Pradeep Kumar Siddappa, Premashish Kar
Department of Medicine,
Maulana Azad Medical College,
New Delhi - 110002, India
Corresponding Author:
Prof. Pradeep Kumar Siddappa
Email: grayneo@yahoo.com
Abstract
Hepatic hydrothorax is defined as significant pleural effusion (usually greater than 500 mL) in a cirrhotic patient, in the absence of underlying pulmonary or cardiac disease. The diagnosis of hepatic hydrothorax should be suspected in a patient with established cirrhosis and portal hypertension, presenting with unilateral pleural effusion, most commonly rightsided. Hydrothorax is uncommon, and is found in 4–6% of all patients with cirrhosis and up to 10% in patients with decompensated cirrhosis. Although ascites is usually present, hydrothorax can occur in the absence of ascites. Patients with hepatic hydrothorax usually have advanced liver disease with portal hypertension and most of them require liver transplantation. Current insight into the pathogenesis of this entity has led to improved treatment modalities such as portosystemic shunts (TIPS) and video-assisted thoracoscopy for closure of diaphragmatic defects. These modalities may provide a bridge towards transplantation.
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48uep6bbphidvals|269 48uep6bbphidcol4|ID 48uep6bbph|2000F98CTab_Articles|Fulltext 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 reduced 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.
Hepatic hydrothorax
Hepatic hydrothorax is defined as a significant pleural effusion, usually greater than 500 mL, in a cirrhotic patient,without an underlying pulmonary or cardiac disease.[1,2] It seems to be a relatively uncommon complication of portal hypertension with an estimated prevalence of 5–12% in patients with cirrhosis of the liver.[3,4] In most cases (85%) hepatic hydrothorax develops on the right side, with 13% of cases occurring on the left side and 2% bilateral[4,5] A study has reported that pleural effusion was present in 10% of chest X-rays in cirrhotic patients.[5] In the vast majority of cases, ascites is also present. It is well known that in cirrhotic patients, a large volume of ascitic fluid is generally well tolerated due to the capacitance of the peritoneal cavity. On the other hand, even modest volumes of pleural fluid can cause significant respiratory symptoms, including dyspnea and chest pain.
Pathogenesis of ascites and hepatic hydrothorax
Most patients with advanced cirrhosis are unable to maintain extracellular fluid volume within normal limits, which results in increased total extracellular fluid volume and subsequent accumulation of fluid in the peritoneal and/or pleural cavities and interstitial tissue.[6,7,8,9] The main factor responsible for this increase in extracellular fluid volume is an abnormal increase in renal sodium reabsorption.[10] Although the exact pathogenesis of abnormal fluid regulation in cirrhosis is unknown, a large body of evidence indicates that it is secondary to arterial splanchnic vasodilation with a subsequent fall in effective arterial blood volume (the volume sensed by arterial and cardiopulmonary receptors).[9,10,11,12] The accumulation of fluid and the abnormalities in renal function are the consequence of the homeostatic activation of vasoconstrictor and antinatriuretic factors triggered to compensate for the relative arterial underfilling. Several mechanisms have been proposed in order to explain the development of hepatic hydrothorax in patients with cirrhosis and portal hypertension (Table 1).
The first three mechanisms fail to explain the right side predominance of hepatic hydrothorax
In 1955, Emerson described for the first time a diaphragmatic fenestration in a patient with cirrhosis and pleural effusion.[10]More recent studies have demonstrated the existence of such diaphragmatic defects in a large number of patients with hepatic hydrothorax.[11,12] Microscopic examination of these defects revealed discontinuities in the collagen bundles that make up the tendinous portion of the diaphragm. Increase in the intra-abdominal pressure, for example, as a result of ascites, coughing, or straining, might lead to small herniations of the peritoneum through these gaps into the pleural cavity. These herniations, also called pleuroperitoneal blebs, may rupture. The ensuing defects, which are typically less than 1 cm in diameter, allow free communication between the peritoneal and pleural space.[6,13]
The leakage of ascitic fluid via diaphragmatic defects seems to explain the pathogenesis of hepatic hydrothorax. The negative intrapleural pressure compared to that of the peritoneal cavity facilitates the one-way transfer of fluid and its subsequent trapping into the pleural space. Hepatic hydrothorax occurs when the accumulation of fluid surpasses the absorptive capacity of the pleura. This theory is further supported by the fact that air, dyes, or radiolabeled substances intra-abdominally injected in patients with hepatic hydrothorax move rapidly into the pleural cavity.[14,15,16,17,18]
Huang et al,[15] classified the diaphragmatic defects stemming from hepatic hydrothorax into 4 morphologic types: type I, no obvious defect; type II, blebs lying on the diaphragm; type III, broken defects (fenestrations) in the diaphragm; and type IV, multiple gaps in the diaphragm.
