Adult Chest Surgery

Chapter 8. Postoperative Management 

Postoperative care of the thoracic surgery patient requires an active rehabilitative approach. Both the type of surgical procedure and the underlying disease can present a significant challenge to postoperative management. An illustration of this approach is early ambulation after surgery. Early postoperative ambulation confers multiple systemic benefits in any surgical setting but is uniquely valuable to the recovering thoracic surgery patient (Table 8-1). Ambulation promotes airway clearance and decreases the risk of pneumonia. These benefits are amplified in patients who have surgically related or underlying lung dysfunction. Thus the nature and extent of surgical resection in thoracic patients require a well-trained staff and specialized equipment for monitoring patient status, which together can have a significant impact on morbidity and mortality.

Table 8-1. BRAT Staging Protocol

Stage

Activity

Room Air O2 Saturation LTP

Room Air O2 Saturation Non-LTP

0

Resting

<85

<90

1

Resting

>85

>90

2

Sitting

>85

>90

3

Standing

>85

>90

4

Walking 1–6 minutes

>85

>90

5

Walking >6 minutes

>85

>90

 

BRAT = Brigham Room Air Tolerance (BRAT) staging protocol. The BRAT assessment was developed to provide a quantifiable measurement of a patient's oxygen saturation level during physical activity. The BRAT stage is determined daily and documented on the patient flow sheet. LTP = lung transplant patient.

PRINCIPLES OF POSTOPERATIVE CARE

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 necessarily 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.

Extubation

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, and (3) decortication or visceral pleurectomy.

Pain

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. Because of the geometry of the thorax and lung, at least one tube should be placed in the apical thorax to facilitate optimal cephalad expansion of the lung and maintain control of the apical space.

The use of suction also should 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 contaminate the pleural space with oral flora.

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. Because the chest contains relatively compliant structures, the larger the space, the bigger is the swing. This may be a sign of 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 chest tube suction apparatus. When there is a sudden loss of suction, it is commonly a result of compression of the tube caused either by the patient or the wheel of the bed. An uncontrolled air leak of approximately 50 L/min usually indicates a system 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. If there is a rush of air through the system, this is a sign that air was inappropriately accumulating in the previous 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.

Fluid Management

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 it 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.

Aspiration

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 consequence of prolonged intubation.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.

Since 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. 8-1). Raising only 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,and some type of tube compression is often required for up to a week after surgery.

Figure 8-1.

 

Reverse Trendelenburg position.

Ventilation

In rare circumstances, it may be beneficial or necessary to ventilate the postoperative patient overnight. Indications for postoperative ventilation include (1) bleeding requiring large-volume replacement, (2) inadequate pain control requiring high-dose parenteral narcotics, and (3) 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.

Atrial Fibrillation

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. 8-2).

Figure 8-2.

 

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.

Because of the frequency of atrial fibrillation in the thoracic surgery population, almost all patients should receive perioperative prophylactic treatment with a beta blocker. 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 treatment of precipitating factors and rate control. 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., AFFIRMand RACE), 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. 8-3). 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.

Figure 8-3.

 
 
 
 

This patient developed hyperperfusion pulmonary edema (A to C) within 4 hours of pneumonectomy and rapid atrial fibrillation within 24 hours. The patient responded to rate control and diuresis.

Antiarrhythmic agents typically are classified by the Vaughn 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)(Table 8-2).

Table 8-2. Vaughn Williams Classification of Antiarrhythmic Agents*

Class

Mechanism

Examples

Effect on Action Potential

Ia

Interfere with Na+ channel

Quinidine

Procainamide

 

II

Slow conduction through atrioventricular node

Esmolol

Propranolol

Metoprolol

 

III

Blocks K+ channel and prolongs repolarization

Amiodorone

Ibutilide

Sotalol

 

IV

Calcium channel blockers slow AV node conduction

Verapamil

Diltiazem

 

V

Other mechanisms

Adenosine

Digoxin

 

 

From reference 6.

Since 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. Because of the common effects of class III or IV agents on the atrioventricular node, a combination of beta blockers and calcium channel blockers must be used with caution to avoid heart block.

Pulmonary Embolism

Thoracic surgery patients have an increased risk of developing deep vein thrombosis (DVT) related to both malignancy-induced hypercoagulability and surgical trauma. 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. Because of the subtleties of establishing a clinical diagnosis, all patients should be treated prophylactically for DVT. 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 formations. Because of these limitations, duplex ultrasound has become the most effective noninvasive tool for diagnosing DVT.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 33–46% 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.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 3–6% 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.

