Current challenges in the recognition, prevention and

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Expert Review of Respiratory Medicine

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Current challenges in the recognition, prevention and treatment of perioperative pulmonary atelectasis Ruben D Restrepo & Jane Braverman To cite this article: Ruben D Restrepo & Jane Braverman (2015) Current challenges in the recognition, prevention and treatment of perioperative pulmonary atelectasis, Expert Review of Respiratory Medicine, 9:1, 97-107, DOI: 10.1586/17476348.2015.996134 To link to this article: http://dx.doi.org/10.1586/17476348.2015.996134

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Date: 12 January 2017, At: 11:28

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Current challenges in the recognition, prevention and treatment of perioperative pulmonary atelectasis Expert Rev. Respir. Med. 9(1), 97–107 (2015)

Ruben D Restrepo*1 and Jane Braverman2 1 Department of Respiratory Care, The University of Texas Health Science Center at San Antonio, MSC 6248, San Antonio, TX 78229, USA 2 187 Malcolm Avenue SE, Minneapolis, MN 55414, USA *Author for correspondence: [email protected]

Innovations in surgery have significantly increased the number of procedures performed every year. While more individuals benefit from better surgical techniques and technology, a larger group of patients previously deemed ineligible for surgery now undergo high-complexity surgical procedures. Despite continuous improvements in the operating room and post-operative care, post-operative pulmonary complications (PPCs) continue to pose a serious threat to successful outcomes. PPCs are common, serious and costly. Growing awareness of the impact of PPCs has led to intensified efforts to understand the underlying causes. Current evidence demonstrates that a high proportion of PPCs are directly traceable to the pre-operative risk for and perioperative development of atelectasis. The substantial costs and losses associated with PPCs demand strategies to reduce their prevalence and impact. Effective interventions will almost certainly produce cost savings that significantly offset current economic and human resource expenditures. The purpose of this review is to describe the most common challenges encountered in the recognition, prevention and management of perioperative atelectasis. Expanding awareness and understanding of the role of atelectasis as a cause of PPCs can reduce their prevalence, impact important clinical outcomes and reduce the financial burden associated with treating these complications. KEYWORDS: atelectasis . hyperinflation therapy . perioperative . pulmonary complication . pulmonary hygiene

The Problem

Atelectasis is a clinically important condition that is often a precursor, contributor, or simply part of other important, and often more severe, post-operative pulmonary complications (PPCs). These complications include, but are not limited to, bronchial obstruction, aspiration pneumonitis, interstitial and/or alveolar edema, gas exchange abnormalities, pneumonia, acute lung injury/respiratory failure, need for reintubation within 48 h, weaning failure, pleural effusion, bronchospasm and pneumothorax [1–3]. Very simply defined, a post-operative pulmonary complication is a pulmonary abnormality that produces identifiable disease or dysfunction

that is clinically significant and adversely affects the clinical course [4,5]. PPCs account for a substantial proportion of prolonged hospitalizations, admissions to the intensive care unit (ICU) and hospital re-admissions, and are associated with increased morbidity, mortality and healthcare expenditure [6–10]. They are considered the leading cause of death and of hospital costs in both cardiothoracic and non-cardiothoracic surgical procedures [11,12]. Reporting the prevalence of PPCs is complicated because reporting decisions are influenced by patient population, institutional criteria, surgical site and the clinical treatment setting. For example, milder abnormalities may resolve quickly and tend not to be counted.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercialNoDerivatives License (http://creativecommons.org/Licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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10.1586/17476348.2015.996134

Ó 2014 The Author(s). Published by Taylor & Francis

ISSN 1747-6348

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Figure 1. AP view of the chest of a patient scheduled for an elective surgical procedure. The image shows no obvious signs of parenchymal lung disease. Figure courtesy of Carlos S Restrepo MD, Professor of Radiology and Director, Cardio-Thoracic Radiology, The University of Texas Health Science Center, San Antonio, TX, USA.