Moreover, the direct passage of peritoneal fluid into the pleural space via diaphragmatic defects explains the rightside predomination of hepatic hydrothorax. Autopsy studies suggest that pleuroperitoneal blebs occur less frequently in the left hemidiaphragm, as it is thicker and more muscular.[16] Intraperitoneal injection of a radiolabeled tracer will confirm the rapid passage of the isotope through the diaphragm and its accumulation in the pleural space of such individuals.
In a recent study by Foschi et al[17] the presence of peritoneal-pleural communications was demonstrated by real time contrast enhanced ultrasound; and these results were comparable to those of a nuclear scan. Contrast enhanced ultrasound is cheaper and can theoretically be performed wherever ultrasound facilities are available.
Clinical presentation and diagnosis
The diagnosis of hepatic hydrothorax should be suspected in a patient with established cirrhosis and portal hypertension, presenting with a unilateral pleural effusion, most commonly right sided.[7,18,19] In most cases, the dominating clinical manifestations are those of cirrhosis and ascites. However, a variety of respiratory symptoms, including dyspnea, nonproductive cough, pleural chest pain, and fatigue due to hypoxemia may also occur. The severity of these symptoms depends on the volume of pleural fluid. Patients rarely present with symptoms and signs of respiratory failure due to acute tension hydrothorax.[20,21] In a minority of cases, pleural effusion may be noted incidentally on a chest radiography performed for other reasons.[22] Several authors have reported cases of unilateral pleural effusions in cirrhotic patients without clinical or even ultrasonic evidence of ascites. In these cases, respiratory symptoms may confuse the clinician leading to extensive diagnostic evaluation, as liver cirrhosis is not commonly considered a distinct cause of pleural effusion.
Pleural fluid examination
As in any patient with significant pleural effusion, a diagnostic thoracocentesis (approximately 40 mL of pleural fluid) should be performed for confirmation of diagnosis and to exclude infection.[23,24] Diagnostic tests to be ordered include cell count, Gram stain and culture of the pleural fluid in blood-culture bottles, serum and fluid protein, albumin, lactate dehydrogenase, and bilirubin. Other tests of the fluid that can be useful, depending on the clinical suspicion, include triglyceride levels, pleural pH, adenosine deaminase levels for tuberculosis , amylase levels , and cytology. The composition of pleural fluid consequent to portal hypertension is transudative and similar to the ascitic fluid, but some differences might be evident due to the different mechanisms of fluid absorption from the pleural space compared to those present in the peritoneal cavity. The characteristics and diagnostic tests and their interpretations for pleural fluid in hepatic hydrothorax are described in Table 2. In uncomplicated hepatic hydrothorax the cell count is less than 500 cells/mm3, and the total protein concentration is less than 2.5 g/dL.
Occasionally chylomicrons are found in the pleural fluid.[25,26] Portal hypertension increases splanchnic lymph flow, and rupture of these vessels may give rise to a hepatic chylothorax in the patient with a pleuroperitoneal communication. Because the lymph is diluted by the ascetic fluid, the triglyceride levels and lymphocyte counts tend to be lower than in other forms of chylothorax, and the fluid retains the characteristics of a transudate.
In patients with cirrhosis and pleural effusion, a thorough investigation for primary cardiopulmonary disorders should be performed. In a recent study a diagnosis other than hepatic hydrothorax was established in 18% of cirrhotics with pleural effusion.
When uncertainty exists concerning the aetiology of a transudative effusion, the finding of an elevated serum soluble Fas ligand may help distinguish a hepatic hydrothorax from one resulting from heart failure in patients with viral cirrhosis.[27][
In cases where the diagnosis of hepatic hydrothorax is in doubt, in particular when pleural effusion is left-sided and/or
ascites is absent an intraperitoneal administration of 99mTchuman serum albumin or 99mTc-sulfur colloid should be performed. The migration of the radioisotope into the pleural cavity within hours confirms the presence of a communication between the pleural and peritoneal spaces. According to a recent study, this technique has sensitivity and specificity rates of 71% and 100%, respectively.[28] Moreover, it can be used even in the absence of ascites, through the ultrasound-guided administration of the radiolabeled substance in a 500-mL volume of normal saline.[29] Finally, other diagnostic modalities, including magnetic resonance imaging, CT chest and thoracoscopy can be performed in order to detect the underlying diaphragmatic defects.[31,32]
Subacute bacterial empyema (SBEM)
Infection of the pleural fluid in cirrhosis is associated with deteriorating prognosis and frequently there are few localizing signs.
