing of alveoli when alveolar expansion measures, including PEEP, are applied. This approach also relies on the avoidance of volutrauma or overdistension, achieved by holding airway pressure and tidal volume within limits. (2) Accurate oxygen administration: oxygen is adjusted throughout the anesthetic procedure as the administration of a high oxygen concentration (to prevent surgical site infection [47 ]) is balanced against the risks of promoting atelectasis [11 ]. However, a recent meta-analysis concluded that applying a high intraoperative FIO2 (over 80%) for this purpose does not promote atelectasis [47 ]. During emergence from anesthesia, applying recruitment maneuvers and 40% oxygen concentration has been shown to improve oxygenation in comparison to administering 100% oxygen due to the development of readsorption atelectasis [48]. (3) Intraoperative nonventilatory measures: this large set of measures includes infection prevention [49 ,50,51], fluid therapy management [52], avoiding transfusion, and using appropriately chosen and accurately dosed anesthetics [52] and neuromuscular blocking agents [20 ]. &&
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(4) Surgical approach: measures for reducing the aggressiveness of procedures have been shown to reduce the risk of PRF [52]. (5) Postoperative strategies: a multimodal approach includes effective analgesia [52,53], physiotherapy [54 ], and early treatment of postoperative hypoxemia [38,55] as the pillars of PRF prevention. &
CONCLUSION PRF, the postoperative complication responsible for the highest number of deaths, is the result of interacting factors related to patient status, kind of surgery, and intraoperative events, which can cause lung damage. The chest wall and lung changes that anesthesia induces promote atelectasis in the dependent parts of the lung, providing the context in which some patients will develop life-threatening PRF. Although lung-protective strategies are always in place, patients at greatest risk of PRF must be identified in the interest of optimizing management if this complication develops. Further studies are therefore needed to improve PRF prediction. New controlled trials assessing intraoperative and postoperative measures to reduce the incidence of PRF are under way, but we already have some evidence for several respiratory and nonrespiratory measures that can be applied perioperatively to reduce PRF risk. Nonetheless, it is imperative to arrive at consensus on the most relevant postoperative time frame for this event and to use arterial blood gas measurements to define PRF in research so that findings can be usefully compared. Until research designs converge, it will remain difficult to apply current knowledge in the actual clinical settings. Acknowledgements Funding: Grant 041610–2003 from the Catalan public television network (TV3) Marathon fund (’Fundacio´ La Marato´ de TV3’), Barcelona, Spain. Mary Ellen Kerans gave advice on English expression in a version of this article. Conflicts of interest There are no conflicts of interest.
REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. Mitchell CK, Smoger SH, Pfeifer MP, et al. Multivariate analysis of factors associated with postoperative pulmonary complications following general elective surgery. Arch Surg 1998; 133:194–198. 2. McAlister FA, Bertsch K, Man J, et al. Incidence of and risk factors for pulmonary complications after nonthoracic surgery. Am J Respir Crit Care Med 2005; 171:514–517.
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Preoperative pulmonary risk stratification for noncardiothoracic surgery: systematic review for the American College of Physicians. Ann Intern Med 2006; 144:581–595. 8. Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA 2012; 307:2526–2533. 9. Tusman G, Bohm SH, Warner DO, et al. Atelectasis and perioperative pulmonary complications in high-risk patients. Curr Opin Anaesthesiol 2012; 25:1–10. 10. Duggan M, Kavanagh BP. Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology 2005; 102:838–854. 11. Hedenstierna G. Oxygen and anesthesia: what lung do we deliver to the && postoperative ward? Acta Anaesthesiol Scand 2012; 56:675–685. An excellent review on the effects and use of perioperative oxygen. 12. Canet J, Ricos M, Vidal F. Early postoperative arterial oxygen desaturation. Determining factors and response to oxygen therapy. Anesth Analg 1989; 69:207–212. 13. Lindberg P, Gunnarsson L, Tokics L, et al. 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A score for predicting unplanned intubation within 3 days – interesting as a starting point for future studies on this event. 18. Gupta H, Gupta PK, Fang X, et al. Development and validation of a risk calculator predicting postoperative respiratory failure. Chest 2011; 140:1207–1215. 19. Hua M, Brady JE, Li G. A scoring system to predict unplanned intubation in & patients having undergone major surgical procedures. Anesth Analg 2012; 115:88–94. A recent risk score with variables similar to those of previous studies. The information on comorbidities and type of surgery is limited. 20. Sasaki N, Meyer MJ, Eikermann M. Postoperative respiratory muscle dysfunc&& tion: pathophysiology and preventive strategies. Anesthesiology 2013; 118:961–978. An excellent and seminal update on the effects on anesthesia and surgery on respiratory muscles. 21. Nishino T, Shirahata M, Yonezawa T, et al. 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Volume 20 Number 1 February 2014
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