Treatment of Primary Fetal Hydrothorax with OK-432 (Picibanil): Outcome in 14 Fetuses and a Review of the Literature.

BACKGROUND: Primary fetal hydrothorax (PFHT) is an uncommon condition with an estimated prevalence of 1 in 10,000/15,000 pregnancies. Therapeutic interventions include thoracocentesis, thoraco-amniotic shunting (TAS), and pleurodesis using OK-432. METHODS: A review of the literature was performed to identify all cases of PFHT treated with TAS and OK-432. All cases of PFHT referred to the Fetal Maternal Unit at Royal Prince Alfred Hospital between 2002 and 2012 were retrospectively reviewed. In the cohort of fetuses treated with OK-432, the main perinatal outcomes evaluated were termination of pregnancy, live birth, neonatal death, and fetal death in utero. Secondary outcomes included gestational age (GA) at diagnosis, GA at treatment, GA at resolution, birth weight, and GA at birth. The development of the children was screened using the Ages and Stages Questionnaires, Version 3 (ASQ-3, 2009). RESULTS: Primary hydrothorax was diagnosed in 31 fetuses, of which 14 had treatment with OK-432. One pregnancy terminated after treatment with OK-432. Survival was 85% (11/13): 100% in fetuses treated with OK-432 without hydrops, and 78% in those treated with hydrops. This compares well to the cases of TAS in the literature with an average survival of 63%: 85% in fetuses without hydrops and 55% with hydrops. The mean GA at birth was 36(+4) weeks and mean birth weight 3,007 g. Eight of the 9 children screened with ASQ-3 scored well within the normal range. CONCLUSION: OK-432 appears to be a valid treatment option in fetuses with PFHT, particularly in those diagnosed at early GAs.

Hepatic hydrothorax.

Hepatic hydrothorax is defined as a pleural effusion in patients with liver cirrhosis in the absence of cardiopulmonary disease. The estimated prevalence among patients with liver cirrhosis is approximately 5-6%. The pathophysiology involves the passage of ascitic fluid from the peritoneal cavity to the pleural space through diaphragmatic defects. The diagnosis is made from clinical presentation and confirmed by diagnostic thoracentesis with pleural fluid analysis. The initial medical management is sodium restriction and diuretics, but liver transplantation provides the only definitive therapy. For patients who are not transplant candidates and those who await organ availability, other therapeutic modalities that are to be considered include transjugular intrahepatic portosystemic shunt placement, videoassisted thoracoscopic surgery repair, pleurodesis, and vasoconstrictors (eg, octreotide and terlipressin). The primary therapeutic goals are to reduce ascitic fluid production and improve symptoms to bridge the time for liver transplantation.

Successful lamivudine monotherapy in an elderly patient suffering from HBV-related decompensated cirrhosis associated with widespread leukocytoclastic vasculitis.

Hepatitis B virus (HBV) infection is known to be responsible for both hepatic and extrahepatic manifestations including dermatitis, polyarthralgias and arthritis, pulmonary disease, aplastic anemia, glomerulonephritis and vasculitis. The mechanism of these extrahepatic disorders is thought to be linked to immune complex disease, but their pathogenesis is poorly clarified. Immunosuppressive treatment could promote viral load and impair hepatic disease, also worsening the vasculitis by enhancing viral antigenemia. Lamivudine is a nucleoside analogue approved for treating chronic hepatitis B, that decreases the amount of viral antigens by suppressing HBV replication. Several reports have suggested lamivudine in the treatment of vasculitis associated with HBV infection, but, although significant inhibition of HBV is achieved in the short term, resistance develops in 15-32 percent annual risk rating. We report an elderly patient whose chronic hepatitis B decompensated cirrhosis with associated refractory hepatic hydrothorax and extensive leukocytoclastic vasculitis was successfully treated with ongoing long-term lamivudine monotherapy.

Bilateral pleural effusions in congestive heart failure.

The salt-avid state that accounts for the clinical syndrome congestive heart failure (CHF) leads to an initial expansion of intra- and subsequent rise in extravascular volumes that can include the appearance of pleural effusion. Herein, we present a 54-year-old man with a dilated cardiomyopathy who was hospitalized because of his CHF, which included bilateral pleural effusions, right hydrothorax greater than left. The pathophysiology of pleural fluid formation in CHF, previously debated, has now reached consensus, albeit not frequently reviewed. This index case offers such an opportunity.

Mycoplasma pneumoniae 23S rRNA A2063G mutation does not influence chest radiography features in children with pneumonia.

