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Multiple pulmonary microemboli complicating pneumonectomy
Multiple Pulmonary Microemboli Complicating Pneumonectomy Christopher M. R. Satur, FRCS, Roderick H. Robertson, FRCR, Philip E. Da Costa, MRCPath, Nigel R. Saunders, FRCS, and Duncan R. Walker, FRCS Departments of Cardiothoracic Surgery, Radiology, and Histopathology, The Killingbeck Hospital, Leeds, England
Pulmonary embolism is widely recognized to complicate abdominal and lower limb orthopedic surgical procedures, but in comparison, it is seldom recognized to hamper the postoperative progress of patients after thoracic operations. We present 4 patients in whom multiple
pulmonary emboli developed after pneumonectomy, 2 of whom were treated successfully. We discuss the mostly atypical presentation and the physiological and clinical consequences, and also suggest a mode of management. (Ann Thorac Surg 1991;52:122-6)
T
pathophysiological changes that resulted. We also suggest a plan of management for early recognition and treatment of these pulmonary emboli.
he three factors constituting Virchow's triad-venous stasis, trauma to vascular endothelium, and altered coagulability-encourage venous thrombosis after operation. Stasis results in hypoxic damage to endothelial cells and a reduced production of prostaglandin I,, which normally inhibits platelet aggregation. Trauma to endothelium reduces production of fibrinolytic activators and thus allows fibrin deposition on the endothelium. Increased production of plasminogen activator inhibitor, interleukin 1 by endothelial cells, and tumor necrosis factor induces a procoagulant state [l].All three components of the triad are present after both extrathoracic and intrathoracic surgical procedures and thus are likely to cause thromboembolic complications after both. Patients at greatest risk of thromboembolic phenomena are those more than 50 years old [2], those who have a neoplasia, and those who have been immobile before and after major surgical procedures [3, 41. Pulmonary emboli complicate as many as 30% of major general surgical procedures and cause the death of 3% of patients after orthopedic procedures [5]. Those patients with compromised pulmonary and cardiac function are prone to suffer the greatest pulmonary and cardiac embarrassment [6,3]. Patients treated by pulmonary resection possess many of the risk factors predisposing to pulmonary emboli and are theoretically likely to suffer marked symptoms; they are, however, seldom recognized to suffer from the complication, the reported incidence being less than 0.5% [7-91. We believe that this statistic may be erroneously low and that cases of pulmonary emboli are unrecognized after major pulmonary resection. The often vague and nonspecific symptoms may be attributed to more common complications such as bronchospasm, atelectasis, pulmonary edema, or pulmonary insufficiency [3]. In this report, we describe the cases of 4 patients seen over a period of 18 months that exemplify this problem, and we discuss the Accepted for publication April 11, 1991 Address correspondence to Mr Satur, Department of Cardiothoracic Surgery, The Killingbeck Hospital, York Rd, Leeds, West Yorkshire, Leeds, LS14 6UQ, England.
0 1991 by The Society of Thoracic Surgeons
Perioperative Management Protocol A standard philosophy for preparation of the patient for lung resection was adhered to. In the presence of neoplasia (patients 1 to 3), the resectability of the tumor was assessed by clinical examination and laboratory investigations. Respiratory function was assessed by spirometry, with all but 1 patient having a forced expiratory volume in 1 second greater than 2.0 Lls, and a ratio of forced expiratory volume in 1 second to forced vital capacity greater than 0.60. In the patient with poor lung function, computed tomography demonstrated almost complete destruction of the lung to be resected. Resections were then performed using similar techniques of stapling major vessels and bronchi. Patients received routine broadspectrum antibiotics for 48 hours after the operation and 5,000 units of calcium heparin subcutaneously twice a day, and were mobilized early.
