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  4. Clinical Research in Hepatic Hydrothorax
 
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Clinical Research in Hepatic Hydrothorax

Date Issued
2005
Date
2005
Author(s)
Huang, Pei-Ming  
DOI
zh-TW
URI
http://ntur.lib.ntu.edu.tw//handle/246246/55461
Abstract
Liver cirrhosis is an important medical research problem in Taiwan, because the prevalence rate is higher than in Western countries. The research on one of the complications of liver cirrhosis, hepatic hydrothorax, includes organ transplantation and diaphragmatic defects and surgical repair. Hepatic hydrothorax is a complex pathophysiological process. It includes multiple steps. Basically, under a long period of high-pressure stress, the diaphragm may produce some streak breaks. The peritoneum may progressively protrude into the pleural cavity and eventually produce blebs or fenestrations. They allow the ascites to communicate with the pleural cavity. These phenomenon, including oozing defects, blebs, or fenestration, may be directly or indirectly observed by means of imaging systems. These findings seem not only to occur in hepatic hydrothorax, occasionally, they have been reported in renal failure patients with continuous peritoneal dialysis. Therefore, the abdominal pressure plays an important role during the formation of diaphragmatic defects. In the model of simple blockade of the trans-diaphragmatic flow, treatment can be divided into medical or surgical management. However, the therapeutic effect of the former may be only attributed to the adhesion between the fully expanded pulmonary parenchyma and the diaphragm in blocking the trans-diaphragmatic flow. On the contrary, the latter, such as organ transplantation or the diaphragm repair model, should correct the underlying situation, including liver cirrhosis or repairing the diaphragmatic defects. In this study, we look at the role of surgical intervention. Part I Studies on the Pathophysiology of Hepatic Hydrothorax Several explanations for the development of hepatic hydrothorax have been proposed including hypoalbuminemia, hypertension of azygous vein, leakage from the thoracic duct, transdiaphragmatic lymphatic migration, and pressure gradient-directed flow through diaphragmatic defects. Thus, we should differentiate the theories. In order to solve this problem, we utilized the imaging modality of video-assisted thoracoscopy to detect the defects. According to the findings of this study, we established a further therapeutic method. The result and conclusion of the first part of the study is as follows: Results: The diaphragmatic defects stemming from the hepatic hydrothorax were classified into four morphologic types: type I: no obvious defect (one patient), type II: blebs lying on the diaphragm (four patients), type III: broken defects (fenestrations) in the diaphragm (eight patients), and type IV: multiple gaps in the diaphragm (one patient). The type of the diaphragmatic defect did not correlate with the volume occupied by the pleural effusion in the preoperative chest x-rays. Conclusion: The findings of this study allow the pathophysiology of hepatic hydrothorax to be directly visualized, and further studies concerning the treatment of hepatic hydrothorax may be based on these mechanisms. Part II Comparison and Setup of Various Modes of Intervention Based on the findings of the first part, the hepatic hydrothorax may be solved after blocking the diaphragmatic defects. Despite numerous case reports describing clinical features and treatments, the optimal management of this condition remains inconclusive. Liver transplantation is the treatment of choice, but the donor is rarely available. Other treatment options include repeated thoracentesis, pleurodesis, peritoneoveous shunts, transjugular intrahepatic portosystemic shunt, and surgical repair of the diaphragmatic leak. Several management techniques are considered as temporary relief of symptoms only, and sometimes result in adverse effects, because there are no available guidelines on therapy based on good evidence. Therefore, most patients receive either aggressive intervention or supportive care. The optimal management, however, remains unclear, and few previous studies have systematically evaluated the effect of therapy on clinical outcome. The aim of this study was to evaluate the impact of medical and surgical interventions on the survival of these patients at National Taiwan University Hospital over the past years. It proves the importance of the patients’ conditions during this process and the principle of surgical treatment. To create an appropriate surgical approach, it was necessary to solve the following issues: (1) The criteria of the surgical model in this study; (2) the duration of surgical intervention lessened to prevent