Ann Thorac Surg 1999;67:1518-1522
© 1999 The Society of Thoracic Surgeons
Collective Reviews
Thoracic complications of peritoneal dialysis
G. Chad Hughes, MDa,
Terry L. Ketchersid, MDa,
Jonathan M. Lenzen, MDa,
James E. Lowe, MDa
a Division of Cardiovascular and Thoracic Surgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA
Address reprint requests to Dr Lowe, Duke University Medical Center, Box 3954, Durham, NC 27710
e-mail: lowe0004{at}mc.duke.edu
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Abstract
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Approximately 20% of the 100,000 patients in the United States currently undergoing dialysis therapy for end-stage renal disease use the technique of peritoneal dialysis. We present a patient on peritoneal dialysis who developed a large posterior mediastinal mass, which on surgical exploration was found to be a paraesophageal hernia sac filled with omentum and dialysis fluid. We use this case as an introduction to review the thoracic complications of peritoneal dialysis.
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Introduction
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There are currently over 100,000 people in the United States with end-stage renal disease maintained on chronic dialysis [1], approximately 20% of whom use peritoneal dialysis [13]. There are several major types of peritoneal dialysis [2, 3], which vary according to patient needs: intermittent peritoneal dialysis (IPD), continuous ambulatory peritoneal dialysis (CAPD), and continuous cyclic peritoneal dialysis (CCPD). IPD involves several 1-hour exchanges per day, whereas in CAPD the dialysate is allowed to dwell for 48-hours before drainage. This cycle is then repeated up to 4 times daily. In CCPD, an automated cycling device performs three or more exchanges at night while the patient sleeps, followed by a single ambulatory cycle the next day [2]. Peritoneal dialysis allows patients fewer lifestyle restrictions, as well as improved blood pressure and fluid and electrolyte control, as compared with hemodialysis [1].
We present a patient who developed a paraesophageal hernia filled with peritoneal dialysate, which masqueraded as a posterior mediastinal mass. This is an extremely rare entity; we were unable to find a previous report in the literature. This case will serve as an introduction to a review of the thoracic complications of peritoneal dialysis.
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Case report
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The patient is a 32-year-old black male with end-stage renal disease secondary to hypertension who has been maintained on peritoneal dialysis since January 1995. A chest roentgenogram performed in July 1997, as part of a prerenal transplant evaluation, was remarkable for a posterior mediastinal mass located in the retrocardiac area (Fig 1). The patient was asymptomatic at that time. The mass was not present on a prior chest film 2.5 years earlier. A computed tomographic (CT) scan of the chest confirmed the presence of an extensive mass in the retrocardiac area of the lower mediastinum extending superiorly to the level of the carina. The upper abdomen and adrenal glands were normal. Bronchoscopy and barium swallow (Fig 2) were unremarkable. The patient was subsequently referred for surgical evaluation. He was taken to the operating room in August 1997, where he underwent a left posterolateral thoracotomy through the seventh intercostal space under general anesthesia. Intraoperative findings were remarkable for a large cystic-appearing posterior mediastinal mass medial to the aorta. The pleura over the mass was incised, and the mass itself was found to be a paraesophageal hernia sac. The hernia defect in the diaphragm measured approximately 1 cm in diameter and was located lateral to the esophagus on the left. A small portion of omentum was found protruding through the defect inside the hernia sac. In addition, the sac was filled with approximately 400 cc of dialysate fluid. The diaphragmatic defect was closed primarily with a running 2-0 nonabsorbable suture. The hernia sac edges were then trimmed and closed in three separate layers. The patient was awakened and extubated in the operating room, and had an uncomplicated postoperative course. His peritoneal dialysis was resumed on postoperative day 1 and was well tolerated. He was discharged to home on postoperative day 5. At 12-month follow-up, the patient is doing well and is currently awaiting renal transplantation.

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Fig 1. Chest roentgenogram demonstrating the retrocardiac mediastinal mass. The mass was not present on a prior film 2.5 years earlier.
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Fig 2. Barium swallow performed at the referring hospital, which failed to demonstrate the large paraesophageal hernia.
