Hidrotórax en Diálisis Peritoneal. A propósito de dos casos / Hydrothorax in peritoneal dialysis: a report of two cases

El hidrotórax como complicación en Diálisis Peritoneal (DP) puede producirse por el paso de líquido de diálisis, de peritoneo a pleura cuando existe una comunicación congénita o adquirida en la barrera diafragmática. Puede ser asintomático o manifestarse con disnea, tos, dolor torácico, disminución del volumen de drenaje o simular un déficit de ultrafiltración. Existe una relación entre el aumento de la Presión Intraperitoneal (PIP) y la aparición de hidrotórax. El diagnóstico se realiza por radiografía de tórax, toracentesis y gammagrafía. Es una complicación seria y poco frecuente que generalmente ocasiona el abandono de la técnica, aunque la realización de pleurodesis química con sustancias esclerosantes (talco, tetraciclinas, sangre) puede ser un tratamiento eficaz para resolver la comunicación pleuroperitoneal. Describimos dos casos de hidrotórax que aparecieron después de tres meses de inicio de la DP, cursaron con derrame pleural derecho, tos, disnea y disminución del volumen de drenaje, el diagnostico se realizo mediante radiografía de tórax, toracentesis y gammagrafía con infusión intraperitoneal del radioisótopo. Los dos casos se resolvieron con la suspensión de la diálisis peritoneal. En base a la relación existente entre la PIP y la aparición de fugas de líquido hacia diferentes cavidades entre ellas la cavidad pleural, podría ser interesante medir y monitorizar los resultados de la Presión Intraperitoneal como parte de la rutina de las actividades enfermeras. Para realizar la gammagrafía, la colaboración entre la Enfermería de DP y Medicina Nuclear permite la administración del radioisótopo de forma segura e indolora (AU)

Hydrothorax as complication in Peritoneal Dialysis (PD) can be produced by the passage of dialysis fluid from the peritoneum to pleura when there is a communication congenital or acquired diaphragmatic wall. It may be asymptomatic or manifest with dyspnea, cough, chest pain, decreased amount of drainage or simulate a deficit of ultrafiltration. There is a relationship between increased intraperitoneal pressure (IP) and the appearance of hydrothorax. The diagnosis is made by chest X-ray, thoracentesis and gammagraphy. It is a serious and rare complication that usually causes the abandonment of techniques while the realization of chemical pleurodesis with sclerosing agents (talc, tetracyclines, blood) can be an effective treatment to solve the pleuroperitoneal communication. We describe two cases of hydrothorax that appeared after three months of start of PD, coursing with right pleural effusion, cough, dyspnea and decreased volume of drainage, the diagnosis was made by chest X-ray, thoracentesis and gammagraphy with intraperitoneal radioisotope infusion. The two cases were resolved with the suspension of peritoneal dialysis. Based on the relationship between the IP and the occurrence of leakage of fluid into different chambers including pleural cavity, it may be interesting to measure and monitor the results of the intraperitoneal pressure as part of the routine activities of nurses. To carry out the gammagraphy, the collaboration between DP nurse and Medicine Nuclear allow the safe and painless administration of the radioisotope (AU)

CD4(+)CD25(-)Foxp3(+) T cells play a role in tuberculous hydrothorax rather than malignant hydrothorax.

