What every physician needs to know:
The respiratory system is particularly vulnerable to the adverse effects of general anesthesia and surgery, and postoperative pulmonary complications are commonly encountered. Overall, pulmonary complications account for approximately 25 percent of deaths in the postoperative period. Pulmonary complications also contribute to increased intensive care and hospital lengths of stay, prolonged recovery times, and increased cost of care.
Classification:
While the list of potential postoperative pulmonary complications is long, most notable among them are the following:
-
Acute respiratory failure
Continue Reading -
Atelectasis
-
Pneumonia
-
Aspiration pneumonitis
-
Transfusion-related acute lung injury (TRALI) and transfusion-associated circulatory overload (TACO)
-
Exacerbation of pre-existing lung disease
-
Pleural effusion
-
Phrenic nerve injury
-
Pulmonary embolism
-
Obstructive sleep apnea
Are you sure your patient has a postoperative pulmonary complication? What should you expect to find?
Clinical hallmarks of common postoperative respiratory complications include:
Acute Respiratory Failure
Acute respiratory failure (ARF) in the postoperative period is usually defined as the continued need for mechanical ventilation beyond 24-48 hours following surgery. ARF may be due to either the inability to wean from the ventilator or the need to reinstitute mechanical ventilatory support following failed extubation. ARF may be due to inadequate oxygenation, inadequate ventilation, or a combination of the two.
Patients who are breathing spontaneously with impending ARF are typically tachypneic with a rapid, shallow breathing pattern. Restlessness, confusion, use of accessory muscles of respiration, and paradoxical thoraco-abdominal movement on inspiration are other signs of respiratory distress. Increasing somnolence may reflect the presence of severe hypercapnia.
Atelectasis
Because of the presence of intrapulmonary shunting, atelectais is typically accompanied by hypoxemia of varying severity. Additional clues to the presence of atelectasis are derived from the physical examination, which usually reveals dullness to percussion and tubular breath sounds over the involved segment.
Pneumonia
Pneumonia should be suspected in the presence of fever, leukocytosis, cough with purulent sputum, and radiographic infiltrates. Clinical findings are nonspecific and, in one autopsy series, provided a correct antemortem diagnosis in only 70 percent of cases.
Aspiration Pneumonitis
Aspiration of gastric contents manifests clinically as fever, tachypnea, and hypoxemia. Radiographic findings include multifocal opacities that occur predominantly in dependent areas of lung. The diagnosis is most firmly established in the setting of a witnessed aspiration, but it should also be considered in patients at risk because of vomiting, impaired consciousness, or impaired swallowing.
Transfusion-Related Acute Lung Injury (TRALI)
TRALI develops within 6 hours of transfusion of blood products. Mild episodes of TRALI present with fever and dyspnea; more severe cases are characterized by respiratory distress, hypoxemia, hypotension, and diffuse opacities noted on chest X-ray.
Transfusion-Associated Circulatory Overload (TACO)
Like TRALI, TACO also develops within 6 hours of transfusion of blood products. Respiratory distress, hypertension, hypoxemia, signs of volume overload on clinical exam such as elevated jugular venous distention and peripheral edema, and diffuse opacities on chest X-ray are characteristic. This should be considered in any patient with underlying cardiac or renal disease who develops respiratory symptoms after transfusion of blood products.
Exacerbation of Pre-existing Lung Disease
Patients with obstructive and/or bronchospastic lung disease, such as chronic obstructive lung disease (COPD) or asthma, may experience an exacerbation of their underlying disease postoperatively. Dyspnea, tachypnea, increased cough with or without sputum production, and wheezing are characteristic.
Patients with interstitial lung disease (ILD), particularly patients with idiopathic pulmonary fibrosis (IPF), are at increased risk of developing exacerbations of their underlying ILD after surgery, particularly thoracic surgery. Signs and symptoms are nonspecific and include respiratory distress, tachypnea, hypoxemia, and new opacities on chest X-ray. The diagnosis should be considered in a patient with a known ILD in whom alternative causes of postoperative pulmonary complications have been excluded.
Pleural Effusion
Pleural effusions are common with an incidence of at least 50% after both abdominal and thoracic surgery. Although common, pleural effusions usually represent incidental findings of minimal clinical significance. Patients may complain of dyspnea and exam may demonstrate decreased breath sounds at the site of the effusion. Chest X-ray findings may range from only mild blunting of the costo-phrenic angle to partial or, in severe cases, complete opacification of the hemithorax.
Phrenic Nerve Injury
Phrenic nerve injury and resultant diaphragmatic paralysis are well-described complications of cardiac and thoracic surgical procedures. Although typically inconsequential in patients with normal underlying pulmonary function, unilateral diaphragmatic paralysis may lead to significant respiratory compromise in patients with chronic lung disease. Bilateral diaphragmatic paralysis, while rare, may be a devastating complication, resulting in hypercapnic respiratory failure requiring prolonged mechanical ventilatory support.
Patients with diaphragmatic dysfunction often complain of orthopnea because of the additional compromise that occurs with loss of gravitational assistance in the supine position. With bilateral diaphragmatic dysfunction, a paradoxical breathing pattern–expansion of the chest wall and inward movement of the abdominal wall during inspiration–may be seen.
Pulmonary Embolism
Pulmonary embolism is typically accompanied by dyspnea, pleuritic chest pain, tachypnea, tachycardia, and hypoxemia. However, these features are commonly present in many postoperative patients as a result of pain and atelectasis. Development of hypotension suggests the presence of massive pulmonary embolism.
Obstructive Sleep Apnea (OSA)
OSA is characterized by repetitive occlusion of the upper airway during sleep, causing episodic hypoxemia and hypercapnia and leading to fragmentation of sleep. The principle daytime symptom is hypersomnolence, but OSA is increasingly identified as a cause or exacerbating factor of coronary artery disease, essential hypertension, diabetes mellitus, and stroke.
OSA in the postoperative period may present with episodic hypoxemia, confusion, cardiac arrhythmias, and even sudden cardiac death. Because of the alterations in oropharyngeal anatomy that commonly accompany obesity and OSA, difficulties with mask ventilation and oropharyngeal intubation are likely to be encountered when anesthesia is induced.
