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Extracardiac Thoracic Complications of Cardiac Surgery
Symposium on Surgery of the Chest
Extracardiac Thoracic Complications of Cardiac Surgery
Donald A. Barnhorst, M.D.
Few thoracic complications are peculiar to cardiac surgery, but they can occur after any surgical approach to the thorax. The more common of these problems will be discussed to aid in recognition of their causes, so that they may be avoided if possible, and methods for their management will be suggested.
STERNOTOMY PROBLEMS Median sternotomy has become the most common approach to the heart for procedures requiring extracorporeal circulation and is used almost exclusively at this institution. The only exception is for correction of atrial septal defects in young girls when right anterolateral thoracotomy may be used. The pain associated with this incision is perhaps a little less than that with lateral thoracotomy, probably because of the shoulder-movement pain accompanying the latter. Two types of pain, however, are unique to median sternotomy. Significant pain occurring beyond the third or fourth day after sternotomy is usually secondary to movement of the sternal halves against each other or to pain in the back resulting from the intraoperative stretching of the costovertebral junctions and their ligamentous attachments. Sternal-movement pain can be minimized by secure wiring of the sternal halves with six or seven 22-gauge wires. Lambert et al. described a helpful technique for securely wiring the sternum when one or both sternal halves have been fractured. Back pain seems to be more common in older patients with osteoarthritis and gradually abates within a week or two. Attention to opening the sternal spreader only as much as is necessary for exposure can lessen this problem in the older patient. Kirsh and associates reported five cases of temporary dysfunction of the brachial plexus developing after median sternotomy. The mechanism is thought to be depression of the clavicles into the retroclavicular space, superior rotation of the first ribs, and resultant stretching of the brachial Surgical Clinics of North America- VoL 53, No.4, August 1973
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plexus secondary to wide retraction of the sternal halves. Manifestations were various motor and sensory abnormalities of the upper extremities, and all patients had spontaneous recovery. Prophylaxis again depends on avoidance of unnecessary spreading of the sternal halves. Infection of the sternotomy wound is a potentially serious problem because of the danger of spread to underlying aortic and cardiac suture lines and prosthetic material. 17 • 20 Superficial infections can be treated by adequate drainage and appropriate antibiotics. If the sternum and anterior mediastinum become involved, it is necessary to reopen the sternum, debride the region, and reclose the sternum over irrigation and drainage catheters. Cheanvechai et al. reviewed three cases of infected sternotomy wounds associated with sternal dehiscence. Their experience supported the conclusion that reclosure of the sternum without debridement and adequate drainage of the mediastinum is unlikely to be successful.
ATELECT ASIS Some degree of pulmonary atelectasis occurs in a high percentage of patients after cardiac procedures. Median sternotomy operations avoiding both pleural spaces have a lower incidence of atelectasis than do operations through a lateral thoracotomy where the lung is retracted and may be inadvertently contused. We prefer not to drain the mediastinum into one of the pleural spaces after operation; in our opinion there is less pulmonary compression by blood and perhaps also less bleeding because of the mild compressive effect of the lateral aspects of the pericardium on the heart. The endotracheal tube is left in place after operation in all patients with marginal hemodynamics and in those more likely to have pulmonary problems, such as patients with mitral valvular disease or primary chronic pulmonary disease. These patients are given assisted ventilation usually for 24 hours or until their hemodynamic and pulmonary status is satisfactory. After extubation, these patients, as well as all others who were extubated in the operating room, are given chest physiotherapy twice daily by a team of trained physiotherapists and more frequently during the day by nurses in the intensive care unit. This therapy includes assistance with coughing and deep breathing, percussion of the chest, and postural drainage. Although the value of prophylactic intermittent positive pressure breathing (IPPB) is difficult to prove, we do give postoperative patients IPPB for 10 minutes every 2 hours during their stay in the intensive care unit, which averages 2 to 3 days. Such therapy is continued beyond this period only for specific indications. We share the current enthusiasm for the llse of continuous positive airway pressure in the postoperative manage,ilent of infants. The details of this technique are thoroughly discussed by Gregory and associates 8 • 9 and by Edmunds et al. and will not be restated here. The need for constant observation of these small patients with tiny, easily obstructed endotracheal tubes, however, must be emphasized.
EXTRACARDIAC THORACIC COMPLICATIONS OF CARDIAC SURGERY
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With this program, the occurrence of major atelectasis has become rare and problems with retained pulmonary secretions are infrequent.