Case Histories
Patient 1 A 53-year-old man with a squamous cell carcinoma of the left main bronchus was treated by resection of the left lung, a procedure that required intrapericardial resection of the superior pulmonary vein. Six days later, marked dyspnea with clinical signs of pulmonary edema developed. The chest roentgenogram showed minor segmental and subsegmental defects suggestive of but not conclusive evidence of emboli, and an electrocardiogram was normal. He was treated with intravenous Frusemide (Antigen Pharmaceuticals Ltd, Roscrea, Ireland) and nebulized Salbutamol (ventolin; Allen L. Hanburys Ltd, Greenford, England), which relieved his symptoms temporarily. Later that day, right-sided pleuritic chest pain accompanied by an audible pleural rub developed. The diagnosis of acute pulmonary emboli was made, and anticoagu0003-4975/91/$3.50
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Ann Thorac Surg 1991;52:122-6
A
123
treated by right pneumonectomy. Two days after operation, he became distressed, dyspneic, and hypotensive, and was believed to be in hypovolemic shock. A clinical examination showed a central venous pressure of 7 cm H,O, and an arterial blood gas analysis demonstrated a pH of 7.37, carbon dioxide tension of 5.27 kPa, and oxygen tension of 7.83 kPa. A chest roentgenogram showed a little patchy consolidation at the left base compatible with minor postoperative infection, insufficient to explain the marked deterioration in his condition. It did not show any evidence of pulmonary emboli or edema. Resuscitation by the infusion of whole blood, administration of face mask oxygen, and intravenous inotropic support was attempted. This achieved temporary improvement in the hemodynamic and ventilatory status. Rapid atrial fibrillation then developed, which was controlled with amiodarone, and later, electrocardiographic changes of cardiac ischemia developed. Mechanical ventilatory support was instituted. He suffered an asystolic cardiac arrest unresponsive to intensive resuscitative measures, and he died. Postmortem examination showed evidence of pulmonary edema and focal hemorrhages within the interstitium related to multiple fresh thromboemboli within the pulmonary arterial branches of the left lung (Fig 2). The emboli involved arteries between 1 and 4 mm in diameter and were consistent with showers of small emboli from the thrombi present in the deep veins of the leg.
Patient 3 This 59-year-old man had a squamous cell carcinoma that originated in the upper lobe, involved the lower lobe of the right lung, and was resected by pneumonectomy. On the third postoperative day, he became dyspneic and had widespread wheezes audible in the left lung and patchy shadowing in the mid and lower zones visible on chest roentgenogram (Fig 3A). Atelectasis, infection, and secondary bronchospasm were the suspected causes; thus, he was treated with broad-spectrum antibiotics and nebulized Salbutamol. Moderate respiratory failure ensued, and a second chest roentgenogram showed more confluB
Fig 1 . Chest roentgenograni ( A ) shoiuing norm1 appearances in the right lung field accompanied by multiple right upper and posterobasal defects on the perfusion scan (B).
lation treatment commenced initially with intravenous heparin and later with warfarin. The following day, a radioisotope pulmonary perfusion scan demonstrated segmental and subsegmental perfusion defects in the apical and basal regions of the lung unmatched by chest roentgenographic changes; emboli were thus highly probable (Fig 1). The patient fully recovered and has remained well 18 months after discharge.
Patient 2 A 57-year-old male patient with poorly differentiated squamous cell carcinoma of the right main bronchus was
Fig 2 . A medium-sized muscular artery containing a recent laminated thrornboembolus.
124
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Ann Thorac Surg 1991;52:122-6
There were large thromboemboli in the pulmonary trunk and the main artery that were adherent and well organized, a s well as smaller emboli in the branch arteries, some old and organized, others fresh (Fig 3B). Thrombi of varying ages were present in the leg veins. Histological examination showed the consolidation to be due to old edema and hemorrhage with organization within airspaces, as well as focal bronchopneumonic change. The major emboli had a degree of organization indicating probable occurrence around the time of operation rather than a more recent event.
Patient 4
A
B Fig 3. ( A ) Chest roentgenogram shoriiiizg nonspecific left niidzone consolidation; changes zcwe demonstrated by clinical history to be ernboli. ( B ) A large arteriole showing obliteration of the lurnen by n plux of thromboembolus undergoing organization and incorporation into the wall.
ence of consolidation more in keeping with cardiac failure and early adult respiratory distress syndrome. Arterial gas analysis demonstrated a respiratory acidosis, a pH of 7.11, and a carbon dioxide tension of 7.23 kPa; thus, mechanical ventilatory support was provided for 48 hours. Respiratory failure recurred 7 days later, when the pulmonary artery wedge pressure measured with a flotation balloon catheter was 20 mm Hg. Artificial ventilation was reinstituted and was continued until the time of death 25 days postoperatively. Terminal events included the development of a bronchopleural fistula, radiological evidence of severe adult respiratory distress syndrome, and finally septicemic shock. At postmortem examination, the left lung was found to be extensively consolidated with partial basal collapse.
