Causes of postoperative hypoxemia

Upper airway obstruction: Upper airway obstruction can occur in the surgical patient, typically because of posterior displacement of the tongue and loss of airway muscular tone (see Table 9.1). Perioperative polypharmacy including opioids and sedatives is responsible for many cases of postoperative airway obstruction. Subclinical residual neuromuscular blockade may present with airway obstruction. As many as 31% of surgical patients arriving in the PACU have demonstrable residual neuromuscular blockade.^[9] Residual neuromuscular blockade is implicated in a majority of hypoxic events in the PACU and many cases of upper airway obstruction.^[10] Gauze throat packs are often used during surgical procedures to prevent the swallowing of blood to decrease the incidence of postoperative nausea and vomiting. Failure to remove the throat pack at the end of surgery may cause sudden airway obstruction in the early postoperative period. Upper airway edema from trauma, angioedema, vocal cord paralysis, and expanding neck hematoma after carotid endarterectomy are less common causes. Most upper airway obstructions may be managed with airway maneuvers including chin lift or jaw thrust. For refractory causes or when the patency of the airway is threatened, endotracheal intubation may be necessary. If endotracheal intubation is not successful in the presence of a postoperative neck hematoma, decompression of the hematoma may be life-saving and should not be delayed.

Stridor: Causes of hypoxia which present with stridor are discussed separately in Chapter 10.

Atelectasis is the most common cause of postoperative hypoxemia (occurring in 45–90% of cases) and is the result of both mechanical and physiological pulmonary changes that accompany general anesthesia. Within 5 minutes of the induction of general anesthesia atelectasis develops and can persist days into the postoperative period.^[11] Three mechanisms have been described that contribute to the development of atelectasis: compression, gas absorption, and surfactant impairment.^[12]

Compression atelectasis results from a reduction in the transthoracic pressure leading to alveolar collapse. This is associated with patient positioning (supine, lithotomy), body habitus, surgical factors (retraction, packing), and surgical site (thoracic, abdominal). Gas absorption atelectasis can result from the use of high oxygen concentrations. Nitrogen makes up 80% of room air and is poorly absorbed, thereby serving to prevent alveolar collapse which may occur when nitrogen is displaced by oxygen. Anesthetic agents and low tidal volumes cause atelectasis by impairing surfactant action leading to increased surface tension. The physiological impact of the three mechanisms is to increase the shunt fraction.

Atelectasis is usually not visible on plain imaging unless severe; CT imaging is more sensitive but rarely necessary. Prevention begins intraoperatively with recruitment maneuvers, positive end-expiratory pressure (PEEP), and utilization of the minimal necessary oxygen concentration.^[13] Supplemental oxygen corrects atelectasis-induced hypoxemia, but may exacerbate the atelectasis, so it should be administered with therapy directed at the atelectasis itself. Simple posture change from supine to upright may decrease atelectasis. Deep breathing maneuvers, including incentive spirometry, deep breathing exercises, intermittent positive pressure breathing, and chest physiotherapy, have been shown to improve atelectasis.^[14]

Pulmonary embolism is more common in the perioperative period, and one must have a high level of suspicion in order to diagnose promptly. Multiple types of pulmonary emboli exist including venous thromboemboli (VTE), air, or fat.

VTE risk is elevated after surgery owing to a derangement in one or more of the components of Virchow’s triad (hypercoagulability, venous stasis, and vessel injury). General anesthesia leads to a state of venous stasis due to immobility and vasodilation from the effect of anesthetic drugs. The surgical stress response leads to a hypercoagulable state, while the surgical intervention itself can lead to direct vessel injury. Major orthopedic procedures of the lower extremity or pelvis are especially high risk for VTE.