HEMORRHAGE In most patients in whom hemorrhage after a cardiac procedure necessitates reoperation, a cardiac source of the bleeding is found and therefore this complication does not precisely fit the requirements of the title of this paper. However, a brief discussion of postoperative bleeding is appropriate as a reminder that hemostasis is necessary at all points in a cardiac surgical procedure. A recent review by Gomes and McGoon indicated a 3% incidence of reexploration necessary for continued bleeding after open-heart surgery. In 75% of patients reexplored, a specific bleeding site was found and the aortotomy was the most frequent site. Closure of the aortotomy in one or two layers did not result in a significant difference in bleeding rates. The fact that a third of the patients were found to be bleeding from the aortotomy stresses the importance of accurate closure of this incision. The sternal incision is suspect in many patients in whom the specific bleeding site is not found. The cut edges of the periosteum should be well cauterized, and bone wax is helpful to seal the marrow spaces. We have not had particular problems with bone wax and use it routinely. The wire holes through the sternum should be inspected before the sternum is closed to make certain they are not bleeding. Care must be taken to avoid lacerating the internal mammary vessels lateral to the sternum when placing wires. Cardiopulmonary bypass does effect changes in the coagulation mechanism but these rapidly revert toward normal after the operative procedure. Prolonged bypass (beyond 3 hours) and cyanotic congenital heart disease are known to be associated with increased bleeding. 7 These factors are seldom of great significance and most often cannot account for bleeding likely due to deficiencies in meticulous surgical hemostasis. In the standard situation we drain the mediastinum with two tubes, one anterior to the heart and one (a right-angle tube) in the midline just below the diaphragmatic surface of the heart. Both are connected to a bottle to which 20 cm of water suction is applied. The tubing is frequently "milked" with a tube stripper to maintain patency, and in questionable circumstances the tubes are irrigated under sterile conditions to ensure their patency. Resnicoff et al. recently reported the use of Fogarty catheters to extract clots from chest tubes. If the patient experiences severe bleeding as soon as he reaches the intensive care unit or if the hourly volume progressively increases, he is returned to the operating room. Decisions for treatment are difficult if the patient steadily bleeds approximately 200 to 300 ml of blood per hour. As long as he is hemodynamically stable, showing no signs of cardiac tamponade, we are inclined to wait several hours hoping for a decline in the rate of bleeding. If the same rate continues for more than 5 hours, it is likely that a significant source of bleeding is present and return of the pa-
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tient to the operating room for surgical investigation is advisable before problems occur.
PLEURAL EFFUSION AND HEMOTHORAX As mentioned earlier, we do not routinely drain the pericardial space into one of the pleural cavities. On occasion, however, and especially on reoperations, a pleural space may be entered inadvertently and opened widely for drainage. A low-lying chest tube usually drains the space satisfactorily. In the rare situation in which a large collection of blood has been trapped in a pleural space and is not retrievable by thoracentesis or thoracostomy tube, we think that limited lateral thoracotomy for removal of the blood and freeing-up of the underlying lung is indicated. This usually can be done safely and satisfactorily a week to 10 days after the initial operation, assuming satisfactory convalescence from the initial cardiac procedure. Varying degrees of pleural effusion occasionally follow the operation, usually as a manifestation of left-heart failure. We limit fluid intake to 500 ml/m2 of body surface on the day of operation and allow only 750 ml/m2 the next day. This total is gradually liberalized to 1,500 to 2,000 ml/day for the remainder of the hospitalization. Sodium intake is restricted to 20 mEq/day and patients are weighed daily. With this program, we see a fairly low incidence of pleural effusion, and in most of the patients the amount of fluid is small. Patients with small collections of fluid can usually be treated with diuretics, which bring about gradual resorption of the fluid. Patients having large collections of fluid must be treated with thoracentesis.
POSTCARDIOTOMY SYNDROME The occurrence of fever, pericardial pain, pleural pain, pulmonary infiltrates, arthralgias, dyspnea, pericardial or pleural effusion, pericardial friction rub, or any combination of these signs and symptoms in cardiac patients after surgical treatment may constitute what has been termed the "postcardiotomy syndrome."4 The cause is unknown, as is the precise incidence. Occurrence of postcardiotomy syndrome has been estimated variously as 10 to 40%, but only an estimate is possible because of the vague nature of findings in most cases. The importance of this syndrome lies in the necessity to differentiate it from more serious problems, such as myocardial infarction, pulmonary embolism, bacterial endocarditis, and pneumonia. The white blood cell count is usually mildly to moderately elevated with an increase in lymphocytes, which is often helpful in differentiating the syndrome from significant bacterial infection. The electrocardiogram may rule out myocardial infarction, and the characteristic elevation of the precordial lead S-T segment associated with pericarditis mayor may not be seen. Treatment depends on the severity of the syndrome, and in many cases no therapy is required. Salicylates, bed rest, and occasionally
EXTRACARDIAC THORACIC COMPLICATIONS OF CARDIAC SURGERY
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steroids are required in more serious cases. In a review of 40 cases of postcardiotomy syndrome by Connolly and Burchell, 13 patients were treated with steroids, 2 of whom became steroid-dependent. Resection of the pericardium in such dependent patients must be considered if their underlying cardiac disease does not make the surgical risk excessive.
