Version May 2024
INTRODUCTION — Respiratory complications are the most common major problem in the immediate postoperative period and the second most common problem requiring intervention (after nausea and vomiting) [1-3]. Etiologies are varied and can be due to abnormalities in the upper airway, lower airway, or lung parenchyma, as well as abnormalities of peripheral nerves and muscles that control breathing. Appropriate monitoring, early diagnosis, and timely management are critical since even potentially fatal respiratory compromise is usually reversible.
This topic will review monitoring, assessment, and management of respiratory problems in adults admitted to the post-anesthesia care unit (PACU). Evaluation of preoperative pulmonary risk, strategies to reduce postoperative pulmonary complications, and management of these complications after PACU discharge are presented separately.
●(See "Evaluation of perioperative pulmonary risk".)
●(See "Strategies to reduce postoperative pulmonary complications in adults".)
●(See "Overview of the management of postoperative pulmonary complications".)
The anesthetic and postoperative management of patients with chronic lung diseases are also discussed separately.
●(See "Anesthesia for adult patients with asthma", section on 'Postoperative management'.)
RESPIRATORY MONITORING AND RISK ASSESSMENT — Airway patency, respiratory rate, and peripheral oxygen (O2) saturation (SpO2) are assessed upon arrival in the post-anesthesia care unit (PACU), with subsequent continuous monitoring of respiratory rate and SpO2, and frequent reassessment of airway patency [4]. Neuromuscular function, mental status, cardiovascular function, temperature, pain, and nausea with vomiting are also assessed initially and periodically; these parameters may affect adequacy of respiration. (See "Overview of post-anesthetic care for adult patients".)
Intraoperative events relevant to the patient's postoperative respiratory status include problems with airway management, ventilation strategy, doses and timing of analgesic and anesthetic agents, and fluid administration. Patients at high risk for developing respiratory complications due to preexisting conditions, surgical procedure, or anesthetic factors are identified by noting the following (see "Strategies to reduce postoperative pulmonary complications in adults", section on 'Risk factors'):
●Patient-related risk factors – Preexisting risk factors include chronic obstructive pulmonary disease (COPD), asthma, obstructive sleep apnea (OSA), obesity, heart failure, pulmonary hypertension, upper respiratory tract infection, tobacco use, neuromuscular disorders, metabolic factors (eg, albumin <3 g/dL, blood urea nitrogen [BUN] >30 mg/dL), and higher American Society of Anesthesiologists (ASA) risk class (table 1).
●Procedure-related risk factors – Risk is increased with thoracic or upper abdominal surgery close to the diaphragm since pulmonary function may be affected [5,6]. Ear, nose, and throat procedures may cause upper airway obstruction, while intracranial procedures may cause altered mental status with resultant hypoventilation or pulmonary aspiration. Other factors that confer risk are severe incisional pain resulting in voluntary restriction of respiratory effort, fluid resuscitation with large volumes, and procedure duration >3 hours.
●Anesthetic risk factors – Patients who had general anesthesia (GA) are more likely to have postoperative pulmonary complications than those who had neuraxial or other regional anesthetic techniques [7,8]. Administration of neuromuscular blocking agents (NMBAs) during GA is a common risk factor due to incomplete reversal [3,9-13]. Administration of opioids may cause respiratory depression [14]. (See 'Opioids and anesthetic agents' below and 'Neuromuscular blocking agents' below.)
INITIAL APPROACH TO RESPIRATORY INSUFFICIENCY — Prompt assessment and management are required for patients who develop respiratory insufficiency to avoid potentially fatal complications.
Signs and symptoms — Clinical features vary because of the variety of conditions that may cause respiratory insufficiency in the immediate postoperative setting. Symptoms and signs are not sensitive or specific.
An awake extubated patient may complain of difficulty breathing or hoarseness. However, symptoms may be mild or absent in a sedated patient. Signs of respiratory insufficiency include:
●Tachypnea (respiratory rate >30 breaths per minute [bpm]), shallow respirations, and/or labored breathing (eg, nasal flaring, use of accessory respiratory muscles with intercostal indrawing and suprasternal or supraclavicular retractions), indicating increased work of breathing and inadequate ventilation. Respiratory arrest may occur when the patient is unable to maintain the increased respiratory effort.
●Bradypnea (respiratory rate <8 bpm) or periods of apnea indicating respiratory depression (typically due to opioids or residual effects of other agents used to produce sedation and/or general anesthesia). (See 'Opioids and anesthetic agents' below.)
●Peripheral arterial oxygen (O2) saturation (SpO2) <93 percent indicating hypoxemia. This may be accompanied by a bluish discoloration of skin and mucous membranes, as well as abnormal breath sounds such as stridor or wheezing. Frank cyanosis does not develop until the level of deoxyhemoglobin reaches 5 g/dL, which corresponds to SpO2 of approximately 67 percent [15]. Provision of supplemental O2 which is common in the immediate postoperative period may prevent decreased SpO2 and cyanosis, thereby delaying recognition of hypoventilation. (See "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure".)
