Postanesthesia Recovery

Loss of Pharyngeal Muscle Tone

The most frequent cause of airway obstruction in the immediate postoperative period is the loss of pharyngeal muscle tone in a sedated or obtunded patient. The persistent effects of inhaled and intravenous (IV) anesthetics, neuromuscular blocking drugs, and opioids all contribute to the loss of pharyngeal tone in this setting.

In an awake patient opening of the upper airway is facilitated by the contraction of the pharyngeal muscles at the same time that negative inspiratory pressure is generated by the diaphragm. As a result, the tongue and soft palate are pulled forward, tenting the airway open during inspiration. This pharyngeal muscle activity is depressed during sleep, and the resulting decrease in tone can promote airway obstruction. A vicious cycle then ensues wherein the collapse of compliant pharyngeal tissue during inspiration produces a reflex compensatory increase in respiratory effort and negative inspiratory pressure that promotes further airway obstruction.

The effort to breathe against an obstructed airway is characterized by a paradoxical breathing pattern consisting of retraction of the sternal notch and exaggerated abdominal muscle activity. Collapse of the chest wall and protrusion of the abdomen with inspiratory effort produce a rocking motion that becomes more prominent with increasing airway obstruction. Obstruction secondary to loss of pharyngeal tone can be relieved by simply opening the airway with the “jaw thrust maneuver” or continuous positive airway pressure (CPAP) applied via a facemask (or both). Support of the airway is needed until the patient has adequately recovered from the effects of drugs administered during anesthesia. If the airway obstruction cannot be overcome by the aforementioned approach, placement of an oropharyngeal or nasopharyngeal airway, a supraglottic airway device, or an endotracheal tube (ETT) may be required.

Residual Neuromuscular Blockade

Postoperative residual neuromuscular blockade is very common, with reported incidences between 20% and 40%. A 2015 study even found that 56% of patients (the majority of whom received neostigmine for neuromuscular blockade reversal) had residual neuromuscular blockade upon arrival in the PACU. When evaluating upper airway obstruction in the PACU, the possibility of residual neuromuscular blockade should be considered in any patient who received neuromuscular blocking drugs during anesthesia. Residual neuromuscular blockade may not be evident upon arrival in the PACU because the diaphragm recovers from neuromuscular blockade before the pharyngeal muscles do. With an ETT in place, end-tidal carbon dioxide concentrations and tidal volumes may indicate adequate ventilation while the ability to maintain a patent upper airway and clear upper airway secretions remains compromised. The stimulation associated with tracheal extubation, followed by the activity of patient transfer to the gurney and subsequent encouragement to breathe deeply, may keep the airway open during transport to the PACU. Only after the patient is calmly resting in the PACU does upper airway obstruction become evident. Even patients treated with intermediate- and short-acting neuromuscular blocking drugs may manifest residual paralysis in the PACU despite what was deemed clinically adequate pharmacologic reversal in the operating room.

The recovery from neuromuscular blockade and the assessment of residual blockade can be done by clinical assessment and by using a nerve stimulator (also see Chapter 11 ). Measurement of the train-of-four (TOF) ratio is a subjective assessment that is often misleading when done by touch or observation alone. The use of quantitative TOF measurement is the most reliable indicator of adequate reversal. Significant signs and symptoms of clinical weakness persist up to a ratio of 0.7, whereas pharyngeal function is not restored to normal until an adductor pollicis TOF ratio is greater than 0.9.

Qualitative TOF measurement and 5-second sustained tetanus at 50 Hz are insensitive and will not detect residual paralysis. In an awake patient clinical assessment of reversal of neuromuscular blockade is preferred to the application of painful TOF or tetanic stimulation. Clinical evaluation includes grip strength, tongue protrusion, ability to lift the legs off the bed, and the ability to lift the head off the bed for a full 5 seconds. Of these maneuvers, the 5-second sustained head lift has been considered to be the standard, reflecting not only generalized motor strength but, more importantly, the patient's ability to maintain and protect the airway. However, studies have shown that the 5-second head lift is remarkably insensitive and should not routinely be used to assess recovery from neuromuscular blockade. The ability to strongly oppose the incisor teeth against a tongue depressor is a more reliable indicator of pharyngeal muscle tone. This maneuver correlates with an average TOF ratio of 0.85.