POSTPERFUSION PULMONARY INSUFFICIENCY This entity has been given different identities depending on the circumstances in which it is found. Therefore, the terms "shock lung," "wet lung," and "postperfusion lung" have been used to descnbe what seems to be the same pathologic process. Since this condition will be discussed in detail elsewhere in this volume, we will mention it only briefly. The syndrome follows massive trauma, situations requiring massive blood transfusions, and extracorporeal circulation. It is characterized by increased effort in breathing, by severe hypoxemia with a large alveolar-arterial oxygen gradient that improves only slightly with the administration of 100% oxygen, and by increased fluid in the tracheobronchial tree. IS. 21 Central venous, pulmonary arterial, and pulmonary capillary wedge pressures may all be normal. The roentgenogram of the chest shows evidence of diffuse, fluffy, alveolar or interstitial infiltrate. The incidence of this syndrome after open-heart surgery is greatest in patients with longstanding heart failure, those with severe aortopulmonary collateral circulation, and in infants. IS However, it seems to be occurring less frequently, perhaps secondary to hemodilution techniques lO and the greater use of filters in extracorporeal circuits. Although the precise etiology of this condition is unclear, the principal pathophysiologic process 21 is most probably increased loss of fluid across the pulmonary capillaries with leakage of fluid into alveoli. This results in inhibition of surfactant leading to alveolar closure and diffuse microatelectasis that eventuates in a decrease in functional residual capacity and a decrease in lung compliance. Oxygen diffusion is further impaired by an increase in pulmonary interstitial fluid. 6 Blood then perfuses unventilated alveoli producing a wide alveolar-arterial oxygen gradient. Management of these patients initially was directed only at increasing the concentration of inspired oxygen. Because of appreciable right-toleft shunt, inspiration of high concentrations of oxygen was ineffective in raising arterial concentration of oxygen. As a result, prolonged use of high fractional concentration of oxygen in inspired gas (F 102) often led to oxygen toxicity, further lung dysfunction, and a vicious cycle with no hope of recovery. The reintroduction of positive end-expiratory pressure ventilation (PEEP) approached the problem at its source. Positive end-expiratory pressure works by opening atelectatic alveoli and increasing the functional residual capacity. Significant improvements in the partial pressure of arterial blood oxygen (P a02) are noted shortly after institution of PEEP,21 and continued improvement occurs presumably as pulmonary extravascular water decreases. Current therapy for the syndrome as now encountered after cardiac surgery is ventilatory support with a volume ventilator using high tidal
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volumes of 12 to 15 ml/kg of body weight. Extra dead space is added if needed to maintain the normal range of partial pressure of carbon dioxide in arterial blood. Fluids are restricted and diuretics are administered, usually beginning with the intravenous injection of 20 to 40 mg of furosemide. This treatment alone is effective in many early or mild cases of the syndrome. 6 If, in spite of these maneuvers, the P a o 2 is still less than 70 mm Hg,t PEEP is added, beginning with a pressure of 5 cm H 20, and is gradually increased to a value as high as 15 cm H 20 if the arterial blood gases indicate unsatisfactory response at lower pressures. Sugerman and associates reported no significant effect on cardiac output, systemic vascular resistance, or pulmonary vascular resistance with PEEP up to 15 cm H 2 0.
PULMONARY EMBOLISM In spite of increased awareness of this complication, it continues to occur with disturbing frequency after all types of surgical procedures. Because of the frequent need for anticoagulants in patients with valvular prostheses and the routine anticoagulation during hospitalization of patients with coronary-bypass grafts, the incidence of pulmonary embolism in cardiac surgical patients is somewhat lower than it might be. In the last 100 consecutive coronary bypass patients on my service, however, there have been three docUIhented episodes of pulmonary embolism, one of which was fatal. Encouraging the bedridden patient to exercise his lower extremities, the use of elastic bandages by patients with known venous disease, early ambulation after operation, and the elective use of anticoagulants after operation in high-risk patients are all valuable measures in the prophylaxis of this disease. If, in spite of these efforts, a pulmonary embolus develops, early diagnosis is important to salvage the patient with a massive insult. Patients with massive pulmonary emboli have few of the classic symptoms and signs of pulmonary embolic disease because infarction of the lung is not yet present. Sudden, severe dyspnea is usually the only symptom. In a cooperative study sponsored by the National Heart and Lung Institute,22 the triad of hemoptysis, pleuritic chest pain, and dyspnea was seen in only 20% of 160 patients with documented acute pulmonary emboli. In another series of patients with major pulmonary emboli,14 the most common symptom was also noted to be dyspnea, with only 25% of the patients experiencing pain in the chest. The most common signs were increased jugular venous pressure, right ventricular lift or gallop, tachypnea, and cyanosis. The electrocardiogram showed right heart strain in only 39% of patients. The difficulty of making the diagnosis on clinical grounds is borne out by the fact that slightly more than half of the patients referred for pulmonary angiography in the British series 14 were found not to have a pulmonary embolus. Acute respiratory diseases and pulmonary vascular congestion caused most of the diagnostic errors.
