The incidence of PACU complications varies with patient population and likely dependent upon a patient’s medical history as well as the anesthesia and procedure performed. The most frequent issues encountered in the PACU setting include the following:

Respiratory complications occur in 2% to 19% of postoperative patients, and many of these are initiated by events in the PACU such as hypoxia, hypoventilation, upper airway obstruction, laryngospasm, bronchospasm, and aspiration.

A. Hypoxemia. General anesthesia is associated with inhibition of hypoxic and hypercapnic ventilatory drive and a reduction in the lung’s functional residual capacity (FRC). These changes may persist for a variable period of time postoperatively and predispose the patient to hypoventilation and hypoxemia. Supplemental oxygen can delay the detection of hypoventilation by pulse oximetry; however, it also reduces the incidence of hypoxia in the postoperative period. The decision to administer supplemental oxygen should be clinically determined for each patient but should generally be applied when transporting the patient from the OR to the PACU. Signs of hypoxemia include dyspnea, cyanosis, altered mental status, agitation, obtundation, tachycardia, hypertension, and arrhythmias. Hypoxemia should be diagnostically ruled out before undertaking specific treatment for these symptoms.

B. Causes of hypoxemia include the following:

1. Atelectasis is a predictable effect of the reduction in the FRC during general anesthesia and can lead to increased intrapulmonary shunting. Obese patients and those undergoing thoracic or upper abdominal procedures are more susceptible to atelectasis. Epidural anesthesia without general anesthesia is associated with little or no atelectasis formation. Deep breathing, intermittent positive-pressure breathing, and incentive spirometry are effective in rapidly reexpanding small areas of alveolar collapse, although their ability to reduce respiratory complications is uncertain. Noninvasive ventilation (NIV) has been shown to decrease atelectasis and improve oxygenation in postoperative patients. Occasionally, hypoxemia may persist and a chest radiograph may reveal a segmental or lobar collapse. Chest physiotherapy or fiberoptic bronchoscopy may help with reinflating the collapsed segment.

2. Hypoventilation causes hypoxemia by promoting alveolar collapse and increasing the partial pressure of CO₂ in the alveolar air.

3. Diffusion hypoxia may occur during washout of nitrous oxide upon emergence from general anesthesia. High-inspired O₂ fraction (FiO₂) by face mask can prevent hypoxemia.

4. Upper airway obstruction is most often caused by inadequate recovery of the airway reflexes and tone and is seen commonly in patients with obesity, preexisting obstructive sleep apnea (OSA) (see section V.C) or residual neuromuscular blockade (see Chapter 13).

5. Bronchospasm may cause hypoventilation, CO₂ retention, and hypoxemia.

6. Aspiration of gastric contents can lead to aspiration pneumonitis and pneumonia (see Chapter 37).

7. Pulmonary edema may occur from cardiac failure, increased pulmonary capillary permeability or persistent exposure to negative pressure. Cardiogenic edema occurs mostly in individuals with preexisting cardiac disease and is characterized by hypoxemia, dyspnea, orthopnea, jugular venous distention, wheezing, and an S₃ gallop. It may be precipitated by fluid overload, dysrhythmias, and myocardial ischemia. A chest radiograph, arterial blood gas, a 12-lead ECG, and troponin level should be obtained. Evaluation by a cardiologist may be indicated, particularly when aggressive management of conditions such as unstable angina or acute valvular disease is being considered. Inotropic agents, diuretics, and vasodilators are the mainstay of treatment. The use of NIV can obviate the need for intubation in patients with severe hypoxia, pending the response to the medical treatment. Noncardiogenic pulmonary edema secondary to sepsis, head injury, aspiration, transfusion
reaction, anaphylaxis, negative pressure pulmonary edema, or upper airway obstruction is characterized by hypoxemia without the signs of left ventricular overload. Negative pressure pulmonary edema happens secondary to persistent upper airway collapse such as laryngospasm, biting down on the endotracheal tube or hypopharyngeal collapse, with continued diaphragmatic activity. Treatment for pulmonary edema generally needs to be continued in an ICU (see Chapter 37).

8. Pneumothorax may cause hypoventilation, hypoxemia, and hemodynamic instability (see section V.B.2.e).

9. Pulmonary embolism seldom occurs in the immediate postoperative period. However, it must be considered in the differential diagnosis of hypoxemia in patients with deep venous thrombosis, cancer, multiple trauma, or with extended periods of immobility.