Beware: there are other diseases that can mimic a postoperative pulmonary complication:
A number of postoperative pulmonary complications may be difficult to distinguish from one another:
Atelectasis
The clinical and radiographic presentation of atelectasis may be virtually indistinguishable from pneumonia. Occasionally, the respiratory distress and hypoxemia associated with atelectasis can be relatively abrupt in onset, and the chest X-ray may be clear if it is obtained before resorption of gas has occurred from non-ventilated areas of lung. In such instances, the presentation may mimic that of pulmonary embolism.
Pneumonia
Atelectasis, pulmonary embolism, acute lung injury, aspiration pneumonitis, and congestive heart failure may share similar clinical and radiographic features with pneumonia.
Aspiration Pneumonitis
Aspiration pneumonitis shares clinical and radiographic features with nosocomial pneumonia. Furthermore, increased use of gastric acid suppressive medications leading to increased gastric bacterial colonization further blurs the lines between these two entities. The absence of witnessed aspiration and the presence of respiratory symptoms beyond 48 hours and purulent secretions, however, argues against aspiration pneumonitis and favors a diagnosis of pneumonia.
Transfusion-Related Acute Lung Injury (TRALI) and Transfusion-Associated Circulatory Overload (TACO)
When dyspnea, hypoxemia, and diffuse pulmonary opacities develop within 6 hours of receiving blood product transfusions, noncardiogenic pulmonary edema in the form of TRALI and cardiogenic pulmonary edema in the form of TACO are both considerations. While other classic transfusion reactions may be associated with fever and dyspnea (because of bronchospasm), they are distinguished from TRALI and TACO by the absence of radiographic opacities on chest X-ray. The presence of fever and hypotension favors a diagnosis of TRALI and the absence of fever in the presence of hypertension, signs of volume overload on exam, and patient history of cardiac or renal disease favor the diagnosis of TACO.
Exacerbation of Pre-existing Lung Disease
Wheezing in patients with COPD or asthma may suggest bronchospasm and an exacerbation of their obstructive lung disease. The presence of wheezing in the absence of abnormalities on chest X-ray favors the diagnosis of bronchospasm. However, bronchospasm may still occur in the presence of chest X-ray abnormalities such as aspiration pneumonitis or pneumonia. Furthermore, wheezing is not specific for bronchospasm and may be seen with cardiogenic pulmonary edema in the absence of bronchospasm.
Because of the nonspecific signs and symptoms, diagnosing an exacerbation of ILD requires exclusion of other causes of postoperative pulmonary complications such as cardiogenic pulmonary edema, pulmonary embolus, atelectasis, etc.
Pleural Effusion
The radiographic signs of a pleural effusion can sometimes mimic those of atelectasis or other causes of opacities on chest X-ray.
Phrenic Nerve Injury
Non-traumatic causes of diaphragmatic dysfunction include critical illness polyneuropathy and myopathy, and myopathy resulting from prolonged use of neuromuscular blocking agents.
Pulmonary Embolism
Pneumonia, atelectasis, aspiration pneumonitis, ARDS, and congestive heart failure share clinical features (e.g., dyspnea, hypoxemia) with pulmonary embolism, but they are usually associated with more pronounced radiographic abnormalities on chest X-ray or chest CT scan.
How and/or why did the patient develop a postoperative pulmonary complication?
Several factors related to surgery adversely affect pulmonary function and may contribute to postoperative respiratory complications:
Acute Respiratory Failure
Effects of General Anesthesia
Administration of general anesthesia by either the inhaled or intravenous route results in a nearly instantaneous loss of diaphragmatic and intercostal muscle tone, cephalad shift of the diaphragm, and decrease in transverse thoracic diameter. These changes result in a 20 percent reduction in functional residual capacity and promote the development of atelectasis. Studies that have employed CT imaging during and after administration of general anesthesia have demonstrated the presence of atelectasis in dependent areas of lung within ten minutes of induction with either inhalational or intravenous anesthetics. The single exception is ketamine, which is unique in maintaining respiratory muscle tone. The inhalational agents commonly used for anesthesia are also respiratory depressants that blunt the response to both hypoxemia and hypercapnia.
In contrast to general anesthesia, neuraxial anesthesia (spinal or epidural) preserves diaphragmatic function and does not blunt the ventilatory response to CO2. Despite these favorable effects on respiratory function and respiratory drive, a clinically significant benefit of neuraxial anesthesia over general anesthesia has not been demonstrated consistently.
Intraoperative Ventilation Strategies
Principles of lung protective mechanical ventilation such as low tidal volume ventilation and the use of positive end expiration pressure (PEEP) to reduce morbidity and mortality in patients with injured lungs with the acute respiratory distress syndrome (ARDS) are well established. Increasingly recognized, however, is that these similar principles when applied to patients receiving mechanical ventilation undergoing routine surgery reduce postoperative pulmonary complications. A meta-analysis of 15 randomized controlled trials involving 2,127 patients demonstrated that lung protective ventilation during general surgery, defined as a tidal volume ventilation of less than 8mL/kg of ideal body weight, reduced postoperative pulmonary complications from to 8.7% from 14.7% for conventional ventilation. The effect size of lung protective ventilation may be even more dramatic in individuals identified to be at intermediate or high risk of postoperative pulmonary complications, as a randomized controlled trial of this at risk patient population undergoing abdominal surgery demonstrated that low tidal volume ventilation reduced postoperative pulmonary complications from 27.5% to 10.5%.
Postoperative Analgesia
Opiates are routinely administered via the parenteral or epidural route for major surgical procedures, particularly those involving the chest or abdomen. The results of studies that compare the effect of epidural and parenteral opiates on pulmonary function conflict: While most document the superior analgesic effect of the epidural route, it is not clear that this analgesic effect results in less impairment in respiratory mechanics or gas exchange or in a lower incidence of pulmonary complication. Both routes of administration are associated with a risk of respiratory depression, with approximately 3 percent of patients developing hypercapnia as a result. Elderly patients are particularly susceptible to the respiratory depressant effects of opiates because of impaired drug metabolism.
Type of Surgery
Cardiothoracic and upper abdominal surgery result in pronounced impairment in pulmonary function in the postoperative period. Within twenty-four hours following upper abdominal surgery, vital capacity declines by 50 percent. While the decline improves over time, significant impairment persists for as long as seven days after surgery. In contrast, vital capacity falls by only 25 percent following lower abdominal procedures and typically returns to normal by the third postoperative day.