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Radioisotope lung scanning has aided in the diagnosis of pulmonary embolus, but this procedure also has limitations. Linton et al. reviewed the cases of 48 patients who were suspected of having a pulmonary embolus and who underwent both lung scanning and pulmonary angiography. If the scan showed negative findings, the likelihood of the patient having an embolus was low;' only 1 of 11 such patients was shown to have an embolus on angiography. However, in 37 scans showing positive findings, there were only 17 documented emboli on angiography. Emphysema, pneumonia, pleural effusion, and atelectasis most frequently accounted for the false-positive scans. The pulmonary scan is a valuable screening test; in the patient in whom significant pulmonary embolism is being considered, however, a follow-up with pulmonary angiography is an essential guide to therapy. Repeat lung scans are then helpful in the follow-up of areas of hypoperfusion. Therapy for the hemodynaInically stable patient with pulmonary embolism consists of rest in bed, oxygen therapy, anticoagulation with intravenous administration of heparin, and close monitoring of hemodynamics and arterial blood gases. Recovery is almost uniform if additional emboli do not occur. If embolization recurs in the adequately anticoagulated patient, interruption of the inferior vena cava is advised since most pulmonary emboli arise in tributaries of the infrarenal cava. In the patient who is critically ill the transvenous umbrella filter has proved to be a valuable device. 15 ,16 In the patient in whom the risk of a general anesthetic is not great, we still prefer a direct retroperitoneal approach to the cava and placement of a partially occluding clip. In the infrequent patient in cardiovascular collapse caused by a massive obstructive embolus, pulmonary embolectomy is the only effective treatment and must be carried out as soon as the diagnosis is definitely established by angiography. To sum up the problem of pulmonary embolism in the postoperative cardiac patient, the possibility of pulmonary embolism must be seriously entertained whenever severe dyspnea develops suddenly. An accurate diagnosis must be obtained as soon as possible and treatment should be carried out as outlined.
SUMMARY Several of the more common problems affecting the postoperative cardiac surgical patient have been discussed. Problems with the wound and with bleeding can often be avoided by constant attention to detail in the operating room. Pulmonary atelectasis can be minimized by a good program of chest physiotherapy early in the postoperative period. Pulmonary insufficiency and pulmonary embolism require alertness in .diagnosis and prompt institution of appropriate therapy.
REFERENCES 1. Brown HS, Turk LN, Hopkins WA: Management of the white lung syndrome. AnnThorac
Surg 13:411-419, 1972
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2. Cheanvechai C, Travisano F, Effler DB: Treatment of infected sternal wounds. Cleve Clin Q 39:43-47,1972 3. Connolly DC, Burchell HB: Pericarditis: a ten year survey. Am J Cardiol 7:7-14,1961 4. Ebert PA: The pericardium. In Surgery of the Chest. Second edition. Edited by JH Gibbon, DC Sabiston, FC Spencer. Philadelphia, WB Saunders Company, 1969, pp 569-571 5. Edmunds LH Jr, Fishman NH, Gregory GA, et al: Cardiac surgery in infants less than six weeks of age. Circulation 46:250-256, 1972 6. Fleming WH, Bowen JC: The use of diuretics in the treatment of early wet lung syndrome. Ann Surg 175:505-509, 1972 7. Gomes MMR, McGoon DC: Bleeding patterns after open-heart surgery. J Thorac Cardiovasc Surg 60:87-97, 1970 8. Gregory GA: Respiratory care of newborn infants. Pediatr Clin North Am 19:311-324, 1971 9. Gregory GA, Kitterman JA, Phibbs RH, et al: Treatment of the idiopathic respiratorydistress syndrome with continuous positive airway pressure. N Engl J Med 284: 13331340,1971 10. Hepps SA, Roe BB, Wright RR, et al: Amelioration of the pulmonary postperfusion syndrome with hemodilution and low molecular weight dextran. Surgery 54:232-241, 1963 11. Kirsh MM, Magee KR, Gago 0, et al: Brachial plexus injury following median sternotomy incision. Ann Thorac Surg 11 :315-319, 1971 12. Lambert CJ, Mitchel BF, Adam M, et al: A modified technique for secure median sternotomy closure. Surgery 69:393,1971 13. Linton DS Jr, Bellon EM, Bodie JF, et al: Comparison of results of pulmonary arteriography and radioisotope lung scanning in the diagnosis of pulmonary emboli. Am J Roentgenol Radium Ther Nucl Med 112:745-748, 1971 14. McDonald IG, Hirsh J, Hale GS, et al: Major pulmonary embolism, a correlation of clinical findings, haemodynamics, pulmonary angiography, and pathological physiology. Br Heart J 34:356-364, 1972 15. Mobin-Uddin K, Callard GM, Bolooki H, et al: Transvenous caval interruption with umbrella filter. N Engl J Med 286:55-58, 1972 16. Mobin-Uddin K, Trinkle JK, Bryant LR: Present status of the inferior vena cava umbrella filter. Surgery 70:914-918, 1971 17. Orringer MB, Murray GF, Haller JA, et al: Median sternotomy and outflow patch infections in total repair of tetralogy of Fallot: report of three cases of survival and a review of the literature. J Thorac Cardiovasc Surg 63:442-448, 1972 18. Parker DJ, Karp RB, Kirklin JW, et al: Lung water and alveolar and capillary volumes after intracardiac surgery. Circulation 45 Suppl 1: 139-146, 1972 19. Resnicoff SA, McReynolds DG, DeWeese JA: A technique for maintaining the patency of chest catheters following open-heart surgery. Ann Thorac Surg 13:190-191, 1972 20. Sanfelippo PM, Danielson GK: Complications associated with median sternotomy. J Thorac Cardiovasc Surg 63:419-423, 1972 21. Sugerman HJ, Olofsson KB, Pollock TW, et al: Continuous positive end-expiratory pressure ventilation (PEEP) for the treatment of diffuse interstitial pulmonary edema. J Trauma 12:263-273, 1972 22. Wenger NK, Stein PD, Willis PW: Massive acute pulmonary embolism: the deceivingly nonspecific manifestations. JAMA 220:843-844, 1972
Extracardiac Thoracic Complications of Cardiac Surgery
Donald A. Barnhorst, M.D.