Objective To measure the rate of the A2063G mutation in the Mycoplasma pneumoniae ( M. pneumoniae) 23S rRNA domain V in children with pneumonia and to determine the correlation between radiographic findings and the presence of the A2063G mutation. Methods Patients who were hospitalized with a confirmed diagnosis of M. pneumoniae pneumonia were enrolled in this study. M. pneumoniae strains were collected for genotype analysis. Chest radiography was performed on all children prior to and following macrolide treatment. Clinical and imaging data were obtained. Results Of 211 patients, 195 (92.42%) harboured M. pneumoniae with the A2063G mutation. No significant differences were identified in inflammation score, chest radiography inflammation absorption grade before and after macrolide treatment, or pulmonary complications (atelectasis, hydrothorax, or pleuritis) prior to macrolide treatment when children were stratified based on the presence or absence of the A2063G mutation. Conclusions A high proportion of children with pneumonia harboured strains of M. pneumoniae with the A2063G mutation in the 23S rRNA domain V. However, no obvious chest radiographic features of M. pneumoniae pneumonia were associated with the A2063G variant.

Refractory hepatic hydrothorax: successful treatment with octreotide.

We report the case of a patient that developed hepatic hydrothorax as the first complication of liver cirrhosis. Due to the lack of response to diuretics, pleurodesis and TIPS, treatment with octreotide was started with resolution of hydrothorax. To the best of our knowledge, this is the third reported case of refractory hepatic hydrothorax with complete and sustained response to octreotide.

[Clinical observation on treatment of cancerous hydrothorax by aiyishu injection].

OBJECTIVE: To investigate the therapeutic effects of Aiyishu Injection (AYSI) on cancerous hydrothorax, quality of life (QOF), and cellular immune function of patients. METHODS: Sixty late-stage cancer patients accompanied hydrothorax were randomly divided into the experimental group (EG) and the control group (CG), with thirty patients in each group. After thoracenteses being carried out in all patients for draining off hydropsy, to the patients in EG, AYSI was medicated, 50 ml by intrathoracic and another 50 ml by intravenous injection; while to the patients in CG chemotherapeutic agent or interleukin-2 (IL-2) was given. The same treatment, thoracentesis and medication, was repeated 3 days later. After 4 weeks, the volume of pleural effusion was measured with B-mode ultrasound to evaluate the therapeutic effects of AYSI. QOF, body weight and T-lymphocyte subsets were compared between the two groups before and after treatment. RESULTS: The clinical efficacy was significantly higher in EG than that in CG (P < 0.01). Besides, QOF was significantly improved (P < 0.05) and levels of CD3+ , CD4+ , CD4+ /CD8+ in peripheral blood increased in EG after treatment, which were significantly different to those in CG (P < 0.01, P < 0.05). CONCLUSION: AYSI has definite therapeutic effects on cancerous hydrothorax, it could improve QOF and cellular immune function in patients with cancer.

Hepatic hydrothorax: pathogenesis, diagnosis, and management.

Hepatic hydrothorax is defined as a pleural effusion in a patient with cirrhosis of the liver and no cardiopulmonary disease. The estimated prevalence of this often debilitating complication in patients with liver cirrhosis is 4% to 10%. Its pathophysiology involves movement of ascitic fluid from the peritoneal cavity into the pleural space through diaphragmatic defects. As a result patients are at increased risk of respiratory infection. Initial management consists of sodium restriction, diuretics, and thoracentesis. A transjugular intrahepatic portosystemic shunt may be required. Because most patients with hepatic hydrothorax have end-stage liver disease, a liver transplant should be considered if these options fail.

Treatment of refractory hepatic hydrothorax with transjugular intrahepatic portosystemic shunt: long-term results in 40 patients.

BACKGROUND/AIMS: Hepatic hydrothorax is a complication of portal hypertension secondary to ascites. In this study, we investigated retrospectively the effects of the transjugular intrahepatic portosystemic shunt (TIPS) on hepatic hydrothorax refractory to diuretic treatment. METHODS: Forty patients (Child-Pugh class B, 24 patients; Child-Pugh class C, 16 patients) with hydrothorax refractory to diuretic treatment, pleurocenteses or pleurodesis were included. The TIPS implantation was successful in all patients, who were then followed for 16 +/- 14 months (range 1 day-54 months). RESULTS: TIPS reduced the portosystemic pressure gradient from 26 +/- 6 to 10 +/- 5 mmHg. In the 17 patients whom we followed for 12 months or longer, improvements were found for the Child--Pugh score (8.6 +/- 1.8 v. 6.7 +/- 1.5), serum albumin concentration (3.1 +/- 0.5 v. 3.6 +/- 0.5 g/l), and urinary sodium excretion (22 +/- 29 v. 89 +/- 43 mmol/24 h) (P< 0.05). Two patients developed severe hepatic encephalopathy requiring shunt occlusion. Hydrothorax improved in 82% of patients and resolved in 71% of patients. Fifty per cent of patients developed shunt insufficiency within 7 +/- 9 months, contributing to a probability of relapse-free 1-year survival of 35%. In these patients, shunt revision resulted in a secondary response rate of 82.3%. The 1-year survival was 64%. Both hydrothorax response and survival showed a significant inverse correlation with age over 60 years (P< 0.01 and P< 0.003, respectively) but not with other biomedical variables. CONCLUSION: TIPS is effective for hydrothorax refractory to diuretic treatment and other standard interventions to bridge the time to transplantation. Patients older than 60 years have a poor response and short survival.