Spontaneous infection within the pleural fluid is known as spontaneous bacterial empyema (SBEM). It is defined as pleural fluid with a PMN cell count >500 cells/mm3 or positive culture with PMN cell count >250 cells/mm3 with exclusion of a parapneumonic effusion.[32]
This type of infection must be considered in any patient with hydrothorax who develops fever, pleuritic pain, encephalopathy, or unexplained deterioration in clinical status. A high index of suspicion is therefore essential for its diagnosis, SBEM can be present in as many as 13% of patients with hepatic hydrothorax on admission with an associated mortality as high as 20% during treatment.[33] It might occur as a result of a direct bacterial spread from the peritoneal cavity. However, in a recent study, nearly 45% of episodes were not associated with spontaneous bacterial peritonitis.33 Moreover, SBEM may occur even in the absence of ascites. In those cases, a transient bacteremia that infects the pleural space can be the underlying pathogenic cause.[34] The aetiology in most cases is infection with Escherichia coli, Streptococcus, Enterococcus, Klebsiella and Pseudomonas. A recent study showed that an analysis of pleural fluid with a reagent strip for leukocyte esterase might represent a rapid, easy-to-use, and inexpensive tool for the diagnosis of SBEM in cirrhotic patients.
The risk factors for developing SBEM in patients with cirrhosis include:
· low levels of pleural fluid C3
· low serum albumin
· pleural fluid total protein, and
· high Child-Pugh score[34]
Management
The vast majority of patients with hepatic hydrothorax have end-stage liver disease. Therefore, they should be considered as potential candidates for orthotopic liver transplantation. Until the performance of transplantation, other therapeutic modalities should be applied in order to relieve symptoms and prevent pulmonary complications. shows the existing therapeutic modalities in patients with hepatic hydrothorax.
Medical management
Hepatic hydrothorax is ascitic fluid that has entered the pleural cavity. Therefore, the principles of medical management are identical to those of ascites in cirrhotic patients.[35] The aim of therapy should be to create and subsequently maintain a negative sodium balance.
Nutritional recommendations
An evaluation by a nutritionist is recommended for appropriate education concerning appropriate calorie and salt intake. A low sodium diet with 70-90 mmol/day is recommended because a more severe restriction is usually unpalatable. Improvement of the nutritional status is of key importance given that patients with advanced cirrhotic disease have a decreased intake of nutrients, decreased absorption of nutrients, increased energy expenditure and altered fuel metabolism, with an accelerated starvation metabolism.[36]
Diuretic therapy
Diet therapy is not sufficient to achieve a negative sodium balance,[37,38] therefore, diuretics are required in the vast majority of cases. The cornerstone of therapy has relied on the administration of diuretics—drugs that increase sodium excretion by reducing the tubular reabsorption of sodium. The diuretic most commonly used in patients with cirrhosis, ascites and hepatic hydrothorax is spironolactone (50-400 mg/day), a drug that inhibits sodium re-absorption by binding to the mineralocorticoid receptor in the renal collecting tubules, thus blocking the effects of aldosterone.[39] Spironolactone can be given in combination with furosemide (20-160 mg/day), which acts by inhibiting the Na+-K+-2Clco- transporter in the loop of Henle.