When a PACU patient demonstrates signs and/or symptoms of muscular weakness in the form of respiratory distress and/or agitation, one must suspect that there could be residual neuromuscular blockade, and prompt review of possible etiologic factors is indicated ( Box 39.2 ). Common factors include respiratory acidosis and hypothermia, alone or in combination. Upper airway obstruction as a result of the residual depressant effects of volatile anesthetics or opioids (or both) may result in progressive respiratory acidosis after the patient is admitted to the PACU and external stimulation is minimized. Simple measures such as warming the patient, airway support, and correction of electrolyte abnormalities can facilitate recovery from neuromuscular blockade.

A 2016 study of one institution's surgical database found that patients who had received neuromuscular blocking drugs but did not receive reversal agents had a 2.3 times greater risk of developing postoperative pneumonia compared with those who did receive reversal agents. The introduction of sugammadex may have a major impact on residual paralysis in patients who received aminosteroid neuromuscular blocking drugs. Although reversal with neostigmine requires a baseline twitch response and the time until the patient has a TOF ratio of ≥0.9 is highly variable, sugammadex can be administered at any depth of neuromuscular blockade and most commonly produces full recovery (TOF ratio ≥0.9) within several minutes after administration (also see Chapter 11 ). The increased availability and use of sugammadex as an alternative to neostigmine will result in a decreased incidence of residual neuromuscular blockade in the PACU. Indeed, a 2020 study comparing sugammadex with neostigmine for neuromuscular blockade reversal confirmed that the risk of postoperative pneumonia, respiratory failure, and other major complications is significantly lower with sugammadex.

Laryngospasm

Laryngospasm refers to a sudden spasm of the vocal cords that completely occludes the laryngeal opening via forceful contractions of the laryngeal muscles. It typically occurs in the transitional period when the extubated patient is emerging from general anesthesia. Although laryngospasm is most likely to occur in the operating room at the time of extubation, patients who arrive in the PACU asleep after general anesthesia are also at risk for laryngospasm upon awakening, triggered by airway irritants such as secretions or blood. Treatment of laryngospasm involves suctioning to remove the stimulus and applying a jaw thrust with CPAP (up to 40 cm H ₂ O) to break the laryngospasm. However, if this fails, immediate skeletal muscle relaxation can be achieved with succinylcholine (0.1 to 1 mg/kg intravenously or 4 mg/kg intramuscularly [IM]). If laryngospasm persists, one should proceed with emergent intubation with a full dose of an induction agent and intubating dose of a muscle relaxant. Because of the risk of causing glottic injury, the anesthesia provider should not attempt to forcibly pass an ETT through a glottis that is closed because of laryngospasm.

Airway Edema or Hematoma

Airway edema is a possible complication of prolonged procedures in the prone or Trendelenburg position, procedures involving the airway and neck (including thyroidectomy, carotid endarterectomy, and cervical spine procedures), and those with large-volume resuscitation. Although facial and scleral edema is an important physical sign that can alert the clinician to the presence of airway edema, visible external signs may not accompany significant edema of pharyngeal tissue. Patients who had a difficult intubation or repeated airway instrumentation may also have increased airway edema. If extubation is to be attempted in these patients in the PACU, evaluation of airway patency must precede removal of the ETT. This is commonly done with a leak test. The patient's ability to breathe around the ETT can be evaluated by suctioning the oral pharynx and deflating the ETT cuff. With occlusion of the proximal end of the ETT, the patient is then asked to breathe around the tube. Satisfactory air movement suggests that the patient's airway will remain patent after tracheal extubation. An alternative method measures the intrathoracic pressure required to produce a leak around the ETT with the cuff deflated. Lastly, when ventilating patients in the volume control mode, one can measure the exhaled tidal volume before and after cuff deflation. The presence of a cuff leak demonstrates the likelihood of successful extubation, but is not a guarantee, just as a failed cuff leak does not rule out a successful extubation. The cuff leak test should not take the place of sound clinical judgment when deciding to safely extubate the patient. If concern for airway compromise is significant, the patient can be extubated with a tracheal tube exchange catheter left in place as a conduit to reintroduce an ETT.

