Management of Postoperative Problems Following Pulmonary and Cardiac Surgery

Management of Postoperative Problems Following Pulmonary and Cardiac Surgery

Management of Postoperative Problems Following Pulmonary and Cardiac Surgery From the Department of Surgery, New England Center Hospital and ...

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Management of Postoperative Problems Following Pulmonary and Cardiac Surgery From the Department of Surgery, New England Center Hospital and
RALPH A. DETERLING, JR., M.D., PH.D., F.A.C.S. Professor and Chairman, Department of Surgery, Tufts University School of Medicine; Surgeon-in-Chief, Tufts-New England Medical Center; Director, First (Tufts) Surgical Service, Boston City Hospital

HAROLD F. RHEINLANDER, M.D., F.A.C.S. Associate Professor of Surgery, Tufts University School of Medicine; Surgeon, Tufts-New England Medical Center; Associate Surgeon, Boston Floating Hospital;'Attending Surgeon, Boston Veterans Administration Hospital

THERE has been a very significant reduction in morbidity and mortality associated with thoracic and cardiac surgery during the past 15 years. Part of thil;; improvement is due to specialized training of the surgeon and to the development of team care .of these patients. Equally important has been the increased emphasis on proper preoperative preparation, adequate blood replacement, improved techniques of anesthesia, availability of effective antibiotic drugs as well as early recognition and treatment of related complications. It is our intent to describe certain of the more common complications following pulmonary and cardiac surgery, and to suggest effective means of dealing with them. Smooth convalescence in the thoracic surgical patient is achieved by prompt restoration of cardiac and pulmonary function. This objective can be attained by maintaining adequate blood volume and cardiac function, by providing a clear airway and fully expanded lung tissue with adequate alveolar ventilation, and by avoiding undue postoperative blood loss. Although similar complications are seen following both pul-

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monary and cardiac surgery, there are specific problems involving each field which will be discussed separately. PROBLEMS FOLLOWING PULMONARY SURGERY

Pneumothorax

Following lobectomy, segmented resection and wedge resections, prompt and full expansion of the residual lung must be achieved. In order to provide egress for air and fluid from the pleural space, intercostal drainage tubes are invariably used. It is our practice to insert a No. 28 plastic catheter through a stab wound in the eighth or ninth interspace in the midaxillary line to drain the inferior aspect of the pleural space in every case. When air leaks are left from raw pulmonary surfaces, an additional plastic catheter is positioned with its tip in the apex of the chest to aspirate residual air. The second catheter may be placed beside the first or through a stab wound in the second intercostal space. These tubes are attached to separate water-seal drainage bottles. When air leaks persist, 12 to 18 cm. of water negative pressure is applied to the catheters to promote more rapid re-expansion of the lung and sealing of the raw surfaces. Persistent air spaces may occur after lobectomy, segmental resection, excision of emphysematous blebs and wedge resections. Adjustment or replacement of the intercostal drainage tubes or the addition of suction may allow the lung to re-expand and obliterate the space. Occasionally such spaces may persist for some time without causing difficulty although they remain potential trouble spots for the development of infection. Following pneumonectomy a single No. 24 plastic catheter may be utilized through the seventh or eighth intercostal space. It remains clamped except for once a day when the pleural pressure is adjusted to minus 5 to 8 cm. of water. It is usually removed on the fifth postoperative day unless the persistent recurrence of positive pleural pressures denotes a bronchial air leak in which case it is attached to a water-seal drainage bottle for decompression of the pleural space. Many surgeons prefer intermittent needle aspirations through the second intercostal space instead of the catheter for the adjustment of intrapleural pressures. Bronchopleural Fistula

Small bronchial fistulas may be diagnosed by persistent air leaks or recurring positive pleural pressures in the pneumonectomized patient. Late fistulas may be suspected by bloody sputum, collapse of a previously expanded lobe or recurrence of an air-fluid level in the chest. Massive fistula following pneumonectomy may be ushered in by sudden copious expectoration of blood-stained fluid and the patient is in danger of drowning in his own pleural fluid.

