Asian Cardiovasc Thorac Ann 2007;15:e35-e37
© 2007 Asia Publishing EXchange Ltd
Differential Ventilation with Spontaneous Respiration for Bilateral Emphysema
Murali Chakravarthy, MD,
Vivek Jawali, MCh
Wockhardt Heart Institute, Bangalore, India
For reprint information contact: Murali Chakravarthy, MD Tel: 91 80 2228 1146 Fax: 91 80 2228 1149 Email: mailchakravarthy{at}gmail.com, Wockhardt Heart Institute, 14 Cunningham Road, Bangalore 560052, Karnataka, India.
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ABSTRACT
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In patients with bilateral bullous disease and empyema in one lung, controlled ventilation may be hazardous and result in severe hypoxia. A 50-year-old man with bullous disease and thoracic empyema on the left side was operated on under general anesthesia with spontaneous respiration using differential lung ventilation.
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INTRODUCTION
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Histologically, bullous emphysema is the presence of emphysematous areas with complete destruction of lung tissue, producing an airspace greater than 1 cm in diameter. Bilateral emphysematous bullous disease can pose anesthetic problems such as hypoxemia, hypercarbia, bronchospasm, spontaneous rupture of the bulla, and pneumothorax.1 In patients with bilateral bullous disease and additional empyema in one of the lungs, controlled ventilation may be hazardous because of the high risk of inducing pneumothorax on the healthy side, causing bilateral collapse of the lungs, resulting in severe hypoxia.
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CASE REPORT
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A 50-year-old man weighing 76 kg and 176 cms tall, presented to a primary care center with acute onset of chest pain and dyspnea. He had a history of smoking. He was found to have left-sided pneumothorax, and his symptoms were relieved by insertion of an intercostal drain. Recurrences necessitated referral to our center with an indwelling drainage tube. On admission, he was comfortable at rest but had dyspnea on minimal activity. Computed tomography revealed multiple bullae in both lungs and collapse of the left lung with hydropneumothorax. The middle and lower lobes of the right lung appeared normal. A diagnosis of chronic obstructive pulmonary disease (COPD) with bilateral bullous disease and left-sided empyema was made. Despite the bilateral bullae, it was decided to decorticate only the left lung. Preoperative blood tests were normal. Resting arterial blood gases while breathing O2 via nasal prongs were: pH 7.356, PaO2 96 mm Hg, PaCO2 45 mm Hg, and standard bicarbonate 24 mEq·L1. Pulmonary function testing was not carried out because of empyema, hydropneumothorax, and the presence of an intercostal drain. The patient was premedicated with 200 µg of fentanyl and 5 mg of midazolam intramuscularly 30 minutes prior to surgery. Peripheral venous access was obtained, and a 16 gauge thoracic epidural catheter was inserted under local anesthesia at the T23 interspace by a midline approach using the loss-of-resistance technique with the patient seated. A 2 mL dose of 2% lidocaine with 1:200,000 adrenaline was administered, and when no untoward reactions were observed, epidural analgesia was achieved with 6 mL of 0.5% bupivacaine and 4 mL of 2% lidocaine with 1:200,000 adrenaline along with 25 µg of fentanyl.
Under local anesthesia, a triple-lumen catheter (Certofix trio V 715, B Braun, Melsungen, Germany) was passed into the right internal jugular vein and a 20 gauge cannula was placed in the left radial artery. Adequate sensory block was confirmed, and an infusion of bupivacaine 0.25% and fentanyl 15 µg·mL1 was given at a rate of 5 mL·hr1. Induction of general anesthesia was initiated with 100 mg of intravenous propofol and spontaneous inhalation of 2.5% of sevoflurane. The vocal cords were sprayed with 2 mL of 4% lidocaine. The trachea was intubated with a left-sided 41F double-lumen endobronchial catheter (Portex, Canterbury, UK), its position was confirmed, and the patient was allowed to breathe spontaneously, inhaling 1.5% to 2% sevoflurane in oxygen. With the patient in the right lateral position, differential lung ventilation was instituted using 2 ventilators while he continued to breathe spontaneously. The dependent (right) lung received 10 cm H2O pressure-support ventilation with a fraction of inspired oxygen (FiO2) of 0.8; this resulted in an exhaled tidal volume of 350 mL; the non-dependent lung received 5 cm H2O of continuous positive airway pressure with FiO2 of 0.8 through a similar ventilator.