Interpretation of clinical studies yielding prevalence data is likewise complicated by lack of a uniform definition of qualifying events. A combination of these factors may explain why prevalence statistics differ dramatically, ranging from 2 to 40% [2,6]. Imprecise data, notwithstanding, the impact of PPCs on patient outcomes is sobering. Hospital length of stay has been consistently reported to be increased by as much as 8 days together with a 2- to 12-fold increase in associated healthcare expenditures [13]. Among those adults who experience respiratory failure, more than 26% die within 30 days [14]. Total expenditures attributable to PPCs, including ICU care, pneumonia management, respiratory therapy, intubation and mechanical ventilation (MV), greatly exceed those of uncomplicated patients. A wellpowered study based upon 2002 data from a single private-sector center comparing the hospital costs of post-surgical patients with and without PPCs found that median charges for those with such complications were US$62,704 (range US$27,959– US$135,463) versus US$5015 (range US$4498–US$5686) for those without any problems [6]. These figures do not include therapeutic services and equipment. Dollar amounts have, of course, increased substantially over the past decade, but have likely remained relatively proportional. The cost of providing MV for patients who need 24-h therapy was estimated in 2003 as US$1500/day [15]. Compelling data from a prospective study of more than 100,000 Veterans Administration patients underscores the importance of predicting and preventing PPCs [16]. An analysis of survival following eight common surgical procedures found that the occurrence of a PPC (or other serious complications) within the first 30 post-operative days was 98

the single most important determinant of survival. Independent of pre-operative patient risk and intraoperative factors, mortality rates related to respiratory complications including pneumonia and failure to wean from MV at 30 days, 1 year and 5 years were 22, 45.9 and 71.4%, respectively. In sharp contrast, death rates for cohorts without complications were 2, 8.7 and 41.1% for the same intervals. These figures demonstrate dramatically decreased longer-term survival among patients following discharge after a PPC event. With understanding of the causes of PPC, most are potentially preventable. It is impossible to overstate the urgency of developing process improvement, bestpractice models and/or guidelines to maximize prevention of these complications. A preponderance of evidence implicates the occurrence of perioperative atelectasis as a key element in the progression to PPCs. Indeed, its presence appears to be a universal finding in PPCs arising from a diverse array of intrinsic and extrinsic contributing factors. Understanding atelectasis, recognizing its risk factors and clinical consequences, and selecting the best therapeutic approaches may significantly reduce prevalence and mitigate the devastating human and economic costs of preventable PPCs. Historical perspectives: focus on atelectasis

In the simplest terms, atelectasis is defined as a reversible alveolar collapse typically resulting from obstruction of the airway serving the affected alveoli. As a consequence, respiratory exchange of carbon dioxide and oxygen is impaired [17–19]. For many decades, surgeons have recognized that patients with previously healthy lungs experience measurable respiratory compromise when exposed to general anesthesia [20]. Routine observations include reduced respiratory system compliance and impaired oxygenation. In 1963, it was first suspected by Bendixen et al. that progressive alveolar collapse, or atelectasis, was the principle cause [21]. Those investigators found that in anesthetized patients, both lung compliance and the partial pressure of arterial oxygen decreased in succession but could be quickly restored with lung expansion maneuvers. However, owing to the limitations of conventional radiology, it has been difficult to verify this concept until the emergence of improved imaging techniques. Appropriate technologies now include computed tomography, MRI, electric impedance tomography, ultrasonography and, most recently, intravital microscopy [22,23]. With the implementation of these methods, it has been shown that 90% of patients undergoing general anesthesia demonstrate atelectasis in the most dependent parts of the lung (FIGURES 1–3) [20,23,24]. It has been further shown that anesthesia-induced atelectasis triggers a cascade of pathophysiological events that may culminate in diffuse alveolar damage, respiratory failure and, in extreme cases, death [5,20,24]. Etiology & pathogenesis of atelectasis

Atelectasis is a critical factor in the pathophysiology of a broad range of PPCs. Virtually all patients undergoing major surgical procedures develop some degree of atelectasis along with measurable alterations in lung function and compromises in pulmonary defense. As a rule, those changes are transitory and Expert Rev. Respir. Med. 9(1), (2015)

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recovery is uneventful. However, subpopulations of patients are significantly more likely to experience problems. Although the etiology of atelectasis in the perioperative setting has not been fully explained, three important ‘physiologic’ mechanisms have been found to cause or contribute to its development. These include compression, alveolar gas resorption and surfactant impairment [18,20,25]. These mechanisms have been found to interact simultaneously in vivo and are explained in detail below [20]. Compression

Mechanical compression of the alveoli is a characteristic effect of general anesthesia that results when the forces that cause the alveoli to collapse are exceeded by the transmural pressure that maintains them in the open state [19,20,26]. In anaesthetized patients, muscle relaxation displaces the diaphragm cephalad. Pleural pressure is then increased in the dependent parts of the lung, resulting in compression of adjacent lung tissue. Other factors that influence development of compression atelectasis include chest geometry, regional diaphragmatic and respiratory muscle changes, altered diaphragmatic dynamics and any condition with the potential to increase intra-abdominal pressures such as a shift of central vascular blood into the abdomen [19,20,25,27]. Alveolar gas resorption

