Postoperative airway and pulmonary complications in adults: Etiologies and initial assessment and stabilization

INTRODUCTION — Respiratory problems are common in the postoperative setting. Appropriate monitoring, early diagnosis, and timely management are critical since even potentially fatal respiratory compromise is usually reversible.

This topic reviews initial diagnostic evaluation and management of acute respiratory compromise during the early postoperative period in the postoperative anesthesia care unit (PACU) or intensive care unit (ICU), or later in the ICU, hospital ward, or rarely in outpatients following hospital discharge. Discussed in other topics are the following:

●Respiratory complications occurring in the operating room during emergence from general anesthesia and immediately after extubation. (See "Emergence from general anesthesia", section on 'Airway or respiratory problems' and "Extubation following anesthesia", section on 'Complications of extubation'.)

●Avoidance of respiratory complications during postoperative transport to the PACU or ICU. (See "Transport of surgical patients", section on 'Respiratory monitoring' and "Transport of surgical patients", section on 'Airway equipment and supplemental oxygen'.)

●Prevention and management of individual postoperative pulmonary complications. (See "Strategies to reduce postoperative pulmonary complications in adults" and "Postoperative airway and pulmonary complications in adults: Management following initial stabilization".)

ETIOLOGIES AND THEIR RISK FACTORS — Etiologies that can result in postoperative respiratory conditions are listed in the table (table 1), most of which occur in the first few hours or days after surgery.

Immediate potentially life-threatening emergencies — The potential for life-threatening postoperative respiratory compromise is greatest in the immediate postoperative setting shortly after transport to the postoperative anesthesia care unit (PACU) or intensive care unit (ICU) but may present later in a hospital ward or ICU (table 1).

After nausea and vomiting, respiratory complications are the most common major problem in the PACU setting, and the second most common problem requiring intervention [1-3].

Hypoventilation — Hypoventilation may occur in the early postoperative period due to residual effects of agents administered in the operating room (anesthetic agents and neuromuscular blocking agents [NMBAs]), or due to central nervous system (CNS) depression from other neurologic causes.

●Residual anesthetic drug effects – Temporary obtundation and central hypoventilation is common in the early postoperative period due to residual effects of opioids or anesthetic and adjunct agents (table 2) [4]. Anesthetic agents act synergistically to cause CNS and respiratory depression [5]. (See "Delayed emergence and emergence delirium in adults", section on 'Consider prolonged drug effects'.)

•Opioids – Opioid analgesics, both systemic and neuraxial, that are administered during the intraoperative and/or postoperative periods cause dose-dependent respiratory depression. Postoperative peripheral oxygen saturation (SpO₂) <95 percent is common [6-9]. (See "Perioperative uses of intravenous opioids in adults: General considerations".)

•Anesthetic agents – Residual intravenous (IV) or inhalation anesthetic agents also commonly contribute to respiratory depression.

•Benzodiazepines – Oversedation caused by benzodiazepines is uncommon in the perioperative setting since the most commonly used agent, midazolam, has a brief duration and is less commonly used than opioids. (See "Benzodiazepine poisoning", section on 'Role of antidote (flumazenil)'.)

Risk factors for prolonged anesthetic drug effects include the following (see "Delayed emergence and emergence delirium in adults", section on 'Risk factors for prolonged drug effects'):

•Older age

•Obesity or very low body weight

•Hepatic or renal insufficiency

•Hypothyroidism

•Hypothermia

•Metabolic derangements

•Potential interactions of anesthetic agents with preoperative prescription drugs, supplements, recreational drugs, or alcohol

Administration of supplemental oxygen to patients with opioid-induced respiratory depression may worsen hypercapnia, which may further depress consciousness [10]. Depression of the hypercapnic drive may lead to carbon dioxide (CO₂) narcosis and worsening obtundation. For this reason, optimal monitoring in the PACU includes use of capnography [11]. (See "Mechanisms, causes, and effects of hypercapnia", section on 'Oxygen-induced hypercapnia' and "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure", section on 'Titration of oxygen'.)

●Residual neuromuscular blockade – Significant muscle weakness caused by residual effects of NMBAs may cause hypoventilation due to significant respiratory muscle weakness. This may impair the patient's ability to take deep breaths, resulting in low tidal volumes and minute ventilation. Postoperative residual neuromuscular block may also lead to diminished protective airway reflexes increasing the risk of aspiration and pneumonia [12]. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Consequences of residual block'.)

●Neurologic disorders – Transient focal neurologic deficits may become apparent after sedation or general anesthesia in patients with prior history of neurologic insult from stroke, a phenomenon known as differential awakening. Rarely, a new neurologic complication (eg, stroke) is the cause of obtundation. Details regarding neurologic evaluation are discussed separately. (See "Delayed emergence and emergence delirium in adults", section on 'Consider neurologic disorders'.)

Acute upper airway obstruction — Most life-threatening emergencies occurring in the immediate postoperative period involve the upper airway and cause symptoms of upper airway obstruction (UAO). UAO can occur in the pharynx, larynx, or large airways (ie, trachea or major bronchi). The signs and symptoms and initial management of UAO are discussed below. (See 'Ensure a patent upper airway and adequate ventilation' below and 'Upper airway disorders' below.)

Etiologies of UAO and their risk factors include the following:

●Laryngospasm – Laryngospasm is a prolonged exaggeration of the glottic closure reflex due to stimulation of the superior laryngeal nerve (a branch of the vagus nerve). Although the cords are adducted, the primary obstruction is caused by tonic contraction of the laryngeal muscles and descent of the epiglottis [13] over the laryngeal inlet.

Risk factors for laryngospasm include:

•Recent extubation (vocal cords may be traumatized during extubation)

•Secretions, blood, or foreign body in the upper airway

•Recent removal from positive pressure ventilation via face mask (presumably due to sudden airway collapse)

●Pharyngeal muscle weakness – Pharyngeal muscle weakness causes the base of the tongue and the tissues of the posterior oropharynx to move toward each other. Many cases are mild but if severe, pharyngeal collapse may be life-threatening.

•Residual effects of NMBAs – Pharyngeal muscle weakness is most often due to residual effect of NMBAs, even if reversal agents such as neostigmine with glycopyrrolate or sugammadex were administered [3,14-21]. Hypothermia may exacerbate this phenomenon [17]. (See "Perioperative temperature management", section on 'Intraoperative hypothermia' and "Perioperative temperature management", section on 'Postoperative temperature derangements'.)

Other risk factors include administration of succinylcholine or mivacurium in a patient who has pseudocholinesterase deficiency, myasthenia gravis and myasthenic syndromes, succinylcholine-induced phase II block, or acidosis. 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'.)

-(See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Reversal of neuromuscular block'.)

