A. Miskovic,
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10 February 2017
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Abstract
Postoperative pulmonary complications (PPCs) are common, costly, and increase patient mortality. Changes to the respiratory system occur immediately on induction of general anaesthesia: respiratory drive and muscle function are altered, lung volumes reduced, and atelectasis develops in > 75% of patients receiving a neuromuscular blocking drug. The respiratory system may take 6 weeks to return to its preoperative state after general anaesthesia for major surgery. Risk factors for PPC development are numerous, and clinicians should be aware of non-modifiable and modifiable factors in order to recognize those at risk and optimize their care. Many validated risk prediction models are described. These have been useful for improving our understanding of PPC development, but there remains inadequate consensus for them to be useful clinically. Preventative measures include preoperative optimization of co-morbidities, smoking cessation, and correction of anaemia, in addition to intraoperative protective ventilation strategies and appropriate management of neuromuscular blocking drugs. Protective ventilation includes low tidal volumes, which must be calculated according to the patient’s ideal body weight. Further evidence for the most beneficial level of PEEP is required, and on-going randomized trials will hopefully provide more information. When PEEP is used, it may be useful to precede this with a recruitment manoeuvre if atelectasis is suspected. For high-risk patients, surgical time should be minimized. After surgery, nasogastric tubes should be avoided and analgesia optimized. A postoperative mobilization, chest physiotherapy, and oral hygiene bundle reduces PPCs.
The term postoperative pulmonary complication (PPC) encompasses almost any complication affecting the respiratory system after anaesthesia and surgery. These complications are defined heterogeneously, occur commonly, have major adverse effects on patients, and are difficult to predict. This paper reviews the current literature regarding PPCs to enable readers to understand better why they occur, identify at-risk patients, and to suggest strategies to reduce their occurrence. This is a narrative rather than systematic review, and because of the amount of literature on the topic of PPCs it has not been possible to include all relevant papers, so we have focused on those which are, in our opinion, most relevant to clinical practice.
Definition and impact of PPCs
Postoperative pulmonary complications can be considered as a composite outcome measure. In 2015, a European joint taskforce published guidelines for perioperative clinical outcome (EPCO) definitions.1 The EPCO-recommended definitions for PPCs are shown in Table 1 alongside other published definitions to demonstrate the variability in the literature. The taskforce considered respiratory infection, respiratory failure, pleural effusion, atelectasis, pneumothorax, bronchospasm, and aspiration pneumonitis to be the composite measures and defined pneumonia, acute respiratory distress syndrome (ARDS), and pulmonary embolus as individual adverse outcomes. Studies evaluating PPCs also use different combinations of these individual outcomes. A systematic review for the American College of Physicians showed almost 60% of 16 studies used a combination of pneumonia and respiratory failure to define PPCs.27
Table 1
European Perioperative Clinical Outcome definitions1 for postoperative pulmonary complications and other defined outcome measures, shown to highlight the variation of definitions in the literature; in particular, respiratory failure and pneumonia. International statistical classification of diseases and related health problems, ninth revision (ICD-9) codes have also been used to define PPCs.2,3 ARDS, acute respiratory distress syndrome; CXR, chest radiograph; EPCO, European Perioperative Clinical Outcome; FIO 2, fraction of inspired oxygen; NIV, non-invasive ventilation; PaO2, partial pressure of oxygen in arterial blood; PPC, postoperative pulmonary complication
Respiratory infection | Antibiotics for suspected infection with one or more of the following: new or changed sputum, new or changed lung opacities, fever, white blood cell count >12 × 109 litre−1 | Two or more of the following for >48 h: new cough/sputum production, physical findings compatible with pneumonia, fever >38 °C, and new infiltrate on CXR7 |
Respiratory failure | Postoperative PaO2 <8 kPa (60 mm Hg) on room air, a PaO2 :FIO2 ratio <40 kPa (300 mm Hg), or arterial oxyhaemoglobin saturation measured with pulse oximetry <90% and requiring oxygen therapy | Ventilator dependence for >1 postoperative day or re-intubation8,9 |
Need for postoperative mechanical ventilation >48 h10–13 | ||
Unplanned re-intubation because of respiratory distress, hypoxia, hypercarbia, or respiratory acidosis within 30 days of surgery10,11,13–15 | ||
Re-intubation within 3 days requiring mechanical ventilation16 | ||
Postoperative acute lung injury17 | ||
ARDS17–19 | ||
Requiring mechanical ventilation within 7 days of surgery20,21 | ||
Requiring NIV22 | ||
Pleural effusion | CXR with blunting of costophrenic angle, loss of sharp silhouette of the ipsilateral hemidiaphragm in upright position, displacement of adjacent anatomical structures, or (in supine position) hazy opacity in one hemithorax with preserved vascular shadows | Pleural effusion requiring thoracocentesis8,9,20 |
Atelectasis | Lung opacification with mediastinal shift, hilum or hemidiaphragm shift towards the affected area, with compensatory hyperinflation in adjacent non-atelectatic lung | Requiring bronchoscopic intervention20 |
Major atelectasis (one or more pulmonary segments)23 | ||
Pneumothorax | Air in the pleural space with no vascular bed surrounding the visceral pleura | Pneumothorax requiring thoracocentesis20,22 |
Bronchospasm | Newly detected expiratory wheeze treated with bronchodilators | Clinical diagnosis resulting in change in therapy89 |
Refractory wheeze requiring parenteral drugs in addition to preoperative regimen24 | ||
Aspiration pneumonitis | Acute lung injury after inhalation of regurgitated gastric contents | |
Pneumonia | CXR with at least one of the following: infiltrate, consolidation, cavitation;plus at least one of the following: fever >38 °C with no other cause, white cell count <4 or > 12 × 109 litre−1, >70 yr of age with altered mental status with no other cause;plus at least two of the following: new purulent/changed sputum, increased secretions/suctioning, new/worse cough/dyspnoea/tachypnoea, rales/bronchial breath sounds, worsening gas exchange | Radiographic change and antibiotics89 |
Antibiotics with new/changed sputum or radiographic change or fever or increased white cell count >12 000 μl−1 4 | ||
Two or more of the following for ≥2 consecutive days: new cough/sputum production, examination compatible with pneumonia, temperature >38 °C, and radiographic change7,23 | ||
New or progressive infiltrate on CXR or crackles or dullness on percussion and any of the following: new purulent/changed sputum, positive blood cultures, isolation of pathogen from sputum20,25 | ||
Positive sputum culture or infiltrate on CXR, and diagnosis of pneumonia or pneumonitis18 | ||
New infiltrate on CXR plus fever, leucocytosis, and positive sputum Gram stain/culture24 | ||
ARDS | Ventilated, bilateral infiltrates on CXR, PaO2:FIO2≤300, minimal evidence of left atrial fluid overload within 7 days of surgery19 | |
Tracheobronchitis | Purulent sputum with normal chest radiograph, no i.v. antibiotics8,9 | |
Pulmonary oedema | Pulmonary congestion/hypostasis, acute oedema of lung, congestive heart failure, fluid overload2,3 | |
Exacerbation of pre-existing lung disease23 | Not further defined | |
Pulmonary embolism23 | Not further defined | |
Death24,26 |
Respiratory infection | Antibiotics for suspected infection with one or more of the following: new or changed sputum, new or changed lung opacities, fever, white blood cell count >12 × 109 litre−1 | Two or more of the following for >48 h: new cough/sputum production, physical findings compatible with pneumonia, fever >38 °C, and new infiltrate on CXR7 |
Respiratory failure | Postoperative PaO2 <8 kPa (60 mm Hg) on room air, a PaO2 :FIO2 ratio <40 kPa (300 mm Hg), or arterial oxyhaemoglobin saturation measured with pulse oximetry <90% and requiring oxygen therapy | Ventilator dependence for >1 postoperative day or re-intubation8,9 |
Need for postoperative mechanical ventilation >48 h10–13 | ||
Unplanned re-intubation because of respiratory distress, hypoxia, hypercarbia, or respiratory acidosis within 30 days of surgery10,11,13–15 | ||
Re-intubation within 3 days requiring mechanical ventilation16 | ||
Postoperative acute lung injury17 | ||
ARDS17–19 | ||
Requiring mechanical ventilation within 7 days of surgery20,21 | ||
Requiring NIV22 | ||
Pleural effusion | CXR with blunting of costophrenic angle, loss of sharp silhouette of the ipsilateral hemidiaphragm in upright position, displacement of adjacent anatomical structures, or (in supine position) hazy opacity in one hemithorax with preserved vascular shadows | Pleural effusion requiring thoracocentesis8,9,20 |
Atelectasis | Lung opacification with mediastinal shift, hilum or hemidiaphragm shift towards the affected area, with compensatory hyperinflation in adjacent non-atelectatic lung | Requiring bronchoscopic intervention20 |
Major atelectasis (one or more pulmonary segments)23 | ||
Pneumothorax | Air in the pleural space with no vascular bed surrounding the visceral pleura | Pneumothorax requiring thoracocentesis20,22 |
Bronchospasm | Newly detected expiratory wheeze treated with bronchodilators | Clinical diagnosis resulting in change in therapy89 |
Refractory wheeze requiring parenteral drugs in addition to preoperative regimen24 | ||
Aspiration pneumonitis | Acute lung injury after inhalation of regurgitated gastric contents | |
Pneumonia | CXR with at least one of the following: infiltrate, consolidation, cavitation;plus at least one of the following: fever >38 °C with no other cause, white cell count <4 or > 12 × 109 litre−1, >70 yr of age with altered mental status with no other cause;plus at least two of the following: new purulent/changed sputum, increased secretions/suctioning, new/worse cough/dyspnoea/tachypnoea, rales/bronchial breath sounds, worsening gas exchange | Radiographic change and antibiotics89 |
Antibiotics with new/changed sputum or radiographic change or fever or increased white cell count >12 000 μl−1 4 | ||
Two or more of the following for ≥2 consecutive days: new cough/sputum production, examination compatible with pneumonia, temperature >38 °C, and radiographic change7,23 | ||
New or progressive infiltrate on CXR or crackles or dullness on percussion and any of the following: new purulent/changed sputum, positive blood cultures, isolation of pathogen from sputum20,25 | ||
Positive sputum culture or infiltrate on CXR, and diagnosis of pneumonia or pneumonitis18 | ||
New infiltrate on CXR plus fever, leucocytosis, and positive sputum Gram stain/culture24 | ||
ARDS | Ventilated, bilateral infiltrates on CXR, PaO2:FIO2≤300, minimal evidence of left atrial fluid overload within 7 days of surgery19 | |
Tracheobronchitis | Purulent sputum with normal chest radiograph, no i.v. antibiotics8,9 | |
Pulmonary oedema | Pulmonary congestion/hypostasis, acute oedema of lung, congestive heart failure, fluid overload2,3 | |
Exacerbation of pre-existing lung disease23 | Not further defined | |
Pulmonary embolism23 | Not further defined | |
Death24,26 |
Table 1
European Perioperative Clinical Outcome definitions1 for postoperative pulmonary complications and other defined outcome measures, shown to highlight the variation of definitions in the literature; in particular, respiratory failure and pneumonia. International statistical classification of diseases and related health problems, ninth revision (ICD-9) codes have also been used to define PPCs.2,3 ARDS, acute respiratory distress syndrome; CXR, chest radiograph; EPCO, European Perioperative Clinical Outcome; FIO2, fraction of inspired oxygen; NIV, non-invasive ventilation; PaO2, partial pressure of oxygen in arterial blood; PPC, postoperative pulmonary complication
Respiratory infection | Antibiotics for suspected infection with one or more of the following: new or changed sputum, new or changed lung opacities, fever, white blood cell count >12 × 109 litre−1 | Two or more of the following for >48 h: new cough/sputum production, physical findings compatible with pneumonia, fever >38 °C, and new infiltrate on CXR7 |
Respiratory failure | Postoperative PaO2 <8 kPa (60 mm Hg) on room air, a PaO2 :FIO2 ratio <40 kPa (300 mm Hg), or arterial oxyhaemoglobin saturation measured with pulse oximetry <90% and requiring oxygen therapy | Ventilator dependence for >1 postoperative day or re-intubation8,9 |
Need for postoperative mechanical ventilation >48 h10–13 | ||
Unplanned re-intubation because of respiratory distress, hypoxia, hypercarbia, or respiratory acidosis within 30 days of surgery10,11,13–15 | ||
Re-intubation within 3 days requiring mechanical ventilation16 | ||
Postoperative acute lung injury17 | ||
ARDS17–19 | ||
Requiring mechanical ventilation within 7 days of surgery20,21 | ||
Requiring NIV22 | ||
Pleural effusion | CXR with blunting of costophrenic angle, loss of sharp silhouette of the ipsilateral hemidiaphragm in upright position, displacement of adjacent anatomical structures, or (in supine position) hazy opacity in one hemithorax with preserved vascular shadows | Pleural effusion requiring thoracocentesis8,9,20 |
Atelectasis | Lung opacification with mediastinal shift, hilum or hemidiaphragm shift towards the affected area, with compensatory hyperinflation in adjacent non-atelectatic lung | Requiring bronchoscopic intervention20 |
Major atelectasis (one or more pulmonary segments)23 | ||
Pneumothorax | Air in the pleural space with no vascular bed surrounding the visceral pleura | Pneumothorax requiring thoracocentesis20,22 |
Bronchospasm | Newly detected expiratory wheeze treated with bronchodilators | Clinical diagnosis resulting in change in therapy89 |
Refractory wheeze requiring parenteral drugs in addition to preoperative regimen24 | ||
Aspiration pneumonitis | Acute lung injury after inhalation of regurgitated gastric contents | |
Pneumonia | CXR with at least one of the following: infiltrate, consolidation, cavitation;plus at least one of the following: fever >38 °C with no other cause, white cell count <4 or > 12 × 109 litre−1, >70 yr of age with altered mental status with no other cause;plus at least two of the following: new purulent/changed sputum, increased secretions/suctioning, new/worse cough/dyspnoea/tachypnoea, rales/bronchial breath sounds, worsening gas exchange | Radiographic change and antibiotics89 |
Antibiotics with new/changed sputum or radiographic change or fever or increased white cell count >12 000 μl−1 4 | ||
Two or more of the following for ≥2 consecutive days: new cough/sputum production, examination compatible with pneumonia, temperature >38 °C, and radiographic change7,23 | ||
New or progressive infiltrate on CXR or crackles or dullness on percussion and any of the following: new purulent/changed sputum, positive blood cultures, isolation of pathogen from sputum20,25 | ||
Positive sputum culture or infiltrate on CXR, and diagnosis of pneumonia or pneumonitis18 | ||
New infiltrate on CXR plus fever, leucocytosis, and positive sputum Gram stain/culture24 | ||
ARDS | Ventilated, bilateral infiltrates on CXR, PaO2:FIO2≤300, minimal evidence of left atrial fluid overload within 7 days of surgery19 | |
Tracheobronchitis | Purulent sputum with normal chest radiograph, no i.v. antibiotics8,9 | |
Pulmonary oedema | Pulmonary congestion/hypostasis, acute oedema of lung, congestive heart failure, fluid overload2,3 | |
Exacerbation of pre-existing lung disease23 | Not further defined | |
Pulmonary embolism23 | Not further defined | |
Death24,26 |
Respiratory infection | Antibiotics for suspected infection with one or more of the following: new or changed sputum, new or changed lung opacities, fever, white blood cell count >12 × 109 litre−1 | Two or more of the following for >48 h: new cough/sputum production, physical findings compatible with pneumonia, fever >38 °C, and new infiltrate on CXR7 |
Respiratory failure | Postoperative PaO2 <8 kPa (60 mm Hg) on room air, a PaO2 :FIO2 ratio <40 kPa (300 mm Hg), or arterial oxyhaemoglobin saturation measured with pulse oximetry <90% and requiring oxygen therapy | Ventilator dependence for >1 postoperative day or re-intubation8,9 |
Need for postoperative mechanical ventilation >48 h10–13 | ||
Unplanned re-intubation because of respiratory distress, hypoxia, hypercarbia, or respiratory acidosis within 30 days of surgery10,11,13–15 | ||
Re-intubation within 3 days requiring mechanical ventilation16 | ||
Postoperative acute lung injury17 | ||
ARDS17–19 | ||
Requiring mechanical ventilation within 7 days of surgery20,21 | ||
Requiring NIV22 | ||
Pleural effusion | CXR with blunting of costophrenic angle, loss of sharp silhouette of the ipsilateral hemidiaphragm in upright position, displacement of adjacent anatomical structures, or (in supine position) hazy opacity in one hemithorax with preserved vascular shadows | Pleural effusion requiring thoracocentesis8,9,20 |
Atelectasis | Lung opacification with mediastinal shift, hilum or hemidiaphragm shift towards the affected area, with compensatory hyperinflation in adjacent non-atelectatic lung | Requiring bronchoscopic intervention20 |
Major atelectasis (one or more pulmonary segments)23 | ||
Pneumothorax | Air in the pleural space with no vascular bed surrounding the visceral pleura | Pneumothorax requiring thoracocentesis20,22 |
Bronchospasm | Newly detected expiratory wheeze treated with bronchodilators | Clinical diagnosis resulting in change in therapy89 |
Refractory wheeze requiring parenteral drugs in addition to preoperative regimen24 | ||
Aspiration pneumonitis | Acute lung injury after inhalation of regurgitated gastric contents | |
Pneumonia | CXR with at least one of the following: infiltrate, consolidation, cavitation;plus at least one of the following: fever >38 °C with no other cause, white cell count <4 or > 12 × 109 litre−1, >70 yr of age with altered mental status with no other cause;plus at least two of the following: new purulent/changed sputum, increased secretions/suctioning, new/worse cough/dyspnoea/tachypnoea, rales/bronchial breath sounds, worsening gas exchange | Radiographic change and antibiotics89 |
Antibiotics with new/changed sputum or radiographic change or fever or increased white cell count >12 000 μl−1 4 | ||
Two or more of the following for ≥2 consecutive days: new cough/sputum production, examination compatible with pneumonia, temperature >38 °C, and radiographic change7,23 | ||
New or progressive infiltrate on CXR or crackles or dullness on percussion and any of the following: new purulent/changed sputum, positive blood cultures, isolation of pathogen from sputum20,25 | ||
Positive sputum culture or infiltrate on CXR, and diagnosis of pneumonia or pneumonitis18 | ||
New infiltrate on CXR plus fever, leucocytosis, and positive sputum Gram stain/culture24 | ||
ARDS | Ventilated, bilateral infiltrates on CXR, PaO2:FIO2≤300, minimal evidence of left atrial fluid overload within 7 days of surgery19 | |
Tracheobronchitis | Purulent sputum with normal chest radiograph, no i.v. antibiotics8,9 | |
Pulmonary oedema | Pulmonary congestion/hypostasis, acute oedema of lung, congestive heart failure, fluid overload2,3 | |
Exacerbation of pre-existing lung disease23 | Not further defined | |
Pulmonary embolism23 | Not further defined | |
Death24,26 |
Incidence
It has been estimated that worldwide >230 million major operations occur annually.28 The incidence of PPCs in major surgery ranges from <1 to 23%.45,78,12,17,20,22,23,29 Several studies have shown pulmonary complications to be more common than cardiac complications,8,30,31 and postoperative respiratory failure is the most common PPC.6,29,Table 2 shows major studies from the last 16 yr, focusing on the varying incidences and mortality, which differ depending on the PPC definitions.47,8,12,20,23,29Table 2 clearly illustrates the wide variation in incidence and mortality rate, mostly caused by a combination of differing definitions (Table 1) and different patient populations, in particular the surgical specialty (see ‘Surgery type’ section below).
