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An intrapericardial approach may be used for radical pneumonectomy to facilitate access to major vessels and allow wider hilar dissection. This technique may result in a large pericardial defect that the surgeon is not able to close after the pneumonectomy is completed. There have been several reports of herniation of the heart[409] through the pericardial opening into the empty hemithorax. The herniation can be into either the right or left hemithorax, and herniation into either side can cause profound cardiac functional impairment; the mortality rate is 50%.
With herniation, the heart protrudes through the defect into one of the hemithoraces, thereby potentially causing twisting of the superior vena cava (superior vena cava syndrome), inferior vena cava (cardiovascular collapse), distal end of the trachea (wheezing), pulmonary veins (pulmonary edema), and pericardial constriction of the heart (myocardial ischemia and ventricular arrhythmia). These symptoms may occur individually or in various combinations.
In most reports, herniation of the heart has occurred either immediately after the patient is turned from the LDP to the supine position (75%) or during the first few hours of postoperative mechanical ventilation. However, this complication can also occur as late as several days after surgery. Events that increase intrapleural pressure in the nonsurgical (ventilated) hemithorax or that decrease intrapleural pressure in the surgical (empty) hemithorax may predispose the patient to cardiac herniation. Positioning the patient so that the empty hemithorax is in a dependent position allows the heart to be pulled by gravity into the empty hemithorax. The use of high levels of pressure and volume during mechanical ventilation of the remaining lung can push the heart into the empty hemithorax. Similarly, coughing can increase pleural pressure in the remaining lung and thereby promote displacement of the heart into the empty hemithorax. Conversely, inadvertently applying suction to a chest drain in the empty hemithorax can pull the heart through a pericardial defect (tension vacuthorax).
The diagnosis of cardiac herniation is made by the sudden appearance of catastrophic symptoms in a patient who had a radical pneumonectomy, the presence of a predisposing condition (see earlier), and a chest radiograph that shows the apex of the heart pointing toward a lateral chest wall at a right angle.[410] A diagnosis of cardiac herniation almost always necessitates immediate re-exploration.
Five conservative measures may improve cardiopulmonary function before and during transfer to the operating room (they are the reverse of the causes of herniation of the heart discussed previously), and they should be instituted as soon as the diagnosis is entertained. First, the patient should be positioned so that the ventilated nonsurgical side is in a dependent position and the empty
Pulmonary torsion refers to rotation of the parenchyma on its bronchovascular pedicle and is thought to be due to increased mobility of a lobe (as may occur to the remaining lobes in one hemithorax after a lobectomy). Any patient with atelectasis or an expanding intrathoracic mass and perhaps with severe chest pain after thoracotomy should have lung torsion added to the differential diagnosis, which also includes intrathoracic bleeding and progressive atelectasis. Because torsion compromises the pulmonary vasculature (both arteries and veins), as well as the bronchi, prompt recognition and surgical intervention are required to avoid the attendant morbidity and mortality (i.e., infarction and gangrene).[410]
A DLT should be inserted before surgery if pulmonary torsion is suspected because during surgical correction of this condition (either completion pneumonectomy or untwisting and stabilization of the lobe to another lobe or chest wall), massive hemorrhage into the airways may occur as a result of release of entrapped blood and continuing bleeding from necrotic lung tissue (i.e., vessels and airways), which would drown the dependent lung and produce severe hypoxia or death. Other intraoperative therapeutic modalities that the anesthesiologist should consider include the use of intravenous steroids to decrease any reactive pulmonary inflammation, the use of PEEP to reexpand atelectatic lung tissue, and saline lavage for the removal of any excess blood that might form clots in the normal airways and thereby obstruct healthy lung parenchyma.
Postoperative bleeding that necessitates emergency thoracotomy [409] may occur in as many as 3% of all thoracotomy patients.[411] The mortality associated with major postoperative bleeding is approximately 23%.[411] Potential sources of major postoperative hemorrhage are bleeding from divided pulmonary arteries and veins because of slippage of surgical ligatures, diffuse bleeding from raw surfaces, and systemic arterial bleeding (bronchial and intercostal arteries).
