Although many principles of postoperative care in the thoracic surgery population are common to other areas of surgery, there are some important differences. For example, fluid management in thoracic patients differs significantly from strategies used in nonthoracic patients. Lung edema and its effect on pulmonary compliance are closely linked to extracellular fluid volume. Many maneuvers made during thoracic surgery result in an increase in lung water. To compensate, it may be appropriate to restrict fluid administration postoperatively. In general, minimizing total body water improves pulmonary compliance and overall lung function.
Mediastinal dissection, whether for mediastinal tumor or esophageal surgery, can be associated with idiopathic pleural and pericardial effusions. Similarly, esophageal surgery, whether for motility disorder, reflux disease, or tumor, is associated with an increased risk for aspiration pneumonia. An additional consequence of esophagectomy is that it entails a complete vagotomy. In the acute setting, the complete vagotomy may result in prolonged dysmotility, enhancing the risk of malnutrition and even aspiration.
The range of issues that affect the recovery period include extubation, pain, air leak/chest tube management, fluid management, aspiration, ventilation, and the prevention of atrial fibrillation or pulmonary embolism. Specific complications related to a particular thoracic procedure may involve thoracic duct injury, vocal cord paralysis, pulmonary edema after lobectomy, esophageal anastomotic leak, and bronchopleural fistula.
Early extubation is the overriding goal of thoracic anesthesia and should be performed immediately after the surgical procedure. Immediate extubation not only improves patient mobilization but also promotes airway clearance. In rare circumstances, it may be beneficial to ventilate the postoperative patient overnight. Indications for postoperative ventilation include (1) bleeding that requires large-volume resuscitation, (2) inadequate pain control requiring high-dose parenteral narcotics, (3) decortication or visceral pleurectomy, and (4) a high-risk airway.
Postoperative pain control is essential for recovery, particularly in patients undergoing thoracotomy or sternotomy. For patients with severely impaired lung function, a preoperative epidural catheter is often indicated, even for thoracoscopic procedures. Chest wall pain can result in a restrictive chest wall and low lung volumes. Diminished forced vital capacity (FVC) and functional residual capacity (FRC) lead to fatigue and eventual hypoxemia. To prevent this consequence of chest wall pain in high-risk lung surgery patients, epidural catheters or, in selected patients, a paraspinal blockade should be used preemptively. Intravenous analgesics are not an acceptable substitute for epidural analgesia. Intravenous narcotics, whether patient-controlled or controlled by nursing, result in inevitable sedation and potential hypercarbia.
Air Leak/Chest Tube Management
Chest drains are used to evacuate fluid that accumulates in the pleural space after surgery. Blood that collects in the pleural space needs to be evacuated because it may compromise lung function. Similarly, air in the pleural space indicates that the lung is inadequately filling the hemithorax, causing a proportionate impairment in lung function.
The amount of suction applied to the chest tube should be the minimum required to obtain full expansion of the lung. Too much suction may exclude the chest tube if locally compliant tissue occludes the holes of the tube. The chest tube also may be excluded if it is poorly positioned, such as in a fissure or in the lateral pleural space. Owing to the geometry of the thorax and lung, at least one chest tube should be placed in the apical thorax to facilitate optimal cephalad expansion of the lung and maintain control of the apical space. Often a basilar tube is also used to complement the apical tube and prevent the accumulation of subpulmonic air or fluid.
Pleural suction, usually applied using a pleural drainage unit, should also be minimized to limit airflow through the pleural space. Depending on the location of the pleural drain relative to the air leak, increasing the suction simply may increase the leak volume. A large ongoing air leak eventually will result in bacterial contamination as oral flora are entrained through the lung and deposited in the pleural space.
Proper chest tube management requires the recognition of several typical clinical situations:
Large swings in the water seal chamber. Tidal ventilation results in big swings in the chest tube water seal when there is a large residual pleural space. The chest contains relatively compliant structures. Therefore, the larger the space, the bigger is the swing. A large swing in the water seal chamber may reflect significant atelectasis or volume loss in the remaining lung.
Chest tube not draining a pneumothorax. The presence of a “paradoxical” pneumothorax implies one of two easily distinguishable clinical scenarios: (1) the unrecognized loss of pleural suction or (2) an air leak sufficiently large to overwhelm the suction provided by the pleural drainage unit. When there is a sudden loss of suction, it is commonly due to compression of the tube by either the patient or the wheel of the bed. An uncontrolled air leak of approximately 50 L/min usually indicates a systemic disconnection or, more ominously, a central airway communication.
