Year : 2010 | Volume
: 3 | Issue : 1 | Page : 58--64
Pleural effusions in children undergoing cardiac surgery
Sachin Talwar, Sandeep Agarwala, Chander Mohan Mittal, Shiv Kumar Choudhary, Balram Airan
Cardiothoracic Center and Department of Pediatric Surgery, All India Institute of Medical Sciences, New Delhi, India
Cardiothoracic Center, All India Institute of Medical Sciences, New Delhi-110 029
Persistent pleural effusions are a source of significant morbidity and mortality following surgery in congenital heart disease. In this review, we discuss the etiology, pathophysiology, and management of this common complication.
|How to cite this article:|
Talwar S, Agarwala S, Mittal CM, Choudhary SK, Airan B. Pleural effusions in children undergoing cardiac surgery.Ann Pediatr Card 2010;3:58-64
|How to cite this URL:|
Talwar S, Agarwala S, Mittal CM, Choudhary SK, Airan B. Pleural effusions in children undergoing cardiac surgery. Ann Pediatr Card [serial online] 2010 [cited 2019 Jul 22 ];3:58-64
Available from: http://www.annalspc.com/text.asp?2010/3/1/58/64368
Pleural effusions are a significant problem following cardiac surgical procedures in children with a reported incidence of more than 25%.  They cause significant morbidity following cardiac surgery in children and contribute to their increased stay in the intensive care unit (ICU) and hospital. In this review, an attempt is made to discuss the etiology, pathophysiology, and general management guidelines for persistent pleural effusions and chylothorax following cardiac surgical procedures in children.
Most of the data on the incidence of persistent effusions is derived from studies which comprise both the adult and pediatric population. In a study by Labidi et al,  of 2892 adult patients (mean age 66 years) undergoing open-heart surgery, 192 (6.6%) had a clinically significant pleural effusion within the first 30 days of the operation. Bocsi et al. reported that out of 75 patients (18 years of age or less) undergoing open-heart surgery, 29 (38.6%) developed a significant pleural effusion.  O'Callaghan et al. demonstrated effusions in 11% of 83 pediatric patients after cardiac surgery.  In our own experience with 348 patients undergoing univentricular repair, significant pleural effusion was encountered in 27% of the patients.  However, in one of the largest studies , involving 1341 pediatric patients undergoing correction of congenital heart disease, 18 (1.3%) were seen to have developed postoperative chylothorax. 
Pleural effusions are particularly common following univentricular palliation (bidirectional cavopulmonary or total cavopulmonary connection) and many studies have addressed the factors predisposed to increasing pleural drainage after the Fontan procedure. , Lower preoperative oxygen saturation, presence of postoperative infection, smaller conduit size, and longer duration of cardiopulmonary bypass have been associated with persistent pleural effusions after the extracardiac Fontan procedure.  Low pulmonary vascular compliance has also been shown to be an important risk factor for prolonged pleural effusion drainage after the extracardiac Fontan procedure.  The absence of a fenestration may also be associated with an increased incidence of pleural effusions following the lateral tunnel Fontan. 
Pleural effusions occur between two membranes: the visceral (inner) layer of the pleura attached to the lungs, and the parietal (outer) layer attached to the chest wall. The 'pleural space' is normally nonexistent and is lubricated by a very small amount of pleural fluid (10 - 20 ml) that provides lubrication between the two layers of the pleura. Fluid (sera) continuously moves from the parietal pleura through the pleural space to be absorbed by the visceral pleura. The fluid is then drained into the lymphatic system. This fluid in the pleural space is minimized by a balance of Starling forces, oncotic pressure in the circulation and negative pressure in the lymphatics of the lungs. Movement of the pleural fluid across the pleural space may be about 5 - 10 litres/day, and derangements in this movement may significantly increase the volume of the pleural fluid.
