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Chylothorax: An assessment of current surgical management
J
THoRAc CARDIOVASC SURG
89:221-227, 1985
Chylothorax: An assessment of current surgical management The development of chylothorax is a serious and often life-threatening clinical entity. Optimal management of this problem has not been wen defmed to date. We reviewed our experience with chylothorax in patients of an ages during the past 10 years. Ages ranged from 2 days to 69 years. The etiologies were traumatic in 17 and congenital or idiopathic in three. Six patients (five infants) were treated nonoperatively with either repeated thoracenteses or chest tube drainage. Fourteen patients (11 infants) lUlderwent operative treatment: transthoracic thoracic duct ligation(five patients), pleuroperitoneal shunting (seven), pleuroperitoneal shunting combined with reoperation on a patient with congenital heart disease (one), and reoperation alone on a patient with congenital heart disease (one). Duration of preoperative therapy ranged from 9 days to 2 months (average 3.3 weeks). Five of six (83.3%) patients treatednonoperatively died. Of the surgicaDy treated group,only twoof 14 (14.3%)died, and 11 of the 12 survivors had resolution of the chylothorax and immediate clinical improvement Our experience suggests that both pediatric and adult patients respond poorly to nonoperative treatment of chylothorax and that this treatment has a high mortality rate. Post-traumatic and congenital chylothorax should be treated operatively after a 6mited trial (1 to 2 weeks) of nonoperative therapy. Pleuroperitoneal shunting may offer a reasonable and effective alternative to thoracotomy and thoracic duct ligation.
Jeffrey W. Milsom, M.D., Irving L. Kron, M.D., Karen S. Rheuban, M.D., and Bradley M. Rodgers, M.D., Charlottesville, Va.
h e ideal treatment of chylothorax is not wellestablished. Its etiologies are diverse, as are opinions as to the type and timing of diagnostic and therapeutic manuevers.':' It is certain that the development of a lymphatic leak in the thorax heralds the need for decisive management if considerable morbidity and mortality are to be avoided." We have reviewed the experience with the treatment of chylothorax at our institution during the past decade. Certain guidelines have emerged that have enhanced both our understanding and treatment of this difficult clinical problem.
Patients and methods The hospital charts and personal physicians' records of all patients with the diagnosis of chylothorax seen at the University of Virginia during the past decade were From the Departments of Surgery and Pediatric Cardiology, University of Virginia Medical Center, Charlottesville, Va. Read at the Tenth Annual Meeting of The Western Thoracic Surgical Association, Maui, Hawaii, June 20-23, 1984. Address for reprints: Irving L. Kron, M.D., Box 181, Department of Surgery, University of Virginia Medical Center, Charlottesville, Va. 22908.
Table I. Etiologies of chylothorax (N = 20) No. of Cause Traumatic: 17 patients Direct interruption of thoracic duct SVC occlusion or obstruction Status after Mustard/Senning procedure Central line insertion/PDA ligation Central line insertion
patients
6 II 3 7 I
Congenital or idiopathic: 3 patients Thoracic lymphangioma RDS/pulmonary interstitial emphysema RDS/neonatal hydrops Legend: SVC, Superior vena eava. PDA, Patent ductus arteriosus. RDS, Respiratory distress syndrome.
reviewed. The patients' ages ranged from 2 days to 69 years. Sixteen of the 20 patients were less than 1 year old. Treatment was undertaken in a nonrandomized fashion by thoracic surgeons. Nonoperative therapy consisted of multiple thoracenteses and/or tube thoracostomy. Total parenteral nutrition was administered to 15 of 221
The Journal of Thoracic and Cardiovascular Surgery
2 2 2 Milsom et al.
Table D. Results of nonoperative treatment of chylothorax Case No.
Disease
68 yr
Left carotid, vertebral, and subclavian artery stenosis
2
42 days
Prematurity, PDA
3
92 days
Prematurity
4
28 days
Prematurity, PDA
5
38 days
Prematurity, PDA
6
40 days
Prematurity, PDA
Operation
Left subclavian and vertebral endarterectomy, subclavian-carotid PTFE conduit Bilateral central venous catheters, PDA ligation Bilateral central venous catheters Right central venous catheter, PDA ligation Left central venous catheter, PDA ligation Bilateral central venous catheters, PDA ligation
Onset after procedure
Treatment
Immediately
Multiple thoracenteses, chest tube for 5 wk
3 wk
Multiple thoracenteses, chest tubes
I wk
Multiple thoracenteses, chest tube
3 wk
Multiple thoracenteses, chest tubes
2V2 wk
Multiple thoracenteses, chest tubes
2 wk
Multiple thoracenteses, chest tubes
Result
Death-sepsis, renal failure
Death-sepsis, respiratory failure Death-sepsis, respiratory failure Survived--effusions resolved Death-sepsis, respiratory failure Death-sepsis, respiratory failure
Legend: PDA, Patent ductus arteriosus.
the 20 patients, although not consistently enough to characterize its effect. Operative therapy included either thoracic duct ligation or pleuroperitoneal shunt insertion. Transthoracic ligation of the thoracic duct was performed in standard fashion by identification and direct suture ligation of the duct at the esophageal hiatus on the right side. If the duct could not be located, all tissue between the aorta and azygos vein was mass ligated, as advocated by Patterson and co-workers.' Pleuroperitonea! shunting was performed by elevating the pertinent hemithorax 30 degrees above the operating table while the patient was maintained in the supine position. The lower chest and upper abdomen were included in the operative field. The Denver double valve peritoneovenous shunt (Denver Biomaterials, Inc., Evergreen, Colo.) was used. After the pumping chamber had been tunneled into the subcutaneous tissues overlying the lower rib margin, the afferent limb of the shunt was inserted into the chest by a small intercostal incision. The efferent limb was then placed into the peritoneal cavity through a small rectus-splitting incision that seals the catheter in the abdomen with a posterior rectus sheath purse-string suture. Situating the pumping chamber directly over a rib facilitates pump-chamber compression. The two groups of patients were compared by Fisher's exact test for nonmatched groups.
Results The etiology of the chylothorax was traumatic in 17 patients and congenital or idiopathic in three patients (Table I). There were 12 male and eight female patients. Nine patients had bilateral chylous effusions. Seven had right-sided and four had left-sided lymphatic collections. Six patients (five infants) were treated nonoperatively (Table II). The oldest patient (68 years) died 5 weeks after initiation of treatment from inanition, renal failure, and sepsis. Five premature infants had superior vena caval thrombus from indwelling central venous catheters, which resulted in chylothorax. Four of the five underwent venography, which demonstrated obstruction of the superior vena cava and innominate vein, including the area of entry of the thoracic duct. In the sole survivor of this group, the effusions resolved spontaneously in 2 weeks and the patient was discharged from the hospital several weeks later. The remaining 14 patients (Table III) were operated upon after an initial period of nonoperative therapy ranging in 13 of them from 4 days to 8 weeks. In one patient with a tracheoesophageal fistula, a large pleural effusion developed on the right side immediately after repair of the fistula. She underwent thoracic duct ligation 24 hours later with complete resolution of the effusion. Both of the older patients who were operated upon
Volume 89 Number 2 February, 1985
Chylothorax
223
Table m. Results of surgical treatment of chylothorax Case No.
