The Postanesthesia Care Unit

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 anesthetics, neuromuscular blocking drugs, and opioids all contribute to the loss of pharyngeal tone in the PACU patient.

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 produces 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. In selected patients, placement of an oral or nasal airway, laryngeal mask airway, or endotracheal tube may be required.

Residual Neuromuscular Blockade

Postoperative residual neuromuscular blockade is unfortunately very common ( Box 80.2 ). The literature reports incidences between 20% and 40% and a recent study even found that 56% of patients 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 on arrival in the PACU because the diaphragm recovers from neuromuscular blockade before the pharyngeal muscles do. With an endotracheal tube 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.

Measurement of the train-of-four (TOF) ratio is a subjective assessment that is often misleading when done by touch or observation alone. A decline in this ratio may not be appreciated until it reaches a value less than 0.4 to 0.5, whereas significant signs and symptoms of clinical weakness persist to a ratio of 0.7. Pharyngeal function is not restored to normal until an adductor pollicis TOF ratio is greater than 0.9.

In the anesthetized patient, a quantitative TOF measurement showing a TOF ratio ≥0.9 is the most reliable indicator of adequate reversal of drug-induced neuromuscular blockade. Qualitative TOF measurement and 5-second sustained tetanus at 50 Hz are insensitive and will not allow detection of fade above an average TOF ratio of 0.31 ± 0.15; 5-second sustained tetanus at 100 Hz is unreliable. 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, the 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 as opposed to 0.60 for the sustained head lift. In a year-long study of 7459 PACU patients who had received general anesthesia, Murphy et al. reported critical respiratory events (CREs) in 61 of them. These events occurred within the first 15 minutes of PACU admission, at which time a TOF ratio was measured. When compared with matched controls, these patients had a significantly lower TOF ratio (0.62 [+0.20]) compared to controls 0.98 [+0.07]). In a recent study, Bulka and associates were able to demonstrate that patients who had received neuromuscular blocking drugs, but did not receive reversal agents, had a 2.26 times higher risk of developing postoperative pneumonia compared to those who did receive reversal agents.

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 a residual neuromuscular blockade and prompt review of possible etiologic factors is indicated (see Box 80.2 ). 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. The approval of sugammadex in the United States by the FDA in December 2015 may have a major impact on residual paralysis in patients who were paralyzed with aminosteroid neuromuscular blocking drugs (sugammadex does not work with benzylisoquinolinium neuromuscular blocking drugs). While reversal with neostigmine requires a baseline twitch response, and the duration 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 within several minutes after administration. In a recent study, reversal with sugammadex resulted in a return of TOF ratio to greater than 0.9 within 5 minutes in 85% of patients with no twitches on TOF stimulation. It is anticipated that 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.

Laryngospasm

Laryngospasm refers to a sudden spasm of the vocal cords that completely occludes the laryngeal opening via forceful tonic contractions of the laryngeal muscles and descent of the epiglottis over the laryngeal inlet. It typically occurs in the transitional period when the extubated patient is emerging from general anesthesia yet not fully awake. Although laryngospasm is most likely to occur in the operating room at the time of tracheal extubation, patients who arrive in the PACU asleep after general anesthesia are also at risk for laryngospasm upon awakening, which is often triggered by airway irritants, such as secretions or blood. Treatment of laryngospasm involves removal of the stimulus (suctioning of secretions, blood) and the application of a jaw thrust maneuver with CPAP (up to 40 cm water [H ₂ O]) is often sufficient stimulation to break the laryngospasm. However, if jaw thrust maneuver and CPAP fail, then immediate skeletal muscle relaxation can be achieved with succinylcholine (0.1-1.0 mg/kg intravenously [IV] or 4 mg/kg intramuscularly [IM]). If these maneuvers fail, one should proceed with a full dose of an induction agent and intubating dose of a muscle relaxant to enable the practitioner to perform an emergent tracheal intubation; attempting to pass a tracheal tube forcibly through a glottis that is closed because of laryngospasm is not acceptable.