Successful treatment of hepatic hydrothorax with octreotide.

Hepatic hydrothorax is a rare complication of cirrhosis. Controlling ascites formation is the goal of therapy. We report the case of an adult patient presenting with alcoholic cirrhosis who developed first a symptomatic hydrothorax, refractory to diuretics and fluid and sodium restriction, and then an hepatorenal syndrome. Treatment consisted of chest tube insertion and 5 days' intravenous infusion of octreotide. Complete clinical and biological data were reviewed. Octreotide administration resulted in an increased urinary outflow and sodium output, concomitant with improved renal function. The patient has been free of symptoms after discharge from hospital for a follow-up period of 5 months. This observation raises interesting issues regarding the possible utility of splanchnic vasoconstrictors, reducing portal hypertension, in the treatment of refractory hepatic hydrothorax.

Radionuclide evaluation of pleural-peritoneal shunt before pleurodesis.

OBJECTIVES: Talc pleurodesis can be offered to patients with hepatic hydrothorax. The authors wanted to determine their patient's eligibility for talc pleurodesis by excluding a pleural-peritoneal shunt. MATERIALS AND METHODS: The authors measured the size of the talc particles and matched them with the radionuclide particle size. After injecting radiopharmaceutical into the pleura, the authors imaged the abdomen for possible migration. RESULTS: In their patient, there was no migration of radionuclide from the thorax into the abdomen. CONCLUSION: Injecting radionuclide into the thoracic cavity and then imaging for an extended period of time is one way to determine whether the patient has a pleural-peritoneal shunt.

[Recurrent breast cancer successfully treated with a weekly dose of paclitaxel--a case report].

The patient was a 46-year-old women who was treated for axillary lymph node recurrence of breast cancer by a variety of methods, including surgery, chemotherapy, and radiotherapy, but who experienced recurrences in the cervical and mediastinal lymph nodes and skin, and developed hydrothorax and ascites. Although the recurrent foci responded to 4 cycles of CAF chemotherapy, there was concern that the foci would become refractory or resistant to chemotherapy. The administration of paclitaxel was therefore initiated. The patient received a dose of paclitaxel once a week for 5 consecutive weeks followed by a 1-week recovery period (one cycle). After two cycles of the paclitaxel treatment, a marked shrinkage of the lymph nodes and complete resolution of the hydrothorax and ascites were observed. Even though the patient exhibited bone marrow suppression and G-CSF was administered twice for neutropenia, there were no adverse effects except mild alopecia, again suggesting the possibility that paclitaxel is effective chemotherapy for recurrent breast cancer.

A 62-year-old female patient with left-sided pleural effusion.

Hepatic hydrothorax is defined as a pleural effusion in patients with liver cirrhosis without primary cardiac, pulmonary or pleural disease. It is a rare but important cause of unilateral-pleural effusion. The prevalence of this complication is 5-10% of the total number of patients with advanced stages of cirrhosis. In most cases (85%), the effusion is right-sided; however, in 13% of cases it can be left-sided and bilateral in 2% of the cases. We present a case of left-sided hepatic hydrothorax in the absence of ascites in a patient with primary biliary cirrhosis. The diagnosis of cirrhosis was confirmed by the biopsy;the patient didn't have any history or any signs or symptoms of cirrhosis prior to her presentation. In the case described, the patient was treated with spirnolactone, furosemide and ursodeoxycholic acid. At follow-up after six months since the diagnosis, she was responding to treatment with no complications. This case emphasizes the importance of considering hepatic hydrothorax as an etiology of a transudative pleural effusion regardless of the presence or absence of ascites inpatients with occult cirrhosis.

Dexamethasone acutely accelerates pleural fluid absorption in mice hydrothoraces.

This study assessed the effect of corticosteroid treatment in the clearance of hydrothoraces in mice. Twenty-four C57BL/6 mice were divided into four groups and were injected intrapleurally with 500 microL sterilized PBS-BSA 1% to create isosmotic hydrothoraces. Two groups served as control and two groups were treated with dexamethasone. The control groups received intraperitoneally PBS, while the corticosteroid treatment groups received dexamethasone (1 mg/kg), both 5 min after the induction of hydrothorax. Control and treated animals were sacrificed 2 and 4 h after the induction of hydrothorax, and pleural fluid volume was measured. The pleural fluid volume 2 and 4 h after the induction of hydrothoraces was significantly lower in the dexamethasone-treated group compared to the untreated group. The rate of pleural fluid absorption 2 and 4 h after the induction of hydrothoraces was significantly higher in the dexamethasone-treated groups. The present study demonstrated that dexamethasone accelerates pleural fluid absorption in induced isosmotic hydrothoraces in mice. This newly reported property of dexamethasone may partly account for the clinical observation of faster resolution of pleural effusions when corticosteroids are administered in patients with pleural effusions of certain etiologies.