Other drugs
Terlipressin
In a recent report by Ibrisim et al, a case of hepatic hydrothorax, which was refractory to thoracic tube drainage and octreotide treatment, was controlled with 5 days of terlipressin therapy associated with albumin. Terlipressin administration resulted in both improvement in renal function and successful resolution of hepatic hydrothorax. Splanchnic vasoconstrictor agents that reduce splanchnic blood flow, increase both central volume and effective renal blood flow. Thus they improve renal function. The report demonstrated that terlipressin, a drug with known benefit in the hepatorenal syndrome, might also be effective in the treatment of hepatic hydrothorax.[40]
Octreotide
A recent report by Barreales, et al[41] describes a patient who 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 initiated which resulted in resolution of the hydrothorax.. There have been similar reports of successful treatment of hydrothorax with octreotide.[42,43,44]
Refractory hydrothorax
Precise criteria for defining refractory hepatic hydrothorax have not been proposed, but criteria for refractory ascites were proposed Moore, et al.[9] Therefore the diagnosis of refractory hepatic hydrothorax should be according to the criteria for refractory ascites. According to these criteria, refractory ascites may be either diuretic resistant (lack of response to dietary sodium restriction and intensive diuretic treatment) or diuretic-intractable (development of diuretic induced complications that preclude the use of an effective diuretic dosage).
Current treatment strategies for refractory ascites include repeated therapeutic paracentesis plus intravenous albumin and TIPS.
Treatment options for refractory hydrothorax
Repeated thoracentesis
Therapeutic thoracentesis is the most effective way of reducing a large effusion.[45,46] It is a simple and effective procedure indicated for relief symptoms of dyspnea in patients with large effusions (2 litres) and those with recurrent or refractory hydrothorax. Contrary to what occurs in the peritoneal cavity, where 2 litres does not cause discomfort, this amount of fluid collection in the pleural cavity causes discomfort and therefore these patients experience rapid relief of symptoms after thoracentesis. In patients with adequate natriuresis (urine sodium >30 mEq/day) a therapeutic thoracentesis followed by diuretics leads to complete resolution of the effusion. However, in those patients with severe sodium retention (urine sodium <10 mEq/day) this measure might need to be repeated often (about every 2 weeks). Angueira and Kadakia[46] found a significant increase in total lung capacity and symptomatic improvement within 2 hours of an average of 3.5 L ascitic fluid removal by paracentesis.
The major risk of this procedure is pneumothorax, which occurs with increasing frequency with serial thoracenteses, increasing from 7.7% at the first therapeutic thoracentesis to 34.7% at the fourth.[47] It is recommended that in most cases no more than 2 L is removed because there is the risk of reexpansion pulmonary oedema or hypotension.[48] Other complications of thoracentesis include pain at puncture site, empyema or soft tissue infection, vasovagal episodes, bleeding hemoptysis, air embolism, laceration of the liver or spleen, and/or subcutaneous emphysema.[49]
Transjugular intrahepatic portosystemic stent-shunt (TIPSS)
The performance of transjugular intrahepatic portosystemic shunts (TIPS) is the procedure of choice in patients with hepatic hydrothorax who do not respond to diuretic treatment and/or repetitive therapeutic thoracentesis. TIPSS is created by placement, under the fluoroscopic guidance of an expandable metal stent in the hepatic parenchyma between the portal and the hepatic venous systems. Therefore, TIPSS reduce portal pressure and addresses the elevated hepatic sinusoidal pressure that leads to ascites.[50,51]
Data in the literature concerning the effectiveness of TIPSS in the management of refractory hepatic hydrothorax are encouraging. TIPSS may lead to a symptomatic improvement in 70-80% of patients with refractory ydrothorax.[52,53,54,55] However, shunt occlusion and hepatic encephalopathy are common complications encountered after the TIPSS placement (25% and 31% of patients, respectively, in a large series). The worsening of pre-existing pulmonary hypertension may also occur. Moreover, an increased mortality rate (20–25%), within the first 2 months after TIPSS placement has been reported. In the vast majority of cases, death is attributed to the complications of end-stage liver disease. A recent study showed that the mortality rates were the same for patients with similar Child–Pugh scores, irrespective of the indication for the procedure.[56]
In a retrospective analysis by Amarapurkar et al,[57] in 23 patients with refractory ascitis/hydrothorax over a span of 10 years, covered (Group B: 11 patients) were compared with uncovered (Group A: 12 patients) TIPSS. Results showed that TIPSS-dysfunction requiring re intervention was significantly more common in Group-A (50%) when compared to Group-B (0%). This showed that covered TIPSS was superior to uncovered TIPSS, because of less TIPSSdysfunction without increasing chances of HE; but failed to offer any survival advantage.
Surgical interventions
Tube thoracostomy with chemical pleurodesis
Tube thoracostomy with subsequent injection of a sclerosing agent, for example, talc, may lead to ablation of the space between the parietal and visceral pleura.[58,59] However, the rates of fluid re-accumulation are extremely high. Moreover, the procedure is associated with a variety of complications, including fever, empyema, chest pain, pneumonia, incomplete re-expansion, and wound infection. Therefore, it is not recommended for the treatment of hepatic hydrothorax in clinical practice.
