I. INTRODUCTION

Postoperative respiratory complications occur commonly and are a significant source of morbidity and mortality. A large Australian review showed respiratory and airway complications occurring in 2.2% of 8,372 postanesthetic care unit (PACU) admissions. Notable complications were inadequate oxygenation and ventilation, upper airway obstruction, and aspiration. Because most respiratory events culminate in hypoxemia as the common pathway, routine use of pulse oximetry in the PACU can lead to timely detection of these complications. However, because most patients receive supplemental oxygen therapy, desaturation may not occur until late in the course of respiratory events, and PACU providers must use other parameters and clinical signs to assist in their assessments of pulmonary status. In the evaluation of the patient with postoperative pulmonary issues, the anesthesiologist in the PACU must decide which issues can continue to be treated in the PACU with the extension of care on the hospital floor or which patients will require triaging to an ICU either for more definitive care or for extensive observation.

II. CONTRIBUTING FACTORS

A. The development of postoperative respiratory complications is a synergy between a patient’s medical condition and the effects of general anesthesia (GA) and surgery on the respiratory system.

1. Patient factors

Age > 70 years, ASA classification ≥ 2, cigarette smoking, malnutrition (serum albumin < 30 g/L), functional dependence, and comorbidities such as underlying chronic respiratory disease, congestive heart failure, and neuromuscular weakness all decrease pulmonary reserve and increase susceptibility to effects of surgery and anesthesia.

a. Patients with asthma have increased risk of bronchospasm, pneumonia, and respiratory failure if history of frequent exacerbations, recent hospitalization, or tracheal intubation for asthma. Complication rates for general versus regional anesthesia were similar in a study of over 1,500 asthmatic patients.

b. Chronic obstructive pulmonary disease (COPD) is associated with high risk of developing postoperative pulmonary complications. Patients can have chronically fatigued respiratory muscles, unrecognized cor pulmonale, and bronchospasm in addition to their fixed obstructive disease.

c. Obstructive sleep apnea (OSA) is greatly affected by anesthesia and surgery, and patients are at risk for more frequent and severe episodes of postoperative hypoxemia. Sedatives and analgesics decrease pharyngeal tone and attenuate responses to hypoxia and hypercarbia. GA alone results in transient alterations in sleep architecture, which combined with use of opioids may be important factors in the development of postoperative sleep disturbance and propensity for obstruction.

d. Smoking cessation should be emphasized in all patients. Carbon monoxide and nicotine normalize after 12 to 48 hours of abstinence. Airway reactivity is reduced after 1 week, and sputum volume is halved at 2 weeks. Stopping smoking 4 to 6 weeks prior to surgery is shown to reduce the overall incidence of perioperative respiratory complications.

2. Surgical factors

a. Thoracic and abdominal surgery (including major vascular surgeries) results in dysfunction of the diaphragm. This occurs via functional disruption of respiratory muscles from surgical incisions and retracting, irritation, or injury of the phrenic and intercostal nerves, and effects of postoperative pain limiting deep breathing. These factors produce a restrictive respiratory pattern in the acute postoperative period. In patients undergoing laparotomy, functional residual capacity (FRC) decreases to approximately 50% of baseline, returning to normal over 1 to 2 weeks. Neurosurgery can affect control of respiration, and surgeries involving the head and neck increase the risk for airway complications postoperatively.

b. The degree of surgical insult such as level of aggressiveness, procedure duration (>3 hours), and amount of blood lost is associated with postoperative pulmonary complications, likely as part of the systemic inflammatory response syndrome, large fluid shifts during resuscitation, and amplification of local factors described earlier. The need for intraoperative blood transfusion is an independent risk factor, as is emergency surgery.

3. Anesthetic factors

a. GA reduces FRC with an immediate and universal development of atelectasis in the dependent parts of the lung. FRC is reduced by approximately 20% under GA with greater reduction in patients with obesity and COPD. This occurs from loss of chest wall muscle tone and upward displacement of the diaphragm causing compression atelectasis. The reduced FRC, in part, also decreases lung compliance and increases airway resistance. The relative reduction in FRC to closing volume produces intrapulmonary shunting and ventilation-perfusion mismatches. Anesthesia is also associated with inhibition of hypoxic and hypercapnic ventilatory drive, which persists for a variable period of time postoperatively and predisposes to hypoventilation and hypoxemia.

b. Epidural anesthesia without GA creates little to no atelectasis formation. Neuraxial techniques may therefore be preferred in high-risk patients.

c. Residual anesthetics, sedatives, and analgesics blunt hypoxic and hypercapnic ventilator drives, predisposing to hypoventilation and hypoxemia.

