Asian Cardiovasc Thorac Ann 2003;11:70-71
© 2003 Asia Publishing EXchange Ltd
Conservative Management of Persistent Pleural Effusion Using Somatostatin
Kiyoshi Haneda, MD,
Yoshimi Shoji, MD,
Tsunenori Katakura, MD1,
Shuichiro Abe, MD2,
Yuki Ogata,
Michio Makabe, MD1
Department of Cardiovascular Surgery
1 Department of Internal Medicine
2 Department of Radiology, Makabe Hospital, Yamoto, Miyagi, Japan
For reprint information contact: Kiyoshi Haneda, MD Tel: 81 225 82 7111 Fax: 81 225 82 7149 email: khaneda{at}itokukai.or.jp Department of Cardiovascular Surgery, Makabe Hospital, 109-4 Shishiishimae, Yamoto, Miyagi 981-0503, Japan.
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ABSTRACT
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Persistent pleural effusion developed in an 81-year-old man with acute pulmonary edema due to myocardial dysfunction. Daily chest tube drainage was 1,000 to 1,400 mL. Despite total parenteral nutrition and albumin supplementation, drainage did not decrease. However, continuous infusion of a somatostatin analog was effective in controlling the effusion.
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INTRODUCTION
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Pleural effusion is a common clinical finding in cardiovascular diseases and cardiothoracic surgery, including congestive heart failure, post-myocardial infarction syndrome, and pericardial disease. Although the morbidity and mortality of patients with pleural effusion are directly related to the cause and the stage of the disease at the time of presentation, persistent effusion frequently causes complications and difficulties in patient management. Conservative treatment with total parenteral nutrition or a low-fat diet containing medium-chain triglycerides is usually tried before surgical treatment. Other methods, including pleurodesis and somatostatin infusion, have also been reported recently.1–5 Here we report a case of persistent pleural effusion where somatostatin therapy was effective.
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CASE REPORT
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An 81-year-old man was admitted in July 2001 for severe dyspnea with foamy and bloody sputum. His medical history included old myocardial infarction and gastric cancer, which was treated with subtotal gastrectomy in 1990. On admission, he was alert but was in cardiopulmonary failure with a respiratory rate above 30 min-1, arterial oxygen tension of 46.2 mm Hg, and arterial systolic pressure of 90 mm Hg. He was intubated and managed with mechanical ventilation under the diagnosis of pulmonary edema caused by myocardial dysfunction. Despite catecholamine administration (dopamine and dobutamine of 15 µg•kg-1•min-1 each), his arterial systolic pressure never exceeded 90 mm Hg, blood gas results did not improve, and urine was not discharged. To remove excess body fluid, continuous hemofiltration was initiated, which resulted in elevated arterial pressure, improvement in blood gas values, and urination.
Serum total protein and albumin levels were as low as 4.1 and 2.7 g•dL-1, respectively. Mild but continuous gastrointestinal bleeding mandated total parenteral nutrition. On the 16th day of admission, fluid accumulation in the left thoracic cavity necessitated drainage, which continued for the following 27 days. Respiratory support, including mechanical ventilation with positive end-expiratory pressure or continuous positive airway pressure, was discontinued on day 31. However, mechanical ventilation was restarted on day 37 because of respiratory failure due to massive fluid accumulation in the right chest. Pleural fluid of 1,000 to 1,400 mL was drained from the right chest tube daily. The serum protein level fell to between 3.4 and 3.6 g•dL-1, unresponsive to daily supplement of albumin. His renal function worsened progressively, with urinary output decreasing to 100 to 300 mL. Body fluid balance was maintained with continuous hemodialysis and hemofiltration. The fluid drained from the chest tube contained total protein and albumin of 0.8 and 0.5 g•dL-1, respectively, total cholesterol of 3 mg•dL-1, lactate dehydrogenase of 106 IU•L-1, but no triglycerides. It also contained 120 cells•µL-1, consisting of almost equal numbers of neutrophils and lymphocytes.
The patient’s condition progressively deteriorated with hypotension and oliguria. To control pleural effusion, continuous infusion of a somatostatin analog (octreotide, 40 µg•kg-1 per day) was initiated on day 59. Drainage gradually decreased to 300 mL over a period of 9 days (Figure 1
). Side effects of somatostatin were not observed. However, the patient died of cardiac and renal failure on day 67.
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DISCUSSION
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The most common cause of increased pleural fluid formation is interstitial edema in the lungs caused by left ventricular failure or adult respiratory distress syndrome. Other, less common mechanisms are elevated pressure in the parietal pleural capillaries, reduced pressure in the pleural space, impaired lymphatic drainage, elevated systemic venous pressure, and increased pleural permeability due to inflammation.6 Although the effusion in our patient was not characteristic of chyle, the lymphatic system in the pleural cavity, including the thoracic duct, was very likely damaged by the elevated systemic venous pressure. Total parenteral nutrition in this patient might have led to chylous fluid not being produced.
Treatment of pleural effusion by pleurodesis using OK-432 (picibanil) with or without minocycline has been reported in cases of esophageal carcinoma and lung cancer,1,2 while continuous infusion of a somatostatin analog has been applied in persistent pleural effusion.3–5 Somatostatin is a peptide that acts as a neurohormone as well as a paracrine agent. It has been suggested that it can reduce chyle flow. Although its mechanism remains to be identified, its effectiveness in treating thoracic duct injuries has been shown experimentally.7 Somatostatin is believed to reduce hepatic, splanchnic, and portal blood flow, as well as inhibit pancreatic secretion, gallbladder contraction, intestinal motility, glucose and amino acid absorption, and gastrointestinal peptide hormone secretion.7 Lymphatic vessels have somatostatin receptors, thus constriction of the vessels with somatostatin may reduce lymph production.5 In our case, continuous somatostatin infusion remarkably reduced pleural fluid formation by about 75%, although the patient later died. Conservative treatment using somatostatin is thus useful for persistent pleural effusion.
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REFERENCES
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- Nishi H, Nakahara M, Ogino N, Nakao K, Lee CM, Tsujimato M. A case of chylothorax following resection of esophageal carcinoma — successful treatment by pleurodesis with OK-432 and minocycline. Jpn J Gastroenterol Surg
1999;32:1203–7.
- Koga Y, Mita Y, Dobashi K, Masuo T, Aihara M, Shimizu Y, et al. Lung cancer with chylothorax successfully treated by chemical pleurodesis with OK-432 [Japanese]. Nihon Kokyuki Gakkai Zasshi
1999;37:627–30.[Medline]
- Rimensberger PC, Müller-Schenker B, Kalangos A, Beghetti M. Treatment of a persistent postoperative chylothorax with somatostatin. Ann Thorac Surg
1998;66:253–4.[Abstract/Free Full Text]
- Kelly RF, Shumway SJ. Conservative management of postoperative chylothorax using somatostatin. Ann Thorac Surg
2000;69:1944–5.[Abstract/Free Full Text]
- Buettiker V, Hug MI, Burger R, Baenziger O. Somatostatin: a new therapeutic option for the treatment of chylothorax. Intensive Care Med
2001;27:1083–6.[Medline]
- Johnson JL. Pleural effusions in cardiovascular disease. Pearls for correlating the evidence with the cause. Postgrad Med
2000;107:95–101.
- Markham KM, Glover JL, Welsh RJ, Lucas RJ, Bendick PJ. Octreotide in the treatment of thoracic duct injuries. Am Surg
2000;66:1165–7.[Medline]
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ABSTRACT
INTRODUCTION