●Anxiety, confusion, or agitation may be caused by hypoxemia and/or hypercapnia. Severe hypoxemia and/or hypercapnia may result in somnolence or obtundation; eventually, myoclonus, seizures, or cardiac arrest may occur.
●Tachycardia and hypertension may be due to sympathetic discharge (ie, "stress response") resulting from hypoxemia and/or hypercapnia. Severe hypoxemia and hypercapnia with acidosis may result in hypotension, bradycardia, or malignant arrhythmias.
Initial assessment — Initial assessment of severity and probable causes of respiratory insufficiency includes a targeted examination, arterial blood gases, and chest radiograph. Risk factors for specific causes of respiratory problems are reviewed. (See 'Respiratory monitoring and risk assessment' above.)
Simultaneously, O2 administration, urgent airway management, and other measures are instituted for life-threatening situations. (See 'Stabilization' below and "Advanced cardiac life support (ACLS) in adults".)
●Is the upper airway patent? – Severe compromise of airway patency requires immediate intervention. (See 'Upper airway obstruction' below.)
Signs of upper airway obstruction and inadequate gas exchange include intercostal and suprasternal retractions, and discoordinated abdominal and chest wall motion during inspiration. Complete upper airway obstruction may be silent, whereas partial obstruction is accompanied by snoring if it is above the larynx or inspiratory stridor if the obstruction is perilaryngeal. The neck and chest are auscultated to distinguish stridor from wheezing; stridor is more prominent over the neck than the chest and is more clearly heard on inspiration than expiration.
●Is there evidence of lower airway or pulmonary pathology on auscultation? – Auscultation of the chest may reveal generalized wheezing due to restriction of air flow below the level of the trachea, typically caused by bronchospasm. However, wheezing may be absent due to very limited air movement in a patient with severe bronchospasm. (See 'Bronchospasm' below.)
A localized wheeze heard on chest auscultation may indicate lower airway obstruction by a mucous plug or foreign body. (See 'Secretion clearance' below and 'Foreign body' below.)
Rales on lung auscultation typically indicate pulmonary edema or atelectasis. Aspiration pneumonitis may present as diffuse crackles. Prominent coarse rhonchi are typically due to airway secretions; these may disappear after coughing, suggesting that the secretions can be effectively cleared. (See 'Pulmonary edema' below and 'Aspiration pneumonitis' below and 'Atelectasis' below and 'Secretion clearance' below.)
●Is the patient obtunded? – Depressed level of consciousness due to opioids, residual anesthetic agents, or a neurologic complication may result in hypoventilation with hypercapnia and hypoxemia which further depresses consciousness. (See 'Central and peripheral nervous system abnormalities' below and "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure", section on 'Clinical features of hypercapnia'.)
Arterial blood gas (ABG) analysis is performed in patients with suspected respiratory insufficiency as soon possible, to determine the presence and severity of abnormal gas exchange (eg, hypoxemia, hypercapnia) and metabolic abnormalities (eg, acidosis). (See "Arterial blood gases", section on 'Interpretation'.)
A chest radiograph obtained at the bedside may reveal:
●Pneumothorax (see "Clinical presentation and diagnosis of pneumothorax", section on 'Diagnostic imaging')
●Pulmonary edema (see "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Chest radiograph')
●Pneumonitis (see "Aspiration pneumonia in adults", section on 'Diagnosis')
●Airway foreign body (see "Airway foreign bodies in adults", section on 'Imaging')
●Atelectasis or pneumonia (see "Radiologic patterns of lobar atelectasis" and "Overview of the management of postoperative pulmonary complications", section on 'Pneumonia')
Stabilization
Supplemental oxygen — Supplemental O2 is immediately provided while assessing potential causes and severity of respiratory insufficiency (table 2). If hypoxemia is not adequately treated with delivery of supplemental O2 by conventional delivery systems, options include a nonrebreather face mask or humidified high-flow O2 delivered via nasal cannulae (HFNC) at up to 60 L/minute. HFNC is employed in selected patients to achieve adequate oxygenation as well as to facilitate ventilation [16-18]. A 2017 meta-analysis noted that O2 delivered via HFNC was as effective as noninvasive positive pressure ventilation (NIV) for avoidance of intubation and mechanical ventilation (3881 patients; 18 studies); however, the majority of studies included were did not involve the immediate postoperative period [19]. Further studies describing the use of HFNC in the post-extubation setting and in medical patients with severe hypoxemic respiratory failure are provided separately:
●(See "Continuous oxygen delivery systems for the acute care of infants, children, and adults".)
Ventilatory support — If necessary, ventilatory support with bag-mask positive pressure ventilation is initiated. (See "Basic airway management in adults", section on 'Bag-mask ventilation'.)
Endotracheal intubation or reintubation and controlled mechanical ventilation may be necessary in some circumstances (algorithm 1). All necessary airway equipment for reintubation should be immediately available in the PACU. Surgical support is typically available in case emergency cricothyrotomy or tracheostomy becomes necessary. (See "Airway management for induction of general anesthesia" and "Management of the difficult airway for general anesthesia in adults" and "Emergency cricothyrotomy (cricothyroidotomy) in adults".)