Few thoracic complications are peculiar to cardiac surgery, but they can occur after any surgical approach to the thorax. The more common of these problems will be discussed to aid in recognition of their causes, so that they may be avoided if possible, and methods for their management will be suggested.
STERNOTOMY PROBLEMS Median sternotomy has become the most common approach to the heart for procedures requiring extracorporeal circulation and is used almost exclusively at this institution. The only exception is for correction of atrial septal defects in young girls when right anterolateral thoracotomy may be used. The pain associated with this incision is perhaps a little less than that with lateral thoracotomy, probably because of the shoulder-movement pain accompanying the latter. Two types of pain, however, are unique to median sternotomy. Significant pain occurring beyond the third or fourth day after sternotomy is usually secondary to movement of the sternal halves against each other or to pain in the back resulting from the intraoperative stretching of the costovertebral junctions and their ligamentous attachments. Sternal-movement pain can be minimized by secure wiring of the sternal halves with six or seven 22-gauge wires. Lambert et al. described a helpful technique for securely wiring the sternum when one or both sternal halves have been fractured. Back pain seems to be more common in older patients with osteoarthritis and gradually abates within a week or two. Attention to opening the sternal spreader only as much as is necessary for exposure can lessen this problem in the older patient. Kirsh and associates reported five cases of temporary dysfunction of the brachial plexus developing after median sternotomy. The mechanism is thought to be depression of the clavicles into the retroclavicular space, superior rotation of the first ribs, and resultant stretching of the brachial Surgical Clinics of North America- VoL 53, No.4, August 1973
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plexus secondary to wide retraction of the sternal halves. Manifestations were various motor and sensory abnormalities of the upper extremities, and all patients had spontaneous recovery. Prophylaxis again depends on avoidance of unnecessary spreading of the sternal halves. Infection of the sternotomy wound is a potentially serious problem because of the danger of spread to underlying aortic and cardiac suture lines and prosthetic material. 17 • 20 Superficial infections can be treated by adequate drainage and appropriate antibiotics. If the sternum and anterior mediastinum become involved, it is necessary to reopen the sternum, debride the region, and reclose the sternum over irrigation and drainage catheters. Cheanvechai et al. reviewed three cases of infected sternotomy wounds associated with sternal dehiscence. Their experience supported the conclusion that reclosure of the sternum without debridement and adequate drainage of the mediastinum is unlikely to be successful.
ATELECT ASIS Some degree of pulmonary atelectasis occurs in a high percentage of patients after cardiac procedures. Median sternotomy operations avoiding both pleural spaces have a lower incidence of atelectasis than do operations through a lateral thoracotomy where the lung is retracted and may be inadvertently contused. We prefer not to drain the mediastinum into one of the pleural spaces after operation; in our opinion there is less pulmonary compression by blood and perhaps also less bleeding because of the mild compressive effect of the lateral aspects of the pericardium on the heart. The endotracheal tube is left in place after operation in all patients with marginal hemodynamics and in those more likely to have pulmonary problems, such as patients with mitral valvular disease or primary chronic pulmonary disease. These patients are given assisted ventilation usually for 24 hours or until their hemodynamic and pulmonary status is satisfactory. After extubation, these patients, as well as all others who were extubated in the operating room, are given chest physiotherapy twice daily by a team of trained physiotherapists and more frequently during the day by nurses in the intensive care unit. This therapy includes assistance with coughing and deep breathing, percussion of the chest, and postural drainage. Although the value of prophylactic intermittent positive pressure breathing (IPPB) is difficult to prove, we do give postoperative patients IPPB for 10 minutes every 2 hours during their stay in the intensive care unit, which averages 2 to 3 days. Such therapy is continued beyond this period only for specific indications. We share the current enthusiasm for the llse of continuous positive airway pressure in the postoperative manage,ilent of infants. The details of this technique are thoroughly discussed by Gregory and associates 8 • 9 and by Edmunds et al. and will not be restated here. The need for constant observation of these small patients with tiny, easily obstructed endotracheal tubes, however, must be emphasized.
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With this program, the occurrence of major atelectasis has become rare and problems with retained pulmonary secretions are infrequent.