Table 2
Incidence and mortality rates of major studies evaluating postoperative pulmonary complications since the year 2000. Prospective studies are followed by retrospective studies in reverse chronological order. Where more than three surgical specialties are included, the term ‘multi-specialty’ is used. Where risk prediction model papers include a training set and a validation set, data from the validation set have been used. AAA, open abdominal aortic aneurysm; ALI, acute lung injury; ARDS, acute respiratory distress syndrome; ARISCAT, Assess Respiratory Risk in Surgical Patients in Catalonia; CXR, chest radiograph; EPCO, European Perioperative Clinical Outcome definition (Table 1); EVAR, endovascular aneurysm repair; PE, pulmonary embolus; PERISCOPE, Prospective Evaluation of a RIsk Score for postoperative pulmonary COmPlications in Europe; PPC, postoperative pulmonary complication; RF, respiratory failure; SpO 2, peripheral oxygen saturation; UPI, unplanned intubation
Canet and colleagues29 | 2015 | Secondary analysis of ‘PERISCOPE’ | RF | 5384 | 4.2 | 10.3 (in hospital) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multi-centre cohort; evaluating PPCs | |||||||
Mazo and colleagues6 | 2014 | ‘PERISCOPE’ | As per EPCO | 5099 | 7.9 | 8.3 (in hospital) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multicentre cohort; external validation of ‘ARISCAT’ | |||||||
Canet and colleagues4 | 2010 | ‘ARISCAT’ | As per EPCO | 2464 | 5.0 | 19.5 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multicentre cohort | |||||||
24.4 (90 day) | |||||||
Scholes and colleagues32 | 2009 | Prospective multi-centre cohort | More than four of the following:
| 268 | 13.0 | Not stated | Upper abdominal |
McAlister and colleagues20 | 2005 | Prospective single-centre cohort | RF, pneumonia, atelectasis, pneumothorax, pleural effusion | 1055 | 2.7 | Not stated | Multi-specialty (non-thoracic) elective, including abdominal |
Yang and colleagues12 | 2015 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | Pneumonia, UPI, or RF | 165 196 | 5.8 | Not stated | Elective major abdominal (non-vascular) |
Jeong and colleagues5 | 2014 | Retrospective single-centre analysis of prospectively collected cohort regarding PPC risk | As per EPCO | 2059 | 6.8 | Not stated | Multi-specialty elective and emergency, including abdominal (open and laparoscopic), vascular, cardiac, and thoracic |
Blum and colleagues19 | 2013 | Retrospective single-centre cohort | ARDS | 50 367 | 0.2 | 27.0 (90 day) | Multi-specialty (non-cardiothoracic) elective and emergency, including abdominal |
Brueckmann and colleagues16 | 2013 | Retrospective single-centre cohort | UPI | 33 769 | 0.43 | 16.0 | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Gupta and colleagues13 | 2013 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | Pneumonia | 211 410 | 1.8 | 17.0 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Li and colleagues18 | 2013 | Retrospective single-centre cohort | Pneumonia, pulmonary oedema, atelectasis, ARDS, pleural effusion | 316 | 18.9 | Not specific to PPC | Elective and emergency infrarenal AAA |
Hua and colleagues14 | 2012 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | UPI | 231 548 | 1.9 | 28.0 (30 day) | Multi-specialty elective and emergency, including major abdominal, vascular (open and EVAR) cardiac, and thoracic |
Kor and colleagues17 | 2011 | Retrospective analysis of prospective single-centre cohort evaluating intraoperative ventilator settings and ALI | ALI/ARDS | 4366 | 2.6 | 14.2 | Multi-specialty elective, including abdominal (open and laparoscopic), vascular, cardiac, and thoracic |
Gupta and colleagues11 | 2011 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | RF, UPI | 211 410 | 2.6 | 25.6 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Ramachandran and colleagues15 | 2011 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | UPI | 222 094 | 0.9 | 9.7 (low-risk group), | Elective multi-specialty (non-cardiac) |
30.6 (high-risk group) | |||||||
Smith and colleagues23 | 2010 | Retrospective single-centre cohort | Pneumonia, acute bronchitis, atelectasis, exacerbation of pre-existing lung disease, RF, PE | 329 | 7.0 | 16.0 (30 day) | Elective and emergency laparotomy, including AAA |
Johnson and colleagues33 | 2007 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | RF, UPI | 180 359 | 3.0 | 26.5 (30 day) | Elective and emergency major vascular and general |
Arozullah and colleagues25 | 2001 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | Pneumonia | 160 805 | 1.5 | 21 (30 day) | Multi-specialty (non-cardiac), including abdominal, vascular, and thoracic |
Arozullah and colleagues34 | 2000 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | RF | 81 719 | 3.4 | 27 (30 day) | Multi-specialty (non-cardiac), including abdominal, vascular, and thoracic |
Canet and colleagues29 | 2015 | Secondary analysis of ‘PERISCOPE’ | RF | 5384 | 4.2 | 10.3 (in hospital) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multi-centre cohort; evaluating PPCs | |||||||
Mazo and colleagues6 | 2014 | ‘PERISCOPE’ | As per EPCO | 5099 | 7.9 | 8.3 (in hospital) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multicentre cohort; external validation of ‘ARISCAT’ | |||||||
Canet and colleagues4 | 2010 | ‘ARISCAT’ | As per EPCO | 2464 | 5.0 | 19.5 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multicentre cohort | |||||||
24.4 (90 day) | |||||||
Scholes and colleagues32 | 2009 | Prospective multi-centre cohort | More than four of the following:
| 268 | 13.0 | Not stated | Upper abdominal |
McAlister and colleagues20 | 2005 | Prospective single-centre cohort | RF, pneumonia, atelectasis, pneumothorax, pleural effusion | 1055 | 2.7 | Not stated | Multi-specialty (non-thoracic) elective, including abdominal |
Yang and colleagues12 | 2015 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | Pneumonia, UPI, or RF | 165 196 | 5.8 | Not stated | Elective major abdominal (non-vascular) |
Jeong and colleagues5 | 2014 | Retrospective single-centre analysis of prospectively collected cohort regarding PPC risk | As per EPCO | 2059 | 6.8 | Not stated | Multi-specialty elective and emergency, including abdominal (open and laparoscopic), vascular, cardiac, and thoracic |
Blum and colleagues19 | 2013 | Retrospective single-centre cohort | ARDS | 50 367 | 0.2 | 27.0 (90 day) | Multi-specialty (non-cardiothoracic) elective and emergency, including abdominal |
Brueckmann and colleagues16 | 2013 | Retrospective single-centre cohort | UPI | 33 769 | 0.43 | 16.0 | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Gupta and colleagues13 | 2013 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | Pneumonia | 211 410 | 1.8 | 17.0 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Li and colleagues18 | 2013 | Retrospective single-centre cohort | Pneumonia, pulmonary oedema, atelectasis, ARDS, pleural effusion | 316 | 18.9 | Not specific to PPC | Elective and emergency infrarenal AAA |
Hua and colleagues14 | 2012 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | UPI | 231 548 | 1.9 | 28.0 (30 day) | Multi-specialty elective and emergency, including major abdominal, vascular (open and EVAR) cardiac, and thoracic |
Kor and colleagues17 | 2011 | Retrospective analysis of prospective single-centre cohort evaluating intraoperative ventilator settings and ALI | ALI/ARDS | 4366 | 2.6 | 14.2 | Multi-specialty elective, including abdominal (open and laparoscopic), vascular, cardiac, and thoracic |
Gupta and colleagues11 | 2011 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | RF, UPI | 211 410 | 2.6 | 25.6 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Ramachandran and colleagues15 | 2011 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | UPI | 222 094 | 0.9 | 9.7 (low-risk group), | Elective multi-specialty (non-cardiac) |
30.6 (high-risk group) | |||||||
Smith and colleagues23 | 2010 | Retrospective single-centre cohort | Pneumonia, acute bronchitis, atelectasis, exacerbation of pre-existing lung disease, RF, PE | 329 | 7.0 | 16.0 (30 day) | Elective and emergency laparotomy, including AAA |
Johnson and colleagues33 | 2007 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | RF, UPI | 180 359 | 3.0 | 26.5 (30 day) | Elective and emergency major vascular and general |
Arozullah and colleagues25 | 2001 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | Pneumonia | 160 805 | 1.5 | 21 (30 day) | Multi-specialty (non-cardiac), including abdominal, vascular, and thoracic |
Arozullah and colleagues34 | 2000 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | RF | 81 719 | 3.4 | 27 (30 day) | Multi-specialty (non-cardiac), including abdominal, vascular, and thoracic |
Table 2
Incidence and mortality rates of major studies evaluating postoperative pulmonary complications since the year 2000. Prospective studies are followed by retrospective studies in reverse chronological order. Where more than three surgical specialties are included, the term ‘multi-specialty’ is used. Where risk prediction model papers include a training set and a validation set, data from the validation set have been used. AAA, open abdominal aortic aneurysm; ALI, acute lung injury; ARDS, acute respiratory distress syndrome; ARISCAT, Assess Respiratory Risk in Surgical Patients in Catalonia; CXR, chest radiograph; EPCO, European Perioperative Clinical Outcome definition (Table 1); EVAR, endovascular aneurysm repair; PE, pulmonary embolus; PERISCOPE, Prospective Evaluation of a RIsk Score for postoperative pulmonary COmPlications in Europe; PPC, postoperative pulmonary complication; RF, respiratory failure; SpO2, peripheral oxygen saturation; UPI, unplanned intubation
Canet and colleagues29 | 2015 | Secondary analysis of ‘PERISCOPE’ | RF | 5384 | 4.2 | 10.3 (in hospital) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multi-centre cohort; evaluating PPCs | |||||||
Mazo and colleagues6 | 2014 | ‘PERISCOPE’ | As per EPCO | 5099 | 7.9 | 8.3 (in hospital) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multicentre cohort; external validation of ‘ARISCAT’ | |||||||
Canet and colleagues4 | 2010 | ‘ARISCAT’ | As per EPCO | 2464 | 5.0 | 19.5 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multicentre cohort | |||||||
24.4 (90 day) | |||||||
Scholes and colleagues32 | 2009 | Prospective multi-centre cohort | More than four of the following:
| 268 | 13.0 | Not stated | Upper abdominal |
McAlister and colleagues20 | 2005 | Prospective single-centre cohort | RF, pneumonia, atelectasis, pneumothorax, pleural effusion | 1055 | 2.7 | Not stated | Multi-specialty (non-thoracic) elective, including abdominal |
Yang and colleagues12 | 2015 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | Pneumonia, UPI, or RF | 165 196 | 5.8 | Not stated | Elective major abdominal (non-vascular) |
Jeong and colleagues5 | 2014 | Retrospective single-centre analysis of prospectively collected cohort regarding PPC risk | As per EPCO | 2059 | 6.8 | Not stated | Multi-specialty elective and emergency, including abdominal (open and laparoscopic), vascular, cardiac, and thoracic |
Blum and colleagues19 | 2013 | Retrospective single-centre cohort | ARDS | 50 367 | 0.2 | 27.0 (90 day) | Multi-specialty (non-cardiothoracic) elective and emergency, including abdominal |
Brueckmann and colleagues16 | 2013 | Retrospective single-centre cohort | UPI | 33 769 | 0.43 | 16.0 | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Gupta and colleagues13 | 2013 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | Pneumonia | 211 410 | 1.8 | 17.0 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Li and colleagues18 | 2013 | Retrospective single-centre cohort | Pneumonia, pulmonary oedema, atelectasis, ARDS, pleural effusion | 316 | 18.9 | Not specific to PPC | Elective and emergency infrarenal AAA |
Hua and colleagues14 | 2012 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | UPI | 231 548 | 1.9 | 28.0 (30 day) | Multi-specialty elective and emergency, including major abdominal, vascular (open and EVAR) cardiac, and thoracic |
Kor and colleagues17 | 2011 | Retrospective analysis of prospective single-centre cohort evaluating intraoperative ventilator settings and ALI | ALI/ARDS | 4366 | 2.6 | 14.2 | Multi-specialty elective, including abdominal (open and laparoscopic), vascular, cardiac, and thoracic |
Gupta and colleagues11 | 2011 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | RF, UPI | 211 410 | 2.6 | 25.6 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Ramachandran and colleagues15 | 2011 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | UPI | 222 094 | 0.9 | 9.7 (low-risk group), | Elective multi-specialty (non-cardiac) |
30.6 (high-risk group) | |||||||
Smith and colleagues23 | 2010 | Retrospective single-centre cohort | Pneumonia, acute bronchitis, atelectasis, exacerbation of pre-existing lung disease, RF, PE | 329 | 7.0 | 16.0 (30 day) | Elective and emergency laparotomy, including AAA |
Johnson and colleagues33 | 2007 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | RF, UPI | 180 359 | 3.0 | 26.5 (30 day) | Elective and emergency major vascular and general |
Arozullah and colleagues25 | 2001 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | Pneumonia | 160 805 | 1.5 | 21 (30 day) | Multi-specialty (non-cardiac), including abdominal, vascular, and thoracic |
Arozullah and colleagues34 | 2000 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | RF | 81 719 | 3.4 | 27 (30 day) | Multi-specialty (non-cardiac), including abdominal, vascular, and thoracic |
Canet and colleagues29 | 2015 | Secondary analysis of ‘PERISCOPE’ | RF | 5384 | 4.2 | 10.3 (in hospital) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multi-centre cohort; evaluating PPCs | |||||||
Mazo and colleagues6 | 2014 | ‘PERISCOPE’ | As per EPCO | 5099 | 7.9 | 8.3 (in hospital) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multicentre cohort; external validation of ‘ARISCAT’ | |||||||
Canet and colleagues4 | 2010 | ‘ARISCAT’ | As per EPCO | 2464 | 5.0 | 19.5 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Prospective multicentre cohort | |||||||
24.4 (90 day) | |||||||
Scholes and colleagues32 | 2009 | Prospective multi-centre cohort | More than four of the following:
| 268 | 13.0 | Not stated | Upper abdominal |
McAlister and colleagues20 | 2005 | Prospective single-centre cohort | RF, pneumonia, atelectasis, pneumothorax, pleural effusion | 1055 | 2.7 | Not stated | Multi-specialty (non-thoracic) elective, including abdominal |
Yang and colleagues12 | 2015 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | Pneumonia, UPI, or RF | 165 196 | 5.8 | Not stated | Elective major abdominal (non-vascular) |
Jeong and colleagues5 | 2014 | Retrospective single-centre analysis of prospectively collected cohort regarding PPC risk | As per EPCO | 2059 | 6.8 | Not stated | Multi-specialty elective and emergency, including abdominal (open and laparoscopic), vascular, cardiac, and thoracic |
Blum and colleagues19 | 2013 | Retrospective single-centre cohort | ARDS | 50 367 | 0.2 | 27.0 (90 day) | Multi-specialty (non-cardiothoracic) elective and emergency, including abdominal |
Brueckmann and colleagues16 | 2013 | Retrospective single-centre cohort | UPI | 33 769 | 0.43 | 16.0 | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Gupta and colleagues13 | 2013 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | Pneumonia | 211 410 | 1.8 | 17.0 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Li and colleagues18 | 2013 | Retrospective single-centre cohort | Pneumonia, pulmonary oedema, atelectasis, ARDS, pleural effusion | 316 | 18.9 | Not specific to PPC | Elective and emergency infrarenal AAA |
Hua and colleagues14 | 2012 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | UPI | 231 548 | 1.9 | 28.0 (30 day) | Multi-specialty elective and emergency, including major abdominal, vascular (open and EVAR) cardiac, and thoracic |