Edema or Hematoma

Airway edema is a possible surgical complication in patients undergoing prolonged procedures in the prone or Trendelenburg position, procedures involving the airway and neck (including thyroidectomy, carotid endarterectomy, and cervical spine procedures ), as well as those in which the patient receives a 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 (see also Chapter 44 ). Patients who have had a difficult intraoperative intubation and/or airway instrumentation may also have increased airway edema from direct injury. If tracheal extubation is to be attempted in these patients in the PACU, then evaluation of airway patency must precede removal of the endotracheal tube. The patient’s ability to breathe around the endotracheal tube can be evaluated by suctioning the oral pharynx and deflating the endotracheal tube cuff. With occlusion of the proximal end of the endotracheal tube, the patient is then asked to breathe around the tube. Good air movement suggests that the patient’s airway will remain patent after tracheal extubation. An alternative method involves measuring the intrathoracic pressure required to produce a leak around the endotracheal tube with the cuff deflated. This method was originally used to evaluate pediatric patients with croup before extubation. When used in patients with general oropharyngeal edema, the safe pressure threshold can be difficult to identify. Lastly, when ventilating patients in the volume control mode, one can measure the exhaled tidal volume before and after cuff deflation. Patients who require reintubation generally have a smaller leak (i.e., less percentage difference between exhaled volume before and after cuff deflation) than those who do not. A difference greater than 15.5% is the advocated cutoff value for extubation of the trachea. The presence of a cuff leak demonstrates the likelihood of successful extubation, not a guarantee, just as a failed cuff leak does not rule out a successful extubation. The cuff leak test does not and should never take the place of sound clinical judgment, as it is neither sensitive nor specific; it may be used as an adjunct to aid in providing another layer of guidance.

In order to facilitate the reduction of airway edema, one may sit the patient upright to ensure adequate venous drainage, and consider administering a diuretic and intravenous dexamethasone (4-8 mg every 6 hours for 24 hours), which may help decrease airway swelling.

External airway compression is most often caused by hematomas following thyroid, parathyroid, or carotid surgical procedures. Patients may complain of pain and/or pressure, dysphagia, and can demonstrate signs of respiratory distress as the pressure from the expanding hematoma within the tissue can disrupt both venous and lymphatic drainage, both of which can further exacerbate airway swelling. Mask ventilation may not be possible in a patient with severe upper airway obstruction resulting from edema or hematoma. In the case of a hematoma, an attempt can be made to decompress the airway by releasing the clips or sutures on the wound and evacuating the hematoma. This maneuver is recommended as a temporizing measure, but it will not effectively decompress the airway if a significant amount of fluid or blood (or both) has infiltrated the tissue planes of the pharyngeal wall. If emergency tracheal intubation is required, then ready access to difficult airway equipment and surgical backup to perform an emergency tracheostomy are crucial, as one should assume increased difficulty secondary to laryngeal and airway edema, possible tracheal deviation, and a compressed tracheal lumen. If the patient is able to move adequate air via spontaneous ventilation, then an awake technique is often preferred as visualization of the cords by direct laryngoscopy may not be possible.

Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) syndrome is an often overlooked cause of airway obstruction in the PACU, given that most patients are actually not obese and the vast majority of patients are undiagnosed at the time of surgery.

It is well known that patients with OSA are at an increased risk of suffering from cardiopulmonary complications as compared to the general population not affected by OSA syndrome. Patients with OSA are particularly prone to airway obstruction and should not be extubated until they are fully awake and following commands. Any redundant compliant pharyngeal tissue in these patients not only increases the incidence of airway obstruction, but can also increase the difficulty of intubation by direct laryngoscopy. Once in the PACU, a patient with OSA whose trachea has been extubated is exquisitely sensitive to opioids and, when possible, continuous regional anesthesia techniques should be used to provide postoperative analgesia. Other opioid-sparing techniques should be utilized, such as scheduled acetaminophen, and use of nonsteroidal antiinflammatory drugs (NSAIDs) when not contraindicated. One may also employ the use of ketamine, dexmedetomidine, and clonidine, all of which can also decrease postoperative opioid requirements. Interestingly, 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.

Another strategy to employ when caring for a patient with OSA is to position them in either an upright (seated, reverse Trendelenburg) or semi-upright position whenever possible, as the supine position is known to worsen OSA.

In addition, the use of goal-directed fluid strategies should be utilized with consideration of lower salt-containing substances, as these patients are more prone to fluid shifts, which can worsen airway edema.

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.

In patients with OSA who are morbidly obese, immediately applying CPAP postextubation in the operating room rather than waiting to apply positive pressure in the PACU may offer additional benefits. In patients undergoing laparoscopic bariatric surgery, Neligan and colleagues compared the application of 10 cm H ₂ O CPAP immediately postextubation to instituting the same CPAP 30 minutes later in the PACU. When compared with matched controls, patients who received immediate CPAP demonstrated improved spirometric lung function (i.e., functional residual capacity [FRC], peak expiratory flow [PEF], and forced expiratory volume [FEV]) at 1 hour and 24 hours postoperatively.