Disease
4
11 mo
5
I wk
Squamous cell carcinoma, RLL Thoracic lymphangioma Tetralogy of Fallot, PFO Complex congenital heart disease Prematurity, PDA
6
3 wk
Prematurity, PDA
7
20 days
8
5 mo
9
3 mo
Prematurity, RDS; interstitial edema Prematurity, RDS; neonatal hydrops Prematurity, RDS; PDA
2
12 yr 3 mo
10 II
12 13 14
3V, mo 46 yr
2 days 7 mo
22 mo
Operation RML and RLL lobectomy
Onset after procedure
Treatment
Result
Immediately
Thoracic duct ligation
Cured Cured
Repair
Immediately
Glenn procedure
3 wk
Thoracic duct ligation, pleurodesis Thoracic duct ligation, pleurodesis Thoracic duct ligation
Central PDA Central PDA
5 wk
Pleuroperitoneal shunt
Cured
3 days
Bilateral pleuroperitoneaI shunt Pleuroperitoneal shunt
Died-progressive heart failure Cured
Pleuroperitoneal shunt
Cured Died, 8 days postop.intraventricular hemorrhage Cured
venous catheter, ligation venous catheter, ligation
Central venous catheter, PDA ligation
1 mo
PleuroperitoneaI shunt
Redo Mustard, bilateral pleuroperitoneal shunt Pleuroperitoneal shunt
TGA; pulmonary artery stenosis Squamous cell carcinoma left lung TEF
Mustard repair
10 wk
Radical left pneumonectomy TEF repair
Immediately
TGA TGA
Senning procedure Mustard procedure
3 days 5 mo
I day
Thoracic duct ligation, pleurodesis Pleuroperitoneal shunt Thoracentesis, redo Mustard
Cured Cured
Cured Cured Cured Cured
Legend: RLL, Right lowerlobe. RML, Right middle lobe. PFO, Patent foramen ovale. PDA, Patent ductus arteriosus. RDS, Respiratory distresssyndrome. TGA, Transposition of the great arteries. TEF, Tracheoesophageal fistula.
failed to thrive during their trial of nonoperative therapy. After right middle and lower lobectomy, a 69year-old patient developed pneumonia and a respiratory arrest and lost 10 pounds during the next 2 weeks, despite the use of parenteral nutrition. He then underwent transthoracic thoracic duct ligation. After a left radical pneumonectomy, a 46-year-old patient gradually became bedridden, had intermittent febrile episodes at home, and lost 44 pounds in the 2 months prior to insertion of a pleuroperitoneal shunt. Both patients rapidly gained weight and returned to normal life-styles after control of the chylothorax. Of the five premature infants who had pleuroperitoneal shunting for chylothoraces, three underwent placementof Broviac catheters within the superior vena cava aswell as ligation of the patent ductus arteriosus prior to onset of effusions. The chylothorax never resolved after shunt insertion in one these infants, a 3-week-old girl. She is the only patient in our series in whom this
occurred. Postoperatively, abdominal distention appeared, but the pleural effusions persisted. Shunt patency was verified by intrapleural injection of 20% diatrizoate sodium (Hypaque, Winthrop Laboratory Division, Sterling Drug, Inc., New York, N. Y.) and by following the dye into the peritoneal cavity radiographically. Nonetheless, the infant died 3 weeks postoperatively of congestive heart failure and respiratory insufficiency. The other death in the series of surgically treated patients occurred in a 3-month-old infant who died of an intraventricular hemorrhage 8 days after pleuroperitoneal shunt insertion. Autopsy revealed a patent shunt and no fluid in the treated hemithorax. Baffle obstruction developed in two children after the Mustard operation for transposition of the great arteries. Both children had bilateral chylous pleural effusions. One patient was cured by operative correction of the vena caval obstruction. The second patient required insertion of bilateral pleuroperitoneal shunts as well as
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Mi/som et al.
The Journal of Thoracic and Cardiovascular Surgery
Fig. 1. A, Patient 13, one month after a Senning procedure for transposition of the great arteries, with persistent right-sided chylothorax. B, The same patient, 10 days after insertion of a pleuroperitoneaI shunt, evidencing a near-complete resolution of the previous chylothorax.
operative correction of the obstruction to resolve the effusions. Pleuroperitoneal shunting alone was successful in managing a chylothorax that developed after the performance of a Senning procedure on a boy with transposition of the great vessels (Fig, 1). The mortality rate in the nonoperative group was 83.3% (5/6 patients); in the operative group, it was 14.3% (2/14 patients). These results are significantly different (p < 0.002).