A 65-year-old woman, who had an aspergilloma that occupied a tuberculous cavity in the right upper lobe of the lung resected in 1975. The residual lung, which was severely damaged by bronchiectasis, was the focus of recurrent infection and was resected in 1990. She was a poor candidate for operation, having an oxygen tension of 8.9 kPa in air, carbon dioxide tension of 5.46 kPa, and a forced expiratory volume in 1 second of 0.9 L/s, 64% of the forced vital capacity. On the second postoperative day, rapid atrial fibrillation developed, requiring treatment with digoxin. Five days later, moderate dyspnea accompanied by a cough productive of purulent sputum and by hemoptysis developed. An electrocardiogram showed atrial fibrillation, and a chest roentgenogram showed a small left posterior basal segmental collapse. Four days of treatment with antibiotics and bronchodilators improved the purulent sputum but did not improve her overall dyspneic state. The arterial blood pH was 7.46, carbon dioxide tension was 4.82 kPa, and oxygen tension was 9.9 kPa on 28% face mask oxygen. Pulmonary emboli were therefore suspected, and anticoagulation was started with substantial benefit. A pulmonary perfusion scan performed 2 days later suggested the presence of pulmonary emboli with a high probability of accuracy. Segmental and subsegmental defects unmatched by acute changes on the chest roentgenogram were demonstrated (Fig 4). There were, however, areas of calcification within the left lung that we are unable to report with certainty in the absence of a ventilation scan, and that were unrelated to the perfusion defects. Hemoptysis persisted, and other features of a bronchopleural fistula developed, including infection within the pleural space. This was successfully treated by fashioning a Clagget window, allowing full resolution of symptomatology .
Comment The cases described clearly demonstrate the difficulties encountered in diagnosing pulmonary emboli after pneumonectomy. The symptoms were not openly attributable to emboli, with only one seen as pleuritic chest pain. All the patients had dyspnea and other symptoms that may have been attributed either to preexisting disease or to other complications of lung operation. Typical abnormalities associated with emboli were not noted on electrocardiograms or on chest roentgenograms; however, pulmo-
Ann Thorac Surg 1991;52:122-6
Fig 4. A perfusion scan showing widespread perfusion defects, particularly i n the apical segment of the left lower lobe.
nary perfusion scans demonstrated segmental defects consistent with serious emboli in 2 patients. The postmortem examinations of 2 patients were conspicuous by the absence of large thrombi occluding major vessels but showed the presence of numerous thrombi occluding small to medium-sized branches of the pulmonary artery. In nonsurgical patients without compromised pulmonary function, an embolus large enough to occlude a main branch artery would not necessarily cause symptoms of the magnitude described here [lo]. Emboli to the residual lung tissue would, however, further obstruct the pulmonary circulation and then cause a low cardiac output, poor exchange of oxygen, and marked symptoms. Occlusion of a main branch artery is reproduced by the procedure of pneumonectomy, and we hypothesize that the latter situation might be mimicked postoperatively when microemboli shower the lung [3, 61. In a study of 156 patients undergoing amputation of part of the lower limb, the presence of pulmonary emboli postoperatively was investigated prospectively. Twenty percent and 12% of the patients were found to have substantial evidence of emboli on a perfusion scan and on angiography, respectively, but less than 2.5% of the total group were symptomatic [ l l ] . Thus, most of these emboli were sufficiently small not to cause hemodynamic com-
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125