PROCEDURE-SPECIFIC COMPLICATIONS

Thoracic Duct Injury

The thoracic duct transports lymph from the intraabdominal triangular dilatation called the cisterna chyli to the junction of the left subclavian vein with the left internal jugular vein in the neck. Although there are many anatomic variants, the thoracic duct typically ascends along the right side of the thoracic vertebra, crossing to the left side at the level of the subcarinal space.

Thoracic duct fluid is composed of chyle and lymph plasma. Chyle is composed of the long-chain fatty acids that are absorbed in the intestines and then secreted in chylomicrons into the intestinal lymphatics. Lymph plasma is composed of serum electrolytes, a relatively high concentration of protein (particularly albumin), and lymphocytes.

The chylous portion of a thoracic duct leak may not manifest until the patient begins eating. Because triglycerides (glycerol plus fatty acids) are the dominant component of chylomicrons, a test for triglycerides is typically abnormal if the patient is receiving enteral nutrition. In the absence of enteral feeding, the triglyceride levels will reflect plasma concentrations.

Patients at increased risk for thoracic duct injury include individuals undergoing esophagectomy or extensive extrapleural or mediastinal dissections. The possibility of a thoracic duct injury should be raised when a patient has (1) chest tube output more than 1 L/day and (2) a recent extrapleural or mediastinal dissection.

The diagnosis of thoracic duct leak can be made after the introduction of enteral feedings. The fluid accumulating in the chest has a milky appearance and elevated triglyceride levels.

Treatment of small accessory duct leaks with relatively low output (1 L/day) can be managed without intervention if adequate nutrition can be maintained. Placing the chest tube on water seal (20 cm H2O resistance) avoids the vacuum-assisted "sump" created by the chest tube. Increased resistance to lymph flow is believed to encourage lymph flow through existing vessels and decrease drainage.

Outputs of 3–5 L/day, however, must be managed aggressively to avoid hypoproteinemia and malnutrition. Although percutaneous decompression or occlusion of the cisterna chyli can be useful, surgical ligation of the main thoracic duct typically is indicated. The thoracic duct has valves and myoepithelial elements. Therefore, the fluid may accumulate under considerable pressure. Because of the possibility of collateral leaks or "blowouts" proximal to the ligation, the ligation is best performed as caudally as possible within the right chest. The ligation typically is performed with a pledget to prevent injury to the duct. Because of pressure generated by the thoracic duct, sclerosis of the pleural space generally is ineffective. Attempts at sclerosis either fail completely or result in loculated pleural collections.

Vocal Cord Paralysis

The recurrent laryngeal nerve is a branch of the vagus nerve that supplies the motor component of the intrinsic muscles of the larynx and a portion of the cricopharyngeus. The recurrent laryngeal nerve also provides a sensory component to the laryngeal mucosa below the vocal cords.

The recurrent laryngeal nerve takes a different course in each hemithorax. The left recurrent laryngeal nerve passes under the aortic arch and along the tracheoesophageal groove. The right recurrent laryngeal nerve loops under the right subclavian artery and ascends to the larynx with a more lateral course than the left nerve (Fig. 8-4).

Figure 8-4.

 

The left recurrent laryngeal nerve passes under the aortic arch along the tracheoesophageal groove. The right recurrent laryngeal nerve loops under the right subclavian artery and ascends to the larynx with a more lateral course than the left nerve.

The left recurrent laryngeal nerve is the nerve most commonly injured in thoracic surgical procedures. The left recurrent laryngeal nerve typically is injured during cervical mediastinoscopy or esophagectomy procedures. Nerve injuries during mediastinoscopy are caused by direct trauma to the nerve or the ill-advised use of electrocautery during the dissection of 2L or 4L lymph nodes. Similarly, recurrent laryngeal nerve injuries during esophagectomy are associated with excessive traction or direct trauma.

The diagnosis of vocal cord paralysis may be delayed because of vocal cord edema in the immediate postoperative period. Usually within 24 hours a patient with vocal cord paralysis will demonstrate a weak voice and unusual effort required with phonation.

The configuration and mobility of the vocal cords are best evaluated using a fiberoptic laryngoscopy. The vocal cord and arytenoid are immobile on the paralyzed side, resulting in a glottal gap with phonation. Although the paralyzed vocal cord may have a variable position, paralyzed vocal cords typically are abducted from the midline. In unusual circumstances, typically those associated with traumatic intubations, vocal cord dysfunction is a consequence of subluxation of the arytenoid.

Spirometry shows abnormalities in the patient's flow-volume loop. Patients with vocal cord paralysis may show blunting or truncation of the inspiratory loop—evidence of extrathoracic airflow obstruction.