Alveolar gas resorption can occur in two ways. The first mechanism involves the physics of oxygen tension in the presence of supplemental oxygen. In the normal state, lung regions that have low ventilation compared with perfusion have low alveolar oxygen tension when the fraction of inspired oxygen is low. During general anesthesia, when the fraction of inspired oxygen is increased with the addition of supplemental oxygen, alveolar oxygen tension (partial pressure of arterial oxygen) also rises. Accordingly, the rate of gas transfer from the alveolus to the capillary is increased and alveolar nitrogen tension decreases. With the loss of inert nitrogen, corresponding increases in oxygen absorption result in diminished alveolar volume [20,28]. The second mechanism is activated in the presence of complete collapse of small airways. In this circumstance, a pocket of gas is trapped in alveoli distal to the obstruction. This pocket gradually collapses because oxygen gas uptake by the mixed venous blood passing through the lung capillaries continues as a result of the diffusion gradient [19,20,25]. Surfactant impairment

Pulmonary surfactant is a phospholipid that reduces alveolar surface tension, thereby increasing alveolar stability and preventing collapse. Anesthesia has been shown to depress the stabilizing properties of surfactant. Repetitive opening and closing of the alveoli during general anesthesia with MV leads to deactivation and reduced availability of the surface active agent, producing an increase in surface tension at the local level and an overall reduction in functional residual capacity (FRC) [20,29,30]. Other factors contributing to development of atelectasis among surgical patients include disruption of normal respiratory muscle activity and loss of lung volumes. informahealthcare.com

Figure 2. AP view of the chest obtained on the second post-operative day. The image shows effaced left hemidiaphragm and dense left retrocardiac opacity consistent with left lower lobe post-op atelectasis. Radiograph courtesy of Carlos S Restrepo MD, Professor of Radiology and Director, Cardio-Thoracic Radiology, The University of Texas Health Science Center, San Antonio, TX, USA.

Diaphragmatic dysfunction

Diaphragmatic dysfunction plays a critical role in progression to PPC. This is especially true in patients undergoing upper abdominal and thoracic surgeries. For reasons unclear, significant post-anesthesia impairment of diaphragmatic contraction often persists for up to a week after surgery in some patients [31]. Increased expiratory muscle activity also occurs commonly both during anesthesia and post-operatively. Such an activity produces a rapid decrease in end-expiratory lung volume. Combined with reduced FRC, these mechanisms intensify the severity of atelectasis [25,32]. Lung volume reduction

Lung volume reduction occurs in any surgical procedure involving general anesthesia. Placing the patient in a supine position leads to a modest reduction of resting lung volume that significantly worsens during induction of general anesthesia due to its effect over FRC [5,33]. A single agent, ketamine, is an exception to this rule since even the deeper level of anesthesia induced by this agent does not affect FRC, ventilation distribution or minute ventilation [34]. Post-surgical deficits in FRC and vital capacity indicate the presence of a restrictive process. In some procedures, these effects are considerable. Abdominal surgery patients lose a great deal of inspiratory and expiratory reserve volume during the first post-operative days, with a 40% reduction in FRC, total lung capacity and forced expired volume in 1 s persisting for at least 1 week post-operatively [31]. Results for coronary bypass patients are similar [35]. Decreases in FRC lead to V/Q mismatch and promote development of atelectasis and hypoxemia. 99

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to be at 5.8-times greater risk for PPCs than low-scoring individuals [43]. However, in the Lawrence analysis of PPC events, patients whose only pulmonary abnormality was microatelectasis were excluded because it was considered clinically unimportant. Occurrences of macroatelectasis were likewise excluded because at that time, its clinical significance was unclear. Although assessments of absolute and relative risk vary significantly depending upon criteria particular to individual evaluation instruments, they all seek to rank patients on the basis of a growing body of data with the goal of implementing appropriate preventive and/or therapeutic interventions [1,4]. To date, no definitive, widely applicable instrument provides a simple and useful score for quantifying risk for PPC. Currently, a large international multicenter observational study addressing this problem is in progress. Designated by the acronym PERISCOPE, the study goals include refining tools to predict PPCs and to more accurately track their incidence among the general surgical population in Europe [44,45]. Outcome measures are a composite of in-hospital fatal and nonfatal adverse respiratory events that include atelectasis. Figure 3. Chest tomographic axial image at the lung base showing air space opacity in the left lower lobe consistent with atelectasis. Chest tomography courtesy of Carlos S Restrepo MD, Professor of Radiology and Director, Cardio-Thoracic Radiology, The University of Texas Health Science Center, San Antonio, TX, USA.