Risk factors for development of pleural effusion are listed in [Table 1]. Pleural effusion may occur in patients with (a) Increased capillary permeability caused by inflammation or infection (b) Increased hydrostatic pressure due to congestive heart failure, increased right-sided pressures or venous hypertension as in superior vena cava (SVC) obstruction (c) Decreased oncotic pressure from hypoalbuminemia, and (d) Increase in the normal negative pressure to a more negative intrathoracic pressure, secondary to atelectasis.
Probably the most common scenarios associated with prolonged pleural effusion after open-heart surgery are following the repair of the Tetralogy of Fallot (TOF) and following univentricular repair. , Systemic venous hypertension is often reflected by high right atrial pressures following repair of TOF, which increases the mean capillary hydrostatic pressure, leading to accumulation of excessive fluid in the pleural space.  In addition many of these patients may have borderline pulmonary artery and peripheral pulmonary artery stenosis, which leads to elevated right atrial pressures. , The presence of residual tricuspid insufficiency, compounds the problem of right heart failure. In patients with TOF and other forms of cyanotic heart disease, the pulmonary vascular anatomy is often abnormal. The muscular pulmonary arteries are thin-walled with medial atrophy and the lumens of the pulmonary arteries, veins, and capillaries are dilated. Once the obstruction to the right ventricular outflow tract is relieved, there is a sudden increase in the pulmonary blood flow resulting in increased intravascular hydrostatic pressure and an increased gradient across the pleural membrane, leading to effusion.  In these patients with preoperative polycythemia, there is an acute hemodilution as a result of surgery, resulting in an increased pulmonary blood flow, which leads to effusion.  Prolonged mechanical ventilation is also associated with an increased incidence of pleural effusion, due to an increase in the intrathoracic pressure, decrease in the intrapleural pressure, and an increase in the systemic venous pressure, which decreases the lymphatic drainage of the pleural cavities, leading to effusion.  Low preoperative oxygen saturation is often a reflection of the poor condition of the patient or a severe degree of obstruction to the right ventricular outflow tract, both of which are correlated with a higher incidence of effusion.
As mentioned above, postoperative pleural effusions are also very common following univentricular palliation and lead to a prolonged hospital stay of these patients. Attempts to address this issue have led to the concept of creating a fenestration in the Fontan pathway. However, the results and views on the role of fenestration in reducing the incidence of pleural effusion are conflicting. ,,,, The advent of extracardiac Fontan operation has not reduced the incidence of effusion significantly following this operation. On the contrary, use of a smaller conduit size during this operation has been associated with a higher incidence of effusion.  Performing this operation without cardiopulmonary bypass has also not altered the frequency of this problem, thus reinforcing the belief that the state of systemic venous hypertension imposed by the Fontan state is an important factor leading to effusions. Protein losing enteropathy following the Fontan operation may further increase the tendency to effusions, by reducing the plasma colloidal oncotic pressure. In addition, the occurrence of diaphragmatic palsy in some of these patients may adversely affect the Fontan circuit and lead to a higher incidence of effusions. The mechanisms of the latter are discussed in the article on diaphragmatic palsy in the same issue of this journal. 
Chylothorax occurs due to a direct trauma to the thoracic duct and the lymphatic system. This usually occurs following a Blalock-Taussig shunt, ligation of patent ducts arteriosus, or following coarctation of aorta repair via a thoracotomy approach.
Postoperative pleural effusions may present in a variety of ways. Many times, the patients are completely asymptomatic and pleural effusions are an incidental finding on chest radiographs. However, depending on the size of the effusions, there may be a dramatic onset of dyspnea, shortness of breath, fever, and chest pain. Larger effusions can even lead to hemodynamic compromise due to cardiac embarrassment. In chylothorax, chest pain and fever are uncommon because chyle is not irritating to the pleural surface. More serious sequelae of chylothorax are malnutrition, weakness, dehydration, metabolic acidosis, and a compromised immunologic status.