plications. Rosenow and associates [3] reported that in medical patients suffering from emboli, the typical triad of acute pleurisy, dyspnea, and hemoptysis is present in only 20% of patients, whereas dyspnea is present in 80%. The correct diagnosis required that emboli were considered in any person with acute nonspecific cardiopulmonary complaints. The differential diagnosis of respiratory failure after pulmonary operation includes pulmonary edema, cardiac failure, infection, bronchospasm, and pulmonary emboli. Correct diagnosis necessitates a clear awareness of fluid balance [ 121, hematological and microbiological variables, and the patients’ preoperative potential for bronchospasm [8]. Pulmonary emboli may, however, be difficult to differentiate from the other problems as it can produce a similar clinical and investigational picture. The hypoxia resulting from emboli may cause reflex bronchospasm typical of asthma or of an exacerbation of chronic obstructive airways disease [3, 13-15]. Airways may be rendered atelectatic and susceptible to secondary infection, causing edema (31. Thus, in the 4 patients described, the initial diagnoses may in fact have been the secondary pathology. Blood gas analysis may help in indicating the presence of emboli by demonstrating recent onset of hypoxia and hypocarbia; measurement of the alveolar-arterial oxygen pressure gradient will, however, be misleading in the presence of the acute ventilatory changes after operation [16].We recommend that a lung scan is performed early if emboli are suggested, a ventilation/perfusion scan being preferable though not ideal. In the presence of marked dyspnea in an unwell patient in the early postoperative period, the ventilation scan will provide poor-quality results [ 171. In addition, the kryptonhbidium required for the investigation is not always readily available to institutions. We are satisfied to complete the full anticoagulation protocol by initially administering intravenous heparin and then oral warfarin if pulmonary emboli are highly likely on clinical assessment, and if segmental perfusion defects unmatched by chest roentgenographic changes are present [17]. We do not believe that pulmonary angiography is a worthwhile procedure in these critically ill patients. However, in the presence of highly probable symptoms and an equivocal perfusion scan, angiography is recommended [ 181. Prophylaxis against thromboembolism is commonly practiced in the field of general surgery [3] and should be considered for use by thoracic surgeons. The measures used include the limitation of the hospitalization period before operation, wearing antiembolic stockings postoperatively, and, most importantly, administration of calcium heparin subcutaneously preoperatively and postoperatively. The latter provides an effective reduction in morbidity and mortality arising from deep vein thromboses or emboli, and greatest protection is afforded if the dose is adjusted to maintain the activated partial thromboplastin time between 31.5 and 36 seconds rather than administering fixed doses (41. Using heparin perioperatively may increase the incidence of postoperative bleeding [ 191, but the magnitude
126
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of this risk in comparison with that from emboli can only be weighed in a randomized trial. Heparin administration may, however, be commenced after active bleeding has ceased, but this is less effective. Over the last 12 months, 94 lung resections have been performed in this institute, 34 of which were by pneumonectomy. Of the total group, 6 patients, all of whom had undergone a pneumonectomy, died. The immediate causes of death were attributed to a massive pulmonary embolus in 2 and to respiratory failure in another 2 in whom postmortem examinations were not performed. Thus, the risk of this complication being a contributory cause of death or of morbidity is substantial and appears to justify that due consideration be given to the role of prophylaxis for and treatment of all patients receiving pulmonary resection by pneumonectomy . In conclusion, pulmonary emboli may seriously complicate the progress of a patient after pneumonectomy while producing few specific symptoms, signs, or abnormalities on investigation. It may masquerade as one of the other more common complications after pneumonectomy and may account for hospital mortality. We believe that its early identification and treatment will reduce hospital morbidity and mortality.
References 1. Risberg 8 . Pathophysiological mechanisms of thromboembolism. Acta Chir Scand Suppl 1988;550:10414. 2. Hume M, Sevitt S, Thomas DP. Venous thrombosis and pulmonary embolism. Cambridge, MA: Harvard University Press, 1970. 3. Rosenow EC 111, Osmundson PJ, Brown ML. Pulmonary embolism. Mayo Clin Proc 1981;56:161-78. 4. Kakkar V. Prevention of venous thrombosis and pulmonary embolism. Am J Cardiol 1990;65:5OC4C. 5. Consensus Conference. Prevention of venous thrombosis and pulmonary embolism. JAMA 1986;256:74&9.