Discussion The ideal management of a patient with chylothorax is unknown. The disease occurs under a variety of situations, and considerable diversity of opinion exists as to which types of chylothorax should be treated operatively: the postsurgical or post-traumatic types only, or the nontraumatic types as well.!" There is also controversy as to whether young children should or should not undergo operation." Prior to Lampson's" report in 1948 of successful control of a traumatic chylothorax by direct ligation of the thoracic duct, the mortality rate for this condition was 45%; nontraumatic chylothorax carried a 100% mortality rate.v" Treatment at that time consisted of thoracentesis and/or tube thoracostomy and possibly a low-fat diet. Goorwitch's" review of chylothorax in 1955 demonstrated no deaths among 15 patients treated operatively and a 19% mortality rate among 16 patients treated nonoperatively. Maloney and Spencer' in 1956 countered a growing
tendency toward immediate operative intervention by demonstrating cures in 11 of 13 young children with postoperative chylothorax who were treated by multiple aspirations of the chyle. Clinical parameters for treatment of this disease were proposed in 1971 by Selle, Snyder, and Schreiber' when they reviewed their experience with 15 patients with chylothorax of various etiologies. They believed that idiopathic chylothorax in neonates and nontraumatic chylothorax should be managed nonoperatively. Traumatic chylothorax was considered for thoracic duct ligation when chyle flow had not diminished over a 2 week period or when nutritional complications appeared imminent. Their series had one death in four patients with traumatic chylothorax treated nonoperatively and no deaths in the four treated operatively. Three of the six patients with nontraumatic chylothorax in their series died of their underlying primary disease. In 1981, Strausser and FIye3 refuted the nonoperative approach to nontraumatic chylothorax and reported on 13 patients with this diagnosis, only three of whom responded to nonoperative therapy. Four of these patients were treated by transthoracic thoracic duct ligation, and three had permanent relief of chylothorax. These series illustrate the controversy in treating this disease. Once the diagnosis of chylothorax is established, a course of therapy should be chosen which will avoid the serious metabolic, nutritional, and immunologic sequellae widely known to this disease and manifested even in several of our surgically treated patients prior to their
Volume 89 Number 2 I=ebruary. 1985
operations.' Nutritional support should be begun early, particularly in the neonate. Nonoperative measures are then instituted, such as thoracentesis and/or tube thoracostomy. If the clinical course is such that no progress is achieved in the first 2 weeks of such treatment, or if the patients' nutritional or metabolic status declines measurably during that time, surgical intervention should be undertaken. There is less agreement on the type of surgical effort to apply. Transthoracic thoracic duct ligation has been the standard therapy and has a greater than 90% probability of correcting the problem. I. 2, 7. 8 In 1978, Adler and Levinsky? reported the successful treatment of two patients with persistent chylothorax by talc pleurodesis. Chylothorax was secondary to lymphosarcoma in one and developed after repair of a dissecting aneurysm in the other. Radiotherapy has been successful in managing chylothorax in patients with mediastinal lymphoma. 10. II Radiotherapy for nonmalignant chylous effusions has been unsuccessful, as has intrapleural instillation of other compounds such as sterile broth chloroazodin (Azochloramid), hypertonic glucose, and nitrogen mus-
tard.' Fibrin glue cured one case of postsurgical chylothorax after extrapleural ligation of a patent ductus arteriosus. 12 Weese and Schouten" reported the use of pleuroperitoneal shunting for malignant pleural effusions in two patients. The shunts worked well and achieved good palliation in both patients. Azizkhan and co-workers 14 reported the first use of pleuroperitoneal shunting in chylothorax in infants, with good results in four of five premature infants, all of whom are included in our study. Our experience suggests that operative intervention is indicated after a minimum trial of nonoperative therapy in both the adult and pediatric age groups. Pleuroperitoneal shunting is a highly effective method of treatment, avoids a major surgical procedure, and perhaps should be the treatment of choice for most patients with chylothorax that has not responded to initial nonoperative management. Thoracic duct ligation or correction of the etiology of the chylothorax is indicated if pleuroperitoneal shunting fails to resolve the chylous leak. REFERENCES Bessone LN, Ferguson TB, Burford TH: Chylothorax. Ann Thorac Surg 12:527-530, 1971 2 Selle JG, Snyder WH, Schreiber JT: Chylothorax.Indications for surgery. Ann Surg 177:245-249, 1973 3 Strausser JL, Flye MW: Management of nontraumatic chylothorax. Ann Thorac Surg 31:520-526, 1981
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4 Maloney JV, Spencer FC: The nonoperative treatment of traumatic chylothorax. Surgery 40: 121-128, 1956 5 Shackelford RT, Fisher AM: Traumatic chylothorax. South Med J 31:766-775, 1938 6 Lampson RS: Traumatic chylothorax. A review of the literature and report of a case treated by mediastinal ligationof the thoracic duct. J THORAC SURG 17:778-791, 1948
7 Patterson GA, Todd TRJ, Delarue NC, lives R, Pearson FG, Cooper JD: Supradiaphragmatic ligation of the thoracic duct in intractable chylous fistula. Ann Thorac Surg 32:44-49, 1981 8 Goorwitch J: Traumatic chylothorax and thoracic duct ligation. Case report and review of the literature. J THORAC SURG 29:467-479, 1955 9 Adler RH, Levinsky L: Persistent chylothorax. J THORAC CARDIOVASC SURG 76:859-864, 1978 10 Swensson NL, Kurohara SS, George FW: Complete regression following abdominal irradiation alone of chylothorax complicating lymphosarcoma with ascites. Radiology 87:635-640, 1966 11 Lowe DK, Fletcher WS, Horowitz 11, Hyman MD: Management of chylothorax secondary to lymphoma. Surg Gynecol Obstet 135:35-38, 1972 12 Stenz) W, Rigler B, Tscheliessnigg HK, Beitzke A, Metgler H: Treatment of postsurgical chylothorax with fibrin glue. Thorac Cardiovasc Surg 31:35-36, 1983 13 Weese JL, Schouten JT: Pleural peritoneal shunts for the treatment of malignant pleural effusions. Surg Gynecol Obstet 154:391-392, 1982 14 Azizkhan RG, Canfield J, Alford BA, Rodgers BM: Pleuroperitoneal shunts in management of neonatal chylothorax. J Pediatr Surg 18:842-850, 1983
Discussion DR. JAMES B. D. MARK Stanford. Calif
I believe the authors' main point is wellmade: Nonoperative treatment of chylothorax, no matter what its etiology, is almost certainly doomed to failure. This concept is gaining wide support. Merlini and his associates from Lausanne, Siwtzerland, have suggested that, in adults, chyle loss of over 500 m1 per day for 5 days or of lesseramounts continuing for 10 days is an indication for operation. In addition, they point out the frequency of late relapse after apparently successful conservative treatment. Let me reorganizethe conceptsof etiology and treatment of chylothorax for the purpose of clarification. The authors have pointed out the frequency of venous obstruction as a major cause of chylothorax, particularly in infants. Elevenof their 20 patients probably belong in this category. Superior vena caval obstruction secondary to central venous catheters seems to play a major role. The most common cause of lymphatic obstruction in our experience is mediastinal lymphadenopathy usually secondary to lymphoma of some sort or late fibrosis secondary to radiation therapy of a previous lymphoma. It is frequently difficult to tell the difference.
The Journal of Thoracic and Cardiovascular Surgery
2 2 6 Milsom et al.