BACKGROUND: Foxp3(+) T cells regulate inflammation and tumorigenesis. However, little is known about the role of different subsets of Foxp3(+) T cells in malignant or tuberculous hydrothorax. METHODS: The numbers of CD4(+)CD25(+)Foxp3(+), CD4(+)CD25(-)Foxp3(+) T cells and the levels of some inflammatory cytokines in patients with tuberculous hydrothorax, malignant hydrothorax, and healthy controls (HCs) were examined by flow cytometry and ELISA. The potential association between the numbers of different subsets of Foxp3 + T cells and the values of clinical measures were analyzed. RESULTS: The numbers of peripheral blood CD4(+)CD25(+)Foxp3(+) T cells were greater in malignant hydrothorax patients than in HCs, but fewer than those of hydrothorax in patients. The percentages of circulating IL-10(+) or LAP(+) CD4(+)CD25(+)Foxp3(+) T cells were higher than in the hydrothorax in patients with malignant hydrothorax. The numbers of circulating CD4(+)CD25(-)Foxp3(+) T cells were significantly fewer in patients with tuberculous hydrothorax than in HCs, and both the numbers of circulating CD4(+)CD25(+)Foxp3(+) and CD4(+)CD25(-)Foxp3(+) T cells were significantly fewer than in the hydrothorax in patients. Significantly higher percentages of circulating IL-10(+) or LAP(+) CD4(+)CD25(+)Foxp3(+) and CD4(+)CD25(-)Foxp3(+) T cells were detected in tuberculous hydrothorax patients. The numbers of CD4(+)CD25(+)Foxp3(+) and CD4(+)CD25(-)Foxp3(+) T cells were associated with hydrothorax adenosine deaminase (ADA) levels in tuberculous hydrothorax patients, while CD4(+)CD25(+)Foxp3(+) T cells were associated with carcino-embryonic antigen (CEA) in malignant hydrothorax patients. The concentrations of serum IL-6 and TGF-ß in the patients were significantly higher than that in the HCs, but lower than that in the corresponding hydrothorax. A similar pattern of IL-10 was observed in different groups, except that there was no significant difference in the levels of serum IL-10 between the tuberculous hydrothorax patients and HCs. CONCLUSIONS: CD4(+)CD25(-)Foxp3(+) T cells, which have lower inhibitory function than CD4(+)CD25(+)Foxp3(+) T cells, may play a role in tuberculous hydrothorax.

Identifying transudates misclassified by Light's criteria.

PURPOSE OF REVIEW: Light's criteria combine three dichotomous tests into a decision rule that is considered positive if any one of the tests is positive. This strategy clearly maximizes sensitivity, although at the expense of specificity. Although Light's criteria identify 98% of pleural exudates, they misclassify about 25% of transudates as exudates. The way to overcome this limitation is discussed in this review. RECENT FINDINGS: Traditionally, measurement of the protein gradient between the serum and pleural fluid has been recommended to decrease the misclassification rate of Light's criteria. A recent study demonstrated that a gradient between the albumin levels in the serum and the pleural fluid more than 1.2 g/dl performs significantly better than a protein gradient more than 3.1 g/dl to correctly categorize mislabeled cardiac effusions (83 vs. 55%). On the other hand, the accuracy of a pleural fluid to serum albumin ratio less than 0.6 excelled when compared with albumin and protein gradients in patients with miscategorized hepatic hydrothoraces (77 vs. 62 vs. 61%). SUMMARY: The simplest strategy to reveal the true transudative nature of heart failure-related effusions, labeled as exudates by Light's criteria, is to calculate the serum to pleural fluid albumin gradient. Conversely, for misclassified hepatic hydrothoraces, measurement of the pleural to serum albumin ratio is recommended. The serum to pleural fluid protein gradient should no longer be considered the preferred test for this purpose.

Solving the Light's criteria misclassification rate of cardiac and hepatic transudates.

BACKGROUND AND OBJECTIVE: Pleural transudates are most commonly due to heart failure (HF) or hepatic hydrothorax (HH), but a number of these effusions are misclassified as exudates by standard (Light's) criteria. The aim of this study was to determine the prevalence of mislabelled transudates and to establish simple alternative parameters to correctly identify them. METHODS: We retrospectively analysed the pleural fluid and serum protein, lactate dehydrogenase and albumin concentrations from 364 cardiac effusions and 102 HH. The serum-to-pleural fluid protein and albumin gradients (serum concentration minus pleural fluid concentration), as well as the pleural fluid-to-serum albumin ratio (pleural fluid concentration divided by the serum concentration) were calculated for the mislabelled transudates. RESULTS: Light's criteria had misclassified more HF-associated effusions than HH (29% vs 18%, P = 0.002). A serum-to-pleural fluid protein gradient >3.1 g/dL correctly identified 55% and 61% of the HF and HH false exudates, respectively. The figures for an albumin gradient >1.2 g/dL were 83% and 62%. Finally, a pleural fluid-to-serum albumin ratio <0.6 had identical accuracy for labelling miscategorized cardiac and liver-related effusions (78% and 77%, respectively). CONCLUSIONS: If the clinical picture is consistent with HF but the pleural fluid meets Light's exudative criteria, the measurement of the albumin rather than the protein gradient is recommended. In the context of cirrhosis, a potentially 'false' exudate is identified better by the pleural fluid-to-serum albumin ratio.