Kor and colleagues17 | 2011 | Retrospective analysis of prospective single-centre cohort evaluating intraoperative ventilator settings and ALI | ALI/ARDS | 4366 | 2.6 | 14.2 | Multi-specialty elective, including abdominal (open and laparoscopic), vascular, cardiac, and thoracic |
Gupta and colleagues11 | 2011 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | RF, UPI | 211 410 | 2.6 | 25.6 (30 day) | Multi-specialty elective and emergency, including abdominal, vascular, cardiac, and thoracic |
Ramachandran and colleagues15 | 2011 | Retrospective analysis of multi-centre prospective cohort (not specific to PPCs) | UPI | 222 094 | 0.9 | 9.7 (low-risk group), | Elective multi-specialty (non-cardiac) |
30.6 (high-risk group) | |||||||
Smith and colleagues23 | 2010 | Retrospective single-centre cohort | Pneumonia, acute bronchitis, atelectasis, exacerbation of pre-existing lung disease, RF, PE | 329 | 7.0 | 16.0 (30 day) | Elective and emergency laparotomy, including AAA |
Johnson and colleagues33 | 2007 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | RF, UPI | 180 359 | 3.0 | 26.5 (30 day) | Elective and emergency major vascular and general |
Arozullah and colleagues25 | 2001 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | Pneumonia | 160 805 | 1.5 | 21 (30 day) | Multi-specialty (non-cardiac), including abdominal, vascular, and thoracic |
Arozullah and colleagues34 | 2000 | Retrospective analysis of multi-centre prospective cohort (non-specific to PPCs) | RF | 81 719 | 3.4 | 27 (30 day) | Multi-specialty (non-cardiac), including abdominal, vascular, and thoracic |
Impact
Mortality is increased in both the short and long term in patients who develop a PPC. One in five patients (14–30%) who have a PPC will die within 30 days of major surgery compared with 0.2–3% without a PPC.46,15,17,23,20,35 The 90 day mortality has been shown to be significantly increased in those with a PPC: 24.4 vs 1.2%.4 An observational study of two large databases shows long-term significant differences in mortality rates with and without PPCs: 45.9 vs 8.7% at 1 yr or 71.4 vs 41.1% at 5 yr.35
Morbidity is also increased by PPCs. Length of hospital stay (LOS) has been shown to be prolonged by 13–17 days.8,23,36 For example, postoperative respiratory failure requiring unplanned re-intubation (mostly occurring within 72 h of surgery)15,21 has been shown to be associated with a considerable increase in morbidity and LOS.15,36
Developing a PPC also increases health-care costs, primarily as a result of increased LOS.22 For example, pneumonia or respiratory failure in a Canadian tertiary hospital resulted in a 41 and 47% increase in cost, respectively.30 The most recent study to evaluate the additional expenditure attributable to PPCs found an incremental cost of $25 498 per admission after gastrointestinal surgery.37 In times of increasing financial restrictions, particularly in the UK, PPCs represent a significant potential source of cost-savings. Anaesthetists and surgeons should therefore be aware of those at risk and adopt preventative measures that may reduce morbidity, mortality, and the cost of a surgical procedure.
Pathophysiology leading to PPCs
Intraoperative changes to the respiratory system
Adverse respiratory effects of general anaesthesia (GA) begin as soon as the patient loses consciousness.38 Central respiratory drive is depressed, causing prolonged apnoea followed by a return of spontaneous ventilation with a dose-dependent reduction in minute ventilation. The ventilatory responses to hypercapnia and hypoxia are significantly impaired even at low doses of anaesthetic drugs.39 As a result, hypercapnia is the norm unless artificial ventilation is used, and severe hypoxaemia occurs if ventilation is challenged by, for example, airway obstruction.
Respiratory muscle function changes immediately after induction. Airway obstruction occurs, there is increased curvature of the spine, cephalad diaphragm displacement in dependent areas, and a reduced cross-sectional area of the chest wall. These changes in end-expiratory muscle tone occur irrespective of whether or not the patient receives a neuromuscular blocking drug (NMBD) and lead to a reduction of functional residual capacity (FRC) of 15–20% compared with the subject’s awake, supine volume.38 The reduced FRC, along with abnormal regional distribution of ventilation during intermittent positive pressure ventilation and reduced cardiac output, leads to altered ventilation perfusion (V̇/Q̇) relationships. Although overall ventilation and perfusion are not particularly abnormal, there are increased areas of both high and low ̇ ratios. The former contribute to alveolar deadspace and a further impairment of carbon dioxide elimination, whereas the latter contribute to impaired oxygenation.
A more significant effect of reduced lung volume with regard to PPCs is the development of atelectasis. This occurs in more than three-quarters of patients receiving GA involving a NMBD,40 and is easily seen on computerized tomography (CT) scans in the dependent areas of the lung irrespective of the patient’s position (Fig. 1). Physiological factors contributing to formation of atelectasis include direct compression of lung tissue, for instance by the displaced diaphragm, airway closure when FRC reduces below closing volume, and rapid absorption of gases from alveoli in lung regions where the airways are narrowed or closed. The last of these factors is exacerbated by the use of high fractional inspired oxygen (FIO2), particularly at values of 1.0. For example, preoxygenation with an FIO2 of 1.0, 0.8, or 0.6 results in 5.6, 1.3, and 0.2% atelectasis, respectively, on cross-sectional area of a CT scan a few minutes after induction.41 Despite these dramatic differences at induction, there is no evidence that use of ‘hyperoxia’ (normally FIO2 of 0.8) throughout a GA with the aim of reducing surgical site infection results in more atelectasis after surgery.42 This suggests that even 20% nitrogen in inspired gas is helpful in preventing alveolar collapse. Strategies that may be used to minimize atelectasis involve avoiding the use of 100% oxygen and maintaining moderate levels of positive airway pressure during expiration to maintain airway patency. Once atelectasis has occurred, recruitment manoeuvres (RMs) are required to re-expand it.43,44
Fig 1
Computerised tomography scans of the chest in two patients during general anaesthesia in the supine (A) and prone (B) positions. Both scans are taken just cephalad of the right diaphragm, and show atelectasis in dependent lung regions irrespective of patient position.
These multiple and universal physiological changes to respiratory function are, in most instances, easily managed during routine GA, with the majority of patients having no respiratory problems beyond a few hours after emergence. Although poorly researched in comparison with intraoperative changes, it is, however, likely that the changes developing in the early stages of the anaesthetic form the pathophysiological basis for subsequent PPCs in at-risk patients, such as older patients with cardiorespiratory co-morbidity undergoing prolonged major surgery.
Postoperative respiratory pathophysiology
Postanaesthesia care unit changes
Hypoxia is common in the postanaesthesia care unit (PACU) and classified by some studies as a PPC in its own right.21 Multiple interacting factors contribute to episodes of desaturation.
(i) Airway obstruction occurs in many patients, exacerbated by the factors below.
(ii) Continued sedation from residual anaesthetic and opioid drugs, or from hypercapnia attributable to continuing central respiratory depression.
(iii) Residual effects of NMBDs. Even when conventional clinical and quantitative neuromuscular junction monitoring indicate adequate recovery, NMBDs may still impair respiratory function. There is impairment of the normal phasic activity of genioglossus, making airway obstruction or increased resistance more likely.45 Co-ordination of pharyngeal and upper oesophageal muscles is abnormal, increasing the risk of aspiration. This has been elegantly demonstrated in healthy awake volunteers given small doses of NMBDs to train-of-four (TOF) ratios of 0.6–0.9,46 the last of these being generally regarded as clinically recovered from a NMBD. At all levels of NMBD block there were significant numbers of subjects with pharyngeal dysfunction, and videofluoroscopy of a swallow found a high incidence of misdirected swallowing and penetration of contrast onto the vocal cords, even with a TOF ratio of 0.9. These events are likely to be much worse in a patent in the PACU who is also sedated. These changes do not result from muscle weakness per se, but illustrate how small changes in the speed and fine control of muscle responses cause failure of crucial reflexes.
(iv) Impairment of ventilatory responses to hypercapnia and hypoxia. Experimental studies in isocapnic subjects show that the hypoxic response is significantly impaired at low doses of anaesthetic drugs (e.g. 0.2 minimal alveolar concentration), but there is wide variation between different agents and experimental conditions.47 In hypercapnic conditions, which are most likely in the clinical situation, the response may be at least partly preserved, but that is not to say that an obstructed patient in the PACU will generate a normal ventilatory response to hypoxia during an episode of airway obstruction.
The reduced FRC and impaired oxygenation normally seen during anaesthesia usually return to normal within a few hours after minor operations, but this is not the case after major surgery. Atelectasis is still present in patients in the PACU. In a small study of 30 patients having peripheral surgery under GA, CT scans were performed 20 min after extubation and showed significant areas of atelectasis still to be present,48 and this was significantly worse if the patient had received 100% oxygen during emergence. A further small study of patients having either inguinal hernia or open cholecystectomy procedures showed CT evidence of atelectasis in nine of 10 subjects at 1 h and in five of 10 at 24 h after surgery.49 Atelectasis on CT scans 24 h after surgery is also more common in morbidly obese patients.50 Although involving only small numbers owing to the challenges of performing chest CT in patients recovering from a recent GA, these studies still suggest that expansion of atelectasis does not reliably occur after surgery. Further indirect evidence of atelectasis in the PACU can be obtained by measuring oxygenation, most easily done with alveolar-to-arterial oxygen difference, which remains substantially elevated 1 h after extubation in patients having major surgery,51 indicating significant venous admixture.
Residual effects of NMBDs may contribute to the inability to re-expand atelectasis in the first few hours after major surgery. Unsurprisingly, residual NMBD activity after GA, defined as a TOF ratio <0.9, is associated with significantly lower values for forced vital capacity (FVC) and peak expiratory flow rate.52 Of more potential relevance to re-expanding atelectasis is a finding in healthy awake volunteers that inspiratory respiratory manoeuvres are more sensitive to NMBD effects than the more usually measured expiratory ones.53 This means that after a dose of a NMBD it takes longer for a patient to recover inspiratory respiratory strength and coordination than to recover normal expiratory activity as demonstrated with FVC or forced expiratory volume in 1 s (FEV1). A TOF ratio of >0.95 was required for a normal forced inspiratory volume in one second, which is the respiratory muscle activity most useful for lung re-expansion.
Respiratory changes beyond the PACU
After major surgery, the restoration of a normal alveolar-to-arterial oxygen difference may take some days, and episodes of hypoxaemia are common. After upper abdominal surgery, FRC usually reaches its lowest value 1–2 days after surgery, before slowly returning to normal values after 5–7 days.54–56 As described above, atelectasis seen on CT scans during anaesthesia persists for at least 24 h in most patients having major surgery. One review of postoperative atelectasis in a heterogeneous group of non-thoracic patients found radiological evidence of atelectasis in 539 of 944 (57%) patients,57 with this incidence showing little sign of improving on postoperative day 3. The presence of atelectasis was not associated with a fever, indicating the difficulty in diagnosing this particular PPC without radiography.
Effort-dependent lung function tests, such as FVC, FEV1, and peak expiratory flow rate, are all reduced significantly after surgery, particularly if the patient has pain.56 The normal activity of most respiratory muscle groups is impaired after major surgery, including the airway muscles, abdominal muscles, and diaphragm.58 Factors contributing to this dysfunction include anaesthetic agents and NMBDs, postoperative analgesic drugs (particularly opioids), pain, disturbed sleep patterns, and the inflammatory response to surgery. The aetiology is more complex than simple muscle weakness and also involves poor co-ordination between muscle groups along with failure of the normal physiological reflexes and control mechanisms on which their activity depends.58
Respiratory control may be abnormal for some weeks after anaesthesia and surgery,59 with, for example, reduced ventilatory responses to hypercapnia and hypoxia. This has major implications for overcoming airway obstruction when asleep and probably explains the particular challenges faced by patients with obstructive sleep apnoea (OSA) in the postoperative period. In one study, the responses were still slightly impaired 6 weeks after surgery, at a time when inflammation, pain, and analgesic use were absent.59 These results suggest plasticity in the respiratory control mechanisms at the time of surgery that takes some time to return to normal.
Sputum retention is common after surgery. General anaesthesia, particularly with a tracheal tube, causes impairment of mucociliary transport in the airways,60 an effect that may persist into the postoperative period.
This combination of reduced FRC, residual atelectasis, an ineffective cough, and abnormal respiratory control, forms an ideal situation for PPCs to develop.
Preoperative risk stratification
Risk prediction models can be used to identify patients at high risk of complications and so may enable more informed consent and optimal perioperative management. Many prediction models for PPCs have been published in the last 5 yr, most of which have limitations as a result of being developed from retrospective databases,5,10,11,13,14,19,25 focused on a single adverse outcome (e.g. pneumonia,13,25 respiratory failure,11,29 unplanned re-intubation,10,14 or acute lung injury/ARDS),17,19 or from a lack of inclusion of intraoperative risk factors. There is therefore no ‘one size fits all’ model for PPC risk stratification.
Here, we describe three related risk prediction models, which were prospective, multicentre trials, using EPCO definitions for composite outcomes. ARISCAT (assess respiratory risk in surgical patients in Catalonia) developed a seven-variable regression model, stratifying patients into low-, intermediate-, and high-risk groups. Respective incidences of PPC development in their validation group were 1.6, 13.3, and 42.1%. The independent variables are low preoperative peripheral oxygen saturation (SpO2; <96%), respiratory infection in the last month, age, preoperative anaemia (<100 g dl−1), intrathoracic/upper abdominal surgery, duration of procedure (>2 h), and emergency surgery.4 Definition of a PPC was the development of at least one of the outcomes subsequently defined by EPCO (Table 1).