HEMORRHAGE In most patients in whom hemorrhage after a cardiac procedure necessitates reoperation, a cardiac source of the bleeding is found and therefore this complication does not precisely fit the requirements of the title of this paper. However, a brief discussion of postoperative bleeding is appropriate as a reminder that hemostasis is necessary at all points in a cardiac surgical procedure. A recent review by Gomes and McGoon indicated a 3% incidence of reexploration necessary for continued bleeding after open-heart surgery. In 75% of patients reexplored, a specific bleeding site was found and the aortotomy was the most frequent site. Closure of the aortotomy in one or two layers did not result in a significant difference in bleeding rates. The fact that a third of the patients were found to be bleeding from the aortotomy stresses the importance of accurate closure of this incision. The sternal incision is suspect in many patients in whom the specific bleeding site is not found. The cut edges of the periosteum should be well cauterized, and bone wax is helpful to seal the marrow spaces. We have not had particular problems with bone wax and use it routinely. The wire holes through the sternum should be inspected before the sternum is closed to make certain they are not bleeding. Care must be taken to avoid lacerating the internal mammary vessels lateral to the sternum when placing wires. Cardiopulmonary bypass does effect changes in the coagulation mechanism but these rapidly revert toward normal after the operative procedure. Prolonged bypass (beyond 3 hours) and cyanotic congenital heart disease are known to be associated with increased bleeding. 7 These factors are seldom of great significance and most often cannot account for bleeding likely due to deficiencies in meticulous surgical hemostasis. In the standard situation we drain the mediastinum with two tubes, one anterior to the heart and one (a right-angle tube) in the midline just below the diaphragmatic surface of the heart. Both are connected to a bottle to which 20 cm of water suction is applied. The tubing is frequently "milked" with a tube stripper to maintain patency, and in questionable circumstances the tubes are irrigated under sterile conditions to ensure their patency. Resnicoff et al. recently reported the use of Fogarty catheters to extract clots from chest tubes. If the patient experiences severe bleeding as soon as he reaches the intensive care unit or if the hourly volume progressively increases, he is returned to the operating room. Decisions for treatment are difficult if the patient steadily bleeds approximately 200 to 300 ml of blood per hour. As long as he is hemodynamically stable, showing no signs of cardiac tamponade, we are inclined to wait several hours hoping for a decline in the rate of bleeding. If the same rate continues for more than 5 hours, it is likely that a significant source of bleeding is present and return of the pa-
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tient to the operating room for surgical investigation is advisable before problems occur.
PLEURAL EFFUSION AND HEMOTHORAX As mentioned earlier, we do not routinely drain the pericardial space into one of the pleural cavities. On occasion, however, and especially on reoperations, a pleural space may be entered inadvertently and opened widely for drainage. A low-lying chest tube usually drains the space satisfactorily. In the rare situation in which a large collection of blood has been trapped in a pleural space and is not retrievable by thoracentesis or thoracostomy tube, we think that limited lateral thoracotomy for removal of the blood and freeing-up of the underlying lung is indicated. This usually can be done safely and satisfactorily a week to 10 days after the initial operation, assuming satisfactory convalescence from the initial cardiac procedure. Varying degrees of pleural effusion occasionally follow the operation, usually as a manifestation of left-heart failure. We limit fluid intake to 500 ml/m2 of body surface on the day of operation and allow only 750 ml/m2 the next day. This total is gradually liberalized to 1,500 to 2,000 ml/day for the remainder of the hospitalization. Sodium intake is restricted to 20 mEq/day and patients are weighed daily. With this program, we see a fairly low incidence of pleural effusion, and in most of the patients the amount of fluid is small. Patients with small collections of fluid can usually be treated with diuretics, which bring about gradual resorption of the fluid. Patients having large collections of fluid must be treated with thoracentesis.
POSTCARDIOTOMY SYNDROME The occurrence of fever, pericardial pain, pleural pain, pulmonary infiltrates, arthralgias, dyspnea, pericardial or pleural effusion, pericardial friction rub, or any combination of these signs and symptoms in cardiac patients after surgical treatment may constitute what has been termed the "postcardiotomy syndrome."4 The cause is unknown, as is the precise incidence. Occurrence of postcardiotomy syndrome has been estimated variously as 10 to 40%, but only an estimate is possible because of the vague nature of findings in most cases. The importance of this syndrome lies in the necessity to differentiate it from more serious problems, such as myocardial infarction, pulmonary embolism, bacterial endocarditis, and pneumonia. The white blood cell count is usually mildly to moderately elevated with an increase in lymphocytes, which is often helpful in differentiating the syndrome from significant bacterial infection. The electrocardiogram may rule out myocardial infarction, and the characteristic elevation of the precordial lead S-T segment associated with pericarditis mayor may not be seen. Treatment depends on the severity of the syndrome, and in many cases no therapy is required. Salicylates, bed rest, and occasionally
EXTRACARDIAC THORACIC COMPLICATIONS OF CARDIAC SURGERY
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steroids are required in more serious cases. In a review of 40 cases of postcardiotomy syndrome by Connolly and Burchell, 13 patients were treated with steroids, 2 of whom became steroid-dependent. Resection of the pericardium in such dependent patients must be considered if their underlying cardiac disease does not make the surgical risk excessive.