The drainage from a patent chest tube is an excellent monitor of the amount of intrathoracic bleeding. In addition, the hematocrit of the usual fluid in the chest drainage is always less than 20%, and intrathoracic bleeding increases the hematocrit to some higher value. Significant hemorrhage, of course, is accompanied by the hemodynamic signs of hypovolemia. Significant hemorrhage cannot always be ruled out by the absence of chest tube drainage because the chest tube may be blocked by clotted blood or otherwise obstructed. Nevertheless, the patient will still show signs and symptoms of hypovolemia and a shift in the mediastinum to the opposite side.
Development of a bronchopleural fistula is a serious complication of pulmonary resection and as recently as 1978 carried a mortality of 23%.[412] The symptoms and signs are variable and depend on the size of the communication, the presence or absence of a chest drain, and the presence of fluid of any sort within the pleural space.
Gross disruption of a bronchial stump is usually signaled by massive bubbling of gas through the chest tube drainage system, if present, tension pneumothorax if the chest tube is not present, hypoxemia, and hypercapnia. Prompt resuscitation is essential and may need to include mechanical and differential or one-lung ventilation with a DLT and support of the circulation. A functioning chest tube, if not present, must be inserted immediately to evacuate the air (to prevent tension pneumothorax) and fluid (to prevent further contamination of the opposite lung) from the pneumonectomy cavity; a needle can decompress the hemithorax while a chest tube is being inserted. The patient should be recumbent, with the normal side in a nondependent position. The stump must be closed surgically as soon as possible.[412]
It should be remembered that tension pneumothorax may occur in the contralateral side if very high inflation pressures are used to expand a previously collapsed lung (as commonly occurs for one-lung ventilation); the tension pneumothorax may become apparent only after closure of the chest. Other causes of acute postoperative contralateral pneumothorax relevant to thoracic surgery include damage to the contralateral pleura during surgery, puncture of the pleura during insertion of a central venous cannula or thoracic epidural needle, or damage to the bronchus by the use of an endobronchial catheter.
Development of a chronic bronchopleural fistula may be expected to occur in 1% to 3% of pulmonary resection patients.[412] A chronic bronchopleural fistula most frequently becomes evident within the first 2 weeks after surgery and may run a fulminating course characterized by sepsis, empyema, purulent sputum, and respiratory insufficiency. Factors that predispose to the formation of a chronic bronchopleural fistula after pulmonary resection are preoperative irradiation, infection, residual neoplasm at the site of closure, and the presence of a long or avascular stump.
Acute respiratory insufficiency (within 30 days of resection) is probably the most common serious complication after pulmonary resection. Recent data from a large thoracic surgery service indicate an incidence of 4.4% after resection of bronchial carcinoma, and in this study, the patients in whom acute respiratory failure developed had a mortality rate of 50%.[413] Mortality from respiratory
First, the remaining lung in either hemithorax may be edematous or soiled with blood, or both. The lung that was dependent during surgery may be edematous and may have aspirated blood (if a DLT was not used) as a result of gravitational effects (in zones 3 and 4). The lung that was nondependent during surgery may be edematous and hemorrhagic because of surgical compression and trauma. Second, the size of the remaining pulmonary vascular bed is decreased; this decrease can lead to pulmonary edema. Treatment of respiratory insufficiency is discussed in detail in Chapter 74 and Chapter 75 .
