Case Reports Ascites and Right Pleural Effusion: Demonstration of a Pentoneo-Pleural Communication Jean Verreault, Serge Lepage, Guy Bisson, and Andre Plante Departments ofNuc/ear Medicine and Internal Medicine, Centre Hospitalier Universitaire, University ofSherbrooke, Sherbrooke, Québec,Canada A 54-yr-oldfemale with known livercirrhosis presented with a right transudative pleural effusion and ascites. To findthe source of pleural fluid,[@“TcJsuIfurcolloidwas injected intraperitoneallyand a serial imagingstudy revealed its passage to the right pleural space on 2-hr and 24-hr images. Mechanisms proposed in the formation of pleural effusion in liver cirrhosis are (a) lymphatic drainage and (b) diaphragmatic defect. Radioisotope migration speed may be a clue for differentiating these two mechanisms, being more rapid in the presence of a diaphragmatic defect. J NucIMed 27:1706—1709,1986 leural effusions occur in 5% to 10% of patients with cluded enlarged liver and evidence of free liquid in the pen cirrhosis of the liver (1 ). In these patients, ascites is toneal cavity. usually evident but a pleural effusion may develop in a The chest x-ray demonstrated a large right pleural effusion. cirrhotic patient in the absence ofdetectable ascites (2). Other laboratory tests were compatible with liver cirrhosis and The effusions are usually right-sided, but may be bilat toxic effects ofalcohol. Thoracentesis revealed a fluid that had the characteristics ofa transudate as did a sample of pentoneal eral or left-sided. The precise mechanism of fluid ac fluid. Forty-eight hours after the thoracentesis of 1,800 cc, the cumulation is not clear. right pleural space was completely refilled (Fig. 1). We describe a case where a peritoneopleural com To prove that right pleural effusion was related to ascites, munication has been demonstrated by radioisotopic 5 mCi of technetium-99m (@mTc) sulfur colloid was injected method. The possible mechanisms involved in the for with aseptic technique into the right lower abdominal cavity. mation of pleural effusion in liver cirrhosis are dis A serial imaging study was done in anterior view at intervals cussed. of 5 mm for 30 mm and at 2 and 24 hr postinjection (Fig. 2). Images were obtained on a large field-of-view camera with an all-purpose, parallel collimator. At 2 hr the radiocolloid ap CASE REPORT peared in the right hemithorax and at 24 hr activity was further increased. It confirmed the presence of a peritoneo A 54-yr-old white female was admitted for progressive pleural communication. The patient responded well to medi dyspnea of recent onset and signs of upper respiratory infec cal therapy and pleural effusion resolvedcompletely in 10 tion. Her past history included a background of considerable days. alcohol ingestion, and a diagnosis of Laennec cirrhosis had been previously made by liver biopsy. On admission, the patient looked chronically ill. She was DISCUSSION afebrile with regular pulse rate of 120/mm and a blood pres sure of 180/100. There were clinical signs of cirrhosis and The association ofhydrothorax with hepatic cirrhosis frank jaundice. Chest examination revealed evidence for a has been recognized for many years but there has been massive right pleural effusion. Other physical findings in much speculation as to its origin. In 1947, Higgins and his colleagues suggested that pleural effusion was related to the fall in the concentra ReceivedDec. 13, 1985;revision accepted Apr. 23, 1986. For reprints contact: Jean Verreault, MD, Dept. of Nuclear tion of plasma proteins (3). In 1958, Morrow, Kantor Medicine,Centre Hospitalier Universitaire, Sherbrooke, Québec, and Armen suggested that the fluid might come from Canada, J 1H-5N4. the blood stream as a result of hypoalbuminemia or 1706 Verreault,Lepage,Bissonetal The Journal of Nuclear Medicine bumin from the peritoneal to pleural spaces in a patient with right hepatic hydrothorax. The autopsy showed no gross defect in the right diaphragm. Since lymphatics are more abundant in the right than £ in the left diaphragm (10), this mechanism might ex plain that hepatic hydrothorax are more frequently right sided. In addition to this, Leak (11) used electron microscopy to show that pores of 4—12 @zin diameter exist between mesothelial cells and diaphragmatic lym phatics. They provide a system of open channels through which fluids and cells may rapidly be removed from the serous cavities. What remains unclear is how and why the fluid leaves the lymphatic system and enters the pleural space instead ofbeing expelled toward the larger collecting vessels. It may result from lym phatic system overload (12). There is strong evidence to support the two mech 4 anisms. We think that each of these can explain the formation of hydrothorax from ascites depending on the case. Lymphatic drainage is probably the first mech anism to occur in reaction to the presence of ascites. It can be the way by which hydrothorax will be formed if there is an overload of the