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If an effective intercostal drainage tube is not already in place, a large catheter should be inserted into the pleural space through a trocar and attached to water-seal drainage. If the fistula is small, persistent drainage may allow the fistula to close and any residual lung expand to fill the pleural cavity. Following pneumonectomy, persistent drainage may be followed by closure of the fistula. If the residual pleural cavity remains sterile the tube may then be removed. If empyema occurs it is occasionally possible to render the pleural cavity sterile by means of repeated injection of the appropriate antibiotic drugs following wruch the catheter can be withdrawn. The incidence of bronchopleural fistula can be lowered after pulmonary resection by meticulous closure of the amputated bronchial stump.21 The stump should never be grasped with forceps or clamps and a minimal number of nonabsorbable simple end-over sutures should be used. Whenever possible it is our practice following pneumonectomy to cover the broncrual stump with a pleural flap dissected from the chest wall. It is occasionally possible to acrueve successful closure of a bronchopleural fistula occurring early in the postoperative course by reamputation and resuture of the bronchus. Atelectasis

Atelectasis is the most frequent cause of fever early in the postoperative course. Collapsed pulmonary parenchyma results from inadequate re-expansion of the lung before the chest is closed, inadequate decompression of the pleural space, or from brachial obstruction by blood or secretions with absorption of distal air. Atelectasis is promoted by direct lung trauma, excessive secretions, inadequate broncrual toilet by the anesthetist at the conclusion of the procedure, and incisional pain which restricts respiratory movements and prevents an effective cough. Preexisting chronic bronchitis and bronchospasm such as exists in the heavy smoker also predispose to this condition. The presence of dehydration, dry atmosphere or inadequately hydrated oxygen, and drying agents such as atropine and scopolamine augment the above mechanisms. In many instances the only sign of difficulty is the presence of rales or limited areas of decreased breath sounds and the chest film may not show any significant abnormalities. Adequate preoperative preparation of the patient for chest surgery can prevent development of atelectasis in many instances. The heavy smoker should abstain from tobacco for at least one week prior to operation. Bronchospasm should be overcome by bronchodilator drugs, using corticosteroids as necessary. The patient with copious bronchial secretions should be placed on a preoperative regimen of postural drainage, with expectorants, wetting agents and mucolytic drugs to aid in clearing secretions. Intermittent positive pressure breathing apparatus may aid in the weak and debilitated individual. Specific bacterial

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invaders in the tracheobronchial tree should be treated by appropriate antibiotic drugs. Finally, preoperative instruction in the mechanics of deep breathing and coughing is extremely valuable. During and at the conclusion of the operation, endotracheal toilet must be meticulous. Sedation with narcotic drugs must be adequate to control incisional pain, but dosages sufficient to cause respiratory depression must be avoided. Intercostal nerve blocks may be effective in promoting free respiratory movements and cough in patients who seem particularly affected by incisional pain. The prophylactic use of humidified vapor, particularly when propylene glycol is used, has been effective in preventing the accumulation of tenacious tracheobronchial secretions. In patients whose cough is inadequate and ineffective, prophylactic endotracheal suction has been helpful. The patient must be routinely encouraged to turn, breathe deeply and cough, particularly during the first few postoperative hours and days. Early ambulation seems to have a beneficial effect in lowering the incidence of atelectasis. Once atelectasis has occurred, the above prophylactic measures must be continued when appropriate. Endotracheal aspiration should be frequent but not prolonged at anyone attempt. Occasionally bronchoscopy will be necessary to clear the air passage, especially if inspissated secretions or blood clots are the obstructing agents. The value of the bedside vaporizer with detergents and wetting agents cannot be overemphasized. Expectorants are also useful and, if bronchospasm is present, bronchodilating drugs should be employed. More recently we have used intermittent or continuous endotracheal instillation of saline, 2 ml. every two hours or 2 drops per minute, through a percutaneously placed small plastic catheter with great effectiveness. When secretions are particularly viscid, the similar administration of 1 or 2 ml. of a 2 per cent solution of acetyl-cysteine four times daily has been successful. 25 Hemorrhage