POSTPERFUSION PULMONARY INSUFFICIENCY This entity has been given different identities depending on the circumstances in which it is found. Therefore, the terms "shock lung," "wet lung," and "postperfusion lung" have been used to descnbe what seems to be the same pathologic process. Since this condition will be discussed in detail elsewhere in this volume, we will mention it only briefly. The syndrome follows massive trauma, situations requiring massive blood transfusions, and extracorporeal circulation. It is characterized by increased effort in breathing, by severe hypoxemia with a large alveolar-arterial oxygen gradient that improves only slightly with the administration of 100% oxygen, and by increased fluid in the tracheobronchial tree. IS. 21 Central venous, pulmonary arterial, and pulmonary capillary wedge pressures may all be normal. The roentgenogram of the chest shows evidence of diffuse, fluffy, alveolar or interstitial infiltrate. The incidence of this syndrome after open-heart surgery is greatest in patients with longstanding heart failure, those with severe aortopulmonary collateral circulation, and in infants. IS However, it seems to be occurring less frequently, perhaps secondary to hemodilution techniques lO and the greater use of filters in extracorporeal circuits. Although the precise etiology of this condition is unclear, the principal pathophysiologic process 21 is most probably increased loss of fluid across the pulmonary capillaries with leakage of fluid into alveoli. This results in inhibition of surfactant leading to alveolar closure and diffuse microatelectasis that eventuates in a decrease in functional residual capacity and a decrease in lung compliance. Oxygen diffusion is further impaired by an increase in pulmonary interstitial fluid. 6 Blood then perfuses unventilated alveoli producing a wide alveolar-arterial oxygen gradient. Management of these patients initially was directed only at increasing the concentration of inspired oxygen. Because of appreciable right-toleft shunt, inspiration of high concentrations of oxygen was ineffective in raising arterial concentration of oxygen. As a result, prolonged use of high fractional concentration of oxygen in inspired gas (F 102) often led to oxygen toxicity, further lung dysfunction, and a vicious cycle with no hope of recovery. The reintroduction of positive end-expiratory pressure ventilation (PEEP) approached the problem at its source. Positive end-expiratory pressure works by opening atelectatic alveoli and increasing the functional residual capacity. Significant improvements in the partial pressure of arterial blood oxygen (P a02) are noted shortly after institution of PEEP,21 and continued improvement occurs presumably as pulmonary extravascular water decreases. Current therapy for the syndrome as now encountered after cardiac surgery is ventilatory support with a volume ventilator using high tidal
942
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volumes of 12 to 15 ml/kg of body weight. Extra dead space is added if needed to maintain the normal range of partial pressure of carbon dioxide in arterial blood. Fluids are restricted and diuretics are administered, usually beginning with the intravenous injection of 20 to 40 mg of furosemide. This treatment alone is effective in many early or mild cases of the syndrome. 6 If, in spite of these maneuvers, the P a o 2 is still less than 70 mm Hg,t PEEP is added, beginning with a pressure of 5 cm H 20, and is gradually increased to a value as high as 15 cm H 20 if the arterial blood gases indicate unsatisfactory response at lower pressures. Sugerman and associates reported no significant effect on cardiac output, systemic vascular resistance, or pulmonary vascular resistance with PEEP up to 15 cm H 2 0.
PULMONARY EMBOLISM In spite of increased awareness of this complication, it continues to occur with disturbing frequency after all types of surgical procedures. Because of the frequent need for anticoagulants in patients with valvular prostheses and the routine anticoagulation during hospitalization of patients with coronary-bypass grafts, the incidence of pulmonary embolism in cardiac surgical patients is somewhat lower than it might be. In the last 100 consecutive coronary bypass patients on my service, however, there have been three docUIhented episodes of pulmonary embolism, one of which was fatal. Encouraging the bedridden patient to exercise his lower extremities, the use of elastic bandages by patients with known venous disease, early ambulation after operation, and the elective use of anticoagulants after operation in high-risk patients are all valuable measures in the prophylaxis of this disease. If, in spite of these efforts, a pulmonary embolus develops, early diagnosis is important to salvage the patient with a massive insult. Patients with massive pulmonary emboli have few of the classic symptoms and signs of pulmonary embolic disease because infarction of the lung is not yet present. Sudden, severe dyspnea is usually the only symptom. In a cooperative study sponsored by the National Heart and Lung Institute,22 the triad of hemoptysis, pleuritic chest pain, and dyspnea was seen in only 20% of 160 patients with documented acute pulmonary emboli. In another series of patients with major pulmonary emboli,14 the most common symptom was also noted to be dyspnea, with only 25% of the patients experiencing pain in the chest. The most common signs were increased jugular venous pressure, right ventricular lift or gallop, tachypnea, and cyanosis. The electrocardiogram showed right heart strain in only 39% of patients. The difficulty of making the diagnosis on clinical grounds is borne out by the fact that slightly more than half of the patients referred for pulmonary angiography in the British series 14 were found not to have a pulmonary embolus. Acute respiratory diseases and pulmonary vascular congestion caused most of the diagnostic errors.
EXTRACARDIAC THORACIC COMPLICATIONS OF CARDIAC SURGERY
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Radioisotope lung scanning has aided in the diagnosis of pulmonary embolus, but this procedure also has limitations. Linton et al. reviewed the cases of 48 patients who were suspected of having a pulmonary embolus and who underwent both lung scanning and pulmonary angiography. If the scan showed negative findings, the likelihood of the patient having an embolus was low;' only 1 of 11 such patients was shown to have an embolus on angiography. However, in 37 scans showing positive findings, there were only 17 documented emboli on angiography. Emphysema, pneumonia, pleural effusion, and atelectasis most frequently accounted for the false-positive scans. The pulmonary scan is a valuable screening test; in the patient in whom significant pulmonary embolism is being considered, however, a follow-up with pulmonary angiography is an essential guide to therapy. Repeat lung scans are then helpful in the follow-up of areas of hypoperfusion. Therapy for the hemodynaInically stable patient with pulmonary embolism consists of rest in bed, oxygen therapy, anticoagulation with intravenous administration of heparin, and close monitoring of hemodynamics and arterial blood gases. Recovery is almost uniform if additional emboli do not occur. If embolization recurs in the adequately anticoagulated patient, interruption of the inferior vena cava is advised since most pulmonary emboli arise in tributaries of the infrarenal cava. In the patient who is critically ill the transvenous umbrella filter has proved to be a valuable device. 15 ,16 In the patient in whom the risk of a general anesthetic is not great, we still prefer a direct retroperitoneal approach to the cava and placement of a partially occluding clip. In the infrequent patient in cardiovascular collapse caused by a massive obstructive embolus, pulmonary embolectomy is the only effective treatment and must be carried out as soon as the diagnosis is definitely established by angiography. To sum up the problem of pulmonary embolism in the postoperative cardiac patient, the possibility of pulmonary embolism must be seriously entertained whenever severe dyspnea develops suddenly. An accurate diagnosis must be obtained as soon as possible and treatment should be carried out as outlined.