NIV should be initiated early, rather than waiting until there is evidence of severe respiratory failure, which may avoid the need for reintubation (table 3) [20-23]. In a 2015 meta-analysis of use of NIV treatment for patients with evidence of acute respiratory failure (ARF) after upper abdominal surgery, continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP) reduced the need for reintubation (risk ratio [RR] 0.25, 95% CI 0.08-0.83) and length of stay in the ICU (approximately two days) compared with standard O2 and medical therapy (two trials; 269 participants) [22]. Similarly, a 2021 review noted that CPAP improves oxygenation and reduces the need for reintubation and mechanical ventilation, as well as reducing apnea, hypopnea frequency, and related hypoxemia after surgery [24]. Older systematic reviews of NIV prophylaxis or treatment of respiratory failure after a variety of surgical procedures came to similar conclusions [20,25]. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications" and "Extubation management in the adult intensive care unit", section on 'Patients at high risk of postextubation respiratory failure'.)
Patients who used preoperative CPAP (eg, patients with obstructive sleep apnea [OSA]) should resume this therapy at the previously prescribed level shortly after arrival in the PACU if there are no contraindications [26]. The CPAP mask may not be appropriate to use on a patient who has undergone repair of facial fractures or other facial surgery. In addition, we also generally avoid NIV after esophageal or gastric resections due to the risk of insufflating a newly created gastroesophageal, gastroduodenal, or gastrojejunal anastomosis. Nevertheless, systematic reviews and case series have reported successful use of NIV after esophagectomy, Roux-en-Y gastric bypass, gastrectomy, or pancreaticoduodenectomy, without evidence of increased anastomotic disruption [22,27,28]. When NIV is selected following esophageal or gastric procedures, low levels of inspiratory pressure are used, with breaks for gastric decompression and careful monitoring for leakage.
Patients receiving NIV are continuously monitored, with reassessment of respiratory status within one to two hours. Those with improving clinical status and gas exchange may continue NIV in the PACU or another monitored setting. Patients who fail to respond within two hours are reintubated with initiation of mechanical ventilation. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) with hypercapnic respiratory acidosis' and "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease", section on 'Failure of noninvasive ventilation'.)
Secretion clearance — Administered O2 should be humidified whenever possible to prevent obstruction of smaller airways by dried secretions. In patients with pain, sedation, or general debilitation limiting ability to effectively cough and expel secretions, oral or nasotracheal suctioning clears tracheal secretions and stimulates coughing. (See "Overview of the management of postoperative pulmonary complications", section on 'Abundant respiratory secretions'.)
Rarely, flexible bronchoscopy with suctioning of the airways may be necessary when secretions, thick mucus plugs, or other foreign bodies interfere with adequate ventilation and/or oxygenation. (See "Flexible bronchoscopy in adults: Indications and contraindications", section on 'Indications'.)
UPPER AIRWAY OBSTRUCTION — Upper airway obstruction can occur in the pharynx, larynx, or large airways. Specific treatment typically confirms the diagnosis and stabilizes the patient.
The following diagnoses are considered in patients with signs of upper airway obstruction in the immediate postoperative period (see 'Initial assessment' above):
Pharyngeal muscular weakness — Residual effect of longer-acting neuromuscular blocking agents (NMBAs) is the most common cause of upper airway obstruction in the post-anesthesia care unit (PACU) [9-11]. This can occur even if reversal agents were administered (eg, neostigmine [with glycopyrrolate] or sugammadex), although such reversal diminishes the likelihood of residual weakness [10,12,29]. Whether choice of the reversal agent affects risk for postoperative pulmonary complications is unclear [30-32]. Detailed discussion of strategies to avoid residual neuromuscular blockade, including reversal of the effects of NMBAs, is available elsewhere. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Avoidance of residual neuromuscular blockade' and "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Reversal of neuromuscular block'.)
Other factors that may contribute to pharyngeal muscle relaxation include the effects of opioids, volatile anesthetics, or other agents with sedative properties [3].
Residual paralysis of pharyngeal muscles (or their relaxation during sleep) causes the base of the tongue and the tissues of the posterior oropharynx to move toward each other, obstructing the supraglottic inlet. As the patient attempts to draw in air, negative pressure generated in the thorax brings the pharyngeal tissues even closer together, further obstructing the airway. Absence of airflow into the trachea manifests as retraction at the sternal notch and paradoxical motion of the abdominal musculature. Severe upper airway obstruction results in oxygen (O2) desaturation, atelectasis, and respiratory failure. This is more likely in patients with obesity, obstructive sleep apnea (OSA), or tonsillar or adenoidal hypertrophy because of excess pharyngeal or nasal soft tissue.
Simple maneuvers may be effective (eg, a chin lift or jaw thrust to bring both the mandible and the base of the tongue forward, thus opening the inlet to the posterior oropharynx, or lateral decubitus positioning). Oropharyngeal or nasopharyngeal airways are useful adjuncts. Nasopharyngeal airways are better tolerated than oral airways at light levels of sedation because of lesser risk of provoking a gag reflex; however, they must be carefully inserted to avoid bleeding from the nasal passages. Such airway support devices are left in place until complete recovery from anesthesia is complete. (See "Basic airway management in adults", section on 'Airway obstruction'.)