The decline in lung function that is associated with upper abdominal surgery is mediated in part by diaphragmatic dysfunction, as documented by a reduction in transdiaphragmatic pressures with tidal breathing and in a shift from abdominal to rib cage breathing. Two theories to explain the observed impairment in diaphragmatic function have been proposed:
1- A primary alteration in diaphragmatic contraction arises from local irritation, inflammation, surgical trauma, or pain. The finding that that external stimulation of the phrenic nerves produces normal maximum transdiaphragmatic pressures in patients who are recovering from upper abdominal surgery argues against this mechanism.
2-The currently favored theory is that diaphragmatic dysfunction results from reduced phrenic nerve output, although what causes diminished neural drive remains a matter of speculation. While general anesthesia is known to depress output from the central respiratory centers and to inhibit synaptic transmission, these effects are transient and modest.
The degree of dysfunction observed after upper abdominal surgery is not seen following general anesthesia with procedures that involve the lower abdomen or the extremities. An inhibitory arc initiated by abdominal nocioceptors for pain is unlikely, since achievement of adequate pain control by epidural opiates fails to improve pulmonary function or diaphragmatic performance consistently.
In contrast, epidural anesthetics like bupivacaine are associated with improved diaphragmatic function. Since these agents produce a sympathetic blockade in addition to pain control, it has been suggested that visceral sympathetic afferents may be responsible for providing an inhibitory signal that attenuates central neural drive and phrenic nerve activity. Supporting this notion of a reflex inhibitory arc is the demonstration in animal models that mechanical gall bladder stimulations strongly inhibit electromyographic activity and motion in the diaphragm.
Cardiac surgery has adverse effects on pulmonary function. Following coronary artery bypass grafting (CABG), lung volumes decrease by approximately 30 percent, and subsequent normalization may take several months. Lung function is more severely affected when internal mammary artery harvesting and grafting are performed. Hypoxemia is common following CABG, falling to a nadir of around 55 mm Hg (room air) on postoperative day two. Shunt fraction increases from 3 percent preoperatively to a peak of 19 percent postoperatively. Underlying the increase in shunt fraction is development of basilar atelectasis, which more pronounced on the left side.
A number of factors have been implicated in the development of post-CABG pulmonary dysfunction and atelectasis: surgical manipulation of the chest wall and resultant decreased chest wall compliance; intraoperative lung retraction and injury of the left lower lobe; intraoperative injury to the phrenic nerves, leading to diaphragmatic dysfunction; and cardiopulmonary bypass-associated development of atelectasis and acute lung injury.
Lung resection surgery has the potential to induce the greatest impairment in lung function. The magnitude of permanent loss in lung function resulting from resection of functioning lung parenchyma can be reliably estimated from preoperative quantitative radionuclide perfusion lung scans performed in conjunction with standard spirometry. In addition, factors in the perioperative period transiently magnify the degree of impairment.
The standard posterolateral thoracotomy incision involves rib retraction and resection, and transection of intercostal, latissimus dorsi, trapezius, and serratus anterior muscles. As a consequence of this extensive trauma to the chest wall, total respiratory compliance drops by as much as 75 percent, the work of breathing increases, and lung volumes decline out of proportion to the loss of functional lung. Following lobectomy or wedge resection via thoracotomy, FEV1 and FVC fall to 25 percent of preoperative values at one hour postoperatively and rise to only 30 percent at twenty-four hours. Use of the more limited muscle-sparing incision is associated with a far less profound impact on lung function.
Atelectasis
Both intraoperative and postoperative mechanisms contribute to the development and persistence of atelectasis. Compression atelectasis and resorption atelectasis are the primary intraoperative mechanisms that contribute to this perioperative pulmonary complication. The development of compression atelectasis is multifactorial to the cephalad displacement of the diaphragm into the thorax, the diaphragmatic dysfunction induced by the surgical manipulation of the thorax and abdomen, and differences in regional ventilation within the lungs during passive ventilation as compared to spontaneous ventilation. During spontaneous ventilation, the lower dependent portion of the diaphragm displaces the most, but after induction of general anesthesia with mechanical ventilation the upper, nondependent portion of the diaphragm is preferentially displaced. It is in the lower, dependent areas of the lungs where postoperative atelectasis tends to occur. Resorption atelectasis occurs as a result of two different mechanisms. It can result from resorption of gasses beyond an occluded airway. In the absence of an occluded airway it can also occur in areas of the lung with low ratios of ventilation compared to perfusion when gases with a high fraction of inspired oxygen are used. In these areas, the net uptake of oxygen into the bloodstream exceeds the efflux of carbon dioxide and the regional influx of ventilated gasses and resorption atelectasis results.
Postoperatively, splinting as a result of pain is a common mechanism contributing to atelectasis. Additionally, phrenic nerve injury complicating thoracic, esophageal, and cardiac surgery is an occasional cause. Mucus plugging of central airways, a problem encountered particularly in patients with weak, ineffective cough, may lead to atelectasis of a segment, lobe, or even an entire lung.
Pneumonia
Microaspiration of oropharyngeal secretions appears to be the predominant mechanism in the pathogenesis of postoperative and nosocomial pneumonia. A critical initiating event is colonization of the oropharynx with gram-negative aerobic bacilli, a process that typically occurs in response to serious illness or surgical stress.
Microaspiration of oropharyngeal organisms is facilitated by the presence of an endotracheal tube, postextubation swallowing dysfunction, and depressed consciousness. The stomach is an additional source of bacteria that may contribute to nosocomial pneumonia especially in patients on gastric acid suppressive medications. Gastroesophageal reflux permits bacteria-laden gastric contents to enter the respiratory tract, either directly or by first colonizing the oropharynx. The simple measure of maintaining patients in a semi-erect position has been shown to significantly reduce the incidence of pneumonia significantly.
Aspiration Pneumonitis
Aspiration occurs when the mechanisms of glottic closure and cough that normally protect the airway are compromised. Acidic gastric contents introduced into the airway are rapidly disseminated throughout the bronchial tree and lung parenchyma, producing an almost instantaneous chemical burn. In addition, acid aspiration triggers a delayed release of inflammatory cytokines and influx of neutrophils, resulting in injury to the alveolar-capillary membrane and accumulation of protein-rich edema fluid in the alveolar interstitium and airspaces. Surfactant is also depleted because of direct acid denaturation and diminished production, with resultant alveolar instability and atelectasis.
The magnitude of lung injury is directly related to the pH and volume of aspirated material. In animal models, a pH of less than 2.5 is necessary to produce lung injury. However, other non-acid constituents of gastric contents, such as bile, are also capable of inducing injury.