In addition to the fatigue associated with ineffectual phonation, vocal cord paralysis is associated with aspiration. In particular, liquids are aspirated during the pharyngeal phase of swallowing. Postswallow aspiration also may occur when the residual food bolus is retained in the piriform sinus on the paralyzed side. The most telling sign of vocal cord paralysis in the thoracic surgical patient is an ineffective cough.

Fatigue and airway clearance are the primary indications for treatment of vocal cord paralysis in the early postoperative period. There are two main approaches to treating vocal cord paralysis.

·   Because some patients may recover nerve function spontaneously, an injection of a temporary or absorbable material is used to stiffen and medialize the vocal cord. The injection can be performed through a laryngoscope under local anesthesia. Teflon also can be injected, but this procedure should be considered permanent.

·   A more definitive solution is a lateral laryngeal implant. This procedure requires an external neck incision, but it can be performed under local anesthesia. The lateral laryngeal implant has a high success rate but is potentially reversible.

Pulmonary Edema after Sleeve Lobectomy

There are three pathophysiologic processes that can contribute to the development of pulmonary edema: (1) imbalance in transpleural fluid filtration (passive Starling forces), (2) impairment of lymphatic drainage, and (3) increases in capillary endothelial permeability.The lung lymph vessels are found both inside (submucosa) and outside (peribronchial) the airways. Surgical procedures that divide the bronchus, such as sleeve resections and lung transplantation, result in a clinically significant impairment of lymphatic drainage.

The balance of Starling forces in the lung results in a small net movement of fluid out of the pulmonary vasculature and into the lung interstitium. This movement of fluid, approximately 10–20 mL/min, represents only approximately 2% of the pulmonary blood flow. In normal circumstances, this excess fluid is removed by the pulmonary lymphatic system. After surgical division of the lung, however, the lymphatic drainage is impaired, and normal Starling forces favor the accumulation of fluid within the affected lung.

The most common site of sleeve resection is the right upper lobe secondary to airway and vascular anatomy. In the average adult, the remaining middle and lower lobes of the reconstructed right lung will accumulate approximately 500 mL of lung water within the first 2 days after surgery. This progressive pulmonary edema typically results in unexpected hypoxemia 2–3 days after sleeve lobectomy. In some patients, hypoxic vasoconstriction of the affected lung results in an apparent "hyperperfusion" pulmonary edema of the contralateral lung.

The treatment of pulmonary edema relies on active reversal of passive Starling forces, namely, a diuresis sufficiently vigorous to cause a net movement of fluid out of the lung interstitium and into the vasculature. Empirical observations after lung transplantation suggest that passive Starling forces will reverse after an acute diuresis equivalent to 20% of the patient's circulating blood volume. In the average 70-kg patient, the total blood volume is 5 L (65 mL/kg for females and 75 mL/kg for males). As a consequence, treatment of pulmonary edema secondary to lymphatic impairment requires a diuresis of approximately 250 mL/h for 4 hours. The clinical complaint of thirst and a serum sodium concentration in the low 140s corroborate the hemoconcentration.

Esophageal Anastomotic Leak

Leaks from a gastroesophageal anastomosis occur most commonly within the first 48 hours or 7–10 days after esophagectomy. Early leaks typically reflect technical complications at the time of surgery. Late anastomotic leaks reflect ischemia of the gastric (or colonic) interposition graft. Ischemic complications are more likely to occur in cervical esophageal anastomoses (20%) than in intrathoracic anastomoses (1%).

Early anastomotic failures are characterized by the drainage of bilious material from the chest drain or the rapid accumulation of a pleural effusion. Accompanying these ominous signs are fever, leukocytosis, and the toxicity of acute mediastinitis.

Late anastomotic leaks usually are associated with subtle signs and symptoms. A slight increase in the blood leukocyte count and tenderness in the neck incision may herald an anastomotic leak. Although cervical esophageal anastomoses are more commonly associated with leaks, these can be drained quite easily by opening up the skin of the neck incision. Prompt drainage of the cervical collection can avoid the septic complications of the leak. Anastomotic leaks appear to be associated with a higher incidence of anastomotic stricture, but a cervical leak is usually not life-threatening.

Bronchopleural Fistula

Bronchopleural fistulas are communications between the central airways and the pleural space. Although all air leaks technically communicate with the central airways, the term bronchopleural fistula usually is reserved for the breakdown of a surgical closure of the lobar or main stem bronchus.