Accumulation of pleural air with decreasing vacuum. When weaning the patient off chest tube suction, one should routinely check for the accumulation of pleural air. This “functional test” occasionally involves increasing the amount of applied vacuum. A rush of air through the drainage system at a higher suction setting implies that the previous setting was inadequate; that is, air was inappropriately accumulating at the lower setting. This test is far more sensitive than chest x-ray to determine the appropriateness of discontinuing suction (so-called water seal).
Small or intermittent air leak. The presence of a very small or intermittent air leak can be difficult to detect. One approach is to reconnect the suction device while the water seal chamber is observed carefully. A rush of air suggests that air was accumulating in the pleural space. A related approach is to clamp the chest tube for a period of time, place the tube back on suction, and then release the clamp while observing the water seal chamber.
A CT scan of the chest may be needed to determine the amount of air in the thoracic cavity and assess the relative advantage of placing additional chest drains (Fig. 8-1).
Chest CT scans showing the presence of intrathoracic air on coronal (A) and sagittal (B) views.
Intraoperative fluid management is critical to maintaining lung compliance. Injudicious fluid administration combined with surgical trauma may lead to a loss of pulmonary compliance and impaired postoperative ventilation. Patients with impaired lung function may require ventilatory support, but ventilation should be avoided whenever possible, because mechanical ventilation can cause a separate set of complications.
Postoperative lung edema and pulmonary compliance are closely related to extracellular fluid volume. This is particularly so in patients recovering from pulmonary resection, where lung tissues have been insulted from the surgical procedure itself. Fluid volumes must be monitored closely. Generally speaking, anything that can be done to minimize total body water in the recovery period will improve pulmonary compliance and overall lung function. Fluid management also plays a role in the surgical resection of mediastinal tumors because mediastinal dissection can be associated with idiopathic pleural or pericardial effusion.
The risk for aspiration pneumonia is particularly high in individuals undergoing esophageal surgery, whether for a motility disorder, reflux disease, or esophageal tumor. Complete vagotomy performed in conjunction with esophagectomy in the acute setting may result in prolonged dysmotility, which enhances the risk of malnutrition and aspiration.
Aspiration causes the tracheobronchial tree to be contaminated with material from the upper digestive tract. The two primary sources of aspirated substances are the oropharynx and the stomach. Oropharyngeal aspiration commonly results in bacterial contamination by anaerobic organisms, alone or in combination with aerobic and/or microaerophilic organisms. In most intensive care settings, the pathogens are hospital-acquired flora that disseminate via oropharyngeal colonization (e.g., enteric gram-negative bacteria and staphylococci).
The aspiration of gastric contents can result in chemical pneumonitis. The degree of pulmonary parenchymal injury depends on the chemical composition and volume of the aspirated material. Even small volumes of aspirated fluid with a pH less than 2.5 have been associated with severe chemical pneumonitis (Mendelson syndrome).1
Oropharyngeal and small-volume gastric aspiration is a common event in healthy individuals. The aspirated material is cleared by airflow (e.g., cough), mucociliary action, and pulmonary phagocytes. A major contributor to airway clearance is sustained airflow. Effective airflow depends on unobstructed airways and adequate lung volumes. Endotracheal tubes or mucus impaction are common reasons for inadequate airflow. Ventilator-associated pneumonias are a well-established and dangerous consequence of prolonged intubation.2 The risk of pneumonia is likely due to both the relative obstruction of mucociliary clearance and the presence of artificial surfaces in the airway. (Bacterial adherence, the so-called biofilm, is a characteristic of many species of bacteria, including Pseudomonas aeruginosa and Staphylococcus aureus.) Inadequate lung volumes result from recumbent posture and immobilization.
The treatment for oropharyngeal and small-volume gastric aspiration is mobilization and ambulation. Ambulation recruits lung volumes and improves airflow. Patients can be ambulated while requiring some ventilatory support, but extubation has the additional benefit of improving airway clearance and removing artificial surfaces within the trachea.