Two large cohort studies demonstrated that patients with OSA who are not treated with positive airway pressure (PAP) preoperatively are at increased risk for cardiopulmonary complications after general and vascular surgery and that PAP therapy was associated with a reduction in postoperative cardiovascular complications. If the patient can tolerate PAP, and their surgical procedure is not a contraindication to its application, patients with OSA should use a PAP device postoperatively.

Alveolar Hypoventilation

Review of the alveolar gas equation demonstrates that hypoventilation alone is sufficient to cause arterial hypoxemia in a patient breathing room air ( Fig. 80.2 ). At sea level, a normocapnic patient breathing room air will have an alveolar oxygen pressure (PAO ₂ ) of 100 mm Hg. Thus, a healthy patient without a significant alveolar-arterial gradient will have a Pao ₂ near 100 mm Hg. In the same patient, an increase in Paco ₂ from 40 to 80 mm Hg (alveolar hypoventilation) results in a Pao ₂ of 50 mm Hg. Hence, even a patient with normal lungs will become hypoxic if allowed to significantly hypoventilate while breathing room air.

Normally, minute ventilation increases linearly by approximately 2 L/min for every 1-mm Hg increase in Paco ₂ . In the immediate postoperative period, the residual effects of inhaled anesthetics, opioids, and sedative-hypnotics can significantly depress this ventilatory response to carbon dioxide. In addition to depressed respiratory drive, the differential diagnosis of postoperative hypoventilation includes generalized weakness due to residual neuromuscular blockade or underlying neuromuscular disease. The presence of restrictive pulmonary conditions, such as preexisting chest wall deformity, postoperative abdominal binding, or abdominal distention, can also contribute to inadequate ventilation.

Arterial hypoxemia secondary to hypercapnia can be reversed by the administration of supplemental oxygen ( Fig. 80.3 ) or by normalizing the patient’s Paco ₂ by external stimulation of the patient to wakefulness, pharmacologic reversal of opioid or benzodiazepine effect, or controlled mechanical ventilation of the patient’s lungs.

Decreased Alveolar Oxygen Pressure

Diffusion hypoxia refers to the rapid diffusion of nitrous oxide into alveoli at the end of a nitrous oxide anesthetic. Nitrous oxide dilutes the alveolar gas and produces a transient decrease in Pao ₂ and Paco ₂ . In a patient breathing room air, the resulting decrease in Pao ₂ can produce arterial hypoxemia while decreased Paco 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 moments in the PACU.

Ventilation-Perfusion Mismatch and Shunt

Hypoxic pulmonary vasoconstriction refers to the attempt of normal lungs to optimally match ventilation and perfusion. 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 used to treat systemic hypertension or improve hemodynamics will blunt hypoxic pulmonary vasoconstriction and contribute to arterial hypoxemia.

Unlike a 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 PAP by facemask can be effective in treating atelectasis.

Increased Venous Admixture

Increased venous admixture typically refers to low cardiac output states. It is due to 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 Pao 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 Pao 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.

Finally, keep in mind that inadequate oxygen delivery may result from an unrecognized disconnection of the oxygen source or empty oxygen tank.

Postobstructive Pulmonary Edema

Postobstructive pulmonary edema (also referred to as negative pressure pulmonary edema, NPPE) is a rare, but significant consequence of laryngospasm and other upper airway obstruction that may follow tracheal extubation at the conclusion of anesthesia and surgery. Laryngospasm is likely the most common cause of postobstructive pulmonary edema in the PACU, but postobstructive pulmonary edema may result from any condition that occludes the upper airway. The etiology of NPPE is multifactorial, but is clearly correlated with the generation of exaggerated negative intrathoracic pressure attributable to forced inspiration against a closed glottis. The resulting negative intrathoracic pressure augments blood flow to the right side of the heart, which in turn dilates and increases hydrostatic pressure gradient across the pulmonary vascular bed, promoting the movement of fluid into the interstitial and alveolar spaces from the pulmonary capillaries. Negative inspiratory pressure will also increase left ventricular afterload, thus decreasing the ejection fraction, which heightens left ventricular end diastolic pressure, left atrial pressure, and pulmonary venous pressure. This chain of events further escalates the development of pulmonary edema via increase of pulmonary hydrostatic pressures. Patients who are muscularly healthy are at increased risk of postobstructive pulmonary edema secondary to their ability to generate significant inspiratory force.

The resulting arterial hypoxemia develops relatively quickly (usually observed 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. The general consensus of postoperative monitoring in these patients ranges anywhere from 2 to 12 hours. Resolution of NPPE typically occurs within 12 to 48 hours when recognized and treated immediately; however, if diagnosis and resulting therapy is delayed, mortality rates can reach 40%. Although it is quite uncommon, pulmonary hemorrhage and hemoptysis have been observed.