Clinical utility of pleural fluid NT-pro brain natriuretic peptide (NT-proBNP) in patients with pleural effusions.

BACKGROUND: Pleural effusion is not a pathognomonic sign and distinguishing between transudates and exudates often presents a diagnostic dilemma. OBJECTIVE: To examine whether the NT pro-brain natriuretic peptide (NT-proBNP) in pleural fluid is a diagnostic tool for determining the cardiac etiology of pleural effusions. METHODS: We measured pleural fluid and serum NT-proBNP levels in a consecutive series of 98 patients with heart failure and in 142 patients with other causes. RESULTS: The median pleural fluid NT-proBNP levels among the heart failure patients were significantly higher (3,310 pg/mL) than hepatic hydrothorax (16 patients, 531 pg/mL), malignant pleural effusion (38 patients, 733 pg/mL), parapneumonic pleural effusion (40 patients, 294 pg/mL), and tuberculous pleural effusion (64 patients, 214 pg/mL) (p<0.001). At a cut-off point of > or = 1,714 pg/mL, the test had a sensitivity of 99%, a specificity of 99 % for the diagnosis of heart failure. There were 28 patients with pleural effusion due to heart failure misclassified as exudates by Light's criteria. Ten cases of misclassified heart failure (36% of 28 patients) showed serum-effusion protein gradient less than 3.1 g/dL; 26 of them exhibited pleural fluid NT-proBNP levels of > or = 1,714 pg/mL. The 26 patients of misclassified heart failure received diuretics before thoracentesis. Pleural fluid NT-proBNP levels were correlated with serum NT-proBNP levels (R(2)=0.928, p<0.001). CONCLUSION: Pleural fluid NT-proBNP may be useful in the diagnosis of pleural effusion resulting from heart failure. The test may be especially useful in heart failure patients with exudates who have been treated with diuretics.

Contribution of lymphatic drainage through stomata to albumin removal from pleural space.

The contribution of lymphatic drainage through the stomata of parietal mesothelium to the overall removal of labeled albumin from the pleural space was found 89% in sheep with very large hydrothoraces (10 ml/kg), a condition involving a approximately 20 times increase in lymphatic drainage [Broaddus et al., J. Appl. Physiol. 64 (1988) 384]. We determined this contribution in anesthetized rabbits with small (0.12 ml/kg) and large (2.4 ml/kg) hydrothoraces of Ringer-albumin with labeled albumin and labeled dextran-2000 kDa. This dextran was used as marker of liquid removal through the stomata because it should essentially leave the pleural space through the stomata only, owing to its size. The removal of labeled albumin by lymphatic drainage through the stomata was 39% of the overall removal in the small hydrothoraces, and 64% in the large ones. Hence, lymphatic drainage through the stomata does not contribute most of protein and liquid removal from the pleural space under physiological conditions, as it has been maintained. It markedly increases with the increase in pleural liquid volume.

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.

Effect of adrenaline and alpha-agonists on net rate of liquid absorption from the pleural space of rabbits.

