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A case is presented of ascites and hydrothorax in association with struma ovarii. Nine previously reported cases are reviewed and the possible causes of the ascites and hydrothorax discussed.
Pulmonary edema and hydrothorax were observed in mature swine that died approximately 5 days after consuming corn screenings. These postmortem observations were reproduced in younger pigs that died within 1 week when fed the corn screenings under experimental conditions. Additionally, pulmonary edema and hydrothorax were induced in a pig that died after receiving 4 daily intravenous injections of fumonisin B1, a toxic metabolite produced by Fusarium moniliforme.
A 28-year-old male patient developed bilateral hydrothorax due to extravasation of fluid into the mediastinum from a subclavian line. The injection of radio-opaque dye through the central venous cannula confirmed spillage into the mediastinum. There was no direct communication between the central venous cannula and the pleural cavities. The hydrothorax appeared to develop as a result of a shift of fluid from the mediastinum into the pleural cavities due to pressure differences in the two compartments. Bilateral chest tubes were inserted, the subclavian cannula was removed and the patient made a good recovery.
Cerebrospinal fluid hydrothorax is a very rare complication following ventriculoperitoneal shunting. The authors report a case of a 3-year-old girl who developed cerebrospinal fluid hydrothorax (caused by migration of the intra-abdominal catheter through the right vertebrocostal trigone of Bochdalek, the one most unlikely to be congenitally patent) and respiratory distress. The patient was successfully treated with thoracocentesis and shunt revision.
BACKGROUND: Hepatic hydrothorax is defined as a pleural effusion that arises in patients with cirrhosis of the liver and no cardiopulmonary disease; it is believed to result from peritoneopleural communication through a defect in the diaphragm. METHODS: Nine patients underwent thoracoscopic pleurodesis. The diaphragmatic defect was detected and corrected in two cases. In all patients, an argon beam coagulator was applied to the diaphragm surface, which was then completely covered with bioabsorbable prostheses. We then spread 3 ml of fibrin glue on the covered diaphragm and sprinkled 5 KE of OK-432 and 100 mg of minocycline hydrochloride in the thoracic cavity. RESULTS: All patients showed clinical improvement. The pleural effusion and breathlessness resolved immediately after pleurodesis. There were two recurrences after 1 and 4 months, respectively. One of these patients improved after repeat pleurodesis; the other was treated conservatively. CONCLUSION: Our new technique of thoracoscopic pleurodesis is an effective and minimally invasive treatment for patients with refractory hepatic hydrothorax.
The purpose of this paper is to describe the risks of ventriculopleural shunt in patients with spina bifida and end-stage-renal-diseases (ESRD), and to describe endoscopic third ventriculostomy as an alternative for the combination of cerebrospinal shunt and dialysis modality. We report a 16-year-old boy with spina bifida on chronic dialysis with a massive unilateral hydrothorax and respiratory distress complicating a ventriculopleural (VPL) shunt. Two thoracocenteses were performed, draining 3200 ml of a clear fluid. The VPL shunt was removed and revised successfully to a third ventriculostomy (TVE). Peritoneal dialysis (PD) was the initial dialysis modality. After 12 months on PD, the patient was transferred to hemodialysis (HD) because of refractory peritonitis. Hydrothorax developed while the patient was on PD, reaching its maximum 2 months after the transference to HD. To our knowledge there has been no other report of ventriculopleural (VPL) shunt failure, and endoscopic TVE, as a cerebrospinal fluid (CSF) diversion alternative in patients on chronic dialysis.