•Oropharyngeal collapse due to obstructive sleep apnea (OSA) – Pharyngeal muscle weakness is more likely to occur and be more severe in patients with obesity, obstructive sleep apnea (OSA), or tonsillar or adenoidal hypertrophy because of excess pharyngeal or nasal soft tissue. OSA can be worsened in the postoperative period following any surgery including upper airway surgery. Oropharyngeal wall weakness associated with NMBA or sedatives, anesthetic-induced blunted hypoxic and hypercapnic drive, and supine positioning may all exacerbate OSA following surgery. Perioperative management of OSA is discussed separately. (See "Postoperative airway and pulmonary complications in adults: Management following initial stabilization", section on 'Oropharyngeal collapse due to obstructive sleep apnea'.)

•Residual anesthetic drug effects – Residual effects of opioids, sedatives, and other anesthetic agents often contribute to obtundation with inability to control pharyngeal musculature and maintain an open airway. Further details are found above. (See 'Hypoventilation' above.)

●Copious secretions – Increased respiratory secretions, inspissation of secretions (ie, mucous plugging) may cause upper airway obstruction, particularly in patients with pre-existing pulmonary pathology. Management of excessive postoperative secretions is discussed separately. (See "Postoperative airway and pulmonary complications in adults: Management following initial stabilization", section on 'Atelectasis'.)

●Upper airway edema – Patients with significant upper airway edema may remain intubated to allow time for resolution. However, upper airway edema may not be appreciated until after extubation.

Risk factors for airway edema include airway or major neck surgery, prolonged head-down or prone positioning, large volumes of fluid resuscitation [22], or history of multiple or traumatic intubation attempts during the current surgery. Rarer causes include anaphylaxis or angioedema. Several common culprit agents which can trigger angioedema include antibiotics, latex, radiocontrast agents, fibrinolytic agents, calcium channel blockers, opioids, angiotensin converting enzyme (ACE) inhibitors, or nonsteroidal anti-inflammatory drugs (table 3). Management of upper airway edema is discussed separately. (See "Postoperative airway and pulmonary complications in adults: Management following initial stabilization", section on 'Upper airway edema'.)

●Oropharyngeal trauma – Trauma in the oropharynx due to a local surgical procedure or after repeated instrumentation of the airway during intubation attempts may lead to bleeding, edema, hypoventilation, and decreased likelihood of successful intubation or reintubation. Prevention and management are discussed in a separate topic. (See "Management of the difficult airway for general anesthesia in adults", section on 'Unanticipated difficult intubation'.)

●Foreign body aspiration – Aspiration of a foreign body or a mucous plug may cause severe airway obstruction as well as laryngospasm and bronchospasm [23,24]. Postoperatively, it is most often due to tooth dislodgement during intubation but can be due to a retained throat pack or suture. Management of foreign body aspiration is discussed separately. (See "Airway foreign bodies in adults", section on 'Life-threatening asphyxiation' and "Airway foreign bodies in adults", section on 'Foreign body removal'.)

●Expanding cervical hematoma – Hematoma formation compressing the upper airway may occur after neck surgery (eg, carotid endarterectomy, thyroidectomy, parathyroidectomy), anterior cervical spine surgery, central venous catheter (CVC) placement in the internal jugular vein, or interscalene block placement [25]. While many cervical hematomas are small, a rapidly expanding hematoma may become life-threatening by causing supraglottic edema due to venous and lymphatic congestion, tracheal deviation, or direct compression of the tracheal lumen below the level of the cricoid cartilage [26]. Management is described below. (See 'Initial stabilization' below.)

●Bilateral vocal cord paralysis – Bilateral vocal cord paralysis is a rare complication of neck surgery due to injury of the bilateral laryngeal nerves. (See "Anesthesia for laryngeal surgery", section on 'Bilateral vocal fold paralysis'.)

Unilateral dysfunction is more common but less likely to be life-threatening and more likely to be asymptomatic, although may be poorly tolerated in patients with underlying lung dysfunction. Further details on vocal cord injury are provided separately. (See "Complications of airway management in adults", section on 'Vocal cord injury'.)

Lower airway pulmonary parenchymal/vascular emergencies — Other life-threatening emergencies that do not involve the upper airway include the following:

●Bronchospasm – Bronchospasm occurring due to an allergic reaction/anaphylaxis to a medication (eg, opiates, antibiotics, latex) (table 4) must be urgently treated (table 5). (See "Perioperative anaphylaxis: Clinical manifestations, etiology, and management".)

Bronchoconstriction can also occur due to reflex constriction of bronchial smooth muscles from tracheal stimulation during airway suctioning, aspiration of gastric contents, the presence of secretions, blood, or a mucous plug or foreign body in the lower airway, and endotracheal reintubation.

Severe postoperative bronchospasm is most likely in patients with underlying asthma, significant smoking history, or obstructive lung disease as the bronchodilatory effect of anesthetics wears off. (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 can be cardiogenic (see "Pathophysiology of cardiogenic pulmonary edema"), noncardiogenic (see "Noncardiogenic pulmonary edema"), or a combination of both. It may present as an emergency in the PACU (eg, cardiogenic pulmonary edema, negative pressure pulmonary edema). Alternatively, the presentation may be more subtle and present after transfer to the floor (eg, fluid overload, acute respiratory distress syndrome, neurogenic pulmonary edema).

The etiology and pathophysiology of cardiogenic and noncardiogenic pulmonary edema are discussed separately (see "Pathophysiology of cardiogenic pulmonary edema" and "Noncardiogenic pulmonary edema"). Issues that are pertinent to pulmonary edema in the postoperative setting are discussed in this section below.

•Cardiogenic – Patients with a history of chronic left heart failure may be predisposed to cardiogenic pulmonary edema, 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). (See "Pathophysiology of cardiogenic pulmonary edema".)

•Negative pressure pulmonary edema – Negative pressure pulmonary edema (NPPE) is one form of noncardiogenic pulmonary edema [27]. NPPE develops when patients forcibly inhale against a closed glottis (ie, Mueller or reverse Valsalva maneuver). As the intrathoracic pressure becomes more negative, blood flow to the right heart increases. The interstitial pressure around the capillaries also becomes more negative, and intravascular fluid is drawn into the interstitial space.

NPPE is most commonly due to acute airway obstruction resulting from laryngospasm, pharyngeal obstruction, or biting of the endotracheal tube during extubation. NPPE classically occurs in the PACU setting and has been estimated to complicate 0.05 to 0.1 percent of all procedures involving intubation and general anesthesia [28]. However, it may also present as a delayed phenomenon following relief of upper airway obstruction (up to 12 hours).

Patients with a predisposition to upper airway obstruction are at the greatest risk for NPPE (eg, obesity, short neck, obstructive sleep apnea, or acromegaly) [29]. However, laryngospasm-induced NPPE following extubation has also been reported in young, healthy, athletic adults [27,30-32].

•Other etiologies of noncardiogenic pulmonary edema – Other causes of noncardiogenic pulmonary edema that can occur in the postoperative setting include the following:

-Fluid overload – Fluid overload may be due to the excess administration of intravascular fluid before, during, and/or following surgery.

-Naloxone administration – (See "Delayed emergence and emergence delirium in adults", section on 'Opioids'.)