PERISCOPE (prospective evaluation of a risk score for postoperative pulmonary complications in Europe) externally validated ARISCAT with good discrimination; c-statistic 0.80 [confidence interval (CI) 0.78–0.82].6 In 2015, secondary analysis of these data (sample size 5384) was used to develop and validate a score to predict postoperative respiratory failure (PRF). The incidence of PRF was 4.2%, and seven factors were used to stratify patients into low-, intermediate-, and high-risk groups, with incidences of PRF of 1.1, 4.6, and 18.8%, respectively. However, the independent variables differ slightly from those found in ARISCAT: low preoperative Sp O2, at least one preoperative respiratory symptom, chronic liver disease, congestive heart failure, intrathoracic/upper abdominal surgery, procedure >2 h, and emergency surgery.29
One other prospective multicentre cohort study, with a small sample size of 268, focused specifically on risk-stratifying patients with upper abdominal incisions.32 They defined PPCs as shown for Scholes and colleagues32 in Table 2. Five independent risk factors were identified in the regression model, including duration of anaesthesia, surgical category, respiratory co-morbidity, current smoker, and predicted maximal oxygen uptake. A score of 2.02 or less derived from a clinical prediction rule was associated with a high risk of PPCs [odds ratio (OR) (CI) 8.41 (3.33–21.26)]. This model requires external validation before clinical implementation. Further risk prediction models have been summarized in Table 2.
These studies highlight the complexity of choosing an appropriate risk prediction model. Although they have undoubtedly furthered our understanding of which patient groups are susceptible to PPCs, the lack of agreement between studies and the complexity of the scoring systems currently make them impractical for routine clinical use.
Who gets postoperative pulmonary complications?
The numerous published non-modifiable and modifiable risk factors that may predict the development of a PPC are shown in Table 3. They can be considered as patient related, procedure related, or laboratory testing risk factors, as categorized by Smetana and colleagues.27 Only the more clinically significant and independent factors are discussed in more detail in this review. These factors are reproducible in multiple studies, and we believe them to be the most clinically relevant.
Table 3
Published risk factors for developing a postoperative pulmonary complication, categorized into patient factors, procedure factors, and laboratory testing (as defined by Smetana and colleagues),27 further divided into non-modifiable and modifiable. Risk factors with strong evidence in the literature are discussed in more detail in the main text. AAA, abdominal aortic aneurysm; CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; CXR, chest X-ray; FEV1, forced expiratory volume in 1 s; FVC, forced vital capacity; GA, general anaesthesia; GORD, gastro-oesophageal reflux disease; NMBDs, neuromuscular blocking drugs; OSA, obstructive sleep apnoea; PACU, postanaesthesia care unit; ‘Positive cough test’, patient takes a deep breath and coughs once, and a positive test=ongoing coughing after the initial cough; TOF, train of four
Non-modifiable | Non-modifiable | Urea >7.5 mmol litre−1 1025 |
Age4–7,10,13,14,18,20,24,25,27,33,36 | Type of surgery:4–7,10–13,15–18,23,25,27,29 | Increased creatinine33 |
Male sex12,19,33 |
| Abnormal liver function tests15 |
ASA ≥II5,11–14,16,19,27,33 | Low preoperative oxygen saturation4,6,29 | |
Functional dependence (frailty)10–13,25,27,34,36 | ‘Positive cough test’20 | |
Acute respiratory infection (within 1 month)4,6 | Abnormal preoperative CXR9,27 | |
Impaired cognition7 | Preoperative anaemia (<100 g litre−1)4,6 | |
Impaired sensorium25 | Low albumin5,10,27 | |
Cerebrovascular accident25 | Emergency (vs elective)4–6,10,11,16,18,19,23,25,29,33,36 | Predicted maximal oxygen uptake32 |
Malignancy7,15 | Duration of procedure6,12,14,20,22,27,29,32 | FEV1:FVC <0.7 and FEV1 <80% of predicted5 |
Weight loss >10% (within 6 months)15,25 | Re-operation18,23,36 | |
Long-term steroid use25 | Multiple GA during admission19 | |
Prolonged hospitalization15 | Modifiable | |
Modifiable | Mechanical ventilation strategy3,19,63–71 | |
Smoking57,12,13,15,25,32,33,61 | GA (vs regional)4,25,27,72 | |
COPD10,12,13,15–19,24,25,27,32,33,36 | Long-acting NMBDs and TOF ratio <0.7 in PACU73 | |
Asthma20,32 | Residual neuromuscular block | |
CHF15,16,18,27,29,33 | Intermediate-acting NMBDs with surgical time <2 h (not antagonized)21 | |
OSA62 | Neostigmine21,74 | |
BMI <18.5 or > 40 kg m−2 15 | Sugammadex with supraglottic airway75,76 | |
BMI >27 kg m−2 7 | Failure to use peripheral nerve stimulator21,74 | |
Hypertension15 | Open abdominal surgery (vs laparoscopic)5,26,77–79 | |
Chronic liver disease29 | Perioperative nasogastric tube18,20,22,23,25,80 | |
Renal failure19 | Intraoperative blood transfusion19,25,36 | |
Ascites12 | ||
Diabetes mellitus15,17 | ||
Alcohol17,25 | ||
GORD17 | ||
Preoperative sepsis13–15,33 | ||
Preoperative shock12 |
Non-modifiable | Non-modifiable | Urea >7.5 mmol litre−1 1025 |
Age4–7,10,13,14,18,20,24,25,27,33,36 | Type of surgery:4–7,10–13,15–18,23,25,27,29 | Increased creatinine33 |
Male sex12,19,33 |
| Abnormal liver function tests15 |
ASA ≥II5,11–14,16,19,27,33 | Low preoperative oxygen saturation4,6,29 | |
Functional dependence (frailty)10–13,25,27,34,36 | ‘Positive cough test’20 | |
Acute respiratory infection (within 1 month)4,6 | Abnormal preoperative CXR9,27 | |
Impaired cognition7 | Preoperative anaemia (<100 g litre−1)4,6 | |
Impaired sensorium25 | Low albumin5,10,27 | |
Cerebrovascular accident25 | Emergency (vs elective)4–6,10,11,16,18,19,23,25,29,33,36 | Predicted maximal oxygen uptake32 |
Malignancy7,15 | Duration of procedure6,12,14,20,22,27,29,32 | FEV1:FVC <0.7 and FEV1 <80% of predicted5 |
Weight loss >10% (within 6 months)15,25 | Re-operation18,23,36 | |
Long-term steroid use25 | Multiple GA during admission19 | |
Prolonged hospitalization15 | Modifiable | |
Modifiable | Mechanical ventilation strategy3,19,63–71 | |
Smoking57,12,13,15,25,32,33,61 | GA (vs regional)4,25,27,72 | |
COPD10,12,13,15–19,24,25,27,32,33,36 | Long-acting NMBDs and TOF ratio <0.7 in PACU73 | |
Asthma20,32 | Residual neuromuscular block | |
CHF15,16,18,27,29,33 | Intermediate-acting NMBDs with surgical time <2 h (not antagonized)21 | |
OSA62 | Neostigmine21,74 | |
BMI <18.5 or > 40 kg m−2 15 | Sugammadex with supraglottic airway75,76 | |
BMI >27 kg m−2 7 | Failure to use peripheral nerve stimulator21,74 | |
Hypertension15 | Open abdominal surgery (vs laparoscopic)5,26,77–79 | |
Chronic liver disease29 | Perioperative nasogastric tube18,20,22,23,25,80 | |
Renal failure19 | Intraoperative blood transfusion19,25,36 | |
Ascites12 | ||
Diabetes mellitus15,17 | ||
Alcohol17,25 | ||
GORD17 | ||
Preoperative sepsis13–15,33 | ||
Preoperative shock12 |
Table 3
Published risk factors for developing a postoperative pulmonary complication, categorized into patient factors, procedure factors, and laboratory testing (as defined by Smetana and colleagues),27 further divided into non-modifiable and modifiable. Risk factors with strong evidence in the literature are discussed in more detail in the main text. AAA, abdominal aortic aneurysm; CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; CXR, chest X-ray; FEV1, forced expiratory volume in 1 s; FVC, forced vital capacity; GA, general anaesthesia; GORD, gastro-oesophageal reflux disease; NMBDs, neuromuscular blocking drugs; OSA, obstructive sleep apnoea; PACU, postanaesthesia care unit; ‘Positive cough test’, patient takes a deep breath and coughs once, and a positive test=ongoing coughing after the initial cough; TOF, train of four
Non-modifiable | Non-modifiable | Urea >7.5 mmol litre−1 1025 |
Age4–7,10,13,14,18,20,24,25,27,33,36 | Type of surgery:4–7,10–13,15–18,23,25,27,29 | Increased creatinine33 |
Male sex12,19,33 |
| Abnormal liver function tests15 |
ASA ≥II5,11–14,16,19,27,33 | Low preoperative oxygen saturation4,6,29 | |
Functional dependence (frailty)10–13,25,27,34,36 | ‘Positive cough test’20 | |
Acute respiratory infection (within 1 month)4,6 | Abnormal preoperative CXR9,27 | |
Impaired cognition7 | Preoperative anaemia (<100 g litre−1)4,6 | |
Impaired sensorium25 | Low albumin5,10,27 | |
Cerebrovascular accident25 | Emergency (vs elective)4–6,10,11,16,18,19,23,25,29,33,36 | Predicted maximal oxygen uptake32 |
Malignancy7,15 | Duration of procedure6,12,14,20,22,27,29,32 | FEV1:FVC <0.7 and FEV1 <80% of predicted5 |
Weight loss >10% (within 6 months)15,25 | Re-operation18,23,36 | |
Long-term steroid use25 | Multiple GA during admission19 | |
Prolonged hospitalization15 | Modifiable | |
Modifiable | Mechanical ventilation strategy3,19,63–71 | |
Smoking57,12,13,15,25,32,33,61 | GA (vs regional)4,25,27,72 | |
COPD10,12,13,15–19,24,25,27,32,33,36 | Long-acting NMBDs and TOF ratio <0.7 in PACU73 | |
Asthma20,32 | Residual neuromuscular block | |
CHF15,16,18,27,29,33 | Intermediate-acting NMBDs with surgical time <2 h (not antagonized)21 | |
OSA62 | Neostigmine21,74 | |
BMI <18.5 or > 40 kg m−2 15 | Sugammadex with supraglottic airway75,76 | |
BMI >27 kg m−2 7 | Failure to use peripheral nerve stimulator21,74 | |
Hypertension15 | Open abdominal surgery (vs laparoscopic)5,26,77–79 | |
Chronic liver disease29 | Perioperative nasogastric tube18,20,22,23,25,80 | |
Renal failure19 | Intraoperative blood transfusion19,25,36 | |
Ascites12 | ||
Diabetes mellitus15,17 | ||
Alcohol17,25 | ||
GORD17 | ||
Preoperative sepsis13–15,33 | ||
Preoperative shock12 |
Non-modifiable | Non-modifiable | Urea >7.5 mmol litre−1 1025 |
Age4–7,10,13,14,18,20,24,25,27,33,36 | Type of surgery:4–7,10–13,15–18,23,25,27,29 | Increased creatinine33 |
Male sex12,19,33 |
| Abnormal liver function tests15 |
ASA ≥II5,11–14,16,19,27,33 | Low preoperative oxygen saturation4,6,29 | |
Functional dependence (frailty)10–13,25,27,34,36 | ‘Positive cough test’20 | |
Acute respiratory infection (within 1 month)4,6 | Abnormal preoperative CXR9,27 | |
Impaired cognition7 | Preoperative anaemia (<100 g litre−1)4,6 | |
Impaired sensorium25 | Low albumin5,10,27 | |
Cerebrovascular accident25 | Emergency (vs elective)4–6,10,11,16,18,19,23,25,29,33,36 | Predicted maximal oxygen uptake32 |
Malignancy7,15 | Duration of procedure6,12,14,20,22,27,29,32 | FEV1:FVC <0.7 and FEV1 <80% of predicted5 |
Weight loss >10% (within 6 months)15,25 | Re-operation18,23,36 | |
Long-term steroid use25 | Multiple GA during admission19 | |
Prolonged hospitalization15 | Modifiable | |
Modifiable | Mechanical ventilation strategy3,19,63–71 | |
Smoking57,12,13,15,25,32,33,61 | GA (vs regional)4,25,27,72 | |
COPD10,12,13,15–19,24,25,27,32,33,36 | Long-acting NMBDs and TOF ratio <0.7 in PACU73 | |
Asthma20,32 | Residual neuromuscular block | |
CHF15,16,18,27,29,33 | Intermediate-acting NMBDs with surgical time <2 h (not antagonized)21 | |
OSA62 | Neostigmine21,74 | |
BMI <18.5 or > 40 kg m−2 15 | Sugammadex with supraglottic airway75,76 | |
BMI >27 kg m−2 7 | Failure to use peripheral nerve stimulator21,74 | |
Hypertension15 | Open abdominal surgery (vs laparoscopic)5,26,77–79 | |
Chronic liver disease29 | Perioperative nasogastric tube18,20,22,23,25,80 | |
Renal failure19 | Intraoperative blood transfusion19,25,36 | |
Ascites12 | ||
Diabetes mellitus15,17 | ||
Alcohol17,25 | ||
GORD17 | ||
Preoperative sepsis13–15,33 | ||
Preoperative shock12 |
Non-modifiable risk factors
Age
Advancing age, even when adjusted for co-morbidity, is predictive of PPCs. Multiple studies have found age >60 or 65 yr to be a risk factor.7,18,20,33 More detailed age stratification shows an increased risk of a PPC as age increases. Compared with patients <60 yr, the OR (95% CI) for a PPC for 60- to 69-yr-olds is 2.1 (1.7–2.6) and for 70- to 79-yr-olds 3.1 (2.1–4.4).27 Above 80 yr of age, the risk increases further to an OR of 5.1 (1.9–13.3) compared with patients <50 yr old.4 These studies have not considered frailty when adjusting for age. Older patients are more likely to be frail, and frailty has also been shown to be associated with PPCs, even when adjusted for age.81 Interest in frailty is increasing, and the results of further studies of PPC occurrence in age-matched frail and non-frail patients will be interesting.
Surgery type
Patients are at high risk of developing PPCs after certain types of surgery.16,25 Compared with ‘other types of surgery’, the incidence of pneumonia is significantly higher after abdominal aortic aneurysm repair [OR (CI) 4.29 (3.34–5.50)], thoracic [3.92 (3.36–4.57)], upper abdominal [2.68 (2.38–3.03)], or neck surgery [2.30 (1.73–3.05)], neurosurgery [2.14 (1.66–2.75)], and major vascular surgery [1.29 (1.10–1.52)].25 ‘Other types of surgery’ included ear, nose, and throat, lower abdominal, urological, peripheral vascular, and spinal surgery as a collective comparator.