Indirect evidence supporting a solute-coupled liquid absorption from the pleural space of rabbits has recently been provided; moreover, the beta 2-adrenoceptor agonist terbutaline has been found to increase this absorption. In this study the effect of adrenaline and alpha-adrenoceptor agonists on net rate of liquid absorption (Jnet) from albumin Ringer hydrothoraces of various sizes has been determined in anaesthetized rabbits. In hydrothoraces with adrenaline (5 x 10(-6) M) the relationship between Jnet and volume of liquid injected was displaced upwards by 0.09 ml h-1 relative to that in control hydrothoraces (P < 0.01). This displacement did not occur with lower adrenaline concentrations or after pretreatment with the beta-blocker propranolol. Hence, this increase in Jnet is mediated by stimulation of beta-receptors. It seems to be caused by an increase in solute-coupled liquid absorption, since beta-agonists inhibit lymphatic activity while, at relatively high concentrations, they may increase active transport. Conversely, the strong stimulation of lymphatic alpha-receptors that should occur with adrenaline after beta-blockade may fail to increase lymphatic drainage, because it has been shown that the increase in contraction frequency of lymphatics may be balanced by the decrease in their stroke volume. Arterial blood pressure during the hydrothoraces with adrenaline was unchanged. In hydrothoraces with the alpha 2-agonist clonidine (5 x 10(-6) M; a less potent agent than adrenaline) the slope of the relationship between Jnet and volume injected increased by 26% (P < 0.01), while its origin did not change. This increase in slope did not occur with a lower clonidine concentration or after pretreatment with the alpha-blocker phentolamine. Hence, it is caused by stimulation of alpha 2-receptors, which probably lead to an increase in lymphatic drainage related to liquid load. In hydrothoraces with the alpha 1-agonist phenylephrine (5 x 10(-6) or 10(-7) M) Jnet was simlar to control values.

Effect on phloridzin on net rate of liquid absorption from the pleural space of rabbits.

Previous indirect findings have suggested the occurrence of solute-coupled liquid absorption from the pleural space, consistent with Na(+)-K(+)-ATPase on the interstitial side plus a Na(+)-H+ and CI(-)-HCO3- double exchange on the luminal side of the pleural mesothelium. To assess whether Na(+)-glucose cotransport also operates on the luminal side, the relationship between net rate of liquid absorption from the right pleural space (Jnet) and volume of liquid injected into this space (0.5, 1 or 2 ml) was determined in anaesthetized rabbits during hydrothoraces with phloridzin (10(-3)M) or with phloridzin plus 4-acetamido-4'-isothiocyanatostilbene-2, 2'-disulphonic acid (SITS; 1.5 x 10(-4)M). The relationship obtained during hydrothoraces with phloridzin was displaced downwards by 0.09 ml h-1 relative to that in control hydrothoraces (P < 0.01). The decrease in Jnet was similar in hydrothoraces of various sizes. The relationship obtained in hydrothoraces with phloridzin plus SITS was displaced downwards by 0.16 ml h-1 relative to that in control hydrothoraces (P < 0.01), i.e. the decrease in Jnet was similar to the sum (0.17 ml h-1) of the decreases in Jnet produced individually by phloridzin and by SITS (0.08 ml h-1). The decrease in Jnet was similar in hydrothoraces of differing size. The above findings are consistent with the occurrence of Na(+)-glucose cotransport on the luminal side of the pleural mesothelium, operating simultaneously with the double exchange also under physiological conditions.

Beta-agonist activation of an amiloride-insensitive transport mechanism in rabbit pleura.

The beta-agonist terbutaline increases the net rate of liquid absorption from hydrothoraces with albumin-Ringer solution: since beta-agonists decrease lymphatic drainage, the effect of terbutaline seems due to an increase in solute-coupled liquid absorption, (Zocchi et al. 1994 Respir. Physiol. 97:347-356). In this research we determined in anesthetized rabbits the rate of volume change in albumin-Ringer hydrothoraces of different size with amiloride plus terbutaline, and compared it with that previously obtained in hydrothoraces with amiloride alone. The net rate of liquid absorption was 0.09 ml/h greater (P < 0.01) with amiloride plus terbutaline than with amiloride alone. This indicates that terbutaline activates an amiloride-insensitive mechanism of Na+ transport. The increase in net rate of liquid absorption produced by terbutaline persisted with bumetanide 10(-6) M and SITS 10(-4) M, disappeared almost completely with bumetanide 10(-5) M, and completely with furosemide 10(-3) M. These findings suggest that the mechanism activated by terbutaline, when the amiloride-sensitive mechanisms of the pleura have been blocked, is a Na(+)-K(+)-2 Cl- or Na(+)-Cl- symport little sensitive to bumetanide.