SUMMARY Several of the more common problems affecting the postoperative cardiac surgical patient have been discussed. Problems with the wound and with bleeding can often be avoided by constant attention to detail in the operating room. Pulmonary atelectasis can be minimized by a good program of chest physiotherapy early in the postoperative period. Pulmonary insufficiency and pulmonary embolism require alertness in .diagnosis and prompt institution of appropriate therapy.
REFERENCES 1. Brown HS, Turk LN, Hopkins WA: Management of the white lung syndrome. AnnThorac
Surg 13:411-419, 1972
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2. Cheanvechai C, Travisano F, Effler DB: Treatment of infected sternal wounds. Cleve Clin Q 39:43-47,1972 3. Connolly DC, Burchell HB: Pericarditis: a ten year survey. Am J Cardiol 7:7-14,1961 4. Ebert PA: The pericardium. In Surgery of the Chest. Second edition. Edited by JH Gibbon, DC Sabiston, FC Spencer. Philadelphia, WB Saunders Company, 1969, pp 569-571 5. Edmunds LH Jr, Fishman NH, Gregory GA, et al: Cardiac surgery in infants less than six weeks of age. Circulation 46:250-256, 1972 6. Fleming WH, Bowen JC: The use of diuretics in the treatment of early wet lung syndrome. Ann Surg 175:505-509, 1972 7. Gomes MMR, McGoon DC: Bleeding patterns after open-heart surgery. J Thorac Cardiovasc Surg 60:87-97, 1970 8. Gregory GA: Respiratory care of newborn infants. Pediatr Clin North Am 19:311-324, 1971 9. Gregory GA, Kitterman JA, Phibbs RH, et al: Treatment of the idiopathic respiratorydistress syndrome with continuous positive airway pressure. N Engl J Med 284: 13331340,1971 10. Hepps SA, Roe BB, Wright RR, et al: Amelioration of the pulmonary postperfusion syndrome with hemodilution and low molecular weight dextran. Surgery 54:232-241, 1963 11. Kirsh MM, Magee KR, Gago 0, et al: Brachial plexus injury following median sternotomy incision. Ann Thorac Surg 11 :315-319, 1971 12. Lambert CJ, Mitchel BF, Adam M, et al: A modified technique for secure median sternotomy closure. Surgery 69:393,1971 13. Linton DS Jr, Bellon EM, Bodie JF, et al: Comparison of results of pulmonary arteriography and radioisotope lung scanning in the diagnosis of pulmonary emboli. Am J Roentgenol Radium Ther Nucl Med 112:745-748, 1971 14. McDonald IG, Hirsh J, Hale GS, et al: Major pulmonary embolism, a correlation of clinical findings, haemodynamics, pulmonary angiography, and pathological physiology. Br Heart J 34:356-364, 1972 15. Mobin-Uddin K, Callard GM, Bolooki H, et al: Transvenous caval interruption with umbrella filter. N Engl J Med 286:55-58, 1972 16. Mobin-Uddin K, Trinkle JK, Bryant LR: Present status of the inferior vena cava umbrella filter. Surgery 70:914-918, 1971 17. Orringer MB, Murray GF, Haller JA, et al: Median sternotomy and outflow patch infections in total repair of tetralogy of Fallot: report of three cases of survival and a review of the literature. J Thorac Cardiovasc Surg 63:442-448, 1972 18. Parker DJ, Karp RB, Kirklin JW, et al: Lung water and alveolar and capillary volumes after intracardiac surgery. Circulation 45 Suppl 1: 139-146, 1972 19. Resnicoff SA, McReynolds DG, DeWeese JA: A technique for maintaining the patency of chest catheters following open-heart surgery. Ann Thorac Surg 13:190-191, 1972 20. Sanfelippo PM, Danielson GK: Complications associated with median sternotomy. J Thorac Cardiovasc Surg 63:419-423, 1972 21. Sugerman HJ, Olofsson KB, Pollock TW, et al: Continuous positive end-expiratory pressure ventilation (PEEP) for the treatment of diffuse interstitial pulmonary edema. J Trauma 12:263-273, 1972 22. Wenger NK, Stein PD, Willis PW: Massive acute pulmonary embolism: the deceivingly nonspecific manifestations. JAMA 220:843-844, 1972