Transfusion-Related Acute Lung Injury (TRALI)
The most clearly identified mechanism of TRALI involves the transfusion of blood products containing leukoagglutinating antibodies. These antibodies are typically present in blood products donated by multiparous women who have been sensitized to foreign HLA or granulocyte antigens during pregnancy. When transfused into a recipient with these same antigens, the antibodies lead to leukoagglutination and activation of recipient granulocytes and monocytes within the pulmonary microvasculature, resulting in acute lung injury of varying severity.
A second mechanism implicated in the development of TRALI is the infusion of biologically active mediators derived from the breakdown of the cellular components of stored blood products.
Transfusion-Associated Circulatory Overload (TACO)
The mechanism by which TACO occurs is an increased hydrostatic pressure within the pulmonary vasculature as a result of increased blood and plasma volume due to blood product transfusion. This leads to the efflux of fluid from the capillaries, first into the pulmonary interstitial space and later into the alveolar space.
Exacerbation of Pre-existing Lung Disease
Bronchospasm, either in isolation or in in patients with asthma or COPD, is a common postoperative pulmonary complication, especially in patients with COPD undergoing thoracic surgery. There are many recognized precipitants of bronchospasm in the perioperative period, including laryngoscopy, both endotracheal intubation and extubation, airway suctioning, tracheal secretions, use of perioperative medications such as opioids that can increase histamine release, or reflex bronchoconstriction in response to the discontinuation of inhaled anesthetics.
The mechanisms leading to an exacerbation of underlying interstitial lung disease as a postoperative pulmonary complication are not known. Purported triggers include ventilator induced lung injury as a result of large intraoperative tidal volumes during mechanical ventilation, high concentrations of inspired oxygen associated, and/or ischemic/reperfusion injury in the setting of single lung ventilation during surgical lung biopsy.
Pleural Effusion
A variety of mechanisms may contribute to the development of pleural effusions during both abdominal or thoracic surgery. In all surgical settings, pleural effusions may result from hypervolemia as a result of intravenous fluid therapy and blood product transfusion in the perioperative period. In cases of abdominal surgery, atelectasis may also contribute as the atelectatic lung promotes a more negative local pleural pressure, thereby favoring the formation of pleural fluid in this space.
During and after abdominal surgery, free peritoneal fluid may also transgress small pores in the diaphragm producing a pleural effusion. Manipulation and irritation of the diaphragm during surgery also promotes the formation of a pleural effusion as pleural effusions are more common in upper abdominal as opposed to lower abdominal surgeries. Furthermore, when surgery within the abdomen has a localized laterality, pleural effusion formation is more common on the same side as the surgery.
Although most pleural effusions in the postoperative period are benign, a pleural effusion may be associated with a pneumonia (i.e. a parapneumonic effusion), a pulmonary embolus, or, uncommonly, a thoracic duct injury (i.e. chylothorax).
Phrenic Nerve Injury
In the past, cold cardioplegia placed in the pericardium to induce cardiac arrest in association with coronary bypass grafting and other cardiac procedures was a common cause of thermal injury to the phrenic nerves. While this technique has fallen out of favor, the phrenics are still vulnerable to injury from traction, ischemia, use of diathermy, and transection during sternal retraction and harvesting of the internal mammary arteries.
Phrenic nerve injury is not restricted to cardiac procedures; it is also seen in association with thoracic surgery, neck surgery, and liver transplantation.
Obstructive Sleep Apnea
OSA results from a combination of anatomical alterations to the upper airway that commonly accompany obesity and diminished neural tone of the pharyngeal musculature responsible for maintaining patency of the airway. The use of anesthetics, opioids, and sedatives in the surgical patient may provoke or exacerbate OSA by further diminishing the activity of the upper airway musculature, blunting arousal from sleep and diminishing the ventilatory response to hypercapnia. The impact of opiates and benzodiazapines on upper airway obstruction is out of proportion to the level of sedation and analgesia achieved.
Which individuals are at greatest risk of developing a postoperative pulmonary complication?
Risk factors for the development of general postoperative pulmonary complications are well established and are generally categorized into patient-related and procedural-related risk factors.
Patient-related risk factors for the development of postoperative pulmonary complications include COPD, age > 60 years, congestive heart failure, New York Health Association functional class of II or greater pulmonary hypertension, smoking, obstructive sleep apnea (OSA), low serum albumin < 3.5 g/dL, American Society of Anesthesiologists (ASA) class of II or greater, or at least partial functional dependence. Some of these merit additional explanation below.
Presence of COPD has been identified as an independent risk factor for postoperative respiratory failure. However, the exact relationship between severity of COPD, or specific preoperative pulmonary function parameters, and risk of postoperative respiratory failure have not been defined. The single exception to this generality is thoracotomy with lobectomy or pneumonectomy, for which a post-resection FEV1 ,defined as the volume of air that can be forced out of the lungs in 1 second after taking a full breath, under 40 percent of predicted is associated with a markedly increased risk of postoperative respiratory failure.
Smoking has been shown to be a risk factor for postoperative pulmonary complications in general and for prolonged mechanical ventilatory support in particular. Smoking does not appear to be simply a surrogate marker for COPD; rather, it poses a risk independent of the magnitude of pulmonary impairment.
American Society of Anesthesiologists (ASA) class of II or greater is associated with a substantial increased risk of postoperative pulmonary complications. In this categorization, with each increase in class from a patient with a mild systemic disease (class II) to a patient with systemic disease that is not incapacitating (III) to a patient with an incapacitating systemic disease that is a constant threat to life (IV), the risk increases.
Procedural-related risk factors include surgical site, length of surgery, emergent surgery, general anesthesia, type of neuromuscular blocker used, and ventilatory strategies during anesthesia. In general, the risk of postoperative pulmonary complications decreases the further the surgical procedural is located from the diaphragm. Head and neck, neurosurgical, aortic aneurysm repair, and vascular surgery also convey an elevated risk. Surgical procedures lasting longer than 3 to 4 hours and the use of pancuronium, a long acting neuromuscular blocker, are also associated with an increased risk of complications.
Acute Respiratory Failure
There are two indices or calculators validated to assist clinicians in quantifying a patient’s risk for postoperative pulmonary failure.