Intrapleural hemorrhage is a serious problem during the postoperative period. Not only may the blood volume be decreased but the accumulated blood causes pulmonary collapse and may form the nidus for an empyema. Bleeding from vascular adhesions to the parietal pleura can be very troublesome and the electrocoagulating current is extremely helpful in aiding hemostasis during operation. If the amount of blood draining into the trap bottle is significant or the early postoperative chest films show an accumulation of fluid, the patient must be watched carefully and every attempt should be made to remove the intrapleural blood by irrigating and adjusting the intercostal drainage tubes. If hemorrhage continues and no clotting defect is apparent, re-exploration should be undertaken and the bleeding vessels ligated. If a clotting defect is discovered, the administration of fresh whole blood or fibrinogen may prove of value.

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Massive hemorrhage during or following pulmonary resection is usually due to the slipping of a ligature from the major pulmonary vessel. The accident may result in a fatality and can be prevented by oversewing the ends of all large pulmonary vessels with a continuous 5-0 arterial silk suture or using a supplementary transfixion ligature. Once a clotted hemothorax has occurred, removal of the pleural collection may be difficult. In some hands the use of enzymes such as Varidase, which liquefy the clot and permit its withdrawal through drainage tubes or large-bore needles, has been successful. If the clot is of significant size, open operation with complete evacuation of the clot and pulmonary decortication to effect complete re-expansion of the compressed lung has been very successful in our experience. Empyema

Empyema following pneumonectomy is fortunately an unusual complication today. It results from contamination of too pleural space at the time of pulmonary resection or from the development of a leak in the bronchial stump. Once the diagnosis of postpneumonectomy empyema has been made, a large-bore intercostal tube should be promptly inserted either by trocar or limited rib resection to empty the pleural space. In favorable cases, the condition has been successfully treated by repeated instillations of the appropriate antibiotic drugs into the pleural cavity, with resulting sterilization of the infection. However, most patients are not so fortunate and prolonged drainage must be maintained until the mediastinum is fixed and the chest wall contracted. Thoracoplasty will then be required to obliterate the residual infected space. Empyema following lobectomy or limited pulmonary resection should also be treated promptly by tube decompression and water-seal drainage. It may be possible by long-term drainage, instillation of fibrinolytic agents and local and general administration of the proper antibiotic drugs to control the infection and re-expand the lung completely. However, following the institution of conservative drainage, many patients will require more radical procedures to obliterate the chronic empyema cavity. These involve either collapse of the chest wall or, preferably, open decortication with re-expansion of the lung and obliteration of the chronically infected space. Miscellaneous Problems

Pulmonary edema following pulmonary resection is a complication almost entirely confined to the older age group and to persons who are in generally poor physical condition. It is treated postoperatively by the usual measures of positive pressure oxygen, venesection, tourniquets, morphine, digitalis, diuretic drugs and other medical measures. A uricular fibrillation occurs following pulmonary surgery in from 10