Subsequent treatment in selected patients (eg, those with OSA or obesity) includes use of continuous positive airway pressure (CPAP) administered via a facemask. Occasionally, patients require reintubation [3]. (See "Anesthesia for the patient with obesity", section on 'Post-anesthesia care unit management'.)
Laryngospasm — Laryngospasm is a prolonged exaggeration of the glottic closure reflex due to stimulation of the superior laryngeal nerve. Although the cords are adducted, the primary obstruction is caused by tonic contraction of the laryngeal muscles and descent of the epiglottis over the laryngeal inlet.
Onset of laryngospasm may occur abruptly after extubation in a patient who is not awake enough to counteract laryngeal reflexes in response to vocal cord irritation due to endotracheal tube removal, secretions, blood, or a foreign body in the upper airway. Laryngospasm can also occur upon cessation of positive pressure ventilation via face mask, presumably due to sudden airway collapse. Partial laryngospasm allows for some air movement and may be difficult to distinguish from other causes of upper airway obstruction. Complete laryngospasm prevents all air movement and may result in severe hypoxemia or negative pressure pulmonary edema.
Simple maneuvers such as a chin lift or jaw thrust are not effective. Treatment of laryngospasm consists of removing the noxious stimulus (eg, by suctioning blood or secretions) and employing positive pressure bag-mask ventilation concurrent with a jaw thrust maneuver [33]. Also, applying pressure with fingertips to the "laryngospasm notch," which is the area between the mastoid process, the ramus of the mandible, and the base of the skull (also known as "Larson’s maneuver") (picture 1) may rapidly reverse laryngospasm [34-36].
If these measures are not successful, a small dose of succinylcholine (0.1 mg/kg IV) is administered by the anesthesia provider to relax the cords. In some patients, it may be necessary to administer an induction agent and an intubating dose of a NMBA to facilitate emergency endotracheal intubation. (See "Rapid sequence intubation in adults for emergency medicine and critical care".)
Airway edema — Risk factors for airway edema include airway or major neck surgery, decreased venous drainage due to prolonged head-down or prone positioning, and large volumes of fluid resuscitation [37]. Although facial and scleral edema may be present in these patients, visible external signs indicating pharyngeal and/or laryngeal edema may be absent. Also, patients who have had multiple or traumatic intubation attempts may develop pharyngeal or laryngeal edema. (See "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients", section on 'Laryngeal injury'.)
For patients with airway edema and none of the risk factors noted above, other causes such as angioedema or anaphylaxis are considered. Angioedema may occur in the perioperative setting due to latex, radiocontrast agents, fibrinolytic agents, calcium channel blockers, opioids, or nonsteroidal antiinflammatory drugs (NSAIDs) (table 4). Treatment of angioedema includes parenteral administration of antihistamines and corticosteroids. Anaphylaxis is treated with epinephrine. (See "An overview of angioedema: Clinical features, diagnosis, and management", section on 'Angioedema in or near the airway' and "Anaphylaxis: Emergency treatment".)
If airway edema is suspected in a patient who remains intubated, an endotracheal tube cuff leak test can be performed during spontaneous ventilation [38,39]. During the cuff leak test, simultaneous direct or video-assisted fiberoptic laryngoscopy enhances detection of laryngeal edema [40]. If the cuff leak is absent or laryngoscopic evidence of edema is present, the endotracheal tube should remain in place. The head is elevated to facilitate venous drainage. A short course of glucocorticoid therapy is also typically administered. Extubation is reconsidered when an air leak around the endotracheal tube becomes apparent. Details regarding the cuff leak test and management of airway edema are available elsewhere. (See "Extubation management in the adult intensive care unit", section on 'Assess risk for postextubation stridor'.)
In extubated patients with mild to moderate symptoms of airway edema, treatment with continuous administration of nebulized epinephrine may avoid the need for reintubation. A diuretic may be administered if fluid overload is suspected to be a contributing cause. Rarely, inhaled heliox is employed to reduce turbulent flow in large airways. (See "Physiology and clinical use of heliox", section on 'Use in adults'.)
Reintubation may be necessary if symptomatic laryngeal edema persists.
Foreign body — Aspiration of a foreign body may cause severe airway obstruction [41,42]. Aspiration is suspected when there is a possibility of retained surgical packs or instruments, dislodged teeth or dentures, or if the cause of upper airway obstruction remains obscure. Relevant data regarding the aspirated foreign body, including the size and shape of the object, location and extent of the obstruction, and stability of the object within the airway may be unknown. Although a chest radiograph may be helpful, a normal radiograph does not necessarily exclude this diagnosis [41,42]. (See "Airway foreign bodies in adults", section on 'Imaging'.)
Direct oropharyngeal laryngoscopy can often identify and retrieve the foreign body. If this is not possible, rigid or fiberoptic bronchoscopy is employed. Although some cooperative patients can tolerate fiberoptic bronchoscopy with local anesthesia, general anesthesia is typically required [43]. An anesthetic induction that maintains spontaneous ventilation is often selected to avoid converting a partial obstruction to a full obstruction. If rigid bronchoscopy is necessary, controlled ventilation using an intravenous anesthetic technique provides optimal conditions. Emergency cricothyrotomy or tracheostomy may be necessary if complete airway obstruction occurs. (See "Airway foreign bodies in adults", section on 'Foreign body removal'.)