The plain chest radiograph is the most commonly performed investigation and may reveal findings ranging from opacification of the entire hemithorax in large effusions or mere blunting of the costophrenic angle in small effusions. The latter may be more apparent in chest radiographs obtained in the upright posture. The lateral decubitus film can also be used to diagnose small effusions. Bedside ultrasonography is also useful to diagnose pleural collections and to differentiate between effusions and lung consolidation or collapse.  High-resolution contrast chest tomograph (HRCT) has been promoted as the gold standard for diagnosis of small pleural collections, but carries a high radiation exposure. We, however, consider it an unnecessary and expensive investigation when a simple chest radiograph is equally informative.
Pleural fluid aspiration (Thoracentesis) using a needle helps in diagnosing the type of effusion and its etiology, which in turn helps to plan the management of pleural effusions. The appearance of the fluid, cell count, and certain biochemical tests as mentioned in [Table 2], aid in the diagnosis.
The pleural fluid aspirate is straw-colored in patients with congestive heart failure and tuberculosis. It is a transudate in heart failure, whereas, it is an exudate in tuberculosis. In hemothorax it is bloody, in parapneumonic effusions it is serosanguinous, and in chylothorax it is milky white in color. Exudative pleural effusion is characterized by any one of the criteria listed in [Table 2].  The cell content of tubercular effusion is predominantly lymphocytes, in acute infective pleural effusion it is neutrophils, and in hemothorax the pleural fluid hematocrit is > 0.5 of the blood hematocrit. Characteristics of pleural effusion due to various causes are detailed herewith:
Effusion in congestive cardiac failure or raised venous pressure
The effusion is a transudate and is serous or straw-colored. It occurs more often on the right side. The effusion occurs because increased amount of lung interstitial fluid exits into the pleural space and overwhelms the capacity of the lymphatics in the parietal pleura to drain the fluid. Diagnostic thoracentesis is performed if effusions are not bilateral, if patient is febrile or has pleuritic chest pain.
This may occur as a late complication of the Fontan procedure leading to liver cirrhosis and ascites.  The predominant mechanism is the direct movement of the peritoneal fluid through small holes within the diaphragm into the pleural space. The effusion is a transudate and is usually right-sided and large enough to produce severe dyspnea.
Protein losing enteropathy
Loss of protein via the gastrointestinal tract occurs in 3.7% of the patients following the Fontan operation and is clinically characterized by fatigue, peripheral edema, pleural and pericardial effusions, ascites, and chronic diarrhea  associated with hypoalbuminemia.
Parapneumonic effusions are associated with bacterial pneumonia or lung abscess. These are exudative effusions and may be blood stained. Pleural effusions more than 10 mm thick on lateral decubitus film require a diagnostic tap. 
Post cardiac injury syndrome
This occurs days to weeks following open-heart surgery. The development of pericardial, pleural, and pulmonary parenchymal inflammation following cardiac injury may be suggested by, fever, dyspnea, pleuropericardial rub, rales, elevated erythrocyte sedimentation rate, leukocytosis, pleural effusion, and pulmonary parenchymal infiltrates.  Nonetheless, these common clinical manifestations and laboratory features of post cardiac injury syndrome (PCIS) are nonspecific. The finding of a bloody, exudative pleural effusion with a pH greater than 7.30 helps to confirm a clinical suspicion of PCIS, but these pleural fluid characteristics are not pathognomonic.  Thus, arriving at a presumptive diagnosis of PCIS currently requires both clinical pattern recognition and exclusion of other diagnoses that may arise in this setting, namely, pulmonary embolism, congestive heart failure, atelectasis, and pneumonia.