The Arozullah respiratory failure index was derived from a study of more than 81,000 patients undergoing elective or emergency non-cardiac procedures. In this study, the overall incidence of postoperative respiratory failure (usually defined as the need for mechanical ventilation beyond forty-eight hours) was 3.4 percent. This study, which identified a number of factors that are independently associated with increased risk (Table 1), derived a scoring system that predicted the likelihood of developing respiratory failure (Table 2). Risk factors identified in this and a multitude of other studies include procedures involving the thorax or upper abdomen, the surgical approach, the presence of COPD, and smoking.
Table 1:
Respiratory failure risk index
Table 2:
Respiratory Failure Index Scores and Predicted Probability of Post-Operative Respiratory Failure
Procedures involving the thorax or upper abdomen. In this category, thoracoabdominal aortic aneurysm repair carries the greatest risk. Other procedures associated with significant risk include abdominal aortic aneurysm repair, upper gastrointerstinal surgery, thoracotomy, and cardiac surgery.
Surgical approach. Use of a transverse abdominal incision carries lower risk than a vertical midline incision does, and laparoscopic surgery appears to be associated with considerably lower risk than conventional open procedures. For thoracic procedures, median sternotomy and muscle-sparing lateral thoracotomy are better tolerated than posterior thoracotomy. As an alternative to conventional cancer surgery, video-assisted thoracoscopic surgery (VATS) in association with wedge resection or segmentectomy appears to be well tolerated by patients with severe lung disease, with only a 4 percent incidence of respiratory failure in one series.
The second index, the Gupta calculator for postoperative respiratory failure, was derived from a dataset of over 200,000 patients in which 6,351 (3.1%) were identified as having postoperative respiratory failure. Logistic regression identified the type of surgery, emergency surgery, dependent functional status, preoperative sepsis, and higher ASA class as significant predictors of respiratory failure. This calculator may be accessed online to help clinicians calculate a patient’s individual risk.
Atelectasis
Factors that predispose to atelectasis include cardiac, thoracic, and abdominal procedures; splinting because of pain; mucus plugging; and phrenic nerve injury.
Pneumonia
The risk of postoperative pneumonia is greatest following standard thoracic and upper abdominal procedures, with an incidence of up to 20 percent in some series. In contrast, an incidence of about 5 percent has been reported in association with lower abdominal procedures. Other factors associated with an increased risk of postoperative pneumonia include low serum albumin level, presence of COPD, extensive smoking history, advanced age, and high-risk status according to the American Society of Anesthesiologists (ASA) rating scale. A direct relationship between duration of surgery and incidence of postoperative pneumonia has also been demonstrated.
Postoperative risk factors include presence of a nasogastric tube, immunosuppression, impaired consciousness, and witnessed aspiration. The most consistently identified risk factor is the need for prolonged mechanical ventilatory support.
Aspiration Pneumonitis
In the surgical patient, the period of maximal vulnerability for aspiration spans from the induction of general anesthesia to full return of consciousness postoperatively. A number of factors enhance the risk of aspiration, pre-eminent among them being depressed consciousness accompanying administration of anesthesia.
Insufflation of air into the stomach during induction may cause gastric distention and promote vomiting. Vomiting can also be induced by stimulation of the posterior oropharynx during intubation and extubation. Reflux of gastric contents is facilitated by medication-induced relaxation of the lower esophageal sphincter, placement of the patient in the supine position, and manipulation of the bowel during abdominal procedures.
At completion of surgery, extubation is commonly performed when the patient, while able to ventilate adequately, may not yet be able to fully protect the airway. Notably, upper airway reflexes remain significantly impaired for up to two hours after recovery from anesthesia. In addition, residual glottic dysfunction can persist for up to eight hours following removal of an endotracheal tube. Although the risk of aspiration diminishes beyond the immediate perioperative period, administration of narcotics poses a persistent risk, as these agents may induce vomiting and depress consciousness.
In a study of 215,000 general anesthetic procedures at the Mayo Clinic, the incidence of aspiration in the immediate perioperative period was 0.03 percent, but the incidence was nearly four times higher in the setting of emergency surgery. Predisposing factors, including intestinal obstruction, swallowing dysfunction, depressed mental status, esophageal surgery, and recent meal, were identified in more than half of the patients who aspirated. The majority of events occurred during insertion of the laryngoscope in preparation for intubation and during extubation.
Transfusion-Related Acute Lung Injury (TRALI)
The true risk of TRALI is difficult to ascertain because this entity is likely underdiagnosed. One study documented an incidence of 0.02 percent per unit and 0.16 percent per patient. Most cases are clustered in the immediate postoperative period when transfusions are frequently required to address blood loss that occurred during surgery.
The risk of TRALI is most closely linked to donor characteristics, rather than to those of the recipient. Use of blood products from female donors carries a significantly greater risk than does that from male donors, and the magnitude of risk is further dictated by the number of pregnancies the donor has undergone. In one study of critically ill patients, two recipient risk factors were also identified: sepsis and history of alcohol abuse.
The risk of TRALI may be greatest with transfusion of plasma-rich blood products (fresh frozen plasma, platelets), but virtually all blood products are capable of precipitating this reaction.
Transfusion-Associated Circulatory Overload (TACO)
Like TRALI, the incidence of TACO is difficult to ascertain as it too is likely underreported. The incidence may range as high as 1% to 8% of all patients receiving blood products. The strongest risk factors for the development of TACO include chronic renal failure, heart failure, number of blood products transfused, and fluid balance per hour.
Exacerbation of Pre-existing Lung Disease
Although bronchospasm in patients with asthma and COPD is a well recognized perioperative pulmonary complication, risk factors for exacerbations of the underlying illnesses of COPD and asthma have not been well studied. One study in patients with COPD who underwent partial lung resection for malignancy found an incidence of exacerbation approaching 50%. Risk factors for the development of exacerbation included male sex and increased GOLD stage classification of obstruction. Patients who developed an exacerbation demonstrated increased subsequent risk of an additional postoperative pulmonary complication, increased length of stay, and increased mortality.
Risk factors for perioperative exacerbations of patients with interstitial lung disease include emergent surgery, lung surgery, and longer anesthesia time. Thoracic surgeries, particularly open surgical lung biopsies and lung resection surgery, are associated with higher rates of exacerbation than abdominal surgeries.
Pleural Effusions
Pleural effusions may have an incidence approximating 50% in abdominal surgeries and are almost universal in post-coronary artery bypass graft surgery. In abdominal surgery, risk factors for the development of pleural effusions include upper vs lower abdominal surgery, the presence of atelectasis, and the presence of free abdominal fluid.
