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Ann Thorac Surg 2002;73:977-979
© 2002 The Society of Thoracic Surgeons

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Case report

Treatment of persistent chylothorax after Norwood procedure with somatostatin

^a Division of Pediatric Cardiothoracic Surgery, Louisiana State University, New Orleans, Louisiana, USA

Accepted for publication May 28, 2001.

* Address reprint requests to Dr Pettitt, Division of Cardiothoracic Surgery, Children’s Hospital, 200 Henry Clay Ave, New Orleans, LA 70118, USA
e-mail: twpettitt{at}aol.com

	Abstract

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A newborn who had undergone Norwood procedure for hypoplastic left heart syndrome developed a voluminous chylothorax that persisted despite weeks of prolonged complete bowel rest, total parenteral nutrition, and effective chest tube drainage. Chest tube output diminished immediately following initiation of intravenous somatostatin, allowing restoration of full enteral feeds and removal of chest tubes within 6 days.

	Introduction

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Postoperative chylothorax can be a morbid and often frustrating complication in infants and children with congenital heart disease. The majority of these patients respond to conservative therapy including bowel rest, total parenteral nutrition, fluid restriction, diuresis, and the gradual reintroduction of fats to their diet. Employing such a conservative approach has enabled us to avoid surgical intervention in the majority of cases; however, weeks may pass before enteral feeds can be resumed. Neonates who develop chylothoraces following cardiac operations have limited reserves and are at increased risk of developing life-threatening complications such as lymphocytopenia, hypoproteinemia, and serious electrolyte and acid-base disturbances. The need for long-term central venous access in the presence of a depressed immune system puts them at risk for sepsis. Aggressive fluid restriction and diuresis may not be well tolerated, and renal failure may ensue. In order to eliminate these adverse effects, intravenous somatostatin has been recently suggested as a new modality for treatment of postoperative chylothorax. We report our experience with a newborn following Norwood procedure who developed a persistent chylothorax that was unresponsive to conservative treatment.

A 37-week gestational age newborn boy, weighing 3.25 kg, was diagnosed with hypoplastic left heart syndrome at birth by echocardiography. Findings included mitral and aortic atresia, a hypoplastic ascending aorta, and an atrial septal defect. The pulmonary veins appeared more dilated than usual, and the atrial septal defect was restrictive (V_max 2.5 m/s); however, the patient was stable on room air, with good perfusion and clear lung fields on roentgenogram.

A Norwood procedure was performed on day 8, initially using a 3.5-mm right-modified Blalock-Taussig shunt (Gore-Tex, W. L. Gore & Associates, Flagstaff, AZ). The child could not be weaned off cardiopulmonary bypass because of unacceptably low arterial oxygen saturations. The shunt was replaced with a 4-mm graft, and the patient was weaned from bypass. Although he required nitric oxide and 100% oxygen to come off bypass, he was weaned of these rapidly as the pulmonary circulation improved during the early postoperative period. During the next several days he demonstrated transient episodes of pulmonary overcirculation associated with decreased systemic perfusion and mild metabolic acidosis. These were managed by a combination of afterload reduction and subambient fractions of inspired oxygen. The patient underwent delayed sternal closure on postoperative day 9 and remained hemodynamically stable.

Clear liquids through a nasojejunal tube were begun on postoperative day 11 and slowly advanced to full-strength Portagen (Mead Johnson and Company, Evansville, IN). Mediastinal and pleural drainage averaged approximately 100 mL/d; however, it tripled as soon as enteral feeds were begun, necessitating their discontinuation (Fig 1). Most of the drainage was from the right pleural chest tube, but the right pleural cavity and mediastinum were in continuity through a breach in the pleura. We were not aware of any obvious injury to any major lymphatic structures during the procedure that would explain this voluminous chylothorax. For the next 2 weeks the patient’s chest tube output averaged 200 mL/d, and his serum protein levels remained low despite total parenteral nutrition and frequent infusions of albumin and fresh frozen plasma. The patient had a mild, persistent acidemia that was thought to be secondary to bicarbonate losses from the chest drainage. Serial Doppler echocardiography showed normal cardiac function with minimal atrioventricular valve regurgitation. The aortic arch and the systemic and pulmonary veins appeared to be unobstructed.

View larger version (19K): [in this window] [in a new window]   Fig 1. Daily chest tube drainage following Norwood procedure. Chest tube drainage increased dramatically following initiation of enteral feeds (closed arrow) and remained high despite complete bowel rest. Chest drainage decreased dramatically following initiation of intravenous somatostatin every 12 hours for 3 days (open arrow). Chest tube output remained low after resuming enteral feeds following somatostatin therapy (dashed arrow).