Abdominal and vascular procedures have repeatedly been shown to be high risk for development of PPCs.47 Laparotomy with an upper abdominal incision may have up to 15 times the risk of a PPC compared with a lower abdominal incision.7,23 Yang and colleagues12 confirmed this finding, with a higher incidence of PPCs with oesophagectomy and other upper abdominal procedures compared with colectomy, but did not comment on whether procedures were laparoscopic or open. Emergency surgery compared with elective surgery confers a two- to six-fold increased risk for a PPC.4,16,23,33 Several multivariate analyses have identified reoperation to result in a four- to seven-fold increase in PPCs compared with one procedure.23,26 Although the surgery type is non-modifiable itself, laparoscopic surgery for both upper and lower gastrointestinal procedures results in fewer PPCs compared with open procedures.26,77–79
Preoperative investigations
Preoperative spirometry and arterial blood gases (ABGs) have traditionally been cited as useful for PPC prediction. However, a systematic review in 2002 found four out of five studies of spirometry values not to be predictive of PPCs.22 The fifth study, in patients undergoing head and neck surgery, found spirometry to be predictive of PPCs only in a univariate analysis. This did not extrapolate in multivariate analysis, suggesting that overall, spirometry results are not a useful predictor for PPC development.82 Three studies evaluated the predictive value of preoperative ABGs; none found hypercarbia to be independently associated with PPCs.22 A later systematic review concluded that patients deemed high risk from spirometry results could easily be identified by clinical assessment alone, and that the evidence is not robust for risk stratification for PPCs with spirometry or ABG for non-cardiothoracic surgery.27 The usefulness of a preoperative chest X-ray (CXR) has likewise had inconsistent results. McAlister and colleagues20 found that patients having a CXR performed at the discretion of a clinician did not have more frequent PPCs, whereas Lawrence and colleagues9 found that having an abnormal preoperative CXR (compared with normal CXR) resulted in an OR (CI) of 3.2 (1.1–9.4) for a PPC. Again, an abnormal CXR is likely to be predictable by clinical assessment, but once an abnormal CXR has been found it is predictive of a PPC.27 The National Institute for Health and Care Excellence (NICE) advises that spirometry and ABGs should be performed only at the request of a senior anaesthetist for ASA score III or IV patients with confirmed or suspected respiratory disease, and that CXRs should not be offered routinely before elective surgery.83
Most recently, low preoperative SpO2 (assessed when supine, breathing room air) was found to be a significant independent risk factor for PPCs. Compared with SpO2≥ 96%, patients with preoperative SpO2 91–95% were twice as likely to get a PPC and those with SpO2≤ 90% 10 times more likely.4 This simple test comes at minimal cost and has been externally validated as part of two further PPC prediction models.6,29
Modifiable risk factors and their management
Co-morbidity
An ASA score of II or higher or a diagnosis of chronic obstructive pulmonary disease (COPD), congestive heart failure, or chronic liver disease are independent risk factors for PPCs.16,18,24,27,29,33 A recent meta-analysis has shown that patients with OSA are more than twice as likely as those without OSA to develop acute respiratory failure after non-cardiac surgery.62
Co-morbidities are modifiable to a certain extent in that preoperative medical optimization is possible. Chronic obstructive pulmonary disease and asthma should be optimally treated with bronchodilators and inhaled or oral steroids. A respiratory infection in the last month is associated more chance of developing a PPC,6 and so elective surgery should be postponed until symptoms and lung function tests are back to baseline,84 unless the surgery is urgent, in which case an individual patient decision must be made, balancing the risks of developing a PPC vs delaying surgery. Perioperative steroid replacement for those on high-dose oral steroids should be considered according to local guidelines as there is a paucity of research evidence to guide this practice.85 Congestive heart failure can be pharmacologically optimized by a cardiologist with the aim of minimizing symptoms and maximizing functional capacity. European Society of Cardiology guidelines for treatment of congestive heart failure have been updated in 2016.86 Patients with severe OSA undergoing elective surgery should be commenced on continuous positive airway pressure (CPAP) treatment and assessed for compliance before elective surgery.87
Smoking
Smoking is a risk factor for PPCs.7,12,15,25,61 A meta-analysis comparing current and ex-smokers (for >4 weeks) showed a statistically significant decrease in PPCs for ex-smokers [relative risk (RR) 0.81, CI 0.70–0.93].88 Four large retrospective cohort studies have used the American College of Surgeons National Surgical Quality Improvement Program (NSQIP) database to collate information on postoperative complications in current, previous (cessation >1 yr), and never smokers undergoing major surgery. Current smokers were more likely to have a PPC compared with ex-smokers, who were in turn more likely than those who had never smoked,88–90 particularly if they had smoked for >10 pack-yr.91 In active smokers, PPC incidence increases incrementally with the number of pack-year smoked,92 significantly so for >20 pack-yr; the adjusted OR (CI) compared with non-smokers was 1.20 (1.05–1.38) for <20 pack-yr, 1.57 (1.45–1.70) for 41–60 pack-yr, and 1.82 (1.70–1.94) for >60 pack-yr.90 Mortality (<30 days after surgery) is increased in current smokers with an OR (CI) of 1.17 (1.10–1.24), but not in non- and ex-smokers, defined as those who have not smoked for 1 yr before surgery.92 In contrast to increased morbidity, ex-smokers do not appear to have increased 30 day mortality, whether there is a 10 or 50 pack-yr history.92
Smoking cessation before major surgery reduces postoperative morbidity.88,89,93 In 2013, NICE published perioperative smoking cessation recommendations, focusing on pharmacological and behavioural support to aid cessation in the preoperative assessment phase.94 Intervention commenced at this stage of the surgical pathway has been shown to be effective in reducing smoking rates on admission and achieving a 30 day postoperative abstinence, especially in a day-surgery setting.95 Patients are almost three times more likely to remain smoke free at 12 months if they have received intensive compared with minimal cessation support.96 Several small studies have looked at the effectiveness of preoperative smoking cessation programmes in terms of reducing postoperative complications, but have not been adequately powered to show reductions in PPCs specifically.97–99 However, once pooled, data show a significant reduction in PPCs [RR (CI) 0.81 (0.70–0.93].88
Timing of smoking cessation is of interest. Cessation for >4 weeks reduces PPCs by 23%, and for >8 weeks by 47%,93 suggesting that maximizing the preoperative smoking cessation period minimizes PPCs.88 Concerns regarding increased sputum production after smoking cessation resulting in increased pulmonary complications have been refuted.100 Further research is required to evaluate any benefit of smoking cessation 1–2 weeks before surgery. Patients undergoing major surgery have been shown to have a spontaneously high rate of permanent smoking cessation, and Shi and Warner101 stated that having surgery should be regarded by all clinicians involved as a ‘teachable moment’ for smokers.
Preoperative anaemia
Approximately one-third of European patients presenting to pre-assessment clinics are anaemic.102 Patients with preoperative anaemia (haemoglobin <100 g litre−1) undergoing any type of surgery have a three-fold increase in the risk of a PPC.4 Autologous blood transfusion itself has also been shown to be independently associated with PPCs,25,36 and therefore alternative means of treating preoperative anaemia should be considered. The cause of anaemia should be established. Treatment options include dietary supplements, such as vitamin B12, folate, and oral or i.v. iron therapy (if oral intolerant or <4 weeks before surgery) for iron-deficiency anaemia.103 Erythropoietin is also an option but is itself associated with perioperative complications.104 Recent UK national guidelines have been published for the management of preoperative anaemia.105 Identification and treatment may diagnose disease, reduce autologous blood transfusion, conserve supplies, reduce PPCs, and avoid other potentially harmful effects of both anaemia and transfusion.
General anaesthesia
General anaesthesia disturbs many aspects of respiratory function, and it may therefore seem obvious that the incidence of PPCs is reduced in patients who have central or peripheral regional anaesthesia (RA) instead. The nature of surgical procedures that necessitate GA is similar to those listed above as being high risk for developing a PPC, which one may think would account for a proportion of the increased risk of GA vs RA. However, studies have shown that even for the same procedure, GA is an independent risk factor for PPCs compared with RA. For example, an overview of Cochrane systematic reviews showed a significant reduction in postoperative pneumonia [RR (CI) 0.45 (0.26–0.79)] although there was no difference in 30 day mortality.72 Likewise, a study including >200 000 veterans undergoing major non-cardiac surgery demonstrated an OR (CI) of 1.56 (1.36–1.80) for GA compared with RA.25 Canet and colleagues4 demonstrated an incidence of 7.5 vs 2.0% of developing at least one PPC with and without GA in their prospective multicentre study of 2464 patients.
A duration of surgery and anaesthesia of >2 h is independently associated with PPC development.4,20 The OR (CI) increased further with increasing operation time, being 4.9 (2.4–10.1) with >2 h and 9.7 (4.7–19.9) when >3 h.4 The authors state that this risk factor could, to some extent, be controlled by the surgeons;4 they do not suggest how, but it seems reasonable that those at high risk of a PPC should have a senior surgeon to minimize operative time.
Intraoperative ventilation strategies
Mechanical ventilation under GA plays a large role in development of PPCs. The benefits of lung-protective artificial ventilation in patients with ARDS are well established.106 Good evidence now exists that the incidence of PPC is significantly reduced when protective ventilation strategies are used in patients with non-injured lungs (i.e. during surgery). Protective ventilation involves consideration of tidal volume (VT), level of PEEP, and use of RMs. There is robust evidence that low VT is protective against PPCs; however, the ideal level of PEEP is more controversial, as many studies do not evaluate PEEP independently from low tidal volumes,65–68 and there are concerns over haemodynamic compromise with high PEEP levels. Also, PEEP is most effective for optimizing lung function when a RM is performed before application of PEEP,107 but RMs have not been evaluated independently of the level of PEEP, and the definition of RM varies between studies (Table 4). In the non-obese patient with healthy lungs, a plateau ‘opening pressure’ of 40 cm H2O for 7–8 s effectively opens all alveoli.44
Table 4
Different recruitment manoeuvres used in individual studies of intraoperative ventilation strategies; described by Güldner and colleagues69 as three different techniques: ‘bag-squeezing’, ‘stepwise increase in tidal volume’, and ‘stepwise increase in PEEP’. CPAP, continuous positive airway pressure; IBW, ideal body weight (see main text for calculation); I:E, inspiratory to expiratory ratio; RM, recruitment manoeuvre; RR, respiratory rate; VT, tidal volume
Severgnini and colleagues (2013)65 | Initial setting: 7 ml kg−1 IBW, RR 6 min−1, PEEP 10 cm H2O, I:E ratio 3:1 |
VT increased in steps of 4 ml kg−1 IBW until plateau pressure 30 cm H2O for three breaths | |
Settings returned to original, with PEEP maintained at 10 cm H2O | |
Futier and colleagues (2013)66 | CPAP 30 cm H2O for 30 s |
Treschan and colleagues (2012)108 | Three manual bag ventilations with a maximal pressure of 40 cm H2O before extubation |
Weingarten and colleagues (2010)109 | Three-step increase in PEEP: |
4–10 cm H2O for three breaths | |
10–15 cm H2O for three breaths | |
15–20 cm H2O for 10 breaths | |
PEEP reduced and maintained at 12 cm H2O | |
Repeated 30 and 60 min after the first RM and hourly thereafter |
Severgnini and colleagues (2013)65 | Initial setting: 7 ml kg−1 IBW, RR 6 min−1, PEEP 10 cm H2O, I:E ratio 3:1 |
VT increased in steps of 4 ml kg−1 IBW until plateau pressure 30 cm H2O for three breaths | |
Settings returned to original, with PEEP maintained at 10 cm H2O | |
Futier and colleagues (2013)66 | CPAP 30 cm H2O for 30 s |
Treschan and colleagues (2012)108 | Three manual bag ventilations with a maximal pressure of 40 cm H2O before extubation |
Weingarten and colleagues (2010)109 | Three-step increase in PEEP: |
4–10 cm H2O for three breaths | |
10–15 cm H2O for three breaths | |
15–20 cm H2O for 10 breaths | |
PEEP reduced and maintained at 12 cm H2O | |
Repeated 30 and 60 min after the first RM and hourly thereafter |
Table 4
Different recruitment manoeuvres used in individual studies of intraoperative ventilation strategies; described by Güldner and colleagues69 as three different techniques: ‘bag-squeezing’, ‘stepwise increase in tidal volume’, and ‘stepwise increase in PEEP’. CPAP, continuous positive airway pressure; IBW, ideal body weight (see main text for calculation); I:E, inspiratory to expiratory ratio; RM, recruitment manoeuvre; RR, respiratory rate; VT, tidal volume
Severgnini and colleagues (2013)65 | Initial setting: 7 ml kg−1 IBW, RR 6 min−1, PEEP 10 cm H2O, I:E ratio 3:1 |
VT increased in steps of 4 ml kg−1 IBW until plateau pressure 30 cm H2O for three breaths | |
Settings returned to original, with PEEP maintained at 10 cm H2O | |
Futier and colleagues (2013)66 | CPAP 30 cm H2O for 30 s |
Treschan and colleagues (2012)108 | Three manual bag ventilations with a maximal pressure of 40 cm H2O before extubation |
Weingarten and colleagues (2010)109 | Three-step increase in PEEP: |
4–10 cm H2O for three breaths | |
10–15 cm H2O for three breaths | |
15–20 cm H2O for 10 breaths | |
PEEP reduced and maintained at 12 cm H2O | |
Repeated 30 and 60 min after the first RM and hourly thereafter |
Severgnini and colleagues (2013)65 | Initial setting: 7 ml kg−1 IBW, RR 6 min−1, PEEP 10 cm H2O, I:E ratio 3:1 |
VT increased in steps of 4 ml kg−1 IBW until plateau pressure 30 cm H2O for three breaths | |
Settings returned to original, with PEEP maintained at 10 cm H2O | |
Futier and colleagues (2013)66 | CPAP 30 cm H2O for 30 s |
Treschan and colleagues (2012)108 | Three manual bag ventilations with a maximal pressure of 40 cm H2O before extubation |
Weingarten and colleagues (2010)109 | Three-step increase in PEEP: |
4–10 cm H2O for three breaths | |
10–15 cm H2O for three breaths | |
15–20 cm H2O for 10 breaths | |
PEEP reduced and maintained at 12 cm H2O | |
Repeated 30 and 60 min after the first RM and hourly thereafter |
Studies with the highest quality evidence focus on open abdominal surgery. The most current expert recommendation (for non-obese patients with normal lungs) is initially to use a low VT (6–8 ml kg−1) with PEEP ≤ 2cm H2O, FIO2 0.4 if oxygen saturations are ≥92%, and respiratory rate titrated to maintain normocarbia.69 In the event of inadequate oxygenation, an algorithm is suggested.69
Evidence continues to be evaluated. A further meta-analysis in 2016 demonstrated reduced lung infection with low VT alone, but when PEEP with RM were performed in combination with low VT, lung infection, atelectasis, and acute lung injury were also reduced.71 PROBESE,110 IPROVE,111 and LAS VEGAS112 are three studies in the recruitment, data collection, and manuscript preparation phases, respectively, which will provide more evidence for protective perioperative ventilation strategies. Additional trials are required to evaluate the role of individualized, higher PEEP levels in the prevention of PPCs in other types of surgery.
Low tidal volume
A recent meta-analysis of 15 randomized controlled trials (RCTs) including 2127 patients undergoing general surgery showed a significant reduction in PPCs between low (< 8 ml kg−1) and high (>8 ml kg−1) VT ventilation, regardless of the PEEP level used.63 A large multicentre observational study from 2006 showed that 18% of patients still received a VT >10 ml kg−1 despite evidence at the time that high VT promoted an inflammatory response and contributed to acute lung injury.113,114 It does, however, appear that there has been a trend for reduced VT over time, probably influenced by evidence from ARDS ventilation strategies. Levin and colleagues64 noted a significant reduction from 9 to 8.3 ml kg−1 (P=0.01) between 2008 and 2011, and a prospective study of 406 patients in the UK in 2016 showed median tidal volumes of 8.4 ml kg−1 predicted body weight.115 Extremes of weight and female sex are risk factors for inadvertent high-volume ventilation.113 116 It must be emphasized that VT in these studies is always set based on predicted or ideal body weight rather than real weight. Previously described calculations for predicted body weight used by the ARDS network are as follows:106
Men: 50+0.91(centimetres of height−152.4)
Women: 45.5+0.91(centimetres of height−152.4)
Evidence for moderate to high PEEP
Several RCTs and a meta-analysis have shown reduced PPCs with low VT and moderate PEEP levels.65–67 Severgnini and colleagues65 compared 9 ml kg−1VT, zero PEEP, and no RMs (standard ventilation) with 7 ml kg−1, 10 cm H2O PEEP, and an RM after induction, disconnection, and before extubation (protective ventilation). This study evaluated 56 patients undergoing open abdominal surgery of >2 h duration. Pulmonary function (FVC and FEV1) and arterial oxygenation in air were improved, atelectasis on CXR reduced, and the ‘Clinical Pulmonary Infection Score’ reduced in the protective ventilation group. No haemodynamic compromise occurred in the protective ventilation group in this small study.65 Futier and colleagues66 compared 10–12 ml kg−1 and zero PEEP (standard) with 6–8 ml kg−1 and 6–8 cm H2O PEEP with a RM every 30 min (protective), in 400 patients undergoing major open or laparoscopic abdominal surgery. The RR (CI) for PPC development in the protective arm was 0.29 (0.14–0.61). Neither study, as mentioned above, differentiates between low VT and higher PEEP as the beneficial component.
An observational study (>29 000 patients) showed an increased 30 day mortality in patients ventilated with low VT (6–8 ml kg−1) and low PEEP [median (range) 4.0 (2.2–5.0) cm H2O], suggesting that low VT may be beneficial only when used with an appropriate level of PEEP.64 Secondary analysis of a recent larger retrospective study of 64 000 ventilated patients undergoing non-cardiac surgery showed zero PEEP to be harmful, and a PEEP of 5 cm H2O with plateau pressures ≤16 cm H2O to be protective against developing PPCs. Interestingly, low VT (<10 ml kg−1) was not protective in this retrospective study.3 Another small observational study of ear, nose, and throat patients showed a PEEP of 5 cm H2O to be insufficient to prevent atelectasis, but PPCs were not evaluated.117 This group suggests that compliance should be monitored during surgery and PEEP set accordingly. Whether this prevents PPCs is questionable.118
Evidence against high PEEP
High PEEP (>10 cm H2O) may not be as important as low VT in protecting against PPCs and may, in fact, be harmful. The above-mentioned low tidal volume meta-analysis63 showed a non-significant risk reduction towards a low PEEP level, a finding that was supported by the PROVHILO study.70 PROVHILO is a large RCT and is the first to compare low VT with high PEEP (12 cm H2O) with RM vs low VT with low PEEP (≤2 cm H2O) without RM. Postoperative pulmonary complications occurred in 40% of the high PEEP group and 39% of the low-PEEP group [RR (CI) 1.01 (0.86–1.20)]. Furthermore, haemodynamic compromise occurred significantly more commonly in the high-PEEP group requiring more fluid and vasopressors. However, fluid loading before RM and high PEEP reduces cardiovascular compromise in obese patients,119 and PROVHILO does not mention the use of fluid loading before RM in the high-PEEP group.70 Hong and colleagues120 demonstrated significantly increased bronchiolar inflammatory markers in pigs exposed to high PEEP levels in comparison to the low-PEEP group, after 8 h of low-volume ventilation without surgery, suggesting that lung injury might result from high PEEP.