Ann Thorac Surg 1991;52:122-6
6. Sabiston DC, Spencer FC. Gibbons’s surgery of the chest, 4th ed. Philadelphia: W.B. Saunders, 1983:21. 7. Deslauriers J, Ginsberg RJ, Dubois P, Beaulieu M, Goldberg M, Piraux M. Current operative morbidity associated with elective surgical resection for lung cancer. Can J Surg 1989; 32:33>9. 8. Kirsh MM, Rotman H, Behrendt DM, Orringer MB, Sloan H. Complications of pulmonary resection. Ann Thorac Surg 1975;20:215-34. 9. Nagasaki F, Flehinger BJ, Martini N. Complications of surgery in the treatment of carcinoma of the lung. Chest 1982;82:25-9. 10. Marshall R, Sabiston DC, Allison PR, Dunnill MS. The immediate and late effects of pulmonary embolism by large thrombi in dogs. Thorax 1963;18:1. 11. Williams JW, Eikman EA, Greenberg S. Asymptomatic pulmonary embolism. A common event in high risk patients. Ann Surg 1982;195:323-7. 2. Zeldin RA, Normandin D, Landtwing D, Peters RM. Postoperative pulmonary edema. J Thorac Cardiovasc Surg 1984;87: 3594. 3. Lippmann M, Fein A. Pulmonary embolism in the patient with chronic obstructive pulmonary disease; a diagnostic dilemma. Chest 1981;79:3942. 4. Windebank WJ. Diagnosing pulmonary thromboembolism. Br Med J 1987;294:1369-70. 5. Windebank WJ, Boyd G, Moran F. Pulmonary embolism presenting as asthma. Br Med J 1973;1:90-4. 16. Cvitanic 0, Marinao PL. Improved use of arterial blood gas analysis in suspected pulmonary embolism. Chest 1989;95: 4a5i. 17. Benetar SR, Immelman EJ, Jeffery P. Pulmonary embolism. Br J Dis Chest 1986;80:31>34. 18. Dalen JE, Brooks HL, Johnson LW, Meister SG, Szucs MM, Dexter L. Pulmonary angiography in acute pulmonary embolism: indications, techniques, and results in 367 patients. Am Heart J 1971;81:175-85. 19. Reilly DT. Prophylactic methods against thromboembolism. Acta Chir Scand Suppl 1988;550:115-8.
Pulmonary embolism is widely recognized to complicate abdominal and lower limb orthopedic surgical procedures, but in comparison, it is seldom recognized to hamper the postoperative progress of patients after thoracic operations. We present 4 patients in whom multiple
pulmonary emboli developed after pneumonectomy, 2 of whom were treated successfully. We discuss the mostly atypical presentation and the physiological and clinical consequences, and also suggest a mode of management. (Ann Thorac Surg 1991;52:122-6)
T
pathophysiological changes that resulted. We also suggest a plan of management for early recognition and treatment of these pulmonary emboli.
he three factors constituting Virchow's triad-venous stasis, trauma to vascular endothelium, and altered coagulability-encourage venous thrombosis after operation. Stasis results in hypoxic damage to endothelial cells and a reduced production of prostaglandin I,, which normally inhibits platelet aggregation. Trauma to endothelium reduces production of fibrinolytic activators and thus allows fibrin deposition on the endothelium. Increased production of plasminogen activator inhibitor, interleukin 1 by endothelial cells, and tumor necrosis factor induces a procoagulant state [l].All three components of the triad are present after both extrathoracic and intrathoracic surgical procedures and thus are likely to cause thromboembolic complications after both. Patients at greatest risk of thromboembolic phenomena are those more than 50 years old [2], those who have a neoplasia, and those who have been immobile before and after major surgical procedures [3, 41. Pulmonary emboli complicate as many as 30% of major general surgical procedures and cause the death of 3% of patients after orthopedic procedures [5]. Those patients with compromised pulmonary and cardiac function are prone to suffer the greatest pulmonary and cardiac embarrassment [6,3]. Patients treated by pulmonary resection possess many of the risk factors predisposing to pulmonary emboli and are theoretically likely to suffer marked symptoms; they are, however, seldom recognized to suffer from the complication, the reported incidence being less than 0.5% [7-91. We believe that this statistic may be erroneously low and that cases of pulmonary emboli are unrecognized after major pulmonary resection. The often vague and nonspecific symptoms may be attributed to more common complications such as bronchospasm, atelectasis, pulmonary edema, or pulmonary insufficiency [3]. In this report, we describe the cases of 4 patients seen over a period of 18 months that exemplify this problem, and we discuss the Accepted for publication April 11, 1991 Address correspondence to Mr Satur, Department of Cardiothoracic Surgery, The Killingbeck Hospital, York Rd, Leeds, West Yorkshire, Leeds, LS14 6UQ, England.