The clinical presentation of VTE can range from asymptomatic, to mild hypoxemia, to cardiovascular collapse, depending on the size and rapidity of embolism development. Typical non-specific signs and symptoms include tachypnea, tachycardia, dyspnea, hypoxia, chest pain, hypotension, and increased dead space ventilation. The latter manifests as an increased PaCO₂ to end-tidal CO₂ gradient as well as hypoxia uncorrected with supplemental oxygen. Signs of right ventricular dysfunction may also be present. Physical exam may demonstrate distended neck veins, increased pulmonic heart sound, and a tricuspid regurgitation murmur. Electrocardiogram (ECG) may demonstrate the classic S1Q3T3 pattern, but may also show T-wave inversion in leads V1–V4, or incomplete or complete right bundle-branch block.^[15] However, it is important to note that the ECG is usually normal after pulmonary embolism, and the most common ECG abnormality is sinus tachycardia, so the more specific signs of acute right heart strain may be absent. Laboratory studies are of limited utility in the postoperative period,^[16] and the diagnosis of pulmonary embolism can be confirmed by imaging studies. CT angiography is the study of choice because of its rapidity and ability to also evaluate the veins of the legs and pelvis for embolic sources. Treatment consists of supportive therapy and anticoagulation is usually administered to prevent further progression of clot formation. If anticoagulation is contraindicated, an inferior vena cava filter should be placed. In hemodynamically unstable patients, thrombolytic therapy as well as catheter or surgical based embolectomy may be considered.^[17]

Venous air embolism (VAE) is associated with surgeries in which air enters the venous circulation via an incision or cannulated vein above the level of the heart. Small air emboli resolve spontaneously, but large quantities of air may cause respiratory embarrassment. Intracardiac air may be associated with a “mill-wheel” murmur. Air embolism may present after surgery and may be associated with central line (CVP) insertion or vascular catheter open to air. Preventing further air entrainment is crucial. Transesophageal echocardiography, pulmonary artery catheters, or precordial Dopplers have a high yield in diagnosis.^[18] Placing the patient in the Trendelenburg position, left side down, to prevent paradoxical cerebral embolism through a patent foramen ovale, and aspiration of intracardiac air from a CVP placed into the right ventricle may be necessary.

Fat emboli and emboli of surgical debris are most commonly seen in orthopedic procedures where fat from bone marrow or debris from cement enters the venous system owing to elevated medullary pressure or surgical manipulation from placement of rods or nails. Symptoms of fat embolism are protean because of the diffuse effect of numerous emboli. Mental status changes are common, and a petechial rash may be observed in about one-half of affected patients. Treatment is supportive with intravenous steroids possibly demonstrating benefit in some trials. Heparin, aspirin, alcohol, hypertonic glucose with insulin, surfactant, clofibrate, α-blockers, corticosteroids, albumin, dextran, and aprotinin have all been advocated in therapy, but none have been shown to improve outcome.^[19]

Pneumothorax is an uncommon but potentially fatal complication after surgery. Pneumothorax can occur spontaneously or iatrogenically from a surgical or barotrauma related to mechanical ventilation. It should be considered in the setting of central line placement (risk: subclavian > internal jugular vein), rib fracture, regional anesthesia (neuraxial, brachial plexus, and intercostal blocks), neck dissections, tracheostomy, nephrectomies, or other retroperitoneal or intraabdominal procedures. Patients with history of emphysema, subpleural blebs, or large bullae can develop pneumothorax with positive pressure ventilation. Pneumothorax can also result from anesthesia machine malfunction or a patient coughing or bucking during positive pressure ventilation.

The clinical presentation of pneumothorax is based on the underlying etiology, but includes chest pain, shortness of breath, and possibly hemoptysis. Physical exam will demonstrate hyperresonance and decreased breath sounds on auscultation and decreased chest excursion on the affected side. Chest radiography and computed tomography can aid in the diagnosis of pneumothorax. If the size of the pneumothorax is relatively small (15% to 20%) it can be managed conservatively with 100% oxygen and radiological follow-up to ensure resolution.^[20] However, if the pneumothorax is larger or the patient is symptomatic, a chest tube should be inserted. Tension pneumothorax can develop if a one-way valve exists in the lungs or pleura such that air enters the pleural space but cannot exit. Needle decompression and chest tube insertion may be necessary.