Recognition of patients at risk

Numerous risk-stratification and prediction models have been developed to identify patients with increased risk for perioperative atelectasis and PPCs. Several of these tools yield a numerical PPC prediction score based upon multivariable logistic analysis of evaluated patient-specific intrinsic and extrinsic risk factors [1,2,11,12,36–42]. These variables are categorized broadly as procedure and treatment-related factors and patient-related factors (BOX 1). Among these systems, the Lawrence Risk Index, published in 1996, offers the advantage of requiring neither spirometry nor arterial blood gases [42]. With this tool, based upon a nested case control study of 2291 patients undergoing elective abdominal surgery between 1982 and 1991, highest-scoring patients are shown Box 1. Risk factors for atelectasis. . . . . . . . . . . .

General anesthesia – type and duration Surgery – type and duration Underlying lung disease Underlying neuromuscular disease Chronic systemic disease or debility Obesity Age Airway mucus retention or mucus plugging Pleural effusion Prolonged bed rest (especially with limited position changes) Shallow breathing (result of pain and splinting)

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Procedure/treatment-related risk factors

Procedure-related variables known to increase the risk for atelectasis and PPCs include type of surgery, duration of operative time, and type and duration of anesthesia [1,2,4]. The incidence of PPCs after thoracic surgery is higher than that after abdominal or peripheral surgery [4]. Procedures associated with significant risk include thoracic resections, coronary artery bypass grafting, upper abdominal operations, head and neck procedures, certain orthopedic procedures including joint replacement and surgery for trauma. Treatment-related factors include type and duration of anesthesia, use of certain medications including immunosuppressive drugs and use of MV [4]. Physiological and psychogenic influences, including treatment-related altered breathing patterns, diaphragmatic weakness, splinting and fear of pain may also contribute to PPCs [4,46]. Patient-related risk factors

Patient-related factors that influence PPCs risk include presence of cardiovascular disease, chronic obstructive pulmonary disease (COPD), neuromuscular/neuromotor disorders, renal failure, malignancy and autoimmune disease [1,2,4,12,47,48]. Additional factors include recent respiratory illness, traumatic injury, a history of tobacco smoking, obesity and age [4,41,49]. Among these, COPD is the single most important risk factor for PPCs [50]. Likelihood of PPCs increases when high-complexity procedures are performed in patients with pre-existing risk for complications [3,4,12]. These factors include symptomatic respiratory disease (abnormal chest examination, wheezing, coughing, sputum production), current smoking, obesity and age. The effects of smoking as a discrete variable independent of COPD are also considerable. Smoking affects the lung at various loci including the bronchi, bronchioles and the lung parenchyma [49]. The effect of tobacco smoke in the larger airways (i.e., the bronchi) alters both the structure and function of the bronchial mucus glands. Exposure to smoke increases both the number and size Expert Rev. Respir. Med. 9(1), (2015)

Current challenges in the recognition, prevention & treatment of perioperative pulmonary atelectasis

of these mucus-secreting glands, resulting in the production and deposition of excess mucus within the lumen of the airway. In response to enlarged, hyperactive mucus glands, as well as to the influx of inflammatory cells, the airway walls become thickened. Correspondingly, the diameter of the airway lumen is reduced and may more easily become congested or plugged with mucus [51]. Atelectasis ensues. Clinical implications of perioperative atelectasis

It is important to understand the harmful effects of atelectasis in order to appreciate its impact on the post-operative clinical course. Such knowledge is critical for identifying and implementing perioperative strategies to minimize PPC events. Even mild atelectasis in surgical patients is associated with a variety of adverse effects and, with progression, may trigger a cascade of serious, often fatal complications. The consequences of atelectasis include, but are not limited to, reduction in lung compliance, hypoxemia, increased pulmonary vascular resistance (PVR), post-operative infection/ pneumonia and acute respiratory failure (ARF) [5,18,20,25,27]. Reduced lung compliance

The reduction in lung volume concomitant with exposure to general anesthesia, surgical positioning and operative maneuvers necessarily leads to an impairment of respiratory mechanics. Respiratory cycles begin with a lower FRC and the energy consumption is increased. The additive effects of atelectasis occur in proportion to severity [20,25]. Hypoxemia

Under anesthesia, alveolar collapse leads to an intrapulmonary shunt, V/Q mismatch and hypoxia [25]. Deterioration of oxygenation correlates with the amount of atelectasis. Likewise, the amount of lung surface affected by atelectasis and the degree of shunt correlate closely with the severity of hypoxia. Atelectasis in the surgical context also contributes to hypoventilation, hypovolemia, low cardiac output, anemia and alterations in the V/Q ratio [52]. Post-operative hypoxemia is the main cause of ARF and subsequent need for re-intubation and MV [53]. Increase in PVR

In healthy individuals, PVR is lowest when the lung volume is equal to FRC [54]. In surgical patients with atelectasis, hypoxia associated with the affected lung regions produces an increase in local PVR. This increase in the vascular resistance is triggered by the hypoxic pulmonary vasoconstriction activated when partial pressure of arterial oxygen and venous mixed blood are reduced and by the physical compression or kinking of large pulmonary vessels. Deleterious effects include increased pulmonary vascular pressure, right ventricular failure and extravasation of fluid at the microvascular level [17,19,20,25].

