Reexpansion Pulmonary Edema After Mediastinal Tumor Removal Naoki Matsumiya, MD, Shuji Dohi,
MD,
Tetsu Kimura,
MD,
and Hiroshi Naito,
MD
Department of Anesthesiology, Institute of Clinical Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan and Department of Anesthesiology, Gifu University School of Medicine, Gifu City, Gifu, Japan
S
udden evacuation of pneumothorax or pulmonary effusion may cause edema of ipsilateral lung (reexpansion pulmonary edema, RPE) (1). Other reports described a more acute form of RPE associated with lung reexpansion after several hours of atelectasis (2,3). Can lung reexpansion after onelung ventilation cause the edema formation of the nondependent lung? We describe a case of RPE that developed immediately after the removal of a mediastinal tumor during one-lung ventilation anesthesia in a young patient.
Case Report A 17-yr-old boy (body weight 58 kg, height 166 cm) was admitted to the hospital because he experienced a sudden sharp pain in his right hemithorax. Chest roentgenogram (Figure 1) and computed tomograph demonstrated an anterior mediastinal tumor, which was scheduled for removal. His serial chest roentgenograms revealed an increase in the size of the mediastinal tumor and partial atelectasis of the right lower lung and atelectasis of the right middle lobe. His electrocardiogram showed right axis deviation. His echocardiogram demonstrated the adjacency of the tumor to the right ventricle. Analysis of arterial blood gases with a fraction of inspired 0, of 0.2 disclosed the following values: pHa 7.39, arterial 0, tension 78 mm Hg, and arterial CO, tension 39 mm Hg. His preoperative pulmonary function studies revealed a forced vital capacity of 3.74 L and a forced expiratory volume in 1 s of 2.91 L. The data of other laboratory tests were unremarkable. Diazepam (10 mg) was given orally 90 min before arrival in the operating room. After the intravenous injection of 100 pg of fentanyl, his cervical epidural space was punctured with a 17-gauge Tuohy needle Accepted for publication June 28, 1991. Address correspondence to Dr. Matsumiya, Department of Anesthesia, Tsuchiura Kyodo Hospital, Tsuchiura City, Ibaraki 300, Japan.
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Anesth Analg 1991;73:64&4
at the C7-T1 intervertebral space, and an epidural catheter was inserted into which 8 mL of 2% lidocaine with epinephrine (1:200,000) was injected. Then general anesthesia was intravenously induced with 300 mg of thiamylal and 100 pg of fentanyl. The trachea and left main bronchus were intubated with a 35F, left-sided, double-lumen endobronchial tube (Bronchocath, National Catheter, New York, N.Y .). The appropriate placement of the endobronchial tube was confirmed with chest auscultation and fiberoptic bronchoscopic examination. The narrowing of the right main bronchus owing to compression by the mediastinal tumor was observed at this time. Anesthesia was maintained with epidural anesthesia with 2% lidocaine with epinephrine, inhalation of nitrous oxide, and intermittent intravenous injection of fentanyl. Pancuronium was injected intravenously to maintain muscle paralysis and facilitate controlled mechanical ventilation. Median sternotomy and right-sided thoracotomy was performed in the supine position. The right middle lobe was compressed totally by the tumor, whereas the right upper lobe was expanding normally with ventilation. The tracheal lumen of the double-lumen tube was disconnected from the anesthesia machine to provide access to air and only the left lung was ventilated with 50% nitrous oxide and 50% oxygen during the procedure of tumor resection. During this period analysis of arterial blood gases remained within normal range (pHa of 7.44, arterial 0, tension of 168 mm Hg, and arterial CO, tension of 34 mm Hg). Removal of the mediastinal tumor was completed uneventfully 2 h later. Analysis of arterial blood gases revealed the following values: pHa 7.38, arterial 0, tension 189 mm Hg, and arterial CO, tension 39 mm Hg with fraction of inspired 0, 0.5. The weight of the tumor was 1030 g. The right lung was deflated for 2 h during tumor removal. Before closure of the thorax, reinflation of the right lung was required to check air leakage and both lungs were expanded with manual positive-pressure ventilation with 20 cm H,O of peak inspiratory pressure. Hemo01991 by the International Anesthesia Research Society 0003-2999191/$3.50
ANESTH ANALG 19!21;73:64&8
CASE REPORTS
647
Figure 2. Chest roentgenogram immediately after the surgery showing unilateral pulmonary edema. Figure 1. Chest roentgenogram showing large mediastinal tumor 1 mo before surgery.