complications; (3) avoiding hepatorenal syndrome, keeping a balance of input and output required in this group; and (4) liver cirrhosis treated perioperatively to decrease the possibility of bias. The results and conclusion of the second part of the study is as follows: Results: Hepatic hydrothorax was diagnosed with four patients in Child-Pugh class A, 20 patients in class B, and 28 patients in class C. There were 28 patients receiving supportive care with thoracentesis for symptom relief. Among the other 24 patients, 16 were treated by chemical pleurodesis (minocycline, picibanil and beta-iodine), 14 underwent surgical interventions (Thoracoscopic pleural onlay, Denver shunt, pleurodectomy or diaphragmatic repair) and six patients received both interventions. Intervention success, defined as resolution of hydrothorax for at least 3 months, was achieved in 37.5% and 42.9% patients of the intervention group by chemical pleurodesis and surgery, respectively, with an overall success rate of 50%. Multivariate analysis showed that only intervention success (P=0.01, hazard ratio=0.25) was an independent predictor of survival benefits. In the surgical model, from October 2003 to March 2005, 10 patients (age, 32–83 years; 6 men and 4 women) with refractory hepatic hydrothorax (Child-Pugh class B~C) underwent thoracoscopic pleura (n=7) or mesh (n=3) onlay reinforcement to repair diaphragmatic defects on which this study focuses, and all patients have since been under follow-up in a prospective observation study. After a mean of 7.7 months of follow-up examinations, no local recurrence occurred in all patients. Two patients died of hemorrhage from esophageal varices two months postoperatively. All patients had better postoperative pulmonary function. Conclusion: For patients with hepatic hydrothorax, aggressive medical or surgical intervention may confer a survival benefit over supportive management, especially when resolution of hydrothorax can be maintained for at least three months. The use of pleura and mesh onlay reinforcement of the diaphragm is an encouraging treatment modality for refractory hepatic hydrothorax. Part III New Diagnostic Method to Detect Diaphragmatic Defects in Hepatic Hydrothorax Early diagnosis and treatment is an important issue to attenuate the poor condition of refractory hepatic hydrothorax. Several diagnostic methods have been reported for diagnosis of hepatic hydrothorax, including biochemical analysis of ascitic and pleural fluid, conventional radi¬ography, radioisotope imaging, indocyanine green dye, magnetic resonance imaging studies, and thoracoscopy. Among these methods, ultrasonography may be considered as the easiest method and has the benefit of real-time diagnosis of anatomical integrity and flow studies across the diaphragm in patients with hepatic hydrothorax with and without massive ascites. The present study was performed in order to directly demonstrate the presence or absence of peritoneo-pleural communication by color Doppler ultrasonography and was verified by video-assisted thoracoscopic surgery. Furthermore, we evaluated the effect of color Doppler ultrasonography in the morphology of diaphragmatic defects and compare with the above studies. The result and conclusion of the third part of the study was as follows: Results: Three patients were found to have transdiaphragmatic flow from the peritoneal to the pleural cavity in color Doppler ultrasonography. Among these ultrasonography positive findings, bleb defects were noted thoracoscopically on the diaphragm, and they had massive pleural effusion in the radiologic study. However, in the diffuse oozing diaphragmatic defect or in the bleb defect without obvious radiologic study, color Doppler ultrasonography seems to be limited. Conclusions: Color Doppler ultrasonography is a simple, safe and rather non invasive method to confirm passage of ascitic fluid across the diaphragm. Color Doppler ultrasonography may play just as an important role in identifying hepatic hydrothorax as the etiology of pleural effusion in patients with chronic liver disease. Summary: The mechanism of hepatic hydrothorax has been proposed such that pleural effusion in cirrhotic patients, and the transdiaphragmatic flow of ascitic fluid through a diaphragmatic defect, is considered the most probable factor. Furthermore, color Doppler ultrasonography is a simple, safe and definitive method to confirm passage of ascitic fluid across the diaphragm. Either aggressive medical or surgical intervention, only intervention success is an independent predictor of survival benefits. Compared with other methods, the reinforcement of diaphragm defects is an encouraging treatment for refractory hepatic hydrothorax.
Subjects
肝硬化
肝性肋膜積水
liver cirrhosis
hepatic hydrothorax
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