-Neurogenic pulmonary edema – (See "Neurogenic pulmonary edema".)

-Acute respiratory distress syndrome (eg, cardiac, and thoracic surgery) – (See "Mechanical ventilation during anesthesia in adults", section on 'Lung protective ventilation during anesthesia'.)

-Transfusion-associated lung injury – (See "Transfusion-related acute lung injury (TRALI)".)

-Reperfusion lung injury (eg, after pulmonary artery thrombectomy) – (See "Chronic thromboembolic pulmonary hypertension: Pulmonary thromboendarterectomy", section on 'Reperfusion pulmonary edema'.)

●Aspiration of gastric contents – Regurgitation and aspiration can occur during induction and intubation for general anesthesia. Aspiration may also occur in the immediate and early postoperative period since anesthetic agents depress airway protective reflexes [33,34]. Aspiration of large-volume, particulate, acidic material or with high bacterial load can result in infection, airway obstruction, acute respiratory distress syndrome, and death. (see "Rapid sequence induction and intubation (RSII) for anesthesia", section on 'Aspiration'). Details regarding management are discussed separately. (See "Postoperative airway and pulmonary complications in adults: Management following initial stabilization", section on 'Aspiration (chemical) pneumonitis'.)

●Tension pneumothorax – Tension pneumothorax may occur, most commonly following cardiothoracic or neck surgery. (See "Pneumothorax in adults: Epidemiology and etiology", section on 'Iatrogenic'.)

●Other lower airway, pulmonary parenchymal, and vascular conditions – Other conditions affecting the lower airway, pulmonary parenchyma, and pulmonary vasculature include atelectasis, pneumonia, pleural effusion, and pulmonary embolism. These entities can present as a life-threatening emergency immediately after surgery but are more commonly encountered within hours to days after surgery, as discussed below. (See 'Early postoperative pulmonary conditions (hours to days)' below.)

Other rare emergencies in the immediate postoperative period include non-venous embolic phenomena and bilateral diaphragmatic paralysis, which are all discussed separately:

•(See "Air embolism", section on 'Surgery and trauma'.)

•(See "Fat embolism syndrome", section on 'Epidemiology and etiology'.)

•(See "Amniotic fluid embolism", section on 'Risk factors'.)

•(See "Diagnostic evaluation of adults with bilateral diaphragm paralysis", section on 'Etiology'.)

Early postoperative pulmonary conditions (hours to days) — Most conditions involving the lower airways or pulmonary parenchyma and vasculature occur several hours or days following surgery (table 1).

●Hypoventilation, bronchospasm, pulmonary edema, aspiration, and pneumothorax – While hypoventilation, bronchospasm, pulmonary edema, aspiration, and pneumothorax can present in the postoperative setting as an acute life-threatening emergency, these etiologies can also present over hours to days in the postoperative wards. For example, patients receiving IV opioids via patient-controlled analgesia (PCA), nurse-administered bolus doses, or a neuraxial infusion in the postoperative period have an ongoing risk of respiratory depression after transfer from the PACU. These etiologies are discussed above. (See 'Hypoventilation' above and 'Lower airway pulmonary parenchymal/vascular emergencies' above.)

●Atelectasis – Atelectasis is one of the most common postoperative pulmonary complications, especially following upper abdominal, thoracic, and cardiac surgeries [35]. Postoperative atelectasis is usually caused by postoperative pain that interferes with spontaneous deep breathing and coughing, as well as decreased compliance of lung tissue, impaired regional ventilation, and/or retained airway secretions, [36,37]. While atelectasis can begin to develop during anesthesia, significant hypoxemia due to postoperative atelectasis tends to occur later, after the patient has left the PACU. (See "Atelectasis: Types and pathogenesis in adults".)

●Pneumonia – All major surgeries place patients at risk for bacterial pneumonia due to the effects of atelectasis, aspiration, and impaired pulmonary secretion clearance, especially abdominal and thoracoabdominal procedures. Risk factors for and typical microbiology (eg, gram-negative bacteria) of hospital-associated pneumonia are described separately. (See "Epidemiology, pathogenesis, microbiology, and diagnosis of hospital-acquired and ventilator-associated pneumonia in adults".)

●Pleural effusion – Small pleural effusions are common during the immediate postoperative period, particularly following upper abdominal surgery (up to 50 percent), and cardiothoracic surgery [38]. However, most are small and do not cause symptoms unless they become infected. The exceptions are patients with rapidly accumulating hemothorax (eg, trauma to the lung during surgery) or chylothorax (eg, esophagectomy, congenial heart surgery). (See "Evaluation and management of pleural effusions following cardiac surgery", section on 'Risk factors' and "Etiology, clinical presentation, and diagnosis of chylothorax", section on 'Traumatic causes (including iatrogenic causes)' and "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Hemothorax'.)

●Pulmonary embolism (PE) – Surgery is a well-known risk factor for PE. The highest risk is in patients undergoing pelvic and lower orthopedic extremity surgery, major vascular surgery, neurosurgery, and cancer surgery. (See "Overview of the causes of venous thrombosis", section on 'Surgery'.)

●Other complications – Tracheal laceration is a rare but well-described complication of endotracheal intubation [39-42]. Laceration is usually minor but can be life-threatening if severe or if rupture occurs. (see "Complications of airway management in adults", section on 'Traumatic complications'). Details regarding management are discussed separately. (See "Postoperative airway and pulmonary complications in adults: Management following initial stabilization", section on 'Rare upper airway disorders'.)

Other rare causes of complications include arytenoid dislocation, temporomandibular joint (TMJ) dislocation, and unilateral vocal cord paralysis. These entities are discussed in separate topics:

•(See "Complications of airway management in adults", section on 'Arytenoid cartilage dislocation'.)

•(See "Complications of airway management in adults", section on 'Temporomandibular joint dislocation'.)

Late postoperative pulmonary conditions (weeks to months) — A small number of pulmonary complications present later and include the following:

●Tracheal stenosis due to traumatic intubation, prolonged intubation or tracheostomy placement – (See "Presentation and diagnostic evaluation of non-life-threatening and nonmalignant subglottic and tracheal stenosis in adults", section on 'Traumatic'.)

●Obstructive pneumonia due lower airway foreign body aspiration – (See "Airway foreign bodies in adults", section on 'Clinical manifestations'.)

●Unilateral diaphragmatic paralysis (eg, cardiothoracic or neck surgery, paravertebral or brachial plexus nerve blocks) – (See "Diagnosis and management of nontraumatic unilateral diaphragmatic paralysis (complete or partial) in adults", section on 'Etiology'.)

INITIAL ASSESSMENT OF RESPIRATORY COMPROMISE

Recognition of significant respiratory compromise — In the postoperative setting, clinical features differ because of the variety of conditions that cause respiratory compromise (table 1). Some patients may present in a stable state (eg, minor desaturation and mild dyspnea), while others may present with significant respiratory decompensation.

