Peritoneal Dialysis International, Vol. 18, pp 5 -10 0896 -8608/98 $300 + 00
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EDITORIAL
HYDROTHORAX IN PERITONEAL DIAL YSIS
H
ydrothorax associated with abnormal commu nications between the peritoneal and abdominal cavities was first described by Meigs, who re ported the coexistence of pleural effusion and ascites associated with ovarian fibroma ( 1). Likewise, Ratnoff, quoted by Popper, gave one of the first descriptions of hydrothorax as a complication of ascites associated with liver cirrhosis (2).
Since then, various authors have approached the study of
"hepatic hydrothorax" (3-9). Recently, several cases have been reported associated with ovarian stimulation (10). As a replacement therapy for chronic renal failure, peritoneal dialysis (PD) involves the abdominal instillation of a variable volume of dialysis solution, giving rise to an
"artificial ascites." The common denominator of all cases of hydrothorax that have been reported is the presence of fluid in the peritoneal cavity combined with an increase in hydrostatic pressure.
With the increasing use of PD as a replacement therapy in chronic renal failure, the number of complications related to PD also has increased (11,12); one of these is hydrothorax associated with anomalous pleuroperitoneal communications. The first descriptions of this complication are credited to Edward, Unger, Finn, and Jowett in the 1960s (13,14). Since then, others have reported such cases and examined different aspects of this complication (15-23).
The prevalence of this complication varies, ranging from 1.6% in Nomoto et al.'s series, which reported 50 cases of hydrothorax in a population of 3195 PD
patients (17); 2.9% in the series studied by Shemin et al.
(18); and as high as 10% in Chow et al.'s series (19). The actual frequency may be much higher because low degrees of hydrothorax may pass unnoticed. Its prevalence is similartothatofhydrothorax observed among cirrhotic patients with ascites but without renal failure (6,7,24).
This complication is serious, although generally not life- threatening. On many occasions, it forces the patient to withdraw from PD and to accept a temporary or permanent transfer to hemodialysis (HD) (11-23). It has been described much more often in women (13-16,22), although only 46% of Nomoto's patients were women. It develops chiefly in the right
hemithorax, indeed 88% of Nomoto's cases were in this location (17).
SYMPTOMS
The most common presentation is immediately after starting PD or a few days later, although cases have been described with a longer latent period, even several years (12,17). Sometimes, it is asymptomatic and is detected accidentally in a routine chest radiograph. In some cases the patient reports only a decrease in ultrafiltration, which indicates that dialysate is collecting in the pleural space. On other occasions, the hydrothorax presents with suddenonset dyspnea and compromised ventilation that requires thoracocentes is. Less common symptoms are pleuritic chest pain, weight gain, and hypotension.
A prominent predisposing factor cited in the literature is polycystic kidney disease, because the kidney's volume decreases abdominal capacity and the subsequent infusion of dialysate increases the hydrostatic pressure (25). It has been proposed that peritonitis increases the incidence of hydrothorax by exacerbating the continuity defects in the perito
neopleural structures; Shemin et al. note that 6% of their hydrothorax patients had suffered peritonitis
(18).
In most cases, no triggering factor is identified. In some instances the condition appeared after coughing fits (26) or in association with tight girdles worn
for reasons of fashion (27).
PATHOGENESIS
Based on the early appearance and the lack of a relationship with the volume infused, some authors believe that the dialysate enters the pleural cavity from the abdominal cavity through hereditary pleura peritoneal communications (8,9,16-23). Autopsies have shown discontinuities in the tendinous portions of the hemidiaphragms (7,8,20,21) and the absence of muscle fibres, which have been replaced by a weaker collagen network (7,8). Assuming that such defects exist, the mechanism behind the hydrothorax
is simple: the physiological negative pressure in the pleural space and the increased positive pressure in the peritoneal cavity caused by the presence of fluid favors the passage of the fluid along the pressure gradient; thereafter, the fluid will remain in the pleural cavity until the gradient disappears. This mechanism explains the development of massive hydrothorax shortly after starting dialysis and the remissions observed after stopping PD, as the pressure gradient has been eliminated.
Other authors, observing the persistence of pleural effusion after abdominal emptying, believe that the passage of fluid is one-way, from the abdomen to the pleura, either because of a valve defect or due to the tamponade action of the subphrenic hepatic capsule (22). However, the late appearance of hydrothorax suggests an acquired mechanism such as a constant increase in intra-abdominal pressure that causes small discontinuities due to the breakage of collagen fibres in the diaphragmatic pleuroperi- toneum; this action gives rise to small "bubbles" that, within a weakened tissue, can break, allowing com- munication between the two cavities (8,12,17,21, 22,28).
Another mechanism that has been postulated is lymph drainage disorders, particularly in the right hemidiaphragm, where this system is most abundant (8,28-30).