Phrenic Nerve Injury
Patients who undergo CABG are at greatest risk for phrenic nerve injury. Other cardiac procedures, lobectomy, lung transplantation, and liver transplantation also carry the risk of phrenic nerve injury.
Pulmonary Embolism
An increased risk of pulmonary embolism accompanies a number of surgical procedures, including upper abdominal, neurosurgical, cardiac, major urological, and lower extremity orthopedic procedures. Nonsurgical risk factors include obesity, immobility, underlying malignancy, and underlying thrombophilic state (e.g., Factor V Leiden mutation).
Obstructive Sleep Apnea
OSA is a common disorder, with moderate to severe disease encountered in up to 7 percent of the adult population. Studies have suggested that approximately 20 percent of the adults who present for elective non-upper airway surgery have OSA; the prevalence exceeds 70 percent in patients undergoing bariatric surgery.
Up to 80 percent of surgical candidates with OSA are undiagnosed prior to their surgical admission, so a high index of suspicion and a careful history and physical are essential in identifying patients at risk. Risk factors for OSA include obesity, older age, male sex, a neck circumference greater than seventeen inches for men and sixteen inches for women, and craniofacial abnormalities like retrognathia and macroglossia. A history of loud snoring, observed apneas, daytime hypersomnolence, and morning headaches also increases the likelihood of underlying OSA.
The risk of OSA-related complications in the postsurgical patient has been most closely linked to use of perioperative opioids.
What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
A number of laboratory studies are useful in determining the presence of common pulmonary complications in surgical patients:
Pneumonia
Leukocytosis is a nearly universal feature of pneumonia, but it is a nonspecific finding. Sputum or tracheal aspirate cultures may be helpful, but each can be contaminated by organisms that colonize the oropharynx and proximal airways.
Transfusion-Related Acute Lung Injury (TRALI)
Demonstration of the presence of leukoagglutinating antibodies in donor blood products provides strong evidence in support of a diagnosis of TRALI in the appropriate setting. Large published series demonstrate the presence of such antibodies in 70-85 percent of cases. Because of the cost and time involved, not all blood banks are willing to perform the necessary testing on donor blood products.
Transfusion-Associated Circulatory Overload (TACO)
A brain-natriuretic peptide (BNP) may be elevated in patients who develop pulmonary edema after blood product transfusion to assist in the diagnosis of carcinogenic pulmonary edema.
Pulmonary Embolism
A negative D-dimer test is helpful in excluding pulmonary embolism only in cases in which the pretest probability is low or moderate. The utility of the d-dimer in postoperative patients is also limited by the high prevalence of positive tests resulting from recent surgery.
An arterial blood gas is of limited value since hypoxemia and a widened arterial-alveolar oxygen gradient will not distinguish among the various other considerations in the differential diagnosis.
An electrocardiogram may be helpful and should be obtained. Sinus tachycardia is a nearly universal finding in patients with pulmonary embolism; its absence (assuming the patient is not on negative chronotropic medications) argues against the diagnosis. Occasionally, pulmonary embolism is heralded by new onset atrial fibrillation, but this rhythm is also commonly seen following cardiothoracic surgical procedures. An S1Q3T3 pattern or new right bundle branch block is indicative of right heart strain and is an important, albeit uncommon, clue to the possible presence of pulmonary embolism.
What imaging studies will be helpful in making or excluding the diagnosis of a postoperative pulmonary complication?
A variety of imaging studies may prove helpful in evaluating postoperative patients in whom there is concern about a pulmonary complication.
Pneumonia
A chest X-ray should be obtained in patients with suspected pneumonia. Demonstration of a new or worsening radiographic opacity suggests the possibility of pneumonia, but similar changes may also be caused by atelectasis, pulmonary edema, aspiration pneumonitis, or pulmonary infarction. Occasionally, a chest CT scan is necessary to demonstrate an opacity that is not apparent on chest X-ray.
Aspiration Pneumonitis
The presence of multifocal airspace opacities that are distributed predominantly in dependent areas of the lungs is strongly suggestive of aspiration, although the finding does not distinguish chemical pneumonitis from pneumonia.
Transfusion-Related Acute Lung Injury (TRALI)
TRALI is associated with the presence of pulmonary opacities on chest X-ray or chest CT, reflecting the presence of noncardiogenic pulmonary edema.
Transfusion-Associated Circulatory Overload (TACO)
Similar to TRALI, a chest X-ray or chest CT will demonstrate interstitial or alveolar opacities. The presence of pleural effusions, especially if bilateral, supports the diagnosis of cardiogenic pulmonary edema.
Exacerbations of Underlying Lung Disease
The absence of pulmonary edema or pleural effusions will aid in the diagnosis of an exacerbation of COPD or asthma by excluding other postoperative pulmonary complications.
Pleural Effusion
A small pleural effusion can be diagnosed on simple chest X-ray by blunting of the costo-phrenic angle(s). Larger pleural effusions will obscure increasing areas of a hemithorax on chest X-ray. In the setting of an opacified hemithorax, deviation of the trachea away from the opacification supports the diagnosis of a pleural effusion. Alternatively, if the trachea is deviated toward the opacified hemithorax the diagnosis of atelectasis is supported.
A lateral decubitus film can be obtained to evaluate for the presence of free flowing pleural fluid to help exclude a complicated pleural effusion (i.e. presence of loculations). Alternatively, ultrasonography or a chest CT can be used to further evaluate pleural effusions.
Phrenic Nerve Injury
Elevation of one or both hemidiaphragms, often with associated basilar atelectasis, is a common, but nonspecific, radiographic clue to the possible presence of phrenic nerve injury. Fluoroscopic inspection of diaphragmatic motion with tidal breathing and a “sniff” maneuver is often helpful in documenting diaphragmatic paralysis. Bedside ultrasound assessment of diaphragmatic motion is an increasingly popular alternative to fluoroscopy.
Pulmonary Embolism
Chest X-ray findings in pulmonary embolism are non-specific and include basilar atelectasis, small pleural effusions, and peripheral wedge-shaped infiltrates indicative of pulmonary infarcts. The chest X-ray is most suggestive of pulmonary embolism when it is normal or only minimally abnormal in the setting of severe hypoxemia. It is also potentially helpful in identifying other causes of hypoxemia and respiratory distress, such as pneumonia, pneumothorax, or ARDS.