Signs of significant respiratory compromise include the following:

●Respiratory distress with 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) indicate increased work of breathing and inadequate ventilation. Paradoxical (ie, inward) motion of abdominal muscles during inspiration can also be seen. Respiratory arrest may occur when the patient is unable to maintain the increased respiratory effort.

●Bradypnea (respiratory rate [RR] <8 bpm), hypercapnia detected with capnography [11], or periods of apnea often indicate hypoventilation and may herald respiratory arrest. Agonal breathing usually indicates ensuing respiratory arrest.

●Abnormal breath sounds such as stridor, inspiratory and expiratory wheezing, or absent air movement often indicate significant respiratory compromise.

●Peripheral oxygen saturation (SpO₂) <90 percent associated with a bluish discoloration of the skin or frank cyanosis indicates poor end-organ oxygenation and significant cardiopulmonary compromise [43].

●Associated hemodynamic instability or malignant rhythm disturbances may be due to severe hypoxemia and hypercapnia with acidosis.

Initial rapid assessment — For patients with respiratory compromise, we quickly assess the following at the bedside:

●Airway patency, respiratory rate and pattern (eg, hyperventilation, hypoventilation, agonal breathing), SpO₂, heart rate and rhythm, and blood pressure. In addition, mental status, skin color, neuromuscular function, temperature, and the presence of pain, nausea, or vomiting are also assessed [44].

●A rapid review of preoperative and intraoperative events relevant to the patient's postoperative respiratory status including problems with airway management, ventilation strategy, doses and timing of analgesic, anesthetic and neuromuscular blocking agents, and fluid or blood product administered. These data help the clinician form an empiric diagnosis that prompts targeted therapy. (See 'Other lifesaving measures' below.)

●In addition, arterial blood gas (ABG) analysis, chest radiography, an electrocardiogram (ECG) tracing and bedside ultrasonography imaging may be performed to help narrow the differential diagnosis. (See 'Narrowing the differential' below.)

This assessment is repeated as needed during the postoperative period if respiratory distress recurs or worsens and provides the clinician with data to stabilize the patient and select appropriate treatment. (See 'Initial stabilization' below.)

Narrowing the differential — Timing of the presentation, clinical findings, and, in some cases, additional tests such as ABG analysis, bedside imaging, and ECG help to narrow the differential diagnosis for postoperative respiratory complications (table 1). Once categorized as hypoventilation, upper airway obstruction (UAO), or lower airway pathology, we next assess for individual etiologies within the category. In most patients, an empiric diagnosis is made with this approach so that targeted therapies can be promptly administered. (See 'Initial stabilization' below.)

When the patient is stable, additional imaging and testing may be useful to confirm the diagnosis (eg, computed chest tomography, sputum sampling, echocardiography, troponin level, lower extremity ultrasonography).

Timing — Most conditions present in the immediate postoperative period shortly after transport to the postoperative anesthesia care unit (PACU) or intensive care unit (ICU), or during the first few hours or days after surgery while still in the ICU or on a hospital ward. The typical time course for specific postoperative complications is listed in the table (table 1). In general, conditions that cause post-anesthetic hypoventilation or UAO after tracheal extubation are more likely to be seen shortly after surgery while the patient is still in the PACU (or ICU), while atelectasis and pneumonia are more likely to be seen later after discharge from these settings. However, overlap can occur. For example, aspiration, pulmonary embolism (PE), bronchospasm, pulmonary edema, and hypoventilation can present immediately or later. (See 'Etiologies and their risk factors' above.)

Occasionally, a complication may become symptomatic weeks or months after a surgical procedure. Examples include tracheal stenosis, obstructive pneumonia due to a foreign body, or unilateral diaphragmatic paralysis. Details are discussed separately. (See "Presentation and diagnostic evaluation of non-life-threatening and nonmalignant subglottic and tracheal stenosis in adults" and "Airway foreign bodies in adults", section on 'Presentation' and "Diagnosis and management of nontraumatic unilateral diaphragmatic paralysis (complete or partial) in adults".)

Suspecting hypoventilation — Bradypnea, hypercapnia, and hypoxemia suggest hypoventilation especially if associated with a depressed level of consciousness. Since SpO₂ does not detect hypoventilation, diagnosis of hypercapnia by capnography, ABG, or venous blood gas (VBG) analysis is necessary [44].

Evidence of hypoventilation should prompt a search for central and peripheral nervous system abnormalities and drugs that can cause hypoventilation (eg, residual neuromuscular blocking agent [NMBA] or anesthetic effects, opioid use). Sudden mental status changes associated with hypercapnia may also suggest stroke or air embolism. (See "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure", section on 'Clinical features of hypercapnia'.)

Distinguishing upper from lower airway and pulmonary disorders — In the sections below, general clinical features and presentation of specific upper airway and lower pulmonary disorders are described to facilitate diagnosis of etiologies.

Upper airway disorders — Upper airway disorders include the following:

●Upper airway obstruction – Upper airway disorders are most frequently due to UAO, which can be partial or complete.

•General features – Other than stridor, many of the features of partial obstruction are nonspecific and can also occur in any patient with respiratory distress (eg, intercostal and suprasternal retractions, paradoxical abdominal motion during inspiration). Snoring may suggest that obstruction is above the larynx, while inspiratory stridor (best heard over the neck during inspiration) suggests peri-laryngeal obstruction.

By contrast, complete UAO may be silent (ie, no air movement) despite the patient's efforts (eg, upward movement of the thoracic cage, abdominal paradox). Lack of air entry may also be due to significant associated bronchospasm. Complete UAO progresses rapidly to cardiopulmonary arrest, if untreated.

•Features that favor specific etiologies – Select features that may support a specific etiology of UAO include the following:

-An intense cough may support foreign body aspiration, and occasionally a foreign body may be seen on chest imaging if radio-opaque (eg, tooth). Clinical features and management of foreign body aspiration are presented separately. (See "Airway foreign bodies in adults".)

-Facial, scleral, and tongue swelling may support upper airway edema due to prone positioning, anaphylaxis, or angioedema. Hypotension and known allergy may also support anaphylaxis. A history of traumatic or multiple intubation attempts or large volume resuscitation may also support upper airway edema. Clinical presentation and management of anaphylaxis (table 5) are discussed separately. (See "An overview of angioedema: Clinical features, diagnosis, and management".)

-An obese body habitus and short neck on examination may support oropharyngeal collapse from obstructive sleep apnea (OSA). If severe hypoxemia or hypercapnia are present, patients may have snoring, periods of apnea, oxygen desaturation during sleep, and mental status changes. Complications and management of OSA in the postoperative period including management of postoperative oropharyngeal collapse are discussed separately. (See "Postoperative management of adults with obstructive sleep apnea".)

-Difficulties achieving hemostasis during surgery and an expanding mass in the neck may suggest cervical hematoma. Clinical presentation and management of a cervical hematoma are provided separately. (See "Complications of carotid endarterectomy", section on 'Cervical hematoma'.)