Although by strict definition tubercular (TB) pleural effusions are not postoperative in nature, we have included a short discussion on these because these effusions are not uncommon in the cardiac intensive care unit in our country, even prior to open-heart surgery. These are thought to be due to a hypersensitivity reaction to the tuberculosis protein in the pleural space. Patients with tubercular pleuritis present with fever, weight loss, dyspnea, and/or pleuritic chest pain. Pleural fluid is straw-colored and exudative, with lymphocytic predominance. The diagnosis is established by demonstrating high levels of TB markers  in pleural fluid (adenosine deaminase > 45IU / l, Gamma interferon > 140 pg/ml or positive polymerase chain reaction-PCR for tuberculosis DNA).
Chylothorax represents chyle in the pleural cavity. Chyle is a lymphatic fluid rich in fat, and its digestive products are absorbed by the intestinal epithelium. Pleural fluid triglyceride levels have been used for diagnosis of chylothorax. Pleural fluid triglyceride levels > 110 mg/dl, presence of chylomicrons, low cholesterol level, and elevated lymphocyte count are diagnostic of a chylothorax.  When the pleural fluid triglyceride level is > 110 mg/dl, there is  When the triglyceride level is between 55 and 110 mg/dl, a lipoprotein analysis is indicated, to detect chylomicrons. Other criteria for chylothorax include a pleural fluid to serum triglyceride ratio > 1, and a pleural fluid to serum cholesterol ratio  Pseudochylothorax, also known as chyliform pleural effusion or cholesterol pleural effusion, is the term applied to pleural fluid that mimics the true chylous pleural effusion in appearance, but lacks the biochemical criteria for chylothorax. In contrast to true chylothorax, it is chronic, and may be present for months to years. Pseudochylothorax is more likely to result from long-standing pleural effusion. The fluid is yellow or opalescent green and may initially be mistaken for a chylous effusion, an empyema, or both.  High cholesterol levels are typical of a pseudochylous pleural effusion. Cholesterol levels are generally > 200 mg/dl and may even exceed 1000 mg/dl.  The fluid may demonstrate rhomboid-shaped cholesterol crystals on microscopy, which do not stain with Sudan III stain. 
Management centers around correction of the underlying cause and drainage of pleural fluid either by needle aspiration or insertion of an intercostal tube.
Pleural effusion secondary to heart failure is managed by diuretic therapy and other drugs used for heart failure. The various drugs and their dosages have been elegantly summarized in a recent review.  They include digoxin, furosemide, spironolactone, captopril, enalapril, losartan, metoprolol, and carvedilol.
Protein losing enteropathy following the Fontan procedure is managed by dietary modifications (high protein and high-medium chain triglycerides), afterload reducing agents, ionotropic agents, heparin, albumin infusions, octreotide, prednisone, creation of atrial fenestration, if required Fontan revision or conversion to a different form, and in refractory cases, cardiac transplantation. 
Parapneumonic effusions that are uncomplicated generally resolve with antibiotics. In case of complicated effusions tube thoracostomy is required along with intravenous antibiotics. In case of loculated effusions instillation of a thrombolytic agent (streptokinase or urokinase) through tube is helpful.  Tubercular effusions are managed by standard anti-tubercular therapy.
Various Options for the management of chylothorax are listed in [Table 3] and a suggested management guideline is listed in the flow chart [Figure 1].
When managing chylothorax conservatively, chest tube drainage of less than 500 ml during the first 24 hours following cessation of oral intake and institution of total parentaral nutrition (TPN) may predict a successful outcome on conservative treatment.  Operative intervention for chylothorax should be considered when: (a) Average daily loss has exceeded 1500 ml/year of age in children for a five-day period,  (b) Chyle flow has not diminished over 14 days, (c) Nutritional depletion, fluid and electrolyte loss, hypolipemia, lymphocytopenia and immunodeficiency appear imminent, and (d) Accumulation of chyle is continuous and more than 5 ml/Kg per day despite chest tube drainage, after all conservative measures.