DIAGNOSI S
Pleural effusions in PD patients may be due to other factors and the pleura peritoneal structures may be normal (31). The most common are salt/water retention with expansion of extracellular volume, heart failure, and hypoproteinemia. One should keep in mind the coexistence of hydrothorax with pleural or lung disease, such as malignancies, tuberculosis, etc.
Mter ruling out these causes, the clinical presentation induces the clinician to suspect the diagnosis of secondary hydrothorax. Chest auscultation shows that there is no ventilatory function over the hydrothorax. The sounds obtained on percussion are dull and vocal vibrations are not transmitted. Posteroanterior and lateral radiographs of the chest reveal the existence of hydrothorax.
The chemical characteristics of the pleural fluid should be compared with those of the patient's blood. It has the characteristics of a transudate, with a protein content less than 30 -35 g/L. Pleural LDH levels are low and glucose content is high, similar to that of the dialysis fluid and higher than the patient's blood sugar level, even if he/she is diabetic. These differences, which are found in major hydrothoraces, are not as evident in minor hydrothorax or in those instances where the evacuation of pleural fluid has
been delayed, because the glucose is reabsorbed via the pleural membrane (28,32). Some authors recommend the assay of D-Iactate in the sample, because this agent is a buffer in the dialysis solution and is not found in the body (12). When the diagnosis is in doubt, one can add a diluted dye (methylene blue, indigo) to the dialysis bag, which, after it has been instilled into the peritoneum, can be detected subsequently in the pleural fluid. In addition to giving false negatives, this technique is not without risk because in some patients it can provoke chemical peritonitis (32) or side effects related to the dye itself (e.g., general reaction, fever, malaise) (33). Consequently, many carry out peritoneography with tradi
tional iodinated contrast (Hypaque, SanofiWinthrop, NY, U.S.A.) and, later, nonionic, isotonic iodinated contrast (lopamidol). While these substances do not damage the peritoneum (34), their diffusion is low.
The currently preferred technique uses radionuclides such as macro aggregate 99Tc added to the dialysis
bag at a dose of 3 -10 mCi. This provides more accurate information about the existence of pleuroperitoneal communications and, sometimes, the precise location of the abnormal communication, while preserving the peritoneum.
The radioactive risk to the patient is low. Mter administration, the patient walks and adopts various lying positions to ensure complete homogenization of the isotope and to assist its passage through the communication.
However, its reliability is not absolute (32,35-39).
TREATMEN T
We will discuss the immediate treatment of the complication and subsequent therapy aimed at closing the pleuroperitoneal communication. If the hydrothorax is severe enough to compromise the patient's ventilatory function, a thoracocentesis must be performed, after which the patient usually improves dramatically. If the hydrothorax is minor , discontinuance of PD will produce a marked reduction in the effusion and bring rapid improvement. If the condition resolves more slowly, the clinician can assume the existence of a valvular communication that is delaying return of the dialysate to the abdomi nal cavity.
Once the acute symptoms have resolved, one should reconsider the wisdom of having a patient with hydrothorax on PD. Mter treating the hydrothorax or in response to the patient's request, there are some authorities who convert the patient to permanent HD, ifhe/she has no formal contraindications to this technique (40-42). If subsequently there is no in crease in intra-abdominal pressure, a recurrence is unlikely. Spontaneous resolution of these hydrothoraces has been reported (43).
Where one cannot arrange even a temporary conversion to another mode of dialysis because of associated pathology or the patient's refusal, some authors suggest that the patient continue on PD but use only hypertonic solutions with "night-time rest" (daytime PD) ( 44). Others use low volume exchanges and others, in addition to this, also dialyze patients in a semisitting position or use only low-volume intermit tent PD ( 45-48).
If a temporary transfer to HD is possible, the PD is stopped and, after obtaining a temporary vascular access (subclavian or jugular central catheter), the patient remains on HD for approximately 4 weeks. Subsequently, PD is resumed with a higher number of lower volume exchanges.
Sometimes, the patient can be put on automated PD, which produces lower increases in intra-abdominal pressure.
These procedures seek to encourage spontaneous closure of the pleuroperitoneal communication by eliminating the pressure gradient between the two cavities.
Some have suggested that the dialysate itself could act as a sclerosant by promoting a "waterproof seal" of the epithelial layers (12,43). In spite of occasional spontaneous resolutions, cure rates are about 40% (49) and recurrences
are common.
In contrast to this "wait-and-see" attitude, one may choose such interventionist procedures as pleurodesis:
adhesion of the pleurae using irritants instilled into the pleural cavity (chemical pleurodesis), by pleurectomy, or by mechanical abrasion of the pleurae. The first technique is the traditional treatment for pneumothorax and pleural effusions caused by other conditions (50). The instilled substances irritate the epithelial surface of the pleurae, giving rise to an inflammatory reaction and pleural fibrosis.