[Dynamics of pleural liquid in hydrothorax].

The basics of pleural liquid dynamics are summarized. The normal pleural cavity contains a small amount of pleural liquid (0.1-0.3 ml/kg). Its protein concentration is about 1.0 g/dl and its pH is 7.6. The normal flow of pleural liquid is gravity dependent, and pleural liquid flows from the costal to the mediastinal region. In experimental hydrothorax, the pleural liquid was removed mainly via lymphatics. The turnover of the pleural liquid is rapid, and it depends on the area of contact between pleural liquid and pleural and on the blood flow to the pleura.

Active Na+ transport and coupled liquid outflow from hydrothoraces of various size.

The net rate of liquid flow and Na+ flux across the pleura was determined in anesthetised rabbit during hydrothoraces 0.5 to 5 ml in size, without and with amiloride. In the hydrothoraces with amiloride the net liquid flow and Na+ flux reversed when the volume injected approached zero. This indicates that the active Na+ transport and the consequent liquid absorption occur also under physiological conditions. The difference between the data obtained without and with amiloride provides the net solute-coupled liquid outflow and active Na+ efflux. These parameters increased linearly with the hydrothorax size up to 2 ml (0.39 ml/h and 54 muEq/h, respectively), and then levelled off. The linear relationship allowed their extrapolation to physiological conditions: 0.15 ml/h (0.07 ml.h-1.kg-1) and 21 muEq/h (0.1 muEq.h-1.cm-2). The increase in these parameters with the hydrothorax size seems due to the protein dilution caused by the Ringer injection, because it did not occur if Ringer was added with albumin to keep the protein concentration in the pleural liquid similar to that under physiological conditions.

Starling forces and lymphatic drainage in pleural liquid and protein exchanges.

Pleural liquid volume and protein concentration (C) were determined in rabbits 60 min after a 2 ml hydrothorax with various albumin concentrations in Ringer, homologous serum or plasma. The absorption rate of the hydrothorax decreased with the increase in colloid osmotic pressure of the pleural liquid (pi), being 0.56 +/- 0.03, 0.32 +/- 0.02 and 0.17 +/- 0.05 ml/h with Ringer, 1.1 and 3 g% albumin, respectively, and nil with 5% albumin, serum or plasma. C increased with Ringer and 1.1% albumin, did not change with 3% albumin, and decreased with 5% albumin, serum or plasma. The protein content in the pleural liquid increased with Ringer, did not change with 1.1% albumin, and decreased with the other hydrothoraces. These findings indicate that with hydrothoraces of this size: (1) the Starling forces plus the solute-coupled liquid absorption [Agostoni and Zocchi (1990) Respir. Physiol. 81: 19-28] provide most of the pleural liquid absorption when pi is less than or equal to physiological; (2) the lymphatic drainage increases with pi, providing most of the liquid outflow when pi is similar to that of plasma. This increase in lymphatic drainage, however, does not compensate for the effects of the changes in Starling forces produced by the increased pi.

Reabsorption of a saline- or plasma-induced hydrothorax.

In supine rabbits injection of 2 ml of saline into the lower right diaphragmatic region increased pleural liquid pressure at the injection point and, to a minor extent, on the costal and mediastinal side, indicating a redistribution of liquid among the pleural compartments. Over a period of 120 min end-expiratory liquid pressure on the diaphragmatic and costal surfaces approached the control value as a result of local reabsorption. No difference in the time course of liquid pressure was found on injection of either saline or homologous plasma. This was confirmed by measuring the volume of saline or plasma remaining in the cavity 90 min after injection; the net absorption flow amounted to 0.22 ml . kg-1 . h-1. These results suggest that local absorption mechanisms are relatively independent of the Starling pressure gradients acting across the pulmonary-perfused (-10.2 and 6.6 cmH2O with saline and plasma, respectively, the negative sign indicating a reabsorption gradient) and systemically perfused mesothelium (3.3 and 20.1 cmH2O with saline and plasma, respectively).