dynamic responses to lung inflation were not remarkable (systolic arterial blood pressure 140-144 mm Hg, heart rate 102-98 beatdmin). Central venous pressure was 7 mm Hg. Small amounts of sputum were aspirated from the right bronchus 30 min later. Thereafter, gasping respiration developed. Immediately after the completion of surgery, copious amounts of frothy pulmonary edema fluid flowed from the right bronchus. A sample of the fluid showed the total protein content to be 3.2 g/dL, with a pulmonary edema-serum protein ratio of 0.71, demonstrating increased pulmonary vascular permeability. No frothy fluid was aspirated from the left bronchus. Analysis of arterial blood gas data revealed the following values: pHa 7.37, arterial 0, tension 373 mm Hg, and arterial CO, tension 41 mm Hg with fraction of inspired O2 1.0. A chest roentgenogram showed diffuse alveolar infiltrates over the right lung field with clear left lung field (Figure 2). The blood loss was 3500 mL during the operation, which lasted for 5 h, and the patient received 4400 mL of crystalloid, 1000 mL of colloid, and 2000 mL of whole blood intravenously. The endobronchial tube was replaced by an endotracheal tube, and the patient was transferred to the intensive care unit where he was treated with controlled mechanical ventilation with 5 cm H,O of peak end-expiratory pressure. Epidural injection of 6 mL of 0.25% bupivacaine and 5 mg of morphine through the epidural catheter provided analgesia. Midazolam was administered for sedation. The aspiration of frothy edema fluid was continued and endotracheal suctioning every 30 min was required. Thereafter systolic arterial blood pressure gradually decreased to 80 mm Hg. With rapid transfusion of
colloid, arterial blood pressure returned to normal. Ten hours later, his condition improved markedly and continuous positive airway pressure was started instead of controlled mechanical ventilation. Over the next 30 h, hemodynamic and respiratory status was stabilized. The trachea was extubated on the following day. Serial chest roentgenograms showed that the pulmonary edema was resolving during the following 3 days. The remainder of his time in the intensive care unit was uneventful.
Discussion This is an unusual case of RPE that developed immediately after the surgical extirpation of an anterior mediastinal tumor during contralateral one-lung ventilation anesthesia. Many factors are associated with the development of RPE. The duration and severity of the lung collapse and the speed of reexpansion are important (1). The duration of lung compression by the mediastinal tumor in this case was more than 80 days before surgery, whereas the duration of lung atelectasis of the right middle lobe was about 20 days. The chest roentgenogram obtained the day before the operation revealed enlargement of the mediastinal tumor to occupy the lower half of the right lung field, and bronchoscopic examination just after endobronchial intubation revealed narrowing of the right main bronchus. Complete collapse of the lung is one risk factor of RPE. This is substantiated by the report that described RPE localized to one lobe that collapsed completely due to pneumothorax, and partially collapsed lobes that did not develop RPE after reexpansion (4). In our case, although a complete airless area was confined to the right middle lobe and the lower
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lobe was partially collapsed, RPE developed in the right lung as showed in Figure 2. Therefore, the complete collapse of the lobe because of compression by the mediastinal tumor was not the sole cause of the development of RPE in our case. Thus, we speculate that complete collapse of the right lung might contribute to the development of RPE. We used one-lung ventilation to avoid the interruption of surgical manipulation owing to lung inflation. Recently, a more acute form of RPE after only 2 h of atelectasis during the thoracic stage of esophagectomy (5) has been reported. Furthermore, one instance of unilateral pulmonary edema after rapid reexpansion of an atelectatic lung of short duration due to accidental placement of the endotracheal