The History of Surgical Procedures for Emphysema
1997; Elsevier BV; Volume: 63; Issue: 2 Linguagem: Inglês
10.1016/s0003-4975(96)01227-1
ISSN1552-6259
Autores Tópico(s)Chronic Obstructive Pulmonary Disease (COPD) Research
ResumoI was sent a humorous greeting card by one of our lung transplant recipients some time ago. On the cover it shows one of life's couch potatoes complaining about her lot in life, with the text, "Life is so hard." On the inside the text reads "It's breathe, breathe, breathe all the time." Well, considering who is on the cover of the card, it is rather humorous. However, there are many for whom its not funny. I am referring to patients suffering from end-stage lung disease, tethered to an oxygen tank, whose life is centered around a wheelchair, for whom each breath is a struggle. It has been exciting that in the last 10 to 12 years there are some new surgical procedures that have brought hope and relief to this group of patients. Today I would like to review with you the evolution of surgical procedures for chronic obstructive pulmonary disease. The anatomic changes associated with emphysema were described two centuries ago. Even earlier, veterinary descriptions of the lungs, in what was termed "broken winded" horses, depicted the changes of emphysema. In a text by Baillie in 1793, there is included a description of emphysematous lungs at autopsy. He noted that "in opening into the chest it is not unusual to find that the lungs do not collapse but that they fill up the cavity completely on each side of the heart. When examined their cells appear full of air so that there is seen upon the surface a prodigious number of small white vesicles" [[1Baillie M. The morbid anatomy of some of the most important parts of the human body. London: Printed for J. Johns and G. Nicol, 1793:314.Google Scholar]]. In his accompanying atlas, Baillie illustrated his autopsy findings. This particular drawing (Fig. 1) is of the lungs of Dr Samuel Johnson, whose autopsy was performed by Dr Baillie. However, it was the famous French physician and anatomist Rene Laennec who systematically described both the clinical and pathologic features of emphysema. In his famous treatise on diseases of the chest first published in the French literature in 1817 [[2Laennec RTH A treatise on the diseases of the chest and of mediate auscultation. Translated by John Forced, MD, FRS. 4th ed. Whittaker & Co, London1834Google Scholar]], Laennec noted that "in pulmonary emphysema the size of the vesicles"—by that he meant the air spaces—"is much increased and less uniform. The greater number equal or exceed the size of a millet seed while some attain the magnitude of a hemp seed, cherry stone, or even fresh beans." He noted that at autopsy "the lungs seem as if confined in their cavity, and when exposed instead of collapsing as usual, they rise in some degree and project beyond the borders of the thorax." He noted that on percussion, "the whole chest yields a very distinct sound, and instead of its natural compressed shape it exhibits an almost round or globular outline, swelling out both before and behind. This conformation of the chest is sufficiently remarkable to have enabled me sometimes to announce the existence of emphysema from simple inspection." Although the pathologic changes associated with emphysema were described 200 years ago, the pathophysiology of chronic obstructive pulmonary disease was poorly understood until the latter half of this century. This lack of understanding, however, did not prevent the trial of numerous operations directed at the consequences of emphysema. Thus Freund, in 1906, observing the fixed state of the thorax, which was capable of very little respiratory movement, proposed costochondrectomy. To improve movement of the chest wall, Freund did a costochondrectomy of the upper ribs on one side, and sometimes on both sides. Others, focusing on the distention of the chest, proposed thoracoplasty to reduce the size of the chest. Noting the depressed, flattened configuration of the diaphragm, physicians made attempts to restore it to a more normal position. These attempts included the use of abdominal belts, as proposed by Gordon in 1934 [[3Gordon B The mechanism and use of abdominal supports and the treatment of pulmonary diseases.Am J Med Sci. 1934; 187: 692-700Crossref Google Scholar]], phrenic crush as proposed by Allison in 1947 [[4Allison PR Giant bullous cysts of the lung.Thorax. 