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Disorders of the Pleura |

Intractable Pleural Effusions Associated With Upper Extremity Deep Vein Thrombosis in a Patient With Advanced Lung Cancer FREE TO VIEW

Kosuke Tsuruno, MD; Kazunori Tobino, MD
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Iizuka Hospital, Iizuka, Japan


Chest. 2015;148(4_MeetingAbstracts):430A. doi:10.1378/chest.2279647
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Abstract

SESSION TITLE: Disorders of the Pleura Global Case Reports

SESSION TYPE: Global Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: Pleural effusion in patients with lung cancer is mostly induced by cancerous dissemination to pleura, superior vena cava syndrome and heart failure. We report here a novel cause of intractable pleural effusion attributed to upper extremity deep vein thrombosis (UEDVT) in a patient with lung cancer.

CASE PRESENTATION: A 62-year-old woman presented to our hospital with shortness of breath and bilateral upper extremity edema. She had been diagnosed with stage IV lung cancer (adenocarcinoma) with bilateral malignant pleural effusion and metastasis to the lung, cervical lymph node, brain, and bone, one year prior. Genetic analysis of the cells from pleural effusion revealed an epidermal growth factor receptor (EGFR) point mutation at exon 21 (L858R), and she was receiving gefitinib treatment for three months. During the treatment, the lung cancer and metastatic lesions were markedly reduced, however, bilateral pleural effusions remained. Her past medical history was otherwise remarkable for uterus myoma. She had a 40 pack-year history of smoking. The vital signs were as follows: heart rate, 85 beats per minute; blood pressure 110/60 mmHg; temperature, 37.4 ℃; respiratory rate, 24 breaths per minute and oxygen saturation, 94 % on room air. Physical examination revealed edema of bilateral upper extremities, neck, and front part of the chest. Both sides of thorax were dull to percussion with decreased breath sounds. Chest X-ray revealed massive bilateral effusions, larger on the right. Thoracentesis of pleural effusion on both sides was performed, and pleural fluid analysis revealed a lymphocytic predominant transudate with negative cytological and microbiological studies. An echocardiography was normal and laboratory results showed a normal blood cell count, electrolytes, kidney and liver function. Plasma thyroid-stimulating hormone and free thyroxin were normal. Contrast-enhanced CT scan revealed thrombosis of the left brachiocephalic and subclavian vein. It was thought that the occluded lymphatic flow in the left venous angle probably contributed to the development of pleural fluid. She required eight more thoracentesis, each at four days interval for the recurrence of large pleural effusion, and on each occasion 1500 ml of transudative fluid containing no malignant cells was removed. Although the general condition of the patient was relatively good, her QOL was decreased for repeated thoracentesis. With this background, we decided to place a pleuroperitoneal shunt (Denver Shunt®, Denver Biomedical Inc, Denver, CO). After the placement of pleuroperitoneal shunt, pleural effusion was improved and the patient became symptom free. No further therapeutic intervention for pleural effusion was required for two months until death, and there were no problems with the pleuroperitoneal shunt during the course.

DISCUSSION: Malignant pleural effusion is commonly seen in patients with lung cancer. There are, however, a number of lung cancer patients in whom identifyfing the aetiology of pleural effusion remains elusive in spite of systematic and repeated testing. The patient’s pleural fluid one year prior was due to malignant pleuritis, however, the pleural fluid at this admission was lymphocytic predominant transudate with negative cytology. This patient had no signs of heart failure, liver or kidney dysfunction, and hypothyroidism. We considered that the thrombotic occlusion of left venous angle led to impairment in lymphatic return, increase in thoracic duct pressure, and finally, accumulation of transudate pleural effusion. Several reports described some patients with massive pleural effusion due to catheter associated severe stenosis of upper extremity deep vein. These reports support our hypothesis, however, to our knowledge, there were no prior reports describing pleural effusion attributed to UEDVT in patients with lung cancer.

CONCLUSIONS: It should be further kept in mind that UEDVT might lead to intractable pleural effusion caused by increase in thoracic duct pressure secondary to the occlusion of venous angle.

Reference #1: Hylton V. et al. Upper−extremity deep vein thrombosis a prospective registry of 592 patients. Circulation 2004;110:1605-1611.

Reference #2: Reha E. et al. Internal jugular vein thrombosis two different etiology. Eur J Gen Med 2005;2(3):123-128.

Reference #3: Enrique M. et al. Unilateral pleural effusions associated with stenosis of left brachiocephalic vein in haemodialysis patients. Nephrol Dial Transplant 2005;20:1257-1259.

DISCLOSURE: The following authors have nothing to disclose: Kosuke Tsuruno, Kazunori Tobino

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