•Vocal cord paralysis – Hoarseness may suggest unilateral vocal cord injury or paralysis. Bilateral paralysis can present as life-threatening UAO requiring tracheostomy. Clinical features and management of vocal cord paralysis are discussed separately. (See "Anesthesia for laryngeal surgery", section on 'Bilateral vocal fold paralysis' and "Complications of airway management in adults", section on 'Injuries of the larynx and vocal cords'.)

•Tracheal laceration or rupture – Tracheal laceration or rupture does not present with the findings of UAO but may have features like pneumothorax such as sudden dyspnea, hypoxemia, subcutaneous emphysema, or pneumomediastinum on imaging. Minor tracheal lacerations with a slow leak may not present until several hours after extubation [41]. Imaging on CT or direct visualization may confirm the diagnosis. (See 'Lower airway disorders and pulmonary parenchymal/vascular disorders' below.)

Notably, chest radiography may be relatively clear in a patient with UAO unless there is underlying lung disease or associated atelectasis.

Lower airway disorders and pulmonary parenchymal/vascular disorders — Lower airway disorders are more likely to present with hypoxemia, dyspnea, lower respiratory tract findings (eg, cough, sputum, wheeze, rales, crackles), and imaging abnormalities (eg, atelectasis, infiltrates). Exceptions include venous thromboembolism where imaging may be normal.

●Pulmonary edema – Acute onset dyspnea with pink or frothy sputum and rarely frank hemoptysis, bilateral crackles and bilateral pulmonary infiltrates on chest imaging is suggestive of pulmonary edema [45-47]. Signs of fluid overload elsewhere such as ankle edema and raised jugular venous pressure or new and abnormal ECG changes may suggest a cardiogenic source, while the absence of these findings in a patient with a history of troublesome extubation may suggest negative pressure pulmonary edema (NPPE). Notably, NPPE may develop immediately or up to 12 hours following relief of upper airway obstruction. Presentation and management of pulmonary edema are provided separately. (See "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Postoperative management' and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults".)

●Atelectasis – Slow onset hypoxemia (or new oxygen requirement) and bilateral infiltrates on chest radiograph as well as crackles that clear after deep inspiration, coughing, or suctioning in a patient with poor expectoration and abundant secretions or mucous plugs suggest atelectasis. Types and management of atelectasis are provided separately. Details regarding management are discussed separately. (See "Postoperative airway and pulmonary complications in adults: Management following initial stabilization", section on 'Atelectasis' and "Atelectasis: Types and pathogenesis in adults" and "Radiologic patterns of lobar atelectasis".)

●Bronchospasm – Wheezing indicating bronchospasm is best heard over the chest during expiration and may be due to secretions, blood, or foreign body in the lower airway or an allergic reaction to a medication. Bronchospasm is more likely with underlying lung disease (eg, asthma, chronic obstructive pulmonary disease [COPD]), especially after the bronchodilatory effect of certain anesthetics has worn off. A localized wheeze heard on chest auscultation may indicate lower airway obstruction by a mucous plug or foreign body. Management of postoperative bronchospasm is discussed separately. (See "Postoperative airway and pulmonary complications in adults: Management following initial stabilization", section on 'Bronchospasm'.)

●Aspiration – Abrupt onset of dyspnea and tachycardia following a witnessed aspiration event in at risk patients (eg, obstetric patients (table 6)) may suggest chemical pneumonitis from aspiration of gastric contents. Patients may also exhibit fever, bronchospasm, crackles or rales, hypoxemia, cyanosis, and/or pink frothy sputum. The rapid onset of these features supports a diagnosis of chemical pneumonitis following aspiration which is akin to "pulmonary acid burn" rather than secondary bacterial infection.

Infiltrates may appear in one or both lower lobes, usually within the first 12 to 24 hours following aspiration. Patients who do not develop symptoms within two hours of aspiration generally do not progress to chemical pneumonitis [34]. However, some patients develop a secondary bacterial infection (ie, aspiration pneumonia) or acute respiratory distress syndrome (ARDS). Clinical presentation and management of aspiration are provided separately. (See "Aspiration pneumonia in adults".)

●Pneumonia – Fever, leukocytosis, dyspnea, sputum/increased secretions, hypoxemia, and pulmonary infiltrates on chest radiograph may suggest postoperative pneumonia. The diagnosis of pneumonia can be challenging in this population since many parenchymal disorders can present similarly including pulmonary edema, pulmonary embolism, acute lung injury, and atelectasis. Clinical judgment and imaging may help distinguish these etiologies. Further details regarding the presentation and management of pneumonia are provided elsewhere. (See "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

The utility of elevated postoperative procalcitonin (PCT) levels as an early biomarker in aiding in the diagnosis of hospital-acquired pneumonia following abdominal surgery is unclear [48]. The role of an elevated PCT level in aiding in the evaluation of postoperative fever is discussed separately. (See "Fever in the surgical patient", section on 'Laboratories'.)

●Embolism – Sudden onset desaturation may support embolic disorders. Some types of surgery are associated with embolic phenomena. Examples include:

•Amniotic fluid embolism (AFE) in patients after labor and delivery

•Fat embolism syndrome (FES) or venous thromboembolism (VTE) after long bone orthopedic surgery

•Air embolism after central venous catheter (CVC) placement

•VTE after cancer or pelvic surgery

Both VTE and AFE may lead to acute right heart systolic dysfunction and dilation, which can be diagnosed with bedside echocardiography. Details regarding diagnosis and management of these disorders are discussed separately:

•(See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".)

•(See "Fat embolism syndrome".)

•(See "Air embolism".)

•(See "Fat embolism syndrome".)

•(See "Intraoperative venous air embolism during neurosurgery".)

●Pneumothorax – Airway deviation and dyspnea following neck, thoracic, or cardiac surgery suggests development of a pneumothorax. Chest imaging or bedside ultrasound may help confirm the suspicion but should not delay urgent management. Details regarding diagnosis and management of pneumothorax are provided separately. (See "Clinical presentation and diagnosis of pneumothorax" and "Initial evaluation and management of blunt thoracic trauma in adults", section on 'Pneumothorax'.)

●Pleural effusion – Postoperative pleural effusions may be evident on chest tube output or chest imaging. (See "Diagnostic evaluation of the hemodynamically stable adult with a pleural effusion".)

INITIAL STABILIZATION — Initial stabilization involves ensuring a patent airway, providing respiratory support, and administering other potentially life-saving therapies for suspected etiologies. Intravenous access should be secured, if not already done.

Ensure a patent upper airway and adequate ventilation — The signs and symptoms of upper airway obstruction (UAO) and hypoventilation are discussed above. (See 'Distinguishing upper from lower airway and pulmonary disorders' above and 'Suspecting hypoventilation' above.)

If UAO or hypoventilation is suspected, the following measures may be appropriate to achieve a fully patent airway and adequate respiration, and/or to select further treatment (table 1):

●Airway support – A chin lift or jaw thrust may successfully open the airway.