After removal of a foreign body, the patient is observed for signs of airway edema or respiratory compromise. (See "Airway foreign bodies in adults", section on 'Follow-up'.)
Vocal cord paralysis — Vocal cord paralysis due to unilateral or bilateral recurrent laryngeal nerve injury can occur after otolaryngologic surgery, thyroidectomy, parathyroidectomy, surgery of the aortic arch or its branches or rigid bronchoscopy [44]. In addition, an inflated endotracheal tube cuff in the subglottic larynx can compress the anterior branch of the recurrent laryngeal nerve between the cricoid and thyroid cartilage, resulting in nerve injury [45].
Injury to the recurrent laryngeal nerve prevents abduction of the ipsilateral vocal cord, which becomes fixed in a paramedian position because of the unopposed action of the cricothyroid muscle. Also, arytenoid avulsion during intubation can result in unilateral vocal cord immobility [46]. Vocal cord paralysis is typically temporary and resolves spontaneously over a period of days to months, unless frank nerve transection has occurred.
In the immediate postoperative period, unilateral paralysis is often asymptomatic. Hoarseness is typically noted immediately after extubation. The resulting increased airway resistance is often tolerated by healthy patients but may create difficulty for patients with pre-existing pulmonary comorbidity. Before discharge from the PACU, otolaryngologic evaluation is warranted if vocal cord paralysis or injury is suspected or confirmed [47].
Bilateral recurrent laryngeal nerve injury can present in much the same way as laryngospasm. Diagnostic laryngoscopy reveals that the vocal cords are in apposition at the midline. Attempted intubation in this setting is traumatic and often unsuccessful. Emergency tracheostomy is the appropriate initial intervention [47,48].
Cervical hematoma — Hematoma formation compressing the upper airway may occur after carotid endarterectomy, thyroidectomy, parathyroidectomy, or other neck surgery. A retropharyngeal hematoma may occur after anterior cervical spine surgery [49]. Although many neck hematomas can be treated conservatively, the patient should be closely monitored for signs of airway compromise. A rapidly expanding hematoma may cause supraglottic edema due to venous and lymphatic congestion or may cause tracheal deviation or directly compress the tracheal lumen below the level of the cricoid cartilage [50]. Although symptoms may be absent until the lumen is <5 mm, compression may rapidly become life-threatening, resulting in a need for emergency airway management and reoperation.
Emergency reintubation may be difficult due to marked tracheal deviation, laryngeal edema, and a small tracheal lumen [51]. Visualization of upper airway anatomy may be further complicated by multiple intubation attempts resulting in oropharyngeal and laryngeal edema or bleeding. The American Society of Anesthesiologists (ASA) has developed guidance for airway management in this setting, as noted in the table (table 5). (See "Anesthesia for adult trauma patients", section on 'Airway management'.)
In many cases (eg, rapid expansion of a neck hematoma), the neck incision should be reopened and hematoma decompressed before attempting reintubation. If not in extremis, the patient is immediately returned to the operating room, where the neck is prepped and draped, sutures or staples are removed under sterile conditions, and the hematoma is evacuated from the wound. Sponges are placed into the wound and pressure is applied by the surgeon to control bleeding during endotracheal intubation, followed by neck reexploration and definitive control of bleeding sites. Rarely, complete airway obstruction necessitates emergency cricothyrotomy or tracheostomy.(See "Complications of carotid endarterectomy", section on 'Cervical hematoma'.)
Obstructive sleep apnea — Airway obstruction due to obstructive sleep apnea (OSA) should be considered in those who carry the diagnosis, as well as in patients with obesity and others with positive OSA screening tests since undiagnosed OSA is prevalent in adult surgical patients. [52,53]. (See "Surgical risk and the preoperative evaluation and management of adults with obstructive sleep apnea", section on 'Screening with a questionnaire'.)
Postoperative management of OSA is discussed separately (algorithm 2). (See "Postoperative management of adults with obstructive sleep apnea".)
LOWER AIRWAY AND PULMONARY COMPLICATIONS — Lower airway or pulmonary complications may result in increased work of breathing or evidence of hypoxemia or hypercarbia, including desaturation (peripheral arterial oxygen [O2] saturation <93 percent) evident on pulse oximetry, with confirmation on arterial blood gas. (See 'Initial assessment' above.)
Auscultation of the lungs may reveal generalized wheezing indicating bronchospasm, rales consistent with pulmonary edema, or crackles which may indicate aspiration pneumonitis. (See 'Initial assessment' above.)
Bronchospasm — Postoperative bronchospasm may occur in patients with chronic obstructive pulmonary disease (COPD) or asthma or may be due to aspiration or an allergic reaction [54,55]. Management of bronchospasm and/or anaphylaxis in the post-anesthesia care unit (PACU) is the same as management in the operating room (table 6). (See "Anesthesia for adult patients with asthma", section on 'Intraoperative bronchospasm' and "Perioperative anaphylaxis: Clinical manifestations, etiology, and management".)