Peak and mean airway pressures and exhaled tidal volume were monitored. The flow-volume and pressure-flow loops were also monitored. The ventilator circuit was disconnected on both sides every 10 min to allow expiration of any trapped gases. Arterial blood gases after positioning the patient were: PaO2 156 mm Hg, PaCO2 36 mm Hg, and pH 7.41. End-tidal CO2 from the dependent lung was 32 mm H2O. After a left anterolateral thoracotomy, the left lung was found to be collapsed and covered with empyema. Decortication was carried out and it was fully inflated at 40 cm H2O with FiO2 of 0.5. After inflation, 4 to 5 bullae appeared on the surface of the lung, which were plicated by clips, minor bronchial openings were identified by underwater air leak and sutured with 5/0 Prolene. Pressure-support ventilation (12 cm H2O) was applied to both lungs with a resultant exhaled tidal volume of 0.6 L. The chest was closed over a single 32F intercostal drainage tube. Isoflurane was discontinued, and the patient was found to be conscious, pain-free, and breathing adequately. Arterial blood gases were: PaO2 250 mm Hg, PaCO2 36 mm Hg, pH 7.36, and end-tidal CO2 31 mm Hg. The patient was extubated and noninvasive pressure-support ventilation was continued at 5 cm H2O and FiO2 of 0.5 via a face mask to prevent atelectasis.
Postoperative chest radiography showed an expanded left lung and no pneumothorax on the right side. Pressure support was discontinued after 3 hours, and the patient was supplemented with O2 via a face mask. Deep-breathing and physiotherapy exercises were started soon after transfer to the intensive care unit. The patient was moved to the ward the next day. Postoperatively, a mixture of fentanyl 5 µg·mL1 in 0.0625% bupivacaine was administered at a rate of 35 mL·hr1 through the epidural catheter for 4 days. The patient was discharged from the hospital on the 5th postoperative day.
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DISCUSSION
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Bullae are air-containing spaces within the lung parenchyma, which result from the destruction of alveolar tissue. Enlargement of bullae is the result of a valve-like mechanism that permits air trapping within the bullae.2 Increased airway resistance, destruction of lung parenchyma, and compression of the surrounding normal lung tissue by bullae in patients with COPD unfavorably affects pulmonary mechanics and gaseous exchange, invariably leading to physical limitation and respiratory failure. Institution of positive-pressure ventilation may lead to rupture of the bullae, life-threatening pneumothorax, and hypoxia. Thus, we used differential lung ventilation in this patient who was breathing spontaneously during decortication of the left lung, to prevent inadvertent pneumothorax on the contralateral side, with potentially catastrophic consequences.
Pneumothorax can be detected by increased airway pressure or by further diminution in breath sounds on the affected side; loss of ventilatory volume during manual ventilation strongly suggests further expansion or rupture of the bullae. The major concerns during ventilation of patients with COPD are prevention of dynamic pulmonary hyperinflation and auto-positive end-expiratory pressure.2 Both can cause hemodynamic consequences such as left ventricular dysfunction and a tamponade effect on the right ventricle. The main determinants are intrinsic (airway resistance and compliance), extrinsic (endotracheal tube and ventilator circuit), and the ventilatory pattern.3 The interval from the induction of anesthesia, when these problems can occur, to the point at which the thoracotomy is completed and the problems can be controlled, should be kept to a minimum. Awake-intubation with topical anesthesia or inhalation induction, and intubation and preservation of spontaneous respiration until completion of thoracotomy, are alternatives that can prevent rupture or expansion of bullae.4
A double-lumen tube allows complete and independent ventilatory control of each lung.1 Immediate discontinuation of ventilation on the side of the pneumothorax would prevent development of tension pneumothorax and hemodynamic instability. The other advantages of a double-lumen tube include selective suctioning and testing of the suture or staple line for leaks, against a known high pressure without increasing lung volume on the non-resected side.2 However, a 3-fold rise in airway pressure resulting in elevation of pulmonary vascular resistance during bulla excision and one-lung ventilation has been described.4 In our case, we chose to use the double-lumen tube because: the occurrence of pneumothorax on the healthy side was very likely, therefore, lung isolation was necessary; following decortication, the lung has to be expanded manually, but the increased airway pressures necessary to expand a chronically collapsed lung may cause pneumothorax on the contralateral side; and during re-expansion of the collapsed lung, rupture of bullae may lead to uncontrolled loss of tidal volume and hypoventilation.
Thoracic surgery in the presence of COPD carries a high risk of pulmonary complications.5 These include pneumonia, respiratory failure, and need for prolonged ventilatory support. Adequate relief from pain and the patients cooperation in chest physiotherapy and incentive spirometry can help to maintain pulmonary function and reduce pulmonary complications.6 Thoracic epidural analgesia ensures pain relief and is thought to improve pulmonary function. Therefore, we continued epidural infusion of bupivacaine and fentanyl for 4 days in the postoperative period. This report highlights the fact that anesthetic management of such cases is difficult.
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REFERENCES
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