Protective ventilation for obese patients
There is mixed evidence as to whether obese patients, as an individual cohort, are at increased risk of PPCs. However, because of altered respiratory physiology in obesity, especially during GA, a specific protective ventilation strategy is recommended, primarily to reduce atelectasis.121 Tidal volume should be 6–8 ml kg−1 based on predicted body weight, along with PEEP ≥5 cm H2O with the use of appropriate RMs. These patients may require a higher opening pressure of up to 55 cm H2O.107 Respiratory rate should be used to control carbon dioxide concentrations and maintain normal pH.121
Inevitably, with such a mass of often conflicting evidence, the ideal ventilator settings during surgery depend on the individual patient. The authors’ opinion is that a small VT of 6–8 ml kg−1, based on ideal body weight, should be used in all patients, and in patients with healthy lungs having open or peripheral surgery, PEEP of >2 cm H2O is unlikely to be required.69 However, many patients have additional respiratory challenges, such as obesity, pneumoperitoneum, or existing lung disease (including current smokers), and more protective ventilation components are then likely to be required.70 Initially, greater levels of PEEP may be used in an attempt to prevent atelectasis and V̇/Q̇ mismatch developing to such an extent that oxygenation becomes impaired even with modestly increased F IO2 (up to 0.6). Finally, when the PEEP level reaches that associated with cardiovascular problems (≥10 cm H2O),70 an RM should be performed before increasing FIO2 or PEEP further.
Postoperative respiratory support with CPAP and nasal high-flow oxygen
A Cochrane review published in 2014 evaluated 10 studies (1981–2007) with 709 patients.122 It concluded that there was insufficient evidence to confirm a benefit of postoperative CPAP after major abdominal surgery, with regard to reducing mortality or major respiratory complications. A meta-analysis, published in 2012, demonstrated non-invasive ventilation to be beneficial in the postoperative period after major surgery (reduced LOS, re-intubation, and pneumonia rates).123 However, the postoperative data from this meta-analysis are heavily weighted by one RCT focusing on cardiac surgery,124 and otherwise evaluate the same studies as the Cochrane review.124 Post-cardiac surgery prophylactic CPAP (10 cm H2O for 6 h) has been shown to reduce PPCs, but did not shorten LOS.124 A recent meta-analysis showed a reduction in respiratory complications [RR (CI) 0.33 (0.16–0.66)] with pre- and postoperative non-invasive ventilation in obese patients, but only a trend towards a reduction in unplanned re-intubation and intensive care admission.125 Further large, high-quality RCTs are required.
Nasal high-flow oxygen is becoming a popular form of well-tolerated non-invasive ventilation for respiratory failure and is being studied for its place in prevention of PPCs. Prophylactic nasal high-flow oxygen may benefit high-risk cardiac patients with respiratory co-morbidity; a trial is in the pre-recruitment phase to determine this.126 However, it does not improve oxygenation or respiratory function or reduce complications after uncomplicated coronary artery bypass graft surgery.127 The results from an RCT comparing nasal high-flow oxygen with standard treatment to prevent hypoxaemia after abdominal surgery are awaited.128
Neuromuscular blocking drugs and their reversal
It is well known that postoperative residual paralysis causes respiratory compromise. The link between NMBDs and PPCs was first described in an audit of 600 000 patients in 1954, showing a mortality rate of 1:370 in patients who received curare vs 1:2100 in those who did not, with 63% of the deaths having a respiratory component.129 More recent studies confirmed this observation. For example, the use of long-duration NMBDs, such as pancuronium, with a TOF ratio <0.7 after extubation is a risk factor for developing a PPC.73 The same study demonstrated that the occurrence of PPCs was not higher with the use of pancuronium when residual block was avoided, or with atracurium and vecuronium, even in the presence of residual block. In contrast, a recent large observational study showed that using intermediate-duration NMBDs is associated with greater likelihood of desaturation in the PACU and unplanned re-intubation, especially if the duration of surgery was <2 h.21 The control cohort in this study underwent similar major surgical procedures, such as cardiac, thoracic, and abdominal surgery, apparently without the use of a NMBD, highlighting the limitation of retrospective analysis of database information. Another group have shown there to be a dose-dependent increase in PPC development with the use of intermediate-duration NMBDs, but the strength of this relationship was lessened by correct management of NMBD reversal.2
Neostigmine, particularly if given to patients whose NMBD activity is low, has respiratory effects of its own, probably resulting from excess acetylcholine causing weakness. When neostigmine is administered without a NMBD, there is impairment of genioglossus function and pharyngeal muscle coordination,130 and decreases in TOF ratio in peripheral muscles.131,132 These changes may translate into clinical problems. Recent evidence suggests that neostigmine is independently associated with PPCs, ascribed by the study authors either to excess acetylcholine or the duration of action of neostigmine being less than the elimination time of the NMBD in certain conditions.21 The odds of developing postoperative pulmonary oedema and re-intubation are increased when neostigmine is used without neuromuscular monitoring.74
Use of peripheral nerve stimulation in conjunction with neostigmine to guide reversal of NMBDs can reduce residual block and therefore PPCs.21,74 There have been recent calls in both the USA and UK to increase the use of mandatory quantitative monitoring of neuromuscular function whenever NMBDs are administered.133,134
Choice of reversal agent is currently limited by cost in the UK; however, the use of sugammadex is becoming increasingly popular for reversal of rocuronium and vecuronium, with the advantage that it can counteract profound neuromuscular block. Sugammadex use has, however, already been linked to adverse outcomes, such as laryngospasm and negative pressure pulmonary oedema with early administration in the presence of a supraglottic airway.75,76 Prospective evidence is conflicting as to whether sugammadex reduces postoperative residual curarization as a direct cause for reducing PPCs.135,136 A small RCT demonstrated reduced PPCs with sugammadex,137 and in a larger retrospective study comparing sugammadex with neostigmine or no reversal, the authors suggest that PPCs may be reduced with the use of sugammadex.138 A trial is currently recruiting to evaluate PPCs after major abdominal surgery, comparing sugammadex and neostigmine.139
These associations between management of NMBDs and PPCs at first seem surprising. The pharmacokinetics of modern NMBDs suggest that they should be having little clinical effect a few hours after emergence, yet PPCs occur more frequently for several days in patients receiving them. In addition to the failure to re-expand intraoperative atelectasis, there are other possible mechanisms by which events early in recovery might influence longer-term respiratory outcomes. These include inadequate clearance of the airway secretions normally associated with manipulation of the airway at emergence, and aspiration of pharyngeal or gastric secretions, the mechanisms of which are described in the above pathophysiology section.
Nasogastric tube
Several of the above-mentioned studies have identified nasogastric tube (NGT) placement as a risk factor for PPCs. Patients undergoing abdominal surgery are five to eight times more likely to have a PPC if an NGT is used in the perioperative period.20,22,23 A meta-analysis showed increased rates of atelectasis and pneumonia with routine use of NGTs.80 They are traditionally left in situ after abdominal surgery to speed return of bowel function, reduce distension, reduce risk of aspiration, and protect anastomoses. Two meta-analyses have shown no benefit in routine NGT placement after elective or emergency open abdominal surgery.80 140 Considering their association with PPCs as described above, their use should therefore be reserved only for symptom relief or specific surgical reasons.
Other preventative measures
Preoperative physiotherapy
A systematic review of 12 controlled trials showed that preoperative aerobic exercise and inspiratory muscle training (IMT) reduced PPCs and LOS in patients undergoing cardiac and abdominal surgery but not joint replacement surgery.141 The RR (CI) for PPCs was 0.4 (0.23–0.72). The authors recommended targeting patients at high risk of developing a PPC in order to instigate preoperative IMT.141 A more recent meta-analysis included additional controlled trials and showed similar outcomes with IMT, with PPCs almost halved [RR (CI) 0.48 (0.26–0.89)] when compared with ‘sham’ or no IMT in patients having cardiac and abdominal surgery.142 A 2015 Cochrane review confirmed a reduction in postoperative atelectasis and pneumonia after cardiac and major abdominal surgery with preoperative IMT compared with none. However, it is emphasized that the quality of evidence is low to moderate because of unavoidable inadequate blinding in the studies.143 These techniques are time consuming and expensive, normally requiring repeated direct supervision of the patient by a physiotherapist, so until the evidence for their use is more robust they should be reserved for only those patients at very high risk of PPCs.
Postoperative physiotherapy and mobilization
I COUGH is a postoperative respiratory care programme that reduces rates of pneumonia and unplanned re-intubation in general and vascular patients.144 The programme starts before surgery, with education in leaflet and video format. Incentive spirometry is prescribed 10 times each hour (three to five efforts each set) during waking hours until discharge, with the device always being in reach and after preoperative technique practice. Four-hourly documentation of incentive spirometry volumes occurs. Patients deep breathe and cough every 2 h. Ideally, patients are sat in a chair, or the head of the bed is elevated >30°, with mobilization three times a day. Oral hygiene is maintained with twice daily teeth brushing and mouthwash. Incentive spirometry alone has not been shown to reduce PPCs after thoracic, cardiac, or abdominal surgery.145,146 A combination of physiotherapy, mobilization, and oral hygiene seems to be more beneficial.
Analgesia
Addition of epidural analgesia to GA significantly reduces the risk of postoperative pneumonia in the general surgical population when compared with systemic opioids alone.72,147 It is especially beneficial for patients with severe COPD having major abdominal surgery, presumably as a result of improved analgesia and reduced opioid consumption. Epidural analgesia improves respiratory function and reduces rates of pneumonia, postoperative ventilation, and unplanned re-intubation.148,149
Obese patients are more likely to have OSA, and those with OSA are at risk of respiratory depression after surgery because of increased sensitivity to opioids and sedatives.121,150 Reduced doses of opioids should therefore be administered to some patients with known or suspected OSA, because opioid dose is correlated with postoperative increases in OSA and therefore the potential for PPCs.150
Conclusion
Postoperative pulmonary complications are common, and although many scoring systems exist to quantify PPC risk, there is no consensus on the best one to use, and they remain too complex to use clinically. Preoperative investigations, with the exception of SpO2 while breathing air, are poor predictors of developing a PPC. Modifiable risk factors include most cardiorespiratory co-morbidities, and these should be optimized before surgery if time allows. Preoperative smoking cessation interventions before surgery reduce PPC incidence, and more intensive cessation support increases their success. Correction of severe preoperative anaemia also improves PPC risk. In the intraoperative period, avoidance of GA in favour of RA will reduce PPC risk. In those receiving a GA, ‘protective ventilation’ should be used, particularly a small VT of 6–8 ml kg−1 of ideal body weight, supplemented with RMs and PEEP if required. The ideal level of PEEP remains controversial, with <5 cm H2O being acceptable in low-risk patients, but higher levels will be required in more challenging patients. The use of NMBDs is associated with PPCs, so these should be avoided if possible, and when used, they should be monitored quantitatively and antagonized with neostigmine only when required. Postoperative non-invasive ventilation may be useful in a small group of high-risk patients, but otherwise avoidance of PPCs after major surgery requires good analgesia and a care bundle of physiotherapy, mobilization, and good oral hygiene. It is our hope that as these strategies become more widely adopted, the incidence of PPCs and their associated morbidity and mortality will reduce.
Authors’ contributions
A.M. and A.L. contributed equally to development, drafting, and final approval of the version to be published, and agree to be accountable for all aspects of the work, ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
Declaration of interest
None declared.
References
1
Jammer
I
Wickboldt
N
Sander
M
, et al. .Standards for definitions and use of outcome measures for clinical effectiveness research in perioperative medicine: European Perioperative Clinical Outcome (EPCO) definitions: a statement from the ESA-ESICM joint taskforce on perioperative outcome measures
.
Eur J Anaesthesiol
2015
;
32
:
88
–
105
2
McLean
DJ
Diaz-Gil
D
Farhan
HN
Ladha
KS
Kurth
T
Eikermann
M.
Dose-dependent association between intermediate-acting neuromuscular-blocking agents and postoperative respiratory complications
.
Anesthesiology
2015
;
122
:
1201
–
13
3
Ladha
K
Vidal Melo
MF
McLean
DJ
, et al. .Intraoperative protective mechanical ventilation and risk of postoperative respiratory complications: hospital based registry study
.
Br Med J
2015
;
351
:
h3646
4
Canet
J
Gallart
L
Gomar
C
, et al. .Prediction of postoperative pulmonary complications in a population-based surgical cohort
.
Anesthesiology
2010
;
113
:
1338
–
50
5
Jeong
B-H
Shin
B
Eom
JS
, et al. .Development of a prediction rule for estimating postoperative pulmonary complications
.
PLoS One
2014
;
9
:
e113656
6
Mazo
V
Sabaté
S
Canet
J
, et al. .Prospective external validation of a predictive score for postoperative pulmonary complications
.
Anesthesiology
2014
;
121
:
219
–
31
7
Brooks-Brunn
JA.
Predictors of postoperative pulmonary complications following abdominal surgery
.
Chest
1997
;
111
:
564
–
71
8
Lawrence
VA
Hilsenbeck
SG
Mulrow
CD
Dhanda
R
Sapp
J
Page
CP.
Incidence and hospital stay for cardiac and pulmonary complications after abdominal surgery
.
J Gen Intern Med
1995
;
10
:
671
–
8
9
Lawrence
VA
Dhanda
R
Hilsenbeck
SG
Page
CP.
Risk of pulmonary complications after elective abdominal surgery
.
Chest
1996
;
110
:
744
–
50
10
Arozullah
AM
Daley
J
Henderson
WG
Khuri
SF.
Multifactorial risk index for predicting postoperative respiratory failure in men after major non cardiac surgery. The National Veterans Administration Surgical Quality Improvement Program
.
Ann Surg
2000
;
232
:
242
–
53
11
Gupta
H
Gupta
P
Fang
X
, et al. .Development and validation of a risk calculator predicting postoperative respiratory failure
.
Chest
2011
;
140
:
1207
–
15
12
Yang
CK
Teng
A
Lee
DY
Rose
K.
Pulmonary complications after major abdominal surgery: national surgical quality improvement program analysis
.
J Surg Res
2015
;
198
:
441
–
9
13
Gupta
H
Gupta
PK
Schuller
D
, et al. .Development and validation of a risk calculator for predicting postoperative pneumonia
.
Mayo Clin Proc
2013
;
88
:
1241
–
9
14
Hua
M
Brady
J
Guohua
L.
A scoring system to predict unplanned intubation in patients having undergone major surgical procedures
.
Anesth Analg
2012
;
115
:
88
–
94
15
Ramachandran
SK
Nafiu
OO
Ghaferi
A
Tremper
KK
Shanks
A
Kheterpal
S.
Independent predictors and outcomes of unanticipated early postoperative tracheal intubation after nonemergent, noncardiac surgery
.
Anesthesiology
2011
;
115
:
44
–
53
16
Brueckmann
B
Villa-Uribe
JL
Bateman
BT
, et al. .Development and validation of a score for prediction of postoperative respiratory complications
.
Anesthesiology
2013
;
118
:
1276
–
85
17
Kor
DJ
Warner
DO
Alsara
A
, et al. .Derivation and diagnostic accuracy of the surgical lung injury prediction model
.
Anesthesiology
2011
;
115
:
117
–
28
18
Li
C
Yang
WH
Zhou
J
, et al. .Risk factors for predicting postoperative complications after open infrarenal abdominal aortic aneurysm repair: results from a single vascular center in China
.
J Clin Anesth
2013
;
25
:
371
–
8
19
Blum
JM
Stentz
MJ
Dechert
R
, et al. .Preoperative and intraoperative predictors of postoperative acute respiratory distress syndrome in a general surgical population
.
Anesthesiology
2013
;
118
:
19
–
29
20
McAlister
FA
Bertsch
K
Man
J
Bradley
J
Jacka
M.