C. Hypoventilation is characterized by inadequate minute ventilation resulting in hypercarbia and acute respiratory acidosis. When severe, hypoventilation can result in hypoxemia, mental status changes, and ultimately apnea. Supplemental oxygen may mask early detection of hypoventilation through pulse oximetry. Therefore, monitoring the ventilatory status of postoperative patients should not rely entirely on pulse oximetry. Etiologies of postoperative hypoventilation may be divided into two groups:

a. All inhaled halogenated agents depress ventilatory drive (see Chapter 12) and may produce hypoventilation in the postoperative period. Opioids are also potent respiratory depressants. All µ-receptor agonists increase the apneic threshold. Overnarcotized patients typically appear pain free, with a slow respiratory rate and a tendency to become apneic if left unstimulated. Large doses of benzodiazepines may also inhibit ventilatory drive. The safest treatment of anesthetic-related hypoventilation is to continue mechanical ventilation until breathing is adequate. Alternatively, pharmacologic reversal may be considered.

1. Opioid-induced hypoventilation can be reversed by naloxone, an opioid antagonist with greatest affinity for the µ-receptor. Doses of 20 to 80 µg IV are titrated to effect. Reversal occurs within 1 to 2 minutes and lasts for 30 to 60 minutes. Naloxone treatment may induce significant side effects such as pain, tachycardia, hypertension, and pulmonary edema. The respiratory depressant effects of the opioids may outlast a single dose of naloxone. Thus, the patient should be monitored for recurrence of opioid-induced hypoventilation. Naloxone should be used cautiously in patients with known or suspected history of chronic opioid use because it may precipitate acute withdrawal.

2. Hypoventilation secondary to benzodiazepines can be reversed by flumazenil (increments of 0.2 to 1 mg IV over 5 minutes, up to a maximum of 5 mg). The onset of reversal occurs within 1 to 2 minutes with peak effect at 6 to 10 minutes. The patients should be followed closely after administration of flumazenil because resedation may occur due to its short 7 to 15 minute half-life. Flumazenil should be used cautiously in patients with chronic benzodiazepine use because it may precipitate seizures.

b. Less common, but potentially life-threatening, causes of decreased ventilatory drive include complications of intracranial and carotid artery surgery, head injuries, and intraoperative stroke (see section VIII).

a. Preexisting respiratory disease is the most important risk factor for postoperative respiratory complications. Chronic obstructive pulmonary disease (COPD) alters the match of ventilation and perfusion, resulting in hypoxemia and hypercapnia. Impaired gas exchange and expiratory flow limitation cause a high ventilatory workload under normal circumstances. Restrictive disease (e.g., pulmonary fibrosis, pleural effusions, obesity, scoliosis, massive ascites, and pregnancy) is associated with fewer complications than COPD, particularly when respiratory muscle strength is preserved and the restrictive defect is extrapulmonary. NIV can be beneficial in COPD and in restrictive pulmonary disease by decreasing the work of breathing, augmenting the ventilatory parameters, and avoiding intubation.

b. Residual neuromuscular blockade is defined as a train-of-four ratio less than 0.9 and suggested by the clinical observations of spasmodic twitching, generalized weakness, upper airway obstruction, or by more subtle signs such as hypoxemia or shallow breathing. Even with modern non-depolarizing neuromuscular blocking agents, approximately 30% of patients are admitted to the PACU with residual neuromuscular blockade. Adequacy of muscle strength can only be definitively assessed with the aid of a quantitative neuromuscular transmission monitor (see Chapter 13). If muscle weakness persists after adequate pharmacologic reversal (e.g., neostigmine 20 to 60 µg/kg up to 5 mg, and glycopyrrolate 0.2 mg per 1 mg of neostigmine administered), it is best to institute or continue mechanical ventilation, administer adequate anxiolysis, and wait for the muscle strength to recover. At this point, special situations such as myasthenia gravis and myasthenic syndromes, pseudocholinesterase deficiency, succinylcholine-induced phase II block, hypothermia, acid-base and electrolyte imbalance, and anticholinesterase inhibitor-induced weakness should be considered.

c. Inadequate analgesia after thoracic or upper abdominal surgery may cause splinting and decreased minute ventilation, resulting in alveolar collapse, hypercapnia, and hypoxemia. This is preventable with early analgesia and encouragement of deep breathing and coughing. Compared with systemic opioids, epidural analgesia may reduce the incidence of respiratory complications (atelectasis, pulmonary infections, or hypoxia).

d. Bronchospasm is common in the pediatric population as well as patients with COPD, asthma, or a recent respiratory tract infection. It is often precipitated by manipulation of the airway, particularly tracheal intubation. Wheezing may also be heard upon chest examination of patients with pulmonary edema, endobronchial intubation, aspiration pneumonitis, and pneumothorax. Treatment is discussed in Chapter 37.

e. Pneumothorax may complicate certain procedures such as thoracotomy, mediastinoscopy, bronchoscopy, high retroperitoneal dissection for nephrectomy or adrenalectomy, laparoscopic surgery, and spinal fusion. Insertion of central venous lines and nerve blocks of the upper extremities are other possible iatrogenic etiologies. Diagnosis is made with a chest radiograph (CXR) in the upright position. In the presence of hemodynamic instability (tension pneumothorax), a needle decompression or tube thoracostomy must be performed emergently even without CXR diagnosis (see Chapter 37).