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Comment
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During their first year of treatment, 50% of patients on peritoneal dialysis (PD) are hospitalized for complications related to this therapy [2]. The thoracic complications of peritoneal dialysis have been recognized as early as the mid-1960s [4] and can be divided into several categories: - Infectious complications
- Bronchitis
- Pneumonia
- Effects on respiratory muscle function
- Decreased maximal inspiratory and expiratory pressures
- Decreased total lung capacity
- Decreased residual volume
- Decreased DLCO
- Cardiovascular complications
- Decreased preload
- Decreased stroke volume and cardiac output
- Hypotension
- Increased intraabdominal pressure
- Acute, massive hydrothorax
- Paraesophageal hernia
- Foramen of Bochdalek hernia
- Foramen of Morgagni hernia
- Boerhaaves syndrome
- Other
- Pulmonary edema
- Uremic pleuritis
- Uremic pericarditis
- Renal osteodystrophy
- Metastatic pulmonary calcifications
Other thoracic complications related to end-stage renal disease and not to peritoneal dialysis per se, such as pulmonary edema, uremic pleuritis and pericarditis, renal osteodystrophy, and metastatic pulmonary calcifications, will not be discussed and have been reviewed in detail elsewhere [5].
Infection
An increased risk of infectious complications has long been recognized in patients with end-stage renal disease [4]. This increased susceptibility is now known to be secondary to depressed humoral and cellular immunity, as well as impaired macrophage function, changes that are not modified by dialytic therapy [5]. Consequently, patients on peritoneal dialysis have an increased incidence of both bronchitis and pneumonia [4, 5]. This increased risk of bronchopulmonary infection may be attributed, at least in part, to impaired pulmonary toilet as outlined below.
Effects on respiratory muscle function
The administration of dialysis fluid into the peritoneal cavity may affect the function of the respiratory muscles due to alterations in their force-length relationship [6]. Maximal inspiratory and expiratory pressures have been shown to decrease significantly during peritoneal dialysis, with a subsequent return to normal after dialysate drainage. Total lung capacity and residual volume are significantly reduced as well [6]. This decrease in lung volumes and ventilatory pressures likely contributes to the commonly observed complications of atelectasis and bronchopneumonia [4, 7]. In fact, basal platelike atelectasis may be seen in up to 50% of patients undergoing peritoneal dialysis [5]. These changes may be aggravated by uremic myopathy and phrenic neuropathy, which lead to further ventilatory insufficiency from diaphragmatic fatigue [8]. In addition, a reduction in carbon monoxide diffusion capacity (DLCO) is common. This may be seen even with a normal chest radiograph and is possibly secondary to subclinical interstitial pulmonary edema [9].
Cardiovascular complications
In addition to coronary artery disease, left ventricular hypertrophy, and myocardial fibrosis, which often accompany the uremic state [10], peritoneal dialysis itself may occasionally have direct effects on the cardiovascular system. The presence of dialysis fluid in the peritoneal cavity has the potential to affect cardiac function by impairing venous return secondary to inferior vena caval compression [1014]. Gotloib and colleagues [12] reported significant reductions in cardiac output and stroke volume with increasing dialysate exchange volumes. However, other studies [13] have found no effect on cardiac function with infusion of up to 3 L of dialysate. More recently, Franklin and associates [14] have found that only patients with left ventricular hypertrophy demonstrated evidence of impaired systolic function with infusion of large volumes of dialysate. This diminished systolic function was felt secondary to impaired ventricular filling, as evidenced by a decrease in end-diastolic left ventricular diameter by echocardiography. From a physiologic standpoint, the results of the latter study seem most plausible, as those patients with hypertrophic ventricles and decreased compliance should be most vulnerable to diminished preload [10]. In summary, the presence of intraperitoneal dialysate does not usually exert a deleterious effect on cardiac function, although there is a potential for such effects with the use of large (> 3 L) volumes in patients with diminished ventricular compliance [10].
Complications related to increased intraabdominal pressure
The most common complications of PD are infectious including both peritonitis and catheter exit site infections. However, the majority of other complications occurring in PD patients are related to an elevation in intraabdominal pressure after infusion of dialysate [15]. The intraabdominal pressure may increase from the normal of 0.5 to 2.2 cm H2O to as high as 10 cm H2O with the infusion of 2 L of dialysate fluid [12, 15]. This increase in intraabdominal pressure then leads to leakage of peritoneal fluid out of the abdominal cavity, as in the development of hydrothorax and thoracic, abdominal, and groin hernias [15].