After pulmonary resection, most surgeons test their bronchial closure by submerging the stump and looking for air bubbles during active ventilation. Because of this practice, early technical failures of stump closure are rare. A more common complication is the breakdown of a pneumonectomy stump in the weeks to months after surgery. The mechanism of bronchopleural fistula in most cases is believed to be the ischemic breakdown of the stump closure with a secondary infection of the distal pleural space. (Supporting this mechanism is the observation that longer stumps are generally located in the "watershed" region of bronchial artery perfusion.) Patients typically present with increasing dyspnea, a new infiltrate in the remaining lung, and a decrease in the air-fluid level in the pneumonectomy space. On questioning, the patient may report brown or rust-colored sputum.

A related complication, but with a more insidious presentation, is the gradual wasting and cachexia associated with chronic empyema. Patients with a chronic pneumonectomy space infection may be afebrile and have a normal leukocyte count. It is not uncommon for a medical oncologist to assume that the patient has a recurrent cancer.

Bronchopleural fistula is treated initially by draining the pneumonectomy space to prevent massive aspiration. Because of the contraction of the pleural space, a tube thoracostomy should be placed at or above the level of the pneumonectomy incision. A useful technique is to direct a right-angled tube into the costophrenic sulcus to optimize drainage of the hemithorax. The procedure should be performed with local anesthesia and spontaneous ventilation.

The suspected fistula should be evaluated by bronchoscopy performed during spontaneous ventilation. Small fistulas may be difficult to see but may be effectively demonstrated by the disappearance of stump fluid during inspection. The space distal to the bronchopleural fistula is, by definition, infected. The use of plugs or glues is rarely helpful because they do not address the primary problem, that is, ischemic breakdown of the airway with secondary space infection. In the setting of a suspected bronchopleural fistula, general anesthesia can be a major risk. General anesthesia and even the positioning of the patient for intubation are associated with increased risk of contamination of the remaining lung. If the pneumonectomy space has been drained, positive-pressure ventilation may be ineffective or result in tension pneumothorax. The loss of effective positive airway pressure in an anesthetized patient will result in a loss of lung volume and progressive hypoxemia. Because the average length of the right main stem bronchus is very short (1.3 ± 0.3 cm), selective intubation of the main stem bronchus is only practical with a remaining left lung.

Even when selective intubation is achieved, it is difficult to maintain. The angle and luminal diameter of the left main stem bronchus result in intermittent tube obstruction or displacement. In addition, the selective intubation of the left main stem bronchus requires a 6F endotracheal tube, which effectively limits bronchoscopic access to the remaining lung.

In the patient with respiratory failure, the management principle is to avoid the circumstance of ongoing soilage of the remaining lung. The problem with tube drainage (with or without irrigation) is that it provides only partial control of the pneumonectomy space. Drainage is limited by the position of the tube or inflammatory loculations within the chest. To ensure adequate drainage and to prevent ongoing contamination of the remaining lung, an open thoracic "window" should be created. A thoracic window or Clagett procedure10 involves the resection of one or more ribs in the dependent lateral chest wall to facilitate irrigation and packing of the empyema space. In contrast to the Clagett procedure, the Eloesser flap was proposed to facilitate drainage of an empyema in the setting of functioning ipsilateral lung tissue requiring spontaneous ventilation11 (see Chap. 2).

Positive-pressure ventilation can be maintained in a patient with a large bronchopleural fistula and a thoracic window by tightly packing the chest with rolls of mineral oil-soaked gauze. The chest must be packed tightly. Dressing changes, usually performed once a day, need to be performed expeditiously.

Most surgeons wait 6 weeks to 6 months before closing the window. During that time, nutrition is optimized, and control of the infection is ensured. Ideally, the fistula is healed before closure of the thoracic window. In addition, patients with malignancy should be restaged radiographically. Closure of the chest wall involves rotation of muscle into the chest to facilitate antibiotic delivery and to minimize the residual space.

SUMMARY

Thoracic surgery creates unique physiologic stresses in the immediate postoperative period. Optimal postoperative management relies on multiple pre- and perioperative interventions. Daily preoperative conditioning programs can improve the patient's exercise capacity and facilitate early ambulation after surgery. Early ambulation after surgery promotes airway clearance and decreases the risk of pneumonia. Early mobility also decreases the risk of pulmonary embolus. Careful attention to fluid management can improve pulmonary compliance and gas exchange in the immediate postoperative period. Cardiac rate and rhythm disturbances are a common feature of postoperative management. Other complications can be directly related to the operative thoracic procedure, such as thoracic duct injury, vocal cord paralysis, pulmonary edema after lobectomy, esophageal anastomotic leak, and bronchopleural fistula. Most of these complications are best managed by a well-equipped facility with a highly trained staff.

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