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to 15 per cent of patients over the age of 50 years. Prompt digitalization will reduce the heart rate but one should be alert to the possibilities of mediastinal shift from accumulations of air or fluid or pulmonary collapse as being the initiating cause. The arrhythmia is usuaJly selflimited and reverts spontaneously with the passage of time unless organic heart disease exists. Subcutaneous emphysema occurs in almost every patient to some extent, as noted by crepitation in the area of the incision. If the emphysema is severe one should check the position and function of the waterseal drainage tubes and insert new ones if necessary to decompress the air leak. Tracheostomy and superior mediastinotomy may be required to prevent airway and great vein obstruction. If ventilatory inSUfficiency is anticipated, either from the preoperative evaluation of the patient or from the extent of the pulmonary reflection, particular attention must be paid to certain aspects of postoperative care. A clear tracheobronchial tree must be maintained at all times. Bronchospasm must be prevented by bronchodilators and corticosteroid drugs if necessary. Any degree of associated cardiac failure should be promptly treated by digitalization, fluid and salt restriction, diuretic drugs and other supportive medical means. Postoperative oxygen therapy, preferably delivered by nasal cannula, is a valuable adjunct.1 5 The residual lung must be fully expanded and the mediastinum maintained in the midline. If respiratory acidosis develops and cannot be reversed by the above measures, endotracheal intubation or tracheotomy must be performed and alveolar ventilation improved by means of a mechanical ventilator such as the Bird, Emerson, Engstrom or Bennett respirators. In such patients repeated evaluation of arterial blood pH, p02 and pC0 2 is helpful in determining the necessity and efficiency of such treatment. PROBLEMS FOLLOWING CARDIAC SURGERY

In addition to the complications which may occur following pulmonary surgery as already described, there are certain complications which are more specifically encountered following surgery of the great vessels or of the heart. Hemorrhage

Following the anastomosis or repair of the aorta or the closure of an opening in the wall of the atrium or ventricle, there can be chronic continued loss of blood from the suture lines if hemostasis is not secure at the time the operation is completed. Great care should be exercised in employing suture material of adequate strength and in placing sutures deeply enough to provide a secure closure. This is particularly true when sutures are placed in a badly di'3eased thoracic aorta or ventricular wall.

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In the case of aortic closure, either a vertical incision or end-to-end anastomosis may be closed adequately in most instances by applying a continuous horizontal mattress suture with the aorta collapsed and under minimal tension. The everted aortic edges should then be oversewn with a continuous suture. When the suture line has been completed, removal of the distal aortic clamp first permits retrograde blood flow under lower pressures to expel air from the vessel and indicates by leakage of blood any areas in the anastomosis which may require additional interrupted sutures. If the tissues are so diseased that sutures will not hold well, one should consider topical application of epoxy resin 7 or Eastman 910. *, I; Serious sudden postoperative hemorrhage can occur through a fracture of the aorta at the site of clamping. This may be evidenced by the sudden passage of blood from the chest tube and rapid development of shock in the patient. Successful resuscitation may be achieved, after very prompt removal of the patient to the operating room, by the intravenous administration of fluids under pressure. Intraaortic transfusion under pressure may be preferred on opening the chest, and cardiac massage should be instituted immediately if necessary. In patients undergoing open heart surgery, complete neutralization of the heparin routinely given during operation is important following completion of cardiopulmonary bypass. In patients with continued bleeding from the suture lines it is important to recheck the clotting time carefully since occasionally there can be a rebound of heparin activity after the patient was given what was considered an adequate dose of protamine sulfate or Polybrene. It also must be recognized that an excess of these agents also interferes with the clotting mechanism and overdosage can result in serious bleeding tendencies. In some patients an actual deficit may occur in one of the clotting factors following perfusion. Clauss and his associates 8 have developed a simple test to determine whether excessive fibrinolytic activity was the basic cause. In these patients prompt administration of fibrinogen in sufficient quantities has been very helpful. In refractory cases the addition of epsilon caprilic acid or Trasylol has had seeming benefits. In prolonged perfusion, platelet deficiencies are regularly observed and fresh blood or platelet preparations are used in our clinic if the perfusion is longer than one hour. When measured bleeding appears massive or when there is minimal loss of blood evident through chest tubes but the patient exhibits pallor, tachycardia and hypotension, serious consideration should be given to immediate re-exploration. Although in some cases no obvious single individual sources of bleeding will be observed, there will be patients with localized brisk blood loss from a suture line of the aorta or heart, or from an intercostal artery. The authors know of at least two children who died in the immediate postoperative period from bleeding coronary

* Distributed by Ethicon, Inc., Somerville, New Jersey.