tube in the right mainstem bronchus was reported (2). Therefore we cannot exclude the possibility that a 2-h collapse of the right lung during one-lung ventilation could contribute to the development of RPE in our case. Most clinical and experimental observations support increased pulmonary vascular permeability as a major factor in the development of RPE (6-8). Possible mechanisms of the increase in pulmonary vascular permeability include anoxic damage to the capillary endothelium and mechanical damage to the blood vessel from overstretching during the process of reexpansion (1,8). Furthermore, a recent study demonstrated a potential role for free radicals provided by neutrophils in the increase in pulmonary vascular permeability as a cause of RPE (9,lO). Free radicals mediate damage in a variety of pathological conditions including ischemia in organs such as myocardium, intestine, and brain (11,12). Reoxygenation of ischemic tissue results in tissue damage (13). One potential mechanism of this reperfusion injury is that oxygen radicals lead to lipid peroxidation and membrane injury. Thus, one-lung ventilation of unilateral lung followed by bilateral lung ventilation may cause ischemia and reperfusion injury in the nonventilated lung and may increase pulmonary vascular permeability. We used cervical epidural anesthesia in addition to light general anesthesia in the present case. Although cervical epidural anesthesia has the possibility of causing cardiovascular changes, thoracic sympathetic blockade created by it using lidocaine is unlikely to affect pulmonary hemodynamics modifying the severity of pulmonary edema. Rather, thoracic epidural
anesthesia could minimize the deterioration in pulmonary oxygenation after oleic acid-induced pulmonary edema in sheep (14). But the effects of this anesthetic technique on pulmonary vascular permeability are unknown. We demonstrated a case of RPE in which collapse of the unilateral lung due to one-lung ventilation and manual reinflation of the collapsed lung were significant factors in its development. The result is often nothing more than a roentgenogram diagnosis of patchy consolidation and usually little or no clinical consequence. However, we should be aware that the institution of one-lung ventilation may cause an increase in pulmonary vascular permeability at the time of bilateral lung ventilation.
References 1. Marfood S, Hix WR, Aaron BL, Blaes P, Watson DC. Reexpan-
sion pulmonary edema. Ann Thorac Surg 1988;45:340-5. 2. Ravin CE, Dahmash NS. Re-expansion pulmonary edema. Chest 1980;77:709-10. 3. Sherman S, Ravikrishnan KP. Unilateral pulmonary edema following reexpansion of pneumothorax of brief duration. Chest 1980;77:714. 4. Vuong TK, Dautheribes C, Robert J, Laaban JP. Reexpansion pulmonary edema localized to a lobe. Chest 1989;95:1170. 5. Waller DA, Turner N. Re-expansion pulmonary oedema. Anaesthesia 1989;44:446-7. 6. Sprung CL, Loewenherz JW, Baier H, Hauser MJ. Evidence for increased permeability in reexpansion pulmonary edema. Am J Med 1981;71:497-500. 7. Marland AM, Glauser FL. Hemodynamic and pulmonary edema protein measurements in a case of reexpansion pulmonary edema. Chest 1982;81:250-1. 8. Pavlin DJ, Nessly ML, Cheney FW. Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits. Am Rev Respir Dis 1981;124:422-7. 9. lackson RM, Veal CF, Alexander CB, Brannen AL, Fulmer JD. Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis. Am Rev Respir Dis 1988;137116571. 10. jackson RM, Veal CF. Review: re-expansion, re-oxygenation, and rethinking. Am J Med Sci 1989;29844-50. 11. McCord J. Oxygen derived free radicals in post ischemic tissue injury. N Engl J Med 1989;312:159-63. 12. Liu TH, Beckman JS, Freeman BA, Hogan EL, Hsu CY. Polyethylene glycol-conjugated superoxide dismutase and catalase reduce ischemic brain injury. Am J Physiol 1989;256: H589-93. 13 Bulkley GB. Free radical-mediated reperfusion injury: a selective review. Br J Cancer 1987;55(SupplVIII):6673. 14 Mayumi T, Gallagher TJ, Kretzman WE. Thoracic epidural blockade-induced pulmonary sympathectomy improves PO2 in an oleic-acid induced model of pulmonary edema. Anesthesiology 1988;69:A852.