0 1991 by The Society of Thoracic Surgeons
Perioperative Management Protocol A standard philosophy for preparation of the patient for lung resection was adhered to. In the presence of neoplasia (patients 1 to 3), the resectability of the tumor was assessed by clinical examination and laboratory investigations. Respiratory function was assessed by spirometry, with all but 1 patient having a forced expiratory volume in 1 second greater than 2.0 Lls, and a ratio of forced expiratory volume in 1 second to forced vital capacity greater than 0.60. In the patient with poor lung function, computed tomography demonstrated almost complete destruction of the lung to be resected. Resections were then performed using similar techniques of stapling major vessels and bronchi. Patients received routine broadspectrum antibiotics for 48 hours after the operation and 5,000 units of calcium heparin subcutaneously twice a day, and were mobilized early.
Case Histories
Patient 1 A 53-year-old man with a squamous cell carcinoma of the left main bronchus was treated by resection of the left lung, a procedure that required intrapericardial resection of the superior pulmonary vein. Six days later, marked dyspnea with clinical signs of pulmonary edema developed. The chest roentgenogram showed minor segmental and subsegmental defects suggestive of but not conclusive evidence of emboli, and an electrocardiogram was normal. He was treated with intravenous Frusemide (Antigen Pharmaceuticals Ltd, Roscrea, Ireland) and nebulized Salbutamol (ventolin; Allen L. Hanburys Ltd, Greenford, England), which relieved his symptoms temporarily. Later that day, right-sided pleuritic chest pain accompanied by an audible pleural rub developed. The diagnosis of acute pulmonary emboli was made, and anticoagu0003-4975/91/$3.50
SATUR ET AL PULMONARY EMBOLI
Ann Thorac Surg 1991;52:122-6
A
123
treated by right pneumonectomy. Two days after operation, he became distressed, dyspneic, and hypotensive, and was believed to be in hypovolemic shock. A clinical examination showed a central venous pressure of 7 cm H,O, and an arterial blood gas analysis demonstrated a pH of 7.37, carbon dioxide tension of 5.27 kPa, and oxygen tension of 7.83 kPa. A chest roentgenogram showed a little patchy consolidation at the left base compatible with minor postoperative infection, insufficient to explain the marked deterioration in his condition. It did not show any evidence of pulmonary emboli or edema. Resuscitation by the infusion of whole blood, administration of face mask oxygen, and intravenous inotropic support was attempted. This achieved temporary improvement in the hemodynamic and ventilatory status. Rapid atrial fibrillation then developed, which was controlled with amiodarone, and later, electrocardiographic changes of cardiac ischemia developed. Mechanical ventilatory support was instituted. He suffered an asystolic cardiac arrest unresponsive to intensive resuscitative measures, and he died. Postmortem examination showed evidence of pulmonary edema and focal hemorrhages within the interstitium related to multiple fresh thromboemboli within the pulmonary arterial branches of the left lung (Fig 2). The emboli involved arteries between 1 and 4 mm in diameter and were consistent with showers of small emboli from the thrombi present in the deep veins of the leg.
Patient 3 This 59-year-old man had a squamous cell carcinoma that originated in the upper lobe, involved the lower lobe of the right lung, and was resected by pneumonectomy. On the third postoperative day, he became dyspneic and had widespread wheezes audible in the left lung and patchy shadowing in the mid and lower zones visible on chest roentgenogram (Fig 3A). Atelectasis, infection, and secondary bronchospasm were the suspected causes; thus, he was treated with broad-spectrum antibiotics and nebulized Salbutamol. Moderate respiratory failure ensued, and a second chest roentgenogram showed more confluB
Fig 1 . Chest roentgenograni ( A ) shoiuing norm1 appearances in the right lung field accompanied by multiple right upper and posterobasal defects on the perfusion scan (B).
lation treatment commenced initially with intravenous heparin and later with warfarin. The following day, a radioisotope pulmonary perfusion scan demonstrated segmental and subsegmental perfusion defects in the apical and basal regions of the lung unmatched by chest roentgenographic changes; emboli were thus highly probable (Fig 1). The patient fully recovered and has remained well 18 months after discharge.
Patient 2 A 57-year-old male patient with poorly differentiated squamous cell carcinoma of the right main bronchus was
Fig 2 . A medium-sized muscular artery containing a recent laminated thrornboembolus.