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arterial branches in the edge of the ventriculotomy. Callaghan and his associates,6 in analyzing the causes of death in their open heart cases, observed late deaths from pericardial tamponade in two patients occurring four and ten days after operation. Should tamponade be suggested by a rising venous pressure, falling blood pressure and tachycardia together with a large cardiac shadow, pericardiocentesis is indicated, but if symptoms recur re-exploration is necessary. Difficulties with cannulation of the common femoral or external iliac artery are another source of hemorrhage in patients undergoing open heart surgery. Jones et al.,13 van der Woude 24 and others have described massive retroperitoneal hemorrhage, extensive aortic dissection and other sequelae from false passage or perforation of the artery by the cannula. These patients lose blood rapidly into the pump via the venous cannulae if the arterial inflow is not operating properly. In Callaghan's series there were four deaths from technical errors during open heart surgery; three were due to cannulae slipping from the left atrium or peripheral artery. Recovery from such an accident requires the immediate removal of the patient from the bypass, resumption of ventilation and rapid blood transfusion. If exsanguination has been massive, the blood volume can be quickly restored by attaching the arterial outflow line of the pump to one of the venous drainage catheters and rapidly transfusing the patient from the pump. Hypovolemia has been a cause of hypotension and inadequate heart action. With certain types of aortic surgery associated with major blood loss or with the shift in circulating blood volume associated with extracorporeal circulation, one should be certain that adequate blood volume has been restored. In addition to simple gravimetric and volumetric estimations, there has been developed a reliable rapid method utilizing isotopes and permitting accurate re-estimations at frequent intervals. 27 However, no method of measurement of blood volume will reflect the sequestered red cell mass and plasma volume which may be seen following cardiopulmonary bypass. l Cardiac Problems

One of the most dramatic and urgent problems is the spontaneous development of cardiac arrest or ventricular fibrillation during the conduct of cardiac or vascular surgery without cardiopulmonary bypass. Cardiac massage should be performed promptly and efficiently. During brief interruptions in massage the pericardium may be opened to provide more effective manipulation. With a damaged myocardium, one should avoid being too forceful in the compression for fear of perforating the heart. Complete emptying of the ventricles at a near-normal rate is preferable. When ventricular fibrillation is present, massage ~hould be carried out to insure good oxygenation of the myocardium, after which electrodes should be placed at the apex and base of the heart and

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repeated brief shocks applied until a beat is restored. Massage is maintained except during the actual period of shock. A flabby heart can be aided by intracardiac injection of calcium chloride, which seems preferable initially to epinephrine. Should cardiac arrest occur in the recovery room with adequate staff and adjacent operating rooms, one may reopen the chest for direct massage. In other hospital areas, however, it may be more appropriate to utilize closed cardiac resuscitation. 6 By either method, a prompt and adequate effort is mandatory. Less critical but of importance after mitral valve surgery is the frequent development of auricular fibrillation. This may occur on the operating table or several days following operation and a question may arise as to when conversion to sinus rhythm should be undertaken. In these patients it is resonable to attempt conversion just before discharge from the hospital. Digitalization alone is seldom effective in restoring normal rhythm and a course of quinidine sulfate is often necessary.4 Attempts at late conversion, three to four months after surgery when atrial size has diminished and pericardial inflammation has subsided, have also been successful in our hands. The recent introduction of the direct current defibrillator appears to have favorably affected the success rate of conversion to sinus rhythm in these patientsJ8 One of the most disappointing and frustrating problems following repair of cardiac defects, particularly that for acquired valvular disease, is inadequate cardiac action. In such cases there is a marked hypotension from an ineffective heart beat, even though the rhythm may be regular. Adequate oxygenation and ventilation together with the use of pressor drugs are indicated. One of the more effective of the new pressor agents is Angiotensin, which permits adequate renal artery flow despite peripheral vasoconstriction. l l Broader use of this drug may prevent the oliguria or renal shutdown occasionally seen as a further complication of inadequate circulation or perfusion. One further measure which may be taken to avoid renal complications is the administration of mannitol during aortic surgery. Perhaps the most distressing complication associated with repair of intracardiac defects is total heart block. The block is usually the result of damage to the conduction bundle during the suture closure of an interventricular septal or ostium primum defect. The location of the conduction system has been well shown by the studies of Truex23 and Reemtsma. 20 Whenever possible these defects should be repaired without induced cardioplegia so that interference with the conduction system can be immediately diagnosed by continuous electrographic monitoring and the offending suture removed. Thung et aJ.22 have recently demonstrated that hypoxia can cause hemorrhage into the conduction system sufficient to produce arrhythmia and sudden death. Obviously this source of difficulty can be eliminated by maintenance of adequate