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risk for progression to ARF requiring MV [16]. Perioperative changes in lung mechanics and breathing patterns weaken the lung defense system, impairing both cough and mucociliary clearance [4,55]. As a consequence, particulate matter, including pathogens, is retained, increasing the risk for pulmonary infection. Although atelectasis is an established predisposing factor in the development of PPCs, it has been difficult to demonstrate a direct link between atelectasis and pneumonia per se in the clinical setting. Experimental evidence, however, supports a significant role in aggravating the course of such infections [20,25,29,30]. van Kaam et al. showed in an animal model that creating surfactant deficiency by whole lung lavage followed by intratracheal instillation of bacteria induced severe pneumonia with bacterial translocation into the blood stream [56]. Control group animals had a mortality rate of almost 80%. In contrast, in one of two experimental groups, pre-treatment with exogenous surfactant before instillation of streptococci attenuated both bacterial growth and translocation and prevented clinical deterioration. A similar outcome was achieved in a second group by reversing atelectasis in lavaged animals via open lung ventilation. Results suggest that minimizing the alveolar collapse by exogenous surfactant and open lung ventilation may reduce the risk of pneumonia and subsequent sepsis in post-surgical and/or ventilated patients. Impaired penetration of antibiotics into lung tissue

The goal of antibiotic therapy in treating lung infections is to achieve therapeutic levels of tissue penetration. Since the perioperative V/Q mismatch associated with atelectasis impedes the distribution of antibiotics into the lung tissue, prophylactic and/or therapeutic antibiotic therapy may not be as effective for the treatment of respiratory infections and/or pneumonia [57]. Therefore, strategies to reverse atelectasis and enhance delivery of drugs to target lung regions are critically needed. Atelectrauma due to acute respiratory distress syndrome

Acute respiratory distress syndrome is characterized by rapidonset bilateral pulmonary infiltrates and hypoxemia of noncardiac origin. Several pathophysiologic phenomena that include volutrauma, barotrauma, biotrauma and atelectrauma explain the complexity of acute respiratory distress syndrome. In the post-surgical setting, the term atelectrauma is used to characterize lung injury mechanisms triggered by atelectasis [58]. In both healthy and atelectatic lung regions, varying degrees of pulmonary damage occur when there is repetitive opening and closing of alveoli [26]. In the presence of atelectasis, damage is proportional to the degree of involvement. The greater the amount of tissue affected by atelectasis, the smaller the portion of lung that must adapt to the tidal volume administered. As a consequence, hyperinflation develops in healthy areas of the lung [26]. Simultaneously, the protective effects of surfactant are diminished by activation of the inflammatory response [59].

Post-operative pneumonia

Atelectasis and infectious complications account for most PPCs [13,24]. This combination of events is important since pneumonia and atelectasis are associated with a 30–50% increase in informahealthcare.com

Acute respiratory failure

Among PPCs, ARF is the most life-threatening event and is defined as a condition in which the gas exchange fails and 101

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oxygen and carbon dioxide cannot be maintained within their normal ranges due to worsening of the V/Q ratio. The degree of deterioration of alveolar compliance and gas exchange is strongly correlated to number of collapsed alveoli when atelectasis is present. Atelectasis causes V/Q mismatch, which ultimately results in compromise of gas exchange and may lead to respiratory failure [24]. In the post-surgical setting, when these patients require positive pressure ventilation and develop ARF, the mortality is high. One study showed that fatal outcomes in patients with ARF after major abdominal surgery may range from 40 to 65%. Survivors experienced 5- and 10-year mortality rates of 50 and 70%, respectively [60]. Another study found that median longterm survival is reduced by 87% when ARF develops in the first 30 post-operative days [13]. As expected, ARF is associated with prolonged ICU and hospital stays and high rates of ventilatorassociated pneumonia [11,24] Pre- & peri-surgical risk management