124
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Ann Thorac Surg 1991;52:122-6
There were large thromboemboli in the pulmonary trunk and the main artery that were adherent and well organized, a s well as smaller emboli in the branch arteries, some old and organized, others fresh (Fig 3B). Thrombi of varying ages were present in the leg veins. Histological examination showed the consolidation to be due to old edema and hemorrhage with organization within airspaces, as well as focal bronchopneumonic change. The major emboli had a degree of organization indicating probable occurrence around the time of operation rather than a more recent event.
Patient 4
A
B Fig 3. ( A ) Chest roentgenogram shoriiiizg nonspecific left niidzone consolidation; changes zcwe demonstrated by clinical history to be ernboli. ( B ) A large arteriole showing obliteration of the lurnen by n plux of thromboembolus undergoing organization and incorporation into the wall.
ence of consolidation more in keeping with cardiac failure and early adult respiratory distress syndrome. Arterial gas analysis demonstrated a respiratory acidosis, a pH of 7.11, and a carbon dioxide tension of 7.23 kPa; thus, mechanical ventilatory support was provided for 48 hours. Respiratory failure recurred 7 days later, when the pulmonary artery wedge pressure measured with a flotation balloon catheter was 20 mm Hg. Artificial ventilation was reinstituted and was continued until the time of death 25 days postoperatively. Terminal events included the development of a bronchopleural fistula, radiological evidence of severe adult respiratory distress syndrome, and finally septicemic shock. At postmortem examination, the left lung was found to be extensively consolidated with partial basal collapse.
A 65-year-old woman, who had an aspergilloma that occupied a tuberculous cavity in the right upper lobe of the lung resected in 1975. The residual lung, which was severely damaged by bronchiectasis, was the focus of recurrent infection and was resected in 1990. She was a poor candidate for operation, having an oxygen tension of 8.9 kPa in air, carbon dioxide tension of 5.46 kPa, and a forced expiratory volume in 1 second of 0.9 L/s, 64% of the forced vital capacity. On the second postoperative day, rapid atrial fibrillation developed, requiring treatment with digoxin. Five days later, moderate dyspnea accompanied by a cough productive of purulent sputum and by hemoptysis developed. An electrocardiogram showed atrial fibrillation, and a chest roentgenogram showed a small left posterior basal segmental collapse. Four days of treatment with antibiotics and bronchodilators improved the purulent sputum but did not improve her overall dyspneic state. The arterial blood pH was 7.46, carbon dioxide tension was 4.82 kPa, and oxygen tension was 9.9 kPa on 28% face mask oxygen. Pulmonary emboli were therefore suspected, and anticoagulation was started with substantial benefit. A pulmonary perfusion scan performed 2 days later suggested the presence of pulmonary emboli with a high probability of accuracy. Segmental and subsegmental defects unmatched by acute changes on the chest roentgenogram were demonstrated (Fig 4). There were, however, areas of calcification within the left lung that we are unable to report with certainty in the absence of a ventilation scan, and that were unrelated to the perfusion defects. Hemoptysis persisted, and other features of a bronchopleural fistula developed, including infection within the pleural space. This was successfully treated by fashioning a Clagget window, allowing full resolution of symptomatology .
Comment The cases described clearly demonstrate the difficulties encountered in diagnosing pulmonary emboli after pneumonectomy. The symptoms were not openly attributable to emboli, with only one seen as pleuritic chest pain. All the patients had dyspnea and other symptoms that may have been attributed either to preexisting disease or to other complications of lung operation. Typical abnormalities associated with emboli were not noted on electrocardiograms or on chest roentgenograms; however, pulmo-
Ann Thorac Surg 1991;52:122-6
Fig 4. A perfusion scan showing widespread perfusion defects, particularly i n the apical segment of the left lower lobe.