Somatostatin or octreotide therapy
Somatostatin is an inhibitor of gastric, pancreatic, and intestinal secretions, and is known to decrease chyle production.  Octreotide, its analog, has been successfully used as a therapeutic adjunct for managing persistent chylothorax in a small number of neonatal patients and a larger number of pediatric patients. , No consensus has been reached as to the optimal route of administration, dose, duration of therapy, or strategy for discontinuation of therapy. The common doses are between 80 - 100 microg/kg/day and early initiation of this therapy has been recommended. 
In the absence of a correctable cause, pleurodesis is recommended for persistent effusions / chylous drainage, unresponsive to medical and conservative measures. Almost all sclerosing agents  can produce fever, tachycardia, chest pain, and nausea. The patient needs to be premedicated with analgesics prior to instillation of the sclerosing agents. Talc is the most effective sclerosing agent used, and is often administered as a slurry. , When administered as a slurry through a chest tube or pleural catheter, it may be as effective as the direct insufflation of talc powder via thoracoscopy.  After drainage of the pleural fluid, the slurry (4 - 6 g of talc in a solution of 100 ml saline with or without lidocaine) is instilled. Adverse reactions include microemboli and granulomatous tissue reactions.  Tetracycline has been commonly used in the past in association with tube thoracostomy  and provides faster pleurodesis and pleural symphysis than chest tube drainage alone; however it is very painful. Doxycycline is an alternative to tetracycline and is equally effective. , Bleomycin (60 units) has been used as an alternative sclerosing agent and may have equivalent effectiveness to tetracycline. It is however, expensive and can have systemic toxicity. 
After placement of the chemical agent, the chest tube should be clamped for a period of two to four hours. During this time, the patient should lie in the following positions; supine, right lateral decubitus position, left lateral decubitus position, and for a period of time in the trendelenburg and reverse trendelenburg positions. Afterward, the chest tube should be unclamped and the residual fluid allowed to drain. This may be repeated a day or two later if high output continues. 
Surgical therapy: Thoracic duct ligation
Lampson first demonstrated that chylothorax could be controlled by ligation of the thoracic duct.  Preoperative administration of lipophilic dye (e.g., Evans blue or cream) helps to locate the site of lymphatic leakage during the procedure. The thoracic duct is identified, isolated, and ligated just above the aortic hiatus between T-8 and T-12,  via a thoracotomy. Alternatively, an abdominal approach to ligate the thoracic duct is recommended, where a thoracic approach is not feasible.  Others have described a posterior extrapleural approach for ligation of the thoracic duct.  Even video-assisted thoracoscopic ligation is an option in bigger children and adults. 
The pleuroperitoneal shunt has also been successfully used to manage persistent pleural drainage following open-heart surgery.  The shunt consists of pleural and peritoneal catheters connected to a manual pumping chamber capable of handling viscous fluid such as chyle. The system contains a one-way valve that allows drainage from the pleura into the peritoneal cavity where the fluid is absorbed. This prevents further loss of chyle and thus reduces the need for TPN.  Occlusion of the shunt occurs by fibrinous debris in 10% and needs replacement. 
Fluoroscopic percutaneous embolization of the thoracic duct
This is a minimally invasive alternative to open surgical ligation of the thoracic duct. Pedal lymphography is performed to opacify the lymphatic duct, for a puncture transabdominally. ,, Once access is obtained, a small catheter (3 - 4 Fr) is used and the contrast is injected to opacify the thoracic duct and collateral branches. Various coils and/or glue are used to occlude the thoracic duct. The success rate is variable, ranging from 45 to 100%. ,
Another approach is to create a diaphragmatic fenestration for resistant chylothorax. , In our experience with two patients aged 5 and 12 years, we found that after thoracotomy, there was a diffuse ooze from the pleural surface rather than a localized leak, which meant that thoracic duct ligation in itself would be inadequate. In these patients, after breaking all loculi and adhesions, a 4 cm Χ 3 cm opening was made in the dome of diaphragm. An appropriately sized patch (polypropylene mesh in the first patient and a polytetrafluoroethylene patch with multiple 4 mm holes in the second patient) was chosen and sutured to the margins of the defect in the diaphragm. In both these patients, the chest tubes were removed on the seventh and fourth day, respectively. This procedure may therefore be a useful adjunct to thoracic duct ligation in managing these patients, when conventional modes of therapy have failed.