Because large-volume gastric aspiration typically is associated with acute respiratory failure, treatment requires long periods of intubation, ventilatory support, and emergent bronchoscopy. Broad-spectrum antibiotic coverage is usually begun at the time of aspiration, because the pulmonary injury is often associated with subsequent superinfection.
All patients benefit from reverse Trendelenburg positioning, which tilts the entire plane of the bed such that the head is elevated with respect to the legs (Fig. 8-2). Merely raising the head end of the bed by 30 degrees is inadequate because it is difficult to maintain the patient in this position and can even increase intraabdominal pressure. Patients who have had a left pneumonectomy are at particular risk for aspiration. The elevated left hemidiaphragm compromises hiatal antireflux mechanisms, and the single remaining lung makes any aspiration life threatening. Other patients at high risk for aspiration are esophagectomy patients. These patients may have prolonged gastrointestinal dysmotility because of acute thoracic vagotomy. To improve drainage of the gastric interposition graft, a pyloroplasty usually is performed,3 and some type of tube compression is often required for up to a week after surgery.
Reverse Trendelenburg position.
In rare circumstances, it may be beneficial or necessary to ventilate the postoperative patient overnight. Indications for postoperative ventilation include (1) a high-risk airway, (2) bleeding requiring large-volume replacement, (3) inadequate pain control requiring high-dose parenteral narcotics, and (4) decortication or visceral pleurectomy.
Postoperative ventilation can be beneficial to patients undergoing decortication or visceral pleurectomy. Both procedures result in a loss of lung compliance secondary to surgical trauma to the parenchyma. In addition, these procedures are often associated with a bloody pleural space and several days of air leak. Overnight ventilation helps to facilitate pleural apposition and minimize the accumulation of blood or air in the pleural space.
Cardiac myocytes undergo transient depolarization and repolarization that is triggered by external (e.g., nerve depolarization) or intracellular stimulation. The cardiac action potential is distinct from those found in nerve or muscle cells. The cardiac action potential is several hundred times longer (200–400 ms), and calcium plays a role in depolarization (Fig. 8-3).
The cardiac action potential consists of five phases. Phase 4 is a resting membrane potential. Phase 0 is the rapid depolarization caused by a transient increase in fast Na+ channel conductance. Phase 1 represents an initial repolarization that is caused by the opening of a special type of K+ channel. Phase 2 reflects a large increase in calcium conductance. Phase 3 occurs with an increase in K+ conductance.
Atrial fibrillation is a common complication of thoracic surgery. Thirty percent of all patients who undergo major thoracic surgery develop atrial dysrhythmias. Almost all these arrhythmias present between 24 and 96 hours after surgery. The mechanism of atrial fibrillation is unknown, but high endogenous catecholamine levels appear to participate.4
Almost all patients undergoing thoracic surgery should receive perioperative prophylactic treatment with a beta blocker, because the frequency of atrial fibrillation is very high in this population. Exclusion criteria for cardioselective beta blockade include severe cardiomyopathy and rare drug insensitivities. A trial of preoperative beta-blocker therapy may be indicated in selected patients to determine the appropriate dosing.
In the acute setting, the initial evaluation of atrial fibrillation should focus on (1) treatment of precipitating factors and (2) rate control.4 Precipitating factors include electrolyte abnormalities, high catecholamine states secondary to pain, and the administration of arrhythmogenic agents (e.g., dopamine or epinephrine).
Supported by clinical trials in nonsurgical settings (e.g., AFFIRM5 and RACE6), the treatment of thoracic surgery patients should emphasize rate control over rhythm control. Acute rhythm control is rarely successful in the immediate postoperative period. Potential reasons for the failure of rhythm control include high endogenous catecholamine levels related to volume depletion and pain. Further, local inflammation after intrapericardial dissection may prevent the return to sinus rhythm. Despite problems with rhythm control in the first week, almost all patients revert to stable spontaneous sinus rhythm within 6 weeks of surgery.
Rapid atrial fibrillation can lead to hyperperfusion pulmonary edema, an important reason to emphasize rate control. In some patients, rapid atrial fibrillation is associated with a fall in cardiac output. This may increase central venous pressures and slightly increase lung water but is not a life-threatening emergency. In contrast, other patients have increased cardiac output caused by an increase in intraventricular conduction. If these patients have a limited vascular bed because of a pneumonectomy or other surgical resection, they may rapidly develop pulmonary edema (Fig. 8-4). The clinical spiral believed to be related to plasma ultrafiltration in excess of oncotic reabsorption or lymphatic drainage results in rapidly progressive pulmonary edema. The treatment is rapid control of heart rate. This may even require the administration of a short-acting beta blocker such as esmolol.