Of the traumatic group, operative trauma is far more frequent as a cause than is nonoperative trauma. Chylothorax secondary to thoracic duct injury at operation usually makes itself known in the very early postoperative period, as Dr. Milsom has indicated. Congenital or idiopathic causes of chylothorax are rare. Three were reported by the authors. It is easy to see from the above analysis that physicians play a major role in the occurrence of chylothorax. Clearly, thoracic duct injury at the time of various intrathoracic procedures should be avoided. Maybe caval thrombosis secondary to central venous catheters can be prevented in some cases by more careful catheter care, but it seems to me that this may have to be lumped in the category of "diseases of medical progress." Central venous catheters have saved many lives,but clearly they are not without risk. Ignorance rather than modesty forbids me from commenting on baffle obstruction secondary to intracardiac repair or complex congenital anomalies. Nonoperative treatment should begin with thoracostomy drainage in most cases along with dietary management and appropriate nutritional support. If one is going to allow oral nutriment, and I question whether this is a good idea, medium-chain triglycerides should be used since they are absorbed directly into the portal system rather than into intestinal lymphatics. I really believe that total parenteral nutrition should be used in essentially all cases in order to provide nutrition, boost immune defenses, and decrease thoracic duct flow. We have tried tetracycline sclerosis in a number of these patients, with little success. If chylothorax is due to obstruction by enlarged mediastinal nodes involvedwith lymphoma or other malignant, diseases, appropriate radiation or chemotherapy is in order but may not be totally successful. Thoracic duct obstruction rarely can be relieved by operation. Operative intervention will generally involve ligation of the thoracic duct, usually by thoracotomy on the side of the chylothorax. The thoracic duct ascends into the right hemithorax through the aortic hiatus along with the aorta and azygos vein. It is generally a single trunk between the eighth and twelfth thoracic vertebrae and between the two aforementioned vascular structures. I would not advise using methylene blue as a method of indentifying the thoracic duct. The leaking blue chyle just stains everything in the territory. We prefer to give the patient some cream by mouth a couple of hours before thoracotomy in order to stimulate the flow of chyle, which aids in identification of the thoracic duct. Communication with the anesthesiologist about this trick may keep him from cancelling the case. We have not done pleuroperitoneaI shunting and I would be interested in hearing further from Dr. Milsom about the long-term fate of these shunts. If such a device is placed in an infant only days or weeks old, one is looking forward to the possibility of having it work not for 5 or 10 years but for 70 years or more. I wonder, also, about the fate of the chyle that goes from the pleural cavity into the peritoneal cavity. Have tracer studies been done to show the fate of the fluid, the proteins, and the cellular elements? How rapidly does the
chyle recirculate and does it become useful to the body's economy? Let me illustrate some of the problems in managing chylothorax by discussing one case. A 62-year-old woman had right-sided chylothorax secondary to lymphoma in mediastinal nodes. She was treated unsuccessfully with chemotherapy and repeated thoracenteses. Finally tube thoracostomy, total parenteral nutrition, and tetracycline sclerosis were all used without success. She finally came to thoracotomy, at which time the thoracic duct was ligated and a decortication was done. Three months after the operation, the chest x-ray film demonstrated no additional fluid accumulation in the right side of the chest. She remains well and active 15 months later. DR. RALPH D. ALLEY Albany, N. Y.
I congratulate the gentlemen from Virginia on their rediscovery of chylothorax and the thoracic duct. That goes for you, too, Jim Mark. Also I would like to say that the little duct has been upstaged in recent years by the stampede of leg veins seeking domicile in the thorax. I have a warm feeling for the thoracic duct because I assisted George Emerson in doing the first intraoperative thoracic ductogram in delineating a cyst of the thoracic duct which was masquerading as a posterior mediastinal tumor on chest film. This episode occurred in New Haven in 1946 or 1947. As this is a paper presented by a resident, I am reminded of the first paper I presented to an important audience as a resident. The setting was the annual meeting of the American Surgical Association at the Chateau Frontenac in Quebec City in the spring of 1948. The title of my paper was "Pharmacologic Factors Influencing Collateral Ventilation." The discussant was Dr. Edward Churchill, Chairman of the Department of Surgery at Harvard University and Surgeon-in-Chief of the Massachusetts General Hospital. When he got up, I experienced severe PVCs. When he got through I was in total heart block! His eloquence and scholarly discussion can best be summarized in the vernacular of Tom Fogarty or Eddie Murphy, who would have reduced what Churchill had to say over several pages to the bottom line as follows: "This is a lot of turkey stuffing." To this day, I do not know which of us was right. I think I was, because I did the laboratory work. Thirty-six years later the tables are turned and, fortunately, what we have just heard is not a lot of turkey stuffing. However, as one member of a team in Albany, New York, who spent many years studying the thoracic duct in health and disease in the 1950s and early 1960s (the thoracic duct and traumatic rupture of aneurysm of the thoracic aorta were specialties of the house), I confess to an eerie feeling that the authors have overlooked a large body of literature that appeared chiefly in the 1950s, much of it emanating from Albany. This literature was not overlooked by F. Henry Ellis, Jr. After he accepted the editorship of the Thoracic Surgical Section of Lewis's System of Surgery in 1960, or thereabouts, he asked my associate, Dr. Harvey W. Kausel, to write the chapter on the thoracic duct. I commend it to your
Volume 89 Number 2 February, 1985
reading, or rereading. Perhaps you will find it arrestingly informative. The use of valved pleuroperitoneal shunting with the Denver shunt is, to me, the novel and exciting contribution of this paper, and warrants further consideration. I foresee a place for its use as the first step, and possibly definitive therapy, for chylothorax, offering promise of resolution short of thoracic duct ligation. Its indications include congenital chylothorax (often bilateral and usually accompanied by chyloascites) and right chylothorax following a cavopulmonary shunt. We have managed two cases of congenital chylothorax by a method suggested by Dr. Robert E. Gross in a telephone consultation. In each instance, a right thoracotomy and oversewing of a myriad of mediastinal chyle leaks with mattress sutures rescued the infant from death by inanition resulting from bilateral, prolonged chest tube drainage of chyle, In these cases, the development of tributaries of the cisterna chyli and its effluent thoracic duct drainage system is arrested at an early gestational stage, and the thoracic duct as a discrete structure is not to be found, The multiple sites of mediastinal chyle leak can be identified by the simple expedient of having the anesthesiologist inject cream into the stomach through a nasogastric tube after the mediastinum has been exposed at operation. Anesthesiologists willingly participate in this maneuver once the airway of the patient is protected by intubation. The same amount of cream administered by mouth at the bedside before the patient is called to the operating room may lead to cancellation of the case for violation of the rule, "nothing by mouth after midnight." The applicability of this approach to intraoperative visualization of the visceral lymphatic system, including the thoracic duct where needed, is self-evident. As predicted by Dr, Gross, in each of these two infants the tense distention of the abdomen resolved spontaneously over a
Chylothorax
227
matter of months. This was a trying period of concern for the parents and all professional attending staff caring for the infants (including the thoracic surgical team, who bore the responsibility for reassuring everyone else). Though the ending was a happy one for each infant, initially the abdomen grew to an alarming degree. Chylothorax may occur on the right side after cavopulmonary shunt, due to relative stenosis at the anastomotic site. This results from marked caval system engorgement after the obligatory side-to-end coupling of a huge superior vena cava and a small pulmonary artery, This in turn results in back-bleeding of chyle through lymphatic tributaries violated by mediastinal dissection. The first step in relief lies in plasmaphoresis (down to a hematocrit value in the high 40s) to reduce viscosity of blood and attendant hydraulic resistance to flow through the cavo-right pulmonary vascular system, If this does not effect regression of chyle leakage, I would favor a trial of the Denver pleuroperitoneal valved shunt. DR. MILSOM (Closing) Thank you very much for your discussions, Dr. Mark and Dr. Alley. As regards the long-term fate of the shunt, we have found that chylothorax, at least in all patients into whom we have placed the shunt, is really a self-limiting disease. In every instance we have been able to remove the shunt within about 3 months after inserting it. For some reason the leakage heals itself, collateral develops (we are not sure exactly why), and we have had no recurrence of chylothorax. Regarding the fate of chyle, Dr. Mark, we have not used tracer studies to follow the chylous fluid beyond the peritoneum. We have used radionuclide studies to verify patency by injecting a technetium-labeled substance into the chest and following it down into the abdomen.