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oxygenation. If heart block persists, a special conductive wire should be inserted into the muscle of the ventricle and a second implanted in the axillary subcutaneous tissue for attachment to an external pacemaker.26 When traumatic heart block occurs in patients after repair of interventricular septal defects, the pacemaker may be required for a few days to three weeks. Medical management of block may be attempted by the use of ephedrine, Isuprel or corticosteroid drugs. In the uncommon case with irreversible block, a small transistorized pacemaker may be implanted in the lateral chest wall as described by Zoll et al,28 and others. Failure of the heart to recover normal function following elective cardiac arrest has occasionally been a cause of death. The toxic properties of the cardioplegic drugs and the destructive influence of anoxia as means of cardioplegia have been demonstrated. When arrest is indicated, the best method appears to be hypothermic cardioplegia as . evidenced by experimental studies in our laboratory.3 This can be achieved with topical Ringer's slush, but when prolonged arrest (i.e., over 30 minutes) is required, intermittent or continuous perfusion of the coronary arteries with cold blood should be provided as well. Metabolic Acidosis

In addition to the renal insufficiency which may be associated with inadequate cardiac action or insufficient perfusion, metabolic acidosis has in the past been a serious postoperative complication following openheart surgery. The accumulation of acid metabolites causes a decreased hydrogen ion concentration and buffer base. Clowes 9 and others have demonstrated the importance of having an adequate flow rate, and one should realize that the length of perfusion also influences the degree of acidosis. Mild generalized hypothermia has been used to reduce the metabolic requirements of the tissues of the body during low-flow cardiopulmonary bypass. However, even under optimal conditions of bypass, metabolic acidosis with increased lactate and pyruvate levels has been shown to occur. These fixed acids are buffered by bicarbonate, phosphate and hemoglobin systems as well as by sodium and potassium shifts. During actual bypass the pH may be maintained in a reasonably normal range by elimination of carbon dioxide by the oxygenator. A significantly reduced base bicarbonate may have occurred by three to five hours post perfusion with lesser and later reductions in pH. Some sudden deaths in the postperfusion period may have actually been the result of an elevated potassium, according to Krasna et al. 17 Bernhard et aP have studied metabolic alterations associated with profound hypothermia and extracorporeal circulation. The decreased hepatocellular activity occurring at temperatures below 30° C. leads to inhibition of lactate metabolism with resultant lacticacidosis. Less