MD,
Tetsu Kimura,
MD,
and Hiroshi Naito,
MD
Department of Anesthesiology, Institute of Clinical Medicine, University of Tsukuba, Tsukuba City, Ibaraki, Japan and Department of Anesthesiology, Gifu University School of Medicine, Gifu City, Gifu, Japan
S
udden evacuation of pneumothorax or pulmonary effusion may cause edema of ipsilateral lung (reexpansion pulmonary edema, RPE) (1). Other reports described a more acute form of RPE associated with lung reexpansion after several hours of atelectasis (2,3). Can lung reexpansion after onelung ventilation cause the edema formation of the nondependent lung? We describe a case of RPE that developed immediately after the removal of a mediastinal tumor during one-lung ventilation anesthesia in a young patient.
Case Report A 17-yr-old boy (body weight 58 kg, height 166 cm) was admitted to the hospital because he experienced a sudden sharp pain in his right hemithorax. Chest roentgenogram (Figure 1) and computed tomograph demonstrated an anterior mediastinal tumor, which was scheduled for removal. His serial chest roentgenograms revealed an increase in the size of the mediastinal tumor and partial atelectasis of the right lower lung and atelectasis of the right middle lobe. His electrocardiogram showed right axis deviation. His echocardiogram demonstrated the adjacency of the tumor to the right ventricle. Analysis of arterial blood gases with a fraction of inspired 0, of 0.2 disclosed the following values: pHa 7.39, arterial 0, tension 78 mm Hg, and arterial CO, tension 39 mm Hg. His preoperative pulmonary function studies revealed a forced vital capacity of 3.74 L and a forced expiratory volume in 1 s of 2.91 L. The data of other laboratory tests were unremarkable. Diazepam (10 mg) was given orally 90 min before arrival in the operating room. After the intravenous injection of 100 pg of fentanyl, his cervical epidural space was punctured with a 17-gauge Tuohy needle Accepted for publication June 28, 1991. Address correspondence to Dr. Matsumiya, Department of Anesthesia, Tsuchiura Kyodo Hospital, Tsuchiura City, Ibaraki 300, Japan.
646
Anesth Analg 1991;73:64&4
at the C7-T1 intervertebral space, and an epidural catheter was inserted into which 8 mL of 2% lidocaine with epinephrine (1:200,000) was injected. Then general anesthesia was intravenously induced with 300 mg of thiamylal and 100 pg of fentanyl. The trachea and left main bronchus were intubated with a 35F, left-sided, double-lumen endobronchial tube (Bronchocath, National Catheter, New York, N.Y .). The appropriate placement of the endobronchial tube was confirmed with chest auscultation and fiberoptic bronchoscopic examination. The narrowing of the right main bronchus owing to compression by the mediastinal tumor was observed at this time. Anesthesia was maintained with epidural anesthesia with 2% lidocaine with epinephrine, inhalation of nitrous oxide, and intermittent intravenous injection of fentanyl. Pancuronium was injected intravenously to maintain muscle paralysis and facilitate controlled mechanical ventilation. Median sternotomy and right-sided thoracotomy was performed in the supine position. The right middle lobe was compressed totally by the tumor, whereas the right upper lobe was expanding normally with ventilation. The tracheal lumen of the double-lumen tube was disconnected from the anesthesia machine to provide access to air and only the left lung was ventilated with 50% nitrous oxide and 50% oxygen during the procedure of tumor resection. During this period analysis of arterial blood gases remained within normal range (pHa of 7.44, arterial 0, tension of 168 mm Hg, and arterial CO, tension of 34 mm Hg). Removal of the mediastinal tumor was completed uneventfully 2 h later. Analysis of arterial blood gases revealed the following values: pHa 7.38, arterial 0, tension 189 mm Hg, and arterial CO, tension 39 mm Hg with fraction of inspired 0, 0.5. The weight of the tumor was 1030 g. The right lung was deflated for 2 h during tumor removal. Before closure of the thorax, reinflation of the right lung was required to check air leakage and both lungs were expanded with manual positive-pressure ventilation with 20 cm H,O of peak inspiratory pressure. Hemo01991 by the International Anesthesia Research Society 0003-2999191/$3.50
ANESTH ANALG 19!21;73:64&8
CASE REPORTS
647
Figure 2. Chest roentgenogram immediately after the surgery showing unilateral pulmonary edema. Figure 1. Chest roentgenogram showing large mediastinal tumor 1 mo before surgery.