Oro- or nasopharyngeal airways are also useful adjuncts. Nasopharyngeal airways are better tolerated than oral airways because of lesser risk of provoking a gag reflex; however, they must be carefully inserted to avoid bleeding from the nasal passages and may be difficult to tolerate in a fully conscious patient. (See "Basic airway management in adults", section on 'Airway obstruction'.)

In some cases, intermittent bag-mask ventilation and agent reversal may be necessary.

●Inspection of the oropharynx and airway – Upper airway inspection may reveal oropharyngeal collapse, airway edema, or external compression by a cervical hematoma. Direct laryngoscopy may be necessary to diagnose and, in some cases, treat etiologies such as laryngospasm, foreign body or mucous plug, or vocal cord paralysis or injury. Less commonly, flexible and/or rigid bronchoscopy may be needed to identify and retrieve an obstructing body below the vocal cords [49].

Examples of conditions that may be rapidly reversed without intubation include the following:

●Hypoventilation – Hypoventilation due to opioids may resolve with frequent stimulation to encourage adequate ventilation, airway support measures (eg, nasopharyngeal airway), or positive pressure ventilation. If symptoms persist, low doses of intravenous (IV) naloxone 40 mcg may be administered, and a continuous infusion of naloxone may be administered to avoid intubation (table 2). Reintubation is rarely necessary. (See "Perioperative uses of intravenous opioids in adults: General considerations", section on 'Prevention and management of adverse opioid effects' and "Acute opioid intoxication in adults", section on 'Management'.)

In rare cases, when benzodiazepine is suspected to be contributing to hypoventilation, IV flumazenil (0.2 mg IV) may be administered and intubation avoided (table 2). (See "Benzodiazepine poisoning", section on 'Role of antidote (flumazenil)'.)

There are no reversal agents for IV sedative-hypnotic agents (eg, dexmedetomidine [50]), or for potent inhalation anesthetic agents (eg, isoflurane).

●NMBA-related pharyngeal weakness – Treatment of pharyngeal weakness due to residual neuromuscular blocking agent (NMBA) by administering reversal agents. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Reversal of neuromuscular block'.)

●OSA-related oropharyngeal collapse – Many patients with oropharyngeal collapse due to obstructive sleep apnea (OSA) may be managed with noninvasive ventilation (NIV) alone. (See "Postoperative management of adults with obstructive sleep apnea" and 'Noninvasive ventilation' below.)

●Obstructing airway lesion – An obstructing foreign body, thrombus, or mucus plug that may be suctioned or removed during oropharyngeal laryngoscopy or bronchoscopy. (See "Airway foreign bodies in adults".)

●Bronchospasm – Treatment of postoperative bronchospasm with inhaled bronchodilators and treatment of the underlying cause (eg, secretions, allergic reaction).

●Laryngospasm – Immediate treatment of laryngospasm by:

•Removing the noxious stimulus (eg, by suctioning blood or secretions) and employing positive pressure bag-mask ventilation concurrent with a jaw thrust maneuver [51].

•Application of pressure with fingertips to the "laryngospasm notch," which may rapidly reverse laryngospasm (also known as "Larson's maneuver") (picture 1) [52-54]. The laryngospasm notch is the area between the mastoid process, the ramus of the mandible, and the base of the skull.

•If these measures fail, an anesthetic dose (eg, 0.5 to 1 mg/kg of propofol) may be administered alone or together with a small dose of succinylcholine (0.1 mg/kg IV) to relax the cords and facilitate positive pressure bag-mask ventilation, but only if the patient is in a monitored setting and the clinician is an expert in airway management.

•Occasionally, if partial laryngospasm is suspected on the hospital floor, nebulized lidocaine (eg, 10 mL of 2 percent solution) or racemic epinephrine (2.25 percent solution; one vial) may be administered, although limited data support this approach [55-57].

In some cases, emergency reintubation may be necessary if the suspected etiology is not easily reversed or is unclear (eg, persistent laryngospasm, inability to retrieve a foreign body in the trachea or bronchi, bilateral diaphragmatic paralysis). We commonly administer an anesthetic 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".)

Other conditions require more invasive emergency measures:

●Cervical hematoma – Most cervical hematomas are mild and can be treated conservatively, with local compression and monitoring for signs of airway compromise. However, a rapidly expanding hematoma requires intubation and reoperation (figure 1). Emergency reintubation in this setting may be difficult due to marked tracheal deviation, laryngeal edema, and a small tracheal lumen [58]. Visualization of upper airway anatomy may be further complicated by multiple intubation attempts resulting in oropharyngeal and laryngeal edema or bleeding [59].

The American Society of Anesthesiologists (ASA) has developed guidance for airway management in patients with airway compression, as noted in the table (table 7). Specific approaches are based on the speed of expansion and presence of airway compromise:

•In patients with evidence of respiratory distress due to airway compromise, the neck incision is immediately reopened on site (eg, postoperative anesthesia care unit [PACU]), and hematoma decompressed before attempting reintubation.

•If the patient is not in distress, the incision is opened under sterile conditions in the operating room before attempting intubation. The patient is subsequently reintubated while the surgeon is applying pressure using sponges to control bleeding. Once the airway is secured, surgical re-exploration is necessary to evacuate the hematoma and control the bleeding source.

•Rarely, complete airway obstruction necessitates emergency cricothyrotomy or tracheostomy.

●Bilateral vocal cord paralysis – In rare cases when bilateral vocal cord paralysis is present or obstruction of the upper airway is complete and irreversible, an emergency tracheostomy is required [60,61]. Intubation in this setting is traumatic and often unsuccessful. (See "Anesthesia for laryngeal surgery", section on 'Bilateral vocal fold paralysis'.)

Provide supplemental oxygen and respiratory support — All patients receive supplemental oxygen to avoid or treat hypoxemia in the immediate postoperative period, especially if any sedative, opioid, or anesthetic agents were administered (see "Overview of post-anesthetic care for adult patients", section on 'Initial assessment and care'). Supplemental oxygen is continued if SpO₂ is low (eg, <93 percent).

Use of supplemental oxygen and respiratory support in patients with persistent hypoxemic respiratory failure are discussed in detail separately (algorithm 1 and table 8). (See "Evaluation and management of the nonventilated, hospitalized adult patient with acute hypoxemia", section on 'Oxygen and respiratory support'.)

Details that are specific to the postoperative patient are discussed in the sections below. (See 'Patients with minimal oxygen needs (eg, ≤6 L/min)' below and 'Mechanical ventilation' below.)

Patients with minimal oxygen needs (eg, ≤6 L/min) — For most spontaneously breathing patients with minimal oxygen needs (eg, ≤6 L/min), supplemental low-flow oxygen is provided while the assessment is ongoing. If facial surgery precludes delivery via nasal cannulae, oxygen delivered via a facemask may be the only option.

Up to approximately 6 L/minute can be delivered accurately through low-flow systems. Higher flows up to 10 to 15 L/minute are also feasible using a low-flow system; however, the exact fraction of inspired oxygen (FiO2) cannot be accurately determined.