Lower extremity venous ultrasonography is an important adjunct test that can be pursued easily at the bedside. Demonstration of a noncompressible vein is a highly sensitive and specific feature of proximal deep vein thrombosis. Documentation of a proximal deep vein thrombosis in a patient with suspected pulmonary embolism provides the necessary justification for initiating treatment and may obviate the need for more expensive and complex studies to demonstrate the presence of clot in the lung.
Bedside echocardiography is another potentially useful study, particularly in patients who are hypotensive. Evidence of a dilated right ventricle in the face of a normal or underfilled left ventricle should raise suspicion for massive pulmonary embolism.
Ventilation-perfusion lung scanning was previously the noninvasive diagnostic procedure of choice in evaluating suspected pulmonary embolism, but it has been largely supplanted by CT angiography (see below). Ventilation-perfusion lung scanning is still occasionally useful in patients with significant renal insufficiency, which precludes administration of intravenous contrast agent. Only when there is concordance between the pretest and the scan-assessed probability of pulmonary embolism can pulmonary embolism be excluded (low/low) or confirmed (high/high) with a high degree of certainty.
CT-angiography has emerged as the procedure of choice in the diagnosis of pulmonary embolism. Since it requires a significant intravenous contrast load, its use is problematic in patients with significant impairment in renal function. Interpretation requires a skilled reader, and results should be viewed in the context of the clinician’s assessment of pretest probability for pulmonary embolism. In this regard, a negative study in the setting of a high pretest probability or a positive study in the setting of a low pretest probability should prompt consideration of additional testing, such as pulmonary angiography.
What diagnostic procedures will be helpful in making or excluding the diagnosis of a postoperative pulmonary complication?
Additional diagnostic procedures are sometimes helpful in problematic cases.
Pneumonia
In intubated patients, bronchoscopy with bronchoalveolar lavage or use of a sheathed brush has been advocated as a means of accurately sampling the lower respiratory tract to ascertain the presence or absence of bacterial pathogens. However, false positive and false negative rates are in the range of 30 percent. If either technique is performed, it is essential to do so prior to the initiation of antibiotics.
Aspiration Pneumonitis
The diagnosis of aspiration pneumonitis is most firmly established in the setting of witnessed vomiting or recovery of gastric contents in the airways via suctioning or bronchoscopy. More often, the diagnosis is based on the presence of a compatible radiographic picture in a patient with risk factors.
Transfusion-Related Acute Lung Injury (TRALI)
See the section on laboratory studies, above.
Transfusion-Associated Circulatory Overload (TACO)
A transthoracic echocardiogram to evaluate heart function can help when cardioogenic pulmonary edema is suspected.
Pleural Effusions
Only selected pleural effusions in the postoperative setting require evaluation with a thoracentesis.
Pleural effusions are an almost universal finding in post-coronary artery bypass graft surgery. They only need to be further evaluated if the effusion is symptomatic, large (> 25% hemithorax), enlarging, or predominantly right sided. If any of these or a pleural effusion in the setting of fever or chest pain is present, a thoracentesis should be performed to evaluate for pleural infection, chylothorax, and hemothorax. Early post-coronary artery bypass graft surgery effusions are typically exudative per Light’s criteria, bloody, with neutrophilic and eosinophilic predominance. Pleural fluid triglycerides should be obtained to evaluate for a chylothorax and pleural fluid pH, glucose, and bacterial gram stain with culture should be obtained to evaluate for pleural infection.
Although pleural effusions may be complications in up to 50% of abdominal surgeries, in one study only approximately 10% were greater than 10 mm and amenable to a thoracentesis. Similar to post-coronary artery bypass graft surgery pleural effusions, a thoracentesis should only be performed when symptomatic, large or enlarging, or there is suspicion for pleural infection, hemothorax, or chylothorax.
Phrenic Nerve Injury
Electrophysiological testing may be performed in cases in which fluoroscopic or ultrasound assessment of diaphragmatic function is nondiagnostic. The phrenic nerve is stimulated transcutaneously in the neck, and the diaphragmatic electromyogram (EMG) is recorded using surface electrodes or by direct puncture of the diaphragm with a recording electrode.
Pulmonary Embolism
See the section on imaging studies, above.
Obstructive Sleep Apnea
Definitive diagnosis of OSA requires performance of overnight polysomnography in a sleep laboratory. Although an appropriate means of screening patients scheduled for elective surgery, this approach is impractical for assessing patients who require more urgent procedures and those who are already hospitalized and awaiting surgery. An alternative diagnostic approach that is increasingly available is use of portable polysomnography equipment for use in the home or at the patient’s bedside.
The most widely available study is overnight oximetry monitoring, where visual inspection of the tracing provides a simple, qualitative assessment of the presence and frequency of desaturations associated with sleep. Because of its lack of specificity, overnight oximetry is not recommended as a diagnostic tool for OSA, but its high sensitivity makes it useful in identifying a preoperative population at increased risk for OSA.
If you decide the patient has a postoperative pulmonary complication, how should the patient be managed?
A variety of therapeutic interventions should be considered in the management of postoperative pulmonary complications.
Atelectasis
Standard pulmonary toilet measures used to treat atelectasis include nebulized albuterol, chest percussion, incentive spirometry, and frequent suctioning of intubated patients.
Fiber-optic bronchoscopy (FOB) has a limited role in the treatment of serious postoperative atelectasis. In one classic study of the efficacy of FOB in this setting, FOB and chest physiotherapy were equally effective in treating atelectasis when an air bronchogram was absent on chest X-ray, presumably signifying proximal airway obstruction from mucus plugging. In contrast, the presence of an air bronchogram is associated with minimal response to either modality.
In the absence of proven superiority of the more invasive approach, simple pulmonary toilet measures should be considered the first-line approach to atelectasis. Bronchoscopy should be reserved for cases in which chest physiotherapy is contraindicated (e.g., chest trauma), poorly tolerated, or unsuccessful, and in instances in which severe hypoxemia demands immediate intervention (which, in many cases, should also include intubation and mechanical ventilation).
Pneumonia
Empiric treatment of nosocomial pneumonia consists of broad-spectrum antibiotics that cover Staphylococcus aureus (including methicillin-resistant strains) and gram-negative bacilli. The specific agents chosen should reflect the particular epidemiologic profile and microbiological susceptibility patterns at the clinician’s institution.
Aspiration Pneumonitis
Treatment of aspiration pneumonitis is supportive and includes correction of hypoxemia using supplemental oxygen and, in more severe cases, mechanical ventilation. Bronchoscopy is indicated only when large airway obstruction by food particles is suspected on the basis of a localized wheeze or lobar atelectasis. Because acid is disseminated and endogenously neutralized within seconds, large-volume bronchoalveolar lavage is ineffective in attenuating the degree of injury and is not recommended.