Other methods, such as video-assisted thoracoscopy with pleurodesis, have been reported with more encouraging results but our experience is limited.[60]
VATS with repair of defects in the diaphragm
A few case reports described the successful surgical repair of diaphragmatic defects responsible for fluid migration into the pleural cavity.[61,62] In a study involving eight patients with refractory hepatic hydrothorax, Moroux et al used videoassisted thoracoscopy in order to repair diaphragmatic defects in addition to pleurodesis. There was a complete response in six cases and no recurrence was detected.[63]
The use of pleura and mesh onlay reinforcementof the diaphragm seems to be an encouraging form of treatment for refractory hepatic hydrothorax.
Peritoneovenous shunts
Peritoneovenous shunting for the management of hepatic hydrothorax has been used in a limited number of patients;[64,65] the results are conflicting. This procedure is associated with serious complications, including hepatic encephalopathy and shunt occlusion that cause significant morbidity and mortality.[66]Therefore, peritoneovenous shunting for the treatment of hepatic hydrothorax was abandoned nearly a decade ago.
Pleurovenous shunts
There have been case reports of success with pleurovenous shunts in patients with refractory hepatic hydrothorax.[67]
Liver transplantation
Recently, Xiol et al studied the outcome of liver transplantation in patients with hepatic hydrothorax. They showed that there were no differences between the hydrothorax group and the control group in the length of surgery, days of mechanical ventilation after surgery, transfusion requirements, and postoperative mortality and long-term survival. Long-term evolution was similar between patients with refractory hepatic hydrothorax or spontaneous bacterial empyema and those with non-complicated hepatic hydrothorax. Therefore, they suggested that hepatic transplantation might be an excellent therapeutic option for patients with hepatic hydrothorax.[68]
Others
Nasal continuous airway pressure (nCPAP)
Conversion of the intra-thoracic pressure from negative to positive might offer a new strategy to control hepatic hydrothorax. The prevalence of snoring is reported to be high, sometimes estimated to be as high as 83%.Therefore, the prevalence of hepatic hydrothorax patients with snoring would also be expected to be high. It has been reported that intrathoracic negative pressure becomes worse when snoring, which exacerbates the hepatic hydrothorax.
There is a case report of successful treatment of refractory hepatic hydrothorax with nCPAP by Takahashi et al.[69
Treatment of subacute bacterial empyema ( SBEM)
In SBEM, therapy with an intravenous third-generation cephalosporin antibiotic (such as ceftriaxone 1-2 g every 24 hours for 7-10 days) should be started after diagnosis. In those with a slow recovery, a repeat thoracentesis is useful to document that the patient is responding. Given that the patients who develop SBEM have approximately a 20% mortality during therapy and that a beneficial effect on mortality has been demonstrated with albumin infusion in the setting of SBP, some authors also use albumin therapy at 1.5 g/kg on day 1 and 1.0 g/kg on day 3 in the setting of SBEM, although albumin infusion has not been specifically studied in the setting of hepatic hydrothorax and SBEM.
Conclusion
Hepatic hydrothorax is an uncommon complication of portal hypertension in patients with liver cirrhosis. The leakage of ascitic fluid via diaphragmatic defects seems to explain the pathogenesis of hepatic hydrothorax. In most cases, dominating clinical manifestations are those of cirrhosis and ascites. However, a variety of respiratory symptoms, including dyspnea, non-productive cough, pleural chest pain, and fatigue due to hypoxemia may also occur. A diagnostic thoracentesis should be performed in any patient with suspected hepatic hydrothorax. In cases where the diagnosis of hepatic hydrothorax is in doubt, an intraperitoneal administration of a radiolabeled substance should be performed. The migration of the radioisotope into the pleural cavity within hours confirms the presence of a communication between the pleural and peritoneal spaces. In the vast majority of cases, patients with hepatic hydrothorax have endstage liver disease. Therefore, they should be considered potential candidates for orthotopic liver transplantation. Until the performance of transplantation, other therapeutic modalities, including a sodium-restricted diet, diuretics, therapeutic thoracentesis, and transjugular intrahepatic portosystemic shunts should be applied in order to relieve symptoms and prevent pulmonary complications.
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