nary perfusion scans demonstrated segmental defects consistent with serious emboli in 2 patients. The postmortem examinations of 2 patients were conspicuous by the absence of large thrombi occluding major vessels but showed the presence of numerous thrombi occluding small to medium-sized branches of the pulmonary artery. In nonsurgical patients without compromised pulmonary function, an embolus large enough to occlude a main branch artery would not necessarily cause symptoms of the magnitude described here [lo]. Emboli to the residual lung tissue would, however, further obstruct the pulmonary circulation and then cause a low cardiac output, poor exchange of oxygen, and marked symptoms. Occlusion of a main branch artery is reproduced by the procedure of pneumonectomy, and we hypothesize that the latter situation might be mimicked postoperatively when microemboli shower the lung [3, 61. In a study of 156 patients undergoing amputation of part of the lower limb, the presence of pulmonary emboli postoperatively was investigated prospectively. Twenty percent and 12% of the patients were found to have substantial evidence of emboli on a perfusion scan and on angiography, respectively, but less than 2.5% of the total group were symptomatic [ l l ] . Thus, most of these emboli were sufficiently small not to cause hemodynamic com-
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125
plications. Rosenow and associates [3] reported that in medical patients suffering from emboli, the typical triad of acute pleurisy, dyspnea, and hemoptysis is present in only 20% of patients, whereas dyspnea is present in 80%. The correct diagnosis required that emboli were considered in any person with acute nonspecific cardiopulmonary complaints. The differential diagnosis of respiratory failure after pulmonary operation includes pulmonary edema, cardiac failure, infection, bronchospasm, and pulmonary emboli. Correct diagnosis necessitates a clear awareness of fluid balance [ 121, hematological and microbiological variables, and the patients’ preoperative potential for bronchospasm [8]. Pulmonary emboli may, however, be difficult to differentiate from the other problems as it can produce a similar clinical and investigational picture. The hypoxia resulting from emboli may cause reflex bronchospasm typical of asthma or of an exacerbation of chronic obstructive airways disease [3, 13-15]. Airways may be rendered atelectatic and susceptible to secondary infection, causing edema (31. Thus, in the 4 patients described, the initial diagnoses may in fact have been the secondary pathology. Blood gas analysis may help in indicating the presence of emboli by demonstrating recent onset of hypoxia and hypocarbia; measurement of the alveolar-arterial oxygen pressure gradient will, however, be misleading in the presence of the acute ventilatory changes after operation [16].We recommend that a lung scan is performed early if emboli are suggested, a ventilation/perfusion scan being preferable though not ideal. In the presence of marked dyspnea in an unwell patient in the early postoperative period, the ventilation scan will provide poor-quality results [ 171. In addition, the kryptonhbidium required for the investigation is not always readily available to institutions. We are satisfied to complete the full anticoagulation protocol by initially administering intravenous heparin and then oral warfarin if pulmonary emboli are highly likely on clinical assessment, and if segmental perfusion defects unmatched by chest roentgenographic changes are present [17]. We do not believe that pulmonary angiography is a worthwhile procedure in these critically ill patients. However, in the presence of highly probable symptoms and an equivocal perfusion scan, angiography is recommended [ 181. Prophylaxis against thromboembolism is commonly practiced in the field of general surgery [3] and should be considered for use by thoracic surgeons. The measures used include the limitation of the hospitalization period before operation, wearing antiembolic stockings postoperatively, and, most importantly, administration of calcium heparin subcutaneously preoperatively and postoperatively. The latter provides an effective reduction in morbidity and mortality arising from deep vein thromboses or emboli, and greatest protection is afforded if the dose is adjusted to maintain the activated partial thromboplastin time between 31.5 and 36 seconds rather than administering fixed doses (41. Using heparin perioperatively may increase the incidence of postoperative bleeding [ 191, but the magnitude
126
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of this risk in comparison with that from emboli can only be weighed in a randomized trial. Heparin administration may, however, be commenced after active bleeding has ceased, but this is less effective. Over the last 12 months, 94 lung resections have been performed in this institute, 34 of which were by pneumonectomy. Of the total group, 6 patients, all of whom had undergone a pneumonectomy, died. The immediate causes of death were attributed to a massive pulmonary embolus in 2 and to respiratory failure in another 2 in whom postmortem examinations were not performed. Thus, the risk of this complication being a contributory cause of death or of morbidity is substantial and appears to justify that due consideration be given to the role of prophylaxis for and treatment of all patients receiving pulmonary resection by pneumonectomy . In conclusion, pulmonary emboli may seriously complicate the progress of a patient after pneumonectomy while producing few specific symptoms, signs, or abnormalities on investigation. It may masquerade as one of the other more common complications after pneumonectomy and may account for hospital mortality. We believe that its early identification and treatment will reduce hospital morbidity and mortality.
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