THoRAc CARDIOVASC SURG
89:221-227, 1985
Chylothorax: An assessment of current surgical management The development of chylothorax is a serious and often life-threatening clinical entity. Optimal management of this problem has not been wen defmed to date. We reviewed our experience with chylothorax in patients of an ages during the past 10 years. Ages ranged from 2 days to 69 years. The etiologies were traumatic in 17 and congenital or idiopathic in three. Six patients (five infants) were treated nonoperatively with either repeated thoracenteses or chest tube drainage. Fourteen patients (11 infants) lUlderwent operative treatment: transthoracic thoracic duct ligation(five patients), pleuroperitoneal shunting (seven), pleuroperitoneal shunting combined with reoperation on a patient with congenital heart disease (one), and reoperation alone on a patient with congenital heart disease (one). Duration of preoperative therapy ranged from 9 days to 2 months (average 3.3 weeks). Five of six (83.3%) patients treatednonoperatively died. Of the surgicaDy treated group,only twoof 14 (14.3%)died, and 11 of the 12 survivors had resolution of the chylothorax and immediate clinical improvement Our experience suggests that both pediatric and adult patients respond poorly to nonoperative treatment of chylothorax and that this treatment has a high mortality rate. Post-traumatic and congenital chylothorax should be treated operatively after a 6mited trial (1 to 2 weeks) of nonoperative therapy. Pleuroperitoneal shunting may offer a reasonable and effective alternative to thoracotomy and thoracic duct ligation.
Jeffrey W. Milsom, M.D., Irving L. Kron, M.D., Karen S. Rheuban, M.D., and Bradley M. Rodgers, M.D., Charlottesville, Va.
h e ideal treatment of chylothorax is not wellestablished. Its etiologies are diverse, as are opinions as to the type and timing of diagnostic and therapeutic manuevers.':' It is certain that the development of a lymphatic leak in the thorax heralds the need for decisive management if considerable morbidity and mortality are to be avoided." We have reviewed the experience with the treatment of chylothorax at our institution during the past decade. Certain guidelines have emerged that have enhanced both our understanding and treatment of this difficult clinical problem.
Patients and methods The hospital charts and personal physicians' records of all patients with the diagnosis of chylothorax seen at the University of Virginia during the past decade were From the Departments of Surgery and Pediatric Cardiology, University of Virginia Medical Center, Charlottesville, Va. Read at the Tenth Annual Meeting of The Western Thoracic Surgical Association, Maui, Hawaii, June 20-23, 1984. Address for reprints: Irving L. Kron, M.D., Box 181, Department of Surgery, University of Virginia Medical Center, Charlottesville, Va. 22908.
Table I. Etiologies of chylothorax (N = 20) No. of Cause Traumatic: 17 patients Direct interruption of thoracic duct SVC occlusion or obstruction Status after Mustard/Senning procedure Central line insertion/PDA ligation Central line insertion
patients
6 II 3 7 I
Congenital or idiopathic: 3 patients Thoracic lymphangioma RDS/pulmonary interstitial emphysema RDS/neonatal hydrops Legend: SVC, Superior vena eava. PDA, Patent ductus arteriosus. RDS, Respiratory distress syndrome.
reviewed. The patients' ages ranged from 2 days to 69 years. Sixteen of the 20 patients were less than 1 year old. Treatment was undertaken in a nonrandomized fashion by thoracic surgeons. Nonoperative therapy consisted of multiple thoracenteses and/or tube thoracostomy. Total parenteral nutrition was administered to 15 of 221
The Journal of Thoracic and Cardiovascular Surgery
2 2 2 Milsom et al.
Table D. Results of nonoperative treatment of chylothorax Case No.
Disease
68 yr
Left carotid, vertebral, and subclavian artery stenosis
2
42 days
Prematurity, PDA
3
92 days
Prematurity
4
28 days
Prematurity, PDA
5
38 days
Prematurity, PDA
6
40 days
Prematurity, PDA
Operation
Left subclavian and vertebral endarterectomy, subclavian-carotid PTFE conduit Bilateral central venous catheters, PDA ligation Bilateral central venous catheters Right central venous catheter, PDA ligation Left central venous catheter, PDA ligation Bilateral central venous catheters, PDA ligation
Onset after procedure
Treatment
Immediately
Multiple thoracenteses, chest tube for 5 wk
3 wk
Multiple thoracenteses, chest tubes
I wk
Multiple thoracenteses, chest tube
3 wk
Multiple thoracenteses, chest tubes
2V2 wk
Multiple thoracenteses, chest tubes
2 wk
Multiple thoracenteses, chest tubes
Result
Death-sepsis, renal failure
Death-sepsis, respiratory failure Death-sepsis, respiratory failure Survived--effusions resolved Death-sepsis, respiratory failure Death-sepsis, respiratory failure
Legend: PDA, Patent ductus arteriosus.
the 20 patients, although not consistently enough to characterize its effect. Operative therapy included either thoracic duct ligation or pleuroperitoneal shunt insertion. Transthoracic ligation of the thoracic duct was performed in standard fashion by identification and direct suture ligation of the duct at the esophageal hiatus on the right side. If the duct could not be located, all tissue between the aorta and azygos vein was mass ligated, as advocated by Patterson and co-workers.' Pleuroperitonea! shunting was performed by elevating the pertinent hemithorax 30 degrees above the operating table while the patient was maintained in the supine position. The lower chest and upper abdomen were included in the operative field. The Denver double valve peritoneovenous shunt (Denver Biomaterials, Inc., Evergreen, Colo.) was used. After the pumping chamber had been tunneled into the subcutaneous tissues overlying the lower rib margin, the afferent limb of the shunt was inserted into the chest by a small intercostal incision. The efferent limb was then placed into the peritoneal cavity through a small rectus-splitting incision that seals the catheter in the abdomen with a posterior rectus sheath purse-string suture. Situating the pumping chamber directly over a rib facilitates pump-chamber compression. The two groups of patients were compared by Fisher's exact test for nonmatched groups.
Results The etiology of the chylothorax was traumatic in 17 patients and congenital or idiopathic in three patients (Table I). There were 12 male and eight female patients. Nine patients had bilateral chylous effusions. Seven had right-sided and four had left-sided lymphatic collections. Six patients (five infants) were treated nonoperatively (Table II). The oldest patient (68 years) died 5 weeks after initiation of treatment from inanition, renal failure, and sepsis. Five premature infants had superior vena caval thrombus from indwelling central venous catheters, which resulted in chylothorax. Four of the five underwent venography, which demonstrated obstruction of the superior vena cava and innominate vein, including the area of entry of the thoracic duct. In the sole survivor of this group, the effusions resolved spontaneously in 2 weeks and the patient was discharged from the hospital several weeks later. The remaining 14 patients (Table III) were operated upon after an initial period of nonoperative therapy ranging in 13 of them from 4 days to 8 weeks. In one patient with a tracheoesophageal fistula, a large pleural effusion developed on the right side immediately after repair of the fistula. She underwent thoracic duct ligation 24 hours later with complete resolution of the effusion. Both of the older patients who were operated upon
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223
Table m. Results of surgical treatment of chylothorax Case No.
