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.
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).
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.9 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 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.