Further details regarding the types of low-flow oxygen that can be provided are discussed elsewhere. (See "Evaluation and management of the nonventilated, hospitalized adult patient with acute hypoxemia", section on 'Patients with minimal oxygen requirements (eg, ≤6 L/min)'.)

Patients requiring advanced respiratory support

Choosing among the options — For patients in whom advanced respiratory support is needed, options include high-flow oxygen delivered via nasal cannulae (HFNC), NIV, or invasive mechanical ventilation.

High-flow oxygen delivered via nasal cannulae

●Indications – A trial of HFNC is often the first option, unless there is a clear indication for NIV (see 'Noninvasive ventilation' below). Data supporting HFNC in this population suggest that HFNC is superior to low-flow oxygen systems and likely equivalent to NIV when compared with intubation, as discussed below.

●Contraindications – Contraindications to HFNC in the postoperative patient include surgery of the face, nose, or airway that preclude an appropriate-fitting nasal cannula. (See "Heated and humidified high-flow nasal oxygen in adults: Practical considerations and potential applications".)

●Initiation – Details regarding the application and use of HFNC as a treatment for acute hypoxemic respiratory failure in medical patients and for prevention of respiratory failure in the immediate postextubation period in critically ill patients are discussed separately. (See "Evaluation and management of the nonventilated, hospitalized adult patient with acute hypoxemia", section on 'Humidified, high-flow oxygen delivered via nasal cannulae (HFNC)' and "Heated and humidified high-flow nasal oxygen in adults: Practical considerations and potential applications" and "Extubation management in the adult intensive care unit", section on 'High-flow oxygen via nasal cannulae'.)

HFNC has been studied in the treatment and prevention of respiratory failure in the postoperative setting [62-67]. Although some studies compared HFNC with NIV, most trials and several meta-analyses compared HFNC with conventional low-flow oxygenation (COT) strategies [65-67]:

•In a 2020 meta-analysis of eight trials, use of HFNC postoperatively lowered reintubation rates compared with COT (relative risk [RR] 0.32, 95% CI 0.12-0.88) and decreased the need to escalate respiratory support (eg, cross over to NIV; RR 0.54, 95% CI 0.31-0.94); however, rates of reintubation were similar when compared with NIV [66]. HFNC had no effect on mortality, intensive care unit (ICU) and length of stay, or rate of postoperative hypoxemia. However, most of the included trials were performed in patients considered to be at high risk of reintubation and HFNC was examined as a preventive rather than therapeutic tool.

•Another 2020 meta-analysis of 14 trials (2568 patients) also reported that HFNC reduced reintubation rates when compared with COT or NIV (RR 0.76, 95% CI 0.57-1.01), and reduced the rate of postoperative complications (RR 0.89, 95% CI 0.75-1.06) and length of hospital stay (mean difference: -0.81; 95% CI -1.34 to -0.29), but without an impact on mortality [65]. However, subgroup analysis reported similar reintubation rates when HFNC was compared with NIV alone (three studies; RR 0.95, 95% CI 0.69 to 1.40).

Noninvasive ventilation

●Indications – Conditions for which NIV has clear benefit include acute cardiogenic pulmonary edema and acute hypercapnic respiratory failure due to an exacerbation of COPD or hypoventilation [68]. These data are discussed separately. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications", section on 'Patients likely to benefit'.)

NIV should also be used in those who required positive airway pressure (PAP) support during sleep preoperatively (eg, patients with OSA). These data are discussed separately. (See "Obstructive sleep apnea: Overview of management in adults", section on 'Efficacy'.)

Furthermore, a trial of NIV may be reasonable if HFNC fails.

Data supporting NIV use in the postoperative population also suggest that NIV is superior to low-flow oxygen and likely equivalent to HFNC. These data are provided below. (See 'Mechanical ventilation' below.)

●Contraindications – Contraindications to NIV are listed in the table (table 9). Contraindications that are specific to the postoperative patient include repair of facial fractures or other facial surgery. In addition, although not an absolute contraindication and little evidence exists to support it, we also generally avoid NIV after tracheal resection/reconstruction or after esophageal or gastric resections due to the risk of insufflating a newly created gastroesophageal, gastroduodenal, or gastrojejunal anastomosis [69-71]. However, if NIV is selected following tracheal, esophageal or gastric procedures, we use low levels of inspiratory pressure, with breaks for gastric decompression and careful monitoring for leakage.

●Initiation – NIV should be initiated early, rather than waiting until there is evidence of severe respiratory failure (table 10) [69,72-74]. We reassess respiratory status within one to two hours. Those with improving clinical status and gas exchange may continue NIV, while those who fail to respond should be reintubated and mechanically ventilated. (See "Noninvasive ventilation in adults with acute respiratory failure: Practical aspects of initiation", section on 'Trial duration and reassessment'.)

Data suggest that NIV lowers intubation rates when NIV is compared with low-flow oxygen.

●Several meta-analyses and randomized trials have demonstrated benefit from NIV compared with low-flow oxygen [69,72,75,76]. As an example, in a 2015 meta-analysis in patients following upper abdominal surgery (as a preventive or treatment measure), NIV reduced the need for reintubation (RR 0.25, 95% CI 0.08-0.83) and length of stay in the ICU (approximately two days) compared with low-flow oxygen [69].

A subsequent randomized trial of 293 patients with hypoxemic respiratory failure following abdominal surgery also reported fewer reintubations in patients treated with NIV compared with low-flow oxygen (33 versus 45 percent) [75]. NIV was also associated with more ventilator-free days (25 versus 23 days), and fewer healthcare-associated infections (31 versus 49 percent) but was not associated with a mortality benefit. Methodologic flaws such as the exclusion of patients requiring immediate reintubation and a lower-than-expected rate of reintubation in the oxygen alone group limits interpretation of this study.

●Limited data suggest that reintubation rates appear to be similar when NIV is compared with HFNC. These data are discussed above. (See 'High-flow oxygen delivered via nasal cannulae' above.)

●Data in OSA patients report benefit from NIV after surgery. These data are discussed separately. (See "Postoperative management of adults with obstructive sleep apnea", section on 'Positive airway pressure therapy'.)

Mechanical ventilation — Methods and indications for ventilatory support other than NIV include the following:

●Bag-mask positive pressure ventilation (PPV) – Ventilatory support with bag-mask PPV (eg, patients with hypoventilation or near cardio-respiratory arrest). (See "Basic airway management in adults", section on 'Bag-mask ventilation'.)

In such patients, bag-mask ventilation may be temporary, and intubation may be avoided if patients have a rapidly reversible cause (eg, expectoration or removal of a foreign body or mucus plug).

●Invasive mechanical ventilation – Continued postoperative invasive mechanical ventilation is typically necessary in patients who were receiving mechanical ventilation in the preoperative period. Furthermore, endotracheal intubation and mechanical ventilation may be necessary in postoperative patients who fail postoperative HFNC and/or NIV, and in those with new or exacerbated postoperative respiratory distress, a compromised airway, hemodynamic instability, or impending life-threatening respiratory or cardiac arrest.