On the basis of current understanding of factors that predispose to PPCs, including those factors discussed in this paper that are associated with an increased likelihood of developing atelectasis, most surgical facilities implement strategies to reduce complications. Although a number of tests may be available to confirm the diagnosis and severity of atelectasis, the clinical impression and a plain radiograph are the only parameters used in most cases. They also help to determine the therapeutic strategy and the response to therapy. Additional tests that could be considered for the diagnosis of atelectasis include high-resolution computed tomography, MRI, lung ultrasound and pulmonary function testing. Making use of the accumulated knowledge, several protocols and guidelines have been created to promote modification of risk and to suggest rational interventions aimed at reducing the prevalence of PPCs [2,7,12,36,39,41,42,61–63].

development of atelectasis and subsequent PPCs is wellrecognized and an extensive body of literature is focused on surveillance and management procedures [4,33,53]. Intraoperative secretion management is critical in MV patients. This is achieved by various methods that include adequate humidification of medical gases and the physical removal of airway secretions via a suction catheter [4]. Non-invasive, individually tailored respiratory support may be an important adjunct in the intraoperative setting. A recent meta-analysis of eight trials that included 1669 patients testing the effect of lung-protective intraoperative ventilator settings on the incidence of PPCs found statistically significant reduction in the incidence of lung injury, pulmonary infection and atelectasis in patients receiving intraoperative MV at lower tidal volumes [66]. These findings are of high importance in light of results of the largest multicenter, international randomized controlled trial (RCT) to date investigating the effects of MV during general anesthesia for open abdominal surgery [67]. In this study, designated by the acronym ‘PROVHILO’, investigators hypothesized that a high level of positive-end expiratory pressure (PEEP) with recruitment maneuvers protects against PPCs in at-risk open abdominal surgery patients receiving MV with low tidal volumes during general anesthesia. The hypothesis was not confirmed. Outcomes revealed high rates of PPCs among patients receiving either higher or lesser amounts of PEEP. PPCs, which included atelectasis as a discrete entity, were reported in 40% of 445 patients in the higher PEEP group versus 39% in the lower PEEP group. Patients in the higher PEEP group developed intraoperative hypotension and required more vasoactive drugs. The current recommended intraoperative protective strategy, consistent with the results of the meta-analysis cited above, should include a low tidal volume and low PEEP without recruitment maneuvers. Post-operative risk management: general

Pre-operative management

Using validated assessment tools, the medical history of surgical candidates is evaluated for factors including pre-existing respiratory and/or systemic disease, smoking history, medication use and other factors identified above. Testing for cough and deep breathing is recommended since poor cough effort is a strong predictor for atelectasis and other PPCs. Preventive interventions

Active tobacco smokers have a significantly heightened risk for PPCs. Smoking cessation 6–8 weeks before surgery has been shown to be beneficial and is strongly encouraged [4,49]. Patients with a chronic pulmonary disease may be prescribed increased doses of bronchodilator therapy to reduce bronchial hyperreactivity and increased airway clearance therapy (ACT) to reduce secretion retention and improve the airway patency [4,55,64,65]. Intraoperative management

Attention to anesthetic technique, ventilator management, fluid monitoring, and surgical technique and duration is fundamental to reduce the risk for atelectasis. The role of anesthesia in 102

Post-surgical interventions to promote optimal recovery vary significantly depending upon the type of surgery and individual patient needs. Among these, adequate pain control and judicious use of nasogastric tubes directly reduce the risk for development of atelectasis and PPCs [62]. Pain control

Post-operative pain control is critical to PPC prevention. Pain contributes to diminishing the lung volumes and restricts the expansion of the lung by impairing the ability to perform deep inspirations and cough effectively [5,43]. Patients in pain have difficulty with mobilization and cooperating with lung expansion maneuvers. Several studies have shown that patients receiving post-operative epidural anesthesia show reduced rates of atelectasis and other PPCs [68,69]. In a recent meta-analysis, Popping et al. evaluated 125 trials (9044 patients, 4525 received epidural analgesia) [70]. The investigators found improvement in a number of respiratory endpoints including a statistically significant reduction in atelectasis in patients treated with epidural analgesia compared to controls. In an RCT, patients receiving epidural anesthesia after major elective surgery were Expert Rev. Respir. Med. 9(1), (2015)

Current challenges in the recognition, prevention & treatment of perioperative pulmonary atelectasis

compared to cohorts who received systemic analgesia (opioids). The epidural anesthesia group experienced a significantly lower rate of respiratory failure [71]. A recent meta-analysis of studies comparing the use of epidural versus systemic anesthesia 24 h or longer post-operatively found that epidural users demonstrated reduced need for prolonged MV or re-intubation, better pulmonary function and decreased rates of pneumonia [72]. Evidence suggests that despite the critical importance of adequate pain control, monitoring for opioid-induced respiratory depression with continuous pulse oximetry and capnography/or/ transcutaneous CO2 should be recommended in all individuals under the effect of potent analgesics, particularly in those using patient-controlled analgesia [72]. Nasogastric decompression