Incidence of and risk factors for pulmonary complications after non-thoracic surgery
.
Am J Respir Crit Care Med
2005
;
171
:
514
–
7
21
Grosse-Sundrup
M
Henneman
JP
Sandberg
WS
, et al. .Intermediate acting non-depolarizing neuromuscular blocking agents and risk of postoperative respiratory complications: prospective propensity score matched cohort study
.
Br Med J
2012
;
345
:
e6329
22
Fisher
BW
Majumdar
SR
McAlister
FA.
Predicting pulmonary complications after nonthoracic surgery: a systematic review of blinded studies
.
Am J Med
2002
;
112
:
219
–
25
23
Smith
PR
Baig
MA
Brito
V
Bader
F
Bergman
MI
Alfonso
A.
Postoperative pulmonary complications after laparotomy
.
Respiration
2010
;
80
:
269
–
74
24
Wong
DH
Weber
EC
Schnell
MJ
Wong
AB
Anderson
CT
Barker
SJ.
Factors associated with postoperative pulmonary complications in patients with severe chronic obstructive pulmonary disease
.
Anesth Analg
1995
;
80
:
276
–
84
25
Arozullah
AM
Khuri
SF
Henderson
WG
Daley
J.
Development and validation of a multifactorial risk index for predicting postoperative pneumonia after major noncardiac surgery
.
Ann Intern Med
2001
;
135
:
847
–
57
26
Antoniou
SA
Antoniou
GA
Koch
OO
Köhler
G
Pointner
R
Granderath
FA.
Laparoscopic versus open obesity surgery: a meta-analysis of pulmonary complications
.
Dig Surg
2015
;
32
:
98
–
107
27
Smetana
GW
Lawrence
VA
Cornell
JE.
Preoperative pulmonary risk stratification for non cardiothoracic surgery: systematic review for the American College of Physicians
.
Ann Intern Med
2006
;
144
:
581
–
95
28
Weiser
TG
Regenbogen
SE
Thompson
KD
, et al. .An estimation of the global volume of surgery: a modelling strategy based on available data
.
Lancet
2008
;
372
:
139
–
44
29
Canet
J
Sabaté
S
Mazo
V
, et al. .Development and validation of a score to predict postoperative respiratory failure in a multicentre European cohort. A prospective, observational study
.
Eur J Anaesthesiol
2015
;
32
:
458
–
70
30
Khan
NA
Quan
H
Bugar
JM
Lemaire
JB
Brant
R
Ghali
WA.
Association of postoperative complications with hospital costs and length of stay in a tertiary care center
.
J Gen Intern Med
2006
;
21
:
177
–
80
31
Lawrence
VA
Hilsenbeck
SG
Noveck
H
Poses
RM
Carson
JL.
Medical complications and outcomes after hip fracture repair
.
Arch Intern Med
2002
;
162
:
2053
–
7
32
Scholes
RL
Browning
L
Sztendur
EM
Denehy
L.
Duration of anaesthesia, type of surgery, respiratory co-morbidity, predicted VO2max and smoking predict postoperative pulmonary complications after upper abdominal surgery: an observational study
.
Aust J Physiother
2009
;
55
:
191
–
8
33
Johnson
RG
Arozullah
AM
Neumayer
L
Henderson
WG
Hosokawa
P
Khuri
SF.
Multivariable predictors of postoperative respiratory failure after general and vascular surgery: results from the patient safety in surgery study
.
J Am Coll Surg
2007
;
204
:
1188
–
98
34
Arozullah
AM
Daley
J
Henderson
WG
Khuri
SF.
Multifactorial risk index for predicting postoperative respiratory failure in men after major noncardiac surgery
.
Ann Surg
2000
;
232
:
242
–
53
35
Khuri
SF
Henderson
WG
DePalma
RG
Mosca
C
Healey
NA
Kumbhani
DJ.
Determinants of long-term survival after major surgery and the adverse effect of postoperative complications
.
Ann Surg
2005
;
242
:
326
–
41
36
Nafiu
OO
Ramachandran
SK
Ackwerh
R
Tremper
KK
Campbell
DA
JrStanley
JC.
Factors associated with and consequences of unplanned post-operative intubation in elderly vascular and general surgery patients
.
Eur J Anaesthesiol
2011
;
28
:
220
–
4
37
Fleisher
LE
Linde-Zwirble
WT.
Incidence, outcome, and attributable resource use associated with pulmonary and cardiac complications after major small and large bowel procedures
.
Perioper Med
2014
;
3
:
7
38
Lumb
AB
, Anaesthesia. In:Lumb
AB.
Nunn’s Applied Respiratory Physiology
, 8th Edn.
London
:
Elsevier
,
2016
;
291
–
318
39
Teppema
LJ
Baby
S.
Anesthetics and control of breathing
.
Respir Physiol Neurobiol
2011
;
177
:
80
–
92
40
Lundquist
H
Hedenstierna
G
Strandberg
A
, et al. .CT-assessment of dependent lung densities in man during general anaesthesia
.
Acta Radiol
1995
;
36
:
626
–
32
41
Edmark
L
Kostova-Aherdan
K
Enlund
M
Hedenstierna
G.
Optimal oxygen concentration during induction of general anesthesia
.
Anesthesiology
2003
;
98
:
28
–
33
42
Hovaguimian
F
Lysakowski
C
Elia
N
Tramèr
MR.
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
–
16
43
Tusman
G
Böhm
SH
Vazquez de Anda
GF
, et al. .‘Alveolar recruitment strategy’ improves arterial oxygenation during general anaesthesia
.
Br J Anaesth
1999
;
82
:
8
–
13
44
Rothen
HU
Neumann
P
Berglund
JE
Valtysson
J
Magnusson
A
Hedenstierna
G.
Dynamics of re-expansion of atelectasis during general anaesthesia
.
Br J Anaesth
1999
;
82
:
551
–
6
45
Herbstreit
F
Peters
J
Eikermann
M.
Impaired upper airway integrity by residual neuromuscular blockade. Increased airway collapsibility and blunted genioglossus muscle activity in response to negative pharyngeal pressure
.
Anesthesiology
2009
;
110
:
1253
–
60
46
Sundman
E
Witt
H
Olsson
R
Ekberg
O
Kuylenstierna
R
Eriksson
LI.
The incidence and mechanisms of pharyngeal and upper esophageal dysfunction in partially paralyzed humans
.
Anesthesiology
2000
;
92
:
977
–
84
47
Pandit
JJ.
The variable effect of low-dose volatile anaesthetics on the acute ventilator response to hypoxia in humans: a quantitative review
.
Anaesthesia
2002
;
57
:
632
–
43
48
Benoit
Z
Wicky
S
Fischer
J-F
, et al. .The effect of increased Fio2 before tracheal extubation on postoperative atelectasis
.
Anesth Analg
2002
;
95
:
1777
–
81
49
Strandberg
A
Tokics
L
Brismar
B
Lundquist
H
Hedenstierna
G.
Atelectasis during anaesthesia and in the postoperative period
.
Acta Anaesthesiol Scand
1986
;
30
:
154
–
8
50
Eichenberger
A-S
Proietti
S
Wicky
S
, et al. .Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem
.
Anesth Analg
2002
;
95
:
1788
–
92
51
Lumb
AB
Bradshaw
K
Gamlin
FMC
Heard
J.
The effect of coughing at extubation on oxygenation in the post-anaesthesia care unit
.
Anaesthesia
2015
;
70
:
416
–
20
52
Kumar
GV
Nair
AM
Murthy
HS
Jalaja
KR
Ramachandra
K
Parameshwara
G.
Residual neuromuscular blockade affects postoperative pulmonary function
.
Anesthesiology
2012
;
117
:
1234
–
44
53
Eikermann
M
Groeben
H
Hüsing
J
Pet
J.
Accelerometry of adductor pollicis muscle predicts recovery of respiratory function from neuromuscular blockade
.
Anesthesiology
2003
;
98
:
1333
–
7
54
Meyers
JR
Lembeck
L
O’Kane
H
Baue
AE.
Changes in functional residual capacity of the lung after operation
.
Arch Surg
1975
;
110
:
576
–
83
55
Craig
DB.
Postoperative recovery of pulmonary function
.
Anesth Analg
1981
;
60
:
46
–
52
56
Liu
S
Carpenter
RL
Neal
JM.
Epidural anesthesia and analgesia: their role in postoperative outcome
.
Anesthesiology
1995
;
82
:
1474
–
506
57
Mavros
MN
Velmahos
GC
Falagas
ME.
Atelectasis as a cause of postoperative fever. Where is the clinical evidence?
Chest
2011
;
140
:
418
–
24
58
Sasaki
N
Meyer
MJ
Eikermann
M.
Postoperative respiratory muscle dysfunction: pathophysiology and preventive strategies
.
Anesthesiology
2013
;
118
:
961
–
78
59
Nieuwenhuijs
D
Bruce
J
Drummond
GB
Warren
PM
Wraith
PK
Dahan
A.
Ventilatory responses after major surgery and high dependency care
.
Br J Anaesth
2012
;
108
:
864
–
71
60
Keller
C
Brimacombe
J.
Bronchial mucus transport velocity in paralyzed anesthetized patients: a comparison of the laryngeal mask airway and cuffed tracheal tube
.
Anesth Analg
1998
;
86
:
1280
–
2
61
Myles
PS
Iacono
GA
Hunt
JO
, et al. .Risk of respiratory complications and wound infection in patients undergoing ambulatory surgery: smokers versus nonsmokers
.
Anesthesiology
2002
;
97
:
842
–
7
62
Kaw
R
Chung
F
Pasupuleti
V
Mehta
J
Gay
PC
Hernandez
AV.
Meta-analysis of the association between obstructive sleep apnoea and postoperative outcome
.
Br J Anaesth
2012
;
109
:
897
–
906
63
Serpa Neto
A
Hemmes
SN
Barbas
CS
, et al. .Protective versus conventional ventilation for surgery. A systematic review and individual patient data meta-analysis
.
Anesthesiology
2015
;
123
:
66
–
78
64
Levin
MA
McCormick
PJ
Lin
HM
Hosseinian
L
Fischer
GW.
Low intraoperative tidal volume ventilation with minimal PEEP is associated with increased mortality
.
Br J Anaesth
2014
;
113
:
97
–
108
65
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
–
21
66
Futier
E
Constantin
JM
Paugam-Burtz
C
, et al. .IMPROVE Study Group: a trial of intra-operative low-tidal-volume ventilation in abdominal surgery
.
N Engl J Med
2013
;
369
:
428
–
37
67
Hemmes
SN
Serpa Neto
A
Schultz
MJ.
Intraoperative ventilatory strategies to prevent postoperative pulmonary complications: a meta-analysis
.
Curr Opin Anesthesiol
2013
;
26
:
126
–
33
68
Gu
W
Wang
F
Liu
J.
Effect of lung-protective ventilation with lower tidal volumes on clinical outcomes among patients undergoing surgery: a meta-analysis of randomized controlled trials
.
CMAJ
2015
;
187
:
E101
–
9
69
Güldner
A
Kiss
T
Serpa Neto
A
, et al. .Intraoperative protective mechanical ventilation for prevention of postoperative pulmonary complications. A comprehensive review of the role of tidal volume, positive end-expiratory pressure, and lung recruitment maneuvers
.
Anesthesiology
2015
;
123
:
692
–
713
70
PROVE Network Investigators for the Clinical Trial Network of the European Society of Anaesthesiology
,
Hemmes
SN
Gama de Abreu
M
Pelosi
P
, et al. .High versus low positive end-expiratory pressure during general anaesthesia for open abdominal surgery (PROVHILO trial): a multicentre randomised controlled trial
.
Lancet
2014
;
384
:
495
–
503
71
Yang
D
Grant
MC
Stone
A
Wu
CL
Wick
ECA.
Meta-analysis of intraoperative ventilation strategies to prevent pulmonary complications: is low tidal volume alone sufficient to protect healthy lungs?
Ann Surg
2016
;
263
:
881
–
7
72
Guay
J
Choi
P
Suresh
S
Albert
N
Kopp
S
Pace
NL.
Neuraxial blockade for the prevention of postoperative mortality and major morbidity: an overview of Cochrane systematic reviews
.
Cochrane Database Syst Rev
2014
;
1
:
CD010108
73
Berg
H
Roed
J
Viby-Mogensen
J
, et al. .Residual neuromuscular block is a risk factor for postoperative pulmonary complications. A prospective, randomised, and blinded study of postoperative pulmonary complications after atracurium, vecuronium and pancuronium
.
Acta Anaesthesiol Scand
1997
;
41
:
1095
–
103
74
Sasaki
M
Meyer
M
Malviya
SA
, et al. .Effects of neostigmine reversal of nondepolarizing neuromuscular blocking agents on postoperative respiratory outcomes; a prospective study
.
Anesthesiology
2014
;
121
:
959
–
68
75
Komasawa
N
Nishihara
I
Minami
T.
Relationship between timing of sugammadex administration and development of laryngospasm during recovery from anaesthesia when using supraglottic devices: a randomised clinical study
.
Eur J Anaesthesiol
2016
;
33
:
691
–
2
76
Ikeda-Miyagawa
Y
Kihara
T
Matsuda
R.
Case of negative pressure pulmonary edema after administration of sugammadex under general anesthesia with laryngeal mask airway
.
Masui
2014
;
63
:
1362
–
5
77
Lee
CZ
Kao
LT
Lin
HC
Wei
PL.
Comparison of clinical outcome between laparoscopic and open right hemicolectomy: a nationwide study
.
World J Surg Oncol
2015
;
13
:
250
78
Bablekos
GD
Michaelides
SA
Analitis
A
Charalabopoulos
KA.
Effects of laparoscopic cholecystectomy on lung function: a systematic review
.
World J Gastroenterol
2014
;
20
:
17603
–
17
79
Jiang
L
Yang
KH
Guan
QL
, et al. .Laparoscopy-assisted gastrectomy versus open gastrectomy for resectable gastric cancer: an update meta-analysis based on randomised controlled trials
.
Surg Endosc
2013
;
27
:
2466
–
80
80
Cheatham
ML
Chapman
WC
Key
SP
Sawyers
JL.
A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy
.
Ann Surg
1995
;
221
:
469
–
78
81
Robinson
TN
Wu
DS
Pointer
L
, et al. .Simple frailty score predicts postoperative complications across surgical specialties
.
Am J Surg
2013
;
206
:
544
–
50
82
Rao
MK
Reilley
TE
Schuller
DE
Young
DC.
Analysis of risk factors for postoperative pulmonary complications in head and neck surgery
.
Laryngoscope
1992
;
102
:
45
–
7
84
Lumb
A
Biercamp
C.
Chronic obstructive pulmonary disease and anaesthesia
.
Contin Educ Anaesth Crit Care Pain
2013
;
14
:
1
–
5
85
Yong
SL
Marik
P
Esposito
M
Coulthard
P.
Supplemental perioperative steroids for surgical patients with adrenal insufficiency
.
Cochrane Database Syst Rev
2009
;
4
:
CD005367
86
Ponikowski
P
Voors
AA
Anker
SD
, et al. .ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
.
Eur Heart J
2016
;
37
:
2129
–
200
87
Association of Anaesthetists of Great Britain and Ireland
.
Peri-operative management of the obese surgical patient 2015
.
Anaesthesia
2015
;
70
:
859
–
76
88
Mills
E
Eyawo
O
Lockhart
I
Kelly
S
Wu
P
Ebbert
JO.
Smoking cessation reduces postoperative complications: a systematic review and meta-analysis
.
Am J Med
2011
;
124
:
144
–
54
89
Schmid
M
Sood
A
Campbell
L
, et al. .Impact of smoking on perioperative outcomes after major surgery
.
Am J Surg
2015
;
210
:
221
–
9
90
Hawn
MT
Houston
TK
Campagna
EJ
, et al. .The attributable risk of smoking on surgical complications
.
Ann Surg
2011
;
254
:
914
–
20
91
Turan
A
Mascha
EJ
Roberman
D
, et al. .Smoking and perioperative outcomes
.
Anesthesiology
2011
;
114
:
837
–
46
92
Musallam
KM
Rosendaal
FR
Zaatari
G
, et al. .Smoking and the risk of mortality and vascular and respiratory events in patients undergoing major surgery
.
JAMA Surg
2013
;
148
:
755
–
62
93
Wong
J
Lam
DP
Abrishami
A
Chan
MTV
Chung
F.
Short-term preoperative smoking cessation and postoperative complications: a systematic review and meta-analysis
.