Pleural effusion causes hypoxia by compression of lung parenchyma by fluid accumulation in the thoracic cavity. Pleural effusions may be exacerbated by fluid shifts after surgery, but rarely have first presentation postoperatively. Exceptions include hemothorax, which may occur after surgical trauma or CVP, and urinothorax, very rarely reported after urinary tract procedures. It is important to remember that hemothorax may occur after unsuccessful attempt at CVP, so the postoperative patient with hemothorax may not have an indwelling CVP.

Bronchospasm is caused by a contraction of the smooth muscles surrounding the bronchial tree. It may present as a component of an allergic reaction, but more commonly it is an isolated non-allergy event. Bronchospasm is more common and more severe in patients with a history of reactive airway disease such as asthma or chronic obstructive pulmonary disease, but can occur in patients with no such history. Other risk factors include history of tobacco exposure, recent respiratory infection, endotracheal intubation, airway manipulation, mechanical or chemical airway irritation, or pulmonary edema.^[19] Clinical presentation may include expiratory wheezing, prolonged expiration, reduced breath sounds, and increased airway pressures during positive pressure ventilation.

The mainstay of treatment is inhaled short-acting β-agonist, such as albuterol, administered via a metered dose inhaler (MDI; 6 to 8 puffs repeated as needed) or nebulizer (5 mg). In the intubated patient, only 10% of the MDI administered reaches the airway while 90% condenses in the circuit; therefore treatment should be based on the clinical response (or appearance of side effects) rather than a set dose. In severe bronchospasm, inhaled agents may be ineffective owing to limited air movement. Important second-line agents include: epinephrine (10–100 mcg IV) titrated to effect, ipratropium bromide (0.5 mg q 6 hr), magnesium sulphate (50 mg/kg IV over 20 min, max 2 g), hydrocortisone 200 mg IV q 6 hr, and ketamine bolus 10–20 mg.^[20]

Pulmonary edema can be classified as either cardiogenic or non-cardiogenic. Cardiogenic pulmonary edema (increased hydrostatic pressure) results from acute left ventricular failure from fluid overload (>1.5 liter), myocardial ischemia or infarction. Patients often carry a history of cardiopulmonary dysfunction such as congestive heart failure, coronary artery disease, cardiomyopathy, arrhythmia, or valvular dysfunction. Non-cardiogenic pulmonary edema (increased permeability) occurs in the setting of acute respiratory distress syndrome, SIRS, sepsis, transfusion, trauma, burns, and aspiration. Damage to the alveolar cells allows fluid to enter the alveolar space, leading to pulmonary edema. Non-cardiac pulmonary edema occurring within 6 hours of the transfusion of blood products should raise suspicion for transfusion-related lung injury (TRALI). TRALI occurs after 1:3,000 transfusions of red cells and is the most common cause of transfusion-related mortality.^[21]

Patients usually present with hypoxemia, tachypnea, dyspnea, tachycardia, or airway secretions (“pink frothy” secretions). Chest auscultation may reveal rales, and chest radiography will demonstrate pulmonary cephalization. Troponin levels and ECG may suggest cardiac ischemia or infarction. Echocardiography can evaluate myocardial function and valvular anatomy. Left ventricular apical ballooning syndrome (Takotsubo cardiomyopathy) is increasingly recognized by the characteristic chest pain, ECG abnormalities indicative of cardiac ischemia, pulmonary edema, and transient echocardiographic abnormalities including ballooning of the ventricular apex with relative sparing of the wall motion at the base of the heart. When there is diagnostic uncertainty, a wedge pressure may aid in the diagnosis. Pulmonary occlusion pressure is usually elevated in cardiogenic pulmonary edema but normal in non-cardiogenic edema. Management is guided by the underlying etiology. In the case of cardiogenic pulmonary edema, treatment consists of diuresis and afterload reduction with further intervention specific to the underlying etiology. In non-cardiogenic edema, lung protective measures should be undertaken in the intubated patient with low peak pressures and low tidal volume ventilation (6 ml/kg of ideal body weight).^[21]