We determined in anesthetised rabbits the net rate of liquid absorption (NRLA) from Ringer or 1% albumin-Ringer hydrothoraces with the beta-blocker propranolol (or nadolol) or the beta-agonist terbutaline. The beta-blocker reduced NRLA by 38% in 2 ml Ringer hydrothoraces, and did not change it in 2 ml albumin-Ringer hydrothoraces; hence, with beta-blocker NRLA became similar in both kinds of hydrothorax (0.31 +/- 0.02 ml/h). Terbutaline decreased NRLA by 25% in 2 ml Ringer hydrothoraces, and increased it by 29% in 2 ml albumin-Ringer hydrothoraces; hence, with terbutaline NRLA became similar in both kinds of hydrothorax (0.40 +/- 0.02 ml/h), and 25% higher than with beta-blocker. Because beta-adrenoreceptor activity inhibits lymphatic smooth muscles and may increase Na+ transport in epithelia, these results suggest that: (1) pleural mesothelium is provided with beta-receptors, which increase Na+ transport and seem activated by protein dilution, (2) beta-receptors of the pleural lymphatics are essentially silent with and without protein dilution, (3) the lymphatic drainage produced by smooth muscle activity is smaller than the increase in solute-coupled liquid absorption caused by mesothelium beta-receptors.
A patient presented to the emergency department with a malignant pleural effusion associated with shortness of breath, and radiographic evidence of mediastinal shift and hypotension. Tube thoracostomy yielded serosanguinous pleural fluid under pressure and after 1 liter of fluid was drained, the patient's hemodynamic status stabilized. The entity of tension hydrothorax is rare but may be life threatening. The treatment should consist of prompt drainage and efforts to prevent recurrence. As physicians become more adept at prolonging the lives of patients with cancer, tension hydrothorax may become more common.
The natural course of patients with cirrhosis is frequently complicated by the accumulation of fluid in the peritoneal or pleural cavities and interstitial tissue. Functional renal abnormalities that occur as a consequence of decreased effective arterial blood volume are responsible for fluid accumulation in the form of ascites and hepatic hydrothorax. Ascites is the most common complication of cirrhosis and poses an increased risk for infections, renal failure and mortality. Patients have a poor prognosis and it is estimated that nearly half will die in approximately 2 years without liver transplantation. Hepatic hydrothorax is defined as a pleural effusion greater than 500 mL (mostly right-sided) in patients with cirrhosis without cardiopulmonary disease; the estimated prevalence is approximately 5-10%. Liver transplantation is the most definitive cure for both conditions in those patients that are suitable candidates. However, the mainstay of therapy for minimizing fluid accumulation in both conditions includes sodium restriction and administration of diuretics. This article reviews the most current concepts of pathogenesis, clinical findings, diagnosis, and treatment of these complications of cirrhosis.
Isolated fetal hydrothorax is an uncommon finding on routine prenatal ultrasound and is associated with a variable prognosis. We believe this is the first report of a patient whose antenatal hydrothorax was associated with both congenital diaphragmatic hernia and congenital pulmonary lymphangiectasia. This rare combination caused significant problems in diagnosis and subsequent treatment.
We report a case of successful, long-term pleurovenous shunt (PVS) in treating refractory nonmalignant hepatic hydrothorax. An 82-year-old woman with liver cirrhosis, hypertension complicated with chronic renal failure while on hemodialysis, presented with progressive dyspnea in association with a recurrent right-sided pleural effusion, occurring secondary to transdiaphragmatic migration of ascites. The diagnosis was established by a demonstration of (99m)Tc-sulphur colloid sequential scintigraphic scan. Despite repetitive thoracenteses and traditional medical treatment, she suffered dyspnea without relief. Denver peritoneovenous shunt was inserted into the right-sided pleural cavity to drain effusion into the subclavian vein without short- and long-term complications. Manually pumping schedule of 10 min was performed twice daily to remove pleural fluid into the venous circulation for maintaining shunt patency. After 19 months of follow-up, the patient is doing well and PVS remains patent without significant pleural effusion. PVS opens a window of opportunity and offers an alternative procedure with minimal invasiveness for high-risk patients with refractory hepatic hydrothorax. It could be an alternative treatment to other conventional surgical interventions.
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.