Nasogastric tube placement, previously used routinely after certain surgical procedures, is currently recommended only for patients demonstrating the need for intestinal decompression. Nasogastric tubes increase the risk for respiratory infection by impairing cough reflex and providing a more direct pathway for oro-pharyngeal bacteria to reach the lungs [3,62,73]. Selective use has been shown to significantly reduce the rates of atelectasis and pneumonia without increasing the risk for aspiration [2,73,74]. Post-operative risk management: respiratory care

Prophylactic respiratory care is provided routinely after major surgery to minimize the adverse effects of surgical trauma and anesthesia on the pulmonary system. As discussed above, decreased lung volumes, atelectasis, altered breathing patterns, diaphragmatic dysfunction and impaired mucociliary clearance contribute significantly to the development of PPCs. A group of therapeutic modalities known as ACTs have been developed to promote lung expansion and secretion mobilization [4,55,65]. They are administered to improve lung volumes, strengthen respiratory muscles, mobilize retained pulmonary secretions and resolve atelectasis. ACT techniques/modalities include incentive spirometry (IS), deep breathing exercises, chest physiotherapy techniques, continuous positive pressure breathing, positive expiratory pressure and airway oscillation therapies including intrapulmonary percussive ventilation and oral high-frequency oscillation techniques. Lung expansion therapy

Lawrence et al. evaluated qualifying RCTs that focused upon strategies to reduce atelectasis, pneumonia and respiratory failure after non-cardiothoracic surgery [62]. Their team then synthesized outcomes data and ranked the ‘strength of evidence’ on a graduated scale. Among the modalities evaluated, lung expansion techniques only received ‘A’ level grade. Data did not permit preference of one technique over another and led only to the conclusion that all lung expansion therapies reduced PPCs by >50% compared with no treatment and that any treatment was superior to no treatment. The Lawrence/Smetana reviews currently serve as the basis for the most recent practice guideline by the American College of Physicians [47]. informahealthcare.com

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A recent literature review of the scientific basis of postoperative respiratory care modalities addresses the considerable variation found in treatment protocols from institution to institution [4]. In addition, the review discusses the therapeutic modalities in current use, appraises supporting evidence and calls for multicenter studies to develop evidence-based standards to optimize reduction of preventable PPCs. The generally poor quality of clinical studies of chest physiotherapy, IS, continuous positive pressure breathing and positive expiratory pressure yield unreliable data, thus precluding definitive judgment. Continuous positive pressure breathing alone was associated with comparatively strong evidence, particularly when used in highrisk patients with hypoxemia. It cannot be overstated that recruitment/expansion of atelectatic lungs is more easily accomplished when acute lung injury has not occurred [23]. Post-operative risk management: a multidisciplinary approach

In a recent study, Cassidy et al. designed, implemented and evaluated a multidisciplinary program. Designated by the acronym ICOUGH (Incentive spirometry, Coughing and deep breathing, Oral care – brushing teeth and using mouthwash twice daily, Understanding – patient and family education, Getting out of bed frequently – at least three-times daily and Head-of-bed elevation), this multidisciplinary approach resulted in a 38.5% reduction of post-operative pneumonia [75]. More consistent lung expansion therapy encouraged by the use of IS may have contributed to the overall reduction in PPCs, as a 25% increase in the use of IS was achieved during their study. This result should be viewed with caution, however, as it has been shown in other studies that IS as monotherapy has limited impact on the reduction of post-operative atelectasis and its routine use should be questioned [76]. It may be that coughing and deep breathing and getting patients out of bed three-times daily were equal or greater contributors to the reduction in PPCs, particularly in light of the growing body of evidence underscoring the importance of early mobilization. Findings in the Cassidy study showed the ICOUGH intervention resulted in an increase in the frequency that patients were out of bed from 19% pre-treatment to 61% with treatment [76,77]. Makhabah et al. recently summarized the positive effects of perioperative physiotherapy to reduce PPCs [65]. These physiotherapy techniques included early mobilization, respiratory muscle training, neuromuscular electrical stimulation, breathing exercises and fast-track rehabilitation [65]. Early mobilization has been a focus of nursing practice and has been associated with an overall reduction in the length of stay and improved clinical outcomes, regardless of the clinical area where the patient is managed [78]. Use of lung expansion therapy is an intuitive approach to treatment with a base of support in the literature. A meta-analysis by Lawrence et al. reported that five RCTs support the use of IS, deep breathing exercises and continuous positive airway pressure to reduce the overall risk of PPCs [62]. Though the quality of the evidence is rated only as fair, positive outcomes provide a rationale to consider lung recruitment therapies to prevent or treat atelectasis [20,33,59,79]. 103