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acidosis is observed with higher temperatures and higher flows. In their clinical experiences, 75 per cent of patients were able to achieve spontaneous correction of the metabolic acidosis. The remainder required additional help, such as the intravenous administration of bicarbonate or Tham. Embolism The development of peripheral arterial embolization during and following mitral valve surgery may demand immediate surgical intervention, provided the embolus is in an accessible artery. In such instances direct embolectomy is the procedure of choice, provided the patient can tolerate such a procedure. Emboli have been successfully removed from the aortic bifurcation, the carotid, femoral and popliteal arteries, and the less common mesenteric arterial embolus may also be directly accessible. Cerebral embolization is not often helped by surgical exploration and in some series 50 per cent of these patients succumb. Management has generally been supportive, although intra-arterial infusion of thrombolytic agents may prove to helpful in the future. Calcific embolization associated with aortic valve surgery has been reported by Glotzer et aU2 and others, and has been the major cause of death in our experience with surgery of the aortic valve. In Callahan's series, calcific cerebral embolus proved fatal in two patients undergoing open-heart surgery. With the use of bubble oxygenators, there has been attributed a danger of cerebral embolization by microbubbles and by antifoam compounds. Concern for this has led to the increasing use of the disc oxygenator in the United States. Technical errors unrelated to the type of pump oxygenator apparatus may lead to cerebral air embolization from trapped gas in the left atrium or ventricle or ascending aorta. Postcardiotomy needle aspiration of the left ventricle through the elevated apex, or from the aorta just proximal to the occluding clamp following ascending aortotomy can prevent such an accident. The authors have seen at least two patients with this complication who recovered completely despite the flat electroencephalographic pattern and immediate postoperative evidence of severe cerebral depression. Postoperative management includes hypothermia, high oxygen concentrations and intermittent CO 2 administration. As a result of a technical error, air can be introduced into the heart from the pump oxygenator, although gravity drainage of the cavae obviates this complication. With an interatrial septal defect present the air can pass to the left side of the heart and to the brain as well as coronary arteries. When significant air embolization has occurred into coronary arteries, the heart will generally fibrillate. The air may be removed either by massage or by transsecting the vessel in its distal portion. Once the air is expelled, normal rhythm is usually easily restored by electric shock.

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Paraplegia

The prolonged occlusion of the thoracic aorta occasionally required for repair of a coarctation with minimal collateral arteries or thoracic aneurysms may so reduce arterial blood flow in the anterior spinal artery that weakness or actual paraplegia results. Perhaps the most simple and effective means of preventing this serious complication is the use of the left atrial to femoral artery bypass as described by Cooley et al.1° This method also reduces the hypertension in the upper extremities and head. However, despite adequate bypass, the blood flow to the anterior spinal area may be curtailed through the division of the lower thoracic intercostal arteries which not infrequently provide the major supply of blood to the anterior spinal artery. For this reason it is desirable to avoid dividing intercostal arteries of TlO, 11 and 12 and even the lumbar arteries at Ll. In case of such complication, a trial of general mild hypothermia may be worthwhile. Respiratory Insufficiency

Pulmonary complications may follow surgery of the great vessels or heart. Although cyanosis may be evidence of an inadequate peripheral circulation following open heart surgery, it may also reflect diffuse atelectasis, as indicated by a large alveolar arterial pC0 2 gradient as reported by Osborn et al. 19 The correction of atelectasis and the use of positive pressure ventilation in instances of inadequate spontaneous ventilation have proved effective in managing this complication. In the earlier days of open-heart surgery, a dreaded postoperative complication was congestive atelectasis. This developed from several hours to a few days post perfusion and was evidenced by increasing dyspnea and respiratory insufficiency. The condition was usually refractory to treatment and at autopsy the lungs were intensely congested and grossly resembled liver. The development of pulmonary capillary damage was emphasized by Kolff and Effier,14 who among others developed the use of the left atrial vent in patients with large pulmonary collateral circulation or hypertension and in patients requiring elective cardiac arrest for correction of aortic or mitral valvular defects. The vent prevented sudden overloading of the pulmonary vascular bed leading to acute pulmonary capillary damage. COMMENT

It would be presumptuous to attempt to describe in any detail the entire range of complications that one may encounter following pulmonary or cardiovascular surgery. In these fields, more than any other, the value of team care of the patient by properly trained and alert nurses and physicians is evident. The hospital should have adequate equipment