If airway edema is deemed significant enough to preclude extubation, the following measures can facilitate resolution of edema: (1) sitting the patient upright to ensure venous drainage and reduce any component of dependent edema, (2) diuretic administration; and (3) IV dexamethasone to decrease airway swelling.

External airway compression is most often caused by hematomas after thyroid, parathyroid, or carotid surgeries. Patients may complain of pain and/or pressure and dysphagia and can demonstrate signs of respiratory distress. Mask ventilation may not be possible in a patient with a large hematoma. An attempt can be made to decompress the airway by releasing the clips or sutures on the wound and evacuating the hematoma. If emergency tracheal intubation is required, then difficult airway equipment and surgical backup to perform an emergency tracheostomy are crucial; one should assume increased difficulty secondary to laryngeal and airway edema and possible tracheal deviation or compression. If the patient is able to spontaneously ventilate, then awake intubation is preferred because visualization of the vocal cords by direct laryngoscopy may not be possible.

Obstructive Sleep Apnea (also see Chapter 48 )

Obstructive sleep apnea (OSA) is an often-overlooked cause of airway obstruction in the PACU, given that the vast majority of patients are undiagnosed at the time of surgery. Patients with OSA have more frequent cardiopulmonary complications and need for intensive care unit (ICU) transfer.

Patients with OSA are particularly prone to airway obstruction and should not be extubated until they are fully awake and following commands. Once in the PACU, a patient with OSA is exquisitely sensitive to opioids, and, when possible, continuous regional anesthesia and multimodal opioid-sparing analgesic (acetaminophen, nonsteroidal anti-inflammatory drugs [NSAIDs], dexmedetomidine) techniques should be used (also see Chapter 40 ). Benzodiazepines can have a greater effect on pharyngeal muscle tone than opioids, and the use of benzodiazepines in the perioperative setting can significantly contribute to airway obstruction in the PACU.

When caring for a patient with OSA, plans should be made preoperatively to provide CPAP in the immediate postoperative period. Patients should be asked to bring their own CPAP machines with them on the day of surgery to enable the equipment to be set up before the patient's arrival in the PACU. ^, Patients who do not routinely use CPAP at home or who do not have their machines with them may require additional attention from the respiratory therapist to ensure proper fit of the CPAP delivery device (mask or nasal airways) and to determine the amount of positive pressure needed to prevent upper airway obstruction. Patients with known or suspected OSA should have continuous pulse oximetry monitoring in the postoperative period.

Alveolar Hypoventilation

Review of the alveolar gas equation demonstrates that hypoventilation alone is sufficient to cause hypoxemia in a patient breathing room air ( Box 39.4 ). At sea level, a normocapnic patient breathing room air will have an alveolar oxygen pressure (P _A o ₂ ) of 100 mm Hg. Thus a healthy patient without a significant alveolar-arterial gradient will have a Pa o ₂ near 100 mm Hg. In the same patient an increase in Pa co ₂ from 40 to 80 mm Hg (from alveolar hypoventilation) results in a P _A o ₂ of 50 mm Hg. Hence, even a patient with normal lungs will become hypoxemic if significant hypoventilation occurs while breathing room air.

Arterial hypoxemia secondary to hypercapnia can be reversed by administering supplemental oxygen or by normalizing the patient's Pa co ₂ by external stimulation to awaken the patient, pharmacologic reversal of opioid or benzodiazepine effect, or controlled mechanical ventilation.

Decreased Alveolar Partial Pressure of Oxygen

Diffusion hypoxia refers to the rapid diffusion of nitrous oxide into alveoli at the end of a nitrous oxide anesthetic (also see Chapter 7 ). Nitrous oxide dilutes the alveolar gas and produces a transient decrease in Pa o ₂ and Pa co ₂ . In a patient breathing room air the resulting decrease in Pa o ₂ can produce arterial hypoxemia, whereas a decreased Pa co ₂ can depress the respiratory drive. In the absence of supplemental oxygen administration diffusion hypoxia can persist for 5 to 10 minutes after discontinuation of a nitrous oxide anesthetic; therefore it may contribute to arterial hypoxemia in the initial minutes in the PACU.