Disease
4
11 mo
5
I wk
Squamous cell carcinoma, RLL Thoracic lymphangioma Tetralogy of Fallot, PFO Complex congenital heart disease Prematurity, PDA
6
3 wk
Prematurity, PDA
7
20 days
8
5 mo
9
3 mo
Prematurity, RDS; interstitial edema Prematurity, RDS; neonatal hydrops Prematurity, RDS; PDA
2
12 yr 3 mo
10 II
12 13 14
3V, mo 46 yr
2 days 7 mo
22 mo
Operation RML and RLL lobectomy
Onset after procedure
Treatment
Result
Immediately
Thoracic duct ligation
Cured Cured
Repair
Immediately
Glenn procedure
3 wk
Thoracic duct ligation, pleurodesis Thoracic duct ligation, pleurodesis Thoracic duct ligation
Central PDA Central PDA
5 wk
Pleuroperitoneal shunt
Cured
3 days
Bilateral pleuroperitoneaI shunt Pleuroperitoneal shunt
Died-progressive heart failure Cured
Pleuroperitoneal shunt
Cured Died, 8 days postop.intraventricular hemorrhage Cured
venous catheter, ligation venous catheter, ligation
Central venous catheter, PDA ligation
1 mo
PleuroperitoneaI shunt
Redo Mustard, bilateral pleuroperitoneal shunt Pleuroperitoneal shunt
TGA; pulmonary artery stenosis Squamous cell carcinoma left lung TEF
Mustard repair
10 wk
Radical left pneumonectomy TEF repair
Immediately
TGA TGA
Senning procedure Mustard procedure
3 days 5 mo
I day
Thoracic duct ligation, pleurodesis Pleuroperitoneal shunt Thoracentesis, redo Mustard
Cured Cured
Cured Cured Cured Cured
Legend: RLL, Right lowerlobe. RML, Right middle lobe. PFO, Patent foramen ovale. PDA, Patent ductus arteriosus. RDS, Respiratory distresssyndrome. TGA, Transposition of the great arteries. TEF, Tracheoesophageal fistula.
failed to thrive during their trial of nonoperative therapy. After right middle and lower lobectomy, a 69year-old patient developed pneumonia and a respiratory arrest and lost 10 pounds during the next 2 weeks, despite the use of parenteral nutrition. He then underwent transthoracic thoracic duct ligation. After a left radical pneumonectomy, a 46-year-old patient gradually became bedridden, had intermittent febrile episodes at home, and lost 44 pounds in the 2 months prior to insertion of a pleuroperitoneal shunt. Both patients rapidly gained weight and returned to normal life-styles after control of the chylothorax. Of the five premature infants who had pleuroperitoneal shunting for chylothoraces, three underwent placementof Broviac catheters within the superior vena cava aswell as ligation of the patent ductus arteriosus prior to onset of effusions. The chylothorax never resolved after shunt insertion in one these infants, a 3-week-old girl. She is the only patient in our series in whom this
occurred. Postoperatively, abdominal distention appeared, but the pleural effusions persisted. Shunt patency was verified by intrapleural injection of 20% diatrizoate sodium (Hypaque, Winthrop Laboratory Division, Sterling Drug, Inc., New York, N. Y.) and by following the dye into the peritoneal cavity radiographically. Nonetheless, the infant died 3 weeks postoperatively of congestive heart failure and respiratory insufficiency. The other death in the series of surgically treated patients occurred in a 3-month-old infant who died of an intraventricular hemorrhage 8 days after pleuroperitoneal shunt insertion. Autopsy revealed a patent shunt and no fluid in the treated hemithorax. Baffle obstruction developed in two children after the Mustard operation for transposition of the great arteries. Both children had bilateral chylous pleural effusions. One patient was cured by operative correction of the vena caval obstruction. The second patient required insertion of bilateral pleuroperitoneal shunts as well as
2 24
Mi/som et al.
The Journal of Thoracic and Cardiovascular Surgery
Fig. 1. A, Patient 13, one month after a Senning procedure for transposition of the great arteries, with persistent right-sided chylothorax. B, The same patient, 10 days after insertion of a pleuroperitoneaI shunt, evidencing a near-complete resolution of the previous chylothorax.
operative correction of the obstruction to resolve the effusions. Pleuroperitoneal shunting alone was successful in managing a chylothorax that developed after the performance of a Senning procedure on a boy with transposition of the great vessels (Fig, 1). The mortality rate in the nonoperative group was 83.3% (5/6 patients); in the operative group, it was 14.3% (2/14 patients). These results are significantly different (p < 0.002).