Persistent pleural effusions and chylothorax are multifactorial and are a significant cause of postoperative morbidity following open-heart surgery in children. It is important to diagnose them early and institute aggressive measures in the early postoperative period to achieve a satisfactory outcome. Management of persistent chylothorax can be particularly challenging, and at times, frustrating.
|1||Labidi M, Baillot R, Dionne B, Lacasse Y, Maltais F, Boulet LP. Pleural effusions following cardiac surgery: Prevalence, risk factors, and clinical features. Chest 2009;136:1604-11.|
|2||Bocsi J, Hambsch J, Osmancik P, Schneider P, Valet G, Tarnok A. Preoperative prediction of pediatric patients with effusions and edema following cardiopulmonary bypass surgery by serological and routine laboratory data. Crit Care 2002;6:226-33.|
|3||O'Callaghan C, Cooke J, Kerr IH, Shinebourne EA. Subpulmonary pleural effusions in children after cardiac surgery. Br Heart J 1985;54:593-5.|
|4||Airan B, Sharma R, Choudhary SK, Mohanty SR, Bhan A, Chowdhari UK, et al. Univentricular repair: Is routine fenestration justified? Ann Thorac Surg 2000;69:1900-6.|
|5||Milonakis M, Chatzis AC, Giannopoulos NM, Contrafouris C, Bobos D, Kirvassilis GV, et al. Etiology and management of chylothorax following pediatric heart surgery. J Card Surg 2009;24:369-73.|
|6||Gupta A, Daggett C, Behera S, Ferraro M, Wells W, Starnes V. Risk factors for persistent pleural effusions after the extracardiac Fontan procedure. J Thorac Cardiovasc Surg 2004;127:1664-9.|
|7||Yun TJ, Im YM, Jung SH, Jhang WK, Park JJ, Seo DM, et al. Pulmonary vascular compliance and pleural effusion duration after the Fontan procedure. Int J Cardiol 2009;133:55-61.|
|8||Liang CM, Hwang B, Lu JH, Lee PC, Weng ZC, Ho TY, et al. Risk factors for prolonged postoperative pleural effusion after repair of tetalogy of Fallot. J Chin Med Assoc 2005;68:406-10.|
|9||Mainwaring RD, Lamberti JJ, Carter TL Jr, Moore JW, Nelson JC. Renin, angiotensin II, and the development of effusions following bidirectional Glenn and Fontan procedures. J Card Surg 1995;10:111-8.|
|10||Vaynblat M, Chiavarelli M, Anderson JE, Rao S, Nudel DB, Cunningham JN Jr. Pleural drainage after repair of tetralogy of Fallot. J Card Surg 1997;12:71-6.|
|11||Virmani R, Roberts WC. Pulmonary arteries in congenital heart disease: A structure-function analysis. Adult Congenital Heart Disease. In: Roberts WC, editor. Philadelphia: FA Davis; 1987. p. 77-130.|
|12||Biondi JW, Schulman DS, Wiedemann HP, Matthay RA. Mechanical heart-lung interaction in an adult respiratory distress syndrome. Clin Chest Med 1990;11:691-714.|
|13||Talwar S, Agarwala S, Mittal CM, Choudhary SK, Airan B. Diaphragmatic palsy after cardiac surgical procedures in patients with congenital heart disease. Ann Pediatr Cardiol 2010. in press.|
|14||Piccoli M, Trambaiolo P, Salustri A, Cerquetani E, Posteraro A, Pastena G, et al. Bedside diagnosis and follow-up of patients with pleural effusion by a hand-carried ultrasound device early after cardiac surgery. Chest 2005;128:3413-20.|