dynamic responses to lung inflation were not remarkable (systolic arterial blood pressure 140-144 mm Hg, heart rate 102-98 beatdmin). Central venous pressure was 7 mm Hg. Small amounts of sputum were aspirated from the right bronchus 30 min later. Thereafter, gasping respiration developed. Immediately after the completion of surgery, copious amounts of frothy pulmonary edema fluid flowed from the right bronchus. A sample of the fluid showed the total protein content to be 3.2 g/dL, with a pulmonary edema-serum protein ratio of 0.71, demonstrating increased pulmonary vascular permeability. No frothy fluid was aspirated from the left bronchus. Analysis of arterial blood gas data revealed the following values: pHa 7.37, arterial 0, tension 373 mm Hg, and arterial CO, tension 41 mm Hg with fraction of inspired O2 1.0. A chest roentgenogram showed diffuse alveolar infiltrates over the right lung field with clear left lung field (Figure 2). The blood loss was 3500 mL during the operation, which lasted for 5 h, and the patient received 4400 mL of crystalloid, 1000 mL of colloid, and 2000 mL of whole blood intravenously. The endobronchial tube was replaced by an endotracheal tube, and the patient was transferred to the intensive care unit where he was treated with controlled mechanical ventilation with 5 cm H,O of peak end-expiratory pressure. Epidural injection of 6 mL of 0.25% bupivacaine and 5 mg of morphine through the epidural catheter provided analgesia. Midazolam was administered for sedation. The aspiration of frothy edema fluid was continued and endotracheal suctioning every 30 min was required. Thereafter systolic arterial blood pressure gradually decreased to 80 mm Hg. With rapid transfusion of
colloid, arterial blood pressure returned to normal. Ten hours later, his condition improved markedly and continuous positive airway pressure was started instead of controlled mechanical ventilation. Over the next 30 h, hemodynamic and respiratory status was stabilized. The trachea was extubated on the following day. Serial chest roentgenograms showed that the pulmonary edema was resolving during the following 3 days. The remainder of his time in the intensive care unit was uneventful.
Discussion This is an unusual case of RPE that developed immediately after the surgical extirpation of an anterior mediastinal tumor during contralateral one-lung ventilation anesthesia. Many factors are associated with the development of RPE. The duration and severity of the lung collapse and the speed of reexpansion are important (1). The duration of lung compression by the mediastinal tumor in this case was more than 80 days before surgery, whereas the duration of lung atelectasis of the right middle lobe was about 20 days. The chest roentgenogram obtained the day before the operation revealed enlargement of the mediastinal tumor to occupy the lower half of the right lung field, and bronchoscopic examination just after endobronchial intubation revealed narrowing of the right main bronchus. Complete collapse of the lung is one risk factor of RPE. This is substantiated by the report that described RPE localized to one lobe that collapsed completely due to pneumothorax, and partially collapsed lobes that did not develop RPE after reexpansion (4). In our case, although a complete airless area was confined to the right middle lobe and the lower
648
CASE REPORTS
ANESTH ANALG 1991;73:6464
lobe was partially collapsed, RPE developed in the right lung as showed in Figure 2. Therefore, the complete collapse of the lobe because of compression by the mediastinal tumor was not the sole cause of the development of RPE in our case. Thus, we speculate that complete collapse of the right lung might contribute to the development of RPE. We used one-lung ventilation to avoid the interruption of surgical manipulation owing to lung inflation. Recently, a more acute form of RPE after only 2 h of atelectasis during the thoracic stage of esophagectomy (5) has been reported. Furthermore, one instance of unilateral pulmonary edema after rapid reexpansion of an atelectatic lung of short duration due to accidental placement of the endotracheal tube in the right