A patient who received intraoperative treatment for severe intraoperative bronchospasm may require a period of postoperative controlled ventilation in the PACU. Similarly, noninvasive ventilation may be beneficial after extubation of a patient with COPD or asthma. (See "Anesthesia for adult patients with asthma", section on 'Postoperative management' and "Anesthesia for patients with chronic obstructive pulmonary disease", section on 'Management of postanesthesia care'.)
Pulmonary edema — Postoperative pulmonary edema may be cardiogenic or noncardiogenic. (See "Overview of the management of postoperative pulmonary complications", section on 'Pulmonary edema'.)
●Cardiogenic pulmonary edema – Cardiogenic pulmonary edema may occur in patients with a history of chronic left or right heart failure, particularly those who had intraoperative myocardial ischemia, fluid overload, or prolonged unfavorable surgical positioning (eg, supine positioning of a patient who cannot tolerate this position while awake). Treatment is discussed separately. (See "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Postoperative management' and "Treatment of acute decompensated heart failure: Specific therapies".)
●Noncardiogenic pulmonary edema – Noncardiogenic pulmonary edema may develop in an otherwise healthy patient due to airway obstruction resulting from laryngospasm, pharyngeal obstruction, or biting that clamps off the endotracheal tube, resulting in negative pressure pulmonary edema. Rarely, flash pulmonary edema is caused by naloxone administration for narcotic reversal. (See 'Opioids and anesthetic agents' below.)
Treatment of noncardiogenic pulmonary edema is supportive with administration of supplemental O2, as well as diuretics if appropriate. Reintubation may be necessary if oxygenation is severely impaired, but a trial of noninvasive continuous positive airway pressure is appropriate if there are no contraindications. (See "Overview of the management of postoperative pulmonary complications", section on 'Pulmonary edema' and 'Ventilatory support' above.)
Aspiration pneumonitis — Chemical pneumonitis may occur during the perioperative period due to aspiration of acidic gastric contents. Anesthetic agents depress airway protective reflexes, which predisposes patients to aspiration. Although risk is highest during induction of anesthesia with endotracheal intubation and with extubation during emergence, aspiration may also occur in the immediate postoperative period [56,57].
Witnessed aspiration is treated with lateral head positioning and suctioning of the oropharynx [58]. Patients with mild or uncertain aspiration are monitored for development of coughing, diffuse crackles on lung auscultation, bronchospasm (treated with bronchodilators), or signs of inadequate oxygenation (treated with supplemental O2) [59]. If severe, mechanical ventilatory support with positive end-expiratory pressure may be necessary. Patients without signs or symptoms within two hours of suspected aspiration are unlikely to develop pulmonary complications [57]. (See "Overview of the management of postoperative pulmonary complications", section on 'Chemical pneumonitis'.)
Tension pneumothorax — Tension pneumothorax is suspected in patients with chest pain, dyspnea, tachypnea, hypoxemia, hypotension, distended neck veins, tracheal deviation, or risk factors that include attempted or actual central line insertion, surgery in the neck or thorax, or chronic lung disease. A standard thoracostomy tube (24 or 28 Fr) is inserted if equipment and personnel are immediately available; otherwise needle thoracostomy should be emergently performed, followed by chest tube placement as soon as possible. (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children", section on 'Tension pneumothorax'.)
Pulmonary embolism — Pulmonary embolism is suspected in patients with acute onset of shortness of breath, hypoxemia, hypotension, and tachycardia. Management is discussed separately. (See "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults".)
Atelectasis — When mild to moderate hypoxemia is thought to be due to atelectasis, treatment is supportive, including adequate analgesia to facilitate deep breathing and coughing [60]. If indicated, noninvasive ventilation techniques may be initiated to prevent or treat atelectasis. (See "Overview of the management of postoperative pulmonary complications", section on 'Atelectasis'.)
Preexisting pneumonia — New onset of postoperative pneumonia rarely occurs in the immediate postoperative period. However, hypoxemia typically worsens in patients with preexisting pneumonia due to the effects of general anesthesia and surgery [61]. Management of postoperative pneumonia is discussed separately. (See "Overview of the management of postoperative pulmonary complications", section on 'Pneumonia'.)
CENTRAL AND PERIPHERAL NERVOUS SYSTEM ABNORMALITIES — Central hypoventilation associated with hypoxemia and hypercapnia may occur in postoperative patients with a depressed level of consciousness due to residual anesthetic drug effects or a neurologic complication [13]. Hypoventilation may also be due to residual peripheral neuromuscular weakness in the post-anesthesia care unit if reversal of neuromuscular blocking agents (NMBAs) was inadequate [9-13]. Hypothermia may exacerbate a depressed level of consciousness and/or residual neuromuscular blockade [13]. (See "Delayed emergence and emergence delirium in adults", section on 'Delayed emergence'.)