|15||Heffner JE, Brown LK, Barbieri CA. Diagnostic value of tests that discriminate between exudative and transudative pleural effusions. Primary Study Investigators. Chest 1997;111:970-80.|
|16||Ghaferi AA, Hutchins GM. Progression of liver pathology in patients undergoing the Fontan procedure: Chronic passive congestion, cardiac cirrhosis, hepatic adenoma, and hepatocellular carcinoma. J Thorac Cardiovasc Surg 2005;129:1348-52.|
|17||Mertens L, Hagler DJ, Sauer U, Somerville J, Gewillig M. Protein-losing enteropathy after the Fontan operation: An international multicentre study. PLE study group. J Thorac Cardiovasc Surg 1998;115:1063-73.|
|18||Colice GL, Curtis A, Deslauriers J, Heffner J, Light R, Littenberg B, et al. Medical and surgical treatment of parapneumonic effusions: An evidence-based guideline. Chest 2000;118:1158-71.|
|19||Stelzner TJ, King TE Jr, Antony VB, Sahn SA. The pleuropulmonary manifestations of the postcardiac injury syndrome. Chest 1983;84:383-7.|
|20|| Kim S, Sahn SA. Postcardiac injury syndrome. An immunologic pleural fluid analysis. Chest 1996;109:570-2.|
|21||Hiraki A, Aoe K, Eda R, Maeda T, Murakami T, Sugi K, et al. Comparison of six biological markers for the diagnosis of tuberculous pleuritis. Chest 2004;125:987-9.|
|22||Nair SK, Petko M, Hayward MP. Aetiology and management of chylothorax in adults. Eur J Cardiothorac Surg 2007;32:362-9. |
|23||Hillerdal G. Chylothorax and pseudochylothorax. Eur Respir J 1997;10:1157-62.|
|24||Hamm H, Pfalzer B, Fabel H. Lipoprotein analysis in a chyliform pleural effusion: Implications for pathogenesis and diagnosis. Respiration 1991;58:294-300.|
|25||Chaturvedi V, Saxena A. Heart failure in children: Clinical aspect and management. Indian J Pediatr 2009;76:195-205.|
|26||Cerfolio RJ, Allen MS, Deschamps C, Trastek VF, Pairolero PC. Post-operative chylothorax. J Thorac Cardiovasc Surg 1996;112:1361-5; discussion 1365-6.|
|27||Selle JG, Snyder WH 3 rd , Schreiber JT. Chylothorax: Indication for surgery. Ann Surg 1973;177:245-9.|
|28||Ulibarri JI, Sanz Y, Fuentes C, Mancha A, Aramendia M, Sanchez S. Reduction of lymphorrhagia from ruptured thoracic duct by somatostatin. Lancet 1990;336:258.|
|29||Helin RD, Angeles ST, Bhat R. Octreotide therapy for chylothorax in infants and children: A brief review. Pediatr Crit Care Med 2006;7:576-9.|
|30|| Schafers SJ, Dresler CM. Update on talc, bleomycin, and the tetracyclines in the treatment of malignant pleural effusions. Pharmacotherapy 1995;15:228-35.|
|31||Zimmer PW, Hill M, Casey K, Harvey E, Low DE. Prospective randomized trial of talc slurry vs bleomycin in pleurodesis for symptomatic malignant pleural effusions. Chest 1997;112:430-4. |
|32||Antony VB. Pathogenesis of malignant pleural effusions and talc pleurodesis. Pneumologie 1999;53:493-8.|
|33||Hartman DL, Gaither JM, Kesler KA, Mylet DM, Brown JW, Mathur PN. Comparison of insufflated talc under thoracoscopic guidance with standard tetracycline and bleomycin pleurodesis for control of malignant pleural effusions. J Thorac Cadiovasc Surg 1993;105:743-7; discussion 747-8.|