OBJECTIVE: The purpose of our study was to determine whether in utero pleural decompression can improve abnormal cardiotocograms resulting from compressive fetal hydrothorax. STUDY DESIGN: We reviewed all cases of fetal hydrothorax referred to our level 3 fetal medicine unit. Highly pathologic cardiotocographic findings were observed in four third-trimester patients. All had mediastinal compression that resulted in skin edema on the upper part of the body. Prenatal therapy was performed on an emergency basis, two with thoracocentesis and two with pleuroamniotic catheters. RESULTS: One patient went into intractable bradycardia on arrival in the department and died in spite of immediate thoracocentesis. The other three recovered, with normal heart rate patterns after pleural decompression. CONCLUSION: Emergency prenatal therapy may reverse fetal distress in utero, allowing time for delivery of uncompromised infants if possible after a complete evaluation of nonimmune hydrops.
Hepatic hydrothorax occurs frequently in ascites arising from communications in the diaphragm between peritoneal and pleural cavities. Numerous treatments have been described but are of limited utility due to invasiveness and poor success rate. We describe a case of hepatic hydrothorax in which the pore in the diaphragm was documented photographically and in which successful resolution was achieved with videothoracoscopic suture ligation and talc pleurodesis.
Two cases of right hepatic hydrothorax occurring in the absence of clinical ascites are reported. Diagnosis was confirmed by the intraperitoneal and intrapleural injection of radioisotope 99mTc-sulfur colloid that demonstrated the one-way transdiaphragmatic flow of fluid from the peritoneal to pleural cavities. In contrast, radioisotope injected into the peritoneal cavity of 5 patients with pleural effusions secondary to pulmonary or cardiac disease failed to traverse the diaphragm and localize in the pleural space. Medical therapy with salt and water restriction and diuretics resulted in both of the patients with hepatic hydrothorax developing signs of intravascular volume depletion without significant mobilization of the pleural fluid. Thoracotomy allowed identification of the diaphragmatic defects that were repaired by chemical and traumatic pleurodesis followed by postoperative peritoneal and pleural drainage. This therapy resulted in complete resolution of the pleural effusions, which have not recurred despite the subsequent development of clinical ascites in both patients.
Primary fetal hydrothorax presents a wide spectrum of severity ranging from small, harmless effusions, to life-threatening thoracic compression. To define natural history and management, we reviewed 32 cases seen at two large perinatal centers from 1980 to 1987. Spontaneous resolution of the effusions was seen in three fetuses, all of whom survived. Three fetuses were electively terminated. The overall mortality was 53%. In the 24 untreated fetuses, sex and the presence of polyhydramnios did not influence mortality, but hydrops, gestational age less than 35 weeks at delivery, and bilateral effusions were associated with a poor prognosis. Five fetuses underwent in utero decompression. In four, thoracentesis was performed, with rapid reaccumulation of the effusion. All four died from pulmonary insufficiency. In the fifth fetus, a thoracoamniotic shunt permanently decompressed the effusion, with resolution of the hydrops, and delivery of a normal viable infant. We conclude that (1) primary fetal hydrothorax may resolve or progress to hydrops, necessitating close follow-up with ultrasound; (2) pulmonary hypoplasia as a result of undrained large pleural effusions may result in neonatal mortality; (3) the gestational age at both diagnosis and delivery, the development of hydrops, and bilaterality of effusions are important prognostic predictors; and (4) the fetus with large effusions and hydrops has a poor prognosis, and thoracic decompression with a thoracoamniotic shunt may prove life saving.
Recurrent hydrothorax complicating peritoneal dialysis has been considered a contraindication to continuing peritoneal dialysis. In the continuous ambulatory peritoneal dialysis (CAPD) population this problem has generally required a change of dialytic modality. Talc poudrage has been attempted to ameliorate the problem but has met with limited success. We report a successful case of intrapleural instillation of tetracycline to induce a pleural symphysis and prevent recurrence of peritoneal dialysis-related hydrothorax in a patient who refused any alternative mode of dialysis. We also review the literature, pathophysiology, epidemiology, diagnosis, and management of this compromising problem.
Tension hydrothorax is rare, with few cases reported in the literature dating back to the late 1960s. We report a case of tension hydrothorax in a patient with a ventriculopleural shunt who improved dramatically after thoracentesis. The discussion includes a brief review of ventriculopleural shunts and pleural physiology.