1947; 2: 169Crossref PubMed Scopus (16) Google Scholar]], and the use of pneumoperitoneum as proposed by Gaensler in 1950 [[5Carter MG Gaensler EA Kyllonen A Pneumoperitoneum in the treatment of pulmonary emphysema.N Engl J Med. 1950; 243: 549-558Crossref PubMed Scopus (23) Google Scholar]]. Actually the abdominal belts and the pneumoperitoneum did improve pulmonary function, but both proved to be rather cumbersome and impractical means of achieving a rather modest improvement. From autopsy findings showing diminished vascularity in emphysematous lungs, Crenshaw and Rowles [[6Crenshaw GL Rowles DF Surgical management of pulmonary emphysema.J Thorax Surg. 1952; 24: 398-410PubMed Google Scholar]], in 1952, proposed pleural abrasion to create systemic-to-pulmonary collateral blood flow in the hopes of improving lung function. Osler Abbott, made famous by the Abbott Award of this Society, in fact proposed denervation of the lung. There were a whole series of denervation experiments and clinical applications. In an article he published in 1953 [[7Abbott OA Hopkins WA Van Fleit W Robinson JS A new approach to pulmonary emphysema.Thorax. 1953; 8: 116-132Crossref PubMed Scopus (18) Google Scholar]], he described pulmonary plexectomy, pulmonary artery, periarterial sympathectomy, upper dorsal sympathectomy, and a partial resection of lung. This was followed by one of the most unphysiologic, controversial, and infamous operations in all of surgical history: glomectomy, the excision of the carotid body for both asthma and emphysema. The initial report by Nakayama [[8Nakayma K Surgical removal of the carotid body for bronchial asthma.Dis Chest. 1961; 40: 595-604Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar]] in 1961 contained almost 4,000 cases done in Japan. A subsequent publication by Dr Richard Overholt [[9Overholt RH Glomectomy for asthma.Dis Chest. 1961; 40: 605-610Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar]] included more than 800 cases. It should be noted that subjectively more than 80% of the patients felt they had benefited from this procedure, which we now know has no physiologic basis. It took several randomized, double-blinded studies in which half of the patients underwent a sham operation and half the glomectomy before the procedure was finally proved worthless. In a 1972 review article in The New England Journal of Medicine [[10Laforet EG Surgical management of chronic obstructive lung disease.N Engl J Med. 1972; 287: 175-177Crossref PubMed Scopus (17) Google Scholar]], Dr Eugene Laforet humorously summarized his perception of the various surgical procedures that had been proposed over the years for treating emphysema. "Thus," he noted, "resection of costal cartilages was proposed in an era when chronic obstructive lung disease was thought to be secondary to a skeletal deformity, and when incidentally chest-wall surgery was in its flower. The results were grim. "Undaunted and starting with a new set of premises surgeons were soon advocating such procedures as thoracoplasty and phrenic nerve interruption, each calculated to reduce the volume of the over-distended lung. The alleged benefits of these maneuvers were frequently lost on patients whose worsened dyspnea left them little energy to debate with their surgeon." Regarding excision of the carotid body, Laforet observed that "unfortunately, for its integrity, it is readily accessible to the scalpel and may even be attacked under local anesthesia. The benefits of its unilateral surgical removal (glomectomy) in [chronic obstructive lung disease] have been extolled with much vigor but little objectivity, although a tortured physiology is often invoked for support." Laforet concluded his article with the observation that "probably the best surgical solution for the patient with crippling and potentially lethal chronic obstructive lung disease would be to start from scratch with a new set of lungs." Indeed, the eminent pulmonary physiologist David Bates in a previous editorial [[11Bates D The other lung [Editorial].N Engl J Med. 1970; 282: 277-279Crossref PubMed Scopus (20) Google Scholar]] had reflected that "any physician who has had the sad task of caring for a patient suffering from advanced pulmonary emphysema must on occasion have wished that human lung transplantation could offer some hope to these unfortunate patients." But it was not for lack of interest, or hard work, that efforts to develop successful lung transplantation had not yet borne fruit. The famous Russian physiologist Demicoff began experimenting in the 1940s with lobar transplantation in dogs. You will remember that he is the person who did heart-lung transplantations without cardiopulmonary bypass 10 years before Gibbons' first successful use of the heart-lung bypass machine in 1953. He did a series of substituting anastomoses and inserted a new heart and set of lungs in a dog and removed the old ones without using bypass. He is best known, of course, for sewing a second head on a dog and having them both barking and eating for several days until the dog died. Henri Metras [[12Metras H Note preliminaire sur la greffe totale du poumon chez le chien.C R Acad Sci (Paris). 