Studies on the role of systemic corticosteroids have been inconclusive, and use of these agents is not warranted.
Use of prophylactic antibiotics is generally discouraged, but they are often employed when there is diagnostic uncertainty as to whether the patient has a chemical pneumonitis or bacterial pneumonia. Since up to 40 percent of patients will develop a superimposed bacterial pneumonia after an aspiration event the clinician must remain vigilant for new fever, new or progressive radiographic opacities, and purulent sputum. Such findings should prompt initiation of broad-spectrum antibiotics.
Transfusion-Related Acute Lung Injury (TRALI)
Treatment of TRALI is supportive; management includes use of supplemental oxygen and, in more severe cases, mechanical ventilation to address hypoxemia.
Transfusion-Associated Circulatory Overload (TACO)
Treatment of TACO is primarily diuresis with the use of loop diuretics in addition to supportive measures with the use of supplemental oxygen.
Exacerbations of Underlying Lung Disease
Short-acting bronchodilators, primarily beta-2-agonists and also inhaled anticholinergics, are the mainstay of treatment for bronchospasm. Systemic corticosteroids may be necessary in more severe cases.
Management of patients with exacerbations of underlying interstitial lung disease is primarily supportive. The use of corticosteroids is common but evidence for efficacy is lacking.
Pleural Effusion
Most pleural effusions in the postoperative setting do not require treatment and will resolve spontaneously. However, if symptomatic, large or enlarging, or concern for a pleural infection, chylothorax, or hemothorax is present, a therapeutic thoracentesis is indicated.
Phrenic Nerve Injury
Patients with diaphragmatic dysfunction are generally well-suited to non-invasive, positive pressure ventilation if they are awake and are able to clear secretions from the respiratory tract effectively. In more severe cases, conventional mechanical ventilation is required. Selected patients with permanent diaphragmatic paralysis may derive symptomatic improvement form surgical plication of the diaphragm.
Pulmonary Embolism
Anticoagulation with heparin is the mainstay of therapy for stable patients without contraindications.
The presence of life-threatening hypoxemia or shock should prompt consideration of thrombolyic therapy, but its use in the postoperative period is limited by the risk of bleeding at the site of recent surgery. This risk appears to fall to an acceptable level beyond the seventh postoperative day, although the exception is intracranial surgery, which precludes use of thrombolytic agents for at least two months.
Several interventional radiology techniques–thrombus fragmentation, suction embolectomy, and intra-embolic infusion of low-dose thrombolytics–and surgical embolectomy are alternative considerations in unstable patients for whom thrombolytics are either contraindicated or unsuccessful.
Placement of a filter in the inferior vena cava should be considered as an adjunct for patients who are hemodynamically unstable and unable to handle additional clot burden, and for patients who have an absolute contraindication to anticoagulation.
Obstructive Sleep Apnea
Surgical candidates with known or suspected OSA should be handled by an anesthesiologist skilled in management of the difficult airway. Awake fiber-optic intubation is sometimes required, and extubation at the completion of surgery should be performed only when the patient is fully awake. Patients should be maintained in a semi-erect, rather than supine, position, as the latter tends to facilitate airway obstruction.
There should be a low threshold for applying a continuous positive airway pressure (CPAP) device following extubation and in the ensuing postoperative period, especially in patients who demonstrate frequent desaturations or apneas. CPAP should also be used at nighttime and with naps.
Opioids should be used with caution; use of non-narcotic analgesics may be helpful in reducing the need for opioids.
What is the prognosis for patients managed in the recommended ways?
The prognosis with postoperative pulmonary complications depends on the specific complication.
Pneumonia
Nosocomial pneumonia is associated with reported mortality rates of 20-50 percent.
Aspiration Pneumonitis
Most patients with aspiration pneumonitis demonstrate progressive radiographic and clinical improvement over several days. However, a subset of patients progress rapidly to ARDS or develop secondary bacterial pneumonias. Aspiration pneumonitis is the third leading cause of anesthesia-related deaths, accounting for 10-30 percent of fatal outcomes. It is a major cause of ARDS in the postsurgical patient. The overall mortality rate associated with massive aspiration approximates 30 percent and exceeds 50 percent in those with initial shock or respiratory arrest, secondary pneumonia, or ARDS.
Transfusion-Related Acute Lung Injury (TRALI)
TRALI tends to be self-limited in most cases, and it is typically characterized by rapid clearing of infiltrates and improved oxygenation within several days. However, a more protracted course of longer than one week may be seen in approximately 20 percent of patients. A mortality rate of 5-10 percent has been reported.
Transfusion-Associated Circulatory Overload (TACO)
TACO, like TRALI, is usually self-limited and improves with diuresis. However, it is associated with increased hospital length of stay and mortality.
Exacerbation of Underlying Lung Disease
Limited data exists regarding the prognosis of patients who experience a COPD exacerbation as a postoperative complication. One study demonstrated patients with COPD who experienced an exacerbation after lung resection for malignancy developed higher rates of additional postoperative pulmonary complications and demonstrated higher mortality compared to patients with COPD who did not experience an exacerbation.
Patients with interstitial lung disease, particularly patients with idiopathic pulmonary fibrosis, who experience an exacerbation of their disease have a poor prognosis. The mortality for a patient with IPF who experiences respiratory failure approaches 50%. Although the overall rate of an exacerbation in all patients with an ILD is small (2.1% in one study), mortality may approach 40%.
Pleural Effusions:
In general, pleural effusions in the postoperative setting are usually incidental findings of minimal clinical significance.
Phrenic nerve injury
The prognosis for full recovery of phrenic nerve and diaphragmatic function is highly favorable with thermal or traction injury, although recovery may take weeks to months.
Obstructive sleep apnea
Several studies have suggested that patients with OSA have a significantly higher rate of postoperative complications than do those without this disorder. The most common postoperative pulmonary complication in OSA is oxygen desaturation. Other reported complications include hypercapnia, increased reintubation rates, delirium, and increased length of stay. Notably, patients with OSA reported in these studies did not routinely receive CPAP postoperatively; rather, CPAP was often initiated only after a complication occurred. While it is assumed that routine use of CPAP postoperatively in all patients with OSA might mitigate the risks of complications, supporting data are lacking.
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.