Hydrothorax
Patients on peritoneal dialysis often develop small, chronic pleural effusions secondary to increased movement of fluid from the peritoneal to pleural spaces via the diaphragmatic lymphatics [4, 7]. However, these small effusions differ from the acute, massive hydrothoraces, which may require the involvement of a thoracic surgeon. First reported in 1967 by Edwards and Unger [16], this complication has been reported to occur in 2% of patients undergoing peritoneal dialysis [17]. Hydrothorax appears to be more common on the right [7, 15, 17], and has been reported to present as life-threatening tension hydrothorax with cardiovascular instability [18]. Early reports stated acute hydrothorax was more common in women [19], possibly secondary to diaphragmatic involvement with endometriosis [20], although a prospective study of over 3,000 patients in Japan found no gender predilection [21]. The pathogenesis is likely related to congenital or acquired defects in the diaphragm, which allow the dialysate to reach the pleural space [7, 15, 19, 21, 22], similar to the etiology of hepatic hydrothorax in cirrhotic patients with ascites [23]. The dialysate is driven across the diaphragm into the negative pressure thorax by the large pressure gradient created by filling the abdominal cavity with fluid [18]. These anatomic defects have been reported to occur more commonly on the right [21], thus explaining the right-sided predominance of this entity.
The usual clinical presentation is that of new onset dyspnea during peritoneal dialysis [7, 21]; however, as many as a quarter of patients will be asymptomatic [21]. Hydrothorax appears to be more common in the first 30 days after starting peritoneal dialysis [21], although it may occur at any time. The diagnosis is initially suspected by finding diminished breath sounds and dullness to percussion on the side of the effusion. Confirmation is made by chest roentgenogram (Fig 3). The source of the pleural fluid is dialysate originating from the peritoneal cavity. This may be confirmed by finding a very high glucose concentration in the pleural fluid as compared with serum, although occasionally the glucose concentration may be only modestly elevated if thoracentesis is not performed immediately after the fluid exchange precipitating the hydrothorax [19]. The fluid should also contain both the L- and D+ isomers of lactate since the dialysate contains a racemic lactate buffer, unlike other endogenous sources of pleural fluid, which contain only the physiologic L- isomer found in mammals [19]. Another method to prove the abdominal origin of the hydrothorax fluid involves the instillation of methylene blue dye into the peritoneal cavity with subsequent pleural detection upon thoracentesis. However, if a large amount of dialysate remains in the abdomen, the dye may be diluted before reaching the thoracic cavity, thus making detection difficult. In addition, instillation of methylene blue into the abdomen has been associated with significant pain, likely secondary to chemical irritation [19, 20]. Other techniques used to confirm the extrathoracic origin of the fluid have included nuclear scans with technetium 99-tagged macroaggregated albumin instilled intraperitoneally [2426] and CT peritoneography [27].

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Fig 3. Chest roentgenogram revealing a massive right hydrothorax in a 42-year-old female with end-stage renal disease secondary to diabetes who presented with progressive shortness of breath approximately 2 weeks after starting peritoneal dialysis.
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The initial management of acute hydrothorax involves a discontinuation of peritoneal dialysis. The dialysis catheter should be allowed to drain all fluid from the abdomen. If the patient experiences any degree of respiratory difficulty, therapeutic thoracentesis should be performed. If the patient is not in respiratory distress, then either diagnostic thoracentesis or CT with intraperitoneal contrast or peritoneal scintigraphy may be considered to confirm the origin of fluid. If thoracentesis is performed, the fluid should be sent for glucose and protein concentration, as well as assay for the D+ and L- isomers of lactate. A high glucose and low protein concentration along with the presence of both lactate isomers in the fluid confirms the origin of the fluid as dialysate [19]. However, the need for thoracentesis in the patient with no respiratory complaints is not absolute. If thoracentesis is not performed, then a follow-up chest roentgenogram should be performed to document resolution of the hydrothorax. Because the diaphragmatic defects may act as a one-way valve [5], the hydrothorax may persist after the drainage of all fluid from the abdomen. In this situation, thoracentesis should be performed.