1950; 231: 1176-1178Google Scholar]], in 1950, reported to the French Academy his pioneering experiments with lung transplantation in dogs, including use of an atrial cuff for the venous anastomosis and direct revascularization of the bronchial artery. But it was Drs James Hardy and Watts Webb who, after many years of laboratory investigation, performed the world's first human lung transplantation at the University of Mississippi in 1963. Although their patient died after 18 days, this event stimulated interest in lung transplantation throughout the world. Unfortunately, the time was not right, and although a number of attempts at human lung transplantation were made throughout the 1960s and early 1970s, interest waned considerably because of universal failure. In 1978, one of those unsuccessful transplantations was performed by my colleagues and myself at the University of Toronto under the direction of my partner, Dr Bill Nelems. My role was primarily to supervise the use of the extracorporeal membrane oxygenator support system, which had been developed for use in patients with severe respiratory failure. Although the transplant procedure was successful, and the patient was subsequently weaned from both the membrane oxygenator and the respirator, he died 3 weeks later of bronchial disruption. His death prompted a review of the world experience, which indicated that virtually all patients surviving 2 weeks or more after lung transplantation had died because of, or in association with, complications of the bronchial anastomosis. We decided not to embark on any more lung transplantations, and it was not until a couple of years later that I became interested in investigating the causes and potential solutions for the airway complications occurring after lung transplantation. With the help of a number of colleagues and research fellows from around the world, we did a series of animal experiments looking at factors affecting bronchial healing. We concluded that the bronchial disruption was not primarily an immunologic event, as had been thought, because it occurred when you reimplanted a lung just as much as when you transplanted a lung. We found that the high doses of prednisone then being used for immunosuppression were clearly prejudicial to the anastomotic healing and that cyclosporine, which was just then becoming available, could be substituted without adverse effect on wound healing. We also found that an omental wrap around the bronchial anastomosis restored blood supply to the severed bronchial circulation within 2 to 3 days and protected the anastomosis from disruption or from bronchovascular fistula if it failed to heal properly. We then began a cautious clinical approach to lung transplantation again in 1983. One major remaining issue was in whom do you perform transplantation? By that time the score was 0 successes for 44 attempts. A deathbed rescue attempt in a patient on a ventilator with multisystem failure is clearly not the environment that is likely to produce success. We decided to choose pulmonary fibrosis, a condition that can be indolent, but once the patients go on oxygen and show arterial desaturation with mild exercise, I can assure you they do not have a year to live. By selecting such a patient, we could try transplantation in a patient who was not yet hospital bound or ventilator dependent yet whose life expectancy was severely limited, justifying the enormous risks involved. Our first attempt was in a 58-year-old man with severe pulmonary fibrosis and a rapidly deteriorating clinical course. The procedure was successful, and for the next 6 years he continued to work regularly. Sadly, he died 61/2 years afterward of renal failure. But thereafter, no one ever had to go through a lung transplantation again without seeing, or at least knowing of, someone who had success. Our first patient was a wonderfully brave pioneer. We thought that pulmonary fibrosis was ideal for single-lung transplantation, because the extensive scarring and loss of compliance in the native lung would help ensure that both blood flow and ventilation were preferentially directed to the transplanted lung. It had been observed, in several unsuccessful single-lung transplantations for emphysema, that the native, overly compliant emphysematous lung received much of the ventilation and then became further distended while the transplanted lung received most of the blood flow, thus creating a ventilation-perfusion mismatch. In the hopes of applying lung transplantation to patients with severe emphysema, and also to septic lung conditions such as cystic fibrosis, we sought ways of replacing both lungs. Initially we employed the combined heart-lung transplantation developed at Stanford but quickly realized that it should not be necessary to replace a patient's heart to transplant two lungs. It did not make sense to replace a heart in someone who did not need a new heart. On the basis of further laboratory and autopsy studies, under the direction of my colleague, Dr Alec Patterson, the first version of a double-lung transplantation was developed and successfully applied. It included the use of a tracheal anastomosis, an atrial anastomosis, and anastomosis of the main pulmonary artery—sort of a heart-lung hold the heart. In fact, 9 years ago this month a woman