Ventilation-Perfusion Mismatch and Shunt

Hypoxic pulmonary vasoconstriction refers to the attempt of normal lungs to optimally match ventilation and perfusion (also see Chapter 5 ). This response constricts vessels in poorly ventilated regions of the lung and directs pulmonary blood flow to well-ventilated alveoli. In the PACU the residual effects of inhaled anesthetics and vasodilators, such as nitroprusside and dobutamine, will blunt hypoxic pulmonary vasoconstriction and contribute to arterial hypoxemia.

Unlike ventilation-perfusion mismatch, a true shunt will not respond to supplemental oxygen. Causes of postoperative pulmonary shunt include atelectasis, pulmonary edema, gastric aspiration, pulmonary emboli, and pneumonia. Of these, atelectasis is probably the most common cause of pulmonary shunting in the immediate postoperative period. Mobilization of the patient to the sitting position, incentive spirometry, and positive airway pressure by facemask can be effective in treating atelectasis.

Increased Venous Admixture

Increased venous admixture typically refers to low cardiac output states. It is caused by the mixing of desaturated venous blood with oxygenated arterial blood. Normally, only 2% to 5% of cardiac output is shunted through the lungs, and this shunted blood with a normal mixed venous saturation has a minimal effect on Pa O ₂ . In low cardiac output states blood returns to the heart severely desaturated. Additionally, the shunt fraction increases significantly in conditions that impede alveolar oxygenation, such as pulmonary edema and atelectasis. Under these conditions, mixing of desaturated shunted blood with saturated arterialized blood decreases Pa O ₂ .

Decreased Diffusion Capacity

A decreased diffusion capacity may reflect the presence of underlying lung disease such as emphysema, interstitial lung disease, pulmonary fibrosis, or primary pulmonary hypertension. In this regard the differential diagnosis of arterial hypoxemia in the PACU must include the contribution of any preexisting pulmonary condition.

Postobstructive Pulmonary Edema

Postobstructive pulmonary edema (also referred to as negative pressure pulmonary edema, NPPE ) is a rare, but significant, consequence of laryngospasm (or, less commonly, other upper airway obstruction) that may follow extubation. The etiology of NPPE is multifactorial but is clearly correlated with the generation of exaggerated negative intrathoracic pressure during inspiration against a closed glottis. The resulting negative intrathoracic pressure augments venous return, which in turn increases pulmonary hydrostatic pressures, promoting the movement of fluid into the interstitial and alveolar spaces from the pulmonary capillaries. Patients who are muscular are at increased risk of postobstructive pulmonary edema secondary to their ability to generate significant inspiratory force.

The resulting arterial hypoxemia develops quickly (usually within 90 minutes of the upper airway obstruction) and is accompanied by dyspnea, pink frothy sputum, and bilateral fluffy infiltrates on the chest radiograph. Treatment is generally supportive and includes supplemental oxygen, diuresis, and, in severe cases initiation of positive-pressure ventilation. These patients should be monitored for 2 to 12 hours postoperatively. When recognized and treated immediately, NPPE typically resolves within 12 to 48 hours; however, if diagnosis and therapy are delayed, mortality rates can reach 40%. Although uncommon, pulmonary hemorrhage and hemoptysis have been observed.

Transfusion-Related Acute Lung Injury

The differential diagnosis of pulmonary edema in the PACU should include TRALI in any patient who intraoperatively received blood products. TRALI usually manifests within 2 to 4 hours after the transfusion of plasma-containing blood products, including packed red blood cells, whole blood, fresh frozen plasma, or platelets. TRALI occurs when recipient neutrophils become activated by donor plasma and then release inflammatory mediators, which cause increased pulmonary vascular permeability resulting in pulmonary edema. Clinical manifestations include fever, pulmonary infiltrates on chest radiograph, cyanosis, and systemic hypotension. The sudden onset of hypoxemic respiratory failure can occur up to 6 hours after the conclusion of the transfusion, and TRALI may first present when the patient is in the PACU.

Treatment is supportive and includes supplemental oxygen and diuresis. Approximately 80% of patients will recover within 48 to 96 hours. Mechanical ventilation may be needed to support hypoxemia and respiratory failure, and vasopressors may be required to treat refractory hypotension.