Discussion The ideal management of a patient with chylothorax is unknown. The disease occurs under a variety of situations, and considerable diversity of opinion exists as to which types of chylothorax should be treated operatively: the postsurgical or post-traumatic types only, or the nontraumatic types as well.!" There is also controversy as to whether young children should or should not undergo operation." Prior to Lampson's" report in 1948 of successful control of a traumatic chylothorax by direct ligation of the thoracic duct, the mortality rate for this condition was 45%; nontraumatic chylothorax carried a 100% mortality rate.v" Treatment at that time consisted of thoracentesis and/or tube thoracostomy and possibly a low-fat diet. Goorwitch's" review of chylothorax in 1955 demonstrated no deaths among 15 patients treated operatively and a 19% mortality rate among 16 patients treated nonoperatively. Maloney and Spencer' in 1956 countered a growing
tendency toward immediate operative intervention by demonstrating cures in 11 of 13 young children with postoperative chylothorax who were treated by multiple aspirations of the chyle. Clinical parameters for treatment of this disease were proposed in 1971 by Selle, Snyder, and Schreiber' when they reviewed their experience with 15 patients with chylothorax of various etiologies. They believed that idiopathic chylothorax in neonates and nontraumatic chylothorax should be managed nonoperatively. Traumatic chylothorax was considered for thoracic duct ligation when chyle flow had not diminished over a 2 week period or when nutritional complications appeared imminent. Their series had one death in four patients with traumatic chylothorax treated nonoperatively and no deaths in the four treated operatively. Three of the six patients with nontraumatic chylothorax in their series died of their underlying primary disease. In 1981, Strausser and FIye3 refuted the nonoperative approach to nontraumatic chylothorax and reported on 13 patients with this diagnosis, only three of whom responded to nonoperative therapy. Four of these patients were treated by transthoracic thoracic duct ligation, and three had permanent relief of chylothorax. These series illustrate the controversy in treating this disease. Once the diagnosis of chylothorax is established, a course of therapy should be chosen which will avoid the serious metabolic, nutritional, and immunologic sequellae widely known to this disease and manifested even in several of our surgically treated patients prior to their
Volume 89 Number 2 I=ebruary. 1985
operations.' Nutritional support should be begun early, particularly in the neonate. Nonoperative measures are then instituted, such as thoracentesis and/or tube thoracostomy. If the clinical course is such that no progress is achieved in the first 2 weeks of such treatment, or if the patients' nutritional or metabolic status declines measurably during that time, surgical intervention should be undertaken. There is less agreement on the type of surgical effort to apply. Transthoracic thoracic duct ligation has been the standard therapy and has a greater than 90% probability of correcting the problem. I. 2, 7. 8 In 1978, Adler and Levinsky? reported the successful treatment of two patients with persistent chylothorax by talc pleurodesis. Chylothorax was secondary to lymphosarcoma in one and developed after repair of a dissecting aneurysm in the other. Radiotherapy has been successful in managing chylothorax in patients with mediastinal lymphoma. 10. II Radiotherapy for nonmalignant chylous effusions has been unsuccessful, as has intrapleural instillation of other compounds such as sterile broth chloroazodin (Azochloramid), hypertonic glucose, and nitrogen mus-
tard.' Fibrin glue cured one case of postsurgical chylothorax after extrapleural ligation of a patent ductus arteriosus. 12 Weese and Schouten" reported the use of pleuroperitoneal shunting for malignant pleural effusions in two patients. The shunts worked well and achieved good palliation in both patients. Azizkhan and co-workers 14 reported the first use of pleuroperitoneal shunting in chylothorax in infants, with good results in four of five premature infants, all of whom are included in our study. Our experience suggests that operative intervention is indicated after a minimum trial of nonoperative therapy in both the adult and pediatric age groups. Pleuroperitoneal shunting is a highly effective method of treatment, avoids a major surgical procedure, and perhaps should be the treatment of choice for most patients with chylothorax that has not responded to initial nonoperative management. Thoracic duct ligation or correction of the etiology of the chylothorax is indicated if pleuroperitoneal shunting fails to resolve the chylous leak. REFERENCES Bessone LN, Ferguson TB, Burford TH: Chylothorax. Ann Thorac Surg 12:527-530, 1971 2 Selle JG, Snyder WH, Schreiber JT: Chylothorax.Indications for surgery. Ann Surg 177:245-249, 1973 3 Strausser JL, Flye MW: Management of nontraumatic chylothorax. Ann Thorac Surg 31:520-526, 1981
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4 Maloney JV, Spencer FC: The nonoperative treatment of traumatic chylothorax. Surgery 40: 121-128, 1956 5 Shackelford RT, Fisher AM: Traumatic chylothorax. South Med J 31:766-775, 1938 6 Lampson RS: Traumatic chylothorax. A review of the literature and report of a case treated by mediastinal ligationof the thoracic duct. J THORAC SURG 17:778-791, 1948
7 Patterson GA, Todd TRJ, Delarue NC, lives R, Pearson FG, Cooper JD: Supradiaphragmatic ligation of the thoracic duct in intractable chylous fistula. Ann Thorac Surg 32:44-49, 1981 8 Goorwitch J: Traumatic chylothorax and thoracic duct ligation. Case report and review of the literature. J THORAC SURG 29:467-479, 1955 9 Adler RH, Levinsky L: Persistent chylothorax. J THORAC CARDIOVASC SURG 76:859-864, 1978 10 Swensson NL, Kurohara SS, George FW: Complete regression following abdominal irradiation alone of chylothorax complicating lymphosarcoma with ascites. Radiology 87:635-640, 1966 11 Lowe DK, Fletcher WS, Horowitz 11, Hyman MD: Management of chylothorax secondary to lymphoma. Surg Gynecol Obstet 135:35-38, 1972 12 Stenz) W, Rigler B, Tscheliessnigg HK, Beitzke A, Metgler H: Treatment of postsurgical chylothorax with fibrin glue. Thorac Cardiovasc Surg 31:35-36, 1983 13 Weese JL, Schouten JT: Pleural peritoneal shunts for the treatment of malignant pleural effusions. Surg Gynecol Obstet 154:391-392, 1982 14 Azizkhan RG, Canfield J, Alford BA, Rodgers BM: Pleuroperitoneal shunts in management of neonatal chylothorax. J Pediatr Surg 18:842-850, 1983
Discussion DR. JAMES B. D. MARK Stanford. Calif
I believe the authors' main point is wellmade: Nonoperative treatment of chylothorax, no matter what its etiology, is almost certainly doomed to failure. This concept is gaining wide support. Merlini and his associates from Lausanne, Siwtzerland, have suggested that, in adults, chyle loss of over 500 m1 per day for 5 days or of lesseramounts continuing for 10 days is an indication for operation. In addition, they point out the frequency of late relapse after apparently successful conservative treatment. Let me reorganizethe conceptsof etiology and treatment of chylothorax for the purpose of clarification. The authors have pointed out the frequency of venous obstruction as a major cause of chylothorax, particularly in infants. Elevenof their 20 patients probably belong in this category. Superior vena caval obstruction secondary to central venous catheters seems to play a major role. The most common cause of lymphatic obstruction in our experience is mediastinal lymphadenopathy usually secondary to lymphoma of some sort or late fibrosis secondary to radiation therapy of a previous lymphoma. It is frequently difficult to tell the difference.
The Journal of Thoracic and Cardiovascular Surgery
2 2 6 Milsom et al.