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Expert commentary

Atelectasis plays a substantial role in the development of PPCs. Recognition of the mechanisms that lead to atelectasis and of its role in triggering a cascade of events resulting in serious PPCs is of critical importance if the goal of preventing or reducing this serious problem is to be realized. Awareness of risk for atelectasis is especially critical in patients with characteristics that are recognized as strong predictors for PPCs. Significant factors include advanced age, abnormal cough, presence of significant systemic and/or pulmonary comorbidities including COPD and/or obstructive sleep apnea, higher American Society of Anesthesologists class and abnormal findings on the chest examination. The number of clinical manifestations and their intensity depends on the severity of atelectasis. Patients may present with dyspnea, cough, intercostal retractions, nasal flaring, tachypnea and diaphoresis. If severe, the physical exam of the chest may reveal decreased chest excursion and either decreased breath sounds or the presence of fine crackles that can clear after deep breathing or cough. Shifting of the trachea and cardiac point of maximum impulse occurs in severe cases of unilateral atelectasis where the pulling forces are strong enough to cause ipsilateral deviations of adjacent intrathoracic structures. Likewise, risk evaluation must consider the site and duration of certain surgical procedures that place patients at higher risk for atelectasis and other PPCs. The type and expected duration of anesthesia must also be factored in. Because clinicians have little control over many of the risk factors that contribute to perioperative atelectasis and subsequent PPCs, they are challenged to identify effective strategies to minimize atelectasis that include lung expansion maneuvers and ACT techniques. Despite ever-increasing understanding of the mechanisms that lead to perioperative atelectasis, robust evidence demonstrating the efficacy of particular prophylactic and

therapeutic interventions persists. The level of scientific evidence derived from RCTs supporting the use of lung expansion and ACT, either alone or in combination, is inadequate. Current recommendations for the use of interventional approaches rely more on clinicians’ judgment, preference and experience than on guidelines resulting from well-conducted clinical trials. Best evidence suggests implementation of a ‘bundle’ approach based on individual patient needs. Increased awareness of the impact of perioperative atelectasis, as well as of the potential usefulness of an array of modalities to minimize complications, is of critical importance in order to identify and test therapeutic approaches that strengthen clinical, quality-of-life and economic outcomes. Five-year view

As the American population ages, and with expanded access to health insurance, the frequency and complexity of surgical procedures performed on higher-risk individuals will increase significantly. High rates of morbidity, hospital re-admission and complication-related mortality must be moderated or societal costs will become unsustainable. We anticipate significant effort over the next five years to identify and implement interventions to prevent or moderate these adverse outcomes. An understanding of the role of atelectasis as an underlying cause of PPCs is fundamental to accomplish this goal. Financial & competing interests disclosure

RD Restrepo and J Braverman are independent consultants for Hill-Rom. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.

Key issues .

Significant excess morbidity, mortality and healthcare costs are directly associated with post-operative pulmonary complications (PPCs). The incidence of PPCs is increasing sharply in proportion to aging, with more medically complex population eligible for higher-risk surgical procedures.

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PPCs are a multifactorial syndrome in which atelectasis plays a significant role. Evidence demonstrates that development of atelectasis is a nearly universal precursor and concomitant feature of PPCs.

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The etiology of atelectasis in the perioperative setting has not been fully explained. However, three major ‘physiologic’ mechanisms – compression, alveolar gas resorption and surfactant impairment – have been identified and are shown to interact simultaneously in vivo. Diaphragmatic dysfunction and lung volume reduction also play a role.

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Prevention or aggressive early management of atelectasis is vital to optimally minimize progression to serious/life-threatening PPCs and unsustainable economic expenditure.

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Pulmonary hygiene measures are provided as Standard of Care for surgical patients. However, the evidence base for a diverse array of largely empirical management strategies that include airway clearance therapy and lung expansion maneuvers remains weak.

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Currently, best evidence suggests that a multifaceted or ‘bundle’ approach to mitigate PPCs yields best results. Understanding the cause/s of atelectasis and incorporating interventions that directly moderate the physiological risks for or consequences of this pathology will likely lead to development of more dependable, scientifically sound therapeutic protocols.

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Expanding awareness and understanding of the role of atelectasis as a cause of PPCs is a fundamental step toward minimizing prevalence, improving clinical outcomes and reducing the financial burden of this potentially preventable complication.

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Current challenges in the recognition, prevention & treatment of perioperative pulmonary atelectasis

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