B. Risk Stratification

Although patients at increased risk for developing postoperative respiratory complications can be identified, it is difficult to quantify their risk with more precision.

1. Laboratory studies, baseline arterial blood gases, pulmonary function testing, and preoperative chest radiograph have not been shown to be helpful, unless there is a question of diagnosis or presence of unexplained symptoms.

2. Predictive pulmonary risk indices for postoperative respiratory failure or pneumonia (Table 17.1) have been developed. The major contributors to patients’ risk remain clinical factors. These results were based on the analysis of Veteran Affairs patient database, which,
although encompassing a high number of patients, was skewed to include mostly male veterans.

III. UPPER AIRWAY OBSTRUCTION

A. Upper airway obstruction is most often caused by inadequate recovery of airway reflexes and muscle tone.

B. Clinical signs typically include poor chest excursion, discoordinate abdominal and chest wall motion during inspiration, and intercostal and suprasternal retraction. Inspiratory stridor and snoring may be present if the obstruction is partial; complete obstruction is silent.

C. At-risk groups are patients with history of OSA, craniofacial abnormalities, redundant soft tissues (obesity), acromegaly, and tonsillar and adenoidal hypertrophy

D. Differential Diagnoses

1. Pharyngeal obstruction from a sagging tongue and poor pharyngeal tone in the semiconscious patient is the most common cause of postoperative airway obstruction. The most studied upper airway dilator muscles are the genioglossus and tensor palatini muscles, both of which are involved in stabilizing airway patency in response to negative pharyngeal pressure during inspiration. Residual anesthetic and neuromuscular blockade can cause dilator muscle dysfunction and airway collapse in the postoperative patient.

a. Pharyngeal obstruction usually responds to simple airway maneuvers including chin tilt and jaw thrust (anteriorly displacing mandible), lateral decubitus positioning, and use of oral- or nasopharyngeal airways. Nasal airways are typically better tolerated, because they do not stimulate the gag reflex.

b. Patients with OSA can benefit from continuous positive airway pressure (CPAP), ideally from the time of extubation onward. It is advantageous for the patient to bring his/her own CPAP machine to the hospital.

2. Laryngeal obstruction

a. Laryngospasm is caused by intense tonic contraction of the laryngeal muscles and descent of the epiglottis over the laryngeal inlet. Laryngospasm in the PACU is generally precipitated by an airway irritant (e.g., secretions, blood) in a patient still emerging from anesthesia. Partial laryngospasm can be difficult to discern from other causes of airway obstruction because some air movement still occurs. Vocal cord paresis can result from recurrent laryngeal nerve (RLN) injury or mechanical injury to the vocal cords. Injury to the RLN prevents abduction of the ipsilateral vocal cord, which fixes in a paramedian position because of unopposed action of the cricothyroid muscle (supplied by the superior laryngeal nerve). The RLN and vocal cords can be injured during thyroid, parathyroid, laryngeal, and thoracic surgery as well as from trauma sustained during rigid bronchoscopy and intubation. Unilateral RNL injury presents typically with hoarseness, with the primary concern being risk of gastric aspiration. Both laryngospasm and vocal cord paresis can be clinically manifested by stridor and extremely high-pitched vocalization. Paradoxical respiration (chest retraction during inspiration while the abdomen is distended) may also be noticed. A brief application of positive pressure ventilation will be efficacious to “break open” the vocal cords if laryngospasm is the problem. If this treatment is not effective, there should be no delay in securing the airway with tracheal intubation especially if bilateral vocal cord abduction from nerve injury is likely. Most vocal cord paralysis is transient, and recovery occurs over the course of weeks to months. Permanent paralysis occurs. Complete laryngospasm and vocal cord paralysis can cause negative pressure pulmonary edema.