Opioids and anesthetic agents — Opioids, benzodiazepines, and most general anesthetic agents have synergistic effects which may cause excessive sedation in the PACU [62]. Because most patients are receiving supplemental oxygen (O2), monitoring of peripheral O2 saturation (SpO2) is an insensitive indicator of hypoventilation [4,63]. Increasing supplemental O2 may worsen hypoventilation and hypercapnia. (See "Delayed emergence and emergence delirium in adults", section on 'Consider prolonged drug effects'.)
●Opioids – Opioid analgesics administered in the intraoperative and/or postoperative periods cause dose-dependent respiratory depression. Postoperative SpO2 <95 percent is common [64-68]. Significant hypoventilation is treated with frequent stimulation to encourage adequate ventilation. If necessary, positive pressure ventilation may be temporarily employed. (See "Perioperative uses of intravenous opioids in adults: General considerations", section on 'Prevention and management of adverse opioid effects'.)
If opioid overdose is determined to be the most likely cause of heavy sedation and persistent bradypnea, particularly if reintubation may be necessary, low doses of naloxone 40 to 80 mcg may be administered (table 7). In most patients, titration of such low doses of naloxone will safely reverse opioid effects while preserving some analgesia. However, sudden reversal of analgesic effects may cause extreme discomfort and a sympathetic surge resulting in hypertension, tachycardia, and myocardial ischemia in susceptible patients. Rarely, flash pulmonary edema can occur after a large dose of naloxone [11]. (See "Acute opioid intoxication in adults", section on 'Management' and 'Pulmonary edema' above.)
●Other anesthetic agents – In addition to opioid effects, hypoxemia in the PACU may be due to residual and synergistic effects of other anesthetic agents. For example, although dexmedetomidine is often used to provide sedation with minimal respiratory depression during surgical procedures, case reports have noted delayed respiratory depression after its use [69]. Depression of the hypercapnic drive may lead to CO2 narcosis and worsening obtundation. There are no reversal agents for IV sedative-hypnotic agents or volatile anesthetic agents. Patients are stimulated frequently to encourage adequate ventilation or stabilized with ventilatory support until the drug effects wear off. (See "Delayed emergence and emergence delirium in adults", section on 'Consider prolonged drug effects'.)
Oversedation caused by benzodiazepines is uncommon in the perioperative setting since the most commonly used agent, midazolam, has a brief duration. In rare cases, IV flumazenil may be administered (table 7). (See "Benzodiazepine poisoning", section on 'Role of antidote (flumazenil)'.)
Neuromuscular blocking agents — In patients who received an NMBA during general anesthesia, signs of postoperative residual neuromuscular blockade include spasmodic twitching, generalized weakness, shallow breathing, upper airway obstruction due to pharyngeal muscular weakness, and/or hypoxemia, as noted above (see 'Pharyngeal muscular weakness' above). Furthermore, one study noted that persistent impairment of the peripheral chemoreflex, with blunting of ventilatory responses to hypoxia, can occur despite complete reversal of rocuronium with neostigmine or sugammadex [70,71].
Inadequacy of muscle strength is best confirmed with the aid of a peripheral nerve stimulator. Additional doses of a reversal agent are administered, if appropriate. Typically, a pseudocholinesterase inhibitor (eg, neostigmine 20 to 70 mcg/kg, up to 5 mg total dose) is administered with an anticholinergic agent to block vagal stimulation (eg, glycopyrrolate 0.2 mg for every 1 mg of neostigmine, up to 1 mg total dose). Dosing for neostigmine (and thus for glycopyrrolate) depends on the degree of neuromuscular blockade at the time of reversal (table 8) (see "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Anticholinesterases'). An alternative reversal agent is sugammadex, which may be selected if rocuronium or vecuronium was administered. The dose of sugammadex should be based on the level of neuromuscular block (table 8). Compared with neostigmine, sugammadex results in faster complete reversal of rocuronium-induced neuromuscular blockade. Complete recovery from neuromuscular blockade is correlated with a train-of-four (TOF) peripheral nerve stimulation ratio of 0.9 (defined as the amplitude of the twitch response to a fourth nerve stimulation relative to the twitch response of the first stimulation). (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Anticholinesterases' and "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Sugammadex'.)
In some patients, persistent neuromuscular blockade may be due to administration of succinylcholine or mivacurium in a patient who has pseudocholinesterase deficiency. Other conditions that result in delayed recovery from neuromuscular blockade include myasthenia gravis and myasthenic syndromes, succinylcholine-induced phase II block, hypothermia, or acidosis. (See "Anesthesia for the patient with myasthenia gravis", section on 'Neuromuscular blocking agents'.)
If muscle weakness persists for any reason after adequate pharmacologic reversal, mechanical ventilation is initiated or continued, with administration of adequate sedation while waiting for recovery of muscle strength.
Stroke — Acute perioperative stroke or other neurologic disorder is an infrequent cause of respiratory depression in the PACU. (See "Delayed emergence and emergence delirium in adults", section on 'Consider neurologic disorders'.)
If an acute neurologic event is suspected in a patient with adequate ventilation, O2 saturation is continuously monitored and supplemental O2 is administered to maintain O2 saturation ≥94 percent [72]. In a patient with severe obtundation or pharyngeal weakness due to a neurologic disorder, endotracheal intubation may be necessary to restore adequate ventilation. Intubation also protects the airway from aspiration.