with severe emphysema underwent the first successful application of this procedure. In 2 weeks she will be enjoying her ninth anniversary and continues to do quite nicely. In fact, the first 3 patients who underwent this operation will all be celebrating their ninth anniversaries in the next few months. In spite of concerns that single-lung transplantation for emphysema was thought to be physiologically unsound, a group under the direction of Dr Andreasen in Paris performed a couple of successful single lung transplantations for emphysema. They were kind enough to send us the information and the postoperative roentgenograms, and their report was encouraging. In retrospect it seems probable that the reason patients were getting into trouble after a single-lung transplantation for emphysema was related to injury to the transplanted lung, such as reperfusion injury or poor donor selection or early rejection, so that the lung became less compliant, which would foster overexpansion of the native lung. But the group in Paris demonstrated you could get away with it. And so we began a series of single-lung transplantations in older patients with emphysema who at the time we did not consider candidates for the bilateral procedure. Fig. 2 is the roentgenogram of the first patient with emphysema to undergo a single-lung transplantation in our program. Fig. 2 is the preoperative film before left lung transplantation, which was done in 1989, and Fig. 2 shows the postoperative result. There is some shift of the mediastinum, but the functional result was excellent. We achieved good success with single-lung transplantations for emphysema—in fact, I believe we had a 90% hospital success rate in the first 50 that were done—so the main stimulus to develop an improved bilateral procedure was the cystic fibrosis population in need of a transplant. The original operation, the en-bloc double-lung transplantation, was technically very difficult. It required prolonged cardiopulmonary bypass; the tracheal anastomosis, notwithstanding an omental wrap, was still the source of major complication in 30% of the patients; and the operation was complex and technically demanding. One of my colleagues, Dr Michael Pasque, observing the routine success we were able to achieve with single-lung transplantations, proposed that we should just do separate single-lung transplantations, one on either side, rather than the complicated en-bloc double procedures. And so we went back to the laboratory and back to the autopsy room and developed what we called the bilateral sequential lung transplantation, restoring the use of an old, historical incision used in the early days of open heart surgery, the bilateral transverse thoracosternotomy. This approach gives superb exposure of both pleural spaces and the mediastinum as well. This incision is far better tolerated than we thought it would be. The first patient to undergo the procedure was a patient with emphysema due to α1-antitrypsin deficiency. You just take out one lung and replace it while the other lung carries the patient. Then you go to the other side of the table and replace the second lung. This has now become the standard method of replacing both lungs for cystic fibrosis patients, for about half the emphysema transplantations and for a number of other conditions. Fig. 3 is a brief summary of the first 259 single and bilateral sequential transplantations that were done since 1988 in St. Louis. There is a 94.5% hospital survival rate. The first 3 years of the survival curve are what I call the ecstasy part of the agony and the ecstasy curve. The agony comes later when chronic rejection sets in, the major limiting step to all organ transplants. Thus, we have a 75% three-year survival but only a 53% five-year survival, very similar to what is achieved with other major organ transplants. If you look at just those patients who had emphysema, the survival is about 5% better all along, with a survival rate of about 80% at 3 years. When I earlier catalogued some of the procedures done in the earlier part of the century for emphysema, I omitted the one procedure that was in fact of proven benefit over the years, namely, the excision of giant emphysematous bullae in the presence of normal underlying compressed lung. In 1989, Connolly and Wilson [[13Connolly JE Wilson A The current status of surgery for bullous emphysema.J Thorac Cardiovasc Surg. 1989; 97: 351-361Abstract Full Text PDF PubMed Google Scholar]] wrote a review article and summarized their experience with 19 patients collected over 33 years. These are not common patients. They emphasized what all of us believed to be true, namely, that such resection should only be done in patients with "incapacitating dyspnea and unequivocal compression of relatively normal underlying lung tissue." They pointed out that in the great majority of emphysema patients there is diffuse involvement of the lungs and surgery has little to offer. In fact, that was the generally