Hypoventilation with severe hypercapnia can lead to hypoxemia by necessarily lowering the alveoral oxygen content. Hypoventilation in the recovery period is common, but usually mild and undiagnosed. Signs usually become apparent at a PaCO₂ above 60 mmHg and include somnolence, slow respiratory rate, labored breathing, tachypnea, and shallow breaths. Mild to moderate hypercapnia leads to sympathetic activation with tachycardia, hypertension, and cardiac irritability, but cardiac depression when hypercapnia becomes severe.

Hypoventilation is usually a result of the depressant effects of the anesthetic agents on respiratory drive. These agents include opioids, benzodiazepines, and anesthetic gases, as well as residual neuromuscular blockade and/or inadequate reversal. In addition to anesthetic drugs, other causes of hypoventilation include splinting, airway obstruction, bronchospasm, and restrictive conditions such as abdominal binders and abdominal distension.

Arterial blood gas tensions will allow one to assess the severity of hypoventilation and respiratory acidosis, and will guide management. Management should target the underlying cause. Patients with severe hypoventilation, obtundation, severe respiratory acidosis, or circulatory depression require intubation. Naloxone can be used to antagonize the respiratory depressant effects of opioids, remembering that most opioids have a longer duration of action than naloxone and will require careful monitoring. Flumazenil may reverse the sedative effects of benzodiazepines, but the reversal of respiratory depression is less reliable. Residual neuromuscular blockade can be ruled out with a sustained head-lift or observation of a train-of-four twitches elicited by a peripheral nerve stimulator in intubated patients, and further anticholinestrase can be given. Respiratory splinting can be mitigated with analgesics.

Hypoxia due to competitive binding to hemoglobin is a rare cause of postoperative hypoxia. Carbon monoxide may be produced when volatile anesthetics contact desiccated baralyme used to scrub carbon dioxide from the system.^[22] Desiccation occurs from air flow through the circuit, so this complication may occur on Monday morning (from a machine running over the weekend) or if anesthesia is conducted in infrequently used outpost locations. Oxygen administration is therapeutic. Methemoglobinemia may occur because of exposure to a variety of medications that may be administered during surgery, but is most often reported after exposure to benzocaine. Cyanosis that does not respond to supplemental oxygen in a patient having received a precipitating medication should raise suspicion for methemoglobinemia. Treatment with methylene blue may be curative.

Right-to-left shunting of pulmonary blood returning poorly oxygenated blood into systemic circulation is a cause of hypoxia refractory to supplemental oxygenation. This may occur in individuals with known intracardiac defects or may occur de novo after surgery. Patients with pulmonary hypertension may experience shunting through a patent foramen ovale or other pathway when systemic pressure falls. Even in the absence of pre-existing pulmonary hypertension, new right-to-left shunts may occur rarely after surgical procedures. Pulmonary resections including pneumonectomy or lobectomy may precipitate right-to-left shunts which develop gradually over months, but on very rare occasions these have occurred acutely in the PACU.^[23] The normal 5% of intrapulmonary shunting may be exaggerated in conditions in which mixed venous oxygen falls, including severe anemia. Treatment of right-to-left shunting is directed at correction of the underlying cause.

Factitious hypoxemia from pulse oximeter failure can occur. Patient movement, interference from ambient light, poor tissue perfusion, or the use of vasopressors may lead to inaccurate readings. The incidence of pulse oximeter failure in the PACU setting is about 1 in every 150 patients.^[24] Poor plethysmography waveform may suggest this etiology, and rotation of the probe to another site may correct this problem.