D. Upper airway obstruction may occur during recovery from anesthesia. Principal signs are the lack of adequate air movement, intercostal and suprasternal retractions, and paradoxical abdominal and chest wall motion during inspiration. Complete upper airway obstruction is silent. Partial obstruction is accompanied by either snoring (if the obstruction is above the larynx) or stridor (if perilaryngeal). Obstruction is more commonly seen in patients with OSA, obesity, tonsillar or adenoidal hypertrophy, or craniofacial abnormalities. Often times, airway obstruction may be relieved with a chin lift or jaw thrust (see Chapter 37). Patients with OSA may benefit from the use of continuous positive airway pressure. Common etiologies for upper airway obstruction include the following:

1. Incomplete recovery from general anesthesia and/or neuromuscular blockade (see section V.B). Decreased strength and coordination of the intrinsic and extrinsic airway musculature causes the tongue to fall backward and occlude the airway. Patency is reestablished by inserting a nasal or oral airway, by manually assisting ventilation, or by intubating the trachea.

2. Laryngospasm may be precipitated by light anesthesia and irritation of the glottis by secretions, blood, or a foreign body (see Chapter 37).

3. Airway edema may be caused by laryngoscopy, bronchoscopy, nasogastric tube insertion, esophagoscopy, or surgery on the head and neck. It may also follow a traumatic intubation, allergic reaction, the administration of large amounts of IV fluids, or prolonged prone position. Children are particularly susceptible to airway obstruction from edema because of the small diameter of their upper airway. The cuff leak test is neither sensitive nor specific and should not be used as the sole determinant for extubation of a patient with suspected airway edema. Treatment of upper airway edema includes the following:

a. Administration of warmed, humidified 100% O₂ by face mask.

b. Head elevation, fluid restriction, and possible diuresis.

c. Nebulization of racemic epinephrine 2.25% solution, 0.5 to 1.0 mL in normal saline, or L-epinephrine, 2 mL of a 1:1,000 solution, which may be repeated in 20 minutes if needed.

d. Dexamethasone, 4 to 8 mg IV every 6 hours for 24 hours.

e. Administration of Heliox (helium:oxygen, 80:20) can dramatically improve gas exchange and the work of breathing by establishing laminar airflow and improving gas exchange at distal alveoli.

f. Reintubation of the trachea must be considered early in the course of suspected airway obstruction as distortion of airway anatomy may occur rapidly, particularly in the setting of allergic reactions.

4. Wound hematoma caused by bleeding at the surgical site may complicate thyroid and parathyroid surgery, neck dissections, and carotid endarterectomy. The pressure caused by an expanding hematoma within the neck tissue planes causes obstruction of venous and lymphatic drainage and massive edema. Patients complain of local pain and pressure, dysphagia, and variable degrees of respiratory distress and may have drainage from the surgical site. Neck wound hematomas must be treated immediately by emergency reexploration and evacuation in the OR. The surgeon should be notified immediately and an OR prepared. The anesthesiologist must support the airway by mask ventilation with 100% O₂, followed by intubation of the trachea under direct vision. If tracheal intubation cannot be rapidly accomplished, opening the wound at the bedside can relieve soft tissue compression of the airway and improve airway patency.

5. Vocal cord (VC) paralysis may occur after thyroid, parathyroid, thoracic, tracheal, and neck surgery or a traumatic endotracheal intubation. VC paralysis may be transient, resulting from manipulation of the recurrent laryngeal nerve, or permanent, from severing the nerve. Unilateral transient VC paralysis is relatively common, and the primary concern is potential aspiration of gastric contents. Permanent unilateral VC paralysis can occur without clinical symptoms as compensatory action of the contralateral VC minimizes the occurrence of aspiration. Bilateral VC paralysis can occur after radical surgery for thyroid or tracheal cancer when neoplastic infiltration makes identification of the recurrent laryngeal nerves difficult. Bilateral VC injury is a rare and serious complication that can lead to complete upper airway obstruction after extubation in the immediate postoperative period. It requires emergency endotracheal intubation (which may be more difficult due to disrupted airway anatomy) and possibly a tracheostomy.

E. The intubated patient presents special considerations. The anesthesiologist in the PACU should establish a plan regarding weaning and extubation or, alternatively, transfer to an ICU. Conditions that could delay the extubation at the end of the surgery include the following:

1. Delayed emergence from general anesthesia due to volatile or IV agents. Reversal may be facilitated pharmacologically for some agents, but generally it is prudent to support ventilation and allow the respiratory depression to resolve spontaneously. The presence of a full stomach mandates additional vigilance in ensuring the recovery of consciousness and pharyngeal reflexes before extubation.