Among the most common of these substances have been:
asbestos-free talc (51); tetracyclines (52); fibrin derivatives such as Tissucol (Immuno AG, Vienna, Austria) with two components: fibrinogen and factor XIII, plus an aprotinin - thrombin solution (53); Nacardia rubra cell-wall skeleton (54) and OK-432 (hemolytic streptococcal derivatives) (55); and, more recently, autologous blood obtained from a peripheral vein (56-59).
The administration of talc and tetracycline re quires prior sedation and analgesia because the procedure is painful and may cause a general reaction with fever, malaise, and, rarely, infection (local and empyema) and respiratory failure (51). Both agents may reach the abdominal cavity and cause peritoneal fibrosis. Talc is insoluble, is not absorbed, and remains indefinitely in the pleural cavity.
Consequently, the results in other types of pleural effusion have been better (51) although, in PD-inducedhydrothorax, the results are equivalent (49).
With fibrin derivatives, the procedure is more laborious and these products may be vehicles for hepatitis B. With autologous blood, the procedure is painless and, in the event of recurrence, can be repeated (58). Under local or general anesthesia and with a short hospital stay (60,61), perhaps with video-assistance (VATS) (62,63), the product is in- stilled directly through the thoracocentesis trocar , with direct thoracoscopy; or it may be done with thoracotomy, which requires general anesthesia. Mter having been administered the fibrosant agent, the patient must remain recumbent, adopting various lying positions (as per Fowler, see Ref. 64) to ensure broad distribution. With these procedures , PD is stopped for about 4 weeks -the time thought to be needed for permanent fibrosis and the oblitera tion of the abnormal communication(s) -and, if necessary, the patient is transferred to HD. At the end of this period, the PD is resumed with small volumes that are gradually increased. However, in spite of this, the failure rates after pleurodesis are high (49).
The most radical approach, used in recurrent cases or sometimes as a first approach if the patient's general condition is good enough, is surgical repair with thoracotomy, which requires general anesthesia (21,49,65,66). The defects are located, sutured, and can be reinforced with prosthetic material such as Teflon (49).
Sometimes, the discontinuities or "bubbles" in the tendinous hemidiaphragms are so small that they are difficult to identify.
With regard to the variability of the results, in their series, Nomotoet al. reported that stopping PD alone or in combination with pleurodesis achieved a 50% success rate;
the remainder ofhis patients were transferred to HD (17).
Mter reviewing Nomoto's report, four studies published between 1982 and 1991, and isolated case reports (17,19,52,67 ,68) -a total of81 episodes and many different treatments Allen and Mat thews ( 49) reported that, of 56 patients who received conservative therapy, 30 were not re- lieved of their hydrothoraces and were transferred to HD (53%); of23 patients treated with pleurodesis, 10 were not relieved (43%), and subsequently, in 2 patients treated with surgery, the hydrothorax disappeared. The results obtained with conservative therapy, and even with pleurodesis, cast doubt on the efficacy of these techniques. Scheldewaert advises us to perform thoracoscopy and, only if the communication is visible, to resort to operation (68).
In our series of 128 patients seen in our PD program between 1986 and 1997, 4 (2 males, 2 females) developed hydrothorax (3.12%). Their average age was 53 years (31 - 78 yr). None had polycystic kidney disease and none had a history of respiratory disease, heart failure, or hypoproteinemia. All pre
sented with sudden-onset dyspnea and decreases in the dialysate volume drained. The effusion was in the right hemithorax in all cases. It appeared early, with a mean of 12 weeks after starting PD (5 -20 weeks). None required thoracocentesis. The hydrothorax decreased markedly within 24 -48 hours. In 3 patients, we found a considerable difference in the glucose content in the pleural fluid and in the blood. In the other patient, the pleural sample was de layed, hence the results cannot be relied upon. In 1 patient, 99Tc scintigraphy was inconclusive. Two
patients were transferred directly to HD; the other 2 had a pleurodesis with autologous blood. Both of these patients had a recurrence and a second pleuro desis. A further recurrence developed in 1 of these patients, who was then transferred to HD; the other withdrew from PD because of catheter-related complications and the result of the repeated sclerosis is unknown.
Our results in the management of hydrothorax have not been encouraging. As noted earlier, different treatment regimens give variable results, but the recurrence rate is high. The operative treatment gives the highest success rate but, in these patients, associated disease makes this approach questionable. Consequently, at present we have no simple, safe tr.eatment that provides good results.
R. Garcia Ramon A. Miguel Carrasco Peritoneal Dialysis Unit Nephrology Department Hospital Clínico
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