mainstem bronchus was reported (2). Therefore we cannot exclude the possibility that a 2-h collapse of the right lung during one-lung ventilation could contribute to the development of RPE in our case. Most clinical and experimental observations support increased pulmonary vascular permeability as a major factor in the development of RPE (6-8). Possible mechanisms of the increase in pulmonary vascular permeability include anoxic damage to the capillary endothelium and mechanical damage to the blood vessel from overstretching during the process of reexpansion (1,8). Furthermore, a recent study demonstrated a potential role for free radicals provided by neutrophils in the increase in pulmonary vascular permeability as a cause of RPE (9,lO). Free radicals mediate damage in a variety of pathological conditions including ischemia in organs such as myocardium, intestine, and brain (11,12). Reoxygenation of ischemic tissue results in tissue damage (13). One potential mechanism of this reperfusion injury is that oxygen radicals lead to lipid peroxidation and membrane injury. Thus, one-lung ventilation of unilateral lung followed by bilateral lung ventilation may cause ischemia and reperfusion injury in the nonventilated lung and may increase pulmonary vascular permeability. We used cervical epidural anesthesia in addition to light general anesthesia in the present case. Although cervical epidural anesthesia has the possibility of causing cardiovascular changes, thoracic sympathetic blockade created by it using lidocaine is unlikely to affect pulmonary hemodynamics modifying the severity of pulmonary edema. Rather, thoracic epidural
anesthesia could minimize the deterioration in pulmonary oxygenation after oleic acid-induced pulmonary edema in sheep (14). But the effects of this anesthetic technique on pulmonary vascular permeability are unknown. We demonstrated a case of RPE in which collapse of the unilateral lung due to one-lung ventilation and manual reinflation of the collapsed lung were significant factors in its development. The result is often nothing more than a roentgenogram diagnosis of patchy consolidation and usually little or no clinical consequence. However, we should be aware that the institution of one-lung ventilation may cause an increase in pulmonary vascular permeability at the time of bilateral lung ventilation.
References 1. Marfood S, Hix WR, Aaron BL, Blaes P, Watson DC. Reexpan-
sion pulmonary edema. Ann Thorac Surg 1988;45:340-5. 2. Ravin CE, Dahmash NS. Re-expansion pulmonary edema. Chest 1980;77:709-10. 3. Sherman S, Ravikrishnan KP. Unilateral pulmonary edema following reexpansion of pneumothorax of brief duration. Chest 1980;77:714. 4. Vuong TK, Dautheribes C, Robert J, Laaban JP. Reexpansion pulmonary edema localized to a lobe. Chest 1989;95:1170. 5. Waller DA, Turner N. Re-expansion pulmonary oedema. Anaesthesia 1989;44:446-7. 6. Sprung CL, Loewenherz JW, Baier H, Hauser MJ. Evidence for increased permeability in reexpansion pulmonary edema. Am J Med 1981;71:497-500. 7. Marland AM, Glauser FL. Hemodynamic and pulmonary edema protein measurements in a case of reexpansion pulmonary edema. Chest 1982;81:250-1. 8. Pavlin DJ, Nessly ML, Cheney FW. Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits. Am Rev Respir Dis 1981;124:422-7. 9. lackson RM, Veal CF, Alexander CB, Brannen AL, Fulmer JD. Re-expansion pulmonary edema. A potential role for free radicals in its pathogenesis. Am Rev Respir Dis 1988;137116571. 10. jackson RM, Veal CF. Review: re-expansion, re-oxygenation, and rethinking. Am J Med Sci 1989;29844-50. 11. McCord J. Oxygen derived free radicals in post ischemic tissue injury. N Engl J Med 1989;312:159-63. 12. Liu TH, Beckman JS, Freeman BA, Hogan EL, Hsu CY. Polyethylene glycol-conjugated superoxide dismutase and catalase reduce ischemic brain injury. Am J Physiol 1989;256: H589-93. 13 Bulkley GB. Free radical-mediated reperfusion injury: a selective review. Br J Cancer 1987;55(SupplVIII):6673. 14 Mayumi T, Gallagher TJ, Kretzman WE. Thoracic epidural blockade-induced pulmonary sympathectomy improves PO2 in an oleic-acid induced model of pulmonary edema. Anesthesiology 1988;69:A852.