Sudden evacuation of a chronic or subacute pneumothorax or pulmonary effusion may cause edema of the ipsilateral lung (reexpansion pulmonary edema).[414] [415] Still other reports describe an even more acute form of reexpansion pulmonary edema associated with lung reexpansion after only several hours of atelectasis,[416] [417] including reexpansion of the nondependent lung after one-lung ventilation to facilitate thoracic surgery[418] [419] [420] [421] and after correction of an inadvertent main stem bronchial intubation.[416] [422]
Most clinical and experimental observations support increased pulmonary vascular permeability as a major factor in the development of reexpansion pulmonary edema.[423] [424] [425] All the aforementioned clinical literature indicates that the rate of reexpansion may be as important as the duration of collapse in the development of reexpansion pulmonary edema.[414] [420] Thus, other mechanisms of reexpansion pulmonary edema include the generation of markedly negative intrathoracic pressure during reexpansion and increased pulmonary capillary pressure and flow on lung reexpansion.[426] Therefore, an important factor in preventing reexpansion pulmonary edema is to reexpand the lung slowly and in a gradual fashion. Treatment of established reexpansion pulmonary edema is mechanical ventilation, PEEP, restriction of fluids, and diuretics.
Major pulmonary resection results in a decrease in the cross-sectional area of the pulmonary vasculature and an increase in RV afterload, which in some patients can result in acute right heart failure. Although patients at risk for right heart failure after pulmonary resection can usually be identified preoperatively, right heart failure may also occur if additional stress, such as infection, increased pulmonary blood flow, and new active pulmonary vasoconstriction (such as that caused by hypoxia, acidosis, vasoactive amines, and peptides), is placed on the right side of the heart.
The diagnosis of selective right heart failure is established when right atrial pressure exceeds left atrial pressure (i.e., pulmonary artery wedge pressure) in the presence of abnormally low cardiac output. In addition, pulmonary hypertension with a pulmonary artery diastolic-wedge pressure gradient will usually be present, along with the systemic signs of left heart failure (oliguria, decreased mentation, peripheral edema). Treatment of acute right heart failure follows the same principles used to treat left-sided failure: control the heart rate, optimize preload and the inotropic state of the right ventricle, and reduce PVR (see Chapter 50 and Chapter 52 ).
Many adults have a patent foramen ovale;[409] at autopsy, the incidence of a probe-patent foramen ovale is highest at 34% during the first 3 decades of life and decreases to 20% by the 9th and 10th decades. Normally, there is no right-to-left shunting across the foramen ovale because left atrial pressure exceeds right atrial pressure; this pressure gradient keeps the one-way flap valve of the foramen ovale pressed against the opening, thereby resulting in a functionally competent seal. If right atrial pressure exceeds left atrial pressure (as may be the result of any factor that increases PVR and RV pressure), the one-way flap valve can open, and right-to-left shunting can occur through the newly opened foramen ovale. [409] Thus, newonset right-to-left shunting across a patent foramen ovale or atrial septal defect after pneumonectomy and lobectomy has been reported as a cause of otherwise unexplained postoperative dyspnea and systemic oxygen desaturation.[409] The use of contrast-enhanced two-dimensional echocardiography combined with a saline bubble injection study is an excellent method of diagnosing this process, if suspected. Contrast angiography and dye dilution curve analysis are other available diagnostic methods. Nonsurgical treatment consists of decreasing right atrial preload and afterload, which permits functional closure of the foramen ovale in most patients.
During radical hilar dissection or excision of mediastinal tumors, the phrenic, vagus, and recurrent laryngeal nerves may be injured accidentally or may be sacrificed deliberately.[409] Phrenic nerve injury leads to respiratory embarrassment by a flail chest effect and also causes elevation of the ipsilateral hemidiaphragm. The diagnosis should be suspected in patients who have relatively clear chest radiographs, have adequate gas exchange, and cannot be weaned from the ventilator. The diagnosis can be confirmed by paradoxical movements of the diaphragm on fluoroscopy. Injury to the vagus nerve causes gastric and intestinal atony, which is not usually problematic in the first few postoperative days. Bilateral partial injury of the recurrent laryngeal nerve causes adductor spasm of the vocal cords, which after extubation may result in upper airway obstruction. This complication must be diagnosed promptly and treated by immediate reintubation and possible tracheotomy until the dysfunction is resolved.
Aside from clamping of the thoracic aorta with resultant spinal cord ischemia, two other causes of paraplegia after thoracotomy can occur. First, damage to the spinal
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