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and facilities for the proper preoperative evaluation and postoperative care of such patients. Also, and more so than in almost any other field, the old adage "An ounce of prevention is worth a pound of cure" is true. The best single bit of advice to the young thoracic surgeon is to be ever vigilant and, once a complication is recognized, to be prompt and aggressive in its management. Those complications which significantly affect respiration and circulation may produce such rapid deleterious effects that hesitation or unreasonable temporizing may well cost the patient his life. REFERENCES 1. Ankeney, J. L. and Murthy, M. B.: A study of the peripheral (IVC and SVC) and central (splanchnic) venous flow rates during extracorporeal bypass. J. Thor. & C.V. Surg. 44: 589, 1962. 2. Bernhard, W. F., Carroll, S. E., Schwarz, H. F. and Gross, R. E.: Metabolic alterations associated with profound hypothermia and extracorporeal circulation in the dog and man. J. Thor. & C.V. Surg. 42: 793, 1961. 3. Bhonslay, S. B., Deterling, R. A., Jr., Wallace, H. W. and Rheinlander, H. F.: Elective cardiac arrest. J. Cardiovasc. Surg. 2: 168, 1961. 4. Black, H., Lown, B. and Bartholomay, A. F.: Value of quinidine in the prevention of arterial fibrillation after mitral valvuloplasty. Circulation 23: 519, 1961. 5. Braunwald, N. S. and Awe, W. C.: Control of hemorrhage from the heart and aorta utilizing a plastic adhesive. Surgery 51: 786, 1962. 6. Callaghan, J. C., Despres, J. P. and Benvenuto, R.: A study of the causes of 60 deaths following total cardiopulmonary bypaEs. J. Thor. & C.V. Surg. 42: 489, 1961. 7. Callow, A. D., Deterling, R. A., Jr., Selverstone, B. and Dehghan, R.: Reinforcement of arterial anastomoses and aneurysms with adherent synthetic resins. Bull. Soc. intern. de chir. 21: 104, 1962. 8. Clauss, R.: Personal communication. 9. Clowes, G. H. A., Jr., Neville, W. E., Hopkins, A., Anjola, J. and Simeone, F. A.: Factors contributing to success or failure in thp. use of a pump oxygenator for complete bypass of the heart and lung. Surgery 36: 557, 1954. 10. Cooley, D. A., DeBakey, M. E. and Morris, G. C., Jr.: Controlled extracorporeal circulation in surgical treatment of aortic aneurysm. Ann. Surg. 146: 473 1957. 11. del Greco, F. and Johnson, D. C.: Clinical experience with Angiotensin II in the treatment of shock. J.A.M.A. 178: 994, 1961. 12. Glotzer, D. J., Shaw, R. S. and Scannell, J. G.: Calcific coronary emboli following open valvuloplasty for aortic stenosis. J. Thor. & C.V. Surg. 43: 434, 1962. 13. Jones, T. W., Vetto, R. R., Winterscheid, L. C., Dollard, D. H. and Merendino, D. A.: Arterial complications incident to cannulation in "open heart surgery." Ann. Surg. 152: 969, 1960. 14. Kolff, W. J. and Effler, D. B.: Causes of failure in open-heart operations. Tr. Am. Soc. Artif. Int. Organs 4: 111, 1958. 15. Kory, R. C., Bergmann, J. C., Sweet, R. D. and Smith, J. R.: Comparative evaluation of oxygen therapy techniques. J.A.M.A. 179: 767, 1962. 16. Kouwenhoven, W. B., Jude, J. R. and Knickerbocker, G. G.: Closed-chest cardiac massage. J.A.M.A. 173: 1064, 1960. 17. Krasna, 1. H, Shuster, M., Baens, H., Kreel, 1. and Baronofsky, 1. D.: A study of acid-base and electrolyte derangements after prolonged cardiopulmonary bypass. J. Thor. & C.V. Surg. 42: 244, 1961. 18. Lown, B., Amarasingham, R. and Newman, J.: A new method for terminating cardiac arrhythmias. J.A.M.A. 182: 548, 1962.

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