lymphatic system. If it is I insufficient, the abdominal pressure increases and may FIGURE 1 cause subsequent rupture ofthe diaphragm. One objec Chest x-ray showing large right pleuraleffusion tion to this assumption may be that pleural effusions can be present in liver cirrhosis without ascites. In these hypertension in the azygous and hemiazygous systems cases, the alternative explanation is that there is con or be secondary to ascites either by direct passage of genital diaphragmatic weakness caused by an insuffi fluid through a diaphragmatic defect or by its transport dent deposition of muscle and tendon bundles. We through the diaphragmatic lymphatics (4). proposed that the clue to distinguish between these two Hypoproteinemia as a sole cause can be eliminated mechanisms may be the use of radioisotope injected for there are many patients, cirrhotic or not, who have intraperitoneally as we did. low serum protein levels but never develop hydrothorax Indeed, when we assume that the radiocolloid in (5). Ifazygous hypertension is present due to collaterals jected intrapentoneally is mixed with ascites fluid and between this system and the portal system, transudation consider that its migration from peritoneal to pleural of fluid into the chest might appear. However, this space was right sided as was the pleural effusion, we cannot explain hydrothorax occurring in Meigs' syn can presume that there is a relationship between ascites drome where there is no portal hypertension. The most fluid and pleural effusion. Furthermore, our proposal probable explanation is that hydrothorax is derived extends to the time required to show accumulation of directly from the peritoneal fluid either through a defect the agent in the pleural space. If it happens within a in the diaphragm or through the lymphatic channels few minutes, as it was reported by Faiyaz and Goyal that penetrate it. (13), a diaphragmatic defect is probably present partic At least three studies (6—8)have provided evidence ularly when the accumulation is as intense as peritoneal that hydrothorax complicating cirrhosis is generated activity. If it takes a longer period of time as was seen from ascites through a diaphragmatic defect acquired for our patient, the peritoneopleural communication as a result of increased intra-abdominal pressure. This may be attributed to diaphragmatic lymphatics partic has been demonstrated either by rapid passage of dye ularly when that accumulation is less intense than per from the ascites into the pleural effusion, induction of itoneal activity. a hydropneumothorax by the intra-abdominal instilla Such a study can be done either by the use of[@mTc1 tion of oxygen, thoracoscopy, or by necropsy findings. sulfur colloid or [99mTc]macroaW@ted albumin. The The other mechanism proposed in literature is that radiopharmaceutical can be injected intraperitoneally peritoneal fluid passes to the pleural space through the at the end of the usual diagnostic or therapeutic peri diaphragmatic lymphatics. Johnston and Rodolfo (9) toneal puncture. It can show the source of pleural support it by the demonstration of unidirectional trans effusions in liver cirrhosis and also in patients with port of carbon particles and radioiodinated serum al peritoneal dialysis (14). We postulate that the speed at Volume27 •Number 11 •November1986 1707 @ ,)s 2@:@. %1@i;@@• @ ... •@:, @ N IPPLE : :@,@‘&@@-4' • @ . .. • • @ LINE . • I @ . @: . @ ...@ .@. @ e . 1. ‘@ ‘ .‘—.@: : ‘.@.: _k@ .;@ ). r'@ @.,. @ —@ .. @. @h@i: @ • @ .,•;@; •@‘‘;!‘@@: £@•@ . ,,‘@ A B . @ S. S .@: @ @-1 C D @::@ FIGURE 2 Serial anterior imagingstudy of abdomen and thorax. A: 5 mm, B: 30 mm, C: 2 hr. D:24 hr after intraperitoneal injection of [@‘TcJsuffurcolloid.Migrationof radioisotope is seen on 2 hr (C)and 24 hr (D)images which the radioisotope migrates from peritoneal to ACKNOWLEDGMENT pleural space may be a clue for differentiation between The authors thank Mrs. LiseCôtéfor her excellentsecre the two pathophysiological mechanisms proposed in tanal assistance. the literature. Such a differentiation may influence the patient's treatment. If transit time is rapid, a macro scopic diaphragmatic defect could be sought. If transit REFERENCES is slow, only medical treatment has to be contemplated. 1. Brody iS: Diseases of the pleura, mediastinum, dia phragm and chest wall. In Cecil TextbookofMedicine, Vol. 1, Wyngaarden and Smith, Philadelphia, Saun ders,1982,p 423 FOOTNOTE 2. Singer JA, Kaplan MM, Katz RL: Cirrhotic pleural effusion in the absence of ascites. Gastroenterology . Picker International, Highland Heights, OH. 73:575—577,1977 1708 Verreauft,Lepage,Bissonetal The Journal of Nudear Medicine 3. Higgins G, Kelsall AR, O'Brien JR. et al: Ascites in 9. Johnston RF, Loo RV: Hepatic hydrothorax: Studies chronic diseases of the liver. QJ Med 16:263—274, to determine the source offluid and report of thirteen 1947 cases.Ann InternMed 61:385—401,I964 4. Morrow CS, Kantor M, Armen RN: Hepatic hydro 10.