Can J Anaesth
2012
;
59
:
268
–
79
94
Smoking cessation in secondary care: acute, maternity and mental health services (NICE public health guidance 48). November
2013
. Available from //www.nice.org.uk/guidance/ph48 (accessed 27 January 2017)
95
Lee
SM
Landry
J
Jones
PM
Buhrmann
O
Morley-Forster
P.
The effectiveness of a perioperative smoking cessation program: a randomized clinical trial
.
Anesth Analg
2013
;
117
:
605
–
13
96
Thomsen
T
Villebro
N
Møller
AM.
Interventions for preoperative smoking cessation
.
Cochrane Database Syst Rev
2010
;
7
:
CD002294
97
Lindström
D
Sadr Azodi
O
Wladis
A
, et al. .Effects of a perioperative smoking cessation intervention on postoperative complications: a randomized trial
.
Ann Surg
2008
;
248
:
739
–
45
98
Møller
AM
Villebro
N
Pedersen
T
Tønnesen
H.
Effect of preoperative smoking intervention on postoperative complications: a randomised clinical trial
.
Lancet
2002
;
359
:
114
–
7
99
Sørensen
LT
Jørgensen
T.
Short-term pre-operative smoking cessation intervention does not affect postoperative complications in colorectal surgery: a randomized clinical trial
.
Colorectal Dis
2003
;
5
:
347
–
52
100
Myers
K
Hajek
P
Hinds
C
McRobbie
H.
Stopping smoking shortly before surgery and postoperative complications: a systematic review and meta-analysis
.
Arch Intern Med
2011
;
171
:
983
–
9
101
Shi
Y
Warner
DO.
Surgery as a teachable moment for smoking cessation
.
Anesthesiology
2010
;
112
:
102
–
7
102
Baron
DM
Hochrieser
H
Posch
M
, et al. .Preoperative anaemia is associated with poor clinical outcome in non-cardiac surgery patients
.
Br J Anaesth
2014
;
113
:
416
–
23
103
Clevenger
B
Richards
T.
Pre-operative anaemia
.
Anaesthesia
2015
;
70
:
20
–
8
104
Unger
EF
Thompson
AM
Blank
MJ
Temple
R.
Erythropoiesis-stimulating agents — time for a reevaluation
.
N Engl J Med
2010
;
362
:
189
–
92
105
Kotzé
A
Harris
A
Baker
C
, et al. .British committee for standards in haematology guidelines on the identification and management of pre-operative anaemia
.
Br J Haematol
2015
;
171
:
322
–
31
106
Acute Respiratory Distress Syndrome Network
.
Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome
.
N Engl J Med
2000
;
342
:
1301
–
8
107
Reinius
H
Jonsson
L
Gustafsson
S
, et al. .Prevention of atelectasis in morbidly obese patients during general anesthesia and paralysis. A computerized tomography study
.
Anesthesiology
2009
;
111
:
979
–
87
108
Treschan
TA
Kaisers
W
Schaefer
MS
, et al. .Ventilation with low tidal volumes during upper abdominal surgery does not improve postoperative lung function
.
Br J Anaesth
2012
;
109
:
263
–
71
109
Weingarten
TN
Whalen
FX
Warner
DO
, et al. .Comparison of two ventilator strategies in elderly patients undergoing major abdominal surgery
.
Br J Anaesth
2010
;
104
:
16
–
22
110
Protective Ventilation With Higher Versus Lower PEEP During General Anesthesia for Surgery in Obese Patients (PROBESE). ClinicalTrials.gov Identifier: NCT02148692
111
Individualized Perioperative Open Lung Ventilatory Strategy (iPROVE). ClinicalTrials.gov Identifier: NCT02158923
112
Local Assessment of Ventilatory Management During General Anesthesia for Surgery (LAS VEGAS). ClinicalTrials.gov Identifier: NCT0160122
113
Jaber
S
Coisel
Y
Chanques
G
, et al. .A multicentre observational study of intra-operative ventilatory management during general anaesthesia: tidal volumes and relation to body weight
.
Anaesthesia
2012
;
67
:
999
–
1008
114
Determann
RM
Royakkers
A
Wolthuis
EK
, et al. .Ventilation with lower tidal volumes as compared with conventional tidal volumes for patients without acute lung injury: a preventive randomized controlled trial
.
Critical Care
2010
;
14
:
R1
115
Patel
JM
Baker
R
Yeung
J
Small
C
;West Midlands-Trainee Research and Audit Network (WM-TRAIN)
.
Intra-operative adherence to lung-protective ventilation: a prospective observational study
.
Perioper Med
2016
;
5
:
8
116
Lellouche
F
Dionne
S
Simard
S
, et al. .High tidal volumes in mechanically ventilated patients increase organ dysfunction after cardiac surgery
.
Anesthesiology
2012
;
116
:
1072
–
82
117
Wirth
S
Baur
M
Spaeth
J
Guttmann
J
Schumann
S.
Intraoperative positive end-expiratory pressure evaluation using the intratidal compliance–volume profile
.
Br J Anaesth
2015
;
114
:
483
–
90
118
Wetterslev
J
Hansen
EG
Roikjaer
O
Kanstrup
IL
Heslet
L.
Optimizing peroperative compliance with PEEP during upper abdominal surgery: effects on perioperative oxygenation and complications in patients without preoperative cardiopulmonary dysfunction
.
Eur J Anaesthesiol
2001
;
18
:
358
–
65
119
Bohm
SH
Thamm
OC
von Sandersleben
A
, et al. .Alveolar recruitment strategy and high positive end-expiratory pressure levels do not affect hemodynamics in morbidly obese intravascular volume-loaded patients
.
Anesth Analg
2009
;
109
:
160
–
3
120
Hong
CM
Da-Zhong
X
Lu
Q
, et al. .Low tidal volume and high positive end-expiratory pressure mechanical ventilation results in increased inflammation and ventilator-associated lung injury in normal lungs
.
Anesth Analg
2010
;
110
:
1652
–
60
121
Hodgson
LE
Murphy
PB
Hart
N.
Respiratory management of the obese patient undergoing surgery
.
J Thorac Dis
2015
;
7
:
943
–
52
122
Ireland
CJ
Chapman
TM
Mathew
SF
Herbison
GP
Zacharias
M.
Continuous positive airway pressure (CPAP) during the postoperative period for prevention of postoperative morbidity and mortality following major abdominal surgery
.
Cochrane Database Syst Rev
2014
;
8
:
CD008930
123
Glossop
AJ
Shephard
N
Bryden
DC
Mills
GH.
Non-invasive ventilation for weaning, avoiding reintubation after extubation and in the postoperative period: a meta-analysis
.
Br J Anaesth
2012
;
109
:
305
–
14
124
Zarbock
A
Mueller
E
Netzer
S
Gabriel
A
Feindt
P
Kindgen-Milles
D.
Prophylactic nasal continuous positive airway pressure following cardiac surgery protects from postoperative pulmonary complications: a prospective, randomized, controlled trial in 500 patients
.
Chest
2009
;
135
:
1252
–
9
125
Carron
M
Zarantonello
F
Tellaroli
P
Ori
C.
Perioperative noninvasive ventilation in obese patients: a qualitative review and meta-analysis
.
Surg Obes Relat Dis
2015
;
12
:
681
–
91
126
High Flow Nasal Oxygen Therapy (Optiflow™) in High-risk Cardiac Surgical Patients. ClincialTrials.gov Identifier: NCT02496923
127
Parke
R
McGuinness
S
Dixon
R
Jull
A.
Open-label, phase II study of routine high-flow nasal oxygen therapy in cardiac surgical patients
.
Br J Anaesth
2013
;
111
:
925
–
31
128
Optiflow® to Prevent Post-Extubation Hypoxemia afteR Abdominal Surgery (the OPERA Trial) (OPERA). ClinicalTrials.gov Identifier: NCT01887015
129
Beecher
H
Todd
DPA.
Study of the deaths associated with anesthesia and surgery
.
Ann Surg
1954
;
140
:
2
–
34
130
Herbstreit
F
Zigrahn
D
Ochterbeck
C
Peters
J
Eikermann
M.
Neostigmine/glycopyrrolate administered after recovery from neuromuscular block increases upper airway collapsibility by decreasing genioglossus muscle activity in response to negative pharyngeal pressure
.
Anesthesiology
2010
;
113
:
1280
–
8
131
Caldwell
JE.
Reversal of residual neuromuscular block with neostigmine at one to four hours after a single intubating dose of vecuronium
.
Anesth Analg
1995
;
80
:
1168
–
74
132
Payne
JP
Hughes
R
Al Azawi
S.
Neuromuscular blockade by neostigmine in anaesthetized man
.
Br J Anaesth
1980
;
52
:
69
–
76
133
AAGBI Working party
.
Recommendations for Standards of Monitoring during Anaesthesia and Recovery 2015
.
London
:
AAGBI
,
2015
134
Brull
SJ
Prielipp
RC.
Reversal of neuromuscular blockade
.
Anesthesiology
2015
;
122
:
1183
–
5
135
Martinez-Ubieto
J
Ortega-Lucea
S
Pascual-Bellosta
A
, et al. .Prospective study of residual neuromuscular block and postoperative respiratory complications in patients reverted with neostigmine versus sugammadex
.
Minerva Anestesiol
2016
;
82
:
735
–
42
136
Cammu
GV
Smet
V
De Jongh
K
Vadeput
D.
A prospective, observational study comparing postoperative residual curarisation and early adverse respiratory events in patients reversed with neostigmine or sugammadex or after apparent spontaneous recovery
.
Anaesth Intensive Care
2012
;
40
:
999
–
1006
137
Sherman
A
Abelansky
Y
Evron
S
Ezri
T.
The effect of sugammadex vs. neostigmine on the postoperative respiratory complications following laparoscopic sleeve gastrectomy
.
Eur J Anaesthesiol
2014
;
31
:
152
138
Ledowski
T
Falke
L
Johnston
F
, et al. .Retrospective investigation of postoperative outcome after reversal of residual neuromuscular blockade: sugammadex, neostigmine or no reversal
.
Eur J Anaesthesiol
2014
;
31
:
423
–
9
139
Effects of Neuromuscular Block Reversal With Sugammadex vs Neostigmine on Postoperative Respiratory Outcomes After Major Abdominal Surgery. ClinicalTrials.gov Identifier: NCT02361060
140
Nelson
R
Edwards
S
Tse
B.
Prophylactic nasogastric decompression after abdominal surgery
.
Cochrane Database Syst Rev
2004
;
3
:
CD004929
141
Valkenet
K
van de Port
IG
Dronkers
JJ
de Vries
WR
Lindeman
E.
The effects of preoperative exercise therapy on postoperative outcome: a systematic review
.
Clin Rehabil
2011
;
25
:
99
–
111
142
Mans
CM
Reeve
JC
Elkins
MR.
Postoperative outcomes following preoperative inspiratory muscle training in patients undergoing cardiothoracic or upper abdominal surgery: a systematic review and meta analysis
.
Clin Rehabil
2015
;
29
:
426
–
38
143
Katsura
M
Kuriyama
A
Takeshima
T
Fukuhara
S
Furukawa
TA.
Preoperative inspiratory muscle training for postoperative pulmonary complications in adults undergoing cardiac and major abdominal surgery
.
Cochrane Database Syst Rev
2015
;
10
:
CD010356
144
Cassidy
MR
Rosenkranz
P
McCabe
K
Rosen
JE
McAneny
D.
I COUGH: reducing postoperative pulmonary complications with a multidisciplinary patient care program
.
JAMA Surg
2013
;
148
:
740
–
5
145
do Nascimento Junior
P
Módolo
NS
Andrade
S
Guimarães
MM
Braz
LG
El Dib
R.
Incentive spirometry for prevention of postoperative pulmonary complications in upper abdominal surgery
.
Cochrane Database Syst Rev
2014
;
2
:
CD006058
146
Agostini
P
Naidu
B
Cieslik
H
, et al. .Effectiveness of incentive spirometry in patients following thoracotomy and lung resection including those at high risk for developing pulmonary complications
.
Thorax
2013
;
68
:
580
–
5
147
Pöpping
DM
Elia
N
Van Aken
HK
, et al. .Impact of epidural analgesia on mortality and morbidity after surgery: systematic review and meta-analysis of randomized controlled trials
.
Ann Surg
2014
;
259
:
1056
–
67
148
Hausman
MS
JrJewell
ES
Engoren
M.
Regional versus general anesthesia in surgical patients with chronic obstructive pulmonary disease: does avoiding general anesthesia reduce the risk of postoperative complications?
Anesth Analg
2015
;
120
:
1405
–
12
149
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
–
21
150
Dawson
D
Singh
M
Chung
F.
The importance of obstructive sleep apnoea management in peri-operative medicine
.
Anaesthesia
2016
;
71
:
251
–
6
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© The Author 2017. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email:
Comments
1 Comment
Aspiration is a major postoperative pulmonary complication
10 May 2017
Réanimation, clinique de Parly 2, Ramsay Générale de Santé, 21 rue Moxouris, 78150 Le Chesnay, France
I read with interest this up-to-date review covering very broad and common topic-postoperative pulmonary complications (PPC).[1] First, diagnosis of tracheobronchitis is difficult and “purulent sputum with normal chest radiograph, no intravenous antibiotics” is false.[2] The chest radiograph may be abnormal (bronchial abnormalities), and antibiotics may actually be needed.[3],[4]
Finally, I would like to emphasize the major role of aspiration in PPC beyond the narrow definition of “acute lung injury after inhalation of regurgitated gastric contents”. Indeed, aspiration pneumonitis as previously defined when gross inhalation is witnessed by the staff and responsible for acute lung injury, is a serious disease.[5] However, “silent” micro aspiration may lead to tracheobronchitis, pneumonia, acute respiratory distress syndrome, respiratory infection and/or failure. As a matter of fact, when invasive ventilation is prolonged, aspiration is supposed to be a major trigger of ventilator-acquired complications.[6],[7] Even when invasive ventilation and intubation are shortened, aspiration may lead to significant PPC. This may be grossly approached by several means to decreasing colonization, aspiration, and/or its consequences that accordingly decrease PPC after surgery with relatively short period of intubation, including eradication of nasal carriage of Meticillin resistant Staphylococcus aureus by nasal mupirocin, and widening the antibiotic prophylaxis with second generation cefalosporin.[8],[9] Thus, any effort to decrease aspiration may translate into decreased PPC, including abovementioned procedures, adequate level of end-expiratory pressure, endotracheal cuff design and pressure, subglottic suction, up-right position (>30 to 45°), limitation of tracheal aspirates and nasogastric tubes whenever possible…[7],[10]
References
1. Miskovic A, Lumb AB. Postoperative pulmonary complications. BJA Br J Anaesth 2017;118(3):317–34.
2. Champion S. Does this Patient Have Ventilator-associated Tracheobronchitis? Am J Med 2014;127(8):e25.
3. Martin-Loeches I, Povoa P, Rodríguez A, et al. Incidence and prognosis of ventilator-associated tracheobronchitis (TAVeM): a multicentre, prospective, observational study. Lancet Respir Med 2015;3(11):859–68.
4. Nseir S, Martin-Loeches I, Makris D, et al.
Impact of appropriate antimicrobial treatment on transition from ventilator-associated tracheobronchitis to ventilator-associated pneumonia. Crit Care 2014;18(3):R129.
5. Lee A, Festic E, Park PK, et al. Characteristics and Outcomes of Patients Hospitalized Following Pulmonary Aspiration. Chest 2014;146(4):899–907.
6. Raghavendran K, Nemzek J, Napolitano LM, Knight PR. Aspiration-induced lung injury: Crit Care Med 2011;39(4):818–26.
7. Jaillette E, Girault C, Brunin G, et al.
Impact of tapered-cuff tracheal tube on microaspiration of gastric contents in intubated critically ill patients: a multicenter cluster-randomized cross-over controlled trial. Intensive Care Med 2017;
8. Perl TM, Cullen JJ, Wenzel RP, et al. Intranasal Mupirocin to Prevent Postoperative Staphylococcus aureus Infections. N Engl J Med 2002;346(24):1871–7.
9. Lador A, Nasir H, Mansur N, et al. Antibiotic prophylaxis in cardiac surgery: systematic review and meta-analysis. J Antimicrob
Chemother 2012;67(3):541–50.
10. Jaillette E, Martin-Loeches I, Artigas A, Nseir S. Optimal care and design of the tracheal cuff in the critically ill patient. Ann Intensive Care 2014;4(1):7.
Submitted on 10/05/2017 6:42 PM GMT