accepted viewpoint. The rationale was to get rid of the space-occupying bullae when there was clear-cut evidence of compression of relatively normal underlying lung, so that "normal" lung could reexpand and resume functioning. There was one person, however, who had a somewhat different approach. That person was Otto Brantigan, Professor of Surgery and Surgical Anatomy at the University of Maryland, who wrote an article in 1959 with his colleagues titled, "A Surgical Approach to Pulmonary Emphysema" [[14Brantigan OC Mueller E Kress MB A surgical approach to pulmonary emphysema.Am Rev Respir Dis. 1959; 80: 194-202PubMed Google Scholar]]. He noted, as had others, that the thorax in the emphysematous patient is more or less fixed in a state of full inspiration and the hemidiaphragms are lowered or depressed. He proposed that by resection of functionally useless areas of the emphysematous lung could be reduced in volume, improving respiratory mechanics and the outward pull on the lung, which he thought would help keep the small airways open. He emphasized that it is an operation directed at restoration of a physiologic principle. It is not concerned with the removal of pathologic tissue, because all of the lung is affected to one degree or another by the emphysematous process, and if you remove all of the pathology you will not have anything left. Brantigan used several techniques to reef up, or excise, the most abnormal portions of the lung. He thought that ideally both lungs should be operated on at the same time but because of the risks proposed staged bilateral procedures 3 months apart. Brantigan combined the operation with radical hilar stripping, which was then in vogue. He observed that his patients felt and functioned better after the operation and in a subsequent publication indicated that the benefit in many patients lasted 5 years or more. Because there was an operative mortality of 16%, and no attempt was made to objectively document the benefit, Brantigan's procedure did not gain acceptance and came in for much criticism. Gaensler and associates [[15Gaensler EA Cugell DW Knudson RJ FitzGerald MX Surgical management of emphysema.Clin Chest Med. 1983; 4: 443-463PubMed Google Scholar]] noted that "although the idea of restoring lung tension and a more negative intrathoracic pressure is attractive, it is difficult to believe that a disease characterized by extensive loss of lung parenchyma can be effectively treated by further resection of lung." In fact, it is a rather odd notion to take people who cannot breathe to the operating room to remove more of their lung. Well, I was not aware of Otto Brantigan's work until about 8 years ago when someone brought it to my attention, and I confess, it sounded a little odd to me as well. However, observations made in the course of our lung transplant program for emphysema give some credence to Brantigan's hypothesis. Fig. 4 is a chest roentgenogram of a woman with severe emphysema who subsequently underwent bilateral lung transplantation. Note the marked distention of the chest with bulging of the lower rib cage—the so-called thoracic waist—the depression and flattening of the hemidiaphragms, and the upward slope of the posterior ribs with broad posterior interspaces. It looks as if someone took a tire pump and inflated this woman's chest. In the early days of lung transplantation we wondered what type of donor lungs might be found for such a recipient. We were concerned that a normal lung would rattle around in the large chest, predisposing to air leaks, effusions, and empyema. We thought we might need to use the largest male donor for the smallest female recipient. It turns out that our concerns were groundless. Fig. 5 shows this same woman several hours later after undergoing sequential bilateral lung transplantation. Note the more normal position of the hemidiaphragms and the reduced distention of the chest. This repeated observation that the chronically distended emphysematous chest could promptly resume a more normal configuration once the distending lungs were removed gave some credence to Brantigan's observations, namely, that downsizing the lung might improve respiratory mechanics. This same phenomenon was also seen after unilateral transplantation for emphysema. We noted that similar changes after single-lung transplantation for emphysema allowed the mediastinum to shift toward the transplant side, decompressing the opposite chest. This in turn improved the position of the diaphragm and chest wall on the side of the remaining, native lung. I believe that is one of the reasons these patients have done so well.Fig. 5The same patient as Fig. 4, several hours after sequential bilateral transplantation. Note marked improvement in diaphragmatic and chest wall position.