Urgent neurologic consultation is obtained to guide further therapy. (See "Initial assessment and management of acute stroke".)
DISCHARGE FROM THE POST-ANESTHESIA CARE UNIT: RESPIRATORY CONSIDERATIONS — Patients remain in the post-anesthesia care unit (PACU) until they are no longer at risk for respiratory depression [4]. For discharge to an unmonitored setting, oxygen (O2) saturation (SpO2) must be adequate and/or recovered to baseline level for at least 15 minutes after administration of the last intravenous opioid or sedative dose, and for at least 15 minutes after discontinuation of supplemental O2. Other criteria for discharge from the PACU are discussed separately (table 9). (See "Overview of post-anesthetic care for adult patients".)
Patients with persistent respiratory compromise may require ongoing respiratory support in a monitored setting after discharge from the PACU (eg, an intensive care unit or transitional unit).
SUMMARY AND RECOMMENDATIONS
●Routine risk assessment and monitoring – Airway patency, respiratory rate, and oxygen (O2) saturation (SpO2) are assessed upon arrival in the post-anesthesia care unit (PACU), with subsequent continuous monitoring of respiratory rate and SpO2, and frequent reassessment of airway patency. Patients at risk for development of respiratory insufficiency due to preexisting conditions, the surgical procedure, or anesthetic factors are identified. (See 'Respiratory monitoring and risk assessment' above.)
●Approach to respiratory insufficiency
•Note signs and symptoms – Symptoms of respiratory insufficiency such as dyspnea and difficulty breathing may be present in an awake patient but may be mild or absent in a sedated patient. Signs of respiratory insufficiency include tachypnea (respiratory rate [RR] >30 breaths per minute [bpm]) or bradypnea (RR <8 bpm), SpO2 <93%, abnormal respiratory sounds, or cyanosis. (See 'Signs and symptoms' above.)
Hypoxemia and hypercapnia may cause anxiety, confusion, and agitation, as well as tachycardia and hypertension. Severe abnormalities may cause somnolence or obtundation, with hypotension, bradycardia, or malignant arrhythmias.
Tension pneumothorax or pulmonary embolism may cause sudden severe hypotension and cardiovascular collapse.
•Perform further assessment – Assessment of a patient with respiratory insufficiency includes a targeted physical examination, arterial blood gases, and chest radiograph to determine whether the cause is likely due to upper airway obstruction, a lower airway or pulmonary complication, or neurologic abnormality. (See 'Initial assessment' above.)
•Stabilize the patient – Supplemental O2 is provided while potential causes and severity of respiratory insufficiency are being assessed (table 2). Some patients may require ventilatory support as well. If there are no contraindications, use of HFNC or noninvasive ventilation is a useful technique to avoid reintubation. (See 'Ventilatory support' above.)
●Treat causes of respiratory insufficiency
•Upper airway obstruction – Causes of upper airway obstruction requiring immediate treatment include pharyngeal muscular weakness, laryngospasm, airway edema, foreign body aspiration, vocal cord paralysis, or cervical hematoma. (See 'Upper airway obstruction' above.)
•Lower airway obstruction or pulmonary causes – Immediate treatment is necessary if hypoxemia and/or hypercapnia develop or work of breathing is increased. These include bronchospasm, pulmonary edema, aspiration pneumonitis, tension pneumothorax, or pulmonary embolus. (See 'Lower airway and pulmonary complications' above.)
•Central and peripheral nervous system causes – Respiratory depression and hypoventilation may be caused by:
-Residual effects of opioids and other anesthetic agents. If opioid overdose is the most likely cause of heavy sedation and persistent bradypnea, we suggest titration of low doses of naloxone 40 to 80 mcg to avoid reintubation (Grade 2C) (table 7). (See 'Opioids and anesthetic agents' above.)
-Inadequate reversal of neuromuscular blocking agents (NMBA) is common in patients admitted to a PACU and may cause pharyngeal muscle weakness, upper airway obstruction, and hypoventilation. If residual NMBA effect is confirmed with a peripheral nerve stimulator, either a pseudocholinesterase inhibitor (eg, neostigmine 20 to 70 mcg/kg, up to 5 mg total dose) is administered with an anticholinergic agent (eg, glycopyrrolate 0.2 mg for every 1 mg of neostigmine, up to 1 mg total dose), or sugammadex may be administered for reversal of rocuronium or vecuronium. (See 'Neuromuscular blocking agents' above.)
-Rarely stroke may be the suspected cause; urgent neurologic consultation is obtained to guide further therapy. (See 'Stroke' above.)
●Criteria for PACU discharge – Patients remain in the PACU until they are no longer at risk for respiratory depression or can be transferred to a monitored setting. SpO2 must be adequate for at least 15 minutes after administration of the last intravenous opioid or sedative dose, and for 15 minutes after discontinuation of supplemental O2, in addition to other standard criteria for PACU discharge (table 9). (See 'Discharge from the post-anesthesia care unit: Respiratory considerations' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Edward George, MD, PhD who contributed to an earlier version of this topic review.
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