This patient developed hyperperfusion pulmonary edema within 4 hours of pneumonectomy and rapid atrial fibrillation within 24 hours. The chest X-rays show the lungs at 1 hour (A), 4 hours (B) and 8 hours (C) after surgery. The CT scan demonstrates the pulmonary edema 12 hours (D) after surgery. The patient responded to rate control and diuresis.
Antiarrhythmic agents typically are classified by the Vaughan Williams classification system. This scheme attempts to classify agents based on their mechanism of action but is limited by the need to account for agents with multiple mechanisms (e.g., sotalol) or active metabolites with disparate functions (e.g., procainamide)7 (Table 8-2).
Table 8-2Vaughan Williams Classification of Antiarrhythmic Agents ||Download (.pdf) Table 8-2Vaughan Williams Classification of Antiarrhythmic Agents
Because most arrhythmias related to surgery in the thorax are self-limited, the focus on rate control means that most patients are treated with class III or IV agents. A combination of beta blockers and calcium channel blockers must be used with caution to avoid heart block, because of the common effects of class III or IV agents on the atrioventricular node.
Pulmonary embolism is a life-threatening complication of DVT. Approximately one-third of patients with an untreated pulmonary embolism eventually will die from an embolic event. Autopsy series suggest that pulmonary embolism is far more common than is recognized clinically. Clot in the deep venous system may not produce diagnostic signs and symptoms. The subtleties of establishing a clinical diagnosis warrant prophylactic treatment for DVT in all thoracic surgery patients. High-risk patients with any clinically significant respiratory insufficiency should undergo periodic noninvasive surveillance by noninvasive imaging.
The following approaches to preventing DVT have proven value: low-dose subcutaneous heparin, intermittent pneumatic compression of the legs, oral anticoagulants, adjusted doses of subcutaneous heparin, graduated compression stockings, and low-molecular-weight heparin. Antiplatelet agents such as aspirin are less effective for preventing DVT. Patients at high risk for DVT include those with any of the following characteristics: age over 60 years, obesity, malignancy, surgery, immobility, pregnancy, and active phlebitis or a history of prior DVT.
Venography cannot be performed repeatedly, and some studies indicate that the radiographic dye actually may promote blood clot formation. These limitations have rendered duplex ultrasound the most effective noninvasive tool for diagnosing DVT.8 Duplex ultrasound can be used most effectively to diagnosis thigh blood clots. The ultrasound uses high-frequency sound waves to image the vein. The procedure can be performed at the bedside without the need for nephrotoxic contrast agents. Gentle compression of the thigh vein with the ultrasound probe can identify rigid or inflexible areas of clot. This study also provides important information about blood flow characteristics.
Pulmonary emboli can originate in virtually any vein in the body. With the availability of increasingly sensitive procedures to test for pulmonary embolism, the current data suggest that nearly every patient with a large vein thrombosis will have some evidence of pulmonary embolism. Approximately half these patients will have no clinical symptoms to suggest pulmonary embolism. Clot arising in the popliteal segment of the femoral vein is the cause of pulmonary embolism in more than 60% of patients. In contrast to earlier beliefs, calf veins are a significant source of DVT. Recent studies have shown that 33% to 46% of patients with calf vein thromboses will develop a pulmonary embolism.
The diagnosis of pulmonary embolism is currently made using helical CT angiography (CTA), also known as PE-CT. CTA has been shown to be more sensitive and specific than radionuclide perfusion scanning.9 Whole-body CTA imaging can establish the diagnosis of both venous thrombosis and pulmonary embolism. Of note, CTA in the lung is insensitive to subsegmental clots, which comprise 3% to 6% of pulmonary emboli.
D-dimer is a blood test that is useful in establishing the diagnosis of pulmonary embolism as well as DVT, acute myocardial infarction, and disseminated intravascular coagulation. D-dimer is formed only when fibrin is cross-linked. Therefore, the release of D-dimer fragments in the blood reflects thrombin and plasmin activity.