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Another observation from the transplant program was that during single-lung transplantation for emphysema, the patient was always well-maintained on the contralateral diseased emphysematous lung and never required institution of cardiopulmonary bypass for reasons of gas exchange. Thus, regardless of how bad the emphysematous destruction, once the thorax was decompressed by deflating one lung, and adequate ventilation to the opposite lung was supplied, albeit by mechanical means, gas exchange was always quite satisfactory. This too seemed to confirm the notion that improved ventilation of an emphysematous lung could lead to improved gas exchange. And so these observations prompted us to look at volume reduction surgery. Candidates for the procedure are patients who are severely dyspneic, who have a distended thorax, and who have what I call "target" areas, namely, some regions with severe destruction where the lung is functionless but is taking up a lot of space. By removing those portions you can improve the function of the rest of the lung by two mechanisms: (1) improved chest wall and diaphragmatic position, which improves mechanics, and (2) redistribution of ventilation, which improves gas exchange. The type of situation most favorable for this procedure is the so-called centriacinar or centrilobular emphysema, where the upper lobe and the superior segment of the lower lobe are most involved, while the middle lobe, lingular, and basal segments are less involved. This pattern of disease is often the case, however, and we are highly selective. We take only 20% of the patients referred. We have chosen to do a bilateral procedure using the median sternotomy approach to achieve the maximum benefit with the least morbidity and greatest operative flexibility. With this approach there is no trauma to any of the chest wall muscles or intercostal nerves, and excellent access to both pleural spaces is provided throughout the procedure. Approximately 30% of the total lung volume is removed on either side, concentrating mainly on the upper lobes except in patients with the α1-antitrypsin deficiency form of emphysema, whose disease is centered in the lower lobes. Persistent air leaks have always been a major problem after excision of emphysematous lung tissue, and this procedure was no exception. We recognized that the air leaks were not coming through the staple lines, but from the puncture of the lung by the most proximal row of staples, which tend to tear through as the lung is reinflated. We found that by applying strips of bovine pericardium to the stapler before its application, so as to buttress the staple lines, we could virtually eliminate this source of air leaks. Ventilation to one lung is suspended and over several minutes the persistent blood flow causes absorption atelectasis in the better parts of the lung, which have preserved blood supply. The most destroyed parts of the lung have little if any blood supply and remain markedly distended. Half or more of the upper lobe is excised, using a continuous buttressed staple line (Fig. 6). The initial line of excision begins on the medial aspect of the right upper lobe near the horizontal fissure. This is followed by successive applications of the stapler producing an inverted U-shaped line of excision, which is carried toward the apex and down the posterolateral aspect of the right upper lobe. Half or more of the bulk of the right upper lobe is removed, but because the remaining lung is folded in by the staple line, the right upper lobe is reduced in volume by about two-thirds. In some cases, when the upper lobe is totally destroyed and the fissures are complete, a lobectomy rather than wedge excision may be performed. This has been done in approximately 10% of the cases. At the end of the excision, inflation of the lung under water usually reveals no air leak whatsoever. The same procedure is then repeated on the opposite side. We often release the parietal pleura from the apex of the chest to produce a so-called pleural tent. Thus, the visceral and parietal pleura can still be in contact with each other to reduce the chances of space problem or a prolonged air leak. The space above the tent fills up with fluid, which is gradually reabsorbed over a few months. The type of patient undergoing this operation is depicted in this summary of our first 100 patients (Table 1). All patients must enroll in a 6- to 8-week supervised pulmonary exercise rehabilitation program before operation to improve stamina and reduce as much as possible the operative risk. The preoperative data I will show during this presentation refer to the data obtained after completion of the rehabilitation program and optimization of medical management. The average preoperative forced expiratory volume in 1 second was somewhat less than 700 mL, or 24% of predicted, with more than 40% of patients having a first-second vital capacity of less than 500 mL. Ninety percent of patients require supplemental oxygen at some time during their daily routine, with more than half of the patients requiring contin
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