|34||Kennedy L, Rusch VW, Strange C, Ginsberg RJ, Sahn SA. Pleurodesis using talc slurry. Chest 1994;106:342-6.|
|35||Martinez Moragon E, Aparicio Urtasun J, Sanchis Aldas J, Fullana Monllor J, Sanchis Moret F, Montalar Salcedo J, et al. Tetracycline pleurodesis for treatment of malignant pleural effusions. Retrospective study of 91 cases. Med Clin (Barc) 1993;101:201-4. |
|36||Herrington JD, Gora-Harper ML, Salley RK. Chemical pleurodesis with doxycycline 1 g. Pharmacotherapy 1996;16:280-5.|
|37||Prevost A, Nazeyrollas P, Milosevic D, Fernandez-Valoni A. Malignant pleural effusions treated with high dose intrapleural doxycycline: Clinical efficacy and tolerance. Oncol Rep 1998;5:363-6.|
|38||Ong KC, Indumathi V, Raghuram J, Ong YY. A comparative study of pleurodesis using talc slurry and bleomycin in the management of malignant pleural effusions. Respirology 2000;5:99-103.|
|39||Putnam JB Jr. Malignant pleural effusions. Surg Clin North Am 2002;82:867-83.|
|40||Lampson RS. Traumatic chylothorax; a review of literature and report of a case treated by mediastinal ligation of thoracic duct. J Thorac Surg 1948;17:778-91.|
|41||Ross JK. A review of surgery of the thoracic duct. Thorax 1961;16:12-21.|
|42||Mason PF, Thorpe JA. Chylothorax: A new surgical strategy. Chest 1993;103:1929.|
|43||Di F, Kun L, Su CQ. Ligation of the thoracic duct without thoracotomy for treatment of postoperative chylothorax: A newly designed surgical procedure. J R Coll Surg Edinb 1995;40:60-1.|
|44||Graham DD, McGahren ED, Tribble CG, Daniel TM, Rodgers BM. Use of video-assisted thoracic surgery in the treatment of chylothorax. Ann Thorac Surg 1994;57:1507-11; discussion 1511-2.|
|45||Milsom JW, Kron IL, Rheuban KS, Rodgers BM. Chylothorax: An assessment of current surgical management. J Thorac Cardiovasc Surg 1985;89:221-7.|
|46||Cummings SP, Wyatt DA, Baker JW, Flanagan TL, Spotnitz WD, Rodgers BM, et al. Successful treatment of postoperative chylothorax using an external pleuroperitoneal shunt. Ann Thorac Surg 1992;54:276-8.|
|47||Rheuban KS, Kron IL, Carpenter MA, Gutgesell HP, Rodgers BM. Pleuroperitoneal shunts for refractive chylothorax after operation for congenital heart disease. Ann Thorac Surg 1992;53:85-7.|
|48||Cope C, Kaiser LR. Management of unremitting chylothorax by percutaneous embolization and blockage of retroperitoneal lymphatic vessels in 42 patients. J Vasc Interv Radiol 2002;13:1139-48.|
|49||Hoffer EK, Bloch RD, Mulligan MS, Borsa JJ, Fontaine AB. Treatment of chylothorax: Percutaneous catheterization and embolisation of the thoracic duct. AJR Am J Roentgenol 2001;176:1040-2.|
|50||Cope C. Management of chylothorax via percutaneous embolization. Curr Opin Pulm Med 2004;10:311-4.|
|51||Talwar S, Choudhary SK, Airan B. Diaphragmatic fenestration for resistant chylothorax. Ann Thorac Surg 2006;82:767-8.|
|52||Durairaj M, Sharma R, Choudhary SK, Bhan A, Venugopal P. Diaphragmatic fenestration for resistant pleural effusions after univentricular repair. Ann Thorac Surg 2002;74:931-2.|