Of the traumatic group, operative trauma is far more frequent as a cause than is nonoperative trauma. Chylothorax secondary to thoracic duct injury at operation usually makes itself known in the very early postoperative period, as Dr. Milsom has indicated. Congenital or idiopathic causes of chylothorax are rare. Three were reported by the authors. It is easy to see from the above analysis that physicians play a major role in the occurrence of chylothorax. Clearly, thoracic duct injury at the time of various intrathoracic procedures should be avoided. Maybe caval thrombosis secondary to central venous catheters can be prevented in some cases by more careful catheter care, but it seems to me that this may have to be lumped in the category of "diseases of medical progress." Central venous catheters have saved many lives,but clearly they are not without risk. Ignorance rather than modesty forbids me from commenting on baffle obstruction secondary to intracardiac repair or complex congenital anomalies. Nonoperative treatment should begin with thoracostomy drainage in most cases along with dietary management and appropriate nutritional support. If one is going to allow oral nutriment, and I question whether this is a good idea, medium-chain triglycerides should be used since they are absorbed directly into the portal system rather than into intestinal lymphatics. I really believe that total parenteral nutrition should be used in essentially all cases in order to provide nutrition, boost immune defenses, and decrease thoracic duct flow. We have tried tetracycline sclerosis in a number of these patients, with little success. If chylothorax is due to obstruction by enlarged mediastinal nodes involvedwith lymphoma or other malignant, diseases, appropriate radiation or chemotherapy is in order but may not be totally successful. Thoracic duct obstruction rarely can be relieved by operation. Operative intervention will generally involve ligation of the thoracic duct, usually by thoracotomy on the side of the chylothorax. The thoracic duct ascends into the right hemithorax through the aortic hiatus along with the aorta and azygos vein. It is generally a single trunk between the eighth and twelfth thoracic vertebrae and between the two aforementioned vascular structures. I would not advise using methylene blue as a method of indentifying the thoracic duct. The leaking blue chyle just stains everything in the territory. We prefer to give the patient some cream by mouth a couple of hours before thoracotomy in order to stimulate the flow of chyle, which aids in identification of the thoracic duct. Communication with the anesthesiologist about this trick may keep him from cancelling the case. We have not done pleuroperitoneaI shunting and I would be interested in hearing further from Dr. Milsom about the long-term fate of these shunts. If such a device is placed in an infant only days or weeks old, one is looking forward to the possibility of having it work not for 5 or 10 years but for 70 years or more. I wonder, also, about the fate of the chyle that goes from the pleural cavity into the peritoneal cavity. Have tracer studies been done to show the fate of the fluid, the proteins, and the cellular elements? How rapidly does the
chyle recirculate and does it become useful to the body's economy? Let me illustrate some of the problems in managing chylothorax by discussing one case. A 62-year-old woman had right-sided chylothorax secondary to lymphoma in mediastinal nodes. She was treated unsuccessfully with chemotherapy and repeated thoracenteses. Finally tube thoracostomy, total parenteral nutrition, and tetracycline sclerosis were all used without success. She finally came to thoracotomy, at which time the thoracic duct was ligated and a decortication was done. Three months after the operation, the chest x-ray film demonstrated no additional fluid accumulation in the right side of the chest. She remains well and active 15 months later. DR. RALPH D. ALLEY Albany, N. Y.
I congratulate the gentlemen from Virginia on their rediscovery of chylothorax and the thoracic duct. That goes for you, too, Jim Mark. Also I would like to say that the little duct has been upstaged in recent years by the stampede of leg veins seeking domicile in the thorax. I have a warm feeling for the thoracic duct because I assisted George Emerson in doing the first intraoperative thoracic ductogram in delineating a cyst of the thoracic duct which was masquerading as a posterior mediastinal tumor on chest film. This episode occurred in New Haven in 1946 or 1947. As this is a paper presented by a resident, I am reminded of the first paper I presented to an important audience as a resident. The setting was the annual meeting of the American Surgical Association at the Chateau Frontenac in Quebec City in the spring of 1948. The title of my paper was "Pharmacologic Factors Influencing Collateral Ventilation." The discussant was Dr. Edward Churchill, Chairman of the Department of Surgery at Harvard University and Surgeon-in-Chief of the Massachusetts General Hospital. When he got up, I experienced severe PVCs. When he got through I was in total heart block! His eloquence and scholarly discussion can best be summarized in the vernacular of Tom Fogarty or Eddie Murphy, who would have reduced what Churchill had to say over several pages to the bottom line as follows: "This is a lot of turkey stuffing." To this day, I do not know which of us was right. I think I was, because I did the laboratory work. Thirty-six years later the tables are turned and, fortunately, what we have just heard is not a lot of turkey stuffing. However, as one member of a team in Albany, New York, who spent many years studying the thoracic duct in health and disease in the 1950s and early 1960s (the thoracic duct and traumatic rupture of aneurysm of the thoracic aorta were specialties of the house), I confess to an eerie feeling that the authors have overlooked a large body of literature that appeared chiefly in the 1950s, much of it emanating from Albany. This literature was not overlooked by F. Henry Ellis, Jr. After he accepted the editorship of the Thoracic Surgical Section of Lewis's System of Surgery in 1960, or thereabouts, he asked my associate, Dr. Harvey W. Kausel, to write the chapter on the thoracic duct. I commend it to your
Volume 89 Number 2 February, 1985
reading, or rereading. Perhaps you will find it arrestingly informative. The use of valved pleuroperitoneal shunting with the Denver shunt is, to me, the novel and exciting contribution of this paper, and warrants further consideration. I foresee a place for its use as the first step, and possibly definitive therapy, for chylothorax, offering promise of resolution short of thoracic duct ligation. Its indications include congenital chylothorax (often bilateral and usually accompanied by chyloascites) and right chylothorax following a cavopulmonary shunt. We have managed two cases of congenital chylothorax by a method suggested by Dr. Robert E. Gross in a telephone consultation. In each instance, a right thoracotomy and oversewing of a myriad of mediastinal chyle leaks with mattress sutures rescued the infant from death by inanition resulting from bilateral, prolonged chest tube drainage of chyle, In these cases, the development of tributaries of the cisterna chyli and its effluent thoracic duct drainage system is arrested at an early gestational stage, and the thoracic duct as a discrete structure is not to be found, The multiple sites of mediastinal chyle leak can be identified by the simple expedient of having the anesthesiologist inject cream into the stomach through a nasogastric tube after the mediastinum has been exposed at operation. Anesthesiologists willingly participate in this maneuver once the airway of the patient is protected by intubation. The same amount of cream administered by mouth at the bedside before the patient is called to the operating room may lead to cancellation of the case for violation of the rule, "nothing by mouth after midnight." The applicability of this approach to intraoperative visualization of the visceral lymphatic system, including the thoracic duct where needed, is self-evident. As predicted by Dr, Gross, in each of these two infants the tense distention of the abdomen resolved spontaneously over a
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227
matter of months. This was a trying period of concern for the parents and all professional attending staff caring for the infants (including the thoracic surgical team, who bore the responsibility for reassuring everyone else). Though the ending was a happy one for each infant, initially the abdomen grew to an alarming degree. Chylothorax may occur on the right side after cavopulmonary shunt, due to relative stenosis at the anastomotic site. This results from marked caval system engorgement after the obligatory side-to-end coupling of a huge superior vena cava and a small pulmonary artery, This in turn results in back-bleeding of chyle through lymphatic tributaries violated by mediastinal dissection. The first step in relief lies in plasmaphoresis (down to a hematocrit value in the high 40s) to reduce viscosity of blood and attendant hydraulic resistance to flow through the cavo-right pulmonary vascular system, If this does not effect regression of chyle leakage, I would favor a trial of the Denver pleuroperitoneal valved shunt. DR. MILSOM (Closing) Thank you very much for your discussions, Dr. Mark and Dr. Alley. As regards the long-term fate of the shunt, we have found that chylothorax, at least in all patients into whom we have placed the shunt, is really a self-limiting disease. In every instance we have been able to remove the shunt within about 3 months after inserting it. For some reason the leakage heals itself, collateral develops (we are not sure exactly why), and we have had no recurrence of chylothorax. Regarding the fate of chyle, Dr. Mark, we have not used tracer studies to follow the chylous fluid beyond the peritoneum. We have used radionuclide studies to verify patency by injecting a technetium-labeled substance into the chest and following it down into the abdomen.