The long-term management of patients after a first episode of acute hydrothorax is controversial. When the complication was first described [7], the occurrence of hydrothorax was considered a contraindication to continuing peritoneal dialysis, as it was felt that hydrothorax would recur. However, subsequent reports have successfully managed the technique by temporary discontinuation of peritoneal dialysis [15, 21, 28], reducing dialysate volumes with dialysis performed in the semirecumbent position [17, 21, 29], chemical pleurodesis [19, 21, 30], as well as direct surgical repair of diaphragmatic defects [26, 2931].
Intrathoracic hernia
Another common complication of peritoneal dialysis is hernia formation [15, 22, 32]. Although the majority of these hernias are abdominal in nature [32], there are several types of hernia involving the thoracic cavity. The first of these is a Morgagni hernia. This hernia appears to occur uncommonly in the peritoneal dialysis population, although Ramos and associates [33] reported the case of a 66-year-old woman who presented with peritonitis and was found to have an ischemic segment of colon incarcerated within a right foramen of Morgagni. Likewise, strangulation and perforation of the transverse colon through the foramen of Bochdalek has been reported as well [34]. These cases may present a diagnostic dilemma because of the difficulty in distinguishing surgical causes of peritonitis from catheter-related causes, which generally respond to conservative therapy with antibiotics. Clinical features that suggest a surgical etiology include [34, 35]: localized abdominal pain, marked tenderness and rigidity, poor general condition, progressive increase in intraperitoneal free air, food-fiber residue in dialysate, and medically refractory peritonitis. In addition, peritoneal fluid cultures growing gram-negative or multiple organisms also favor an intestinal source [2, 32, 33, 35, 36]. A standard postero-anterior and lateral chest radiograph should reveal an air-fluid level above the diaphragm, thus suggesting the diagnosis [33]. CT scanning may be useful as well to make the diagnosis and rule out other intraabdominal pathology [35].
The third type of hernia involving the thoracic cavity and potentially complicating peritoneal dialysis is paraesophageal hernia, as in the case presented. As mentioned, we were unable to find another case in the literature, and consequently we assume this to be a rare complication of PD. However, the diagnosis should be considered in any patient on peritoneal dialysis presenting with a mediastinal mass. Because of the risk of bowel incarceration and strangulation within the hernia sac, the mere presence of this lesion is an indication for surgical intervention [37].
Distal esophageal rupture
A final rare thoracic complication of PD is distal esophageal perforation. Level and colleagues [38] recently reported a case of spontaneous esophageal rupture in a CAPD patient with chronic renal failure secondary to scleroderma. They hypothesized that the combination of esophageal dyskinesia from scleroderma, increased intraabdominal pressure from the peritoneal dialysate, and vomiting secondary to uremia led to Boerhaaves syndrome.
Perioperative complications
Patients on dialysis therapy for end-stage renal disease undergo operative procedures at a rate exceeding that of the remainder of the population. In addition, perioperative complication rates in these patients are exceedingly high, occurring in up to two-thirds of patients [3941]. Because cardiothoracic surgeons perform a proportion of these procedures, a brief review of these complications is in order. Hyperkalemia is the most commonly occurring postoperative complication, seen in approximately 20%30% of patients [39, 41]. Along with cardiac arrhythmias and respiratory failure, these complications occur most frequently in the early postoperative period. Fluid overload and hemodynamic instability are usually manifest in the first postoperative day. Other commonly occurring complications including sepsis, pneumonia, hemorrhage, and wound complications are seen later in the postoperative period [39]. The most common causes of perioperative death in these patients are hyperkalemia, sepsis, and bleeding [41]. Overall, surgery in uremic patients on PD can be performed with acceptable rates of morbidity and mortality as long as potential complications are anticipated and preventive measures taken [41].
In summary, patients on peritoneal dialysis are susceptible to multiple complications of their therapy, many of which involve the thoracic cavity. Of greatest interest to cardiothoracic surgeons are acute, massive hydrothorax, diaphragmatic hernias, and esophageal perforation, all of which may require surgical intervention. In addition, peritoneal dialysis patients undergoing surgery are more likely to have perioperative complications, and a knowledge of these potential pitfalls is essential.
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