Rarely, an emergency cricothyrotomy or tracheostomy is necessary (eg, bilateral vocal cord paralysis, irreversible and complete obstruction of the upper airway). (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".)

There are no efficacy data comparing invasive mechanical ventilation with NIV or HFNC.

Other lifesaving measures — Therapies that may be needed to treat specific emergencies include:

●Reversal of NMBAs, opioids, or benzodiazepines if residual effects are suspected (table 2) – (See "Clinical use of neuromuscular blocking agents in anesthesia", section on 'Reversal of neuromuscular block' and "Delayed emergence and emergence delirium in adults", section on 'Consider prolonged drug effects'.)

●Treatment of bronchospasm with bronchodilators – (See "Anesthesia for adult patients with asthma", section on 'Intraoperative bronchospasm' and "Postoperative airway and pulmonary complications in adults: Management following initial stabilization", section on 'Bronchospasm'.)

●Treatment of anaphylaxis (table 5) – (See "Perioperative anaphylaxis: Clinical manifestations, etiology, and management", section on 'Initial management'.)

●Chest tube insertion to treat pneumothorax – (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Tension pneumothorax'.)

●Administration of a diuretic to treat cardiogenic pulmonary edema – (See "Cardiovascular problems in the post-anesthesia care unit (PACU)", section on 'Decompensated heart failure' and "Approach to diagnosis and evaluation of acute decompensated heart failure in adults".)

DISPOSITION — Once the patient is stable and diagnostic investigations ongoing, a decision needs to be made regarding disposition. This decision should be made on a case-by-case basis and take into consideration staffing, acuity, risk of recurrence, and need for close observation.

Patients remain in the post-anesthesia care unit (PACU) until they are no longer at risk for respiratory depression and meet other discharge criteria to an unmonitored setting (table 11) [44]. Peripheral oxygen saturation (SpO₂) should 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 oxygen. Criteria for discharge from the PACU are discussed separately. (See "Overview of post-anesthetic care for adult patients", section on 'Discharge from the post-anesthesia care unit'.)

By contrast, some patients with persistent respiratory compromise on the hospital floor or PACU may require ongoing respiratory support in a monitored setting (eg, an intensive care or transitional care unit) and further management. Details are discussed separately. (See "Postoperative airway and pulmonary complications in adults: Management following initial stabilization".)

SUMMARY AND RECOMMENDATIONS

●Immediate emergencies – The potential for life-threatening postoperative respiratory compromise is greatest in the immediate postoperative setting shortly after transport to the post-anesthesia care unit (PACU) or intensive care unit (ICU) but may present later in a hospital ward or ICU. These include (table 1) (see 'Immediate potentially life-threatening emergencies' above):

•Hypoventilation – (See 'Hypoventilation' above.)

-Opioids and residual intravenous (IV) or inhalation anesthetic agents and adjuncts

-Residual effects of a neuromuscular blocking agent (NMBA)

-Neurologic disorders

•Acute upper airway obstruction (UAO) – (See 'Acute upper airway obstruction' above.)

-Laryngospasm

-Pharyngeal muscle weakness due to NMBA effects including oropharyngeal collapse due to obstructive sleep apnea, or residual anesthetic effects

-Copious secretions

-Upper airway edema

-Oropharyngeal trauma

-Foreign body aspiration

-Expanding cervical hematoma

-Bilateral vocal cord paralysis

•Lower airway or pulmonary parenchymal/vascular emergencies – (See 'Lower airway disorders and pulmonary parenchymal/vascular disorders' above.)

-Bronchospasm

-Pulmonary edema (cardiogenic or noncardiogenic)

-Aspiration of gastric contents

-Pneumothorax

-Other conditions such as pulmonary embolism, pneumonia, atelectasis, or pleural effusion

-Rare emergencies such as non-venous air or fluid emboli and bilateral diaphragmatic paralysis

●Early postoperative conditions – Conditions that are more likely to present hours to days after surgery, rather than during the immediate postoperative period, include hypoventilation, bronchospasm, pulmonary edema, aspiration, pneumothorax, atelectasis, pneumonia, pleural effusion, pulmonary embolism, and rare traumatic complications such as tracheal laceration, arytenoid dislocation, unilateral vocal cord paralysis, and temporomandibular joint (TMJ) dislocation. These conditions are described above, while management is described in a separate topic. (See 'Early postoperative pulmonary conditions (hours to days)' above.)

●Late postoperative conditions – A small number of pulmonary complications rarely present later in the weeks and months following surgery. These include tracheal stenosis, obstructive pneumonia due to foreign body aspiration, and unilateral diaphragmatic paralysis. (See 'Late postoperative pulmonary conditions (weeks to months)' above.)

●Initial assessment – We quickly assess the following (see 'Initial rapid assessment' above):

•Airway patency, respiratory rate and pattern (eg, hyperventilation, hypoventilation, agonal breathing), peripheral oxygen saturation (SpO₂), heart rate and rhythm, and blood pressure, as well as mental status, skin color, neuromuscular function, and temperature.

•Intraoperative events including timing and doses of medications and fluids administered and results of any tests (eg, arterial blood gas [ABG] analysis, chest radiography, and electrocardiogram [ECG] tracing, and bedside ultrasonography imaging).

•Signs of significant respiratory compromise requiring urgent attention such as respiratory distress, bradypnea or agonal breathing, stridor and limited air movement, low SpO₂ (<90 percent) with signs of end-organ perfusion, and hemodynamic instability. (See 'Recognition of significant respiratory compromise' above.)

•Signs of hypoventilation (eg, bradypnea, hypercapnia, hypoxemia, depressed level of consciousness); signs of UAO including respiratory distress with stridor or limited air movement; signs of lower airway disorders including hypoxemia, dyspnea, lower respiratory tract examination findings, and imaging abnormalities. Other findings suggestive of specific etiologies are listed in the table (table 1). (See 'Narrowing the differential' above.)

•Initial stabilization – Patients with life-threatening postoperative respiratory compromise should be immediately treated with airway support including chin lift or jaw thrust, and/or an oro- or nasal-pharyngeal airway or bag-mask ventilation together with emergency treatment of the suspected underlying etiology. (See 'Ensure a patent upper airway and adequate ventilation' above and 'Other lifesaving measures' above.)

●Supplemental oxygen (O₂) and respiratory support – Supplemental low-flow O₂ is provided to most patients (table 8). Some patients require additional respiratory support such as O₂ delivered via high-flow nasal cannulae (HFNC), noninvasive ventilation (NIV) if there are no contraindications (table 9 and table 10), or mechanical ventilation. (See 'Provide supplemental oxygen and respiratory support' above and 'Choosing among the options' above.)

●Disposition – Patients remain in the PACU until they are no longer at risk for respiratory depression or can be transferred to a monitored setting (table 11). Patients with persistent respiratory compromise on the floor or PACU may require ongoing respiratory support in a monitored setting (eg, ICU or transitional care unit). (See 'Disposition' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Edward George, MD, PhD who contributed to an earlier version of this topic review.