	Comment

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Postoperative chylothorax in newborns with congenital heart disease is a major complication that requires prolonged hospitalization and that may jeopardize the surgical outcome. The etiology of chylothorax formation in children following operations for congenital heart disease cannot be simply explained by injury to the main thoracic duct, especially because most procedures are done through a median sternotomy. However, extensive mediastinal dissection, which is often required, may disrupt microscopic lymphatic channels, which in the presence of some degree of "lymphatic hypertension" is the most likely substrate for chylothorax formation. In our experience, patients at the greatest risk of developing chylothorax are those with single ventricle physiology or significant right-sided dysfunction. Patients with cavopulmonary connections may have residual systemic venous hypertension, which, when transmitted to the lymphatic system, may promote chylothorax formation. Similarly, patients undergoing repair of tetralogy of Fallot complicated by right-sided dysfunction would also be expected to have some degree of systemic venous hypertension. Pulmonary vascular congestion, from either overcirculation or pulmonary venous obstruction (as was probably the case for the patient described in this report) could also predispose to lymphatic hypertension within the lung itself, contributing to chylothorax formation.

Conservative therapy for chylothorax focuses on reducing chyle formation. Eliminating fats from the diet will reduce the transport of triglycerides and chylomicrons in chyle, but it does not stop the continued absorption of fluid from the intestinal lacteals. Therefore, complete bowel rest would help prevent neurohormonal stimulation of digestive secretions. Somatostatin reduces gastric, pancreatic, and intestinal secretions. It also appears to reduce intestinal absorption and decrease hepatic venous pressure gradient and splanchnic blood flow [1]. Any of these mechanisms would be potentially beneficial in reducing chyle production.

There have been several anecdotal reports in the literature [2–4] of somatostatin being used for chylothorax complicating adult thoracic procedures. In each of these reports, the chylothorax was thought to be related to injury of the thoracic duct or major accessory lymphatic channels. The response to somatostatin was dramatic, allowing resumption of enteral feeds and removal of chest drains. What is even more intriguing is the seemingly long-lasting effect on chyle production by somatostatin in these case reports, even after it was discontinued. Whether the somatostatin permanently changed the lymph dynamics or the "leaks" simply sealed themselves during the period of reduced flow needs further study.

The use of somatostatin for chylothorax following an operation for congenital heart disease has been reported only once before, in a 4-month-old child with transposition of the great arteries who underwent a Senning procedure [5]. This patient was given somatostatin as a continuous, intravenous infusion (3.5 to 7 µg · kg^-1 · h^-1) for more than 14 days, during which time the chest tube drainage gradually stopped. Our patient, who was only 1 month old at the time of treatment, had a remarkable response to only 5 µg (1.6 µg/kg), given twice daily for a total of 3 days. Although somatostatin appears to be a safe drug to administer, caution needs to be used. We have tried using somatostatin in 2 other patients but discontinued it because of elevated liver function tests and vomiting in one and flulike symptoms in the other.

Early surgical intervention has been advocated for small babies with persistent chylothorax [6]. However, thoracic duct ligation, pleurodesis, or pleuroperitoneal shunt are not guaranteed to solve the problem. Further, they expose an already compromised patient to the risks of another operation. We have seen at least 1 patient with chylothorax develop a chyloperitoneum following thoracic duct ligation, which was just as debilitating. Admittedly, this case report represents just 1 patient with a relatively short follow-up period. However, it would appear that somatostatin may be a useful adjunct to conventional therapy for postoperative chylothorax, especially in small babies and neonates, who are at the greatest danger of succumbing to this serious complication, and may obviate the need for surgical reintervention.

	References

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1. Davis S.N., Granner D.K. Insulin, oral hypoglycemic agents, and the pharmacology of the endocrine pancreas. In: Gilman A.G., Hardman J.G., Limbird L.E., Molionoff P.B., Ruddon R.W., eds. Goodman and Gilman’s the pharmacological basis of therapeutics, 9th ed New York: Pergamon Press, 1996:1512-1513.
2. Ulibarri J.I., Sanz Y., Fuentes C., Mancha A., Aramendia M., Sanchez S. Reduction of lymphorrhagia from ruptured thoracic duct by somatostatin. Lancet 1990;335:258.[Medline]
3. Collard J.M., Laterre P.F., Boemer F., Reynaert M., Ponlot R. Conservative treatment of postsurgical lymphatic leaks with somatostatin-14. Chest 2000;117:902-905.[Abstract/Free Full Text]
4. Kelly R.F., Shumway S.J. Conservative management of postoperative chylothorax using somatostatin. Ann Thorac Surg 2000;69:1944-1945.[Abstract/Free Full Text]
5. Rimensberger P.C., Muller-Schenker B., Kalangos A., Beghetti M. Treatment of a persistent postoperative chylothorax with somatostatin. Ann Thorac Surg 1998;66:253-254.[Abstract/Free Full Text]
6. Azizkhan R.G., Canfield J., Alford B.A., Rodgers B.M. Pleuroperitoneal shunts in the management of neonatal chylothorax. J Pediatr Surg 1983;18:842-850.[Medline]

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Timothy W. Pettitt Joseph Caspi Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pettitt, T. W. Articles by Borne, A. Search for Related Content PubMed PubMed Citation Articles by Pettitt, T. W. Articles by Borne, A.